FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Hirota, M
Watanabe, K
Hamada, S
Sun, YP
Strizzi, L
Mancino, M
Nagaoka, T
Gonzales, M
Seno, M
Bianco, C
Salomon, DS
AF Hirota, Morihisa
Watanabe, Kazuhide
Hamada, Shin
Sun, Youping
Strizzi, Luigi
Mancino, Mario
Nagaoka, Tadahiro
Gonzales, Monica
Seno, Masaharu
Bianco, Caterina
Salomon, David S.
TI Smad2 functions as a co-activator of canonical Wnt/beta-catenin
signaling pathway independent of Smad4 through histone acetyltransferase
activity of p300
SO CELLULAR SIGNALLING
LA English
DT Article
DE activin; beta-catenin; smads; Tcf/Lef; TGF-beta; Wnt
ID TUMOR-SUPPRESSOR SMAD4/DPC4; GROWTH-FACTOR-BETA; TGF-BETA;
BREAST-CANCER; WNT PATHWAY; TRANSCRIPTIONAL ACTIVATION; INTESTINAL
TUMORIGENESIS; COLORECTAL-CANCER; CELLULAR INVASION; IN-VIVO
AB Both canonical Wnt/beta-catenin and TGF beta/Smad signaling pathways coordinately regulate pattern formation during embryogenesis as well as tumor progression. Evidence of cross-talk between these two pathways has been reported. Here we demonstrated that the Activin-like kinase 4 (Alk4)/Smad2 pathway facilitates the transcriptional activity of the oncogenic Wnt/beta-catenin/Tcf4 pathway through a novel Smad4-independent mechanism. Upon activation, Smad2 physically interacted with Tcf4, beta-catenin and the co-activator p300 to enhance transcriptional activity of beta-catenin/Tcf4 through the histone acetyltransferase activity of p300. Transactivation by Smad2 was independent of a Smad-binding element (SBE) and Smad4. Indeed, the enhancement of beta-catenin/Tcf4 transcriptional activity by activated Smad2 was negatively regulated by the presence of Smad4. Moreover, a tumor-derived missense mutant of Smad2, lacking the ability to bind to Smad4 was still able to enhance the Tcf4 transcriptional reporter in the presence of p-catenin and Tcf4. Our findings suggest that Smad2 may function as an activator of canonical Wnt/beta-catenin/Tcf4 signaling through a SBE/Smad4-independent pathway. Published by Elsevier Inc.
C1 [Hirota, Morihisa; Watanabe, Kazuhide; Hamada, Shin; Sun, Youping; Strizzi, Luigi; Mancino, Mario; Nagaoka, Tadahiro; Gonzales, Monica; Bianco, Caterina; Salomon, David S.] NCI, Tumor Growth Factor Sect, Mammary Biol & Tumorigenesis Lab, Canc Res Ctr,Natl Inst Hlth, Bethesda, MD 20892 USA.
[Hirota, Morihisa; Watanabe, Kazuhide] Tohoku Univ, Div Gastroenterol, Sendai, Miyagi 9810933, Japan.
[Strizzi, Luigi] Northwestern Univ, Feinberg Sch Med, Childrens Mem Res Ctr, Robert H Lurie Canc Ctr, Chicago, IL 60611 USA.
[Seno, Masaharu] Okayama Univ, Lab Nanobiotechnol, Dept Med & Bioengn Sci, Okayama, Japan.
[Sun, Youping] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
[Mancino, Mario] Oncol Res Ctr, Mercogliano, AV, Italy.
RP Watanabe, K (reprint author), Bldg 37,Rm 1112,37 Convent Dr, Bethesda, MD 20892 USA.
EM watanabek@mail.nih.gov
RI SENO, Masaharu /B-2092-2011;
OI SENO, Masaharu /0000-0001-8547-6259; Nagaoka,
Tadahiro/0000-0002-9391-0243
FU Intramural NIH HHS [Z01 BC009003-25]
NR 54
TC 28
Z9 29
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0898-6568
J9 CELL SIGNAL
JI Cell. Signal.
PD SEP
PY 2008
VL 20
IS 9
BP 1632
EP 1641
DI 10.1016/j.cellsig.2008.05.003
PG 10
WC Cell Biology
SC Cell Biology
GA 336MQ
UT WOS:000258368400006
PM 18595660
ER
PT J
AU Botello-Harbaum, M
Nansel, T
Haynie, DL
Iannotti, RJ
Simons-Morton, B
AF Botello-Harbaum, M.
Nansel, T.
Haynie, D. L.
Iannotti, R. J.
Simons-Morton, B.
TI Responsive parenting is associated with improved type 1 diabetes-related
quality of life
SO CHILD CARE HEALTH AND DEVELOPMENT
LA English
DT Review
DE parenting style; quality of life; responsiveness; type 1 diabetes
ID METABOLIC-CONTROL; SELF-CARE; ADOLESCENTS; STYLES; CHILDREN;
INVOLVEMENT; ADHERENCE; COMPETENCE; ADJUSTMENT; MANAGEMENT
AB Background Improved quality of life is an important treatment goal for children and adolescents with type 1 diabetes. While previous research supports a relationship between family environment and quality of life, little research has addressed the relationship of parenting style constructs to quality of life in children with chronic disease. The present investigation assesses the relationship of parent responsiveness and demandingness with diabetes-related quality of life among children and adolescents with type 1 diabetes.
Methods Baseline and 12-month follow-up self-report assessments were collected on a sample of 81 children with type 1 diabetes participating in an efficacy trial of a behavioural intervention to enhance adherence. The sample had a mean age of 13.3 years (SD = 1.7) and duration of diabetes of 7.7 years (SD = 3.7). Multiple regression analyses were conducted to determine the relationship of parent responsiveness and demandingness to diabetes-related quality of life at each time point.
Results After adjusting for demographic and diabetes characteristics, as well as diabetes-specific parent-child behaviours, parent responsiveness was significantly associated with baseline diabetes-related quality of life (beta = 0.23; P = 0.04). This relationship was sustained at 12-month follow-up (beta = 0.22; P = 0.04) after adjusting for baseline quality of life and treatment group assignment, suggesting that parent responsiveness is associated with improved quality of life.
Conclusions Findings indicate the importance of a supportive and emotionally warm parenting style in promoting improved quality of life for children with type 1 diabetes. Appropriate parenting skills should be an element of diabetes family management health care.
C1 [Botello-Harbaum, M.; Nansel, T.; Haynie, D. L.; Iannotti, R. J.; Simons-Morton, B.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol & Stat, Prevent Res Branch, Bethesda, MD USA.
RP Nansel, T (reprint author), NICHD, Prevent Res Branch, DESPR, NIH, MSC 7510,6100 Execut Blvd, Bethesda, MD 20852 USA.
EM nanselt@mail.nih.gov
OI Nansel, Tonja/0000-0002-8298-7595; Simons-Morton,
Bruce/0000-0003-1099-6617; Haynie, Denise/0000-0002-8270-6079
FU Intramural NIH HHS [Z01 HD008741-06, Z99 HD999999]
NR 43
TC 17
Z9 18
U1 3
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0305-1862
J9 CHILD CARE HLTH DEV
JI Child Care Health Dev.
PD SEP
PY 2008
VL 34
IS 5
BP 675
EP 681
DI 10.1111/j.1365-2214.2008.00855.x
PG 7
WC Psychology, Developmental; Pediatrics
SC Psychology; Pediatrics
GA 335GS
UT WOS:000258279400018
PM 18796059
ER
PT J
AU Wainer, IW
AF Wainer, Irving W.
TI Investigation of molecular recognition in biological systems using
cellular membrane affinity chromatography
SO CHIMICA OGGI-CHEMISTRY TODAY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTOR; CATION TRANSPORTER HOCT1; CHIRAL
STATIONARY-PHASE; NONCOMPETITIVE INHIBITORS; IDENTIFICATION; DOCKING;
BINDING; COLUMN
AB Cellular membrane affinity chromatography (CMAC) columns have been created through the immobilization of cellular membrane fragments on liquid chromatographic supports. A CMAC column containing the human organic cation transporter, CMAC(hOCT1) column, has been used to study the stereoselective binding of competitive inhibitors. The chromatographic data obtained using the CMAC( hOCT1) column was to develop a pharmacophore model that described the stereoselectivity. The results indicate that a dynamic chiral recognition model based upon conformational adjustments between the inhibitors and hOCT1 is responsible for the observed steroeselectivity.
C1 NIA, NIH, Gerontol Res Ctr, Baltimore, MD 21224 USA.
RP Wainer, IW (reprint author), NIA, NIH, Gerontol Res Ctr, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
FU National Institute on Aging Intramural Research Program
FX This work was supported by funding from the National Institute on Aging
Intramural Research Program.
NR 22
TC 2
Z9 2
U1 0
U2 1
PU TEKNOSCIENZE PUBL
PI MILANO
PA VIALE BRIANZA 22, 20127 MILANO, ITALY
SN 1973-8250
J9 CHIM OGGI
JI Chim. Oggi-Chem. Today
PD SEP-OCT
PY 2008
VL 26
IS 5
SU 1
BP 19
EP 22
PG 3
WC Biotechnology & Applied Microbiology; Chemistry, Multidisciplinary
SC Biotechnology & Applied Microbiology; Chemistry
GA 356XS
UT WOS:000259811500007
PM 19430544
ER
PT J
AU Marraccini, P
Brass, DM
Hollingsworth, JW
Maruoka, S
Garantziotis, S
Schwartz, DA
AF Marraccini, P.
Brass, D. M.
Hollingsworth, J. W.
Maruoka, S.
Garantziotis, S.
Schwartz, D. A.
TI Bakery flour dust exposure causes non-allergic inflammation and enhances
allergic airway inflammation in mice
SO CLINICAL AND EXPERIMENTAL ALLERGY
LA English
DT Article
DE allergic asthma; baker's asthma; endotoxin; flour dust; LPS;
occupational airways disease; toll-like receptor 4
ID WHEAT-FLOUR; ASTHMA; SENSITIZATION; WORKERS; PREVENTION; SYMPTOMS;
DISEASE
AB Background Baker's asthma is one of the most commonly reported occupational lung diseases in countries where fresh bread is baked daily in large quantities, and is characterized by rhinitis, bronchial hyperresponsiveness, and reversible airflow obstruction. Epidemiological studies have identified pre-existing atopy as an important risk factor for developing baker's asthma, yet the aetiology and pathogenesis of baker's asthma remain poorly understood.
Objective We sought to develop a mouse model of baker's asthma that could be used to characterize the development and progression of baker's asthma.
Methods We were unable to sensitize mice to bakery flour dust or flour dust extract. We assessed total inflammatory cells, cellular differential, total serum IgE and the pro-inflammatory cytokine response to oropharyngeally instilled bakery flour dust or flour dust extract by itself or in the context of ovalbumin (OVA) sensitization and challenge.
Results Both bakery flour dust and flour dust extract consistently elicited a neutrophilic inflammation in a Toll-like receptor 4-independent manner; suggesting that endotoxin is not playing a role in the inflammatory response to flour dust. Moreover, bakery flour dust and dust extract significantly enhance the inflammatory response in OVA-sensitized and challenged mice.
Conclusions Bakery flour dust and flour dust extract are strongly pro-inflammatory and can cause non-allergic airway inflammation and can enhance allergen-mediated airway inflammation.
C1 [Brass, D. M.; Maruoka, S.] Duke Univ, Med Ctr, Neonatal & Perinatal Res Inst, Dept Pediat,Neonatol Div, Durham, NC 27710 USA.
[Marraccini, P.] Fdn Maggiore Policlin Hosp Mangiagalli & Regina E, Prevent & Occupat Med Dept, Unit Environm & Occupat, Milan, Italy.
[Hollingsworth, J. W.] Duke Univ, Med Ctr, Div Pulm Allergy & Crit Care Med, Durham, NC 27710 USA.
[Schwartz, D. A.] Natl Inst Environm Hlth Sci, NHLBI, Lab Environm Lung Dis, Res Triangle Pk, NC USA.
RP Brass, DM (reprint author), Duke Univ, Med Ctr, Neonatal & Perinatal Res Inst, Dept Pediat,Neonatol Div, Box 3373, Durham, NC 27710 USA.
EM david.brass@duke.edu
RI Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
FU National Heart, Lung and Blood Institute [HL91335]; National Institute
of Environmental Health Sciences [ES11961]; National Institute of
Allergy and Infectious Diseases [AI058161]
FX Funding Support: This research was supported, in part, by the Intramural
Research Program of the National Heart, Lung and Blood Institute; the
National Institute of Environmental Health Sciences and by grants from
the National Institute of Environmental Health Sciences (ES11961); the
National Heart, Lung, and Blood Institute (HL91335) and the National
Institute of Allergy and Infectious Diseases (AI058161).
NR 29
TC 10
Z9 10
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0954-7894
J9 CLIN EXP ALLERGY
JI Clin. Exp. Allergy
PD SEP
PY 2008
VL 38
IS 9
BP 1526
EP 1535
DI 10.1111/j.1365-2222.2008.03038.x
PG 10
WC Allergy; Immunology
SC Allergy; Immunology
GA 341PS
UT WOS:000258727400015
PM 18564331
ER
PT J
AU Keller, JE
AF Keller, James E.
TI Characterization of new formalin-detoxified botulinum neurotoxin toxoids
SO CLINICAL AND VACCINE IMMUNOLOGY
LA English
DT Article
ID CLOSTRIDIUM-BOTULINUM; INTERNATIONAL STANDARDS; IMMUNOLOGICAL RESPONSE;
IMMUNE GLOBULIN; SEROTYPE-A; B TOXINS; VACCINE; FORMALDEHYDE;
ANTITOXINS; TOXICITY
AB Antigenicities of several formalin-detoxified botulinum neurotoxin preparations were measured by inhibition and sandwich enzyme-linked immunosorbent assay (ELISA), and immunogenicity was studied in mice. The toxoids were derived primarily from the serotype A 150-kDa neurotoxin protein, while one toxoid was derived from the naturally occurring 900-kDa toxin-hemagglutinin complex. Antigenicity was severely compromised in two commercially available toxoids. A variety of new toxoids were synthesized in-house by optimizing formaldehyde reaction conditions. Three of the resulting toxoids were found to be antigenically identical to the native toxin, as measured by inhibition ELISA, in spite of showing a reduction of toxicity by more than 100,000-fold. Sandwich ELISAs indicated that the in-house toxoids were two-to threefold less antigenic than the neurotoxin compared to commercial toxoids, which were about 100-fold less antigenic. Mice were immunized twice, on day 0 and day 14. By day 28, relatively high toxin-specific immunoglobulin G (IgG) titers were detected in animals that had received any of the in-house toxoids, with greater than 99% being IgG1 and the remainder being IgG2. These immunized mice remained asymptomatic after being challenged with 50 to 1,000,000 50% lethal dose (LD50) units of the 900-kDa neurotoxin. In contrast, animals immunized with several different batches of commercially available toxoids did not develop measurable toxin-specific antibody titers. However, these mice survived neurotoxin challenges with 2 LD50 units but died when challenged with 6 LD50 units. Neutralizing titers measured from pools of sera generated with the in-house toxoid preparations ranged from 2.5 to 5 U/ml. In terms of predicting immunogenicity, inhibition ELISAs comparing each formalin toxoid to the parent toxin provided good insight for screening the new toxoids as well as for estimating their relative in vivo potencies. Inhibition ELISA data indicate that those toxoids that most closely resemble the native toxin are highly immunogenic and protective. The superior quality of these new toxoids makes them useful tools for continued use in ELISA development and for antitoxin production.
C1 US FDA, Lab Resp & Special Pathogens, Div Bacterial Parasit & Allergen Prod, Off Vaccines Res & Review,Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA.
RP Keller, JE (reprint author), US FDA, Lab Resp & Special Pathogens, Div Bacterial Parasit & Allergen Prod, Off Vaccines Res & Review,Ctr Biol Evaluat & Res, HFM-434,Bldg 29,Room 122,29 Lincoln Dr,NIH Campus, Bethesda, MD 20892 USA.
EM james.keller@fda.hhs.gov
FU FDA/CBER; FDA/CBER-NIAID/NIH [Y1-AI-6153-01, 224-06-1322]
FX Much of the ELISA analysis was performed by Pravina Mattoo (FDA/CBER)
and Adaku Iwueze. Dan Li (FDA/CBER) assisted with determining mouse
neutralization titers. Christine Anderson (FDA/CBER) provided the
standard equine antitoxin, and Juan Arciniega (FDA/CBER) provided
valuable discussion and advice during the writing of this paper. D.
Sesardic (NIBSC, United Kingdom) and R. Jones (NIBSC, United Kingdom)
provided valued assistance to confirm some of the neutralizing titer
data. Michael Goodnough and Carl Malizio (Metabiologics, Inc.) provided
very helpful information on the preparation of the commercial toxoid and
subsequently performed confirmatory testing by immunizing mice with
botulinum toxoids and challenging with botulinum toxin.; This work was
supported by intramural FDA/CBER funding and by FDA/CBER-NIAID/NIH
interagency agreement no. Y1-AI-6153-01/no.224-06-1322.; The findings
and conclusions in this article have not been formally disseminated by
the Food and Drug Administration and should not be construed to
represent any agency determination or policy.
NR 36
TC 17
Z9 17
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1556-6811
J9 CLIN VACCINE IMMUNOL
JI Clin. Vaccine Immunol.
PD SEP
PY 2008
VL 15
IS 9
BP 1374
EP 1379
DI 10.1128/CVI.00117-08
PG 6
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 344UF
UT WOS:000258952100010
PM 18667637
ER
PT J
AU Chinnaiyan, P
Cerna, D
Burgan, WE
Beam, K
Williams, ES
Camphausen, K
Tofilon, PJ
AF Chinnaiyan, Prakash
Cerna, David
Burgan, William E.
Beam, Katie
Williams, Eli S.
Camphausen, Kevin
Tofilon, Philip J.
TI Postradiation sensitization of the histone deacetylase inhibitor
valproic acid
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HUMAN GLIOBLASTOMA CELLS; DNA-DAMAGE REPAIR; GAMMA-H2AX FOCI;
IONIZING-RADIATION; CHROMATIN DYNAMICS; PROTEIN 53BP1;
RADIOSENSITIZATION; CANCER; HDAC; P53
AB Purpose: Preclinical studies evaluating histone deacetylase (HDAC) inhibitor-induced radiosensitization have largely focused on the preirradiation setting based on the assumption that enhanced radiosensitivity was mediated by changes in gene expression. Our previous investigations identified maximal radiosensitization when cells were exposed to HDAC inhibitors in both the preradiation and postradiation setting. We now expand on these studies to determine whether postirradiation exposure alone affects radiosensitivity.
Experimental Design: The effects of the HDAC inhibitor valproic acid (VA) on postirradiation sensitivity in human glioma cell lines were evaluated using a clonogenic assay, exposing cells to VA up to 24 h after irradiation. DNA damage repair was evaluated using gamma H2AX and 53BP1 foci and cell cycle phase distribution was analyzed by flow cytometry. Western blot of acetylated gamma H2AX was done following histone extraction on AUT gels.
Results: VA enhanced radiosensitivity when delivered up to 24 h after irradiation. Cells accumulated in G(2)-M following irradiation, although they returned to baseline at 24 h, mitigating the role of cell cycle redistribution in postirradiation sensitization by VA. At 12 h after irradiation, significant gamma H2AX and 53BP1 foci dispersal was shown in the control, although cells exposed to VA after irradiation maintained foci expression. VA alone had no effect on the acetylation or phosphorylation of H2AX, although it did acetylate radiation-induced gamma H2AX.
Conclusions: These results indicate that VA enhances radiosensitivity at times up to 24 h after irradiation, which has direct clinical application.
C1 [Chinnaiyan, Prakash] H Lee Moffitt Canc Ctr & Res Inst, Div Radiat Oncol Neurooncol Expt Therapeut, Tampa, FL 33612 USA.
[Williams, Eli S.; Tofilon, Philip J.] H Lee Moffitt Canc Ctr & Res Inst, Drug Discovery Program, Tampa, FL 33612 USA.
[Camphausen, Kevin] NCI, Radiat Oncol Branch, Bethesda, MD 20892 USA.
[Cerna, David; Burgan, William E.; Beam, Katie] NCI, Mol Radiat Therapeut Branch, Bethesda, MD 20892 USA.
[Burgan, William E.; Beam, Katie] NCI, Sci Applicat Int Corp Frederick, Frederick, MD 21701 USA.
RP Chinnaiyan, P (reprint author), H Lee Moffitt Canc Ctr & Res Inst, Div Radiat Oncol Neurooncol Expt Therapeut, SRB3,12902 Magnolia Dr, Tampa, FL 33612 USA.
EM prakash.chinnaiyan@moffitt.org
FU Intramural NIH HHS [ZIA SC010373-10]
NR 31
TC 57
Z9 58
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD SEP 1
PY 2008
VL 14
IS 17
BP 5410
EP 5415
DI 10.1158/1078-0432.CCR-08-0643
PG 6
WC Oncology
SC Oncology
GA 347UG
UT WOS:000259166000013
PM 18765532
ER
PT J
AU Bilke, S
Chen, QR
Wei, JS
Khan, J
AF Bilke, Sven
Chen, Qing-Rong
Wei, Jun S.
Khan, Javed
TI Whole chromosome alterations predict survival in high-risk neuroblastoma
without MYCN amplification
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID PEDIATRIC-ONCOLOGY-GROUP; GENE-EXPRESSION; GENOMIC ALTERATIONS;
ARRAY-CGH; STRATIFICATION; PROGNOSIS; PROFILES; PATTERNS; TUMORS; STAGE
AB Purpose: Patients with stage IV neuroblastoma over the age of 500 days without MYCN amplification have a survival rate of < 30% and there are currently no reliable means of predicting which of these patients will survive or succumb to the disease. The goal of this study is to develop a DNA copy number-based prognostic profile for these patients.
Experimental Design: We have used comparative genomic hybridization to identify genome copy number changes that can predict outcome in patients with stage IV neuroblastoma without MYCN amplification.
Results: A strong correlation of patient survival with the presence of whole chromosome changes (WCC >= 2) was observed, even in the group of patients older than 500 days at time of diagnosis. This novel prognostic marker showed a significant dependence on the date of diagnosis; patients with WCC >= 2 diagnosed after 1998 had a significantly higher probability of survival compared with those diagnosed earlier. At the same time, no such time dependence was found among the samples with WCC < 2, suggesting that medical progress patients in recent years has particularly benefited those patients with a stage IV non - MYCN-amplified disease if WCC >= 2 were present.
Conclusions: In this pilot study, we present a novel prognostic marker for survival of high-risk neuroblastoma patients over the age of 500 days without MYCN amplification and diagnosed after 1998. Further validation study is required to establish this risk stratification for these patients.
C1 [Bilke, Sven; Khan, Javed] NCI, Canc Genet Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Bilke, Sven; Chen, Qing-Rong; Wei, Jun S.; Khan, Javed] NCI, Oncogenom Sect, Pediat Oncol Branch, Adv Technol Ctr, Gaithersburg, MD USA.
[Chen, Qing-Rong] NCI, Adv Biomed Comp Ctr, Sci Applicat Int Corp Frederick Inc, Frederick, MD 21701 USA.
RP Khan, J (reprint author), NCI, Canc Genet Branch, Ctr Canc Res, 8717 Grovemont Circle,Room 134E, Bethesda, MD 20892 USA.
EM khanjav@mail.nih.gov
RI Khan, Javed/P-9157-2014
OI Khan, Javed/0000-0002-5858-0488
FU Intramural NIH HHS [Z01 BC010592-03, Z99 CA999999]; NCI NIH HHS
[N01-CO-12400, N01CO12400]
NR 27
TC 6
Z9 6
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD SEP 1
PY 2008
VL 14
IS 17
BP 5540
EP 5547
DI 10.1158/1078-0432.CCR-07-4461
PG 8
WC Oncology
SC Oncology
GA 347UG
UT WOS:000259166000027
PM 18765546
ER
PT J
AU Smith, FO
Downey, SG
Klapper, JA
Yang, JC
Sherry, RM
Royal, RE
Kammula, US
Hughes, MS
Restifo, NP
Levy, CL
White, DE
Steinberg, SM
Rosenberg, SA
AF Smith, Franz O.
Downey, Stephanie G.
Klapper, Jacob A.
Yang, James C.
Sherry, Richard M.
Royal, Richard E.
Kammula, Uclai S.
Hughes, Marybeth S.
Restifo, Nicholas P.
Levy, Catherine L.
White, Donald E.
Steinberg, Seth M.
Rosenberg, Steven A.
TI Treatment of metastatic melanoma using interleukin-2 alone or in
conjunction with vaccines
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HIGH-DOSE INTERLEUKIN-2; RENAL-CELL-CANCER; GP100 MELANOMA; RECOMBINANT
INTERLEUKIN-2; BOLUS INTERLEUKIN-2; INTERFERON-ALPHA; T-LYMPHOCYTES;
ANTIGEN; IDENTIFICATION; GUIDELINES
AB Purpose: To identify prognostic factors associated with survival beyond 4 years and overall response in patients with metastatic melanoma treated with high-dose bolus i.v. interleukin-2 (IL-2) given either alone or in combination with a variety of melanoma vaccines.
Study Design: 684 consecutive patients with metastatic melanoma received high-dose bolus i.v. IL-2 either alone or in conjunction with a variety of melanoma vaccines. Treatments occurred between August 1, 1985 and January 1, 2006.
Results: The overall objective response rate was 13% for patients receiving IL-2 alone and 16% for patients who received IL-2 with vaccine. In patients treated with IL-2 alone (n = 305) and IL-2 with vaccine (n = 379), having an objective response was associated with survival beyond 4 years (P < 0.0001). No pretreatment factors could be identified that were strongly associated with increased rate of objective response or long-term survival in patients receiving IL-2 alone. In patients receiving IL-2 with vaccines, there were increased response rates in patients with s.c. or cutaneous disease only and lower response rates with visceral disease only. Patients who received the gp100: 209-217 (210 M) peptide plus IL-2 showed a strong trend to increased objective responses compared with IL-2 alone (22% versus 12.8%; P = 0.01) and also compared with patients who received a variety of vaccines that did not include this immunogenic peptide (13.8%; P = 0.009).
Conclusion: IL-2 can produce a modest response rate in patients with metastatic melanoma including patients with durable complete responses. S.c. or cutaneous disease only and vaccination with gp100:209-217(210M) peptide was associated with significant increase in response rates.
C1 [Smith, Franz O.; Downey, Stephanie G.; Klapper, Jacob A.; Yang, James C.; Sherry, Richard M.; Royal, Richard E.; Kammula, Uclai S.; Hughes, Marybeth S.; Restifo, Nicholas P.; Levy, Catherine L.; White, Donald E.; Rosenberg, Steven A.] NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Dept Biostat, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Data Management Sect, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Rosenberg, SA (reprint author), NCI, Surg Branch, Ctr Canc Res, NIH, Room 3-3940,10 Ctr Dr, Bethesda, MD 20892 USA.
EM franz_smith@nih.gov
RI Restifo, Nicholas/A-5713-2008;
OI Restifo, Nicholas P./0000-0003-4229-4580
FU Intramural NIH HHS [Z01 SC003811-33]
NR 28
TC 114
Z9 120
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD SEP 1
PY 2008
VL 14
IS 17
BP 5610
EP 5618
DI 10.1158/1078-0432.CCR-08-0116
PG 9
WC Oncology
SC Oncology
GA 347UG
UT WOS:000259166000036
PM 18765555
ER
PT J
AU Kurkjian, C
Murgo, AJ
Kummar, S
AF Kurkjian, Carla
Murgo, Anthony J.
Kummar, Shivaani
TI Treatment of recurrent metastatic colon cancer in the age of modern
adjuvant therapy
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE metastasis; oxaliplatin; platinum resistance; recurrence
ID ADVANCED COLORECTAL-CANCER; PHASE-III TRIAL; STAGE-II; OVARIAN-CANCER;
OXALIPLATIN RESISTANCE; CHEMOTHERAPY; FLUOROURACIL; LEUCOVORIN;
CISPLATIN; IRINOTECAN
AB The treatment of patients with metastatic colon cancer has evolved tremendously over the past 10 years, with improved overall survival (OS) rates as a result of the advent of several important agents. Following the results of important adjuvant trials, the incorporation of oxaliplatin into the adjuvant setting has significantly increased the disease-free survival and OS rates in patients who undergo curative resection. However, still a significant number of patients will present with recurrent disease after being treated with oxaliplatin-containing chemotherapy regimens. Herein, we present approaches to the chemotherapeutic management of such patients with a review of the literature.
C1 [Murgo, Anthony J.; Kummar, Shivaani] NCI, Med Oncol Branch, Clin Res Ctr, Bethesda, MD 20892 USA.
[Kurkjian, Carla; Murgo, Anthony J.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Kummar, S (reprint author), NCI, Med Oncol Branch, Clin Res Ctr, 10 Ctr Dr,10-12N226, Bethesda, MD 20892 USA.
EM kummars@mail.nih.gov
NR 31
TC 4
Z9 4
U1 0
U2 0
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD SEP
PY 2008
VL 7
IS 5
BP 321
EP 324
DI 10.3816/CCC.2008.n.042
PG 4
WC Oncology
SC Oncology
GA 348UJ
UT WOS:000259235300005
PM 18794064
ER
PT J
AU Tadjine, M
Lampron, A
Ouadi, L
Horvath, A
Stratakis, CA
Bourdeau, I
AF Tadjine, Mimi
Lampron, Antoine
Ouadi, Lydia
Horvath, Anelia
Stratakis, Constantine A.
Bourdeau, Isabelle
TI Detection of somatic beta-catenin mutations in primary pigmented nodular
adrenocortical disease (PPNAD)
SO CLINICAL ENDOCRINOLOGY
LA English
DT Article
ID MACRONODULAR ADRENAL-HYPERPLASIA; WNT SIGNALING PATHWAY; CARNEY COMPLEX;
GENE; FREQUENT; CANCER; HETEROGENEITY; ADENOMAS; PDE11A; TUMORS
AB Background Primary pigmented nodular adrenocortical disease (PPNAD) leads to Cushing syndrome (CS) and is often associated with Carney complex (CNC). Genetic alterations of the type 1-alpha regulatory subunit of cAMP-dependent protein kinase A (PRKAR1A) and phosphodiesterase 11A4 (PDE11A) genes have been found in PPNAD. Recent studies have demonstrated that beta-catenin mutations are frequent in adrenocortical adenomas and carcinomas and that the Wnt-signalling pathway is involved in PPNAD tumorigenesis. We hypothesized that adrenocortical adenomas that form in the context of PPNAD may harbour beta-catenin mutations.
Methods We studied 18 patients with CS secondary to PPNAD who were screened for germline PRKAR1A and PDE11A mutations. Tumor DNA was extracted from pigmented adrenocortical adenoma and nodular adrenal hyperplasia. Mutation analysis of exons 3 and 5 of beta-catenin was performed using polymerase chain reaction and direct sequencing. Sections from formalin-fixed, paraffin-embedded tumour samples were studied by immunohistochemistry with an antibody against beta-catenin.
Results Nine patients were carrying germline PRKAR1A mutations and one patient had a PDE11A mutation. We found somatic beta-catenin mutations in 2 of 18 patients (11%). In both cases, the mutations occurred in relatively large adenomas that had formed in the background of PPNAD. Tumor DNA analysis revealed a heterozygous ACC-to-GCC missense mutation in codon 41 (T41A) and a TCT-to-CCT missense mutation in codon 45 (S45P) of exon 3 of the beta-catenin gene that was confirmed at the cDNA level. There were no alterations in the DNA of PPNAD-adjacent tissues and lymphocytes from the patients, indicating somatic events. Immunohistochemistry showed nuclear accumulation of beta-catenin in more than 90% of cells in adenomatous tissue whereas no nuclear immunoreactivity was detected in adjacent PPNAD nodular cells. Nuclear translocation of beta-catenin protein in the PPNAD adenoma suggests activation of the Wnt-beta-catenin pathway in PPNAD.
Conclusions We report, for the first time, beta-catenin mutations in adenomas associated with PPNAD, further implicating Wnt-beta-catenin signalling in tumorigenesis linked to bilateral adrenal hyperplasias.
C1 [Tadjine, Mimi; Lampron, Antoine; Ouadi, Lydia; Bourdeau, Isabelle] CHUM Hotel Dieu, Div Endocrinol, Dept Med, Res Ctr, Montreal, PQ H2W 1T7, Canada.
[Horvath, Anelia; Stratakis, Constantine A.] NICHD, Pediat Endocrinol Interinst Training Program, NIH, Bethesda, MD USA.
RP Bourdeau, I (reprint author), CHUM Hotel Dieu, Div Endocrinol, Dept Med, Res Ctr, 3850 St Urbain St, Montreal, PQ H2W 1T7, Canada.
EM isabelle.bourdeau@umontreal.ca
RI Levesque, Isabelle/A-1899-2012
FU Fonds de la Recherche en Sante du Quebec [FRSQ-6519/5360]; Cancer
Research Society; National Institute of Child Health of Human
Development (NICHD)
FX We are grateful to Dr Andre Lacroix, Centre hospitalier de l'Universite
de Montreal (CHUM), Montreal, Quebec, Canada, for providing
adrenocortical samples. We thank Dr Anne-Marie Mess-Masson and members
of her laboratory for their assistance in the immunohistochemical
studies as well as the MacDonald Stewart Foundation for photographic
support. The editing of our manuscript by Mr Ovid Da Silva, Research
Support Office, Research Centre, CHUM, is acknowledged. This study was
supported by Grant FRSQ-6519/5360 from Fonds de la Recherche en Sante du
Quebec (PI: Dr I. B.) and The Cancer Research Society ( PI: Dr I. B.),
and, in part, by the National Institute of Child Health of Human
Development (NICHD) intramural program (to Dr C. A. S.).
NR 25
TC 54
Z9 55
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0300-0664
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD SEP
PY 2008
VL 69
IS 3
BP 367
EP 373
DI 10.1111/j.1365-2265.2008.03273.x
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 337MW
UT WOS:000258441200003
PM 18419788
ER
PT J
AU Malik, M
Webb, J
Catherino, WH
AF Malik, Minnie
Webb, Joy
Catherino, William H.
TI Retinoic acid treatment of human leiomyoma cells transformed the cell
phenotype to one strongly resembling myometrial cells
SO CLINICAL ENDOCRINOLOGY
LA English
DT Article
ID SMOOTH-MUSCLE-CELLS; GROWTH-FACTOR-BETA; UTERINE LEIOMYOMAS;
EXTRACELLULAR-MATRIX; GENE-EXPRESSION; TGF-BETA; PROMYELOCYTIC LEUKEMIA;
TUMOR; PROLIFERATION; TGF-BETA-3
AB Background Uterine leiomyomas are clinically significant tumours that may develop due to an altered differentiation pathway. We have previously identified a dysregulated retinoic acid (RA) pathway that reduced retinoic exposure in human leiomyoma surgical specimens, and have shown that the leiomyoma phenotype was characterized by excessive and disorganized extracellular matrix (ECM).
Objective The goal of this study was to determine the impact of RA exposure on the disrupted ECM phenotype of leiomyomas.
Design and methods Study of immortalized and molecularly confirmed cells generated from surgical specimens of spontaneous uterine leiomyoma and matched myometrium.
Results Immortalized leiomyoma and myometrial cells retained the molecular characteristics of their progenitor tissue. Proliferation of leiomyoma cells was inhibited by all-trans retinoic acid (ATRA). Furthermore, there was a dose-dependent decrease in soluble extracellular collagen protein in ATRA-treated leiomyoma cells. Exposure of leiomyoma cells to ATRA resulted in a dose-dependent inhibition of templates for specific ECM protein production including collagen 1, collagen 4, fibronectin and versican. Notably, expression levels in treated leiomyoma cells approached those found in myometrial cells. These mRNA alterations translated into altered protein. Down-regulation was also observed among the RA pathway genes such as CYP26A1 with exposure to ATRA. Finally, ATRA down-regulated TGF-beta 3 mRNA expression and the TGF-beta regulated genes in leiomyoma cells.
Conclusion Exposure of leiomyomas to ATRA down-regulated cell proliferation, ECM formation, RA metabolism and TGF-beta regulation, suggesting that RA exposure can alter the leiomyoma phenotype to one that more closely approximates normal myometrium.
C1 [Malik, Minnie; Webb, Joy; Catherino, William H.] Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bethesda, MD 20814 USA.
[Catherino, William H.] NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA.
RP Catherino, WH (reprint author), Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bldg A, Room 3078,4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM wcatherino@usuhs.mil
OI Malik, Minnie/0000-0003-1129-6575
FU Intramural NIH HHS
NR 45
TC 35
Z9 36
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0300-0664
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD SEP
PY 2008
VL 69
IS 3
BP 462
EP 470
DI 10.1111/j.1365-2265.2008.03207.x
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 337MW
UT WOS:000258441200017
PM 18248652
ER
PT J
AU Takahashi, M
Furihata, M
Akimitsu, N
Watanabe, M
Kaul, S
Yumoto, N
Okada, T
AF Takahashi, Munehisa
Furihata, Mutsuo
Akimitsu, Nobuyoshi
Watanabe, Morihiro
Kaul, Sunil
Yumoto, Noboru
Okada, Tomoko
TI A highly bone marrow metastatic murine breast cancer model established
through in vivo selection exhibits enhanced anchorage-independent growth
and cell migration mediated by ICAM-1
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE breast cancer; metastasis; bone marrow; anchorage-independent growth;
migration; ICAM-1
ID COMPLEX CLASS-II; TUMOR-CELLS; EXPRESSION; IMMUNOTHERAPY; INVASIVENESS;
INHIBITION; INVASION; VITRO; CD43; SUBPOPULATIONS
AB To understand the mechanisms underlying bone marrow metastasis precisely, we established the highly metastatic 4T1E/M3 murine breast cancer cell line. 4T1 murine breast cancer cells were transfected with the neomycin resistance gene, selected in G418, intravenously injected into mice, and harvested from bone marrow. By repeating this protocol three times, we established the 4T1E/M3 cells. The clonality of 4T1E/M3 cells was markedly high confirmed by genomic southern analysis using neo-gene probe. When tissues harvested from mice after intravenous injection of 4T1E/M3 cells were examined histologically, markedly enhanced bone marrow metastasis was observed; 77% of spines from 4T1E/M3-injected mouse showed metastasis as compared to 14% metastasis seen with the parent cells. In vitro, 4T1E/M3 cells attached more strongly to the plastic plate and to bone marrow-derived endothelial cells. DNA micro arrays, real time RT-PCR and FACS analyses revealed that the expression of ICAM-1 and beta 2 integrin was upregulated in 4T1E/M3 cells at both the mRNA and cell surface protein levels. 4T1E/M3 cells also showed greater anchorage-independent proliferation in soft agar, and migrated markedly faster than the parent cells in wound healing assays. Anti-ICAM-1 antibodies strongly inhibited both the colony formation and the migration activity of 4T1E/M3 suggesting the importance of the role of ICAM-1. Our newly established highly metastatic 4T1E/M3 cells may provide a potentially powerful tool to study the molecular mechanisms of bone marrow metastasis and to identify new molecular targets for therapeutic interventions.
C1 [Takahashi, Munehisa; Akimitsu, Nobuyoshi; Okada, Tomoko] Natl Inst Adv Ind Sci & Technol, Inst Biol Resources & Funct, Tsukuba, Ibaraki 3058566, Japan.
[Furihata, Mutsuo] Kochi Med Sch, Dept Pathol, Nanko Ku, Kochi 7838505, Japan.
[Watanabe, Morihiro] NCI, Expt Immunol Lab, Ft Detrick, MD 21702 USA.
[Kaul, Sunil] Natl Inst Adv Ind Sci & Technol, Res Inst Cell Engn, Tsukuba, Ibaraki 3058562, Japan.
[Yumoto, Noboru] Natl Inst Adv Ind Sci & Technol, Tsukuba, Ibaraki 3058568, Japan.
RP Okada, T (reprint author), Natl Inst Adv Ind Sci & Technol, Inst Biol Resources & Funct, 1-1-1 Higashi, Tsukuba, Ibaraki 3058566, Japan.
EM t.okada@aist.go.jp
NR 45
TC 30
Z9 30
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD SEP
PY 2008
VL 25
IS 5
BP 517
EP 529
DI 10.1007/s10585-008-9163-5
PG 13
WC Oncology
SC Oncology
GA 327HE
UT WOS:000257719400003
PM 18340424
ER
PT J
AU Fleisher, TA
Notarangelo, LD
AF Fleisher, Thomas A.
Notarangelo, Luigi D.
TI What does it take to call it a pathogenic mutation?
SO CLINICAL IMMUNOLOGY
LA English
DT Editorial Material
ID X-LINKED AGAMMAGLOBULINEMIA; IDENTIFICATION; PHENOTYPE; BTK
C1 [Fleisher, Thomas A.] NIH, Ctr Clin, Dept Lab Med, Bethesda, MD 20892 USA.
[Notarangelo, Luigi D.] Childrens Hosp, Div Immunol, Boston, MA 02115 USA.
RP Fleisher, TA (reprint author), NIH, Ctr Clin, Dept Lab Med, Bethesda, MD 20892 USA.
EM tfleishe@mail.nih.gov
RI Notarangelo, Luigi/F-9718-2016
OI Notarangelo, Luigi/0000-0002-8335-0262
NR 12
TC 7
Z9 7
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD SEP
PY 2008
VL 128
IS 3
BP 285
EP 286
DI 10.1016/j.clim.2008.04.013
PG 2
WC Immunology
SC Immunology
GA 341SB
UT WOS:000258734100001
PM 18617443
ER
PT J
AU Segal, BH
Herbrecht, R
Stevens, DA
Ostrosky-Zeichner, L
Sobel, J
Viscoli, C
Walsh, TJ
Maertens, J
Patterson, TF
Perfect, JR
Dupont, B
Wingard, JR
Calandra, T
Kauffman, CA
Graybill, JR
Baden, LR
Pappas, PG
Bennett, JE
Kontoyiannis, DP
Cordonnier, C
Viviani, MA
Bille, J
Almyroudis, NG
Wheat, LJ
Graninger, W
Bow, EJ
Holland, SM
Kullberg, BJ
Dismukes, WE
De Pauw, BE
AF Segal, Brahm H.
Herbrecht, Raoul
Stevens, David A.
Ostrosky-Zeichner, Luis
Sobel, Jack
Viscoli, Claudio
Walsh, Thomas J.
Maertens, Johan
Patterson, Thomas F.
Perfect, John R.
Dupont, Bertrand
Wingard, John R.
Calandra, Thierry
Kauffman, Carol A.
Graybill, John R.
Baden, Lindsey R.
Pappas, Peter G.
Bennett, John E.
Kontoyiannis, Dimitrios P.
Cordonnier, Catherine
Viviani, Maria Anna
Bille, Jacques
Almyroudis, Nikolaos G.
Wheat, L. Joseph
Graninger, Wolfgang
Bow, Eric J.
Holland, Steven M.
Kullberg, Bart-Jan
Dismukes, William E.
De Pauw, Ben E.
TI Defining responses to therapy and study outcomes in clinical trials of
invasive fungal diseases: Mycoses study group and European Organization
for Research and Treatment of Cancer consensus criteria
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Editorial Material
ID RECONSTITUTION INFLAMMATORY SYNDROME;
ACQUIRED-IMMUNODEFICIENCY-SYNDROME; CELL TRANSPLANT RECIPIENTS;
BETA-D-GLUCAN; AMPHOTERICIN-B; PULMONARY ASPERGILLOSIS;
BACTERIAL-MENINGITIS; ANTIFUNGAL THERAPY; DISSEMINATED HISTOPLASMOSIS;
CRYPTOCOCCAL MENINGITIS
AB Invasive fungal diseases (IFDs) have become major causes of morbidity and mortality among highly immunocompromised patients. Authoritative consensus criteria to diagnose IFD have been useful in establishing eligibility criteria for antifungal trials. There is an important need for generation of consensus definitions of outcomes of IFD that will form a standard for evaluating treatment success and failure in clinical trials. Therefore, an expert international panel consisting of the Mycoses Study Group and the European Organization for Research and Treatment of Cancer was convened to propose guidelines for assessing treatment responses in clinical trials of IFDs and for defining study outcomes. Major fungal diseases that are discussed include invasive disease due to Candida species, Aspergillus species and other molds, Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis. We also discuss potential pitfalls in assessing outcome, such as conflicting clinical, radiological, and/or mycological data and gaps in knowledge.
C1 [Segal, Brahm H.; Almyroudis, Nikolaos G.] Roswell Pk Canc Inst, Dept Med, Buffalo, NY 14263 USA.
[Perfect, John R.] Duke Univ, Med Ctr, Durham, NC USA.
[Kontoyiannis, Dimitrios P.] Univ Texas MD Anderson Canc Ctr, San Antonio, TX USA.
[Ostrosky-Zeichner, Luis] Univ Texas Hlth Sci Ctr Houston, San Antonio, TX USA.
[Patterson, Thomas F.; Graybill, John R.] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, San Antonio, TX 78229 USA.
[Kauffman, Carol A.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Sobel, Jack] Wayne State Univ, Sch Med, Detroit, MI USA.
[Wingard, John R.] Univ Florida, Coll Med, Gainesville, FL USA.
[Stevens, David A.] Santa Clara Valley Med Ctr, San Jose, CA 95128 USA.
[Herbrecht, Raoul] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Pappas, Peter G.; Dismukes, William E.] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
[Walsh, Thomas J.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Bennett, John E.; Holland, Steven M.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Wheat, L. Joseph] MiraVista Diagnost MiraBella Technol, Indianapolis, IN USA.
[Baden, Lindsey R.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst,Div Infect Dis, Cambridge, MA 02138 USA.
[Bow, Eric J.] Univ Manitoba, Winnipeg, MB, Canada.
[De Pauw, Ben E.] Univ Med Ctr St Raboud, Nijmegen, Netherlands.
[Kullberg, Bart-Jan] Univ Nijmegen, Med Ctr, Dept Med, Nijmegen, Netherlands.
[Kullberg, Bart-Jan] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Bille, Jacques] Univ Lausanne Hosp, Inst Microbiol, Lausanne, Switzerland.
[Calandra, Thierry] CHU Vaudois, Dept Med, Infect Dis Serv, CH-1011 Lausanne, Switzerland.
[Calandra, Thierry] Univ Lausanne, Lausanne, Switzerland.
[Herbrecht, Raoul] Hosp Hautepierre, Dept Hematol & Oncol, Strasbourg, France.
[Dupont, Bertrand] Hop Necker Enfants Malad, Paris, France.
[Cordonnier, Catherine] Hop Henri Mondor, APHP, F-94010 Creteil, France.
[Cordonnier, Catherine] Univ Paris 12, Creteil, France.
[Graninger, Wolfgang] Med Univ Vienna, Vienna, Austria.
[Graninger, Wolfgang] Univ Hosp Vienna, Div Infect Dis, Vienna, Austria.
[Viviani, Maria Anna] Univ Milan, Dept Publ Hlth Microbiol & Virol, Sect Publ Hlth, Milan, Italy.
[Viscoli, Claudio] Univ Genoa, Genoa, Italy.
[Viscoli, Claudio] San Martino Univ Hosp, Div Infect Dis, Genoa, Italy.
[Maertens, Johan] Univ Hosp Gasthuisberg, Dept Hematol, Acute Leukemia & Hematopoiet Stem Cell Transplant, B-3000 Louvain, Belgium.
RP Segal, BH (reprint author), Roswell Pk Canc Inst, Dept Med, Elm & Carlton Sts, Buffalo, NY 14263 USA.
EM brahm.segal@roswellpark.org
RI Herbrecht, Raoul/D-3471-2013; Kullberg, Bart Jan/C-8520-2013; Calandra,
Thierry/D-9017-2015;
OI Calandra, Thierry/0000-0003-3051-1285; Herbrecht,
Raoul/0000-0002-9381-4876
FU Intramural NIH HHS [Z01 AI000654-16]
NR 78
TC 172
Z9 185
U1 1
U2 9
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
EI 1537-6591
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD SEP 1
PY 2008
VL 47
IS 5
BP 674
EP 683
DI 10.1086/590566
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 333VN
UT WOS:000258181000013
PM 18637757
ER
PT J
AU Xie, DW
Joffe, MM
Brunelli, SM
Beck, G
Chertow, GM
Fink, JC
Greene, T
Hsu, CY
Kusek, JW
Landis, R
Lash, J
Levey, AS
O'Conner, A
Ojo, A
Rahman, M
Townsend, RR
Wang, H
Feldman, HI
AF Xie, Dawei
Joffe, Marshall M.
Brunelli, Steven M.
Beck, Gerald
Chertow, Glenn M.
Fink, Jeffrey C.
Greene, Tom
Hsu, Chi-yuan
Kusek, John W.
Landis, Richard
Lash, James
Levey, Andrew S.
O'Conner, Andrew
Ojo, Akinlolu
Rahman, Mahboob
Townsend, Raymond R.
Wang, Hao
Feldman, Harold I.
TI A comparison of change in measured and estimated glomerular filtration
rate in patients with nondiabetic kidney disease
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID DIETARY-PROTEIN RESTRICTION; TYPE-2 DIABETIC-PATIENTS; RENAL-FUNCTION
DECLINE; SERUM CYSTATIN-C; PREDICTION EQUATIONS; AFRICAN-AMERICAN;
CREATININE; GFR; NEPHROPATHY; PROGRESSION
AB Background and objectives: All glomerular filtration rate (GFR) estimating equations have been developed from cross-sectional data. The aims of this study were to examine the concordance between use of measured GFR (mGFR) and estimated GFR (eGFR) in tracking changes in kidney function over time among patients with moderately severe chronic kidney disease.
Design, setting, participants, & measurements: A retrospective cohort study of subjects who had been enrolled in the MDRD Study A and who had two or more contemporaneous assessments of mGFR and eGFR (n = 542; mGFR range, 25 to 55 ml/min per 1.73 m(2)) during the chronic phase (month 4 and afterwards). mGFR was based on urinary iothalamate clearance; eGFR was based on the 4-variable MDRD Study equation. Temporal changes in GFR were assessed by within-subject linear regression of time on GFR.
Results: Median follow-up time for all subjects was 2.6 yr; median number of GFR measurements was six. The eGFR slope tended to underestimate measured decrements in GFR. The absolute value of the difference in mGFR and eGFR slopes was <= 2 ml/min per 1.73 m(2) per yr among 58.3% of subjects; the remainder of subjects had larger absolute differences. Among the 22 variables studied, none predicted a systematic difference between mGFR slope and eGFR slope.
Conclusions: Although eGFR and mGFR exhibited similar relationships to 22 baseline variables, the overall bias seen in the full cohort suggests that clinicians and researchers should exercise caution when interpreting eGFR slope as a marker of progression of kidney disease.
C1 [Xie, Dawei; Joffe, Marshall M.; Brunelli, Steven M.; Landis, Richard; Wang, Hao; Feldman, Harold I.] Univ Penn, Ctr Clin Epidemiol & Biostat, Sch Med, Philadelphia, PA 19104 USA.
[Brunelli, Steven M.; Townsend, Raymond R.; Feldman, Harold I.] Univ Penn, Dept Med, Sch Med, Philadelphia, PA 19104 USA.
[Beck, Gerald] Cleveland Clin Fdn, Dept Quantitat Hlth Sci, Cleveland, OH 44195 USA.
[Chertow, Glenn M.] Stanford Univ, Sch Med, Div Nephrol, Palo Alto, CA 94304 USA.
[Fink, Jeffrey C.] Univ Maryland, Sch Med, Div Nephrol, Baltimore, MD 21201 USA.
[Greene, Tom] Univ Utah, Sch Med, Div Clin Epidemiol, Salt Lake City, UT USA.
[Hsu, Chi-yuan] Univ Calif San Francisco, Sch Med, Div Nephrol, San Francisco, CA USA.
[Kusek, John W.] NIDDK, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD USA.
[Lash, James] Univ Illinois, Sch Med, Div Nephrol, Chicago, IL USA.
[Levey, Andrew S.] Tufts Univ, Sch Med, Div Nephrol, Boston, MA 02111 USA.
[O'Conner, Andrew] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Emergency Med, New Brunswick, NJ USA.
[Ojo, Akinlolu] Univ Michigan, Sch Med, Div Nephrol, Ann Arbor, MI USA.
[Rahman, Mahboob] Case Western Reserve Univ, Sch Med, Div Nephrol & Hypertens, Cleveland, OH USA.
RP Feldman, HI (reprint author), Univ Penn, Ctr Clin Epidemiol & Biostat, Sch Med, 923 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM hfeldman@mail.med.upenn.edu
RI Landis, J. Richard/A-9330-2010;
OI Fink, Jeffrey/0000-0002-5622-5052
FU NIDDK NIH HHS [R01 DK072231]
NR 24
TC 40
Z9 40
U1 0
U2 1
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD SEP
PY 2008
VL 3
IS 5
BP 1332
EP 1338
DI 10.2215/CJN.05631207
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 342AR
UT WOS:000258757500020
PM 18667734
ER
PT J
AU Xu, S
Kruecker, J
Turkbey, B
Glossop, N
Singh, AK
Choyke, P
Pinto, P
Wood, BJ
AF Xu, Sheng
Kruecker, Jochen
Turkbey, Baris
Glossop, Neil
Singh, Anurag K.
Choyke, Peter
Pinto, Peter
Wood, Bradford J.
TI Real-time MRI-TRUS fusion for guidance of targeted prostate biopsies
SO COMPUTER AIDED SURGERY
LA English
DT Article; Proceedings Paper
CT 10th International Conference on Medical Image Computing and
Computer-Assisted Intervention (MICCAI 2007)
CY OCT 29-NOV 02, 2007
CL Brisbane, AUSTRALIA
DE Motion compensation; prostate biopsy; tracking; image registration
ID ELASTIC REGISTRATION; ULTRASONOGRAPHY; IMAGES; SYSTEM
AB Targeted prostate biopsy is challenging because no currently established imaging modality is both accurate for prostate cancer diagnosis and cost-effective for real-time procedure guidance. A system that fuses real-time transrectal ultrasound images with previously acquired endorectal coil MRI images for prostate biopsy guidance is presented here. The system uses electromagnetic tracking and intraoperative image registration to superimpose the MRI data on the ultrasound image. Prostate motion is tracked and compensated for without the need for fiducial markers. The accuracy of the system in phantom studies was shown to be 2.4 +/- 1.2 mm. The fusion system has been used in more than 20 patients to guide biopsies with almost no modification of the conventional protocol. Retrospective clinical evaluation suggests that clinically acceptable spatial accuracy can be achieved.
C1 [Xu, Sheng; Kruecker, Jochen] Philips Res N Amer, Briarcliff Manor, NY USA.
[Glossop, Neil] Traxtal Inc, Toronto, ON, Canada.
RP Xu, S (reprint author), Philips Res N Amer, NIH, Clin Sites Res Program, Ctr Clin, Bldg 10,Room 1C-504X,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM sheng.xu@philips.com
FU Intramural NIH HHS [Z99 CL999999]
NR 17
TC 142
Z9 148
U1 4
U2 18
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1092-9088
J9 COMPUT AIDED SURG
JI Comput. Aided Surg.
PD SEP
PY 2008
VL 13
IS 5
SI SI
BP 255
EP 264
DI 10.1080/10929080802364645
PG 10
GA 372RD
UT WOS:000260918200003
PM 18821344
ER
PT J
AU Richesson, RL
Fung, KW
Krischer, JP
AF Richesson, Rachel L.
Fung, Kin Wah
Krischer, Jeffrey P.
TI Heterogeneous but "standard" coding systems for adverse events: Issues
in achieving interoperability between apples and oranges
SO CONTEMPORARY CLINICAL TRIALS
LA English
DT Article
DE biomedical research; adverse effects; informatics; forms and records
control; terminology; Systematized Nomenclature of Medicine
ID CLINICAL-RESEARCH; MEDDRA
AB Monitoring adverse events (AEs) is an important part of clinical research and a crucial target for data standards. The representation of adverse events themselves requires the use of controlled vocabularies with thousands of needed clinical concepts. Several data standards for adverse events currently exist, each with a strong user base. The structure and features of these current adverse event data standards (including terminologies and classifications) are different, so comparisons and evaluations are not straightforward, nor are strategies for their harmonization. Three different data standards - the Medical Dictionary for Regulatory Activities (MedDRA) and the Systematized Nomenclature of Medicine Clinical Terms (SNOMED CT) terminologies, and Common Terminology Criteria for Adverse Events (CTCAE) classification - are explored as candidate representations for AEs. This paper describes the structural features of each coding system, their content and relationship to the Unified Medical Language System (UMLS), and unsettled issues for future interoperability of these standards. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Richesson, Rachel L.; Krischer, Jeffrey P.] Univ S Florida, Coll Med, Dept Pediat, Tampa, FL 33612 USA.
[Fung, Kin Wah] Natl Lib Med, Bethesda, MD USA.
RP Richesson, RL (reprint author), Univ S Florida, Coll Med, Dept Pediat, 3650 Spectrum Blvd,Suite 100, Tampa, FL 33612 USA.
EM richesrl@epi.usf.edu
FU NCRR NIH HHS [U54 RR019259-02, U54 RR019259, RR019259]
NR 30
TC 8
Z9 8
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1551-7144
J9 CONTEMP CLIN TRIALS
JI Contemp. Clin. Trials
PD SEP
PY 2008
VL 29
IS 5
BP 635
EP 645
DI 10.1016/j.cct.2008.02.004
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 351KY
UT WOS:000259424400002
PM 18406213
ER
PT J
AU Beigel, JH
AF Beigel, John H.
TI Influenza
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE influenza; avian flu; pandemic; pneumonia; complications; treatment
ID COMMUNITY-ACQUIRED PNEUMONIA; A VIRUS-INFECTION; NEURAMINIDASE INHIBITOR
OSELTAMIVIR; RESISTANT STAPHYLOCOCCUS-AUREUS; RANDOMIZED
CONTROLLED-TRIAL; ACUTE RESPIRATORY SYNDROME; UNITED-STATES; ORAL
OSELTAMIVIR; IMMUNOCOMPROMISED PATIENTS; REQUIRING HOSPITALIZATION
AB Objective: Influenza is a major concern for intensivists in all communities in the U.S. While there is considerable concern whether or not the country will be ready for a pandemic influenza, even seasonal influenza poses a major challenge to hospitals. The objective of this review is to summarize current knowledge of influenza with emphasis on the issues that intensivist will encounter.
Setting: Intensive care unit in a 450-bed, tertiary care, teaching hospital.
Methods: Source data were obtained from a PubMed search of the medical literature. PubMed "related articles" search strategies were likewise employed frequently.
Summary and Conclusions: Seasonal influenza causes more than 200,000 hospitalizations and 41,000 deaths in the U.S. every year, and is the seventh leading cause of death in the U.S. Despite this impact there is a shortcoming in knowledge of influenza among many health care workers, and a paucity of clinical data and studies to guide therapy. Intensivists need to recognize the importance of seasonal influenza as a cause of severe morbidity and mortality. This review summarizes current knowledge of the diagnosis, complications, therapy, and infection control measures associated with influenza.
C1 NIAID, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Beigel, JH (reprint author), NIAID, Natl Inst Hlth, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jbeigel@niaid.nih.gov
RI Chiang, Vincent, Ming-Hsien/D-4312-2016
OI Chiang, Vincent, Ming-Hsien/0000-0002-2029-7863
FU Intramural Program of the NIH; National Allergy and Infectious Diseases
Institute and Critical Care Medicine Department, Clinical Center;
National Institutes of Health
FX This research was supported, in part, by the Intramural Program of the
NIH, National Allergy and Infectious Diseases Institute and Critical
Care Medicine Department, Clinical Center, National Institutes of
Health.
NR 88
TC 42
Z9 46
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD SEP
PY 2008
VL 36
IS 9
BP 2660
EP 2666
DI 10.1097/CCM.0b013e318180b039
PG 7
WC Critical Care Medicine
SC General & Internal Medicine
GA 345TV
UT WOS:000259020800024
PM 18679129
ER
PT J
AU Carson, JL
Reynolds, RC
Klein, HG
AF Carson, Jeffrey L.
Reynolds, Richard C.
Klein, Harvey G.
TI Bad bad blood?
SO CRITICAL CARE MEDICINE
LA English
DT Editorial Material
DE blood transfusion
ID TRANSFUSION; OUTCOMES; TRIAL
C1 [Carson, Jeffrey L.; Reynolds, Richard C.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Div Gen Internal Med, New Brunswick, NJ USA.
[Klein, Harvey G.] NIH, Ctr Clin, Dept Transfus Med, Bethesda, MD 20892 USA.
RP Carson, JL (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Div Gen Internal Med, New Brunswick, NJ USA.
NR 6
TC 13
Z9 13
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD SEP
PY 2008
VL 36
IS 9
BP 2707
EP 2708
DI 10.1097/CCM.0b013e3181843ee7
PG 2
WC Critical Care Medicine
SC General & Internal Medicine
GA 345TV
UT WOS:000259020800045
PM 18728495
ER
PT J
AU Shurin, SB
AF Shurin, Susan B.
TI The Genome-wide Association Studies Data Sharing Policy
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Editorial Material
C1 NHLBI, Bethesda, MD 20892 USA.
RP Shurin, SB (reprint author), NHLBI, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1752-8054
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD SEP
PY 2008
VL 1
IS 2
BP 91
EP 91
DI 10.1111/j.1752-8062.2008.00044.x
PG 1
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 532RT
UT WOS:000272767900007
PM 20443825
ER
PT J
AU Korman, BD
Kastner, DL
Gregersen, PK
Remmers, EF
AF Korman, Benjamin D.
Kastner, Daniel L.
Gregersen, Peter K.
Remmers, Elaine F.
TI STAT4: Genetics, mechanisms, and implications for autoimmunity
SO CURRENT ALLERGY AND ASTHMA REPORTS
LA English
DT Review
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; TYROSINE-PHOSPHATASE PTPN22; GENOME-WIDE
ASSOCIATION; RHEUMATOID-ARTHRITIS; RISK LOCUS; VARIANTS; ASTHMA;
RESPONSES; DISEASES; POLYMORPHISMS
AB Recent advances in genetics and technology have led to breakthroughs in understanding the genes that predispose individuals to autoimmune diseases. A common haplotype of the signal transducer and activator of transcription 4 (STAT4) gene has been shown to be associated with susceptibility to rheumatoid arthritis, systemic lupus erythematosus, and primary Sjogren's syndrome. STAT4 is a transcription factor that transduces interleukin-12, interleukin-23, and type I interferon cytokine signals in T cells and monocytes, leading to T-helper type I and T-helper type 17 differentiation, monocyte activation, and interferon-gamma production. Although the evidence for this association is very strong and well replicated, the exact mechanism by which polymorphisms in this gene lead to disease remains unknown. In concert with the identification of other disease-associated loci, elucidating how the variant form of STAT4 modulates immune function should lead to an improved understanding of the pathophysiology of autoimmunity.
C1 [Remmers, Elaine F.] NIAMSD, Bethesda, MD 20892 USA.
RP Remmers, EF (reprint author), NIAMSD, 9 Mem Dr,NIH Bldg,Room 1W108, Bethesda, MD 20892 USA.
EM remmerse@mail.nih.gov
FU National institutes of Health (NIH) [NO1-AR-2-2263, RO1 AR44422];
National Institute of Arthritis, Musculoskeletal, and Skin Diseases; NIH
Clinical Research Program
FX This work was supported by the National institutes of Health (NIH)
NO1-AR-2-2263 and RO1 AR44422 awards to Dr. Gregersen and by the
Intramural Program of the National Institute of Arthritis,
Musculoskeletal, and Skin Diseases. Dr. Korman was supported by the NIH
Clinical Research Program, a public private partnership between the
Foundation for the NIH and Pfizer.
NR 43
TC 81
Z9 84
U1 2
U2 18
PU CURRENT SCIENCE INC
PI PHILADELPHIA
PA 400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA
SN 1529-7322
J9 CURR ALLERGY ASTHM R
JI Curr. Allergy Asthma Rep.
PD SEP
PY 2008
VL 8
IS 5
BP 398
EP 403
DI 10.1007/s11882-008-0077-8
PG 6
WC Allergy; Immunology
SC Allergy; Immunology
GA 338ZI
UT WOS:000258547500005
PM 18682104
ER
PT J
AU Kakizaki, S
Yamazaki, Y
Takizawa, D
Negishi, M
AF Kakizaki, Satoru
Yamazaki, Yuichi
Takizawa, Daichi
Negishi, Masahiko
TI New insights on the xenobiotic-sensing nuclear receptors in liver
diseases - CAR and PXR-
SO CURRENT DRUG METABOLISM
LA English
DT Review
DE nuclear receptor; constitutive androstane receptor; pregnane X receptor;
liver disease
ID PREGNANE-X-RECEPTOR; CONSTITUTIVE ANDROSTANE RECEPTOR; THYROID-HORMONE
METABOLISM; RESISTANCE-ASSOCIATED PROTEIN-3; INFLAMMATORY-BOWEL-DISEASE;
PRIMARY BILIARY-CIRRHOSIS; DRUG-INDUCED OSTEOMALACIA; NF-KAPPA-B;
CROSS-TALK; RAT-LIVER
AB The xenobiotic receptors CAR and PXR constitute two important members of the NRII nuclear receptor family. They function as sensors of toxic byproducts derived from the endogenous metabolism and of exogenous chemicals, in order to enhance their elimination. They regulate numerous genes which are involved in drug and xenobiotic metabolism, including Phase I (cytochrome P450), Phase II (conjugation catalyzed by sulfotransferases, glucuronosyltransferases and glutathione S-transferases), and transporters ( multidrug resistance proteins, multidrug resistance-associated proteins, and organic anion-transporting polypeptides). Although CAR and PXR were initially characterized as xenosensors, it is now evident that CAR and PXR also trigger pleiotropic effects on physiological or pathological functions. Recent studies have shown that the activation of CAR and PXR alters lipid metabolism, glucose homeostasis, and inflammation. Therefore, in addition to regulating drug elimination pathways, they also play important roles in regulating metabolic pathways. As a result, these receptors may be closely associated with the pathogenesis of many diseases. However, the pathophysiological roles of CAR and PXR are not fully understood. The purpose of this review is to discuss the physiological and pathological roles of CAR and PXR in liver diseases.
C1 [Kakizaki, Satoru; Yamazaki, Yuichi; Takizawa, Daichi] Gunma Univ, Grad Sch Med, Dept Med & Mol Sci, Gunma 3718511, Japan.
[Negishi, Masahiko] Natl Inst Environm Hlth Sci, Pharmacogenet Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Kakizaki, S (reprint author), Gunma Univ, Grad Sch Med, Dept Med & Mol Sci, 3-39-15 Showa Machi, Gunma 3718511, Japan.
EM kakizaki@showa.gunma-u.ac.jp
NR 119
TC 60
Z9 62
U1 1
U2 6
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-2002
J9 CURR DRUG METAB
JI Curr. Drug Metab.
PD SEP
PY 2008
VL 9
IS 7
BP 614
EP 621
DI 10.2174/138920008785821666
PG 8
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 351TA
UT WOS:000259447600005
PM 18781913
ER
PT J
AU Foster, PS
Rosenberg, HF
Asquith, KL
Kumar, RK
AF Foster, Paul S.
Rosenberg, Helene F.
Asquith, Kelly L.
Kumar, Rakesh K.
TI Targeting eosinophils in asthma
SO CURRENT MOLECULAR MEDICINE
LA English
DT Review
DE asthma; eosinophils; antiviral defense; interleukin-5 receptor;
beta-common subunit
ID BONE-MARROW EOSINOPHILOPOIESIS; ALLERGIC AIRWAY INFLAMMATION;
RESPIRATORY SYNCYTIAL VIRUS; COLONY-STIMULATING FACTOR; PERSISTENT
ASTHMA; EPITHELIAL-CELLS; MOUSE MODEL; IN-VITRO; MONOCLONAL-ANTIBODY;
HUMAN INTERLEUKIN-5
AB Recruitment of eosinophils has long been recognized as a hallmark of the inflammatory response in asthma. However, the functions of this population of cells in host defense remain poorly understood. Eosinophils play an important part in the inflammatory response and have key regulatory roles in the afferent arm of the immune response. More recently, eosinophils have been demonstrated to participate in host defense against respiratory viruses. The specific contributions of eosinophils to the pathophysiology of asthma remain controversial. However, the balance of evidence indicates that they have a significant role in the disease, suggesting that they may be appropriate targets for therapy. Towards this end, a novel intervention of considerable potential interest is the use of an antibody directed against the common chain of the receptor for interleukin-3, interleukin-5 and granulocyte-macrophage colony-stimulating factor. However, eliminating eosinophils may not be a risk-free therapeutic strategy, as there is potentially an increased likelihood of respiratory viral infections. This may predispose to the development of acute exacerbations of asthma, an outcome that would have significant clinical implications.
C1 [Foster, Paul S.] Univ Newcastle, Ctr Asthma & Resp Dis, Fac Hlth, Discipline Immunol & Microbiol, Newcastle, NSW 2300, Australia.
[Foster, Paul S.] Australian Natl Univ, John Curtin Sch Med Res, Div Mol Biosci, Canberra, ACT 2601, Australia.
[Rosenberg, Helene F.] NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA.
[Kumar, Rakesh K.] Univ New S Wales, Sch Med Sci, Dept Pathol, Sydney, NSW, Australia.
RP Foster, PS (reprint author), Univ Newcastle, Ctr Asthma & Resp Dis, Fac Hlth, Discipline Immunol & Microbiol, 5th Floor David Maddison Clin Sci Bldg,Cnr Watt &, Newcastle, NSW 2300, Australia.
EM Paul.Foster@newcastle.edu.au
RI Kumar, Rakesh/J-6124-2012; Foster, Paul/G-5057-2013
OI Kumar, Rakesh/0000-0002-9531-8411;
FU Intramural NIH HHS [Z99 AI999999, ZIA AI000941-08, ZIA AI000943-08]
NR 90
TC 18
Z9 19
U1 2
U2 4
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1566-5240
J9 CURR MOL MED
JI Curr. Mol. Med.
PD SEP
PY 2008
VL 8
IS 6
BP 585
EP 590
DI 10.2174/156652408785748013
PG 6
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 351SQ
UT WOS:000259446600014
PM 18781965
ER
PT J
AU Kurkjian, C
Kummar, S
Murgo, AJ
AF Kurkjian, Carlo
Kummar, Shivaani
Murgo, Anthony J.
TI DNA Methylation: Its Role in Cancer Development and Therapy
SO CURRENT PROBLEMS IN CANCER
LA English
DT Review
ID ACUTE MYELOID-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; CPG ISLAND
METHYLATION; CHRONIC LYMPHOCYTIC-LEUKEMIA; ABERRANT PROMOTER
METHYLATION; ACUTE LYMPHOBLASTIC-LEUKEMIA; TUMOR-SUPPRESSOR GENES;
RENAL-CELL CARCINOMA; HELICOBACTER-PYLORI ERADICATION; LOW-DOSE
5-AZA-2'-DEOXYCYTIDINE
C1 [Kurkjian, Carlo] NCI, Div Canc Treatment & Diagnosis, Adv Dev Therapeut Training Program, Bethesda, MD USA.
[Kummar, Shivaani] Yale Univ, Ctr Canc, New Haven, CT USA.
[Kummar, Shivaani] NCI, Med Oncol Branch, Ctr Clin Res, Bethesda, MD USA.
[Kummar, Shivaani] Yale Univ, Dept Pharmacol, New Haven, CT 06520 USA.
[Murgo, Anthony J.] Uniformed Serv Univ Hlth Sci, Bethesda, MD USA.
[Murgo, Anthony J.] W Virginia Univ, Sch Med, Morgantown, WV 26506 USA.
[Murgo, Anthony J.] W Virginia Univ, Hematol Oncol Sect, Morgantown, WV 26506 USA.
[Murgo, Anthony J.] US FDA, Div Oncol Drug Prod, Rockville, MD 20857 USA.
RP Kurkjian, C (reprint author), NCI, Div Canc Treatment & Diagnosis, Adv Dev Therapeut Training Program, Bethesda, MD USA.
NR 256
TC 28
Z9 35
U1 0
U2 10
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0147-0272
EI 1535-6345
J9 CURR PROB CANCER
JI Curr. Probl. Cancer
PD SEP-OCT
PY 2008
VL 32
IS 5
BP 185
EP 235
DI 10.1016/j.currproblcancer.2008.08.002
PG 51
WC Oncology
SC Oncology
GA 360ZL
UT WOS:000260097200002
PM 18926281
ER
PT J
AU Longmire, M
Choyke, PL
Kobayashi, H
AF Longmire, Michelle
Choyke, Peter L.
Kobayashi, Hisataka
TI Dendrimer-based contrast agents for molecular imaging
SO CURRENT TOPICS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE dendrimer; contrast agent; molecular imaging; nanomedicine; magnetic
resonance imaging; optical imaging; radionuclide imaging; multiple
modalities
ID MAGNETIC-RESONANCE; IN-VIVO; MRI; CORES; MICE; GENERATION; CHEMISTRY;
DELIVERY
AB The extensive adaptability of dendrimer-based contrast agents is ideal for the molecular imaging of organs and other target-specific locations. The ability of literally atom-by-atom modification on cores, interiors, and surface groups, permits the rational manipulation of dendrimer-based agents in order to optimize their physical characteristics, biodistribution, receptor-mediated targeting, and controlled release of the payload. Such modifications enable agents to localize preferentially to areas or organs of interest for facilitating target-specific imaging as well as assume excretion pathways that do not interfere with desired applications. Recent innovations in dendrimer research have increased agent directibility and new synthetic chemistry approaches have increased efficiency of production as well as led to the creation of novel dendrimer-based contrast agents. In addition, by taking advantage of the numerous attachment sites available on the surface of a single dendrimer molecule, new synthetic chemistry techniques have led to the development of multi-modality magnetic resonance, radionuclide, and fluorescence imaging agents for molecular imaging. Herein we discuss advances in dendrimer-based contrast agents for molecular imaging focusing mainly on the chemical design as applied to optical, magnetic resonance, computer tomography, radionuclide, and multi-modality imaging.
C1 [Longmire, Michelle; Choyke, Peter L.; Kobayashi, Hisataka] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
RP Kobayashi, H (reprint author), NCI, Mol Imaging Program, NIH, Bldg 10,Room 1B40,MSC 1088, Bethesda, MD 20892 USA.
EM kobayash@mail.nih.gov
FU Intramural Research Program of the NIH; National Cancer Institute;
Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 27
TC 59
Z9 62
U1 0
U2 20
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1568-0266
J9 CURR TOP MED CHEM
JI Curr. Top. Med. Chem.
PD SEP
PY 2008
VL 8
IS 14
BP 1180
EP 1186
DI 10.2174/156802608785849021
PG 7
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 352MN
UT WOS:000259501400004
PM 18855704
ER
PT J
AU Trinchieri, G
AF Trinchieri, Giorgio
TI Role of pro-inflammatory cytokines in carcinogenesis
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Trinchieri, Giorgio] NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 231
EP 231
DI 10.1016/j.cyto.2008.07.020
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900003
ER
PT J
AU Thomas, E
Hu, ZY
Dong, S
Feld, JJ
Liang, TJ
AF Thomas, Emmanuel
Hu, Zongyi
Dong, Stephen
Feld, Jordan J.
Liang, T. Jake
TI A novel innate immune antiviral mechanism of action of ribavirin in
mammalian cells contributes to efficacy of combination therapy for
hepatitis C
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Thomas, Emmanuel; Hu, Zongyi; Dong, Stephen; Feld, Jordan J.; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 237
EP 237
DI 10.1016/j.cyto.2008.07.042
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900021
ER
PT J
AU Tsuno, T
Mejido, J
Zhao, TM
Morrow, A
Zoon, KC
AF Tsuno, Takaya
Mejido, Josef
Zhao, Tongmao
Morrow, Angel
Zoon, Kathryn C.
TI Roles of JAK-STAT pathway factors in antiproliferative activities of
human IFN-alpha and IFN-gamma: A comprehensive assessment in human
ovarian adenocarcinoma OVCAR3 cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Tsuno, Takaya; Mejido, Josef; Zhao, Tongmao; Morrow, Angel; Zoon, Kathryn C.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 237
EP 237
DI 10.1016/j.cyto.2008.07.043
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900022
ER
PT J
AU Bekisz, J
Mejido, J
Veenstra, T
Zoon, K
AF Bekisz, Joseph
Mejido, Josef
Veenstra, Timothy
Zoon, Kathryn
TI Gene and protein expression observed after treatment of Daudi cells with
IFN-alpha 2c and IFN-alpha 21 beta
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Bekisz, Joseph; Mejido, Josef; Zoon, Kathryn] NIAID, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Veenstra, Timothy] SAIC Frederick Inc, Natl Canc Inst, Frederick, MD 21702 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 240
EP 240
DI 10.1016/j.cyto.2008.07.055
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900034
ER
PT J
AU Morrow, AN
Schmeisser, H
Tsuno, T
Zoon, KC
AF Morrow, Anzel N.
Schmeisser, Hana
Tsuno, Takaya
Zoon, Kathryn C.
TI Induction of ISGF3 in response to interferon gamma in human cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Morrow, Anzel N.; Schmeisser, Hana; Tsuno, Takaya; Zoon, Kathryn C.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 240
EP 241
DI 10.1016/j.cyto.2008.07.058
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900037
ER
PT J
AU Schmeisser, H
Mejido, J
Zoon, KC
AF Schmeisser, Hana
Mejido, Josef
Zoon, Kathryn C.
TI Identification of IFN-alpha-induced genes and proteins that are
associated with antiviral activity in Daudi cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Schmeisser, Hana; Mejido, Josef; Zoon, Kathryn C.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 240
EP 240
DI 10.1016/j.cyto.2008.07.057
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900036
ER
PT J
AU Masters, SL
Aksentijevich, I
Ferguson, PJ
Booty, MG
Laurence, A
Pham, H
Stone, DL
Cowen, EW
Plass, N
Bing, XY
Clarke, GI
Ohson, K
Ei-Shanti, HI
van Royen, A
Frenk, J
AF Masters, Seth L.
Aksentijevich, Ivona
Ferguson, Polly J.
Booty, Matthew G.
Laurence, Arian
Pham, Hang
Stone, Deborah L.
Cowen, Edward W.
Plass, Nicole
Bing, Xinyu
Clarke, Gillian I.
Ohson, Kamal
Ei-Shanti, Hatem I.
van Royen, Annet
Frenk, Joost
TI Mutations in the interleulkin-1 receptor antagonist cause a new
autoinflammatory disease
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Masters, Seth L.; Aksentijevich, Ivona; Booty, Matthew G.] Genet & Genom Branch, Bethesda, MD USA.
[Pham, Hang; Stone, Deborah L.; Plass, Nicole] Off Clin Director, Bethesda, MD USA.
[Laurence, Arian] NIAMSD, Mol Immunol & Inflammat Branch, Bethesda, MD 20892 USA.
[Cowen, Edward W.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Ferguson, Polly J.; Bing, Xinyu; Ei-Shanti, Hatem I.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Ei-Shanti, Hatem I.] Shafallah Med Genet Ctr, Doha, Qatar.
[van Royen, Annet] Univ Med Ctr, Div Pediat, Dept Gen Pediat, Utrecht, Netherlands.
[Ohson, Kamal] Mem Univ Newfoundland, Dept Med, St John, NF A1C 5S7, Canada.
[Clarke, Gillian I.] Div Dermatol, St John, NF, Canada.
RI Laurence, Arian/A-8770-2009
OI Laurence, Arian/0000-0003-0942-8292
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 244
EP 245
DI 10.1016/j.cyto.2008.07.075
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900053
ER
PT J
AU Siegel, RM
Kahle, E
Acharya, K
Fuss, I
Wang, E
Meylan, F
AF Siegel, Richard M.
Kahle, Erin
Acharya, Krishika
Fuss, Ivan
Wang, Eddie
Meylan, Francoise
TI TL1A-DR3 interactions drive immunopathology mediated by multiple T-cell
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Siegel, Richard M.; Kahle, Erin; Acharya, Krishika; Meylan, Francoise] Ist Super Sanita, Dept Infect Parasit & Immune Mediated Dis, I-00161 Rome, Italy.
[Fuss, Ivan] NIAID, Mucosal Immun Sect, Host Def Lab, NIH, Bethesda, MD 20892 USA.
[Wang, Eddie] Cardiff Univ, Sch Med, Cardiff, Wales.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 246
EP 246
DI 10.1016/j.cyto.2008.07.082
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900060
ER
PT J
AU Schwartz, B
Anton, K
Koltchev, D
Skawinski, M
Clark, W
Lavoie, T
Izotova, LS
Lembo, D
Day, P
Pang, S
Schiller, JT
Pestka, S
AF Schwartz, Barbara
Anton, Kevin
Koltchev, Dolly
Skawinski, Michael
Clark, William
Lavoie, Thomas
Izotova, Lara S.
Lembo, David
Day, Patricia
Pang, Susana
Schiller, John T.
Pestka, Sidney
TI Ultra human interferons exhibit higher activity than the standard
interferons in prevention of human papillomavirus infection in cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Schwartz, Barbara; Anton, Kevin; Pestka, Sidney] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Mol Genet Microbiol & Immunol, Piscataway, NJ 08854 USA.
[Koltchev, Dolly; Skawinski, Michael; Clark, William; Lavoie, Thomas; Izotova, Lara S.; Pestka, Sidney] PBL Biotechnol Labs, Piscataway, NJ 08854 USA.
[Lembo, David] Univ Turin, Dept Publ Hlth & Microbiol, I-10126 Turin, Italy.
[Day, Patricia; Pang, Susana; Schiller, John T.] NCI, NIH, Cellular Oncol Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 261
EP 261
DI 10.1016/j.cyto.2008.07.150
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900128
ER
PT J
AU Sato, N
Waldmann, TA
Tagaya, Y
AF Sato, Noriko
Waldmann, Thomas A.
Tagaya, Yutaka
TI Cytokine responses of naive T-cells requires special permission by
accessory cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Sato, Noriko; Waldmann, Thomas A.; Tagaya, Yutaka] NCI, NIH, Metab Branch, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 267
EP 267
DI 10.1016/j.cyto.2008.07.173
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900150
ER
PT J
AU Borrego, F
Narayanan, S
Tang, XB
Alvarez, Y
Coligan, JE
AF Borrego, Francisco
Narayanan, Sriram
Tang, Xiaobin
Alvarez, Yelina
Coligan, John E.
TI The immunomodulatory CD300A receptor is differentially expressed on
human TH1 and TH17 cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Borrego, Francisco; Narayanan, Sriram; Tang, Xiaobin; Alvarez, Yelina; Coligan, John E.] NIAID, Receptor Cell Biol Sect, Immunogenet Lab, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 272
EP 272
DI 10.1016/j.cyto.2008.07.198
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900174
ER
PT J
AU Boirivant, M
Amendola, A
Butera, A
Sanchez, M
Xu, LL
Marinaro, M
Kitani, A
Di Giacinto, C
Strober, W
Fuss, IJ
AF Boirivant, Monica
Amendola, Antonello
Butera, Alessia
Sanchez, Massimo
Xu, Lili
Marinaro, Mariarosaria
Kitani, Atsushi
Di Giacinto, Claudia
Strober, Warren
Fuss, Ivan J.
TI A transient breach in the epithelial barrier leads to regulatory T-cell
generation and resistance to TNBS-colitis induction
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Boirivant, Monica; Amendola, Antonello; Butera, Alessia; Marinaro, Mariarosaria; Di Giacinto, Claudia] Ist Super Sanita, Dept Infect Parasit & Immunemed Dis, Immunemed Dis Sect, I-00161 Rome, Italy.
[Sanchez, Massimo] Ist Super Sanita, Dept Cell Biol & Neurosci, I-00161 Rome, Italy.
[Xu, Lili; Kitani, Atsushi; Strober, Warren; Fuss, Ivan J.] NIAID, Mucosal Immun Sect, Host Def Lab, Bethesda, MD 20892 USA.
RI BOIRIVANT, MONICA/B-9977-2016; AMENDOLA, ANTONELLO/B-9979-2016
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 273
EP 273
DI 10.1016/j.cyto.2008.07.203
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900179
ER
PT J
AU Pandiyan, P
Lenardo, M
AF Pandiyan, Pushpa
Lenardo, Michael
TI cytokines control CD4+CD25+Foxp3+regulatory T-cell survival and their
mechanism of suppression
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Pandiyan, Pushpa; Lenardo, Michael] NIAID, Immunol Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 273
EP 273
DI 10.1016/j.cyto.2008.07.201
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900177
ER
PT J
AU Ozato, K
Tailor, P
Ramakrishna, L
Chang, TH
Kubota, T
Matsuoka, M
Morse, CH
AF Ozato, Keiko
Tailor, Prafullakumar
Ramakrishna, Lakshimi
Chang, Tsung Hsien
Kubota, Toru
Matsuoka, Mayumi
Morse, C. Herbert, III
TI The mechanism of interferon gene transcription in dendritic cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Ozato, Keiko; Tailor, Prafullakumar; Ramakrishna, Lakshimi; Chang, Tsung Hsien; Kubota, Toru; Matsuoka, Mayumi] NICHD, Program Genom Differentiat, Bethesda, MD USA.
[Kubota, Toru; Matsuoka, Mayumi] Natl Inst Infect Dis, Tokyo, Japan.
[Morse, C. Herbert, III] NIAID, Immunopathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 277
EP 277
DI 10.1016/j.cyto.2008.07.219
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900194
ER
PT J
AU Savan, R
Yalamanchili, R
Hakim, S
Young, HA
AF Savan, Ram
Yalamanchili, Rajesh
Hakim, Shakeeb
Young, Howard A.
TI The Role of miRNAs in the regulation of interferon-gamma gene expression
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Savan, Ram; Yalamanchili, Rajesh; Hakim, Shakeeb; Young, Howard A.] NCI, Canc & Inflammat Program, Expt Immunol Lab, Ctr Canc Res, Frederick, MD 21702 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 278
EP 278
DI 10.1016/j.cyto.2008.07.224
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900198
ER
PT J
AU O'Shea, J
AF O'Shea, Jahn
TI Cytokine signaling and T-cell differentiation
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [O'Shea, Jahn] NIAMS, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 279
EP 279
DI 10.1016/j.cyto.2008.07.230
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900203
ER
PT J
AU Kennedy, MA
Nechaev, S
Gilchrist, DA
Muse, GW
Chinenov, Y
Adelman, K
Rogatsky, I
AF Kennedy, Megan A.
Nechaev, Sergei
Gilchrist, Daniel A.
Muse, Ginger W.
Chinenov, Yurii
Adelman, Karen
Rogatsky, Inez
TI Regulation of TNF alpha gene transcription at the post-initiation step
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Kennedy, Megan A.; Chinenov, Yurii; Rogatsky, Inez] Cornell Univ, Weill Med Coll, Dept Microbiol & Immunol, New York, NY 10021 USA.
[Kennedy, Megan A.; Chinenov, Yurii; Rogatsky, Inez] Cornell Univ, Hosp Special Surg, Weill Med Coll, New York, NY 10021 USA.
[Nechaev, Sergei; Gilchrist, Daniel A.; Muse, Ginger W.; Adelman, Karen] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 280
EP 280
DI 10.1016/j.cyto.2008.07.234
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900206
ER
PT J
AU Klaschik, S
Tross, D
Klinman, DM
AF Klaschik, Sven
Tross, Debra
Klinman, Dennis M.
TI Inductive and suppressive networks regulate TLR19-dependent gene
expression in vivo
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Klaschik, Sven; Tross, Debra; Klinman, Dennis M.] NCI, Expt Immunol Lab, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 1
U2 6
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 283
EP 283
DI 10.1016/j.cyto.2008.07.248
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900220
ER
PT J
AU Petrenko, L
Klaschik, S
Shirota, H
Klinman, DM
AF Petrenko, Lev
Klaschik, Sven
Shirota, Hidekazu
Klinman, Dennis M.
TI Synergistic up-regulation of cytokine encoding genes by CpG
oligonucleotides plus poly (I:C)
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Petrenko, Lev; Klaschik, Sven; Shirota, Hidekazu; Klinman, Dennis M.] NCI, Expt Immunol Lab, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 284
EP 284
DI 10.1016/j.cyto.2008.07.250
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900222
ER
PT J
AU Gamero, AM
Scarzello, AJ
Young, MR
Mentor-Marcel, R
Babe, G
Wise, J
Colburn, NH
AF Gamero, Ana M.
Scarzello, Anthony J.
Young, Matthew R.
Mentor-Marcel, Roycelynn
Babe, Gerd
Wise, Jennifer
Colburn, Nancy H.
TI STAT2 Contributes to inflammation-induced colorectal cancer
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Gamero, Ana M.] Temple Univ, Sch Med, Dept Biochem, Philadelphia, PA 19140 USA.
[Scarzello, Anthony J.] NCI, Expt Immunol Lab, Canc & Inflammat Program, NIH, Frederick, MD 21701 USA.
[Young, Matthew R.; Mentor-Marcel, Roycelynn; Babe, Gerd; Wise, Jennifer; Colburn, Nancy H.] NCI, Lab Canc Prevent, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 290
EP 290
DI 10.1016/j.cyto.2008.07.279
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900250
ER
PT J
AU Snyder, GA
Jiang, JS
Xiao, T
AF Snyder, Greg A.
Jiang, Jiansheng
Xiao, Tsan
TI Mechanism of TOLL/IL-1 receptor domain dimerization and signaling
revealed by a crystal structure of the MYD88
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Snyder, Greg A.; Jiang, Jiansheng; Xiao, Tsan] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RI Xiao, Tsan/A-8590-2010
NR 0
TC 0
Z9 1
U1 0
U2 2
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 291
EP 291
DI 10.1016/j.cyto.2008.07.282
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900252
ER
PT J
AU Dufour, F
Sasseville, AMJ
Chabaud, S
Siegel, RM
Massie, B
Largelier, Y
AF Dufour, Florent
Sasseville, A. Marie-Josee
Chabaud, Stephane
Siegel, Richard M.
Massie, Bernard
Largelier, Yves
TI The R1 subunit of Herpes simplex virus type 2 ribonucleotide reductase
protects cells against TNF-alpha and double-stranded-RNA-induced
apoptosis by direct interaction with procaspase-8
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Dufour, Florent; Sasseville, A. Marie-Josee; Chabaud, Stephane; Largelier, Yves] CHU Montreal, Ctr Rech, Montreal, PQ, Canada.
[Dufour, Florent; Sasseville, A. Marie-Josee; Chabaud, Stephane; Largelier, Yves] Hop Notre Dame De Bon Secours, Inst Canc Montreal, Montreal, PQ, Canada.
[Massie, Bernard; Largelier, Yves] Univ Montreal, Dept Microbiol & Immunol, Montreal, PQ H3C 3J7, Canada.
[Massie, Bernard] Inst Rech Biotechnol, Montreal, PQ, Canada.
[Siegel, Richard M.] NIAMS, Immunoregulat Unit, Autoimmun Branch, NIH, Bethesda, MA USA.
[Massie, Bernard] Univ Quebec, Inst Armand Frappier, INRS, Laval, PQ, Canada.
[Largelier, Yves] Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 300
EP 300
DI 10.1016/j.cyto.2008.07.322
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900291
ER
PT J
AU Feldmann, H
AF Feldmann, Heinz
TI Ebola and Marburg viruses: Immunopathology and immunoprotection
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Feldmann, Heinz] NIAID, Rocky Mt Labs, Virol Lab, NIH, Hamilton, MT 59840 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 302
EP 302
DI 10.1016/j.cyto.2008.07.330
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900298
ER
PT J
AU Leonard, W
AF Leonard, Warren
TI Signaling and gene regulation by gamma c-dependent cytokines
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Leonard, Warren] NHLBI, Lab Mol Immunol, Div Intramural Res, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 304
EP 304
DI 10.1016/j.cyto.2008.07.335
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900302
ER
PT J
AU Shevach, EM
Huter, E
Tran, D
Andersson, J
AF Shevach, Ethan M.
Huter, Eva
Tran, Dar
Andersson, John
TI Control of immune responses by natural and adaptive regulatory T cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Shevach, Ethan M.; Huter, Eva; Tran, Dar; Andersson, John] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 305
EP 305
DI 10.1016/j.cyto.2008.07.339
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900306
ER
PT J
AU Li, WQ
Guszczynski, T
Hixon, J
Durum, SK
AF Li, Wenqing
Guszczynski, Tad
Hixon, Julie
Durum, Scott K.
TI Development and maintenance of T-cell requires post-translational
regulation of anti-apoptotic MCL-1 and pro-apoptotic BIM by IL-7
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Li, Wenqing; Hixon, Julie; Durum, Scott K.] NCI, Lab Mol Immunoregulat Canc & Inflammat Program, CCR, NIH, Frederick, MD 21701 USA.
[Guszczynski, Tad] NCI, Lab Cell & Dev Signaling, CCR, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 306
EP 306
DI 10.1016/j.cyto.2008.07.344
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900310
ER
PT J
AU Hodge, DL
Berthet, C
Subleski, J
Bere, W
Chen, X
Coppola, V
Buschman, M
Wolfe, T
Shuggi, I
Young, HA
AF Hodge, Deborah L.
Berthet, Cyril
Subleski, Jeff
Bere, William
Chen, Xin
Coppola, Vincenzo
Buschman, Matthew
Wolfe, Thomas
Shuggi, Isabelle
Young, Howard A.
TI IFN-gamma 3 ' untranslated region AU-RICH element-deleted mice have
altered immune structure and function
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Hodge, Deborah L.; Subleski, Jeff; Bere, William; Buschman, Matthew; Wolfe, Thomas; Shuggi, Isabelle; Young, Howard A.] NCI, Expt Immunol Lab, Canc Res Ctr, Frederick, MD 21702 USA.
[Berthet, Cyril; Coppola, Vincenzo] NCI, Mouse Canc Genet Program, Canc Res Ctr, Frederick, MD 21702 USA.
[Chen, Xin] NCI, Mol Immunoregulat Lab, Canc Res Ctr, Frederick, MD 21702 USA.
RI Coppola, Vincenzo/E-2917-2011; Chen, Xin/I-6601-2015
OI Coppola, Vincenzo/0000-0001-6163-1779; Chen, Xin/0000-0002-2628-4027
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 313
EP 313
DI 10.1016/j.cyto.2008.07.376
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900341
ER
PT J
AU Mielke, LA
Elkins, K
Starr, R
Hilton, DJ
Tsichlis, P
O'Shea, JJ
Watford, WT
AF Mielke, Lisa A.
Elkins, Karen
Starr, Robyn
Hilton, Douglas J.
Tsichlis, Philip
O'Shea, John J.
Watford, Wendy T.
TI Receptor and cell-specific function of MAP3K8/TPL2 in innate immune
signaling and cytokine production
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Mielke, Lisa A.; O'Shea, John J.; Watford, Wendy T.] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
[Mielke, Lisa A.; Hilton, Douglas J.] Walter & Eliza Hall Inst Med Res, Div Mol Med, Parkville, Vic, Australia.
[Mielke, Lisa A.] Univ Melbourne, Dept Med Biol, Melbourne, Vic 3010, Australia.
[Elkins, Karen] US FDA, CEBR, Div Bacterial Parasit & Allergen Prod, Rockville, MD 20857 USA.
[Starr, Robyn] St Vincents Inst, Signal Transduct Lab, Melbourne, Vic, Australia.
[Tsichlis, Philip] Tufts Univ New England Med Ctr, Mol Oncol Res Inst, Boston, MA USA.
RI Hilton, Douglas/C-7250-2013
OI Hilton, Douglas/0000-0002-7698-2392
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 314
EP 314
DI 10.1016/j.cyto.2008.07.381
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900346
ER
PT J
AU Brann, TW
Yang, J
Huang, DW
Frank, A
Lempicki, RA
Baseler, MW
Kottilili, S
Lane, HC
Imamichi, T
AF Brann, Terrence W.
Yang, Jun
Huang, Da-Wei
Frank, Astrid
Lempicki, Richard A.
Baseler, Michael W.
Kottilili, Shaym
Lane, H. Clifford
Imamichi, Tom
TI IL-27 is a novel anti-viral cytokine that inhibits replication of HIV-1
and HCV
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Brann, Terrence W.; Imamichi, Tom] NCI, Lab Human Retrovirol, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Yang, Jun; Huang, Da-Wei; Lempicki, Richard A.] NCI, Lab Immunopathogenesis & Bioinformat, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Frank, Astrid; Kottilili, Shaym; Lane, H. Clifford] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Baseler, Michael W.] NCI, AIDS Monitoring Lab, SAIC Frederick Inc, Frederick, MD 21701 USA.
RI Lempicki, Richard/E-1844-2012
OI Lempicki, Richard/0000-0002-7059-409X
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 320
EP 321
DI 10.1016/j.cyto.2008.07.408
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900372
ER
PT J
AU Baron, S
Poast, J
Suzuki, F
Kobayashi, M
Clouse, K
Bacot, S
Tiffany, L
Lankford, C
Boekhoudt, G
Morrow, A
Fey, S
Schmeisser, H
Bekisz, J
Zoon, K
AF Baron, Samuel
Poast, Joyce
Suzuki, Fujio
Kobayashi, Makiko
Clouse, Kathleen
Bacot, Sylvia
Tiffany, Linda
Lankford, Carla
Boekhoudt, Gunther
Morrow, Angel
Fey, Samuel
Schmeisser, Hana
Bekisz, Joseph
Zoon, Kathryn
TI Innate immunity: Preclinical study of eradication of tumor cells by
IFN-activated monocytes in vitro and in vivo
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Baron, Samuel; Poast, Joyce] Univ Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX USA.
[Baron, Samuel; Suzuki, Fujio; Kobayashi, Makiko] Univ Texas Med Branch, Dept Internal Med, Galveston, TX USA.
[Clouse, Kathleen; Bacot, Sylvia; Tiffany, Linda; Lankford, Carla; Boekhoudt, Gunther] US FDA, Bethesda, MD 20014 USA.
[Baron, Samuel; Morrow, Angel; Fey, Samuel; Schmeisser, Hana; Bekisz, Joseph; Zoon, Kathryn] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 322
EP 322
DI 10.1016/j.cyto.2008.07.415
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900379
ER
PT J
AU Wilhelm, C
Di Mascio, M
Hu, ZH
Srinivasula, S
Thaker, V
Adelsberger, J
Rupert, A
Baseler, M
Tagaya, Y
Roby, G
Rehm, C
Follmann, D
Lane, C
Catalfarno, M
AF Wilhelm, Christopher
Di Mascio, Michele
Hu, Zonghui
Srinivasula, Sharat
Thaker, Vishakha
Adelsberger, Joseph
Rupert, Adam
Baseler, Michael
Tagaya, Yutaka
Roby, Gregg
Rehm, Catherine
Follmann, Dean
Lane, Clifford
Catalfarno, Marta
TI HIV Infection leads to increased proliferation of T-cells by two
distinct pathways that differentially affect CD4 and CD8 T-cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 7th Joint Conference of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytoklin-Research
CY OCT 12-16, 2008
CL Montreal, CANADA
SP Int Cytokine Soc, Int Soc Interferon & Cytokin Res
C1 [Wilhelm, Christopher; Thaker, Vishakha; Roby, Gregg; Rehm, Catherine; Lane, Clifford; Catalfarno, Marta] NIAID, CMRS, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Di Mascio, Michele; Hu, Zonghui; Follmann, Dean] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Srinivasula, Sharat] NCI, Biostat Res Branch, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Adelsberger, Joseph; Rupert, Adam; Baseler, Michael] NCI, AIDS Monitoring Labs, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Tagaya, Yutaka] NCI, Metab Branch, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD SEP
PY 2008
VL 43
IS 3
BP 322
EP 322
DI 10.1016/j.cyto.2008.07.416
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 362QT
UT WOS:000260212900380
ER
PT J
AU Hendee, WR
Cleary, K
Ehman, RL
Fullerton, GD
Grundfest, WS
Haller, J
Kelley, CA
Meyer, AE
Murphy, RF
Phillips, W
Torchilin, VP
AF Hendee, William R.
Cleary, Kevin
Ehman, Richard L.
Fullerton, Gary D.
Grundfest, Warren S.
Haller, John
Kelley, Christine A.
Meyer, Anne E.
Murphy, Robert F.
Phillips, William
Torchilin, Vladimir P.
TI Bioengineering and Imaging Research Opportunities Workshop V: A summary
on imaging and characterizing structure and function in native and
engineered tissues
SO CYTOMETRY PART A
LA English
DT Editorial Material
DE tissue engineering; functional; molecular and structural imaging;
imaging of engineered tissues; targeted cell, gene, and drug delivery;
single-cell measurements; emerging imaging technologies
ID MAGNETIC-RESONANCE ELASTOGRAPHY; CANCER-THERAPY; WHITE PAPER;
MICROSCOPY; RECOMMENDATIONS; VISUALIZATION; SYSTEMS
AB The Fifth Bioengineering and Imaging Research Opportunities Workshop (BIROW V) was held on January 18-19, 2008. As with previous BIROW meetings, the purpose of BIROW V was to identify and characterize research and engineering opportunities in biomedical engineering and imaging. The topic of this BIROW meeting was Imaging and Characterizing Structure and Function in Native and Engineered Tissues. Under this topic, four areas were explored in depth: 1) Heterogeneous single-cell measurements and their integration into tissue and organism models; 2) Functional, molecular, and structural imaging of engineered tissue in vitro and in vivo; 3) New technologies for characterizing cells and tissues in situ; 4) Imaging for targeted cell, gene, and drug delivery. (C) 2008 international Society for Advancement of Cytometry.
C1 [Hendee, William R.] Med Coll Wisconsin, Dept Radiol, Milwaukee, WI 53226 USA.
[Cleary, Kevin] Georgetown Univ, Dept Radiol, Imaging Sci & Informat Syst Ctr, Washington, DC USA.
[Ehman, Richard L.] Mayo Clin, Dept Radiol, Rochester, MI USA.
[Fullerton, Gary D.] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, San Antonio, TX 78229 USA.
[Grundfest, Warren S.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Haller, John] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
[Kelley, Christine A.] Natl Inst Biomed Imaging & Bioengn, Div Discovery Sci & Technol, NIH, Bethesda, MD USA.
[Meyer, Anne E.] SUNY Buffalo, Biomat Grad Program, Buffalo, NY USA.
[Murphy, Robert F.] Carnegie Mellon Univ, Lane Ctr Computat Biol, Pittsburgh, PA 15213 USA.
[Phillips, William] Univ Texas Med Ctr, Dept Radiol, San Antonio, TX USA.
[Torchilin, Vladimir P.] Northeastern Univ, Dept Pharmaceut Sci, Boston, MA 02115 USA.
[Torchilin, Vladimir P.] Northeastern Univ, Ctr Pharmaceut Biotechnol & Nanomed, Boston, MA 02115 USA.
RP Hendee, WR (reprint author), Med Coll Wisconsin, Dept Radiol, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
EM whendee@mcw.edu
NR 26
TC 3
Z9 3
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1552-4922
J9 CYTOM PART A
JI Cytom. Part A
PD SEP
PY 2008
VL 73A
IS 9
BP 779
EP 784
DI 10.1002/cyto.a.20568
PG 6
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 343XV
UT WOS:000258890500002
PM 18677767
ER
PT J
AU Roederer, M
Moody, MA
AF Roederer, Mario
Moody, M. Anthony
TI PolyChromatic plots: Graphical display of multidimensional data
SO CYTOMETRY PART A
LA English
DT Article
ID SYSTEMS; POINTS; SPACE
AB Limitations of graphical displays as well as human perception make the presentation and analysis of multidimensional data challenging. Graphical display of information on paper or by current projectors is perforce limited to two dimensions; the encoding of information from other dimensions must be overloaded into the two physical dimensions. A number of alternative means of encoding this information have been implemented, such as offsetting data points at an angle (e.g., three-dimensional projections onto a two-dimensional surface) or generating derived parameters that are combinations of other variables (e.g., principal components). Here, we explore the use of color to encode additional dimensions of data. PolyChromatic Plots are standard dot plots, where the color of each event is defined by the values of one, two, or three of the measurements for that event. The measurements for these parameters are mapped onto an intensity value for each primary color (red, green, or blue) based on different functions. In addition, differential weighting of the priority with which overlapping events are displayed can be defined by these same measurements. PolyChromatic Plots can encode up to five independent dimensions of data in a single display. By altering the color mapping function and the priority function, very different displays that highlight or de-emphasize populations of events can be generated. As for standard black-and-white dot plots, frequency information can be significantly biased by this display; care must be taken to ensure appropriate interpretation of the displays. PolyChromatic Plots are a powerful display type that enables rapid data exploration. By virtue of encoding as many as five dimensions of data independently, an enormous amount of information can be gleaned from the displays. In many ways, the display performs somewhat like an unsupervised cluster algorithm, by highlighting events of similar distributions in multivariate space. Published 2008 Wiley-Liss, Inc.
C1 [Roederer, Mario] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Moody, M. Anthony] Duke Univ, Dept Pediat, Sch Med, Durham, NC 27706 USA.
RP Roederer, M (reprint author), NIH, Vaccine Res Ctr, 40 Convent Dr,Room 5509, Bethesda, MD 20892 USA.
EM Roederer@nih.gov
OI Moody, Tony/0000-0002-3890-5855
FU Intramural NIH HHS [Z01 AI005020-06]
NR 11
TC 10
Z9 11
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4922
J9 CYTOM PART A
JI Cytom. Part A
PD SEP
PY 2008
VL 73A
IS 9
BP 868
EP 874
DI 10.1002/cyto.a.20610
PG 7
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 343XV
UT WOS:000258890500012
PM 18629844
ER
PT J
AU El-Bizri, N
Guignabert, C
Wang, L
Cheng, A
Stankunas, K
Chang, CP
Mishina, Y
Rabinovitch, M
AF El-Bizri, Nesrine
Guignabert, Christophe
Wang, Lingli
Cheng, Alexander
Stankunas, Kryn
Chang, Ching-Pin
Mishina, Yuji
Rabinovitch, Marlene
TI SM22 alpha-targeted deletion of bone morphogenetic protein receptor 1A
in mice impairs cardiac and vascular development, and influences
organogenesis
SO DEVELOPMENT
LA English
DT Article
DE Bmpr1a (Alk3); vasculogenesis; heart development; craniofacial
development; matrix metalloproteinase (metallopeptidase); MMP2; MMP9;
smooth muscle cell proliferation; pericyte apoptosis; SM22 alpha
(transgelin, Tagln); mouse
ID PRIMARY PULMONARY-HYPERTENSION; MATRIX METALLOPROTEINASE-2 EXPRESSION;
ABDOMINAL AORTIC-ANEURYSMS; MUSCLE-CELL MIGRATION; RAT CAROTID-ARTERY;
SMOOTH-MUSCLE; ENDOCARDIAL CUSHION; KNOCKOUT MICE; MOUSE EMBRYOS;
TGF-BETA
AB Expression of bone morphogenetic protein receptor 1A (BMPR1A) is attenuated in the lung vessels of patients with pulmonary arterial hypertension, but the functional impact of this abnormality is unknown. We ablated Bmpr1a in cardiomyocytes and vascular smooth muscle cells (VSMCs) by breeding mice possessing a loxP allele of Bmpr1a (Bmpr1a(flox)) expressing R26R with SM22 alpha-Cre mice. SM22 alpha-Cre;R26R;Bmpr1a(flox/flox) mice died soon after embryonic day 11 (E11) with massive vascular and pericardial hemorrhage and impaired brain development. At E10.5, SM22 alpha-Cre;R26R;Bmpr1a(flox/flox) embryos showed thinning of the myocardium associated with reduced cell proliferation. These embryos also had severe dilatation of the aorta and large vessels with impaired investment of SMCs that was also related to reduced proliferation. SM22 alpha-Cre;R26R;Bmpr1a(flox/flox) mice showed collapsed telencephalon in association with impaired clearing of brain microvessels in areas where reduced apoptosis was observed. Transcript and protein levels of matrix metalloproteinase (MMP) 2 and 9 were reduced in E9.5 and E10.5 SM22 alpha-Cre; R26R;Bmpr1a(flox/flox) embryos, respectively. Knock-down of BMPR1A by RNA interference in human pulmonary artery SMCs reduced MMP2 and MMP9 activity, attenuated serum-induced proliferation, and impaired PDGF-BB-directed migration. RNA interference of MMP2 or MMP9 recapitulated these abnormalities, supporting a functional interaction between BMP signaling and MMP expression. In human brain microvascular pericytes, knock-down of BMPR1A reduced MMP2 activity and knock-down of either BMPR1A or MMP2 caused resistance to apoptosis. Thus, loss of Bmpr1a, by decreasing MMP2 and/or MMP9 activity, can account for vascular dilatation and persistence of brain microvessels, leading to the impaired organogenesis documented in the brain.
C1 [El-Bizri, Nesrine; Guignabert, Christophe; Wang, Lingli; Cheng, Alexander; Rabinovitch, Marlene] Stanford Univ, Sch Med, Cardiopulmonary Res Program, Vera Moulton Wall Ctr Pulm Vasc Dis, Stanford, CA 94305 USA.
[El-Bizri, Nesrine; Guignabert, Christophe; Wang, Lingli; Cheng, Alexander; Rabinovitch, Marlene] Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA.
[Stankunas, Kryn; Chang, Ching-Pin] Stanford Univ, Sch Med, Dept Med, Stanford, CA 94305 USA.
[Mishina, Yuji] Natl Inst Environm Hlth Sci, Reprod & Dev Toxicol Lab, Mol Dev Biol Grp, Res Triangle Pk, NC USA.
RP Rabinovitch, M (reprint author), Stanford Univ, Sch Med, Cardiopulmonary Res Program, Vera Moulton Wall Ctr Pulm Vasc Dis, Stanford, CA 94305 USA.
EM marlener@stanford.edu
FU Intramural NIH HHS; NHLBI NIH HHS [HL085345, R01 HL074186, R01
HL074186-01A1, R01 HL074186-02, R01 HL074186-03, R01 HL074186-04, R01
HL074186-05, R01 HL085345, R01 HL087118, R01 HL087118-01A1]
NR 61
TC 27
Z9 27
U1 1
U2 3
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0950-1991
J9 DEVELOPMENT
JI Development
PD SEP 1
PY 2008
VL 135
IS 17
BP 2981
EP 2991
DI 10.1242/dev.017863
PG 11
WC Developmental Biology
SC Developmental Biology
GA 336WL
UT WOS:000258395500016
PM 18667463
ER
PT J
AU Crowe, SL
Blair, RJR
AF Crowe, S. L.
Blair, R. J. R.
TI The development of antisocial behavior: What can we learn from
functional neuroimaging studies?
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Review
ID POSTTRAUMATIC-STRESS-DISORDER; INTERMITTENT EXPLOSIVE DISORDER;
POSITRON-EMISSION TOMOGRAPHY; CALLOUS-UNEMOTIONAL TRAITS;
CEREBRAL-BLOOD-FLOW; VENTROMEDIAL PREFRONTAL CORTEX; PEDIATRIC BIPOLAR
DISORDER; VOXEL-BASED MORPHOMETRY; CHILDHOOD SEXUAL-ABUSE; TEMPORAL-LOBE
EPILEPSY
AB The recent development of low-risk imaging technologies. such as functional magnetic resonance imaging (fMRI), have had a significant impact on the investigation of psychopathologies in children and adolescents. This review considers what we can infer from fMRI work regarding the development of conduct disorder (CD) and oppositional defiant disorder (ODD). We make two central assumptions that are grounded in the empirical literature. First the diagnoses of CD and ODD identify individuals with heterogeneous pathologies: that is, different developmental pathologies can receive a and ODD identify individuals with heterogeneous pathologies: that is, different developmental pathologies can receive a CDD or ODD diagnosis. This is indicated by the comorbidities associated with CD/ODD. some of which appear to be mutually exclusive at the biological level (e.g., posttraumatic stress disorder [PTSD] and psychopathic tendencies). Second, two populations of antisocial individuals can be identified: those that show an increased risk for only reactive aggression and those that show an increased risk for both reactive and instrumental aggression. We review the fMRI data indicating that particular comorbidities of CD/ODD (i.e., mood and anxiety conditions such as childhood bipolar disorder and PTSD) are associated with either increased responsiveness of neural regions implicated in the basic response to threat (e.g., the amygdala) or decreased responsiveness in regions of frontal cortex (e.g., ventromedial frontal cortex) that are implicated in the regulation of the basic threat response. We suggest why such pathology would increase the risk for reactive aggression and, in turn, lead to the association with a CD/ODD diagnosis. We also review the literature on psychopathic tendencies, a condition where the individual is at significantly elevated risk for both reactive and instrumental aggression. We show that in individuals with psychopathic tendencies, the functioning of the amygdala in stimulus-reinforcement learning and of the ventromedial frontal cortex in the representation of reinforcement expectancies is impaired. We suggest why such pathology would increase the risk for reactive and instrumental aggression and thus also lead to the association with a CD/ODD diagnosis.
C1 [Blair, R. J. R.] NIMH, Mood & Anxiety Program, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Blair, RJR (reprint author), NIMH, Mood & Anxiety Program, Natl Inst Hlth, 15 K N Dr, Bethesda, MD 20892 USA.
EM blairj@intra.nimh.nih.gov
FU Intramural NIH HHS
NR 142
TC 57
Z9 59
U1 9
U2 30
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD FAL
PY 2008
VL 20
IS 4
BP 1145
EP 1159
DI 10.1017/S0954579408000540
PG 15
WC Psychology, Developmental
SC Psychology
GA 373SU
UT WOS:000260993800007
PM 18838035
ER
PT J
AU Lenroot, RK
Giedd, JN
AF Lenroot, Rhoshel K.
Giedd, Jay N.
TI The changing impact of genes and environment on brain development during
childhood and adolescence: Initial findings from a neuroimaging study of
pediatric twins
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Review
ID STRESSFUL LIFE EVENTS; MONOZYGOTIC TWINS; CORTICAL THICKNESS; MALTREATED
CHILDREN; UNAFFECTED SIBLINGS; ONSET SCHIZOPHRENIA; MAJOR DEPRESSION;
DIZYGOTIC TWINS; EEG COHERENCE; CHORION TYPE
AB Human brain development is created through continuing complex interactions of genetic and environmental influences. The challenge of linking specific genetic or environmental risk factors to typical or atypical behaviors has led to interest in using brain structural features as an intermediate phenotype. Twin studies in adults have found that many aspects of brain anatomy are highly heritable. demonstrating that genetic factors provide a significant contribution to variation in brain structures. Less is known about the relative impact of genes and environment while the brain is actively developing. We summarize results from the ongoing National Institute of Mental Health child and adolescent twin study that suggest that heritability of different brain areas changes over the course of development in a regionally specific fashion. Areas associated with more complex reasoning abilities become increasingly heritable with maturation. The potential mechanisms by which gene-environment interactions may affect heritability values during development is discussed.
C1 [Giedd, Jay N.] NIMH, Child Psychiat Branch, Brain Imaging Unit, Bethesda, MD 20892 USA.
RP Giedd, JN (reprint author), NIMH, Child Psychiat Branch, Brain Imaging Unit, 10 Ctr Dr,MSC 1600,Bldg 10,Room 4C110, Bethesda, MD 20892 USA.
EM jg@nih.gov
RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978
FU Intramural NIH HHS [ZIA MH002794-08]
NR 113
TC 44
Z9 44
U1 6
U2 17
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD FAL
PY 2008
VL 20
IS 4
BP 1161
EP 1175
DI 10.1017/S0954579408000552
PG 15
WC Psychology, Developmental
SC Psychology
GA 373SU
UT WOS:000260993800008
PM 18838036
ER
PT J
AU Maheu, FS
Mazzone, L
Merke, DP
Keil, M
Stratakis, CA
Pine, DS
Ernst, M
AF Maheu, Francoise S.
Mazzone, Luigi
Merke, Deborah P.
Keil, Margaret
Stratakis, Constantine A.
Pine, Daniel S.
Ernst, Monique
TI Altered amygdala and hippocampus function in adolescents with
hypercortisolemia: A functional magnetic resonance imaging study of
Cushing syndrome
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID MAJOR DEPRESSIVE DISORDER; MEMORY CONSOLIDATION; CORTISOL SECRETION;
COGNITIVE DECLINE; ANIMAL-MODELS; STRESS; CHILDREN; BRAIN; FMRI;
EXPERIENCE
AB Chronic elevations of endogenous cortisol levels have been shown to alter medial temporal cortical structures and to be accompanied by declarative memory impairments and depressive symptons in human adults. These effects of elevated endogenous levels of cortisol have not been directly Studied in adolescents. Because adolescents with Cushing syndrome show endogenous elevations in cortisol, they, represent a unique natural model to study the effects of prolonged hypercortisolemia on brain fuction. and memory and affective processes during this developmental stage. Using functional magnetic resonance imaging (fMRI), we compared 12 adolescents with Cushing syndrome with 22 healthy control adolescents on amygdala and anterior hippocampus activation during an emotional faces encoding task. None of these adolescents manifested depressive symptoms. Encoding Success was assessed using a memory recognition test performed after the scan. The fMRI analyses followed all event-related design and were conducted using the SPM99 platform. Compared to healthy adolescents, patients with Cushing syndrome showed greater left amygdala and right anterior hippocampus activation during Successful face encoding. Memory performance for faces recognition did riot differ between groups. This first study of cerebral function in adolescents with chronic endogeneous hypercortisolemia due to Cushing syndrome demonstrates the presence of functional alterations in amygdala and hippocampus, which are not associated with affective or memory impairments. Such findings need to be followed by work examining the role of age and related brain maturational stage on these effects, as well as the identification of possible protective factors conferring resilience to affective and cognitive consequences in this disease and/or during this stage of cerebral development.
C1 [Ernst, Monique] NIMH, Mon Ernst Emot Dev & Affec Neurosci Branch, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
RP Ernst, M (reprint author), NIMH, Mon Ernst Emot Dev & Affec Neurosci Branch, Mood & Anxiety Disorders Program, 15K N Dr,Room 118, Bethesda, MD 20892 USA.
EM ernstm@mail.nih.gov
FU Intramural NIH HHS [ZIA HD000642-13]
NR 58
TC 26
Z9 26
U1 2
U2 8
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD FAL
PY 2008
VL 20
IS 4
BP 1177
EP 1189
DI 10.1017/S0954579408000564
PG 13
WC Psychology, Developmental
SC Psychology
GA 373SU
UT WOS:000260993800009
PM 18838037
ER
PT J
AU Sperber, SM
Dawid, IB
AF Sperber, Steven M.
Dawid, Igor B.
TI barx1 is necessary for ectomesenchyme proliferation and
osteochondroprogenitor condensation in the zebrafish pharyngeal arches
SO DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE Barx1; pharyngogenesis; viscerocranium; zebrafish; pharyngeal arches;
neural crest; chondrogenesis; cartilage; BMP; FGF
ID CRANIOFACIAL DEVELOPMENT; HOMEOBOX GENE; CARTILAGE MORPHOGENESIS;
VASCULAR DEVELOPMENT; SKELETAL DEVELOPMENT; LIMB DEVELOPMENT; BRANCHIAL
ARCH; EXPRESSION; FGF; CHONDROGENESIS
AB Barx1 modulates cellular adhesion molecule expression and participates in specification of tooth-types, but little is understood of its role in patterning the pharyngeal arches. We examined barx1 expression during zebrafish craniofacial development and performed a functional analysis using antisense morpholino Oligonucleotides. Barx1 is expressed in the rhombencephalic neural crest, the pharyngeal arches, the pectoral fill buds and the gut in contrast to its paralogue barx2, which is most prominently expressed ill the arch epithelium. Additionally, barx1 transient expression was observed in the posterior lateral line ganglia and developing trunk/tail. We show that Barx1 is necessary for proliferation of the arch osteochondrogenic progenitors, and that morphants exhibit diminished and dysmorphic arch cartilage elements due to reductions in chondrocyte differentiation and condensation. Attenuation of Barx1 results in lost arch expression of osteochondrogenic markers col2al, runx2a and chondromodulin, as well as odontogenic marker dlx2b. Further, loss of barx1 positively influenced gdf5 and chordin, markets of jaw joint patterning. FGF signaling is required for maintaining barx1 expression, and that ectopic BMP4 induces expression of barx1 ill the intermediate region of the second pharyngeal arch. Together, these results indicate ail essential role for barx1 at early stages of chondrogenesis within the developing zebrafish viscerocranium. Published by Elsevier Inc.
C1 [Sperber, Steven M.; Dawid, Igor B.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Mol Genet Lab, Bethesda, MD 20892 USA.
RP Sperber, SM (reprint author), Natl Inst Child Hlth, Mol Genet Lab, Bldg 6B,Room 422,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM sperbers@mail.nih.gov
FU NICHD; NIH
FX We thank Pfizer Inc. for the generous gift of the SU5402, Dr. Chisa
Shukunami for chondromodulin, Dr. Matthias Hammerschmidt for the lia
embryos: Drs. Tom Sargent and Ting Luo for the inca probe. Dr. Marc
Ekker for the dlx2b probe, our laboratory colleagues for their helpful
discussions, Dr. G.H. Sperber and the NIH Fellows Editorial Board for
their comments oil the manuscript, and Mark Rath and John Gonzales for
their assistance with zebrafish husbandry. This research has been
supported by the Intramural Program of the NICHD, NIH.
NR 71
TC 35
Z9 36
U1 1
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0012-1606
J9 DEV BIOL
JI Dev. Biol.
PD SEP 1
PY 2008
VL 321
IS 1
BP 101
EP 110
DI 10.1016/j.ydbio.2008.06.004
PG 10
WC Developmental Biology
SC Developmental Biology
GA 341JP
UT WOS:000258710800009
PM 18590717
ER
PT J
AU Moore, AF
Jablonski, KA
McAteer, JB
Saxena, R
Pollin, TI
Franks, PW
Hanson, RL
Shuldiner, AR
Knowler, WC
Altshuler, D
Florez, JC
AF Moore, Allan F.
Jablonski, Kathleen A.
McAteer, Jarred B.
Saxena, Richa
Pollin, Toni I.
Franks, Paul W.
Hanson, Robert L.
Shuldiner, Alan R.
Knowler, William C.
Altshuler, David
Florez, Jose C.
CA Diabetes Prevent Program Res Grp
TI Extension of type 2 diabetes genome-wide association scan results in the
Diabetes Prevention Program
SO DIABETES
LA English
DT Article
ID BETA-CELL FUNCTION; INSULIN-RESISTANCE; GLUCOSE-TOLERANCE; VARIANTS;
SUSCEPTIBILITY; LOCI; POLYMORPHISMS; SECRETION; CDKAL1; GENES
AB OBJECTIVE-Genome-wide association scans (GWASs) have identified novel diabetes-associated genes. We evaluated how these variants impact diabetes incidence, quantitative glycemic traits, and response to preventive interventions in 3,548 Subjects at high risk of type 2 diabetes enrolled in the Diabetes Prevention Program (DPP), which examined the effects of lifestyle intervention, metformin, and troglitazone versus placebo.
RESEARCH DESIGN AND METHODS-We genotyped selected single nucleotide polymorphisms (SNPs) in or near diabetes-associated loci, including EXT2, CDKAL1, CDKN2A/B, IGF2BP2, HHEX, LOC387761, and SLC30A8 in DPP participants and performed Cox regression analyses using genotype, intervention, and their interactions as predictors of diabetes incidence. We evaluated their effect on insulin resistance and secretion at 1 year.
RESULTS-None of the selected SNPs were associated with increased diabetes incidence in this population. After adjustments for ethnicity, baseline insulin secretion was lower in subjects with the risk genotype at HHEX rs1111875 (P = 0.01); there were no significant differences in baseline insulin sensitivity. Both at baseline and at 1 year, subjects with the risk genotype at, LOC387761 had paradoxically increased insulin secretion; adjustment for self-reported effinicity abolished these differences. In ethnicity-adjusted analyses, we noted a nominal differential improvement in P-cell function for carriers of the protective genotype at CDKN2A/B after 1 year of troglitazone treatment (P = 0.01) and possibly lifestyle modification (P = 0.05).
CONCLUSIONS-We were unable to replicate the GWAS findings regarding diabetes risk in the DPP. We did observe genotype associations with differences in baseline insulin secretion at the HHEX locus and a possible pharmacogenetic interaction at CDKNA2/B.
C1 [Moore, Allan F.; McAteer, Jarred B.; Saxena, Richa; Altshuler, David; Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Dept Med, Boston, MA 02114 USA.
[Moore, Allan F.; Altshuler, David; Florez, Jose C.] Massachusetts Gen Hosp, Ctr Diabet, Dept Med, Boston, MA 02114 USA.
[Moore, Allan F.; Altshuler, David; Florez, Jose C.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Moore, Allan F.; McAteer, Jarred B.; Saxena, Richa; Altshuler, David; Florez, Jose C.] Broad Inst Harvard, Program Med & Populat Genet, Cambridge, MA USA.
[Moore, Allan F.; McAteer, Jarred B.; Saxena, Richa; Altshuler, David; Florez, Jose C.] MIT, Cambridge, MA 02139 USA.
[Jablonski, Kathleen A.] George Washington Univ, Ctr Biostat, Rockville, MD USA.
[Pollin, Toni I.; Shuldiner, Alan R.] Univ Maryland, Sch Med, Dept Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA.
[Franks, Paul W.] Umea Univ Hosp, Genet Epidemiol & Clin Res Grp, Dept Publ Hlth & Clin Med, Div Med, S-90185 Umea, Sweden.
[Hanson, Robert L.; Knowler, William C.] Natl Inst Diabet & Digest & Kidney Dis, Diabet Epidemiol & Clin Res Sect, Phoenix, AZ USA.
[Altshuler, David] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
RP Florez, JC (reprint author), Massachusetts Gen Hosp, Ctr Human Genet Res, Dept Med, Boston, MA 02114 USA.
EM dppmail@biostat.bsc.gwuj.edu
RI Altshuler, David/A-4476-2009; de Bakker, Paul/B-8730-2009; Hanson,
Robert/O-3238-2015; Uwaifo, Gabriel/M-2361-2016
OI Altshuler, David/0000-0002-7250-4107; de Bakker,
Paul/0000-0001-7735-7858; Hanson, Robert/0000-0002-4252-7068; Uwaifo,
Gabriel/0000-0002-6962-9304
FU National Institutes of Health [R01-DK-072041]; Doris Duke Charitable
Foundation Distinguished Scientist Clinical Award; NIH Research Career
Award [K23-DK-65978-04]; The National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK); NIDDK; Indian Health Service;
Office of Research on Minority Health; National Institute of Child
Health and Human Development; National Institute on Aging; Centers for
Disease Control and Prevention; Office of Research on Women's Health;
American Diabetes Association; McKesson BioServices; Matthews Media
Group; Henry M. Jackson Foundation
FX K.A.J. has received National Institutes of Health (NIH) Grant
R01-DK-072041. T.I.P. has received NIH Grant R01-DK-072041. A.R.S. has
received NIH Grant R01-DK-072041. D.A. has received NIH Grant
R01-DK-072041 and a Doris Duke Charitable Foundation Distinguished
Scientist Clinical Award. J.C.F. has received NIH Grant R01-DK-072041
and NIH Research Career Award K23-DK-65978-04. The National Institute of
Diabetes and Digestive and Kidney Diseases (NIDDK) of the NIH provided
funding to the clinical centers and the coordinating center for the
design and conduct of the study, collection, management, analysis, and
interpretation of the data. The Southwestern American Indian Centers
were supported directly by the NIDDK and the Indian Health Service. The
General Clinical Research Center Program, National Center for Research
Resources supported data collection at many of the clinical centers.
Funding for data collection and participant support was also provided by
the Office of Research on Minority Health, the National Institute of
Child Health and Human Development, the National Institute on Aging, the
Centers for Disease Control and Prevention, the Office of Research on
Women's Health, and the American Diabetes Association. Bristol-Myers
Squibb and Parke-Davis provided medication. This research was also
supported in part by the intramural research program of the NIDDK.
LifeScan, Health O Meter, Hoechst Marion Roussel, Merck-Medco Managed
Care, Merck, Nike Sports Marketing, Slim Fast Foods, and Quaker Oats
donated materials, equipment, or medicines for concomitant conditions.
McKesson BioServices, Matthews Media Group, and the Henry M. Jackson
Foundation provided support services under subcontract with the
coordinating center. The opinions expressed are those of the
investigators and do not necessarily reflect the views of the Indian
Health Service or other funding agencies. A complete list of centers,
investigators, and staff can be found in the online appendix. We
gratefully acknowledge the commitment and dedication of all participants
in the DPP, without whom this work would not have been possible.
NR 26
TC 60
Z9 61
U1 1
U2 6
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD SEP
PY 2008
VL 57
IS 9
BP 2503
EP 2510
DI 10.2337/db08-0284
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 343QP
UT WOS:000258869000029
PM 18544707
ER
PT J
AU Bainbridge, KE
Cowie, CC
Rust, KF
Fradkin, JE
AF Bainbridge, Kathleen E.
Cowie, Catherine C.
Rust, Keith F.
Fradkin, Judith E.
TI Mitigating case mix factors by choice of glycemic control performance
measure threshold
SO DIABETES CARE
LA English
DT Article; Proceedings Paper
CT Joint Statistical Meetings of the American-Statistical-Association
CY JUL 29-AUG 02, 2007
CL Salt Lake City, UT
SP Amer Stat Assoc
ID QUALITY-OF-CARE; ETHNIC-DIFFERENCES; DIABETES CARE; US ADULTS; RACE;
TARGETS; A1C
AB OBJECTIVE - Performance measures are tools for assessing quality of care but may be influenced by patient factors. We investigated how currently endorsed performance measures for glycemic control in diabetes may be influenced by case Mix composition. We assessed differences in A1C performance measure threshold attainment by case mix factors for A1C >9% and examined how lowering the threshold to A1C >8% or >7% changed these differences.
RESEARCH DESIGN AND METHODS - Using data from the 1.999-2002 National Health and Nutrition Examination Survey for 843 adults self-reporting diabetes, we computed the mean difference in A1C threshold attainment of >9, >8, and >7% by various case mix factors. The mean difference is the average percentage point difference in threshold attainment for population groups compared with that for the overall population.
RESULTS - Diabetes medication was the only factor for which the difference in threshold attainment increased at lower thresholds, with mean differences of 5.7 percentage points at A1C >9% (reference), 10.1 percentage points at A1C >8% (P < 0.05), and 14.1 percentage points at A1C >7% (P < 0.001).
CONCLUSIONS - As 87% of U.S. adults have A1C <9%, a performance measure threshold of >9% will not drive major improvements in glycemic control. Lower thresholds do not exacerbate differences in threshold attainment for most factors. Reporting by diabetes medication use may compensate for heterogeneous case mix when a performance measure threshold of A1C >8% or lower is used.
C1 [Bainbridge, Kathleen E.] Social & Sci Syst, Silver Spring, MD USA.
[Cowie, Catherine C.; Fradkin, Judith E.] Natl Inst Diabet & Digest & Kidney Dis, Bethesda, MD USA.
[Rust, Keith F.] Westat Corp, Rockville, MD USA.
RP Bainbridge, KE (reprint author), Social & Sci Syst, Silver Spring, MD USA.
EM kbainbridge@s-3.com
FU NIAAA NIH HHS [HHSN267200700001C]; NIDDK NIH HHS [N001-DK-1-2478]; NLM
NIH HHS [HHSN267200700001G]; PHS HHS [HHSN267200700001G]
NR 28
TC 13
Z9 13
U1 0
U2 1
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD SEP
PY 2008
VL 31
IS 9
BP 1754
EP 1760
DI 10.2337/dc07-2010
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 343QN
UT WOS:000258868800010
PM 18509211
ER
PT J
AU Strotmeyer, ES
De Rekeneire, N
Schwartz, AV
Faulkner, KA
Resnick, HE
Goodpaster, BH
Shorr, RI
Vinik, AI
Harris, TB
Newman, AB
AF Strotmeyer, Elsa S.
De Rekeneire, Nathalie
Schwartz, Ann V.
Faulkner, Kimberly A.
Resnick, Helaine E.
Goodpaster, Bret H.
Shorr, Ronald I.
Vinik, Aaron I.
Harris, Tamara B.
Newman, Anne B.
CA Health ABC Study
TI The relationship of reduced peripheral nerve function and diabetes with
physical performance in older white and black adults - The Health,
Aging, and Body Composition (Health ABC) Study
SO DIABETES CARE
LA English
DT Article
ID WOMENS HEALTH; AGE; DISABILITY; NEUROPATHY; FOOT; ASSOCIATION;
IMPAIRMENTS; DYSFUNCTION; MUSCLES; DISEASE
AB OBJECTIVE - Poor peripheral nerve function is prevalent in diabetes and older populations, and it has great potential to contribute to poor physical performance.
RESEARCH DESIGN AND METHODS - Cross-sectional analyses were done for the Health, Aging, and Body Composition (Health ABC) Study participants (n = 2,364; 48% men; 38% black; aged 73-82 years). Sensory and motor peripheral nerve function in legs/feet was assessed by 10- and 1.4-g monofilament perception, vibration detection, and peroneal motor nerve conduction amplitude and velocity. The Health ABC lower-extremity performance battery was a supplemented version of the Established Populations for the Epidemiologic Studies of the Elderly battery (chair stands, standing balance, and 6-m walk), adding increased stand duration, single foot stand, and narrow walk.
RESULTS - Diabetic participants had fewer chair stands (0.34 vs. 0.36 stands/s), shorter standing balance time (0.69 vs. 0.75 ratio), slower usual walking speed (1.11 vs. 1.14 m/s), slower narrow walking speed (0.80 vs. 0.90 m/s), and lower performance battery score (6.43 vs. 6.93) (all P < 0.05). Peripheral nerve function was associated with each physical performance measure independently. After addition of peripheral nerve function in fully adjusted models, diabetes remained significantly related to a lower performance battery score and slower narrow walking speed but not to chair stands, standing balance, or usual walking speed.
CONCLUSIONS - Poor peripheral nerve function accounts for a portion of worse physical performance in diabetes and may be directly associated with physical performance in older diabetic and nondiabetic adults. The impact of peripheral nerve function on incident disability should be evaluated in older adults.
C1 [Strotmeyer, Elsa S.; Faulkner, Kimberly A.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
[De Rekeneire, Nathalie] Epictr, Paris, France.
[Schwartz, Ann V.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Resnick, Helaine E.] Amer Assoc Homes & Serv Aging, Washington, DC USA.
[Goodpaster, Bret H.] Univ Pittsburgh, Sch Med, Div Endocrinol & Metab, Pittsburgh, PA USA.
[Shorr, Ronald I.] Univ Florida, Geriatr Res Educ & Clin Ctr, N Florida S Georgia Vet Hlth Syst, Gainesville, FL USA.
[Shorr, Ronald I.] Univ Florida, Dept Aging & Geriatr, Gainesville, FL USA.
[Vinik, Aaron I.] Eastern Virginia Med Sch, Norfolk, VA 23501 USA.
[Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
[Newman, Anne B.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Newman, Anne B.] Univ Pittsburgh, Grad Sch Publ Hlth, Div Geriatr Med, Pittsburgh, PA USA.
[Newman, Anne B.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
RP Strotmeyer, ES (reprint author), Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
EM strotmeyere@edc.pitt.edu
RI Strotmeyer, Elsa/F-3015-2014; Newman, Anne/C-6408-2013;
OI Newman, Anne/0000-0002-0106-1150; Strotmeyer, Elsa/0000-0002-4093-6036
FU National Institute on Aging [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6-2106, 1-R01-AG 028050]; Intramural Research Program of the
National Institutes of Health; National Institute on Aging; University
of Pittsburgh Claude D. Pepper Older Americans Independence Center
[P30-AG024827]; American Diabetes Association [1-04-JF-46]
FX This work was funded by the National Institute on Aging (contracts
N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106) and 1-R01-AG 028050 (to
E.S.S.) and supported in part by the Intramural Research Program of the
National Institutes of Health, National Institute on Aging, the
University of Pittsburgh Claude D. Pepper Older Americans Independence
Center (P30-AG024827) Pilot Grant (to E.S.S.), and the American Diabetes
Association (1-04-JF-46 to E.S.S.).
NR 24
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U1 1
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PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD SEP
PY 2008
VL 31
IS 9
BP 1767
EP 1772
DI 10.2337/dc08-0433
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 343QN
UT WOS:000258868800012
PM 18535192
ER
PT J
AU Nettleton, JA
Steffen, LM
Ni, H
Liu, K
Jacobs, DR
AF Nettleton, Jennifer A.
Steffen, Lyn M.
Ni, Hanyu
Liu, Kiang
Jacobs, David R., Jr.
TI Dietary patterns and risk of incident type 2 diabetes in the
Multi-Ethnic Study of Atherosclerosis (MESA)
SO DIABETES CARE
LA English
DT Article
ID SWEETENED BEVERAGES; INSULIN-RESISTANCE; METABOLIC SYNDROME;
FOOD-CONSUMPTION; WOMEN; MEN; MELLITUS; COHORT
AB OBJECTIVE - We characterized dietary patterns and their relation to incident type 2 diabetes in 5,011 participants from the Multi-Ethnic Study of Atherosclerosis (MESA).
RESEARCH DESIGN AND METHODS - White, black, Hispanic, and Chinese adults, aged 45-84 years and free of cardiovascular disease and diabetes, completed food frequency questionnaires at baseline (2000-2002). Incident type 2 diabetes was defined at three follow-up exams (2002-2003, 2004-2005, and 2005-2007) as fasting glucose > 126 mg/dl, self-reported type 2 diabetes, or use of diabetes medication. Two types of dietary patterns were studied: four empirically derived (principal components analysis) and one author-defined (low-risk food pattern) as the weighted sum of whole grains, vegetables, nuts/seeds, low-fat dairy, coffee (positively weighted), red meat, processed meat, high-fat dairy, and soda (negatively weighted).
RESULTS - The empirically derived dietary pattern characterized by high intake of tomatoes, beans, refined grains, high-fat dairy, and red meat was associated with an 18% greater risk (hazard ratio per 1-score SD 1.18 [95% CI 1.06-1.321; P-trend = 0.004), whereas the empirically derived dietary pattern characterized by high intake of whole grains, fruit, nuts/seeds, green leafy vegetables, and low-fat dairy was associated with a 15% lower diabetes risk (0.85 [0.76-0.95] P-trend = 0.005). The low-risk food pattern was also inversely associated with diabetes risk (0.87 [0.81-0.99]; P-trend = 0.04). Individual component food groups were not independently associated with diabetes risk. Associations were not modified by sex or race/ethnicity.
CONCLUSIONS - Multiple food groups collectively influence type 2 diabetes risk beyond that of the individual food groups themselves.
C1 [Nettleton, Jennifer A.] Univ Texas Hlth Sci Ctr Houston, Div Epidemiol & Dis Control, Houston, TX USA.
[Ni, Hanyu] NHLBI, NIH, Minneapolis, MN USA.
[Liu, Kiang] Northwestern Univ, Sch Med, Chicago, IL USA.
[Jacobs, David R., Jr.] Univ Oslo, Dept Nutr, Oslo, Norway.
RP Nettleton, JA (reprint author), Univ Texas Hlth Sci Ctr Houston, Div Epidemiol & Dis Control, Houston, TX USA.
EM jennifer.a.nettleton@uth.tmc.edu
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95165,
N01-HC-95169]
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95165 and N01-HC-95169 from the National Heart, Lung, and Blood
Institute.; The authors thank the other investigators, the staff, and
the participants of the MESA study for their valuable contributions (a
full list of participating Multi-Ethnic Study of Atherosclerosis
investigators and institutions can be found at
http://www.mesa-nhlbi.org).
NR 26
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U1 1
U2 9
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD SEP
PY 2008
VL 31
IS 9
BP 1777
EP 1782
DI 10.2337/dc08-0760
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 343QN
UT WOS:000258868800014
PM 18544792
ER
PT J
AU Burbelo, PD
Hirai, H
Leahy, H
Lernmark, A
Ivarsson, SA
Iadarola, MJ
Notkins, AL
AF Burbelo, Peter D.
Hirai, Hiroki
Leahy, Hannah
Lernmark, Ake
Ivarsson, Sten A.
Iadarola, Michael J.
Notkins, Abner Louis
TI A new luminescence assay for autoantibodies to mammalian cell-prepared
insulinoma-associated protein 2
SO DIABETES CARE
LA English
DT Article
ID IA-2
AB OBJECTIVE - Insulinoma-associated protein 2 (IA-2) is a major autoantigen in type I diabetes, and IA-2 autoantibodies are routinely detected by a liquid-phase radioimmunoprecipitation assay. The present experiments were initiated to develop a new assay that does not require the use of radioisotopes or autoantigens prepared in bacteria or by in vitro transcription/translation.
RESEARCH DESIGN AND METHODS - IA-2 luciferase fusion protein was expressed in mammalian cells and assayed for autoantibodies by liquid-phase luciferase immunoprecipitation.
RESULTS - Our study showed that there was no significant difference between the luciferase immunoprecipitation and the radioimmunoprecipitation assays in sensitivity and specificity, and comparison of the two assays revealed a high correlation coefficient (R-2 = 0.805).
CONCLUSIONS - The luciferase system offers a robust, inexpensive, nonradioactive method for the detection of autoantibodies to mammalian cell-prepared IA-2 and could be of practical value at the clinical level.
C1 [Burbelo, Peter D.; Leahy, Hannah; Iadarola, Michael J.] Natl Inst Dent & Craniolacial Res, Sensory Biol Branch, Natl Inst Hlth, Bethesda, MD USA.
[Hirai, Hiroki; Notkins, Abner Louis] Natl Inst Dental & Craniofacial Res, Oral Infect & Immun Branch, Natl Inst Hlth, Bethesda, MD USA.
[Lernmark, Ake] Univ Washington, Dept Clin Sci, RH Williams Lab, Seattle, WA 98195 USA.
[Ivarsson, Sten A.] Lund Univ, Univ Hosp MAS, Dept Clin Sci, Malmo, Sweden.
RP Iadarola, MJ (reprint author), Natl Inst Dent & Craniolacial Res, Sensory Biol Branch, Natl Inst Hlth, Bethesda, MD USA.
EM miadarol@mail.nih.gov; anotkins@mail.nih.gov
FU Intramural Research Program of the National Institute of Dental and
Craniofacial Research; National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Dental and Craniofacial Research, National
Institutes of Health.
NR 7
TC 20
Z9 21
U1 0
U2 0
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD SEP
PY 2008
VL 31
IS 9
BP 1824
EP 1826
DI 10.2337/dc08-0286
PG 3
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 343QN
UT WOS:000258868800022
PM 18535195
ER
PT J
AU O'Sullivan, EP
McDermott, JH
Murphy, MS
Sen, S
Walsh, CH
AF O'Sullivan, E. P.
McDermott, J. H.
Murphy, M. S.
Sen, S.
Walsh, C. H.
TI Declining prevalence of diabetes mellitus in hereditary haemochromatosis
- The result of earlier diagnosis
SO DIABETES RESEARCH AND CLINICAL PRACTICE
LA English
DT Article
DE prevalence; diabetes; hereditary haemochromatosis
ID INSULIN; MUTATIONS; GLUCOSE; POPULATION; SECONDARY; GENE
AB Aims: The aims of this study were to describe the prevalence and clinical features of diabetes in hereditary haemochromatosis (HH), with particular emphasis to how this has changed since the introduction of genetic testing in 1996.
Subjects and methods: Two hundred and thirty-seven patients were diagnosed with HH (based on elevated iron indices and liver biopsy or genetic testing) by a single physician, and all biochemical and clinical data recorded from diagnosis to the end of the study.
Results: The prevalence of diabetes (21.9%) was lower than most previously published studies. There was a significantly greater prevalence of diabetes and cirrhosis in those diagnosed before the introduction of genetic testing, p < 0.001. The type of genetic mutation for HH, degree of ferritin elevation at diagnosis, or the presence of cirrhosis was not predictive for the development of diabetes. Iron depletion did not result in an improvement in glycaemic control or reduction in insulin requirements in the majority of patients.
Conclusions: This is one of the largest published series of diabetes in HH. Because the occurrence of diabetes in patients with HH reduces life expectancy, our finding of a lower prevalence of diabetes is expected to translate into a greater survival rate in these patients. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [O'Sullivan, E. P.; Walsh, C. H.] Univ Hosp, S Infirm Victoria, Dept Endocrinol & Diabet, Cork, Ireland.
[McDermott, J. H.] Connolly Hosp, Dublin, Ireland.
[Murphy, M. S.] Univ Coll Hosp, Galway, Ireland.
[Sen, S.] NIDDK, NIH, Bethesda, MD USA.
RP O'Sullivan, EP (reprint author), Beaumont Hosp, Diabet Day Ctr, Dept Diabet, Dublin 9, Ireland.
EM eoinosullivan@beaumont.ie
NR 21
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U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0168-8227
J9 DIABETES RES CLIN PR
JI Diabetes Res. Clin. Pract.
PD SEP
PY 2008
VL 81
IS 3
BP 316
EP 320
DI 10.1016/j.diabres.2008.05.001
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 350XY
UT WOS:000259388300008
PM 18565609
ER
PT J
AU Montori-Grau, M
Minor, R
Lerin, C
Allard, J
Garcia-Martinez, C
de Cabo, R
Gomez-Foix, AM
AF Montori-Grau, M.
Minor, R.
Lerin, C.
Allard, J.
Garcia-Martinez, C.
de Cabo, R.
Gomez-Foix, A. M.
TI Effects of aging and calorie restriction on rat skeletal muscle glycogen
synthase and glycogen phosphorylase
SO DIABETOLOGIA
LA English
DT Meeting Abstract
C1 [Montori-Grau, M.; Garcia-Martinez, C.; Gomez-Foix, A. M.] Univ Barcelona, E-08007 Barcelona, Spain.
[Lerin, C.] Joslin Diabet Ctr, Div Res, Boston, MA 02215 USA.
[Minor, R.; Allard, J.; de Cabo, R.] NIA, Lab Expt Gerontol, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD SEP
PY 2008
VL 51
SU 1
MA 646
BP S261
EP S261
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 340QN
UT WOS:000258660200645
ER
PT J
AU Perry, JRB
Melzer, D
Maggio, M
Hernandez, D
Singleton, A
Ferrucci, L
Palmer, C
Bennett, A
Ruokonen, A
Panicker, V
Jarvelin, MR
Hattersley, A
McCarthy, M
Frayling, T
AF Perry, J. R. B.
Melzer, D.
Maggio, M.
Hernandez, D.
Singleton, A.
Ferrucci, L.
Palmer, C.
Bennett, A.
Ruokonen, A.
Panicker, V.
Jarvelin, M. -R.
Hattersley, A.
McCarthy, M.
Frayling, T.
TI A Mendelian randomisation study provides initial evidence that sex
hormone binding globulin (SHBG) levels alter type 2 diabetes risk
SO DIABETOLOGIA
LA English
DT Meeting Abstract
C1 [Perry, J. R. B.; Melzer, D.; Hattersley, A.; Frayling, T.] Peninsula Med Sch, Exeter, Devon, England.
[Maggio, M.] NIA, NIH, Baltimore, MD 21224 USA.
[Hernandez, D.; Singleton, A.] NIA, Neurogenet Lab, Bethesda, MD 20892 USA.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Bethesda, MD 20892 USA.
[Palmer, C.] Univ Dundee, Biomed Res Ctr, Dundee DD1 4HN, Scotland.
[Bennett, A.; McCarthy, M.] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
[Ruokonen, A.] Univ Oulu, Oulu, Finland.
[Panicker, V.] Univ Bristol, Henry Wellcome Labs Integrat Neurosci & Endocrino, Bristol BS8 1TH, Avon, England.
[Jarvelin, M. -R.] Univ London Imperial Coll Sci Technol & Med, London, England.
RI Singleton, Andrew/C-3010-2009; Perez , Claudio Alejandro/F-8310-2010
OI Perez , Claudio Alejandro/0000-0001-9688-184X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD SEP
PY 2008
VL 51
SU 1
MA 309
BP S131
EP S131
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 340QN
UT WOS:000258660200309
ER
PT J
AU Rayner, NW
Prokopenko, I
Groves, CJ
Zeggini, E
Hanson, RL
Mitchell, BD
Jia, W
Ng, M
Froguel, P
Chan, J
Bogardus, C
Elbein, SC
Shuldiner, AR
McCarthy, MI
AF Rayner, N. W.
Prokopenko, I.
Groves, C. J.
Zeggini, E.
Hanson, R. L.
Mitchell, B. D.
Jia, W.
Ng, M.
Froguel, P.
Chan, J.
Bogardus, C.
Elbein, S. C.
Shuldiner, A. R.
McCarthy, M. I.
CA Int Type Diabet lq Consortium
TI Large-scale follow-up study does not confirm putative association
signals in the NOS1AP and PKLR gene regions on chromosome 1q with type 2
diabetes
SO DIABETOLOGIA
LA English
DT Meeting Abstract
C1 [Rayner, N. W.; Prokopenko, I.; Groves, C. J.; Zeggini, E.; McCarthy, M. I.] Univ Oxford, WTCHG, Oxford OX1 2JD, England.
[Hanson, R. L.; Bogardus, C.] NIH, NIDDK, Phoenix, AZ USA.
[Mitchell, B. D.; Shuldiner, A. R.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Jia, W.] Shanghai Diabet Inst, Dept Endocrinol & Metab, Shanghai, Peoples R China.
[Ng, M.] Chinese Univ Hong Kong, Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China.
[Elbein, S. C.] Univ Arkansas, Div Endocrinol & Metab, Little Rock, AR 72204 USA.
RI Hanson, Robert/O-3238-2015; Chan, Juliana /B-7918-2016
OI Hanson, Robert/0000-0002-4252-7068; Chan, Juliana /0000-0003-1325-1194
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD SEP
PY 2008
VL 51
SU 1
MA 301
BP S128
EP S128
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 340QN
UT WOS:000258660200301
ER
PT J
AU Brynczka, C
Merrick, BA
AF Brynczka, Christopher
Merrick, B. Alex
TI The p53 transcriptional target gene wnt7b contributes to NGF-inducible
neurite outgrowth in neuronal PC12 cells
SO DIFFERENTIATION
LA English
DT Article
DE wnt7b; wnt; p53; PC12; NGF; neurite; JNK; Fzd
ID NEURAL PRECURSOR CELLS; BETA-CATENIN; PHEOCHROMOCYTOMA CELLS; INT-1
PROTOONCOGENE; NERVOUS-SYSTEM; DIFFERENTIATION; EXPRESSION; ACTIVATION;
PROTEIN; GROWTH
AB Differentiation of PC12 cells by nerve growth factor (NGF) is characterized by changes in signal transduction pathways leading to growth arrest and neurite extension. The transcription factor p53, involved in regulating cell cycle and apoptosis, is also activated during PC12 differentiation and contributes to each of these processes but the mechanisms are incompletely understood. NGF signaling stabilizes p53 protein expression, which enables its transcriptional regulation of target genes, including the newly identified target, wnt7b, a member of the wnt family of secreted morphogens. We tested the hypothesis that wnt7b expression is a factor in NGF-dependent neurite outgrowth of differentiating PC12 cells. Wnt7b transcript and protein levels are increased following NGF treatment in a p53-dependent manner, as demonstrated by a reduction in wnt7b protein levels following stable shRNA-mediated silencing of p53. In addition, overexpressed human tp53 was capable of inducing marked wnt7b expression in neuronal PC12 cells but tp53 overexpression did not elevate wnt7b levels in several tested human tumor cell lines. Ectopic wnt7b overexpression was sufficient to rescue neurite outgrowth in NGF-treated p53-silenced PC12 cells, which could be blocked by c-Jun N-terminal kinase (JNK) inhibition with SP600125 and did not involve beta-catenin nuclear translocation. Addition of sFRP1 to differentiation medium inhibited wnt7b-dependent phosphorylation of JNK, demonstrating that wnt7b is secreted and signals through a JNK-dependent mechanism in PC12 cells. We further identify an NGF-inducible subset of wnt receptors that likely supports wnt7b-mediated neurite extension in PC12 cells. In conclusion, wnt7b is a novel p53-regulated neuritogenic factor in PC12 cells that in conjunction with NGF-regulated Fzd expression is involved in p53-dependent neurite outgrowth through noncanonical JNK signaling.
C1 [Brynczka, Christopher; Merrick, B. Alex] NIEHS, Natl Ctr Toxicogenom, NIH, Res Triangle Pk, NC 27709 USA.
[Brynczka, Christopher] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27606 USA.
RP Merrick, BA (reprint author), NIEHS, Natl Ctr Toxicogenom, NIH, Res Triangle Pk, NC 27709 USA.
EM merrick@niehs.nih.gov
FU Intramural Research Program of the NIH; National Institute of
Environmental Health Sciences
FX This work was supported by the Intramural Research Program of the NIH,
National Institute of Environmental Health Sciences. We thank Dr. Kevin
E. Gerrish and Dr. Serena M. Dudek for critical review of this
manuscript.
NR 64
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U1 0
U2 6
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0301-4681
J9 DIFFERENTIATION
JI Differentiation
PD SEP
PY 2008
VL 76
IS 7
BP 795
EP 808
DI 10.1111/j.1432-0436.2007.00261.x
PG 14
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 339MJ
UT WOS:000258581400005
PM 18177422
ER
PT J
AU Chang, MC
Grieder, FB
AF Chang, Michael C.
Grieder, Franziska B.
TI The baffling multitude of disease models for the study of human disease
- how can the scientist navigate the huge amount of data and receive
guidance?
SO DISEASE MODELS & MECHANISMS
LA English
DT Editorial Material
ID MEDICINE; HEALTH
AB Funding from external sources is the lifeline for most biomedical research scientists. In the USA, the National Institutes of Health (NIH), composed of 27 institutes and centers, is the primary federal agency for conducting and supporting medical research. One of these centers, the National Center for Research Resources (NCRR) provides financial support and resources to clinical or translational scientists working to understand human disease. Through the Division of Comparative Medicine, the NCRR funds projects focused on the development and use of model organisms to understand, diagnose, prevent and treat disease. Here, officials within the NCRR's Division of Comparative Medicine discuss some of the funding opportunities and resources available to researchers who use model organisms, and their perspectives on the future of model organism research.
C1 [Chang, Michael C.; Grieder, Franziska B.] NIH, Natl Ctr Res Resources, Div Comparat Med, Bethesda, MD 20892 USA.
RP Grieder, FB (reprint author), NIH, Natl Ctr Res Resources, Div Comparat Med, 6701 Democracy Blvd, Bethesda, MD 20892 USA.
EM griederf@mail.nih.gov
NR 2
TC 1
Z9 1
U1 0
U2 0
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 1754-8403
J9 DIS MODEL MECH
JI Dis. Model. Mech.
PD SEP-OCT
PY 2008
VL 1
IS 2-3
BP 99
EP 102
DI 10.1242/dmm.001354
PG 4
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 474AH
UT WOS:000268254100009
PM 19048071
ER
PT J
AU Gearhart, PJ
AF Gearhart, Patricia J.
TI Response to "Mutation frequency vs. mutation patterns: A comparison of
the results in spleen and Peyer's patches"
SO DNA REPAIR
LA English
DT Letter
ID SOMATIC HYPERMUTATION; IG GENES
C1 NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Gearhart, PJ (reprint author), NIA, Lab Mol Gerontol, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM gearhartp@grc.nia.nih.gov
FU Intramural NIH HHS [Z01 AG000732-12]
NR 7
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
J9 DNA REPAIR
JI DNA Repair
PD SEP 1
PY 2008
VL 7
IS 9
BP 1411
EP 1412
DI 10.1016/j.dnarep.2008.06.001
PG 2
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 347JK
UT WOS:000259136300003
PM 19727317
ER
PT J
AU Hwang, JY
Smith, S
Ceschia, A
Torres-Rosell, J
Aragon, L
Myung, K
AF Hwang, Ji-Young
Smith, Stephanie
Ceschia, Audrey
Torres-Rosell, Jordi
Aragon, Luis
Myung, Kyungjae
TI Smc5-Smc6 complex suppresses gross chromosomal rearrangements mediated
by break-induced replications
SO DNA REPAIR
LA English
DT Article
DE Smc5-Smc6; gross chromosomal rearrangement; break-induced replication;
checkpoints; translocations
ID DOUBLE-STRAND BREAKS; DNA-DAMAGE CHECKPOINTS; SACCHAROMYCES-CEREVISIAE
HOMOLOG; S-PHASE PROGRESSION; GENOME INSTABILITY; SUMO MODIFICATION; SMC
PROTEINS; TELOMERE ELONGATION; DEFECTIVE-MUTANTS; BLOOMS-SYNDROME
AB Translocations in chromosomes alter genetic information. Although the frequent translocations observed in many tumors suggest the altered genetic information by translocation could promote tumorigenesis, the mechanisms for how translocations are suppressed and produced are poorly understood. The smc6-9 mutation increased the translocation class gross chromosomal rearrangement (GCR). Translocations produced in the smc6-9 strain are unique because they are non-reciprocal and dependent on break-induced replication (BIR) and independent of non-homologous endjoining. The high incidence of translocations near repetitive sequences such as 6 sequences, ARS, tRNA genes, and telomeres in the smc6-9 strain indicates that Smc5-Smc6 suppresses translocations by reducing DNA damage at repetitive sequences. Synergistic enhancements of translocations in strains defective in DNA damage checkpoints by the smc6-9 mutation without affecting de novo telomere addition class GCR suggest that Smc5-Smc6 defines a new pathway to suppress GCR formation. Published by Elsevier B.V.
C1 [Hwang, Ji-Young; Smith, Stephanie; Myung, Kyungjae] NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Ceschia, Audrey; Torres-Rosell, Jordi; Aragon, Luis] Univ London Imperial Coll Sci Technol & Med, Ctr Clin Sci, Cell Cycle Grp, MRC, London, England.
RP Myung, K (reprint author), NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, NIH, Bldg 49,Room 4A22, Bethesda, MD 20892 USA.
EM kmyung@nhgri.nih.gov
RI Torres-Rosell, Jordi/A-4213-2010;
OI Torres-Rosell, Jordi/0000-0003-1308-6926; Hwang,
Ji-Young/0000-0001-8044-1989
FU National Human Genome Research Institute, National Institutes of Health;
Medical Research Council UK
FX We thank S. Lee (U. Texas San Antonio) for helpful discussion; X. Zhao
(Sloan Kettering Cancer Center) for the mms21-11 strain; the NIH fellows
editorial board for comments on the manuscript; J. Fekecs (NHGRI) for
figure preparation. K.M. especially thanks E. Cho. This research was
supported by the intramural research program of the National Human
Genome Research Institute, National Institutes of Health (to K.M.) and
the Medical Research Council UK (to L.A.).
NR 71
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U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
J9 DNA REPAIR
JI DNA Repair
PD SEP 1
PY 2008
VL 7
IS 9
BP 1426
EP 1436
DI 10.1016/j.dnarep.2008.05.006
PG 11
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 347JK
UT WOS:000259136300005
PM 18585101
ER
PT J
AU Martomo, SA
Saribasak, H
Yokoi, M
Hanaoka, F
Gearhart, PJ
AF Martomo, Stella A.
Saribasak, Huseyin
Yokoi, Masayuki
Hanaoka, Fumio
Gearhart, Patricia J.
TI Reevaluation of the role of DNA polymerase theta in somatic
hypermutation of immunoglobulin genes
SO DNA REPAIR
LA English
DT Article
DE somatic hypermutation; class switch recombination; immunoglobulin gene;
DNA polymerase theta; DNA polymerase eta
ID CLASS-SWITCH RECOMBINATION; ANTIBODY GENES; IG GENES; MICE; ETA;
DIVERSIFICATION; MUTATIONS; MECHANISMS; FREQUENCY; REGIONS
AB DNA polymerase theta has been implicated in the process of somatic hypermutation in immunoglobulin variable genes based on several reports of alterations in the frequency and spectra of mutations from Polq(-/-) mice. However, these studies have contrasting results on mutation frequencies and the types of nucleotide substitutions, which question the role of polymerase theta in hypermutation. DNA polymerase eta has a dominant effect on mutation and may substitute in the absence of polymerase theta to affect the pattern. Therefore, we have examined mutation in mice deficient for both polymerases theta and eta. The mutation frequencies in rearranged variable genes from Peyer's patches were similar in wild type, Polq-/-, Polh(-/-), and Polq(-/-) Polh(-/-) mice. The types of substitutions were also similar between wild type and Polq-/- clones, and between Polh(-/-) and Polq(-/-)Polh(-/-) clones. Furthermore, there was no difference in heavy chain class switching in splenic B cells from the four groups of mice. These results indicate that polymerase theta does not play a significant role in the generation of somatic mutation in immunoglobulin genes. Published by Elsevier B.V
C1 [Martomo, Stella A.; Saribasak, Huseyin; Gearhart, Patricia J.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
[Yokoi, Masayuki; Hanaoka, Fumio] Gakushuin Univ, Fac Sci, Toshima Ku, Tokyo 1718588, Japan.
RP Gearhart, PJ (reprint author), NIA, Lab Mol Gerontol, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM gearhartp@grc.nia.nih.gov
RI Saribasak, Huseyin/C-9331-2012
OI Saribasak, Huseyin/0000-0003-0055-062X
FU Intramural Research Program of the NIH, National Institute on Aging
FX We thank J. Chrest, C. Morris, and R. Wersto for flow cytometry; the
entire staff of the Comparative Medicine Section for mouse breeding;
William Yang for technical help, and Robert Maul for comments. mice
heterozygous for pol theta were graciously provided by John Schimenti .
This research was supported by the Intramural Research Program of the
NIH, National Institute on Aging.
NR 28
TC 33
Z9 35
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
J9 DNA REPAIR
JI DNA Repair
PD SEP 1
PY 2008
VL 7
IS 9
BP 1603
EP 1608
DI 10.1016/j.dnarep.2008.04.002
PG 6
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 347JK
UT WOS:000259136300018
PM 18485835
ER
PT J
AU Ghitza, UE
Epstein, DH
Preston, KL
AF Ghitza, Udi E.
Epstein, David H.
Preston, Kenzie L.
TI Self-report of illicit benzodiazepine use on the Addiction Severity
Index predicts treatment outcome
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE contingency management; cocaine abuse; heroin abuse; opiate;
benzodiazepine
ID METHADONE-MAINTENANCE TREATMENT; SUBSTANCE USE DISORDERS; RISK-TAKING
BEHAVIOR; INJECTING DRUG-USERS; COCAINE ABSTINENCE; SOCIAL-ADJUSTMENT;
CONTINGENCY MANAGEMENT; FOLLOW-UP; DEPENDENT PATIENTS; RANDOMIZED-TRIAL
AB The relationship between pre-treatment illicit benzodiazepine use (days of use in the last 30) assessed on the Addiction Severity Index (ASI) and treatment outcome was investigated by retrospective analysis of data from two controlled clinical trials in 361 methadone maintained cocaine/opiate users randomly assigned to 12-week voucher- or prize-based contingency management (CM) or control interventions. Based on screening ASI, participants were identified as non-users (BZD-N; 0 days of use) or users (BZD-U; >0 days of use). Outcome measures were: urine drug screens (thrice weekly): quality of life and self-reported HIV-risk behaviors (every 2 weeks): and current DSM-IV diagnosis of cocaine and heroin dependence (study exit). In the CM group, BZD-U had significantly worse outcomes on in-treatment cocaine use, quality-of-life scores, needle-sharing behaviors, and current heroin dependence diagnoses at study exit compared to BZD-N. In the control group. BZD-U had significantly higher in-treatment cocaine use but did not differ from BZD-N on psychosocial measures. Thus, in a sample of non-dependent BZD users, self-reported illicit BZD use on the ASI, even at low levels, predicted worse outcome on cocaine use and blunted response to CM. Published by Elsevier Ireland Ltd.
C1 [Ghitza, Udi E.; Epstein, David H.; Preston, Kenzie L.] NIDA, Clin Pharmacol & Therapeut Res Branch, Treatment Sect, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
RP Ghitza, UE (reprint author), NIDA, Clin Pharmacol & Therapeut Res Branch, Treatment Sect, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
EM ghitzau@intra.nida.nih.gov
RI Preston, Kenzie/J-5830-2013
OI Preston, Kenzie/0000-0003-0603-2479
FU Intramural NIH HHS [Z01 DA000234-15]
NR 56
TC 9
Z9 9
U1 1
U2 8
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD SEP 1
PY 2008
VL 97
IS 1-2
BP 150
EP 157
DI 10.1016/j.drugalcdep.2008.04.003
PG 8
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 335RQ
UT WOS:000258308100015
PM 18499354
ER
PT J
AU Yu, E
Miotto, K
Akerele, E
Montgomery, A
Elkashef, A
Walsh, R
Montoya, I
Fischman, MW
Collins, J
McSherry, F
Boardman, K
Davies, DK
O'Brien, CP
Ling, W
Kleber, H
Herman, BH
AF Yu, Elmer
Miotto, Karen
Akerele, Evaristo
Montgomery, Ann
Elkashef, Ahmed
Walsh, Robert
Montoya, Ivan
Fischman, Marian W.
Collins, Joseph
McSherry, Frances
Boardman, Kathy
Davies, David K.
O'Brien, Charles P.
Ling, Walter
Kleber, Herbert
Herman, Barbara H.
TI A Phase 3 placebo-controlled, double-blind, multi-site trial of the
alpha-2-adrenergic agonist, lofexidine, for opioid withdrawal
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE lofexidine; alpha-2-adrenergic agonist; opioid withdrawal treatment;
phase 3; placebo-controlled; double-blind; multi-site trail
ID RANDOMIZED CONTROLLED-TRIAL; OPIATE WITHDRAWAL; DETOXIFICATION;
CLONIDINE; ADDICTION; METHADONE; RAT; MORPHINE; NEURONS; LOCUS
AB Context: Lofexidine is an alpha-2-adrenergic receptor agonist that is approved in the United Kingdom for the treatment of opioid withdrawal symptoms. Lofexidine has been reported to have more significant effects on decreasing opioid withdrawal symptoms with less hypotension than clonidine. Objective: To demonstrate that lofexidine is well tolerated and effective in the alleviation of observationally defined opioid withdrawal symptoms in opioid dependent individuals Undergoing medically supervised opioid detoxification as compared to placebo. Design: An inpatient, Phase 3. placebo-controlled. double-blind. randomized mufti-site trial with three phases: (1) opioid agonist stabilization phase (days 1-3), (2) detoxification/medication or placebo phase (clays 4-8). and (3) post detoxification/medication phase (days 9-11). Subjects: Sixty-eight opioid dependent subjects were enrolled at three sites with 35 randomized to lofexidine and 33 to placebo. Main outcome measure: Modified Himmelsbach Opiate Withdrawal Scale (MHOWS) on study day 5 (second opioid detoxification treatment day). Results: Due to significant findings. the study was terminated early. On the study clay 5 MHOWS. Subjects treated with lofexidine had significantly lower scores (equating to fewer/less severe withdrawal symptoms) than placebo subjects (least squares means 19.5 +/- 2.1 versus 30.9 +/- 2.7; p=0.0019). Lofexidine subjects had significantly better retention in treatment than placebo subjects (38.2% versus 15.2%; Log rank test p=0.01). Conclusions: Lofexidine is well tolerated and more efficacious than placebo for reducing opioid withdrawal symptoms in inpatients undergoing medically supervised opioid detoxification. Published by Elsevier Ireland Ltd.
