FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Francis, SA Schneeberger, EE Lynch, RD AF Francis, SA Schneeberger, EE Lynch, RD TI Reduction of MDCK cell cholesterol (CH) alters steady state transepithelial electrical resistance (TER) and increases diacylglycerol (DAG) content. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. UNIV LOWELL,DEPT BIOL SCI,LOWELL,MA 01854. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 1997 VL 8 SU S BP 1191 EP 1191 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601191 ER PT J AU Wang, JH AF Wang, JH TI Crystal structures of IG superfamily proteins as integrin ligands. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 1997 VL 8 SU S BP 1378 EP 1378 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601374 ER PT J AU Wagner, DD Dong, ZM AF Wagner, DD Dong, ZM TI Leukocyte adhesion molecules in normal physiology and in disease. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 1997 VL 8 SU S BP 1380 EP 1380 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601375 ER PT J AU GonzalezAgosti, C Murthy, A Cordero, E Pinney, D Candia, C Solomon, F Gusella, JF Ramesh, V AF GonzalezAgosti, C Murthy, A Cordero, E Pinney, D Candia, C Solomon, F Gusella, JF Ramesh, V TI Identification and characterization of a novel interactor for merlin that interacts with the ERM proteins. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MIT,CTR CANC RES,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,MOL NEUROGENET UNIT,CHARLESTOWN,MA 02129. NR 0 TC 0 Z9 0 U1 1 U2 1 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 NOV PY 1997 VL 8 SU S BP 1598 EP 1598 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09601596 ER PT J AU Herndon, ME Lawler, J AF Herndon, ME Lawler, J TI Chondroitin sulfate binding to thombospondin-1 is restricted to the C-terminal region of the molecule. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 BETH ISRAEL DEACONES MED CTR,DEPT EXPT PATHOL,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 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 NOV PY 1997 VL 8 SU S BP 2291 EP 2291 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602284 ER PT J AU Johnson, MR Denhez, F Perkins, LA AF Johnson, MR Denhez, F Perkins, LA TI The Drosophila nonreceptor protein tyrosine phosphatase, corkscrew, is essential for patterning throughout development SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT SURG RES LABS,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 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 NOV PY 1997 VL 8 SU S BP 2570 EP 2570 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602564 ER PT J AU Lian, JP Huang, RY Robinson, DR Badwey, JA AF Lian, JP Huang, RY Robinson, DR Badwey, JA TI Regulation of the p21-activated protein kinase(Paks) in neutrophils by sphingolipids. SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 BOSTON BIOMED RES INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 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 NOV PY 1997 VL 8 SU S BP 2637 EP 2637 PG 1 WC Cell Biology SC Cell Biology GA YF096 UT WOS:A1997YF09602630 ER PT J AU Hooi, SC Koenig, JI Abraczinskas, DR Kaplan, LM AF Hooi, SC Koenig, JI Abraczinskas, DR Kaplan, LM TI Regulation of anterior pituitary galanin gene expression by thyroid hormone SO MOLECULAR BRAIN RESEARCH LA English DT Article DE galanin; gene expression; pituitary; hypothalamus; thyroid hormone ID VASOACTIVE INTESTINAL POLYPEPTIDE; GROWTH-HORMONE; TRANSCRIPTION FACTOR; POSSIBLE INVOLVEMENT; MEDIAN-EMINENCE; MALE-RAT; SECRETION; ESTROGEN; PROTEIN; RELEASE AB Thyroid hormone is required for basal and estrogen-induced expression of anterior pituitary galanin. Steady-state anterior pituitary galanin mRNA levels decreased 6-fold in hypothyroid rats after 3 weeks of treatment. Similarly, hypothyroidism resulted in a 2.6-fold decrease in estrogen induction of galanin gene expression. The effect of thyroid hormone on anterior pituitary galanin gene expression appears to be exerted, at least in part, at the pituitary itself. Transient expression assays in GH(3) cells suggest the involvement of transcriptional mechanisms in the regulation of galanin gene expression by thyroid hormone. A region between -41 and -132 bp upstream of the transcriptional start site confers thyroid hormone responsiveness to the galanin gene. Gel-mobility shift assays show specific binding of 'SPI-like' proteins in GH(3) nuclear extracts to this region of the galanin gene. This binding was greatly enhanced by thyroid hormone. (C) 1997 Elsevier Science B.V. C1 UNIV MARYLAND,SCH MED,MARYLAND PSYCHIAT RES CTR,BALTIMORE,MD 21228. MASSACHUSETTS GEN HOSP,DEPT MED,GI UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP Hooi, SC (reprint author), NATL UNIV SINGAPORE,FAC SCI,DEPT PHYSIOL,10 KENT RIDGE CRESCENT,SINGAPORE 119260,SINGAPORE. RI Hooi, Shing/C-8588-2012 NR 33 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD NOV PY 1997 VL 51 IS 1-2 BP 15 EP 22 DI 10.1016/S0169-328X(97)00191-5 PG 8 WC Neurosciences SC Neurosciences & Neurology GA YJ738 UT WOS:A1997YJ73800003 ER PT J AU Lee, SB Kolquist, KA Nichols, K Englert, C Maheswaran, S Ladanyi, M Gerald, WL Haber, DA AF Lee, SB Kolquist, KA Nichols, K Englert, C Maheswaran, S Ladanyi, M Gerald, WL Haber, DA TI The EWS-WT1 translocation product induces PDGFA in desmoplastic small round-cell tumour SO NATURE GENETICS LA English DT Article ID FACTOR-A-CHAIN; GROWTH-FACTOR; WILMS-TUMOR; GENE-PRODUCT; TRANSCRIPTION FACTOR; SUBNUCLEAR LOCALIZATION; SUPPRESSOR WT1; FUSION; BINDING; RECEPTOR AB Chromosomal translocations resulting in chimaeric transcription factors underlie specific malignancies, but few authentic target genes regulated by these fusion proteins have been identified. Desmoplastic small round-cell tumour (DSRT) is a multiphenotypic primitive tumour characterized by massive reactive fibrosis surrounding nests of tumour cells(1). The t(11;22)(p13;q12) chromosomal translocation that defines DSRT produces a chimaeric protein containing the potential transactivation domain of the Ewing-sarcoma protein (EWS) fused to zinc fingers 2-4 of the Wilms tumour suppressor and transcriptional repressor WT1 (refs 2,3). By analogy with other EWS fusion products, the EWS-WT1 chimaera may encode a transcriptional activator whose target genes overlap with those repressed by WT1 (ref. 4). To characterize its functional properties, we generated osteosarcoma cell lines with tightly regulated inducible expression of EWS-WT1. Expression of EWS-WT1 induced the expression of endogenous platelet-derived growth factor-A (PDGFA), a potent secreted mitogen and chemoattractant whose promoter contains the many potential WT1-binding sites(5,6). Native PDGFA was not regulated by wild-type WT1, indicating a difference in target gene specificity between this tumour suppressor and its oncogenic derivative. PDGFA was expressed within tumour cells in primary DSRT specimens, but it was absent in Wilms tumours expressing WT1 and Ewing sarcomas with an EWS-Fli translocation. We conclude that the oncogenic fusion of EWS to WT1 in DSRT results in the induction of PDGFA, a potent fibroblast growth factor that contributes to the characteristic reactive fibrosis associated with this unique tumour. C1 MASSACHUSETTS GEN HOSP,CTR CANC,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. MEM SLOAN KETTERING CANC CTR,DEPT PATHOL,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,DEPT HUMAN GENET,NEW YORK,NY 10021. FU NCI NIH HHS [CA60376, CA71167, CA 68273] NR 31 TC 91 Z9 96 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD NOV PY 1997 VL 17 IS 3 BP 309 EP 313 DI 10.1038/ng1197-309 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA YD667 UT WOS:A1997YD66700025 PM 9354795 ER PT J AU Jain, RK Schlenger, K Hockel, M Yuan, F AF Jain, RK Schlenger, K Hockel, M Yuan, F TI Quantitative angiogenesis assays: Progress and problems SO NATURE MEDICINE LA English DT Review ID FIBROBLAST GROWTH-FACTOR; VASCULAR-PERMEABILITY FACTOR; TUMOR ANGIOGENESIS; ENDOTHELIAL-CELLS; MICROVASCULAR ARCHITECTURE; NEOPLASTIC TRANSFORMATION; MAMMARY-GLAND; NORMAL TISSUE; NUDE-MICE; IN-VIVO C1 UNIV MAINZ,DEPT GYNECOL & OBSTET,D-55101 MAINZ,GERMANY. DUKE UNIV,DEPT BIOMED ENGN,DURHAM,NC 27708. RP Jain, RK (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114, USA. RI Yuan, Fan/A-1287-2011 FU NCI NIH HHS [R35-CA-56591] NR 82 TC 293 Z9 306 U1 0 U2 23 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 1997 VL 3 IS 11 BP 1203 EP 1208 DI 10.1038/nm1197-1203 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA YD896 UT WOS:A1997YD89600027 PM 9359693 ER PT J AU Perez, GI Knudson, CM Leykin, L Korsmeyer, SJ Tilly, JL AF Perez, GI Knudson, CM Leykin, L Korsmeyer, SJ Tilly, JL TI Apoptosis-associated signaling pathways are required for chemotherapy-mediated female germ cell destruction SO NATURE MEDICINE LA English DT Article ID DAUNORUBICIN-INDUCED APOPTOSIS; GRANULOSA-CELLS; PRIMORDIAL FOLLICLES; ICE/CED-3 PROTEASE; P53 PROTEIN; RAT OVARY; IN-VIVO; DEATH; BCL-2; EXPRESSION AB Female sterility resulting from oocyte destruction is an unfortunate, and in many cases inevitable, consequence of chemotherapy. We show that unfertilized mouse oocytes exposed to therapeutic levels of the antitumor drug, doxorubicin (DXR), undergo apoptosis; however, fertilized oocytes do not initiate apoptosis, but enter cell-cycle arrest, when treated with DXR. Apoptosis induced by DXR in oocytes is blocked by sphingosine-1-phosphate, an inhibitor of ceramide-promoted cell death. Oocytes from Bax-deficient, but not p53-null, female mice display complete resistance to DXR-induced apoptosis in vivo and in vitro. Pretreatment of oocytes with a specific peptide inhibitor of caspases also abrogates the apoptotic response to DXR. These findings indicate that oocyte destruction caused by chemotherapy can be prevented by manipulation of apoptosis-associated signaling pathways. C1 MASSACHUSETTS GEN HOSP,VINCENT CTR REPROD BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02114. WASHINGTON UNIV,SCH MED,DEPT MED,DIV MOL ONCOL,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT PATHOL,DIV MOL ONCOL,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,ST LOUIS,MO 63110. FU NCI NIH HHS [R01-CA49712]; NIA NIH HHS [R01-AG12279]; NICHD NIH HHS [R01-HD34226] NR 48 TC 231 Z9 235 U1 0 U2 11 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 1997 VL 3 IS 11 BP 1228 EP 1232 DI 10.1038/nm1197-1228 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA YD896 UT WOS:A1997YD89600031 PM 9359697 ER PT J AU Schacter, DL Buckner, RL Koutstaal, W Dale, AM Rosen, BR AF Schacter, DL Buckner, RL Koutstaal, W Dale, AM Rosen, BR TI Late onset of anterior prefrontal activity during true and false recognition: An event-related fMRI study SO NEUROIMAGE LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; MEMORY RETRIEVAL; EPISODIC MEMORY; ILLUSIONS; BRAIN; WORDS AB Previous studies using PET and fMRI to examine memory retrieval have been limited by the requirement to test different types of items in separate blocks and to average data across items and response types within blocks. We used recently developed procedures for analyzing event-related mixed trial data from fMRI experiments to compare brain activity during true recognition of previously studied words and false recognition of semantic associates. A previous PET study using blocked testing procedures reported similarities and differences in rCBF patterns associated with true and false recognition (Schacter ct al., 1996a). We examined brain activity during blocked testing of studied words and nonstudied semantic associates (similar to PET), and also during event-related mixed trials, where studied words and nonstudied semantic associates are intermixed. Six subjects initially heard lists of semantically related words and were later tested for old/new recognition with studied words and nonstudied semantic associates, either in separate blocks or intermixed randomly for the event-related analysis. Compared to a fixation control condition, a variety of regions previously reported in the PET study showed significant activation for both true and false recognition, including anterior prefrontal, frontal opercular, medial parietal, and visual cortex extending into hippocampal/parahippocampal regions. Differences across trial types were not clearly present. Event-related analyses of time course data show a relatively late onset and sustained duration for anterior prefrontal signal changes compared to signal changes in other activated regions. Further study is needed to resolve whether this late onset originates from variance in hemodynamic response properties or is attributable to delayed neural activity. The delayed onset is consistent with the idea that anterior prefrontal regions participate in postretrieval monitoring processes. (C) 1997 Academic Press. C1 Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA. Harvard Univ, Dept Radiol, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Nucl Magnet Resonance Ctr, Boston, MA 02114 USA. RP Schacter, DL (reprint author), Harvard Univ, Dept Psychol, 33 Kirkland St, Cambridge, MA 02138 USA. RI Dale, Anders/A-5180-2010; OI Schacter, Daniel/0000-0002-2460-6061 FU NIA NIH HHS [AG08441]; NIDCD NIH HHS [DC03245-01] NR 36 TC 279 Z9 279 U1 4 U2 16 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PD NOV PY 1997 VL 6 IS 4 BP 259 EP 269 DI 10.1006/nimg.1997.0305 PG 11 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA YM327 UT WOS:000071052500004 PM 9417969 ER PT J AU Kosslyn, SM Thompson, WL Alpert, NM AF Kosslyn, SM Thompson, WL Alpert, NM TI Neural systems shared by visual imagery and visual perception: A positron emission tomography study SO NEUROIMAGE LA English DT Article ID MENTAL-IMAGERY; INFEROTEMPORAL CORTEX; EXTRASTRIATE CORTEX; IDENTIFYING OBJECTS; UNILATERAL NEGLECT; HUMAN BRAIN; ATTENTION; MEMORY; PATTERNS; MONKEY AB Subjects participated in perceptual and imagery tasks while their brains were scanned using positron emission tomography. In the perceptual conditions, subjects judged whether names were appropriate for pictures. In one condition, the objects were pictured from canonical perspectives and could be recognized at first glance; in the other, the objects were pictured from noncanonical perspectives and were not immediately recognizable. In this second condition, we assume that top-down processing is used to evaluate the names. In the imagery conditions, subjects saw a grid with a single X mark; a lowercase letter was presented before the grid. In the baseline condition, they simply responded when they saw the stimulus, whereas in the imagery condition they visualized the corresponding block letter in the grid and decided whether it would have covered the X if it were physically present. Fourteen areas were activated in common by both tasks, only 1 of which may not be involved in visual processing (the precentral gyrus); in addition, 2 were activated in perception but not imagery, and 5 were activated in imagery but not perception. Thus, two-thirds of the activated areas were activated in common. (C) 1997 Academic Press. C1 Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA. RP Kosslyn, SM (reprint author), 832 William James Hall,33 Kirtland St, Cambridge, MA 02138 USA. NR 65 TC 173 Z9 181 U1 3 U2 10 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 NOV PY 1997 VL 6 IS 4 BP 320 EP 334 DI 10.1006/nimg.1997.0295 PG 15 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA YM327 UT WOS:000071052500009 PM 9417974 ER PT J AU Moskowitz, MA Cutrer, FM AF Moskowitz, MA Cutrer, FM TI Attacking migraine headache from beginning to end SO NEUROLOGY LA English DT Editorial Material ID SUBCUTANEOUS SUMATRIPTAN C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. RP Moskowitz, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL & NEUROSURG,149 13TH ST,ROOM 6403,CHARLESTOWN,MA 02129, USA. RI Moskowitz, Michael/D-9916-2011 NR 13 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV PY 1997 VL 49 IS 5 BP 1193 EP 1195 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA YF844 UT WOS:A1997YF84400001 PM 9371890 ER PT J AU Seeck, M Mainwaring, N Cosgrove, N Blume, H Dubuisson, D Mesulam, MM Schomer, DL AF Seeck, M Mainwaring, N Cosgrove, N Blume, H Dubuisson, D Mesulam, MM Schomer, DL TI Neurophysiologic correlates of implicit face memory in intracranial visual evoked potentials SO NEUROLOGY LA English DT Article ID NEUROCOGNITIVE NETWORKS; TEMPORAL CORTEX; RECOGNITION; HIPPOCAMPUS AB Visual evoked potentials were recorded in the amygdala, hippocampus, mid- and inferotemporal cortex, orbitofrontal cortex, and lateral frontal cortex of seven epileptic patients while they were engaged in a difficult task requiring the discrimination between repeated and nonrepeated faces. The explicit recognition of previously seen faces was at chance levels, as measured by the accuracy of push-button responses. Nevertheless, all subjects showed clear-cut differential evoked responses to repeated versus nonrepeated faces, indicating implicit encoding of the distinction between the two types of stimuli. Differential responses mere more frequent in neocortical recording sites (especially in the mid- and inferotemporal leads) than in limbic recording sites such as the amygdala and hippocampus. The authors conclude that implicit encoding processes are modulated by neocortical visual association areas of the temporal lobes. C1 BETH ISRAEL HOSP,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. RP Seeck, M (reprint author), UNIV GENEVA,HOP CANTONAL,NEUROL CLIN,LAB EXPLORAT PRECHIRURG EPILEPSIES,UNITE EEG,CH-1211 GENEVA 14,SWITZERLAND. NR 16 TC 19 Z9 20 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV PY 1997 VL 49 IS 5 BP 1312 EP 1316 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA YF844 UT WOS:A1997YF84400025 PM 9371914 ER PT J AU Gillespie, PG Corey, DP AF Gillespie, PG Corey, DP TI Myosin and adaptation by hair cells SO NEURON LA English DT Review ID MECHANOELECTRICAL TRANSDUCTION; BULLFROGS SACCULUS; BLOCK ADAPTATION C1 JOHNS HOPKINS UNIV,DEPT NEUROSCI,BALTIMORE,MD 21205. MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,DEPT NEUROBIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,BOSTON,MA 02114. RP Gillespie, PG (reprint author), JOHNS HOPKINS UNIV,DEPT PHYSIOL,BALTIMORE,MD 21205, USA. OI Corey, David/0000-0003-4497-6016; Barr-Gillespie, Peter/0000-0002-9787-5860 NR 15 TC 80 Z9 81 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD NOV PY 1997 VL 19 IS 5 BP 955 EP 958 DI 10.1016/S0896-6273(00)80387-6 PG 4 WC Neurosciences SC Neurosciences & Neurology GA YH594 UT WOS:A1997YH59400003 PM 9390509 ER PT J AU Ong, HT Tieman, J Albert, M Jolesz, F Sandor, T AF Ong, HT Tieman, J Albert, M Jolesz, F Sandor, T TI Semi-automated extraction of brain contours from MRI SO NEURORADIOLOGY LA English DT Article DE brain volume measurement; magnetic resonance imaging; contour extraction; image processing ID SEGMENTATION; IMAGES; HIPPOCAMPAL; ATROPHY; DISEASE; SCANS; HEAD AB We compared brain volumes computed by trained operators using the BRAIN-MAP algorithm, which automatically extracts the contours of the brain from gradient-echo magnetic resonance images, The images of 19 subjects randomly selected from a group of normals and a group of patients with dementia were included. BRAIN-MAP found brain perimeters that were on the average ca. 3 % tighter than those obtained by two experienced operators. Between-operator and within-operator reproducibility of the analyses were also estimated and found to be (-0.13 +/- 0.51) % and (-0.63 +/- 0.08) %, respectively. Replicate volume measurement by the computer alone provided a reproducibility of (0.44 +/- 0.46) %. C1 BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. FU NIA NIH HHS [P01-AG04953] NR 16 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0028-3940 J9 NEURORADIOLOGY JI Neuroradiology PD NOV PY 1997 VL 39 IS 11 BP 797 EP 803 PG 7 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA YJ372 UT WOS:A1997YJ37200007 PM 9406206 ER PT J AU Bogdanov, A Petherick, P Marecos, E Weissleder, R AF Bogdanov, A Petherick, P Marecos, E Weissleder, R TI In vivo localization of diglycylcysteine-bearing synthetic peptides by nuclear imaging of oxotechnetate transchelation SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article DE diglycylcysteine; gene expression; imaging; technetium-99m; oxotechnetate ID SINGLE-CHAIN FV; MONOCLONAL-ANTIBODIES; MONOAMINE-OXIDASE; TC-99M; GLUCOHEPTONATE; STABILITY; PROTEINS; SITE AB A phenomenon of in vivo transchelation of oxotechnetate from a complex with glucoheptonic acid to synthetic peptides bearing oxotechnetate-binding motifs and a technique for in vivo visualization of these peptides are described. Using two model peptides bearing two tandem diglycylcysteine (GGC) motifs (P1) or three GGC motifs (P2), we demonstrated that: (i) these peptides efficiently transchelated oxo-[Tc-99m]technetate from a complex with glucoheptonic acid in vitro (a complex with peptides was stable at least 24 h; radiochemical purity exceeded 95% by high performance liquid chromatography); (ii) injection of peptides into the rectus femoris muscle (at 0.5-1 mu mol of SH groups) followed by an intravenous injection of Tc-99m glucoheptonate (0.25-0.5 mCi per animal) yielded visualization of the injected muscle by nuclear imaging within 1 h after injection; (iii) the experimental/control (contralateral) thigh muscle ratio was 1.80 +/- 0.05 for peptide P1 and 3.0 +/- 0.1 for P2; (iv) the injection of a control peptide P2 with SH groups covalently modified with N-ethylmaleimide resulted in a ratio of 1.4 +/- 0.2. These findings argue for specific association of oxo [Tc-99m]technetate with free thiols within the binding motif of injected peptides in vivo. In vivo transchelation of oxo-[Tc-99m]technetate may be useful for the purpose of noninvasive imaging of gene expression, i.e., when the expression product bears GGC motifs. (C) 1997 Elsevier Science Inc. RP Bogdanov, A (reprint author), MASSACHUSETTS GEN HOSP,CTR MOL IMAGING RES,THIRTEENTH ST,BOSTON,MA 02129, USA. NR 28 TC 9 Z9 10 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD NOV PY 1997 VL 24 IS 8 BP 739 EP 742 DI 10.1016/S0969-8051(97)00117-0 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA YE966 UT WOS:A1997YE96600007 PM 9428599 ER PT J AU Uvin, SC Caliendo, AM AF Uvin, SC Caliendo, AM TI Cervicovaginal human immunodeficiency virus secretion and plasma viral load in human immunodeficiency virus-seropositive women SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID CERVICAL SECRETIONS; GENITAL SECRETIONS; MENSTRUAL-CYCLE; INFECTED WOMEN; DISEASE STAGE; RISK; AIDS; DNA AB Objective: To evaluate human immunodeficiency virus (HIV)-1 RNA burden in paired plasma and cervicovaginal lavage specimens and to assess the relation of plasma HIV-1 RNA level, CD4 cell count, and antiretroviral therapy with cervicovaginal HIV-1 viral load. Methods: Paired blood and cervicovaginal lavage specimens were collected from 72 HIV-infected women. Quantitation of HIV-1 RNA from plasma and cervicovaginal lavage specimens was performed by using the nucleic acid sequence-based amplification assay. Analyses examined relations between cervicovaginal HIV-1 RNA and plasma HIV-1 RNA level, CD4 count, and antiretroviral therapy. Results: Plasma HIV-1 RNA was detectable in 61 of 72 women (85%), with copy numbers ranging from 330 to 1,600,000 copies/mL. Twenty-eight of 72 (39%) had detectable HIV-1 RNA in cervicovaginal lavage specimens, ranging from 320 to 440,000 copies/mL. The cervicovaginal lavage HIV-1 RNA level was detectable in 9%, 29%, 52%, and 53% of the women with plasma HIV-1 RNA of less than 400, 400-9999, 10,000-100,000, and more than 100,000 copies, respectively (P = .043). Among women with CD4 counts of less than 200, 200-500, and greater than 500/mm(3), cervicovaginal lavage HIV-1 RNA was detected in 67%, 32%, and 25% of subjects, respectively (P = .018). Among women receiving antiretroviral therapy, cervicovaginal lavage revealed HIV-1 RNA in 67%, 31%, and 25% with CD4 cell counts of less than 200, 200-500, and more than 500/mm(3), respectively (P = .042). Conclusion: The presence of HIV-1 RNA in cervicovaginal lavage correlates significantly with the level of HIV-1 RNA in plasma and negatively with CD4 cell count. (C) 1997 by The American College of Obstetricians and Gynecologists. C1 MASSACHUSETTS GEN HOSP,MICROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP Uvin, SC (reprint author), BROWN UNIV,MIRIAM HOSP,CTR IMMUNOL,164 SUMMIT AVE,PROVIDENCE,RI 02906, USA. FU NICHD NIH HHS [HD 33215] NR 20 TC 29 Z9 29 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD NOV PY 1997 VL 90 IS 5 BP 739 EP 743 DI 10.1016/S0029-7844(97)00411-0 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA YB816 UT WOS:A1997YB81600008 PM 9351756 ER PT J AU Frenkel, REP Shin, DH Epstein, DL Hertzmark, E Bohn, JL Hong, YJ AF Frenkel, REP Shin, DH Epstein, DL Hertzmark, E Bohn, JL Hong, YJ TI Laser trabeculoplasty: How little is enough? SO OPHTHALMIC SURGERY AND LASERS LA English DT Article ID OPEN-ANGLE GLAUCOMA; INTRAOCULAR-PRESSURE; MONKEYS; COMPLICATIONS; THERAPY AB BACKGROUND AND OBJECTIVE: The optimal number of laser applications for argon laser trabeculoplasty in patients with primary open-angle glaucoma has not been established. The purpose of this study was to determine the fewest number of burns necessary for clinically effective intraocular pressure reduction for these patients. PATIENTS AND METHODS: Using a prospective, randomized, collaborative study, the authors examined the relationship between the number of laser trabeculoplasty burns and intraocular pressure for patients with primary open-angle glaucoma. A total of 122 patients received either 50 burns to half of the trabecular meshwork (group 1) or 35 burns to one third of the trabecular meshwork (group 2). RESULTS: The mean baseline intraocular pressures were similar between group 1 (22.3 +/- 4.1 mm Hg [mean +/- SDI) and group 2 (22.8 +/- 5.0 mm Hg) (P = .58). Intraocular pressure reduction at 9 to 12 months, although significant in both groups (group I: 4.4 +/- 3.0 mm Hg, P <.0001; group 2: 3.9 +/- 5.1 mm Hg, P <.0001), did not differ significantly between the two groups (P = .63). CONCLUSION: This study demonstrated that 35 burns may be as clinically effective as 50 burns in reducing the intraocular pressure in primary open-angle glaucoma patients. C1 MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,GLAUCOMA SERV,BOSTON,MA. WAYNE STATE UNIV,SCH MED,KRESGE EYE INST,DETROIT,MI 48201. DUKE UNIV,CTR EYE,DURHAM,NC. HARVARD UNIV,SCH PUBL HLTH,BROOKLINE,MA. YON SEI UNIV,DEPT OPHTHALMOL,SEOUL,SOUTH KOREA. RP Frenkel, REP (reprint author), EYE RES FDN,E FLORIDA EYE INST,309 E OSCEOLA ST,SUITE 104,STUART,FL 34994, USA. NR 24 TC 6 Z9 6 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD NOV PY 1997 VL 28 IS 11 BP 900 EP 904 PG 5 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA YE160 UT WOS:A1997YE16000003 PM 9387175 ER PT J AU Gragoudas, ES Egan, KM AF Gragoudas, ES Egan, KM TI Metastatic risk for distinct patterns of postirradiation local recurrence of posterior uveal melanoma - Discussion SO OPHTHALMOLOGY LA English DT Editorial Material RP Gragoudas, ES (reprint author), MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD NOV PY 1997 VL 104 IS 11 BP 1792 EP 1793 PG 2 WC Ophthalmology SC Ophthalmology GA YF417 UT WOS:A1997YF41700024 ER PT J AU Akpek, EK Merchant, A Pinar, V Foster, CS AF Akpek, EK Merchant, A Pinar, V Foster, CS TI Ocular rosacea - Patient characteristics and follow-up SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT Castroviejo-Cornea-Society Meeting CY OCT, 1996 CL CHICAGO, IL SP Castroviejo Cornea Soc ID METRONIDAZOLE AB Purpose: The purpose of this report is to review the presenting symptoms and signs, treatment regimens used, complications encountered, and outcome in a cohort of patients with ocular rosacea, Methods: The medical records of 131 patients with a diagnosis of ocular rosacea were reviewed retrospectively. Data were entered in a tabulated form, and a descriptive analysis was performed. Results: The age range at presentation was between 23, and 85 years (mean, 56 years). Cutaneous manifestations of rosacea were present in 112 of the patients at their first visit. The most common presenting symptoms were foreign body sensation and burning, and the most common signs were telangiectasia and irregularity of lid margins, and meibomian gland dysfunction, Thirteen patients had decreased visual acuity at the time of presentation due to corneal complications. Six of these patients required penetrating keratoplasty during the course of their disease. Seven patients had severe cicatrizing conjunctivitis at the time of referral. One hundred thirteen patients were treated with oral tetracycline derivatives. Seven patients were left with visual acuity less than 20/400, and one patient underwent enucleation for corneal perforation and endophthalmitis. Conclusions: Ocular rosacea is a common disease involving the skin and the eyes, It is widely underdiagnosed by many ophthalmologists despite the blinding potential. Successful therapy requires a multidisciplinary approach. C1 MASSACHUSETTS EYE & EAR INFIRM,SERV IMMUNOL,DEPT IMMUNOL,BOSTON,MA 02114. DOKUZ EYLUL UNIV,DEPT OPHTHALMOL,IZMIR,TURKEY. NR 26 TC 108 Z9 115 U1 1 U2 6 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD NOV PY 1997 VL 104 IS 11 BP 1863 EP 1867 PG 5 WC Ophthalmology SC Ophthalmology GA YF417 UT WOS:A1997YF41700037 PM 9373118 ER PT J AU Boppart, SA Bouma, BE Pitris, C Tearney, GJ Fujimoto, JG Brezinski, ME AF Boppart, SA Bouma, BE Pitris, C Tearney, GJ Fujimoto, JG Brezinski, ME TI Forward-imaging instruments for optical coherence tomography SO OPTICS LETTERS LA English DT Article AB We discuss the design and implementation of forward-imaging instruments for optical coherence tomography (OCT), which require the delivery, scanning, and collection of single-spatial-mode optical radiation. A hand-held surgical probe for use in open surgery can provide cross-sectional images of subsurface tissue before surgical incisions are made. A rigid laparoscope for minimally invasive surgical OCT imaging provides a simultaneous en face view of the area being imaged. OCT imaging is demonstrated on in vitro human specimens. (C) 1997 Optical Society of America. C1 MIT,ELECT RES LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP Boppart, SA (reprint author), MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139, USA. RI Boppart, Stephen/C-7338-2009; OI Pitris, Costas/0000-0002-5559-1050 NR 11 TC 123 Z9 126 U1 1 U2 7 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 SN 0146-9592 J9 OPT LETT JI Opt. Lett. PD NOV 1 PY 1997 VL 22 IS 21 BP 1618 EP 1620 DI 10.1364/OL.22.001618 PG 3 WC Optics SC Optics GA YE155 UT WOS:A1997YE15500013 PM 18188315 ER PT J AU Teknos, TN Megerian, CA Rauch, SD AF Teknos, TN Megerian, CA Rauch, SD TI Hemangioma of the middle ear SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID MANAGEMENT; TUMORS C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02115. NR 4 TC 5 Z9 5 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD NOV PY 1997 VL 117 IS 5 BP 573 EP 574 DI 10.1016/S0194-5998(97)70033-0 PG 2 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA YF816 UT WOS:A1997YF81600025 PM 9374186 ER PT J AU Herrera, CR Lewin, A Fiddes, R Friedman, J Linn, W Baker, T Balanoff, D Beach, CL AF Herrera, CR Lewin, A Fiddes, R Friedman, J Linn, W Baker, T Balanoff, D Beach, CL TI Long-acting diltiazem CD is safe and effective in a hypertensive Mexican-American population SO PHARMACOTHERAPY LA English DT Article ID ONCE-DAILY DILTIAZEM; NON-HISPANIC WHITES; HEALTH AB Study Objective. To evaluate the safety and effectiveness of diltiazem CD for reducing blood pressure in Mexican-American patients with mild to moderate hypertension. Design. Randomized, double-blind, placebo-controlled trial. Setting. Twelve clinical sites in the United States. Patients. Patients with baseline diastolic blood pressures between 95 and 115 mm Hg. Interventions. Patients were treated with an average daily dose of diltiazem CD 246 mg (60 patients) or placebo (58 patients) to achieve a trough diastolic blood pressure below 90 mm Hg. Measurements and Main Results. Diltiazem CD significantly reduced mean diastolic blood pressure compared with placebo, -8.2 versus -4.1 mm Hg, respectively (p=0.0025). Diastolic blood pressure below 90 mm Hg or a reduction of 10 mm Hg or more was achieved by 57% of diltiazem CD versus 28% of placebo recipients. Systolic blood pressure and heart rate were also reduced with diltiazem CD. Adverse events were mild, with similar frequency for diltiazem CD (15%) and placebo (19%). Conclusion. Diltiazem CD is safe and effective in hypertensive Mexican-Americans, and diastolic blood pressure reductions compare with those in non-Hispanic white patients. C1 NATL RES INST,LOS ANGELES,CA. SO CALIF RES INST,WHITTIER,CA. HLTH CARE PARTNERS MED GRP,LOS ANGELES,CA. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. HOECHST MARION ROUSSEL,US MED RES,KANSAS CITY,MO. RP Herrera, CR (reprint author), UNIV TEXAS,DEPT INTERNAL MED,64331 FANNIN ST,MSB 1-122,HOUSTON,TX 77030, USA. NR 13 TC 6 Z9 6 U1 0 U2 0 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER BOX 806 171 HARRISON AVE, BOSTON, MA 02111 SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD NOV-DEC PY 1997 VL 17 IS 6 BP 1254 EP 1259 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YG522 UT WOS:A1997YG52200011 PM 9399608 ER PT J AU Leupold, D Kochevar, IE AF Leupold, D Kochevar, IE TI Multiphoton photochemistry in biological systems introduction SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID LIGHT-HARVESTING COMPLEX; ENERGY-TRANSFER PROCESSES; CRYSTAL-STRUCTURE; SPECTROSCOPY; PHYTOCHROME; ABSORPTION; FLUORESCENCE; EXCITATION; MICROSCOPY; MECHANISM C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. RP Leupold, D (reprint author), MAX BORN INST NICHTLINEARE OPT & KURZZEITSPEKTROS,RUDOWER CHAUSSEE 6,PF 1107,D-12474 BERLIN,GERMANY. NR 42 TC 8 Z9 8 U1 1 U2 2 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD NOV PY 1997 VL 66 IS 5 BP 562 EP 565 DI 10.1111/j.1751-1097.1997.tb03189.x PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA YG526 UT WOS:A1997YG52600008 ER PT J AU Noel, PH Pugh, JA Larme, AC Marsh, G AF Noel, PH Pugh, JA Larme, AC Marsh, G TI The use of traditional plant medicines for non-insulin dependent diabetes mellitus in South Texas SO PHYTOTHERAPY RESEARCH LA English DT Article DE NIDDM; Opuntia streptacantha; Cnidoscolus chayamansa; Eriobotrya japonica; Aloe vera ID FOLK MEDICINE; OPUNTIA SP AB The use of traditional plant medicines, as well as the factors associated with their use, were documented in 662 outpatients with non-insulin dependent diabetes mellitus enrolled at six primary care clinics in South Texas. Forty-nine percent of the patients reported using alternative treatments for their diabetes, which included 61 different traditional plant medicines. The four most commonly reported were nopal (Opuntia streptacantha) or the prickly pear cactus, chaya (Cnidoscolus chayamansa), mispero (Eriobotrya japonica) or loquat, and savila (Aloe vera). Logistic regression was used to develop a multivariate model which indicated that alternative medicine use is positively associated with age and diabetes-related 'hassles', and was more likely among border residents and individuals who were born in Mexico. Disease severity was not associated with the use of alternative treatments when controlling for other variables. Users of alternative treatments also appeared just as likely to adhere to orthodox biomedical treatment recommendations as non-users. While preliminary reports ire the literature suggest that some of the identified plants have hypoglycaemic properties, information is limited or nonexistent for many of the other plants. Given their preponderance in this region, some of these plants should he targeted for further investigation to document their efficacy or to screen for toxicity. (C) 1997 John Wiley & Sons, Ltd. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,ALMMVA,SAN ANTONIO,TX 78284. RP Noel, PH (reprint author), UNIV TEXAS,HLTH SCI CTR,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. OI Pugh, Jacqueline/0000-0003-4933-141X NR 26 TC 22 Z9 25 U1 2 U2 12 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0951-418X J9 PHYTOTHER RES JI Phytother. Res. PD NOV PY 1997 VL 11 IS 7 BP 512 EP 517 DI 10.1002/(SICI)1099-1573(199711)11:7<512::AID-PTR149>3.0.CO;2-H PG 6 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YC979 UT WOS:A1997YC97900008 ER PT J AU Rockett, HRH Breitenbach, M Frazier, AL Witschi, J Wolf, AM Field, AE Colditz, GA AF Rockett, HRH Breitenbach, M Frazier, AL Witschi, J Wolf, AM Field, AE Colditz, GA TI Validation of a youth/adolescent food frequency questionnaire SO PREVENTIVE MEDICINE LA English DT Article DE children and adolescents; food frequency questionnaire; validation; nutritional assessment ID DIETARY ASSESSMENT; VALIDITY; ADOLESCENTS; CHILDREN; REPRODUCIBILITY; RECALL; NUTRITION; PATTERNS; DESIGN; RECORD AB Background. To address limited longitudinal nutrition data on children and adolescents, a self-administered food frequency questionnaire was designed for older children and adolescents. Initially, the Youth/Adolescent Questionnaire (YAQ) was developed and demonstrated to be reproducible, This study was conducted to evaluate its validity. Methods. The form was administered twice to a sample of 261 youths (ages 9 to 18) at an approximate interval of 1 year (1993-1994), and three 24-hr dietary recalls were collected during this period, Pearson correlation coefficients were calculated on nutrient data. Results. Validity was first evaluated by comparing the average of the three 24-hr recalls to the average of the two YAQs. Similar mean nutrients were found by both methods. Correlation coefficients between the mean energy-adjusted nutrients computed by the two methods ranged from 0.21 for sodium to 0.58 for folate. After correction for within-person error, the average correlation coefficient was 0.54, similar to that found among adults. Conclusion. A simple self-administered questionnaire completed by older children and adolescents can provide nutritional information about this age group. (C) 1997 Academic Press. C1 CHILDRENS HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02115. DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02138. HARVARD UNIV,SCH MED,BOSTON,MA 02138. RP Rockett, HRH (reprint author), BRIGHAM & WOMENS HOSP,CHANNING LAB,181 LONGWOOD AVE,BOSTON,MA 02115, USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NIDDK NIH HHS [DK46200] NR 31 TC 420 Z9 422 U1 4 U2 22 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0091-7435 J9 PREV MED JI Prev. Med. PD NOV-DEC PY 1997 VL 26 IS 6 BP 808 EP 816 DI 10.1006/pmed.1997.0200 PG 9 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA YH616 UT WOS:A1997YH61600006 PM 9388792 ER PT J AU Deutsch, TF AF Deutsch, TF TI Lasers and optics in health care SO PROCEEDINGS OF THE IEEE LA English DT Article ID INDUCED FLUORESCENCE; IN-VITRO; 5-AMINOLEVULINIC ACID; COHERENCE TOMOGRAPHY; CORONARY-ARTERY; BLADDER-CANCER; SPECTROSCOPY; MICROSCOPY; DIAGNOSIS; TISSUE AB Lasers and optics have affected health care in a myriad of ways. This paper surveys their impact on three aspects of health care: Ij surgery and medicine, 2) biology, and 3) biotechnology. In surgery, fiber optics have enabled the development of endoscopes, which allow access to most sites within the body. Endoscopes have, in turn, led to the development of minimally invasive therapy, which is charging the practice of surgery. Optics contributes to biology via new techniques for visualization, measurement and analysis, and manipulation. In biotechnology, broadly defined as the measurement, manipulation, and manufacture of large biologically significant molecules such as proteins and DNA, optical methods have become important in genetic sequencing and pharmaceutical development. C1 HARVARD UNIV, SCH MED, CAMBRIDGE, MA 02138 USA. RP MASSACHUSETTS GEN HOSP, WELLMAN LABS PHOTOMED, DEPT DERMATOL, BOSTON, MA 02114 USA. NR 80 TC 6 Z9 6 U1 0 U2 2 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA SN 0018-9219 EI 1558-2256 J9 P IEEE JI Proc. IEEE PD NOV PY 1997 VL 85 IS 11 BP 1797 EP 1816 DI 10.1109/5.649658 PG 20 WC Engineering, Electrical & Electronic SC Engineering GA YG524 UT WOS:A1997YG52400013 ER PT J AU Bernstein, JG AF Bernstein, JG TI Current psychotherapeutic drugs, 1st edition - Klein,DF, Rowland,LP SO PSYCHIATRIC SERVICES LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 5 TC 0 Z9 0 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1075-2730 J9 PSYCHIATR SERV JI Psychiatr. Serv. PD NOV PY 1997 VL 48 IS 11 BP 1479 EP 1479 PG 1 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA YE213 UT WOS:A1997YE21300040 ER PT J AU Murray, G AF Murray, G TI Clinical assessment of malingering and deception SO PSYCHOSOMATICS LA English DT Book Review C1 Massachusetts Gen Hosp, Psychiat Fellowship Program, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Murray, G (reprint author), Massachusetts Gen Hosp, Psychiat Fellowship Program, Boston, MA 02114 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 USA SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD NOV-DEC PY 1997 VL 38 IS 6 BP 585 EP 585 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA YL755 UT WOS:000070989600012 ER PT J AU Solbiati, L Goldberg, SN Ierace, T Livraghi, T Meloni, F Dellanoce, M Sironi, S Gazelle, GS AF Solbiati, L Goldberg, SN Ierace, T Livraghi, T Meloni, F Dellanoce, M Sironi, S Gazelle, GS TI Hepatic metastases: Percutaneous radio-frequency ablation with cooled-tip electrodes SO RADIOLOGY LA English DT Article DE liver neoplasms, secondary; liver neoplasms, therapy; radio-frequency (RF) ablation ID RADIOFREQUENCY TISSUE ABLATION; HEPATOCELLULAR-CARCINOMA; MICROWAVE COAGULATION; THERMAL ABLATION; EXPERIENCE; TEMPERATURE; CANCER; TUMORS; SIZE AB PURPOSE: To assess the feasibility and safety of using cooled-tip electrodes to increase the volume of coagulation necrosis obtained or reduce the number of treatment sessions necessary with percutaneous tumor radio-frequency (RF) ablation. MATERIALS AND METHODS: Twenty-nine patients with 44 hepatic metastases (1.3-5.1 cm diameter) from colorectal (n = 22), gastric (n = 5), pancreatic (n = 1), or breast (n = 1) carcinoma were treated with RF ablation using cooled-tip, 18-gauge electrodes with 2-3 cm tip exposure. Each tumor was treated in one or two treatment sessions. RESULTS: Technical success, ablation of all visualized tumor, was achieved in 40 (91%) metastases. Findings at computed tomography (CT) and magnetic resonance (MR) imaging performed 3-6 months after treatment confirmed complete necrosis of the entire metastasis in 66%. Disease-free survival was 50% at 12 months and 33% at 18 months, with localized progression of disease in 34% of treated lesions. Overall survival was 100%, 94%, and 89% at 6, 12, and 18 months, respectively. Only one complication, self-limited hemorrhage, was seen. CONCLUSION: Use of cooled-tip electrodes was a safe and feasible adjunct for tumor RF ablation therapy that produced larger volumes of coagulation necrosis with fewer electrode insertions than is produced with other RF ablation techniques. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA. OSPED CIVILE,DEPT RADIOL,VIMERCATE,ITALY. UNIV MILAN,OSPED SAN RAFFAELE,DEPT RADIOL,I-20127 MILAN,ITALY. RP Solbiati, L (reprint author), OSPED GEN,DEPT RADIOL,PIAZZALE SOLARO 3,I-21052 BUSTO ARSIZIO,VA,ITALY. OI meloni, maria franca/0000-0001-7485-7400; Solbiati, Luigi/0000-0002-3109-1449 NR 20 TC 445 Z9 467 U1 0 U2 7 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD NOV PY 1997 VL 205 IS 2 BP 367 EP 373 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA YD151 UT WOS:A1997YD15100014 PM 9356616 ER PT J AU Niklason, LT Christian, BT Niklason, LE Kopans, DB Castleberry, DE OpsahlOng, BH Landberg, CE Slanetz, PJ Giardino, AA Moore, R Albagli, D DeJule, MC Fitzgerald, PF Fobare, DF Giambattista, BW Kwasnick, RF Liu, JQ Lubowski, SJ Possin, GE Richotte, JF Wei, CY Wirth, RF AF Niklason, LT Christian, BT Niklason, LE Kopans, DB Castleberry, DE OpsahlOng, BH Landberg, CE Slanetz, PJ Giardino, AA Moore, R Albagli, D DeJule, MC Fitzgerald, PF Fobare, DF Giambattista, BW Kwasnick, RF Liu, JQ Lubowski, SJ Possin, GE Richotte, JF Wei, CY Wirth, RF TI Digital Tomosynthesis in breast imaging SO RADIOLOGY LA English DT Article; Proceedings Paper CT 82nd Scientific Assembly and Annual Meeting of the Radiological-Society-of-North-America CY DEC 01-06, 1996 CL CHICAGO, IL SP Radiol Soc N Amer DE breast neoplasms, radiography; breast radiography, radiation dose; breast radiography, technology; radiography, digital; radiography, technology ID SUBTRACTION ANGIOGRAPHY; CANCER DETECTION; MAMMOGRAPHY; RADIOGRAPHS; TOMOGRAPHY; REMOVAL; OCCULT AB PURPOSE: To describe and evaluate a method of tomosynthesis breast imaging with a full-field digital mammographic system. MATERIALS AND METHODS: In this tomosynthesis method, low-radiation-dose images were acquired as the x-ray source was moved in an are above the stationary breast and digital detector. A step-and-expose method of imaging was used. Breast tomosynthesis and conventional images of two imaging phantoms and four mastectomy specimens were obtained. Three experienced readers scored the relative lesion visibility, lesion margin visibility, and confidence in the classification of six lesions. RESULTS: Tomosynthesis image-reconstruction algorithms allow tomographic imaging of the entire breast from a single are of the x-ray source and at a radiation dose comparable with that in single-view mammography. Except for images of a large mass in a fatty breast, the tomosynthesis images were superior to the conventional images. CONCLUSION: Digital mammographic systems make breast tomosynthesis possible. Tomosynthesis may improve the specificity of mammography with improved lesion margin visibility and may improve early breast cancer detection, especially in women with radiographically dense breasts. C1 KETTERING MEM HOSP,DEPT NUCL MED,KETTERING,OH. GE CO,CORP RES & DEV,SCHENECTADY,NY 12301. RP Niklason, LT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL SCI,EDWARDS 517,50 BLOSSOM ST,BOSTON,MA 02114, USA. OI Slanetz, Priscilla/0000-0003-1248-5116 NR 39 TC 477 Z9 490 U1 3 U2 26 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD NOV PY 1997 VL 205 IS 2 BP 399 EP 406 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA YD151 UT WOS:A1997YD15100018 PM 9356620 ER PT J AU Bashir, A Gray, ML Boutin, RD Burstein, D AF Bashir, A Gray, ML Boutin, RD Burstein, D TI Glycosaminoglycan in articular cartilage: In vivo assessment with delayed Gd(DTPA)(2-)-enhanced MR imaging SO RADIOLOGY LA English DT Article DE arthritis, degenerative; cartilage; gadolinium; gadoteridol; magnetic resonance (MR), contrast enhancement ID DEGRADATION; ENHANCEMENT; COLLAGEN; FLUID; MODEL; KNEE AB PURPOSE: To investigate the feasibility of applying magnetic resonance (MR) imaging with use of an anionic compound, Gd(DTPA)(2-) (gadolinium diethylenetriaminepentaacetic acid), for measuring glycosaminoglycan concentration in human cartilage in clinical studies. MATERIALS AND METHODS: Penetration of Gd(DTPA)(2-) into cartilage was monitored through sequential T1-calculated images obtained after intraarticular (n = 2) or intravenous (n = 2) injection. T1-weighted and T1-calculated image series were then obtained in seven volunteers (nine knees) after penetration of Gd(DTPA)(2-) into cartilage. If T1 was heterogeneous on Gd(DTPA)(2-)-enhanced images, images were also obtained after penetration of the cartilage with the nonionic contrast agent, gadoteridol. RESULTS: Gd(DTPA)(2-) penetrated cartilage from the articular surface after intraarticular injection and from both the articular surface and the subchondral bone after intravenous injection. The latter resulted in shorter overall penetration time. T1 values on Gd(DTPA)(2-)-enhanced images were homogeneous in four knees, but in five knees T1 differences of up to 30% were observed. These T1 differences were not seen in the presence of gadoteridol. These variations in T1 reflected about 50% variations in glycosaminoglycan. CONCLUSION: The data suggest that Gd(DTPA)(2-)-enhanced MR imaging has potential for monitoring glycosaminoglycan content of cartilage in vivo. C1 BETH ISRAEL DEACONESS MED CTR,CHARLES A DANA RES INST,DEPT RADIOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. MIT,DEPT ELECT ENGN & COMP SCI,CONTINUUM ELECTROMECH GRP,ELECTROMAGNET & ELECT SYST LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BOSTON,MA 02114. HARVARD MASSACHUSETTS INST TECHNOL,DIV HLTH SCI & TECHNOL,CAMBRIDGE,ENGLAND. FU NIAMS NIH HHS [AR41713, AR42773] NR 31 TC 313 Z9 321 U1 3 U2 14 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD NOV PY 1997 VL 205 IS 2 BP 551 EP 558 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA YD151 UT WOS:A1997YD15100042 PM 9356644 ER PT J AU Pribill, I Barnes, GT Chen, JM Church, D Buckler, A Baxendale, S Bates, GP Lehrach, H Gusella, MJ Duyao, MP Ambrose, CM Gusella, JF MacDonald, ME AF Pribill, I Barnes, GT Chen, JM Church, D Buckler, A Baxendale, S Bates, GP Lehrach, H Gusella, MJ Duyao, MP Ambrose, CM Gusella, JF MacDonald, ME TI Exon trapping and sequence-based methods of gene finding in transcript mapping of human 4p16.3 SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID HUNTINGTONS-DISEASE GENE; YEAST ARTIFICIAL CHROMOSOMES; CANDIDATE REGION; DNA; CLONING; PROTEIN; CDNA; MAP; AMPLIFICATION; IDENTIFICATION AB We have applied exert amplification GRAIL2 exon prediction and EST database searching to a 2 Mb segment of chromosome 4p16.3. Experimental and computational methods of identifying exons were comparable in efficiency and apparent false positive rate, brit were complementary in gene identification, revealing distinct overlapping sets of expressed sequences. EST searching was most powerful when we considered only those ESTs that show evidence of splicing relative to the genomic sequence. The combination of the three gene finding methods produced a transcription map of 30 loci in this segment of 4p16,3 that includes known human genes, homologs of loci identified in rodents and several anonymous transcripts, including a putative novel DNA polymerase and a gene related to Drosophila ash 1. While most of the genes in the region have been found, our data suggest that even with the entire DNA sequence available, complete saturation of the transcript map will require additional, focused experimental effort. C1 Massachusetts Gen Hosp, Mol Neurogenet Unit, Charlestown, MA 02129 USA. Imperial Canc Res Fund, London WC2A 3PX, England. RP Pribill, I (reprint author), Genos Biosci, La Jolla, CA 92037 USA. RI Bates, Gillian/E-1146-2012 OI Bates, Gillian/0000-0002-4041-6305 FU NHGRI NIH HHS [HG00169, HG00672]; NINDS NIH HHS [NS16367]; Wellcome Trust NR 43 TC 2 Z9 3 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD NOV PY 1997 VL 23 IS 6 BP 413 EP 427 DI 10.1007/BF02673751 PG 15 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA ZX840 UT WOS:000074560700005 PM 9661704 ER PT J AU Rordorf, G Cramer, SC Efird, JT Schwamm, LH Buonanno, F Koroshetz, WJ AF Rordorf, G Cramer, SC Efird, JT Schwamm, LH Buonanno, F Koroshetz, WJ TI Pharmacological elevation of blood pressure in acute stroke - Clinical effects and safety SO STROKE LA English DT Article DE hypertension; phenylephrine; stenosis; stroke management ID ANEURYSMAL SUBARACHNOID HEMORRHAGE; CEREBRAL-ARTERY OCCLUSION; AMERICAN-HEART-ASSOCIATION; HEALTH-CARE PROFESSIONALS; SPECIAL WRITING GROUP; INDUCED HYPERTENSION; COMPUTED-TOMOGRAPHY; ISCHEMIC DEFICITS; VOLUME EXPANSION; BRAIN EDEMA AB Background and Purpose Lowering of blood pressure can adversely affect ischemic symptoms iri acute stroke. The aim of our study was to determine whether induced hypertension in stroke is safe and to examine its effects on neurological deficits in patients presenting with acute cerebral ischemia. Methods We retrospectively reviewed all patients admitted to our neurological intensive care unit with the diagnosis of ischemic stroke over a 2.5-year period. Thirty-three patients were not given a presser agent (Ph-group), while 30 were treated with phenylephrine (Ph+ group) in an attempt to improve cerebral perfusion. Results Baseline characteristics showed few differences between the Ph+ and Ph-groups. Intracerebral hemorrhage, brain edema, cardiac morbidity, and mortality were not increased in the Ph+ group. In 10 of 30 Ph+ patients, a systolic blood pressure threshold was identified below which ischemic deficits worsened and above which deficits improved. The mean threshold was 156 mm Hg (range, 120 to 190 mm Hg). The mean number of stenotic/occluded cerebral arteries was greater in those Ph+ patients with an identified clinical blood pressure threshold (mean, 2.1 per patient) than in Ph+ patients without a threshold (mean, 1.2 per patient; P<.05). Conclusions The results suggest that careful use of phenylephrine-induced hypertension is not associated with an increase in morbidity or mortality in acute stroke. Although based on a retrospective analysis of clinical practice, this report suggests that a subset of patients, particularly those with multiple stenosis of cerebral arteries, may improve neurologically upon elevation of the blood pressure. C1 MASSACHUSETTS GEN HOSP,STROKE SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,CLIN INVESTIGATOR TRAINING PROGRAM,BOSTON,MA 02115. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. RP Rordorf, G (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,GRB 1256,FRUIT ST,BOSTON,MA 02114, USA. OI Schwamm, Lee/0000-0003-0592-9145 NR 59 TC 123 Z9 126 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD NOV PY 1997 VL 28 IS 11 BP 2133 EP 2138 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA YE841 UT WOS:A1997YE84100004 PM 9368553 ER PT J AU Cramer, SC Nelles, G Schaechter, JD Kaplan, JD Finklestein, SP AF Cramer, SC Nelles, G Schaechter, JD Kaplan, JD Finklestein, SP TI Computerized measurement of motor performance after stroke SO STROKE LA English DT Article DE diagnosis; motor activity; stroke assessment ID CEREBRAL INFARCTION; RECOVERY; SCALES; CORTEX AB Background and Purpose Stroke scales usually convert motor status to a score along an ordinal scale and do not provide a permanent recording of motor performance. Computerized methods sensitive to small changes in neurological status may be of value for studying and measuring stroke recovery. Methods We developed a computerized dynamometer and tested 23 stroke subjects and 12 elderly control subjects on three motor tasks: sustained squeezing, repetitive squeezing, and index finger tapping. For each subject, scores on the Fugl-Meyer and National Institutes of Health stroke scales were also obtained. Results Sustained squeezing by the paretic hand of stroke subjects was weaker (9.2 kg) than the unaffected hand (20.2 kg; P<.0005), as well as control dominant (23.1 kg; P<.0005) and nondominant (19.9 kg; P<.005) hands. Paretic index finger tapping was slower (2.5 Hz) than the unaffected hand (4.2 Hz; P<.01), as well as control dominant (4.7 Hz; P<.0005) and nondominant (4.9 Hz; P<.0005) hands. Many features of dynamometer data correlated significantly with stroke subjects' Fugl-Meyer scores, including sustained squeeze maximum force (rho=.91) and integral of force over 5 seconds (rho=.91); repetitive squeeze mean force (rho=.92) and mean frequency (rho=.73); and index finger tap mean frequency (rho=.83). Correlation of these motor parameters with National Institutes of Health stroke scale score was weaker in all cases, a consequence of the scoring of nonmotor deficits on this scale. Dynamometer measurements showed excellent interrater (r=.99) and intrarater (r=.97) reliability. Conclusions The degree of motor deficit quantitated with the dynamometer is strongly associated with the extent of neurological abnormality measured with the use of two standardized stroke scales. The computerized dynamometer rapidly measures motor function along a continuous, linear scale and produces a permanent recording of hand motor performance accessible for subsequent analyses. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,SPAULDING REHABIL HOSP,BOSTON,MA. NORTHEASTERN UNIV,BOUVE COLL PHARM & HLTH SCI,BOSTON,MA 02115. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,CLIN INVESTIGATOR TRAINING PROGRAM,BOSTON,MA 02115. PFIZER INC,BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. MASSACHUSETTS GEN HOSP,SPAULDING NEURO RECOVERY PROGRAM,BOSTON,MA 02114. NR 26 TC 36 Z9 36 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD NOV PY 1997 VL 28 IS 11 BP 2162 EP 2168 PG 7 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA YE841 UT WOS:A1997YE84100009 PM 9368558 ER PT J AU Goldbaum, AM Woog, JJ AF Goldbaum, AM Woog, JJ TI The CO2 laser in oculoplastic surgery SO SURVEY OF OPHTHALMOLOGY LA English DT Review DE blepharoplasty; carbon dioxide laser; continuous-wave laser; cutaneous laser; resurfacing; incisional surgery; ptosis repair; pulsed laser; thermal injury; tissue ablation ID CARBON-DIOXIDE LASER; CO2-LASER TISSUE ABLATION; TRICHLOROACETIC-ACID; THERMAL-DAMAGE; HIGH-ENERGY; SKIN; BLEPHAROPLASTY; COMPLICATIONS; RHYTIDES; DURATION AB The introduction of a new generation of carbon dioxide (CO2) lasers has permitted the development of new approaches toward certain oculoplastic disorders and procedures. The high absorption of this infrared laser by tissue water assists oculoplastic surgeons in performing incisional and excisional procedures precisely and with relatively good hemostasis. The development of new scanned continuous-wave or pulsed delivery systems has facilitated controlled tissue ablation with decreased collateral thermal injury during cutaneous resurfacing procedures. The unique characteristics of the CO2 laser mandate special attention to protection of the patient and surgical team, and careful preparation and training will help the prospective laser surgeon to successfully address the learning curve associated with this new technology. Although long-term follow-up is limited, results reported to date suggest that the CO2 laser represents an important addition to the armamentarium of the oculoplastic surgeon. (C) 1997 by Elsevier Science Inc. All rights reserved. C1 OPHTHALM CONSULTANTS BOSTON,CTR EYE RES,BOSTON,MA 02114. TUFTS UNIV NEW ENGLAND MED CTR,DEPT OPHTHALMOL,BOSTON,MA 02111. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. TUFTS UNIV,SCH MED,BOSTON,MA 02111. NEW YORK EYE & EAR INFIRM,NEW YORK,NY 10003. MANHATTAN EYE EAR & THROAT HOSP,NEW YORK,NY 10021. NR 55 TC 9 Z9 9 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0039-6257 J9 SURV OPHTHALMOL JI Surv. Ophthalmol. PD NOV-DEC PY 1997 VL 42 IS 3 BP 255 EP 267 DI 10.1016/S0039-6257(97)00097-0 PG 13 WC Ophthalmology SC Ophthalmology GA YH916 UT WOS:A1997YH91600005 PM 9406371 ER PT J AU Bagot, M Martinel, I Charue, D Weill, F Boulland, ML Wechsler, J Freeman, GJ Bensussan, A Boumsell, L AF Bagot, M Martinel, I Charue, D Weill, F Boulland, ML Wechsler, J Freeman, GJ Bensussan, A Boumsell, L TI CD101 is expressed by skin dendritic cells - Role in T-lymphocyte activation SO TISSUE ANTIGENS LA English DT Article DE co-stimulatory molecule; dendritic cell; FACS (staining); skin ID EPIDERMAL LANGERHANS CELLS; LEUKOCYTE SURFACE PROTEIN; ADHESION MOLECULES; ANTIGEN; PHENOTYPE; MIGRATION; MEMBRANE; INVITRO; SUBSETS; DERMIS AB CD101 was first described in our laboratory using two different monoclonal antibodies, BA27 and BB27, recognizing a 140-kDa disulfide-bonded homodimeric polypeptide on a small subset of circulating T lymphocytes and on most activated T cells in vitro. Further, it has been reported that most intestinal mucosal T lymphocytes expressed CD101. The gene coding for-the CD101 antigen has been cloned and found to be identical to the gene coding for the recently described V7 antigen, corresponding to a type I trans-membrane protein with seven immunoglobulin-like loops in its extracellular domain. To define surface proteins that are involved in skin dendritic cell (DC) localization or function, we looked for the expression of CD101 on skin DC migrating from human skin explants. The majority of these DC had a phenotype of Langerhans cell (LC)-like mature DC, i.e., HLA-DR(+)CD1a(+)CD1c(+)CD11a(+) CcD11c(+)CD40(+)CD50(+)CD54(+)CD58(+) CD80(+)CD83(+)CD86(+). We found that CD101 was expressed by a major subset of these HLA-DR(+)CD1a(+)CD1c(+) LC-like skin DC. Next, we studied the effect of anti-CD101 monoclonal antibodies on primary allogeneic and on soluble antigen-specific mixed skin DC-lymphocyte reactions. We showed that two different monoclonal antibodies, BB27 and V7.1, inhibited the T-lymphocyte proliferative responses and that the inhibitory effect was overcome by high doses of exogenous IL-2. As both DC and T lymphocytes expressed CD101 molecules, we determined that the inhibitory effect was achieved both at the responder T-cell level and at the DC level. Thus, CD101 which is expressed on a subset of circulating T lymphocytes, has also been found on a subpopulation of LC-like DC. This molecule plays a major role in the activation of T cells by skin DC. C1 UNIV PARIS 12, DEPT PATHOL, HOP HENRI MONDOR, F-94010 CRETEIL, FRANCE. DANA FARBER CANC INST, BOSTON, MA 02115 USA. RP Bagot, M (reprint author), UNIV PARIS 12, INSERM U448, HOP HENRI MONDOR, IM3, 51 AVE MARECHAL LATTRE TASSIGNY, F-94010 CRETEIL, FRANCE. RI Bensussan, Armand/E-5434-2017 NR 33 TC 10 Z9 11 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD NOV PY 1997 VL 50 IS 5 BP 439 EP 448 DI 10.1111/j.1399-0039.1997.tb02898.x PG 10 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA YC439 UT WOS:A1997YC43900003 PM 9389317 ER PT J AU Rettig, MB Said, JW Berenson, JR AF Rettig, MB Said, JW Berenson, JR TI Multiple myeloma and Kaposi's sarcoma-associated herpesvirus - a paracrine model of tumorigenesis? Response SO TRENDS IN MICROBIOLOGY LA English DT Article ID DENDRITIC CELLS; INTERLEUKIN-6 RP Rettig, MB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DIV HEMATOL & ONCOL,11301 WILSHIRE BLVD,111-H,LOS ANGELES,CA 90073, USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0966-842X J9 TRENDS MICROBIOL JI Trends Microbiol. PD NOV PY 1997 VL 5 IS 11 BP 425 EP 426 DI 10.1016/S0966-842X(97)01148-7 PG 2 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA YF711 UT WOS:A1997YF71100003 ER PT J AU Bromley, B Lieberman, E Benacerraf, BR AF Bromley, B Lieberman, E Benacerraf, BR TI The incorporation of maternal age into the sonographic scoring index for the detection at 14-20 weeks of fetuses with Down's syndrome SO ULTRASOUND IN OBSTETRICS & GYNECOLOGY LA English DT Article DE maternal age; sonographic scoring index; Down's syndrome ID AUTOSOMAL TRISOMY; RISK; TRIMESTER AB Sonographic markers for Down's syndrome have been useful in the identification of affected fetuses. In this study, we evaluated the accuracy of an expanded scoring index that included recently described sonographic markers as well as maternal age to optimize identification of fetuses with Down's syndrome. Over a 27-month period we performed 4075 genetic amniocenteses for advanced maternal age or an abnormal triple panel. Prior to each amniocentesis, a complete sonographic assessment of the fetus was performed including a structural survey and fetal biometry. Each patient was assigned a score based on the sonographic markers in a previously reported scoring system, modified by the addition of an echogenic intracardiac focus. The sonographic scoring system was then combined with the assignment of additional points based on maternal age. Karyotypic results were obtained subsequent to the scans, and Down's syndrome fetuses and a control group of normal fetuses were compared. Fifty-three fetuses with Down's syndrome were identified by karyotype and compared to a control group of 177 normal fetuses. A score of greater than or equal to 2 as a criterion for a positive test resulted in the identification of 75.4% of fetuses with Down's syndrome, with a 5.7% false-positive rate. A score of greater than or equal to 2 increased the sensitivity to 83.0%, with a false-positive rate of 17.5%. The age-adjusted modification resulted in the identification of 86.8% of fetuses with Down's syndrome, with a false-positive rate of 27.1%. It is for the individual patient and her practitioner to weigh the risks and benefits in selecting her options for prenatal diagnosis. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Obstet & Gynecol, Boston, MA USA. RP Bromley, B (reprint author), Diagnost Ultrasound Associates, 333 Longwood Ave, Boston, MA 02115 USA. NR 14 TC 54 Z9 54 U1 0 U2 1 PU PARTHENON PUBLISHING GROUP PI CARNFORTH LANCASHIRE PA CASTERTON HALL, CARNFORTH LANCASHIRE LA6 2LA, ENGLAND SN 0960-7692 J9 ULTRASOUND OBST GYN JI Ultrasound Obstet. Gynecol. PD NOV PY 1997 VL 10 IS 5 BP 321 EP 324 DI 10.1046/j.1469-0705.1997.10050321.x PG 4 WC Acoustics; Obstetrics & Gynecology; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Obstetrics & Gynecology; Radiology, Nuclear Medicine & Medical Imaging GA YP309 UT WOS:000071264000006 PM 9444045 ER PT J AU Stampfer, DS McDougal, WS McGovern, FJ AF Stampfer, DS McDougal, WS McGovern, FJ TI Metabolic and nutritional complications SO UROLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID URINARY INTESTINAL DIVERSION; SOLUTE TRANSPORT; SEGMENTS; ACIDOSIS; RATS AB The use of gastrointestinal segments for construction of a urinary conduit or reservoir has become a widely practiced technique in reconstructive urology. This article reviews basic intestinal transport, metabolic and nutritional complications relevant to particular gastrointestinal segments, and clinical relevance and treatment. RP Stampfer, DS (reprint author), MASSACHUSETTS GEN HOSP,1 HAWTHORNE PL,BOSTON,MA 02114, USA. NR 37 TC 25 Z9 26 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0094-0143 J9 UROL CLIN N AM JI Urol. Clin. N. Am. PD NOV PY 1997 VL 24 IS 4 BP 715 EP & DI 10.1016/S0094-0143(05)70413-4 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA YH864 UT WOS:A1997YH86400003 PM 9391524 ER PT J AU Optenberg, SA Clark, JY Brawer, MK Thompson, IM Stein, CR Friedrichs, P AF Optenberg, SA Clark, JY Brawer, MK Thompson, IM Stein, CR Friedrichs, P TI Development of a decision-making tool to predict risk of prostate cancer: The Cancer of the Prostate Risk Index (CAPRI) test SO UROLOGY LA English DT Article; Proceedings Paper CT 92nd Annual Meeting of the American-Urological-Association CY APR 12-17, 1997 CL NEW ORLEANS, LA SP Amer Urolog Assoc ID DIGITAL RECTAL EXAMINATION; REFERENCE RANGES; UNITED-STATES; ANTIGEN; MEN; CARCINOMA; DIAGNOSIS; BLACK; RACE; OLD AB Objectives. To provide a simple and reliable clinical prediction for an individual patient's overall risk of cancer at biopsy by deriving an easily implemented test based on a generalizable model. Four variables are analyzed for inclusion in the model: prostate-specific antigen (PSA) level, digital rectal examination (DRE) results, race, and age. Methods. Two populations were used to develop and validate the test: a model (n = 633) and an independent, geographically separate, external population (n = 766). Pathology records for patients who underwent prostate biopsy between 1991 and 1995 were reviewed and screened for the presence of PSA and DRE results. Records where age and race could be determined were extracted. Multiple logistic regression was used with an iterative approach to optimize each test factor. The Wald chi-square test, receiver operating characteristic (ROC) curve, and Hosmer-Lemingshaw test were used to evaluate the model's predictive capability in the two populations. Results. The model and external populations were significantly different for racial mix, PSA level, age, and biopsy detection rate, providing diverse populations to validate the test. Within a combined model, PSA, DRE, race, and age all demonstrated independent capability to predict cancer at biopsy. Predictive power of the overall test was high within the model population (ROC 80.8%), with minimal loss of power in the external population. The test demonstrated no significant lack of fit in either population. Conclusions. Within a combined test, PSA, DRE, race, and age all contribute significantly to prediction of prostate cancer at biopsy in an individual patient. The test depicts individual risk in an easily understood, visually provocative manner and should assist the clinician and patient in reaching a decision as to whether biopsy is appropriate. C1 WILFORD HALL USAF MED CTR,DEPT UROL,SAN ANTONIO,TX 78236. BROOKE ARMY MED CTR,DEPT SURG,FT SAM HOUSTON,TX 78234. VET AFFAIRS PUGET SOUND HLTH CARE SYST,SEATTLE,WA. UNIV WASHINGTON,DEPT UROL,SEATTLE,WA 98195. RP Optenberg, SA (reprint author), USA,MED DEPT CTR & SCH,CTR HEALTHCARE EDUC & STUDIES,1608 STANLEY RD,BLDG 2268,FT SAM HOUSTON,TX 78234, USA. OI Clark, Joseph/0000-0002-3817-4343 NR 22 TC 23 Z9 23 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD NOV PY 1997 VL 50 IS 5 BP 665 EP 672 DI 10.1016/S0090-4295(97)00451-2 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA YG346 UT WOS:A1997YG34600002 PM 9372872 ER PT J AU Moon, TD Hagen, L Heisey, DM AF Moon, TD Hagen, L Heisey, DM TI Urinary symptomatology in younger men SO UROLOGY LA English DT Article ID BENIGN PROSTATIC HYPERPLASIA; SYMPTOMS; AGE AB Objectives. We surveyed a ''population'' of younger men (20 to 49 years old) for lower urinary tract symptomatology and for symptomatology associated with prostatitis. Methods. A National Guard unit was surveyed by mail with a 58-question urinary symptom questionnaire. Surveys were returned anonymously by mail. Results. International Prostate Symptom Score (IPSS) of 8 or greater was seen in 5% of men in their 20s and rose to 15% of those in their 40s. Approximately 5% (0% to 7%) reported a history of prostatitis. Caffeine caused symptoms in 2% to 13%, while exercise and smoking were not associated with symptoms. Individual prostatitis symptoms were only seen occasionally across this age group. Conclusions. As measured by the IPSS, urinary symptoms increased during the 20 to 49-year age period. A history of prostatitis is much less common than most nonpopulation studies suggest. (C) 1997, Elsevier Science Inc. All rights reserved. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,SURG SERV,MADISON,WI. RP Moon, TD (reprint author), UNIV WISCONSIN,DEPT SURG,DIV UROL,G5343 CSC,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 12 TC 48 Z9 49 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD NOV PY 1997 VL 50 IS 5 BP 700 EP 703 DI 10.1016/S0090-4295(97)00336-1 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA YG346 UT WOS:A1997YG34600010 PM 9372878 ER PT J AU Koenig, F McGovern, FJ AF Koenig, F McGovern, FJ TI Fluorescence detection of bladder carcinoma SO UROLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RP Koenig, F (reprint author), MASSACHUSETTS GEN HOSP,DEPT UROL,50 BLOSSOM ST,BOSTON,MA 02114, USA. NR 0 TC 18 Z9 18 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD NOV PY 1997 VL 50 IS 5 BP 778 EP 779 DI 10.1016/S0090-4295(97)00409-3 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA YG346 UT WOS:A1997YG34600024 PM 9372892 ER PT J AU Carlson, KJ AF Carlson, KJ TI Primary care for women under managed care: Clinical issues SO WOMENS HEALTH ISSUES LA English DT Article; Proceedings Paper CT Symposium on Womens Primary Care - Clinical and Provider Issues CY FEB 07, 1997 CL WASHINGTON, D.C. SP Jacobs Inst Womens Hlth ID CHRONIC PELVIC PAIN; FEE-FOR-SERVICE; HEALTH-CARE; MEDICAL OUTCOMES; PATIENT OUTCOMES; BREAST-CANCER; QUALITY; TRIAL; HMO; SEX C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA. RP Carlson, KJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA. NR 40 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 1049-3867 J9 WOMEN HEALTH ISS JI Womens Health Iss. PD NOV-DEC PY 1997 VL 7 IS 6 BP 349 EP 361 DI 10.1016/S1049-3867(97)00075-3 PG 13 WC Public, Environmental & Occupational Health; Women's Studies SC Public, Environmental & Occupational Health; Women's Studies GA YM269 UT WOS:000071046700002 PM 9439196 ER PT J AU Cooper, DKC Thall, AD AF Cooper, DKC Thall, AD TI Xenoantigens and xenoantibodies: Their modification SO WORLD JOURNAL OF SURGERY LA English DT Article ID ALPHA-GALACTOSYL EPITOPES; NATURAL ANTIBODIES; DISCORDANT XENOTRANSPLANTATION; ORGAN XENOTRANSPLANTATION; GAL ANTIBODY; PIG; OLIGOSACCHARIDES; BABOON; CELLS; COMPLEMENT AB The hyperacute rejection of pig organs by primates, including humans, results from antibody-mediated complement activation. Protection from complement injury still leads to delayed rejection, which results from other mechanisms that may also be dependent on the presence of antibody. Anti-pig antibodies are directed largely, if not entirely, against alpha-galactose (alpha Gal) epitopes on pig vascular endothelium. Prevention of antibody-antigen binding is being attempted by methods that (1) alter antigen expression on the donor organ or (2) deplete the potential recipient of anti-alpha Gal antibody. To date, most progress has been made in depleting antibody by extracorporeal immunoadsorption using immuno-affinity columns of synthetic alpha Gal oligosaccharides. A pig organ transplanted into a recipient baboon depleted of antibody functions for several days-in contrast to minutes to hours in unmodified baboons. The return of antibody, however, results in rejection of the graft. Pharmacologic immunosuppressive agents are relatively ineffective for prolonged suppression of anti-alpha Gal production. Total-body irradiation and splenectomy are proving more successful. Studies are continuing with the aim of achieving a state of B cell tolerance toward alpha Gal epitopes. C1 BIOTRANSPLANT INC,CHARLESTOWN,MA 02129. RP Cooper, DKC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 48 TC 15 Z9 15 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2313 J9 WORLD J SURG JI World J.Surg. PD NOV-DEC PY 1997 VL 21 IS 9 BP 901 EP 906 PG 6 WC Surgery SC Surgery GA YC063 UT WOS:A1997YC06300002 PM 9361502 ER PT J AU Sykes, M Zhao, Y Yang, YG AF Sykes, M Zhao, Y Yang, YG TI Tolerance induction for xenotransplantation SO WORLD JOURNAL OF SURGERY LA English DT Article ID NONLETHAL PREPARATIVE REGIMEN; INTRATHYMIC CLONAL DELETION; BONE-MARROW TRANSPLANTATION; HUMAN T-CELLS; LONG-TERM; ALLOGRAFT-REJECTION; TRANSGENIC MICE; NONMYELOABLATIVE REGIMEN; MONOCLONAL-ANTIBODY; XENOGENEIC BARRIER AB The transplantation of donor hematopoietic tissue prior to organ xenografting has the potential to induce lasting T cell tolerance and, possibly, tolerance of natural antibody-producing B cells. However, the development of specific and nontoxic methods of overcoming the immunologic and physiologic barriers to xenogeneic marrow engraftment is a major challenge that must be met before this goal can be achieved. A greater understanding of the species specificity of molecular interactions important for hematopoiesis and cell homing is a first step toward transcending these physiologic barriers. Perhaps most promising is the potential associated with the use of nonprimate xenogeneic donors genetically engineered to make donor tissues more readily capable of surviving and, in the case of hematopoietic cells, competing with host tissues for survival in a human environment. RP Sykes, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129, USA. FU NHLBI NIH HHS [R01HL46532, R01HL49915]; NIAID NIH HHS [P01AI39755] NR 73 TC 19 Z9 20 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2313 J9 WORLD J SURG JI World J.Surg. PD NOV-DEC PY 1997 VL 21 IS 9 BP 932 EP 938 PG 7 WC Surgery SC Surgery GA YC063 UT WOS:A1997YC06300007 PM 9361507 ER PT J AU Seebach, JD Waneck, GL AF Seebach, JD Waneck, GL TI Natural killer cells in xenotransplantation SO XENOTRANSPLANTATION LA English DT Review DE natural killer cell; xenotransplantation; MHC; porcine; endothelial cell; adhesion; animal models ID CARDIAC XENOGRAFT REJECTION; PORCINE ENDOTHELIAL-CELLS; HUMAN T-CELLS; MEDIATED CYTOTOXICITY; NK CELLS; DISCORDANT XENOGRAFT; DIRECT ACTIVATION; GRAFT-REJECTION; PIG; LYMPHOCYTES C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02129 USA. RP Seebach, JD (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Transplantat Biol Res Ctr, MGH E,Bldg 149-0919,13th St, Boston, MA 02129 USA. NR 102 TC 49 Z9 50 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0908-665X J9 XENOTRANSPLANTATION JI Xenotransplantation PD NOV PY 1997 VL 4 IS 4 BP 201 EP 211 DI 10.1111/j.1399-3089.1997.tb00184.x PG 11 WC Medicine, Research & Experimental; Transplantation SC Research & Experimental Medicine; Transplantation GA YN056 UT WOS:000071128700001 ER PT J AU Yang, YG Sergio, JJ Sykes, M AF Yang, YG Sergio, JJ Sykes, M TI Engraftment of discordant xenogeneic swine bone marrow cells in immunodeficient mice SO XENOTRANSPLANTATION LA English DT Article DE xenotransplantation; bone marrow transplantation; chimerism; cytokine; swine; mouse ID IMMUNE-DEFICIENT MICE; HEMATOPOIETIC STEM-CELLS; SCID MICE; MONOCLONAL-ANTIBODIES; PECULIAR IMMUNOBIOLOGY; GRAFT-REJECTION; T-CELLS; TRANSPLANTATION; MOUSE; RECONSTITUTION AB We have recently demonstrated that swine bone marrow cells (BMC) can engraft in C.B-17 scid mice. While engraftment is enhanced by providing donor-specific porcine cytokines, the level of swine hematopoiesis declines between 3 and 6 weeks post-transplant. In the present study, the utility of several strains of immunodeficient mice as recipients of swine hematopoietic cells has been determined by comparing levels of swine bone marrow engraftment at 3 weeks after bone marrow transplant. Irradiated recipients were injected with 1x10(8) swine BMC and were treated daily with porcine cytokines. The presence of swine cells in BMT recipients was detected by flow cytometry and marrow colony-forming assays. Recombination activating gene-1 (RAG-l)-deficient mice were not permissive for the engraftment of swine BMC, even with administration of increased doses of whole body irradiation, or with depleting anti-NK cell antibody. In contrast, NOD-scid mice showed improved swine BMC engraftment compared to C.B-17 scid mice. Levels of swine class I+, myeloid, and CD2(+) cells in bone marrow, spleen, and peripheral blood, and the number of porcine myeloid progenitor cells was significantly higher in NOD-scid recipients than in simultaneous C.B-17 scid recipients, In addition, the sera from C.B-17 scid mice markedly inhibited the proliferation of swine BMC in vitro., A weaker inhibitory effect was also mediated by sera from RAG-1-deficient! mice, but not by sera from NOD-scid mice. Together, our results indicate that multiple host elements resist xenogeneic hematopoietic engraftment and function, some of which are clearly independent of host T, B, or NK cells. Understanding the basis for the advantage of NOD-scid mice as recipients of discordant xenogeneic porcine BMC will help to identify these elements. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp,BMT Sect, Transplantat Biol Res Ctr,Surg Serv, Boston, MA 02129 USA. RP Sykes, M (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp,BMT Sect, Transplantat Biol Res Ctr,Surg Serv, MGH E,Bldg 149-5102,13th St, Boston, MA 02129 USA. NR 44 TC 10 Z9 11 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0908-665X J9 XENOTRANSPLANTATION JI Xenotransplantation PD NOV PY 1997 VL 4 IS 4 BP 235 EP 244 DI 10.1111/j.1399-3089.1997.tb00188.x PG 10 WC Medicine, Research & Experimental; Transplantation SC Research & Experimental Medicine; Transplantation GA YN056 UT WOS:000071128700005 ER PT J AU Sawada, T Friedman, T Iacomini, J AF Sawada, T Friedman, T Iacomini, J TI Conditions permitting short-term engraftment of human T cells in RAG-1 mutant mice SO XENOTRANSPLANTATION LA English DT Article DE RAG-1; human T cells; engraftment ID PERIPHERAL-BLOOD LYMPHOCYTES; COMBINED IMMUNE-DEFICIENCY; PBL-SCID MICE; MUTATION; MOUSE; REPAIR; XENOTRANSPLANTATION; REJECTION; RADIATION AB The ability to reconstitute RAG-1 deficient (R-) mice with human peripheral blood cells was examined using four different host preparative regimens. Our results indicate that while untreated R-mice could be reconstituted with human cells, pre-conditioning with either 5Gy whole body irradiation (WBI) or anti-asialo GM1 rabbit anti-serum led to an increase in the frequency of CD45(+) human cells that could be detected in the circulation. Pre-conditioning with both anti-asialo GM1; and WBI led to a further increase in the frequency of circulating human cells in reconstituted R- mice. Human CD45(+) cells were detected in the spleen and lymph nodes, but not the thymus of reconstituted mice pre-conditioned with WBI and anti-asialo GM1. Our results suggest that mouse NK cells and a limitation in physical space are limiting factors mediating resistance to human cell engraftment in R- mice. C1 Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02129 USA. Harvard Univ, Sch Med, Boston, MA 02129 USA. RP Iacomini, J (reprint author), Massachusetts Gen Hosp, Transplantat Biol Res Ctr, MGH-E,Bldg 149-9019,13th St, Boston, MA 02129 USA. NR 27 TC 1 Z9 1 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0908-665X J9 XENOTRANSPLANTATION JI Xenotransplantation PD NOV PY 1997 VL 4 IS 4 BP 245 EP 251 DI 10.1111/j.1399-3089.1997.tb00189.x PG 7 WC Medicine, Research & Experimental; Transplantation SC Research & Experimental Medicine; Transplantation GA YN056 UT WOS:000071128700006 ER PT J AU Auchincloss, H AF Auchincloss, H TI Literature update 1997, part 2 SO XENOTRANSPLANTATION LA English DT Review C1 Massachusetts Gen Hosp, Transplantat Unit, Surg Serv, Boston, MA 02114 USA. RP Auchincloss, H (reprint author), Massachusetts Gen Hosp, Transplantat Unit, Surg Serv, GRB 504, Boston, MA 02114 USA. NR 124 TC 0 Z9 0 U1 0 U2 3 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0908-665X J9 XENOTRANSPLANTATION JI Xenotransplantation PD NOV PY 1997 VL 4 IS 4 BP 267 EP 274 DI 10.1111/j.1399-3089.1997.tb00192.x PG 8 WC Medicine, Research & Experimental; Transplantation SC Research & Experimental Medicine; Transplantation GA YN056 UT WOS:000071128700009 ER PT J AU Testa, CM Hollingsworth, ZR Shinozaki, H Penney, JB Young, AB AF Testa, CM Hollingsworth, ZR Shinozaki, H Penney, JB Young, AB TI Selective metabotropic receptor agonists distinguish non-ionotropic glutamate binding sites SO BRAIN RESEARCH LA English DT Article DE L-CCG-II; DCG-IV; DHPG; metabotropic glutamate receptor; autoradiography ID RAT SPINAL-CORD; CYCLIC-AMP FORMATION; INOSITOL PHOSPHOLIPID HYDROLYSIS; KAINIC ACID BINDING; SIGNAL-TRANSDUCTION; MOLECULAR CHARACTERIZATION; CORTICAL-NEURONS; OLFACTORY-BULB; DCG-IV; BRAIN AB Metabotropic glutamate receptors (mGluRs) are thought to mediate diverse processes in brain including synaptic plasticity and excitotoxicity. These receptors are often divided into three groups by their pharmacological profiles. [H-3]Glutamate binding in the presence of compounds selective for ionotropic glutamate receptors can be used as a general assay for these receptors; subtypes of this non-ionotropic [H-3]glutamate binding differ in both pharmacology and anatomical distribution, and are differentially sensitive to quisqualate. The characteristics of these binding sites are consistent with those of group 1 (high-affinity quisqualate) and group 2 (low-affinity quisqualate) mGluRs. Under our assay conditions, no [H-3]glutamate binding to group 3-like (L-AP4 sensitive) sites could be demonstrated. We have attempted to characterize particular agents which may selectively measure [H-3]glutamate binding to mGluR subtypes, We used two isomers of 2-(carboxycyclopropyl)glycine, L-CCG-I and L-CCG-II, and the (2S,1'R,2'R,3'R) isomer of 2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV) as competitors of non-ionotropic [H-3]glutamate binding sites. DCG-IV clearly distinguishes two binding sites. Quantitative levels of DCG-IV binding by anatomic region correlate with quisqualate-defined binding subtypes: high-affinity DCG-IV binding correlates with low-affinity quisqualate binding, whereas low-affinity DCG-IV binding correlates with high-affinity quisqualate binding. L-CCG-II displaces only one type of non-ionotropic [3H]glutamate binding, corresponding to high-affinity quisqualate binding. Therefore DCG-IV and L-CCG-II at appropriate concentrations appear to distinguish binding to putative group 2 vs. group 1 mGluRs, L-CCG-I displaces both high-and low-affinity quisqualate binding sites, but unlike the other two compounds, does not clearly distinguish between them. (C) 1997 Elsevier Science B.V. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. TOKYO METROPOLITAN INST MED SCI,BUNKYO KU,TOKYO 113,JAPAN. FU NIA NIH HHS [AG13617, AG11337]; NINDS NIH HHS [NS31579] NR 51 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD OCT 31 PY 1997 VL 773 IS 1-2 BP 15 EP 27 DI 10.1016/S0006-8993(97)00818-4 PG 13 WC Neurosciences SC Neurosciences & Neurology GA YG696 UT WOS:A1997YG69600003 PM 9409700 ER PT J AU Burks, DJ Pons, S Towery, H SmithHall, J Myers, MG Yenush, L White, MF AF Burks, DJ Pons, S Towery, H SmithHall, J Myers, MG Yenush, L White, MF TI Heterologous pleckstrin homology domains do not couple IRS-1 to the insulin receptor SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BRUTONS TYROSINE KINASE; PH DOMAINS; SUBSTRATE-1; DYNAMIN; BINDING; PROTEIN; ACTIVATION; SUBUNITS; REGION AB Pleckstrin homology (PH) domains occur in many signaling proteins, including substrates for the insulin receptor tyrosine kinase (IRS proteins). Based on the hypothesis that PH domains may have a common function such as membrane targeting we tested the ability of PH domains from other signaling molecules to link IRS-1 to the insulin receptor. Chimeric IRS-1 proteins containing a homologous PH domain derived from other HRS proteins (IRS-2 or Gab-1) were tyrosine phosphorylated normally in response to insulin. In contrast, heterologous PH domains from the beta-adrenergic receptor kinase, phospholipase C gamma, or spectrin failed to mediate tyrosine phosphorylation of chimeric IRS-1 proteins, even in cells expressing high levels of insulin receptor. Moreover, IRS-1 proteins containing heterologous PH domains did not bind phosphorylated NPEY motifs derived from the insulin receptor, suggesting that the presence of these structures interfered with the function of the adjacent PTB binding domain. Thus, tyrosine phosphorylation of IRS-1 by the insulin receptor specifically requires a PH domain derived from IRS proteins. C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. RI Pons , Sebastian/K-7794-2014; Yenush, Lynne/J-8815-2014 OI Pons , Sebastian/0000-0003-1027-0621; Yenush, Lynne/0000-0001-8589-7002 FU NIDDK NIH HHS [DK43808, T32 DK 07260, P30 DK36836] NR 34 TC 47 Z9 47 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 31 PY 1997 VL 272 IS 44 BP 27716 EP 27721 DI 10.1074/jbc.272.44.27716 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YD473 UT WOS:A1997YD47300039 PM 9346913 ER PT J AU Elser, B Kriz, W Bonventre, JV Englert, C Witzgall, R AF Elser, B Kriz, W Bonventre, JV Englert, C Witzgall, R TI The Kruppel-associated box (KRAB) zinc finger protein Kid-1 and the Wilms' tumor protein WT1, two transcriptional repressor proteins, bind to heteroduplex DNA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GENE-PRODUCT; DOMAIN; SUBFAMILY; SEQUENCE; SITES AB Zinc finger proteins of the Cys(2)His(2) class represent a large group of DNA-binding proteins. A major subfamily of those proteins, the Kruppel-associated box (KRAB) domain-containing Cys(2)His(2)-zinc finger proteins, have been described as potent transcriptional repressors. So far, however, no DNA-binding sites for KRAB domain-containing zinc finger proteins have been isolated. Using a polymerase chain reaction-based selection strategy with double-and single-stranded DNA, we failed to reveal a binding site for Kid-1, one member of KRAB-zinc finger proteins. Binding of Kid-1 both to single-and homoduplex double-stranded DNA was negligible. We now present evidence that Kid-1 binds to heteroduplex DNA. Similar to Kid-1, the non-KRAB-zinc finger protein WT1 also bound avidly to heteroduplex DNA (both the -KTS and +KTS splice variant of WT1), whereas the POU domain protein Oct-6, the ets domain protein Ets-1 and the RING finger of BRCA-1 did not bind to heteroduplex DNA. Binding of WT1 to heteroduplex DNA was markedly reduced in naturally occurring mutants. The recognition of certain DNA structures by transcriptional repressor proteins may therefore represent a more common phenomenon than previously thought. C1 UNIV HEIDELBERG,INST ANAT & CELL BIOL 1,D-69120 HEIDELBERG,GERMANY. HARVARD UNIV,SCH MED,DEPT MED,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP,RENAL UNIT,CHARLESTOWN,MA 02129. FORSCHUNGSZENTRUM KARLSRUHE,INST GENET,D-76021 KARLSRUHE,GERMANY. NR 32 TC 17 Z9 18 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 31 PY 1997 VL 272 IS 44 BP 27908 EP 27912 DI 10.1074/jbc.272.44.27908 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YD473 UT WOS:A1997YD47300065 PM 9346939 ER PT J AU Orlando, LR LuthiCarter, R Standaert, DG Coyle, JT Penney, JB Young, AB AF Orlando, LR LuthiCarter, R Standaert, DG Coyle, JT Penney, JB Young, AB TI N-acetylaspartylglutamate (NAAG) protects against rat striatal quinolinic acid lesions in vivo SO NEUROSCIENCE LETTERS LA English DT Article DE quinolinic acid; excitotoxicity; striatum; N-acetylaspartylglutamate; N-methyl-D-aspartate receptors; metabotropic glutamate receptors ID METABOTROPIC GLUTAMATE RECEPTORS; IN-VITRO; NEUROTOXICITY; NEURONS; MODULATION; DISEASE; AGONIST AB We examined the effects of N-acetylaspartylglutamate (NAAG), an endogenous peptide thought to be involved in neurotransmission and neuromodulation, on striatal quinolinate lesions, a rodent model of Huntington's disease. We found that NAAG (500 and 1000 nmol) co-injected with quinolinic acid significantly reduced lesion volumes (by 50% and 65%, respectively). A 1000 nmol dose of the non-hydrolyzable analogue, beta-NAAG, also reduced quinolinic acid lesion volumes by 78.4%, indicating that the protection observed was not secondary to cleavage of NAAG into N-acetyl-aspartate (NAA) and glutamate. Likewise, co-injection of both NAA and glutamate (1000 nmol each) with quinolinic acid did not significantly alter the size of lesions. NAAG's protective effect may be mediated through actions on N-methyl-D-aspartate receptors or metabotropic glutamate receptors. (C) 1997 Elsevier Science Ireland Ltd. C1 HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. OI Standaert, David/0000-0003-2921-8348 FU NIA NIH HHS [AG11337, AG13617]; NINDS NIH HHS [NS31579] NR 24 TC 32 Z9 32 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD OCT 31 PY 1997 VL 236 IS 2 BP 91 EP 94 DI 10.1016/S0304-3940(97)00769-6 PG 4 WC Neurosciences SC Neurosciences & Neurology GA YH839 UT WOS:A1997YH83900008 PM 9404819 ER PT J AU Mercurio, F Zhu, HY Murray, BW Shevchenko, A Bennett, BL Li, JW Young, DB Barbosa, M Mann, M AF Mercurio, F Zhu, HY Murray, BW Shevchenko, A Bennett, BL Li, JW Young, DB Barbosa, M Mann, M TI IKK-1 and IKK-2: Cytokine-activated I kappa B kinases essential for NF-kappa B activation SO SCIENCE LA English DT Article ID TRANSCRIPTION FACTORS; ALPHA PROTEOLYSIS; MASS-SPECTROMETRY; PHOSPHORYLATION; PROTEINS; UBIQUITINATION; DEGRADATION; SIGNAL; FAMILY; IDENTIFICATION AB Activation of the transcription factor nuclear factor kappa B (NF-kappa B) is controlled by sequential phosphorylation, ubiquitination, and degradation of its inhibitory subunit I kappa B. A large multiprotein complex, the I kappa B kinase (IKK) signalsome, was purified from Hela cells and found to contain a cytokine-inducible I kappa B kinase activity that phosphorylates I kappa B-alpha and I kappa B-beta. Two components of the IKK signalsome, IKK-1 and IKK-2, were identified as closely related protein serine kinases containing leucine zipper and helix-loop-helix protein interaction motifs. Mutant versions of IKK-2 had pronounced effects on RelA nuclear translocation and NF-kappa B-dependent reporter activity, consistent with a critical role for the IKK kinases in the NF-kappa B signaling pathway. C1 EUROPEAN MOL BIOL LAB,D-69012 HEIDELBERG,GERMANY. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP Mercurio, F (reprint author), SIGNAL PHARMACEUT INC,5555 OBERLIN AVE,SAN DIEGO,CA 92121, USA. RI Mann, Matthias/A-3454-2013 OI Mann, Matthias/0000-0003-1292-4799 NR 41 TC 1625 Z9 1668 U1 1 U2 21 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 31 PY 1997 VL 278 IS 5339 BP 860 EP 866 DI 10.1126/science.278.5339.860 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YD479 UT WOS:A1997YD47900046 PM 9346484 ER PT J AU Ghosh, PM Mott, GE GhoshChoudhury, N Radnik, RA Stapleton, ML Ghidoni, JJ Kreisberg, JI AF Ghosh, PM Mott, GE GhoshChoudhury, N Radnik, RA Stapleton, ML Ghidoni, JJ Kreisberg, JI TI Lovastatin induces apoptosis by inhibiting mitotic and post-mitotic events in cultured mesangial cells SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE mesangial cell; protein prenylation; RhoA; geranylgeraniol; farnesol; cytokinesis ID FOCAL ADHESION KINASE; GTP-BINDING PROTEINS; POSTTRANSLATIONAL MODIFICATIONS; TYROSINE PHOSPHORYLATION; COMPETITIVE INHIBITOR; STRESS FIBERS; RHO; GROWTH; REDUCTASE; GERANYLGERANYLATION AB Lovastatin, an inhibitor of protein prenylation, was reported to inhibit DNA synthesis and induce apoptosis in cultured cells. This report describes the morphological consequences of lovastatin treatment. Lovastatin (50 mu M) induced mesangial cell rounding and disassembly of actin stress fibers within 24 to 48 h. After 48 to 72 h of lovastatin treatment, the cells detached from the substratum and underwent apoptotic cell death as evidenced by condensed nuclear chromatin, nuclear fragmentation, cell blebbing and decrease in cell size. Time lapse cinematography revealed that lovastatin caused cell rounding by either inhibiting cytokinesis or cell spreading following cytokinesis. Lovastatin-induced cell rounding, detachment, and apoptosis were dependent upon cell proliferation. These effects were prevented by serum deprivation to inhibit cell proliferation or by plating cells at densities which resulted in contact inhibition of cell growth. Lovastatin-induced mesangial cell rounding and apoptosis were also prevented by the inclusion of the isoprenoids all-trans-farnesol or all-trans-geranylgeraniol in the incubation medium. These results indicate that the effects of lovastatin were mediated by inhibition of protein isoprenylation because exogenous all-trans-geranylgeraniol can be used only in protein prenylation. The small GTP-binding protein RhoA, which may be important for cell spreading and cytokinesis, accumulated in the cytosol following treatment with lovastatin, suggestive of its inactivation. This effect was also prevented by the inclusion of either farnesol or geranylgeraniol in the incubation medium. Thus, lovastatin-induced apoptosis in mesangial cells occurs by interfering with prenylation dependent mitotic and post-mitotic events. (C) 1997 Elsevier Science B.V. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. S TEXAS VET HLTH CARE SYST,RES & DEV SERV,SAN ANTONIO,TX. NR 38 TC 58 Z9 63 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4889 J9 BBA-MOL CELL RES JI Biochim. Biophys. Acta-Mol. Cell Res. PD OCT 30 PY 1997 VL 1359 IS 1 BP 13 EP 24 DI 10.1016/S0167-4889(97)00091-8 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA YG699 UT WOS:A1997YG69900002 PM 9398081 ER PT J AU Ogg, S Paradis, S Gottlieb, S Patterson, GI Lee, L Tissenbaum, HA Ruvkun, G AF Ogg, S Paradis, S Gottlieb, S Patterson, GI Lee, L Tissenbaum, HA Ruvkun, G TI The Fork head transcription factor DAF-16 transduces insulin-like metabolic and longevity signals in C-elegans SO NATURE LA English DT Article ID DAUER LARVA DEVELOPMENT; CAENORHABDITIS-ELEGANS; ALVEOLAR RHABDOMYOSARCOMA; INTERACTING GENES; EXPRESSION; GROWTH; TRANSLOCATION; SUPPRESSES; PROTEINS; HOMOLOG AB In mammals, insulin signalling regulates glucose transport together with the expression and activity of various metabolic enzymes. In the nematode Caenorhabditis elegans, a related pathway regulates metabolism, development and longevity(1,2). Wild-type animals enter the developmentally arrested dauer stage in response to high levels of a secreted pheromone(3), accumulating large amounts of fat in their intestines and hypodermis. Mutants in DAF-2 (a homologue of the mammalian insulin receptor) and AGE-1 (a homologue of the catalytic subunit of mammalian phosphatidylinositol 3-OH kinase) arrest development at the dauer stage(3), Moreover, animals bearing weak or temperature-sensitive mutations in daf-2 and age-1 can develop reproductively, but nevertheless show increased energy storage and longevity(1,2,4,5). Here we show that null mutations in daf-16 suppress the effects of mutations in daf-2 or age-1; lack of daf-16 bypasses the need for this insulin receptor-like signalling pathway. The principal role of DAF-2/AGE-1 signalling is thus to antagonize DAF-16. daf-16 is widely expressed and encodes three members of the Fork head family of transcription factors, The DAF-2 pathway acts synergistically with the pathway activated by a nematode TGF-beta-type signal, DAF-7, suggesting that DAF-16 cooperates with nematode SMAD proteins in regulating the transcription of key metabolic and developmental control genes. The probable human orthologues of DAF-16, FKHR and AFX, may also act downstream of insulin signalling and cooperate with TGF-beta effecters in mediating metabolic regulation. These genes may be dysregulated in diabetes. C1 MASSACHUSETTS GEN HOSP,DEPT MOL BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. NR 30 TC 1208 Z9 1236 U1 12 U2 83 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD OCT 30 PY 1997 VL 389 IS 6654 BP 994 EP 999 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YD299 UT WOS:A1997YD29900062 PM 9353126 ER PT J AU Caplan, LR Mohr, JP Kistler, JP Koroshetz, W AF Caplan, LR Mohr, JP Kistler, JP Koroshetz, W TI Should thrombolytic therapy be the first-line treatment for acute ischemic stroke? Thrombolysis - Not a panacea for ischemic stroke SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material C1 NEUROL INST,NEW YORK,NY 10032. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Caplan, LR (reprint author), TUFTS UNIV NEW ENGLAND MED CTR,DEPT NEUROL,314,750 WASHINGTON ST,BOSTON,MA 02111, USA. NR 7 TC 135 Z9 137 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 30 PY 1997 VL 337 IS 18 BP 1309 EP 1310 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA YC920 UT WOS:A1997YC92000012 PM 9345084 ER PT J AU Goff, DC Wine, L AF Goff, DC Wine, L TI Glutamate in schizophrenia: clinical and research implications SO SCHIZOPHRENIA RESEARCH LA English DT Article DE glutamate; schizophrenia; amino acids; D-cycloserine; glycine ID EXCITATORY AMINO-ACIDS; D-ASPARTATE RECEPTOR; CONVENTIONAL NEUROLEPTIC TREATMENT; NMDA INTERVENTION STRATEGY; GLYCINE ADJUVANT THERAPY; PREFRONTAL CORTEX; DOPAMINE RELEASE; D-CYCLOSERINE; CEREBROSPINAL-FLUID; NEGATIVE SYMPTOMS AB The excitatory amino acids, glutamate and aspartate, are of interest to schizophrenia research because of their roles in neurodevelopment, neurotoxicity and neurotransmission. Recent evidence suggests that densities of glutamatergic receptors and the ratios of subunits composing these receptors may be altered in schizophrenia, although it is unclear whether these changes are primary or compensatory. Agents acting at the phencyclidine binding site of the NMDA receptor produce symptoms of schizophrenia in normal subjects, and precipitate relapse in patients with schizophrenia. The improvement of negative symptoms with agents acting at the glycine modulatory site of the NMDA receptor, as well as preliminary evidence that clozapine may differ from conventional neuroleptic agents in its effects on glutamatergic systems, suggest that clinical implications may follow from this model. While geriatric patients may be at increased risk for glutamate-mediated neurotoxicity, very little is known about the specific relevance of this model to geriatric patients with schizophrenia. (C) 1997 Elsevier Science B.V. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PSYCHOT DISORDERS PROGRAM,BOSTON,MA. FU NIMH NIH HHS [R01 MH54245] NR 93 TC 73 Z9 76 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD OCT 30 PY 1997 VL 27 IS 2-3 BP 157 EP 168 DI 10.1016/S0920-9964(97)00079-0 PG 12 WC Psychiatry SC Psychiatry GA YH234 UT WOS:A1997YH23400006 PM 9416645 ER PT J AU Dryja, TP AF Dryja, TP TI Gene-based approach to human gene-phenotype correlations SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID RECESSIVE RETINITIS-PIGMENTOSA; STRAND CONFORMATION POLYMORPHISM; STATIONARY NIGHT BLINDNESS; PERIPHERIN-RDS GENE; HUMAN COLOR-VISION; ALPHA-SUBUNIT; MOLECULAR-GENETICS; CGMP PHOSPHODIESTERASE; ROD PHOSPHODIESTERASE; RHODOPSIN GENE AB Elucidating the genetic basis of human phenotypes is a major goal of contemporary geneticists. Logically, two fundamental and contrasting approaches are available, one that begins with a phenotype and concludes with the identification of a responsible gene or genes; the other that begins with a gene and works toward identifying one or more phenotypes resulting from allelic variation of it. This paper provides a conceptual overview of phenotype-based vs. gene-based procedures with emphasis on gene-based methods. A key feature of a gene-based approach is that laboratory effort first is devoted to developing an assay for mutations in the gene under regard; the assay then is applied to the evaluation of large numbers of unrelated individuals with a variety of phenotypes that are deemed potentially resulting from alleles at the gene. No effort is directed toward chromosomally mapping the loci responsible for the phenotypes scanned. Example is made of my laboratory's successful use of a gene-based approach to identify genes causing hereditary diseases of the retina such as retinitis pigmentosa. Reductions in the cost and improvements in the speed of scanning individuals for DNA sequence anomalies may make a gene-based approach an efficient alternative to phenotype-based approaches to correlating genes with phenotypes. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP Dryja, TP (reprint author), HARVARD UNIV,SCH MED,OCULAR MOL GENET INST,243 CHARLES ST,BOSTON,MA 02114, USA. NR 54 TC 36 Z9 37 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 28 PY 1997 VL 94 IS 22 BP 12117 EP 12121 DI 10.1073/pnas.94.22.12117 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YD506 UT WOS:A1997YD50600067 PM 9342372 ER PT J AU Richardson, JH Waldmann, TA Sodroski, JG Marasco, WA AF Richardson, JH Waldmann, TA Sodroski, JG Marasco, WA TI Inducible knockout of the interleukin-2 receptor alpha chain: Expression of the high-affinity IL-2 receptor is not required for the in vitro growth of HTLV-I-transformed cell lines SO VIROLOGY LA English DT Article ID LEUKEMIA-LYMPHOMA VIRUS; HUMAN T-CELLS; ANTI-TAC; INFECTED-CELLS; MESSENGER-RNA; BETA-CHAIN; LYMPHOCYTES; ANTIBODIES; ACTIVATION; DISTINCT AB Adult T cell leukemia (ATL) is an aggressive malignancy that is associated with HTLV-I infection and characterized by constitutive expression of the high-affinity interleukin-2 receptor. The cu subunit of the high-affinity receptor (IL-2R alpha), which is normally present only on activated T cells, is specifically upregulated by HTLV-I and constitutively expressed on fresh leukemic cells from ATL patients as well as cell lines transformed by HTLV-I in vitro. Here we directly address the functional significance of IL-2R alpha expression in HTLV-I transformed cell lines by using an endoplasmic reticulum-targeted single-chain antibody to inhibit the cell surface expression of IL-2 alpha. Using constitutive and tetracycline-repressible systems to express the ER-targeted antibody against IL-2R alpha, we have reduced cell surface expression of IL-2R alpha by more that 2 logs of mean fluorescence intensity to virtually undetectable levels in the IL-2-independent HTLV-I-transformed cell lines C8166-45 and HUT102. No toxicity was associated with the intracellular retention of IL-2R alpha, and the growth rate of the IL-2R alpha-negative cells was in each case comparable to that of the parental cell line. We conclude that cell surface expression of IL-2R alpha is dispensable for the in vitro growth of these HTLV-l-transformed cells. (C) 1997 Academic Press. C1 DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. NCI,METAB BRANCH,NIH,BETHESDA,MD 20892. NR 45 TC 14 Z9 16 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD OCT 27 PY 1997 VL 237 IS 2 BP 209 EP 216 DI 10.1006/viro.1997.8779 PG 8 WC Virology SC Virology GA YF073 UT WOS:A1997YF07300003 PM 9356333 ER PT J AU Campbell, AJ Robertson, MC Gardner, MM Norton, RN Tilyard, MW Buchner, DM AF Campbell, AJ Robertson, MC Gardner, MM Norton, RN Tilyard, MW Buchner, DM TI Randomised controlled trial of a general practice programme of home based exercise to prevent falls in elderly women SO BRITISH MEDICAL JOURNAL LA English DT Article ID FICSIT TRIALS; OLDER ADULTS; RISK-FACTORS; TAI-CHI; COMMUNITY; BALANCE; INTERVENTION; STRENGTH AB Objective: To assess the effectiveness of a home exercise programme of strength and balance retraining exercises in reducing falls and injuries in elderly women. Design: Randomised controlled trial of an individually tailored programme of physical therapy in the home (exercise group, n=116) compared with the usual care and an equal number of social visits (control group, n=117). Setting 17 general practices in Dunedin, New Zealand. Subjects: Women aged 80 years and older living in the community and registered with a general practice in Dunedin. Main outcome measures: Number of falls and injuries related to falls and time between falls during one year of follow up; changes in muscle strength and balance measures after six months. Results: After one year there were 152 falls in the control group and 88 falls in the exercise group. The mean (SD) rate of falls was lower in the exercise than the control group (0.87 (1.29) v 1.34 (1.93) falls per year respectively; difference 0.47; 95% confidence interval 0.04 to 0.90). The relative hazard for the first four falls in the exercise group compared with the control group was 0.68 (0.52 to 0.90). The relative hazard for a first fall with injury in the exercise group compared with the control group was 0.61 (0.39 to 0.97). After six months, balance had improved in the exercise group (difference between groups in change in balance score 0.43 (0.21 to 0.65). Conclusions: An individual programme of strength and balance retraining exercises improved physical function and was effective in reducing falls and injuries in women 80 years and older. C1 UNIV AUCKLAND,SCH MED,INJURY PREVENT RES CTR,AUCKLAND,NEW ZEALAND. UNIV OTAGO SCH MED,DUNEDIN SCH MED,DEPT GEN PRACTICE,DUNEDIN,NEW ZEALAND. VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA 98108. RP Campbell, AJ (reprint author), UNIV OTAGO SCH MED,DUNEDIN SCH MED,DEPT MED,POB 913,DUNEDIN,NEW ZEALAND. RI Robertson, Mary Clare/A-3964-2009 NR 24 TC 515 Z9 535 U1 10 U2 49 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0959-8138 J9 BRIT MED J JI Br. Med. J. PD OCT 25 PY 1997 VL 315 IS 7115 BP 1065 EP 1069 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA YD445 UT WOS:A1997YD44500027 PM 9366737 ER PT J AU Belding, MA Iguchi, MY Morral, AR McLellan, AT AF Belding, MA Iguchi, MY Morral, AR McLellan, AT TI Assessing the helping alliance and its impact in the treatment of opiate dependence SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE helping alliance; therapeutic alliance; heroin dependence; methadone maintenance; treatment ID THERAPEUTIC ALLIANCE; PSYCHOTHERAPY; DETOXIFICATION; DETERMINANTS; DEPRESSION; THERAPIST; COUNSELOR; PROGRAM; SUCCESS AB This study assesses the relationship between the patient-counselor helping alliance (HA) and progress in methadone maintenance treatment. Questionnaire measures of HA were administered to 57 patients 1 and 3 months after admission. Three-month HA measures (especially counselors' ratings) predicted reductions in drug use as measured by weekly urinalysis results and 6-month self-report data. HA was unrelated to treatment retention or improvement in psychiatric symptomatology. Moreover, controlling for urinalysis results in the previous month rendered insignificant the correlations between 3-month HA and subsequent drug use. Thus, this evaluation of the HA's unique contribution to the prediction of outcome suggests that the development of a positive HA may be more a marker of treatment progress than a necessary precursor of positive outcomes in the methadone maintenance treatment setting. (C) 1997 Elsevier Science Ireland Ltd. C1 ALLEGHENY UNIV HLTH SCI,MCP HAHNEMANN UNIV,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19102. RP Belding, MA (reprint author), UNIV PENN,SCH MED,DEPT PSYCHIAT,CTR STUDIES ADDICT,PHILADELPHIA VET AFFAIRS MED CTR,BLDG 7,PHILADELPHIA,PA 19104, USA. RI Iguchi, Martin/A-7848-2009 FU NIDA NIH HHS [P50 DA07705, R01 DA06096] NR 21 TC 33 Z9 33 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD OCT 25 PY 1997 VL 48 IS 1 BP 51 EP 59 DI 10.1016/S0376-8716(97)00103-8 PG 9 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA XY392 UT WOS:A1997XY39200007 PM 9330921 ER PT J AU Kavka, AI Green, JBA AF Kavka, AI Green, JBA TI Tales of tails: Brachyury and the T-box genes SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER LA English DT Review ID CONSERVED PROTEIN MOTIF; MESODERM FORMATION; MOUSE BRACHYURY; XENOPUS EMBRYOS; EXPRESSION PATTERN; ZEBRAFISH HOMOLOG; T(BRACHYURY) GENE; INDUCTION; CELLS; GASTRULATION RP Kavka, AI (reprint author), DANA FARBER CANC INST,44 BINNEY ST,ROOM B455,BOSTON,MA 02215, USA. RI Green, Jeremy/F-3630-2010 OI Green, Jeremy/0000-0002-6102-2620 NR 82 TC 23 Z9 23 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-419X J9 BBA-REV CANCER JI Biochim. Biophys. Acta-Rev. Cancer PD OCT 24 PY 1997 VL 1333 IS 2 BP F73 EP F84 DI 10.1016/S0304-419X(97)00016-4 PG 12 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA YG523 UT WOS:A1997YG52300002 PM 9395282 ER PT J AU Kharbanda, S Yuan, ZM Weichselbaum, R Kufe, D AF Kharbanda, S Yuan, ZM Weichselbaum, R Kufe, D TI Functional role for the c-Abl protein tyrosine kinase in the cellular response to genotoxic stress SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER LA English DT Article ID NF-KAPPA-B; RADIATION-INDUCED APOPTOSIS; MYELOID-LEUKEMIA CELLS; DNA-DAMAGING AGENTS; IONIZING-RADIATION; ATAXIA-TELANGIECTASIA; BINDING-ACTIVITY; PHOSPHATIDYLINOSITOL 3-KINASE; GAMMA-RADIATION; JNK ACTIVATION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. NR 89 TC 9 Z9 9 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-419X J9 BBA-REV CANCER JI Biochim. Biophys. Acta-Rev. Cancer PD OCT 24 PY 1997 VL 1333 IS 2 BP O1 EP O7 DI 10.1016/S0304-419X(97)00020-6 PG 7 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA YG523 UT WOS:A1997YG52300006 PM 9395286 ER PT J AU Passani, LA Vonsattel, JPG Coyle, JT AF Passani, LA Vonsattel, JPG Coyle, JT TI Distribution of N-acetylaspartylglutamate immunoreactivity in human brain and its alteration in neurodegenerative disease SO BRAIN RESEARCH LA English DT Article DE Alzheimer's disease; Huntington's disease; N-acetylaspartylglutamate; glutamate; peptide; microglia; striatum; cerebral ID ACETYL-ASPARTYL-GLUTAMATE; ENHANCED CARBODIIMIDE FIXATION; ACIDIC DIPEPTIDASE ACTIVITY; HUNTINGTONS-DISEASE; AMINO-ACIDS; RAT-BRAIN; ALZHEIMERS-DISEASE; PYRAMIDAL NEURONS; ACETYLASPARTATE IMMUNOREACTIVITIES; POSTMORTEM CHANGES AB The dipeptide N-acetylaspartylglutamate (NAAG) may be involved in the process of glutamatergic signaling by both acting at glutamate receptors and as a glutamate protransmitter. In the present study we determined the cellular localization and distribution of NAAG-like immunoreactivity (NAAG-LI) in normal human brain and in neurodegenerative disorders to ascertain the degree of NAAG's colocalization to putative glutamatergic pathways. Immunohistochemistry with an antibody against NAAG was performed on control, Huntington's disease (HD) and Alzheimer's disease (AD) human autopsy and biopsy brain sections from the cerebral cortex, hippocampus, amygdala, neostriatum, brainstem and spinal cord. In normal human brain, NAAG-LI was widespread localized to putative glutamatergic pyramidal neurons of the cerebral cortex and hippocampus. Punctate NAAG-LI was present in areas known to receive neuronal glutamatergic input, such as layer IV of the cerebral cortex, striatal neuropil, and the outer portion of the molecular layer of the hippocampal dentate gyrus. In the two pathologic brain regions examined, the HD neostriatum and the AD temporal cortex, we observed a widespread loss of NAAG-LI neurons. In addition NAAG-LI reactive microglia surrounding plaques were seen in AD temporal cortex but not in the HD striatum. Our results suggest that NAAG is substantially localized to putative glutamatergic pathways in human brain and that NAAG-LI neurons are vulnerable to the neurodegenerative process in HD and AD. (C) 1997 Elsevier Science B.V. C1 MASSACHUSETTS GEN HOSP,LAB MOL & DEV NEUROSCI,CHARLESTOWN,MA. MASSACHUSETTS GEN HOSP,LAB MOL NEUROPATHOL,CHARLESTOWN,MA. HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA. FU NIMH NIH HHS [MH-572901, MH/NS31862] NR 66 TC 31 Z9 32 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD OCT 24 PY 1997 VL 772 IS 1-2 BP 9 EP 22 DI 10.1016/S0006-8993(97)00784-1 PG 14 WC Neurosciences SC Neurosciences & Neurology GA YG083 UT WOS:A1997YG08300002 PM 9406950 ER PT J AU Chen, CM Xie, Y Stevenson, MA Auron, PE Calderwood, SK AF Chen, CM Xie, Y Stevenson, MA Auron, PE Calderwood, SK TI Heat shock factor 1 represses Ras-induced transcriptional activation of the c-fos gene SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SERUM RESPONSE ELEMENT; PROMOTER ELEMENTS; HSP70 GENE; EXPRESSION; PROTEIN; BINDING; PHOSPHORYLATION; ONCOGENES; CELLS; EUKARYOTES AB Heat shock factor 1, the critical molecular regulator of the stress response is conserved throughout eukaryotic organisms and activates the transcription of heat shock genes. We now show that heat shock factor 1 inhibits the expression of c-fos, an immediate early gene that controls responses to extracellular stimuli for growth and differentiation. Heat shock factor 1 inhibits the transcription of the c-fos gene and antagonizes the activating effects of the signal transducing protein Has on the c-fos promoter and on the promoter of another Has responsive gene uPA. This property was specific for heat shock factor 1; c-fos repression was not seen with the structurally related protein heat shock factor 2, Repression involved different molecular mechanisms compared with those involved in transcriptional activation by heat shock factor 1 and specifically did not require binding to the c-fos promoter. Thus, in addition to its known role as a transcriptional activator of the cellular heat shock response, heat shock factor 1 also antagonizes the expression of Fos, a key component of the ubiquitous AP-1 transcription factor complex and as such could influence multiple aspects of cell regulation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,CTR BLOOD RES,BOSTON,MA 02115. FU NCI NIH HHS [CA50642, CA31303, CA4707] NR 38 TC 64 Z9 66 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 24 PY 1997 VL 272 IS 43 BP 26803 EP 26806 DI 10.1074/jbc.272.43.26803 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YC659 UT WOS:A1997YC65900003 PM 9341107 ER PT J AU Hocker, M Henihan, RJ Rosewicz, S Riecken, EO Zhang, ZS Koh, TJ Wang, TC AF Hocker, M Henihan, RJ Rosewicz, S Riecken, EO Zhang, ZS Koh, TJ Wang, TC TI Gastrin and phorbol 12-myristate 13-acetate regulate the human histidine decarboxylase promoter through raf-dependent activation of extracellular signal-regulated kinase-related signaling pathways in gastric cancer cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE; MAP KINASE; C-JUN; IN-VIVO; HA-RAS; CHOLECYSTOKININ; RECEPTOR; PHOSPHORYLATION; EXPRESSION; TRANSFORMATION AB Gastrin stimulates transcription of the human histidine decarboxylase (HDC) gene through binding to the G-protein-coupled cholecystokinin-B/gastrin receptor. We have explored the possibility that mitogen-activated protein kinase cascades play a role in mediating the effects of gastrin on transcription in a gastric cancer (AGS-B) cell line. Gastrin and phorbol 12-myristate 13-acetate (PMA) treatment of AGS-B cells was found to increase the phosphorylation of tyrosine residues of extracellular signal-regulated kinases (ERKs) 1 and 2 and increase ERK activity as determined by the in vitro phosphorylation of myelin basic protein. Reporter gene assays also demonstrated that gastrin and PMA stimulated Elk-1- and c-Myc-dependent transactivation, consistent with gastrin and PMA-induced activation of ERKs. Overexpression of wild type ERK-1 and ERK-2 or activation of endogenous ERKs using activated MEK-1 (mitogen-activated protein kinase kinase or ERK kinase) overexpression stimulated HDC promoter activity in a dose-dependent fashion. Interruption of the ERK-related pathway using expression vectors for kinase-deficient ERKs or an ERK-specific phosphatase (PAC-1) blocked gastrin and PMA-stimulated HDC promoter activity. In contrast, inhibition of the Jun kinase pathway using an interfering dominant negative SEK-1 (stress-activated protein kinase/ERK-1) mutant did not inhibit HDC promoter activity. Furthermore, whereas gastrin stimulated phosphorylation of She proteins and association with Grb2, activation of the HDC promoter was not influenced by expression of dominant negative Ras (N15 or N17) proteins. However, gastrin stimulated Raf-1 kinase activity, and activation of the HDC promoter was blocked by coexpression of a dominant negative Raf-1 construct. Overall, these data demonstrate that gastrin regulates HDC transcription in a Raf-dependent, Ras-independent fashion predominantly through activation of the ERK-related pathway. C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NCI NIH HHS [CA67463]; NIDDK NIH HHS [DK48077] NR 43 TC 69 Z9 70 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 24 PY 1997 VL 272 IS 43 BP 27015 EP 27024 DI 10.1074/jbc.272.43.27015 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YC659 UT WOS:A1997YC65900036 PM 9341140 ER PT J AU Rosowsky, A Papoulis, AT Queener, SF AF Rosowsky, A Papoulis, AT Queener, SF TI 2,4-Diaminothieno [2,3-d]pyrimidine lipophilic antifolates as inhibitors of Pneumocystis carinii and Toxoplasma gondii dihydrofolate reductase SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; ANTITUMOR-ACTIVITY; PIRITREXIM; DAPSONE; ANALOGS; POTENT; TRIMETREXATE; COMBINATION; BRODIMOPRIM; INFECTIONS AB Ten previously unreported 2,4-diaminothieno[2,3-d]pyrimidine lipophilic dihydrofolate reductase inhibitors were synthesized as potential inhibitors of Pneumocystis carinii and Toxoplasma gondii dihydrofolate reductase. Pivaloylation of 2,4-diamino-5-methylthieno[2,3-d]pyrimidine followed by dibromination with N-bromosuccinimide in the presence of benzoyl peroxide gave 2,4-bis(pivaloylamino)-6-bromo-5-(bromomethyl)thieno[2,3-d]pyrimidine, which after condensation with substituted anilines or N-methylanilines and deprotection with base yielded 2,4-diamino-6-bromo-5-[(substituted anilino)methyl]thieno[2,3-d]pyrimidines. Removal of the B-bromo substituent was accomplished with sodium borohydride and palladium chloride. The reaction yields were generally good to excellent. The products were tested as inhibitors of dihydrofolate reductase (DHFR) from P. carinii, T. gondii, and rat liver. Although the IC50 could not be reached for the 6-unsubstituted compounds because of their extremely poor solubility, three of the five 6-bromo derivatives were soluble enough to allow the IC50 to be determined against all three enzymes. 2,4-Diamino-5-[3,5-dichloro-4-(1-pyrrolo)anilino]methyl]-6-bromothieno[2,3-d]pyrimidine was the most active of the 6-bromo derivatives, with an IC50 of 7.5 mu M against P. carinii DHFR, but showed no selectivity for either P. carinii or T. gondii DHFR relative to the enzyme from rat liver. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOL PHARMACOL,BOSTON,MA 02115. INDIANA UNIV,SCH MED,DEPT PHARMACOL & TOXICOL,INDIANAPOLIS,IN 46202. RP Rosowsky, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [N01-AI35171, R01-AI29904] NR 35 TC 37 Z9 38 U1 1 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD OCT 24 PY 1997 VL 40 IS 22 BP 3694 EP 3699 DI 10.1021/jm970399a PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA YD599 UT WOS:A1997YD59900026 PM 9357537 ER PT J AU Dieckmann, T Butcher, SE Sassanfar, M Szostak, JW Feigon, J AF Dieckmann, T Butcher, SE Sassanfar, M Szostak, JW Feigon, J TI Mutant ATP-binding RNA aptamers reveal the structural basis for ligand binding SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE NMR; RNA structure; binding constants; RNA folding; in vitro selection ID MOLECULAR RECOGNITION; NMR-SPECTROSCOPY; COMPLEX; POLYMERASE; EVOLUTION; NETWORKS; SPECTRA; FILTERS; MOTIF AB The solution structure of the ATP-binding RNA aptamer has recently been determined by NMR spectroscopy. The three-dimensional fold of the molecule is determined tio a large extent by stacking and hydrogen bond interactions. In the course of the structure determination it was discovered that several highly conserved nucleotides in the binding pocket can be substituted while retaining binding under NMR conditions. These surprising findings allow a closer look at the interactions that determine stability and specificity of the aptamer as well as local structural features of the molecule. The binding properties of ATP binder mutants and modified ligand molecules are explored using NMR spectroscopy, column binding studies and molecular modeling. We present additional evidence and new insights regarding the network of hydrogen bonds that defines the structure and determines stability and specificity of the aptamer. (C) 1997 Academic Press Limited. C1 UNIV CALIF LOS ANGELES,DEPT CHEM & BIOCHEM,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,INST MOL BIOL,LOS ANGELES,CA 90095. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOL BIOL,BOSTON,MA 02114. RI Dieckmann, Thorsten/F-1949-2010 FU NIGMS NIH HHS [GM37254] NR 29 TC 31 Z9 32 U1 1 U2 8 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD OCT 24 PY 1997 VL 273 IS 2 BP 467 EP 478 DI 10.1006/jmbi.1997.1329 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YD510 UT WOS:A1997YD51000009 PM 9344753 ER PT J AU Sager, PT AF Sager, PT TI Atrial fibrillation: Antiarrhythmic therapy versus rate control with antithrombotic therapy SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Changing Trends in Antiarrhythmic Therapy - Worldwide Experience with Class III Agents CY NOV 10-10, 1996 CL NEW ORLEANS, LA SP UCLA Sch Med, Berlex Lab ID RADIOFREQUENCY CATHETER MODIFICATION; RAPID VENTRICULAR RESPONSE; RANDOMIZED CONTROL TRIALS; ADVANCED HEART-FAILURE; SINUS RHYTHM; DOUBLE-BLIND; SUPRAVENTRICULAR ARRHYTHMIAS; ELECTRICAL CARDIOVERSION; ATRIOVENTRICULAR NODE; MECHANICAL FUNCTION AB Atrial fibrillation is a major health problem in the United States, but the best strategies for treating it have not been rigorously determined in clinical studies. Specifically, there is a paucity of data comparing the approach of maintaining sinus rhythm using prophylactic antiarrhythmic drug therapy with the approach of controlling the ventricular response to atrial fibrillation while reducing embolic events with concomitant antithrombotic therapy. Until ongoing randomized trials are completed, which patients benefit most from a specific approach cannot be determined with certainty. In general, the most reasonable strategies include (1) the restoration of sinus rhythm (without prophylactic antiarrhythmic therapy) after the patient's first episode of atrial fibrillation; and (2) the maintenance of sinus rhythm (including the use of prophylactic antiarrhythmic therapy) in patients who remain symptomatic despite adequate rate control, and who are not at high risk for proarrhythmia and/or are unlikely to maintain sinus rhythm. The risks and benefits need to be carefully weighed in patients with truly asymptomatic atrial fibrillation. Many patients may require multiple attempts to maintain sinus rhythm. Current investigative treatment modalities (e.g., ablation techniques, atrial implantable cardioverter-defibrillators, new antiarrhythmic agents) are likely to alter the current approaches to atrial fibrillation. (C) 1997 by Excerpta Medica, Inc. C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90024 USA. RP Sager, PT (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, DIV CARDIOL, WILSHIRE & SAWTELLE BLVD, LOS ANGELES, CA 90073 USA. NR 85 TC 4 Z9 5 U1 0 U2 0 PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC PI BRIDGEWATER PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA SN 0002-9149 EI 1879-1913 J9 AM J CARDIOL JI Am. J. Cardiol. PD OCT 23 PY 1997 VL 80 SI 8A BP G74 EP G81 DI 10.1016/S0002-9149(97)00716-9 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YC886 UT WOS:A1997YC88600009 PM 9354414 ER PT J AU Singh, BN Breithardt, G AF Singh, BN Breithardt, G TI Changing trends in antiarrhythmic therapy: Worldwide experience with class III agents - Introduction SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Editorial Material C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. RP Singh, BN (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DIV CARDIOL 111E,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD OCT 23 PY 1997 VL 80 SI 8A BP G1 EP G3 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YC886 UT WOS:A1997YC88600001 PM 9354406 ER PT J AU Singh, BN AF Singh, BN TI Controlling cardiac arrhythmias: An overview with a historical perspective SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Changing Trends in Antiarrhythmic Therapy - Worldwide Experience with Class III Agents CY NOV 10, 1996 CL NEW ORLEANS, LA SP UCLA Sch Med, Berlex Lab ID CONGESTIVE-HEART-FAILURE; ACUTE MYOCARDIAL-INFARCTION; ANTIARRHYTHMIC DRUGS; VENTRICULAR TACHYARRHYTHMIAS; DOUBLE-BLIND; INTRAVENOUS AMIODARONE; SINUS RHYTHM; SUDDEN-DEATH; SOTALOL; ATRIAL AB During the past decade, several developments in our knowledge of antiarrhythmic drugs have had a major influence on our approach to their use. These developments may be summarized as follows: (1) it has become clear that arrhythmias merit treatment only for the relief of symptoms, with improved quality of life, and for prolongation of survival by reducing arrhythmic deaths; (2) suppression of arrhythmias-symptomatic or asymptomatic-may not necessarily decrease mortality, the net impact on mortality being agent-specific; (3) antiarrhythmic drugs have the propensity to decrease as well as to increase cardiac arrhythmias (producing proarrhythmias); (4) the most important determinant of arrhythmia mortality is the degree and nature of ventricular dysfunction; and (5) only controlled trials have the potential to establish the effect of treatment on mortality in patients with cardiac arrhythmias. To these considerations must be added the advances in nonpharmacologic approaches to controlling cardiac arrhythmias. These include catheter ablation of cardiac arrhythmias, certain surgical techniques that in selected patients offer prospects of cure, and the development of implantable ventricular and atrial cardioverter defibrillators, which allow rite evaluation of drugs versus placebo against the background of the defibrillator. This is particularly germane in the case of life-threatening symptomatic ventricular arrhythmias such as sustained ventricular tachycardia and ventricular fibrillation. Antiarrhythmic drugs and implantable devices in the control of arrhythmias cannot be considered in isolation. Their role in mortality reduction needs to be defined alone as well as in combination by controlled clinical trials. (C) 1997 by Excerpta Medica, Inc. C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. RP Singh, BN (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DIV CARDIOL 111E,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 78 TC 11 Z9 11 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD OCT 23 PY 1997 VL 80 SI 8A BP G4 EP G15 DI 10.1016/S0002-9149(97)00709-1 PG 12 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YC886 UT WOS:A1997YC88600002 PM 9354407 ER PT J AU Wain, JC Boiselle, PM Mark, EJ AF Wain, JC Boiselle, PM Mark, EJ TI A 75-year-old man with chest pain, hemoptysis, and a pulmonary lesion - Inhalation of a sprig (arborvitae), causing purulent bronchiectasis and chronic organizing pneumonia SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID FLEXIBLE FIBEROPTIC BRONCHOSCOPY; NEEDLE ASPIRATION; LUNG LESIONS; SOLITARY; NODULE; THORACOSCOPY; DIAGNOSIS; BIOPSY C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. RP Wain, JC (reprint author), MASSACHUSETTS GEN HOSP,LUNG TRANSPLANT SERV,BOSTON,MA 02114, USA. NR 29 TC 8 Z9 8 U1 1 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 23 PY 1997 VL 337 IS 17 BP 1220 EP 1226 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA YB718 UT WOS:A1997YB71800008 ER PT J AU Farrer, LA Cupples, LA Haines, JL Hyman, B Kukull, WA Mayeux, R Myers, RH PericakVance, MA Risch, N vanDuijn, CM AF Farrer, LA Cupples, LA Haines, JL Hyman, B Kukull, WA Mayeux, R Myers, RH PericakVance, MA Risch, N vanDuijn, CM TI Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease - A meta-analysis SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID E ALLELE EPSILON-4; EARLY-ONSET ALZHEIMERS; LEWY BODY DISEASE; VASCULAR DEMENTIA; E POLYMORPHISM; RISK FACTOR; JAPANESE PATIENTS; PREDICTIVE VALUE; SENILE DEMENTIA; TYPE-4 ALLELE AB Objective.-To examine more closely the association between apolipoprotein E (APOE) genotype and Alzheimer disease (AD) by age and sex in populations of various ethnic and racial denominations. Data Sources.-Forty research teams contributed data on APOE genotype, sex, age at disease onset, and ethnic background for 5930 patients who met criteria for probable or definite AD and 8607 controls without dementia who were recruited from clinical, community, and brain bank sources. Main Outcome Measures.-Odds ratios (ORs) and 95% confidence intervals (CIs) for AD, adjusted for age and study and stratified by major ethnic group (Caucasian, African American, Hispanic, and Japanese) and source, were computed for APOE genotypes epsilon 2/epsilon 2, epsilon 2/epsilon 3, epsilon 2/epsilon 4, epsilon 3/epsilon 4, and epsilon 4/epsilon 4 relative to the epsilon 3/epsilon 3 group. The influence of age and sex on the OR for each genotype was assessed using logistic regression procedures. Results.-Among Caucasian subjects from clinic-or autopsy-based studies, the risk of AD was significantly increased for people with genotypes epsilon 2/epsilon 4 (OR=2.6, 95% CI=1.6-4.0), epsilon 3/epsilon 4 (OR=3.2, 95% Cl=2.8-3.8), and epsilon 4/epsilon 4 (OR=14.9, 95% CI=10.8-20.6); whereas, the ORs were decreased for people with genotypes epsilon 2/epsilon 2 (OR=0.6, 95% CI=0.2-2.0) and epsilon 2/epsilon 3 (OR=0.6, 95% CI=0.5-0.8). The APOE epsilon 4-AD association was weaker among African Americans and Hispanics, but there was significant heterogeneity in ORs among studies of African Americans (P<.03), The APOE epsilon 4-AD association in Japanese subjects was stronger than in Caucasian subjects (epsilon 3/epsilon 4: OR=5.6, 95% CI=3.9-8.0; epsilon 4/epsilon 4, OR=33.1, 95% CI=13.6-80.5). The epsilon 2/epsilon 3 genotype appears equally protective across ethnic groups. We also found that among Caucasians, APOE genotype distributions are similar in groups of patients with AD whose diagnoses were determined clinically or by autopsy. In addition, we found that the APOE epsilon 4 effect is evident at all ages between 40 and 90 years but diminishes after age 70 years and that the risk of AD associated with a given genotype varies with sex. Conclusions.-The APOE epsilon 4 allele represents a major risk factor for AD in all ethnic groups studied, across all ages between 40 and 90 years, and in both men and women, The association between APOE epsilon 4 and AD in African Americans requires clarification, and the attenuated effect of APOE epsilon 4 in Hispanics should be investigated further. C1 BOSTON UNIV,SCH MED,DEPT BIOSTAT & EPIDEMIOL,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,MOL NEUROGENET UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195. COLUMBIA UNIV,GERTRUDE H SERGIEVSKY CTR,NEW YORK,NY 10027. COLUMBIA UNIV,DEPT NEUROL,NEW YORK,NY. DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710. STANFORD UNIV,SCH MED,DEPT GENET,STANFORD,CA 94305. ERASMUS UNIV ROTTERDAM,DEPT EPIDEMIOL,ROTTERDAM,NETHERLANDS. RP Farrer, LA (reprint author), BOSTON UNIV,SCH MED,DEPT NEUROL,80 E CONCORD ST,BOSTON,MA 02118, USA. RI Haines, Jonathan/C-3374-2012; OI Kukull, Walter/0000-0001-8761-9014; Farrer, Lindsay/0000-0001-5533-4225 FU NIA NIH HHS [AG-09029, U24 AG021886]; Telethon [E.0482] NR 85 TC 1815 Z9 1868 U1 17 U2 150 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 22 PY 1997 VL 278 IS 16 BP 1349 EP 1356 DI 10.1001/jama.278.16.1349 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA YA905 UT WOS:A1997YA90500037 PM 9343467 ER PT J AU Hanson, RN Choi, SW Elmaleh, DR Fischman, AJ AF Hanson, RN Choi, SW Elmaleh, DR Fischman, AJ TI Synthesis and evaluation of novel-N-2-(bis-arylmethoxy)ethyl-N'-aralkyl-alpha,omega-alkanediamines as potent and selective dopamine reuptake inhibitors: Seco analogs of GBR12935 and GBR12909 SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID TRANSPORTERS AB A series of analogs of the N-L[2-bis arylmethoxy]-N'-phenylpropyl-piperazines GBR12909 and 12935 was synthesized and evaluated as inhibitors of synaptic monoamine transporters. The data indicated that all of the new compounds demonstrated a selectivity for the dopamine transporter compared to the other monoamine transporters with IC50 values approaching 10 nM. The results suggest that the internal piperazine moiety is not required for activity and may be replaced with a more flexible diamine unit. (C) 1997 Elsevier Science Ltd. C1 MASSACHUSETTS GEN HOSP,DIV NUCL MED,DEPT RADIOPHARMACEUT CHEM,BOSTON,MA 02114. RP Hanson, RN (reprint author), NORTHEASTERN UNIV,BOUVE COLL PHARM & HLTH SCI,DEPT PHARMACEUT SCI,BOSTON,MA 02115, USA. NR 16 TC 8 Z9 8 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD OCT 21 PY 1997 VL 7 IS 20 BP 2559 EP 2564 DI 10.1016/S0960-894X(97)10053-1 PG 6 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA YF105 UT WOS:A1997YF10500001 ER PT J AU LItalien, GJ Paul, SD Cambria, RP Hendel, RC Leppo, JA Fleisher, LA Brown, KA Cohen, MC Eagle, KA AF LItalien, GJ Paul, SD Cambria, RP Hendel, RC Leppo, JA Fleisher, LA Brown, KA Cohen, MC Eagle, KA TI Longterm cardiac event free survival in patients undergoing carotid endarterectomy, aortic surgery, and peripheral surgery: Is there a difference? SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NORTHEASTERN UNIV,BOSTON,MA 02115. UNIV VERMONT,BURLINGTON,VT. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. UNIV MICHIGAN,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 63 EP 63 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000063 ER PT J AU Otsuji, Y Handschumacher, MD LielCohen, N Tanabe, H Jiang, L Schwammenthal, E Guerrero, JL Nicholls, LA Viahakes, GJ Levine, RA AF Otsuji, Y Handschumacher, MD LielCohen, N Tanabe, H Jiang, L Schwammenthal, E Guerrero, JL Nicholls, LA Viahakes, GJ Levine, RA TI Mechanism of functional ischemic mitral regurgitation: In vivo validation of the leaflet tethering hypothesis by three dimensional echocardiography SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV NEBRASKA,MED CTR,OMAHA,NE. CHAIM SHEBA MED CTR,IL-52621 TEL HASHOMER,ISRAEL. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 172 EP 172 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000172 ER PT J AU Harrington, EO Pearlman, JD Doyle, KE Ware, JA AF Harrington, EO Pearlman, JD Doyle, KE Ware, JA TI Conditional expression of PKC pseudosubstrate peptides in intact endothelial cells alters their growth and formation in capillaries SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BIDMC,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 243 EP 243 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000243 ER PT J AU Fagan, KA Sato, K Tyler, RC Morris, KG Huang, PL McMurtry, IF Rodman, DM AF Fagan, KA Sato, K Tyler, RC Morris, KG Huang, PL McMurtry, IF Rodman, DM TI Endothelial nitric oxide synthase (eNOS) knock-out mice develop pulmonary hypertension. SO CIRCULATION LA English DT Meeting Abstract C1 UNIV COLORADO,DENVER,CO 80202. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 334 EP 334 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000333 ER PT J AU Yamada, K Choo, JK Erhorn, AE Allan, JS Slisz, JK Sachs, DH Madsen, JC AF Yamada, K Choo, JK Erhorn, AE Allan, JS Slisz, JK Sachs, DH Madsen, JC TI Mechanisms of tolerance induction and prevention of cardiac allograft vasculopathy (CAV) in heart/kidney recipients. SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 354 EP 354 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000353 ER PT J AU Stafford, RS Singer, DE AF Stafford, RS Singer, DE TI Rate control and sinus rhythm maintenance in atrial fibrillation: National trends in medication use, 1980-94 SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 420 EP 420 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000424 ER PT J AU Larsen, GC McAnulty, JH Hallstrom, A Marchant, C Shein, M Akiyama, T Brodsky, M Baessler, C Pinski, SL Jennings, CA Morris, M AF Larsen, GC McAnulty, JH Hallstrom, A Marchant, C Shein, M Akiyama, T Brodsky, M Baessler, C Pinski, SL Jennings, CA Morris, M TI Hospitalization charges in the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial: The AVID economic analysis study SO CIRCULATION LA English DT Meeting Abstract C1 PORTLAND VA MED CTR,PORTLAND,OR. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. UNIV WASHINGTON,SEATTLE,WA 98195. US FDA,ROCKVILLE,MD 20857. UNIV ROCHESTER,ROCHESTER,NY. UNIV CALIF,ORANGE,CA. MED COLL PENN & HAHNEMANN UNIV,LIKOFF INST,PHILADELPHIA,PA. CLEVELAND CLIN FDN,CLEVELAND,OH 44195. NATL INST HLTH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 424 EP 424 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000423 ER PT J AU Wilkoff, BL Shih, HT Friedman, PL Page, RL Klein, RC Dalamagas, H Nora, M Larsen, GC Baessler, C Morris, M Jennings, C AF Wilkoff, BL Shih, HT Friedman, PL Page, RL Klein, RC Dalamagas, H Nora, M Larsen, GC Baessler, C Morris, M Jennings, C TI Multivariate predictors of hospital length of stay in patients with severe ventricular arrhythmias: Antiarrhythmics versus implantable defibrillators registry study SO CIRCULATION LA English DT Meeting Abstract C1 CLEVELAND CLIN FDN,CLEVELAND,OH 44195. UNIV TEXAS,HOUSTON,TX. HARVARD UNIV,BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. UNIV TEXAS,DALLAS,TX 75230. UNIV UTAH,SALT LAKE CITY,UT. ST FRANCIS HOSP & MED CTR,HARTFORD,OH. MIDWEST HEART SPECIALISTS,LOMBARD,IL. PORTLAND VA MED CTR,PORTLAND,OR. MED COLL PENN & HAHNEMANN UNIV,LIKOFF INST,PHILADELPHIA,PA. UNIV WASHINGTON,SEATTLE,WA 98195. NHLBI,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 425 EP 425 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000430 ER PT J AU Lehmann, KG Brown, BG Melkert, R AF Lehmann, KG Brown, BG Melkert, R TI Occult luminal narrowing in coronary artery disease: Severity, predictors, and impact on interventions SO CIRCULATION LA English DT Meeting Abstract C1 VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. UNIV WASHINGTON,SEATTLE,WA 98195. CARDIALYSIS,ROTTERDAM,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 429 EP 429 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000428 ER PT J AU Otsuji, Y Guerrero, JL LielCohen, N Sullivan, S Schwammenthal, E Jiang, L Viahakes, GJ Handschumacher, MD AF Otsuji, Y Guerrero, JL LielCohen, N Sullivan, S Schwammenthal, E Jiang, L Viahakes, GJ Handschumacher, MD TI Mechanistic insights from three-dimensional echocardiography for functional mitral regurgitation: Direct in vivo demonstration of increased demand for leaflet area to cover the mitral annulus SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CHAIM SHEBA MED CTR,IL-52621 TEL HASHOMER,ISRAEL. UNIV NEBRASKA,MED CTR,OMAHA,NE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 452 EP 452 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000451 ER PT J AU Hung, J Otsuji, Y Handschumacher, MD Schwammenthal, E Levine, RA AF Hung, J Otsuji, Y Handschumacher, MD Schwammenthal, E Levine, RA TI Mechanism of dynamic regurgitant orifice area variation in functional mitral regurgitation: Physiologic insights from the proximal flow convergence technique SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CHAIM SHEBA MED CTR,IL-52621 TEL HASHOMER,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 454 EP 454 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000453 ER PT J AU Siegel, AJ Lewandrowski, K AF Siegel, AJ Lewandrowski, K TI Positive rapid assays for cardiac markers including troponin I in asymptomatic marathon runners after competition SO CIRCULATION LA English DT Meeting Abstract C1 MCLEAN HOSP,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 468 EP 468 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000467 ER PT J AU Ellis, SG Serruys, PW Popma, JJ Teirstein, PS Ricci, DR Gold, HK Effron, MB AF Ellis, SG Serruys, PW Popma, JJ Teirstein, PS Ricci, DR Gold, HK Effron, MB TI Can abciximab prevent neointimal proliferation in Palmaz-Schatz stents? The final ERASER results SO CIRCULATION LA English DT Meeting Abstract C1 CLEVELAND CLIN FDN,CLEVELAND,OH 44195. ERASMUS UNIV ROTTERDAM,ROTTERDAM,NETHERLANDS. WASHINGTON HOSP,WASHINGTON,DC. SCRIPPS CLIN,LA JOLLA,CA 92037. VANCOUVER HOSP,VANCOUVER,BC,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ELI LILLY & CO,INDIANAPOLIS,IN 46285. RI Effron, Mark/P-9300-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 476 EP 476 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000475 ER PT J AU Wong, H Yang, D Nikazy, J Hill, JS Schotz, MC AF Wong, H Yang, D Nikazy, J Hill, JS Schotz, MC TI Lipoprotein lipase subunit orientation and domain interaction during lipolysis SO CIRCULATION LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 609 EP 609 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000596 ER PT J AU Kharbanda, S Arbustini, E Kolodgie, FD Khaw, BA Semigran, MJ Dec, GW Kufe, DW Narula, J AF Kharbanda, S Arbustini, E Kolodgie, FD Khaw, BA Semigran, MJ Dec, GW Kufe, DW Narula, J TI Release of cytochrome c from mitochondria, activation of caspases and apoptosis in explanted cardiomyopathic hearts from cardiac allograft recipients SO CIRCULATION LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. INST PATHOL ANAT,PAVIA,ITALY. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NORTHEASTERN UNIV,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 647 EP 647 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000634 ER PT J AU Matsui, T Hajjar, RJ Kang, JX Rosenzweig, A AF Matsui, T Hajjar, RJ Kang, JX Rosenzweig, A TI Pl 3-kinase prevents post ischemic cardiocyte apoptosis in vitro SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 653 EP 653 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000647 ER PT J AU Chlumsky, LJ KolibalPegher, SS Brady, CA Cohen, SA AF Chlumsky, LJ KolibalPegher, SS Brady, CA Cohen, SA TI Sodium channel subtype steady state mRNA levels may not predict functional protein expression SO CIRCULATION LA English DT Meeting Abstract C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 675 EP 675 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000662 ER PT J AU Otsuji, Y Nathan, N Handschumacher, MD Coulter, S LielCohen, N DAmbra, M Vlahakes, GJ Akins, CW Levine, RA AF Otsuji, Y Nathan, N Handschumacher, MD Coulter, S LielCohen, N DAmbra, M Vlahakes, GJ Akins, CW Levine, RA TI Mechanism of ischemic mitral regurgitation: Intraoperative evaluation of leaflet tethering geometry by three-dimensional echocardiography SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 869 EP 869 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000865 ER PT J AU Philbin, EF Jenkins, PL Nichols, M DiSalvo, TG AF Philbin, EF Jenkins, PL Nichols, M DiSalvo, TG TI Influence of race and gender on hospital process of care and outcomes in heart failure SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BASSETT HEALTHCARE,COOPERSTOWN,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 881 EP 881 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000879 ER PT J AU Haupert, GT Titus, J Wang, Y Gallagher, RT Torchiana, DF AF Haupert, GT Titus, J Wang, Y Gallagher, RT Torchiana, DF TI Na,K-ATPase inhibitor from bovine hypothalamus has an equivalent inotropic effect to ouabain in isolated perfused guinea pig hearts SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BION INC,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 890 EP 890 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000893 ER PT J AU Han, XQ Opel, DJ Huang, PL Fishman, MC Kelly, RA AF Han, XQ Opel, DJ Huang, PL Fishman, MC Kelly, RA TI Targeted disruption of eNOS impairs muscarinic cholinergic regulation of ICa-L in murine ventricular myocytes SO CIRCULATION LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 940 EP 940 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000934 ER PT J AU Moroi, M Garabedian, HD Moons, L Carmeliet, P Collen, D Gold, HK AF Moroi, M Garabedian, HD Moons, L Carmeliet, P Collen, D Gold, HK TI Effects of disruption of genes encoding the plasminogen/plasmin system on vascular neointimal formation in mice SO CIRCULATION LA English DT Meeting Abstract C1 TOHO UNIV,OHASHI HOSP,TOKYO 153,JAPAN. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CTR TRANSGENE TECHNOL & GENE THERAPY,LOUVAIN,BELGIUM. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 947 EP 947 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88000941 ER PT J AU Stuart, EM Welty, FK Huddleston, JS Ennis, MF Goyer, L OMeara, MC Zuttermeister, PC Resurreccion, LAC Friedman, R AF Stuart, EM Welty, FK Huddleston, JS Ennis, MF Goyer, L OMeara, MC Zuttermeister, PC Resurreccion, LAC Friedman, R TI An integrated multiple risk reduction program: Psychosocial and behavioral outcomes SO CIRCULATION LA English DT Meeting Abstract C1 BIDMC,MIND BODY MED INST,BOSTON,MA. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1058 EP 1058 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001056 ER PT J AU Rankin, SH Carroll, DL Arnstein, P Robinson, E Buselli, EF Capasso, V Castle, J Simon, M Berry, D Currier, E AF Rankin, SH Carroll, DL Arnstein, P Robinson, E Buselli, EF Capasso, V Castle, J Simon, M Berry, D Currier, E TI Change in health outcomes after myocardial infarction: The influence of age and gender in unpartnered elders SO CIRCULATION LA English DT Meeting Abstract C1 BOSTON COLL,CHESTNUT HILL,MA 02167. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MIND BODY MED INSTE,BIDMC,BOSTON,MA. NORTHEASTERN UNIV,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1059 EP 1059 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001057 ER PT J AU Tseng, WYI Reese, TG Weisskoff, RM Brady, TJ Dinsmore, RE Wedeen, VJ AF Tseng, WYI Reese, TG Weisskoff, RM Brady, TJ Dinsmore, RE Wedeen, VJ TI Mapping myocardial fiber and sheet function in humans by magnetic resonance imaging (MRI) SO CIRCULATION LA English DT Meeting Abstract C1 MIT,CAMBRIDGE,MA 02139. MGH NMR CTR,CAMBRIDGE,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1096 EP 1096 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001094 ER PT J AU Quinn, DA Fogel, RB Smith, CD Laposata, M Thompson, BT Johnson, SM Waltman, AC Hales, CA AF Quinn, DA Fogel, RB Smith, CD Laposata, M Thompson, BT Johnson, SM Waltman, AC Hales, CA TI Latex agglutination assay for D-dimers in the diagnosis of pulmonary embolism SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1330 EP 1330 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001338 ER PT J AU Fischman, DL Savage, MP Penn, IM Rehmann, DE Dempsey, CM Goldberg, S AF Fischman, DL Savage, MP Penn, IM Rehmann, DE Dempsey, CM Goldberg, S TI Have current stenting techniques improved the long term outcome of coronary stents in smaller vessels? SO CIRCULATION LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. UNIV BRITISH COLUMBIA,VANCOUVER,BC V5Z 1M9,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1523 EP 1523 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001521 ER PT J AU Madsen, JC Yamada, K Allan, JS Choo, JK Erhorn, AE Pins, MR Vesga, L Slisz, JK Sachs, DH AF Madsen, JC Yamada, K Allan, JS Choo, JK Erhorn, AE Pins, MR Vesga, L Slisz, JK Sachs, DH TI Prevention of cardiac allograft vasculopathy across class I MHC disparities by the induction of transplantation tolerance SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NORTHWESTERN UNIV,CHICAGO,IL 60611. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1671 EP 1671 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001665 ER PT J AU Koelling, TM Poncelet, BP Schmidt, CJ Kwong, KK Reese, TG Brady, TJ Kantor, HL Weisskoff, RM AF Koelling, TM Poncelet, BP Schmidt, CJ Kwong, KK Reese, TG Brady, TJ Kantor, HL Weisskoff, RM TI Oxygen-sensitive magnetic resonance imaging: Assessment of myocardial perfusion reserve in swine SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1698 EP 1698 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001691 ER PT J AU Mahdi, NA Lopez, JC Leon, MN Pathan, A Harrell, LC Palacios, IF AF Mahdi, NA Lopez, JC Leon, MN Pathan, A Harrell, LC Palacios, IF TI Primary stenting in acute myocardial infarction: A comparison with primary PTCA with stent bailout SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1825 EP 1825 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001816 ER PT J AU Jang, IK AF Jang, IK TI A randomized study of argatroban vs heparin as adjunctive therapy to tissue plasminogen activator in acute myocardial infarction: MINT (Myocardial Infarction with Novastan and TPA) study SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1845 EP 1845 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001841 ER PT J AU LloydJones, DM Camargo, CA Giugliano, RP Walsh, CR Lager, RA ODonnell, CJ AF LloydJones, DM Camargo, CA Giugliano, RP Walsh, CR Lager, RA ODonnell, CJ TI Clinical characteristics and prognosis of patients with normal creatine kinase but elevated MB isoenzyme fraction SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. RI Lloyd-Jones, Donald/C-5899-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1855 EP 1855 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001852 ER PT J AU Halperin, BD Brodsky, MA Lancaster, S Raitt, M Kron, J Akiyama, T Englestein, ED Jodanath, R Mitchell, LB Daubert, JP AF Halperin, BD Brodsky, MA Lancaster, S Raitt, M Kron, J Akiyama, T Englestein, ED Jodanath, R Mitchell, LB Daubert, JP TI Prognostic value of baseline electrophysiology studies - The Antiarrhythmics Versus Implantable Defibrillators (AVID) Trial SO CIRCULATION LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. UNIV CALIF,ORANGE,CA. AVID COORDINATING CTR,SEATTLE,WA. PORTLAND VA MED CTR,PORTLAND,OR. UNIV ROCHESTER,ROCHESTER,NY. KRANNERT INST,INDIANAPOLIS,IN. N SHORE UNIV HOSP,CORNELL UNIV MED COLL,DIV BIOSTAT,MANHASSET,NY 11030. FOOTHILLS PROV GEN HOSP,CALGARY,AB T2N 2T9,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1865 EP 1865 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001856 ER PT J AU OMeara, MC Zuttermeister, PC Casey, A Huddleston, JS Buselli, EF Moran, MD Friedman, R Baltos, P Stuart, EM AF OMeara, MC Zuttermeister, PC Casey, A Huddleston, JS Buselli, EF Moran, MD Friedman, R Baltos, P Stuart, EM TI Gender-specific lipid changes with weight loss SO CIRCULATION LA English DT Meeting Abstract C1 MIND BODY MED INST,BIDMC,BOSTON,MA. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1955 EP 1955 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001946 ER PT J AU Stuart, EM OMeara, MC Huddleston, JS Ennis, MF Zuttermeister, PC Resurreccion, LAC Friedman, R Welty, FK AF Stuart, EM OMeara, MC Huddleston, JS Ennis, MF Zuttermeister, PC Resurreccion, LAC Friedman, R Welty, FK TI An integrated approach to multiple risk reduction: Comparison of outcomes from ''Heart and Sole'' and the Ornish Intensive Lifestyle Management Programs SO CIRCULATION LA English DT Meeting Abstract C1 MIND BODY MED INST,BIDMC,BOSTON,MA. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1956 EP 1956 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001947 ER PT J AU Yoshida, M Szente, BE Kiely, JM Rosenzweig, A Gimbrone, MA AF Yoshida, M Szente, BE Kiely, JM Rosenzweig, A Gimbrone, MA TI Phosphorylation of the cytoplasmic domain of E-selectin is regulated during leukocyte adhesion SO CIRCULATION LA English DT Meeting Abstract C1 TOKYO MED & DENT UNIV,TOKYO 113,JAPAN. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 1987 EP 1987 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88001978 ER PT J AU Willmore, TM Gallahue, F Cramner, H Linder, J Ladenson, JH Lewis, L Jaffe, AS AF Willmore, TM Gallahue, F Cramner, H Linder, J Ladenson, JH Lewis, L Jaffe, AS TI Influence of cardiac troponin I in emergency department patients SO CIRCULATION LA English DT Meeting Abstract C1 WASHINGTON UNIV,ST LOUIS,MO. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. WASHINGTON UNIV,ST LOUIS,MO. SUNY SYRACUSE,SYRACUSE,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2033 EP 2033 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002024 ER PT J AU Hylek, EM Skates, SJ Heiman, H Sheehan, MA Singer, DE AF Hylek, EM Skates, SJ Heiman, H Sheehan, MA Singer, DE TI Risk factors for excessive anticoagulation among outpatients taking warfarin SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2103 EP 2103 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002094 ER PT J AU Hashimoto, A Fischman, AJ Moroi, M Gold, HK Yasuda, T AF Hashimoto, A Fischman, AJ Moroi, M Gold, HK Yasuda, T TI Dual energy SPECT with Fluorine-18-deoxyglucose and Technethium-99m-Sestamibi for the detection of transiently depressed cardiac function after acute myocardial infarction SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2107 EP 2107 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002098 ER PT J AU Gallik, DM Meissner, MD Communale, M Singer, I Hanin, L AF Gallik, DM Meissner, MD Communale, M Singer, I Hanin, L TI Favorable hemodynamic effects of Amio-Aqueous(R), a new formulation of intravenous amiodarone SO CIRCULATION LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. WAYNE STATE UNIV,HARPER HOSP,DETROIT,MI. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. UNIV LOUISVILLE HOSP,LOUISVILLE,KY. ACAD PHARMACEUT,CHICAGO,IL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2147 EP 2147 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002138 ER PT J AU Hashimoto, A Abraham, SA Fischman, AJ Force, TL Palmer, EL Rabito, CA Scott, JA Zervos, GD Yasuda, T AF Hashimoto, A Abraham, SA Fischman, AJ Force, TL Palmer, EL Rabito, CA Scott, JA Zervos, GD Yasuda, T TI Reliability of stress ECG finding in patients who achieved an extraordinary level of exercise SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2174 EP 2174 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002164 ER PT J AU Pathan, A Lopez, JC Leon, MN Mahdi, NA Simosa, H McMellon, C Palacios, IF AF Pathan, A Lopez, JC Leon, MN Mahdi, NA Simosa, H McMellon, C Palacios, IF TI Is redo valvuloplasty a good option for patients with restenosis after percutaneous mitral valvuloplasty? SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2222 EP 2222 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002212 ER PT J AU Leon, MN Pathan, A Lopez, JC Mahdi, NA Simosa, H Palacios, IF AF Leon, MN Pathan, A Lopez, JC Mahdi, NA Simosa, H Palacios, IF TI Immediate outcome of Inoue vs double balloon percutaneous mitral valvotomy: The Massachusetts General Hospital experience. SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2224 EP 2224 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002214 ER PT J AU LopezCuellar, JC Leon, MN Pathan, A Mahdi, NA Simosa, H McMellon, C Harrell, LC Palacios, IF AF LopezCuellar, JC Leon, MN Pathan, A Mahdi, NA Simosa, H McMellon, C Harrell, LC Palacios, IF TI Ten year follow-up of optimal candidates for percutaneous mitral balloon valvuloplasty SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2225 EP 2225 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002215 ER PT J AU Paul, SD Lambrew, CT Barron, HV Hilbe, J Rogers, WJ Fifer, MA AF Paul, SD Lambrew, CT Barron, HV Hilbe, J Rogers, WJ Fifer, MA TI Development and validation of a clinical index for mortality after acute myocardial infarction in a cohort of 44,826 diabetics: Ischemic chest pain predicts low risk SO CIRCULATION LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. UNIV VERMONT,BURLINGTON,VT 05405. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. UNIV ARIZONA,TUCSON,AZ 85721. UNIV ALABAMA,BIRMINGHAM,AL. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2270 EP 2270 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002259 ER PT J AU Strain, JE Fischman, DL Savage, MP Rehmann, DE Ellis, SG Penn, IM Goldberg, S Moses, JW AF Strain, JE Fischman, DL Savage, MP Rehmann, DE Ellis, SG Penn, IM Goldberg, S Moses, JW TI More restenosis with IVUS-guided stenting: STRESS III IVUS substudy results SO CIRCULATION LA English DT Meeting Abstract C1 LENOX HILL HOSP,NEW YORK,NY 10021. THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107. CLEVELAND CLIN FDN,CLEVELAND,OH 44195. UNIV BRITISH COLUMBIA,VANCOUVER,BC V5Z 1M9,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2287 EP 2287 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002275 ER PT J AU Shworak, NW Liu, J Fritze, LMS Schwartz, JJ Zhang, LJ Rosenberg, RD AF Shworak, NW Liu, J Fritze, LMS Schwartz, JJ Zhang, LJ Rosenberg, RD TI Control of the synthesis of anticoagulant heparan sulfate: Molecular cloning and expression of the rate limiting enzyme, 3-O-sulfotransferase SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BIDMC,BOSTON,MA. MIT,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2300 EP 2300 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002288 ER PT J AU London, B Wang, DW Hill, JA Bennett, PB Fishman, MC AF London, B Wang, DW Hill, JA Bennett, PB Fishman, MC TI The transient outward current (I-to) in targeted mice lacking Kv1.4 SO CIRCULATION LA English DT Meeting Abstract C1 UNIV PITTSBURGH,PITTSBURGH,PA. VANDERBILT UNIV,NASHVILLE,TN. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2355 EP 2355 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002343 ER PT J AU Lipshultz, SE Lipsitz, SR Sallan, SE Mone, SM Gelber, RD Cohen, SD AF Lipshultz, SE Lipsitz, SR Sallan, SE Mone, SM Gelber, RD Cohen, SD TI Is enalapril beneficial in doxorubicin-treated long-term survivors of childhood cancer? SO CIRCULATION LA English DT Meeting Abstract C1 UNIV ROCHESTER,ROCHESTER,NY. DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2438 EP 2438 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002425 ER PT J AU Mathier, MA Conner, DA Vatner, DE Asai, K Shannon, RP Vatner, SF Seidman, CE Seidman, JG AF Mathier, MA Conner, DA Vatner, DE Asai, K Shannon, RP Vatner, SF Seidman, CE Seidman, JG TI Enhanced left ventricular contractile responses to acute beta-adrenergic stimulation in a beta-arrestin-1 knockout mouse SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. ALLEGHENY UNIV HLTH SCI,PITTSBURGH,PA. ALLEGHENY GEN HOSP,PITTSBURGH,PA 15212. NR 0 TC 0 Z9 0 U1 0 U2 4 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2488 EP 2488 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002475 ER PT J AU Mathier, MA Lozano, PM Shannon, RP AF Mathier, MA Lozano, PM Shannon, RP TI Angiotensin converting enzyme inhibition selectively improves subendocardial perfusion in conscious dogs with heart failure SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NERPRC,SOUTHBOROUGH,MA. ALLEGHENY GEN HOSP,PITTSBURGH,PA 15212. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2531 EP 2531 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002517 ER PT J AU Cohen, MC Stafford, RS AF Cohen, MC Stafford, RS TI Treadmill testing: Impact of gender, race, and insurance on test ordering SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2574 EP 2574 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002560 ER PT J AU Koren, MJ Buda, C Henry, W Ellison, WT Milas, JM Morgan, M Sprinkle, L McGreevy, MJ Goldberg, RK Gerry, S Barrett, M Connolly, S Morrison, L Abrahamson, DC Somogyi, C Weiss, RJ Abisalih, DN Ridley, C Browne, KF McGowan, N Hariman, RJ Tully, M Bissett, J May, R Heywood, JT Fabbri, S Crawford, W Platt, M Bramlet, D Morgan, C Dillon, MC Roark, S Marquis, N Page, RL Canby, RC Horton, RP Ash, G Shettigar, UR Barbier, G Appunn, D Leonelli, F McFarland, T Rajkovich, K Pritchett, ELC Tormey, MA Walker, JL Carley, JE Tracy, DM Anderson, JL Karagounis, LA Summers, K Barker, AH Fowles, RE Preece, MJ Doran, EN Roy, D Talajic, M Dubuc, M Beaudoin, D Fujimura, O Aceron, D Onufer, J Barciano, R Cameron, D Weller, B Drehobl, M Brodkin, J Joswig, B Barker, M Schu, D Kremers, MS Whisnant, D Lurie, M Brinkley, A Pollak, SJ Nicholls, S Bloomfield, D DeStefano, M King, N Geris, B Green, M Tang, ASL Luce, M ElShahawy, M Wagner, M Rudge, J Steinberg, JS Tan, E Yee, R Klein, GJ Braney, M Backes, R Miller, K Branco, M Myers, D Suggs, T Shah, A Heus, B Trizzino, C Grossman, WJ Fletcher, K Loh, IK Smith, C DeGennaro, K Singer, I Cicic, A Langan, MN Gomes, JA Mehta, D Pe, E Sager, PT Ploss, D Attin, M Lueken, M Gray, RJ Chelliah, NN Hagen, K Carter, D Gray, C Curtis, AB Conti, JB Salvetti, L Sheldon, R Ritchie, D Ellenbogen, K Wood, MA Michaels, N Hall, JH Fausset, D Linden, P Schulman, C Gershengorn, K Saltz, S Kinsman, E Jacobson, K Littell, F Mossberg, J Dauw, K Karlsberg, RP Gerez, T Tobis, FM Rasmussen, E Carlson, M Walker, B Silverman, B Banasik, S Rubin, M Busch, J Hack, TC Criasia, M Florek, R Hamlin, M Friedman, J Dinning, A Misaljevic, Y Keller, M Trajillo, N Anderson, D Wagshal, A Rofino, K Motta, M Block, LS Wistran, DC Grogan, EW Sommerfeldt, B Rothrock, D Baron, S Stedfield, S Swenson, L Gilbert, B Bernstein, V Kerr, C MacDonald, K Mooney, S Bilsker, MS Kamerman, M Bradley, J Peacock, T Chen, PS Goodman, JS Peter, CT Schoenbaum, M Conte, S Curlee, P Booker, R DiCarlo, LA Kappler, JH Winston, SA Adolphson, M Henthorn, R Lipps, J Ibanez, K Johnson, WB Polich, M Martin, DT Woodhead, G Moore, SL Mishak, S Manholt, S Noll, HE Kelley, JG Perlman, R Guido, J Stambler, B Sargent, D Stein, J Willis, R Stoever, WW Cotham, P Mason, K Gaber, J Winters, SL Curwin, JH Banas, JS Enright, LJ Brodsky, M Chaim, S Carlson, H Furka, E Daubert, J Akiyama, T Flynn, D Ocampo, C Erdin, RA Heiges, TA Kadel, K Stucky, ED Rittenhouse, M McAnulty, J Timberg, J McNeer, JF Smith, B Murray, KT Norris, K Edgett, C Sorenson, JL Adelman, B Stoner, D Offenberg, H Arnow, L Thind, G Faughn, C Williams, D Hendricks, E Friedman, B Payne, W Fuenzalida, CE Washam, M Heinsimer, J Lentini, MG Weinberg, DM Fox, C McCown, R Cook, FS ODonoghue, S Fenton, J Chung, M Kidwell, GA Jaeger, FJ Holmes, DR Morant, VA Trohman, RG Wilkoff, BL Pinski, SL Tchou, PJ Holmes, D Kerin, NZ Faitel, K Stamato, NJ Whiting, D Bhalla, RK Hicks, T Bianchi, P Hamilton, W Chilson, D Baxter, J Contrafatto, DS Afshari, D Guarnieri, T Bolderman, K Margolis, PD Durham, J Martin, HM Wayand, CE McGrew, F Wilson, B Nademanee, K Smith, S Sharma, A ONeill, G Skadsen, A Ware, D Malmberg, G Wilson, M Bednarczyk, E Bateson, M Zinn, PD Robles, E Cullors, D Crossley, G DavisOBrien, K Frishman, WH Root, L Blanco, B Furia, S Goodman, L JonesLanier, S Kocheril, A Winecoff, A Packer, D Cosberg, K Barbey, JT HewettMeulman, J Wertheimer, J Fierstein, J Benene, C Hurwitz, J Alexander, L Wimberly, B Overweg, N Mejia, V Pacifico, A Farrell, M Steinman, R ValMejias, J Patterson, P Wilson, J Enright, L Dyckman, E Harris, B Raines, P Paul, T Blackman, T Porterfield, JG Porterfield, LM Roth, J Vagnoni, J AF Koren, MJ Buda, C Henry, W Ellison, WT Milas, JM Morgan, M Sprinkle, L McGreevy, MJ Goldberg, RK Gerry, S Barrett, M Connolly, S Morrison, L Abrahamson, DC Somogyi, C Weiss, RJ Abisalih, DN Ridley, C Browne, KF McGowan, N Hariman, RJ Tully, M Bissett, J May, R Heywood, JT Fabbri, S Crawford, W Platt, M Bramlet, D Morgan, C Dillon, MC Roark, S Marquis, N Page, RL Canby, RC Horton, RP Ash, G Shettigar, UR Barbier, G Appunn, D Leonelli, F McFarland, T Rajkovich, K Pritchett, ELC Tormey, MA Walker, JL Carley, JE Tracy, DM Anderson, JL Karagounis, LA Summers, K Barker, AH Fowles, RE Preece, MJ Doran, EN Roy, D Talajic, M Dubuc, M Beaudoin, D Fujimura, O Aceron, D Onufer, J Barciano, R Cameron, D Weller, B Drehobl, M Brodkin, J Joswig, B Barker, M Schu, D Kremers, MS Whisnant, D Lurie, M Brinkley, A Pollak, SJ Nicholls, S Bloomfield, D DeStefano, M King, N Geris, B Green, M Tang, ASL Luce, M ElShahawy, M Wagner, M Rudge, J Steinberg, JS Tan, E Yee, R Klein, GJ Braney, M Backes, R Miller, K Branco, M Myers, D Suggs, T Shah, A Heus, B Trizzino, C Grossman, WJ Fletcher, K Loh, IK Smith, C DeGennaro, K Singer, I Cicic, A Langan, MN Gomes, JA Mehta, D Pe, E Sager, PT Ploss, D Attin, M Lueken, M Gray, RJ Chelliah, NN Hagen, K Carter, D Gray, C Curtis, AB Conti, JB Salvetti, L Sheldon, R Ritchie, D Ellenbogen, K Wood, MA Michaels, N Hall, JH Fausset, D Linden, P Schulman, C Gershengorn, K Saltz, S Kinsman, E Jacobson, K Littell, F Mossberg, J Dauw, K Karlsberg, RP Gerez, T Tobis, FM Rasmussen, E Carlson, M Walker, B Silverman, B Banasik, S Rubin, M Busch, J Hack, TC Criasia, M Florek, R Hamlin, M Friedman, J Dinning, A Misaljevic, Y Keller, M Trajillo, N Anderson, D Wagshal, A Rofino, K Motta, M Block, LS Wistran, DC Grogan, EW Sommerfeldt, B Rothrock, D Baron, S Stedfield, S Swenson, L Gilbert, B Bernstein, V Kerr, C MacDonald, K Mooney, S Bilsker, MS Kamerman, M Bradley, J Peacock, T Chen, PS Goodman, JS Peter, CT Schoenbaum, M Conte, S Curlee, P Booker, R DiCarlo, LA Kappler, JH Winston, SA Adolphson, M Henthorn, R Lipps, J Ibanez, K Johnson, WB Polich, M Martin, DT Woodhead, G Moore, SL Mishak, S Manholt, S Noll, HE Kelley, JG Perlman, R Guido, J Stambler, B Sargent, D Stein, J Willis, R Stoever, WW Cotham, P Mason, K Gaber, J Winters, SL Curwin, JH Banas, JS Enright, LJ Brodsky, M Chaim, S Carlson, H Furka, E Daubert, J Akiyama, T Flynn, D Ocampo, C Erdin, RA Heiges, TA Kadel, K Stucky, ED Rittenhouse, M McAnulty, J Timberg, J McNeer, JF Smith, B Murray, KT Norris, K Edgett, C Sorenson, JL Adelman, B Stoner, D Offenberg, H Arnow, L Thind, G Faughn, C Williams, D Hendricks, E Friedman, B Payne, W Fuenzalida, CE Washam, M Heinsimer, J Lentini, MG Weinberg, DM Fox, C McCown, R Cook, FS ODonoghue, S Fenton, J Chung, M Kidwell, GA Jaeger, FJ Holmes, DR Morant, VA Trohman, RG Wilkoff, BL Pinski, SL Tchou, PJ Holmes, D Kerin, NZ Faitel, K Stamato, NJ Whiting, D Bhalla, RK Hicks, T Bianchi, P Hamilton, W Chilson, D Baxter, J Contrafatto, DS Afshari, D Guarnieri, T Bolderman, K Margolis, PD Durham, J Martin, HM Wayand, CE McGrew, F Wilson, B Nademanee, K Smith, S Sharma, A ONeill, G Skadsen, A Ware, D Malmberg, G Wilson, M Bednarczyk, E Bateson, M Zinn, PD Robles, E Cullors, D Crossley, G DavisOBrien, K Frishman, WH Root, L Blanco, B Furia, S Goodman, L JonesLanier, S Kocheril, A Winecoff, A Packer, D Cosberg, K Barbey, JT HewettMeulman, J Wertheimer, J Fierstein, J Benene, C Hurwitz, J Alexander, L Wimberly, B Overweg, N Mejia, V Pacifico, A Farrell, M Steinman, R ValMejias, J Patterson, P Wilson, J Enright, L Dyckman, E Harris, B Raines, P Paul, T Blackman, T Porterfield, JG Porterfield, LM Roth, J Vagnoni, J TI Treatment of atrial fibrillation and paroxysmal supraventricular tachycardia with bidisomide SO CIRCULATION LA English DT Article DE antiarrhythmia agents; arrhythmia; fibrillation; tachycardia ID ANTIARRHYTHMIC AGENT; FLECAINIDE; SC-40230; THERAPY; PLACEBO AB Background Atrial fibrillation and paroxysmal supraventricular tachycardia are common disorders of the heart rhythm for which antiarrhythmic drug therapy is commonly prescribed. The Atrial Fibrillation Investigation with Bidisomide (AFIB) study was a randomized, placebo-controlled clinical trial designed to accomplish three goals in a single protocol: (1) to determine the efficacy of the antiarrhythmic drug bidisomide in the treatment of these two arrhythmias; (2) to establish the appropriate dose range for bidisomide; and (3) to detect an adverse mortality effect of bidisomide if one were present in patients with atrial fibrillation. Methods and Results In this clinical trial, 1227 patients with atrial fibrillation and 187 with paroxysmal supraventricular tachycardia were randomly assigned to bidisomide (200, 400, or 600 mg BID) or placebo; patient groups with each arrhythmia were analyzed separately. Symptomatic recurrences of atrial fibrillation and paroxysmal supraventricular tachycardia were documented with the use of transtelephonic ECG monitoring. The time to the first symptomatic arrhythmia recurrence was measured in each patient and compared among treatment groups. Among the atrial fibrillation patients, there was no significant difference in the time to first symptomatic recurrence between the placebo group and any of the three bidisomide treatment groups; the hazard ratios (placebo:treatment) were 1.19, 1.03, and 1.14 for bidisomide 200, 400, and 600 mg BID, respectively. Among paroxysmal supraventricular tachycardia patients, there was a similar lack of a significant treatment effect; the hazard ratios were 1.30, 1.93, and 1.59 for bidisomide 200, 400, and 600 mg BID, respectively. In the primary safety analysis of mortality, 3 of 493 patients taking placebo died, compared with 9 of 488 patients taking one of the two higher doses of bidisomide (P>.10). Conclusions Bidisomide in the doses tested did not have a clinically important antiarrhythmic effect. The AFIB study provided a novel clinical trial design to test antiarrhythmic drugs for both safety and efficacy. C1 DUKE UNIV,MED CTR,DUKE S HOSP,DURHAM,NC 27710. JACKSONVILLE CARDIOVASC CLIN,JACKSONVILLE,FL. UPSTATE CLIN RES INC,GREER,SC. CARDIOL MED GRP SAN DIEGO,LA MESA,CA. MCMASTER UNIV,HAMILTON,ON,CANADA. ORANGE CTY HEART INST,ORANGE,CA. ANDROSCOGGIN CARDIOL ASSOCIATES,AUBURN,ME. WATSON CLIN,LAKELAND,FL. EDWARD HINES JR VET ADM HOSP,HINES,IL 60141. UNIV ARKANSAS MED SCI,LITTLE ROCK,AR 72205. LOMA LINDA UNIV,JERRY L PETTIS MEM VET HOSP,LOMA LINDA,CA 92357. MONTGOMERY CARDIOVASC ASSOCIATES PA,MONTGOMERY,AL. CARDIOL CONSULTANTS RES,ST PETERSBURG,FL. CARDIOL ASSOCIATES GAINESVILLE,GAINESVILLE,FL. UNIV TEXAS,SW MED CTR,DALLAS,TX. VET ADM MED CTR,BAY PINES,FL. UNIV KENTUCKY,MED CTR,LEXINGTON,KY. UNIV UTAH,LATTER DAY ST HOSP,SALT LAKE CITY,UT 84143. SALT LAKE CLIN RES FDN,SALT LAKE CITY,UT. MONTREAL HEART INST,MONTREAL,PQ H1T 1C8,CANADA. UNIV CALIF SAN DIEGO,MED CTR,SAN DIEGO,CA 92103. CARDIOVASC ASSOCIATES LTD,NORFOLK,VA. TORONTO HOSP,TORONTO,ON M5T 2S8,CANADA. CTR HLTH CARE,SAN DIEGO,CA. PRESBYTERIAN HOSP HEART CTR,CHARLOTTE,NC. CENT FLORIDA CARDIOL GRP PA,ORLANDO,FL. ST VINCENTS MED CTR,STATEN ISL,NY. OTTAWA CIVIC HOSP,OTTAWA,ON K1Y 4E9,CANADA. ST LUKES ROOSEVELT HOSP,NEW YORK,NY. UNIV WESTERN ONTARIO,UNIV HOSP,LONDON,ON N6A 5A5,CANADA. N CENT HEART INST,SIOUX FALLS,SD. W FLORIDA MED CTR CLIN PA,PENSACOLA,FL. HCA LOS ROBLES MED CTR,VENTURA HEART INST,THOUSAND OAKS,CA. UNIV LOUISVILLE,LOUISVILLE,KY 40292. MT SINAI MED CTR,NEW YORK,NY 10029. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV N DAKOTA,UNITED HOSP,GRAND FORKS,ND 58201. UNIV FLORIDA,GAINESVILLE,FL. CALGARY GEN HOSP,CALGARY,AB,CANADA. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. MED RES CONSORTIUM,INDIANAPOLIS,IN. CARDIOL ASSOCIATES GREATER BOSTON,BROOKLINE,MA. OREGON RES GRP,EUGENE,OR. CARDIOVASC RES INST SO CALIF,BEVERLY HILLS,CA. CASE WESTERN RESERVE UNIV,UNIV HOSP CLEVELAND,CLEVELAND,OH 44106. NORTHSIDE HOSP,ATLANTA,GA. LEE COAST RES CTR INC,FT MYERS,FL. GOOD SAMARITAN HOSP,PORTLAND,OR 97209. HEALTHCARE PARTNERS,LOS ANGELES,CA. VET ADM MED CTR,DENVER,CO 80220. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA. CARDIOL PHYSICIANS INC,SALEM,MA. JACKSON FDN MED RES,MADISON,WI. ST PAUL RAMSEY MED CTR,ST PAUL,MN 55101. UNIV BRITISH COLUMBIA HOSP,VANCOUVER,BC,CANADA. UNIV MIAMI,CORAL GABLES,FL 33124. DOCTORS CLIN,VERO BEACH,FL. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. ST MARYS HOSP,GRAND JCT,CO. MICHIGAN HEART & VASC INST,YPSILANTI,MI. CHRIST HOSP,CARDIOVASC RES CTR,CINCINNATI,OH 45219. IOWA HEART CTR,DES MOINES,IA. LAHEY CLIN FDN,BURLINGTON,MA. N OHIO HEART CTR,ELYRIA,OH. SHARP REES STEALY MED CTR,SAN DIEGO,CA. PARTNERS MED RES,BALTIMORE,MD. MCGUIRE DEPT VET AFFAIRS MED CTR,RICHMOND,VA. MERCY HOSP,MED CTR,SAN DIEGO,CA. HEALTHCARE RES CONSULTANTS,TULSA,OK. MORRISTOWN MEM HOSP,MORRISTOWN,NJ 07962. UNIV CALIF IRVINE,IRVINE MED CTR,ORANGE,CA 92668. UNIV ROCHESTER,MED CTR,ROCHESTER,NY 14627. NORTHSIDE CARDIOL,SPOKANE,WA. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. VANDERBILT UNIV,MED CTR,NASHVILLE,TN. SW MED GRP,LAS VEGAS,NV. HALIFAX CLIN RES CTR,DAYTONA BEACH,FL. UNIV LOUISVILLE,HLTH SCI CTR,LOUISVILLE,KY 40292. ATLANTIC INST CLIN RES,DAYTONA BEACH,FL. VET ADM MED CTR,MED RES SERV,KANSAS CITY,MO. WESTERN HEART SPECIALISTS PC,DENVER,CO. ST JOSEPH MERCY HOSP OAKLAND,PONTIAC,MI. CARDIOL ASSOCIATES MED GRP,ANAHEIM,CA. WASHINGTON HOSP CTR,WASHINGTON,DC 20010. CLEVELAND CLIN FDN,CLEVELAND,OH 44195. SINAI HOSP,DETROIT,MI 48235. INLAND CARDIOL ASSOCIATES PS,SPOKANE,WA. ST FRANCIS REG MED CTR,PITTSBURGH,PA. MIDATLANTIC CARDIOVASC CONSULTANTS PA,BALTIMORE,MD. OKLAHOMA HEART INC,TULSA,OK. TAMPA MED RES ASSOCIATES INC,TAMPA,FL. CARDIOL GRP MEMPHIS PA,MEMPHIS,TN. DENVER GEN HOSP,DENVER,CO. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. MILLARD FILLMORE HOSP,BUFFALO,NY 14209. CARDIOL CLIN SAN ANTONIO PA,SAN ANTONIO,TX. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC. MONTEFIORE HOSP & MED CTR,ALBERT EINSTEIN COLL MED HOSP,BRONX,NY 10461. MEM MED CTR INC,SAVANNAH,GA. MED COLL GEORGIA,AUGUSTA,GA 30912. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. GEORGETOWN UNIV,WASHINGTON,DC. ALBERT EINSTEIN MED CTR,PHILADELPHIA,PA 19141. PRESBYTERIAN HEART INST,DALLAS,TX. EASTSIDE COMPREHENS MED SERV,NEW YORK,NY. TEXAS ARRHYTHMIA INST,HOUSTON,TX. ST JOHNS HOSP,DETROIT,MI. GALICHIA MED CTR,WICHITA,KS. GOOD SAMARITAN HOSP,CINCINNATI,OH. SE CLIN RESOURCES,ATLANTA,GA. CARDIOL ASSOCIATES LEXINGTON,LEXINGTON,KY. FUTURE HEALTHCARE,BIRMINGHAM,AL. ARRHYTHMIA CONSULTANTS,MEMPHIS,TN. MED COLL WISCONSIN,MILWAUKEE,WI 53226. RI Page, Richard/L-5501-2014 OI Page, Richard/0000-0001-5603-1330 NR 18 TC 17 Z9 17 U1 2 U2 12 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 BP 2625 EP 2632 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC671 UT WOS:A1997YC67100027 ER PT J AU Grimes, RY Levine, RA Yoganathan, AP Saranno, ME AF Grimes, RY Levine, RA Yoganathan, AP Saranno, ME TI Relevance of systolic pulmonary venous flow reversal in severe mitral regurgitation: A combined computer modeling and clinical study SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GEORGIA INST TECHNOL,ATLANTA,GA 30332. MAYO CLIN,ROCHESTER,MN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2631 EP 2631 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002617 ER PT J AU Lipshultz, SE Rifai, N Sallan, SE Lipsitz, SR Dalton, V Sacks, DB Ottlinger, ME AF Lipshultz, SE Rifai, N Sallan, SE Lipsitz, SR Dalton, V Sacks, DB Ottlinger, ME TI Predictive value of cardiac troponin T in pediatric patients at risk for myocardial injury SO CIRCULATION LA English DT Article DE myocardial infarction; pediatrics; doxorubicin; heart defects, congenital; troponin T ID SPONTANEOUSLY HYPERTENSIVE RATS; CREATINE-KINASE; HEART-SURGERY; DOXORUBICIN; MB; TRANSPLANTATION; CARDIOTOXICITY; INFARCTION; MECHANICS; RELEASE AB Background Biochemical markers have not been routinely used in children at risk for myocardial damage. Yet, because of somatic growth and the duration of survival, a low level of myocardial damage may ultimately be of more consequence in children than in adults. Methods and Results We investigated the utility of cardiac troponin T (cTnT) blood levels (CARDIAC T ELISA Troponin T, Boehringer Mannheim Corp) in 51 consecutively sampled patients from 1 day to 34 years of age (median=5.7 years) undergoing cardiovascular (n=19) or noncardiovascular (n=17) surgery or who received doxorubicin for acute lymphoblastic leukemia (ALL) (n=15). Minimum detectable cTnT elevations were 0.03 ng/mL. cTnT was measurable in children of all ages with myocyte damage. In patients who underwent cardiovascular surgery, a correlation was noted between a score of increasing surgical severity and the mean level of postoperative cTnT (r =.79, P<.0001). Postoperative cTnT levels were elevated in children who completed cardiovascular surgery with an open chest compared with those with a closed chest (P=.0083). In addition, cTnT levels before cardiovascular surgery predicted postoperative survival (P=.007). cTnT elevations were observed after initial doxorubicin therapy for ALL. The magnitude of elevation predicted left ventricular dilatation (r=.80 when variables were treated as continuous, P=.003) and wall thinning (r =.61, P=.044) 9 months later. Conclusions Elevations of blood cTnT in children relate to the severity of myocardial damage and predict subsequent subclinical and clinical cardiac morbidity and mortality. C1 CHILDRENS HOSP,DEPT CARDIOL,BOSTON,MA 02115. CHILDRENS HOSP,DEPT LAB MED,BOSTON,MA 02115. CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. VET ADM MED CTR,BOSTON,MA. BOSTON UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02118. OI Sacks, David/0000-0003-3100-0735 FU NCI NIH HHS [CA34183, CA68484]; NHLBI NIH HHS [HR96041] NR 33 TC 222 Z9 229 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 BP 2641 EP 2648 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC671 UT WOS:A1997YC67100029 PM 9355905 ER PT J AU Gold, HK Kereiakes, DJ Dinsmore, RE Martin, LH Lausten, D Broderick, TM Anderson, KM Garabedian, HD Leinbach, RC AF Gold, HK Kereiakes, DJ Dinsmore, RE Martin, LH Lausten, D Broderick, TM Anderson, KM Garabedian, HD Leinbach, RC TI A randomized, placebo-controlled crossover trial of ReoPro alone or combined with low-dose plasminogen activator for coronary reperfusion in patients with acute myocardial infarction: Preliminary results SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. LINDNER CARDIOVASC RES,CINCINNATI,OH. OHIO HEART HLTH CTR,CINCINNATI,OH. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2649 EP 2649 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002635 ER PT J AU Nagashima, M Shinoka, T Nollert, G ShumTim, D Roth, SJ Hickey, PR Kirchhoff, A Burke, PR Springer, TA Mayer, JE AF Nagashima, M Shinoka, T Nollert, G ShumTim, D Roth, SJ Hickey, PR Kirchhoff, A Burke, PR Springer, TA Mayer, JE TI Effect of antibody to P-selectin on recovery of neonatal lamb hearts after hypothermic ischemia SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2685 EP 2685 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002671 ER PT J AU Shi, CW Lee, WS Russell, ME Zhang, D Fletcher, DL Newell, JB Haber, E AF Shi, CW Lee, WS Russell, ME Zhang, D Fletcher, DL Newell, JB Haber, E TI Hypercholesterolemia exacerbates transplant arteriosclerosis via increased neointimal smooth muscle cell accumulation - Studies in apolipoprotein E knockout mice SO CIRCULATION LA English DT Article DE vasculature; transplantation; muscle, smooth; hypercholesterolemia ID CARDIAC ALLOGRAFTS; HEART-TRANSPLANTATION; ATHEROSCLEROSIS; INTERLEUKIN-8; EXPRESSION; REJECTION; PATHOGENESIS; DISEASE; LESIONS; N51 AB Background Hypercholesterolemia is thought to be a significant risk factor for coronary vasculopathy in cardiac transplant recipients. Methods and Results. We examined the development of arteriosclerosis in mouse carotid artery loops allografted from B.10A(2R) (H-2(h2)) donors to normocholesterolemic C57BL/6J (H-2(b)) recipients and hypercholesterolemic C57BL/6J recipients in which the apolipoprotein (apo) E gene had been knocked out. Luminal occlusion and cross-sectional neointimal area were greater in arteries allografted into hypercholesterolemic recipients at 15 and 30 days after transplantation. We also measured cellular and extracellular matrix components of the neointima by computerized planimetry of the fractional areas subtended by smooth muscle cells (anti-alpha-actin stain), collagen (Masson's trichrome), lipid (oil red O), and leukocytes (anti-CD45). The neointimal area stained for smooth muscle cells was significantly greater in hypercholesterolemic recipients than in normocholesterolemic recipients at 15 and 30 days after allografting. Lipid contributed to neointimal area to a lesser degree, and there was no significant increase in the contribution of collagen or leukocytes. Conclusions Smooth muscle cell accumulation appears to be the principal contributor to the increase in neointimal area observed in arteries allografted into hypercholesterolemic mice. C1 HARVARD UNIV,SCH PUBL HLTH,CARDIOVASC BIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. BRIGHAM & WOMENS HOSP,DIV CARDIOVASC,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CARDIAC COMP CTR,BOSTON,MA 02114. NR 29 TC 26 Z9 26 U1 1 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 BP 2722 EP 2728 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC671 UT WOS:A1997YC67100039 PM 9355915 ER PT J AU Molnar, A Bonventre, J Pombo, C Kyriakis, J Force, TL AF Molnar, A Bonventre, J Pombo, C Kyriakis, J Force, TL TI The Ste20-like oxidant stress response kinase-1 induces cell cycle arrest in G1via a p38 MAP kinase independent pathway SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2727 EP 2727 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002710 ER PT J AU Gerszten, RE Yoshida, M Gimbrone, MA Rosenzweig, A AF Gerszten, RE Yoshida, M Gimbrone, MA Rosenzweig, A TI E-selectin dependent adhesion is exempt from the inhibitory effect of interleukin-8 SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2761 EP 2761 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002742 ER PT J AU Ritchie, JL Maynard, C Every, NR Chapko, MK Martin, DC AF Ritchie, JL Maynard, C Every, NR Chapko, MK Martin, DC TI Coronary angioplasty volumes and outcomes in the healthcare cost and utilization project SO CIRCULATION LA English DT Meeting Abstract C1 VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. UNIV WASHINGTON,SEATTLE,WA 98195. SEATTLE VA,SEATTLE,WA. RI Maynard, Charles/N-3906-2015 OI Maynard, Charles/0000-0002-1644-7814 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2831 EP 2831 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002813 ER PT J AU Lehmann, KG HeathLange, SJ Ferris, ST AF Lehmann, KG HeathLange, SJ Ferris, ST TI Randomized comparison of hemostasis techniques following invasive cardiovascular procedures SO CIRCULATION LA English DT Meeting Abstract C1 VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2959 EP 2959 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002941 ER PT J AU Giugliano, RP Cannon, CP McCabe, CH vandeWerf, FJ Braunwald, E AF Giugliano, RP Cannon, CP McCabe, CH vandeWerf, FJ Braunwald, E TI Lower dose heparin with thrombolysis is associated with lower rates of intracranial hemorrhage: Results from TIMI 10B and ASSENT I SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. UNIV ZIEKENHUIS LEUVEN,LOUVAIN,BELGIUM. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 2996 EP 2996 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88002978 ER PT J AU LielCohen, N Otsuji, Y Vlahakes, GJ Akins, CW Levine, RA AF LielCohen, N Otsuji, Y Vlahakes, GJ Akins, CW Levine, RA TI Functional ischemic mitral regurgitation can persist despite ring annuloplasty: Mechanistic insights SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3026 EP 3026 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003007 ER PT J AU Feener, EP Bouchie, J Hansen, H AF Feener, EP Bouchie, J Hansen, H TI Atrial natriuretic factor is a potent inhibitor of plasminogen activator inhibitor-1 expression in vascular smooth muscle cells SO CIRCULATION LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3047 EP 3047 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003028 ER PT J AU Murohara, T Asahara, T Silver, M Keaney, M Magner, M Yang, JH Chen, DH Chen, DF Symes, JF Huang, PL Isner, JM AF Murohara, T Asahara, T Silver, M Keaney, M Magner, M Yang, JH Chen, DH Chen, DF Symes, JF Huang, PL Isner, JM TI Essential role of endothelial nitric oxide synthase in angiogenesis in vivo SO CIRCULATION LA English DT Meeting Abstract C1 ST ELISABETH MED CTR,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ST ELISABETH MED CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3080 EP 3080 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003061 ER PT J AU Laham, RJ Tofukuji, M Selke, FW Simons, M AF Laham, RJ Tofukuji, M Selke, FW Simons, M TI Vascular endothelial growth factor (VEGF) affects microvessels but not epicardial coronary arteries and veins SO CIRCULATION LA English DT Meeting Abstract C1 BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. HARVARD UNIV,SCH MED,BIDMC,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3081 EP 3081 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003062 ER PT J AU Rithcie, JL Maynard, C Every, NR Chapko, MK Martin, DC AF Rithcie, JL Maynard, C Every, NR Chapko, MK Martin, DC TI Coronary angioplasty volumes and outcomes in the health can cost and utilization project SO CIRCULATION LA English DT Meeting Abstract C1 VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. UNIV WASHINGTON,SEATTLE,WA 98195. SEATTLE VA,SEATTLE,WA. RI Maynard, Charles/N-3906-2015 OI Maynard, Charles/0000-0002-1644-7814 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3145 EP 3145 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003126 ER PT J AU Stafford, RS Blumenthal, D AF Stafford, RS Blumenthal, D TI Specialty differences in cardiovascular disease prevention practices SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3147 EP 3147 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003128 ER PT J AU Gold, HK Garabedian, HD Guerrero, JL Sullivan, S Zawadzka, A Dinsmore, J Edge, ASB Dersimonian, H AF Gold, HK Garabedian, HD Guerrero, JL Sullivan, S Zawadzka, A Dinsmore, J Edge, ASB Dersimonian, H TI Cellular therapy for myocardial repair: Successful transplantation of human myoblasts by intracoronary injection into the canine heart after acute myocardial infarction SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. DIACRIN INC,CHARLESTOWN,MA. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3170 EP 3170 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003151 ER PT J AU Brezinski, ME Tearney, GJ Boppart, SA Bouma, BE Pitris, C Southern, JF Fujimoto, JG AF Brezinski, ME Tearney, GJ Boppart, SA Bouma, BE Pitris, C Southern, JF Fujimoto, JG TI Ultrahigh resolution catheter based in vivo imaging of the rabbit aorta with optical coherence tomography SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. SINAI SAMARITAN MED CTR,MILWAUKEE,WI. RI Boppart, Stephen/C-7338-2009 NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3294 EP 3294 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003274 ER PT J AU Moreno, PR Palacios, IF Pathan, A Fuster, V Fallon, JT AF Moreno, PR Palacios, IF Pathan, A Fuster, V Fallon, JT TI Histological comparison of in stent and post-PTCA restenotic tissue SO CIRCULATION LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MT SINAI HOSP,NEW YORK,NY 10029. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3299 EP 3299 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003287 ER PT J AU WoodcockMitchell, J Marutsuka, K Holt, RE Gold, HK Sobel, BE AF WoodcockMitchell, J Marutsuka, K Holt, RE Gold, HK Sobel, BE TI Differential expression of fibrinolytic system proteins in coronary atheroma from type II diabetic and non diabetic subjects SO CIRCULATION LA English DT Meeting Abstract C1 UNIV VERMONT,BURLINGTON,VT. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3302 EP 3302 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003290 ER PT J AU Rodriguez, AE Bernardi, VH Ayala, FP Marchand, EM Pardinas, CA Santaera, OA Mauvecin, CE Vogel, DF Palacios, IF AF Rodriguez, AE Bernardi, VH Ayala, FP Marchand, EM Pardinas, CA Santaera, OA Mauvecin, CE Vogel, DF Palacios, IF TI Optimal coronary balloon angioplasty vs stent (OCBAS): Angiographic long term follow up results of a randomized trial SO CIRCULATION LA English DT Meeting Abstract C1 OTAMENDI ANCHORENA HOSP,BUENOS AIRES,DF,ARGENTINA. UNIV CHILE,SANTIAGO,CHILE. UNIV CATTOLICA,SANTIAGO,CHILE. INST CARDIOL,MONTEVIDEO,URUGUAY. HOSP ESPANOL,BAHIA BLANCA,ARGENTINA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3311 EP 3311 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003299 ER PT J AU Philbin, EF Jenkins, PL Nichols, M DiSalvo, TG AF Philbin, EF Jenkins, PL Nichols, M DiSalvo, TG TI HMO management of congestive heart failure: Resource use, process of care and clinical outcomes SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BASSETT HEALTHCARE,COOPERSTOWN,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3449 EP 3449 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003434 ER PT J AU Goldberg, LR Dec, GW DiSalvo, TG Philbin, EF AF Goldberg, LR Dec, GW DiSalvo, TG Philbin, EF TI Managed care for acute myocardial infarction: Higher procedure use, lower charges and equivalent clinical outcomes SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3452 EP 3452 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003437 ER PT J AU Wilensky, RL Lehmann, KG Werner, JA Chambers, JW Harlamert, E Dillon, JC AF Wilensky, RL Lehmann, KG Werner, JA Chambers, JW Harlamert, E Dillon, JC TI The Biostent trial: A randomized, double-blind, prospective, multi-center trial evaluating the safety and tolerability of locally delivered cytochalasin B for prophylaxis of angioplasty restenosis SO CIRCULATION LA English DT Meeting Abstract C1 UNIV PENN,PHILADELPHIA,PA 19104. VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. PROVIDENCE HEART GRP,SEATTLE,WA. UNIV WASHINGTON,SEATTLE,WA 98195. COMMUNITY HOSP E,INDIANAPOLIS,IN. INDIANA UNIV,INDIANAPOLIS,IN 46204. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3641 EP 3641 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003622 ER PT J AU Goldberg, S Schwartz, RS Mann, JT Sketch, MH Feldman, RL Midei, MG Safian, RD Brown, CL Rogers, EW Savage, MP Gebhardt, S Murphy, BE AF Goldberg, S Schwartz, RS Mann, JT Sketch, MH Feldman, RL Midei, MG Safian, RD Brown, CL Rogers, EW Savage, MP Gebhardt, S Murphy, BE TI Comparison of a novel self-expanding nitinol stent (RADIUS(TM)) with a balloon expandable (Palmaz-Schatz(TM)) stent: Initial results of a randomized trial (SCORES) SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MAYO CLIN,ROCHESTER,MN. WAKE HEART ASSOCIATES,RALEIGH,NC. DUKE UNIV,DURHAM,NC 27706. MUNROE REG MED CTR,OCALA,FL. ST JOSEPHS MED CTR,BALTIMORE,MD. WILLIAM BEAUMONT HOSP,ROYAL OAK,MI 48072. PIEDMONT HOSP FUQUA HEART CTR,ATLANTA,GA. SACRED HEART HOSP,PENSACOLA,FL. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3664 EP 3664 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003645 ER PT J AU Myerson, M Weil, HFC Healthcare, A Philbin, EF Jenkins, PL Nichols, M Reed, RG Francis, CK Pearson, TA AF Myerson, M Weil, HFC Healthcare, A Philbin, EF Jenkins, PL Nichols, M Reed, RG Francis, CK Pearson, TA TI Is lipoprotein (a) associated with myocardial infarction (MI) independent of its atherogenic effects? SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BASSETT HEALTHCARE,COOPERSTOWN,NY. COLUMBIA UNIV COLL PHYS & SURG,HARLEM HOSP CTR,NEW YORK,NY 10032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3674 EP 3674 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003655 ER PT J AU Myerson, M Weil, HFC Philbin, EF Groff, A Jenkins, PL Nichols, M Reed, RG Francis, CK Pearson, TA AF Myerson, M Weil, HFC Philbin, EF Groff, A Jenkins, PL Nichols, M Reed, RG Francis, CK Pearson, TA TI Lipoprotein (a) and sinking pre-beta lipoprotein band: Are they equivalent in their prediction of coronary heart disease? SO CIRCULATION LA English DT Meeting Abstract C1 BASSETT HEALTHCARE,COOPERSTOWN,NY. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. COLUMBIA UNIV COLL PHYS & SURG,HARLEM HOSP CTR,NEW YORK,NY 10032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3675 EP 3675 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003656 ER PT J AU Echenhagen, T Vandercasteele, G Huang, P Fischmeister, R AF Echenhagen, T Vandercasteele, G Huang, P Fischmeister, R TI Targeted disruption of the NOS III gene does not alter the contractile response to isoprenaline or carbachol in isolated muscle preparations SO CIRCULATION LA English DT Meeting Abstract C1 UNIV HAMBURG HOSP,D-2000 HAMBURG,GERMANY. INSERM,U446,CHATENAYMALABRY,FRANCE. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3778 EP 3778 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003759 ER PT J AU Torchiana, DF Newell, JB Bohmer, RM AF Torchiana, DF Newell, JB Bohmer, RM TI Hospital readmission rates following coronary bypass surgery: A statewide study SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3793 EP 3793 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003774 ER PT J AU Yu, GS Lu, YC Gulick, T AF Yu, GS Lu, YC Gulick, T TI Cloning, expression, and genetic analysis of human and S-cerevisiae carnitine/acylcarnitine translocases SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3869 EP 3869 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003845 ER PT J AU Yu, GS Lu, YC Gulick, T AF Yu, GS Lu, YC Gulick, T TI Expression of novel carnitine palmitoyltransferase I mRNA splicing variants in human heart: Implications for myocardial fatty acid beta-oxidative metabolism SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3871 EP 3871 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003847 ER PT J AU ScherrerCrosbie, M Steudel, W Hunziker, PR Foster, GP Zapol, WM Picard, MH AF ScherrerCrosbie, M Steudel, W Hunziker, PR Foster, GP Zapol, WM Picard, MH TI Validation of three dimensional transesophageal echocardiography for right ventricular volumes and function in mice SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3909 EP 3909 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003885 ER PT J AU Hunziker, PR Klug, MA Crosbie, MS LielCohen, N Handschumacher, MD Benton, SA Picard, MH AF Hunziker, PR Klug, MA Crosbie, MS LielCohen, N Handschumacher, MD Benton, SA Picard, MH TI Dynamic holographic imaging of the beating human heart SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3910 EP 3910 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003886 ER PT J AU ScherrerCrosbie, M Steudel, W Hunziker, PR Foster, GP Zapol, WM Picard, MH AF ScherrerCrosbie, M Steudel, W Hunziker, PR Foster, GP Zapol, WM Picard, MH TI Validation of transesophageal echocardiography for the assessment of right ventricular hypertrophy in the mouse SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3912 EP 3912 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003888 ER PT J AU Crawford, MH Ferry, DR Deedwania, PC Pepine, CJ Lehmann, KG Boden, WE AF Crawford, MH Ferry, DR Deedwania, PC Pepine, CJ Lehmann, KG Boden, WE TI Complications of revascularization in non Q-wave myocardial infarction patients: Results of the VA trial SO CIRCULATION LA English DT Meeting Abstract C1 UNIV NEW MEXICO,ALBUQUERQUE,NM 87131. VET ADM MED CTR,FRESNO,CA. UNIV FLORIDA,GAINESVILLE,FL. VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. VET ADM MED CTR,SYRACUSE,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3919 EP 3919 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003895 ER PT J AU Michaels, AD Barron, HV Maynard, C Every, NR AF Michaels, AD Barron, HV Maynard, C Every, NR TI Clinical predictors of ACE inhibitor use after acute myocardial infarction: Experience from the Second National Registry of Myocardial Infarction (NRMI 2) SO CIRCULATION LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. UNIV WASHINGTON,SEATTLE,WA 98195. RI Maynard, Charles/N-3906-2015 OI Maynard, Charles/0000-0002-1644-7814 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 3950 EP 3950 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88003926 ER PT J AU Han, RO Schmidt, U Gold, HK DiSalvo, TG Zapol, WM Bloch, KD Semigran, MJ AF Han, RO Schmidt, U Gold, HK DiSalvo, TG Zapol, WM Bloch, KD Semigran, MJ TI Inhaled nitric oxide combined with the cGMP-specific phosphodiesterase inhibitor zaprinast eliminates cyclic reocclusion in a canine model of platelet-mediated coronary thrombosis after thrombolysis SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 4050 EP 4050 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88004018 ER PT J AU Schmidt, U Han, RO Guerrero, JL Zapol, WM Bloch, KD Semigran, MJ AF Schmidt, U Han, RO Guerrero, JL Zapol, WM Bloch, KD Semigran, MJ TI Dipyridamole augments the antithrombotic effects of inhaled nitric oxide in a canine model of platelet mediated coronary artery occlusion after thrombolysis SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 4051 EP 4051 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88004019 ER PT J AU Filippov, G Bloch, KD AF Filippov, G Bloch, KD TI Cytokines decrease soluble guanylate cyclase subunit mRNA levels via a nitric oxide-independent mechanism SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 21 PY 1997 VL 96 IS 8 SU S BP 4072 EP 4072 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YC880 UT WOS:A1997YC88004040 ER PT J AU Yauch, RL Felsenfeld, DP Kraeft, SK Chen, LB Sheetz, MP Hemler, ME AF Yauch, RL Felsenfeld, DP Kraeft, SK Chen, LB Sheetz, MP Hemler, ME TI Mutational evidence for control of cell adhesion through integrin diffusion/clustering, independent of ligand binding SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID SUBUNIT CYTOPLASMIC DOMAIN; MEDIATED ADHESION; BETA(1) INTEGRIN; AFFINITY STATES; T-LYMPHOCYTES; VLA-4; RECEPTOR; ALPHA; DISTINCT; LFA-1 AB Previous studies have shown that integrin a chain tails make strong positive contributions to integrin-mediated cell adhesion. We now show here that integrin alpha(4) tail deletion markedly impairs static cell adhesion by a mechanism that does not involve altered binding of soluble vascular cell adhesion molecule 1 ligand. Instead, truncation of the alpha(4) cytoplasmic domain caused a severe deficiency in integrin accumulation into cell surface clusters, as induced by ligand and/or antibodies. Further-more, alpha(4) tail deletion also significantly decreased the membrane diffusivity of alpha(4) beta(1), as determined by a single particle tracking technique. Notably, low doses of cytochalasin D partially restored the deficiency in cell adhesion seen upon alpha(4) tail deletion. Together, these results suggest that alpha(4) tail deletion exposes the beta(1), cytoplasmic domain, leading to cytoskeletal associations that apparently restrict integrin lateral diffusion and accumulation into clusters, thus causing reduced static cell adhesion. Our demonstration of integrin adhesive activity regulated through receptor diffusion/clustering (rather than through altered Ligand binding affinity) may be highly relevant towards the understanding of inside-out signaling mechanisms for beta(1) integrins. C1 DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. DANA FARBER CANC INST,DIV MOL & CELLULAR BIOL,BOSTON,MA 02115. DUKE UNIV,MED CTR,DEPT CELL BIOL,DURHAM,NC 27710. FU NIAID NIH HHS [AI09490, F32 AI009490]; NIGMS NIH HHS [GM46526] NR 45 TC 129 Z9 134 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD OCT 20 PY 1997 VL 186 IS 8 BP 1347 EP 1355 DI 10.1084/jem.186.8.1347 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA YC950 UT WOS:A1997YC95000019 PM 9334374 ER PT J AU Doranz, BJ GrovitFerbas, K Sharron, MP Mao, SH Goetz, MB Daar, ES Doms, RW OBrien, WA AF Doranz, BJ GrovitFerbas, K Sharron, MP Mao, SH Goetz, MB Daar, ES Doms, RW OBrien, WA TI A small-molecule inhibitor directed against the chemokine receptor CXCR4 prevents its use as an HIV-1 coreceptor SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; INFECTION; ENTRY; INDIVIDUALS; CCR5; GENE; MIP-1-ALPHA; PROGRESSION; LESTR/FUSIN; REPLICATION AB The chemokine receptor CXCR4 is the major coreceptor used for cellular entry by T cell-tropic human immunodeficiency virus (HIV)-1 strains, whereas CCR5 is used by macrophage (M)-tropic strains. Here we show that a small-molecule inhibitor, ALX40-4C, inhibits HIV-1 envelope (Env)-mediated membrane fusion and viral entry directly at the level of coreceptor use. ALX40-4C inhibited HIV-1 use of the coreceptor CXCR4 by T-and dual-tropic HIV-1 strains, whereas use of CCR5 by M-and dual-tropic strains was not inhibited. Dual-tropic viruses capable of using both CXCR4 and CCR5 were inhibited by ALX40-4C only when cells expressed CXCR4 alone. ALX40-4C blocked stromal-derived factor (SDF)-1 alpha-mediated activation of CXCR4 and binding of the monoclonal antibody 12G5 to cells expressing CXCR4. Overlap of the ALX40-4C binding site with that of 12G5 and SDF implicates direct blocking of Env interactions, rather than downregulation of receptor, as the mechanism of inhibition. Thus, ALX40-4C represents a small-molecule inhibitor of HIV-1 infection that acts directly against a chemokine receptor at the level of Env-mediated membrane fusion. C1 UNIV TEXAS,MED BRANCH,DEPT MED,GALVESTON,TX 77555. UNIV PENN,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. OI Goetz, Matthew/0000-0003-4542-992X FU NIAID NIH HHS [AI-38225, AI-40880, R01 AI040880, T32 AI007388]; NINDS NIH HHS [NS-35705] NR 34 TC 290 Z9 295 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD OCT 20 PY 1997 VL 186 IS 8 BP 1395 EP 1400 DI 10.1084/jem.186.8.1395 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA YC950 UT WOS:A1997YC95000025 PM 9334380 ER PT J AU Fishman, MC Olson, EN AF Fishman, MC Olson, EN TI Parsing the heart: Genetic modules for organ assembly SO CELL LA English DT Review ID MORPHOGENESIS; DROSOPHILA; TINMAN C1 UNIV TEXAS,SW MED CTR,DEPT MOL BIOL & ONCOL,DALLAS,TX 75235. RP Fishman, MC (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,CHARLESTOWN,MA 02129, USA. NR 20 TC 120 Z9 120 U1 2 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD OCT 17 PY 1997 VL 91 IS 2 BP 153 EP 156 DI 10.1016/S0092-8674(00)80397-9 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA YC350 UT WOS:A1997YC35000002 PM 9346232 ER PT J AU Hara, K Yonezawa, K Kozlowski, MT Sugimoto, T Andrabi, K Weng, QP Kasuga, M Nishimoto, I Avruch, J AF Hara, K Yonezawa, K Kozlowski, MT Sugimoto, T Andrabi, K Weng, QP Kasuga, M Nishimoto, I Avruch, J TI Regulation of eIF-4E BP1 phosphorylation by mTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID P70 S6 KINASE; PHOSPHATIDYLINOSITOL 3-KINASE; MAMMALIAN PROTEIN; SERINE RESIDUE; RAPAMYCIN; YEAST; COMPLEX; TARGET; FKBP12-RAPAMYCIN; FKBP12 AB The proteins eIF-4E BP1 and p70 S6 kinase each undergo an insulin/mitogen-stimulated phosphorylation in situ that is partially inhibited by rapamycin. Previous work has established that the protein known as mTOR/RAFT-1/FRAP is the target through which the rapamycin.FKBP12 complex acts to dephosphorylate/deactivate the p70 S6 kinase; thus, some mTOR mutants that have lost the ability to bind to the rapamycin.FKBP12 complex in vitro can protect the p70 S6 kinase against rapamycin-induced dephosphorylation/deactivation in situ, We show herein that such mTOR mutants also protect eIF-4E BP1 against rapamycin-induced dephosphorylation, and for both p70 S6 kinase and eIF-4E BP1, such protection requires that the rapamycin-resistant mTOR variant retains an active catalytic domain, In contrast, mutants of p70 S6 kinase rendered intrinsically resistant to inhibition by rapamycin in situ are not able to protect coexpressed eIF-4E BP1 from rapamycin-induced dephosphorylation. We conclude that mTOR is an upstream regulator of eIF-4E BP1 as well as the p70 S6 kinase; moreover, these two mTOR targets are regulated in a parallel rather than sequential manner. C1 MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. KOBE UNIV,BIOSIGNAL RES CTR,KOBE,HYOGO 657,JAPAN. KOBE UNIV,SCH MED,DEPT INTERNAL MED 2,KOBE,HYOGO 657,JAPAN. KEIO UNIV,SCH MED,DEPT PHARMACOL & NEUROSCI,TOKYO 160,JAPAN. FU NIDDK NIH HHS [DK17776] NR 33 TC 314 Z9 316 U1 1 U2 10 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 17 PY 1997 VL 272 IS 42 BP 26457 EP 26463 DI 10.1074/jbc.272.42.26457 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YB139 UT WOS:A1997YB13900056 PM 9334222 ER PT J AU Huang, XD Atwood, CS Moir, RD Hartshorn, MA Vonsattel, JP Tanzi, RE Bush, AI AF Huang, XD Atwood, CS Moir, RD Hartshorn, MA Vonsattel, JP Tanzi, RE Bush, AI TI Zinc-induced Alzheimer's A beta 1-40 aggregation is mediated by conformational factors SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BETA-AMYLOID PEPTIDES; PROTEIN-PRECURSOR; CORTICAL-NEURONS; DISEASE BRAINS; NEUROTOXICITY; DEPOSITION; PATHOGENESIS; FRAGMENTS; PLATELETS; CLEAVAGE AB The heterogeneous precipitates of A beta that accumulate in the brain cortex in Alzheimer's disease possess varying degrees of resistance to resolubilization. We previously found that A beta 1-40 is rapidly precipitated in vitro by physiological concentrations of zinc, a neurochemical that is highly abundant in brain compartments where A beta is most likely to precipitate. We now present evidence that the zinc-induced precipitation of A beta is mediated by a peptide dimer and favored by conditions that promote alpha-helical and diminish beta-sheet conformations. The manner in which the synthetic peptide is solubilized was critical to its behavior in vitro. Zinc-induced A beta aggregation was dependent upon the presence of NaCl, was enhanced when the peptide stock solution was stored frozen. The A beta aggregates induced by zinc were reversible by chelation, but could then be reprecipitated by zinc for several cycles, indicating that the peptide's conformation is probably preserved in the zinc-mediated assembly. In contrast, A beta aggregates induced by low pH (5.5) were not resolubilized by returning the pH milieu to 7.4. The zinc-A beta interaction exhibits features resembling the gelation process of zinc-mediated fibrin assembly, suggesting that, in events such as clot formation or injury, reversible A beta assembly could be physiologically purposive. Such a mechanism is contemplated in the early evolution of diffuse plaques in Alzheimer's disease and suggests a possible therapeutic strategy for the resolubilization of some forms of A beta deposit in the disease. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,GENET & AGING UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RI Bush, Ashley/A-1186-2007 OI Bush, Ashley/0000-0001-8259-9069 FU NIA NIH HHS [1R29AG126801] NR 52 TC 259 Z9 267 U1 1 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 17 PY 1997 VL 272 IS 42 BP 26464 EP 26470 DI 10.1074/jbc.272.42.26464 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YB139 UT WOS:A1997YB13900057 PM 9334223 ER PT J AU Buchsbaum, MS Trestman, RL Hazlett, E Siegel, BV Schaefer, CH LuuHsia, C Tang, C Herrera, S Solimando, AC Losonczy, M Serby, M Silverman, J Siever, LJ AF Buchsbaum, MS Trestman, RL Hazlett, E Siegel, BV Schaefer, CH LuuHsia, C Tang, C Herrera, S Solimando, AC Losonczy, M Serby, M Silverman, J Siever, LJ TI Regional cerebral blood flow during the Wisconsin Card Sort Test in schizotypal personality disorder SO SCHIZOPHRENIA RESEARCH LA English DT Article DE single photon emission computed tomography; frontal lobe; neuropsychology; schizophrenia ID DORSOLATERAL PREFRONTAL CORTEX; HIPPOCAMPAL PYRAMIDAL CELL; FRONTAL-LOBE LESIONS; SCHIZOPHRENIC-PATIENTS; PHYSIOLOGICAL DYSFUNCTION; TEST-PERFORMANCE; ACTIVATION; SPECT; ABNORMALITIES; AMPHETAMINE AB Regional cerebral blood flow (rCBF) was measured by single photon emission computed tomography in 10 patients with schizotypal personality disorder (SPD) and nine age-and sex-matched normal volunteers. Subjects performed both the Wisconsin Card Sort Test (WCST) and a control task, the Symbol Matching Test (SMT). Four-way analyses of variance were performed to assess relative rCBF of the prefrontal cortex and of the medial temporal region. Normal volunteers showed more marked activation in the precentral gyrus, while SPD patients showed greater activation in the middle frontal gyrus. Relative flow in the left prefrontal cortex was correlated with better WCST performance in normal volunteers. SPD patients, however, showed no such correlations in the left prefrontal cortex, but demonstrated correlations of good and bad performance with CBF in the right middle and inferior frontal gyrus, respectively. Thus, at least some SPD patients demonstrate abnormal patterns of prefrontal activation, perhaps as a compensation for dysfunction in other regions. (C) 1997 Elsevier Science B.V. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90073. W LOS ANGELES DEPT VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. BRONX VET AFFAIRS MED CTR,DEPT PSYCHIAT,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,DEPT NUCL MED,BRONX,NY 10468. FDR VET AFFAIRS MED CTR,PSYCHIAT SERV,MONTROSE,NY 10548. RP Buchsbaum, MS (reprint author), CUNY MT SINAI SCH MED,DEPT PSYCHIAT,BOX 1505,1 GUSTAVE L LEVY PL,NEW YORK,NY 10029, USA. FU NIMH NIH HHS [5R37MH42827-02, MH40071] NR 44 TC 44 Z9 44 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD OCT 17 PY 1997 VL 27 IS 1 BP 21 EP 28 DI 10.1016/S0920-9964(97)00081-9 PG 8 WC Psychiatry SC Psychiatry GA YD369 UT WOS:A1997YD36900003 PM 9373891 ER PT J AU Buchsbaum, MS Yang, S Hazlett, E Siegel, BV Germans, M Haznedar, M OFlaithbheartaigh, S Wei, TC Silverman, J Siever, LJ AF Buchsbaum, MS Yang, S Hazlett, E Siegel, BV Germans, M Haznedar, M OFlaithbheartaigh, S Wei, TC Silverman, J Siever, LJ TI Ventricular volume and asymmetry in schizotypal personality disorder and schizophrenia assessed with magnetic resonance imaging SO SCHIZOPHRENIA RESEARCH LA English DT Article DE temporal horn; laterality; ventricle-brain ratio; memory; duration of illness ID DEVELOPMENTAL BRAIN ABNORMALITIES; DORSOLATERAL PREFRONTAL CORTEX; STRUCTURED INTERVIEW; COMPUTED-TOMOGRAPHY; ENLARGEMENT; DEFICITS; MOTHERS; RISK; DYSFUNCTION; DIAGNOSIS AB Magnetic resonance imaging (MRI) was performed in 12 patients with schizotypal personality disorder (SPD), 11 patients with chronic schizophrenia, and 23 age- and sex-matched normal volunteers. MRI slices were acquired in the axial plane at 1.2-mm intervals, and the ventricles were traced on every other slice. The lateral ventricular system was divided into the anterior horn, temporal horn, and dorsal lateral ventricle. Schizophrenic patients had larger left anterior and temporal horns than the normal volunteers. Size of the left anterior and temporal horn in SPD patients was intermediate between those of normal volunteers and schizophrenic patients and differed significantly from schizophrenic patients. The left-minus-right difference was larger in schizophrenic patients than in normal volunteers or SPD patients. Thus, in their structural brain characteristics, as well as in their clinical symptomatology, SPD patients evidence, in attenuated form, abnormalities resembling those found in full-ledged schizophrenia. The findings suggest that decreased left hemispheric volume, in frontal and temporal regions, may characterize both psychotic and non-psychotic disorders of the schizophrenia spectrum. (C) 1997 Elsevier Science B.V. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. DVA MED CTR,PSYCHIAT SERV,BRONX,NY 10468. RP Buchsbaum, MS (reprint author), CUNY MT SINAI SCH MED,DEPT PSYCHIAT,BOX 1505,1 GUSTAVE L LEVY PL,NEW YORK,NY 10029, USA. FU NIMH NIH HHS [MH42827, MH48858, MH40071] NR 43 TC 82 Z9 82 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD OCT 17 PY 1997 VL 27 IS 1 BP 45 EP 53 DI 10.1016/S0920-9964(97)00087-X PG 9 WC Psychiatry SC Psychiatry GA YD369 UT WOS:A1997YD36900006 PM 9373894 ER PT J AU Finch, CE Tanzi, RE AF Finch, CE Tanzi, RE TI Genetics of aging SO SCIENCE LA English DT Article ID CAENORHABDITIS-ELEGANS; ALZHEIMERS-DISEASE; SACCHAROMYCES-CEREVISIAE; HUMAN LONGEVITY; LIFE-SPAN; OXIDATIVE STRESS; TRANSGENIC MICE; CELL-DEATH; AGE; SENESCENCE AB The role of genetics in determining life-span is complex and paradoxical, Although the heritability of life-span is relatively minor, some genetic variants significantly modify senescence of mammals and invertebrates, with both positive and negative impacts on age-related disorders and life-spans, In certain examples, the gene variants alter metabolic pathways, which could thereby mediate interactions with nutritional and other environmental factors that influence life-span, Given the relatively minor effect and variable penetrance of genetic risk factors that appear to affect survival and health at advanced ages, life-style and other environmental influences may profoundly modify outcomes of aging. C1 UNIV SO CALIF,DEPT BIOL SCI,LOS ANGELES,CA 90089. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,GENET & AGING UNIT,CHARLESTOWN,MA 02129. RP Finch, CE (reprint author), UNIV SO CALIF,ETHEL PERCY ANDRUS GERONTOL CTR,NEUROGERONTOL DIV,3715 MCCLINTOCK AVE,LOS ANGELES,CA 90089, USA. NR 89 TC 283 Z9 292 U1 2 U2 18 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 17 PY 1997 VL 278 IS 5337 BP 407 EP 411 DI 10.1126/science.278.5337.407 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YB355 UT WOS:A1997YB35500031 PM 9334291 ER PT J AU Bonni, A Sun, Y NadalVicens, M Bhatt, A Frank, DA Rozovsky, I Stahl, N Yancopoulos, GD Greenberg, ME AF Bonni, A Sun, Y NadalVicens, M Bhatt, A Frank, DA Rozovsky, I Stahl, N Yancopoulos, GD Greenberg, ME TI Regulation of gliogenesis in the central nervous system by the JAK-STAT signaling pathway SO SCIENCE LA English DT Article ID LEUKEMIA INHIBITORY FACTOR; FIBRILLARY ACIDIC PROTEIN; CEREBRAL-CORTEX; CNTF RECEPTOR; TRANSCRIPTION; CELLS; GENE; GFAP; DIFFERENTIATION; NEUROGENESIS AB A mechanism by which members of the ciliary neurotrophic factor (CNTF)-leukemia inhibitory factor cytokine family regulate gliogenesis in the developing mammalian central nervous system was characterized, Activation of the CNTF receptor promoted differentiation of cerebral cortical precursor cells into astrocytes and inhibited differentiation of cortical precursors along a neuronal lineage, Although CNTF stimulated both the Janus kinase-signal transducer and activator of transcription (JAK-STAT) and Ras-mitogen-activated protein kinase signaling pathways in cortical precursor cells, the JAK-STAT signaling pathway selectively enhanced differentiation of these precursors along a glial lineage, These findings suggest that cytokine activation of the JAK-STAT signaling pathway may be a mechanism by which cell fate is controlled during mammalian development. C1 CHILDRENS HOSP,DIV NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. UNIV SO CALIF,ETHEL PERCY ANDRUS GERONTOL CTR,NEUROGERONTOL DIV,LOS ANGELES,CA 90089. UNIV SO CALIF,DEPT SCI BIOL,LOS ANGELES,CA 90089. REGENERON PHARMACEUT INC,TARRYTOWN,NY 10591. FU NCI NIH HHS [R01 CA43855]; NICHD NIH HHS [NIHP30-HD 18655] NR 35 TC 656 Z9 676 U1 3 U2 27 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 17 PY 1997 VL 278 IS 5337 BP 477 EP 483 DI 10.1126/science.278.5337.477 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YB355 UT WOS:A1997YB35500049 PM 9334309 ER PT J AU Huang, YY Yuan, ZM Ishiko, T Nakada, S Utsugisawa, T Kato, T Kharbanda, S Kufe, DW AF Huang, YY Yuan, ZM Ishiko, T Nakada, S Utsugisawa, T Kato, T Kharbanda, S Kufe, DW TI Pro-apoptotic effect of the c-Abl tyrosine kinase in the cellular response to 1-beta-D-arabinofuranosylcytosine SO ONCOGENE LA English DT Article DE ara-C; c-Abl kinase; apoptosis; p53 ID NF-KAPPA-B; ACTIVATED PROTEIN-KINASE; INDEPENDENT MECHANISMS; DNA-DAMAGE; P53; STRESS; CYCLE; GROWTH; DEATH; LOCALIZATION AB Treatment of cells with the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents is associated with activation of the c-Abl protein tyrosine kinase. The functional role of c-Abl in the response to DNA damage, however, remains unclear. The present studies demonstrate that cells expressing a dominant negative, kinase-inactive c-Abl (K-R) are resistant to killing by ara-C. The expression of c-Abl (K-R) blocked ara-C-induced apoptosis by a mechanism that is at least in part independent of the p53 tumor suppressor. Cells null for c-Abl also exhibited resistance to induction of apoptosis. These findings provide support for a pro-apoptotic function of c-Abl in the response to certain genotoxic drugs. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA66996, CA29431] NR 34 TC 39 Z9 39 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 16 PY 1997 VL 15 IS 16 BP 1947 EP 1952 DI 10.1038/sj.onc.1201376 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA YA872 UT WOS:A1997YA87200009 PM 9365241 ER PT J AU Matchar, DB Samsa, GP Matthews, JR Ancukiewicz, M Parmigiani, G Hasselblad, V Wolf, PA DAgostino, RB Lipscomb, J AF Matchar, DB Samsa, GP Matthews, JR Ancukiewicz, M Parmigiani, G Hasselblad, V Wolf, PA DAgostino, RB Lipscomb, J TI The stroke prevention policy model: Linking evidence and clinical decisions SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID COST-EFFECTIVENESS; MEDICINE AB Simulation models that support decision and cost-effectiveness analysis can further the goals of evidence-based medicine by facilitating the synthesis of information from several sources into a single comprehensive structure. The Stroke Prevention Policy Model (SPPM) performs this function for the clinical and policy questions that surround stroke prevention. This paper first describes the basic structure and functions of the SPPM, concentrating on the role of large databases (broadly defined as any database that contains many patients, regardless of study design) in providing the SPPM inputs. Next, recognizing that the use of modeling continues to be a source of some controversy in the medical community, it; discusses the philosophical underpinnings of the SPPM. Finally, it discusses conclusions in the context of both stroke prevention and other complex medical decisions. We conclude that despite the difficulties in developing comprehensive models (for example, the length and complexity of model development and validation processes, the proprietary nature of data sources, and the necessity for developing new software), the benefits of such models exceed the costs of continuing to rely on more conventional methods. Although they should not replace the clinician in decision making; comprehensive models based on the best available evidence from large databases can support decision making in medicine. C1 DUKE UNIV,MED CTR,SCH MED,DEPT COMMUNITY & FAMILY MED,DIV BIOMETRY,DURHAM,NC 27705. MASSACHUSETTS GEN HOSP,DEPT MED,DIV RADIAT ONCOL,BOSTON,MA 02114. DUKE UNIV,INST STAT & DECIS SCI,DURHAM,NC 27708. BOSTON UNIV,SCH MED,DEPT MED,BOSTON,MA 02118. BOSTON UNIV,SCH MED,EVANS MEM DEPT CLIN RES,PREVENT MED & EPIDEMIOL SECT,BOSTON,MA 02118. BOSTON UNIV,COLL ARTS & SCI,DEPT MATH,BOSTON,MA 02215. DUKE UNIV,SANFORD INST PUBL POLICY,DURHAM,NC 27708. BOSTON UNIV,MED CTR,BOSTON,MA. RP Matchar, DB (reprint author), DUKE UNIV,CTR CLIN HLTH POLICY RES,1ST UNION TOWER,SUITE 230,2200 W MAIN ST,DURHAM,NC 27705, USA. OI Matthews, J Rosser/0000-0002-8304-2948; Matchar, David/0000-0003-3020-2108 FU NHLBI NIH HHS [N01-HL-38038]; NINDS NIH HHS [2-RO1-NS-17950-16]; PHS HHS [282-81-0028] NR 32 TC 48 Z9 48 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD OCT 15 PY 1997 VL 127 IS 8 BP 704 EP 711 PN 2 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA YB385 UT WOS:A1997YB38500009 PM 9382384 ER PT J AU McHorney, CA AF McHorney, CA TI Generic health measurement: Past accomplishments and a measurement paradigm for the 21st century SO ANNALS OF INTERNAL MEDICINE LA English DT Review ID SICKNESS IMPACT PROFILE; QUALITY-OF-LIFE; FUNCTIONAL STATUS; RASCH ANALYSIS; PRIMARY CARE; RHEUMATOID-ARTHRITIS; POPULATION SURVEY; ITEM SELECTION; RESPONSE RATES; SURVEY SF-36 AB Generic health surveys have been proposed for use in increasingly diverse applications and populations. This paper describes the history of generic tools in the past 30 years and suggests a more modern measurement platform for advances in the 21st century. Many generic tools lack the precision required for effective health care decision making. A meaningful goal for the next era of development of generic measures should be the generation of equiprecise measurement for generic health concepts. Equiprecise tests yield measures of equal precision at all levels of the underlying construct. Equiprecise measurement can be achieved through conjoint use of computerized-adaptive testing as the survey platform and item response theory as the measurement theory. C1 UNIV WISCONSIN,SCH MED,MADISON,WI. RP McHorney, CA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL & LAB MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 102 TC 153 Z9 155 U1 23 U2 29 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD OCT 15 PY 1997 VL 127 IS 8 BP 743 EP 750 PN 2 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA YB385 UT WOS:A1997YB38500016 PM 9382391 ER PT J AU Weisdorf, DJ Billett, AL Hannan, P Ritz, J Sallan, SE Steinbuch, M Ramsay, NKC AF Weisdorf, DJ Billett, AL Hannan, P Ritz, J Sallan, SE Steinbuch, M Ramsay, NKC TI Autologous versus unrelated donor allogeneic marrow transplantation for acute lymphoblastic leukemia SO BLOOD LA English DT Article ID VERSUS-HOST DISEASE; BONE-MARROW; HIGH-RISK; IDENTICAL SIBLINGS; PLUS COMPLEMENT; 1ST REMISSION; FOLLOW-UP; CHEMOTHERAPY; ADULTS; CHILDREN AB Bone marrow transplantation (BMT) can cure patients with high-risk or recurrent acute lymphoblastic leukemia (ALL). Those lacking a related donor can receive either autologous or histocompatible unrelated donor (URD) marrow. Autotransplantation may result in higher risk of relapse, whereas URD allografts, although associated with serious posttransplant toxicities, may reduce relapse risk. Six years (1987 to 1993) of consecutive autologous BMT (University of Minnesota, Dana Farber Cancer Institute; n = 214) were compared with URD transplants (National Marrow Donor Program; n = 337). Most transplants (70% autologous, 48% URD) were in early remission (first or second complete remission [CR1 or CR2]); 376 patients (75% autologous, 64% URD) were less than 18 years old. Autologous BMT led to significantly lower transplant-related mortality (TRM; relative risk [RR] 0.35; P = .001). URD transplantation offered greater protection against relapse (autologous RR 3.1; P = .001). Patients greater than 18 years old, women, and BMT recipients beyond CR2 had higher TRM, whereas adults, BMT recipients in CR2+, or BMT recipients during 1991 through 1993 had significantly more relapse. After 25 months median follow-up, 100 URD and 56 autologous recipients survive leukemia free. URD BMT in CR2 resulted in superior disease-free survival (DFS), especially for adult patients. Multivariate analysis showed superior DFS for children, men, and BMT during CR1 or 2. Autologous and URD BMT can extend survival for a minority of patients unlikely to be cured by chemotherapy, and the results with either technique are comparable. Greater toxicity and TRM after URD BMT are counterbalanced by better protection against relapse. Prospective studies addressing additional clinical variables are needed to guide clinical decision making about transplant choices for patients with ALL. (C) 1997 by The American Society of Hematology. C1 UNIV MINNESOTA,DEPT MED,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT PEDIAT,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,BONE MARROW TRANSPLANT PROGRAM,MINNEAPOLIS,MN 55455. DANA FARBER CANC INST,BOSTON,MA 02115. NATL MARROW DONOR PROGRAM,MINNEAPOLIS,MN. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA21737, CA66996, CA68484] NR 38 TC 65 Z9 65 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 1997 VL 90 IS 8 BP 2962 EP 2968 PG 7 WC Hematology SC Hematology GA YC736 UT WOS:A1997YC73600010 PM 9376576 ER PT J AU Aguiar, RCT Chase, A Coulthard, S Macdonald, DHC Carapeti, M Reiter, A Sohal, J Lennard, A Goldman, JM Cross, NCP AF Aguiar, RCT Chase, A Coulthard, S Macdonald, DHC Carapeti, M Reiter, A Sohal, J Lennard, A Goldman, JM Cross, NCP TI Abnormalities of chromosome band 8p11 in leukemia: Two clinical syndromes can be distinguished on the basis of MOZ involvement SO BLOOD LA English DT Article ID ACUTE MONOCYTIC LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; MYELOPROLIFERATIVE DISORDER; MYELOMONOCYTIC LEUKEMIA; TRANSLOCATION; FUSION; GENE; PROTEIN; CBP; BCR AB Two distinct leukemia syndromes are associated with abnormalities of chromosome band 8p11. First, a myeloproliferative disorder with features characteristic of both chronic myeloid leukemia and non-Hodgkin's lymphoma and second, an acute myeloid leukemia (AML) with French-American-British (FAB) M4/5 morphology and prominent erythrophagocytosis. The two syndromes are exemplified by a t(8;13)(p11;q12) and a t(8;16)(p11;p13), respectively, but cytogenetic variants of both have been described. Recently, the t(8;16) has been cloned and shown to fuse the MOZ gene at 8p11 to the CBP gene at 16p13. We have used fluorescence in situ hybridization (FISH), Southern blotting, and reverse transcriptase-polymerase chain reaction (RT-PCR) to refine the 8p11 breakpoint in three cases with t(8;13)(p11;q12) and in a single case of AML-M5 with a clinical picture apparently identical to that found in patients with a t(8;16), but characterized by an inv(8)(p11q13). FISH analysis was performed with several 8p11 CEPH yeast artificial chromosome (YAC) clones. YAC 782H11 was centromeric to the one case with t(8;13) tested, but was telomeric to the inv(8). YAC 847B12 was telomeric to both the t(8;13) and the inv(8), whereas YAC 829D12 was centromeric to the t(8;13), but split by the inv(8). Southern blotting and PCR of YAC 829D12 showed that it contained the MOZ gene. A 900-bp MOZ fragment encompassing the published t(8;16) breakpoint was amplified by PCR from normal peripheral blood leukocyte cDNA and used to probe Southern blots of patient DNA. A rearrangement was detected in the case with inv(8), but not in any of the three cases with t(8;13). Southern blotting with a CBP probe and RT-PCR with MOZ and CBP primers suggested that the inv(8) does not result in a cryptic MOZ-CBP fusion. It is likely, therefore, that MOZ is fused to a novel gene at 8q13 in this case, We conclude that the t(8;13) breakpoint is flanked by YACs 782H11 and 847B12 and is at least 1 Mb telomeric to MOZ. MOZ is involved, however, in a new variant of the t(8;16). (C) 1997 by The American Society of Hematology. C1 HAMMERSMITH HOSP,ROYAL POSTGRAD MED SCH,LRF CTR ADULT LEUKAEMIA,LONDON W12 0NN,ENGLAND. DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. ROYAL VICTORIA INFIRM,DEPT HAEMATOL,NEWCASTLE TYNE NE1 4LP,TYNE & WEAR,ENGLAND. RI Cross, Nicholas/B-4817-2009 OI Cross, Nicholas/0000-0001-5481-2555 NR 33 TC 74 Z9 75 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 1997 VL 90 IS 8 BP 3130 EP 3135 PG 6 WC Hematology SC Hematology GA YC736 UT WOS:A1997YC73600028 PM 9376594 ER PT J AU Still, IH Chernova, O Hurd, D Stone, RM Cowell, JK AF Still, IH Chernova, O Hurd, D Stone, RM Cowell, JK TI Molecular characterization of the t(8;13)(p11;q12) translocation associated with an atypical myeloproliferative disorder: Evidence for three discrete loci involved in myeloid leukemias on 8p11 SO BLOOD LA English DT Article ID ACUTE MONOCYTIC LEUKEMIA; MYELOMONOCYTIC LEUKEMIA; LYMPHOBLASTIC LYMPHOMA; REGION; MAP; T(8; IDENTIFICATION; CHROMOSOME-13; ABNORMALITIES; MYELOFIBROSIS AB A reciprocal chromosome translocation between 13q12 and 8p11 is the consistent cytogenetic abnormality seen in a nonspecific myeloproliferative disorder that is associated with T-cell leukemia/lymphoma and peripheral blood eosinophilia. Detailed molecular analyses of the translocation breakpoints associated with this rearrangement have not been reported to date, We have now generated somatic cell hybrids from a newly described patient with this specific structural rearrangement and analyzed the breakpoints on the derivative chromosomes, We have shown that the breakpoint on chromosome 13 lies within a 300- to 500-kb region defined by the KIAA177 gene and D13S1123 marker, In addition, we have identified a 1.2-Mb YAC, 959A4, that crosses the translocation breakpoint on the short arm of chromosome 8 in this patient. The location of this breakpoint in 8p11 is distinct from the t(8;16) and t(8;22) translocations associated with M4/M5 myeloid leukemias, and suggests that three distinct loci located within 8p11 are involved in the pathogenesis of myeloid neoplasias. (C) 1997 by The American Society of Hematology. C1 CLEVELAND CLIN FDN,RES INST,DEPT NEUROSCI NC30,CLEVELAND,OH 44195. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC. DANA FARBER CANC INST,BOSTON,MA 02115. OI Cowell, John/0000-0002-2079-5950 NR 28 TC 44 Z9 46 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 1997 VL 90 IS 8 BP 3136 EP 3141 PG 6 WC Hematology SC Hematology GA YC736 UT WOS:A1997YC73600029 PM 9376595 ER PT J AU Tsukada, J Misago, M Serino, Y Ogawa, R Murakami, S Nakanishi, M Tonai, S Kominato, Y Morimoto, I Auron, PE Eto, S AF Tsukada, J Misago, M Serino, Y Ogawa, R Murakami, S Nakanishi, M Tonai, S Kominato, Y Morimoto, I Auron, PE Eto, S TI Human T-cell leukemia virus type I tax transactivates the promoter of human prointerleukin-1 beta gene through association with two transcription factors, nuclear factor-interleukin-6 and Spi-1 SO BLOOD LA English DT Article ID NF-KAPPA-B; HTLV-I; DNA-BINDING; INTERLEUKIN-8 GENE; ACTIVATION DOMAIN; TRANS-ACTIVATION; INFECTED-CELLS; IL-1-BETA GENE; ESSENTIAL SITE; BZIP PROTEINS AB The human T-cell leukemia virus type I (HTLV-I), which infects a wide variety of mammalian cells including monocytes and macrophages, encodes a transactivating protein designated as Tax. We now report that Tax induces the human prointerleukin-1 beta (IL1B) gene promoter in monocytic cells. In our transient transfection assays using human THP-1 monocytic cells, a chloramphenicol acetyltransferase (CAT) construct containing the IL1B promoter sequence between positions -131 and +12 showed an approximately 90-fold increase in activity following cotransfection of a Tax expression vector. Moreover, Tax synergized with lipopolysaccharide (LPS) to induce the IL1B promoter activity. Analyses of specific nucleotide substitutions further indicated that the Tax-induced transcriptional activation requires two transcription factor binding motifs within the IL1B promoter; one is a binding site for nuclear factor (NF)-IL6 (CCAAT/enhancer binding protein beta, C/EBP beta), which belongs to the basic region-leucine zipper (bZIP) family and the other for Spi-1 (PU.1), which is an Ets family protein found principally in monocytes, macrophages, and B lymphocytes. In electrophoretic mobility shift assays (EMSA) using in vivo THP-1 nuclear extracts, Tax expression in THP-1 monocytic cells significantly increased binding of the two factors to their target IL1B promoter sequences. However, in contrast to NF-IL6 and Spi-1, DNA binding activity of Oct-1, an ubiquitously expressed octamer-binding protein was not affected by Tax. Additional EMSA using in vitro translated proteins also showed that recombinant Tax enhances DNA binding of both of recombinant NF-IL6 and Spi-1 proteins. These data were supported by our glutathione S-transferase (GST)-pull-down data, which indicated that Tax physically interacts with the two proteins. Based on the results obtained from the present study, we conclude that the IL1B promoter is a Tax-responsive sequence as a result of ability of Tax to induce binding of NF-IL6 and Spi-1 to the IL1B promoter sequence through protein-protein interaction. (C) 1997 by The American Society of Hematology. C1 UNIV OCCUPAT & ENVIRONM HLTH,SCH HLTH SCI,KITAKYUSHU,FUKUOKA 807,JAPAN. TOYAMA MED & PHARMACEUT UNIV,TOYAMA,JAPAN. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP Tsukada, J (reprint author), UNIV OCCUPAT & ENVIRONM HLTH,SCH MED,DEPT INTERNAL MED 1,YAHATANISHI KU,1-1 ISEIGAOKA,KITAKYUSHU,FUKUOKA 807,JAPAN. NR 66 TC 33 Z9 33 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 1997 VL 90 IS 8 BP 3142 EP 3153 PG 12 WC Hematology SC Hematology GA YC736 UT WOS:A1997YC73600030 PM 9376596 ER PT J AU Hill, GR Crawford, JM Cooke, KR Brinson, YS Pan, LY Ferrara, JLM AF Hill, GR Crawford, JM Cooke, KR Brinson, YS Pan, LY Ferrara, JLM TI Total body irradiation and acute graft-versus-host disease: The role of gastrointestinal damage and inflammatory cytokines SO BLOOD LA English DT Article ID TUMOR-NECROSIS-FACTOR; BONE-MARROW TRANSPLANTATION; DONOR T-CELLS; FACTOR-ALPHA; IONIZING-RADIATION; MYELOID-LEUKEMIA; APLASTIC-ANEMIA; SCID MICE; ENDOTOXIN; CYCLOPHOSPHAMIDE AB The influence of bone marrow transplantation (BMT) conditioning regimens on the incidence and severity of graft-versus-host disease (GVHD) has been suggested in clinical BMT. Using murine BMT models, we show here an increase in GVHD severity in several donor-recipient strain combinations after intensification of the conditioning regimen by increasing the total body irradiation (TBI) dose from 900 cGy to 1,300 cGy. Increased GVHD was mediated by systemic increases in tumor necrosis factor alpha (TNF alpha). Histologic analysis of gastrointestinal tracts showed synergistic damage by increased TBI and allogeneic donor cells that permitted increased translocation of lipopolysacharide (LPS) into the systemic circulation. In vitro, LPS triggered excess TNF alpha from macrophages primed by the GVH reaction. In addition, macrophages isolated within 4 hours of conditioning were primed in proportion to the TBI dose itself to secrete TNF alpha. Thus, the higher TBI dose increased macrophage priming and increased gut damage after allogeneic BMT, causing higher systemic levels of inflammatory cytokines and subsequent severe GVHD. These data highlight the importance of conditioning in GVHD pathophysiology and suggest that interventions to prevent LPS stimulation of primed macrophages may limit the severity of GVHD after intensive conditioning for allogeneic BMI. (C) 1997 by The American Society of Hematology. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. YALE UNIV,SCH MED,DEPT PATHOL,NEW HAVEN,CT. RI Hill, Geoffrey/O-2630-2016 OI Hill, Geoffrey/0000-0003-2994-0429 FU NCI NIH HHS [CA39542]; NHLBI NIH HHS [HL55162] NR 51 TC 519 Z9 527 U1 3 U2 9 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 15 PY 1997 VL 90 IS 8 BP 3204 EP 3213 PG 10 WC Hematology SC Hematology GA YC736 UT WOS:A1997YC73600038 PM 9376604 ER PT J AU Waters, GS Caplan, D AF Waters, GS Caplan, D TI The role of working memory in sentence processing: Evidence from Parkinson's disease SO BRAIN AND LANGUAGE LA English DT Meeting Abstract ID COMPREHENSION; CAPACITY C1 MCGILL UNIV,SCH COMMUN SCI & DISORDERS,MONTREAL,PQ H3A 2T5,CANADA. MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,BOSTON,MA 02114. NR 2 TC 8 Z9 8 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD OCT 15 PY 1997 VL 60 IS 1 BP 64 EP 66 PG 3 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA YA053 UT WOS:A1997YA05300022 ER PT J AU Caplan, D Alpert, N Waters, G AF Caplan, D Alpert, N Waters, G TI Effects of syntactic structure and number of propositions on patterns of regional cerebral blood flow SO BRAIN AND LANGUAGE LA English DT Meeting Abstract ID COMPREHENSION C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROPSYCHOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. NR 4 TC 1 Z9 1 U1 3 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD OCT 15 PY 1997 VL 60 IS 1 BP 66 EP 69 PG 4 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA YA053 UT WOS:A1997YA05300023 ER PT J AU Melvold, J Kohn, SE AF Melvold, J Kohn, SE TI So alike and yet so different: Evidence for two distinct lexical-phonological deficits in fluent aphasia SO BRAIN AND LANGUAGE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 3 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD OCT 15 PY 1997 VL 60 IS 1 BP 137 EP 140 PG 4 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA YA053 UT WOS:A1997YA05300047 ER PT J AU Titone, D Wingfield, A Caplan, D Waters, G Prentice, K AF Titone, D Wingfield, A Caplan, D Waters, G Prentice, K TI Discourse encoding strategies of right hemisphere damaged patients SO BRAIN AND LANGUAGE LA English DT Meeting Abstract C1 BRANDEIS UNIV,WALTHAM,MA 02254. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MCGILL UNIV,MONTREAL,PQ H3A 2T5,CANADA. NR 5 TC 0 Z9 0 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD OCT 15 PY 1997 VL 60 IS 1 BP 183 EP 185 PG 3 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA YA053 UT WOS:A1997YA05300065 ER PT J AU Roodman, GD AF Roodman, GD TI Mechanisms of bone lesions in multiple myeloma and lymphoma SO CANCER LA English DT Article; Proceedings Paper CT Symposium on Skeletal Complications of Malignancy CY APR 19-20, 1997 CL NIH, NATCHER CTR, BETHESDA, MD SP Paget Fdn HO NIH, NATCHER CTR DE myeloma; lymphoma; 1,25-(OH)(2)D-3; parathyroid hormone related protein; bone lesions; interleukin-1 ID T-CELL LEUKEMIA; HORMONE-RELATED PROTEIN; MARROW STROMAL CELLS; INTERLEUKIN-6 SECRETION; ADHESION MOLECULES; PAGETS-DISEASE; GIANT-CELLS; TUMOR-CELLS; HYPERCALCEMIA; RESORPTION AB BACKGROUND. Bone lesions and hypercalcemia occur rarely in patients with hematologic malignancies, except those patients with multiple myeloma and adult T-cell leukemia/lymphoma (ATL) associated with the human T-cell leukemia/lymphoma virus-1 (HTLV-1) virus. The primary mechanism for bone destruction in patients with myeloma and lymphoma is increased osteoclastic bone resorption. In patients with multiple myeloma, new bone formation is also inhibited. Mediators including lymphotoxin, interleukin-1 beta, parathyroid hormone related protein (PTHrP), and interleukin-6, produced by the myeloma cells or by marrow stromal cells in response to myeloma cells, have been implicated as osteoclast-activating factors (OAF) in multiple myeloma. However, most studies to identify OAF produced by myeloma cells have been inconclusive. METHODS. To try to identify the OAF produced by myeloma cells, we developed an in vivo model of human myeloma bone disease using the ARH-77 myeloma cell line transplanted into severe combined immunodeficiency mice. RESULTS. We found that a novel cytokine(s) may be responsible for bone destruction. Interleukin-1 and PTHrP mediate bone destruction in patients with ATL. These factors can be detected in media conditioned by ATL cells or by lymphocytes infected with HTLV-1. Furthermore, serum PTHrP levels are increased in ATL patients. In patients with Hodgkin's disease or other types of non-Hodgkin's lymphoma, 1,25-(OH)(2)D-3 or PTHrP is produced by the lymphoma cells and mediates bone destruction. Chemotherapy or resection of the lymphoma decreases 1,25-(OH)2D(3) levels and hypercalcemia in these patients. CONCLUSION. Thus, OAF produced locally by the tumor or the marrow microenvironment play an important role in the bone destruction seen in patients with hematologic malignancies. (C) 1997 American Cancer Society. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED HEMATOL,SAN ANTONIO,TX 78284. FU NCI NIH HHS [CA 69136-01A1] NR 38 TC 117 Z9 119 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD OCT 15 PY 1997 VL 80 IS 8 SU S BP 1557 EP 1563 DI 10.1002/(SICI)1097-0142(19971015)80:8+<1557::AID-CNCR5>3.3.CO;2-K PG 7 WC Oncology SC Oncology GA YA765 UT WOS:A1997YA76500006 PM 9362422 ER PT J AU Rosenthal, DI AF Rosenthal, DI TI Radiologic diagnosis of bone metastases SO CANCER LA English DT Article; Proceedings Paper CT Symposium on Skeletal Complications of Malignancy CY APR 19-20, 1997 CL NIH, NATCHER CTR, BETHESDA, MD SP Paget Fdn HO NIH, NATCHER CTR ID QUANTITATIVE COMPUTED-TOMOGRAPHY; VERTEBRAL METASTASES; SKELETAL SCINTIGRAPHY; PERCUTANEOUS BIOPSY; BREAST-CANCER; CT GUIDANCE; MR; SARCOMA; LESIONS; MALIGNANCIES AB Metastatic cancer often involves the skeleton. Tumor most often reaches the bones by hematogenous spread; however, direct extension from the primary tumor or from another site of metastasis, as well as lymphatic dissemination, may occur. Clinical features depend on the affected sites and the extent of disease. The radioisotope bone scan has been the preferred imaging screening modality. Magnetic resonance imaging is probably more sensitive in the detection of axial lesions, but additional development is needed before it can replace the isotope scan in evaluation of the long bones. For patients presenting with metastatic disease, the appearance of the lesions may help to guide the search for a primary. Some helpful patterns include lyric and sclerotic lesions, ''expanded'' lesions, ''pseudosarcomatous'' lesions, acral lesions, and soft tissue ossification. Evaluation of response to therapy is problematic. Progressive sclerosis of a lyric focus generally indicates a positive response. Pitfalls in the evaluation of response include the ''flare'' phenomenon, which has been observed on radioisotope scans early in the course of therapy. (C) 1997 American Cancer Society. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Rosenthal, DI (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,WHITE 239,BOSTON,MA 02114, USA. NR 36 TC 87 Z9 91 U1 2 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD OCT 15 PY 1997 VL 80 IS 8 SU S BP 1595 EP 1607 DI 10.1002/(SICI)1097-0142(19971015)80:8+<1595::AID-CNCR10>3.0.CO;2-V PG 13 WC Oncology SC Oncology GA YA765 UT WOS:A1997YA76500011 PM 9362427 ER PT J AU Berenson, JR AF Berenson, JR TI Bisphosphonates in multiple myeloma SO CANCER LA English DT Article; Proceedings Paper CT Symposium on Skeletal Complications of Malignancy CY APR 19-20, 1997 CL NIH, NATCHER CTR, BETHESDA, MD SP Paget Fdn HO NIH, NATCHER CTR DE multiple myeloma; bisphosphonates; etidronate; clodronate; pamidronate ID BREAST-CANCER; BONE METASTASES; MULTICENTER TRIAL; IN-VIVO; PAMIDRONATE; CLODRONATE; RESORPTION; PLACEBO AB The major clinical manifestations of multiple myeloma are related to enhanced bone destruction resulting in osteolytic lesions, osteoporosis, and pathologic fractures in most patients as well as hypercalcemia and spinal cord compression in many individuals. These patients frequently require radiation therapy or surgery. In an attempt to reduce these complications, bisphosphonates have been evaluated in several large randomized trials in patients also receiving chemotherapy. Oral etidronate given daily showed no clinical benefit, whereas the use of oral clodronate daily did reduce the development of new osteolytic lesions but did not significantly affect bone pain or rates of pathologic fractures. A large, randomized, double-blind study was conducted in which Stage III multiple myeloma patients received either pamidronate (90 mg) or placebo as a 4-hour infusion every 4 weeks for 21 cycles in addition to antimyeloma chemotherapy. The proportion of patients with at least one skeletal complication was significantly reduced in the pamidronate group compared with the placebo group. Although survival was not different between the pamidronate and placebo groups overall, patients in whom first-line chemotherapy had failed when they entered the trial lived longer with pamidronate treatment than those receiving placebo. Patients who received pamidronate had significant decreases in bone pain, had less analgesic drug use, and had better Eastern Cooperative Oncology Group performance status than patients receiving placebo. Pamidronate was safe and well tolerated during the trial. (C) 1997 American Cancer Society. C1 UNIV CALIF LOS ANGELES,JONSSON COMPREHENS CANC CTR,SCH MED,LOS ANGELES,CA 90024. RP Berenson, JR (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DIV MED ONCOL,111H,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 28 TC 27 Z9 27 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD OCT 15 PY 1997 VL 80 IS 8 SU S BP 1661 EP 1667 PG 7 WC Oncology SC Oncology GA YA765 UT WOS:A1997YA76500017 PM 9362433 ER PT J AU Zhang, M Magit, D Pardee, AB Sager, R AF Zhang, M Magit, D Pardee, AB Sager, R TI Re-expression of elafin in 21MT2 breast carcinomas by phorbol 12-myristate 13-acetate is mediated by the Ap1 site in the elafin promoter SO CANCER RESEARCH LA English DT Article ID MAMMARY EPITHELIAL-CELLS; PROTEIN-KINASE-C; PLASMINOGEN-ACTIVATOR INHIBITOR; DIFFERENTIAL EXPRESSION; TRANSCRIPTION FACTOR; ELASTASE INHIBITOR; BINDING-SITES; RETINOIC ACID; DNA-BINDING; GENE AB elafin is a unique elastase inhibitor. It is differentially expressed at the transcriptional level in human normal mammary epithelial cells and carcinomas. The elafin gene is induced by PIMA in 21MT2 breast tumor cells. By deletion analysis and mutagenesis, we have identified the Ap1 site in the promoter as the cis element mediating transcriptional activation of elafin in 70N normal breast cells and its induction by phorbol 12-myristate 13-acetate (PMA) in 21MT2 breast tumors. PIMA treatment induces AP1 factor expression, which binds to the Ap1 site of the elafin promoter, Mutation of this Ap1 abolishes the capability of induction by PMA. Furthermore, our data provide a basis for therapeutic manipulation of proteinase inhibitors such as elafin. C1 DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 51 TC 17 Z9 17 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1997 VL 57 IS 20 BP 4631 EP 4636 PG 6 WC Oncology SC Oncology GA YA360 UT WOS:A1997YA36000032 PM 9377579 ER PT J AU Patterson, GI Koweek, A Wong, A Liu, YX Ruvkun, G AF Patterson, GI Koweek, A Wong, A Liu, YX Ruvkun, G TI The DAF-3 Smad protein antagonizes TGF-beta-related receptor signaling in the Caenorhabditis elegans dauer pathway SO GENES & DEVELOPMENT LA English DT Article DE diapause; neuroendocrine; TGF-beta signaling ID GROWTH-FACTOR-BETA; C-ELEGANS; MAD PROTEINS; CELL LINEAGE; CHEMOSENSORY NEURONS; LARVAL DEVELOPMENT; GENE; EXPRESSION; DROSOPHILA; PHEROMONE AB Signals from TGF-beta superfamily receptors are transduced to the nucleus by Smad proteins, which transcriptionally activate target genes. In Caenorhabditis elegans, defects in a TGF-beta-related pathway cause a reversible developmental arrest and metabolic shift at the dauer larval stage. Null mutations in daf-3 suppress mutations in genes encoding this TGF-beta signal, its receptors, and associated Smad signal transduction proteins. daf-3 encodes a Smad protein that is most closely related to mammalian DPC4, and is expressed throughout development in many of the tissues that are remodeled during dauer development. DAF-4, the type II TGF-beta receptor in this pathway, is also expressed in remodeled tissues. These data suggest that the DAF-7 signal from sensory neurons acts as a neuroendocrine signal throughout the body to directly regulate developmental and metabolic shifts in tissues that are remodeled during dauer formation. A full-length functional DAF-3/GFP fusion protein is predominantly cytoplasmic, and this localization is independent of activity of the upstream TGF-beta-related pathway. However, this fusion protein is associated with chromosomes in mitotic cells, suggesting that DAF-3 binds DNA directly or indirectly. DAF-3 transgenes also interfere with dauer formation, perhaps attributable to a dosage effect. A truncated DAF-3/GFP fusion protein that is predominantly nuclear interferes with dauer formation, implying a role for DAF-3 in the nucleus. These data suggest that DAF-7 signal transduction antagonizes or modifies DAF-3 Smad activity in the nucleus to induce reproductive development; when DAF-7 signals are disabled, unmodified DAF-3 Smad activity mediates dauer arrest and its associated metabolic shift. Therefore, daf-3 is unique in that it is antagonized, rather than activated, by a TGF-beta pathway. C1 HARVARD UNIV,SCH MED,DEPT MOL BIOL,MASSACHUSETTS GEN HOSP,DEPT GENET,BOSTON,MA 02114. FU NIA NIH HHS [R01 AG014161, R01 AG14161] NR 49 TC 140 Z9 150 U1 1 U2 5 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD OCT 15 PY 1997 VL 11 IS 20 BP 2679 EP 2690 DI 10.1101/gad.11.20.2679 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA YB614 UT WOS:A1997YB61400008 PM 9334330 ER PT J AU Hu, G Zhang, S Vidal, M LaBaer, J Xu, T Fearon, ER AF Hu, G Zhang, S Vidal, M LaBaer, J Xu, T Fearon, ER TI Mammalian homologs of seven in absentia regulate DCC via the ubiquitin-proteasome pathway SO GENES & DEVELOPMENT LA English DT Article DE DCC; mammalian homologs; Drosophila sina gene; ubiquitin-proteasome pathway ID SIGNAL-TRANSDUCTION PATHWAY; FAT-FACETS GENE; COLORECTAL-CANCER; CONJUGATING ENZYME; DROSOPHILA EYE; CELL FATE; NEURONAL DIFFERENTIATION; TYROSINE KINASE; NERVOUS-SYSTEM; AXON GUIDANCE AB DCC (deleted in colorectal cancer) is postulated to function as transmembrane receptor for the axon and cell guidance factor netrin-1. We report here that the DCC cytoplasmic domain binds to proteins encoded by mammalian homologs of the Drosophila seven in absentia (sina) gene, as well as Drosophila Sina. Sina has a critical role in R7 photoreceptor development and shows upward of 85% amino acid identity with its mammalian homologs (termed Siahs), but the function of the Sina/Siah proteins has not been defined. We sought, therefore, to characterize further their interaction with DCC. Immunofluorescence studies suggested the Sina/Siah proteins localized predominantly in the cytoplasm and in association with DCC. DCC was found to be ubiquitinated and the Sina/Siah proteins regulated its expression. Proteasome inhibitors blocked the effects of Sina/Siah on DCC, and the Sina/Siah proteins interacted with ubiquitin-conjugating enzymes (Ubcs). A mutant Siah protein lacking the amino-terminal Ubc-binding sequences complexed with DCC, but did not degrade it. The in vivo interaction between Sina/Siah and DCC was confirmed through studies of transgenic Drosophila lines in which DCC and Sina were ectopically expressed in the eye. Taken together, the data imply that the Sina/Siah proteins regulate DCC and perhaps other proteins via the ubiquitin-proteasome pathway. C1 UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,DIV MOL MED & GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT PATHOL,ANN ARBOR,MI 48109. YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06536. YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06536. MASSACHUSETTS GEN HOSP,CTR CANC,CHARLESTOWN,MA 02129. RI Tang, Amy/L-3226-2016 OI Tang, Amy/0000-0002-5772-2878 FU NCI NIH HHS [CA70097] NR 62 TC 164 Z9 169 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD OCT 15 PY 1997 VL 11 IS 20 BP 2701 EP 2714 DI 10.1101/gad.11.20.2701 PG 14 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA YB614 UT WOS:A1997YB61400010 PM 9334332 ER PT J AU Nobile, C Marchi, J Nigro, V Roberts, RG Danieli, GA AF Nobile, C Marchi, J Nigro, V Roberts, RG Danieli, GA TI Exon-intron organization of the human dystrophin gene SO GENOMICS LA English DT Article ID BECKER MUSCULAR-DYSTROPHY; MOLECULAR-BASIS; DMD GENE; DUCHENNE; DELETION; LOCUS; BRAIN; TRANSCRIPT; CHROMOSOME; PROMOTER AB Analysis of the exon-intron organization of the human dystrophin gene has been hampered by its enormous size. By using a YAC-based exon mapping approach and long PCR, we have succeeded in defining the size of the gene and its organization. Our results, compared with data on the distribution of deletion breakpoints by intron, elucidate the topography of the intragenic deletion-prone regions. Within the central high-frequency deletion region, the small, 6.6-kb, intron 49 shows a much higher density of deletion breakpoints than intron 44, which was previously believed to coincide with the mast mutable zone of the gene. On the other hand, in the proximal part of the gene, deletion breakpoints do not preferentially occur in a few introns, but are spread over a large DNA segment containing introns 2 to 42. (C) 1997 Academic Press. C1 IST NAZL RIC CANC,LAB GENET POPOLAZ,I-07040 S MARIA LA PALMA,SASSARI,ITALY. UNIV NAPLES,IST PATOL GEN,I-80138 NAPLES,ITALY. MASSACHUSETTS GEN HOSP,HHMI LABS,BOSTON,MA 02114. UNIV PADUA,DIPARTIMENTO BIOL,I-35122 PADUA,ITALY. RP Nobile, C (reprint author), CNR,IST GENET MOL,CASELLA POSTALE,I-07040 S MARIA LA PALMA,SASSARI,ITALY. RI Roberts, Roland/C-3596-2009; OI Roberts, Roland/0000-0001-6636-1579; Nigro, Vincenzo/0000-0002-3378-5006 FU Telethon [445, 899] NR 25 TC 26 Z9 29 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD OCT 15 PY 1997 VL 45 IS 2 BP 421 EP 424 DI 10.1006/geno.1997.4911 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA YC792 UT WOS:A1997YC79200027 PM 9344670 ER PT J AU McKinnon, WC Baty, BJ Bennett, RL Magee, M NeufeldKaiser, WA Peters, KF Sawyer, JC Schneider, KA AF McKinnon, WC Baty, BJ Bennett, RL Magee, M NeufeldKaiser, WA Peters, KF Sawyer, JC Schneider, KA TI Predisposition genetic testing for late-onset disorders in adults - A position paper of the National Society of Genetic Counselors SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID HUNTINGTONS-DISEASE; COLORECTAL-CANCER; INFORMED CONSENT; OVARIAN-CANCER; FAMILY HISTORY; BRCA1; PROTOCOL; BREAST; SUSCEPTIBILITY; MODEL C1 UNIV VERMONT,COLL MED,DEPT PEDIAT,BURLINGTON,VT. UNIV UTAH,MED CTR,DEPT PEDIAT,SALT LAKE CITY,UT. UNIV WASHINGTON,DIV MED GENET,SEATTLE,WA 98195. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,CTR HUMAN & MOL GENET,NEWARK,NJ 07103. ODESSA CHILDRENS CLIN,COMPREHENS SICKLE CELL PROGRAM,SEATTLE,WA. NIH,NATL CTR HUMAN GENOME RES,MED GENET BRANCH,BETHESDA,MD 20892. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT BEHAV SCI,HOUSTON,TX. DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA 02115. FU NCI NIH HHS [CA63681]; NCRR NIH HHS [RR00064]; NHGRI NIH HHS [HG00199] NR 60 TC 75 Z9 75 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 15 PY 1997 VL 278 IS 15 BP 1217 EP 1220 DI 10.1001/jama.278.15.1217 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA XZ709 UT WOS:A1997XZ70900002 PM 9333247 ER PT J AU PericakVance, MA Bass, MP Yamaoka, LH Gaskell, PC Scott, WK Terwedow, HA Menold, MM Conneally, PM Small, GW Vance, JM Saunders, AM Roses, AD Haines, JL AF PericakVance, MA Bass, MP Yamaoka, LH Gaskell, PC Scott, WK Terwedow, HA Menold, MM Conneally, PM Small, GW Vance, JM Saunders, AM Roses, AD Haines, JL TI Complete genomic screen in late-onset familial Alzheimer disease - Evidence for a new locus on chromosome 12 SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID AFFECTED RELATIVE PAIRS; LINKAGE STRATEGIES; ALLELE; GENE; TRAITS; POLYMORPHISM; ASSOCIATION; DIAGNOSIS AB Context.-Four genetic loci have been identified as contributing to Alzheimer disease (AD), including the amyloid precursor protein gene, the presenilin 1 gene, the presenilin 2 gene, and the apolipoprotein E gene, but do not account for all the genetic risk for AD. Objective.-To identify additional genetic risk factors for late-onset AD. Design.-A complete genomic screen was performed (N=280 markers). Critical values for chromosomal regional follow-up were a P value of .05 or less for affected relative pair analysis or sibpair analysis, a parametric lod score of 1.0 or greater, or both. Regional follow-up included analysis of additional markers and a second data set. Setting.-Clinic populations in the continental United States. Patients.-From a series of multiplex families affected with late-onset (greater than or equal to 60 years) AD ascertained during the last 14 years (National Insititute of Neurological Disorders and Stroke-Alzheimer's Disease and Related Disorders Association diagnostic criteria) and for which DNA has been obtained, a subset of 16 families (135 total family members, 52 of whom were patients with AD) was used for the genomic screen. A second subset of 38 families (216 total family members, 89 of whom were patients with AD) was used for the follow-up analysis. Main Outcome Measures.-Linkage analysis results generated using both genetic model-dependent (led score) and model-independent methods. Results.-Fifteen chromosomal regions warranted initial follow-up. Follow-up analyses revealed 4 regions of continued interest on chromosomes 4, 6, 12, and 20, with the strongest results observed for chromosome 12. Peak 2-point affecteds-only rod scores (n=54) were 1.3, 1.6, 2.7, and 2.2 and affected relative pairs P values (n=54) were .04, .03, .14, and .04 for D125373, D12S1057, D1251042, and D12S390, respectively. Sibpair analysis (n=54) resulted in maximum lod scores (MLSs) of 1.5, 2.6, 3.2, and 2.3 for these markers, with a peak multipoint MLS of 3.5. A priori stratification by APOEgenotype identified 27 families that had at least 1 member with AD whose genotype did not contain an APOE*4 allele. Analysis of these 27 families resulted in MLSs of 1.0, 2.4, 3.7, and 3.3 and a peak multipoint MLS of 3.9. Conclusions.-A complete genomic screen in families affected with late-onset AD identified 4 regions of interest after follow-up. Chromosome 12 gave the strongest and most consistent results with a peak multipoint MLS of 3.5, suggesting that this region contains a new susceptibility gene for AD. Additional analyses are necessary to identify the chromosome 12 susceptibility gene for AD and to follow up the regions of interest on chromosomes 4, 6, and 20. C1 MASSACHUSETTS GEN HOSP,MOL NEUROGENET UNIT,CHARLESTOWN,MA. INDIANA UNIV,MED CTR,DEPT MED & MOL GENET,INDIANAPOLIS,IN. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA. RP PericakVance, MA (reprint author), DUKE UNIV,MED CTR,MED GENET SECT,DEPT MED,BOX 3445,DURHAM,NC 27710, USA. RI Scott, William/A-7593-2009; Haines, Jonathan/C-3374-2012 FU NIA NIH HHS [U24 AG021886] NR 31 TC 289 Z9 292 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 15 PY 1997 VL 278 IS 15 BP 1237 EP 1241 DI 10.1001/jama.278.15.1237 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA XZ709 UT WOS:A1997XZ70900028 PM 9333264 ER PT J AU ShattuckEidens, D Oliphant, A McClure, M McBride, C Gupte, J Rubano, T Pruss, D Tavtigian, SV Teng, DHF Adey, N Staebell, M Gumpper, K Lundstrom, R Hulick, M Kelly, M Holmen, J Lingenfelter, B Manley, S Fujimura, F Luce, M Ward, B CannonAlbright, L Steele, L Offit, K Gilewski, T Norton, L Brown, K Schulz, C Hampel, H Schluger, A Giulotto, E Zoli, W Ravaioli, A Nevanlinna, H Pyrhonen, S Rowley, P Loader, S Osborne, MP Daly, M Tepler, I Weinstein, PL Scalia, JL Michaelson, R Scott, RJ Radice, P Pierotti, MA Garber, JE Isaacs, C Peshkin, B Lippman, ME Dosik, MH Caligo, MA Greenstein, RM Pilarski, R Weber, B Burgemeister, R Frank, TS Skolnick, MH Thomas, A AF ShattuckEidens, D Oliphant, A McClure, M McBride, C Gupte, J Rubano, T Pruss, D Tavtigian, SV Teng, DHF Adey, N Staebell, M Gumpper, K Lundstrom, R Hulick, M Kelly, M Holmen, J Lingenfelter, B Manley, S Fujimura, F Luce, M Ward, B CannonAlbright, L Steele, L Offit, K Gilewski, T Norton, L Brown, K Schulz, C Hampel, H Schluger, A Giulotto, E Zoli, W Ravaioli, A Nevanlinna, H Pyrhonen, S Rowley, P Loader, S Osborne, MP Daly, M Tepler, I Weinstein, PL Scalia, JL Michaelson, R Scott, RJ Radice, P Pierotti, MA Garber, JE Isaacs, C Peshkin, B Lippman, ME Dosik, MH Caligo, MA Greenstein, RM Pilarski, R Weber, B Burgemeister, R Frank, TS Skolnick, MH Thomas, A TI BRCA 1 sequence analysis in women at high risk for susceptibility mutations - Risk factor analysis and implications for genetic testing SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID BREAST-CANCER FAMILIES; PROTEIN TRUNCATION TEST; OVARIAN-CANCER; STRONG CANDIDATE; POLYMORPHISMS; FREQUENCY AB Context.-A mutation in the BRCA1 gene may confer substantial risk for breast and/or ovarian cancer, However, knowledge regarding all possible mutations and the relationship between risk factors and mutations is incomplete. Objectives.-To identify BRCA1 mutations and to determine factors that best predict presence of a deleterious BRCA1 mutation in patients with breast and/or ovarian cancer. Design.-A complete sequence analysis of the BRCA1 coding sequence and flanking intronic regions was performed in 798 women in a collaborative effort involving institutions from the United States, Italy, Germany, Finland, and Switzerland. Participants.-Institutions selected 798 persons representing families (1 person for each family) thought to be at elevated a priori risk of BRCA1 mutation due to potential risk factors, such as multiple cases of breast cancer, early age of breast cancer diagnosis, and cases of ovarian cancer, No participant was from a family in which genetic markers showed linkage to the BRCA1 locus. Major Outcome Measures.-Sequence variants detected in this sample are presented along with analyses designed to determine predictive characteristics of those testing positive for BRCA1 mutations. Results.-In 102 women (12.8%), clearly deleterious mutations were detected. Fifty new genetic alterations were found including 24 deleterious mutations, 24 variants of unknown significance, and 2 rare polymorphisms. In a subset of 71 Ashkenazi Jewish women, only 2 distinct deleterious mutations were found: 185delAG in 17 cases and 5382insC in 7 cases. A bias in prior reports for mutations in exon 11 was revealed, Characteristics of a patient's specific diagnosis (unilateral or bilateral breast cancer, with or without ovarian cancer), early age at diagnosis, Ashkenazi Jewish ethnicity, and family history of cancer were positively associated with the probability of her carrying a deleterious BRCA1 mutation. Conclusions.-Using logistic regression analysis, we provide a method for evaluating the probability of a woman's carrying a deleterious BRCA1 mutation for a wide range of cases, which can be an important tool for clinicians as they incorporate genetic susceptibility testing into their medical practice. C1 MYRIAD GENET INC,SALT LAKE CITY,UT 84108. MYRIAD GENET LABS INC,SALT LAKE CITY,UT. UNIV UTAH,DEPT MED INFORMAT,SALT LAKE CITY,UT 84112. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY. UNIV PAVIA,DEPT GENET & MICROBIOL,I-27100 PAVIA,ITALY. OSPED GB MORGAGNI L PIERANTONE,DEPT MED ONCOL,FORLI,ITALY. IST ONCOL ROMAGNOLO,FORLI,ITALY. OSPED INFERMI RIMINI,DEPT ONCOL,RIMINI,ITALY. UNIV HELSINKI,CENT HOSP,DEPT OBSTET & GYNECOL,FIN-00290 HELSINKI,FINLAND. UNIV HELSINKI,CENT HOSP,DEPT ONCOL,HELSINKI,FINLAND. UNIV ROCHESTER,ROCHESTER,NY. STRANG CANC PREVENT CTR,NEW YORK,NY. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. BENNETT CANC CTR,STAMFORD,CT. CANC CTR ST BARNABAS,LIVINGSTON,NJ. KANTONSSPITAL,DEPT FORSCH,CH-4031 BASEL,SWITZERLAND. IST NAZL STUDIO & CURA TUMORI,I-20133 MILAN,ITALY. DANA FARBER CANC INST,BOSTON,MA 02115. GEORGETOWN UNIV,MED CTR,LOMBARDI CANC CTR,WASHINGTON,DC 20007. N SHORE HEMATOL ONCOL ASSOCIATES PC,SETAUKET,NY. IST ANAT PATOL,PISA,ITALY. UNIV CONNECTICUT,HLTH SCI CTR,DIV HUMAN GENET,FARMINGTON,CT. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. RI Radice, Paolo/O-3119-2013; Pilarski, Robert/E-3871-2011; OI GIULOTTO, ELENA/0000-0002-4705-2049; Pierotti, Marco Alessandro/0000-0002-7431-8332; albright, lisa/0000-0003-2602-3668; Thomas, Alun/0000-0001-5650-7044 FU NCI NIH HHS [CA-55914] NR 29 TC 293 Z9 294 U1 2 U2 18 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 15 PY 1997 VL 278 IS 15 BP 1242 EP 1250 DI 10.1001/jama.278.15.1242 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA XZ709 UT WOS:A1997XZ70900029 PM 9333265 ER PT J AU Wong, FL Boice, JD Abramson, DH Tarone, RE Kleinerman, RA Stovall, M Goldman, MB Seddon, JM Tarbell, N Fraumeni, JF Li, FP AF Wong, FL Boice, JD Abramson, DH Tarone, RE Kleinerman, RA Stovall, M Goldman, MB Seddon, JM Tarbell, N Fraumeni, JF Li, FP TI Cancer incidence after retinoblastoma - Radiation dose and sarcoma risk SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID SOFT-TISSUE SARCOMAS; BILATERAL RETINOBLASTOMA; HEREDITARY RETINOBLASTOMA; TRILATERAL RETINOBLASTOMA; SURVIVORS; TUMORS; RADIOTHERAPY; NEOPLASMS; CARCINOMAS; MORTALITY AB Context.-There is a substantial risk of a second cancer for persons with hereditary retinoblastoma, which is enhanced by radiotherapy. Objective.-To examine long-term risk of new primary cancers in survivors of childhood retinoblastoma and quantify the role of radiotherapy in sarcoma development. Design.-Cohort incidence study of patients with retinoblastoma followed for a median of 20 years, and nested case-control study of a radiation dose-response relationship for bone and soft tissue sarcomas. Setting/Participants.-A total of 1604 patients with retinoblastoma who survived at least 1 year after diagnosis, identified from hospital records in Massachusetts and New York during 1914 to 1984. Results.-Incidence of subsequent cancers was statistically significantly elevated only in the 961 patients with hereditary retinoblastoma, in whom 190 cancers were diagnosed, vs 6.3 expected in the general population (relative risk [RR], 30 [95% confidence interval, 26-47]), Cumulative incidence (+/-SE) of a second cancer at 50 years after diagnosis was 51.0% (+/-6.2%) for hereditary retinoblastoma, and 5.0% (+/-3.0%) for nonhereditary retinoblastoma. All 114 sarcomas of diverse histologic types occurred in patients with hereditary retinoblastoma. For soft tissue sarcomas, the RRs showed a stepwise increase at all dose categories, and were statistically significant at 10 to 29.9 Gy and 30 to 59.9 Gy. A radiation risk for all sarcomas combined was evident at doses above 5 Gy, rising to 10.7-fold at doses of 60 Gy or greater (P<.05). Conclusions.-Genetic predisposition has a substantial impact on risk of subsequent cancers in retinoblastoma patients, which is further increased by radiation treatment. A radiation dose-response relationship is demonstrated for all sarcomas and, for the first time in humans, for soft tissue sarcomas. Retinoblastoma patients should be examined for new cancers and followed into later life to determine whether their extraordinary cancer risk extends to common cancers of adulthood. C1 NCI,DIV CANC EPIDEMIOL & GENET,NIH,ROCKVILLE,MD 20892. UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX. NEW YORK HOSP,CORNELL MED CTR,NEW YORK,NY 10021. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA 02115. RI Wong, Fuhin/M-8360-2013; OI Kleinerman, Ruth/0000-0001-7415-2478 FU NCI NIH HHS [N01-CP-85604, N02-CP-33013] NR 38 TC 369 Z9 377 U1 2 U2 6 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 15 PY 1997 VL 278 IS 15 BP 1262 EP 1267 DI 10.1001/jama.278.15.1262 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA XZ709 UT WOS:A1997XZ70900032 PM 9333268 ER PT J AU Lay, JD Tsao, CJ Chen, JY Kadin, ME Su, IJ AF Lay, JD Tsao, CJ Chen, JY Kadin, ME Su, IJ TI Upregulation of tumor necrosis factor-alpha gene by Epstein-Barr virus and activation of macrophages in Epstein-Barr virus-infected T cells in the pathogenesis of hemophagocytic syndrome SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE tumor necrosis factor-alpha; Epstein-Barr virus; T/NK cell lymphoma; hemophagocytic syndrome ID MALIGNANT HISTIOCYTOSIS; INTERFERON-GAMMA; LYMPHOMA; EXPRESSION; LYMPHOHISTIOCYTOSIS; PHAGOCYTOSIS; HYPERLIPIDEMIA; PROLIFERATION; INTERLEUKIN-6; RETICULOSIS AB A potentially fatal hemophagocytic syndrome has been noted in patients with malignant lymphomas, particularly in EBV-infected T cell lymphoma, Cytokines, such as interferon-gamma (IFN-gamma), TNF-alpha, and IL-1 alpha, are elevated in patients' sera. To verify whether infection of T cells by EBV will upregulate specific cytokine genes and subsequently activate macrophages leading to hemophagocytic syndrome, we studied the transcripts of TNF-alpha, IFN-gamma, and IL-1 alpha in EBV-infected and EBV-negative lymphoma tissues, By reverse transcription PCR analysis, transcripts of TNF-alpha were detected in 8 (57%) of 14 EBV-infected T cell lymphomas, higher than that detected in EBV-negative T cell lymphoma (one of six, 17%), EBV-positive B cell lymphoma (two of five, 40%) and EBV-negative B cell lymphomas (one of seven, 14%). Transcripts of IFN-gamma were consistently detected in T cell lymphoma and occasionally in B cell lymphoma, but were independent of EBV status. IL-1 alpha expression was not detectable in any category. Consistent with these in vivo observations, in vitro EBV infection of T cell lymphoma lines caused upregulation of TNF-alpha gene, and increased secretion of TNF-alpha, but not IFN-gamma or IL-1 alpha. Expression of TNF-alpha, IFN-gamma, and IL-1 alpha was not changed by EBV infection of B cell lymphoma lines. To identify the specific cytokine(s) responsible for macrophage activation, culture supernatants from EBV-infected T cells were cocultured with a monocytic cell line U937 for 24 h. Enhanced phagocytosis and secretion of TNF-alpha, IFN-gamma, and IL-1 alpha by U937 cells were observed, and could be inhibited to a large extent by anti-TNF-alpha (70%), less effectively by anti-IFN-gamma (31%), but almost completely by the combination of anti-TNF-alpha and anti-IFN-gamma (85%). Taken together, the in vivo and in vitro observations suggest that infection of T cells by EBV selectively upregulates the TNF-alpha expression which, in combination with IFN-gamma and probably other cytokines, can activate macrophages. This study not only highlights a probable pathogenesis for virus-associated hemophagocytic syndrome, but also suggests that anti-TNF-alpha will have therapeutic potential in the context of their fatal syndrome. C1 NATL CHENG KUNG UNIV HOSP,DEPT PATHOL,TAINAN 704,TAIWAN. NATL CHENG KUNG UNIV HOSP,DEPT INTERNAL MED,TAINAN 704,TAIWAN. COLL MED,TAINAN 704,TAIWAN. NATL TAIWAN UNIV,COLL MED,GRAD INST MICROBIOL,TAIPEI 100,TAIWAN. NATL TAIWAN UNIV,COLL MED,GRAD INST PATHOL,TAIPEI 100,TAIWAN. BETH ISRAEL DEACONNESS MED CTR,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Su, Ih-Jen/B-2655-2010; Chen, Jen-Yang/D-2085-2010 NR 47 TC 169 Z9 177 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT 15 PY 1997 VL 100 IS 8 BP 1969 EP 1979 DI 10.1172/JCI119728 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YC366 UT WOS:A1997YC36600009 PM 9329960 ER PT J AU Gerard, C Frossard, JL Bhatia, M Saluja, A Gerard, NP Lu, B Steer, M AF Gerard, C Frossard, JL Bhatia, M Saluja, A Gerard, NP Lu, B Steer, M TI Targeted disruption of the beta-chemokine receptor CCR1 protects against pancreatitis-associated lung injury SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE MIP1 alpha/RANTES receptor; caerulein; gene deletion; respiratory distress; systemic immune response syndrome ID INFLAMMATORY RESPONSE; MICE LACKING; NEUTROPHIL; INFECTION; HOMOLOG AB beta-Chemokines and their receptors mediate the trafficking and activation of a variety of leukocytes including the lymphocyte and macrophage. An array of no less than eight beta-chemokine receptors has been identified, four of which are capable of recognizing the chemokines MIP1 alpha and RANTES. Genetic deletion of one of the MIP1 alpha and RANTES receptors, CCR5, is associated with protection from infection with HIV-1 in humans, while deletion of the ligand MIP1 alpha protects against Coxsackie virus-associated myocarditis. In this report we show that the deletion of another receptor for MIP1 alpha and RANTES, the CCR1 receptor, is associated with protection from pulmonary inflammation secondary to acute pancreatitis in the mouse. The protection from lung injury is associated with decreased levels of TNF-alpha in a temporal sequence indicating that the activation of the CCR1 receptor is an early event in the systemic inflammatory response syndrome. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,BETH ISRAEL DEACONNESS MED CTR,DEPT PEDIAT,BOSTON,MA 02115. BETH ISRAEL DEACONNESS MED CTR,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. RP Gerard, C (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,BETH ISRAEL DEACONNESS MED CTR,DEPT MED,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-52503]; NIAID NIH HHS [AI-39759]; NIDDK NIH HHS [DK-31396] NR 19 TC 168 Z9 173 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT 15 PY 1997 VL 100 IS 8 BP 2022 EP 2027 DI 10.1172/JCI119734 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YC366 UT WOS:A1997YC36600015 PM 9329966 ER PT J AU Weber, C Springer, TA AF Weber, C Springer, TA TI Neutrophil accumulation on activated, surface-adherent platelets in flow is mediated by interaction of Mac-1 with fibrinogen bound to alpha IIb beta 3 and stimulated by platelet-activating factor SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE platelets; polymorphonuclear leukocytes; integrins; selectins; chemokines ID GLYCOPROTEIN-IIB/IIIA COMPLEX; P-SELECTIN; MONOCLONAL-ANTIBODIES; GLANZMANN THROMBASTHENIA; IMMOBILIZED PLATELETS; LEUKOCYTE ACTIVATION; HUMAN-MONOCYTES; CC CHEMOKINES; IRAQI-JEWISH; CD11B CD18 AB We have studied the pathways that lead to arrest and firm adhesion of rolling PMN on activated, surface-adherent platelets, Stable arrest and adhesion strengthening of PMN on thrombin-stimulated, surface-adherent platelets in flow required distinct Ca2+- and Mg2+-dependent regions of Mac-1 (alpha M beta 2), and involved interactions of Mac-1 with fibrinogen, which was bound to platelets via alpha IIb beta 3. Mac-1 also bound to other unidentified ligands on platelets, which were not intracellular adhesion molecule-2 (ICAM-2), heparin, or heparan-sulfate proteoglycans, This was shown by inhibition with mAbs or peptides, by treatment of platelets with heparitinase, and by using platelets with defective alpha IIB beta 3 from a patient with Glanzmann thrombasthenia. Tethering of PMN on platelet ICAM-2 via LFA-1 (alpha L beta 2) was observed, which may facilitate the transition between rolling on selectins and Mac-1-dependent arrest. Arrest and adhesion strengthening was pertussis toxin sensitive and in flow was mainly induced by platelet-activating factor but not through activation of the chemokine receptor CXCR2. In stasis, spreading occurred and the CXCR2 contributed to firm adhesion. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02215. OI Weber, Christian/0000-0003-4610-8714 FU NHLBI NIH HHS [HL-48675] NR 62 TC 233 Z9 237 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT 15 PY 1997 VL 100 IS 8 BP 2085 EP 2093 DI 10.1172/JCI119742 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YC366 UT WOS:A1997YC36600023 PM 9329974 ER PT J AU Kitayama, J Fuhlbrigge, RC Puri, KD Springer, TA AF Kitayama, J Fuhlbrigge, RC Puri, KD Springer, TA TI P-selectin, L-selectin, and alpha(4) integrin have distinct roles in eosinophil tethering and arrest on vascular endothelial cells under physiological flow conditions SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LEUKOCYTE ADHESION MOLECULE-1; IN-VITRO; NONSTATIC CONDITIONS; SUPPORTS NEUTROPHIL; HYDRODYNAMIC SHEAR; ROLLING ADHESIONS; EXPRESSION; LIGAND; RECEPTOR; INFLAMMATION AB The adhesive interactions of eosinophils with purified E-, P-, and L-selectins; vascular cell adhesion molecule-1 molecule; and HUVEC were examined in shear flow. Compared with neutrophils, eosinophils showed markedly less binding to E-selectin, but significantly stronger avidity for P-selectin. Both cell types showed a similar level of tethering and rolling on L-selectin. Eosinophils tethered and arrested abruptly on vascular cell adhesion molecule-1. However, some of the tethers were detached within several seconds; this was prevented by stimulation with eotaxin. Eosinophils also showed immediate arrest on HUVEC stimulated with 100 U/ml TNF-alpha for 6 h. Treatment with L-selectin mAb decreased eosinophil accumulation on the HUVEC by abrogating secondary tethers through interactions between flowing and attached eosinophils. mAb to P-selectin but not to E-selectin strongly inhibited primary tethers and accumulation of eosinophils. mAb to the integrin alpha(4) subunit inhibited arrest, induced rolling or detachment of tethered eosinophils, and resulted in partial reduction of eosinophil accumulation. mAb to the integrin beta(2) subunit had only a slight effect, whereas treatment with mAb to the integrin alpha(4) and beta(2) subunits together abolished rolling interactions as well as arrest, and thus almost totally inhibited eosinophil accumulation. Our data indicate that P-selectin, but not E-selectin, is directly involved in eosinophil tethering on inflammatory endothelium while L-selectin mainly mediates intereosinophil interaction. VLA-4 has a crucial role in eosinophil arrest, and arrest is enhanced by exposure to chemoattractants. C1 HOWARD MED SCH,CTR BLOOD RES,BOSTON,MA 02115. FU NHLBI NIH HHS [HL48675] NR 71 TC 104 Z9 108 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 15 PY 1997 VL 159 IS 8 BP 3929 EP 3939 PG 11 WC Immunology SC Immunology GA XZ994 UT WOS:A1997XZ99400030 PM 9378981 ER PT J AU Weber, C Lu, CF Casasnovas, JM Springer, TA AF Weber, C Lu, CF Casasnovas, JM Springer, TA TI Role of alpha(L)beta(2) integrin avidity in transendothelial chemotaxis of mononuclear cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MONOCYTE CHEMOATTRACTANT PROTEIN-1; INTERCELLULAR-ADHESION MOLECULE-1; FUNCTION-ASSOCIATED ANTIGEN-1; CYTOPLASMIC DOMAIN; MAC-1 CD11B/CD18; T-CELLS; MONOCLONAL-ANTIBODY; HUMAN-NEUTROPHILS; LYMPHOCYTES-T; CC CHEMOKINES AB The leukocyte integrin alpha(L) beta(2) (LFA-1) is important in transendothelial migration, Since it is not fully understood how LFA-1 mediates transmigration, We studied the effects of alpha(L) and beta(2) cytoplasmic domain mutants that alter LFA-1 adhesiveness for intercellular adhesion molecule-1, Monocyte chemotactic protein-1 (MCP-1) induced LFA-1-dependent transendothelial migration of Jurkat and J-beta 2.7 transfectants coexpressing the MCP-1 receptor CCR2B and wild-type alpha(L). No transendothelial chemotaxis was observed with truncation mutants of the alpha(L) cytoplasmic tail, which rendered LFA-1 constitutively active or locked LFA-1 in a low avidity state unresponsive to cellular activation, Moreover, transendothelial chemotaxis of lymphoblastoid SLA transfectants was abolished by truncation of the beta(2) cytoplasmic domain, but not by mutation of its TTT motif, which is important in phorbol ester-induced adhesion, These data indicate that transmigration may require both alpha(L) and beta(2) cytoplasmic domains, We further show that MCP-1-induced transendothelial chemotaxis of PBMC was inhibited by sustained activation of LFA-1 with Mn2+ or a stimulatory mAb to beta(2). Dimeric soluble intercellular adhesion molecule-1 also reduced transendothelial chemotaxis of PBMC, Taken together, our data suggest that transendothelial chemotaxis of mononuclear cells may involve dynamic changes in LFA-1 avidity. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RI Casasnovas, Jose/L-6299-2014; OI Casasnovas, Jose/0000-0002-2873-6410; Weber, Christian/0000-0003-4610-8714 FU NCI NIH HHS [CA31798] NR 48 TC 53 Z9 53 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 15 PY 1997 VL 159 IS 8 BP 3968 EP 3975 PG 8 WC Immunology SC Immunology GA XZ994 UT WOS:A1997XZ99400034 PM 9378985 ER PT J AU Atlas, SJ Volinn, E AF Atlas, SJ Volinn, E TI Classics from the spine literature revisited: A randomized trial of 2 versus 7 days of recommended bed rest for acute low back pain SO SPINE LA English DT Article DE acute low back pain; bed rest; randomized controlled trial; review; treatment ID ACUTE MYOCARDIAL-INFARCTION; MEDICAL LITERATURE; CLINICAL-TRIAL; USERS GUIDES; THERAPY; PREVENTION; PATTERNS; ARTICLE AB Study Design. Review of a trial of bed rest for patients with acute low back pain. Objectives. To assess the validity and results of the study, and their applicability to and influence on current clinical practice and recommendations. Summary of Background Data. Although bed rest has been a cornerstone of treatment for acute low back pain, historically this recommendation was largely based on ''expert opinion.'' In 1986, Deyo et al. published a randomized study of 2 versus 7 days of recommended bed rest for acute low back pain. Despite results from this and other studies, current clinical practice and treatment recommendations continue to overemphasize bed rest. Methods. The study was reviewed using structured criteria adopted from the medical literature that focus on the validity of the study design, the results of the treatment, and the relevance of the findings to clinical practice. Results. Two hundred and three patients were randomized to 2 versus 7 days of recommended bed rest. Groups were similar at baseline evaluation. Outcomes assessed at 3 and 12 weeks were similar between groups, except that patients receiving a recommendation for 2 days of bed rest had significantly fewer days of work absence than those recommended 7 days. Limitations of the study included poor compliance with recommended bed rest, especially in the 7-day group, a marginal sample size without information on relevant confidence intervals, and patient characteristics that may have affected the generalizability of these findings to others with acute low back pain. Conclusions. Despite limitations, this study provided strong evidence that less bed rest was associated with similar outcomes for acute low back pain along with quicker return to work. Results from this and other studies support a shift away from bed rest as a primary recommendation in the initial management of low back pain. In spite of this, bed rest recommendations for episodes of low back pain remain common. Additional efforts are needed to change clinical practice. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,MED SERV,GEN INTERNAL MED UNIT,BOSTON,MA. LIBERTY MUTUAL RES CTR SAFETY & HLTH,HOPKINTON,MA. RP Atlas, SJ (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,MED SERV,MED PRACTICES EVALUAT CTR,50 STANIFORD ST,BOSTON,MA 02114, USA. NR 30 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-2436 J9 SPINE JI SPINE PD OCT 15 PY 1997 VL 22 IS 20 BP 2331 EP 2337 DI 10.1097/00007632-199710150-00002 PG 7 WC Clinical Neurology; Orthopedics SC Neurosciences & Neurology; Orthopedics GA YC853 UT WOS:A1997YC85300002 PM 9355212 ER PT J AU Pascual, M Thadhani, R Chung, RT Williams, WW Meehan, S TolkoffRubin, N Colvin, R Cosimi, AB AF Pascual, M Thadhani, R Chung, RT Williams, WW Meehan, S TolkoffRubin, N Colvin, R Cosimi, AB TI Nephrotic syndrome after liver transplantation in a patient with hepatitis C virus-associated glomerulonephritis SO TRANSPLANTATION LA English DT Article ID MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS; INFECTION; CRYOGLOBULINEMIA; THERAPY AB In recent years, hepatitis C virus infection has been reported to be typically associated with membrane-proliferative glomerulonephritis and less frequently with membranous nephropathy. Treatment of hepatitis C with interferon-alpha can reduce viremia and improve renal disease. After liver transplantation for hepatitis C virus-associated liver failure, standard immunosuppressive protocols result in a significant increase in hepatitis C viremia. In this report we describe a patient with end-stage liver disease and biopsy-proven hepatitis C-associated glomerulonephritis who underwent liver transplantation. Within 1 month after transplantation, he developed a severe nephrotic syndrome that paralleled a marked increase in viremia. We discuss the possible pathogenic relationship between hepatitis C virus infection and the nephrotic syndrome that followed liver transplantation. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP Pascual, M (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,BOX MZ-70,55 FRUIT ST,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [K08DK02209] NR 20 TC 29 Z9 29 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD OCT 15 PY 1997 VL 64 IS 7 BP 1073 EP 1076 DI 10.1097/00007890-199710150-00022 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA YB065 UT WOS:A1997YB06500022 PM 9381532 ER PT J AU Qi, LJ Leung, AT Xiong, YT Marx, KA AbouSamra, AB AF Qi, LJ Leung, AT Xiong, YT Marx, KA AbouSamra, AB TI Extracellular cysteines of the corticotropin-releasing factor receptor are critical for ligand interaction SO BIOCHEMISTRY LA English DT Article ID ADENYLATE-CYCLASE ACTIVITY; SITE-DIRECTED MUTAGENESIS; HORMONE-RELATED PEPTIDE; PARATHYROID-HORMONE; BETA-2-ADRENERGIC RECEPTOR; FUNCTIONAL EXPRESSION; PITUITARY-GLAND; DISULFIDE BOND; CRF RECEPTOR; RAT-BRAIN AB The corticotropin-releasing factor receptor (CRF-R) contains six conserved cysteines in its amino-terminal domain (C30, C44, C54, C68, C87, and C102) and one cysteine in its first and second extracellular loops (C188 and C258, respectively). Additionally, several other cysteines are located in the transmembrane domains (C128, C211, C233, and C364) and first intracellular loop (C150). Reduction of disulfide bonds with DTT decreased CRF binding to detergent-solubilized membranes, suggesting an important role for disulfide bonds in ligand recognition. Therefore, site-directed mutagenesis was used to introduce single and paired Cys (C) to Ser (S) or Ala (A) mutations. A silent nine amino acid tag from c myc was introduced in the amino terminus of the mouse CRF-R. With the exception of C258S and C188S/C258S mutations, all C to S or to A receptor mutants had good surface expression that was at least 52.5% of control. C30S, C54S, and C30S/C54S mutations had good CRF binding and CRF-stimulated cAMP accumulation. No CRF binding was detected for the C44S, C68S, C87S, C102S, C188S, C258S, C30S/C44S, C30S/C68S, C54S/C68S, C87S/C102S, and C188S/C258S mutants, while CRF-stimulated cAMP accumulation occurred with high EC50 values. In particular, receptors carrying double mutations, C44S/C102S and C68S/C87%, had an improved signaling property as compared to receptors carrying the respective single cysteine mutations. These data, together with the effects of DTT on CRF binding, indicate that disulfide bridges are important for receptor functions. Functional data from single and paired cysteine mutations suggest potential pairings between C44 and C102, C68 and C87, and C188 and C258 that are critical for ligand-receptor interactions. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. UNIV LOWELL,DEPT CHEM,LOWELL,MA 01854. RI Leung, Albert/H-6030-2013; OI Abou-Samra, Abdul/0000-0001-8735-1142 FU NIDDK NIH HHS [NIDDK 45020] NR 36 TC 55 Z9 55 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 14 PY 1997 VL 36 IS 41 BP 12442 EP 12448 DI 10.1021/bi970997r PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YB019 UT WOS:A1997YB01900007 PM 9376348 ER PT J AU Williams, KP Liu, XH Schumacher, TNM Lin, HY Ausiello, DA Kim, PS Bartel, DP AF Williams, KP Liu, XH Schumacher, TNM Lin, HY Ausiello, DA Kim, PS Bartel, DP TI Bioactive and nuclease-resistant L-DNA ligand of vasopressin SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID H-3 LABELED OLIGONUCLEOTIDES; CELL-LINE LLC-PK1; RECEPTOR TRANSITION; ALPHA-L; RNA; SELECTION; BINDING; OLIGODEOXYNUCLEOTIDES; PHOSPHOROTHIOATE; PHARMACOKINETICS AB In vitro selection experiments have produced nucleic acid ligands (aptamers) that bind tightly and specifically to a great variety of target biomolecules, The utility of aptamers is often limited by their vulnerability to nucleases present in biological materials, One way to circumvent this problem is to select an aptamer that binds the enantiomer of the target, then synthesize the enantiomer of the aptamer as a nuclease-insensitive ligand of the normal target, We have so identified a mirror-image single-stranded DNA that binds the peptide hormone vasopressin and have demonstrated its stability to nucleases and its bioactivity as a vasopressin antagonist in cell culture. C1 MIT,WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. MIT,DEPT BIOL,CAMBRIDGE,MA 02142. HOWARD HUGHES MED INST,CAMBRIDGE CTR 9,CAMBRIDGE,MA 02142. MASSACHUSETTS GEN HOSP,DEPT MED,PROGRAM MEMBRANE BIOL,RENAL UNIT,CHARLESTOWN,MA 02129. NR 37 TC 123 Z9 126 U1 4 U2 22 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 14 PY 1997 VL 94 IS 21 BP 11285 EP 11290 DI 10.1073/pnas.94.21.11285 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YA930 UT WOS:A1997YA93000040 PM 9326601 ER PT J AU Yang, OO Tran, AC Kalams, SA Johnson, RP Roberts, MR Walker, BD AF Yang, OO Tran, AC Kalams, SA Johnson, RP Roberts, MR Walker, BD TI Lysis of HIV-1-infected cells and inhibition of viral replication by universal receptor T cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; HEPATITIS-B VIRUS; LYMPHOCYTE ACTIVITY; HIV-1 INFECTION; INTRACELLULAR INACTIVATION; FINE SPECIFICITY; CTL; RESPONSES; PEPTIDE; MECHANISM AB Increasing evidence suggests that HIV-1-specific cytotoxic T lymphocytes (CTLs) are a key host immune response to HIV-1 infection. Generation of CTL responses for prevention or therapy of HIV-1 infection has several intrinsic technical barriers such as antigen expression and presentation, the varying HLA restrictions between different individuals, and the potential for viral escape by sequence variation or surface molecule alteration on infected cells. A strategy to circumvent these limitations is the construction of a chimeric T cell receptor containing human CD4 or HIV-1-specific Ig sequences linked to the signaling domain of the T cell receptor zeta chain (universal T cell receptor). CD8(+) CTLs transduced with this universal receptor can then bind and lyse infected cells that express surface HIV-1 gp120. We evaluated the ability of universal-receptor-bearing CD8(+) cells from a seronegative donor to lyse acutely infected cells and inhibit HIV-1 replication in vitro. The kinetics of lysis and efficiency of inhibition were comparable to that of naturally occurring HIV-1-specific CTL clones isolated from infected individuals. Further study will be required to determine the utility of these cells as a therapeutic strategy in vivo. C1 MASSACHUSETTS GEN HOSP,AIDS RES CTR,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. CELL GENESYS INC,FOSTER CITY,CA 94404. RP Yang, OO (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,ROOM 5234,149 13TH ST,CHARLESTOWN,MA 02129, USA. FU NIAID NIH HHS [AI 30914, AI 28568, F32 AI 09280-01, F32 AI009270, R01 AI028568, R01 AI030914, R37 AI028568] NR 47 TC 72 Z9 74 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 14 PY 1997 VL 94 IS 21 BP 11478 EP 11483 DI 10.1073/pnas.94.21.11478 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA YA930 UT WOS:A1997YA93000074 PM 9326635 ER PT J AU Campbell, A Villavicencio, AT Yeghiayan, SK Balikian, R Baldessarini, RJ AF Campbell, A Villavicencio, AT Yeghiayan, SK Balikian, R Baldessarini, RJ TI Mapping of locomotor behavioral arousal induced by microinjections of dopamine within nucleus accumbens septi of rat forebrain SO BRAIN RESEARCH LA English DT Article DE arousal; accumbens; dopamine; microinjection; nucleus accumbens septi ID PHASEOLUS-VULGARIS LEUCOAGGLUTININ; VENTRAL STRIATUM; EFFERENT PROJECTIONS; TOPOGRAPHICAL ORGANIZATION; COMPARTMENTAL ORGANIZATION; CHOLINERGIC NEURONS; CAUDATE-PUTAMEN; D-AMPHETAMINE; RECEPTORS; SHELL AB Dopamine (DA) at ca. ED50 (16 mu g) or saline was stereotaxically microinjected unilaterally 2 h after pretreatment with an MAO inhibitor into left or right nucleus accumbens septi of 697 freely moving rats (1394 injections) to define subregions involved in DA-induced behavioral arousal throughout the anatomical extent of the accumbens. Locomotion was quantified electronically and behavioral responses were assigned to histologically verified injection sites; postural or stereotyped behaviors characteristic of DA injections in caudate-putamen did not occur. Screening with 60 injections across mid-accumbens (2.2-3.2 mm rostral to bregma) indicated that locomotion was elicited non-homogeneously, and was particularly intense dorsomedially. Sites yielding intense arousal and their inactive surround were mapped along the rostrocaudal axis (1.4-4.2 mm anterior to bregma) in coronal sections. Responses to DA showed lateral symmetry and were similar across rostrocaudal levels, with intense responses in dorsomedial accumbens along its border with the caudate-putamen. This functional localization does not coincide closely with reported distributions of DA or its receptors, nor with histologically or histochemically defined core-shell regions of this limbic structure. Nucleus accumbens in rat brain thus appears to be organized functionally into distinct subregions differing markedly in ability to produce locomotor hyperactivity in response to exogenous DA. (C) 1997 Elsevier Science B.V. C1 HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR 309,NEUROPHARMACOL LAB,BELMONT,MA 02178. FU NIMH NIH HHS [MH-47370, MH31154, MH-34006] NR 70 TC 28 Z9 28 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD OCT 10 PY 1997 VL 771 IS 1 BP 55 EP 62 DI 10.1016/S0006-8993(97)00777-4 PG 8 WC Neurosciences SC Neurosciences & Neurology GA YD132 UT WOS:A1997YD13200007 PM 9383008 ER PT J AU Aronson, D Dufresne, SD Goodyear, LJ AF Aronson, D Dufresne, SD Goodyear, LJ TI Contractile activity stimulates the c-Jun NH2-terminal kinase pathway in rat skeletal muscle SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ACTIVATED-PROTEIN-KINASE; SIGNAL-TRANSDUCTION PATHWAY; MAP KINASE; CARDIAC MYOCYTES; GENE-EXPRESSION; MECHANICAL-STRESS; GAMMA-RADIATION; JNK ACTIVATION; PHOSPHORYLATION; FOS AB Contractile activity plays a critical role in the regulation of gene transcription in skeletal muscle, which in turn determines muscle functional capabilities. However, little is known about the molecular signaling mechanisms that convert contractile activity into gene regulatory responses in skeletal muscle. In the current study we determined the effects of contractile activity in vivo on the c-Jun NH2-terminal kinase (JNK) pathway, a signaling cascade that has been implicated in the regulation of transcription. Electrical stimulation of the sciatic nerve to produce contractions in anaesthetized rats increased JNK activity by up to 7-fold above basal. Maximal enzyme activity occurred at 15 min of contraction and remained elevated at 60 min of contraction. The upstream activators of JNK, the mitogen-activated protein kinase kinase 4 and the mitogen-activated protein kinase kinase kinase 1 followed a similar time course of activation in response to contractile activity. In contrast, contraction induced a rapid and transient activation of the extracellular-regulated kinase pathway, indicating that the regulation of JNK signaling is distinct from that of extracellular-regulated kinase. The activation of the JNK signaling cascade was temporally associated with an increased expression of c-jun mRNA. These results demonstrate that contractile activity regulates JNK activity in skeletal muscle and suggest that activation of JNK may regulate contraction-induced gene expression in skeletal muscle. C1 BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. RI Aronson, Doron/F-3390-2010 FU NIAMS NIH HHS [AR-42238] NR 40 TC 65 Z9 68 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 10 PY 1997 VL 272 IS 41 BP 25636 EP 25640 DI 10.1074/jbc.272.41.25636 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YA358 UT WOS:A1997YA35800040 PM 9325285 ER PT J AU Clarkson, WD Corbett, AH Paschal, BM Kent, HM McCoy, AJ Gerace, L Silver, PA Stewart, M AF Clarkson, WD Corbett, AH Paschal, BM Kent, HM McCoy, AJ Gerace, L Silver, PA Stewart, M TI Nuclear protein import is decreased by engineered mutants of nuclear transport factor 2 (NTF2) that do not bind GDP-Ran SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE nucleocytoplasmic transport; nuclear pores; GTPase; protein-protein interactions; protein engineering ID PORE COMPLEX; KARYOPHERIN-ALPHA; NUCLEOCYTOPLASMIC TRANSPORT; CRYSTAL-STRUCTURE; P62 COMPLEX; GTP; YEAST; IDENTIFICATION; RAN/TC4; BETA AB Nuclear transport factor 2 (NTF2) is associated with the translocation stage of nuclear protein import and binds both to nuclear pore proteins (nucleoporins) containing phenylalanine-rich repeats and to the Ras family GTPase Ran. In tl-tis study we probed the role of the NTF2-Ran interaction in nuclear protein import using site-directed mutants of NTF2 that interfere with its interaction with GDP-Ran. The design of these mutants was based on the X-ray crystal structure of NTF2 and was concentrated on conserved residues in and around the molecule's hydrophobic cavity. The mutant NTF2 cDNAs were expressed in Escherichia coli. Purified mutant proteins retained the interaction with FxFG-repeat nucleoporins, but several mutants in the negatively charged residues that surround the NTF2 cavity or in residues in the cavity itself were unable to bind GDP-Ran in vitro. The crystal structure of the E42K mutant protein in showed significant structural changes only in this side-chain, indicating that it participated directly in the interaction with GDP-Ran. In permeabilised cell nuclear protein Import assays, only wild-type NTF2 and mutants that bound GDP-Ran were functional. Furthermore, when the NTF2 E42K and D92N/D94N NTF2 mutants that failed to bind GDP-Ran in vitro were substituted for the chromosomal yeast NTF2, the yeast cells became non-viable, whereas yeast substituted with human NTF2 remained viable. We conclude that interaction between NTF2 and GDP-Ran is important for efficient nuclear protein import. (C) 1997 Academic Press Limited. C1 MRC, MOL BIOL LAB, CAMBRIDGE CB2 2QH, ENGLAND. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOL PHARMACOL, BOSTON, MA 02115 USA. DANA FARBER CANC INST, BOSTON, MA 02115 USA. EMORY UNIV, SCH MED, DEPT BIOCHEM, ATLANTA, GA 30322 USA. UNIV VIRGINIA, CTR CELL SIGNALLING, HSC, CHARLOTTESVILLE, VA 22908 USA. SCRIPPS RES INST, DEPT CELLULAR BIOL, LA JOLLA, CA 92037 USA. Scripps Res Inst, DEPT MOL BIOL, LA JOLLA, CA 92037 USA. FU NIGMS NIH HHS [GM41955] NR 62 TC 55 Z9 57 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD OCT 10 PY 1997 VL 272 IS 5 BP 716 EP 730 DI 10.1006/jmbi.1997.1255 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YB267 UT WOS:A1997YB26700006 PM 9368653 ER PT J AU Quinn, LS Haugk, KL Damon, SE AF Quinn, LS Haugk, KL Damon, SE TI Interleukin-15 stimulates C2 skeletal myoblast differentiation SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID FACTOR-BINDING-PROTEIN; GROWTH FACTOR-II; IL-2 RECEPTOR; BETA-CHAIN; EXPRESSION; MUSCLE; PROLIFERATION; CLONING AB Interleukin-15 (IL-15) is a cytokine which is highly expressed in skeletal muscle, and which stimulates muscle protein accretion in cultured skeletal muscle fibers. Using parental C2 skeletal myoblasts, no significant effects of IL-15 on skeletal muscle differentiation were observed. To test the hypothesis that IL-15 may stimulate skeletal muscle differentiation if the strong differentiation-inducing effects of autocrine insulin-like growth factor (IGF) production were inhibited, a C2 myoblast subline (C2-pBP4) was stably transfected with an expression vector for rat IGF binding protein-4 (IGFBP-4). Differentiation responses to autocrine and exogenous IGFs in C2-BP4 myoblasts were reduced 3- to 4-fold in C2-BP4 cultures compared to C2-pLXSN cultures, a subline transfected with a control plasmid. Addition of IL-15 to C2-pBP4 myoblasts doubled the number of differentiated muscle cells which arose. These findings indicate that IL-15 can stimulate myogenic differentiation in conditions in which the strongly differentiative effects of the IGFs are inhibited. The differentiative activity of IL-15 may be of physiological significance in conditions in which IGF concentrations are low or in which the IGFs are sequestered by binding proteins. (C) 1997 Academic Press. C1 UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. RP Quinn, LS (reprint author), VA PUGET SOUND HLTH CARE SYST,CTR GERIATR RES EDUC & CLIN,TACOMA,WA 98493, USA. FU NIA NIH HHS [AG 13280]; NICHD NIH HHS [N01-HD-6-2915] NR 18 TC 34 Z9 36 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 9 PY 1997 VL 239 IS 1 BP 6 EP 10 DI 10.1006/bbrc.1997.7414 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA YB131 UT WOS:A1997YB13100002 PM 9345260 ER PT J AU Tallman, MS Andersen, JW Schiffer, CA Appelbaum, FR Feusner, JH Ogden, A Shepherd, L Willman, C Bloomfield, CD Rowe, JM Wiernik, PH AF Tallman, MS Andersen, JW Schiffer, CA Appelbaum, FR Feusner, JH Ogden, A Shepherd, L Willman, C Bloomfield, CD Rowe, JM Wiernik, PH TI All-trans-retinoic acid in acute promyelocytic leukemia SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article; Proceedings Paper CT 36th Meeting of the American-Society-of-Hematology CY DEC 01-05, 1995 CL SEATTLE, WA SP Amer soc Hematol ID ACUTE MYELOID-LEUKEMIA; DIFFERENTIATION THERAPY; REMISSION INDUCTION; RESIDUAL DISEASE; RAR-ALPHA; TRANSLOCATION; CHEMOTHERAPY; EXPERIENCE; DIAGNOSIS; REDUCTION AB Background All-trans-retinoic acid induces complete remission in acute promyelocytic leukemia. However, it is not clear whether induction therapy with all-trans-retinoic acid is superior to chemotherapy alone or whether maintenance treatment with all-trans-retinoic acid improves outcome. Methods Three hundred forty-six patients with previously untreated acute promyelocytic leukemia were randomly assigned to receive all-trans-retinoic acid or daunorubicin plus cytarabine as induction treatment. Patients who had a complete remission received consolidation therapy consisting of one cycle of treatment identical to the induction chemotherapy, then high-dose cytarabine plus daunorubicin. Patients still in complete remission after two cycles of consolidation therapy were then randomly assigned to maintenance treatment with all-trans-retinoic acid or to observation. Results Of the 174 patients treated with chemotherapy, 120 (69 percent) had a complete remission, as did 124 of the 172 (72 percent) given all-trans-retinoic acid (P=0.56). When both induction and maintenance treatments were taken into account, the estimated rates of disease-free survival at one, two, and three years were 77, 61, and 55 percent, respectively, for patients assigned to chemotherapy then all-trans-retinoic acid; 86, 75, and 75 percent for all-trans-retinoic acid then all-trans-retinoic acid; 75, 60, and 60 percent for all-trans-retinoic acid then observation; and 29, 18, and 18 percent for chemotherapy then observation. By intention-to-treat analysis, the rates of overall survival at one, two, and three years after entry into the study were 75, 57, and 50 percent, respectively, among patients assigned to chemotherapy, and 82, 72, and 67 percent among those assigned to all-trans-retinoic acid (P=0.003). Conclusions All-trans-retinoic acid as induction or maintenance treatment improves disease-free and overall survival as compared with chemotherapy alone and should be included in the treatment of acute promyelocytic leukemia. (C) 1997, Massachusetts Medical Society. C1 DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MARYLAND,SCH MED,GREENEBAUM CANC CTR,BALTIMORE,MD 21201. UNIV WASHINGTON,FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98195. CHILDRENS HOSP OAKLAND,OAKLAND,CA 94609. TEXAN CHILDRENS CANC CTR,HOUSTON,TX. NATL CANC INST,CANADA CLIN TRIALS GRP,KINGSTON,ON,CANADA. UNIV NEW MEXICO,ALBUQUERQUE,NM 87131. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. UNIV ROCHESTER,ROCHESTER,NY. MONTEFIORE MED CTR,ALBERT EINSTEIN CANC CTR,BRONX,NY 10467. RP Tallman, MS (reprint author), NORTHWESTERN UNIV,SCH MED,DIV HEMATOL ONCOL,ROBERT H LURIE CANC CTR,233 E ERIE ST,SUITE 700,CHICAGO,IL 60611, USA. NR 37 TC 639 Z9 661 U1 0 U2 6 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 9 PY 1997 VL 337 IS 15 BP 1021 EP 1028 DI 10.1056/NEJM199710093371501 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA XZ844 UT WOS:A1997XZ84400001 PM 9321529 ER PT J AU Rigotti, NA DiFranza, JR Chang, YC Tisdale, T Kemp, B Singer, DE AF Rigotti, NA DiFranza, JR Chang, YC Tisdale, T Kemp, B Singer, DE TI The effect of enforcing tobacco-sales laws on adolescents' access to tobacco and smoking behavior SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CIGARETTE SALES; YOUTH ACCESS; MINORS; ENFORCEMENT; PREVENTION AB Background Enforcing laws banning tobacco sales to miners is widely advocated as a way to reduce young people's access to tobacco and tobacco use. Whether this approach is successful is not known. Methods In a two-year controlled study, we assessed sales of tobacco to miners and young people's access to and use of tobacco in six Massachusetts communities. Three communities (the intervention group) enforced tobacco-sales laws, whereas three matched communities (the control group) did not. To assess compliance with the law, miners working for the study investigators attempted to purchase tobacco from all retail vendors in each community every six months. Three annual anonymous surveys of a total of 22,021 students in grades 9 through 12 (response rate, 84 percent) measured access to tobacco and smoking behavior. Results At base line, 68 percent of 487 vendors sold tobacco to miners. Compliance with the law improved significantly faster in the intervention communities than in the controls (P<0.001). By the study's end, 82 percent of the merchants in the intervention communities complied with the law, as compared with 45 percent in the control communities (P<0.001). However, adolescents under 18 years old reported only a small drop in their ability to purchase tobacco and no decline in its use. Communities with and those without enforcement programs did not differ with respect to these outcomes. Conclusions Enforcing tobacco-sales laws improved merchants' compliance and reduced illegal sales to miners but did not alter adolescents' perceived access to tobacco or their smoking. Test purchases of tobacco do not accurately reflect adolescents' self-reported access to tobacco, and reducing illegal sales to less than 20 percent of attempts - the goal of a new federal law - may not decrease young people's access to or use of tobacco. (C) 1997, Massachusetts Medical Society. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, TOBACCO RES & TREATMENT CTR, BOSTON, MA 02114 USA. UNIV MASSACHUSETTS, MED CTR, DEPT FAMILY & COMMUNITY MED, WORCESTER, MA USA. RP Rigotti, NA (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED, GEN INTERNAL MED UNIT,50 STANIFORD ST, 9TH FL, BOSTON, MA 02114 USA. FU NCI NIH HHS [CA01673] NR 37 TC 167 Z9 168 U1 0 U2 4 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 9 PY 1997 VL 337 IS 15 BP 1044 EP 1051 DI 10.1056/NEJM199710093371505 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA XZ844 UT WOS:A1997XZ84400005 PM 9321533 ER PT J AU Stone, RM Mark, EJ Ferry, JA Truong, MT Zachary, KC AF Stone, RM Mark, EJ Ferry, JA Truong, MT Zachary, KC TI A 67-year-old renal-transplant recipient with anemia, leukopenia, and pulmonary lesions - Post-transplantation lymphoproliferative disorder, monomorphic B-cell type. Bronchiolitis obliterans SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID EPSTEIN-BARR-VIRUS; BONE-MARROW TRANSPLANTATION; ORGAN-TRANSPLANTATION; IMMUNOCOMPROMISED HOSTS; DISEASE; INFECTIONS; LYMPHOMA; SPECTRUM; PATIENT; CYCLOSPORINE C1 DANA FARBER CANC INST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, CAMBRIDGE, MA 02138 USA. RP Stone, RM (reprint author), BRIGHAM & WOMENS HOSP, 75 FRANCIS ST, BOSTON, MA 02115 USA. NR 46 TC 5 Z9 5 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 9 PY 1997 VL 337 IS 15 BP 1065 EP 1074 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA XZ844 UT WOS:A1997XZ84400008 ER PT J AU Petty, MA Elands, J Johnson, MP Linnik, MD Hamel, E Moskowitz, MA Lee, WS McCarty, DR Hibert, M Baron, BM AF Petty, MA Elands, J Johnson, MP Linnik, MD Hamel, E Moskowitz, MA Lee, WS McCarty, DR Hibert, M Baron, BM TI The selectivity of MDL 74,721 in models of neurogenic versus vascular components of migraine SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE 5-HT receptor pharmacology; migraine model; aminotetralin; cerebrovascular regulation; inflammation, neurogenic ID BOVINE CEREBRAL-ARTERIES; 5-HT1D BINDING-SITES; DURA-MATER; PLASMA EXTRAVASATION; TRIGEMINAL GANGLIA; BLOOD-VESSELS; MESSENGER-RNA; SUMATRIPTAN; RECEPTORS; SEROTONIN AB MDL 74,721 (R)-2-(N1,N1-dipropylamino)-8-methylaminosulfonylmethyl-1,2,3,4-tetrahydronaphthalene, a sulfonamidotetralin, has been found to exhibit a 10000-fold greater potency in neurogenic versus vascular models of migraine. Sumatriptan, a relatively pure 5-HT1D/5-HT1B receptor agonist, also showed higher potency versus neurogenic inflammation. However, for sumatriptan the potency difference (100-fold) in the two pathophysiological models was less pronounced than seen for MDL 74,721. The affinity profile of MDL 74,721 at 5-HT1 receptor subtypes may in part explain its ability to differentiate these two physiological responses. MDL 74,721 demonstrated nanomolar affinity for 5-HT1A (12.7 +/- 0.3 nM) and 5-HT1D (41.3 +/- 10.9 nM) but considerably lower affinity for 5-HT1B receptors (>1000 nM). Serotonin-like activity was seen in in vitro functional assays including inhibition of forskolin-stimulated cAMP accumulation in human 5-HT1D receptor-transfected fibroblasts or eliciting vasoconstriction in isolated human pial arteries. The intrinsic activity (relative to 5-HTEAmax) and affinity (pD(2)) for the human cerebrovascular 5-HT receptors were: 5-HT (100%, 7.51 +/- 0.49), sumatriptan (94%, 6.85 +/- 0.1) and MDL 74,721 (66%, 5.70 +/- 0.23), In anaesthetised cats, treatment with MDL 74,721 resulted in a dose-related reduction in the percentage of carotid flow going through the arteriovenous anastomoses to the lungs, with an ED50 of 0.3 mg/kg i.v., the same as sumatriptan. However, in the guinea-pig neurogenic model, MDL 74,721 inhibited plasma protein extravasation with an ED50 of 0.023 mu g/kg compared to 2.5 mu g/kg for sumatriptan. MDL 74,721 was also effective in this model (in rats) after oral administration. In conclusion, MDL 74,721 demonstrates a preclinical profile consistent with anti-migraine efficacy, Its marked preference for inhibiting neurogenic inflammation makes this compound a useful tool for assessing the relative contribution of this pathophysiological mechanism to the human disease state. (C) 1997 Elsevier Science B.V. C1 MARION MERRELL,F-67080 STRASBOURG,FRANCE. HOECHST MARION ROUSSEL INC,CINCINNATI,OH 45215. MCGILL UNIV,MONTREAL NEUROL INST,MONTREAL,PQ,CANADA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. RI Moskowitz, Michael/D-9916-2011 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 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD OCT 8 PY 1997 VL 336 IS 2-3 BP 127 EP 136 DI 10.1016/S0014-2999(97)01218-1 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YC679 UT WOS:A1997YC67900004 PM 9384224 ER PT J AU Aretz, HT Colvin, RB AF Aretz, HT Colvin, RB TI Endomyocardial biopsies - An early warning system for chronic transplant arteriopathy SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID CORONARY-ARTERY DISEASE; CARDIAC TRANSPLANTATION; MOUSE HEARTS; ALLOGRAFT-REJECTION; ATHEROSCLEROSIS; ULTRASOUND; PATHOLOGY RP Aretz, HT (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,COX 5,100 BLOSSOM ST,BOSTON,MA 02114, USA. NR 17 TC 3 Z9 3 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 8 PY 1997 VL 278 IS 14 BP 1197 EP 1198 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA XY422 UT WOS:A1997XY42200042 PM 9326484 ER PT J AU Neubauer, S Horn, M Cramer, M Harre, K Newell, JB Peters, W Pabst, T Ertl, G Hahn, D Ingwall, JS Kochsiek, K AF Neubauer, S Horn, M Cramer, M Harre, K Newell, JB Peters, W Pabst, T Ertl, G Hahn, D Ingwall, JS Kochsiek, K TI Myocardial phosphocreatine-to-ATP ratio is a predictor of mortality in patients with dilated cardiomyopathy SO CIRCULATION LA English DT Article DE spectroscopy, magnetic resonance; mortality; heart failure; metabolism ID MAGNETIC-RESONANCE SPECTROSCOPY; CONGESTIVE-HEART-FAILURE; CORONARY-ARTERY DISEASE; P-31 MR SPECTROSCOPY; DECREASED ENERGY RESERVE; CREATINE-KINASE REACTION; BIOENERGETIC CONSEQUENCES; CARDIAC METABOLISM; SKELETAL-MUSCLES; INFARCTION AB Background In patients with heart failure due to dilated cardiomyopathy, cardiac energy metabolism is impaired, as indicated by a reduction of the myocardial phosphocreatine-to-ATP ratio, measured noninvasively by P-31-MR spectroscopy. The purpose of this study was to test whether the phosphocreatine-to-ATP ratio also offers prognostic information in terms of mortality prediction as well as how this index compares with well-known mortality predictors such as left ventricular ejection fraction (LVEF) or New York Heart Association (NYHA) class. Methods and Results Thirty-nine patients with dilated cardiomyopathy were followed up for 928 +/- 85 days (2.5 years). At study entry, LVEF and NYHA class were determined, and the cardiac phosphocreatine-to-ATP ratio was measured by localized P-31-MR spectroscopy of the anterior myocardium. During the study period, total mortality was 26%. Patients were divided into two groups, one with a normal phosphocreatine-to-ATP ratio (>1.60; mean +/- SE, 1.98 +/- 0.07; n=19; healthy volunteers: 1.94 +/- 0.11, n=30) and one with a reduced phosphocreatine-to-ATP ratio (<1.60; 1.30 +/- 0.05; n=20). At reevaluation (mean, 2.5 years), 8 of 20 patients with reduced phosphocreatine-to-ATP ratios had died, all of cardiovascular causes (total and cardiovascular mortality, 40%). Of the 19 patients with normal phosphocreatine-to-ATP ratios, 2 had died (total mortality, 11%), one of cardiovascular causes (cardiovascular mortality, 5%). Kaplan-Meier analysis showed significantly reduced total (P = .036) and cardiovascular (P = .016) mortality for patients with normal versus patients with low phosphocreatine-to-ATP ratios. A Cox model for multivariate analysis showed that the phosphocreatine-to-ATP ratio and NYHA class offered significant independent prognostic information on cardiovascular mortality. Conclusions The myocardial phosphocreatine-to-ATP ratio, measured noninvasively with P-31-MR spectroscopy, is a predictor of both total and cardiovascular mortality in patients with dilated cardiomyopathy. C1 UNIV WURZBURG, DEPT RADIOL, D-97080 WURZBURG, GERMANY. MASSACHUSETTS GEN HOSP, CARDIAC COMP CTR, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, NMR LAB PHYSIOL CHEM, BOSTON, MA USA. RP Neubauer, S (reprint author), UNIV WURZBURG, MED KLIN, DEPT MED, JOSEF SCHNEIDER STR 2, D-97080 WURZBURG, GERMANY. RI Neubauer, Stefan/B-8448-2011 NR 45 TC 376 Z9 379 U1 2 U2 15 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 7 PY 1997 VL 96 IS 7 BP 2190 EP 2196 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YA098 UT WOS:A1997YA09800015 PM 9337189 ER PT J AU Byers, PH Duvic, M Atkinson, M Robinow, M Smith, LT Krane, SM Greally, MT Ludman, M Matalon, R Pauker, S Quanbeck, D Schwarze, U AF Byers, PH Duvic, M Atkinson, M Robinow, M Smith, LT Krane, SM Greally, MT Ludman, M Matalon, R Pauker, S Quanbeck, D Schwarze, U TI Ehlers-Danlos syndrome type VIIA and VIIB result from splice-junction mutations or genomic deletions that involve exon 6 in the COL1A1 and COL1A2 genes of type I collagen SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Ehlers-Danlos syndrome; Ehlers-Danlos syndrome type VII; collagen; procollagen; exon skipping; exon deletion; alternative splicing; congenital hip dislocation ID PROCOLLAGEN N-PROTEINASE; HUMAN DERMATOSPARAXIS; BASE SUBSTITUTION; CLINICAL-FEATURES; ACCEPTOR SITE; AMINO-ACIDS; PATIENT; CHAIN; FORM; PHENOTYPE AB Ehlers-Danlos syndrome (EDS) type VII results from defects in the conversion of type I procollagen to collagen as a consequence of mutations in the substrate that alter the protease cleavage site (EDS type VIIA and VIIB) or in the protease itself (EDS type VIIC), We identified seven additional families in which EDS type VII is either dominantly inherited (one family with EDS type VIIB) or due to new dominant mutations (one family with EDS type VIIA and five families with EDS type VIIB), In six families, the mutations alter the consensus splice junctions, and, in the seventh family, the exon is deleted entirely, The COL1A1 mutation produced the most severe phenotypic effects, whereas those in the COL1A2 gene, regardless of the location or effect, produced congenital hip dislocation and other joint instability that was sometimes very marked, Fractures are seen in some people with EDS type VII, consistent with alterations in mineral deposition on collagen fibrils in bony tissues, These new findings expand the array of mutations known to cause EDS type VII and provide insight into genotype/phenotype relationships in these genes. (C) 1997 Wiley-Liss, Inc. C1 UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT BIOL STRUCT,SEATTLE,WA 98195. UNIV TEXAS,SCH MED,DEPT DERMATOL,HOUSTON,TX. CHILDRENS HOSP & MED CTR,DEPT PEDIAT,DAYTON,OH. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. EASTERN VIRGINIA MED SCH,DEPT PEDIAT,NORFOLK,VA 23501. DALHOUSIE UNIV,DEPT PEDIAT MED GENET,HALIFAX,NS,CANADA. MIAMI CHILDRENS HOSP,MIAMI,FL. HARVARD COMMUN HLTH PLAN,BOSTON,MA. SHRINERS HOSP CRIPPLED CHILDREN,MINNEAPOLIS,MN. RP Byers, PH (reprint author), UNIV WASHINGTON,DEPT PATHOL,BOX 357470,SEATTLE,WA 98195, USA. OI Byers, Peter H./0000-0001-7786-7030 FU NIAMS NIH HHS [AR 21557, AR 03564] NR 43 TC 47 Z9 51 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 3 PY 1997 VL 72 IS 1 BP 94 EP 105 DI 10.1002/(SICI)1096-8628(19971003)72:1<94::AID-AJMG20>3.0.CO;2-O PG 12 WC Genetics & Heredity SC Genetics & Heredity GA XU368 UT WOS:A1997XU36800020 PM 9295084 ER PT J AU Jin, SF Kharbanda, S Mayer, B Kufe, D Weaver, DT AF Jin, SF Kharbanda, S Mayer, B Kufe, D Weaver, DT TI Binding of Ku and c-Abl at the kinase homology region of DNA-dependent protein kinase catalytic subunit SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID STRAND-BREAK REPAIR; V(D)J RECOMBINATION; TYROSINE KINASE; END; PHOSPHORYLATION; AUTOANTIGEN; DEFECTS; DOMAINS; COMPLEX; CELLS AB The DNA-dependent protein kinase (DNA-PK) con trols the repair of double-stranded DNA breaks in mammalian cells. The protein kinase subunit of DNA-PK (DNA-PKcs) is targeted to DNA breaks by association with the Hu DNA-binding heterodimer. Here we show that a Ku association site is present at the carboxyl terminus of DNA-PKcs (amino acids 3002-3850) near the protein kinase domain. Correspondingly, the nuclear c-Abl tyrosine kinase that associates with DNA-PK also binds to the kinase homology domain. The c-Abl SH3 domain binds to amino acids 3414-3850 of DNA-PKcs. c-Abl phosphorylates C-terminal fragments of DNA-PKcs, particularly amino acids 3414-3850. c-Abl phosphorylation of DNA-PKcs disassociates the DNA-PKcs.Ku complex. Thus, Ku and c-Abl provide opposing functions with regard to DNA-PK activity. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOL GENET,BOSTON,MA 02115. CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. FU NCI NIH HHS [CA54326] NR 28 TC 77 Z9 78 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 3 PY 1997 VL 272 IS 40 BP 24763 EP 24766 DI 10.1074/jbc.272.40.24763 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA XY970 UT WOS:A1997XY97000010 PM 9312071 ER PT J AU Ikezu, T Okamoto, T Yonezawa, K Tompkins, RG Martyn, JAJ AF Ikezu, T Okamoto, T Yonezawa, K Tompkins, RG Martyn, JAJ TI Analysis of thermal injury-induced insulin resistance in rodents - Implication of postreceptor mechanisms SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TUMOR-NECROSIS-FACTOR; FACTOR-ALPHA; PHOSPHATIDYLINOSITOL 3-KINASE; SKELETAL-MUSCLE; RECEPTOR SUBSTRATE-1; BURN INJURY; TNF-ALPHA; SIGNAL-TRANSDUCTION; GLUCOSE-TRANSPORT; PROTEIN-SYNTHESIS AB Burn injury is associated with insulin resistance. The molecular basis of this resistance was investigated by examining insulin receptor signaling in rats after thermal injury. The impaired insulin-stimulated transport of [H-3]2-deoxyglucose into soleus muscle strips confirmed the insulin resistance following burns. In vivo insulin-stimulated phosphoinositide 3-kinase activity, pivotal, in translocation of GLUT4, was decreased in burns when assessed by its insulin receptor substrate-1 (IRS-1)-associated activity. Insulin-induced tyrosine kinase activity of insulin receptor (IR) and tyrosine phosphorylation of IRS-I were also attenuated, Immunoprecipitated IR, however, appeared to have normal insulin-responsive kinase activity. Finally, immunoprecipitated IRS-I was tested for its effect on partially purified recombinant IR and was found to inhibit its kinase activity. This inhibitory effect of IRS-1 was abolished by prior treatment of IRS-1 with alkaline phosphatase, indicating that burn injury-related hyperphosphorylation of IRS-1 is similar to that observed in TNF alpha-induced inhibition of LR signaling All of these changes were observed in the absence of quantitative changes in IR, IRS-1, and phosphoinositide 3-kinase. Alterations in postreceptor insulin signaling, therefore, may be responsible for the insulin resistance after thermal injury. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT ANESTHESIOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT SURG,BOSTON,MA 02114. KOBE UNIV,BIOSIGNAL RES CTR,KOBE,HYOGO 657,JAPAN. FU NIGMS NIH HHS [GM 55032-01, GM 31569-15] NR 50 TC 72 Z9 83 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 3 PY 1997 VL 272 IS 40 BP 25289 EP 25295 DI 10.1074/jbc.272.40.25289 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA XY970 UT WOS:A1997XY97000085 PM 9312146 ER PT J AU Navder, KP Baraona, E Lieber, CS AF Navder, KP Baraona, E Lieber, CS TI Polyenylphosphatidylcholine decreases alcoholic hyperlipemia without affecting the alcohol-induced rise of HDL-cholesterol SO LIFE SCIENCES LA English DT Article DE polyenylphosphatidylcholine; alcohol; serum lipoproteins; rats ID HYPERCHOLESTEROLEMIC RATS; POLYUNSATURATED LECITHIN; PLASMA-CHOLESTEROL; SERUM-CHOLESTEROL; CORN-OIL; LIPOPROTEINS; METABOLISM; ABSORPTION; LIPIDS; PATHOGENESIS AB In ethanol-fed rats, supplementation of the diet with soybean polyenylphosphatidylcholine (3 g/liter for 21 days) markedly decreased postprandial VLDL-triglycerides and both VLDL- and LDL-cholesterol levels, whereas it maintained high levels of HDL-cholesterol, compared to an equivalent intake of choline and polyunsaturated fatty acids. By contrast, there were no changes in the serum lipoproteins of the pair-fed controls. The prevention of alcoholic hypertriglyceridemia was associated with marked attenuation of the alcoholic fatty liver and it occurred despite a slight increase in fat absorption. Thus, the administration of polyenylphosphatidylcholine not only attenuates the hepatotoxicity of ethanol, but also increases the HDL/LDL cholesterol ratio, which may be beneficial for the prevention of atherosclerosis and coronary heart disease. C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,BRONX,NY 10468. MT SINAI SCH MED,BRONX,NY 10468. CUNY HUNTER COLL,DEPT FOOD SCI & NUTR,NEW YORK,NY 10010. FU NIAAA NIH HHS [AA05934, AA11115] NR 41 TC 19 Z9 22 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PD OCT 3 PY 1997 VL 61 IS 19 BP 1907 EP 1914 DI 10.1016/S0024-3205(97)00830-8 PG 8 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA YA565 UT WOS:A1997YA56500005 PM 9364195 ER PT J AU Boussiotis, VA Freeman, GJ Berezovskaya, A Barber, DL Nadler, LM AF Boussiotis, VA Freeman, GJ Berezovskaya, A Barber, DL Nadler, LM TI Maintenance of human T cell anergy: Blocking of IL-2 gene transcription by activated Rap1 SO SCIENCE LA English DT Article ID PROTEIN-TYROSINE KINASE; NUCLEOTIDE DISSOCIATION STIMULATOR; CBL PROTOONCOGENE PRODUCT; SIGNAL-TRANSDUCTION; ANTIGEN RECEPTOR; C-CBL; PHOSPHATIDYLINOSITOL 3-KINASE; SUPPRESSOR ACTIVITY; INSULIN-RECEPTOR; MAMMALIAN-CELLS AB In the absence of costimulation, T cells activated through their antigen receptor become unresponsive (anergic) and do not transcribe the gene encoding interleukin-2 (IL-2) when restimulated with antigen. Anergic alloantigen-specific human T cells contained phosphorylated Cbl that coimmunoprecipitated with Fyn. The adapter protein CrkL was associated with both phosphorylated Cbl and the guanidine nucleotide-releasing factor G3G, which catalyzes guanosine triphosphate (GTP) exchange on Rap1. Active Rap1 (GTP-bound form) was present in anergic cells, Forced expression of low amounts of Rap1-GTP in Jurkat T cells recapitulated the anergic defect and blocked T cell antigen receptor (TCR)- and CD28-mediated IL-2 gene transcription. Therefore, Rap1 functions as a negative regulator of TCR-mediated IL-2 gene transcription and may be responsible for the specific defect in IL-2 production in T cell anergy. C1 HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. ONTARIO CANC INST,DIV CELLULAR & MOL BIOL,TORONTO,ON M5G 2M9,CANADA. RP Boussiotis, VA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT ADULT ONCOL,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL 54785]; NIAID NIH HHS [AI 35225, AI39671] NR 77 TC 372 Z9 379 U1 0 U2 3 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 3 PY 1997 VL 278 IS 5335 BP 124 EP 128 DI 10.1126/science.278.5335.124 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA XZ124 UT WOS:A1997XZ12400053 PM 9311917 ER PT J AU Weir, GC Sharma, A Zangen, DH BonnerWeir, S AF Weir, GC Sharma, A Zangen, DH BonnerWeir, S TI Transcription factor abnormalities as a cause of beta cell dysfunction in diabetes: a hypothesis SO ACTA DIABETOLOGICA LA English DT Article; Proceedings Paper CT 6th International Milano Meeting on Diabetes CY MAR 21-23, 1996 CL UNIV MILAN, MILAN, ITALY HO UNIV MILAN DE diabetes; beta cell; insulin secretion; glucotoxicity; PDX-1 ID INSULIN GENE-TRANSCRIPTION; RAT PANCREATIC-ISLETS; GLYCEROL PHOSPHATE DEHYDROGENASE; GLUCOSE TRANSPORTER ISOFORMS; CHRONIC EXPOSURE; MESSENGER-RNA; HOMEODOMAIN PROTEIN; TRANSGENIC MICE; HIT CELLS; CONTROL ELEMENT AB Well-characterized defects in insulin secretion, most notably a loss of glucose-induced insulin secretion, are found in virtually all forms of NIDDM, as well as in early IDDM. Similar abnormalities have been found in all animal models of diabetes in which they have been studied. A novel hypothesis is being proposed to explain the mechanisms responsible for these alterations. Many abnormalities in the various steps of glucose-induced insulin secretion have been identified in rodent models of diabetes, but none by itself seems sufficient to explain the defects. These include a loss of GLUT2, glycogen accumulation, glucose recycling, abnormal glucokinase or hexokinase, altered mitochondrial glycerol phosphate dehydrogenase (mGPDH) activity, abnormal ion channel function and beta cell degranulation. We propose that optimal secretory function is dependent upon the unique differentiation of beta cells that is maintained by a set of transcription factors and that this control is disrupted by the diabetic state. Therefore, we propose that key transcription factors are affected even when beta cells are stressed by insulin resistance in very earliest stages of diabetes and that the abnormality becomes more severe as full-blown diabetes develops, which leads to loss of beta cell differentiation and a resultant derangement of insulin secretion. C1 HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA. JOSLIN DIABET CTR,BOSTON,MA 02215. RP Weir, GC (reprint author), HARVARD UNIV,SCH MED,BETH ISRAEL DEACONESS MED CTR,DEPT MED,JOSLIN DIABET CTR,BOSTON,MA, USA. FU NIDDK NIH HHS [DK-35449] NR 92 TC 28 Z9 29 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0940-5429 J9 ACTA DIABETOL JI Acta Diabetol. PD OCT PY 1997 VL 34 IS 3 BP 177 EP 184 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YF729 UT WOS:A1997YF72900001 PM 9401638 ER PT J AU Lein, M Stephan, C Jung, K Koenig, F Schnorr, D Loening, SA AF Lein, M Stephan, C Jung, K Koenig, F Schnorr, D Loening, SA TI Ratio of free-PSA/total-PSA: An indicator for differentiation between patients with prostate cancer and benign prostatic hyperplasia SO AKTUELLE UROLOGIE LA German DT Article DE prostate cancer; prostate-specific antigen; free PSA; discrimination limits ID ENZYMATIC-ACTIVITY; REFERENCE RANGES; ANTIGEN LEVELS; SERUM; ALPHA-1-ANTICHYMOTRYPSIN; COMPLEX; PERFORMANCE; ASSAYS; ALPHA(1)-ANTICHYMOTRYPSIN; STANDARDIZATION AB A survey on literature data concerning free prostate specific antigen and the corresponding cut-offs for f-PSA/t-PSA differentiating patients suffering from prostate carcinoma and benign prostatic hyperplasia is given. The essential importance of the diagnostic criterion for establishing the cut-off value is demonstrated. On the basis of own data, the application of the parameter f-PSA/t-PSA is recommended as additional criterion. F-PSA and t-PSA were determined in serum samples of 149 patients (45 with prostate cancer, 50 with benign prostate hyperplasia, 54 healthy controls) using the IMMULITE test. According to the IMMULITE test results, median values for t-PSA (f-PSA) were 1.59 (0.29) mu g/l in healthy men, 7.90 (0.80) mu g/l in patients with PCa and 4.30 (0.81) mu g/l in patients with benign prostatic hyperplasia. The percentage of f-PSA (f-PSA/t-PSA) was significantly lower in patients with PCa (median value: 9.5% in the IMMULITE test) compared to patients with BPH (21.2%) and healthy controls (23.7%). The receiver-operation-characteristics analyzis (ROC) shows, compared to t-PSA alone, obtaining the percentage of f-PSA significantly improves the ability to differentiate between PCa and BPH as well as healthy controls. For reasons of diagnostic efficiency, a cut-off for the percentage of f-PSA (f-PSA%) of 15% is suggested for the IMMULITE test. C1 Humboldt Univ, Fak Med, Klin & Poliklin Urol, Univ Klinikum Charite, D-1040 Berlin, Germany. RP Lein, M (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 48 TC 2 Z9 2 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0001-7868 J9 AKTUEL UROL JI Aktuelle Urol. PD OCT PY 1997 VL 28 IS 6 BP 323 EP 328 DI 10.1055/s-2008-1054297 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA YL645 UT WOS:000070977200004 ER PT J AU Brezinski, ME Tearney, G Boppart, SA Bouma, B Weissman, NJ Pitris, C Fujimoto, JG AF Brezinski, ME Tearney, G Boppart, SA Bouma, B Weissman, NJ Pitris, C Fujimoto, JG TI Micron scale catheter based in vivo and in vitro imaging with optical coherence SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GEORGETOWN UNIV,BOSTON,MA. MIT,BOSTON,MA. RI Boppart, Stephen/C-7338-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD OCT PY 1997 VL 80 SI 7A BP TCT3 EP TCT3 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YC885 UT WOS:A1997YC88500003 ER PT J AU Kiesz, RS Rozek, MM Mego, DM Miller, LA OLeary, E Patel, V SaundersWebb, E Ebersole, DG Chilton, R AF Kiesz, RS Rozek, MM Mego, DM Miller, LA OLeary, E Patel, V SaundersWebb, E Ebersole, DG Chilton, R TI Acute directional coronary atherectomy prior to stenting: Long term angiographic results. SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,S TEXAS VET HLTH SYST,AUDIE MURPHY DIV,SAN ANTONIO,TX. BROOKE ARMY MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD OCT PY 1997 VL 80 SI 7A BP TCT83 EP TCT83 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YC885 UT WOS:A1997YC88500083 ER PT J AU Porch, JV Jain, K Reilly, A Valdez, C Mazariegos, M Ziegler, TR Solomons, N Smith, RJ AF Porch, JV Jain, K Reilly, A Valdez, C Mazariegos, M Ziegler, TR Solomons, N Smith, RJ TI Aging, physical activity, insulin-like growth factor I, and body composition in Guatemalan women SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE growth hormone; insulin-like growth factor I; body composition; bioelectrical impedance analysis; physical activity; elderly; Guatemala; aging ID HEAVY-RESISTANCE EXERCISE; REPUBLIC-OF-GUATEMALA; IGF-I; HORMONAL RESPONSES; PROLONGED EXERCISE; SOMATOMEDIN-C; ELDERLY MEN; OLDER MEN; AGE; SECRETION AB Aging is associated with diminished secretion of growth hormone and the major endogenous mediator of growth hormone action, insulin-like growth factor I(IGF-I). Aging is also associated with decreased physical activity. Alterations in body composition characteristic of the aging process (increased fat mass and decreased lean body mass) may be related to the decline in anabolic effects of IGF-I with aging, decreased physical activity, or both. Guatemalan women often maintain a high level of physical activity during aging. The purpose of this study was to determine whether IGF-I concentrations correlated with physical activity level (determined by standardized scoring of a self-report questionnaire) and body composition (determined by bioelectrical impedance analysis) in elderly Guatemalan women. In 112 women aged 20-87 y, we found a progressively lower serum IGF-I with age (r = -0.732). In subjects > 60 y of age, the self-reported activity level was associated with a lower percentage body fat (P < 0.001) but there was no significant relation between physical activity level and either lean body mass or IGF-I. We conclude that there is a significant age-related decline in serum IGF-I concentrations in Guatemalan women, similar to that observed in both men and women in the United States. An increased level of physical activity in the elderly Guatemalan population was associated with reduced body fat but did not modify the expected reduction in circulating IGF-I concentrations that occurs with aging. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,JOSLIN RES LAB,BOSTON,MA 02215. CTR STUDIES SENSORY IMPAIRMENT AGING & METAB,GUATEMALA CITY,GUATEMALA. FU NIDDK NIH HHS [DK50411, DK48503] NR 44 TC 12 Z9 13 U1 0 U2 0 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD OCT PY 1997 VL 66 IS 4 BP 874 EP 879 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA XY491 UT WOS:A1997XY49100019 PM 9322563 ER PT J AU Bridges, AJ Lorden, TE Havighurst, TC AF Bridges, AJ Lorden, TE Havighurst, TC TI Autoantibody testing for connective tissue diseases - Comparison of immunodiffusion, immunoblot, and enzyme immunoassay SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE autoantibody; enzyme immunoassay; immunoblot; connective tissue disease; systemic lupus erythematosus; Sjogren's syndrome ID SYSTEMIC LUPUS-ERYTHEMATOSUS; AUTOIMMUNE-DISEASES; REVISED CRITERIA; ANTIBODIES; CLASSIFICATION; ELISA AB We evaluated 500 consecutive patient serum samples for the presence of six autoantibodies by three antibody detection methods: immunodiffusion, immunoblot, and enzyme immunoassay. Clinical data were reviewed for each patient with positive antibody test results. Serum samples from 60 patients revealed antibodies to Sm, ribonucleoprotein (RNP), SSA/Ro, SSB/La, Scl-70, or Jo-1. There were 7 false-positive test results (1%). All three methods detected autoantibodies in 36 (68%) of 53 patients with connective tissue disease. Immunoblot was the most sensitive method to detect autoantibodies (92%). Enzyme immunoassay and immunodiffusion were less sensitive (81% and 74%, respectively). Antiribonucleoprotein and anti-SSB/La antibodies were more often detected by immunoblotting, whereas anti-SSA/Ro antibodies were more often detected by enzyme immunoassay. Newer antibody detection methods (immunoblot and enzyme immunoassay) are less time consuming than immunodiffusion and show good interassay sensitivity without loss of specificity. A combination of immunoblot and enzyme immunoassay yielded excellent assay sensitivity (100%) and specificity (99%) for detection of autoantibodies. C1 UNIV WISCONSIN,SCH MED,DEPT MED,CLIN IMMUNOL SERV,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT BIOSTAT,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. NR 19 TC 13 Z9 15 U1 0 U2 0 PU AMER SOC CLIN PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON ST, CHICAGO, IL 60612 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD OCT PY 1997 VL 108 IS 4 BP 406 EP 410 PG 5 WC Pathology SC Pathology GA XX434 UT WOS:A1997XX43400007 PM 9322593 ER PT J AU Fanburg, JC Rosenberg, AE Weaver, DL Leslie, KO Mann, KG Taatjes, DJ Tracy, RP AF Fanburg, JC Rosenberg, AE Weaver, DL Leslie, KO Mann, KG Taatjes, DJ Tracy, RP TI Osteocalcin and osteonectin immunoreactivity in the diagnosis of osteosarcoma SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE osteosarcoma; osteocalcin (bone Gla protein); osteonectin; immunohistochemistry; monoclonal antibodies ID OSTEOGENIC BONE-TUMORS; IMMUNOHISTOCHEMICAL LOCALIZATION; IMMUNOELECTRON MICROSCOPY; ADJUVANT CHEMOTHERAPY; MONOCLONAL-ANTIBODIES; BASEMENT-MEMBRANE; BOVINE BONE; GLA-PROTEIN; CALF BONE; SPARC AB Osteosarcomas (OSAs) can be difficult to distinguish histologically from tumors with significantly different biologic potentials and treatment protocols. The correct diagnosis of OSA relies on identification of malignant osteoblasts that are capable of producing neoplastic bone. To determine the use of immunohistochemistry for the diagnosis of OSA, 106 tumors from the Massachusetts General Hospital and the University of Vermont were immunostained with monoclonal antiosteocalcin (OC) and antiosteonectin (ON) antibodies. They included 42 OSAs, 25 non-bone-forming sarcomas, 24 other malignant tumors including lymphomas, carcinomas, and melanomas, and 15 benign bone tumors. Cytoplasmic staining with OC showed 70% sensitivity and 100% specificity, while staining with ON showed 90% sensitivity and 54% specificity for bone-forming tumors, consistently staining cell types other than osteoblasts. Of the OSAs, 83% demonstrated matrix staining with one or both antibodies, whereas dense collagen was negative for both antibodies in all tumors. We conclude that tumor cell cytoplasmic staining with monoclonal OC may be helpful in distinguishing OSAs from other malignancies, and staining of extracellular matrix for OC and ON antibodies concurrently may help distinguish bone matrix from dense collagen. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405. UNIV VERMONT,DEPT BIOCHEM,BURLINGTON,VT 05405. RP Fanburg, JC (reprint author), ARMED FORCES INST PATHOL,DEPT SOFT TISSUE PATHOL,BLDG 54,ROOM 3075,14TH ST & ALASKA AVE NW,WASHINGTON,DC 20306, USA. FU NIA NIH HHS [AG-08777] NR 50 TC 42 Z9 45 U1 0 U2 0 PU AMER SOC CLIN PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON ST, CHICAGO, IL 60612 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD OCT PY 1997 VL 108 IS 4 BP 464 EP 473 PG 10 WC Pathology SC Pathology GA XX434 UT WOS:A1997XX43400015 PM 9322601 ER PT J AU Tearney, GJ Brezinski, ME Southern, JF Bouma, BE Boppart, SA Fujimoto, JG AF Tearney, GJ Brezinski, ME Southern, JF Bouma, BE Boppart, SA Fujimoto, JG TI Optical biopsy in human gastrointestinal tissue using optical coherence tomography SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID ENDOSCOPIC ULTRASONOGRAPHY; INTRADUCTAL ULTRASONOGRAPHY; PANCREATIC-CANCER; DIAGNOSIS; ULTRASOUND; DISEASES AB Objectives: Optical coherence tomography (OCT) is a new technique for performing high-resolution, cross-sectional tomographic imaging in human tissue, OCT is somewhat analogous to ultrasound B mode imaging except that it uses light rather than acoustical waves. OCT has over 10 times the resolution of currently available clinical high-resolution imaging technologies, In this work, we investigate the capability of OCT to differentiate the architectural morphology of gastrointestinal tissue with the long-term objective of extending OCT to endoscopic based diagnostics, Methods: Normal and diseased gastrointestinal tissues were taken postmortem and imaged using OCT, Images were compared with corresponding histology to confirm tissue identity and suggest the mechanisms that produce tissue contrast. Results: Microstructure was delineated in different tissues, including the esophagus and colon, at 16 +/- 1 mu m resolution, higher than any clinically available cross-sectional imaging technology, Differentiation of tissue layers, such as the mucosa, submucosa, and muscularis were achieved because of their different optical properties, Conclusions: The ability of OCT to provide high-resolution in situ imaging of gastrointestinal microstructure, without the need for excisional biopsy, suggests the feasibility of using OCT as a powerful diagnostic imaging technology, which can be integrated with conventional endoscopy. C1 MIT,DEPT ELECT ENGN & COMP SCI,ELECT RES LAB,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA. RI Boppart, Stephen/C-7338-2009 FU NEI NIH HHS [9-RO1-EY11289-10]; NHLBI NIH HHS [1-R29-HL55686-01A1] NR 20 TC 114 Z9 116 U1 0 U2 12 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD OCT PY 1997 VL 92 IS 10 BP 1800 EP 1804 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XZ848 UT WOS:A1997XZ84800008 PM 9382040 ER PT J AU Allikmets, R Shroyer, NF Singh, N Seddon, JM Lewis, RA Bernstein, P Peiffer, A Zabriskie, N Li, Y Hutchinson, A Dean, M Lupski, JR Leppert, M AF Allikmets, R Shroyer, NF Singh, N Seddon, JM Lewis, RA Bernstein, P Peiffer, A Zabriskie, N Li, Y Hutchinson, A Dean, M Lupski, JR Leppert, M TI The Stargardt disease gene (ABCR) is mutated in age-related macular degeneration. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, Frederick, MD USA. SAIC Frederick, Frederick, MD USA. Baylor Coll Med, Houston, TX 77030 USA. Univ Utah, Moran Eye Ctr, Salt Lake City, UT 84112 USA. Univ Utah, Eccles Inst Human Genet, Salt Lake City, UT 84112 USA. Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 6 BP A3 EP A3 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000007 ER PT J AU Baser, ME MacCollin, MM Evans, DGR Allen, J Jackler, RK Sujansky, E Rubenstein, AE Louis, DN AF Baser, ME MacCollin, MM Evans, DGR Allen, J Jackler, RK Sujansky, E Rubenstein, AE Louis, DN TI Malignant nervous system tumors in neurofibromatosis 2. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. St Marys Hosp, Manchester M13 0JH, Lancs, England. Beth Israel Hosp, New York, NY USA. Univ Calif San Francisco, Sch Med, San Francisco, CA 94143 USA. Univ Colorado, Sch Med, Denver, CO USA. Mt Sinai Sch Med, New York, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 321 BP A60 EP A60 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000320 ER PT J AU Bass, MP Scott, WK Terwedow, HA Menold, MM Aboudonia, S Yamaoka, LH Gaskell, PC Conneally, PM Schamel, M Small, GW Vance, JM Saunders, AM Roses, AD Haines, JL Pericak-Vance, MA AF Bass, MP Scott, WK Terwedow, HA Menold, MM Aboudonia, S Yamaoka, LH Gaskell, PC Conneally, PM Schamel, M Small, GW Vance, JM Saunders, AM Roses, AD Haines, JL Pericak-Vance, MA TI The chromosome 12 AD locus is restricted to large late-onset pedigrees. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Duke Univ, Med Ctr, Durham, NC 27706 USA. Massachusetts Gen Hosp, Charlestown, MA USA. Indiana Univ, Med Ctr, Indianapolis, IN USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Vanderbilt Univ, Med Ctr, Nashville, TN USA. RI Scott, William/A-7593-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1553 BP A267 EP A267 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001557 ER PT J AU Beauchamp, RL Pinney, DM Candia, C Murthy, V Gonzalez-Agosti, C Ramesh, V AF Beauchamp, RL Pinney, DM Candia, C Murthy, V Gonzalez-Agosti, C Ramesh, V TI Developmental expression analysis of tuberin isoforms. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 322 BP A60 EP A60 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000323 ER PT J AU Benoit, E Tsao, H Dryja, TP Haluska, FG AF Benoit, E Tsao, H Dryja, TP Haluska, FG TI Retinoblastoma tumors lacking identified RB1 alterations do not carry mutations in p16/CDKN2A or CDK4, other elements of the pRB pathway. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 324 BP A61 EP A61 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000327 ER PT J AU Blakley, PM Hoar, RM Holmes, LB AF Blakley, PM Hoar, RM Holmes, LB TI Prenatal counseling for "anatomic variants" detected by sonography. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Genet & Teratol Unit, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 2203 BP A376 EP A376 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446002205 ER PT J AU Calzonetti, T White, JK Weaver, MA Vrbanac, V Gusella, JF MacDonald, ME AF Calzonetti, T White, JK Weaver, MA Vrbanac, V Gusella, JF MacDonald, ME TI Huntingtin is required at several stages of murine embryogenesis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Mol Neurogenet Unit, Charlestown, MA 02129 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1782 BP A305 EP A305 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001785 ER PT J AU Chen, ZY Derfler, B Hasson, T Schwender, B Corey, DP AF Chen, ZY Derfler, B Hasson, T Schwender, B Corey, DP TI Cloning and characterization of a new member of myosin VII family: Myosin VIIb. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Dept Neurobiol, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA 02114 USA. Howard Hughes Med Inst, Boston, MA 02114 USA. Yale Univ, Dept Biol, New Haven, CT 06520 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 966 BP A168 EP A168 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000966 ER PT J AU Collins, JS Perry, RT Watson, B Vanichanan, CJ Blacker, D Meyers, DA Albert, MS Tanzi, R Bassett, SS Rodes, L Go, RCP AF Collins, JS Perry, RT Watson, B Vanichanan, CJ Blacker, D Meyers, DA Albert, MS Tanzi, R Bassett, SS Rodes, L Go, RCP TI Linkage of D6S305 in Alzheimer disease families containing APOE E4/E4 genotypes - The NIHM genetics initiative AD study group. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Alabama, Birmingham, AL USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 2333 BP A399 EP A399 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446002335 ER PT J AU Coulon, V Feilotter, HE Boag, AH Dorion-Bonnet, F Duboue, B Latham, WCW Eng, C Longy, M Mulligan, LM AF Coulon, V Feilotter, HE Boag, AH Dorion-Bonnet, F Duboue, B Latham, WCW Eng, C Longy, M Mulligan, LM TI Loss of heterozygosity of chromosomal region 10q23 in human sporadic breast carcinoma. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Inst Bergonie, Oncol Mol Lab, F-33076 Bordeaux, France. Queens Univ, Dept Pathol, Kingston, ON K7L 3N6, Canada. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Human Canc Genet Unit, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Program Populat Sci,Dept Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 335 BP A63 EP A63 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000336 ER PT J AU Dahla, PLM Marsh, DJ Zheng, Z Zedenius, J Komminoth, P Parsons, R Longy, M Larsson, C Eng, C AF Dahla, PLM Marsh, DJ Zheng, Z Zedenius, J Komminoth, P Parsons, R Longy, M Larsson, C Eng, C TI Mutation and deletion analysis of the Cowden disease gene, PTEN, in sporadic nonmedullary thyroid tumors. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Karolinska Hosp, Dept Mol Med, S-10401 Stockholm, Sweden. Karolinska Hosp, Dept Surg, S-10401 Stockholm, Sweden. Univ Zurich, Dept Pathol, CH-8006 Zurich, Switzerland. Columbia Univ, Ctr Canc, Dept Pathol, New York, NY 10027 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 338 BP A63 EP A63 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000340 ER PT J AU Emmons, KM Kalkbrenner, KJ Kieffer, SA Schrag, D Patenaude, AF Light, T Schneider, KA Garber, JE AF Emmons, KM Kalkbrenner, KJ Kieffer, SA Schrag, D Patenaude, AF Light, T Schneider, KA Garber, JE TI Cancer risk behaviors among a sample of patients presenting for genetic testing. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Dana Farber Canc Inst, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1082 BP A188 EP A188 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001086 ER PT J AU Eng, C Marsh, D Liaw, D Dahia, P Li, J Zheng, Z Tsou, H Peacocke, M Gorlin, R Parsons, R AF Eng, C Marsh, D Liaw, D Dahia, P Li, J Zheng, Z Tsou, H Peacocke, M Gorlin, R Parsons, R TI Germline mutations of the PTEN gene in Cowden disease and Bannayan-Zonana syndrome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Columbia Univ, Ctr Canc, New York, NY 10027 USA. Univ Minnesota, Minneapolis, MN 55455 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 69 BP A15 EP A15 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000069 ER PT J AU Feilotter, HE Nagal, MA Boag, AH Eng, C Mulligan, LM AF Feilotter, HE Nagal, MA Boag, AH Eng, C Mulligan, LM TI Analysis of the PTEN coding region in primary prostate carcinomas. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Queens Univ, Dept Pathol, Kingston, ON K7L 3N6, Canada. Univ Sao Paulo, Fac Med, Dept Radiol, Disciplina Oncol, Sao Paulo, Brazil. Harvard Univ, Sch Med, Dept Adult Oncol, Human Canc Genet Unit, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med,Program Populat Sci, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 348 BP A65 EP A65 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000351 ER PT J AU Hagstrom, SA Dryja, TP AF Hagstrom, SA Dryja, TP TI Somatic recombination map of 13cen-q14. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1619 BP A278 EP A278 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001623 ER PT J AU Haines, JL Oksenberg, JR Rimmler, JB Lincoln, R Bazyk, A Leber, LA Hauser, SL Terwedow, HA Pericak-Vance, MA AF Haines, JL Oksenberg, JR Rimmler, JB Lincoln, R Bazyk, A Leber, LA Hauser, SL Terwedow, HA Pericak-Vance, MA TI Examination of the MHC in multiple sclerosis (MS). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Vanderbilt Univ, Nashville, TN USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Duke Univ, Med Ctr, Durham, NC 27706 USA. RI Hauser, Stephen/J-2978-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 209 BP A40 EP A40 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000210 ER PT J AU Haluska, FG Benoit, E Huebner, K Haber, D Tsao, H AF Haluska, FG Benoit, E Huebner, K Haber, D Tsao, H TI Involvement of the novel tumor suppressor PTEN in the pathogenesis of malignant melanoma. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Thomas Jefferson Univ, Med Ctr, Philadelphia, PA 19107 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 363 BP A67 EP A67 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000362 ER PT J AU Hiller, EH Parmigiani, G Berry, DA Chittenden, AB Fox, E Kieffer, SA Mahoney, KE Schneider, KA Schrag, D Garber, JE AF Hiller, EH Parmigiani, G Berry, DA Chittenden, AB Fox, E Kieffer, SA Mahoney, KE Schneider, KA Schrag, D Garber, JE TI Validity testing of a computer model for calculating carrier probabilities of BRCA1 and BRCA2 mutations. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Duke Univ, ISDS, Durham, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1280 BP A221 EP A221 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001281 ER PT J AU Kieffer, SA Schneider, KA Patenaude, AF Emmons, KM Hiller, EH Mahoney, KE Schrag, D Kalkbrenner, KJ Light, TE Weber, BL Garber, JE AF Kieffer, SA Schneider, KA Patenaude, AF Emmons, KM Hiller, EH Mahoney, KE Schrag, D Kalkbrenner, KJ Light, TE Weber, BL Garber, JE TI Cancer risk perception and surveillance behaviors in a population presenting for BRCA1 and BRCA2 testing. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DFCI, Boston, MA USA. Univ Penn, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 113 BP A23 EP A23 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000113 ER PT J AU Kramer, P Zareparsi, S Kaye, J Camicioli, R Nutt, J Litt, M Payami, H AF Kramer, P Zareparsi, S Kaye, J Camicioli, R Nutt, J Litt, M Payami, H TI Exclusion of the locus for Parkinson's disease on Chromosome 4 in three families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Portland Vet Affairs Med Ctr, Portland, OR USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1639 BP A281 EP A281 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001642 ER PT J AU Kupfer, GM Naf, D Suliman, A Pulsipher, M D'Andrea, AD AF Kupfer, GM Naf, D Suliman, A Pulsipher, M D'Andrea, AD TI The Fanconi anemia proteins, FAA and FAC bind and form a nuclear complex. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Harvard Univ, Childrens Hosp, Sch Med, Dept Pediat, Boston, MA 02115 USA. Harvard Univ, Childrens Hosp, Sch Med, Dana Farber Canc Inst,Div Pediat Oncol, Boston, MA 02115 USA. Harvard Univ, Childrens Hosp, Sch Med, Dana Farber Canc Inst,Div Cellular & Mol Biol, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 248 BP A47 EP A47 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000249 ER PT J AU Kwiatkowski, DJ Henske, EP Kwiatkowska, J Young, J Burley, M Jeremiah, S Woodward, K Nahmias, J Fox, M Ekong, R Wolfe, J Povey, S Osborne, J Snell, RG Cheadle, JP Jones, AC Tachataki, M Ravine, D Sampson, JR Reeve, MP Richardson, P Wilmer, F Munro, C Hawkins, TL Sepp, T Ali, JBM Ward, S Green, AJ Yates, JRW Short, MP Haines, JH Jozwiak, S van Slegtenhorst, M de Hoogt, R Hermans, C Nellist, M Janssen, B Verhoef, S Lindhout, D van den Ouweland, A Halley, D AF Kwiatkowski, DJ Henske, EP Kwiatkowska, J Young, J Burley, M Jeremiah, S Woodward, K Nahmias, J Fox, M Ekong, R Wolfe, J Povey, S Osborne, J Snell, RG Cheadle, JP Jones, AC Tachataki, M Ravine, D Sampson, JR Reeve, MP Richardson, P Wilmer, F Munro, C Hawkins, TL Sepp, T Ali, JBM Ward, S Green, AJ Yates, JRW Short, MP Haines, JH Jozwiak, S van Slegtenhorst, M de Hoogt, R Hermans, C Nellist, M Janssen, B Verhoef, S Lindhout, D van den Ouweland, A Halley, D TI Identification of the tuberous sclerosis gene (TSC1) on chromosome 9q34. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Brigham & Womens Hosp, Div Expt Med & Med Oncol, Boston, MA 02115 USA. UCL, Galton Lab, London WC1E 6BT, England. UCL, MRC, Human Biochem Genet Unit, London WC1E 6BT, England. Univ Bath, Bath BA2 7AY, Avon, England. Cardiff Univ, Inst Med Genet, Cardiff CF4 4XN, S Glam, Wales. MIT, Whitehead Inst, Ctr Genome Res, Cambridge, MA USA. Univ Cambridge, Dept Pathol, Addenbrookes NHS Trust, Cambridge CB2 1QP, England. Univ Cambridge, Dept Med Genet, Addenbrookes NHS Trust, Cambridge CB2 1QP, England. Univ Chicago, Sch Med, Dept Child Neurol, Chicago, IL 60637 USA. Massachusetts Gen Hosp, Mol Neurogenet Unit, Boston, MA 02114 USA. Childrens Hlth Ctr, Div Child Neurol, Warsaw, Poland. Erasmus Univ, Dept Clin Genet, NL-3000 DR Rotterdam, Netherlands. Univ Hosp, Rotterdam, Netherlands. RI Ravine, David/A-6797-2008; MOHD ALI, JOHARI/B-5259-2010 OI MOHD ALI, JOHARI/0000-0002-6884-4280 NR 0 TC 0 Z9 0 U1 2 U2 6 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 7 BP A4 EP A4 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000008 ER PT J AU Larson, GP Zhang, G Ding, S Foldenauer, K Udar, N Gatti, RA Neuberg, D Lunetta, K Longmate, J Flanagan, S Krontiris, TG AF Larson, GP Zhang, G Ding, S Foldenauer, K Udar, N Gatti, RA Neuberg, D Lunetta, K Longmate, J Flanagan, S Krontiris, TG TI An allelic variant at the ATM locus is implicated in breast cancer susceptibility SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 City Hope Natl Med Ctr, Beckman Res Inst, Div Mol Med, Duarte, CA 91010 USA. City Hope Natl Med Ctr, Beckman Res Inst, Div Neurosci, Duarte, CA 91010 USA. City Hope Natl Med Ctr, Beckman Res Inst, Div Informat Sci, Duarte, CA 91010 USA. Univ Calif Los Angeles, Sch Med, Dept Pathol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Sch Med, Dept Ophthalmol, Los Angeles, CA 90095 USA. Dana Farber Canc Inst, Dept Biostat Sci, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 385 BP A71 EP A71 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000385 ER PT J AU Liebert, CB Mull, J LeBel, A MacCormack, K Gill, S Leyne, M Moody, D Buckler, A Maayan, C Blumenfeld, A Axelrod, F Gusella, JF Slaugenhaupt, SA AF Liebert, CB Mull, J LeBel, A MacCormack, K Gill, S Leyne, M Moody, D Buckler, A Maayan, C Blumenfeld, A Axelrod, F Gusella, JF Slaugenhaupt, SA TI Cloning of a novel band 4.1 superfamily gene from the Familial Dysautonomia candidate region on human chromosome 9. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Sequana Inc, La Jolla, CA USA. Hadassah Univ Hosp, IL-91120 Jerusalem, Israel. NYU, Sch Med, New York, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1014 BP A176 EP A176 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001014 ER PT J AU Lockwood, SK Sims, KB AF Lockwood, SK Sims, KB TI A protein with two immunoglobulin domains interacts with the Norrie disease gene product norrin. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Ctr Neurosci, Charlestown, MA 02129 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 903 BP A158 EP A158 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000907 ER PT J AU Lunetta, KL AF Lunetta, KL TI Effect of non-amplifying ("null") alleles on affected and discordant sib pair linkage analyses. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Harvard Univ, Dana Farber Canc Inst, Boston, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1650 BP A283 EP A283 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001651 ER PT J AU Malecki, M Casey, P Antonellis, A Ji, L Yang, Y Wantman, M Warram, JH Krolewski, AS AF Malecki, M Casey, P Antonellis, A Ji, L Yang, Y Wantman, M Warram, JH Krolewski, AS TI Exclusion of the Hepatocyte Nuclear Factor-4 alpha as a candidate gene for late onset NIDDM that is linked with chromosome 20q12-13.1 in Caucasian families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Joslin Diabet Ctr, Boston, MA 02215 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1654 BP A284 EP A284 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001656 ER PT J AU Myers, SM Eng, C Hession, C Cate, R Kogon, MD Mulligan, LM AF Myers, SM Eng, C Hession, C Cate, R Kogon, MD Mulligan, LM TI The physical structures of GDNFR-alpha and NDNR-alpha. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Dana Farber Canc Inst, Div Canc Epidemiol & Control, Boston, MA 02115 USA. Queens Univ, Dept Pathol, Kingston, ON K7L 3N6, Canada. Biogen Inc, Dept Mol Biol, Cambridge, MA 02142 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 2231 BP A381 EP A381 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446002231 ER PT J AU Ozelius, LJ Hewett, JW Shalish, C Page, CE Bressman, SB Kramer, PL deLeon, D Buckler, AJ Brin, MF Corey, DP Fahn, S Risch, NJ Gusella, JF Breakefield, XO AF Ozelius, LJ Hewett, JW Shalish, C Page, CE Bressman, SB Kramer, PL deLeon, D Buckler, AJ Brin, MF Corey, DP Fahn, S Risch, NJ Gusella, JF Breakefield, XO TI Early onset torsion dystonia gene (DYT1) encodes an ATP-binding protein. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. Columbia Presbyterian Med Ctr, New York, NY 10032 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Mt Sinai Med Ctr, New York, NY 10029 USA. Stanford Univ, Stanford, CA 94305 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 46 BP A11 EP A11 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000049 ER PT J AU Peel, D Kolodner, R Li, F Anton-Culver, H AF Peel, D Kolodner, R Li, F Anton-Culver, H TI Relationship between replication error (RER) and MSH2/MLH1 gene mutation in population based HNPCC kindreds. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Calif Irvine, Div Epidemiol, Irvine, CA 92697 USA. Dana Farber Canc Inst, Div Human Canc Genet, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1203 BP A208 EP A208 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001204 ER PT J AU Pivnick, EK Shaefer, GB Lin, AE Park, VM Tolley, EA Lawrence, MD Huson, SM AF Pivnick, EK Shaefer, GB Lin, AE Park, VM Tolley, EA Lawrence, MD Huson, SM TI Delineation of a common facial appearance in neurofibromatosis type 1 (NF1). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Tennessee, Memphis, TN USA. Univ Nebraska, Omaha, NE 68182 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Lebonheur Childrens Med Ctr, Memphis, TN USA. Oxford Radcliffe Hosp, Oxford, England. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 616 BP A110 EP A110 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000618 ER PT J AU Rebbeck, TR Blackwood, MA Walker, AH White, DL Godwin, AK Daly, MB Garber, JE Weber, BL Narod, SA AF Rebbeck, TR Blackwood, MA Walker, AH White, DL Godwin, AK Daly, MB Garber, JE Weber, BL Narod, SA TI Association of breast cancer incidence with NAT2 genotype and smoking in BRCA1 mutation carriers. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Penn, Philadelphia, PA 19104 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Womens Coll Hosp, Toronto, ON M5S 1B2, Canada. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 242 BP A46 EP A46 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000243 ER PT J AU Rimmler, JB Gaskell, PC Aboudonia, S Welsh-Bohmer, K Jackson, CE Schamel, M Yamaoka, L Haines, JL Pericak-Vance, MA AF Rimmler, JB Gaskell, PC Aboudonia, S Welsh-Bohmer, K Jackson, CE Schamel, M Yamaoka, L Haines, JL Pericak-Vance, MA TI A genomic screen in extended Amish families supports a locus on chromosome 12 for Alzheimer disease (AD). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Duke Univ, Med Ctr, Durham, NC 27706 USA. Henry Ford Hosp, Detroit, MI 48202 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Vanderbilt Univ, Med Ctr, Nashville, TN USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1705 BP A292 EP A292 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001708 ER PT J AU Rogus, JJ Lunetta, KL AF Rogus, JJ Lunetta, KL TI Asymptotic properties and power of linkage tests for discordant and transplant sib pairs. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Harvard Univ, Sch Publ Hlth, Program Populat Genet, Boston, MA 02115 USA. Dana Farber Canc Inst, Div Biostat, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1210 BP A209 EP A209 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001213 ER PT J AU Schneider, KA McDermet, M AF Schneider, KA McDermet, M TI Differences in informed consent and genetic counseling practices in cancer susceptibility testing. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Genzyme, Tarrytown, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 110 BP A22 EP A22 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000111 ER PT J AU Schwartz, CE Hunter, AGW Holmes, LB Guttormsen, SA Tackels, DC Kemp, L Torres, ST Du, YZ Stevenson, RE Weitkamp, LR AF Schwartz, CE Hunter, AGW Holmes, LB Guttormsen, SA Tackels, DC Kemp, L Torres, ST Du, YZ Stevenson, RE Weitkamp, LR TI The methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism: An example of heterozygote advantage by natural selection SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Greenwood Genet Ctr, Self Res Inst, Greenwood, SC 29646 USA. Childrens Hosp Eastern Ontario, Dept Genet, Ottawa, ON K1H 8L1, Canada. Massachusetts Gen Hosp, Serv Pediat, Genet & Teratol Unit, Boston, MA 02114 USA. Univ Rochester, Med Ctr, Div Genet, Rochester, NY 14642 USA. NR 0 TC 0 Z9 0 U1 1 U2 4 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1220 BP A211 EP A211 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001224 ER PT J AU Siddique, T Pericak-Vance, MA Caliendo, J Hong, ST Hung, WY Kaplan, J McKenna-Yasek, D Rimmler, JB Sapp, P Saunders, AM Scott, WK Siddique, N Haines, JL Brown, RH AF Siddique, T Pericak-Vance, MA Caliendo, J Hong, ST Hung, WY Kaplan, J McKenna-Yasek, D Rimmler, JB Sapp, P Saunders, AM Scott, WK Siddique, N Haines, JL Brown, RH TI Lack of association between apolipoprotein E (APOE) genotype and sporadic amyotrophic lateral sclerosis (ALS). SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Northwestern Univ, Sch Med, Chicago, IL USA. Duke Univ, Med Ctr, Durham, NC 27706 USA. Massachusetts Gen Hosp, Charlestown, MA USA. MIT, Boston, MA USA. Vanderbilt Univ, Med Ctr, Nashville, TN USA. RI Scott, William/A-7593-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1718 BP A294 EP A294 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001718 ER PT J AU Sippel, KC Fraioli, RE Smith, GD Schalkoff, ME Dryja, TP AF Sippel, KC Fraioli, RE Smith, GD Schalkoff, ME Dryja, TP TI Frequent somatic and germ-line mosaicism in retinoblastoma: relevance to genetic counseling. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA. Boston Fertil Ctr, Brookline, MA USA. Univ Chicago, Chicago, IL 60637 USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 75 BP A16 EP A16 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000075 ER PT J AU Stoler, JM Holmes, LB AF Stoler, JM Holmes, LB TI Alcohol dehydrogenase (ADH2) genotypes in infants with fetal alcohol effects. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Genet & Teratol Unit, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 2270 BP A388 EP A388 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446002271 ER PT J AU Ticho, BS Oh, SP Li, E AF Ticho, BS Oh, SP Li, E TI The genetics of left-right asymmetry and heterotaxy elucidated by a mouse knock-out of the TGF beta activin receptor IIB which is a model for asplenia syndrome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 940 BP A164 EP A164 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000941 ER PT J AU Tsao, H Benoit, E Huebner, K Thiele, C Haluska, FG AF Tsao, H Benoit, E Huebner, K Thiele, C Haluska, FG TI Identification of novel mutations in the exon of CDK4 containing the p16-binding region. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Thomas Jefferson Med Ctr, Philadelphia, PA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 467 BP A85 EP A85 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000471 ER PT J AU Tsou, HC Teng, D Ping, XL Broncolini, V Davis, T Hu, R Xie, XX Gruener, AC Schrager, AC Christiano, AC Eng, C Steck, P Ott, J Tavitigian, S Peacocke, M AF Tsou, HC Teng, D Ping, XL Broncolini, V Davis, T Hu, R Xie, XX Gruener, AC Schrager, AC Christiano, AC Eng, C Steck, P Ott, J Tavitigian, S Peacocke, M TI Role of MMAC1 mutations in early onset breast cancer: Causative in association with Cowden's syndrome and excluded in BRCA1-negative cases SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Texas, MD Anderson Cancer Ctr, Dept Pathol, Brain Tumor Ctr, Houston, TX 77030 USA. Univ Texas, MD Anderson Cancer Ctr, Dept Neurooncol, Brain Tumor Ctr, Houston, TX 77030 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Columbia Univ Coll Phys & Surg, Dept Dermatol, New York, NY 10032 USA. Myriad Genet Inc, Salt Lake City, UT 84108 USA. Rockefeller Univ, Lab Stat Genet, New York, NY 10021 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 468 BP A85 EP A85 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000469 ER PT J AU Weitzel, JN Larson, G Ding, S Goodman, A Grendys, EC Ball, HG Krontiris, TG AF Weitzel, JN Larson, G Ding, S Goodman, A Grendys, EC Ball, HG Krontiris, TG TI Rare HRAS1 minisatellite alleles contribute to sporadic epithelial ovarian cancer risk SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 New England Med Ctr, Boston, MA 02111 USA. City Hope Natl Med Ctr, Duarte, CA 91010 USA. Beckman Res Inst, Duarte, CA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 484 BP A88 EP A88 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446000486 ER PT J AU Wheeler, VC Ryan, A Auerbach, A Calzonetti, T Duyao, MP White, JK Vrbanac, V Allen, MJ Gusella, JF Srinidhi, J Joyner, AL MacDonald, ME AF Wheeler, VC Ryan, A Auerbach, A Calzonetti, T Duyao, MP White, JK Vrbanac, V Allen, MJ Gusella, JF Srinidhi, J Joyner, AL MacDonald, ME TI Inheritance of the Huntington's disease CAG repeat in mice. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp East, Mol Neurogenet Unit, Charlestown, MA USA. NYU, Med Ctr, Skirball Inst Biomol Med, Dev Genet Program, New York, NY 10016 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1892 BP A323 EP A323 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001894 ER PT J AU White, JK Auerbach, W Calzonetti, T Weaver, M Vrbanac, V Vonsattel, JP Gusella, JF Joyner, AL MacDonald, ME AF White, JK Auerbach, W Calzonetti, T Weaver, M Vrbanac, V Vonsattel, JP Gusella, JF Joyner, AL MacDonald, ME TI Huntingtin function is required for mouse brain development and is not impaired by the Huntington's disease CAG expansion mutation. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Massachusetts Gen Hosp, Mol Neurogenet Unit, Charlestown, MA 02129 USA. Massachusetts Gen Hosp, Lab Mol Neuropathol, Charlestown, MA 02129 USA. NYU Med Ctr, Skirball Inst Biomol Med, Dev Genet Program, New York, NY 10016 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 1893 BP A324 EP A324 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446001895 ER PT J AU Wilkin, DJ Liberfarb, R Mortier, GR Warman, M Cohn, DH Francomano, CA AF Wilkin, DJ Liberfarb, R Mortier, GR Warman, M Cohn, DH Francomano, CA TI Genetic heterogeneity in Stickler syndrome: phenotypic exploration. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NHGRI, NIH, Bethesda, MD USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. State Univ Ghent Hosp, Ctr Med Genet, B-9000 Ghent, Belgium. Case Western Reserve Univ, Cleveland, OH 44106 USA. Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA. RI Mortier, Geert/D-2542-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 2055 BP A351 EP A351 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446002057 ER PT J AU Yang, Y Antonellis, A Malecki, M Wantman, M Warram, JH Krolewski, AS AF Yang, Y Antonellis, A Malecki, M Wantman, M Warram, JH Krolewski, AS TI Mutation screening of the HNF-1 alpha gene in North American MODY families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Joslin Diabet Ctr, Boston, MA 02215 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1997 VL 61 IS 4 SU S MA 2061 BP A352 EP A352 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA YQ995 UT WOS:000071446002063 ER PT J AU Chow, MT DiSilvestro, VA Yung, CY Nawab, ZM Leehey, DJ Ing, TS AF Chow, MT DiSilvestro, VA Yung, CY Nawab, ZM Leehey, DJ Ing, TS TI Treatment of acute methanol intoxication with hemodialysis using an ethanol-enriched, bicarbonate-based dialysate SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE methanol; bicarbonate; hemodialysis; ethanol; dialysate ID THERAPY AB A patient poisoned with methanol was successfully hemodialyzed with an ethanol-enriched, bicarbonate-based dialysate, Along with a concomitant intravenous infusion of ethanol, the ethanol-enriched dialytic procedure was able to maintain an intradialytic plasma ethanol level of 80 to 102 mg/dL. The patient recovered without any sequelae of methanol intoxication. (C) 1997 by the National Kidney Foundation, Inc. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,DEPT MED,HINES,IL 60141. LOYOLA UNIV,DEPT MED,CHICAGO,IL 60611. LOYOLA UNIV,STRITCH SCH MED,MAYWOOD,IL 60153. NR 15 TC 22 Z9 24 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD OCT PY 1997 VL 30 IS 4 BP 568 EP 570 DI 10.1016/S0272-6386(97)90318-8 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA YA577 UT WOS:A1997YA57700019 PM 9328374 ER PT J AU Andrist, LC AF Andrist, LC TI Genital herpes: Overcoming barriers to diagnosis and treatment SO AMERICAN JOURNAL OF NURSING LA English DT Article RP Andrist, LC (reprint author), MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,GRAD PROGRAM NURSING,BOSTON,MA 02114, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-936X J9 AM J NURS JI Am. J. Nurs. PD OCT PY 1997 VL 97 IS 10 BP AAA16 EP & PG 4 WC Nursing SC Nursing GA XZ851 UT WOS:A1997XZ85100008 ER PT J AU Clermont, AC Aiello, LP Mori, F Aiello, LM Bursell, SE AF Clermont, AC Aiello, LP Mori, F Aiello, LM Bursell, SE TI Vascular endothelial growth factor and severity of nonproliferative diabetic retinopathy mediate retinal hemodynamics in vivo: A potential role for vascular endothelial growth factor in the progression of nonproliferative diabetic retinopathy SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID VIDEO FLUORESCEIN ANGIOGRAPHY; BLOOD-FLOW; PERMEABILITY FACTOR; MELLITUS; CIRCULATION; CELLS; RATS; NEOVASCULARIZATION; COMPLICATIONS; EXPRESSION AB PURPOSE: To determine the effect of vascular endothelial growth factor and retinopathy level on retinal hemodynamics in nondiabetic and diabetic rats and to evaluate retinal hemodynamics in nondiabetic and diabetic patients. METHODS: Forty-eight diabetic and 22 nondiabetic patients had their diabetic retinopathy levels determined from fundus photographs according to Early Treatment Diabetic Retinopathy Study (ETDRS). Fluorescein angiograms were recorded from the left eye by video fluorescein angiography. Retinal blood flow was calculated from the digitized angiograms. Human recombinant vascular endothelial growth factor or vehicle alone was injected intravitreally into 13 nondiabetic and 11 diabetic rats. RESULTS: Retinal blood flow decreased 33% in patients with ETDRS retinopathy level 10 compared with control patients (P = .001) and increased sequentially in more advanced stages of retinopathy, with a strong correlation between retinal blood flow and retinopathy level (r(2) = 0.434, P = .001). Tn the diabetic rats, retinal blood flow was decreased 35.6% (P = .01). Vascular endothelial growth factor maximally increased retinal blood flow by 36.1% in nondiabetic rats after 25 minutes (P = .001) and by 73.7% in diabetic rats after only 5 minutes (P = .01) and caused a greater response in diabetic than in nondiabetic rats. CONCLUSIONS: Retinal blood flow increases with advancing nonproliferative diabetic retinopathy in humans, and diabetes accentuates the vascular endothelial growth factor-induced increase in retinal blood flow and venous dilation in rats. Vascular endothelial growth factor may contribute to the changes in retinal hemodynamics and morphology observed in early diabetic retinopathy. C1 JOSLIN DIABET CTR, BEETHAM EYE INST, DIV RES, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, DEPT OPHTHALMOL, BOSTON, MA USA. FU NEI NIH HHS [EY10827, EY09602]; PHS HHS [36836] NR 64 TC 100 Z9 104 U1 1 U2 4 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD OCT PY 1997 VL 124 IS 4 BP 433 EP 446 PG 14 WC Ophthalmology SC Ophthalmology GA XZ001 UT WOS:A1997XZ00100001 PM 9323935 ER PT J AU Stewart, WC Cohen, JS Netland, PA Weiss, H Nussbaum, LL Abrams, D Schwartz, G Hughes, P Adelson, A Brink, M Myers, M Bahr, R Dowling, JL Richards, F Geltzer, A Hofmann, J SnadyMcCoy, L Bartnik, LA Beneke, J Barr, L Muroski, D Neal, J Clevenger, C Summitt, B Lee, A Cohen, J Riccio, KA Luechauer, A DuBiner, H Cribbs, S Laibovitz, R Neck, K Mundorf, T Otero, D Vivolo, DA Schwartz, L Carmichael, P Conner, R Nowinski, T Kesselring, J Bollenbach, A Foley, A Stewart, W Stewart, J Schwartz, A Latham, BD AF Stewart, WC Cohen, JS Netland, PA Weiss, H Nussbaum, LL Abrams, D Schwartz, G Hughes, P Adelson, A Brink, M Myers, M Bahr, R Dowling, JL Richards, F Geltzer, A Hofmann, J SnadyMcCoy, L Bartnik, LA Beneke, J Barr, L Muroski, D Neal, J Clevenger, C Summitt, B Lee, A Cohen, J Riccio, KA Luechauer, A DuBiner, H Cribbs, S Laibovitz, R Neck, K Mundorf, T Otero, D Vivolo, DA Schwartz, L Carmichael, P Conner, R Nowinski, T Kesselring, J Bollenbach, A Foley, A Stewart, W Stewart, J Schwartz, A Latham, BD TI Efficacy of carteolol hydrochloride 1% vs timolol maleate 0.5% in patients with increased intraocular pressure SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID OPHTHALMIC BETA-BLOCKERS; OPEN-ANGLE GLAUCOMA; OCULAR HYPERTENSION; HEALTHY-VOLUNTEERS; 2-PERCENT AB PURPOSE: To evaluate the ocular hypotensive effect and safety of carteolol hydrochloride 1% vs timolol maleate 0.5%, METHODS: One hundred seventy sir; patients with ocular hypertension of primary open angle glaucoma were randomly assigned to receive either carteolol 1% twice a day or timolol maleate 0.5% solution twice a day in a randomized, double-masked, multicenter, parallel-group, active control comparison trial during a 3-month period, RESULTS: After 12 weeks, carteolol 1% reduced the mean +/- SE intraocular pressure from 25.0 +/- 0.3 to 19.5 +/- 0.3 mm Ng; timolol maleate 0.5% reduced the mean intraocular pressure from 25.2 +/- 0.3 to 19.6 +/- 0.3 mm Hg. The mean difference in trough intraocular pressure between carteolol and timolol maleate of -0.14 rum Hg was not. significantly (P = .745) different (95% confidence limits, -0.97 to 0.70 mm Hg). Trough pulse and blood pressure also showed no consistent statistically significant differences between groups. The 2-hour postdose pulse, however, demonstrated a greater decrease in the timolol maleate than in the carteolol group (P < .001). Systemic and ocular signs and symptoms mere similar between the groups except that: the number of treatment emergent reports of bradycardia was greater in the timolol maleate group (P = .039), and the carteolol group reported fewer ocular symptoms than the timolol maleate group did (P < .01). CONCLUSIONS: Both carteolol 1% and timolol maleate 0.5% are highly effective in lowering intraocular pressure when measured at the end of the dosing interval, Carteolol 1% demonstrates an ocular hypotensive effect and safety profile similar to those of timolol maleate 0.5% solution. C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. CINCINNATI EYE INST,CINCINNATI,OH. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. WASHINGTON HOSP CTR,WASHINGTON,DC 20010. GEORGETOWN UNIV,CTR SIGHT,WASHINGTON,DC. OTSUKA AMER PHARMACEUT INC,ROCKVILLE,MD. NR 21 TC 17 Z9 17 U1 0 U2 1 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD OCT PY 1997 VL 124 IS 4 BP 498 EP 505 PG 8 WC Ophthalmology SC Ophthalmology GA XZ001 UT WOS:A1997XZ00100006 PM 9323940 ER PT J AU Abrass, CK Spicer, D Berfield, AK StJohn, PL Abrahamson, DR AF Abrass, CK Spicer, D Berfield, AK StJohn, PL Abrahamson, DR TI Diabetes induces changes in glomerular development and laminin-beta 2 (s-laminin) expression SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID RAT MESANGIAL CELLS; EXTRACELLULAR-MATRIX; BASEMENT-MEMBRANE; DEVELOPING KIDNEY; NEUROMUSCULAR-JUNCTION; GROWTH-FACTORS; MESSENGER-RNA; HIGH GLUCOSE; IN-VITRO; COLLAGEN AB Offspring of diabetic mothers have developmental renal abnormalities; thus, we investigated the effects of the diabetic milieu on kidney development. Four groups of host rats, including insulin-deficient and insulin-treated streptozotocin-induced diabetic rats, normal controls, and insulin-treated nondiabetic rats, were prepared. After 38 days, rats received ocular implants of E14 fetal rat kidneys. Nine days later the fetal kidney grafts were harvested for analysis of glomerular development and expression of fibronectin, laminin, laminin-beta 2, and alpha-smooth muscle actin and m170, two additional markers of mesangial maturation. The rate of glomerular maturation was delayed in grafts placed in hyperglycemic, insulin-deficient diabetic rats. These glomeruli contained few mesangial cells or matrix, and laminin-beta 2 expression was reduced as compared with controls. Mesangial expression of alpha-smooth muscle actin and m170 was not detected. In contrast, grafts placed in insulin-treated diabetic animals had increased numbers of mesangial cells and expanded mesangial matrix. The content of laminin-beta 2 and expression of m170 and alpha-smooth muscle actin were also increased in these grafts. These data show that hyperglycemia and insulin status influence laminin isoform expression and play important roles in mesangial development. C1 VET AFFAIRS PUGET SOUND HLTH CARE SYST,DEPT MED,DIV NEPHROL,SEATTLE,WA 98108. UNIV WASHINGTON,SCH MED,SEATTLE,WA. UNIV ALABAMA,DEPT CELL BIOL,BIRMINGHAM,AL 35294. FU NIDDK NIH HHS [R01 DK34972, R01 DK49771, R01 DK37891] NR 43 TC 24 Z9 24 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD OCT PY 1997 VL 151 IS 4 BP 1131 EP 1140 PG 10 WC Pathology SC Pathology GA XZ753 UT WOS:A1997XZ75300028 PM 9327747 ER PT J AU Ullian, ME Raymond, JR Willingham, MC Paul, RV AF Ullian, ME Raymond, JR Willingham, MC Paul, RV TI Regulation of vascular angiotensin II receptors by EGF SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY LA English DT Article DE vascular smooth muscle cells; mitogen-activated protein kinase; G proteins ID SMOOTH-MUSCLE CELLS; GROWTH-FACTOR; PHOSPHOLIPASE-C; KINASE INHIBITORS; BINDING; RAT; ALDOSTERONE; PHOSPHORYLATION; PROTEIN; PROLIFERATION AB After vascular endothelial injury, angiotensin II (ANG II) plays a role in the resulting hypertrophic response, and expression of epidermal growth factor (EGF) is enhanced. Therefore, we tested the possibility that EGF regulates vascular ANG II action and receptor expression. Incubation of cultured aortic vascular smooth muscle cells (VSMC) with EGF (or basic fibroblast growth factor but not platelet-derived growth factor isoforms) resulted in concentration-dependent (1-50 ng/ml EGF), time-dependent (> 8 h), and reversible decreases in ANG II surface receptor density. For example, a 50% reduction was observed after exposure to 50 ng/ml EGF for 24 h. Incubation of cultured VSMC with 50 ng/ml EGF for 24 h resulted in a 77% reduction in ANG II-stimulated inositol phosphate formation. EGF not only prevented but also reversed ANG II receptor upregulation by 100 nM corticosterone. The specific tyrosine kinase inhibitor tyrphostin A48 (50 mu M) reduced EGF-stimulated thymidine incorporation and EGF-stimulated phosphorylation of mitogen-activated protein kinase but did not prevent EGF from reducing ANG II receptor density. Neither pertussis toxin (100 ng/ml) nor downregulation of protein kinase C by phorbol myristate acetate (100 nM for 24 h) prevented EGF from reducing ANG; II receptor density. In summary, EGF is a potent negative regulator of vascular ANG II surface receptor density and ANG II action by mechanisms that do not appear to include tyrosine phorphorylation, pertussis toxin-sensitive G proteins, or phorbol ester-sensitive protein kinase C. The possibility that EGF shifts the cell culture phenotype to one that exhibits reduced surface ANG II density cannot be eliminated by the present studies. C1 RALPH H JOHNSON VET AFFAIRS MED CTR, DEPT MED, DIV NEPHROL, CHARLESTON, SC 29425 USA. RALPH H JOHNSON VET AFFAIRS MED CTR, DEPT PATHOL, CHARLESTON, SC 29425 USA. RP Ullian, ME (reprint author), MED UNIV S CAROLINA, DEPT MED, DIV NEPHROL, CLIN SCI BLDG 829, 171 ASHLEY AVE, CHARLESTON, SC 29425 USA. FU NIDDK NIH HHS [DK-52448] NR 26 TC 17 Z9 17 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6143 J9 AM J PHYSIOL-CELL PH JI Am. J. Physiol.-Cell Physiol. PD OCT PY 1997 VL 273 IS 4 BP C1241 EP C1249 PG 9 WC Cell Biology; Physiology SC Cell Biology; Physiology GA YB153 UT WOS:A1997YB15300016 PM 9357768 ER PT J AU Rosenberg, IM Goke, M Kanai, M Reinecker, HC Podolsky, SK AF Rosenberg, IM Goke, M Kanai, M Reinecker, HC Podolsky, SK TI Epithelial cell kinase-B61: an autocrine loop modulating intestinal epithelial migration and barrier function SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE growth factors; cytokines; receptors; differentiation ID PROTEIN-TYROSINE KINASE; GROWTH-FACTOR; CDNA CLONING; RECEPTOR; IDENTIFICATION; EXPRESSION; FAMILY; GENE; ECK; LIGAND AB Epithelial cell kinase (Eck) is a member of a large family of receptor tyrosine kinases whose functions remain largely unknown. Expression and regulation of Eck and its cognate ligand B61 were analyzed in the human colonic adenocarcinoma cell line Caco-2. Immunocytochemical staining demonstrated coexpression of Eck and B61 in the same cells, suggestive of an autocrine loop. Eck levels were maximal in preconfluent cells. In contrast, B61 levels were barely detectable in preconfluent cells and increased progressively after the cells reached confluence. Caco-2 cells cultured in the presence of added B61 showed a significant reduction in the levels of dipeptidyl peptidase and sucrase-isomaltase mRNA, markers of Caco-2 cell differentiation. Cytokines interleukin-1 beta (IL-1 beta), basic fibroblast growth factor, IL-2, epidermal growth factor, and transforming growth factor-beta modulated steady-state levels of Eck and B61 mRNA and regulated Eck activation as assessed by tyrosine phosphorylation. Functionally, stimulation of Eck by B61 resulted in increased proliferation, enhanced barrier function, and enhanced restitution of injured epithelial monolayers. These results suggest that the Eck-B61 interaction, a target of regulatory peptides, plays a role in intestinal epithelial cell development, migration, and barrier function, contributing to homeostasis and preservation of continuity of the epithelial barrier. C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, DEPT MED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, DEPT MED, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK-43351, DK-41552, DK-51003] NR 36 TC 87 Z9 94 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 EI 1522-1547 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD OCT PY 1997 VL 273 IS 4 BP G824 EP G832 PG 9 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA YC068 UT WOS:A1997YC06800009 PM 9357823 ER PT J AU DeSanctis, GT Mehta, S Kobzik, L Yandava, C Jiao, AP Huang, PL Drazen, JM AF DeSanctis, GT Mehta, S Kobzik, L Yandava, C Jiao, AP Huang, PL Drazen, JM TI Contribution of type I NOS to expired gas NO and bronchial responsiveness in mice SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY LA English DT Article DE asthma; bronchoconstriction; neuronal nitric oxide synthase; knockout; nitric oxide ID NITRIC-OXIDE SYNTHASE; AIRWAY HYPERRESPONSIVENESS; ASTHMATIC-PATIENTS; NEURONS; IMMUNOREACTIVITY; LOCALIZATION; RELAXATION; INHIBITOR AB Nitric oxide (NO) can be measured in the expired gas of humans and animals, but the source of expired NO (FENO) and the functional contribution of the various known isoforms of NO synthase (NOS) to the NO measured in the expired air is not known. FENO was measured in the expired air of mice during mechanical ventilation via a tracheal cannula. FENO was significantly higher in wild-type B6SV129J +/+ mice than in mice with a targeted deletion of type I (neural) NOS (nNOS, -/-) (6.3 +/- 0.9 vs. 3.9 +/- 0.4 partsroillion, P = 0.0345, for +/+ and -/- mice, respectively), indicating that similar to 40% of the NO in expired air in B6SV129 mice is derived from nNOS. Airway responsiveness to methacholine (MCh), assessed by the log of the effective dose of MCh for a doubling of pulmonary resistance from baseline (ED200RL), was significantly lower in the -/- nNOS mice than in the wild-type mice (logED(200)R(L), 2.24 +/- 0.07 vs. 2.51 +/- 0.06 mu g/kg, respectively; P = 0.003). These findings indicate that nNOS significantly contributes to baseline FENO and promotes airway hyperresponsiveness in the mouse. C1 BRIGHAM & WOMENS HOSP, DEPT MED, DIV PULM & CRIT CARE, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, CARDIAC UNIT, BOSTON, MA 02115 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, CARDIOVASC RES CTR, BOSTON, MA 02115 USA. UNIV WESTERN ONTARIO, LONDON HLTH SCI CTR VICTORIA CAMPUS, DEPT MED, DIV RESP, LONDON, ON N6A 4G5, CANADA. FU NHLBI NIH HHS [HL-36110]; NINDS NIH HHS [NS-33335] NR 28 TC 56 Z9 58 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1040-0605 J9 AM J PHYSIOL-LUNG C JI Am. J. Physiol.-Lung Cell. Mol. Physiol. PD OCT PY 1997 VL 273 IS 4 BP L883 EP L888 PG 6 WC Physiology; Respiratory System SC Physiology; Respiratory System GA YA436 UT WOS:A1997YA43600022 PM 9357865 ER PT J AU Reed, JAH Rice, WR Zsengeller, ZK Wert, SE Dranoff, G Whitsett, JA AF Reed, JAH Rice, WR Zsengeller, ZK Wert, SE Dranoff, G Whitsett, JA TI GM-CSF enhances lung growth and causes alveolar type II epithelial cell hyperplasia in transgenic mice SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY LA English DT Article DE proliferation; alveolar macrophage; morphometric analysis; lung injury and repair; lung growth factor ID COLONY-STIMULATING FACTOR; RECEPTOR-DEFICIENT MICE; IN-VIVO; SP-A; PROLIFERATION; EXPRESSION; GENE; DIFFERENTIATION; HEMATOPOIESIS; PROTEINOSIS AB The human surfactant protein (SP)-C gene promoter was used to direct expression of mouse granulocyte macrophage colony-stimulating factor (GM-CSF; SP-C-GM mice) in lung epithelial cells in GM-CSF-replete (GM+/+) or GM-CSF null mutant (GM-/-) mice. Lung weight and volume were significantly increased in SP-C-GM mice compared with GM+/+ or GM-/- control mice. Immunohistochemical staining demonstrated marked type II cell hyperplasia, and immunofluorescent labeling for proliferating cell nuclear antigen was increased in type II cells of SP-C-GM mice. Abundance of type II cells per mouse lung was increased three-to fourfold in SP-C-GM mice compared with GM+/+ and GM-/- mice. GM-CSF increased bromodeoxyuridine labeling of isolated type II cells in vitro. Type II cells, alveolar macrophages, and endothelial and bronchiolar epithelial cells were stained by antibodies to the GM-CSF receptor ol-subunit in both GM+/+ mice and GM-CSF gene-targeted mice that are also homozygous for the SP-C-GM transgene. High levels of GM-CSF expression in type II cells of transgenic mice increased lung size and caused type II cell hyperplasia, demonstrating an unexpected role for the molecule in the regulation of type II cell proliferation and differentiation. C1 CHILDRENS HOSP, MED CTR, DIV PULM BIOL, CINCINNATI, OH 45229 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. NR 36 TC 68 Z9 68 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1040-0605 J9 AM J PHYSIOL-LUNG C JI Am. J. Physiol.-Lung Cell. Mol. Physiol. PD OCT PY 1997 VL 273 IS 4 BP L715 EP L725 PG 11 WC Physiology; Respiratory System SC Physiology; Respiratory System GA YA436 UT WOS:A1997YA43600002 ER PT J AU Gunning, M Solomon, RJ Epstein, FH Silva, P AF Gunning, M Solomon, RJ Epstein, FH Silva, P TI Role of guanylyl cyclase receptors for CNP in salt secretion by shark rectal gland SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article DE Squalus acanthias; HS-142-1; oxygen consumption ID ATRIAL-NATRIURETIC-PEPTIDE; SQUALUS-ACANTHIAS; MICROBIAL ORIGIN; GLOMERULAR HYPERFILTRATION; NONPEPTIDE ANTAGONIST; VOLUME EXPANSION; HS-142-1; RATS; CELLS; POLYSACCHARIDE AB The role of C-type natriuretic peptide (CNP) and its guanylyl cyclase-linked receptors in mediating salt secretion by the rectal gland of the spiny dogfish shark (Squalus acanthias) was investigated using HS-142-1, a competitive inhibitor of the binding of natriuretic peptides to their guanylyl cyclase receptors. CNP binds to receptors and activates guanylyl cyclase in rectal gland membranes in a way that is inhibited by HS-142-1. Guanylyl cyclase activation in rectal gland membranes is far more sensitive to CNP than to atrial natriuretic peptide, whereas the reverse is true for membranes derived from mammalian (rabbit) renal collecting duct cells. HS-142-1 inhibited the stimulatory effect of CNP on ouabain-inhibitable oxygen consumption by rectal gland tubules. In explanted rectal glands continuously perfused with blood from intact donor sharks, HS-142-1 inhibited the increase in salt secretion normally provoked by infusing isotonic saline solutions into the donor animal. These results strongly support the view that CNP released into the systemic circulation in response to volume expansion mediates the secretion of chloride by the rectal gland via receptors linked to guanylyl cyclase. C1 HARVARD UNIV, SCH MED, JOSLIN DIABET CTR, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, BETH ISRAEL DEACONESS MED CTR, DEPT MED, BOSTON, MA 02215 USA. MT DESERT ISL BIOL LAB, SALSBURY COVE, ME 04672 USA. FU NIDDK NIH HHS [DK-18078, DK-16684]; NIEHS NIH HHS [ES-O3828] NR 30 TC 6 Z9 6 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regul. Integr. Comp. Physiol. PD OCT PY 1997 VL 273 IS 4 BP R1400 EP R1406 PG 7 WC Physiology SC Physiology GA YA447 UT WOS:A1997YA44700025 PM 9362305 ER PT J AU Alper, SL StuartTilley, AK Biemesderfer, D Shmukler, BE Brown, D AF Alper, SL StuartTilley, AK Biemesderfer, D Shmukler, BE Brown, D TI Immunolocalization of AE2 anion exchanger in rat kidney SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY LA English DT Article DE chloride/bicarbonate exchange; immunomicroscopy; macula densa; thin limbs of Henle; thick limb of Henle; collecting duct; epitope unmasking ID COLLECTING DUCT; INTERCALATED CELLS; CL-/HCO3 EXCHANGER; MESSENGER-RNAS; BAND-3; MEMBRANE; ATPASE; IDENTIFICATION; LOCALIZATION; POLYPEPTIDE AB The cellular and subcellular localizations of the AE2 anion exchanger in rat kidney have remained elusive despite detection of moderately abundant AE2 mRNA and AE2 polypeptide in all kidney regions. In this report a simple epitope unmasking technique has allowed the immunolocalization of AE2 antigenic sites in basolateral membranes of several rat kidney tubular epithelial cells. AE2 immunostaining was faint or absent in the glomerulus and proximal tubule, present in descending and ascending thin limbs, and stronger in the medullary thick ascending limb (MTAL). A lower staining intensity was found in cortical thick ascending limbs and even less in the distal convoluted tubule. In contrast, there was an enhanced staining in the macula densa. In principal cells (PC) of the connecting segment, AE2 was undetectable but gradually increased in intensity along the collecting duct, with strongest staining in inner medullary collecting duct (IMCD) PC. A sodium dodecyl sulfate-sensitive AE2-related Golgi epitope was also detected in some interstitial and endothelial cells of the inner medulla and in epithelial cells of IMCD and MTAL. Colchicine treatment of the intact animal altered the distribution of this Golgi-associated epitope but left plasmalemmal AE2 undisturbed. Reverse transcription-polymerase chain reaction detected AE2a, AE2b, and AE2c2 but not AE2c1 transcripts in rat kidney mRNA. The results suggest a widespread occurrence of the AE2 protein in several renal epithelial cell types. C1 BETH ISRAEL DEACONESS MED CTR, RENAL UNIT, BOSTON, MA 02215 USA. MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, DEPT CELL BIOL, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02215 USA. YALE UNIV, SCH MED, NEPHROL SECT, NEW HAVEN, CT 06520 USA. YALE UNIV, SCH MED, DEPT MED, NEW HAVEN, CT 06520 USA. YALE UNIV, SCH MED, DEPT PHYSIOL, NEW HAVEN, CT 06520 USA. RP Alper, SL (reprint author), BETH ISRAEL DEACONESS MED CTR, MOL MED UNIT, RW763 E CAMPUS, 330 BROOKLINE AVE, BOSTON, MA 02215 USA. FU NIDDK NIH HHS [DK-43495, DK-42956, DK-51059] NR 40 TC 98 Z9 98 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1931-857X J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Physiol. PD OCT PY 1997 VL 273 IS 4 BP F601 EP F614 PG 14 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA YA441 UT WOS:A1997YA44100013 PM 9362338 ER PT J AU OSullivan, RL Keuthen, NJ Christenson, GA Mansueto, CS Stein, DJ Swedo, SE AF OSullivan, RL Keuthen, NJ Christenson, GA Mansueto, CS Stein, DJ Swedo, SE TI Trichotillomania: Behavioral symptom or clinical syndrome? SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Editorial Material ID OBSESSIVE-COMPULSIVE DISORDER; MGH HAIRPULLING SCALE; DOUBLE-BLIND; HAIR PULLERS; FLUOXETINE; CLOMIPRAMINE; CROSSOVER C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA. UNIV MINNESOTA,BOYNTON HLTH CTR,DEPT PSYCHIAT,MINNEAPOLIS,MN. BOWIE STATE UNIV,BOWIE,MD. UNIV STELLENBOSCH,DEPT PSYCHIAT,ZA-7600 STELLENBOSCH,SOUTH AFRICA. NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. RI Citations, TLC SAB/C-4006-2011; OI Stein, Dan/0000-0001-7218-7810 NR 52 TC 24 Z9 24 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD OCT PY 1997 VL 154 IS 10 BP 1442 EP 1449 PG 8 WC Psychiatry SC Psychiatry GA XY997 UT WOS:A1997XY99700018 PM 9326829 ER PT J AU Chew, FS AlSinan, AA AF Chew, FS AlSinan, AA TI Periosteal osteosarcoma of the tibia SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP Chew, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 4 TC 3 Z9 3 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD OCT PY 1997 VL 169 IS 4 BP 1034 EP 1034 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA XW981 UT WOS:A1997XW98100021 PM 9308458 ER PT J AU Eble, JN Amin, MB Young, RH AF Eble, JN Amin, MB Young, RH TI Epithelioid angiomyolipoma of the kidney - A report of five cases with a prominent and diagnostically confusing epithelioid smooth muscle component SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE kidney; angiomyolipoma; epithelioid cells; melanoma-associated antigens; immunohistochemistry ID HEPATIC ANGIOMYOLIPOMA; RENAL ANGIOMYOLIPOMA; HMB-45 REACTIVITY; LYMPHANGIOMYOMATOSIS; TRANSFORMATION; FAMILY; TUMOR AB We report five angiomyolipomas with a prominent component of epithelioid smooth muscle cells that occurred in patients from 20 to 48 (mean, 36) years of age. The tumors often posed problems in diagnosis, particularly with regard to distinction from renal cell carcinoma. Two patients had tuberous sclerosis. Two patients with more than 5 years' follow-up are alive and well. The epithelioid smooth muscle cells typically formed sheets that in two tumors were traversed by hyaline cords. The epithelioid cells ranged from medium sized and polygonal with slightly pleomorphic nuclei and eosinophilic cytoplasm to giant cells with prominent nucleoli. Hemorrhage, necrosis, and clusters of foamy macrophages were present in three tumors. Mitotic figures were easy to find in two of the tumors, but they were absent in the others. Obvious elements of typical angiomyolipoma were present in two tumors. The others contained only scattered, thick-walled blood vessels or a few fat cells suggestive of typical angiomyolipoma. None of the tumors was positive for low-or high-molecular-weight cytokeratins or epithelial membrane antigen. Actin was detected in the epithelioid areas in four tumors. Melanoma-associated antigens related to the gp100-cl gene product, HMB-45 and HMB-50, were present in all the tumors. Another melanoma-associated antigen, CD63 (NKI/C3), also was present in all the tumors, a finding suggesting that angiomyolipoma has features in common with melanoma beyond premelanosomal structures. C1 INDIANA UNIV,SCH MED,INDIANAPOLIS,IN. HENRY FORD HOSP,DETROIT,MI 48202. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Eble, JN (reprint author), RICHARD L ROUDEBUSH VET AFFAIRS MED CTR,1481 W 10TH ST,INDIANAPOLIS,IN 46202, USA. NR 23 TC 173 Z9 185 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD OCT PY 1997 VL 21 IS 10 BP 1123 EP 1130 DI 10.1097/00000478-199710000-00001 PG 8 WC Pathology; Surgery SC Pathology; Surgery GA YB150 UT WOS:A1997YB15000001 PM 9331283 ER PT J AU Ronnett, BM Kurman, RJ Shmookler, BM Sugarbaker, PH Young, RH AF Ronnett, BM Kurman, RJ Shmookler, BM Sugarbaker, PH Young, RH TI The morphologic spectrum of ovarian metastases of appendiceal adenocarcinomas - A clinicopathologic and immunohistochemical analysis of tumors often misinterpreted as primary ovarian tumors or metastatic tumors from other gastrointestinal sites SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE ovary; metastases; appendix; mucinous adenocarcinoma; signet ring cell carcinoma; krukenberg tumor; immunohistochemistry ID BILATERAL KRUKENBERG TUMORS; CRYPT CELL-CARCINOMA; MUCINOUS TUMORS; PSEUDOMYXOMA-PERITONEI; VERMIFORM APPENDIX; ORIGIN; CYTOKERATIN-7; EMPHASIS; CYSTADENOCARCINOMA; EXPRESSION AB Twenty cases of ovarian metastases derived from appendiceal adenocarcinomas were analyzed. The most common presentation was a pelvic mass. The appendiceal and ovarian tumors were diagnosed concurrently in 15 cases; in the remaining five, the ovarian tumors were diagnosed before the appendiceal tumor. The appendiceal adenocarcinomas demonstrated four morphologic patterns: 1) signet ring cell type, with or without glandular or goblet cell differentiation (14 cases); 2) mixed signer ring cell and intestinal type (two cases); 3) intestinal type (two cases); and 4) typical colorectal type (two cases). The ovarian tumors were bilateral in 16 cases and were histologically similar to the associated appendiceal tumor in each case. Ovarian metastases that demonstrate signet ring cell, glandular, and goblet cell differentiation mimic metastases from gastric adenocarcinoma. Those that are derived from well-differentiated mucinous appendiceal adenocarcinomas mimic primary ovarian mucinous tumors and metastases from the pancreas and biliary tract. Metastases of appendiceal adenocarcinomas of colorectal type simulate both metastatic colorectal carcinoma and primary ovarian endometrioid carcinomas. The appendiceal and ovarian tumors were immunophenotypically identical in each case. Approximately 50% of the appendiceal and ovarian tumors were positive for cytokeratin 7 (CK 7), and all were positive for cytokeratin 20 (CK 20). CK 20 positivity of the ovarian tumors is consistent with gastrointestinal origin; CK 7 positivity does not confirm ovarian origin, because appendiceal carcinomas are positive in 50% of cases. Metastatic appendiceal adenocarcinoma should be considered in the differential diagnosis of mucinous ovarian tumors with signet ring cell, goblet cell, or intestinal type differentiation, especially when these tumors are associated with extraovarian disease and are bilateral. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT OBSTET & GYNECOL,BALTIMORE,MD 21205. WASHINGTON HOSP CTR,DEPT PATHOL,WASHINGTON,DC 20010. WASHINGTON HOSP CTR,DEPT SURG,WASHINGTON,DC 20010. WASHINGTON HOSP CTR,INST CANC,WASHINGTON,DC 20010. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA. RP Ronnett, BM (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205, USA. NR 55 TC 97 Z9 98 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD OCT PY 1997 VL 21 IS 10 BP 1144 EP 1155 DI 10.1097/00000478-199710000-00004 PG 12 WC Pathology; Surgery SC Pathology; Surgery GA YB150 UT WOS:A1997YB15000004 PM 9331286 ER PT J AU Oliva, E Ferry, JA Young, RH Prat, J Srigley, JR Scully, RE AF Oliva, E Ferry, JA Young, RH Prat, J Srigley, JR Scully, RE TI Granulocytic sarcoma of the female genital tract: A clinicopathologic study of 11 cases SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE granulocytic sarcoma; chloroma; myeloid leukemia; ovary; vagina; uterus ID MYELOID CELL TUMORS; EMBEDDED TISSUE-SECTIONS; MYELOMONOCYTIC LEUKEMIA; PRIMARY MANIFESTATION; OVARY; LYMPHOMAS; CHLOROMA; CERVIX; VAGINA; UTERUS AB Eleven patients, 13 to 76 (mean, 40) years of age, had granulocytic sarcoma of the female genital tract (FGT) (ovary, seven cases; vagina, three cases; cervix, one case). In nine cases, the FGT involvement was the initial clinical presentation of the disease, and in the other two cases, the FGT involvement was discovered during a relapse of acute myeloid leukemia. The tumors ranged from 0.5 to 14 (mean, 7.5) cm in greatest dimension. Two ovarian tumors were bilateral, and three were green. Microscopic examination revealed a predominantly diffuse pattern of growth, but cords and pseudoacinar spaces were also present focally in several cases. Sclerosis was seen in five tumors and was prominent in one. Prominent myeloid differentiation was readily recognizable on routinely stained sections in three cases, whereas the neoplastic cells in the other cases were primitive with only rare eosinophilic myelocytes. All 11 tumors were positive for chloroacetate esterase, nine of nine were strongly and diffusely positive for lysozyme, eight of eight for myeloperoxidase, seven of seven for CD68, and six of six for CD43. Examination of bone marrow or peripheral blood performed after the diagnosis of FGT involvement revealed acute myeloid leukemia in three of five cases. Two of these patients died of disease, 1 and 16 months after the initial diagnosis, and the third, who received chemotherapy, is alive and free of disease 8 months after the initial diagnosis. One of the two patients with negative bone marrow had recurrent granulocytic sarcoma 30 months after diagnosis and died of sepsis 1 month later; no residual disease was noted at autopsy. The other patient is alive and free of disease 18 months after the diagnosis. One of the four remaining patients with primary FGT involvement who did not have a bone marrow biopsy died of leukemia 24 months later; no follow-up information is available for the other three patients. One of the two patients with a prior diagnosis of acute myeloid leukemia was alive with disease 26 months later; follow-up is not available for the second patient. The diagnosis was often difficult in these cases, the most com mon problem being distinction from malignant lymphoma, but carcinoma, granulosa cell tumor, and, rarely, other tumors were considered. Immunohistochemical and enzyme histochemical staining were useful in establishing the diagnosis, although suspicion of the diagnosis on examination of routinely stained sections was of paramount importance. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HOSP STA CREU & ST PAU,BARCELONA,SPAIN. CREDIT VALLEY HOSP,MISSISSAUGA,ON,CANADA. RP Oliva, E (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,32 FRUIT ST,BOSTON,MA 02114, USA. RI Prat, Jaime/G-4679-2011 NR 44 TC 48 Z9 58 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD OCT PY 1997 VL 21 IS 10 BP 1156 EP 1165 DI 10.1097/00000478-199710000-00005 PG 10 WC Pathology; Surgery SC Pathology; Surgery GA YB150 UT WOS:A1997YB15000005 PM 9331287 ER PT J AU Prus, D Rosenberg, AE Blumenfeld, A Udassin, R Neeman, Z Young, RH Ariel, I AF Prus, D Rosenberg, AE Blumenfeld, A Udassin, R Neeman, Z Young, RH Ariel, I TI Infantile hemangioendothelioma of the ovary: A monodermal teratoma or a neoplasm of ovarian somatic cells? SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE ovarian tumor; infantile hemangioendothelioma; congenital tumor; monodermal teratoma ID HEMANGIOMA; ORIGIN; GENETICS; BIOLOGY; MARKERS; TUMOR; DNA AB Vascular tumors of the female genital tract are uncommon, and only a few cases have been reported in the ovary. We describe herein, an unusual tumor of the ovary: infantile hemangioendothelioma (cellular hemangioma of infancy) in a newborn. The tumor consisted of well-formed blood vessels and proliferating endothelial cells that were arranged in solid cordlike structures. The tumor permeated the ovarian stroma and entrapped normal ovarian follicles. By immunohistochemistry the neoplastic cells expressed factor VIII, CD34, and alpha smooth-muscle actin, and ultrastructurally they had the features of endothelial cells that were focally associated with pericytes. We examined simple sequence repeat (SSR) polymorphic markers in the tumor tissue, as well as in the patient's and parents' blood. The informative SSR markers were found to be identical in the tumor and in the patient's somatic cells. We suggest that the tumor described herein is a congenital infantile hemangioendothelioma arising from ovarian parenchymal cells rather than a teratoma originating from germ cells. A similar morphologic lesion has been described recently in the ovary and interpreted as monodermal teratoma composed of vascular tissue. C1 HADASSAH UNIV HOSP,MOL BIOL UNIT,IL-91120 JERUSALEM,ISRAEL. HADASSAH UNIV HOSP,DEPT PEDIAT SURG,IL-91120 JERUSALEM,ISRAEL. HEBREW UNIV JERUSALEM,HADASSAH MED SCH,IL-91010 JERUSALEM,ISRAEL. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA. RP Prus, D (reprint author), HADASSAH UNIV HOSP,DEPT PATHOL,MT SCOPUS,POB 24035,IL-91240 JERUSALEM,ISRAEL. NR 29 TC 12 Z9 13 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD OCT PY 1997 VL 21 IS 10 BP 1231 EP 1235 DI 10.1097/00000478-199710000-00015 PG 5 WC Pathology; Surgery SC Pathology; Surgery GA YB150 UT WOS:A1997YB15000015 PM 9331297 ER PT J AU Rosow, CE AF Rosow, CE TI Methylnaltrexone - Reversing the gastrointestinal effects of opioids SO ANESTHESIOLOGY LA English DT Editorial Material DE opioid; gastric emptying; smooth muscle; methylnaltrexone C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA & CRIT CARE,BOSTON,MA 02114. RP Rosow, CE (reprint author), HARVARD UNIV,SCH MED,55 FRUIT ST,BOSTON,MA 02114, USA. NR 4 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD OCT PY 1997 VL 87 IS 4 BP 736 EP 737 DI 10.1097/00000542-199710000-00003 PG 2 WC Anesthesiology SC Anesthesiology GA YD117 UT WOS:A1997YD11700003 PM 9357871 ER PT J AU Gan, TJ Glass, PS Windsor, A Payne, F Rosow, C Sebel, P Manberg, P Howell, S Sanderson, I Ray, J Elidrissi, C Wilkes, N Calhoun, P Connors, P Alfille, P Shapiro, L Denman, W Dershwitz, M Clifford, J Embree, P Sigl, J AF Gan, TJ Glass, PS Windsor, A Payne, F Rosow, C Sebel, P Manberg, P Howell, S Sanderson, I Ray, J Elidrissi, C Wilkes, N Calhoun, P Connors, P Alfille, P Shapiro, L Denman, W Dershwitz, M Clifford, J Embree, P Sigl, J TI Bispectral index monitoring allows faster emergence and improved recovery from propofol, alfentanil, and nitrous oxide anesthesia SO ANESTHESIOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-of-Anesthesiologists CY OCT 17-25, 1996 CL NEW ORLEANS, LA SP Amer Soc Anesthesiologists DE anesthetics, intravenous, alfentanil, nitrous oxide, propofol; measurement techniques, bispectral index; outcome, anesthesia; recovery, emergence time ID SEDATION HYPNOSIS; MOVEMENT; EEG; VOLUNTEERS AB Background: The bispectral index (BIS), a parameter derived from the electroencephalograph (EEG), has been shown to correlate with increasing sedation and loss of consciousness. This study determined whether addition of BLS monitoring to standard anesthetic practice results in improvements in the conduct of anesthesia or in patient outcomes. Methods: Three hundred two patients receiving a propofolalfentanil-nitrous oxide anesthetic were studied at four institutions. Thirty-four patients were initially enrolled to determine preexisting anesthetic practice and patient outcomes at each institution. Subsequent patients were randomized to either standard clinical practice (SP group), or standard practice plus BIS monitoring (BIS group). In all patients, the anesthesiologist attempted to provide a stable anesthetic with the fastest possible recovery. BIS was recorded for all patients, but viewed only in the BIS group. In the BIS group, propofol infusions were adjusted to achieve a target BIS between 45-60, increasing to 60-75 during the final 15 min of the case. In the SP group, propofol dose adjustments were made based only on standard clinical signs. Drug use, intraoperative responses, and patient recovery parameters were recorded. Results: Demographics were similar between groups. Com pared with the SP group, patients in the BIS group required lower normalized propofol infusion rates (134 vs. 116 mu g.kg(-1).min(-1); P < 0.001), were extubated sooner (11.22 vs. 7.25 min; P < 0.003), had a higher percentage of patients oriented on arrival to PACU (43% vs. 23%; P < 0.02), had better postanesthesia care unit (PACU) nursing assessments (P < 0.001), and became eligible for discharge sooner (37.77 us. 31.70 min; P < 0.04). There was no significant difference in the incidence of intraoperative responses between the groups. Conclusions: Titrating propofol with BIS monitoring during balanced anesthesia decreased propofol use and significantly improved recovery. Intraoperative course was not changed. These findings indicate that the use of BIS may be valuable in guiding the administration of propofol intraoperatively. C1 EMORY UNIV, GRADY HLTH SYST, DEPT ANESTHESIOL, ATLANTA, GA 30322 USA. UNIV N CAROLINA, DEPT ANESTHESIOL, CHAPEL HILL, NC USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, DEPT ANESTHESIOL, BOSTON, MA USA. ASPECT MED SYST, DEPT ANESTHESIOL, NATICK, MA USA. RP Gan, TJ (reprint author), DUKE UNIV, MED CTR, DEPT ANESTHESIOL, BOX 3094, DURHAM, NC 27710 USA. NR 18 TC 341 Z9 364 U1 0 U2 7 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-3022 EI 1528-1175 J9 ANESTHESIOLOGY JI Anesthesiology PD OCT PY 1997 VL 87 IS 4 BP 808 EP 815 DI 10.1097/00000542-199710000-00014 PG 8 WC Anesthesiology SC Anesthesiology GA YD117 UT WOS:A1997YD11700014 PM 9357882 ER PT J AU Patrick, DL Pearlman, RA Starks, HE Cain, KC Cole, WG Uhlmann, RF AF Patrick, DL Pearlman, RA Starks, HE Cain, KC Cole, WG Uhlmann, RF TI Validation of preferences for life-sustaining treatment: Implications for advance care planning SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE advance directives; life support care; health status; treatment outcomes ID STATES WORSE; DIRECTIVES; ATTITUDES; STABILITY; CHOICES; QUALITY; VALUES; DEATH AB Background: Treatment preferences established before life-threatening illness occurs may differ from actual decisions because of changes in preferences or poor understanding of the link between prospective preferences and outcomes. Objective: To evaluate the validity of prospective treatment preferences by examining their concordance with ratings of health states. Design: Survey of seven cohorts of persons with diverse health status. Home-and hospital-based interviews were conducted at baseline and at 6, 18, and 30 months. Setting: The greater Seattle area. Participants: Younger and older well adults; persons with chronic conditions, terminal cancer, or AIDS; stroke survivors; and nursing home residents. Measurements: Concordance between six treatment preferences and five health state ratings (on a seven-point scale) was assessed by using logistic regression to measure the increase in odds of treatment refusal for each one-point change in health state ratings. Preferences were considered concordant if treatments were refused in health states rated as worse than death and were accepted in health states rated as better than death. Reasons for discordance were elicited at the final interview. Results: The probability of refusal of prospective treatment was strongly related to health state ratings. Odds ratios ranged from 1.7 to 1.9 (P < 0.001) for every treatment. When patients were shown their discordant preferences, they had a coherent explanation or changed their health state rating or treatment preference to make the two concordant. Conclusions: Prospective life-sustaining treatment preferences show high convergent validity. For most persons, treatment preferences are grounded in a consistent belief system. Concordance and discordance between treatment preferences and health state ratings offer clinicians the opportunity to explore patients' Values and reasoning. C1 VET AFFAIRS PUGET SOUND HLTH CARE SYST,SEATTLE,WA 98108. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. RP Patrick, DL (reprint author), UNIV WASHINGTON,DEPT HLTH SERV,BOX 357660,SEATTLE,WA 98195, USA. FU AHRQ HHS [HS06343] NR 25 TC 77 Z9 81 U1 1 U2 6 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD OCT 1 PY 1997 VL 127 IS 7 BP 509 EP & PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA XY733 UT WOS:A1997XY73300002 PM 9313018 ER PT J AU Sapp, E Schwarz, C Chase, K Bhide, PG Young, AB Penney, J Vonsattel, JP Aronin, N DiFiglia, M AF Sapp, E Schwarz, C Chase, K Bhide, PG Young, AB Penney, J Vonsattel, JP Aronin, N DiFiglia, M TI Huntingtin localization in brains of normal and Huntington's disease patients SO ANNALS OF NEUROLOGY LA English DT Article ID ENDOSOMAL-LYSOSOMAL SYSTEM; STRIATAL NEURONS; PROJECTION NEURONS; TRINUCLEOTIDE REPEAT; MUTANT HUNTINGTIN; PREFERENTIAL LOSS; IN-VIVO; EXPRESSION; GENE; IMMUNOREACTIVITY AB The immunohistochemical localization of huntingtin was examined in the Huntington's disease (HD) brain with an antibody that recognizes the wild-type and mutant proteins. Neuronal staining was reduced in areas of the HD striatum depleted of medium-sized neurons; large striatal neurons, which are spared in HD, retained normal levels of huntingtin expression. Neuronal labeling was markedly reduced in both segments of the globus pallidus including in brains with minimal loss of pallidal neurons. In some HD cortical and striatal neurons with normal looking morphology, huntingtin was associated with punctate cytoplasmic granules that at the ultrastructural level resembled the multivesicular body, an organelle involved in retrograde transport and protein degradation. Some immunoreactive processes showed blebbing and segmentation similar to that induced experimentally by hypoxic-ischemic or excitotoxic injury. Huntingtin staining was more concentrated in the perinuclear cytoplasm and reduced or absent in processes of atrophic cortical neurons. Nuclear staining was also evident. Fibers in the subcortical white matter of HD patients had significantly increased huntingtin immunoreactivity compared with those of controls. Results suggest that there may be changes in the neuronal expression and transport of wild-type and/or mutant huntingtin at early and late stages of neuronal degeneration in affected areas of the HD brain. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA. FU NINDS NIH HHS [NS 16367, NS 31579] NR 45 TC 226 Z9 229 U1 0 U2 8 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD OCT PY 1997 VL 42 IS 4 BP 604 EP 612 DI 10.1002/ana.410420411 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA YA463 UT WOS:A1997YA46300010 PM 9382472 ER PT J AU Beal, MF Ferrante, RJ Browne, SE Matthews, RT Kowall, NW Brown, RH AF Beal, MF Ferrante, RJ Browne, SE Matthews, RT Kowall, NW Brown, RH TI Increased 3-nitrotyrosine in both sporadic and familial amyotrophic lateral sclerosis SO ANNALS OF NEUROLOGY LA English DT Article ID MOTOR-NEURON DISEASE; SUPEROXIDE-DISMUTASE GENE; NEUROFILAMENT SUBUNIT; TRANSGENIC MICE; NITRIC-OXIDE; TYROSINE PHOSPHORYLATION; HYDROGEN-PEROXIDE; OXIDATIVE DAMAGE; SOD1 MUTATION; MOUSE MODEL AB The pathogenesis of neuronal degeneration in both sporadic and familial amyotrophic lateral sclerosis (ALS) associated mutations in superoxide dismutase may involve oxidative stress. A leading candidate as a mediator of oxidative stress is peroxynitrite, which is formed by the reaction of superoxide with nitric oxide. 3-Nitrotyrosine is a relatively specific marker for oxidative damage mediated by peroxynitrite, In the present study, biochemical measurements showed increased concentrations of 3-nitrotyrosine and 3-nitro-4-hydroxyphenylacetic acid in the lumbar and thoracic spinal cord of ALS patients. Increased 3-nitrotyrosine immunoreactivity was observed in motor neurons of both sporadic and familial ALS patients. Neurologic control patients with cerebral ischemia also showed increased 3-nitrotyrosine immunoreactivity, These findings suggest that peroxynitrite-mediated oxidative damage may play a role in the pathogenesis of both sporadic and familial ALS. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,DAY NEUROMUSCULAR LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,BEDFORD,MA. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02118. RP Beal, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,32 FRUIT ST,BOSTON,MA 02114, USA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NIA NIH HHS [P01 AG11337, P01 AG12992]; NINDS NIH HHS [P01 NS31248-01] NR 43 TC 335 Z9 341 U1 0 U2 6 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD OCT PY 1997 VL 42 IS 4 BP 644 EP 654 DI 10.1002/ana.410420416 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA YA463 UT WOS:A1997YA46300015 PM 9382477 ER PT J AU Zareparsi, S Kaye, J Camicioli, R Grimslid, H Oken, B Litt, M Nutt, J Bird, T Schellenberg, G Payami, H AF Zareparsi, S Kaye, J Camicioli, R Grimslid, H Oken, B Litt, M Nutt, J Bird, T Schellenberg, G Payami, H TI Modulation of the age at onset of Parkinson's disease by apolipoprotein E genotypes SO ANNALS OF NEUROLOGY LA English DT Article ID ALZHEIMERS-DISEASE; EPSILON-4 ALLELE; DEMENTIA; FREQUENCY; GENE; INDIVIDUALS; RISK AB Parkinson's disease (PD) patients often develop dementia, and Alzheimer's disease (AD) patients frequently develop parkinsonian signs. The apolipoprotein E epsilon 4 allele is associated with increased risk and earlier onset of AD. We studied 137 unrelated white PD patients. Those with epsilon 4 had the earliest onset (52.7 +/- 9.8 years), epsilon 3/epsilon 3 patients had an intermediate onset (56.1 +/- 11.1 years), and those with epsilon 2 had the latest onset (59.1 +/- 13.4 years). The age at onset distribution for epsilon 4/epsilon- was significantly earlier than for epsilon 3/epsilon 3 and epsilon 2/epsilon 3. These preliminary results suggest that apolipoprotein E genotypes modulate the age at onset of PD. C1 OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT BIOCHEM & MOL BIOL,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. UNIV WASHINGTON,DEPT NEUROL,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT PHARMACOL,SEATTLE,WA 98195. RP Zareparsi, S (reprint author), OREGON HLTH SCI UNIV,CDW2,DEPT MOL & MED GENET,745 SW GAINES RD,PORTLAND,OR 97201, USA. OI Kaye, Jeffrey/0000-0002-9971-3478; Camicioli, Richard/0000-0003-2977-8660 FU NIA NIH HHS [AG05136, AG0817] NR 24 TC 47 Z9 47 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD OCT PY 1997 VL 42 IS 4 BP 655 EP 658 DI 10.1002/ana.410420417 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA YA463 UT WOS:A1997YA46300016 PM 9382478 ER PT J AU Comcowich, SA Spitzer, TR Tsunoda, SM AF Comcowich, SA Spitzer, TR Tsunoda, SM TI Ursodiol to prevent hepatic venoocclusive disease SO ANNALS OF PHARMACOTHERAPY LA English DT Article ID BONE-MARROW TRANSPLANTATION; VENO-OCCLUSIVE DISEASE; CONTROLLED TRIAL; LIVER; BUSULFAN; PHARMACOKINETICS C1 NORTHEASTERN UNIV,BOUVE COLL PHARM & HLTH SCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BONE MARROW TRANSPLANT PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 22 TC 5 Z9 5 U1 0 U2 0 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 1060-0280 J9 ANN PHARMACOTHER JI Ann. Pharmacother. PD OCT PY 1997 VL 31 IS 10 BP 1249 EP 1252 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YA808 UT WOS:A1997YA80800019 PM 9337452 ER PT J AU Zgraggen, K Rivera, JA Compton, CC Pins, M Werner, J FernandezdelCastillo, C Rattner, DW Lewandrowski, KB Rustgi, AK Warshaw, AL AF Zgraggen, K Rivera, JA Compton, CC Pins, M Werner, J FernandezdelCastillo, C Rattner, DW Lewandrowski, KB Rustgi, AK Warshaw, AL TI Prevalence of activating K-ras mutations in the evolutionary stages of neoplasia in intraductal papillary mucinous tumors of the pancreas SO ANNALS OF SURGERY LA English DT Article; Proceedings Paper CT 117th Annual Scientific Session of the American-Surgical-Association CY APR 17-19, 1997 CL QUEBEC CITY, CANADA SP Amer Surg Assoc ID HYPERSECRETING NEOPLASMS; ONCOGENE ACTIVATION; CYSTIC NEOPLASMS; POINT MUTATION; P53 MUTATIONS; GENE; CARCINOMA; FREQUENCY; CANCER; ADENOCARCINOMA AB Objective The purpose of the study was to determine the prevalence of activating K-ras mutations in the pancreas of patients with intraductal papillary mucinous tumors (IPMT) and to analyze their relation to the degree of site-specific histopathologic abnormality. Background Intraductal papillary mucinous tumors of the pancreas have a biologic behavior that is significantly different from pancreatic ductal adenocarcinoma. Activating K-ras mutations, which may be important events in a multistage process of carcinogenesis, have been reported in IPMT. Methods Forty-six different histologic specimens (comprising normal pancreatic ducts, hyperplasia, low-grade dysplasia, high-grade dysplasia-carcinoma in situ, and carcinoma) from 16 patients with IPMT and 9 specimens from patients with pancreatic ductal adenocarcinomas were designated by a pathologist. Genomic DNA was extracted from paraffin-embedded tissue sections after microdissection. The K-ras gene was amplified by polymerase chain reaction and subjected to DNA sequencing. Results The K-ras mutations were detected in at least one specimen in 13 (81.2%) of 16 patients with IPMT. All mutations were found in codon 12. No codon 13 mutations were detected. The relative frequency of K-ras mutations in the different stages of IPMT was 16.7% in normal epithelium and papillary hyperplasia, 28.6% in low-grade dysplasia, and 57.1% in high-grade dysplasia-carcinoma in situ and invasive carcinoma. The K-ras mutations were detected in 6 (66%) of 9 pancreatic ductal adenocarcinomas. Conclusions The K-ras codon 12 point mutations are as frequent in IPMT as in ductal adenocarcinoma. A stepwise increase in the frequency of codon 12 mutations correlated with the stage of neoplastic evolution to cancer. This finding is consistent with an important role of K-ras gene mutations in the transformation from normal epithelium to invasive carcinoma in the majority of patients with IPMT. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 44 TC 154 Z9 154 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD OCT PY 1997 VL 226 IS 4 BP 491 EP 498 DI 10.1097/00000658-199710000-00010 PG 8 WC Surgery SC Surgery GA YC231 UT WOS:A1997YC23100019 PM 9351717 ER PT J AU Allan, JS Choo, JK Vesga, L Arn, JS Pins, MR Sachs, DH Madsen, JC AF Allan, JS Choo, JK Vesga, L Arn, JS Pins, MR Sachs, DH Madsen, JC TI Cardiac allograft vasculopathy is abrogated anti-CD8 monoclonal antibody therapy SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT 33rd Annual Meeting of the Society-of-Thoracic-Surgeons CY FEB 03-05, 1997 CL SAN DIEGO, CA SP Soc Thorac Surgeons ID MAJOR HISTOCOMPATIBILITY COMPLEX; TRANSPLANTED MOUSE HEARTS; MINIATURE SWINE; CORONARY ATHEROSCLEROSIS; TIME-COURSE AB Background. Cardiac allograft vasculopathy, a diffuse and accelerated form of arteriosclerosis, is a major cause of graft loss or heart transplant recipient death after the first transplant year. This study examined the effects of depleting host CD8+ T lymphocytes on the development of cardiac allograft vasculopathy in miniature swine. Methods. Cardiac allografts were heterotopically transplanted across a major histocompatibility complex class I barrier in partially inbred miniature swine and monitored for rejection by serial biopsies, electrocardiograms, and echocardiograms. Four control animals received cyclosporine on postoperative days 0 to 11. Another four miniswine were given 14.5 mg/kg of 76-2-11 (a mouse anti-swine CD8 monoclonal antibody) on postoperative day 0, in addition to a 12-day course of cyclosporine. Host CD8+ T cells and circulating 76-2-11 monoclonal antibodies were monitored by now cytometry. Results. As compared with cyclosporine-treated control animals, swine receiving 76-2-11 demonstrated near-complete depletion of peripheral CD8+ T cells by postoperative day 2, which persisted for 14 to 18 days. Mean allograft survival of the antibody-treated group and the control group was not statistically different (33 days versus 39 days, respectively) and both groups demonstrated severe interstitial rejection at necropsy. Control animals demonstrated florid intimal thickening of large and small arteries at necropsy. However, swine treated with 76-2-11 showed no intimal proliferation. Conclusions. Depletion of host CD8+ T cells prevents or delays the development of intimal proliferation in miniature swine. CD8+ lymphocytes play an important role in the early development of cardiac allograft vasculopathy in large animals. (C) 1997 by The Society of Thoracic Surgeons. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,CARDIAC SURG UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02114. FU NHLBI NIH HHS [R01-HL54211] NR 22 TC 37 Z9 37 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD OCT PY 1997 VL 64 IS 4 BP 1019 EP 1025 DI 10.1016/S0003-4975(97)00796-0 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA YC220 UT WOS:A1997YC22000027 PM 9354520 ER PT J AU Pogue, BW Lilge, L Patterson, MS Wilson, BC Hasan, T AF Pogue, BW Lilge, L Patterson, MS Wilson, BC Hasan, T TI Absorbed photodynamic dose from pulsed versus continuous wave light examined with tissue-simulating dosimeters SO APPLIED OPTICS LA English DT Article DE photodynamic therapy; photosensitizer; benzoporphyrin derivative; tissue optical property; tissue phantom ID NORMAL RAT-LIVER; PHTHALOCYANINE SENSITIZATION; OPTICAL-PROPERTIES; THERAPY; DIFFUSION; PHANTOMS; INVIVO; TUMOR; GENERATION; DEPENDENCE AB A dosimetric system has been developed to measure the spatially resolved light dose absorbed by a photosensitizer in a tissue-simulating medium. These gelatin-based dosimeters had macroscopic optical scattering and absorption properties that are typical for homogeneous tissue and contained the photosensitizer benzoporphyrin derivative monoacid (BPD-MA). A reporter molecule, 2'7'-dichlorofluorescin diacetate (DCF-DA), served as an actinometer, which could be photosensitized by BPD-MA. to generate a highly fluorescent photoproduct. The relative photosensitizing efficiencies of high-intensity pulsed and cw laser light were compared in these tissue-simulating dosimeters. These measurements demonstrate an increase in penetration for pulsed Light as compared with cw light in the dosimeters. A numerical simulation of the light propagation based on optical diffusion theory was used along with the energy levels of the photosensitizer molecule to examine the mechanisms involved in the absorbed dose. The increased penetration of high-intensity pulsed light was due to a transient decrease in the absorption of the photosensitizer, resulting from saturation of the photosensitizer optical transitions. This study provides the first direct comparison of the photodynamic dose absorbed by a photosensitizer using both high-intensity pulsed and cw laser light in a tissue-simulating medium. These measurements demonstrate that a small increase in depth of treatment is possible with pulsed laser Light as compared with cw laser light simply on the basis of the unique photochemistry of the photosensitizer. However, this effect still needs to be examined carefully in tumor tissue, where other biological or chemical effects may become significant. (C) 1997 Optical Society of America. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL, WELLMAN LABS PHOTOMED, BOSTON, MA 02114 USA. PRINCESS MARGARET HOSP, ONTARIO CANC INST, TORONTO, ON M5G 2M9, CANADA. MCMASTER UNIV, HAMILTON, ON L8V 5C2, CANADA. HAMILTON REG CANC CTR, HAMILTON, ON L8V 5C2, CANADA. RI Patterson, Michael/A-9882-2010; Lilge, lothar/J-6434-2013 OI Patterson, Michael/0000-0002-6398-0742; NR 47 TC 29 Z9 29 U1 1 U2 4 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA SN 0003-6935 J9 APPL OPTICS JI Appl. Optics PD OCT 1 PY 1997 VL 36 IS 28 BP 7257 EP 7269 DI 10.1364/AO.36.007257 PG 13 WC Optics SC Optics GA XX496 UT WOS:A1997XX49600022 PM 18264235 ER PT J AU Clatworthy, AE GomezIsla, T Rebeck, GW Wallace, RB Hyman, BT AF Clatworthy, AE GomezIsla, T Rebeck, GW Wallace, RB Hyman, BT TI Lack of association of a polymorphism in the low-density lipoprotein receptor-related protein gene with Alzheimer disease SO ARCHIVES OF NEUROLOGY LA English DT Article ID APOLIPOPROTEIN-E; NEURITE OUTGROWTH; ALLELE AB Background: The apolipoprotein E epsilon 4 (ApoE epsilon 4) allele is associated with an increased risk for development of Alzheimer disease (AD). We hypothesized that polymorphisms in proteins that interact with ApoE also might have an impact on the likelihood of AD developing. We examined a polymorphism in the gene for the low-density lipoprotein receptor-related protein (LRP), because LRP is a major ApoE receptor in the brain that also mediates binding and degradation of secreted Kunitz protease inhibitor forms of amyloid precursor protein. Subjects and Design: The LRP genotypes in 2 groups were studied. The first group consisted of 130 patients with probable or definite AD (mean+/-SD age, 78.2+/-8.9 years) and 64 nondemented, control subjects (mean+/-SD age, 81.7+/-12.3 years) who were primarily the spouses of the patients. The second group consisted of individuals from a population-based, epidemiologic study, including 38 cognitively impaired individuals (mean+/-SD age, 79.9+/-4.1 years) and 93 nondemented controls (mean+/-SD age, 78.7+/-4.4 years). Finally, 22 brains with a neuropathological diagnosis of AD were evaluated for neuronal loss, beta-amyloid deposition, and neurofibrillary tangle number and compared with the LRP genotype Results: No genetic disequilibrium in LRP allele frequencies between controls and patients with AD or cognitive impairment was observed. No interaction between the ApoE epsilon 4 and LRP genotypes was observed in patients with AD. Moreover, the LRP genotype did not correlate with degree of neuronal loss, beta-amyloid deposition, or neurofibrillary tangle number in individuals examined using quantitative neuropathological techniques. Conclusion: This LRP gene polymorphism is not linked with the pathophysiological changes of AD. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,ALZHEIMER UNIT,CHARLESTOWN,MA 02129. UNIV IOWA,COLL MED,DEPT PREVENT MED,IOWA CITY,IA. FU NIA NIH HHS [AG-12406, AG-02106, P50 AG-05134] NR 20 TC 41 Z9 43 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD OCT PY 1997 VL 54 IS 10 BP 1289 EP 1292 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA YA805 UT WOS:A1997YA80500015 PM 9341576 ER PT J AU Compton, CC Sobin, LH AF Compton, CC Sobin, LH TI Protocol for the examination of specimens removed from patients with gastrointestinal lymphoma - A basis for checklists SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID EUROPEAN-AMERICAN CLASSIFICATION; PRIMARY GASTRIC LYMPHOMAS; NON-HODGKINS LYMPHOMAS; PROGNOSTIC FACTORS; MANAGEMENT; NEOPLASMS; FEATURES; SURGERY; THERAPY; DISEASE C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. ARMED FORCES INST PATHOL,DIV GASTROINTESTINAL PATHOL,WASHINGTON,DC 20306. NR 42 TC 7 Z9 7 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD OCT PY 1997 VL 121 IS 10 BP 1042 EP 1047 PG 6 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA YB125 UT WOS:A1997YB12500004 PM 9341582 ER PT J AU Jordan, CD Flotte, TJ Wright, SW MacKool, B Duncan, LM AF Jordan, CD Flotte, TJ Wright, SW MacKool, B Duncan, LM TI Necrobiosis lipoidica in a diabetic intravenous drug user SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article AB Necrobiosis lipoidica occurs most commonly on the lower extremities in patients with diabetes; lesions typically occur in the pretibial region. Although the pathogenesis of necrobiosis lipoidica remains unclear, both external trauma and vascular damage have been proposed as contributing to the development of this disorder. We report polarizable foreign material in small blood vessels and multinucleated histiocytes in lesions of necrobiosis lipoidica. This phenomenon occurred in a patient who was both diabetic and an intravenous drug user. C1 MASSACHUSETTS GEN HOSP,DERMATOPATHOL UNIT,DEPT PATHOL,BOSTON,MA 02114. SUNY HLTH SCI CTR,DEPT PATHOL,SYRACUSE,NY 13210. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 8 TC 2 Z9 2 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD OCT PY 1997 VL 121 IS 10 BP 1093 EP 1095 PG 3 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA YB125 UT WOS:A1997YB12500012 PM 9341590 ER PT J AU McGibbon, CA Krebs, DE Mann, RW AF McGibbon, CA Krebs, DE Mann, RW TI In vivo hip pressures during cane and load-carrying gait SO ARTHRITIS CARE AND RESEARCH LA English DT Article; Proceedings Paper CT 1st Annual North-American-Society-of-Gait-and-Clinical-Motion-Analysis CY APR, 1996 CL BIRMINGHAM, AL SP North Amer Soc Gait & Clin Motion DE hip pressure; gait; cane; load carriage ID ACETABULAR CONTACT PRESSURES; INVIVO; REHABILITATION; PHASE; JOINT AB Objective. To test the hypotheses that carrying a load reduces hip contact pressure ipsilateral to the load and that using a cane when carrying a load further reduces hip contact pressure. Methods. A Moore-type endoprosthesis with 13 femoral-head pressure transducers was implanted in a human subject following a Garden III fracture. Hip contact pressures were measured during unaided, cane-aided, and load-carrying gait over two years. Results. Relative to unloaded gait, contact pressures increased significantly when ipsilateral to the carried load. Using a contralateral cane when carrying the load reduced ipsilateral posterior-superior contact pressure; however, the hip contralateral to the load experienced significantly higher than normal pressures. Conclusions. Ipsilaterally carried loads may not always provide stress protection of the arthritic hip. Using a cane opposite to the load may aid in restoring normal pressures to the ipsilateral hip, but may expose the contralateral hip to a significant stress burden. C1 INST HLTH PROFESS,GRAD PROGRAM PHYS THERAPY,BOSTON,MA. MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. RP McGibbon, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,BIOMOT LAB,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [R01-AR40036]; NICHD NIH HHS [R01-HD30063] NR 26 TC 15 Z9 15 U1 0 U2 0 PU AMER COLL RHEUMATOLOGY PI ATLANTA PA 60 EXECUTIVE PARK SOUTH, STE 150, ATLANTA, GA 30329 SN 0893-7524 J9 ARTHRIT CARE RES JI Arthritis Care Res. PD OCT PY 1997 VL 10 IS 5 BP 300 EP 307 DI 10.1002/art.1790100504 PG 8 WC Rheumatology SC Rheumatology GA YC003 UT WOS:A1997YC00300003 PM 9362596 ER PT J AU Tackson, SJ Krebs, DE Harris, BA AF Tackson, SJ Krebs, DE Harris, BA TI Acetabular pressures during hip arthritis exercises SO ARTHRITIS CARE AND RESEARCH LA English DT Article DE osteoarthritis; exercise; hip joint; acetabulum; contact pressure ID RHEUMATOID-ARTHRITIS; CONTACT PRESSURES; OSTEOARTHRITIS; CARTILAGE; WALKING; JOINT; KNEE AB Objective. To examine in vivo maximum acetabular contact pressures during gait and hip arthritis exercises recommended by clinicians and the Arthritis Foundation. Methods. Acetabular contact pressure data were collected for 2.5 years, at 3-4-month intervals, from an instrumented endoprosthesis implanted in an 84-year-old male who had sustained a left hip fracture. Maximum pressure data were compared for each activity. Results. Mean pressures ranged from 9.0 +/- 2.3 megapascals (MPa) during maximum isometric hip abduction, 9.0 +/- 0.8 MPa during standing right hip abduction, and 8.9 +/- 2.8 MPa during standing left hip abduction to 1.2 +/- 0.3 MPa during quiet standing. Free-speed gait pressure averaged 5.6 +/- 0.9 MPa. The maximum mean pressure during side-lying hip abduction and straight leg raise at 30 degrees/second were less than the same activities at 60 degrees/second. Conclusions. These in vivo hip pressure measurements challenge traditional protocols for patients with hip osteoarthritis and provide quantitative data as a framework for designing exercise programs. Maxim um isometric hip exercise and standing exercise generated much higher hip pressures, and are therefore probably more stressful to acetabular cartilage, than gait or stationary cycling. Clinicians must consider exercise velocity because of its direct correlation with hip contact pressure. Walking generated fewer pressure than most activities studied and, given its other benefits, is therefore probably beneficial for patients with hip osteoarthritis. C1 MASSACHUSETTS GEN HOSP,BIOMOT LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02138. FU NICHD NIH HHS [R01HD30063] NR 59 TC 18 Z9 18 U1 0 U2 2 PU AMER COLL RHEUMATOLOGY PI ATLANTA PA 60 EXECUTIVE PARK SOUTH, STE 150, ATLANTA, GA 30329 SN 0893-7524 J9 ARTHRIT CARE RES JI Arthritis Care Res. PD OCT PY 1997 VL 10 IS 5 BP 308 EP 319 DI 10.1002/art.1790100505 PG 12 WC Rheumatology SC Rheumatology GA YC003 UT WOS:A1997YC00300004 PM 9362597 ER PT J AU Escary, JL Choy, HA Reue, K Schotz, MC AF Escary, JL Choy, HA Reue, K Schotz, MC TI Hormone-sensitive lipase overexpression increases cholesteryl-ester hydrolysis in macrophage foam cells SO ATHEROSCLEROSIS LA English DT Meeting Abstract C1 W LOS ANGELES VA MED CTR,LIPID RES LAB,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0021-9150 J9 ATHEROSCLEROSIS JI Atherosclerosis PD OCT PY 1997 VL 134 IS 1-2 SI SI BP 230 EP 230 DI 10.1016/S0021-9150(97)89225-8 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA XY106 UT WOS:A1997XY10601057 ER PT J AU Moore, KJ Andersson, LP Freeman, MW AF Moore, KJ Andersson, LP Freeman, MW TI Embryonic stem cell differentiated macrophages: A model system for the evaluation of macrophage foam cell formation and function SO ATHEROSCLEROSIS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0021-9150 J9 ATHEROSCLEROSIS JI Atherosclerosis PD OCT PY 1997 VL 134 IS 1-2 SI SI BP 234 EP 234 DI 10.1016/S0021-9150(97)89246-5 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA XY106 UT WOS:A1997XY10601078 ER PT J AU Yoshida, M Chien, LJ Rosenzweig, A Numano, F Gimbrone, MA AF Yoshida, M Chien, LJ Rosenzweig, A Numano, F Gimbrone, MA TI E-selectin overexpression on human vascular endothelium via adenoviral mediated gene transfer: A novel model for inflammation and atherosclerosis SO ATHEROSCLEROSIS LA English DT Meeting Abstract C1 TOKYO MED & DENT UNIV,MED RES INST,DEPT MOL GENET,TOKYO,JAPAN. TOKYO MED & DENT UNIV,DEPT MED,TOKYO 113,JAPAN. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV VASC RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0021-9150 J9 ATHEROSCLEROSIS JI Atherosclerosis PD OCT PY 1997 VL 134 IS 1-2 SI SI BP 248 EP 248 DI 10.1016/S0021-9150(97)89313-6 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA XY106 UT WOS:A1997XY10601144 ER PT J AU Gonschior, P Vogel-Wiens, C Goetz, AE Huehns, TY Breger, F Gerheuser, F Fleuchaus, M Welsch, U Sroka, R Dellian, M Lehr, HA Hofling, B AF Gonschior, P Vogel-Wiens, C Goetz, AE Huehns, TY Breger, F Gerheuser, F Fleuchaus, M Welsch, U Sroka, R Dellian, M Lehr, HA Hofling, B TI Endovascular catheter-delivered photodynamic therapy in an experimental response to injury model SO BASIC RESEARCH IN CARDIOLOGY LA English DT Article DE restenosis; photodynamic therapy; angioplasty; local drug delivery ID EXPERIMENTAL INTIMAL HYPERPLASIA; DRUG-DELIVERY; ANGIOPLASTY AB Background: The effectiveness of local endovascular photodynamic therapy (PDT) in preventing tissue. hyperplasia was evaluated in a vascular injury model. Methods: Standardized unidirectional arterial injury with a directional atherectomy catheter was performed in porcine arteries (n = 180). Animals (n = 72) were randomly allocated to unidirectional injury only (Group 1), injury followed by drug delivery of photosensitizer with a porous balloon (Group 2), or by local exposure to monochromatic light (Group 3). In Group I, injury was followed by local drug delivery of photosensitizer and subsequent exposure to light (PDT), kip to 21 days after treatment, all experimental vessels were excised, fixed and processed for histology immunohistochemistry and transmission electron microscopy. Results: After-vascular injury an inflammatory and myoproliferative response was observed in Groups 1, 2 and 3 (mean tissue hyperplasia/media ratio 1.0 +/- 0.5 at 21 days, area tissue hyperplasia: 1.57 +/- 0.9 mm(2)). Proliferation in injured vascular segments (Group 1-3) reached a maximum at 7 days, with 6 %. Only in Group 4, after injury followed by photodynamic therapy, was there no significant vascular response (mean tissue hyperplasia/media ratio 0.3 +/- 0.2; area tissue hyperplasia: 0.1 +/- 0.05 mm(2) p < 0.001, proliferating cells 0.3 %). Conclusion: Vascular response after unidirectional injury was suppressed only by endovascular photodynamic therapy. C1 Univ Munich, Klinikum Grosshadern, Dept Med, D-81377 Munich, Germany. Univ Munich, Klinikum Grosshadern, Inst Anesthesia, D-81377 Munich, Germany. Inst Anat, D-80336 Munich, Germany. GSF Laser Res Dept, D-81377 Munich, Germany. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, Boston, MA 01772 USA. Univ Washington, Dept Pathol, Seattle, WA 98195 USA. RP Gonschior, P (reprint author), Univ Munich, Klinikum Grosshadern, Dept Med, Marchioninistr 15, D-81377 Munich, Germany. RI Sroka, Ronald/I-2765-2013 NR 23 TC 7 Z9 10 U1 0 U2 0 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PLATZ DER DEUTSCHEN EINHEIT 25, D-64293 DARMSTADT, GERMANY SN 0300-8428 J9 BASIC RES CARDIOL JI Basic Res. Cardiol. PD OCT PY 1997 VL 92 IS 5 BP 310 EP 319 DI 10.1007/BF00788943 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YM872 UT WOS:000071110100003 PM 9486352 ER PT J AU Polla, BS Richard, MJ Robinson, DR Maresca, B AF Polla, BS Richard, MJ Robinson, DR Maresca, B TI Effects of membrane fatty acids on thermal and oxidative injury in the human premonocytic line U937 SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE dietary fatty acids; heat shock proteins; reactive oxygen species; lipid peroxidation; human cells; cellular thermometer ID HEAT-SHOCK RESPONSE; HUMAN MONOCYTES-MACROPHAGES; LIPID-COMPOSITION; PROTEIN-SYNTHESIS; INTERFERON-GAMMA; TEMPERATURE; ACTIVATION; CALCIUM; HSP70; CELLS AB Heat shock (HS) proteins (HSP) function as molecular chaperones and protect cells from thermal and oxidative injury. The signals leading to HSP synthesis, i.e. the ''cellular thermometer(s),'' are still a matter of debate. In the human premonocytic line U937, we investigated the effects of specific modification of membrane fatty acid (FA) composition by incubation with various saturated and unsaturated fatty acids (UFA) on the HS response and on hydrogen peroxide (H2O2)-induced cell death. FA readily incorporated into U937 cell membranes. UFA did not modulate the HS response but potentiated H2O2-mediated damage, while pre-exposure to HS protected the UFA-treated cells from this increased H2O2 toxicity. (C) 1997 Elsevier Science Inc. C1 MASSACHUSETTS GEN HOSP,DEPT MED,ARTHRIT UNIT,BOSTON,MA 02114. INT INST GENET & BIOPHYS,I-80125 NAPLES,ITALY. CHRU,BIOCHIM LAB C,GREPO,F-38000 GRENOBLE,FRANCE. RP Polla, BS (reprint author), UNIV PARIS 05,UFR COCHIN PORT ROYAL,PHYSIOL RESP LAB,24 RUE FAUBOURG ST JACQUES,F-75014 PARIS,FRANCE. NR 37 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD OCT 1 PY 1997 VL 54 IS 7 BP 773 EP 780 DI 10.1016/S0006-2952(97)00246-3 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA XX782 UT WOS:A1997XX78200004 PM 9353131 ER PT J AU Sheng, M Wyszynski, M AF Sheng, M Wyszynski, M TI Ion channel targeting in neurons SO BIOESSAYS LA English DT Review ID TUMOR-SUPPRESSOR GENE; HETEROMULTIMERIC K+ CHANNELS; NMDA RECEPTOR SUBUNITS; RAT-BRAIN; GUANYLATE KINASES; GLYCINE RECEPTOR; SODIUM-CHANNELS; SUBCELLULAR-LOCALIZATION; CLUSTERING ACTIVITY; PSD-95 FAMILY AB Electrical signaling by neurons depends on the precisely ordered distribution of a wide variety of ion channels on the neuronal surface. The mechanisms underlying the targeting of particular classes of ion channels to specific subcellular sites are poorly understood. Recent studies have identified a new class of protein-protein interaction mediated by PDZ domains, protein binding modules that recognize specific sequences at the C terminus of membrane proteins. The PDZ domains of a family of synaptic cytoskeleton-associated proteins, typified by PSD-95, bind to the intracellular C-terminal tails of NMDA receptors and Shaker-type K+ channels. This interaction appears to be important in the clustering and localization of these ion channels at synaptic sites. Recognition of specific C-terminal peptide sequences by different PDZ domain-containing proteins may be a general mechanism for differential targeting of proteins to a variety of subcellular locations. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROBIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP Sheng, M (reprint author), HOWARD HUGHES MED INST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA66268-02]; NINDS NIH HHS [R01 NS35050] NR 63 TC 127 Z9 127 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD OCT PY 1997 VL 19 IS 10 BP 847 EP 853 DI 10.1002/bies.950191004 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA YB455 UT WOS:A1997YB45500003 PM 9363678 ER PT J AU Fava, M Uebelacker, LA Alpert, JE Nierenberg, AA Pava, JA Rosenbaum, JF AF Fava, M Uebelacker, LA Alpert, JE Nierenberg, AA Pava, JA Rosenbaum, JF TI Major depressive subtypes and treatment response SO BIOLOGICAL PSYCHIATRY LA English DT Article DE major depression; atypical depression; melancholic depression; anxious depression; subtypes ID PERSONALITY-DISORDER; ANGER ATTACKS; FLUOXETINE TREATMENT; ATYPICAL DEPRESSION; DOUBLE-BLIND; ANXIOUS DEPRESSION; FOLLOW-UP; MELANCHOLIA; ANTIDEPRESSANTS; OUTPATIENTS AB The purpose of this study was to investigate the relationships between depressive subtypes and response to fluoxetine treatment in a large cohort of outpatients. We studied 294 outpatients with major depressive disorder who were then treated with fluoxetine 20 mg/day for 8 weeks, Treatment outcome was evaluated with the Hamilton Depression Raring Scale (HDRS)-17, the Clinical Global Impressions-Severity, and with the HDRS-8; the latter is proposed to be a relatively more specific measure of depression severity than the HDRS-17, We assessed the relationships between degree of treatment response and several depressive subtypes (melancholic, atypical, hostile, and anxious depression, double depression, and depression with comorbid personality disorders), after adjusting for baseline depression severity. We found that nonanxious depressives (patients without any comorbid anxiety disorder) improved slightly but significantly more during treatment than anxious depressives on all outcome measures. Melancholic depression was associated with slightly less improvement on the HDRS-17 only, whereas the other subtypes of depression were not associated with differences in treatment outcome. (C) 1997 Society of Biological Psychiatry. RP Fava, M (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,DEPRESS RES PROGRAM,15 PARKMAN ST,BOSTON,MA 02114, USA. OI Alpert, Jonathan/0000-0002-4332-908X FU NIMH NIH HHS [R01 MH48483-01] NR 46 TC 171 Z9 175 U1 0 U2 9 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD OCT 1 PY 1997 VL 42 IS 7 BP 568 EP 576 DI 10.1016/S0006-3223(96)00440-4 PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA XX204 UT WOS:A1997XX20400005 PM 9376453 ER PT J AU Uddin, S Fish, EN Sher, D Gardziola, C Colamonici, OR Kellum, M Pitha, PM White, MF Platanias, LC AF Uddin, S Fish, EN Sher, D Gardziola, C Colamonici, OR Kellum, M Pitha, PM White, MF Platanias, LC TI The IRS-pathway operates distinctively from the stat-pathway in hematopoietic cells and transduces common and distinct signals during engagement of the insulin or interferon-alpha receptors SO BLOOD LA English DT Article ID DEPENDENT TYROSINE PHOSPHORYLATION; VAV PROTOONCOGENE PRODUCT; JAK KINASES; TRANSCRIPTION FACTOR; DOCKING PROTEIN; IFN-ALPHA; SUBSTRATE-1; ACTIVATION; GAMMA; GENE AB Binding of interferon-cu (IFN-LU) to its receptor on hematopoietic cells activates the signal transducers and activators of transcription (Stat)- and insulin receptor substrate (IRS)pathways, and regulates expression of antiproliferative and antiviral activities. However, it remains unknown whether these two pathways cooperate in the generation of IFN-cu responses or function independently, and whether IRS-proteins transduce distinct downstream signals in response to IFNs or insulin/insulin-like growth factor (IGF)-1-mediated activation. Our data show that in response to IFN-cu treatment, IRS-1 functions selectively as a docking protein for the SH2 domains of the p85 subunit of the Pl 3'-kinase, but not the SH2 domain of Grb-2 which is engaged during insulin/lGF-1 signaling. In studies with THP-1 human myelomonocytic cells and 32D mouse myeloid cells, which are IRS-defective, we found that the IFN-alpha-regulated activation of Stat-1, Stat-2, and Stat-3 does not require the function of the IRS-system. Furthermore, THP-1 cells are responsive to the protective effect of IFN-LU against vesicular stomatitis virus, Both 32D and THP-1 cells were resistant to the growth inhibitory effect of IFN-alpha, but this effect was not reversible by expression of IRS-1 or IRS-2 alone in 32D cells. Taken altogether these data show that: (1) The IRS-system transduces common and distinct signals in response to IFN-alpha or insulin/IGF-1 stimulation of hematopoietic cells. (2) The IRS-pathway operates separately from the Stat-pathway, and its function is not essential for the generation of the antiviral effect of IFN-alpha. (3) Neither the IRS-nor the Stat-pathways alone are sufficient to mediate the antiproliferative effects of IFN-alpha in hematopoietic cells, and additional signaling elements are required. (C) 1997 by The American Society of Hematology. C1 UNIV ILLINOIS,HEMATOL ONCOL SECT,DEPT MED,CHICAGO,IL 60607. UNIV TORONTO,DEPT MED GENET & MICROBIOL,TORONTO,ON,CANADA. LOYOLA UNIV,DIV HEMATOL ONCOL,CHICAGO,IL 60611. HINES VA HOSP,MAYWOOD,IL. UNIV TENNESSEE,DEPT PATHOL,MEMPHIS,TN. JOHNS HOPKINS UNIV,CTR ONCOL,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. FU NCI NIH HHS [CA73381]; NIDDK NIH HHS [DK43808, DK38712] NR 51 TC 90 Z9 90 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD OCT 1 PY 1997 VL 90 IS 7 BP 2574 EP 2582 PG 9 WC Hematology SC Hematology GA XY703 UT WOS:A1997XY70300009 PM 9326223 ER PT J AU Cooke, KR Nishinakamura, R Martin, TR Kobzik, L Brewer, J Whitsett, JA Bungard, D Murray, R Ferrara, JLM AF Cooke, KR Nishinakamura, R Martin, TR Kobzik, L Brewer, J Whitsett, JA Bungard, D Murray, R Ferrara, JLM TI Persistence of pulmonary pathology and abnormal lung function in IL-3/GM-CSF/IL-5 beta c receptor-deficient mice despite correction of alveolar proteinosis after BMT SO BONE MARROW TRANSPLANTATION LA English DT Article DE lung; PFTs; pathology; beta c deficient; BMT ID BONE-MARROW TRANSPLANTATION; IDIOPATHIC PNEUMONIA; IMMUNE-RESPONSE; DISEASE; FAILURE; MOUSE AB Mice deficient for the IL-3/GM-CSF/IL-5 beta c receptor (beta cR KO) develop lung disease similar to that seen in human pulmonary alveolar proteinosis (PAP) which includes lymphocytic infiltration around airways and vessels and the progressive accumulation of surfactant and macrophages within the alveolar space, We investigated bone marrow transplantation (BMT) as a curative treatment of PAP in beta cR KO mice by semiquantitative histologic analysis and evaluation of pulmonary function, BMT from wild-type (WT) donors into lethally irradiated beta cR KO recipients (WT --> KO) led to the complete resolution of alveolar protein accumulation and to normalization of BAL fluid cellularity and macrophage morphology, However, detailed microscopic analysis of lung tissue revealed the persistence of significant cellular infiltrates in WT --> KO recipients which were equivalent to those seen in KO --> KO animals, Evaluation of pulmonary function demonstrated that only dynamic compliance (C-dyn) and not airway conductance (G(L)) was significantly improved in the WT --> KO group compared to KO --> KO animals and that both of these measurements remained significantly abnormal when compared to WT --> WT controls. We conclude, that although BMT for PAP reverses alveolar macrophage and protein accumulation, it does not decrease the interstitial inflammatory component of this disease. The importance of this residual pathology is demonstrated by the incomplete correction of alveolar function (C-dyn) and lack of improvement in increased airway resistance (G(L)). These findings may have important implications with regard to the extent that BMT can be considered a potential curative procedure for this clinical disorder. C1 CHILDRENS HOSP,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV RESP,BOSTON,MA 02115. CHILDRENS HOSP,DIV PULM BIOL,CINCINNATI,OH 45229. DNAX RES INST MOL & CELLULAR BIOL INC,PALO ALTO,CA 94304. RP Cooke, KR (reprint author), DANA FARBER CANC INST,DIV PEDIAT ONCOL,D1638,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA39542]; NHLBI NIH HHS [HL55162]; NIDDK NIH HHS [DK39512] NR 31 TC 28 Z9 28 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD OCT PY 1997 VL 20 IS 8 BP 657 EP 662 DI 10.1038/sj.bmt.1700958 PG 6 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA YD131 UT WOS:A1997YD13100006 PM 9383229 ER PT J AU Eming, SA Morgan, JR Berger, A AF Eming, SA Morgan, JR Berger, A TI Gene therapy for tissue repair: approaches and prospects SO BRITISH JOURNAL OF PLASTIC SURGERY LA English DT Article ID FIBROBLAST GROWTH-FACTOR; GENETICALLY-MODIFIED KERATINOCYTES; CULTURED EPIDERMAL-KERATINOCYTES; ADENOVIRUS-MEDIATED TRANSFER; MUSCLE CELL-PROLIFERATION; MODIFIED SKIN FIBROBLASTS; CHRONIC LEG ULCERS; IN-VIVO; ENDOTHELIAL-CELLS; SYSTEMIC DELIVERY AB Recent advances in molecular biology have resulted in the development of new technologies for the introduction and expression of genes in human somatic cells. This emerging field, known as gene therapy, is broadly defined as the transfer of genetic material to cells/tissues in order to achieve a therapeutic effect for inherited as well as acquired diseases. We and others are exploring the potential application of this technology to tissue repair. One primary focus has been to transfer genes encoding wound healing growth factors, a broad class of proteins which control local events in tissues such as cell proliferation, cell migration and the formation of extracellular matrix. Using several different strategies for gene transfer, wound healing growth factor genes have been introduced and expressed in cells and tissues in vitro as well as in vivo. Various experimental models of wound healing and tissue repair have been used to evaluate the efficacy of this new and exciting approach to tissue repair. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,SURG SERV,CAMBRIDGE,MA 02137. KRANKENHAUS OSTSTADT,DEPT PLAST SURG,D-30659 HANNOVER,GERMANY. UNIV HANNOVER,DEPT PLAST SURG,HANNOVER,GERMANY. OI Morgan, Jeffrey/0000-0002-7546-3443 FU NIAMS NIH HHS [AR42012-01A1]; NICHD NIH HHS [HD 28528-01] NR 91 TC 25 Z9 25 U1 1 U2 2 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0007-1226 J9 BRIT J PLAST SURG JI Br. J. Plast. Surg. PD OCT PY 1997 VL 50 IS 7 BP 491 EP 500 DI 10.1016/S0007-1226(97)91297-2 PG 10 WC Surgery SC Surgery GA YD124 UT WOS:A1997YD12400004 PM 9422946 ER PT J AU Lewandrowski, KU Tomford, WW Michaud, NA Schomacker, KT Deutsch, TF AF Lewandrowski, KU Tomford, WW Michaud, NA Schomacker, KT Deutsch, TF TI An electron microscopic study on the process of acid demineralization of cortical bone SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE acid demineralization; cortical bone; advancing-reaction-front theory ID ALLOGRAFTS AB Demineralization has been shown to foster osteoinductive properties of cortical bone grafts, yet little is known about the process of demineralization and how to control it. The purpose of this study was to investigate the process of cortical bone demineralization by using scanning electron microscopy to evaluate how hydrochloric acid demineralizes cortical bone. Results showed that in the demineralization of diaphyseal cortical bone specimens using hydrochloric acid, a uniformly thick circumferential band of demineralized bone matrix surrounds an inner undecalcified bone core as the process of demineralization occurs. The interface between the demineralized and mineralized section of the bone specimens was extremely sharp. This interface between demineralized and undemineralized bone was noted to advance as a reaction front with increasing demineralization which resulted in continuous shrinkage of the inner cortical bone core. This study suggests that cortical bone demineralization can be best described using an advancing reaction front theory, and this explanation can be used for implementation of the concept of controlled demineralization. C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RP Lewandrowski, KU (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED RES LAB,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [AR-21896] NR 12 TC 8 Z9 10 U1 1 U2 5 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD OCT PY 1997 VL 61 IS 4 BP 294 EP 297 DI 10.1007/s002239900338 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XX355 UT WOS:A1997XX35500007 PM 9312199 ER PT J AU OhtaniFujita, N Dryja, TP Rapaport, JM Fujita, T Matsumura, S Ozasa, K Watanabe, Y Hayashi, K Maeda, K Kinoshita, S Matsumura, T Ohnishi, Y Hotta, Y Takahashi, R Kato, MV Ishizaki, K Sasaki, MS Horsthemke, B Minoda, K Sakai, T AF OhtaniFujita, N Dryja, TP Rapaport, JM Fujita, T Matsumura, S Ozasa, K Watanabe, Y Hayashi, K Maeda, K Kinoshita, S Matsumura, T Ohnishi, Y Hotta, Y Takahashi, R Kato, MV Ishizaki, K Sasaki, MS Horsthemke, B Minoda, K Sakai, T TI Hypermethylation in the retinoblastoma gene is associated with unilateral, sporadic retinoblastoma SO CANCER GENETICS AND CYTOGENETICS LA English DT Article ID TUMOR-SUPPRESSOR GENE; DNA METHYLATION; SUSCEPTIBILITY GENE; PARENTAL ORIGIN; HUMAN CANCERS; RB1 PROMOTER; MUTATIONS; EXPRESSION; CARCINOMA; ALLELE AB We previously reported 9 unilateral, sporadic retinoblastomas with hypermethylation in the 5' region of the RE gene, and we found that CpG methylation in the RE promoter inhibits the binding of the retinoblastoma binding factor I (RBF-1) and the activating transcription factor (ATF)-like factors, thereby resulting in a considerable reduction in RE promoter activity. In this study, we screened for hypermethylation in 121 additional cases of retinoblastoma, and found 5 tumors with hypermethylation, including 4 unilateral, sporadic tumors, and one hereditary tumor. The hereditary tumor had a germline deletion of one allele, and the hypermethylation was an acquired, epigenetic change in the other allele. Another tumor had hypermethylation restricted to approximately 800 base pairs in the RS promoter region including the essential RBF-1 and A TF sites. The frequency of hypermethylation in unilateral, sporadic tumors was 9.3% combining our previous and present examinations (13 among 140), whereas the frequency was 1.0% in bilateral hereditary tumors (one among 101). The statistical analyses using the chi-square test indicated significant correlation between hypermethylation and unilateral, sporadic tumors (p < 0.05). These results suggest that hypermethylation in the RE gene is always an acquired, epigenetic change and causes about 9% of unilateral, sporadic tumors. (C) Elsevier Science Inc., 1997. C1 KYOTO PREFECTURAL UNIV MED,DEPT PREVENT MED,KAMIKYO KU,KAMIGYO KU,KYOTO 602,JAPAN. KYOTO PREFECTURAL UNIV MED,DEPT OPHTHALMOL,KYOTO 602,JAPAN. KYOTO PREFECTURAL UNIV MED,DEPT PEDIAT,KYOTO 602,JAPAN. KYOTO UNIV,DEPT PATHOL 2,KYOTO 606,JAPAN. KYOTO UNIV,CTR RADIAT BIOL,KYOTO 606,JAPAN. WAKAYAMA MED COLL,DEPT OPHTHALMOL,WAKAYAMA 640,JAPAN. JUTENDO UNIV,SCH MED,DEPT OPHTHALMOL,TOKYO,JAPAN. TEIKYO UNIV,SCH MED,DEPT OPHTHALMOL,ICHIHARA HOSP,CHIBA,JAPAN. UNIV ESSEN GESAMTHSCH KLINIKUM,INST HUMAN GENET,D-4300 ESSEN,GERMANY. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA. RI Kato, Mitsuo/D-5411-2009; OI Kato, Mitsuo/0000-0002-1783-1084 FU NEI NIH HHS [EY05321] NR 25 TC 82 Z9 88 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0165-4608 J9 CANCER GENET CYTOGEN JI Cancer Genet. Cytogenet. PD OCT 1 PY 1997 VL 98 IS 1 BP 43 EP 49 DI 10.1016/S0165-4608(96)00395-0 PG 7 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA XW702 UT WOS:A1997XW70200008 PM 9309117 ER PT J AU Teng, DHF Perry, WL Hogan, JK Baumgard, M Bell, R Berry, S Davis, T Frank, D Frye, C Hattier, T Hu, R Jammulapati, S Janecki, T Leavitt, A Mitchell, JT Pero, R Sexton, D Schroeder, M Su, PH Swedlund, B Kyriakis, JM Avruch, J Bartel, P Wong, AKC Oliphant, A Thomas, A Skolnick, MH Tavtigian, SV AF Teng, DHF Perry, WL Hogan, JK Baumgard, M Bell, R Berry, S Davis, T Frank, D Frye, C Hattier, T Hu, R Jammulapati, S Janecki, T Leavitt, A Mitchell, JT Pero, R Sexton, D Schroeder, M Su, PH Swedlund, B Kyriakis, JM Avruch, J Bartel, P Wong, AKC Oliphant, A Thomas, A Skolnick, MH Tavtigian, SV TI Human mitogen-activated protein kinase kinase 4 as a candidate tumor suppressor SO CANCER RESEARCH LA English DT Article ID CELL-DEATH; PANCREATIC-CARCINOMA; INDUCED APOPTOSIS; BRCA2 REGION; C-JUN; STRESS; MAP; MUTATIONS; PATHWAYS; P53 AB Mitogen-activated protein kinases function in signal transduction pathways that are involved in controlling key cellular processes in many organisms. A mammalian member of this kinase family, MKK4/JNRK1/SEK1, has been reported to link upstream MEKK1 to downstream stress-activated protein kinase/JNK1 and p38 mitogen-activated protein kinase, This mitogen-activated protein kinase pathway has been implicated in the signal transduction of cytokine-and stress-induced apoptosis in a variety of cell types, Here, we report that two human tumor cell lines, derived from pancreatic carcinoma and lung carcinoma, harbor homozygous deletions that eliminate coding portions of the MKK4 locus at 17p, located approximately 10 cM centromeric of p53. In addition, in a set of 88 human cancer cell lines prescreened for loss of heterozygosity, we detected two nonsense and three missense sequence variants of MKK4 in cancer cell lines derived from human pancreatic, breast, colon, and testis cells, In vitro biochemical assays revealed that, when stimulated by MEKK1, four of the five altered MKK4 proteins lacked the ability to phosphorylate stress-activated protein kinase. Thus, the incidence of coding mutations of MKK4 in the set of cell lines is 6 of 213 (similar to 3%). These findings suggest that MKK4 may function as a suppressor of tumorigenesis or metastasis in certain types of cells. C1 MASSACHUSETTS GEN HOSP,DEPT MED,DIABET UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT MED,MED SERV,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP Teng, DHF (reprint author), MYRIAD GENET INC,390 WAKARA WAY,SALT LAKE CITY,UT 84108, USA. OI Thomas, Alun/0000-0001-5650-7044 NR 29 TC 154 Z9 161 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 1 PY 1997 VL 57 IS 19 BP 4177 EP 4182 PG 6 WC Oncology SC Oncology GA XZ011 UT WOS:A1997XZ01100008 PM 9331070 ER PT J AU Hanna, NN Mauceri, HJ Wayne, JD Hallahan, DE Kufe, DW Weichselbaum, RR AF Hanna, NN Mauceri, HJ Wayne, JD Hallahan, DE Kufe, DW Weichselbaum, RR TI Virally directed cytosine deaminase/5-fluorocytosine gene therapy enhances radiation response in human cancer xenografts SO CANCER RESEARCH LA English DT Article ID THYMIDINE KINASE GENE; TISSUE-SPECIFIC EXPRESSION; MALIGNANT BRAIN-TUMORS; DEAMINASE SUICIDE GENE; IN-VIVO; SELECTIVE ENHANCEMENT; CARCINOMA-CELLS; 5-FLUOROURACIL; 5-FLUOROCYTOSINE; GANCICLOVIR AB Gene therapy combined with radiation therapy to enhance selectively radiation cytotoxicity in malignant cells represents a new approach for cancer treatment, We investigated the efficacy of adenoviral (Ad5)-directed cytosine deaminase/5-fluorocytosine (CD/5-FC) enzyme/prodrug gene therapy to enhance selectively the tumoricidal action of ionizing radiation in human cancer xenografts derived from a human squamous carcinoma cell line (SQ-20B). Tumor xenografts grown in hindlimbs of nude mice were transfected with an adenoviral vector (Ad.CMV.CD) containing the cytosine deaminase (CD) gene under the control of a cytomegalovirus (CMV) promoter, Mice were injected i.p. with 800 mg/kg of 5-FC for 12 days, and tumors were treated with fractionated radiation at a dose of 5 Gy/day to a total dose of 50 Gy, In larger tumors with a mean volume of 1069 mm(3), marked tumor regression to 11% of the original tumor volume was observed at day 21 (P = 0.01), The volumetric regression of smaller tumors with a mean volume of 199 mm(3), which received the same combined treatment protocol, was significant at day 12 (P = 0.014), However, unlike large tumors, regression of the smaller tumors continued until day 36 (P = 0.01), with 43% cured at day 26, No cures or significant volumetric reduction in size was observed in tumors treated with radiation alone; Ad.CMV.CD with or without radiation; or with Ad.CMV.CD and 5-FC, These results suggest that the CD/5-FC gene therapy approach is an effective radiosensitizing strategy and may lead to substantial improvement in local tumor control that would translate into improved cure rates and better survival. C1 UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,PRITZKER SCH MED,CHICAGO,IL 60637. UNIV CHICAGO,PRITZKER SCH MED,DEPT SURG,CHICAGO,IL 60637. DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA41068, T32CA09516] NR 59 TC 73 Z9 78 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 1 PY 1997 VL 57 IS 19 BP 4205 EP 4209 PG 5 WC Oncology SC Oncology GA XZ011 UT WOS:A1997XZ01100014 PM 9331076 ER PT J AU Chmura, SJ Mauceri, HJ Advani, S Heimann, R Beckett, MA Nodzenski, E Quintans, J Kufe, DW Weichselbaum, RR AF Chmura, SJ Mauceri, HJ Advani, S Heimann, R Beckett, MA Nodzenski, E Quintans, J Kufe, DW Weichselbaum, RR TI Decreasing the apoptotic threshold of tumor cells through protein kinase C inhibition and sphingomyelinase activation increases tumor killing by ionizing radiation SO CANCER RESEARCH LA English DT Article ID NECROSIS-FACTOR; TERMINAL DIFFERENTIATION; SIGNAL-TRANSDUCTION; CONFERS RESISTANCE; CANCER-THERAPY; P53 STATUS; IN-VIVO; CERAMIDE; DEATH; LINES AB Approximately 30% of cancer deaths result from the failure to control local and regional tumors, The goal of radiotherapy is to maximize local and regional tumor cell killing while minimizing normal tissue destruction, Attempts to enhance radiation-mediated tumor cell killing using halogenated pyrimidines, antimetabolites, and other DNA-damaging agents or sensitizers of hypoxic tumor cells have met with only modest clinical success, In an unique strategy to modify tumor radiosensitivity, we used an inhibitor of the protein kinase C group A and B isoforms, chelerythrine chloride (chelerythrine), to enhance the killing effects of ionizing radiation (IR), protein kinase C activity plays a central role in cellular proliferation, differentiation, and apoptosis, Chelerythrine increases sphingomyelinase activity and enhances IR-mediated cell killing through induction or apoptotic tumor cell death in a radioresistant tumor model both in vitro and in vivo. Although previous reports have suggested that IR-mediated apoptosis correlates with tumor volume reduction, me demonstrate for the first time that lowering the apoptotic threshold increases tumor cell killing in vivo. C1 UNIV CHICAGO,DEPT PATHOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. UNIV CHICAGO,DIV BIOL SCI,CHICAGO,IL 60637. UNIV CHICAGO,PRITZKER SCH MED,CHICAGO,IL 60637. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [5-R01-CA42596, 5-R01-CA41068]; NIGMS NIH HHS [GM07183] NR 60 TC 85 Z9 87 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 1 PY 1997 VL 57 IS 19 BP 4340 EP 4347 PG 8 WC Oncology SC Oncology GA XZ011 UT WOS:A1997XZ01100034 PM 9331096 ER PT J AU Miyama, S Takahashi, T Nowakowski, RS Caviness, VS AF Miyama, S Takahashi, T Nowakowski, RS Caviness, VS TI Gradient in the duration of the G1 phase in the murine neocortical proliferative epithelium SO CEREBRAL CORTEX LA English DT Article ID DEVELOPING CEREBRAL-CORTEX; CELL-CYCLE; VISUAL-CORTEX; MOUSE; PATTERNS; ORGANIZATION; DISPERSION; WALL; HISTOGENESIS; FOREBRAIN AB Neuronogenesis in the neocortical pseudostratified ventricular epithelium (PVE) is initiated rostrolaterally acid progresses caudo-medially as development progresses. Here we have measured the cytokinetic parameters and the fractional neuronal output parameter, a, of laterally located early-maturing regions over the principal embryonic days (E12-E15) of neocortical neuronogenesis in the mouse. These measures are compared with ones previously made of a medial, late-maturing portion of fire PVE. Laterally, as medially, the duration of the neuronogenetic interval is 6 days and comprises 11 integer cell cycles. Also, in both lateral acid medial areas the length of G1 phase (T-G1) increases nearly 4-fold and is the only cell cycle parameter to change, a progresses essentially identically laterally and medially with respect to the succession of integer cell cycles. Most importantly, from E12 to E13 there is a steeply declining lateral to medial gradient in T-G1. The gradient is due both to the lateral to medial graded stage of neuronogenesis and to the stepwise increase in T-G1 with each integer cycle during the neuronogenetic interval. To our knowledge this gradient in T-G1 of the cerebral PVE is the first cell biological gradient to be demonstrated experimentally in such an extensive proliferative epithelial sheet. We suggest that this gradient in T-G1 is the cellular mechanism for positionally encoding a protomap of the neocortex within the PVE. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. KEIO UNIV,SCH MED,DEPT PEDIAT,TOKYO 160,JAPAN. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT NEUROSCI & CELL BIOL,PISCATAWAY,NJ 08854. RI Nowakowski, Richard/C-3217-2016 FU NINDS NIH HHS [NS33443, NS12005] NR 63 TC 73 Z9 73 U1 1 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 1047-3211 J9 CEREB CORTEX JI Cereb. Cortex PD OCT-NOV PY 1997 VL 7 IS 7 BP 678 EP 689 DI 10.1093/cercor/7.7.678 PG 12 WC Neurosciences SC Neurosciences & Neurology GA YB886 UT WOS:A1997YB88600006 PM 9373022 ER PT J AU MarquesMagallanes, JA Koyal, SN Cooper, CB Kleerup, EC Tashkin, DP AF MarquesMagallanes, JA Koyal, SN Cooper, CB Kleerup, EC Tashkin, DP TI Impact of habitual cocaine smoking on the physiologic response to maximum exercise SO CHEST LA English DT Article DE cardiovascular response; cocaine smoking; crack; gas exchange; maximum exercise; ventilatory response ID GAS-EXCHANGE; ENDURANCE; RATS; CATECHOLAMINE; WITHDRAWAL; CRACK; USERS AB Background: Habitual smoking of alkaloidal cocaine (crack) has been reported to be associated with a number of cardiopulmonary complications that may not be clinically obvious but could potentially interfere with normal physiologic responses to exercise and thus impair maximum exercise performance. Study objective: To evaluate the impact of regular use of cocaine on maximum exercise. Design: Observational study in crack users and age- and gender-matched control subjects. Subjects: Thirty-five habitual cocaine smokers (21 male and 14 female) and 29 age-matched sedentary control nonsmokers of cocaine (15 male and 14 female), all of whom were in good general health. Methods: In these subjects, we compared physiologic responses to symptom-limited, incremental maximal exercise performed on a cycle ergometer using a ramp protocol. Comparisons were made for men and women separately. Results: For both men and women, long-term cocaine smokers had a reduced aerobic capacity (maximum oxygen consumption) compared with control nonsmokers but did not show evidence of ventilatory limitation, reduced gas exchange threshold, increased physiologic dead space, or gas exchange abnormality at maximum exercise compared with the healthy control subjects. Although cocaine smokers had reduced maximum heart rates compared with control subjects, the relationship between submaximal heart rate and oxygen uptake was normal, indicating a normal cardiovascular response pattern. However, effort perception was similar between the two groups despite the difference in heart rate at maximum exercise, suggesting the possibility of perceptual dysfunction for effort. Differences in aerobic capacity between the crack users and nonusers could not be explained by differences in physical fitness or altered perception of dyspnea. Conclusion: In the subjects we studied, long-term cocaine smoking was associated with reduced maximum exercise performance, probably due to poor motivation or altered effort perception. No other identifiable physiologic abnormality appeared to limit exercise in the habitual crack users. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHYSIOL,LOS ANGELES,CA 90095. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. FU NIDA NIH HHS [R01 DA008254, R01 DA08254] NR 29 TC 11 Z9 11 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 BP 1008 EP 1016 DI 10.1378/chest.112.4.1008 PG 9 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA351 UT WOS:A1997YA35100025 PM 9377910 ER PT J AU Anderson, IC AF Anderson, IC TI Limited-stage small cell lung cancer - A case report SO CHEST LA English DT Article; Proceedings Paper CT Harvard-Medical-School Symposium on Multimodality Therapy of Chest Malignancies - Update 96 CY MAR 28-29, 1996 CL BOSTON, MA SP Harvard Med Sch, Dept Oncol, Harvard Med Sch, Dana Farber Canc Inst, Harvard Med Sch, Div Thorac Surg, Brigham & Womens Hosp, Harvard Joint Ctr Radiat Therapy AB Because small cell lung cancer (SCLC) is very responsive to chemotherapy, an attempt at treatment is warranted even in poor-prognosis patients with limited-stage disease. Concurrent thoracic radiotherapy and prophylactic cranial irradiation should be considered in such cases. A case report of an elderly, debilitated patient with limited-stage SCLC is presented, and his management is discussed. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. RP Anderson, IC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,THORAC ONCOL PROGRAM,44 BINNEY ST,BOSTON,MA 02115, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 SU S BP S249 EP S250 DI 10.1378/chest.112.4_Supplement.249S PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA767 UT WOS:A1997YA76700016 PM 9337298 ER PT J AU Baldini, EH Strauss, GM AF Baldini, EH Strauss, GM TI Women and lung cancer - Waiting to exhale SO CHEST LA English DT Article; Proceedings Paper CT Harvard-Medical-School Symposium on Multimodality Therapy of Chest Malignancies - Update 96 CY MAR 28-29, 1996 CL BOSTON, MA SP Harvard Med Sch, Dept Oncol, Harvard Med Sch, Dana Farber Canc Inst, Harvard Med Sch, Div Thorac Surg, Brigham & Womens Hosp, Harvard Joint Ctr Radiat Therapy ID SMALL-CELL CARCINOMA; CIGARETTE-SMOKING; NONSMOKING WOMEN; FOLLOW-UP; HISTOLOGIC TYPE; SEX-DIFFERENCES; UNITED-STATES; HIGHER RISK; NEW-JERSEY; SMOKERS AB Lung cancer is now the leading cause of cancer deaths among women, In the United States, 64,300 women are expected to die of lung cancer in 1996, Smoking is responsible for about 80% of lung cancer cases, Unfortunately, the prevalence of smoking among women remains unacceptably high at about 22% and is expected to surpass the rate in men by the year 2000, Smoking rates are highest among young girls and the less educated, Whether lung cancer represents a different disease in women than in men is unclear, Data are conflicting regarding the magnitude of the relative risk of developing lung cancer due to smoking between the genders, There appears to be a difference in the relative distribution of lung cancer histologic features between men and women that is not explained entirely by differences in smoking patterns, Women who smoke appear to be at higher risk of developing small cell lung cancer than squamous cell lung cancer, whereas men who smoke have a similar risk for the two histologic conditions, Furthermore, women smelters are more likely to develop adenocarcinoma of the lung, and estrogens may play a causative role in this phenomenon. Data are unclear regarding whether the outcome of lung cancer treatment differs between genders. Solutions to the lung cancer epidemic among US women include (1) prevention of the disease by reducing smoking rates, (2) improving early detection methods, and (3) exploring new therapeutic strategies. C1 DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. RP Baldini, EH (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOINT CTR RADIAT THERAPY,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 64 TC 45 Z9 49 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 SU S BP S229 EP S234 DI 10.1378/chest.112.4_Supplement.229S PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA767 UT WOS:A1997YA76700012 PM 9337294 ER PT J AU Elias, AD AF Elias, AD TI Small cell lung cancer - State-of-the-art therapy in 1996 SO CHEST LA English DT Article; Proceedings Paper CT Harvard-Medical-School Symposium on Multimodality Therapy of Chest Malignancies - Update 96 CY MAR 28-29, 1996 CL BOSTON, MA SP Harvard Med Sch, Dept Oncol, Harvard Med Sch, Dana Farber Canc Inst, Harvard Med Sch, Div Thorac Surg, Brigham & Womens Hosp, Harvard Joint Ctr Radiat Therapy ID PROPHYLACTIC CRANIAL IRRADIATION; PHASE-III TRIAL; RANDOMIZED TRIAL; BRONCHOGENIC-CARCINOMA; DOSE CYCLOPHOSPHAMIDE; THORACIC IRRADIATION; UNTREATED PATIENTS; FREE SURVIVAL; CHEMOTHERAPY; ETOPOSIDE AB Small cell lung cancer (SCLC) occurs almost exclusively in smokers and represents 15 to 25% of all lung cancer histologic findings. It is distinguished from non-small cell lung cancer by its rapid tumor doubling time, high growth fraction, and early development of widespread metastases. Since patients with SCLC usually present with disseminated disease, treatment strategies have focused on systemic therapy, Single-agent and combination chemotherapy, as well as combined-modality therapy, have produced high response rates (80 to 100% for limited disease; 60 to 80% for extensive disease), but these tend to he short-lived (median duration, 6 to 8 months). Survival beyond 5 years occurs in only 3 to 8% of all patients with SCLC. At least 15 to 20 different chemotherapeutic agents have shown major activity against SCLC in both the untreated and relapsed settings, including etoposide, teniposide, cisplatin, carboplatin, ifosfamide, cyclophosphamide, vincristine, and doxorubicin. This paper reviews state-of-the-art treatment strategies being employed in the treatment of SCLC, including those incorporating high-dose intensive therapy, salvage therapy, new agents, thoracic radiotherapy, prophylactic cranial, radiotherapy, surgical resection, and biologic response modifiers. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Elias, AD (reprint author), DANA FARBER CANC INST,DIV CLIN PHARMACOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 52 TC 56 Z9 59 U1 2 U2 3 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 SU S BP S251 EP S258 DI 10.1378/chest.112.4_Supplement.251S PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA767 UT WOS:A1997YA76700017 PM 9337299 ER PT J AU Frei, E AF Frei, E TI Non-small cell lung cancer - Novel treatment strategies SO CHEST LA English DT Article; Proceedings Paper CT Harvard-Medical-School Symposium on Multimodality Therapy of Chest Malignancies - Update 96 CY MAR 28-29, 1996 CL BOSTON, MA SP Harvard Med Sch, Dept Oncol, Harvard Med Sch, Dana Farber Canc Inst, Harvard Med Sch, Div Thorac Surg, Brigham & Womens Hosp, Harvard Joint Ctr Radiat Therapy ID RANDOMIZED TRIAL; CHEMOTHERAPY AB Prevention of cigarette smoking and early lung cancer detection remain important in our approach to the control of non-small cell lung cancer (NSCLC). In recent years, chemotherapy has emerged as a viable option in the treatment of NSCLC. The most impressive and widely confirmed evidence for this is the fact that chemotherapy can eradicate NSCLC micrometastases, Indeed, in some studies employing neoadjuvant chemotherapy followed by local surgery, pathology-confirmed complete remission rates as high as 20% have been reported, New agents showing preliminary activity in NSCLC include paclitaxel, vinorelbine, gemcitabine, and irinotecan (CPT-11). Certainly, however, there remains a need for novel, effective single-agent and combination chemotherapies, The seed/soil tumor concept, in which the seed consists of the tumor cells per se and the soil is the stroma containing the seeds, has proven helpful in devising new treatment strategies, Such strategies may include the use of antisoil agents, including antiangiogenesis, anti-invasion, and antimetastasis agents, both separately and particularly in conjunction with established antitumor agents, New therapeutic targets and methods of antitumor agent development based on modern molecular biology and pharmacology will protide a greater opportunity to improve the treatment of NSCLC. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. RP Frei, E (reprint author), DANA FARBER CANC INST,DIV CANC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 8 TC 2 Z9 2 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 SU S BP S266 EP S268 DI 10.1378/chest.112.4_Supplement.266S PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA767 UT WOS:A1997YA76700019 PM 9337301 ER PT J AU Mentzer, SJ Swanson, SJ DeCamp, MM Bueno, R Sugarbaker, DJ AF Mentzer, SJ Swanson, SJ DeCamp, MM Bueno, R Sugarbaker, DJ TI Mediastinoscopy, thoracoscopy, and video-assisted thoracic surgery in the diagnosis and staging of lung cancer SO CHEST LA English DT Article; Proceedings Paper CT Harvard-Medical-School Symposium on Multimodality Therapy of Chest Malignancies - Update 96 CY MAR 28-29, 1996 CL BOSTON, MA SP Harvard Med Sch, Dept Oncol, Harvard Med Sch, Dana Farber Canc Inst, Harvard Med Sch, Div Thorac Surg, Brigham & Womens Hosp, Harvard Joint Ctr Radiat Therapy ID BRONCHOGENIC-CARCINOMA AB The intrathoracic staging of lung cancer involves assessment of the primary tumor and potential sites of metastases. Imaging studies of the chest are sensitive in detecting intrathoracic abnormalities, but specific staging information generally requires a tissue biopsy. The instruments used to obtain this information include the bronchoscope, mediastinoscope, add thoracoscope, The complementary application of these instruments can provide valuable staging information while limiting the morbidity of surgical staging. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP Mentzer, SJ (reprint author), HARVARD UNIV,DIV THORAC SURG,BRIGHAM & WOMENS HOSP,SCH MED,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL47078] NR 10 TC 22 Z9 22 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 SU S BP S239 EP S241 DI 10.1378/chest.112.4_Supplement.239S PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA767 UT WOS:A1997YA76700014 PM 9337296 ER PT J AU Shaffer, K AF Shaffer, K TI Radiologic evaluation in lung cancer - Diagnosis and staging SO CHEST LA English DT Article; Proceedings Paper CT Harvard-Medical-School Symposium on Multimodality Therapy of Chest Malignancies - Update 96 CY MAR 28-29, 1996 CL BOSTON, MA SP Harvard Med Sch, Dept Oncol, Harvard Med Sch, Dana Farber Canc Inst, Harvard Med Sch, Div Thorac Surg, Brigham & Womens Hosp, Harvard Joint Ctr Radiat Therapy ID LABELED MONOCLONAL-ANTIBODY; COMPUTED-TOMOGRAPHY; BRONCHOGENIC-CARCINOMA; PULMONARY NODULES; CT; IMMUNOSCINTIGRAPHY; METASTASES; STANDARD; SPECT AB Radiology and surgery are not competing but are complementary modalities in the care of patients with lung cancer. In certain areas, such as evaluation of the solitary pulmonary nodule, radiologic studies can have an important impact on patient care. Mediastinal staging with imaging studies is inexact, and CT may be most effective as a road map for more definitive surgical staging. MRI currently offers no advantages over CT in staging of the mediastinum but can be helpful in evaluation of parts of the chest not well demonstrated on axial images. A discussion of newer nuclear medicine imaging modalities is included. C1 DANA FARBER CANC INST,DEPT ONCORADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. NR 28 TC 11 Z9 11 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 SU S BP S235 EP S238 DI 10.1378/chest.112.4_Supplement.235S PG 4 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA767 UT WOS:A1997YA76700013 PM 9337295 ER PT J AU Strauss, GM AF Strauss, GM TI Measuring effectiveness of lung cancer screening - From consensus to controversy and back SO CHEST LA English DT Article; Proceedings Paper CT Harvard-Medical-School Symposium on Multimodality Therapy of Chest Malignancies - Update 96 CY MAR 28-29, 1996 CL BOSTON, MA SP Harvard Med Sch, Dept Oncol, Harvard Med Sch, Dana Farber Canc Inst, Harvard Med Sch, Div Thorac Surg, Brigham & Womens Hosp, Harvard Joint Ctr Radiat Therapy ID FECAL-OCCULT-BLOOD; RANDOMIZED CONTROLLED TRIAL; LOCALIZED PROSTATE-CANCER; BREAST-CANCER; COLORECTAL-CANCER; MOLECULAR EPIDEMIOLOGY; DEATH RATES; FOLLOW-UP; MAMMOGRAPHY; SURVIVAL AB Background: While intense controversy exists regarding screening for breast, colorectal, and prostate cancer, a consensus exists regarding lung cancer screening. All organizations recommend against any efforts to detect early lung cancer because each of four randomized controlled trials (RCTs) has failed to demonstrate a significant reduction in lung cancer mortality as a result of screening. Synthesis: Disease-specific mortality is assumed to represent the best measure of screening effectiveness in RCTs, because it is not subject to confounding by lead time, length, or overdiagnosis biases. However, the effects of these biases are predictable, so accurate assessments of the degree of confounding by these biases can be made. Moreover, the ability of mortality to accurately reflect cancer death rates depends on the ability of randomization to create experimental and control populations that have an equal risk of dying of the disease under study, except insofar as early detection may reduce that risk. Because the majority of participants in screening trials never develop the disease under investigation, small absolute differences in disease risk between groups often persist despite randomization, and such differences translate into much larger proportional differences in the size of subgroups at risk for disease-specific mortality. This effect confounds the ability of disease-specific mortality to accurately measure screening effectiveness. Results: A total of 18 RCTs have been conducted to evaluate screening for breast, colorectal, and lung cancer. In the only two RCTs that reported a significant mortality reduction for screening mammography in breast cancer, and in the one RCT that reported a significant mortality reduction for fecal occult blood screening in colorectal cancer, population differences led mortality comparisons to overestimate the effectiveness of screening. In lung cancer, no significant mortality reductions have been reported (to my knowledge), but in the two RCTs most directly addressing the effectiveness of chest radiograph (CXR) screening, population differences led mortality comparisons to underestimate the ability of CXRs to reduce the risk of crying of lung cancer. Although mortality is believed to be the best measure of outcome, not a single example can be cited as definitive proof of efficacy for any screening strategy. Thus, screening cannot be recommended for any cancer on the basis of consistent reductions in mortality in RCTs. Analysis: Current policy, which calls for no early detection efforts for lung cancer, implicitly accepts the validity of two contradictory assertions. Conventional wisdom maintains that lung cancer is a highly virulent disease and that metastases are present: at inception; accordingly, early detection is ineffective. However, RCTs suggest that lung cancer is an indolent disease and that radiographically detected lesions are clinically unimportant; accordingly, early detection is unnecessary. Such contradictions mandate some rethinking of the fundamental assumptions underlying screening evaluation. Conclusions: Considerable evidence suggests that annual CXR screening could result: in a dramatic reduction in lung cancer mortality in our society. However, proper interpretation of the data depends completely on how screening effectiveness is measured. Given the enormous public health importance of this issue, a consensus conference is recommended to determine whether lung cancer screening can save lives. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. RP Strauss, GM (reprint author), MEM HOSP,DIV HEMATOL ONCOL,119 BELMONT ST,WORCESTER,MA 01605, USA. NR 90 TC 41 Z9 41 U1 1 U2 3 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 SU S BP S216 EP S228 DI 10.1378/chest.112.4_Supplement.216S PG 13 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA767 UT WOS:A1997YA76700011 PM 9337293 ER PT J AU Sugarbaker, DJ Garcia, JP AF Sugarbaker, DJ Garcia, JP TI Multimodality therapy for malignant pleural mesothelioma SO CHEST LA English DT Article; Proceedings Paper CT Harvard-Medical-School Symposium on Multimodality Therapy of Chest Malignancies - Update 96 CY MAR 28-29, 1996 CL BOSTON, MA SP Harvard Med Sch, Dept Oncol, Harvard Med Sch, Dana Farber Canc Inst, Harvard Med Sch, Div Thorac Surg, Brigham & Womens Hosp, Harvard Joint Ctr Radiat Therapy ID EXTRAPLEURAL PNEUMONECTOMY; UNITED-STATES; DIFFUSE; EXPERIENCE; PATTERNS AB Mesothelioma is a rare disease for which neither single modality nor bimodality therapy improves survival. For this reason, from 1980 to 1995, we used trimodality therapy in an attempt to improve survival in selected patients at Brigham and Women's Hospital and Dana-Farber Cancer Institute, One hundred twenty patients underwent trimodality treatment involving extrapleural pneumonectomy followed by combination chemoradiotherapy, Twenty-seven women and 93 men (mean age, 56 years) were evaluable for response and treatment-related morbidity. The operative mortality rate was 5%, and 22% of patients experienced major morbidity, Cell type and nodal status were significant prognostic variables, The respective 2- and 5-year survival rates were 45% and 22% overall, 70% and 37% for patients with epithelial cell type, 20% and 0% for patients with sarcomatous or mixed-histologic-type tumors, and 74% and 39% for patients who were node-negative with epithelial histologic type. Positive resection margins impacted survival only in the case of full-thickness, transdiaphragmatic invasion. A revised staging system stratified survival with median intervals of 22, 17, and 11 months for stages I, II, and III disease, respectively (p=0.04). Thus, extrapleural pneumonectomy with adjuvant therapy is appropriate and effective treatment for patients with stage I disease according to the revised staging system. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP Sugarbaker, DJ (reprint author), HARVARD UNIV,DIV THORAC SURG,BRIGHAM & WOMENS HOSP,SCH MED,THORAC ONCOL PROGRAM,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 19 TC 14 Z9 15 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD OCT PY 1997 VL 112 IS 4 SU S BP S272 EP S275 DI 10.1378/chest.112.4_Supplement.272S PG 4 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA YA767 UT WOS:A1997YA76700021 PM 9337303 ER PT J AU McGibbon, CA Riley, PO Krebs, DE AF McGibbon, CA Riley, PO Krebs, DE TI Comparison of hip center estimation using in-vivo and ex-vivo measurements from the same subject SO CLINICAL BIOMECHANICS LA English DT Article DE hip joint center; motion analysis; anatomical scaling; photogrammetry ID JOINT CENTER LOCATION; MUSCLE FORCES; GAIT ANALYSIS; PREDICTION; LANDMARKS; WALKING; MODEL AB Objective. To evaluate the accuracy of locating the hip center (HIPC) by comparing in-vivo estimations to posthumous HIPC measurement in the same subject. Background. Numerous techniques have been used to locate the HIPC in living subjects and in cadavers. There are no published reports, however, which have compared measurements of the HIPC obtained in-vivo and ex-vivo for the same subject. Design and methods. Bilateral hip centers (HIPC) were estimated for an elderly male patient seven times over 32 months in a gait laboratory using a technique which combines kinematic data and static pointing. The patient's pelvis was recovered posthumously and analytical photogrammetry used to estimate the HIPC locations. Published methods which scale anatomical measurements to locate the HIPC were compared to our ex-vivo and in-vivo measurements. Results. HIPC precision was 0.94 cm for the in-vivo measurements (N = 7 trial days) and 0.15 cm for the ex-vivo measurements (N = 6 photogrammetry trials). The resultant error between ex-vivo and in-vivo estimates of HIPC position was 1.17 cm. Resultant errors in locating the HIPC using published anatomical scaling factors ranged between 1.48 cm and 5.37 cm. Conclusions. Although we have been unable to compare in-vivo and ex-vivo HIPC measurements for more than one subject, results of our analysis suggest that using anatomical scaling to locate the HIPC may result in unsatisfactory subject-specific estimates of the HIPC. Relevance Accurate measurement of the hip joint center (HIPC) is paramount for application of inverse dynamic models in clinical movement analysis. (C) 1997 Elsevier Science Ltd. All rights reserved. C1 Massachusetts Gen Hosp, Dept Orthopaed, Biomot Lab, Boston, MA 02114 USA. Spaulding Rehabil Hosp, Boston, MA USA. Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Boston, MA USA. RP McGibbon, CA (reprint author), Massachusetts Gen Hosp, Dept Orthopaed, Biomot Lab, Boston, MA 02114 USA. EM McGibbon.Chris@mgh.harvard.edu RI Riley, Patrick/B-3053-2009 NR 22 TC 5 Z9 5 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0268-0033 J9 CLIN BIOMECH JI Clin. Biomech. PD OCT-DEC PY 1997 VL 12 IS 7-8 BP 491 EP 495 DI 10.1016/S0268-0033(97)00058-2 PG 5 WC Engineering, Biomedical; Orthopedics; Sport Sciences SC Engineering; Orthopedics; Sport Sciences GA ZK517 UT WOS:000073330400010 ER PT J AU Mironova, M Virella, G VirellaLowell, I LopesVirella, MF AF Mironova, M Virella, G VirellaLowell, I LopesVirella, MF TI Anti-modified LDL antibodies and LDL-containing immune complexes in IDDM patients and healthy controls SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID LOW-DENSITY-LIPOPROTEIN; MONOCYTE-DERIVED MACROPHAGES; FOAM CELL-FORMATION; HUMAN RED-CELLS; DIABETES-MELLITUS; AUTOANTIBODIES; ATHEROSCLEROSIS; PROTEINS; PLASMA; GLYCOSYLATION AB Antibodies to oxidized LDL (ox-LDL) and LDL containing immune complexes (LDL-IC) have been reported to be associated with the presence or progression of arteriosclerosis. We screened for anti-modified LDL antibodies and isolated soluble IC by precipitation with 3.5% (w/v) polyethylene glycol (PEG) 6000 in two groups. The patient group was constituted by 16 insulin-dependent diabetes mellitus subjects free of macrovascular complications. The control group was constituted by 16 healthy, age-, gender-, race-, and body mass index-matched nondiabetic subjects. We detected anti-ox-LDL antibodies and anti-malondialdehyde-modified LDL antibodies with similar levels in patients and controls, while the levels of anti-glycated LDL antibodies were very low, but slightly higher in diabetics than in healthy controls. Isolated LDL-IC were adsorbed to red blood cells (RBC) and incubated with human macrophages for 18 hr at 37 degrees C. Under those experimental conditions, RBC-adsorbed IC are taken up by macrophages but the RBC remain intact and are not ingested. Slightly higher levels of cholesteryl ester (CE) accumulation were measured in macrophages incubated with RBC to which we adsorbed IC isolated from diabetics (15.4 +/- 2.5 mu g/mg of protein, mean +/- SEM) than in macrophages incubated with IC isolated from controls (12.5 +/- 1.6 mu g/mg of protein, mean +/- SEM), but the difference did not reach statistical significance. PEG-precipitable IC isolated from both normal and diabetic subjects led, in some instances, to the transformation of macrophages into foam cells. Significant correlations were observed between CE accumulation and the content of apo B (P < 0.0001), total cholesterol (P = 0.0004), IgG (P = 0.015), and IgA (P = 0.015) in the isolated IC. The correlation between CE accumulation and the content of apo B in isolated IC was stronger in diabetics than in the control group (r = 0.759 vs r = 0.500). Fractionation of isolated IC in immobilized protein A/G yielded immunoglobulin-rich fractions which contained cholesterol and IgG anti-ox-LDL antibodies. The cholesterol content of these fractions was significantly correlated (P = 0.001) with CE accumulation. In conclusion, both diabetics and normal individuals have circulating IC whose atherogenic potential appears to be related to the presence of LDL and antibodies of the IgG and IgA isotypes. (C) 1997 Academic Press. C1 MED UNIV S CAROLINA,DEPT MICROBIOL & IMMUNOL,CHARLESTON,SC 29401. MED UNIV S CAROLINA,RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. RP Mironova, M (reprint author), MED UNIV S CAROLINA,DEPT MED,DIV ENDOCRINOL METAB & MED GENET,CHARLESTON,SC 29401, USA. FU NHLBI NIH HHS [HL46815] NR 37 TC 40 Z9 40 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD OCT PY 1997 VL 85 IS 1 BP 73 EP 82 DI 10.1006/clin.1997.4404 PG 10 WC Immunology; Pathology SC Immunology; Pathology GA YA706 UT WOS:A1997YA70600010 PM 9325072 ER PT J AU Rao, PM Rhea, JT Novelline, RA AF Rao, PM Rhea, JT Novelline, RA TI Appendiceal and peri-appendiceal air at CT: Prevalence, appearance and clinical significance SO CLINICAL RADIOLOGY LA English DT Article ID DIAGNOSIS AB Aim: Appendiceal air has been reported as both a sign of appendicitis and of a normal appendix both at plain radiography and computed tomography (CT), It is the aim of this investigation to determine the prevalence, range of appearances, and significance of appendiceal and peri-appendiceal air at CT, Patients and Methods: Appendiceal CT scans of 100 patients with proven appendicitis and 100 patients with a normal appendix were reviewed for the presence of appendiceal and peri-appendiceal air, All cases mere correlated with surgical and pathological findings or clinical follow-up, Results: In 100 CT cases of appendicitis, appendiceal and/or peri-appendiceal air was present in one or more forms in 31% of cases, When present, it appeared as intraluminal air bubbles (38.7%) or air-fluid levels (22.6%), appendolith air (41.9%), intramural air (16.1%), peri-appendiceal air bubbles (12.9%), or extraluminal air-fluid level(s) (29.0%), Intramural and extraluminal air correlated with perforation in 60% and 100%, respectively, In 100 CT cases of a normal appendix, air was present in 57%, It was always intraluminal and appeared as small bubbles of air (52.6%), a tubular-shaped air collection (43.9%), or as an air-fluid level (3.5%), The appendiceal lumen was either airless (43%), or minimally (32%), moderately (18%), or completely filled with air (7%). Conclusion: Air is a common finding at appendiceal CT in both the normal and inflamed appendix, Intraluminal air is seen in both appendicitis and normal appendices, and cannot be presumed to indicate a patent lumen and thus a normal appendix, Appendolith, intramural and peri-appendiceal air appear diagnostic of appendicitis. RP Rao, PM (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 18 TC 36 Z9 36 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0009-9260 J9 CLIN RADIOL JI Clin. Radiol. PD OCT PY 1997 VL 52 IS 10 BP 750 EP 754 DI 10.1016/S0009-9260(97)80153-5 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA YB777 UT WOS:A1997YB77700004 PM 9366533 ER PT J AU Ahern, DK Lohr, BA AF Ahern, DK Lohr, BA TI Psychosocial factors in sports injury rehabilitation SO CLINICS IN SPORTS MEDICINE LA English DT Article ID LIFE STRESS; MODERATOR VARIABLES; PERFORMANCE; REHEARSAL; EVENTS AB Recent research in sport psychology and behavioral medicine has highlighted the importance of psychosocial factors in sports performance and in the prevention, management, and rehabilitation of sports injury. This article presents an overview of the psychosocial and behavioral risk factors known to contribute to sports injury risk and rehabilitation, as well as guidelines for assessment and treatment of sports injury from a biopsychosocial perspective. Finally, areas for future research and clinical practice are discussed, particularly regarding the role of psychology within the sports medicine team. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP Ahern, DK (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BEHAV MED UNIT,15 PARKMAN ST,WACC 816,BOSTON,MA 02114, USA. NR 55 TC 12 Z9 13 U1 0 U2 14 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0278-5919 J9 CLIN SPORT MED JI Clin. Sports Med. PD OCT PY 1997 VL 16 IS 4 BP 755 EP & DI 10.1016/S0278-5919(05)70052-1 PG 15 WC Sport Sciences SC Sport Sciences GA YA081 UT WOS:A1997YA08100011 PM 9330812 ER PT J AU Fichtner, CG Poddig, BE deVito, RA AF Fichtner, CG Poddig, BE deVito, RA TI Post-traumatic stress disorder - Pathophysiological aspects and pharmacological approaches to treatment SO CNS DRUGS LA English DT Review ID VIETNAM COMBAT VETERANS; GLUCOCORTICOID RECEPTOR NUMBER; CONCURRENT PSYCHIATRIC-ILLNESS; PLATELET ADENYLATE-CYCLASE; PLASMA BETA-ENDORPHIN; MONOAMINE-OXIDASE; WAR NEUROSIS; PSYCHOPHARMACOLOGICAL TREATMENT; PSYCHOPHYSIOLOGICAL RESPONSES; CATECHOLAMINE EXCRETION AB Post-traumatic stress disorder (PTSD) is a syndrome of psychophysiological sequelae occurring in the aftermath of severe emotional trauma. Phenomenologically, symptoms occur in 3 clusters: re-experiencing, avoidance and hyperarousal. Other psychiatric disorders such as depression, panic disorder and substance abuse frequently co-occur with PTSD. Treatment strategies for PTSD are often multimodal and attempt to integrate biological, behavioural, cognitive, psychodynamic and social formulations. Pharmacotherapy must target specific symptoms in all 3 clusters, and address the presence of comorbid psychiatric disorders. Psychotropic medication can facilitate psychotherapeutic work, or serve as the primary modality in a biologically based approach to treatment. Specific medications used in the treatment of PTSD span a broad spectrum of pharmacological agents. The most empirically studied agents, tricyclic antidepressants and monoamine oxidase inhibitors, demonstrate a definite but limited impact on specific PTSD symptoms. For the patient who presents in an acute symptomatic state, benzodiazepine anxiolytics may be appropriate. For longer term treatment, selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs), particularly fluoxetine, appear to have broader spectrum therapeutic effects on specific PTSD symptom clusters. Both antidepressants and anxiolytics have, in some studies, shown beneficial effects on depressive symptoms and anxiety, without measurable impact on the symptoms more specific to PTSD. Maintenance pharmacotherapy frequently requires a multidrug regimen; an SSRI may serve as the primary agent, with adjunctive agents targeting residual hyperarousal and re-experiencing symptoms. Benzodiazepines, sedating tricyclic or antihistamine compounds, and the noradrenergic drugs clonidine and propranolol are used in this way. Buspirone, a serotonergic anxiolytic, may serve a similar role for some patients, and cyproheptadine in particular appears to be helpful for nightmares. The antikindling agents carbamazepine and valproic acid (sodium valproate) have also been reported to be beneficial, and may provide an alternative for patients with persistent hyper-reactivity and explosiveness that have not responded to other treatments. C1 FINCH UNIV HLTH SCI CHICAGO MED SCH, DEPT PSYCHIAT & BEHAV SCI, CHICAGO, IL USA. US DEPT VET AFFAIRS, VET AFFAIRS EDWARD HINES JR HOSP, SERV PHARM, HINES, IL 60141 USA. LOYOLA UNIV, STRITCH SCH MED, DEPT PSYCHIAT, MAYWOOD, IL 60153 USA. RP Fichtner, CG (reprint author), ILLINOIS DEPT HUMAN SERV, DIV CLIN SCI, 100 W RANDOLPH ST, SUITE 6-400, CHICAGO, IL 60601 USA. NR 239 TC 17 Z9 17 U1 2 U2 4 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PD OCT PY 1997 VL 8 IS 4 BP 293 EP 322 DI 10.2165/00023210-199708040-00004 PG 30 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA YA335 UT WOS:A1997YA33500004 ER PT J AU Goldstein, O Asher, C Cragoe, E Kleyman, TR Garty, H AF Goldstein, O Asher, C Cragoe, E Kleyman, TR Garty, H TI An aldosterone regulated chicken intestine protein with high affinity to amiloride SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR & INTEGRATIVE PHYSIOLOGY LA English DT Article; Proceedings Paper CT 4th Abildgaard Symposium on Intestinal NaCl and SCFA Transport CY AUG 19-22, 1995 CL ROYAL VET & AGR UNIV, COPENHAGEN, DENMARK HO ROYAL VET & AGR UNIV DE amiloride-binding protein; epithelial transport; ion transport; Na+ channel; NaCl intake ID EPITHELIAL SODIUM-CHANNEL; SENSITIVE NA+ CHANNEL; MEMBRANE-VESICLES; BINDING-PROTEIN; TIGHT EPITHELIA; ION-TRANSPORT; H-3 PHENAMIL; EXPRESSION; CLONING; ANALOGS AB The pattern of chicken intestine amiloride-binding proteins was determined using the photoreactive amiloride analogue 2'-methoxy-5'-nitrobenzamil (NMBA) and a polyclonal anti-amiloride antibody. At 10(-7)M, NMBA inhibits similar to 62% of the Na+ channel activity. At this concentration the amiloride analogue labels a number of membrane proteins, and in particular a 40-45 kDa polypeptide denoted ABP40. Incorporation of NMBA into ABP40 could be prevented by a 100-fold excess of benzamil, but not by a 1000-fold excess of 5-(N-ethyl-N-isopropyl)-amiloride. Labeling of ABP40 was intense in membranes derived from salt-deprived chickens and similar to 5-fold weaker in membranes from salt-repleted animals. Because of its small size, ABP40 is not likely to be an avian Na+ channel subunit, yet this amiloride-binding protein could be involved in the response to aldosterone. (C) 1997 Elsevier Science Inc. C1 WEIZMANN INST SCI, DEPT MEMBRANE RES & BIOPHYS, IL-76100 REHOVOT, ISRAEL. UNIV PENN, DEPT PHYSIOL & MED, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA 19104 USA. NR 45 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1095-6433 EI 1531-4332 J9 COMP BIOCHEM PHYS A JI Comp. Biochem. Physiol. A-Mol. Integr. Physiol. PD OCT PY 1997 VL 118 IS 2 BP 201 EP 208 DI 10.1016/S0300-9629(97)00067-4 PG 8 WC Biochemistry & Molecular Biology; Physiology; Zoology SC Biochemistry & Molecular Biology; Physiology; Zoology GA XY783 UT WOS:A1997XY78300003 PM 9366044 ER PT J AU Goldstein, G AF Goldstein, G TI Clinical neuropsychology of alcoholism - Knight,RG, Longmore,BE SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review RP Goldstein, G (reprint author), VET AFFAIRS PITTSBURGH HEALTHCARE SYST,PITTSBURGH,PA, USA. NR 4 TC 0 Z9 0 U1 0 U2 3 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD OCT PY 1997 VL 42 IS 10 BP 918 EP 919 PG 2 WC Psychology, Multidisciplinary SC Psychology GA XZ236 UT WOS:A1997XZ23600028 ER PT J AU Burgeson, RE Christiano, AM AF Burgeson, RE Christiano, AM TI The dermal-epidermal junction SO CURRENT OPINION IN CELL BIOLOGY LA English DT Article ID BULLOUS PEMPHIGOID ANTIGEN; BENIGN EPIDERMOLYSIS-BULLOSA; VII COLLAGEN; ANCHORING FIBRILS; HEMIDESMOSOMES; LAMININ-5; AUTOANTIBODIES; COMPONENT; MUTATIONS; ADHESION AB Recent insights into the structure and function of the dermal-epidermal junction have resulted from two converging lines of experimental evidence, namely, the study of inherited blistering disorders of the skin, in which mutations in genes encoding proteins of this region have been discovered, and the targeted ablation of the same genes in knockout mouse models. In addition to these studies, elegant analyses of the cell biology of the hemidesmosome/anchoring filament complex have revealed not only functionally important interactions between structural protein components, but also the role of certain of these proteins in mediating cell adhesion, migration, and signal transduction of messages from the extracellular matrix into the keratinocyte. Our current understanding of the dermal-epidermal junction forms a new model encapsulating the nature both of the hemidesmosomal attachment structures and of the interhemidesmosomal attachments that are mediated by differential cell type specific expression of proteins of the cutaneous adhesion zone. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT DERMATOL,NEW YORK,NY 10032. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA 02129. NR 49 TC 175 Z9 178 U1 1 U2 10 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0955-0674 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD OCT PY 1997 VL 9 IS 5 BP 651 EP 658 DI 10.1016/S0955-0674(97)80118-4 PG 8 WC Cell Biology SC Cell Biology GA XX922 UT WOS:A1997XX92200008 PM 9330868 ER PT J AU Kolanus, W Seed, B AF Kolanus, W Seed, B TI Integrins and inside-out signal transduction: converging signals from PKC and PIP3 SO CURRENT OPINION IN CELL BIOLOGY LA English DT Article ID SUBUNIT CYTOPLASMIC DOMAIN; FUNCTION-ASSOCIATED ANTIGEN-1; STIMULATED LIGAND-BINDING; PROTEIN-KINASE-C; CELL-ADHESION; ALPHA-ACTININ; PHOSPHATIDYLINOSITOL 3-KINASE; MONOCLONAL-ANTIBODIES; LEUKOCYTE INTEGRINS; CROSS-LINKING AB Recent studies have identified molecules that interact with integrins and appear to participate in the signaling pathways that regulate integrin adhesiveness. Clues provided by studies of these molecules point to the integration by integrins of signal transduction pathways implicated in cell division and activation. C1 MASSACHUSETTS GEN HOSP,DEPT MOL BIOL,BOSTON,MA 02114. RP Kolanus, W (reprint author), UNIV MUNICH,GENZENTRUM,MOL BIOL LAB,D-81337 MUNICH,GERMANY. NR 77 TC 121 Z9 123 U1 0 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0955-0674 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD OCT PY 1997 VL 9 IS 5 BP 725 EP 731 DI 10.1016/S0955-0674(97)80127-5 PG 7 WC Cell Biology SC Cell Biology GA XX922 UT WOS:A1997XX92200017 PM 9330877 ER PT J AU Kim, TW Tanzi, RE AF Kim, TW Tanzi, RE TI Presenilins and Alzheimer's disease SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Article ID AMYLOID-BETA-PROTEIN; IN-VIVO; CAENORHABDITIS-ELEGANS; MISSENSE MUTATIONS; GENE; APOPTOSIS; DEPOSITION AB Mutations in the genes encoding the presenilins cause the majority of early-onset cases of Alzheimer's disease (AD). The identification of the presenilin genes has provided new opportunities for elucidating the molecular mechanisms underlying the etiology and pathogenesis of AD. Recent progress has been made in attempts to understand the normal and pathological functions of the presenilins, emphasizing the effects of presenilin familial AD mutations on the amyloid beta-protein precursor, the presenilins themselves, and apoptotic cell death. RP Kim, TW (reprint author), MASSACHUSETTS GEN HOSP,GENET & AGING UNIT,149 13TH ST,CHARLESTOWN,MA 02129, USA. NR 60 TC 43 Z9 43 U1 1 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-4388 J9 CURR OPIN NEUROBIOL JI Curr. Opin. Neurobiol. PD OCT PY 1997 VL 7 IS 5 BP 683 EP 688 DI 10.1016/S0959-4388(97)80089-X PG 6 WC Neurosciences SC Neurosciences & Neurology GA YG690 UT WOS:A1997YG69000013 PM 9384549 ER PT J AU DeMaria, MA Johnson, RP Rosenzweig, M AF DeMaria, MA Johnson, RP Rosenzweig, M TI Four color immunofluorescence detection using two 488-nm lasers on a Becton Dickinson FACS vantage flow cytometer SO CYTOMETRY LA English DT Article DE four color immunofluorescence; FACS; vantage; 488-nm laser ID LYMPHOCYTE AB Multiparameter flow cytometric analysis is sometimes limited by the availability of directly conjugated monoclonal antibodies or streptavidin-conjugated secondary reagents, While many manufacturers offer a wide variety of monoclonal antibodies or streptavidin reagents directly conjugated to 488-nm excitable fluorochromes, there are not many available that are directly conjugated to 360-nm (UV) or 630-nm (HeNe) excitable fluorochromes. For this reason we attempted to develop a four color immunofluorescence staining protocol on a FACS Vantage using four 488-nm excitable fluorochromes, The fixed configuration of the FAGS Vantage limits the feasibility of using four 488-nm excitable fluorochrome simultaneously because of the five fluorescence detectors, two are always electronically delayed This means that only three signals - FL1, FL2, and FL3 - can be detected off the primary 488-nm laser beam, FL4 and FL5 are always delayed, only detecting signals off the second laser beam, Our instrument is configured with an ILT air cooled 488-nm laser in the second position that is used in order to conserve she Coherent Enterprise laser when using only 488-nm excitable fluorochromes, Because of this, we were able Ito develop a four-color immunofluorescence staining protocol using only 488-nm excitable fluorochromes. (C) 1997 Wiley-Liss, Inc. C1 HARVARD UNIV,NEW ENGLAND REG PRIMATE RES CTR,SCH MED,DIV IMMUNOL,SOUTHBOROUGH,MA 01772. MASSACHUSETTS GEN HOSP,CTR AIDS RES,CHARLESTOWN,MA. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,CHARLESTOWN,MA. FU NCRR NIH HHS [RR00168] NR 4 TC 2 Z9 2 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0196-4763 J9 CYTOMETRY JI Cytometry PD OCT 1 PY 1997 VL 29 IS 2 BP 178 EP 181 PG 4 WC Biochemical Research Methods; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA XZ811 UT WOS:A1997XZ81100011 PM 9332825 ER PT J AU Meigs, JB DAgostino, RB Wilson, PWF Cupples, LA Nathan, DM Singer, DE AF Meigs, JB DAgostino, RB Wilson, PWF Cupples, LA Nathan, DM Singer, DE TI Risk variable clustering in the insulin resistance syndrome - The Framingham Offspring Study SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; IMPAIRED GLUCOSE-TOLERANCE; CORONARY-HEART-DISEASE; BODY-FAT DISTRIBUTION; SYNDROME SYNDROME-X; CARDIOVASCULAR-DISEASE; BLOOD-PRESSURE; ESSENTIAL-HYPERTENSION; METABOLIC SYNDROME; HYPERINSULINEMIA AB Insulin resistance has been hypothesized to unify the clustering of hypertension, glucose intolerance, hyperinsulinemia, increased levels of triglyceride and decreased HDL cholesterol, and central and overall obesity We tested this hypothesis with factor analysis, a statistical technique that should identify one factor if a single process underlies the clustering of these risk variables, From 2,458 nondiabetic subjects of the Framingham Offspring Study, we collected clinical data, fasting and 2-h postchallenge glucose and insulin levels, and fasting lipid levels, We performed factor analyses separately for men and women in the entire population and among subgroups with features of the insulin resistance syndrome, Subjects ranged in age from 26 to 82 years (mean age 54); 53% were women, 13.4% had impaired glucose tolerance, 27.6% had hypertension, 40% were obese, and 11.6% mere hyperinsulinemic, defined by elevated fasting insulin levels. Underlying the clustering of these risk variables were three factors, Fasting and 2-h postchallenge insulin levels, fasting triglyceride and HDL cholesterol levels, BMI, and waist-to-hip ratio were associated with one factor, Fasting and 2-h levels of glucose and insulin were associated with a second factor, Systolic blood pressure, diastolic blood pressure, and BMI were associated with a third factor, Results were similar for men and women and for all subgroups, These results were consistent with more than one independent physiological process underlying risk variable clustering: a central metabolic syndrome (characterized by hyperinsulinemia, dyslipidemia, and obesity), glucose intolerance, and hypertension. Glucose intolerance and hypertension were linked to the central syndrome through shared correlations with insulin levels and obesity insulin resistance (reflected by hyperinsulinemia) alone did not appear to underlie all features of the insulin resistance syndrome. C1 MASSACHUSETTS GEN HOSP,DEPT MED,DIABET UNIT,BOSTON,MA 02114. BOSTON UNIV,DEPT MATH STAT,BOSTON,MA 02215. BOSTON UNIV,CONSULTING UNIT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. BOSTON UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL & BIOSTAT,BOSTON,MA. BOSTON UNIV,SCH MED,BOSTON,MA. NHLBI,NIH,FRAMINGHAM HEART STUDY,FRAMINGHAM,MA. RP Meigs, JB (reprint author), MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT S50 9,DEPT MED,BOSTON,MA 02114, USA. NR 61 TC 367 Z9 384 U1 0 U2 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD OCT PY 1997 VL 46 IS 10 BP 1594 EP 1600 DI 10.2337/diabetes.46.10.1594 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XX800 UT WOS:A1997XX80000010 PM 9313755 ER PT J AU Punglia, RS Lu, M Hsu, J Kuroki, M Tolentino, MJ Keough, K Levy, AP Levy, NS Goldberg, MA DAmato, RJ Adamis, AP AF Punglia, RS Lu, M Hsu, J Kuroki, M Tolentino, MJ Keough, K Levy, AP Levy, NS Goldberg, MA DAmato, RJ Adamis, AP TI Regulation of vascular endothelial growth factor expression by insulin-like growth factor I SO DIABETES LA English DT Article ID PROLIFERATIVE DIABETIC-RETINOPATHY; PERMEABILITY FACTOR; MESSENGER-RNA; RETINAL NEOVASCULARIZATION; IRIS NEOVASCULARIZATION; ANGIOGENIC AGENT; NONHUMAN PRIMATE; EPITHELIAL-CELLS; FACTOR VEGF; FACTOR GENE AB Insulin-like growth factor I (IGF-I) and vascular endothelial growth factor (VEGF) levels are correlated with retinal ischemia-associated intraocular neovascularization in humans, Since VEGF is required for iris and retinal neovascularization in animal models of retinal ischemia, we tested whether IGF-I could act as an indirect angiogenic factor by increasing VEGF gene expression, IGF-I increased retinal pigment epithelial (RPE) cell VEGF mRNA in a concentration-dependent manner with an EC50 of 7 nmol/l (53.6 ng/ml), RPE and bovine smooth muscle cells exposed to 50 nmol/l (383 ng/ml) IGF-I achieved peak VEGF mRNA expression within 2 h. IGF-I-treated RPE cells increased VEGF protein levels in conditioned media and stimulated capillary endothelial cell proliferation, Blockade of the IGF-I receptor with a neutralizing antibody abrogated the VEGF increases in RPE cells, Further, hypoxia-mediated and IGF-I-mediated increases in VEGF mRNA and protein levels were additive in RPE cells, and the hypoxia-induced VEGF increases were independent of endogenous IGF-I. VEGF promoter activity was enhanced by IGF-I in RPE cells, but VEGF transcript half-life was unaltered, In summary, the supplementation of RPE and smooth muscle cell cultures with IGF-I at 5-100 nmol/l increased VEGF mRNA and secreted protein levels, The VEGF increases in RPE cells occurred primarily through enhanced transcription of the VEGF gene and via the IGF-I receptor, Elevated IGF-I levels may promote neovascularization through increased retinal VEGF gene expression. C1 HARVARD UNIV, MASSACHUSETTS EYE & EAR INFIRM, SCH MED, DEPT OPHTHALMOL, BOSTON, MA 02114 USA. HARVARD UNIV, CHILDRENS HOSP, SCH MED, SURG RES LAB, BOSTON, MA 02115 USA. OMIYA MED CTR, JICHI MED SCH, DEPT MED, OMIYA, SAITAMA, JAPAN. HARVARD UNIV, BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED, HEMATOL ONCOL DIV, BOSTON, MA 02115 USA. FU PHS HHS [NEI 00325] NR 54 TC 144 Z9 148 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0012-1797 EI 1939-327X J9 DIABETES JI Diabetes PD OCT PY 1997 VL 46 IS 10 BP 1619 EP 1626 DI 10.2337/diabetes.46.10.1619 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XX800 UT WOS:A1997XX80000014 PM 9313759 ER PT J AU Bjorklund, A Yaney, G McGarry, JD Weir, G AF Bjorklund, A Yaney, G McGarry, JD Weir, G TI Fatty acids and beta-cell function SO DIABETOLOGIA LA English DT Article; Proceedings Paper CT 4th World Conference on Diabetes Research CY MAR 15-19, 1997 CL ATHENS, GREECE SP Novo Nordisk A/S Pharmaceut, Eli Lilly & Co, Amylin Pharmaceut, Bayer Corp, Becton Dickinson & Co, Boehringer Mannheim GmbH, Bristol Myers Squibb Co, Lifescan Inc, Novartis Pharmaceut, Hoechst AG, Grp Rech Int Servier, Pfizer US Pharmaceut Grp, Wyeth Ayerst Int Inc ID INDUCED INSULIN-SECRETION; CHAIN ACYL-COA; RAT C1 UNIV TEXAS,SW MED CTR,DEPT INTERNAL MED,DALLAS,TX 75235. KAROLINSKA INST,DEPT MOL MED,S-10401 STOCKHOLM,SWEDEN. BOSTON MED CTR,EVANS DEPT MED,BOSTON,MA. JOSLIN DIABET CTR,BOSTON,MA 02215. NR 12 TC 20 Z9 21 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD OCT PY 1997 VL 40 SU 3 BP B21 EP B26 DI 10.1007/s001250051392 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XY886 UT WOS:A1997XY88600005 PM 9345641 ER PT J AU Caprio, S Wong, S Alberti, KGMM King, G AF Caprio, S Wong, S Alberti, KGMM King, G TI Cardiovascular complications of diabetes SO DIABETOLOGIA LA English DT Article; Proceedings Paper CT 4th World Conference on Diabetes Research CY MAR 15-19, 1997 CL ATHENS, GREECE SP Novo Nordisk A/S Pharmaceut, Eli Lilly & Co, Amylin Pharmaceut, Bayer Corp, Becton Dickinson & Co, Boehringer Mannheim GmbH, Bristol Myers Squibb Co, Lifescan Inc, Novartis Pharmaceut, Hoechst AG, Grp Rech Int Servier, Pfizer US Pharmaceut Grp, Wyeth Ayerst Int Inc ID CORONARY HEART-DISEASE; POPULATION; MORTALITY; BETA; GENE C1 JOSLIN DIABET CTR,BOSTON,MA 02215. YALE UNIV,SCH MED,NEW HAVEN,CT 06520. UNIV NEWCASTLE UPON TYNE,HUMAN DIABET & METAB RES CTR,NEWCASTLE TYNE NE1 7RU,TYNE & WEAR,ENGLAND. HARVARD UNIV,SCH MED,BOSTON,MA. NR 14 TC 17 Z9 19 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD OCT PY 1997 VL 40 SU 3 BP B78 EP B82 DI 10.1007/s001250051411 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XY886 UT WOS:A1997XY88600016 PM 9345652 ER PT J AU Corbett, J Serup, P BonnerWeir, S Nielsen, JH AF Corbett, J Serup, P BonnerWeir, S Nielsen, JH TI Beta-cell ontogeny: growth and death SO DIABETOLOGIA LA English DT Article; Proceedings Paper CT 4th World Conference on Diabetes Research CY MAR 15-19, 1997 CL ATHENS, GREECE SP Novo Nordisk A/S Pharmaceut, Eli Lilly & Co, Amylin Pharmaceut, Bayer Corp, Becton Dickinson & Co, Boehringer Mannheim GmbH, Bristol Myers Squibb Co, Lifescan Inc, Novartis Pharmaceut, Hoechst AG, Grp Rech Int Servier, Pfizer US Pharmaceut Grp, Wyeth Ayerst Int Inc ID GENE; INTERLEUKIN-1; EXPRESSION; PANCREAS C1 HAGEDORN RES INST,DK-2820 GENTOFTE,DENMARK. WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. JOSLIN DIABET CTR,BOSTON,MA 02215. RI Serup, Palle/A-7407-2011 OI Serup, Palle/0000-0002-0858-590X NR 12 TC 20 Z9 20 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD OCT PY 1997 VL 40 SU 3 BP B27 EP B32 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XY886 UT WOS:A1997XY88600006 PM 9345642 ER PT J AU Heesom, KJ Harbeck, M Kahn, CR Denton, RM AF Heesom, KJ Harbeck, M Kahn, CR Denton, RM TI Insulin action on metabolism SO DIABETOLOGIA LA English DT Article; Proceedings Paper CT 4th World Conference on Diabetes Research CY MAR 15-19, 1997 CL ATHENS, GREECE SP Novo Nordisk A/S Pharmaceut, Eli Lilly & Co, Amylin Pharmaceut, Bayer Corp, Becton Dickinson & Co, Boehringer Mannheim GmbH, Bristol Myers Squibb Co, Lifescan Inc, Novartis Pharmaceut, Hoechst AG, Grp Rech Int Servier, Pfizer US Pharmaceut Grp, Wyeth Ayerst Int Inc C1 UNIV BRISTOL,SCH MED SCI,DEPT BIOCHEM,BRISTOL BS8 1TD,AVON,ENGLAND. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. JOSLIN DIABET CTR,BOSTON,MA 02215. NR 0 TC 12 Z9 12 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD OCT PY 1997 VL 40 SU 3 BP B3 EP B9 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XY886 UT WOS:A1997XY88600002 PM 9345638 ER PT J AU Salinsky, MC AF Salinsky, MC TI A practical analysis of computer based seizure detection during continuous video-EEG monitoring SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE electroencephalography; telemetry; epilepsy; seizure; computer aided diagnosis ID EPILEPTIC SEIZURES AB Computer based seizure detection (CSD) systems improve the efficiency of CCTV-EEG monitoring by capturing epileptic seizures which would have otherwise been missed. We prospectively evaluated the yield of a commercial CSD system in 83 consecutive CCTV-EEG admissions. All seizures were coded as to the method of detection. The percentage of seizures detected only by CSD was calculated for each patient, and the impact on length of hospital stay was estimated. Overall, 33% of epileptic seizures were signaled by the patient, 45% were directly observed by family or medical personnel, and 22% were captured only by CSD. Forty admissions (48%) had at least one seizure captured only by CSD. The majority of these events were clinical and electrographic seizures (73%) and the remainder were purely electrographic. Five admissions concluded with all seizures captured only by CSD. We estimated an average saving of 1.3 hospital days per admission, based on the percentage of seizures captured only by CSD. (C) 1997 Elsevier Science Ireland Ltd. C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP Salinsky, MC (reprint author), OREGON HLTH SCI UNIV,EPILEPSY CTR CDW3,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. NR 11 TC 19 Z9 19 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD OCT PY 1997 VL 103 IS 4 BP 445 EP 449 DI 10.1016/S0013-4694(97)00025-4 PG 5 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA YE154 UT WOS:A1997YE15400005 PM 9368489 ER PT J AU Strother, D van Hoff, J Rao, PV Smith, EI Shamberger, RC Halperin, EC Murray, KJ Castleberry, RP AF Strother, D van Hoff, J Rao, PV Smith, EI Shamberger, RC Halperin, EC Murray, KJ Castleberry, RP TI Event-free survival of children with biologically favourable neuroblastoma based on the degree of initial tumour resection: Results from the Pediatric Oncology Group SO EUROPEAN JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT Meeting on Advances in Neuroblastoma Research - 1996 CY MAY 22-25, 1996 CL PHILADELPHIA, PENNSYLVANIA DE stage 2B/3 neuroblastoma; chemotherapy; surgery; Shimada; histology ID NEURO-BLASTOMA; STAGE-III; SURGERY; CHEMOTHERAPY AB We analysed the 2-year event-free survival (EFS) of 49 patients 1 year of age and older, with stage 2B or 3 neuroblastoma, treated on Pediatric Oncology Group protocols 8742 and 9244, with respect to the degree of tumour resection at diagnosis. The 2-year EFS rate for 21 children whose tumours were completely resected at diagnosis was 85% (SE = 10%) compared with an EFS rate of 70% (SE = 9%) for the 28 children whose tumours were incompletely resected at diagnosis. Despite the observed trend in favour of complete resection, these EFS curves were not statistically significantly different (P = 0.259). Patients with favourable Shimada histology tumours had an EFS rate of 92% (SE = 7%) compared with a rate of 58% (SE = 15%) for patients with unfavourable histology tumours. EFS curves for the two histologic groups were significantly different (P = 0.009). The impact of aggressive surgery and adjuvant chemotherapy on the outcome of patients with biologically favourable regional neuroblastoma is still unclear. (C) 1997 Elsevier Science Ltd. C1 Pediat Oncol Grp Off, Chicago, IL 60611 USA. Baylor Coll Med, Texas Childrens Canc Ctr, Houston, TX 77030 USA. Yale Univ, Sch Med, New Haven, CT USA. Pediat Oncol Grp Stat Off, Gainesville, FL USA. Univ Florida, Gainesville, FL USA. Univ Texas, SW Med Ctr, Dallas, TX USA. Dana Farber Canc Inst, Boston, MA 02115 USA. Duke Univ, Med Ctr, Durham, NC USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. Univ Alabama, Birmingham, AL USA. RP Strother, D (reprint author), Pediat Oncol Grp Off, 645 N Michigan Ave,Ste 910, Chicago, IL 60611 USA. FU NCI NIH HHS [CA 69428, CA 29139, CA 03161] NR 8 TC 25 Z9 25 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD OCT PY 1997 VL 33 IS 12 BP 2121 EP 2125 DI 10.1016/S0959-8049(97)00293-1 PG 5 WC Oncology SC Oncology GA YM917 UT WOS:000071114800046 PM 9516866 ER PT J AU Peterfreund, RA Gies, EK Fink, JS AF Peterfreund, RA Gies, EK Fink, JS TI Protein kinase C regulates adenosine A2a receptor mRNA expression in SH-SY5Y cells SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE adenosine receptor; phorbol ester; protein kinase C; SH-SY5Y neuroblastoma cell; cAMP ID HUMAN NEUROBLASTOMA-CELLS; MESSENGER-RNA; PC12 CELLS; GH3 CELLS; RAT-BRAIN; DESENSITIZATION; DIFFERENTIATION; ACTIVATION; INHIBITOR; AGONIST AB Protein kinase C regulates mRNAs encoding several G protein-linked receptors but its role in adenosine A2a receptor expression is not known. We tested the hypothesis that protein kinase C activated by tetradecanoyl phorbol acetate (TPA) regulates adenosine A2a receptor mRNA levels. SH-SY5Y human neuroblastoma cells express adenosine receptors which positively couple to adenylyl cyclase with a pharmacologic profile expected of the A2a subtype. Northern blotting demonstrated an adenosine A2a receptor mRNA species of similar molecular size in SH-SY5Y cells and in human brain. TPA increased adenosine A2a receptor mRNA in a dose-and time-dependent fashion. Transcription or translation inhibition prevented increases in adenosine A2a receptor mRNA. Bisindolylmaleimide blocked TPA effects. Adenosine A2a receptor mRNA stability was unchanged by TPA. This study identifies a human neuroblastoma cell line expressing functional adenosine A2a receptors. Protein kinase C activation appears to enhance transcription of the adenosine A2a receptor gene. (C) 1997 Elsevier Science B.V. C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIA & CRIT CARE,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP Peterfreund, RA (reprint author), MASSACHUSETTS GEN HOSP,MOL NEUROBIOL LAB,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS31579] NR 41 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD OCT 1 PY 1997 VL 336 IS 1 BP 71 EP 80 DI 10.1016/S0014-2999(97)01194-1 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YC455 UT WOS:A1997YC45500010 PM 9384256 ER PT J AU Royall, DR Cordes, J Polk, M AF Royall, DR Cordes, J Polk, M TI Executive control and the comprehension of medical information by elderly retirees SO EXPERIMENTAL AGING RESEARCH LA English DT Article ID MINI-MENTAL-STATE; ALZHEIMERS-DISEASE; COMPETENCE; IMPAIRMENT; BEHAVIOR AB This study examined the independent contributions of executive control function, general cognition, age, education, and medication usage to the comprehension of medical information. Randomly selected elderly retirees (N = 105) more than 70 years of age completed the Executive Interview (EXIT25), the Mini-Mental State Exam (MMSE), and the Hopkins Competency Assessment Test (HCAT), Cognitive measures were stronger predictors of HCAT scores than age, education, or number of prescribed medications. A discriminant model bused on EXIT25 and MMSE scores correctly classified 91% of subjects relative to their HCAT scores. It was concluded that executive impairment is strongly associated with impaired comprehension of medical information, As many as 88% of probable Alzheimer's disease patients, 69% of institutionalized elderly retirees, and 49% of noninstitutionalized retirees may be impaired in their ability to comprehend medical information, even when it has been presented well below their educational level. C1 UNIV TEXAS,HLTH SCI CTR,DIV CLIN PHARMACOL,SAN ANTONIO,TX. RP Royall, DR (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,S TEXAS VET HEALTHCARE SYST,SAN ANTONIO,TX 78284, USA. NR 31 TC 59 Z9 59 U1 0 U2 0 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0361-073X J9 EXP AGING RES JI Exp. Aging Res. PD OCT-DEC PY 1997 VL 23 IS 4 BP 301 EP 313 DI 10.1080/03610739708254033 PG 13 WC Geriatrics & Gerontology; Psychology SC Geriatrics & Gerontology; Psychology GA YC446 UT WOS:A1997YC44600001 PM 9352289 ER PT J AU Cornford, EM Varesi, JB Hyman, S Damian, RT Raleigh, MJ AF Cornford, EM Varesi, JB Hyman, S Damian, RT Raleigh, MJ TI Mitochondrial content of choroid plexus epithelium SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE blood-CSF barrier mitochondrial volume; digital electron microscopy; cuboidal epithelium; rat; mouse; rabbit; monkey ID BLOOD-BRAIN-BARRIER; ENDOTHELIAL-CELL MITOCHONDRIA; MORPHOMETRIC ANALYSIS; GLUCOSE-TRANSPORTER; RAT; ULTRASTRUCTURE; NUMBER; LOCALIZATION; MICROVESSELS; MEMBRANES AB The objective of the present study was to examine the apparent work capacity of one of the two separate membrane systems (the blood-cerebrospinal fluid barrier) that isolate the mammalian brain extracellular fluid (and cerebrospinal fluid, CSF) from plasma. Digitized analyses of electron-microscopic images provided estimates of mitochondrial volumes, which were expressed as a percentage of the cell cytoplasm. We recorded a high mitochondrial content of 12-15% in the cuboidal epithelium of primate choroid plexus, which was consistent in vervet, rhesus, and squirrel monkeys, as well as in baboons. Similarly high mitochondrial contents were observed in the rabbit, rat, and mouse choroid plexus. It has been postulated that the high mitochondrial content of brain endothelium is associated with maintaining the ionic gradients within the central nervous system. We observed that the mitochondrial content of the choroid plexus (where CSF is produced) was slightly higher than in (prior measurements of) the blood-brain barrier (BBB). In addition, surface areas at the apical borders of the choroid plexus epithelia (where the Na(+)K(+)ATPase activity has been localized) were increased 7- to 13-fold over the basal borders, in the primate species examined. The observation of high mitochondrial volumes in choroid plexus cells is consistent with the suggestion that increased mitochondrial densities seen in choroidal epithelia and BBB capillaries provide a metabolic work capability for both secretory activities and maintaining ionic gradients across blood-CSF barriers. C1 W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,SW REG VA EPILEPSY CTR W12B,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90095. UNIV CALIF SANTA BARBARA,SCH ENGN,SANTA BARBARA,CA 93106. UNIV CALIF LOS ANGELES,SCH MED,INST BRAIN RES,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90095. RP Cornford, EM (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,SW REG VA EPILEPSY CTR W12B,LOS ANGELES,CA 90073, USA. FU NINDS NIH HHS [NS 25554] NR 28 TC 27 Z9 28 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PD OCT PY 1997 VL 116 IS 3 BP 399 EP 405 DI 10.1007/PL00005768 PG 7 WC Neurosciences SC Neurosciences & Neurology GA YC086 UT WOS:A1997YC08600003 PM 9372289 ER PT J AU Gorry, MC Gabbaizedeh, D Furey, W Gates, LK Preston, RA Aston, CE Zhang, YZ Ulrich, C Ehrlich, GD Whitcomb, DC AF Gorry, MC Gabbaizedeh, D Furey, W Gates, LK Preston, RA Aston, CE Zhang, YZ Ulrich, C Ehrlich, GD Whitcomb, DC TI Mutations in the cationic trypsinogen gene are associated with recurrent acute and chronic pancreatitis SO GASTROENTEROLOGY LA English DT Article ID HEREDITARY PANCREATITIS; LINKAGE ANALYSIS; DNA-SEQUENCE; LONG ARM; MAPS; SPHINCTER; ODDI AB Background & Aims: We recently identified a single R117H mutation in the cationic trypsinogen gene in several kindreds with an inherited form of acute and chronic pancreatitis (HP1), providing strong evidence that trypsin plays a central role in premature zymogen activation and pancreatitis, However, not all families studied have this mutation, The aim of this study was to determine the disease-causing mutation in kindreds with hereditary pancreatitis that lack the previously identified mutation. Methods: Clinical features of the HP1 kindreds were compared with those of the new kindreds (HP2), and genetic linkage analysis, screening for mutations through DNA sequencing, and screening an unaffected population were performed. Results: The onset of symptoms was delayed and hospitalizations were fewer in HP2 compared with HP1(P < 0.05). Linkage of the disease gene to chromosome 7q35 was established (logarithm of the odds, 3.73), Mutational screening identified a single A to T mutation resulting in an asparagine to isoleucine transition mutation at position 21 (N21I) in cationic trypsinogen. The mutation was absent in 94 unrelated individuals, representing 188 unique chromosomes. Conclusions: The identification of a second mutation in the cationic trypsinogen gene (HP2) suggests a dominant role of trypsin in premature protease activation-mediated forms of acute pancreatitis. The pathogenesis of hereditary pancreatitis also suggests that chronic pancreatitis may result from recurrent acute pancreatitis. C1 UNIV PITTSBURGH,DEPT MED,DIV GASTROENTEROL & HEPATOL,PITTSBURGH,PA 15261. UNIV PITTSBURGH,DEPT CRYSTALLOG,PITTSBURGH,PA 15261. UNIV PITTSBURGH,DEPT PATHOL,PITTSBURGH,PA 15261. UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA 15261. UNIV PITTSBURGH,DEPT CELL BIOL & PHYSIOL,PITTSBURGH,PA 15261. VET AFFAIRS PITTSBURGH HLTH CARE SYST,PITTSBURGH,PA. CHILDRENS HOSP PITTSBURGH,DEPT PEDIAT OTOLARYNGOL,PITTSBURGH,PA 15213. UNIV KENTUCKY,DEPT MED,LEXINGTON,KY 40506. UNIV CINCINNATI,DEPT MED,CINCINNATI,OH 45221. FU NIDCD NIH HHS [R01 DC02148]; NIDDK NIH HHS [R01 DK50236, R03 DK51954] NR 35 TC 309 Z9 312 U1 1 U2 7 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD OCT PY 1997 VL 113 IS 4 BP 1063 EP 1068 DI 10.1053/gast.1997.v113.pm9322498 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YB027 UT WOS:A1997YB02700007 PM 9322498 ER PT J AU Quirk, DM Rattner, DW FernandezdelCastillo, C Warshaw, AL Brugge, WR AF Quirk, DM Rattner, DW FernandezdelCastillo, C Warshaw, AL Brugge, WR TI The use of endoscopic ultrasonography to reduce the cost of treating ampullary tumors SO GASTROINTESTINAL ENDOSCOPY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-for-Gastrointestinal-Endoscopy CY MAY 19-22, 1996 CL SAN FRANCISCO, CA SP Amer Soc Gastrointestinal Endoscopy ID LOCAL RESECTION; RADICAL RESECTION; VILLOUS TUMORS; CARCINOMA; VATER; PAPILLA; PANCREATODUODENECTOMY; ENDOSONOGRAPHY; EXCISION AB Background: Local excision of selected ampullary tumors may result in the same benefit as Whipple resection with less morbidity and mortality, The purpose of this study was to determine if endoscopic ultrasonography could aid in the selection of patients for local resection and to determine if there was a significant cost: difference between the two surgical procedures, Methods: In this retrospective study of 32 patients who underwent surgery for ampullary tumors, endoscopic ultrasonography staging was performed in 18 patients, Resected specimens were used to determine pathologic staging. Local disease was defined as stage T2NO or less, Cost data were available for 20 patients. Results: The sensitivity and specificity of endoscopic ultrasonography for differentiating local from advanced ampullary tumors were both 83%. The median total cost for a local resection was $9314 versus $16,017 for a Whipple resection (p < 0.0017). Conclusion: Endoscopic ultrasonography is an effective tool for identifying patients with localized ampullary tumors. The cost of a local resection for ampullary tumors is significantly less than that of a Whipple resection. The use of endoscopic ultrasonography to select patients for local resection may be a cost-effective technique in the management of patients with ampullary tumors. C1 MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT GEN SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 26 TC 20 Z9 25 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD OCT PY 1997 VL 46 IS 4 BP 334 EP 337 DI 10.1016/S0016-5107(97)70121-4 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YB205 UT WOS:A1997YB20500008 PM 9351037 ER PT J AU Yasothornsrikul, S Wendy, JD Cramer, G Kimbrell, DA Dearolf, CR AF Yasothornsrikul, S Wendy, JD Cramer, G Kimbrell, DA Dearolf, CR TI viking: identification and characterization of a second type IV collagen in Drosophila SO GENE LA English DT Article DE Drosophila gene; extracellular matrix; in-situ hybridization ID BASEMENT-MEMBRANE COLLAGEN; ALPHA-2(IV) COLLAGEN; STRUCTURAL ORGANIZATION; CAENORHABDITIS-ELEGANS; EXTRACELLULAR-MATRIX; GLOBULAR DOMAIN; CELL-DEATH; GENE; CHAIN; MELANOGASTER AB We have taken an enhancer trap approach to identify genes that are expressed in hematopoietic cells and tissues of Drosophila. We conducted a molecular analysis of two P-element insertion strains that have reporter gene expression in embryonic hemocytes, strain 197 and viking(ICO). This analysis has determined that viking encodes a collagen type IV gene, alpha 2(IV). The viking locus is located adjacent to the previously described DCg1, which encodes collagen alpha 1(IV), and in the opposite orientation. The alpha 2(IV) and alpha 1(IV) collagens are structurally very similar to one another, and to vertebrate type TV collagens. In early development, viking and DCg1 are transcribed in the same tissue-specific pattern, primarily in the hemocytes and fat body cells. Our results suggest that both the alpha 1 and alpha 2 collagen IV chains may contribute to basement membranes in Drosophila. This work also provides the foundation for a more complete genetic dissection of collagen type IV molecules and their developmental function in Drosophila. (C) 1997 Elsevier Science B.V. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEV GENET GRP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,CANC BIOL SECT,BOSTON,MA 02115. UNIV HOUSTON,DEPT BIOL,HOUSTON,TX 77204. FU NCI NIH HHS [CA73158]; NHLBI NIH HHS [HL48823] NR 51 TC 62 Z9 62 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD OCT 1 PY 1997 VL 198 IS 1-2 BP 17 EP 25 DI 10.1016/S0378-1119(97)00274-6 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA YA834 UT WOS:A1997YA83400003 PM 9370260 ER PT J AU Gong, J Chen, L Chen, D Kashiwaba, M Manome, Y Tanaka, T Kufe, D AF Gong, J Chen, L Chen, D Kashiwaba, M Manome, Y Tanaka, T Kufe, D TI Induction of antigen-specific antitumor immunity with adenovirus-transduced dendritic cells SO GENE THERAPY LA English DT Article DE dendritic cells; adenovirus; transduction; antitumor immunity; DF3/MUC1 ID CARCINOMA-ASSOCIATED ANTIGEN; CYTOTOXIC T-LYMPHOCYTES; DF3; PEPTIDE; MUCIN; GENE; EPISIALIN; REACTIVITY; EXPRESSION; DF3/MUC1 AB Transduction of dendritic cells (DC) can result in presentation of tumor-associated antigens and induction of immunity against undefined epitopes. The present studies demonstrate adenovirus (Ad)-mediated transduction of the beta-galactosidase gene in mouse DC. Similar transductions have been obtained with the gene encoding the DF3/MUC1 tumor-associated antigen. We show that the Ad-transduced DC are functional in primary allogeneic mixed lymphocyte reactions. Mice immunized with Ad-transduced DC develop cytotoxic T lymphocytes that are specific for the beta-galactosidase or DF3/MUC1 antigens. The results also demonstrate that Ad.MUC1-transduced DC induce a specific response which inhibits the growth of DF3/MUC1-positive tumors. These findings support the usefulness of Ad-transduced DC for in vivo immunization against tumor-associated antigens. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA38493] NR 26 TC 99 Z9 103 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0969-7128 J9 GENE THER JI Gene Ther. PD OCT PY 1997 VL 4 IS 10 BP 1023 EP 1028 DI 10.1038/sj.gt.3300496 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA XZ210 UT WOS:A1997XZ21000004 PM 9415307 ER PT J AU Wen, ST VanEtten, RA AF Wen, ST VanEtten, RA TI The PAG gene product, a stress-induced protein with antioxidant properties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity SO GENES & DEVELOPMENT LA English DT Article DE c-Abl; Bcr-Abl; Philadelphia chromosome; two-hybrid system; SH3 binding protein ID THIOL-SPECIFIC ANTIOXIDANT; MURINE ERYTHROLEUKEMIA-CELLS; BCR-ABL; TRANSFORMING ABILITY; REGULATORY DOMAIN; SH3 DOMAINS; BINDING; CLONING; MOUSE; SRC AB Biochemical and genetic evidence suggests that the tyrosine kinase activity of c-Abl is tightly regulated in vivo by a cellular factor binding to the Src homology 3 (SH3) domain of Abl. We used the yeast two-hybrid system to identify a gene, FAG, whose protein product (Fag) interacts specifically with the Abl SH3 domain. Fag, also known as macrophage 23-kD stress protein (MSP23), is a member of a novel family of proteins with antioxidant activity implicated in the cellular response to oxidative stress and in control of cell proliferation and differentiation. In a co-expression assay, Fag associates with c-Abl in vivo and inhibits tyrosine phosphorylation induced by overexpression of c-Abl. Inhibition requires the Abl SH3 and kinase domains and is not observed with other Abl SH3-binding proteins. Expression of Fag also inhibits the in vitro kinase activity of c-Abl, but not SH3-mutated Abl or v-Abl. When transfected in NIH-3T3 cells, Fag is localized to nucleus and cytoplasm and rescues the cytostatic effect induced by c-Abl. These observations suggest Fag is a physiological inhibitor of c-Abl in vivo. C1 HARVARD UNIV,SCH MED,DEPT GENET,CTR BLOOD RES,BOSTON,MA 02115. NR 74 TC 208 Z9 213 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD OCT 1 PY 1997 VL 11 IS 19 BP 2456 EP 2467 DI 10.1101/gad.11.19.2456 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA YB597 UT WOS:A1997YB59700002 PM 9334312 ER PT J AU Polymenis, M Schmidt, EV AF Polymenis, M Schmidt, EV TI Coupling of cell division to cell growth by translational control of the G(1) cyclin CLN3 in yeast SO GENES & DEVELOPMENT LA English DT Article DE primer extension; prt1; cyclin; CLN3; uORF; translation ID POLYMERASE CHAIN-REACTION; SACCHAROMYCES-CEREVISIAE; PROTEIN-SYNTHESIS; BUDDING YEAST; INCREASED EXPRESSION; SIGNALING PATHWAY; PRT1 MUTATIONS; MESSENGER-RNAS; G1 CYCLINS; C-MYC AB The eukaryotic cell cycle is driven by a cascade of cyclins and kinase partners including the G(1) cyclin Cln3p in yeast. As the first step in this cascade, Cln3p is uniquely positioned to determine the critical growth-rate threshold for division. To analyze factors regulating CLN3 expression, we identified a short upstream open reading frame (uORF) in the 5' leader of CLN3 mRNA as a translational control element. This control element is critical for the growth-dependent regulation of Cln3p synthesis because it specifically represses CLN3 expression during conditions of diminished protein synthesis or slow growth. Inactivation of the uORF accelerates the completion of Start and entry into the fell cycle suggesting that translational regulation of CLN3 provides a mechanism coupling cell growth and division. C1 MASSACHUSETTS GEN HOSP,MGH CANC CTR,CHARLESTOWN,MA 02129. MASSACHUSETTS GEN HOSP,SERV PEDIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02114. FU NCI NIH HHS [R01-CA63117, R01 CA063117] NR 60 TC 206 Z9 207 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD OCT 1 PY 1997 VL 11 IS 19 BP 2522 EP 2531 DI 10.1101/gad.11.19.2522 PG 10 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA YB597 UT WOS:A1997YB59700007 PM 9334317 ER PT J AU Kessler, MM Henry, MF Shen, E Zhao, J Gross, S Silver, PA Moore, CL AF Kessler, MM Henry, MF Shen, E Zhao, J Gross, S Silver, PA Moore, CL TI Hrp1, a sequence-specific RNA-binding protein that shuttles between the nucleus and the cytoplasm, is required for mRNA 3'-end formation in yeast SO GENES & DEVELOPMENT LA English DT Article DE HRP1; hnRNP; mRNA polyadenylation; RNA processing; mRNA export ID PRE-MESSENGER-RNA; CLEAVAGE FACTOR-I; SACCHAROMYCES-CEREVISIAE; POLY(A) POLYMERASE; POLYADENYLATION FACTOR; 3' END; GENE; PURIFICATION; SIMILARITY; SUBUNIT AB In yeast, four factors (CF I, CF II, PF I, and PAP) are required for accurate pre-mRNA cleavage and polyadenylation in vitro. CF I can be separated further into CF IA and CF IB. Here we show that CF IB is the 73-kD Hrp1 protein. Recombinant Hrp1p made in Escherichia coli provides full CF IB function in both cleavage and poly(A) addition assays. Consistent with the presence of two RRM-type motifs, Hrp1p can be UV cross-linked to RNA, and this specific interaction requires the (UA), polyadenylation efficiency element. Furthermore, the CF II factor enhances the binding of Hrp1p to the RNA precursor. A temperature-sensitive mutant in HRP1 yields mRNAs with shorter poly(A) tails when grown at the nonpermissive temperature. Genetic analyses indicate that Hrp1p interacts with Rna15p and Rna14g, two components of CF 1A. The HRP1 gene was originally isolated as a suppressor of a temperature-sensitive npl3 allele, a gene encoding a protein involved in mRNA export. Like Npl3p, Hrp1p shuttles between the nucleus and cytoplasm, providing a potential link between 3'-end processing and mRNA export from the nucleus. C1 TUFTS UNIV, SCH MED, DEPT MOL BIOL & MICROBIOL, BOSTON, MA 02111 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOL PHARMACOL, BOSTON, MA 02115 USA. DANA FARBER CANC INST, BOSTON, MA 02115 USA. FU NIGMS NIH HHS [R01 GM036373, R01 GM041752, R01 GM36373, R01 GM41752] NR 60 TC 170 Z9 174 U1 0 U2 3 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 EI 1549-5477 J9 GENE DEV JI Genes Dev. PD OCT 1 PY 1997 VL 11 IS 19 BP 2545 EP 2556 DI 10.1101/gad.11.19.2545 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA YB597 UT WOS:A1997YB59700009 PM 9334319 ER PT J AU Newburg, DS Warren, CD Chaturvedi, P Ye, S Newburg, AR Tilden, C Oftedal, OT AF Newburg, DS Warren, CD Chaturvedi, P Ye, S Newburg, AR Tilden, C Oftedal, OT TI Milk oligosaccharide profiles of humans and other mammals SO GLYCOBIOLOGY LA English DT Meeting Abstract C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BOSTON UNIV,SCH MED,BOSTON,MA 02118. SMITHSONIAN INST,NATL ZOOL PK,WASHINGTON,DC 20008. NR 0 TC 1 Z9 1 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0959-6658 J9 GLYCOBIOLOGY JI Glycobiology PD OCT PY 1997 VL 7 IS 7 BP 98 EP 98 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YA478 UT WOS:A1997YA47800114 ER PT J AU Chaturvedi, P Warren, CD Ye, S Pickering, LK Newburg, DS AF Chaturvedi, P Warren, CD Ye, S Pickering, LK Newburg, DS TI Intestinal absorption and excretion of human milk oligosaccharides SO GLYCOBIOLOGY LA English DT Meeting Abstract C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,WALTHAM,MA 02254. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. BOSTON UNIV,SCH MED,BOSTON,MA 02118. EASTERN VIRGINIA MED SCH,NORFOLK,VA 23510. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0959-6658 J9 GLYCOBIOLOGY JI Glycobiology PD OCT PY 1997 VL 7 IS 7 BP 99 EP 99 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YA478 UT WOS:A1997YA47800113 ER PT J AU Wiederschain, GY Newburg, DS AF Wiederschain, GY Newburg, DS TI Human milk enzymes may modify endogenous complex carbohydrates SO GLYCOBIOLOGY LA English DT Meeting Abstract C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,WALTHAM,MA 02254. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0959-6658 J9 GLYCOBIOLOGY JI Glycobiology PD OCT PY 1997 VL 7 IS 7 BP 101 EP 101 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YA478 UT WOS:A1997YA47800116 ER PT J AU Wagner, G Wyss, DF Choi, JS Sun, J Freund, C Li, J Knoppers, MH Willis, KJ Arulanandam, ARN Smolyar, A Reinherz, EL AF Wagner, G Wyss, DF Choi, JS Sun, J Freund, C Li, J Knoppers, MH Willis, KJ Arulanandam, ARN Smolyar, A Reinherz, EL TI Structure and significance of the N-linked high-mannose glycan in human CD2 SO GLYCOBIOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOL PHARMACOL,BOSTON,MA 02115. PROCEPT INC,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0959-6658 J9 GLYCOBIOLOGY JI Glycobiology PD OCT PY 1997 VL 7 IS 7 BP 147 EP 147 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA YA478 UT WOS:A1997YA47800161 ER PT J AU Naliboff, BD Munakata, J Fullerton, S Gracely, RH Kodner, A Harraf, F Mayer, EA AF Naliboff, BD Munakata, J Fullerton, S Gracely, RH Kodner, A Harraf, F Mayer, EA TI Evidence for two distinct perceptual alterations in irritable bowel syndrome SO GUT LA English DT Article DE irritable bowel syndrome; visceral hypersensitivity; pain threshold ID RECTAL SENSITIVITY; DISTENSION; MOTILITY; PAIN AB Background and aims-Visceral hyperalgesia has been implicated as a factor contributing to symptom generation in irritable bowel syndrome (IBS). However, previous studies using intestinal balloon distension have used psychophysical procedures which do not provide adequate and unbiased measures of visceral sensitivity. Methods-Three psychophysical tasks were examined in 45 patients with IBS (positive Rome criteria) and 14 controls using rectal balloon distension with a computerised distension device. Discomfort threshold and tolerance were assessed during an ascending series of phasic pressure stimuli and during an interactive threshold tracking procedure. In addition, stimulus response functions were generated from intensity and unpleasantness ratings of the rectal distensions. Results-Discomfort threshold and tolerance for the ascending stimuli were significantly lower for the patients with IBS compared with the controls. In contrast, discomfort thresholds during the tracking procedure and stimulus response curves for the ascending series were not different between the groups. A factor analysis of the psychophysical data was consistent with the presence of two distinct and unrelated perceptual alterations related to rectal distension: hypervigilance for visceral stimuli, manifested as lowered response criteria for using the descriptor ''discomfort''; and rectal hypersensitivity, manifested as a lower discomfort threshold and left shift of the stimulus response curves. Conclusions-Patients with IBS as a group have a greater propensity to label visceral sensations negatively and show a lower tolerance for rectal balloon distension. A subgroup of patients also have baseline rectal hypersensitivity, assessed by unbiased measures of discomfort threshold and stimulus intensity judgements. C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90073. NIDR,NAB,DEPT MED,NIH,BETHESDA,MD 20892. NIDR,NAB,DEPT PHYSIOL,NIH,BETHESDA,MD 20892. NIDR,NAB,DEPT PSYCHOL,NIH,BETHESDA,MD 20892. NIDR,NAB,NEUROPATH PAIN & PAIN ASSESSMENT SECT,NIH,BETHESDA,MD 20892. RP Naliboff, BD (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,CURE DIGEST DIS RES CTR,NEUROENTER DIS PROGRAM,LOS ANGELES,CA 90073, USA. FU NIDDK NIH HHS [DK48351] NR 32 TC 278 Z9 281 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0017-5749 J9 GUT JI Gut PD OCT PY 1997 VL 41 IS 4 BP 505 EP 512 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YB236 UT WOS:A1997YB23600018 PM 9391250 ER PT J AU Mahida, YR Beltinger, J Makh, S Goke, M Gray, T Podolsky, DK Hawkey, CJ AF Mahida, YR Beltinger, J Makh, S Goke, M Gray, T Podolsky, DK Hawkey, CJ TI Adult human colonic subepithelial myofibroblasts express extracellular matrix proteins & cyclooxygenase-1 & -2 SO GUT LA English DT Meeting Abstract C1 UNIV NOTTINGHAM HOSP,QUEENS MED CTR,DIV GASTROENTEROL,NOTTINGHAM NG7 2UH,ENGLAND. UNIV NOTTINGHAM HOSP,QUEENS MED CTR,DIV PATHOL,NOTTINGHAM NG7 2UH,ENGLAND. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0017-5749 J9 GUT JI Gut PD OCT PY 1997 VL 41 SU 3 BP A29 EP A29 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YB966 UT WOS:A1997YB96600119 ER PT J AU Miyamoto, MI Hutter, AM Blum, JH Torchiana, DF AF Miyamoto, MI Hutter, AM Blum, JH Torchiana, DF TI Cardiac conduction abnormalities preceding transoesophageal echocardiographic evidence of perivalvar extension of infection in a case of Salmonella prosthetic valve endocarditis SO HEART LA English DT Article DE endocarditis; Salmonella enteritidis; heart block AB A 59 year old African-American man developed complete heart block in association with Salmonella enteritidis prosthetic valve endocarditis. Severe cardiac conduction abnormalities signalled the presence of perivalvar extension of infection before development of evidence of abscess by transoesophageal echocardiography. Cardiac conduction temporarily returned after debridement and aortic homograft placement. This case emphasises the value of electrocardiographic monitoring in the detection of perivalvar extension of infection complicating infective endocarditis, even in the era of sophisticated imaging modalities. C1 MASSACHUSETTS GEN HOSP, INFECT DIS UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CARDIAC SURG UNIT, BOSTON, MA 02114 USA. RP Miyamoto, MI (reprint author), MASSACHUSETTS GEN HOSP, CARDIAC UNIT, BOSTON, MA 02114 USA. NR 5 TC 7 Z9 8 U1 0 U2 0 PU BMJ PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 1355-6037 EI 1468-201X J9 HEART JI Heart PD OCT PY 1997 VL 78 IS 4 BP 416 EP 418 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YC552 UT WOS:A1997YC55200024 PM 9404262 ER PT J AU Zaman, A Hapke, R Flora, K Rosen, H Benner, K AF Zaman, A Hapke, R Flora, K Rosen, H Benner, K TI Factors predicting the presence of esophageal and gastric varices in patients with advanced liver disease. SO HEPATOLOGY LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. PORTLAND VA MED CTR,PORTLAND,OR. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 29 EP 29 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400029 ER PT J AU Perrillo, R Rakela, J Martin, P Levy, G Schiff, E Wright, T Dienstag, J Gish, R Villeneuve, JP Caldwell, S Brown, N Self, P AF Perrillo, R Rakela, J Martin, P Levy, G Schiff, E Wright, T Dienstag, J Gish, R Villeneuve, JP Caldwell, S Brown, N Self, P TI Long term lamivudine therapy of patients with recurrent hepatitis B post liver transplantation. SO HEPATOLOGY LA English DT Meeting Abstract C1 UNIV PITTSBURGH,ALTON OCHSNER MED FDN & OCHSNER CLIN,PITTSBURGH,PA 15260. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. TORONTO HOSP,TORONTO,ON M5T 2S8,CANADA. UNIV MIAMI,CORAL GABLES,FL 33124. UCSF,SAN FRANCISCO,CA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CALIF PACIFIC MED CTR,SAN FRANCISCO,CA. HOSP ST LUC,MONTREAL,PQ,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 196 EP 196 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400196 ER PT J AU Mitic, L Fanning, AS Schneeberger, E Anderson, JM AF Mitic, L Fanning, AS Schneeberger, E Anderson, JM TI Targeting of connexin-occludin chimeras to tight junctions. SO HEPATOLOGY LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT CELL BIOL,NEW HAVEN,CT 06520. YALE UNIV,SCH MED,DEPT INTERNAL MED,NEW HAVEN,CT 06520. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 207 EP 207 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400206 ER PT J AU Encke, J Putlitz, JZ Heintges, T Wands, JR AF Encke, J Putlitz, JZ Heintges, T Wands, JR TI Total chemical synthesis with oligodeoxyneucleotides of the 3' untranslated region of hepatitis C virus. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 324 EP 324 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400324 ER PT J AU Melegari, M Scaglioni, PP Wands, JR AF Melegari, M Scaglioni, PP Wands, JR TI Biological properties of hepatitis B viral genomes with mutation in the precore promoter and ORF SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 364 EP 364 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400364 ER PT J AU Putlitz, JZ Wands, JR AF Putlitz, JZ Wands, JR TI A novel deletion mutant of hepatitis B virus detected in a patient with chronic hepatitis. SO HEPATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CHARLESTOWN,MA. MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 365 EP 365 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400365 ER PT J AU Geissler, M Bruss, V Blum, HE Wands, J AF Geissler, M Bruss, V Blum, HE Wands, J TI Influence of hepatitis B virus envelope antigen secretion and retention of cellular and humoral immune responses in the context of genetic immunization. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. UNIV HOSP,DEPT MED,FREIBURG,GERMANY. UNIV GOTTINGEN,DEPT MED MICROBIOL,D-3400 GOTTINGEN,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 380 EP 380 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400380 ER PT J AU Geissler, M Blum, HE Wands, J AF Geissler, M Blum, HE Wands, J TI Differential cellular and humoral immune responses to hepatitis B virus large and middle envelope proteins after genetic immunizations augmented with IL-2 and GM-CSF expressing plasmids. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. UNIV HOSP,DEPT MED,FREIBURG,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 381 EP 381 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400381 ER PT J AU Geissler, M Gesien, A Wands, J AF Geissler, M Gesien, A Wands, J TI Chronic ethanol effects on cellular immune responses to hepatitis B virus envelope protein: An immunologic mechanism for induction of persistent viral infection in alcoholics. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. UNIV HOSP,DEPT MED,FREIBURG,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 382 EP 382 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400383 ER PT J AU Tong, S Li, J Wands, JR AF Tong, S Li, J Wands, JR TI P170 is a cell surface binding receptor for duck hepatitis B virus. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 383 EP 383 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400382 ER PT J AU Banerjee, K Tanaka, S Wands, JR delaMonte, SM AF Banerjee, K Tanaka, S Wands, JR delaMonte, SM TI Selective inhibition of tyrosyl phosphorylation of human insulin receptor substrate-1 on exposure to ethanol in HCC cells. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEMATOL LAB,CHARLESTOWN,MA 02129. KYUSHU UNIV,FAC MED,DEPT SURG 2,FUKUOKA 812,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 499 EP 499 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400498 ER PT J AU Ito, T Sasaki, Y Horimoto, M Hayashi, N Hori, M Wands, JR AF Ito, T Sasaki, Y Horimoto, M Hayashi, N Hori, M Wands, JR TI Acquisition of resistance to apoptosis by insulin receptor substrate-1 (IRS-1) overexpression. SO HEPATOLOGY LA English DT Meeting Abstract C1 OSAKA UNIV,SCH MED,DEPT MED 1,OSAKA 553,JAPAN. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 505 EP 505 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400505 ER PT J AU Heintges, T Putlitz, JZ Wands, JR AF Heintges, T Putlitz, JZ Wands, JR TI Cloning, recombinant expression, characterization and sequencing of monoclonal antibodies against hepatitis C virus core protein. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 519 EP 519 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400518 ER PT J AU Perrillo, R Rakela, J Martin, P Wright, T Levy, G Schiff, E Dienstag, J Gish, R Dickson, R Adams, P Brown, N Self, P AF Perrillo, R Rakela, J Martin, P Wright, T Levy, G Schiff, E Dienstag, J Gish, R Dickson, R Adams, P Brown, N Self, P TI Lamivudine for suppression and/or prevention of hepatitis B when given pre/post liver transplantation (OLT). SO HEPATOLOGY LA English DT Meeting Abstract C1 UNIV PITTSBURGH,ALTON OCHSNER MED FDN & OCHSNER CLIN,PITTSBURGH,PA 15260. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. TORONTO HOSP,TORONTO,ON M5T 2S8,CANADA. UNIV MIAMI,CORAL GABLES,FL 33124. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CA PAC MED CTR,SAN FRANCISCO,CA. UNIV FLORIDA,GAINESVILLE,FL 32611. UNIV WESTERN ONTARIO,LONDON,ON N6A 3K7,CANADA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 526 EP 526 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400527 ER PT J AU Heintges, T Encke, J Putlitz, JZ Wands, JR AF Heintges, T Encke, J Putlitz, JZ Wands, JR TI Assembly of a cDNA encoding the entire genome of hepatitis C virus. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 680 EP 680 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400680 ER PT J AU Chung, RT Kaplan, LM AF Chung, RT Kaplan, LM TI Identification of a cellular protein that binds selectively to the conserved 3'-terminal structure of the HCV genome. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 683 EP 683 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400682 ER PT J AU Mohr, L Yoon, SK Eastman, SJ Scheule, RK Chu, Q Scaglioni, PP Heintges, T Wands, JR AF Mohr, L Yoon, SK Eastman, SJ Scheule, RK Chu, Q Scaglioni, PP Heintges, T Wands, JR TI In vivo gene delivery to the liver and to intrahepatic tumors with cationic liposomes in nude mice. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MGH CANC CTR,MOL HEPATOL LAB,CHARLESTOWN,MA. GENZYME CORP,FRAMINGHAM,MA 01701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 938 EP 938 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400939 ER PT J AU Mohr, L Schauer, JI Boutin, RH Moradpour, D Wands, JR AF Mohr, L Schauer, JI Boutin, RH Moradpour, D Wands, JR TI Targeted gene delivery to hepatocellular carcinoma cells using a monoclonal antibody based nonviral gene delivery system. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MGH CANC CTR,MOL HEPATOL LAB,CHARLESTOWN,MA. APOLLON INC,MALVERN,PA 19355. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 941 EP 941 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400941 ER PT J AU Melegari, M Scaglioni, PP Wands, JR AF Melegari, M Scaglioni, PP Wands, JR TI Hepatitis B virus mutants induced by 3TC and famciclovir are replication defective SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA 02129. HARVARD UNIV,SCH MED,CHARLESTOWN,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 959 EP 959 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400958 ER PT J AU Mohr, L Tanaka, S delaMonte, S Wands, JR AF Mohr, L Tanaka, S delaMonte, S Wands, JR TI Proliferative response of hepatocytes to human insulin receptor substrate-1 (h-IRS-1) overexpression in the liver of transgenic mice. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MGH CANC CTR,MOL HEPATOL LAB,CHARLESTOWN,MA. KYUSHU UNIV,FAC MED,DEPT SURG 2,FUKUOKA 812,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 976 EP 976 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400976 ER PT J AU Mohr, L Tanaka, S Wands, JR AF Mohr, L Tanaka, S Wands, JR TI Chronic ethanol feeding inhibits hepatocyte proliferation via the insulin receptor substrate-1 (h-IRS-1) signal transduction cascade in transgenic mice SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. KYUSHU UNIV,DEPT SURG 2,FUKUOKA 812,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 977 EP 977 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400977 ER PT J AU delaMonte, SM Ganju, N Tanaka, S Brown, NV Wands, JR AF delaMonte, SM Ganju, N Tanaka, S Brown, NV Wands, JR TI Ethanol-inhibition of insulin-stimulated GAPDH expression is mediated through specific motifs of insulin receptor substrate-1. SO HEPATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MGH CANC CTR,MOL HEPATOL LAB,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 978 EP 978 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87400979 ER PT J AU Koziel, MJ Wong, DKH Dudley, D Houghton, M Walker, BD AF Koziel, MJ Wong, DKH Dudley, D Houghton, M Walker, BD TI Hepatitis C virus-specific cytolytic T lymphocyte (CTL) and T helper cell responses in seronegative individuals SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BETH ISRAEL DEACONESS MED CTR,BOSTON,MA. CHIRON CORP,EMERYVILLE,CA 94608. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 1110 EP 1110 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87401111 ER PT J AU Putlitz, JZ Wands, JR AF Putlitz, JZ Wands, JR TI Cloning, bacterial expression and characterization of immunoglobulin variable regions from a murine monoclonal antibody directed against hepatitis B virus surface protein. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 1189 EP 1189 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87401189 ER PT J AU Garrett, L Dienstag, JL Gauthier, J Condreay, L Crowther, L Gelb, L Schiff, ER Brown, NA AF Garrett, L Dienstag, JL Gauthier, J Condreay, L Crowther, L Gelb, L Schiff, ER Brown, NA TI Hepatitis B e-antigen (HBeAg) seroconversion in two patients with evidence of genotypic resistance following extended lamivudine treatment. SO HEPATOLOGY LA English DT Meeting Abstract C1 GLAXO WELLCOME,RES TRIANGLE PK,NC. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. WASHINGTON UNIV,ST LOUIS,MO. UNIV MIAMI,MIAMI,FL 33152. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 1209 EP 1209 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87401209 ER PT J AU Yoon, SK Scaglioni, PP Mohr, L Melegari, MM Armentano, D delaMonte, S Wands, JR AF Yoon, SK Scaglioni, PP Mohr, L Melegari, MM Armentano, D delaMonte, S Wands, JR TI Adenovirus mediated gene transfer and expression in mouse liver. SO HEPATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,CHARLESTOWN,MA. GENZYME CORP,FRAMINGHAM,MA 01701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD OCT PY 1997 VL 26 IS 4 SU S BP 2018 EP 2018 PN 2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA XY874 UT WOS:A1997XY87402019 ER PT J AU Delgado, JC Hameed, A Yunis, JJ Bhol, K Rojas, AI Rehman, SB Khan, AA Ahmad, M Alper, CA Ahmed, AR Yunis, EJ AF Delgado, JC Hameed, A Yunis, JJ Bhol, K Rojas, AI Rehman, SB Khan, AA Ahmad, M Alper, CA Ahmed, AR Yunis, EJ TI Pemphigus vulgaris autoantibody response is linked to HLA-DQB1*0503 in Pakistani patients SO HUMAN IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; PCR-RFLP METHOD; CLASS-II GENES; HLA-DRB1 ALLELES; JEWISH PATIENTS; SELF-PEPTIDES; SUSCEPTIBILITY; MOLECULES; BINDING; AUTOIMMUNITY AB Pemphigus vulgaris (PV) is an autoimmune disease of the skin and mucous membranes characterized by an autoantibody response against an epidermal cadherin. We performed high resolution HLA class II typing in 19 patients with PV from Rawalpindi, Pakistan and 19 non-Jewish European PV patients from Boston by sequence-specific oligonucleotide probe hybridization. The results were compared with two separate ethnically matched control populations. We found that PV patients from Pakistan had significantly increased frequencies of DRB1*1404 (P = 0.01), DQA1*0101 (P = 0.02), and DQB1*0503 (P = 0.01). Among the patients of non-Jewish European ancestry, DRB1*1401 (P < 10(-6)) DQA1*0101 (P < 10(-5)) and DQB1*0503 (P < 10(-6)), were increased in PV patients. Formal linkage analysis between the major histocompatibility complex and the PV antibody was performed in 67 relatives of the 19 Pakistani patients. The results showed strong evidence for linkage of HLA-DRB1*1404, DQA1*0101, DQB1*0503, with the presence of PV antibody in relatives' families with a significant logarithm of the odds score of 6.06. Based on the three dimensional structure of class II molecules, we propose that HLA-DQA1*0101 and DQB1*0503, encode a negatively charged P9 peptide binding pocket of the DQ molecule and are significantly associated with susceptibility to PV in non-Jewish populations. (C) American Society for Histocompatibility and Immunogenetics, 1997. Published by Elsevier Science Inc. C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Army Med Coll, Dept Dermatol, Rawalpindi, Pakistan. Univ Nacl Colombia, Dept Genet, Santa Fe, Colombia. Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Dent Med, Boston, MA 02115 USA. RP Yunis, EJ (reprint author), 44 Binney St, Boston, MA 02115 USA. EM Edmond_J._Yunis@dfci.harvard.edu FU NEI NIH HHS [EY08379]; NHLBI NIH HHS [HL29583]; NIDCR NIH HHS [DE09978] NR 35 TC 41 Z9 41 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0198-8859 EI 1879-1166 J9 HUM IMMUNOL JI Hum. Immunol. PD OCT PY 1997 VL 57 IS 2 BP 110 EP 119 DI 10.1016/S0198-8859(97)00203-6 PG 10 WC Immunology SC Immunology GA YN916 UT WOS:000071221600005 PM 9438202 ER PT J AU Wu, L Nichogiannopoulou, A Shortman, K Georgopoulos, K AF Wu, L Nichogiannopoulou, A Shortman, K Georgopoulos, K TI Cell-autonomous defects in dendritic cell populations of Ikaros mutant mice point to a developmental relationship with the lymphoid lineage SO IMMUNITY LA English DT Article ID COLONY-STIMULATING FACTOR; PRECURSOR CELLS; MOUSE THYMUS; TRANSCRIPTION FACTOR; CD8 EXPRESSION; TNF-ALPHA; T-CELLS; GENE; COMMITMENT; LIGAND AB The transcription factor Ikaros is a major determinant of lymphocyte differentiation. Mice homozygous for an Ikaros dominat-negative (DN-/-) mutation lack all cells of lymphoid origin, including T, B, and natural killer (NK) cells. Mice homozygous for an Ikaros null allele lack B and NK cells but display specific defects in T lymphocytes. Nonetheless, both Ikaros mutant lines make an excess of monocytes and macrophages. Here we report that the production of subsets of antigen-presenting dendritic cells (DCs) is also defective. By constructing bone marrow chimeras, we demonstrate that the Ikaros-mediated defect in lymphocytes and DCs is intrinsic to their precursors and is not environment dependent. The selective defects in DCs manifested with the Ikaros null mutation suggest a tight linkage between development of T cells and CD8 alpha(+) DCs. The complete lack of DCs in the lymphoid organs of Ikaros DN-/- micke points to an essential role for the Ikaros gene family in the development of all DCs. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,CHARLESTOWN,MA 02129. RP Wu, L (reprint author), WALTER & ELIZA HALL INST MED RES,MELBOURNE,VIC 3050,AUSTRALIA. FU NIAID NIH HHS [R01-AI33062-09] NR 28 TC 162 Z9 165 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD OCT PY 1997 VL 7 IS 4 BP 483 EP 492 DI 10.1016/S1074-7613(00)80370-2 PG 10 WC Immunology SC Immunology GA YD593 UT WOS:A1997YD59300005 PM 9354469 ER PT J AU Sleckman, BP Bardon, CG Ferrini, R Davidson, L Alt, FW AF Sleckman, BP Bardon, CG Ferrini, R Davidson, L Alt, FW TI Function of the TCR alpha enhancer in alpha beta and gamma delta T cells SO IMMUNITY LA English DT Article ID RECEPTOR ALPHA/DELTA-LOCUS; CHAIN GENE REARRANGEMENT; V(D)J RECOMBINATION; TRANSCRIPTIONAL ENHANCER; THYMOCYTE DEVELOPMENT; TARGETED DELETION; INTRON ENHANCER; 3' END; GENOMIC ORGANIZATION; ATTACHMENT REGION AB We have used gene targeted mutational approaches to assess the role of the T cell receptor alpha (TCR alpha) enhancer (E alpha) in the control of TCR alpha. and TCR delta gene rearrangement and expression. We show that E alpha functions in cis to promote V alpha to J alpha rearrangement across the entire J alpha locus, a distance of greater than 70 kb. We also show that E alpha is required for normal alpha beta T cell development; in this lineage, E alpha is required for germline J alpha expression, for normal expression levels of rearranged V alpha J alpha genes, and for expression of a diverse V alpha repertoire. In gamma delta T cells, E alpha is not required for V delta DJ delta rearrangement, but, surprisingly, is required for normal expression levels of mature V delta DJ delta transcripts and for expression of germline J alpha transcripts. Our findings imply that E alpha function is not limited to the TCR alpha components of the TCR alpha/delta locus or to the alpha beta lineage; rather, E alpha function is important in both alpha beta and gamma delta lineage T cells. C1 CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. FU NIAID NIH HHS [AI-01297-01, AI-20047] NR 72 TC 159 Z9 159 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD OCT PY 1997 VL 7 IS 4 BP 505 EP 515 DI 10.1016/S1074-7613(00)80372-6 PG 11 WC Immunology SC Immunology GA YD593 UT WOS:A1997YD59300007 PM 9354471 ER PT J AU Dimarcq, JL Imler, JL Lanot, R Ezekowitz, RAB Hoffmann, JA Janeway, CA Lagueux, M AF Dimarcq, JL Imler, JL Lanot, R Ezekowitz, RAB Hoffmann, JA Janeway, CA Lagueux, M TI Treatment of l(2)mbn Drosophila tumorous blood cells with the steroid hormone ecdysone amplifies the inducibility of antimicrobial peptide gene expression SO INSECT BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article DE ecdysone; insect immunity; L(2)mbn cells; phagocytosis; antimicrobial peptides; macrophage ID INSECT IMMUNITY; TRANSMEMBRANE PROTEIN; EMBRYONIC POLARITY; INNATE IMMUNITY; DIPTERICIN GENE; DORSAL; SEQUENCE; CECROPIN; MELANOGASTER; RESISTANCE AB Insects rely on both humoral and cellular mechanisms to defend themselves against microbial infections, The humoral response involves synthesis of a battery of potent antimicrobial peptides by the fat body and, to a lesser extent, by blood cells. The cellular response on the other hand consists of phagocytosis of small microorganisms and melanization and encapsulation of larger parasites. The l(2)mbn cell line, established from tumorous larval hemocytes, represents a system of choice to dissect the molecular events controlling cellular immunity. We report here that l(2)mbn cells can be efficiently induced to differentiate in adherent, macrophage-like cells by treatment with 20-hydroxyecdysone. Ecdysone treatment increases both the phagocytic capacity of l(2)mbn cells and their competence to express antimicrobial genes in response to immune challenge. We also report that expression of several regulatory molecules thought to be involved in the immune response is up-regulated by ecdysone in l(2)mbn cells. (C) 1997 Elsevier Science Ltd. All rights reserved. C1 Inst Biol Mol & Cellulaire, CNRS, UPR 9022, F-67084 Strasbourg, France. Massachusetts Gen Hosp, Boston, MA 02114 USA. Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06510 USA. RP Imler, JL (reprint author), Inst Biol Mol & Cellulaire, CNRS, UPR 9022, 15 Rue Rene Descartes, F-67084 Strasbourg, France. EM imler@ibmc.u-strasbg.fr NR 44 TC 83 Z9 89 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0965-1748 EI 1879-0240 J9 INSECT BIOCHEM MOLEC JI Insect Biochem. Mol. Biol. PD OCT PY 1997 VL 27 IS 10 BP 877 EP 886 DI 10.1016/S0965-1748(97)00072-6 PG 10 WC Biochemistry & Molecular Biology; Entomology SC Biochemistry & Molecular Biology; Entomology GA YV176 UT WOS:000071797000008 PM 9474784 ER PT J AU Koyasu, S Clayton, LK Lerner, A Heiken, H Parkes, A Reinherz, EL AF Koyasu, S Clayton, LK Lerner, A Heiken, H Parkes, A Reinherz, EL TI Pre-TCR signaling components trigger transcriptional activation of a rearranged TCR alpha gene locus and silencing of the pre-TCR alpha locus: implications for intrathymic differentiation SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE allelic exclusion; rag-2(-/-) mice; TCR transgenic mice; T cell development; V alpha 14 ID T-CELL DEVELOPMENT; BETA-CHAIN EXPRESSION; ALLELIC EXCLUSION; RECEPTOR GENES; MICE; LYMPHOCYTES; ANTIGEN; THYMOCYTES; SEQUENCE; ONTOGENY AB A rearranged TCR alpha transgene remains transcriptionally inactive in rag-2(-/-) thymocytes but can be induced by CD3-mediated signals with concomitant maturation of double-negative (DN) thymocytes to the CD4(+)CD8(+) double-positive (DP) stage, Reciprocally, the same signals silence pre-TCR alpha (pT alpha) expression, In normal C57BL/6 thymocytes, TCR alpha expression is not detected in DN thymocytes while, in contrast, TCR beta expression is initiated at the most immature c-kit(+)CD44(+)CD25(-) stage and continues throughout thymocyte development, pT alpha expression is first detected at the intermediate c-kit(+/-)CD44(+)CD25(+) DN stage, increases during transition to the more mature c-kit(-)CD44(-)CD25(+) stage and is lost at the DP stage, Thus, although TCR beta and pT alpha expression are independent, the pre-TCR complex mediates signals controlling the appearance of alpha beta TCR through selective regulation of TCR alpha and pT alpha genes. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. RI Koyasu, Shigeo/J-5583-2015 OI Koyasu, Shigeo/0000-0001-9585-3038 FU NIAID NIH HHS [AI33017, AI19807] NR 33 TC 25 Z9 25 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD OCT PY 1997 VL 9 IS 10 BP 1475 EP 1480 DI 10.1093/intimm/9.10.1475 PG 6 WC Immunology SC Immunology GA YD178 UT WOS:A1997YD17800008 PM 9352352 ER PT J AU Raaphorst, FM Raman, CS Tami, J Fischbach, M Sanz, I AF Raaphorst, FM Raman, CS Tami, J Fischbach, M Sanz, I TI Human Ig heavy chain CDR3 regions in adult bone marrow pre-B cells display an adult phenotype of diversity: evidence for structural selection of D-H amino acid sequences SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE antigen receptor; B lymphocyte; repertoire; VDJ rearrangement ID COMPLEMENTARITY-DETERMINING REGIONS; ANTIBODY-ANTIGEN COMPLEXES; PREFERENTIAL UTILIZATION; V(D)J RECOMBINATION; 3-DIMENSIONAL STRUCTURE; HYPERVARIABLE REGIONS; V(H) SEGMENTS; GENE SEGMENTS; FETAL LIVER; REPERTOIRE AB Ig repertoires generated at various developmental stages differ markedly in diversity. It is well documented that Ig H chain genes in human fetal liver are limited with regard to N-regional diversity and use of diversity elements. It is unclear whether these characteristics persist in pre-B cell H chain genes of adult bone marrow. Using Ig H chain CDR3 fingerprinting and sequence analysis, we analyzed the diversity of Ig H chain third complementarity determining regions (HCDR3) in adult bone marrow pre-B and mature a lymphocytes. pre-B cell HCDR3 sequences exhibited adult characteristics with respect to HCDR3 size, distribution of N regions and usage of diversity elements. This suggested that pre-B cells in adults are distinct from fetal a cell precursors with regard to Ig H chain diversification mechanisms. At the DNA sequence level, HCDR3 diversity in mature a cells was similar to that in pre-B cells, pre-B HCDR3s, however, frequently contained a consecutive stretch of hydrophobic amino acids, which were rare in mature a cells. We propose that highly hydrophobic pre-B HCDR3s may be negatively selected on the basis of structural limitations imposed by the antigen binding site. At the same time, usage of hydrophilic HCDR3 sequences (thought to support HCDR3 loop formation) may be promoted by positive selection. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. S TEXAS VET HLTH CARE SYST,AUDIE L MURPHY DIV,SAN ANTONIO,TX 78284. OI Raman, C. S./0000-0002-1036-3193 NR 64 TC 47 Z9 47 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD OCT PY 1997 VL 9 IS 10 BP 1503 EP 1515 DI 10.1093/intimm/9.10.1503 PG 13 WC Immunology SC Immunology GA YD178 UT WOS:A1997YD17800011 PM 9352355 ER PT J AU Mizuta, R Cheng, HL Gao, YJ Alt, FW AF Mizuta, R Cheng, HL Gao, YJ Alt, FW TI Molecular genetic characterization of XRCC4 function SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE DNA-dependent protein kinase; double-strand break repair; V(D)J recombination; XRCC4 ID DEPENDENT PROTEIN-KINASE; V(D)J RECOMBINATION; RAG2 PROTEINS; DNA-REPAIR; 12/23-RULE; MUTATION; DEFECTS; STEPS; CELLS; KU80 AB XRCC4 is a generally expressed protein of 334 amino acids that is involved in the repair of DNA double-strand breaks and in V(D)J recombination, but its function is unknown. In this study, we have used a mutational approach and the yeast two-hybrid method to perform an initial characterization of this protein, We show that the XRCC4 protein is located in the nucleus, We also demonstrate that several potential phosphorylation sites are not required for XRCC4 function in a transient V(D)J recombination assay, In addition, we show that XRCC4 forms a homodimer in vivo with the homodimerization domain being located within amino acids 115-204. Finally, we define a core domain of XRCC4 that functions in V(D)J recombination and comprises amino acids 18-204, Potential functions of XRCC4 are discussed. C1 CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. FU NIAID NIH HHS [AI315714] NR 20 TC 36 Z9 36 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD OCT PY 1997 VL 9 IS 10 BP 1607 EP 1613 DI 10.1093/intimm/9.10.1607 PG 7 WC Immunology SC Immunology GA YD178 UT WOS:A1997YD17800023 PM 9352367 ER PT J AU Ferry, JA AF Ferry, JA TI Adenoid basal carcinoma of the uterine cervix - Evolution of a distinctive clinicopathologic entity SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Editorial Material ID MESONEPHRIC REMNANTS C1 Massachusetts Gen Hosp, Dept Pathol, James Homer Wright Pathol Labs, Boston, MA 02114 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. RP Ferry, JA (reprint author), Massachusetts Gen Hosp, Dept Pathol, James Homer Wright Pathol Labs, Boston, MA 02114 USA. NR 10 TC 11 Z9 12 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD OCT PY 1997 VL 16 IS 4 BP 299 EP 300 DI 10.1097/00004347-199710000-00001 PG 2 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA YU404 UT WOS:000071713700001 PM 9421066 ER PT J AU Nielsen, GP Young, RH Prat, J Scully, RE AF Nielsen, GP Young, RH Prat, J Scully, RE TI Primary angiosarcoma of the ovary - A report of seven cases and review of the literature SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Review DE ovary; angiosarcoma; dermoid cyst ID GERM-CELL TUMORS; EPITHELIOID ANGIOSARCOMA; UTERUS; HEMANGIOMA; SARCOMAS AB Seven primary ovarian angiosarcomas were diagnosed in 7 patients 20 to 32 (mean 26) years of age. The most common clinical presentation was abdominal pain and distention. Three tumors were in the right ovary and 3 in the left: one was bilateral. Four tumors were Stage I and 3 Stage III. The tumors were brown and hemorrhagic, ranging in maximum dimension from 6 to 13 (average 10) cm. Microscopically, 5 tumors were pure angiosarcomas and 2 were associated with a dermoid cyst. Follow-up information ranging from 2 months to 9 (average 3.6) years was available for 5 patients. Three patients, all with Stage III disease, died of tumor (1 with a pure angiosarcoma, 2 with tumors arising in a dermoid cyst) 2, 15, and 30 months postoperatively. Two patients with Stage I disease and follow-up data were alive and healthy 5.5 and 9 years postoperatively. The differential diagnosis of these tumors is discussed and the literature reviewed. C1 Harvard Univ, Dept Pathol, Massachusetts Gen Hosp, Sch Med,James Homer Wright Pathol Labs, Boston, MA 02114 USA. RP Nielsen, GP (reprint author), Harvard Univ, Dept Pathol, Massachusetts Gen Hosp, Sch Med,James Homer Wright Pathol Labs, Fruit St, Boston, MA 02114 USA. RI Prat, Jaime/G-4679-2011 NR 37 TC 38 Z9 42 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD OCT PY 1997 VL 16 IS 4 BP 378 EP 382 DI 10.1097/00004347-199710000-00014 PG 5 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA YU404 UT WOS:000071713700013 PM 9421078 ER PT J AU Nielsen, GP Young, RH AF Nielsen, GP Young, RH TI Fibromatosis of soft tissue type involving the female genital tract - A report of two cases SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE ovary; vulva; fibromatosis-soft-tissue-type ID AGGRESSIVE ANGIOMYXOMA; OVARY AB Two cases of soft tissue-type fibromatosis of the female genital tract are described. One involved the vulva of a 19-year-old woman, and was approximately 6.0 cm in greatest dimension and had a rubbery consistency with a gray-white, whorled cut surface. Microscopically, it had infiltrating borders and extended to the ischio-rectal region. All gross tumor was resected. There was no evidence of recurrent disease 6 years later. The other tumor involved primarily the ovary of a 20-year-old woman. It was 24 cm in greatest dimension and infiltrated the mesentery, psoas muscle, and iliac vessels. The tumor was resected along with the sigmoid colon and the patient was free of disease 3 months later. Fibromatosis of the female genital tract, histologically identical to the soft tissue lesion and distinct from so-called "ovarian fibromatosis," should be included in the differential diagnosis of low-grade spindle cell lesions of this region. C1 Harvard Univ, Dept Pathol, Massachusetts Gen Hosp, Sch Med,James Homer Pathol Labs, Boston, MA 02114 USA. RP Nielsen, GP (reprint author), Harvard Univ, Dept Pathol, Massachusetts Gen Hosp, Sch Med,James Homer Pathol Labs, Fruit St, Boston, MA 02114 USA. NR 13 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD OCT PY 1997 VL 16 IS 4 BP 383 EP 386 DI 10.1097/00004347-199710000-00015 PG 4 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA YU404 UT WOS:000071713700014 PM 9421079 ER PT J AU Tao, ML Barnes, PD Billett, AL Leong, T Shrieve, DC Scott, RM Tarbell, NJ AF Tao, ML Barnes, PD Billett, AL Leong, T Shrieve, DC Scott, RM Tarbell, NJ TI Childhood optic chiasm gliomas: Radiographic response following radiotherapy and long-term clinical outcome SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT 37th Annual Meeting of the American-Society-for-Therapeutic-Radiology-and-Oncology CY OCT 07-11, 1995 CL MIAMI BEACH, FL SP Amer Soc Therapeut Radiol & Oncol DE optic chiasm; glioma; radiotherapy; magnetic resonance imaging ID RADIATION-THERAPY; NEUROFIBROMATOSIS TYPE-1; NERVE GLIOMA; BRAIN-TUMOR; MANAGEMENT; CHILDREN; IRRADIATION; PATHWAYS; ASTROCYTOMA AB Purpose: In children with chiasmal gliomas, radiation therapy can arrest progressive visual and neurologic impairment. We examined the radiographic response and clinical outcomes after irradiation. Methods and Materials: Forty-two children (median age at diagnosis, 6.6 years) with chiasmal gliomas were managed as follows: 11 asymptomatic patients with neurofibromatosis-1 (NF-1) were observed only; 2 patients, less than 3 years old, underwent surgery and chemotherapy to delay irradiation; and 29 patients with progressive disease received radiation with or without prior surgery or chemotherapy. Time to radiographic response, long-term tumor control and late sequelae were reviewed for the 29 irradiated patients. Results: The probability of at least 50% radiographic response at 24 months after irradiation was 18.1% and increased to 38.2% by 48 months and 45.9% by 60 months. By actuarial analysis, the median time for such radiographic response was 62 months. For the 29 irradiated patients, the 10-year freedom from progression and overall survival rates were 100% and 89%, respectively (median follow-up for surviving patients, 108 months). Stabilization or improvement in vision occurred in 81% of 26 evaluable irradiated patients. Conclusions: Notable radiographic response may be observed years after irradiation. Radiation therapy provides excellent long-term tumor control and vision preservation or improvement in the majority of patients with progressive chiasmal gliomas. (C) 1997 Elsevier Science Inc. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROSURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. NR 40 TC 49 Z9 50 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 1 PY 1997 VL 39 IS 3 BP 579 EP 587 DI 10.1016/S0360-3016(97)00359-3 PG 9 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA YA917 UT WOS:A1997YA91700009 PM 9336136 ER PT J AU Constantinou, EC Daly, W Fung, CY Willett, CG Kaufman, DS DeLaney, TF AF Constantinou, EC Daly, W Fung, CY Willett, CG Kaufman, DS DeLaney, TF TI Time-dose considerations in the treatment of anal cancer SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT 38th Meeting of the American-Society-for-Therapeutic-Radiology-and-Oncology CY OCT 27-31, 1996 CL LOS ANGELES, CA SP Amer Soc Therapeut Radiol & Oncol DE anal cancer; chemoradiation; dose response; hemoglobin ID THERAPY; 5-FLUOROURACIL; CHEMORADIATION; RADIOTHERAPY; RADIATION; CARCINOMA; MITOMYCIN; CISPLATIN AB Purpose: To analyze the impact of patient and treatment parameters in concurrent chemoradiation treatment for anal carcinoma. Methods and Materials: Retrospective review of 50 MO anal cancer patients treated from 1984-1994. Most patients received concurrent 5-FU, mitomycin, and radiation. Local control and disease-free/overall survival were determined and analyzed according to patient and treatment parameters. Results: With 43 month median follow-up, projected overall survival is 66% at 5 and 8 years. Disease-free survival is 67% at 5 years and 59% at 8 years. Local control is 70% at 5 and 8 years. Doses of greater than or equal to 54 Gy are associated with improved 5-year survival (84 vs. 47%, p = 0.02), disease-free survival (74 v. 56%, p = 0.09), and local control (77 vs. 61%, p = 0.04). Although local control, disease-free survival, and overall survival were improved in patients whose overall treatment time was <40 days, this was not statistically significant. Outcome in the four patients with pretreatment hemoglobin (Hgb) <10 appeared worse with 3-year overall survival 50 vs. 68% (p = 0.07), disease-free survival 0 vs. 67% (p = 0.11), and local control 0 vs. 74% (p = 0.05). Projected 5-year overall survival, relapse-free survival, and local control in 4 HIV(+) patients is 0, 75, and 75%. Multivariate analysis reveals that dose (p = 0.02) and Hgb (p = 0.05) independently affect local control, dose (p = 0.02) affects disease-free survival, and dose (p = 0.01), Hgb (p = 0.03), T-stage (p = 0.03), and HIV-status (0.07) independently influence overall survival. Conclusion: Radiation doses of greater than or equal to 54 Gy are associated with significantly improved survival and local control in anal cancer patients treated with chemoradiation. Overall treatment times of less than 40 days are associated with a trend towards improved outcome, but this is not significant. Pretreatment hemoglobin <10 is associated with worse treatment outcome. Survival of HIV (+) patient is poor, but the majority of such patients in this series died of intercurrent disease with their anal carcinomas controlled by chemoradiation. (C) 1997 Elsevier Science Inc. C1 BOSTON UNIV,MED CTR,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02118. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HEMATOL ONCOL UNIT,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. NR 20 TC 77 Z9 80 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 1 PY 1997 VL 39 IS 3 BP 651 EP 657 DI 10.1016/S0360-3016(97)00329-5 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA YA917 UT WOS:A1997YA91700018 PM 9336145 ER PT J AU Budach, W Gioioso, D Taghian, A Stuschke, M Suit, HD AF Budach, W Gioioso, D Taghian, A Stuschke, M Suit, HD TI Repopulation capacity during fractionated irradiation of squamous cell carcinomas and glioblastomas in vitro SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE repopulation; radiation; squamous cell carcinoma; glioblastoma ID LOCAL TUMOR-CONTROL; TREATMENT TIME; DOUBLING TIME; NECK TUMORS; T-POT; RADIOTHERAPY; HEAD; CANCER; TCD50 AB Purpose: Determination of clonogenic cell proliferation of three highly malignant squamous cell carcinomas (SCC) and two glioblastoma cell lines during a 20-day course of fractionated irradiation under in vitro conditions, Methods and Materials: Tumor cells in exponential growth phase were plated in 24-well plastic flasks and irradiated 24 h after plating with 250 kV x-rays at room temperature, Six fractions with single doses between 0.6 and 9 Gy were administered in 1.67, 5, 10, 15, and 20 days, Colony growth was monitored for at least 60 days after completion of irradiation, Wells with confluent colonies were considered as ''recurrences'' and wells without colonies as ''controlled.'' The dose required to control 50% of irradiated wells (WCD50) was estimated by a logistic regression for the different overall treatment times, The effective doubling time of clonogenic cells (T-eff), was determined by a direct fit using the maximum likelihood method, Results: The increase of WCD50 within 18.3 days was highly significant for all tumor cell lines accounting for 7.9 and 12.0 Gy in the two glioblastoma cell lines and for 12.7, 14.0, and 21.7 Gy in the three SCC cell lines, The corresponding T(eff)s were 4.4 and 2.0 days for glioblastoma cell lines and 2.4, 4.2, and 1.8 days for SCC cell lines, Population doubling times (PDT) of untreated tumor cells ranged from 1.0 to 1.9 days, showing no correlation with T(eff)s. T-eff was significantly longer than PDT in three of five tumor cell lines, No significant differences were observed comparing glioblastomas and SCC, Increase of WCD50 with time did not correlate with T-eff but with T-eff* InSF2 (surviving fraction at 2 Gy), Conclusion: The intrinsic ability of SCC and glioblastoma cells to repopulate during fractionated irradiation could be demonstrated, Repopulation induced dose loss per day depends on T-eff and intrinsic radiation sensitivity, proliferation during treatment was decelerated compared to pretreatment PDT in the majority of cell lines, Pretreatment cell kinetics did not predict for tumor cell proliferation during treatment. (C) 1997 Elsevier Science Inc. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. FU NCI NIH HHS [CA-13311] NR 28 TC 34 Z9 35 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 1 PY 1997 VL 39 IS 3 BP 743 EP 750 DI 10.1016/S0360-3016(97)00362-3 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA YA917 UT WOS:A1997YA91700031 PM 9336158 ER PT J AU Weiser, MR Pechet, TTV Williams, JP Ma, MH Frenette, PS Moore, FD Kobzik, L Hines, RO Wagner, DD Carroll, MC Hechtman, HB AF Weiser, MR Pechet, TTV Williams, JP Ma, MH Frenette, PS Moore, FD Kobzik, L Hines, RO Wagner, DD Carroll, MC Hechtman, HB TI Experimental murine acid aspiration injury is mediated by neutrophils and the alternative complement pathway SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE complement activation; transgenic mice; inflammation; pneumonia; selectins ID RESPIRATORY-DISTRESS SYNDROME; INDUCED LUNG INJURY; P-SELECTIN; MICE DEFICIENT; EXPRESSION; LEUKOTRIENE-B4; MECHANISMS; EMIGRATION; PULMONARY; INFECTION AB Acid aspiration may result in the development of the acute respiratory distress syndrome, an event associated with significant morbidity and mortality. Although once attributed to direct distal airway injury, the pulmonary failure after acid aspiration is more complex and involves an inflammatory injury mediated by complement (C) and polymorphonuclear leukocytes. This study examines the injurious inflammatory cascades that are activated after acid aspiration. The role of neutrophils was defined by immunodepletion before aspiration, which reduced injury by 59%. The injury was not modified in either P-or E-selectin-knockout mice, indicating that these adhesion molecules were not operative. C activation after aspiration was documented with immunochemistry by C3 deposition on injured alveolar pneumocytes. Animals in which C activation was inhibited with soluble C receptor type 1 (sCR1) had a 54% reduction in injury, similar to the level of protection seen in CS-knockout mice (58%). However C4-knockout mice were not protected from injury, indicating that C activation is mediated by the alternative pathway. Finally, an additive effect of neutrophils and C was demonstrated whereby neutropenic animals that were treated with sCR1 showed an 85% reduction in injury. Thus acid aspiration injury is mediated be neurophils and the alternative C pathway. C1 BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. RI Frenette, Paul/J-8272-2012 FU NIGMS NIH HHS [GM-07560-18, GM-35141-09, GM-52585-01] NR 27 TC 34 Z9 35 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD OCT PY 1997 VL 83 IS 4 BP 1090 EP 1095 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA XZ835 UT WOS:A1997XZ83500008 PM 9338415 ER PT J AU Liu, AM OConnor, DO Harris, WH AF Liu, AM OConnor, DO Harris, WH TI Comparison of cerclage techniques using a hose clamp versus monofilament cerclage wire or cable SO JOURNAL OF ARTHROPLASTY LA English DT Article DE wire; cable; hose damp; cerclage technique; trochanteric osteotomy ID GRIP SYSTEM AB To assess the compressive force generated by different techniques of cerclage wiring, the compression produced by 6 different cerclage techniques, including monofilament wires, Dall-Miles cables (Howmedica, Rutherford, NJ), and hose clamps, was measured. Tests were performed on both a polysulfone cylinder model and a cadaver bone model. The hose clamp generated significantly higher compression force than any other cerclage device tested. Doubled wires produced similar compressive force as the cables. As the hose clamp is the least expensive and produces the maximum compression, it may be advantageous in instances in which maximum compression is desirable as a temporary device, but because it is not implantable, it must be replaced by other techniques prior to wound closure. The Dall-Miles cable is expensive and its compressive force can be equaled at lower cost by a doubled wire. The use of a single strand of monofilament wire was the least effective. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. NR 7 TC 7 Z9 7 U1 0 U2 1 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0883-5403 J9 J ARTHROPLASTY JI J. Arthroplast. PD OCT PY 1997 VL 12 IS 7 BP 772 EP 776 DI 10.1016/S0883-5403(97)90007-3 PG 5 WC Orthopedics SC Orthopedics GA YB802 UT WOS:A1997YB80200008 PM 9355006 ER PT J AU Pal, L Shifren, JL Isaacson, KB Chang, YC Marean, M Leykin, L Toth, TL AF Pal, L Shifren, JL Isaacson, KB Chang, YC Marean, M Leykin, L Toth, TL TI Outcome of IVF in DES-exposed daughters: Experience in the 90s SO JOURNAL OF ASSISTED REPRODUCTION AND GENETICS LA English DT Article DE diethylstilbestrol; infertility; in vitro fertilization; implantation; pregnancy; assisted reproduction ID INVITRO FERTILIZATION; DIETHYLSTILBESTROL; ENDOMETRIUM; WOMEN; IMPLANTATION; CYCLES AB Purpose: The outcome of in vitro fertilization (IVF) in a group of infertile women with a history of in utero exposure to diethylstilbestrol (DES) was analyzed. Records from an academic NF program were retrospectively reviewed. Methods: Seventeen infertile women with a self-reported history of exposure to DES in utero, attending the NF unit at Massachusetts General Hospital (MGH) for assisted reproductive technology (ART), underwent 27 NF cycles. Analysis of the outcome of NF including implantation and ongoing pregnancy rates was performed. The data were compared with results from a group of 20 infertile patients with idiopathic infertility undergoing 27 NF cycles at MGH during the same period. The patients in the two groups were matched for age, basal day 3 levels of follicle stimulating hormone and serum estradiol, and the number and quality of embryos transferred, Results: The response to controlled ovarian hyperstimulation was comparable in the two groups, Significantly lower implantation and ongoing pregnancy rates following IVF and embryo transfer were seen in the utero DES-exposed group compared to the control patients. Conclusions: Infertile patients with a history of in utero exposure to DES exhibit a significantly impaired implantation rate following IVE and the outcome of ART remains poor. RP Pal, L (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,IVF UNIT,DIV REPROD ENDOCRINOL & INFERTIL,VBK 2,BOSTON,MA 02114, USA. NR 18 TC 8 Z9 8 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 1058-0468 J9 J ASSIST REPROD GEN JI J. Assist. Reprod. Genet. PD OCT PY 1997 VL 14 IS 9 BP 513 EP 517 DI 10.1023/A:1021175326230 PG 5 WC Genetics & Heredity; Obstetrics & Gynecology; Reproductive Biology SC Genetics & Heredity; Obstetrics & Gynecology; Reproductive Biology GA YH534 UT WOS:A1997YH53400008 PM 9401869 ER PT J AU Hashim, SR Fontaine, A He, SQ Levine, RA Yoganathan, AP AF Hashim, SR Fontaine, A He, SQ Levine, RA Yoganathan, AP TI A three-component force vector cell for in vitro quantification of the force exerted by the papillary muscle on the left ventricular wall SO JOURNAL OF BIOMECHANICS LA English DT Article DE mitral valve; regurgitation; tethering force; coapting force; papillary muscles AB Recent clinical studies indicate that functional mitral regurgitation, which is a common complication in patients who suffer from ischemic heart disease, is related to an increase in the tethering forces acting on the mitral valve leaflets. Alterations in the valvular assembly, displacement of the papillary muscles or dilatation of the mitral valve annulus can disrupt the normal force balance on the mitral leaflets and result in an abnormal coaptation geometry with incomplete mitral leaflet closure. The force balance imposed on the mitral leaflets is created by the coapting forces generated by the transmitral pressure difference and the tethering forces at the leaflet attachments. A unique force vector cell capable of accurately measuring the three-component force vector applied by the papillary muscle on the left-ventricular wall was designed and manufactured to permit quantification of the alteration in the force balance acting on the mitral leaflets, and to allow for the study of the influence of papillary muscle displacement on mitral regurgitation. (C) 1997 Elsevier Science Ltd. C1 GEORGIA INST TECHNOL,SCH CHEM ENGN,CARDIOVASC FLUID MECH LAB,ATLANTA,GA 30332. GEORGIA INST TECHNOL,INST BIOENGN & BIOSCI,ATLANTA,GA 30332. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 8 TC 9 Z9 10 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9290 J9 J BIOMECH JI J. Biomech. PD OCT PY 1997 VL 30 IS 10 BP 1071 EP 1075 DI 10.1016/S0021-9290(97)00066-3 PG 5 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA YF899 UT WOS:A1997YF89900010 PM 9391876 ER PT J AU Weiss, MA Ukiyama, E King, CY AF Weiss, MA Ukiyama, E King, CY TI The SRY cantilever motif discriminates between sequence- and structure-specific DNA recognition: Alanine mutagenesis of an HMG box SO JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS LA English DT Article ID BINDING PROPERTIES; CRYSTAL-STRUCTURE; MOLECULAR-BASIS; MINOR-GROOVE; DOMAIN; TRANSCRIPTION; JUNCTION; PROTEIN; COMPLEXES; MECHANISM AB The high-mobility-group (HMG) box defines a DNA-bending motif conserved among architectural transcription factors. A ''hydrophobic wedge'' at the protein surface provides a mechanism of DNA bending: disruption of base stacking by insertion of a sidechain ''cantilever.'' First described in the mammalian testis-determining factor SRY, the cantilever motif consists of adjacent aromatic and nonpolar sidechains at the crux of the HMG box (residues 12 and 13). Here, the role of these side chains in DNA recognition is investigated by alanine mutagenesis. F12A and I13A substitutions in the SRY HMG box each permit native folding and thermal stability (as monitored by circular dichroism and H-1-NMR) but eliminate sequence-specific DNA-binding activity (as detected by gel-mobility shift). On binding to the sharp angles of a four-way DNA junction (4WJ), however, the substitutions each promote formation of a high-molecular-weight aggregate, presumably by DNA-dependent oligomerization. The substitutions have opposite effects on initial binding to the 4WJ: whereas such binding is attenuated ten-fold by F12A, it is enhanced by I13A. A foreshortened ''alanine cantilever'', not observed among specific HMG boxes, occurs in a non-specific domain (HMG-1A) and may enhance architecture-selective DNA recognition. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. RP Weiss, MA (reprint author), UNIV CHICAGO,DEPT BIOCHEM & MOL BIOL & CHEM,CHICAGO,IL 60637, USA. NR 32 TC 13 Z9 13 U1 0 U2 1 PU ADENINE PRESS INC PI GUILDERLAND PA PO BOX 355/340, GUILDERLAND, NY 12084 SN 0739-1102 J9 J BIOMOL STRUCT DYN JI J. Biomol. Struct. Dyn. PD OCT PY 1997 VL 15 IS 2 BP 177 EP 184 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA YH369 UT WOS:A1997YH36900004 PM 9399148 ER PT J AU Toma, CD Ashkar, S Gray, ML Schaffer, JL Gerstenfeld, LC AF Toma, CD Ashkar, S Gray, ML Schaffer, JL Gerstenfeld, LC TI Signal transduction of mechanical stimuli is dependent on microfilament integrity: Identification of osteopontin as a mechanically induced gene in osteoblasts SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID 44-KILODALTON BONE PHOSPHOPROTEIN; EXTRACELLULAR-MATRIX; CHICKEN OSTEOPONTIN; EMBRYONIC CHICK; CELL-SURFACE; EXPRESSION; SIALOPROTEIN; PATHWAYS; STRAIN; RNA AB Mechanical perturbation has been shown to modulate a wide variety of changes in second message signals and patterns of gene expression in osteoblasts. Embryonic chick osteoblasts were subjected to a dynamic spatially uniform biaxial strain (1.3% applied strain) at 0.25 Hz for a single 2-h period, and osteopontin (OPN), an Arg-Gly-Asp (RGD)-containing protein, was shown to be a mechanoresponsive gene. Expression of opn mRNA reached a maximal 4-fold increase 9 h after the end of the mechanical perturbation that was not inhibited by cycloheximide, thus demonstrating that mechanoinduction of opn expression is a primary response through the activation of pre-existing transcriptional factors, The signal transduction pathways, which mediated the increased expression of opn in response to mechanical stimuli, were shown to be dependent on the activation of a tyrosine kinase(s) and protein kinase A (PKA) or a PKA-like kinase, Selective inhibition of protein kinase C (PKC) had no effect on the mechanoinduction of osteopontin even though opn has been demonstrated to be an early response gene to phorbol 12-myristate 13-acetate (PMA) stimulation, Mechanotransduction was dependent on microfilament integrity since cytochalasin-D blocked the up-regulation of the opn expression; however, microfilament disruption had no effect on the PMA induction of the gene, The microtubule component of the cytoskeleton was not related to the mechanism of signal transduction involved in controlling opn expression in response to mechanical stimulation since colchicine did not block opn expression. Mechanical stimulus,vas shown to activate focal adhesion kinase (FAK), which specifically became associated with the cytoskeleton after mechanical perturbation, and its association with the cytoskeleton was dependent on tyrosine kinase activity, In conclusion, these results demonstrate that the signal transduction pathway for mechanical activation of opn is uniquely dependent on the structural integrity of the microfilament component of the cytoskeleton, In contrast, the PKC pathway, which also activates this gene in osteoblasts, acts independently of the cytoskeleton in the transduction of its activity. C1 CHILDRENS HOSP,LAB STUDY SKELETAL DISORDERS & REHABIL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02115. MIT,HARVARD MIT DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02139. MIT,ARTHRIT UNIT,MASSACHUSETTS GEN HOSP,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. OI /0000-0002-0477-1211 NR 72 TC 130 Z9 137 U1 0 U2 3 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD OCT PY 1997 VL 12 IS 10 BP 1626 EP 1636 DI 10.1359/jbmr.1997.12.10.1626 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XY467 UT WOS:A1997XY46700011 PM 9333123 ER PT J AU Silver, K Walston, J Plotnick, L Taylor, SI Kahn, CR Shuldiner, AR AF Silver, K Walston, J Plotnick, L Taylor, SI Kahn, CR Shuldiner, AR TI Molecular scanning of beta-3-adrenergic receptor gene in total congenital lipoatrophic diabetes mellitus SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID INSULIN-RECEPTOR; THERMOGENESIS; MUTATIONS AB Total congenital lipoatrophic diabetes is characterized by absence of subcutaneous adipose tissue, hypertriglyceridemia, and insulin resistance. We hypothesized that mutations in the beta-3-adrenergic receptor (beta 3AR) gene might result in the lipoatrophic phenotype by preventing triglyceride storage in adipocytes; thereby, resulting in secondary insulin resistance. We screened the beta 3AR gene in 7 subjects with total congenital lipoatropic diabetes. We found a heterozygous substitution of a guanine to cytosine at position -153 (G-153C) in the 5'-untranslated region of 3 African-American lipoatrophic siblings and 1 sibling without lipoatrophy but with insulin resistance. To determine whether the base change was related to the lipoatrophic phenotype, we genotyped 69 African-Americans without lipoatrophy and found the G-153C substitution in 2 control subjects (allele frequency = 0.01). No other single-stranded polymorphism variants were found in any of the 7 lipoatrophic subjects. Direct sequencing of both alleles of 1 lipoatrophic subject demonstrated a thymidine insertion at position -300 in both alleles. All lipoatrophic subjects along with 20 African-American control subjects were homozygous for the base insertion, suggesting an error in the published sequence. In conclusion, mutations in the beta 3AR gene do not appear to be involved in the development of congenital total lipoatrophy. C1 JOHNS HOPKINS UNIV, SCH MED, DIV ENDOCRINOL & METAB, BALTIMORE, MD 21287 USA. JOHNS HOPKINS UNIV, SCH MED, DIV GERIATR MED & GERONTOL, BALTIMORE, MD 21287 USA. JOHNS HOPKINS UNIV, SCH MED, DIV PEDIAT ENDOCRINOL, BALTIMORE, MD 21287 USA. NIDDKD, DIABET BRANCH, NIH, BETHESDA, MD 20892 USA. JOSLIN DIABET CTR, BOSTON, MA 02215 USA. FU NIDDK NIH HHS [1F32DK09340-01] NR 16 TC 10 Z9 11 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 OCT PY 1997 VL 82 IS 10 BP 3395 EP 3398 DI 10.1210/jc.82.10.3395 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YA002 UT WOS:A1997YA00200042 PM 9329375 ER PT J AU Asch, DA Jedrziewski, MK Christakis, NA AF Asch, DA Jedrziewski, MK Christakis, NA TI Response rates to mail surveys published in medical journals SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE cost-effectiveness; data collection; epidemiology; financial incentives; health services research; mailed survey; research design; response bias; survey methods ID INCENTIVES; NONRESPONDENTS; METAANALYSIS; STRATEGIES; BEHAVIOR; BIAS AB Objective. The purpose of this study was to characterize response rates for mail surveys published in medical journals; to determine how the response rate among subjects who are typical targets of mail surveys varies; and to evaluate the contribution of several techniques used by investigators to enhance response rates. Methods. One hundred seventy-eight manuscripts published in 1991, representing 321 distinct mail surveys, were abstracted to determine response rates and survey techniques. In a follow-up mail survey, 113 authors of these manuscripts provided supplementary information. Results. The mean response rate among mail surveys published in medical journals is approximately 60%. However, response rates vary according to subject studied and techniques used. Published surveys of physicians have a mean response rate of only 54%, and those of non-physicians have a mean response rate of 68%. In addition, multivariable models suggest that written reminders provided with a copy of the instrument and telephone reminders are each associated with response rates about 13% higher than surveys that do not use these techniques. Other techniques, such as anonymity and financial incentives, are not associated with higher response rates. Conclusions. Although several mail survey techniques are associated with higher response rates, response rates to published mail surveys tend to be moderate. However, a survey's response rate is at best an indirect indication of the extent of non-respondent bias. Investigators, journal editors, and readers should devote more attention to assessments of bias, and less to specific response rate thresholds. (C) 1997 Elsevier Science Inc. C1 UNIV CHICAGO,DEPT SOCIOL,CHICAGO,IL 60637. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DIV GEN INTERNAL MED,PHILADELPHIA,PA 19104. RP Asch, DA (reprint author), UNIV CHICAGO,MED CTR,DIV GEN INTERNAL MED,GEN INTERNAL MED SECT,5841 S MARYLAND AVE,MC 6098,CHICAGO,IL 60637, USA. RI Christakis, Nicholas/B-6690-2008; Christakis, Nicholas/C-3205-2009 NR 19 TC 1336 Z9 1344 U1 1 U2 40 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD OCT PY 1997 VL 50 IS 10 BP 1129 EP 1136 DI 10.1016/S0895-4356(97)00126-1 PG 8 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA YA673 UT WOS:A1997YA67300008 PM 9368521 ER PT J AU Okuda, K DAndrea, A VanEtten, RA Griffin, JD AF Okuda, K DAndrea, A VanEtten, RA Griffin, JD TI A chimeric receptor/oncogene that can be regulated by a ligand in vitro and in vivo SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE chronic myelogenous leukemia; BCR/ABL; oncogene; erythropoietin ID CHRONIC MYELOGENOUS LEUKEMIA; HEMATOPOIETIC-CELL LINES; CHRONIC MYELOID-LEUKEMIA; ABL TYROSINE KINASE; FOCAL ADHESION PROTEINS; ERYTHROPOIETIN RECEPTOR; C-ABL; PHILADELPHIA-CHROMOSOME; SIGNAL-TRANSDUCTION; BCR GENE AB The BCR/ABL oncogene encodes an activated tyrosine kinase that causes human chronic myelogenous leukemia. The mechanism of transformation, however, is complex and not well understood, One of the important contributions of BCR to transformation is believed to be dimerization or oligomerization of ABL, thereby activating ABL tyrosine kinase activity, We reasoned that if ABL was dimerized through other mechanisms, activation of the tyrosine kinase activity should also result, and the activated kinase may also be transforming, Erythropoietin is known to activate its receptor by causing dimerization, and therefore a synthetic oncogene was created by linking the extracytoplasmic and transmembrane domains of the EPO receptor with c-ABL, This chimeric receptor was stably expressed in Ba/F3 cells and, in the absence of EPO, had no detectable biological effect on the cells, EPO, however, induced a rapid, dose-dependent activation of ABL tyrosine kinase activity and phosphorylation of several cellular proteins, The major target proteins have been identified, and are very similar to the known substrates of BCR/ABL, including Shc, CBL, CRKL, and several proteins in the cytoskeleton, EPO treatment also resulted in biological effects that were remarkably similar to those of BCR/ABL, including improved viability, altered integrin function, and a weak mitogenic signal, The biological effects were in part dose-dependent, in that low EPO concentrations enhanced viability but did not cause proliferation. At high EPO doses, kinase activation was maximal, and a mitogenic effect was also revealed, In nude mice, Ba/F3 cells expressing this chimeric receptor did not cause detectable disease-without administration of pharmacologic doses of EPO, If EPO was given intraperitoneally 5 days a week, however, a dose-dependent lethal leukemia resulted, This ligand-regulatable oncogene mimics some of the biological effects of BCR/ABL, and analysis of ABL mutants in this system will be useful to dissect the signaling pathways that cause CML. C1 CHILDRENS HOSP,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. CHILDRENS HOSP,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA66996]; NIDDK NIH HHS [DK560654] NR 50 TC 8 Z9 8 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT 1 PY 1997 VL 100 IS 7 BP 1708 EP 1715 DI 10.1172/JCI119695 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YA424 UT WOS:A1997YA42400006 PM 9312168 ER PT J AU Gukovskaya, AS Gukovsky, I Zaninovic, V Song, M Sandoval, D Gukovsky, S Pandol, SJ AF Gukovskaya, AS Gukovsky, I Zaninovic, V Song, M Sandoval, D Gukovsky, S Pandol, SJ TI Pancreatic acinar cells produce, release, and respond to tumor necrosis factor-alpha - Role in regulating cell death and pancreatitis SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE TNF alpha; apoptosis; NF-kappa B; TNF alpha receptor; pancreatitis ID PLATELET-ACTIVATING-FACTOR; NF-KAPPA-B; TNF-ALPHA; MONOCLONAL-ANTIBODIES; MOLECULAR MECHANISMS; FACTOR RECEPTORS; EXPRESSION; APOPTOSIS; CYTOKINE; RAT AB The aim of this study was to determine whether tumor necrosis factor-alpha (TNF alpha) and receptors for TNF alpha are expressed in the exocrine pancreas, and whether pancreatic acinar cells release and respond to TNF alpha. Reverse transcription PCR, immunoprecipitation, and Western blot analysis demonstrated the presence of TNF alpha and 55- and 75-kD TNF alpha receptors in pancreas from control rats, rats with experimental pancreatitis induced by supramaximal doses of cerulein, and in isolated pancreatic acini. Immunohistochemistry showed TNF alpha presence in pancreatic acinar cells. ELISA and bioassay measurements of TNF alpha indicated its release from pancreatic acinar cells during incubation in primary culture. Acinar cells responded to TNF alpha. TNF alpha potentiated NF-kappa B translocation into the nucleus and stimulated apoptosis in isolated acini while not affecting LDH release, In vivo studies demonstrated that neutralization of TNF alpha with an antibody produced a mild improvement in the parameters of cerulein-induced pancreatitis. However, TNF alpha neutralization greatly inhibited apoptosis in a modification of the cerulein model of pancreatitis which is associated with a high percentage of apoptotic cell death. The results indicate that pancreatic acinar cells produce, release, and respond to TNF alpha. This cytokine regulates apoptosis in both isolated pancreatic acini and experimental pancreatitis. C1 UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90073. RP Gukovskaya, AS (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,BLDG 258,ROOM 340,LOS ANGELES,CA 90073, USA. NR 56 TC 270 Z9 279 U1 2 U2 10 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT 1 PY 1997 VL 100 IS 7 BP 1853 EP 1862 DI 10.1172/JCI119714 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YA424 UT WOS:A1997YA42400025 PM 9312187 ER PT J AU Peraldi, P Xu, M Spiegelman, BM AF Peraldi, P Xu, M Spiegelman, BM TI Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE insulin resistance; insulin signaling; antidiabetic drugs; NIDDM adipocytes ID ACTIVATED RECEPTOR-GAMMA; TYROSINE KINASE-ACTIVITY; PHOSPHATIDYLINOSITOL 3-KINASE; 3T3-L1 ADIPOCYTES; GENE-EXPRESSION; TNF-ALPHA; GLUCOSE-TOLERANCE; ADIPOSE-TISSUE; AGENT CS-045; RESISTANCE AB TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity, This cytokine induces insulin resistance, at least in part, through inhibition of the tyrosine kinase activity of the insulin receptor. Recently, a new class of compounds, the antidiabetic thiazolidinediones (TZDs), has been shown to improve insulin resistance in obesity and non-insulin-dependent diabetes mellitus in both rodents and man, Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). That this effect of TZDs operates through activation of the nuclear receptor PPAR gamma/RXR complex is shown by the fact that similar effects are observed with other PPAR gamma/RXR ligands such as 15 deoxy Delta(12,14)PGJ2 and LG268. The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. RI Peraldi, Pascal/O-4592-2016 OI Peraldi, Pascal/0000-0003-0205-9252 FU NIDDK NIH HHS [DK 42539] NR 48 TC 248 Z9 259 U1 1 U2 5 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD OCT 1 PY 1997 VL 100 IS 7 BP 1863 EP 1869 DI 10.1172/JCI119715 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YA424 UT WOS:A1997YA42400026 PM 9312188 ER PT J AU ElZimaity, HMT Itani, K Graham, DY AF ElZimaity, HMT Itani, K Graham, DY TI Early diagnosis of signet ring cell carcinoma of the stomach: role of the Genta stain SO JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE signet ring cell; Genta stain; gastric carcinoma; early diagnosis ID GASTRIC-CARCINOMA; YOUNG AB Signet ring cell carcinoma is a poorly differentiated adenocarcinoma in which the tumour cells invade singly or in small groups. Early stages of the disease can be missed easily when using regular haematoxylin and eosin staining. This is a report of a case in which routine screening of gastric biopsies with the Genta stain was responsible for rapid identification of signet ring carcinoma. The patient, a 29 year old woman, had a large portion of the antrum excised surgically for signet ring cell gastric carcinoma. Follow up endoscopy six years later showed no evidence of tumour. Twenty six large cup biopsies were obtained and a single focus of signet ring tumour cells infiltrating the surface mucosa in single files was seen. The diagnosis was missed on haematoxylin and eosin stain by three senior pathologists but owing to the Alcian blue component of the Genta stain the tumour cells were recognised easily. Thus, the Genta stain not only facilitates detection of Helicobacter pylori but also allows for simultaneous visualisation of gastric morphology as well as signet ring carcinoma that can be missed with conventional stains. C1 BAYLOR COLL MED,VA MED CTR,DEPT SURG,HOUSTON,TX 77030. RP ElZimaity, HMT (reprint author), BAYLOR COLL MED,VA MED CTR 111D,DEPT MED,2002 HOLCOMBE BLVD,ROOM 3A352,HOUSTON,TX 77030, USA. NR 14 TC 13 Z9 14 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0021-9746 J9 J CLIN PATHOL JI J. Clin. Pathol. PD OCT PY 1997 VL 50 IS 10 BP 867 EP 868 DI 10.1136/jcp.50.10.867 PG 2 WC Pathology SC Pathology GA YC587 UT WOS:A1997YC58700017 PM 9462273 ER PT J AU Haffajee, AD Cugini, MA Dibart, S Smith, C Kent, RL Socransky, SS AF Haffajee, AD Cugini, MA Dibart, S Smith, C Kent, RL Socransky, SS TI Clinical and microbiological features of subjects with adult periodontitis who responded poorly to scaling and root planing SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE periodontal diseases; periodontitis; treatment; scaling and root planing; microbiology ID LOCALIZED JUVENILE PERIODONTITIS; ACTINOMYCETEMCOMITANS-ASSOCIATED PERIODONTITIS; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; REFRACTORY PERIODONTITIS; SYSTEMIC TETRACYCLINE; TOOTH LOSS; LONG-TERM; THERAPY; METRONIDAZOLE; SUPPRESSION AB In a previous report, it was shown that scaling and root planing (SRP) decreased mean pocket depth and attachment level in subjects with adult periodontitis, as well as the levels and prevalence of Bacteroides forsythus, Porphyromonas gingivalis and Treponema denticola. However, a subset of subjects in that study exhibited mean loss of attachment following SRP. The purpose of the present investigation was to seek clinical and microbiological differences between subjects who responded well or poorly to SRP. 57 subjects with adult periodontitis were treated by full-mouth SRP under local anaesthetic. Clinical assessments of plaque, redness, suppuration, BOP, pocket depth and attachment level were made at 6 sites per tooth prior to and 3 months post-SRP. Attachment level measurements were repeated at each visit and differences in means between visits used to assess change. 18 subjects showed mean attachment loss 3 months post-SRP (poor response group), while 39 showed mean attachment level gain (good response group). The prevalence and levels of 40 subgingival taxa in subgingival plaque samples from the mesiobuccal site of each tooth (maximum 28 sites) in each subject prior to and 3 months post-SRP were assessed using checkerboard DNA-DNA hybridization. The prevalence of each species was computed for each subject and averaged across subjects in the 2 treatment-response groups at each visit. Differences between groups were sought using the Mann-Whitney test. There were no statistically significant differences between the 2 response groups in any clinical parameter prior to therapy. Subjects in the good response group showed more attachment level gain at sites with baseline pocket depths of <4 mm, 4-6 and >6 mm than poor response subjects. Of 40 species evaluated, A. naeslundii genospecies 2 (A. viscosus), T. denticola, C. gracilis and C. rectus were significantly higher and more prevalent pre-therapy in the good response subjects. Mean attachment level change post SRP could be predicted using multiple linear regression with A. naeslundii genospecies 2 (A. viscosus) and T. denticola as the predictor variables (r(2)=0.373, p<0.00001). Sites that gained >2 mm of attachment post therapy showed a significant decrease in the counts of P. gingivalis (7.5+/-3.5 to 0.2+/-0.2x10(5)), T. denticola (8.2+/-3.5 to 1.8+/-1.1x10(5)) and B. forsythus (11.1+/-5.7 to 0.3+/-0.2x10(5)). The data of the present investigation indicate that SRP is most effective in subjects and sites with high levels of the subgingival species that this therapy affects. C1 FORSYTH DENT CTR,DEPT BIOSTAT,BOSTON,MA 02115. RP Haffajee, AD (reprint author), FORSYTH DENT CTR,DEPT PERIODONTOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-04881] NR 27 TC 64 Z9 69 U1 0 U2 5 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD OCT PY 1997 VL 24 IS 10 BP 767 EP 776 DI 10.1111/j.1600-051X.1997.tb00195.x PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA XY261 UT WOS:A1997XY26100009 PM 9350562 ER PT J AU Rosenbaum, JF Moroz, G Bowden, CL AF Rosenbaum, JF Moroz, G Bowden, CL TI Clonazepam in the treatment of panic disorder with or without agoraphobia: A dose-response study of efficacy, safety, and discontinuance SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID BENZODIAZEPINE TREATMENT; DOUBLE-BLIND; SHORT-TERM; ALPRAZOLAM; PLASMA; TRIAL AB In this multicenter, parallel-group, placebo-controlled fixed-dose study, the efficacy, safety, dosing characteristics, and discontinuation of clonazepam were analyzed in patients with panic disorder. Four hundred thirteen patients were randomly assigned to receive placebo or one of five fixed daily dosages of clonazepam (0.5 mg;, 1.0 mg, 2.0 mg, 3.0 mg, and 4.0 mg). After 3 weeks of dose escalation, the fixed dose was given for 6 weeks (the dose-maintenance phase) and then was tapered during a 7-week discontinuance phase. The completion rates for the dose-maintenance phase ranged from 59 to 85%, for the clonazepam groups (74% for the placebo group). Efficacy measurements at the end of the dose-maintenance phase indicated clinical improvement in all treatment groups but with a clear differentiation of the four higher doses of clonazepam horn the 0.5-mg dose and placebo. The minimum effective dosage, as determined by the Williams' test, was 1.0 mg daily. Dose-response analysis showed that daily dosages of 1.0 mg and higher were equally efficacious in reducing the number of panic attacks. All treatments mere well tolerated. Somnolence and ataxia were reported more often by patients in the 3.0- and 4.0-mg groups; depression, dizziness, fatigue, and irritability, although not showing dose-relatedness, were reported by more patients taking clonazepam than placebo. During the discontinuance phase, most patients worsened from their condition at the end of the dose-maintenance phase but did not revert to that at baseline. In addition, with the tapering schedule chosen for this study, patients in all treatment groups tolerated the discontinuance of clonazepam. Daily dosages of 1.0 to 2.0 mg of clonazepam offered the best balance of therapeutic benefit and tolerability. C1 HOFFMANN LA ROCHE INC, DEPT CLIN SCI, NUTLEY, NJ 07110 USA. UNIV TEXAS, HLTH SCI CTR, DEPT PSYCHIAT, SAN ANTONIO, TX USA. RP Rosenbaum, JF (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT PSYCHIAT, 15 PARKMAN ST, BOSTON, MA 02114 USA. RI Maddock, Richard/F-3761-2012 NR 27 TC 49 Z9 52 U1 0 U2 6 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD OCT PY 1997 VL 17 IS 5 BP 390 EP 400 DI 10.1097/00004714-199710000-00008 PG 11 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA XY987 UT WOS:A1997XY98700009 PM 9315990 ER PT J AU Greene, RW Biederman, J Faraone, SV Sienna, M GarciaJetton, J AF Greene, RW Biederman, J Faraone, SV Sienna, M GarciaJetton, J TI Adolescent outcome of boys with attention-deficit/hyperactivity disorder and social disability: Results from a 4-year longitudinal follow-up study SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT 43rd Annual Meeting of the American-Academy-of-Child-and-Adolescent-Psychiatry CY 1996 CL PHILADELPHIA, PA SP Amer Acad Child & Adolescent Psychiat ID DEFICIT HYPERACTIVITY DISORDER; PSYCHIATRIC-DISORDERS; LEARNING-DISABILITIES; ADJUSTMENT INVENTORY; SOCIOMETRIC STATUS; RESEARCH CRITERIA; RIGHT-HEMISPHERE; PEER RELATIONS; CHILDREN; MECHANISMS AB IQ-achievement discrepancy methodology similar to that used in defining learning disabilities has recently been used to identify a subset of boys with attention-deficit/hyperactivity disorder (ADHD) evidencing marked impairment in social functioning. In this study, 2 issues were examined: (a) What is the longitudinal outcome of boys with ADHD identified at baseline as ''socially disabled''? (b) Is social disability at baseline a significant predictor of severe long-term outcomes (such as substance use disorders) in bogs with ADHD? if so, are its predictive relationships accounted for by renditions that are comorbid with ADI-LD? Results showed that, at follow-up, boys with ADHD who also had social disability evidenced significantly higher rates of mood, anxiety, disruptive, and substance use disorders, compared with nonsocially disabled boys with ADHD and comparison boys without ADHD. Findings also showed that social disability at baseline in boys with ADHD was a significant predictor of later conduct disorder and most substance use disorders after baseline mood and conduct disorders and behavior checklist ratings of aggressive behavior and attention problems were controlled. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Greene, RW (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,ACC-75,BOSTON,MA 02114, USA. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01 MH-41314-01A2] NR 53 TC 108 Z9 110 U1 0 U2 8 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0022-006X J9 J CONSULT CLIN PSYCH JI J. Consult. Clin. Psychol. PD OCT PY 1997 VL 65 IS 5 BP 758 EP 767 DI 10.1037/0022-006X.65.5.758 PG 10 WC Psychology, Clinical SC Psychology GA YA397 UT WOS:A1997YA39700007 PM 9337495 ER PT J AU Bostic, JQ Muriel, AC Hack, S Weinstein, S Herzog, D AF Bostic, JQ Muriel, AC Hack, S Weinstein, S Herzog, D TI Anorexia nervosa in a 7-year-old girl SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE anorexia nervosa; childhood eating disorders ID EATING DISORDERS; BULIMIA NERVOSA; ONSET; SCHOOL; ADOLESCENCE; POPULATION; ATTITUDES; FEATURES; THINNESS AB We report on a 7-year-old girl with anorexia nervosa and consider factors contributing to this early emergence. Cognitive differences in younger children can alter their understanding of this illness, so we chronicled this girl's treatment because it diverged from practices used with older patients. Accordingly, effective interventions in very young anorexics might require modifications of treatments used in postpubertal populations. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. BELLEVUE MED CTR,DEPT PSYCHIAT,NEW YORK,NY. NYU,NEW YORK,NY. MCLEAN HOSP,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,BOSTON,MA 02114. RP Bostic, JQ (reprint author), MASSACHUSETTS GEN HOSP,DEPT CHILD PSYCHIAT,15 PARKMAN ST,WAC 725,BOSTON,MA 02114, USA. NR 35 TC 4 Z9 4 U1 2 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD OCT PY 1997 VL 18 IS 5 BP 331 EP 333 DI 10.1097/00004703-199710000-00008 PG 3 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA YA865 UT WOS:A1997YA86500008 PM 9349976 ER PT J AU Wands, JR Geissler, M Putlitz, JZU Blum, H VonWeizsacker, F Mohr, L Yoon, SK Melegari, M Scaglioni, PP AF Wands, JR Geissler, M Putlitz, JZU Blum, H VonWeizsacker, F Mohr, L Yoon, SK Melegari, M Scaglioni, PP TI Nucleic acid-based antiviral and gene therapy of chronic hepatitis B infection SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY LA English DT Article; Proceedings Paper CT International Symposium on Hepatology CY 1996 CL TAIPEI, TAIWAN DE antisense RNA and DNA; gene therapy; viral hepatitis B ID HUMAN-IMMUNODEFICIENCY-VIRUS; CYTOTOXIC T-LYMPHOCYTES; ANTISENSE OLIGODEOXYNUCLEOTIDES; SURFACE-ANTIGEN; DNA VACCINATION; RNA ENZYMES; IMMUNE-RESPONSES; TRANSGENIC MICE; REPLICATION; INHIBITION AB Persistent hepatitis B virus (HBV) infection often leads to the development of chronic hepatitis, cirrhosis and hepatocellular carcinoma. There is a need to develop new antiviral approaches for the treatment of this disease. We have explored various nucleic acid-based strategies designed to inhibit HBV replication including: the use of antisense RNA and DNA constructs, DNA-based immunization techniques to stimulate broad-based cellular immune responses with particular emphasis on the generation of cytotoxic lymphocyte (CTL) activity to viral structural proteins, hammerhead ribozymes to cleave HBV pregenomic RNA in vitro and dominant negative HBV core mutant proteins as inhibitors of nucleocapsid Formation within cells. In order to optimize these antiviral effects, various novel expression vectors have been developed to deliver such DNA constructs to cells. For example, adenoviral vectors carrying genes that encode far dominant negative proteins have been employed to transfect hepatocytes in vitro and in vivo. In addition, plasmid vectors have been produced to promote expression of HBV structural genes following injection into muscle cells as a means to stimulate the host's cellular and humoral immune response in the context of histocompatibility antigen (HLA) class I and II antigen presentation, These experimental approaches may have important implications for the generation of efficient antiviral effect during chronic HBV infection. C1 HARVARD UNIV,SCH MED,CHARLESTOWN,MA. UNIV FREIBURG,MED KLIN,INNERE MED ABT 2,D-7800 FREIBURG,GERMANY. RP Wands, JR (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOL HEPATOL LAB,149 13TH ST,CHARLESTOWN,MA 02129, USA. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-02169] NR 68 TC 23 Z9 26 U1 0 U2 0 PU BLACKWELL SCIENCE PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON VICTORIA 3053, AUSTRALIA SN 0815-9319 J9 J GASTROEN HEPATOL JI J. Gastroenterol. Hepatol. PD OCT PY 1997 VL 12 IS 9-10 BP S354 EP S369 DI 10.1111/j.1440-1746.1997.tb00521.x PG 16 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YK841 UT WOS:A1997YK84100038 PM 9407358 ER PT J AU Mendez, MF Perryman, KM Miller, BL Swartz, JR Cummings, JL AF Mendez, MF Perryman, KM Miller, BL Swartz, JR Cummings, JL TI Compulsive behaviors as presenting symptoms of frontotemporal dementia SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID FRONTAL-LOBE DEMENTIA; CEREBRAL BLOOD-FLOW; NON-ALZHEIMER TYPE; CAUDATE-NUCLEUS; PICKS-DISEASE; DISORDER; DEGENERATION; PROVOCATION; SPECT; SCALE AB Frontotemporal dementia (FTD) is a common neurodegenerative dementia syndrome. Compulsive behaviors frequently occur in FTD and may be presenting symptoms of this disorder. This study evaluated compulsive behaviors as presenting symptoms in 29 patients with FTD compared to 48 patients with Alzheimer's disease (ADI enrolled in the UCLA Alzheimer's Disease Center, The FTD patients met the Lund and Manchester criteria for FTD and had predominant frontal hypoperfusion on single-photon emission computer tomography neuroimaging. The AD patients met National Institute of Neurological and Communicative Disorders-Alzheimer's Disease and Related Disorders criteria for clinically probable AD. Compulsive behaviors occurred in 11 FTD patients (38%) versus 5 AD patients (10%) (chi(2) = 6.73, P < .01). This difference persisted after controlling for the younger age of the FTD group. There was a range of compulsive behaviors, with the most frequent being repetitive checking activities. Compulsive behaviors are common presenting symptoms among FTD patients and may result from an inability to inhibit urges to perform compulsive movements from damage to frontal-striatal circuits. C1 W Los Angeles Vet Affairs Med Ctr, Neurobehav Unit 691 116AF, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Harbor UCLA Med Ctr, Los Angeles, CA USA. RP Mendez, MF (reprint author), W Los Angeles Vet Affairs Med Ctr, Neurobehav Unit 691 116AF, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA. FU NIA NIH HHS [AG10123] NR 41 TC 49 Z9 49 U1 0 U2 2 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD OCT PY 1997 VL 10 IS 4 BP 154 EP 157 PG 4 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA YQ720 UT WOS:000071416500004 PM 9453681 ER PT J AU Pascualy, M Tsuang, D Shores, M Agustin, C Krause, E Spain, W Bird, T Peskind, E AF Pascualy, M Tsuang, D Shores, M Agustin, C Krause, E Spain, W Bird, T Peskind, E TI Frontal-complex partial status epilepticus misdiagnosed as bipolar affective disorder in a 75-year-old man SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID PARTIAL SEIZURES; ORIGIN AB The incidence and prevalence of epilepsy increases with age, with the majority of cases having a known cause, and approximately half of elderly patients with epilepsy experiencing complex partial seizures that often present initially as neuropsychiatric symptoms. This presentation often delays diagnosis of the epileptiform disorder. To illustrate, we present the case of a 75-year-old man who was initially misdiagnosed with bipolar affective disorder later to be revealed as a frontal lobe seizure disorder. C1 VA Puget Sound Hlth Care Syst, Mental Hlth Serv 116, Seattle, WA 98108 USA. VA Puget Sound Hlth Care Syst, Neurol Serv, Seattle, WA 98108 USA. VA Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ & Clin, Seattle, WA 98108 USA. Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. RP Pascualy, M (reprint author), VA Puget Sound Hlth Care Syst, Mental Hlth Serv 116, 1660 S Columbian Way, Seattle, WA 98108 USA. RI Tsuang, Debby/L-7234-2016 OI Tsuang, Debby/0000-0002-4716-1894 NR 12 TC 2 Z9 3 U1 0 U2 0 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD OCT PY 1997 VL 10 IS 4 BP 158 EP 160 PG 3 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA YQ720 UT WOS:000071416500005 PM 9453682 ER PT J AU Go, RCP Duke, LW Harrell, LE Cody, H Bassett, SS Folstein, MF Albert, MS Foster, JL Sharrow, NA Blacker, D AF Go, RCP Duke, LW Harrell, LE Cody, H Bassett, SS Folstein, MF Albert, MS Foster, JL Sharrow, NA Blacker, D TI Development and validation of a structured telephone interview for dementia assessment (STIDA): The NIMH genetics initiative SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article AB As part of the NIMH Genetics Initiative Alzheimer's Disease (AD) Study Group, a brief structured telephone interview to distinguish individuals with normal cognitive functioning from those with changes in cognition and daily functioning suggestive of early AD was developed. The Structured Telephone Interview for Dementia Assessment (STIDA), yields a dementia score between 0 and 81 (higher scores indicating greater impairment). Subscales corresponding to the subscales of the Clinical Dementia Rating Scale (CDR) can be derived. The STIDA performed well as a screening instrument for mildly demented individuals. When a score of 10 or more (based on informant interview and subject testing) was used to identify mildly impaired individuals, the STIDA had a sensitivity of .93 and a specificity of .92 for a clinician-derived CDR of 0.5 or more. The STIDA was also capable of accurately assessing the level of dementia. STIDA-derived CDR ratings agreed with clinician-derived CDR scores in 23 of 28 cases, corresponding to an unweighted kappa of .71 and a weighted kappa of .81. A much-abbreviated short STIDA that could be administered directly to the subject was able to detect possible impairment with a sensitivity of .93 and a specificity of .77. These results suggest that the short STIDA provides a sensitive and fairly specific telephone screen for dementia, and that the full STIDA, consisting of an interview with a knowledgeable informant and subject testing, approximates the success of a face-to-face clinical interview, and provides reliable and valid screening and staging of dementia over the telephone. C1 Univ Alabama, Sch Publ Hlth, Dept Psychol, Birmingham, AL 35294 USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Johns Hopkins Sch Med, Baltimore, MD USA. Harvard Univ, Sch Med, Boston, MA USA. RP Go, RCP (reprint author), 720 S 20th St,TH 202A, Birmingham, AL 35294 USA. FU NIA NIH HHS [R01-AG10163]; NIMH NIH HHS [U01-MH46281, U01-MH46373] NR 9 TC 28 Z9 29 U1 0 U2 1 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD OCT PY 1997 VL 10 IS 4 BP 161 EP 167 PG 7 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA YQ720 UT WOS:000071416500006 PM 9453683 ER PT J AU Seebach, JD Comrack, C Germana, S LeGuern, C Sachs, DH DerSimonian, H AF Seebach, JD Comrack, C Germana, S LeGuern, C Sachs, DH DerSimonian, H TI HLA-Cw3 expression on porcine endothelial cells protects against xenogeneic cytotoxicity mediated by a subset of human NK cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NATURAL-KILLER-CELLS; MHC CLASS-I; HLA-C; MONOCLONAL-ANTIBODIES; XENOGRAFT REJECTION; GENE-PRODUCTS; TARGET-CELLS; MOLECULES; RECOGNITION; RECEPTORS AB There is increasing evidence that NK cells make an important contribution to human anti-porcine xenogeneic cytotoxicity. Most allogeneic as well as autologous normal cells are not susceptible to NK cell-mediated cytotoxicity because they express inhibitory molecules encoded within the MHC class I loci. The protective signal is delivered to NK cells through killer cell-inhibitory receptors expressing different MHC class I specificities, It has been proposed that xenogeneic target cells may be susceptible to NK cell-mediated lysis because their MHC class I molecules fail to be recognized by human killer cell-inhibitory receptors, To explore this hypothesis, we examined the effect of human MHC class I expression on porcine target cell lysis by human NK cells, An immortalized porcine bone marrow-derived endothelial cell line (2A2) was transfected with three different human MHC class I allelic genes (HLA-A2, -B27, or -Cw3), The cytotoxic activity of several CL183(+) NK clones, which lysed untransfected porcine cells effectively, was substantially blocked by the presence of HLA-Cw3. In contrast, HLA-Cw3-positive cells were not protected against lysis by CL183(-)EB6(+) NK clones, The expression of HLA-B27 or HLA-A2 molecules on pig target cells did not provide substantial protection from lysis by any of the NK clones tested, In addition to confirming the hypothetical basis of NK cell-mediated killing of xenogeneic targets, these results have practical implications as an approach to overcoming NK cell-mediated cytotoxicity, which may be an obstacle to pig-to-human xenotransplantation. RP Seebach, JD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149-9019,BOSTON,MA 02129, USA. NR 40 TC 95 Z9 99 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 1 PY 1997 VL 159 IS 7 BP 3655 EP 3661 PG 7 WC Immunology SC Immunology GA XY461 UT WOS:A1997XY46100065 PM 9317166 ER PT J AU Koziel, MJ Wong, DKH Dudley, D Houghton, M Walker, BD AF Koziel, MJ Wong, DKH Dudley, D Houghton, M Walker, BD TI Hepatitis C virus-specific cytolytic T lymphocyte and T helper cell responses in seronegative persons SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID MEDIATED IMMUNE-RESPONSE; NUCLEOCAPSID ANTIGEN; INFECTED PATIENTS; FINE SPECIFICITY; RECOGNIZE; TYPE-1; INDUCTION; EPITOPES; PEPTIDES; BINDING AB Hepatitis C virus (HCV) is a common infection worldwide, and in most persons, it leads to persistent viremia and liver damage. Efforts to identify the correlates of protective immunity are hampered by this high rate of persistent infection in both infected humans and the only animal model, the chimpanzee. Peripheral blood mononuclear cells from seronegative persons were stimulated with synthetic peptides that represent epitopes recognized by HCV-specific cytotoxic T lymphocytes (CTL) after natural infection. In addition, CD4(+) proliferative responses to recombinant HCV proteins were examined in these same persons. CTL responses directed against a peptide epitope of HCV and proliferative responses in 2 HCV-seronegative persons with possible occupational exposure to HCV were found. These otherwise healthy persons were not viremic, suggesting that they may have recovered from acute HCV infection. Characterization of virus-specific immune responses in exposed but seronegative persons may provide important clues as to the nature of protective immunity in HCV. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. CHIRON CORP,EMERYVILLE,CA 94608. FU NIAID NIH HHS [AI-01210, AI-31563] NR 47 TC 115 Z9 117 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD OCT PY 1997 VL 176 IS 4 BP 859 EP 866 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA XZ465 UT WOS:A1997XZ46500003 PM 9333142 ER PT J AU Rossetti, RG Seiler, CM DeLuca, P Laposata, M Zurier, RB AF Rossetti, RG Seiler, CM DeLuca, P Laposata, M Zurier, RB TI Oral administration of unsaturated fatty acids: effects on human peripheral blood T lymphocyte proliferation SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE rheumatoid arthritis; gammalinolenic acid ID GAMMA-LINOLENIC ACID; IL-2 GENE-EXPRESSION; RHEUMATOID-ARTHRITIS; INDEPENDENT MECHANISM; CELL-PROLIFERATION; SUPPRESSION; INHIBITION; ACTIVATION AB Oils enriched in certain polyunsaturated fatty acids suppress joint pain and swelling in rheumatoid arthritis (RA) patients, Because T lymphocyte activation is important to propagation of joint tissue injury in patients with RA, we examined the effects of fatty acids administered by mouth in vivo on proliferation of human lymphocytes activated through the T cell receptor complex. T cell proliferation was reduced after oral administration of 2.4 g gammalinolenic acid in capsules of borage seed oil, Oral administration of coils enriched in Linoleic acid, the parent n-6 fatty acid, and alpha linolenic acid, the parent n-3 fatty acid, did not influence grwth of stimulated cells, Fatty acid analyses indicated that suppression of lynmphocyte proliferation after gammalinolenic acid administration was associated with increased plasma and peripheral blood mononuclear cell concentrations of gammalinolenic acid and dihomogammalinolenic acid. C1 UNIV MASSACHUSETTS,MED CTR,DIV RHEUMATOL,WORCESTER,MA 01655. MASSACHUSETTS GEN HOSP,DIV CLIN LABS,BOSTON,MA 02114. FU NIAMS NIH HHS [T32 AR7572, AR 38501] NR 30 TC 34 Z9 36 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD OCT PY 1997 VL 62 IS 4 BP 438 EP 443 PG 6 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YA004 UT WOS:A1997YA00400003 PM 9335312 ER PT J AU Kupatt, C Weber, C Wolf, DA Becker, BF Smith, TW Kelly, RA AF Kupatt, C Weber, C Wolf, DA Becker, BF Smith, TW Kelly, RA TI Nitric oxide attenuates reoxygenation-induced ICAM-1 expression in coronary microvascular endothelium: Role of NF kappa B SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE transcription factors; adhesion molecules; antioxidants; proteasome inhibitor; AP-1 ID INTERCELLULAR-ADHESION MOLECULE-1; NECROSIS-FACTOR-ALPHA; LEUKOCYTE ADHESION; MYOCARDIAL-ISCHEMIA; REPERFUSION INJURY; MONOCLONAL-ANTIBODY; TRANSCRIPTIONAL REGULATION; BIND NEUTROPHILS; BETA-2 INTEGRINS; OXYGEN RADICALS AB Enhanced leukocyte adhesion has been shown to occur in postischemic reperfused hearts due to the upregulation of specific cell-surface adhesion molecules. Therefore, we investigated the influence of 4 h of reoxygenation after 20 h of hypoxia on ICAM-1 induction in primary cultures of rat coronary microvascular endothelial cells (CMEC). ICAM-1 surface expression as well as oxygen free radical formation were measured by now cytometry. Changes in ICAM-1 mRNA levels were assessed by Northern blot and activation of NF kappa B and AP-1 signalling were analysed by electrophoretic mobility shift assays (EMSA) in CMEC lysates. Although hypoxia alone did not affect cell-surface ICAM-1 expression, 4 h of reoxygenation induced a significant upregulation of ICAM-1. ICAM-1 mRNA could not be found after hypoxia alone, but could be detected as early as 1 h following reoxygenation. Unlike AP-1, the activation of which could be detected in CMEC lysates following hypoxia alone, NF kappa B binding activity was induced only following reoxygenation, concurrent with an increase in the formation of reactive oxygen species (ROS). A proteasome inhibitor, nor-Leu (25 mu M) inhibited NF kappa B activation by reoxygenation and ICAM-1 expression. Blockade of endogenous nitric oxide (NO) synthesis in CMEC with L-nitroarginine (10 mu M) accentuated post-reoxygenation ICAM-1 expression. Finally an exogenous NO donor, s-nitrosoacetyl-penicillamine (SNAP 100 mu M), suppressed the generation of ROS upon reoxygenation, and blocked the activation of NF kappa B and the upregulation of ICAM-1. Thus, ICAM-1 upregulation in CMEC primary cultures is not induced by hypoxia alone, but appears shortly after reoxygenation in the absence of exogenous cytokines or inflammatory cells. Because upregulation of AP-1 through hypoxia alone did not affect ICAM-1 expression, we conclude that redox-sensitive NF kappa B activation triggers ICAM-1 upregulation. NO inhibits reoxygenation-specific ICAM-1 upregulation, most likely by diminishing oxidative stress that leads-to NF kappa B activation. (C) 1997 Academic Press Limited. C1 BRIGHAM & WOMENS HOSP, DEPT MED, DIV CARDIOVASC, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, CTR BLOOD RES, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT CELL BIOL, BOSTON, MA 02115 USA. UNIV MUNICH, DEPT PHYSIOL, D-80336 MUNICH, GERMANY. FU NHLBI NIH HHS [HL 36141, HL52320] NR 49 TC 59 Z9 62 U1 0 U2 2 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD OCT PY 1997 VL 29 IS 10 BP 2599 EP 2609 DI 10.1006/jmcc.1997.0439 PG 11 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA YC586 UT WOS:A1997YC58600001 PM 9344755 ER PT J AU Schultz, D Su, XF Bishop, SP Billadello, J DellItalia, LJ AF Schultz, D Su, XF Bishop, SP Billadello, J DellItalia, LJ TI Selective induction of the creatine kinase-B gene in chronic volume overload hypertrophy is not affected by ACE-inhibitor therapy SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE creatine kinase; mitral regurgitation; angiotensin converting enzyme inhibitor; congestive heart failure; left ventricular hypertrophy ID COMPLETE NUCLEOTIDE-SEQUENCE; CORONARY-ARTERY OCCLUSION; MITRAL REGURGITATION; CARDIAC-HYPERTROPHY; DEVELOPMENTAL REGULATION; MYOCARDIAL-INFARCTION; PRESSURE OVERLOAD; MESSENGER-RNAS; HEART-FAILURE; EXPRESSION AB Hypertrophied and failing myocardium has been shown to undergo creatine kinase. (CK) isoform switching, resulting in increased MB and BB components, We tested the hypothesis that chronic volume overload hypertrophy due to mitral regurgitation in the dog causes CK isoenzyme switching and that this could be reversed by angiotensin converting enzyme inhibitor therapy. Thirteen adult mongrel dogs had mitral regurgitation induced by mitral valvular chordal rupture: six were treated with ramipril for 4 months and seven were untreated for 4 months. Twelve dogs were sham-operated: six received ramipril for 3 months and six were untreated. Left ventricular end-diastolic volume increased from 58 +/- 4 to 104 +/- 10 ml in untreated (P<0.001) and from 55 +/- 3 to 91 +/- 6 ml in treated dogs (P<0.01) as LV mass/volume ratio decreased in both untreated (1.60 +/- 0.07 to 1.13 +/- 0.08 g/ml, P<0.001) and treated dogs (1.44 +/- 0.06 to 1.20 +/- 0.08 g/ml, P<0.01). CK-MB isoform was 7.4 +/- 1.1% in normal shams and increased to 13.5 +/- 1.9% and 18.1 +/- 3.0% in both treated and untreated mitral regurgitation dogs; respectively (P<0.05). Steady state CK-B mRNA increased three fold in treated and untreated dogs with mitral regurgitation (P<0.003) compared to normals, while CK-M mRNA expression did not differ in all groups. Thus, chronic volume overload hypertrophy of mitral regurgitation induces CK isoform switching by selective induction of the CK-B gene, and ramipril therapy does not affect this isoform switch. This may reflect a response to increased diastolic stress and more efficient energy utilization in the volume overloaded myocardium. (C) 1997 Academic Press Limited. C1 UNIV ALABAMA, BIRMINGHAM VET AFFAIRS MED CTR, DEPT MED, DIV CARDIOVASC DIS HYPERTENS & VASC BIOL, BIRMINGHAM, AL 35294 USA. AUBURN COLL VET MED, AUBURN, AL 36849 USA. WASHINGTON UNIV, DEPT MED, DIV CARDIOVASC DIS, ST LOUIS, MO 63110 USA. FU NHLBI NIH HHS [2T32HL07457-16A1, HL54816]; NICHD NIH HHS [HD SCOR HL 17667] NR 39 TC 10 Z9 10 U1 2 U2 2 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD OCT PY 1997 VL 29 IS 10 BP 2665 EP 2673 DI 10.1006/jmcc.1997.0498 PG 9 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA YC586 UT WOS:A1997YC58600007 PM 9344761 ER PT J AU Hyman, BT Trojanowski, JQ AF Hyman, BT Trojanowski, JQ TI Editorial on consensus recommendations for the postmortem diagnosis of Alzheimer disease from the National Institute on Aging and the Reagan Institute working group on diagnostic criteria for the neuropathological assessment of Alzheimer disease SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA. UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,CTR NEURODEGENERAT DIS RES,PHILADELPHIA,PA 19104. RP Hyman, BT (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,ALZHEIMERS UNIT,149 13TH ST CNY 6405,CHARLESTOWN,MA 02129, USA. NR 9 TC 445 Z9 450 U1 2 U2 8 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD OCT PY 1997 VL 56 IS 10 BP 1095 EP 1097 DI 10.1097/00005072-199710000-00002 PG 3 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA XZ763 UT WOS:A1997XZ76300002 PM 9329452 ER PT J AU Maintz, D Fiedler, K Koopmann, J Rollbrocker, B Nechev, S Lenartz, D Stangl, AP Louis, DN Schramm, J Wiestler, OD vonDeimling, A AF Maintz, D Fiedler, K Koopmann, J Rollbrocker, B Nechev, S Lenartz, D Stangl, AP Louis, DN Schramm, J Wiestler, OD vonDeimling, A TI Molecular genetic evidence for subtypes of oligoastrocytomas SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE allelic loss; astrocytoma; LOH; mutation; oligoastrocytoma; oligodendroglioma; TP53 ID TUMOR-SUPPRESSOR GENE; OLIGODENDROGLIAL TUMORS; HUMAN ASTROCYTOMAS; HUMAN GLIOMAS; GRADE-III; TP53 GENE; P53; MUTATIONS; 1P; HETEROZYGOSITY AB The histogenesis of oligoastrocytomas remains controversial, with some data arguing similarity of oligoastrocytomas to astrocytic tumors, and other data suggesting closer relationships with oligodendroglial neoplasms. Since the molecular genetic changes in astrocytomas differ from those of oligodendrogliomas, we characterized 120 astrocytic and oligodendroglial tumors, including 38 oligoastrocytomas, for genetic alterations that occur disproportionately between astrocytomas and oligodendrogliomas, i.e. TP53 gene mutations and allelic loss of chromosomes Ip, 17p and 19q. As previously reported, TP53 mutations were common in astrocytic gliomas, occurring in approximately half of WHO grade II and III astrocytomas, but in only 5% of WHO grades II and III oligodendrogliomas. Allelic losses of chromosomes Ip and 19q, however, were common in oligodendrogliomas (41% and 63%), but less frequent in astrocytomas (9% and 35%). Oligoastrocytomas showed TP53 mutations in 12/38 (32%) cases and allelic losses of chromosomes Ip and 19q in 52% and 70%, respectively. Most importantly, TP53 mutations and allelic losses on chromosomes Ip and 19q were inversely correlated in oligoastrocytomas (p < 0.011 and p < 0.019). These data suggest the existence of two genetic subsets of oligoastrocytomas, one genetically related to astrocytomas and the other genetically related to oligodendrogliomas. Histologically, those oligoastrocytomas with TP53 mutations were more often astrocytoma-predominant, while those with chromosome 19q loss were more often oligodendroglioma-predominant. C1 UNIV BONN,MED CTR,DEPT NEUROPATHOL,D-5300 BONN,GERMANY. HOSP COLOGNE MERHEIM,DEPT NEUROSURG,COLOGNE,GERMANY. UNIV KLINIKEN BONN,INST NEUROPATHOL,DEPT NEUROSURG,D-53105 BONN,GERMANY. MASSACHUSETTS GEN HOSP,CS KUBLIK LAB NEUROPATHOL & MOL NEUROONCOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X FU NCI NIH HHS [CA57683] NR 21 TC 180 Z9 184 U1 0 U2 2 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD OCT PY 1997 VL 56 IS 10 BP 1098 EP 1104 DI 10.1097/00005072-199710000-00003 PG 7 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA XZ763 UT WOS:A1997XZ76300003 PM 9329453 ER PT J AU Lee, BW Kelsey, KT Hashimoto, D Yakes, B Seitz, T Christiani, DC AF Lee, BW Kelsey, KT Hashimoto, D Yakes, B Seitz, T Christiani, DC TI The prevalence of pulmonary and upper respiratory tract symptoms and spirometric test findings among newspaper pressroom workers exposed to solvents SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Article ID TRADE-UNION MEMBERS; PRINTING INDUSTRY; MALIGNANT-MELANOMA; MANCHESTER; MORTALITY; PRINTERS; CANCER AB To investigate the relationship between exposure to organic solvents and the presence of pulmonary and upper respiratory tract mucous membrane symptoms, we conducted a cross-sectional study of 215 newspaper pressroom workers who were occupationally exposed to organic solvent and lubricant mixtures. Thirty-four compositors, who were not occupationally exposed to the solvents or lubricants, served as controls. Pressroom workers and compositors underwent spirometric testing and were also asked about the presence of cough, phlegm, hemoptysis, dyspnea, wheezing, chest tightness, nose or throat irritation, eye irritation, and sinus trouble. The spirometric results did not significantly differ between the two groups. However the pressroom workers were significantly more likely to report pulmonary or upper respiratory tract mucous membrane symptoms than were compositors (P < 0.005). Ain exposure-response relationship could be demonstrated when comparing the number of solvents exposed with the total number of symptoms (P < 0.001). Similarly, an exposure-response relationship could be demonstrated when comparing the frequency of use of each of the seven solvents with the total number of symptoms (P < 0.002). Each of these findings was supported in a multivariable linear regression model that adjusted for potential confounders such as age, smoking history, and number of years in the industry. A high prevalence of these symptoms was reported even though the degree of exposure to solvents and lubricants was within the current permissible exposure limits. C1 HARVARD UNIV,SCH PUBL HLTH,OCCUPAT HLTH PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS RESP HOSP,OCCUPAT HLTH SERV,S BRAINTREE,MA. HARVARD UNIV,SCH PUBL HLTH,LAB RADIOL,BOSTON,MA 02115. NIOSH,CINCINNATI,OH 45226. RI Kelsey, Karl/I-1252-2014 FU NIEHS NIH HHS [ES00002, 5 T32 ESO7069] NR 21 TC 11 Z9 11 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1076-2752 J9 J OCCUP ENVIRON MED JI J. Occup. Environ. Med. PD OCT PY 1997 VL 39 IS 10 BP 960 EP 969 DI 10.1097/00043764-199710000-00008 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YA641 UT WOS:A1997YA64100006 PM 9343761 ER PT J AU Hu, SX Merayo-Lloves, J Zhao, TZ Foster, CS AF Hu, SX Merayo-Lloves, J Zhao, TZ Foster, CS TI Potent inhibitory effect of tetrandrine on experimental allergic conjunctivitis in mice SO JOURNAL OF OCULAR PHARMACOLOGY AND THERAPEUTICS LA English DT Article ID PLANT ALKALOID TETRANDRINE; PLATELET-ACTIVATING-FACTOR; TUMOR-NECROSIS-FACTOR; BISBENZYLISOQUINOLINE ALKALOIDS; GUINEA-PIG; BERBAMINE; INTERLEUKIN-1; INFLAMMATION; PHOSPHOLIPASE-A2; CHALLENGE AB This study investigated the effectiveness of tetrandrine (TDR) on experimental allergic conjunctivitis secondary to ragweed pollen. SWR/J mice were divided as follows: group 1, normal controls; group 2, sensitized but untreated; group 3, sensitized, buffered saline (BS)-treated; and group 4, sensitized, TDR-treated. The last three groups were exposed to ragweed through topical contact on the nasal and conjunctival mucosae followed by challenge with the allergen on the conjunctiva. Groups 3 and 4 received doses of BS and TDR, respectively. The allergic conjunctivitis was evaluated by scoring of the clinical signs and histopathology, mRNA gene expression of interleukin 1 beta (IL-1 beta) and IL-5 in the conjunctiva was analyzed by polymerase chain reaction techniques. All mice exposed to ragweed developed allergic conjunctivitis clinically and histologically. The conjunctivitis was significantly modulated by intraperitoneal injection of a new anti-inflammatory agent, TDR. Histopathologic analysis demonstrated that TDR strikingly reduced the conjunctival eosinophil infiltration and the number of intact and degranulating mast cells. IL-1 beta and IL-5 mRNA gene expression in the conjunctiva of TDR-treated mice was dramatically down-regulated compared with untreated and BS-treated controls. The results indicated that TDR may have potential clinical use in the treatment of conjunctivitis. C1 Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med,Dept Ophthalmol, Serv Immunol,Rhoads Mol & Hilles Immunol Labs, Boston, MA 02114 USA. RP Foster, CS (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med,Dept Ophthalmol, Serv Immunol,Rhoads Mol & Hilles Immunol Labs, 243 Charles St, Boston, MA 02114 USA. NR 32 TC 2 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1080-7683 J9 J OCUL PHARMACOL TH JI J. Ocular Pharmacol. Ther. PD OCT PY 1997 VL 13 IS 5 BP 435 EP 444 DI 10.1089/jop.1997.13.435 PG 10 WC Ophthalmology; Pharmacology & Pharmacy SC Ophthalmology; Pharmacology & Pharmacy GA YP841 UT WOS:000071321000005 PM 9326725 ER PT J AU Cove, JA Lhowe, DW Jupiter, JB Siliski, JM AF Cove, JA Lhowe, DW Jupiter, JB Siliski, JM TI The management of femoral diaphyseal nonunions SO JOURNAL OF ORTHOPAEDIC TRAUMA LA English DT Article DE external fixation; femur; fracture; infection; plate fixation; vascularized fibula transfer ID OPEN FRACTURES; RECONSTRUCTION; FEMUR AB Objective: To assess the efficacy of treatment and develop an algorithm for management of nonunions of the femoral diaphysis. Study Design: Retrospective. Setting: University hospital. Methods: Forty-four patients treated at one institution for nonunion of the femoral diaphysis were studied. Thirteen of these patients had a history of infection. After debridement (where appropriate) and repair of the femoral: nonunion, followup averaged twenty-eight months (range, 24 to 108 months). All patients were examined at final follow-up. Results: Thirty-three patients achieved union after one procedure, and eight patients achieved union after additional procedures. One patient underwent above-knee amputation, and two patients remained ununited at the time of their final follow-up. Time to union averaged 11.8 months. Seventeen patients healed with more than two centimeters of shortening, and ten patients lost more than 30 degrees of knee flexion. Conclusion: Established femoral diaphyseal nonunions can be treated effectively, even in the presence of chronic sepsis: Selective use of a vascularized fibula transfer has proven beneficial in addressing intercalary defects. Plate fixation, with or without a vascularized fibula transfer, has been the predominant mode of skeletal stabilization in more complex reconstructions. C1 Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA. RP Lhowe, DW (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, ACC 525, Boston, MA 02114 USA. NR 23 TC 26 Z9 27 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 0890-5339 J9 J ORTHOP TRAUMA JI J. Orthop. Trauma PD OCT PY 1997 VL 11 IS 7 BP 513 EP 520 DI 10.1097/00005131-199710000-00009 PG 8 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA YQ620 UT WOS:000071406100009 PM 9334953 ER PT J AU Marcus, KC Grien, HE Shamberger, RC Gebhardt, MC PerezAtayde, A Silver, B Tarbell, NJ AF Marcus, KC Grien, HE Shamberger, RC Gebhardt, MC PerezAtayde, A Silver, B Tarbell, NJ TI Childhood soft tissue sarcoma: A 20-year experience SO JOURNAL OF PEDIATRICS LA English DT Article ID RESEARCH-HOSPITAL EXPERIENCE; LIMB-SPARING SURGERY; ADJUVANT CHEMOTHERAPY; RADIOTHERAPY; CHILDREN; EXTREMITY AB Purpose: To evaluate the disease-free and overall survival of pediatric patients with nonrhabdomyosarcoma soft-tissue sarcomas. Methods: We retrospectively analyzed the records of 67 pediatric patients with a diagnosis of nonrhabdomyosarcoma soft tissue sarcoma treated with curative intent between 1970 and 1992. Median follow-up time for the 52 survivors was 120 months (range, 7 to 277 months). Fifty-nine patients received external beam radiotherapy, in a median dose of 5400 cCy (range, 1800 to 6560 cGy.) All patients underwent an initial surgical procedure. Eighteen patients had gross residual disease, and 15 had gross total excision with microscopic residual disease or positive margins. Adjuvant chemotherapy was administered to 44 patients (65%). Results: The actuarial 10-year freedom from progression or recurrence and overall survival rates were 76% and 75%, and the 20-year rates were the same. Of 18 patients with gross residual disease, 9 (50%) had local progression and 6 died of local-only disease. By contrast, only one patient with microscopic residual disease who received postoperative radiotherapy had a local recurrence. The disease-free survival rate also correlated with histologic grade. Conclusions: As with adult soft tissue sarcomas, gross residual disease predicts local failure. Our results suggest that pediatric patients with soft tissue sarcomas treated with surgery and postoperative radiotherapy generally have a favorable overall survival rate. C1 HARVARD UNIV, CHILDRENS HOSP, DANA FARBER CANC INST, SCH MED, BOSTON, MA 02115 USA. HARVARD UNIV, CHILDRENS HOSP, DEPT ORTHOPED SURG, SCH MED, BOSTON, MA 02115 USA. HARVARD UNIV, CHILDRENS HOSP, DEPT PATHOL, SCH MED, BOSTON, MA 02115 USA. HARVARD UNIV, CHILDRENS HOSP, DIV HEMATOL ONCOL, SCH MED, BOSTON, MA 02115 USA. RP Marcus, KC (reprint author), HARVARD UNIV, DEPT RADIAT ONCOL,JOINT CTR RADIAT ONCOL, CHILDRENS HOSP,SCH MED, 300 LONGWOOD AVE, BOSTON, MA 02115 USA. NR 19 TC 23 Z9 24 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD OCT PY 1997 VL 131 IS 4 BP 603 EP 607 DI 10.1016/S0022-3476(97)70070-2 PG 5 WC Pediatrics SC Pediatrics GA YG843 UT WOS:A1997YG84300023 PM 9386667 ER PT J AU Dawson, TM Starkebaum, G AF Dawson, TM Starkebaum, G TI Colchicine induced rhabdomyolysis SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE colchicine; rhabdomyolysis; gout ID FAMILIAL MEDITERRANEAN FEVER; RENAL-FAILURE; MYOPATHY; NEUROPATHY AB A 59-year-old man with chronic obstructive pulmonary disease (COPD)? atrial fibrillation, and gout developed acute dyspnea, cough, and diffuse muscle aches and pains. He had commenced colchicine (0.6 mg bid po), for the first time, one month earlier for recurrent gout attacks. Clinical examination revealed atrial fibrillation, an exacerbation of his pulmonary disease, render muscles, especially calves, and diffuse muscle weakness. Laboratory results included creatinine phosphokinase 6961 U/l (1% MB), microscopic hematuria, myoglobinuria, elevated creatinine 1.6 mg/dl, and blood urea nitrogen 17 mg/dl. COPD and atrial fibrillation were treated and colchicine was discontinued. The patient made a full recovery. This 2nd reported case of colchicine induced rhabdomyolysis is the first reported in the treatment of gout. C1 UNIV WASHINGTON,DIV RHEUMATOL,SEATTLE,WA 98195. RP Dawson, TM (reprint author), VA PUGET SOUND HLTH CARE SYST,MED SERV,DEPT MED,ARTHRITIS SECT,1600 S COLUMBIAN WAY,SEATTLE,WA 98108, USA. NR 13 TC 18 Z9 18 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD OCT PY 1997 VL 24 IS 10 BP 2045 EP 2046 PG 2 WC Rheumatology SC Rheumatology GA XY693 UT WOS:A1997XY69300033 PM 9330953 ER PT J AU Beresin, EV AF Beresin, EV TI Child and adolescent psychiatry residency training: Current issues and controversies SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE child; adolescent; psychiatry residency training ID PROGRAM AB Objective: To examine major current influences on child and adolescent psychiatry (CAP) residency training, highlighting the most common problems. Potential solutions and unresolved dilemmas are presented. Method: Data were gathered from empirical studies, review articles, national census data, and discussions over the past decade at national meetings on recruitment of residents and faculty; clinical, didactic, and research training; the impact of managed care and changes in graduate medical education funding; and the professional development of CAP residents. Results: Overall there are significant problems recruiting U.S. medical students and attracting faculty into CAP training programs. Economic forces, including decreased reimbursements from managed care and the federal government, are threatening the survival and vitality of training programs. Managed care is harmful for sound residency training and identity formation of the child and adolescent psychiatrist. Conclusions: The integrity of CAP residency training in the future will depend on increased efforts of teaching hospitals acid programs to develop fiscally viable systems of care integrated with residency training; seek new sources of training subsidies; modify traditional models of clinical and didactic curricula; and foster greater collaboration between training programs locally and nationally. C1 MCLEAN HOSP,BOSTON,MA. RP Beresin, EV (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BULFINCH 449,BOSTON,MA 02114, USA. NR 22 TC 14 Z9 14 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD OCT PY 1997 VL 36 IS 10 BP 1339 EP 1348 DI 10.1097/00004583-199710000-00015 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA XZ473 UT WOS:A1997XZ47300015 PM 9334546 ER PT J AU Faraone, SV Biederman, J Mennin, D Wozniak, J Spencer, T AF Faraone, SV Biederman, J Mennin, D Wozniak, J Spencer, T TI Attention-deficit hyperactivity disorder with bipolar disorder: A familial subtype? SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE attention-deficit hyperactivity disorder; bipolar disorder; genetics; comorbidity; nosology ID PSYCHIATRIC STATUS; JUVENILE MANIA; RISK-FACTORS; FOLLOW-UP; CHILDREN; COMORBIDITY; ONSET; PSYCHOPATHOLOGY; HETEROGENEITY; ADOLESCENTS AB Objective: To clarify the nosological status of children with attention-deficit hyperactivity disorder (ADHD) who also satisfy diagnostic criteria for bipolar disorder (BPD). Method: Blind raters and structured psychiatric interviews were used to examine 140 children with ADHD, a sample of 120 non-ADHD comparisons, and their 822 first-degree relatives, Data analyses tested specific hypotheses about the familial relationship between ADHD and BPD. Results: After stratifying the ADHD sample into those with and without BPD, the authors found that (1) relatives of both ADHD subgroups were at significantly greater risk for ADHD than relatives of non-ADHD controls; (2) the two subgroups did not differ significantly from one another in their relatives' risk for ADHD; (3) a fivefold elevated risk for BPD was observed among relatives when the proband child had BPD but not when the proband had ADHD alone; (4) an elevated risk for major depression with severe impairment was found for relatives of ADHD+BPD probands; (5) both ADHD and BPD occurred in the same relatives more often than expected by chance alone; and (6) there was a trend for random mating between ADHD parents and those with mania. Conclusions: The data suggest that comorbid ADHD with BPD is familially distinct from other forms of ADHD and may be related to what others have termed childhood-onset BPD. C1 MASSACHUSETTS GEN HOSP, PSYCHIAT SERV, PEDIAT PSYCHOPHARMACOL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT PSYCHIAT, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PSYCHIAT, BROCKTON W ROXBURY VET AFFAIRS MED CTR, BOSTON, MA USA. MASSACHUSETTS HLTH CTR, BOSTON, MA USA. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01 MH41314-07] NR 41 TC 201 Z9 205 U1 2 U2 9 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD OCT PY 1997 VL 36 IS 10 BP 1378 EP 1387 DI 10.1097/00004583-199710000-00020 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA XZ473 UT WOS:A1997XZ47300020 PM 9334551 ER PT J AU Khuri, SF Daley, J Henderson, W Hur, K Gibbs, JO Barbour, G Demakis, J Irvin, G Stremple, JF Grover, F McDonald, G Passaro, E Fabri, PJ Spencer, J Hammermeister, K Aust, JB AF Khuri, SF Daley, J Henderson, W Hur, K Gibbs, JO Barbour, G Demakis, J Irvin, G Stremple, JF Grover, F McDonald, G Passaro, E Fabri, PJ Spencer, J Hammermeister, K Aust, JB TI Risk adjustment of the postoperative mortality rate for the comparative assessment of the quality of surgical care: Results of the National Veterans Affairs Surgical Risk Study SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS LA English DT Article ID HOSPITAL DISCHARGE DATA; CARDIAC-SURGERY; CARDIOVASCULAR MEDICINE; PROGNOSTIC PREDICTION; OPERATIVE MORBIDITY; RELATIVE VALUES; OUTCOMES; INDEX; IMPROVEMENT; PATIENT AB Background: The National Veterans Affairs Surgical Risk Study was designed to collect reliable, valid data on patient risk and outcomes for major surgery in the Veterans Health Administration and to report comparative risk-adjusted postoperative mortality rates for surgical services in Veterans Health Administration. Study Design: This cohort study was conducted in 44 Veterans Affairs Medical Centers. Included were 87,078 major noncardiac operations performed under general, spinal, or epidural anesthesia between October 1, 1991, and December 31, 1993. The main outcomes measure was all-cause mortality within 30 days after the index procedure. Multivariable logistic regression risk-adjustment models for all operations and for eight surgical subspecialties were developed. Risk-adjusted surgical mortality rates were expressed as observed-to-expected ratios and were compared with unadjusted 30-day postoperative mortality rates. Results: Patient risk factors predictive of postoperative mortality included serum albumin level, American So-ciety of Anesthesia class, emergency operation, and 31 additional preoperative variables. Considerable variability in unadjusted mortality rates for all operations was observed across the 44 hospitals (1.2-5.4%). After risk adjustment, observed-to-expected ratios ranged from 0.49 to 1.53. Rank order correlation of the hospitals by unadjusted and risk-adjusted mortality rates for all operations was 0.64. Ninety-three percent of the hospitals changed rank after risk adjustment, 50% by more than 5 and 25% by more than 10. Conclusions: The Department of Veterans Affairs has successfully implemented a system for the prospective collection and comparative reporting of risk-adjusted postoperative mortality rates after major noncardiac operations. Risk adjustment had an appreciable impact on the rank ordering of the hospitals and provided a means for monitoring and potentially improving the quality of surgical care. (C) 1997 by the American College of Surgeons. C1 HARVARD UNIV,SCH MED,BOSTON,MA. BETH ISRAEL MED CTR,DIV GEN MED & PRIMARY CARE,BOSTON,MA. HINES VA CTR COOPERAT STUDIES HLTH SERV,HINES,IL. WASHINGTON VA MED CTR,WASHINGTON,DC. GEORGE WASHINGTON UNIV,SCH MED,DEPT MED,WASHINGTON,DC. UNIV MIAMI,DEPT SURG,MIAMI,FL 33152. MIAMI VA MED CTR,MIAMI,FL. PITTSBURGH VA MED CTR,PITTSBURGH,PA. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA. DENVER VA MED CTR,DENVER,CO. UNIV COLORADO,HLTH SCI CTR,DENVER,CO. DEPT VET AFFAIRS HEADQUARTERS,DEPT SURG,WASHINGTON,DC. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. TAMPA VA MED CTR,TAMPA,FL. UNIV S FLORIDA,COLL MED,TAMPA,FL. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RP Khuri, SF (reprint author), VET AFFAIRS MED CTR,1400 VFW PKWY,W ROXBURY,MA 02132, USA. NR 54 TC 429 Z9 431 U1 3 U2 7 PU AMER COLL SURGEONS PI CHICAGO PA 54 EAST ERIE ST, CHICAGO, IL 60611 SN 1072-7515 J9 J AM COLL SURGEONS JI J. Am. Coll. Surg. PD OCT PY 1997 VL 185 IS 4 BP 315 EP 327 DI 10.1016/S1072-7515(01)00938-3 PG 13 WC Surgery SC Surgery GA XZ460 UT WOS:A1997XZ46000001 PM 9328380 ER PT J AU Daley, J Khuri, SF Henderson, W Hur, K Gibbs, JO Barbour, G Demakis, J Irvin, G Stremple, JF Grover, F McDonald, G Passaro, E Fabri, PJ Spencer, J Hammermeister, K Aust, JB Oprian, C AF Daley, J Khuri, SF Henderson, W Hur, K Gibbs, JO Barbour, G Demakis, J Irvin, G Stremple, JF Grover, F McDonald, G Passaro, E Fabri, PJ Spencer, J Hammermeister, K Aust, JB Oprian, C TI Risk adjustment of the postoperative morbidity rate for the comparative assessment of the quality of surgical care: Results of the National Veterans Affairs Surgical Risk Study SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS LA English DT Article ID HOSPITAL DISCHARGE DATA; ARTERY BYPASS-SURGERY; CARDIAC-SURGERY; HEALTH-CARE; CONTINUOUS IMPROVEMENT; PROGNOSTIC PREDICTION; PROSPECTIVE PAYMENT; ADVERSE EVENTS; MORTALITY; COMPLICATIONS AB Background: The National Veterans Affairs Surgical Risk Study was designed to collect reliable, valid data on patient risk and outcomes for major surgery in the Veterans Health Administration and to report comparative risk-adjusted postoperative mortality and morbidity rates for surgical services in the Veterans Health Administration. Study Design: This was a cohort study conducted at 44 Veterans Affairs Medical Centers closely affiliated with university medical centers. Included were 87,078 major noncardiac operations performed under general, spinal, or epidural anesthesia between October 1, 1991, and December 31, 1993. The main outcomes measures in this report are 21 postoperative adverse events (morbidities) occurring within 30 days after the index procedure. Multivariable logistic regression risk-adjustment models for all operations and for eight surgical subspecialties were developed, Results: Patient risk factors predictive of postoperative morbidity included serum albumin level, American Society of Anesthesia class, the complexity of the operation, and 17 other preoperative risk variables. Wide variation in the unadjusted rates of one or more postoperative morbidities for all operations was observed across the 44 hospitals (7.4-28.4%). Risk-adjusted observed-to-expected ratios ranged from 0.49 to 1.46. The Spearman rank order correlation between the ranking of the hospitals based on unadjusted morbidity rates and risk-adjusted observed-to-expected ratios for all operations was 0.87. There was little or no correlation between the rank order of the hospitals by risk-adjusted morbidity and risk-adjusted mortality. Conclusions: The Department of Veterans Affairs has successfully implemented a system for the prospective collection and comparative reporting of postoperative mortality and morbidity rates after major noncardiac operations. Risk adjustment had only a modest effect on the rank order of the hospitals. (C) 1997 by the American College of Surgeons. C1 HARVARD UNIV,SCH MED,BOSTON,MA. BETH ISRAEL MED CTR,DIV GEN MED & PRIMARY CARE,BOSTON,MA. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HINES VA CTR COOPERAT STUDIES HLTH SERV,HINES,IL. WASHINGTON VA MED CTR,WASHINGTON,DC. GEORGE WASHINGTON UNIV,SCH MED,WASHINGTON,DC. UNIV MIAMI,DEPT SURG,MIAMI,FL 33152. UNIV MIAMI,SCH MED,MIAMI,FL 33152. MIAMI VA MED CTR,MIAMI,FL. PITTSBURGH VA MED CTR,PITTSBURGH,PA. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA. DENVER VA MED CTR,DENVER,CO. UNIV COLORADO,HLTH SCI CTR,DENVER,CO. DEPT VET AFFAIRS HEADQUARTERS,DEPT SURG,WASHINGTON,DC. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. TAMPA VA MED CTR,TAMPA,FL. UNIV S FLORIDA,COLL MED,TAMPA,FL. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. RP Daley, J (reprint author), BROCKTON W ROXBURY VET AFFAIRS MED CTR,1400 VFW PKWY,W ROXBURY,MA 02132, USA. NR 53 TC 342 Z9 346 U1 4 U2 7 PU AMER COLL SURGEONS PI CHICAGO PA 54 EAST ERIE ST, CHICAGO, IL 60611 SN 1072-7515 J9 J AM COLL SURGEONS JI J. Am. Coll. Surg. PD OCT PY 1997 VL 185 IS 4 BP 328 EP 340 DI 10.1016/S1072-7515(01)00939-5 PG 13 WC Surgery SC Surgery GA XZ460 UT WOS:A1997XZ46000002 PM 9328381 ER PT J AU Haverstock, BD Barth, LD Jacobs, AM AF Haverstock, BD Barth, LD Jacobs, AM TI Ankle arthrodesis following avascular necrosis of the talus in a patient with lupus SO JOURNAL OF THE AMERICAN PODIATRIC MEDICAL ASSOCIATION LA English DT Article ID ISCHEMIC NECROSIS; EARLY DIAGNOSIS; OSTEONECROSIS; ERYTHEMATOSUS; BONE AB Avascular necrosis of bone is a common manifestation of systemic lupus erythematosus, particularly in those patients receiving corticosteroids. The authors review the pathogenesis and diagnosis of avascular necrosis and describe an ankle arthrodesis in a patient with systemic lupus erythematosus who developed avascular necrosis of the talus. C1 DEACONESS MED CTR,DEPT PODIATR MED & SURG,ST LOUIS,MO. NR 56 TC 4 Z9 4 U1 0 U2 0 PU AMER PODIATRIC MED ASSN PI BETHESDA PA 9312 OLD GEORGETOWN ROAD, BETHESDA, MD 20814-1621 SN 0003-0538 J9 J AM PODIAT MED ASSN JI J. Am. Podiatr. Med. Assoc. PD OCT PY 1997 VL 87 IS 10 BP 483 EP 489 PG 7 WC Orthopedics SC Orthopedics GA YB573 UT WOS:A1997YB57300006 PM 9351319 ER PT J AU Curhan, GC Willett, WC Rimm, EB Stampfer, MJ AF Curhan, GC Willett, WC Rimm, EB Stampfer, MJ TI Family history and risk of kidney stones SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID FOOD FREQUENCY QUESTIONNAIRE; CALCIUM; NEPHROLITHIASIS; DISEASE; REPRODUCIBILITY; VALIDITY AB Kidney stones develop more frequently in individuals with a family history of kidney stones than in those without a family history; however, little information is available regarding whether the increased risk is attributable to genetic factors, environmental exposures, or some combination. In this report, the relation between family history and risk of kidney stone formation was studied in a cohort of 37,999 male participants in the Health Professionals Follow-up Study. Information on family history, kidney stone formation, and other exposures of interest, including dietary intake, was obtained by mailed questionnaires. A family history of-kidney stones was much more common in men with a personal history of stones at baseline in 1986 than in those without a history of stones (age-adjusted prevalence odds ratio, 3.16; 95% confidence interval [CI], 2.90 to 3.45). During 8 yr of follow-up, 795 incident cases of stones were documented. After adjusting for a variety of risk factors, the relative risk of incident stone formation in men with a positive family history, compared with those without, was 2.57 (95% CI, 2.19 to 3.02). Family history did not modify the inverse association between dietary calcium intake and the risk of stone formation. These results suggest that a family history of kidney stones substantially increases the risk of stone formation. In addition, these data suggest that dietary calcium restriction may increase the risk of stone formation, even among individuals with a family history of kidney stones. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP Curhan, GC (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,665 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA55075]; NHLBI NIH HHS [HL35464]; NIDDK NIH HHS [DK45362] NR 21 TC 122 Z9 131 U1 0 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD OCT PY 1997 VL 8 IS 10 BP 1568 EP 1573 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA XY974 UT WOS:A1997XY97400010 PM 9335385 ER PT J AU Patel, A Dorey, F Franklin, J deKernion, JB AF Patel, A Dorey, F Franklin, J deKernion, JB TI Recurrence patterns after radical retropubic prostatectomy: Clinical usefulness of prostate specific antigen doubling times and log slope prostate specific antigen SO JOURNAL OF UROLOGY LA English DT Article DE prostate; prostate-specific antigen; prostatectomy; linear models; recurrence ID LOCAL RECURRENCE; CANCER; ADENOCARCINOMA; PROGRESSION; LEUPROLIDE; FLUTAMIDE; THERAPY; RATES AB Purpose: We studied the correlation between prostate specific antigen (PSA) doubling time or, equivalently, log slope PSA and clinical recurrence in patients with detectable PSA after radical retropubic prostatectomy who were followed expectantly. Materials and Methods: In patients with PSA recurrence after radical retropubic prostatectomy log slope PSA was determined from the difference in the 2 log PSA values divided by the time between readings in months. For a given slope the corresponding PSA doubling time was calculated as log x 2 divided by the slope of the log PSA line. When the initial PSA value was considerably greater than 0.4 ng./ml., the log slope PSA plot was extrapolated to determine the time point at which PSA would have become detectable (0.4 ng./ml.). The relationship between these values, and the time and pattern of clinical recurrence were studied. Results: In this series of 77 patients 80% with PSA doubling time of 6 months or greater remained clinically disease-free compared to 64% with PSA doubling time less than 6 months. PSA doubling time had better correlation with time to clinical recurrence after PSA became detectable (p <0.001 Cox proportional hazards model) than Gleason sum, pathological stage or margin status. Biochemical recurrence within 3 months was associated with early clinical recurrence (p <0.002). In addition, short PSA doubling time, that is a high log slope, regardless of the time at which PSA became positive was strongly associated with clinical recurrence (p <0.001). Distant recurrence was invariably associated with short PSA doubling time. Conversely, local recurrence reliably correlated with long PSA doubling time, that is a low log slope. Conclusions: After PSA became detectable PSA doubling time or, equivalently, log slope PSA, was a better indicator of the risk and time to clinical recurrence after radical retropubic prostatectomy than preoperative PSA, specimen Gleason sum or pathological stage. Hormone treatment may be targeted to patients at high risk for early metastatic clinical recurrence, appropriately timed radiation can be offered for proved local recurrence in those with long PSA doubling time and expectant treatment may be proposed for those with long PSA doubling time who remain clinically disease-free. Frequent and expensive imaging does not appear to be cost-effective in this latter group. C1 UNIV CALIF LOS ANGELES,DEPT UROL ONCOL & BIOSTAT,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,DEPT UROL ONCOL,LOS ANGELES,CA 90073. RP Patel, A (reprint author), UNIV CALIF LOS ANGELES,DEPT UROL,LOS ANGELES,CA 90024, USA. NR 21 TC 207 Z9 211 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD OCT PY 1997 VL 158 IS 4 BP 1441 EP 1445 DI 10.1016/S0022-5347(01)64238-1 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA XV524 UT WOS:A1997XV52400034 PM 9302139 ER PT J AU Liu, HM Wu, XY Xiao, HL Conway, JA Kappes, JC AF Liu, HM Wu, XY Xiao, HL Conway, JA Kappes, JC TI Incorporation of functional human immunodeficiency virus type 1 integrase into virions independent of the Gag-Pol precursor protein SO JOURNAL OF VIROLOGY LA English DT Article ID VIRAL NUCLEIC-ACIDS; REVERSE-TRANSCRIPTASE; DNA INVITRO; GENETIC-ANALYSIS; CELL-LINE; EXPRESSION; MUTANTS; LOCALIZATION; REPLICATION; INFECTION AB Retroviral integrase (IN) is expressed and incorporated into virions as part of the Gag-Pol polyprotein precursor. IN catalyzes integration of the proviral DNA into host cell chromosomes during the early stages of the virus life cycle, and as a component of Gag-Pol, it is involved in virion morphogenesis during late stages. It is unknown whether the scheme, conserved among retroviruses, for expressing and incorporating IN as a component of the Gag-Pol precursor protein is necessary for its function in the infected cell after viral entry. We have developed human immunodeficiency virus (HIV) virion-associated accessory proteins (Vpr and Vpx) as vehicles to deliver both foreign and viral proteins into the virus particle by their expression in trans as heterologous fusion proteins (X. Wu, et al., J. virol. 69:3389-3398, 1995; X. Wu, et al., J. Virol. 