FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Lasser, R Siegel, E Dukoff, R Sunderland, T AF Lasser, R Siegel, E Dukoff, R Sunderland, T TI Diagnosis and treatment of geriatric depression SO CNS DRUGS LA English DT Review ID BEREAVEMENT-RELATED DEPRESSION; RECURRENT MAJOR DEPRESSION; LATE-LIFE DEPRESSION; CONSENSUS DEVELOPMENT CONFERENCE; SELECTIVE REUPTAKE INHIBITORS; PLACEBO-CONTROLLED TRIAL; AGE-OF-ONSET; ELDERLY PATIENTS; DOUBLE-BLIND; COMPLICATED GRIEF AB Geriatric depression is a common psychiatric illness affecting as many as one-third of the older population. With the growing number of elderly in many countries of the world, the morbidity and mortality associated with untreated and partially treated depression is of great concern from both a medical and economic perspective. Depression in the elderly often presents with more somatic or anxious features and less of the subjective sadness expressed by younger groups. In addition, in the elderly, depressive-spectrum disorders (which include minor depression, dysthymia, mixed anxiety/depression, bereavement-related depression and even suicidal ideation) are generally under-recognised and undertreated by health professionals. The clinical mismatch between high prevalence but undertreatment stems from patient and physician attitudes toward depression as a 'normal' response to aging and loss, diagnostically confusing medical illness-related symptomatology, and noncompliance with prescribed treatment. Furthermore, late-onset depression may hold special prognostic value in the elderly, with the relationship between late-onset depression and cerebrovascular events and progressive dementing illness being particularly strong. Therapeutically, then has been a recent expansion in the pharmacological tools that can be used to treat depression. A variety of new agents are now available that have adverse effect, pharmacodynamic and target-receptor profiles that differ from the older agents. For example, newer drugs that block the serotonin (5-hydroxytryptamine; 5-HT) transporter have supplanted older agents that cause more frequent and toxic adverse effects. These newer agents have also focused attention on the impact of polypharmacy on the hepatic cytochrome P450 system, which is responsible for drug metabolism and elimination. Electroconvulsive therapy and psychotherapy remain effective nonpharmacological treatments for geriatric depression. Generally, the opportunities for therapeutic intervention in geriatric depression suggest that greater diagnostic attention and more widespread application of treatments for this increasingly prevalent disorder continue to be needed. C1 NIMH, Geriatr Psychiat Branch, NIH, Ctr Clin, Bethesda, MD 20892 USA. Catholic Univ Amer, Dept Psychol, Washington, DC 20064 USA. RP Lasser, R (reprint author), NIMH, Geriatr Psychiat Branch, NIH, Ctr Clin, Bldg 10,Rm 3D41,10 Ctr Dr,MSC 1264, Bethesda, MD 20892 USA. NR 136 TC 10 Z9 10 U1 3 U2 7 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 JAN PY 1998 VL 9 IS 1 BP 17 EP 30 DI 10.2165/00023210-199809010-00003 PG 14 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA YU159 UT WOS:000071688200003 ER PT S AU Murphy, EH Robbins, TW Friedman, E Kosofsky, BE Gingras, JL Delaney-Black, V Ferriero, D Chiriboga, C Chasnoff, I Covington, C Tyler, R Koren, G Maza, P Wright, L Karmel, B AF Murphy, EH Robbins, TW Friedman, E Kosofsky, BE Gingras, JL Delaney-Black, V Ferriero, D Chiriboga, C Chasnoff, I Covington, C Tyler, R Koren, G Maza, P Wright, L Karmel, B BE Harvey, JA Kosofsky, BE TI Round table 4. Levels of vulnerability in functional deficits: Specificity of dysfunctional brain systems SO COCAINE: EFFECTS ON THE DEVELOPING BRAIN SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Editorial Material CT Conference on Cocaine - Effects on the Developing Brain CY SEP 16-19, 1997 CL WASHINGTON, D.C. SP New York Acad Sci, Allegheny Univ Hlth Sci, Natl Inst Drug Abuse, Nat Inst Child & Human Dev, NIMH, March Dimes, Culpeper Fdn C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Columbia Univ, New York, NY 10027 USA. Univ Chicago, Chicago, IL 60637 USA. Univ Detroit Mercy, Detroit, MI 48221 USA. Univ Toronto, Toronto, ON, Canada. NIDA, Lexington, KY USA. RP Murphy, EH (reprint author), Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-127-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 846 BP 289 EP 295 PG 7 WC Substance Abuse; Developmental Biology; Multidisciplinary Sciences; Clinical Neurology SC Substance Abuse; Developmental Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BL26F UT WOS:000074931100023 PM 9668415 ER PT S AU Kaltenbach, K Finnegan, L AF Kaltenbach, K Finnegan, L BE Harvey, JA Kosofsky, BE TI Prevention and treatment issues for pregnant cocaine-dependent women and their infants SO COCAINE: EFFECTS ON THE DEVELOPING BRAIN SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Cocaine - Effects on the Developing Brain CY SEP 16-19, 1997 CL WASHINGTON, D.C. SP New York Acad Sci, Allegheny Univ Hlth Sci, Natl Inst Drug Abuse, Nat Inst Child & Human Dev, NIMH, March Dimes, Culpeper Fdn ID ADDICTION AB The increase in cocaine use among pregnant women has created significant challenges for treatment providers. Drug-dependent women tend to neglect general health and prenatal care. Perinatal management is often difficult due to medical, obstetrical, and psychiatric complications. Research has demonstrated that comprehensive care, including high risk obstetrical care, psychosocial services, and addiction treatment can reduce complications associated with perinatal substance abuse. Research investigating the effectiveness of residential and outpatient treatment for pregnant cocaine-dependent women also suggests that many biopsychosocial characteristics and issues influence treatment outcomes. Homelessness and psychiatric illness require a more intensive level of care, and abstinence is difficult to maintain for many women in outpatient treatment as they continue to live in drug-using environments. To optimize the benefit of comprehensive services, services should be provided within a multilevel model of substance abuse treatment including long- and short-term residential, intensive outpatient, and outpatient settings. C1 Thomas Jefferson Univ, Jefferson Med Coll, Dept Pediat, Philadelphia, PA 19107 USA. NIH, Woments Hlt Initiat, Bethesda, MD 20892 USA. RP Kaltenbach, K (reprint author), Thomas Jefferson Univ, Jefferson Med Coll, Dept Pediat, 1201 Chestnut St,9th Floor, Philadelphia, PA 19107 USA. EM kaltenb1@jeflin.tju.edu NR 23 TC 17 Z9 17 U1 0 U2 6 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-127-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 846 BP 329 EP 334 DI 10.1111/j.1749-6632.1998.tb09749.x PG 6 WC Substance Abuse; Developmental Biology; Multidisciplinary Sciences; Clinical Neurology SC Substance Abuse; Developmental Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BL26F UT WOS:000074931100027 PM 9668419 ER PT S AU Coyle, J Lester, BM Koren, G Chasnoff, IJ Kaltenbach, K Karmel, B Weinberg, N Snyder-Keller, A Wright, L Lubin, D Smeriglio, V Frank, D AF Coyle, J Lester, BM Koren, G Chasnoff, IJ Kaltenbach, K Karmel, B Weinberg, N Snyder-Keller, A Wright, L Lubin, D Smeriglio, V Frank, D BE Harvey, JA Kosofsky, BE TI Round table 5. Nature-nurture issues SO COCAINE: EFFECTS ON THE DEVELOPING BRAIN SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Editorial Material CT Conference on Cocaine - Effects on the Developing Brain CY SEP 16-19, 1997 CL WASHINGTON, D.C. SP New York Acad Sci, Allegheny Univ Hlth Sci, Natl Inst Drug Abuse, Nat Inst Child & Human Dev, NIMH, March Dimes, Culpeper Fdn C1 NIDA, Lexington, KY 40583 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-127-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 846 BP 341 EP 347 PG 7 WC Substance Abuse; Developmental Biology; Multidisciplinary Sciences; Clinical Neurology SC Substance Abuse; Developmental Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BL26F UT WOS:000074931100029 PM 9668421 ER PT S AU Maza, PL Wright, LL Bauer, CR Shankaran, S Bada, HS Lester, B Krause-Steinrauf, H Smeriglio, VL Bowler, A Katsikiotis, V AF Maza, PL Wright, LL Bauer, CR Shankaran, S Bada, HS Lester, B Krause-Steinrauf, H Smeriglio, VL Bowler, A Katsikiotis, V BE Harvey, JA Kosofsky, BE TI Maternal lifestyles study (MLS) - Caretaking environment and stability of substance-exposed infants at one month corrected age SO COCAINE: EFFECTS ON THE DEVELOPING BRAIN SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Cocaine - Effects on the Developing Brain CY SEP 16-19, 1997 CL WASHINGTON, D.C. SP New York Acad Sci, Allegheny Univ Hlth Sci, Natl Inst Drug Abuse, Nat Inst Child & Human Dev, NIMH, March Dimes, Culpeper Fdn ID LOW-BIRTH-WEIGHT; CHILDREN; COCAINE; MOTHERS; DRUGS; LIFE; HOME C1 Childrens Bur, Adm Children Youth & Families, Washington, DC 20013 USA. NICHD, Rockville, MD 20852 USA. Univ Miami, Jackson Mem Hosp, Sch Med, Dept Pediat,Maternal Lifestyles Study, Miami, FL 33136 USA. Wayne State Univ, Childrens Hosp Michigan, Sch Med, Div Neonatal & Perinatal Med, Detroit, MI 48201 USA. Univ Tennessee, Sch Med, EH Crump Hosp, New Born Ctr, Memphis, TN 38163 USA. Brown Univ, Women & Infants Hosp, Dept Pediat, Providence, RI 02905 USA. George Washington Univ, Ctr Biostat, Rockville, MD 20852 USA. NIDA, Clin Med Branch, Rockville, MD 20857 USA. RP Maza, PL (reprint author), Childrens Bur, Adm Children Youth & Families, Box 1182, Washington, DC 20013 USA. NR 23 TC 4 Z9 4 U1 1 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-127-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 846 BP 358 EP 361 DI 10.1111/j.1749-6632.1998.tb09754.x PG 4 WC Substance Abuse; Developmental Biology; Multidisciplinary Sciences; Clinical Neurology SC Substance Abuse; Developmental Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BL26F UT WOS:000074931100032 PM 9668424 ER PT S AU Sparenborg, S AF Sparenborg, S BE Harvey, JA Kosofsky, BE TI Mortality in neonatal rats is increased by moderate prenatal exposure to some monoamine reuptake inhibitors - A brief review SO COCAINE: EFFECTS ON THE DEVELOPING BRAIN SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Cocaine - Effects on the Developing Brain CY SEP 16-19, 1997 CL WASHINGTON, D.C. SP New York Acad Sci, Allegheny Univ Hlth Sci, Natl Inst Drug Abuse, Nat Inst Child & Human Dev, NIMH, March Dimes, Culpeper Fdn ID COCAINE C1 NIDA, Pharmacol & Toxicol Branch, Medicat Dev Div, NIH, Rockville, MD 20857 USA. RP Sparenborg, S (reprint author), Room 11A-55,5600 Fishers Lane, Rockville, MD 20857 USA. EM ss292q@nih.gov NR 16 TC 0 Z9 0 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-127-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 846 BP 423 EP 426 DI 10.1111/j.1749-6632.1998.tb09771.x PG 4 WC Substance