C1 [Yu, Elmer; O'Brien, Charles P.] Univ Penn, Philadelphia, PA 19104 USA.
[Miotto, Karen; Ling, Walter] Univ Calif Los Angeles, David Geffen Sch Med, Long Beach Vet Affairs Med Ctr, Los Angeles, CA 90025 USA.
[Akerele, Evaristo; Fischman, Marian W.; Kleber, Herbert] Columbia Univ Coll Phys & Surg, New York, NY 10032 USA.
[Akerele, Evaristo; Fischman, Marian W.; Kleber, Herbert] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Montgomery, Ann; Elkashef, Ahmed; Walsh, Robert; Montoya, Ivan; Herman, Barbara H.] NIDA, DPMCDA, NIH, Bethesda, MD 20892 USA.
[Collins, Joseph; McSherry, Frances] VA Med Ctr, Dept Vet Affairs Cooperat Studies Program, Perry Point, MD 21902 USA.
[Boardman, Kathy] VACSPCRPCC, Albuquerque, NM 87106 USA.
[Davies, David K.] Britannia Pharmaceut Ltd, Surrey RH1 6YS, England.
RP Yu, E (reprint author), Univ Penn, Philadelphia VAMC 116,Univ & Woodland Ave, Philadelphia, PA 19104 USA.
EM yu_e@mail.trc.upenn.edu
FU Intramural NIH HHS [Z99 DA999999]; NIDA NIH HHS [P50 DA 09236, P50
DA009236, P50 DA009236-05S1, P60 DA 005186, P60 DA005186, P60
DA005186-13, Y1 DA 1001]
NR 42
TC 20
Z9 20
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD SEP 1
PY 2008
VL 97
IS 1-2
BP 158
EP 168
DI 10.1016/j.drugalcdep.2008.04.002
PG 11
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 335RQ
UT WOS:000258308100016
PM 18508207
ER
PT J
AU Eckelman, WC
Reba, RC
Kellof, GJ
AF Eckelman, William C.
Reba, Richard C.
Kellof, Gary J.
TI Targeted imaging: an important biomarker for understanding disease
progression in the era of personalized medicine
SO DRUG DISCOVERY TODAY
LA English
DT Review
ID POSITRON-EMISSION-TOMOGRAPHY; GASTROINTESTINAL STROMAL TUMOR; IN-VIVO;
IMATINIB MESYLATE; DRUG DISCOVERY; GLUCOSE-UTILIZATION;
MALIGNANT-TUMORS; HER2 EXPRESSION; RECEPTOR; PET
AB The key to applying targeted imaging to personalized medicine is the choice of the right radiolabeled probe for the right target for the right disease following the lead of pharmaceutical development. The imaging approach differs depending on whether the target is a single disease control point (e.g. a specific receptor or transport protein linked to the mechanistic activity of a drug) or a general disease control point applicable to a number of treatment paradigms (e.g. proliferation, angiogenesis,inflammation). But in either case, the number of control points must be small given the time constraints on molecular imaging procedures in the clinic. Regardless of the choice, the radiotracer must be validated as binding the target with the appropriate pharmacokinetics and pharmacodynamics for effective external imaging. Such an imaging agent developed in concert with drug development has a built in synergy that will accelerate the drug development process, targeted imaging and personalized medicine as well.
C1 [Eckelman, William C.] Mol Tracer LLC, Bethesda, MD 20814 USA.
[Reba, Richard C.] NIH, Bethesda, MD 20892 USA.
[Kellof, Gary J.] NCI, Bethesda, MD 20892 USA.
RP Eckelman, WC (reprint author), Mol Tracer LLC, Bethesda, MD 20814 USA.
EM wceckelman@verizon.net
NR 71
TC 30
Z9 31
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6446
J9 DRUG DISCOV TODAY
JI Drug Discov. Today
PD SEP
PY 2008
VL 13
IS 17-18
BP 748
EP 759
DI 10.1016/j.drudis.2008.05.009
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 356PP
UT WOS:000259790400003
PM 18617011
ER
PT J
AU Sharma, S
Ou, JH
Strom, S
Mattison, D
Caritis, S
Venkataramanan, R
AF Sharma, Shringi
Ou, Junhai
Strom, Stephen
Mattison, Don
Caritis, Steve
Venkataramanan, Raman
TI Identification of enzymes involved in the metabolism of 17
alpha-hydroxyprogesterone caproate: An effective agent for prevention of
preterm birth
SO DRUG METABOLISM AND DISPOSITION
LA English
DT Article
ID CYTOCHROME-P450 3A4; PREGNANCY; INDUCTION; DELIVERY
AB Preterm delivery, that is delivery before 37 completed weeks of gestation, is the major determinant of neonatal morbidity and mortality. Until recently, no effective therapies for prevention of preterm birth existed. In a recent multicentered trial, 17 alpha-hydroxyprogesterone caproate (17-OHPC) reduced the rate of preterm birth by 33% in a group of high-risk women. Limited pharmacologic data exist for this drug. The recommended dose is empiric; the metabolic pathways are not well defined especially in pregnant women; and the fetal exposure has not been quantified. To define the metabolic pathways of 17-OHPC we used human liver microsomes (HLMs), fresh human hepatocytes (FHHs), and expressed enzymes. HLMs in the presence of NADPH generated three metabolites, whereas two major metabolites were observed with FHHs. Metabolism of 17-OHPC was significantly inhibited by the CYP3A4 inhibitors ketoconazole and troleandomycin in HLM and FHH. Metabolism of 17-OHPC was significantly greater in FHH treated with the CYP3A inducers, rifampin and phenobarbital. Furthermore, studies with expressed enzymes showed that 17-OHPC is metabolized exclusively by CYP3A4 and CYP3A5. The caproic acid ester was intact in the major metabolites generated, indicating that 17-OHPC is not converted to the primary progesterone metabolite, 17 alpha-hydroxyprogesterone. In summary, this study shows that 17-OHPC is metabolized by CYP3A. Because CYP3A is involved in the oxidative metabolism of numerous commonly used drugs, 17-OHPC may be involved in clinically relevant metabolic drug interactions with coadministered CYP3A inhibitors or inducers.
C1 [Sharma, Shringi; Ou, Junhai; Venkataramanan, Raman] Univ Pittsburgh, Sch Pharm, Dept Pharmaceut Sci, Pittsburgh, PA 15261 USA.
[Strom, Stephen; Venkataramanan, Raman] Univ Pittsburgh, Sch Pharm, Dept Pathol, Pittsburgh, PA 15261 USA.
[Mattison, Don] NICHHD, Ctr Res Mothers & Children, OPRU Network, Bethesda, MD 20892 USA.
[Caritis, Steve] Magee Womens Hosp, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA USA.
RP Venkataramanan, R (reprint author), Univ Pittsburgh, Sch Pharm, Dept Pharmaceut Sci, 731 Salk Hall,3501 Terrace St, Pittsburgh, PA 15261 USA.
EM rv@pitt.edu
RI Mattison, Donald/C-2015-2009; Mattison, Donald/L-4661-2013;
OI Mattison, Donald/0000-0001-5623-0874; caritis,
steve/0000-0002-2169-0712; Strom, Stephen/0000-0002-2889-3387
FU NICHD NIH HHS [HD-047905-2]
NR 17
TC 19
Z9 19
U1 0
U2 0
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0090-9556
EI 1521-009X
J9 DRUG METAB DISPOS
JI Drug Metab. Dispos.
PD SEP
PY 2008
VL 36
IS 9
BP 1896
EP 1902
DI 10.1124/dmd.108.021444
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 339WK
UT WOS:000258607800019
PM 18573861
ER
PT J
AU Jessup, CM
Bohannan, BJM
AF Jessup, Christine M.
Bohannan, Brendan J. M.
TI The shape of an ecological trade-off varies with environment
SO ECOLOGY LETTERS
LA English
DT Article
DE adaptive dynamics; bacteria; bacteriophage; divergent selection;
Escherichia coli; microbial ecology; parasitoid-host; pathogen-host;
predator-prey; trade-off
ID FREQUENCY-DEPENDENT SELECTION; TERM EXPERIMENTAL EVOLUTION; LARVAL
COMPETITIVE ABILITY; LOTKA-VOLTERRA SYSTEMS; ESCHERICHIA-COLI K-12;
DROSOPHILA-MELANOGASTER; PARASITOID RESISTANCE; RESOURCE ENRICHMENT;
QUANTILE REGRESSION; ADAPTIVE DYNAMICS
AB Central to most theories that explain the diversity of life is the concept that organisms face trade-offs. Theoretical work has shown that the precise shape of a trade-off relationship affects evolutionary predictions. One common trade-off is that between competitive ability and resistance to predators, parasitoids, pathogens or herbivores. We used a microbial experimental system to elucidate the shape of the relationship between parasitoid resistance and competitive ability. For each of 86 bacteriophage-resistant isolates of the bacterium Escherichia coli B, we measured the degree of resistance to bacteriophage T2 (a viral parasitoid) and relative competitive ability in both the resource environment in which strains were isolated and in two alternate environments. We observed that environmental change can alter trade-off shape, and that different physiological mechanisms can lead to different trade-off shapes and different sensitivities to environmental change. These results highlight the important interaction between environment and trade-off shape in affecting ecological and evolutionary dynamics.
C1 [Jessup, Christine M.] Stanford Univ, Dept Biol Sci, Stanford, CA 94305 USA.
[Bohannan, Brendan J. M.] Univ Oregon, Ctr Ecol & Evolutionary Biol, Eugene, OR 97403 USA.
RP Jessup, CM (reprint author), NIH, Int Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA.
EM cjessup@stanfordalumni.org
FU National Science Foundation [DEB-0408108, DEB-0515598, DEB-0129942]
FX This work was supported by the National Science Foundation (DEB-0408108,
DEB-0515598, and DEB-0129942). David Ackerly, Craig Criddle, Samantha
Forde and Fiorenza Micheli, and three anonymous referees provided
insightful comments on this manuscript. Ellen Edenberg, Weronika Patena,
Alike Wiser and Steve Biller assisted with preliminary experiments.
Discussions with Mike Quance guided the development of the resistance
assay used in these experiments. We are particularly grateful to David
Ackerly for valuable suggestions regarding statistical analysis and data
interpretation.
NR 65
TC 32
Z9 32
U1 4
U2 45
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1461-023X
J9 ECOL LETT
JI Ecol. Lett.
PD SEP
PY 2008
VL 11
IS 9
BP 947
EP 959
DI 10.1111/j.1461-0248.2008.01205.x
PG 13
WC Ecology
SC Environmental Sciences & Ecology
GA 349EB
UT WOS:000259263000007
PM 18557986
ER
PT J
AU Costa-Mattioli, M
Bidinosti, M
Dever, TE
AF Costa-Mattioli, Mauro
Bidinosti, Michael
Dever, Thomas E.
TI Getting the message in protein synthesis - Keystone Symposium on
Translational Regulatory Mechanisms
SO EMBO REPORTS
LA English
DT Editorial Material
DE initiation factor; learning and memory; miRNA; mRNA stability;
translational control
ID MESSENGER-RNA DECAY; INITIATION-FACTORS; RIBOSOMAL-SUBUNIT; SUBSTRATE
RECOGNITION; SYNAPTIC PLASTICITY; EIF2-ALPHA KINASE; PHOSPHORYLATION;
NONSENSE; RELEASE; CELLS
C1 [Dever, Thomas E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
[Costa-Mattioli, Mauro; Bidinosti, Michael] McGill Univ, Dept Biochem, Montreal, PQ H3G 1Y6, Canada.
[Costa-Mattioli, Mauro; Bidinosti, Michael] McGill Univ, McGill Canc Ctr, Montreal, PQ H3G 1Y6, Canada.
RP Dever, TE (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
EM tdever@nih.gov
OI Dever, Thomas/0000-0001-7120-9678
NR 37
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1469-221X
J9 EMBO REP
JI EMBO Rep.
PD SEP
PY 2008
VL 9
IS 10
BP 954
EP 959
DI 10.1038/embor.2008.165
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 355AX
UT WOS:000259682100006
PM 18758437
ER
PT J
AU Csanady, L
Mindell, JA
AF Csanady, Laszlo
Mindell, Joseph A.
TI The twain shall meet: channels, transporters and things between -
Meeting on Membrane Transport in Flux: The Ambiguous Interface between
Channels and Pumps
SO EMBO REPORTS
LA English
DT Editorial Material
DE channel; coupling; gates; occluded state; transporter
ID ANTHRAX TOXIN; GLUTAMATE TRANSPORTER; PROTEIN TRANSLOCATION; ABC
TRANSPORTER; SELECTIVITY; HOMOLOG; DRIVEN; SODIUM
C1 [Csanady, Laszlo] Semmelweis Univ, Dept Med Biochem, H-1088 Budapest, Hungary.
[Mindell, Joseph A.] NINDS, Membrane Transport Biophys Unit, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Csanady, L (reprint author), Semmelweis Univ, Dept Med Biochem, Puskin U 9, H-1088 Budapest, Hungary.
EM csanady@puskin.sote.hu; mindellj@ninds.nih.gov
OI Csanady, Laszlo/0000-0002-6547-5889; Mindell, Joseph/0000-0002-6952-8247
NR 17
TC 3
Z9 3
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1469-221X
J9 EMBO REP
JI EMBO Rep.
PD SEP
PY 2008
VL 9
IS 10
BP 960
EP 965
DI 10.1038/embor.2008.172
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 355AX
UT WOS:000259682100007
PM 18772896
ER
PT J
AU Morens, DM
AF Morens, David M.
TI In memoriam: Michael B. Gregg (1930-2008)
SO EMERGING INFECTIOUS DISEASES
LA English
DT Biographical-Item
C1 NIAID, Natl Inst Hlth, Off Director, Bethesda, MD 20892 USA.
RP Morens, DM (reprint author), NIAID, Natl Inst Hlth, Off Director, Bldg 31,Rm 7A-03,31 Ctr Dr,Mailstop 2520, Bethesda, MD 20892 USA.
EM dm270q@nih.gov
NR 0
TC 1
Z9 1
U1 0
U2 0
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD SEP
PY 2008
VL 14
IS 9
BP 1476
EP 1478
DI 10.3201/eid1409080952
PG 3
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 345JE
UT WOS:000258991700027
PM 18760025
ER
PT J
AU Usdin, TB
Paciga, M
Riordan, T
Kuo, J
Parmelee, A
Petukova, G
Camerini-Otero, RD
Mezey, E
AF Usdin, Ted B.
Paciga, Mark
Riordan, Tim
Kuo, Jonathan
Parmelee, Alissa
Petukova, Galina
Camerini-Otero, R. Daniel
Mezey, Eva
TI Tuberoinfundibular peptide of 39 residues is required for germ cell
development
SO ENDOCRINOLOGY
LA English
DT Article
ID CHROMOSOME SYNAPSIS; NERVOUS-SYSTEM; FEMALE MICE; EXPRESSION; MEIOSIS;
RECEPTOR; RAT; GENE; ENDOCRINE; HOMOLOG
AB Tuberoinfundibular peptide of 39 residues (TIP39) was identified as a PTH 2 receptor ligand. We report that mice with deletion of Tifp39, the gene encoding TIP39, are sterile. Testes contained Leydig and Sertoli cells and spermatogonia but no spermatids. Labeling chromosome spreads with antibodies to proteins involved in recombination showed that spermatogonia do not complete prophase of meiosis I. Chromosomes were observed at different stages of recombination in single nuclei, a defect not previously described with mutations in genes known to be specifically involved in DNA replication and recombination. TIP39 was previously shown to be expressed in neurons projecting to the hypothalamus and within the testes. LH and FSH were slightly elevated in Tifp39(-/-) mice, suggesting intact hypothalamic function. We found using in situ hybridization that the genes encoding TIP39 and the PTH 2 receptor are expressed in a stage-specific manner within seminiferous tubules. Using immunohistochemistry and quantitative RT-PCR, TIP39 expression is greatest in mature testes, and appears most abundant in postmeiotic spermatids, but TIP39 protein and mRNA can be detected before any cells have completed meiosis. We used mice that express Cre recombinase under control of a spermatid-specific promoter to express selectively a cDNA encoding TIP39 in the testes of Tifp39(-/-) mice. Spermatid production and fertility were rescued, demonstrating that the defect in Tifp39(-/-) mice was due to the loss of TIP39. These results show that TIP39 is essential for germ cell development and suggest that it may act as an autocrine or paracrine agent within the gonads.
C1 [Usdin, Ted B.; Paciga, Mark; Riordan, Tim; Kuo, Jonathan] NIMH, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Petukova, Galina; Camerini-Otero, R. Daniel] NIDDK, Bethesda, MD 20892 USA.
[Parmelee, Alissa; Mezey, Eva] Natl Inst Dent & Craniofacial Res, Bethesda, MD 20892 USA.
RP Usdin, TB (reprint author), Bldg 35,35 Convent Dr,MSC 3728, Bethesda, MD 20892 USA.
EM usdint@mail.nih.gov
FU Intramural Program of the National Institutes of Health; National
Institute of Mental Health
FX This research was supported by the Intramural Program of the National
Institutes of Health, National Institute of Mental Health.
NR 44
TC 15
Z9 15
U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD SEP
PY 2008
VL 149
IS 9
BP 4292
EP 4300
DI 10.1210/en.2008-0419
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 340QT
UT WOS:000258660800008
PM 18483145
ER
PT J
AU Muniyappa, R
Iantorno, M
Quon, MJ
AF Muniyappa, Ranganath
Iantorno, Micaela
Quon, Michael J.
TI An Integrated View of Insulin Resistance and Endothelial Dysfunction
SO ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA
LA English
DT Review
ID NITRIC-OXIDE SYNTHASE; TYPE-2 DIABETES-MELLITUS; MUSCLE GLUCOSE-UPTAKE;
C-REACTIVE PROTEIN; CARDIOVASCULAR RISK-FACTORS;
POLYCYSTIC-OVARY-SYNDROME; CORONARY-ARTERY-DISEASE; FLOW-MEDIATED
DILATION; HUMAN SKELETAL-MUSCLE; ORAL VITAMIN-C
AB Endothelial dysfunction and insulin resistance are frequently comorbid states. Vasodilator actions of insulin are mediated by phosphatidylinositol 3-kinase (PI3K)-dependent signaling pathways that stimulate production of nitric oxide from vascular endothelium. This helps to couple metabolic and hemodynamic homeostasis under healthy conditions. In pathologic states, shared causal factors, including glucotoxicity, lipotoxicity, and inflammation selectively impair PI3K-dependent insulin signaling pathways that contribute to reciprocal relationships between insulin resistance and endothelial dysfunction. This article discusses the implications of pathway-selective insulin resistance in vascular endothelium, interactions between endothelial dysfunction and insulin resistance, and therapeutic interventions that may simultaneously improve both metabolic and cardiovascular physiology in insulin-resistant conditions.
C1 [Muniyappa, Ranganath; Iantorno, Micaela; Quon, Michael J.] NIH, Diabet Unit, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
RP Quon, MJ (reprint author), NIH, Diabet Unit, Natl Ctr Complementary & Alternat Med, 9 Mem Dr,Bldg 9,Room 1N-105,MSC 0920, Bethesda, MD 20892 USA.
EM quonm@nih.gov
OI Quon, Michael/0000-0002-9601-9915; Quon , Michael /0000-0002-5289-3707
FU Intramural Research Program; NCCAM; NIH
FX This work was supported by the Intramural Research Program, NCCAM, NIH.
NR 148
TC 76
Z9 79
U1 0
U2 9
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8529
EI 1558-4410
J9 ENDOCRIN METAB CLIN
JI Endocrinol. Metabol. Clin. North Amer.
PD SEP
PY 2008
VL 37
IS 3
BP 685
EP +
DI 10.1016/j.ecl.2008.06.001
PG 29
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 357WJ
UT WOS:000259877600010
PM 18775359
ER
PT J
AU Bjornstad, ON
Grenfell, BT
AF Bjornstad, Ottar N.
Grenfell, Bryan T.
TI Hazards, spatial transmission and timing of outbreaks in epidemic
metapopulations
SO ENVIRONMENTAL AND ECOLOGICAL STATISTICS
LA English
DT Article; Proceedings Paper
CT Spring Meeting of the Eastern North American Region of the
International-Biometric-Society
CY MAR 20-23, 2005
CL Austin, TX
SP Int Biomet Soc, Eastern N Amer Reg
DE measles; inter-epidemic periods; TSIR model; disease ecology; population
dynamics
ID MEASLES METAPOPULATION; COMMUNITY SIZE; TIME-SERIES; DYNAMICS; DISEASES;
MODEL; STOCHASTICITY; DETERMINISM; HIERARCHIES; STATES
AB Highly infectious, immunizing pathogens can cause violent local outbreaks that are followed by the agent's extinction as it runs out of susceptible hosts. For these pathogens, regional persistence can only be secured through spatial transmission and geographically asynchronous epidemics. In this paper we develop a hazard model for the waiting time between epidemics. We use the model, first, to discuss the predictability in timing of epidemics, and, second, to estimate the strength of spatial transmission. Based on the hazard model, we conclude that highly epidemic pathogens can at times be predictable in the sense that the waiting-time distribution between outbreaks is probabilistically bounded; The greater the spatial transmission the more periodic the outbreak dynamics. When we analyze the historical records of measles outbreaks in England and Wales between 1944 and 1965, we find the waiting-time between epidemics to depend inversely on community size. This is because large communities are much more tightly coupled to the regional metapopulation. The model further help identify the most important areas for spatial transmission. We conclude that the data on absence of these pathogens is the key to understanding spatial spread.
C1 [Bjornstad, Ottar N.] Penn State Univ, Dept Entomol, University Pk, PA 16802 USA.
[Bjornstad, Ottar N.; Grenfell, Bryan T.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Bjornstad, Ottar N.; Grenfell, Bryan T.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Bjornstad, ON (reprint author), Penn State Univ, Dept Entomol, University Pk, PA 16802 USA.
EM onb1@psu.edu
RI Bjornstad, Ottar/I-4518-2012
NR 30
TC 8
Z9 8
U1 2
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1352-8505
EI 1573-3009
J9 ENVIRON ECOL STAT
JI Environ. Ecol. Stat.
PD SEP
PY 2008
VL 15
IS 3
BP 265
EP 277
DI 10.1007/s10651-007-0059-3
PG 13
WC Environmental Sciences; Mathematics, Interdisciplinary Applications;
Statistics & Probability
SC Environmental Sciences & Ecology; Mathematics
GA 334TI
UT WOS:000258243700002
ER
PT J
AU Kan, HD
London, SJ
Chen, GH
Zhang, YH
Song, GX
Zhao, NQ
Jiang, LL
Chen, BH
AF Kan, Haidong
London, Stephanie J.
Chen, Guohai
Zhang, Yunhui
Song, Guixiang
Zhao, Naiqing
Jiang, Lili
Chen, Bingheng
TI Season, sex, age, and education as modifiers of the effects of outdoor
air pollution on daily mortality in Shanghai, China: The Public Health
and Air Pollution in Asia (PAPA) study
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE air pollution; modifiers; mortality; time-series studies
ID CASE-CROSSOVER ANALYSIS; TIME-SERIES ANALYSIS; PARTICULATE MATTER;
SENSITIVITY-ANALYSIS; NATIONAL MORBIDITY; EXPOLIS-HELSINKI; EUROPEAN
CITIES; WESTERN-EUROPE; APHEA PROJECT; US CITIES
AB BACKGROUND: Various factors can modify the health effects of outdoor air pollution. Prior findings about modifiers are inconsistent, and most of these studies were conducted in developed countries.
OBJECTIVES: We conducted a time-series analysis to examine the modifying effect of season, sex, age, and education on the association between outdoor air pollutants [particulate matter < 10 mu m in aerodynamic diameter (PM10), sulfur dioxide, nitrogen dioxide, and ozone] and daily mortality in Shanghai, China, using 4 years of daily data (2001-2004).
METHODS: Using a natural spline model to analyze the data, we examined effects of air pollution for the warm season (April-September) and cool season (October-March) separately. For total mortality, we examined the association stratified by sex and age. Stratified analysis by educational attainment was conducted for total, cardiovascular, and respiratory mortality.
RESULTS: Outdoor air pollution was associated with mortality from all causes and from cardiorespiratory diseases in Shanghai. An increase of 10 mu g/m(3) in a 2-day average concentration of PM10, SO2, NO2, and O-3 corresponds to increases in all-cause mortality of 0.25% [95% confidence interval (CI), 0.14-0.37), 0.95% (95% CI, 0.62-1.28), 0.97% (95% CI, 0.66-1.27), and 0.31% (95% CI, 0.04-0.58), respectively. The effects of air pollutants were more evident in the cool season than in the warm season, and females and the elderly were more vulnerable to outdoor air pollution. Effects of air pollution were generally greater in residents with low educational attainment (illiterate or primary school) compared with those with high educational attainment (middle school or above).
CONCLUSIONS: Season, sex, age, and education may modify the health effects of outdoor air pollution in Shanghai. These findings provide new information about the effects of modifiers on the relationship between daily mortality and air pollution in developing countries mid may have implications for local environmental and social policies.
C1 [Kan, Haidong; Zhang, Yunhui; Chen, Bingheng] Fudan Univ, Dept Environm Hlth, Sch Publ Hlth, Shanghai 200032, Peoples R China.
[Kan, Haidong; London, Stephanie J.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, US Dept HHS, Res Triangle Pk, NC USA.
[Chen, Guohai] Shanghai Environm Monitoring Ctr, Shanghai, Peoples R China.
[Song, Guixiang; Jiang, Lili] Shanghai Municipal Ctr Dis Control & Prevent, Shanghai, Peoples R China.
[Zhao, Naiqing] Fudan Univ, Sch Publ Hlth, Dept Hlth Stat, Shanghai 200433, Peoples R China.
RP Kan, HD (reprint author), Fudan Univ, Dept Environm Hlth, Sch Publ Hlth, Shanghai 200032, Peoples R China.
EM haidongkan@gmail.com
OI London, Stephanie/0000-0003-4911-5290
FU Intramural NIH HHS
NR 52
TC 177
Z9 205
U1 14
U2 68
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD SEP
PY 2008
VL 116
IS 9
BP 1183
EP 1188
DI 10.1289/ehp.10851
PG 6
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 345TP
UT WOS:000259020100032
PM 18795161
ER
PT J
AU Wong, CM
Vichit-Vadakan, N
Kan, HD
Qian, ZM
AF Wong, Chit-Ming
Vichit-Vadakan, Nuntavarn
Kan, Haidong
Qian, Zhengmin
CA PAPA Project Teams
TI Public Health and Air Pollution in Asia (PAPA): A multicity study of
short-term effects of air pollution on mortality
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE air pollution; Bangkok; Hong Kong; mortality; Shanghai; time-series
analysis; Wuhan
ID PARTICULATE MATTER; NITROGEN-DIOXIDE; APHEA PROJECT; TIME-SERIES;
EXPOSURE; BANGKOK; CITIES; ASSOCIATIONS; POLLUTANTS; THAILAND
AB BACKGROUND AND OBJECTIVES: Although the deleterious effects of air pollution from fossil fuel combustion have been demonstrated in many Western nations, fewer studies have been conducted in Asia. The Public Health and Air Pollution in Asia (PAPA) project assessed the effects of short-term exposure to air pollution on daily mortality in Bangkok, Thailand, and in three cities in China: Hong Kong, Shanghai, and Wuhan.
METHODS: Poisson regression models incorporating natural spline smoothing functions were used to adjust for seasonality and other time-varying covariates that might confound the association between air pollution and mortality. Effect estimates were determined for each city and then for the cities combined using a random effects method.
RESULTS: In individual cities, associations were detected between most of the pollutants [nitrogen dioxide, sulfur dioxide, particulate matter <= 10 mu m in aerodynamic diameter (PM10), and ozone] and most health outcomes under study (i.e., all natural-cause, cardiovascular, and respiratory mortality). The city-combined effects of the four pollutants tended to be equal or greater than those identified in studies conducted in Western industrial nations. In addition, residents of Asian cities are likely to have higher exposures to air pollution than those in Western industrial nations because they spend more time outdoors and less time in air conditioning.
CONCLUSIONS: Although the social and environmental conditions may be quite different, it is reasonable to apply estimates derived from previous health effect of air pollution studies in the West to Asia.
C1 [Wong, Chit-Ming] Univ Hong Kong, Dept Community Med, Sch Publ Hlth, Hong Kong, Hong Kong, Peoples R China.
[Vichit-Vadakan, Nuntavarn] Thammasat Univ, Fac Publ Hlth, Pathum Thani, Thailand.
[Kan, Haidong] Fudan Univ, Sch Publ Hlth, Shanghai 200433, Peoples R China.
[Kan, Haidong] Natl Inst Environm Hlth Sci, Epidemiol Branch, Res Triangle Pk, NC USA.
[Qian, Zhengmin] Penn State Univ, Coll Med, Hershey, PA USA.
[Qian, Zhengmin] Geisinger Ctr Hlth Res, Danville, PA USA.
RP Wong, CM (reprint author), Univ Hong Kong, Dept Community Med, Sch Publ Hlth, 5-F William MW Mong Block,21 Sassoon Rd, Hong Kong, Hong Kong, Peoples R China.
EM hrmrwcm@hkucc.hku.hk
RI Wong, Chit Ming/C-4438-2009;
OI Thomas, Graham Neil/0000-0002-2777-1847; London,
Stephanie/0000-0003-4911-5290
NR 28
TC 171
Z9 192
U1 10
U2 82
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD SEP
PY 2008
VL 116
IS 9
BP 1195
EP 1202
DI 10.1289/ehp.11257
PG 8
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 345TP
UT WOS:000259020100034
PM 18795163
ER
PT J
AU Tinkle, SS
AF Tinkle, Sally S.
TI Nanotechnology: Collaborative opportunities for ecotoxicology and
environmental health
SO ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY
LA English
DT Editorial Material
C1 Natl Inst Environm Hlth Sci, Natl Inst Hlth, Durham, NC USA.
RP Tinkle, SS (reprint author), Natl Inst Environm Hlth Sci, Natl Inst Hlth, Durham, NC USA.
NR 4
TC 6
Z9 6
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0730-7268
J9 ENVIRON TOXICOL CHEM
JI Environ. Toxicol. Chem.
PD SEP
PY 2008
VL 27
IS 9
BP 1823
EP 1824
DI 10.1897/08-266.1
PG 2
WC Environmental Sciences; Toxicology
SC Environmental Sciences & Ecology; Toxicology
GA 335WT
UT WOS:000258325000001
PM 19086312
ER
PT J
AU Hoffman, CS
Mendola, P
Savitz, DA
Herring, AH
Loomis, D
Hartmann, KE
Singer, PC
Weinberg, HS
Olshan, AF
AF Hoffman, Caroline S.
Mendola, Pauline
Savitz, David A.
Herring, Amy H.
Loomis, Dana
Hartmann, Katherine E.
Singer, Philip C.
Weinberg, Howard S.
Olshan, Andrew F.
TI Drinking water disinfection by-product exposure and fetal growth
SO EPIDEMIOLOGY
LA English
DT Article
ID ADVERSE PREGNANCY OUTCOMES; BIRTH-WEIGHT; TRIHALOMETHANE LEVELS;
GESTATIONAL-AGE; UNITED-STATES; CONTAMINANTS; ASSOCIATION; CONSUMPTION;
POPULATION; CHLOROFORM
AB Previous studies suggest that elevated exposure 10 drinking water disinfection by-products (DBPs)-in particular, total trihalomethanes (TTHMs-may lead to fetal growth restriction. We examined the effects of exposure to TTHMs, haloacetic acids, and total organic halide oil the probability of delivering small-for-gestational-age (SGA) infant and on birth weight al term.
Methods: Women early fit pregnancy (: 12 weeks' gestation) or planning a pregnancy were enrolled in a prospective pregnancy study conducted in 3 US communities from 2000 through 2004. Weekly (or biweekly) water samples were collected at each site as well as individual-level participant data. Associations between DBP exposures (T-THMs, halolacetic acids. total organic halide) and fetal growth Were assessed Using log-binomial regression for SGA (it 1958) and linear regression For term birth weight (it - 1854). We conducted I Bayesian analysis to examine associations between individual DBP species and fetal growth.
Results: Haloacetic acids and total organic halide were not associated with SGA or term birth weight. The probability of delivering an SGA infant was elevated when comparing women with an average third-trimester residential TTHM concentration >= 80 mu g/L to women with exposure <80 mu g/L (risk ratio = 2.0 [95% confidence interval 1.1-3.6]), but not when examining other exposure contrasts. Bayesian analyses did not support l Consistent association,growth although these analyses between any DBP species and fetal g were based oil small sample sizes.
Conclusions: Our results do not suggest an adverse effect of haloacetic acid or total organic halide exposure oil fetal growth. All association ol'TTI-INI with SGA was seen only for average r sid tial concentrations above the current( extraordinary standard.
C1 [Hoffman, Caroline S.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Mendola, Pauline] US EPA, Human Studies Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA.
[Savitz, David A.] Mt Sinai Sch Med, Dept Community & Preventat Med, New York, NY USA.
[Herring, Amy H.] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Herring, Amy H.] Univ N Carolina, Carolina Populat Ctr, Chapel Hill, NC USA.
[Loomis, Dana] Univ Nevada, Sch Publ Hlth, Reno, NV 89557 USA.
[Hartmann, Katherine E.] Vanderbilt Univ, Med Ctr, Dept Obstet & Gynecol, Nashville, TN 37232 USA.
[Hartmann, Katherine E.] Vanderbilt Univ, Med Ctr, Inst Med & Publ Hlth, Nashville, TN USA.
[Singer, Philip C.; Weinberg, Howard S.; Olshan, Andrew F.] Univ N Carolina, Dept Environm Sci & Engn, Chapel Hill, NC USA.
RP Hoffman, CS (reprint author), Natl Inst Environm Hlth Sci, POB 12233,MD EC-21, Res Triangle Pk, NC 27709 USA.
EM dilworthch@niehs.nih.gov
OI Mendola, Pauline/0000-0001-5330-2844
FU NIEHS NIH HHS [5-T32-ES07018]; PHS HHS [P30E510126]
NR 41
TC 49
Z9 53
U1 2
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD SEP
PY 2008
VL 19
IS 5
BP 729
EP 737
DI 10.1097/EDE.0b013e3181812bd4
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 341KB
UT WOS:000258712000014
PM 18633330
ER
PT J
AU Kinoshita-Moleka, R
Smith, JS
Atibu, J
Tshefu, A
Hemingway-Foday, J
Hobbs, M
Bartz, J
Koch, MA
Rimoin, AW
Ryder, RW
AF Kinoshita-Moleka, R.
Smith, J. S.
Atibu, J.
Tshefu, A.
Hemingway-Foday, J.
Hobbs, M.
Bartz, J.
Koch, M. A.
Rimoin, A. W.
Ryder, R. W.
TI Low prevalence of HIV and other selected sexually transmitted infections
in 2004 in pregnant women from Kinshasa, the Democratic Republic of the
Congo
SO EPIDEMIOLOGY AND INFECTION
LA English
DT Article
ID SUB-SAHARAN AFRICA; POPULATIONS; SUBTYPES; NIGERIA; SPREAD
AB This study examined the prevalence of HIV and other sexually transmitted infections (STIs) in pregnant women in Kinshasa, the Democratic Republic of the Congo (DRC). Between April and July 2004., antenatal attendees at two of the largest maternity clinics in Kinshasa were tested to identify HIV status, syphilis, Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG). HIV seroprevalence was 1.9 % in 2082 women. With PCR techniques, CT and NG infections were also uncommon in the first 529 women (1.7% and 0.4%, respectively). No active syphilis infection case was identified by Treponema pallidum haemagglutination assay (TPHA) and rapid plasma reagin test (RPR). A woman's risk of HIV infection was significantly associated with her reporting a male partner having had other female sexual partners (OR 2.7, 95 % CI 1.2-6.2). The continuing low seroprevalence of HIV in pregnant women from Kinshasa was confirmed. Understanding factors associated with this phenomenon could help prevent a future HIV epidemic in low HIV transmission areas in Africa.
C1 [Kinoshita-Moleka, R.; Smith, J. S.; Ryder, R. W.] Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27515 USA.
[Kinoshita-Moleka, R.; Atibu, J.] UNC DRC Program, Kinshasa, Zaire.
[Tshefu, A.] Kinshasa Sch Publ Hlth, Kinshasa, Zaire.
[Hemingway-Foday, J.; Bartz, J.; Koch, M. A.] RTI Int, Res Triangle Pk, NC USA.
[Hobbs, M.; Ryder, R. W.] Univ N Carolina, Sch Med, Chapel Hill, NC USA.
[Rimoin, A. W.] NIH, Bethesda, MD 20892 USA.
[Rimoin, A. W.] Univ Calif Los Angeles, Dept Epidemiol, Sch Publ Hlth, Los Angeles, CA USA.
RP Smith, JS (reprint author), Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27515 USA.
EM jennifers@unc.edu
FU Global Network for Women's and Children's Health Research [NICHD U01
HD043475-01]; Bill & Melinda Gates Foundation; Center for AIDS Research
[5 P30 A1050410-07 NIAID]; North Carolina STI; Topical Microbicide
Cooperative Research Center [5 U19 AI031496-14]
FX The authors acknowledge K. Rich (UNC-CH Microbiology Laboratory) and S.
Edidi (DRC National AIDS Reference Laboratory) for laboratory technical
support. G. Mpanya, M. Onyamboko, and K. Mwandagalirwa worked in the
planning and implementation phases of the study. This work was financed
by the Global Network for Women's and Children's Health Research (NICHD
U01 HD043475-01) and the Bill & Melinda Gates Foundation. J. Smith was
supported through a Center for AIDS Research grant (5 P30 A1050410-07
NIAID). Logistical support for STI testing was provided by the North
Carolina STI and Topical Microbicide Cooperative Research Center grant
(5 U19 AI031496-14).
NR 28
TC 12
Z9 12
U1 0
U2 2
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0950-2688
J9 EPIDEMIOL INFECT
JI Epidemiol. Infect.
PD SEP
PY 2008
VL 136
IS 9
BP 1290
EP 1296
DI 10.1017/S095026S807009818
PG 7
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 350DI
UT WOS:000259332400019
PM 18028581
ER
PT J
AU Probstfield, JL
Wright, JT
Einhorn, PT
Pressel, S
Davis, BR
AF Probstfield, J. L.
Wright, J. T.
Einhorn, P. T.
Pressel, S.
Davis, B. R.
CA ALLHAT Investigators
TI ALLHAT findings revisited 5 years later in the context of subsequent
analyses
SO EUROPEAN HEART JOURNAL
LA English
DT Meeting Abstract
C1 [Probstfield, J. L.] Univ Washington, Seattle, WA 98195 USA.
[Wright, J. T.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Einhorn, P. T.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Pressel, S.; Davis, B. R.] Univ Texas Houston, Sch Publ Hlth, Houston, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
J9 EUR HEART J
JI Eur. Heart J.
PD SEP
PY 2008
VL 29
SU 1
BP 511
EP 511
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA V28TG
UT WOS:000208702502458
ER
PT J
AU Koh, K
Oh, P
Quon, M
Han, S
Chung, W
Shin, E
AF Koh, K.
Oh, P.
Quon, M.
Han, S.
Chung, W.
Shin, E.
TI Significant differential metabolic effects of lipophilic and hydrophilic
statins in hypercholesterolemic patients
SO EUROPEAN HEART JOURNAL
LA English
DT Meeting Abstract
C1 [Koh, K.] Gachon Med Sch, Div Cardiol, Gil Heart Ctr, Inchon, South Korea.
[Oh, P.; Han, S.; Chung, W.; Shin, E.] Gachon Univ, Gil Med Ctr, Inchon, South Korea.
[Quon, M.] NIH, Diabet Unit, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
J9 EUR HEART J
JI Eur. Heart J.
PD SEP
PY 2008
VL 29
SU 1
BP 614
EP 615
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA V28TG
UT WOS:000208702503163
ER
PT J
AU Montero, CI
Shea, YR
Jones, PA
Harrington, SM
Tooke, NE
Witebsky, FG
Murray, PR
AF Montero, C. I.
Shea, Y. R.
Jones, P. A.
Harrington, S. M.
Tooke, N. E.
Witebsky, F. G.
Murray, P. R.
TI Evaluation of Pyrosequencing (R) technology for the identification of
clinically relevant non-dematiaceous yeasts and related species
SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES
LA English
DT Article
ID MOLECULAR-IDENTIFICATION; CRYPTOCOCCUS-NEOFORMANS;
TRICHOSPORON-PULLULANS; CANDIDA-ORTHOPSILOSIS; FUNGAL PATHOGENS;
METAPSILOSIS; PARAPSILOSIS; INFECTION; DISEASE; COMPLEX
AB Pyrosequencing was used to identify 133 isolates of clinically relevant non-dematiaceous yeasts. These included 97 ATCC strains (42 type strains), seven UAMH strains, and 29 clinical isolates. Isolates belonged to the following genera: Candida (18 species), Trichosporon (10), Cryptococcus (7), Malassezia (3), Rhodotorula (2), Geotrichum (1), Blastoschizomyces (1), and Kodamaea (1). Amplicons of a hyper-variable ITS region were obtained and analyzed using Pyrosequencing technology. The data were evaluated by a BLAST search against the GenBank database and correlated with data obtained by conventional cycle sequencing of the ITS1-5.8S-ITS2 region. Cycle sequencing identified 78.9% of the isolates to the species level. Pyrosequencing technology identified 69.1%. In 90.1% of all of the strains tested, the identification results of both sequencing methods were identical. Most Candida isolates can be identified to the species level by Pyrosequencing. Trichosporon species and some Cryptococcus species cannot be differentiated at the species level. Pyrosequencing can be used for the reliable identification of most commonly isolated non-dematiaceous yeasts, with a reduction of cost per identification compared to conventional sequencing.
C1 [Montero, C. I.; Shea, Y. R.; Jones, P. A.; Witebsky, F. G.; Murray, P. R.] NIH, Microbiol Serv, Dept Lab Med, Clin Ctr,US Dept HHS, Bethesda, MD 20892 USA.
[Harrington, S. M.] Albany Med Ctr, Dept Clin Microbiol, Albany, NY 12208 USA.
[Tooke, N. E.] Biotage AB, S-75318 Uppsala, Sweden.
RP Montero, CI (reprint author), NIH, Microbiol Serv, Dept Lab Med, Clin Ctr,US Dept HHS, 10 Ctr Dr,MSC 1508, Bethesda, MD 20892 USA.
EM monteroc@cc.nih.gov
FU NIH Clinical Center
FX We thank Patricia S. Conville, Department of Laboratory Medicine, Warren
Grant Magnuson Clinical Center, NIH, for her technical assistance. This
research was supported by the Intramural Research Program of the NIH
Clinical Center. The views expressed herein are those of the authors and
should not be construed as those of the U. S. Department of Health and
Human Services.
NR 37
TC 26
Z9 30
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0934-9723
J9 EUR J CLIN MICROBIOL
JI Eur. J. Clin. Microbiol. Infect. Dis.
PD SEP
PY 2008
VL 27
IS 9
BP 821
EP 830
DI 10.1007/s10096-008-0510-x
PG 10
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 337RK
UT WOS:000258453000008
PM 18421488
ER
PT J
AU de Snoo, FA
Hottenga, JJ
Gillanders, EM
Sandkuijl, LA
Jones, MP
Bergman, W
van der Drift, C
van Leeuwen, I
van Mourik, L
ter Huurne, JAC
Frants, RR
Willemze, R
Breuning, MH
Trent, JM
Gruis, NA
AF de Snoo, Femke A.
Hottenga, Jouke-Jan
Gillanders, Elizabeth M.
Sandkuijl, Loudewijk A.
Jones, Mary Pat
Bergman, Wilma
van der Drift, Clasine
van Leeuwen, Inge
van Mourik, Lenny
ter Huurne, Jeanet A. C.
Frants, Rune R.
Willemze, Rein
Breuning, Martijn H.
Trent, Jeffrey M.
Gruis, Nelleke A.
TI Genome-wide linkage scan for atypical nevi in p16-Leiden melanoma
families
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE nevus gene; familial melanoma; linkage
ID FAMMM SYNDROME FAMILIES; GERMLINE MUTATION; CDKN2A MUTATIONS;
SUSCEPTIBILITY; PENETRANCE; CANCER; GENE; TWIN; COUNT; MAP
AB In most Dutch melanoma families, a founder deletion in the melanoma susceptibility gene CDKN2A (which encodes p16) is present. This founder deletion (p16-Leiden) accounts for a significant proportion of the increased melanoma risk. However, it does not account for the Atypical Nevus (AN) phenotype that segregates in both p16-Leiden carriers and non-carriers. The AN-affected p16-Leiden family members are therefore a unique valuable resource for unraveling the genetic etiology of the AN phenotype, which is considered both a risk factor and a precursor lesion for melanoma. In this study, we performed a genome-wide scan for linkage in four p16-Leiden melanoma pedigrees, classifying family members with five or more AN as affected. The strongest evidence for an atypical nevus susceptibility gene was mapped to chromosome band 7q21.3 (two-point LOD score 2.751), a region containing candidate gene CDK6.
C1 [de Snoo, Femke A.; van Mourik, Lenny; ter Huurne, Jeanet A. C.; Frants, Rune R.; Breuning, Martijn H.] Leiden Univ, Med Ctr, Dept Human, NL-2333 ZA Leiden, Netherlands.
[de Snoo, Femke A.; van Mourik, Lenny; ter Huurne, Jeanet A. C.; Frants, Rune R.; Breuning, Martijn H.] Leiden Univ, Med Ctr, Dept Clin Genet, NL-2333 ZA Leiden, Netherlands.
[Hottenga, Jouke-Jan; Gruis, Nelleke A.] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands.
[Gillanders, Elizabeth M.; Jones, Mary Pat] NHGRI, Inherited Dis Res Branch, NIH, Dept Hlth & Human Serv, Baltimore, MD USA.
[Sandkuijl, Loudewijk A.] Leiden Univ, Med Ctr, Dept Med Stat, Leiden, Netherlands.
[Bergman, Wilma; van der Drift, Clasine; van Leeuwen, Inge; Willemze, Rein] Leiden Univ, Med Ctr, Dept Dermatol, Leiden, Netherlands.
[Trent, Jeffrey M.] Translat Genom Res Inst, Phoenix, AZ USA.
RP de Snoo, FA (reprint author), Leiden Univ, Med Ctr, Ctr Human & Clin Genet, Dept Clin Genet, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
EM desnoo@lumc.nl
OI Gruis, Nelleke/0000-0002-5210-9150
FU Dutch Cancer Society [RUL 99-1932]; Aspasia fellowship of the
Netherlands organization for Scientific Research
FX We are indebted to the family members for their past and recent
participation in our research. FAS is supported by the Dutch Cancer
Society (RUL 99-1932); NAG is a recipient of an Aspasia fellowship of
the Netherlands organization for Scientific Research.
NR 26
TC 11
Z9 11
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD SEP
PY 2008
VL 16
IS 9
BP 1135
EP 1141
DI 10.1038/ejhg.2008.72
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 344LX
UT WOS:000258929800016
PM 18398432
ER
PT J
AU Jatav, V
Mishra, P
Kashaw, S
Stables, JP
AF Jatav, Varsha
Mishra, Pradeep
Kashaw, Sushil
Stables, J. P.
TI CNS depressant and anticonvulsant activities of some novel
3-[5-substituted 1,3,4-thiadiazole-2-yl]-2-styryl quinazoline-4(3H)-ones
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Styryl quinazoline-4(3H)-ones; 1,3,4-Thiadiazole; MES; Subcutaneous
pentylenetetrazole induced seizure; CNS depressants
ID SEMICARBAZONES; DERIVATIVES; AGENTS
AB A series of new 3-[5-substituted phenyl-1,3,4-thiadiazole-2-yl]-2-styryl quinazoline-4(3H)-ones were synthesized and evaluated for anticonvulsant, sedative-hypnotic and CNS depression activities. After i.p. injection to mice or rat at doses of 30, 100, and 300 mg/kg body weight 2-styryl quinazolin-4(3H)-ones derivatives were examined in the maximal electroshock (MES) induced seizures and subcutaneous pentylenetetrazole (scPTZ) induced seizure models in mice. Rotorod method was employed to determine the neurotoxicity. Out of 18 compounds only 4a, 4e and 4p showed anticonvulsant activity in one or more test models. All except 4l and 4q exhibited significant sedative-hypnotic activity via actophotometer screen. Forced swim pool method to determine CNS depressant activity resulted in some potent compounds. It can be concluded that synthesized compounds exhibited better sedative-hypnotic and CNS depressant activities than anticonvulsant activity. (C) 2007 Elsevier Masson SAS. All rights reserved.
C1 [Jatav, Varsha; Mishra, Pradeep; Kashaw, Sushil] Dr HSG Univ, Pharmaceut Chem Div, Dept Pharmaceut Sci, Sagar 470003, Madhya Pradesh, India.
[Stables, J. P.] NIH, Preclin Pharmacol Sect, Epilepsy Branch, Bethesda, MD 20892 USA.
RP Kashaw, S (reprint author), Dr HSG Univ, Pharmaceut Chem Div, Dept Pharmaceut Sci, Sagar 470003, Madhya Pradesh, India.
EM sushilkashaw@gmail.com
NR 22
TC 84
Z9 85
U1 0
U2 1
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0223-5234
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD SEP
PY 2008
VL 43
IS 9
BP 1945
EP 1954
DI 10.1016/j.ejmech.2007.12.003
PG 10
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 360RC
UT WOS:000260074200016
PM 18222569
ER
PT J
AU Lauretani, F
Semba, RD
Dayhoff-Brannigan, M
Corsi, AM
Di Iorio, A
Buiatti, E
Bandinelli, S
Guralnik, JM
Ferrucci, L
AF Lauretani, Fulvio
Semba, Richard D.
Dayhoff-Brannigan, Margaret
Corsi, Anna Maria
Di Iorio, Angelo
Buiatti, Eva
Bandinelli, Stefania
Guralnik, Jack M.
Ferrucci, Luigi
TI Low total plasma carotenoids are independent predictors of mortality
among older persons - The InCHIANTI study
SO EUROPEAN JOURNAL OF NUTRITION
LA English
DT Article
DE aging; carotenoids; fruits; mortality; vegetables
ID CARDIOVASCULAR-DISEASE MORTALITY; CORONARY-HEART-DISEASE;
ALPHA-TOCOPHEROL; ANTIOXIDANT VITAMINS; SERUM CAROTENOIDS;
BETA-CAROTENE; ALL-CAUSE; POPULATION; CANCER; NUTRITION
AB Background Plasma carotenoids are considered a valid biological marker for fruit and vegetable dietary intake. Recent studies show that low carotenoid levels are associated with a high risk of inflammation, cancer, and cardiovascular disease. Aim of the study To determine whether low plasma carotenoids are associated with increased mortality among older adults. Methods Longitudinal study among 1,043 adults, 65 years and older, in the InCHIANTI study, a population-based cohort of adults living in the community in the Tuscany region, Italy. Results Mean total carotenoid concentration was 1.80 mu mol/l. During eight years of follow-up, 310 (29.7%) of participants died. Eight-year survival was lower in the lowest compared with the highest tertile of total serum carotenoids (P < 0.0001 by Mantel-Haenszel chi-square). In a multivariate Cox proportional hazards model adjusted for age, education, smoking, body mass index, energy intake, and chronic diseases, adults in the highest tertile of plasma carotenoids at enrollment had lower mortality compared to those in the lowest tertile (Hazards Ratio obtained by considering carotenoids level as an ordinal variable 0.81, 95%; CI 0.65-0.99; P for trend = 0.046). Conclusions Low plasma carotenoids are an independent risk factor for mortality among older adults living in the community.
C1 [Lauretani, Fulvio] Univ Hosp Parma, Geriatr Unit, Parma, Italy.
[Lauretani, Fulvio; Corsi, Anna Maria; Buiatti, Eva] Tuscany Reg Agcy, Florence, Italy.
[Semba, Richard D.; Dayhoff-Brannigan, Margaret] Johns Hopkins Sch Med, Baltimore, MD USA.
[Di Iorio, Angelo] Univ G dAnnunzio, Lab Clin Epidemiol, Chieti, Italy.
[Bandinelli, Stefania] Azienda Sanit Firenze, Florence, Italy.
[Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Ferrucci, Luigi] NIA, Clin Res Branch, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
RP Lauretani, F (reprint author), Univ Hosp Parma, Geriatr Unit, Parma, Italy.
EM flauretani@ao.pr.it
RI Lauretani, Fulvio/K-5115-2016
OI Lauretani, Fulvio/0000-0002-5287-9972
FU National Institute on Aging [N01-AG-916413, N01-AG-821336, N01-AG5
-0002]; NIA [R01 AG027012]; Intramural Research Program; National
Institute on Aging, NIH
FX This work was supported by National Institute on Aging Contracts
N01-AG-916413, N01-AG-821336, N01-AG5 -0002, and NIA Grant R01 AG027012.
This research was supported in part by the Intramural Research Program,
National Institute on Aging, NIH.
NR 33
TC 26
Z9 26
U1 0
U2 0
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1436-6207
J9 EUR J NUTR
JI Eur. J. Nutr.
PD SEP
PY 2008
VL 47
IS 6
BP 335
EP 340
DI 10.1007/s00394-008-0732-9
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 342BA
UT WOS:000258758400007
PM 18709473
ER
PT J
AU Akhmadeeva, L
Andreeva, VA
Sussman, S
Khusnutdinova, Z
Simons-Morton, BG
AF Akhmadeeva, Leila
Andreeva, Valentina A.
Sussman, Steve
Khusnutdinova, Zolya
Simons-Morton, Bruce G.
TI Need and possibilities for seat belt use promotion in Bashkortostan,
Russia
SO EVALUATION & THE HEALTH PROFESSIONS
LA English
DT Article
DE seat belts; health promotion; Bashkortostan; Russia
ID TRANSPORTATION SAFETY; ENFORCEMENT; LAWS; LEGISLATION; PROGRAM; RATES;
CHILD
AB Bashkortostan is a republic in the Russian Federation with a population of 4.1 million. As with other health behaviors, the prevalence of seat belt use is low, which may account in part for the very high rate of motor-vehicle-related mortality in this republic. The authors discuss the need and potential for translating seat belt promotion programming from other Russian regions and other countries to Bashkortostan. The authors conclude that current policies developed in other countries could work well in the republic, if they are enforced. Meanwhile, initiatives such as the Sakhalin Road Safety Partnership offer great potential for translation in Bashkortostan as well as in other regions with similarly low seat belt use prevalence.
C1 [Akhmadeeva, Leila] Bashkir State Med Univ, Ufa, Russia.
[Andreeva, Valentina A.; Sussman, Steve] Univ So Calif, Los Angeles, CA USA.
[Khusnutdinova, Zolya] Bashkir State Pedag Univ, Ufa, Russia.
[Simons-Morton, Bruce G.] NICHHD, Bethesda, MD 20892 USA.
RP Akhmadeeva, L (reprint author), Bashkir State Med Univ, Ufa, Russia.
OI Akhmadeeva, Leila/0000-0002-1177-6424; Simons-Morton,
Bruce/0000-0003-1099-6617
FU Intramural NIH HHS [Z99 HD999999]
NR 36
TC 4
Z9 4
U1 3
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0163-2787
J9 EVAL HEALTH PROF
JI Eval. Health Prof.
PD SEP
PY 2008
VL 31
IS 3
BP 282
EP 289
DI 10.1177/0163278708320167
PG 8
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 335KL
UT WOS:000258289400005
PM 18559882
ER
PT J
AU Lopez-Lluch, G
Irusta, PM
Navas, P
de Cabo, R
AF Lopez-Lluch, Guillermo
Irusta, Pablo M.
Navas, Placido
de Cabo, Rafael
TI Mitochondrial biogenesis and healthy aging
SO EXPERIMENTAL GERONTOLOGY
LA English
DT Review
DE aging; calorie restriction; mitochondrial biogenesis; PGC-1 alpha
ID ACTIVATED PROTEIN-KINASE; MUSCLE OXIDATIVE CAPACITY; RAT
SKELETAL-MUSCLE; THYROID-HORMONE; SACCHAROMYCES-CEREVISIAE; CALORIC
RESTRICTION; NITRIC-OXIDE; TRANSCRIPTIONAL REPRESSION; CELLULAR
DIFFERENTIATION; NEUROSPORA-CRASSA
AB Aging is associated with an overall loss of function at the level of the whole organism that has origins in cellular deterioration. Most cellular components, including mitochondria, require continuous recycling and regeneration throughout the lifespan. Mitochondria are particularly susceptive to damage over time as they are the major bioenergetic machinery and source of oxidative stress in cells. Effective control of mitochondrial biogenesis and turnover, therefore, becomes critical for the maintenance of energy production, the prevention of endogenous oxidative stress and the promotion of healthy aging. Multiple endogenous and exogenous factors regulate mitochondrial biogenesis through the peroxisome proliferator-activated receptor gamma coactivator-1 alpha (KC-1 alpha). Activators of PGC-1 alpha include nitric oxide, CREB and AMPK. Calorie restriction (CR) and resveratrol, a proposed CR mimetic, also increase mitochondrial biogenesis through activation of PGC-1 alpha. Moderate exercise also mimics CR by inducing mitochondrial biogenesis. Negative regulators of PGC-1 alpha such as RIP140 and 160MBP suppress mitochondrial biogenesis. Another mechanism involved in mitochondrial maintenance is mitochondrial fission/fusion and this process also involves an increasing number of regulatory proteins. Dysfunction of either biogenesis or fission/fusion of mitochondria is associated with diseases of the neuromuscular system and aging, and a greater understanding of the regulation of these processes should help us to ultimately control the aging process. Published by Elsevier Inc.
C1 [de Cabo, Rafael] NIA, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA.
[Lopez-Lluch, Guillermo; Navas, Placido] Univ Pablo Olavide, CSIC, CABD, Seville 41013, Spain.
[Irusta, Pablo M.] Georgetown Univ, Med Ctr, Dept Human Sci, Washington, DC 20057 USA.
RP de Cabo, R (reprint author), NIA, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA.
EM decabora@grc.nia.nih.gov
RI de Cabo, Rafael/E-7996-2010; Lopez-Lluch, Guillermo/N-4742-2014; de
Cabo, Rafael/J-5230-2016;
OI Lopez-Lluch, Guillermo/0000-0001-9830-8502; de Cabo,
Rafael/0000-0002-3354-2442; , rafael/0000-0003-2830-5693
FU Intramural NIH HHS [Z01 AG000368-03]
NR 84
TC 157
Z9 163
U1 4
U2 21
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0531-5565
J9 EXP GERONTOL
JI Exp. Gerontol.
PD SEP
PY 2008
VL 43
IS 9
BP 813
EP 819
DI 10.1016/j.exger.2008.06.014
PG 7
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 351QF
UT WOS:000259438400002
PM 18662766
ER
PT J
AU Tang, SC
Lathia, JD
Selvaraj, PK
Jo, DG
Mughal, MR
Cheng, A
Siler, DA
Markesbery, WR
Arumugam, TV
Mattson, MP
AF Tang, Sung-Chun
Lathia, Justin D.
Selvaraj, Pradeep K.
Jo, Dong-Gyu
Mughal, Mohamed R.
Cheng, Aiwu
Siler, Dominic A.
Markesbery, William R.
Arumugam, Thiruma V.
Mattson, Mark P.
TI Toll-like receptor-4 mediates neuronal apoptosis induced by amyloid
beta-peptide and the membrane lipid peroxidation product
4-hydroxynonenal
SO EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE toll-like receptors; amyloid beta-peptide; 4-hydroxynonenal; neuron;
cell death
ID FOCAL CEREBRAL-ISCHEMIA; INNATE IMMUNE DEFENSE; ALZHEIMERS-DISEASE;
SIGNALING PATHWAYS; OXIDATIVE STRESS; NERVOUS-SYSTEM; COMPLEMENT
ACTIVATION; BRAIN-INJURY; INFLAMMATION; TOLL-LIKE-RECEPTOR-4
AB The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited to immune cells. We recently found that neurons express several TLRs, and that the levels of TLR2 and TLR4 are increased in neurons in response to energy deprivation. Here we report that TLR4 expression increases in neurons when exposed to amyloid beta-peptide (A beta 1-42) or the lipid pet-oxidation product 4-hydroxynonenal (HNE). Neuronal apoptosis triggered by A beta and HNE was mediated by jun N-terminal kinase (JNK); neurons from TLR4 mutant mice exhibited reduced JNK and caspase-3 activation and were protected against apoptosis induced by A beta and HNE. Levels of TLR4 were decreased in inferior parietal cortex tissue specimens from end-stage AD patients compared to aged-matched Control Subjects, possibly as the result of loss of neurons expressing TLR4. Our findings Suggest that TLR4 signaling increases the vulnerability of neurons to A beta and oxidative stress in AD, and identify TLR4 as a potential therapeutic target for AD. Published by Elsevier Inc.
C1 [Tang, Sung-Chun; Lathia, Justin D.; Jo, Dong-Gyu; Mughal, Mohamed R.; Cheng, Aiwu; Siler, Dominic A.; Mattson, Mark P.] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
[Tang, Sung-Chun] Natl Taiwan Univ Hosp, Stoke Ctr, Dept Neurol, Taipei, Taiwan.
[Tang, Sung-Chun] Natl Taiwan Univ Hosp, Dept Neurol, Yun Liin Branch, Taipei, Taiwan.
[Jo, Dong-Gyu] Sungkyunkwan Univ, Coll Pharm, Suwon, South Korea.
[Markesbery, William R.] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA.
[Selvaraj, Pradeep K.; Arumugam, Thiruma V.] Texas Tech Univ, Hlth Sci Ctr, Dept Pharmaceut Sci, Sch Pharm, Amarillo, TX USA.
[Mattson, Mark P.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov
RI Arumugam, Thiruma/C-7969-2009; Arumugam, Thiruma/B-4898-2011; Mattson,
Mark/F-6038-2012;
OI Tang, Sung-Chun/0000-0003-3731-5973
FU Intramural Research Program of the National Institute on Aging; National
Institutes of Health
FX We wish to thank Hiayang Zhu and Ouyang Xin for their excellent
technical support. This work was supported by Intramural Research
Program of the National Institute on Aging, National Institutes of
Health.
NR 55
TC 134
Z9 144
U1 5
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4886
J9 EXP NEUROL
JI Exp. Neurol.
PD SEP
PY 2008
VL 213
IS 1
BP 114
EP 121
DI 10.1016/j.expneurol.2008.05.014
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 344QX
UT WOS:000258943500014
PM 18586243
ER
PT J
AU Wolf, RC
Sambataro, F
Vasic, N
Shonfeldt-Lecuona, C
Ecker, D
Landwehrmeyer, B
AF Wolf, Robert Christian
Sambataro, Fabio
Vasic, Nenad
Shoenfeldt-Lecuona, Carlos
Ecker, Daniel
Landwehrmeyer, Bernhard
TI Aberrant connectivity of lateral prefrontal networks in presymptomatic
Huntington's disease
SO EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE premanifest Huntington's disease; working memory; striatum; independent
component analysis; functional magnetic resonance imaging
ID INDEPENDENT COMPONENT ANALYSIS; EVENT-RELATED FMRI; WORKING-MEMORY;
COGNITIVE DEFICITS; BRAIN; DYSFUNCTION; CORTEX; NEUROPATHOLOGY;
ABNORMALITIES; EXPRESSION
AB In clinically presymptomatic individuals with the Huntington's disease (HD) gene mutation, functional neuroimaging data have suggested a dysfuuction Of multiple cortical and subcortical regions including the prefrontal and parietal cortex, as well as the striatum. Although it has been hypothesized that these activation differences most likely reflect aberrant corticostriatal circuits, the functional Coupling of neural networks associated with cognitive performance has not been investigated so far. In this Study, we used functional magnetic resonance imaging (fMRI) and multivariate analytic techniques to investigate memory-related patterns of functional connectivity in healthy controls (n = 16) and pre-HD individuals (n = 16). Independent component analyses (ICA) revealed distinct bilateral frontostriatal and frontoparietal networks that were activated during a verbal working memory paradigm in both healthy controls and pre-HD subjects. Compared with healthy controls, pre-HD individuals exhibited lower functional connectivity in left lateral prefrontal and parietal regions as well as in the bilateral putamen. Functional connectivity indices in the left putamen were negatively correlated with the CAG repeat size and the UHDRS behavioral score, and positively correlated with the predicted years to manifest symptom onset. The connectivity of the right putamen was negatively correlated with the UHDRS motor score. In pre-HD individuals, these results suggest ail early frontostriatal and frontoparietal deficit of dissociable functional networks associated with executive processing. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Wolf, Robert Christian; Vasic, Nenad; Shoenfeldt-Lecuona, Carlos] Univ Ulm, Dept Psychiat & Psychotherapy 3, D-89075 Ulm, Germany.
[Sambataro, Fabio] Univ Bari, Dept Psychiat, I-70121 Bari, Italy.
[Ecker, Daniel; Landwehrmeyer, Bernhard] Univ Ulm, Dept Neurol, D-89069 Ulm, Germany.
[Sambataro, Fabio] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Wolf, RC (reprint author), Univ Ulm, Dept Psychiat & Psychotherapy 3, Leimgrubenweg 12-14, D-89075 Ulm, Germany.
EM christian.wolf@uni-ulm.de
RI Sambataro, Fabio/E-3426-2010;
OI Sambataro, Fabio/0000-0003-2102-416X; Landwehrmeyer, Georg
Bernhard/0000-0003-3375-790X
FU European Huntington's Disease Network (EHDN)
FX This study was supported by the European Huntington's Disease Network
(EHDN). The authors are grateful to Beate Englet and Sebastian Satzinger
for their assistance with the data collection.
NR 54
TC 58
Z9 58
U1 1
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4886
J9 EXP NEUROL
JI Exp. Neurol.
PD SEP
PY 2008
VL 213
IS 1
BP 137
EP 144
DI 10.1016/j.expneurol.2008.05.017
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 344QX
UT WOS:000258943500017
PM 18588876
ER
PT J
AU Ostera, G
Tokumasu, F
Oliveira, F
Sa, J
Furuya, T
Teixeira, C
Dvorak, J
AF Ostera, Graciela
Tokumasu, Fuyuki
Oliveira, Fabiano
Sa, Juliana
Furuya, Tetsuya
Teixeira, Clarissa
Dvorak, James
TI Plasmodium falciparum: Food vacuole localization of nitric oxide-derived
species in intraerythrocytic stages of the malaria parasite
SO EXPERIMENTAL PARASITOLOGY
LA English
DT Article
DE Plasmodium falciparum; nitric oxide
ID SYNTHASE; IDENTIFICATION; HEMOGLOBIN; ERYTHROCYTES
AB Nitric oxide (NO) has diverse biological functions. Numerous studies have documented NO's biosynthetic pathway in a wide variety of organisms. Little is known, however, about NO production in intraerythrocytic Plasmodium falciparum. Using diaminorhodamine-4-methyl acetoxymethylester (DAR-4M AM), a fluorescent indicator, we obtained direct evidence of NO and NO-derived reactive nitrogen species (RNS) production in intraerythrocytic P.falciparum parasites, as well as in isolated food vacuoles from trophozoite stage parasites. We preliminarily identified two gene sequences that might be implicated in NO synthesis in intra erythrocytic P.falciparum. We showed localization of the protein product of one of these two genes, a molecule that is structurally similar to a plant nitrate reductase, in trophozoite food vacuole membranes. We confirmed previous reports on the antiproliferative effect of NOS (nitric oxide synthase) inhibitors in A falciparum cultures; however, we did not obtain evidence that NOS inhibitors had the ability to inhibit RNS production or that there is an active NOS in mature forms of the parasite. We concluded that a nitrate reductase activity produce NO and NO-derived RNS in or around the food vacuole in A falciparum parasites. The food vacuole is a critical parasitic compartment involved in hemoglobin degradation, heme detoxification and a target for antimalarial drug action. Characterization of this relatively unexplored synthetic activity could provide important clues into poorly understood metabolic processes of the malaria parasite. Published by Elsevier Inc.
C1 [Ostera, Graciela; Tokumasu, Fuyuki; Dvorak, James] NIAID, Biophys & Biochem Parasitol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
[Oliveira, Fabiano; Teixeira, Clarissa] NIAID, Vector Mol Biol Unit, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Sa, Juliana] NIAID, Malaria Genet Sect, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Furuya, Tetsuya] NIAID, Malaria Genom Sect, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
RP Ostera, G (reprint author), NIAID, Biophys & Biochem Parasitol Sect, Lab Malaria & Vector Res, NIH, 12735 Twinbrook Pkwy,Twinbrook 3,Room 2W-09, Rockville, MD 20852 USA.
EM gostera@niaid.nih.gov
RI Oliveira, Fabiano/B-4251-2009; Furuya, Tetsuya/J-5916-2013; Furuya,
Tetsuya/H-2412-2013
OI Oliveira, Fabiano/0000-0002-7924-8038; Tokumasu,
Fuyuki/0000-0003-2790-1071; Furuya, Tetsuya/0000-0003-3979-7072
FU Intramural NIH HHS [Z99 AI999999]
NR 23
TC 13
Z9 13
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4894
J9 EXP PARASITOL
JI Exp. Parasitol.
PD SEP
PY 2008
VL 120
IS 1
BP 29
EP 38
DI 10.1016/j.exppara.2008.04.014
PG 10
WC Parasitology
SC Parasitology
GA 347DC
UT WOS:000259119800005
PM 18504040
ER
PT J
AU Patterson, LJ
Robert-Guroff, M
AF Patterson, L. Jean
Robert-Guroff, Marjorie
TI Replicating adenovirus vector prime/protein boost strategies for HIV
vaccine development
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Review
DE animal models; HIV vaccine; mucosal immunity; multigenic priming;
protein boost; replication competent adenovirus vectors
ID SIMIAN-IMMUNODEFICIENCY-VIRUS; VESICULAR STOMATITIS-VIRUS; CELLULAR
IMMUNE-RESPONSES; HOST-RANGE MUTANT; CD4(+) T-CELLS; DIPLOID TISSUE
CULTURE; RHESUS MACAQUES; NEUTRALIZING ANTIBODIES; RECOMBINANT
ADENOVIRUS; AIDS VACCINE
AB Background: In recent years the HIV vaccine field introduced a number of promising vaccine candidates into human clinical trials. Objective: To briefly discuss the advances made in vaccine development and HIV pathogenesis and give an overview of the body of work our lab has generated in multiple animal models on replication-competent Adenovirus recombinant vaccines. Methods: Emphasis is placed on comparative examination of vaccine components, routes of immunization and challenge models using replicating Adenovirus vectors. Results/conclusion: The findings make the case that replicating Adenovirus vectors are superior in priming multiple arms of the immune system, and in conjunction with protein boosting, have resulted in dramatic protective efficacy leading to their advancement to Phase I trials. Implications of the recent halting of the Merck Ad5-HIV Phase IIb clinical trial of our vaccine approach and other vectored vaccines are discussed.
C1 [Patterson, L. Jean; Robert-Guroff, Marjorie] NCI, Natl Inst Hlth, Vaccine Branch, Bethesda, MD 20892 USA.
RP Robert-Guroff, M (reprint author), NCI, Natl Inst Hlth, Vaccine Branch, 41 Medlars Dr Bldg 41,Room D804, Bethesda, MD 20892 USA.
EM guroffm@mail.nih.gov
FU National Institutes of Health; National Cancer Institute
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute.
NR 136
TC 28
Z9 28
U1 0
U2 4
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1471-2598
J9 EXPERT OPIN BIOL TH
JI Expert Opin. Biol. Ther.
PD SEP
PY 2008
VL 8
IS 9
BP 1347
EP 1363
DI 10.1517/14712590802256991
PG 17
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA 348LW
UT WOS:000259213000008
PM 18694354
ER
PT J
AU Zarate, CA
Manji, HK
AF Zarate, Carlos A., Jr.
Manji, Husseini K.
TI Riluzole in psychiatry: a systematic review of the literature
SO EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY
LA English
DT Review
DE antidepressant; anxiety disorder; bipolar disorder; depression;
glutamate; mania; plasticity; psychiatry; riluzole; treatment
ID AMYOTROPHIC-LATERAL-SCLEROSIS; OPEN-LABEL TRIAL; NEUROPROTECTIVE AGENT
RILUZOLE; OBSESSIVE-COMPULSIVE DISORDER; MAJOR DEPRESSIVE DISORDER;
CELLULAR PLASTICITY CASCADES; GENERALIZED ANXIETY DISORDER;
SODIUM-CHANNEL BLOCKERS; SPINAL-CORD-INJURY;
UDP-GLUCURONOSYLTRANSFERASES
AB Background: The glutamate system seems to be an important contributor to the pathophysiology of mood and anxiety disorders. Thus, glutamatergic modulators are reasonable candidate drugs to test in patients with mood and anxiety disorders. Riluzole, a neuroprotective agent with anticonvulsant properties approved for the treatment of amyotrophic lateral sclerosis (ALS) is one such agent. Objective: To assess the potential risks and benefits of riluzole treatment in psychiatric patients. Methods: A PubMed search was performed using the keywords 'riluzole', 'inhibitor of glutamate release' and 'glutamatergic modulator' to identify all clinical studies and case reports involving riluzole in psychiatric patients. Results/conclusion: Riluzole's side effect profile is favorable and preliminary results regarding riluzole for the treatment of severe mood, anxiety and impulsive disorders are encouraging.
C1 [Zarate, Carlos A., Jr.; Manji, Husseini K.] NIMH, Lab Mol Pathophysiol & Expt Therapeut, Mood & Anxiety Disorders Res Program, Bethesda, MD 20892 USA.
RP Zarate, CA (reprint author), 10 Ctr Dr,Mark O Hatfield CRC,Unit 7 SE,Rm 7-3445, Bethesda, MD 20892 USA.
EM zaratec@mail.nih.gov
FU Intramural NIH HHS [Z01 MH002828-05, Z01 MH002857-03]
NR 92
TC 35
Z9 36
U1 0
U2 7
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1742-5255
J9 EXPERT OPIN DRUG MET
JI Expert Opin. Drug Metab. Toxicol.
PD SEP
PY 2008
VL 4
IS 9
BP 1223
EP 1234
DI 10.1517/17425250802340946
PG 12
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 348LZ
UT WOS:000259213300008
PM 18721116
ER
PT J
AU Miller, S
Stagl, J
Wallerstedt, DB
Ryan, M
Mansky, PJ
AF Miller, Scott
Stagl, Jamie
Wallerstedt, Dawn B.
Ryan, Mary
Mansky, Patrick J.
TI Botanicals used in complementary and alternative medicine treatment of
cancer: clinical science and future perspectives
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Review
DE botanical; cancer symptoms; cancer treatment; clinical trials;
complementary and alternative medicine
ID CHRONIC MYELOGENOUS LEUKEMIA; FACTOR-KAPPA-B; TRADITIONAL CHINESE
MEDICINE; QUALITY-OF-LIFE; WITHANIA-SOMNIFERA; BREAST-CANCER; ADJUVANT
IMMUNOCHEMOTHERAPY; COLORECTAL-CANCER; POLYSACCHARIDE-K; CHRONIC-PHASE
AB Background: Botanicals and herbal combinations are among the most common complementary and alternative medicine (CAM) approaches used by cancer patients both for cancer treatment and management of cancer symptoms. Despite their widespread use, however, the safety and efficacy of many botanicals has not been established in controlled clinical trials. Objectives: This article reviews the published evidence for the safety and clinical benefit of botanicals used in the treatment of cancer and cancer symptom management and describes the continuing clinical trials of botanicals with applications in oncology. Methods: Literature searches were conducted in PubMed, EMBASE, Cochrane Clinical Trials databases, Pharmaprojects and CRISP (Computer Retrieval of Information on Scientific Projects) clinical trials databases. Conclusion: A number of botanicals have shown promise for cancer symptom management but need further study. A limited number of multi-agent nutritional supplement approaches are being explored in clinical trials. Botanical immunomodulators and botanical products shown to affect pathways of angiogenesis, apoptosis and cell signaling in vitro have stimulated research interest and may broaden the range of available cancer treatments.
C1 [Miller, Scott; Stagl, Jamie; Wallerstedt, Dawn B.; Mansky, Patrick J.] Natl Inst Hlth, DHHS, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Ryan, Mary] Natl Inst Hlth Lib, Bethesda, MD 20892 USA.
RP Mansky, PJ (reprint author), Natl Inst Hlth, DHHS, Natl Ctr Complementary & Alternat Med, 10 Ctr Dr,CRC,Room 4-1741,MSC 1302, Bethesda, MD 20892 USA.
EM manskyp@mail.nih.gov
FU NIH; NCCAM
FX This research was supported in part by the Intramural Research Program
of the NIH, NCCAM. Conclusions drawn and recommendations for future
directions made are the opinions of the authors and do not represent the
view of the National Center for Complementary and Alternative Medicine.
NR 99
TC 10
Z9 10
U1 0
U2 5
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1354-3784
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD SEP
PY 2008
VL 17
IS 9
BP 1353
EP 1364
DI 10.1517/13543780802323464
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 343VD
UT WOS:000258882500007
PM 18694368
ER
PT J
AU Brown, M
Cohen, J
Arun, P
Chen, Z
Van Waes, C
AF Brown, Matthew
Cohen, Jonah
Arun, Pattatheyil
Chen, Zhong
Van Waes, Carter
TI NF-kappa B in carcinoma therapy and prevention
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
DE aspirin; BMS-345541; bortezomib; carcinoma; CHS-828; dexamethasone;
inhibitor-kappaB; MLN-120B; NF-kappa B; NSAIDs; proteasome; sulindac
ID SQUAMOUS-CELL CARCINOMA; PROSTATE-CANCER CELLS; PROTEIN-KINASE CK2;
PROTEASOME INHIBITOR BORTEZOMIB; MULTIPLE-MYELOMA; BREAST-CANCER;
TRANSCRIPTIONAL ACTIVITY; TUMOR-GROWTH; IN-VIVO; SIGNALING PATHWAY
AB Background: NF-kappa B includes a family of signal-activated transcription factors that normally regulate responses to injury and infection but which are aberrantly activated in many carcinomas. Objective: To review the activation and role of NF-kappa B in pathogenesis and as a target for treatment and prevention in carcinoma. Methods: Evidence from experimental, epidemiological, preclinical studies and clinical trials cited in the literature are reviewed. Results/conclusion: Cumulative evidence implicates NF-kappa B in cell survival, inflammation, angiogenesis, spread and therapeutic resistance during tumor development, progression and metastasis of carcinomas. Non-specific natural and synthetic agents that inhibit NF-kappa B have demonstrated activity and safety in prevention or therapy. NF-kappa B-activating kinases and the proteasome are under investigation for targeted prevention and therapy of carcinoma.
C1 [Brown, Matthew; Cohen, Jonah; Arun, Pattatheyil; Chen, Zhong; Van Waes, Carter] Natl Inst Deafncss & Other Commun Disorders, Head & Neck Surg Branch, Bethesda, MD 20892 USA.
[Van Waes, Carter] NCI, Ctr Canc Res, Radiat Oncol Branch, Bethesda, MD 20892 USA.
[Van Waes, Carter] Natl Inst Deafness & Other Commun Disorders, NIH, Head & Neck Surg Branch, Bethesda, MD 20892 USA.
RP Van Waes, C (reprint author), Natl Inst Deafncss & Other Commun Disorders, Head & Neck Surg Branch, Bethesda, MD 20892 USA.
EM vanwaesc@nidcd.nih.gov
FU NIDCD intramural project [ZOI-DC-00016]; NCI-Millennium Pharmaceuticals
Cooperative Research and Development Agreement [00676]
FX The authors would like to thank Shivaani Kummar and James F Battey for
reading the manuscript. This research was supported by NIDCD intramural
project ZOI-DC-00016, NCI-Millennium Pharmaceuticals Cooperative
Research and Development Agreement 00676 (CM, NIH-Pfizer Clinical
Research Training Program (MB), and Howard Hughes Medical Institute
Research Scholars Program (JC).
NR 122
TC 47
Z9 49
U1 0
U2 1
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1472-8222
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD SEP
PY 2008
VL 12
IS 9
BP 1109
EP 1122
DI 10.1517/14728220802287810
PG 14
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 343LY
UT WOS:000258856500005
PM 18694378
ER
PT J
AU Arbab, AS
Janic, B
Knight, RA
Anderson, SA
Pawelczyk, E
Rad, AM
Read, EJ
Pandit, SD
Frank, JA
AF Arbab, Ali S.
Janic, Branislava
Knight, Robert A.
Anderson, Stasia A.
Pawelczyk, Edyta
Rad, Ali M.
Read, Elizabeth J.
Pandit, Sunil D.
Frank, Joseph A.
TI Detection of migration of locally implanted AC133(+) stem cells by
cellular magnetic resonance imaging with histological findings
SO FASEB JOURNAL
LA English
DT Article
DE MRI; magnetically labeled AC133(+) cells; tumors; angiogenesis
ID ENDOTHELIAL PROGENITOR CELLS; HYPOXIA-INDUCIBLE FACTOR-1-ALPHA;
BONE-MARROW; PRECURSOR CELLS; GROWTH-FACTOR; TUMOR ANGIOGENESIS;
IN-VITRO; POSTNATAL NEOVASCULARIZATION; BLOOD; CANCER
AB This study investigated the factors responsible for migration and homing of magnetically labeled AC133(+) cells at the sites of active angiogenesis in tumor. AC133(+) cells labeled with ferumoxide-protamine sulfate were mixed with either rat glioma or human melanoma cells and implanted in flank of nude mice. An MRI of the tumors including surrounding tissues was performed. Tumor sections were stained for Prussian blue (PB), platelet-derived growth factor (PDGF), hypoxia-inducible factor-1 alpha (HIF-1 alpha), stromal cell derived factor-1 (SDF-1), matrix metalloproteinase-2 (MMP-2), vascular endothelial growth factor (VEGF), and endothelial markers. Fresh snap-frozen strips from the central and peripheral parts of the tumor were collected for Western blotting. MRIs demonstrated hypointense regions at the periphery of the tumors where the PB(+)/AC133(+) cells were positive for endothelial cells markers. At the sites of PB(+)/AC133(+) cells, both HIF-1 alpha and SDF-1 were strongly positive and PDGF and MMP-2 showed generalized expression in the tumor and surrounding tissues. There was no significant association of PB(+)/AC133(+) cell localization and VEGF expression in tumor cells. Western blot demonstrated strong expression of the SDF-1, MMP-2, and PDGF at the peripheral parts of the tumors. HIF-1 alpha was expressed at both the periphery and central parts of the tumor. This work demonstrates that magnetically labeled cells can be used as probes for MRI and histological identification of administered cells.
C1 [Arbab, Ali S.; Janic, Branislava; Knight, Robert A.; Rad, Ali M.] Henry Ford Hosp, Dept Radiol, Mol & Cellular Imaging Lab, Detroit, MI 48202 USA.
[Anderson, Stasia A.] NHLBI, Mouse Core Imaging Facil, Bethesda, MD 20892 USA.
[Pawelczyk, Edyta; Frank, Joseph A.] NIH, Expt Neuroimaging Sect, Lab Diagnost Radiol Res, Bethesda, MD 20892 USA.
[Read, Elizabeth J.] NIH, Cell Proc Sect, Dept Transfus Med, Bethesda, MD 20892 USA.
[Pandit, Sunil D.] NIH, Mol Imaging Lab, Ctr Clin, Bethesda, MD 20892 USA.
RP Arbab, AS (reprint author), Henry Ford Hlth Syst, Dept Radiol, 1 Ford Pl,2F,Box 82, Detroit, MI 48202 USA.
EM saali@rad.hfh.edu
FU Intramural Research Program; National Institutes of Health
[5R01CA122031]
FX We thank Gene T. Yocum for help during the labeling of AC133+
cells at the National Institutes of Health. We thank Dr. A. S. M.
Iskander for help in sectioning of collected tumor samples and
collection of AC133+ cells from cord blood, and Dr. Hanh M.
Khuu for supervision during collection of AC133+ from
volunteers. This work was supported in part by the Intramural Research
Program of the Clinical Center at the National Institutes of Health and
an extramural funding grant (5R01CA122031).
NR 54
TC 41
Z9 44
U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD SEP
PY 2008
VL 22
IS 9
BP 3234
EP 3246
DI 10.1096/fj.07-105676
PG 13
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 342CD
UT WOS:000258761300016
PM 18556461
ER
PT J
AU Donzelli, S
Espey, MG
Flores-Santana, W
Switzer, CH
Yeh, GC
Huang, JM
Stuehr, DJ
King, SB
Miranda, KM
Wink, DA
AF Donzelli, Sonia
Espey, Michael Graham
Flores-Santana, Wilmarie
Switzer, Christopher H.
Yeh, Grace C.
Huang, Jinming
Stuehr, Dennis J.
King, S. Bruce
Miranda, Katrina M.
Wink, David A.
TI Generation of nitroxyl by heme protein-mediated peroxidation of
hydroxylamine but not N-hydroxy-L-arginine
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE heme; peroxidase; hydroxylamine; N-hydroxy-L-arginine; nitroxyl;
suffinamide
ID NITRIC-OXIDE SYNTHASE; CARDIAC SARCOPLASMIC-RETICULUM; DETERRENT AGENT
CYANAMIDE; IN-VIVO; ANGELIS SALT; ALDEHYDE DEHYDROGENASE;
SODIUM-NITROPRUSSIDE; SUPEROXIDE-DISMUTASE; GUANYLATE-CYCLASE; OXIDATIVE
STRESS
AB The chemical reactivity, toxicology, and pharmacological responses to nitroxyl (HNO) are often distinctly different from those of nitric oxide (NO). The discovery that HNO donors may have pharmacological Utility for treatment of cardiovascular disorders such as heart failure and ischemia reperfusion has led to increased speculation of potential endogenous pathways for HNO biosynthesis. Here, the ability of heme proteins to utilize H2O2 to oxidize hydroxylamine (NH2OH) or N-hydroxy-L-arginine (NOHA) to HNO was examined. Formation of HNO was evaluated with a recently developed selective assay in which the reaction products ill the presence of reduced glutathione (GSH) were quantified by HPLC. Release of HNO from the heme pocket was indicated by formation of sulfinamide (GS(O)NH2), While the yields of nitrite and nitrate signified the degree of intramolecular recombination of HNO with the heme. Formation of GS(O)NH2 was observed upon oxidation of NH2OH, whereas NOHA, the primary intermediate in oxidation of L-arginine by NO synthase, was apparently resistant to oxidation by the heme proteins utilized. In the presence of NH2OH, the highest yields of GS(O)NH2 were observed with proteins in which the heme was coordinated to a histidine (horseradish peroxidase, lactoperoxidase, myeloperoxidase, myoglobin, and hemoglobin) in contrast to a tyrosine (catalase) or cysteine (cytochrome P450). That peroxidation of NH2OH by horseradish peroxidase produced free HNO, which was able to affect intracellular targets, was verified by conversion of 4,5-diaminofluorescein to the corresponding fluorophore within intact cells. (c) Published by Elsevier Inc.
C1 [Donzelli, Sonia; Espey, Michael Graham; Flores-Santana, Wilmarie; Switzer, Christopher H.; Wink, David A.] NCI, Tumor Biol Sect, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
[Yeh, Grace C.] NCI, Cellular Defense & Carcinogenesis Sect, Lab Metab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Huang, Jinming; King, S. Bruce] Wake Forest Univ, Dept Chem, Winston Salem, NC 27109 USA.
[Stuehr, Dennis J.] Lerner Res Inst, Dept Pathobiol, Cleveland, OH 44195 USA.
[Miranda, Katrina M.] Univ Arizona, Dept Chem, Tucson, AZ 85721 USA.
RP Wink, DA (reprint author), NCI, Tumor Biol Sect, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
EM sdonzell@uke.uni-hamburg.de; wink@mail.nih.gov
RI Switzer, Christopher/D-9203-2013; Miranda, Katrina/B-7823-2009
FU National Institutes of Health National Cancer Institute; Center for
Cancer Research (DW); National Institutes of Health [R01-GM076247]
FX The authors acknowledge the technical assistance of D. Janie Salmon and
Derek Hollman (UA). The research was Supported by the Intramural
Research Program of the National Institutes of Health National Cancer
Institute and the Center for Cancer Research (DW) and National
Institutes of Health Grant R01-GM076247 (KIVI).
NR 69
TC 46
Z9 46
U1 1
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD SEP 1
PY 2008
VL 45
IS 5
BP 578
EP 584
DI 10.1016/j.freeradbiomed.2008.04.036
PG 7
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 345KK
UT WOS:000258995200005
PM 18503778
ER
PT J
AU Jeong, YC
Walker, NJ
Burgin, DE
Kissling, G
Gupta, M
Kupper, L
Birnbaum, LS
Swenberg, JA
AF Jeong, Yo-Chan
Walker, Nigel J.
Burgin, Deborah E.
Kissling, Grace
Gupta, Mayetri
Kupper, Lawrence
Birnbaum, Linda S.
Swenberg, James A.
TI Accumulation of M(1)dG DNA adducts after chronic exposure to PCBs, but
not from acute exposure to polychlorinated aromatic hydrocarbons
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE polychlorinated aromatic hydrocarbons; PCBs; TCDD; oxidative DNA lesion;
M(1)dG; carcinogenesis
ID TOXIC EQUIVALENCY FACTORS; DIOXIN-LIKE COMPOUNDS; SPRAGUE-DAWLEY RATS;
BIPHENYLS PCBS; OXIDATIVE STRESS; RISK ASSESSMENT; FACTORS TEFS;
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN; 2,2',4,4',5,5'-HEXACHLOROBIPHENYL;
TCDD
AB Oxidative DNA damage is one of the key events thought to be involved in mutation and cancer. The present study examined the accumulation of M(1)dC, 3-(2'-deoxy-beta-D-erythro-pentofuranosyl)-pyrimido[1,2-a]-purin-10(3H)-one, DNA adducts after single dose or 1-year exposure to polyhalogenated aromatic hydrocarbons (PHAH) in order to evaluate the potential role of oxidative DNA damage in PHAH toxicity and carcinogenicity. The effect of PHAH exposure on the number of M(1)dG adducts was explored initially in female mice exposed to a single dose of either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or a PHAH mixture. This study demonstrated that a single exposure to PHAH had no significant effect on the number of M(1)dG adducts compared to the corn oil control group. The role of M(1)dG adducts in polychlorinated biphenyl (PCB)-inducecl toxicity and carcinogenicity was further investigated in rats exposed for a year to PCB 153, PCB 126, or a mixture of the two. PCB 153, at doses up to 3000 mu g/kg/day. had no significant effect on the number of M(1)dG adducts in liver and brain tissues from the exposed rats compared to controls. However, 1000 ng/kg/day of PCB 126 resulted in M(1)dG adduct accumulation in the liver. More importantly, coadministration of equal proportions of PCB 153 and PCB 126 resulted in dose-dependent increases in M(1)dG adduct accumulation in the liver from 300 to 1000 ng/kg/day of PCB 126 with 300-1000 mu g/kg/day of PCB 153. Interestingly, the coadministration of different amounts of PCB 153 with fixed amounts of PCB 126 demonstrated more M(1)dG adduct accumulation with higher doses of PCB 153. These results are consistent with the results from cancer bioassays that demonstrated a synergistic effect between PCB 126 and PCB 153 on toxicity and tumor development. In summary, the results from the present Study Support the hypothesis that oxidative DNA damage plays a key role in toxicity and carcinogenicity following long-term PCB exposure. (c) 2008 Elsevier Inc. All rights reserved.
C1 [Jeong, Yo-Chan; Swenberg, James A.] Univ N Carolina, Dept Environm Sci & Engn, Chapel Hill, NC 27599 USA.
[Walker, Nigel J.; Kissling, Grace] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
[Burgin, Deborah E.; Birnbaum, Linda S.] NHEERL, USEPA, ORD, ETD, Res Triangle Pk, NC 27709 USA.
[Gupta, Mayetri; Kupper, Lawrence] Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
RP Swenberg, JA (reprint author), Univ N Carolina, Dept Environm Sci & Engn, Room 253C,Rosenau Hall,CB 7431, Chapel Hill, NC 27599 USA.
EM jswenber@email.unc.edu
RI Walker, Nigel/D-6583-2012
OI Walker, Nigel/0000-0002-9111-6855
FU NIEHS Superfund Basic Research Program [P42-ES05948]; NIH [R42-ESII746,
P30-ES10126]; NHEERL-DESE Training in Environmental Sciences Research;
EPA [CT902908, T32-ES07126]
FX We thank Drs. Barohny Eun, Michael Wyde, and Ivan Rusyn for a critical
reading of the manuscript; Dr. Valeriy V. Afonin for his technical
assistance in DNA isolation; and Daniela Sotres-Alvarez for her
assistance in statistical analyses. This research Was Supported in part
by the NIEHS Superfund Basic Research Program P42-ES05948, NIH Grants
R42-ESII746 and P30-ES10126, and the Intramural Research Program of the
NIH and NIEHS. Partial funding was provided by the NHEERL-DESE Training
in Environmental Sciences Research, EPA CT902908 and T32-ES07126. The
information in this document has been subjected to review and approved
for publication by the National Health and Environmental Effects
Research Laboratory, U.S. Environmental Protection Agency, and by NIEHS,
NIH. Approval does not signify that the contents reflect the views of
the Agency, nor does mention of trade names or commercial products
constitute endorsement or recommendation for use.
NR 46
TC 22
Z9 23
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD SEP 1
PY 2008
VL 45
IS 5
BP 585
EP 591
DI 10.1016/j.freeradbiomed.2008.04.043
PG 7
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 345KK
UT WOS:000258995200006
PM 18534201
ER
PT J
AU Pi, JB
Diwan, BA
Sun, Y
Liu, J
Qu, W
He, YY
Styblo, M
Waalkes, MP
AF Pi, Jingbo
Diwan, Bhalchandra A.
Sun, Yang
Liu, Jie
Qu, Wei
He, Yuying
Styblo, Miroslav
Waalkes, Michael P.
TI Arsenic-induced malignant transformation of human keratinocytes:
Involvement of Nrf2
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE arsenic; carcinogenesis; Nrf2; oxidative stress; CK2
ID OXIDATIVE DNA-DAMAGE; PROTEIN-KINASE CK2; UROTHELIAL CELLS; LUNG-CANCER;
SKIN; APOPTOSIS; ACTIVATION; EXPRESSION; STRESS; MICE
AB Arsenic is a well-known human skin carcinogen but the underlying mechanisms of carcinogenesis are unclear. Transcription factor Nrf2-mediated antioxidant response represents a critical cellular defense mechanism, and emerging data suggest that constitutive activation of Nrf2 contributes to malignant phenotype. In the present study when an immortalized. nontumorigenic human keratinocyte cell line (HaCaT) was continuously exposed to an environmentally relevant level of inorganic arsenite (100 nM) for 28 weeks, malignant transformation occurred as evidenced by the formation of highly aggressive squamous cell carcinoma after inoculation into nude mice. To investigate the mechanisms involved, a broad array of biomarkers for transformation were assessed in these arsenic-transformed cells (termed As-TM). In addition to increased secretion of matrix metalloproteinase-9 (MMP-9), a set of markers for squamous differentiation and skin keratinization, including keratin-1, keratin-10, involucrin, and loricrin, were significantly elevated in As-TM cells. Furthermore, As-TM cells showed increased intracellular glutathione and elevated expression of Nrf2 and its target genes, as well as generalized apoptotic resistance. In contrast to increased basal Nrf2 activity in As-TM cells, a diminished Nrf2-mediated antioxidant response induced by acute exposure to high doses of arsenite or tert-butyl hydroxyquinone occurred. The findings that multiple biomarkers for malignant transformation observed in As-TM cells, including MMP-9 and cytokeratins, are potentially regulated by NFf2 suggest that Constitutive Nrf2 activation may be involved in arsenic carcinogenesis of skin. The weakened Nrf2 activation in response to oxidative stressors observed in As-TM cells, coupled with acquired apoptotic resistance, would potentially have increased the likelihood of transmittable oxidative DNA damage and fixation of mutational/DNA damage events. (c) 2008 Elsevier Inc. All rights reserved.
C1 [Pi, Jingbo] Hamner Inst Hlth Sci, Div Translat Biol, Res Triangle Pk, NC 27709 USA.
[Pi, Jingbo; Sun, Yang; Liu, Jie; Qu, Wei; Waalkes, Michael P.] NIEHS, Comparat Carcinogenesis Lab, NCI, NIH, Res Triangle Pk, NC 27709 USA.
[Diwan, Bhalchandra A.] NCI, Basic Res Program, Sci Applicat Int Corp Frederick, Frederick, MD 21702 USA.
[He, Yuying] NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA.
[Styblo, Miroslav] Univ N Carolina, Dept Nutr, Chapel Hill, NC 27599 USA.
RP Pi, JB (reprint author), Hamner Inst Hlth Sci, Div Translat Biol, Res Triangle Pk, NC 27709 USA.
EM jpi@thehamner.org; waalkes@niehs.nih.gov
FU Intramural NIH HHS; NCI NIH HHS [N01-CO-124000]; NIDDK NIH HHS [K01
DK076788, K01 DK076788-01A1]
NR 50
TC 79
Z9 88
U1 1
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD SEP 1
PY 2008
VL 45
IS 5
BP 651
EP 658
DI 10.1016/j.freeradbiomed.2008.05.020
PG 8
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 345KK
UT WOS:000258995200014
PM 18572023
ER
PT J
AU Jia, YP
Alayash, AI
AF Jia, Yiping
Alayash, Abdu I.
TI Effects of (-)-epigallocatechin gallate on the redox reactions of human
hemoglobin
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE (-)-epigallocatechin gallate; blood substitutes; hemoglobin
ID CROSS-LINKED HEMOGLOBIN; GREEN TEA EXTRACT; CARRIERS BLOOD SUBSTITUTES;
OXIDE PRODUCING REACTIONS; NITRIC-OXIDE; OXYGEN CARRIERS;
EPIGALLOCATECHIN GALLATE; HYDROGEN-PEROXIDE; (-)-EPICATECHIN GALLATE;
METABOLIC-ACIDOSIS
AB The toxicity of a cellular hemoglobin (Hb)-based therapeutics has been attributed in part to the uncontrolled oxidative reactions. A variety of antioxidant Strategies to ameliorate potential oxidative damage in vivo have been suggested. We have examined the effects of (-)-epigallocatechin gallate (EGCG), a green tea polyphenol compound widely regarded as a chain-breaking antioxidant. on the oxidative stability of diaspirin crosslinked Hb (DBBF) and its cytotoxic ferryl intermediate. DBBF (ferrous) was rapidly oxidized to the ferric form in the presence of EGCG relative to the normal spontaneous oxidation of this Hb. The fast elimination of ferrous Hb is probably due to the ability of EGCG to produce hydrogen peroxide (H2O2) as these reactions were almost completely reversed by the addition of catalase and superoxide dismutase to the reaction medium. EGCG, however, effectively reduced ferryl back to ferric Hb in a biphasic kinetic reaction at physiological pH. At acidic pH where the autoreduction of protonated ferryl Hb is enhanced, a monophasic reduction process of the ferry] heme is achieved. A balance between pro and antioxidant properties of EGCG should be taken into account if EGCG is used in combination therapy with redox active acellular Hbs. Published by Elsevier Inc.
C1 [Jia, Yiping; Alayash, Abdu I.] US FDA, LBVB, CBER, Div Hematol, Bethesda, MD 20892 USA.
RP Jia, YP (reprint author), US FDA, LBVB, CBER, Div Hematol, NIH Campus,8800 Rockville Pike,Bldg 29,Rm 129, Bethesda, MD 20892 USA.
EM yiping.jia@fda.hhs.gov
NR 68
TC 13
Z9 14
U1 3
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD SEP 1
PY 2008
VL 45
IS 5
BP 659
EP 666
DI 10.1016/j.freeradbiomed.2008.05.010
PG 8
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 345KK
UT WOS:000258995200015
PM 18539156
ER
PT J
AU Hussain, SP
AF Hussain, S. Perwez
TI Inflammation and cancer: Is AID aiding?
SO GASTROENTEROLOGY
LA English
DT Editorial Material
ID INDUCED CYTIDINE DEAMINASE; ACTIVATION; EXPRESSION; MICRORNA-155;
MALIGNANCIES
C1 NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Hussain, SP (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [Z99 CA999999]
NR 15
TC 2
Z9 3
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD SEP
PY 2008
VL 135
IS 3
BP 736
EP 737
DI 10.1053/j.gastro.2008.07.035
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 346WC
UT WOS:000259099300009
PM 18692057
ER
PT J
AU Baege, AC
Fink, D
Baker, C
Niederhuber, J
AF Baege, A. C.
Fink, D.
Baker, C.
Niederhuber, J.
TI Isolation, characterization, and potential role of cervical stem cells
in HPV-induced cervical carcinogenesis
SO GEBURTSHILFE UND FRAUENHEILKUNDE
LA English
DT Meeting Abstract
DE HPV; HPV infection; carcinogenesis; cervical cancer; stem cells
C1 [Baege, A. C.; Fink, D.] Univ Spital Zurich, Klin Gynakol, Zurich, Switzerland.
[Baker, C.; Niederhuber, J.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0016-5751
J9 GEBURTSH FRAUENHEILK
JI Geburtshilfe Frauenheilkd.
PD SEP
PY 2008
VL 68
SU 1
BP S143
EP S143
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 353OO
UT WOS:000259577500593
ER
PT J
AU Ortiz, M
Kaessmann, H
Zhang, K
Bashirova, A
Carrington, M
Quintana-Murci, L
Telenti, A
AF Ortiz, M.
Kaessmann, H.
Zhang, K.
Bashirova, A.
Carrington, M.
Quintana-Murci, L.
Telenti, A.
TI The evolutionary history of the CD209 (DC-SIGN) family in humans and
non-human primates
SO GENES AND IMMUNITY
LA English
DT Article
DE C-type lectins; HIV; Ebola; mycobacteria; innate immunity; DC-SIGN
ID AMINO-ACID SITES; POSITIVE SELECTION; TYPE-1 INFECTION; INNATE-IMMUNITY;
POLYMORPHISMS; RECEPTORS; DOMAIN; SUSCEPTIBILITY; TRIM5-ALPHA;
LIKELIHOOD
AB The CD209 gene family that encodes C-type lectins in primates includes CD209 (DC-SIGN), CD209L (L-SIGN) and CD209L2. Understanding the evolution of these genes can help understand the duplication events generating this family, the process leading to the repeated neck region and identify protein domains under selective pressure. We compiled sequences from 14 primates representing 40 million years of evolution and from three non-primate mammal species. Phylogenetic analyses used Bayesian inference, and nucleotide substitutional patterns were assessed by codon-based maximum likelihood. Analyses suggest that CD209 genes emerged from a first duplication event in the common ancestor of anthropoids, yielding CD209L2 and an ancestral CD209 gene, which, in turn, duplicated in the common Old World primate ancestor, giving rise to CD209L and CD209. K(A)/K(S) values averaged over the entire tree were 0.43 (CD209), 0.52 (CD209L) and 0.35 (CD209L2), consistent with overall signatures of purifying selection. We also assessed the Toll-like receptor (TLR) gene family, which shares with CD209 genes a common profile of evolutionary constraint. The general feature of purifying selection of CD209 genes, despite an apparent redundancy (gene absence and gene loss), may reflect the need to faithfully recognize a multiplicity of pathogen motifs, commensals and a number of self-antigens.
C1 [Ortiz, M.; Zhang, K.; Telenti, A.] Univ Lausanne, Inst Microbiol, Lausanne, Switzerland.
[Kaessmann, H.] Univ Lausanne, Ctr Integrat Genom, Lausanne, Switzerland.
[Bashirova, A.] USA, Med Res Inst Infect Dis, Lab Mol Immunol, Frederick, MD USA.
[Carrington, M.] NCI, SAIC Frederick Inc, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Quintana-Murci, L.] Inst Pasteur, CNRS, URA3012, Paris, France.
RP Telenti, A (reprint author), CHU Vaudois, Inst Microbiol, Bugnon 48, CH-1011 Lausanne, Switzerland.
EM amalio.telenti@chuv.ch
RI Kaessmann, Henrik/B-4989-2013;
OI Quintana-Murci, Lluis/0000-0003-2429-6320
FU Swiss National Science Foundation; Faculty of Biology and Medicine of
the University of Lausanne; National Cancer Institute; National
Institutes of Health [N01-CO-12400]; Intramural Research Program of the
NIH; Center for Cancer Research
FX We thank Keith Mansfield and Kuei-Chin Lin from the New England Primate
Center, and Charles Buillard and Eugene Chabloz from the Zoo of Servion
for materials. This work was funded by the Swiss National Science
Foundation and a grant for interdisciplinary research from the Faculty
of Biology and Medicine of the University of Lausanne. This project has
been funded in whole or in part with federal funds from the National
Cancer Institute, National Institutes of Health, under contract
N01-CO-12400. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products or
organizations imply endorsement by the US Government. This research was
supported in part by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research.
NR 32
TC 18
Z9 19
U1 1
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1466-4879
J9 GENES IMMUN
JI Genes Immun.
PD SEP
PY 2008
VL 9
IS 6
BP 483
EP 492
DI 10.1038/gene.2008.40
PG 10
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA 344LM
UT WOS:000258928500001
PM 18528403
ER
PT J
AU Belanger, S
Tai, LH
Anderson, SK
Makrigiannis, AP
AF Belanger, S.
Tai, L-H
Anderson, S. K.
Makrigiannis, A. P.
TI Ly49 cluster sequence analysis in a mouse model of diabetes: an expanded
repertoire of activating receptors in the NOD genome
SO GENES AND IMMUNITY
LA English
DT Article
DE Ly49; diabetes; natural killer cells; comparative immunology/evolution;
cell surface molecules
ID NATURAL-KILLER-CELL; NK CELLS; LY-49D RECEPTOR; MICE; GENE; RECOGNITION;
H-2D(D); PHOSPHORYLATION; CYTOMEGALOVIRUS; COMPLEX
AB The mouse Ly49 and human killer cell immunoglobulin-like receptors (KIR) gene clusters encode activating and inhibitory class I MHC receptors on natural killer (NK) cells. A direct correlation between the presence of multiple activating KIR and various human autoimmune diseases including diabetes has been shown. Previous studies have implicated NK cell receptors in the development of diabetes in the non-obese diabetic ( NOD) inbred mouse strain. To assess the contribution of Ly49 to NOD disease acceleration the Ly49 gene cluster of these mice was sequenced. Remarkably, the NOD Ly49 haplotype encodes the largest haplotype and the most functional activating Ly49 of any known mouse strain. These activating Ly49 include three Ly49p-related and two Ly49h-related genes. The NOD cluster contains large regions highly homologous to both C57BL/6 and 129 haplotypes, suggesting unequal crossing over as a mechanism of Ly49 haplotype evolution. Interestingly, the 129-like region has duplicated in the NOD genome. Thus, the NOD Ly49 cluster is a unique mix of elements seen in previously characterized Ly49 haplotypes resulting in a disproportionately large number of functional activating Ly49 genes. Finally, the functionality of activating Ly49 in NOD mice was confirmed in cytotoxicity assays.
C1 [Belanger, S.; Tai, L-H; Makrigiannis, A. P.] Univ Montreal, Inst Rech Clin Montreal, Lab Mol Immunol, Montreal, PQ H2W 1R7, Canada.
[Belanger, S.; Tai, L-H; Makrigiannis, A. P.] McGill Univ, Dept Microbiol & Immunol, Montreal, PQ, Canada.
[Anderson, S. K.] SAIC Frederick Inc, NCI, Basic Res Program, Frederick, MD USA.
RP Makrigiannis, AP (reprint author), Univ Montreal, Inst Rech Clin Montreal, Lab Mol Immunol, Rm 1340,110 Ave Pins Ouest, Montreal, PQ H2W 1R7, Canada.
EM makriga@ircm.qc.ca
RI Anderson, Stephen/B-1727-2012
OI Anderson, Stephen/0000-0002-7856-4266
FU Canadian Institutes of Health Research [CIHR MOP 62841]; Intramural
Research Program of the NIH; National Cancer Institute; Center for
Cancer Research; National Institutes of Health [NO1-CO-12400]; Fonds de
la recherche en sante du Quebec; CIHR Cancer Training Program; CIHR
FX We thank Christophe Benoist for his essential aid in initiating the
sequencing of the NOD Ly49 region. We also thank Dr Silvia Vidal for her
help with MCMV plaque assays and reagents. We gratefully acknowledge the
genome sequencing efforts of The Wellcome Trust Sanger Institute. This
work was supported by an Operating Grant from the Canadian Institutes of
Health Research (CIHR MOP 62841). This research was supported in part by
the Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research. This project has also been funded in part
with Federal funds from the National Cancer Institute, National
Institutes of Health, under contract no. NO1-CO-12400. SB is supported
by a scholarship from the Fonds de la recherche en sante du Quebec. L-HT
is supported by a CIHR Cancer Training Program scholarship. APM is
supported by a New Investigator Award from the CIHR.
NR 51
TC 25
Z9 25
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1466-4879
J9 GENES IMMUN
JI Genes Immun.
PD SEP
PY 2008
VL 9
IS 6
BP 509
EP 521
DI 10.1038/gene.2008.43
PG 13
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA 344LM
UT WOS:000258928500004
PM 18528402
ER
PT J
AU Szamecz, B
Rutkai, E
Cuchalova, L
Munzarova, V
Herrmannova, A
Nielsen, KH
Burela, L
Hinnebusch, AG
Valasek, L
AF Szamecz, Bela
Rutkai, Edit
Cuchalova, Lucie
Munzarova, Vanda
Herrmannova, Anna
Nielsen, Klaus H.
Burela, Laxminarayana
Hinnebusch, Alan G.
Valasek, Leos
TI eIF3a cooperates with sequences 5 ' of uORF1 to promote resumption of
scanning by post-termination ribosomes for reinitiation on GCN4 mRNA
SO GENES & DEVELOPMENT
LA English
DT Article
DE translation initiation; reinitiation; eIF3; 40S ribosomal subunit; GCN4;
short uORF
ID EUKARYOTIC TRANSLATION INITIATION; START CODON SELECTION; OPEN READING
FRAME; IN-VIVO; RECOGNITION MOTIF; 40S SUBUNITS; STOP CODONS; BINDING;
YEAST; COMPLEXES
AB Yeast initiation factor eIF3 ( eukaryotic initiation factor 3) has been implicated in multiple steps of translation initiation. Previously, we showed that the N-terminal domain (NTD) of eIF3a interacts with the small ribosomal protein RPS0A located near the mRNA exit channel, where eIF3 is proposed to reside. Here, we demonstrate that a partial deletion of the RPS0A-binding domain of eIF3a impairs translation initiation and reduces binding of eIF3 and associated eIFs to native preinitiation complexes in vivo. Strikingly, it also severely blocks the induction of GCN4 translation that occurs via reinitiation. Detailed examination unveiled a novel reinitiation defect resulting from an inability of 40S ribosomes to resume scanning after terminating at the first upstream ORF (uORF1). Genetic analysis reveals a functional interaction between the eIF3a-NTD and sequences 5 ' of uORF1 that is critically required to enhance reinitiation. We further demonstrate that these stimulatory sequences must be positioned precisely relative to the uORF1 stop codon and that reinitiation efficiency after uORF1 declines with its increasing length. Together, our results suggest that eIF3 is retained on ribosomes throughout uORF1 translation and, upon termination, interacts with its 5 ' enhancer at the mRNA exit channel to stabilize mRNA association with post-termination 40S subunits and enable resumption of scanning for reinitiation downstream.
C1 [Szamecz, Bela; Rutkai, Edit; Cuchalova, Lucie; Munzarova, Vanda; Herrmannova, Anna; Valasek, Leos] Inst Microbiol AVCR, Lab Regulat Gene Express, Prague 14220, Czech Republic.
[Nielsen, Klaus H.] Univ Aarhus, Dept Mol Biol, Ctr mRNP Biogenesis & Metab, DK-8000 Aarhus, Denmark.
[Burela, Laxminarayana; Hinnebusch, Alan G.] NICHHD, Lab Gene Regulat & Dev, Bethesda, MD 20892 USA.
RP Valasek, L (reprint author), Inst Microbiol AVCR, Lab Regulat Gene Express, Videnska 1083, Prague 14220, Czech Republic.
EM valasekl@biomed.cas.cz
RI Herrmannova, Anna/I-1745-2014; Valasek, Leos/I-5743-2014; Cuchalova,
Lucie/H-4650-2014
FU Wellcome Trusts [076456/Z/05/Z]; Howard Hughes Medical Institute;
Fogarty International Center [R01 TW007271]; Purkyne from the Academy of
Sciences of the Czech Republic; Institute Research Concept
[AV0Z50200510]; National Institutes of Health
FX We are thankful to Libor Krasny for critical reading of the manuscript,
to the members of the Valasek and Krasny laboratories for helpful
suggestions, and to Olga Krydova, Anna Delijannisova, and Ilona
Krupickova for technical and administrative assistance. This research
was supported for the most part by The Wellcome Trusts Grant
076456/Z/05/Z, and partly also by the Howard Hughes Medical Institute,
by NIH Research Grant R01 TW007271 funded by the Fogarty International
Center, by the Fellowship of Jan E. Purkyne from the Academy of Sciences
of the Czech Republic, by the Institute Research Concept AV0Z50200510,
and by the Intramural Research Program of the National Institutes of
Health.
NR 39
TC 63
Z9 64
U1 1
U2 4
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD SEP 1
PY 2008
VL 22
IS 17
BP 2414
EP 2425
DI 10.1101/gad.480508
PG 12
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 343TM
UT WOS:000258878100012
PM 18765792
ER
PT J
AU Mackwan, RR
Carver, GT
Kissling, GE
Drake, JW
Grogan, DW
AF Mackwan, Reena R.
Carver, Geraldine T.
Kissling, Grace E.
Drake, John W.
Grogan, Dennis W.
TI The rate and character of spontaneous mutation in Thermus thermophilus
SO GENETICS
LA English
DT Article
ID ARCHAEON SULFOLOBUS-ACIDOCALDARIUS; DNA-BINDING PROTEIN; EXTREME
THERMOPHILE; COMPARATIVE GENOMICS; FRAMESHIFT MUTATION; POLYMERASES;
REPAIR; IDENTIFICATION; PURIFICATION; EXPRESSION
AB Selection of spontaneous, loss-of-function mutations at two chromosomal loci (pyrF and pyrE) enabled the first molecular-level of replication fidelity in the extremely thermophilic bacterium Thermus thermophilus. Two different methods yielded similar mutation rates, mutational spectra determined by sequencing of independent mutants revealed a variety of replication errors distributed throughout the target genes. The genomic mutation rate estimated from these targets, 0.00097 +/- 0.00052 per replication, was lower than corresponding estimates from mesophilic microorganisms, primarily because of a low rate of base substitution.. However, both the rate and spectrum of spontaneous mutations T. thermophilus resembled those of the thermoacidophilic archaeon Sulfolobus acidocaldarius, despite important molecular differences between these two thermophiles mid their genomes.
C1 [Mackwan, Reena R.; Grogan, Dennis W.] Univ Cincinnati, Dept Biol Sci, Cincinnati, OH 45221 USA.
[Carver, Geraldine T.; Drake, John W.] Natl Inst Environm Hlth Sci, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
[Kissling, Grace E.] Natl Inst Environm Hlth Sci, Biostat Branch, Res Triangle Pk, NC 27709 USA.
RP Grogan, DW (reprint author), Univ Cincinnati, Dept Biol Sci, 614 Rieveschl Hall ML 0006,Clifton Court, Cincinnati, OH 45221 USA.
EM grogandw@email.uc.edu
FU National Science Foundation [MCB 9733103, MCB 0543910]; National
Institutes of Health National Institute of Environmental Health Sciences
FX We thank Marilyn Diaz and Tom Kunkel for critical readings of the
manuscript. This work was supported by National Science Foundation
grants MCB 9733103 and MCB 0543910 to D.W.G. and by the Intramural
Research Program of the National Institutes of Health National Institute
of Environmental Health Sciences.
NR 39
TC 15
Z9 15
U1 0
U2 5
PU GENETICS
PI BALTIMORE
PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD SEP
PY 2008
VL 180
IS 1
BP 17
EP 25
DI 10.1534/genetics.108.089086
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 356DI
UT WOS:000259758500003
PM 18723895
ER
PT J
AU Eydmann, T
Sommariva, E
Inagawa, T
Mian, S
Klar, AJS
Dalgaard, JZ
AF Eydmann, T.
Sommariva, E.
Inagawa, T.
Mian, S.
Klar, A. J. S.
Dalgaard, J. Z.
TI Rtf1-mediated eukaryotic site-specific replication termination
SO GENETICS
LA English
DT Article
ID RNA-POLYMERASE-I; TRANS-ACTING FACTORS; SACCHAROMYCES-CEREVISIAE;
SCHIZOSACCHAROMYCES-POMBE; TRANSCRIPTION TERMINATION; DNA-REPLICATION;
FISSION YEAST; RIBOSOMAL DNA; FORK ARREST; ESCHERICHIA-COLI
AB The molecular mechanisms mediating eukaryotic replication termination and pausing remain largely unknown. Here we present the molecular characterization of Rtf1 that mediates site-specific replication termination at the polar Schizosaccharomyces pombe barrier RTS1. We show that Rtf1 possesses two chimeric myb/SANT domains: one is able to interact with the repeated motifs encoded by the RTS1 element as well as the elements enhancer region, while the other shows only a weak DNT binding activity. In addition we show that the C-terminal tail of Rtf1 mediates self-interaction, and deletion of this tail has a dominant phenotype. Finally, we identify a point imitation in Rtf1 domain I that converts the RTS1 element into a replication barrier of the opposite polarity. Together our data establish that multiple protein DNA and protein-protein interactions between Rtf1 molecules and both the repeated motifs and the enhancer region of RTS1 are required for site-specific termination at the RTS1 element.
C1 [Eydmann, T.; Sommariva, E.; Inagawa, T.; Dalgaard, J. Z.] Marie Curie Res Inst, Oxted RH8 0TL, Surrey, England.
[Mian, S.] Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA 94720 USA.
[Klar, A. J. S.] NCI, Gene Regulat & Chromosome Biol Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA.
RP Dalgaard, JZ (reprint author), Marie Curie Res Inst, Oxted RH8 0TL, Surrey, England.
EM j.dalgaard@mcri.ac.uk
RI Sommariva, Elena/K-4078-2016
OI Sommariva, Elena/0000-0003-2172-4051
FU National Cancer Institute of the National Institutes of Health; Marie
Curie Cancer Care; Association of International Cancer Research
FX We thank our colleagues at the Marie Curie Research Institute for
helpful suggestions and interactions. A special thanks to Rob Cross,
Natalie Mansfield, S. Jack Carlisle, Doug Drummond, Sonya Vengrova, and
Michael Bonaduce for technical assistance. This work was supported by
the Intramural Research Program of the National Cancer Institute of the
National Institutes of Health (A.J.S.K.), the Marie Curie Cancer Care
(J.Z.D.) and the Association of International Cancer Research (J.Z.D.).
NR 55
TC 25
Z9 27
U1 0
U2 2
PU GENETICS SOCIETY AMERICA
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 0016-6731
EI 1943-2631
J9 GENETICS
JI Genetics
PD SEP
PY 2008
VL 180
IS 1
BP 27
EP 39
DI 10.1534/genetics.108.089243
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 356DI
UT WOS:000259758500004
PM 18723894
ER
PT J
AU Frydrychova, RC
Mason, JM
Archer, TK
AF Frydrychova, Radmila Capkova
Mason, James M.
Archer, Trevor K.
TI HP1 is distributed within distinct chromatin domains at drosophila
telomeres
SO GENETICS
LA English
DT Article
ID POSITION-EFFECT VARIEGATION; HET-A; HETEROCHROMATIN PROTEIN-1;
MELANOGASTER TELOMERES; LYSINE-9 METHYLATION; DIFFERENT MECHANISMS;
FUNCTIONAL-ANALYSIS; CHROMOSOME ENDS; DNA-SEQUENCES; GENE
AB Telomeric regions In Drosophila are Composed of till-cc subdomains. A chromosome cap distinguishes the chromosome end from a DNA double-strand break; an an-ay of retrotransposons, HeT-A, TART, and TAHRE (HTT), maintains telomere length by targeted transposition to chromosome ends; and telomere-associated sequence (TAS), which consists of a mosaic of complex repeated sequences, has been identified as a source of gene silencing. Heterochromatin protein 1 (HP1) and HP1-ORC-associated protein (HOAP) are major protein components of the telomere cap in Drosophila and are required for telomere- protein stability. Besides the chromosome cap, HP1 is also localized along the HTT array and in TAS. Mutants for Su(var)205, the gene encoding HP1, have decreased the HP1 level in the HTT array and increased transcription of individual HeT-A elements. This suggests that HP1 levels directly affect HeT-A activity along, the HTT array, although they have little or no effect on transcription of a while reporter gene in the HTT. Chromatin immunoprecipitation to identify other heterochromatic proteins indicates that TAS and the HTT array may be distinct from either heterochromatin or euchromatin.
C1 [Archer, Trevor K.] NIEHS, Mol Carcinogenesis Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Frydrychova, Radmila Capkova; Mason, James M.] NIEHS, Mol Genet Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Archer, TK (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, DHHS, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM archer1@niehs.nih.gov
RI Capkova Frydrychova, Radmila/H-4187-2014
FU National Institutes of Health National Institute of Environmental Health
Sciences
FX We thank Karen Adelman and Daniel Menendez for critical reading of: the
manuscript. and Harald Biessmann for providing sequences of EY and KG
insertions and comments to the manuscript. This research was supported
by the Intramural Research Program of National Institutes of Health
National Institute of Environmental Health Sciences.
NR 56
TC 18
Z9 18
U1 0
U2 3
PU GENETICS
PI BALTIMORE
PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD SEP
PY 2008
VL 180
IS 1
BP 121
EP 131
DI 10.1534/genetics.108.090647
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 356DI
UT WOS:000259758500012
PM 18723888
ER
PT J
AU Zaykin, DV
Pudovkin, A
Weir, BS
AF Zaykin, Dmitri V.
Pudovkin, Alexander
Weir, Bruce S.
TI Correlation-based inference for linkage disequilibrium with multiple
alleles
SO GENETICS
LA English
DT Article
ID GOODNESS-OF-FIT; RANDOMLY MATING POPULATIONS; GAMETIC DISEQUILIBRIUM;
TESTS; LOCI; ASSOCIATION; FREQUENCIES; STATISTICS; PREDICTORS; PATTERNS
AB The correlation between alleles at a pair of genetic loci is a measure of linkage disequilibrium. The square of the sample correlation multiplied by sample size provides the usual test statistic for the hypothesis of no disequilibrium for loci with two alleles and this relation has proved useful for study design and marker selection. Nevertheless, this relation holds only in a diallelic case, and an extension to multiple alleles has not been made. Here we introduce a similar statistic, R-z, which leads to correlaiton -based test for loci with multiple alleles: for a pair of loci with k and m alleles, and a sample of n individuals, the approximate distribution of n(k-1) (m-1)/(km)R-2 under independence between loci is chi(2)((k-1)(m-1)). One advantage of this statistic is that is can be interpreted as the total correlation between a pair of loci. When the phase of two-locus genotypes is know, the approach is equivalent to a test for the overall correlation between rows and columns in a contingency table. In the phase-known case, R-2 is strong competitor to approaches such as Pearson's chi square, Fisher's exact test, and a test based on Cressie and Read's power divergence statistic. We combine this approach with our previous composite-disequilibrium measures to address the case when the genotypic phase is unknown. Calculation os the new multiallele test statistic and its P-value is very simple and utilizes the approximate distribution of R-2. We provide a computer program that evaluates approximate as well as "exact" permutational P-values.
C1 [Zaykin, Dmitri V.] Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC 27709 USA.
[Pudovkin, Alexander] Russian Acad Sci, Inst Marine Biol, Vladivostok 690041, Russia.
[Weir, Bruce S.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
RP Zaykin, DV (reprint author), Natl Inst Environm Hlth Sci, NIH, MD A3-03,South Bldg 101-B356B,POB 12233, Res Triangle Pk, NC 27709 USA.
EM zaykind@niehs.nih.gov
FU National Institutes of Health (NIH) [GM 07591]; National Institute of
Environmental Health Sciences
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health (NIH), National Institute of
Environmental Health Sciences, and by NIH GM 07591.
NR 40
TC 41
Z9 41
U1 0
U2 6
PU GENETICS
PI BALTIMORE
PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD SEP
PY 2008
VL 180
IS 1
BP 533
EP 545
DI 10.1534/genetics.108.089409
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 356DI
UT WOS:000259758500043
PM 18757931
ER
PT J
AU Walser, JC
Ponger, L
Furano, AV
AF Walser, Jean-Claude
Ponger, Loic
Furano, Anthony V.
TI CpG dinucleotides and the mutation rate of non-CpG DNA
SO GENOME RESEARCH
LA English
DT Article
ID HUMAN GENOME; LINE-1 RETROTRANSPOSONS; CYTOSINE METHYLATION; MOLECULAR
EVOLUTION; NUCLEOTIDE-SEQUENCE; CHIMPANZEE GENOMES; LOCAL SIMILARITY;
MAMMALIAN GENOME; FOREIGN DNA; GC-CONTENT
AB The neutral mutation rate is equal to the base substitution rate when the latter is not affected by natural selection. Differences between these rates may reveal that factors such as natural selection, linkage, or a mutator locus are affecting a given sequence. We examined the neutral base substitution rate by measuring the sequence divergence of similar to 30,000 pairs of inactive orthologous L1 retrotransposon sequences interspersed throughout the human and chimpanzee genomes. In contrast to other studies, we related ortholog divergence to the time ( age) that the L1 sequences resided in the genome prior to the chimpanzee and human speciation. As expected, the younger orthologs contained more hypermutable CpGs than the older ones because of their conversion to TpGs (and CpAs). Consequently, the younger orthologs accumulated more CpG mutations than the older ones during the similar to 5 million years since the human and chimpanzee lineages separated. But during this same time, the younger orthologs also accumulated more non-CpG mutations than the older ones. In fact, non-CpG and CpG mutations showed an almost perfect (R-2 = 0.98) correlation for similar to 97% of the ortholog pairs. The correlation is independent of G + C content, recombination rate, and chromosomal location. Therefore, it likely reflects an intrinsic effect of CpGs, or mutations thereof, on non-CpG DNA rather than the joint manifestation of the chromosomal environment. The CpG effect is not uniform for all regions of non-CpG DNA. Therefore, the mutation rate of non-CpG DNA is contingent to varying extents on local CpG content. Aside from their implications for mutational mechanisms, these results indicate that a precise determination of a uniform genome-wide neutral mutation rate may not be attainable.
C1 [Walser, Jean-Claude; Furano, Anthony V.] NIDDK, Sect Genom Struct & Funct, Lab Mol & Cellular Biol, NIH, Bethesda, MD 20892 USA.
[Ponger, Loic] Museum Natl Hist Nat, UMS Regulat & Dynam Genomes 503, F-75005 Paris 5, France.
RP Furano, AV (reprint author), NIDDK, Sect Genom Struct & Funct, Lab Mol & Cellular Biol, NIH, Bethesda, MD 20892 USA.
EM avf@helix.nih.gov
FU NIH; NIDDK; National Museum of Natural History, France
FX We thank Deborah M. Hinton and Natalia Wesolowska for their valuable
suggestions during the preparation of the manuscript. We are grateful to
the UCSC Genome Browser Database group for providing various sequences
files and programs. Furthermore, we thank Marcos Antezana (U. Chicago)
for stimulating discussions on mutational aspects of the response to
foreign DNA in eukaryotes. The Intramural Research Program of the NIH,
NIDDK, funded A. V. F. and J.-C.W., and the National Museum of Natural
History, France funded L. P.
NR 73
TC 30
Z9 30
U1 1
U2 2
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD SEP
PY 2008
VL 18
IS 9
BP 1403
EP 1414
DI 10.1101/gr.076455.108
PG 12
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 342AH
UT WOS:000258756500003
PM 18550801
ER
PT J
AU Johnson, CC
Kessel, B
Riley, TL
Ragard, LR
Williams, CR
Xu, JL
Buys, SS
AF Johnson, Christine C.
Kessel, Bruce
Riley, Thomas L.
Ragard, Lawrence R.
Williams, Craig R.
Xu, Jian-Lun
Buys, Saundra S.
CA PLCO Project Team
TI The epidemiology of CA-125 in women without evidence of ovarian cancer
in the prostate, lung, colorectal and ovarian cancer (PLCO) screening
trial
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE epidemiology; CA-125; race/ethnicity
ID HEALTHY POSTMENOPAUSAL WOMEN; HORMONE REPLACEMENT THERAPY; SERUM CA-125;
TUMOR-MARKERS; ANTIGEN CA125; ENDOMETRIUM; RECRUITMENT; RISK; GENE
AB Objective. To determine the epidemiology of CA-125 in women without ovarian cancer.
Methods. We analyzed demographic, medical and lifestyle characteristics related to CA-125, measured using the Centocor CA-125II RIA assay, among 25,608 multi-ethnic U.S. women aged 55-74 years enrolled in a cancer screening trial and found to have no evidence of ovarian cancer.
Results. Mean CA-125 level was 11.9 U/ml (SD 8.3); median 10.0 U/ml, interquartile range 8.0-14.0. High levels, using the clinical cut point of >= 35 U/ml, were associated with increased age (p<0.001) and former smoking (p<0.021), while hysterectomy and obesity were protective (p<0.001). Mean levels were higher with increasing age (p<0.001), ever use of hormone therapy (p<0.001), former smoking (p<0.017) and history of breast cancer (p<0.002), but lower (p<0.001) with non-White status, previous hysterectomy, current smoking, and obesity. Current hormone therapy use was not associated with CA-125 in women without a uterus.
Conclusion. In post-menopausal women without ovarian cancer, CA-125 level is influenced by a number of factors, including race/ethnicity, age, hysterectomy, smoking history and obesity. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Johnson, Christine C.] Henry Ford Hosp, Josephine Ford Canc Ctr, Detroit, MI 48202 USA.
[Kessel, Bruce] Pacific Hlth Res Inst, Honolulu, HI USA.
[Kessel, Bruce] Univ Hawaii, Honolulu, HI 96822 USA.
[Riley, Thomas L.; Williams, Craig R.] Informat Management Syst, Rockville, MD USA.
[Ragard, Lawrence R.] Westat Corp, Rockville, MD USA.
[Xu, Jian-Lun] NCI, Biometry Res Grp, Canc Prevent Div, NIH,DHHS, Bethesda, MD 20892 USA.
[Buys, Saundra S.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA.
RP Johnson, CC (reprint author), Henry Ford Hosp, Josephine Ford Canc Ctr, 1 Ford Pl,5C, Detroit, MI 48202 USA.
EM cjohnso1@hfhs.org
OI Kessel, Bruce/0000-0001-9979-2068; Johnson, Christine
Cole/0000-0002-6864-6604
FU NCI NIH HHS [N01 CN25404, N01 CN25512, N01 CN25516, N01 CN25522, N01
CN75022]
NR 31
TC 40
Z9 42
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD SEP
PY 2008
VL 110
IS 3
BP 383
EP 389
DI 10.1016/j.ygyno.2008.05.006
PG 7
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 349XN
UT WOS:000259316700018
PM 18586313
ER
PT J
AU Patel, KV
AF Patel, Kushang V.
TI Variability and heritability of hemoglobin concentration: an opportunity
to improve understanding of anemia in older adults
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Editorial Material
ID UNEXPLAINED ANEMIA; MORTALITY; HOSPITALIZATION; ERYTHROPOIETIN;
DEFINITION; IMPACT; STATES
C1 NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
RP Patel, KV (reprint author), NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
EM patelku@mail.hih.gov
FU Intramural NIH HHS
NR 20
TC 7
Z9 7
U1 0
U2 0
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOL-HEMATOL J
JI Haematol-Hematol. J.
PD SEP
PY 2008
VL 93
IS 9
BP 1281
EP 1283
DI 10.3324/haematol.13692
PG 3
WC Hematology
SC Hematology
GA 347DF
UT WOS:000259120100001
PM 18757846
ER
PT J
AU Salaverria, I
Zettl, A
Beaa, S
Hartmann, EM
Dave, SS
Wright, GW
Boerma, EJ
Kluin, PM
Ott, G
Chan, WC
Weisenburger, DD
Lopez-Guillermo, A
Gascoyne, RD
Delabie, J
Rimsza, LM
Braziel, RM
Jaffe, ES
Staudt, LM
Mueller-Hermelink, HK
Campo, E
Rosenwald, A
AF Salaverria, Itziar
Zettl, Andreas
Bea, Silvia
Hartmann, Elena M.
Dave, Sandeep S.
Wright, George W.
Boerma, Evert-Jan
Kluin, Philip M.
Ott, German
Chan, Wing C.
Weisenburger, Dennis D.
Lopez-Guillermo, Armando
Gascoyne, Randy D.
Delabie, Jan
Rimsza, Lisa M.
Braziel, Rita M.
Jaffe, Elaine S.
Staudt, Louis M.
Mueller-Hermelink, Hans Konrad
Campo, Elias
Rosenwald, Andreas
CA LLMPP
TI Chromosomal alterations detected by comparative genomic hybridization in
subgroups of gene expression-defined Burkitt's lymphoma
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Article
DE Burkitt's lymphoma; comparative genomic hybridization; DLBCL; gene
expression
ID B-CELL LYMPHOMA; MOLECULAR PATHOGENESIS; ABNORMALITIES; ABERRATIONS;
ADOLESCENTS; PROGNOSIS; ADULTS
AB Background
Burkitt's lymphoma is an aggressive B-cell lymphoma characterized by typical morph 0 logical, immunophenotypic and molecular features. Gene expression profiling provided a molecular signature of Burkitt's lymphoma, but also demonstrated that a subset of aggressive B-cell lymphomas not fulfilling the current World Health Organization criteria for the diagnosis of Burkitt's lymphoma nonetheless show a molecular signature of Burkitt's lymphoma ('discrepant Burkitt's lymphoma'). Given the different treatment of Burkitt's lymphoma and diffuse large B-cell lymphomas we investigated molecular differences within gene expression-defined Burkitt's lymphoma.
Design and Methods
We studied tumors from 51 Burkitt's lymphoma patients, comprising 26 with classic Burkitt's lymphoma, 17 with atypical Burkitt's lymphoma and 8 with 'discrepant Burkitt's lymphoma', by comparative genomic hybridization and gene expression profiling.
Results
Classic and atypical Burkitt's lymphoma (excluding 'discrepant Burkitt's lymphoma'), in adult and pediatric cases do not differ in underlying genomic imbalances or gene expression suggesting that these subgroups are molecularly homogeneous. 'Discrepant Burkitt's lymphoma', however, differ dramatically in the absolute number of alterations from classic/atypical Burkitt's lymphoma and from diffuse large B-cell lymphoma. Moreover, this category includes lymphomas that carry both the t(14;18) and t(8;14) translocations and are clinically characterized by presentation in adult patients and an aggressive course.
Conclusions
Pediatric and adult Burkitt's lymphoma are molecularly homogeneous, whereas 'discrepant Burkitt's lymphoma' differ in underlying genetic and clinical features from typical/atypical Burkitt's lymphoma. 'Discrepant Burkitt's lymphoma' may therefore form a distinct genetic subgroup of aggressive B-cell lymphomas, which show poor response to multi-agent chemotherapy.
C1 [Zettl, Andreas; Hartmann, Elena M.; Ott, German; Mueller-Hermelink, Hans Konrad; Rosenwald, Andreas] Univ Wurzburg, Inst Pathol, D-97080 Wurzburg, Germany.
[Salaverria, Itziar; Bea, Silvia; Campo, Elias] Univ Barcelona, Dept Pathol, Barcelona, Spain.
[Dave, Sandeep S.; Staudt, Louis M.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
[Wright, George W.] NCI, Biometr Res Branch, NIH, Bethesda, MD 20892 USA.
[Boerma, Evert-Jan; Kluin, Philip M.] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol, NL-9713 AV Groningen, Netherlands.
[Chan, Wing C.; Weisenburger, Dennis D.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
[Lopez-Guillermo, Armando] Univ Barcelona, Hematol Hosp Clin, Barcelona, Spain.
[Gascoyne, Randy D.] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Delabie, Jan] Norwegian Radium Hosp, Norway Hosp Clin, Oslo, Norway.
[Rimsza, Lisa M.] Univ Arizona, Dept Pathol, Tucson, AZ USA.
[Braziel, Rita M.] Oregon Hlth & Sci Univ, Dept Pathol, Portland, OR 97201 USA.
[Jaffe, Elaine S.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Ott, German] Robert Bosch Krankenhaus, Inst Clin Pathol, Stuttgart, Germany.
RP Rosenwald, A (reprint author), Univ Wurzburg, Inst Pathol, Josef Schneider Str 2, D-97080 Wurzburg, Germany.
EM Rosenwald@mail.uni-wuerzburg.de
RI SALAVERRIA, ITZIAR/L-2246-2015; Bea, Silvia/K-7699-2014;
OI SALAVERRIA, ITZIAR/0000-0002-2427-9822; Delabie,
Jan/0000-0001-5023-0689; Bea, Silvia/0000-0001-7192-2385; Campo,
elias/0000-0001-9850-9793
FU Spanish Comision Interministerial de Ciencia y Tecnologia (CICYT)
[SAF05/5855]; Instituto de Salud Carlos III Red Tematica de
Investigacion Cooperativa de Cancer; Interdisciplinary Center for
Clinical Research (IZKF) of the University of Wurzburg, Germany; NIH
[U01-CA84967]; National Cancer Institute, Bethesda, MD, USA
FX supported by grants from the Spanish Comision Interministerial de
Ciencia y Tecnologia (CICYT) SAF05/5855, Instituto de Salud Carlos III
Red Tematica de Investigacion Cooperativa de Cancer, by the
Interdisciplinary Center for Clinical Research (IZKF) of the University
of Wurzburg, Germany (AR, EH), and by an NIH grant (U01-CA84967) from
the National Cancer Institute, Bethesda, MD, USA, (WCC, AR, EC, GO,
HKMH).
NR 20
TC 45
Z9 46
U1 1
U2 5
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOL-HEMATOL J
JI Haematol-Hematol. J.
PD SEP
PY 2008
VL 93
IS 9
BP 1327
EP 1334
DI 10.3324/haematol.13071
PG 8
WC Hematology
SC Hematology
GA 347DF
UT WOS:000259120100009
PM 18698080
ER
PT J
AU Choi, CW
Chung, YJ
Slape, C
Aplan, PD
AF Choi, Chul Won
Chung, Yang Jo
Slape, Christopher
Aplan, Peter D.
TI Impaired differentiation and apoptosis of hematopoietic precursors in a
mouse model of myelodysplastic syndrome
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Article
DE myelodysplastic syndromes; mouse model; NUP98; HOXD13; apoptosis
ID IN-VITRO PROLIFERATION; PROGENITORS; CELLS; MDS; CULTURES; FAS
AB Expression of a NUP98-HOXD13 (NHD13) fusion gene, initially identified in a patient with myelodysplastic syndrome, leads to a highly penetrant myelodysplastic syndrome in mice that recapitulates all of the key features of the human disease. Expansion of undifferentiated lineage negative (lin(neg)) hematopoietic precursors that express NHD13 was markedly inhibited (30-fold) in vitro. Decreased expansion was accompanied by decreased production of terminally differentiated cells, indicating impaired differentiation of NHD13 precursors Rather than differentiate, the majority (80%) of NHD13 lin(neg) precursors underwent apoptotic cell death when induced to differentiate. These findings demonstrate that NHD13 lin(neg) cells provide a tractable in vitro system for studies of myelodysplastic syndrome.
C1 [Choi, Chul Won; Chung, Yang Jo; Slape, Christopher; Aplan, Peter D.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Aplan, PD (reprint author), Navy 8,Room 5101,8901 Wisconsin Ave, Bethesda, MD 20889 USA.
EM aplanp@mail.nih.gov
RI Slape, Christopher/H-8586-2016; Aplan, Peter/K-9064-2016
OI Slape, Christopher/0000-0002-8407-3092;
FU NIH; NCI
FX we would like to thank Dave Caudell, Helge Hartung, Sarah Beachy, Dwayne
Barber, and Eli Estey for helpful discussion. This research was
supported by the Intramural Research Program of the NIH, NCI.
NR 19
TC 13
Z9 13
U1 0
U2 0
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOL-HEMATOL J
JI Haematol-Hematol. J.
PD SEP
PY 2008
VL 93
IS 9
BP 1394
EP 1397
DI 10.3324/haematol.13042
PG 4
WC Hematology
SC Hematology
GA 347DF
UT WOS:000259120100020
PM 18603548
ER
PT J
AU Resnik, DB
AF Resnik, David B.
TI The Sex Kitten of Bioethics? Research Ethics Comes of Age
SO HASTINGS CENTER REPORT
LA English
DT Letter
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Resnik, DB (reprint author), NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU HASTINGS CENTER
PI BRIARCLIFF MANOR
PA 255 ELM ROAD, BRIARCLIFF MANOR, NY 10510 USA
SN 0093-0334
J9 HASTINGS CENT REP
JI Hastings Cent. Rep.
PD SEP-OCT
PY 2008
VL 38
IS 5
BP 5
EP 6
PG 2
WC Ethics; Health Care Sciences & Services; Medical Ethics; Social
Sciences, Biomedical
SC Social Sciences - Other Topics; Health Care Sciences & Services; Medical
Ethics; Biomedical Social Sciences
GA 357LZ
UT WOS:000259848600006
ER
PT J
AU Schelbert, EB
Vaughan-Sarrazin, MS
Welke, KF
Rosenthal, GE
AF Schelbert, E. B.
Vaughan-Sarrazin, M. S.
Welke, K. F.
Rosenthal, G. E.
TI Valve type and long-term outcomes after aortic valve replacement in
older patients
SO HEART
LA English
DT Article
ID PROSTHETIC HEART-VALVES; MEDICARE CLAIMS DATA; ADMINISTRATIVE DATA;
PORCINE BIOPROSTHESES; OPERATIVE MORTALITY; MECHANICAL VALVE;
RANDOMIZED-TRIAL; NEXT-GENERATION; UNITED-STATES; CABG SURGERY
AB Objective: To compare outcomes after aortic valve replacement (AVR) according to valve type specifically in older patients since valve-related risks are age-dependent; two randomised trials comparing mechanical and bioprosthetic valves found better outcomes with mechanical valves, but the samples were small and the patients were considerably younger than most who undergo AVR.
Design: Cohort study.
Setting: 1199 US hospitals.
Patients: Patients 65 years and older undergoing AVR during 1991-2003 (n = 307 054) identified through Medicare claims data.
Main outcome measures: Relative hazard ratios associated with bioprosthetic valves of (1) death (n = 131 719); (2) readmission for haemorrhage (n = 31 186), stroke (n = 25 051) or embolism (n = 5870); (3) reoperation (n = 4216); and (4) death or reoperation (reoperation free survival) in Cox regression analyses adjusting for demographic and clinical factors and hospital-level effects.
Results: Overall, 36% of AVR patients received bioprosthetic valves. Bioprosthetic valve recipients were older (77 vs 75 years, p<0.001) and generally had higher comorbidity. Bioprosthetic valve recipients had a slightly lower adjusted hazard ratios of death (HR = 0.97; 95% CI 0.95 to 0.98); readmission for haemorrhage, stroke or embolism (HR = 0.90, 95% CI 0.88 to 0.92); and death or reoperation (HR = 0.97, 95% CI 0.96 to 0.98), but a higher hazard ratio of reoperation (HR = 1.25, 95% CI 1.16 to 1.35). However, overall mortality and complication rates were more than 20 and 10 times higher, respectively, than the overall reoperation rate.
Conclusions: In older patients undergoing AVR, bioprosthetic valve recipients had slightly lower risks of death and complications, but a higher risk of reoperation. Given the low reoperation rate, these data suggest that bioprosthetic valves may be preferred in older patients.
C1 [Schelbert, E. B.] Univ Iowa, Dept Internal Med, Div Cardiovasc Dis, Carver Coll Med, Iowa City, IA 52242 USA.
[Vaughan-Sarrazin, M. S.; Rosenthal, G. E.] Univ Iowa, Dept Internal Med, Div Gen Internal Med, Carver Coll Med, Iowa City, IA 52242 USA.
[Vaughan-Sarrazin, M. S.; Rosenthal, G. E.] Iowa City VA Med Ctr, CRIISP, Iowa City, IA USA.
[Welke, K. F.] Oregon Hlth & Sci Univ, Div Cardiothorac Surg, Dept Surg, Portland, OR USA.
RP Schelbert, EB (reprint author), NHLBI, NIH, 10 Ctr Dr,Room B1D416,MSC 1061, Bethesda, MD 20892 USA.
EM schelberteb@nhlbi.nih.gov
OI Vaughan Sarrazin, Mary/0000-0001-8717-1061
FU NHLBI NIH HHS [K30HL04117-01A1]
NR 40
TC 21
Z9 21
U1 1
U2 2
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1355-6037
J9 HEART
JI Heart
PD SEP
PY 2008
VL 94
IS 9
BP 1181
EP 1188
DI 10.1136/hrt.2007.127506
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 337PH
UT WOS:000258447500021
PM 18070945
ER
PT J
AU Hosgood, HD
Baris, D
Zhang, Y
Zhu, Y
Zheng, T
Yeager, M
Welch, R
Zahm, S
Chanock, S
Rothman, N
Lan, Q
AF Hosgood, H. Dean, III
Baris, Dalsu
Zhang, Yawei
Zhu, Yong
Zheng, Tongzhang
Yeager, Meredith
Welch, Robert
Zahm, Shelia
Chanock, Stephen
Rothman, Nathaniel
Lan, Qing
TI Caspase polymorphisms and genetic susceptibility to multiple myeloma
SO HEMATOLOGICAL ONCOLOGY
LA English
DT Article
DE multiple myeloma; caspase; variant; polymorphism; snp : risk factors
ID LUNG-CANCER; CONNECTICUT WOMEN; BREAST-CANCER; IN-VIVO; APOPTOSIS; RISK;
ASSOCIATION; DEATH; ACTIVATION; VARIANTS
AB Multiple myeloma is a haematological malignency, characterized by clonal expansion of plastma cells. However, little is known about the cause of multiple rnyeloma. Cancer cells must avoid apoptosis to ensure unregulated tumour formation and growth. The highly conserved caspase cascade is essential to the regulation of the apoptotic pathway. To examine if five single nucleotide polymorphisms (SNPs) in four caspase genes [CASP3 Ex8-280 C > A (rs6948), CASP3 Ex8 + 567 T > c (rs1049216), CASP8 Ex14-271 A > T (rs13113). CASP9 Ex5 + 32 G > A (rs1052576), CASPIO Ex3-171 A > G (rs39001150)] alter multiple myeloma risk, we conducted a population-based case-control study of women (128 cases; 516 controls) in Connecticut. Compared to individuals with the TT genotype of CASP3 Ex8 + 567 T > C, subjects with the CC genotype had a five-fold decreased risk of multiple myeloma (odds ratio (OR)(cc) = 0.2, 95% confidence interval (CI)=0.0-1.0). Further, individuals with the AG and AA genotypes of CASP9 Ex5+32 G > A also experienced a decreased risk of multiple myeloma (ORAG=0.8, 95% CI=0.5-1.3; ORAA=0.5, 95% CI=03-0.9, p-trend=0.02). While no previous study has evaluated the association between caspase genes and multiple myeloma, studies have found associations with lung, breast, esophageal, gastric, colorectal and cervical cancers. Our parallel study of non-Hodgkin lymphoma, which utilized the same controls, found strong evidence that caspase genes play a key role in lymphogenesis. The protective associations observed in two key caspase genes suggest that genetic variation in CASP genes may play an important role in the aetiology of multiple myeloma. Copyright (C) 2008 John Wiley & Sons, Ltd.
C1 [Hosgood, H. Dean, III; Baris, Dalsu; Zahm, Shelia; Chanock, Stephen; Rothman, Nathaniel; Lan, Qing] NCI, Div Canc Epidemiol & Genet, Occupat & Environm Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
[Hosgood, H. Dean, III; Zhang, Yawei; Zhu, Yong; Zheng, Tongzhang] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Yeager, Meredith; Welch, Robert] NCI, SAIC Frederick Inc, Adv Technol Program, Div Canc Epidemiol & Genet,Core Genotyping Facil, Frederick, MD 21701 USA.
[Chanock, Stephen] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Hosgood, HD (reprint author), NCI, Div Canc Epidemiol & Genet, Occupat & Environm Epidemiol Branch, NIH, 6120 Execut Blvd,EPS 8118,MCS 7240, Bethesda, MD 20892 USA.
EM hosgoodd@mail.nihgov
RI Zahm, Shelia/B-5025-2015
FU Yale University-National Cancer Institute Partnership Pre-Doctoral
Fellowship Training Program [NCI TU2 CA 105666]; National Cancer
Institute; National Institutes of Health [N01-CO-12400]
FX This work was supported in pan by the Yale University-National Cancer
Institute Partnership Pre-Doctoral Fellowship Training Program (NCI TU2
CA 105666). This project has been funded in whole or in part with
federal funds from the National Cancer Institute, National Institutes of
Health, under contract N01-CO-12400. The content of this publication
does not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products or organizations imply endorsement by the US Government.
NR 33
TC 30
Z9 32
U1 0
U2 2
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0278-0232
J9 HEMATOL ONCOL
JI Hematol. Oncol.
PD SEP
PY 2008
VL 26
IS 3
BP 148
EP 151
DI 10.1002/hon.852
PG 4
WC Oncology; Hematology
SC Oncology; Hematology
GA 356CQ
UT WOS:000259756700004
PM 18381704
ER
PT J
AU Kato, T
Choi, Y
Elmowalid, G
Sapp, RK
Barth, H
Furusaka, A
Mishiro, S
Wakita, T
Krawczynski, K
Liang, TJ
AF Kato, Takanobu
Choi, Youkyung
Elmowalid, Gamal
Sapp, Ronda K.
Barth, Heidi
Furusaka, Akihiro
Mishiro, Shunji
Wakita, Takaji
Krawczynski, Krzysztof
Liang, T. Jake
TI Hepatitis C virus JFH-1 strain infection in chimpanzees is associated
with low pathogenicity and emergence of an adaptive mutation
SO HEPATOLOGY
LA English
DT Article
ID B VIRAL-HEPATITIS; FULMINANT NON-A; CELL-CULTURE; MOLECULAR CLONE;
EFFICIENT REPLICATION; HUH-7 CELLS; IN-VIVO; RNA; PARTICLES; NS2
AB The identification of the hepatitis C virus (HCV) strain JFH-1 enabled the successful development of infectious cell culture systems. Although this strain replicates efficiently and produces infectious virus in cell culture, the replication capacity and pathogenesis in vivo are still undefined. To assess the in vivo phenotype of the JFH-1 virus, cell culture-generated JFH-1 virus (JFH-1cc) and patient serum from which JFH-1 was isolated were inoculated into chimpanzees. Both animals became HCV RNA-positive 3 days after inoculation but showed low-level viremia and no evidence of hepatitis. HCV viremia persisted 8 and 34 weeks in JFH-1cc and patient serum-infected chimpanzees, respectively. Immunological analysis revealed that HCV-specific immune responses were similarly induced in both animals. Sequencing of HCV at various times of infection indicated more substitutions in the patient serum-inoculated chimpanzee, and the higher level of sequence variations seemed to be associated with a prolonged infection in this animal. A common mutation G838R in the NS2 region emerged early in both chimpanzees. This mutation enhances viral assembly, leading to an increase in viral production in transfected or infected cells. Conclusion: Our study shows that the HCV JFH-1 strain causes attenuated infection and low pathogenicity in chimpanzees and is capable of adapting in vivo with a unique mutation conferring an enhanced replicative phenotype.
C1 [Kato, Takanobu; Elmowalid, Gamal; Sapp, Ronda K.; Barth, Heidi; Liang, T. Jake] NIDDKD, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Kato, Takanobu; Mishiro, Shunji] Toshiba Gen Hosp, Dept Med Sci, Tokyo, Japan.
[Kato, Takanobu; Wakita, Takaji] Natl Inst Infect Dis, Dept Virol 2, Shinjuku Ku, Tokyo 1628640, Japan.
[Choi, Youkyung; Krawczynski, Krzysztof] Ctr Dis Control & Prevent, Div Viral Hepatitis, Atlanta, GA USA.
[Furusaka, Akihiro] Jikei Univ, Sch Med, Dept Internal Med, Tokyo, Japan.
RP Liang, TJ (reprint author), NIDDKD, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
EM JakeL@bdgl0.niddk.nih.gov
FU Intramural NIH HHS [Z01 DK054504-11]
NR 46
TC 35
Z9 35
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD SEP
PY 2008
VL 48
IS 3
BP 732
EP 740
DI 10.1002/hep.22422
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 344QJ
UT WOS:000258942100006
PM 18712792
ER
PT J
AU Balan, V
Ruppert, K
Demetris, AJ
Ledneva, T
Duquesnoy, RJ
Detre, KM
Wei, YL
Rakela, J
Schafer, DF
Roberts, JP
Everhart, JE
Wiesner, RH
AF Balan, Vijayan
Ruppert, Kris
Demetris, A. Jake
Ledneva, Tatiana
Duquesnoy, Rene J.
Detre, Katherine M.
Wei, Yuling L.
Rakela, Jorge
Schafer, Daniel F.
Roberts, John P.
Everhart, James E.
Wiesner, Russell H.
TI Long-term outcome of human leukocyte antigen mismatching in liver
transplantation: Results of the National Institute of Diabetes and
Digestive and Kidney Diseases Liver Transplantation Database
SO HEPATOLOGY
LA English
DT Article
ID HEPATITIS-C; GRAFT-SURVIVAL; HLA COMPATIBILITY; RETROSPECTIVE ANALYSIS;
PATIENT SURVIVAL; ACUTE REJECTION; RISK-FACTORS; IMPACT;
HISTOCOMPATIBILITY; IDENTIFICATION
AB A perfect or nearly perfect human lettkocyte antigen (HI-A) match has been associated with better immediate and long-term survival of diseased donor kidney transplants. However, the effect of HLA matching for hepatic allografts remains poorly defined. Using data from the National Institutes of Diabetes and Digestive and Kidney Diseases Liver Transplantation Database, we investigated the association between HLA mismatches and hepatic allograft survival, disease recurrence, and immunosuppression interactions. A, B, and DR loci were used to calculate total mismatch scores of 0 (no mismatches in any loci) to 6 (mismatches in all loci). Seven hundred ninety-nine adults (male, 55%; female, 45%) underwent 883 liver transplants. The 10-year graft survival according to total mismatch score was as follows: 0-2, 60%; 3-4, 54%; and 5-6, 57%. There was a negative effect of mismatching at the A locus on patient survival, with shorter survival for patients with I or 2 mismatches compared with 0 mismatches [P = 0.05, hazard ratio (HR) = 1.6]. Patients on tacrolimus with I or 2 mismatches at B or DR loci appeared to have increased rates of patient and graft survival compared to patients with 0 mismatches, with the appearance of a protective effect of tacrolimus (HR = 0.67). The effect of HILA mismatching was more pronounced on certain disease recurrences. DR-locus mismatch increased recurrence of autoimmune hepatitis (P = 0.01, HR = 4.2) and primary biliary cirrhosis (P = 0.04, HR = 2). Mismatch in the A locus was associated with more recurrence of hepatitis C virus (P = 0.01, HR = 1.6) and primary sclerosing cholangitis (P = 0.03, HR = 2.9). Conclusion: Mismatching at the A locus decreases patient survival in liver transplant recipients, and mismatching at the DR and A loci affects recurrence of autoimmune liver diseases and hepatitis C, respectively.
C1 [Balan, Vijayan; Rakela, Jorge] Mayo Clin, Dept Transplantat Med, Phoenix, AZ USA.
[Ruppert, Kris; Demetris, A. Jake; Ledneva, Tatiana; Detre, Katherine M.; Wei, Yuling L.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Duquesnoy, Rene J.] Univ Pittsburgh, Sch Med, Div Transplantat Pathol, Pittsburgh, PA USA.
[Schafer, Daniel F.] Univ Nebraska Med Ctr, Dept Med, Omaha, NE USA.
[Schafer, Daniel F.] Univ Nebraska Med Ctr, Dept Surg, Omaha, NE USA.
[Roberts, John P.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Roberts, John P.] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94143 USA.
[Everhart, James E.] NIDDKD, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
[Wiesner, Russell H.] Mayo Clin & Mayo Fdn, Dept Med, Rochester, MN 55905 USA.
[Wiesner, Russell H.] Mayo Clin & Mayo Fdn, Dept Surg, Rochester, MN 55905 USA.
RP Balan, V (reprint author), Mayo Clin, 13400 E Shea Blvd, Scottsdale, AZ 85259 USA.
EM balan.vijayan@mayo.edu
RI Ruppert, Kristine/C-2555-2016
OI Ruppert, Kristine/0000-0002-3008-6584
FU National Institute of Diabetey and Digestive and Kidney Diseases [DK
55883]
FX This work was supported by National Institute of Diabetey and Digestive
and Kidney Diseases grant DK 55883.
NR 43
TC 34
Z9 34
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD SEP
PY 2008
VL 48
IS 3
BP 878
EP 888
DI 10.1002/hep.22435
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 344QJ
UT WOS:000258942100021
PM 18752327
ER
PT J
AU Masson, MJ
Carpenter, LD
Graf, ML
Pohl, LR
AF Masson, Mary Jane
Carpenter, Leah D.
Graf, Mary L.
Pohl, Lance R.
TI Pathogenic role of natural killer T and natural killer cells in
acetaminophen-induced liver injury in mice is dependent on the presence
of dimethyl sulfoxide
SO HEPATOLOGY
LA English
DT Article
ID INNATE IMMUNE-SYSTEM; NKT CELLS; HEPATIC-INJURY; INDUCED HEPATOTOXICITY;
MACROPHAGE-MIGRATION; DEFICIENT MICE; MURINE MODEL; MOUSE MODEL; MAJOR
ROLE; DIMETHYLSULFOXIDE
AB Dimethyl sulfoxide (DMSO) is commonly used in biological studies to dissolve drugs and enzyme inhibitors with low solubility. Although DMSO is generally thought of as being relatively inert, it can induce biological effects that are often overlooked. An example that highlights this potential problem is found in a recent report demonstrating a pathogenic role for natural killer T (NKT) and natural killer (NK) cells in acetaminophen-induced liver injury (AILI) in C57131/6 mice in which DMSO was used to facilitate acetaminophen (APAP) dissolution. We report that NKT and NK cells do not play a pathologic role in AILI in C57131/6 mice in the absence of DMSO. Although AILI was significantly attenuated in mice depleted of NKT and NK cells prior to APAP treatment in the presence of DMSO, no such effect was observed when APAP was dissolved in saline. Because of this unexpected finding, the effects of DMSO on hepatic NKT and NK cells were subsequently investigated. When given alone, DMSO activated hepatic NKT and NK cells in vivo as evidenced by increased NKT cell numbers and higher intracellular levels of the cytotoxic effector molecules interferon-gamma (IFN-gamma) and granzyme B in both cell types. Similarly, when used as a solvent for APAP, DMSO again increased NKT cell numbers and induced IFN-gamma and granzyme B expression in both cell types. Conclusion: These data demonstrate a previously unappreciated effect of DMSO on hepatic NKT and NK cells, suggesting that DMSO should be used cautiously in experiments involving these cells.
C1 [Masson, Mary Jane; Carpenter, Leah D.; Graf, Mary L.; Pohl, Lance R.] NHLBI, Mol & Cellular Toxicol Sect, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Masson, MJ (reprint author), NHLBI, Mol & Cellular Toxicol Sect, Lab Mol Immunol, NIH, 10 Ctr Dr,Bldg 10,Room 8N110, Bethesda, MD 20892 USA.
EM massonm@nhlbi.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Heart, Lung, and Blood Institute
FX Supported by the Intramural Research Program of the National Institutes
of Health and the National Heart, Lung, and Blood Institute.
NR 49
TC 57
Z9 57
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD SEP
PY 2008
VL 48
IS 3
BP 889
EP 897
DI 10.1002/hep.22400
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 344QJ
UT WOS:000258942100022
PM 18712839
ER
PT J
AU Yeager, M
Xiao, NQ
Hayes, RB
Bouffard, P
Desany, B
Burdett, L
Orr, N
Matthews, C
Qi, LQ
Crenshaw, A
Markovic, Z
Fredrikson, KM
Jacobs, KB
Amundadottir, L
Jarvie, TP
Hunter, DJ
Hoover, R
Thomas, G
Harkins, TT
Chanock, SJ
AF Yeager, Meredith
Xiao, Nianqing
Hayes, Richard B.
Bouffard, Pascal
Desany, Brian
Burdett, Laura
Orr, Nick
Matthews, Casey
Qi, Liqun
Crenshaw, Andrew
Markovic, Zdenek
Fredrikson, Karin M.
Jacobs, Kevin B.
Amundadottir, Laufey
Jarvie, Thomas P.
Hunter, David J.
Hoover, Robert
Thomas, Gilles
Harkins, Timothy T.
Chanock, Stephen J.
TI Comprehensive resequence analysis of a 136 kb region of human chromosome
8q24 associated with prostate and colon cancers
SO HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; COLORECTAL-CANCER; GENETIC ALTERATIONS;
BREAST-CANCER; RISK LOCUS; SUSCEPTIBILITY; VARIANT; SEQUENCES; INSIGHTS;
SCAN
AB Recently, genome-wide association studies have identified loci across a segment of chromosome 8q24 ( 128,100,000-128,700,000) associated with the risk of breast, colon and prostate cancers. At least three regions of 8q24 have been independently associated with prostate cancer risk; the most centromeric of which appears to be population specific. Haplotypes in two contiguous but independent loci, marked by rs6983267 and rs1447295, have been identified in the Cancer Genetic Markers of Susceptibility project (http://cgems.cancer.gov), which genotyped more than 5,000 prostate cancer cases and 5,000 controls of European origin. The rs6983267 locus is also strongly associated with colorectal cancer. To ascertain a comprehensive catalog of common single-nucleotide polymorphisms (SNPs) across the two regions, we conducted a resequence analysis of 136 kb (chr8: 128,473,000 128,609,802) using the Roche/454 next-generation sequencing technology in 39 prostate cancer cases and 40 controls of European origin. We have characterized a comprehensive catalog of common (MAF > 1%) SNPs within this region, including 442 novel SNPs and have determined the pattern of linkage disequilibrium across the region. Our study has generated a detailed map of genetic variation across the region, which should be useful for choosing SNPs for fine mapping of association signals in 8q24 and investigations of the functional consequences of select common variants.
C1 [Yeager, Meredith] NCI, Adv Technol Ctr, Gaithersburg, MD 20877 USA.
[Yeager, Meredith; Xiao, Nianqing; Burdett, Laura; Matthews, Casey; Qi, Liqun; Crenshaw, Andrew; Amundadottir, Laufey] NCI Frederick, SAIC Frederick Inc, Adv Technol Program, Core Genotyping Facil, Ft Detrick, MD 21702 USA.
[Yeager, Meredith; Xiao, Nianqing; Hayes, Richard B.; Burdett, Laura; Matthews, Casey; Crenshaw, Andrew; Amundadottir, Laufey; Hunter, David J.; Hoover, Robert; Thomas, Gilles; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Bouffard, Pascal; Desany, Brian; Markovic, Zdenek; Jarvie, Thomas P.] Life Sci 454, Branford, CT USA.
[Orr, Nick; Chanock, Stephen J.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH,DHHS, Bethesda, MD 20892 USA.
[Jacobs, Kevin B.] Bioinformed Consulting Serv, Gaithersburg, MD USA.
[Hunter, David J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Fredrikson, Karin M.; Harkins, Timothy T.] Roche Appl Sci, Indianapolis, IN USA.
RP Yeager, M (reprint author), NCI, Adv Technol Ctr, 8717 Grovemont Circle, Gaithersburg, MD 20877 USA.
EM yeagerm@mail.nih.gov
RI Amundadottir, Laufey/L-7656-2016;
OI Amundadottir, Laufey/0000-0003-1859-8971; Hayes,
Richard/0000-0002-0918-661X
FU National Cancer Institute; National Institutes of Health [N01-CO-12400]
FX The authors would like to recognize the contribution of the late Robert
A. Welch to the conception, execution, and analysis of this project.
This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract N01-CO-12400. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the US Government.
NR 28
TC 77
Z9 79
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
J9 HUM GENET
JI Hum. Genet.
PD SEP
PY 2008
VL 124
IS 2
BP 161
EP 170
DI 10.1007/s00439-008-0535-3
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 342BJ
UT WOS:000258759300006
PM 18704501
ER
PT J
AU Berndt, SI
Potter, JD
Hazra, A
Yeager, M
Thomas, G
Makar, KW
Welch, R
Cross, AJ
Huang, WY
Schoen, RE
Giovannucci, E
Chan, AT
Chanock, SJ
Peters, U
Hunter, DJ
Hayes, RB
AF Berndt, Sonja I.
Potter, John D.
Hazra, Aditi
Yeager, Meredith
Thomas, Gilles
Makar, Karen W.
Welch, Robert
Cross, Amanda J.
Huang, Wen-Yi
Schoen, Robert E.
Giovannucci, Edward
Chan, Andrew T.
Chanock, Stephen J.
Peters, Ulrike
Hunter, David J.
Hayes, Richard B.
TI Pooled analysis of genetic variation at chromosome 8q24 and colorectal
neoplasia risk
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; PROSTATE-CANCER RISK; ADENOMATOUS POLYPS;
LINKAGE PHASE; COLON-CANCER; C-MYC; METAANALYSIS; VARIANT; LOCUS;
POPULATION
AB Several different genetic variants at chromosome 8q24 have been related to prostate, breast and colorectal cancer risk with evidence of region-specific risk differentials for various tumor types. We investigated the association between 15 polymorphisms located in 8q24 regions associated with cancer risk in a pooled analysis of 2587 colorectal adenoma cases, 547 colorectal cancer cases and 2798 controls of European descent from four studies. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) for the associations. Three polymorphisms (rs10808555, rs6983267 and rs7837328) located between 128.47 and 128.54 Mb were found to be associated with colorectal tumor risk. The association was strongest for the previously reported rs6983267 variant and was similar for both adenoma (OR(per allele) = 1.16, 95% CI: 1.07-1.25, P = 0.0002) and cancer (OR(per allele) = 1.17, 95% CI: 1.01-1.35, P = 0.03). The strength of the association of the regional haplotype containing variant alleles at rs10808555, rs6983267 and rs7837328 but not rs10505476 was greater than that of any single variant of both adenoma (OR = 1.27, P = 0.0001) and cancer (OR = 1.26, P = 0.03). The risk associated with rs6983267 was stronger for multiple adenomas (OR(per allele) = 1.29, P = 5.6 x 10(-6)) than for single adenoma (ORper allele = 1.10, P = 0.03) with P(heterogeneity) = 0.008. This study confirms the association between colorectal neoplasia and the 8q24 polymorphisms located between 128.47 and 128.54 Mb and suggests a role for these variants in the formation of multiple adenomas.