70:3378-3384, 1996; X. Wu, et al., EMBO J. 16:5113-5122, 1977). To analyze IN function independent of its expression as a part of Gag-Pol, we expressed and incorporated IN into HIV type 1 (HIV-1) virions in trans as a fusion partner of Vpr (Vpr-IN). Our results demonstrate that the Vpr-IN fusion protein is efficiently incorporated into virions and then processed by the viral protease to liberate the IN protein. Virus derived from IN-minus provirus is noninfectious. However, this defect is overcome by trans complementation with the Vpr-IN fusion protein. Moreover, complemented virions are able to replicate through a complete cycle of infection, included formation of the provirus (integration). These results show, for the first time, that full IN function can be provided in trans, independent of its expression and incorporation into virions as a component of Gag-Pol. This finding also indicates that the IN domain of Gag-Pol is not required for the formation of infectious virions when IN is provided in trans. The ability to incorporate functional IN into retroviral particles in trans will provide unique opportunities to explore the function of this critical enzyme in a biologically relevant context, i.e., in infected cells as part of the nucleoprotein/preintegration complex. C1 UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. BIRMINGHAM VET AFFAIRS MED CTR,RES SERV,BIRMINGHAM,AL 35233. FU NIAID NIH HHS [AI31816, P30-AI-27767] NR 32 TC 28 Z9 28 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD OCT PY 1997 VL 71 IS 10 BP 7704 EP 7710 PG 7 WC Virology SC Virology GA XW142 UT WOS:A1997XW14200068 PM 9311854 ER PT J AU Johnson, RP Glickman, RL Yang, JQ Kaur, A Dion, JT Mulligan, MJ Desrosiers, RC AF Johnson, RP Glickman, RL Yang, JQ Kaur, A Dion, JT Mulligan, MJ Desrosiers, RC TI Induction of vigorous cytotoxic T-lymphocyte responses by live attenuated simian immunodeficiency virus SO JOURNAL OF VIROLOGY LA English DT Article ID BLOOD MONONUCLEAR-CELLS; RECOMBINANT VACCINIA VIRUS; LOW VIRAL LOAD; RHESUS-MONKEYS; HIV-1 INFECTION; NEUTRALIZING ANTIBODIES; DELETION MUTANT; MACAQUES; SIV; PROTECTION AB Although live attenuated vaccine strains of simian immunodeficiency virus (Sn) have proven highly effective in protecting macaques against challenge with pathogenic SIV strains, little is known about the mechanisms of protective immunity induced by these vaccines, We examined cytotoxic T-lymphocyte (CTL) responses against SIV in animals infected with SIVmac239 Delta nef (deficient in nef) or STVmac239 Delta 3 (deficient in nef, vpr, and upstream sequences in U3), To enhance detection of SN-specific CTL activity, we stimulated peripheral blood mononuclear cells with autologous B-lymphoblastoid cell lines which had been infected with recombinant vaccinia viruses expressing SIV proteins and subsequently inactivated with psoralen and UV light. Animals chronically infected with SIV239 Delta nef or SN239 Delta 3 mounted vigorous CTL responses against the SIV Gag and Env proteins, This CTL activity was major histocompatibility class restricted and mediated by CD8(+) T lymphocytes, CTL responses persisted at relatively high levels for more than 6 Sears after infection, Limiting dilution precursor frequency assays demonstrated that the frequency of SN-specific CTLs was as high as 234 CTL precursors per 100,000 cells, Animals acutely infected with SN239 Delta nef developed CTL activity by day 14 after infection, coincident with decreases in viral load, Animals acutely infected with SIV239 Delta 3 developed CTL responses within 4 weeks of infection, Thus, vaccination of juvenile or adult animals with SN239 Delta nef or SN239 Delta 3 results in the induction of a vigorous CTL response which arises early in the course of infection and persists for gears after a single inoculation of virus. C1 HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,DIV MICROBIOL,SOUTHBOROUGH,MA 01772. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,AIDS RES CTR,BOSTON,MA 02115. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294. RP Johnson, RP (reprint author), HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,DIV IMMUNOL,1 PINE HILL DR,POB 9102,SOUTHBOROUGH,MA 01772, USA. FU NCRR NIH HHS [RR 00055, RR 00168]; NIAID NIH HHS [AI35365] NR 67 TC 127 Z9 127 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD OCT PY 1997 VL 71 IS 10 BP 7711 EP 7718 PG 8 WC Virology SC Virology GA XW142 UT WOS:A1997XW14200069 PM 9311855 ER PT J AU Geller, SE Bernstein, SJ Harlow, SD AF Geller, SE Bernstein, SJ Harlow, SD TI The decision-making process for the treatment of abnormal uterine bleeding SO JOURNAL OF WOMENS HEALTH LA English DT Article ID SMALL-AREA VARIATIONS; MEFENAMIC-ACID; UNITED-STATES; MEDICAL-CARE; HYSTERECTOMY; OUTCOMES; PATIENT; MENORRHAGIA; PREFERENCES; INFORMATION AB This pilot study was conducted to investigate the treatment decision-making process of patients and physicians for abnormal uterine bleeding (AUB). Frequently, women with AUB are referred for hysterectomy without diagnostic workup, alternative therapeutic management, or patient input (i.e., patient treatment preferences). Variations in treatment strategies used for patients may be related to a number of factors external to the patient's underlying disease. However, little is known about which factors are most influential or about the extent to which they influence physicians',and patients' decisions. We prospectively followed the management and treatment of 52 women with complaints of AUB and examined differences in treatment among these patients. Extensive previsit interviews were conducted with these women to identify each patient's symptoms, health status, functional status, and preferences for and expectations of treatment. We then conducted telephone interviews within a week of the visit and again 9-12 months later to determine the treatment plan, patient level of participation in and satisfaction with the treatment, symptoms, and functional status. Overall, our findings suggest that patients want to be involved in making treatment decisions and that when women were presented with alternatives to hysterectomy, many chose alternative medical therapy or other surgical procedures. In addition, women reported that these alternative treatments produced significant improvement in symptom intensity and functioning. Increased patient participation in decision making enhanced patient satisfaction. These findings suggest that hysterectomy rates may be decreased by offering women alternative treatments and by finding ways to increase women's participation in their treatment decisions. C1 UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,ANN ARBOR,MI. US DEPT VET AFFAIRS,ANN ARBOR,MI. UNIV MICHIGAN,SCH PUBL HLTH,DEPT EPIDEMIOL,ANN ARBOR,MI 48109. RP Geller, SE (reprint author), UNIV ILLINOIS,SCH PUBL HLTH,DEPT COMMUNITY HLTH SCI,2035 W TAYLOR,CHICAGO,IL 60612, USA. NR 33 TC 13 Z9 13 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1059-7115 J9 J WOMENS HEALTH JI J. Womens Health PD OCT PY 1997 VL 6 IS 5 BP 559 EP 567 DI 10.1089/jwh.1997.6.559 PG 9 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 YE674 UT WOS:A1997YE67400012 PM 9356979 ER PT J AU Lieberthal, W AF Lieberthal, W TI Biology of acute renal failure: Therapeutic implications SO KIDNEY INTERNATIONAL LA English DT Editorial Material ID PROGRAMMED CELL-DEATH; ACUTE TUBULAR-NECROSIS; NITRIC-OXIDE SYNTHASE; EPITHELIAL-CELLS; RECEPTOR ANTAGONIST; LEUKOCYTE ADHESION; PROXIMAL TUBULE; GENE-EXPRESSION; RELAXING FACTOR; GROWTH-FACTORS C1 TUFTS UNIV NEW ENGLAND MED CTR, DIV NEPHROL, BOSTON, MA 02111 USA. TUFTS UNIV, SCH MED, BOSTON, MA 02111 USA. JOSLIN DIABET CTR, RENAL UNIT, BOSTON, MA 02215 USA. RP Lieberthal, W (reprint author), BOSTON UNIV, MED CTR, RENAL SECT, 88 E NEWTON ST, BOSTON, MA 02118 USA. NR 108 TC 45 Z9 47 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 EI 1523-1755 J9 KIDNEY INT JI Kidney Int. PD OCT PY 1997 VL 52 IS 4 BP 1102 EP 1115 DI 10.1038/ki.1997.435 PG 14 WC Urology & Nephrology SC Urology & Nephrology GA XY564 UT WOS:A1997XY56400028 ER PT J AU Shapiro, JI AF Shapiro, JI TI Pathogenesis of cardiac dysfunction during metabolic acidosis: Therapeutic implications SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT Conference Honoring Dr. Robert W Schrier CY NOV 09, 1996 CL DENVER, CO DE intracellular pH; adenosine triphosphate; acidosis; mitochondria; cardiac function ID NUCLEAR MAGNETIC-RESONANCE; HYPOXIC LACTIC-ACIDOSIS; SODIUM-BICARBONATE; SYSTEMIC ACIDOSIS; SKELETAL-MUSCLE; ISOLATED HEART; PH RESPONSES; CARBICARB; RAT; BRAIN C1 UNIV COLORADO,SCH MED,DEPT MED,DENVER VA MED CTR,DENVER,CO. UNIV COLORADO,SCH MED,DEPT RADIOL,DENVER,CO. UNIV COLORADO,SCH MED,WEBB WARING INST BIOMED RES,GILES FILLEY RES LAB,DENVER,CO. NR 33 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD OCT PY 1997 SU 61 BP S47 EP S51 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA XX137 UT WOS:A1997XX13700014 ER PT J AU Youssef, TF Poe, DS AF Youssef, TF Poe, DS TI Endoscope-assisted second-stage tympanomastoidectomy SO LARYNGOSCOPE LA English DT Article; Proceedings Paper CT Meeting of the Eastern Section of the American-Laryngological-Rhinological-and-Otological-Society CY JAN 31-FEB 02, 1997 CL BOSTON, MA SP Amer Laryngol Rhinol & Otol Soc, E Sect ID EAR SURGERY AB Intact canal wall mastoidectomy techniques for cholesteatoma are often followed by a planned second look for residual disease and possible ossicular reconstruction. Endoscopic techniques may reduce morbidity but introduce new concerns. Twenty-five consecutive second-look procedures were performed from July 1994 to July 1996 utilizing endoscopes in 19 cases and avoiding or terminating their use in the others because of known difficult anatomy, inadequate exposure, or excessive bleeding. Thirteen cases were prospectively explored first through a planned exclusively endoscopic approach and then opened for a conventional second look in comparison. In one of the 13 cases, endoscopy was abandoned. There were no cases in which endoscopy yielded a false-negative result. Endoscopes underestimated the size of recurrence in one case. Our experience, indications, and precautions for endoscope-assisted second-stage tympanomastoidectomy are presented. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. NR 5 TC 21 Z9 26 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD OCT PY 1997 VL 107 IS 10 BP 1341 EP 1344 DI 10.1097/00005537-199710000-00009 PG 4 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA XZ927 UT WOS:A1997XZ92700009 PM 9331310 ER PT J AU Voena, C Ladetto, M Astolfi, M Provan, D Gribben, JG Boccadoro, M Pileri, A Corradini, P AF Voena, C Ladetto, M Astolfi, M Provan, D Gribben, JG Boccadoro, M Pileri, A Corradini, P TI A novel nested-PCR strategy for the detection of rearranged immunoglobulin heavy-chain genes in B cell tumors SO LEUKEMIA LA English DT Article DE B cell malignancies; IgH nested-PCR; minimal residual disease ID ACUTE LYMPHOBLASTIC-LEUKEMIA; MINIMAL RESIDUAL DISEASE; DOSE SEQUENTIAL CHEMORADIOTHERAPY; ACUTE PROMYELOCYTIC LEUKEMIA; BONE-MARROW TRANSPLANTATION; MULTIPLE-MYELOMA; CLINICAL-SIGNIFICANCE; RELEVANCE; LYMPHOMAS; RELAPSE AB Several methods have been developed for the detection of minimal residual disease (MRD) in B cell tumors. Chromosomal translocations or the rearrangement of the immunoglobulin heavy chain (IgH) and T cell receptor genes are generally employed. We report a novel PCR method to detect MRD using IgH genes. IgH rearranged variable region (VDJ) were amplified from tumor specimens using consensus primers for variable and joining region genes. Complementarity-determining regions (CDR) were identified and used to generate tumor-specific primers. Two-round amplifications using primers derived from CDRs and joining or constant regions were performed for MRD detection. IgH nested-PCR approach was tested on a panel of 75 B cell tumors including acute lymphoblastic and chronic lymphocytic leukemias, non-Hodgkin's lymphomas and multiple myelomas. A VDJ sequence was obtained in 62 out of 75 cases (83%). Sensitivity using DNA or cDNA templates was 10(-5) and (-6), respectively. This method is specific and sensitive and provides a simple, non-radioactive approach for the evaluation of MRD in B cell tumors. C1 UNIV TURIN,DIPARTIMENTO MED & ONCOL SPERIMENTALE,DIV EMATOL,AZIENDA OSPED SAN GIOVANNI BATTISTA,TURIN,ITALY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. OI LADETTO, Marco/0000-0002-8283-2681 NR 31 TC 74 Z9 75 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD OCT PY 1997 VL 11 IS 10 BP 1793 EP 1798 DI 10.1038/sj.leu.2400801 PG 6 WC Oncology; Hematology SC Oncology; Hematology GA YA291 UT WOS:A1997YA29100028 PM 9324303 ER PT J AU Avraham, S Avraham, H AF Avraham, S Avraham, H TI Characterization of the novel focal adhesion kinase RAFTK in hematopoietic cells SO LEUKEMIA & LYMPHOMA LA English DT Review DE novel focal adhesion kinase; RAFTK; hematopoietic cells ID PROTEIN-TYROSINE KINASE; INTEGRIN-DEPENDENT PHOSPHORYLATION; SIGNAL-TRANSDUCTION; KAPOSIS-SARCOMA; GROWTH-FACTOR; INFLAMMATORY CYTOKINES; ACTIN CYTOSKELETON; TRANSFORMED-CELLS; MOLECULAR-CLONING; ACTIVATION AB Protein tyrosine kinases (PTKs) mediate signals that respond to many pivotal cellular functions. Tyrosine phosphorylation, controlled by the coordinated actions of protein tyrosine phosphatases (PTPs) and PTKs, is a critical control mechanism for various physiological processes, including cell growth, differentiation, metabolism, cell cycle regulation and cytoskeleton function. The focal adhesion kinase (FAK) is a widely expressed non-receptor tyrosine kinase that is implicated in integrin-mediated signaling and plays a role in signal transduction pathways mediating cell adhesion, motility and anchorage-independent growth. Recently, we and others have identified a novel protein tyrosine kinase termed RAFTK, (also known as Pyk2 or Cak-beta), which is related to FAK. This review describes the role of RAFTK in various signaling cascades mainly in reference to hematopoietic cell lineages. C1 HARVARD UNIV,INST MED,BIDMC,DIV EXPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL51456, HL55445] NR 79 TC 24 Z9 24 U1 0 U2 4 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-8194 J9 LEUKEMIA LYMPHOMA JI Leuk. Lymphoma PD OCT PY 1997 VL 27 IS 3-4 BP 247 EP 256 PG 10 WC Oncology; Hematology SC Oncology; Hematology GA YG894 UT WOS:A1997YG89400006 PM 9402324 ER PT J AU Klingenspor, M Bodnar, J Welch, C Xia, XR Lusis, AJ Reue, K AF Klingenspor, M Bodnar, J Welch, C Xia, XR Lusis, AJ Reue, K TI Localization of ubiquitin gene family members to mouse Chromosomes 5, 11, and 18 SO MAMMALIAN GENOME LA English DT Article ID POLYUBIQUITIN GENE; UBB C1 W LOS ANGELES VET AFFAIRS MED CTR,LIPID RES LAB,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,INST MOL BIOL,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,DEPT MICROBIOL & MOL GENET,LOS ANGELES,CA 90095. RI Klingenspor, Martin/D-6930-2011; OI Klingenspor, Martin/0000-0002-4502-6664 FU NHLBI NIH HHS [HL28481] NR 10 TC 1 Z9 1 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD OCT PY 1997 VL 8 IS 10 BP 789 EP 790 DI 10.1007/s003359900572 PG 2 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA XY081 UT WOS:A1997XY08100022 PM 9321482 ER PT J AU Gulli, G Rossetti, L DeFronzo, RA AF Gulli, G Rossetti, L DeFronzo, RA TI Hyperamylinemia is associated with hyperinsulinemia in the glucose-tolerant, insulin-resistant offspring of two Mexican-American non-insulin-dependent diabetic parents SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID ISLET AMYLOID POLYPEPTIDE; PERFUSED RAT PANCREAS; BETA-CELL; EUGLYCEMIC CLAMP; INCREASED RISK; AMYLIN; SECRETION; SENSITIVITY; MELLITUS; INVIVO AB Several investigations have presented evidence that amylin inhibits insulin Secretion and induces insulin resistance both in vitro and in vivo. However, basal and postmeal amylin concentrations proved similar in non-insulin-dependent diabetes mellitus (NIDDM) patients and controls. Since hyperglycemia may alter both amylin and insulin secretion, we examined basal and glucose-stimulated amylin secretion in eight glucose-tolerant, insulin-resistant Mexican-American subjects with both parents affected with NIDDM (offspring) and correlated the findings with the insulin sensitivity data acquired by an insulin clamp. Eight offspring and eight Mexican-Americans without any family history of diabetes (controls) underwent measurement of fat free mass ((H2O)-H-3 dilution method), 180-minutes, 75-g oral glucose tolerance test (OGTT), and 40-mU/m(2), 180-minute euglycemic insulin clamp associated with H-3 - glucose infusion and indirect calorimetry. Fasting amylin was significantly increased in offspring versus controls (11.5 +/- 1.4 v 7.0 +/- 0.8 pmol/L, P < .05). After glucose ingestion, both total (3,073 +/- 257 v 1,870 +/- 202 pmol.L-1.min(-1), P < .01) and incremental (1,075 +/- 170 v 518 +/- 124 pmol.L-1.min(-1), P < .05) arias under the curve (AUCs) of amylin concentration were significantly greater in offspring. The amylin to insulin molar ratio was similar in offspring and controls at all time points. Basal and postglucose insulin and C-peptide concentrations were significantly increased in the offspring. No correlation was found between fasting amylin, postglucose amylin AUC or IAUC, and any measured parameter of glucose metabolism during a euglycemic-hyperinsulinemic clamp (total glucose disposal, 7.21 +/- 0,73 v 11.03 +/- 0.54; P < .001; nonoxidative glucose disposal, 3.17 +/- 0.59 v 6.33 +/- 0.56, P < .002; glucose oxidation, 4.05 +/- 0.46 v 4.71 +/- 0.21, P = NS; hepatic glucose production, 0.29 +/- 0.16 v 0.01, +/- 0.11, = NS; all mg.min(-1).kg(-1) fat-free mass, offspring v controls). In conclusion, these data do not support a causal role for amylin in the genesis of insulin resistance in NIDDM. Copyright (C) 1997 by W.B. Saunders Company. C1 UNIV TEXAS,HLTH SCI CTR,DIV DIABET,SAN ANTONIO,TX. YESHIVA UNIV,ALBERT EINSTEIN COLL MED,DIV ENDOCRINOL,BRONX,NY. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK-24092] NR 47 TC 12 Z9 12 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD OCT PY 1997 VL 46 IS 10 BP 1157 EP 1161 DI 10.1016/S0026-0495(97)90209-2 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA XY568 UT WOS:A1997XY56800011 PM 9322799 ER PT J AU Nielsen, GP OConnell, JX Dickersin, GR Rosenberg, AE AF Nielsen, GP OConnell, JX Dickersin, GR Rosenberg, AE TI Solitary fibrous tumor of soft tissue: A report of 15 cases, including 5 malignant examples with light microscopic, immunohistochemical, and ultrastructural data SO MODERN PATHOLOGY LA English DT Article DE soft tissue; solitary fibrous tumor; vulva ID UPPER RESPIRATORY-TRACT; DERMATOFIBROSARCOMA PROTUBERANS; DESMOPLASTIC FIBROBLASTOMA; AMIANTHOID FIBERS; PERIPHERAL-NERVE; PLEURA; MESOTHELIOMA; BENIGN; CD34; MEDIASTINUM AB We describe 15 soft tissue solitary fibrous tumors (SFTs) occurring in patients 24 to 78 years old (average, 50.6 yr). Ten tumors were benign and arose in the head and neck area (three tumors), thigh (two), vulva (two), upper arm (one), lower leg (one), and retroperitoneum (one). Five tumors were histologically malignant and arose in the thigh (two), abdominal wall (one), buttock (one), and retroperitoneum (one). All of the tumors were grossly well circumscribed. The benign tumors measured from 2 to 10 cm (average, 4.8 cm) and the malignant ones from 3 to 5.5 cm (average, 4.3 cm) in greatest diameter. Microscopically, the benign tumors showed areas of hypercellularity with variable amounts of collagenous and myxoid stroma; one had amianthoid fibers. The malignant tumors were composed of cytologically atypical cells enmeshed in a collagenous or myxoid extracellular matrix. Ultrastructural study of three benign and three malignant tumors showed fibroblastic differentiation; one benign tumor showed myofibroblastic differentiation. Immunohistochemically, all of the tumors examined were immunoreactive for vimentin, and seven of nine were positive for CD34, including all of the malignant ones. There was focal staining for muscle actin in two benign tumors and for Leu-7 in one benign tumor; there was no staining for cytokeratin, desmin, S-100 protein, epithelial membrane antigen, or smooth muscle actin in any of the examined tissues. Follow-up was available for eight patients for 6 to 21 months (average, 12 mo). No tumor recurred locally or metastasized. The SFTs reported herein support the experiences of others who recently described these tumors in the somatic soft tissues, In addition, our series highlights the occurrence of malignant SFTs in the soft tissues, SFTs should be separated from other spindle cell sarcomas, with which they can be confused. C1 VANCOUVER HOSP & HLTH SCI CTR,DEPT PATHOL,VANCOUVER,BC V5Z 1M9,CANADA. RP Nielsen, GP (reprint author), HARVARD UNIV,DEPT PATHOL,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT PATHOL LABS,FRUIT ST,BOSTON,MA 02114, USA. NR 72 TC 138 Z9 147 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD OCT PY 1997 VL 10 IS 10 BP 1028 EP 1037 PG 10 WC Pathology SC Pathology GA YB118 UT WOS:A1997YB11800010 PM 9346183 ER PT J AU Ding, HF Bustin, M Hansen, U AF Ding, HF Bustin, M Hansen, U TI Alleviation of histone H1-mediated transcriptional repression and chromatin compaction by the acidic activation region in chromosomal protein HMG-14 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID RNA-POLYMERASE-II; NEWBORN GUINEA-PIGS; ACTIVE CHROMATIN; NUCLEOSOME CORES; IN-VIVO; BINDING; DNA; GENES; COMPLEX; REPLICATION AB Histone H1 promotes the generation of a condensed, transcriptionally inactive, higher order chromatin structure. Consequently histone H1 activity must be antagonized in order to convert chromatin to a transcriptionally competent, more extended structure. Using simian virus 40 minichromosomes as a model system, we now demonstrate that the nonhistone chromosomal protein HMG-14, which is known to preferentially associate with active chromatin, completely alleviates histone H1-mediated inhibition of transcription by RNA polymerase II. HMG-14 also partially disrupts histone H1-dependent compaction of chromatin. Bath the transcriptional enhancement and chromatin-unfolding activities of HMG-14 are mediated through its acidic, C-terminal region. Strikingly, transcriptional and structural activities of HMG-14 are maintained upon replacement of the C-terminal fragment by acidic regions from either GAL4 or HMG-2. These data support the model that the acidic C terminus of HMG-14 is involved in unfolding higher-order chromatin structure to facilitate transcriptional activation of mammalian genes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOL GENET,B411,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOL GENET,BOSTON,MA 02115. NCI,MOL CARCINOGENESIS LAB,NIH,BETHESDA,MD 20892. RI Bustin, Michael/G-6155-2015 FU NCI NIH HHS [5T32CA0936] NR 74 TC 70 Z9 73 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD OCT PY 1997 VL 17 IS 10 BP 5843 EP 5855 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA XX658 UT WOS:A1997XX65800018 PM 9315642 ER PT J AU Waeber, C Moskowitz, MA AF Waeber, C Moskowitz, MA TI 5-Hydroxytryptamine(1A) and 5-hydroxytryptamine(1B) receptors stimulate [S-35]guanosine-5'-O-(3-thio)triphosphate binding to rodent brain sections as visualized by in vitro autoradiography SO MOLECULAR PHARMACOLOGY LA English DT Article ID GAMMA-S BINDING; GUANOSINE 5'-O-(GAMMA-THIO)TRIPHOSPHATE BINDING; RAT-BRAIN; G-PROTEINS; GUANOSINE-5'-O-(3-THIO)TRIPHOSPHATE BINDING; SIGNAL-TRANSDUCTION; GUINEA-PIG; GTP; LOCALIZATION; SEROTONIN AB [S-35]Guanosine-5'-O-(3-thio)triphosphate ([S-35]GTP gamma S) binding to G proteins was measured by in vitro autoradiography in guinea pig and rat brain sections after activation by 5-hydroxytryptamine (5-HT) receptor agonists. 5-Carboxamidotryptamine stimulated binding strongly in hippocampus and lateral septum and weakly in substantia nigra. This effect was blocked in the substantia nigra by the 5-HT1B/1D receptor antagonist GR-127,935 and in the former two regions by the 5-HT1A antagonist NAN-190. 5-HT1B/1D receptor agonists stimulated binding in substantia nigra and in areas containing 5-HT1A receptors. In guinea pig substantia nigra, 5-(nonyloxy)-tryptamine maximally stimulated [S-35]GTP gamma S binding by 54%, with an EC50 value of 62 nM; at 100 mu M, this agonist increased binding by similar to 200% in hippocampus (with a 2-fold weaker EC50 value). The distribution of [H-3]8-OH-DPAT binding sites was identical to that of the [S-35]GTP gamma S labeling stimulated by the 5-HT1A agonist (R)-8-hydroxy-2-dipropylaminotetralin [(R)-8-OH-DPAT)]. (R)-8-OH-DPAT, (S)-8-OH-DPAT, and buspirone stimulated [S-35]GTP gamma S binding in hippocampus by 340%, 140%, and 78%, with EC50 values of 71, 51, and 132 nM. Enhanced [S-35]GTP gamma S binding was not detected in the presence of 5-HT1F, 5-HT2, 5-HT4, and 5-HT7 receptor agonists, Because activation of mu-opioid, muscarinic M-2, histamine H-3, and cannabinoid receptors was also visualized successfully, these data suggest that only receptors coupled to pertussis toxin-sensitive G proteins can be seen by [S-35]GTP gamma S binding autoradiography. This study also shows that different 5-HT receptors coupled to these proteins can show a wide range of [S-35]GTP gamma S binding stimulation. Although the functional significance of these variations is unclear, this technique offers advantages over receptor autoradiography because it does not require high affinity radioligands and provides a measure of agonist efficacies in various brain regions. RP Waeber, C (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,NEUROL SERV,DEPT SURG,CHARLESTOWN,MA 02129, USA. RI Moskowitz, Michael/D-9916-2011; Waeber, Christian/A-8333-2009 OI Waeber, Christian/0000-0001-6078-0027 FU NINDS NIH HHS [1-P01-NS35611-01] NR 30 TC 59 Z9 59 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD OCT PY 1997 VL 52 IS 4 BP 623 EP 631 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA YA268 UT WOS:A1997YA26800010 PM 9380025 ER PT J AU Pereira, L Andrikopoulos, K Tian, J Lee, SY Keene, DR Ono, R Reinhardt, DP Sakai, LY Biery, NJ Bunton, T Dietz, HC Ramirez, F AF Pereira, L Andrikopoulos, K Tian, J Lee, SY Keene, DR Ono, R Reinhardt, DP Sakai, LY Biery, NJ Bunton, T Dietz, HC Ramirez, F TI Targetting of the gene encoding fibrillin-1 recapitulates the vascular aspect of Marfan syndrome SO NATURE GENETICS LA English DT Article ID DEVELOPING MOUSE AORTA; MICROFIBRILS; MUTATIONS; ORGANIZATION; COMPONENT; EXPRESSION; DELETION; REVEALS; MATRIX AB Aortic aneurysm and dissection account for about 2% of all deaths in industrialized countries; they are also components of several genetic diseases, including Marfan syndrome (MFS)(1). The vascular phenotype of MFS results from mutations in fibrillin-1 (FBN1), the major constituent of extracellular microfibrils(2,3). Microfibrils, either associated with or devoid of elastin, give rise to a variety of extracellular networks in elastic and non-elastic tissues(3). It is believed that microfibrils regulate elastic fibre formation by guiding tropo-elastin deposition during embryogenesis and early post-natal life(4). Hence, vascular disease in MFS is thought to result when FBN1 mutations preclude elastic fibre maturation by disrupting microfibrillar assembly, Here we report a gene-targetting experiment in mice that indicates that fibrillin-1 microfibrils are predominantly engaged in tissue homeostasis rather than elastic matrix assembly. This finding, in turn, suggests that aortic dilation is due primarily to the failure by the microfibrillar array of the adventitia to sustain physiological haemodynamic stress, and that disruption of the elastic network of the media is a secondary event. C1 CUNY MT SINAI SCH MED,BROOKDALE CTR DEV & MOL BIOL,NEW YORK,NY 10029. UNIV SAO PAULO,INST BIOCIENCIAS,DEPT BIOL,BR-05508 SAO PAULO,BRAZIL. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. SHRINERS HOSP CHILDREN,PORTLAND,OR 97201. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MOL BIOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT GENET,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT COMPARAT MED & PATHOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,HOWARD HUGHES MED INST,BALTIMORE,MD 21205. RI Pereira, Lygia/C-1049-2012; Reinhardt, Dieter/A-3102-2008 OI Pereira, Lygia/0000-0002-0002-725X; Reinhardt, Dieter/0000-0001-6535-9872 FU NIAMS NIH HHS [AR41135, AR42044] NR 27 TC 241 Z9 247 U1 6 U2 17 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD OCT PY 1997 VL 17 IS 2 BP 218 EP 222 DI 10.1038/ng1097-218 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA XZ555 UT WOS:A1997XZ55500033 PM 9326947 ER PT J AU Parr, MJ Manome, Y Tanaka, T Wen, P Kufe, DW Kaelin, WG Fine, HA AF Parr, MJ Manome, Y Tanaka, T Wen, P Kufe, DW Kaelin, WG Fine, HA TI Tumor-selective transgene expression in vivo mediated by an E2F-responsive adenoviral vector SO NATURE MEDICINE LA English DT Article ID RETINOBLASTOMA PROTEIN; CDK4 AMPLIFICATION; BRAIN-TUMORS; E2F-1 GENE; DELETION; DNA; GLIOBLASTOMAS; TRANSCRIPTION; PROGRESSION; MAJORITY AB Recent data suggest that many tumors, such as malignant gliomas, have disrupted pRB function, either because of RB-1 gene mutations or as a result of mutations affecting upstream regulators of pRB such as cyclin D1 or pl6/INK4a/MTS1 (ref. 1-5). Tumor suppression by pRB has been linked to its ability to repress E2F-responsive promoters such as the E2F-1 promoter(6,7). Thus, a prediction, which has not yet been demonstrated experimentally in vivo, is that EaF-responsive promoters should be more active in tumor cells relative to normal cells because of an excess of ''free'' E2F and loss of pRB/E2F repressor complexes. We demonstrate that adenoviral vectors that contain transgenes driven by the E2F-1 promoter can mediate tumor-selective gene expression in vivo, allowing for eradication of established gliomas with significantly less normal tissue toxicity than seen with standard adenoviral vectors. Our data indicate that de-repression of the E2F-1 promoter occurs in cancer cells in vivo, a finding that can be exploited to design viral vectors that mediate tumor-selective gene expression. C1 HARVARD UNIV,SCH MED,CTR NEUROONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,LAB CANC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,LAB NEOPLAST DIS MECHANISMS,DANA FARBER CANC INST,BOSTON,MA 02115. NR 24 TC 133 Z9 136 U1 1 U2 3 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD OCT PY 1997 VL 3 IS 10 BP 1145 EP 1149 DI 10.1038/nm1097-1145 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA XZ287 UT WOS:A1997XZ28700043 PM 9334729 ER PT J AU Kingston, RE AF Kingston, RE TI A snapshot of a dynamic nuclear building block SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID TRANSCRIPTION; YEAST; CHROMATIN; PROMOTER; COMPLEX; DOMAINS; MODEL; GENE; SIR3; H3 AB How does DNA in chromatin become accessible? The recent report of a nucleosome core particle structure offers insights into the dynamic interactions between chromatin and regulatory protein complexes. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. RP Kingston, RE (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOL BIOL,BOSTON,MA 02114, USA. NR 12 TC 9 Z9 9 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD OCT PY 1997 VL 4 IS 10 BP 763 EP 766 DI 10.1038/nsb1097-763 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA YA203 UT WOS:A1997YA20300002 PM 9334735 ER PT J AU Beal, MF AF Beal, MF TI New techniques for investigating mitochondrial DNA in neurodegenerative diseases SO NEUROLOGY LA English DT Editorial Material ID HEREDITARY OPTIC NEUROPATHY; COMPLEX-I DEFECT; MTDNA-LESS CELLS; MUTATION; RESPIRATION C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Beal, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV WRN 408,NEUROCHEM LAB,32 FRUIT ST,BOSTON,MA 02114, USA. NR 12 TC 5 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD OCT PY 1997 VL 49 IS 4 BP 907 EP 908 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA YC431 UT WOS:A1997YC43100001 PM 9339665 ER PT J AU Thomas, U Kim, E Kuhlendahl, S Koh, YH Gundelfinger, ED Sheng, M Garner, CC Budnik, V AF Thomas, U Kim, E Kuhlendahl, S Koh, YH Gundelfinger, ED Sheng, M Garner, CC Budnik, V TI Synaptic clustering of the cell adhesion molecule fasciclin II by discs-large and its role in the regulation of presynaptic structure SO NEURON LA English DT Article ID TUMOR-SUPPRESSOR GENE; DENSITY PROTEIN PSD-95; NMDA RECEPTOR SUBUNITS; FUNCTIONAL COMPONENTS; NEUROMUSCULAR-JUNCTIONS; DROSOPHILA-MELANOGASTER; GUANYLATE KINASES; CHANNEL PROTEINS; EMBRYONIC NEURON; MOTOR AXONS AB The cell adhesion molecule Fasciclin II (FASII) is involved in synapse development and plasticity. Here we provide genetic and biochemical evidence that proper localization of FASII at type I glutamatergic synapses of the Drosophila neuromuscular junction is mediated by binding between the intracellular tSXV bearing C-terminal tail of FASII and the PDZ1-2 domains of Discs-Large (DLG). Moreover, mutations in fasII and/or dig have similar effects on presynaptic ultrastructure, suggesting their functional involvement in a common developmental pathway. DLG can directly mediate a biochemical complex and a macroscopic cluster of FASII and Shaker Kf channels in heterologous cells. These results indicate a central role for DLG in the structural organization and downstream signaling mechanisms of cell adhesion molecules and ion channels at synapses. C1 UNIV MASSACHUSETTS,DEPT BIOL,AMHERST,MA 01003. FED INST NEUROBIOL,DEPT NEUROCHEM & MOL BIOL,D-39118 MAGDEBURG,GERMANY. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROBIOL,BOSTON,MA 02114. UNIV ALABAMA,DEPT NEUROBIOL,BIRMINGHAM,AL 35294. RI Kim, Eunjoon/C-1566-2011 FU NIA NIH HHS [AG12978-02]; NICHD NIH HHS [P50 HD32901]; NINDS NIH HHS [R01 NS030072, R01 NS30072] NR 66 TC 159 Z9 160 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD OCT PY 1997 VL 19 IS 4 BP 787 EP 799 DI 10.1016/S0896-6273(00)80961-7 PG 13 WC Neurosciences SC Neurosciences & Neurology GA YD189 UT WOS:A1997YD18900007 PM 9354326 ER PT J AU Postle, BR Locascio, JJ Corkin, S Growdon, JH AF Postle, BR Locascio, JJ Corkin, S Growdon, JH TI The time course of spatial and object learning in Parkinson's disease SO NEUROPSYCHOLOGIA LA English DT Article DE working memory; memory; dopamine; basal ganglia; caudate nucleus ID MONKEYS MACACA-FASCICULARIS; WORKING-MEMORY; FRONTAL-CORTEX; BASAL GANGLIA; COGNITIVE FUNCTION; PREFRONTAL CORTEX; PREMOTOR CORTEX; DISSOCIATION; DEFICITS; LESIONS AB Parkinson's disease (PD) is characterized by spatial memory dysfunction, but the selectivity of the deficit remains unclear. We addressed this issue by comparing performance on spatial and object variants of a conditional associative learning task, and by analysing the data with time series analytical techniques. The 11 PD subjects and 15 normal control subjects learned stimulus-stimulus pairings through trial-and-error learning. PD subjects were selectively impaired on the spatial condition: they required more trials to achieve criterion, learned at a slower rate and displayed a working memory deficit. The groups did not differ in the object condition. These results suggest a distinction between material-specific spatial and object visual memory systems. Further, they indicate that spatial learning and memory are selectively impaired in early PD, suggesting that interactions between the basal ganglia and prefrontal cortex are important for the mediation of high-level cognition. (C) 1997 Elsevier Science Ltd. C1 MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. MIT,CLIN RES CTR,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. FU NCRR NIH HHS [RR00088]; NIA NIH HHS [AG 06605, AG08812] NR 63 TC 46 Z9 48 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PD OCT PY 1997 VL 35 IS 10 BP 1413 EP 1422 DI 10.1016/S0028-3932(97)00054-7 PG 10 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA YA205 UT WOS:A1997YA20500011 PM 9347488 ER PT J AU Abad, JC An, B Power, WJ Foster, CS Azar, DT Talamo, JH AF Abad, JC An, B Power, WJ Foster, CS Azar, DT Talamo, JH TI A prospective evaluation of alcohol assisted versus mechanical epithelial removal before photorefractive keratectomy SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 100th Annual Meeting of the American-Academy-of-Ophthalmology CY OCT 27-31, 1996 CL CHICAGO, IL SP Amer Acad Ophthalmol ID CORNEAL EPITHELIUM; EXCIMER-LASER; KERATOCYTE LOSS; DEEPITHELIALIZATION; RABBITS; SURFACE; MYOPIA; INJURY AB Objective: The purpose of the study is to compare alcohol-assisted versus mechanical debridement of the corneal epithelium before photorefractive keratectomy (PRK) for low-to-moderate myopia. Design: A prospective study was performed on a group of consecutive patients operated on at the Massachusetts Eye and Ear Infirmary from February to April 1996 and followed for 6 months. Participants: Eighty patients (eyes) were divided in 2 groups: 40 alcohol and 40 mechanical. Intervention: The patients underwent PRK for myopia (-1.5 to -7.5 diopters) with a Summit Apex excimer laser. The corneal epithelium was removed either with 20% ethanol or with a scalpel blade. Main Outcome Measures: The two groups were compared for epithelial removal time, epithelial defect size at the end of surgery, and rate of re-epithelialization. Uncorrected visual acuity (UCVA), refractive outcome, best-corrected visual acuity (BCVA), and subjective haze were measured at 4 days and at 1, 3, and 6 months. In an additional short-term study, 40 patients (20 alcohol, 20 mechanical) had intraoperative pachymetry performed. Results: Alcohol-assisted de-epithelialization was faster than mechanical debridement (107 [+/-20.6 standard deviation] versus 141 [+/-30.5] seconds [P < 0.0001]) and led to a more circumscribed and reproducible epithelial defect at the end of surgery (87,739 [+/-11,852] versus 103,518 [+/-33,942] square pixels [t test, P = 0.04; f test, P = 0.001]). At 4 days, 95% of the alcohol-treated patients had healed compared with 78% of the mechanically scraped patients (Fisher's exact test, P = 0.04). The alcohol group had a better UCVA at 4 days (logarithm of the minimum angle of resolution UCVA 0.36 [+/-0.22] versus 0.51 [+/-0.26]) and at 1 month (0.14 [+/-0.17] versus 0.22 [+/-0.16] [Mann-Whitney U test, P = 0.02 and P = 0.03]) but equalized at 3 months (0.10 [+/-0.14] versus 0.13 [+/-0.16]) and at 6 months (0.11 [+/-0.15] versus 0.14 [+/-0.13] [Mann-Whitney U test, P = 0.23 and P = 0.34]). There was a trend toward less subjective haze in the alcohol-treated patients over the course of the study (area under the curve, 71.9 [+/-35.3] versus 87.9 [+/-33.8] [Mann-Whitney U test, P = 0.07]). The difference from target was equivalent in both groups at 6 months (-0.22 [+/-0.58] diopter in the alcohol group and -0.43 [+/-0.52] diopter in the mechanical group [t test, P = 0.14; f test, P = 0.57]). There were no differences in intraoperative pachymetry, corneal uniformity index as calculated from the corneal topography, and loss of BCVA between the two groups. Conclusions: Twenty percent ethanol is a simple, safe, and effective alternative to mechanical scraping before PRK and appears to be associated with a quicker visual rehabilitation. C1 HARVARD UNIV,SCH MED,CORNEA & REFRACT SERV,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA. HARVARD UNIV,SCH MED,IMMUNOL & UVEITIS SERV,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA. CORNEA CONSULTANTS,BOSTON,MA. NR 25 TC 45 Z9 45 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD OCT PY 1997 VL 104 IS 10 BP 1566 EP 1574 PG 9 WC Ophthalmology SC Ophthalmology GA XZ283 UT WOS:A1997XZ28300022 PM 9331192 ER PT J AU Dana, MR Schaumberg, DA Moyes, AL Gomes, JAP AF Dana, MR Schaumberg, DA Moyes, AL Gomes, JAP TI Corneal transplantation in children with Peters anomaly and mesenchymal dysgeneses SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT Centennial Meeting of the American-Academy-of-Ophthalmology CY OCT 27-31, 1996 CL CHICAGO, IL SP Amer Acad Ophthalmol ID PENETRATING KERATOPLASTY; PEDIATRIC KERATOPLASTY; INFANTS AB Objective: The purpose of the study is to describe graft and visual outcomes of penetrating keratoplasty among young children with Peters anomaly and associated mesenchymal dysgeneses. Design: The design was a multicenter retrospective analysis of the indications and outcome in pediatric keratoplasty. Participants: The records of all children aged 12 years and younger who underwent penetrating keratoplasty for mesenchymal dysgenesis between January 1975 and May 1993 at the participating centers were reviewed. Measures: The data were analyzed regarding graft survival and postoperative visual acuity. Results: Forty-seven corneal transplants in 36 eyes of 29 patients with mesenchymal dysgenesis were studied. The majority of eyes operated on (30) had Peters anomaly (83%). Patients' mean age at the time of keratoplasty was 7 months. After a mean followup period of 38 months, 61% of eyes retained full graft clarity. One and 3-year survival rates were 79% (95% confidence interval [CI] = 65%-93%) and 62% (95% CI = 45%-79%), respectively. Postoperative corneal ulcers/nonhealing epithelial defects (P = 0.03), and additional noncorneal surgical procedures at the time of transplantation (P = 0.05) were associated with graft failure. Provision of postoperative optical aids (P = 0.01) was associated with better postoperative visual acuity levels. Conclusions: Penetrating keratoplasty for Peters anomaly and related mesenchymal dysgeneses in young children has a reasonable chance of success during the critical years of visual maturation and is associated with satisfactory visual results in one third to half the cases. The data suggest that complicated cases requiring additional surgical procedures have a worse prognosis. C1 MASSACHUSETTS EYE & EAR INFIRM,CORNEA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,SCHEPENS EYE RES INST,BOSTON,MA. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV OPHTHALMOL,CORNEA & OCULAR IMMUNOL SERV,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV PREVENT MED,BOSTON,MA 02115. KANSAS CITY EYE ASSOCIATES,KANSAS CITY,KS. UNIV KANSAS,MED CTR,SCH MED,DEPT OPHTHALMOL,KANSAS CITY,KS 66103. THOMAS JEFFERSON UNIV,WILLS EYE HOSP,PHILADELPHIA,PA 19107. NR 16 TC 31 Z9 33 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD OCT PY 1997 VL 104 IS 10 BP 1580 EP 1586 PG 7 WC Ophthalmology SC Ophthalmology GA XZ283 UT WOS:A1997XZ28300025 PM 9331194 ER PT J AU Haimovici, R Gragoudas, ES Duker, JS Sjaarda, RN Eliott, D AF Haimovici, R Gragoudas, ES Duker, JS Sjaarda, RN Eliott, D TI Central serous chorioretinopathy associated with inhaled or intranasal corticosteroids SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT Combined Meeting of the Club-Jules-Gonin / Retina-Society CY SEP 05, 1996 CL BERNE, SWITZERLAND SP Club Jules Gonin, Retina Soc ID BULLOUS RETINAL-DETACHMENT; BETA-ADRENERGIC RECEPTORS; BECLOMETHASONE DIPROPIONATE; HYPERTENSIVE CHOROIDOPATHY; MALIGNANT HYPERTENSION; ASTHMATIC-CHILDREN; PIGMENT EPITHELIUM; FUNDUS LESIONS; A BEHAVIOR; GLUCOCORTICOIDS AB Objective: The purpose of the study is to investigate the relationship between inhaled or intranasal adrenergic agonists and corticosteroids and the development of central serous chorioretinopathy (CSC). Design: The medical records of three patients with CSC who were found to use inhaled adrenergic agents or corticosteroids or both were identified prospectively. A survey of members of the Retina, Macula, and Vitreous societies and the National Registry of Drug-induced Ocular Side Effects identified three additional cases. Results: Six patients with CSC were found to be chronic users of corticosteroid (four patients) or both beta adrenergic agonist and corticosteroid (two patients) metered dose inhalers or nasal sprays. in three cases, there was a close temporal correlation between the use of a corticosteroid nasal spray and the development of CSC. Conclusions: These findings suggest that, in patients who are susceptible, the periocular or systemic absorption of inhaled corticosteroids may be sufficient to produce CSC in humans, supporting previous hypotheses regarding the pathogenesis of the disorder, Further studies are needed to confirm this association and to determine whether inhaled adrenergic agents also contribute to the development of this disorder. Patients in whom CSC develops while using corticosteroid inhalers or nasal sprays should be alerted to the possible relationship between CSC and these agents. C1 HARVARD UNIV, MASSACHUSETTS EYE & EAR INFIRM, SCH MED, BOSTON, MA USA. NEW ENGLAND EYE CTR, BOSTON, MA USA. RETINA SPECIALISTS, BALTIMORE, MD USA. WAYNE STATE UNIV, KRESGE EYE INST, DETROIT, MI USA. RP Haimovici, R (reprint author), BOSTON UNIV, SCH MED, DEPT OPHTHALMOL, DOB-10, 720 HARRISON AVE, BOSTON, MA 02114 USA. NR 68 TC 76 Z9 81 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0161-6420 EI 1549-4713 J9 OPHTHALMOLOGY JI Ophthalmology PD OCT PY 1997 VL 104 IS 10 BP 1653 EP 1660 PG 8 WC Ophthalmology SC Ophthalmology GA XZ283 UT WOS:A1997XZ28300039 PM 9331207 ER PT J AU Sakellari, D Socransky, SS Dibart, S Eftimiadi, C Taubman, MA AF Sakellari, D Socransky, SS Dibart, S Eftimiadi, C Taubman, MA TI Estimation of serum antibody to subgingival species using checkerboard immunoblotting SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE periodontal disease; antibody; assay; quantification; chemiluminescence ID GINGIVAL CREVICULAR FLUID; RAPIDLY PROGRESSIVE PERIODONTITIS; LOCALIZED JUVENILE PERIODONTITIS; DEPENDENT CHEMI-LUMINESCENCE; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; ORAL MICROORGANISMS; ADULT PERIODONTITIS; DNA HYBRIDIZATION; YOUNG-ADULTS; RESPONSES AB Measurement of serum antibody to subgingival bacterial species has been useful in discriminating possible periodontal pathogens and in assessing the host's immune response to subgingival species. An immunoassay system was developed to measure the level of serum antibody to multiple subgingival species in multiple serum samples on a single nitrocellulose membrane. The principle steps of the assay are the following: I) binding of antigens from bacterial preparations and protein A in parallel lanes on nitrocellulose membranes; 2) incubation of known concentrations of human immunoglobulin as well as various dilutions of serum from patients in lanes perpendicular to the antigen lanes; 3) incubation of the membrane with a peroxidase-conjugated second antibody; 4) detection of positive reactions by enhanced chemiluminescence. Emitted light was captured on a photographic him in which the positive reactions appeared as squares at the intersections of antigens with appropriate antibody. Antibody was quantified using a laser densitometer to compare the signal intensity of unknown samples with the ones generated by known amounts of human immunoglobulin captured on the same membrane. The assay permitted simultaneous screening and/or quantification of antibody in as many as 45 serum samples against up to 45 bacterial species. The mean and standard error of the coefficients of variation for replicates within an assay averaged 7.3 +/- 2.3%. Coefficients of Variation of the assay run on different days for serum antibody to a range of subgingival species averaged 10.1 +/- 2.1%. Checkerboard immunoblotting is a simple and rapid immunoassay to permit quantification and/or screening of antibody to multiple subgingival species or antigens in multiple serum samples. C1 FORSYTH DENT CTR,DEPT PERIODONTOL & IMMUNOL,BOSTON,MA 02115. UNIV THESSALONIKI,SCH DENT,DEPT PERIODONTOL,THESSALONIKI,GREECE. RI SAKELLARI, DIMITRA/F-3299-2011; Eftimiadi, Costantino/F-3491-2015 OI Eftimiadi, Costantino/0000-0003-1510-4614 FU NIDCR NIH HHS [DE-03420, DE-04881] NR 54 TC 42 Z9 42 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD OCT PY 1997 VL 12 IS 5 BP 303 EP 310 DI 10.1111/j.1399-302X.1997.tb00395.x PG 8 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA XX512 UT WOS:A1997XX51200007 PM 9467384 ER PT J AU Loovis, CF Schall, DG Teter, DL AF Loovis, CF Schall, DG Teter, DL TI The role of assistive devices in the rehabilitation of hearing impairment SO OTOLARYNGOLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID BENEFIT AB Formal investigation and clinical experience have revealed success in the use of assistive devices in aiding speech understanding where conventional amplification alone has failed. The long-term benefits of this technology are keeping people, particularly the elderly, socially engaged and independent. To accomplish this end, hearing health care professionals have not only to arm themselves with a rapidly advancing, complex array of technical tools, but also to apply them efficaciously. This article provides an overview of these tools, the procedures for using them, the criteria for selecting them, and the resources for obtaining them. A discussion of the various types of assistive devices and their application is followed by a review of the principles for selection and fitting and concludes with a review of the modern role of the hearing health care provider. C1 VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA. MADIGAN ARMY MED CTR,DEPT OTOLARYNGOL HEAD & NECK SURG,TACOMA,WA 98431. DARREL L TETER & ASSOCIATES INC,HIGHLANDS RANCH,CO. NR 38 TC 5 Z9 5 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0030-6665 J9 OTOLARYNG CLIN N AM JI Otolaryngol. Clin. N. Am. PD OCT PY 1997 VL 30 IS 5 BP 803 EP & PG 46 WC Otorhinolaryngology SC Otorhinolaryngology GA YB166 UT WOS:A1997YB16600010 PM 9295255 ER PT J AU Eibling, DE Boyd, EM AF Eibling, DE Boyd, EM TI Rehabilitation of lower cranial nerve deficits SO OTOLARYNGOLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID VOCAL CORD PARALYSIS; RADICAL NECK DISSECTION; PASSY-MUIR VALVE; INTRACTABLE ASPIRATION; TRACHEOSTOMY; THYROPLASTY; DYSPHAGIA; INJECTION; PRESSURE; SURGERY AB Lower cranial nerve deficits following skull base surgery can be accompanied by significant morbidity, especially if the vagus nerve has been sacrificed or injured. Loss of pharyngeal function and glottic closure can result in dysphagia and aspiration. Left untreated, these can result in the major morbidity for the patient following skull base surgery. The authors discuss the management of lower cranial nerve deficits, with emphasis on rehabilitation of swallowing function and prevention of aspiration following vagal injury. C1 UNIV PITTSBURGH,SCH MED,VA PITTSBURGH HLTH CARE SYST,DEPT OTOLARYNGOL,PITTSBURGH,PA. WILFORD HALL USAF MED CTR,DEPT OTOLARYNGOL,LACKLAND AFB,TX 78236. NR 32 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0030-6665 J9 OTOLARYNG CLIN N AM JI Otolaryngol. Clin. N. Am. PD OCT PY 1997 VL 30 IS 5 BP 865 EP & PG 12 WC Otorhinolaryngology SC Otorhinolaryngology GA YB166 UT WOS:A1997YB16600012 PM 9295257 ER PT J AU Meyer, JH Lake, R AF Meyer, JH Lake, R TI Mismatch of duodenal deliveries of dietary fat and pancreatin from enterically coated microspheres SO PANCREAS LA English DT Article DE pancreatic insufficiency; steatorrhea; treatment ID CYSTIC-FIBROSIS; ENZYME PREPARATION; CANINE MODEL; SOLID-LIQUID; INSUFFICIENCY; ABSORPTION; LIPASE; MEALS AB Gastric emptying of dietary fat is affected by both chemical and physical factors; but when ingested as a free oil or an aqueous emulsion, fat may empty most rapidly immediately after the meal. In contrast, gastric transit of 1- to 3-mm spheres (like those of enterically coated pancreatins) is known to vary inversely with sphere diameter; and spheres leave the stomach initially slowly, if their diameter is greater than or equal to 1.6 mm. Our objective was to determine whether 2-mm microspheres of Pancrease would empty much more slowly than free or emulsified oil and whether 1.2-mm microspheres of Creon would empty as fast as free oil. We used a gamma camera to track the concurrent gastric emptying of I-123-labeled oil and In-113m-labeled spheres of Pancrease or Creon in pancreatic-insufficient subjects with cystic fibrosis who ingested 20 g of free oil in spaghetti meals or 20 g of oil emulsified in a milk meal. We found that either type of oil emptied rapidly initially but slowed later, whereas either dosage form emptied slowly initially but rapidly later. Unexpectedly, the smaller spheres of Creon emptied about the same as Pancrease did after the spaghetti meal. For example, 50% of oil but <25% of either dosage form had left the stomach by 90 min after the meals. Both dosage forms were lipophilic, forming aggregates in vitro. We concluded that the gastric emptying of either dosage form frequently lagged behind the emptying of oil from ordinary meals. We speculated that the similar transits of the 1.2-mm Creon and the 2-mm Pancrease resulted from aggregation of these microspheres in the presence of free oil. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,DEPT NUCL MED,LOS ANGELES,CA 90073. SEPULVEDA VA MED CTR,DEPT MED,LOS ANGELES,CA. SEPULVEDA VA MED CTR,DEPT NUCL MED,LOS ANGELES,CA. NR 28 TC 19 Z9 19 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0885-3177 J9 PANCREAS JI Pancreas PD OCT PY 1997 VL 15 IS 3 BP 226 EP 235 DI 10.1097/00006676-199710000-00003 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YJ775 UT WOS:A1997YJ77500003 PM 9336785 ER PT J AU Torok, TJ Kilgore, PE Clarke, MJ Holman, RC Bresee, JS Glass, RI Odom, J Goodenough, F Nelson, R Hardy, C Inderlied, CB Bovey, S Hartin, MS Margesson, K Lee, MH Robinson, CC Egbertson, S Huber, KM Reichwein, B Julian, SL Marchetti, NJ Christensen, ML Mazza, A Smaron, MF Frank, A Mason, TJ Swack, NS Creek, PA Luttrell, D Sundin, DR Doucet, C Jamison, RM Morin, M Hammond, PG Spencer, S Doveikis, SA Turner, N Guskey, L Humphries, JE Abel, D Bonnot, T Buller, R Hanauer, JM Norberg, L Yam, P Cavalieri, S Kelly, D Rantz, H Aiazzi, DK Fortier, WF Vasallo, M Perez, G Oty, GW Armstrong, GV RiepenhoffTalty, M Leonardi, G Lipson, SN Hartley, C Miller, SE Ulmer, G AF Torok, TJ Kilgore, PE Clarke, MJ Holman, RC Bresee, JS Glass, RI Odom, J Goodenough, F Nelson, R Hardy, C Inderlied, CB Bovey, S Hartin, MS Margesson, K Lee, MH Robinson, CC Egbertson, S Huber, KM Reichwein, B Julian, SL Marchetti, NJ Christensen, ML Mazza, A Smaron, MF Frank, A Mason, TJ Swack, NS Creek, PA Luttrell, D Sundin, DR Doucet, C Jamison, RM Morin, M Hammond, PG Spencer, S Doveikis, SA Turner, N Guskey, L Humphries, JE Abel, D Bonnot, T Buller, R Hanauer, JM Norberg, L Yam, P Cavalieri, S Kelly, D Rantz, H Aiazzi, DK Fortier, WF Vasallo, M Perez, G Oty, GW Armstrong, GV RiepenhoffTalty, M Leonardi, G Lipson, SN Hartley, C Miller, SE Ulmer, G TI Visualizing geographic and temporal trends in rotavirus activity in the United States, 1991 to 1996 SO PEDIATRIC INFECTIOUS DISEASE JOURNAL LA English DT Article DE diarrhea; disease outbreaks; epidemiology; gastroenteritis; kriging; rotavirus infections; seasons; spatial analysis; surveillance; United States ID CHILDREN; EPIDEMIC; IMMUNIZATION; MORTALITY; MORBIDITY; FRANCE AB Background. Rotavirus is the leading cause of severe pediatric gastroenteritis worldwide, A vaccine may soon be licensed for use in the United States to prevent this disease, To characterize US geographic and temporal trends in rotavirus activity, we made contour maps showing the timing of peak rotavirus activity. Methods, From July, 1991, through June, 1996, 79 laboratories participating in the National Respiratory and Enteric Virus Surveillance System reported on a weekly basis the number of stool specimens that tested positive for rotavirus, The peak weeks in rotavirus detections from each laboratory were mapped using kriging, a modeling technique originally developed for geostatistics. Results, During the B-year period 118 716 fecal specimens were examined, of which 27 616 (23%) were positive for rotavirus. Timing of rotavirus activity varied by geographic location in a characteristic pattern in which peak activity occurred first in the Southwest from October through December and last in the Northeast in April or May, The Northwest exhibited considerable year-to-year variability (range, December to May) in the timing of peak activity, whereas the temporal pattern in the remainder of the contiguous 48 states was relatively constant, Conclusion, Kriging is a useful method for visualizing geographic and temporal trends in rotavirus activity in the United States, This analysis confirmed trends reported in previous years, and it also identified unexpected variability in the timing of peak rotavirus activity in the Northwest, The causes of the seasonal differences in rotavirus activity by region are unknown, Tracking of laboratory detections of rotavirus may provide an effective surveillance tool to assess the impact of a rotavirus vaccination campaign in the United States. C1 CTR DIS CONTROL & PREVENT,DIV VIRAL & RICKETTSIAL DIS,NATL CTR INFECT DIS,ATLANTA,GA 30333. UNIV ALABAMA,BIRMINGHAM,AL. UNIV ARIZONA,MED CTR,TUCSON,AZ. ARKANSAS CHILDRENS HOSP,LITTLE ROCK,AR 72202. LONG BEACH MEM MED CTR,LONG BEACH,CA. CHILDRENS HOSP LOS ANGELES,LOS ANGELES,CA 90027. UNIV CALIF LOS ANGELES,MED CTR,LOS ANGELES,CA 90024. CHILDRENS HOSP,SAN DIEGO,CA. UNIV CALIF SAN DIEGO,MED CTR,RAPID DIAGNOST LAB,SAN DIEGO,CA 92103. UCSF,MT ZION MED CTR,SAN FRANCISCO,CA. STANFORD UNIV HOSP,STANFORD,CA 94305. UNIV CALIF LOS ANGELES,HARBOR MED CTR,TORRANCE,CA 90509. CHILDRENS HOSP,DENVER,CO 80218. CONNECTICUT DEPT HLTH SERV,HARTFORD,CT. YALE NEW HAVEN MED CTR,NEW HAVEN,CT 06504. MED CTR DELAWARE,NEWARK,DE. EMORY,EGLESTON CHILDRENS HOSP,ATLANTA,GA. UNIV HAWAII,SCH MED,HONOLULU,HI 96822. CHILDRENS MEM HOSP,CHICAGO,IL 60614. COOK CTY HOSP,CHICAGO,IL 60612. UNIV CHICAGO,MED CTR,CHICAGO,IL 60637. UNIV ILLINOIS,SCH MED,CHICAGO,IL. INDIANA UNIV HOSP,INDIANAPOLIS,IN 46202. UNIV IOWA,STATE HYG LAB,IOWA CITY,IA. UNIV KANSAS,MED CTR,KANSAS CITY,KS 66103. ALLIANT HLTH SYST,LOUISVILLE,KY. CHAR HOSP NEW ORLEANS,NEW ORLEANS,LA. CHILDRENS HOSP,NEW ORLEANS,LA. LOUISIANA STATE UNIV,MED CTR,SHREVEPORT,LA. MAINE MED CTR,PORTLAND,ME 04102. MARYLAND DEPT HLTH & MENTAL HYG,BALTIMORE,MD. CHILDRENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV MICHIGAN,MED CTR,ANN ARBOR,MI. MICHIGAN DEPT PUBL HLTH,LANSING,MI 48909. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. CHILDRENS MERCY HOSP,KANSAS CITY,MO 64108. ST LOUIS UNIV,CARDINAL GLENNON CHILDRENS HOSP,ST LOUIS,MO. WASHINGTON UNIV,SCH MED,ST LOUIS,MO. MISSOURI DEPT HLTH,JEFFERSON CITY,MO. COMMUNITY MED CTR,MISSOULA,MT. CHILDRENS MEM HOSP,OMAHA,NE. ST JOSEPHS HOSP,OMAHA,NE. UNIV NEBRASKA,MED CTR,OMAHA,NE. ASSOCIATED PATHOL LABS,LAS VEGAS,NV. WASHOE CITY MED CTR,RENO,NV. CONCORD HOSP,CONCORD,NH. HACKENSACK MED CTR,HACKENSACK,NJ 07604. ST MICHAELS HOSP,NEWARK,NJ 07102. NEW MEXICO DEPT HLTH,ALBUQUERQUE,NM. NEW YORK STATE DEPT HLTH,ALBANY,NY. SUNY COLL BUFFALO,CHILDRENS HOSP BUFFALO,BUFFALO,NY 14222. NASSAU CTY MED CTR,E MEADOW,NY 11554. N SHORE UNIV HOSP,MANHASSET,NY 11030. UNIV N CAROLINA,CHAPEL HILL,NC. DUKE UNIV,MED CTR,DURHAM,NC. FARGO CLIN LTD,FARGO,ND. METROHLTH MED CTR,CLEVELAND,OH. CHILDRENS HOSP OKLAHOMA,OKLAHOMA CITY,OK. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. GEISINGER MED CTR,DANVILLE,PA 17822. RHODE ISL HOSP,PROVIDENCE,RI. RICHLAND MEM HOSP,COLUMBIA,SC. GREENVILLE MEM HOSP,GREENVILLE,SC. UNIV S DAKOTA,SCH MED,SIOUX FALLS,SD. VANDERBILT UNIV,NASHVILLE,TN. VANDERBILT UNIV,MED CTR,NASHVILLE,TN. DRISCOLL FDN CHILDRENS HOSP,CORPUS CHRISTI,TX. PROVIDENCE MEM HOSP,EL PASO,TX. ARMSTRONG LAB,BROOKS AFB,TX 78235. UNIV HOSP,S TEXAS MED CTR,SAN ANTONIO,TX. UNIV UTAH,SCH MED,PRIMARY CHILDRENS MED CTR,SALT LAKE CITY,UT. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. UNIV WASHINGTON,CHILDRENS HOSP,SEATTLE,WA 98195. CHARLESTON AREA MED CTR,CHARLESTON,WV. W VIRGINIA UNIV HOSP,MORGANTOWN,WV. UNIV WISCONSIN,WISCONSIN STATE LAB HYG,MADISON,WI 53706. CHILDRENS HOSP WISCONSIN,MILWAUKEE,WI 53201. MILWAUKEE HLTH DEPT,MILWAUKEE,WI. CLIN LABS,CHEYENNE,WY. RI Kilgore, Paul/L-1462-2013 OI Kilgore, Paul/0000-0003-3214-4482 NR 17 TC 74 Z9 82 U1 0 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0891-3668 J9 PEDIATR INFECT DIS J JI Pediatr. Infect. Dis. J. PD OCT PY 1997 VL 16 IS 10 BP 941 EP 946 DI 10.1097/00006454-199710000-00007 PG 6 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA YA647 UT WOS:A1997YA64700006 PM 9380468 ER PT J AU So, GM Kosofsky, BE Southern, JF AF So, GM Kosofsky, BE Southern, JF TI Acute hydrocephalus following carbon monoxide poisoning SO PEDIATRIC NEUROLOGY LA English DT Article ID COMPUTED TOMOGRAPHIC FINDINGS; INTOXICATION; BRAIN; FEATURES; CT AB Carbon monoxide remains a significant cause of poisoning in children, Cerebral edema is often the cause of significant morbidity and mortality in exposed children, While lesions of the basal ganglia have been well documented, the advent of neuroimaging has allowed antemortem demonstration of infarctions of the globus pallidus and putamen with carbon monoxide intoxication, Acute hydrocephalus following carbon monoxide poisoning has been a rare occurrence, We report a 2 year 6 month-old boy who, to our knowledge, represents the first reported case in which repeat computed tomography documented the evolution of hydrocephalus due to carbon monoxide exposure in a child. (C) 1997 by Elsevier Science Inc. All rights reserved. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA. SINAI SAMARITAN HOSP,DEPT PATHOL,MILWAUKEE,WI. NR 20 TC 7 Z9 7 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0887-8994 J9 PEDIATR NEUROL JI Pediatr. Neurol. PD OCT PY 1997 VL 17 IS 3 BP 270 EP 273 DI 10.1016/S0887-8994(97)00097-0 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA YG006 UT WOS:A1997YG00600014 PM 9390708 ER PT J AU Sheridan, RL Ryan, CM Petras, LM Lydon, MK Weber, JM Tompkins, RG AF Sheridan, RL Ryan, CM Petras, LM Lydon, MK Weber, JM Tompkins, RG TI Burns in children younger than two years of age: An experience with 200 consecutive admissions SO PEDIATRICS LA English DT Article ID MORTALITY C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP Sheridan, RL (reprint author), SHRINERS BURN INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 7 TC 17 Z9 19 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD OCT PY 1997 VL 100 IS 4 BP 721 EP 723 DI 10.1542/peds.100.4.721 PG 3 WC Pediatrics SC Pediatrics GA XZ079 UT WOS:A1997XZ07900032 PM 9310533 ER PT J AU Alora, MBT Fitzpatrick, TB Taylor, CR AF Alora, MBT Fitzpatrick, TB Taylor, CR TI Total body heliotherapy SO PHOTODERMATOLOGY PHOTOIMMUNOLOGY & PHOTOMEDICINE LA English DT Article DE Tan-thru (TM) bathing suit; minimal erythema dose (MED); SPF AB Sunlight has long been known to be beneficial for a variety of skin diseases. Patients with psoriasis and eczema frequently employ ambient heliotherapy to control their conditions. However, social norms do not permit a person to expose the entire body in public, thus placing severe restrictions on the utility of this modality for the treatment of generalized psoriasis, for example, Tan-Thru(TM) bathing suits, designed to attract those who wish to tan without an accentuated "tan line", are reported to absorb ultraviolet (UV) rays up to a maximum equivalent of a sun protection factor (SPF) 10 sunblock, thus offering approximately 89% protection while in use, according to their manufacturer. If so, this bathing suit may allow patients with W-responsive skin dermatoses to achieve full body exposure in a socially acceptable manner. The objective of this study was to verify the SPF and to determine the actual transmittance to skin covered by a Tan-Thru(TM) bathing suit. Ten healthy adult subjects were recruited for this investigation, UVB minimal erythema dose (MED) was determined on unaffected gluteal or lower back skin, once with and once without the swimsuit on. Our results showed that the mean SPF afforded by the bathing suit was in fact 4.9 (range 4.5-5.6). In conclusion, theoretically, the Tan-Thru(TM) bathing suits could allow enough UVB penetration under ambient conditions to be beneficial for patients with UVB responsive conditions. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol,Wellman Labs Photomed, Boston, MA 02114 USA. RP Taylor, CR (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol,Wellman Labs Photomed, Boston, MA 02114 USA. NR 2 TC 2 Z9 2 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0905-4383 J9 PHOTODERMATOL PHOTO JI Photodermatol. Photoimmunol. Photomed. PD OCT-DEC PY 1997 VL 13 IS 5-6 BP 178 EP 180 PG 3 WC Dermatology SC Dermatology GA YY898 UT WOS:000072198500004 PM 9542753 ER PT J AU Morrow, NS Schall, M Grijalva, CV Geiselman, PJ Garrick, T Nuccion, S Novin, D AF Morrow, NS Schall, M Grijalva, CV Geiselman, PJ Garrick, T Nuccion, S Novin, D TI Body temperature and wheel running predict survival times in rats exposed to activity-stress SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE activity-stress; body temperature; wheel running; anorexia nervosa ID ACTIVITY-BASED ANOREXIA; ULCER AB The relationship between restricted feeding, core body temperature (T-b), wheel running, survival, and gastric erosion formation was examined in female rats exposed to activity-stress. Core body temperature and gross motor activity were telemetrically monitored in four groups of rats that had free access to running wheels and in one group that was not allowed to run on the wheels. Twenty-four hours prior to the onset of hypothermia and predicted mortality, different groups were left undisturbed, warmed with a heal lamp, denied access to running wheels, or euthanized. Length of survival in wheel-running rats varied from 2 to 12 days. During the first day of food deprivation, premorbid changes in the variability of T-b during the diurnal period and the mean number of wheel revolutions during the nocturnal period were strongly predictive of length of survival. Warming rats with a heat lamp or preventing rats from ever running on the wheel increased the length of survival and attenuated gastric erosion formation. only rats that were warmed had a greater likelihood of survival. Gastric pathology was also reduced in rats that were euthanized prior to becoming moribund. Rats that were left undisturbed or locked from the running wheel over the last 24 h of testing became moribund and had extensive gastric mucosal damage. These results indicate that thermoregulatory disturbances induced by restricted feeding and not wheel running alone are critical in determining survival and the degree of gastric mucosal injury in rats exposed to activity-stress. Results further suggest that predisposing factors may put some rats at risk for the development of activity-stress-induced mortality. (C) 1997 Elsevier Science Inc. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90095. UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CURE,DIGEST DIS RES CTR,LOS ANGELES,CA 90073. TULANE UNIV,DEPT PSYCHOL,NEW ORLEANS,LA 70118. LOUISIANA STATE UNIV,DEPT PSYCHOL,BATON ROUGE,LA 70808. LOUISIANA STATE UNIV,PENNINGTON BIOMED RES CTR,BATON ROUGE,LA 70808. FU NIDDK NIH HHS [DK 41301, K04DK01897]; PHS HHS [5T32M17140] NR 26 TC 24 Z9 24 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD OCT PY 1997 VL 62 IS 4 BP 815 EP 825 DI 10.1016/S0031-9384(97)00243-6 PG 11 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA XT845 UT WOS:A1997XT84500020 PM 9284503 ER PT J AU Rubin, JP Yaremchuk, MJ AF Rubin, JP Yaremchuk, MJ TI Complications and toxicities of implantable biomaterials used in facial reconstructive and aesthetic surgery: A comprehensive review of the literature SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-of-Plastic-and-Reconstructive-Surgeons CY NOV, 1996 CL DALLAS, TX SP Amer Soc Plast & Reconstruct Surgeons ID ORBITAL FLOOR FRACTURES; MALIGNANT FIBROUS HISTIOCYTOMA; RIGID INTERNAL-FIXATION; POLYTETRAFLUOROETHYLENE GORE-TEX; POLY(L-LACTIDE) BONE PLATES; CONNECTIVE-TISSUE DISEASES; TOTAL HIP-REPLACEMENT; STAINLESS-STEEL WIRE; LAG SCREW FIXATION; MANDIBULAR FRACTURES AB The use of implantable biomaterials has become an integral part of aesthetic and reconstructive surgery of the face. Metals are used for fracture fixation devices, whereas polymers are used primarily for bone or soft-tissue substitution. This review of the scientific literature examines the risks and complications of these materials. First, iue present an overview of commonly used materials. Second, we address general considerations of toxicity relevant to all biomaterials. Third, we present data from a large number of clinical series on the incidence of complications for individual materials used in specific applications. C1 MASSACHUSETTS GEN HOSP, DEPT SURG, DIV PLAST & RECONSTRUCT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 244 TC 136 Z9 141 U1 0 U2 7 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD OCT PY 1997 VL 100 IS 5 BP 1336 EP 1353 DI 10.1097/00006534-199710000-00043 PG 18 WC Surgery SC Surgery GA XY996 UT WOS:A1997XY99600043 PM 9326803 ER PT J AU Athey, JL OMalley, P Henderson, DP Ball, JW AF Athey, JL OMalley, P Henderson, DP Ball, JW TI Emergency medical services for children: Beyond lights and sirens SO PROFESSIONAL PSYCHOLOGY-RESEARCH AND PRACTICE LA English DT Article ID PEDIATRIC TRAUMA; RESPONSES; FAMILIES; PATIENT AB This article describes the history of emergency medical services for children and identifies important mental health issues. It discusses the roles of psychologists in such services, including intervening with children and their families during times of crisis, helping others who are providing the physical care of children to mitigate rather than exacerbate children's emotional distress, and attending to the emotional needs of health care providers who treat children. C1 UNIV CALIF LOS ANGELES,REI HARBOR,MED CTR,LOS ANGELES,CA 90024. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Athey, JL (reprint author), US PHS,EMERGENCY MED SERV CHILDREN PROGRAM,DEPT HLTH & HUMAN SERV,ROOM 18A-39,ROCKVILLE,MD 20857, USA. NR 26 TC 7 Z9 7 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7028 J9 PROF PSYCHOL-RES PR JI Prof. Psychol.-Res. Pract. PD OCT PY 1997 VL 28 IS 5 BP 464 EP 470 DI 10.1037//0735-7028.28.5.464 PG 7 WC Psychology, Multidisciplinary SC Psychology GA XX770 UT WOS:A1997XX77000011 ER PT J AU Muszbek, L Racz, E Laposata, M AF Muszbek, L Racz, E Laposata, M TI Posttranslational modification of proteins with fatty acids in platelets SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article; Proceedings Paper CT ETRO-ISSFAL Symposium CY JUL 10-13, 1996 CL MAASTRICHT UNIV, MAASTRICHT, NETHERLANDS SP European Thrombosis Res Org, Int Soc Study Fatty Acids & Lipids HO MAASTRICHT UNIV ID COVALENT MODIFICATION; THIOESTER LINKAGES; GLYCOPROTEIN-IX; PALMITIC ACID; ACYLATION; PALMITOYLATION; IDENTIFICATION; MYRISTOYLATION; PALMITYLATION; ARACHIDONATE AB Direct modification of proteins by fatty acid can occur as cotranslational N-myristoylation of an N-terminal glycine residue or as posttranslational thioesterification of cysteine residue(s), Platelets provide an excellent model system for studying the posttranslational type of modification in the absence of active protein synthesis and in the absence of protein synthesis-related protein modifications with lipids. Using this model system it was shown that thioesterification of proteins with fatty acid is less specific for palmitate than it was thought earlier and that other saturated, mono- and even polyunsaturated long chain fatty acids can also participate. The chain length and the extent of unsaturation of the protein-linked fatty acid moiety can, very likely, modulate hydrophobic protein-membrane lipid and protein-protein interactions. CD9, HLA class I glycoprotein, glycoproteins Ib, IX and IV, P-selectin and a subunits of G proteins have been demonstrated unequivocally as S-fatty acid acylated platelet proteins. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. RP Muszbek, L (reprint author), DEBRECEN UNIV MED,SCH MED,DEPT CLIN CHEM,POB 40,H-4012 DEBRECEN,HUNGARY. NR 43 TC 5 Z9 5 U1 0 U2 2 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD OCT PY 1997 VL 57 IS 4-5 BP 359 EP 366 DI 10.1016/S0952-3278(97)90411-7 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA YL257 UT WOS:A1997YL25700003 PM 9430379 ER PT J AU Rosenzweig, AC Brandstetter, H Whittington, DA Nordlund, P Lippard, SJ Frederick, CA AF Rosenzweig, AC Brandstetter, H Whittington, DA Nordlund, P Lippard, SJ Frederick, CA TI Crystal structures of the methane monooxygenase hydroxylase from Methylococcus capsulatus (Bath): Implications for substrate gating and component interactions SO PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS LA English DT Article DE nonheme iron enzyme; dinuclear iron center; leucine gate; reductase binding site; protein crystallography ID METHYLOSINUS-TRICHOSPORIUM OB3B; MONO-OXYGENASE; PROTEIN; OXIDATION; OXO; IDENTIFICATION; HYDROCARBONS; RESOLUTION; REDUCTASE; CENTERS AB The crystal structure of the nonheme iron-containing hydroxylase component of methane monooxygenase hydroxylase (MMOH) from Methylococcus capsulatus (Bath) has been solved in two crystal forms, one of which was refined to 1.7 Angstrom resolution. The enzyme is composed of two copies each of three subunits (alpha(2) beta(2) gamma(2)), and all three subunits are almost completely alpha-helical, with the exception of two beta hairpin structures in the alpha subunit. The active site of each alpha subunit contains one dinuclear iron center, housed in a four-helix bundle, The two iron atoms are octahedrally coordinated by 2 histidine and 4 glutamic acid residues as well as by a bridging hydroxide ion, a terminal water molecule, and at 4 degrees C, a bridging acetate ion, which is replaced at -160 degrees C with a bridging water molecule, Comparison of the results for two crystal forms demonstrates overall conservation and relative orientation of the domain structures, The most prominent structural difference identified between the two crystal forms is in an altered side chain conformation for Leu 110 at the active site cavity, We suggest that this residue serves as one component of a hydrophobic gate controlling access of substrates to and products from the active site, The leucine gate may be responsible for the effect of the B protein component on the reactivity of the reduced hydroxylase with dioxygen, A potential reductase binding site has been assigned based on an analysis of crystal packing in the two forms and corroborated by inhibition studies with a synthetic peptide corresponding to the proposed docking position. (C) 1997 Wiley-Liss, Inc. C1 MIT, DEPT CHEM, CAMBRIDGE, MA 02139 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOL PHARMACOL, BOSTON, MA 02115 USA. DANA FARBER CANC INST, BOSTON, MA 02115 USA. UNIV STOCKHOLM, DEPT MOL BIOL, S-10691 STOCKHOLM, SWEDEN. RI Brandstetter, Hans/E-6754-2011 OI Brandstetter, Hans/0000-0002-6089-3045 FU NIGMS NIH HHS [GM48388, GM32134] NR 48 TC 130 Z9 131 U1 1 U2 11 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0887-3585 EI 1097-0134 J9 PROTEINS JI Proteins PD OCT PY 1997 VL 29 IS 2 BP 141 EP 152 DI 10.1002/(SICI)1097-0134(199710)29:2<141::AID-PROT2>3.3.CO;2-W PG 12 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA XZ547 UT WOS:A1997XZ54700002 PM 9329079 ER PT J AU Grachev, ID AF Grachev, ID TI MRI-based morphometric topographic parcellation of human neocortex in trichotillomania SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE brain volumetrics; cuneal cortex; inferior frontal gyrus; magnetic resonance imaging; morphology; neocortex; topographic parcellation; trichotillomania ID OBSESSIVE-COMPULSIVE DISORDER; DORSOLATERAL PREFRONTAL CORTEX; POSITRON EMISSION TOMOGRAPHY; BASAL GANGLIA; TOURETTES-SYNDROME; RHESUS-MONKEY; SYMPTOM PROVOCATION; ABNORMALITIES; ORGANIZATION; STIMULI AB The purpose of the present study was to test specific hypotheses regarding volumetric changes of the neocortex between 10 female trichotillomania (TTM) subjects and 10 female normal controls. A standard three-dimensional (3-D) brain coordinate system was imposed over each newly acquired native magnetic resonance imaging (MRI) scan for positional normalization and 3-D shape/geometric localization analyses were based on the midpoints of anterior and posterior commissures, and the longitudinal fissure. The brain segmentation method, using well-characterized semiautomated intensity and differential contour algorithms by signal intensity-frequency histograms, was used blind to segment the principal gray and white matter structures. The segmented neocortical ribbon was subdivided into 48 regions (i.e. parcellation units) per hemisphere via a new method of morphometric topographic parcellation. There were no significant volumetric changes of the precentral gyrus, postcentral gyrus, supplementary motor cortex or opercular cortex in TTM patients compared with control subjects. A broader analysis as a hypothesis-generating post-hoc effort showed that TTM subjects exhibited significantly reduced left inferior frontal gyrus Volume of 27% (t = 2.21, d.f. = 18, P = 0.04) and enlarged right cuneal cortex volume of 40% (t = -2.30, d.f. = 18, P = 0.03) compared to normal controls. This is the first report of a structural neocortex abnormality in TTM. Results are discussed in terms of the behavioral specialization of these two brain neocortical regions and the complex interractions between visual and sensorimotor cortices. The results also showed the feasibility of the MRI-based morphometric topographic parcellation for investigation of the human neocortex in neuroscience research. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,PSYCHIAT NEUROSCI PROGRAM,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,PSYCHIAT NEUROSCI PROGRAM,BOSTON,MA. RI Rohlf, F/A-8710-2008 NR 76 TC 20 Z9 21 U1 3 U2 4 PU BLACKWELL SCIENCE PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON VICTORIA 3053, AUSTRALIA SN 1323-1316 J9 PSYCHIAT CLIN NEUROS JI Psychiatry Clin. Neurosci. PD OCT PY 1997 VL 51 IS 5 BP 315 EP 321 DI 10.1111/j.1440-1819.1997.tb03205.x PG 7 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA YG374 UT WOS:A1997YG37400009 PM 9413880 ER PT J AU Melany, ML Grant, EG Duerinckx, AJ Watts, TM Levine, BS AF Melany, ML Grant, EG Duerinckx, AJ Watts, TM Levine, BS TI Ability of a phase shift US contrast agent to improve imaging of the main renal arteries SO RADIOLOGY LA English DT Article DE ultrasound (US), contrast media; ultrasound (US), Doppler studies; hypertension, renovascular; renal arteries, stenosis or obstruction ID DOWNSTREAM CIRCULATION; SLOWED SYSTOLE; STENOSIS; DIAGNOSIS; TARDUS; ANGIOGRAPHY; ENHANCEMENT; SONOGRAPHY; PATTERN AB PURPOSE: To evaluate the ability of a phase shift contrast agent to improve Doppler sonographic imaging of the main renal arteries in cases of suspected renal artery stenosis. MATERIALS AND METHODS: In 25 patients in whom renal artery stenosis was suspected, baseline Doppler sonography was performed followed by two studies performed after blinded administration of contrast material or placebo (saline). Each kidney (n = 45) was evaluated for (n) visualization of the main renal artery on a scale of 0-4, (b) presence of accessory renal arteries, and (c) direct Doppler sonographic findings suggestive of renal artery stenosis. Correlative magnetic resonance angiography was performed in 24 patients, and angiograms were obtained in eight kidneys with stenosis at one or both imaging studies. RESULTS: Contrast enhancement was observed in 23 patients. Enhancement was 8-20 minutes. Renal artery visualization scores improved from a mean of 2.56 and 2.71 on baseline and noncontrast scans, respectively, to 3.69 after administration of contrast material. Contrast-enhanced images depicted seven kidneys with accessory renal arteries not seen at other studies. Two of eight cases of stenosis were seen only with contrast-enhanced sonography. CONCLUSION: Use of the phase shift contrast agent appears to enable a reduction in the number of equivocal findings of renal artery stenosis. C1 UNIV CALIF LOS ANGELES,DEPT INTERNAL MED,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,DEPT RADIOL,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,DEPT INTERNAL MED,LOS ANGELES,CA. RP Melany, ML (reprint author), UNIV CALIF LOS ANGELES,DEPT RADIOL SCI,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 22 TC 29 Z9 34 U1 1 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD OCT PY 1997 VL 205 IS 1 BP 147 EP 152 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA XX266 UT WOS:A1997XX26600026 PM 9314976 ER PT J AU Freston, JW Ahnen, DJ Czinn, SJ Earnest, DL Farthing, MJ Gorbach, SL Hunt, RH Sandler, RS Schuster, MM AF Freston, JW Ahnen, DJ Czinn, SJ Earnest, DL Farthing, MJ Gorbach, SL Hunt, RH Sandler, RS Schuster, MM TI Review and analysis of the effects of Olestra, a dietary fat substitute, on gastrointestinal function and symptoms SO REGULATORY TOXICOLOGY AND PHARMACOLOGY LA English DT Review ID SORBITOL INTOLERANCE; NONABSORBABLE LIPIDS; SUCROSE POLYESTER; PREVALENCE; DISEASE; ENERGY; HEALTH; ABSORPTION; ADULTS; RAT AB Olestra, a dietary fat substitute, was recently made available to consumers in savory snacks in three cities. Early reports of gastrointestinal complaints attributed to olestra attracted media coverage and fostered confusion among physicians and consumers about the nature of olestra and its effects on the digestive system, We reviewed all published studies of olestra's gastrointestinal effects and all relevant unpublished studies submitted to the Food and Drug Administration. Each study was analyzed by a group of expert gastroenterologists and epidemiologists. The symptoms reported with olestra ingestion are similar to those reported with ingestion of fiber and sorbitol, although the mechanisms involved in changing stool characteristics differ among these food additives. Olestra's effects on stool habit and characteristics are due to its presence in the stool. Large amounts are more likely to induce gastrointestinal symptoms than small amounts. There is no evidence that olestra induces pathological change in bowel function: there is no increased fluid or electrolyte nor is there altered gastrointestinal motility or microflora, Olestra and triglyceride ingestion resulted in a similar frequency of symptoms in normal adults and children and in people with chronic inflammatory bowel disease in remission, Olestra traverses the digestive tract intact to become a stool additive. Some subjects develop a change in bowel habit and stool characteristics due to the presence of more olestra in the stool, These changes resemble those associated with ingestion of sorbitol and fiber. (C) 1997 Academic Press. C1 UNIV COLORADO,SCH MED,DENVER,CO. DENVER VA MED CTR,DEPT MED,DENVER,CO. CASE WESTERN RESERVE UNIV,SCH MED,DEPT PEDIAT,CLEVELAND,OH 44106. UNIV ARIZONA,HLTH SCI CTR,DEPT MED,TUCSON,AZ 85721. ST BARTHOLOMEWS & ROYAL LONDON SCH MED & DENT,DIGEST DIS RES CTR,LONDON,ENGLAND. TUFTS UNIV,SCH MED,DEPT COMMUNITY HLTH,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT MED,BOSTON,MA 02111. MCMASTER UNIV,DEPT MED,HAMILTON,ON L8S 4L8,CANADA. UNIV N CAROLINA,DEPT MED,CHAPEL HILL,NC 27515. JOHNS HOPKINS UNIV,BAYVIEW MED CTR,DEPT MED,BALTIMORE,MD 21218. RP Freston, JW (reprint author), UNIV CONNECTICUT,CTR HLTH,DEPT MED,FARMINGTON,CT 06032, USA. NR 36 TC 17 Z9 17 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0273-2300 J9 REGUL TOXICOL PHARM JI Regul. Toxicol. Pharmacol. PD OCT PY 1997 VL 26 IS 2 BP 210 EP 218 DI 10.1006/rtph.1997.1165 PG 9 WC Medicine, Legal; Pharmacology & Pharmacy; Toxicology SC Legal Medicine; Pharmacology & Pharmacy; Toxicology GA YH056 UT WOS:A1997YH05600008 PM 9356284 ER PT J AU Badr, MS Kawak, A Skatrud, JB Morrell, MJ Zahn, BR Babcock, MA AF Badr, MS Kawak, A Skatrud, JB Morrell, MJ Zahn, BR Babcock, MA TI Effect of induced hypocapnic hypopnea on upper airway patency in humans during NREM sleep SO RESPIRATION PHYSIOLOGY LA English DT Article DE control of breathing, reduced ventilatory drive; mammals, humans; sleep, upper airway patency; upper airways, patency, hypopnea ID TOTAL PULMONARY RESISTANCE; HYPOXIA; OBSTRUCTION; APNEA AB We wished to determine the effect of reduced ventilatory drive (hypopnea) on upper airway patency in humans during non-rapid-eye-movement (NREM) sleep. We studied nine subjects (58 trials) spanning the spectrum of susceptibility to upper airway collapse including normals, snorers and patients with mild sleep apnea. Hypocapnic hypopnea was induced by abrupt cessation of brief (1 min) nasal mechanical hyperventilation. Surface inspiratory EMG (EMG(insp)) was used as an index of drive. Upper airway resistance and supraglottic pressure-flow plots were used as indexes of upper airway patency. Termination of nasal mechanical ventilation resulted in reduced (V) over dot E to 49% of pre-mechanical ventilation eupneic control. Upper airway resistance at a fixed flow did not change significantly in inspiration or expiration. Likewise, pressure-flow plots showed no increase in upper airway resistance except in one subject. However, maximum flow ((V) over dot max) decreased during hypopnea in four subjects who demonstrated inspiratory flow-limitation (IFL) during eupneic control. in contrast, no IFL was noted in subjects who showed no evidence of IFL during eupnea. We concluded: (1) Reduced ventilatory drive does not compromise upper airway patency in normal subjects during NREM sleep; (2) the reduction in (V) over dot max during hypopnea in subjects with IFL during eupneic control, suggests that reduced drive is associated with increased upper airway compliance in these subjects; and (3) upper airway susceptibility to narrowing/closure is an important determinant of the response to induced hypopnea during NREM sleep. (C) 1997 Elsevier Science B.V. C1 UNIV WISCONSIN,SCH MED,WILLIAM S MIDDLETON MEM VET HOSP,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT PREVENT MED,MADISON,WI. WAYNE STATE UNIV,SCH MED,DEPT MED,DETROIT,MI 48201. RP Badr, MS (reprint author), DETROIT VA MED CTR,4646 JOHN R,DETROIT,MI 48201, USA. FU NHLBI NIH HHS [HL-07654]; PHS HHS [R29 53443, P01 42242] NR 15 TC 34 Z9 34 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0034-5687 J9 RESP PHYSIOL JI Respir. Physiol. PD OCT PY 1997 VL 110 IS 1 BP 33 EP 45 DI 10.1016/S0034-5687(97)00072-8 PG 13 WC Physiology; Respiratory System SC Physiology; Respiratory System GA YD149 UT WOS:A1997YD14900004 PM 9361150 ER PT J AU Sparacia, G Gonzalez, RG Buonanno, F Sorensen, AG Lagalla, R DeMaria, M AF Sparacia, G Gonzalez, RG Buonanno, F Sorensen, AG Lagalla, R DeMaria, M TI Diagnosis of acute human stroke by diffusion weighted imaging (DWI): Comparison with conventional imaging modality SO RIVISTA DI NEURORADIOLOGIA LA Italian DT Article; Proceedings Paper CT XIVth National Congress of the Associazione-Italiana-di-Neuroradiologia CY OCT 16-18, 1997 CL CONSENTIA, ITALY SP Assoc Italiana Neuroradiol DE brain; infarction; MRI; CT; diffusion weighted imaging (DWI) ID PLANAR AB Stroke is the third leading cause of death and is a major cause of long-term disability. Neuroprotective treatment within a 4-hour <> has proved highly efficacious in reducing morbility and mortality in animal model. It is with this background that the need for emergent diagnosis and therapy of acute stroke in strongly suggested. Computed tomography (CT) shows the parenchymal changes of acute stroke too late to be helpful, and its role has been primarily to evaluate the possibility of intracerebral or subarachnoid hemorrhage. While conventional magnetic resonance (MR) imaging can demonstrate parenchymal abnormalities 4-6 hours after ischemia, newer techniques such as diffusion-weighted MR imaging (DWI) hold promise that a diagnosis of ischemia can be made within minutes after the acute event. In this article compares different aspects of hyperacute cerebral ischemia depicted at diffusion-weighted imaging before infarction is depicted at conventional MR or CT scans. DWI techniques may improve stroke diagnosis and may contribute to advances in treatment. C1 UNIV PALERMO,IST RADIOL P CIGNOLINI,I-90133 PALERMO,ITALY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA. OI Sparacia, Gianvincenzo/0000-0002-4787-1634 NR 5 TC 0 Z9 0 U1 0 U2 1 PU EDIZIONI CENTAURO PI BOLOGNA PA VIA DEL PRATELLO, 8, 40122 BOLOGNA, ITALY SN 1120-9976 J9 RIV NEURORADIOL JI Riv. Neuroradiol. PD OCT PY 1997 VL 10 SU 2 BP 47 EP 50 PG 4 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA YE854 UT WOS:A1997YE85400012 ER PT J AU Clark, JW AF Clark, JW TI Perspectives on new chemotherapeutic agents in the treatment of colorectal cancer SO SEMINARS IN ONCOLOGY LA English DT Review ID CLINICAL-TRIALS; MURINE TUMORS; PHASE-II; 5-FLUOROURACIL; LEUCOVORIN; FLUOROURACIL; AZIDOTHYMIDINE; CYTOTOXICITY; IMMUNOTHERAPY; ANGIOGENESIS C1 Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Clark, JW (reprint author), Massachusetts Gen Hosp, Dept Hematol Oncol, Cox,Room 640,100 Blossom St, Boston, MA 02114 USA. NR 54 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD OCT PY 1997 VL 24 IS 5 SU 18 BP 19 EP 24 PG 6 WC Oncology SC Oncology GA YP511 UT WOS:000071285100004 ER PT J AU Spiro, IJ Gebhardt, MC Jennings, LC Mankin, HJ Harmon, DC Suit, HD AF Spiro, IJ Gebhardt, MC Jennings, LC Mankin, HJ Harmon, DC Suit, HD TI Prognostic factors for local control of sarcomas of the soft tissues managed by radiation and surgery SO SEMINARS IN ONCOLOGY LA English DT Review ID PROSPECTIVE RANDOMIZED TRIAL; LIMB-SPARING SURGERY; ADJUVANT CHEMOTHERAPY; INTRAOPERATIVE RADIOTHERAPY; POSTOPERATIVE RADIOTHERAPY; SUPERFICIAL TRUNK; SURGICAL MARGINS; EXTREMITY; THERAPY; ADULT C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED ONCOL,BOSTON,MA 02114. RP Spiro, IJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,FRUIT ST,BOSTON,MA 02114, USA. NR 29 TC 38 Z9 41 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD OCT PY 1997 VL 24 IS 5 BP 540 EP 546 PG 7 WC Oncology SC Oncology GA YB531 UT WOS:A1997YB53100007 PM 9344320 ER PT J AU Willett, CG AF Willett, CG TI The role of radiation therapy and 5-fluorouracil in colon and rectal cancer SO SEMINARS IN RADIATION ONCOLOGY LA English DT Article ID ADJUVANT THERAPY; CARCINOMA; FLUOROURACIL; CHEMOTHERAPY; FAILURE RP Willett, CG (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 01890, USA. NR 24 TC 8 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1053-4296 J9 SEMIN RADIAT ONCOL JI Semin. Radiat. Oncol. PD OCT PY 1997 VL 7 IS 4 BP 300 EP 305 DI 10.1016/S1053-4296(97)80029-X PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA YB859 UT WOS:A1997YB85900008 ER PT J AU Can, U Furie, KL Suwanwela, N Southern, JF Macdonald, NR Ogilvy, CS Buonanno, FS Koroshetz, WJ Kistler, JP AF Can, U Furie, KL Suwanwela, N Southern, JF Macdonald, NR Ogilvy, CS Buonanno, FS Koroshetz, WJ Kistler, JP TI Transcranial Doppler ultrasound criteria for hemodynamically significant internal carotid artery stenosis based on residual lumen diameter calculated from en bloc endarterectomy specimens SO STROKE LA English DT Article DE transcranial Doppler; carotid arteries; pathology; diagnostic imaging ID NONINVASIVE ASSESSMENT; CEREBRAL-ISCHEMIA; DISEASE; FLOW; ANGIOGRAPHY; SONOGRAPHY; PATHOLOGY; OCCLUSION AB Background and Purpose Transcranial Doppler (TCD) is often used in conjunction with carotid duplex ultrasonography (CDUS) to evaluate the hemodynamic significance of internal carotid artery (ICA) stenosis. We examined the sensitivity and specificity of TCD criteria for detection of a hemodynamically significant stenosis (residual lumen diameter <1.5 mm) at the origin of the ICA. Methods We selected patients who underwent carotid endarterectomy (CEA) and had preoperative TCD data available. Eighty-one patients underwent transorbital evaluation, 49 of whom also had transtemporal TCD performed. The endarterectomy specimens were removed en bloc and sectioned, and the minimal residual lumen diameter calculated by computer analysis. Results For the transorbital approach, the strongest indicators of a residual lumen diameter <1.5 mm were reversed flow in the ipsilateral ophthalmic artery and a >50% peak systolic velocity difference between the carotid siphons (distal ICAs) in patients with unilateral ICA origin stenosis. They were 100% specific and 31% and 26% sensitive, respectively. For the transtemporal approach in patients with a unilateral stenosis, a >35% difference in ipsilateral middle cerebral artery (MCA) peak systolic velocity relative to the contralateral MCA or a >50% difference in contralateral anterior cerebral artery (ACA) peak systolic velocity relative to the ipsilateral ACA were 100% specific for identifying a residual lumen diameter of <1.5 mm. Sensitivities were 32% and 43%, respectively. Irrespective of contralateral stenosis, a >35% difference in ipsilateral MCA peak systolic velocity relative to the ipsilateral posterior cerebral artery had a 100% specificity and a 23% sensitivity for detecting a <1.5 mm minimal residual lumen diameter. Conclusions Although the TCD sensitivity for detecting a hemodynamically significant stenosis is relatively low, it can be highly specific (up to 100%). We conclude that TCD enhances the specificity of highly sensitive CDUS criteria for detecting a hemodynamically significant ICE stenosis. C1 MASSACHUSETTS GEN HOSP,VASC LAB,STROKE SERV,CEREBROVASC SECT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,STROKE SERV,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. NR 36 TC 20 Z9 21 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD OCT PY 1997 VL 28 IS 10 BP 1966 EP 1971 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA YD025 UT WOS:A1997YD02500022 PM 9341705 ER PT J AU Finklestein, SP AF Finklestein, SP TI Rapid induction of vascular endothelial growth factor gene expression after transient middle cerebral artery occlusion in rats - Comment SO STROKE LA English DT Editorial Material RP Finklestein, SP (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,CNS GROWTH FACTOR RES LAB,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD OCT PY 1997 VL 28 IS 10 BP 2044 EP 2044 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA YD025 UT WOS:A1997YD02500039 ER PT J AU Sakaguchi, N Yoshimura, M Hershman, JM Nishikawa, M Inada, M AF Sakaguchi, N Yoshimura, M Hershman, JM Nishikawa, M Inada, M TI Paracrine effect of human chorionic gonadotropin ectopically produced from papillary thyroid cancer cells on growth and function of FRTL-5 rat thyroid cells SO THYROID LA English DT Article ID HUMAN TSH RECEPTORS; CARCINOMA; HORMONE AB It is well known that human chorionic gonadotropin (hCG) is sometimes secreted from nontrophoblastic neoplasms. To elucidate the role of ectopic hCG, we investigated the effect of hCG produced from a papillary thyroid cancer cell line (B-CPAP cells) on stimulation and growth promotion of FRTL-5 rat thyroid cells. Ectopic hCG contained in the culture medium of B-CPAP cells was purified using gel filtration and bioassayed for thyrotropic activity in FRTL-5 cells. Addition of ectopic hCG (up to 5.2 x 10(4) IU/L) increased cyclic adenosine monophosphate (cAMP) accumulation and H-3-thymidine incorporation in FRTL-5 cells dose dependently. These effects were almost as potent as the stimulation induced by standard hCG CR-127. After the absorption of the ectopic hCG by anti-hCG-beta monoclonal antibody, the cAMP accumulation was significantly decreased. Analysis of ectopic hCG isoforms with different isoelectric points indicated the predominance of the acidic hCG isoform with isoelectric point (pI) 3.8-3.2 that is the major isoform of standard hCG. Basic isoforms (pI 5.7-5.3) with higher thyrotropic potency were also detected. These results indicate that the ectopic hCG secreted from papillary thyroid cancer cells possess intrinsic thyroid-stimulating and growth-promoting activity. The ectopic hCG may act as an autocrine-paracrine factor in nontrophoblastic neoplasms. C1 W LOS ANGELES VET AFFAIRS MED CTR, DIV ENDOCRINOL & METAB, LOS ANGELES, CA 90073 USA. RP Sakaguchi, N (reprint author), KANSAI MED UNIV, DEPT INTERNAL MED 2, HEMODIALYSIS CTR, 10-15 FUMIZONOCHO, MORIGUCHI, OSAKA 570, JAPAN. NR 19 TC 3 Z9 4 U1 0 U2 0 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1050-7256 EI 1557-9077 J9 THYROID JI Thyroid PD OCT PY 1997 VL 7 IS 5 BP 779 EP 782 DI 10.1089/thy.1997.7.779 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YD729 UT WOS:A1997YD72900014 PM 9349584 ER PT J AU Yu, N Ohashi, M Alosco, S Granja, C Salazar, M Hegland, J Yunis, E AF Yu, N Ohashi, M Alosco, S Granja, C Salazar, M Hegland, J Yunis, E TI Accurate typing of HLA-A antigens and analysis of serological deficiencies SO TISSUE ANTIGENS LA English DT Article DE HLA typing; PCR-SSOP; PCR-SSP; serology ID PRIMERS PCR-SSP; GENOMIC DNA; TRANSPLANTATION; AMPLIFICATION; ALLELES; FAMILY; LOCUS AB We are reporting the results of HLA-A typing by PCR-SSOP complemented by PCR-SSP of samples obtained from the National Marrow Donor Program (NMDP). These samples were a representative group from 2486 tested in duplicate by serology. A total of 390 samples gave HLA-A discrepant results. Comparing the molecular typing results of 238 samples (samples with available DNA) with the serological typing results, 54 homozygotes and 184 heterozygotes produced a total of 422 assignments by molecular methods. We found assignment discrepancies in 147/422 (35%) in laboratory 1 and 144/422 (34%) in laboratory 2 (a combined group of 4 NMDP laboratories; laboratory 1 is not included), The serological discrepancies found were of 3 categories: a) false negatives, b) incomplete typing (discrepancies due to the level of resolution within a cross-reactive or CREG group) and c) false positives. Major problems were identified using serology for typing HLA-A antigens: a) inability to identify all WHO-recognized specificities, more frequently in non-Caucasians or in HLA-A specificities known to be found more frequently in non-Caucasians for laboratory 1 and incorrect assignments of A19 specificities in laboratory 2, b) incorrect assignments in cells with poor viability and c) false-positive assignments in homozygotes. We propose a possible strategy to type HLA-A specificities with two steps: a) a minimum of serology for typing specificities for common CREG groups: A1, A2, A3, A11, A9, A10, A28, A19, However, a given laboratory can determine the level of serological assignments needed as a first step. And b) molecular methods to identify splits: A23, A24, A29, A30. A31, A32, A33, A34, A36, A66, A74 and A80, The technique described is useful for large-scale bone marrow donor typings for cells with poor viability, and for resolving ambiguous results including false-positive assignments of homozygous cells. C1 NATL MARROW DONOR PROGRAM,MINNEAPOLIS,MN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP Yu, N (reprint author), AMER RED CROSS,BLOOD SERV,NEW ENGLAND REG,HLA LAB,180 RUSTCRAFT RD,DEDHAM,MA 02026, USA. NR 16 TC 18 Z9 25 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD OCT PY 1997 VL 50 IS 4 BP 380 EP 386 DI 10.1111/j.1399-0039.1997.tb02891.x PG 7 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA XY345 UT WOS:A1997XY34500013 PM 9349623 ER EF