Abuse; Developmental Biology; Multidisciplinary Sciences; Clinical Neurology SC Substance Abuse; Developmental Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BL26F UT WOS:000074931100049 PM 9668441 ER PT S AU Bada, HS Bauer, CR Shankaran, S Lester, B Wright, LL Verter, J Smeriglio, VL Finnegan, LP Maza, PL AF Bada, HS Bauer, CR Shankaran, S Lester, B Wright, LL Verter, J Smeriglio, VL Finnegan, LP Maza, PL BE Harvey, JA Kosofsky, BE TI Central and autonomic nervous systems' signs associated with in utero exposure to cocaine/opiates SO COCAINE: EFFECTS ON THE DEVELOPING BRAIN SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Cocaine - Effects on the Developing Brain CY SEP 16-19, 1997 CL WASHINGTON, D.C. SP New York Acad Sci, Allegheny Univ Hlth Sci, Natl Inst Drug Abuse, Nat Inst Child & Human Dev, NIMH, March Dimes, Culpeper Fdn ID COCAINE C1 Univ Tennessee, Memphis, TN 38163 USA. Univ Miami, Miami, FL 33152 USA. Wright State Univ, Detroit, MI USA. Brown Univ, Providence, RI 02912 USA. NICHHD, Bethesda, MD USA. George Washington Univ, Washington, DC USA. NIDA, Lexington, KY USA. Ctr Subst Abuse Treatment, Rockville, MD USA. RP Bada, HS (reprint author), Newborn Ctr, 853 Jefferson Ave,Room 201, Memphis, TN 38163 USA. NR 5 TC 1 Z9 1 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-127-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 846 BP 431 EP 434 DI 10.1111/j.1749-6632.1998.tb09773.x PG 4 WC Substance Abuse; Developmental Biology; Multidisciplinary Sciences; Clinical Neurology SC Substance Abuse; Developmental Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BL26F UT WOS:000074931100051 PM 9668443 ER PT J AU Adhya, S Geanacopoulos, M Lewis, DEA Roy, S Aki, T AF Adhya, S Geanacopoulos, M Lewis, DEA Roy, S Aki, T TI Transcription regulation by repressosome and by RNA polymerase contact SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposium on Quantitative Biology - Mechanisms of Transcription CY 1998 CL NEW YORK, NEW YORK SP Amgren Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, Forest Labs Inc, Genentech Inc, Genet Inst, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Eli Lilly & Co, Merck Genome Res Inst, Novartis Pharma Res, Novo Nardisk Biotech Inc, ZymoGenet Inc, OSI Pharmaceut Inc, Pall Corp, Paarke Davis Pharmaceut Res, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Scherring Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC, Plant Corp Associates, Amer Cyanamid Co, Monsanto Co, Pioneer Hi-Bred Int Inc, Westvaco Corp ID SITE-SPECIFIC RECOMBINATION; ESCHERICHIA-COLI K-12; DNA-BINDING PROTEINS; GAL REPRESSOR; HU PROTEIN; CRYSTAL-STRUCTURE; GALACTOSE OPERON; GENE-EXPRESSION; COMPLEX; ACTIVATION C1 NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RP Adhya, S (reprint author), NCI, Mol Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA. RI Aki, Tsunehiro/B-6719-2012 OI Aki, Tsunehiro/0000-0001-9753-2043 NR 58 TC 30 Z9 30 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1998 VL 63 BP 1 EP 9 DI 10.1101/sqb.1998.63.1 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 208MJ UT WOS:000080994900003 PM 10384265 ER PT J AU Wade, PA Jones, PL Vermaak, D Veenstra, GJC Imhof, A Sera, T Tse, C Ge, H Shi, YB Hansen, JC Wolffe, AP AF Wade, PA Jones, PL Vermaak, D Veenstra, GJC Imhof, A Sera, T Tse, C Ge, H Shi, YB Hansen, JC Wolffe, AP TI Histone deacetylase directs the dominant silencing of transcription in chromatin: Association with MeCP2 and the Mi-2 chromodomain SWI SNF ATPase SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposium on Quantitative Biology - Mechanisms of Transcription CY 1998 CL NEW YORK, NEW YORK SP Amgren Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, Forest Labs Inc, Genentech Inc, Genet Inst, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Eli Lilly & Co, Merck Genome Res Inst, Novartis Pharma Res, Novo Nardisk Biotech Inc, ZymoGenet Inc, OSI Pharmaceut Inc, Pall Corp, Paarke Davis Pharmaceut Res, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Scherring Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC, Plant Corp Associates, Amer Cyanamid Co, Monsanto Co, Pioneer Hi-Bred Int Inc, Westvaco Corp ID RNA-POLYMERASE-II; NUCLEOSOME CORE PARTICLE; XENOPUS-LAEVIS; IN-VIVO; REPRESS TRANSCRIPTION; NEGATIVE REGULATOR; TERMINAL DOMAIN; FACTOR ACCESS; YEAST GCN5P; DNA-BINDING C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Univ Texas, Hlth Sci Ctr, Dept Biochem, San Antonio, TX 78284 USA. RP Wade, PA (reprint author), NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. RI Veenstra, Gert Jan C./D-4963-2012 OI Veenstra, Gert Jan C./0000-0002-7787-4940 NR 72 TC 56 Z9 56 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1998 VL 63 BP 435 EP 445 DI 10.1101/sqb.1998.63.435 PG 11 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 208MJ UT WOS:000080994900046 PM 10384308 ER PT J AU Kotani, T Zhang, X Schiltz, RL Ogryzko, VV Howard, T Swanson, MJ Vassilev, A Zhang, H Yamauchi, J Howard, BH Qin, J Nakatani, Y AF Kotani, T Zhang, X Schiltz, RL Ogryzko, VV Howard, T Swanson, MJ Vassilev, A Zhang, H Yamauchi, J Howard, BH Qin, J Nakatani, Y TI TBP-associated factors in the PCAF histone acetylase complex SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposium on Quantitative Biology - Mechanisms of Transcription CY 1998 CL NEW YORK, NEW YORK SP Amgren Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, Forest Labs Inc, Genentech Inc, Genet Inst, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Eli Lilly & Co, Merck Genome Res Inst, Novartis Pharma Res, Novo Nardisk Biotech Inc, ZymoGenet Inc, OSI Pharmaceut Inc, Pall Corp, Paarke Davis Pharmaceut Res, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Scherring Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC, Plant Corp Associates, Amer Cyanamid Co, Monsanto Co, Pioneer Hi-Bred Int Inc, Westvaco Corp ID NUCLEOSOME CORE PARTICLE; RETINOBLASTOMA PROTEIN; CELL-CYCLE; TRANSCRIPTIONAL ACTIVATION; REPRESS TRANSCRIPTION; YEAST; INTERACTS; COACTIVATORS; GCN5; DNA C1 NICHHD, Lab Mol Growth Regulat, NIH, Bethesda, MD 20892 USA. NICHHD, Biophys Chem Lab, NIH, Bethesda, MD 20892 USA. RP Kotani, T (reprint author), Nara Inst Sci & Technol, Plant Mol Genet Lab, 8916-5 Takayama, Nara 63001, Japan. RI Ogryzko, Vasily/M-6665-2015 OI Ogryzko, Vasily/0000-0002-8548-1389 NR 53 TC 5 Z9 5 U1 1 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1998 VL 63 BP 493 EP 499 DI 10.1101/sqb.1998.63.493 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 208MJ UT WOS:000080994900051 PM 10384313 ER PT J AU Bell, A Boyes, J Chung, J Pikaart, M Prioleau, MN Recillas, F Saitoh, N Felsenfeld, G AF Bell, A Boyes, J Chung, J Pikaart, M Prioleau, MN Recillas, F Saitoh, N Felsenfeld, G TI The establishment of active chromatin domains SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposium on Quantitative Biology - Mechanisms of Transcription CY 1998 CL NEW YORK, NEW YORK SP Amgren Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, Forest Labs Inc, Genentech Inc, Genet Inst, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Eli Lilly & Co, Merck Genome Res Inst, Novartis Pharma Res, Novo Nardisk Biotech Inc, ZymoGenet Inc, OSI Pharmaceut Inc, Pall Corp, Paarke Davis Pharmaceut Res, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Scherring Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC, Plant Corp Associates, Amer Cyanamid Co, Monsanto Co, Pioneer Hi-Bred Int Inc, Westvaco Corp ID BETA-GLOBIN LOCUS; TRANSCRIPTION FACTOR GATA-1; HYPERSENSITIVE SITES; BINDING DOMAIN; DNA-BINDING; GENE; ENHANCER; PROTEIN; COMPLEX; DROSOPHILA C1 NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RP Bell, A (reprint author), Inst Canc Res, Chester Beatty Labs, Sect Gene Funct & Regulat, 237 Fulham Rd, London SW3 6JB, England. RI Prioleau, Marie-Noelle/G-9824-2014 NR 30 TC 7 Z9 7 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1998 VL 63 BP 509 EP 514 DI 10.1101/sqb.1998.63.509 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 208MJ UT WOS:000080994900053 PM 10384315 ER PT J AU Wu, C Tsukiyama, T Gdula, D Georgel, P Martinez-Balbas, M Mizuguchi, G Ossipow, V Sandaltzopoulos, R Wang, HM AF Wu, C Tsukiyama, T Gdula, D Georgel, P Martinez-Balbas, M Mizuguchi, G Ossipow, V Sandaltzopoulos, R Wang, HM TI ATP-dependent remodeling of chromatin SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT Cold Spring Harbor Symposium on Quantitative Biology - Mechanisms of Transcription CY 1998 CL NEW YORK, NEW YORK SP Amgren Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med Inc, Diagnost Prod Corp, Forest Labs Inc, Genentech Inc, Genet Inst, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Eli Lilly & Co, Merck Genome Res Inst, Novartis Pharma Res, Novo Nardisk Biotech Inc, ZymoGenet Inc, OSI Pharmaceut Inc, Pall Corp, Paarke Davis Pharmaceut Res, Perkin Elmer Corp, Appl Biosyst Div, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Scherring Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC, Plant Corp Associates, Amer Cyanamid Co, Monsanto Co, Pioneer Hi-Bred Int Inc, Westvaco Corp ID POLYMERASE-II TRANSCRIPTION; SOLUBLE NUCLEAR FRACTION; HEAT-SHOCK PROMOTER; DROSOPHILA EMBRYOS; HISTONE METABOLISM; NUCLEOSOME; PROTEIN; ACTIVATION; COMPLEX; BINDING C1 NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. RP Wu, C (reprint author), Fred Hutchinson Canc Res Ctr, Div Basic Sci, 1100 Fairview Ave N,POB 19024, Seattle, WA 98109 USA. OI Martinez-Balbas, Marian/0000-0003-0173-0964 FU NCI NIH HHS [Z01CB05263] NR 46 TC 18 Z9 19 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1998 VL 63 BP 525 EP 534 DI 10.1101/sqb.1998.63.525 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 208MJ UT WOS:000080994900055 PM 10384317 ER PT J AU Yu, KF AF Yu, KF TI On estimating subpopulation means SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE subpopulation; mixture; classification; clustering; fuzzy partition; estimation; regression; unbiasedness AB A sample is taken from a population consisting of K subpopulations. The observations consist of two components (P,Y) where Y is of real interests and P is a conditional probability to help identify as to which subpopulation the observations come from. A general estimation procedure for estimating the subpopulation means of Y is introduced. It is the regression coefficient estimation when Y is regressed on the conditional probability. When the conditional probability is accurately given, the estimator is unbiased. The notion of a fuzzy partition is introduced. It is suggested that the estimation procedure using a fuzzy partition will reduce the bias. A simulation study is conducted to compare the proposed estimator (estimator after fuzzy classification) with the usual estimator (estimator after hard classification) and Selen's (1986) estimator. C1 NICHHD, Biometry & Math Stat Branch, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD 20892 USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0361-0926 J9 COMMUN STAT-THEOR M JI Commun. Stat.