C1 [Berndt, Sonja I.; Yeager, Meredith; Thomas, Gilles; Welch, Robert; Cross, Amanda J.; Huang, Wen-Yi; Chanock, Stephen J.; Hayes, Richard B.] Natl Canc Inst, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Potter, John D.; Makar, Karen W.; Peters, Ulrike] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Potter, John D.; Peters, Ulrike] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Hazra, Aditi; Giovannucci, Edward; Hunter, David J.] Harvard Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Yeager, Meredith; Welch, Robert] SAIC Frederick Inc, Adv Technol Program, Natl Canc Inst Frederick, Frederick, MD 21702 USA.
[Schoen, Robert E.] Univ Pittsburgh, Dept Med, Pittsburgh, PA 15260 USA.
[Schoen, Robert E.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15260 USA.
[Schoen, Robert E.] Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15260 USA.
[Giovannucci, Edward; Hunter, David J.] Harvard Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Giovannucci, Edward; Chan, Andrew T.; Hunter, David J.] Harvard Univ, Sch Med, Channing Lab, Brigham & Womens Hosp,Dept Med, Boston, MA 02115 USA.
[Chan, Andrew T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
RP Berndt, SI (reprint author), Natl Canc Inst, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 8116,MSC 7240, Bethesda, MD 20892 USA.
EM berndts@mail.nih.gov
OI Potter, John/0000-0001-5439-1500; Hayes, Richard/0000-0002-0918-661X
FU Intramural Research Program of the Division of Cancer Epidemiology and
Genetics; National Cancer Institute; National Institutes of Health
[N01-CO-12400, CA87969, CA55075, CA059045]
FX This study was supported by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute,
National Institutes of Health; National Cancer Institute, National
Institutes of Health under contract N01-CO-12400; and National
Institutes of Health research grants CA87969, CA55075 and CA059045.
NR 35
TC 51
Z9 53
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD SEP 1
PY 2008
VL 17
IS 17
BP 2665
EP 2672
DI 10.1093/hmg/ddn166
PG 8
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 343PW
UT WOS:000258867000008
PM 18535017
ER
PT J
AU Vergarajauregui, S
Connelly, PS
Daniels, MP
Puertollano, R
AF Vergarajauregui, Silvia
Connelly, Patricia S.
Daniels, Mathew P.
Puertollano, Rosa
TI Autophagic dysfunction in mucolipidosis type IV patients
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID NEURODEGENERATIVE DISEASE; CATION CHANNEL; FRONTOTEMPORAL DEMENTIA;
MEMBRANE-PROTEIN; TRAFFICKING; MUTATIONS; GENE; IDENTIFICATION; MICE;
MACROAUTOPHAGY
AB Mutations in Mucolipin 1 (MCOLN1) have been linked to mucolipidosis type IV (MLIV), a lysosomal storage disease characterized by several neurological and ophthalmological abnormalities. It has been proposed that MCOLN1 might regulate transport of membrane components in the late endosomal-lysosomal pathway; however, the mechanisms by which defects of MCOLN1 function result in mental and psychomotor retardation remain largely unknown. In this study, we show constitutive activation of autophagy in fibroblasts obtained from MLIV patients. Accumulation of autophagosomes in MLIV cells was due to the increased de novo autophagosome formation and to delayed fusion of autophagosomes with late endosomes/lysosomes. Impairment of the autophagic pathway led to increased levels and aggregation of p62, suggesting that abnormal accumulation of ubiquitin proteins may contribute to the neurodegeneration observed in MLIV patients. In addition, we found that delivery of platelet-derived growth factor receptor to lysosomes is delayed in MCOLN1-deficient cells, suggesting that MCOLN1 is necessary for efficient fusion of both autophagosomes and late endosomes with lysosomes. Our data are in agreement with recent evidence showing that autophagic defects may be a common characteristic of many neurodegenerative disorders.
C1 [Vergarajauregui, Silvia; Puertollano, Rosa] NHLBI, Natl Inst Hlth, Cell Biol Lab, Bethesda, MD 20892 USA.
[Connelly, Patricia S.; Daniels, Mathew P.] NHLBI, Natl Inst Hlth, Electron Microscopy Core Facil, Bethesda, MD 20892 USA.
RP Puertollano, R (reprint author), NHLBI, Natl Inst Hlth, Cell Biol Lab, Bethesda, MD 20892 USA.
EM puertolr@mail.nih.gov
FU Intramural Research Program of the NIH; National Heart, Lung, and Blood
Institute (NHLBI)
FX This project was supported by the Intramural Research Program of the
NIH, National Heart, Lung, and Blood Institute (NHLBI).
NR 57
TC 78
Z9 79
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD SEP 1
PY 2008
VL 17
IS 17
BP 2723
EP 2737
DI 10.1093/hmg/ddn174
PG 15
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 343PW
UT WOS:000258867000014
PM 18550655
ER
PT J
AU Ingelsson, E
Pencina, MJ
Levy, D
Aragam, J
Mitchell, GF
Benjamin, EJ
Vasan, RS
AF Ingelsson, Erik
Pencina, Michael J.
Levy, Daniel
Aragam, Jayashri
Mitchell, Gary F.
Benjamin, Emelia J.
Vasan, Ramachandran S.
TI Aortic root diameter and longitudinal blood pressure tracking
SO HYPERTENSION
LA English
DT Article
DE blood pressure; aorta; hypertension
ID TARGET ORGAN DAMAGE; SYSTOLIC HYPERTENSION; PULSE PRESSURE; FLOW
RELATIONSHIP; WAVE REFLECTION; DILATATION; SIZE; DETERMINANTS;
PATHOGENESIS; HYPERTROPHY
AB Proximal aortic diameter, including aortic root ( AoR) diameter, has been inversely related to pulse pressure in cross-sectional studies. So, investigators have hypothesized that a smaller AoR diameter may increase the risk of developing hypertension. Prospective studies are lacking to test this hypothesis. We measured AoR diameter in 3195 Framingham Study participants ( mean age: 49 years; 57% women; 8460 person-examinations) free from hypertension and previous cardiovascular disease who underwent routine echocardiography. We related AoR to hypertension incidence and blood pressure ( BP) progression ( increment of >= 1 category, as defined by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure). On follow- up ( median: 4 years), 1267 individuals ( 15%; 661 women) developed hypertension, and 2978 participants experienced BP progression ( 35%; 1588 women). In logistic regression models adjusted for age, sex, and height, AoR was positively associated with hypertension incidence ( odds ratio: 1.15; 95% CI: 1.08 to 1.23) and BP progression ( odds ratio: 1.09; 95% CI: 1.04 to 1.14) on follow- up. However, adjustment for other factors known to influence BP tracking ( baseline systolic and diastolic BP, smoking, diabetes, and weight) rendered these relations statistically nonsignificant ( odds ratio: 1.03; 95% CI: 0.96 to 1.11 for hypertension incidence; odds ratio: 1.03; 95% CI: 0.97 to 1.08 for BP progression). In our large community- based sample of nonhypertensive individuals, AoR diameter was not associated with hypertension incidence or BP progression prospectively after adjustment for potential confounders. Our prospective study does not support the notion that a smaller AoR predisposes to hypertension.
C1 [Ingelsson, Erik; Pencina, Michael J.; Levy, Daniel; Aragam, Jayashri; Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Framingham Study, Framingham, MA USA.
[Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Evans Mem Dept Med, Framingham, MA USA.
[Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Whitaker Cardiovasc Inst, Framingham, MA USA.
[Ingelsson, Erik] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Pencina, Michael J.] Boston Univ, Dept Math, Boston, MA 02215 USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Aragam, Jayashri] Vet Adm Hosp, W Roxbury, MA USA.
[Mitchell, Gary F.] Cardiovasc Engn Inc, Holliston, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA.
RP Vasan, RS (reprint author), Framingham Heart Dis Epidemiol Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM vasan@bu.edu
OI Ramachandran, Vasan/0000-0001-7357-5970; Benjamin,
Emelia/0000-0003-4076-2336
FU Swedish Society of Medicine and the Swedish Heart-Lung Foundation;
National Institutes of Health/National Heart, Lung, and Blood Institute
[N01-HC-25195, 6R01-NS 17950, HL080124, 2K24HL4334]
FX This work was supported by the Swedish Society of Medicine and the
Swedish Heart-Lung Foundation (E. I.) and the National Institutes of
Health/National Heart, Lung, and Blood Institute contracts N01-HC-
25195, 6R01-NS 17950 (E. J. B.), HL080124, and 2K24HL4334 (R. S. V.).
NR 25
TC 12
Z9 13
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD SEP
PY 2008
VL 52
IS 3
BP 473
EP 477
DI 10.1161/HYPERTENSIONAHA.108.114157
PG 5
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 339XB
UT WOS:000258609500009
PM 18663156
ER
PT J
AU Erim, Z
Lin, W
AF Erim, Zeynep
Lin, Winsean
TI Decomposition of intramuscular EMG signals using a heuristic fuzzy
expert system
SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING
LA English
DT Article
DE action potential (AP); classification; decomposition; electromyography
(EMG); expert system; fuzzy logic; intramuscular; motor unit (MU)
ID ACTION-POTENTIALS; RESOLUTION
AB Although increasingly sophisticated algorithms have been proposed to decompose intramuscular electromyography signals into the concurrent activities of individual motor units (MUs), the human operator is still able to improve decomposition results by visual inspection. The rationale for this paper was to combine components from previous decomposition procedures in an expert systems approach utilizing fuzzy logic and attempting to replicate the thought process of an accomplished decomposer in order to minimize the user interaction subsequently needed to enhance decomposition results. The decomposition procedure is discussed and examples are given of the type of information it can yield. The method has been used to identify the discharge activities of up to 15 MUs with up to 95% accuracy.
C1 [Erim, Zeynep; Lin, Winsean] Rehabil Inst Chicago, Sensory Motor Performance Program, Chicago, IL 60611 USA.
[Erim, Zeynep] Northwestern Univ, Feinberg Sch Med, Dept Phys Med & Rehabil, Chicago, IL 60611 USA.
RP Erim, Z (reprint author), NIH, Natl Inst Biomed Imaging & Bioengn, Bethesda, MD 20892 USA.
EM erimz@mail.nih.gov
FU NICHD NIH HHS [K25HD043993]
NR 17
TC 15
Z9 16
U1 0
U2 1
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0018-9294
J9 IEEE T BIO-MED ENG
JI IEEE Trans. Biomed. Eng.
PD SEP
PY 2008
VL 55
IS 9
BP 2180
EP 2189
DI 10.1109/FBME.2008.923915
PG 10
WC Engineering, Biomedical
SC Engineering
GA 341NW
UT WOS:000258722200008
PM 18713687
ER
PT J
AU Pham, TD
Wang, HH
Zhou, XB
Beck, D
Brandl, M
Hoehn, G
Azok, J
Brennan, ML
Hazen, SL
Li, K
Wong, STC
AF Pham, Tuan D.
Wang, Honghui
Zhou, Xiaobo
Beck, Dominik
Brandl, Miriam
Hoehn, Gerard
Azok, Joseph
Brennan, Marie-Luise
Hazen, Stanley L.
Li, King
Wong, Stephen T. C.
TI Computational prediction models for early detection of risk of
cardiovascular events using mass spectrometry data
SO IEEE TRANSACTIONS ON INFORMATION TECHNOLOGY IN BIOMEDICINE
LA English
DT Article
DE cardiovascular risk; early disease detection; mass spectrometry (MS);
prediction models; proteomics
ID OVARIAN-CANCER; PROTEOMIC PATTERNS; HUMAN SERUM; CLASSIFICATION;
IDENTIFICATION; DISCOVERY; SELECTION; MARKERS; SPEECH
AB Early prediction of the risk of cardiovascular events in patients with chest pain is critical in order to provide appropriate medical care for those with positive diagnosis. This paper introduces a computational methodology for predicting such events in the context of robust computerized classification using mass spectrometry data of blood samples collected from patients in emergency departments. We applied the computational theories of statistical and geostatistical linear prediction models to extract effective features of the mass spectra and a simple decision logic to classify disease and control samples for the purpose of early detection. While the statistical and geostatistical techniques provide better results than those obtained from some other methods, the geostatistical approach yields superior results in terms of sensitivity and specificity in various designs of the data set for validation, training, and testing. The proposed computational strategies are very promising for predicting major adverse cardiac events within six months.
C1 [Pham, Tuan D.; Beck, Dominik; Brandl, Miriam] Univ New S Wales, Sch Informat Technol & Elect Engn, ADFA, Canberra, ACT 2006, Australia.
[Wang, Honghui; Hoehn, Gerard; Azok, Joseph; Li, King] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Zhou, Xiaobo; Wong, Stephen T. C.] Harvard Univ, Sch Med, HCNR, Ctr Bioinformat, Boston, MA 02115 USA.
[Brennan, Marie-Luise; Hazen, Stanley L.] Cleveland Clin Fdn, Ctr Cardiovasc Diagnost & Prevent, Cleveland, OH 44195 USA.
RP Pham, TD (reprint author), Univ New S Wales, Sch Informat Technol & Elect Engn, ADFA, Canberra, ACT 2006, Australia.
EM t.pham@adfa.edu.au; hwang2@cc.nih.gov; xiaobo_zhou@hms.harvard.edu;
d.beck@adfa.edu.au; m.brandl@adfa.edu.au; ghoehn@cc.nih.gov;
brennam@ccf.org; hazens@ccf.org; kli@tmhs.org;
stephen_wong@hms.harvard.edu
NR 39
TC 11
Z9 11
U1 1
U2 4
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 1089-7771
J9 IEEE T INF TECHNOL B
JI IEEE T. Inf. Technol. Biomed.
PD SEP
PY 2008
VL 12
IS 5
BP 636
EP 643
DI 10.1109/TITB.2007.908756
PG 8
WC Computer Science, Information Systems; Computer Science,
Interdisciplinary Applications; Mathematical & Computational Biology;
Medical Informatics
SC Computer Science; Mathematical & Computational Biology; Medical
Informatics
GA 353MI
UT WOS:000259571700010
PM 18779078
ER
PT J
AU Tan, S
Yao, JH
Ward, MM
Yao, L
Summers, RM
AF Tan, Sovira
Yao, Jianhua
Ward, Michael M.
Yao, Lawrence
Summers, Ronald M.
TI Computer aided evaluation of Ankylosing Spondylitis using
high-resolution CT
SO IEEE TRANSACTIONS ON MEDICAL IMAGING
LA English
DT Article
DE level sets on nonplanar manifolds; multiscale vertebra segmentation;
ridgelines/crestlines; semi-synthetic digital phantoms
ID SEGMENTATION METHOD; 3-D SEGMENTATION; ACTIVE CONTOURS; CREST LINES;
IMAGES; SURFACES; MESHES; MODEL; CURVES; SPINE
AB Ankylosing Spondylitis is a disease characterized by abnormal bone structures (syndesmophytes) growing at intervertebral disk spaces. Because this growth is so slow as to be undetectable on plain radiographs taken over years, it is desirable to resort to computerized techniques to complement qualitative human judgment with precise quantitative measures. We developed an algorithm with minimal user intervention that provides such measures using high-resolution computed tomography (CT) images. To the best of our knowledge it is the first time that determination of the disease's status is attempted by direct measurement of the syndesmophytes. The first part of our algorithm segments the whole vertebral body using a 3-D multiscale cascade of successive level sets. The second part extracts the continuous ridgeline of the vertebral body where syndesmophytes are located. For that we designed a novel level set implementation capable of evolving on the isosurface of an object represented by a triangular mesh using curvature features. The third part of the algorithm segments the syndesmophytes from the vertebral body using local cutting planes and quantitates them. We present experimental work (lone with 10 patients from each of which we processed five vertebrae. The results of our algorithm were validated by comparison with a semi-quantitative evaluation made by a medical expert who visually inspected the CT scans. Correlation between the two evaluations was found to be 0.936 (p < 10(-18)).
C1 [Tan, Sovira; Ward, Michael M.] NIAMSD, NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Yao, Jianhua; Yao, Lawrence; Summers, Ronald M.] NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA.
RP Tan, S (reprint author), NIAMSD, NIH, Ctr Clin, Bethesda, MD 20892 USA.
EM tanso@mail.nih.gov
FU National Institutes of Health; Clinical Center; National Institute of
Arthritis and Musculoskeletal and Skin diseases
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, Clinical Center and the National
Institute of Arthritis and Musculoskeletal and Skin diseases.
NR 53
TC 20
Z9 20
U1 1
U2 3
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0278-0062
EI 1558-254X
J9 IEEE T MED IMAGING
JI IEEE Trans. Med. Imaging
PD SEP
PY 2008
VL 27
IS 9
BP 1252
EP 1267
DI 10.1109/TMI.2008.920612
PG 16
WC Computer Science, Interdisciplinary Applications; Engineering,
Biomedical; Engineering, Electrical & Electronic; Imaging Science &
Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging
SC Computer Science; Engineering; Imaging Science & Photographic
Technology; Radiology, Nuclear Medicine & Medical Imaging
GA 344TF
UT WOS:000258949500007
PM 18779065
ER
PT J
AU Hu, CH
Zhou, QF
Shung, KK
AF Hu, Chang-hong
Zhou, Qifa
Shung, K. Kirk
TI Design and implementation of high frequency ultrasound pulsed-wave
Doppler using FPGA
SO IEEE TRANSACTIONS ON ULTRASONICS FERROELECTRICS AND FREQUENCY CONTROL
LA English
DT Article
ID DIGITAL BEAMFORMER; BLOOD-FLOW; ARRAY; TRANSDUCERS
AB The development of a field-programmable gate array (FPGA)-based pulsed-wave Doppler processing approach in pure digital domain is reported in this paper. After the ultrasound signals are digitized, directional Doppler frequency shifts are obtained with a digital-down converter followed by a low-pass filter. A Doppler spectrum is then calculated using the complex fast Fourier transform core inside the FPGA. In this approach, a pulsed-wave Doppler implementation core with reconfigurable and real-time processing capability is achieved.
C1 [Hu, Chang-hong] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
RP Hu, CH (reprint author), Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
EM changhoh@usc.edu
FU NIBIB NIH HHS [P41 EB002182-12, P41 EB002182, P41-EB2182]
NR 9
TC 9
Z9 12
U1 0
U2 5
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA
SN 0885-3010
J9 IEEE T ULTRASON FERR
JI IEEE Trans. Ultrason. Ferroelectr. Freq. Control
PD SEP
PY 2008
VL 55
IS 9
BP 2109
EP 2111
DI 10.1109/TUFFC.904
PG 3
WC Acoustics; Engineering, Electrical & Electronic
SC Acoustics; Engineering
GA 344FR
UT WOS:000258912800027
PM 18986909
ER
PT J
AU Catalfamo, M
Tai, XG
Karpova, T
McNally, J
Henkart, PA
AF Catalfamo, Marta
Tai, Xuguang
Karpova, Tatiana
McNally, James
Henkart, Pierre A.
TI TcR-induced regulated secretion leads to surface expression of CTLA-4 in
CD4(+)CD25(+) T cells
SO IMMUNOLOGY
LA English
DT Article
DE cytotoxic T-lymphocyte-associated antigen-4; human CD4(+) T cells;
regulated exocytosis; secretory lysosome
ID LYMPHOCYTE-ACTIVATION; GRANULE EXOCYTOSIS; SELF-TOLERANCE; CD4(+);
PATHWAY; CD28; IDENTIFICATION; STIMULATION; COMPARTMENT; RECEPTOR
AB In this study we show that CD4(+) T cells develop a functional regulated secretory compartment after differentiation into effector cells, as shown by their increased expression and T-cell receptor-induced exocytosis of lysosomal and cytotoxic effector proteins. We tested the hypothesis that activation-induced surface cytotoxic T-lymphocyte-associated antigen (CTLA-4) expression in CD4(+)CD25(+) regulatory T cells occurs via a similar regulated secretory pathway. Fluorescence microscopy showed that internal CTLA-4 in these cells was stored in a vesicular compartment distinct from lysosomal vesicles. Rapid activation-induced CTLA-4 surface expression in mouse CD4(+)CD25(+) T cells is independent of protein synthesis and Rab-27a. When antigen-dependent T-cell-antigen-presenting cell (APC) conjugates were analysed for surface distribution of CD86 on APC, a higher concentration of CD86 molecules was observed in the synapse of APC conjugated to CD4(+)CD25(+) cells than APC conjugated to CD4(+)CD25(-) cells. These results demonstrate that fast delivery of mediators by the regulated secretory pathway in CD4(+) T cells can be used to perform other functions that are not involved in cytotoxic function but that can influence/regulate other cells.
C1 [Catalfamo, Marta] NIAID, CMRS, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Catalfamo, Marta; Tai, Xuguang; Henkart, Pierre A.] NCI, Expt Immunol Branch, Bethesda, MD 20892 USA.
[Karpova, Tatiana; McNally, James] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
RP Catalfamo, M (reprint author), NIAID, CMRS, Immunoregulat Lab, NIH, Bldg 10,Room 11B01, Bethesda, MD 20892 USA.
EM catalfam@mail.nih.gov
NR 30
TC 14
Z9 14
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0019-2805
J9 IMMUNOLOGY
JI Immunology
PD SEP
PY 2008
VL 125
IS 1
BP 70
EP 79
DI 10.1111/j.1365-2567.2008.02822.x
PG 10
WC Immunology
SC Immunology
GA 335AR
UT WOS:000258263700008
PM 18397268
ER
PT J
AU Yu, SQ
Xie, H
Datta, A
Naidu, N
Gu, XX
AF Yu, Shengqing
Xie, Hang
Datta, Anup
Naidu, Natasha
Gu, Xin-Xing
TI Galactose residues on the lipooligosaccharide of Moraxella catarrhalis
26404 form the epitope recognized by the bactericidal antiserum from
conjugate vaccination
SO INFECTION AND IMMUNITY
LA English
DT Article
ID BRANHAMELLA-CATARRHALIS; MONOCLONAL-ANTIBODY; SEROTYPE-C;
LIPOPOLYSACCHARIDE ANTIGENS; HAEMOPHILUS-INFLUENZAE; VACCINES;
POLYSACCHARIDE; STRAINS; PROTEIN; OLIGOSACCHARIDES
AB Lipooligosaccharide (LOS) from Moraxella catarrhalis has the potential to elicit bactericidal antibodies against the pathogen. We generated LOS-based conjugate vaccines that elicited bactericidal antibodies in animal models. However, epitopes on the LOS recognized by the functional anti-LOS antibodies remain unidentified. In this study, a mutant strain, D4, which lost the recognition by a bactericidal anti-LOS rabbit serum in Western blotting was generated from a serotype C strain 26404 by random transposon mutagenesis. Sequence analysis revealed there was an insertion of a kanamycin resistance gene in the lgt2 gene of D4, which encodes beta(1-4)-galactosyltransferase. An isogenic lgt2 mutant, 26404lgt2, was constructed. Structural analysis indicated that the mutant strain produced a truncated LOS lacking terminal galactoses from 4- and 6-linked oligosaccharide chains of strain 26404. Further studies showed that the antiserum lost the recognition of both mutant cells and LOSs in Western blotting, an enzyme-linked immunosorbent assay (ELISA), or a flow cytometry assay. The antiserum also lost the ability to kill the mutant strain in a bactericidal assay, whereas it showed a bactericidal titer of 1:80 to strain 26404. In an inhibition ELISA, D-(+)-galactose or 26404lgt2 LOS showed no inhibition. However, the 26404 LOS and a serotype A O35E LOS with terminal galactoses on its 6-linked oligosaccharide chain showed > 90% inhibition, while a serotype B 26397 LOS showed > 60% inhibition. These studies suggest that the terminal alpha-Gal-(1 -> 4)-beta-Gal on the 6-linked oligosaccharide chain of 26404 LOS plays a critical role in forming the epitope recognized by the bactericidal antiserum induced by immunization with our conjugate vaccine.
C1 [Yu, Shengqing; Xie, Hang; Gu, Xin-Xing] Natl Inst Deafness & Other Commun Disorders, Vaccine Res Facil, Rockville, MD 20850 USA.
[Datta, Anup; Naidu, Natasha] Univ Calif San Diego, Glycotechnol Core Resource, Glycobiol Res & Training Ctr, La Jolla, CA 92093 USA.
RP Gu, XX (reprint author), 5 Res Court,Room 2A31, Rockville, MD 20850 USA.
EM guxx@nidcd.nih.gov
OI DATTA, ANUP/0000-0002-3796-6891
FU NIH, NIDCD
FX We thank Eric J. Hansen and John C. McMichael (retired from Wyeth
Vaccines, New York) for kindly supplying Moraxella catarrhalis strains.;
This research was supported by the intramural research program of the
NIH, NIDCD.
NR 43
TC 9
Z9 13
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD SEP
PY 2008
VL 76
IS 9
BP 4251
EP 4258
DI 10.1128/IAI.01570-07
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 340TI
UT WOS:000258667500047
PM 18559429
ER
PT J
AU Zhang, Y
Murtha, J
Roberts, MA
Siegel, RM
Bliska, JB
AF Zhang, Yue
Murtha, James
Roberts, Margaret A.
Siegel, Richard M.
Bliska, James B.
TI Type III secretion decreases bacterial and host survival following
phagocytosis of Yersinia pseudotuberculosis by macrophages
SO INFECTION AND IMMUNITY
LA English
DT Article
ID PROTEIN-TYROSINE-PHOSPHATASE; NECROSIS-FACTOR-ALPHA; VIRULENCE
DETERMINANT; EFFECTOR PROTEIN; KINASE ACTIVATION; INDUCED APOPTOSIS;
GAMMA-INTERFERON; OUTER PROTEINS; YOP2B PROTEIN; RHO-GTPASES
AB Yersinia pseudotuberculosis uses a plasmid (pYV)-encoded type III secretion system (T3SS) to translocate a set of effectors called Yops into infected host cells. YopJ functions to induce apoptosis, and YopT, YopE, and YopH act to antagonize phagocytosis in macrophages. Because Yops do not completely block phagocytosis and Y. pseudotuberculosis can replicate in macrophages, it is important to determine if the T3SS modulates host responses to intracellular bacteria. Isogenic pYV-cured, pYV(+) wild-type, and yop mutant Y. pseudotuberculosis strains were allowed to infect bone marrow-derived murine macrophages at a low multiplicity of infection under conditions in which the survival of extracellular bacteria was prevented. Phagocytosis, the intracellular survival of the bacteria, and the apoptosis of the infected macrophages were analyzed. Forty percent of cell-associated wild-type bacteria were intracellular after a 20-min infection, allowing the study of the macrophage response to internalized pYV(+) Y. pseudotuberculosis. Interestingly, macrophages restricted survival of pYV(+) but not pYV-cured or Delta yopB Y. pseudotuberculosis within phagosomes: only a small fraction of the pYV(+) bacteria internalized replicated by 24 h. In addition, similar to 20% of macrophages infected with wild-type pYV(+) Y. pseudotuberculosis died of apoptosis after 20 h. Analysis of yop mutants expressing catalytically inactive effectors revealed that YopJ was important for apoptosis, while a role for YopE, YopH, and YopT in modulating macrophage responses to intracellular bacteria could not be identified. Apoptosis was reduced in Toll-like receptor 4-deficient macrophages, indicating that cell death required signaling through this receptor. Treatment of macrophages harboring intracellular pYV(+) Y. pseudotuberculosis with chloramphenicol reduced apoptosis, indicating that the de novo bacterial protein synthesis was necessary for cell death. Our finding that the presence of a functional T3SS impacts the survival of both bacterium and host following phagocytosis of Y. pseudotuberculosis suggests new roles for the T3SS in Yersinia pathogenesis.
C1 [Zhang, Yue; Murtha, James; Bliska, James B.] SUNY Stony Brook, Ctr Infect Dis, Stony Brook, NY 11794 USA.
[Zhang, Yue; Murtha, James; Bliska, James B.] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA.
[Roberts, Margaret A.; Siegel, Richard M.] Natl Inst Arthrit, Natl Inst Hlth, Autoimmun Branch, Immunoregulat Unit, Bethesda, MD 20892 USA.
RP Zhang, Y (reprint author), SUNY Stony Brook, Ctr Infect Dis, Stony Brook, NY 11794 USA.
EM yzhang@ms.cc.sunysb.edu
FU National Institutes of Health [AI043389]; NIAID National Institutes of
Health intramural biodefense research [Y2-AI-3739]; NIAMS intramural
research
FX We thank Susan von Horn and Guo-Wei Tian at the Central Microscopy
Imaging Center at Stony Brook University for assistance with electron
microscopy and confocal microscopy, respectively; Kim Orth at the
University of Texas Southwestern Medical Center for providing YopJ
proteins used for antibody production; Wei-Xing Zong for stimulating
discussion and suggestions; Hana Fukuto, Joseph McPhee, Celine Pujol,
Adrianus van der Velden, and Gloria Viboud for comments and suggestions;
and Galina Romanov for excellent technical assistance.; This work is
supported by grants from the National Institutes of Health (AI043389)
awarded to J.B.B., by NIAID National Institutes of Health intramural
biodefense research grant Y2-AI-3739 to R.M.S., and by NIAMS intramural
research funding to R.M.S.
NR 57
TC 22
Z9 23
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD SEP
PY 2008
VL 76
IS 9
BP 4299
EP 4310
DI 10.1128/IAI.00183-08
PG 12
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 340TI
UT WOS:000258667500052
PM 18591234
ER
PT J
AU Lehmann, T
Diabate, A
AF Lehmann, Tovi
Diabate, Abdoulaye
TI The molecular forms of Anopheles gambiae: A phenotypic perspective
SO INFECTION GENETICS AND EVOLUTION
LA English
DT Review
DE Anopheles gambiae; Malaria; Mating behavior; Predation; Reproductive
isolation; Divergent selection; Ecological speciation; Swarm
ID DNA-SEQUENCE VARIATION; WEST-AFRICA; GENETIC DIFFERENTIATION;
CHROMOSOMAL FORMS; BURKINA-FASO; REPRODUCTIVE ISOLATION; INCIPIENT
SPECIATION; INSECTICIDE RESISTANCE; SYMPATRIC SPECIATION; MALARIA
TRANSMISSION
AB The African malaria mosquito Anopheles gambiae is undergoing speciation, being split into the M and S molecular forms. Speciation is the main process promoting biological diversity, thus, new vector species might complicate disease transmission. Genetic differentiation between the molecular forms has been extensively studied, but phenotypic differences between them, the evolutionary forces that generated divergence, and the mechanisms that maintain their genetic isolation have only recently been addressed. Here, we review recent studies suggesting that selection mediated by larval predation and competition promoted divergence between temporary and permanent freshwater habitats. These differences explain the sharp discontinuity in distribution of the molecular forms between rice fields and surrounding savanna, but they can also explain the concurrent cline between humid and and environments due to the dependence on permanent habitats in the latter. Although less pronounced, differences in adult body size, reproductive output, and longevity also suggest that the molecular forms have adapted to distinct niches. Reproductive isolation between the molecular forms is achieved by spatial swarm segregation, although within-swarm mate recognition appears to play a role in certain locations. The implications of these results to disease transmission and control are discussed and many of the gaps in our understanding are highlighted. Published by Elsevier B.V.
C1 [Lehmann, Tovi; Diabate, Abdoulaye] NIAID, Lab Malaria & Vector Res, NIH, MS 8132, Rockville, MD USA.
RP Lehmann, T (reprint author), NIAID, Lab Malaria & Vector Res, NIH, MS 8132, 12735 Twinbrook Pkwy, Rockville, MD USA.
EM tlehmann@niaid.nih.gov
FU National Institutes of Health; National Institute of Allergy and
Infectious Diseases
FX We thank Drs. Frederic Simard, Nicholas Manoukis, Cecilia Coscaron,
Frederic Tripet, Adama Dao, Jen Hume, and Bill Hawley, for helpful
comments and discussions on earlier versions of this paper. Special
thanks to Drs. Nora Besansky, Nicholas Manoukis, Frederic Simard, and to
Mr. Adama Dao and colleagues at MRTC, Mali for sharing unpublished data.
This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases.
NR 101
TC 84
Z9 86
U1 2
U2 20
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-1348
EI 1567-7257
J9 INFECT GENET EVOL
JI Infect. Genet. Evol.
PD SEP
PY 2008
VL 8
IS 5
BP 737
EP 746
DI 10.1016/j.meegid.2008.06.003
PG 10
WC Infectious Diseases
SC Infectious Diseases
GA 361XK
UT WOS:000260160900029
PM 18640289
ER
PT J
AU Dworkin, MS
Schwan, TG
Anderson, DE
Borchardt, SM
AF Dworkin, Mark S.
Schwan, Tom G.
Anderson, Donald E.
Borchardt, Stephanie M.
TI Tick-borne relapsing fever
SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA
LA English
DT Article
ID SPIROCHETE BORRELIA-HERMSII; UNITED-STATES; LYME-DISEASE; PHYLOGENETIC
ANALYSIS; INTERSTATE OUTBREAK; ANTIGENIC VARIATION; BRITISH-COLUMBIA;
NORTH-AMERICA; GRAND-CANYON; IDENTIFICATION
AB Each year, many residents of And visitors to endemic regions of the western United States are exposed to the tick vectors of tick-borne relapsing fever (TBRF), Ornithodoros hermsi, Ornithodoros turicata, or Ornithodoros parkeri. This disease is remarkable because the human host is unaware of the tick bite, usually becomes very ill, may experience an exacerbation of symptoms rather than improvement shortly after beginning appropriate treatment, and, despite often high numbers of the etiologic organism in the blood, rarely dies as a result of the illness. Although relapsing fever is acquired in many parts of the world, this article focuses primarily on knowledge about TBRF in North America.
C1 [Dworkin, Mark S.] Univ Illinois, Div Epidemiol & Biostat, Sch Publ Hlth, Chicago, IL 60612 USA.
[Schwan, Tom G.] NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Anderson, Donald E.] Washington State Univ, Coll Pharm, Spokane, WA 99223 USA.
[Borchardt, Stephanie M.] Fargo Vet Adm Med Ctr, Fargo, ND 58102 USA.
RP Dworkin, MS (reprint author), Univ Illinois, Div Epidemiol & Biostat, Sch Publ Hlth, 1603 W Taylor St, Chicago, IL 60612 USA.
EM mdworkin@uic.edu
FU Intramural NIH HHS [Z01 AI000492-21]
NR 67
TC 56
Z9 60
U1 0
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0891-5520
EI 1557-9824
J9 INFECT DIS CLIN N AM
JI Infect. Dis. Clin. North Am.
PD SEP
PY 2008
VL 22
IS 3
BP 449
EP +
DI 10.1016/j.idc.2008.03.006
PG 21
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 354DN
UT WOS:000259619200006
PM 18755384
ER
PT J
AU Lin, J
DiCuccio, M
Grigoryan, V
Wilbur, WJ
AF Lin, Jimmy
DiCuccio, Michael
Grigoryan, Vahan
Wilbur, W. John
TI Navigating information spaces: A case study of related article search in
PubMed
SO INFORMATION PROCESSING & MANAGEMENT
LA English
DT Article
DE MEDLINE; TREC genomics; browsing; interactive IR
ID EXPLORATION; RETRIEVAL; NETWORKS
AB The concept of an "information space" provides a powerful metaphor for guiding the design of interactive retrieval systems. We present a case study of related article search, a browsing tool designed to help users navigate the information space defined by results of the PubMed (R) search engine. This feature leverages content-similarity links that tie MEDLINE (R) citations together in a vast document network. We examine the effectiveness of related article search from two perspectives: a topological analysis of networks generated from information needs represented in the TREC 2005 genomics track and a query log analysis of real PubMed users. Together, data suggest that related article search is a useful feature and that browsing related articles has become an integral part of how users interact with PubMed. Published by Elsevier Ltd.
C1 [Lin, Jimmy] Univ Maryland, iSch, College Pk, MD 20742 USA.
[Lin, Jimmy; DiCuccio, Michael; Grigoryan, Vahan; Wilbur, W. John] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
RP Lin, J (reprint author), Univ Maryland, iSch, College Pk, MD 20742 USA.
EM jimmylin@umd.edu; dicuccio@ncbi.nlm.nih.gov; grigoryv@ncbi.nlm.nih.gov;
wilbur@ncbi.nlm.nih.gov
NR 29
TC 6
Z9 6
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4573
J9 INFORM PROCESS MANAG
JI Inf. Process. Manage.
PD SEP
PY 2008
VL 44
IS 5
BP 1771
EP 1783
DI 10.1016/j.ipm.2008.04.002
PG 13
WC Computer Science, Information Systems; Information Science & Library
Science
SC Computer Science; Information Science & Library Science
GA 342UA
UT WOS:000258807800010
ER
PT J
AU Mans, BJ
Ribeiro, JMC
AF Mans, Ben J.
Ribeiro, Jose M. C.
TI Function, mechanism and evolution of the moubatin-clade of soft tick
lipocalins
SO INSECT BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Article
DE Ornithodoros moubata; Ornithodoros savignyi; Moubatin; TSGP2; TSGP3;
Platelet aggregation; Thromboxane A(2); Complement C5 inhibitor
ID ORNITHODOROS-MOUBATA; PLATELET-AGGREGATION; GRANULE BIOGENESIS;
IXODES-SCAPULARIS; BINDING PROTEINS; SALIVARY-GLANDS; FAMILY; INHIBITOR;
CLONING; EXPRESSION
AB The "moubatin-clade" of soft tick lipocalins, although monophyletic, shows clear signs of paralogy as indicated by the various functions associated with this protein family. This includes anti-platelet (moubatin), anti-complement (OMCI) and toxic (TSGP2) activities in the vertebrate host. In order to understand the evolution of function and how it relates to the various paralogs in this clade, we characterized a number of different proteins in regard to undefined function and mechanism. By utilizing gain-of-function for TSGP2 and loss-of-function for TSGP3, we show that inhibition of collagen-induced platelet aggregation by moubatin and TSGP3 is due to scavenging of thromboxane A(2). Moubatin, TSGP2 and TSGP3 are also able to bind leukotriene B-4 With high affinity. TSGP2 and TSGP3, but not moubatin, binds complement C5, with kinetics that indicates that conformation change occurs during interaction. A conserved loop and histidine residue in the sequences of OMCI, TSGP2 and TSGP3 are implicated in the interaction with complement C5. The data presented suggest that the ancestral function evolved in this clade was aimed at inhibition of vasoconstriction, platelet aggregation and neutrophil aggregation, primarily by scavenging of thromboxane A(2) and leukotriene B-4. C5 complement targeting activity evolved within this clade, probably within the Old World Ornithodorinae. The moubatin-clade itself most probably derived from the related histamine and serotonin-binding lipocalin sub-family that is conserved within the Argasidae. (c) 2008 Elsevier Ltd. All rights reserved.
C1 [Mans, Ben J.; Ribeiro, Jose M. C.] NIH, Lab Malaria & Vector Res, Rockville, MD 20852 USA.
RP Mans, BJ (reprint author), Agr Res Council, Onderstepoort Vet Inst, ZA-0110 Onderstepoort, South Africa.
EM mansb@arc.agric.za
OI Mans, Ben/0000-0002-0177-0029; Ribeiro, Jose/0000-0002-9107-0818
FU NIAID; National Institutes of Health
FX Dr. Carl Hammer of the Research and Technology Branch of the NIAID is
thanked for mass spectrometry analysis of the recombinant proteins. This
work was supported by the intramural research program of the NIAID,
National Institutes of Health.
NR 42
TC 50
Z9 50
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0965-1748
J9 INSECT BIOCHEM MOLEC
JI Insect Biochem. Mol. Biol.
PD SEP
PY 2008
VL 38
IS 9
BP 841
EP 852
DI 10.1016/j.ibmb.2008.06.007
PG 12
WC Biochemistry & Molecular Biology; Entomology
SC Biochemistry & Molecular Biology; Entomology
GA 358CT
UT WOS:000259894900004
PM 18694828
ER
PT J
AU Mans, BJ
Ribeiro, JMC
AF Mans, Ben J.
Ribeiro, Jose M. C.
TI A novel clade of cysteinyl leukotriene scavengers in soft ticks
SO INSECT BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Article
DE Argas monolakensis; Ornithodoros savignyi; TSGP4; AM-33; Vasodilator;
Leukotrienes; Mast cell; Basophil
ID ORNITHODOROS-SAVIGNYI; HOST INTERACTIONS; BINDING PROTEINS;
SALIVARY-GLANDS; SAND TAMPAN; EVOLUTION; FAMILY; PERSPECTIVE; TOXICOSES;
HISTAMINE
AB Inflammation is an important vertebrate defense mechanism against ecto-parasites for which ticks have evolved numerous mechanisms of modulation. AM-33 and TSGP4, related lipocalins from the soft ticks Argas monolakensis and Ornithodoros savignyi bind cysteinyl leukotrienes with high affinity as measured by isothermal titration calorimetry. This was confirmed in a smooth muscle bioassay that measured contraction of guinea pig ileum induced by leukotriene C-4 where both proteins inhibited contraction effectively. Conservation of this function in two diverse soft tick genera suggests that scavenging of cysteinyl leukotrienes evolved in the ancestral soft tick lineage. In addition soft ticks also evolved mechanisms that target other mediators of inflammation that include scavenging of histamine, serotonin, leukotriene B-4, thromboxane A(2), ATP and inhibition of the complement cascade. Inhibitors of blood-coagulation and platelet aggregation were also present in the ancestral soft tick lineage. Because histamine and cysteinyl leukotrienes are mainly produced by mast cells and basophils, and these cells are important in the mediation of tick rejection reactions, these findings indicate an ancient antagonistic relationship between ticks and the immune system. As such, modulation of the hemostatic system as well as inflammation was important adaptive responses in the evolution of a blood-feeding lifestyle in soft ticks. (c) 2008 Elsevier Ltd. All rights reserved.
C1 [Mans, Ben J.; Ribeiro, Jose M. C.] NIH, Lab Malaria & Vector Res, Rockville, MD 20852 USA.
RP Mans, BJ (reprint author), Agr Res Council, Onderstepoort Vet Inst, ZA-0110 Onderstepoort, South Africa.
EM mansb@arc.agric.za
OI Mans, Ben/0000-0002-0177-0029; Ribeiro, Jose/0000-0002-9107-0818
FU MAID; National Institutes of Health
FX Dr. Carl Hammer and Mark Garfield of the Research and Technology Branch
of the NIAID are thanked for mass spectrometry analysis and Edman
sequencing of the recombinant proteins. This work was supported by the
intramural research program of the MAID, National Institutes of Health.
NR 41
TC 36
Z9 36
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0965-1748
J9 INSECT BIOCHEM MOLEC
JI Insect Biochem. Mol. Biol.
PD SEP
PY 2008
VL 38
IS 9
BP 862
EP 870
DI 10.1016/j.ibmb.2008.06.002
PG 9
WC Biochemistry & Molecular Biology; Entomology
SC Biochemistry & Molecular Biology; Entomology
GA 358CT
UT WOS:000259894900006
PM 18675910
ER
PT J
AU Hsiao, AF
Wong, MD
Miller, MF
Ambs, AH
Goldstein, MS
Smith, A
Ballard-Barbash, R
Becerra, LS
Cheng, EM
Wenger, NS
AF Hsiao, An-Fu
Wong, Mitchell D.
Miller, Melissa F.
Ambs, Anita H.
Goldstein, Michael S.
Smith, Ashley
Ballard-Barbash, Rachel
Becerra, Lida S.
Cheng, Eric M.
Wenger, Neil S.
TI Role of religiosity and spirituality in complementary and alternative
medicine use among cancer survivors in California
SO INTEGRATIVE CANCER THERAPIES
LA English
DT Article
DE CAM; integrative medicine; spirituality; religiosity; survivors
ID HEALTH-CARE; ETHNIC-DIFFERENCES; ONCOLOGY; PREVALENCE; ADULTS
AB Objectives. Cancer survivors often turn to religion, spirituality, and complementary and alternative medicine (CAM) because they perceive these areas as being more holistic and patient-centered than conventional medicine. Because increased religiosity and spirituality have been found to be associated with higher CAM use in the general population, it was hypothesized that these factors would be important predictors of CAM use in cancer survivors. Design and Subjects. The study included a subsample of 1844 people with cancer or a history of cancer from the 2003 California Health Interview Survey of CAM, a cross-sectional survey of a population-based sample of adults in California. Prevalence and predictors of religious/spiritual forms of CAM (R/S CAM) and nonreligious/nonspiritual forms of CAM (non-R/S CAM) were compared. Multivariate logistic regression was used to identify the predictors of R/S CAM and non-R/S CAM. Results. Nearly two thirds of participants reported using at least 1 type of R/S CAM, and 85% reported ever using non-R/S CAM. The majority of cancer survivors reported that they were very/moderately religious or spiritual. Both religiosity and spirituality were strongly related to non-R/S CAM use, but in opposite directions. Very or moderately religious cancer survivors were less likely (odds ratio = 0.30; 95% confidence interval, 0.12-0.40) than nonreligious cancer survivors to use non-R/S CAM. In contrast, very or moderately spiritual cancer survivors were more likely (odds ratio = 2.42; 95% confidence interval, 1.16-6.02) than nonspiritual cancer survivors to use non-R/S CAM. Conclusions. The use of R/S CAM and non-R/S CAM is very high in cancer survivors. It may be helpful for clinicians to ascertain their patients' use of these types of CAM to integrate all forms of care used to managing their cancer.
C1 [Hsiao, An-Fu] VA Long Beach Healthcare Syst, Long Beach, CA 90822 USA.
[Hsiao, An-Fu] Univ Calif Irvine, Ctr Hlth Policy Res, Irvine, CA USA.
[Wong, Mitchell D.] Univ Calif Los Angeles, Div Gen Internal Med, Los Angeles, CA USA.
[Wong, Mitchell D.; Wenger, Neil S.] Univ Calif Los Angeles, Hlth Serv Res, Los Angeles, CA USA.
[Miller, Melissa F.; Ambs, Anita H.; Smith, Ashley; Ballard-Barbash, Rachel] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Goldstein, Michael S.] Univ Calif Los Angeles, Dept Community Hlth Sci, Los Angeles, CA USA.
[Becerra, Lida S.] Univ Calif Los Angeles, Ctr Hlth Policy & Res, Los Angeles, CA USA.
[Cheng, Eric M.] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA USA.
[Cheng, Eric M.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
RP Hsiao, AF (reprint author), VA Long Beach Healthcare Syst, 5901 E 7th St,Mail Code 11-111, Long Beach, CA 90822 USA.
EM anfu.hsiao@va.gov
OI Wong, Mitchell/0000-0002-4800-8410
FU National Institutes of Health (NIH); National Center of Complementary
and Alternative Medicine [R21 AT002248-01]; NCCAM [R21-AT002248-01];
National Cancer institute (NCI) [NO2-PC-95057]
FX We thank Victor Gonzalez for his technical assistance. We thank UCLA
Center for Health Policy Research for their assistance in carrying out
the research. FUNDING/GRANT INFORMATION: Dr. Hsiao was supported by
National Institutes of Health (NIH), National Center of Complementary
and Alternative Medicine (R21 AT002248-01). This publication was made
possible by Grant No. R21-AT002248-01 from NCCAM. The collection of data
used in this study was supported by the National Cancer institute (NCI)
under contract NO2-PC-95057 awarded to the UCLA Center for Health Policy
Research. The contents of this manuscript are solely the responsibility
of the authors and do not necessarily represent the official views of
the NCCAM, NCI, or the NIH.
NR 36
TC 20
Z9 21
U1 1
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1534-7354
J9 INTEGR CANCER THER
JI Integr. Cancer Ther.
PD SEP
PY 2008
VL 7
IS 3
BP 139
EP 146
DI 10.1177/1534735408322847
PG 8
WC Oncology; Integrative & Complementary Medicine
SC Oncology; Integrative & Complementary Medicine
GA 351PQ
UT WOS:000259436800004
PM 18815145
ER
PT J
AU Miller, MA
Miller, WA
Conrad, PA
James, ER
Melli, AC
Leutenegger, CM
Dabritz, HA
Packham, AE
Paradies, D
Harris, M
Ames, J
Jessup, DA
Worcester, K
Grigg, ME
AF Miller, M. A.
Miller, W. A.
Conrad, P. A.
James, E. R.
Melli, A. C.
Leutenegger, C. M.
Dabritz, H. A.
Packham, A. E.
Paradies, D.
Harris, M.
Ames, J.
Jessup, D. A.
Worcester, K.
Grigg, M. E.
TI Type X Toxoplasma gondii in a wild mussel and terrestrial carnivores
from coastal California: New linkages between terrestrial mammals,
runoff and toxoplasmosis of sea otters
SO INTERNATIONAL JOURNAL FOR PARASITOLOGY
LA English
DT Article
DE Toxoplasma gondii; Type X; B1; 18S rDNA; SAG1; GRA6; otter; felid;
mussel
ID ENHYDRA-LUTRIS-NEREIS; OYSTERS CRASSOSTREA-VIRGINICA; WATERBORNE
TOXOPLASMOSIS; SEXUAL RECOMBINATION; DRINKING-WATER; OOCYSTS; MARINE;
SPP.; CRYPTOSPORIDIUM; PROTOZOAN
AB Sea otters in California are commonly infected with Toxoplasma gondii. A unique Type X strain is responsible for 72% of otter infections, but its prevalence in terrestrial animals and marine invertebrates inhabiting the same area was unknown. Between 2000 and 2005, 45 terrestrial carnivores (lions, bobcats, domestic cats and foxes) and 1396 invertebrates (mussels, clams and worms) were screened for T gondii using PCR and DNA sequencing to determine the phylogeographic distribution of T gondii archetypal 1, 11, 111 and Type X genotypes. Marine bivalves have been shown to concentrate T gondii oocysts in the laboratory, but a comprehensive survey of wild invertebrates has not been reported. A California mussel from an estuary draining into Monterey Bay was confirmed positive for Type X T gondii by multilocus PCR and DNA sequencing at the B1 and SAG1 loci. This mussel was collected from nearshore marine waters just after the first significant rainfall event in the fall of 2002. Of 45 carnivores tested at the B1, SAG1, and GRA6 typing loci, 15 had PCR-confirmed T gondii infection; 11 possessed alleles consistent with infection by archetypal Type I, II or III strains and 4 possessed alleles consistent with Type X T gondii infection. No non-canonical alleles were identified. The four T gondii strains with Type X alleles were identified from two mountain lions, a bobcat and a fox residing in coastal watersheds adjacent to sea otter habitat near Monterey Bay and Estero Bay. Confirmation of Type X T. gondii in coastal-dwelling felids, canids, a marine bivalve and nearshore-dwelling sea otters supports the hypotheses that feline faecal contamination is flowing from land to sea through surface runoff, and that otters can be infected with T gondii via consumption of filter-feeding marine invertebrates. (c) 2008 Australian Society for Parasitology Inc. Published by Elsevier Ltd. All rights reserved.
C1 [Miller, M. A.; Harris, M.; Ames, J.; Jessup, D. A.] Marine Wildlife Vet Care & Res Ctr, Calif Dept Fish & Game, Santa Cruz, CA 95060 USA.
[Miller, W. A.; Conrad, P. A.; Melli, A. C.; Packham, A. E.] Univ Calif Davis, Sch Vet Med, Dept Pathol Microbiol & Immunol, Davis, CA 95616 USA.
[James, E. R.] Univ British Columbia, Dept Med, Vancouver, BC V5C 3J5, Canada.
[Leutenegger, C. M.] IDEXX Reference Labs, W Sacramento, CA 95605 USA.
[Dabritz, H. A.] Infant Botulism Treatment & Prevent Program, Calif Dept Publ Hlth, Richmond, CA 94804 USA.
[Paradies, D.] Bay Fdn Morro Bay, Morro Bay, CA 93442 USA.
[Worcester, K.] Reg Water Qual Control Board Cent Coast, San Luis Obispo, CA 93401 USA.
[Grigg, M. E.] NIAID, Mol Parasitol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Miller, MA (reprint author), Marine Wildlife Vet Care & Res Ctr, Calif Dept Fish & Game, 1451 Shaffer Rd, Santa Cruz, CA 95060 USA.
EM mmiller@ospr.dfg.ca.gov
RI James, Erick/D-4725-2012
FU Morris Animal Foundation; National Sea Grant; Central Coast Regional
Water Quality Control Board; Duke Power and the Morro Bay Water
Treatment Plant; National Science Foundation; Intramural Research
Program of the NIH; NIAID
FX Financial support was provided by the Morris Animal Foundation (MAM,
PAC, HAD), National Sea Grant (MAM and PAC), CDFG (MAM and DAJ), the
Central Coast Regional Water Quality Control Board, Duke Power and the
Morro Bay Water Treatment Plant (MAM, DAJ, PAC and WAM) and the National
Science Foundation (MEG). This research was supported in part by the
Intramural Research Program of the NIH and NIAID (MEG). We are grateful
to the wardens, biologists and staff of CDFG, California State Parks,
USDA-Wildlife Protection Services, the Elkhorn Slough Reserve, Monterey
SPCA, Moss Landing Yacht Club, Elkhorn Slough Safari Tours, Morro Bay
Water Treatment Plant, UC Davis, UC Santa Cruz, the Central Coast Water
Quality Control Board and the Morro Bay Harbor Patrol for their
enthusiastic collaboration and support. In particular, we thank Adam
Schneider, Alexis Fisher, Bruce Keough, Dave Paradies, Debbie
Brownstein, Elene Dorfmeier, Eva Berberich, Erin Dodd, Francesca Batac,
Larry White, Nancy Wagner, Sara Miller, Sharon Toy-Choutka and Tricia
Wilson for assistance with data collection, specimen transport,
necropsies and manuscript preparation. We would especially like to thank
Ms. Betty White-Ludden for her long-term support of sea otter research.;
The cover photo was provided by Mr. Frank Balthis.
NR 55
TC 101
Z9 103
U1 5
U2 50
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0020-7519
J9 INT J PARASITOL
JI Int. J. Parasit.
PD SEP
PY 2008
VL 38
IS 11
BP 1319
EP 1328
DI 10.1016/j.ijpara.2008.02.005
PG 10
WC Parasitology
SC Parasitology
GA 345TU
UT WOS:000259020700009
PM 18452923
ER
PT J
AU Ahn, J
Moslehi, R
Weinstein, SJ
Snyder, K
Virtamo, J
Albanes, D
AF Ahn, Jiyoung
Moslehi, Roxana
Weinstein, Stephanie J.
Snyder, Kirk
Virtamo, Jarmo
Albanes, Demetrius
TI Family history of prostate cancer and prostate cancer risk in the
Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE family history; prostate cancer; height; weight; alpha-tocopherol;
retinol; beta-carotene
ID NATIONWIDE REGISTER COHORT; POPULATION-BASED COHORT; BREAST-CANCER;
FOLLOW-UP; SWEDEN; MEN; HEALTH; CARCINOMA; MEAT; AGE
AB Prostate cancer family history has been associated with increased risk of the malignancy. Most prior studies have been retrospective and subject to recall bias, however, and data evaluating interactions with other important risk factors are limited. We examined the relationship between a family history of prostate cancer and prostate cancer risk in relation to body size, micronutrients and other exposures in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study cohort of Finnish male smokers. Family history of cancer information was self-reported once during the study in 1991, and anthropometry was measured by trained personnel. Among 19,652 men with complete data, 1,111 incident cases were identified during up to 12.3 years of follow-up. A first-degree family history of prostate cancer was associated with an overall relative risk (RR) of 1.91 (95% CI = 1.49-2.47) and a RR of 4.16 (95% CI = 2.67-6.49) for advanced disease (stage : 3), adjusted for age and trial intervention. Our data also suggest that to some degree, height, body mass index, and serum a-tocopherol and P-carotene modify the family history and prostate cancer association, although the interactions were not statistically significant. Supplementation with vitamin E or beta-carotene did not modify the family history-prostate cancer association. This study provides additional evidence that family history is a significant risk factor for prostate cancer. Published 2008 Wiley-Liss, Inc.
C1 [Albanes, Demetrius] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Snyder, Kirk] Informat Management Serv Inc, Silver Spring, MD USA.
[Virtamo, Jarmo] Natl Publ Hlth Inst, Dept Hlth Promot & Chron Dis Prevent, Helsinki, Finland.
RP Albanes, D (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, EPS-3044,6120 Execut Blvd, Bethesda, MD 20892 USA.
EM daa@nih.gov
RI Albanes, Demetrius/B-9749-2015
FU CCR NIH HHS [N01-RC-37004, N01-RC-45035]; Intramural NIH HHS; NCI NIH
HHS [N01-CN-45165]
NR 38
TC 18
Z9 18
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD SEP 1
PY 2008
VL 123
IS 5
BP 1154
EP 1159
DI 10.1002/ijc.23591
PG 6
WC Oncology
SC Oncology
GA 334TE
UT WOS:000258243300022
PM 18546266
ER
PT J
AU Shamir, L
AF Shamir, Lior
TI Evaluation of face datasets as tools for assessing the performance of
face recognition methods
SO INTERNATIONAL JOURNAL OF COMPUTER VISION
LA English
DT Article
DE face recognition; biometrics; FERET
ID QUANTITATIVE-ANALYSIS; INFORMATICS; ALGORITHMS; IMAGES
AB Face datasets are considered a primary tool for evaluating the efficacy of face recognition methods. Here we show that in many of the commonly used face datasets, face images can be recognized accurately at a rate significantly higher than random even when no face, hair or clothes features appear in the image. The experiments were done by cutting a small background area from each face image, so that each face dataset provided a new image dataset which included only seemingly blank images. Then, an image classification method was used in order to check the classification accuracy. Experimental results show that the classification accuracy ranged between 13.5% (color FERET) to 99% (YaleB). These results indicate that the performance of face recognition methods measured using face image datasets may be biased. Compilable source code used for this experiment is freely available for download via the Internet.
C1 NIA, NIH, Genet Lab, Baltimore, MD 21224 USA.
RP Shamir, L (reprint author), NIA, NIH, Genet Lab, 333 Cassell Dr, Baltimore, MD 21224 USA.
EM shamirl@mail.nih.gov
FU Intramural NIH HHS [NIH0012688432]
NR 32
TC 22
Z9 22
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0920-5691
EI 1573-1405
J9 INT J COMPUT VISION
JI Int. J. Comput. Vis.
PD SEP
PY 2008
VL 79
IS 3
BP 225
EP 230
DI 10.1007/s11263-008-0143-7
PG 6
WC Computer Science, Artificial Intelligence
SC Computer Science
GA 310KW
UT WOS:000256529500001
PM 18776952
ER
PT J
AU Kretschmer, D
Gleske, AK
Rautenberg, M
van Strijp, J
Otto, M
Peschel, A
AF Kretschmer, D.
Gleske, A. K.
Rautenberg, M.
van Strijp, J.
Otto, M.
Peschel, A.
TI The leukocidal phenol-soluble modulin (PSM) peptides of Staphylococcus
aureus represent a novel type of leukocyte attractants
SO INTERNATIONAL JOURNAL OF MEDICAL MICROBIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
Deutschen-Gesellschaft-fur-Hygiene-und-Mikrobiologie
CY SEP 21-24, 2008
CL Dresden, GERMANY
SP Deutsch Gesell Hygiene & Mikrobiol
C1 [Kretschmer, D.; Gleske, A. K.; Rautenberg, M.; Peschel, A.] Univ Tubingen, Tubingen, Germany.
[van Strijp, J.] Univ Med Ctr Utrecht, Eijkman Winkler Inst, Utrecht, Netherlands.
[Otto, M.] NIAID, Rocky Mt Labs, Lab Human Bacterial Pathogenesis, US NIH, Hamilton, MT 59840 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 1438-4221
J9 INT J MED MICROBIOL
JI Int. J. Med. Microbiol.
PD SEP
PY 2008
VL 298
SU 45
BP 45
EP 45
PG 1
WC Microbiology; Virology
SC Microbiology; Virology
GA 353SV
UT WOS:000259589400175
ER
PT J
AU Lee, KY
Choi, SY
Bae, JW
Kim, S
Chung, KW
Drayna, D
Kim, UK
Lee, SH
AF Lee, K. Y.
Choi, S. Y.
Bae, J. W.
Kim, S.
Chung, K. W.
Drayna, D.
Kim, U. K.
Lee, S. H.
TI Molecular analysis of the GJB2, GJB6 and SLC26A4 genes in Korean
deafness patients
SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY
LA English
DT Article
DE connexin; hearing loss; Koreans; mutation; Pendred syndrome
ID CONNEXIN 26 GENE; NONSYNDROMIC HEARING-LOSS; PENDRED-SYNDROME;
VESTIBULAR AQUEDUCT; RECESSIVE DEAFNESS; CHILDHOOD DEAFNESS;
HIGH-FREQUENCY; UNITED-STATES; PDS GENE; MUTATIONS
AB Objectives: Mutations in the GJB2, GJB6 and SLC26A4 genes are a frequent cause of hearing toss in a number of populations. However, little is known about the genetic causes of hearing toss in the Korean population.
Methods: We sequenced the GJB2 and GJB6 genes to examine the rote of mutations in these genes in 22 hearing loss patients. We also sequenced the SLC26A4 gene in seven patients with inner ear malformations, including enlarged vestibular aqueduct (EVA) revealed by computer tomography.
Results: Coding sequence mutations in GJB2 were identified in 13.6% of the patients screened. Two different mutations, 235delC and T86R were found in three unrelated patients. The 235delC was the most prevalent mutation with an allele frequency of 6.9% in our patient group. No mutations, including 342-kb deletion, were found in GJB6 gene. Three different variants of SLC26A4 were identified in the EVA patients, including one novel. mutation. Four EVA patients carried two mutant alleles of SLC26A4, and at least one allele in all patients was the H723R mutation, which accounted for 75% of all mutant alleles.
Conclusions: Our results suggest that GJB2 and SLC26A4 mutations together make up a major cause of congenital hearing loss in the Korean population. Further studies may be able to identify other common variants that account for a significant fraction of hearing toss in the Korean population. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Lee, K. Y.; Lee, S. H.] Kyungpook Natl Univ, Coll Med, Dept Otolaryngol, Taegu 702701, South Korea.
[Choi, S. Y.; Bae, J. W.; Kim, U. K.] Kyungpook Natl Univ, Coll Nat Sci, Dept Biol, Taegu 702701, South Korea.
[Kim, S.] Deagu Fatima Hosp, Dept Otolaryngol, Taegu 701600, South Korea.
[Chung, K. W.] Kongju Natl Univ, Dept Biol Sci, Kong Ju 314701, South Korea.
[Drayna, D.] Natl Inst Deafness & Other Commun Disorders, NIH, Rockville, MD 20850 USA.
RP Lee, KY (reprint author), Kyungpook Natl Univ, Coll Med, Dept Otolaryngol, Taegu 702701, South Korea.
EM drlky@hanmail.net; kimuk@knu.ac.kr
FU Korea Science and Engineering Foundation (KOSEF); Korean government
(MOST) [R01-2008-000-10431-0]; Kyungpook National University Hospital;
Korean Ministry of Education
FX We thank all the subjects who participated in the present study. We also
thank Young-Jun Choi and Jung Ree Lee for collecting:) patients and
family members. This work was supported by the Korea Science and
Engineering Foundation (KOSEF) grant funded by the Korean government
(MOST) (No. R01-2008-000-10431-0). This work was supported by BioMedical
Research Institute grant, Kyungpook National University Hospital (2007).
SY Choi and JW Bae were supported by the Korean Ministry of Education
through the Brain Korea 21 project.
NR 46
TC 40
Z9 43
U1 0
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0165-5876
J9 INT J PEDIATR OTORHI
JI Int. J. Pediatr. Otorhinolaryngol.
PD SEP
PY 2008
VL 72
IS 9
BP 1301
EP 1309
DI 10.1016/j.ijport.2008.05.007
PG 9
WC Otorhinolaryngology; Pediatrics
SC Otorhinolaryngology; Pediatrics
GA 347IW
UT WOS:000259134800001
PM 18585793
ER
PT J
AU Bondar, IV
Leopold, DA
Logothetis, NK
AF Bondar, I. V.
Leopold, D. A.
Logothetis, N. K.
TI Stability of neuronal representation in inferotemporal cortex: Long-term
single neurons study by chronically implanted microelectrodes
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Bondar, I. V.] RAS, Inst Higher Nervous Act & Neurophysiol, Moscow 117901, Russia.
[Leopold, D. A.] NIMH, Unit Cognit Neurophysiol & Imaging, Bethesda, MD 20892 USA.
[Logothetis, N. K.] Max Planck Inst Biol Cybernet, Tubingen, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 172
EP 172
DI 10.1016/j.ijpsycho.2008.05.447
PG 1
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700119
ER
PT J
AU Furey, ML
AF Furey, M. L.
TI Influence of muscarinic cholinergic receptors on mood, attention and
emotional stimulus processing in affective disorders
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Furey, M. L.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 187
EP 187
DI 10.1016/j.ijpsycho.2008.05.499
PG 1
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700171
ER
PT J
AU Pietrini, P
Furey, ML
AF Pietrini, P.
Furey, M. L.
TI The role of the cholinergic system in physiological and pathological
conditions
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Pietrini, P.] Univ Pisa, Dept Expt Pathol Med Biotechnol Infectivol & Epid, Lab Clin Biochem & Mol Biol, Pisa, Italy.
[Furey, M. L.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 187
EP 187
DI 10.1016/j.ijpsycho.2008.05.498
PG 1
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700170
ER
PT J
AU Ricciardi, E
Pietrini, P
Furey, ML
AF Ricciardi, E.
Pietrini, P.
Furey, M. L.
TI Cholinergic modulation on brain response to working memory as task
difficulty increases in young and older subjects
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Ricciardi, E.; Pietrini, P.] Univ Pisa, Dept Expt Pathol Med Biotechnol Infectivol & Epid, Lab Clin Biochem & Mol Biol, Pisa, Italy.
[Furey, M. L.] NIMH, NIH, Bethesda, MD 20892 USA.
RI Furey, Maura/H-5273-2013; Ricciardi, Emiliano/E-6929-2011
OI Ricciardi, Emiliano/0000-0002-7178-9534
NR 2
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 187
EP 188
DI 10.1016/j.ijpsycho.2008.05.500
PG 2
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700172
ER
PT J
AU Nugent, AC
Bain, EE
Sollers, JJ
Thayer, JF
Drevets, WC
AF Nugent, A. C.
Bain, E. E.
Sollers, J. J.
Thayer, J. F.
Drevets, W. C.
TI Alterations in neural correlates of autonomic control in females with
and without major depressive disorder
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Nugent, A. C.; Drevets, W. C.] NIMH, Bethesda, MD USA.
[Bain, E. E.] Abbott Labs, Abbott Pk, IL 60064 USA.
[Sollers, J. J.; Thayer, J. F.] Ohio State Univ, Columbus, OH 43210 USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 194
EP 194
DI 10.1016/j.ijpsycho.2008.05.524
PG 1
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700196
ER
PT J
AU Nugent, AC
Bain, EE
Thayer, JF
Sollers, JJ
Drevets, WC
AF Nugent, A. C.
Bain, E. E.
Thayer, J. F.
Sollers, J. J.
Drevets, W. C.
TI Alterations in neural correlates of autonomic control in females with
major depressive disorder
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Nugent, A. C.; Drevets, W. C.] NIMH, NIH, Bethesda, MD 20892 USA.
[Bain, E. E.] Abbott Labs, Abbott Pk, IL 60064 USA.
[Thayer, J. F.; Sollers, J. J.] Ohio State Univ, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 195
EP 195
DI 10.1016/j.ijpsycho.2008.05.526
PG 1
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700198
ER
PT J
AU Leopold, DA
Wilke, M
Maier, A
AF Leopold, D. A.
Wilke, M.
Maier, A.
TI Neural correlates of perception measured with fMRl and microelectrodes
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Leopold, D. A.; Wilke, M.; Maier, A.] NIMH, Neuropsychol Lab, Bethesda, MD 20892 USA.
RI Maier, Alexander/B-7489-2009
OI Maier, Alexander/0000-0002-7250-502X
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 199
EP 200
DI 10.1016/j.ijpsycho.2008.05.543
PG 2
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700215
ER
PT J
AU Duncan, CC
Mirsky, AF
AF Duncan, C. C.
Mirsky, A. F.
TI Auditory P300 is more sensitive than visual P300 to the attention
impairment in absence epilepsy
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Duncan, C. C.] Uniformed Serv Univ Hlth Sci, Dept Psychiat, Lab Clin Psychophysiol, Bethesda, MD 20814 USA.
[Mirsky, A. F.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 207
EP 207
DI 10.1016/j.ijpsycho.2008.05.011
PG 1
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700234
ER
PT J
AU Rota, G
Turicchia, L
Veit, R
Guazzelli, M
Birbaumer, N
Dogil, G
AF Rota, G.
Turicchia, L.
Veit, R.
Guazzelli, M.
Birbaumer, N.
Dogil, G.
TI Perceptual learning of speech processed by a Cochlear Implant simulator
- An fMRI investigation
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Meeting Abstract
CT 14th World Congress of Psychophysiology the Olympics of the Brain
CY SEP 08-13, 2008
CL St Petersburg, RUSSIA
SP Int Org Psychophysiol
C1 [Rota, G.; Guazzelli, M.] Univ Pisa, Dept Psychiat Neurobiol Pharmacol & Biotechnol, Pisa, Italy.
[Turicchia, L.] MIT, Elect Res Lab, Cambridge, MA 02139 USA.
[Rota, G.; Veit, R.; Birbaumer, N.] Univ Tubingen, Inst Med Psychol & Behav Neurobiol, Tubingen, Germany.
[Veit, R.] Max Planck Inst Biol Cybernet, Tubingen, Germany.
[Birbaumer, N.] NINDS, NIH, Human Cort Physiol Sect, Bethesda, MD 20892 USA.
[Rota, G.; Dogil, G.] Univ Stuttgart, Inst Natural Language Proc, Stuttgart, Germany.
RI Veit, Ralf/F-8907-2012
OI Veit, Ralf/0000-0001-9860-642X
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD SEP
PY 2008
VL 69
IS 3
BP 225
EP 226
DI 10.1016/j.ijpsycho.2008.05.072
PG 2
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 336VU
UT WOS:000258393700294
ER
PT J
AU Cisneros, GA
Tholander, SNI
Parisel, O
Darden, TA
Elking, D
Perera, L
Piquemal, JP
AF Cisneros, G. A.
Tholander, S. Na-Im
Parisel, O.
Darden, T. A.
Elking, D.
Perera, L.
Piquemal, J. -P.
TI Simple formulas for improved point-charge electrostatics in classical
force fields and hybrid quantum mechanical/molecular mechanical
embedding
SO INTERNATIONAL JOURNAL OF QUANTUM CHEMISTRY
LA English
DT Article; Proceedings Paper
CT 3rd International Theoretical Biophysics Symposium
CY JUN 16-20, 2007
CL Cetraro, ITALY
DE electrostatics; force fields; QM/MM; embedding; penetration energy;
reaction path
ID INTERMOLECULAR INTERACTION ENERGY; POLARIZABLE MOLECULAR-MECHANICS;
FRAGMENT POTENTIAL METHOD; PARTICLE MESH EWALD; 4-OXALOCROTONATE
TAUTOMERASE; SIMULATION; DENSITY; HYDROGEN; MODEL; ATOMS
AB We present a simple damping scheme for point-charge electrostatics that could be used directly in classical force fields. The approach acts at the charge (or monopole) level only and allows the inclusion of short-range electrostatic penetration effects at a very low cost. Results are compared with density functional theory Coulomb intermolecular interaction energies and with several other methods such as distributed multipoles, damped distributed multipoles, and transferable Hermite-Gaussian densities. Realistic trends in the interactions are observed for atom-centered Mertz-Kollman corrected point-charge distributions. The approach allows increasing the selectivity of parameters in the case of metal complexes. In addition, two QM/MM calculations are presented where the damping function is employed to include the MM atoms located at the QM/MM boundary. The first calculation corresponds to the gas-phase proton transfer of aspartic acid through water and the second is the first step of the reaction catalyzed by the 4-oxalocrotonate tautomerase (4OT) enzyme. First, improved agreement is observed when using the damping approach compared with the conventional excluded charge method or when including all charges in the calculation. Second, in the case of 4OT, the damped charge approach is in agreement with previous calculations, whereas including all charges gives a significantly higher energy barrier. In both cases, no reparameterization of the van der Waals part of the force field was performed. (c) 2008 Wiley Periodicals, Inc.
C1 [Tholander, S. Na-Im; Parisel, O.; Piquemal, J. -P.] Univ Paris 06, UPMC, Chim Theor Lab, UMR 7616, F-75005 Paris, France.
[Cisneros, G. A.; Darden, T. A.; Elking, D.; Perera, L.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
[Tholander, S. Na-Im; Parisel, O.; Piquemal, J. -P.] CNRS, Chim Theor Lab, UMR 7616, F-75005 Paris, France.
RP Piquemal, JP (reprint author), Univ Paris 06, UPMC, Chim Theor Lab, UMR 7616, Case Courrier 137,4 Pl Jussieu, F-75005 Paris, France.
EM jpp@lct.jussieu.fr
RI Cisneros, Gerardo/B-3128-2010; Piquemal, Jean-Philip/B-9901-2009;
perera, Lalith/B-6879-2012
OI Piquemal, Jean-Philip/0000-0001-6615-9426; perera,
Lalith/0000-0003-0823-1631
FU Intramural NIH HHS [NIH0011757912]
NR 57
TC 37
Z9 37
U1 1
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7608
EI 1097-461X
J9 INT J QUANTUM CHEM
JI Int. J. Quantum Chem.
PD SEP
PY 2008
VL 108
IS 11
BP 1905
EP 1912
DI 10.1002/qua.21675
PG 8
WC Chemistry, Physical; Mathematics, Interdisciplinary Applications;
Physics, Atomic, Molecular & Chemical
SC Chemistry; Mathematics; Physics
GA 326EY
UT WOS:000257642300005
PM 19606279
ER
PT J
AU Simone, CB
Vapiwala, N
Hampshire, MK
Metz, JM
AF Simone, Charles B., II
Vapiwala, Neha
Hampshire, Margaret K.
Metz, James M.
TI Internet-based survey evaluating use of pain medications and attitudes
of radiation oncology patients toward pain intervention
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE quality of life; pain management; Internet; analgesic; pain
ID CANCER PAIN; BREAST-CANCER; HEALTH-CARE; MANAGEMENT; INFORMATION;
BARRIERS; PHYSICIANS; THERAPIES; ANXIETY; COMPLEMENTARY
AB Purpose: Pain is it common symptom among cancer patients, yet many patients do not receive adequate pain management. Few data exist quantifying analgesic use by radiation oncology patients. This study evaluated the causes of pain in cancer patients and investigated the reasons patients fail to receive optimal analgesic therapy.
Methods and Materials: An institutional review board-approved, Internet-based questionnaire assessing analgesic use and pain control was posted on the OncoLink (available at www.oncolink.org) Website. Between November 2005 and April 2006, 243 patients responded. They were predominantly women (73%), white (71%), and educated beyond high school (67%) and had breast (38%), lung (6%), or ovarian (6%) cancer. This analysis evaluated the 106 patients (44%) who underwent radiotherapy.
Results: Of the 106 patients, 58% reported pain from their cancer treatment, and 46% reported pain directly from their cancer. The pain was chronic in 51% and intermittent in 33%. Most (80%) did not use medication to manage their pain. Analgesic use was significantly less in patients with greater education levels (11% vs. 36%, p = 0.002), witha trend toward lower use by whites (16% vs. 32%, p = 0.082) and women (17% vs. 29%, p = 0.178). The reasons for not taking analgesics included healthcare provider not recommending medication (87%), fear of addiction or dependence (79%), and inability to pay (79%). Participants experiencing pain, but not taking analgesics, pursued alternative therapies for relief.
Conclusions: Many radiation oncology patients experience pain from their disease and cancer treatment. Most study participants did not use analgesics because of concerns of addiction, cost, or failure of the radiation oncologist to recommend medication. Healthcare providers should have open discussions with their patients regarding pain symptoms and treatment. (C) 2008 Elsevier Inc.
C1 [Simone, Charles B., II] NCI, Natl Inst Hlth, Radiat Oncol Branch, Bethesda, MD 20892 USA.
[Simone, Charles B., II; Vapiwala, Neha; Hampshire, Margaret K.; Metz, James M.] Hosp Univ Penn, Dept Radiat Oncol, Philadelphia, PA 19104 USA.
RP Simone, CB (reprint author), NCI, Natl Inst Hlth, Radiat Oncol Branch, Bldg 10-CRC,Rm B2-3500,10 Ctr Dr, Bethesda, MD 20892 USA.
EM simonec@mial.nih.gov
RI Vapiwala, Neha/A-5445-2010
NR 53
TC 9
Z9 9
U1 3
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD SEP 1
PY 2008
VL 72
IS 1
BP 127
EP 133
DI 10.1016/j.ijrobp.2008.03.071
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 341UX
UT WOS:000258741700023
PM 18547743
ER
PT J
AU Wang, HB
Wang, N
Chen, RY
Sharp, GB
Ma, YL
Wang, GX
Ding, GW
Wu, ZL
AF Wang, Haibo
Wang, Ning
Chen, Ray Y.
Sharp, Gerald B.
Ma, Yanling
Wang, Guixiang
Ding, Guowei
Wu, Zhenglai
TI Prevalence and predictors of herpes simplex virus type 2 infection among
female sex workers in Yunnan Province, China
SO INTERNATIONAL JOURNAL OF STD & AIDS
LA English
DT Article
DE herpes simplex virus type 2 (HSV-2); female sex worker; condom; sexually
transmitted infection; China
ID SEXUALLY-TRANSMITTED INFECTIONS; RISK-FACTORS; WOMEN; HIV-1;
ACQUISITION; METAANALYSIS; MEN; SEROPREVALENCE; EPIDEMIOLOGY; HIV/AIDS
AB The objective of this study was to determine the seroprevalence of herpes simplex virus type 2 (HSV-2), and to evaluate the relationship between HSV-2 infection and sociodemographic factors and the sexual practices of female sex workers (FSWs) in Kaiyuan city, Yunnan Province, China. This cross-sectional study involved 737 FSWs and was carried out from March to May 2006 with confidential interviews and laboratory tests for HSV-2 and other sexually transmitted infections (STI). HSV-2 was the most common STI (68%), followed by Chlamydia trachomatis (26%), Trichomonas vaginalis (11%), Neisseria gonorrhoeae (8%) and syphilis (7%). Prevalence of HIV-1 was 10.3%. Adjusted odds ratios of HSV-2 seroprevalence were 2.6 (95% CI [confidence interval]: 1.30-5.38) for HIV-1 infection, 2.0 (95% CI: 1.33-3.16) for vaginal douching, 2.0 (95% CI: 0.45-0.86) for condom breaking or failing off during sexual intercourse with the ciient in the previous week, 1.8 (95% CI: 1.07-3.18) for >= 5 years of commercial sex work, 1.6 (95% CI: 1.08-2.33) for >= 5 clients in the previous week, 0.6 (95% CI: 0.45-0.86) for >= 9 years of education. This study identifies a very high prevalence of HSV-2 infections among FSWs in Yunnan Province, with only a few who reported a prior history of genital herpes. HSV-2 serological screening and suppressive therapy should be considered for study populations. Education on the importance of diagnosis, treatment and prevention may help control the spread of HSV-2 infection.
C1 [Wang, Haibo; Wang, Ning; Ding, Guowei] Chinese Ctr Dis Control & Prevent, Natl Ctr AIDS STD Prevent & Control, Beijing 100050, Peoples R China.
[Chen, Ray Y.; Sharp, Gerald B.] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Ma, Yanling] Yunnan Ctr Dis Control & Prevent, Dept AIDS, Kaiyuan, Yunnan, Peoples R China.
[Wang, Guixiang] Kaiyuan Ctr Dis Control & Prevent, Kaiyuan, Yunnan, Peoples R China.
[Wu, Zhenglai] Peking Union Med Coll, Dept Epidemiol, Beijing 100021, Peoples R China.
RP Wang, N (reprint author), Chinese Ctr Dis Control & Prevent, Natl Ctr AIDS STD Prevent & Control, 27 Nanwei Rd, Beijing 100050, Peoples R China.
EM wangnbj@163.com
OI Chen, Ray/0000-0001-6344-1442
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health [U19 AI51915-05]
FX This study was funded by a grant from the National Institute of Allergy
and Infectious Diseases, National Institutes of Health (U19 AI51915-05).
NR 33
TC 29
Z9 34
U1 1
U2 8
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON W1G 0AE, ENGLAND
SN 0956-4624
J9 INT J STD AIDS
JI Int. J. STD AIDS
PD SEP
PY 2008
VL 19
IS 9
BP 635
EP 639
DI 10.1258/ijsa.2008.008013
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 350SZ
UT WOS:000259374700014
PM 18725558
ER
PT J
AU Leng, K
Lonsdorf, A
Hartmann, M
AF Leng, K.
Lonsdorf, A.
Hartmann, M.
TI Fatal outcome of nevirapine-associated toxic epidermal necrolysis
SO INTERNATIONAL JOURNAL OF STD & AIDS
LA English
DT Article
DE HIV; nevirapine; TEN; rash
ID STEVENS-JOHNSON-SYNDROME; HYPERSENSITIVITY
AB The irregular use of antiretroviral therapy (ART) can result in ART-resistance but can also lead to a sensitization between agents with a cross-sensitivity. We report a case of nevirapine-associated toxic epidermal necrolysis resulting in death in an HIV-infected man.
C1 [Leng, K.; Hartmann, M.] Univ Heidelberg, Dept Dermatol, D-6900 Heidelberg, Germany.
[Lonsdorf, A.] NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Leng, K (reprint author), Univ Hautklin, Vossstr 2, D-69115 Heidelberg, Germany.
EM katharina.leng@med.uni-heidelberg.de
NR 7
TC 4
Z9 5
U1 0
U2 0
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON W1G 0AE, ENGLAND
SN 0956-4624
J9 INT J STD AIDS
JI Int. J. STD AIDS
PD SEP
PY 2008
VL 19
IS 9
BP 642
EP 643
DI 10.1258/ijsa.2008.008062
PG 2
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 350SZ
UT WOS:000259374700016
PM 18725560
ER
PT J
AU Nunez-Troconis, J
Velasquez, J
Mindiola, R
Munroe, D
AF Nunez-Troconis, Jose
Velasquez, Jesvy
Mindiola, Raimy
Munroe, David
TI Educational level and cervical cancer screening programs in a Venezuelan
urban area
SO INVESTIGACION CLINICA
LA English
DT Article
DE Pap smear; educational level; cervical cancer screening program;
Venezuela
ID HUMAN-PAPILLOMAVIRUS; PREVENTION; COVERAGE; WOMEN; CARE
AB The purpose of this study was to investigate, in a group of Venezuelan women, the knowledge and understanding of the purpose of the Pap smear and the correlation of this knowledge with their educational level. Women were recruited for a cervical cancer screening program and answered a questionnaire concerning what a Pap smear is used for. Three hundred one women were included in the study. Two hundred eighty six women (95%) answered that they knew about Pap smear. Two hundred sixty eight patients (89%) knew that the Pap smear is used for cervical cancer screening. One hundred sixteen women (38.5%) had a low educational level. One hundred and four of them (89.7%) knew that Pap smear is used to screen cervical cancer. Ninety two percent of women who did not complete elementary school had the knowledge of the purpose of vaginal cytology. Two hundred eighty one patients (93%) mentioned that they had at least one Pap smear. One hundred sixty four patients (58.3%) reported to have >= 4 Pap smears in their life time. Two hundred fifty seven women (91.5%) remembered when the first Pap smear was taken. Twenty one patients (7%) had a Pap smear for the first time. The conclusions are: 1) low educational level in an urban area is not a limitation for knowing about and having a cervical cytology test taken; 2) high percentage of Venezuelan women in an urban area know what the Pap smear is used for.
C1 [Nunez-Troconis, Jose] Univ Zulia, Manuel Noriega Trigo Hosp, Dept Obstet & Gynecol, Maracaibo 4011, Venezuela.
[Velasquez, Jesvy; Mindiola, Raimy] Univ Zulia, Fac Med, Reg Lab Virol Reference, Maracaibo 4011, Venezuela.
[Munroe, David] SAIC Frederick Inc, Natl Canc Inst, Lab Mol Technol, Frederick, MD USA.
RP Nunez-Troconis, J (reprint author), Univ Zulia, Fac Med, Dept Obstet & Gynecol, Ave 20, Maracaibo 4011, Venezuela.
EM jnunezt@cantv.net
FU National Cancer Institute; National Institutes of Health [N01-C0-12400];
Fogarty Foundation/NCI/PAHO
FX This project has been funded in whole or in part with Federal Funds from
the National Cancer Institute, National Institutes of Health, under
Contract N01-C0-12400. The content of this publication does not
necessarily reflect the view or policies of the Department of Health and
Human Services, nor does mention of trades names, commercial products,
or organizations imply endorsement by the U.S. Government. Dr.
Nunez-Trocoms is supported by a scholarship from Fogarty
Foundation/NCI/PAHO.; We thank all the members of Social Service and
nurses who work at the Gynecological Out-Patient Clinic of Manuel
Noriega Trigo Hospital for their assistant and help.
NR 21
TC 1
Z9 1
U1 0
U2 7
PU INST INVESTIGACION CLINICA
PI MARACAIBO
PA APARTADO 23, MARACAIBO 4001-A, VENEZUELA
SN 0535-5133
J9 INVEST CLIN
JI Invest. Clin.
PD SEP
PY 2008
VL 49
IS 3
BP 331
EP 339
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 349AQ
UT WOS:000259251600006
PM 18846774
ER
PT J
AU Huang, LL
Coleman, HR
Kim, J
de Monasterio, F
Wong, WT
Schleicher, RL
Ferris, FL
Chew, EY
AF Huang, Lynn L.
Coleman, Hanna R.
Kim, Jonghyeon
de Monasterio, Francisco
Wong, Wai T.
Schleicher, Rosemary L.
Ferris, Frederick L., III
Chew, Emily Y.
TI Oral supplementation of lutein/zeaxanthin and omega-3 long chain
polyunsaturated fatty acids in persons aged 60 years or older, with or
without AMD
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID MACULAR DEGENERATION; VITAMIN-E; LUTEIN SUPPLEMENTATION; ALPHA-CAROTENE;
BETA-CAROTENE; UNITED-STATES; BIOAVAILABILITY; PREVALENCE; DISEASE;
HEALTH
AB PURPOSE. Increased dietary intake of lutein/zeaxanthin and omega-long-chain polyunsaturated fatty acids (omega-3 LCPUFA) was found to be associated with reduced risk of advanced age-related macular degeneration (AMD). The purpose of the study was to examine the effect of oral supplementation of omega-3 LCPUFA on changes in serum levels of lutein/zeaxanthin during supplementation in persons 60 years of age and older, with or without AMD.
METHODS. Forty participants with AMD of various degrees of severity received lutein (10 mg) and zeaxanthin (2 mg) daily and were equally randomized to receive omega-3 LCPUFA (350 mg docosahexaenoic acid [DHA] and 650 mg eicosapentaenoic acid [EPA]) or placebo for 6 months. Serum levels of lutein, zeaxanthin, and omega-3 LCPUFAs and macular pigment optical densities were measured at baseline, 1 week, and 1, 3, 6, and 9 months.
RESULTS. By month 6, the median serum levels of lutein/zeaxanthin increased by two- to threefold compared with baseline. Increases in serum levels of lutein/zeaxanthin did not differ by omega-3 LCPUFA treatment (P > 0.5). After 1 month, in the omega-3 LCPUFA-treated group, the median levels of DHA and EPA increased and the placebo group had no changes. At month 6, participants with AMD had a lower increase in serum lutein concentration than did those without AMD (P < 0.05).
CONCLUSIONS. The addition of omega-3 LCPUFA to oral supplementation of lutein/zeaxanthin did not change the serum levels of lutein and zeaxanthin. A long-term large clinical trial is necessary to investigate the benefits and adverse effects of these factors for the treatment of AMD.
C1 [Chew, Emily Y.] NEI, CRC, NIH, Div Epidemiol & Clin Res,Clin Trials Branch, Bethesda, MD 20892 USA.
[de Monasterio, Francisco] NEI, NIH, Off Clin Director, Bethesda, MD 20892 USA.
[Kim, Jonghyeon] EMMES Corp, Rockville, MD USA.
[Schleicher, Rosemary L.] Ctr Dis Control & Prevent, Atlanta, GA USA.
RP Chew, EY (reprint author), NEI, CRC, NIH, Div Epidemiol & Clin Res,Clin Trials Branch, Bldg 10,Room 3-2531,10 Ctr Dr,MSC 1204, Bethesda, MD 20892 USA.
EM echew@nei.nih.gov
RI Sanguansri, Luz/B-6630-2011; Wong, Wai/B-6118-2017
OI Sanguansri, Luz/0000-0003-1908-7604; Wong, Wai/0000-0003-0681-4016
FU National Eye Institute; Pfizer Pharmaceuticals Group, Bethesda; NIH;
Pfizer; National Institutes of Health
FX Supported by the intramural funds of the National Eye Institute; and a
grant to the Foundation for the NIH from Pfizer Pharmaceuticals Group,
Bethesda, MD (LLH), with a public-private partnership supported jointly
by the NIH and Pfizer. LLH is a Clinical Research Training Program
Scholar at the National Institutes of Health.
NR 19
TC 23
Z9 24
U1 4
U2 8
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD SEP
PY 2008
VL 49
IS 9
BP 3864
EP 3869
DI 10.1167/iovs.07-1420
PG 6
WC Ophthalmology
SC Ophthalmology
GA 344AB
UT WOS:000258896500017
PM 18450596
ER
PT J
AU Lee, JE
Liang, KJ
Fariss, RN
Wong, WT
AF Lee, Jung Eun
Liang, Katharine J.
Fariss, Robert N.
Wong, Wai T.
TI Ex vivo dynamic imaging of retinal microglia using time-lapse confocal
microscopy
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID MACULAR DEGENERATION; IN-VIVO; DIABETIC-RETINOPATHY; DENDRITIC CELLS;
ACTIVATION; BRAIN; MOUSE; NEUROTOXICITY; BEHAVIOR; DISEASE
AB PURPOSE. Retinal microglia have been implicated in the pathogenesis of various retinal diseases, but their basic function and cellular phenotype remain incompletely understood. Here, the authors used a novel ex vivo retinal imaging preparation to examine the behavioral phenotype of living retinal microglia in intact tissue and in response to injury.
METHODS. Fluorescence-labeled microglia in retinal explants from CX3CR1(+/GFP) transgenic mice were observed using time-lapse confocal imaging. High spatial and temporal resolution imaging parameters were used to follow dynamic microglial behavior in real time.
RESULTS. Under normal conditions, resting retinal microglia are not static in structure but instead exhibit extensive structural dynamism in their cellular processes. Process movements are highly random in direction but are balanced to maintain overall cellular symmetry and arbor size. At rest, however, these exuberant process movements do not result in overt cellular migration. After focal laser injury, microglial processes increase significantly in their motility and direct themselves toward the injury site. Microglia rapidly transition their morphologies from symmetric to polarized toward the laser lesion. Microglia also transition from a fixed to a migratory phenotype, translocating through tissue while retaining their ramified morphology.
CONCLUSIONS. Retinal microglia normally occupying uninjured tissue display a continuous, dynamic behavior that suggests functions of tissue surveillance and intercellular communication. Microglial behavior is highly regulated by, and immediately responsive to, focal tissue injury and may constitute a therapeutic cellular response to focal laser photocoagulation. Ex vivo live imaging in the retina is an experimental approach well suited to the study of dynamic aspects of microglial physiology.
C1 [Lee, Jung Eun; Liang, Katharine J.; Wong, Wai T.] NEI, Natl Inst Hlth, Off Sci Director, Bethesda, MD 20892 USA.
[Lee, Jung Eun; Liang, Katharine J.] NEI, Natl Inst Hlth, Div Epidemiol & Clin Res, Bethesda, MD 20892 USA.
RP Wong, WT (reprint author), NEI, Natl Inst Hlth, Off Sci Director, Room 217,7 Mem Dr, Bethesda, MD 20892 USA.
EM wongw@nei.nih.gov
RI Wong, Wai/B-6118-2017
OI Wong, Wai/0000-0003-0681-4016
FU Howard Hughes Medical Institute (JEL); National Eye Institute Intramural
Research Program
FX Supported by the Howard Hughes Medical Institute (JEL) and the National
Eye Institute Intramural Research Program.
NR 31
TC 72
Z9 73
U1 2
U2 5
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD SEP
PY 2008
VL 49
IS 9
BP 4169
EP 4176
DI 10.1167/iovs.08-2076
PG 8
WC Ophthalmology
SC Ophthalmology
GA 344AB
UT WOS:000258896500057
PM 18487378
ER
PT J
AU Fontainhas, AM
Townes-Anderson, E
AF Fontainhas, Aurora M.
Townes-Anderson, Ellen
TI RhoA and its role in synaptic structural plasticity of isolated
salamander photoreceptors
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID GTP-BINDING PROTEINS; MYELIN-ASSOCIATED GLYCOPROTEIN;
CENTRAL-NERVOUS-SYSTEM; ENHANCES AXONAL REGENERATION;
SPINAL-CORD-INJURY; MYOSIN-II ACTIVITY; RETINAL-DETACHMENT; IN-VITRO;
LYSOPHOSPHATIDIC ACID; DEPENDENT MECHANISM
AB PURPOSE. Adult salamander photoreceptors retract existing axons and extend new neuritic processes in vitro. In mammalian retina, similar forms of structural plasticity occur in injury and disease. The authors asked whether RhoA is present in photoreceptor axon terminals and whether activity in the RhoA-ROCK pathway contributes to the structural plasticity observed in rod and cone cells.
METHODS. Antibodies against RhoA were used to immunolabel Western blots sections and isolated neurons from salamander retina. Isolated photoreceptors were treated with lysophosphatidic acid (LPA; a RhoA activator) or Y27632 (an inhibitor of RhoA effector ROCK) for the first 24 hours, the first 3 days, or the last 24 hours of culture. Growth and retraction were assessed with time-lapse and image analyses.
RESULTS. RhoA protein was found throughout the retina, including in rod and cone synaptic terminals. When treated with LPA, photoreceptors significantly reduced the growth of new neuritic processes and presynaptic varicosities and retracted growth at the highest LPA concentrations. When treated with Y27632, rod cells significantly increased the number of varicosities, whereas cone cells increased process growth. Treatment with Y27632 also dramatically reduced retraction of the existing axon, which occurs spontaneously in rod cells during the first 24 hours of culture.
CONCLUSIONS. Thus, RhoA-ROCK activity reduces and retracts neuritic growth, but inhibition of activity increases neuritic development and blocks retraction. The results suggest that RhoA activation contributes to axon retraction by rod cells after retinal detachment, whereas inhibition of RhoA contributes to the neuritic sprouting seen in reattached and degenerating retina.
C1 [Fontainhas, Aurora M.] UMDNJ Grad Sch Biomed Sci, Program Integrat Neurosci, Newark, NJ USA.
[Fontainhas, Aurora M.] Rutgers State Univ, Newark, NJ 07102 USA.
[Townes-Anderson, Ellen] UMDNJ New Jersey Med Sch, Dept Neurol & Neurosci, Newark, NJ USA.
RP Fontainhas, AM (reprint author), NEI, Natl Inst Hlth, 7 Mem Dr, Bethesda, MD 20892 USA.
EM fontainhasa@nei.nih.gov
FU National Eye Institute [EY012031]; F. M. Kirby Foundation
FX Supported by National Eye Institute Grant EY012031 and by the F. M.
Kirby Foundation.
NR 89
TC 11
Z9 11
U1 0
U2 1
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD SEP
PY 2008
VL 49
IS 9
BP 4177
EP 4187
DI 10.1167/iovs.07-1580
PG 11
WC Ophthalmology
SC Ophthalmology
GA 344AB
UT WOS:000258896500058
PM 18503000
ER
PT J
AU Jones, SD
Teigen, PM
AF Jones, Susan D.
Teigen, Philip M.
TI Anthrax in transit - Practical experience and intellectual exchange
SO ISIS
LA English
DT Review
ID VACCINE
AB Focusing on three Anglo-American outbreaks of industrial anthrax, this essay engages the question of how local circumstances influenced the transmission of scientific knowledge in the late nineteenth century. Walpole (Massachusetts), Glasgow, and Bradford (Yorkshire) served as important nodes of transnational investigation into anthrax. Knowledge about the morphology and behavior of Bacillus anthracis changed little while in transit between these nodes, even during complex debates about the nature of bacterial morphology, disease causation, and spontaneous generation. Working independently of their more famous counterparts (Robert Koch and Louis Pasteur), Anglo-American anthrax investigators used visual representations of anthrax bacilli to persuade their peers that a specific, identifiable cause produced all forms of anthrax-malignant pustule (cutaneous anthrax), intestinal anthrax, and woolsorter's disease (pneumonic anthrax). By the late 1870s, this point of view also supported what we would today call an ecological notion of the disease's origins in the interactions of people, animals, and microorganisms in the context of global commerce.
C1 [Jones, Susan D.] Univ Minnesota, Program Hist Sci Technol & Med, St Paul, MN 55108 USA.
[Jones, Susan D.] Univ Minnesota, Dept Ecol Evolut & Behav, St Paul, MN 55108 USA.
[Teigen, Philip M.] Natl Lib Med, Hist Med Div, Bethesda, MD 20894 USA.
RP Jones, SD (reprint author), Univ Minnesota, Program Hist Sci Technol & Med, 1987 Upper Buford Circle, St Paul, MN 55108 USA.
NR 110
TC 6
Z9 8
U1 0
U2 3
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0021-1753
J9 ISIS
JI Isis
PD SEP
PY 2008
VL 99
IS 3
BP 455
EP 485
DI 10.1086/591709
PG 31
WC History & Philosophy Of Science
SC History & Philosophy of Science
GA 357KH
UT WOS:000259844200001
PM 18959192
ER
PT J
AU Konstam, MA
AF Konstam, Marvin A.
TI Patterns of Ventricular Remodeling After Myocardial Infarction Clues
Toward Linkage Between Mechanism and Morbidity
SO JACC-CARDIOVASCULAR IMAGING
LA English
DT Editorial Material
DE myocardial infarction; ventricular remodeling; hypertension;
echocardiography; cardiovascular risk
C1 [Konstam, Marvin A.] NHLBI, Div Cardiovasc Dis, Bethesda, MD 20892 USA.
[Konstam, Marvin A.] Tufts Univ, Boston, MA 02111 USA.
[Konstam, Marvin A.] Tufts Med Ctr, Div Cardiol, Boston, MA USA.
RP Konstam, MA (reprint author), NHLBI, Div Cardiovasc Dis, MSC 7940,6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM konstamm@nhlbi.nih.gov
NR 12
TC 2
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-878X
J9 JACC-CARDIOVASC IMAG
JI JACC-Cardiovasc. Imag.
PD SEP
PY 2008
VL 1
IS 5
BP 592
EP 594
DI 10.1016/j.jcmg.2008.07.005
PG 3
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA V13EL
UT WOS:000207650000006
PM 19356486
ER
PT J
CA NIHM Multisite HIV STD Prevent Tri
TI The role of community advisory boards (CABs) in Project Eban
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE African American couples; community advisory board; culturally
congruent; HIV; behavioral prevention
ID PROTECTING COMMUNITIES; PREVENTION PROGRAM; PUBLIC-HEALTH; HIV;
COLLABORATION; RESEARCHERS; FAMILIES; YOUTH
AB Objective: To describe tire theoretical principles that guided the establishment of Project Ebans community Advisory Boards (CABs), their functions, and composition the selection and recruitment processes; lessons learned; and recommendations on the use of CABs in multisite HIV clinical trial Studies.
Methods: In the first year of Project Eban's implementation, each of the 4 sites formed a local CAB. Member recruitment took place during the first 6 months of the study. On average, each site's CAB consisted of 13-19 stakeholders, with a total of 62 members for the multisite study, including leaders of HIV-AIDS-related community-based organizations (CBOs), hospital-based HIV/AIDS service providers, HIV/AIDS network leaders in minority communities, CBOs that serve predominantly black communities, and consumers.
Results: Each of the CAB members has expressed a strong commitment to assisting in the conduct of the research. CABs are integral to the success of the study and their input is highly respected and used to improve the quality of the research.
Conclusions: This article highlights the importance of CABs in the conduct of HIV multisite clinical trials and their roles in making the study culturally congruent to meet the needs of the black community in dealing with the HIV epidemic.
C1 [NIHM Multisite HIV STD Prevent Tri] NIMH, Ctr Mental Hlth Res AIDS, Div AIDS & Hlth & Behav Res, Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 27
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD SEP 1
PY 2008
VL 49
SU 1
BP S68
EP S74
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 343JB
UT WOS:000258848300009
ER
PT J
CA NIHM Multisite HIV STD Prevent Tri
TI Supervision of facilitators in a multisite study: Goals, process, and
outcomes
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE African American couples; behavioral interventions; cognitive behavior
therapy; empowerment; supervision
AB Objective: To describe the aims, implementation, and desired Outcomes of facilitator Supervision for both interventions (treatment and control) in Project Eban and to present the Eban Theoretical Framework for Supervision that guided the facilitators' Supervision. The qualifications and training of Supervisors and facilitators are also described.
Design: This article provides a detailed description of supervision in a multisite behavioral intervention trial. The Eban Theoretical Framework for Supervision is guided by 3 theories: cognitive behavior therapy, the Model of Life-Long Supervision, and the empowerment model of culturally responsive Supervision.
Methods: Supervision is based oil the Eban Theoretical Framework for Supervision, which provides guidelines for implementing both interventions using goals, process, and outcomes.
Results: Because of effective supervision, the interventions were implemented with fidelity to the protocol and were standard across the Multiple Sites.
Conclusions: Supervision of facilitators is a crucial aspect of multisite intervention research quality assurance. It provides them with expert advice, optimizes the effectiveness of facilitators, and increases adherence to the protocol across Multiple Sites. Based oil the experience in this trial, some of the challenges that arise when conducting a multisite randomized control trial and how they call be handled by implementing the Eban Theoretical Framework for Supervision are described.
C1 [NIHM Multisite HIV STD Prevent Tri] NIMH, Ctr Mental Hlth Res AIDS, Div AIDS & Hlth & Behav Res, Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 15
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD SEP 1
PY 2008
VL 49
SU 1
BP S59
EP S67
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 343JB
UT WOS:000258848300008
ER
PT J
CA NIMH Multisite HIV STD Prevent Tri
TI Designing an audio computer-assisted self-interview (ACASI) system in a
multisite trial: A brief report
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE ACASI; AIDS; Audio Computer-Assisted Self-Interview; HIV; intervention
ID REPRODUCTIVE HEALTH RESEARCH; RIO-DE-JANEIRO; DRUG-USE; SEXUAL-BEHAVIOR;
RANDOMIZED-TRIAL; RISK BEHAVIORS; HIV RISK; POPULATION; COLLECTION;
WOMEN
AB Objective: To describe the advantages and limitations of an audio computer-assisted self-interview (ACASI) system in a multisite trial with African American couples and to present the steps in designing, testing, and implementing a system.
Methods: The ACASI system evolved from a paper and pencil interview that was pilot tested. Based oil this initial work, the paper and pencil inter-view was translated into storyboards that were the basis of the development of ACASI system. Storyboards consisted of 1 page per question and provided the programmers with the test of the question. valid responses, and any instructions that were to be read to the participants. Storyboards were further translated into flow diagrams representing each module of the survey and illustrating the skip patterns used to navigate a participant through the survey. Provisions were also made to insert a face-to-lace interview into the ACASI assessment process, to elicit sexual abuse history data. which typically requires specially trained data collectors with active listening skills to help participants reframe and coordinate times. places and, emotionally difficult Memories.
Results: The ACASI was successfully developed and implemented in the main trial. During an exit interview, respondents indicated that they liked using the ACASI and indicating that they favored it as the method to answer questions.
Conclusions: It is feasible to implement an ACASI system in a multisite study in a timely and efficient way.
C1 [NIMH Multisite HIV STD Prevent Tri] NIMH, Ctr Mental Hlth Res AIDS, Div AIDS & Hlth & Behav Res, Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 43
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD SEP 1
PY 2008
VL 49
SU 1
BP S52
EP S58
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 343JB
UT WOS:000258848300007
ER
PT J
CA NIMH Multisite HIV STD Prevent Tri
TI Measure of HIV/STD risk-reduction: Strategies for enhancing the utility
of behavioral and biological outcome measures for African American
couples
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE African American; behavioral and biological outcome measures;
biomarkers; couples; heterosexual
ID SEXUALLY-TRANSMITTED-DISEASES; LIGASE CHAIN-REACTION; RANDOMIZED
CONTROLLED-TRIAL; CONDOM-USE ERRORS; PREVENTION INTERVENTIONS; REACTION
ASSAY; INFECTION; HIV; URINE; WOMEN
AB Objective: Numerous studies have discussed the value of including biological outcome measures as a complement to behavioral outcome measure to assess the efficacy of HIV risk-reduction interventions. This article highlights strategies used to minimize the limitations of including both self-reported sexual behaviors and biologically confirmed Sexually transmitted diseases as Primary outcome measures in all HIV/sexually transmitted disease (STD) prevention program for African American serodiscordant couples (Eban).
Design: Couples receiving all HIV intervention condition (Eban) were compared with couples receiving a time-equivalent General Health Promotion condition oil behavioral and biological outcomes. Both behavioral and biological data were collected at baseline, immediately post intervention, and at 6 and 12 months post-intervention.
Methods: Literature reviews, Consulting other researchers who conducted couples studies, Our investigative team's experience in previous HIV interventions, and formative work were used to develop procedures to minimize potential limitations associated with the inclusion of behavioral and biological outcome measures for Eban.
Results: Given the strengths Of including behavioral and biological Outcome measures, the Eban study chose to have both measures serve as primary outcomes. The primary behavioral outcome for the trial is the proportion of protected vaginal and anal intercourse episodes that Occurred within the index Couple in 90 days before each follow-tip assessment and over the 12-month postintervention follow-up period. The primary biological outcome is the proportion of participants (male or female study partners,) with an incident STD) (Chlamydia, gonorrhea, or trichomoniasis) over the 12-month postintervention follow-up Period.
Conclusions: Employing procedures to minimize limitations of using self-reported Sexual behaviors and STDs as complementary primary Outcomes enhances their utility as measures of the efficacy of HIV/STD prevention interventions.
C1 [NIMH Multisite HIV STD Prevent Tri] NIMH, Ctr Mental Hlth Res AIDS, Div AIDS & Hlth & Behav Res, Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 46
TC 0
Z9 0
U1 3
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD SEP 1
PY 2008
VL 49
SU 1
BP S35
EP S41
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 343JB
UT WOS:000258848300005
ER
PT J
CA NIMH Multisite HIV STD Prevent Tri
TI Eban Health Promotion Intervention: Conceptual basis and procedures
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE African American; behavioral intervention; fruit and vegetable
consumption; HIV; medical adherence; physical activity
AB Objective: This article concerns the health promotion intervention that served as the comparison condition in Project E-ban, the NIMH Multisite HIV/STD prevention Trial for African American Couples. Considerable research has documented the high rates of chronic diseases, including heart disease, cancer, stroke, and diabetes, among African Americans. Many of these diseases are tied to behavioral risk factors-the things that people do or do not do, their diet, the amount of exercise they get and their substance use practices.
Design: The Eban Health Promotion Intervention was designed to increase healthful behaviors, including physical activity. healthful dietary practices, ceasing cigarette smoking and alcohol abuse. practicing early detection and screening behaviors, and improving medication adherence. As a comparison condition, the Eban Health Promotion Intervention was designed to be structurally similar to the Eban HIV/STD Risk Reduction Intervention.
Methods: This article describes the intervention and how it was developed, integrating, social cognitive theory with information collected in formative research to ensure that the intervention was appropriate for African Americans affected by HIV
Conclusion: Project Eban not only tests the efficacy of an HIV/STD risk reduction intervention for African American serodiscordant couples, but also tests the efficacy of ail intervention addressing many of the other health problems common in this Population.
C1 [NIMH Multisite HIV STD Prevent Tri] NIMH, Ctr Mental Hlth Res AIDS, Div AIDS & Hlth & Behav Res, Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 7
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
EI 1077-9450
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD SEP 1
PY 2008
VL 49
SU 1
BP S28
EP S34
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 343JB
UT WOS:000258848300004
ER
PT J
CA NIMH Multisite HIV STD Prevent Tri
TI Formative study to develop the Eban treatment and comparison
interventions for couples
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE African American couples; behavioral intervention; culturally congruent;
focus groups; HIV; sexual behavior
ID SERODISCORDANT HETEROSEXUAL COUPLES; RISK REDUCTION INTERVENTION;
AFRICAN-AMERICAN WOMEN; CHILD SEXUAL-ABUSE; HIV-INFECTION; CONDOM USE;
PREVENTION; BEHAVIORS; SUPPORT; TRANSMISSION
AB Objective: To describe formative and pilot-testing research that generated themes and procedures. curricula, and critical measures for a randomized clinical trial testing a Risk Reduction Intervention for HIV-serodiscordant African American couples (project Eban).
Design: This article describes the themes that emerged from discussions with African American serodiscordant couples about HIV-related risks from focus groups with 11 couples and pilot study results with 32 couples across 4 sites.
Methods: In step 1, focus groups examined the need for a Risk Reduction Intervention for HIV-serodiscordant African American Couples and confirmed 4 themes that formed the basis for the intervention curriculum and study format. In step 2, a Pilot Study refined the clinical trial procedures, for this population and tested critical measures and selected portions of the curriculum for both the treatment and the comparison interventions.
Results: Based oil these findings, stigma and psychological distress, barriers to condom use. insufficient support from community and service organisations,and the lack of skills that emphasize individual and relationship protection were ultimately integrated into the Risk Reduction Intervention.
Conclusions: Pilot study findings highlighted the importance of examining gender and ethnicity in HIV-impacted couples along with factors that heightened HIV-related risk behaviors that affect couples' skills and psychological adjustment. The goal was to ensure that a skill-based, culturally congruent, relationship-centered intervention could be understood and of interest to couples. Future analyses in the main trial will be discussed.
C1 NIMH, Ctr Mental Hlth Res AIDS, Div AIDS & Hlth & Behav Res, Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 43
TC 0
Z9 0
U1 3
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD SEP 1
PY 2008
VL 49
SU 1
BP S42
EP S51
PG 10
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 343JB
UT WOS:000258848300006
ER
PT J
CA NIMH Multisite HIV STD Prevent Tri
TI Eban HIV/STD risk reduction intervention: Conceptual basis and
procedures
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE African American; behavioral intervention; couple-level; culturally
congruent; HIV sexual behavior
ID HUMAN-IMMUNODEFICIENCY-VIRUS; AMERICAN ADOLESCENT GIRLS; HIV-PREVENTION;
HETEROSEXUAL COUPLES; CONDOM USE; WOMEN; EFFICACY; BEHAVIOR; SEX; AFRICA
AB Objective: To describe the Eban HIV/STD Risk Reduction Intervention being evaluated in the NIMH Multisite HIV/STD Prevention trial for heterosexual African American Couples, including the integrated theoretical framework, the structure, core elements and procedures of the intervention, and how the content was shaped by Culturally congruent concepts to address the needs of the Study target population.
Design: The Eban HIV/STD) Risk Reduction Intervention is designed to address multilevel individual, interpersonal-, and community-level factors that contribute to HIV/STD transmission risk behaviors all-tong heterosexual African American couples who are HIV serodiscordant.
Methods: The Eban HIV/STD Risk Reduction Intervention employs a mixed modality, couple-based approach that is based oil an integrated ecological Framework incorporating social cognitive theory and uses ail Afrocentric paradigm that is informed by previous evidence-based Couples HIV prevention interventions. For this randomized controlled trial, African American serodiscordant Couples were recruited from 4 urban sites (Atlanta, Los Angeles, New York, and Philadelphia) and were randomized to either the Eban HIV/STD Risk Reduction Intervention (treatment condition) or a Health Promotion Intervention that served as an attentional control condition. Both interventions had 4 individual couple sessions and 4 group) sessions, but only the treatment condition was focused oil reducing HIV/STD risk behaviors. Behavioral and biological data were collected at baseline, immediately after the intervention, and at 6 and 12 months. The theoretical framework, core elements, and content of each session are described and lessons learned from this intervention trial are discussed.
Results: Ail HIV prevention intervention combining couple and group sessions can be feasibly implemented with African American HIV-serodiscordant Couples Who remain at high risk of HIV/STD transmission. The lessons carried from the trial Suggest that the participants responded very well to both the couple and the group sessions. Participant feedback Suggests that the cultural congruence of the intervention and use of African American cofacilitators made them feel comfortable disclosing risky behaviors. Participant feedback also Suggests that the intervention's couple-based focus oil enhancing dyadic communication and (decision-making skills was key to helping the couples work together to overcome barriers to using condoms.
Conclusions: Participant and facilitator evaluations of the Eban Risk Reduction Intervention suggest that couples responded well to the Afrocentric content and mixed modalities of the intervention sessions. Couple sessions were optimal for enhancing interpersonal and microlevel factors, including communication problem solving and decision making.
C1 [NIMH Multisite HIV STD Prevent Tri] NIMH, Ctr Mental Hlth Res AIDS, Div AIDS & Hlth & Behav Res, Natl Inst Hlth, Bethesda, MD 20892 USA.
FU NIMH NIH HHS [P50 MH073453, U10 MH078819-03, U10 MH078819]
NR 58
TC 0
Z9 0
U1 2
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD SEP 1
PY 2008
VL 49
SU 1
BP S15
EP S27
DI 10.1097/QAI.0b013e318184255d
PG 13
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 343JB
UT WOS:000258848300003
PM 18724186
ER
PT J
CA NIMH Multisite HIV STD Prevent Tri
TI Methodological overview of an African American couple-based HIV/STD
Prevention Trial
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE AIDS; behavioral intervention; clinical trial; HIV; HIV-serodiscordant
couples; STDs
ID HUMAN-IMMUNODEFICIENCY-VIRUS; RISK REDUCTION INTERVENTION; MAIN SEXUAL
PARTNERS; HETEROSEXUAL COUPLES; MINORITY WOMEN; CONDOM USE; HIV;
BEHAVIOR; AIDS; TRANSMISSION
AB Objective: to provide in overview of the National Institute of Mental Health Multisite HIV/sexually transmitted disease (STD) Prevention Trial for African American Couples conducted in 4 urban areas: Atlanta, Los Angeles, New York, and Philadelphia. The rationale, study design methods, proposed data analyses, and study management are described.
Design: This is a 2-arm randomized trial, implementing a modified randomized block design, to evaluate the efficacy of a couples-based intervention designed for HIV-serodiscordant African American Couples.
Methods: The Study phases consisted of formative work, pilot Studies, and a randomized clinical trial. The sample is 535 HIV-serodiscordant heterosexual African American Couples. There are 2 theoretically derived behavioral interventions with 8 group and individual sessions: the Eban HIV/STD Risk Reduction Intervention (treatment) versus the Eban Health Promotion Intervention (control). The treatment intervention was Couples based and focused on HIV/STD risk reduction whereas the control was individual based and focused oil health promotion. The 2 study conditions were Structurally similar in length and types of activities. At baseline, participants completed an audio computer assisted self-interview and interviewer-administered questionnaire and provided biological specimens to assess tor STDs. Similar follow-up assessments were conducted immediately after the intervention, at 6 months, and at 12 months.
Results: The trial results will be analyzed across the 4 sites by randomization assignment. Generalized estimating equations and mixed-effects modeling are planned to test: (1) file effects of the intervention oil STD incidence and condom use and oil mediator variables of these Outcomes and (2) whether the effects of the intervention differ depending oil key moderator variables (eg, gender of the HIV-seropositive partners, length of relationship, psychological distress, sexual abuse history, and Substance abuse history).
Conclusions: The lessons learned From the design and conduct of this clinical trial provide guidelines for future couples-based clinical trials in HIV/STD risk reduction and call be generalized to other couples-based behavioral interventions.
C1 NIMH, Ctr Mental Hlth Res AIDS, Div AIDS & Hlth & Behav Res, Natl Inst Hlth, Bethesda, MD 20892 USA.
FU NIMH NIH HHS [U10 MH078819, U10 MH078819-03, P50 MH073453]
NR 48
TC 0
Z9 0
U1 3
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD SEP 1
PY 2008
VL 49
SU 1
BP S3
EP S14
DI 10.1097/QAI.0b013e3181842570
PG 12
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 343JB
UT WOS:000258848300002
PM 18724188
ER
PT J
AU Henderson, WA
Fall-Dickson, JM
Schlenk, EA
Kim, KH
Matthews, JT
Erlen, JA
AF Henderson, Wendy A.
Fall-Dickson, Jane M.
Schlenk, Elizabeth A.
Kim, Kevin H.
Matthews, Judith T.
Erlen, Judith A.
TI Effects of liver disease on the well-being of persons living with HIV
SO JANAC-JOURNAL OF THE ASSOCIATION OF NURSES IN AIDS CARE
LA English
DT Article
DE HIV; liver disease; quality of life; well-being
ID QUALITY-OF-LIFE; CHRONIC HEPATITIS-C; MEDICAL OUTCOMES; VIRUS-INFECTION;
COINFECTION; THERAPY; IMPACT
AB Clinical evidence suggests that patients with liver disease and HIV have poorer quality of life (QOL). Because little research exists to support this observation, this study examined the relationships between people with HIV and liver disorders and their QOL. Cella's multidimensional (functional, social,emotional, physical) conceptualization of QOL guided this study. The sample included 80 participants with liver disorders and HIV; 48.8% had chronic or permanent hepatitis. Cella's four dimensions significantly correlated with QOL: functional, r = .329, p < .01; social, r = .636, p < .01; emotional, r = -.549, p < .01; and physical, r = -.480, p < .01. Linear regression analysis with QOL as the dependent variable and the four dimensions as predictors resulted in significant associations explaining approximately 50% of the variance (R-2 = .532). Confirmatory factor analysis supported Cella's model with the four subdomains loading on one factor (QOL). Understanding the multiple dimensions of QOL may assist in developing interventions for patients with HIV and comorbid liver disorders.
C1 [Henderson, Wendy A.] NINR, Biobehav Unit, Symptom Management Branch, NIH, Bethesda, MD 20892 USA.
[Fall-Dickson, Jane M.] NINR, Mucosal Injury Unit, Symptom Management Branch, NIH, Bethesda, MD 20892 USA.
[Schlenk, Elizabeth A.; Matthews, Judith T.; Erlen, Judith A.] Univ Pittsburgh, Sch Nursing, Dept Hlth & Community Syst, Pittsburgh, PA 15260 USA.
[Kim, Kevin H.] Univ Pittsburgh, Sch Educ, Pittsburgh, PA 15260 USA.
RP Henderson, WA (reprint author), NINR, Biobehav Unit, Symptom Management Branch, NIH, Bethesda, MD 20892 USA.
OI Schlenk, Elizabeth/0000-0001-7361-1951; Henderson,
Wendy/0000-0003-3924-7118
FU National Institute of Nursing Research (NINR); National Institutes of
Health (NIH); Department of Health and Human Services [NINR 1R01
NR047491]; Center for Research in Chronic Disorders [P30NR03924]; NIH
Clinical and Translational Fellowship [1 TL1 RR 024155-01]; Sigma Theta
Tau International and Association for Nurses in AIDS Care 2006 Research
Award; Sigma Theta Tau, Epsilon Phi 2006 Research Award
FX Sincere gratitude goes to the persons living with HIV who participated
in the study. The authors thank Donna Caruthers, PhD, RN, Project
Director, Michelle Meyers, BSN, RN, Recruitment Coordinator, Alison
Colbert, PhD, MSN, RN, Graduate Student Assistant, and Angela Martino,
BSN, student assistant, for their assistance. They also thank Dr. Lisa
A. Morrow and Tara J. Taylor for reviewing the manuscript.; Support for
this study was provided from a grant to the parent study from the
National Institute of Nursing Research (NINR), National Institutes of
Health (NIH), Department of Health and Human Services (NINR 1R01
NR047491, Primary Investigator: Dr. Judith A. Erlen), and the
NINR-funded Center for Research in Chronic Disorders (P30NR03924). Dr.
Wendy A. Henderson's efforts were also supported by the NIH Clinical and
Translational Fellowship (1 TL1 RR 024155-01), Sigma Theta Tau
International and Association for Nurses in AIDS Care 2006 Research
Award, Sigma Theta Tau, Epsilon Phi 2006 Research Award, and by endowed
scholarships from Dr. Corrine Barnes, Dr. Rose Constantino, and the
Pennsylvania Higher Education Funds for graduate studies in nursing. The
opinions expressed are those of the authors and do not represent the
position of the NIH or the U.S. Government.
NR 27
TC 1
Z9 2
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1055-3290
J9 J ASSOC NURSE AIDS C
JI J. Assoc. Nurses Aids Care
PD SEP-OCT
PY 2008
VL 19
IS 5
BP 368
EP 374
DI 10.1016/j.jana.2008.05.004
PG 7
WC Nursing
SC Nursing
GA 350XW
UT WOS:000259388100006
PM 18762144
ER
PT J
AU Mahajan, R
El-Omar, EM
Lissowska, J
Grillo, P
Rabkin, CS
Baccarelli, A
Yeager, M
Sobin, LH
Zatonski, W
Channock, SJ
Chow, WH
Hou, LF
AF Mahajan, Rajeev
El-Omar, Emad M.
Lissowska, Jolanta
Grillo, Paolo
Rabkin, Charles S.
Baccarelli, Andrea
Yeager, Meredith
Sobin, Leslie H.
Zatonski, Witold
Channock, Stephen J.
Chow, Wong-Ho
Hou, Lifang
TI Genetic variants in t helper cell type 1, 2 and 3 pathways and gastric
cancer risk in a Polish population
SO JAPANESE JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE gastric cancer; T helper cell pathways; polymorphism
ID SINGLE NUCLEOTIDE POLYMORPHISMS; HELICOBACTER-PYLORI INFECTION;
NON-HODGKIN-LYMPHOMA; CTLA4 GENE; MULTIPLE-SCLEROSIS; KOREAN POPULATION;
STOMACH-CANCER; ORAL TOLERANCE; TNF-ALPHA; TGF-BETA
AB Host immune responses are known determinants of gastric cancer susceptibility. We previously reported an increased gastric cancer risk associated with common variants of several T helper type 1 (Th1) cytokine genes in a population-based case-control study in Warsaw, Poland. In the present study, we augmented our investigation to include additional Th1 genes as well as key genes in the Th2 and Th3 pathways. Analysis of 378 cases and 435 age- and sex-matched controls revealed associations for polymorphisms in the Th1 IL7R gene and one polymorphism in the Th2 IL5 gene. The odd ratios (ORs) for IL7R rs1494555 were 1.4 [95% confidence interval (CI), 1.0-1.9] for A/G and 1.5 (95% CI, 1.0-2.4) for G/G carriers relative to A/A carriers (P = 0.04). The ORs for IL5 rs2069812 were 0.9 (95% CI, 0.7-1.3) for C/T and 0.6 (95% CI, 0.3-1.0) T/T carriers compared with C/C carriers (P = 0.03). These results suggest that IL5 rs2069812 and IL7R rs1389832, rs1494556 and rs1494555 polymorphisms may contribute to gastric cancer etiology.
C1 [Hou, Lifang] Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Mahajan, Rajeev; Rabkin, Charles S.; Channock, Stephen J.; Chow, Wong-Ho; Hou, Lifang] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[El-Omar, Emad M.] Univ Aberdeen, Dept Med & Therapeut, Inst Med Sci, Aberdeen, Scotland.
[Lissowska, Jolanta; Zatonski, Witold] Ctr Canc, Div Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta; Zatonski, Witold] M Sklodowska Curie Inst Oncol, Warsaw, Poland.
[Grillo, Paolo; Baccarelli, Andrea] Univ Milan, Maggiore Hosp IRCCS Fdn, EPOCA Epidemiol Res Ctr, Milan, Italy.
[Yeager, Meredith; Channock, Stephen J.] Natl Canc Inst, Adv Technol Ctr, Core Genotyping Facil, Gaithersburg, MD USA.
[Sobin, Leslie H.] Armed Forces Inst Pathol, Div Gastrointestinal Pathol, Washington, DC 20306 USA.
RP Hou, LF (reprint author), Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, 680 N Lake Shore Dr, Chicago, IL 60611 USA.
EM l-hou@northwestern.edu
RI Kim, Seongman/N-6910-2014;
OI Baccarelli, Andrea/0000-0002-3436-0640; Lissowska,
Jolanta/0000-0003-2695-5799
FU National Cancer Institute, National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health.
NR 69
TC 17
Z9 20
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0368-2811
J9 JPN J CLIN ONCOL
JI Jpn. J. Clin. Oncol.
PD SEP
PY 2008
VL 38
IS 9
BP 626
EP 633
DI 10.1093/jjco/hyn075
PG 8
WC Oncology
SC Oncology
GA 348II
UT WOS:000259203800008
PM 18687755
ER
PT J
AU Macones, GA
Hankins, GDV
Spong, CY
Hauth, J
Moore, T
AF Macones, George A.
Hankins, Gary D. V.
Spong, Catherine Y.
Hauth, John
Moore, Thomas
TI The 2008 National Institute of Child Health and Human Development
workshop report on electronic fetal monitoring: Update on definitions,
interpretation, and research guidelines
SO JOGNN-JOURNAL OF OBSTETRIC GYNECOLOGIC AND NEONATAL NURSING
LA English
DT Article
DE fetal heart tracings; uterine contractions; electronic fetal heart rate;
monitoring
AB In April 2008, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the American College of Obstetricians and Gynecologists, and the Society for Maternal-Fetal Medicine partnered to sponsor a 2-day workshop to revisit nomenclature, interpretation, and research recommendations for intrapartum electronic fetal heart rate monitoring. Participants included obstetric experts and representatives from relevant stakeholder groups and organizations. This article provides a summary of the discussions at the workshop. This includes a discussion of terminology and nomenclature for the description of fetal heart tracings and uterine contractions for use in clinical practice and research. A three-tier system for fetal heart rate tracing interpretation is also described. Lastly, prioritized topics for future research are provided.
C1 Washington Univ, Dept Obstet & Gynecol, St Louis, MO 63110 USA.
Univ Texas Med Branch, Dept Obstet & Gynecol, Galveston, TX USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
Univ Alabama Birmingham, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
Univ Calif San Diego, Dept Obstet & Gynecol, San Diego, CA 92103 USA.
RP Macones, GA (reprint author), Washington Univ, Dept Obstet & Gynecol, St Louis, MO 63110 USA.
EM maconesg@wustl.edu
NR 8
TC 59
Z9 62
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0884-2175
J9 JOGNN-J OBST GYN NEO
JI JOGNN
PD SEP-OCT
PY 2008
VL 37
IS 5
BP 510
EP 515
DI 10.1111/j.1552-6909.2008.00284.x
PG 6
WC Nursing; Obstetrics & Gynecology
SC Nursing; Obstetrics & Gynecology
GA 347OT
UT WOS:000259151600002
PM 18761565
ER
PT J
AU Freeman, MP
Davis, M
Sinha, P
Wisner, KL
Hibbeln, JR
Gelenberg, AJ
AF Freeman, Marlene P.
Davis, Melinda
Sinha, Pniti
Wisner, Katherine L.
Hibbeln, Joseph R.
Gelenberg, Alan J.
TI Omega-3 fatty acids and supportive psychotherapy for perinatal
depression: A randomized placebo-controlled study
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Article
DE perinatal; depression; postpartum; pregnancy; omega-3; supportive
psychotherapy
ID SEROTONIN-REUPTAKE INHIBITORS; FATTY-ACID STATUS; POSTPARTUM DEPRESSION;
POSTNATAL DEPRESSION; SEAFOOD CONSUMPTION; FISH CONSUMPTION;
PREGNANT-WOMEN; BIRTH-DEFECTS; DHA CONTENT; TRIAL
AB Background: Perinatal major depressive disorder (MDD), including antenatal and postpartum depression, is common and has serious consequences. This study was designed to investigate the feasibility, safety, and efficacy of omega-3 fatty acids for perinatal depression in addition to supportive psychotherapy.
Methods: Perinatal women with MDD were randomized to eicosapentacnoic (EPA) and docosahexaenoic acids (DHA), 1.9g/day, or placebo for 8weeks. A manualized supportive psychotherapy was provided to all subjects. Symptoms were assessed with the Hamilton Rating Scale for Depression (HAM-D) and Edinburgh Postnatal Depression Scale (EPDS) biweekly.
Results: Fifty-nine women enrolled; N = 51 had two data collection points that allowed for evaluation of efficacy. Omega-3 fatty acids were well tolerated. Participants in both groups experienced significant decreases in EPDS and HAM-D scores (P < .0001) from baseline. We did not find a benefit of omega-3 fatty acids over placebo. Dietary omega-3 fatty acid intake was low among participants.
Limitations: The ability to detect an effect of omega-3 fatty acids may have been limited by sample size, study length, or dose. The benefits of supportive psychotherapy may have limited the ability to detect an effect of omega-3 fatty acids.
Conclusions: There was no significant difference between omega-3 fatty acids and placebo in this study in which all participants received supportive psychotherapy. The manualized supportive psychotherapy warrants further study. The low intake of dietary omega-3 fatty acids among participants is of concern, in consideration of the widely established health advantages in utero and in infants. (C) 2007 Elsevier B.V. All rights reserved.
C1 [Freeman, Marlene P.] Univ Texas SW Med Ctr Dallas, Womens Mental Hlth Ctr, Dept Psychiat, Dallas, TX 75390 USA.
[Freeman, Marlene P.; Sinha, Pniti; Gelenberg, Alan J.] Univ Arizona, Dept Psychiat, Coll Med, Tucson, AZ 85721 USA.
[Davis, Melinda] Univ Arizona, Dept Pediat, Coll Med, Tucson, AZ 85721 USA.
[Wisner, Katherine L.] Univ Pittsburgh, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Wisner, Katherine L.] Univ Pittsburgh, Western Psychiat Inst & Clin, Dept Obstet & Gynecol, Pittsburgh, PA 15260 USA.
[Wisner, Katherine L.] Univ Pittsburgh, Western Psychiat Inst & Clin, Dept Epidemiol, Pittsburgh, PA 15260 USA.
[Hibbeln, Joseph R.] NIAAA, Bethesda, MD 20892 USA.
RP Freeman, MP (reprint author), Univ Texas SW Med Ctr Dallas, Womens Mental Hlth Ctr, Dept Psychiat, Dallas, TX 75390 USA.
EM marlene.freeman@utsouthwestern.edu
FU NIMH NIH HHS [K23 MH066265, K23MH066265]
NR 40
TC 94
Z9 98
U1 1
U2 17
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0327
J9 J AFFECT DISORDERS
JI J. Affect. Disord.
PD SEP
PY 2008
VL 110
IS 1-2
BP 142
EP 148
DI 10.1016/j.jad.2007.12.228
PG 7
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 343JX
UT WOS:000258850600016
PM 18206247
ER
PT J
AU Rooks, RN
Simonsick, EM
Klesges, LM
Newman, AB
Ayonayon, HN
Harris, TB
AF Rooks, Ronica N.
Simonsick, Eleanor M.
Klesges, Lisa M.
Newman, Anne B.
Ayonayon, Hilsa N.
Harris, Tamara B.
TI Racial disparities in health care access and cardiovascular disease
indicators in black and white older adults in the health ABC study
SO JOURNAL OF AGING AND HEALTH
LA English
DT Article
DE racial disparities; health insurance; access to care; socioeconomic
status; cardiovascular disease
ID QUALITY-OF-LIFE; LONG-TERM-CARE; MEXICAN-AMERICANS; NORTH-CAROLINA;
MEDICAL-CARE; RACE; HYPERTENSION; MORTALITY; SERVICES; ASSOCIATION
AB Objective: Black adults consistently exhibit higher rates of and poorer health outcomes due to cardiovascular disease (CVD) than other racial groups, independent of differences in socioeconomic status (SES). Whether factors related to health care access can further explain racial disparities in CVD has not been thoroughly examined. Method: Using logistic regression, the authors examined racial and health care (i.e., health insurance and access to care) associations with CVD indicators (i.e., hypertension, low ankle-arm index, and left ventricular hypertrophy) in the Health, Aging, and Body Composition Study, a longitudinal study of well-functioning older adults. Results: Older Black versus White adults had significantly worse health care. Overall, health care reduced the significant association between being Black and CVD only slightly, while race remained strongly associated with CVD after adjusting for demographics, SES, body mass index, and comorbidity. Discussion: Research on health care quality may contribute to our understanding of these disparities.
C1 [Rooks, Ronica N.] Univ Colorado, Dept Hlth & Behav Sci, Denver, CO 80217 USA.
[Simonsick, Eleanor M.; Harris, Tamara B.] NIA, Bethesda, MD 20892 USA.
[Klesges, Lisa M.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Ayonayon, Hilsa N.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Rooks, RN (reprint author), Univ Colorado, Dept Hlth & Behav Sci, POB 173364,CB 188, Denver, CO 80217 USA.
EM ronica.rooks@cudenver.edu
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
FU Intramural NIH HHS [Z01 AG007390-02]; NIA NIH HHS [N01-AG-6-2106,
N01-AG-6-2101, N01-AG-6-2103]
NR 49
TC 29
Z9 29
U1 3
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0898-2643
J9 J AGING HEALTH
JI J. Aging Health
PD SEP
PY 2008
VL 20
IS 6
BP 599
EP 614
DI 10.1177/0898264308321023
PG 16
WC Gerontology; Health Policy & Services
SC Geriatrics & Gerontology; Health Care Sciences & Services
GA 339IK
UT WOS:000258571100001
PM 18625758
ER
PT J
AU Huang, L
Chen, MH
Yu, F
Neal, PR
Anderson, GJ
AF Huang, Lan
Chen, Ming-Hui
Yu, Fang
Neal, Paul R.
Anderson, Gregory J.
TI On modeling repeated binary responses and time-dependent missing
covariates
SO JOURNAL OF AGRICULTURAL BIOLOGICAL AND ENVIRONMENTAL STATISTICS
LA English
DT Article
DE flower intensity; generalized linear mixed model (GLMM); missing at
random; Monte Carlo EM algorithm; model assessment; Tilia; weather
conditions
ID GENERALIZED LINEAR-MODELS; MIXED MODELS; EM ALGORITHM; REGRESSION;
INFERENCE; ECOLOGY; DROPOUT
AB We develop a novel modeling strategy for analyzing data with repeated binary responses over time as well as time-dependent missing covariates. We assume that covariates are missing at random (MAR). We use the generalized linear mixed logistic regression model for the repeated binary responses and then propose a joint model for time-dependent missing covariates using information from different sources. A Monte Carlo EM algorithm is developed for computing the maximum likelihood estimates. We propose an extended version of the AlC criterion to identify the important factors that may explain the binary responses, A real plant dataset is used to motivate and illustrate the proposed methodology.
C1 [Huang, Lan] NCI, Stat Res & Applicat Branch, Div Canc Control & Populat Sci, Rockville, MD 20852 USA.
[Chen, Ming-Hui] Univ Connecticut, Dept Stat, Storrs, CT 06269 USA.
[Yu, Fang] Univ Nebraska Med Ctr, Dept Biostat, Coll Publ Hlth, Omaha, NE 68198 USA.
[Anderson, Gregory J.] Univ Connecticut, Dept Ecol & Evolutionary Biol, Storrs, CT 06269 USA.
RP Huang, L (reprint author), NCI, Stat Res & Applicat Branch, Div Canc Control & Populat Sci, Rockville, MD 20852 USA.
EM ming-hui.chen@uconn.edu
RI Yu, Fang/B-9874-2013
FU NIH [GM 70335, CA 74015]
FX The authors thank the editor. an associate editor, and two referees, for
their constructive comments and suggestions which led to improvements
it) this article. Dr. Chen's research was partially suppoprted by NIH
grants #GM 70335 and #CA 74015.
NR 27
TC 1
Z9 1
U1 0
U2 4
PU AMER STATISTICAL ASSOC & INT BIOMETRIC SOC
PI WASHINGTON
PA 1444 I ST NW, STE 700, WASHINGTON, DC 20005 USA
SN 1085-7117
J9 J AGR BIOL ENVIR ST
JI J. Agric. Biol. Environ. Stat.
PD SEP
PY 2008
VL 13
IS 3
BP 270
EP 293
DI 10.1198/108571108X338023
PG 24
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA 343HC
UT WOS:000258843100003
ER
PT J
AU Ciencewicki, J
Trivedi, S
Kleeberger, SR
AF Ciencewicki, Jonathan
Trivedi, Shweta
Kleeberger, Steven R.
TI Oxidants and the pathogenesis of lung diseases
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Review
DE oxidative stress; antioxidant; genetics; susceptibility; infant;
reproductive outcome; premature; children; elderly; asthma; chronic
obstructive pulmonary disease; ozone; pollutants; particulates; PM;
acute respiratory distress syndrome; hyperoxia; SNP; single nucleotide
polymorphism
ID OBSTRUCTIVE PULMONARY-DISEASE; RESPIRATORY-DISTRESS-SYNDROME;
LOW-BIRTH-WEIGHT; EXHALED BREATH CONDENSATE; DIESEL EXHAUST PARTICLES;
AMBIENT AIR-POLLUTION; SURFACTANT PROTEIN-A; ACUTE OZONE EXPOSURE; LIPID
OZONATION PRODUCTS; GLUTATHIONE-S-TRANSFERASE
AB The increasing number of population-based and epiderniologic associations between oxidant pollutant exposures and cardiopulmonary disease exacerbation, decrements in pulmonary function, and mortality underscores the important detrimental effects of oxidants on public health. Because inhaled oxidants initiate a number of pathologic processes, including inflammation of the airways, which may contribute to the pathogenesis and/or exacerbation of airways disease, it is critical to understand the mechanisms through which exogenous and endogenous oxidants interact with molecules in the cells, tissues, and epithelial lining fluid of the lung. Furthermore, it is clear that interindividual variation in response to a given exposure also exists across an individual lifetime. Because of the potential impact that oxidant exposures may have on reproductive outcomes and infant, child, and adult health, identification of the intrinsic and extrinsic factors that may influence susceptibility to oxidants remains an important issue. In this review, we discuss mechanisms of oxidant stress in the lung, the role of oxidants in lung disease pathogenesis and exacerbation (eg, asthma, chronic obstructive pulmonary disease, and acute respiratory distress syndrome), and the potential risk factors (eg, age, genetics) for enhanced susceptibility to oxidant-induced disease.
C1 [Ciencewicki, Jonathan; Trivedi, Shweta; Kleeberger, Steven R.] NIEHS, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA.
RP Kleeberger, SR (reprint author), NIEHS, Lab Resp Biol, NIH, 111 TW Alexander Dr,Bldg 101,Rm D240, Res Triangle Pk, NC 27709 USA.
EM kleeber1@niehs.nih.gov
FU National Institute of Environmental Health Sciences, National Institutes
of Health, Department of Health and Human Services.
FX Supported by the Division of Intramural Research at the National
Institute of Environmental Health Sciences, National Institutes of
Health, Department of Health and Human Services.
NR 182
TC 164
Z9 168
U1 3
U2 28
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD SEP
PY 2008
VL 122
IS 3
BP 456
EP 468
DI 10.1016/j.jaci.2008.08.004
PG 13
WC Allergy; Immunology
SC Allergy; Immunology
GA 348TW
UT WOS:000259234000002
PM 18774381
ER
PT J
AU MacPherson, H
Nahin, R
Paterson, C
Cassidy, CM
Lewith, GT
Hammerschlag, R
AF MacPherson, Hugh
Nahin, Richard
Paterson, Charlotte
Cassidy, Claire M.
Lewith, George T.
Hammerschlag, Richard
TI Developments in Acupuncture Research: Big-Picture Perspectives from the
Leading Edge
SO JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE
LA English
DT Article; Proceedings Paper
CT Annual Conference of the Society-for-Acupuncture-Research
CY NOV 09-11, 2007
CL Univ Maryland, Baltimore, MD
SP Soc Acupuncture Res, Natl Ctr Complementary Med, NCCAM
HO Univ Maryland
ID CHINESE MEDICINE USERS; WHOLE SYSTEMS RESEARCH; ALTERNATIVE MEDICINE;
UNITED-STATES; HEALTH-CARE; COMPLEMENTARY; MODEL
AB On November 8-9, 2007, the Society for Acupuncture Research (SAR) hosted an international conference to mark the tenth anniversary of the landmark NIH [National Institutes of Health] Consensus Development Conference on Acupuncture. More than 300 acupuncture researchers, practitioners, students, funding agency personnel, and health policy analysts from 20 countries attended the SAR meeting held at the University of Maryland School of Medicine, Baltimore, MD. This paper summarizes important invited lectures in the area of how the field has developed in the past decade, along with a focus on appropriate strategies for advancing the field. Specific topics include: the impact of the 1997 NIH Acupuncture Consensus Conference on acupuncture research; whole-system strategies for developing the evidence without distorting the medicine; use of qualitative research methods to explore acupuncture as a complex intervention; use of qualitative research approaches to explore some "missing" topics in acupuncture research; and the impact of acupuncture research on clinical practice. A concluding section focuses on future directions in acupuncture research.
C1 [MacPherson, Hugh] Univ York, Dept Hlth Sci, York YO10 5DD, N Yorkshire, England.
[Nahin, Richard] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Paterson, Charlotte] Univ Exeter, Peninsular Med Sch, Exeter, Devon, England.
[Cassidy, Claire M.] Windpath Healing Works LLC, Bethesda, MD USA.
[Lewith, George T.] Univ Southampton, Southampton, Hants, England.
[Hammerschlag, Richard] Oregon Coll Oriental Med, Portland, OR USA.
RP MacPherson, H (reprint author), Univ York, Dept Hlth Sci, Seebohm Rowntree Bldg, York YO10 5DD, N Yorkshire, England.
EM hm18@york.ac.uk
OI Nahin, Richard/0000-0002-3682-4816; Lewith, George/0000-0002-2364-3960;
MacPherson, Hugh/0000-0003-4255-4768
FU Medical Research Council [G106/1095]
NR 37
TC 15
Z9 15
U1 0
U2 5
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1075-5535
J9 J ALTERN COMPLEM MED
JI J. Altern. Complement Med.
PD SEP
PY 2008
VL 14
IS 7
BP 883
EP 887
DI 10.1089/acm.2008.SAR-5
PG 5
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA 363RD
UT WOS:000260283500014
PM 18803497
ER
PT J
AU Riley, W
Obermayer, J
Jean-Mary, J
AF Riley, William
Obermayer, Jami
Jean-Mary, Jersino
TI Internet and mobile phone text messaging intervention for college
smokers
SO JOURNAL OF AMERICAN COLLEGE HEALTH
LA English
DT Article
DE college health; health education; smoking cessation; text messaging
ID SMOKING-CESSATION PROGRAM; RANDOMIZED-TRIAL; COMPUTER; STUDENTS; MODEL;
ADOLESCENTS; PREVENTION; TELEPHONE
AB Objective: -The authors developed a smoking cessation program using mobile phone text messaging to provide tailored and stage-specific messages to college smokers. Participants and Methods: The authors recruited 31 daily smokers who desired to quit front a college campus and asked them to use an Internet and mobile phone text messaging program to quit smoking. Results: Six weeks after program initiation, 45% reported abstinence with 42% abstinent based on cotinine verification. Continued smokers reported significantly reduced smoking rates and dependence. Overall, participants accepted the text messages. Conclusions: These results replicate findings from ail earlier study and indicate that mobile phone text messaging, is a potentially efficacious and easily disseminated method for providing cessation interventions to young adult smokers.
C1 [Riley, William; Obermayer, Jami; Jean-Mary, Jersino] PICS Inc, Reston, VA USA.
RP Riley, W (reprint author), NIMH, 6001 Execut Blvd,MSC 9615, Bethesda, MD 20892 USA.
EM wiriley@mail.nih.gov
RI Emchi, Karma/Q-1952-2016
NR 29
TC 65
Z9 67
U1 3
U2 19
PU HELDREF PUBLICATIONS
PI WASHINGTON
PA 1319 EIGHTEENTH ST NW, WASHINGTON, DC 20036-1802 USA
SN 0744-8481
J9 J AM COLL HEALTH
JI J. Am. Coll. Health
PD SEP-OCT
PY 2008
VL 57
IS 2
BP 245
EP 248
DI 10.3200/JACH.57.2.245-248
PG 4
WC Education & Educational Research; Public, Environmental & Occupational
Health
SC Education & Educational Research; Public, Environmental & Occupational
Health
GA 352PH
UT WOS:000259508900014
PM 18809542
ER
PT J
AU Villar, R
Vicente, E
Solano, B
Perez-Silanes, S
Aldana, I
Maddry, JA
Lenaerts, AJ
Franzblau, SG
Cho, SH
Monge, A
Goldman, RC
AF Villar, Raquel
Vicente, Esther
Solano, Beatriz
Perez-Silanes, Silvia
Aldana, Ignacio
Maddry, Joseph A.
Lenaerts, Anne J.
Franzblau, Scott G.
Cho, Sang-Hyun
Monge, Antonio
Goldman, Robert C.
TI In vitro and in vivo antimycobacterial activities of ketone and amide
derivatives of quinoxaline 1,4-di-N-oxide
SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY
LA English
DT Article; Proceedings Paper
CT 38th World Conference on Lung Health of the
International-Union-Against-Tuberculosis-and-Lung-Disease
CY NOV 08-12, 2007
CL Cape Town, SOUTH AFRICA
SP Int Union Against Tuberculosis & Lung Dis
DE antitubercular drugs; resistance; in vivo efficacy
ID EXTENSIVELY DRUG-RESISTANT; MYCOBACTERIUM-TUBERCULOSIS AGENTS;
GENE-DISRUPTED MICE; ALAMAR BLUE ASSAY; QUINOXALINE-2-CARBONITRILE
1,4-DI-N-OXIDE; ANTITUBERCULOSIS ACTIVITY; COENZYME F-420; BOVIS BCG;
TB; BIOSYNTHESIS
AB Objectives: To evaluate a novel series of quinoxaline 1,4-di-N-oxides for in vitro activity against Mycobacterium tuberculosis and for efficacy in a mouse model of tuberculosis (TB).
Methods: Ketone and amide derivatives of quinoxaline 1,4-di-N-oxide were evaluated in in vitro and in vivo tests including: (i) activity against M. tuberculosis resistant to currently used antitubercular drugs including multidrug-resistant strains (MDR-TB resistant to isoniazid and rifampicin); (ii) activity against non-replicating persistent (NRP) bacteria; (iii) MBC; (iv) maximum tolerated dose, oral bioavailability and in vivo efficacy in mice; and (v) potential for cross-resistance with another bioreduced drug, PA-824.
Results: Ten compounds were tested on single drug-resistant M. tuberculosis. In general, all compounds were active with ratios of MICs against resistant and non-resistant strains of <= 4.00. One compound, 5, was orally active in a murine model of TB, bactericidal, active against NRP bacteria and active on MDR-TB and poly drug-resistant clinical isolates (resistant to 3-5 antitubercular drugs).
Conclusions: Quinoxaline 1,4-di-N-oxides represent a new class of orally active antitubercular drugs. They are likely bioreduced to an active metabolite, but the pathway of bacterial activation was different from PA-824, a bioreducible nitroimidazole in clinical trials. Compound 5 was bactericidal and active on NRP organisms indicating that activation occurred in both growing and non-replicating bacteria leading to cell death. The presence of NRP bacteria is believed to be a major factor responsible for the prolonged nature of antitubercular therapy. If the bactericidal activity and activity on non-replicating bacteria in vitro translate to in vivo conditions, quinoxaline 1,4-di-N-oxides may offer a path to shortened therapy.
C1 [Goldman, Robert C.] NIAID, Div Aids, Therapeut Res Program, Bethesda, MD 20892 USA.
[Villar, Raquel; Vicente, Esther; Solano, Beatriz; Perez-Silanes, Silvia; Aldana, Ignacio; Monge, Antonio] Univ Navarra, CIFA, Unidad Invest & Desarrollo Medicamentos, E-31080 Pamplona, Spain.
[Maddry, Joseph A.] So Res Inst, Birmingham, AL 35255 USA.
[Lenaerts, Anne J.] Colorado State Univ, Dept Microbiol Immunol & Pathol, Ft Collins, CO 80523 USA.
[Franzblau, Scott G.; Cho, Sang-Hyun] Univ Illinois, Inst TB Res, Chicago, IL 60612 USA.
RP Goldman, RC (reprint author), NIAID, Div Aids, Therapeut Res Program, Bethesda, MD 20892 USA.
EM rgoldman@niaid.nih.gov
RI Perez-Silanes, Silvia/B-5284-2008; Vicente, Esther/P-2308-2016;
Lenaerts, Anne/F-1353-2017;
OI Perez-Silanes, Silvia/0000-0002-6284-4546; Vicente,
Esther/0000-0002-1061-2292; Franzblau, Scott/0000-0002-8698-0243
FU NIAID NIH HHS [N01 AI095385, N01 AI095364, N01-AI-95364, N01-AI-95385]
NR 32
TC 37
Z9 39
U1 1
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-7453
J9 J ANTIMICROB CHEMOTH
JI J. Antimicrob. Chemother.
PD SEP
PY 2008
VL 62
IS 3
BP 547
EP 554
DI 10.1093/jac/dkn214
PG 8
WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
GA 337ZD
UT WOS:000258473200022
PM 18502817
ER
PT J
AU Rajter, R
French, RH
Podgornik, R
Ching, WY
Parsegian, VA
AF Rajter, Rick
French, Roger H.
Podgornik, Rudi
Ching, W. Y.
Parsegian, V. Adrian
TI Spectral mixing formulations for van der Waals-London dispersion
interactions between multicomponent carbon nanotubes
SO JOURNAL OF APPLIED PHYSICS
LA English
DT Article
ID ELECTRONIC-STRUCTURE; OPTICAL-PROPERTIES; HAMAKER CONSTANTS;
SPECTROSCOPIC ELLIPSOMETRY; DIELECTRIC FUNCTION; WATER; FORCES; SYSTEMS;
VACUUM; FIELD
AB Recognition of spatially varying optical properties is a necessity when studying the van der Waals-London dispersion (vdW-Ld) interactions of carbon nanotubes (CNTs) that have surfactant coatings, tubes within tubes, and/or substantial core sizes. The ideal way to address these radially dependent optical properties would be to have an analytical add-a-layer solution in cylindrical coordinates similar to the one readily available for the plane-plane geometry. However, such a formulation does not exist nor does it appear trivial to be obtained exactly. The best and most pragmatic alternative for end-users is to take the optical spectra of the many components and to use a spectral mixing formulation so as to create effective solid-cylinder spectra for use in the far-limit regime. The near-limit regime at "contact" is dominated by the optical properties of the outermost layer, and thus no spectral mixing is required. Specifically we use a combination of a parallel capacitor in the axial direction and the Bruggeman effective medium in the radial direction. We then analyze the impact of using this mixing formulation upon the effective vdW-Ld spectra and the resulting Hamaker coefficients for small and large diameter single walled CNTs (SWCNTs) in both the near- and far-limit regions. We also test the spectra of a [16,0,s+7,0,s] muldwalled CNT (MWCNT) with an effective MWCNT spectrum created by mixing its [16, 0, s] and [7, 0, s] SWCNT components to demonstrate nonlinear coupling effects that exist between neighboring layers. Although this paper is primarily on nanotubes, the strategies, implementation, and analysis presented are applicable and likely necessary to any system where one needs to resolve spatially varying optical properties in a, particular Lifshitz formulation. (C) 2008 American Institute of Physics.
C1 [Rajter, Rick] MIT, Dept Mat Sci & Engn, Cambridge, MA 02139 USA.
[French, Roger H.] DuPont Co Inc, Cent Res, Expt Stn, Wilmington, DE 19880 USA.
[Podgornik, Rudi] Univ Ljubljana, Fac Math & Phys, Ljubljana, Slovenia.
[Podgornik, Rudi] Jozef Stefan Inst, Dept Theoret Phys, SI-1000 Ljubljana, Slovenia.
[Ching, W. Y.] Univ Missouri, Dept Phys, Kansas City, MO 64110 USA.
[Parsegian, V. Adrian] NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA.
RP Rajter, R (reprint author), MIT, Dept Mat Sci & Engn, Room 13-5046, Cambridge, MA 02139 USA.
EM rickrajter@alum.mit.edu
RI Ching, Wai-Yim/B-4686-2009; French, Roger/E-1986-2011; Podgornik,
Rudolf/C-6209-2008
OI Ching, Wai-Yim/0000-0001-7738-8822; French, Roger/0000-0002-6162-0532;
Podgornik, Rudolf/0000-0002-3855-4637
NR 41
TC 10
Z9 10
U1 1
U2 10
PU AMER INST PHYSICS
PI MELVILLE
PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1,
MELVILLE, NY 11747-4501 USA
SN 0021-8979
J9 J APPL PHYS
JI J. Appl. Phys.
PD SEP 1
PY 2008
VL 104
IS 5
AR 053513
DI 10.1063/1.2975207
PG 13
WC Physics, Applied
SC Physics
GA 357NO
UT WOS:000259853600043
ER
PT J
AU Scichilone, N
La Sala, A
Bellia, M
Fallano, K
Togias, A
Brown, RH
Midiri, M
Bellia, V
AF Scichilone, Nicola
La Sala, Alba
Bellia, Maria
Fallano, Katherine
Togias, Alkis
Brown, Robert H.
Midiri, Massimo
Bellia, Vincenzo
TI The airway response to deep inspirations decreases with COPD severity
and is associated with airway distensibility assessed by computed
tomography
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE high-resolution computed tomography; methacholine; airway-parenchyma
interdependence; bronchoprovocation; hyperinflation
ID OBSTRUCTIVE LUNG-DISEASE; SMOOTH-MUSCLE; METHACHOLINE CHALLENGE;
ASTHMATIC SUBJECTS; HEALTHY-SUBJECTS; EXPIRATORY FLOW; INFLATION;
RESPONSIVENESS; CALIBER
AB In patients with mild chronic obstructive pulmonary disease (COPD), the effect of deep inspirations (DIs) to reverse methacholine-induced bronchoconstriction is largely attenuated. In this study, we tested the hypothesis that the effectiveness of DI is reduced with increasing disease severity and that this is associated with a reduction in the ability of DI to distend the airways. Fifteen subjects [Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I-II: n = 7; GOLD stage III-IV: n = 8] underwent methacholine bronchoprovocation in the absence of DI, followed by DI. The effectiveness of DI was assessed by their ability to improve inspiratory vital capacity and forced expiratory volume in 1 s (FEV1). To evaluate airway distensibility, two sets of high-resolution computed tomography scans [at residual volume (RV) and at total lung capacity] were obtained before the challenge. In addition, mean parenchymal density was calculated on the high-resolution computed tomography scans. We found a strong correlation between the response to DI and baseline FEV1 %predicted (r(2) = 0.70, P < 0.0001) or baseline FEV1/forced vital capacity (r(2) = 0.57, P = 0.001). RV % predicted and functional residual capacity %predicted correlated inversely (r(2) = 0.33, P = 0.02 and r(2) = 0.32, P = 0.03, respectively), and parenchymal density at RV correlated directly (r(2) = 0.30, P = 0.03), with the response to DI. Finally, the effect of DI correlated to the change in large airway area from RV to total lung capacity (r(2) = 0.44, P = 0.01). We conclude that loss of the effects of DI is strongly associated with COPD severity and speculate that the reduction in the effectiveness of DI is due to the failure to expand the lungs because of the hyperinflated state and/or the parenchymal damage that prevents distension of the airways with lung inflation.
C1 [Scichilone, Nicola; La Sala, Alba; Bellia, Vincenzo] Univ Palermo, Dipartimento Med Pneumol Fisiol & Ntr Umana, Sez Pneumol & Med, I-90146 Palermo, Italy.
[Bellia, Maria; Midiri, Massimo] Univ Palermo, Dipartimento Biotecnol & Med Legale, Sez Sci Radiol, I-90146 Palermo, Italy.
[Fallano, Katherine; Brown, Robert H.] Johns Hopkins Univ, Dept Environm Hlth Sci, Baltimore, MD 21205 USA.
[Togias, Alkis] Natl Inst Allergy & Infect Dis, Natl Inst Hlth, Bethesda, MD USA.
RP Scichilone, N (reprint author), Univ Palermo, Dipartimento Med Pneumol Fisiol & Ntr Umana, Sez Pneumol & Med, Via Trabucco 180, I-90146 Palermo, Italy.
EM n.scichilone@libero.it
OI Scichilone, Nicola/0000-0001-6400-6573
FU University of Palermo, Palermo, Italy
FX The study was funded by the University of Palermo, Palermo, Italy.
NR 26
TC 12
Z9 13
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD SEP
PY 2008
VL 105
IS 3
BP 832
EP 838
DI 10.1152/japplphysiol.01307.2007
PG 7
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 345ZT
UT WOS:000259038900009
PM 18617628
ER
PT J
AU Liu, DM
Metter, EJ
Ferrucci, L
Roth, SM
AF Liu, Dongmei
Metter, E. Jeffrey
Ferrucci, Luigi
Roth, Stephen M.
TI TNF promoter polymorphisms associated with muscle phenotypes in humans
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE genetics; skeletal muscle; inflammation; cytokine; tumor necrosis
factor-alpha
ID TUMOR-NECROSIS-FACTOR; SKELETAL-MUSCLE; FACTOR-ALPHA; PROTEIN-SYNTHESIS;
CIRCULATING LEVELS; BEHCETS-DISEASE; ELDERLY-MEN; OLDEST-OLD; AGE;
SARCOPENIA
AB Tumor necrosis factor-alpha (TNF-alpha) is a potent catabolic factor to skeletal muscle. Single-nucleotide polymorphisms (SNPs) in the promoter region of the TNF-alpha coding gene, TNF, have been implicated in the interindividual variation in TNF-alpha production via transcriptional regulation. The present study investigated the association of muscle phenotypes with five TNF promoter SNPs, which potentially have biological significance. Female and male volunteers (n = 1,050) from the Baltimore Longitudinal Study of Aging were genotyped, and their regional and total body muscle mass, and arm and leg muscle strength were measured. Results indicated that putative high-expression alleles at positions -1031 and -863, individually or in combination in the haplotype 1031C-863A-857C-308G-238G, were associated with lower muscle mass in men. Specifically, carriers of -1031C, compared with noncarriers, exhibited lower arm muscle mass (6.4 +/- 0.1 vs. 6.8 +/- 0.1 kg, P = 0.01) and appendicular skeletal muscle mass (ASM) (24.3 +/- 0.4 vs. 25.4 +/- 0.2 kg, P = 0.02), with leg muscle mass and the ASM index (ASMI; kg/m(2)) also tending to be lower (P = 0.06 and 0.07). Similarly, -863A allele carriers (linked with -1031), compared with noncarriers, exhibited lower arm muscle mass (6.4 +/- 0.1 vs. 6.8 +/- 0.1 kg, P = 0.04). Carriers of the haplotype 1031C-863A-857C-308G-238G, compared with noncarriers, exhibited lower arm muscle mass (6.3 +/- 0.2 vs. 6.8 +/- 0.1 kg, P < 0.01), trunk muscle mass (25.7 +/- 0.5 vs. 26.9 +/- 0.3 kg, P < 0.05), and ASM (24.1 +/- 0.5 vs. 25.3 +/- 0.2 kg, P < 0.025), with tendencies for lower leg muscle mass and ASMI (P = 0.07 and 0.08). Results indicate that genetic variation in the TNF locus may contribute to the interindividual variation in muscle phenotypes in men.
C1 [Liu, Dongmei; Roth, Stephen M.] Univ Maryland, Sch Publ Hlth, Dept Kinesiol, College Pk, MD 20742 USA.
[Metter, E. Jeffrey; Ferrucci, Luigi] Harbor Hosp, Natl Inst Aging, Clin Res Branch, Baltimore, MD USA.
RP Roth, SM (reprint author), Univ Maryland, Sch Publ Hlth, Dept Kinesiol, 2134 SPH Bldg, College Pk, MD 20742 USA.
EM sroth1@umd.edu
RI Liu, Dongmei/C-1525-2012;
OI Roth, Stephen/0000-0002-7841-3695
FU National Institutes of Health [AG-021500, AG-022791]
FX The BLSA research was conducted as a component of the Intramural
Research Program of the National Institute on Aging. This work was
further sponsored by National Institutes of Health Grants AG-021500 and
AG-022791.
NR 51
TC 10
Z9 10
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD SEP
PY 2008
VL 105
IS 3
BP 859
EP 867
DI 10.1152/japplphysiol.90655.2008
PG 9
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 345ZT
UT WOS:000259038900013
PM 18635873
ER
PT J
AU Minshew, NJ
Hobson, JA
AF Minshew, Nancy J.
Hobson, Jessica A.
TI Sensory sensitivities and performance on sensory perceptual tasks in
high-functioning individuals with autism
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE autism; sensory sensitivities; sensory perception; sensory neglect
ID CHILDHOOD AUTISM; INFANTILE-AUTISM; DEVELOPMENTAL DISORDERS; SENTENCE
COMPREHENSION; SPECTRUM DISORDERS; DISTURBED-CHILDREN; MOTOR
INTEGRATION; ASPERGER-SYNDROME; ABNORMALITIES; CONNECTIVITY
AB Most reports of sensory symptoms in autism are second hand or observational, and there is little evidence of a neurological basis. Sixty individuals with high-functioning autism and 61 matched typical participants were administered a sensory questionnaire and neuropsychological tests of elementary and higher cortical sensory perception. Thirty-two percent of autism participants endorsed more sensory sensitivity items than any control participants. Both groups made few errors on elementary sensory perception items. Controls made few errors on higher cortical sensory perception items, but 30% of the autism participants made high numbers of errors. These findings support the common occurrence of sensory symptoms in high functioning autism based on first person report, and the presence of neurological abnormalities in higher cortical sensory perception.
C1 [Minshew, Nancy J.] Univ Pittsburgh, Sch Med, NICHD, Collaborat Program Excellence Autism, Pittsburgh, PA 15213 USA.
[Minshew, Nancy J.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA.
[Minshew, Nancy J.] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15213 USA.
[Hobson, Jessica A.] UCL, Inst Child Hlth, London, England.
RP Minshew, NJ (reprint author), Univ Pittsburgh, Sch Med, NICHD, Collaborat Program Excellence Autism, 3811 OHara St,Suite 300 Webster Hall, Pittsburgh, PA 15213 USA.
EM minshewnj@upmc.edu
FU NICHD NIH HHS [U19 HD035469-09, P01 HD035469, P50 HD055748, U19
HD035469, U19 HD035469-07, U19 HD035469-10, HD35469, U19 HD035469-06,
U19 HD035469-08]
NR 85
TC 32
Z9 32
U1 4
U2 21
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD SEP
PY 2008
VL 38
IS 8
BP 1485
EP 1498
DI 10.1007/s10803-007-0528-4
PG 14
WC Psychology, Developmental
SC Psychology
GA 338TI
UT WOS:000258531400008
PM 18302014
ER
PT J
AU Yeh, S
Wroblewski, K
Buggage, R
Li, Z
Kurup, SK
Sen, HN
Dahr, S
Sran, P
Reed, GF
Robinson, R
Ragheb, JA
Waldmann, TA
Nussenblatt, RB
AF Yeh, Steven
Wroblewski, Keith
Buggage, Ronald
Li, Zhuqing
Kurup, Shree K.
Sen, Hatice Nida
Dahr, Sam
Sran, Pushpa
Reed, George F.
Robinson, Randy
Ragheb, Jack A.
Waldmann, Thomas A.
Nussenblatt, Robert B.
TI High-dose humanized anti-IL-2 receptor alpha antibody (daclizumab) for
the treatment of active, non-infectious uveitis
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Daclizumab; Posterior uveitis; Panuveitis; Intermediate uveitis;
Interleukin-2
ID PREVENT ACUTE REJECTION; IL-2 RECEPTOR; MYCOPHENOLATE-MOFETIL;
TRANSPLANT RECIPIENTS; RENAL-TRANSPLANTATION; LUNG TRANSPLANTATION;
POSTERIOR UVEITIS; CLINICAL-TRIAL; T(H)17 CELLS; T-CELLS
AB Purpose: This study was designed to provide preliminary data regarding the safety and efficacy of high-dose humanized anti-IL-2 receptor (daclizumab) therapy for the treatment of active intermediate, posterior or panuveitis.
Methods: Five patients were recruited into this non-randomized, prospective pilot study of high-dose intravenous induction daclizumab therapy given at doses of 8 mg/kg at day 0 and 4 mg/kg at day 14. Patients who did not meet a safety endpoint at the 3-week follow-up evaluation were given the option of continuing therapy with subcutaneous daclizumab at 2 mg/kg every 4 weeks for 52 weeks. The primary outcome assessed was a two-step decrease in vitreous haze at day 21. Secondary outcomes evaluated included best-corrected visual acuity, retinal thickness as measured by optical coherence tomography, retinal vascular leakage assessed by fluorescein angiography, anterior chamber and vitreous cellular inflammation.
Results: Four male patients and one female patient were enrolled. Diagnoses included birdshot retinochoroidopathy (two patients), Vogt-Koyanagi-Harada's disease, bilateral idiopathic panuveitis and bilateral idiopathic intermediate uveitis. By the 4th week, four of five patients demonstrated a two-step decrease in vitreous haze. The other participant did not meet this criterion until week 20, but all five patients maintained stability in vitreous haze grade throughout their follow-up periods. At enrollment, mean visual acuity (10 eyes in 5 patients) was 69.2 ETDRS letters and following treatment was 78.2 letters (p < 0.12). Anterior chamber cell, vitreous cell, and vitreous haze also improved in the majority of eyes. Adverse events were generally mild except for one episode of left-lower lobe pneumonia requiring hospitalization and treatment.
Conclusion: This is the first demonstration that high-dose daclizumab can reduce inflammation in active uveitis. Daclizumab was well tolerated but there may be a potential increased risk of infection associated with immunosuppression. All five patients demonstrated a decrease in vitreous haze and measures of intraocular inflammation at final follow-up. The results of this small, non-randomized pilot study support the consideration of high-dose daclizumab therapy in cases of active posterior uveitis. Published by Elsevier Ltd.
C1 [Yeh, Steven; Wroblewski, Keith; Buggage, Ronald; Li, Zhuqing; Kurup, Shree K.; Sen, Hatice Nida; Dahr, Sam; Sran, Pushpa; Ragheb, Jack A.; Nussenblatt, Robert B.] NEI, NIH, Immunol Lab, Bethesda, MD 20892 USA.
[Reed, George F.] NIH, Dept Biometry & Epidemiol, Bethesda, MD 20892 USA.
[Robinson, Randy] BioPharma Inc, Prot Design Lab, Redwood City, CA USA.
[Waldmann, Thomas A.] NCI, NIH, Bethesda, MD 20892 USA.
RP Nussenblatt, RB (reprint author), NEI, NIH, Immunol Lab, Bldg 10,10 Ctr Dr, Bethesda, MD 20892 USA.
EM drbob@nei.nih.gov
FU National Eye Institute; National Institutes of Health; Heed Ophthalmic
Foundation
FX This research was funded in part by the Intramural Research Program of
the National Eye Institute, National Institutes of Health. S.Y. is
supported in part by the Heed Ophthalmic Foundation. Daclizumab was
provided by PDL BioPharma (Redwood City, CA).
NR 26
TC 43
Z9 43
U1 1
U2 1
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
J9 J AUTOIMMUN
JI J. Autoimmun.
PD SEP
PY 2008
VL 31
IS 2
BP 91
EP 97
DI 10.1016/j.jaut.2008.05.001
PG 7
WC Immunology
SC Immunology
GA 357XO
UT WOS:000259880700001
PM 18571896
ER
PT J
AU Hawes, JJ
Nerva, JD
Reilly, KM
AF Hawes, Jessica J.
Nerva, John D.
Reilly, Karlyne M.
TI Novel dual-reporter preclinical screen for antiastrocytoma agents
identifies cytostatic and cytotoxic compounds
SO JOURNAL OF BIOMOLECULAR SCREENING
LA English
DT Article
DE astrocytoma; Nf1; p53; E2F1; luciferase
ID NEUROFIBROMATOSIS TYPE-1; GLIOBLASTOMA-MULTIFORME; P53 MUTATIONS; GENE;
PROLIFERATION; CHEMOTHERAPY; ASTROCYTOMA; BOUVARDIN; PATHWAY; GLIOMAS
AB Astrocytoma/glioblastoma is the most common malignant form of brain cancer and is Often unresponsive to current pharmacological therapies and Surgical interventions. Despite several potential therapeutic agents against astrocytoma and glioblastoma, there are currently no effective therapies for astrocytoma, creating a great need for the identification of effective antitumor agents. The authors have developed a novel dual-reporter system in Trp53/Nf1-null astrocytoma cells to simultaneously and rapidly assay cell viability and cell cycle progression as evidenced by activity of the human E2F1 promoter in vitro. The dual-reporter high-throughput assay was used to screen experimental therapeutics for activity in Trp53/Nf1-null astrocytoma. Several compounds were identified demonstrating selectivity for astrocytoma over primary astrocytes. The dual-reporter system described here may be a valuable tool for identifying potential antitumor treatments that specifically target astrocytoma.
C1 [Hawes, Jessica J.; Nerva, John D.; Reilly, Karlyne M.] NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA.
RP Reilly, KM (reprint author), NCI, Mouse Canc Genet Program, W 7th St Ft Detrick,POB B,Bldg 560,Rm 32-20, Frederick, MD 21702 USA.
EM kreilly@ncifcrf.gov
FU Intralflural Research Program of the National Institutes of Health
(NIH); National Cancer Institute
FX This research was supported by the Intralflural Research Program of the
National Institutes of Health (NIH), National Cancer Institute. This
research was performed while JJH held a National Research Council
Research Associateship Award at the National Cancer Institute. All
experiments were conducted in compliance with the current laws of the
United States.
NR 28
TC 9
Z9 9
U1 2
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1087-0571
J9 J BIOMOL SCREEN
JI J. Biomol. Screen
PD SEP
PY 2008
VL 13
IS 8
BP 795
EP 803
DI 10.1177/1087057108321085
PG 9
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Chemistry
GA 352MS
UT WOS:000259501900007
PM 18664715
ER
PT J
AU Aragon, AB
Jackson, WM
Onodera, J
Tuan, RS
Nesti, LJ
AF Aragon, A. B.
Jackson, W. M.
Onodera, J.
Tuan, R. S.
Nesti, L. J.
TI Gene Expression in Blast-Injured Muscle: Insights into the Mechanism of
Heterotopic Ossification.
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Aragon, A. B.; Nesti, L. J.] Walter Reed Army Med Ctr, Dept Orthopaed & Rehabil, Washington, DC 20307 USA.
[Jackson, W. M.; Onodera, J.; Tuan, R. S.] NIAMSD, Cartilage Biol & Orthopaed Branch, Bethesda, MD 20892 USA.
RI Onodera, Jun/D-7142-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S281
EP S281
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001428
ER
PT J
AU Cabral, WA
Barnes, AM
Rotimi, CN
Porter, D
Bailey-Wilson, J
Brody, L
Martini, JC
AF Cabral, W. A.
Barnes, A. M.
Rotimi, C. N.
Porter, D.
Bailey-Wilson, J.
Brody, L.
Martini, J. C.
TI Recurring Mutation Causing Severe/Lethal Recessive Type VIII
Osteogenesis Imperfecta in African-Americans Originated in West Africa
More than 300 Years Ago
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Cabral, W. A.; Barnes, A. M.; Martini, J. C.] NICHD, Bone & Extracellular Matrix Branch, NIH, Bethesda, MD USA.
[Rotimi, C. N.; Bailey-Wilson, J.] NHGRI, Inherited Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Porter, D.] NHGRI, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA.
[Brody, L.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S183
EP S183
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001058
ER
PT J
AU Chang, W
Barnes, AM
Cabral, WA
Marini, JC
AF Chang, W.
Barnes, A. M.
Cabral, W. A.
Marini, J. C.
TI Prolyl 3-Hydroxylase 1 and CRTAP are Mutually Stabilizing in the
Endoplasmic Reticulum Collagen Prolyl 3-Hydroxylation Complex
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Chang, W.; Barnes, A. M.; Cabral, W. A.; Marini, J. C.] NICHD, Bone & Extracellular Matrix Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S15
EP S15
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000050
ER
PT J
AU Chen, J
Bi, Y
Young, MF
Wadhwa, S
AF Chen, J.
Bi, Y.
Young, M. F.
Wadhwa, S.
TI Identification And Characterization of 3.6 Col I Positive Cells from
Mouse Temporomandibular Joint
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Chen, J.; Wadhwa, S.] Univ Connecticut, Ctr Hlth, Farmington, CT USA.
[Bi, Y.; Young, M. F.] Natl Inst Dent & Craniofacial Res, Craniofacial & Skeletal Dis Branch, US Natl Inst Hlth, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S274
EP S274
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001399
ER
PT J
AU Collin-Osdoby, P
Uveges, TE
Cabral, WA
Goldberg, L
Gronowicz, GA
Osdoby, P
Marini, JC
AF Collin-Osdoby, P.
Uveges, T. E.
Cabral, W. A.
Goldberg, L.
Gronowicz, G. A.
Osdoby, P.
Marini, J. C.
TI Increased Osteoclasts in Brtl Mouse Model for Osteogenesis Imperfecta
Are Independent of Decreased Osteoblast Matrix Production and RANKL/OPG
Ratio, but Are Associated with Increased Osteoclast Precursors in
Marrow.
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Collin-Osdoby, P.; Goldberg, L.; Osdoby, P.] Washington Univ, Dept Biol, St Louis, MO 63130 USA.
[Collin-Osdoby, P.; Goldberg, L.; Osdoby, P.] Washington Univ, Div Bone & Mineral Metab, St Louis, MO 63130 USA.
[Uveges, T. E.; Cabral, W. A.; Marini, J. C.] NICHD, Bone & Extracellular Matrix Branch, NIH, Bethesda, MD USA.
[Gronowicz, G. A.] Univ Connecticut, Ctr Hlth, Dept Orthopaed Surg, Farmington, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S292
EP S292
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001473
ER
PT J
AU Daley, ELH
McBride, DJ
Uveges, TE
Kuznetsova, NV
Leikin, S
Marini, JC
Goldstein, SA
AF Daley, E. L. H.
McBride, D. J.
Uveges, T. E.
Kuznetsova, N. V.
Leikin, S.
Marini, J. C.
Goldstein, S. A.
TI Age-Associated Changes in the Material Properties of the G610C (Amish)
OI Mouse Model
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Daley, E. L. H.; Goldstein, S. A.] Univ Michigan, Ann Arbor, MI 48109 USA.
[McBride, D. J.] Univ Maryland, Baltimore, MD 21201 USA.
[Uveges, T. E.; Kuznetsova, N. V.; Leikin, S.; Marini, J. C.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S182
EP S182
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001051
ER
PT J
AU Duverger, O
Lee, D
Hassan, MQ
Chen, SX
Jaisser, F
Lian, JB
Morasso, MI
AF Duverger, O.
Lee, D.
Hassan, M. Q.
Chen, S. X.
Jaisser, F.
Lian, J. B.
Morasso, M. I.
TI Molecular Consequences of a Mutant Dlx3 Affecting Bone Homeostasis in
Tricho-Dento-Osseous Syndrome
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Duverger, O.; Lee, D.; Chen, S. X.; Morasso, M. I.] NIAAMS, NIH, Bethesda, MD USA.
[Hassan, M. Q.; Lian, J. B.] UMass Med Sch, Worcester, MA USA.
[Jaisser, F.] Coll France, F-75231 Paris, France.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S76
EP S76
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000273
ER
PT J
AU Gafni, RI
Bhattacharyya, N
Brahim, JS
Dumitrescu, CE
Theman, TA
Kelly, MH
Molinolo, AA
Collins, MT
AF Gafni, R. I.
Bhattacharyya, N.
Brahim, J. S.
Dumitrescu, C. E.
Theman, T. A.
Kelly, M. H.
Molinolo, A. A.
Collins, M. T.
TI Evidence Supporting the Necessity of
UDP-N-acetyl-alpha-D-galactosamine-polypeptide
N-acetylgalactosaminyl-transferase 3 (GalNac-T3) in the Processing of
Fibroblast Growth Factor 23 (FGF23) in Humans
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Gafni, R. I.; Bhattacharyya, N.; Brahim, J. S.; Dumitrescu, C. E.; Theman, T. A.; Kelly, M. H.; Molinolo, A. A.; Collins, M. T.] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S173
EP S173
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001018
ER
PT J
AU Gudnason, V
Aspelund, T
Smith, AV
Siggeirsdottir, K
Eiriksdottir, G
Jonsson, BY
Lang, TF
Launer, LJ
Harris, TB
AF Gudnason, V.
Aspelund, T.
Smith, A. V.
Siggeirsdottir, K.
Eiriksdottir, G.
Jonsson, B. Y.
Lang, T. F.
Launer, L. J.
Harris, T. B.
TI Use of Genetic Markers in Prediction of Fractures
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Gudnason, V.; Aspelund, T.; Smith, A. V.; Siggeirsdottir, K.; Eiriksdottir, G.] Iceland Heart Assoc, Kopavogur, Iceland.
[Jonsson, B. Y.] Univ Hosp, Malmo, Sweden.
[Lang, T. F.] UCSF, San Francisco, CA USA.
[Launer, L. J.; Harris, T. B.] NIA, Bethesda, MD 20892 USA.
RI Aspelund, Thor/F-4826-2011; Aspelund, Thor/C-5983-2008; Gudnason,
Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S27
EP S27
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000095
ER
PT J
AU Han, S
Makareeva, E
Kuznetsova, NV
DeRidder, AM
Sutter, MB
McBride, DJ
Phillips, CL
Schwartze, U
Pace, JM
Byers, PH
Visse, R
Nagase, H
Leikin, S
AF Han, S.
Makareeva, E.
Kuznetsova, N. V.
DeRidder, A. M.
Sutter, M. B.
McBride, D. J.
Phillips, C. L.
Schwartze, U.
Pace, J. M.
Byers, P. H.
Visse, R.
Nagase, H.
Leikin, S.
TI Do Type I Collagen Homotrimers Contribute to Osteoporosis by Altering
Bone Remodeling?
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Han, S.; Makareeva, E.; Kuznetsova, N. V.; DeRidder, A. M.; Sutter, M. B.; Leikin, S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[McBride, D. J.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Phillips, C. L.] Univ Missouri, Dept Biochem, Columbia, MO USA.
[Schwartze, U.; Pace, J. M.; Byers, P. H.] Univ Washington, Dept Pathol, Seattle, WA 98195 USA.
[Visse, R.; Nagase, H.] Univ London Imperial Coll Sci Technol & Med, Kennedy Inst Rheumatol, London, England.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S162
EP S162
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000579
ER
PT J
AU Ichikawa, S
Sorenson, AH
Fritz, TA
Moh, A
Mackenzie, DS
Hui, SL
Econs, MJ
AF Ichikawa, S.
Sorenson, A. H.
Fritz, T. A.
Moh, A.
Mackenzie, D. S.
Hui, S. L.
Econs, M. J.
TI Ablation of the Galnt3 Gene in Mice Leads to Low Circulating Fgf23
Concentrations and Hyperphosphatemia Despite Increased Fgf23 Gene
Expression
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Ichikawa, S.; Sorenson, A. H.; Moh, A.; Mackenzie, D. S.; Hui, S. L.; Econs, M. J.] Indiana Univ, Sch Med, Indianapolis, IN USA.
[Fritz, T. A.] NIDDK, Sect Biol Chem, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S6
EP S6
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000019
ER
PT J
AU Islam, MS
Chen, I
Adams, D
Xi, J
Li, H
Kronenberg, M
Duffin, M
Morasso, M
Reichenberger, E
Lichtler, AC
AF Islam, M. S.
Chen, I.
Adams, D.
Xi, J.
Li, H.
Kronenberg, M.
Duffin, M.
Morasso, M.
Reichenberger, E.
Lichtler, A. C.
TI High Bone Mass Phenotype in the Bone Specific Dlx3 Knock Out mice.
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Islam, M. S.] Univ Minnesota, Minneapolis, MN USA.
[Chen, I.; Adams, D.; Xi, J.; Li, H.; Kronenberg, M.; Duffin, M.; Morasso, M.; Lichtler, A. C.] Univ Connecticut, Farmington, CT USA.
[Morasso, M.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S380
EP S381
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411002164
ER
PT J
AU Kiel, DP
Hannan, MT
Barton, BA
Lang, TF
Bouxsein, ML
Brown, K
Shane, E
Magaziner, J
Zimmerman, S
Harris, T
Rubin, CT
AF Kiel, D. P.
Hannan, M. T.
Barton, B. A.
Lang, T. F.
Bouxsein, M. L.
Brown, K.
Shane, E.
Magaziner, J.
Zimmerman, S.
Harris, T.
Rubin, C. T.
TI The "Vibes" Trial: Low Magnitude Mechanical Stimulation (LMMS) to
Improve Bone Mineral Density (BMD).
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Kiel, D. P.; Hannan, M. T.] Hebrew Rehab Ctr, IFAR, Boston, MA USA.
[Barton, B. A.; Brown, K.] Maryland Med Res Inst, Baltimore, MD USA.
[Lang, T. F.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Bouxsein, M. L.] BIDMC, Ortho Biomech Lab, Boston, MA USA.
[Shane, E.] Columbia Univ, New York, NY USA.
[Magaziner, J.] Univ MD, Baltimore, MD USA.
[Zimmerman, S.] UNC, Cecil G Sheps Ctr Hlth Serv Res, Chapel Hill, NC USA.
[Harris, T.] NIA, Washington, DC USA.
[Rubin, C. T.] SUNY Stony Brook, Stony Brook, NY 11794 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S474
EP S474
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411002531
ER
PT J
AU Lang, TF
Hughes, T
Sigurdsson, S
Sigurdsson, G
Harris, TB
Siggeirsdottir, K
Gudnason, V
Launer, L
AF Lang, T. F.
Hughes, T.
Sigurdsson, S.
Sigurdsson, G.
Harris, T. B.
Siggeirsdottir, K.
Gudnason, V.
Launer, L.
TI Proximal Femoral Fragility and Age-Related White Matter Lesions by Brain
MRI in Elderly Subjects: the Age Gene/Environment Susceptibility
Study-Reykjavik
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Lang, T. F.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Hughes, T.; Harris, T. B.; Launer, L.] NIA, Lab Epidemiol & Biometry, Bethesda, MD 20892 USA.
[Sigurdsson, G.] Landspitali, Endocrinol, Reykjavik, Iceland.
[Sigurdsson, S.; Siggeirsdottir, K.; Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S28
EP S28
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000097
ER
PT J
AU Marini, JC
Abukhaled, MK
Cintas, HL
Obafemi, AA
Troendle, JF
Letocha, AD
Reynolds, JC
Paul, S
AF Marini, J. C.
Abukhaled, M. K.
Cintas, H. L.
Obafemi, A. A.
Troendle, J. F.
Letocha, A. D.
Reynolds, J. C.
Paul, S.
TI Randomized Dose Comparison of Pamidronate in Children with Types III and
IV Osteogenesis Imperfecta: 3 vs 6 Month Cycles.
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Marini, J. C.; Abukhaled, M. K.; Obafemi, A. A.; Letocha, A. D.] NICHHD, Bone & Extracellular Matrix Branch, NIH, Bethesda, MD 20892 USA.
[Cintas, H. L.; Paul, S.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Troendle, J. F.] NICHHD, Biometry & Math Stat Branch, NIH, Bethesda, MD 20892 USA.
[Reynolds, J. C.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S370
EP S370
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411002130
ER
PT J
AU Matsunobu, T
Kulkarni, AB
Karlsson, S
Yamada, Y
AF Matsunobu, T.
Kulkarni, A. B.
Karlsson, S.
Yamada, Y.
TI Critical Role of TGF-beta Signaling Pathways in Skeletal Development
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Matsunobu, T.; Kulkarni, A. B.; Yamada, Y.] Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, NIH, Bethesda, MD USA.
[Karlsson, S.] Lund Univ, Lund Strateg Ctr Stem Cell Biol & Cell Therapy, Lund, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S24
EP S24
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000080
ER
PT J
AU Ou, G
Isales, C
Hamrick, M
Ding, K
Yang, S
Gonzalez, F
Kream, B
Shi, X
AF Ou, G.
Isales, C.
Hamrick, M.
Ding, K.
Yang, S.
Gonzalez, F.
Kream, B.
Shi, X.
TI Targeted Disruption of PPAR gamma in Bone Marrow Stromal Cells Reveals
Its Role in Aging-Induced Bone Loss.
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Ou, G.; Isales, C.; Ding, K.; Shi, X.] Med Coll Georgia, Inst Mol Med & Genet, Augusta, GA 30912 USA.
[Isales, C.] Med Coll Georgia, Dept Orthopaed, Augusta, GA 30912 USA.
[Yang, S.] Wayne State Univ, Dept Orthopaed Surg, Detroit, MI USA.
[Gonzalez, F.] NCI, Mol Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Kream, B.] Univ Connecticut, Ctr Hlth, Dept Med & Genet, Farmington, CT USA.
[Kream, B.] Univ Connecticut, Ctr Hlth, Dept Dev Biol, Farmington, CT USA.
[Shi, X.] Med Coll Georgia, Dept Pathol, Augusta, GA 30912 USA.
RI Isales, Carlos/J-9902-2013; Hamrick, Mark/K-1131-2016
OI Isales, Carlos/0000-0002-4480-3484;
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S42
EP S42
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000149
ER
PT J
AU Oz, OK
Hajibeigi, A
Korach, K
Chambon, P
Zerwekh, J
AF Oz, O. K.
Hajibeigi, A.
Korach, K.
Chambon, P.
Zerwekh, J.
TI Regulation of Renal Klotho: The Importance of ER alpha
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Oz, O. K.; Hajibeigi, A.; Zerwekh, J.] UT SW Med Ctr, Dallas, TX USA.
[Korach, K.] NIEHS, NIH, Environm Dis Med Program, Res Triangle Pk, NC 27709 USA.
[Chambon, P.] Univ Strasbourg 1, CNRS, UMR 7104, INSERM,U596, Strasbourg, France.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S175
EP S175
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001025
ER
PT J
AU Panaroni, C
Gioia, R
Lupi, A
Farina, A
Casasco, M
Perilli, E
Baruffaldi, F
Cetta, G
Goldstein, SA
Kreider, J
Villa, I
Rossi, A
Marini, JC
Frattini, A
Vezzoni, P
Forlino, A
AF Panaroni, C.
Gioia, R.
Lupi, A.
Farina, A.
Casasco, M.
Perilli, E.
Baruffaldi, F.
Cetta, G.
Goldstein, S. A.
Kreider, J.
Villa, I.
Rossi, A.
Marini, J. C.
Frattini, A.
Vezzoni, P.
Forlino, A.
TI In utero Stem Cell Therapy as Treatment for Classical Osteogenesis
Imperfecta Using the Knock In Murine Model BrtIIV
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Panaroni, C.; Gioia, R.; Lupi, A.; Baruffaldi, F.; Cetta, G.; Rossi, A.; Forlino, A.] Univ Pavia, Dept Biochem, I-27100 Pavia, Italy.
[Farina, A.; Casasco, M.] Univ Pavia, Dept Expt Med, I-27100 Pavia, Italy.
[Perilli, E.] Ist Ortoped Rizzoli, Lab Tecnol Med, Bologna, Italy.
Univ Michigan, Orthopaed Res Labs, Ann Arbor, MI 48109 USA.
[Villa, I.] Ist Sci San Raffaele, Bone Metab Unit, I-20132 Milan, Italy.
[Marini, J. C.] NICHD, BEMB, Bethesda, MD USA.
[Frattini, A.] Ist Clin Humanitas, Milan, Italy.
[Vezzoni, P.] Ist Clin Rozzano, Milan, Italy.
RI Rossi, Antonio/E-9935-2012; Forlino, Antonella/H-5385-2015
OI Forlino, Antonella/0000-0002-6385-1182
NR 0
TC 0
Z9 0
U1 0
U2 6
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S129
EP S129
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000464
ER
PT J
AU Raggio, CL
Fishbein, KW
Carter, EM
Kim, M
Pleshko, N
Spencer, RG
AF Raggio, C. L.
Fishbein, K. W.
Carter, E. M.
Kim, M.
Pleshko, N.
Spencer, R. G.
TI Identification of Skin Abnormalities in Osteogenesis Imperfecta Patients
by Magnetic Resonance Imaging-A Pilot Study
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Carter, E. M.] Hosp Special Surg, Kathryn O & Alan C Greenberg Ctr Skeletal Dysplas, New York, NY 10021 USA.
[Spencer, R. G.] NIA, Nucl Magnet Resonance Unit, NIH, Baltimore, MD 21224 USA.
[Kim, M.] Hosp Special Surg, Mineralized Tissue Lab, New York, NY 10021 USA.
[Pleshko, N.] Exponent, Biomech, Philadelphia, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S240
EP S240
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001260
ER
PT J
AU Rianon, N
Lang, T
Sigurdsson, G
Siggeirsdottir, K
Eiriksdottir, G
Sigurdsson, S
Jonsson, B
Gudnason, V
Harris, T
AF Rianon, N.
Lang, T.
Sigurdsson, G.
Siggeirsdottir, K.
Eiriksdottir, G.
Sigurdsson, S.
Jonsson, B.
Gudnason, V.
Harris, T.
TI A Composite Bone Score with QCT Bone Measurements and Fracture History.
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Rianon, N.; Harris, T.] NIA, LEDB, Bethesda, MD 20892 USA.
[Lang, T.] UCSF, San Francisco, CA USA.
[Sigurdsson, G.; Gudnason, V.] Univ Iceland, Reykjavik, Iceland.
[Siggeirsdottir, K.; Eiriksdottir, G.; Sigurdsson, S.] Iceland Heart Assoc, Kopavogur, Iceland.
[Jonsson, B.] Orthoped Univ Hosp, Malmo, Sweden.
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S314
EP S314
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411001552
ER
PT J
AU Saito, H
Ellwanger, K
Clement-Lacroix, P
Hesse, E
Maltry, N
Niedermeyer, J
Lee, RW
Rawadi, G
Westphal, H
Niehrs, C
Baron, R
AF Saito, H.
Ellwanger, K.
Clement-Lacroix, P.
Hesse, E.
Maltry, N.
Niedermeyer, J.
Lee, R. W.
Rawadi, G.
Westphal, H.
Niehrs, C.
Baron, R.
TI Deletion of the Dkk1 Co-receptors Kremen 1 and Kremen 2 in Mice Leads to
Increased Bone Formation and Bone Mass
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Saito, H.; Hesse, E.; Baron, R.] Harvard Univ, Sch Dent Med, Boston, MA 02115 USA.
[Ellwanger, K.; Niedermeyer, J.; Lee, R. W.; Niehrs, C.] DKFZ, Heidelberg, Germany.
[Westphal, H.] NICHHD, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S2
EP S2
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000005
ER
PT J
AU Samelson, EJ
Massaro, JM
Fox, CS
Tucker, KL
Booth, SL
Wang, TJ
Broe, KE
Berry, SD
Hannan, MT
McLean, RR
Cupples, LA
O'Donnell, CJ
Kiel, DP
AF Samelson, E. J.
Massaro, J. M.
Fox, C. S.
Tucker, K. L.
Booth, S. L.
Wang, T. J.
Broe, K. E.
Berry, S. D.
Hannan, M. T.
McLean, R. R.
Cupples, L. A.
O'Donnell, C. J.
Kiel, D. P.
TI Calcium Intake Is Not Associated with Increased Coronary Artery
Calcification: The Framingham QCT Study.
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Samelson, E. J.; Broe, K. E.; Berry, S. D.; Hannan, M. T.; McLean, R. R.; Kiel, D. P.] Harvard Univ, Sch Med, Inst Aging Res, Boston, MA USA.
[Massaro, J. M.; Cupples, L. A.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Fox, C. S.; O'Donnell, C. J.] NHLBI, Framingham, MA USA.
[Tucker, K. L.; Booth, S. L.] Tufts Univ, Boston, MA 02111 USA.
[Wang, T. J.] Harvard Univ, Sch Med, MA Gen Hosp, Boston, MA USA.
RI Tucker, Katherine/A-4545-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S58
EP S58
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000208
ER
PT J
AU Sigurdsson, G
Aspelund, T
Siggeirsdottir, K
Jonsson, B
Mogensen, B
Sigurdsson, S
Launer, L
Harris, TB
Lang, TF
Gudnason, V
AF Sigurdsson, G.
Aspelund, T.
Siggeirsdottir, K.
Jonsson, B.
Mogensen, B.
Sigurdsson, S.
Launer, L.
Harris, T. B.
Lang, T. F.
Gudnason, V.
TI Prediction of Incidental Low Trauma Limb Fractures in Older Men and
Women with Quantitative CT(QCT) Variables of Bone and Muscles in
Mid-Thigh: The AGES-Reykjavik Study
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Sigurdsson, G.; Aspelund, T.; Siggeirsdottir, K.; Jonsson, B.; Mogensen, B.; Sigurdsson, S.; Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
[Launer, L.; Harris, T. B.] NIA, Intramural Res Program, Bethesda, MD 20892 USA.
[Gudnason, V.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RI Aspelund, Thor/F-4826-2011; Aspelund, Thor/C-5983-2008; Gudnason,
Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S118
EP S118
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000424
ER
PT J
AU Theman, TA
Collins, MT
Dempster, DW
Zhou, H
Reynolds, JC
Brahim, JS
Roschger, P
Klaushofer, K
Winer, KK
AF Theman, T. A.
Collins, M. T.
Dempster, D. W.
Zhou, H.
Reynolds, J. C.
Brahim, J. S.
Roschger, P.
Klaushofer, K.
Winer, K. K.
TI Safety and Efficacy of Long-Term Parathyroid Hormone Replacement in a
Pediatric Patient with Inherited Hypoparathyroidism: Skeletal and Renal
Outcomes
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Theman, T. A.; Collins, M. T.] NIDCR, Skeletal Clin Studies Unit, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA.
[Dempster, D. W.; Zhou, H.] Helen Hayes Hosp, Reg Bone Ctr, W Haverstraw, NY USA.
[Reynolds, J. C.] NIH, Nucl Med CC, Bethesda, MD 20892 USA.
[Roschger, P.; Klaushofer, K.] Hanusch Hosp, Ludwig Boltzmann Inst Osteol, Vienna, Austria.
[Winer, K. K.] NICHD, ENGB, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S103
EP S103
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000368
ER
PT J
AU von Marschall, Z
Fisher, LW
AF von Marschall, Z.
Fisher, L. W.
TI Specific Forms of DMPI Support Attachment and Haptotactic Migration via
alpha V beta 3 but not alpha V beta 5 Integrin
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [von Marschall, Z.; Fisher, L. W.] NIH, CSDB, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S97
EP S97
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000348
ER
PT J
AU Wu, JY
Maes, C
Chen, M
Weinstein, LS
Kronenberg, HM
AF Wu, J. Y.
Maes, C.
Chen, M.
Weinstein, L. S.
Kronenberg, H. M.
TI Deletion of the G Protein Subunit Gs alpha in Early Osteoblasts Leads to
Accelerated Osteoblast Maturation and Formation of Woven Bone with
Abnormal Osteocytes, Resulting in Severe Osteoporosis
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Wu, J. Y.; Maes, C.; Kronenberg, H. M.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Chen, M.; Weinstein, L. S.] NIDDK, Metab Dis Branch, Bethesda, MD USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S71
EP S71
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000255
ER
PT J
AU Yang, W
Harris, MA
Cui, Y
Skinner, C
Chen, X
Lai, Y
Lichtler, A
Kream, B
Mishina, Y
Harris, SE
AF Yang, W.
Harris, M. A.
Cui, Y.
Skinner, C.
Chen, X.
Lai, Y.
Lichtler, A.
Kream, B.
Mishina, Y.
Harris, S. E.
TI Conditional Deletion of BMP2 Gene in Early Osteoblasts Leads to
Reduction in the Total Bone Marrow (BM) Mesenchymal Stem Cells and Their
Capacity to Form Osteoblast Precursors
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Yang, W.; Harris, M. A.; Cui, Y.; Skinner, C.; Chen, X.; Lai, Y.; Harris, S. E.] U Texas HSC San Antonio, San Antonio, TX USA.
[Lichtler, A.; Kream, B.] U Connecticut Med CTR, Farmington, CT USA.
[Mishina, Y.] NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S33
EP S33
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000115
ER
PT J
AU Zemel, B
Kalkwarf, H
Gilsanz, V
Lappe, J
Oberfield, S
Shepherd, J
Mahboubi, S
Frederick, M
Winer, K
AF Zemel, B.
Kalkwarf, H.
Gilsanz, V.
Lappe, J.
Oberfield, S.
Shepherd, J.
Mahboubi, S.
Frederick, M.
Winer, K.
TI A Clinical Tool for Adjusting BMD Z-Scores for Body Size in Growing
Children?
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Zemel, B.] Univ Penn, Philadelphia, PA 19104 USA.
[Kalkwarf, H.] Cincinnati Childrens Med Ctr, Cincinnati, OR USA.
[Gilsanz, V.] Los Angeles Childrens Hosp, Los Angeles, CA USA.
[Lappe, J.] Creighton Univ, Omaha, NE 68178 USA.
[Oberfield, S.] Columbia Univ, New York, NY USA.
[Shepherd, J.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Mahboubi, S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Frederick, M.] CTASC, Baltimore, MD USA.
[Winer, K.] NICHD, Bethesda, MD USA.
RI Zemel, Babette/D-1117-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S30
EP S31
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000106
ER
PT J
AU Zhao, L
Huang, J
Guo, R
Chen, D
Zhang, YE
Boyce, BF
Xing, L
AF Zhao, L.
Huang, J.
Guo, R.
Chen, D.
Zhang, Y. E.
Boyce, B. F.
Xing, L.
TI Age-related Bone Loss in Mice Associated with Ubiquitin Ligase Smurf1
Degradation of JunB Protein and Reduced Osteoblast Proliferation
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Meeting Abstract
CT 30th Annual Meeting of the
American-Society-for-Bone-and-Mineral-Research
CY SEP 12-16, 2008
CL Montreal, CANADA
SP Amer Soc Bone & Mineral Res
C1 [Zhao, L.; Guo, R.; Boyce, B. F.; Xing, L.] Univ Rochester, Med Ctr, Dept Pathol & Lab Med, Rochester, NY 14642 USA.
[Huang, J.; Chen, D.] Univ Rochester, Med Ctr, Dept Orthopaed, Rochester, NY 14642 USA.
[Zhang, Y. E.] NCI, Cellular & Mol Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RI Huang, Jian/B-3146-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC BONE & MINERAL RES
PI WASHINGTON
PA 2025 M ST, N W, STE 800, WASHINGTON, DC 20036-3309 USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD SEP
PY 2008
VL 23
BP S33
EP S33
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 351FX
UT WOS:000259411000114
ER
PT J
AU Touz, MC
Ropolo, AS
Rivero, MR
Vranych, CV
Conrad, JT
Svard, SG
Nash, TE
AF Carolina Touz, Maria
Silvana Ropolo, Andrea
Romina Rivero, Maria
Veronica Vranych, Cecilia
Conrad, John Thomas
Svard, Staffan Gunnar
Nash, Theodore Elliott
TI Arginine deiminase has multiple regulatory roles in the biology of
Giardia lamblia
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE arginine deiminase; citrullination; sumoylation; antigenic variation;
encystation; gene regulation
ID INTESTINAL EPITHELIAL-CELLS; SURFACE PROTEIN; ANTIGENIC VARIATION;
PERIPHERAL VACUOLES; CITRULLINE RESIDUES; ANTIBODIES; DIFFERENTIATION;
PALMITOYLATION; IDENTIFICATION; CYTOTOXICITY
AB The protozoan parasite Giardia lamblia uses arginine deiminase (ADI) to produce energy from free L-arginine under anaerobic conditions. In this work, we demonstrate that, in addition to its known role as a metabolic enzyme, it also functions as a peptidylarginine deiminase, converting protein-bound arginine into citrulline. G. lamblia ADI specifically binds to and citrullinates the arginine in the conserved CRGKA tail of variant-specific surface proteins (VSPs), affecting both antigenic switching and antibody-mediated cell death. During encystation, ADI translocates from the cytoplasm to the nuclei and appears to play a regulatory role in the expression of encystation-specific genes. ADI is also sumoylated, which might modulate its activity. Our findings reveal a dual role played by ADI and define novel regulatory pathways used by Giardia for survival.
C1 [Carolina Touz, Maria; Silvana Ropolo, Andrea; Romina Rivero, Maria; Veronica Vranych, Cecilia] INIMEC CONICET, Inst Invest Med Mercedes & Martin Ferreyra, Cordoba, Argentina.
[Conrad, John Thomas; Nash, Theodore Elliott] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Svard, Staffan Gunnar] Uppsala Univ, Dept Cell & Mol Biol, SE-75124 Uppsala, Sweden.
RP Touz, MC (reprint author), INIMEC CONICET, Inst Invest Med Mercedes & Martin Ferreyra, Friuli 2434, Cordoba, Argentina.
EM ctouz@immf.uncor.edu
FU Agencia Nacional para la Promocion de la Ciencia y Tecnolog a FONCyT
Jovenes PICT2004; National Institutes of Allergy and Infectious
Diseases, National Institutes of Health
FX Adrian Hehl is acknowledged for his collaboration in the production of
anti-ADI pAb, and Alfredo Caceres and laboratory members for providing
numerous reagents. This work was partially supported by the Agencia
Nacional para la Promocion de la Ciencia y Tecnolog a FONCyT Jovenes
PICT2004. This research was also supported in part by the Intramural
Research Program of the National Institutes of Allergy and Infectious
Diseases, National Institutes of Health.
NR 44
TC 40
Z9 44
U1 0
U2 8
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD SEP 1
PY 2008
VL 121
IS 17
BP 2930
EP 2938
DI 10.1242/jcs.026963
PG 9
WC Cell Biology
SC Cell Biology
GA 339SC
UT WOS:000258596600016
PM 18697833
ER
PT J
AU Bauge, C
Beauchef, G
Leclercq, S
Kim, SJ
Pujol, JP
Galera, P
Boumediene, K
AF Bauge, C.
Beauchef, G.
Leclercq, S.
Kim, S. J.
Pujol, J. P.
Galera, P.
Boumediene, K.
TI NF kappa B mediates IL-1 beta-induced down-regulation of T beta RII
through the modulation of Sp3 expression
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE interleukin-1; TGF beta receptors; Sp transcription factors; NF kappa B
ID GROWTH-FACTOR-BETA; COLLAGEN GENE-EXPRESSION; II RECEPTOR GENE;
ARTICULAR CHONDROCYTES; TRANSFORMING GROWTH-FACTOR-BETA-1; TRANSCRIPTION
FACTORS; ACTIVATION; PROMOTER; CELLS; RESPONSIVENESS
AB We previously showed that interleukin-1 beta (IL-1 beta) down-regulation of type II TGF beta receptor (T beta RII) involves NF kappa B pathway and requires de novo synthesis of a yet unknown protein. Here, we demonstrate that this effect is mediated through Sp1 site located at position -25 of human T beta RII promoter. Inhibition of transcription factors binding (decoy oligonucleotides or mithramycin) abolished IL-1 beta effect. EMSA and ChIP revealed that this treatment induced Sp3 binding to cis-sequence whereby IL-1 beta exerts its transcriptional effects whereas it decreased that of Sp1. Moreover, although the cytokine did not modulate Sp1 expression, it increased that of Sp3 via NF kappa B pathway. Experiments of gain and loss of function clearly showed that Sp3 inhibited T beta RII expression whereas its silencing abolished IL-1 beta effect. In addition, both Sp1 and Sp3 were found to interact with NF kappa B, which therefore may indirectly interact with T beta RII promoter. Altogether, these data suggest that IL-1 beta decreases T beta RII expression by inducing Sp3 via NF kappa B and its binding on core promote at the expense of Sp1, which could explain the loss of cell responsiveness in certain conditions. These findings bring new insights in the knowledge of the interference between two antagonistic transduction pathways involved in multiple physiopathological processes.
C1 [Boumediene, K.] Univ Caen, IFR ICORE 146, Lab Connect Tissue Biochem, F-14032 Caen, France.
[Leclercq, S.] St Martin Private Clin, Dept Orthopaed Surg, Caen, France.
[Pujol, J. P.] NCI, Chemoprevent Lab, Bethesda, MD 20892 USA.
RP Boumediene, K (reprint author), Univ Caen, IFR ICORE 146, Lab Connect Tissue Biochem, F-14032 Caen, France.
EM karim.boumediene@unicaen.fr
OI BOUMEDIENE, Karim/0000-0001-6517-8318; BAUGE,
Catherine/0000-0001-5642-998X
FU French Ministry of Education and Research (MENRT)
FX We thank Dr Jalinot (Laboratoire de Biologie Moleculaire et Cellulaire,
ENS, Lyon, France), Dr Suske (Institut fur Molekularbiologie and
tumorforschung, Marburg, Germany) and Dr Kim (National Cancer Institute,
Bethesda, MD, USA) for providing pEVR2-p65, pEVR2-Sp1, pCMV-Sp3 and T
beta RII promoter constructs, respectively. C. Bauge was a recipient of
a fellow from French Ministry of Education and Research (MENRT).
NR 27
TC 14
Z9 16
U1 0
U2 0
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 1582-1838
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD SEP-OCT
PY 2008
VL 12
IS 5A
BP 1754
EP 1766
DI 10.1111/j.1582-4934.2007.00173.x
PG 13
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 361EB
UT WOS:000260109200035
PM 18053089
ER
PT J
AU Liu, A
Yoshioka, KI
Salerno, V
Hsieh, P
AF Liu, Angen
Yoshioka, Ken-ichi
Salerno, Vincenzo
Hsieh, Peggy
TI The mismatch repair-mediated cell cycle checkpoint response to
fluorodeoxyuridine
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Article
DE mismatch repair; 5-Fluouracil; DNA damage; ATR; colorectal cancer
ID COLORECTAL-CANCER PROGNOSIS; DNA-DAMAGE-RESPONSE;
MICROSATELLITE-INSTABILITY; BASE-EXCISION; TUMOR-CELLS; HMUTS-ALPHA;
MUTS-ALPHA; ATR KINASE; CYTOTOXICITY; 5-FLUOROURACIL
AB The loss of DNA mismatch repair (MMR) is responsible for hereditary nonpolyposis colorectal cancer and a subset of sporadic tumors. Acquired resistance or tolerance to some anti-cancer drugs occurs when MMR function is impaired. 5-Fluorouracil (FU), an anti-cancer drug used in the treatment of advanced colorectal and other cancers, and its metabolites are incorporated into RNA and DNA and inhibit thymidylate synthase resulting in depletion of dTTP and incorporation in DNA of uracil. Although the MMR deficiency has been implicated in tolerance to FU, the mechanism of cell killing remains unclear. Here, we examine the cellular response to fluorodeoxyuridine (FdU) and the role of the MMR system. After brief exposure of cells to low closes of FdU, MMR mediates DNA damage signaling during S-phase and triggers arrest: in G2/M in the first cell cycle in a manner requiring MctS alpha, MutL alpha, and DNA replication. Cell cycle arrest is mediated by ATR kinase and results in phosphorylation of Chk1 and SMC1. MutS alpha binds FdU:G mispairs in vitro consistent with its being a DNA damage sensor. Prolonged treatment with FdU results in an irreversible arrest in G2 Chat is independent of MMR status and leads to the accumulation of DNA lesions that are targeted by the base excision repair (BER) pathway. Thus, MMR can act as a direct sensor of FdU-mediated DNA lesions eliciting cell cycle arrest via the ATR/Chk1 pathway. However, at higher levels of damage, other damage surveillance pathways such as BER also play important roles.
C1 [Liu, Angen; Yoshioka, Ken-ichi; Salerno, Vincenzo; Hsieh, Peggy] NIDDK, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
RP Hsieh, P (reprint author), NIDDK, Genet & Biochem Branch, NIH, Bldg 5,Room 324, Bethesda, MD 20892 USA.
EM ph52x@nih.gov
FU Baylor University Medical Center; Massachusetts General Hospital; NIEHS,
NIH; Intramural Research Program of the National Institute of Diabetes
and Digestive and Kidney Diseases
FX We are grateful to Richard Boland (Baylor University Medical Center) for
providing us HCT116 3-6 cells, Paul Nghiem (Massachusetts General
Hospital) for providing ATR-wt and ATR-kd U20S cells, and Tom Kunkel
(NIEHS, NIH) for providing HEC59 and HEC59 2-4 cells used in this study.
This work was funded by the Intramural Research Program of the National
Institute of Diabetes and Digestive and Kidney Diseases, NIH.
NR 39
TC 31
Z9 31
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0730-2312
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD SEP 1
PY 2008
VL 105
IS 1
BP 245
EP 254
DI 10.1002/jcb.21824
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 346ZX
UT WOS:000259109200027
PM 18543256
ER
PT J
AU Deshet, N
Lupu-Meiri, M
Espinoza, I
Fili, O
Shapira, Y
Lupu, R
Gershengorn, MC
Oron, Y
AF Deshet, Naamit
Lupu-Meiri, Monica
Espinoza, Ingrid
Fili, Oded
Shapira, Yuval
Lupu, Ruth
Gershengorn, Marvin C.
Oron, Yoram
TI Plasminogen-induced aggregation of PANC-1 cells requires conversion to
plasmin and is inhibited by enclogenous plasminogen activator
inhibitor-1
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID UROKINASE RECEPTOR; SERINE-PROTEASE; PRECURSOR CELLS; PAI-1 GENE;
SYSTEM; CANCER; PROUROKINASE; FIBRINOLYSIS; PERMEABILITY; VITRONECTIN
AB PANC-1 cells express proteinase-activated receptors (PARs)-1, -2, and respond to their activation by transient elevation of cytosolic [Ca2+]and accelerated aggregation (Wei et al., 2006, J Cell Physiol 206:322-328). We studied the effect of plasminogen (PGN), an inactive precursor of the PAR-1-activating protease, plasmin (PN) on aggregation of pancreatic adenocarcinoma (PDAC) cells. A single dose of PGN time- and dose-dependently promoted PANC-1 cells aggregation in serum-free medium, while PN did not. PANC-1 cells express urokinase plasminogen activator (uPA), which continuously converted PGN to PN. This activity and PGN-induced aggregation were inhibited by the uPA inhibitor amiloride. PGN-incluced aggregation was also inhibited by alpha-antiplasmin and by the PN inhibitor epsilon-aminocaproic acid (EACA). Direct assay of uPA activity revealed very low rate, markedly enhanced in the presence of PGN. Moreover, in PGN activator inhibitor I-deficient PANC-1 cells, uPA activity and PGN-induced aggregation were markedly potentiated. Two additional human PDAC cell lines, MiaPaCa and Colo347, were assayed for PGN-induced aggregation. Both cell lines responded by aggregation and exhibited PGN-enhanced uPA activity. We hypothesized that the continuous conversion of PGN to PN by enclogenous uPA is limited by PN's degradation and negatively controlled by enclogenously produced PAI-1. Indeed, we found that PANC-1 cells inactivate PN with t 1/2 of approximately 7 h, while the continuous addition of PN promoted aggregation. Our data suggest that PANC-1 cells possess intrinsic, PAI-1-sensitive mechanism for promotion of aggregation and differentiation by prolonged exposure to PGN and, possibly, additional precursors of PARs agonists.
C1 [Deshet, Naamit; Lupu-Meiri, Monica; Fili, Oded; Shapira, Yuval; Oron, Yoram] Tel Aviv Univ, Sackler Fac Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel.
[Espinoza, Ingrid; Lupu, Ruth] Evanston NW Healthcare Res Inst, Dept Med, Evanston, IL USA.
[Gershengorn, Marvin C.] NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD USA.
RP Oron, Y (reprint author), Tel Aviv Univ, Sackler Fac Med, Dept Physiol & Pharmacol, IL-69978 Tel Aviv, Israel.
EM medfair@post.tau.ac.il
NR 42
TC 5
Z9 5
U1 1
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0021-9541
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD SEP
PY 2008
VL 216
IS 3
BP 632
EP 639
DI 10.1002/jcp.21441
PG 8
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 335EK
UT WOS:000258273400008
PM 18366077
ER
PT J
AU Strizzi, L
Mancino, M
Bianco, C
Raafat, A
Gonzales, M
Booth, BW
Watanabe, K
Nagaoka, T
Mack, DL
Howard, B
Callahan, R
Smith, GH
Salomon, DS
AF Strizzi, Luigi
Mancino, Mario
Bianco, Caterina
Raafat, Ahmed
Gonzales, Monica
Booth, Brian W.
Watanabe, Kazuhide
Nagaoka, Tadahiro
Mack, David L.
Howard, Beatrice
Callahan, Robert
Smith, Gilbert H.
Salomon, David S.
TI Netrin-1 can affect morphogenesis and differentiation of the mouse
mammary gland
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID EMBRYONIC STEM-CELLS; BETA-CASEIN GENE; EPITHELIAL-CELLS; TRANSGENIC
MICE; IN-VITRO; HUMAN CRIPTO-1; ADULT STEM; EXPRESSION; GROWTH;
PLURIPOTENCY
AB Netrin-1 has been shown to regulate the function of the EGF-like protein Cripto-1 (Cr-1) and affect mammary gland development. Since Cr-1 is a target gene of Nanog and Oct4, we investigated the relationship between Netrin-1 and Cr-1, Nanog and Oct4 during different stages of development in the mouse mammary gland. Results from histological analysis show that exogenous Netrin-1 was able to induce formation of alveolar-like structures within the mammary gland terminal end buds of virgin transgenic Cripto-1 mice and enhance mammary gland alveologenesis in early pregnant FVB/N mice. Results from immunostaining and Western blot analysis show that Netrin-1, Nanog and Oct4 are expressed in the mouse embryonic mammary anlage epithelium while Cripto-1 is predominantly expressed outside this structure in the surrounding mesenchyme. We find that in lactating mammary glands of postnatal FVB/N mice, Netrin-1 expression is highest while Cripto-1 and Nanog levels are lowest indicating that Netrin-1 may perform a role in the mammary gland during lactation. HC-II mouse mammary epithelial cells stimulated with lactogenic hormones and exogenous soluble Netrin-1 showed increased beta-casein expression as compared to control thus supporting the potential role for Netrin-1 during functional differentiation of mouse mammary epithelial cells. Finally, mouse ES cells treated with exogenous soluble Netrin-1 showed reduced levels of Nanog and Cripto-1 and higher levels of beta-III tubulin during differentiation. These results suggest that Netrin-1 may facilitate functional differentiation of mammary epithelial cells and possibly affect the expression of Nanog and/or Cripto-1 in multipotent cells that may reside in the mammary gland.
C1 [Strizzi, Luigi; Mancino, Mario; Bianco, Caterina; Raafat, Ahmed; Gonzales, Monica; Booth, Brian W.; Watanabe, Kazuhide; Nagaoka, Tadahiro; Mack, David L.; Callahan, Robert; Smith, Gilbert H.; Salomon, David S.] NCI, Tumor Growth Factor Sect, Mammary Biol & Tumorigenesis Lab, Bethesda, MD 20892 USA.
[Howard, Beatrice] Inst Canc Res, Breakthrough Breast Canc Res Ctr, London SW3 6JB, England.
RP Salomon, DS (reprint author), NCI, Tumor Growth Factor Sect, Mammary Biol & Tumorigenesis Lab, 37 Convent Dr,Bldg 37,Room 1112, Bethesda, MD 20892 USA.
EM salomond@mail.nih.gov
OI Nagaoka, Tadahiro/0000-0002-9391-0243
FU Intramural NIH HHS [Z01 BC009003-25]
NR 49
TC 13
Z9 13
U1 0
U2 3
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0021-9541
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD SEP
PY 2008
VL 216
IS 3
BP 824
EP 834
DI 10.1002/jcp.21462
PG 11
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 335EK
UT WOS:000258273400029
PM 18425773
ER
PT J
AU Miller, BT
Singh, RP
Klauda, JB
Hodoscek, M
Brooks, BR
Woodcock, HL
AF Miller, Benjamin T.
Singh, Rishi P.
Klauda, Jeffery B.
Hodoscek, Milan
Brooks, Bernard R.
Woodcock, H. Lee, III
TI CHARMMing: A new, flexible web portal for CHARMM
SO JOURNAL OF CHEMICAL INFORMATION AND MODELING
LA English
DT Article
ID MOLECULAR-DYNAMICS SIMULATION; BINDING-SITES; CONSERVATION; POTENTIALS;
ALGORITHMS; PREDICTION; PRESSURE; PROTEINS; QUANTUM; SYSTEMS
AB A new web portal for the CHARMM macromolecular modeling package, CHARMMing (CHARMM interface and graphics, http://www.charmming.org), is presented. This tool provides a user-friendly interface for the preparation, submission, monitoring, and visualization of molecular simulations (i.e., energy minimization, solvation, and dynamics). The infrastructure used to implement the web application is described. Two additional programs have been developed and integrated with CHARMMing: GENRTF, which is employed to define structural features not supported by the standard CHARMM force field, and a job broker, which is used to provide a portable method for using grid and Cluster computing with CHARMMing. The use of the program is described with three proteins: 1YJP, 1O1O, and 1UFY. Source code is provided allowing CHARMMing to be downloaded, installed, and used by supercomputing centers and research groups that have a CHARMM license. Although no software can replace a scientist's own judgment and experience, CHARMMing eases the introduction of newcomers to the molecular modeling discipline by providing a graphical method for running simulations.
C1 [Miller, Benjamin T.; Singh, Rishi P.; Klauda, Jeffery B.; Brooks, Bernard R.; Woodcock, H. Lee, III] NHLBI, Natl Inst Hlth, Lab Computat Biol, Bethesda, MD 20892 USA.
[Hodoscek, Milan] Natl Inst Chem, Ctr Mol Modeling, SI-1000 Ljubljana, Slovenia.
RP Woodcock, HL (reprint author), NHLBI, Natl Inst Hlth, Lab Computat Biol, Bldg 10, Bethesda, MD 20892 USA.
EM hlwood@nih.gov
RI Woodc, Henry/D-9275-2011;
OI Woodcock, Henry/0000-0003-3539-273X; Miller,
Benjamin/0000-0003-1647-0122
FU NIH; NHLBI
FX We wish to acknowledge Richard M. Venable and Xiongwu Wu for their
assistance With preparing the CHARMM input scripts. We also wish to
thank the developers of Django (an open source web application
framework). Jmol (used for visualization). Ajax Tabs (used to provide
the tabbed user interface), Bubble tooltips (provides context-sensitive
help), Prototype (a Javascript framework), SDMenu (for the side menu),
TableKit (For table sorting), and GreyBox (for various display
functionality). This research was supported by the Intramural Research
Program of the NIH, NHLBI.
NR 47
TC 57
Z9 57
U1 0
U2 10
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1549-9596
J9 J CHEM INF MODEL
JI J. Chem Inf. Model.
PD SEP
PY 2008
VL 48
IS 9
BP 1920
EP 1929
DI 10.1021/ci800133b
PG 10
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Computer Science,
Information Systems; Computer Science, Interdisciplinary Applications
SC Pharmacology & Pharmacy; Chemistry; Computer Science
GA 351BH
UT WOS:000259398500018
PM 18698840
ER
PT J
AU Brenner, D
Bago, AG
Gallatz, K
Palkovits, M
Usdin, TB
Dobolyi, A
AF Brenner, David
Bago, Attila G.
Gallatz, Katallin
Palkovits, Miklos
Usdin, Ted Bjoern
Dobolyi, Arpad
TI Tuberoinfundibular peptide of 39 residues in the embryonic and early
postnatal rat brain
SO JOURNAL OF CHEMICAL NEUROANATOMY
LA English
DT Article
DE neuropeptide; transient expression; ontogeny; medial paralemniscal
nucleus; amygdalo-hippocampal transitional zone; posterior intralaminar
thalamic nucleus
ID PARATHYROID-HORMONE; PTH2 RECEPTOR; EXPRESSION; FOREBRAIN; NEURONS;
TIP39; EJACULATION; IDENTIFICATION; HYPOTHALAMUS; ORGANIZATION
AB Tuberoinfundibular peptide of 39 residues (TIP39) was identified as the endogenous ligand of parathyroid hormone 2 receptor. We have recently demonstrated that TIP39 expression in adult rat brain is confined to the subparafascicular area of the thalamus with a few cells extending laterally into the posterior intralaminar thalamic nucleus (PIL), and the medial paralemniscal nucleus (MPL) in the lateral pontomesencephalic tegmentum. During postnatal development, TIP39 expression increases until postnatal (lay 33 (PND-33), then decreases, and almost completely disappears by PND-125. Here, we report the expression of TIP39 during early brain development. TIP39-immunoreactive (TIP39-ir) neurons in the subparafascicular area first appeared at PND-1. In contrast, TIP39-ir neurons were detectable in the MPL at embryonic day 14.5 (ED-14.5), and the intensity of their labeling increased thereafter. We also identified TIP39-ir neurons between ED-16.5 and PND-5 in two additional brain areas, the PIL and the amygdalo-hippocampal transitional zone (AHi). We confirmed the specificity of TIP39 immunolabeling by demonstrating TIP39 mRNA using in situ hybridization histochemistry. In the PIL, TIP39 neurons are located medial to the CGRP group as demonstrated by double immunolabeling. All TIP39-ir neurons in the AHi and most TIP39-ir neurons in the PIL disappear during early postnatal development. The adult pattern of TIP39-ir fibers emerge during postnatal development. However, fibers emanating from PIL can be followed in the supraoptic decussations towards the hypothalamus at ED-18.5. These TIP39-ir fibers disappear by PND-1. The complex pattern of TIP39 expression during early brain development suggests the involvement of TIP39 in transient functions during ontogeny. (c) 2008 Elsevier B.V. All rights reserved.
C1 [Brenner, David; Bago, Attila G.; Gallatz, Katallin; Palkovits, Miklos; Dobolyi, Arpad] Semmelweis Univ, Dept Anat Histol & Embryol, Neuromorphol and Neuroendocrine Res Lab, H-1094 Budapest, Hungary.
[Brenner, David; Bago, Attila G.; Gallatz, Katallin; Palkovits, Miklos; Dobolyi, Arpad] Hungarian Acad Sci, H-1094 Budapest, Hungary.
[Bago, Attila G.] Natl Inst Neurosurg, H-1145 Budapest, Hungary.
[Usdin, Ted Bjoern] NIMH, Sect Fundamental Neurosci, Bethesda, MD 20892 USA.
RP Dobolyi, A (reprint author), Semmelweis Univ, Dept Anat Histol & Embryol, Neuromorphol and Neuroendocrine Res Lab, H-1094 Budapest, Hungary.
EM dobolyi@ana.sote.hu
RI Palkovits, Miklos/F-2707-2013;
OI Palkovits, Miklos/0000-0003-0578-0387
FU Hungarian Science Foundation [OTKA K67646]
FX We appreciate the technical assistance of Erzsebet Tarnokne Voros and
Frigyesne Helfferich. Support was provided by the Hungarian Science
Foundation (OTKA K67646) for A.D. Arpad Dobolyi is a grantee of the
Bolyai Janos Scholarship.
NR 38
TC 4
Z9 4
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0891-0618
J9 J CHEM NEUROANAT
JI J. Chem. Neuroanat.
PD SEP
PY 2008
VL 36
IS 1
BP 59
EP 68
DI 10.1016/j.jchemneu.2008.04.001
PG 10
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 337JT
UT WOS:000258433100007
PM 18495420
ER
PT J
AU Winer, KK
Sinaii, N
Peterson, D
Sainz, B
Cutler, GB
AF Winer, Karen K.
Sinaii, Ninet
Peterson, Donna
Sainz, Bruno, Jr.
Cutler, Gordon B., Jr.
TI Effects of once versus twice-daily parathyroid hormone 1-34 therapy in
children with hypoparathyroidism
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID PARATHYROID-HORMONE 1-34; LONG-TERM TREATMENT; PHOSPHATE-METABOLISM;
VITAMIN-D; BONE; CALCIUM; 1,25-DIHYDROXYVITAMIN-D3; CALCITRIOL;
HYPERCALCIURIA; OSTEOPOROSIS
AB Context: Hypoparathyroidism is among the few hormonal insufficiency states not treated with replacement of the missing hormone. Long-term conventional therapy with vitamin D and analogs may lead to nephrocalcinosis and renal insufficiency.
Objective: Our objective was to compare the response of once-daily vs. twice-daily PTH 1-34 treatment in children with hypoparathyroidism.
Setting: The study was conducted at a clinical research center.
Subjects: Fourteen children ages 4-17 yr with chronic hypoparathyroidism were studied. Study
Design: This was a randomized cross-over trial, lasting 28 wk, which compared two dose regimens, once-daily vs. twice-daily PTH1-34. Each 14-wk study arm was divided into a 2-wk inpatient dose-adjustment phase and a 12-wk outpatient phase.
Results: Mean predose serum calcium was maintained at levels just below the normal range. Repeated serum measures over a 24-h period showed that twice-daily PTH 1-34 increased serum calcium and magnesium levels more effectively than a once-daily dose. This was especially evident during the second half of the day (12-24 h). PTH 1-34 normalized mean 24-h urine calcium excretion on both treatment schedules. This was achieved with half the PTH 1-34 dose during the twice-daily regimen compared with the once-daily regimen ( twice-daily, 25 +/- 15 mu g/d vs. once-daily, 58 +/- 28 mu g/d; P < 0.001).
Conclusions: We conclude that a twice-daily PTH1-34 regimen provides a more effective treatment of hypoparathyroidism compared with once-daily treatment because it reduces the variation in serum calcium levels and accomplishes this at a lower total daily PTH 1-34 dose. The results showed, as in the previous study of adult patients with hypoparathyroidism, that a twice-daily regimen produced significantly improved metabolic control compared with once-daily PTH 1-34.
C1 [Winer, Karen K.] NICHHD, NIH, Ctr Res Mothers & Children, Endocrinol Nutr & Growth Branch, Bethesda, MD 20892 USA.
[Sinaii, Ninet] Natl Inst Hlth, Biostat & Clin Epidemiol Serv, Ctr Clin, Bethesda, MD USA.
RP Winer, KK (reprint author), NICHHD, NIH, Ctr Res Mothers & Children, Endocrinol Nutr & Growth Branch, Bldg 6100,Room 4B11, Bethesda, MD 20892 USA.
EM winerk@mail.nih.gov
FU National Institutes of Health Clinical Center
FX We thank the National Institutes of Health Clinical Center fellows and
nursing staff for their contributions and support. We also thank
nutritionist Nancy Sebring for her contributions.
NR 23
TC 52
Z9 55
U1 0
U2 2
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD SEP
PY 2008
VL 93
IS 9
BP 3389
EP 3395
DI 10.1210/jc.2007-2552
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 344TV
UT WOS:000258951100021
PM 18492754
ER
PT J
AU Florio, P
Romero, R
Chaiworapongsa, T
Kusanovic, JP
Torricelli, M
Lowry, PJ
Petraglia, F
AF Florio, Pasquale
Romero, Roberto
Chaiworapongsa, Tinnakorn
Kusanovic, Juan Pedro
Torricelli, Michela
Lowry, Phil J.
Petraglia, Felice
TI Amniotic fluid and umbilical cord plasma corticotropin-releasing factor
(CRF), CRF-binding protein, adrenocorticotropin, and cortisol
concentrations in intraamniotic infection and inflammation at term
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID MATERNAL PLASMA; HUMAN PLACENTA; PREGNANT-WOMEN; HORMONE; PRETERM;
LABOR; ASSOCIATION; MECHANISM; CYTOKINES; PEPTIDES
AB Context: Pregnant tissues express corticotropin-releasing factor (CRF), a peptide modulating fetal and placental ACTH and cortisol secretion. These actions are modulated by the locally expressed CRF-binding protein (CRF-BP).
Objective: The objective of the study was to determine whether CRF, CRF-BP, ACTH, and cortisol concentrations change in amniotic fluid and umbilical cord plasma in the presence of intraamniotic infection/inflammation (IAI) in women with spontaneous labor at term.
Design: This was a cross-sectional study.
Setting: The study was conducted at a tertiary referral center for obstetric care.
Patients: Patients included women in active labor at term with (n = 39) and without (controls; n = 78) IAI.
Main Outcome Measures: Amniotic fluid and umbilical cord plasma concentrations of CRF, CRF-BP, ACTH, and cortisol measured by RIA and immunoradiometric assays were measured.
Results: In patients with IAI, amniotic fluid CRF (0.97 +/- 0.18 ng/ml) and CRF-BP (33.06 +/- 5.54 nmol/liter) concentrations were significantly (P < 0.001) higher than in controls (CRF: 0.32 +/- 0.04 ng/ml; CRF-BP: 14.69 +/- 2.79 ml). The umbilical cord plasma CRF and CRF-BP concentrations were significantly (P < 0.001 for all) higher in women with IAI than in controls (CRF: 2.96 +/- 0.35 ng/ml vs. 0.38 +/- 0.18 ng/ml; CRF-BP: 152.12 +/- 5.94 nmol/liter vs. 106.9 +/- 5.97 nmol/liter). In contrast, amniotic fluid and umbilical cord plasma ACTH and cortisol concentrations did not differ between groups.
Conclusions: Amniotic fluid and umbilical cord plasma CRF and CRF-BP concentrations are increased in women with spontaneous labor at term and IAI. CRF-BP may modulate CRF actions on ACTH and cortisol secretion, playing a pivotal role in limiting the inflammatory process and thus avoiding an overactivation of the fetal/placental hypothalamus-pituitary-adrenal axis at birth.
C1 [Florio, Pasquale; Torricelli, Michela; Petraglia, Felice] Univ Siena, Chair Obstet & Gynecol, Dept Pediat Obstet & Reprod Med, I-53100 Siena, Italy.
[Romero, Roberto; Chaiworapongsa, Tinnakorn; Kusanovic, Juan Pedro] NICHHD, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20814 USA.
[Romero, Roberto; Chaiworapongsa, Tinnakorn; Kusanovic, Juan Pedro] NICHHD, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI 48202 USA.
Wayne State Univ, Hutzel Hosp, Dept Obstet & Gynecol, Detroit, MI 48202 USA.
[Lowry, Phil J.] Univ Reading, Sch Anim & Microbial Sci, Reading RG6 6UR, England.
RP Florio, P (reprint author), Univ Siena, Chair Obstet & Gynecol, Dept Pediat Obstet & Reprod Med, Policlin Le Scotte Viale Bracci, I-53100 Siena, Italy.
EM florio@unisi.it
RI Torricelli, Michela/N-1785-2016; PETRAGLIA, Felice/K-6535-2016
OI Torricelli, Michela/0000-0001-8608-9875; PETRAGLIA,
Felice/0000-0002-8851-625X
FU Italian Ministry of University and Scientific Research; University of
Siena
FX The work was partially supported by grants from the Italian Ministry of
University and Scientific Research and the University of Siena ( to F.
P.). The funding sources had no role in the design and conduct of the
study; collection, management, analysis, and interpretation of the data;
and preparation, review, and approval of the manuscript.
NR 31
TC 6
Z9 6
U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD SEP
PY 2008
VL 93
IS 9
BP 3604
EP 3609
DI 10.1210/jc.2007-2843
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 344TV
UT WOS:000258951100052
PM 18559919
ER
PT J
AU Ma, L
Hanson, RL
Que, LN
Mack, JL
Franks, PW
Infante, AM
Kobes, S
Bogardus, C
Baier, LJ
AF Ma, Lijun
Hanson, Robert L.
Que, Lorem N.
Mack, Janel L.
Franks, Paul W.
Infante, Aniello M.
Kobes, Sayuko
Bogardus, Clifton
Baier, Leslie J.
TI Association analysis of Kruppel-like factor 11 variants with type 2
diabetes in Pima Indians
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID TRANSCRIPTION FACTOR KLF11; PANCREATIC-CANCER; CELL-GROWTH; BETA;
MECHANISM; MELLITUS; LOCI
AB Context: Kruppel-like factor 11 (KLF11) is a transcription factor of the zinc finger domain family that has been shown to regulate expression of the insulin gene. An initial study reported that a KLF11 variant predicting a Q62R was associated with type 2 diabetes (T2D) in French Caucasians; however, subsequent studies have failed to identify an association between this variant and T2D in subjects from a similar Northern-European ancestry.
Objective: We sought to determine whether the Q62R or other variants within KLF11 were associated with T2D in Pima Indians, a population with an extremely high prevalence of this disease.
Design, Setting, and Subjects: KLF11 was sequenced in 24 Pima Indians to identify potentially novel variants. There were 18 variants genotyped in a family-based sample of 1337 Pima Indians to analyze the linkage disequilibrium pattern of this gene and identify representative variants. Four representative variants were further genotyped in a population-based sample of 3501 full-heritage Pima Indians for association analyses. Among these subjects, 413 had undergone metabolic studies when they were nondiabetic to measure traits that predict T2D.
Results: Neither the Q62R nor any other common variant in KLF11 was associated with T2D in the Pima population. In addition, no variant was associated with insulin secretion or insulin-stimulated glucose disposal rate.
Conclusions: Common variation in KLF11 variation does not appear to influence the population-based risk for developing T2D among full-heritage Pima Indians. Thus, KLF11 is unlikely to play a major role in the etiology of T2D among this Native American population.
C1 [Ma, Lijun; Hanson, Robert L.; Que, Lorem N.; Mack, Janel L.; Franks, Paul W.; Infante, Aniello M.; Kobes, Sayuko; Bogardus, Clifton; Baier, Leslie J.] NIDDK, Diabet Mol Genet Sect, Phoenix Epidemiol & Clin Res Branch, NIH,Dept Hlth & Human Serv, Phoenix, AZ 85004 USA.
[Franks, Paul W.] Umea Univ Hosp, Genet Epidemiol & Clin Res Grp, Dept Publ Hlth & Clin Med, Div Med, SE-90187 Umea, Sweden.
RP Baier, LJ (reprint author), NIDDK, Diabet Mol Genet Sect, Phoenix Epidemiol & Clin Res Branch, NIH,Dept Hlth & Human Serv, 445 N 5th St,Suite 210, Phoenix, AZ 85004 USA.
EM lbaier@phx.niddk.nih.gov
RI Hanson, Robert/O-3238-2015;
OI Hanson, Robert/0000-0002-4252-7068; Franks, Paul/0000-0002-0520-7604
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health
FX This study was also supported by the intramural research program of
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health.
NR 16
TC 7
Z9 8
U1 0
U2 1
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD SEP
PY 2008
VL 93
IS 9
BP 3644
EP 3649
DI 10.1210/jc.2008-0546
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 344TV
UT WOS:000258951100058
PM 18593768
ER
PT J
AU Kim, SJ
Zhang, ZJ
Sarkar, C
Tsai, PC
Lee, YC
Dye, L
Mukherjee, AB
AF Kim, Sung-Jo
Zhang, Zhongjian
Sarkar, Chinmoy
Tsai, Pei-Chih
Lee, Yi-Ching
Dye, Louis
Mukherjee, Anil B.
TI Palmitoyl protein thioesterase-1 deficiency impairs synaptic vesicle
recycling at nerve terminals, contributing to neuropathology in humans
and mice
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID NEURONAL CEROID-LIPOFUSCINOSIS; MEMBRANE-FUSION; HIPPOCAMPAL-NEURONS;
HUNTINGTONS-DISEASE; MOLECULAR-CLONING; SYNAPTOTAGMIN-I; GOLGI
MEMBRANES; KNOCKOUT MICE; ENDOCYTOSIS; EXOCYTOSIS
AB Neuronal ceroid lipofuscinoses represent the most common childhood neurodegenerative storage disorders. Infantile neuronal ceroid lipofuscinosis (INCL) is caused by palmitoyl protein thioesterase-1 (PPT1) deficiency. Although INCL patients show signs of abnormal neurotransmission, manifested by myoclonus and seizures, the molecular mechanisms by which PPT1 deficiency causes this abnormality remain obscure. Neurotransmission relies on repeated cycles of exo- and endocytosis of the synaptic vesicles (SVs), in which several palmitoylated proteins play critical roles. These proteins facilitate membrane fusion, which is required for neurotransmitter exocytosis, recycling of the fused SV membrane components, and regeneration of fresh vesicles. However, palmitoylated proteins require depalmitoylation for recycling. Using postmortem brain tissues from an INCL patient and tissue from the PPT1-knockout (PPT1-KO) mice that mimic INCL, we report here that PPT1 deficiency caused persistent membrane anchorage of the palmitoylated SV proteins, which hindered the recycling of the vesicle components that normally fuse with the presynaptic plasma membrane during SV exocytosis. Thus, the regeneration of fresh SVs, essential for maintaining the SV pool size at the synapses, was impaired, leading to a progressive loss of readily releasable SVs and abnormal neurotransmission. This abnormality may contribute to INCL neuropathology.
C1 [Kim, Sung-Jo; Zhang, Zhongjian; Sarkar, Chinmoy; Tsai, Pei-Chih; Lee, Yi-Ching; Mukherjee, Anil B.] NICHHD, NIH, Sect Dev Genet, Heritable Disorders Branch, Bethesda, MD 20892 USA.
[Dye, Louis] NICHHD, NIH, Microscopy & Imaging Core, Bethesda, MD 20892 USA.
RP Mukherjee, AB (reprint author), NICHHD, NIH, Sect Dev Genet, Heritable Disorders Branch, Bldg 10,Room 9D42,10 Ctr Dr, Bethesda, MD 20892 USA.
EM mukherja@exchange.nih.gov
FU NICHD; NIH
FX We thank J.Y. Chou, I. Owens,J.T. Russell, and S.W. Levin For critical
review of the manuscript and helpful suggestions. The statistical
analysis of the SV data by H. Wei is gratefully acknowledged. We are
also grateful to V. Schram (Microscopy and Imaging Core, National
Institute of Child Health and Human Development [NICHD]) for confocal
microscopy and L. Holtzclaw (Section on Cellular and Synaptic
Physiology, NICHD) for her expert assistance with the perfusion of the
triouse brain. Brain autopsy tissue samples were obtained from the Human
Brain and Spinal Fluid Resource Center at the VA West Los Angeles
Healthcare Center (Los Angeles, California, USA), which is sponsored by
the National institute of Neurological Disorders and Stroke/National
Institute of Mental Health, National Multiple Sciences Society, and the
Department of Veterans Affairs. This research was supported in whole by
the intramural Research Program of the NICHD, NIH.
NR 69
TC 52
Z9 52
U1 0
U2 5
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD SEP
PY 2008
VL 118
IS 9
BP 3075
EP 3086
DI 10.1172/JCI33482
PG 12
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 344OF
UT WOS:000258936500012
PM 18704195
ER
PT J
AU Osei-Hyiaman, D
Liu, J
Zhou, L
Godlewski, G
Harvey-White, J
Jeong, WI
Batkai, S
Marsicano, G
Lutz, B
Buettner, C
Kunos, G
AF Osei-Hyiaman, Douglas
Liu, Jie
Zhou, Liang
Godlewski, Grzegorz
Harvey-White, Judith
Jeong, Won-il
Batkai, Sandor
Marsicano, Giovanni
Lutz, Beat
Buettner, Christoph
Kunos, George
TI Hepatic CB(1) receptor is required for development of diet-induced
steatosis, dyslipidemia, and insulin and leptin resistance in mice
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID FATTY-ACID OXIDATION; REDUCED FOOD-INTAKE; INDUCED OBESITY;
RISK-FACTORS; ANTAGONIST SR141716; OVERWEIGHT PATIENTS;
ENERGY-EXPENDITURE; WISTAR RATS; BODY-WEIGHT; ZUCKER RATS
AB Diet-induced obesity is associated with fatty liver, insulin resistance, leptin resistance, and changes in plasma lipid profile. Endocannabinoids have been implicated in the development of these associated phenotypes, because mice deficient for the cannabinoid receptor CB, (CB1(-/-)) do not display these changes in association with diet-induced obesity. The target tissues that mediate these effects, however, remain unknown. We therefore investigated the relative role of hepatic versus extrahepatic CBI receptors in the metabolic consequences of a high-fat diet, using liver-specific CBI knockout (LCB1(-/-)) mice. LCB1(-/-) mice fed a high-fat diet developed a similar degree of obesity as that of wild-type mice, but, similar to CB1(-/-) mice, had less steatosis, hyperglycemia, dyslipidemia, and insulin and leptin resistance than did wild-type mice fed a high-fat diet. CBI agonist-induced increase in de novo hepatic lipogenesis and decrease in the activity of carnitine paimitoyltransferase-1 and total energy expenditure were absent in both CB1(-/-) and LCB1(-/-) mice. We conclude that endocannabinoid activation of hepatic CB, receptors contributes to the diet-induced steatosis and associated hormonal and metabolic changes, but not to the increase in adiposity, observed with high-fat diet feeding. Theses studies suggest that peripheral CBI receptors could be selectively targeted for the treatment of fatty liver, impaired glucose homeostasis, and dyslipidemia in order to minimize the neuropsychiatric side effects of nonselective CB, blockade during treatment of obesity-associated conditions.
C1 [Osei-Hyiaman, Douglas; Liu, Jie; Zhou, Liang; Godlewski, Grzegorz; Harvey-White, Judith; Jeong, Won-il; Batkai, Sandor; Kunos, George] NIAAA, Lab Physiol Studies, NIH, Bethesda, MD USA.
[Marsicano, Giovanni] Univ Bordeaux 2, U862, INSERM, Magendie Ctr, F-33076 Bordeaux, France.
[Lutz, Beat] Johannes Gutenberg Univ Mainz, Dept Physiol Chem, D-6500 Mainz, Germany.
[Buettner, Christoph] Mt Sinai Sch Med, Dept Med, New York, NY USA.
RP Kunos, G (reprint author), NIAAA, 5625 Fishers Lane, Rockville, MD 20852 USA.
EM gkunos@mail.nih.gov
RI Batkai, Sandor/G-3889-2010; JEONG, WON IL/B-6615-2011; Batkai,
Sandor/H-7983-2014
FU National Institute on Alcohol Abuse and Alcoholism, NIH; AVENIR; INSERM
FX We thank Keming Xiong for expert technical assistance. This study was
supported by Funds from the intramural research program of the National
Institute on Alcohol Abuse and Alcoholism, NIH. G. Marsicano is
supported by an AVENIR grant of INSERM in partnership with Foundation
Bettencourt-Schueller.
NR 42
TC 228
Z9 231
U1 1
U2 12
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD SEP
PY 2008
VL 118
IS 9
BP 3160
EP 3169
DI 10.1172/JCI34827
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 344OF
UT WOS:000258936500020
PM 18677409
ER
PT J
AU Mitchell, C
Jennings, C
Brambilla, D
Aldrovandi, G
Amedee, AM
Beck, I
Bremer, JW
Coombs, R
Decker, D
Fiscus, S
Fitzgibbon, J
Luzuriaga, K
Moye, J
Palumbo, P
Reichelderfer, P
Somasundaran, M
Stevens, W
Frenkel, L
AF Mitchell, Caroline
Jennings, Cheryl
Brambilla, Donald
Aldrovandi, Grace
Amedee, Angela Martin
Beck, Ingrid
Bremer, James W.
Coombs, Robert
Decker, Don
Fiscus, Susan
Fitzgibbon, Joseph
Luzuriaga, Katherine
Moye, John
Palumbo, Paul
Reichelderfer, Patricia
Somasundaran, Mohan
Stevens, Wendy
Frenkel, Lisa
CA IMPAACT Network
TI Diminished human immunodeficiency virus type 1 DNA yield from dried
blood spots after storage in a humid incubator at 37 degrees C compared
to-20 degrees C
SO JOURNAL OF CLINICAL MICROBIOLOGY
LA English
DT Article
ID POLYMERASE CHAIN-REACTION; SUBTYPE-B DNA; HIV-INFECTION; FILTER-PAPER;
INFANTS; DIAGNOSIS; STABILITY; SAMPLES; MOTHERS; MORTALITY
AB Collecting whole blood on filter paper simplifies the processing, transport, and storage of specimens used for the diagnosis of human immunodeficiency virus type 1 (HIV-1) and other tests. Specimens may be collected in tropical or rural areas with minimal facilities for handling specimens. To compare simulated tropical conditions with freezer storage, we examined the stability of HIV-1 DNA in dried blood spots (DBS) stored in humid heat and at -20 degrees C. DBS were created by spotting 50-mu l aliquots of whole blood on 903 filter paper. DNA was extracted from DBS at baseline and after 2, 6, or 12 months of storage at -20 degrees C or at 37 degrees C with similar to 85% humidity. The DNA was tested undiluted or diluted using the Amplicor HIV-1 DNA PCR (Roche), version 1.5. Each reaction was scored positive, negative, or indeterminate based on optical density. Results were compared between storage conditions and over time. A total of 1,832 reactions from 916 DBS were analyzed, including 100 DBS at baseline, 418 stored at -20 degrees C, and 398 stored at 37 degrees C. A chi-square test showed fewer positive reactions for DBS stored at 37 degrees C (55%) than for those stored at -20 degrees C (78%) (P < 0.0001). Samples stored at -20 degrees C showed little change in the probability of detection of HIV-1 DNA over time; the odds ratio (OR) was 0.93 after storage for 1 year. Samples stored at 37 degrees C demonstrated a significant change in detection at 1 year (OR, 0.29). We conclude that exposure of DBS to 37 degrees C and high humidity impaired the recovery of HIV-1 DNA from DBS, whereas DNA recovery was preserved when DBS were stored frozen.
C1 [Beck, Ingrid; Frenkel, Lisa] Seattle Childrens Hosp Res Inst, Seattle, WA 98109 USA.
[Mitchell, Caroline; Coombs, Robert; Frenkel, Lisa] Univ Washington, Seattle, WA 98195 USA.
[Jennings, Cheryl; Bremer, James W.] Rush Univ, Virol Qual Assurance Lab, Chicago, IL 60612 USA.
[Brambilla, Donald] New England Res Inst, Watertown, MA 02172 USA.
[Luzuriaga, Katherine; Somasundaran, Mohan] Univ Massachusetts, Worcester, MA 01605 USA.
[Aldrovandi, Grace] Univ So Calif, Los Angeles, CA USA.
[Aldrovandi, Grace; Decker, Don] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Amedee, Angela Martin] Louisiana State Univ, New Orleans, LA USA.
[Fiscus, Susan] Univ N Carolina, Chapel Hill, NC USA.
[Fitzgibbon, Joseph] NIAID, Bethesda, MD 20892 USA.
[Moye, John; Reichelderfer, Patricia] NICHHD, Bethesda, MD 20892 USA.
[Palumbo, Paul] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
[Stevens, Wendy] Univ Witwatersrand, Johannesburg, South Africa.
RP Frenkel, L (reprint author), Seattle Childrens Hosp Res Inst, 1900 9th Ave, Seattle, WA 98109 USA.
EM lfrenkel@u.washington.edu
OI moye, john/0000-0001-9976-8586
FU Children's LA [HD 40777]; NIH [U01 AI068632-01]; DAIDS [N01-AI-5044,
U01AI068632, U01 AI068632, NO1-HD-3-3612]
FX This project was funded by Children's LA grant HD 40777 (to G. A.) and
NIH awards U01 AI068632-01 (to G. A.), N01-AI-5044 DAIDS (to J.W.B.),
U01AI068632 (to S. F.), U01 AI068632 (to L. F.), and NO1-HD-3-3612 (to
L. F.).
NR 16
TC 13
Z9 14
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0095-1137
J9 J CLIN MICROBIOL
JI J. Clin. Microbiol.
PD SEP
PY 2008
VL 46
IS 9
BP 2945
EP 2949
DI 10.1128/JCM.00359-08
PG 5
WC Microbiology
SC Microbiology
GA 344FS
UT WOS:000258912900020
PM 18614660
ER
PT J
AU Krull, KR
Okcu, MF
Potter, B
Jain, N
Dreyer, Z
Kamdar, K
Brouwers, P
AF Krull, Kevin R.
Okcu, M. Fatih
Potter, Brian
Jain, Neelam
Dreyer, ZoAnn
Kamdar, Kala
Brouwers, Pim
TI Screening for neurocognitive impairment in pediatric cancer long-term
survivors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; COGNITIVE IMPAIRMENT; INITIAL VALIDATION;
CHILDHOOD-CANCER; NORMATIVE DATA; PERFORMANCE; DEMENTIA; CHILDREN;
ASSOCIATION; STRATEGIES
AB Purpose Recent studies suggest that up to 40% of childhood cancer survivors may experience neurocognitive problems, a finding that has led the Children's Oncology Group to recommend regular evaluation. However, for a variety of reasons, including costs, time restraints, health insurance, and access to professional resources, these guidelines are often difficult to implement. We report reliability and validity data on a brief neurocognitive screening method that could be used to routinely screen patients in need of comprehensive follow-up.
Patients and Methods Two hundred forty consecutive patients were screened during their annual visits to a long-term survivor clinic using standard neurocognitive measures and brief parent rating. From this total, 48 patients had a second screening, and 52 patients had a comprehensive follow-up evaluation. Test-retest reliability and predictive and discriminative validity were examined.
Results Good test-retest reliability was demonstrated, with an overall r = 0.72 and all individual subtest correlations greater than r = 0.40. Although means tended to improve from first to second testing, no significant changes were detected (all P >.10). The screen accurately predicted global intellect (F-6,F-45 = 11.81, P < .0001), reading skills (F-6,F-45 = 4.74, P < .001), and mathematics (F-6,F-45 = 3.35, P < .008). Parent rating was a marginal indicator of global intellect only.
Conclusion The brief neurocognitive screening was a better predictor of child functioning than specific parent rating. This brief measure, which can be completed in 30 minutes, is a practical and reliable method to identify cancer survivors in need of further neurocognitive follow-up.
C1 Texas Childrens Hosp, Dept Child Psychol, Houston, TX 77030 USA.
Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
Texas Childrens Canc Ctr, Houston, TX USA.
NIMH, Div AIDS & Hlth & Behav Res, Rockville, MD 20857 USA.
RP Krull, KR (reprint author), St Jude Childrens Hosp, Dept Epidemiol & Canc Control, 332 N Lauderdale St,MS 735, Memphis, TN 38105 USA.
EM kevin.krull@stjude.org
NR 38
TC 39
Z9 39
U1 2
U2 5
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD SEP 1
PY 2008
VL 26
IS 25
BP 4138
EP 4143
DI 10.1200/JCO.2008.16.8864
PG 6
WC Oncology
SC Oncology
GA 350KB
UT WOS:000259350200013
PM 18757327
ER
PT J
AU Egorin, M
Ramanathan, RK
Gibbons, J
Petros, W
Ivy, SP
Remick, SC
AF Egorin, Merrill
Ramanathan, Ramesh K.
Gibbons, Joseph
Petros, William
Ivy, S. Percy
Remick, Scot C.
TI Inhibition of imatinib transport by uremic toxins during renal failure -
In reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
ID DYSFUNCTION WORKING GROUP; ADVANCED MALIGNANCIES; VARYING DEGREES;
PHASE-I; MESYLATE; LIVER
C1 [Egorin, Merrill] Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15260 USA.
[Ramanathan, Ramesh K.] Scottsdale Clin Res Inst, Translat Genom Inst, Scottsdale, AZ USA.
[Gibbons, Joseph] Case Comprehens Canc Ctr, Cleveland, OH USA.
[Petros, William; Remick, Scot C.] Mary Babb Randolph Canc Ctr, Morgantown, WV USA.
[Ivy, S. Percy] NCI, Bethesda, MD 20892 USA.
RP Egorin, M (reprint author), Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15260 USA.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD SEP 1
PY 2008
VL 26
IS 25
BP 4227
EP 4228
DI 10.1200/JCO.2008.18.5470
PG 2
WC Oncology
SC Oncology
GA 350KB
UT WOS:000259350200035
ER
PT J
AU Brar, S
Leu, J
Kim, Y
Venitz, J
AF Brar, S.
Leu, J.
Kim, Y.
Venitz, J.
TI Effects of smoking and gender on tetrahydroisoquinolines (TIQ) and
beta-carbolines in a healthy population
SO JOURNAL OF CLINICAL PHARMACOLOGY
LA English
DT Meeting Abstract
CT 37th Annual Meeting of the American-College-of-Clinical-Pharmacology
CY SEP 14-16, 2008
CL Philadelphia, PA
SP Amer Coll Clin Pharmacol
C1 NIAAA, NIH, Bethesda, MD USA.
Virginia Commonwealth Univ, Dept Pharmaceut, Richmond, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0091-2700
J9 J CLIN PHARMACOL
JI J. Clin. Pharmacol.
PD SEP
PY 2008
VL 48
IS 9
MA 100
BP 1122
EP 1122
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 341MT
UT WOS:000258719300099
ER
PT J
AU Kim, Y
Herion, D
George, DT
Venitz, J
AF Kim, Y.
Herion, D.
George, D. T.
Venitz, J.
TI Effects of smoking on R- and S-salsolinol and dopamine in a healthy
population and during alcohol detoxification
SO JOURNAL OF CLINICAL PHARMACOLOGY
LA English
DT Meeting Abstract
CT 37th Annual Meeting of the American-College-of-Clinical-Pharmacology
CY SEP 14-16, 2008
CL Philadelphia, PA
SP Amer Coll Clin Pharmacol
C1 NIAAA, NIH, Bethesda, MD USA.
Virginia Commonwealth Univ, Dept Pharmaceut, Richmond, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0091-2700
J9 J CLIN PHARMACOL
JI J. Clin. Pharmacol.
PD SEP
PY 2008
VL 48
IS 9
MA 101
BP 1122
EP 1122
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 341MT
UT WOS:000258719300100
ER
PT J
AU Hasin, DS
Keyes, KM
Alderson, D
Wang, S
Aharonovich, E
Grant, BE
AF Hasin, Deborah S.
Keyes, Katherine M.
Alderson, Donald
Wang, Shuang
Aharonovich, Efrat
Grant, Bridget E.
TI Cannabis withdrawal in the United States: Results from NESARC
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID ALCOHOL-USE DISORDER; NATIONAL EPIDEMIOLOGIC SURVEY; INTERVIEW SCHEDULE
AUDADIS; SUBSTANCE USE DISORDERS; GENERAL-POPULATION SAMPLE; DSM-IV
ALCOHOL; MARIJUANA WITHDRAWAL; DRUG-USE; ABSTINENCE SYMPTOMS; SMOKED
MARIJUANA
AB Objective: Although cannabis is the most widely abused illicit drug, little is known about the prevalence of cannabis withdrawal and its factor structure, clinical validity, and psychiatric correlates in the general population.
Method: National Epidemiologic Survey on Alcohol and Related Conditions participants were assessed, in 2001-2002, with structured in-person interviews covering substance history, DSM-IV Axis I and 11 disorders, and withdrawal symptoms after cessation of use. Of these, 2613 had been frequent cannabis users (>= 3 times/week), and a "cannabis-only" subset (N = 1119) never binge-drank or used other drugs 3 times/week.
Results: In the full sample and subset, 44.3% (SE = 1.19) and 44.2% (SE = 1.75), respectively, experienced ! 2 cannabis withdrawal symptoms, while 34.4% (SE = 1.21) and 34.1% (SE = 1.76), respectively, experienced ! 3 symptoms. The symptoms formed 2 factors, one characterized by weakness, hypersomnia, and psychomotor retardation and the second by anxiety, restlessness, depression, and insomnia. Both symptom types were associated with significant distress/impairment (p < .01), substance use to relieve/avoid cannabis withdrawal symptoms (p < .01), and quantity of cannabis use (among the cannabis-only users p < .05). Panic (p < .01) and personality (p <= .01) disorders were associated with anxiety symptoms in both samples, family history of drug problems was associated with weakness symptoms in the subset (p = .01), and depression was associated with both sets of symptoms in the subset (p < .05).
Conclusion: Cannabis withdrawal was prevalent and clinically significant among a representative sample of frequent cannabis users. Similar results in the subset without polysubstance abuse confirmed the specificity of symptoms to cannabis. Cannabis withdrawal should be added to DSM-V, and the etiology and treatment implications of cannabis withdrawal symptoms should be investigated.
C1 [Hasin, Deborah S.; Keyes, Katherine M.; Alderson, Donald; Wang, Shuang; Aharonovich, Efrat] Columbia Univ, New York State Psychiat Inst, Mailman Sch Publ Hlth, New York, NY 10032 USA.
[Grant, Bridget E.] NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, US Dept HHS,NIH, Bethesda, MD USA.
RP Hasin, DS (reprint author), Columbia Univ, New York State Psychiat Inst, Mailman Sch Publ Hlth, 1051 Riverside Dr,Box 123, New York, NY 10032 USA.
EM dsh2@columbia.edu
FU National Institute on Alcohol Abuse and Alcoholism (NIAAA), Bethesda, Md
[K05 AA014223]; National Institute on Drug Abuse (NIDA), Bethesda, Md
[R01 DA018652]; National Institutes of Health, NIAAA
FX The National epidemiologic Survey on Alcohol and Related Conditions was
conducted and funded by the National Institute on Alcohol Abuse and
Alcoholism (NIAAA), Bethesda, Md., with supplemental funding by the
National Institute on Drug Abuse (NIDA). Bethesda, Md. This study was
funded in part by the Intramural Program of the National Institutes of
Health, NIAAA. This research was supported in part by grants from the
NIAAA (K05 AA014223) and the NIDA (R01 DA018652) and support from New
York State Psychiatric Institute.; The authors thank Vialerie Richmond,
M.A., New York State Psychiatric Institute, New York, for manuscript
preparation and editorial assistance. Ms. Richmond reports no financial
or other relationships relevant to the subject of this article.; The
views and opinions expressed in this report are those of the authors and
should not be construed to represent the views of any sponsoring
organization, agencies, or the U.S. government.; The authors report no
additional financial or other relationships relevant to the subject of
this article.
NR 45
TC 63
Z9 65
U1 2
U2 7
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 240008, MEMPHIS, TN 38124 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD SEP
PY 2008
VL 69
IS 9
BP 1354
EP 1363
PG 10
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 355NV
UT WOS:000259716500002
PM 19012815
ER
PT J
AU Guyer, AE
Monk, CS
McClure-Tone, EB
Nelson, EE
Roberson-Nay, R
Adler, AD
Fromm, SJ
Leibenluft, E
Pine, DS
Ernst, M
AF Guyer, Amanda E.
Monk, Christopher S.
McClure-Tone, Erin B.
Nelson, Eric E.
Roberson-Nay, Roxann
Adler, Abby D.
Fromm, Stephen J.
Leibenluft, Ellen
Pine, Daniel S.
Ernst, Monique
TI A developmental examination of amygdala response to facial expressions
SO JOURNAL OF COGNITIVE NEUROSCIENCE
LA English
DT Article
ID FUSIFORM FACE AREA; EVENT-RELATED FMRI; HUMAN BRAIN; ANTERIOR CINGULATE;
PREFRONTAL CORTEX; FUNCTIONAL CONNECTIVITY; EMOTIONAL RESPONSES; NEURAL
RESPONSES; ADOLESCENT BRAIN; SOCIAL-BEHAVIOR
AB Several lines of evidence implicate the amygdala in face emotion processing, particularly for fearful facial expressions. Related findings suggest that face-emotion processing engages the amygdala within an interconnected circuitry that can be studied using a functional-connectivity approach. Past work also underscores important functional changes in the amygdala during development. Taken together, prior research on amygdala function and development reveals a need for more work examining developmental changes in the amygdala's response to fearful faces and in amygdala functional connectivity during face processing. The present study used event-related functional magnetic resonance imaging to compare 31 adolescents (9-17 years old) and 30 adults (21-40 years old) on activation to fearful faces in the amygdala and other regions implicated in face processing. Moreover, these data were used to compare patterns of amygdala functional connectivity in adolescents and adults. During passive viewing, adolescents demonstrated greater amygdala and fusiform activation to fearful faces than did adults. Functional connectivity analysis revealed stronger connectivity between the amygdala and the hippocampus in adults than in adolescents. Within each group, variability in age did not correlate with amygdala response, and sex-related developmental differences in amygdala response were not found. Eye movement data collected outside of the magnetic resonance imaging scanner using the same task suggested that developmental differences in amygdala activation were not attributable to differences in eye-gaze patterns. Amygdala hyperactivation in response to fearful faces may explain increased vulnerability to affective disorders in adolescence; stronger amygdala - hippocampus connectivity in adults than adolescents may reflect maturation in learning or habituation to facial expressions.
C1 [Guyer, Amanda E.] NIMH, MAP, NIH, Bethesda, MD 20892 USA.
[Monk, Christopher S.] Univ Michigan, Ann Arbor, MI 48109 USA.
[McClure-Tone, Erin B.] Georgia State Univ, Atlanta, GA 30303 USA.
[Roberson-Nay, Roxann] Virginia Commonwealth Univ, Richmond, VA 23284 USA.
RP Guyer, AE (reprint author), NIMH, MAP, NIH, 15K N Dr,Room 208,MSC 2670, Bethesda, MD 20892 USA.
EM amandaguyer@mail.nih.gov
RI Nelson, Eric/B-8980-2008
OI Nelson, Eric/0000-0002-3376-2453
FU Intramural Research Program of the National Institute of Mental Health;
National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Mental Health, National Institutes of Health.
NR 94
TC 153
Z9 154
U1 8
U2 35
PU MIT PRESS
PI CAMBRIDGE
PA 55 HAYWARD STREET, CAMBRIDGE, MA 02142 USA
SN 0898-929X
J9 J COGNITIVE NEUROSCI
JI J. Cogn. Neurosci.
PD SEP
PY 2008
VL 20
IS 9
BP 1565
EP 1582
DI 10.1162/jocn.2008.20114
PG 18
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 341EB
UT WOS:000258695900004
PM 18345988
ER
PT J
AU Zhao, Y
Flandin, P
Long, JE
Dela Cuesta, M
Westphal, H
Rubenstein, JLR
AF Zhao, Yangu
Flandin, Pierre
Long, Jason E.
Dela Cuesta, Melissa
Westphal, Heiner
Rubenstein, John L. R.
TI Distinct molecular pathways for development of telencephalic interneuron
subtypes revealed through analysis of Lhx6 mutants
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE Lhx6; Dlx; GABAergic; interneuron; NPY
ID CORTICAL GABAERGIC INTERNEURONS; FOREBRAIN CHOLINERGIC NEURONS; MEDIAL
GANGLIONIC EMINENCE; LIM-HOMEOBOX GENE; CELL-MIGRATION; DLX GENES;
TRANSCRIPTION FACTORS; DEVELOPING NEOCORTEX; BASAL FOREBRAIN;
CEREBRAL-CORTEX
AB Here we analyze the role of the Lhx6 lim-homeobox transcription factor in regulating the development of subsets of neocortical, hippocampal, and striatal interneurons. An Lhx6 loss-of-function allele, which expresses placental alkaline phosphatase (PLAP), allowed analysis of the development and fate of Lhx6-expressing interneurons in mice lacking this homeobox transcription factor. There are Lhx6(+)-;Dlx(+) and Lhx6(-);Dlx(+) subtypes of tangentially migrating interneurons. Most interneurons in Lhx6(PLAP/PLAP) mutants migrate to the cortex, although less efficiently, and exhibit defects in populating the marginal zone and superficial parts of the neocortical plate. By contrast, migration to superficial parts of the hippocampus is not seriously affected. Furthermore, whereas parvalbumin(+) and somatostatin(+) interneurons do not differentiate, NPY(+) interneurons are present; we suggest that these NPY(+) interneurons are derived from the Lhx6(-);Dlx(+) subtype. Striatal interneurons show deficits distinct from pallial interneurons, including a reduction in the NPY(+) subtype. We provide evidence that Lhx6 mediates these effects through promoting expression of receptors that regulate interneuron migration (ErbB4, CXCR4, and CXCR7), and through promoting the expression of transcription factors either known (Arx) or implicated (bMaf, Cux2, and NPAS1) in controlling interneuron development.
C1 [Rubenstein, John L. R.] Univ Calif San Francisco, Nina Ireland Lab Dev Neurobiol, Dept Psychiat, San Francisco, CA 94143 USA.
[Zhao, Yangu; Dela Cuesta, Melissa; Westphal, Heiner] NICHHD, Lab Mammalian Genes & Dev, Bethesda, MD 20892 USA.
RP Rubenstein, JLR (reprint author), Univ Calif San Francisco, Nina Ireland Lab Dev Neurobiol, Dept Psychiat, 2nd Floor S,Room GD 284C,1550 4th St, San Francisco, CA 94143 USA.
EM john.rubenstein@ucsf.edu
FU Nina Ireland; Larry L. Hillblom Foundation; National Institute of Mental
Health [RO1 MH49428-01, K05 MH065670]; Swiss National Science Foundation
[PA00A-117463, PBGEA-112882]; Intramural Research Program of the
National Institute of Child Health and Human Development
FX Grant sponsor: Nina Ireland (to J.L.R.R.); Grant sponsor: the Larry L.
Hillblom Foundation (to J.L.R.R.); Grant sponsor: the National Institute
of Mental Health; Grant numbers: RO1 MH49428-01 and K05 MH065670 (to
J.L.R.R.); Grant sponsor: the Swiss National Science Foundation; Grant
numbers: PA00A-117463 and PBGEA-112882 (to P.F.); Grant sponsor: the
Intramural Research Program of the National Institute of Child Health
and Human Development (to H.W.).
NR 71
TC 113
Z9 114
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0021-9967
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD SEP 1
PY 2008
VL 510
IS 1
BP 79
EP 99
DI 10.1002/cne.21772
PG 21
WC Neurosciences; Zoology
SC Neurosciences & Neurology; Zoology
GA 338CG
UT WOS:000258481900005
PM 18613121
ER
PT J
AU Schneidman-Duhovny, D
Dror, O
Inbar, Y
Nussinov, R
Wolfson, HJ
AF Schneidman-Duhovny, Dina
Dror, Oranit
Inbar, Yuval
Nussinov, Ruth
Wolfson, Haim J.
TI Deterministic pharmacophore detection via multiple flexible alignment of
drug-like molecules
SO JOURNAL OF COMPUTATIONAL BIOLOGY
LA English
DT Article; Proceedings Paper
CT 11th Annual International Conference on Research in Computational
Molecular Biology
CY APR 21-25, 2007
CL Oakland, CA
SP AFFYMETRIX, BioNovo, Genentech, Int Soc Computat Biol, Helicos, Merck, Roche, Wyeth, ARIADNE, QB3 Calif Inst Quantitat Biomed Res
DE computer-aided drug design (CADD); rational drug discovery; 3D molecular
similarity; 3D molecular superposition
ID SIZED MOLECULES; IDENTIFICATION; SUPERPOSITION; 3D; SETS; SUBSTRUCTURES;
SEARCH; DESIGN
AB We present a novel highly efficient method for the detection of a pharmacophore from a set of drug-like ligands that interact with a target receptor. A pharmacophore is a spatial arrangement of physico-chemical features in a ligand that is essential for the interaction with a specific receptor. In the absence of a known three-dimensional (3D) receptor structure, a pharmacophore can be identified from a multiple structural alignment of ligand molecules. The key advantages of the presented algorithm are: (a) its ability to multiply align flexible ligands in a deterministic manner, (b) its ability to focus on subsets of the input ligands, which may share a large common substructure, resulting in the detection of both outlier molecules and alternative binding modes, and (c) its computational efficiency, which allows to detect pharmacophores shared by a large number of molecules on a standard PC. The algorithm was extensively tested on a dataset of almost 80 ligands acting on 12 different receptors. The results, which were achieved using a set of standard default parameters, were consistent with reference pharmacophores that were derived from the bound ligand-receptor complexes. The pharmacophores detected by the algorithm are expected to be a key component in the discovery of new leads by screening large databases of drug-like molecules. A user-friendly web interface is available at http://bioinfo3d.cs.tau.ac.il/pharma. Supplementary material can be found at http://bioinfo3d.cs.tau.ac.il/pharma/reduction/.
C1 [Schneidman-Duhovny, Dina; Dror, Oranit; Inbar, Yuval; Wolfson, Haim J.] Tel Aviv Univ, Sch Comp Sci, Raymond & Beverly Sackler Fac Exact Sci, IL-69978 Tel Aviv, Israel.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Fac Med, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel.
[Nussinov, Ruth] NCI, Ctr Canc Res, SAIC Frederick Inc, Basic Res Program,Nanobiol Program, Frederick, MD 21701 USA.
RP Dror, O (reprint author), Tel Aviv Univ, Sch Comp Sci, Raymond & Beverly Sackler Fac Exact Sci, Haim Levanon St, IL-69978 Tel Aviv, Israel.
EM oranit@post.tau.ac.il
RI Wolfson, Haim/A-1837-2011
FU Intramural NIH HHS [Z01 BC010442-06]; NCI NIH HHS [N01-CO-12400,
N01CO12400]; NIAID NIH HHS [1UC1AI067231, UC1 AI067231]
NR 32
TC 18
Z9 19
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1066-5277
J9 J COMPUT BIOL
JI J. Comput. Biol.
PD SEP
PY 2008
VL 15
IS 7
BP 737
EP 754
DI 10.1089/cmb.2007.0130
PG 18
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 351TW
UT WOS:000259449800007
PM 18662104
ER
PT J
AU Mabley, JG
Pacher, P
Murthy, KGK
Williams, W
Southan, GJ
Salzman, AL
Szabo, C
AF Mabley, Jon G.
Pacher, Pal
Murthy, Kanneganti G. K.
Williams, William
Southan, Garry J.
Salzman, Andrew L.
Szabo, Csaba
TI The novel inosine analogue, INO-2002, protects against diabetes
development in multiple low-dose streptozotocin and non-obese diabetic
mouse models of type I diabetes
SO JOURNAL OF ENDOCRINOLOGY
LA English
DT Article
ID POLY(ADP-RIBOSE) POLYMERASE ACTIVATION; BETA-CELL DESTRUCTION;
ADP-RIBOSE POLYMERASE; NITRIC-OXIDE SYNTHASE; NOD MICE;
MYCOPHENOLATE-MOFETIL; DOWN-REGULATION; REPERFUSION INJURY; RADICAL
SCAVENGER; IMPROVES SURVIVAL
AB Endogenous purines including inosine have been shown to exert immunomodulatory and anti-inflammatory effects in a variety of disease models. The dosage of inosine required for protection is very high because of the rapid metabolism of inosine in vivo. The aim of this study was to determine whether a metabolic-resistant purine analogue, INO-2002, exerts anti-inflammatory effects in two animal models of type I diabetes. Type I diabetes was induced chemically with streptozotocin or genetically using the non-obese diabetic (NOD) female mouse model. Mice were treated with INO-2002 or inosine as required at 30, 100, or 200 mg/kg per day, while blood glucose and diabetes incidence were monitored. The effect of INO-2002 on the pancreatic cytokine profile was also determined. INO-2002 reduced both the hyperglycaemia and incidence of diabetes in both streptozotocin-induced and spontaneous diabetes in NOD mice. INO-2002 proved to be more effective in protecting against diabetes than the naturally occurring purine, inosine, when administered at the same dose. INO-2002 treatment decreased pancreatic levels of interleukin (IL)-12 and tumour necrosis factor-alpha, while increasing levels of IL-4 and IL-10. INO-2002 also reduced pancreatic levels of the chemokine MIP-1 alpha. The inosine analogue, INO-2002, was protected more effectively than the naturally occurring purine, inosine, against development of diabetes in two separate animal models. INO-2002 exerts protective effects by changing the pancreatic cytokine expression from a destructive Th1 to a protective Th2 profile. The use of analogues of inosine such as INO-2002 should be considered as a potential preventative therapy in individuals susceptible to developing type I diabetes.
C1 [Mabley, Jon G.] Univ Brighton, Sch Pharm & Biomol Sci, Brighton BN2 4GJ, E Sussex, England.
[Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Murthy, Kanneganti G. K.; Williams, William; Southan, Garry J.; Salzman, Andrew L.] Inotek Pharmaceut Corp, Beverly, MA 01915 USA.
[Szabo, Csaba] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA.
RP Mabley, JG (reprint author), Univ Brighton, Sch Pharm & Biomol Sci, Cockcroft Bldg,Lewes Rd, Brighton BN2 4GJ, E Sussex, England.
EM j.g.mabley@brighton.ac.uk
RI Mabley, Jon/D-2296-2010; Pacher, Pal/B-6378-2008
OI Pacher, Pal/0000-0001-7036-8108
FU National Institutes of Health [1R43 DK59676]
FX This study was supported by a grant from the National Institutes of
Health (1R43 DK59676) to G J S.
NR 51
TC 6
Z9 6
U1 0
U2 1
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 0022-0795
EI 1479-6805
J9 J ENDOCRINOL
JI J. Endocrinol.
PD SEP
PY 2008
VL 198
IS 3
BP 581
EP 589
DI 10.1677/JOE-07-0511
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 365OL
UT WOS:000260416500014
PM 18562629
ER
PT J
AU Cooper, R
Hardy, R
Guralnik, J
Richards, M
Kuh, D
AF Cooper, R.
Hardy, R.
Guralnik, J.
Richards, M.
Kuh, D.
TI Cognitive function across life and mid-life physical performance:
Findings from a British birth cohort study
SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH
LA English
DT Meeting Abstract
C1 [Cooper, R.; Hardy, R.; Richards, M.; Kuh, D.] UCL Royal Free & Univ Coll Med Sch, Dept Epidemiol & Publ Hlth, MRC Unit Lifelong Hlth Ageing, London, England.
[Guralnik, J.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0143-005X
J9 J EPIDEMIOL COMMUN H
JI J. Epidemiol. Community Health
PD SEP
PY 2008
VL 62
MA 021
BP A8
EP A8
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 343CG
UT WOS:000258829600022
ER
PT J
AU Tom, SE
Kuh, D
Guralink, JM
Mishra, G
AF Tom, S. E.
Kuh, D.
Guralink, J. M.
Mishra, G.
TI Patterns in trouble sleeping among women at midlife: Results from a
British prospective cohort study
SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH
LA English
DT Meeting Abstract
C1 [Tom, S. E.; Guralink, J. M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD USA.
[Tom, S. E.; Kuh, D.; Mishra, G.] UCL Royal Free & Univ Coll Med Sch, MRC Unit Lifelong Hlth & Ageing, London, England.
RI Mishra, Gita/F-8052-2011
OI Mishra, Gita/0000-0001-9610-5904
NR 0
TC 0
Z9 0
U1 0
U2 0
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0143-005X
J9 J EPIDEMIOL COMMUN H
JI J. Epidemiol. Community Health
PD SEP
PY 2008
VL 62
MA 022
BP A8
EP A9
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 343CG
UT WOS:000258829600023
ER
PT J
AU Takizawa, M
Tolarova, H
Li, Z
Dubois, W
Lim, S
Callen, E
Franco, S
Mosaico, M
Feigenbaum, L
Alt, FW
Nussenzweig, A
Potter, M
Casellas, R
AF Takizawa, Makiko
Tolarova, Helena
Li, Zhiyu
Dubois, Wendy
Lim, Susan
Callen, Elsa
Franco, Sonia
Mosaico, Maria
Feigenbaum, Lionel
Alt, Frederick W.
Nussenzweig, Andre
Potter, Michael
Casellas, Rafael
TI AID expression levels determine the extent of cMyc oncogenic
translocations and the incidence of B cell tumor development
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID CLASS-SWITCH RECOMBINATION; INDUCED CYTIDINE DEAMINASE;
ACTIVATION-INDUCED DEAMINASE; SOMATIC HYPERMUTATION; DNA BREAKS;
CHROMOSOME BREAKS; PATHWAY; REGION; MICRORNA-155; MECHANISMS
AB Immunoglobulin (Ig) isotype switching is a recombination event that changes the constant domain of antibody genes and is catalyzed by activation-induced cytidine deaminase (AID). Upon recruitment to Ig genes, AID deaminates cytidines at switch (S) recombination sites, leading to the formation of DNA breaks. In addition to their role in isotype switching, AID-induced lesions promote Igh-cMyc chromosomal translocations and tumor development. However, cMyc translocations are also present in lymphocytes from healthy humans and mice, and thus, it remains unclear whether AID directly contributes to the dynamics of B cell transformation. Using a plasmacytoma mouse model, we show that AID(+/-) mice have reduced AID expression levels and display haploinsufficiency both in the context of isotype switching and plasmacytomagenesis. At the Ig loci, AID(+/-) lymphocytes show impaired intra- and inter-switch recombination, and a substantial decrease in the frequency of S mutations and chromosomal breaks. In AID(+/-) mice, these defects correlate with a marked decrease in the accumulation of B cell clones carrying Igh-cMyc translocations during tumor latency. These results thus provide a causality link between the extent of AID enzymatic activity, the number of emerging Igh-cMyc-translocated cells, and the incidence of B cell transformation.
C1 [Dubois, Wendy; Potter, Michael] NCI, Genet Lab, NIH, Bethesda, MD 20892 USA.
[Takizawa, Makiko; Tolarova, Helena; Li, Zhiyu; Lim, Susan; Casellas, Rafael] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Franco, Sonia; Alt, Frederick W.] Childrens Hosp, CBR Inst Biomed Res, Boston, MA 02115 USA.
[Franco, Sonia; Alt, Frederick W.] Howard Hughes Med Inst, Boston, MA 02115 USA.
[Mosaico, Maria; Feigenbaum, Lionel] NCI, Lab Anim Sci Program, SAIC, NIH, Frederick, MD 21702 USA.
RP Potter, M (reprint author), NCI, Genet Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM potter@helix.nih.gov; casellar@mail.nih.gov
FU NIAMS; NCI; NIH
FX This research was supported in part by the Intramural Research Program
of NIAMS and NCI of the NIH.
NR 35
TC 90
Z9 93
U1 0
U2 3
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD SEP 1
PY 2008
VL 205
IS 9
BP 1949
EP 1957
DI 10.1084/jem.20081007
PG 9
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 354RI
UT WOS:000259656300002
PM 18678733
ER
PT J
AU Andersson, J
Tran, DQ
Pesu, M
Davidson, TS
Ramsey, H
O'Shea, JJ
Shevach, EM
AF Andersson, John
Tran, Dat Q.
Pesu, Marko
Davidson, Todd S.
Ramsey, Heather
O'Shea, John J.
Shevach, Ethan M.
TI CD4(+)FoxP3(+) regulatory T cells confer infectious tolerance in a
TGF-beta-dependent manner
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID TRANSCRIPTION FACTOR FOXP3; GROWTH-FACTOR-BETA; DENDRITIC CELLS; CUTTING
EDGE; INDUCTION; EXPRESSION; MICE; AUTOIMMUNITY; SUPPRESSION; SCURFIN
AB CD4(+)FoxP3(+) regulatory T (T reg) cells comprise a separate lineage of T cells that are essential for maintaining immunological tolerance to self. The molecular mechanism(s) by which T reg cells mediate their suppressive effects remains poorly understood. One molecule that has been extensively studied in T reg cell suppression is transforming growth factor (TGF)-beta, but its importance remains controversial. We found that TGF-beta complexed to latency-associated peptide (LAP) is expressed on the cell surface of activated but not resting T reg cells. T reg cell LAP-TGF-beta plays an important role in the suppression of the proliferation of activated T cells, but it is not required for the suppression of naive T cell activation. More importantly, T reg cell-derived TGF-beta could generate de novo CD4(+)FoxP3(+) T cells in vitro from naive precursors in a cell contact-dependent, antigen-presenting cell-independent and alpha(V) integrin-independent manner. The newly induced CD4(+)FoxP3(+) T cells are suppressive both in vitro and in vivo. Transfer of activated antigen-specific T reg cells with naive antigen-specific responder T cells to normal recipients, followed by immunization, also results in induction of FoxP3 expression in the responder cells. T reg cell-mediated generation of functional CD4(+)FoxP3(+) cells via this TGF-beta-dependent pathway may represent a major mechanism as to how T reg cells maintain tolerance and expand their suppressive abilities.
C1 [Andersson, John; Tran, Dat Q.; Davidson, Todd S.; Ramsey, Heather; Shevach, Ethan M.] NIAID, Immunol Lab, Bethesda, MD 20892 USA.
[Pesu, Marko; O'Shea, John J.] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
RP Shevach, EM (reprint author), NIAID, Immunol Lab, Bldg 10, Bethesda, MD 20892 USA.
EM eshevach@niaid.nih.gov
RI Andersson, John/A-4436-2009; Pesu, marko/L-6344-2013;
OI Andersson, John/0000-0003-2799-6349
FU NIAID Intramural Research Program
FX The NIAID Intramural Research Program has supported this work.
NR 31
TC 172
Z9 179
U1 0
U2 5
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
J9 J EXP MED
JI J. Exp. Med.
PD SEP 1
PY 2008
VL 205
IS 9
BP 1975
EP 1981
DI 10.1084/jem.20080308
PG 7
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 354RI
UT WOS:000259656300005
PM 18710931
ER
PT J
AU Kirk, KL
AF Kirk, Kenneth L.
TI Editorial for special issue of JFC on Biomedicinal Chemistry
SO JOURNAL OF FLUORINE CHEMISTRY
LA English
DT Editorial Material
C1 NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RP Kirk, KL (reprint author), NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM kennethk@bdg8.niddk.nih.gov
FU Intramural NIH HHS [Z01 DK031134-01]
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0022-1139
J9 J FLUORINE CHEM
JI J. Fluor. Chem.
PD SEP
PY 2008
VL 129
IS 9
SI SI
BP 730
EP 730
DI 10.1016/j.jfluchem.2008.07.007
PG 1
WC Chemistry, Inorganic & Nuclear; Chemistry, Organic
SC Chemistry
GA 357ZO
UT WOS:000259886100001
PM 19727326
ER
PT J
AU Kiesewetter, DO
Kramer-Marek, G
Ma, Y
Capala, J
AF Kiesewetter, Dale O.
Kramer-Marek, Gabriela
Ma, Ying
Capala, Jacek
TI Radiolabeling of HER2-specific Affibody (R) molecule with F-18
SO JOURNAL OF FLUORINE CHEMISTRY
LA English
DT Article
DE Fluorine-18; HER2; Breast cancer; Affibody (R) molecule
ID REACTIVE F-18-LABELING AGENT; HER2 EXPRESSION; BREAST-CANCER;
MALIGNANT-TUMORS; TRIS(2-CARBOXYETHYL)PHOSPHINE; MALEIMIDE; PEPTIDES;
PROTEINS; THERAPY; TRACER
AB The presence of human epidermal growth factor type 2 (HER2)on 20-30% of human breast cancer is a prognostic indicator of more rapid disease progression and a therapeutic indicator for anti-HER2 monoclonal antibodies. Because the literature has demonstrated some discordance between primary and metastatic tumors in the same patient for expression of the HER2 marker, we set out to develop an imaging agent that could be used to assess the marker concentration in vivo in an individual patient. The pharmaceutical company Affibody (R) AB has optimized the specificity of Affibody (R) molecules for HER2. Two Affibody" molecules, a 7 kDa and an 8 kDa protein, were designed with a single carboxy terminal cysteine in order to provide a specific location for the purposes of labeling for various types of imaging. We have prepared [(18)F]FBEM utilizing a coupling reaction between [(18)F]fluorobenzoic acid and aminoethylmaleimide. We then optimized the conjugation of this radiolabeled maleimide to the free sulfhydryl of cysteine by incubating at pH 7.4 in phosphate buffered saline containing 0.1% sodium ascorbate. An overall uncorrected yield of radiolabeled Affibody (R) molecule of approximately 10% from [(18)F]fluoride was achieved in a 2 h synthesis. These conjugated Affibody (R) molecules were obtained with a specific activity of 2.51 +/- 0.92 MBq/mu g. Characterization of the product by HPLC-MS Supported the conjugation of [(18)F]FBEM with the Affibody (R) molecule. The radiolabeled Affibody" molecule retained its binding specificity as demonstrated by successful imaging of xenografts expressing HER2. Published by Elsevier B.V.
C1 [Kiesewetter, Dale O.; Ma, Ying] NIBIB, PRG, IR, Positron Emiss Tomog Radiochem Grp, Bethesda, MD 20892 USA.
[Kramer-Marek, Gabriela; Capala, Jacek] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Kiesewetter, DO (reprint author), NIBIB, PRG, IR, Positron Emiss Tomog Radiochem Grp, 10 Ctr Dr,MSC 1180,10-1C401, Bethesda, MD 20892 USA.
EM dk7k@nih.gov
FU NIH; National Cancer Institute (NCI); National Institute of Biomedical
Imaging and Bioengineering (NIBIB); Affibody AB (Sweden)
FX This research was supported in part by the intramural research program
of the NIH, including the National Cancer Institute (NCI) and the
National Institute of Biomedical Imaging and Bioengineering (NIBIB). In
addition, partial support was provided by a co-operative research and
development agreement with Affibody AB (Sweden). The authors acknowledge
the NIH/CC cyclotron facility for isotope production and Dr. Jurgen
Seidel for assistance with the ATLAS. The contents of this publication
do not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government.
NR 24
TC 29
Z9 29
U1 3
U2 8
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0022-1139
J9 J FLUORINE CHEM
JI J. Fluor. Chem.
PD SEP
PY 2008
VL 129
IS 9
SI SI
BP 799
EP 806
DI 10.1016/j.jfluchem.2008.06.021
PG 8
WC Chemistry, Inorganic & Nuclear; Chemistry, Organic
SC Chemistry
GA 357ZO
UT WOS:000259886100009
PM 19727427
ER
PT J
AU Hajduch, J
Cramer, JC
Kirk, KL
AF Hajduch, Jan
Cramer, John C.
Kirk, Kenneth L.
TI An enantioselective synthesis of (S)-4-fluorohistidine
SO JOURNAL OF FLUORINE CHEMISTRY
LA English
DT Article
DE Schollkopf diasteroselective alkylation; Photochemical Schiemann
reaction; Fluoroimidazole; Microwave reaction
ID DIAZONIUM SALTS; PHOTOCHEMISTRY
AB We report a new synthesis of enantiomerically pure (S)-4-fluorohisitidine based on diastereoselective alkylation of MOM-protected 4-fluoro-5-bromomethyl imidazole using the Schollkopf bis-lactim amino acid synthesis. Improvements in procedures for preparation of key intermediates are also described. (S)4-Fluorohisitidine prepared by this new method was identical in all respects to material prepared by previous procedures. Published by Elsevier B.V.
C1 [Hajduch, Jan; Cramer, John C.; Kirk, Kenneth L.] NIDDK, Bioorgan Chem Lab, NIH, DHHS, Bethesda, MD 20892 USA.
RP Kirk, KL (reprint author), NIDDK, Bioorgan Chem Lab, NIH, DHHS, Bethesda, MD 20892 USA.
EM kennethk@bdg8.niddk.nih.gov
FU NIDDK
FX This research was supported by the intramural research funds of NIDDK.
NR 12
TC 3
Z9 3
U1 1
U2 14
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0022-1139
J9 J FLUORINE CHEM
JI J. Fluor. Chem.
PD SEP
PY 2008
VL 129
IS 9
BP 807
EP 810
DI 10.1016/j.jfluchem.2008.04.011
PG 4
WC Chemistry, Inorganic & Nuclear; Chemistry, Organic
SC Chemistry
GA 357ZO
UT WOS:000259886100010
PM 19727329
ER
PT J
AU Fujiwara, T
Yin, B
Jin, MX
Kirk, KL
Takeuchi, Y
AF Fujiwara, Tomoya
Yin, Bin
Jin, Meixiang
Kirk, Kenneth L.
Takeuchi, Yoshio
TI Synthetic studies of 3-(3-fluorooxindol-3-yl)-L-alanine
SO JOURNAL OF FLUORINE CHEMISTRY
LA English
DT Article
DE Epimerization; Fluorooxindole; Hydroxyoxindole; Indole; Oxindole;
Oxindolylalanine; Selectfluor (TM); Tryptophan
ID GROWTH-HORMONE SECRETAGOGUES; TRYPTOPHAN INDOLE-LYASE;
OXINDOLYL-L-ALANINE; SACC. TC 1093; 2-ARYL-2-FLUOROPROPIONIC ACIDS;
PROTEASOME INHIBITORS; PYRIDOXAL-PHOSPHATE; ANALOGS; ALKALOIDS;
2,3-DIHYDRO-L-TRYPTOPHAN
AB Oxidative fluorination of several protected tryptophans 8b-g with Selectfluor (TM) proceeded smoothly in aqueous media to give a diastereomeric mixture of the corresponding 3-fluorooxindoles 9b-g. Attempted deprotection of the 3-fluorooxindoles 9b-g under various conditions did not afford 3-(3-fluorooxindol-3-yl)-L-alanine (6). Reaction of the suitably protected tryptophan derivative 16 with Selectfluor (TM) produced the fluorinated product 17. Simultaneous cleavage of all protective groups of 17 under acidic conditions successfully gave the target compound 6 in excellent yield. (c) 2008 Elsevier B.V. All rights reserved.
C1 [Fujiwara, Tomoya; Yin, Bin; Jin, Meixiang; Takeuchi, Yoshio] Toyama Univ, Grad Sch Med & Pharmaceut Sci Res, Toyama 9300194, Japan.
[Kirk, Kenneth L.] NIDDK, Bioorgan Chem Lab, NIH, DHHS, Bethesda, MD 20892 USA.
RP Fujiwara, T (reprint author), Toyama Univ, Grad Sch Med & Pharmaceut Sci Res, Sugitani 2630, Toyama 9300194, Japan.
EM tfuji@pha.u-toyama.ac.jp
FU NIDDK, NIH
FX KLK acknowledges support from the intramural research funds of NIDDK,
NIH.
NR 38
TC 12
Z9 12
U1 0
U2 4
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0022-1139
J9 J FLUORINE CHEM
JI J. Fluor. Chem.
PD SEP
PY 2008
VL 129
IS 9
BP 829
EP 835
DI 10.1016/j.jfluchem.2008.06.026
PG 7
WC Chemistry, Inorganic & Nuclear; Chemistry, Organic
SC Chemistry
GA 357ZO
UT WOS:000259886100013
PM 19122889
ER
PT J
AU Hruschka, S
Yoshida, S
Kirk, KL
Haufe, G
AF Hruschka, Svenja
Yoshida, Shinichi
Kirk, Kenneth L.
Haufe, Guenter
TI Fluorinated phenylcyclopropylamines Part 6. Effects of electron
withdrawing or donating aryl substituents on the inhibition of tyramine
oxidase from Arthrobacter sp by diastereomeric
2-aryl-2-fluoro-cyclopropylamines
SO JOURNAL OF FLUORINE CHEMISTRY
LA English
DT Article
DE Cyclopropylamines; Fluorine; Monoamine oxidase inhibitors; Microbial
tyramine oxidase; Arthrobacter sp
ID ANTIDEPRESSANT DRUG TRANYLCYPROMINE; DEPENDENT AMINE OXIDASES; CATALYTIC
MECHANISM; MONOAMINE OXIDASES; QUINONE; MODEL; RING; SSAO
AB Diastereomeric arylcyclopropylamines substituted with fluorine in the 2-position and with electron donating or electron withdrawing groups at the aromatic ring were evaluated as inhibitors of microbial tyramine oxidase. The trans-isomers were consistently more potent inhibitors of the enzyme than the cis-isomers. Electron donating substituents increased the potency of tyramine oxidase inhibition, while electron withdrawing substituents decreased the activity. The results obtained are discussed in terms of pK(a) and log D values of the inhibitors as well as the mechanism of action of tranylcypromines and the geometry of the active site of the enzyme. (c) 2008 Elsevier B.V. All rights reserved.
C1 [Hruschka, Svenja; Haufe, Guenter] Univ Munster, Inst Organ Chem, D-48149 Munster, Germany.
[Hruschka, Svenja; Haufe, Guenter] Univ Munster, Int NRW Grad Sch Chem, D-48149 Munster, Germany.
[Yoshida, Shinichi] Tottori Inst Ind Technol, Tottori 6891112, Japan.
[Kirk, Kenneth L.] NIDDK, Bioorgan Chem Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Haufe, G (reprint author), Univ Munster, Inst Organ Chem, Corrensstr 40, D-48149 Munster, Germany.
EM haufe@uni-muenster.de
FU DFG; International NRW Graduate School of Chemistry; Intramural Research
Funds of NIDDK, NIH; Tottoti Prefectural Government, Japan
FX This research was partially supported by the DFG as a contribution from
the Sonderforschungsbereich 424, the International NRW Graduate School
of Chemistry, the Intramural Research Funds of NIDDK, NIH, and the
research grant of Tottoti Prefectural Government, Japan.
NR 28
TC 5
Z9 5
U1 0
U2 2
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0022-1139
J9 J FLUORINE CHEM
JI J. Fluor. Chem.
PD SEP
PY 2008
VL 129
IS 9
SI SI
BP 875
EP 880
DI 10.1016/j.jfluchem.2008.06.023
PG 6
WC Chemistry, Inorganic & Nuclear; Chemistry, Organic
SC Chemistry
GA 357ZO
UT WOS:000259886100018
PM 19727324
ER
PT J
AU Marotta, F
Yadav, H
Gumaste, U
Signorelli, P
Minelli, E
Marandola, P
AF Marotta, F.
Yadav, H.
Gumaste, U.
Signorelli, P.
Minelli, E.
Marandola, P.
TI Protective nutragenomic effect of a phytocompound on oxidative stress
and DNA fragmentation against paracetamol-induced liver damage
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Meeting Abstract
C1 [Marotta, F.; Signorelli, P.; Marandola, P.] GAIA Age Management Fdn, Nutraceut Nutrigenom Unit, Pavia, Italy.
[Yadav, H.] NIDDK, NIH, Bethesda, MD USA.
[Gumaste, U.] Agharkar Res Inst, Pune, Maharashtra, India.
[Marotta, F.; Minelli, E.] Univ Milan, WHO, Cntr Biotech & Nat Med, I-20122 Milan, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 0815-9319
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD SEP
PY 2008
VL 23
SU 5
BP A48
EP A48
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 350OD
UT WOS:000259361200165
ER
PT J
AU Kronman, AC
Ash, AS
Freund, KM
Hanchate, A
Emanuel, EJ
AF Kronman, Andrea C.
Ash, Arlene S.
Freund, Karen M.
Hanchate, Amresh
Emanuel, Ezekiel J.
TI Can primary care visits reduce hospital utilization among medicare
beneficiaries at the end of life?
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE end-of-life care; health services research; primary care
AB BACKGROUND: Medical care at the end of life is often expensive and ineffective.
OBJECTIVE: To explore associations between primary care and hospital utilization at the end of life.
DESIGN: Retrospective analysis of Medicare data. We measured hospital utilization during the final 6 months of life and the number of primary care physician visits in the 12 preceding months. Multivariate cluster analysis adjusted for the effects of demographics, comorbidities, and geography in end-of-life healthcare utilization.
SUBJECTS: National random sample of 78,356 Medicare beneficiaries aged 66+ who died in 2001. Non-whites were over-sampled. All subjects with complete Medicare data for 18 months prior to death were retained, except for those in the End Stage Renal Disease program.
MEASUREMENTS: Hospital days, costs, in-hospital death, and presence of two types of preventable hospital admissions (Ambulatory Care Sensitive Conditions) during the final 6 months of life.
RESULTS: Sample characteristics: 38% had 0 primary care visits; 22%, 1-2; 19%, 3-5; 10%, 6-8; and 11%, 9+ visits. More primary care visits in the preceding year were associated with fewer hospital days at end of life (15.3 days for those with no primary care visits vs. 13.4 for those with >= 9 visits, P < 0.001), lower costs ($24,400 vs. $23,400, P < 0.05), less in-hospital death (44% vs. 40%, P < 0.01), and fewer preventable hospitalizations for those with congestive heart failure (adjusted odds ratio, aOR = 0.82, P < 0.001) and chronic obstructive pulmonary disease (aOR = 0.81, P = 0.02).
CONCLUSIONS: Primary care visits in the preceding year are associated with less, and less costly, end-of-life hospital utilization. Increased primary care access for Medicare beneficiaries may decrease costs and improve quality at the end of life.
C1 [Kronman, Andrea C.; Ash, Arlene S.; Freund, Karen M.; Hanchate, Amresh] Boston Univ, Med Ctr, Evans Dept Med, Gen Internal Med Sect,Womens Hlth & Hlth Care Res, Boston, MA 02118 USA.
[Kronman, Andrea C.; Ash, Arlene S.; Freund, Karen M.; Hanchate, Amresh] Boston Univ, Med Ctr, Womens Interdisciplinary Res Ctr, Boston, MA 02118 USA.
[Emanuel, Ezekiel J.] NIH, Dept Clin Bioeth, Warren Magnuson Clin Ctr, Bethesda, MD 20892 USA.
RP Kronman, AC (reprint author), Boston Univ, Med Ctr, Evans Dept Med, Gen Internal Med Sect,Womens Hlth & Hlth Care Res, 801 Massachusetts Ave,Suite 470, Boston, MA 02118 USA.
EM Andrea.Kronman@bmc.org
OI Hanchate, Amresh/0000-0002-7038-4463; Freund, Karen/0000-0002-9049-5574
FU Mentored Clinical Scientist Development Program Award (Building
Interdisciplinary Careers in Women's Health Research); National
Institutes of Health [K12 HD04344, T32 HP 10028]; National Institutes of
Health
FX This work was presented at the Academy Health Annual Research Meeting in
Orlando, FL, on 4 June 2006 and received the Mack Lipkin Sr. Associate
Member Award for Outstanding Scientific Presentation at the National
Meeting for the Society of General Internal Medicine in Los Angeles, CA,
on 26 April 2006. The authors thank Drs. Jim Burgess and John Pagliaro
for their support with manuscript preparation, and Jenn Fonda for
support with computer programming. Dr. Kronman is supported by a
Mentored Clinical Scientist Development Program Award ( Building
Interdisciplinary Careers in Women's Health Research) from the National
Institutes of Health (K12 HD04344, Karen Freund, Principal
Investigator). Dr. Kronman was supported by an Institutional National
Research Service Award from the National Institutes of Health (T32 HP
10028, Rob Friedman, Principal Investigator) when this research was
performed.
NR 37
TC 28
Z9 29
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD SEP
PY 2008
VL 23
IS 9
BP 1330
EP 1335
DI 10.1007/s11606-008-0638-5
PG 6
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 339LJ
UT WOS:000258578800006
PM 18506545
ER
PT J
AU Tilburt, JC
Emanuel, EJ
Miller, FG
AF Tilburt, Jon C.
Emanuel, Ezekiel J.
Miller, Franklin G.
TI Does the evidence make a difference in consumer behavior? Sales of
supplements before and after publication of negative research results
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE complementary therapies; health behaviors; dietary supplements
ID RANDOMIZED CONTROLLED-TRIAL; ST-JOHNS-WORT; BENIGN PROSTATIC
HYPERPLASIA; VITAMIN-E; HYPERICUM EXTRACT; MAJOR DEPRESSION;
CLINICAL-TRIALS; SAW PALMETTO; DOUBLE-BLIND; EFFICACY
AB OBJECTIVE: To determine if the public consumption of herbs, vitamins, and supplements changes in light of emerging negative evidence.
METHODS: We describe trends in annual US sales of five major supplements in temporal relationship with publication of research from three top US general medical journals published from 2001 through early 2006 and the number of news citations associated with each publication using the Lexus-Nexis database.
RESULTS: In four of five supplements (St. John's wort, echinacea, saw palmetto, and glucosamine), there was little or no change in sales trends after publication of research results. In one instance, however, dramatic changes in sales occurred following publication of data suggesting harm from high doses of vitamin E.
CONCLUSION: Results reporting harm may have a greater impact on supplement consumption than those demonstrating lack of efficacy. In order for clinical trial evidence to influence public behavior, there needs to be a better understanding of the factors that influence the translation of evidence in the public.
C1 [Tilburt, Jon C.; Emanuel, Ezekiel J.; Miller, Franklin G.] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
[Tilburt, Jon C.] Mayo Clin, Div Gen Internal Med, Rochester, MN USA.
[Tilburt, Jon C.] Mayo Clin, Program Professionalism & Bioeth, Rochester, MN USA.
RP Tilburt, JC (reprint author), NIH, Dept Bioeth, Bldg 10, Bethesda, MD 20892 USA.
EM tilburt.jon@mayo.edu
FU Department of Bioethics, National Institutes of Health, Bethesda
FX Funding for this research was provided by the Department of Bioethics,
National Institutes of Health, Bethesda, MD. Statistical support was
provided by Joel Verter and Heidi Christ-Schmidt at Statistic
Collaborative, Inc., Washington, D. C.
NR 28
TC 14
Z9 14
U1 1
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD SEP
PY 2008
VL 23
IS 9
BP 1495
EP 1498
DI 10.1007/s11606-008-0704-z
PG 4
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 339LJ
UT WOS:000258578800033
PM 18618194
ER
PT J
AU Hoelzer, K
Shackelton, LA
Parrish, CR
Holmes, EC
AF Hoelzer, Karin
Shackelton, Laura A.
Parrish, Colin R.
Holmes, Edward C.
TI Phylogenetic analysis reveals the emergence, evolution and dispersal of
carnivore parvoviruses
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Article
ID FELINE PANLEUKOPENIA VIRUS; CANINE TRANSFERRIN RECEPTOR;
POLYMERASE-CHAIN-REACTION; HOST-RANGE; MINUTE VIRUS; MURINE CELLS; RNA
VIRUS; NS2; MICE; DNA
AB Canine parvovirus (CPV), first recognized as an emerging virus of dogs in 1978, resulted from a successful cross-species transmission. CPV emerged from the endemic feline panleukopenia virus (FPV), or from a closely related parvovirus of another host. Here we refine our current understanding of the evolution and population dynamics of FPV and CPV. By analysing nearly full-length viral sequences we show that the majority of substitutions distinguishing CPV from FPV are located in the capsid protein gene, and that this gene is under positive selection in CPV, resulting in a significantly elevated rate of molecular evolution. This provides strong phylogenetic, evidence for a prominent role of the viral capsid in host adaptation. In addition, an analysis of the population dynamics of more recent CPV reveals, on a global scale, a strongly spatially subdivided CPV population with little viral movement among countries and a relatively constant population size. Such limited viral migration contrasts with the global spread of the virus observed during the early phase of the CPV pandemic, but corresponds to the more endemic nature of current CPV infections.
C1 [Hoelzer, Karin; Parrish, Colin R.] Cornell Univ, Dept Microbiol & Immunol, Coll Vet Med, Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
[Shackelton, Laura A.; Holmes, Edward C.] Penn State Univ, Ctr Infect Dis Dynam, Dept Biol, Mueller Lab, University Pk, PA 16802 USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Hoelzer, K (reprint author), Cornell Univ, Dept Microbiol & Immunol, Coll Vet Med, Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
EM kh294@cornell.edu
RI Hoelzer, Karin/A-8230-2010;
OI Holmes, Edward/0000-0001-9596-3552
FU NIH [GM080533, AI028385]
FX Leland E. Carmichael and Edward Dubovi provided clinical samples, and
Wendy S. Weichert and Nell Bond provided excellent technical support.
Christian Nelson provided valuable help with the three-dimensional
representation of the positively selected capsid residues. This work was
supported by NIH grants GM080533 to E. C. H. and AI028385 to C. R. P.
NR 45
TC 72
Z9 78
U1 0
U2 10
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
J9 J GEN VIROL
JI J. Gen. Virol.
PD SEP
PY 2008
VL 89
BP 2280
EP 2289
DI 10.1099/vir.0.2008/002055-0
PN 9
PG 10
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 349MT
UT WOS:000259285600025
PM 18753238
ER
PT J
AU Marques, R
Antunes, I
Eksmond, U
Stoye, J
Hasenkrug, K
Kassiotis, G
AF Marques, Rute
Antunes, Ines
Eksmond, Urszula
Stoye, Jonathan
Hasenkrug, Kim
Kassiotis, George
TI B lymphocyte activation by coinfection prevents immune control of Friend
virus infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID DEHYDROGENASE-ELEVATING VIRUS; MURINE LEUKEMIA VIRUSES; FOCUS-FORMING
VIRUS; INDUCED ERYTHROLEUKEMIA; POLYCLONAL ACTIVATION; RETROVIRAL
INFECTION; VIRAL-INFECTIONS; RESISTANT MICE; SENDAI VIRUS; T-CELLS
AB Although the adaptive immune response almost invariably fails to completely eliminate retroviral infections, it can exert significant protection from disease and long-term control of viral replication. Friend virus (FV), a mouse retrovirus, causes persistent infection in all strains of mice and erythroleukaemia in susceptible strains, the course of which can be strongly influenced by both genetic and extrinsic factors. In this study we examine the impact of coinfection on the requirements for immune control of FV infection. We show that congenic C57BL/6 mice, in which the introduction of an allele of the Friend virus susceptibility 2 gene provides the potential for FV-induced leukemia development, effectively resist FV infection, and both T cell- and Ab-dependent mechanisms contribute to their resistance. However, we further demonstrate that coinfection with lactate dehydrogenase-elevating virus (LDV) renders these otherwise immunocompetent mice highly susceptible to FV infection and subsequent disease. The presence of LDV delays induction of FV-specific neutralizing Abs and counteracts the protective contribution of adaptive immunity. Importantly, the disease-enhancing effect of LDV coinfection requires the presence of a polyclonal B cell repertoire and is reproduced by direct polyclonal B cell activation. Thus, immune activation by coinfecting pathogens or their product's can contribute to the pathogenicity of retroviral infection.
C1 [Marques, Rute; Antunes, Ines; Eksmond, Urszula; Kassiotis, George] Natl Inst Med Res, MRC, Div Immunoregulat, London NW7 1AA, England.
[Stoye, Jonathan] Natl Inst Med Res, MRC, Div Virol, London NW7 1AA, England.
[Hasenkrug, Kim] NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, NIH, Hamilton, MT 59840 USA.
RP Kassiotis, G (reprint author), Natl Inst Med Res, MRC, Div Immunoregulat, Ridgeway,Mill Hill, London NW7 1AA, England.
EM gkassio@nimr.mrc.ac.uk
FU U.K.'s Medical Research Council; Portuguese Foundation of Science and
Technology [SFRH/BD/15208/2004]
FX This work was supported by the U.K.'s Medical Research Council and the
Portuguese Foundation of Science and Technology (SFRH/BD/15208/2004 to
I.A.).
NR 59
TC 23
Z9 25
U1 0
U2 0
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD SEP 1
PY 2008
VL 181
IS 5
BP 3432
EP 3440
PG 9
WC Immunology
SC Immunology
GA 352QJ
UT WOS:000259511800053
PM 18714015
ER
PT J
AU Permar, SR
Kang, HH
Carville, A
Mansfield, KG
Gelman, RS
Rao, SS
Whitney, JB
Letvin, NL
AF Permar, Sallie R.
Kang, Helen H.
Carville, Angela
Mansfield, Keith G.
Gelman, Rebecca S.
Rao, Srinivas S.
Whitney, James B.
Letvin, Norman L.
TI Potent simian immunodeficiency virus-specific cellular immune responses
in the breast milk of simian immunodeficiency virus-infected, lactating
rhesus monkeys
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TO-CHILD TRANSMISSION; LYMPHOCYTE-RESPONSES; HUMAN COLOSTRUM;
HIV-1-INFECTED WOMEN; HIV TRANSMISSION; DENDRITIC CELLS; POOLED
ANALYSIS; MACACA-MULATTA; TYPE-1; MASTITIS
AB Breast milk transmission of HIV is a leading cause of infant HIV/AIDS in the developing world. Remarkably, only a small minority of breastfeeding infants born to HIV-infected mothers contract HIV via breast milk exposure, raising the possibility that immune factors in the breast milk confer protection to the infants who remain uninfected. To model HIV-specific immunity in breast milk, lactation was pharmacologically induced in Mamu-A*01(+) female rhesus monkeys. The composition of lymphocyte subsets in hormone-induced lactation breast milk was found to be similar to that in natural lactation breast milk. Hormone-induced lactating monkeys were inoculated i.v. with SIVmac251 and CD8(+) T lymphocytes specific for two immunodominant SIV epitopes, Gag p11C and Tat TL8, and SIV viral load were monitored in peripheral blood and breast milk during acute infection. The breast milk viral load was 1-2 logs lower than plasma viral load through peak and set point of viremia. Surprisingly, whereas the kinetics of the SIV-specific cellular immunity in breast milk mirrored that of the blood, the peak magnitude of the SIV-specific CD8(+) T lymphocyte response in breast milk was more than twice as high as the cellular immune response in the blood. Furthermore, the appearance of the SIV-specific CD8(+) T lymphocyte response in breast milk was associated with a reduction in breast milk viral load, and this response remained higher than that in the blood after viral set point. This robust viral-specific cellular immune response in breast milk may contribute to control of breast milk virus replication.
C1 [Permar, Sallie R.; Kang, Helen H.; Whitney, James B.; Letvin, Norman L.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Viral Pathogenesis, Boston, MA 02115 USA.
[Permar, Sallie R.] Harvard Univ, Sch Med, Div Infect Dis, Childrens Hosp Boston, Boston, MA 02115 USA.
[Carville, Angela; Mansfield, Keith G.] Harvard Univ, Sch Med, New England Reg Primate Res Ctr, Southborough, MA 01772 USA.
[Gelman, Rebecca S.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Rao, Srinivas S.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
RP Permar, SR (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Viral Pathogenesis, 330 Brookline Ave,Res E, Boston, MA 02115 USA.
EM sallie.permar@childrens.harvard.edu
FU Center for HIV/AIDS Vaccine Immunology [R01AI067854]; Fred Lovejoy
Research and Education Fund; Children's Hospital House Officer Research
Award; Pediatric Infectious Disease Society/St. Jude Children's Hospital
Basic Science Research Award; Harvard Center for AIDS Research
[P30AI060354]
FX This work was supported by the Center for HIV/AIDS Vaccine Immunology
(to S.R.P. and N.L.L.; R01AI067854), the Fred Lovejoy Research and
Education Fund (to S.R.P.), the Children's Hospital House Officer
Research Award (to S.R.P.), the Pediatric Infectious Disease Society/St.
Jude Children's Hospital Basic Science Research Award (to S.R.P.), and
the Harvard Center for AIDS Research (to R.S.G.: P30AI060354).
NR 55
TC 23
Z9 23
U1 1
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD SEP 1
PY 2008
VL 181
IS 5
BP 3643
EP 3650
PG 8
WC Immunology
SC Immunology
GA 352QJ
UT WOS:000259511800077
PM 18714039
ER
PT J
AU Kutty, G
Maldarelli, F
Achaz, G
Kovacs, JA
AF Kutty, Geetha
Maldarelli, Frank
Achaz, Guillaume
Kovacs, Joseph A.
TI Variation in the major surface glycoprotein genes in Pneumocystis
jirovecii
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; ANTIGENIC VARIATION; EXPRESSION SITE;
TRYPANOSOMA-BRUCEI; CARINII; IDENTIFICATION; MICE; VARIANTS; MULTIPLE;
RECOMBINATION
AB The genome of Pneumocystis, which causes life-threatening pneumonia in immunosuppressed patients, contains a multicopy gene family that encodes the major surface glycoprotein (Msg). Pneumocystis can vary the expressed Msg, presumably as a mechanism to avoid host immune responses. Analysis of 24 msg-gene sequences obtained from a singlehumanisolate of Pneumocystis demonstrated that the sequences segregate into 2 branches. Results of a number of analyses suggest that recombination between msg genes is an important mechanism for generating msg diversity. Intrabranch recombination occurred more frequently than interbranch recombination. Restriction-fragment length polymorphism analysis of human isolates of Pneumocystis demonstrated substantial variation in the repertoire of the msg-gene family, variation that was not observed in laboratory isolates of Pneumocystis in rats or mice; this may be the result of examining outbred versus captive populations. Increased diversity in the Msg repertoire, generated in part by recombination, increases the potential for antigenic variation in this abundant surface protein.
C1 [Kutty, Geetha; Kovacs, Joseph A.] Natl Inst Hlth, Ctr Clin, Dept Crit Care Med, Bethesda, MD USA.
[Maldarelli, Frank] NCI, Natl Inst Hlth, HIV Drug Resistance Program, Frederick, MD 21701 USA.
[Achaz, Guillaume] UMR 7138, Paris, France.
[Achaz, Guillaume] Atelier Bioinformat, Paris, France.
[Achaz, Guillaume] Univ Paris 06, Paris, France.
RP Kovacs, JA (reprint author), Bldg 10,Rm 2C145,MSC 1662, Bethesda, MD 20892 USA.
EM jkovacs@nih.gov
FU Intramural NIH HHS [Z01 BC010819-01, Z01 CL000146-14]
NR 45
TC 20
Z9 20
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD SEP 1
PY 2008
VL 198
IS 5
BP 741
EP 749
DI 10.1086/590433
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 336KW
UT WOS:000258363700017
PM 18627244
ER
PT J
AU Miller, FG
AF Miller, Franklin G.
TI Research on medical records without informed consent
SO JOURNAL OF LAW MEDICINE & ETHICS
LA English
DT Article
ID SELECTION BIAS; INFORMATION; PRIVACY
AB Observational research involving access to personally identifiable data in medical records has often been conducted without informed consent, owing to practical barriers to soliciting consent and concerns about selection bias. Nevertheless, medical records research without informed consent appears to conflict with basic ethical norms relating to clinical research and personal privacy. This article analyzes the scope of these norms and provides an ethical justification for research using personally identifiable medical information without consent.
C1 Natl Inst Hlth, Dept Bioeth, Bethesda, MD 20892 USA.
RP Miller, FG (reprint author), Natl Inst Hlth, Dept Bioeth, Bethesda, MD 20892 USA.
NR 27
TC 21
Z9 21
U1 3
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1073-1105
J9 J LAW MED ETHICS
JI J. Law Med. Ethics
PD FAL
PY 2008
VL 36
IS 3
BP 560
EP +
DI 10.1111/j.1748-720X.2008.304.x
PG 8
WC Ethics; Law; Medical Ethics; Medicine, Legal
SC Social Sciences - Other Topics; Government & Law; Medical Ethics; Legal
Medicine
GA 341AC
UT WOS:000258685100016
PM 18840249
ER
PT J
AU Johnson, TR
Rothenberg, ME
Graham, BS
AF Johnson, Teresa R.
Rothenberg, Marc E.
Graham, Barney S.
TI Pulmonary eosinophilia requires interleukin-5, eotaxin-1, and CD4+T
cells in mice immunized with respiratory syncytial virus G glycoprotein
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE vaccine; pathogenesis; cytokines; chemokines; immunoregulation
ID AIRWAY EPITHELIAL-CELLS; BALB/C MICE; TISSUE EOSINOPHILIA; T-CELLS;
CATIONIC PROTEIN; SUPEROXIDE ANION; RSV CHALLENGE; LUNG-DISEASE;
IFN-GAMMA; INFECTION
AB Severe illness, type 2 cytokine production, and pulmonary eosinophilia are adverse immune responses resulting from respiratory syncytial virus (RSV) challenge of vvGs-immunized mice. We have shown IL-4 and IL-13 activity must be simultaneously inhibited to reduce disease severity. We now address the contributions of IL-5, eotaxin-1, and CD4+ and CD8+ T cells to the induction of disease-enhancing immune responses. Depletion of CD4+ T cells during immunization prevented IL-4, IL-13, and eotaxin-1 production, diminished eosinophilia, and reduced weight loss. Conversely, CD8+ T cell depletion did not decrease eosinophilia, weight loss, or type 2 cytokines but did dramatically reduce mucus production and increase eotaxin production. Anti-IL-5 administration at immunization or challenge significantly decreased pulmonary eosinophilia. Strikingly, there were not concomitant decreases in weight loss. Following RSV challenge eotaxin-1-deficient mice immunized with vvGs exhibited significantly less eosinophilia without decreased weight loss or type 2 cytokine production. We conclude CD4+ T cell production of IL-5 and induction of eotaxin-1 are required for vvGs-induced eosinophilia following RSV challenge, while CD8+ T cells appear to down-regulate eotaxin-1 and mucus production. In summary, we demonstrate that pulmonary eosinophilia 1) is a by-product of memory CD4+ T cell activation, 2) does not necessarily correlate with mucus production, and, most importantly, 3) is not required for the RSV G-induced illness in mice. These findings have important implications for the evaluation of candidate RSV vaccines.
C1 [Johnson, Teresa R.; Graham, Barney S.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Rothenberg, Marc E.] Cincinnati Childrens Hosp, Med Ctr, Dept Pediat, Div Allergy & Immunol, Cincinnati, OH USA.
RP Johnson, TR (reprint author), NIAID, Vaccine Res Ctr, NIH, Bldg 40,Rm 2614,40 Convent Dr,MSC 3017, Bethesda, MD 20892 USA.
EM teresaj@nih.gov
NR 65
TC 14
Z9 15
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD SEP 1
PY 2008
VL 84
IS 3
BP 748
EP 759
DI 10.1189/jlb.0907621
PG 12
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 338RH
UT WOS:000258525500021
PM 18519743
ER
PT J
AU Demar, JC
DiMartino, C
Baca, AW
Lefkowitz, W
Salem, N
AF Demar, James C., Jr.
DiMartino, Carmine
Baca, Adam W.
Lefkowitz, William
Salem, Norman, Jr.
TI Effect of dietary docosahexaenoic acid on biosynthesis of
docosahexaenoic acid from alpha-linolenic acid in young rats
SO JOURNAL OF LIPID RESEARCH
LA English
DT Article
DE essential fatty acids; lipid metabolism; early development; infant
formula composition
ID N-3 FATTY-ACIDS; TERM INFANTS; EICOSAPENTAENOIC ACID; DOCOSAPENTAENOIC
ACID; DEVELOPING BRAIN; VISUAL-ACUITY; PEROXISOMAL RETROCONVERSION;
NUTRITIONAL DEPRIVATION; DELTA-6 DESATURASE; LIVER CONVERSION
AB Docosahexaenoic acid (DHA), a crucial nervous system n-3 PUFA, may be obtained in the diet or synthesized in vivo from dietary alpha-linolenic acid (LNA). We addressed whether DHA synthesis is regulated by the availability of dietary DHA in artificially reared rat pups, during p8 to p28 development. Over 20 days, one group of rat pups was continuously fed deuterium-labeled LNA (d5-LNA) and no other n-3 PUFA (d5-LNA diet), and a second group of rat pups was fed a d5-LNA diet with unlabeled DHA (d5-LNA + DHA diet). The rat pups were then euthanized, and the total amount of deuterium-labeled docosahexaenoic acid (d5-DHA) (synthesized DHA) as well as other n-3 fatty acids present in various body tissues, was quantified. In the d5-LNA 1 DHA group, the presence of dietary DHA led to a marked decrease (3- to 5-fold) in the total amount of d5-DHA that accumulated in all tissues that we examined, except in adipose. Overall, DHA accretion from d5-DHA was generally diminished by availability of dietary preformed DHA, inasmuch as this was found to be the predominant source of tissue DHA. When preformed DHA was unavailable, d5-DHA and unlabeled DHA were preferentially accreted in some tissues along with a net loss of unlabeled DHA from other organs.-DeMar, Jr., J. C., C. DiMartino, A. W. Baca, W. Lefkowitz, and N. Salem, Jr. Effect of dietary docosahexaenoic acid on biosynthesis of docosahexaenoic acid from alpha-linolenic acid in young rats.
C1 [Demar, James C., Jr.; DiMartino, Carmine; Baca, Adam W.; Salem, Norman, Jr.] NIAAA, Sect Nutr Neurosci, Lab Membrane Biochem & Biophys, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Lefkowitz, William] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
RP Salem, N (reprint author), NIAAA, Sect Nutr Neurosci, Lab Membrane Biochem & Biophys, Natl Inst Hlth, Bethesda, MD 20892 USA.
EM nsalem@niaaa.nih.gov
FU Intramural Research Program of the National Institute on Alcohol Abuse
and Alcoholism
FX This project was supported by the Intramural Research Program of the
National Institute on Alcohol Abuse and Alcoholism.
NR 96
TC 23
Z9 25
U1 3
U2 8
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0022-2275
J9 J LIPID RES
JI J. Lipid Res.
PD SEP
PY 2008
VL 49
IS 9
BP 1963
EP 1980
DI 10.1194/jlr.M800117-JLR200
PG 18
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 337YX
UT WOS:000258472500012
PM 18469302
ER
PT J
AU Farias, SE
Basselin, M
Chang, L
Heidenreich, KA
Rapoport, SI
Murphy, RC
AF Farias, Santiago E.
Basselin, Mireille
Chang, Lisa
Heidenreich, Kim A.
Rapoport, Stanley I.
Murphy, Robert C.
TI Formation of eicosanoids, E-2/D-2 isoprostanes, and docosanoids
following decapitation-induced ischemia, measured in
high-energy-microwaved rat brain
SO JOURNAL OF LIPID RESEARCH
LA English
DT Article
DE arachidonic; docosahexaenoic; eicosanoids; docosanoids; isoprostanes;
brain ischemia
ID FREE FATTY-ACIDS; ALPHA-LINOLENIC ACID; DOCOSAHEXAENOIC ACID;
CEREBRAL-ISCHEMIA; ARACHIDONIC-ACID; MOUSE-BRAIN; LIPID-PEROXIDATION;
MASS-SPECTROMETRY; OXIDATIVE STRESS; GENE-EXPRESSION
AB Inflammatory lipid mediators derived from arachidonic acid (AA) and docosahexaenoic acid (DHA) modify the pathophysiology of brain ischemia. The goal of this work was to investigate the formation of eicosanoids and docosanoids generated from AA and DHA, respectively, during no-flow cerebral ischemia. Rats were subjected to head-focused microwave irradiation 5 min following decapitation (complete ischemia) or prior to decapitation (controls). Brain lipids were extracted and analyzed by reverse-phase liquid chromatography-tandem mass spectrometry. After complete ischemia, brain AA, DHA, and docosapentaenoic acid concentrations increased 18-, 5- and 4-fold compared with controls, respectively. Prostaglandin E-2 (PGE(2)) and PGD(2) could not be detected in control microwaved rat brain, suggesting little endogenous PGE(2)/D-2 production in the brain in the absence of experimental manipulation. Concentrations of thromboxane B-2, E-2/D-2-isoprostanes, 5-hydroxyeicosatetraenoic acid (5-HETE), 5-oxo-eicosatetraenoic acid, and 12-HETE were significantly elevated in ischemic brains. In addition, DHA products such as mono-, di- and trihydroxy-DHA were detected in control and ischemic brains. Monohydroxy-DHA, identified as 17-hydroxy-DHA and thought to be the immediate precursor of neuroprotectin D-1, was 6.5-fold higher in ischemic than in control brain. The present study demonstrated increased formation of eicosanoids, E-2/D-2-IsoPs, and docosanoids following cerebral ischemia. A balance of these lipid mediators may mediate immediate events of ischemic injury and recovery.-Farias, S. E., M. Basselin, L. Chang, K. A. Heidenreich, S. I. Rapoport, and R. C. Murphy. Formation of eicosanoids, E-2/D-2 isoprostanes, and docosanoids following decapitation-induced ischemia, measured in high-energy-microwaved rat brain.
C1 [Farias, Santiago E.; Heidenreich, Kim A.; Murphy, Robert C.] Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Aurora, CO 80045 USA.
[Basselin, Mireille; Chang, Lisa; Rapoport, Stanley I.] NIA, Brain Physiol & Metab Sect, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Murphy, RC (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Aurora, CO 80045 USA.
EM Robert.Murphy@uchsc.edu
FU Heart, Lung and Blood Institute; National Institutes of Health
[HL-025785]; General Medical Sciences [GM-069338]; Intramural Research
Program of the National Institute on Aging
FX This work was supported in part by the Heart, Lung and Blood Institute,
National Institutes of Health, Grant HL-025785, and a grant from General
Medical Sciences (GM-069338) (Lipid Maps), as well as by the Intramural
Research Program of the National Institute on Aging, National Institutes
of Health. No author has a conflict of interest or financial interest
with regard to this work.
NR 61
TC 47
Z9 48
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0022-2275
EI 1539-7262
J9 J LIPID RES
JI J. Lipid Res.
PD SEP
PY 2008
VL 49
IS 9
BP 1990
EP 2000
DI 10.1194/jlr.M800200-JLR200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 337YX
UT WOS:000258472500014
PM 18503030
ER
PT J
AU Detsky, JS
Graham, JJ
Vijayaraghavan, R
Biswas, L
Stainsby, JA
Guttman, MA
Wright, GA
Dick, AJ
AF Detsky, Jay S.
Graham, John J.
Vijayaraghavan, Ram
Biswas, Labonny
Stainsby, Jeffrey A.
Guttman, Michael A.
Wright, Graham A.
Dick, Alexander J.
TI Free-breathing, nongated real-time delayed enhancement MRI of myocardial
infarcts: A comparison with conventional delayed enhancement
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE MRI; delayed enhancement; real-time; myocardial infarct; SSFP
ID INVERSION-RECOVERY TRUEFISP; STATE FREE PRECESSION; MAGNETIC-RESONANCE;
CONTRAST
AB Purpose: To compare a free-breathing, nongated, and black-blood real-time delayed enhancement (RT-DE) sequence to the conventional inversion recovery gradient echo (IR-GRE) sequence for delayed enhancement MRI.
Materials and Methods: Twenty-three patients with suspected myocardial infarct (MI) were examined using both the IR-GRE and RT-DE imaging sequences. The sensitivity and specificity of RT-DE for detecting MI, using IR-GRE as the gold standard, was determined. The contrast-to-noise ratios (CNR) between the two techniques were also compared.
Results: RT-DE had a high sensitivity and specificity (94% and 98%, respectively) for identifying MI. The total acquisition time to image the entire left ventricle was significantly shorter using RT-DE than IR-GRE (5.6 +/- 0.9 versus 11.5 +/- 1.9 min). RT-DE had a slightly lower infarct-myocardium CNR but a higher infarct-blood CNR than IR-GRE imaging. Compared with IR-GRE, RT-DE accurately measured total infarct sizes.
Conclusion: RT-DE can be used for delayed enhancement imaging during free-breathing and without cardiac gating.
C1 [Detsky, Jay S.; Biswas, Labonny; Wright, Graham A.; Dick, Alexander J.] Sunnybrook Hlth Sci Ctr, Imaging Res Program, Toronto, ON M4N 3M5, Canada.
[Detsky, Jay S.; Wright, Graham A.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
[Graham, John J.; Vijayaraghavan, Ram; Dick, Alexander J.] Sunnybrook Hlth Sci Ctr, Schulich Heart Program, Toronto, ON M4N 3M5, Canada.
[Stainsby, Jeffrey A.] GE Healthcare, Mississauga, ON, Canada.
[Guttman, Michael A.] NIH, Bethesda, MD 20892 USA.
RP Detsky, JS (reprint author), Sunnybrook Hlth Sci Ctr, Imaging Res Program, S605,2075 Bayview Ave, Toronto, ON M4N 3M5, Canada.
EM jay.detsky@sri.utoronto.ca
FU Canadian Institutes of Health Research Grant [CIHR-MOP-36477]
FX Contract grant sponsor: the Canadian Institutes of Health Research Grant
#CIHR-MOP-36477.
NR 17
TC 5
Z9 5
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1053-1807
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD SEP
PY 2008
VL 28
IS 3
BP 621
EP 625
DI 10.1002/jmri.21505
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 346ZA
UT WOS:000259106900009
PM 18777543
ER
PT J
AU Callahan, R
Smith, GH
AF Callahan, Robert
Smith, Gilbert H.
TI The mouse as a model for mammary tumorigenesis: History and current
aspects
SO JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA
LA English
DT Editorial Material
C1 [Callahan, Robert; Smith, Gilbert H.] NCI, Bethesda, MD 20892 USA.
RP Smith, GH (reprint author), NCI, Bethesda, MD 20892 USA.
EM smithg@mail.nih.gov
NR 0
TC 3
Z9 3
U1 0
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1083-3021
J9 J MAMMARY GLAND BIOL
JI J. Mammary Gland Biol. Neoplasia
PD SEP
PY 2008
VL 13
IS 3
BP 269
EP 269
DI 10.1007/s10911-008-9094-4
PG 1
WC Oncology; Endocrinology & Metabolism; Physiology
SC Oncology; Endocrinology & Metabolism; Physiology
GA 342RZ
UT WOS:000258802500001
PM 18712586
ER
PT J
AU Callahan, R
Smith, GH
AF Callahan, Robert
Smith, Gilbert H.
TI Common integration sites for MMTV in viral induced mouse mammary tumors
SO JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA
LA English
DT Article
DE mammary tumors; cancer; mouse mammary tumor virus
ID HUMAN BREAST-CANCER; POLYMERASE CHAIN-REACTION; TEMPLATE DNA STRANDS;
TRUNCATED INT3 GENE; TRANSGENIC MICE; INSERTIONAL MUTAGENESIS;
EPITHELIAL-CELLS; NOTCH-GENE; GLAND ADENOCARCINOMAS; STEM-CELLS
AB The paradigm of mammary cancer induction by the mouse mammary tumor virus (MMTV) is used to illustrate the body of evidence that supports the hypothesis that mammary epithelial stem/progenitor cells represent targets for oncogenic transformation. It is argued that this is not a special case applicable only to MMTV-induced mammary cancer, because MMTV acts as an environmental mutagen producing random interruptions in the somatic DNA of infected cells by insertion of proviral DNA copies. In addition to disrupting the host genome, the proviral DNA also influences gene expression through its associated enhancer sequences over significant inter-genomic distances. Genes commonly affected by MMTV insertion in multiple individual tumors include, the Wnt, FGF, RSpo gene families as well as eIF3e and Notch4. All of these gene families are known to play essential roles in stem cell maintenance and behavior in a variety of organs. The MMTV-induced mutations accumulate in cells that are long-lived and possess the properties of stem cells, namely, self-renewal and the capacity to produce divergent epithelial progeny through asymmetric division. The evidence shows that epithelial cells with these properties are present in normal mammary glands, may be infected with MMTV, become transformed to produce epithelial hyperplasia through MMTV-induced mutagenesis and progress to frank mammary malignancy. Retroviral marking via MMTV proviral insertion demonstrates that this process progresses from a single mammary epithelial cell that possesses all of the features ascribed to tissue-specific stem cells.
C1 [Smith, Gilbert H.] NCI, Bethesda, MD 20892 USA.
[Callahan, Robert] NCI, Mammary Gland Biol & Tumorigenesis Lab, Bethesda, MD 20892 USA.
RP Smith, GH (reprint author), NCI, Bldg 37 Room 1112A,MSC 4254, Bethesda, MD 20892 USA.
EM gs4d@nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 86
TC 26
Z9 26
U1 0
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1083-3021
J9 J MAMMARY GLAND BIOL
JI J. Mammary Gland Biol. Neoplasia
PD SEP
PY 2008
VL 13
IS 3
BP 309
EP 321
DI 10.1007/s10911-008-9092-6
PG 13
WC Oncology; Endocrinology & Metabolism; Physiology
SC Oncology; Endocrinology & Metabolism; Physiology
GA 342RZ
UT WOS:000258802500006
PM 18709449
ER
PT J
AU Winter, SF
Hunter, KW
AF Winter, Scott F.
Hunter, Kent W.
TI Mouse modifier genes in mammary tumorigenesis and metastasis
SO JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA
LA English
DT Article
DE breast cancer; mouse models; metastasis; genetics; polymorphism;
quantitative trait loci
ID BREAST-CANCER METASTASIS; PEUTZ-JEGHERS-SYNDROME; TUMOR PROGRESSION;
GLAND DEVELOPMENT; COWDEN DISEASE; SUSCEPTIBILITY; MUTATIONS; BRCA1;
RISK; DISSEMINATION
AB Tumorigenesis and metastasis are complex multistep processes. In addition to the numerous somatic mutations that facilitate cancer progression, there is abundant evidence that an individual's genetic background not only contributes to overall cancer risk, but also specifically influences metastatic potential. The handful of human susceptibility genes that have been identified thus far do not fully account for hereditary cancer risk, and the discovery of additional susceptibility loci using population based studies is complex, time-consuming and expensive. Therefore, we and others have used a variety of mouse models to identify novel candidate susceptibility genes. Here we review how these mouse models have contributed to our understanding of the role of genetic background in modifying tumorigenesis and metastasis susceptibility.
C1 [Winter, Scott F.; Hunter, Kent W.] NCI, Lab Canc Biol & Genet, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Hunter, KW (reprint author), 37 Convent Dr,Rm 5046, Bethesda, MD 20892 USA.
EM hunterk@mail.nih.gov
NR 57
TC 11
Z9 11
U1 0
U2 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1083-3021
J9 J MAMMARY GLAND BIOL
JI J. Mammary Gland Biol. Neoplasia
PD SEP
PY 2008
VL 13
IS 3
BP 337
EP 342
DI 10.1007/s10911-008-9089-1
PG 6
WC Oncology; Endocrinology & Metabolism; Physiology
SC Oncology; Endocrinology & Metabolism; Physiology
GA 342RZ
UT WOS:000258802500008
PM 18661105
ER
PT J
AU Wertheimer, A
Miller, FG
AF Wertheimer, A.
Miller, F. G.
TI Payment for research participation: a coercive offer?
SO JOURNAL OF MEDICAL ETHICS
LA English
DT Article
AB Payment for research participation has raised ethical concerns, especially with respect to its potential for coercion. We argue that characterising payment for research participation as coercive is misguided, because offers of benefit cannot constitute coercion. In this article we analyse the concept of coercion, refute mistaken conceptions of coercion and explain why the offer of payment for research participation is never coercive but in some cases may produce undue inducement.
C1 [Wertheimer, A.; Miller, F. G.] NCI, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Miller, FG (reprint author), NCI, Dept Bioeth, Ctr Clin, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM fmiller@nih.gov
NR 13
TC 44
Z9 44
U1 1
U2 3
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0306-6800
J9 J MED ETHICS
JI J. Med. Ethics
PD SEP 1
PY 2008
VL 34
IS 5
BP 389
EP 392
DI 10.1136/jme.2007.021857
PG 4
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA 294PS
UT WOS:000255418600019
PM 18448723
ER
PT J
AU Resnick, DB
AF Resnick, D. B.
TI Increasing the amount of payment to research subjects
SO JOURNAL OF MEDICAL ETHICS
LA English
DT Article
AB This article discusses some ethical issues that can arise when researchers decide to increase the amount of payment offered to research subjects to boost enrollment. Would increasing the amount of payment be unfair to subjects who have already consented to participate in the study? This article considers how five different models of payment-the free market model, the wage payment model, the reimbursement model, the appreciation model, and the fair benefits model-would approach this issue. The article also considers several practical problems related to changing the amount of payment, including determining whether there is enough money in the budget to offer additional payments to subjects who have already enrolled, ascertaining how difficult it will be to re-contact subjects, and developing a plan of action for responding to subjects who find out they are receiving less money and demand an explanation.