-Theory Methods PY 1998 VL 27 IS 1 BP 235 EP 273 DI 10.1080/03610929808832663 PG 39 WC Statistics & Probability SC Mathematics GA YY145 UT WOS:000072117800018 ER PT J AU Chen, TT Simon, RM Korn, EL Anderson, SJ Lindblad, AS Wieand, HS Douglass, HO Fisher, B Hamilton, JM Friedman, MA AF Chen, TT Simon, RM Korn, EL Anderson, SJ Lindblad, AS Wieand, HS Douglass, HO Fisher, B Hamilton, JM Friedman, MA TI Investigation of disease-free survival as a surrogate endpoint for survival in cancer clinical trials SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article; Proceedings Paper CT Symposium on Applied Statistics CY MAY, 1997 CL RUTGERS UNIV, NEW BRUNSWICK, NEW JERSEY HO RUTGERS UNIV DE stochastic model; exponential; colorectal-adjuvant; conditional independence ID SURGICAL ADJUVANT THERAPY; COLON-CANCER; LARGE-BOWEL; END-POINTS; CARCINOMA; FLUOROURACIL; LEVAMISOLE; CHEMOTHERAPY AB A stochastic model with exponential components is used to describe out data collected from a phase III cancer clinical trial. Criteria which guarantee that disease-free survival (DFS) can be used as a surrogate for overall survival are explored under this model. We examine several colorectal adjuvant clinical trials and find that these conditions are not satisfied. The relationship between the hazard ratio of DFS for an active treatment versus a control treatment and the cumulative hazard ratio of survival for the same two treatments is then explored. An almost linear relationship is found such that a hazard ratio for DFS of less than a threshold R corresponds to a non-null treatment effect on survival. The threshold value R is determined for our colorectal adjuvant trial data. Based on this relationship, a one-sided test of equal hazard rate of survival is equivalent to a test of hazard ratio of DFS small than R. This approach assumes that recurrence information is unbiasedly and accurately assessed; an assumption which is sometimes difficult to ensure for multicenter clinical trials, particularly for interim analyses. C1 NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA. Univ Pittsburgh, NSABP Headquarter, Pittsburgh, PA USA. EMMES Corp, GITSG Stat Off, Potomac, MD USA. Mayo Clin, NCCTG Stat Off, Rochester, MN USA. New York State Dept Hlth, Roswell Pk Mem Inst, Buffalo, NY 14263 USA. Univ Pittsburgh, Pittsburgh, PA USA. OI Anderson, Stewart/0000-0001-8948-0650 NR 26 TC 7 Z9 7 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0361-0926 J9 COMMUN STAT-THEOR M JI Commun. Stat.-Theory Methods PY 1998 VL 27 IS 6 BP 1363 EP 1378 DI 10.1080/03610929808832163 PG 16 WC Statistics & Probability SC Mathematics GA ZQ428 UT WOS:000073860500007 ER PT J AU Horowitz, AM AF Horowitz, AM TI Response to Weinstein: Public health issues in early childhood caries SO COMMUNITY DENTISTRY AND ORAL EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT Conference on Early Childhood Caries CY OCT, 1997 CL BETHESDA, MARYLAND DE case definition; early childhood caries; epidemiology; etiology; hypomineralized teeth; primary dentition ID MUTANS-STREPTOCOCCI; CHINESE CHILDREN; DENTAL-CARIES; HYPOPLASIA; PREVALENCE; DENTITION AB Dr Weinstein's thoughtful overview of public health issues in early childhood caries (ECC) provides an excellent basis for further exploration. For public health to focus on a given problem several factors must be addressed: the disease must be widespread; the etiology or the prevention of the disease or condition must be known; this knowledge is not being applied; and resources for interventions must be available. Currently, appropriate data are not available for ECC and the problem is exacerbated because there is no case definition for the disease. Therefore it is difficult to make public health policy to address this disease. With the knowledge of case definition, prevalence, and efficacy of treatment, we are more likely to engender interest and funding for ECC. Studies in other countries have demonstrated that children who are malnourished, have low birthweight or both, Likely will have hypomineralized primary teeth and thus at risk of ECC. Low birth-weight infants (less than 2500 g) currently constitute over 7% of all US births. The impact of low birth-weight on oral health is not known. Weinstein favors the use of operator-applied preventive agents, yet Little evidence is available on the safety and effectiveness of these agents among infants and young children. Further, they are unlikely to be cost-effective and they require frequent appointments, which is often difficult for poor families to manage. Community interventions hold the greatest promise for preventing ECC because larger numbers of people can be reached than in private practice clinical settings. C1 NIDR, Bethesda, MD 20892 USA. RP Horowitz, AM (reprint author), Bldg 45,Room 3AN-44B,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 21 TC 10 Z9 10 U1 1 U2 4 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0301-5661 J9 COMMUNITY DENT ORAL JI Community Dentist. Oral Epidemiol. PY 1998 VL 26 SU 1 BP 91 EP 95 PG 5 WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health GA ZY505 UT WOS:000074628500011 PM 9671205 ER PT J AU Maina, JN Wood, CM Hogstrand, C Hopkins, TE Luo, YH Gibbs, PDL Walsh, PJ AF Maina, JN Wood, CM Hogstrand, C Hopkins, TE Luo, YH Gibbs, PDL Walsh, PJ TI Structure and function of the axillary organ of the gulf toadfish, Opsanus beta (Goode and Bean) SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR AND INTEGRATIVE PHYSIOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the Society-for-Experimental-Biology on Structure and Function in Comparative Physiology - a Tribute to Pierre Laurent CY MAR 25-26, 1996 CL UNIV LANCASTER, LANCASTER, ENGLAND SP Soc Expt Biol, Anim Respirat & Osmoregulat Grp HO UNIV LANCASTER DE axillary organ; gulf toadfish; Opsanus beta; pheromones; anti-microbial compounds; toxins AB The structure of the axillary organ of a batrachoidid species, the gulf toadfish (Opsanus beta Goode and Bean 1879), has been examined and several simple experiments designed to elucidate its function performed. Electron microscopy (EM) studies revealed cells and structures suggesting secretory and iono regulatory roles (e.g., abundant intracytoplasmic secretory particles, rough endoplasmic reticulum, sparse Golgi bodies, indented epithelial cells with microvilli, numerous endocytotic vesicles, etc.). Our physiological experiments allowed us to reach several conclusions: the organs do not excrete significant quantities of urea relative to other areas of the fish (head and gills), the organs do not secrets a substance that is toxic to a teleost test fish (Gambusia affinis), the secretions do not induce short-term modifications in locomotory activity of other gull toadfish (e.g., by pheromonal means) and the secretions do not inhibit the growth of several species of microorganisms in culture, The function of the organ and its secretions remains unknown, representing a fertile area for research on structure and function in comparative physiology. COMP BIOCHEM PHYSIOL 119A;1:17-26, 1998. (C) 1998 Elsevier Science Inc. C1 Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, Div Marine Biol & Fisheries, NIEHS Marine & Freshwater Biomed Sci Ctr, Miami, FL 33149 USA. Univ Nairobi, Dept Vet Anat, Nairobi, Kenya. McMaster Univ, Dept Biol, Hamilton, ON L8S 4K1, Canada. Univ Kentucky, TH Morgan Sch Biol Sci, Lexington, KY 40506 USA. Rookery Bay Natl Estuarine Res Reserve, Naples, FL 33962 USA. RP Walsh, PJ (reprint author), Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, Div Marine Biol & Fisheries, NIEHS Marine & Freshwater Biomed Sci Ctr, Miami, FL 33149 USA. EM pwalsh@rsmas.miami.edu RI Hogstrand, Christer/C-9041-2013 NR 19 TC 2 Z9 2 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 1095-6433 J9 COMP BIOCHEM PHYS A JI Comp. Biochem. Physiol. A-Mol. Integr. Physiol. PD JAN PY 1998 VL 119 IS 1 BP 17 EP 26 DI 10.1016/S1095-6433(97)00410-8 PG 10 WC Biochemistry & Molecular Biology; Physiology; Zoology SC Biochemistry & Molecular Biology; Physiology; Zoology GA ZZ685 UT WOS:000074756400004 PM 11253782 ER PT B AU Butera, RJ Rinzel, J Smith, JC AF Butera, RJ Rinzel, J Smith, JC BE Bower, JM TI Novel frequency control in a population of bursting neurons with excitatory synaptic coupling SO COMPUTATIONAL NEUROSCIENCE: TRENDS IN RESEARCH LA English DT Proceedings Paper CT 6th Annual Computational Neuroscience Conference CY JUL 06-10, 1997 CL BIG SKY, MT C1 NIDDK, Math Res Branch, NIH, Bethesda, MD 20892 USA. RP Butera, RJ (reprint author), NIDDK, Math Res Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA BN 0-306-45919-1 PY 1998 BP 331 EP 336 PG 6 WC Mathematics, Applied; Neurosciences SC Mathematics; Neurosciences & Neurology GA BL45V UT WOS:000075569500055 ER PT J AU Wilbur, WJ AF Wilbur, WJ TI Accurate Monte Carlo estimation of very small p-values in Markov chains SO COMPUTATIONAL STATISTICS LA English DT Article ID KNOWLEDGE-BASED POTENTIALS; PROTEIN STRUCTURES; RECOGNITION AB There are many events in the real world that are far from random. If we could assign significance levels to them based on a rigorous random model, such p-values must be very small indeed. Why should we be interested in such small numbers? Basically because the number -log(2)(pval) is an estimate of the expected amount of information in bits that must be added to the random model to determine the event in question. Such self information provides an estimate of the complexity of the event and may serve to rank events in order of interest prior to human examination. In some cases we can determine very small p-values from closed formulas. In other cases the appropriate random model is sufficiently complicated that we cannot do so. We present here an algorithm that allows one to calculate very small p-values for some complicated random models that can be realized as Markov processes. Three examples are given illustrating the performance of the algorithm. C1 Natl Lib Med, Bethesda, MD 20894 USA. RP Wilbur, WJ (reprint author), Natl Lib Med, Bldg 38A,Rm 8S806,8600 Rockville Pike, Bethesda, MD 20894 USA. NR 14 TC 5 Z9 5 U1 0 U2 0 PU PHYSICA VERLAG GMBH PI HEIDELBERG PA TIERGARTENSTRASSE 17, 69121 HEIDELBERG, GERMANY SN 0943-4062 J9 COMPUTATION STAT JI Comput. Stat. PY 1998 VL 13 IS 2 BP 153 EP 168 PG 16 WC Statistics & Probability SC Mathematics GA ZY324 UT WOS:000074608900001 ER PT J AU Aguilar, RC Blank, VC Retegui, LA Roguin, LP AF Aguilar, RC Blank, VC Retegui, LA Roguin, LP TI Detection of negative allosteric effects between monoclonal antibodies by using an antigenic model-builder computer program SO COMPUTERS IN BIOLOGY AND MEDICINE LA English DT Article DE antigenic maps; monoclonal antibodies; epitopes; allosteric effects; expert module ID HUMAN GROWTH-HORMONE; SURFACE AB The ability of monoclonal antibodies (MAb) to bind or not simultaneously to the antigen (Ag) is used to establish antigenic maps considering that two different MAb do not bind to the Ag when the corresponding epitopes are overlapped (steric effect). Nevertheless, MAb inducing negative allosteric effect on the Ag could prevent the binding of the second MAb even if it is directed to a separate epitope. We report here that a knowledge-based expert module included in our previously described antigenic model-builder program (MAPAG) was able to differentiate between steric and negative allosteric effects between some MAb. (C) 1998 Elsevier Science Ltd. All rights reserved. C1 UBA, CONICET, Fac Farm & Bioquim, Inst Quim & Fisicoquim Biol, Buenos Aires, DF, Argentina. RP NICHD, Cell Biol & Metab Branch, NIH Bldg,18T,Room 101, Bethesda, MD 20892 USA. NR 16 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0010-4825 EI 1879-0534 J9 COMPUT BIOL MED JI Comput. Biol. Med. PD JAN PY 1998 VL 28 IS 1 BP 61 EP 73 DI 10.1016/S0010-4825(97)00042-5 PG 13 WC Biology; Computer Science, Interdisciplinary Applications; Engineering, Biomedical; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Computer Science; Engineering; Mathematical & Computational Biology GA ZV156 UT WOS:000074275300005 PM 9644574 ER PT S AU Long, LR Thoma, GR AF Long, LR Thoma, GR BE Matthews, MB TI Internet access to digital medical x-rays by image features and associated text SO CONFERENCE RECORD OF THE THIRTY-SECOND ASILOMAR CONFERENCE ON SIGNALS, SYSTEMS & COMPUTERS, VOLS 1 AND 2 SE CONFERENCE RECORD OF THE ASILOMAR CONFERENCE ON SIGNALS, SYSTEMS AND COMPUTERS LA English DT Proceedings Paper CT 32nd Asilomar Conference on Signals, Systems and Computers CY NOV 01-04, 1998 CL PACIFIC GROVE, CA SP Naval Postgrad Sch, Monterey, San Jose State Univ, San Jose, Monterey Bay Aquarium Res Inst, IEEE Signal Proc Soc DE World Wide Web; biomedical; informatics; Internet; database; spine; digital image; morphometry; x-ray image; image query by content; NHANES; NLM; NCHS; NIAMS ID VERTEBRAL MORPHOMETRY AB The Web-based Medical Information retrieval System (WebMIRS) allows Internet access to databases containing 17,000 digitised x-ray spine images and associated textual data from National Health and Nutrition examination Surveys (NHANES). WebMIRS allows SQL query of the text, and viewing of the returned text records and images using a standard browser. We are segmenting a subset of the vertebrae, using techniques from vertebral morphometry. From this, we will derive and add to the database vertebral features. This image-derived data will enhance the user's data access capability by enabling the creation of combined SQL/image-content queries. C1 Natl Lib Med, Bethesda, MD 20894 USA. RP Long, LR (reprint author), Natl Lib Med, Bethesda, MD 20894 USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1058-6393 BN 0-7803-5149-5 J9 CONF REC ASILOMAR C PY 1998 BP 900 EP 904 PG 5 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Engineering, Electrical & Electronic; Telecommunications SC Computer Science; Engineering; Telecommunications GA BM43X UT WOS:000078743600169 ER PT J AU Lee, SK Krebsbach, P Zeichner-David, M Slavkin, HC Yamada, KM Yamada, Y AF Lee, S. K. Krebsbach, P. Zeichner-David, M. Slavkin, H. C. Yamada, K. M. Yamada, Y. TI Ameloblastin: Gene Structure, Expression of Isoforms, and Role in Enamel Formation SO CONNECTIVE TISSUE RESEARCH LA English DT Article C1 [Lee, S. K.; Krebsbach, P.; Slavkin, H. C.; Yamada, K. M.; Yamada, Y.] NIDR, NIH, Bethesda, MD 20892 USA. [Zeichner-David, M.] USC, CCMB, Los Angeles, CA 90033 USA. RP Lee, SK (reprint author), NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0300-8207 J9 CONNECT TISSUE RES JI Connect. Tissue Res. PY 1998 VL 39 IS 1-3 BP 1 EP 1 DI 10.3109/03008209809023906 PG 1 WC Cell Biology; Orthopedics SC Cell Biology; Orthopedics GA V13AS UT WOS:000207640300003 ER PT J AU Simmons, D Gu, TT Krebsbach, PH Yamada, Y MacDougall, M AF Simmons, D. Gu, T. T. Krebsbach, P. H. Yamada, Y. MacDougall, M. TI Identification and Characterization of a cDNA for Mouse Ameloblastin SO CONNECTIVE TISSUE RESEARCH LA English DT Article DE Enamel; ameloblast; ameloblastin; mineralization; alternative splicing AB Ameloblastin was first identified as one of the most abundant novel transcripts from a random screening of a rat incisor cDNA library. In situ hybridization experiments have shown ameloblastin expression to be specific to ameloblasts, with highest levels in secretory and maturation stage ameloblasts and cells of the epithelial root sheath. Ameloblastin has been identified as a candidate gene for the local hypoplastic form of autosomal dominant amelogenesis imperfecta, by virtue of it's location within the critical disease locus. The purpose of this study was to isolate a full length mouse ameloblastin cDNA and determine its temporal expression pattern during odontogenesis. A newborn mouse molar cDNA library was screened using a rat ameloblastin cDNA probe. Positive clones were confirmed by PCR analysis with ameloblastin-specific primers, and their size determined with vector-specific primers. Phage clones were rescued to phagemid using Exassist helper phage and the nucleotide sequence determined. We report here the identification of two clones, exhibiting alternative splicing of the putative open reading frame, and use of multiple polyadenylation signals. Nucleotide sequence analysis indicated a high degree of similarity to rat ameloblastin, rat amelin 1 and 2 and porcine sheathlin. Reverse transcriptase-PCR analysis using mouse first and second mandibular molar mRNA indicated initial expression at E-14. This is one day after the initial expression of tuftelin (E-13) and one day prior to that of amelogenin (E-15). C1 [Simmons, D.; Gu, T. T.; MacDougall, M.] Univ Texas Hlth Sci Ctr San Antonio, Sch Dent, San Antonio, TX 78229 USA. [Krebsbach, P. H.] Univ Michigan, Sch Dent, Ann Arbor, MI 48109 USA. [Yamada, Y.] Natl Inst Dental Res, Bethesda, MD USA. RP MacDougall, M (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Sch Dent, San Antonio, TX 78229 USA. FU NIDCR NIH HHS [DE02848, DE09875] NR 20 TC 17 Z9 19 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0300-8207 J9 CONNECT TISSUE RES JI Connect. Tissue Res. PY 1998 VL 39 IS 1-3 BP 3 EP 12 DI 10.3109/03008209809023907 PG 10 WC Cell Biology; Orthopedics SC Cell Biology; Orthopedics GA V13AS UT WOS:000207640300004 PM 11062984 ER PT J AU Deutsch, D Nanci, A Robinson, C Zeichner-David, M Rosenbloom, J Lee, SK Simmer, JP MacDougall, M DenBesten, P Bashir, MM Kozawa, Y Bosshardt, DD Chen, WY Diekwisch, T Hubbard, MJ Snead, ML Hand, A Kirkham, J Mocetti, P Gibson, C AF Deutsch, D Nanci, A Robinson, C Zeichner-David, M Rosenbloom, J Lee, SK Simmer, JP MacDougall, M DenBesten, P Bashir, MM Kozawa, Y Bosshardt, DD Chen, WY Diekwisch, T Hubbard, MJ Snead, ML Hand, A Kirkham, J Mocetti, P Gibson, C TI Session 1. Ameloblast cell biology - Discussion SO CONNECTIVE TISSUE RESEARCH LA English DT Editorial Material C1 Hebrew Univ Jerusalem, Hadassah Fac Dent Med, Jerusalem, Israel. Univ Montreal, Fac Med Dent, Dept Stomatol, Montreal, PQ H3C 3J7, Canada. Univ Leeds, Sch Dent, Dept Oral Biol, Leeds LS2 9LU, W Yorkshire, England. Univ So Calif, Ctr Craniofacial Mol Biol, Los Angeles, CA 90033 USA. Univ Penn, Sch Dent Med, Dept Anat & Histol, Philadelphia, PA 19104 USA. NIDR, NIH, Bethesda, MD 20892 USA. Univ Texas, Sch Dent, Dept Pediat Dent, San Antonio, TX 78284 USA. Univ Calif San Francisco, Sch Dent, Dept Pediat Dent, San Francisco, CA 94143 USA. Nihon Univ, Sch Dent, Dept Oral Anat 2, Matsudo, Chiba 271, Japan. Univ Montreal, Fac Med Dent, Lab Microscopie Elect, Montreal, PQ H3C 3J7, Canada. McGill Univ, Fac Dent, Montreal, PQ H3A 2B2, Canada. Baylor Coll Dent, Dept Biomed Sci, Dallas, TX 75266 USA. Univ Otago, Dept Biochem, Dunedin, New Zealand. Univ Connecticut, Ctr Hlth, Farmington, CT USA. Univ Rome, Policlin Umberto I, Dept Expt Med & Pathol, I-00161 Rome, Italy. Univ Paris, Fac Chirurg Dent, F-92120 Paris, France. RP Deutsch, D (reprint author), Hebrew Univ Jerusalem, Hadassah Fac Dent Med, POB 1172, Jerusalem, Israel. RI Zeichner-David, Margarita/A-6567-2008 NR 0 TC 2 Z9 2 U1 0 U2 0 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 0300-8207 J9 CONNECT TISSUE RES JI Connect. Tissue Res. PY 1998 VL 38 IS 1-4 BP 35 EP 41 PG 7 WC Cell Biology; Orthopedics SC Cell Biology; Orthopedics GA 145WF UT WOS:000077394100006 ER PT J AU Simmer Deutsch Kuboki Lee Plate Robinson Rosenbloom Iijima Diekwisch Fincham Boyde Snead Goldberg Smith Aoba AF Simmer Deutsch Kuboki Lee Plate Robinson Rosenbloom Iijima Diekwisch Fincham Boyde Snead Goldberg Smith Aoba TI Two new in vitro calcification systems showing the higher calcifiability of enamel proteins than dentin and bone matrices - Discussion SO CONNECTIVE TISSUE RESEARCH LA English DT Editorial Material C1 Univ Texas, Sch Dent, Dept Pediat Dent, San Antonio, TX 78284 USA. Hebrew Univ Jerusalem, Hadassah Fac Dent Med, Jerusalem, Israel. Hokkaido Univ, Sch Dent, Dept Anat, Kita Ku, Sapporo, Hokkaido 060, Japan. NIDR, NIH, Bethesda, MD 20892 USA. Univ Munster, Inst Phys, D-48149 Munster, Germany. Univ Leeds, Sch Dent, Dept Oral Biol, Leeds LS2 9LU, W Yorkshire, England. Univ Penn, Sch Dent Med, Dept Anat & Histol, Philadelphia, PA 19104 USA. Asahi Univ, Sch Dent, Gifu 50102, Japan. Baylor Coll Dent, Dept Biomed Sci, Dallas, TX 75266 USA. Univ So Calif, Ctr Craniofacial Mol Biol, Los Angeles, CA 90033 USA. UCL, Dept Anat & Dev Biol, London WC1E 6BT, England. Univ Paris, Fac Chirurg Dent, F-92120 Paris, France. McGill Univ, Fac Dent, Montreal, PQ H3A 2B2, Canada. Nippon Dent Univ Tokyo, Dept Pathol, Chiyoda Ku, Tokyo 102, Japan. RP Simmer (reprint author), Univ Texas, Sch Dent, Dept Pediat Dent, 7703 Floyd Curl Dr, San Antonio, TX 78284 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 0300-8207 J9 CONNECT TISSUE RES JI Connect. Tissue Res. PY 1998 VL 38 IS 1-4 BP 201 EP 205 PG 5 WC Cell Biology; Orthopedics SC Cell Biology; Orthopedics GA 145WF UT WOS:000077394100023 ER PT J AU Takahashi, K Yamane, A Bringas, P Caton, J Slavkin, HC Zeichner-David, M AF Takahashi, K Yamane, A Bringas, P Caton, J Slavkin, HC Zeichner-David, M TI Induction of amelogenin and ameloblastin by insulin and insulin-like growth factors (IGF-I and IGF-II) during embryonic mouse tooth development in vitro SO CONNECTIVE TISSUE RESEARCH LA English DT Article; Proceedings Paper CT 6th International Symposium on the Composition, Properties and Fundamental Structure of Tooth Enamel CY MAY 11-15, 1997 CL LAKE ARROWHEAD, CA DE tooth development; amelogenesis; gene expression; insulin; insulin-like growth