C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Resnick, DB (reprint author), NIEHS, NIH, Box 12233,NH06, Res Triangle Pk, NC 27709 USA.
EM resnikd@niehs.nih.gov
FU NIEHS/NIH
FX This research was supported by the intramural programme of the
NIEHS/NIH. It does not represent the views of the NIEHS or NIH. I am a
grateful to C Grady and an anonymous reviewer for helpful comments.
NR 16
TC 5
Z9 5
U1 1
U2 2
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0306-6800
J9 J MED ETHICS
JI J. Med. Ethics
PD SEP
PY 2008
VL 34
IS 9
AR e14
DI 10.1136/jme.2007.022699
PG 4
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA 343CE
UT WOS:000258829400031
PM 18757614
ER
PT J
AU Shalowitz, DI
Miller, FG
AF Shalowitz, D. I.
Miller, F. G.
TI The search for clarity in communicating research results to study
participants
SO JOURNAL OF MEDICAL ETHICS
LA English
DT Article
ID CLINICAL-RESEARCH; DUTY
AB Current guidelines on investigators' responsibilities to communicate research results to study participants may differ on (1) whether investigators should proactively re-contact participants, (2) the type of results to be offered, (3) the need for clinical relevance before disclosure, and (4) the stage of research at which results should be offered. Lack of consistency on these issues, however, does not undermine investigators' obligation to offer to disclose research results: an obligation rooted firmly in the principle of respect for research participants.
C1 [Shalowitz, D. I.] Univ Michigan, Sch Med, Bioeth Program, Ann Arbor, MI 48109 USA.
[Miller, F. G.] NIH, Dept Bioeth, Bethesda, MD USA.
RP Shalowitz, DI (reprint author), Univ Michigan, Sch Med, Bioeth Program, N17C27 SPC 5429,300 N Ingalls St, Ann Arbor, MI 48109 USA.
EM dshalowi@med.umich.edu
RI Shalowitz, David/A-7432-2009;
OI Shalowitz, David/0000-0002-5189-4687
NR 13
TC 20
Z9 20
U1 0
U2 4
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0306-6800
J9 J MED ETHICS
JI J. Med. Ethics
PD SEP
PY 2008
VL 34
IS 9
AR e17
DI 10.1136/jme.2008.025122
PG 2
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA 343CE
UT WOS:000258829400034
PM 18757617
ER
PT J
AU Muenke, M
AF Muenke, Maximilian
TI Hedgehog signaling and normal and abnormal brain development in humans
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Meeting Abstract
CT British Human Genetics Conference
CY SEP 15-17, 2008
CL Univ York, York, ENGLAND
HO Univ York
C1 [Muenke, Maximilian] NHGRI, Med Genet Branch, Natl Inst Hlth, Dept Hlth & Human Serv, Bethesda, MD USA.
EM mmuenke@nhgri.nih.gov
NR 5
TC 0
Z9 0
U1 0
U2 0
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
J9 J MED GENET
JI J. Med. Genet.
PD SEP
PY 2008
VL 45
BP S15
EP S15
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA 351PM
UT WOS:000259436400003
ER
PT J
AU Murray, JC
Shi, M
Mostowska, A
Mansilla, MA
Christensen, K
Marazita, M
Cooper, M
Lidral, A
Rahimov, F
Suzuki, S
AF Murray, Jeffrey C.
Shi, M.
Mostowska, A.
Mansilla, M. A.
Christensen, K.
Marazita, M.
Cooper, M.
Lidral, A.
Rahimov, F.
Suzuki, S.
TI Cleft Palate
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Meeting Abstract
CT British Human Genetics Conference
CY SEP 15-17, 2008
CL Univ York, York, ENGLAND
HO Univ York
C1 [Murray, Jeffrey C.; Mansilla, M. A.; Rahimov, F.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Shi, M.] NIEHS, Natl Inst Hlth, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Mostowska, A.] Univ Med Sci, Dept Biochem & Mol Biol, PL-60781 Poznan, Poland.
[Christensen, K.] Univ So Denmark, Inst Publ Hlth, DK-5000 Odense, Denmark.
[Marazita, M.; Cooper, M.] Sch Dent Med, Ctr Craniofacial & Dent Genet, Dept Oral Biol, Pittsburgh, PA 15219 USA.
[Lidral, A.] Univ Iowa, Dept Orthodont, Iowa City, IA 52242 USA.
[Suzuki, S.] Aichi Gakuin Univ, Sch Dent, Nagoya, Aichi 4648651, Japan.
EM jeff-murray@uiowa.edu
RI Mostowska, Adrianna/J-6719-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
J9 J MED GENET
JI J. Med. Genet.
PD SEP
PY 2008
VL 45
BP S15
EP S15
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA 351PM
UT WOS:000259436400002
ER
PT J
AU Garcia, GL
Parent, CA
AF Garcia, G. L.
Parent, C. A.
TI Signal relay during chemotaxis
SO JOURNAL OF MICROSCOPY
LA English
DT Article; Proceedings Paper
CT 6th Abercrombie Symposium on Cell Motility
CY SEP 09-12, 2007
CL St Catherines Coll, Oxford, ENGLAND
HO St Catherines Coll
DE cAMP; chemotaxis; Dictyostelium discoideum
ID PROTEIN-MEDIATED ACTIVATION; ADENYLYL-CYCLASE; DICTYOSTELIUM-DISCOIDEUM;
CHEMOATTRACTANT RECEPTOR; CELL POLARITY; CYTOSOLIC REGULATOR;
LEUKOTRIENE B-4; CAMP SYNTHESIS; LEADING-EDGE; LIVING CELLS
AB The ability of cells to migrate in response to external cues, a process known as chemotaxis, is a fundamental phenomenon in biology. It is exhibited by a wide variety of cell types in the context of embryogenesis, angiogenesis, inflammation, wound heating and many other complex physiological processes. Here, we discuss the signals that control the directed migration of the social amoebae Dictyostelium discoideum both as single cells and in the context of group migration. This multi-cellular organism has served as an excellent model system to decipher amoeboid-like leukocyte migration and has played a key role in establishing signalling paradigms in the chemotaxis field. We envision that Dictyostelium will continue to bring forward basic knowledge as we seek to understand the mechanisms regulating group cell migration.
C1 [Garcia, G. L.; Parent, C. A.] NCI, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Parent, CA (reprint author), NCI, Cellular & Mol Biol Lab, NIH, 37 Convent Dr,Bldg 37,Rm 2066, Bethesda, MD 20892 USA.
EM parentc@mail.nih.gov
FU Intramural NIH HHS [Z01 BC010418-08]
NR 62
TC 20
Z9 20
U1 2
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-2720
EI 1365-2818
J9 J MICROSC-OXFORD
JI J. Microsc..
PD SEP
PY 2008
VL 231
IS 3
BP 529
EP 534
DI 10.1111/j.1365-2818.2008.02066.x
PG 6
WC Microscopy
SC Microscopy
GA 354AJ
UT WOS:000259611000020
PM 18755009
ER
PT J
AU Schinkovitz, A
Pro, SM
Main, M
Chen, SN
Jaki, BU
Lankin, DC
Pauli, GF
AF Schinkovitz, Andreas
Pro, Samuel M.
Main, Matthew
Chen, Shao-Nong
Jaki, Birgit U.
Lankin, David C.
Pauli, Guido F.
TI Dynamic nature of the ligustilide complex
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID ANGELICA-SINENSIS; COUNTERCURRENT SEPARATION; MASS-SPECTROMETRY;
CHUANXIONG; CHROMATOGRAPHY; EXTRACTION; PHTHALIDE; PRODUCTS; ROOTS;
VASODILATATION
AB Monomeric phthalides such as Z-ligustilide (1) and Z-butylidenephthalide (2) are major constituents of medicinal plants of the Apiaceae family. While I has been associated with a variety of observed biological effects, it is also known for its instability and rapid chemical degradation. For the purpose of isolating pure 1 and 2, a gentle and rapid two-step countercurrent isolation procedure was developed. From a supercritical CO(2) fluid extract of Angelica sinensis roots, the phthalides were isolated with high GC-MS purities of 99.4% for 1 and 98.9% for 2 and consistently lower qHNMR purities of 98.1 % and 96.4%, respectively. Taking advantage of molarity-based qHNMR methodology, a time-resolved study of the dynamic changes and residual complexity of pure 1 was conducted. GC-MS and (qH)NMR analysis of artificially degraded 1 provided evidence for the phthalide degradation pathways and optimized storing conditions. Parallel qHNMR analysis led to the recognition of variations in time- and process-dependent sample purity and has impact on the overall assessment of time-dependent changes in complex natural products systems. The study underscores the importance of independent quantitative monitoring as a prerequisite for the biological evaluation of labile natural products such as monomeric phthalides.
C1 [Schinkovitz, Andreas; Main, Matthew; Chen, Shao-Nong; Lankin, David C.; Pauli, Guido F.] Univ Illinois, NIH, Ctr Bot Dietary Supplements Res, Chicago, IL 60612 USA.
[Schinkovitz, Andreas; Main, Matthew; Chen, Shao-Nong; Lankin, David C.; Pauli, Guido F.] Univ Illinois, Program Collaborat Res Pharmaceut Sci, Dept Med Chem & Pharmacognosy, Chicago, IL 60612 USA.
[Pro, Samuel M.; Jaki, Birgit U.; Pauli, Guido F.] Univ Illinois, Inst TB Res, Coll Pharm, Chicago, IL 60612 USA.
RP Pauli, GF (reprint author), Univ Illinois, NIH, Ctr Bot Dietary Supplements Res, Chicago, IL 60612 USA.
EM gfp@uic.edu
OI Pauli, Guido/0000-0003-1022-4326
FU the National Center for Complementary and Alternative Medicine (NCCAM)
[P50 AT00 155]; the Office of Dietary Supplements (ODS)
FX Research was supported by grant number P50 AT00 155 from the National
Center for Complementary and Alternative Medicine (NCCAM) and the Office
of Dietary Supplements (ODS).
NR 38
TC 17
Z9 17
U1 0
U2 11
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD SEP
PY 2008
VL 71
IS 9
BP 1604
EP 1611
DI 10.1021/np800137n
PG 8
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA 353NO
UT WOS:000259574900019
PM 18781813
ER
PT J
AU Bokesch, HR
Wamiru, A
Le Grice, SFJ
Beutler, JA
Mckee, TC
McMahon, JB
AF Bokesch, Heidi R.
Wamiru, Antony
Le Grice, Stuart F. J.
Beutler, John A.
McKee, Tawnya C.
McMahon, James B.
TI HIV-1 ribonuclease H inhibitory phenolic glycosides from Eugenia
hyemalis
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID FLAVONOL GLYCOSIDES; GALLOTANNINS; CONSTITUENTS; PLANT
AB Three new galloyl arbutins, hyemalosides A-C (1-3), along with nine known compounds were isolated from the evergreen tree Eugenia hyemalis. The structures of compounds 1-3 were determined by analysis of NMR and MS data. Compounds 1-3 inhibited HIV-1 RNase H in vitro with IC(50) values of 1.46, > 18, and 1.19 mu M, respectively. However, in a XTT-based cell viability assay using the human T-cell line CEM-SS infected with HIV-1(RT), none of the compounds inhibited the cytopathic effect of HIV-1 infection at the highest dose tested (20 mu g/mL).
C1 [Bokesch, Heidi R.; Wamiru, Antony; Beutler, John A.; McKee, Tawnya C.; McMahon, James B.] NCI, Mol Targets Dev Program, Frederick, MD 21702 USA.
[Bokesch, Heidi R.; Wamiru, Antony] NCI, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Le Grice, Stuart F. J.] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
RP Mckee, TC (reprint author), NCI, Mol Targets Dev Program, Frederick, MD 21702 USA.
EM mckee@ncifcrf.gov
RI Beutler, John/B-1141-2009
OI Beutler, John/0000-0002-4646-1924
FU National Cancer Institute; National Institutes of Health [N01-CO-12400];
NIH; Center for Cancer Research
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract N01-CO-12400. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government.
This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research. We
thank N. Trushell (NYBG) and G. Cragg (NPB) for the contract collection,
T. McCloud for extractions, and J. Wilson for the HIV cytopathicity
assay.
NR 16
TC 19
Z9 20
U1 0
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD SEP
PY 2008
VL 71
IS 9
BP 1634
EP 1636
DI 10.1021/np8002518
PG 3
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA 353NO
UT WOS:000259574900026
PM 18763827
ER
PT J
AU Agnati, LF
Baldelli, E
Andreoli, N
Woods, AS
Vellani, V
Marcellino, D
Guidolin, D
Fuxe, K
AF Agnati, L. F.
Baldelli, E.
Andreoli, N.
Woods, A. S.
Vellani, V.
Marcellino, D.
Guidolin, D.
Fuxe, K.
TI On the key role played by altered protein conformation in Parkinson's
disease
SO JOURNAL OF NEURAL TRANSMISSION
LA English
DT Article
DE Parkinson's disease; disordered proteins; protein mosaics
ID CENTRAL-NERVOUS-SYSTEM; ALPHA-SYNUCLEIN; ALZHEIMERS-DISEASE;
AMYLOID-BETA; NEURODEGENERATIVE DISEASES; MITOCHONDRIAL DYSFUNCTION;
INTRINSIC DISORDER; SUBSTANTIA-NIGRA; BRAIN PATHOLOGY; BODY FORMATION
AB On the basis of the previously proposed hierarchic organisation of the central nervous system (CNS) and of its syntropic behaviour, a view of neurodegenerative diseases focusing on the assemblage of abnormal multimeric proteins (pathologic protein mosaics (PMs)) is proposed. Thus, the main focus of the present paper is on Parkinson's disease (PD) as a neurodegenerative disease, which has as crucial feature protein conformational alterations and formation of pathological PMs. Two interconnected cellular dysfunctions are discussed as main pathogenic factors of PD syndromes, namely mitochondrial deficits (i.e. energy failure, especially critical for Substantia Nigra DA neurons) and conformational protein alterations (due to genetic or environmental causes). Conformational protein alterations can trigger pathological phenomena via the loss and/or the gain of new functions. In particular, altered proteins can lead to the formation of abnormal PMs, which can, inter alia, cause distortion of cellular structures, toxic functions and/or formation of improper membrane ion channels. In view of the fact that disordered proteins can easily acquire unwanted conformation, the "disorder index" (DI) for proteins involved in PD has been evaluated. It has been found that both alpha-synuclein and tau-protein have high DI. This datum is in agreement with the observation that these two proteins synergistically promote polymerisation of each other into amyloid fibrils, favouring the formation of Lewy bodies.
C1 [Agnati, L. F.; Baldelli, E.; Andreoli, N.; Vellani, V.] Univ Modena, Dept Biomed Sci, Physiol Sect, I-41100 Modena, Italy.
[Woods, A. S.] Natl Inst Drug Abuse, Behav Neurosci Branch, NIH, DHHS, Baltimore, MD 20817 USA.
[Marcellino, D.; Fuxe, K.] Karolinska Inst, Div Cellular & Mol Neurochem, Dept Neurosci, S-17177 Stockholm, Sweden.
[Guidolin, D.] Univ Padua, Dept Anat & Physiol, I-35121 Padua, Italy.
[Agnati, L. F.] IRCCS, I-30126 Venice, Italy.
RP Agnati, LF (reprint author), Univ Modena, Dept Biomed Sci, Physiol Sect, I-41100 Modena, Italy.
EM luigiagnati@tin.it
RI Vellani, Vittorio/H-1100-2016;
OI Vellani, Vittorio/0000-0002-3581-6654; Fuxe, Kjell/0000-0001-8491-4288;
Guidolin, Diego/0000-0003-2133-3552; Marcellino,
Daniel/0000-0002-4618-7267
FU IRCCS; PRIN
FX The work has been supported by an IRCCS and a PRIN grant. Thanks to
Dott. A. Percesepe (Dep. of Medical Genetic) for suggestions on the
Table.
NR 93
TC 5
Z9 5
U1 0
U2 1
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0300-9564
J9 J NEURAL TRANSM
JI J. Neural Transm.
PD SEP
PY 2008
VL 115
IS 9
BP 1285
EP 1299
DI 10.1007/s00702-008-0072-1
PG 15
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 342BO
UT WOS:000258759800008
PM 18528629
ER
PT J
AU Fadul, CE
Wen, PY
Kim, L
Olson, JJ
AF Fadul, Camilo E.
Wen, Patrick Y.
Kim, Lyndon
Olson, Jeffrey J.
TI Cytotoxic chemotherapeutic management of newly diagnosed glioblastoma
multiforme
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Article
ID HIGH-GRADE GLIOMAS; OPERATED ASTROCYTOMAS GRADE-3;
EXTERNAL-BEAM-RADIOTHERAPY; RESISTANCE IN-VITRO; FACTOR-KAPPA-B;
MALIGNANT GLIOMA; PHASE-II; RADIATION-THERAPY; RANDOMIZED TRIAL;
POSTOPERATIVE TREATMENT
C1 [Olson, Jeffrey J.] Emory Univ, Sch Med, Dept Neurosurg, Atlanta, GA 30322 USA.
[Fadul, Camilo E.] Dartmouth Hitchcock Med Ctr, Norris Cotton Canc Ctr, Neurooncol Program, Dartmouth Med Sch, Lebanon, NH 03766 USA.
[Wen, Patrick Y.] Brigham & Womens Hosp, Ctr Neurooncol, Dana Farber Brigham & Womens Canc Ctr, Boston, MA 02115 USA.
[Wen, Patrick Y.] Brigham & Womens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Kim, Lyndon] NCI, Neurooncol Branch, NIH, Bethesda, MD 20892 USA.
RP Olson, JJ (reprint author), Emory Univ, Sch Med, Dept Neurosurg, 1365B Clifton Rd,NE,Ste 6200, Atlanta, GA 30322 USA.
EM jeffrey.olson@emoryhealthcare.org
RI Mendez, Pedro /J-8955-2016
OI Mendez, Pedro /0000-0001-6713-7907
NR 79
TC 12
Z9 12
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD SEP
PY 2008
VL 89
IS 3
BP 339
EP 357
DI 10.1007/s11060-008-9615-4
PG 19
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 339XW
UT WOS:000258611600006
PM 18712284
ER
PT J
AU Kanungo, J
Zheng, YL
Amin, ND
Pant, HC
AF Kanungo, Jyotshnabala
Zheng, Ya-Li
Amin, Niranjana D.
Pant, Harish C.
TI The Notch signaling inhibitor DAPT down-regulates cdk5 activity and
modulates the distribution of neuronal cytoskeletal proteins
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE cdk5; neurofilament; Notch signaling; tau
ID CYCLIN-DEPENDENT KINASE-5; NEUROFILAMENT AXONAL-TRANSPORT;
GAMMA-SECRETASE INHIBITOR; TAU-PROTEIN; ALZHEIMERS-DISEASE; ACTIVATOR
P35; UP-REGULATION; PHOSPHORYLATION; DIFFERENTIATION; CELLS
AB Notch signaling is critical for the development of the nervous system. Cyclin-dependent kinase 5 (cdk5) is a neuronal kinase involved in neuronal development and phosphorylates a number of neuronal cytoskeletal proteins. To determine the relationship between Notch and cdk5 signaling, we tested the effects of the Notch inhibitor, N-[N-(3,5-difluorophenacetyl)-1-alanyl]-S-phenylglycine t-butyl ester (DAPT) on cdk5 expression, activity and cytoskeletal protein distribution in the rat cortical neurons in primary cultures. Neurons treated with 10 mu M DAPT showed attenuated cdk5 activity in spite of an up-regulation of cdk5 protein level, consistent with a phenomenon reported in the cdk5 transgenic mice. Immunoblot and immunofluorescence analyses showed an increased level of cdk5, but not p35. Phospho-tau and phospho-neurofilament showed a shift from axons to cell bodies in DAPT-treated cells. DAPT-induced attenuation of cdk5 activity was restored by over-expression of p35 indicating that it interacted with cdk5 and up-regulated nascent cdk5 activity. p35 over-expression also rescued DAPT-induced translocation of phospho-tau and phospho-neurofilament. Immunoprecipitation followed by immunoblotting demonstrated that DAPT does not disrupt cdk5 and p35 interaction. Moreover, DAPT up-regulated neurogenin that is negatively regulated by Notch, and down-regulated Hes1, a downstream target of Notch, suggesting that Notch signaling in the cortical neurons was disrupted. Semi-quantitative and quantitative RT-PCR analyses confirmed that DAPT up-regulated cdk5 expression at the transcriptional level. These results establish a link between Notch signaling and cdk5 expression regulating neuronal cytoskeletal protein dynamics.
C1 [Kanungo, Jyotshnabala; Zheng, Ya-Li; Amin, Niranjana D.; Pant, Harish C.] NINDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA.
RP Pant, HC (reprint author), NINDS, Neurochem Lab, NIH, Bldg 49,Rm 2A28,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM panth@ninds.nih.gov
FU Intramural NIH HHS [Z01 NS002725-21]
NR 48
TC 16
Z9 17
U1 2
U2 12
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3042
J9 J NEUROCHEM
JI J. Neurochem.
PD SEP
PY 2008
VL 106
IS 5
BP 2236
EP 2248
DI 10.1111/j.1471-4159.2008.05551.x
PG 13
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 336JL
UT WOS:000258360000022
PM 18662245
ER
PT J
AU Sveinbjornsdottir, S
Sigurdsson, S
Aspelund, T
Kjartansson, O
Eiriksdottir, G
Valtysdottir, B
Lopez, OL
van Buchem, MA
Jonsson, PV
Gudnason, V
Launer, LJ
AF Sveinbjornsdottir, S.
Sigurdsson, S.
Aspelund, T.
Kjartansson, O.
Eiriksdottir, G.
Valtysdottir, B.
Lopez, O. L.
van Buchem, M. A.
Jonsson, P. V.
Gudnason, V.
Launer, L. J.
TI Cerebral microbleeds in the population based AGES-Reykjavik study:
prevalence and location
SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
LA English
DT Article
ID T2-ASTERISK-WEIGHTED MR-IMAGES; INTRACEREBRAL HEMORRHAGE; ASYMPTOMATIC
MICROBLEEDS; AMYLOID ANGIOPATHY; ALZHEIMERS-DISEASE; ISCHEMIC-STROKE;
MICROHEMORRHAGES; ASSOCIATION; LEUKOARAIOSIS; SEVERITY
AB Background and purpose: Incidental foci of signal loss suggestive of cerebral microbleeds (CMBs) are frequent findings on gradient echo T2* weighted MRI (T2* MRI) of patients with haemorrhagic or ischaemic stroke. There are few prevalence data on older populations. This paper reports on the prevalence and location of CMBs in a community based cohort of older men and women (born 1907-1935) who participated in the Age Gene/ Environment Susceptibility (AGES)-Reykjavik Study, a population based cohort study that followed the Reykjavik Study
Methods: As part of the examination, all eligible and consenting cohort members underwent a full brain MRI, and blood was drawn for genotyping. Results are based on the first 1962 men (n= 820) and women (n= 1142), mean age 76 years, with complete MRI and demographic information available.
Results: Evidence of CMBs was found in 218 participants (11.1% (95% CI 9.8% to 12.6%)); men had significantly more CMBs than women (14.4% vs 8.8%; p= 0.0002, age adjusted). The prevalence of CMBs increased with age (p= 0.0001) in both men (p= 0.006) and women (p= 0.007). CMBs were located in the cerebral lobes (70%), the basal ganglia region (10.5%) and infratentorium (18.6%). Having a CMB was significantly associated with a homozygote Apo E epsilon 4 epsilon 4 genotype (p= 0.01).
Conclusion: Cerebral microbleeds are common in older persons. The association with homozygote Apo E epsilon 4 genotype and finding a relative predominance in the parietal lobes might indicate an association with amyloid angiopathy.
C1 [Sveinbjornsdottir, S.; Kjartansson, O.; Jonsson, P. V.] Landspitali Univ Hosp, Dept Neurol, IS-108 Reykjavik, Iceland.
[Sveinbjornsdottir, S.; Kjartansson, O.; Jonsson, P. V.] Landspitali Univ Hosp, Dept Radiol, IS-108 Reykjavik, Iceland.
[Sveinbjornsdottir, S.; Jonsson, P. V.; Gudnason, V.] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Sveinbjornsdottir, S.; Sigurdsson, S.; Aspelund, T.; Kjartansson, O.; Eiriksdottir, G.; Valtysdottir, B.; Jonsson, P. V.; Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
[Lopez, O. L.] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA.
[Lopez, O. L.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15261 USA.
[van Buchem, M. A.] Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands.
[Launer, L. J.] NIA, Bethesda, MD 20892 USA.
RP Sveinbjornsdottir, S (reprint author), Landspitali Univ Hosp, Dept Neurol, C12, IS-108 Reykjavik, Iceland.
EM sigurls@landspitali.is
RI Aspelund, Thor/C-5983-2008; Aspelund, Thor/F-4826-2011; Gudnason,
Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
Vilmundur/0000-0001-5696-0084
FU Intramural NIH HHS; NIA NIH HHS [N01-AG-1-2100]
NR 33
TC 90
Z9 92
U1 0
U2 3
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-3050
J9 J NEUROL NEUROSUR PS
JI J. Neurol. Neurosurg. Psychiatry
PD SEP
PY 2008
VL 79
IS 9
BP 1002
EP 1006
DI 10.1136/jnnp.2007.121913
PG 5
WC Clinical Neurology; Psychiatry; Surgery
SC Neurosciences & Neurology; Psychiatry; Surgery
GA 337ZG
UT WOS:000258473600008
PM 18270235
ER
PT J
AU Isoda, M
Hikosaka, O
AF Isoda, Masaki
Hikosaka, Okihide
TI A neural correlate of motivational conflict in the superior colliculus
of the macaque
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
ID SUPPLEMENTARY EYE FIELD; ANTERIOR CINGULATE CORTEX; MEDIAL
FRONTAL-CORTEX; PRIMATE CAUDATE-NUCLEUS; VISUAL-SEARCH TASK; BASAL
GANGLIA; NEURONAL-ACTIVITY; CORTICOSTRIATAL PROJECTIONS; RESPONSE BIAS;
MONKEY
AB Behavior is controlled by both external instructions and internal motives, but the actions demanded by each may be different. A common consequence of such a conflict is a delay in decision making and subsequent motor responses. It is unknown, however, what neural mechanisms underlie motivational conflict and associated response delay. To answer this question, we recorded single-neuron activity in the superior colliculus (SC) as macaque monkeys performed a visually guided, asymmetrically rewarded saccade task. A peripheral spot of light at one of two opposing positions was illuminated to indicate a saccade target. In a given block of trials, one position was associated with a big reward and the other with a small reward. The big-reward position was alternated across blocks. Behavioral analyses revealed that small-reward trials created a conflict between the instructed saccade to one position and the internally motivated, yet invalid saccade to the opposite position. We found that movement neurons in the SC temporally exhibited bursting activity after the appearance of the small-reward target opposite their movement field. This transient activity predicted the amount of response delay for upcoming saccades. Our data suggest that motivational conflict activates movement neurons in both colliculi, thereby delaying saccade initiation through intercollicular inhibitory interactions.
C1 [Isoda, Masaki] RIKEN, Lab Symbol Cognit Dev, Brain Sci Inst, Wako, Saitama 3510198, Japan.
[Isoda, Masaki; Hikosaka, Okihide] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
RP Isoda, M (reprint author), RIKEN, Lab Symbol Cognit Dev, Brain Sci Inst, 2-1 Hirosawa, Wako, Saitama 3510198, Japan.
EM isodam@brain.riken.jp
FU National Eye Institute
FX This work was supported by the intramural research program of the
National Eye Institute.
NR 60
TC 11
Z9 12
U1 3
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD SEP
PY 2008
VL 100
IS 3
BP 1332
EP 1342
DI 10.1152/jn.90275.2008
PG 11
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 345YR
UT WOS:000259034900017
PM 18596188
ER
PT J
AU Huey, ED
Zahn, R
Krueger, F
Moll, J
Kapogiannis, D
Wassermann, EM
Grafman, J
AF Huey, Edward D.
Zahn, Roland
Krueger, Frank
Moll, Jorge
Kapogiannis, Dimitrios
Wassermann, Eric M.
Grafman, Jordan
TI A Psychological and Neuroanatomical Model of Obsessive-Compulsive
Disorder
SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES
LA English
DT Review
ID ANTERIOR CINGULATE CORTEX; CEREBRAL-BLOOD-FLOW; POSITRON EMISSION
TOMOGRAPHY; HUMAN ORBITOFRONTAL CORTEX; BASAL GANGLIA LESIONS;
MAGNETIC-RESONANCE; SYMPTOM PROVOCATION; PREFRONTAL CORTEX; MATTER
ABNORMALITIES; ANXIETY DISORDERS
AB Imaging, surgical, and lesion studies suggest that the prefrontal cortex (orbitofrontal and anterior cingulate cortexes), basal ganglia, and thalamus are involved in the pathogenesis of obsessive-compulsive disorder (OCD). On the basis of these findings several models of OCD have been developed, but have had difficulty fully integrating the psychological and neuroanatomical findings of OCD. Recent research in the field of cognitive neuroscience on the normal function of these brain areas demonstrates the role of the orbitofrontal cortex in reward, the anterior cingulate cortex in error detection, the basal ganglia in affecting the threshold for activation of motor and behavioral programs, and the prefrontal cortex in storing memories of behavioral sequences (called "structured event complexes" or SECs). The authors propose that the initiation of these SECs can be accompanied by anxiety that is relieved with completion of the SEC, and that a deficit in this process could be responsible for many of the symptoms of OCD. Specifically, the anxiety can form the basis of an obsession, and a compulsion can be an attempt to receive relief from the anxiety by repeating parts of, or an entire, SEC. The authors discuss empiric support for, and specific experimental predictions of, this model. The authors believe that this model explains the specific symptoms, and integrates the psychology and neuroanatomy of OCD better than previous models.
C1 [Huey, Edward D.; Zahn, Roland; Krueger, Frank; Moll, Jorge; Kapogiannis, Dimitrios; Wassermann, Eric M.; Grafman, Jordan] NINDS, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
[Huey, Edward D.] Litwin Zucker Res Ctr, Study Alzheimers Dis & Memory Disorders, Great Neck, NY USA.
[Moll, Jorge] LABS Or Hosp Network, Cognit & Behav Neurosci Unit, Rio De Janeiro, Brazil.
[Wassermann, Eric M.] NINDS, Brain Stimulat Unit, NIH, Bethesda, MD 20892 USA.
RP Grafman, J (reprint author), NINDS, Cognit Neurosci Sect, NIH, Bldg 10,Rm 7D43,MSC 1440, Bethesda, MD 20892 USA.
EM grafmanj@ninds.nih.gov
RI Zahn, Roland/C-4665-2008; Moll, Jorge/B-2654-2013;
OI Zahn, Roland/0000-0002-8447-1453; Grafman, Jordan H./0000-0001-8645-4457
FU NIH; NINDS; NIMH
FX We thank Ben Greenberg and Anthony Pinto of Brown University for their
very helpful comments and Nicole Armstrong for her help with manuscript
preparation. This research was supported by the Intramural Research
Program of NIH, NINDS, and NIMH.
NR 155
TC 60
Z9 60
U1 7
U2 21
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0895-0172
J9 J NEUROPSYCH CLIN N
JI J. Neuropsychiatr. Clin. Neurosci.
PD FAL
PY 2008
VL 20
IS 4
BP 390
EP 408
PG 19
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 399CV
UT WOS:000262778900002
PM 19196924
ER
PT J
AU Li, J
Okamoto, H
Yin, C
Jagannathan, J
Takizawa, J
Aoki, S
Glasker, S
Rushing, EJ
Vortmeyer, AO
Oldfield, EH
Yamanaka, R
Zhuang, ZP
AF Li, Jie
Okamoto, Hiroaki
Yin, Chunyue
Jagannathan, Jay
Takizawa, Jun
Aoki, Sadao
Glaesker, Sven
Rushing, Elisabeth J.
Vortmeyer, Alexander O.
Oldfield, Edward H.
Yamanaka, Ryuya
Zhuang, Zhengping
TI Proteomic characterization of primary diffuse large B-cell lymphomas in
the central nervous system - Laboratory investigation
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE B-cell lymphoma; gel electrophoresis; proteomics; sporadic systemic
lymphoma; Western blot
ID PROTEIN DISULFIDE-ISOMERASE; CLASSICAL HODGKINS-DISEASE; PRIMARY
MALIGNANT-LYMPHOMA; REED-STERNBERG CELLS; PRIMARY CNS LYMPHOMA;
IMMUNOGLOBULIN TRANSCRIPTION; ENERGY-METABOLISM; WHITE-MATTER;
IMMUNOCOMPETENT PATIENTS; GLIOBLASTOMA-MULTIFORME
AB Object. The lack of primary lymphoid tissue within the central nervous system (CNS) confounds our understanding of the pathogenesis of primary CNS lymphomas (PCNSLs). Comparing the protein expression of PCNSLs and sporadic systemic lymphomas (SSLs) provides a useful strategy for identifying a molecular signature that characterizes disease-associated features and provides information regarding tumor initiation and progression.
Methods. Seven diffuse large B-cell PCNSLs were selected to undergo 2D gel electrophoresis, and profiled proteomes from these PCNSLs were compared with those from 7 diffuse large B-cell SSLs. Distinguishing proteins were sequenced using mass spectrometry.
Results. Two-dimensional get electrophoresis identified an average of 706 proteins from each specimen. Computerized gel analysis and manual reconfirmation revealed a 96% similarity in the proteomes of PCNSLs and SSLs. Comparative analysis identified 9 proteins significantly overexpressed (p < 0.05) and 16 proteins downregulated in PCNSLs. The proteomic findings were further validated using Western blot and immunohistochemical staining.
Conclusions. The similarities in proteomic patterns between PCNSLs and SSLs suggest that these tumor types share structural similarities, acquired during differentiation. The ultimate fate of lymphomatous cells (CNS vs systemic) may be related to differentially expressed proteins, which function in homing and host processing. Elucidating the roles of these differentially expressed proteins will prove valuable in understanding the pathogenesis of PCNSL.
C1 [Li, Jie; Okamoto, Hiroaki; Yin, Chunyue; Jagannathan, Jay; Glaesker, Sven; Vortmeyer, Alexander O.; Oldfield, Edward H.; Zhuang, Zhengping] Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bethesda, MD USA.
[Takizawa, Jun; Aoki, Sadao] Niigata Univ, Div Hematol, Grad Sch Med & Dent Sci, Niigata, Japan.
[Rushing, Elisabeth J.] USAF, Inst Pathol, Dept Neuropathol & Ophthalm Pathol, Washington, DC 20330 USA.
[Yamanaka, Ryuya] Niigata Univ, Brain Res Inst, Dept Neurosurg, Niigata 95021, Japan.
[Jagannathan, Jay] Univ Virginia Hlth Syst, Dept Neurosurg, Charlottesville, VA USA.
RP Zhuang, ZP (reprint author), Room 5D37,10 Ctr Dr, Bethesda, MD 20892 USA.
EM zhuangp@ninds.nih.gov
FU National Institute of Neurological Disorders and Stroke; National
Institutes of Health, Bethesda, Maryland
FX This research was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, National
Institutes of Health, Bethesda, Maryland.
NR 66
TC 4
Z9 5
U1 0
U2 4
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD SEP
PY 2008
VL 109
IS 3
BP 536
EP 546
DI 10.3171/JNS/2008/109/9/0536
PG 11
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 344CX
UT WOS:000258904400027
PM 18759588
ER
PT J
AU Jagannathan, J
Walbridge, S
Butman, JA
Oldfield, EH
Lonser, RR
AF Jagannathan, Jay
Walbridge, Stuart
Butman, John A.
Oldfield, Edward H.
Lonser, Russell R.
TI Effect of ependymal and pial surfaces on convection-enhanced delivery.
Laboratory investigation
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE cerebrospinal fluid; convection-enhanced delivery; ependyma; imaging;
Macaca fascicularis; Macaca mulatta; pia mater; ventricle
ID PRIMATE BRAIN; COMPUTERIZED-TOMOGRAPHY; REAL-TIME; INFUSION; STEM;
GLUCOCEREBROSIDASE; MACROMOLECULES; PERFUSION; PROTEIN; DISEASE
AB Object. Convection-enhanced delivery (CED) is increasingly used to investigate new treatments for central nervous system disorders. Although the properties of CED are well established in normal gray and white matter central nervous system structures, the effects on drug distribution imposed by ependymal and pial surfaces are not precisely defined. To determine the effect of these anatomical boundaries on CED, the authors infused low MW and high MW tracers for MR imaging near ependymal (periventricular) and pial (pericisternal) surfaces.
Methods. Five primates underwent CED of Gd-diethylenetriamine pentaacetic acid (Gd-DTPA; MW 590 D) or Gd-bound albumin (Gd-albumin; MW 72,000 D) during serial real-time MR imaging (FLAIR and T1-weighted sequences). Periventricular (caudate) infusions were performed unilaterally in I animal (volume of infusion [Vi] 57 mu l) and bilaterally in 1 animal with Gd-DTPA (Vi = 40 mu l on each side), and bilaterally in 1 animal with Gd-albumin (Vi = 80 mu l on each side). Pericisternal infusions were performed in 2 animals with Gd-DTPA (Vi = 190 mu l) or with Gd-albumin (Vi = 185 mu l) (1 animal each). Clinical effects, MR imaging, and histology were analyzed.
Results. Large regions of the brain and brainstem were perfused with both tracers. Intraparenchymal distribution was successfully tracked in real time by using T1-weighted MR imaging. During infusion, the volume of distribution (Vd) increased linearly (R-2 = 0.98) with periventricular (mean Vd/Vi ratio +/- standard deviation; 4.5 +/- 0.5) and pericisternal (5.2 +/- 0.3) Vi, but did so only until the leading edge of distribution reached the ependymal or pial surfaces, respectively. After the infusate reached either surface, the Vd/Vi decreased significantly (ependyma 2.9 +/- 0.8, pia mater 3.6 +/- 1.0; p < 0.05) and infusate entry into the ventricular or cisternal cerebrospinal fluid (CSF) was identified on FLAIR but not on T1-weighted MR images.
Conclusions. Ependymal and pial boundaries are permeable to small and large molecules delivered interstitially by convection. Once infusate reaches these surfaces, a portion enters the adjacent ventricular or cisternal CSF and the tissue Vd/Vi ratio decreases. Although T1-weighted MR imaging is best for tracking intraparenchymal infusate distribution, FLAIR MR imaging is the most sensitive and accurate for detecting entry of Gd-labeled imaging compounds into CSF during CED.
C1 [Jagannathan, Jay; Walbridge, Stuart; Oldfield, Edward H.; Lonser, Russell R.] Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Butman, John A.] NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD USA.
[Jagannathan, Jay; Oldfield, Edward H.] Univ Virginia, Dept Neurosurg, Univ Virginia Hlth Syst, Charlottesville, VA USA.
RP Lonser, RR (reprint author), Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bldg 10,Room 5D37, Bethesda, MD 20892 USA.
EM lonserr@ninds.nih.gov
RI Butman, John/A-2694-2008;
OI Butman, John/0000-0002-1547-9195
FU National Institute of Neurological Disorders; Stroke at the National
Institutes of Health
FX Support for this research was provided by the Intramural Research
Program of the National Institute of Neurological Disorders and Stroke
at the National Institutes of Health.
NR 20
TC 24
Z9 24
U1 0
U2 2
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD SEP
PY 2008
VL 109
IS 3
BP 547
EP 552
DI 10.3171/JNS/2008/109/9/0547
PG 6
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 344CX
UT WOS:000258904400028
PM 18759589
ER
PT J
AU Lonser, RR
AF Lonser, Russell R.
TI Metastasis in von Hippel-Lindau disease - Response
SO JOURNAL OF NEUROSURGERY
LA English
DT Letter
C1 NIH, Bethesda, MD 20892 USA.
RP Lonser, RR (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD SEP
PY 2008
VL 109
IS 3
BP 568
EP 569
DI 10.3171/JNS/2008/109/9/0568
PG 2
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 344CX
UT WOS:000258904400032
ER
PT J
AU Lonser, RR
Kim, HJ
AF Lonser, Russell R.
Kim, H. Jeffrey
TI Endolymphatic sac tumors - Response
SO JOURNAL OF NEUROSURGERY
LA English
DT Letter
ID HIPPEL-LINDAU-DISEASE
C1 [Lonser, Russell R.; Kim, H. Jeffrey] NIH, Bethesda, MD 20892 USA.
[Kim, H. Jeffrey] Georgetown Univ, Med Ctr, Washington, DC 20007 USA.
RP Lonser, RR (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 5
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD SEP
PY 2008
VL 109
IS 3
BP 570
EP 570
DI 10.3171/JNS/2008/109/9/0569
PG 1
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 344CX
UT WOS:000258904400034
ER
PT J
AU Esposito, G
Giovacchini, G
Liow, JS
Bhattacharjee, AK
Greenstein, D
Schapiro, M
Hallett, M
Herscovitch, P
Eckelman, WC
Carson, RE
Rapoport, SI
AF Esposito, Giuseppe
Giovacchini, Giampiero
Liow, Jeih-San
Bhattacharjee, Abesh K.
Greenstein, Dede
Schapiro, Mark
Hallett, Mark
Herscovitch, Peter
Eckelman, William C.
Carson, Richard E.
Rapoport, Stanley I.
TI Imaging neuroinflammation in Alzheimer's disease with radiolabeled
arachidonic acid and PET
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE arachidonic; neuroinflammation; PET; Alzheimer's imaging
ID POSITRON-EMISSION-TOMOGRAPHY; FALSE DISCOVERY RATE; PHOSPHOLIPASE A(2);
NEURODEGENERATIVE DISEASES; BRAIN PHOSPHOLIPIDS; BLOOD-FLOW; ACTIVATED
MICROGLIA; RAT; METABOLISM; VOLUME
AB Incorporation coefficients (K(star)) of arachidonic acid (AA) in the brain are increased in a rat model of neuroinflammation, as are other markers of AA metabolism. Data also indicate that neuroinflammation contributes to Alzheimer's disease (AD). On the basis of these observations, K(star) for AA was hypothesized to be elevated in patients with AD. Methods: A total of 8 patients with AD with an average (+/-SD) Mini-Mental State Examination score of 14.7 +/- 8.4 (mean age, 71.7 +/- 11.2 y) and 9 controls with a normal Mini-Mental State Examination score (mean age, 68.7 +/- 5.6 y) were studied. Each subject received a (15)O-water PET scan of regional cerebral blood flow, followed after 15 min by a 1-(11)C-AA scan of regional K(star) for AA. Results: In the patients with AD, compared with control subjects, global gray matter K(star) for AA (corrected or uncorrected for the partial-volume error [PVE]) was significantly elevated, whereas only PVE-uncorrected global cerebral blood flow was reduced significantly (P < 0.05). A false-discovery-rate procedure indicated that PVE-corrected K(star) for AA was increased in 78 of 90 identified hemispheric gray matter regions. PVE-corrected regional cerebral blood flow, although decreased in 12 regions at P < 0.01 by an unpaired t test, did not survive the false-discovery-rate procedure. The surviving K(star) increments were widespread in the neocortex but were absent in caudate, pallidum, and thalamic regions. Conclusion: These preliminary results show that K(star) for AA is widely elevated in the AD brain, particularly in regions reported to have high densities of senile (neuritic) plaques with activated microglia. To the extent that the elevations represent upregulated AA metabolism associated with neuroinflammation, PET with 1-(11)C-AA could be used to examine neuroinflammation in patients with AD and other brain diseases.
C1 [Esposito, Giuseppe; Giovacchini, Giampiero; Liow, Jeih-San; Bhattacharjee, Abesh K.; Schapiro, Mark; Rapoport, Stanley I.] NIA, Natl Inst Hlth, Brain Physiol & Metab Sect, Bethesda, MD 20892 USA.
[Giovacchini, Giampiero] Univ Milano Bicocca, Ctr Mol Bioimaging, Milan, Italy.
[Liow, Jeih-San] NIMH, Natl Inst Hlth, Mol Imaging Branch, Bethesda, MD 20892 USA.
[Greenstein, Dede] NIMH, Natl Inst Hlth, Child Psychiat Branch, Bethesda, MD 20892 USA.
[Schapiro, Mark] Cincinnati Childrens Hosp, Med Ctr, Dept Pediat Neurol, Cincinnati, OH USA.
[Hallett, Mark] NINDS, Natl Inst Hlth, Human Motor Control Sect, Med Neurol Branch, Bethesda, MD 20892 USA.
[Herscovitch, Peter; Eckelman, William C.; Carson, Richard E.] Natl Inst Hlth, Ctr Clin, Dept Positron Emiss Tomog, Bethesda, MD USA.
[Eckelman, William C.] Mol Tracer LLC, Bethesda, MD USA.
[Carson, Richard E.] Yale Univ, Sch Med, Yale PET Ctr, New Haven, CT USA.
RP Rapoport, SI (reprint author), NIA, Natl Inst Hlth, Brain Physiol & Metab Sect, Bldg 9,Room IS128, Bethesda, MD 20892 USA.
EM sir@helix.nih.gov
RI Carson, Richard/H-3250-2011
OI Carson, Richard/0000-0002-9338-7966
FU Intramural Programs of the National Institute on Aging; National
Institute of Neurological Disorders and Stroke; National Institute of
Mental Health; National Institutes of Health, Bethesda, Maryland
FX We thank Dr. Madhav Thambisetty for his helpful comments about the
manuscript. This work was supported by the Intramural Programs of the
National Institute on Aging, the National Institute of Neurological
Disorders and Stroke, the National Institute of Mental Health, and the
PET Department of the Clinical Center at the National Institutes of
Health, Bethesda, Maryland.
NR 46
TC 74
Z9 76
U1 0
U2 6
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD SEP
PY 2008
VL 49
IS 9
BP 1414
EP 1421
DI 10.2967/jnumed.107.049619
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 346CQ
UT WOS:000259046400020
PM 18703605
ER
PT J
AU Sojkova, J
Beason-Held, L
Zhou, Y
An, Y
Kraut, MA
Ye, W
Ferrucci, L
Mathis, CA
Klunk, WE
Wong, DF
Resnick, SM
AF Sojkoval, Jitka
Beason-Held, Lori
Zhou, Yun
An, Yang
Kraut, Michael A.
Ye, Weigo
Ferrucci, Luigi
Mathis, Chester A.
Klunk, William E.
Wong, Dean F.
Resnick, Susan M.
TI Longitudinal cerebral blood flow and amyloid deposition: An emerging
pattern?
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE PIB; CBF; longitudinal; positron emission tomography; aging
ID MILD COGNITIVE IMPAIRMENT; EARLY ALZHEIMERS-DISEASE; PITTSBURGH
COMPOUND-B; REFERENCE TISSUE MODEL; SPATIAL CONSTRAINT; ELDERLY
SUBJECTS; OLDER-ADULTS; PET; DEMENTIA; BRAIN
AB Although cerebral amyloid deposition may precede cognitive impairment by decades, the relationship between amyloid deposition and longitudinal change in neuronal function has not, to our knowledge, been studied. The aim of this article was to determine whether individuals without dementia with high and low amyloid burden show different patterns of longitudinal regional cerebral blood flow (rCBF) changes in the years preceding measurement of amyloid deposition. Methods: Twenty-eight participants without dementia (mean age +/- SD, 82.5 +/- 4.8 y; 6 mildly impaired) from the Baltimore Longitudinal Study of Aging underwent yearly resting-state (15)O-H(2)O PET scans for up to 8 y. (11)C-PIB images of amyloid deposition were acquired on average 10.8 +/- 0.8 y after the first CBF scan. (11)C-PIB distribution volume ratios of regions of interest were estimated by fitting a reference-tissue model to the measured time-activity curves. On the basis of mean cortical distribution volume ratios, participants were divided into groups with high or low (11)C-PIB retention. Differences in longitudinal rCBF changes between high-and low-(11)C-PIB groups were investigated by voxel-based analysis. Results: Longitudinal rCBF changes differed significantly between high- (n = 10) and low- (n = 18) (11)C-PIB groups (P <= 0.001). Greater longitudinal decreases in rCBF in the high-(11)C-PIB group than in the low-(11)C-PIB group were seen in right anterior to middle cingulate, right supramarginal gyrus, left thalamus, and midbrain bilaterally. Greater increases in rCBF overtime in the high-(11)C-PIB group were found in left medial and inferior frontal gyri, right precuneus, left inferior parietal lobule, and left postcentral gyrus. Conclusion: In this group of older adults without dementia, those with high (11)C-PIB show greater longitudinal declines in rCBF in certain areas, representing regions with greater decrements in neuronal function. Greater longitudinal increases in rCBF are also observed in those with higher amyloid load and may represent an attempt to preserve neuronal function in these regions.
C1 [Sojkoval, Jitka; Beason-Held, Lori; An, Yang; Ferrucci, Luigi; Resnick, Susan M.] NIA, Lab Personal & Cognit, NIH, Biomed Ctr,IRP, Baltimore, MD 21224 USA.
[Sojkoval, Jitka; Zhou, Yun; Kraut, Michael A.; Ye, Weigo; Wong, Dean F.] Johns Hopkins Univ, Dept Radiol, Baltimore, MD USA.
[Mathis, Chester A.] Univ Pittsburgh, Dept Radiol, Pittsburgh, PA 15260 USA.
[Klunk, William E.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA.
[Wong, Dean F.] Johns Hopkins Univ, Dept Psychiat, Baltimore, MD USA.
[Wong, Dean F.] Johns Hopkins Univ, Dept Environm Hlth Sci, Baltimore, MD 21205 USA.
RP Resnick, SM (reprint author), NIA, Lab Personal & Cognit, NIH, Biomed Ctr,IRP, Suite 100,Room 04B336,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM susan.resnick@nih.gov
OI Klunk, William/0000-0001-5512-0251
FU National Institutes of Health (NIH) [N01-AG-3-2124, K24 DA00412]; NIA;
PIB
FX We thank the staff of the PET facility at Johns Hopkins University and
the neuroimaging staff of the National Institute on Aging (NIA) for
their assistance. This research was supported by the Intramural Research
Program of the National Institutes of Health (NIH), by the NIA, and by
NIH grants N01-AG-3-2124 and K24 DA00412. GE Healthcare holds a license
agreement with the University of Pittsburgh based on the PIB technology
described in this manuscript. Drs. Klunk and Mathis are co-inventors of
PIB and, as such, have a financial interest in this license agreement.
NR 38
TC 33
Z9 33
U1 0
U2 0
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD SEP
PY 2008
VL 49
IS 9
BP 1465
EP 1471
DI 10.2967/jnumed.108.051946
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 346CQ
UT WOS:000259046400027
PM 18703614
ER
PT J
AU Yang, K
Lamprecht, SA
Shinozaki, H
Fan, K
Yan, W
Newmark, HL
Kopelovich, L
Edelmann, W
Jin, B
Gravaghi, C
Augenlicht, L
Kucherlapati, R
Lipkin, M
AF Yang, Kan
Lamprecht, Sergio A.
Shinozaki, Hiroharu
Fan, Kunhua
Yan, WanCai
Newmark, Harold L.
Kopelovich, Levy
Edelmann, Winfried
Jin, Bo
Gravaghi, Claudia
Augenlicht, Leonard
Kucherlapati, Raju
Lipkin, Martin
TI Dietary calcium and cholecalciferol modulate cyclin D1 expression,
apoptosis, and tumorigenesis in intestine of adenomatous polyposis
coli1638N/+ mice
SO JOURNAL OF NUTRITION
LA English
DT Article
ID FAMILIAL ADENOMATOUS POLYPOSIS; VITAMIN-D; COLON-CANCER;
COLORECTAL-CANCER; SENSING RECEPTOR; GENE-EXPRESSION; MOUSE MODELS; APC;
PREVENTION; CELLS
AB Both epidemiological and experimental findings have indicated that components of Western diets influence colonic tumorigenesis. Among dietary constituents, calcium and cholecalciferol have emerged as promising chemopreventive agents. We have demonstrated that a Western-style diet (WD) with low levels of calcium and cholecalciferol and high levels of (n-6) PUFA, increased the incidence of neoplasia in mouse intestine compared with a standard AIN-76A diet; models included wild-type mice and mice with targeted mutations. In the present study, adenomatous polyposis coli (Apc)(1638N/+) mice carrying a heterozygous Apc mutation were fed either an AIN-76A diet, a WD, or a WD supplemented with calcium and cholecalciferol (WD/Ca/VitD3). Diets were fed for 24 wk and effects on cellular and molecular events were assessed by performing immunohistochemistry in colonic epithelium along the crypt-to-surface continuum. Feeding WD to Apc(1638N/+) mice not only enhanced cyclin D1 expression in colonic epithelium compared with AIN-76A treatment as previously reported but also significantly increased the expression of the antiapoptotic protein B-cell lymphoma 2(Bcl-2) concomitantly with a decrease in the proapoptotic Bcl2-associated X protein and the number of apoptotic epithelial cells. WD treatment enhanced mutant Apc-driven small intestinal carcinogenesis and also resulted in the formation of a small number of colonic adenomas (0.16 +/- 0.09; P < 0.05). By contrast, the WD/Ca/VitD3 diet reversed WD-induced growth, promoting changes in colonic epithelium. Importantly, Apc(1638N/+) mice fed the WD/Ca/VitD3 diet did not develop colonic tumors, further indicating that dietary calcium and cholecalciferol have a key role in the chemoprevention of colorectal neoplasia in this mouse model of human colon cancer.
C1 [Yang, Kan; Lamprecht, Sergio A.; Shinozaki, Hiroharu; Fan, Kunhua; Gravaghi, Claudia; Lipkin, Martin] Cornell Univ, Weill Med Coll, Dept Med Gastroenterol & Hepatol, Strang Canc Res Lab, New York, NY 10065 USA.
[Yan, WanCai; Edelmann, Winfried; Jin, Bo; Augenlicht, Leonard] Albert Einstein Coll Med, Bronx, NY 10461 USA.
[Newmark, Harold L.] Rutgers State Univ, Dept Biol Chem, Piscataway, NJ 08854 USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Kucherlapati, Raju] Harvard Partners Ctr Genet & Genom, Boston, MA 02115 USA.
RP Lipkin, M (reprint author), Cornell Univ, Weill Med Coll, Dept Med Gastroenterol & Hepatol, Strang Canc Res Lab, New York, NY 10065 USA.
EM lipkin@mail.rockefeller.edu
FU NO [N01-CN-43302, N01-CN-43308, U54-CA100926, CA84301, ES-11040]
FX Supported by NO awards N01-CN-43302, N01-CN-43308, U54-CA100926,
CA84301, and ES-11040,
NR 39
TC 27
Z9 27
U1 0
U2 1
PU AMER SOC NUTRITIONAL SCIENCE
PI BETHESDA
PA 9650 ROCKVILLE PIKE, RM L-2407A, BETHESDA, MD 20814 USA
SN 0022-3166
J9 J NUTR
JI J. Nutr.
PD SEP
PY 2008
VL 138
IS 9
BP 1658
EP 1663
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 342RU
UT WOS:000258802000012
PM 18716166
ER
PT J
AU Freedman, LS
Guenther, PN
Krebs-Smith, SM
Kott, PS
AF Freedman, Laurence S.
Guenther, Patricia N.
Krebs-Smith, Susan M.
Kott, Phillip S.
TI A population's mean Healthy Eating Index-2005 scores are best estimated
by the score of the population ratio when one 24-hour recall is
available
SO JOURNAL OF NUTRITION
LA English
DT Article
ID FOODS
AB he USDA Healthy Eating Index-2005 (HEI-2005) is a tool to quantify and evaluate the quality of diet consumed by the U.S. population. It comprises 12 components, expressed as ratios of a food group or nutrient to energy intake. The components are scored on a scale from 0 to M, where M is 5, 10, or 20. Ideally, the HEI-2005 is calculated or the basis of the usual dietary intake of an individual. Intake data, collected via a 24-h recall, are often available for only 1 d for each individual. In this article, we examine how best to estimate a population's mean usual HEI-2005 component and total scores when 1 d of dietary information is available for a sample of individuals from the population. Three methods are considered: the mean of individual scores, the score of the mean of individual ratios, and the score of the ratio of total food group or nutrient intake to total energy intake, which we call the Population ratio. We investigate via computer simulation which method is the least biased. The simulations are based on statistical modeling of the distributions of intakes reported by 738 women participating in the Eating at America's Table Study. The results show that overall, the score of the population ratio is the preferred method. We therefore recommend that the quality of the U.S. population's diet be assessed and monitored using this method.
C1 [Freedman, Laurence S.] Gertner Inst Epidemiol & Hlth Policy Res, IL-52161 Tel Hashomer, Israel.
[Guenther, Patricia N.] USDA, Ctr Nutr Policy & Promot, Alexandria, VA 22302 USA.
[Krebs-Smith, Susan M.] NCI, Bethesda, MD 20892 USA.
[Kott, Phillip S.] Natl Agr Stat Serv, Fairfax, VA 22030 USA.
RP Freedman, LS (reprint author), Gertner Inst Epidemiol & Hlth Policy Res, IL-52161 Tel Hashomer, Israel.
EM lsf@actcom.co.il
FU Intramural NIH HHS [Z99 CA999999]
NR 8
TC 33
Z9 34
U1 0
U2 4
PU AMER SOC NUTRITIONAL SCIENCE
PI BETHESDA
PA 9650 ROCKVILLE PIKE, RM L-2407A, BETHESDA, MD 20814 USA
SN 0022-3166
J9 J NUTR
JI J. Nutr.
PD SEP
PY 2008
VL 138
IS 9
BP 1725
EP 1729
PG 5
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 342RU
UT WOS:000258802000022
PM 18716176
ER
PT J
AU McGrath, PJ
Walco, GA
Turk, DC
Dworkin, RH
Brown, MT
Davidson, K
Eccleston, C
Finley, GA
Goldschneider, K
Haverkos, L
Hertz, SH
Ljungman, G
Palermo, T
Rappaport, BA
Rhodes, T
Schechter, N
Scott, J
Sethna, N
Svensson, OK
Stinson, J
von Baeyer, CL
Walker, L
Weisman, S
White, RE
Zajicek, A
Zeltzer, L
AF McGrath, Patrick J.
Walco, Gary A.
Turk, Dennis C.
Dworkin, Robert H.
Brown, Mark T.
Davidson, Karina
Eccleston, Christopher
Finley, G. Allen
Goldschneider, Kenneth
Haverkos, Lynne
Hertz, Sharon H.
Ljungman, Gustaf
Palermo, Tonya
Rappaport, Bob A.
Rhodes, Thomas
Schechter, Neil
Scott, Jane
Sethna, Navil
Svensson, Ola K.
Stinson, Jennifer
von Baeyer, Carl L.
Walker, Lynn
Weisman, Steven
White, Richard E.
Zajicek, Anne
Zeltzer, Lonnie
TI Core outcome domains and measures for pediatric acute and
chronic/recurrent pain clinical trials: PedIMMPACT recommendations
SO JOURNAL OF PAIN
LA English
DT Article
DE acute pain; chronic pain; children; adolescents; pediatric; clinical
trials; randomized controlled trials; assessment; outcomes;
health-related quality of life; physical functioning; emotional
functioning; global ratings; adverse events; IMMPACT
ID QUALITY-OF-LIFE; FUNCTIONAL DISABILITY INVENTORY; SCHOOL-AGED CHILDREN;
SICKLE-CELL-DISEASE; POSTOPERATIVE PAIN; PSYCHOMETRIC PROPERTIES;
SELF-REPORT; IMMPACT RECOMMENDATIONS; BEHAVIORAL DISTRESS; INITIAL
VALIDATION
AB Under the auspices of the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMPACT), 26 professionals from academia, governmental agencies, and the pharmaceutical industry participated in a 2-stage Delphi poll and a consensus meeting that identified core outcome domains and measures that should be considered in clinical trials of treatments for acute and chronic pain in children and adolescents. Consensus was refined by consultation with the international pediatric pain community through announcement of our recommendations on the Pediatric Pain List and inviting and incorporating comments from external sources. There was consensus that investigators conducting pediatric acute pain clinical trials should consider assessing outcomes in pain intensity; global judgment of satisfaction with treatment; symptoms and adverse events; physical recovery; emotional response; and economic factors. There was also agreement that investigators conducting pediatric clinical trials in chronic and recurrent pain should consider assessing outcomes in pain intensity; physical functioning; emotional functioning; role functioning; symptoms and adverse events; global judgment of satisfaction with treatment; sleep; and economic factors. Specific measures or measurement strategies were recommended for different age groups for each domain.
Perspective: Based on systematic review and consensus of experts, core domains and measures for clinical trials to treat pain in children and adolescents were defined. This will assist in comparison and pooling of data and promote evidence-based treatment, encourage complete reporting of outcomes, simplify the review of proposals and manuscripts, and facilitate clinicians making informed decisions regarding treatment. (C) 2008 by the American Pain Society.
C1 [Walco, Gary A.] Hackensack Univ, Joseph M Sanzari Childrens Hosp, Med Ctr, Hackensack, NJ 07601 USA.
[McGrath, Patrick J.; Finley, G. Allen] Dalhousie Univ, Halifax, NS, Canada.
[McGrath, Patrick J.; Finley, G. Allen] IWK Hlth Ctr, Halifax, NS, Canada.
[Turk, Dennis C.] Univ Washington, Seattle, WA 98195 USA.
[Dworkin, Robert H.] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
[Brown, Mark T.] Pfizer Inc, Ann Arbor, MI USA.
[Davidson, Karina] Columbia Univ, New York, NY USA.
[Eccleston, Christopher] Univ Bath, Bath BA2 7AY, Avon, England.
[Goldschneider, Kenneth] Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA.
[Haverkos, Lynne; Zajicek, Anne] NIH NICHD, Bethesda, MD USA.
[Hertz, Sharon H.; Rappaport, Bob A.; Scott, Jane] US FDA, Rockville, MD 20857 USA.
[Ljungman, Gustaf] Uppsala Univ, Childrens Hosp, Uppsala, Sweden.
[Palermo, Tonya] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Rhodes, Thomas] Merck & Co Inc, Blue Bell, PA USA.
[Schechter, Neil] St Francis Hosp & Med Ctr, Hartford, CT USA.
[Sethna, Navil] Harvard Univ, Sch Med, Childrens Hosp, Boston, MA 02115 USA.
[Svensson, Ola K.] AstraZeneca, Stockholm, Sweden.
[Stinson, Jennifer] Univ Toronto, Toronto, ON, Canada.
[Stinson, Jennifer] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[von Baeyer, Carl L.] Univ Saskatchewan, Saskatoon, SK, Canada.
[Walker, Lynn] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Weisman, Steven] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
[Weisman, Steven] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[White, Richard E.] Endo Pharmaceut, Chadds Ford, PA USA.
[White, Richard E.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Walco, GA (reprint author), Hackensack Univ, Joseph M Sanzari Childrens Hosp, Med Ctr, 30 Prospect Ave, Hackensack, NJ 07601 USA.
EM gwalco@humed.com
OI Ljungman, Gustaf/0000-0002-4949-2494; von Baeyer,
Carl/0000-0002-6308-1966; Zeltzer, Lonnie/0000-0001-9306-9450;
Eccleston, Christopher/0000-0003-0698-1543; McGrath,
Patrick/0000-0002-9568-2571
NR 80
TC 271
Z9 274
U1 4
U2 17
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1526-5900
J9 J PAIN
JI J. Pain
PD SEP
PY 2008
VL 9
IS 9
BP 771
EP 783
DI 10.1016/j.jpain.2008.04.007
PG 13
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 347WN
UT WOS:000259172200002
PM 18562251
ER
PT J
AU Wysocki, T
Iannotti, R
Weissberg-Benchell, J
Laffel, L
Hood, K
Anderson, B
Chen, R
AF Wysocki, Tim
Iannotti, Ronald
Weissberg-Benchell, Jill
Laffel, Lori
Hood, Korey
Anderson, Barbara
Chen, Rusan
CA Family Management Childhood Diabet
TI Diabetes problem solving by youths with type 1 diabetes and their
caregivers: Measurement, validation, and longitudinal associations with
glycemic control
SO JOURNAL OF PEDIATRIC PSYCHOLOGY
LA English
DT Article
DE adolescents; children; diabetes; problem solving
ID BLOOD-GLUCOSE DATA; SELF-MANAGEMENT; CHILDREN; ADOLESCENTS; ADHERENCE;
MELLITUS; IDDM
AB Objectives This article introduces a new measure of problem-solving skills of youths with type 1 diabetes (T1DM) and adult caregivers in correcting glycemic fluctuations. Methods The Diabetes Problem Solving Interview (DPSI), a structured interview, was validated during a pilot study of a behavioral intervention. DPSI data and measures of diabetes management were obtained at baseline from 114 youths (ages 9-14.5) and 109 caregivers. Glycosylated hemoglobin (HbA(1c)) was measured quarterly over 9 months. Results Results confirmed the psychometric adequacy of the DPSI. For caregivers, but not youths, low DPSI scores (indicating poor problem-solving skills) were significantly associated with worse HbA(1c) over 9 months. Conclusions The DPSI has clinical and research utility as a measure of diabetes problem-solving skills. Identification and targeted remediation of caregivers deficient diabetes problem-solving skills or promotion of youths utilization of these skills could possibly enhance glycemic control in youths with T1DM.
C1 [Wysocki, Tim] Nemours Childrens Clin, Ctr Pediat Psychol Res, Jacksonville, FL 32207 USA.
[Iannotti, Ronald] NICHHD, Bethesda, MD 20892 USA.
[Weissberg-Benchell, Jill] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Anderson, Barbara] Texas Childrens Hosp, Houston, TX 77030 USA.
[Chen, Rusan] Georgetown Univ, Washington, DC 20057 USA.
RP Wysocki, T (reprint author), Nemours Childrens Clin, Ctr Pediat Psychol Res, 807 Childrens Way, Jacksonville, FL 32207 USA.
EM twysocki@nemours.org
RI Chen, Robert/B-3899-2009
OI Chen, Robert/0000-0002-8371-8629
FU Intramural NIH HHS; NICHD NIH HHS [N01 HD003364]
NR 27
TC 43
Z9 46
U1 4
U2 12
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0146-8693
J9 J PEDIATR PSYCHOL
JI J. Pediatr. Psychol.
PD SEP
PY 2008
VL 33
IS 8
BP 875
EP 884
DI 10.1093/jpepsy/jsn024
PG 10
WC Psychology, Developmental
SC Psychology
GA 333GP
UT WOS:000258141300009
PM 18346973
ER
PT J
AU Oh, W
Perritt, R
Shankaran, S
Merritts, M
Donovan, EF
Ehrenkranz, RA
O'Shea, TM
Tyson, JE
Laptook, AR
Das, A
Higgins, RD
AF Oh, William
Perritt, Rebecca
Shankaran, Seetha
Merritts, Matthew
Donovan, Edward F.
Ehrenkranz, Richard A.
O'Shea, T. Michael
Tyson, Jon E.
Laptook, Abbot R.
Das, Abhik
Higgins, Rosemary D.
TI Association between urinary lactate to creatinine ratio and
neurodevelopmental outcome in term infants with hypoxic-ischemic
encephalopathy
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID NEWBORN-INFANTS; ASPHYXIA
AB Objective To assess the association between urinary lactate to creatinine ratio (ULCR) and neurodevelopmental outcome in term infants with hypoxic ischemic encephalopathy and examine the effect of hypothermia on the change in ULCR.
Study design Spot urine samples were collected in 58 term infants (28 hypothermia, 30 control subjects) with hypoxic ischemic encephalopathy. Urinary lactate and creatinine were measured by using (1)H nuclear magnetic, resonance spectroscopy and expressed as ULCR. Survivors were examined at 18 months of age.
Results The ULCR was significantly higher in infants who died or had moderate/severe neurodevelopmental disability. Logistic regression analysis controlling for hypothermia and severity of encephalopathy confirmed the association (aqjusted odds ratio, 5.52; 95% CI, 1.36, 22.42; P < .02). Considerable overlap in ULCR was observed between infants with normal/mild disability and those who died or survived with moderate/severe disability. ULCR fell significantly between 6 and 24 hours and 48 and 72 hours of age for all infants. The magnitude of decline did not differ between hypothermia and control groups.
Conclusions High ULCR is associated with death or moderate/severe neurodevelopmental disability. Significant overlap in values between the normal/mild and moderate/severe disability groups limits predictive value of this measure. Whole-body hypothermia did not affect the decline in ULCR.
C1 [Oh, William] Brown Univ, Dept Pediat, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Perritt, Rebecca; Das, Abhik] Res Triangle Int, Res Triangle Pk, NC USA.
[Shankaran, Seetha] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[Merritts, Matthew] Southwestern Univ, Dept Nucl Imaging, Dallas, TX USA.
[Donovan, Edward F.] Univ Cincinnati, Dept Pediat, Cincinnati, OH 45221 USA.
[Ehrenkranz, Richard A.] Yale Univ, Dept Pediat, New Haven, CT 06520 USA.
[O'Shea, T. Michael] Wake Forest Univ, Dept Pediat, Wake Forest, NC USA.
[Tyson, Jon E.] Univ Texas Houston, Dept Pediat, Providence, RI USA.
[Laptook, Abbot R.] Brown Univ, Dept Pediat, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Higgins, Rosemary D.] NICHD, NIH, NICHD Neonatal Res Network, Bethesda, MD USA.
RP Oh, W (reprint author), Women & Infants Hosp Rhode Isl, Brown Med Sch, Dept Pediat, 101 Dudley St,Suite 1100, Providence, RI 02905 USA.
EM woh@wihri.org
FU Neonatal Research Network NICHD
FX Supported by Neonatal Research Network NICHD. The list of grant support
for each participating center is available at WWW. jpeds.com. Authors
declare no conflict of interest.
NR 10
TC 8
Z9 8
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD SEP
PY 2008
VL 153
IS 3
BP 375
EP 378
DI 10.1016/j.jpeds.2008.03.041
PG 4
WC Pediatrics
SC Pediatrics
GA 348JV
UT WOS:000259207700017
PM 18534246
ER
PT J
AU Flanigan, EY
Aros, S
Bueno, MF
Conley, M
Troendle, JF
Cassorla, F
Mills, JL
AF Flanigan, Elizabeth Y.
Aros, Sofia
Ferraz Bueno, Maria
Conley, Mary
Troendle, James F.
Cassorla, Fernando
Mills, James L.
TI Eye malformations in children with heavy alcohol exposure in utero
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID EYEGROUND MALFORMATIONS; OCULAR MANIFESTATIONS; IMAGE-ANALYSIS;
OPTIC-NERVE; FETAL; MOTHERS; INVOLVEMENT
AB Objective To determine whether children who do not develop fetal alcohol syndrome (FAS) despite heavy alcohol exposure are at risk for eye abnormalities.
Study design We screened 9628 pregnant women and identified 101 women who were drinking >= 2 oz of absolute alcohol per day and 101 nondrinking control women. We followed 43 exposed and 55 control offspring between age 4 and 9 years, performing masked standardized ophthalomologic examinations.
Results The groups did not differ in their rates of impaired visual acuity, refractory errors, ptosis, epicanthal folds, or short palpebral fissures. Biomicroscopy examination was normal in all exposed subjects; cataracts were detected in 2 control subjects (4%) but in no exposed subjects. Arterial tortuosity was seen in 7 exposed subjects (16%) and in 8 control subjects (15%). Optic nerve hypoplasia was not detected in any subject.
Conclusions Previous research has found that children with FAS have a high incidence of serious ophthalmologic defects; our data indicate that the risk is limited to children with FAS and does not extend to children exposed to high levels of alcohol prenatally who do not develop FAS. Eye examinations are unlikely to clarify the diagnosis in children suspected of having alcohol-related damage.
C1 [Flanigan, Elizabeth Y.; Conley, Mary; Troendle, James F.; Mills, James L.] NICHD, NIH, DHHS, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA.
[Aros, Sofia] Univ Chile, San Borja Arriaran Clin Hosp, Sch Med, Dept Pediat, Santiago, Chile.
[Ferraz Bueno, Maria] Univ Chile, JJ Aguirre Hosp, Santiago, Chile.
[Flanigan, Elizabeth Y.] Uniformed Serv Univ Hlth Sci, Dept Pediat, Bethesda, MD 20814 USA.
[Flanigan, Elizabeth Y.] Walter Reed Army Med Ctr, Dept Pediat, Washington, DC 20307 USA.
[Cassorla, Fernando] Univ Chile, Sch Med, Inst Maternal & Child Res, Santiago, Chile.
RP Flanigan, EY (reprint author), NICHD, NIH, DHHS, Div Epidemiol Stat & Prevent Res, 6100 Execut Blvd,Room 7B03, Bethesda, MD 20892 USA.
EM eflanigan@usuhs.mil
FU National Institute of Child Health; Human Development's Intramural
Research Program [OHSR-96-04]
FX Supported by the National Institute of Child Health and Human
Development's Intramural Research Program and protocol/project
OHSR-96-04.
NR 35
TC 8
Z9 9
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD SEP
PY 2008
VL 153
IS 3
BP 391
EP 395
DI 10.1016/j.jpeds.2008.04.024
PG 5
WC Pediatrics
SC Pediatrics
GA 348JV
UT WOS:000259207700020
PM 18571671
ER
PT J
AU Roeloffs, R
Wickenden, AD
Crean, C
Werness, S
McNaughton-Smith, G
Stables, J
McNamara, JO
Ghodadra, N
Rigdon, GC
AF Roeloffs, Rosemarie
Wickenden, Alan D.
Crean, Christopher
Werness, Stephen
McNaughton-Smith, Grant
Stables, James
McNamara, James O.
Ghodadra, Neil
Rigdon, Greg C.
TI In vivo profile of ICA-27243
[N-(6-Chloro-pyridin-3-yl)-3,4-difluoro-benzamide], a potent and
selective KCNQ2/Q3 (Kv7.2/Kv7.3) activator in rodent anticonvulsant
models
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID POTASSIUM CHANNEL GENE; PRECLINICAL EVALUATION; SEIZURE MODEL; DUP 996;
EPILEPSY; RETIGABINE; LINOPIRDINE; MUTATION; D-23129; DRUG
AB Openers or activators of neuronal KCNQ2/Q3 potassium channels decrease neuronal excitability and may provide benefit in the treatment of disorders of neuronal excitability such as epilepsy. In the present study, we evaluate the effects of ICA-27243 [N-(6-chloro-pyridin-3-yl)-3,4-difluoro-benzamide], an orally bioavailable, potent, and selective KCNQ2/Q3 opener, in a broad range of rodent seizure models. ICA-27243 was effective against maximal electroshock (MES) and pentylenetetrazole (PTZ)-induced seizures in both rats (MES, ED(50) = 1.5 mg/kg p.o.; PTZ, ED(50) = 2.2 mg/kg p.o.) and mice (MES, ED(50) = 8.6 mg/kg p.o.; PTZ, ED(50) = 3.9 mg/kg p.o.) in the rat amygdala kindling model of partial seizures (full protection from seizure at 9 mg/kg p.o.) and in the 6-Hz model of psychomotor seizures in mice (active at 10 mg/kg i.p.). Antiseizure efficacy in all models was observed at doses significantly less than those shown to effect open-field locomotor activity (rat ED(50) = 40 mg/kg p.o.) or ability to remain on a Rotorod (no effect in rat at doses up to 100 mg/kg p. o.). There was no evidence of cognition impairment as measured in the Morris water maze in the rat (10 and 30 mg/kg p. o.), nor was there evidence of the development of tolerance after multiple doses of ICA-27243. Our findings suggest that selective KCNQ2/Q3 opening activity in the absence of effects on KCNQ3/Q5 or GABA-activated channels may be sufficient for broad-spectrum antiepileptic activity in rodents.
C1 [Roeloffs, Rosemarie; Wickenden, Alan D.; Crean, Christopher; Werness, Stephen; McNaughton-Smith, Grant; Rigdon, Greg C.] Icagen Inc, Durham, NC 27703 USA.
[Stables, James] NINDS, Anticonvulsant Screening Program, NIH, Rockville, MD USA.
[McNamara, James O.; Ghodadra, Neil] Duke Univ, Sch Med, Dept Neurobiol, Durham, NC USA.
RP Roeloffs, R (reprint author), Icagen Inc, 4222 Emperor Blvd,Suite 350, Durham, NC 27703 USA.
EM rroeloffs@icagen.com
FU Icagen
FX R.R., S.W., and G.C.R. are employees of Icagen, Inc. and are owners of
Icagen stock and Icagen stock options. A. D. W., G. M.-S., and C. C. are
former Icagen employees who received Icagen stock option grants as part
of their compensation. Rat amygdala kindling studies were conducted in
the laboratory of J.O.M. by N.G. (Duke University Medical School,
Durham, NC), and these studies were supported by a grant from Icagen. In
addition, J.O.M. declares that he has served as an advisor to Icagen,
that his compensation has included options for shares in Icagen, and
that he currently owns shares in the company.
NR 41
TC 37
Z9 38
U1 1
U2 4
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD SEP
PY 2008
VL 326
IS 3
BP 818
EP 828
DI 10.1124/jpet.108.137794
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 338RB
UT WOS:000258524400016
PM 18577704
ER
PT J
AU Witkin, JM
Levant, B
Zapata, A
Kaminski, R
Gasior, M
AF Witkin, J. M.
Levant, B.
Zapata, A.
Kaminski, R.
Gasior, M.
TI The dopamine D(3)/D(2) agonist (+)-PD-128,907 [(R-(+)-trans3,4a,
10b-tetrahydro-4-propyl-2H, 5H-[1] benzopyrano[4,3-b]1,4-oxazin-9-ol)]
protects against acute and cocaine-kindled seizures in mice: Further
evidence for the involvement of D(3) receptors
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID WILD-TYPE MICE; LOCOMOTOR-ACTIVITY; NUCLEUS-ACCUMBENS; BODY-TEMPERATURE;
BRAIN REWARD; D3; SENSITIZATION; RATS; ANTAGONISTS; ANTICONVULSANT
AB Previous findings have demonstrated a protective role for dopamine D(3)/D(2) receptor agonists in the convulsant and lethal effects of acutely administered cocaine. Data are provided here to establish that the protection occurs through a D(3) linked mechanism and that protection is extended to seizure kindling. The D(3) antagonist SB-277011-A [4-quinolinecarboxamide, N[ trans-4-[2-(6-cyano-3,4-dihydro-2(1H)-isoquinolinyl) ethyl]cyclohexyl]-(9CI)] prevented the anticonvulsant effect of the D(3)/D(2) receptor agonist (+)-PD-128,907 [(R-(+)-trans-3,4a, 10-btetrahydro4-propyl-2H, 5H-[1] benzopyrano[4,3-b]-1,4-oxazin-9-ol)] on cocaine-induced seizures. The protection afforded by the D(3)/D(2) agonist, (+)-PD-128,907, was eliminated in D(3) receptor-deficient mice. In D 2 receptor knockout mice, the anticonvulsant effects of (+)-PD-128,907 were preserved. (+)PD-128,907 also prevented the acquisition and expression of cocaine-kindled seizures engendered by repeated daily dosing with 60 mg/ kg cocaine. (+)-PD-128,907 also blocked the seizures induced in mice fully seizure kindled to cocaine. Although repeated dosing with cocaine increased the potency of cocaine to produce seizures and lethality (decreased ED 50 values), daily coadministration of (+)-PD-128,907 significantly prevented this potency shift. In mice treated daily with cocaine and (+)-PD128,907, the density, but not the affinity, of D 3 receptors was increased. The specificity with which (+)-PD-128,907 acts upon this cocaine-driven process was demonstrated by the lack of a significant effect of (+)-PD-128,907 on seizure kindling to a GABA A receptor antagonist, pentylenetetrazol. Taken together and with literature findings, the data indicate that dopamine D 3 receptors function in the initiation of a dampening mechanism against the toxic effects of cocaine, a finding that might have relevance to psychiatric disorders of drug dependence, schizophrenia, and bipolar depression.
C1 [Witkin, J. M.] Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA.
[Levant, B.] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66103 USA.
[Zapata, A.; Kaminski, R.; Gasior, M.] NIDA, Behav Neurosci Branch, NIH, Baltimore, MD USA.
RP Witkin, JM (reprint author), Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA.
EM jwitkin@lilly.com
NR 50
TC 8
Z9 8
U1 1
U2 3
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD SEP
PY 2008
VL 326
IS 3
BP 930
EP 938
DI 10.1124/jpet.108.139212
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 338RB
UT WOS:000258524400029
PM 18566292
ER
PT J
AU Do Carmo, GP
Polt, R
Bilsky, EJ
Rice, KC
Negus, SS
AF Do Carmo, Gail Pereira
Polt, Robin
Bilsky, Edward J.
Rice, Kenner C.
Negus, S. Stevens
TI Behavioral pharmacology of the mu/delta opioid glycopeptide MMP2200 in
rhesus monkeys
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID BLOOD-BRAIN-BARRIER; CAPSAICIN-INDUCED ALLODYNIA; TAIL-WITHDRAWAL
PROCEDURE; THERMAL NOCICEPTION; UNANESTHETIZED PRIMATES; AGONIST SNC80;
RECEPTORS; MORPHINE; RAT; ANTINOCICEPTION
AB H(2)N-Tyr-D-Thr-Gly-Phe-Leu-Ser-(O-beta-D-lactose)-CONH(2) (MMP2200) is a novel glycopeptide opioid agonist with similar affinities for mu and delta receptors. Glycosylation promoted brain penetration and production of centrally mediated behavioral effects in mice; however, it is unknown whether the magnitude of enhanced brain penetration is sufficient to permit central mediation of drug effects and production of synergistic mu/delta antinociceptive interactions after systemic administration in primates. To address this issue, the present study compared the effects of MMP2200 and the mu-agonist morphine in four behavioral procedures in rhesus monkeys. In an assay of thermal nociception, morphine (1.0-5.6 mg/kg) produced dose-dependent antinociception, whereas MMP2200 (10-56 mg/kg) was ineffective. In an assay of capsaicin-induced thermal allodynia, both morphine (0.01-1.0 mg/kg) and MMP2200 (0.032 -3.2 mg/ kg) produced dose-dependent antiallodynic effects. MMP2200-induced antiallodynia was blocked by the moderately mu-selective antagonist naltrexone (0.01 mg/kg), the delta-selective antagonist naltrindole (1.0 mg/kg), and the peripherally selective opioid antagonist quaternary naltrexone ( 0.32 mg/ kg). In an assay of schedulecontrolled behavior, both morphine (0.01 -1.0 mg/kg) and MMP2200 (10-56 mg/kg) decreased response rates. Morphine effects were antagonized by naltrexone (0.001-0.01 mg/ kg); however, the effects of MMP2200 were not antagonized by either naltrexone ( 0.01 mg/ kg) or naltrindole ( 1.0 mg/kg). In an assay of drug self-administration, morphine (0.0032-0.32 mg/kg/injection) produced reinforcing effects, whereas MMP2200 (0.032 -0.32 mg/kg/injection) did not. These results suggest that systemically administered MMP2200 acted as a peripheral, mu/delta-opioid agonist with limited distribution to the central nervous system in rhesus monkeys. These results also suggest the existence of species differences in the pharmacokinetics and brain penetration of glycopeptides.
C1 [Negus, S. Stevens] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA.
[Do Carmo, Gail Pereira; Negus, S. Stevens] Harvard Univ, Sch Med, McLean Hosp, Alcohol & Drug Abuse Res Ctr, Belmont, MA 02178 USA.
[Polt, Robin] Univ Arizona, Tucson, AZ USA.
[Bilsky, Edward J.] Univ New England, Biddeford, ME USA.
[Rice, Kenner C.] Natl Inst Drug Abuse, Chem Biol Res Branch, Bethesda, MD USA.
[Rice, Kenner C.] NIAAA, NIH, US Dept Hlth & Human Serv, Bethesda, MD USA.
RP Negus, SS (reprint author), Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, 410 N 12th St,POB 980613, Richmond, VA 23298 USA.
EM ssnegus@vcu.edu
OI Bilsky, Edward/0000-0002-4664-5256
FU Intramural NIH HHS; NIDA NIH HHS [R01 DA011460-09, R01 DA011460,
R01-DA11460]; NINDS NIH HHS [R01 NS052727, R01-NS052727, R01
NS052727-01A2]
NR 39
TC 15
Z9 15
U1 0
U2 1
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD SEP
PY 2008
VL 326
IS 3
BP 939
EP 948
DI 10.1124/jpet.108.138180
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 338RB
UT WOS:000258524400030
PM 18511649
ER
PT J
AU Wu, T
Chan, P
Hallett, M
AF Wu, Tao
Chan, Piu
Hallett, Mark
TI Modifications of the interactions in the motor networks when a movement
becomes automatic
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; FUNCTIONAL MRI; EFFECTIVE CONNECTIVITY;
BRAIN ACTIVATION; FRONTAL-CORTEX; SEQUENTIAL-PROCEDURES; VISUOMOTOR
SEQUENCE; MEDIAL WALL; AREAS; FMRI
AB A crucial feature of the motor system is the ability to control some movements automatically. We have previously shown that all parts of the motor networks reduce their activity with automaticity, and, while this change may indicate increased efficiency in terms of neural processing, it is not clear how motor skill can be maintained after a reduction of neural activity. In the current study, we used functional MRI (fMRI) to investigate influences on the effective connectivity of the brain motor networks when movements become automatic. Subjects practiced a sequential movement until they could execute it automatically, and task-related brain fMRI activation was measured before and after they achieved automaticity. Using the psychophysiological interaction (PPI) method, we found that the cerebellum, cingulate motor area, supplementary motor area, and putamen had significantly greater connectivity, whereas the precuneus had less connectivity in the motor networks at the automatic stage. Our findings demonstrate that the importance of the attention networks decrease when movements become automatic. Moreover, the process of automaticity is accompanied by a strengthened interaction of central motor networks even though the magnitude of the activation is decreased. We speculate that this increase in connectivity reflects more efficient neural coding of movement at the automatic stage.
C1 [Wu, Tao; Chan, Piu] Capital Med Univ, Xuanwu Hosp, Minist Educ,Dept Neurol, Key Lab Neurodegenerate Disorder,Beijing Inst Ger, Beijing, Peoples R China.
[Hallett, Mark] NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Hallett, M (reprint author), Bldg 10,Rm 5N226,10 Ctr Dr,MSC 1428, Bethesda, MD 20892 USA.
EM hallettm@ninds.nih.gov
FU National Institute of Neurological Disorders and Stroke Intramural
Competitive Fellowship; National Science Foundation of China [30570530];
NINDS, NIH
FX T. Wu was supported by a National Institute of Neurological Disorders
and Stroke Intramural Competitive Fellowship. This work was partially
supported by the National Science Foundation of China, Grant no.
30570530. In addition, this work was supported in part by the Intramural
Research Program of the NINDS, NIH.
NR 66
TC 44
Z9 44
U1 0
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3751
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD SEP 1
PY 2008
VL 586
IS 17
BP 4295
EP 4304
DI 10.1113/jphysiol.2008.153445
PG 10
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 347NO
UT WOS:000259148500024
PM 18617569
ER
PT J
AU Jin, GX
Zhou, XB
Wang, HH
Zhao, H
Cui, K
Zhang, XS
Chen, LN
Hazen, SL
Li, K
Wong, STC
AF Jin, Guangxu
Zhou, Xiaobo
Wang, Honghui
Zhao, Hong
Cui, Kemi
Zhang, Xiang-Sun
Chen, Luonan
Hazen, Stanley L.
Li, King
Wong, Stephen T. C.
TI The knowledge-integrated network biomarkers discovery for Major Adverse
Cardiac Events
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE proteomics; mass spectrometry; MACE; network biomarker; cross
validation; systems biology
ID PROSTATE-CANCER PROGRESSION; METASTATIC BREAST-CANCER; CROSS-VALIDATION;
PROTEIN-INTERACTION; MASS-SPECTROMETRY; PROTEOMICS; IDENTIFICATION;
SERUM; COMPLEX; HER2
AB The mass spectrometry (MS) technology in clinical proteomics is very promising for discovery of new biomarkers for diseases management. To overcome the obstacles of data noises in MS analysis, we proposed a new approach of knowledge-integrated biomarker discovery using data from Major Adverse Cardiac Events (MACE) patients. We first built up a cardiovascular-related network based on protein information coming from protein annotations in Uniprot, protein-protein interaction (PPI), and signal transduction database. Distinct from the previous machine learning methods in MS data processing, we then used statistical methods to discover biomarkers in cardiovascular-related network. Through the tradeoff between known protein information and data noises in mass spectrometry data, we finally could firmly identify those high-confident biomarkers. Most importantly, aided by protein-protein interaction network, that is, cardiovascular-related network, we proposed a new type of biomarkers, that is, network biomarkers, composed of a set of proteins and the interactions among them. The candidate network biomarkers can classify the two groups of patients more accurately than current single ones without consideration of biological molecular interaction.
C1 [Zhou, Xiaobo] Methodist Hosp, Inst Res, Ctr Biotechnol & Informat, Houston, TX 77030 USA.
Cornell Univ, Houston, TX 77030 USA.
[Jin, Guangxu; Zhang, Xiang-Sun] Chinese Acad Sci, Acad Math & Syst Sci, Beijing 100080, Peoples R China.
[Li, King] Methodist Hosp, Dept Radiol, Houston, TX 77030 USA.
[Wang, Honghui] Natl Inst Hlth, Ctr Clin, Bethesda, MD 20892 USA.
[Chen, Luonan] Osaka Sangyo Univ, Dept Elect Engn, Osaka 5748530, Japan.
[Hazen, Stanley L.] CCF, Ctr Cardiovasc Diagnost & Prevent, Cleveland, OH 44195 USA.
RP Zhou, XB (reprint author), Methodist Hosp, Inst Res, Ctr Biotechnol & Informat, 6535 Fannin, Houston, TX 77030 USA.
EM XZhou@thms.org
RI Jin, Guangxu/B-4627-2012
OI Jin, Guangxu/0000-0002-6616-6981
FU Methodist Research Institute, Cornell University; The Methodist
Hospital; NIH [R01LM08696, R01LM009161, R01AG028928]
FX This research is funded by the Bioinformatics Core Research Grant at The
Methodist Research Institute, Cornell University. Dr. Zhou is partially
funded by The Methodist Hospital Scholarship Award. He and Dr. Wong are
also partially funded by NIH grants R01LM08696, R01LM009161, and
R01AG028928.
NR 37
TC 27
Z9 27
U1 0
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
J9 J PROTEOME RES
JI J. Proteome Res.
PD SEP
PY 2008
VL 7
IS 9
BP 4013
EP 4021
DI 10.1021/pr8002886
PG 9
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 345RZ
UT WOS:000259015500036
PM 18665624
ER
PT J
AU Cascella, NG
Testa, SM
Meyer, SM
Rao, VA
Diaz-Asper, CM
Pearlson, GD
Schretlen, DJ
AF Cascella, Nicola G.
Testa, S. Marc
Meyer, Stephen M.
Rao, Vani A.
Diaz-Asper, Catherine M.
Pearlson, Godfrey D.
Schretlen, David J.
TI Neuropsychological impairment in deficit vs. non-deficit schizophrenia
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE schizophrenia; deficit syndrome; cognitive testing; neuropsychology
ID NEGATIVE SYMPTOMS; NONDEFICIT FORMS; COGNITIVE DEFICITS; BIPOLAR
DISORDER; VERBAL FLUENCY; PERFORMANCE; VALIDATION; PATTERNS
AB This study aimed to assess the severity and specificity of cognitive impairments that affect individuals with deficit versus non-deficit schizophrenia.
We compared 26 patients with the deficit subtype of schizophrenia (SZ-D) and 79 with non-deficit schizophrenia (SZ-ND) to 316 healthy adults (NC). All study participants completed a battery with 19 individual cognitive measures. After adjusting their test performance for age, sex, race, education and estimated premorbid IQ, we derived regression-based T-scores for each measure and the six derived cognitive domains including attention, psychomotor speed, executive function, verbal fluency, visual memory, and verbal memory.
Multivariate analyses of variance revealed Significant group effects for every individual measure and domain of cognitive functioning (all ps < 0.001). Post hoc comparisons revealed that patients with SZ-D performed significantly worse than NCs in every cognitive domain. They also produced lower scores than the SZ-ND group in every domain, but only the difference for verbal fluency reached statistical significance. The correlations of the effect sizes shown by the SZ-D and SZ-ND patients were of intermediate magnitude for the individual tests (r = 0.56, p < 0.01) and higher, but not statistically significant for the cognitive domains (r = 0.79, p = 0.06).
Patients with SZ-D demonstrate cognitive deficits that are both common and distinct from those shown by patients with SZ-ND. Their impairment of verbal fluency is consistent with the observation that poverty of speech is a clinically significant feature of patients with SZ-D. (C) 2007 Elsevier Ltd. All rights reserved.
C1 [Cascella, Nicola G.; Testa, S. Marc; Meyer, Stephen M.; Rao, Vani A.; Diaz-Asper, Catherine M.; Pearlson, Godfrey D.; Schretlen, David J.] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21287 USA.
[Schretlen, David J.] Johns Hopkins Univ, Sch Med, Dept Radiol & Radiol Sci, Baltimore, MD 21287 USA.
[Diaz-Asper, Catherine M.] NIMH, NIH, Bethesda, MD 20892 USA.
[Pearlson, Godfrey D.] Hartford Hosp Inst Living, Olin Neuropsychiat Res Ctr, Hartford, CT USA.
[Pearlson, Godfrey D.] Yale Univ, Sch Med, New Haven, CT USA.
RP Cascella, NG (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, 600 N Wolfe St,Meyer 144, Baltimore, MD 21287 USA.
EM cascella@jhmi.edu
FU NARSAD; NIH [MH60504, MH43775]; NIMH; Stanley Foundation
FX Funding for this study was provided by NARSAD Young Investigator Award
to NGC, NARSAD award to DJS, Stanley Foundation to NGC and NIH (MH60504
and MH43775) to GDP and DJS.; NARSAD, NIMH, and Stanley Foundation had
no further role in study design; in the collection, analysis and
interpretation of data; in the writing of the report; and in the
decision to submit the paper for publication.
NR 42
TC 14
Z9 14
U1 3
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD SEP
PY 2008
VL 42
IS 11
BP 930
EP 937
DI 10.1016/j.jpsychires.2007.10.002
PG 8
WC Psychiatry
SC Psychiatry
GA 342QJ
UT WOS:000258798300007
PM 18021807
ER
PT J
AU Dye, BA
Nowjack-Raymer, R
Barker, LK
Nunn, JH
Steele, JG
Tan, S
Lewis, BG
Beltran-Aguilar, ED
AF Dye, B. A.
Nowjack-Raymer, R.
Barker, L. K.
Nunn, J. H.
Steele, J. G.
Tan, S.
Lewis, B. G.
Beltran-Aguilar, E. D.
TI Overview and Quality Assurance for the Oral Health Component of the
National Health and Nutrition Examination Survey (NHANES), 2003-04
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Article
DE NHANES; oral health; dental public health; epidemiology; data
reliability; quality assurance
ID DENTAL EROSION; TOOTH WEAR; ETIOLOGY
AB The 2003-04 National Health and Nutrition Examination Survey (NHANES) was a collaborative effort involving 28 federal funding partners with the National Center for Health Statistics. The collaborators for the 2003-04 NHANES oral health component included the National Institute of Dental and Craniofacial Research and the National Center for Chronic Disease Prevention and Health Promotion, Division of Oral Health. Oral health data are available on 8,272 persons aged 2 years or older. This report provides an overview of the 2003-04 oral health component including content descriptions and procedures for oral health assessments conducted for the first time in a national survey in the United States. These assessments include posterior functional contacts, tooth wear, and oral health-related quality of life. This report also provides evaluations of data quality in terms of examiner reliability statistics (percent agreements, kappas, and correlation coefficients) for various NHANES 2003-04 oral health examination components and analytical recommendations for producing 6-year estimates using the previous two NHANES data collection components (1999-2000 and 2001-02).
C1 [Dye, B. A.] Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, CDC, NHANES Program, Hyattsville, MD 20782 USA.
[Dye, B. A.] Univ Maryland, Sch Dent, Baltimore, MD 21201 USA.
Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
[Barker, L. K.; Beltran-Aguilar, E. D.] Ctr Dis Control & Prevent, Natl Ctr Chron Dis Prevent & Hlth Promot, Div Oral Hlth, Atlanta, GA USA.
[Nunn, J. H.] Univ Dublin, Trinity Coll, Dent Sch & Hosp, Dept Publ & Child Dent Hlth, Dublin, Ireland.
[Steele, J. G.] Newcastle Univ, Sch Dent, Dept Restorat Dent, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
RP Dye, BA (reprint author), Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, CDC, NHANES Program, 3311 Toledo Rd,RM 4416, Hyattsville, MD 20782 USA.
EM bfd1@cdc.gov
OI Nunn, June/0000-0003-4481-544X
FU NHANES; NIH/NIDCR; CDC/National Center for Health Promotion and Disease
Prevention; Division of Oral Health; CDC/NCHS
FX The 2003-04 NHANES oral health component was a funding and content
collaborative effort between the NIH/NIDCR, the CDC/National Center for
Health Promotion and Disease Prevention, Division of Oral Health, and
the CDC/NCHS.
NR 24
TC 31
Z9 31
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD FAL
PY 2008
VL 68
IS 4
BP 218
EP 226
DI 10.1111/j.1752-7325.2007.00076.x
PG 9
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 380BU
UT WOS:000261441400006
PM 18248340
ER
PT J
AU Arnold, JI
Gray, NE
Jacobowitz, K
Viswanathan, L
Cheung, PW
McFann, KK
Le, H
Blackman, MR
AF Arnold, Julia I.
Gray, Nora E.
Jacobowitz, Ketzela
Viswanathan, Lavanya
Cheung, Pui W.
McFann, Kimberly K.
Le, Hanh
Blackman, Marc R.
TI Human prostate stromal cells stimulate increased PSA production in
DHEA-treated prostate cancer epithelial cells
SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Article
DE DHEA; stromal; prostate; PSA; coculture
ID PERIPHERAL TARGET TISSUES; GROWTH-FACTOR; COCULTURE MODEL;
DEHYDROEPIANDROSTERONE; ANDROGENS; MEN; PROGRESSION; EXPRESSION;
ESTROGENS; INTRACRINOLOGY
AB Dehydroepiandrosterone (DHEA) is commonly used as a dietary supplement and may affect prostate pathophysiology when metabolized to androgens and/or estrogens. Human prostate LAPC-4 cancer cells with a wild type androgen receptor (AR) were treated with DHEA, androgens dihydrotestosterone (DHT), T, or R1881), and E-2 and assayed for prostate specific antigen (PSA) protein and gene expression. In LAPC-4 monocultures, DHEA and E-2 induced little or no increase in PSA protein or mRNA expression compared to androgen-treated cells. When prostate cancer-associated (6S) stromal cells were added in coculture, DHEA stimulated LAPC-4 cell PSA protein secretion to levels approaching induction by DHT. Also, DHEA induced 15-fold more PSA mRNA in LAPC-4 cocultures than in monocultures. LAPC-4 proliferation was increased 2-3-fold when cocultured with 6S stromal cells regardless of hormone treatment. DHEA-treated 6S stromal cells exhibited a dose- and time-dependent increase in T secretion, demonstrating stromal cell metabolism of DHEA to T. Coculture with non-cancerous stroma did not induce LAPC-4 PSA production, suggesting a differential modulation of DHEA effect in a cancer-associated prostate stromal environment. This coculture model provides a research approach to reveal detailed endocrine. intracrine, and paracrine signaling between stromal and epithelial cells that regulate tissue homeostasis within the prostate, and the role of the tumor microenvironment in cancer progression. Published by Elsevier Ltd.
C1 [Arnold, Julia I.; Gray, Nora E.; Jacobowitz, Ketzela; Viswanathan, Lavanya; Cheung, Pui W.; Le, Hanh; Blackman, Marc R.] NCCAM, Endocrinol Sect, LCI, Div Intramural Res,NIH, Bethesda, MD 20892 USA.
[McFann, Kimberly K.] Univ Colorado, Hlth Sci Ctr, Denver, CO 80232 USA.
RP Arnold, JI (reprint author), NCCAM, Endocrinol Sect, LCI, Div Intramural Res,NIH, 9000 Rockville Pike 10-2B47, Bethesda, MD 20892 USA.
EM jarnold@mail.nih.gov
FU Intramural Research Program; National Center for Complementary and
Alternative Medicine; National Institutes of Health, Bethesda, MD
FX The authors thank Dr. Charles Sawyers (UCLA) for providing the LAPC-4
cells, Dr. John Isaacs (Johns Hopkins School of Medicine) for providing
the primary prostate stromal cells (5S, 6S, 9S, 12S) and Dr. Vernon
Steele (NIH-NCI) and Dr. Angela Brodie (University of Maryland) for
their constructive comments upon reviewing this manuscript. This work
was supported by the Intramural Research Program, National Center for
Complementary and Alternative Medicine, National Institutes of Health,
Bethesda, MD.
NR 40
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U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-0760
J9 J STEROID BIOCHEM
JI J. Steroid Biochem. Mol. Biol.
PD SEP
PY 2008
VL 111
IS 3-5
BP 240
EP 246
DI 10.1016/j.jsbmb.2008.06.008
PG 7
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 351YO
UT WOS:000259462100011
PM 18621129
ER
PT J
AU Condon, TP
Miner, LL
Balmer, CW
Pintello, D
AF Condon, Timothy P.
Miner, Lucinda L.
Balmer, Curtis W.
Pintello, Denise
TI Blending addiction research and practice: Strategies for technology
transfer
SO JOURNAL OF SUBSTANCE ABUSE TREATMENT
LA English
DT Article
DE addiction treatment; technology transfer; evidence-based practices;
Clinical Trials Network (CTN); Addiction Technology Transfer Center
(ATTC)
ID CLINICAL-TRIALS NETWORK; SUBSTANCE-ABUSE; DETOXIFICATION; INCENTIVES;
PROGRAMS
AB Consistent with traditional conceptions of technology transfer, efforts to translate substance abuse and addiction research into treatment practice have typically relied on the passive dissemination of research findings. The large gap between addiction research and practice, however, indicates that there are many barriers to successful technology transfer and that dissemination alone is not sufficient to produce lasting changes in addiction treatment. To accelerate the translation of research into practice, the National Institute on Drug Abuse launched the Blending Initiative in 2001. In part a collaboration with the Substance Abuse and Mental Health Services Administration/Center for Substance Abuse Treatment's Addiction Technology Transfer Center program, this initiative aims to improve the development, effectiveness, and usability of evidence-based practices and reduce the obstacles to their timely adoption and implementation. (C) 2008 Published by Elsevier Inc.
C1 [Condon, Timothy P.; Miner, Lucinda L.; Pintello, Denise] Natl Inst Drug Abuse, Bethesda, MD 20892 USA.
[Balmer, Curtis W.] JRS Int Inc, Silver Spring, MD 20910 USA.
RP Condon, TP (reprint author), Natl Inst Drug Abuse, 6001 Execut Blvd,Rm 5274, Bethesda, MD 20892 USA.
EM tc52x@nih.gov
NR 14
TC 24
Z9 24
U1 3
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0740-5472
J9 J SUBST ABUSE TREAT
JI J. Subst. Abus. Treat.
PD SEP
PY 2008
VL 35
IS 2
BP 156
EP 160
DI 10.1016/j.jsat.2007.09.004
PG 5
WC Psychology, Clinical; Substance Abuse
SC Psychology; Substance Abuse
GA 342QR
UT WOS:000258799100007
PM 18337054
ER
PT J
AU Janjanin, S
Li, WJ
Morgan, MT
Shanti, RA
Tuan, RS
AF Janjanin, Sasa
Li, Wan-Ju
Morgan, Meredith T.
Shanti, Rabie A.
Tuan, Rocky S.
TI Mold-shaped, nanofiber scaffold-based cartilage engineering using human
mesenchymal stem cells and bioreactor
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE mesenchymal stem cells; tissue engineering; cartilage; nanofibers;
nanofibrous scaffolds; mold; bioreactor; plastic and reconstructive
surgery
ID CHONDROGENIC DIFFERENTIATION; TISSUE; CHONDROCYTES; AGAROSE;
FABRICATION; EXPRESSION
AB Background. Mesenchymal stem cell (MSC)-based tissue engineering is a promising future alternative to autologous cartilage grafting. This study evaluates the potential of using MSCs, seeded into electrospun, biodegradable polymeric nanofibrous scaffolds, to engineer cartilage with defined dimensions and shape, similar to grafts used for subcutaneous implantation in plastic and reconstructive surgery.
Materials and methods. Human bone marrow derived MSCs seeded onto nanofibrous scaffolds and placed in custom-designed molds were cultured for up to 42 days in bioreactors. Chondrogenesis was induced with either transforming growth factor-beta 1 (TGF-beta I) alone or in combination with insulin-like growth factor-I (IGF-I).
Results. Constructs exhibited hyaline cartilage histology with desired thickness and shape as well as favorable tissue integrity and shape retention, suggesting the presence of elastic tissue. Time-dependent increase in cartilage matrix gene expression was seen in both types of culture: at Day 42, TGF-beta 1/IGF-I treated cultures showed higher collagen Type 2 and aggrecan expression. Both culture conditions showed significant time-dependent increase in sulfated glycosaminoglycan and hydroxyproline contents. TGF-beta 1/IGF-I-treated samples were significantly stiffer; with equilibrium compressive Young's modulus values reaching 17 kPa by Day 42.
Conclusions. The successful ex vivo development of geometrically defined cartilaginous construct using customized molding suggests the potential of cell-based cartilage tissue for reconstructive surgery. (c) 2008 Elsevier Inc. All rights reserved.
C1 [Janjanin, Sasa; Li, Wan-Ju; Morgan, Meredith T.; Shanti, Rabie A.; Tuan, Rocky S.] NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Janjanin, Sasa] Zagreb Clin Hosp Ctr, Dept Otorhinolaryngol Head & Neck Surg, Zagreb, Croatia.
[Shanti, Rabie A.] NIH, Howard Hughes Med Inst, Res Scholars Program, Bethesda, MD 20892 USA.
RP Tuan, RS (reprint author), NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, Dept Hlth & Human Serv, Bldg 50,Room 1523,MSC 8022, Bethesda, MD 20892 USA.
EM tuanr@mail.nih.gov
FU NIH [ZO1 41131]; U.S. Department of State
FX This work is supported by the Intramural Research Program of NIAMS, NIH
(Grant ZO1 41131). Sasa Janjanin is a recipient of the Fulbright
Scholarship of the U.S. Department of State.
NR 31
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U1 4
U2 23
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
J9 J SURG RES
JI J. Surg. Res.
PD SEP
PY 2008
VL 149
IS 1
BP 47
EP 56
DI 10.1016/j.jss.2007.12.788
PG 10
WC Surgery
SC Surgery
GA 340GD
UT WOS:000258633200008
PM 18316094
ER
PT J
AU Iwasa, KH
Sul, B
AF Iwasa, Kuni H.
Sul, Bora
TI Effect of the cochlear microphonic on the limiting frequency of the
mammalian ear
SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA
LA English
DT Article
ID OUTER HAIR CELL; GUINEA-PIG COCHLEA; BASILAR-MEMBRANE; MOTILITY;
CURRENTS; ELECTROMOTILITY; AMPLIFICATION; POTENTIALS; AMPLIFIER;
TRANSDUCTION
AB Electromotility is a basis for cochlear amplifier, which controls the sensitivity of the mammalian ear and contributes to its frequency selectivity. Because it is driven by the receptor potential, its frequency characteristics are determined by the low-pass RC filter intrinsic to the cell, which has a corner frequency about 1/10th of the operating frequency. This filter significantly decreases the efficiency of electromotility as an amplifier. The present paper examines a proposal that the cochlear microphonic, the voltage drop across the extracellular medium by the receptor current, contributes to overcome this problem. It is found that this effect can improve frequency dependence. However, this effect alone is too small to enhance the effectiveness of electromotility beyond 10 kHz in the mammalian ear. (C) 2008 Acoustical Society of America.
C1 [Iwasa, Kuni H.; Sul, Bora] NIDCD, Biophys Sect, NIH, Rockville, MD 20850 USA.
RP Iwasa, KH (reprint author), NIDCD, Biophys Sect, NIH, 5 Res Ct,Rm 1B03, Rockville, MD 20850 USA.
EM kits@nih.gov; Bulb@nidcd.nih.gov
OI Iwasa, Kuni/0000-0002-9397-7704
FU NIDCD; NIH
FX The authors thank Richard Chadwick and two anonymous reviewers for
valuable comments. This research was supported by the Intramural
Research Program of the NIDCD, NIH.
NR 29
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U1 0
U2 3
PU ACOUSTICAL SOC AMER AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0001-4966
J9 J ACOUST SOC AM
JI J. Acoust. Soc. Am.
PD SEP
PY 2008
VL 124
IS 3
BP 1607
EP 1612
DI 10.1121/1.2953317
PN 1
PG 6
WC Acoustics; Audiology & Speech-Language Pathology
SC Acoustics; Audiology & Speech-Language Pathology
GA 356PQ
UT WOS:000259790500023
PM 19045652
ER
PT J
AU Towbin, K
AF Towbin, Kenneth
TI Paying attention to stimulants: Height, weight, and cardiovascular
monitoring in clinical practice
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Editorial Material
ID AMERICAN-HEART-ASSOCIATION; SUDDEN-DEATH; GROWTH; DISORDER; CHILDREN;
METHYLPHENIDATE; ADOLESCENTS; STATEMENT; CLONIDINE; COUNCIL
C1 [Towbin, Kenneth] NIMH, Emot & Dev Branch, Mood & Anxiety Disorder Program, NIH, Bethesda, MD 20892 USA.
[Towbin, Kenneth] US Dept HHS, Washington, DC 20201 USA.
RP Towbin, K (reprint author), NIMH, Emot & Dev Branch, Mood & Anxiety Disorder Program, NIH, CRC Room 1-3633,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM Kenneth.Towbin@nih.gov
NR 20
TC 7
Z9 7
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD SEP
PY 2008
VL 47
IS 9
BP 977
EP 980
DI 10.1097/CHI.0b013e31817e0eb9
PG 4
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 341VE
UT WOS:000258742500001
PM 18580503
ER
PT J
AU Perdue, KA
Copeland, MK
Karjala, Z
Cheng, LI
Ward, JM
Elkins, WR
AF Perdue, Kathy A.
Copeland, Michelle K.
Karjala, Zuzana
Cheng, Lily I.
Ward, Jerrold M.
Elkins, William R.
TI Suboptimal Ability of Dirty-bedding Sentinels to Detect Spironucleus
muris in a Colony of Mice with Genetic Manipulations of the Adaptive
Immune System
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Article
ID T-CELL DEVELOPMENT; LABORATORY MICE; GIARDIA-MURIS; SYPHACIA-OBVELATA;
HOST SPECIFICITY; MOUSE COLONY; NUDE-MICE; HEXAMITIASIS; INFECTION; TCR
AB Spironucleus muris is an unacceptable infectious agent for most rodent colonies. Exposure of sentinel mice to dirty bedding and examination of sentinel intestinal smears was not sufficient for identification of the extent of spironucleosis within 1 mouse room. Clinical abnormalities were not reported in the animals housed in the room despite extensive breeding and a preponderance of mice genetically engineered to have nonfunctional T and B cells. In addition, researchers reported that the infection had not altered their research data. During investigation of the outbreak, direct intestinal smears performed on related animals (conspecifics, offspring, or siblings) revealed that immunodeficient mice often tested negative whereas the immunocompetent cohort tested positive. In this study, we used culled colony animals and compared direct intestinal exam test results with histologic results. The comparison showed the extent of false negatives that may occur when direct intestinal exam alone is used to detect this protozoon. Sensitivity of the direct intestinal exam for detection of S. muris was calculated to be 71%, while histology sensitivity was 91%. In light of the study results and an extensive literature review, we revised our health surveillance plan so that the age and duration of exposure to dirty bedding among sentinel mice is varied at the time of testing.
C1 [Perdue, Kathy A.; Copeland, Michelle K.; Cheng, Lily I.; Ward, Jerrold M.; Elkins, William R.] NIAID, Comparat Med Branch, Div Intramural Res, Bethesda, MD 20892 USA.
[Karjala, Zuzana] NIH, Hlth Surveillance Lab, Diagnost & Res Serv Branch, Div Vet Resources,Off Res Serv, Bethesda, MD 20892 USA.
RP Perdue, KA (reprint author), NIAID, Comparat Med Branch, Div Intramural Res, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kperdue@niaid.nih.gov
FU National Institute of Allergy and Infectious Disease
FX We wish to thank Dr BJ Fowlkes, Dr Karen Laky, and Ms Sharron Evans,
RSSIII, for providing cull animals for testing, assisting with the
animal submission, and providing individual animal data needed for the
study; Ms Remina Greenfield for Figure 1; Ms. Elizabeth M. Williams and
Mr. Lawrence J. Faucette for tissue processing assistance; and Mr Omar
Feliciano, Senior Technician, and the rest of the 14B South caretaking
and technical staff for all of their hard work and assistance with this
study. This research was supported by the Intramural Research Program of
the National Institute of Allergy and Infectious Disease and the Office
of Research Services (National Institutes of Health, Bethesda, MD). The
views and opinions provided are those of the authors and do not reflect
the official policy or positions of the National Institutes of Health,
the Department of Health and Human Services, or the United States
Government.
NR 45
TC 2
Z9 2
U1 0
U2 1
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 10
EP 17
PG 8
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500003
PM 18947164
ER
PT J
AU Fain, MA
Karjala, Z
Perdue, KA
Copeland, MK
Cheng, LI
Elkins, WR
AF Fain, Michele A.
Karjala, Zuzana
Perdue, Kathy A.
Copeland, Michelle K.
Cheng, Lily I.
Elkins, William R.
TI Detection of Spironucleus muris in Unpreserved Mouse Tissue and Fecal
Samples by Using a PCR Assay
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Article
ID LABORATORY MICE; GIARDIA-MURIS; HEXAMITIASIS; EXCYSTATION; INFECTIONS;
STRAINS
AB The purpose of this study was to develop a rapid DNA isolation method and a sensitive and specific PCR assay for detecting Spironucleus muris in mouse tissue and fecal samples. A PCR assay based on the carboxy terminus of the elongation factor la gene was developed; the PCR product was confirmed by nucleic acid sequencing and nested PCR. The new PCR assay then was used to test feces from animals that had been screened for S. muris by using direct intestinal examination and histology. The PCR assay was determined to be a more sensitive test than either direct intestinal examination or intestinal histology. To our knowledge, this assay represents the first use of a PCR-based diagnostic screening method to confirm the presence of S. muris in murine tissue and fecal samples.
C1 [Fain, Michele A.; Perdue, Kathy A.; Copeland, Michelle K.; Cheng, Lily I.; Elkins, William R.] NIAID, Comparat Med Branch, Bethesda, MD 20892 USA.
[Karjala, Zuzana] NIH, Hlth Surveillance Lab, Diagnost & Res Serv Branch, Div Vet Resources,Off Res Serv, Bethesda, MD 20892 USA.
RP Perdue, KA (reprint author), NIAID, Comparat Med Branch, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kperdue@niaid.nih.gov
FU National Institute of Allergy and Infectious Disease
FX We wish to think Dr BJ Fowlkes, Dr Karen Laky, Ms Sharron Evans, RSSIIl,
for providing cull animals for testing; Ms Elizabeth M Williams for
tissue processing assistance; Mr Jeremy Dathe of Lofstrand Labs for his
superior service; Ms Roman Tesfaye for her help with the figures; and Dr
Gerry Shea for his scientific assistance. This research was supported by
the Intramural Research Program of the National Institute of Allergy and
Infectious Disease (National Institutes of Health, Bethesda, MD). The
views and opinions provided are those of the authors and do not reflect
the official policy or positions of the National Institutes of Health,
the Department of Health and Human Services, or the United States
Government.
NR 26
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U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 39
EP 43
PG 5
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500008
PM 18947169
ER
PT J
AU DeMuro, K
AF DeMuro, K.
TI New Approach to Quality Assurance
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [DeMuro, K.] SoBran, Bethesda, MD USA.
[DeMuro, K.] NIH, DVR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 92
EP 92
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500071
ER
PT J
AU McGee, K
Patel, D
McKenna, J
Banks, F
Sekou, S
Prevost, K
Barnard, D
Skopets, B
AF McGee, K.
Patel, D.
McKenna, J.
Banks, F.
Sekou, S.
Prevost, K.
Barnard, D.
Skopets, B.
TI Use of Dietary Fiber in the Management of Chronic and Reoccurring
Diarrhea in Pigtail Macaques (Macaca nemestrina)
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [McGee, K.; Patel, D.; McKenna, J.; Banks, F.; Sekou, S.] NIH, SoBran Inc, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 104
EP 105
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500104
ER
PT J
AU Caviness, GF
Thigpen, JE
Locklear, J
Whiteside, TE
Grant, MG
Forsythe, DB
AF Caviness, G. F.
Thigpen, J. E.
Locklear, J.
Whiteside, T. E.
Grant, M. G.
Forsythe, D. B.
TI Incidence of Mycoplasma Contaminants in Cell Cultures: Detection and
Growth on Trypticase Soy Agar Containing 5% Sheep Blood
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Caviness, G. F.; Thigpen, J. E.; Locklear, J.; Whiteside, T. E.; Grant, M. G.; Forsythe, D. B.] NIH, Res Triangle Pk, NC USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 106
EP 106
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500108
ER
PT J
AU Locklear, J
Caviness, GF
Thigpen, JE
Whiteside, TE
Grant, MG
Forsythe, DB
AF Locklear, J.
Caviness, G. F.
Thigpen, J. E.
Whiteside, T. E.
Grant, M. G.
Forsythe, D. B.
TI Arthropod Detection during Screening of Sentinel Mice
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Locklear, J.; Caviness, G. F.; Thigpen, J. E.; Whiteside, T. E.; Grant, M. G.; Forsythe, D. B.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 106
EP 107
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500110
ER
PT J
AU Thigpen, JE
Hobbs, BA
Cliffordz, CB
Grant, MG
Myers, MB
Forsythe, DB
AF Thigpen, J. E.
Hobbs, B. A.
Cliffordz, C. B.
Grant, M. G.
Myers, M. B.
Forsythe, D. B.
TI Background Lesions in Homozygous and Heterozygous Mice of Two Stocks,
Crl:NU-Fox(nu) and CA:CD1-Foxn1(nu), Used as Sentinels
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Thigpen, J. E.; Hobbs, B. A.; Grant, M. G.; Myers, M. B.; Forsythe, D. B.] NIEHS, Comparat Med Branch, Res Triangle Pk, NC 27709 USA.
[Cliffordz, C. B.] Charles River, Wilmington, DE USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 107
EP 107
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500112
ER
PT J
AU Davis, BA
Graninger, H
Hitt, ND
AF Davis, B. A.
Graninger, H.
Hitt, N. D.
TI Novel Cage Flag System for Identifying Special Husbandry Requests
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Davis, B. A.; Graninger, H.; Hitt, N. D.] NINDS, AHCS, Germantown, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 117
EP 117
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500141
ER
PT J
AU Pinkney, J
Smith, D
Burkholder, T
AF Pinkney, J.
Smith, D.
Burkholder, T.
TI Fur Mite Treatment 101: Labor, Time Management, and Project Coordination
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Pinkney, J.] SoBran, Bethesda, MD USA.
[Pinkney, J.; Smith, D.; Burkholder, T.] NIH, DVR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 127
EP 127
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500170
ER
PT J
AU Mensch, J
AF Mensch, J.
TI Supplemental Care for ERCC-1-deficient Mice
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Mensch, J.] SoBran Inc, Rockville, MD USA.
[Mensch, J.] FLAC, NIAAA, OLAS, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 130
EP 130
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500177
ER
PT J
AU Rosa, MC
Perez, D
Sabol-Jones, M
Hitt, ND
AF Rosa, M. C.
Perez, D.
Sabol-Jones, M.
Hitt, N. D.
TI Systematic Approach to Solving Breeding Colony Problems
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Rosa, M. C.; Perez, D.; Sabol-Jones, M.; Hitt, N. D.] NINDS, NIH, AHCS, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 134
EP 135
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500190
ER
PT J
AU Huntsberry, M
AF Huntsberry, M.
TI Enhancements to the Canine Socialization and Training Program
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Huntsberry, M.] SoBran, Bethesda, MD USA.
[Huntsberry, M.] NIH, DVR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 5
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 135
EP 135
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500191
ER
PT J
AU Savane, S
AF Savane, S.
TI Use of Flashlights in Old World Nonhuman Primate Health Monitoring
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Savane, S.] SoBran, Bethesda, MD USA.
[Savane, S.] NIH, DVR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 140
EP 140
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500206
ER
PT J
AU Thigpen, JE
Padilla-Banks, E
Kissling, G
Caviness, GF
WIuteside, TE
Locklear, J
Grant, MG
Forsythe, DB
AF Thigpen, J. E.
Padilla-Banks, E.
Kissling, G.
Caviness, G. F.
WIuteside, T. E.
Locklear, J.
Grant, M. G.
Forsythe, D. B.
TI Commercially Available Corn-cob Bedding Naturally Contaminated with
Zearalenone Significantly Advances the Time of Vaginal Opening in
Immature CD-1 Mice
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Thigpen, J. E.; Padilla-Banks, E.; Kissling, G.; Caviness, G. F.; WIuteside, T. E.; Locklear, J.; Grant, M. G.; Forsythe, D. B.] NIH, Res Triangle Pk, NC USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 159
EP 159
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500255
ER
PT J
AU Hagelin, K
Young, J
Mattison, J
Ingram, D
AF Hagelin, K.
Young, J.
Mattison, J.
Ingram, D.
TI Locomotor Activity in Rhesus Macaques (Macaca mulatta) on Long-term
Calorie Restriction
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Hagelin, K.; Young, J.] NIHAC SoBran Inc, Div Vet Resources, Poolesville, MD USA.
[Mattison, J.] NIA, Lab Expt Gerontol, Poolesville, MD USA.
[Ingram, D.] Pennington Biomed Res Ctr, Nutr Neurosci & Aging Lab, Baton Rouge, LA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 161
EP 161
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500260
ER
PT J
AU Blair, R
Hoogstraten-Miller, SL
Mueller, K
Schwartzberg, P
AF Blair, R.
Hoogstraten-Miller, S. L.
Mueller, K.
Schwartzberg, P.
TI Alternative Method for Intrathymic Injections in Mice
SO JOURNAL OF THE AMERICAN ASSOCIATION FOR LABORATORY ANIMAL SCIENCE
LA English
DT Meeting Abstract
C1 [Hoogstraten-Miller, S. L.] NHGRI, Off Lab Anim Med, NIH, Bethesda, MD 20892 USA.
[Blair, R.; Mueller, K.; Schwartzberg, P.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1559-6109
J9 J AM ASSOC LAB ANIM
JI J. Amer. Assoc. Lab. Anim. Sci.
PD SEP
PY 2008
VL 47
IS 5
BP 171
EP 171
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 361MJ
UT WOS:000260131500286
ER
PT J
AU Goode, PS
FitzGerald, MP
Richter, HE
Whitehead, WE
Nygaard, I
Wren, PA
Zyczynski, HM
Cundiff, G
Menefee, S
Senka, JM
Gao, X
Weber, AM
AF Goode, Patricia S.
FitzGerald, Mary P.
Richter, Holly E.
Whitehead, William E.
Nygaard, Ingrid
Wren, Patricia A.
Zyczynski, Halina M.
Cundiff, Geoffrey
Menefee, Shawn
Senka, Judith M.
Gao, Xin
Weber, Anne M.
CA Pelvic Floor Disorders Network
TI Enhancing participation of older women in surgical trials
SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
LA English
DT Article
ID PELVIC ORGAN PROLAPSE; RECRUITMENT STRATEGIES; CLINICAL-TRIAL;
STRESS-INCONTINENCE; ADULTS; DYSFUNCTION; DEPRESSION; EXCLUSION; PEOPLE
AB BACKGROUND: Older participants are often excluded from clinical trials, precluding a representative sample.
STUDY DESIGN: Using qualitative and quantitative methods, we examined recruitment and retention of older women with pelvic organ prolapse in two surgical trials: the randomized Colpopexy And Urinary Reduction Efforts (CARE) study and the Longitudinal Pelvic Symptoms and Patient Satisfaction After Colpocleisis cohort study. Using focus groups, we developed a questionnaire addressing factors facilitating and impeding the recruitment and retention of older study participants and administered it to research staff. Enrollment-to-surgery ratios, missed visit rates, and dropout rates for older and younger participants were compared using Fisher's exact test, with cut-points of 70 and 80 years for the CARE and Colpocleisis studies, respectively.
RESULTS: Questionnaires were completed by 23 physician investigators and I I nurses or coordinators (92% response rate). Respondents indicated it was more difficult to recruit older research participants (32%), obtain informed con sent (56%), and retain participants to study completion (50%). Challenges to recruitment included caregiver involvement in the decision to participate and participant comorbidities. Perceived barriers to retention were transportation, caregiver availability, and participant fatigue. Data quality was challenged by sensory and cognitive impairment, resulting in a change from telephone inter-views to in-person visits in the Colpocleisis study. Older participants did not have higher dropout rates than younger participants. There were no differences in missed in-person visits or telephone interview rates between age groups.
CONCLUSIONS: Strategies, albeit unstudied, could assist investigators in planning surgical trials-that successfully enroll and retain older women.
C1 [Goode, Patricia S.] Univ Alabama, Birmingham VA Med Ctr, Dept Med, Birmingham, AL 35233 USA.
[Richter, Holly E.] Univ Alabama, Dept Obstet & Gynecol, Birmingham, AL 35233 USA.
[Goode, Patricia S.] Vet Affairs Med Ctr, Atlanta Geriatr Res Educ & Clin Ctr, Birmingham, AL USA.
[FitzGerald, Mary P.] Loyola Univ, Med Ctr, Dept Obstet & Gynecol, Maywood, IL 60153 USA.
[Whitehead, William E.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Nygaard, Ingrid] Univ Utah, Hlth Sci Ctr, Dept Obstet & Gynecol, Salt Lake City, UT USA.
[Wren, Patricia A.] Oakland Univ, Dept Hlth Behav Hlth Educ, Rochester, MI 48063 USA.
[Zyczynski, Halina M.] Univ Pittsburgh, Magee Womens Hosp, Dept Obstet & Gynecol, Pittsburgh, PA 15213 USA.
[Cundiff, Geoffrey] Univ British Columbia, Dept Obstet & Gynaecol, Vancouver, BC V5Z 1M9, Canada.
[Menefee, Shawn] Univ Calif San Diego, Dept Obstet & Gynecol, San Diego, CA 92103 USA.
[Senka, Judith M.] Northwestern Univ, Evanston Hosp, Dept Obstet & Gynecol, Evanston, IL 60201 USA.
[Gao, Xin] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Weber, Anne M.] NICHHD, NIH, Bethesda, MD 20892 USA.
RP Goode, PS (reprint author), Univ Alabama, Birmingham VA Med Ctr, Dept Med, 11G,700 S 19th St, Birmingham, AL 35233 USA.
FU National Institute of Child Health and Human Development [U01 HD41249,
U10 HD41268, U10 HD41248, U10 HD41250, U10 HD41261, U10 HD41263, U10
HD41269, U10 HD41267]
FX Supported by grants from the National Institute of Child Health and
Human Development (U01 HD41249, U10 HD41268, U10 HD41248, U10 HD41250,
U10 HD41261, U10 HD41263, U10 HD41269, and U10 HD41267).
NR 26
TC 10
Z9 11
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1072-7515
J9 J AM COLL SURGEONS
JI J. Am. Coll. Surg.
PD SEP
PY 2008
VL 207
IS 3
BP 303
EP 311
DI 10.1016/j.jamcollsurg.2008.03.012
PG 9
WC Surgery
SC Surgery
GA 349FD
UT WOS:000259265800001
PM 18722933
ER
PT J
AU Heaton, TE
Peranteau, WH
Bauer, TR
Zoltick, PW
Hickstein, DD
Flake, AW
AF Heaton, Todd Erin
Peranteau, William H.
Bauer, Thomas R.
Zoltick, Philip W.
Hickstein, Dennis D.
Flake, Alan W.
TI High level chimerism and donor specific tolerance achieved in the canine
model by in utero hematopoietic cell transplantation followed by
postnatal minimal conditioning bone marrow transplantation
SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
LA English
DT Meeting Abstract
CT 94th Annual Clinical Congress of the American-College-of-Surgeons/63rd
Annual Sessions of the Owen H Wangensteen Forum on Fundamental Surgical
Problems
CY OCT 12-16, 2008
CL San Francisco, CA
SP Amer Coll Surg
C1 [Heaton, Todd Erin; Peranteau, William H.; Bauer, Thomas R.; Zoltick, Philip W.; Hickstein, Dennis D.; Flake, Alan W.] Childrens Hosp Philadelphia, NIH, Bethesda, MD USA.
RI Heaton, Todd/E-5197-2016
OI Heaton, Todd/0000-0003-3515-0028
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1072-7515
J9 J AM COLL SURGEONS
JI J. Am. Coll. Surg.
PD SEP
PY 2008
VL 207
IS 3
SU S
BP S105
EP S105
DI 10.1016/j.jamcollsurg.2008.06.268
PG 1
WC Surgery
SC Surgery
GA 349NV
UT WOS:000259288500234
ER
PT J
AU Rovner, AJ
Stallings, VA
Kawchak, DA
Schall, JI
Ohene-Frempong, K
Zemel, BS
AF Rovner, Alisha J.
Stallings, Virginia A.
Kawchak, Deborah A.
Schall, Joan I.
Ohene-Frempong, Kwakij
Zemel, Babette S.
TI High risk of vitamin D deficiency in children with sickle cell disease
SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION
LA English
DT Article
ID ADOLESCENT GIRLS; 25-HYDROXYVITAMIN-D; OUTCOMES
AB Vitamin D is a particularly concerning nutrient for children with homozygous SS sickle cell disease (SCD-SS) due to their increased skin melanin concentrations, reduced levels of physical activity, and poor vitamin D intake. The goal of this study was to compare the vitamin D status of children with SCD-SS to healthy African-American children living in the same geographic area. Growth, dietary intake, serum 25-hydroxyvitamin D [25(OH)D], and intact parathyroid hormone (iPTH) concentrations were measured in 61 African-American subjects with SCD-SS and 89 healthy African-American control subjects age 5 to 18 years from the Philadelphia, PA, region (latitude 39.95 degrees N). Median serum 25(OH)D concentrations were 15 ng/mL (95% confidence interval [Cl]: 13, 17) in subjects with SCD-SS and 21 ng/mL (95% CI: 18, 22) in healthy control subjects (P<0.0002). Vitamin D deficiency [25(OH)D<11 mg/mL] was found in 33% of subjects with SCD-SS and 9% of healthy control subjects (P<0.001); 25% of subjects with SCD-SS and 17% of healthy control subjects had elevated iPTH [(>59 rho g/mL), P<0.05]. Ninety-three percent of subjects with SCD-SS and 90% of healthy subjects had vitamin D insufficiency [25(OH)D<30 mg/mL]. The risk of vitamin D deficiency among subjects with SCD-SS was 5.3 (95% CI: 2.5, 8.2) times greater than control subjects, adjusted for season and age. Poor vitamin D status was prevalent in children with SCD-SS and healthy African-American children living in the same geographic area. However, children with SCD-SS were at greater risk for vitamin D deficiency than healthy African-American children.
C1 [Zemel, Babette S.] Childrens Hosp Philadelphia, Div Gastroenterol Hepatol, Philadelphia, PA 19104 USA.
[Rovner, Alisha J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent, Rockville, MD USA.
[Schall, Joan I.] Childrens Hosp Philadelphia, Nutr & Growth Lab, Philadelphia, PA 19104 USA.
[Zemel, Babette S.] Childrens Hosp Philadelphia, Div Gastroenterol Hepatol, Philadelphia, PA 19104 USA.
[Ohene-Frempong, Kwakij] Childrens Hosp Philadelphia, Div Hematol, Philadelphia, PA 19104 USA.
RP Zemel, BS (reprint author), Childrens Hosp Philadelphia, Div Gastroenterol Hepatol, CHOP N,Room 1560,34th & Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM zemel@email.chop.edu
RI Zemel, Babette/D-1117-2009
FU General Clinical Research Center [5-MO1-RR-000240]; Comprehensive Sickle
Cell Center [1354 HL 70596-3]; Nutrition Center at The Children's
Hospital of Philadelphia; American Society for Parenteral and Enteral
Nutrition
FX Funding for this research was provided by the General Clinical Research
Center (5-MO1-RR-000240), Comprehensive Sickle Cell Center (1354 HL
70596-3), the Nutrition Center at The Children's Hospital of
Philadelphia, and the Richard Fleming Grant from the American Society
for Parenteral and Enteral Nutrition.; We greatly appreciate the
children and their families from the Comprehensive Sickle Cell Center at
The Children's Hospital of Philadelphia for participating in this study.
We acknowledge the staff of the General Clinical Research Center for
drawing the blood and storing and shipping the samples, Richard Reitz,
MD, and his lab staff at Quest Nichols Institute (San Juan Capistrano,
CA) for conducting the vitamin D and PTH analyses, Kimberly O'Brien,
PhD, for serving as thesis advisor for Alisha Rovner, PhD (these data
were collected as part of a doctoral dissertation), and Dei Macleod for
her assistance in the manuscript preparation.
NR 23
TC 29
Z9 32
U1 0
U2 0
PU AMER DIETETIC ASSOC
PI CHICAGO
PA 120 S RIVERSIDE PLZ, STE 2000, CHICAGO, IL 60606-6995 USA
SN 0002-8223
J9 J AM DIET ASSOC
JI J. Am. Diet. Assoc.
PD SEP
PY 2008
VL 108
IS 9
BP 1512
EP 1516
DI 10.1016/j.jada.2008.06.433
PG 5
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 346DR
UT WOS:000259049100023
PM 18755325
ER
PT J
AU Bassim, CW
Gibson, G
Ward, T
Paphides, BM
DeNucci, DJ
AF Bassim, Carol W.
Gibson, Gretchen
Ward, Timothy
Paphides, Brian M.
DeNucci, Donald J.
TI Modification of the risk of mortality from pneumonia with oral hygiene
care
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE long-term care; nursing home; oral hygiene; oral care; pneumonia
ID LONG-TERM-CARE; VENTILATOR-ASSOCIATED PNEUMONIA; HOME-ACQUIRED
PNEUMONIA; NURSING-HOME; ASPIRATION PNEUMONIA; RESPIRATORY PATHOGENS;
NOSOCOMIAL INFECTIONS; DENTAL PLAQUE; OLDER-ADULTS; HEALTH-CARE
AB OBJECTIVES: To investigate the associations between the assignment of an oral hygiene aide staff member and risk factors for mortality from pneumonia in a nursing home and to test the hypothesis that this care would affect the incidence of mortality from pneumonia.
DESIGN: Electronic medical records.
SETTING:Nursing home.
PARTICIPANTS: One hundred forty-three residents of a Veterans Affairs Medical Center (VAMC) nursing home.
METHODS: The electronic medical records of 143 residents of a VAMC nursing home were analyzed for risk factors for pneumonia. A certified nursing assistant had been assigned to provide oral hygiene care for residents on two of four nursing home wards. Researchers performed a longitudinal analysis of resident's medical records to investigate the association between the assignment of an oral hygiene aide with the risk of mortality from pneumonia.
RESULTS: Initially, the group that received oral care, an older and less functionally able group, showed approximately the same incidence of mortality from pneumonia as the group that did not receive oral care, but when the data were adjusted for the risk factors found to be significant for mortality from pneumonia, the odds of dying from pneumonia in the group that did not receive oral care was more than three times that of the group that did receive oral care (odds ratio=3.57, P=.03). Modified risk factors included age, functionality, cognitive function, and clinical concern about aspiration pneumonia.
CONCLUSION: Oral hygiene nursing aide intervention may be an efficient risk factor modifier of mortality from nursing home-associated pneumonia.
C1 [Bassim, Carol W.; DeNucci, Donald J.] Dental Serv, Washington, DC USA.
[Bassim, Carol W.; DeNucci, Donald J.] Vet Affairs Med Ctr, Washington, DC 20422 USA.
[Gibson, Gretchen] Fayetteville Vet Affaires Med Ctr, Dent Serv, Fayetteville, AR USA.
[Ward, Timothy; DeNucci, Donald J.] Dept Vet Affairs, Off Dent, Washington, DC USA.
[Paphides, Brian M.] N Florida S Georgia Vet Hlth Syst, Vet Affairs Med Ctr, Dent Serv, Lake City, FL USA.
RP Bassim, CW (reprint author), NIH NIDCR CRC, 10 Ctr Dr Bldg 10,Rm 1N-118,MSC 1191, Bethesda, MD 20892 USA.
EM bassimc@mail.nih.gov
FU Dental Research Fellowship
FX This work was supported by a Dental Research Fellowship through the
Veterans Affairs Office of Academic Affiliations. We would like to thank
the dental and long-term care staff of the Lake City, Florida, VAMC for
their service for our veterans.
NR 51
TC 36
Z9 36
U1 1
U2 6
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD SEP
PY 2008
VL 56
IS 9
BP 1601
EP 1607
DI 10.1111/j.1532-5415.2008.01825.x
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 347PC
UT WOS:000259152500002
PM 18691286
ER
PT J
AU Unruh, ML
Newman, AB
Larive, B
Dew, MA
Miskulin, DC
Greene, T
Beddhu, S
Rocco, MV
Kusek, JW
Meyer, KB
AF Unruh, Mark L.
Newman, Anne B.
Larive, Brett
Dew, Mary Amanda
Miskulin, Dana C.
Greene, Tom
Beddhu, Srinivasan
Rocco, Michael V.
Kusek, John W.
Meyer, Klemens B.
CA Hemodialysis Study Grp
TI The influence of age on changes in health-related quality of life over
three years in a cohort undergoing hemodialysis
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE hemodialysis; quality of life; aging; chronic health conditions
ID STAGE RENAL-DISEASE; CHRONIC DIALYSIS; MEMBRANE FLUX; PSYCHOSOCIAL
FACTORS; FUNCTIONAL HEALTH; KIDNEY-DISEASE; SURVIVAL; HEMO; ADEQUACY;
OUTCOMES
AB OBJECTIVES: To assess the extent to which persons aged 70 and older undergoing hemodialysis (HD) had greater changes in health-related quality of life (HRQOL) over 3 years than younger patients undergoing HD.
DESIGN: Longitudinal.
SETTING: The Hemodialysis Study (HEMO Study) was a randomized, clinical trial of the effects of HD dose and membrane flux on mortality and morbidity in patients undergoing chronic dialysis.
PARTICIPANTS: Secondary analysis of the HEMO Study.
MEASUREMENTS: Participants completed the Index of Well-Being (IWB) and the Kidney Disease Quality of Life-Long Form (KDQOL-LF), which also includes the Medical Outcomes Study 36-item Short Form Questionnaire (SF-36) annually. Changes in subjects those aged 70 and older were compared with changes in subjects aged 55 to 69 and 18 to 54.
RESULTS: At baseline, 1,813 (98%) of HEMO participants completed HRQOL surveys. Their mean age was 58, 56% were female, 64% were black, and mean duration of dialysis was 3.8 years. In subjects with HRQOL data at the first three annual assessments, there were no substantial mean declines in the SF-36 Physical or Mental Component Summary scales over 3 years. In models incorporating effects of attrition, the differences in average change over 3 years between patients undergoing HD aged 70 and older and the younger cohorts were small in magnitude. There were high rates of adverse HRQOL events in all age groups and significantly higher composite event rates of death or clinically significant decline in HRQOL over 3 years was found in subjects aged 70 and older.
CONCLUSION: Although HRQOL was impaired in the population undergoing HD, HRQOL scores at baseline reflect a better-preserved multidimensional quality of life in respondents in the HEMO Study aged 70 and older than in younger patients undergoing HD. There was no substantial relationship between age and average decline in HRQOL score over 3 years in participants in the HEMO Study.
C1 [Unruh, Mark L.; Newman, Anne B.; Dew, Mary Amanda] Univ Pittsburgh, Med Ctr, Dept Med, Pittsburgh, PA USA.
[Newman, Anne B.] Univ Pittsburgh, Med Ctr, Dept Epidemiol, Pittsburgh, PA USA.
[Larive, Brett; Greene, Tom] Cleveland Clin Fdn, Dept Biostat, Cleveland, OH 44195 USA.
[Miskulin, Dana C.; Meyer, Klemens B.] Tufts Univ New England Med Ctr, Div Kidney Dis & Hypertens, Boston, MA USA.
[Beddhu, Srinivasan] Univ Utah, Div Nephrol & Hypertens, Salt Lake City, UT USA.
[Beddhu, Srinivasan] Vet Affairs Salt Lake City Hlth Care Syst, Salt Lake City, UT USA.
[Rocco, Michael V.] Wake Forest Univ, Bowman Gray Sch Med, Div Nephrol & Hypertens, Winston Salem, NC USA.
[Kusek, John W.] NIDDK, Bethesda, MD USA.
RP Unruh, ML (reprint author), Renal Electrolyte Div, A908 Scaife Hall, Pittsburgh, PA 15261 USA.
EM unruh@pitt.edu
RI Newman, Anne/C-6408-2013;
OI Newman, Anne/0000-0002-0106-1150; Meyer, Klemens/0000-0001-5253-4950
FU National Kidney Foundation; Baxter Extramural Grant Program [DK077785,
DK66006]; National Institutes of Diabetes; Digestive and Kidney Diseases
(NIDDK) [U01DK 46109, U01 DK 46114, U01DK 46126, U01DK 46143, U01DK
49240, U01DK 49241, UO1DK 49242, U01DK 49243, U01DK49244, U01DK 49249,
U01DK 49252, U01DK 49254, U01DK 49259, U01DK 49261, U01DK 49264, U01DK
49271]; Dialysis Clinics Incorporated, Baxter; Consultants Merck and
Qualitymetric KBM; Dialysis Clinic Inc; ESRD Network of New England,
Inc., Amgen; Board of Directors of ESRD Network of New England; Forum of
ESRD Networks; Merck; GersonLehrman; NIDDK; Covidien
FX Conflict of Interest: Dr. Unruh was supported by Fresenius Medical Care
Young Investigator Grant of the National Kidney Foundation, Baxter
Extramural Grant Program, DK077785 and DK66006.; TheHEMOStudy is
supported by the National Institutes of Diabetes, Digestive and Kidney
Diseases (NIDDK) via cooperative agreements: U01DK 46109, U01 DK 46114,
U01DK 46126, U01DK 46143, U01DK 49240, U01DK 49241, UO1DK 49242, U01DK
49243, U01DK, 49244, U01DK 49249, U01DK 49252, U01DK 49254, U01DK 49259,
U01DK 49261, U01DK 49264, U01DK 49271.; MLU: Grant support from Dialysis
Clinics Incorporated, Baxter Extramural Grant Fund; Consultants Merck
and Qualitymetric KBM: Salary support from Dialysis Clinic Inc.;
honoraria from ESRD Network of New England, Inc., Amgen, National Kidney
Foundation; member of Board of Directors of ESRD Network of New England
and Forum of ESRD Networks; consulting for Merck, GersonLehrman, Primary
Insight; grant support from the NIDDK and Covidien. DCM: Salary support
from Dialysis Clinic Inc. MVR: Grant support from NIDDK; consultant for
Amgen, DaVita, Hoffman LaRoche, Rennaissance Health Care.
NR 57
TC 45
Z9 52
U1 0
U2 10
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD SEP
PY 2008
VL 56
IS 9
BP 1608
EP 1617
DI 10.1111/j.1532-5415.2008.01849.x
PG 10
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 347PC
UT WOS:000259152500003
PM 18721224
ER
PT J
AU Chaves, PHM
Varadhan, R
Lipsitz, LA
Stein, PK
Windham, G
Tian, J
Fleisher, LA
Guralnik, JM
Fried, LP
AF Chaves, Paulo H. M.
Varadhan, Ravi
Lipsitz, Lewis A.
Stein, Phyllis K.
Windham, Gwen
Tian, Jing
Fleisher, Lee A.
Guralnik, Jack M.
Fried, Linda P.
TI Physiological complexity underlying heart rate dynamics and frailty
status in community-dwelling older women
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE frailty; approximate entropy; heart rate variability; elderly;
physiological complexity
ID RATE-VARIABILITY; MYOCARDIAL-INFARCTION; APPROXIMATE ENTROPY; CHAOS
THEORY; DISEASE; HEALTH; PREDICTOR; MORTALITY; INFLAMMATION; DYSFUNCTION
AB OBJECTIVES: To assess whether less physiological complexity underlying regulation of heart rate dynamics, as indicated by lower approximate entropy for heart rate (ApEn(HR)), is associated with frailty. For supporting validity, relationships between frailty and traditional linear indices of heart rate variability (HRV) were also assessed.
DESIGN: Cross-sectional.
SETTING: Women's Health and Aging Study I, a community-based observational study, 1992 to 1995.
PARTICIPANTS: Subset of 389 community-dwelling women aged years and older with moderate to severe disability with ApEn(HR) data (convenience sampling).
MEASUREMENTS: Electrocardiographic Holter recordings obtained over 2- to 3-hour periods were processed for ApEn(HR) and HRV measures. ApEn(HR) is a nonlinear statistic that quantifies the regularity of heart rate fluctuations over time. Lower ApEn(HR) is characteristic of heart rate time series containing a high proportion of repetitive patterns. Frailty was defined according to validated phenotype criteria.
RESULTS: Median ApEn(HR) was lower in frail than in nonfrail subjects (P=.02). Lower ApEn(HR) (top quartile) was associated with lower likelihood of frailty than higher ApEn(HR) (bottom three quartiles) (odds ratio=0.47, 95% confidence interval=0.26-0.86), even after adjustment for major confounders. Frailty was consistently associated with lower HRV as assessed using time- and frequency-domain indices.
CONCLUSION: This study supports the notion that less physiological complexity marks frailty and provides an empirical basis to the concept of frailty as a syndrome of homeostatic impairment. Future research will determine whether noninvasive measures of physiological complexity underlying heart rate dynamics might be useful for screening and monitoring of clinical vulnerability in older adults.
C1 [Chaves, Paulo H. M.; Varadhan, Ravi; Tian, Jing] Johns Hopkins Univ, Ctr Aging & Hlth, Baltimore, MD USA.
[Chaves, Paulo H. M.; Varadhan, Ravi; Tian, Jing] Johns Hopkins Univ, Div Geriatr Med & Gerontol, Baltimore, MD USA.
[Chaves, Paulo H. M.; Varadhan, Ravi; Tian, Jing] Johns Hopkins Univ, Dept Med, Baltimore, MD USA.
[Chaves, Paulo H. M.] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Chaves, Paulo H. M.] Univ Estado Rio De Janeiro, UNATI Ctr Studies Aging & Care Elderly, Rio De Janeiro, Brazil.
[Lipsitz, Lewis A.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
[Lipsitz, Lewis A.] Hebrew Senior Life, Dept Geriatr Med, Boston, MA USA.
[Stein, Phyllis K.] Washington Univ, Sch Med, St Louis, MO USA.
[Windham, Gwen] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
[Fleisher, Lee A.] Univ Penn, Sch Med, Dept Anesthesiol & Crit Care, Philadelphia, PA 19104 USA.
[Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Fried, Linda P.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
RP Chaves, PHM (reprint author), Johns Hopkins Ctr Aging & Hlth, 2024 E Monument St,Suite 2-700, Baltimore, MD 21205 USA.
EM pchaves@jhsph.edu
FU Johns Hopkins Older Americans Independence Center-National Institute on
Aging (NIA) [P30 AG021334]; National Institutes of Health (NIH)-NIA [R37
AG19905]; Intramural Research Program, NIA, NIH; NIA [AG025037]
FX Conflict of Interest: The editor in chief has reviewed the conflict of
interest checklist provided by the authors and has determined that the
authors have no financial or any other kind of personal conflicts with
this manuscript. This research supported by Johns Hopkins Older
Americans Independence Center-National Institute on Aging (NIA) Grant
P30 AG021334; National Institutes of Health (NIH)-NIA Grant R37 AG19905;
the Intramural Research Program, NIA, NIH; and NIA Grant AG025037.
NR 30
TC 27
Z9 27
U1 2
U2 6
PU BLACKWELL PUBLISHING
PI OXFORD
PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD SEP
PY 2008
VL 56
IS 9
BP 1698
EP 1703
DI 10.1111/j.1532-5415.2008.01858.x
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 347PC
UT WOS:000259152500016
PM 19166446
ER
PT J
AU Young, CLE
Chaon, BC
Shan, QA
Lobo, NF
Collins, FH
AF Young, Catherine L. E.
Chaon, Benjamin C.
Shan, Qiuqi A.
Lobo, Neil F.
Collins, Frank H.
TI A checklist of the mosquitoes of Indiana with notes on the cryptic
species complexes Anopheles quadrimaculatus s.l. and Anopheles
punctipennis
SO JOURNAL OF THE AMERICAN MOSQUITO CONTROL ASSOCIATION
LA English
DT Article
DE mosquito; Indiana; cryptic species; Anopheles; new state records
ID WEST-NILE-VIRUS; OCHLEROTATUS-J.-JAPONICUS; EXPERIMENTAL TRANSMISSION;
ENCEPHALITIS-VIRUS; VECTOR COMPETENCE; AEDES-ALBOPICTUS; NEARCTIC
REGION; UNITED-STATES; CULICIDAE; DIPTERA
AB The checklist of the mosquito species reported to occur in the state of Indiana is updated to include a number of new records and new classifications. Specimens of the cryptic species complex Anopheles quadrimaculatus s.l. are identified as An. quadrimaculatus s.s., and specimens of An. punctipennis are identified as the Eastern form of the species.
C1 [Young, Catherine L. E.; Lobo, Neil F.; Collins, Frank H.] Univ Notre Dame, Dept Biol Sci, Notre Dame, IN 46556 USA.
[Chaon, Benjamin C.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Shan, Qiuqi A.] Princeton Univ, Frist Campus Ctr 3593, Princeton, NJ 08544 USA.
RP Young, CLE (reprint author), Univ Notre Dame, Dept Biol Sci, Notre Dame, IN 46556 USA.
NR 33
TC 0
Z9 0
U1 0
U2 3
PU AMER MOSQUITO CONTROL ASSOC
PI MOUNT LAUREL
PA 15000 COMMERCE PARKWAY, SUITE C, MOUNT LAUREL, NJ 08054 USA
SN 8756-971X
EI 1943-6270
J9 J AM MOSQUITO CONTR
JI J. Am. Mosq. Control Assoc.
PD SEP
PY 2008
VL 24
IS 3
BP 450
EP 452
DI 10.2987/5669.1
PG 3
WC Entomology
SC Entomology
GA 351XX
UT WOS:000259460400018
PM 18939701
ER
PT J
AU Chen, JB
Ayyagari, R
Chatterjee, N
Pee, DY
Schairer, C
Byrne, C
Benichou, J
Gail, MH
AF Chen, Jinbo
Ayyagari, Rajeev
Chatterjee, Nilanjan
Pee, David Y.
Schairer, Catherine
Byrne, Celia
Benichou, Jacques
Gail, Mitchell H.
TI Breast Cancer Relative Hazard Estimates From Case-Control and Cohort
Designs With Missing Data on Mammographic Density
SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION
LA English
DT Article
DE Missing at random; Piecewise exponential model; Pseudo-likelihood;
Two-phase stratified case-control study
ID 2-STAGE CASE-CONTROL; MAXIMUM-LIKELIHOOD; LOGISTIC-REGRESSION; RISK;
MODELS; VALIDATION; 2-PHASE; DISEASE; WOMEN
AB We analyzed data from the Breast Cancer Detection Demonstration Project (BCDDP) to obtain multivariate relative hazard models for breast cancer that included mammographic density (MD) in addition to standard risk factors. Data from the BCDDP were collected from a stratified case-control study in the screening phase (1973-1980) and from follow-up of three subcohorts in the follow-up phase (1980-1995). For both phases. MD measurements were only available for about half the women who developed breast cancer (cases) and a small fraction of noncases. We used a logistic regression model for the stratified case-control study and developed a general pseudo-likelihood approach to accommodate missing covariate data (MD) by adapting the method of Scott and Wild and Breslow and Holubkov. We showed that this method was substantially more efficient than a previously proposed weghted-likelihood method. We assumed piecewise exponential models for the analysis of each subcohort, with the missing covariate (MD) distribution conditional on the observed information modeled with polytomous logistic regression. We developed an EM algorithm for estimation, which allowed for time-varying covariates, incomplete follow-up, and left truncation. We analyzed the three follow-up subcohorts separately and then combined the relative hazard models from the case-control and cohort data. The final model included main effects for MD, weight, age at first live birth, number of previous breast biopsies, and number of sisters or mother with breast cancer and was more discriminating (higher concordance) than the original model of Gail et al., which included standard risk jfactors but not MD. In a spearate work, we combined this relative hazard model with other data to project absolute breast cancer risk.
C1 [Chen, Jinbo] Univ Penn, Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Chatterjee, Nilanjan; Schairer, Catherine; Gail, Mitchell H.] Natl Canc Inst, Div Canc Epidemiol & Genet, Biostat Branch, Rockville, MD 20852 USA.
[Ayyagari, Rajeev; Pee, David Y.] Informat Management Serv Inc, Rockville, MD 20852 USA.
[Byrne, Celia] Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
[Benichou, Jacques] Univ Rouen, Rouen, France.
RP Chen, JB (reprint author), Univ Penn, Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
EM jinboche@mail.med.upenn.edu
RI Byrne, Celia/K-2964-2015
OI Byrne, Celia/0000-0001-8289-4252
NR 26
TC 3
Z9 3
U1 0
U2 6
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 732 N WASHINGTON ST, ALEXANDRIA, VA 22314-1943 USA
SN 0162-1459
J9 J AM STAT ASSOC
JI J. Am. Stat. Assoc.
PD SEP
PY 2008
VL 103
IS 483
BP 976
EP 988
DI 10.1198/016214508000000120
PG 13
WC Statistics & Probability
SC Mathematics
GA 362JJ
UT WOS:000260193700007
ER
PT J
AU Luo, S
Crainiceanu, CM
Louis, TA
Chatterjee, N
AF Luo, Sheng
Crainiceanu, Ciprian M.
Louis, Thomas A.
Chatterjee, Nilanjan
TI Analysis of Smoking Cessation Patterns Using a Stochastic Mixed-Effects
Model With a Latent Cured State
SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION
LA English
DT Article
DE Cure model; Mixed-effects model; Recurrent events; Smoking cessation;
Stochastic transition model
ID 2-STATE MARKOV-PROCESSES; MIXTURE-MODELS; CENSORED SAMPLE;
SURVIVAL-DATA; RISK-FACTORS; MORTALITY; CANCER; RATES; EPIDEMIOLOGY;
INDIVIDUALS
AB We develop a mixed model to capture the complex stochastic nature of tobacco abuse and dependence. This model describes transition processes among addiction and nonaddiction stages. An important innovation of our model is allowing an unobserved cure state, or permanent quitting, in contrast to transient quitting. This distinction is necessary to model data from situations where censoring prevents unambiguous determination that a person has been "cured," Moreover, the processes that described transient and permanent quitting are likely to be different and have different policy-making implications. For example, when analyzing factors that influence smoking and can be targeted by interventions, it is more important to target those factors that are associated with permanent quitting rather than transient quitting.
We apply our methodology to the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) study, a large (29,133 participants) longitudinal cohort study. While ATBC was designed as a cancer prevention study. It contains unique information about the smoking status of each participant during every 4-month period of the study. These data are used to model smoking cessation patterns using a discrete-time stochastic mixed-effects model with threee states: smoking, transient cessation, and permanent cessation (absorbent state). Random participant-specific transition probabilities among these states are used to account for participant-to-participant heterogeneity. Another important innovation in our article is to design computationally practical methods for dealing with the size of the dataset and complexity of the models. This is achieved using the marginal likelihood obtained by integrating over the Beta distribution of random effects
C1 [Luo, Sheng; Crainiceanu, Ciprian M.; Louis, Thomas A.] Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
[Chatterjee, Nilanjan] NCI, NIH, Biostat Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
RP Luo, S (reprint author), Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
EM sluo@jhsph.edu
FU NIDDK NIH HHS [R01 DK061662, R01 DK061662-05]
NR 47
TC 5
Z9 5
U1 0
U2 1
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 1429 DUKE ST, ALEXANDRIA, VA 22314 USA
SN 0162-1459
J9 J AM STAT ASSOC
JI J. Am. Stat. Assoc.
PD SEP
PY 2008
VL 103
IS 483
BP 1002
EP 1013
DI 10.1198/016214507000001030
PG 12
WC Statistics & Probability
SC Mathematics
GA 362JJ
UT WOS:000260193700009
PM 19305513
ER
PT J
AU Rodriguez, A
Dunson, DB
Gelfand, AE
AF Rodriguez, Abel
Dunson, David B.
Gelfand, Alan E.
TI The Nested Dirichlet Process
SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION
LA English
DT Article
DE In multicenter studies subjects in different centers may have different
outcome distribution. This article is motivated by the problem of
nonparametric modeling of these distributions, borrowing information
across centers while also allowing centers to be clustered, Starting
with a stick-breaking representation of the Dricichlet process (DP). we
replace that random atoms with random probability measures drawn from a
DP. This results in a nested DP prior, which can be placed on the
collection of distributions for the different centers with centers drawn
from the same DP component authomatically clustered together.
Theorectical properties are discussed and an efficient Markov chain
Monte Carlo algorithm is developed for computation. The methods are
illustrated using a simulation study and an application to quality of
care in U.S hospitals.
ID FINITE NORMAL MIXTURES; PROBABILITY-MEASURES; BAYESIAN-INFERENCE;
SAMPLING METHODS; PROCESS MODELS; DISTRIBUTIONS; HETEROGENEITY;
REGRESSION; PRIORS
C1 [Rodriguez, Abel] Univ Calif Santa Cruz, Dept Appl Math & Stat, Santa Cruz, CA 95064 USA.
[Dunson, David B.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Gelfand, Alan E.] Duke Univ, Inst Stat & Decis Sci, Durham, NC 27708 USA.
RP Rodriguez, A (reprint author), Univ Calif Santa Cruz, Dept Appl Math & Stat, Santa Cruz, CA 95064 USA.
EM abel@soe.ucsc.edu; dunson1@niehs.nih.gov; alan@isds.duke.edu
NR 55
TC 64
Z9 65
U1 0
U2 5
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 1429 DUKE ST, ALEXANDRIA, VA 22314 USA
SN 0162-1459
J9 J AM STAT ASSOC
JI J. Am. Stat. Assoc.
PD SEP
PY 2008
VL 103
IS 483
BP 1131
EP 1144
DI 10.1198/016214508000000553
PG 14
WC Statistics & Probability
SC Mathematics
GA 362JJ
UT WOS:000260193700019
ER
PT J
AU Rodriguez, A
Dunson, DB
Gelfand, AE
AF Rodriguez, Abel
Dunson, David B.
Gelfand, Alan E.
TI The Nested Dirichlet Process Rejoinder
SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION
LA English
DT Editorial Material
C1 [Rodriguez, Abel] Univ Calif Santa Cruz, Dept Appl Math & Stat, Santa Cruz, CA 95064 USA.
[Dunson, David B.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Gelfand, Alan E.] Duke Univ, Inst Stat & Decis Sci, Durham, NC 27708 USA.
RP Rodriguez, A (reprint author), Univ Calif Santa Cruz, Dept Appl Math & Stat, Santa Cruz, CA 95064 USA.
EM abel@soe.ucsc.edu; dunson1@niehs.nih.gov; alan@isds.duke.edu
NR 7
TC 0
Z9 0
U1 1
U2 1
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 1429 DUKE ST, ALEXANDRIA, VA 22314 USA
SN 0162-1459
J9 J AM STAT ASSOC
JI J. Am. Stat. Assoc.
PD SEP
PY 2008
VL 103
IS 483
BP 1153
EP 1154
DI 10.1198/016214508000000616
PG 2
WC Statistics & Probability
SC Mathematics
GA 362JJ
UT WOS:000260193700025
ER
PT J
AU Huang, CY
Qin, J
Follmann, DA
AF Huang, Chiung-Yu
Qin, Jing
Follmann, Dean A.
TI Empirical Likelihood-Based Estimation of the Treatment Effect in a
Pretest- Posttest Study
SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION
LA English
DT Article
DE Auxiliary information; Biased sampling; Casual inference; Observational
study; Survey sampling
ID MISSING RESPONSE; AUXILIARY INFORMATION; RESEARCH DESIGNS; INFERENCE
AB The pretest-posttest study design is commonly used in medical and social science research to assess the effect of a treatment or an intervention. Recently, interest has been rising in developing inference procedures that improve efficiency while relaxing assumptions used in the pretest-posttest data analysis, especially when the posttest measurement might be missing. In this article we propose a semiparametric estimation procedure based on empirical likelihood (EL) that incorporates the common baseline covariate information to improve efficiency. The proposed method also yields an asymptotically unbiased estimate of the response distribution. Thus functions of the response distribution, such as the median, can be estimated straightforwardly, and the EL method can provide a more appealing estimate of the treatment effect for skewed data.We show that, compared with existing methods, the proposed EL estimator has appealing theoretical properties, especially when the working model for the underlying relationship between the pretest and posttest measurements is misspecified. A series of simulation studies demonstrates that the EL-based estimator outerperforms its competitors when the working model is misspecified and the data are missing at random. We illustrate the methods by analyzing data from an AIDS clinical trial (ACTG 175).
C1 [Huang, Chiung-Yu; Qin, Jing; Follmann, Dean A.] NIAID, NIH, Biostat Res Branch, Bethesda, MD 20892 USA.
RP Huang, CY (reprint author), NIAID, NIH, Biostat Res Branch, Bethesda, MD 20892 USA.
EM huangchi@niaid.nih.gov; jingqin@niaid.nih.gov; dfollmann@niaid.nih.gov
FU Intramural NIH HHS [Z99 AI999999]
NR 30
TC 6
Z9 6
U1 0
U2 3
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 1429 DUKE ST, ALEXANDRIA, VA 22314 USA
SN 0162-1459
J9 J AM STAT ASSOC
JI J. Am. Stat. Assoc.
PD SEP
PY 2008
VL 103
IS 483
BP 1270
EP 1280
DI 10.1198/016214508000000625
PG 11
WC Statistics & Probability
SC Mathematics
GA 362JJ
UT WOS:000260193700036
PM 23729942
ER
PT J
AU Goedert, JJ
Scoppio, BM
Pfeiffer, R
Neve, L
Federici, AB
Long, LR
Dolan, BM
Brambati, M
Bellinvia, M
Lauria, C
Preiss, L
Boneschi, V
Whitby, D
Brambilla, L
AF Goedert, J. J.
Scoppio, B. M.
Pfeiffer, R.
Neve, L.
Federici, A. B.
Long, L. R.
Dolan, B. M.
Brambati, M.
Bellinvia, M.
Lauria, C.
Preiss, L.
Boneschi, V.
Whitby, D.
Brambilla, L.
TI Treatment of classic Kaposi sarcoma with a nicotine dermal patch: a
phase II clinical trial
SO JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY AND VENEREOLOGY
LA English
DT Article
DE drug delivery systems; Kaposi sarcoma; smoking
ID ACTIVE ANTIRETROVIRAL THERAPY; 0.1-PERCENT ALITRETINOIN GEL; TRANSDERMAL
NICOTINE; 9-CIS-RETINOIC ACID; ULCERATIVE-COLITIS; VERRUCA-VULGARIS;
DUCT TAPE; AIDS; CHEMOTHERAPY; EFFICACY
AB Background Kaposi sarcoma (KS), a malignancy of dermal endothelial cells that is caused by human herpesvirus 8 (HHV8) infection, is sensitive to perturbations of immunity. Nicotine might be effective against KS because of its immunologic and vascular effects and because smoking is associated with a low risk of KS.
Objective and study design We conducted a masked, randomized phase 2 clinical trial of transdermal nicotine and placebo patches to assess the safety and efficacy of nicotine against classic KS (cKS).
Subjects and methods Three cKS lesions, predominantly nodules, in each of 24 non-smoking patients were randomly assigned to 15 weeks continuous treatment with nicotine patch (escalated to 7 mg), identical masked placebo patch or no patch. Changes in lesion area and elevation from baseline through six follow-up visits, by direct measurement and by two independent readers using digital photographs of the lesions, were compared using non-parametric and regression methods. Changes in longitudinal levels of HHV8 antibodies and DNA in blood cells were similarly assessed.
Results There were no systemic or serious adverse events, and compliance was good. One patient resumed smoking and discontinued patches, and two patients withdrew at week 12 for unrelated indications. Six (29%) of the remaining 21 suspended use of patches to relieve local skin irritation; four of these six completed the trial at reduced dose. Treatment assignment was not associated with significant or consistent changes in cKS lesion area or elevation, HHV8 viral load or antibodies.
Conclusion Transdermal nicotine and placebo patches caused no serious toxicities but had no demonstrable effect on nodular cKS lesions or HHV8 levels.
C1 [Goedert, J. J.; Pfeiffer, R.; Dolan, B. M.] NCI, Viral Epidemiol Branch, Div Canc Epidemiol and Genet, Rockville, MD 20852 USA.
[Goedert, J. J.; Pfeiffer, R.; Dolan, B. M.] NCI, Biostat Branch, Div Canc Epidemiol and Genet, Rockville, MD 20852 USA.
[Scoppio, B. M.; Federici, A. B.; Brambati, M.; Bellinvia, M.; Boneschi, V.; Brambilla, L.] Regina Elena Fdn, IRCCS Fdn Maggiore Policlin Hosp, Dept Med & Med Specialties, Angelo Bianchi Bonomi Hemophilia Thrombosis Ctr, Milan, Italy.
[Scoppio, B. M.; Federici, A. B.; Brambati, M.; Bellinvia, M.; Boneschi, V.; Brambilla, L.] Regina Elena Fdn, IRCCS Fdn Maggiore Policlin Hosp, Dept Med & Med Specialties, Inst Dermatol Sci, Milan, Italy.
[Neve, L.; Long, L. R.] Natl Lib Med, Commun Engn Branch, Bethesda, MD USA.
[Lauria, C.] Lega Italiana Lotta Contro I Tumori RG, Ragusa, Italy.
[Preiss, L.] RTI Int, Rockville, MD USA.
[Preiss, L.] RTI Int, Buenos Aires, DF, Argentina.
[Whitby, D.] NCI, SAIC Frederick, AIDS Vaccine Program, Viral Oncol Sect, Frederick, MD 21701 USA.
RP Goedert, JJ (reprint author), NCI, Viral Epidemiol Branch, Div Canc Epidemiol and Genet, 6120 Execut Blvd Room 7066, Rockville, MD 20852 USA.