factors; tuftelin; amelogenin; ameloblastin ID ELASTIN GENE; EXPRESSION; CELLS; QUANTITATION; DISRUPTION; PROTEIN; DENTIN; BETA; PCR; RNA AB Insulin and insulin-like growth factors (IGF-I and IGF-II) are considered pleiotropic, acting as both mitogen and differentiation factors. Several investigators have demonstrated the expression of insulin, IGFs, their cognate receptors and IGF binding proteins during tooth morphogenesis, Previous work done in our laboratory indicated that exogenous insulin and IGFs induce the accumulation of enamel extracellular matrix on mouse mandibular molars cultured in a serumless, chemically defined medium. In order to determine the level of control of these factors in the induction of enamel biomineralization, we designed experiments to quantitate mRNAs for enamel specific-gene products. Mandibular first molars (M1) obtained from E15 Swiss Webster mice were placed in organ culture in the presence of insulin (1000 ng/ml), IGF-I (100 ng/ml) or IGF-II (100 ng/ml) for 6, 12 and 18-days. At termination date, the RNA was extracted and the concentration of mRNAs for amelogenin, tuftelin and ameloblastin were determined using a quantitative competitive reverse transcription-polymerase chain reaction (RT-PCR) technique (PCR mimic), Our results showed that after 6-days in culture; treatment with insulin, IGF-I and IGF-II increased the synthesis of amelogenin and ameloblastin. In contrast, the expression of tuftelin mRNA was not affected by either factor. In conclusion, our studies showed that the increase in enamel matrix formation by overexpression of IGFs is the result of transcriptional regulation of enamel specific proteins like amelogenin and ameloblastin but not tuftelin, These studies also suggest that the regulatory mechanisms controlling tuftelin gene expression are different than the mechanisms regulating ameloblastin and amelogenin transcription. C1 Univ So Calif, Ctr Craniofacial Mol Biol, Sch Dent, Los Angeles, CA 90033 USA. NIAMSD, Craniofacial Dev Sect, NIH, Bethesda, MD 20892 USA. Tsurumi Univ, Sch Dent Med, Dept Pharmacol, Yokohama, Kanagawa, Japan. RP Zeichner-David, M (reprint author), Univ So Calif, Ctr Craniofacial Mol Biol, Sch Dent, 2250 Alcazar St, Los Angeles, CA 90033 USA. RI Zeichner-David, Margarita/A-6567-2008 FU NIDCR NIH HHS [DEO6425] NR 25 TC 19 Z9 19 U1 0 U2 2 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 0300-8207 J9 CONNECT TISSUE RES JI Connect. Tissue Res. PY 1998 VL 38 IS 1-4 BP 269 EP 278 DI 10.3109/03008209809017047 PG 10 WC Cell Biology; Orthopedics SC Cell Biology; Orthopedics GA 145WF UT WOS:000077394100031 PM 11063034 ER PT J AU Robinson, C Boyde, A Hubbard, MJ Rosenbloom, J Deutsch, D Bonass, WA MacDougall, M Paine, CT Lee Snead, ML Wright Bartlett, JD Bashir, MM Zeichner-David, M Gibson, C Simmer, JP Mednieks, MI AF Robinson, C Boyde, A Hubbard, MJ Rosenbloom, J Deutsch, D Bonass, WA MacDougall, M Paine, CT Lee Snead, ML Wright Bartlett, JD Bashir, MM Zeichner-David, M Gibson, C Simmer, JP Mednieks, MI TI Session 6: Ameloblast gene products: 2 - Discussion SO CONNECTIVE TISSUE RESEARCH LA English DT Editorial Material C1 Univ Leeds, Sch Dent, Dept Oral Biol, Leeds LS2 9LU, W Yorkshire, England. UCL, Dept Anat & Dev Biol, London WC1E 6BT, England. Univ Otago, Dept Biochem, Dunedin, New Zealand. Univ Penn, Sch Dent Med, Dept Anat & Histol, Philadelphia, PA 19104 USA. Hebrew Univ Jerusalem, Hadassah Fac Dent Med, Jerusalem, Israel. Univ Texas, Dept Pediat Dent, Sch Dent, San Antonio, TX 78284 USA. Univ So Calif, Ctr Craniofacial Mol Biol, Los Angeles, CA 90033 USA. NIDR, NIH, Bethesda, MD 20892 USA. Univ N Carolina, Sch Dent, Dept Pediat Dent, Chapel Hill, NC 27599 USA. Forsyth Dent Ctr, Dept Biomineralizat, Boston, MA 02115 USA. Univ Illinois, Coll Dent, Dept Oral Biol, Chicago, IL 60612 USA. RP Robinson, C (reprint author), Univ Leeds, Sch Dent, Dept Oral Biol, Clarendon Way, Leeds LS2 9LU, W Yorkshire, England. RI Zeichner-David, Margarita/A-6567-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 0300-8207 J9 CONNECT TISSUE RES JI Connect. Tissue Res. PY 1998 VL 38 IS 1-4 BP 295 EP 303 PG 9 WC Cell Biology; Orthopedics SC Cell Biology; Orthopedics GA 145WF UT WOS:000077394100034 ER PT J AU Lamb, ME AF Lamb, ME TI Generative fathering: Beyond deficit perspectives SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review C1 NICHHD, Sect Social & Emot Dev, Bethesda, MD 20892 USA. RP Lamb, ME (reprint author), NICHHD, Sect Social & Emot Dev, Bethesda, MD 20892 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD JAN PY 1998 VL 43 IS 1 BP 49 EP 50 PG 2 WC Psychology, Multidisciplinary SC Psychology GA YR417 UT WOS:000071493200034 ER PT S AU Bodine, DM Dunbar, CE Girard, LJ Seidel, NE Cline, AP Donahue, RE Orlic, D AF Bodine, DM Dunbar, CE Girard, LJ Seidel, NE Cline, AP Donahue, RE Orlic, D BE Cohen, AR TI Improved amphotropic retrovirus-mediated gene transfer into hematopoietic stem cells SO COOLEYS ANEMIA: SEVENTH SYMPOSIUM SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Cooleys Anemia Symposium CY MAY 30-JUN 02, 1997 CL CAMBRIDGE, MASSACHUSETTS SP New York Acad Sci, Cooleys Anemia Fdn, NIH, NHLBI, NIH, Natl Inst Diabet & Digest & Kidney Dis, Apotex Res Inc, NIH, NICHHD ID COLONY-STIMULATING FACTOR; HUMAN ADENOSINE-DEAMINASE; BONE-MARROW CELLS; UMBILICAL-CORD BLOOD; LONG-TERM EXPRESSION; APE LEUKEMIA-VIRUS; PERIPHERAL-BLOOD; PROGENITOR CELLS; MURINE RETROVIRUSES; C-KIT AB The efficiency of amphotropic retrovirus-mediated gene transfer into human Hematopoietic Stem Cells (HSC) is less than 1%. This has impeded gene therapy for hematopoietic diseases,(1-3) In this study we demonstrate that populations of mouse and human HSC contain low to undetectable levels of the amphotropic virus receptor mRNA (ampho R mRNA), and are resistant to transduction with amphotropic retroviral vectors. In a subpopulation of mouse HSC expressing 7-fold higher levels of ampho R mRNA, transduction with amphotropic retrovirus vectors was 30-fold higher. We conclude that retrovirus transduction of HSC correlates with ampho R mRNA levels, Our results predict that alternative sources of HSC or retroviruses will be required for human gene therapy of hematopoietic diseases. One alternative source of stem cells is from individuals treated with cytokines, We have previously shown that mice treated with G-CSF and SCF have an immediate increase in peripheral blood HSC immediately after treatment, followed by a 10-fold increase in bone marrow HSC 14 days after treatment.(4) In this report we show that when rhesus monkey bone marrow cells collected 14 days after G-CSF and SCF treatment were transduced with amphotropic retroviruses, gene transfer levels were approximately 10%, which was easily detected by Southern blot analysis, We conclude that the increased gene transfer may be the result of increased expression of the amphotropic retrovirus receptor, increased numbers of cycling HSC or both. C1 NIH, Hematopoiesis Sect, Lab Gene Transfer, Natl Ctr Human Genome Res, Bethesda, MD 20892 USA. NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. RP Bodine, DM (reprint author), Natl Ctr Genome Res, Nitt, Hematopoiesis Sect, LGT, 49 Covent Dr,MSC 4442,Bldg 49,Rm 3A14, Bethesda, MD 20892 USA. NR 42 TC 15 Z9 15 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-121-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 850 BP 139 EP 150 DI 10.1111/j.1749-6632.1998.tb10471.x PG 12 WC Genetics & Heredity; Hematology; Multidisciplinary Sciences; Transplantation SC Genetics & Heredity; Hematology; Science & Technology - Other Topics; Transplantation GA BL26J UT WOS:000074933900016 PM 9668536 ER PT S AU Kollia, P Fibach, E Politou, M Noguchi, CT Schechter, AN Loukopoulos, D AF Kollia, P Fibach, E Politou, M Noguchi, CT Schechter, AN Loukopoulos, D BE Cohen, AR TI Hydroxyurea and hemin affect both the transcriptional and post-transcriptional mechanisms of some globin genes in human adult erythroid cells SO COOLEYS ANEMIA: SEVENTH SYMPOSIUM SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Cooleys Anemia Symposium CY MAY 30-JUN 02, 1997 CL CAMBRIDGE, MASSACHUSETTS SP New York Acad Sci, Cooleys Anemia Fdn, NIH, NHLBI, NIH, Natl Inst Diabet & Digest & Kidney Dis, Apotex Res Inc, NIH, NICHHD ID FETAL HEMOGLOBIN; PROGENITORS; DISEASE C1 Univ Athens, Laikon Hosp, Dept Med 1, GR-11527 Athens, Greece. NIDDK, Biol Chem Lab, NIH, Bethesda, MD USA. RP Kollia, P (reprint author), Univ Athens, Laikon Hosp, Dept Med 1, Agiou Thoma 17, GR-11527 Athens, Greece. OI Schechter, Alan N/0000-0002-5235-9408 NR 6 TC 7 Z9 8 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-121-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 850 BP 449 EP 451 DI 10.1111/j.1749-6632.1998.tb10517.x PG 3 WC Genetics & Heredity; Hematology; Multidisciplinary Sciences; Transplantation SC Genetics & Heredity; Hematology; Science & Technology - Other Topics; Transplantation GA BL26J UT WOS:000074933900062 PM 9668580 ER PT J AU Decker, CF Masur, H AF Decker, CF Masur, H TI Pneumonia in AIDS patients in the critical care unit SO CRITICAL CARE CLINICS LA English DT Review ID PNEUMOCYSTIS-CARINII PNEUMONIA; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; HIV-INFECTED PATIENTS; IMMUNE-DEFICIENCY SYNDROME; AEROSOLIZED PENTAMIDINE PROPHYLAXIS; BRONCHOALVEOLAR LAVAGE FLUID; POLYMERASE CHAIN-REACTION; ACUTE RESPIRATORY-FAILURE; BLOOD-INSTITUTE WORKSHOP; IN-HOSPITAL MORTALITY AB Despite advances in prophylaxis and the reduction of mortality and morbidity resulting from highly active antiretroviral therapy, neumocystis pneumonia remains a common problem in HIV-infected patients. There are many possible causes for the continued prevalence of this condition. This article examines the characteristics, and some of the complex causes of P. carinii pneumonia in AIDS patients. C1 Natl Naval Med Ctr, Div Infect Dis, Bethesda, MD USA. RP Masur, H (reprint author), NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20889 USA. NR 148 TC 1 Z9 1 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0749-0704 J9 CRIT CARE CLIN JI Crit. Care Clin. PD JAN PY 1998 VL 14 IS 1 BP 135 EP + DI 10.1016/S0749-0704(05)70386-9 PG 24 WC Critical Care Medicine SC General & Internal Medicine GA YQ427 UT WOS:000071386100010 PM 9448983 ER PT J AU Sherman, LA Theobald, M Morgan, D Hernandez, J Bacik, I Yewdell, J Bennink, J Biggs, J AF Sherman, LA Theobald, M Morgan, D Hernandez, J Bacik, I Yewdell, J Bennink, J Biggs, J TI Strategies for tumor elimination by cytotoxic T lymphocytes SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Article; Proceedings Paper CT 9th International Symposium on the Immunobiology of Proteins and Peptides CY MAY 20-25, 1997 CL WHISTLER, CANADA SP Bristol Myers Squib, Amer Autoimmune Related Dis Assoc, Corixa, Cytel, Schering Plough Res Inst, Chiron Corp, Chiron Therapeut, Ciba Geigy, Genet Inst, NABI, Amgen, Pangaea Pharm, Anergen, StressGen Biotechnol, Medimmune, Bachem, Multiple Peptide Syst, Zeneca, Immune Response Corp, Peninsula Lab DE p53; HLA-transgenic mice; tumor antigens; tolerance; cytotoxic T lymphocytes ID INFILTRATING LYMPHOCYTES; HER-2/NEU PROTOONCOGENE; HLA-A2 MELANOMAS; WILD-TYPE; IN-VIVO; P53; ANTIGEN; PEPTIDE; CELLS; IDENTIFICATION AB Despite differences in their tissue of origin, many tumors share high level expression of certain tumor-associated proteins. Our laboratory has focused on the possibility of utilizing antigenic components of these proteins as a focus for T-cell immunotherapy of cancer. The advantage of targeting such commonly expressed proteins is the fact that such therapy could be of value in eliminating many different types of tumors. A potential barrier in the identification of T-cell epitopes derived from these proteins and presented by tumor cells is the fact that these proteins are also expressed at low levels in some normal tissues, and therefore, self-tolerance may eliminate T cells that are capable of recognizing these epitopes with high avidity. We have utilized two different murine model systems to explore the extent to which self-tolerance may limit the immune response to a tumor-specific antigen. The first compared the ability of mice deficient in expression of murine p53 (p53 knock-out mice) and normal mice, to respond against several epitopes of the p53 protein. The second model compares the ability of conventional mice with transgenic mice that express the influenza hemagglutinin in the periphery to respond to a dominant antigenic peptide of this transgene product. In both models we have investigated the effect self-tolerance has on elimination of tumors expressing the toleragen. C1 UNIV MAINZ, D-6500 MAINZ, GERMANY. NIAID, VIRAL DIS LAB, BETHESDA, MD 20892 USA. RP Scripps Res Inst, DEPT IMMUNOL, 10550 N TORREY PINES RD, LA JOLLA, CA 92037 USA. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 28 TC 32 Z9 32 U1 0 U2 1 PU BEGELL HOUSE INC PI DANBURY PA 50 NORTH ST, DANBURY, CT 06810 USA SN 1040-8401 EI 2162-6472 J9 CRIT REV IMMUNOL JI Crit. Rev. Immunol. PY 1998 VL 18 IS 1-2 BP 47 EP 54 PG 8 WC Immunology SC Immunology GA YK969 UT WOS:A1998YK96900006 PM 9419447 ER PT J AU Rivoltini, L Loftus, DJ Squarcina, P Castelli, C Rini, F Arienti, F Belli, F Marincola, FM Geisler, C Borsatti, A Appella, E Parmiani, G AF Rivoltini, L Loftus, DJ Squarcina, P Castelli, C Rini, F Arienti, F Belli, F Marincola, FM Geisler, C Borsatti, A Appella, E Parmiani, G TI Recognition of melanoma-derived antigens by CTL: Possible mechanisms involved in down-regulating anti-tumor T-cell reactivity SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Article; Proceedings Paper CT 9th International Symposium on the Immunobiology of Proteins and Peptides CY MAY 20-25, 1997 CL WHISTLER, CANADA SP Bristol Myers Squib, Amer Autoimmune Related Dis Assoc, Corixa, Cytel, Schering Plough Res Inst, Chiron Corp, Chiron Therapeut, Ciba Geigy, Genet Inst, NABI, Amgen, Pangaea Pharm, Anergen, StressGen Biotechnol, Medimmune, Bachem, Multiple Peptide Syst, Zeneca, Immune Response Corp, Peninsula Lab DE immunotherapy; peptides; antagonism ID INFILTRATING LYMPHOCYTES; PERIPHERAL-BLOOD; HEALTHY DONORS; IN-VIVO; PEPTIDE; IDENTIFICATION; RESPONSES; GENES; STIMULATION; ANTAGONISTS AB Several T cell-recognized epitopes presented by melanoma cells have been identified recently. Despite the large array of epitopes potentially available for clinical use, it is still unclear which of these antigens could be effective in mediating anti-tumor responses when used as a vaccine. Preliminary studies showed that immunization of melanoma patients with epitopes derived from proteins of the MAGE family may result in significant clinical regressions. However, no sign of systemic immunization could be observed in peripheral blood of treated patients. Conversely, significant immunization (detected as increased anti specific CTL activity in peripheral blood) was obtained by vaccinating KLA-A2.1+ melanoma patients with the immunodominant epitope (residues 27-35) of the differentiation antigen MART-1, but this immunization was not accompanied by a significant clinical response. To implement immunotherapeuties capable of significantly impacting disease outcome, it is necessary to identify the potential mechanisms responsible for the failure of some antigens to mediate significant anti-tumor responses in vivo. In the case of the MART-1(27-35) epitope, we hypothesize that one of these mechanisms may be related to the existence of natural analogs of this peptide in other human normal proteins. C1 NCI, SURG BRANCH, NIH, BETHESDA, MD 20892 USA. UNIV COPENHAGEN, COPENHAGEN, DENMARK. IST RIC FARMACOL MARIO NEGRI, MILAN, ITALY. RP IST NAZL TUMORI, VIA VENEZIAN 1, I-20133 MILAN, ITALY. RI Geisler, Carsten/A-7056-2012; castelli, chiara/K-6899-2012 OI castelli, chiara/0000-0001-6891-8350 NR 24 TC 27 Z9 28 U1 0 U2 2 PU BEGELL HOUSE INC PI DANBURY PA 50 NORTH ST, DANBURY, CT 06810 USA SN 1040-8401 EI 2162-6472 J9 CRIT REV IMMUNOL JI Crit. Rev. Immunol. PY 1998 VL 18 IS 1-2 BP 55 EP 63 PG 9 WC Immunology SC Immunology GA YK969 UT WOS:A1998YK96900007 PM 9419448 ER PT J AU Hall, FS AF Hall, FS TI Social deprivation of neonatal, adolescent, and adult rats has distinct neurochemical and behavioral consequences SO CRITICAL REVIEWS IN NEUROBIOLOGY LA English DT Review DE social isolation; social deprivation; maternal deprivation; dopamine; serotonin; animal models ID LONG-TERM ISOLATION; CORTICOSTEROID RECEPTOR-BINDING; INDUCED ADRENOCORTICAL-RESPONSE; NEGATIVE FEEDBACK SENSITIVITY; EARLY MATERNAL SEPARATION; ADRENAL STRESS RESPONSES; ISOLATION-REARED RATS; ELEVATED PLUS-MAZE; GROUP-HOUSED RATS; MALE WISTAR RATS AB This review examines the consequences of social deprivation on brain chemistry and behavior on rats. Although social deprivation produces wide-ranging behavioral and neurochemical effects, it appears that these effects are determined by a number of factors, the most critical factor being the age or developmental stage during the period of deprivation. Roughly, the effects examined in this review may be separated into three major developmental stages and each is related to deprivation of specific types of social interaction: preweaning/neonatal, postweaning/adolescent, and adult. The effects of social deprivation during each of these stages appears to be neurochemically and behaviorally specific. However, much of the research to date has failed to examine deprivation during specific stages, often combining deprivation of different types. Nonetheless, these modifications of experience produce animals of differing phenotypes, which could be characterized as pathological in nature in many instances, and may model particular aspects of human psychopathologies or perhaps the propensity to develop those phenotypic features. C1 NIAAA, DICBR, Clin Studies Lab, Bethesda, MD 20892 USA. RP Hall, FS (reprint author), NIAAA, DICBR, Clin Studies Lab, Bethesda, MD 20892 USA. RI Hall, Frank/C-3036-2013 OI Hall, Frank/0000-0002-0822-4063 NR 263 TC 311 Z9 317 U1 3 U2 33 PU BEGELL HOUSE INC PI REDDING PA 50 CROSS HIGHWAY, REDDING, CT 06896 USA SN 0892-0915 J9 CRIT REV NEUROBIOL JI Crit. Rev. Neurobiol. PY 1998 VL 12 IS 1-2 BP 129 EP 162 PG 34 WC Neurosciences SC Neurosciences & Neurology GA YQ262 UT WOS:000071367700005 PM 9444483 ER PT J AU Shippenberg, TS Elmer, GI AF Shippenberg, TS Elmer, GI TI The neurobiology of opiate reinforcement SO CRITICAL REVIEWS IN NEUROBIOLOGY LA English DT Review DE opiate reinforcement; opioid peptides; self-administration; conditioned place preference; microdialysis; voltametry ID CONDITIONED PLACE-PREFERENCE; VENTRAL TEGMENTAL AREA; MU-OPIOID RECEPTORS; MESOLIMBIC DOPAMINE SYSTEM; RAT NUCLEUS-ACCUMBENS; SUPEROXIDE-DISMUTASE MICE; MEDIAL PREFRONTAL CORTEX; IN-VIVO MICRODIALYSIS; INDIRECT 5-HT AGONIST; KAINIC ACID LESIONS AB This article provides a basic introduction into two commonly used behavioral paradigms used for the assessment of the reinforcing and rewarding effects of drugs in experimental animals. Behavioral as well as neurochemical data regarding the neural basis of opiate reward are then critically reviewed in order to evaluate the neuroanatomical and neurochemical substrates mediating the primary and conditioned reinforcing effects of opiates as well as current hypotheses of drug-induced reward and aversion. C1 NIDA, Integrat Neurosci Unit, Behav Neurosci Lab, Intramural Res Program,NIH, Baltimore, MD 21224 USA. Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Dept Psychiat, Baltimore, MD 21228 USA. RP Shippenberg, TS (reprint author), NIDA, Integrat Neurosci Unit, Behav Neurosci Lab, Intramural Res Program,NIH, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. FU NIDA NIH HHS [DA11888-01] NR 237 TC 76 Z9 78 U1 2 U2 6 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 USA SN 0892-0915 J9 CRIT REV NEUROBIOL JI Crit. Rev. Neurobiol. PY 1998 VL 12 IS 4 BP 267 EP 303 PG 37 WC Neurosciences SC Neurosciences & Neurology GA 159UD UT WOS:000078192300001 PM 10348612 ER PT J AU Braccio, L Camparini, M Graziosi, P Baratta, G Ferrigno, L Williams, SL Rosmini, F Sperduto, RD Maraini, G AF Braccio, L Camparini, M Graziosi, P Baratta, G Ferrigno, L Williams, SL Rosmini, F Sperduto, RD Maraini, G TI An independent evaluation of the age-related eye disease study (AREDS) cataract grading system SO CURRENT EYE RESEARCH LA English DT Article DE cataract grading system; cataract types; reproducibility; grading error; longitudinal studies ID II LOCS-II; LENS OPACITIES; PROGRESSION AB Purpose. To assess intra-and interobserver reproducibility of the Age-Related Eye Disease Study (AREDS) system for grading lens opacities and to provide data on its capacity to reliably detect changes in lens status. Methods. Independent and replicate grading of 40 sets of lens photographs (one slit-lamp and two retroillumination photographs) were performed by three experienced observers. Patients were participants in the Collaborative Italian-American Clinical Trial of Nutritional Supplements which is testing the effect of a mineral-multivitamin supplement on age-related cataract (CTNS). Scatterplots and intraclass correlation were used to assess measurement error. Results. Analysis revealed good intra-and interobserver reproducibility of the system. Greatest intraobserver measurement error showed 100% of pairs within 10% areal difference for cortical cataract, 97.5% within 15%, areal difference for posterior subcapsular cataract, and 100% within 1 density unit difference for nuclear opacity. Greatest interobserver measurement error showed 95% of pairs within 10% areal difference for cortical cataract, 97.5% within 15% areal difference for posterior subcapsular cataract, and 