EM goedertj@mail.nih.gov
RI Pfeiffer, Ruth /F-4748-2011
FU NIH Intramural Research Program [N02-CP-55504, N01-CO-12400]
FX We thank the Data and Safety Monitoring Board: Drs Damiano Abeni (
Chair), Gianni Baliva and Paolo Marchetti, all of whom are at the
Istituto Dermatopatico Dell'Immacolata, Rome, Italy. We are grateful to
Joseph A. Matthias and Dr Carolyn M. Dresler, GlaxoSmithKline Consumer
Healthcare, for donation of the patches; to Mss. Julie Russell Grey and
Judith Lichaa for random allocation and masking of the nicotine and
placebo patches; to Noelle Richa (RTI International) for masking and
randomization of the digital photograph files; to Marianne Ardini ( RTI
International) for forms development and operations management; and to
Georgina Mbisa and Vickie Marshall, Viral Oncology Section,
SAIC-Frederick, for HHV8 antibody titres and for HHV8 and EBV viral load
measurements, respectively. This study is supported in part by the NIH
Intramural Research Program through contracts N02-CP-55504 and
N01-CO-12400.
NR 43
TC 7
Z9 7
U1 2
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0926-9959
J9 J EUR ACAD DERMATOL
JI J. Eur. Acad. Dermatol. Venereol.
PD SEP
PY 2008
VL 22
IS 9
BP 1101
EP 1109
DI 10.1111/j.1468-3083.2008.02720.x
PG 9
WC Dermatology
SC Dermatology
GA 337NS
UT WOS:000258443400011
PM 18384551
ER
PT J
AU Choong, NW
Mauer, AM
Haraf, DJ
Lester, E
Hoffman, PC
Kozloff, M
Lin, S
Dancey, JE
Szeto, L
Grushko, T
Olopade, OI
Salgia, R
Vokes, EE
AF Choong, Nicholas W.
Mauer, Ann M.
Haraf, Daniel J.
Lester, Eric
Hoffman, Philip C.
Kozloff, Mark
Lin, Shang
Dancey, Janet E.
Szeto, Livia
Grushko, Tatyana
Olopade, Olufunmilayo I.
Salgia, Ravi
Vokes, Everett E.
TI Phase I trial of erlotinib-based multimodality therapy for inoperable
stage III non-small cell lung cancer
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article; Proceedings Paper
CT 41st Annual Meeting of the American-Society-of-Clinical-Oncology
CY MAY 13-17, 2005
CL Orlando, FL
SP Amer Soc Clin Oncol
DE non-small cell lung cancer; chemoradiotherapy; multimodality therapy;
erlotinib; epidermal-growth factor inhibitor
ID GROWTH-FACTOR RECEPTOR; TYROSINE KINASE INHIBITOR; CARCINOMA-CELLS;
PHARMACODYNAMIC SEPARATION; RADIATION RESPONSE; GEFITINIB; GENE;
CHEMOTHERAPY; COMBINATION; CISPLATIN
AB Introduction: This Phase I trial aimed to determine the maximum-tolerated-dose of erlotinib administered with two standard chemoradiotherapy regimens for non-small cell lung cancer.
Methods: Unresectable stage III non-small cell lung cancer patients were enrolled in this 2-arm close-escalation Study. Erlotinib, given only during chemoradiotherapy, was escalated front 50 to 150 mg/d in 3 to 6 patient cohorts. Arm A: erlotinib with cisplatin (50 mg/m(2) IV days 1, 8, 29, 36), etoposide (50 mg/m(2) IV days 1-5, 29-33) and chest radiotherapy (66 Gy, 2 Gy/d) followed by docetaxel (75 mg/m(2) 2 IV Q21 d) for 3 cycles. Arm B: induction carboplatin (AUC 6) and paclitaxel (200 mg/m(2)) for two 21-d cycles then radiotherapy with erlotinib, carboplatin (AUC = 2/wk) and paclitaxel (50 mg/m(2)/wk).
Results: Seventeen patients were treated in each arm. Patient characteristics: performance status 0 to 24 patients, I to 10 patients, median age 63 years. adenocarcinoma 21% and female 14 patients. Dose-escalation of erlotinib to 150 mg/d was possible oil both chemoradiotherapy regimens. Grade 3/4 leukopenia and neutropenia were predominant toxicities in both arms. Grade 3 chemoradiotherapy toxicities in at-in A were esophagitis (3 patients), vomiting (1), ototoxicity (1), diarrhea (2), dehydration (3), pneumonitis (1) and arm B was esophagitis (6). Seven patients (21%) developed rash (all grade 1/2). Median survival times for patients oil Ann A and B were 10.2 and 13.7 months, respectively. Three-year overall survival in patients with and Without rash were 53% and 10%, respectively (log-rank P = 0.0807). Epidermal growth factor receptor IHC or FISH positive patients showed no significant overall survival difference.
Conclusion: Addition of standard-dose erlotinib to chemoradiotherapy is feasible Without evident increase in toxicities. However, the survival data are disappointing ill this unselected patient Population and does not Support further investigation of this approach.
C1 [Choong, Nicholas W.; Hoffman, Philip C.; Szeto, Livia; Grushko, Tatyana; Olopade, Olufunmilayo I.; Salgia, Ravi; Vokes, Everett E.] Univ Chicago, Med Ctr, Hematol Oncol Sect, Chicago, IL 60615 USA.
[Choong, Nicholas W.; Hoffman, Philip C.; Szeto, Livia; Grushko, Tatyana; Olopade, Olufunmilayo I.; Salgia, Ravi; Vokes, Everett E.] Univ Chicago, Med Ctr, Phase Network 2, Chicago, IL 60615 USA.
[Choong, Nicholas W.] Med Coll Wisconsin, Div Neoplast Dis, Milwaukee, WI 53226 USA.
[Mauer, Ann M.] Advocate Illinois Mason Med Ctr, Creticos Canc Ctr, Chicago, IL USA.
[Haraf, Daniel J.; Vokes, Everett E.] Univ Chicago, Med Ctr, Dept Radiat Biol & Cellular Oncol, Chicago, IL 60615 USA.
[Lester, Eric] Oncol Care Associates, St Joseph, MI USA.
[Kozloff, Mark] Ingalls Hosp, Harvey, IL USA.
[Lin, Shang] Univ Chicago, Dept Hlth Studies, Chicago, IL 60615 USA.
[Dancey, Janet E.] NCI, Invest Drug Branch, Canc Therapy Evaluat Program, Div Canc Treatments & Diag, Rockville, MD USA.
RP Vokes, EE (reprint author), Univ Chicago, Med Ctr, Hematol Oncol Sect, MC 2115,5841 S Maryland Ave, Chicago, IL 60615 USA.
EM evokes@medicine.bsd.uchicago.edu
FU NCI NIH HHS [N01 CM-07003-74, T32 CA009566-15, T32 CA009566, P30
CA14599-32, P30 CA014599, N01 CM007003]
NR 44
TC 40
Z9 43
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD SEP
PY 2008
VL 3
IS 9
BP 1003
EP 1011
DI 10.1097/JTO.0b013e31818396a4
PG 9
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 347TV
UT WOS:000259164900011
PM 18758303
ER
PT J
AU Gill, JM
Page, GG
Sharps, P
Campbell, JC
AF Gill, Jessica M.
Page, Gayle G.
Sharps, Phyllis
Campbell, Jacquelyn C.
TI Experiences of traumatic events and associations with PTSD and
depression development in urban health care-seeking women
SO JOURNAL OF URBAN HEALTH-BULLETIN OF THE NEW YORK ACADEMY OF MEDICINE
LA English
DT Article
DE PTSD; depression; trauma; urban; women
ID POSTTRAUMATIC-STRESS-DISORDER; INTIMATE PARTNER VIOLENCE; CHILD
SEXUAL-ABUSE; PERSONALITY-DISORDER; GENDER-DIFFERENCES;
AFRICAN-AMERICANS; MAJOR DEPRESSION; SUBSTANCE-ABUSE; MENTAL-HEALTH;
COMORBIDITY
AB Posttraumatic stress disorder (PTSD) is an anxiety disorder that occurs after a traumatic event and has been linked to psychiatric and physical health declines. Rates of PTSD are far higher in individuals with low incomes and who reside in urban areas compared to the general population. In this study, 250 urban health care-seeking women were interviewed for a diagnosis of PTSD, major depressive disorder, and also the experience of traumatic events. Multivariate logistic regressions were used to determine the associations between traumatic events and PTSD development. Survival analysis was used to determine if PTSD developed from assaultive and nonassaultive events differed in symptom duration. Eighty-six percent of women reported at least one traumatic event, 14.8% of women were diagnosed with current PTSD, and 19.6% with past PTSD. More than half of women with PTSD had comorbid depression. Assaultive traumatic events were most predictive of PTSD development. More than two thirds of the women who developed PTSD developed chronic PTSD. Women who developed PTSD from assaultive events experienced PTSD for at least twice the duration of women who developed PTSD from nonassaultive events. In conclusion, PTSD was very prevalent in urban health care-seeking women. Assaultive violence was most predictive of PTSD development and also nonremittance.
C1 [Gill, Jessica M.] NINR, NIH, Bethesda, MD 20892 USA.
[Page, Gayle G.; Sharps, Phyllis; Campbell, Jacquelyn C.] Johns Hopkins Univ, Sch Nursing, Baltimore, MD USA.
RP Gill, JM (reprint author), NINR, NIH, 10 Ctr Dr,10 CRC 2-1339, Bethesda, MD 20892 USA.
EM gillj@mail.nih.gov
FU National Institute for Nursing Research (NINR) [F31 NR009166, T32 NR
07968]
FX Funding for this research was provided by the following sources:
Individual National Research Service Award (NRSA) F31 NR009166 funded
through the National Institute for Nursing Research (NINR);
Institutional Training Grant funded through NINR T32 NR 07968: Health
Disparities in Underserved Populations; The Freedom from Fear Sharon
Davies Memorial Grant; Sigma Theta Tau, Beta Nu Chapter, Small Grant
Award.
NR 57
TC 11
Z9 12
U1 7
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1099-3460
J9 J URBAN HEALTH
JI J. Urban Health
PD SEP
PY 2008
VL 85
IS 5
BP 693
EP 706
DI 10.1007/s11524-008-9290-y
PG 14
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 343GS
UT WOS:000258842000006
PM 18581238
ER
PT J
AU Kaplan, SA
Roehrborn, CG
McConnell, JD
Meehan, AG
Surynawanshi, S
Lee, JY
Rotonda, J
Kusek, JW
Nyberg, LM
AF Kaplan, Steven A.
Roehrborn, Claus G.
McConnell, John D.
Meehan, Alan G.
Surynawanshi, Shailaja
Lee, Jeannette Y.
Rotonda, Jennifer
Kusek, John W.
Nyberg, Leroy M., Jr.
CA Med Therapy Prostat Symptoms Res G
TI Long-term treatment with finasteride results in a clinically significant
reduction in total prostate volume compared to placebo over the full
range of baseline prostate sizes in men enrolled in the MTOPS trial
SO JOURNAL OF UROLOGY
LA English
DT Article
DE prostatic hyperplasia; urinary tract; doxazosin; finasteride; combined
modality therapy
ID THERAPY
AB Purpose: In the present analysis we examined data from the MTOPS (Medical Therapy of Prostatic Symptoms) trial to determine the effect of long-term finasteride treatment, either alone or in combination with doxazosin, on total prostate volume across the full range of baseline total prostate volume values in men enrolled in this study.
Materials and Methods: In this trial a total of 3,047 patients with lower urinary tract symptoms were randomized to placebo, doxazosin (4 to 8 mg), finasteride (5 mg) or the combination of doxazosin and finasteride (average length of treatment 4.5 years). Total prostate volume was measured by transrectal ultrasound in all patients at baseline, yearly and at study end or at termination of participation.
Results: Long-term treatment with finasteride led to a consistent reduction of approximately 25% in total prostate volume compared to placebo in men with a relatively small prostate (less than 25 to 30 ml), as well as in those with a moderate size (30 to less than 40 ml) or enlarged prostate (40 ml or greater) at baseline.
Conclusions: In this MTOPS data analysis long-term (more than 4 years) treatment with finasteride, either alone or in combination with doxazosin, led to a consistent, clinically significant reduction in total prostate volume compared to placebo in patients with lower urinary tract symptoms and benign prostatic hyperplasia whose baseline prostate size ranged from relatively small (less than 25 to 30 ml) to enlarged (40 ml or greater).
C1 [Kaplan, Steven A.] Cornell Univ, Inst Bladder & Prostate Hlth, Weill Cornell Med Coll, New York, NY 10021 USA.
[Roehrborn, Claus G.; McConnell, John D.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Meehan, Alan G.; Surynawanshi, Shailaja; Rotonda, Jennifer] Merck Res Labs, Rahway, NJ USA.
[Lee, Jeannette Y.] Univ Alabama, Birmingham, AL USA.
[Kusek, John W.; Nyberg, Leroy M., Jr.] NIDDK, Bethesda, MD USA.
RP Kaplan, SA (reprint author), Cornell Univ, Inst Bladder & Prostate Hlth, Weill Cornell Med Coll, 1300 York Ave,F9 W,Box 261, New York, NY 10021 USA.
EM kaplans@med.cornell.edu
FU NIDDK NIH HHS [U01 DK46468, U01 DK 49912, U01 DK41418, U01 DK46416, U01
DK46429, U01 DK46431, U01 DK46437, U01 DK46472, U01 DK49880, U01
DK49921, U01 DK49951, U01 DK49954, U01 DK49960, U01 DK49961, U01
DK49963, U01 DK49964, U01 DK49971, U01 DK49977, U01 DK49980]
NR 3
TC 32
Z9 34
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
J9 J UROLOGY
JI J. Urol.
PD SEP
PY 2008
VL 180
IS 3
BP 1030
EP 1032
DI 10.1016/j.juro.2008.05.004
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 337TV
UT WOS:000258459300061
PM 18639298
ER
PT J
AU Elagha, AA
Kocaturk, O
Guttman, MA
Ozturk, C
Kim, AH
Burton, GW
Kim, JH
Raman, VK
Raval, AN
Wright, VJ
Schenke, WH
McVeigh, ER
Lederman, RJ
AF Elagha, Abdalla A.
Kocaturk, Ozgur
Guttman, Michael A.
Ozturk, Cengizhan
Kim, Ann H.
Burton, George W.
Kim, June H.
Raman, Venkatesh K.
Raval, Amish N.
Wright, Victor J.
Schenke, William H.
McVeigh, Elliot R.
Lederman, Robert J.
TI Real-time MR imaging-guided laser atrial septal puncture in swine
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID LEFT-HEART CATHETERIZATION; TRANSSEPTAL PUNCTURE; RESONANCE; EXPERIENCE;
ANGIOPLASTY; FLUOROSCOPY; SAFETY; FEASIBILITY; COARCTATION
AB PURPOSE: The authors performed this study to report their initial preclinical experience with real-time magnetic resonance (MR) imaging-guided atrial septal puncture by using a MR imaging-conspicuous blunt laser catheter that perforates only when energized.
MATERIALS AND METHODS: The authors customized a 0.9-mm clinical excimer laser catheter with a receiver coil to impart MR imaging visibility at 1.5 T. Seven swine underwent laser transseptal puncture under real-time MR imaging. MR imaging signal-to-noise ratio profiles of the device were obtained in vitro. Tissue traversal force was tested with a calibrated meter. Position was corroborated with pressure measurements, oximetry, angiography, and necropsy. Intentional non-target perforation simulated serious complication.
RESULTS: Embedded MR imaging antennae accurately reflected the position of the laser catheter tip and profile in vitro and in vivo. Despite having an increased profile from the microcoil, the 0.9-mm laser catheter traversed in vitro targets with similar force (0.22 N +/- 0.03) compared with the unmodified laser. Laser puncture of the atrial septum was successful and accurate in all animals. The laser was activated an average of 3.8 seconds +/- 0.4 before traversal. There were no sequelae after 6 hours of observation. Necropsy revealed 0.9-mm holes in the fossa ovalis in all animals. Intentional perforation of the aorta and atrial free wall was evident immediately.
CONCLUSIONS: MR imaging-guided laser puncture of the interatrial septum is feasible in swine and offers controlled delivery of perforation energy by using an otherwise blunt catheter. Instantaneous soft tissue imaging provides immediate feedback on safety.
C1 [Elagha, Abdalla A.; Kocaturk, Ozgur; Guttman, Michael A.; Ozturk, Cengizhan; Kim, Ann H.; Kim, June H.; Raman, Venkatesh K.; Raval, Amish N.; Wright, Victor J.; Schenke, William H.; McVeigh, Elliot R.; Lederman, Robert J.] NHLBI, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Burton, George W.] Spectranetics, Colorado Springs, CO USA.
RP Lederman, RJ (reprint author), NHLBI, Div Intramural Res, NIH, Bldg 10,Rm 2C713, Bethesda, MD 20892 USA.
EM ledermar@nhlbi.nih.gov
RI Ozturk, Cengizhan/A-6177-2016;
OI Ozturk, Cengizhan/0000-0002-6966-0774; lederman,
robert/0000-0003-1202-6673; Elagha, Abdalla/0000-0003-3136-2293
FU NHLBI Division of Intramural Research [Z01-HL005062-04 CVB]
FX The authors thank Kathy Lucas and Joni Taylor for their animal care and
support and Parag V. Karmarkar for assistance with decoupling circuitry.
Spectranetics customized laser catheters under a Collaborative Research
and Development Agreement with the National Heart Lung and Blood
Institute. Supported by the NHLBI Division of Intramural Research
(Z01-HL005062-04 CVB),
NR 36
TC 6
Z9 6
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
EI 1535-7732
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD SEP
PY 2008
VL 19
IS 9
BP 1347
EP 1353
DI 10.1016/j.jvir.2008.05.007
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 346FU
UT WOS:000259054900013
PM 18725098
ER
PT J
AU Tseng, FC
Edlin, BR
Zhang, M
Kral, A
Busch, MP
Ortiz-Conde, BA
Welzel, TM
O'Brien, TR
AF Tseng, F. -C.
Edlin, B. R.
Zhang, M.
Kral, A.
Busch, M. P.
Ortiz-Conde, B. A.
Welzel, T. M.
O'Brien, T. R.
TI The inverse relationship between chronic HBV and HCV infections among
injection drug users is associated with decades of age and drug use
SO JOURNAL OF VIRAL HEPATITIS
LA English
DT Article; Proceedings Paper
CT Digestive Disease Week Meeting/106th Annual Meeting of the
American-Gastroenterological-Association
CY MAY 14-19, 2005
CL Chicago, IL
SP Amer Gastroenterol Assoc
DE epidemiology; hepatitis B virus; hepatitis C virus; injection drug use;
United States; viral suppression
ID HEPATITIS-C VIRUS; B-VIRUS; SAN-FRANCISCO; HEPATOCELLULAR-CARCINOMA;
LIVER-DISEASE; DELTA VIRUSES; CORE PROTEIN; FOLLOW-UP; PREVALENCE; RISK
AB Infection with hepatitis C virus (HCV) may suppress co-infection with hepatitis B virus (HBV) during acute or chronic HBV infection. We examined relationships between HBV infection, HCV infection and other factors among injection drug users (IDUs) with antibodies to both viruses. Participants enrolled in a cross-sectional study during 1998-2000 were considered to have been infected with HBV if they had core antibody, to be chronically infected if they had hepatitis B surface antigen (HBsAg), to have been infected with HCV if they had HCV antibody and to be chronically infected if they had HCV RNA. Among 1694 participants with antibody to both viruses, HBsAg prevalence decreased with increasing age among those positive for HCV RNA [from 4.55% in those 18-29 years to 1.03% in those >= 50 years old (P(trend) = 0.02)], but not among those who were negative for HCV RNA. Chronic HBV infection was less common overall among those with chronic HCV infection (odds ratio [OR], 0.25; P < 0.0001), but this inverse relationship was much stronger in the oldest (> 50 years; OR = 0.15) than the youngest (18-29 years; OR = 0.81) participants (P(trend) = 0.03). Similar results were obtained when duration of injection drug use was substituted for age (P(trend) = 0.05). Among IDUs who have acquired both HBV and HCV, chronic HBV infection is much less common among those with chronic HCV infection, but this inverse relationship increases markedly with increasing years of age and injection drug use. Co-infection with HCV may enhance the resolution of HBsAg during the chronic phases of these infections.
C1 [O'Brien, T. R.] Natl Canc Inst, Div Canc Epidemiol & Genet, Adv Technol Ctr, Bethesda, MD 20892 USA.
[Edlin, B. R.; Kral, A.; Busch, M. P.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Edlin, B. R.] Cornell Univ, Weill Med Coll, New York, NY 10021 USA.
[Kral, A.] RTI Int, San Francisco Reg Off, San Francisco, CA USA.
[Busch, M. P.] Blood Syst Res Inst, San Francisco, CA USA.
[Ortiz-Conde, B. A.] NCI, Viral Oncol Sect, AIDS Vaccine Program, SAIC Frederick, Frederick, MD 21701 USA.
RP O'Brien, TR (reprint author), Natl Canc Inst, Div Canc Epidemiol & Genet, Adv Technol Ctr, Room 225A,MSC 4605 8717,Grovemont Circle, Bethesda, MD 20892 USA.
EM obrient@mail.nih.gov
RI Tseng, Fan-Chen/D-2097-2010;
OI Edlin, Brian/0000-0001-8172-8797
FU CSAT SAMHSA HHS [H79-TI12103]; Intramural NIH HHS; NCI NIH HHS
[N01CO12400, N02-CP-91027, N01-CO-12400]; NIDA NIH HHS [R01 DA009532,
R01 DA012109, R01-DA16159, R01-DA09532, R01 DA016159, R01 DA013245, R01
DA009532-08, R01-DA13245]
NR 43
TC 11
Z9 12
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1352-0504
J9 J VIRAL HEPATITIS
JI J. Viral Hepatitis
PD SEP
PY 2008
VL 15
IS 9
BP 690
EP 698
DI 10.1111/j.1365-2893.2008.01005.x
PG 9
WC Gastroenterology & Hepatology; Infectious Diseases; Virology
SC Gastroenterology & Hepatology; Infectious Diseases; Virology
GA 336QX
UT WOS:000258380800010
PM 18507757
ER
PT J
AU Chen, JB
Pathak, VK
Peng, WQ
Hu, WS
AF Chen, Jianbo
Pathak, Vinay K.
Peng, Weiqun
Hu, Wei-Shau
TI Capsid proteins from human immunodeficiency virus type 1 and simian
immunodeficiency virus SIVmac can coassemble into mature cores of
infectious viruses
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MURINE LEUKEMIA-VIRUS; HIV-1 INFECTION; RETROVIRAL RESTRICTION;
NONDIVIDING CELLS; VIRAL REPLICATION; TRIM5-ALPHA; REF1;
RECONSTRUCTIONS; ORGANIZATION; LENTIVIRUS
AB We have recently shown that the Gag polyproteins from human immunodeficiency virus type 1 (HIV-1) and HIV-2 can coassemble and functionally complement each other. During virion maturation, the Gag polyproteins undergo proteolytic cleavage to release mature proteins including capsid (CA), which refolds and forms the outer shell of a cone-shaped mature core. Less than one-half of the CA proteins present within the HIV-1 virion are required to form the mature core. Therefore, it is unclear whether the mature core in virions containing both HIV-1 and HIV-2 Gag consists of CA proteins from a single virus or from both viruses. To determine whether CA proteins from two different viruses can coassemble into mature cores of infectious viruses, we exploited the specificity of the tripartite motif 5 alpha protein from the rhesus monkey (rhTRIM5 alpha) for cores containing HIV-1 CA (hCA) but not the simian immunodeficiency virus SIVmac CA protein (sCA). If hCA and sCA cannot coassemble into the same core when equal amounts of sCA and hCA are coexpressed, the infectivities of such virus preparations in cells should be inhibited less than twofold by rhTRIM5 alpha.. However, if hCA and sCA can coassemble into the same core structure to form a mixed core, rhTRIM5 alpha would be able to recognize such cores and significantly restrict virus infectivity. We examined the restriction phenotypes of viruses containing both hCA and sCA. Our results indicate that hCA and sCA can coassemble into the same mature core to produce infectious virus. To our knowledge, this is the first demonstration of functional coassembly of heterologous CA protein into the retroviral core.
C1 [Chen, Jianbo; Pathak, Vinay K.; Hu, Wei-Shau] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Peng, Weiqun] George Washington Univ, Dept Phys, Washington, DC 20052 USA.
RP Hu, WS (reprint author), NCI, HIV Drug Resistance Program, POB B,Bldg 535,Room 336, Frederick, MD 21702 USA.
EM whu@ncifcrf.gov
RI Chen, Jianbo/N-3737-2014
OI Chen, Jianbo/0000-0001-6491-6577
FU NIH [IATAP]; Center for Cancer Research, National Cancer Institute
FX We thank Anne Arthur for her expert editorial help, Matthew Stremlau and
Joseph Sodroski for the generous gifts of TRIM5 alpha and control cell
lines, and Eric Freed and Alan Rein for their input and critical reading
of the manuscript. This research was supported by the Intramural
Research Program of the NIH, including an IATAP grant, and the Center
for Cancer Research, National Cancer Institute.
NR 55
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8253
EP 8261
DI 10.1128/JVI.02663-07
PG 9
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600002
PM 18579598
ER
PT J
AU Liu, MH
Yang, LP
Zhang, L
Liu, BY
Merling, R
Xia, Z
Giam, CZ
AF Liu, Meihong
Yang, Liangpeng
Zhang, Ling
Liu, Baoying
Merling, Randall
Xia, Zheng
Giam, Chou-Zen
TI Human T-cell leukemia virus type 1 infection leads to arrest in the G(1)
phase of the cell cycle
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HTLV-I TAX; ANAPHASE-PROMOTING COMPLEX; ONCOGENE PRODUCT TAX;
NF-KAPPA-B; CENTROSOME OVERDUPLICATION; MOLECULAR MECHANISM; DEPENDENT
KINASES; CDK INHIBITORS; ONCOPROTEIN; ACTIVATION
AB Infection by the human T-cell leukemia virus type 1 (HTLV-1) is thought to cause dysregulated T-cell proliferation, which in turn leads to adult T-cell leukemia/lymphoma. Early cellular changes after HTLV-1 infection have been difficult to study due to the poorly infectious nature of HTLV-1 and the need for cell-to-cell contact for HTLV-1 transmission. Using a series of reporter systems, we show that HeLa cells cease proliferation within one or two division cycles after infection by HTLV-1 or transduction of the HTLV-1 tax gene. HTLV-1-infected HeLa cells, like their tax-transduced counterparts, expressed high levels of p21(CIP1/WAF1) and p27(KIP1), developed mitotic abnormalities, and became arrested in G, in senescence. In contrast, cells of a human osteosarcoma lineage (HOS) continued to divide after HTLV-1 infection or Tax expression, albeit at a reduced growth rate and with mitotic aberrations. Unique to HOS cells is the dramatic reduction of p21(CIP1/WAF1) and p27(KIP1) expression, which is in part associated with the constitutive activation of the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) pathway. The loss of p21(CIP1/WAF1) and p27(KIP1) in HOS cells apparently allows HTLV-1- and Tax-induced G, arrest to be bypassed. Finally, HTLV-1 infection and Tax expression also cause human SupT1 T cells to arrest in the G, phase of the cell cycle. These results suggest that productive HTLV-1 infection ordinarily leads to Tax-mediated G, arrest. However, T cells containing somatic mutations that inactivate p21(CIP1/WAF1) and p27(KIP1) may continue to proliferate after HTLV-I infection and Tax expression. These infected cells can expand clonally, accumulate additional chromosomal abnormalities, and progress to cancer.
C1 [Liu, Meihong; Yang, Liangpeng; Zhang, Ling; Merling, Randall; Xia, Zheng; Giam, Chou-Zen] Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20814 USA.
[Liu, Baoying] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Giam, CZ (reprint author), Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM cgiam@usuhs.mil
FU National Institutes of Health [R01CA115884]
FX We thank K. Wolcott and K. Lund of the Uniformed Services University
Biomedical Instrumentation Center for help with flow cytometry and K. S.
Jones of SAIC-Frederick of National Cancer Institute for helpful
discussions.; This work was supported by a grant (R01CA115884) from the
National Institutes of Health.
NR 45
TC 35
Z9 37
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8442
EP 8455
DI 10.1128/JVI.00091-08
PG 14
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600020
PM 18596104
ER
PT J
AU Jung, KJ
Dasgupta, A
Huang, K
Jeong, SJ
Pise-Masison, C
Gurova, KV
Brady, JN
AF Jung, Kyung-Jin
Dasgupta, Arindam
Huang, Keven
Jeong, Soo-Jin
Pise-Masison, Cynthia
Gurova, Katerina V.
Brady, John N.
TI Small-molecule inhibitor which reactivates p53 in human T-cell leukemia
virus type 1-transformed cells
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NF-KAPPA-B; I TAX PROTEIN; TRANSGENIC MICE; HTLV-1-TRANSFORMED CELLS;
GENE-EXPRESSION; ACTIVATION; TRANSFORMATION; PHOSPHORYLATION;
ONCOPROTEIN; HTLV-1
AB Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent of the aggressive and fatal disease adult T-cell leukemia. Previous studies have demonstrated that the HTLV-1-encoded Tax protein inhibits the function of tumor suppressor p53 through a Tax-induced NF-kappa B pathway. Given these attributes, we were interested in the activity of small-molecule inhibitor 9-aminoacridine (9AA), an anticancer drug that targets two important stress response pathways, NF-kappa B and p53. In the present study, we have examined the effects of 9AA on HTLV-1 -transformed cells. Treatment of HTLV-1-transformed cells with 9AA resulted in a dramatic decrease in cell viability. Consistent with these results, we observed an increase in the percentage of cells in sub-G, and an increase in the number of cells positive by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling assay following treatment of HTLV-1-transformed cells with 9AA. In each assay, HTLV-1-transformed cells C8166, Hut102, and MT2 were more sensitive to treatment with 9AA than control CEM and peripheral blood mononuclear cells. Analyzing p53 function, we demonstrate that treatment of HTLV-1 -transformed cells with 9AA resulted in an increase in p53 protein and activation of p53 transcription activity. Of significance, 9AA-induced cell death could be blocked by introduction of a p53 small interfering RNA, linking p53 activity and cell death. These results suggest that Tax-repressed p53 function in HTLV-1-transformed cells is "druggable" and can be restored by treatment with 9AA. The fact that 9AA induces p53 and inhibits NF-kappa B suggests a promising strategy for the treatment of HTLV-1-transformed cells.
C1 [Jung, Kyung-Jin; Dasgupta, Arindam; Huang, Keven; Jeong, Soo-Jin; Pise-Masison, Cynthia; Brady, John N.] NCI, Virus Tumor Biol Sect, Cellular Oncol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Gurova, Katerina V.] Cleveland Biolabs Inc, Anticanc Drug Discovery Lab, Buffalo, NY 14203 USA.
RP Brady, JN (reprint author), NCI, Virus Tumor Biol Sect, Cellular Oncol Lab, Ctr Canc Res,NIH, Bldg 41,Room B201, Bethesda, MD 20892 USA.
EM bradyj@exchange.nih.gov
NR 49
TC 19
Z9 20
U1 1
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8537
EP 8547
DI 10.1128/JVI.00690-08
PG 11
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600029
PM 18550670
ER
PT J
AU Chang, KW
Oh, J
Alvord, WG
Hughes, SH
AF Chang, Kevin W.
Oh, Jangsuk
Alvord, W. Gregory
Hughes, Stephen H.
TI The effects of alternate polypurine tracts (PPTs) and mutations of
sequences adjacent to the PPT on viral replication and cleavage
specificity of the Rous sarcoma virus reverse transcriptase
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; RNASE-H CLEAVAGE; STRAND DNA-SYNTHESIS;
PRIMER BINDING-SITE; IN-VIVO; RIBONUCLEASE-H; CRYSTAL-STRUCTURE;
CELL-LINE; TYPE-1; INTEGRATION
AB We previously reported that a mutant Rous sarcoma virus (RSV) with an alternate polypurine tract (PPT), DuckHepBFlipPPT, had unexpectedly high titers and that the PPT was miscleaved primarily at one position following a GA dinucleotide by the RNase H of reverse transcriptase (RT). This miscleavage resulted in a portion of the 3' end of the PPT (5'-ATGTA) being added to the end of U3 of the linear viral DNA. To better understand the RNase H cleavage by RSV RT, we made a number of mutations within the DuckHepBFlipPPT and in the sequences adjacent to the PPT. Deleting the entire ATGTA sequence from the DuckHepBFlipPPT increased the relative titer to wild-type levels, while point mutations within the ATGTA sequence reduced the relative titer but had minimal effects on the cleavage specificity. However, mutating a sequence 5' of ATGTA affected the relative titer of the virus and caused the RNase H of RSV RT to lose the ability to cleave the PPT specifically. In addition, although mutations in the conserved stretch of thymidine residues upstream of the PPT did not affect the relative titer or cleavage specificity, the mutation of some of the nucleotides immediately upstream of the PPT did affect the titer and cleavage specificity. Taken together, our studies show that the structure of the PPT in the context of the cognate RT, rather than a specific sequence, is important for the proper cleavage by RSV RT.
C1 [Chang, Kevin W.; Oh, Jangsuk; Hughes, Stephen H.] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Alvord, W. Gregory] NCI, Data Management Serv, Frederick, MD 21702 USA.
[Oh, Jangsuk] NHLBI, Bethesda, MD 20892 USA.
RP Hughes, SH (reprint author), NCI, HIV Drug Resistance Program, POB 8,Bldg 539,Rm 130A, Frederick, MD 21702 USA.
EM hughes@ncifcrf.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX We thank Teresa Burdette for help with the preparation of the manuscript
and Tammy L. Schroyer from the Scientific Publications Graphics and
Media, SAIC-Frederick office for help with the preparation of the
figures.; Research was Supported by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research.
NR 35
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8592
EP 8604
DI 10.1128/JVI.00499-08
PG 13
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600034
PM 18562520
ER
PT J
AU Bisht, H
Weisberg, AS
Moss, B
AF Bisht, Himani
Weisberg, Andrea S.
Moss, Bernard
TI Vaccinia virus L1 protein is required for cell entry and membrane fusion
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID ENVELOPE PROTEIN; VIRION MEMBRANE; MATURE VIRION; GENE; IDENTIFICATION;
POXVIRUSES; EXPRESSION; ANTIBODIES; COMPONENT; TOPOLOGY
AB Genetic and biochemical studies have provided evidence for an entry/fusion complex (EFC) comprised of at least eight viral proteins (A16, A21, A28, G3, G9, H2, J5, and L5) that together with an associated protein (F9) participates in entry of vaccinia virus (VACV) into cells. The genes encoding these proteins are conserved in all poxviruses, are expressed late in infection, and are components of the mature virion membrane but are not required for viral morphogenesis. In addition, all but one component has intramolecular disulfides that are formed by the poxvirus cytoplasmic redox system. The L1 protein has each of the characteristics enumerated above except that it has been reported to be essential for virus assembly. To further investigate the role of L1, we constructed a recombinant VACV (vL1Ri) that inducibly expresses L1. In the absence of inducer, L1 synthesis was repressed and vL1Ri was unable to form plaques or produce infectious progeny. Unexpectedly, assembly and morphogenesis appeared normal and the noninfectious virus particles were indistinguishable from wild-type VACV as determined by transmission electron microscopy and analysis of the component polypeptides. Notably, the L1-deficient virions were able to attach to cells but the cores failed to penetrate into the cytoplasm. In addition, cells infected with vL1Ri in the absence of inducer did not form syncytia following brief low-pH treatment even though extracellular virus was produced. Coimmunoprecipitation experiments demonstrated that L1 interacted with the EFC and indirectly with F9, suggesting that L1 is an additional component of the viral entry apparatus.
C1 [Bisht, Himani; Weisberg, Andrea S.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, 33 N Dr, Bethesda, MD 20892 USA.
EM bmoss@nih.gov
FU Division of Intramural Research; MAID; NIH
FX We thank Mariano Esteban, Geoffrey Smith, and Gary Cohen for their
generosity in providing antibodies; Norman Cooper and Catherine Cotter
for tissue Culture cells; Timothy R. Wagenaar for vA28i/F9TAP virus;
Arban Domi for help in confocal microscopy and the entry assay; and
Tatiana G. Scrikevich for useful discussions.; The study was Supported
by the Division of Intramural Research, MAID, NIH.
NR 41
TC 42
Z9 44
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8687
EP 8694
DI 10.1128/JVI.00852-08
PG 8
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600042
PM 18596103
ER
PT J
AU McCormack, JC
Yuan, XF
Yingling, YG
Kasprzak, W
Zamora, RE
Shapiro, BA
Simon, AE
AF McCormack, John C.
Yuan, Xuefeng
Yingling, Yaroslava G.
Kasprzak, Wojciech
Zamora, Rodolfo E.
Shapiro, Bruce A.
Simon, Anne E.
TI Structural domains within the 3 ' untranslated region of Turnip crinkle
virus
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MINUS-STRAND SYNTHESIS; PARALLEL GENETIC ALGORITHM; CHLOROTIC-RINGSPOT
VIRUS; RNA STRUCTURE-ANALYSIS; 3' END; TRANSLATIONAL ENHANCEMENT; VIRAL
REPLICATION; STEM-LOOP; REGION; INITIATION
AB The genomes of positive-strand RNA viruses undergo conformational shifts that complicate efforts to equate structures with function. We have initiated a detailed analysis of secondary and tertiary elements within the 3' end of Turnip crinkle virus (TCV) that are required for viral accumulation in vivo. MPGAfold, a massively parallel genetic algorithm, suggested the presence of five hairpins (H4a, H4b, and previously identified hairpins H4, H5, and Pr) and one H-type pseudoknot (Psi(3)) within the 3 '-terminal 194 nucleotides (nt). In vivo compensatory mutagenesis analyses confirmed the existence of H4a, H4b, Psi(3) and a second pseudoknot (Psi(2)) previously identified in a TCV satellite RNA. In-line structure probing of the 194-nt fragment supported the coexistence of H4, H4a, H4b, Psi(3) and a pseudoknot that connects H5 and the 3' end (Psi(1)). Stepwise replacements of TCV elements with the comparable elements from Cardamine chlorotic fleck virus indicated that the complete 142-nt 3' end, and subsets containing Psi(3), H4a, and H4b or Psi(3), H4a, H4b, H5, and Psi(2), form functional domains for virus accumulation in vivo. A new 3-D molecular modeling protocol (RNA2D3D) predicted that H4a, H4b, H5, Psi(3), and Psi(2) are capable of simultaneous existence and bears some resemblance to a tRNA. The related Japanese iris necrotic ring virus does not have comparable domains. These results provide a framework for determining how interconnected elements participate in processes that require 3' untranslated region sequences such as translation and replication.
C1 [McCormack, John C.; Yuan, Xuefeng; Zamora, Rodolfo E.; Simon, Anne E.] Univ Maryland, Dept Cell Biol & Mol Genet, College Pk, MD 20742 USA.
[Yingling, Yaroslava G.; Shapiro, Bruce A.] NCI, Ctr Canc Res Nanobiol Program, Frederick, MD 21702 USA.
[Kasprzak, Wojciech] NCI, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Simon, AE (reprint author), Univ Maryland, Dept Cell Biol & Mol Genet, College Pk, MD 20742 USA.
EM simona@umd.edu
RI Yingling, Yaroslava/B-2901-2008
OI Yingling, Yaroslava/0000-0002-8557-9992
FU U.S. Public Health Service [GM 061515-05A2/G120CD, GM 61515-01];
National Science Foundation [MCB-0086952]; NIH Institutional Training
[T32-AI51967-01]; Intramural Research Program; National Cancer
Institute; Center for Cancer Research; National Institutes of Health
[NO1-CO-12400]; National Cancer Institute's Advanced Biomedical
Computing Center
FX We are very grateful 10 Ping Yu for providing LIS with T7 RNA
polymerase.; This work was supported by grants from the U.S. Public
Health Service (GM 061515-05A2/G120CD and GM 61515-01) and the National
Science Foundation (MCB-0086952) to A.E.S. J.C.M. was Supported by NIH
Institutional Training Grant no. T32-AI51967-01. This research was
Supported in part by the Intramural Research Program of NIH, National
Cancer Institute, Center for Cancer Research. This publication has been
funded in part with federal funds from the National Cancer Institute,
National Institutes of Health, under contract no. NO1-CO-12400. The
computational support was provided in part by the National Cancer
Institute's Advanced Biomedical Computing Center.; The content Of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, nor does the mention of trade
names, commercial products, or organizations imply endorsement by the
U.S. government.
NR 47
TC 40
Z9 40
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8706
EP 8720
DI 10.1128/JVI.00416-08
PG 15
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600044
PM 18579599
ER
PT J
AU Munir, S
Le Nouen, C
Luongo, C
Buchholz, UJ
Collins, PL
Bukreyev, A
AF Munir, Shirin
Le Nouen, Cyril
Luongo, Cindy
Buchholz, Ursula J.
Collins, Peter L.
Bukreyev, Alexander
TI Nonstructural proteins 1 and 2 of respiratory syncytial virus suppress
maturation of human dendritic cells
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NF-KAPPA-B; INTERFERON REGULATORY FACTOR-3; HUMAN ALVEOLAR MACROPHAGES;
AIRWAY EPITHELIAL-CELLS; TUMOR-NECROSIS-FACTOR; WILD-TYPE SV5; CD4
T-CELLS; I INTERFERON; ADAPTIVE IMMUNITY; CYTOKINE PRODUCTION
AB Human respiratory syncytial virus (RSV) is the most important agent of serious pediatric respiratory tract disease worldwide. One of the main characteristics of RSV is that it readily reinfects and causes disease throughout life without the need for significant antigenic change. The virus encodes nonstructural protein 1 (NS1) and NS2, which are known to suppress type I interferon (IFN) production and signaling. In the present study, we monitored the maturation of human monocyte-derived myeloiel dendritic cells (DC) following inoculation with recombinant RSVs bearing deletions of the NS1 and/or NS2 proteins and expressing enhanced green fluorescent protein. Deletion of the NS1 protein resulted in increased expression of cell surface markers of DC maturation and an increase in the expression of multiple cytokines and chemokines. This effect was enhanced somewhat by further deletion of the NS2 protein, although deletion of NS2 alone did not have a significant effect. The upregulation was largely inhibited by pretreatment with a blocking antibody against the type I IFN receptor, suggesting that suppression of DC maturation by NS1/2 is, at least in part, a result of IFN antagonism mediated by these proteins. Therefore, this study identified another effect of the NS1 and NS2 proteins. The observed suppression of DC maturation may result in decreased antigen presentation and T-lymphocyte activation, leading to incomplete and/or weak immune responses that might contribute to RSV reinfection.
C1 [Munir, Shirin; Le Nouen, Cyril; Luongo, Cindy; Buchholz, Ursula J.; Collins, Peter L.; Bukreyev, Alexander] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Bukreyev, A (reprint author), NIAID, Infect Dis Lab, NIH, Bldg 50,Room 6505,50 S Dr,MSC 8007, Bethesda, MD 20892 USA.
EM AB176v@nih.gov
FU Intramural Research Program of NIAID, NIH
FX We thank Ronald Rabin and Brian Murphy for reviewing the manuscript and
for useful suggestions. We also thank Christine Winter for sequencing of
the viral constructs, Lijuan Yang for ELISAs, and David Stephany for
help with flow cytometry.; This study was funded as a part of the
Intramural Research Program of NIAID, NIH.
NR 91
TC 50
Z9 54
U1 1
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8780
EP 8796
DI 10.1128/JVI.00630-08
PG 17
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600050
PM 18562519
ER
PT J
AU Sun, Y
Santra, S
Schmitz, JE
Roederer, M
Letvin, NL
AF Sun, Yue
Santra, Sampa
Schmitz, Joern E.
Roederer, Mario
Letvin, Norman L.
TI Magnitude and quality of vaccine-elicited T-cell responses in the
control of immunodeficiency virus replication in rhesus monkeys
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID LYMPHOCYTE RESPONSES; HIV VACCINES; AIDS VACCINE; DNA; VECTORS;
IMMUNOGENICITY; IMMUNIZATION; VOLUNTEERS; PHENOTYPE; INFECTION
AB While a diversity of immunogens that elicit qualitatively different cellular immune responses are being assessed in clinical human immunodeficiency virus vaccine trials, the consequences of those varied responses for viral control remain poorly understood. In the present study, we evaluated the induction (if virus-specific T-cell responses in rhesus monkeys using a series of diverse vaccine vectors. We assessed both the magnitude and the functional profile of the virus-specific CD8(+) T cells by measuring gamma interferon, interleukin-2, and tumor necrosis factor alpha production. We found that the different vectors generated virus-specific T-cell responses of different magnitudes and with different functional profiles. Heterologous prime-boost vaccine regimens induced particularly high-frequency virus-specific T-cell responses with polyfunctional repertoires. Yet, immediately after a pathogenic simian-human immunodeficiency virus (SHIV) challenge, no significant differences were observed between these cohorts of vaccinated monkeys in the magnitudes or the functional profiles of their virus-specific CD8(+) T cells. This finding suggests that the high viral load shapes the functional repertoire of the cellular immune response during primary infection. Nevertheless, in all vaccination regimens, higher frequency and more polyfunctional vaccine-elicited virus-specific CD8(+) T-cell responses were associated with better viral control after SHIV challenge. These observations highlight the contributions of both the quality and the magnitude (of vaccine-elicited cellular immune responses in the control of immunodeficiency virus replication.
C1 [Sun, Yue; Santra, Sampa; Schmitz, Joern E.; Letvin, Norman L.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med,Div Viral Pathogenesis, Boston, MA 02215 USA.
[Roederer, Mario; Letvin, Norman L.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Letvin, NL (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med,Div Viral Pathogenesis, RE113,POB 15732, Boston, MA 02215 USA.
EM nletvin@bidmc.harvard.edu
FU Vaccine Research Centerr, NIAID, NIH; Harvard Medical School [A1060354];
NIH [NOI-AI30033]
FX We are grateful to Mark Cavabyab, Avi-Hai Hovav, Robert Seder, John
Mascola, and Gary Nabel for helpful conversations and Michelle Lifton
for technical assistance.; This work wits supported in part by funds
front the intramural research program of the Vaccine Research Center,
NIAID, NIH; the Harvard Medical School CFAR grant A1060354; and the NIH
grant NOI-AI30033.
NR 23
TC 27
Z9 28
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8812
EP 8819
DI 10.1128/JVI.00204-08
PG 8
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600052
PM 18579590
ER
PT J
AU Peterson, KE
Pourciau, S
Du, M
LaCasse, R
Pathmajeyan, M
Poulsen, D
Agbandje-McKenna, M
Wehrly, K
Chesebro, B
AF Peterson, Karin E.
Pourciau, Susan
Du, Min
LaCasse, Rachel
Pathmajeyan, Melissa
Poulsen, David
Agbandje-McKenna, Mavis
Wehrly, Kathy
Chesebro, Bruce
TI Neurovirulence of polytropic murine retrovirus is influenced by two
separate regions on opposite sides of the envelope protein receptor
binding domain
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID INDUCED SPONGIFORM NEURODEGENERATION; ENDOPLASMIC-RETICULUM STRESS;
LEUKEMIA-VIRUS-TB; NEUROLOGIC DISEASE; SYNCYTIUM FORMATION; MICROGLIAL
CELLS; BRAIN; INDUCTION; INFECTION; GENE
AB Changes in the envelope proteins of retroviruses can alter the ability of these viruses to infect the central nervous system (CNS) and induce neurological disease. In the present study, nine envelope residues were found to influence neurovirulence of the Friend murine polytropic retrovirus Fr98. When projected on a three-dimensional model, these residues were clustered in two spatially separated groups, one in variable region B of the receptor binding site and the other on the opposite side of the envelope. Further studies indicated a role for these residues in virus replication in the CNS, although the residues did not affect viral entry.
C1 [Peterson, Karin E.; Pourciau, Susan; Du, Min] Louisiana State Univ, Sch Vet Med, Dept Pathobiol Sci, Baton Rouge, LA 70803 USA.
[LaCasse, Rachel; Pathmajeyan, Melissa; Wehrly, Kathy; Chesebro, Bruce] NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, Hamilton, MT 59840 USA.
[Poulsen, David] Univ Montana, Ctr Struct & Funct Neurosci, Dept Biomed & Pharmaceut Sci, Missoula, MT 59801 USA.
[Agbandje-McKenna, Mavis] Univ Florida, Dept Biochem & Mol Biol, Gainesville, FL USA.
RP Peterson, KE (reprint author), Louisiana State Univ, Sch Vet Med, Dept Pathobiol Sci, Skip Bertman Dr, Baton Rouge, LA 70803 USA.
EM petersonka@niaid.nih.gov
RI Peterson, Karin/D-1492-2016
OI Peterson, Karin/0000-0003-4177-7249
FU Intramural Research Program of the NIAID, NIH; National Center for
Research Resources [IP20RRO20159]
FX We thank Scott Hughes for technical assistance, Anita Mora and Gary
Hettrick for graphics assistance, and Kim Hasenkrug and John Portis for
helpful suggestions with the manuscript.; This research was supported in
part by the Intramural Research Program of the NIAID, NIH, and in part
by the National Center for Research Resources (grant IP20RRO20159).
NR 24
TC 5
Z9 5
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8906
EP 8910
DI 10.1128/JVI.02134-07
PG 5
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600064
PM 18579597
ER
PT J
AU Schmidt, M
Govindasamy, L
Afione, S
Kaludov, N
Agbandje-McKenna, M
Chiorini, JA
AF Schmidt, Michael
Govindasamy, Lakshmanan
Afione, Sandra
Kaludov, Nick
Agbandje-McKenna, Mavis
Chiorini, John A.
TI Molecular characterization of the heparin-dependent transduction domain
on the capsid of a novel adeno-associated virus isolate, AAV(VR-942)
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID EFFICIENT TRANSDUCTION; SULFATE PROTEOGLYCAN; AAV SEROTYPES; BINDING;
TYPE-2; IDENTIFICATION; SPECIFICITY; VECTORS; CLONING; STOCKS
AB A new adeno-associated virus (AAV), referred to as AAV(VR-942), has been isolated as a contaminant of adenovirus strain simian virus 17. The sequence of the rep gene places it in the AAV serotype 2 (AAV2) complementation group, while the capsid is only 88% identical to that of AAV2. High-level AAV(VR-942) transduction activity requires cell surface heparan sulfate proteoglycans, although AAV(VR-942) lacks residues equivalent to the AAV2 R585 and R588 amino acid residues essential for mediating the interaction of AAV2 with the heparan sulfate proteoglycan receptor. Instead, AAV(VR-942) uses a distinct transduction region. This finding shows that distinct domains on different AAV isolates can be responsible for the same activities.
C1 [Govindasamy, Lakshmanan; Agbandje-McKenna, Mavis] Univ Florida, Coll Med, Dept Biochem & Mol Biol, Struct Biol Ctr,McKnight Brain Inst, Gainesville, FL 32610 USA.
[Schmidt, Michael; Afione, Sandra; Kaludov, Nick; Chiorini, John A.] Natl Inst Dent & Cranifacial Res, Gene Therapy & Therapeut Branch, Bethesda, MD 20892 USA.
RP Agbandje-McKenna, M (reprint author), Univ Florida, Coll Med, Dept Biochem & Mol Biol, Struct Biol Ctr,McKnight Brain Inst, Gainesville, FL 32610 USA.
EM jchiorini@dir.nidcr.nih
FU Intramural Research Program of the NIH and NIDCR [NIH R01 GM082946, NIH
P01 HL51811]
FX We thank the NIDCR sequencing core facility and Danielle Mandikian for
their excellent assistance.; This research was supported by funds from
the Intramural Research Program of the NIH and NIDCR to J.A.C. and
grants NIH R01 GM082946 and NIH P01 HL51811 to M.A.-M.
NR 19
TC 19
Z9 19
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8911
EP 8916
DI 10.1128/JVI.00672-08
PG 6
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600065
PM 18524816
ER
PT J
AU Young, NS
Zhi, N
Wong, S
AF Young, Neal S.
Zhi, Ning
Wong, Susan
TI Human B19 erythrovirus in vitro replication: What's new? Authors' reply
SO JOURNAL OF VIROLOGY
LA English
DT Letter
ID HUMAN PARVOVIRUS B19; CELLS; INVITRO; PROTEIN
C1 [Young, Neal S.; Zhi, Ning; Wong, Susan] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Young, NS (reprint author), NHLBI, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM youngn@nhlbi.nih.gov
NR 12
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 17
BP 8952
EP 8953
PG 2
WC Virology
SC Virology
GA 339UU
UT WOS:000258603600074
ER
PT J
AU Bartlett, EJ
Cruz, AM
Esker, J
Castano, A
Schomacker, H
Surman, SR
Hennessey, M
Boonyaratanakornkit, J
Pickles, RJ
Collins, PL
Murphy, BR
Schmidt, AC
AF Bartlett, Emmalene J.
Cruz, Ann-Marie
Esker, Janice
Castano, Adam
Schomacker, Henrick
Surman, Sonja R.
Hennessey, Margaret
Boonyaratanakornkit, Jim
Pickles, Raymond J.
Collins, Peter L.
Murphy, Brian R.
Schmidt, Alexander C.
TI Human parainfluenza virus type 1 C proteins are nonessential proteins
that inhibit the host interferon and apoptotic responses and are
required for efficient replication in nonhuman primates
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RESPIRATORY SYNCYTIAL VIRUS; ACUTE OTITIS-MEDIA; NF-KAPPA-B;
SENDAI-VIRUS; VACCINE CANDIDATES; NS1 PROTEIN; REVERSE GENETICS;
EPITHELIAL-CELLS; YOUNG-CHILDREN; RNA-SYNTHESIS
AB Recombinant human parainfluenza virus type 1 (rHPIV1) was modified to create rHPIV1-P(C-), a virus in which expression of the C proteins (C ', C, Y1, and Y2) was silenced without affecting the amino acid sequence of the P protein. Infectious rHPIV1-P(C-) was readily recovered from cDNA, indicating that the four C proteins were not essential for virus replication. Early during infection in vitro, rHPIV1-P(C-) replicated as efficiently as wild-type (wt) HPIV1, but its titer subsequently decreased coincident with the onset of an extensive cytopathic effect not observed with wt rHPIV1. rHPIV1-P(C-) infection, but not wt rHPIV1 infection, induced caspase 3 activation and nuclear fragmentation in LLC-MK2 cells, identifying the HPIV1 C proteins as inhibitors of apoptosis. In contrast to wt rHPIV1, rHPIV1-P(C-) and rHPIV1-C(F170S), a mutant encoding an F170S substitution in C, induced interferon (IFN) and did not inhibit IFN signaling in vitro. However, only rHPIV1-P(C-) induced apoptosis. Thus, the anti-IFN and antiapoptosis activities of HPIV1 were separable: both activities are disabled in rHPIV1-P(C-), whereas only the anti-IFN activity is disabled in rHPIV1-C(F170S). In African green monkeys (AGMs), rHPIV1-P(C-) was considerably more attenuated than rHPIV1-C(F170S), suggesting that disabling the anti-IFN and antiapoptotic activities of HPIV1 had additive effects on attenuation in vivo. Although rHPIV1-P(C-) protected against challenge with wt HPIV1, its highly restricted replication in AGMs and in primary human airway epithelial cell cultures suggests that it might be overattenuated for use as a vaccine. Thus, the C proteins of HPIV1 are nonessential but have anti-IFN and antiapoptosis activities required for virulence in primates.
C1 [Bartlett, Emmalene J.; Cruz, Ann-Marie; Esker, Janice; Castano, Adam; Schomacker, Henrick; Surman, Sonja R.; Boonyaratanakornkit, Jim; Collins, Peter L.; Murphy, Brian R.; Schmidt, Alexander C.] NIAID, Infect Dis Lab, Resp Viruses Sect, NIH,US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Hennessey, Margaret; Pickles, Raymond J.] Univ N Carolina, Cyst Fibrosis Pulm Res & Treatment Ctr, Chapel Hill, NC 27599 USA.
[Hennessey, Margaret; Pickles, Raymond J.] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA.
RP Schmidt, AC (reprint author), NIAID, Infect Dis Lab, Resp Viruses Sect, NIH,US Dept Hlth & Human Serv, Bldg 50,Room 6511,50 S Dr,MSC 8007, Bethesda, MD 20892 USA.
EM schmidta@niaid.nih.gov
FU NIAID Intramural Program; National Institutes of Health (NIH) [NIH R01
HL77844-1]
FX We thank Brad Finneyfrock and Marisa St. Claire, Bioqual, Inc., for
carrying out the primate studies. We are grateful to the bioimaging and
flow cytometry groups, especially Lily Koo and David Stephany, within
the Research Technology Branch at NIAID for their excellent support. We
are also grateful to the directors and teams of the UNC Cystic Fibrosis
Center Tissue Culture Core and to Susan Burkett for technical
assistance. John Hiscott, McGill University, provided the VSV-GFP, and
Yasuhiko Ito, Mie University School of Medicine, Mie, Japan, provided
the mouse anti-HPIV1 HN (8.2.2A and 4.5) antibodies.; This project was
funded as a part of the NIAID Intramural Program and National Institutes
of Health (NIH) and by grant NIH R01 HL77844-1.
NR 73
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Z9 27
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 18
BP 8965
EP 8977
DI 10.1128/JVI.00853-08
PG 13
WC Virology
SC Virology
GA 347OX
UT WOS:000259152000002
PM 18614629
ER
PT J
AU Brumme, ZL
Brumme, CJ
Carlson, J
Streeck, H
John, M
Eichbaum, Q
Block, BL
Baker, B
Kadie, C
Markowitz, M
Jessen, H
Kelleher, AD
Rosenberg, E
Kaldor, J
Yuki, Y
Carrington, M
Allen, TM
Mallal, S
Altfeld, M
Heckerman, D
Walker, BD
AF Brumme, Zabrina L.
Brumme, Chanson J.
Carlson, Jonathan
Streeck, Hendrik
John, Mina
Eichbaum, Quentin
Block, Brian L.
Baker, Brett
Kadie, Carl
Markowitz, Martin
Jessen, Heiko
Kelleher, Anthony D.
Rosenberg, Eric
Kaldor, John
Yuki, Yuko
Carrington, Mary
Allen, Todd M.
Mallal, Simon
Altfeld, Marcus
Heckerman, David
Walker, Bruce D.
TI Marked epitope- and allele- specific differences in rates of mutation in
human immunodeficiency type 1 (HIV-1) Gag, Pol, and Nef cytotoxic
T-lymphocyte epitopes in acute/early HIV-1 infection
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID LONG-TERM NONPROGRESSORS; VIRUS TYPE-1; CELL RESPONSES; VIRAL LOAD;
VACCINE DESIGN; P24 GAG; DISEASE PROGRESSION; ESCAPE MUTATIONS;
IMMUNE-RESPONSES; POPULATION-LEVEL
AB During acute human immunodeficiency virus type 1 (HIV-1) infection, early host cellular immune responses drive viral evolution. The rates and extent of these mutations, however, remain incompletely characterized. In a cohort of 98 individuals newly infected with HIV-1 subtype B, we longitudinally characterized the rates and extent of HLA-mediated escape and reversion in Gag, Pol, and Nef using a rational definition of HLA-attributable mutation based on the analysis of a large independent subtype B data set. We demonstrate rapid and dramatic HIV evolution in response to immune pressures that in general reflect established cytotoxic T-lymphocyte (CTL) response hierarchies in early infection. On a population level, HLA-driven evolution was observed in similar to 80% of published CTL epitopes. Five of the 10 most rapidly evolving epitopes were restricted by protective HLA alleles (HLA-B* 13/B* 51/B* 57/B* 5801; P = 0.01), supporting the importance of a strong early CTL response in HIV control. Consistent with known fitness costs of escape, B* 57-associated mutations in Gag were among the most rapidly reverting positions upon transmission to non-B* 57-expressing individuals, whereas many other HLA-associated polymorphisms displayed slow or negligible reversion. Overall, an estimated minimum of 30% of observed substitutions in Gag/Pol and 60% in Nef were attributable to HLA-associated escape and reversion events. Results underscore the dominant role of immune pressures in driving early within-host HIV evolution. Dramatic differences in escape and reversion rates across codons, genes, and HLA restrictions are observed, highlighting the complexity of viral adaptation to the host immune response.
C1 [Brumme, Zabrina L.; Brumme, Chanson J.; Streeck, Hendrik; Eichbaum, Quentin; Block, Brian L.; Baker, Brett; Rosenberg, Eric; Allen, Todd M.; Altfeld, Marcus; Walker, Bruce D.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Partners AIDS Res Ctr, Charlestown, MA 02129 USA.
[Carlson, Jonathan; Kadie, Carl; Heckerman, David] Microsoft Res, Redmond, WA USA.
[Carlson, Jonathan] Univ Washington, Dept Comp Sci, Seattle, WA 98195 USA.
[John, Mina; Mallal, Simon] Royal Perth Hosp, Ctr Clin Immunol & Biomed Stat, Perth, WA, Australia.
[John, Mina; Mallal, Simon] Murdoch Univ, Perth, WA, Australia.
[Markowitz, Martin] Aaron Diamond AIDS Res Ctr, New York, NY USA.
[Jessen, Heiko] Jessen Praxis, Berlin, Germany.
[Kelleher, Anthony D.; Kaldor, John] Univ New S Wales, Natl Ctr HIV Epidemiol & Clin Res, Sydney, NSW, Australia.
[Yuki, Yuko; Carrington, Mary] NCI, Canc & Inflammat Program, Expt Immunol Lab, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Walker, Bruce D.] Howard Hughes Med Inst, Chevy Chase, MD USA.
RP Brumme, ZL (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Partners AIDS Res Ctr, 149 13th St, Charlestown, MA 02129 USA.
EM zbrumme@partners.org
RI Allen, Todd/F-5473-2011; Kaldor, John /D-4545-2011;
OI Brumme, Chanson/0000-0003-2722-5288
FU Howard Hughes Medical Institute; NCI NIH HHS [N01-CO-12400, N01CO12400];
NIAID NIH HHS [R01AI50429, P30 AI060354, R01 AI050429, U01 AI052403,
U01AI052403]
NR 78
TC 127
Z9 131
U1 1
U2 8
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD SEP
PY 2008
VL 82
IS 18
BP 9216
EP 9227
DI 10.1128/JVI.01041-08
PG 12
WC Virology
SC Virology
GA 347OX
UT WOS:000259152000026
PM 18614631
ER
PT J
AU Shaw, LJ
Merz, CNB
Bittner, V
Kip, K
Johnson, BD
Reis, SE
Kelsey, SF
Olson, M
Mankad, S
Sharaf, BL
Rogers, WJ
Pohost, GM
Sopko, G
Pepine, CJ
AF Shaw, Leslee J.
Merz, C. Noel Bairey
Bittner, Vera
Kip, Kevin
Johnson, B. Delia
Reis, Steven E.
Kelsey, Sheryl F.
Olson, Marian
Mankad, Sunil
Sharaf, Barry L.
Rogers, William J.
Pohost, Gerald M.
Sopko, George
Pepine, Carl J.
CA WISE Investigators
TI Importance of socioeconomic status as a predictor of cardiovascular
outcome and costs of care in women with suspected myocardial ischemia.
Results from the National Institutes of Health, National Heart, Lung and
Blood Institute-sponsored Women's Ischemia Syndrome Evaluation (WISE)
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID CORONARY-ARTERY DISEASE; FUNCTIONAL-CAPACITY; ETHNIC-DIFFERENCES;
RISK-FACTORS; SOCIAL-CLASS; CHEST PAIN; ATHEROSCLEROSIS; INEQUALITIES;
MORTALITY; POSITION
AB Background: For women, who are more likely to live in poverty, defining the clinical and economic impact of socioeconomic factors may aid in defining redistributive policies to improve healthcare quality.
Methods. The NIH-NHLBI-sponsored Women's Ischemia Syndrome Evaluation (WISE) enrolled 819 women referred for clinically indicated coronary angiography. This study's primary end point was to evaluate the independent contribution of socioeconomic factors on the estimation of time to cardiovascular death or myocardial infarction (MI) (n = 79) using Cox proportional hazards models. Secondary aims included an examination of cardiovascular costs and quality of life within socioeconomic subsets of women.
Results: In univariable models, socioeconomic factors associated with an elevated risk of cardiovascular death or MI included an annual household income <$20,000 (p = 0.0001), <9th grade education (p = 0.002), being African American, Hispanic, Asian, or American Indian (p = 0.016), on Medicaid, Medicare, or other public health insurance (p < 0.0001), unmarried (p = 0.001.), unemployed or employed part-time (p < 0.0001), and working in a service job (p = 0.003). Of these socioeconomic factors, income (p = 0.006) remained a significant predictor of cardiovascular death or MI in risk-adjusted models that controlled for angiographic coronary disease, chest pain symptoms, and cardiac risk factors. Low-income women, with an annual household income <$20,000, were more often uninsured or on public insurance (p < 0.0001) yet had the highest 5-year hospitalization and drug treatment costs (p < 0.0001). Only 17% of low-income women had prescription drug coverage (vs. >= 50% of higher-income households, p < 0.0001), and 64% required >= 2 anti-ischemic medications during follow-up (compared with 45% of those earning >=$50,000, p < 0.0001).
Conclusions: Economic disadvantage prominently affects cardiovascular disease outcomes for women with chest pain symptoms. These results further support a profound intertwining between poverty and poor health. Cardiovascular disease management strategies should focus on policies that track unmet healthcare needs and worsening clinical status for low-income women.
C1 [Shaw, Leslee J.] Emory Univ, Sch Med, Dept Med, Div Cardiol,Emory Program Cardiovasc Outcome Res, Atlanta, GA 30306 USA.
[Merz, C. Noel Bairey] Cedars Sinai Med Ctr, Cedars Sinai Res Inst, Los Angeles, CA 90048 USA.
[Bittner, Vera; Rogers, William J.] Univ Alabama, Dept Med, Div Cardiovasc Dis, Birmingham, AL 35294 USA.
[Kip, Kevin; Johnson, B. Delia; Kelsey, Sheryl F.; Olson, Marian] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Reis, Steven E.] Univ Pittsburgh, Med Ctr, Cardiovasc Inst, Pittsburgh, PA USA.
[Mankad, Sunil] Allegheny Univ Hlth Sci, Dept Med, Div Cardiol, Pittsburgh, PA USA.
[Sharaf, Barry L.] Rhode Isl Hosp, Div Cardiol, Providence, RI USA.
[Pohost, Gerald M.] Univ So Calif, Div Cardiol, Los Angeles, CA USA.
[Sopko, George] NHLBI, NIH, Bethesda, MD 20892 USA.
[Pepine, Carl J.] Univ Florida, Dept Med, Div Cardiol, Gainesville, FL USA.
RP Shaw, LJ (reprint author), Emory Univ, Sch Med, Dept Med, Div Cardiol,Emory Program Cardiovasc Outcome Res, Suite 1 North,1256 Briarcliff Rd NE, Atlanta, GA 30306 USA.
EM leslee.shaw@emory.edu
RI Reis, Steven/J-3957-2014
FU National Heart, Lung and Blood Institutes [N01-HV-68161, N01-HV-68162,
N01-HV-68163, N01-HV-68164]; National Center for Research Resources
[MO1-RR00425]; Gustavus and Louis Pfeiffer Research Foundation,
Denville, New Jersey; The Women's Guild of Cedars-Sinai Medical Center,
Los Angeles, California; The Ladies Hospital Aid Society of Western
Pennsylvania, Pittsburgh, Pennsylvania; QMED, Inc., Laurence Harbor, New
Jersey; [U0164829]; [U01 HL649141]; [U01 HL649241]
FX This work was supported by contracts from the National Heart, Lung and
Blood Institutes, Nos. N01-HV-68161, N01-HV-68162, N01-HV-68163, and
N01-HV-68164, grants U0164829, U01 HL649141, and U01 HL649241, a GCRC
grant MO1-RR00425 from the National Center for Research Resources, and
grants from the Gustavus and Louis Pfeiffer Research Foundation,
Denville, New Jersey, The Women's Guild of Cedars-Sinai Medical Center,
Los Angeles, California, The Ladies Hospital Aid Society of Western
Pennsylvania, Pittsburgh, Pennsylvania, and QMED, Inc., Laurence Harbor,
New Jersey.
NR 38
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Z9 14
U1 2
U2 10
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD SEP
PY 2008
VL 17
IS 7
BP 1081
EP 1092
DI 10.1089/jwh.2007.0596
PG 12
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 354KT
UT WOS:000259639200005
PM 18774893
ER
PT J
AU Augustson, EM
Barzani, D
Rutten, LJF
Marcus, S
AF Augustson, Erik M.
Barzani, Dilyara
Rutten, Lila J. Finney
Marcus, Stephen
TI Gender differences among hardcore smokers: An analysis of the Tobacco
Use Supplement of the Current Population Survey
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID SMOKING-CESSATION; NICOTINE DEPENDENCE; WORKPLACE SMOKING; MATERNAL
SMOKING; SYNDROME SCALE; BIRTH-WEIGHT; INTERVENTION; RESTRICTIONS;
PREVALENCE; HOUSEHOLD
AB Background: Despite significant declines in smoking rates in the United States, a substantial percentage of adults continue to smoke. Improved understanding of current smokers and their contact with sources of cessation support future tobacco control efforts. Recent evidence suggests that hardcore smokers, established smokers without a history of quit attempts, have less contact with cessation support. Although gender is among the major factors that influence smoking cessation, no research is available on gender differences among hardcore smokers.
Methods: Demographic, environmental, and smoking-related characteristics of female hardcore smokers and male hardcore smokers and other female smokers were examined. Data from 17,777smokers from the 2003 Current Population Survey Tobacco Use Supplement were analyzed.
Results. Compared with female hardcore smokers, male hardcore smokers were more likely to have contact with smoking restrictions at work (OR = 1.69) and at home (OR = 1.45). Compared with female hardcore smokers, female other smokers were more likely to have seen a healthcare provider during the past year who advised them to quit smoking (OR = 1.39) and more likely to have smoking restrictions at work (OR = 1.25) and at home (OR = 2.32)). Measures of nicotine dependence suggested that female hardcore smokers were less dependent than male hardcore smokers but more dependent than other female smokers.
Conclusions: The sociodemographic and healthcare access variations in tobacco use identified in our analyses have significant public health implications and underscore the vital need for clinical and scientific advances in tobacco use prevention and control efforts.
C1 [Augustson, Erik M.] NCI, Tobacco Control Res Branch, DCCPS EPN 4039B, Bethesda, MD 20892 USA.
[Barzani, Dilyara] Kurdistan Reg Govt, Minist Hlth, Kurdistan, Iraq.
[Rutten, Lila J. Finney] NCI, Hlth Commun & Informat Res Branch, Bethesda, MD 20892 USA.
RP Augustson, EM (reprint author), NCI, Tobacco Control Res Branch, DCCPS EPN 4039B, 6130 Execut Blvd,MSC 7337, Bethesda, MD 20892 USA.
EM augustse@mail.nih.gov
NR 38
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Z9 11
U1 1
U2 6
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD SEP
PY 2008
VL 17
IS 7
BP 1167
EP 1173
DI 10.1089/jwh.2007.0535
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 354KT
UT WOS:000259639200013
PM 18707532
ER
PT J
AU McCarthy, EP
Pencina, MJ
Kelly-Hayes, M
Evans, JC
Oberacker, EJ
D'Agostino, RB
Burns, RB
Murabito, JM
AF McCarthy, Ellen P.
Pencina, Michael J.
Kelly-Hayes, Margaret
Evans, Jane C.
Oberacker, Elizabeth J.
D'Agostino, Ralph B., Sr.
Burns, Risa B.
Murabito, Joanne M.
TI Advance Care Planning and Health Care Preferences of Community-Dwelling
Elders: The Framingham Heart Study
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article; Proceedings Paper
CT 28th Annual Meeting of the Society-of-General-Internal-Medicine
CY MAY 11-14, 2005
CL New Orleans, LA
SP Soc Gen Internal Med
DE Advance directives; Geriatrics; End-of-life care; Patient-centered care;
Decision making
ID OF-LIFE CARE; SERIOUSLY ILL PATIENTS; DECISION-MAKING;
CARDIOPULMONARY-RESUSCITATION; CANCER-PATIENTS; DIRECTIVES;
COMMUNICATION; ETHNICITY; DISCUSSIONS; DISPARITIES
AB Objective. The study objective was to describe self-reported advance care planning, health care preferences, use of advance directives, and health perceptions in a very elderly community-dwelling sample.
Methods. We interviewed surviving participants of the original cohort of the Framingham Heart Study who were cognitively intact and attended a routine research examination between February 2004 and October 2005. Participants were queried about discussions about end-of-life care, preferences for care, documentation of advance directives, and health perceptions.
Results. Among 220 community-dwelling respondents, 67% were women with a mean age of 88 years (range 84-100 years). Overall, 69% discussed their wishes for medical care at the end of life with someone, but only 17% discussed their wishes with a physician or health care provider. Two thirds had a health care proxy, 55% had a living will, and 41% had both. Most (80%) respondents preferred comfort care over life-extending care, and 71% preferred to die at home; however, substantially fewer respondents said they would rather die than receive specific life-prolonging interventions (chronic ventilator [63%] or feeding tube [64%]). Many were willing to endure distressing health states, with fewer than half indicating that they would rather die than live out their life in a great deal of pain (46%) or be confused and/or forgetful (45%) all of the time.
Conclusions. Although the vast majority of very elderly community-dwellers in this sample appear to prefer comfort measures at the end of life, many said they were willing to endure specific life-prolonging interventions and distressing health states to avoid death. Our results highlight the need for physicians to better understand patients' preferences and goals of care to help them make informed decisions at the end of life.
C1 [McCarthy, Ellen P.; Burns, Risa B.] Harvard Univ, Sch Med, Dept Med, Div Gen Med & Primary Care,Beth Israel Deaconess, Boston, MA USA.
[Pencina, Michael J.; Kelly-Hayes, Margaret; Evans, Jane C.; Oberacker, Elizabeth J.; D'Agostino, Ralph B., Sr.; Murabito, Joanne M.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Pencina, Michael J.; Evans, Jane C.; D'Agostino, Ralph B., Sr.] Boston Univ, Dept Math & Stat, Stat Consulting Unit, Boston, MA 02215 USA.
[Murabito, Joanne M.] Boston Univ, Sch Med, Gen Internal Med Sect, Dept Med,Boston Med Ctr, Boston, MA 02215 USA.
RP McCarthy, EP (reprint author), Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care, Dept Med, 1309 Beacon St,Suite 220, Brookline, MA 02446 USA.
EM emccarth@bidmc.harvard.edu
FU NHLBI NIH HHS [N01 HC025195, N01-HC-25195, N01HC25195]; NIA NIH HHS [R01
AG008122, R01 AG008122-19, R01 AG08122]; NINDS NIH HHS [R01 NS017950,
R01 NS017950-27, R01 NS17950]
NR 54
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U1 2
U2 12
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD SEP
PY 2008
VL 63
IS 9
BP 951
EP 959
PG 9
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 360RI
UT WOS:000260074800008
PM 18840800
ER
PT J
AU Miller, FG
Gluck, JP
Wendler, D
AF Miller, Franklin G.
Gluck, John P., Jr.
Wendler, David
TI Debriefing and accountability in deceptive research
SO KENNEDY INSTITUTE OF ETHICS JOURNAL
LA English
DT Article
ID PSYCHOLOGICAL-RESEARCH; RESEARCH PARTICIPANTS; INFORMED CONSENT; ETHICAL
ISSUES; PAIN
AB Debriefing is a standard ethical requirement for human research involving the use of deception. Little systematic attention, however, has been devoted to explaining the ethical significance of debriefing and the specific ethical functions that it serves. In this article, we develop an account of debriefing as a tool of moral accountability for the prima facie wrong of deception. Specifically, we contend that debriefing should include a responsibility to promote transparency by explaining the deception and its rationale, to provide an apology to subjects for infringing the principle of respect for persons, and to offer subjects an opportunity to withdraw their data. We also present recommendations concerning the discussion of deception in scientific articles reporting the results of research using deception.
C1 [Miller, Franklin G.] NIMH, Bethesda, MD 20892 USA.
[Miller, Franklin G.; Gluck, John P., Jr.] Georgetown Univ, Kennedy Inst Eth, Washington, DC 20057 USA.
[Gluck, John P., Jr.] Univ New Mexico, Dept Psychol, Albuquerque, NM 87131 USA.
[Miller, Franklin G.; Wendler, David] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
RP Miller, FG (reprint author), NIH, Dept Bioeth, Bldg 10, Bethesda, MD 20892 USA.
NR 30
TC 16
Z9 16
U1 0
U2 6
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
21218-4363 USA
SN 1054-6863
J9 KENNEDY INST ETHIC J
JI Kennedy Inst. Ethics J.
PD SEP
PY 2008
VL 18
IS 3
BP 235
EP 251
PG 17
WC Ethics; Philosophy; Social Issues
SC Social Sciences - Other Topics; Philosophy; Social Issues
GA 355WC
UT WOS:000259738900002
PM 18935922
ER
PT J
AU Zhou, H
Cheruvanky, A
Hu, XZ
Matsumoto, T
Hiramatsu, N
Cho, ME
Berger, A
Leelahavanichkul, A
Doi, K
Chawla, LS
Illei, GG
Kopp, JB
Balow, JE
Austin, HA
Yuen, PST
Star, RA
AF Zhou, Hua
Cheruvanky, Anita
Hu, Xuzhen
Matsumoto, Takayuki
Hiramatsu, Noriyuki
Cho, Monique E.
Berger, Alexandra
Leelahavanichkul, Asada
Doi, Kent
Chawla, Lakhmir S.
Illei, Gabor G.
Kopp, Jeffrey B.
Balow, James E.
Austin, Howard A., III
Yuen, Peter S. T.
Star, Robert A.
TI Urinary exosomal transcription factors, a new class of biomarkers for
renal disease
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE exosomes; transcription factor; ATF3; AKI; WT-1; FSGS
ID ACUTE KIDNEY INJURY; GELATINASE-ASSOCIATED LIPOCALIN;
GLOMERULAR-FILTRATION-RATE; MESSENGER-RNA EXPRESSION; GENE-EXPRESSION;
CARDIAC-SURGERY; CYSTATIN-C; ISCHEMIA-REPERFUSION; DIAGNOSTIC MARKER;
SERUM CREATININE
AB Urinary exosomes are excreted from all nephron segments and constitute a rich source of intracellular kidney injury biomarkers. To study whether they contain transcription factors, we collected urine from two acute kidney injury models (cisplatin or ischemia-reperfusion), two podocyte injury models (puromycin-treated rats or podocin-Vpr transgenic mice) and from patients with focal segmental glomerulosclerosis, acute kidney injury and matched controls. Exosomes were isolated by differential centrifugation and found to contain activating transcription factor 3 (ATF3) and Wilms Tumor 1 (WT-1) proteins detected by Western blot. These factors were found in the concentrated exosomal fraction, but not in whole urine. ATF3 was continuously present in urine exosomes of the rat models following acute injury at times earlier than the increase in serum creatinine. ATF3 was found in exosomes isolated from patients with acute kidney injury but not from patients with chronic kidney disease or controls. Urinary WT-1 was present in animal models before significant glomerular sclerosis and in 9/10 patients with focal segmental glomerulosclerosis but not in 8 controls. Our findings suggest that transcription factor ATF3 may provide a novel renal tubular cell biomarker for acute kidney injury while WT-1 may detect early podocyte injury. Measurement of urinary exosomal transcription factors may offer insight into cellular regulatory pathways.
C1 [Zhou, Hua; Cheruvanky, Anita; Hu, Xuzhen; Leelahavanichkul, Asada; Doi, Kent; Yuen, Peter S. T.; Star, Robert A.] NIDDK, Renal Diagnost & Therapeut Unit, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Matsumoto, Takayuki; Hiramatsu, Noriyuki; Cho, Monique E.; Kopp, Jeffrey B.; Balow, James E.; Austin, Howard A., III] NIDDK, Kidney Dis Sect, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Berger, Alexandra; Chawla, Lakhmir S.] George Washington Univ, Dept Med, Div Renal Dis & Hypertens, Washington, DC USA.
[Illei, Gabor G.] NIDCR, Gene Therapy & Therapeut Branch, Natl Inst Hlth, Bethesda, MD USA.
RP Star, RA (reprint author), NIDDK, Renal Diagnost & Therapeut Unit, Natl Inst Hlth, 10 Ctr Dr,Bldg 10,Room 3N108, Bethesda, MD 20892 USA.
EM Robert_Star@nih.gov
RI Yuen, Peter/B-1954-2008;
OI Yuen, Peter/0000-0001-9557-3909; Kopp, Jeffrey/0000-0001-9052-186X
FU Intramural Research Program of NIH; NIDDK
FX This research was supported by the Intramural Research Program of NIH,
NIDDK. We thank Bertrand Jaber and Orfeas Liangos for insightful
suggestions.
NR 62
TC 89
Z9 94
U1 0
U2 10
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
J9 KIDNEY INT
JI Kidney Int.
PD SEP
PY 2008
VL 74
IS 5
BP 613
EP 621
DI 10.1038/ki.2008.206
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 338TM
UT WOS:000258531800013
PM 18509321
ER
PT J
AU Murkunde, YV
Kalaiselvan, P
Vijayakumar, S
Hemalatha, K
Maronpot, RR
Herbert, RA
Wells, MY
AF Murkunde, Yogeshkumar V.
Kalaiselvan, Ponnusamy
Vijayakumar, Subramaniyan
Hemalatha, Kuppusamy
Maronpot, Robert R.
Herbert, Ronald A.
Wells, Monique Y.
TI Brain lesion in a Wistar rat
SO LAB ANIMAL
LA English
DT Article
C1 [Murkunde, Yogeshkumar V.; Kalaiselvan, Ponnusamy; Vijayakumar, Subramaniyan; Hemalatha, Kuppusamy] Int Inst Biotechnol & Toxicol, Dept Pathol, Padappai 601301, Tamil Nadu, India.
[Maronpot, Robert R.; Herbert, Ronald A.] Natl Inst Environm Hlth Sci, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA.
[Wells, Monique Y.] Toxicol Pathol Serv Inc, F-75005 Paris, France.
RP Murkunde, YV (reprint author), Int Inst Biotechnol & Toxicol, Dept Pathol, Padappai 601301, Tamil Nadu, India.
EM fippat@giasmd01.vsnl.net.in
RI pasuvalingam, visha/B-5717-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0093-7355
J9 LAB ANIMAL
JI Lab Anim.
PD SEP
PY 2008
VL 37
IS 9
BP 401
EP 401
DI 10.1038/laban0908-401
PG 1
WC Veterinary Sciences
SC Veterinary Sciences
GA 340QW
UT WOS:000258661100005
PM 18719690
ER
PT J
AU Huntsberry, ME
Charles, D
Adams, KM
Weed, JL
AF Huntsberry, Mary E.
Charles, Debbie
Adams, Kristina M.
Weed, James L.
TI The foraging ball as a quick and easy enrichment device for pigs (Sus
scrofa)
SO LAB ANIMAL
LA English
DT Article
ID ENVIRONMENTAL ENRICHMENT; AGGRESSIVE-BEHAVIOR; FINISHING PIGS; GROWING
PIGS; WEANED PIGS; SYSTEMS; TOY
AB Providing research pigs with enrichment objects can encourage species-typical behavior such as rooting and foraging. The authors gave pigs hard plastic 'foraging balls' that resembled enrichment devices commonly used for nonhuman primates. Holes were custom-drilled into the balls, and animal caretakers filled them with palatable food items such as jellybeans, unsalted peanuts, cereal, Beggin' Strips, primate biscuits and dog biscuits. Staff members suspended the balls from chains in pigs' enclosures, ensuring that toys did not touch the floor. All pigs manipulated the balls and were able to obtain treats that were supplemental to their standard diet. The simple and effective enrichment device was easily incorporated into the daily routines of research facilities, with little disruption to schedules.
C1 [Huntsberry, Mary E.] SoBran Inc, Bethesda, MD USA.
[Huntsberry, Mary E.; Weed, James L.] NIH, Div Vet Resources, ORS, DHHS, Bethesda, MD USA.
[Charles, Debbie] Tuskegee Univ, Coll Vet Med, Tuskegee, AL 36088 USA.
[Adams, Kristina M.] ARS, USDA, NAL, AWIC, Beltsville, MD USA.
RP Huntsberry, ME (reprint author), SoBran Inc, Bethesda, MD USA.
EM huntsmar@mail.nih.gov
FU Intramural NIH HHS
NR 28
TC 0
Z9 0
U1 2
U2 17
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0093-7355
J9 LAB ANIMAL
JI Lab Anim.
PD SEP
PY 2008
VL 37
IS 9
BP 411
EP 414
DI 10.1038/laban0908-411
PG 4
WC Veterinary Sciences
SC Veterinary Sciences
GA 340QW
UT WOS:000258661100007
PM 18719693
ER
PT J
AU Qiu, J
Ai, L
Ramachandran, C
Yao, B
Gopalakrishnan, S
Fields, CR
Delmas, AL
Dyer, LM
Melnick, SJ
Yachnis, AT
Schwartz, PH
Fine, HA
Brown, KD
Robertson, KD
AF Qiu, Jingxin
Ai, Lingbao
Ramachandran, Cheppail
Yao, Bing
Gopalakrishnan, Suhasni
Fields, C. Robert
Delmas, Amber L.
Dyer, Lisa M.
Melnick, Steven J.
Yachnis, Anthony T.
Schwartz, Philip H.
Fine, Howard A.
Brown, Kevin D.
Robertson, Keith D.
TI Invasion suppressor cystatin E/M (CST6): high-level cell type-specific
expression in normal brain and epigenetic silencing in gliomas
SO LABORATORY INVESTIGATION
LA English
DT Article
DE cell invasion; CST6; cystatin E/M; DNA methylation; glioma; neural stem
cell
ID HUMAN GLIOBLASTOMA CELLS; CATHEPSIN-B EXPRESSION; HISTONE DEACETYLASE
INHIBITION; CYSTEINE PROTEINASE-INHIBITOR; ABERRANT DNA METHYLATION;
TUMOR STEM-CELLS; GENE-EXPRESSION; MALIGNANT GLIOMA; BREAST-CANCER;
DOWN-REGULATION
AB DNA hypermethylation-mediated gene silencing is a frequent and early contributor to aberrant cell growth and invasion in cancer. Malignant gliomas are the most common primary brain tumors in adults and the second most common tumor in children. Morbidity and mortality are high in glioma patients because tumors are resistant to treatment and are highly invasive into surrounding brain tissue rendering complete surgical resection impossible. Invasiveness is regulated by the interplay between secreted proteases ( eg, cathepsins) and their endogenous inhibitors ( cystatins). In our previous studies we identified cystatin E/ M ( CST6) as a frequent target of epigenetic silencing in glioma. Cystatin E/ M is a potent inhibitor of cathepsin B, which is frequently overexpressed in glioma. Here, we study the expression of cystatin E/ M in normal brain and show that it is highly and moderately expressed in oligodendrocytes and astrocytes, respectively, but not in neurons. Consistent with this, the CST6 promoter is hypomethylated in all normal samples using methylation- specific PCR, bisulfite genomic sequencing, and pyrosequencing. In contrast, 78% of 28 primary brain tumors demonstrated reduced/ absent cystatin E/ M expression using a tissue microarray and this reduced expression correlated with CST6 promoter hypermethylation. Interestingly, CST6 was expressed in neural stem cells ( NSC) and markedly induced upon differentiation, whereas a glioma tumor initiating cell ( TIC) line was completely blocked for CST6 expression by promoter methylation. Analysis of primary pediatric brain tumor- derived lines also showed CST6 downregulation and methylation in nearly 100% of 12 cases. Finally, ectopic expression of cystatin E/ M in glioma lines reduced cell motility and invasion. These results demonstrate that epigenetic silencing of CST6 is frequent in adult and pediatric brain tumors and occurs in TICs, which are thought to give rise to the tumor. CST6 methylation may therefore represent a novel prognostic marker and therapeutic target specifically altered in TICs.
C1 [Ai, Lingbao; Yao, Bing; Gopalakrishnan, Suhasni; Fields, C. Robert; Delmas, Amber L.; Dyer, Lisa M.; Brown, Kevin D.; Robertson, Keith D.] Univ Florida, Dept Biochem & Mol Biol, UF Shands Canc Ctr, Program Canc Genet Epigenet & Tumor Virol,Coll Me, Gainesville, FL 32610 USA.
Univ Florida, Dept Pathol, UF Shands Canc Ctr, Program Canc Genet Epigenet & Tumor Virol,Coll Me, Gainesville, FL 32610 USA.
[Ramachandran, Cheppail; Melnick, Steven J.] Miami Childrens Hosp, Dept Pathol, Miami, FL USA.
[Schwartz, Philip H.] Childrens Hosp Orange Cty, Res Inst, Orange, CA 92668 USA.
[Fine, Howard A.] NCI, Neurooncol Branch, NIH, Bethesda, MD 20892 USA.
RP Robertson, KD (reprint author), Univ Florida, Dept Biochem & Mol Biol, UF Shands Canc Ctr, Program Canc Genet Epigenet & Tumor Virol,Coll Me, 1600 SW Archer Rd, Gainesville, FL 32610 USA.
EM keithr@ufl.edu
FU NCI NIH HHS [R01CA114229, R01CA102289, R01 CA114229, R01 CA102289, R01
CA114229-03, R01 CA114229-04]
NR 68
TC 30
Z9 32
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD SEP
PY 2008
VL 88
IS 9
BP 910
EP 925
DI 10.1038/labinvest.2008.66
PG 16
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 340HK
UT WOS:000258636500001
PM 18607344
ER
PT J
AU Davis, AR
Shields, AD
Brigman, JL
Norcross, M
McElligott, ZA
Holmes, A
Winder, DG
AF Davis, Adeola R.
Shields, Angela D.
Brigman, Jonathan L.
Norcross, Maxine
McElligott, Zoe A.
Holmes, Andrew
Winder, Danny G.
TI Yohimbine impairs extinction of cocaine-conditioned place preference in
an alpha(2)-adrenergic receptor independent process
SO LEARNING & MEMORY
LA English
DT Article
ID SYMPATHETIC-NERVOUS-SYSTEM; RAT RELAPSE MODEL; STRIA TERMINALIS; FEAR
EXTINCTION; BED NUCLEUS; FACILITATES EXTINCTION; POTENTIATED STARTLE;
INFRALIMBIC CORTEX; RECEPTOR SUBTYPES; 5-HT1A RECEPTORS
AB Extinction, a form of learning that has the ability to reshape learned behavior based on new experiences, has been heavily studied utilizing fear learning paradigms. Mechanisms underlying extinction of positive-valence associations, such as drug self-administration and place preference, are poorly understood yet may have important relevance to addiction treatment. Data suggest a major role for the noradrenergic system in extinction of fear-based learning. Employing both pharmacological and genetic approaches, we investigated the role of the alpha(2)-adrenergic receptor (alpha(2)-AR) in extinction of cocaine-conditioned place preference (CPP) and glutamatergic transmission in the bed nucleus of the stria terminalis (BNST). We found that pre-extinction systemic treatment with the alpha(2)-AR antagonist yohimbine impaired cocaine CPP extinction in C57BL/6J mice, an effect that was not mimicked by the more selective alpha(2)-AR antagonist, atipamezole. Moreover, alpha(2)A-AR knockout mice exhibited similar cocaine CPP extinction and exacerbated extinction impairing effects of yohimbine. Using acute brain slices and electrophysiological approaches, we found that yohimbine produces a slowly evolving depression of glutamatergic transmission in the BNST that was not mimicked by atipamezole. Further, this action was extant in slices from alpha(2)A-AR knockout mice. Our data strongly suggest that extinction-modifying effects of yohimbine are unlikely to be due to actions at alpha(2)A-ARs.
C1 [Davis, Adeola R.; McElligott, Zoe A.; Winder, Danny G.] Vanderbilt Univ, Med Ctr, Vanderbilt Brain Inst, Nashville, TN 37232 USA.
[Shields, Angela D.; Winder, Danny G.] Vanderbilt Univ, Med Ctr, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
[Brigman, Jonathan L.; Norcross, Maxine; Holmes, Andrew] NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
[Winder, Danny G.] Vanderbilt Univ, Med Ctr, Kennedy Ctr Human Dev, Nashville, TN 37232 USA.
RP Winder, DG (reprint author), Vanderbilt Univ, Med Ctr, Vanderbilt Brain Inst, Nashville, TN 37232 USA.
EM danny.winder@vanderbilt.edu
RI Winder, Danny/H-4857-2013; Brigman, Jonathan/O-4978-2016
FU NIDA; National Institute on Alcohol Abuse and Alcoholism
FX We thank Dr. Chris Olsen for a critical reading of the manuscript and
William Nobis for writing a helpful script to gather data. Research was
supported by NIDA (D. G. W.), NIDA supplement (A. D. and D. G. W.), and
the Intramural Research Program of the National Institute on Alcohol
Abuse and Alcoholism (A. H., J. B., and M. N.).
NR 54
TC 21
Z9 22
U1 1
U2 2
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1072-0502
J9 LEARN MEMORY
JI Learn. Mem.
PD SEP
PY 2008
VL 15
IS 9
BP 667
EP 676
DI 10.1101/lm.1079308
PG 10
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 355HW
UT WOS:000259701000008
PM 18772254
ER
PT J
AU Yong, ASM
Keyvanfar, K
Eniafe, R
Savani, BN
Rezvani, K
Sloand, EM
Goldman, JM
Barrett, AJ
AF Yong, A. S. M.
Keyvanfar, K.
Eniafe, R.
Savani, B. N.
Rezvani, K.
Sloand, E. M.
Goldman, J. M.
Barrett, A. J.
TI Hematopoietic stem cells and progenitors of chronic myeloid leukemia
express leukemia-associated antigens: implications for the
graft-versus-leukemia effect and peptide vaccine-based immunotherapy
SO LEUKEMIA
LA English
DT Article
DE chronic myeloid leukemia; CD34+progenitor cells; leukemia-associated
antigens; graft-versus-leukemia effect
ID CYTOTOXIC T-LYMPHOCYTES; CHRONIC MYELOGENOUS LEUKEMIA; CD34(+) CELLS;
GENE TRANSCRIPTS; CD7 EXPRESSION; CML PATIENTS; TRANSPLANTATION; WT1;
RESPONSES; PROTEINASE-3
AB The cure of chronic myeloid leukemia (CML) patients following allogeneic stem cell transplantation (SCT) is attributed to graft-versus-leukemia (GVL) effects targeting alloantigens and/or leukemia-associated antigens (LAA) on leukemia cells. To assess the potential of LAA-peptide vaccines in eliminating leukemia in CML patients, we measured WT1, PR3, ELA2 and PRAME expression in CD34+ progenitor subpopulations in CML patients and compared them with minor histocompatibility antigens (mHAgs) HA1 and SMCY. All CD34+ subpopulations expressed similar levels of mHAgs irrespective of disease phase, suggesting that in the SCT setting, mHAgs are the best target for GVL. Furthermore, WT1 was consistently over-expressed in advanced phase (AdP) CML in all CD34+ subpopulations, and mature progenitors of chronic phase (CP) CML compared to healthy individuals. PRAME overexpression was limited to more mature AdP-CML progenitors only. Conversely, only CP-CML progenitors had PR3 overexpression, suggesting that PR1-peptide vaccines are only appropriate in CP-CML. Surface expression of WT1 protein in the most primitive hematopoietic stem cells in AdP-CML suggest that they could be targets for WT1 peptide-based vaccines, which in combination with PRAME, could additionally improve targeting differentiated progeny, and benefit patients responding suboptimally to tyrosine kinase inhibitors, or enhance GVL effects in SCT patients.
C1 [Yong, A. S. M.; Keyvanfar, K.; Eniafe, R.; Savani, B. N.; Rezvani, K.; Sloand, E. M.; Goldman, J. M.; Barrett, A. J.] NHLBI, Stem Cell Allotransplantat Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Yong, ASM (reprint author), NHLBI, Stem Cell Allotransplantat Sect, Hematol Branch, NIH, Bldg 10-CRC,Rm 3-5140,10 Ctr Dr,MSC 1202, Bethesda, MD 20892 USA.
EM yonga@nhlbi.nih.gov
FU Intramural Research Program of the National Heart, Lung and Blood
Institute of the NIH
FX We thank Ms Loretta Pfannes for technical advice on the assessment of
WT1 surface protein by flowcytometry. This research was supported by the
Intramural Research Program of the National Heart, Lung and Blood
Institute of the NIH.
NR 33
TC 33
Z9 35
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD SEP
PY 2008
VL 22
IS 9
BP 1721
EP 1727
DI 10.1038/leu.2008.161
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 346KH
UT WOS:000259066900010
PM 18548092
ER
PT J
AU Arons, E
Suntum, T
Margulies, I
Yuan, C
Stetler-Stevenson, M
Kreitman, RJ
AF Arons, Evgeny
Suntum, Tara
Margulies, Inger
Yuan, Constance
Stetler-Stevenson, Maryalice
Kreitman, Robert J.
TI PRAME expression in hairy cell leukemia
SO LEUKEMIA RESEARCH
LA English
DT Article
DE hairy cell leukemia; real-time PCR; chronic lymphocytic leukemia; PRAME;
TaqMan; minimal residual disease
ID MINIMAL RESIDUAL DISEASE; CHRONIC LYMPHOCYTIC-LEUKEMIA;
POLYMERASE-CHAIN-REACTION; TUMOR-ASSOCIATED ANTIGENS; ACUTE
MYELOID-LEUKEMIA; MESSENGER-RNA LEVELS; GENE-EXPRESSION; CLINICAL
IMPORTANCE; MALIGNANCIES; MELANOMA
AB PRAME has been proposed as a useful marker for solid tumors and acute B-cell malignancies. Several studies demonstrate expression in CLL. To further examine its B-cell tumor distribution, we studied PRAME in both CLL and hairy cell leukemia (HCL). While by conventional PCR only 8% of 37 HCL and 27% of 22 CLL patients were positive, nearly all patients and normal donors expressed PRAME by real-time quantitative (TaqMan) PCR. We conclude that HCL and CLL differ in PRAME overexpression, and that basal normal expression of PRAME may limit its usefulness for following patients with minimal residual CLL or HCL. Published by Elsevier Ltd.
C1 [Kreitman, Robert J.] NCI, Mol Biol Lab, Ctr Canc Res, Clin Immunotherapy Sect,NIH, Bethesda, MD 20892 USA.
NCI, Clin Pathol Lab, Ctr Canc Res, Clin Immunotherapy Sect,NIH, Bethesda, MD 20892 USA.
RP Kreitman, RJ (reprint author), NCI, Mol Biol Lab, Ctr Canc Res, Clin Immunotherapy Sect,NIH, 9000 Rockville Pike,Bldg 37,Room 5124B, Bethesda, MD 20892 USA.
EM kreitmar@mail.nih.gov
FU Intramural NIH HHS [Z01 BC010301-10, Z99 CA999999]
NR 41
TC 4
Z9 5
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2126
J9 LEUKEMIA RES
JI Leuk. Res.
PD SEP
PY 2008
VL 32
IS 9
BP 1400
EP 1406
DI 10.1016/j.leukres.2007.12.010
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 312EB
UT WOS:000256650800010
PM 18295331
ER
PT J
AU Adams, DK
Mullineaux, LS
AF Adams, Diane K.
Mullineaux, Lauren S.
TI Supply of gastropod larvae to hydrothermal vents reflects transport from
local larval sources
SO LIMNOLOGY AND OCEANOGRAPHY
LA English
DT Article
ID EAST PACIFIC RISE; COMMUNITY STRUCTURE; MUSSEL BEDS; DISPERSAL;
RECRUITMENT; PATTERNS; SETTLEMENT; ECOLOGY; WATERS; RIDGE
AB Variation in larval supply to disjunct marine populations can provide insight into larval transport and delivery mechanisms, especially when compared with observations of physical transport. Daily variability in larval supply at two mussel-dominated hydrothermal vents, East Wall and Choo Choo, near 9 degrees 50'N, East Pacific Rise, was quantified concurrently with hydrodynamic observations to investigate local dispersal processes. The magnitude and temporal variation in supply differed between the two vent sites despite their close proximity, 1.6 km. Larval supply was relatively high and uninterrupted at East Wall compared to low and episodic at Choo Choo. Observed variation in larval supply was compared to predictions based on advective transport from larval sources at neighboring vents. Variation in larval supply at Choo Choo correlated with along-axis southward currents, consistent with larval transport from a northern larval source. Larval supply to East Wall appeared to be independent of current velocities, suggesting that larvae came from multiple sources north of and south of and possibly including East Wall. Transport of larvae from discrete local sources can explain differences in larval supply to vent communities, even on spatial scales of kilometers.
C1 [Adams, Diane K.; Mullineaux, Lauren S.] Woods Hole Oceanog Inst, Woods Hole, MA 02543 USA.
[Adams, Diane K.] Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA.
RP Adams, DK (reprint author), Woods Hole Oceanog Inst, 266 Woods Hole Rd, Woods Hole, MA 02543 USA.
EM adamsdi@mail.nih.gov
RI Adams, Diane/E-7831-2015
OI Adams, Diane/0000-0001-6638-5781
FU Woods Hole Oceanographic Institution Deep Ocean Exploration Institute;
S. Beaulieu, National Science Foundation [OCE-0424953]; National Defense
Science and Engineering Graduate
FX Funding was provided by a Woods Hole Oceanographic Institution Deep
Ocean Exploration Institute grant to L. M. and S. Beaulieu, National
Science Foundation grant OCE-0424953 to L. M., and a National Defense
Science and Engineering Graduate fellowship to D. A.
NR 38
TC 23
Z9 23
U1 2
U2 12
PU AMER SOC LIMNOLOGY OCEANOGRAPHY
PI WACO
PA 5400 BOSQUE BLVD, STE 680, WACO, TX 76710-4446 USA
SN 0024-3590
J9 LIMNOL OCEANOGR
JI Limnol. Oceanogr.
PD SEP
PY 2008
VL 53
IS 5
BP 1945
EP 1955
DI 10.4319/lo.2008.53.5.1945
PG 11
WC Limnology; Oceanography
SC Marine & Freshwater Biology; Oceanography
GA 350MG
UT WOS:000259356000021
ER
PT J
AU Campsen, J
Blei, AT
Emond, JC
Everhart, JE
Freise, CE
Lok, AS
Saab, S
Wisniewski, KA
Trotter, JF
AF Campsen, Jeffrey
Blei, Andres T.
Emond, Jean C.
Everhart, James E.
Freise, Chris E.
Lok, Anna S.
Saab, Sammy
Wisniewski, Karen A.
Trotter, James F.
CA Adult-to-Adult Living Donor Liver
TI Outcomes of living donor liver transplantation for acute liver failure:
The adult-to-adult living donor liver transplantation cohort study
SO LIVER TRANSPLANTATION
LA English
DT Article
ID FULMINANT HEPATIC-FAILURE; UNITED-STATES
AB For acute liver failure (ALF), living donor liver transplantation (LDLT) may reduce waiting time and provide better timing compared to deceased donor liver transplantation (DDLT). However, there are concerns that a partial graft would result in reduced survival of critically ill LDLT recipients and that the rapid evolution of ALF would lead to selection of inappropriate donors. We report outcomes for ALF patients (and their donors) evaluated for LDLT between 1998 and April 2007 from the Adult-to-Adult Living Donor Liver Transplantation Cohort. Of the 1201 potential LDLT recipients, 14 had ALF, only 6 of whom had an identified cause. The median time from listing to first donor evaluation was 1.5 days, and the median time from evaluation to transplantation was 1 day. One patient recovered without liver transplant, 3 of 10 LDLT recipients died, and 1 of 3 DDLT recipients died. Five of the 10 living donors had a total of 7 posttransplant complications. In conclusion, LDLT is rarely performed for ALF, but in selected patients it may be associated with acceptable recipient mortality and donor morbidity.
C1 [Campsen, Jeffrey; Trotter, James F.] Univ Colorado, Div Transplant Surg, Aurora, CO USA.
[Blei, Andres T.] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
[Emond, Jean C.] Columbia Presbyterian Med Ctr, Dept Surg, New York, NY 10032 USA.
[Everhart, James E.] NIDDK, NIH, Bethesda, MD USA.
[Freise, Chris E.] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94143 USA.
[Lok, Anna S.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Saab, Sammy] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Saab, Sammy] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA.
[Wisniewski, Karen A.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
RP Trotter, JF (reprint author), Univ Colorado Hosp, 1635 N Ursula,Campus Box 154, Aurora, CO 80262 USA.
EM james.trotter@uchsc.edu
RI Lok, Anna /B-8292-2009;
OI Yang, Shuman/0000-0002-9638-0890
FU National Institutes of Health [U01-DK62536, U01-DK62444, U01-DK62467,
U01-DK62483, U01-DK62484, U01-DK62494, U01-DK62496, U01-DK62498,
U01-DK62505, U01-DK62531]; American Society of Transplant Surgeons;
Health Resources and Services Administration; U.S. Department of Health
and Human Services
FX This study was supported in part by the National Institutes of Health
(National Institute of Diabetes and Digestive and Kidney Diseases grant
numbers U01-DK62536, U01-DK62444. U01-DK62467. U01-DK62483, U01-DK62484.
U01-DK62494, U01-DK62496, U01-DK62498. U01-DK62505. and U01-DK62531),
the American Society of Transplant Surgeons, and the Health Resources
and Services Administration. U.S. Department of Health and Human
Services.
NR 20
TC 40
Z9 41
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1527-6465
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD SEP
PY 2008
VL 14
IS 9
BP 1273
EP 1280
DI 10.1002/lt.21500
PG 8
WC Gastroenterology & Hepatology; Surgery; Transplantation
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA 346NY
UT WOS:000259076700009
PM 18756453
ER
PT J
AU Shen, M
Chapman, RS
He, XZ
Liu, LZ
Lai, H
Chen, W
Lan, Q
AF Shen, Min
Chapman, Robert S.
He, Xingzhou
Liu, Larry Z.
Lai, Hong
Chen, Wei
Lan, Qing
TI Dietary factors, food contamination and lung cancer risk in Xuanwei,
China
SO LUNG CANCER
LA English
DT Article
DE risk factor; lung cancer; indoor air pollution; case-control study; food
contamination; polycyclic aromatic hydrocarbon
ID POLYCYCLIC AROMATIC-HYDROCARBONS; DNA ADDUCT FORMATION; COAL-TAR;
BIOREMEDIATION; METABOLISM
AB Background: In rural. Xuanwei County, China, the high incidence of Lung cancer is attributable largely to burning smoky coal indoors for heating and cooking without adequate ventilation. Such burning generates very high levels of indoor air pollutants, including carcinogenic polycyclic aromatic hydrocarbons, which could contaminate foodstuffs in the home. Thus, residents could be exposed to carcinogenic coat emissions not only via inhalation but also via ingestion of these foodstuffs. Methods: A population-based case-control. study of 498 Lung cancer patients and 498 controls was conducted from 1985 through 1990 in Xuanwei. The interviewer-administered study questionnaire queried the frequency of food items commonly consumed in this region. Overall and sex-specific multiple logistic regression models were constructed to estimate Odds ratios (OR) and 95% confidence intervals (CI) for consumption of these foods. Results: Intake of rice, green vegetables, mushrooms and fresh meat was associated with an increased risk of lung cancer. In contrast, intake of corn, buckwheat, radishes, peppers, melons, pickled vegetables, and salt-preserved meats was associated with reduced risk. The detrimental. effect of ingesting green vegetables (OR, 2.39; 95% CI, 1.28-4.48) is consistent with previous reports. Conclusions: These findings suggest that in Xuanwei, food contamination by environmental polycyclic aromatic hydrocarbons may be an important risk factor for Lung cancer, and that differential contamination of foods by polycyclic aromatic hydrocarbons possibly explained the different associations with lung cancer risk. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Shen, Min] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Chapman, Robert S.] Chulalongkorn Univ, Coll Publ Hlth, Bangkok, Thailand.
[He, Xingzhou] Chinese Ctr Dis Control & Prevent, Inst Environm Hlth & Engn, Beijing, Peoples R China.
[Liu, Larry Z.] Cornell Univ, Weill Med Coll, Dept Publ Hlth, New York, NY 10021 USA.
[Lai, Hong] Johns Hopkins Univ, Wilmer Eye Inst, Baltimore, MD 21218 USA.
[Chen, Wei] Forest Labs Inc, Harborside Financial Ctr, Jersey City, NJ USA.
RP Shen, M (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, 6120 Execut Blvd,EPS 8122,MSC 7240, Bethesda, MD 20892 USA.
EM shenmi@mail.nih.gov
NR 18
TC 15
Z9 17
U1 2
U2 9
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0169-5002
J9 LUNG CANCER
JI Lung Cancer
PD SEP
PY 2008
VL 61
IS 3
BP 275
EP 282
DI 10.1016/j.lungcan.2007.12.024
PG 8
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 356TN
UT WOS:000259800600001
PM 18304686
ER
PT J
AU Hagberg, GE
Bianciardi, M
Brainovich, V
Cassara, AM
Maraviglia, B
AF Hagberg, Gisela E.
Bianciardi, Marta
Brainovich, Valentina
Cassara, Antonino Mario
Maraviglia, Bruno
TI The effect of physiological noise in phase functional magnetic resonance
imaging: from blood oxygen level-dependent effects to direct detection
of neuronal currents
SO MAGNETIC RESONANCE IMAGING
LA English
DT Article; Proceedings Paper
CT International School on Magnetic Resonance and Brain Function
CY MAY 06-13, 2007
CL Erice, ITALY
DE fMRI; phase; physiological noise; BOLD; nc-MRI; human; brain
ID INDUCED B-0 FLUCTUATIONS; ECHO-PLANAR; HUMAN BRAIN; MRI DETECTION; 1.5
T; FMRI; BOLD; RESPIRATION; COMPLEX; SIGNAL
AB Recently, the possibility to use both magnitude and phase image sets for the statistical evaluation of fMRI has been proposed, with the prospective of increasing both statistical power and the spatial specificity. In the present work, several issues that affect the spatial and temporal stability in fMRI phase time series in the presence of physiologic noise processes are reviewed, discussed and illustrated by experiments performed at 3 T. The observed phase value is a fingerprint of the underlying voxel averaged magnetic field variations. Those related to physiological processes can be considered static or dynamic in relation to the temporal scale of a 2D acquisition and will play out on different spatial scales as well: globally across the entire images slice, and locally depending on the constituents and their relative fractions inside the MRI voxel. The 'static' respiration-induced effects lead to magneto-mechanic scan-to-scan variations in the global magnetic field but may also contribute to local BOLD fluctuations due to respiration-related variations in arterial carbon dioxide. Likewise, the 'dynamic' cardiac-related effects will lead to global susceptibility effects caused by pulsatile motion of the brain as well as local blood pressure-related changes in BOLD and changes in blood flow velocity. Finally, subject motion may lead to variations in both local and global tissue susceptibility that will be especially pronounced close to air cavities. Since dissimilar manifestations of physiological processes can be expected in phase and in magnitude images, a direct relationship between phase and magnitude scan-to-scan fluctuations cannot be assumed a priori. Therefore three different models were defined for the phase stability, each dependent on the relation between phase and magnitude variations and the best will depend on the underlying noise processes. By experiments on healthy volunteers at rest, we showed that phase stability depends on the type of post-processing and can be improved by reducing the low-frequency respiration-induced mechano-magnetic effects. Although the manifestations of physiological noise were in general more pronounced in phase than in magnitude images, due to phase wraps and global Bo effects, we Suggest that a phase stability similar to that found in magnitude could theoretically be achieved by adequate correction methods. Moreover, as suggested by out-experimental data regarding BOLD-related phase effects, phase stability could even supersede magnitude stability in voxels covering dense microvascular networks with BOLD-related fluctuations as the dominant noise contributor. In the interest of the quality of both BOLD-based and nc-MRI methods, future studies are required to find alternative methods that can improve phase stability, designed to match the temporal and spatial scale of the underlying neuronal activity. (c) 2008 Elsevier Inc. All rights reserved.
C1 [Hagberg, Gisela E.; Bianciardi, Marta; Brainovich, Valentina] Fdn Santa Lucia IRCCS, Lab Neuroimaging, I-00179 Rome, Italy.
[Cassara, Antonino Mario; Maraviglia, Bruno] Univ Roma La Sapienza, Dept Phys, I-00185 Rome, Italy.
[Cassara, Antonino Mario; Maraviglia, Bruno] Museo Storico Fis, I-00184 Rome, Italy.
[Cassara, Antonino Mario; Maraviglia, Bruno] Ctr Studi & Ric, I-00184 Rome, Italy.
[Bianciardi, Marta] NINDS, Adv MRI Sect, NIH, Bethesda, MD 20892 USA.
RP Hagberg, GE (reprint author), Fdn Santa Lucia IRCCS, Lab Neuroimaging, I-00179 Rome, Italy.
EM g.hagberg@hsantalucia.it
RI Hagberg, Gisela/A-2134-2010;
OI Hagberg, Gisela/0000-0003-2176-7086; Cassara, Antonino
Mario/0000-0003-3375-7440; Maraviglia, Bruno/0000-0003-2354-8039
NR 39
TC 20
Z9 20
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0730-725X
J9 MAGN RESON IMAGING
JI Magn. Reson. Imaging
PD SEP
PY 2008
VL 26
IS 7
BP 1026
EP 1040
DI 10.1016/j.mri.2008.01.010
PG 15
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 342TN
UT WOS:000258806500022
PM 18479875
ER
PT J
AU Goelman, G
Pelled, G
Dodd, S
Koretsky, A
AF Goelman, Gadi
Pelled, Galit
Dodd, Steve
Koretsky, Alan
TI Tracking the effects of crusher gradients on gradient-echo BOLD signal
in space and time during rat sensory stimulation
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE spatiotemporal dynamic; BOLD signal; somatosensory stimulation; rat;
extravascular/intravascular weighting; CBV versus CBF
ID RADIAL CORRELATION CONTRAST; CEREBRAL BLOOD-VOLUME; FUNCTIONAL MRI;
WEIGHTED FMRI; IN-VIVO; SOMATOSENSORY CORTEX; SPATIAL LOCALIZATION;
COLUMNAR RESOLUTION; NEURONAL-ACTIVITY; BRAIN ACTIVATION
AB A unique method to map the effect of crusher gradients in space and time on the gradient echo blood oxygen level dependent (BOLD) signal is introduced. Using the Radial Correlation Contrast (RCC) analysis method, amplitude-RCC maps at different time segments and different gradient strengths were obtained. The ratio of amplitude-RCC cluster volumes, with and without crusher gradients, showed a temporal dependency with stronger volume reduction for stimulation-onset versus stimulation-decline. Aside from signal-to-noise ratio reduction in diffusion weighted images, the average temporal patterns were equal. Comparison of the data with and without crushers showed a stronger reduction in local coherence for stimulationon-set times. We hypothesize that the stimulation decline was weighted by extravascular effects originating in expanded veins due to their larger volume and long range susceptibility which couples neighboring voxels. The ratio of amplitude-RCC with and without crushers calculated for each voxel at each time segment yielded a spatial-temporal mapping of the crusher effect. These maps suggest that early stimulation-onset (similar to 9 s) is weighted by flow; later a dynamic steady-state between intra- and extravascular effects is obtained. Stimulation-decline was dominated by extravascular effects, and at late stimulation decline as well as at early stimulation onset, clusters were small and localized to expected site of neuronal activity.
C1 [Goelman, Gadi] Hadassah Hebrew Univ, Med Ctr, Dept Med Biophys & Nucl Med, IMRI MRS Lab,Human Biol Res Ctr, IL-91120 Jerusalem, Israel.
[Pelled, Galit; Dodd, Steve; Koretsky, Alan] NINDS, Lab Funct & Mol Imaging, Bethesda, MD 20892 USA.
RP Goelman, G (reprint author), Hadassah Hebrew Univ, Med Ctr, Dept Med Biophys & Nucl Med, IMRI MRS Lab,Human Biol Res Ctr, POB 1200, IL-91120 Jerusalem, Israel.
EM gadig@hadassah.org.il
RI Koretsky, Alan/C-7940-2015
OI Koretsky, Alan/0000-0002-8085-4756
FU Israel Science Foundation [184/05]
FX Grant sponsor: the Israel Science Foundation; Grant number: 184/05.
NR 34
TC 2
Z9 2
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD SEP
PY 2008
VL 60
IS 3
BP 548
EP 554
DI 10.1002/mrm.21666
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 346FL
UT WOS:000259053900007
PM 18727038
ER
PT J
AU Bennett, KM
Zhou, H
Sumner, JP
Dodd, SJ
Bouraoud, N
Doi, K
Star, RA
Koretsky, AP
AF Bennett, Kevin M.
Zhou, Hua
Sumner, James P.
Dodd, Stephen J.
Bouraoud, Nadia
Doi, Kent
Star, Robert A.
Koretsky, Alan P.
TI MRI of the basement membrane using charged nanoparticles as contrast
agents
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE basement membrane; cationic contrast agents; nanoparticles; kidney
ID NEPHROGENIC SYSTEMIC FIBROSIS; CELL-SURFACE CHARGE; ANIONIC SITES;
ENHANCED MRI; AMINONUCLEOSIDE NEPHROSIS; PREFERENTIAL DISTRIBUTION;
CAPILLARY ENDOTHELIUM; CATIONIZED FERRITIN; LUMINAL SURFACE;
KIDNEY-FUNCTION
AB The integrity of the basement membrane is essential for tissue cellular growth and is often altered in disease. In this work a method for noninvasively detecting the structural integrity of the basement membrane, based on the delivery of cationic iron-oxide nanoparticles, was developed. Cationic particles accumulate due to the highly negative charge of proteoglycans in the basement membrane. The kidney was used to test this technique because of its highly fenestrated endothelia and well-established disease models to manipulate the basement membrane charge barrier. After systemic injection of cationic or native ferritin (CF or NF) in rats, ex vivo and in vivo MRI showed selective accumulation of CF, but not NF, causing a 60% reduction in signal intensity in cortex at the location of individual glomeruli. Immunofluorescence and electron microscopy demonstrated that this CF accumulation was localized to the glomerular basement membrane (GBM). In a model of GBM breakdown during focal and segmental glomerulosclerosis, MRI showed reduced single glomerular accumulation of CIF, but a diffuse accumulation of CIF in the kidney tubules caused by leakage of CIF through the glomerulus. Cationic contrast agents can be used to target the basement membrane and detect the breakdown of the basement membrane in disease.
C1 [Bennett, Kevin M.; Sumner, James P.; Dodd, Stephen J.; Bouraoud, Nadia; Koretsky, Alan P.] NINDS, Natl Inst Hlth, Lab Funct & Mol Imaging, Bethesda, MD 20892 USA.
[Zhou, Hua; Doi, Kent; Star, Robert A.] NINDS, Natl Inst Hlth, Renal Diagnost & Therapeut Unit, Bethesda, MD 20892 USA.
RP Bennett, KM (reprint author), Arizona State Univ, Dept Bioengn, 501 E Tyler,ECG Bldg,Room 334, Tempe, AZ 85286 USA.
EM kevin.m.bennett@asu.edu
RI Koretsky, Alan/C-7940-2015
OI Koretsky, Alan/0000-0002-8085-4756
FU Intramural Research Programs of the NIH/NINDS; NIDDK
FX Grant sponsor: Intramural Research Programs of the NIH/NINDS and NIDDK.
NR 46
TC 36
Z9 36
U1 0
U2 3
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD SEP
PY 2008
VL 60
IS 3
BP 564
EP 574
DI 10.1002/mrm.21684
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 346FL
UT WOS:000259053900009
PM 18727041
ER
PT J
AU Dahnke, H
Liu, W
Herzka, D
Frank, JA
Schaeffter, T
AF Dahnke, Hannes
Liu, Wei
Herzka, Daniel
Frank, Joseph A.
Schaeffter, Tobias
TI Susceptibility gradient mapping (SGM): A new postprocessing method for
positive contrast generation applied to superparamagnetic iron oxide
particle (SPIO)-labeled cells
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE susceptibility; positive contrast; SPIO; labeled cells
ID ATHEROSCLEROTIC PLAQUE; LYMPH-NODES; MRI; AGENT; CATHETERS; TRACKING;
SYSTEM
AB Local susceptibility gradients result in a dephasing of the precessing magnetic moments and thus in a fast decay of the NMR signals. In particular, cells labeled with superparamagnetic iron oxide particles (SPIOs) induce hypointensities, making the in vivo detection of labeled cells from such a negative image contrast difficult. In this work, a new method is proposed to selectively turn this negative contrast into a positive contrast. The proposed method calculates the susceptibility gradient and visualizes it in a parametric map directly from a regular gradient-echo image dataset. The susceptibility gradient map is determined in a postprocessing step, requiring no dedicated pulse sequences or adaptation of the sequence before and during image acquisition. Phantom experiments demonstrated that local susceptibility differences can be quantified. In vivo experiments showed the feasibility of the method for tracking of SPIO-labeled cells. The method bears the potential also for usage in other applications, including the detection of contrast agents and interventional devices as well as metal implants.
C1 [Dahnke, Hannes] Philips Res Europe, Sector Med Imaging Syst, D-22335 Hamburg, Germany.
[Liu, Wei; Herzka, Daniel] Philips Res N Amer, Briarcliff Manor, NY USA.
[Frank, Joseph A.] Natl Inst Hlth, Bethesda, MD USA.
[Schaeffter, Tobias] Kings Coll London, Div Imaging Sci, London WC2R 2LS, England.
RP Dahnke, H (reprint author), Philips Res Europe, Sector Med Imaging Syst, Roentgenstr 24-26, D-22335 Hamburg, Germany.
EM hannes.dahnke@philips.com
OI Herzka, Daniel/0000-0002-9400-7814; Schaeffter,
Tobias/0000-0003-1310-2631
FU Intramural Program of the Clinical Center; German BMBF [13N8896]
FX Grant sponsor: Intramural Program of the Clinical Center at the NIH;
Grant sponsor: German BMBF; Grant number: 13N8896.
NR 27
TC 75
Z9 75
U1 1
U2 13
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD SEP
PY 2008
VL 60
IS 3
BP 595
EP 603
DI 10.1002/mrm.21478
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 346FL
UT WOS:000259053900013
PM 18727097
ER
PT J
AU Watkins, SM
Reich, A
Fleming, LE
Hammond, R
AF Watkins, Sharon M.
Reich, Andrew
Fleming, Lora E.
Hammond, Roberta
TI Neurotoxic shellfish poisoning
SO MARINE DRUGS
LA English
DT Review
DE neurotoxic shellfish Poisoning; NSP; brevetoxins; harmful algal blooms
(HABs); Karenia brevis; epidemiology; human health; red tide
ID FLORIDA RED TIDE; OYSTER CRASSOSTREA-VIRGINICA; HARMFUL ALGAL BLOOMS;
KARENIA-BREVIS; NEW-ZEALAND; BREVETOXIN METABOLISM; GYMNODINIUM-BREVE;
AEROSOLIZED BREVETOXINS; AUSTROVENUS-STUTCHBURYI; DINOFLAGELLATE TOXINS
AB Neurotoxic shellfish poisoning (NSP) is caused by consumption of molluscan shellfish contaminated with brevetoxins primarily produced by the dinoflagellate, Karenia brevis. Blooms of K. brevis, called Florida red tide, occur frequently along the Gulf of Mexico. Many shellfish beds in the US (and other nations) are routinely monitored for presence of K. brevis and other brevetoxin-producing organisms. As a result, few NSP cases are reported annually from the US. However, infrequent larger outbreaks do occur. Cases are usually associated with recreationally-harvested shellfish collected during or post red tide blooms. Brevetoxins are neurotoxins which activate voltage-sensitive sodium channels causing sodium influx and nerve membrane depolarization. No fatalities have been reported, but hospitalizations occur. NSP involves a cluster of gastrointestinal and neurological symptoms: nausea and vomiting, paresthesias of the mouth, lips and tongue as well as distal paresthesias, ataxia, slurred speech and dizziness. Neurological symptoms can progress to partial paralysis; respiratory distress has been recorded. Recent research has implicated new species of harmful algal bloom organisms which produce brevetoxins, identified additional marine species which accumulate brevetoxins, and has provided additional information on the toxicity and analysis of brevetoxins. A review of the known epidemiology and recommendations for improved NSP prevention are presented.
C1 [Watkins, Sharon M.; Reich, Andrew] Florida Dept Hlth, Div Environm Hlth, Aquat Toxins Program, Tallahassee, FL 32399 USA.
[Fleming, Lora E.] Univ Miami, NSF, NIEHS, Oceans & Human Hlth Ctr,Rosenstiel Sch Marine & A, Miami, FL 33136 USA.
[Hammond, Roberta] Florida Dept Hlth, Div Environm Hlth, Food & Waterborne Dis Program, Tallahassee, FL 32399 USA.
RP Watkins, SM (reprint author), Florida Dept Hlth, Div Environm Hlth, Aquat Toxins Program, Tallahassee, FL 32399 USA.
EM Sharon_Watkins@doh.state.fl.us
FU the Florida Department of Health; the Centers for Disease Control and
Prevention (CDC); National Science Foundation; National Institute of
Environmental Health Sciences Oceans and Human Health Center at the
University of Miami Rosenstiel School [NSF 0CE0432368, NIEHS 1 P50
ES12736]; National Institute of Environmental Health Sciences Red Tide
POI [P01 ES 10594]
FX The funding for this study was provided by the Florida Department of
Health and the Centers for Disease Control and Prevention (CDC), as well
as the National Science Foundation and National Institute of
Environmental Health Sciences Oceans and Human Health Center at the
University of Miami Rosenstiel School (NSF 0CE0432368; NIEHS 1 P50
ES12736) and the National Institute of Environmental Health Sciences Red
Tide POI (P01 ES 10594).
NR 136
TC 77
Z9 79
U1 10
U2 40
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1660-3397
J9 MAR DRUGS
JI Mar. Drugs
PD SEP
PY 2008
VL 6
IS 3
BP 431
EP 455
DI 10.3390/md20080021
PG 25
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 354RO
UT WOS:000259656900003
PM 19005578
ER
PT J
AU Friedman, MA
Fleming, LE
Fernandez, M
Bienfang, P
Schrank, K
Dickey, R
Bottein, MY
Backer, L
Ayyar, R
Weisman, R
Watkins, S
Granade, R
Reich, A
AF Friedman, Melissa A.
Fleming, Lora E.
Fernandez, Mercedes
Bienfang, Paul
Schrank, Kathleen
Dickey, Robert
Bottein, Marie-Yasmine
Backer, Lorraine
Ayyar, Ram
Weisman, Richard
Watkins, Sharon
Granade, Ray
Reich, Andrew
TI Ciguatera fish poisoning: Treatment, prevention and management
SO MARINE DRUGS
LA English
DT Review
DE ciguatera fish poisoning; ciguatoxin; harmful algal bloom (HAB);
treatment human health; marine toxins
ID COMMON-SOURCE OUTBREAK; STATES VIRGIN-ISLANDS; INDIAN-OCEAN; SYMPTOMATIC
IMPROVEMENT; CARIBBEAN CIGUATOXINS; PACIFIC CIGUATOXIN-1;
CLINICAL-FEATURES; BREVETOXINS; TOXINS; DISEASE
AB Ciguatera Fish Poisoning (CFP) is the most frequently reported seafood-toxin illness in the world, and it causes substantial physical and functional impact. It produces a myriad of gastrointestinal, neurologic and/or cardiovascular symptoms which last days to weeks, or even months. Although there are reports of symptom amelioration with some interventions ( e. g. IV mannitol), the appropriate treatment for CFP remains unclear to many physicians. We review the literature on the treatments for CFP, including randomized controlled studies and anecdotal reports. The article is intended to clarify treatment options, and provide information about management and prevention of CFP, for emergency room physicians, poison control information providers, other health care providers, and patients.
C1 [Friedman, Melissa A.] Mt Sinai Med Ctr, Miami Beach, FL 33140 USA.
[Friedman, Melissa A.; Fleming, Lora E.] NIEHS, NSF, Oceans & Human Hlth Ctr, Rosenstiel Sch Marine & Atmospher Sci, Miami, FL 33136 USA.
[Fernandez, Mercedes] Carlos Albizu Univ, Miami, FL 33172 USA.
[Bienfang, Paul] Univ Hawaii, Honolulu, HI 96822 USA.
[Schrank, Kathleen] Univ Miami, Dept Med, Jackson Mem Med Ctr, Miami, FL 33136 USA.
[Dickey, Robert; Granade, Ray] US FDA, Div Seafood Sci & Technol, Ctr Food Safety & Nutr, Dauphin Isl, AL 36528 USA.
[Bottein, Marie-Yasmine] NOAA, Natl Ocean Serv, Ctr Coastal Environm Hlth & Biomol Res, Charleston, SC 29412 USA.
[Backer, Lorraine] Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Atlanta, GA 30341 USA.
[Ayyar, Ram] Univ Miami, Dept Neurol, Miami, FL 33136 USA.
[Weisman, Richard] Florida Poison Informat Ctr, Miami, FL 33136 USA.
[Watkins, Sharon; Reich, Andrew] Florida Dept Hlth, Div Environm Hlth, Aquat Toxins Program, Tallahassee, FL 32399 USA.
RP Friedman, MA (reprint author), Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, NSF, NIEHS,Oceans & Human Hlth Ctr, 4600 Rickenbacker Causeway,E Grosvenor Bldg,E211, Key Biscayne, FL 33149 USA.
EM melissafried@yahoo.com
FU National Science Foundation (NSF) [NSF 0CE0432368]; National Institute
of Environmental Health Sciences [NIEHS P50 ES12736]; Florida Dept of
Health Aquatic Toxins Program; Centers for Disease Control and
Prevention (CDC)
FX This publication was made possible through the National Science
Foundation (NSF) National Institute of Environmental Health Sciences
Center for Oceans and Human Health (COHH) program at the University of
Miami (NSF 0CE0432368; NIEHS P50 ES12736), as well as with funding from
the Florida Dept of Health Aquatic Toxins Program and the Centers for
Disease Control and Prevention (CDC).
NR 106
TC 86
Z9 91
U1 6
U2 35
PU MOLECULAR DIVERSITY PRESERVATION INT
PI BASEL
PA MATTHAEUSSTRASSE 11, CH-4057 BASEL, SWITZERLAND
SN 1660-3397
J9 MAR DRUGS
JI Mar. Drugs
PD SEP
PY 2008
VL 6
IS 3
BP 456
EP 479
DI 10.3390/md20080022
PG 24
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 354RO
UT WOS:000259656900004
PM 19005579
ER
PT J
AU Macchi, C
Molino-Lova, R
Polcaro, P
Guarducci, L
Lauretani, F
Cecchi, F
Bandinelli, S
Guralnik, JM
Ferrucci, L
AF Macchi, Claudio
Molino-Lova, Raffaele
Polcaro, Paola
Guarducci, Lorenzo
Lauretani, Fulvio
Cecchi, Francesca
Bandinelli, Stefania
Guralnik, Jack M.
Ferrucci, Luigi
TI Higher circulating levels of uric acid are prospectively associated with
better muscle function in older persons
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Article
DE uric acid; antioxidants; sarcopenia; muscle strength; elderly
ID CORONARY-HEART-DISEASE; LOWER-EXTREMITY FUNCTION; PHYSICAL PERFORMANCE;
CARDIOVASCULAR RISK; INSULIN-RESISTANCE; BLOOD-PRESSURE; GRIP STRENGTH;
MORTALITY; DISABILITY; SARCOPENIA
AB Background: Previous studies have shown that oxidative protein damage is independently associated with low grip strength and that dietary intake and circulating levels of antioxiclant vitamins are positive predictors of muscle strength among older persons. Since uric acid (LIA), has strong antioxidant properties, we tested the hypothesis that UA levels is cross-sectionaly associated with muscle strength and protective against the decline of strength over the aging process.
Subjects and methods: 789 InCHIANTI Study participants underwent baseline serum UA, handgrip and knee extension torque measurements. Of these, 497 participants (226 men and 271 women, mean age 76.0 +/- 5.4 years) also had follow-up strength measures. Lifestyle, comorbidities, nutritional profile, inflammatory markers and other laboratory measures were considered as potential confounders. Results: Follow-up strength measures significantly increased across baseline UA tertiles. After adjusting for potential confounders and analogous baseline strength measures, higher baseline UA levels still remained significantly associated with higher follow-up strength measures.
Conclusions: Our findings suggest that higher levels ofUA might represent a protective reaction aimed at counteracting the excessive production offree radicals that cause muscle protein damage and eventually contribute to the decline of muscle mass and strength. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Macchi, Claudio; Molino-Lova, Raffaele; Polcaro, Paola; Guarducci, Lorenzo; Cecchi, Francesca] Fdn Don C Gnocchi, I-50020 Florence, Italy.
[Lauretani, Fulvio] Tuscany Hlth Reg Agcy, Florence, Italy.
[Bandinelli, Stefania] ASF, Geriatr Rehabil Unit, Florence, Italy.
[Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Ferrucci, Luigi] NIA, Clin Res Branch, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
RP Molino-Lova, R (reprint author), Fdn Don C Gnocchi, Via Imprunetana 124, I-50020 Florence, Italy.
EM rmolino@dongnocchi.it
RI Lauretani, Fulvio/K-5115-2016;
OI Lauretani, Fulvio/0000-0002-5287-9972; Cecchi,
Franco/0000-0002-2035-5621
FU Intramural NIH HHS [Z99 HD999999]; NIA NIH HHS [N01 AG050002, N01
AG821336, N01 AG916413, N01-AG-821336, Z01 AG000971-01]; NIMHD NIH HHS
[263 MD821336, 263 MD9164 13, R01 MD009164]
NR 48
TC 14
Z9 15
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing Dev.
PD SEP
PY 2008
VL 129
IS 9
BP 522
EP 527
DI 10.1016/j.mad.2008.04.008
PG 6
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 334QT
UT WOS:000258237000003
PM 18534661
ER
PT J
AU Shamir, L
Orlov, N
Eckley, DM
Macura, TJ
Goldberg, IG
AF Shamir, Lior
Orlov, Nikita
Eckley, David Mark
Macura, Tomasz J.
Goldberg, Ilya G.
TI IICBU 2008: a proposed benchmark suite for biological image analysis
SO MEDICAL & BIOLOGICAL ENGINEERING & COMPUTING
LA English
DT Article
DE biological imaging; image analysis; image datasets; benchmarks
ID SUBCELLULAR STRUCTURES; ELECTRON-MICROSCOPY; DATABASE; PATTERNS
AB New technology for automated biological image acquisition has introduced the need for effective biological image analysis methods. These algorithms are constantly being developed by pattern recognition and machine vision experts, who tailor general computer vision techniques to the specific needs of biological imaging. However, computer scientists do not always have access to biological image datasets that can be used for computer vision research, and biologist collaborators who can assist in defining the biological questions are not always available. Here, we propose a publicly available benchmark suite of biological image datasets that can be used by machine vision experts for developing and evaluating biological image analysis methods. The suite represents a set of practical real-life imaging problems in biology, and offers examples of organelles, cells and tissues, imaged at different magnifications and different contrast techniques. All datasets are available for free download at http://ome.grc.nia.nih.gov/iicbu2008.
C1 [Shamir, Lior; Orlov, Nikita; Eckley, David Mark; Macura, Tomasz J.; Goldberg, Ilya G.] NIA, Genet Lab, Image Informat & Computat Biol Unit, NIH, Baltimore, MD 21224 USA.
[Macura, Tomasz J.] Univ Cambridge, Comp Lab, Cambridge CB2 3QG, England.
RP Shamir, L (reprint author), NIA, Genet Lab, Image Informat & Computat Biol Unit, NIH, 333 Cassell Dr, Baltimore, MD 21224 USA.
EM shamirl@mail.nih.gov
RI Goldberg, Ilya/H-5307-2011;
OI Goldberg, Ilya/0000-0001-8514-6110; Eckley, D. Mark/0000-0003-2296-5164
FU NIH; National Institute on Aging
FX This research was supported by the Intramural Research Program of the
NIH, National Institute on Aging. The datasets Hela and CHO are from
Murphy lab, CMU. The dataset Pollen was contributed by Andrew Duller,
Henry Lamb and Ian France, and the dataset Binucleate was provided by
Aaron Straight, Stanford U. We would also like to thank Cathy Wolkow and
Wendy Iser for their assistance with the acquisition and definition of
the Terminal Bulb Aging and C. elegans Muscle Aging datasets, and Elaine
Jaffe for providing the data for the Lymphoma dataset.
NR 8
TC 42
Z9 42
U1 0
U2 0
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0140-0118
J9 MED BIOL ENG COMPUT
JI Med. Biol. Eng. Comput.
PD SEP
PY 2008
VL 46
IS 9
BP 943
EP 947
DI 10.1007/s11517-008-0380-5
PG 5
WC Computer Science, Interdisciplinary Applications; Engineering,
Biomedical; Mathematical & Computational Biology; Medical Informatics
SC Computer Science; Engineering; Mathematical & Computational Biology;
Medical Informatics
GA 343GY
UT WOS:000258842700012
PM 18668273
ER
PT J
AU Carney, PA
Hoffman, RM
Lieberman, DA
Hornbrook, MC
Dietrich, AJ
Klabunde, CN
AF Carney, Patricia A.
Hoffman, Richard M.
Lieberman, David A.
Hornbrook, Mark C.
Dietrich, Allen J.
Klabunde, Carrie N.
TI Data systems to evaluate colorectal cancer screening practices and
outcomes at the population level
SO MEDICAL CARE
LA English
DT Editorial Material
ID NATIONAL ENDOSCOPIC DATABASE; UNITED-STATES; MAMMOGRAPHY; PERFORMANCE;
COLONOSCOPY; CONSORTIUM; SURVEILLANCE; GUIDELINES; RATIONALE; SETTINGS
C1 [Carney, Patricia A.] Oregon Hlth & Sci Univ, Dept Family Med, Portland, OR 97239 USA.
[Carney, Patricia A.] Oregon Hlth & Sci Univ, Dept Publ Hlth & Prevent Med, Portland, OR 97239 USA.
[Lieberman, David A.] Oregon Hlth & Sci Univ, Div Gastroenterol, Dept Med, Portland, OR 97239 USA.
[Hoffman, Richard M.] Univ New Mexico, Hlth Sci Ctr, New Mexico Vet Adm Hlth Care Syst, Albuquerque, NM 87131 USA.
[Hornbrook, Mark C.] Kaiser Permanente NW, Ctr Hlth Res, Portland, OR USA.
[Dietrich, Allen J.] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dept Community & Family Med, Hanover, NH 03756 USA.
[Klabunde, Carrie N.] NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Carney, PA (reprint author), Oregon Hlth & Sci Univ, Dept Family Med, 3181 Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM carneyp@ohsu.edu
NR 25
TC 4
Z9 4
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD SEP
PY 2008
VL 46
IS 9
SU 1
BP S132
EP S137
DI 10.1097/MLR.0b013e31817f7355
PG 6
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 344RR
UT WOS:000258945500019
PM 18725825
ER
PT J
AU Klabunde, CN
Lanier, D
Meissner, HI
Breslau, ES
Brown, ML
AF Klabunde, Carrie N.
Lanier, David
Meissner, Helen I.
Breslau, Erica S.
Brown, Martin L.
TI Improving colorectal cancer screening through research in primary care
settings - Introduction
SO MEDICAL CARE
LA English
DT Editorial Material
ID PREVENTIVE SERVICES; UNITED-STATES; GUIDELINES; FUTURE; RATIONALE;
DELIVERY; MEDICINE
C1 [Klabunde, Carrie N.; Brown, Martin L.] NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Lanier, David] Agcy Healthcare Res & Qual, Ctr Primary Care Prevent & Clin Partnerships, Rockville, MD USA.
[Meissner, Helen I.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Breslau, Erica S.] NCI, Div Canc Control & Populat Sci, Behav Res Program, Appl Canc Screening Res Branch, Bethesda, MD 20892 USA.
RP Klabunde, CN (reprint author), NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Execut Plaza N Room 4005,6130 Execut Blvd, Bethesda, MD 20892 USA.
EM klabundc@mail.nih.gov
NR 50
TC 11
Z9 11
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD SEP
PY 2008
VL 46
IS 9
SU 1
BP S1
EP S4
DI 10.1097/MLR.0b013e3181805e2a
PG 4
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 344RR
UT WOS:000258945500001
PM 18725819
ER
PT J
AU Miglioretti, DL
Rutter, CM
Bradford, SC
Zauber, AG
Kessler, LG
Feuer, EJ
Grossman, DC
AF Miglioretti, Diana L.
Mutter, Carolyn M.
Bradford, Susan Carol
Zauber, Ann G.
Kessler, Larry G.
Feuer, Eric J.
Grossman, David C.
TI Improvement in the Diagnostic Evaluation of a Positive Fecal Occult
Blood Test in an Integrated Health Care Organization
SO MEDICAL CARE
LA English
DT Article
DE fecal occult blood test; colorectal cancer screening; diagnostic
follow-up
ID IMPROVING PRIMARY-CARE; COLORECTAL-CANCER; FOLLOW-UP; CLINICAL
GUIDELINES; CHRONIC ILLNESS; UNITED-STATES; PREVENTION; RATIONALE;
MORTALITY; TRIAL
AB Background: Screening for fecal occult blood can be effective in reducing colorectal cancer mortality only if positive tests are appropriately followed up with complete diagnostic evaluation (ie, colonoscopy or flexible sigmoidoscopy with double contrast barium enema) and treatment.
Objectives: To examine whether rates of complete diagnostic evaluation after a positive fecal occult blood test (FOBT) have improved over time after the implementation of tracking systems and physician guidelines within a large integrated health care organization.
Research Design: From 1993 to 2005, 8513 positive FOBTs were identified on 8291 enrollees aged 50-79 of a large health care system. Automated records were used to identify repeat FOBTs, colonoscopy, flexible sigmoidoscopy, and double-contrast barium enema within 1 year after the positive FOBT. National rates of complete diagnostic evaluation were estimated from the 2005 National Health Interview Survey.
Results: In this integrated health care organization, the percentage of positive FOBTs followed by complete diagnostic evaluation within 1 year increased from 57-64% in 1993-1996 to 82-86% from 2000-2005. Use of repeat FOBT after a positive FOBT decreased from 28-31% in 1993-1996 to 6-11% in 2000-2005. Based on the National Health Interview Survey, only 52% of positive FOBTs in 2000-2005 were followed by omplete diagnostic evaluation nationally.
Conclusions: Adherence to recommendations for complete diagnostic evaluation after a positive FOBT has greatly improved over time in an integrated group medical practice. Through the use of tracking systems and screening guidelines, it may be possible to reach levels of follow-up that are comparable to those observed in randomized trials.
C1 [Miglioretti, Diana L.; Mutter, Carolyn M.; Grossman, David C.] Grp Hlth Ctr Hlth Studies, Seattle, WA 98101 USA.
[Bradford, Susan Carol; Grossman, David C.] Grp Hlth Cooperat Puget Sound, Dept Clin Improvement & Prevent, Seattle, WA USA.
[Zauber, Ann G.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY USA.
[Kessler, Larry G.] Ctr Devices & Radiol Hlth Food & Drug Adm, Off Sci & Engn Labs, Silver Spring, MD USA.
[Feuer, Eric J.] Natl Canc Inst, Stat Res & Applicat Branch, Div Canc Control & Populat Sci, Bethesda, MD USA.
RP Miglioretti, DL (reprint author), Grp Hlth Ctr Hlth Studies, 1730 Minor Ave,Suite 1600, Seattle, WA 98101 USA.
EM miglioretti.d@ghc.org
FU National Cancer Institute [U01 CA-97427, U01 CA-97426]
FX Supported by the National Cancer Institute grants U01 CA-97427 and U01
CA-97426.
NR 27
TC 28
Z9 28
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD SEP
PY 2008
VL 46
IS 9
SU 1
BP S91
EP S96
DI 10.1097/MLR.0b013e31817946c8
PG 6
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 344RR
UT WOS:000258945500022
PM 18725839
ER
PT J
AU Srinivasan, S
Kerner, J
AF Srinivasan, Shobha
Kerner, Jon
TI Meeting the needs of diverse populations - An overview and commentary
SO MEDICAL CARE
LA English
DT Editorial Material
ID CANCER SCREENING RATES; COLORECTAL-CANCER; UNITED-STATES;
RACIAL-DISCRIMINATION; INTERVENTION RESEARCH; SOCIOECONOMIC-STATUS;
PREVENTIVE CARE; HEALTH-CARE; DISPARITIES; BARRIERS
C1 [Srinivasan, Shobha; Kerner, Jon] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Srinivasan, S (reprint author), NCI, Div Canc Control & Populat Sci, 6130 Execut Blvd,EPN 6126, Bethesda, MD 20892 USA.
EM ss688k@nih.gov
NR 52
TC 2
Z9 2
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD SEP
PY 2008
VL 46
IS 9
SU 1
BP S30
EP S35
DI 10.1097/MLR.0b013e31817f0d12
PG 6
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 344RR
UT WOS:000258945500006
PM 18725830
ER
PT J
AU Taplin, SH
Haggstrom, D
Jacobs, T
Determan, A
Granger, J
Montalvo, W
Snyder, WM
Lockhart, S
Calvo, A
AF Taplin, Stephen H.
Haggstrom, David
Jacobs, Tracy
Determan, Ada
Granger, Jennifer
Montalvo, Wanda
Snyder, William M.
Lockhart, Susan
Calvo, Ahmed
TI Implementing colorectal cancer screening in community health centers -
Addressing cancer health disparities through a Regional Cancer
Collaborative
SO MEDICAL CARE
LA English
DT Article
DE colorectal cancer screening; quality improvement; health disparities
ID CHRONIC CARE MODEL; INCREASE MAMMOGRAPHY USE; IMPROVING DIABETES CARE;
SERVICES TASK-FORCE; CERVICAL-CANCER; QUALITY IMPROVEMENT; CHRONIC
ILLNESS; BREAST; INTERVENTIONS; SYSTEM
AB Background: The population served by Federally Qualified Health Centers (FQHCs) has lower levels of cancer screening compared with the general population and suffers a disproportionate cancer burden. To address these disparities, 3 federal agencies and a primary care association established and tested the feasibility of a Regional Cancer Collaborative (RCC) in 2005.
Methods: RCC faculty implemented a learning model to improve cancer screening across 4 FQHCs that met explicit organizational readiness criteria. Regional faculty trained "care process leaders," who worked with primary care teams to plan and implement practice changes. FQHCs monitored progress across the following measures of screening implementation: self-management goal-setting; number and percent screened for breast, cervical, and colorectal cancer; percent timely results notification; and percent abnormal screens evaluated within 90 days. Progress and plans were reviewed in regular teleconferences. FQHCs were encouraged to create local communities of practice (LCOP) involving community resources to support cancer screening and to participate in a monthly teleconference that linked the LCOPs into a regional community of practice. Summary reports and administrative data facilitated a process evaluation of the RCC. chi(2) test and test of trends compared baseline and follow-up screening rates.
Results: The RCC taught the collaborative process using process leader training, teleconferences, 2 regional meetings, and local process improvement efforts. All organizations created clinical tracking capabilities and 3 of the 4 established LCOPs, which met monthly in an regional community of practice. Screening documentation increased for all 3 cancers from 2005 to 2007. Colorectal cancer screening increased from 8.6% to 21.2%.
Conclusions: A regional plan to enable collaborative learning for cancer screening implementation is feasible, and improvements in screening rates can occur among carefully selected organizations.
C1 [Taplin, Stephen H.] NCI, Bethesda, MD 20892 USA.
[Haggstrom, David] Indiana Univ, Ctr Hlth Serv & Outcomes Res, Regenstrief Inst, Bloomington, IN 47405 USA.
[Haggstrom, David] Indiana Univ, Sch Med, Dept Internal Med, Div Gen Internal Med & Geriatr, Bloomington, IN 47405 USA.
[Haggstrom, David] Indiana Univ, Ctr Canc, Indianapolis, IN 46204 USA.
[Jacobs, Tracy] IHI, Cambridge, MA USA.
[Determan, Ada; Calvo, Ahmed] HRSA, Rockville, MD USA.
[Granger, Jennifer] CHCACT, Newington, CT USA.
[Montalvo, Wanda] Community Hlth Ctr Assoc New York, New York, NY USA.
[Snyder, William M.] Social Capital Grp, Cambridge, MA USA.
[Lockhart, Susan] Ctr Dis Control & Prevent CDC, Atlanta, GA USA.
RP Taplin, SH (reprint author), 6130 Execut Blvd,MSC 7344, Bethesda, MD 20892 USA.
EM taplins@mail.nih.gov
FU Inter-Agency-Agreement between HRSA; CDC
FX Supported by an Inter-Agency-Agreement between HRSA and the CDC for
support of the teams, faculty, and infrastructure; in-kind contributions
from the National Cancer Institute for the time, travel, and activity of
Dr. Taplin; from HRSA for the infrastructure of the internet based
Knowledge Management System for sharing of insights and data as well as
in kind contribution of staff time, travel, and activity of Dr Calvo and
Ada Determan; and in kind support from CDC with regards to staff time,,
travel, and activity of Dr. Susan Lockhart.
NR 43
TC 36
Z9 37
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD SEP
PY 2008
VL 46
IS 9
SU 1
BP S74
EP S83
DI 10.1097/MLR.0b013e31817fdf68
PG 10
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 344RR
UT WOS:000258945500012
PM 18725837
ER
PT J
AU Vernon, SW
Meissner, HI
AF Vernon, Sally W.
Meissner, Helen I.
TI Evaluating approaches to increase uptake of colorectal cancer screening
- Lessons learned from pilot studies in diverse primary care settings
SO MEDICAL CARE
LA English
DT Editorial Material
ID CERVICAL-CANCER; UNITED-STATES; TASK-FORCE; INTERVENTIONS; METAANALYSIS;
FUTURE; HEALTH; RISK; STRATEGIES; MEDICINE
C1 [Vernon, Sally W.] Univ Texas Houston, Sch Publ Hlth, Ctr Hlth Promot & Prevent Res, Div Hlth Promot & Behav Sci, Houston, TX 77030 USA.
[Meissner, Helen I.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
RP Vernon, SW (reprint author), Univ Texas Houston, Sch Publ Hlth, Ctr Hlth Promot & Prevent Res, Div Hlth Promot & Behav Sci, 7000 Fannin,Suite 2560, Houston, TX 77030 USA.
EM sally.w.vemon@uth.tmc.edu
NR 27
TC 7
Z9 7
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD SEP
PY 2008
VL 46
IS 9
SU 1
BP S97
EP S102
DI 10.1097/MLR.0b013e31817eb346
PG 6
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 344RR
UT WOS:000258945500014
PM 18725840
ER
PT J
AU Zauber, AG
Levin, TR
Jaffe, CC
Galen, BA
Ransohoff, DF
Brown, ML
AF Zauber, Ann G.
Levin, Theodore R.
Jaffe, C. Carl
Galen, Barbara A.
Ransohoff, David F.
Brown, Martin L.
TI Implications of new colorectal cancer screening technologies for primary
care practice
SO MEDICAL CARE
LA English
DT Editorial Material
ID FECAL-OCCULT-BLOOD; SOCIETY-TASK-FORCE; PROXIMAL COLONIC NEOPLASIA;
COLLEGE-OF-RADIOLOGY; ASYMPTOMATIC ADULTS; ADENOMATOUS POLYPS; CLINICAL
GUIDELINES; JOINT GUIDELINE; UNITED-STATES; HUMAN DNA
C1 [Zauber, Ann G.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10065 USA.
[Levin, Theodore R.] Kaiser Permanente, Med Ctr, Dept Gastroenterol, Walnut Creek, CA USA.
[Jaffe, C. Carl; Galen, Barbara A.] NCI, Canc Imaging Program, Bethesda, MD 20892 USA.
[Ransohoff, David F.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Brown, Martin L.] NCI, Div Canc Control & Populat Sci, Hlth Serv & Econ Branch, Bethesda, MD 20892 USA.
RP Zauber, AG (reprint author), Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, 307 E 63rd St, New York, NY 10065 USA.
EM zaubera@mskcc.org
FU NCI NIH HHS [U01 CA097426]
NR 70
TC 8
Z9 8
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD SEP
PY 2008
VL 46
IS 9
SU 1
BP S138
EP S146
DI 10.1097/MLR.0b013e31818192ef
PG 9
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 344RR
UT WOS:000258945500020
PM 18725826
ER
PT J
AU Yao, JH
Chen, D
AF Yao, Jianhua
Chen, David
TI Live level set: A hybrid method of livewire and level set for medical
image segmentation
SO MEDICAL PHYSICS
LA English
DT Article
DE livewire; level set; medical image segmentation
ID SHAPE; LANE
AB Livewire and level set are popular methods for medical image segmentation. In this article, the authors propose a hybrid method of livewire and level set, termed the live level set (LLS). The LLS replaces the one graph update iteration in the classic livewire with two iterations of graph updates. The first iteration generates an initial contour for a level set computation. The level set distance is then factored back into the cost function in the second iteration of graph update. The authors validated LLS using synthetic images. The results show that the performance of the LLS is superior to both the classic live wire and traditional level set methods in terms of accuracy, reproducibility, smoothness and running time. They also qualitatively evaluated the LLS using real clinical data. (C) 2008 American Association of Physicists in Medicine.
C1 [Yao, Jianhua; Chen, David] NIH, Warren Grant Magnuson Clin Ctr, Dept Diagnost Radiol, Bethesda, MD 20892 USA.
[Chen, David] Stanford Univ, Stanford, CA 94305 USA.
RP Yao, JH (reprint author), NIH, Warren Grant Magnuson Clin Ctr, Dept Diagnost Radiol, Bldg 10, Bethesda, MD 20892 USA.
EM jyao@cc.nih.gov
FU Intramural Research Program of the National Institutes of Health; Warren
G. Magnuson Clinical Center
FX The authors thank Dr. Ronald Summers for support of the project and
critical reviews of the article. This research was supported by the
Intramural Research Program of the National Institutes of Health, Warren
G. Magnuson Clinical Center.
NR 25
TC 4
Z9 5
U1 0
U2 1
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD SEP
PY 2008
VL 35
IS 9
BP 4112
EP 4120
DI 10.1118/1.2968876
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 342GQ
UT WOS:000258773000033
PM 18841864
ER
PT J
AU Steiner, AZ
Baird, DD
Kesner, JS
AF Steiner, Anne Z.
Baird, Donna D.
Kesner, James S.
TI Mother's menopausal age is associated with her daughter's early
follicular phase urinary follicle-stimulating hormone level
SO MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY
LA English
DT Article
DE follicle-stimulating hormone; menopause; maternal age at menopause
ID PREMATURE OVARIAN FAILURE; LUTEINIZING-HORMONE; REPRODUCTIVE LIFE;
WOMEN; RESERVE; PERIMENOPAUSE; VARIABILITY; POPULATION; TRANSITION;
SMOKING
AB Objective: Early follicular phase follicle-stimulating hormone (FSH), a marker of ovarian reserve, has been used to predict time to menopause. A mother's age at menopause is related to her daughter's age at menopause, possibly because of genetic factors. In this study we sought to determine the relationship between maternal age at menopause and early follicular phase FSH of premenopausal daughters.
Design: The Uterine Fibroid Study enrolled women randomly selected from a prepaid health plan, collected questionnaire data, and obtained earl), follicular phase urine samples for a Subset of participants. For this secondary analysis, premenopausal women between the ages of 35 and 46 years, who provided a urine sample on cycle day 2, 3, 4, or 5 and their mother's age at natural menopause (n = 182) were selected from the original cohort. Initially bivariate analysis and subsequently regression modeling were performed to assess the independent relationship between maternal age at menopause and urinary creatinine-corrected FSH.
Results: Unadjusted analyses and those adjusting for age (mean +/- SD, 405 +/- 3.2 y), smoking status (16% current smokers), and body mass index (26.8 +/- 6.9 kg/m(2)) showed a significant association between maternal age at menopause and daughter's urinary FSH level (P < 0.04). Women whose mothers experienced earlier menopause had higher urinary FSH levels.
Conclusions: The significantly increased FSH values among women whose mothers experienced early menopause is consistent with previously reported associations between mother's and daughter's age of menopause. FSH, a marker of ovarian reserve, is influenced by both genetic and environmental factors. Future epidemiologic studies on FSH should include collection of information on maternal age at menopause.
C1 [Steiner, Anne Z.] Univ N Carolina, Sch Med, Dept Obstet & Gynecol, Chapel Hill, NC 27515 USA.
[Baird, Donna D.] NIEHS, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Kesner, James S.] NIOSH, Biomonitoring & Hlth Assessment Branch, Div Appl Res & Technol, Cincinnati, OH 45226 USA.
RP Steiner, AZ (reprint author), Univ N Carolina, Sch Med, Dept Obstet & Gynecol, CB 7570,Old Clin Bldg, Chapel Hill, NC 27515 USA.
EM asteiner@med.unc.edu
RI Baird, Donna/D-5214-2017
OI Baird, Donna/0000-0002-5544-2653
FU National Institutes of Health; National Institute of Environmental
Health Sciences; Office of Research on Minority Health; Reproductive
Health Research Career Development Center [5K12 HD050113-02]
FX This study was funded as intramural research at the National Institutes
of Health, National Institute of Environmental Health Sciences with
support from the Office of Research on Minority Health and by Women's
Reproductive Health Research Career Development Center Grant 5K12
HD050113-02 at the University of North Carolina.
NR 31
TC 6
Z9 6
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1072-3714
EI 1530-0374
J9 MENOPAUSE
JI Menopause-J. N. Am. Menopause Soc.
PD SEP-OCT
PY 2008
VL 15
IS 5
BP 940
EP 944
DI 10.1097/gme.0b013e31816429e5
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 347BJ
UT WOS:000259113500022
PM 18779679
ER
PT J
AU Parrish, CR
Holmes, EC
Morens, DM
Park, EC
Burke, DS
Calisher, CH
Laughlin, CA
Saif, LJ
Daszak, P
AF Parrish, Colin R.
Holmes, Edward C.
Morens, David M.
Park, Eun-Chung
Burke, Donald S.
Calisher, Charles H.
Laughlin, Catherine A.
Saif, Linda J.
Daszak, Peter
TI Cross-species virus transmission and the emergence of new epidemic
diseases
SO MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS
LA English
DT Review
ID INFLUENZA-A VIRUS; RESPIRATORY SYNDROME CORONAVIRUS; EMERGING
INFECTIOUS-DISEASES; CANINE TRANSFERRIN RECEPTOR; HOST-RANGE; AVIAN
INFLUENZA; SARS CORONAVIRUS; PUBLIC-HEALTH; RNA VIRUSES; FELINE
PARVOVIRUSES
AB Host range is a viral property reflecting natural hosts that are infected either as part of a principal transmission cycle or, less commonly, as "spillover" infections into alternative hosts. Rarely, viruses gain the ability to spread efficiently within a new host that was not previously exposed or susceptible. These transfers involve either increased exposure or the acquisition of variations that allow them to overcome barriers to infection of the new hosts. In these cases, devastating outbreaks can result. Steps involved in transfers of viruses to new hosts include contact between the virus and the host, infection of an initial individual leading to amplification and an outbreak, and the generation within the original or new host of viral variants that have the ability to spread efficiently between individuals in populations of the new host. Here we review what is known about host switching leading to viral emergence from known examples, considering the evolutionary mechanisms, virus-host interactions, host range barriers to infection, and processes that allow efficient host-to-host transmission in the new host population.
C1 [Parrish, Colin R.] Cornell Univ, Coll Vet Med, James A Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
[Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Park, Eun-Chung; Laughlin, Catherine A.] NIAID, NIH, Virol Branch, Bethesda, MD 20892 USA.
[Burke, Donald S.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15261 USA.
[Calisher, Charles H.] Colorado State Univ, Coll Vet Med & Biomed Sci, Dept Microbiol Immunol & Pathol, Arthropod Borne & Infect Dis Lab, Ft Collins, CO 80523 USA.
[Saif, Linda J.] Ohio State Univ, Ohio Agr Res & Dev Ctr, Food Anim Hlth Res Program, Wooster, OH 44691 USA.
[Daszak, Peter] Consortium Conservat Med, New York, NY 10001 USA.
RP Parrish, CR (reprint author), Cornell Univ, Coll Vet Med, James A Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
EM crp3@cornell.edu
OI /0000-0002-5704-8094; Holmes, Edward/0000-0001-9596-3552
FU National Institutes of Allergy and Infectious Diseases; U. S. National
Institutes of Health
FX This review in part summarizes a meeting (Emergence of new epidemic
viruses through host switching, 6 to 8 September 2005, Washington, DC)
sponsored by the National Institutes of Allergy and Infectious Diseases
and the Office of Rare Diseases of the U. S. National Institutes of
Health.
NR 157
TC 219
Z9 226
U1 12
U2 120
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1092-2172
J9 MICROBIOL MOL BIOL R
JI Microbiol. Mol. Biol. Rev.
PD SEP
PY 2008
VL 72
IS 3
BP 457
EP +
DI 10.1128/MMBR.00004-08
PG 15
WC Microbiology
SC Microbiology
GA 344TW
UT WOS:000258951200004
PM 18772285
ER
PT J
AU To, KKW
Zhan, ZR
Litman, T
Bates, SE
AF To, Kenneth K. W.
Zhan, Zhirong
Litman, Thomas
Bates, Susan E.
TI Regulation of ABCG2 expression at the 3 ' untranslated region of its
mRNA through modulation of transcript stability and protein translation
by a putative MicroRNA in the s1 colon cancer cell line
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID AU-RICH ELEMENT; 3'-UNTRANSLATED REGION; MULTIDRUG-RESISTANCE;
DRUG-RESISTANCE; DOWN-REGULATION; GENE; IDENTIFICATION; BINDING;
OVEREXPRESSION; TRANSPORTER
AB ABCG2 is recognized as an important efflux transporter in clinical pharmacology and is potentially important in resistance to chemotherapeutic drugs. To identify epigenetic mechanisms regulating ABCG2 mRNA expression at its 3' untranslated region (3'UTR), we performed 3' rapid amplification of cDNA ends with the S1 parental colon cancer cell line and its drug-resistant ABCG2-overexpressing counterpart. We found that the 3'UTR is > 1,500 bp longer in parental cells and, using the miRBase TARGETs database, identified a putative microRNA (miRNA) binding site, distinct from the recently reported hsa-miR520h site, in the portion of the 3'UTR missing from ABCG2 mRNA in the resistant cells. We hypothesized that the binding of a putative miRNA at the 3'UTR of ABCG2 suppresses the expression of ABCG2. In resistant S1MI80 cells, the miRNA cannot bind to ABCG2 mRNA because of the shorter 3'UTR, and thus, mRNA degradation and/or repression on protein translation is relieved, contributing to overexpression of ABCG2. This hypothesis was rigorously tested by reporter gene assays, mutational analysis at the miRNA binding sites, and forced expression of miRNA inhibitors or mimics. The removal of this epigenetic regulation by miRNA could be involved in the overexpression of ABCG2 in drug-resistant cancer cells.
C1 [To, Kenneth K. W.; Zhan, Zhirong; Bates, Susan E.] NCI, Mol Therapeut Sect, Med Oncol Branch, Ctr Canc Res,Natl Inst Hlth, Bethesda, MD 20892 USA.
[Litman, Thomas] Exiqon AS, DK-2950 Vedboek, Denmark.
RP To, KKW (reprint author), NCI, Mol Therapeut Sect, Med Oncol Branch, Ctr Canc Res,Natl Inst Hlth, Bldg 10,Room 13N220,10 Ctr Dr, Bethesda, MD 20892 USA.
EM tok@mail.nih.gov
RI To, Kenneth /M-4500-2013
OI To, Kenneth /0000-0003-2755-0283
FU NIH; National Cancer Institute; Center for Cancer Research
FX This research was supported by the intramural research program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 56
TC 95
Z9 106
U1 0
U2 10
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD SEP
PY 2008
VL 28
IS 17
BP 5147
EP 5161
DI 10.1128/MCB.00331-08
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 341DY
UT WOS:000258695600002
PM 18573883
ER
PT J
AU Shao, JY
Welch, WJ
DiProspero, NA
Diamond, MI
AF Shao, Jieya
Welch, William J.
DiProspero, Nicholas A.
Diamond, Marc I.
TI Phosphorylation of profilin by ROCK1 regulates polyglutamine aggregation
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID TRANSGENIC MOUSE MODEL; RHO-ASSOCIATED KINASE; ACTIN-BINDING SITE;
HUNTINGTONS-DISEASE; PROTEIN-KINASE; MOTOR DEFICITS; LIM-KINASE;
INHIBITOR; RECEPTOR; DYNAMICS
AB Y-27632, an inhibitor of the Rho-associated kinase ROCK, is a therapeutic lead for Huntington disease (HD). The downstream targets that mediate its inhibitory effects on huntingtin (Htt)aggregation and toxicity are unknown. We have identified profilin, a small actin-binding factor that also interacts with Htt, as being a direct target of the ROCK1 isoform. The overexpression of profilin reduces the aggregation of polyglutamine-expanded Htt and androgen receptor (AR) peptides. This requires profilin's G-actin binding activity and its direct interaction with Htt, which are both inhibited by the ROCK1-mediated phosphorylation of profilin at Ser-137. Y-27632 blocks the phosphorylation of profilin in HEK293 cells and primary neurons, which maintains profilin in an active state. The knockdown of profilin blocks the inhibitory effect of Y-27632 on both AR and Htt aggregation. A signaling pathway from ROCK1 to profilin thus controls polyglutamine protein aggregation and is targeted by a promising therapeutic lead for HD.
C1 [Shao, Jieya; Diamond, Marc I.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
[Shao, Jieya; Diamond, Marc I.] Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA.
[Welch, William J.] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94143 USA.
[DiProspero, Nicholas A.] NIH, Neurogenet Branch, Bethesda, MD 20892 USA.
RP Diamond, MI (reprint author), Univ Calif San Francisco, Dept Neurol, GH-S572B,600 16th St, San Francisco, CA 94143 USA.
EM marc.diamond@ucsf.edu
NR 54
TC 61
Z9 64
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD SEP
PY 2008
VL 28
IS 17
BP 5196
EP 5208
DI 10.1128/MCB.00079-08
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 341DY
UT WOS:000258695600006
PM 18573880
ER
PT J
AU Maceyka, M
Alvarez, SE
Milstien, S
Spiegel, S
AF Maceyka, Michael
Alvarez, Sergio E.
Milstien, Sheldon
Spiegel, Sarah
TI Filamin A links sphingosine kinase 1 and sphingosine-1-phosphate
receptor 1 at lamellipodia to orchestrate cell migration
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID PROTEIN-COUPLED RECEPTOR; EPIDERMAL-GROWTH-FACTOR; SMOOTH-MUSCLE-CELLS;
PLASMA-MEMBRANE; DEPENDENT TRANSLOCATION; P21-ACTIVATED KINASES;
LYMPHOID ORGANS; PHOSPHORYLATION; ACTIVATION; BINDING
AB Sphingosine kinase 1 (SphK1) catalyzes the phosphorylation of sphingosine to produce the potent lipid mediator sphingosine-1-phosphate (S1P), which plays a critical role in cell motility via its cell surface receptors. Here, we have identified filamin A (FLNa), an actin-cross-linking protein involved in cell movement, as a bona fide SphK1-interacting protein. Heregulin stimulated SphK1 activity only in FLNa-expressing A7 melanoma cells but not in FLNa-deficient cells and induced its translocation and colocalization with FLNa at lamellipodia. SphK1 was required for heregulin-induced migration, lamellipodia formation, activation of PAK1, and subsequent FLNa phosphorylation. S1P directly stimulated PAK1 kinase, suggesting that it may be a target of intracellularly generated S1P. Heregulin also induced colocalization of S1P(1) (promotility S1P receptor) but not S1P(2), with SphK1 and FLNa at membrane ruffles. Moreover, an S1P1 antagonist inhibited the lamellipodia formation induced by heregulin. Hence, FLNa links SphK1 and S1P1 to locally influence the dynamics of actin cytoskeletal structures by orchestrating the concerted actions of the triumvirate of SphK1, FLNa, and PAK1, each of which requires and/or regulates the actions of the others, at lamellipodia to promote cell movement.
C1 [Maceyka, Michael; Alvarez, Sergio E.; Spiegel, Sarah] Virginia Commonwealth Univ, Sch Med, Dept Biochem & Mol Biol, Richmond, VA 23298 USA.
[Maceyka, Michael; Alvarez, Sergio E.; Spiegel, Sarah] Virginia Commonwealth Univ, Sch Med, Massey Canc Ctr, Richmond, VA 23298 USA.
[Milstien, Sheldon] NIMH, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Spiegel, S (reprint author), Virginia Commonwealth Univ, Sch Med, Dept Biochem & Mol Biol, POB 980614,1101 E Marshall St, Richmond, VA 23298 USA.
EM sspiegel@vcu.edu
FU NCI [R01CA61774, 5T32 CA085159-04]; NIMH Intramural Research; NIH [P30
CA16059]
FX This work was supported by NCI grants R01CA61774 (to S. S.) and 5T32
CA085159-04 (to M. M.) and the NIMH Intramural Research Program (S. M.).
Confocal microscopy was supported in part by NIH grant P30 CA16059 to
the Massey Cancer Center.
NR 47
TC 51
Z9 52
U1 0
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD SEP
PY 2008
VL 28
IS 18
BP 5687
EP 5697
DI 10.1128/MCB.00465-08
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 344TU
UT WOS:000258951000011
PM 18644866
ER
PT J
AU Bandyopadhyay, U
Kaushik, S
Varticovski, L
Cuervo, AM
AF Bandyopadhyay, Urmi
Kaushik, Susmita
Varticovski, Lyuba
Cuervo, Ana Maria
TI The chaperone-mediated autophagy receptor organizes in dynamic protein
complexes at the lysosomal membrane
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID RAT-LIVER LYSOSOMES; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; MOLECULAR
CHAPERONE; SELECTIVE UPTAKE; DEGRADATION; FIBROBLASTS
AB Chaperone-mediated autophagy (CMA) is a selective type of autophagy by which specific cytosolic proteins are sent to lysosomes for degradation. Substrate proteins bind to the lysosomal membrane through the lysosome-associated membrane protein type 2A (LAMP-2A), one of the three splice variants of the lamp2 gene, and this binding is limiting for their degradation via CMA. However, the mechanisms of substrate binding and uptake remain unknown. We report here that LAMP-2A organizes at the lysosomal membrane into protein complexes of different sizes. The assembly and disassembly of these complexes are a very dynamic process directly related to CMA activity. Substrate proteins only bind to monomeric LAMP-2A, while the efficient translocation of substrates requires the formation of a particular high-molecular-weight LAMP-2A complex. The two major chaperones related to CMA, hsc70 and hsp90, play critical roles in the functional dynamics of the LAMP-2A complexes at the lysosomal membrane. Thus, we have identified a novel function for hsc70 in the disassembly of LAMP-2A from these complexes, whereas the presence of lysosome-associated hsp90 is essential to preserve the stability of LAMP-2A at the lysosomal membrane.
C1 [Bandyopadhyay, Urmi; Kaushik, Susmita; Cuervo, Ana Maria] Albert Einstein Coll Med, Dept Dev & Mol Biol, Marion Bessin Liver Res Ctr, Bronx, NY 10461 USA.
[Bandyopadhyay, Urmi; Kaushik, Susmita; Cuervo, Ana Maria] Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Anat & Struct Biol, Bronx, NY 10461 USA.
[Varticovski, Lyuba] NCI, Human Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Cuervo, AM (reprint author), Albert Einstein Coll Med, Dept Dev & Mol Biol, Marion Bessin Liver Res Ctr, Ullmann Bldg Room 611D,1300 Morris Pk Ave, Bronx, NY 10461 USA.
EM amcuervo@aecom.yu.edu
RI Bandyopadhyay, Urmi/A-3944-2015
OI Bandyopadhyay, Urmi/0000-0003-3438-8923
FU NIH/NIA [AG021904, AG25355, DK041918]; Ellison Medical Foundation
FX This work was supported by NIH/NIA grants AG021904, AG25355, and
DK041918 and by an Ellison Medical Foundation award.
NR 37
TC 142
Z9 145
U1 3
U2 8
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
EI 1098-5549
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD SEP
PY 2008
VL 28
IS 18
BP 5747
EP 5763
DI 10.1128/MCB.02070-07
PG 17
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 344TU
UT WOS:000258951000016
PM 18644871
ER
PT J
AU Park, JJ
Cawley, NX
Loh, YP
AF Park, Joshua J.
Cawley, Niamh X.
Loh, Y. Peng
TI A bi-directional carboxypeptidase E-driven transport mechanism controls
BDNF vesicle homeostasis in hippocampal neurons
SO MOLECULAR AND CELLULAR NEUROSCIENCE
LA English
DT Article
DE carboxypeptidase E; cytoplasmic tail; BDNF vesicle transport; dynactin
ID RETROGRADE AXONAL-TRANSPORT; ACTIVITY-DEPENDENT SECRETION; PROHORMONE
SORTING RECEPTOR; NEUROTROPHIC FACTOR; VESICULAR TRANSPORT;
CAENORHABDITIS-ELEGANS; CYTOPLASMIC DYNEIN; CORTICAL-NEURONS; DYNACTIN;
GRANULES
AB Anterograde transport of brain-derived neurotrophic factor (BDNF) vesicles from the soma to neurite terminals is necessary for activity-dependent secretion of BDNF to mediate synaptic plasticity, memory and learning, and retrograde BDNF transport back to the soma for recycling. in our study, overexpression of the cytoplasmic tail of the carboxypeptidase E (CPE) found in BDNF vesicles significantly reduced localization of BDNF in neurites of hippocampal neurons. Live-cell imaging showed that the velocity and distance of movement of fluorescent protein-tagged CPE- or BDNF-containing vesicles were reduced in both directions. in pulldown assays, the CPE tail interacted with dynactin along With kinesin-2 and kinesin-3. and cytoplasmic dynein. Competition assays using a CPE tail peptide verified specific interaction between the CPE tail and dynactin. Thus, the CPE cytoplasmic tail binds dynactin that recruits kinesins or dynein for driving bidirectional transport of BDNF vesicle to maintain vesicle homeostasis and secretion in hippocampal neurons. Published by Elsevier Inc.
C1 [Park, Joshua J.; Cawley, Niamh X.; Loh, Y. Peng] NICHHD, Cellular Neurobiol Sect, Dev Neurobiol Program, NIH, Bethesda, MD 20892 USA.
RP Loh, YP (reprint author), NICHHD, Cellular Neurobiol Sect, Dev Neurobiol Program, NIH, Bethesda, MD 20892 USA.
EM lohp@mail.nih.gov
FU NICHD; NIH
FX We thank Dr. Bai Lu (NICHD, NIH), Dr. Joel Rosenbaum (Yale University),
Dr.Trina Schroer(Johns Hopkins University),and Dr. Jennifer
Lippincott-Schwartz (NICHD, NIH) for their suggestions and critical
reading of the manuscript. We also thank Drs. Hong Lou, Guhan Nagappan
and Hisatsugu Koshimizu, all from NICHD for their technical assistance
and helpful discussions. We thank Dr. Vincent Schram and Chip Dye in the
NICHD Microscopy Imaging Core for their technical support. This research
was supported by the Intramural Research Program of the NICHD, NIH.
NR 39
TC 32
Z9 32
U1 0
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1044-7431
J9 MOL CELL NEUROSCI
JI Mol. Cell. Neurosci.
PD SEP
PY 2008
VL 39
IS 1
BP 63
EP 73
DI 10.1016/j.mcn.2008.05.016
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 346EX
UT WOS:000259052500007
PM 18573344
ER
PT J
AU Wang, PY
Seabold, GK
Wenthold, R
AF Wang, Philip Y.
Seabold, Gail K.
Wenthold, Robert.
TI Synaptic adhesion-like molecules (SALMs) promote neurite outgrowth
SO MOLECULAR AND CELLULAR NEUROSCIENCE
LA English
DT Article
ID FIBROBLAST-GROWTH-FACTOR; LEUCINE-RICH REPEATS; N-CADHERIN; EXCITATORY
SYNAPSES; NMDA RECEPTOR; TRANSMEMBRANE PROTEINS; HIPPOCAMPAL-NEURONS;
SURFACE EXPRESSION; AXONAL GROWTH; FAMILY
AB SALMs are a family of five adhesion molecules whose expression is largely restricted to the CNS. Initial reports showed that SALM1 functions in neurite Outgrowth while SALM2 is involved in synapse formation. To investigate the function of SALMs in detail, we asked if all five are involved in neurite outgrowth. Expression of epitope-tagged Proteins in cultured hippocampal neurons showed that SALMs are distributed throughout neurons, including axons, dendrites, and growth cones. Over-expression of each SALM resulted in enhanced neurite outgrowth, but with different phenotypes. Neurite Outgrowth could be reduced by applying antibodies targeting the extracellular leucine rich regions of SALMs and with RNAi. Through over-expression of deletion constructs, we found that the C-terminal PDZ binding domains of SALMs 1-3 are required for most aspects Of neurite outgrowth. In addition, by using a chimera of SALMs 2 and 4, we found that the N-terminus is also-involved in neurite outgrowth. Published by Elsevier Inc.
C1 [Wang, Philip Y.; Seabold, Gail K.; Wenthold, Robert.] NIDCD, Neurochem Lab, NIH, Bethesda, MD 20892 USA.
[Wang, Philip Y.] Univ Maryland, Dept Biol, Coll Chem & Life Sci, College Pk, MD 20742 USA.
[Wang, Philip Y.] Univ Maryland, Neurosci & Cognit Sci Program, College Pk, MD 20742 USA.
RP Wenthold, R (reprint author), NIDCD, Neurochem Lab, NIH, 50 S Dr,MSC 8027,Bldg 50,Room 4140, Bethesda, MD 20892 USA.
EM wenthold@nidcd.nih.gov
FU National Institute on Deafness and Other Communication Disorders (NIDCD)
FX We are grateful to Dr. Kai Chang, Dr. Ya-Xian Wang, and Ms. Linna Ge for
their excellent technical assistance. We would like to thank Dr. Ronald
Petralia, Dr. Rana Al-Hallaq, and members of the Wenthold lab for their
invaluable discussions and suggestions on the preparation of this
manuscript. This work was supported by the National Institute on
Deafness and Other Communication Disorders (NIDCD) Intramural Research
Program.
NR 47
TC 22
Z9 28
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1044-7431
J9 MOL CELL NEUROSCI
JI Mol. Cell. Neurosci.
PD SEP
PY 2008
VL 39
IS 1
BP 83
EP 94
DI 10.1016/j.mcn.2008.05.019
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 346EX
UT WOS:000259052500009
PM 18585462
ER
PT J
AU Prasad, AB
Allard, MW
Green, ED
AF Prasad, Arjun B.
Allard, Marc W.
Green, Eric D.
CA NISC Comparat Sequencing Program
TI Confirming the phylogeny of mammals by use of large comparative sequence
data sets
SO MOLECULAR BIOLOGY AND EVOLUTION
LA English
DT Article
DE Placentalia; Eutheria; Mammalia; mammalian phylogeny; phylogenomics;
Atlantogenata; molecular systematics
ID NEW-WORLD MONKEYS; PLACENTAL MAMMALS; MITOCHONDRIAL GENOMES;
MAXIMUM-LIKELIHOOD; EUTHERIAN RELATIONSHIPS; BAYESIAN PHYLOGENETICS;
EVOLUTIONARY HISTORY; MULTIPLE ALIGNMENTS; MOLECULAR EVIDENCE; PRIMATE
PHYLOGENY
AB The ongoing generation of prodigious amounts of genomic sequence data from myriad vertebrates is providing unparalleled opportunities for establishing definitive phylogenetic relationships among species. The size and complexities of such comparative sequence data sets not only allow smaller and more difficult branches to be resolved but also present unique challenges, including large computational requirements and the negative consequences of systematic biases. To explore these issues and to clarify the phylogenetic relationships among mammals, we have analyzed a large data set of over 60 megabase pairs (Mb) of high-quality genomic sequence, which we generated from 41 mammals and 3 other vertebrates. All sequences are orthologous to a 1.9-Mb region of the human genome that encompasses the cystic fibrosis transmembrane conductance regulator gene (CFTR). To understand the characteristics and challenges associated with phylogenetic analyses of such a large data set, we partitioned the sequence data in several ways and utilized maximum likelihood, maximum parsimony, and Neighbor-Joining algorithms, implemented in parallel on Linux clusters. These studies yielded well-supported phylogenetic trees, largely confirming other recent molecular phylogenetic analyses. Our results provide support for rooting the placental mammal tree between Atlantogenata (Xenarthra and Afrotheria) and Boreoeutheria (Euarchontoglires and Laurasiatheria), illustrate the difficulty in resolving some branches even with large amounts of data (e.g., in the case of Laurasiatheria), and demonstrate the valuable role that very large comparative sequence data sets can play in refining our understanding of the evolutionary relationships of vertebrates.
C1 [Prasad, Arjun B.; Green, Eric D.] NHGRI, Gen Technol Branch, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Green, Eric D.; NISC Comparat Sequencing Program] NHGRI, NIH Intramural Sequencing Ctr, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Prasad, Arjun B.] George Washington Univ, Integrated Biosci Program, Washington, DC 20052 USA.
[Allard, Marc W.] George Washington Univ, Dept Biol Sci, Washington, DC 20052 USA.
RP Green, ED (reprint author), NHGRI, Gen Technol Branch, Natl Inst Hlth, Bethesda, MD 20892 USA.
EM egreen@nhgri.nih.gov
RI Prasad, Arjun/C-6736-2008;
OI Prasad, Arjun/0000-0002-1343-8664
FU Intramural NIH HHS [Z01 HG000196-07, Z99 HG999999]
NR 95
TC 166
Z9 170
U1 9
U2 49
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0737-4038
EI 1537-1719
J9 MOL BIOL EVOL
JI Mol. Biol. Evol.
PD SEP
PY 2008
VL 25
IS 9
BP 1795
EP 1808
DI 10.1093/molbev/msn104
PG 14
WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics &
Heredity
GA 337ZF
UT WOS:000258473400002
PM 18453548
ER
PT J
AU Chen, J
Xiao, L
Rao, JN
Zou, T
Liu, L
Bellavance, E
Gorospe, M
Wang, JY
AF Chen, Jie
Xiao, Lan
Rao, Jaladanki N.
Zou, Tongtong
Liu, Lan
Bellavance, Emily
Gorospe, Myriam
Wang, Jian-Ying
TI JunD represses transcription and translation of the tight junction
protein zona occludens-1 modulating intestinal epithelial barrier
function
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID ANTIGEN-RELATED PROTEIN; AU-RICH-ELEMENT; MESSENGER-RNA; POLYAMINE
DEPLETION; OXIDATIVE STRESS; GENE-EXPRESSION; HUMAN-CELLS; C-JUN;
BINDING; ZO-1
AB The AP-1 transcription factor JunD is highly expressed in intestinal epithelial cells, but its exact role in maintaining the integrity of intestinal epithelial barrier remains unknown. The tight junction (TJ) protein zonula occludens (ZO)-1 links the intracellular domain of TJ-transmembrane proteins occludin, claudins, and junctional adhesion molecules to many cytoplasmic proteins and the actin cytoskeleton and is crucial for assembly of the TJ complex. Here, we show that JunD negatively regulates expression of ZO-1 and is implicated in the regulation of intestinal epithelial barrier function. Increased JunD levels by ectopic overexpression of the junD gene or by depleting cellular polyamines repressed ZO-1 expression and increased epithelial paracellular permeability. JunD regulated ZO-1 expression at the levels of transcription and translation. Transcriptional repression of ZO-1 by JunD was mediated through cAMP response element-binding protein-binding site within its proximal region of the ZO-1-promoter, whereas induced JunD inhibited ZO- 1 mRNA translation by enhancing the interaction of the ZO-13'-untranslated region with RNA-binding protein T cell-restricted intracellular antigen 1-related protein. These results indicate that JunD is a biological suppressor of ZO- 1 expression in intestinal epithelial cells and plays a critical role in maintaining epithelial barrier function.
C1 [Chen, Jie; Xiao, Lan; Rao, Jaladanki N.; Zou, Tongtong; Liu, Lan; Bellavance, Emily; Wang, Jian-Ying] Univ Maryland, Sch Med, Dept Surg, Cell Biol Grp, Baltimore, MD 21201 USA.
[Wang, Jian-Ying] Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA.
[Chen, Jie; Xiao, Lan; Rao, Jaladanki N.; Zou, Tongtong; Liu, Lan; Bellavance, Emily; Wang, Jian-Ying] Baltimore Vet Affairs Med Ctr, Baltimore, MD 21201 USA.
[Gorospe, Myriam] NIA, Natl Inst Hlth, Intramural Res Program, Cellular & Mol Biol Lab, Baltimore, MD 21224 USA.
RP Wang, JY (reprint author), Univ Maryland, Sch Med, Dept Surg, Cell Biol Grp, Baltimore, MD 21201 USA.
EM jwang@smail.umaryland.edu
FU Department of Veterans Affairs; National Institutes of Health [DK-57819,
DK-61972, DK-68491]; National Institute on Aging-Intramural Research
Program, National Institutes of Health
FX This work was supported by a Merit Review grant (to J.-Y.W.) from the
Department of Veterans Affairs and by National Institutes of Health
grants DK-57819, DK-61972, and DK-68491 (to J.-Y.W.). J.-Y.W. is a
Research Career Scientist, Medical Research Service, U. S. Department of
Veterans Affairs. M. G. is supported by the National Institute on
Aging-Intramural Research Program, National Institutes of Health.
NR 65
TC 36
Z9 39
U1 1
U2 3
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD SEP
PY 2008
VL 19
IS 9
BP 3701
EP 3712
DI 10.1091/mbc.E08-02-0175
PG 12
WC Cell Biology
SC Cell Biology
GA 348AM
UT WOS:000259183200008
PM 18562690
ER
PT J
AU Yeh, CH
Hung, LY
Hsu, C
Le, SY
Lee, PT
Liao, WL
Lin, YT
Chang, WC
Tseng, JT
AF Yeh, Chiu-Hung
Hung, Liang-Yi
Hsu, Chin
Le, Shu-Yun
Lee, Pin-Tse
Liao, Wan-Lin
Lin, Yi-Tseng
Chang, Wen-Chang
Tseng, Joseph T.
TI RNA-binding protein HuR interacts with thrombomodulin 5 ' untranslated
region and represses internal ribosome entry site-mediated translation
under IL-1 beta treatment
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; ENDOTHELIAL-CELLS; 5'-UNTRANSLATED REGION;
SECONDARY STRUCTURE; GENE-EXPRESSION; TISSUE-FACTOR; INITIATION; SEPSIS;
INFLAMMATION; MECHANISM
AB Reduction in host-activated protein C levels and resultant microvascular thrombosis highlight the important functional role of protein C anticoagulant system in the pathogenesis of sepsis and septic shock. Thrombomodulin (TM) is a critical factor to activate protein C in mediating the anticoagulation and anti-inflammation effects. However, TM protein content is decreased in inflammation and sepsis, and the mechanism is still not well defined. In this report, we identified that the TM 5' untranslated region (UTR) bearing the internal ribosome entry site (IRES) element controls TM protein expression. Using RNA probe pulldown assay, HuR was demonstrated to interact with the TM 5'UTR. Overexpression of HuR protein inhibited the activity of TM IRES, whereas on the other hand, reducing the HuR protein level reversed this effect. When cells were treated with IL-1 beta, the IRES activity was suppressed and accompanied by an increased interaction between HuR and TM 5'UTR. In the animal model of sepsis, we found the TM protein expression level to be decreased while concurrently observing the increased interaction between HuR and TM mRNA in liver tissue. In summary, HuR plays an important role in suppression of TM protein synthesis in IL-1 beta treatment and sepsis.
C1 [Yeh, Chiu-Hung; Hung, Liang-Yi; Chang, Wen-Chang; Tseng, Joseph T.] Natl Cheng Kung Univ, Dept Pharmacol, Tainan 701, Taiwan.
[Lee, Pin-Tse] Natl Cheng Kung Univ, Inst Basic Med Sci, Coll Med, Tainan 701, Taiwan.
[Hung, Liang-Yi; Liao, Wan-Lin] Natl Cheng Kung Univ, Inst Biosignal Transduct, Tainan 701, Taiwan.
[Tseng, Joseph T.] Natl Cheng Kung Univ, Inst Bioinformat, Coll Biosci & Biotechnol, Tainan 701, Taiwan.
[Tseng, Joseph T.] Natl Cheng Kung Univ, Ctr Gene Regulat & Signal Transduct Res, Tainan 701, Taiwan.
[Hsu, Chin] Kaohsiung Med Univ, Dept Physiol, Grad Inst Physiol & Mol Med, Kaohsiung, Taiwan.
[Lin, Yi-Tseng] Kaohsiung Med Univ, Grad Inst Med, Sch Med, Kaohsiung, Taiwan.
[Le, Shu-Yun] Natl Canc Inst, Natl Inst Hlth, Ctr Canc Res, Nanobiol Program, Frederick, MD 21702 USA.
RP Tseng, JT (reprint author), Natl Cheng Kung Univ, Dept Pharmacol, Tainan 701, Taiwan.
EM wcchang@mail.ncku.edu.tw; tctseng@mail.ncku.edu.tw
RI Hsu, Chin/C-7283-2009
FU National Science Council [NSC 94-2311-B-006-004, NSC
95-2320-B-006-066MY3]; National Cheng-Kung University Project of
Promoting Academic Excellence and Developing World Class Research
Center; Intramural Research Program of the National Institutes of
Health, National Cancer Institute, Center for Cancer Research
FX We thank Professor Anne Willis (School of Pharmacy, The University of
Nottingham, United Kingdom) for kindly providing the pRF, pRMF, pRHRVF,
and phpRF constructs. This work was supported by National Science
Council Grant NSC 94-2311-B-006-004 and NSC 95-2320-B-006-066MY3 of
Taiwan, National Cheng-Kung University Project of Promoting Academic
Excellence and Developing World Class Research Center, and in part by
the Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research.
NR 48
TC 25
Z9 25
U1 0
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD SEP
PY 2008
VL 19
IS 9
BP 3812
EP 3822
DI 10.1091/mbc.E07-09-0962
PG 11
WC Cell Biology
SC Cell Biology
GA 348AM
UT WOS:000259183200018
PM 18579691
ER
PT J
AU Cheng, WH
Muftic, D
Muftuoglu, M
Dawut, L
Morris, C
Helleday, T
Shiloh, Y
Bohr, VA
AF Cheng, Wen-Hsing
Muftic, Diana
Muftuoglu, Meltem
Dawut, Lale
Morris, Christa
Helleday, Thomas
Shiloh, Yosef
Bohr, Vilhelm A.
TI WRN is required for ATM activation and the S-phase checkpoint in
response to interstrand cross-link-induced DNA double-strand breaks
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID WERNER-SYNDROME PROTEIN; COLLAPSED REPLICATION FORKS;
TELANGIECTASIA-MUTATED ATM; SYNDROME GENE-PRODUCT; HOMOLOGOUS
RECOMBINATION; ATAXIA-TELANGIECTASIA; CELLULAR-RESPONSE; SYNDROME CELLS;
CHROMATIN-STRUCTURE; TOPOISOMERASE-I
AB Werner syndrome (WS)is a human genetic disorder characterized by extensive clinical features of premature aging. Ataxia-telengiectasia (A-T) is a multisystem human genomic instability syndrome that includes premature aging in some of the patients. WRN and ATM, the proteins defective in WS and A-T, respectively, play significant roles in the maintenance of genomic stability and are involved in several DNA metabolic pathways. A role for WRN in DNA repair has been proposed; however, this study provides evidence that WRN is also involved in ATM pathway activation and in a S-phase checkpoint in cells exposed to DNA interstrand cross-link-induced double-strand breaks. Depletion of WRN in such cells by RNA interference results in an intra-S checkpoint defect, and interferes with activation of ATM as well as downstream phosphorylation of ATM target proteins. Treatment of cells under replication stress with the ATM kinase inhibitor KU 55933 results in a S-phase checkpoint defect similar to that observed in WRN shRNA cells. Moreover, gamma H2AX levels are higher in WRN shRNA cells than in control cells 6 and 16 h after exposure to psoralen DNA cross-links. These results suggest that WRN and ATM participate in a replication checkpoint response, in which WRN facilitates ATM activation in cells with psoralen DNA cross-link-induced collapsed replication forks.
C1 [Cheng, Wen-Hsing; Muftic, Diana; Muftuoglu, Meltem; Dawut, Lale; Bohr, Vilhelm A.] NIA, NIH, Lab Mol Gerontol, Baltimore, MD 21224 USA.
[Morris, Christa] NIA, NIH, Flow Cytometry Unit, Baltimore, MD 21224 USA.
[Cheng, Wen-Hsing] Univ Maryland, Dept Nutr & Food Sci, College Pk, MD 20742 USA.
[Muftic, Diana; Helleday, Thomas] Stockholm Univ, Dept Genet Microbiol & Toxicol, Arrhenius Lab, S-10691 Stockholm, Sweden.
[Shiloh, Yosef] Tel Aviv Univ, Sackler Sch Med, Dept Human Mol Genet & Biochem, David & Inez Myers Lab Genet Res, IL-69978 Tel Aviv, Israel.
RP Bohr, VA (reprint author), NIA, NIH, Lab Mol Gerontol, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
RI Helleday, Thomas/D-5224-2013;
OI Helleday, Thomas/0000-0002-7384-092X
FU Intramural Research Program of the National Institutes of Health;
National Institute on Aging; Lilly Lawski Foundation
FX We thank G. Smith and A. May for materials and technical support; F.
Indig and R. Earley for confocal microscope; and S. A. Martomo, A.
Balajan, R. Wersto, and Y. Liu for comments. This research was supported
by the Intramural Research Program of the National Institutes of Health,
National Institute on Aging, and Lilly Lawski Foundation (D.M.).
NR 77
TC 46
Z9 46
U1 0
U2 4
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD SEP
PY 2008
VL 19
IS 9
BP 3923
EP 3933
DI 10.1091/mbc.E07-07-0698
PG 11
WC Cell Biology
SC Cell Biology
GA 348AM
UT WOS:000259183200027
PM 18596239
ER
PT J
AU Guirouilh-Barbat, J
Redon, C
Pommier, Y
AF Guirouilh-Barbat, Josee
Redon, Christophe
Pommier, Yves
TI Transcription-coupled DNA double-strand breaks are mediated via the
nucleotide excision repair and the Mre11-Rad50-Nbs1 complex
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID DEPENDENT PROTEIN-KINASE; BLOOMS-SYNDROME HELICASE; SOFT-TISSUE
SARCOMAS; HISTONE H2AX; HOMOLOGOUS RECOMBINATION; CARIBBEAN TUNICATE;
DAMAGE RESPONSE; ATM ACTIVATION; MRE11 COMPLEX; ECTEINASCIDIN-743 ET-743
AB The cellular activity of Yondelis (trabectedin, Ecteinascidin 743, Et743) is known to depend on transcription-coupled nucleotide excision repair (TCR). However, the subsequent cellular effects of Et743 are not fully understood. Here we show that Et743 induces both transcription-and replication-coupled DNA double-strand breaks (DSBs) that are detectible by neutral COMET assay and as gamma-H2AX foci that colocalize with 53BP1, Mre11, Ser(1981)-pATM, and Thr(68)-pChk2. The transcription coupled-DSBs (TC-DSBs) induced by Et743 depended both on TCR and Mre11-Rad50-Nbs1 (MRN) and were associated with DNA-PK-dependent gamma-H2AX foci. In contrast to DNA-PK, ATM phosphorylated H2AX both in NER-proficient and -deficient cells, but its full activation was dependent on H2AX as well as DNA-PK, suggesting a positive feedback loop: DNA-PK-gamma-H2AX-ATM. Knocking-out H2AX or inactivating DNA-PK reduced Et743's antiproliferative activity, whereas ATM and MRN tended to act as survival factors. Our results highlight the interplays between ATM and DNA-PK and their impacts on H2AX phosphorylation and cell survival. They also suggest that gamma-H2AX may serve as a biomarker in patients treated with Et743 and that molecular profiling of tumors for TCR, MRN, ATM, and DNA-PK might be useful to anticipate tumor response to Et743 treatment.
C1 [Guirouilh-Barbat, Josee; Redon, Christophe; Pommier, Yves] NCI, NIH, Ctr Canc Res, Mol Pharmacol Lab, Bethesda, MD 20892 USA.
RP Pommier, Y (reprint author), NCI, NIH, Ctr Canc Res, Mol Pharmacol Lab, Bethesda, MD 20892 USA.
EM pommier@nih.gov
FU National Cancer Institute (NCI) Intramural Program; Center for Cancer
Research, NCI; National Institutes of Health
FX We thank Drs. Chiara Conti, Andrew Jobson, Olivier Sordet, and Kurt W.
Kohn for critical reading of the manuscript and suggestions during the
course of these experiments. We also thank Dr. Roger Griffin, Department
of Chemistry, University of Newcastle, and Dr. Ian Hickson, KuDos
Pharmaceuticals. for generously providing the ATM and DNA-PK small
molecule inhibitors. This work was supported by the National Cancer
Institute (NCI) Intramural Program, Center for Cancer Research, NCI,
National Institutes of Health.
NR 70
TC 45
Z9 47
U1 0
U2 5
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD SEP
PY 2008
VL 19
IS 9
BP 3969
EP 3981
DI 10.1091/mbc.E08-02-0215
PG 13
WC Cell Biology
SC Cell Biology
GA 348AM
UT WOS:000259183200031
PM 18632984
ER
PT J
AU Bryan, L
Paugh, BS
Kapitonov, D
Wilczynska, KM
Alvarez, SM
Singh, SK
Milstien, S
Spiegel, S
Kordula, T
AF Bryan, Lauren
Paugh, Barbara S.
Kapitonov, Dmitri
Wilczynska, Katarzyna M.
Alvarez, Silvina M.
Singh, Sandeep K.
Milstien, Sheldon
Spiegel, Sarah
Kordula, Tomasz
TI Sphingosine-1-phosphate and interleukin-1 independently regulate
plasminogen activator inhibitor-1 and urokinase-type plasminogen
activator receptor expression in glioblastoma cells: Implications for
invasiveness
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID EPIDERMAL-GROWTH-FACTOR; HUMAN-BRAIN-TUMORS; PROTEIN-COUPLED RECEPTOR;
GASTRIC-CANCER CELLS; SPHINGOSINE KINASE-1; SIGNALING PATHWAYS; GENE
AMPLIFICATION; XENOGRAFT MODEL; INVASION; MULTIFORME
AB Glioblastoma multiforme is an invasive primary brain tumor, which evades the current standard treatments. The invasion of glioblastoma cells into healthy brain tissue partly depends on the proteolytic and nonproteolytic activities of the plasminogen activator system proteins, including the urokinase-type plasminogen activator (uPA), plasminogen activator inhibitor 1 (PAI-1), and a receptor for uPA (uPAR). Here we show that sphingosine-1-phosphate (S1P) and the inflammatory mediator interleukin-1 (IL-1) increase the mRNA and protein expression of PAI-1 and uPAR and enhance the invasion of U373 glioblastoma cells. Although IL-1 enhanced the expression of sphingosine kinase 1 (Sphk1), the enzyme that produces S1P, down-regulation of SphK1 had no effect on the IL-1-induced uPAR or PAI-1 mRNA expression, suggesting that these actions of IL-1 are independent of S1P production. Indeed, the S1P-induced mRNA expression of uPAR and PAI-1 was blocked by the S1P(2) receptor antagonist JTE013 and by the down-regulation Of S1P2 using siRNA. Accordingly, the inhibition of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 and Rho-kinase, two downstream signaling cascades activated by S1P(2), blocked the activation of PAI-1 and uPAR mRNA expression by S1P. More importantly, the attachment of glioblastoma cells was inhibited by the addition of exogenous PAI-1 or siRNA to uPAR, whereas the invasion of glioblastoma cells induced by S1P or IL-1 correlated with their ability to enhance the expression of PAI-1 and uPAR. Collectively, these results indicate that S1P and IL-1 activate distinct pathways leading to the mRNA and protein expression of PAI-1 and uPAR, which are important for glioblastoma invasiveness.
C1 [Bryan, Lauren; Paugh, Barbara S.; Kapitonov, Dmitri; Wilczynska, Katarzyna M.; Alvarez, Silvina M.; Singh, Sandeep K.; Spiegel, Sarah; Kordula, Tomasz] Virginia Commonwealth Univ, Sch Med, Dept Biochem & Mol Biol, Richmond, VA 23298 USA.
[Milstien, Sheldon] NIMH, Bethesda, MD 20892 USA.
RP Kordula, T (reprint author), Virginia Commonwealth Univ, Sch Med, Dept Biochem & Mol Biol, Richmond, VA 23298 USA.
EM tkordula@vcu.edu
RI Paugh, Barbara/B-3625-2009
FU NIH [R01 NS044118]; Massey Cancer Center, Virginia Commonwealth
University [R01 CA61774]; National Institute of Mental Health Intramural
Research Program
FX NIH grant R01 NS044118 (T. Kordula); the Pilot Project grant from the
Massey Cancer Center, Virginia Commonwealth University (T. Kordula);
grant R01 CA61774 (S. Spiegel); and the National Institute of Mental
Health Intramural Research Program (S. Milstien).
NR 55
TC 29
Z9 30
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD SEP
PY 2008
VL 6
IS 9
BP 1469
EP 1477
DI 10.1158/1541-7786.MCR-08-0082
PG 9
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 359WB
UT WOS:000260017800009
PM 18819934
ER
PT J
AU Liang, XJ
Finkel, T
Shen, DW
Yin, JJ
Aszalos, A
Gottesman, MM
AF Liang, Xing-Jie
Finkel, Toren
Shen, Ding-Wu
Yin, Jun-Jie
Aszalos, Adorjan
Gottesman, Michael M.
TI SIRT1 contributes in part to cisplatin resistance in cancer cells by
altering mitochondrial metabolism
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID LIFE-SPAN EXTENSION; CALORIE RESTRICTION; CELLULAR PHARMACOLOGY;
MULTIDRUG-RESISTANCE; REDUCED EXPRESSION; CROSS-RESISTANCE; REGULATES
SIRT1; LINES; DEACETYLASE; PROTEINS
AB Tumors frequently develop resistance to cisplatin, a platinum drug used as a cornerstone of present-day chemotherapy regimens, significantly decreasing its usefulness in the clinic. Although it is known that cisplatin-resistant (CP-r) cancer cells commonly grow more slowly and exhibit reduced uptake of various compounds, including nutrients, the effect of tumor metabolism on cisplatin resistance is unclear. It was found that in CP-r cells, uptake of 2-deoxyglucose was reduced due to dysfunction and altered morphology of mitochondria compared with cisplatin-sensitive parental cancer cells. The CP-r cells overexpressed SIRT1, a histone deacetylase that plays a central role in DNA damage response and transcriptional silencing. Incubation of drug-sensitive cells in low glucose medium induced the expression of SIRT1 and increased cellular resistance to cisplatin. Reduced SIRT1 expression by a SIRT1 SMART small interfering RNA duplex sensitized the >20-fold resistant CP-r cells to cisplatin treatment 1.5- to 2-fold, and SIRT1 overexpression by SIRT1 cDNA transfection increased cisplatin resistance in cisplatin-sensitive cells by 2- to 3-fold. Our findings therefore suggest that reduced glucose use and altered mitochondrial metabolism mediated by SIRT1 is one of several alterations that contribute to cellular resistance to cisplatin.
C1 [Liang, Xing-Jie] Natl Ctr Nanosci & Technol China, Div Nanomed & Nanobiol, Lab Nanobiomed & Nanosafety, Beijing 100190, Peoples R China.
[Finkel, Toren] NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA.
[Liang, Xing-Jie; Shen, Ding-Wu; Aszalos, Adorjan; Gottesman, Michael M.] NCI, Cell Biol Lab, Bethesda, MD 20892 USA.
[Yin, Jun-Jie] US FDA, Instrumentat & Biophys Branch, Ctr Food Safety & Appl Nutr, College Pk, MD USA.
RP Liang, XJ (reprint author), Natl Ctr Nanosci & Technol China, Div Nanomed & Nanobiol, Lab Nanobiomed & Nanosafety, Beijing 100190, Peoples R China.
EM liangxj@nanoctr.cn
RI Yin, Jun Jie /E-5619-2014
FU NIH; National Cancer Institute; Chinese Academy of Sciences [07165111ZX]
FX Intramural Research Program of the NIH, National Cancer Institute and
Chinese Academy of Sciences "Hundred Talents Program" (07165111ZX).
NR 34
TC 51
Z9 52
U1 0
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD SEP
PY 2008
VL 6
IS 9
BP 1499
EP 1506
DI 10.1158/1541-7786.MCR-07-2130
PG 8
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 359WB
UT WOS:000260017800012
PM 18723829
ER
PT J
AU Paccione, RJ
Miyazaki, H
Patel, V
Waseern, A
Gutkind, JS
Zehner, ZE
Yeudall, WA
AF Paccione, Rachel J.
Miyazaki, Hiroshi
Patel, Vyomesh
Waseern, Ahmad
Gutkind, J. Silvio
Zehner, Zendra E.
Yeudall, W. Andrew
TI Keratin down-regulation in vimentin-positive cancer cells is reversible
by vimentin RNA interference, which inhibits growth and motility
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID EPITHELIAL-MESENCHYMAL TRANSITION; HUMAN BREAST-CANCER; NF-KAPPA-B;
GENE-EXPRESSION; INTERMEDIATE FILAMENTS; TUMOR PROGRESSION;
CARCINOMA-CELLS; IN-VITRO; METASTASIS; INVASION
AB At later stages of tumor progression, epithelial carcinogenesis is associated with transition to a mesenchymal phenotype, which may contribute to the more aggressive properties of cancer cells and may be stimulated by growth factors such as epidermal growth factor and transforming growth factors-beta. Previously, we found that cells derived from a nodal metastatic squamous cell carcinoma are highly proliferative and motile in vitro and tumorigenic in vivo. In the current study, we have investigated the role of vimentin in proliferation and motility. Cells derived from nodal metastasis express high levels of vimentin, which is undetectable in tumor cells derived from a synchronous primary lesion of tongue. Vimentin expression was enhanced by epidermal growth factor and transforming growth factor-beta both independently and in combination. Use of RNA interference resulted in the generation of stable cell lines that express constitutively low levels of vimentin. RNA interference-mediated vimentin knockdown reduced cellular proliferation, migration, and invasion through a basement membrane substitute by 3-fold compared with nontargeting controls. In addition, cells with reduced vimentin reexpressed differentiation-specific keratins K 13, K 14, and K 15 as a result of increased gene transcription as judged by quantitative PCR and promoter-reporter assays. Furthermore, cells in which vimentin expression was reduced showed a greatly decreased tumorigenic potential, as tumors developing from these cells were 70% smaller than those from control cells. The data suggest that reversal of the mesenchymal phenotype by inhibiting vimentin expression results in reexpression of epithelial characteristics and reduced tumor aggressiveness.
C1 [Paccione, Rachel J.; Miyazaki, Hiroshi; Yeudall, W. Andrew] Philips Inst Oral & Craniofacial Mol Biol, Richmond, VA 23298 USA.
[Paccione, Rachel J.; Zehner, Zendra E.; Yeudall, W. Andrew] Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Richmond, VA USA.
[Zehner, Zendra E.; Yeudall, W. Andrew] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
[Patel, Vyomesh; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, Bethesda, MD USA.
[Waseern, Ahmad] Barts & London Queen Marys Sch Med & Dent, Inst Cell & Mol Sci, Ctr Clin & Diagnost Oral Sci, London, England.
RP Yeudall, WA (reprint author), Philips Inst Oral & Craniofacial Mol Biol, POB 980566, Richmond, VA 23298 USA.
EM wayeudall@vcu.edu
RI Gutkind, J. Silvio/A-1053-2009
FU Philip Morris External Research Program UK Medical Research Council
[COSB1A1R]; Medical Research Council
FX Philip Morris External Research Program UK Medical Research Council
(COSB1A1R); Philip Morris USA (W.A. Yeudall) and Medical Research
Council (A. Waseem).
NR 50
TC 47
Z9 53
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD SEP
PY 2008
VL 7
IS 9
BP 2894
EP 2903
DI 10.1158/1535-7163.MCT-08-0450
PG 10
WC Oncology
SC Oncology
GA 350XP
UT WOS:000259387300031
PM 18790770
ER
PT J
AU Okabe, M
Szakacs, G
Reimers, MA
Suzuki, T
Hall, MD
Abe, T
Weinstein, JN
Gottesman, MM
AF Okabe, Mitsunori
Szakacs, Gergely
Reimers, Mark A.
Suzuki, Toshihiro
Hall, Matthew D.
Abe, Takaaki
Weinstein, John N.
Gottesman, Michael M.
TI Profiling SLCO and SLC22 genes in the NCI-60 cancer cell lines to
identify drug uptake transporters
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID ORGANIC CATION TRANSPORTERS; MULTIDRUG-RESISTANCE; MOLECULAR
PHARMACOLOGY; MEMBRANE TRANSPORTERS; EXPRESSION; CISPLATIN;
CHEMOSENSITIVITY; SENSITIVITY; FAMILY; CHEMORESISTANCE
AB Molecular and pharmacologic profiling of the NCI-60 cell panel offers the possibility of identifying pathways involved in drug resistance or sensitivity. Of these, decreased uptake of anticancer drugs mediated by efflux transporters represents one of the best studied mechanisms. Previous studies have also shown that uptake transporters can influence cytotoxicity by altering the cellular uptake of anticancer drugs. Using quantitative real-time PCR, we measured the mRNA expression of two solute carrier (SLC) families, the organic cation/zwitterion transporters (SLC22 family) and the organic anion transporters (SLCO family), totaling 23 genes in normal tissues and the NCI-60 cell panel. By correlating the mRNA expression pattern of the SLCO and SLC22 family member gene products with the growth-inhibitory profiles of 1,429 anticancer drugs and drug candidate compounds tested on the NCI-60 cell lines, we identified SLC proteins that are likely to play a dominant role in drug sensitivity. To substantiate some of the SLC-drug pairs for which the SLC member was predicted to be sensitizing, follow-up experiments were performed using engineered and characterized cell lines overexpressing SLC22A4 (OCTN1). As predicted by the statistical correlations, expression of SLC22A4 resulted in increased cellular uptake and heightened sensitivity to mitoxantrone and doxorubicin. Our results indicate that the gene expression database can be used to identify SLCO and SLC22 family members that confer sensitivity to cancer cells.
C1 [Okabe, Mitsunori; Szakacs, Gergely; Suzuki, Toshihiro; Hall, Matthew D.; Gottesman, Michael M.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Reimers, Mark A.; Weinstein, John N.] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Szakacs, Gergely] Hungarian Acad Sci, Inst Enzymol, Biol Res Ctr, Budapest, Hungary.
[Reimers, Mark A.] Virginia Commonwealth Univ, Dept Biostat, Richmond, VA USA.
[Suzuki, Toshihiro] Meiji Pharmaceut Univ, Dept Analyt Biochem, Tokyo, Japan.
[Abe, Takaaki] Tohoku Univ, Grad Sch Med, Dept Med, Div Nephrol Endocrinol & Vasc Med, Sendai, Miyagi, Japan.
RP Gottesman, MM (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM mgottesman@nih.gov
RI Szakacs, Gergely/A-2580-2009; Hall, Matthew/B-2132-2010
OI Szakacs, Gergely/0000-0002-9311-7827;
FU NIH, National Cancer Institute; Japan Society for the Promotion of
Science; Leukemia and Lymphoma Society
FX Intramural Research Program of the NIH, National Cancer Institute, and
Japan Society for the Promotion of Science. G. Szakacs is a Bolyai
fellow and a special fellow of the Leukemia and Lymphoma Society.
NR 40
TC 73
Z9 75
U1 3
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD SEP
PY 2008
VL 7
IS 9
BP 3081
EP 3091
DI 10.1158/1535-7163.MCT-08-0539
PG 11
WC Oncology
SC Oncology
GA 350XP
UT WOS:000259387300050
PM 18790787
ER
PT J
AU Risek, B
Bilski, P
Rice, AB
Schrader, WT
AF Risek, Boris
Bilski, Piotr
Rice, Annette B.
Schrader, William T.
TI Androgen receptor-mediated apoptosis is regulated by photoactivatable
androgen receptor ligands
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID INDEPENDENT PROSTATE-CANCER; LONG-LIVED RADICALS; CELL-DEATH; VITAMIN-C;
SINGLET OXYGEN; LNCAP CELLS; OXIDATIVE STRESS; BYSTANDER CELLS; BINDING
DOMAIN; MUTATION
AB We have studied nonsteroidal ligands of the human androgen receptor (hAR) and have shown elsewhere that when photoactivated by visible light they collide with O(2) to yield singlet oxygens ((1)O(2)) in vitro. Here we report cell killing after brief light activation ( 405 nm) of 1,2,3,4-tetrahydro-2,2-dimethyl-6-( trifluoromethyl)-8- pyridono[ 5,6-g] quinoline (TDPQ) in human prostate tumor cells. TDPQ/AR complexes were required for the death response because AR-positive LNCaP cells were killed, whereas AR-negative PC-3 cells were resistant. Excess dihydrotestosterone (DHT) blocked the TDPQ effect when the two were added together; irradiation of cells containing DHT alone had no effect. When LNCaP AR expression was suppressed using small interfering oligonucleotides targeting AR, photocytotoxicity was diminished. Conversely, stable transfection of hAR into PC-3 results were obtained using a structural isomer of TDPQ, and also the synthetic steroidal AR ligand R1881. Cell death occurred via apoptosis as demonstrated by annexin V immunostaining, nuclear condensation, and caspase inhibition. Death involved oxidative stress, because it was prevented by addition of the antioxidant ascorbic acid during photoactivation. Detection of elevated levels of 8-hydroxy-2'-deoxyguanosine in nuclei of irradiated cells indicated oxidative DNA damage. Apoptosis spread into adjacent nonirradiated cells by direct cell-cell contacts, indicative of a bystander effect. Other photoactivatable ligands are described, implying a general method for ablation of cells bearing specific nuclear hormone receptors.
C1 [Risek, Boris; Rice, Annette B.; Schrader, William T.] NIEHS, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC 27709 USA.
[Bilski, Piotr] NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA.
RP Schrader, WT (reprint author), NIEHS, Reprod & Dev Toxicol Lab, 3 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM schrader@niehs.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Institute of Environmental Health Sciences
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences.
NR 54
TC 5
Z9 5
U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD SEP
PY 2008
VL 22
IS 9
BP 2099
EP 2115
DI 10.1210/me.2007-0426
PG 17
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 343LX
UT WOS:000258856400009
PM 18562628
ER
PT J
AU Schoser, B
Bruno, C
Schneider, HC
Shin, YS
Podskarbi, T
Goldfarb, L
Muller-Felber, W
Muller-Hocker, J
AF Schoser, Benedikt
Bruno, Claudio
Schneider, Hans-Christian
Shin, Yoon S.
Podskarbi, Teodor
Goldfarb, Lev
Mueller-Felber, Wolfgang
Mueller-Hoecker, Josef
TI Unclassified polysaccharidosis of the heart and skeletal muscle in
siblings
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Article
DE glycogenosis type 4; idiopathic polysaccharide storage disease;
polyglucosan body; cardiomyopathy; heart transplantation
ID GLYCOGEN-STORAGE-DISEASE; HYPERTROPHIC CARDIOMYOPATHY; IV GLYCOGENOSIS;
AMYLOPECTINOSIS; MYOPATHY; SEQUENCE; LIGHT
AB We describe a 15-year-old boy and his 19-year-old sister with progressive dilated cardiomyopathy and mild non-progressive proximal lower limb myopathy, secondary to the accumulation of amylopectin-like fibrillar glycogen, (polyglucosan) bodies, in heart and skeletal muscle. Evidence of idiopathic amylopectinosis or polysaccharidosis was demonstrated in heart and skeletal muscle tissue by histology, electron microscopy, biochemical, and genetic analysis. In both siblings the heart muscle stored PAS-positive, proteinase-k resistant and partly diastase resistant granulo-filamentous material, simulating polyglucosan bodies. Glycogen branching enzyme activity, and phosphofructokinase enzyme activity, measured in skeletal muscle tissue and explanted heart tissue were all within the normal limits, however glycogen content was elevated. Furthermore, GBE1, PRKAG2, desmin, alpha beta-crystallin, ZASP, myotilin, and LAMP-2 gene sequencing revealed no mutation, excluding e.g. glycogen storage disease type 4 and desmin-related myofibrillar cardiomyopathies. In both patients the diagnosis of an idiopathic polysaccharidosis with progressive dilated cardiomyopathy was made, requiring heart transplantation at age 13 and 14, respectively. Both patients belong to an autosomal recessive group of biochemically and genetically unclassified severe vacuolar glycogen storage disease of the heart and skeletal muscle. Up to now unidentified glycogen synthesis or glycogen degradation pathways are supposed to contribute to this idiopathic glycogen storage disease. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Schoser, Benedikt] Univ Munich, Dept Neurol, Friedrich Baur Inst, D-80336 Munich, Germany.
[Bruno, Claudio] Univ Genoa, Dept Pediat, Neuromuscular Dis Unit, Genoa, Italy.
[Schneider, Hans-Christian] Community Hosp Reutlingen, Dept Pediat, Reutlingen, Germany.
[Shin, Yoon S.; Podskarbi, Teodor] Mol Genet & Metab Lab, Munich, Germany.
[Goldfarb, Lev] NIH, Bethesda, MD 20892 USA.
[Mueller-Felber, Wolfgang] Univ Munich, Dept Neuropediat, Friedrich Baur Inst, D-80336 Munich, Germany.
[Mueller-Hoecker, Josef] Univ Munich, Dept Pathol, D-80336 Munich, Germany.
RP Schoser, B (reprint author), Univ Munich, Dept Neurol, Friedrich Baur Inst, Ziemssenstr 1A, D-80336 Munich, Germany.
EM bschoser@med.uni-muenchen.de
RI Bruno, Claudio/A-3148-2015;
OI Bruno, Claudio/0000-0002-3426-2901; Schoser,
Benedikt/0000-0002-2757-8131
FU Intramural NIH HHS [Z01 NS002973-09]
NR 20
TC 7
Z9 7
U1 0
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD SEP-OCT
PY 2008
VL 95
IS 1-2
BP 52
EP 58
DI 10.1016/j.ymgme.2008.07.005
PG 7
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 358TS
UT WOS:000259941000009
PM 18691923
ER
PT J
AU Buccafusca, R
Venditti, CP
Kenyon, LC
Johanson, RA
Van Bockstaele, E
Ren, J
Pagliardini, S
Minarcik, J
Golden, JA
Coady, MJ
Greer, JJ
Berry, GT
AF Buccafusca, Roberto
Venditti, Charles P.
Kenyon, Lawrence C.
Johanson, Roy A.
Van Bockstaele, Elisabeth
Ren, Jun
Pagliardini, Silvia
Minarcik, Jeremy
Golden, Jeffrey A.
Coady, Michael J.
Greer, John J.
Berry, Gerard T.
TI Characterization of the null murine sodium/myo-inositol cotransporter 1
(Smit1 or Slc5a3) phenotype: Myo-inositol rescue is independent of
expression of its cognate mitochondrial ribosomal protein subunit 6
(Mrps6) gene and of phosphatidylinositol levels in neonatal brain
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Article
DE myo-inositol; phosphatidylinositol; Slc5a3 or Smit1; Mprs6; knockout;
MALDI-TOF MS; central apnea; development; lithium; galactosemia
ID ARTHROGRYPOSIS MULTIPLEX CONGENITA; DOWN-SYNDROME; LITHIUM;
MONOPHOSPHATASE; IDENTIFICATION; MECHANISM; HYPERTONICITY; GALACTOSEMIA;
METABOLISM; PHOSPHATES
AB Ablation of the murine Slc5a3 gene results in severe myo-inositol (Ins) deficiency and congenital central apnea due to abnormal respiratory rhythmogenesis. The lethal knockout phenotype may be rescued by supplementing the maternal drinking water with 1% Ins. In order to test the hypothesis that Ins deficiency leads to inositide deficiencies, which are corrected by prenatal treatment, we measured the effects of Ins rescue on Ins, phosphatidylinositol (PtdIns) and myo-inositol polyphosphate levels in brains of E18.5 knockout fetuses. As the Slc5a3 gene structure is unique in the sodium/solute cotransporter (SLC5) family, and exon 1 is shared with the mitochondrial ribosomal protein subunit 6 (Mrps6) gene, we also sought to determine whether expression of its cognate Mrps6 gene is abnormal in knockout fetuses. The mean level of Ins was increased by 92% in brains of rescued Slc5a3 knockout fetuses (0.48 versus 0.25 nmol/mg), but was still greatly reduced in comparison to wildtype (6.97 nmol/mg). The Ptdlns, InSP(5) and InsP(6) levels were normal without treatment. Mrps6 gene expression was unaffected in the E18.5 knockout fetuses. This enigmatic model is not associated with neonatal PtdIns deficiency and rescue of the phenotype may be accomplished without restoration of Ins. The biochemical mechanism that both uniformly leads to death and allows for Ins rescue remains unknown. In conclusion, in neonatal brain tissue, Mrps6 gene expression may not be contingent on function of its embedded Slc5a3 gene, while inositide deficiency may not be the mechanism of lethal apnea in null Slc5a3 mice. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Buccafusca, Roberto; Berry, Gerard T.] Childrens Hosp, Div Genet, Boston, MA 02115 USA.
[Buccafusca, Roberto; Johanson, Roy A.; Berry, Gerard T.] Thomas Jefferson Univ, Dept Pediat, Philadelphia, PA 19107 USA.
[Venditti, Charles P.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Van Bockstaele, Elisabeth] Thomas Jefferson Univ, Farber Inst Neurosci, Philadelphia, PA 19107 USA.
[Ren, Jun; Pagliardini, Silvia; Greer, John J.] Univ Alberta, Dept Physiol, Edmonton, AB T6G 2M7, Canada.
[Minarcik, Jeremy; Golden, Jeffrey A.] Univ Penn, Childrens Hosp Philadelphia, Sch Med, Dept Pathol, Philadelphia, PA 19104 USA.
[Coady, Michael J.] Univ Montreal, Dept Phys, Montreal, PQ H3C 3J7, Canada.
RP Berry, GT (reprint author), Childrens Hosp, Div Genet, Enders Bldg,Room 507,300 Longwood Ave, Boston, MA 02115 USA.
EM gerard.berry@childrens.harvard.edu
NR 77
TC 15
Z9 15
U1 1
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD SEP-OCT
PY 2008
VL 95
IS 1-2
BP 81
EP 95
DI 10.1016/j.ymgme.2008.05.008
PG 15
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 358TS
UT WOS:000259941000013
PM 18675571
ER
PT J
AU Sameni, M
Dosescu, J
Yamada, KM
Sloane, BF
Cavallo-Medved, D
AF Sameni, Mansoureh
Dosescu, Julie
Yamada, Kenneth M.
Sloane, Bonnie F.
Cavallo-Medved, Dora
TI Functional Live-Cell Imaging Demonstrates that beta(1)-Integrin Promotes
Type IV Collagen Degradation by Breast and Prostate Cancer Cells
SO MOLECULAR IMAGING
LA English
DT Article
ID COLORECTAL-CARCINOMA CELLS; CATHEPSIN-B; PLASMINOGEN-ACTIVATOR; IN-VIVO;
MATRIX-METALLOPROTEINASE; PERICELLULAR PROTEOLYSIS; 3-DIMENSIONAL
COLLAGEN; INTEGRIN EXPRESSION; MMP-13 EXPRESSION; BETA(1) INTEGRIN
AB The ability of tumor cells to adhere to, migrate on, and remodel extracellular matrices is mediated by cell surface receptors such as beta(1)-integrins. Here we conducted functional live-cell imaging in real time to investigate the effects of modulating beta(1)-integrin expression and function on proteolytic remodeling of the extracellular matrix. Human breast and prostate cancer cells were grown on reconstituted basement membrane containing a quenched fluorescent form of collagen IV. Generation of cleavage products and the resulting increases in fluorescence were imaged and quantified. Decreases in the expression and activity of beta(1)-integrin reduced digestion of quenched fluorescent-collagen IV by the breast and prostate cancer cells and correspondingly their invasion through and migration on reconstituted basement membrane. Decreased extracellular matrix degradation also was associated with changes in the constituents of proteolytic pathways: decreases in secretion of the cysteine protease cathepsin B, the matrix metalloproteinase (MMP)-13, and tissue inhibitors of metalloproteinases (TIMP)-1 and 2; a decrease in expression of MMP-14 or membrane type 1 MMP; and an increase in secretion of TIMP-3. This is the first study to demonstrate through functional live-cell imaging that downregulation of beta(1)-integrin expression and function reduces proteolysis of collagen IV by breast and prostate cancer cells.
C1 [Cavallo-Medved, Dora] Wayne State Univ, Sch Med, Dept Pharmacol, Detroit, MI 48201 USA.
Wayne State Univ, Sch Med, Barbara Ann Karmanos Canc Inst, Detroit, MI 48201 USA.
Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA.
RP Cavallo-Medved, D (reprint author), Wayne State Univ, Sch Med, Dept Pharmacol, 540 E Canfield, Detroit, MI 48201 USA.
EM dcavallo@med.wayne.edu
FU National Institutes of Health (NIH) [CA 56586, P30 CA 22453, P30 ES
06639, U54 RR02084330]; Department of Defense [PC991261]
FX This work was supported by National Institutes of Health (NIH) grant CA
56586 and Department of Defense Award PC991261. The Microscopy and
Imaging Resource Center is supported, in part, by NIH Center grants P30
CA 22453, P30 ES 06639, and U54 RR02084330. K.M.Y. was supported in part
by the intramural Research Program of the NIH, National Institute of
Dental and Craniofacial Research.
NR 49
TC 23
Z9 23
U1 0
U2 3
PU B C DECKER INC
PI HAMILTON
PA 69 JOHN STREET SOUTH, STE 310, HAMILTON, ONTARIO L8N 2B9, CANADA
SN 1535-3508
J9 MOL IMAGING
JI Mol. Imaging
PD SEP-OCT
PY 2008
VL 7
IS 5
BP 199
EP 213
DI 10.2310/7290.2008.00019
PG 15
WC Biochemical Research Methods; Radiology, Nuclear Medicine & Medical
Imaging
SC Biochemistry & Molecular Biology; Radiology, Nuclear Medicine & Medical
Imaging
GA 389EI
UT WOS:000262073300001
PM 19123990
ER
PT J
AU Bar, C
Zabel, R
Liu, SH
Stark, MJR
Schaffrath, R
AF Baer, Christian
Zabel, Rene
Liu, Shihui
Stark, Michael J. R.
Schaffrath, Raffael
TI A versatile partner of eukaryotic protein complexes that is involved in
multiple biological processes: Kti11/Dph3
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID KLUYVEROMYCES-LACTIS ZYMOCIN; SACCHAROMYCES-CEREVISIAE REVEALS;
ADP-RIBOSYLATING TOXINS; DIPHTHERIA-TOXIN; TRANSFER-RNA; TRANSLATION
ELONGATION-FACTOR-2; ELONGATOR COMPLEX; TRANSCRIPTIONAL ELONGATION;
DIPHTHAMIDE BIOSYNTHESIS; GAMMA-TOXIN
AB The Kluyveromyces lactis killer toxin zymocin insensitive 11 (KTI11) gene from Saccharomyces cerevisiae is allelic with the diphthamide synthesis 3 (DPH3) locus. Here, we present evidence that the KTI11 gene product is a versatile partner of proteins and operates in multiple biological processes. Notably, Kti11 immune precipitates contain Elp2 and Elp5, two subunits of the Elongator complex which is involved in transcription, tRNA modification and zymocin toxicity. KTI11 deletion phenocopies Elongator-minus cells and causes antisuppression of nonsense and missense suppressor tRNAs (SUP4, SOE1), zymocin resistance and protection against the tRNase attack of zymocin. In addition and unlike Elongator mutants, kti11 mutants resist diphtheria toxin (DT), protect against ADP-ribosylation of eukaryotic translation elongation factor 2 (eEF2) by DT and induce resistance against sordarin, an eEF2 poisoning antifungal. The latter phenotype applies to all diphthamide mutants (dph1-dph5) tested and Kti11/Dph3 physically interacts with diphthamide synthesis factors Dph1 and Dph2, presumably as part of a trimeric complex. Moreover, we present a separation of function mutation in KTI11, kti11-1, which dissociates zymocin resistance from DT sensitivity. It encodes a C-terminal Kti11 truncation that almost entirely abolishes Elongator interaction without affecting association with Kti13, another Kti11 partner protein.
C1 [Baer, Christian; Zabel, Rene; Schaffrath, Raffael] Univ Halle Wittenberg, Inst Genet, D-06120 Halle, Germany.
[Liu, Shihui] Natl Inst Allergy & Infect Dis, Bacteria Toxins & Therapeut Sect, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Stark, Michael J. R.] Univ Dundee, Coll Life Sci, Wellcome Trust Ctr Gene Regulat & Express, Dundee DD1 5EH, Scotland.
RP Schaffrath, R (reprint author), Univ Leicester, Dept Genet, Leicester LE1 7RH, Leics, England.
EM rs240@le.ac.uk
RI Stark, Michael/B-2815-2014
OI Stark, Michael/0000-0001-9086-191X
NR 59
TC 22
Z9 22
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0950-382X
EI 1365-2958
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD SEP
PY 2008
VL 69
IS 5
BP 1221
EP 1233
DI 10.1111/j.1365-2958.2008.06350.x
PG 13
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 334LG
UT WOS:000258222700011
PM 18627462
ER
PT J
AU Zhang, A
Rosner, JL
Martin, RG
AF Zhang, Aixia
Rosner, Judah L.
Martin, Robert G.
TI Transcriptional activation by MarA, SoxS and Rob of two tolC promoters
using one binding site: a complex promoter configuration for tolC in
Escherichia coli
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID EFFLUX PUMP; MICROARRAY DATA; REGULON; PROTEIN; SYSTEM; ORIENTATION;
RESISTANCE; SEQUENCE; OPERON; K-12
AB The Escherichia coli tolC encodes a major outer membrane protein with multiple functions in export (e.g. diverse xenobiotics, haemolysin) and as an attachment site for phage and colicins. tolC is regulated in part by MarA, SoxS and Rob, three paralogous transcriptional activators which bind a sequence called the marbox and which activate multiple antibiotic and superoxide resistance functions. Two previously identified tolC promoters, p1 and p2, are not regulated by MarA, SoxS or Rob but p2 is activated by EvgAS and PhoPQ which also regulate other functions. Using transcriptional fusions and primer extension assays, we show here that tolC has two additional strong overlapping promoters, p3 and p4, which are downstream of p1, p2 and the marbox and are activated by MarA, SoxS and Rob. p3 and p4 are configured so that a single marbox suffices to activate transcription from both promoters. At the p3 promoter, the marbox is separated by 20 bp from the -10 hexamer for RNA polymerase but at the p4 promoter, the same marbox is separated by 30 bp from the -10 hexamer. The multiple tolC promoters may allow the cell to respond to diverse environments by co-ordinating tolC transcription with other appropriate functions.
C1 [Rosner, Judah L.; Martin, Robert G.] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Zhang, Aixia] NICHHD, Cell Biol & Metab Branch, Bethesda, MD 20892 USA.
RP Rosner, JL (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM jlrosner@helix.nih.gov
FU NIH
FX We thank G. Storz for discussions. This research was supported by the
Intramural Research Program of the NIH.
NR 29
TC 16
Z9 17
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD SEP
PY 2008
VL 69
IS 6
BP 1450
EP 1455
DI 10.1111/j.1365-2958.2008.06371.x
PG 6
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 339VX
UT WOS:000258606500012
PM 18673442
ER
PT J
AU Ge, Y
Byun, JS
De Luca, P
Gueron, G
Yabe, IM
Sadiq-Ali, SG
Figg, WD
Quintero, J
Haggerty, CM
Li, QQ
De Siervi, A
Gardner, K
AF Ge, Yun
Byun, Jung S.
De Luca, Paola
Gueron, Geraldine
Yabe, Idalia M.
Sadiq-Ali, Sara G.
Figg, William D.
Quintero, Jesse
Haggerty, Cynthia M.
Li, Quentin Q.
De Siervi, Adriana
Gardner, Kevin
TI Combinatorial antileukemic disruption of oxidative homeostasis and
mitochondrial stability by the redox reactive thalidomide
2-(2,4-difluoro-phenyl)-4,5,6,7-tetrafluoro-1H-isoindole-1,3(2H)-dione
(CPS49) and flavopiridol
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID DEPENDENT KINASE INHIBITOR; NF-KAPPA-B; INDUCED APOPTOSIS; CANCER-CELLS;
S-PHASE; CYCLIN; ANALOGS; TRANSCRIPTION; MECHANISM; NECROSIS
AB 2-(2,4-Difluoro-phenyl)-4,5,6,7-tetrafluoro-1H-isoindole-1,3(2H)-dione (CPS49) is a member of a recently identified class of redox-reactive thalidomide analogs that show selective killing of leukemic cells by increasing intracellular reactive oxygen species (ROS) and targeting multiple transcriptional pathways. Flavopiridol is a semisynthetic flavonoid that inhibits cyclin-dependent kinases and also shows selective lethality against leukemic cells. The purpose of this study is to explore the efficacy and mechanism of action of the combinatorial use of the redox-reactive thalidomide CPS49 and the cyclin-dependent kinase inhibitor flavopiridol as a selective antileukemic therapeutic strategy. In combination, CPS49 and flavopiridol were found to induce selective cytotoxicity associated with mitochondrial dysfunction and elevations of ROS in leukemic cells ranging from additive to synergistic activity at low micromolar concentrations. Highest synergy was observed at the level of ROS generation with a strong correlation between cell-specific cytotoxicity and reciprocal coupling of drug-induced ROS elevation with glutathione depletion. Examination of the transcriptional targeting of CPS49 and flavopiridol combinations reveals that the drugs act in concert to initiate a cell specific transcriptional program that manipulates nuclear factor-kappa B (NF-kappa B), E2F-1, and p73 activity to promote enhanced mitochondrial instability by simultaneously elevating the expression of the proapoptotic factors BAX, BAD, p73, and PUMA while depressing expression of the antiapoptotic genes MCL1, XIAP, BCL-xL, SURVIVIN, and MDM2. The coadministration of CPS49 and flavopiridol acts through coordinate targeting of transcriptional pathways that enforce selective mitochondrial dysfunction and ROS elevation and is therefore a promising new therapeutic combination that warrants further preclinical exploration.
C1 [Ge, Yun; Byun, Jung S.; Yabe, Idalia M.; Sadiq-Ali, Sara G.; Quintero, Jesse; Haggerty, Cynthia M.; Li, Quentin Q.; De Siervi, Adriana; Gardner, Kevin] NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
[Figg, William D.] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
[De Luca, Paola; Gueron, Geraldine; De Siervi, Adriana] Univ Buenos Aires, Dept Biochem, RA-1053 Buenos Aires, DF, Argentina.
RP Gardner, K (reprint author), NCI, Lab Receptor Biol & Gene Express, Bldg 41,Rm 41-D305, Bethesda, MD 20892 USA.
EM gardnerk@mail.nih.gov
RI Figg Sr, William/M-2411-2016
FU National Cancer Institutes; National Institutes of Health
FX This work was funded through intramural research program of the National
Cancer Institutes, National Institutes of Health.
NR 42
TC 10
Z9 10
U1 0
U2 1
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD SEP
PY 2008
VL 74
IS 3
BP 872
EP 883
DI 10.1124/mol.107.040808
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 340HU
UT WOS:000258637500033
PM 18556456
ER
PT J
AU Surapureddi, S
Rana, R
Reddy, JK
Goldstein, JA
AF Surapureddi, Sailesh
Rana, Ritu
Reddy, Janardan K.
Goldstein, Joyce A.
TI Nuclear receptor coactivator 6 mediates the synergistic activation of
human cytochrome P-4502C9 by the constitutive androstane receptor and
hepatic nuclear factor-4 alpha
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID PREGNANE-X-RECEPTOR; INTERACTING PROTEIN PRIP; HUMAN CYP2B6 GENE;
NUCLEAR-RECEPTOR; CROSS-TALK; TRANSCRIPTIONAL REGULATION; COACTIVATOR
PRIP; MOUSE-LIVER; GLUCOCORTICOID RECEPTOR; SIGNAL COINTEGRATOR-2
AB Nuclear receptor coactivator 6 (NCOA6) also known as PRIP/RAP250/ASC-2 anchors a steady-state complex of cofactors and function as a transcriptional coactivator for certain nuclear receptors. This is the first study to identify NCOA6 as a hepatic nuclear factor 4 alpha (HNF4 alpha)-interacting protein. CYP2C9 is an important enzyme that metabolizes both commonly used therapeutic drugs and important endogenous compounds. We have shown previously that constitutive androstane receptor (CAR) (a xenobiotic-sensing receptor) up-regulates the CYP2C9 promoter through binding to a distal site, whereas HNF4 alpha transcriptionally up-regulates CYP2C9 via proximal sites. We demonstrate ligand-enhanced synergistic cross-talk between CAR and HNF4 alpha. We identify NCOA6 as crucial to the underlying mechanism of this cross-talk. NCOA6 was identified as an HNF4 alpha-interacting protein in this study using a yeast two-hybrid screen and GST pull-down assays. Furthermore, we identified NCOA6, CAR, and other coactivators as part of a mega complex of cofactors associated with HNF4 alpha in HepG2 cells. Although the interaction of NCOA6 with CAR is specifically through the first LXXLL motif of NCOA6, both LXXLL motifs are involved in its interaction with HNF4 alpha. Silencing of NCOA6 abrogated the synergistic activation of the CYP2C9 promoter and the synergistic induction of the CYP2C9 gene by CAR-HNF4 alpha. Chromatin immunoprecipitation analysis revealed that NCOA6 can pull down both the proximal HNF4 alpha and distal CAR binding sites of the CYP2C9 promoter and provides the basis for the recruitment of other cofactors. We conclude that the coactivator NCOA6 mediates the mechanism of the synergistic activation of the CYP2C9 gene by CAR and HNF4 alpha.
C1 [Surapureddi, Sailesh; Rana, Ritu; Goldstein, Joyce A.] NIEHS, Pharmacol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Reddy, Janardan K.] Northwestern Univ, Feinberg Sch Med, Dept Pathol, Chicago, IL USA.
RP Goldstein, JA (reprint author), NIEHS, Pharmacol Lab, NIH, A3-02,POB 12233, Res Triangle Pk, NC 27709 USA.
EM goldste1@niehs.nih.gov
RI Rana, Ritu/F-2591-2011; Goldstein, Joyce/A-6681-2012
FU National Institutes of Health [CA104578]; National Institute of
Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
National Institutes of Health and National Institute of Environmental
Health Sciences (to S. S., R. R., and J. A. G.) and in part by National
Institutes of Health grant CA104578 (to J. K. R.).
NR 59
TC 24
Z9 24
U1 0
U2 0
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD SEP
PY 2008
VL 74
IS 3
BP 913
EP 923
DI 10.1124/mol.108.048983
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 340HU
UT WOS:000258637500037
PM 18552123
ER
PT J
AU Phillips, M
Ladouceur, C
Drevets, W
AF Phillips, M. L.
Ladouceur, C. D.
Drevets, W. C.
TI A neural model of voluntary and automatic emotion regulation:
implications for understanding the pathophysiology and neurodevelopment
of bipolar disorder
SO MOLECULAR PSYCHIATRY
LA English
DT Review
DE emotion regulation; voluntary emotion regulation; automatic emotion
regulation; affective neuroscience; neurodevelopment; bipolar disorder
ID MEDIAL PREFRONTAL CORTEX; ANTERIOR CINGULATE CORTEX; VOXEL-BASED
MORPHOMETRY; GRAY-MATTER VOLUME; EVENT-RELATED FMRI; COMPARATIVE
CYTOARCHITECTONIC ANALYSIS; CORTICOCORTICAL CONNECTION PATTERNS; HUMAN
FRONTAL-CORTEX; WORKING-MEMORY TASK; FACIAL EXPRESSIONS
AB The ability to regulate emotions is an important part of adaptive functioning in society. Advances in cognitive and affective neuroscience and biological psychiatry have facilitated examination of neural systems that may be important for emotion regulation. In this critical review we first develop a neural model of emotion regulation that includes neural systems implicated in different voluntary and automatic emotion regulatory subprocesses. We then use this model as a theoretical framework to examine functional neural abnormalities in these neural systems that may predispose to the development of a major psychiatric disorder characterized by severe emotion dysregulation, bipolar disorder.
C1 [Phillips, M. L.; Ladouceur, C. D.; Drevets, W. C.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA.
[Phillips, M. L.] Cardiff Univ, Sch Med, Dept Psychol Med, Cardiff, S Glam, Wales.
[Drevets, W. C.] NIMH, Sect Neuroimaging Mood & Anxiety Disorders, NIH, Bethesda, MD 20892 USA.
RP Phillips, M (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, 121 Meyran Ave, Pittsburgh, PA 15213 USA.
EM phillipsml@upmc.edu
RI Ladouceur, C/H-3124-2016
FU NIMH [R01( MH076971-01)]; NARSAD Independent Investigator Award; NARSAD
Young Investigator Award; NIMH DIRP
FX This study was supported by NIMH, R01( MH076971-01) to MLP; NARSAD
Independent Investigator Award to MLP; NARSAD Young Investigator Award
to CDL and NIMH DIRP support for WCD.
NR 213
TC 481
Z9 490
U1 17
U2 89
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD SEP
PY 2008
VL 13
IS 9
BP 833
EP 857
DI 10.1038/mp.2008.65
PG 25
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 339IJ
UT WOS:000258571000003
PM 18574483
ER
PT J
AU Shaltiel, G
Maeng, S
Malkesman, O
Pearson, B
Schloesser, R
Tragon, T
Rogawski, M
Gasior, M
Luckenbaugh, D
Chen, G
Manji, H
AF Shaltiel, G.
Maeng, S.
Malkesman, O.
Pearson, B.
Schloesser, R. J.
Tragon, T.
Rogawski, M.
Gasior, M.
Luckenbaugh, D.
Chen, G.
Manji, H. K.
TI Evidence for the involvement of the kainate receptor subunit GluR6
(GRIK2) in mediating behavioral displays related to behavioral symptoms
of mania
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE glutamate receptor 6 (GluR6); kainate receptors (KARs); mood-related
behaviors; bipolar disorder (BPD); knockout mice (KO); lithium
ID BIPOLAR AFFECTIVE-DISORDER; METABOTROPIC REGULATION; SYNAPTIC
PLASTICITY; SURFACE EXPRESSION; SUICIDAL-BEHAVIOR; MAJOR DEPRESSION;
CHROMOSOMES 6Q; ANIMAL-MODELS; MICE LACKING; MAP KINASE
AB The glutamate receptor 6 (GluR6 or GRIK2, one of the kainate receptors) gene resides in a genetic linkage region (6q21) associated with bipolar disorder (BPD), but its function in affective regulation is unknown. Compared with wild-type (WT) and GluR5 knockout ( KO) mice, GluR6 KO mice were more active in multiple tests and super responsive to amphetamine. In a battery of specific tests, GluR6 KO mice also exhibited less anxious or more risk-taking type behavior and less despair-type manifestations, and they also had more aggressive displays. Chronic treatment with lithium, a classic antimanic mood stabilizer, reduced hyperactivity, aggressive displays and some risk-taking type behavior in GluR6 KO mice. Hippocampal and prefrontal cortical membrane levels of GluR5 and KA-2 receptors were decreased in GluR6 KO mice, and chronic lithium treatment did not affect these decreases. The membrane levels of other glutamatergic receptors were not significantly altered by GluR6 ablation or chronic lithium treatment. Together, these biochemical and behavioral results suggest a unique role for GluR6 in controlling abnormalities related to the behavioral symptoms of mania, such as hyperactivity or psychomotor agitation, aggressiveness, driven or increased goal-directed pursuits, risk taking and supersensitivity to psychostimulants. Whether GluR6 perturbation is involved in the mood elevation or thought disturbance of mania and the cyclicity of BPD are unknown. The molecular mechanism underlying the behavioral effects of lithium in GluR6 KO mice remains to be elucidated.
C1 [Shaltiel, G.; Maeng, S.; Malkesman, O.; Pearson, B.; Schloesser, R. J.; Tragon, T.; Luckenbaugh, D.; Chen, G.; Manji, H. K.] NIMH, Mol Pathophysiol Lab, NIH, Bethesda, MD 20892 USA.
[Rogawski, M.; Gasior, M.] NINDS, Epilepsy Res Sect, NIH, Bethesda, MD 20892 USA.
RP Manji, H (reprint author), NIMH, Mol Pathophysiol Lab, NIH, Bldg 35,Room 1C-912,35 Convent Dr MSC-3711, Bethesda, MD 20892 USA.
EM manjih@mail.nih.gov
RI Rogawski, Michael/B-6353-2009; Chen, Guang/A-2570-2017;
OI Rogawski, Michael/0000-0002-3296-8193; Pearson,
Brandon/0000-0003-4807-137X
FU Intramural Program of the NIMH
FX We thank Ioline Henter for providing outstanding editorial assistance.
This work was supported by the Intramural Program of the NIMH.
NR 58
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Z9 91
U1 2
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD SEP
PY 2008
VL 13
IS 9
BP 858
EP 872
DI 10.1038/mp.2008.20
PG 15
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 339IJ
UT WOS:000258571000004
PM 18332879
ER
PT J
AU Nicodemus, KK
Marenco, S
Batten, AJ
Vakkalanka, R
Egan, MF
Straub, RE
Weinberger, DR
AF Nicodemus, K. K.
Marenco, S.
Batten, A. J.
Vakkalanka, R.
Egan, M. F.
Straub, R. E.
Weinberger, D. R.
TI Serious obstetric complications interact with
hypoxia-regulated/vascular-expression genes to influence schizophrenia
risk
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE schizophrenia; obstetric complications; hypoxia; AKT1; genes
ID FETAL GENOTYPE INCOMPATIBILITY; INDIVIDUAL PATIENT DATA; HIPPOCAMPAL
VOLUME; PROSPECTIVE COHORT; MATERNAL RECALL; EARLY-ONSET; BIRTH;
SIBLINGS; METAANALYSIS; SUSCEPTIBILITY
AB The etiology of schizophrenia is thought to include both epistasis and gene-environment interactions. We sought to test whether a set of schizophrenia candidate genes regulated by hypoxia or involved in vascular function in the brain (AKT1, BDNF, CAPON, CHRNA7, COMT, DTNBP1, GAD1, GRM3, NOTCH4, NRG1, PRODH, RGS4, TNF-alpha) interacted with serious obstetric complications to influence risk for schizophrenia. A family-based study of transmission disequilibrium was conducted in 116 trios. Twenty-nine probands had at least one serious obstetric complication (OC) using the McNeil-Sjostrom Scale, and many of the OCs reported were associated with the potential for fetal hypoxia. Analyses were conducted using conditional logistic regression and a likelihood ratio test (LRT) between nested models was performed to assess significance. Of the 13 genes examined, four (AKT1 (three SNPs), BDNF (two SNPs), DTNBP1 (one SNP) and GRM3 (one SNP)) showed significant evidence for gene-by-environment interaction (LRT P-values ranged from 0.011 to 0.037). Although our sample size was modest and the power to detect interactions was limited, we report significant evidence for genes involved in neurovascular function or regulated by hypoxia interacting with the presence of serious obstetric complications to increase risk for schizophrenia.
C1 [Nicodemus, K. K.; Marenco, S.; Batten, A. J.; Vakkalanka, R.; Egan, M. F.; Straub, R. E.; Weinberger, D. R.] NIMH, Cognit & Psyhcosis Program, IRP, NIH, Bethesda, MD 20892 USA.
RP Weinberger, DR (reprint author), NIMH, Cognit & Psyhcosis Program, IRP, NIH, Room 4S-235,10 Ctr Dr, Bethesda, MD 20892 USA.
EM weinberd@mail.nih.gov
RI Marenco, Stefano/A-2409-2008
OI Marenco, Stefano/0000-0002-2488-2365
NR 39
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U1 2
U2 11
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD SEP
PY 2008
VL 13
IS 9
BP 873
EP 877
DI 10.1038/sj.mp.4002153
PG 5
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 339IJ
UT WOS:000258571000005
PM 18195713
ER
PT J
AU Hu, JQ
Renaud, G
Golmes, T
Ferris, A
Hendrie, PC
Donahue, RE
Hughes, SH
Wolfsberg, TG
Russell, DW
Dunbar, CE
AF Hu, Jingqiong
Renaud, Gabriel
Golmes, Theotonius
Ferris, Andrea
Hendrie, Paul C.
Donahue, Robert E.
Hughes, Stephen H.
Wolfsberg, Tyra G.
Russell, David W.
Dunbar, Cynthia E.
TI Reduced genotoxicity of avian sarcoma leukosis virus vectors in rhesus
long-term repopulating cells compared to standard murine retrovirus
vectors
SO MOLECULAR THERAPY
LA English
DT Article
ID CHRONIC GRANULOMATOUS-DISEASE; GENE-THERAPY; HEMATOPOIETIC-CELLS;
INSERTIONAL MUTAGENESIS; PROGENITOR CELLS; MACAQUE GENOME; HOT-SPOTS;
INTEGRATION; SCID-X1; STEM
AB Insertional mutagenesis continues to be a major concern in hematopoietic stem-cell gene therapy. Nonconventional gene transfer vectors with more favorable integration features in comparison with conventional retrovirus and lentivirus vectors are being developed and optimized. In this study, we report for the first time a systematic analysis of 198 avian sarcoma leukosis virus (ASLV) insertion sites identified in rhesus long-term repopulating cells, and a comparison of ASLV insertion patterns to Moloney murine leukemia virus (MLV) (n = 396) and simian immunodeficiency virus (SIV) (n = 289) using the newly released rhesus genome databank. Despite a weak preference toward gene-coding regions, ASLV integration is nonclustered, does not favor gene-rich regions, transcription start sites, or CpG islands. There was no propensity for ASLV insertions within or near proto-oncogenes, and most importantly, no insertions close to or within the Mds1-Evi1 locus, which is in contrast to the significant over-representation of this insertion site for MLV vectors in the same transplantation model. Furthermore, ASLV long terminal repeats (LTRs) do not have detectable promoter and enhancer activity in a quantitative luciferase assay to measure neighboring gene activation. The combination of these features is unique for ASLV and suggests that optimized vectors based on this virus could be useful and safe for gene transfer to hematopoietic stem cells and progenitor cells.
C1 [Hu, Jingqiong; Golmes, Theotonius; Donahue, Robert E.; Dunbar, Cynthia E.] NHLBI, Mol Hematopoiesis Sect, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Renaud, Gabriel; Wolfsberg, Tyra G.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
[Ferris, Andrea; Hughes, Stephen H.] NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA.
[Hendrie, Paul C.; Russell, David W.] Univ Washington, Dept Med, Div Hematol, Seattle, WA 98195 USA.
RP Dunbar, CE (reprint author), NHLBI, Mol Hematopoiesis Sect, Hematol Branch, NIH, Bldg 10 CRC,Room 4-5132,10 Ctr Dr, Bethesda, MD 20892 USA.
EM dunbarc@nhlbi.nih.gov
FU National Heart, Lung, Blood Institute; National Human Genome Research
Institute; National Cancer Institute of the National Institutes of
Health
FX The authors thank Stephanie Sellers for assistance with CD34+ cell
purification and culture, and the staff of the 5 Research Court primate
facility for excellent animal care. This work is supported by intramural
research program of National Heart, Lung, Blood Institute, National
Human Genome Research Institute, and National Cancer Institute of the
National Institutes of Health.
NR 34
TC 28
Z9 29
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1525-0016
J9 MOL THER
JI Mol. Ther.
PD SEP
PY 2008
VL 16
IS 9
BP 1617
EP 1623
DI 10.1038/mt.2008.135
PG 7
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 342KG
UT WOS:000258782400016
PM 18578011
ER
PT J
AU Ma, ZZ
Xu, W
Jensen, NH
Roth, BL
Liu-Chen, LY
Lee, DYW
AF Ma, Zhong-Ze
Xu, Wei
Jensen, Niels H.
Roth, Bryan L.
Liu-Chen, Lee-Yuan
Lee, David Y. W.
TI Isoquinoline alkaloids isolated from Corydalis yanhusuo and their
binding affinities at the dopamine D(1) receptor
SO MOLECULES
LA English
DT Article
DE Corydalis yanhusuo; isoquinoline alkaloids; d/l ratio; chiral HPLC;
dopamine receptor
ID TETRAHYDROPALMATINE; BUPRENORPHINE; RATS; TETRAHYDROPROTOBERBERINES;
CHROMATOGRAPHY; OPIATE; ENANTIOMERS; ADDICTION; STRIATUM; EXTRACT
AB Bioactivity-guided fractionation of Corydalis yanhusuo has resulted in the isolation of eight known isoquinoline alkaloids - tetrahydropalmatine, isocorypalmine, stylopine, corydaline, columbamine, coptisin, 13-methylpalmatine, and dehydrocorybulbine. The tertiary alkaloids were further analyzed by chiral HPLC to determine the ratios of d-and l-isomers. The isolated compounds were screened for their binding affinities at the dopamine D(1) receptor. Isocorypalmine had the highest affinity (K(i) = 83 nM). The structure-affinity relationships of these alkaloids are discussed.
C1 [Ma, Zhong-Ze; Lee, David Y. W.] Harvard Univ, McLean Hosp, Sch Med, Bioorgan & Nat Prod Lab, Belmont, MA 02478 USA.
[Xu, Wei; Liu-Chen, Lee-Yuan] Temple Univ, Sch Med, Dept Pharmacol, Philadelphia, PA 19140 USA.
[Xu, Wei; Liu-Chen, Lee-Yuan] Temple Univ, Sch Med, Ctr Subst Abuse Res, Philadelphia, PA 19140 USA.
[Jensen, Niels H.; Roth, Bryan L.] Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Jensen, Niels H.; Roth, Bryan L.] Univ N Carolina, Sch Med, Ctr Neurobiol, Div Med Chem & Nat Prod, Chapel Hill, NC 27599 USA.
[Jensen, Niels H.; Roth, Bryan L.] Univ N Carolina, NIMH, Psychoact Drug Screening Program, Sch Med, Chapel Hill, NC 27599 USA.
RP Lee, DYW (reprint author), Harvard Univ, McLean Hosp, Sch Med, Bioorgan & Nat Prod Lab, 115 Mill St, Belmont, MA 02478 USA.
EM wxu00001@temple.edu; niels_h_jensen@hotmail.com; bryan_roth@med.unc.edu;
lliuche@temple.edu; dlee@mclean.harvard.edu
RI Roth, Bryan/F-3928-2010
FU NCCAM/NIAAA [P01-AT-002038-04]
FX This work was supported by Center of Excellence Research Program
(P01-AT-002038-04, NCCAM/NIAAA) to D.Y.L.
NR 40
TC 32
Z9 35
U1 5
U2 26
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1420-3049
J9 MOLECULES
JI Molecules
PD SEP
PY 2008
VL 13
IS 9
BP 2303
EP 2312
DI 10.3390/molecules13092303
PG 10
WC Chemistry, Organic
SC Chemistry
GA 355UY
UT WOS:000259735800018
PM 18830156
ER
PT J
AU Blumberg, RS
Li, L
Nusrat, A
Parkos, CA
Rubin, DC
Carrington, JL
AF Blumberg, R. S.
Li, L.
Nusrat, A.
Parkos, C. A.
Rubin, D. C.
Carrington, J. L.
TI Recent insights into the integration of the intestinal epithelium within
the mucosal environment in health and disease
SO MUCOSAL IMMUNOLOGY
LA English
DT Article
ID MOUSE SMALL-INTESTINE; STEM-CELLS; CROHNS-DISEASE; IMMUNE HOMEOSTASIS;
ULCERATIVE-COLITIS; EXPRESSION; SUSCEPTIBILITY; PATHOGENESIS;
INFLAMMATION; ASSOCIATION
C1 [Carrington, J. L.] NIDDK, Bethesda, MD 20892 USA.
[Blumberg, R. S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Gastroenterol Div, Boston, MA USA.
[Li, L.] Stowers Inst Med Res, Kansas City, MO USA.
[Nusrat, A.; Parkos, C. A.] Emory Univ, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
[Rubin, D. C.] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
RP Carrington, JL (reprint author), NIDDK, Bethesda, MD 20892 USA.
EM carringj@mail.nih.gov
RI Nusrat, Asma/B-3887-2009; Parkos, Charles/B-3896-2009
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Institutes of Health, the Public Health Service; Department of
Health and Human Services
FX The Workshop on Local Influences on Health and Repair of Intestinal
Epithelium was supported by the National Institute of Diabetes and
Digestive and Kidney Diseases. The following speakers contributed to the
research presentations and discussions described in this manuscript:
Maria Abreu, James M. Anderson, David Artis, Jean-Francois Beaulieu,
Jeffrey Brown, Sean Colgan, Deborah Gumucio, Susan J. Henning, Calvin
Kuo, Andrew Leiter, W. James Nelson, Andre Ouellette, Charalabos
Pothoulakis, Don Powell, Derek Radisky, John Rioux, R. Balfour Sartor,
Ramesh Shivdasani, Thaddeus Stappenbeck, Makoto Taketo, and Melissa
Wong. The opinions expressed herein are those of the authors and do not
necessarily reflect the views of the National Institutes of Health, the
Public Health Service, or the Department of Health and Human Services.
NR 38
TC 10
Z9 11
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1933-0219
J9 MUCOSAL IMMUNOL
JI Mucosal Immunol.
PD SEP
PY 2008
VL 1
IS 5
BP 330
EP 334
DI 10.1038/mi.2008.29
PG 5
WC Immunology
SC Immunology
GA 366HK
UT WOS:000260471200002
PM 19079196
ER
PT J
AU Sheth, PM
Chege, D
Shin, LYY
Huibner, S
Yue, FY
Loutfy, M
Halpenny, R
Persad, D
Kovacs, C
Chun, TW
Kandel, G
Ostrowski, M
Kaul, R
AF Sheth, P. M.
Chege, D.
Shin, L. Y. Y.
Huibner, S.
Yue, F-Y
Loutfy, M.
Halpenny, R.
Persad, D.
Kovacs, C.
Chun, T-W
Kandel, G.
Ostrowski, M.
Kaul, R.
TI Immune reconstitution in the sigmoid colon after long-term HIV therapy
SO MUCOSAL IMMUNOLOGY
LA English
DT Article
ID T-CELL DEPLETION; VIRUS TYPE-1 INFECTION; GASTROINTESTINAL-TRACT;
LYMPHOID-TISSUE; ANTIRETROVIRAL THERAPY; SIV INFECTION; MUCOSAL; CD4(+);
RESPONSES; DISEASE
AB Early and profound CD4+ T-cell depletion in gut-associated lymphoid tissue (GALT) may drive Human Immunodeficiency Virus (HIV) immunopathogenesis, and GALT immune reconstitution on highly active antiretroviral therapy (HAART) may be suboptimal. Blood and sigmoid colon biopsies were collected from HAART-treated individuals with undetectable blood HIV RNA for >= 4 years and from uninfected controls. HIV proviral levels and T-cell phenotype/function were examined in both compartments. CD4+ T-cell reconstitution in the sigmoid, including CD4+ T cells expressing CCR5, exceeded that in blood and did not differ from uninfected controls. Sigmoid HIV proviral load was not correlated with CD4+ reconsitution, but was correlated with the degree of mucosal CD8+ T-cell immune activation. Colonic Gag-specific T-cell responses were common, but were not associated with proviral load or immune activation. In this select study population, long-term HAART was associated with complete CD4+ T-cell reconstitution in sigmoid colon. However, colonic immune activation may drive ongoing HIV replication.
C1 [Sheth, P. M.; Chege, D.; Shin, L. Y. Y.; Huibner, S.; Kaul, R.] Univ Toronto, Dept Med, Toronto, ON, Canada.
[Yue, F-Y; Ostrowski, M.] Univ Toronto, Dept Immunol, Toronto, ON, Canada.
[Yue, F-Y; Loutfy, M.; Halpenny, R.; Persad, D.; Kovacs, C.] Canadian Immunodeficiency Res Collaborat, Toronto, ON, Canada.
[Chun, T-W] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Chun, T-W] NIAID, Off Clin Res, NIH, Bethesda, MD 20892 USA.
[Kandel, G.] St Michaels Hosp, Div Gastroenterol, Toronto, ON M5B 1W8, Canada.
[Kaul, R.] Univ Hlth Network, Dept Med, Toronto, ON, Canada.
RP Sheth, PM (reprint author), Univ Toronto, Dept Med, Toronto, ON, Canada.
EM prameet.sheth@utoronto.ca
FU Ontario HIV Treatment Network; CIHR [HOP-81735, HET-85518]; Canadian
Research Chair Program; Gilead Pharmaceuticals
FX This work was supported in part by the Ontario HIV Treatment Network (P.
S., salary award); the CIHR (R. K., HOP-81735 and HET-85518); the
Canadian Research Chair Program (R. K., salary support); and an
unrestricted research grant from Gilead Pharmaceuticals (M. O., C. K.,
and T. C.). Study sponsors played no role in study design, collection or
analysis of data, interpretation of results, writing of the manuscript,
or decision to submit for publication.
NR 37
TC 41
Z9 41
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1933-0219
J9 MUCOSAL IMMUNOL
JI Mucosal Immunol.
PD SEP
PY 2008
VL 1
IS 5
BP 382
EP 388
DI 10.1038/mi.2008.23
PG 7
WC Immunology
SC Immunology
GA 366HK
UT WOS:000260471200008
PM 19079202
ER
PT J
AU Abrahamsson, S
Packer, A
Oh, U
Burt, RK
Muraro, PA
AF Abrahamsson, Sofia
Packer, Amy
Oh, Unsong
Burt, Richard K.
Muraro, Paolo A.
TI Dose matters: different immunological effects following a reduced- or
high-intensity autologous hematopoietic stem cell transplantation
regimen in patients with multiple sclerosis
SO MULTIPLE SCLEROSIS
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the
Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of
the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th
Congress of the
Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis
CY SEP 17-20, 2008
CL Montreal, CANADA
SP Amer Comm Treatment & Res Multiple Scleros, European Comm Treatment & Res Multiple Scleros, Latin Amer Comm Treatment & Res Multiple Scleros
C1 [Abrahamsson, Sofia; Muraro, Paolo A.] Univ London Imperial Coll Sci Technol & Med, London, England.
[Packer, Amy; Oh, Unsong] NIH, Bethesda, MD 20892 USA.
[Burt, Richard K.] Northwestern Univ, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER
JI Mult. Scler.
PD SEP
PY 2008
VL 14
BP S23
EP S23
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 354YL
UT WOS:000259675700065
ER
PT J
AU Ohayon, J
Oh, U
Richert, ND
McFarland, H
AF Ohayon, Joan
Oh, Unsong
Richert, Nancy D.
McFarland, Henry
TI central nervous system vasculitis in a Subject with multiple sclerosis
on daclizumab monotherapy
SO MULTIPLE SCLEROSIS
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the
Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of
the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th
Congress of the
Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis
CY SEP 17-20, 2008
CL Montreal, CANADA
SP Amer Comm Treatment & Res Multiple Scleros, European Comm Treatment & Res Multiple Scleros, Latin Amer Comm Treatment & Res Multiple Scleros
C1 [Ohayon, Joan; Oh, Unsong; Richert, Nancy D.; McFarland, Henry] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER
JI Mult. Scler.
PD SEP
PY 2008
VL 14
BP S170
EP S170
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 354YL
UT WOS:000259675700558
ER
PT J
AU Richert, ND
Dinacci, D
Ostuni, J
McFarland, H
AF Richert, Nancy D.
Dinacci, Daria
Ostuni, John
McFarland, Henry
TI Whole brain magnetization transfer histogram metrics predict clinical
disability in multiple sclerosis patients: a 5-year follow-up study
SO MULTIPLE SCLEROSIS
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the
Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of
the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th
Congress of the
Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis
CY SEP 17-20, 2008
CL Montreal, CANADA
SP Amer Comm Treatment & Res Multiple Scleros, European Comm Treatment & Res Multiple Scleros, Latin Amer Comm Treatment & Res Multiple Scleros
C1 [Richert, Nancy D.; Ostuni, John; McFarland, Henry] NIH, Neuroimmunol Branch, Bethesda, MD 20892 USA.
[Dinacci, Daria] Univ Naples 2, Naples, Italy.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER
JI Mult. Scler.
PD SEP
PY 2008
VL 14
BP S17
EP S18
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 354YL
UT WOS:000259675700046
ER
PT J
AU Salman, Z
Evangelou, I
Talagala, SL
Ikonomidou, V
Stern, S
Hill, R
Gallo, A
Ohayon, J
Kane, R
McFarland, H
Bagnato, F
AF Salman, Zeena
Evangelou, Iordanis
Talagala, S. Lalith
Ikonomidou, Vasiliki
Stern, Susan
Hill, Rence
Gallo, Antonio
Ohayon, Joan
Kane, Robert
McFarland, Henry
Bagnato, Francesca
TI Cortical lesions in patients with multiple sclerosis: their relation
with cortical atrophy and impact on Physical and cognitive impairment
SO MULTIPLE SCLEROSIS
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the
Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of
the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th
Congress of the
Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis
CY SEP 17-20, 2008
CL Montreal, CANADA
SP Amer Comm Treatment & Res Multiple Scleros, European Comm Treatment & Res Multiple Scleros, Latin Amer Comm Treatment & Res Multiple Scleros
C1 [Salman, Zeena; Evangelou, Iordanis; Talagala, S. Lalith; Ikonomidou, Vasiliki; Stern, Susan; Hill, Rence; Gallo, Antonio; Ohayon, Joan; Kane, Robert; McFarland, Henry; Bagnato, Francesca] NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER
JI Mult. Scler.
PD SEP
PY 2008
VL 14
BP S217
EP S217
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 354YL
UT WOS:000259675700714
ER
PT J
AU Sormani, MP
Bonzano, L
Roccatagliata, L
Bruzzi, P
AF Sormani, Maria Pia
Bonzano, Laura
Roccatagliata, Luca
Bruzzi, Paolo
TI Imaging metrics that predict outcomes
SO MULTIPLE SCLEROSIS
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the
Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of
the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th
Congress of the
Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis
CY SEP 17-20, 2008
CL Montreal, CANADA
SP Amer Comm Treatment & Res Multiple Scleros, European Comm Treatment & Res Multiple Scleros, Latin Amer Comm Treatment & Res Multiple Scleros
C1 [Sormani, Maria Pia] Univ Genoa, Dept Hlth Sci, Genoa, Italy.
[Bonzano, Laura; Roccatagliata, Luca] Univ Genoa, Dept Neurosci Ophthalmol & Genet, Genoa, Italy.
[Bonzano, Laura; Roccatagliata, Luca] Univ Genoa, Magnet Resonance Ctr Nervous Syst Dis, Genoa, Italy.
[Bruzzi, Paolo] Natl Canc Inst, Dept Epidemiol & Prevent, Genoa, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER
JI Mult. Scler.
PD SEP
PY 2008
VL 14
BP S19
EP S19
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 354YL
UT WOS:000259675700051
ER
PT J
AU Cofield, SS
Jenkins, TM
Conwit, R
Cutter, G
Wolinsky, J
Lublin, F
AF Cofield, Stacey S.
Jenkins, Todd M.
Conwit, Robin
Cutter, Gary
Wolinsky, Jerry
Lublin, Fred
TI Optic neuritis and contrast letter acuity at baseline in CombiRx
SO MULTIPLE SCLEROSIS JOURNAL
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the
Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of
the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th
Congress of the
Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis
CY SEP 17-20, 2008
CL Montreal, CANADA
SP Amer Comm Treatment & Res Multiple Sclerosis, European Comm Treatment & Res Multiple Sclerosis, Latin Amer Comm Treatment & Res Multiple Sclerosis
C1 [Cofield, Stacey S.; Jenkins, Todd M.; Cutter, Gary] Univ Alabama, Birmingham, AL USA.
[Lublin, Fred] Mt Sinai Sch Med, New York, NY USA.
[Wolinsky, Jerry] Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
[Conwit, Robin] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER J
JI Mult. Scler. J.
PD SEP
PY 2008
VL 14
SU 1
BP S62
EP S62
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 354YL
UT WOS:000259675700190
ER
PT J
AU Cofield, SS
Cutter, G
Conwit, R
Wolinsky, J
Lublin, F
AF Cofield, Stacey S.
Cutter, Gary
Conwit, Robin
Wolinsky, Jerry
Lublin, Fred
TI Race, ethnicity, country of origin and infections in CombiRx
SO MULTIPLE SCLEROSIS JOURNAL
LA English
DT Meeting Abstract
CT 13th Annual Meeting of the
Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of
the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th
Congress of the
Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis
CY SEP 17-20, 2008
CL Montreal, CANADA
SP Amer Comm Treatment & Res Multiple Sclerosis, European Comm Treatment & Res Multiple Sclerosis, Latin Amer Comm Treatment & Res Multiple Sclerosis
C1 [Cofield, Stacey S.; Cutter, Gary] Univ Alabama, Birmingham, AL USA.
[Lublin, Fred] Mt Sinai Sch Med, New York, NY USA.
[Wolinsky, Jerry] Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
[Conwit, Robin] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER J
JI Mult. Scler. J.
PD SEP
PY 2008
VL 14
SU 1
BP S62
EP S62
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 354YL
UT WOS:000259675700191
ER
PT J
AU Ahn, J
Berndt, SI
Wacholder, S
Kraft, P
Kibel, AS
Yeager, M
Albanes, D
Giovannucci, E
Stampfer, MJ
Virtamo, J
Thun, MJ
Feigelson, HS
Cancel-Tassin, G
Cussenot, O
Thomas, G
Hunter, DJ
Fraumeni, JF
Hoover, RN
Chanock, SJ
Hayes, RB
AF Ahn, Jiyoung
Berndt, Sonja I.
Wacholder, Sholom
Kraft, Peter
Kibel, Adam S.
Yeager, Meredith
Albanes, Demetrius
Giovannucci, Edward
Stampfer, Meir J.
Virtamo, Jarmo
Thun, Michael J.
Feigelson, Heather Spencer
Cancel-Tassin, Geraldine
Cussenot, Olivier
Thomas, Gilles
Hunter, David J.
Fraumeni, Joseph F., Jr.
Hoover, Robert N.
Chanock, Stephen J.
Hayes, Richard B.
TI Variation in KLK genes, prostate-specific antigen and risk of prostate
cancer
SO NATURE GENETICS
LA English
DT Letter
ID SUSCEPTIBILITY; POLYMORPHISM; ASSOCIATION; PROMOTER
C1 [Ahn, Jiyoung; Berndt, Sonja I.; Wacholder, Sholom; Yeager, Meredith; Albanes, Demetrius; Thomas, Gilles; Hunter, David J.; Fraumeni, Joseph F., Jr.; Hoover, Robert N.; Chanock, Stephen J.; Hayes, Richard B.] Natl Canc Inst, Natl Inst Hlth, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Kraft, Peter; Hunter, David J.] Harvard Univ, Sch Publ Hlth, Program Mol & Genet Epidemiol, Dept Epidemiol, Boston, MA 02115 USA.
[Kibel, Adam S.] Washington Univ, Sch Med, Div Urol Surg, St Louis, MO 63110 USA.
[Giovannucci, Edward; Stampfer, Meir J.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Giovannucci, Edward; Stampfer, Meir J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Giovannucci, Edward; Stampfer, Meir J.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Giovannucci, Edward; Stampfer, Meir J.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Virtamo, Jarmo] Natl Publ Hlth Inst, Dept Hlth Promot & Chron Dis Prevent, FIN-0030 Helsinki, Finland.
[Thun, Michael J.; Feigelson, Heather Spencer] Amer Canc Soc, Dept Epidemiol & Surveillance Res, Atlanta, GA 30329 USA.
[Cancel-Tassin, Geraldine; Cussenot, Olivier] CeRePP Hop Tenon, AP HP, F-75020 Paris, France.
RP Hayes, RB (reprint author), Natl Canc Inst, Natl Inst Hlth, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM Hayesr@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015;
OI Hayes, Richard/0000-0002-0918-661X; Cancel-Tassin,
Geraldine/0000-0002-9583-6382
FU CCR NIH HHS [N01RC37004, N01-RC-45035]; Intramural NIH HHS [ZIA
CP010152-11]; NCI NIH HHS [CA55075, N01 CN045165, N01-CO-12400,
U01CA098233, N01CO12400, P01 CA055075, R01 CA112028, R01CA112028, U01
CA098233, U01 CA098710]
NR 10
TC 61
Z9 62
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD SEP
PY 2008
VL 40
IS 9
BP 1032
EP 1034
DI 10.1038/ng0908-1032
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 342CC
UT WOS:000258761200002
PM 19165914
ER
PT J
AU O'Donovan, MC
Craddock, N
Norton, N
Williams, H
Peirce, T
Moskvina, V
Nikolov, I
Hamshere, M
Carroll, L
Georgieva, L
Dwyer, S
Holmans, P
Marchini, JL
Spencer, CCA
Howie, B
Leung, HT
Hartmann, AM
Moller, HJ
Morris, DW
Shi, YY
Feng, GY
Hoffmann, P
Propping, P
Vasilescu, C
Maier, W
Rietschel, M
Zammit, S
Schumacher, J
Quinn, EM
Schulze, TG
Williams, NM
Giegling, I
Iwata, N
Ikeda, M
Darvasi, A
Shifman, S
He, L
Duan, J
Sanders, AR
Levinson, DF
Gejman, PV
Cichon, S
Nothen, MM
Gill, M
Corvin, A
Rujescu, D
Kirov, G
Owen, MJ
AF O'Donovan, Michael C.
Craddock, Nicholas
Norton, Nadine
Williams, Hywel
Peirce, Timothy
Moskvina, Valentina
Nikolov, Ivan
Hamshere, Marian
Carroll, Liam
Georgieva, Lyudmila
Dwyer, Sarah
Holmans, Peter
Marchini, Jonathan L.
Spencer, Chris C. A.
Howie, Bryan
Leung, Hin-Tak
Hartmann, Annette M.
Moeller, Hans-Juergen
Morris, Derek W.
Shi, YongYong
Feng, GuoYin
Hoffmann, Per
Propping, Peter
Vasilescu, Catalina
Maier, Wolfgang
Rietschel, Marcella
Zammit, Stanley
Schumacher, Johannes
Quinn, Emma M.
Schulze, Thomas G.
Williams, Nigel M.
Giegling, Ina
Iwata, Nakao
Ikeda, Masashi
Darvasi, Ariel
Shifman, Sagiv
He, Lin
Duan, Jubao
Sanders, Alan R.
Levinson, Douglas F.
Gejman, Pablo V.
Cichon, Sven
Noethen, Markus M.
Gill, Michael
Corvin, Aiden
Rujescu, Dan
Kirov, George
Owen, Michael J.
CA Mol Genetics Of Schizophrenia Coll
TI Identification of loci associated with schizophrenia by genome-wide
association and follow-up
SO NATURE GENETICS
LA English
DT Article
AB We carried out a genome-wide association study of schizophrenia (479 cases, 2,937 controls) and tested loci with P < 10(-5) in up to 16,726 additional subjects. Of 12 loci followed up, 3 had strong independent support (P < 5 x 10(-4)), and the overall pattern of replication was unlikely to occur by chance (P < 9 x 10(-8)). Meta-analysis provided strongest evidence for association around ZNF804A (P = 1.61 x 10(-7)) and this strengthened when the affected phenotype included bipolar disorder (P = 9.96 x 10(-9)).
C1 [O'Donovan, Michael C.; Craddock, Nicholas; Norton, Nadine; Williams, Hywel; Peirce, Timothy; Moskvina, Valentina; Nikolov, Ivan; Hamshere, Marian; Carroll, Liam; Georgieva, Lyudmila; Dwyer, Sarah; Holmans, Peter; Zammit, Stanley; Williams, Nigel M.; Kirov, George; Owen, Michael J.] Cardiff Univ, Sch Med, Dept Psychol Med, Cardiff CF14 4XN, England.
[Marchini, Jonathan L.; Spencer, Chris C. A.; Howie, Bryan] Univ Oxford, Dept Stat, Oxford OX1 3TG, England.
[Leung, Hin-Tak] Univ Cambridge, Dept Med Genet, Wellcome Trust Diabet & Inflammat Lab, Juvenile Diabet Res Fdn, Cambridge CB2 0XY, England.
[Hartmann, Annette M.; Giegling, Ina; Rujescu, Dan] Univ Munich, Div Mol & Clin Neurbiol, D-80336 Munich, Germany.
[Moeller, Hans-Juergen] Univ Munich, Dept Psychiat, D-80336 Munich, Germany.
[Morris, Derek W.; Quinn, Emma M.; Gill, Michael; Corvin, Aiden] Univ Dublin Trinity Coll, Sch Med, Neuropsychiat Genet Res Grp, Dublin 8, Ireland.
[Shi, YongYong] Shanghai Jiao Tong Univ, BioX Ctr, Shanghai 200030, Peoples R China.
[Feng, GuoYin] Shanghai Inst Mental Hlth, Shanghai 200030, Peoples R China.
[Hoffmann, Per; Vasilescu, Catalina; Cichon, Sven; Noethen, Markus M.] Univ Bonn, Dept Gen, Life & Brain Ctr, D-53105 Bonn, Germany.
[Propping, Peter; Cichon, Sven; Noethen, Markus M.] Univ Bonn, Inst Human Genet, D-53105 Bonn, Germany.
[Maier, Wolfgang] Univ Bonn, Dept Psychiat, D-53105 Bonn, Germany.
[Rietschel, Marcella] Cent Inst Mental Hlth, Div Genet Epidemiol Psychiat, D-68159 Mannheim, Germany.
[Schumacher, Johannes; Schulze, Thomas G.] US Natl Inst Mental Hlth, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Iwata, Nakao; Ikeda, Masashi] Fujita Hlth Univ, Sch Med, Dept Psychiat, Aichi 4701192, Japan.
[Iwata, Nakao; Ikeda, Masashi] Japan Sci & Technol Agcy, CREST, Saitama 3320012, Japan.
[Darvasi, Ariel; Shifman, Sagiv] Hebrew Univ Jerusalem, Inst Life Sci, Dept Genet, IL-91904 Jerusalem, Israel.
[He, Lin] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Shanghai 200031, Peoples R China.
[Duan, Jubao; Sanders, Alan R.; Gejman, Pablo V.] Northwestern Univ, Ctr Psychiat Genet, Evanston, IL 60201 USA.
[Duan, Jubao; Sanders, Alan R.; Gejman, Pablo V.] Northwestern Univ, Feinberg Sch Med, Evanston, IL 60201 USA.
[Levinson, Douglas F.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
RP O'Donovan, MC (reprint author), Cardiff Univ, Sch Med, Dept Psychol Med, Cardiff CF14 4XN, England.
EM wpcmod@cf.ac.uk; wpcmjo@cf.ac.uk
RI turton, miranda/F-4682-2011; Schulze, Thomas/H-2157-2013; Cichon,
Sven/H-8803-2013; Cichon, Sven/B-9618-2014; Holmans, Peter/F-4518-2015;
Schumacher, Johannes/F-4970-2015; Shifman, Sagiv/D-8749-2017;
OI Buccola, Nancy/0000-0003-1378-4636; Escott-Price,
Valentina/0000-0003-1784-5483; Nothen, Markus/0000-0002-8770-2464;
Hoffmann, Per/0000-0002-6573-983X; Morris, Derek/0000-0002-3413-570X;
Gill, Michael/0000-0003-0206-5337; Cichon, Sven/0000-0002-9475-086X;
Cichon, Sven/0000-0002-9475-086X; Holmans, Peter/0000-0003-0870-9412;
Schumacher, Johannes/0000-0001-9217-6457; Shifman,
Sagiv/0000-0003-4071-5361; Corvin, Aiden/0000-0001-6717-4089; O'Donovan,
Michael/0000-0001-7073-2379; Zammit, Stanley/0000-0002-2647-9211
FU MRC; Wellcome Trust; Science Foundation Ireland; Health Research Board
(Ireland); National Genomic Network of the 'Bundesministerium fur
Bildung und Forschung' (BMBF); Alfried Krupp von Bohlen und
Halbach-Stiftung; GlaxoSmithKline.
FX The UK research was supported by grants from the MRC and the Wellcome
Trust. We are grateful to the Wellcome Trust Case Control Consortium for
access to control genotypes (and to the individuals acknowledged in that
respect in ref. 4) and their contribution to the genome-wide study, and
to the Welsh e-Science Centre at Cardiff University for access to
computing resources for some of this work. In Dublin, the research was
supported by Science Foundation Ireland, the Health Research Board
(Ireland) and the Wellcome Trust. We are grateful to J. Waddington for
sample recruitment. Irish controls were supplied by J. McPartlin and the
Trinity College Biobank. In Bonn and Mannheim, the work was supported by
the National Genomic Network of the 'Bundesministerium fur Bildung und
Forschung' (BMBF) and the Alfried Krupp von Bohlen und Halbach-Stiftung.
We also thank the Department of Psychiatry, LMU Munich for clinical
characterization of the Munich subjects and the processing of the
samples. Recruitment in Munich was partially supported by
GlaxoSmithKline. The Ashkenazi samples are part of the Hebrew University
Genetic Resource.
NR 10
TC 628
Z9 652
U1 6
U2 54
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD SEP
PY 2008
VL 40
IS 9
BP 1053
EP 1055
DI 10.1038/ng.201
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 342CC
UT WOS:000258761200014
PM 18677311
ER
PT J
AU Zody, MC
Jiang, Z
Fung, HC
Antonacci, F
Hillier, LW
Cardone, MF
Graves, TA
Kidd, JM
Cheng, Z
Abouelleil, A
Chen, L
Wallis, J
Glasscock, J
Wilson, RK
Reily, AD
Duckworth, J
Ventura, M
Hardy, J
Warren, WC
Eichler, EE
AF Zody, Michael C.
Jiang, Zhaoshi
Fung, Hon-Chung
Antonacci, Francesca
Hillier, LaDeana W.
Cardone, Maria Francesca
Graves, Tina A.
Kidd, Jeffrey M.
Cheng, Ze
Abouelleil, Amr
Chen, Lin
Wallis, John
Glasscock, Jarret
Wilson, Richard K.
Reily, Amy Denise
Duckworth, Jaime
Ventura, Mario
Hardy, John
Warren, Wesley C.
Eichler, Evan E.
TI Evolutionary toggling of the MAPT 17q21.31 inversion region
SO NATURE GENETICS
LA English
DT Article
ID PROGRESSIVE SUPRANUCLEAR PALSY; RECENT SEGMENTAL DUPLICATIONS;
HUMAN-GENOME; COPY-NUMBER; HUMAN-POPULATIONS; COMMON INVERSION;
GENE-EXPRESSION; DNA-SEQUENCE; TAU-GENE; HAPLOTYPE
AB Using comparative sequencing approaches, we investigated the evolutionary history of the European-enriched 17q21.31 MAPT inversion polymorphism. We present a detailed, BAC-based sequence assembly of the inverted human H2 haplotype and compare it to the sequence structure and genetic variation of the corresponding 1.5-Mb region for the noninverted H1 human haplotype and that of chimpanzee and orangutan. We found that inversion of the MAPT region is similarly polymorphic in other great ape species, and we present evidence that the inversions occurred independently in chimpanzees and humans. In humans, the inversion breakpoints correspond to core duplications with the LRRC37 gene family. Our analysis favors the H2 configuration and sequence haplotype as the likely great ape and human ancestral state, with inversion recurrences during primate evolution. We show that the H2 architecture has evolved more extensive sequence homology, perhaps explaining its tendency to undergo microdeletion associated with mental retardation in European populations.
C1 [Hillier, LaDeana W.; Graves, Tina A.; Wallis, John; Glasscock, Jarret; Wilson, Richard K.; Reily, Amy Denise; Warren, Wesley C.] Washington Univ, Sch Med, Genome Sequencing Ctr, St Louis, MO 63108 USA.
[Zody, Michael C.] MIT, Broad Inst, Cambridge, MA 02142 USA.
[Zody, Michael C.] Harvard Univ, Cambridge, MA 02142 USA.
[Zody, Michael C.] Uppsala Univ, Dept Med Biochem & Microbiol, SE-75124 Uppsala, Sweden.
[Jiang, Zhaoshi; Antonacci, Francesca; Kidd, Jeffrey M.; Cheng, Ze; Chen, Lin; Eichler, Evan E.] Univ Washington, Howard Hughes Med Inst, Dept Genome Sci, Seattle, WA 98195 USA.
[Fung, Hon-Chung; Hardy, John] UCL, Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England.
[Fung, Hon-Chung; Hardy, John] UCL, Reta Lila Weston Labs, London WC1N 3BG, England.
[Fung, Hon-Chung] Chang Gung Univ, Chang Gung Mem Hosp, Dept Neurol, Taipei 10591, Taiwan.
[Fung, Hon-Chung] Chang Gung Univ, Coll Med, Taipei 10591, Taiwan.
[Cardone, Maria Francesca; Ventura, Mario] Univ Bari, Dept Genet & Microbiol, I-70126 Bari, Italy.
[Duckworth, Jaime] Natl Inst Aging, Natl Inst Hlth, Neurogenet Lab, Bethesda, MD 20892 USA.
RP Warren, WC (reprint author), Washington Univ, Sch Med, Genome Sequencing Ctr, Campus Box 8501,4444 Forest Pk Ave, St Louis, MO 63108 USA.
EM wwarren@watson.wustl.edu; eee@gs.washington.edu
RI Ventura, Mario/E-6420-2011; Hardy, John/C-2451-2009; Cardone, Maria
Francesca/G-8818-2012; Antonacci, Francesca/F-5457-2013;
OI Ventura, Mario/0000-0001-7762-8777; Cardone, Maria
Francesca/0000-0002-7597-7313; Antonacci, Francesca/0000-0002-5833-6186;
Kidd, Jeffrey/0000-0002-9631-1465
FU National Human Genome Research Institute; National Institute on Aging,
National Institutes of Health, Department of Health and Human Services
[Z01 AG000957-05]; NIH [GM058815, HG002385]; Rosetta Inpharmatics
Fellowship (Merck Laboratories); Howard Hughes Medical Institute
FX We thank T. Marques, D. Reich, A. Navarro, N. Patterson, S. McCarroll,
T. Brown and K. Augustyn for critical comments and valuable discussions
in the preparation of this manuscript; C. Alkan for providing
computational assistance; and members of the Broad Institute Sequence
Platform (BISP) and Washington University Genome Sequencing Center
(WUGSC) for generating clone-based sequencing data for this project. M.
C. Z., A. A., W. C. W., L. W. H., T. A. G., R. K. W., A. D. R., J. W.,
J. G. and the BISP and WUGSC were supported by grants from the National
Human Genome Research Institute. This work was supported in part by the
Intramural Research Program of the National Institute on Aging, National
Institutes of Health, Department of Health and Human Services, project
number Z01 AG000957-05. This work was supported by NIH grants GM058815
and HG002385 to E. E. E. and a Rosetta Inpharmatics Fellowship (Merck
Laboratories) to Z. J. E. E. E. is an investigator of the Howard Hughes
Medical Institute.
NR 45
TC 101
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U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD SEP
PY 2008
VL 40
IS 9
BP 1076
EP 1083
DI 10.1038/ng.193
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 342CC
UT WOS:000258761200020
PM 19165922
ER
PT J
AU Kim, C
Sano, Y
Todorova, K
Carlson, BA
Arpa, L
Celada, A
Lawrence, T
Otsu, K
Brissette, JL
Arthur, JSC
Park, JM
AF Kim, Chun
Sano, Yasuyo
Todorova, Kristina
Carlson, Bradley A.
Arpa, Luis
Celada, Antonio
Lawrence, Toby
Otsu, Kinya
Brissette, Janice L.
Arthur, J. Simon C.
Park, Jin Mo
TI The kinase p38 alpha serves cell type-specific inflammatory functions in
skin injury and coordinates pro- and anti-inflammatory gene expression
SO NATURE IMMUNOLOGY
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; INNATE IMMUNE-RESPONSES; P38 MAP KINASE;
NF-KAPPA-B; SUBSTRATE-SPECIFICITY; MACROPHAGE APOPTOSIS; INHIBITION;
STRESS; INTERLEUKIN-10; PHOSPHATASE-1
AB The mitogen-activated protein kinase p38 mediates cellular responses to injurious stress and immune signaling. Among the many p38 isoforms, p38 alpha is the most widely expressed in adult tissues and can be targeted by various pharmacological inhibitors. Here we investigated how p38 alpha activation is linked to cell type-specific outputs in mouse models of cutaneous inflammation. We found that both myeloid and epithelial p38 alpha elicit inflammatory responses, yet p38 alpha signaling in each cell type served distinct inflammatory functions and varied depending on the mode of skin irritation. In addition, myeloid p38 alpha limited acute inflammation via activation of anti-inflammatory gene expression dependent on mitogen -and stress-activated kinases. Our results suggest a dual function for p38 alpha in the regulation of inflammation and show mixed potential for its inhibition as a therapeutic strategy.
C1 [Kim, Chun; Sano, Yasuyo; Todorova, Kristina; Brissette, Janice L.; Park, Jin Mo] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA.
[Kim, Chun; Sano, Yasuyo; Todorova, Kristina; Brissette, Janice L.; Park, Jin Mo] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Carlson, Bradley A.] NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,Natl Inst Hlth, Bethesda, MD 20892 USA.
[Arpa, Luis; Celada, Antonio] Univ Barcelona, E-08028 Barcelona, Spain.
[Arpa, Luis; Celada, Antonio] Inst Biomed Res, Macrophage Biol Grp, Barcelona 08028, Spain.
[Lawrence, Toby] Barts & London Queen Marys Sch Med & Dent, Ctr Translat Oncol, Inst Canc, London EC1M 6BQ, England.
[Lawrence, Toby] Barts & London Queen Marys Sch Med & Dent, Ctr Translat Oncol, CR UK Clin Ctr, London EC1M 6BQ, England.
[Otsu, Kinya] Osaka Univ, Grad Sch Med, Dept Cardiovasc Med, Suita, Osaka 5650871, Japan.
[Arthur, J. Simon C.] Univ Dundee, MRC, Prot Phosphorylat Unit, Sir James Black Ctr, Dundee DD1 5EH, Scotland.
RP Park, JM (reprint author), Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA.
EM jmpark@cbrc2.mgh.harvard.edu
RI Arthur, J. Simon/B-8058-2010; Lawrence, Toby/F-4461-2015
OI Arthur, J. Simon/0000-0002-8135-1958;
FU Cutaneous Biology Research Center; US National Institutes of Health
[DK043351]; Center for the Study of Inflammatory Bowel Disease at
Massachusetts General Hospital
FX We thank S. Krane (Massachusetts General Hospital) for the
MMP-13-specific antibody and advice on its use; D. Ginsburg (University
of Michigan School of Medicine) for the PAI-2-specific antibody; R.
Bravo (Bristol-Myers Squibb Pharmaceutical Research Institute) and C.
Caelles (Institute for Research in Biomedicine, Barcelona) for Dusp1-KO
mice; and M. Karin for discussion about Jnk-activation mechanisms in p38
alpha-deficient cells. Supported by the Cutaneous Biology Research
Center through the Massachusetts General Hospital-Shiseido Agreement (J.
M. P.), the US National Institutes of Health (DK043351 to D. Podolsky)
and the Center for the Study of Inflammatory Bowel Disease at
Massachusetts General Hospital (J. M. P.).
NR 50
TC 126
Z9 128
U1 2
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD SEP
PY 2008
VL 9
IS 9
BP 1019
EP 1027
DI 10.1038/ni.1640
PG 9
WC Immunology
SC Immunology
GA 339DZ
UT WOS:000258559600014
PM 18677317
ER
PT J
AU Pobezinskaya, YL
Kim, YS
Choksi, S
Morgan, MJ
Li, T
Liu, CY
Liu, ZG
AF Pobezinskaya, Yelena L.
Kim, You-Sun
Choksi, Swati
Morgan, Michael J.
Li, Tao
Liu, Chengyu
Liu, Zhenggang
TI The function of TRADD in signaling through tumor necrosis factor
receptor 1 and TRIF-dependent Toll-like receptors
SO NATURE IMMUNOLOGY
LA English
DT Article
ID NF-KAPPA-B; INDUCED CELL-DEATH; DOMAIN KINASE RIP; TNF RECEPTOR;
MEDIATED APOPTOSIS; ACTIVATION; PROTEIN; MICE; PATHWAY; TRANSDUCTION
AB The physiological function of the adaptor protein TRADD remains unclear because of the unavailability of a TRADD-deficient animal model. By generating TRADD-deficient mice, we found here that TRADD serves an important function in tumor necrosis factor receptor 1 (TNFR1) signaling by orchestrating the formation of TNFR1 signaling complexes. TRADD was essential for TNFR1 signaling in mouse embryonic fibroblasts but was partially dispensable in macrophages; abundant expression of the adaptor RIP in macrophages may have allowed some transmission of TNFR1 signals in the absence of TRADD. Although morphologically normal, TRADD-deficient mice were resistant to toxicity induced by TNF, lipopolysaccharide and polyinosinic-polycytidylic acid. TRADD was also required for TRIF-dependent Toll-like receptor signaling in mouse embryonic fibroblasts but not macrophages. Our findings definitively establish the biological function of TRADD in TNF signaling.
C1 [Pobezinskaya, Yelena L.; Kim, You-Sun; Choksi, Swati; Morgan, Michael J.; Li, Tao; Liu, Zhenggang] NCI, Cell & Canc Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Liu, Chengyu] NHLBI, Transgen Core Facil, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Liu, ZG (reprint author), NCI, Cell & Canc Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
EM zgliu@helix.nih.gov
FU Center for Cancer Research (US National Cancer Institute)
FX We thank W. C. Yeh and T. W. Mak (University of Toronto, Canada) for
Traf2-/- MEFs; H. Nakano (Juntento University, Japan) for
Traf5-/- and Traf2-/- Traf5-/- MEFs; L.
Tessarollo (US National Cancer Institute) for the pLTM260 vector; A.
Singer (US National Cancer Institute) for the pKO Scrambler 917 TK
vector; and L. Pobezinsky for suggestions. Supported by the Intramural
Research Program of Center for Cancer Research (US National Cancer
Institute).
NR 40
TC 106
Z9 110
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD SEP
PY 2008
VL 9
IS 9
BP 1047
EP 1054
DI 10.1038/ni.1639
PG 8
WC Immunology
SC Immunology
GA 339DZ
UT WOS:000258559600017
PM 18641653
ER
PT J
AU Drew, PJ
Duyn, JH
Golanov, E
Kleinfeld, D
AF Drew, Patrick J.
Duyn, Jeff H.
Golanov, Eugene
Kleinfeld, David
TI Finding coherence in spontaneous oscillations
SO NATURE NEUROSCIENCE
LA English
DT Editorial Material
ID VISUAL-CORTEX; BOLD SIGNAL; FLUCTUATIONS; RESPONSES; BEHAVIOR; NEURONS
C1 [Drew, Patrick J.; Kleinfeld, David] Univ Calif San Diego, Dept Phys, La Jolla, CA 92093 USA.
[Golanov, Eugene] NINDS, Extramural Res Program, Bethesda, MD 20892 USA.
RP Drew, PJ (reprint author), Univ Calif San Diego, Dept Phys, La Jolla, CA 92093 USA.
EM dk@physics.ucsd.edu
RI Duyn, Jozef/F-2483-2010; Golanov, Eugene/B-6462-2011;
OI Golanov, Eugene/0000-0003-0220-822X; Drew, Patrick/0000-0002-7483-7378
NR 15
TC 21
Z9 21
U1 1
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1097-6256
J9 NAT NEUROSCI
JI Nat. Neurosci.
PD SEP
PY 2008
VL 11
IS 9
BP 991
EP 993
DI 10.1038/nn0908-991
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA 341NA
UT WOS:000258720000004
PM 18725901
ER
PT J
AU Hasko, G
Linden, J
Cronstein, B
Pacher, P
AF Hasko, Gyorgy
Linden, Joel
Cronstein, Bruce
Pacher, Pal
TI Adenosine receptors: therapeutic aspects for inflammatory and immune
diseases
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Review
ID ISCHEMIA-REPERFUSION INJURY; MARROW-DERIVED CELLS; REGULATORY T-CELLS;
SUPEROXIDE ANION GENERATION; MURINE SEPTIC PERITONITIS; ENDOTHELIAL
GROWTH-FACTOR; HUMAN DENDRITIC CELLS; IFN-GAMMA PRODUCTION; TNF-ALPHA
PRODUCTION; HUMAN MAST-CELLS
AB Adenosine is a key endogenous molecule that regulates tissue function by activating four G-protein-coupled adenosine receptors: A(1), A(2A), A(2B) and A(3). Cells of the immune system express these receptors and are responsive to the modulatory effects of adenosine in an inflammatory environment. Animal models of asthma, ischaemia, arthritis, sepsis, inflammatory bowel disease and wound healing have helped to elucidate the regulatory roles of the various adenosine receptors in dictating the development and progression of disease. This recent heightened awareness of the role of adenosine in the control of immune and inflammatory systems has generated excitement regarding the potential use of adenosine-receptor-based therapies in the treatment of infection, autoimmunity, ischaemia and degenerative diseases.
C1 [Hasko, Gyorgy] Univ Med & Dent New Jersey, Dept Surg, New Jersey Med Sch, Newark, NJ 07103 USA.
[Linden, Joel] Univ Virginia, Dept Med, Charlottesville, VA 22908 USA.
[Linden, Joel] Univ Virginia, Cardiovasc Res Ctr, Charlottesville, VA 22908 USA.
[Cronstein, Bruce] NYU, Sch Med, Dept Med, New York, NY 10016 USA.
[Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, Bethesda, MD 20892 USA.
RP Hasko, G (reprint author), Univ Med & Dent New Jersey, Dept Surg, New Jersey Med Sch, 185 S Orange Ave, Newark, NJ 07103 USA.
EM haskoge@umdnj.edu
RI Pacher, Pal/B-6378-2008
OI Pacher, Pal/0000-0001-7036-8108
FU National Institutes of Health (NIH) [R01GM66189]; Intramural Research
Program of NIH; National Institute on Alcohol Abuse and Alcoholism
FX This work was supported by the National Institutes of Health (NIH) Grant
R01GM66189 and the Intramural Research Program of NIH, National
Institute on Alcohol Abuse and Alcoholism.
NR 130
TC 478
Z9 490
U1 4
U2 45
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD SEP
PY 2008
VL 7
IS 9
BP 759
EP 770
DI 10.1038/nrd2638
PG 12
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA 344GV
UT WOS:000258915800018
PM 18758473
ER
PT J
AU Singh, K
Gittis, AG
Nguyen, P
Gowda, DC
Miller, LH
Garboczi, DN
AF Singh, Kavita
Gittis, Apostolos G.
Nguyen, Phuc
Gowda, D. Channe
Miller, Louis H.
Garboczi, David N.
TI Structure of the DBL3x domain of pregnancy-associated malaria protein
VAR2CSA complexed with chondroitin sulfate A
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID FALCIPARUM-INFECTED ERYTHROCYTES; N-TERMINAL DOMAIN;
PLASMODIUM-FALCIPARUM; HUMAN PLACENTA; VACCINE CANDIDATE; DIFFRACTION
DATA; ADHERENCE; RECEPTOR; BINDING; SURFACE
AB Plasmodium falciparum-infected erythrocytes bind to chondroitin sulfate A (CSA) in the placenta via the VAR2CSA protein, a member of the P. falciparum erythrocyte membrane protein-1 family, leading to life-threatening malaria in pregnant women with severe effects on their fetuses and newborns. Here we describe the structure of the CSA binding DBL3x domain, a Duffy binding-like (DBL) domain of VAR2CSA. By forming a complex of DBL3x with CSA oligosaccharides and determining its structure, we have identified the CSA binding site to be a cluster of conserved positively charged residues on subdomain 2 and subdomain 3. Mutation or chemical modification of lysine residues at the site markedly diminished CSA binding to DBL3x. The location of the CSA binding site is an important step forward in the molecular understanding of pregnancy-associated malaria and offers a new target for vaccine development.
C1 [Singh, Kavita; Gittis, Apostolos G.; Nguyen, Phuc; Garboczi, David N.] NIAID, Struct Biol Sect, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Gowda, D. Channe] Penn State Univ, Coll Med, Dept Biochem & Mol Biol, Hershey, PA 17033 USA.
[Miller, Louis H.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD 20852 USA.
RP Singh, K (reprint author), NIAID, Struct Biol Sect, Immunogenet Lab, NIH, 12441 Parklawn Dr, Rockville, MD 20852 USA.
EM ksingh@niaid.nih.gov; dgarboczi@niaid.nih.gov
FU US Department of Energy; Office of Science; Office of Basic Energy
Sciences [W-31-109-Eng-38]; US National Institutes of Health; National
Institute of Allergy and Infectious Diseases [AI45086]
FX We thank A. Diouf and C. A. Long (Laboratory of Malaria and Vector
Research, National Institute of Allergy and Infectious Diseases) for
screening monoclonal antibodies, J.F. Andersen for helping with ITC, S.
Madala for giving assistance with flow cytometry, H.-P. Su for advising
on molecular biology, J.M. Moore for helping with initial protein
purification and J.D. Smith (Seattle Biomedical Research Institute) for
giving us the A4 genomic DNA. X-ray data were collected at the SBC-CAT
and SER-CAT beamlines at the Advanced Photon Source supported by the US
Department of Energy, Office of Science, Office of Basic Energy
Sciences, under contract W-31-109-Eng-38. This work was supported by the
Intramural Research Program of the US National Institutes of Health,
National Institute of Allergy and Infectious Diseases and by grant
AI45086 for work performed in the laboratory of D. C. Gowda.
NR 39
TC 61
Z9 62
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD SEP
PY 2008
VL 15
IS 9
BP 932
EP 938
DI 10.1038/nsmb.1479
PG 7
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 344LL
UT WOS:000258928400012
PM 19172746
ER
PT J
AU Downs, JL
Mattison, JA
Ingram, DK
Urbanski, HF
AF Downs, Jodi L.
Mattison, Julie A.
Ingram, Donald K.
Urbanski, Henryk F.
TI Effect of age and caloric restriction on circadian adrenal steroid
rhythms in rhesus macaques
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE adrenal steroids; aging; caloric restriction; circadian; cortisol;
DHEAS; endocrine rhythms; primate
ID DEHYDROEPIANDROSTERONE-SULFATE; LIFE-SPAN; IDENTIFYING BIOMARKERS;
DIETARY RESTRICTION; NUTRITIONAL-STATUS; OXIDATIVE STRESS; FOOD
RESTRICTION; BLOOD-CHEMISTRY; MONKEYS; LONGEVITY
AB Dietary caloric restriction (CR) slows aging, extends lifespan, and reduces the occurrence of age-related diseases in short-lived species. However, it is unclear whether CR can exert similar beneficial effects in long-lived species, like primates. Our objective was to determine if CR could attenuate purported age-related changes in the 24-h release of adrenal steroids. To this end, we examined 24-h plasma profiles of cortisol, and dehydroepiandrosterone sulfate (DHEAS) in young and old, mate and female rhesus macaques (Macaca mulatta) subjected to either ad libitum (AL)-feeding or CR (70% of AL) for 2-4 years. Hormone profiles from young monkeys showed pronounced 24-h rhythms. 'Cortisol concentrations were higher in old mates but not females, whereas DHEAS rhythms were dampened with age in both sexes. The cortisol rhythms of old CR males resembled those of young control males. However, CR failed to prevent age-related declines in DHEAS and further dampened DHEAS rhythms in both sexes. Apart from the partial attenuation of the age-related cortisol elevation in the old males, 24-h adrenal steroid rhythms did not benefit from late-onset CR. Published by Elsevier Inc.
C1 [Downs, Jodi L.; Urbanski, Henryk F.] Oregon Reg Primate Res Ctr, Div Neurosci, Beaverton, OR 97006 USA.
[Downs, Jodi L.; Urbanski, Henryk F.] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Portland, OR 97239 USA.
[Downs, Jodi L.; Urbanski, Henryk F.] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97239 USA.
[Mattison, Julie A.; Ingram, Donald K.] NIA, Intramural Res Program, Lab Expt Gerontol, Baltimore, MD 21224 USA.
[Ingram, Donald K.] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Nutr Neurosci & Aging Lab, Baton Rouge, LA 70808 USA.
RP Urbanski, HF (reprint author), Oregon Reg Primate Res Ctr, Div Neurosci, 505 NW 185th Ave, Beaverton, OR 97006 USA.
EM urbanski@ohsu.edu
FU NCRR NIH HHS [P51 RR000163, K01 RR000163, P51 RR000163-450158, P51
RR000163-486757, RR-00163]; NIA NIH HHS [AG-023477, AG-029612, AG-19914,
R01 AG019914, R01 AG019914-04, R01 AG029612, R01 AG029612-01A1, T32
AG023477]; NICHD NIH HHS [HD-29186, R01 HD029186, R01 HD029186-09]
NR 53
TC 26
Z9 26
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD SEP
PY 2008
VL 29
IS 9
BP 1412
EP 1422
DI 10.1016/j.neurobiolaging.2007.03.01
PG 11
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 331UF
UT WOS:000258037400012
PM 17420071
ER
PT J
AU Nolte, MW
Loscher, W
Herden, C
Freed, WJ
Gernert, M
AF Nolte, Marc W.
Loescher, Wolfgang
Herden, Christiane
Freed, William J.
Gernert, Manuela
TI Benefits and risks of intranigral transplantation of GABA-producing
cells subsequent to the establishment of kindling-induced seizures
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
DE substantia nigra pars reticulata; basal ganglia; seizures; genetically
engineered cells; gene therapy; neural transplantation; grafting;
kindling
ID TEMPORAL-LOBE EPILEPSY; LARGE T-ANTIGEN; FETAL GABAERGIC NEURONS;
SUBSTANTIA-NIGRA; ELECTRICAL STIMULATION; BEHAVIORAL SEIZURES; PIRIFORM
CORTEX; BASAL GANGLIA; TSA58 ALLELE; RATS
AB Neural transplantation has been investigated experimentally and clinically for the purpose of developing new treatment options for intractable epilepsy. In the present study we assessed the anticonvulsant efficacy and safety of bilateral allotransplantation of genetically engineered striatal GABAergic rat cell lines into the substantia nigra pars reticulata (SNr). Rats with previously-established seizures, induced by amygdala kindling, were used as a model of temporal lobe epilepsy. Three cell lines were transplanted: (1) immortalized GABAergic cells (M213-20) derived from embryonic rat striatum; (2) M213-20 cells (CL4) transfected with human GAD67 cDNA to obtain higher GABA synthesis than the parent cell line; and (3) control cells (121-11), also derived from embryonic rat striatum, but which did not show GAD expression. A second control group received injections of medium alone. Transplantation of M213-20 cells into the SNr of kindled rats resulted in significant but transient anticonvulsant effects. Neither control cells nor medium induced anticonvulsant effects. Strong tissue reactions were, however, induced in the host brain of kindled but not of non-kindled rats, and only in animals that received grafts of genetically modified CL4 cells. These tissue reactions included graft rejection, massive infiltration of inflammatory immune cells, and gliosis. The anticonvulsant effect of M213-20 cells emphasizes the feasibility of local manipulations of seizures by intranigral transplantation of GABA-producing cells. On the other hand, the present data suggest that kindling-induced activation of microglia in the SNr can enhance immune reactions to transplanted cells. In this case, under conditions of further immunological stimulation by CL4 cells, transfected with a human cDNA, substantial immune reactions occurred. Thus, it appears that the condition of the host brain and the production of foreign proteins by transplanted cells have to be considered in estimating the risks of rejection of transplants into the brain. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Loescher, Wolfgang; Gernert, Manuela] Univ Vet Med Hannover, Dept Pharmacol Toxicol & Pharm, D-30559 Hannover, Germany.
[Herden, Christiane] Univ Vet Med Hannover, Inst Pathol, D-30559 Hannover, Germany.
[Loescher, Wolfgang; Gernert, Manuela] Ctr Syst Neurosci, Hannover, Germany.
[Nolte, Marc W.] Abbott GmbH & Co KG, Dept Pharmacol, D-67061 Ludwigshafen, Germany.
[Freed, William J.] NIDA, IRP, NIH, DHHS, Baltimore, MD 21224 USA.
RP Gernert, M (reprint author), Univ Vet Med Hannover, Dept Pharmacol Toxicol & Pharm, Bunteweg 17, D-30559 Hannover, Germany.
EM manuela.gernert@tiho-hannover.de
FU German National Academic Foundation; NIDA IRP; NIH; DHHS
FX We are grateful to Michael Wei beta ing for excellent help in cell
culture. We thank Holger Volk for crucial help in immunohistology. Horst
Briese did a wonderful job in adapting a probe holder needed during the
stereotaxic transplantation procedure. The assistance of Christiane
Bartling is gratefully acknowledged. We thank Prof. Dr. Claudia Grothe
and Marco Timmer (both Dept. of Neuroanatomy, Medical School Hannover,
Germany) for methodological advice with the microtransplantation
technique. The research was supported in part by a grant of the German
National Academic Foundation to MWN and in part by the NIDA IRP, NIH,
DHHS.
NR 69
TC 17
Z9 17
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
EI 1095-953X
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD SEP
PY 2008
VL 31
IS 3
BP 342
EP 354
DI 10.1016/j.nbd.2008.05.010
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 343NY
UT WOS:000258862000007
PM 18632280
ER
PT J
AU Stranahan, AM
Lee, K
Pistell, PJ
Nelson, CM
Readal, N
Miller, MG
Spangler, EL
Ingram, DK
Mattson, MP
AF Stranahan, Alexis M.
Lee, Kim
Pistell, Paul J.
Nelson, Christopher M.
Readal, Nathaniel
Miller, Marshall G.
Spangler, Edward L.
Ingram, Donald K.
Mattson, Mark P.
TI Accelerated cognitive aging in diabetic rats is prevented by lowering
corticosterone levels
SO NEUROBIOLOGY OF LEARNING AND MEMORY
LA English
DT Article
DE stress; streptozocin; hippocampus; stone maze; aging
ID ADRENAL-STEROID RECEPTORS; MEMORY; IMPAIRMENT; ANTAGONISM; STRESS
AB Diabetes and normal aging are both characterized by increases in levels of glucocorticoids. Because long-term exposure to elevated glucocorticoids can be detrimental to hippocampal function, we evaluated the performance of young diabetic rats in the 14-unit T-maze, a task that is sensitive to hippocampal deficits. To assess the contribution of diabetes-induced elevations in corticosterone levels, we examined maze learning in diabetic rats that had levels of corticosterone 'clamped' through adrenalectomy and low-dose corticosterone replacement. For comparison, we also tested a separate group of young and aged rats in the maze. Adrenally intact diabetic rats learned poorly in the 14-unit T-maze. Preventing the increases in corticosterone levels that accompanies the onset of experimental diabetes also prevented deficits in complex maze learning. The pattern of errors made by adrenally intact diabetic rats was similar to the pattern of errors made by aged rats, suggesting that the cognitive profiles of diabetic and aged rats share common features. Published by Elsevier Inc.
C1 [Stranahan, Alexis M.; Lee, Kim; Mattson, Mark P.] Natl Inst Aging Intramural Res Program, Neurosci Lab, Cellular & Mol Neurosci Sect, Baltimore, MD USA.
[Pistell, Paul J.; Nelson, Christopher M.; Readal, Nathaniel; Miller, Marshall G.; Spangler, Edward L.; Ingram, Donald K.] Natl Inst Aging Intramural Res Program, Lab Expt Gerontol, Baltimore, MD USA.
[Pistell, Paul J.; Ingram, Donald K.] Pennington Biomed Res Ctr, Nutr Neurosci & Aging Lab, Baton Rouge, LA USA.
RP Mattson, MP (reprint author), Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
EM mattsonm@grc.nia.gov
RI Mattson, Mark/F-6038-2012;
OI Lee, Kim/0000-0002-5675-1896
FU National Institute on Aging Intramural Research
FX This research was supported by the National Institute on Aging
Intramural Research Program.
NR 13
TC 32
Z9 32
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1074-7427
J9 NEUROBIOL LEARN MEM
JI Neurobiol. Learn. Mem.
PD SEP
PY 2008
VL 90
IS 2
BP 479
EP 483
DI 10.1016/j.nlm.2008.05.005
PG 5
WC Behavioral Sciences; Neurosciences; Psychology; Psychology,
Multidisciplinary
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 347BT
UT WOS:000259114700025
PM 18579418
ER
PT J
AU Goldstein, DS
Holmes, C
Axelrod, FB
AF Goldstein, David S.
Holmes, Courtney
Axelrod, Felicia B.
TI Plasma catechols in familial dysautonomia: A long-term follow-up study
SO NEUROCHEMICAL RESEARCH
LA English
DT Article
DE familial dysautonomia; dihydroxyphenylglycol; norepinephrine; DOPA;
sympathetic nervous system
ID DOPAMINE-BETA-HYDROXYLASE; NOREPINEPHRINE; HUMANS;
DIHYDROXYPHENYLALANINE
AB This study tested whether familial dysautonomia (FD) involves progressive loss of noradrenergic nerves. Plasma levels of catechols, including dihydroxyphenylglycol (DHPG), norepinephrine (NE), dopamine (DA), and DOPA, were measured in 7 adult patients with FD and 50 healthy control subjects. FD patients were re-tested after a mean follow-up period of 13 years. Compared to controls, FD patients had low plasma levels of DHPG (P < 0.001), high DOPA and DA levels (P = 0.01, P = 0.0002), and high NE:DHPG (P < 0.0001), DA:NE (P = 0.0003), and DOPA:DHPG (P < 0.0001) ratios. At follow-up there were no changes in plasma levels of individual catechols; however, there were further increases in DOPA:DHPG ratios (mean 24 +/- 7%, P = 0.01). In FD, plasma catechol profiles are sufficiently stable, at least over a decade, to be used as a biomarker of disease involvement. An increasing DOPA:DHPG ratio suggests slight but consistent, progressive loss of noradrenergic neurons.
C1 [Goldstein, David S.; Holmes, Courtney] NINDS, NIH, Clin Neurocardiol Sect, Bethesda, MD 20892 USA.
[Axelrod, Felicia B.] NYU, Sch Med, Dysauton Ctr, Dept Pediat, New York, NY USA.
RP Goldstein, DS (reprint author), NINDS, NIH, Clin Neurocardiol Sect, Bldg 10 Room 6N252,10 Ctr Dr MSC-1620, Bethesda, MD 20892 USA.
EM goldsteind@ninds.nih.gov
FU Intramural NIH HHS [Z01 NS003033-02, Z01 NS003034-01, , Z99 NS999999]
NR 20
TC 6
Z9 6
U1 0
U2 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-3190
J9 NEUROCHEM RES
JI Neurochem. Res.
PD SEP
PY 2008
VL 33
IS 9
BP 1889
EP 1893
DI 10.1007/s11064-008-9662-4
PG 5
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 332EJ
UT WOS:000258064900028
PM 18357519
ER
PT J
AU Wu, CWW
Gu, H
Lu, HB
Stein, EA
Chen, JH
Yang, YH
AF Wu, Changwei W.
Gu, Hong
Lu, Hanbing
Stein, Elliot A.
Chen, Jyh-Horng
Yang, Yihong
TI Frequency specificity of functional connectivity in brain networks
SO NEUROIMAGE
LA English
DT Article
ID RESTING-STATE NETWORKS; MONKEY VISUAL-CORTEX; FLUCTUATIONS;
OSCILLATIONS; FMRI; MRI; CORRELATE; DISEASE; SIGNAL
AB Synchronized low-frequency spontaneous fluctuations of the functional MRI (fMRI) signal have been shown to be associated with electroencephalography (EEG) power fluctuations in multiple brain networks within predefined frequency bands. However, it remains unclear whether frequency-specific characteristics exist in the resting-state fMRI signal. in this study, fMRI signals in five functional brain networks (sensorimotor, 'default mode', visual, amygdala, and hippocampus) were decomposed into various frequency bands within a low-frequency range (0-0.24 Hz). Results show that the correlations in cortical networks concentrate within ultra-low frequencies (0.01-0.06 Hz) while connections within limbic networks distribute over a wider frequency range (0.01-0.14 Hz), suggesting distinct frequency-specific features in the resting-state PORI signal within these functional networks. Moreover, the connectivity decay rates along the frequency bands are positively Correlated with the physical distances between connected brain regions and seed points. This distance-frequency relationship might be attributed to a larger attenuation of synchrony of brain regions separated with longer distance and/or connected with more synaptic steps. Published by Elsevier Inc.
C1 [Wu, Changwei W.; Gu, Hong; Lu, Hanbing; Stein, Elliot A.; Yang, Yihong] Natl Inst Drug Abuse, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
[Wu, Changwei W.; Chen, Jyh-Horng] Natl Taiwan Univ, Dept Elect Engn, Interdisciplinary MRI MRS Lab, Taipei, Taiwan.
RP Yang, YH (reprint author), Natl Inst Drug Abuse, Neuroimaging Branch, NIH, Room 7A709,Suite 200,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM jhchen@ntu.edu.tw; YihongYang@intra.nida.nih.gov
FU National Institute on Drug Abuse (NIDA); National Institute of Health
(NIH)
FX This work was supported by the Intramural Research Program of the
National Institute on Drug Abuse (NIDA), National Institute of Health
(NIH). We would like to thank Mark Lowe and Erik Beall of the Cleveland
Clinic Foundation for providing software to correct for physiological
noise, Thomas Ross of the National Institute on Drug Abuse and Michael
Fox of Washington University for their helpful discussions on data
analysis.
NR 28
TC 52
Z9 54
U1 2
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD SEP
PY 2008
VL 42
IS 3
BP 1047
EP 1055
DI 10.1016/j.neuroimage.2008.05.035
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 343PA
UT WOS:000258864800001
PM 18632288
ER
PT J
AU Tavares, JVT
Clark, L
Furey, ML
Williams, GB
Sahakian, BJ
Drevets, WC
AF Tavares, Joana V. Taylor
Clark, Luke
Furey, Maura L.
Williams, Guy B.
Sahakian, Barbara J.
Drevets, Wayne C.
TI Neural basis of abnormal response to negative feedback in unmedicated
mood disorders
SO NEUROIMAGE
LA English
DT Article; Proceedings Paper
CT 45th Annual Meeting of the American-College-of-Neuropsychopharmacology
CY DEC 03-07, 2006
CL Hollywood, FL
SP Amer Coll Neuropsychopharmacol
ID MEDIAL PREFRONTAL CORTEX; MAJOR DEPRESSIVE DISORDER; EVENT-RELATED FMRI;
UNIPOLAR DEPRESSION; BIPOLAR DISORDER; GLUCOSE-METABOLISM; BLOOD-FLOW;
PERFORMANCE; AMYGDALA; EMOTION
AB Depressed individuals show hypersensitivity to negative feedback during cognitive testing, which can precipitate subsequent errors and thereby impair a broad range of cognitive abilities. We studied the neural mechanisms underlying this feedback hypersensitivity using functional magnetic resonance imaging (fMRI) with a reversal learning task that required subjects to ignore misleading negative feedback on some trials. Thirteen depressed subjects with major depressive disorder (MDD), 12 depressed subjects with bipolar disorder (BD) and 15 healthy controls participated. The MDD group, but not the BD group, demonstrated enhanced sensitivity to negative feedback compared to controls, as indicated by the rates of rule reversal following misleading negative feedback. In the control and BD groups, hemodynamic activity was significantly higher in the dorsomedial and ventrolateral prefrontal cortices during reversal shifting, and significantly lower in the right amygdala in response to negative feedback. The extent to which the amygdala showed less activity during negative feedback correlated inversely with the behavioral tendency to reverse after misleading feedback. This effect was not present in the MDD group, who also failed to recruit the prefrontal cortex during behavioral reversal. Hypersensitivity to negative feedback is present in unmedicated depressed patients with MDD. Disrupted top-down control by the prefrontal cortex of the amygdala may underlie this abnormal response to negative feedback in unipolar depression. (c) 2008 Elsevier Inc. All rights reserved.
C1 [Clark, Luke] Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England.
[Tavares, Joana V. Taylor; Sahakian, Barbara J.] Univ Cambridge, Addenbrookes Hosp, Dept Psychiat, Cambridge CB2 2QQ, England.
[Tavares, Joana V. Taylor; Williams, Guy B.] Univ Cambridge, Wolfson Brain Imaging Ctr, Cambridge CB2 2QQ, England.
[Tavares, Joana V. Taylor; Clark, Luke; Sahakian, Barbara J.] Univ Cambridge, Behav & Clin Neurosci Inst, Cambridge CB2 2QQ, England.
[Tavares, Joana V. Taylor; Furey, Maura L.; Drevets, Wayne C.] NIMH, Sect Neuroimaging Mood & Anxiety Disorders, NIH, Bethesda, MD 20892 USA.
RP Clark, L (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England.
EM lc260@cam.ac.uk
RI Furey, Maura/H-5273-2013
NR 45
TC 95
Z9 96
U1 5
U2 18
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD SEP
PY 2008
VL 42
IS 3
BP 1118
EP 1126
DI 10.1016/j.neuroimage.2008.05.049
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 343PA
UT WOS:000258864800007
ER
PT J
AU Tang, H
Pavel, J
Saavedra, JM
Brimijoin, S
AF Tang, Hui
Pavel, Jaroslav
Saavedra, Juan M.
Brimijoin, Stephen
TI Angiotensin II type 1 receptors may not influence response of spinal
autonomic neurons to axonal damage
SO NEUROLOGICAL RESEARCH
LA English
DT Article
DE Candesartan; immunohistochemistry; sympathetic nervous system;
neurodegeneration; primary sensory neurons
ID SPONTANEOUSLY HYPERTENSIVE-RATS; ACETYLCHOLINESTERASE ANTIBODIES; AT(1)
RECEPTORS; BINDING-SITES; BRAIN; ANTAGONIST; BLOCKADE; CORD;
HYPERTROPHY; ISCHEMIA
AB Objectives: Angiotensin II can promote cell stress, and the expression of its AT(1) receptor is characteristic of neuronal populations that die off in multiple systems atrophy and Parkinson's disease. To explore the possible significance of these facts, we undertook to: (1) clarify the distribution of AT(1) in rat neurons; (2) use selective antagonists as a means of determining whether AT(1) activation predisposes stressed neurons to die.
Methods: AT(1)-expression was examined by immunohistochemistry and by autoradiography for [(125) I]-sarcosine(1)-angiotensin II binding in sensory, motor and autonomic neurons. To induce cell loss in a specific neuronal population, rats were given systemic i.v. injection of antiacetylcholinesterase antibodies, which cause a delayed death of pre-ganglionic sympathetic neurons in the intermediolateral nucleus (IML). As pharmacologic intervention, some immunolesioned rats were treated with the selective AT(1) antagonist, Candesartan.
Results: Immunohistochemistry and autoradiography revealed AT(1) expression in dorsal root ganglia, superior cervical ganglion. In the dorsal horn of the spinal cord, AT(1) immunostainining and angiotensin binding were both prominent. In ventral horn and IML, immunoreactivity for AT(1) and choline acetyltransferase co-localized in pre-ganglionic sympathetic and somatic motor neurons. Immunolesion caused over 50% loss of IML perikarya within 3 months. Concurrent treatment with the AT(1) antagonist, Candesartan, did not affect the outcome.
Discussion: AT(1) expression is surprisingly widespread in sensory, autonomic and somatic motor neurons of the rat. This expression may be important to the normal physiology of these systems. Present data, however, do not support the concept that AT(1) activation contributes to the loss of autonomic neurons after axonal damage. [Neurol Res 2008; 30: 751-760]
C1 [Tang, Hui; Brimijoin, Stephen] Mayo Fdn, Dept Mol Pharmacol & Expt Therapeut, Rochester, MN USA.
[Pavel, Jaroslav; Saavedra, Juan M.] NIMH, Clin Sci Lab, Pharmacol Sect, Bethesda, MD 20892 USA.
RP Brimijoin, S (reprint author), Mayo Clin, Dept Mol Pharmacol & Expt Therapeut, 200 1st St SW, Rochester, MN 55905 USA.
EM Brimijoin@mayo.edu
FU NINDS [NS 32352]
FX We thank Professor B. K. Hartman for supplying the antiChAT antibody.
This work was supported by an NINDS Program Project Grant on Autonomic
Disorders (grant no. NS 32352).
NR 27
TC 5
Z9 5
U1 0
U2 4
PU MANEY PUBLISHING
PI LEEDS
PA STE 1C, JOSEPHS WELL, HANOVER WALK, LEEDS LS3 1AB, W YORKS, ENGLAND
SN 0161-6412
J9 NEUROL RES
JI Neurol. Res.
PD SEP
PY 2008
VL 30
IS 7
BP 751
EP 760
DI 10.1179/174313208X298020
PG 10
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 358FE
UT WOS:000259901700016
PM 18498681
ER
PT J
AU Mattson, MP
Wan, RQ
AF Mattson, Mark P.
Wan, Ruiqian
TI Neurotrophic factors in autonomic nervous system plasticity and
dysfunction
SO NEUROMOLECULAR MEDICINE
LA English
DT Review
DE BDNF; NGF; CNTF; sympathetic; parasympathetic; Parkinson's disease;
Alzheimer's disease
ID HEART-RATE-VARIABILITY; FIBROBLAST-GROWTH-FACTOR; SYMPATHETIC
PREGANGLIONIC NEURONS; TRANSGENIC MOUSE MODEL; GDNF FAMILY LIGANDS;
ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; DIETARY RESTRICTION;
HUNTINGTONS-DISEASE; CALORIC RESTRICTION
AB During development, neurotrophic factors are known to play important roles in regulating the survival of neurons in the autonomic nervous system (ANS) and the formation of their synaptic connectivity with their peripheral targets in the cardiovascular, digestive, and other organ systems. Emerging findings suggest that neurotrophic factors may also affect the functionality of the ANS during adult life and may, in part, mediate the effects of environmental factors such as exercise and dietary energy intake on ANS neurons and target cells. In this article, we describe the evidence that ANS neurons express receptors for multiple neurotrophic factors, and data suggesting that activation of those receptors can modify plasticity in the ANS. Neurotrophic factors that may regulate ANS function include brain-derived neurotrophic factor, nerve growth factor, insulin-like growth factors, and ciliary neurotrophic factor. The possibility that perturbed neurotrophic factor signaling is involved in the pathogenesis of ANS dysfunction in some neurological disorders is considered, together with implications for neurotrophic factor-based therapeutic interventions.
C1 [Mattson, Mark P.; Wan, Ruiqian] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
EM mattsonm@grc.nia.nih.gov
RI Mattson, Mark/F-6038-2012
FU Intramural NIH HHS
NR 154
TC 11
Z9 12
U1 0
U2 10
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1535-1084
J9 NEUROMOL MED
JI Neuromol. Med.
PD SEP
PY 2008
VL 10
IS 3
BP 157
EP 168
DI 10.1007/s12017-007-8021-y
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 337SR
UT WOS:000258456300003
PM 18172785
ER
PT J
AU McBain, CJ
AF McBain, C. J.
TI mGluR7: A fulcrum for state-dependent presynaptic metaplasticity
SO NEUROPHARMACOLOGY
LA English
DT Meeting Abstract
CT 6th International mGluR Meeting
CY SEP 14-19, 2008
CL Taormina, ITALY
C1 [McBain, C. J.] NICHD, Program Dev Neurobiol, NIH, Ctr Neurosci, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD SEP
PY 2008
VL 55
IS 4
MA 84
BP 610
EP 610
PG 1
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 353CX
UT WOS:000259544800114
ER
PT J
AU Pelkey, KA
Topolnik, L
Yuan, XQ
Lacaille, JC
McBaiin, CJ
AF Pelkey, K. A.
Topolnik, L.
Yuan, X. Q.
Lacaille, J. C.
McBaiin, C. J.
TI State-dependent cAMP sensitivity of presynaptic function controlled by
mGluR7 activation and internalization
SO NEUROPHARMACOLOGY
LA English
DT Meeting Abstract
CT 6th International mGluR Meeting
CY SEP 14-19, 2008
CL Taormina, ITALY
C1 [Pelkey, K. A.; Yuan, X. Q.; McBaiin, C. J.] NICHHD, Natl Inst Hlth, Lab Cellular & Synapt Neurophysiol, Bethesda, MD 20892 USA.
[Topolnik, L.; Lacaille, J. C.] Univ Montreal, Nerveux Cent, Dept Physiol, Grp Rech Syst, Montreal, PQ H3C 3J7, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD SEP
PY 2008
VL 55
IS 4
MA 106
BP 617
EP 617
PG 1
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 353CX
UT WOS:000259544800136
ER
PT J
AU Gardiner, JM
Brandt, KR
Baddeley, AD
Vargha-Khadem, F
Mishkin, M
AF Gardiner, John M.
Brandt, Karen R.
Baddeley, Alan D.
Vargha-Khadem, Faraneh
Mishkin, Mortimer
TI Charting the acquisition of semantic knowledge in a case of
developmental amnesia
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE developmental amnesia; episodic memory; semantic memory; hippocampus;
learning
ID RECOGNITION MEMORY; HIPPOCAMPAL PATHOLOGY; INFORMATION
AB We report the acquisition and recall of novel facts by Jon, a young adult with early onset developmental amnesia whose episodic memory is gravely impaired due to selective bilateral hippocampal damage. Jon succeeded in learning some novel facts but compared with a control group his intertrial retention was impaired during acquisition and, except for the most frequently repeated facts, he was also less accurate in correctly sourcing these facts to the experiment. The results further support the hypothesis that despite a severely compromised episodic memory and hippocampal system, there is nevertheless the capacity to accrue semantic knowledge available to recall. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Brandt, Karen R.] Univ Keele, Dept Psychol, Keele ST5 5BG, Staffs, England.
[Gardiner, John M.] Univ Sussex, Brighton BN1 9RH, E Sussex, England.
[Baddeley, Alan D.] Univ York, York YO10 5DD, N Yorkshire, England.
[Vargha-Khadem, Faraneh] Great Ormond St Hosp Sick Children, London WC1N 3JH, England.
[Vargha-Khadem, Faraneh] UCL, London, England.
[Mishkin, Mortimer] NIMH, NIH, DHHS, Bethesda, MD, England.
RP Brandt, KR (reprint author), Univ Keele, Dept Psychol, Keele ST5 5BG, Staffs, England.
EM k.r.brandt@psy.keele.ac.uk
RI Vargha-Khadem, Faraneh/C-2558-2008
FU Economic and Social Research Council [R000223887]; NIMH/NIH
FX We are grateful to Jon and to his parents for their very willing
cooperation. This research was supported by a grant from the Economic
and Social Research Council (ESRC Grant R000223887). It was also
supported in part by the Intramural Program of the NIMH/NIH. We thank
them for their support.
NR 15
TC 23
Z9 23
U1 3
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD SEP
PY 2008
VL 46
IS 11
BP 2865
EP 2868
DI 10.1016/j.neuropsychologia.2008.05.021
PG 4
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 339YB
UT WOS:000258612100030
PM 18589461
ER
PT J
AU Jensen, NH
Rodriguiz, RM
Caron, MG
Wetsel, WC
Rothman, RB
Roth, BL
AF Jensen, Niels H.
Rodriguiz, Ramona M.
Caron, Marc G.
Wetsel, William C.
Rothman, Richard B.
Roth, Bryan L.
TI N-Desalkylquetiapine, a potent norepinephrine reuptake inhibitor and
partial 5-HT1A agonist, as a putative mediator of quetiapine's
antidepressant activity
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE quetiapine; N-Desalkylquetiapine; norepinephrine reuptake inhibitor;
antidepressant; antipsychotic
ID ATYPICAL ANTIPSYCHOTIC-DRUGS; BIPOLAR-II DEPRESSION; INDUCED
WEIGHT-GAIN; CLINICAL PHARMACOKINETICS; DOUBLE-BLIND; MICE;
SCHIZOPHRENIA; RECEPTORS; SEROTONIN; BLOCKADE
AB Quetiapine is an atypical antipsychotic drug that is also US FDA approved for treating bipolar depression, albeit by an unknown mechanism. To discover the potential mechanism for this apparently unique action, we screened quetiapine, its metabolite N-Desalkylquetiapine, and dibenzo[b,f][ 1,4] thiazepine-11(10-H)-one (DBTO) against a large panel of G-protein - coupled receptors, ion channels, and neurotransmitter transporters. DBTO was inactive at all tested molecular targets. N-Desalkylquetiapine had a high affinity (3.4 nM) for the histamine H-1 receptor and moderate affinities (10 - 100 nM) for the norepinephrine reuptake transporter (NET), the serotonin 5-HT1A, 5-HT1E, 5-HT2A, 5-HT2B, 5-HT7 receptors, the alpha(1B)-adrenergic receptor, and the M-1, M-3, and M-5 muscarinic receptors. The compound had low affinities (100-1000 nM) for the 5-HT1D, 5-HT2C, 5-HT3, 5-HT5, 5-HT6, alpha(1A), alpha(2A), alpha(2B), alpha(2C), H-2, M-2, M-4, and dopamine D-1, D-2, D-3, and D-4 receptors. N-Desalkylquetiapine potently inhibited human NE transporter with a K-i of 12 nM, about 100-fold more potent than quetiapine itself. N-Desalkylquetiapine was also 10-fold more potent and more efficacious than quetiapine at the 5-HT1A receptor. N-Desalkylquetiapine was an antagonist at 5-HT2A, 5-HT2B, 5-HT2C, alpha(1A), alpha(1D), alpha(2A), alpha(2C), H-1, M-1, M-3, and M-5 receptors. In the mouse tail suspension test, N-Desalkylquetiapine displayed potent antidepressant-like activity in VMAT2 heterozygous mice at doses as low as 0.1 mg/kg. These data strongly suggest that the antidepressant activity of quetiapine is mediated, at least in part, by its metabolite N-Desalkylquetiapine through NET inhibition and partial 5-HT1A agonism. Possible contributions of this metabolite to the side effects of quetiapine are discussed.
C1 [Jensen, Niels H.; Roth, Bryan L.] Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Rodriguiz, Ramona M.; Wetsel, William C.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC USA.
[Rodriguiz, Ramona M.; Wetsel, William C.] Duke Univ, Med Ctr, Mouse Behav & Neuroendocrine Anal Core Facil, Durham, NC USA.
[Caron, Marc G.; Wetsel, William C.] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA.
[Caron, Marc G.; Wetsel, William C.] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA.
[Rothman, Richard B.] NIDA, NIH, Intramural Res Program, Clin Psychopharmacol Sect, Baltimore, MD USA.
[Roth, Bryan L.] Univ N Carolina, Sch Med, NIMH Psychoact Drug Screening Program, Chapel Hill, NC USA.
RP Roth, BL (reprint author), Univ N Carolina, Sch Med, Dept Pharmacol, 8032 Burnett Womack Bldg,CB 7365, Chapel Hill, NC 27599 USA.
EM bryan_roth@med.unc.edu
RI Roth, Bryan/F-3928-2010
FU Intramural NIH HHS; NIMH NIH HHS [R01MH60451, R01MH61887, UF1MH 082441,
N01MH32004, R01MH57635]
NR 43
TC 181
Z9 185
U1 1
U2 11
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD SEP
PY 2008
VL 33
IS 10
BP 2303
EP 2312
DI 10.1038/sj.npp.1301646
PG 10
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 336WM
UT WOS:000258395600001
PM 18059438
ER
PT J
AU Floel, A
Hummel, F
Duque, J
Knecht, S
Cohen, LG
AF Floel, Agnes
Hummel, Friedhelm
Duque, Julie
Knecht, Stefan
Cohen, Leonardo G.
TI Influence of somatosensory input on interhemispheric interactions in
patients with chronic stroke
SO NEUROREHABILITATION AND NEURAL REPAIR
LA English
DT Article
DE anesthesia; interhemispheric inhibition; neurorehabilitation; motor;
stroke
ID TRANSCRANIAL MAGNETIC STIMULATION; PRIMARY MOTOR CORTEX; TRANSCALLOSAL
INHIBITION; INTRACORTICAL CIRCUITS; CLINICAL-APPLICATION; DORSAL
PREMOTOR; HAND; RECOVERY; MUSCLE; EXCITABILITY
AB Background. Ischemia-induced Cutaneous anesthesia of the healthy hand in patients with chronic stroke elicits transient improvements of motor performance in the contralateral, paretic hand. Objective. The present Study was designed to investigate one of the possible mechanisms underlying this effect. Methods. The authors evaluated the effects of transient ischemic Cutaneous anesthesia of the healthy hand (target intervention) and healthy foot (control intervention) on transcranial magnetic stimulation-induced interhemispheric inhibition from the contralesional onto the ipsilesional primary motor cortex (M1). Ten subjects with chronic, predominantly subcortical stroke with motor impairment were assessed. Results. Cutaneous anesthesia of the intact hand but not the intact leg resulted in reduction of the inhibitory drive from the contralesional to the ipsilesional M1 both at rest and immediately preceding movements of the paretic hand. Changes in premovement interhemispheric inhibition showed a trend for correlation with improvements in finger-tapping speed in the paretic hand. Conclusion. The findings Suggest that modulation of interhemispheric inhibitory interactions between the contralesional and ipsilesional M1, either primarily or secondary to intrahemispheric excitability changes in either hemisphere, may contribute to performance improvements with cutaneous anesthesia of the intact hand. The present Study provides additional insight into the mechanisms by which rehabilitative interventions focused on training one hand and restraining the other may operate after chronic stroke.
C1 [Floel, Agnes; Hummel, Friedhelm; Duque, Julie; Cohen, Leonardo G.] NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20817 USA.
[Floel, Agnes; Hummel, Friedhelm; Duque, Julie; Cohen, Leonardo G.] NINDS, Stroke Neurorehabil Clin, NIH, Bethesda, MD 20817 USA.
[Floel, Agnes; Knecht, Stefan] Univ Munster, Dept Neurol, Munster, Germany.
RP Cohen, LG (reprint author), NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20817 USA.
EM cohenl@ninds.nih.gov
RI Floel, Agnes/A-9426-2017;
OI Knecht, Stefan/0000-0003-1056-9228
FU National Institute of Neurological Disorders and Stroke; Deutsche
Forschungsgemeinschaft [Fl 379-1/1, Fl 379-4/1]; Bundesministerium for
Bildung und Forschung [01GW0520]; Nordrhein-Westfalen Ministry of
Education and Research; Innovative Medizinische Forschung Munster
[FL110605]
FX We thank S. Ravindran for help with patient recruitment, N. Dang for
providing technical help, and C. Breitenstein for helpful discussions on
the manuscript.; This work was supported by the intramural research
program of the National Institute of Neurological Disorders and Stroke,
the Deutsche Forschungsgemeinschaft to AF (Fl 379-1/1, Fl 379-4/1), the
Bundesministerium for Bildung und Forschung to AF (01GW0520, part 4),
the Nordrhein-Westfalen Ministry of Education and Research to AF (Lise
Meitner Stipendium), and the Innovative Medizinische Forschung Munster
to AF (FL110605).; None of the authors reports any potential conflict of
interest.
NR 55
TC 30
Z9 30
U1 0
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1545-9683
J9 NEUROREHAB NEURAL RE
JI Neurorehabil. Neural Repair
PD SEP-OCT
PY 2008
VL 22
IS 5
BP 477
EP 485
DI 10.1177/1545968308316388
PG 9
WC Clinical Neurology; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 343QE
UT WOS:000258867900006
PM 18645188
ER
PT J
AU Adamec, R
Holmes, A
Blundell, J
AF Adamec, Robert
Holmes, Andrew
Blundell, Jacqueline
TI Vulnerability to lasting anxiogenic effects of brief exposure to
predator stimuli: Sex, serotonin and other factors-Relevance to PTSD
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Article; Proceedings Paper
CT Satellite Symposium on Olfaction and Aversive Emotions held in
Conjunction with the International-Behavioral-Neuroscience-Society
CY JUN, 2007
CL Rio de Janeiro, BRAZIL
SP Int Behav Neurosci Soc
DE Amygdala; Anxiety; Cat exposure; Cat odor exposure; Elevated plus maze;
Lasting effects; 5-HTT knockout mice; Limbic neuroplasticity; mPFC;
Mice; 5-HT1A; 5-HT2A; PTSD; Startle; SERT
ID POSTTRAUMATIC-STRESS-DISORDER; TRANSPORTER KNOCKOUT MICE; LONG-TERM
POTENTIATION; ANXIETY-LIKE BEHAVIOR; NATIONAL COMORBIDITY SURVEY; 5-HT
TRANSPORTER; TRAUMATIC STRESS; CAT ODOR; NEUROENDOCRINE RESPONSES;
SYSTEMIC INJECTIONS
AB Lasting anxiogenic effects of predator stress in rodents may model aspects of post-traumatic stress disorder (PTSD). There is a link between genetic variation in the serotonin (5-HT) transporter (SERT) and anxiety in humans, promoting the generation of SERT knockout mice. This review brings together studies of SERT knockout male mice, normal female mice, and different 5-HT receptors in predator stress effects on anxiety. These studies provide for a link between vulnerability to the anxiogenic effects of predator stress and abnormalities of 5-HT transmission induced by a life long reduction in 5-HT reuptake in male mice, which creates a vulnerability like that seen in normal female mice. Data reviewed suggest abnormalities in 5-HT transmission contribute to vulnerability to lasting anxiogenic effects of species relevant stressors. To the extent to which predator stress effects model aspects of PTSD, and in the light of relevant human literature, these considerations implicate abnormalities of 5-HT transmission in vulnerability to PTSD per se, and as a potential contributor to enhanced female vulnerability to PTSD. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Adamec, Robert; Blundell, Jacqueline] Mem Univ Newfoundland, Dept Psychol, St John, NF A1B 3X9, Canada.
[Holmes, Andrew] NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIMH,NIH, Bethesda, MD 20892 USA.
RP Adamec, R (reprint author), Mem Univ Newfoundland, Dept Psychol, 232 Elizabeth Ave, St John, NF A1B 3X9, Canada.
EM radamec@mun.ca
FU Intramural NIH HHS [Z01 AA000411-04]
NR 96
TC 38
Z9 38
U1 4
U2 17
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD SEP
PY 2008
VL 32
IS 7
SI SI
BP 1287
EP 1292
DI 10.1016/j.neubiorev.2008.05.005
PG 6
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 363PK
UT WOS:000260279000010
PM 18550167
ER
PT J
AU Holmes, A
AF Holmes, Andrew
TI Genetic variation in cortico-amygdala serotonin function and risk for
stress-related disease
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Article; Proceedings Paper
CT Satellite Symposium on Olfaction and Aversive Emotions held in
Conjunction with the International-Behavioral-Neuroscience-Society
CY JUN, 2007
CL Rio de Janeiro, BRAZIL
SP Int Behav Neurosci Soc
DE Stress; Gene; Strain; Mouse; Inbred; Serotonin; Serotonin transporter;
Tryptophan hydroxylase; VMAT2; MAOA; 5-HT1A; 5-HT1B; 5-HT2A; 5-HT2C;
5-HT3; Prefrontal cortex; Hippocampus; Amygdala; Anxiety; Depression;
Emergence test; Forced swim test; Restraint
ID DORSAL RAPHE NUCLEUS; MEDIAL PREFRONTAL CORTEX; RECEPTOR KNOCKOUT MICE;
ELEVATED PLUS-MAZE; RAT BASOLATERAL AMYGDALA; CENTRAL-NERVOUS-SYSTEM;
ANXIETY-LIKE BEHAVIOR; PITUITARY-ADRENAL AXIS; FORCED SWIMMING TEST;
POSTSYNAPTIC 5-HT1A RECEPTORS
AB The serotonin system is strongly implicated in the pathophysiology and therapeutic alleviation of stress-related disorders such as anxiety and depression. Serotonergic modulation of the acute response to stress and the adaptation to chronic stress is mediated by a myriad of molecules controlling serotonin neuron development (Pet-1), synthesis (tryptophan hydroxylase I and 2 isozymes), packaging (vesicular monoamine transporter 2), actions at presynaptic and postsynaptic receptors (5-HT1A, 5-HT1B, 5-HT2A, 5-HT2C, 5-HT3A, 5-HT4, 5-HT5A, 5-HT6, 5-HT7), reuptake (serotonin transporter), and degradation (monoamine oxidase A). A growing body of evidence from preclinical rodents models, and especially genetically modified mice and inbred mouse strains, has provided significant insight into how genetic variation in these molecules can affect the development and function of a key neural circuit between the dorsal raphe nucleus, medial prefrontal cortex and amygdala. By extension, such variation is hypothesized to have a major influence on individual differences in the stress response and risk for stress-related disease in humans. The current article provides an update on this rapidly evolving field of research. Published by Elsevier Ltd.
C1 NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
RP Holmes, A (reprint author), NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, 5625 Fishers Lane,Room 2N09, Rockville, MD 20852 USA.
EM holmesan@mail.nih.gov
FU Intramural NIH HHS [Z01 AA000411-04]
NR 489
TC 155
Z9 158
U1 6
U2 23
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD SEP
PY 2008
VL 32
IS 7
SI SI
BP 1293
EP 1314
DI 10.1016/j.neubiorev.2008.03.006
PG 22
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 363PK
UT WOS:000260279000011
PM 18439676
ER
PT J
AU Liu, YX
Qin, LY
Wilson, B
Wu, XF
Qian, L
Granholm, AC
Crews, FT
Hong, JS
AF Liu, Yuxin
Qin, Liya
Wilson, Belinda
Wu, Xuefei
Qian, Li
Granholm, Ann-Charlotte
Crews, Fulton T.
Hong, Jau-Shyong
TI Endotoxin induces a delayed loss of TH-IR neurons in substantia nigra
and motor behavioral deficits
SO NEUROTOXICOLOGY
LA English
DT Article; Proceedings Paper
CT 24th International Neurotoxicology Conference on Environmental
Etiologies of Neurological Disorders - Modifiers of Risk
CY NOV 11-14, 2007
CL San Antonio, TX
SP Natl Inst Environm Hlth Sci, EOHSI, ASA, ATSDR, March Dimes, Autism Speaks, Elsevier, Charles River Lab, John Merch Fund, CTEH, Soc Toxicol, INND, Inst Childrens Environm Hlth, Hammer, Inst Hlth Sci, Morris Cranmer, UAMS, VA Res Dev, Arkansas Childrens Hosp
DE Lipopolysaccharide; Neurodegeneration; Parkinson's disease; TH-IR
neurons; Rotarod test
ID PARKINSONS-DISEASE; MICROGLIAL ACTIVATION; DOPAMINERGIC-NEURONS;
ESTROGEN; EXPOSURE; NEUROTOXICITY; INFLAMMATION; MECHANISMS; EXPRESSION;
SEPSIS
AB We have previously reported that a single injection of endotoxin, lipopolysaccharide (LPS, 5 mg/kg, i.p.), causes a delayed and progressive loss of TH-IR neurons in the substantia nigra (SN) in C57BL/six male mice. In this study, we determined sex differences and behavioral deficits accompanying the loss of TH-IR neurons in response to peripheral LPS injection. A single injection of LPS (5 mg/kg, i.p.) failed to produce any loss of TH-IR neurons in the SN of female mice over a 12-month period. To determine if multiple-injections were required, female mice received five injections of LPS (5 mg/kg, i.p.) at either weekly or monthly intervals. Behavioral motor ability and TH-IR neuronal loss were determined after the first injection of LPS. We found significant differences in both behavioral activities and neuronal loss between these two injection paradigms. Between 7 and 20 months after the first injection of LPS, progressive behavioral changes, measured by rotor-rod and open-field activities, and neuronal loss in SN were observed in monthly injected, but not in weekly injected mice. In addition, reduced rotor-rod ability in monthly injected mice were restored following treatment of L-dopa/carbidopa (30 mg/3 mg/kg), i.p.). Approximately 40 and 50% loss of TH-IR neurons at 9 and 20 months, respectively, was observed after exposure to LPS, suggesting that the behavioral deficit is related to loss of dopamine function in the nigra-striatal pathway. More intense immuno-staining of alpha-synuclein and inflammatory markets were detected in brain sections exposed to LPS. In conclusion, these results show that multi-LPS monthly injections can induce a delayed and progressive loss of TH-IR neurons and motor deficits which resemble the progressive nature of Parkinson's disease. Further, the present study reveals a clear sex difference: female mice are more resistant to LPS than male mice. Repeated monthly LPS injections are required to cause both motor behavioral deficits and DA neuronal loss in female mice. Published by Elsevier Inc.
C1 [Liu, Yuxin; Wilson, Belinda; Wu, Xuefei; Qian, Li; Hong, Jau-Shyong] Natl Inst Environm Hlth Sci, Neuropharmacol Sect, Res Triangle Pk, NC 27709 USA.
[Liu, Yuxin; Qin, Liya; Crews, Fulton T.] Univ N Carolina, Sch Med, Bowles Ctr Alcohol Studies, Chapel Hill, NC 27599 USA.
[Qian, Li] Univ N Carolina, Comprehens Ctr Inflammatory Disorders, Chapel Hill, NC 27599 USA.
[Granholm, Ann-Charlotte] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA.
RP Hong, JS (reprint author), Natl Inst Environm Hlth Sci, Neuropharmacol Sect, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM hong3@niehs.nih.gov
FU Intramural NIH HHS; NIA NIH HHS [AG023630, P01 AG023630, P01
AG023630-03]
NR 32
TC 28
Z9 28
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0161-813X
J9 NEUROTOXICOLOGY
JI Neurotoxicology
PD SEP
PY 2008
VL 29
IS 5
SI SI
BP 864
EP 870
DI 10.1016/j.neuro.2008.02.014
PG 7
WC Neurosciences; Pharmacology & Pharmacy; Toxicology
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology
GA 366XE
UT WOS:000260516100014
PM 18471886
ER
PT J
AU Wink, DA
Ridnour, LA
Hussain, SP
Harris, CC
AF Wink, David A.
Ridnour, Lisa A.
Hussain, S. Perwez
Harris, Curtis C.
TI The reemergence of nitric oxide and cancer - Preface
SO NITRIC OXIDE-BIOLOGY AND CHEMISTRY
LA English
DT Editorial Material
ID WOODCHUCK HEPATITIS-VIRUS; ENDOTHELIAL GROWTH-FACTOR; BLOOD-PRESSURE;
NITRATE BIOSYNTHESIS; SYNTHASE ACTIVITY; MUTATION SPECTRA; DIETARY
NITRATE; MARMOTA-MONAX; TUMOR-GROWTH; HUMAN-CELLS
C1 [Wink, David A.; Ridnour, Lisa A.] NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
[Hussain, S. Perwez; Harris, Curtis C.] NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
RP Wink, DA (reprint author), NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
EM wink@mail.nih.gov
FU Intramural NIH HHS [Z01 BC010033-12]
NR 52
TC 60
Z9 61
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1089-8603
J9 NITRIC OXIDE-BIOL CH
JI Nitric Oxide-Biol. Chem.
PD SEP
PY 2008
VL 19
IS 2
BP 65
EP 67
DI 10.1016/j.niox.2008.05.003
PG 3
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 330UW
UT WOS:000257969300001
PM 18638716
ER
PT J
AU Ridnour, LA
Thomas, DD
Switzer, C
Flores-Santana, W
Isenberg, JS
Ambs, S
Roberts, DD
Wink, DA
AF Ridnour, Lisa A.
Thomas, Douglas D.
Switzer, Christopher
Flores-Santana, Wilmarie
Isenberg, Jeffrey S.
Ambs, Stefan
Roberts, David D.
Wink, David A.
TI Molecular mechanisms for discrete nitric oxide levels in cancer
SO NITRIC OXIDE-BIOLOGY AND CHEMISTRY
LA English
DT Review
DE nitric oxide; cancer; angiogenesis; treatment; nitrosative stress
ID SIGNAL-REGULATED KINASE; HUMAN BREAST-CANCER; CELL RESPONSES; POOR
SURVIVAL; WOUND REPAIR; THROMBOSPONDIN-1; MACROPHAGE; PATHWAY; P53;
ANGIOGENESIS
AB Nitric oxide (NO) has been invoked in nearly every normal and pathological condition associated with human physiology. in tumor biology, nitrogen oxides have both positive and negative affects as they have been implicated in both promoting and preventing cancer. Our work has focused on NO chemistry and how it correlates with cytotoxicity and cancer. Toward this end, we have studied both concentration- and time-dependent NO regulation of specific signaling pathways in response to defined nitrosative stress levels that may occur within the tumor microenvironment. Threshold levels of NO required for activation and stabilization of key proteins involved in carcinogenesis including p53, ERK, Akt and HIF have been identified. Importantly, threshold NO levels are further influenced by reactive oxygen species (ROS) including superoxide, which can shift or attenuate NO-mediated signaling as observed in both tumor and endothelial cells. Our studies have been extended to determine levels of NO that are critical during angiogenic response through regulation of the anti-angiogenic agent thrombospondin-1 (TSP-1) and pro-angiogenic agent matrix metalloproteinase-9 (MMP-9). The quantification of redox events at the cellular level has revealed potential mechanisms that may either limit or potentiate tumor growth, and helped define the positive and negative function of nitric oxide in cancer. Published by Elsevier Inc.
C1 [Ridnour, Lisa A.; Switzer, Christopher; Flores-Santana, Wilmarie; Wink, David A.] NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
[Thomas, Douglas D.] Univ Illinois, Sch Pharm, Dept Med Chem & Pharmacol, Chicago, IL USA.
[Isenberg, Jeffrey S.; Roberts, David D.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Ambs, Stefan] NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
RP Ridnour, LA (reprint author), NCI, Radiat Biol Branch, NIH, Bldg 10,Room B3-B35, Bethesda, MD 20892 USA.
EM ridnourl@mail.nih.gov; wink@mail.nih.gov
RI Roberts, David/A-9699-2008; Switzer, Christopher/D-9203-2013
OI Roberts, David/0000-0002-2481-2981;
FU Intramural NIH HHS [Z01 SC007281-14]
NR 34
TC 66
Z9 69
U1 1
U2 10
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1089-8603
J9 NITRIC OXIDE-BIOL CH
JI Nitric Oxide-Biol. Chem.
PD SEP
PY 2008
VL 19
IS 2
BP 73
EP 76
DI 10.1016/j.niox.2008.04.006
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 330UW
UT WOS:000257969300003
PM 18472020
ER
PT J
AU Li, JT
Zhang, Y
Kong, L
Liu, QR
Wei, LP
AF Li, Jiong-Tang
Zhang, Yong
Kong, Lei
Liu, Qing-Rong
Wei, Liping
TI Trans-natural antisense transcripts including noncoding RNAs in 10
species: implications for expression regulation
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID ESCHERICHIA-COLI; HUMAN-GENOME; MESSENGER-RNA; MOUSE OOCYTES; MAMMALIAN
GENOME; GENE-EXPRESSION; PREDICTION; PROTEIN; SENSE; EVOLUTION
AB Natural antisense transcripts are at least partially complementary to their sense transcripts. Cis-Sense/Antisense pairs (cis-SAs) have been extensively characterized and known to play diverse regulatory roles, whereas trans-Sense/Antisense pairs (trans-SAs) in animals are poorly studied. We identified long trans-SAs in human and nine other animals, using ESTs to increase coverage significantly over previous studies. The percentage of transcriptional units (TUs) involved in trans-SAs among all TUs was as high as 4.13%. Particularly 2896 human TUs (or 2.89% of all human TUs) were involved in 3327 trans-SAs. Sequence complementarities over multiple segments with predicted RNA hybridization indicated that some trans-SAs might have sophisticated RNA-RNA pairing patterns. One-fourth of human trans-SAs involved noncoding TUs, suggesting that many noncoding RNAs may function by a trans-acting antisense mechanism. TUs in trans-SAs were statistically significantly enriched in nucleic acid binding, ion/protein binding and transport and signal transduction functions and pathways; a significant number of human trans-SAs showed concordant or reciprocal expression pattern; a significant number of human trans-SAs were conserved in mouse. This evidence suggests important regulatory functions of trans-SAs. In 30 cases, trans-SAs were related to cis-SAs through paralogues, suggesting a possible mechanism for the origin of trans-SAs. All trans-SAs are available at http://trans.cbi.pku.edu.cn/.
C1 [Li, Jiong-Tang; Zhang, Yong; Kong, Lei; Wei, Liping] Peking Univ, Ctr Bioinformat, Natl Lab Prot Engn & Plant Genet Engn, Coll Life Sci, Beijing 100871, Peoples R China.
[Liu, Qing-Rong] NIDA IRP, DHHS, Mol Neurobiol Branch, NIH, Baltimore, MD 21224 USA.
RP Wei, LP (reprint author), Peking Univ, Ctr Bioinformat, Natl Lab Prot Engn & Plant Genet Engn, Coll Life Sci, Beijing 100871, Peoples R China.
EM weilp@mail.cbi.pku.edu.cn
RI Liu, Qing-Rong/A-3059-2012
OI Liu, Qing-Rong/0000-0001-8477-6452
FU China Ministry of Science and Technology [2006AA02Z334, 2006AA0 2Z314,
2006AA02A312, 2007AA02Z165]; Basic Research Programs [2006CB910404,
2007CB946904]; China Ministry of Education [B06001]; National Institutes
of Health (NIH)-Intramural Research Program; National Institute on Drug
Abuse
FX We are grateful to Drs Manyuan Long, Jane Wu, Louis Tao, Zicai Liang and
Ge Gao for insightful suggestions. We thank Dr Laurie Goodman for
proofreading the manuscript. This work was supported by China Ministry
of Science and Technology 863 Hi-Tech Research and Development Programs
(No. 2006AA02Z334, 2006AA0 2Z314, 2006AA02A312, 2007AA02Z165) and 973
Basic Research Programs (No. 2006CB910404, 2007CB946904), and China
Ministry of Education 111 project (No. B06001). This study was also
supported in part by the National Institutes of Health (NIH)-Intramural
Research Program, National Institute on Drug Abuse. Funding to pay the
Open Access publication charges for this article was provided by China
Ministry of Education 111 Project (No. B06001).
NR 75
TC 27
Z9 31
U1 0
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP
PY 2008
VL 36
IS 15
BP 4833
EP 4844
DI 10.1093/nar/gkn470
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 343OW
UT WOS:000258864400009
PM 18653530
ER
PT J
AU Bukowy, Z
Harrigan, JA
Ramsden, DA
Tudek, B
Bohr, VA
Stevnsner, T
AF Bukowy, Zuzanna
Harrigan, Jeanine A.
Ramsden, Dale A.
Tudek, Barbara
Bohr, Vilhelm A.
Stevnsner, Tinna
TI WRN Exonuclease activity is blocked by specific oxidatively induced base
lesions positioned in either DNA strand
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID WERNER-SYNDROME PROTEIN; ABASIC SITE RECOGNITION; ESCHERICHIA-COLI;
FUNCTIONAL INTERACTION; DAMAGED DNA; MAJOR HUMAN; APURINIC/APYRIMIDINIC
ENDONUCLEASE; CRYSTAL-STRUCTURE; EXCISION-REPAIR; RECQ HELICASES
AB Werner syndrome (WS) is a premature aging disorder caused by mutations in the WS gene (WRN). Although WRN has been suggested to play an important role in DNA metabolic pathways, such as recombination, replication and repair, its precise role still remains to be determined. WRN possesses ATPase, helicase and exonuclease activities. Previous studies have shown that the WRN exonuclease is inhibited in vitro by certain lesions induced by oxidative stress and positioned in the digested strand of the substrate. The presence of the 70/86 Ku heterodimer (Ku), participating in the repair of double-strand breaks (DSBs), alleviates WRN exonuclease blockage imposed by the oxidatively induced DNA lesions. The current study demonstrates that WRN exonuclease is inhibited by several additional oxidized bases, and that Ku stimulates the WRN exonuclease to bypass these lesions. Specific lesions present in the non-digested strand were shown also to inhibit the progression of the WRN exonuclease; however, Ku was not able to stimulate WRN exonuclease to bypass these lesions. Thus, this study considerably broadens the spectrum of lesions which block WRN exonuclease progression, shows a blocking effect of lesions in the non-digested strand, and supports a function for WRN and Ku in a DNA damage processing pathway.
C1 [Bukowy, Zuzanna; Stevnsner, Tinna] Univ Aarhus, Dept Mol Biol, Danish Ctr Mol Gerontol, DK-8000 Aarhus C, Denmark.
[Harrigan, Jeanine A.; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, Natl Inst Hlth, Baltimore, MD 21224 USA.
[Ramsden, Dale A.] Univ N Carolina, Dept Biochem & Biophys, Chapel Hill, NC 27599 USA.
[Tudek, Barbara] Polish Acad Sci, Inst Biochem & Biophys, Warsaw, Poland.
[Tudek, Barbara] Warsaw Univ, Inst Genet & Biotechnol, Warsaw, Poland.
RP Stevnsner, T (reprint author), Univ Aarhus, Dept Mol Biol, Danish Ctr Mol Gerontol, DK-8000 Aarhus C, Denmark.
EM tvs@mb.au.dk
FU National Institute of Health/National Institute on Aging Intramural
Program; European Union Research Training Network [HPRN-CT-2002-00240];
Danish Research Council [22-03-0253]; Danish Cancer Society [DP05024];
NovoNordisk Foundation; The Danish Aging Research Center
FX We thank Susanne Trillingsgaard Veno for help with performing the assays
with Fapy lesions. This work was supported in part by the National
Institute of Health/National Institute on Aging Intramural Program. It
was furthermore supported by the European Union Research Training
Network programme (contract no. HPRN-CT-2002-00240), as well as the
Danish Research Council (22-03-0253), the Danish Cancer Society
(DP05024), The NovoNordisk Foundation, and The Danish Aging Research
Center. Funding to pay the Open Access publication charges for this
article was provided by Danish Cancer Society.
NR 67
TC 18
Z9 20
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP
PY 2008
VL 36
IS 15
BP 4975
EP 4987
DI 10.1093/nar/gkn468
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 343OW
UT WOS:000258864400021
PM 18658245
ER
PT J
AU Tozluoglu, M
Karaca, E
Haliloglu, T
Nussinov, R
AF Tozluoglu, Melda
Karaca, Ezgi
Haliloglu, Turkan
Nussinov, Ruth
TI Cataloging and organizing p73 interactions in cell cycle arrest and
apoptosis
SO NUCLEIC ACIDS RESEARCH
LA English
DT Review
ID MOLECULAR INTERACTION MAP; TRANSCRIPTION FACTOR FAMILY; TUMOR-SUPPRESSOR
PROTEIN; YES-ASSOCIATED PROTEIN; ABL TYROSINE KINASE; P53 HOMOLOG P73;
VIRUS TYPE-I; DNA-DAMAGE; C-ABL; PHYSICAL INTERACTION
AB We have compiled the p73-mediated cell cycle arrest and apoptosis pathways. p73 is a member of the p53 family, consisting of p53, p63 and p73. p73 exists in several isoforms, presenting different domain structures. p73 functions not only as a tumor suppressor in apoptosis but also as differentiator in embryo development. p53 mutations are responsible for half of the human cancers; p73 can partially substitute mutant p53 as tumor suppressor. The pathways we assembled create a p73-centered network consisting of 53 proteins and 176 interactions. We clustered our network into five functional categories: Upregulation, Activation, Suppression, ranscriptional Activity and Degradation. Our literature searches led to discovering proteins (c-Jun and pRb) with apparent opposing functional effects; these indicate either currently missing proteins and interactions or experimental misidentification or functional annotation. For convenience, here we present the p73 network using the molecular interaction map (MIM) notation. The p73 MIM is unique amongst MIMs, since it further implements detailed domain features. We highlight shared pathways between p53 and p73. We expect that the compiled and organized network would be useful to p53 family-based studies.
C1 [Tozluoglu, Melda; Karaca, Ezgi; Haliloglu, Turkan] Bogazici Univ, Polymer Res Ctr, TR-80815 Bebek, Turkey.
[Tozluoglu, Melda; Karaca, Ezgi; Haliloglu, Turkan] Bogazici Univ, Dept Chem Engn, TR-80815 Bebek, Turkey.
[Nussinov, Ruth] SAIC Frederick Inc, Ctr Canc Res Nanobiol Program, NCI Frederick, Basic Res Program, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Sackler Inst Mol Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel.
RP Haliloglu, T (reprint author), Bogazici Univ, Polymer Res Ctr, TR-80815 Bebek, Turkey.
EM turkan@prc.boun.edu.tr; ruthn@ncifcrf.gov
FU Turkish Academy of Sciences (TUBA); Scientific and Technological
Research Council of Turkey [TUBITAK, 107T382]; National Cancer
Institute; National Institutes of Health [N01-CO-12400]; Center for
Cancer Research; NCI [N01-CO-12400]; NIH; [EU FP6-2004-ACC-SSA-2
(517991)]
FX We are grateful to Dr Kurt Kohn for suggesting the project to us.
Moreover, Dr Kohn and Dr Mirit Aladjem followed the project making many
useful comments. We would like to acknowledge financial support from the
following sources: EU FP6-2004-ACC-SSA-2 (517991); Turkish Academy of
Sciences (TUBA); The Scientific and Technological Research Council of
Turkey (TUBITAK, 107T382). This project has been funded in whole or in
part with Federal funds from the National Cancer Institute, National
Institutes of Health (N01-CO-12400). The content of this publication
does not necessarily reflect the views or policies of the Department of
Health and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U. S. Government.
This research was supported (in part) by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research.
Funding to pay the Open Access publication charges for this article was
provided by NCI contract N01-CO-12400.
NR 125
TC 15
Z9 16
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP
PY 2008
VL 36
IS 15
BP 5033
EP 5049
DI 10.1093/nar/gkn481
PG 17
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 343OW
UT WOS:000258864400026
PM 18660513
ER
PT J
AU Bauman, JD
Das, K
Ho, WC
Baweja, M
Himmel, DM
Clark, AD
Oren, DA
Boyer, PL
Hughes, SH
Shatkin, AJ
Arnold, E
AF Bauman, Joseph D.
Das, Kalyan
Ho, William C.
Baweja, Mukta
Himmel, Daniel M.
Clark, Arthur D., Jr.
Oren, Deena A.
Boyer, Paul L.
Hughes, Stephen H.
Shatkin, Aaron J.
Arnold, Eddy
TI Crystal engineering of HIV-1 reverse transcriptase for structure-based
drug design
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HIGH-RESOLUTION STRUCTURES; PROTEIN
CRYSTALLIZATION; POSITIONAL ADAPTABILITY; ANGSTROM RESOLUTION; OVERLAP
EXTENSION; INHIBITORS; CRYSTALLOGRAPHY; RESISTANCE; FRAGMENT
AB HIV-1 reverse transcriptase (RT) is a primary target for anti-AIDS drugs. Structures of HIV-1 RT, usually determined at 2.53.0 resolution, are important for understanding enzyme function and mechanisms of drug resistance in addition to being helpful in the design of RT inhibitors. Despite hundreds of attempts, it was not possible to obtain the structure of a complex of HIV-1 RT with TMC278, a nonnucleoside RT inhibitor (NNRTI) in advanced clinical trials. A systematic and iterative protein crystal engineering approach was developed to optimize RT for obtaining crystals in complexes with TMC278 and other NNRTIs that diffract X-rays to 1.8 resolution. Another form of engineered RT was optimized to produce a high-resolution apo-RT crystal form, reported here at 1.85 resolution, with a distinct RT conformation. Engineered RTs were mutagenized using a new, flexible and cost effective method called methylated overlap-extension ligation independent cloning. Our analysis suggests that reducing the solvent content, increasing lattice contacts, and stabilizing the internal low-energy conformations of RT are critical for the growth of crystals that diffract to high resolution. The new RTs enable rapid crystallization and yield high-resolution structures that are useful in designing/developing new anti-AIDS drugs.
C1 [Bauman, Joseph D.; Das, Kalyan; Ho, William C.; Baweja, Mukta; Himmel, Daniel M.; Clark, Arthur D., Jr.; Oren, Deena A.; Shatkin, Aaron J.; Arnold, Eddy] Rutgers State Univ, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA.
[Bauman, Joseph D.; Das, Kalyan; Ho, William C.; Himmel, Daniel M.; Clark, Arthur D., Jr.; Oren, Deena A.; Arnold, Eddy] Rutgers State Univ, Dept Chem & Chem Biol, Piscataway, NJ 08854 USA.
[Boyer, Paul L.; Hughes, Stephen H.] NCI, Frederick Canc Res & Dev Ctr, Frederick, MD USA.
RP Arnold, E (reprint author), Rutgers State Univ, Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA.
EM arnold@cabm.rutgers.edu
FU NIH
FX We acknowledge personnel at the Cornell High Energy Synchrotron Source
(CHESS), Brookhaven National Laboratory (BNL), Advanced Photon Source
Argonne National Laboratory (APS) and Liang Tong of Columbia University
for support of data collection. Members of our laboratories provided
valuable discussions and assistance, including Stefan Sara. anos, Chhaya
Dharia, Chun Chu, Rajiv Bandwar, ThomasActon, Sergio Martinez and Jason
Schifano. E. A. is grateful to the National Institutes of Health (Grants
AI 27690 MERIT Award and P01 GM 066671) for support of RT structural
studies. S. H. H. was supported by the Intramural Research Program of
National Institutes of Health, National Cancer Institute, Center for
Cancer Research and National Institute of General Medical Sciences.
Funding to pay Open Access publication charges for this article was
provided by the NIH.
NR 31
TC 54
Z9 58
U1 0
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP
PY 2008
VL 36
IS 15
BP 5083
EP 5092
DI 10.1093/nar/gkn464
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 343OW
UT WOS:000258864400030
PM 18676450
ER
PT J
AU Kulkarni, A
McNeill, DR
Gleichmann, M
Mattson, MP
Wilson, DM
AF Kulkarni, Avanti
McNeill, Daniel R.
Gleichmann, Marc
Mattson, Mark P.
Wilson, David M., III
TI XRCC1 protects against the lethality of induced oxidative DNA damage in
nondividing neural cells
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID STRAND BREAK REPAIR; BASE EXCISION-REPAIR; OXYGEN FREE-RADICALS;
CHROMOSOMAL-ABERRATIONS; SPINOCEREBELLAR ATAXIA; NEUROBLASTOMA SH-SY5Y;
GENE-PRODUCT; MUTANT-CELLS; APRATAXIN; RESISTANCE
AB XRCC1 is a critical scaffold protein that orchestrates efficient single-strand break repair (SSBR). Recent data has found an association of XRCC1 with proteins causally linked to human spinocerebellar ataxiasaprataxin and tyrosyl-DNA phosphodiesterase 1implicating SSBR in protection against neuronal cell loss and neurodegenerative disease. We demonstrate herein that shRNA lentiviral-mediated XRCC1 knockdown in human SH-SY5Y neuroblastoma cells results in a largely selective increase in sensitivity of the nondividing (i.e. terminally differentiated) cell population to the redox-cycling agents, menadione and paraquat; this reduced survival was accompanied by an accumulation of DNA strand breaks. Using hypoxanthinexanthine oxidase as the oxidizing method, XRCC1 deficiency affected both dividing and nondividing SH-SY5Y cells, with a greater effect on survival seen in the former case, suggesting that the spectrum of oxidative DNA damage created dictates the specific contribution of XRCC1 to cellular resistance. Primary XRCC1 heterozygous mouse cerebellar granule cells exhibit increased strand break accumulation and reduced survival due to increased apoptosis following menadione treatment. Moreover, knockdown of XRCC1 in primary human fetal brain neurons leads to enhanced sensitivity to menadione, as indicated by increased levels of DNA strand breaks relative to control cells. The cumulative results implicate XRCC1, and more broadly SSBR, in the protection of nondividing neuronal cells from the genotoxic consequences of oxidative stress.
C1 [Kulkarni, Avanti; McNeill, Daniel R.; Wilson, David M., III] NIA, NIH, Lab Mol Gerontol, Baltimore, MD 21224 USA.
[Gleichmann, Marc; Mattson, Mark P.] NIA, NIH, Neurosci Lab, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Wilson, DM (reprint author), NIA, NIH, Lab Mol Gerontol, 251 Bayview Blvd,Suite 100, Baltimore, MD 21224 USA.
EM wilsonda@mail.nih.gov
RI Mattson, Mark/F-6038-2012
FU Intramural Research Program of the NIH; National Institute on Aging
FX We thank P. Pistell (Pennington Research Institute) for supervising the
animal behavioral studies, A. Nath (Johns Hopkins) for providing the
human mixed glialneuronal cell populations, H. Nguyen (Stanford
University) for assisting in some of the early mouse brain cell studies,
and Z. Guo (NIA) for helpful discussion. We also thank Drs L. Weissman
and J- L. Yang (NIA) for critical reading of the manuscript. Funding to
pay Open Access publication charges for this article was provided by the
Intramural Research Program of the NIH, National Institute on Aging.
NR 51
TC 26
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U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP
PY 2008
VL 36
IS 15
BP 5111
EP 5121
DI 10.1093/nar/gkn480
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 343OW
UT WOS:000258864400033
PM 18682529
ER
PT J
AU Jothi, R
Cuddapah, S
Barski, A
Cui, K
Zhao, K
AF Jothi, Raja
Cuddapah, Suresh
Barski, Artem
Cui, Kairong
Zhao, Keji
TI Genome-wide identification of in vivo protein-DNA binding sites from
ChIP-Seq data
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID RESTRICTIVE SILENCER FACTOR; TRANSCRIPTIONAL REPRESSOR; ZINC FINGERS;
CTCF; CHROMATIN; GENES; EPIGENETICS; INSULATORS; MOTIFS; CELLS
AB ChIP-Seq, which combines chromatin immunoprecipitation (ChIP) with ultra high-throughput massively parallel sequencing, is increasingly being used for mapping proteinDNA interactions in-vivo on a genome scale. Typically, short sequence reads from ChIP-Seq are mapped to a reference genome for further analysis. Although genomic regions enriched with mapped reads could be inferred as approximate binding regions, short read lengths (similar to 25-50 nt) pose challenges for determining the exact binding sites within these regions. Here, we present SISSRs ((S) under bar ite Identification from (S) under bar hort (S) under bar equence (R) under bar Reads), a novel algorithm for precise identification of binding sites from short reads generated from ChIP-Seq experiments. The sensitivity and specificity of SISSRs are demonstrated by applying it on ChIP-Seq data for three widely studied and well-characterized human transcription factors: CTCF (CCCTC-binding factor), NRSF (neuron-restrictive silencer factor) and STAT1 (signal transducer and activator of transcription protein 1). We identified 26 814, 5813 and 73 956 binding sites for CTCF, NRSF and STAT1 proteins, respectively, which is 32, 299 and 78 more than that inferred previously for the respective proteins. Motif analysis revealed that an overwhelming majority of the identified binding sites contained the previously established consensus binding sequence for the respective proteins, thus attesting for SISSRs accuracy. SISSRs sensitivity and precision facilitated further analyses of ChIP-Seq data revealing interesting insights, which we believe will serve as guidance for designing ChIP-Seq experiments to map in vivo proteinDNA interactions. We also show that tag densities at the binding sites are a good indicator of proteinDNA binding affinity, which could be used to distinguish and characterize strong and weak binding sites. Using tag density as an indicator of DNA-binding affinity, we have identified core residues within the NRSF and CTCF binding sites that are critical for a stronger DNA binding.
C1 [Jothi, Raja; Cuddapah, Suresh; Barski, Artem; Cui, Kairong; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20894 USA.
RP Zhao, K (reprint author), NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20894 USA.
EM zhaok@nhlbi.nih.gov
RI Jothi, Raja/G-3780-2015;
OI Barski, Artem/0000-0002-1861-5316
FU National Heart Lung and Blood Institute, National Institutes of Health
FX The authors would like to thank Dustin E Schones for suggestions and
critical reading of the article, and Warren J Leonard, Tae-Young Roh,
Gang Wei and Zhibin Wang for useful comments. This study was funded by
Intramural Research Program of the National Heart Lung and Blood
Institute, National Institutes of Health. Funding to pay the Open Access
publication charges for this article was provided by the Intramural
Research Program of the National Institutes of Health.
NR 29
TC 343
Z9 356
U1 4
U2 42
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD SEP
PY 2008
VL 36
IS 16
BP 5221
EP 5231
DI 10.1093/nar/gkn488
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 348JA
UT WOS:000259205600016
PM 18684996
ER
PT J
AU Newlin, K
Melkus, GD
Tappen, R
Chyun, D
Koenig, HG
AF Newlin, Kelley
Melkus, Gail D.
Tappen, Ruth
Chyun, Deborah
Koenig, Harold G.
TI Relationships of religion and spirituality to glycemic control in Black
women with type 2 diabetes
SO NURSING RESEARCH
LA English
DT Article
DE glycemic control; religion; spirituality; type 2 diabetes
ID SOCIAL SUPPORT; AFRICAN-AMERICANS; SELF-MANAGEMENT; DEPRESSIVE SYMPTOMS;
PHYSICAL HEALTH; BLOOD-PRESSURE; CARE PROFILE; STRESS; INVOLVEMENT;
ADULTS
AB Background: Although religion and spirituality are prominent in the lives of Black women with type 2 diabetes (T2DM), there is little research on the relationships of religion and spirituality to glycemic control (GC) in this population.
Objective: To examine the relations of religion and spirituality to GC.
Methods: Using a cross-sectional, descriptive, correlational design, a convenience sample of 109 Black women with T2DM was recruited. Measures of demographic (age, income, and education), clinical (body mass index and use of diabetes medications), psychosocial (emotional distress and social support), religion and spirituality (religious and existential wellbeing), and GC (hemoglobin A1c) factors were collected. A theoretical model, based on the work of Koenig, McCullough, and Larson (2001), informed linear regression analyses to examine the relations of religion and spirituality to GC, with psychosocial factors as putative mediators.
Results: With age (beta = -.133, SE = .020, p = .145), income (beta = .020, SE = .139, p = .853), education (beta = -.221, SE = .204, p = .040), body mass index (beta = .237, SE = .031, p = .011), and diabetes medications (beta = .338, SE = .216, p < .001) held constant, religion and spirituality demonstrated significant relations with GC (beta = .289, SE = .032, p = .028 and beta = -.358, SE = .030, p = .006, respectively). Evidence of emotional distress and social support as mediators in the relationships of religion and spirituality to GC was lacking.
Discussion: Religion and spirituality were related to GC, with 4 evidence of psychosocial mediation lacking, thereby forcing revision of the model for the study population. Research is warranted to validate the findings, with further examination of theoretical mediators linking religion and spirituality to GC. Findings suggest that religion and spirituality be addressed in diabetes care to improve GC in Black women with T2DM.
C1 [Newlin, Kelley] Florida Atlantic Univ, Christine E Lynn Coll Nursing, Natl Inst Nursing Res Postdoctoral Fellow, Boca Raton, FL 33431 USA.
[Melkus, Gail D.] Yale Univ, Sch Nursing, New Haven, CT 06536 USA.
[Chyun, Deborah] Yale Univ, Coll Nursing, New Haven, CT 06536 USA.
[Koenig, Harold G.] Duke Univ, Med Ctr, Durham, NC USA.
RP Newlin, K (reprint author), Florida Atlantic Univ, Christine E Lynn Coll Nursing, Natl Inst Nursing Res Postdoctoral Fellow, 777 Glades Rd, Boca Raton, FL 33431 USA.
EM knewlin@fau.edu
RI Koenig, Harold/F-7379-2011
FU National Institute of Nursing Research [F31 NR008190, F32 NR010043,
R01NR05341]
FX This study was supported by the National Institute of Nursing Research
(Grant F31 NR008190, F32 NR010043, and R01NR05341).
NR 41
TC 22
Z9 22
U1 4
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-6562
J9 NURS RES
JI Nurs. Res.
PD SEP-OCT
PY 2008
VL 57
IS 5
BP 331
EP 339
DI 10.1097/01.NNR.0000313497.10154.66
PG 9
WC Nursing
SC Nursing
GA 352CG
UT WOS:000259472200005
PM 18794717
ER
PT J
AU Erichsen, HC
Peters, U
Eck, P
Welch, R
Schoen, RE
Yeager, M
Levine, M
Hayes, RB
Chanock, S
AF Erichsen, Hans Christian
Peters, Ulrike
Eck, Peter
Welch, Robert
Schoen, Robert E.
Yeager, Meredith
Levine, Mark
Hayes, Richard B.
Chanock, Stephen
TI Genetic Variation in Sodium-Dependent Vitamin C Transporters SLC23A1 and
SLC23A2 and Risk of Advanced Colorectal Adenoma
SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
LA English
DT Article
ID ASCORBIC-ACID; DEHYDROASCORBIC ACID; HAPLOTYPE FREQUENCIES; ANTIOXIDANT
VITAMINS; HUMAN NEUTROPHILS; RANDOMIZED TRIAL; RECURRENCE; POLYPS;
PREVENTION
AB Previous observational studies suggest that vitamin C may reduce risk of colorectal cancer. Vitamin C transport is facilitated by membrane bound sodium-dependent transporters, SVCT1 (encoded by SLC23A1) and SVCT2 (encoded by SLC23A2). To investigate if common genetic variants in these two genes are associated with risk of colorectal tumor development, we conducted a case-control study of 656 Caucasian advanced distal colorectal adenoma cases and 665 Caucasian sigmoidoscopy-negative controls nested within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. The analysis of common single nucleotide polymorphisms in SLC23A1 revealed no association. For SLC23A2, overall, there was no association with baplotypes, but two SNPs located in intron 8 and exon 11 could be associated (odds ratio = 0.49, 95% confidence interval = 0.25-0.95 for haplotype G-C vs. haplotype C-C). The findings should be confirmed in follow-up studies, and further investigation is required to probe the functional basis of this finding.
C1 [Erichsen, Hans Christian] NCI, Sect Genom Variat, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Peters, Ulrike; Hayes, Richard B.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Peters, Ulrike] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Peters, Ulrike] Univ Washington, Seattle, WA 98195 USA.
[Eck, Peter; Levine, Mark] NIDDKD, Mol & Clin Nutr Sect, Bethesda, MD 20892 USA.
[Welch, Robert; Yeager, Meredith; Chanock, Stephen] NCI, Core Genotyping Facil, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Schoen, Robert E.] Univ Pittsburgh, Pittsburgh, PA USA.
RP Chanock, S (reprint author), NCI, Sect Genom Variat, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
EM sc83a@nih.gov
OI Eck, Peter/0000-0003-2371-9774; Hayes, Richard/0000-0002-0918-661X
FU Intramural NIH HHS [Z01 DK053211-01]
NR 35
TC 19
Z9 20
U1 0
U2 1
PU LAWRENCE ERLBAUM ASSOC INC-TAYLOR & FRANCIS
PI PHILADELPHIA
PA 325 CHESTNUT STREET, STE 800, PHILADELPHIA, PA 19106 USA
SN 0163-5581
J9 NUTR CANCER
JI Nutr. Cancer
PD SEP-OCT
PY 2008
VL 60
IS 5
BP 652
EP 659
DI 10.1080/01635580802033110
PG 8
WC Oncology; Nutrition & Dietetics
SC Oncology; Nutrition & Dietetics
GA 359ES
UT WOS:000259969800014
PM 18791929
ER
PT J
AU Watters, JL
Satia, JA
Kupper, LL
AF Watters, Joanne L.
Satia, Jessie A.
Kupper, Lawrence L.
TI Correlates of antioxidant nutrients and oxidative DNA damage differ by
race in a cross-sectional study of healthy African American and white
adults
SO NUTRITION RESEARCH
LA English
DT Article
DE oxidative stress; carotenoids; vitamin C; vitamin E; African Americans;
humans
ID SERUM CONCENTRATIONS; BETA-CAROTENE; VEGETABLE CONSUMPTION; DISEASE
MORTALITY; ALPHA-TOCOPHEROL; VITAMIN-C; BASE-LINE; SMOKING; CANCER;
FRUIT
AB Although antioxidant nutrients and oxidative DNA damage have been associated with carcinogenesis, few studies have investigated the factors that influence antioxidant intake and oxidative DNA damage in racially diverse populations. Demographic, behavioral, and diet-related psychosocial correlates of plasma antioxidant (carotenoids, vitamin C, and vitamin E) concentrations and oxidative DNA damage were examined using data from a cross-sectional study of 147 generally healthy, nonsmoking African American and white adults in North Carolina, aged 20 to 45 years. All participants completed self-administered demographic, diet, and health questionnaires and provided semifasting (>= 6hours) blood samples. Multivariate regression analyses were computed separately for each race to determine associations between the potential correlates with plasma antioxidant concentrations and oxidative DNA damage, separately. Our findings suggest appreciable differences by race. Only a few factors (age, supplement use, and several psychosocial factors) were associated with antioxidant concentrations in African Americans, whereas these and additional factors, including physical activity, waist circumference, and passive smoke exposure, were associated with antioxidant concentrations in whites. For oxidative DNA damage, passive smoke exposure was significantly associated with oxidative DNA damage in African Americans, and age and alcohol were significant in whites. In addition, the regression models generally explained more of the variance in plasma antioxidant concentrations and oxidative DNA damage in whites than in African Americans. Considering the salient correlates differed by race, this work has important implications for the design and implementation of future research studies investigating antioxidant nutrients and/or oxidative stress, especially those in racially diverse populations. Published by Elsevier Inc.
C1 [Watters, Joanne L.] Natl Canc Inst, Canc Prevent Fellowship Program, Off Prevent Oncol, Canc Prevent Div, Rockville, MD 20852 USA.
[Satia, Jessie A.] Univ N Carolina, Dept Nutr, Chapel Hill, NC 27599 USA.
[Satia, Jessie A.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Satia, Jessie A.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Satia, Jessie A.] Univ N Carolina, Ctr Gastrointestinal Biol & Dis, Div Digest Dis & Nutr, Chapel Hill, NC 27599 USA.
[Kupper, Lawrence L.] Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
EM wattersj@mail.nih.gov
FU [R03 CA108276]; [K22 CA96556]; [T32 CA72319]; [P30ES010126];
[DK56350]; [RROO046]
FX This study was supported in part by the following grants: R03 CA108276,
K22 CA96556, T32 CA72319, P30ES010126, DK56350, and RROO046.
NR 50
TC 8
Z9 8
U1 1
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0271-5317
J9 NUTR RES
JI Nutr. Res.
PD SEP
PY 2008
VL 28
IS 9
BP 565
EP 576
DI 10.1016/j.nutres.2008.06.005
PG 12
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 344SD
UT WOS:000258946700001
PM 19083461
ER
PT J
AU Koska, J
Stefan, N
Votruba, SB
Smith, SR
Krakoff, J
Bunt, JC
AF Koska, Juraj
Stefan, Norbert
Votruba, Susanne B.
Smith, Steven R.
Krakoff, Jonathan
Bunt, Joy C.
TI Distribution of subcutaneous fat predicts insulin action in obesity in
sex-specific manner
SO OBESITY
LA English
DT Article
ID VISCERAL ADIPOSE-TISSUE; PIMA-INDIANS; REGIONAL DIFFERENCES; BODY-FAT;
METABOLIC COMPLICATIONS; ABDOMINAL ADIPOSITY; MUSCLE COMPOSITION;
GLUCOSE-TOLERANCE; RESISTANCE; WOMEN
AB The pattern of adipose tissue (AT) distribution is an important predictor of metabolic risk. The aim of this study was to analyze the association of peripheral (insulin-mediated glucose disposal - M) and hepatic (suppression of endogenous glucose production - EGP) insulin action with abdominal (subcutaneous abdominal AT-SAAT, intraabdominal AT - IAA70 and thigh AT depots in obese individuals. Fifty-seven Pima Indians with normal glucose tolerance underwent magnetic resonance imaging (MRI) and euglycemic-hyperinsulinemic clamp. M was negatively related to intraperitoneal IAAT (P = 0.02) and deep SAAT (P = 0.03). Suppression of EGP was negatively related to total (P < 0.05) or deep SAAT (P < 0.05 and P = 0.01, respectively), and total or intraperitoneal IAAT (P = 0.009 and P = 0.002, respectively). A significant interaction with sex was found in the association between superficial SAAT and M, so that in women, but not men, M negatively correlated with superficial SAAT (P = 0.02). In stepwise regression analysis, both M (r(2) = 0.09) and EGP suppression (r(2) = 0.17) were associated only with intraperitoneal IAAT in the whole group. In the sex-specific analysis (because of the significant interaction), lower M was associated with higher deep SAAT (r(2) = 0.15) in combination with lower superficial SAAT (r(2) = 0.09) in men, and with higher superficial SAAT (r(2) = 0.29) in combination with lower thigh subcutaneous AT (r(2) = 0.16) in women. Although intraperitoneal IAAT and deep SAAT were major predictors of peripheral and hepatic insulin action in obese Pima Indians, the largest variance in M rate was explained in a sex-specific manner by relative size of subcutaneous AT depots.
C1 [Koska, Juraj; Stefan, Norbert; Votruba, Susanne B.; Krakoff, Jonathan; Bunt, Joy C.] NIDDK, Obes & Diabet Clin Res Sect, NIH, DHHS, Phoenix, AZ 85014 USA.
[Stefan, Norbert] Univ Tubingen, Div Endocrinol, Dept Internal Med, Tubingen, Germany.
[Smith, Steven R.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
RP Koska, J (reprint author), NIDDK, Obes & Diabet Clin Res Sect, NIH, DHHS, Phoenix, AZ 85014 USA.
EM jkrakoff@mail.nih.gov
OI Stefan, Norbert/0000-0002-2186-9595
FU NIDDK/NIH/DHHS
FX This work was funded by the intramural research program of the
NIDDK/NIH/DHHS We gratefully acknowledge Thomas Brookshire, PA; Kathy
Trinidad, RN; and nursing and dietary staff of the National Institutes
of Health (NIH) metabolic unit for the care of the volunteers. We thank
Ann Nelson and magnetic resonance imaging (MRI) staff at The Banner
Health Good Samaritan Medical Center for help in MRI data acquisition.
We are grateful to the members and leaders of the Gila River Indian
Community for their continuing cooperation in our studies. We thank Jeff
Curtis, MD for helpful comments on the manuscript.
NR 40
TC 20
Z9 20
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD SEP
PY 2008
VL 16
IS 9
BP 2003
EP 2009
DI 10.1038/oby.2008.292
PG 7
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 345KP
UT WOS:000258996000004
PM 18551127
ER
PT J
AU El-Mohandes, AAE
Kiely, M
Joseph, JG
Subramanian, S
Johnson, AA
Blake, SM
Gantz, MG
El-Khorazaty, MN
AF El-Mohandes, Ayman A. E.
Kiely, Michele
Joseph, Jill G.
Subramanian, Siva
Johnson, Allan A.
Blake, Susan M.
Gantz, Marie G.
El-Khorazaty, M. Nabil
TI An intervention to improve postpartum outcomes in African-American
mothers - A randomized controlled trial
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the
Pediatric-Academic-Societies/Society-of-Pediatric-Research
CY MAY 05-08, 2007
CL Toronto, CANADA
SP Pediat Acad Soc
ID INTIMATE PARTNER VIOLENCE; ENVIRONMENTAL TOBACCO-SMOKE;
LOW-BIRTH-WEIGHT; BEHAVIORAL INTERVENTION; DOMESTIC VIOLENCE;
PREGNANT-WOMEN; PRIMARY-CARE; DEPRESSION; CESSATION; PREVENTION
AB OBJECTIVE: To evaluate the efficacy of an integrated multiple risk intervention, delivered mainly during pregnancy, in reducing such risks (cigarette smoking, environmental tobacco smoke exposure, depression, and intimate partner violence) postpartum.
METHODS: Data from this randomized controlled trial were collected prenatally and on average 10 weeks postpartum in six prenatal care sites in the District of Columbia. African Americans were screened, recruited, and randomly assigned to the behavioral intervention or usual care. Clinic-based, individually tailored counseling was delivered to intervention women. The outcome measures were number of risks reported postpartum and reduction of these risks between baseline and postpartum.
RESULTS: The intervention was effective in significantly reducing the number of risks reported in the postpartum period. In bivariate analyses, the intervention group was more successful in resolving all risks (47% compared with 35%, P=.007, number needed to treat=9, 95% confidence interval [CI] 5-31) and in resolving some risks (63% compared with 54%, P=.009, number needed to treat=11, 95% CI 7-43) as compared with the usual care group. In logistic regression analyses, women in the intervention group were more likely to resolve all risks (odds ratio 1.86, 95% CI 1.25-2.75, number needed to treat=7, 95% CI 4-19) and resolve at least one risk (odds ratio 1.60, 95% CI 1.15-2.22, number needed to treat=9, 95% CI 6-29).
CONCLUSION: An integrated multiple risk factor intervention addressing psychosocial and behavioral risks delivered mainly during pregnancy can have beneficial effects in risk reduction postpartum.
C1 [El-Mohandes, Ayman A. E.] George Washington Univ, Dept Prevent & Community Hlth, Sch Publ Hlth & Hlth Serv, Med Ctr, Washington, DC 20037 USA.
Georgetown Univ, Washington, DC USA.
Childrens Natl Med Ctr, Washington, DC 20010 USA.
NIH, Bethesda, MD 20892 USA.
Howard Univ, Washington, DC 20059 USA.
Res Triangle Inst Int, Rockville, MD USA.
RP El-Mohandes, AAE (reprint author), George Washington Univ, Dept Prevent & Community Hlth, Sch Publ Hlth & Hlth Serv, Med Ctr, 2175 K St, Washington, DC 20037 USA.
EM sphaxe@gwumc.edu
FU Intramural NIH HHS [Z99 HD999999]; NICHD NIH HHS [U18 HD031206-07,
3U18HD030445, 3U18HD030447, 3U18HD031919, 5U18HD036104, 5U18HD31206, U18
HD030445, U18 HD030445-07, U18 HD030447, U18 HD030447-07, U18 HD031206,
U18 HD031919, U18 HD031919-07, U18 HD036104, U18 HD036104-02]
NR 55
TC 35
Z9 36
U1 1
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
EI 1873-233X
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD SEP
PY 2008
VL 112
IS 3
BP 611
EP 620
DI 10.1097/AOG.0b013e3181834b10
PG 10
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 347YZ
UT WOS:000259179100016
PM 18757660
ER
PT J
AU Castle, PE
Cox, JT
Schiffman, M
Wheeler, CM
Solomon, D
AF Castle, Philip E.
Cox, J. Thomas
Schiffman, Mark
Wheeler, Cosette M.
Solomon, Diane
TI Factors influencing histologic confirmation of high-grade squamous
intraepithelial lesion cytology
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS DNA; CERVICAL-CANCER; CONSENSUS GUIDELINES; WOMEN;
MANAGEMENT; CARCINOGENICITY; PARTICIPANTS; METAANALYSIS; COLPOSCOPY;
NEOPLASIA
AB OBJECTIVE: To examine the predictors of histologic confirmation of high-grade squamous intraepithelial lesion (HSIL) cytology occurring in follow-up of young women originally referred into a trial because of less severe cytology.
METHODS: We used enrollment HSIL cytology (N=411) as read by clinical center pathologists for women participating in the ASCUS-LSIL Triage Study (ALTS). The primary outcome was histologic cervical intraepithelial neoplasia (CIN) grade 3 and early cancer (n = 195; 191 CIN 3 and four cancers) as diagnosed by the Pathology Quality Control Group during the 2-year duration of ALTS.
RESULTS: The 2-year absolute risk of CIN 3 or worse after an HSIL cytology was 47.4% (95% confidence interval 42.5-52.4%). The 2-year absolute risk of CIN 3 or worse was lowest (14.3%) for women who were human papillomavirus (HPV)-16-negative, had colposcopic impression of less than low-grade, and whose HSIL cytology as called by the clinical center was not also called HSIL or equivocal HSIL cytology by the Pathology Quality Control Group. The 2-year absolute risk of CIN 3 or worse was highest (82.4%) for women who were HPV16-positive, had colposcopic impression of low-grade or worse, and whose HSIL cytology also was called HSIL or equivocal HSIL cytology by the Pathology Quality Control Group.
CONCLUSION: Histologic confirmation of precancer among young women with HSIL cytology was more likely when other risk factors (eg, HPV16) for cervical precancer were present.
C1 [Castle, Philip E.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
NCI, Canc Prevent Div, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
Univ Calif Santa Barbara, Gynecol & Colposcopy Clin, Student Hlth Serv, Santa Barbara, CA 93106 USA.
Univ New Mexico, Hlth Sci Ctr, Dept Obstet & Gynecol, Sch Med, Albuquerque, NM 87131 USA.
Univ New Mexico, Hlth Sci Ctr, Dept Mol Genet & Microbiol, Sch Med, Albuquerque, NM 87131 USA.
RP Castle, PE (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd,Room 5004,MSC 7234, Bethesda, MD 20892 USA.
EM castlep@mail.nih.gov
FU National Institutes of Health (NIH); National Cancer Institute; NIH
Department of Health and Human Services [CN-55753, CN-55754, CN-55155,
CN55156, CN-55157, CN-55758, CN-55159, CN-55105]
FX Supported in part by the Intramural Research Program of the National
Institutes of Health (NIH), National Cancer Institute. The ASCUS-LSIL
Triage Study was supported by the National Cancer Institute, NIH
Department of Health and Human Services contracts CN-55753, CN-55754,
CN-55155, CN55156, CN-55157, CN-55758, CN-55159, and CN-55105. Some of
the equipment and supplies used in these studies was donated or provided
at reduced cost by Digene Corporation (Gaithersburg, AID), Cytyc
Corporation (Marlborough, MAI), National Testing Laboratories (Fenton,
MO), DenVu (Tucson, AZ), BD Diagnostics-TriPath (Burlington, NC), and
Roche Molecular Systems Inc. (Alameda, CA).
NR 21
TC 7
Z9 7
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD SEP
PY 2008
VL 112
IS 3
BP 637
EP 645
DI 10.1097/AOG.0b013e3181834637
PG 9
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 347YZ
UT WOS:000259179100019
PM 18757663
ER
PT J
AU Gibson, M
Spong, CY
Simonsen, SE
Martin, S
Scott, JR
AF Gibson, Mark
Spong, Catherine Y.
Simonsen, Sara Ellis
Martin, Sheryl
Scott, James R.
TI Author perception of peer review
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY; MANUSCRIPTS; ACCEPTANCE; FEEDBACK;
EDITORS; IMPACT
AB OBJECTIVE: To survey authors submitting manuscripts to a leading specialty journal regarding their assessment of editorial review. The study sought factors affecting authors' satisfaction and whether authors rated the journal review processes differently from the commentary provided by different reviewers.
METHODS: Participation in an online survey was offered to 445 corresponding authors of research manuscripts submitted consecutively during a 7-month period. All manuscripts received full editorial review. The survey instrument asked authors to rate six aspects of editorial comments from each of two to four reviewers and three aspects of the review process. in addition, the survey queried overall satisfaction and likelihood of submission of future manuscripts based on review experience.
RESULTS: Higher ratings for overall satisfaction with manuscript review were given by authors of accepted compared with rejected manuscripts (98% compared with 80%, P<.001). Authors rated processes for submission and review more highly than editorial commentary (88% compared with 69%, P<.001), and this difference was greater among authors of rejected manuscripts. The extent to which reviewers focused on important aspects of submitted manuscripts received the lowest ratings from authors. Authors' ratings of reviewers' comments differentiated between reviewers and did not correlate with ratings of reviews by the journal's senior editors.
CONCLUSION: Author feedback was more favorable among authors of accepted manuscripts, and responses differentiated among aspects of editorial review and reviewers. Author feedback may provide a means for monitoring and improvement of processes for editorial review and reviewer commentary.
C1 [Gibson, Mark] Univ Utah, Dept Obstet & Gynecol, Sch Med, Salt Lake City, UT 84132 USA.
NICHHD, Pregnancy & Perinatol Branch, NIH, Bethesda, MD 20892 USA.
Univ Utah, Dept Family & Prevent Med, Sch Med, Publ Hlth Program, Salt Lake City, UT 84132 USA.
RP Gibson, M (reprint author), Univ Utah, Dept Obstet & Gynecol, Sch Med, 30 N 1900 E,Room 2B200, Salt Lake City, UT 84132 USA.
EM mark.gibson@hsc.ulah.edu
NR 14
TC 8
Z9 9
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD SEP
PY 2008
VL 112
IS 3
BP 646
EP 651
DI 10.1097/AOG.0b013e31818425d4
PG 6
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 347YZ
UT WOS:000259179100020
PM 18757664
ER
PT J
AU Macones, GA
Hankins, GDV
Spong, CY
Hauth, J
Moore, T
AF Macones, George A.
Hankins, Gary D. V.
Spong, Catherine Y.
Hauth, John
Moore, Thomas
TI The 2008 National Institute of Child Health and Human Development
workshop report on electronic fetal monitoring - Update on definitions,
interpretation, and research guidelines
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Editorial Material
C1 [Macones, George A.] Washington Univ, Dept Obstet & Gynecol, St Louis, MO 63110 USA.
Univ Texas Med Branch, Dept Obstet & Gynecol, Galveston, TX USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
Univ Alabama, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
Univ Calif San Diego, Dept Obstet & Gynecol, San Diego, CA 92103 USA.
RP Macones, GA (reprint author), Washington Univ, Dept Obstet & Gynecol, St Louis, MO 63110 USA.
EM maconesg@wustl.edu
NR 8
TC 235
Z9 253
U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD SEP
PY 2008
VL 112
IS 3
BP 661
EP 666
DI 10.1097/AOG.0b013e3181841395
PG 6
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 347YZ
UT WOS:000259179100022
PM 18757666
ER
PT J
AU Browne, H
Manipalviratn, S
Armstrong, A
AF Browne, Hyacinth
Manipalviratn, Somjate
Armstrong, Alicia
TI Using an intrauterine device in immunocompromised women
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Editorial Material
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; HIV-1-INFECTED WOMEN; HIV
AB Intrauterine devices (IUDs) are a viable treatment option for immunocompromised women who need contraception or menses suppression. They may also be an alternative treatment for women who have a contraindication to estrogen use. A review of the literature on IUD use in this population is sparse, but currently available data suggest that immunocompromised women are not at greater risk of developing pelvic infections.
C1 [Browne, Hyacinth; Manipalviratn, Somjate; Armstrong, Alicia] NICHHD, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RP Browne, H (reprint author), NICHD, Program Reprod & Adult Endocrinol, NIH, CRC 1 E,Rm 1-E-3140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM brownehy@mail.nih.gov
FU Intramural NIH HHS [NIH0012449348]; PHS HHS [NIH0012449348]
NR 13
TC 9
Z9 9
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD SEP
PY 2008
VL 112
IS 3
BP 667
EP 669
DI 10.1097/AOG.0b013e318183464e
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 347YZ
UT WOS:000259179100023
PM 18757667
ER
PT J
AU Levens, ED
Nieman, LK
AF Levens, Eric D.
Nieman, Lynnette K.
TI CDB-2914 for uterine leiomyomata treatment: A randomized controlled
trial - Reply
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Letter
ID MIFEPRISTONE
C1 [Levens, Eric D.; Nieman, Lynnette K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, Bethesda, MD USA.
RP Levens, ED (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, Bethesda, MD USA.
NR 4
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD SEP
PY 2008
VL 112
IS 3
BP 707
EP 708
DI 10.1097/AOG.0b013e318186496b
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 347YZ
UT WOS:000259179100038
ER
PT J
AU Aquino-Jarquin, G
Benitez-Hess, ML
DiPaolo, JA
Alvarez-Salas, LM
AF Aquino-Jarquin, Guillermo
Benitez-Hess, Maria Luisa
DiPaolo, Joseph A.
Alvarez-Salas, Luis M.
TI A triplex ribozyme expression system based on a single hairpin ribozyme
SO OLIGONUCLEOTIDES
LA English
DT Article
ID RNA; INHIBITION; HAMMERHEAD; CLEAVAGE; VIRUS; GENE; REPLICATION;
SEQUENCES; DESIGN; AGENTS
AB Triplex ribozyme (RZ) con C gurations allow for the individual activity of trans-acting RZs in multiple expression cassettes (multiplex), thereby increasing target cleavage relative to conventionally expressed RZs. Although hairpin RZs have been advantageously compared to hammerhead RZs, their longer size and structural features complicated triplex design. We present a triplex expression system based on a single hairpin RZ with trans-cleavage capability and simple engineering. The system was tested in vitro using cis-and trans-cleavage kinetic assays against a known target RNA from HPV-16 E6/E7 mRNA. Single and multiplex triplex RZ constructs were more efficient in cleaving the target than tandem-cloned hairpin RZs, suggesting that the release of individual RZs enhanced trans-cleavage kinetics. Multiplex systems constructed with two different hairpin RZs resulted in better trans-cleavage compared to standard double-RZ constructs. In addition, the triplex RZ performed cis-and trans-cleavage in cervical cancer cells. The use of triplex con C gurations with multiplex RZs permit differential targeting of the same or different RNA, thus improving potential use against unstable targets. This prototype will provide the basis for the development of future RZ-based therapies and technologies.
C1 [Aquino-Jarquin, Guillermo; Benitez-Hess, Maria Luisa; Alvarez-Salas, Luis M.] CINVESTAV, Lab Terapia Genica, Dept Genet & Mol Biol, Mexico City 07360, DF, Mexico.
[DiPaolo, Joseph A.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Alvarez-Salas, LM (reprint author), CINVESTAV, Lab Terapia Genica, Dept Genet & Mol Biol, Mexico City 07360, DF, Mexico.
EM lalvarez@cinvestav.mx
FU CONACyT [45715Z]; Intramural Research Program of the Center for Cancer
Research; NCI/NIH
FX We thank Victor Hugo Rosales-Garcia for cell sorting. This research was
partially supported by CONACyT (Grant No. 45715Z) and by the Intramural
Research Program of the Center for Cancer Research, NCI/NIH.
NR 24
TC 3
Z9 3
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1545-4576
J9 OLIGONUCLEOTIDES
JI Oligonucleotides
PD SEP
PY 2008
VL 18
IS 3
BP 213
EP 223
DI 10.1089/oli.2008.0130
PG 11
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA 360JU
UT WOS:000260054600002
PM 18707243
ER
PT J
AU Abu-Asab, MS
Chaouchi, M
Amri, H
AF Abu-Asab, Mones S.
Chaouchi, Mohamed
Amri, Hakima
TI Phylogenetic modeling of heterogeneous gene-expression microarray data
from cancerous specimens
SO OMICS-A JOURNAL OF INTEGRATIVE BIOLOGY
LA English
DT Article
ID B-CELL LYMPHOMA; MOLECULAR CLASSIFICATION; DIFFERENTIAL EXPRESSION;
COLORECTAL-CANCER; LIKELIHOOD; REVEALS; TUMORS; PATHOGENESIS; PARSIMONY;
PATHWAYS
AB The qualitative dimension of gene expression data and its heterogeneous nature in cancerous specimens can be accounted for by phylogenetic modeling that incorporates the directionality of altered gene expressions, complex patterns of expressions among a group of specimens, and data-based rather than specimen-based gene linkage. Our phylogenetic modeling approach is a double algorithmic technique that includes polarity assessment that brings out the qualitative value of the data, followed by maximum parsimony analysis that is most suitable for the data heterogeneity of cancer gene expression. We demonstrate that polarity assessment of expression values into derived and ancestral states, via outgroup comparison, reduces experimental noise; reveals dichotomously expressed asynchronous genes; and allows data pooling as well as comparability of intra- and interplatforms. Parsimony phylogenetic analysis of the polarized values produces a multidimensional classification of specimens into clades that reveal shared derived gene expressions (the synapomorphies); provides better assessment of ontogenic pathways and phyletic relatedness of specimens; efficiently utilizes dichotomously expressed genes; produces highly predictive class recognition; illustrates gene linkage and multiple developmental pathways; provides higher concordance between gene lists; and projects the direction of change among specimens. Further implication of this phylogenetic approach is that it may transform microarray into diagnostic, prognostic, and predictive tool.
C1 [Chaouchi, Mohamed; Amri, Hakima] Georgetown Univ, Sch Med, Dept Physiol & Biophys, Washington, DC 20007 USA.
[Abu-Asab, Mones S.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Amri, H (reprint author), Georgetown Univ, Sch Med, Dept Physiol & Biophys, Washington, DC 20007 USA.
EM amrih@georgetwon.edu
OI Abu-Asab, Mones/0000-0002-4047-1232
FU Intramural NIH HHS [Z99 CA999999]
NR 39
TC 6
Z9 6
U1 0
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1536-2310
EI 1557-8100
J9 OMICS
JI OMICS
PD SEP
PY 2008
VL 12
IS 3
BP 183
EP 199
DI 10.1089/omi.2008.0010
PG 17
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 348TI
UT WOS:000259232600003
PM 18699725
ER
PT J
AU Wei, JS
Song, YK
Durinck, S
Chen, QR
Cheuk, ATC
Tsang, P
Zhang, Q
Thiele, CJ
Slack, A
Shohet, J
Khan, J
AF Wei, J. S.
Song, Y. K.
Durinck, S.
Chen, Q-R
Cheuk, A. T. C.
Tsang, P.
Zhang, Q.
Thiele, C. J.
Slack, A.
Shohet, J.
Khan, J.
TI The MYCN oncogene is a direct target of miR-34a
SO ONCOGENE
LA English
DT Article
DE microRNA; miR-34a; MYCN; 1p36 LOH; neuroblastoma; translation regulation
ID TUMOR-SUPPRESSOR GENE; HUMAN NEUROBLASTOMA-CELLS; N-MYC; EXPRESSION
PROFILES; FREQUENT DELETIONS; CONSENSUS REGION; TRANSGENIC MICE;
NERVOUS-SYSTEM; CHROMOSOME 1P; APOPTOSIS
AB Loss of 1p36 heterozygosity commonly occurs with MYCN amplification in neuroblastoma tumors, and both are associated with an aggressive phenotype. Database searches identified five microRNAs that map to the commonly deleted region of 1p36 and we hypothesized that the loss of one or more of these microRNAs contributes to the malignant phenotype of MYCN-amplified tumors. By bioinformatic analysis, we identified that three out of the five microRNAs target MYCN and of these miR-34a caused the most significant suppression of cell growth through increased apoptosis and decreased DNA synthesis in neuroblastoma cell lines with MYCN amplification. Quantitative RT-PCR showed that neuroblastoma tumors with 1p36 loss expressed lower level of miR-34a than those with normal copies of 1p36. Furthermore, we demonstrated that MYCN is a direct target of miR-34a. Finally, using a series of mRNA expression pro. ling experiments, we identified other potential direct targets of miR-34a, and pathway analysis demonstrated that miR- 34a suppresses cell-cycle genes and induces several neural-related genes. This study demonstrates one important regulatory role of miR-34a in cell growth and MYCN suppression in neuroblastoma.
C1 [Wei, J. S.; Song, Y. K.; Durinck, S.; Chen, Q-R; Cheuk, A. T. C.; Tsang, P.; Zhang, Q.; Khan, J.] Natl Canc Inst, Oncogenom Sect, Pediat Oncol Branch, Adv Technol Ctr, Gaithersburg, MD 20892 USA.
[Chen, Q-R] NCI, Adv Biomed Comp Ctr, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Thiele, C. J.] Natl Canc Inst, Cell & Mol Biol Sect, Pediat Oncol Branch, Bethesda, MD USA.
[Slack, A.; Shohet, J.] Baylor Coll Med, Dept Pediat, Hematol Oncol Sect, Houston, TX 77030 USA.
RP Khan, J (reprint author), Natl Canc Inst, Oncogenom Sect, Pediat Oncol Branch, Adv Technol Ctr, Room 134E,8717 Grovemont Circle, Gaithersburg, MD 20892 USA.
EM khanjav@mail.nih.gov
RI Khan, Javed/P-9157-2014
OI Khan, Javed/0000-0002-5858-0488
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research
FX We thank Dr Joon-Yong Chung and Xinyu Wen, MS for their excellent
technical support. We also thank Dr John Maris, Dr Wendy London
(Children's Oncology Group, Philadelphia, PA, USA) and Dr Steven Qualman
(Cooperative Human Tissue Network, Columbus, OH, USA) for the NB tumor
samples, and for invaluable discussion of this study with Dr John Maris
and his group. This study is supported by the Intramural Research
Program of the National Institutes of Health, National Cancer Institute,
Center for Cancer Research. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial products
or organizations imply endorsement by the US government.
NR 66
TC 159
Z9 166
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD SEP
PY 2008
VL 27
IS 39
BP 5204
EP 5213
DI 10.1038/onc.2008.154
PG 10
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 344GO
UT WOS:000258915100004
PM 18504438
ER
PT J
AU Parchen, DA
Castro, K
Herringa, C
Ness, E
Bevans, M
AF Parchen, Debra A.
Castro, Kathleen
Herringa, Cynthia
Ness, Elizabeth
Bevans, Margaret
TI Developing outcomes for an oncology nurse internship program
SO ONCOLOGY NURSING FORUM
LA English
DT Editorial Material
C1 [Parchen, Debra A.; Castro, Kathleen; Herringa, Cynthia] NIH, Nursing & Patient Care Serv Clin Ctr, Bethesda, MD 20892 USA.
[Ness, Elizabeth] Natl Canc Inst, Ctr Canc Res, NIH, Bethesda, MD USA.
NIH, Nursing & Patient Care Serv, Ctr Clin, Bethesda, MD USA.
RP Parchen, DA (reprint author), NIH, Nursing & Patient Care Serv Clin Ctr, Bethesda, MD 20892 USA.
EM dparchen@cc.nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 22
TC 1
Z9 1
U1 0
U2 0
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 0190-535X
J9 ONCOL NURS FORUM
JI Oncol. Nurs. Forum
PD SEP
PY 2008
VL 35
IS 5
BP 753
EP 756
DI 10.1188/08.ONF.753-756
PG 4
WC Oncology; Nursing
SC Oncology; Nursing
GA 347BB
UT WOS:000259112700005
PM 18765321
ER
PT J
AU Cecchi, F
Mannoni, A
Molino-Lova, R
Ceppatelli, S
Benvenuti, E
Bandinelli, S
Lauretani, F
Macchi, C
Ferrucci, L
AF Cecchi, F.
Mannoni, A.
Molino-Lova, R.
Ceppatelli, S.
Benvenuti, E.
Bandinelli, S.
Lauretani, F.
Macchi, C.
Ferrucci, L.
TI Epidemiology of hip and knee pain in a community based sample of Italian
persons aged 65 and older
SO OSTEOARTHRITIS AND CARTILAGE
LA English
DT Article
DE hip pain; knee pain; older persons; prevalence; correlates
ID NUTRITION EXAMINATION SURVEY; 3RD NATIONAL-HEALTH; QUALITY-OF-LIFE;
MUSCULOSKELETAL PAIN; DISABLED WOMEN; JOINT PAIN; BACK-PAIN;
OSTEOARTHRITIS; DISABILITY; ADULTS
AB Objective: To describe prevalence, characteristics and correlates of hip pain (HP) and knee pain (KP) in an Italian community based cohort aged 65 and older (65+).
Method: Baseline survey (1998-2000), population-based study in the Chianti area (Tuscany, Italy); 1299 persons aged 65+ were selected from the city registry of Greve in Chianti and Bagno a Ripoli (multistage sampling method); 1006 participants (564 women and 442 men, age 75.2 +/- 7.1) provided information for this analysis. Persons reporting HP/KP in the past 4 weeks were recorded and their Western Ontario and M Master University Osteoarthritis Index pain score (WPS-range 0-20) calculated. Potential correlates of HP/KP, including clinical, lifestyle c and psycho-social features and physical measures, were tested in age- and gender-adjusted regression analyses and then entered a multivariate regression model.
Results: HP was reported by 11.9% participants, while 22.4% reported KP and 7.2% both conditions. Climbing/descending stairs and walking Were the activities eliciting more severe pain in either condition. Average WPSs were 5.6 +/- 3.5 for HP and 5.4 +/- 10.4 for KP. Both HP and KP wore related to back pain, reduced hip abduction, reduced muscle power and increased trunk flexibility. HP was also related to KP and poor self-rated health (SRH), while KP to HP, foot pain, high body mass index, reduced knee passive flexion and knee extension torque, low education.
Conclusion: In a community sample of an Italian persons aged 65+, the prevalence of KP almost doubled that of HP. While both conditions were related to pain in other joints and specific joint impairment, only HP was related to poor SRH, and only KP to mechanical overload. (C) 2008 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
C1 [Cecchi, F.; Molino-Lova, R.; Ceppatelli, S.; Macchi, C.] Sci Inst Recovery & Care, Fdn Don Carlo Gnocchi, Outpatient Rehabil Dept, IRCCS, I-50141 Florence, Italy.
[Mannoni, A.] ASF, Qual Improvement Network, Rheumatol Unit, Florence, Italy.
[Benvenuti, E.; Bandinelli, S.] ASF, Geriatr Unit, Florence, Italy.
[Lauretani, F.] Tuscany Hlth Reg Agcy, Florence, Italy.
[Macchi, C.] Univ Florence, Dept Crit Care Med & Surg, I-50121 Florence, Italy.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD USA.
RP Cecchi, F (reprint author), Sci Inst Recovery & Care, Fdn Don Carlo Gnocchi, Outpatient Rehabil Dept, IRCCS, Caccini 18, I-50141 Florence, Italy.
EM francescacec-chi2002@libero.it
RI Lauretani, Fulvio/K-5115-2016;
OI Lauretani, Fulvio/0000-0002-5287-9972; Cecchi,
Franco/0000-0002-2035-5621
FU Italian Ministry of Health [ICS 110.1\RS97.71]; U.S. National Institute
on Aging [N01-AG-916413, N01-AG-821336, 263 MID 9164 13, 263 MID
821336]; NIH, USA
FX The manuscript submitted does not contain information about medical
device(s)/drug(s). Funds were received in support of this work. No
benefits in any form have been or will be received from a commercial
party related directly or indirectly to the subject of this manuscript.
The InCHIANTI Study was supported as a "targeted project" (ICS
110.1\RS97.71) by the Italian Ministry of Health, by the U.S. National
Institute on Aging (Contracts N01-AG-916413, N01-AG-821336 and Contracts
263 MID 9164 13 and 263 MID 821336) and in part by the Intramural
Research Program, National Institute on Aging, NIH, USA.
NR 50
TC 13
Z9 17
U1 2
U2 7
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 1063-4584
J9 OSTEOARTHR CARTILAGE
JI Osteoarthritis Cartilage
PD SEP
PY 2008
VL 16
IS 9
BP 1039
EP 1046
DI 10.1016/j.joca.2008.01.008
PG 8
WC Orthopedics; Rheumatology
SC Orthopedics; Rheumatology
GA 350UT
UT WOS:000259379400011
PM 18343164
ER
PT J
AU Schisterman, EF
Vexler, A
AF Schisterman, Enrique F.
Vexler, Albert
TI To pool or not to pool, from whether to when: applications of pooling to
biospecimens subject to a limit of detection
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Article
DE biological samples; pooling design; sampling strategy; detection
threshold; Monte Carlo simulations
ID MEASUREMENT ERROR; EXPOSURE; SAMPLES; CURVE
AB Pooling of biological specimens has been utilised as a cost-efficient sampling strategy, but cost is not the unique limiting factor in biomarker development and evaluation. We examine the effect of different sampling strategies of biospecimens for exposure assessment that cannot be detected below a detection threshold (DT). The paper compares use of pooled samples to a randomly selected sample from a cohort in order to evaluate the efficiency of parameter estimates.
The proposed approach shows that a pooling design is more efficient than a random sample strategy under certain circumstances. Moreover, because pooling minimises the amount of information lost below the DT, the use of pooled data is preferable (in a context of a parametric estimation) to using all available individual measurements, for certain values of the DT. We propose a combined design, which applies pooled and unpooled biospecimens, in order to capture the strengths of the different sampling strategies and overcome instrument limitations (i.e. DT). Several Monte Carlo simulations and an example based on actual biomarker data illustrate the results of the article.
C1 [Schisterman, Enrique F.; Vexler, Albert] NICHHD, NIH, Div Epidemiol Stat & Prevent Res, Rockville, MD 20852 USA.
RP Schisterman, EF (reprint author), NICHHD, NIH, Div Epidemiol Stat & Prevent Res, 6100 Execut Blvd,7B03N, Rockville, MD 20852 USA.
EM schistee@mail.nih.gov
OI Schisterman, Enrique/0000-0003-3757-641X
FU Intramural NIH HHS [Z01 HD008761-05]
NR 19
TC 23
Z9 23
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-5022
EI 1365-3016
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD SEP
PY 2008
VL 22
IS 5
BP 486
EP 496
DI 10.1111/j.1365-3016.2008.00956.x
PG 11
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA 349ED
UT WOS:000259263200008
PM 18782255
ER
PT J
AU Keir, ST
Morton, CL
Billups, C
Smith, MA
Houghton, PJ
Gururangan, S
AF Keir, Stephen T.
Morton, Christopher L.
Billups, Catherine
Smith, Malcolm A.
Houghton, Peter J.
Gururangan, Sridharan
TI Initial testing of VNP40101M (Cloretazine (R)) by the pediatric
preclinical testing program
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE developmental therapeutics; preclinical testing; VNP40101 M
ID SULFONYLHYDRAZINE ALKYLATING AGENT; PHASE-I; REFRACTORY LEUKEMIA; CANCER
MODELS; CELL-LINES; CYTOTOXICITY; TUMORS; VIVO
AB VNP40101M is a novel alkylating agent that yields two reactive compounds (a chloroethylating species and methylisocyanate) and has demonstrated activity against a wide spectrum of tumor xenografts. VNP40101M was tested against an in vivo panel of five pediatric brain tumor xenografts at a dose of 18 mg/kg/day administered for 5 days. O-6-methylguanine-DNA methyltransferase (MGMT) levels of xenografts were assessed by Western blot analysis. Only one xenograft (GBM2), which lacked detectable MGMT expression, demonstrated an objective response to VNP40101M. VNP4010M antitumor activity was observed only in the absence of MGMT expression, with resistance to VNP4010M seen even with low MGMT expression.
C1 [Gururangan, Sridharan] Duke Univ, Med Ctr, Preston Robert Tisch Brain Tumor Ctr, Dept Pediat, Durham, NC 27710 USA.
[Morton, Christopher L.; Billups, Catherine; Houghton, Peter J.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Gururangan, Sridharan] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA.
RP Gururangan, S (reprint author), Duke Univ, Med Ctr, Preston Robert Tisch Brain Tumor Ctr, Dept Pediat, 047 Baker House,Trent Dr, Durham, NC 27710 USA.
EM gurur002@mc.duke.edu
RI Houghton, Peter/E-3265-2011
FU NCI NIH HHS [CA108786, N01 CM042216, N01-CM-42216, N01CM42216, P30
CA021765, CA21765, P50 CA108786]
NR 16
TC 7
Z9 7
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD SEP
PY 2008
VL 51
IS 3
BP 439
EP 441
DI 10.1002/pbc.21620
PG 3
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 329YU
UT WOS:000257907300029
PM 18493996
ER
PT J
AU Chilongozi, D
Wang, L
Brown, L
Taha, T
Valentine, M
Emel, L
Sinkala, M
Kafulafula, G
Noor, RA
Read, JS
Brown, ER
Goldenberg, RL
Hoffman, I
AF Chilongozi, Duvid
Wang, Lei
Brown, Lillian
Taha, Taha
Valentine, Melgan
Emel, Lynda
Sinkala, Moses
Kafulafula, George
Noor, Ramadhani A.
Read, Jennifer S.
Brown, Elizabeth R.
Goldenberg, Robert L.
Hoffman, Irving
CA HIVNET 024 Study Team
TI Morbidity and mortality among a cohort of human immunodeficiency virus
type 1-infected and uninfected pregnant women and their infants from
Malawi, Zambia, and Tanzania
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE HIV-1 infection; infant mortality; maternal morbidity and mortality;
sub-Saharan Africa; pregnant women
ID ANTIRETROVIRAL THERAPY; SCALING-UP; CHORIOAMNIONITIS; TRANSMISSION;
ANTIBIOTICS; OUTCOMES; MOTHERS; AFRICA; UGANDA; TRIAL
AB Background: Morbidity and mortality patterns among pregnant women and their infants (before antiretroviral therapy was widely available) determines HIV-1 diagnostic, monitoring, and care interventions.
Methods: Data from mothers and their infants enrolled in a trial of antibiotics to reduce mother-to-child-transmission of HIV-1 at 4 sub-Saharan African sites were analyzed. Women were enrolled during pregnancy and follow-up continued until the infants reached 12 months of age. We describe maternal and infant morbidity and mortality in a cohort of HIV-1-infected and HIV-1-uninfected mothers. Maternal and infant factors associated with mortality risk in the infants were assessed using Cox proportional hazard modeling.
Results: Among 2292 HIV-1-infected mothers, 166 (7.2%) had a serious adverse event (SAE) and 42 (1.8%) died, whereas no deaths Occurred among the 331 HIV-1 uninfected mothers. Four hundred twenty-four (17.8%) of 2383 infants had an SAE and 349 (16.4%) died before the end of follow-up. Infants with early HIV-1 infection (birth to 4-6 weeks) had the highest mortality. Among infants born to HIV-1-infected women, maternal morbidity and mortality (P 0.0001), baseline CD4 Count (P = 0.0002), and baseline plasma HIV-1 RNA concentration (P < 0.0001) were significant predictors of infant mortality in multivariate analyses.
Conclusions: The high mortality among infants with early HIV-1 infection supports access to HIV-1 diagnostics and appropriate early treatment for all infants of HIV-1-infected mothers. The significant association between stage of maternal HIV-1 infection and infant mortality supports routine CD4 Counts at the time of prenatal HIV-1 testing.
C1 [Chilongozi, Duvid] Univ N Carolina Project, Lilongwe, Malawi.
[Wang, Lei; Emel, Lynda] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA.
[Brown, Lillian] Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC 27599 USA.
[Hoffman, Irving] Univ N Carolina, Div Infect Dis, Chapel Hill, NC 27599 USA.
[Taha, Taha] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Valentine, Melgan] Family Hlth Int, Res Triangle Pk, NC 27709 USA.
[Sinkala, Moses] Ctr Infect Dis Res Zambia, Lusaka, Zambia.
[Sinkala, Moses; Goldenberg, Robert L.] Univ Alabama, Dept Obstet & Gynecol, Birmingham, AL USA.
[Kafulafula, George] Univ Malawi, Coll Med, Dept Obstet & Gynaecol, Blantyre, Malawi.
[Noor, Ramadhani A.] Muhimbili Univ, Dar Es Salaam, Tanzania.
[Read, Jennifer S.] NICHHD, Pediat Adolescent & Maternal AIDS Branch, Seattle, WA USA.
[Brown, Elizabeth R.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
RP Hoffman, I (reprint author), Univ N Carolina, Div Infect Dis, 130 Mason Farm Rd, Chapel Hill, NC 27599 USA.
EM hoffmani@med.unc.edu
RI Brown, Elizabeth/A-8984-2008
FU HIV Network for Prevention Trials (HIVNET); U.S. National Institute of
Allergy and Infectious Diseases (NIAID); National Institutes of Health;
Department of Health and Human Services [N01-Al-35173, N01-Al-45200,
N01-Al-35173-117/412]; U.S. National Institute of Allergy and Infectious
Diseases; National Institute of Child Health and Human Development
National Institute Oil Drug Abuse; National Institute of Mental Health;
Harvard University [U01-Al-48006]; Johns Hopkins University
[U01-Al-48005]; University of Alabama Birmingham [U01-Al-47972]
FX This study was supported by the HIV Network for Prevention Trials
(HIVNET) and sponsored by the U.S. National Institute of Allergy and
Infectious Diseases (NIAID), the National Institutes of Health, and
Department of Health and Human Services, through contract #N01-Al-35173
with Family Health International: contract #N01-Al-45200 with Fred
Hutchinson Cancer Research Center, and subcontract #N01-Al-35173-117/412
with Johns Hopkins University. This work was also sponsored by the U.S.
National Institute of Allergy and Infectious Diseases, National
Institute of Child Health and Human Development National Institute Oil
Drug Abuse. National Institute Of Mental Health and the Office of AIDS
Research at the National Institutes of Health.. U.S. Department of
Health aid Human Services, Harvard University (U01-Al-48006), Johns
Hopkins University (U01-Al-48005), and the University of Alabama
Birmingham (U01-Al-47972). Boehringer Ingelheim GMBH, Ingelheim,
Germany) for the study provided by Boehringer Ingelheim Pharmaceuticals,
Incorporated.
NR 16
TC 59
Z9 59
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD SEP
PY 2008
VL 27
IS 9
BP 808
EP 814
DI 10.1097/INF.0b013e31817109a4
PG 7
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 343OE
UT WOS:000258862600007
PM 18679152
ER
PT J
AU Hayden, R
Pounds, S
Knapp, K
Petraitiene, R
Schaufele, RL
Sein, T
Walsh, TJ
AF Hayden, Randall
Pounds, Stanley
Knapp, Katherine
Petraitiene, Ruta
Schaufele, Robert L.
Sein, Tin
Walsh, Thomas J.
TI Galactomannan antigenemia in pediatric oncology patients with invasive
aspergillosis
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE aspergillosis; galactomannan; pediatric oncology
ID LINKED-IMMUNOSORBENT-ASSAY; CHRONIC GRANULOMATOUS-DISEASE; CELL
TRANSPLANT RECIPIENTS; TIME PCR ASSAY; PULMONARY ASPERGILLOSIS;
FUNGAL-INFECTIONS; ENZYME-IMMUNOASSAY; ANTIFUNGAL THERAPY; NEUTROPENIC
PATIENTS; EARLY-DIAGNOSIS
AB Background: Diagnosing invasive aspergillosis is difficult but might be improved by detection of circulating galactomannan. Although galactomannan antigenemia has been well studied ill the detection of invasive aspergillosis ill adult patients, little is known about the expression of circulating galactomannan in immunocompromised children with invasive aspergillosis.
Methods: We studied the expression of galactomannan antigen by enzyme immunoassay (EIA) ill 990 sserum samples from 56 pediatric oncology patients (ages 3 months to 18 years) of whom 17 had proven or probable invasive aspergillosis defined by the European Organization for Research and Treatment of Cancer-Mycoses Study Group criteria. Any sample with a galactomannan EIA Galactomannan index value of >= 0.5 was considered positive.
Results: At least 1 serum sample was positive for 11 of 17 pediatric oncology patients (65.7% sensitivity, 95% confidence interval: 38.3-85.7) with invasive aspergillosis. Galactomannan HA was positive in 99 of 304 samples from patients with proven or probable invasive aspergillosis, and 7 of 686 (1.0%) samples from 39 control subjects resulted in a positive galactomannan EIA result. At least I sample tested positive in 5 of the 39 controls (12.8%. 95% confidence interval: 4.3-27.4). No significant association between accuracy and patient age vas observed. Among the 7 evaluable galactomannan-positive patients with IA, the galactomannan EIA produced a positive result before clinical or radiographic evidence of infection in 6 cases, with a lead-time to diagnosis ranging from 1 day to 34 days (median: 10 clays). In the remaining case, a positive galactomannan vas observed on the same clay as diagnosis by non-EIA methods.
Conclusions: The presence of circulating galactomannan is predictive of invasive aspergillosis in most pediatric oncology patients. Galactomannan antigenemia may precede clinical, microbiologic, oradiographic evidence of invasive aspergillosis.
C1 [Petraitiene, Ruta; Schaufele, Robert L.; Sein, Tin; Walsh, Thomas J.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Hayden, Randall] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38101 USA.
[Pounds, Stanley] St Jude Childrens Res Hosp, Dept Biostat, Memphis, TN 38101 USA.
[Knapp, Katherine] St Jude Childrens Res Hosp, Dept Infect Dis, Memphis, TN 38101 USA.
SAIC Frederick Inc, Lab Anim Sci Program, Frederick, MD USA.
RP Walsh, TJ (reprint author), NCI, Pediat Oncol Branch, CRC 1-5750,10 Ctr Dr, Bethesda, MD 20892 USA.
EM walsht@mail.nih.gov
OI Pounds, Stanley/0000-0002-9167-2114
FU American Lebanese Syrian Associated Charities (ALSAC); National Cancer
Institute, Bethesda, MD
FX The authors thank Diane Brand for assistance in clinical data extraction
and the staff of the Clinical Microbiology Laboratory of St. Jude
Children's Research Hospital. This study was supported in part by the
American Lebanese Syrian Associated Charities (ALSAC) and by the
Intramural Research Program of the National Cancer Institute, Bethesda,
MD.
NR 52
TC 39
Z9 40
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD SEP
PY 2008
VL 27
IS 9
BP 815
EP 819
DI 10.1097/INF.0b013e31817197ab
PG 5
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 343OE
UT WOS:000258862600008
PM 18703991
ER
PT J
AU Chang, M
Parker, EA
Muller, TJM
Haenen, C
Mistry, M
Finkielstain, GP
Murphy-Ryan, M
Barnes, KM
Sundaram, R
Baron, J
AF Chang, Maria
Parker, Elizabeth A.
Muller, Tessa J. M.
Haenen, Caroline
Mistry, Maanasi
Finkielstain, Gabriela P.
Murphy-Ryan, Maureen
Barnes, Kevin M.
Sundaram, Rajeshwari
Baron, Jeffrey
TI Changes in cell-cycle kinetics responsible for limiting somatic growth
in mice
SO PEDIATRIC RESEARCH
LA English
DT Article
ID POSTNATAL GROWTH; RAT; BROMODEOXYURIDINE; CHILDREN; LENGTHS; NUMBER
AB In mammals, the rate of somatic growth is rapid ill early postnatal life but then slows with age, approaching zero as the animal approaches adult body size. To investigate the underlying changes in cell-cycle kinetics, [methyl-H-3]thymidine and 5'-bromo-2'deoxyuridine were used to double-label proliferating cells in 1-, 2-, and 3-wk-old mice for four weeks. Proliferation of renal tubular epithelial cells and hepatocytes decreased with age. The average cell-cycle time did not increase in liver and increased only 1.7 fold in kidney. The fraction of cells in S-phase that will divide again declined approximately 10 fold with age. Concurrently, average cell area increased approximately 2 told. The findings suggest that somatic growth deceleration primarily results not from an increase in cell-cycle time but from a decrease in growth fraction (fraction of cells that continue to proliferate). During the deceleration phase. cells appear to reach it proliferative limit and undergo their final cell divisions, staggered over time. Concomitantly, cells enlarge to a greater volume, perhaps because they are relieved of the size constraint imposed by cell division. In conclusion. a decline in growth fraction with age causes somatic growth deceleration and thus Sets a fundamental limit on adult body size.
C1 [Baron, Jeffrey] NICHD, NIH, Sect Growth & Dev, Bethesda, MD 20892 USA.
[Sundaram, Rajeshwari] NIH, Biometry & Math Stat Branch, Bethesda, MD 20892 USA.
RP Baron, J (reprint author), NICHD, NIH, Sect Growth & Dev, Bldg CRC,Room 1-3330,10 Ctr Dr MSC 1103, Bethesda, MD 20892 USA.
EM jeffrey.baron@nih.gov
OI Sundaram, Rajeshwari/0000-0002-6918-5002
FU National Institute of Child Health and Human Development; NIH
FX This research was supported by the Intramural Research Program of the
National Institute of Child Health and Human Development, NIH.
NR 18
TC 17
Z9 17
U1 0
U2 3
PU INT PEDIATRIC RESEARCH FOUNDATION, INC
PI BALTIMORE
PA 351 W CAMDEN ST, BALTIMORE, MD 21201-2436 USA
SN 0031-3998
J9 PEDIATR RES
JI Pediatr. Res.
PD SEP
PY 2008
VL 64
IS 3
BP 240
EP 245
DI 10.1203/PDR.0b013e318180e47a
PG 6
WC Pediatrics
SC Pediatrics
GA 344DR
UT WOS:000258906700005
PM 18535488
ER
PT J
AU Kahana, SY
Frazier, TW
Drotar, D
AF Kahana, Shoshana Y.
Frazier, Thomas W.
Drotar, Dennis
TI Preliminary quantitative investigation of predictors of treatment
non-adherence in pediatric transplantation: A brief report
SO PEDIATRIC TRANSPLANTATION
LA English
DT Article
DE non-adherence; transplantation; pediatric; predictor
ID HEART-LUNG TRANSPLANTATION; LIVER-TRANSPLANT; RENAL-TRANSPLANTATION;
MEDICATION ADHERENCE; RECIPIENTS; NONCOMPLIANCE; CHILDREN; ADOLESCENTS;
VARIABLES
AB The examination of predictors of non-adherence in transplantation populations offers the potential to identify high-risk individuals and concomitantly generate effective adherence-promoting interventions. The present paper aggregated quantitative estimates of various correlates of treatment adherence in studies of pediatric transplantation. Seventeen studies and three classes of predictors of non-adherence, including demographic, psychosocial, and treatment-related predictors, were included in the current analyses. The weighted means effect sizes for the demographic factors were in the small to medium range (female gender mean d = 0.35, 95% CI = 0.32-0.38, n = 8; mean age d = 0.55, 95% CI = 0.52-0.58, n = 7), suggesting that older youth and males tended to display more non-adherence behaviors than younger youth and females, respectively. Several psychosocial factors exhibited large to very large relationships with non-adherence, in particular comorbid psychiatric conditions (mean d = 1.04, 95% CI = 0.66-1.42, n = 3) and child self-responsibility for medication (mean d = 0.88, 95% CI = 0.53-1.23, n = 3). Finally, prior treatment/grafts (mean d = 0.17, 95% CI = -0.15-0.49, n = 3) and donor source (mean d = 0.33, 95% CI = -0.10-0.76, n = 4) exhibited small, non-significant relationships with non-adherence. Limitations of the study are discussed as are future directions for research.
C1 [Kahana, Shoshana Y.; Drotar, Dennis] Cincinnati Childrens Hosp, Med Ctr, Div Behav Med & Clin Psychol, Ctr Promot Adherence & Self Management, Cincinnati, OH USA.
[Frazier, Thomas W.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
RP Kahana, SY (reprint author), NIMH, Div Dev Translat Res, 6001 Execut Blvd,MSC 9617,Room 6190, Bethesda, MD 20892 USA.
EM sykahana@gmail.com
NR 33
TC 25
Z9 26
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1397-3142
J9 PEDIATR TRANSPLANT
JI Pediatr. Transplant.
PD SEP
PY 2008
VL 12
IS 6
BP 656
EP 660
DI 10.1111/j.1399-3046.2007.00864.x
PG 5
WC Pediatrics; Transplantation
SC Pediatrics; Transplantation
GA 335JW
UT WOS:000258287900009
PM 18798360
ER
PT J
AU Laptook, A
Tyson, J
Shankaran, S
McDonald, S
Ehrenkranz, R
Fanaroff, A
Donovan, E
Goldberg, R
O'Shea, TM
Higgins, RD
Poole, WK
AF Laptook, Abbot
Tyson, Jon
Shankaran, Seetha
McDonald, Scott
Ehrenkranz, Richard
Fanaroff, Avroy
Donovan, Edward
Goldberg, Ronald
O'Shea, T. Michael
Higgins, Rosemary D.
Poole, W. Kenneth
CA Natl Inst Child Hlth Human Dev Neo
TI Elevated temperature after hypoxic-ischemic encephalopathy: Risk factor
for adverse outcomes
SO PEDIATRICS
LA English
DT Article
DE hypoxic-ischemic encephalopathy; neurologic outcome; temperature
ID NEONATAL ENCEPHALOPATHY; BRAIN TEMPERATURE; FOREBRAIN ISCHEMIA;
CEREBRAL-ISCHEMIA; BIRTH-WEIGHT; ACUTE STROKE; HYPERTHERMIA;
HYPOTHERMIA; INFANTS; INJURY
AB OBJECTIVE. The goal was to determine whether the risk of death or moderate/severe disability in term infants with hypoxic-ischemic encephalopathy increases with relatively high esophageal or skin temperature occurring between 6 and 78 hours after birth.
METHODS. This was an observational secondary study within the National Institute of Child Health and Human Development Neonatal Research Network randomized trial comparing whole-body cooling and usual care (control) for term infants with hypoxic-ischemic encephalopathy. Esophageal and skin temperatures were recorded serially for 72 hours. Each infant's temperatures for each site were rank ordered. The high temperature was defined for each infant as the mean of all temperature measurements in the upper quartile. The low temperature was similarly defined as the mean of the lower quartile. Outcomes were related to temperatures in 3 logistic regression analyses for the high, median, and low temperatures at each temperature site for each group, with adjustment for the level of encephalopathy, gender, gestational age, and race.
RESULTS. In control infants, the mean esophageal temperature was 37.2 +/- 0.7 degrees C over the 72-hour period, and 63%, 22%, and 8% of all temperatures were >37 degrees C, > 37.5 degrees C, and >38 degrees C, respectively. The mean skin temperature was 36.5 +/- 0.8 degrees C, and 12%, 5%, and 2% of all temperatures were >37 degrees C, >37.5 degrees C, and >38 degrees C, respectively. The odds of death or disability were increased 3.6-4 fold for each 1 degrees C increase in the highest quartile of skin or esophageal temperatures. There were no associations between temperatures and outcomes in the cooling-treated group.
CONCLUSIONS. Relatively high temperatures during usual care after hypoxia-ischemia were associated with increased risk of adverse outcomes. The results may reflect underlying brain injury and/or adverse effects of temperature on outcomes.
C1 [Laptook, Abbot] Women & Infants Hosp Rhode Isl, Dept Pediat, Providence, RI 02906 USA.
[Tyson, Jon] Univ Texas Houston, Dept Pediat, Houston, TX USA.
[Shankaran, Seetha] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[McDonald, Scott; Poole, W. Kenneth] RTI Int, Dept Stat & Epidemiol, Res Triangle Pk, NC USA.
[Ehrenkranz, Richard] Yale Univ, Dept Pediat, New Haven, CT 06520 USA.
[Fanaroff, Avroy] Case Western Reserve Univ, Dept Pediat, Cleveland, OH 44106 USA.
[Donovan, Edward] Univ Cincinnati, Dept Pediat, Cincinnati, OH 45221 USA.
[Goldberg, Ronald] Duke Univ, Dept Pediat, Durham, NC 27706 USA.
[O'Shea, T. Michael] Wake Forest Univ, Dept Pediat, Winston Salem, NC 27109 USA.
[Higgins, Rosemary D.] NICHHD, Bethesda, MD 20892 USA.
RP Laptook, A (reprint author), Women & Infants Hosp Rhode Isl, Dept Pediat, 101 Dudley St, Providence, RI 02906 USA.
EM alaptook@wihri.org
RI Myers , Gary /I-4901-2013
OI Myers , Gary /0000-0003-4317-015X
FU National Institutes of Health [U10 HD34216, U10 HD27853, U10 HD27871,
U10 HD40461, U10 HD40689, U10 HD27856, U10 HD27904, U10 HD40498, U10
HD40521, U10 HD36790, U10 HD21385, U10 HD27880, U10 HD27851, U10 HD
21373]; General Clinical Research Center [M01 RR 08084, M01 RR 00125,
M01 RR 00750, M01 RR 00070, M01 RR 0039-43, M01RR 00039, 5 M01 RR00044]
FX This work was supported in part by National Institutes of Health grants
U10 HD34216, U10 HD27853, U10 HD27871, U10 HD40461, U10 HD40689, U10
HD27856, U10 HD27904, U10 HD40498, U10 HD40521, U10 HD36790, U10
HD21385, U10 HD27880, U10 HD27851, and U10 HD 21373 and General Clinical
Research Center grants M01 RR 08084, M01 RR 00125, M01 RR 00750, M01 RR
00070, M01 RR 0039-43, M01RR 00039, and 5 M01 RR00044.
NR 36
TC 71
Z9 72
U1 0
U2 0
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD SEP
PY 2008
VL 122
IS 3
BP 491
EP 499
DI 10.1542/peds.2007-1673
PG 9
WC Pediatrics
SC Pediatrics
GA 342ZR
UT WOS:000258822600003
PM 18762517
ER
PT J
AU Cole, CR
Hansen, NI
Higgins, RD
Ziegler, TR
Stoll, BJ
AF Cole, Conrad R.
Hansen, Nellie I.
Higgins, Rosemary D.
Ziegler, Thomas R.
Stoll, Barbara J.
CA Eunice Kennedy Shriver NICHD Neona
TI Very low birth weight preterm infants with surgical short bowel
syndrome: Incidence, morbidity and mortality, and growth outcomes at 18
to 22 months
SO PEDIATRICS
LA English
DT Article
DE short bowel syndrome; preterm; necrotizing enterocolitis; nutrition
ID NEONATAL RESEARCH NETWORK; HOME PARENTERAL-NUTRITION; NECROTIZING
ENTEROCOLITIS; INTESTINAL RESECTION; UNITED-STATES; CHILDREN;
MANAGEMENT; EPIDEMIOLOGY; DEPENDENCE; DURATION
AB OBJECTIVES. The objective of this study was to determine the (1) incidence of short bowel syndrome in very low birth weight (< 1500 g) infants, (2) associated morbidity and mortality during initial hospitalization, and (3) impact on short-term growth and nutrition in extremely low birth weight (< 1000 g) infants.
METHODS. Infants who were born from January 1, 2002, through June 30, 2005, and enrolled in the National Institute of Child Health and Human Development Neonatal Research Network were studied. Risk factors for developing short bowel syndrome as a result of partial bowel resection (surgical short bowel syndrome) and outcomes were evaluated for all neonates until hospital discharge, death, or 120 days. Extremely low birth weight survivors were further evaluated at 18 to 22 months' corrected age for feeding methods and growth.
RESULTS. The incidence of surgical short bowel syndrome in this cohort of 12 316 very low birth weight infants was 0.7%. Necrotizing enterocolitis was the most common diagnosis associated with surgical short bowel syndrome. More very low birth weight infants with short bowel syndrome (20%) died during initial hospitalization than those without necrotizing enterocolitis or short bowel syndrome (12%) but fewer than the infants with surgical necrotizing enterocolitis without short bowel syndrome (53%). Among 5657 extremely low birth weight infants, the incidence of surgical short bowel syndrome was 1.1%. At 18 to 22 months, extremely low birth weight infants with short bowel syndrome were more likely to still require tube feeding (33%) and to have been rehospitalized (79%). Moreover, these infants had growth delay with shorter lengths and smaller head circumferences than infants without necrotizing enterocolitis or short bowel syndrome.
CONCLUSIONS. Short bowel syndrome is rare in neonates but has a high mortality rate. At 18 to 22 months' corrected age, extremely low birth weight infants with short bowel syndrome were more likely to have growth failure than infants without short bowel syndrome.
C1 [Cole, Conrad R.] Emory Univ, Sch Med, Div Pediat Gastroenterol Hepatol & Nutr, Dept Pediat, Atlanta, GA 30322 USA.
[Cole, Conrad R.; Stoll, Barbara J.] Emory Univ, Sch Med, Dept Med, Atlanta, GA 30322 USA.
[Hansen, Nellie I.] RTI Int, Res Triangle Pk, NC USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Cole, CR (reprint author), Emory Univ, Sch Med, Div Pediat Gastroenterol Hepatol & Nutr, Dept Pediat, 2015 Uppergate Dr, Atlanta, GA 30322 USA.
EM conrad_cole@oz.ped.emory.edu
RI Myers , Gary /I-4901-2013
OI Myers , Gary /0000-0003-4317-015X
FU NCATS NIH HHS [KL2 TR000455, UL1 TR000454]; NCRR NIH HHS [M01 RR6022,
1KL2RR025009, 5K12RR017643, K12 RR017643, K24 RR023356, K24 RR023356-03,
KL2 RR025009, M01 RR000039, M01 RR000039-475518, M01 RR006022, M01
RR007122, M01 RR008084, M01 RR016587, M01 RR16587, M01 RR30, M01 RR39,
M01 RR44, M01 RR633, M01 RR70, M01 RR7122, M01 RR750, M01 RR80, M01
RR8084, UL1 RR024139, UL1 RR24139]; NICHD NIH HHS [U01 HD036790, U01
HD36790, U10 HD021364, U10 HD021373, U10 HD021385, U10 HD021397, U10
HD027851, U10 HD027853, U10 HD027856, U10 HD027871, U10 HD027880, U10
HD027904, U10 HD034216, U10 HD040461, U10 HD040492, U10 HD040498, U10
HD040521, U10 HD040689, U10 HD21364, U10 HD21373, U10 HD21385, U10
HD21397, U10 HD27851, U10 HD27853, U10 HD27856, U10 HD27871, U10
HD27880, U10 HD27904, U10 HD34216, U10 HD40461, U10 HD40492, U10
HD40498, U10 HD40521, U10 HD40689]
NR 37
TC 54
Z9 55
U1 0
U2 3
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD SEP
PY 2008
VL 122
IS 3
BP E573
EP E582
DI 10.1542/peds.2007-3449
PG 10
WC Pediatrics
SC Pediatrics
GA 342ZR
UT WOS:000258822600058
PM 18762491
ER
PT J
AU Ferreira-Gonzalez, A
Teutsch, S
Williams, MS
Au, SM
FitzGerald, KT
Miller, PS
Fomous, C
AF Ferreira-Gonzalez, Andrea
Teutsch, Steven
Williams, Marc S.
Au, Sylvia M.
FitzGerald, Kevin T.
Miller, Paul Steven
Fomous, Cathy
CA Secretarys Advisory Comm Genetics
TI US system of oversight for genetic testing: a report from the
Secretary's Advisory Committee on Genetics, Health and Society
SO PERSONALIZED MEDICINE
LA English
DT Article
DE analytical validity; CLIA; clinical decision support; clinical utility;
clinical validity; genetic testing; health communication; oversight;
proficiency testing; USFDA
AB As genetic testing technology is integrated into healthcare, increasingly detailed information about individual and population genetic variation is available to patients and providers. Health professionals use genetic testing to diagnose or assess the risk of disease in individuals, families and populations and to guide healthcare decisions. Consumers are beginning to explore personalized genomic services in an effort to learn more about their risk for common diseases. Scientific and technological advances in genetic testing, as with any newly introduced medical technology, present certain challenges to existing frameworks of oversight. in addition, the growing use of genetic testing will require a significant investment in evidence-based assessments to understand the validity and utility of these tests in clinical and personal decisionmaking. To optimize the use of genetic testing in healthcare, all sectors of the oversight system need to be strengthened and yet remain flexible in order to adapt to advances that will inevitably increase the range of genetic tests and methodologies.
C1 [Fomous, Cathy] NIH, Off Biotechnol Act, Bethesda, MD 20892 USA.
[Ferreira-Gonzalez, Andrea] Virginia Commonwealth Univ, Richmond, VA 23284 USA.
[Teutsch, Steven] Merck & Co Inc, Whitehouse Stn, NJ USA.
[FitzGerald, Kevin T.] Georgetown Univ, Washington, DC 20057 USA.
[Miller, Paul Steven] Univ Washington, Sch Law, Seattle, WA 98195 USA.
RP Fomous, C (reprint author), NIH, Off Biotechnol Act, 6705 Rockledge Dr,Suite 750, Bethesda, MD 20892 USA.
EM cfomous@od.nih.gov
OI Williams, Marc/0000-0001-6165-8701
FU Intramural NIH HHS [Z99 OD999999]
NR 3
TC 6
Z9 6
U1 0
U2 1
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1741-0541
J9 PERS MED
JI Pers. Med.
PD SEP
PY 2008
VL 5
IS 5
BP 521
EP 528
DI 10.2217/17410541.5.5.521
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 349JZ
UT WOS:000259278400019
PM 20490368
ER
PT J
AU Janakiram, NB
Indranie, C
Malisetty, SV
Jagan, P
Steele, VE
Rao, CV
AF Janakiram, Naveena B.
Indranie, Cooma
Malisetty, Swamy V.
Jagan, Patlolla
Steele, Vernon E.
Rao, Chinthalapally V.
TI Chemoprevention of Colon Carcinogenesis by Oleanolic Acid and Its Analog
in Male F344 Rats and Modulation of COX-2 and Apoptosis in Human Colon
HT-29 Cancer Cells
SO PHARMACEUTICAL RESEARCH
LA English
DT Article
DE chemoprevention; colon cancer; COX-2; iNOS; triterpenoids
ID ABERRANT CRYPT FOCI; NITRIC-OXIDE; URSOLIC ACID; CYCLOOXYGENASE-2
INHIBITOR; INCREASED EXPRESSION; COLORECTAL-CANCER; AZOXYMETHANE; RISK;
PREVENTION; CELECOXIB
AB Purpose. To assess the chemopreventive effect of oleanolic acid (ONA) and its synthetic analog 18 alpha-olean-12-ene-3 beta-23,28-triol (OT) on azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) in F344 rats and understand anti-inflammatory properties and apoptosis effects in HT29 colon cancer cells and Raw 264.7 macrophage cell lines.
Methods. Five week-old male F344 rats were fed a control diet or experimental diets containing two doses of ONA (750 and 1,500 ppm) and OT (250 and 500 ppm). After 1 week, all animals were s.c. injected with AOM (15 mg/kg body weight, once weekly for 2 weeks). At 14 weeks of age, all rats were killed and colons were evaluated for ACF. Cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) expressions and apoptosis were assessed in cell lines exposed to OT using western blots and 4',6-diamidino-2-phenylindole staining.
Results. Administration of ONA and OT inhibited mean colonic ACF and multi-crypt AC/foci in a dose dependent manner (p < 0.001-0.0001). OT blocked the COX-2 expression induced by phorbol 12-myristate 13-acetate in a dose-dependent manner and induced apoptosis in HT-29 cancer cells, and suppressed iNOS activation in RAW264.7 macrophages.
Conclusions. ONA and OT possess chemopreventive activity against colon carcinogenesis in rat and OT inhibits the COX-2 and iNOS and induces apoptosis in cell lines.
C1 [Janakiram, Naveena B.; Indranie, Cooma; Malisetty, Swamy V.; Jagan, Patlolla; Rao, Chinthalapally V.] Univ Oklahoma, Hlth Sci Ctr, OU Canc Inst, Hem Onc Sect,Dept Med, Oklahoma City, OK 73104 USA.
[Steele, Vernon E.] NCI, Chemoprevent Agent Dev Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
RP Rao, CV (reprint author), Univ Oklahoma, Hlth Sci Ctr, OU Canc Inst, Hem Onc Sect,Dept Med, Oklahoma City, OK 73104 USA.
EM cv-rao@ouhsc.edu
RI Chinthalapally, Rao/B-3633-2010
FU NCI
FX We gratefully acknowledge NCI chemoprevention drug development
repository for providing oleanolic acid analog OT. We also extend our
thanks to Ms. Alyson Atchison for editing this article.
NR 36
TC 29
Z9 31
U1 1
U2 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0724-8741
J9 PHARM RES-DORD
JI Pharm. Res.
PD SEP
PY 2008
VL 25
IS 9
BP 2151
EP 2157
DI 10.1007/s11095-008-9582-7
PG 7
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
SC Chemistry; Pharmacology & Pharmacy
GA 337AR
UT WOS:000258408400019
PM 18408893
ER
PT J
AU Shin, SH
Kluepfel-Stahl, S
Cooney, AM
Kaneski, CR
Quirk, JM
Schiffmann, R
Brady, RO
Murray, GJ
AF Shin, Sang H.
Kluepfel-Stahl, Stefanie
Cooney, Adele M.
Kaneski, Christine R.
Quirk, Jane M.
Schiffmann, Raphael
Brady, Roscoe O.
Murray, Gary J.
TI Prediction of response of mutated alpha-galactosidase A to a
pharmacological chaperone
SO PHARMACOGENETICS AND GENOMICS
LA English
DT Article
DE alpha-galactosidase A; Fabry disease; lysosomal storage disorders;
molecular chaperone; molecular mechanisms of pharmacological action;
pharmacological chaperone
ID FABRY-DISEASE; ENZYME-ACTIVITY; DEFECT; GENE; MUTATIONS; STORAGE; STROKE
AB Objective To examine the relationship between types and locations of mutations of the enzyme alpha-galactosidase (Gal) A in Fabry disease and the response to the pharmacological chaperone 1-deoxygalactonojirimycin (DGJ)
Methods T cells grown from normal individuals or from patients with Fabry disease were tested for response to treatment with DGJ by increased activity of alpha-Gal A.
Results Cells from normal controls responded with a 28% increase in alpha-Gal A activity, whereas response in Fabry individuals was mutation dependent ranging from no increase to fully normal activity. Nine truncation mutations (all nonresponsive) and 31 missense mutations were tested. Three groups of missense mutations were categorized: responders with activity more than 25% of normal, nonresponders, with less than 7% and an intermediate response group. In normal cells and in responders an increase in the mature lysosomal form of alpha-Gal A was observed after DGJ treatment. Nonresponders showed little or no protein with or without DGJ. The intermediate response group showed an increase in band intensity but incomplete processing of the enzyme to the mature form.
Conclusion Mapping the missense mutations to the structure of alpha-Gal A identified several factors that may influence response. Mutations in regions that are not in alpha-helix or beta-sheets, neither involved in disulfide bonds nor with an identified functional or structural role were more likely to respond. Predictability is, however, not precise and testing of each mutation for response to pharmacological chaperone therapy is necessary for Fabry disease and related lysosomal storage disorders.
C1 [Shin, Sang H.; Kluepfel-Stahl, Stefanie; Cooney, Adele M.; Kaneski, Christine R.; Quirk, Jane M.; Schiffmann, Raphael; Brady, Roscoe O.; Murray, Gary J.] Natl Inst Neurol Disorders & Stroke, Dev & Metab Neurol Branch, Bethesda, MD USA.
RP Murray, GJ (reprint author), NIH, Bldg 10,Room 3D04, Bethesda, MD 20891 USA.
EM murrayg@mail.nih.gov
OI Kaneski, Christine/0000-0003-1453-2502
FU National Institute of Neurologic Disorders and Stroke; National
Institutes of Health; The Public Health Service and Amicus Therapeutics,
Inc [01956]
FX This study was supported in part by the Intramural Program of the
National Institute of Neurologic Disorders and Stroke, National
Institutes of Health. The Public Health Service and Amicus Therapeutics,
Inc. have a Cooperative Research and Development Agreement, #01956. The
authors thank Dr Greg Pastores at New York University for genotyping
some of the patients' samples. The authors appreciate Gregory Zirzow at
NINDS for technical assistance. The contribution of both the patients
and volunteers who participated in this study is gratefully
acknowledged.
NR 22
TC 30
Z9 31
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1744-6872
J9 PHARMACOGENET GENOM
JI Pharmacogenet. Genomics
PD SEP
PY 2008
VL 18
IS 9
BP 773
EP 780
DI 10.1097/FPC.0b013e32830500f4
PG 8
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
& Pharmacy
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology
& Pharmacy
GA 342GE
UT WOS:000258771800004
PM 18698230
ER
PT J
AU Mamedova, LK
Wang, R
Besada, P
Liang, BT
Jacobson, KA
AF Mamedova, Liaman K.
Wang, Ruibo
Besada, Pedro
Liang, Bruce T.
Jacobson, Kenneth A.
TI Attenuation of apoptosis in vitro and ischemia/reperfusion injury in
vivo in mouse skeletal muscle by P2Y(6) receptor activation
SO PHARMACOLOGICAL RESEARCH
LA English
DT Article
DE Ischemia; Uracil nucleotide; G protein-coupled receptor; Tumor necrosis
factor; Skeletal muscle; UDP
ID PROTEIN-KINASE-C; NF-KAPPA-B; NUCLEOTIDE RECEPTORS; MUSCULAR-DYSTROPHY;
DERIVATIVES; ALPHA; CELLS; ASTROCYTES; PATHWAYS; SURVIVAL
AB Activation of the G(q)-coupled P2Y(6) receptor heterologously expressed in astrocytes significantly attenuates apoptosis induced by tumor necrosis factor alpha (TNF alpha). We have extended the analysis of P2Y(6) receptor-induced cytoprotection to mouse skeletal muscle cells endogenously expressing this receptor. The endogenous P2Y(6) receptor agonist UDP and synthetic agonist MRS2693 protected C2C12 skeletal muscle cells against apoptosis in a concentration-dependent manner (0.1-10 nM) as determined by propidium iodide staining, histochemical analysis using hematoxylin and Hoechst 33258, and DNA fragmentation. The insurmountable P2Y(6) receptor antagonist MRS2578 blocked the protection. TNF alpha-induced apoptosis in C2C12 cells correlated with activation of the transcription factor NF-kappa B. The NF-kappa B activation was attenuated by 10 nM MRS2693, which activated the antiapoptic ERK1/2 pathway. In an in vivo mouse hindlimb model, MRS2693 protected against skeletal muscle ischemia/reperfusion injury. The P2Y(6) receptor is a novel cytoprotective receptor that deserves further exploration in ameliorating skeletal muscle injury. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Mamedova, Liaman K.; Besada, Pedro; Jacobson, Kenneth A.] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Mamedova, Liaman K.] Kansas State Univ, Dept Anim Sci & Ind, Manhattan, KS 66506 USA.
[Wang, Ruibo; Liang, Bruce T.] Univ Connecticut, Ctr Hlth, Pat & Jim Calhoun Cardiol Ctr, Farmington, CT 06030 USA.
RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bldg 8A,Rm B1A 19, Bethesda, MD 20892 USA.
EM kajacobs@helix.nih.gov
RI Besada Pereira, Pedro/E-6051-2012; Jacobson, Kenneth/A-1530-2009
OI Besada Pereira, Pedro/0000-0002-9985-9063; Jacobson,
Kenneth/0000-0001-8104-1493
FU NIH; National Institute of Diabetes and Digestive and Kidney Diseases
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Diabetes and Digestive and Kidney Diseases.
We thank Cara Heller (NIDDK) for proofreading this manuscript.
NR 29
TC 18
Z9 20
U1 1
U2 2
PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
J9 PHARMACOL RES
JI Pharmacol. Res.
PD SEP-OCT
PY 2008
VL 58
IS 3-4
BP 232
EP 239
DI 10.1016/j.phrs.2008.08.004
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 375RT
UT WOS:000261131700009
PM 18805489
ER
PT J
AU Zhao, BZ
Bilski, PJ
He, YY
Feng, L
Chignell, CF
AF Zhao, Baozhong
Bilski, Piotr J.
He, Yu-Ying
Feng, Li
Chignell, Colin F.
TI Photo-induced reactive oxygen species generation by different
water-soluble fullerenes (C(60)) and their cytotoxicity in human
keratinocytes
SO PHOTOCHEMISTRY AND PHOTOBIOLOGY
LA English
DT Article
ID SINGLET OXYGEN; GAMMA-CYCLODEXTRIN; MOLECULAR-OXYGEN; C60; IRRADIATION;
OXIDATION; SYSTEM; AZIDE; ACID; NADH
AB In this study we report the phototoxicity toward HaCaT keratinocytes that results from the photogeneration of superoxide and singlet oxygen ((1)O(2)) by four different "water-soluble" fullerene (C(60)) preparations-monomeric (gamma-CyD)(2)/C(60) (gamma-cyclodextrin bicapped C(60)) and three aggregated forms-THF/nC(60) (prepared by solvent exchange from THF solution); Son/nC(60) (prepared by sonication of a toluene/water mixture); and gamma-CyD/nC(60) (prepared by heating the [gamma-CyD](2)/C(60) aqueous solution). Our results demonstrate that all four C(60) preparations photogenerate (1)O(2) efficiently. However, the properties of C(60)-generated (1)O(2), including its availability for reactions in solution, are markedly different for the monomeric and aggregated forms. (1)O(2) produced by monomeric (gamma-CyD)(2)/C(60) is quenchable by NaN(3) and its quantum yield in D(2)O, which is only weakly dependent on oxygen concentration, is as high as C(60) in toluene. In contrast, (1)O(2) generated from aggregated C(60) is not quenchable by NaN(3), exhibits a solvent-independent short-lived lifetime (ca 2.9 mu s), is highly sensitive to oxygen concentration while its phosphorescence is redshifted. All these features indicate that (1)O(2) is sequestered inside the C(60) aggregates, which may explain why these preparations were not phototoxic toward HaCaT cells. Electron paramagnetic resonance studies demonstrated the generation of the C(60) anion radical (C(60)(center dot-)) when (gamma-CyD)(2)/C(60) was irradiated (lambda > 300 nm) in the presence of a reducing agent (NADH); spin trapping experiments (lambda > 400 nm) with 5,5-dimethyl-1-pyrroline N-oxide clearly showed the generation of superoxide resulting from the reaction of C(60)(center dot-) with oxygen. In vitro tests with HaCaT keratinocytes provided evidence that (gamma-CyD)(2)/C(60) phototoxicity is mainly mediated by (1)O(2) (Type II mechanism) with only a minor contribution from free radicals (Type I mechanism).
C1 [Zhao, Baozhong; Bilski, Piotr J.; He, Yu-Ying; Feng, Li; Chignell, Colin F.] NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA.
RP Zhao, BZ (reprint author), NIEHS, Lab Pharmacol & Chem, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM zhaob2@niehs.nih.gov
RI Zhao, Baozhong/B-5865-2011
FU Intramural Research Program of the NIH; National Institute of
Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences. The authors
are indebted to Dr. Ann Motten and Dr. Albert Wielgus, NIEHS, for
critical reading of the manuscript, to Ms. D. Sutton and Mr. J. Horton,
NIEHS, for the TEM pictures and to Mr. Wayneho Kam for Matrox Inspector
analysis of the TEM particle size.
NR 37
TC 30
Z9 30
U1 2
U2 23
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0031-8655
J9 PHOTOCHEM PHOTOBIOL
JI Photochem. Photobiol.
PD SEP-OCT
PY 2008
VL 84
IS 5
BP 1215
EP 1223
DI 10.1111/j.1751-1097.2008.00333.x
PG 9
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 342LL
UT WOS:000258785500021
PM 18399919
ER
PT J
AU Chignell, CF
Sik, RH
Bilski, PJ
AF Chignell, Colin F.
Sik, Robert H.
Bilski, Piotr J.
TI The photosensitizing potential of compact fluorescent vs incandescent
light bulbs
SO PHOTOCHEMISTRY AND PHOTOBIOLOGY
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; PORPHYRIA-CUTANEA-TARDA; SKIN-LESIONS;
IRRADIATION
AB Recently an article about the new energy-saving compact fluorescent light (CFL) bulbs appeared in Parade magazine [Rosenfeld, I. (2008) ParadeFeb 3, 22]. Under the heading "Bright Lights, Bad Headache?" the writer states that "new research suggests some dangers" involving these lights because they are fluorescent and "can aggravate skin rashes in people with lups, eczema, dermatitis or porphyria." We measured the emission spectrum of a 14 W compact fluorescent bulb (with the same luminous flux as a 60 W incandescent bulb) and compared it to 60 W soft white incandescent and cool white fluorescent (CWF) bulbs. Our results clearly show that the spectral irradiance of the compact fluorescent bulb is similar to that of the CWF bulb; both exhibit sharp Hg emission lines at 365 nm (very weak), 404 nm (weak), 435 nm (moderate) and 543 nm (strong). In contrast, the emission of the incandescent bulb begins at 375 nm and then increases monotonically to above 750 nm. From their respective absorption spectra we calculated the potential photosensitization indices of protoporphyrin IX (PPIX; a prototypic porphyria skin photosensitizer) and riboflavin (a putative lens photosensitizer) vs 14 W compact fluorescent, CWF and 60 W incandescent bulbs. A higher photosensitization index would indicate a greater chance that the light/photosensitizer combination would cause photosensitization of the skin or eyes. We found that for PPIX and riboflavin the photosensitization index of the compact fluorescent bulb is less than half that of the 60 W incandescent bulb. These results suggest that substitution of a compact fluorescent bulb for an incandescent bulb of the same luminous flux should not increase the phototoxicity of skin porphyrins or lens riboflavin.
C1 [Chignell, Colin F.; Sik, Robert H.; Bilski, Piotr J.] NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA.
RP Chignell, CF (reprint author), NIEHS, Lab Pharmacol & Chem, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM chignell@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences. The authors
are indebted to Dr. Ann Motten, Dr. Albert Wielgus, NIEHS, for critical
reading of the manuscript.
NR 12
TC 11
Z9 11
U1 2
U2 19
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0031-8655
J9 PHOTOCHEM PHOTOBIOL
JI Photochem. Photobiol.
PD SEP-OCT
PY 2008
VL 84
IS 5
BP 1291
EP 1293
DI 10.1111/j.1751-1097.2008.00366.x
PG 3
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 342LL
UT WOS:000258785500032
PM 18494761
ER
PT J
AU Munday, JN
Capasso, F
Parsegian, VA
Bezrukov, SM
AF Munday, J. N.
Capasso, Federico
Parsegian, V. Adrian
Bezrukov, Sergey M.
TI Measurements of the Casimir-Lifshitz force in fluids: The effect of
electrostatic forces and Debye screening
SO PHYSICAL REVIEW A
LA English
DT Article
ID MICROELECTROMECHANICAL SYSTEMS; ATTRACTIVE FORCES; HAMAKER CONSTANTS;
MU-M; SPHERE; SOLIDS; RANGE
AB We present detailed measurements of the Casimir-Lifshitz force between two gold surfaces (a sphere and a plate) immersed in ethanol and study the effect of residual electrostatic forces, which are dominated by static fields within the apparatus and can be reduced with proper shielding. Electrostatic forces are further reduced by Debye screening through the addition of salt ions to the liquid. Additionally, the salt leads to a reduction of the Casimir-Lifshitz force by screening the zero-frequency contribution to the force; however, the effect is small between gold surfaces at the measured separations and within experimental error. An improved calibration procedure is described and compared with previous methods. Finally, the experimental results are compared with Lifshitz's theory and found to be consistent for the materials used in the experiment.
C1 [Munday, J. N.] Harvard Univ, Dept Phys, Cambridge, MA 02138 USA.
[Capasso, Federico] Harvard Univ, Sch Engn & Appl Sci, Cambridge, MA 02138 USA.
[Parsegian, V. Adrian; Bezrukov, Sergey M.] NIH, Bethesda, MD 20892 USA.
RP Munday, JN (reprint author), Harvard Univ, Dept Phys, Cambridge, MA 02138 USA.
RI Munday, Jeremy/E-6512-2016
OI Munday, Jeremy/0000-0002-0881-9876
FU NSEC [PHY-0117795]; Center for Nanoscale Systems at Harvard University;
Intramural Research Program of the NIH; Eunice Kennedy Shriver National
Institute of Child Health and Human Development; NSF
FX The authors would like to acknowledge R. Podgornik, J. Zimmerberg, G.
Carugno, and M. B. Romanowsky for helpful discussions. This project was
partially supported by NSEC, under NSF Contract No. PHY-0117795, the
Center for Nanoscale Systems at Harvard University, and the Intramural
Research Program of the NIH, Eunice Kennedy Shriver National Institute
of Child Health and Human Development. J.N.M. gratefully acknowledges
financial support from the NSF.
NR 40
TC 21
Z9 21
U1 2
U2 16
PU AMER PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 1050-2947
J9 PHYS REV A
JI Phys. Rev. A
PD SEP
PY 2008
VL 78
IS 3
AR 032109
DI 10.1103/PhysRevA.78.032109
PG 8
WC Optics; Physics, Atomic, Molecular & Chemical
SC Optics; Physics
GA 355DO
UT WOS:000259689400021
ER
PT J
AU Imudia, AN
Kilburn, BA
Petkova, A
Edwin, SS
Romero, R
Armant, DR
AF Imudia, A. N.
Kilburn, B. A.
Petkova, A.
Edwin, S. S.
Romero, R.
Armant, D. R.
TI Expression of heparin-binding EGF-like growth factor in term chorionic
villous explants and its role in trophoblast survival
SO PLACENTA
LA English
DT Article
DE trophoblast; term villous explants; cell death; growth factors; hypoxia;
preeclampsia
ID OXYGEN-TENSION; IN-VITRO; APOPTOSIS; PREECLAMPSIA; ENDOMETRIAL; CELLS;
CYTOTROPHOBLASTS; DIFFERENTIATION; PLACENTATION; IMPLANTATION
AB Heparin-bincling EGF-like growth factor (HBEGF) induces trophoblast extravillous differentiation and prevents apoptosis. These functions are compromised in preeclampsia. Because HBEGF is downregulated in placentas delivered by women with preeclampsia, we have examined its expression and cytoprotective activity in term villous explants. Chorionic villous explants prepared from non-pathological placentas collected by cesarean section at term were cultured at either 20% or 2% O(2) and treated with the HBEGF antagonist CRM197 or recombinant HBEGF. Paraffin sections were assayed for trophoblast death, proliferation and HBEGF expression using the TUNEL method, immunohistochemistry for nuclear Ki67 expression and semi-quantitative immunohistochemistry with image analysis, respectively. Trophoblast cell death was increased significantly after 8 h of culture with CRM 197 or by culture for 2 h at 2% O(2). Exogenous HBEGF prevented cell death due to hypoxia. Proliferative capacity was not affected by culture at either 20% or 2% O(2). Contrary to first trimester placenta, term trophoblasts do not elevate HBEGF expression in response to hypoxia. However, low endogenous levels of HBEGF are required to maintain survival. Therefore, HBEGF-mediated signaling significantly reduces trophoblast cell death at term and its deficiency in preeclampsia could negatively impact trophoblast survival. Published by Elsevier Ltd.
C1 [Armant, D. R.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, CS Mott Ctr, Detroit, MI 48201 USA.
[Edwin, S. S.; Romero, R.] NICHHD, Perinatol Res Branch, NIH, Bethesda, MD 20892 USA.
[Romero, R.] Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI 48201 USA.
[Armant, D. R.] NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA.
RP Armant, DR (reprint author), Wayne State Univ, Sch Med, Dept Obstet & Gynecol, CS Mott Ctr, 275 E Hancock Ave, Detroit, MI 48201 USA.
EM d.armant@wayne.edu
OI Armant, D. Randall/0000-0001-5904-9325
FU National Institute of Child Health and Human Development; National
Institutes of Health; DHHS
FX We thank Mr. Michael Kruger for conducting the statistical analyses.
This work was supported by the intramural research program of the
National Institute of Child Health and Human Development, National
Institutes of Health, DHHS.
NR 36
TC 13
Z9 14
U1 0
U2 1
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0143-4004
J9 PLACENTA
JI Placenta
PD SEP
PY 2008
VL 29
IS 9
BP 784
EP 789
DI 10.1016/j.placenta.2008.06.013
PG 6
WC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology
SC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology
GA 355MI
UT WOS:000259712600003
PM 18691754
ER
PT J
AU Antonellis, A
Huynh, JL
Lee-Lin, SQ
Vinton, RM
Renaud, G
Loftus, SK
Elliot, G
Wolfsberg, TG
Green, ED
McCallion, AS
Pavan, WJ
AF Antonellis, Anthony
Huynh, Jimmy L.
Lee-Lin, Shih-Queen
Vinton, Ryan M.
Renaud, Gabriel
Loftus, Stacie K.
Elliot, Gene
Wolfsberg, Tyra G.
Green, Eric D.
McCallion, Andrew S.
Pavan, William J.
TI Identification of Neural Crest and Glial Enhancers at the Mouse Sox10
Locus through Transgenesis in Zebrafish
SO PLOS GENETICS
LA English
DT Article
ID TRANSCRIPTION FACTOR SOX10; DORSAL-ROOT GANGLIA; HIRSCHSPRUNG-DISEASE;
REGULATORY ELEMENTS; GENE DESERTS; EXPRESSION; SEQUENCE; CELLS;
DIFFERENTIATION; MUTATIONS
AB Sox10 is a dynamically regulated transcription factor gene that is essential for the development of neural crest-derived and oligodendroglial populations. Developmental genes often require multiple regulatory sequences that integrate discrete and overlapping functions to coordinate their expression. To identify Sox10 cis-regulatory elements, we integrated multiple model systems, including cell-based screens and transposon-mediated transgensis in zebrafish, to scrutinize mammalian conserved, noncoding genomic segments at the mouse Sox10 locus. We demonstrate that eight of 11 Sox10 genomic elements direct reporter gene expression in transgenic zebrafish similar to patterns observed in transgenic mice, despite an absence of observable sequence conservation between mice and zebrafish. Multiple segments direct expression in overlapping populations of neural crest derivatives and glial cells, ranging from pan-Sox10 and pan-neural crest regulatory control to the modulation of expression in subpopulations of Sox10-expressing cells, including developing melanocytes and Schwann cells. Several sequences demonstrate overlapping spatial control, yet direct expression in incompletely overlapping developmental intervals. We were able to partially explain neural crest expression patterns by the presence of head to head SoxE family binding sites within two of the elements. Moreover, we were able to use this transcription factor binding site signature to identify the corresponding zebrafish enhancers in the absence of overall sequence homology. We demonstrate the utility of zebrafish transgenesis as a high-fidelity surrogate in the dissection of mammalian gene regulation, especially those with dynamically controlled developmental expression.
C1 [Antonellis, Anthony; Lee-Lin, Shih-Queen; Renaud, Gabriel; Wolfsberg, Tyra G.; Green, Eric D.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
[Loftus, Stacie K.; Elliot, Gene; Pavan, William J.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Huynh, Jimmy L.; Vinton, Ryan M.; McCallion, Andrew S.] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Dept Mol & Comparat Pathobiol, Baltimore, MD USA.
RP Antonellis, A (reprint author), NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
EM andy@jhmi.edu
FU National Human Genome Research Institute's (NHGRI) Intramural Research
Program (WJP); NIH (NIGMS) (ASM)
FX This work was supported by the National Human Genome Research
Institute's (NHGRI) Intramural Research Program (WJP) and by sponsored
funds from the NIH (NIGMS) (ASM).
NR 41
TC 64
Z9 65
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD SEP
PY 2008
VL 4
IS 9
AR e1000174
DI 10.1371/journal.pgen.1000174
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 365MR
UT WOS:000260411200025
PM 18773071
ER
PT J
AU Buac, K
Watkins-Chow, DE
Loftus, SK
Larson, DM
Incao, A
Gibney, G
Pavan, WJ
AF Buac, Kristina
Watkins-Chow, Dawn E.
Loftus, Stacie K.
Larson, Denise M.
Incao, Arturo
Gibney, Gretchen
Pavan, William J.
TI A Sox10 Expression Screen Identifies an Amino Acid Essential for Erbb3
Function
SO PLOS GENETICS
LA English
DT Article
ID EPIDERMAL-GROWTH-FACTOR; TRANSCRIPTIONAL REGULATION;
WAARDENBURG-SYNDROME; CRYSTAL-STRUCTURE; GLIAL-CELLS; MUTATIONS;
RECEPTOR; PROTEIN; MOUSE; HEREGULIN
AB The neural crest (NC) is a population of embryonic stem cells that gives rise to numerous cell types, including the glia and neurons of the peripheral and enteric nervous systems and the melanocytes of the skin and hair. Mutations in genes and genetic pathways regulating NC development lead to a wide spectrum of human developmental disorders collectively called neurocristopathies. To identify molecular pathways regulating NC development and to understand how alterations in these processes lead to disease, we established an N-ethyl-N-nitrosourea (ENU) mutagenesis screen utilizing a mouse model sensitized for NC defects, Sox10(LacZ/+). Out of 71 pedigrees analyzed, we identified and mapped four heritable loci, called modifier of Sox10 expression pattern 1-4 (msp1-4), which show altered NC patterning. In homozygous msp1 embryos, Sox10(LacZ) expression is absent in cranial ganglia, cranial nerves, and the sympathetic chain; however, the development of other Sox10-expressing cells appears unaffected by the mutation. Linkage analysis, sequencing, and complementation testing confirmed that msp1 is a new allele of the receptor tyrosine kinase Erbb3, Erbb3(msp1), that carries a single amino acid substitution in the extracellular region of the protein. The ENU-induced mutation does not alter protein expression, however, it is sufficient to impair ERBB3 signaling such that the embryonic defects observed in msp1 resemble those of Erbb3 null alleles. Biochemical analysis of the mutant protein showed that ERBB3 is expressed on the cell surface, but its ligand-induced phosphorylation is dramatically reduced by the msp1 mutation. These findings highlight the importance of the mutated residue for ERBB3 receptor function and activation. This study underscores the utility of using an ENU mutagenesis to identify genetic pathways regulating NC development and to dissect the roles of discrete protein domains, both of which contribute to a better understanding of gene function in a cellular and developmental setting.
C1 [Buac, Kristina; Watkins-Chow, Dawn E.; Loftus, Stacie K.; Larson, Denise M.; Incao, Arturo; Pavan, William J.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Buac, Kristina] George Washington Univ, Washington, DC USA.
[Gibney, Gretchen] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
RP Buac, K (reprint author), NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
EM bpavan@mail.nih.gov
OI Watkins-Chow, Dawn/0000-0002-4355-0868
FU National Institutes of Health [N01-HG-65403]; National Human Genome
Research Institute; National Institutes of Health (USA)
FX CIDR is fully funded through a federal contract from the National
Institutes of Health to The Johns Hopkins University, contract number
N01-HG-65403. This research was supported in part by the Intramural
Research Program of the National Human Genome Research Institute,
National Institutes of Health (USA).
NR 44
TC 10
Z9 10
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD SEP
PY 2008
VL 4
IS 9
AR e1000177
DI 10.1371/journal.pgen.1000177
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 365MR
UT WOS:000260411200028
PM 18773073
ER
PT J
AU Karp, DR
Carlin, S
Cook-Deegan, R
Ford, DE
Geller, G
Glass, DN
Greely, H
Guthridge, J
Kahn, J
Kaslow, R
Kraft, C
MacQueen, K
Malin, B
Scheuerman, RH
Sugarman, J
AF Karp, David R.
Carlin, Shelley
Cook-Deegan, Robert
Ford, Daniel E.
Geller, Gail
Glass, David N.
Greely, Hank
Guthridge, Joel
Kahn, Jeffrey
Kaslow, Richard
Kraft, Cheryl
MacQueen, Kathleen
Malin, Bradley
Scheuerman, Richard H.
Sugarman, Jeremy
TI Ethical and Practical Issues Associated with Aggregating Databases
SO PLOS MEDICINE
LA English
DT Review
ID INFORMATION; GENOMICS; PRIVACY; PROJECT
C1 [Karp, David R.] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
[Carlin, Shelley] Univ Texas SW Med Ctr Dallas, Inst Review Board, Dallas, TX 75390 USA.
[Cook-Deegan, Robert] Duke Univ, Inst Genome Sci & Policy, Durham, NC USA.
[Sugarman, Jeremy] Johns Hopkins Univ, Berman Inst Bioeth, Dept Med, Baltimore, MD USA.
[Glass, David N.] Univ Cincinnati, Dept Pediat, Cincinnati, OH 45221 USA.
[Greely, Hank] Stanford Law Sch, Stanford, CA USA.
[Guthridge, Joel] Oklahoma Med Res Fdn, Arthrit & Immunol Res Program, Oklahoma City, OK 73104 USA.
[Kahn, Jeffrey] Univ Minnesota, Ctr Bioeth, Minneapolis, MN USA.
[Kaslow, Richard] Univ Alabama, Sch Publ Hlth, Birmingham, AL 35294 USA.
[Kraft, Cheryl] NIAID, Div Allergy Immunol & Transplantat, NIH, Rockville, MD USA.
[MacQueen, Kathleen] Family Hlth Int, Res Triangle Pk, NC 27709 USA.
[Malin, Bradley] Vanderbilt Univ, Sch Med, Dept Biomed Informat, Nashville, TN 37212 USA.
[Scheuerman, Richard H.] Univ Texas SW Med Ctr Dallas, Dept Pathol, Dallas, TX 75390 USA.
[Scheuerman, Richard H.] Univ Texas SW Med Ctr Dallas, Div Biomed Informat, Dallas, TX 75390 USA.
[Sugarman, Jeremy] Johns Hopkins Univ, Dept Hlth Policy & Management, Baltimore, MD 21218 USA.
[Ford, Daniel E.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RP Karp, DR (reprint author), Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
EM david.karp@utsouthwestern.edu
OI Cook-Deegan, Robert/0000-0002-8251-4237
FU NIAID NIH HHS [N01-AI40076, N01AI40076]
NR 21
TC 21
Z9 21
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1549-1277
J9 PLOS MED
JI PLos Med.
PD SEP
PY 2008
VL 5
IS 9
BP 1333
EP 1337
AR e190
DI 10.1371/journal.pmed.0050190
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 365XG
UT WOS:000260442300008
PM 18816162
ER
PT J
AU Ingavale, SS
Chang, YC
Lee, H
McClelland, CM
Leong, ML
Kwon-Chung, KJ
AF Ingavale, Susham S.
Chang, Yun C.
Lee, Hyeseung
McClelland, Carol M.
Leong, Madeline L.
Kwon-Chung, Kyung J.
TI Importance of mitochondria in survival of Cryptococcus neoformans under
low oxygen conditions and tolerance to cobalt chloride
SO PLOS PATHOGENS
LA English
DT Article
ID YEAST SACCHAROMYCES-CEREVISIAE; HYPOXIA-MIMICKING AGENT; INDUCIBLE
FACTOR-I; OXIDATIVE STRESS; SUPEROXIDE-PRODUCTION; STEROL HOMEOSTASIS;
NEUROSPORA CRASSA; ADP/ATP CARRIER; NITRIC-OXIDE; COMPLEX-III
AB Cryptococcus neoformans is an environmental fungal pathogen that requires atmospheric levels of oxygen for optimal growth. For the fungus to be able to establish an infection, it must adapt to the low oxygen concentrations in the host environment compared to its natural habitat. In order to investigate the oxygen sensing mechanism in C. neoformans, we screened T-DNA insertional mutants for hypoxia-mimetic cobalt chloride (CoCl(2))-sensitive mutants. All the CoCl(2)-sensitive mutants had a growth defect under low oxygen conditions at 37 degrees C. The majority of mutants are compromised in their mitochondrial function, which is reflected by their reduced rate of respiration. Some of the mutants are also defective in mitochondrial membrane permeability, suggesting the importance of an intact respiratory system for survival under both high concentrations of CoCl(2) as well as low oxygen conditions. In addition, the mutants tend to accumulate intracellular reactive oxygen species (ROS), and all mutants show sensitivity to various ROS generating chemicals. Gene expression analysis revealed the involvement of several pathways in response to cobalt chloride. Our findings indicate cobalt chloride sensitivity and/or sensitivity to low oxygen conditions are linked to mitochondrial function, sterol and iron homeostasis, ubiquitination, and the ability of cells to respond to ROS. These findings imply that multiple pathways are involved in oxygen sensing in C. neoformans.
C1 [Ingavale, Susham S.; Chang, Yun C.; Lee, Hyeseung; McClelland, Carol M.; Leong, Madeline L.; Kwon-Chung, Kyung J.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Kwon-Chung, KJ (reprint author), NIAID, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM June_Kwon-Chung@nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Bethesda, Maryland, United States of America
FX This study was supported by funds from the intramural program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Bethesda, Maryland, United States of America.
NR 69
TC 33
Z9 34
U1 2
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD SEP
PY 2008
VL 4
IS 9
AR e1000155
DI 10.1371/journal.ppat.1000155
PG 14
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 356MW
UT WOS:000259783300012
PM 18802457
ER
PT J
AU Klein, MM
Gittis, AG
Su, HP
Makobongo, MO
Moore, JM
Singh, S
Miller, LH
Garboczi, DN
AF Klein, Michael M.
Gittis, Apostolos G.
Su, Hua-Poo
Makobongo, Morris O.
Moore, Jaime M.
Singh, Sanjay
Miller, Louis H.
Garboczi, David N.
TI The cysteine-rich interdomain region from the highly variable Plasmodium
falciparum erythrocyte membrane protein-1 exhibits a conserved structure
SO PLOS PATHOGENS
LA English
DT Article
ID FALCIPARUM-INFECTED ERYTHROCYTES; INTERCELLULAR-ADHESION MOLECULE-1;
PARASITE PLASMODIUM-FALCIPARUM; PREGNANCY-ASSOCIATED MALARIA; MEMBRANE
PROTEIN-1 FAMILY; BINDING-LIKE DOMAINS; RED-BLOOD-CELLS; VAR GENES;
ANTIGENIC VARIATION; SEVERE DISEASE
AB Plasmodium falciparum malaria parasites, living in red blood cells, express proteins of the erythrocyte membrane protein-1 (PfEMP1) family on the red blood cell surface. The binding of PfEMP1 molecules to human cell surface receptors mediates the adherence of infected red blood cells to human tissues. The sequences of the 60 PfEMP1 genes in each parasite genome vary greatly from parasite to parasite, yet the variant PfEMP1 proteins maintain receptor binding. Almost all parasites isolated directly from patients bind the human CD36 receptor. Of the several kinds of highly polymorphic cysteine-rich interdomain region (CIDR) domains classified by sequence, only the CIDR1 alpha domains bind CD36. Here we describe the CD36-binding portion of a CIDR1 alpha domain, MC179, as a bundle of three alpha-helices that are connected by a loop and three additional helices. The MC179 structure, containing seven conserved cysteines and 10 conserved hydrophobic residues, predicts similar structures for the hundreds of CIDR sequences from the many genome sequences now known. Comparison of MC179 with the CIDR domains in the genome of the P. falciparum 3D7 strain provides insights into CIDR domain structure. The CIDR1 alpha three-helix bundle exhibits less than 20% sequence identity with the three-helix bundles of Duffy-binding like (DBL) domains, but the two kinds of bundles are almost identical. Despite the enormous diversity of PfEMP1 sequences, the CIDR1 alpha and DBL protein structures, taken together, predict that a PfEMP1 molecule is a polymer of three-helix bundles elaborated by a variety of connecting helices and loops. From the structures also comes the insight that DBL1 alpha domains are approximately 100 residues larger and that CIDR1 alpha domains are approximately 100 residues smaller than sequence alignments predict. This new understanding of PfEMP1 structure will allow the use of better-defined PfEMP1 domains for functional studies, for the design of candidate vaccines, and for understanding the molecular basis of cytoadherence.
C1 [Klein, Michael M.; Gittis, Apostolos G.; Su, Hua-Poo; Moore, Jaime M.; Garboczi, David N.] NIAID, Immunogenet Lab, Struct Biol Sect, NIH, Rockville, MD 20852 USA.
[Makobongo, Morris O.; Singh, Sanjay; Miller, Louis H.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA.
RP Garboczi, DN (reprint author), NIAID, Immunogenet Lab, Struct Biol Sect, NIH, Rockville, MD 20852 USA.
EM dgarboczi@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 64
TC 31
Z9 31
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD SEP
PY 2008
VL 4
IS 9
AR e1000147
DI 10.1371/journal.ppat.1000147
PG 14
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 356MW
UT WOS:000259783300005
PM 18773118
ER
PT J
AU Schelhaas, M
Ewers, H
Rajamaki, ML
Day, PM
Schiller, JT
Helenius, A
AF Schelhaas, Mario
Ewers, Helge
Rajamaki, Minna-Liisa
Day, Patricia M.
Schiller, John T.
Helenius, Ari
TI Human papillomavirus type 16 entry: Retrograde cell surface transport
along actin-rich protrusions
SO PLOS PATHOGENS
LA English
DT Article
ID VIRUS-LIKE PARTICLES; HEPARAN-SULFATE PROTEOGLYCANS; NEURONAL GROWTH
CONES; MURINE POLYOMA-VIRUS; HUMAN KERATINOCYTES; HOST-CELLS; RECEPTORS;
NEUTRALIZATION; ENDOCYTOSIS; FILOPODIA
AB The lateral mobility of individual, incoming human papillomavirus type 16 pseudoviruses (PsV) bound to live HeLa cells was studied by single particle tracking using fluorescence video microscopy. The trajectories were computationally analyzed in terms of diffusion rate and mode of motion as described by the moment scaling spectrum. Four distinct modes of mobility were seen: confined movement in small zones (30-60 nm in diameter), confined movement with a slow drift, fast random motion with transient confinement, and linear, directed movement for long distances. The directed movement was most prominent on actin-rich cell protrusions such as filopodia or retraction fibres, where the rate was similar to that measured for actin retrograde flow. It was, moreover, sensitive to perturbants of actin retrograde flow such as cytochalasin D, jasplakinolide, and blebbistatin. We found that transport along actin protrusions significantly enhanced HPV-16 infection in sparse tissue culture, cells suggesting a role for in vivo infection of basal keratinocytes during wound healing.
C1 [Schelhaas, Mario; Ewers, Helge; Helenius, Ari] ETH, Inst Biochem, Zurich, Switzerland.
[Rajamaki, Minna-Liisa] Univ Helsinki, Dept Appl Biol, Helsinki, Finland.
[Day, Patricia M.; Schiller, John T.] NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
RP Helenius, A (reprint author), ETH, Inst Biochem, Zurich, Switzerland.
EM ari.helenius@bc.biol.ethz.ch
RI Ewers, Helge/I-3455-2012;
OI Ewers, Helge/0000-0003-3948-4332
FU German Science Foundation (DFG) [SCHE 1552/1-1]; Academy of Finland
[204104]; ETH Zurich; Fondation Andromac (Liechtenstein); Swiss National
Science Foundation (SNF)
FX M. S. was supported by the German Science Foundation (DFG, grant SCHE
1552/1-1). M. L. R. was supported by the Academy of Finland (grant
204104). A. H. was supported by the ETH Zurich, the Fondation Andromac
(Liechtenstein), and by the Swiss National Science Foundation (SNF).
NR 49
TC 78
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U1 3
U2 17
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD SEP
PY 2008
VL 4
IS 9
AR e1000148
DI 10.1371/journal.ppat.1000148
PG 14
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 356MW
UT WOS:000259783300006
PM 18773072
ER
PT J
AU Signore, C
Mills, JL
Qian, C
Yu, KF
Rana, S
Karmnanchi, SA
Levine, RJ
AF Signore, Caroline
Mills, James L.
Qian, Cong
Yu, Kai F.
Rana, Sarosh
Karmnanchi, S. Ananth
Levine, Richard J.
TI Circulating soluble endoglin and placental abruption
SO PRENATAL DIAGNOSIS
LA English
DT Article
DE abruptio placentae; preclampsia; gestational hypertension; endoglin;
angiogenic factors
ID GROWTH-FACTOR; ANGIOGENIC FACTORS; UNITED-STATES; ANTIANGIOGENIC
FACTORS; TYROSINE KINASE-1; PREECLAMPSIA; RISK; PREGNANCIES
AB Objective Our objective was to investigate whether serum concentrations of a novel anti-angiogenic factor, soluble endoglin (sEng), could predict placental abruption.
Methods In a nested case-control study of nulliparous pregnancies, we examined levels of sEng in serum collected prospectively from 31 women who later developed placental abruption and from 31 normal controls. All serum specimens were collected before the onset of hypertension or abruption and before labor or delivery. Serum sEng was compared within three gestational age intervals: early- (< 20 weeks), mid- (21-32 weeks), and late (>= 33 weeks) pregnancy.
Results There was no significant difference in sEng between abruption cases and controls in early pregnancy. sEng was significantly elvated among abruption cases at 21-32 weeks (10.7 vs 5.9 ng/mL, P < 0.01). Subgroup analyses revealed no differences in sEng concentrations at any gestational age interval between cases with abruption without hypertension and healthy controls. Among women who developed hypertension and palcental abruption. sEng was not significantly increased in early pregnancy, but was in mid-pregnancy (19.3 vs 5.5 ng/mL, P=0.002) and in late pregnancy (15.6 vs 9.5 ng/mL, P=0.04).
Conclusions Serum levels of the anti-angiogenic factor sEng are elevated prior to the development of hypertension and placental abruption. These elevations are not apparent until the late second trimester (26-27 weeks, on average), but they persist from this time in gestation onward. sEng may be useful for identifying pregnant women at risk for abruption and hypertension. Published in 2008 by John Wiley & Sons, Ltd.
C1 [Signore, Caroline; Mills, James L.; Levine, Richard J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, NICHD,NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Qian, Cong] Allied Technol Grp, Rockville, MD USA.
[Yu, Kai F.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biometry & Math Stat Branch, Div Epidemiol Stat & Prevent Res, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Rana, Sarosh] Women & Infants Hosp Rhode Isl, Dept Obstet & Gynecol, Div Maternal Fetal Med, Providence, RI 02908 USA.
[Rana, Sarosh; Karmnanchi, S. Ananth] Harvard Univ, Sch Med, Dept Med, Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Karmnanchi, S. Ananth] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Obstet & Gynecol, Boston, MA USA.
RP Levine, RJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, NICHD,NIH,Dept Hlth & Human Serv, Bldg 6100,Rm 7B03, Bethesda, MD 20892 USA.
EM LevineRJ@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institutes of Health; National Institute of Child
Health and Human Development [N01-HD-1-3121, -3122, -3123, -3124, -3125,
3126, N01-HD-3154, N01-HD-5-3246]; National Heart, lung and Blood
Institute [HL079594]
FX This research was supported by funds from the intramural research
program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development, National Institutes of Health. The CPEP trial was
supported by contracts (N01-HD-1-3121, -3122, -3123 -3124, -3125, and
-3126, N01-HD-3154; and N01-HD-5-3246) with the National Institute of
Child Health and Human Development, with cofunding from the National
Heart, Lung, and Blood Institute. Dr. Karumanchi is supported by R01
grant HL079594 from the National Heart, lung and Blood Institute.; Dr.
Karumanchi reports being named the coinventor of multiple provisional
patents that have been filed by Beth Israel Deaconess Medical Center for
the diagnosis and treatment of preeclampsia. These patents have been
nonexclusively licensed to several companies. Dr. Karumanchi reports
having served as a consultant to Abbott, Beckman Coulter, and Johnson &
Johnson.
NR 20
TC 24
Z9 24
U1 0
U2 1
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0197-3851
J9 PRENATAL DIAG
JI Prenat. Diagn.
PD SEP
PY 2008
VL 28
IS 9
BP 852
EP 858
DI 10.1002/pd.2065
PG 7
WC Genetics & Heredity; Obstetrics & Gynecology
SC Genetics & Heredity; Obstetrics & Gynecology
GA 355PE
UT WOS:000259720000012
PM 18702104
ER
PT J
AU Berrigan, D
McKinnon, RA
AF Berrigan, David
McKinnon, Robin A.
TI Built environment and health
SO PREVENTIVE MEDICINE
LA English
DT Editorial Material
ID LESSONS
C1 [Berrigan, David] NCI, Off Assoc Director, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[McKinnon, Robin A.] NCI, Risk Factor Monitoring & Methods Branch, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Berrigan, D (reprint author), NCI, Off Assoc Director, Appl Res Program, Div Canc Control & Populat Sci, Execut Plaza N, Bethesda, MD 20892 USA.
EM berrigad@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 11
TC 9
Z9 9
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
J9 PREV MED
JI Prev. Med.
PD SEP
PY 2008
VL 47
IS 3
BP 239
EP 240
DI 10.1016/j.ypmed.2008.07.010
PG 2
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 355MG
UT WOS:000259712400001
PM 18694780
ER
PT J
AU Kruger, J
Ham, SA
Berrigan, D
Ballard-Barbash, R
AF Kruger, Judy
Ham, Sandra A.
Berrigan, David
Ballard-Barbash, Rachel
TI Prevalence of transportation and leisure walking among US adults
SO PREVENTIVE MEDICINE
LA English
DT Article
DE walking; physical activity; transportation
ID PHYSICAL-ACTIVITY; PUBLIC-HEALTH; UNITED-STATES; RECOMMENDATIONS
AB Objective. This paper aims to contrast the demographic correlates of leisure and transportation walking.
Methods. Using data from the 2005 National Health Interview Survey (n=31,482), this paper reports on the prevalence of transportation walking and leisure walking for U.S. adults and examines the variation in prevalence across different socio-demographic groups. The prevalence of transportation walking and leisure walking for U.S. adults (>= 5 days/week for >= 30 min/day) was calculated using data from the 2005 National Health Interview Survey.
Results. In the United States, 41.5% of adults walked for leisure and 28.2% walked for transportation in intervals of at least 10 min. The highest prevalence of transportation walking was among black non-Hispanic men (36.0%) and Asian/Native Hawaiian/Pacific Islander women (40.5%). The highest prevalence of leisure walking was among Asian/Native Hawaiian/Pacific Islander men (42.0%) and white non-Hispanic women (46.6%). Leisure walking was most prevalent among respondents with higher incomes and education levels, whereas transportation walking increased in prevalence with education level but decreased with income level. Based on the findings, 6% of U.S. adults were considered regularly active (>= 5 days/week for >= 30 min/day) by walking for transportation and 9% were regularly active by walking for leisure.
Conclusion. Leisure and transportation walking have distinctly different demographic correlates. These differences should guide interventions aimed at influencing walking for different purposes. Published by Elsevier Inc.
C1 [Kruger, Judy; Ham, Sandra A.] Ctr Dis Control & Prevent, Phys Act & Hlth Branch, Div Nutr, Phys Act & Obes, Atlanta, GA 30341 USA.
[Berrigan, David; Ballard-Barbash, Rachel] NCI, Div Canc Control & Populat Sci, Appl Res Program, Bethesda, MD USA.
RP Kruger, J (reprint author), Ctr Dis Control & Prevent, Phys Act & Hlth Branch, Div Nutr, Phys Act & Obes, 4770 Buford Highway,NE MS K-46, Atlanta, GA 30341 USA.
EM ezk0@cdc.gov
NR 19
TC 50
Z9 53
U1 1
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0091-7435
J9 PREV MED
JI Prev. Med.
PD SEP
PY 2008
VL 47
IS 3
BP 329
EP 334
DI 10.1016/j.ypmed.2008.02.018
PG 6
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 355MG
UT WOS:000259712400018
PM 18445507
ER
EF