97.5% within 1.5 density unit difference for nuclear opacity. Conclusions. The AREDS lens opacities grading system appears to be sufficiently reliable to detect changes of at least 10% areal involvement for cortical, 15% areal involvement for posterior subcapsular, and 1.0 units for nuclear opacities. It therefore seems sufficiently sensitive to adequately monitor progression of lens opacities in a longitudinal study of patients with early cataract. Its applicability in a population with advanced or complex mixed opacities must await further testing. C1 Univ Parma, Inst Ophthalmol, I-43100 Parma, Italy. Ist Super Sanita, Epidemiol & Biostat Lab, I-00161 Rome, Italy. NEI, NIH, Bethesda, MD 20892 USA. RP Maraini, G (reprint author), Univ Parma, Inst Ophthalmol, Via Gramsci 14, I-43100 Parma, Italy. EM maraini@ipruniv.cce.unipr.it FU NEI NIH HHS [N01-EY-5-2100] NR 10 TC 4 Z9 4 U1 0 U2 0 PU AEOLUS PRESS PI BUREN PA PO BOX 740, 4116 ZJ BUREN, NETHERLANDS SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD JAN PY 1998 VL 17 IS 1 BP 53 EP 59 DI 10.1076/ceyr.17.1.53.5259 PG 7 WC Ophthalmology SC Ophthalmology GA YR231 UT WOS:000071474100008 PM 9472471 ER PT J AU Tack, CJJ Lenders, JWM Goldstein, DS Lutterman, JA Smits, P Thien, T AF Tack, CJJ Lenders, JWM Goldstein, DS Lutterman, JA Smits, P Thien, T TI Haemodynamic actions of insulin SO CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION LA English DT Review ID SYMPATHETIC NERVOUS-SYSTEM; MUSCLE BLOOD-FLOW; DEPENDENT DIABETES-MELLITUS; MEDIATED GLUCOSE-UPTAKE; BORDERLINE HYPERTENSIVE HUMANS; POSITRON EMISSION TOMOGRAPHY; HUMAN SKELETAL-MUSCLE; HUMAN FOREARM; INDUCED VASODILATION; NITRIC-OXIDE AB Several lines of evidence indicate a significant association between insulin and cardiovascular disease, This association might be explained by direct (cardio)vascular effects of insulin. Two hemodynamic actions of insulin are discussed in this review; it induces direct vasodilation in skeletal muscle and stimulation of the sympathetic nervous system, These closely linked effects normally offset each other. Although more insight has been obtained into responses in insulin-resistant individuals and possible mechanisms, direct evidence to support a causative role for insulin is not yet available. C1 Univ Nijmegen Hosp, Dept Med, Div Gen Internal Med, NL-6500 HB Nijmegen, Netherlands. Univ Nijmegen Hosp, Dept Pharmacol, NL-6500 HB Nijmegen, Netherlands. NINDS, NIH, Clin Neurosci Branch, Bethesda, MD 20892 USA. RP Tack, CJJ (reprint author), Univ Nijmegen Hosp, Dept Med, Div Gen Internal Med, POB 9101, NL-6500 HB Nijmegen, Netherlands. EM c.tack@aig.azn.nl RI Tack, Cees/A-2368-2014; Lenders, J.W.M./L-4487-2015 NR 126 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1062-4821 J9 CURR OPIN NEPHROL HY JI Curr. Opin. Nephrol. Hypertens. PD JAN PY 1998 VL 7 IS 1 BP 99 EP 106 PG 8 WC Urology & Nephrology; Peripheral Vascular Disease SC Urology & Nephrology; Cardiovascular System & Cardiology GA YQ812 UT WOS:000071425600016 PM 9442370 ER PT B AU Bennett, MC Rose, GM AF Bennett, MC Rose, GM BE Lima, FG TI Behavioral, electrophysiological, and biochemical consequences of chronic cytochrome oxidase inhibition in rats SO CYTOCHROME OXIDASE IN NEURONAL METABOLISM AND ALZHEIMER'S DISEASE LA English DT Proceedings Paper CT International Symposium on Cytochrome Oxidase in Neuronal Metabolism and Alzheimer's Disease at the 27th Meeting of the Society-for-Neuroscience CY OCT 28, 1997 CL NEW ORLEANS, LA SP Soc Neurosci AB The mitochondrial enzyme cytochrome oxidase (C.O.) is an essential catalyst fbr electron transfer in oxidative phosphorylation. Recent clinical studies have shown that C.O. activity is reduced in both blood platelets and in the brains of patients with Alzheimer's disease (A.D.), suggesting that a decline in the efficiency of this enzyme could impair cognition. We explored this idea by chronically treating rats with sodium azide, using doses that inhibited C.O. but not other electron transport chain enzymes. Our initial studies demonstrated that selective C.O. inhibition produced deficits in learning tasks, including spatial learning, but did not alter basic sensorimotor function. Azide treatment also disrupted hippocampal long-term potentiation, a potential memory encoding mechanism. Both these effects may have been the consequence of a reduction in membrane bound protein kinase C activity that was observed in the hippocampus, but not in frontal or temporal cortex or cerebellum. Further work revealed that the stress hormone, corticosterone, potentiated azide-induced inhibition of C.O. and the resulting cognitive deficits. Thus, manipulation of C.O. activity in rats to mimic biochemical conditions observed in patients with A.D. caused impairments in learning and memory. C1 NINDS, Expt Therapeut Branch, NIH, Bethesda, MD 20892 USA. RP Bennett, MC (reprint author), NINDS, Expt Therapeut Branch, NIH, Bldg 10,Rm 6C-103,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA BN 0-306-46024-6 PY 1998 BP 217 EP 232 PG 16 WC Cell Biology; Clinical Neurology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA BL91L UT WOS:000077132300008 ER PT J AU Pack, SD Pak, E Tanigami, A Ledbetter, DH Fukuda, MN AF Pack, SD Pak, E Tanigami, A Ledbetter, DH Fukuda, MN TI Assignment of the bystin gene BYSL to human chromosome band 6p21.1 by in situ hybridization SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID PROTEIN C1 Burnham Inst, La Jolla, CA 92037 USA. NCI, NIH, Bethesda, MD 20892 USA. OtsukaGEN Inst, Tokushima, Japan. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. RP Fukuda, MN (reprint author), Burnham Inst, 10901 N Torrey Pines Rd, La Jolla, CA 92037 USA. RI Pack, Svetlana/C-2020-2014 FU NICHD NIH HHS [HD34108] NR 6 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 83 IS 1-2 BP 76 EP 77 DI 10.1159/000015131 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 165WC UT WOS:000078544000026 PM 9925933 ER PT J AU Nash, WG Wienberg, J Ferguson-Smith, MA Menninger, JC O'Brien, SJ AF Nash, WG Wienberg, J Ferguson-Smith, MA Menninger, JC O'Brien, SJ TI Comparative genomics: tracking chromosome evolution in the family Ursidae using reciprocal chromosome painting SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID ZOO-FISH ANALYSIS; DNA LIBRARIES; KARYOTYPE; HOMOLOGIES; SEGMENTS; MAMMALS; PORCINE; CAT AB The Ursidae family includes eight species, the karyotype of which diverges somewhat, in both chromosome number and morphology, from that of other families in the order Carnivora. The combination of consensus molecular phylogeny and high-resolution trypsin G-banded karyotype analysis has suggested that ancestral chromosomal fissions and at least two fusion events are associated with the development of the different ursid species. Here, we revisit this hypothesis by hybridizing reciprocal chromosome painting probes derived from the giant panda (Ailuropoda melanoleuca), domestic cat (Felis catus), and man (Homo sapiens) to representative bear species karyotypes. Comparative analysis of the different chromosome segment homologies allowed reconstruction of the genomic composition of a putative ancestral bear karyotype based upon the recognition of 39 chromosome segments defined by painting as the smallest conserved evolutionary unit segments (pSCEUS) among these species. The different pSCEUS combinations occurring among modern bear species support and extend the postulated sequence of chromosomal rearrangements and provide a framework to propose patterns of genome reorganization among carnivores and other mammal radiations. C1 Natl Canc Inst, Frederick Canc Res & Dev Ctr, Lab Genom Divers, Frederick, MD 21701 USA. H&W Cytogenet Serv, Lovettsville, VA USA. Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England. NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, SAIC Frederick, Frederick, MD USA. RP O'Brien, SJ (reprint author), Natl Canc Inst, Frederick Canc Res & Dev Ctr, Lab Genom Divers, Bldg 560,Room 21-105, Frederick, MD 21701 USA. EM obrien@ncifcrf.gov NR 30 TC 64 Z9 70 U1 0 U2 10 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 83 IS 3-4 BP 182 EP 192 DI 10.1159/000015176 PG 11 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 175BX UT WOS:000079073000004 PM 10072575 ER PT J AU Jensen, MR Audolfsson, T Keck, CL Zimonjic, DB Thorgeirsson, SS AF Jensen, MR Audolfsson, T Keck, CL Zimonjic, DB Thorgeirsson, SS TI Assignment of the cyclin I gene (Ccni) to mouse chromosome 5E3.3-F1.3 by in situ hybridization SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID LOCALIZATION C1 NCI, NIH, Expt Carcinogenesis Lab, Div Basic Sci, Bethesda, MD 20892 USA. RP Thorgeirsson, SS (reprint author), NCI, NIH, Expt Carcinogenesis Lab, Div Basic Sci, Bldg 37,Room 3C28,37 Convent Dr MSC4255, Bethesda, MD 20892 USA. RI Jensen, Michael/E-9677-2011 NR 5 TC 1 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 83 IS 3-4 BP 242 EP 243 DI 10.1159/000015192 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 175BX UT WOS:000079073000020 PM 10072591 ER PT J AU Leonard, JC Toji, LH Beiswanger, CM Beck, JC AF Leonard, JC Toji, LH Beiswanger, CM Beck, JC TI A panel of lymphoblastoid cell cultures from probands with Williams syndrome and their parents SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 Coriell Inst Med Res, Coriell Cell Repositories, NIGMS Human Genet Mutant Cell Repository, Camden, NJ USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 82 IS 1-2 BP 144 EP 144 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 129BZ UT WOS:000076444500069 ER PT J AU Barlund, M Nupponen, NN Karhu, R Tanner, MM Paavola, P Kallioniemi, OP Kallioniemi, A AF Barlund, M Nupponen, NN Karhu, R Tanner, MM Paavola, P Kallioniemi, OP Kallioniemi, A TI Molecular cytogenetic mapping of 24 CEPH YACs and 24 gene-specific large insert probes to chromosome 17 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID COMPARATIVE GENOMIC HYBRIDIZATION; HUMAN BREAST-CANCER; LOSSES; AMPLIFICATION; PATTERNS; REGIONS; GAINS; CARCINOMAS; TUMORS AB Defining boundaries of chromosomal rearrangements at the molecular level would benefit from landmarks that link the cytogenetic map to physical, genetic, and transcript maps, as well as from large-insert FISH probes for such loci to detect numerical and structural rearrangements in metaphase or interphase cells. Here, we determined the locations of 24 genetically mapped CEPH-Mega YACs along the FLpter scale (fractional length from p-telomere) by quantitative fluorescence in situ hybridization analysis. This generated a set of cytogenetically mapped probes for chromosome 17 with an average spacing of about 5 cM. We then developed large-insert YAC, BAG, PAC, or P1 clones to the following 24 known genes, and determined refined map locations along the same FLpter scale: pter-TP53-TOP3-cen-TNFAIP1-ERBB2-TOP2A-BRCA1 -TCF11-NME1-HLF-ZNF1 47/CLN80-BCL5/MPO/SFRS1 -TBX2-PECAM1-DDX5/PRKCA-ICAM2-GH1/PRKAR1A-GRB2-CDK3/FKHL13-qter. Taken together, these 48 cytogenetically mapped large-insert probes provide tools for the molecular analysis of chromosome 17 rearrangements, such as mapping amplification, deletion, and translocation breakpoints in this chromosome, in cancer and other diseases. C1 Natl Human Genome Res Inst, Canc Genet Branch, NIH, Bethesda, MD 20892 USA. Univ Tampere, Inst Med Technol, Canc Genet Lab, FIN-33101 Tampere, Finland. Tampere Univ Hosp, FIN-33101 Tampere, Finland. Natl Publ Hlth Inst, Dept Human Mol Genet, Helsinki, Finland. RP Kallioniemi, A (reprint author), Natl Human Genome Res Inst, Canc Genet Branch, NIH, 49 Convent Dr,MSC-4470,Room 4A24, Bethesda, MD 20892 USA. RI Kallioniemi, Olli/H-5111-2011; Kallioniemi, Olli/H-4738-2012; OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Anne/0000-0003-3552-8158 NR 15 TC 9 Z9 9 U1 2 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 82 IS 3-4 BP 189 EP 191 DI 10.1159/000015096 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 152UW UT WOS:000077796000009 PM 9858813 ER PT J AU Rajcan-Separovic, E Barcelo, JM Korneluk, RG AF Rajcan-Separovic, E Barcelo, JM Korneluk, RG TI Fluorescence in situ hybridization analysis of the replication properties of the myotonic dystrophy protein kinase (DMPK) gene region SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID TRIPLET REPEAT EXPANSION; LOCI; DOMAINS AB Myotonic dystrophy (DM) is caused by an expansion of a CTG repeat sequence in the 3' noncoding region of a protein kinase gene (DMPK) at 19q13.3. We used in situ hybridization to analyse the replication timing of the genomic region containing DMPK in fibroblasts and myoblasts from controls and myotonic dystrophy patients. In this method the relative proportion of singlet to doublet hybridization signals is used to infer the relative time of replication of specific loci or regions. Our results show that in cells from normal individuals approximately 65% of signals appear as doublers, indicating early replication. In DM patients with a number of CTG repeats ranging from about 600-1800 we observed a significant increase of singlet-doublets compared to the background level. These results suggest the existence of replication alternations and/or structural differences between the normal and mutant alleles induced by the presence of the DM mutation. C1 British Columbia Childrens Hosp, Vancouver, BC V6H 3V4, Canada. NICHHD, Cell Biol & Metab Branch, Bethesda, MD 20892 USA. Childrens Hosp Eastern Ontario, Mol Genet Res Lab, Ottawa, ON K1H 8L1, Canada. RP Rajcan-Separovic, E (reprint author), British Columbia Childrens Hosp, 4480 Oak St, Vancouver, BC V6H 3V4, Canada. EM eseparovic@wpog.childhosp.bc.ca; bob@mgcheo.med.uottawa.ca NR 18 TC 1 Z9 1 U1 0 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 82 IS 3-4 BP 247 EP 250 DI 10.1159/000015111 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 152UW UT WOS:000077796000024 PM 9858828 ER PT J AU Takai, S Lorenzi, MV Long, JE Yamada, K Miki, T AF Takai, S Lorenzi, MV Long, JE Yamada, K Miki, T TI Assignment of the Ect2 protooncogene to mouse chromosome band 3B by in situ hybridization SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID FLUORESCENCE INSITU HYBRIDIZATION; GENE; LEUKEMIA C1 Int Med Ctr Japan, Res Inst, Dept Genet, Shinjuku Ku, Tokyo 162, Japan. NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA. RP Takai, S (reprint author), Int Med Ctr Japan, Res Inst, Dept Genet, Shinjuku Ku, 1-21-1 Toyama, Tokyo 162, Japan. NR 9 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 81 IS 1 BP 83 EP 84 DI 10.1159/000014994 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 105KQ UT WOS:000075072600018 PM 9691182 ER PT J AU Palitti, F Pichierri, P Bassi, L Franchitto, A De Santis, LP Balajee, AS AF Palitti, F Pichierri, P Bassi, L Franchitto, A De Santis, LP Balajee, AS TI Effect of DNA-topoisomerase II inhibitors (VP-16 and m-AMSA) and X-rays on Werner's syndrome cells SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 Univ Tuscia, Dipartimento Agrobiol & Agrochim, I-01100 Viterbo, Italy. NIA, Genet Mol Lab, NIH, Baltimore, MD 21224 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 81 IS 2 SU S MA P220 BP 163 EP 163 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 115GH UT WOS:000075654800245 ER PT J AU Modi, WS Amarante, MRV Hanson, M Womack, JE Chidambaram, A AF Modi, WS Amarante, MRV Hanson, M Womack, JE Chidambaram, A TI Assignment of the mouse and cow CXC chemokine genes SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID CYTOKINES AB Gene specific PCR primers were constructed for five mouse and three bovine CXC chemokine genes. The mouse genes were assigned using SSCP analyses of the Jackson BSS backcross panel to two groups on chromosome 5. One group containing Gro1 and Mip2 cosegregated with reference markers Alb1 and Btc, and was positioned 2.2 cM proximal to a group comprising Ifi10, Mig, and Scyb5. The bovine genes IL8, GRO1, and GRO3, mapped using bovine x hamster somatic cell hybrids, were all found to be located on chromosome 6. The locations of these genes in these two animal species are consistent with the positions in humans (4q13-->q21), and previous syntenic relationships among these three mammals. C1 NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Frederick, MD 21702 USA. Texas A&M Univ, Coll Vet Med, Dept Vet Pathobiol, College Stn, TX 77843 USA. RP Modi, WS (reprint author), NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Frederick, MD 21702 USA. RI Amarante, Monica/N-7828-2013 NR 12 TC 15 Z9 15 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 81 IS 3-4 BP 213 EP 216 DI 10.1159/000015033 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 118EA UT WOS:000075824400015 PM 9730606 ER PT J AU Schoenborn, MA Jenkins, NA Copeland, NG Gilbert, DJ Gayle, RB Maliszewski, CR AF Schoenborn, MA Jenkins, NA Copeland, NG Gilbert, DJ Gayle, RB Maliszewski, CR TI Gene structure and chromosome location of mouse Cd39 coding for an ecto-apyrase SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID CELL ACTIVATION ANTIGEN; ATP-DIPHOSPHOHYDROLASE; CLONING; HOMOLOGY; IDENTIFICATION; BRAIN; MAP C1 Immunex Res & Dev Corp, Seattle, WA 98101 USA. NCI, Frederick Canc Res & Dev Ctr, Mammalian Genet Lab, Frederick, MD 21702 USA. RP Schoenborn, MA (reprint author), Immunex Res & Dev Corp, 51 Univ St, Seattle, WA 98101 USA. NR 12 TC 5 Z9 6 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1998 VL 81 IS 3-4 BP 287 EP 289 DI 10.1159/000015049 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 118EA UT WOS:000075824400031 PM 9730622 ER PT J AU Reed, E AF Reed, E TI Nucleotide excision repair and anti-cancer chemotherapy SO CYTOTECHNOLOGY LA English DT Article DE DNA adduct; ERCC1; nucleotide excision repair; ovarian cancer; platinum compounds ID HUMAN OVARIAN-CANCER; MESSENGER-RNA LEVELS; PLATINUM-BASED CHEMOTHERAPY; ACQUIRED CISPLATIN RESISTANCE; PATIENTS RECEIVING CISPLATIN; INTERSTRAND CROSS-LINKS; DNA-ADDUCT FORMATION; MISMATCH REPAIR; LEUKOCYTE DNA; GENE ERCC-1 AB DNA repair is an important effector of anti-cancer drug resistance. In recent years, it has become apparent that DNA repair is an extremely complex process. Processes within DNA repair that may contribute to one or more drug resistance phenotypes include; O-6-alkyltransferase activity, base excision repair, mismatch repair, nucleotide excision repair, and gene specific repair. Clearly, several of these processes may show increased activity within any single cell, or tumor, at any one time. This review attempts to touch briefly upon the question of the distinctions between each of these specific pathways: and then seeks to expand on nucleotide excision repair as a possible effector of cellular and clinical resistance to platinum-based anticancer therapy. C1 NCI, Med Ovarian Canc Sect, Med Branch, Div Clin Sci, Bethesda, MD 20892 USA. RP Reed, E (reprint author), NCI, Med Ovarian Canc Sect, Med Branch, Div Clin Sci, Bldg 10,Room 12N226, Bethesda, MD 20892 USA. NR 94 TC 28 Z9 28 U1 1 U2 3 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0920-9069 J9 CYTOTECHNOLOGY JI Cytotechnology PY 1998 VL 27 IS 1-3 BP 187 EP 201 DI 10.1023/A:1008016922425 PG 15 WC Biotechnology & Applied Microbiology; Cell Biology SC Biotechnology & Applied Microbiology; Cell Biology GA 155UJ UT WOS:000077964500013 PM 19002792 ER PT J AU Wu, DK Nunes, FD Choo, D AF Wu, DK Nunes, FD Choo, D TI Axial specification for sensory organs versus non-sensory structures of the chicken inner ear SO DEVELOPMENT LA English DT Article DE inner ear development; gene expression; sensory organ ID GENE; EXPRESSION; EMBRYO AB A mature inner ear is a complex labyrinth containing multiple sensory organs and nonsensory structures in a fixed configuration. Any perturbation in the structure of the labyrinth will undoubtedly lead to functional deficits. Therefore, it is important to understand molecularly how and when the position of each inner ear component is determined during development, To address this issue, each axis of the otocyst (embryonic day 2.5, E2.5, stage 16-17) was changed systematically at an age when axial information of the inner ear is predicted to be fixed based on gene expression patterns, Transplanted inner ears were analyzed at E4.5 for gene expression of BMP4 (bone morphogenetic protein), SOHo-1 (sensory organ homeobox-l), Otx1 (cognate of Drosophila orthodenticle gene),p75NGFR (nerve growth factor receptor) and Msx1 (muscle segment homeobox), or at E9 for their gross anatomy and sensory organ formation, Our results showed that axial specification in the chick inner ear occurs later than expected and patterning of sensory organs in the inner ear was first specified along the anterior/posterior (A/P) axis, followed by the dorsal/ventral (D/V) axis, Whereas the A/P axis of the sensory organs was fixed at the time of transplantation, the A/P axis for most non-sensory structures was not and was able to be re-specified according to the new axial information from the host. The D/V axis for the inner ear was not fixed at the time of transplantation. The asynchronous specification of the A/P and D/V axes of the chick inner ear suggests that sensory organ formation is a multi-step phenomenon, rather than a single inductive event. C1 Natl Inst Deafness & Other Commun Disorders, Rockville, MD 20850 USA. RP Wu, DK (reprint author), Natl Inst Deafness & Other Commun Disorders, Rockville, MD 20850 USA. RI Nunes, Fabio/B-4543-2011 OI Nunes, Fabio/0000-0002-7785-6785 NR 29 TC 60 Z9 62 U1 0 U2 6 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD JAN PY 1998 VL 125 IS 1 BP 11 EP 20 PG 10 WC Developmental Biology SC Developmental Biology GA YT861 UT WOS:000071652400002 PM 9389659 ER PT J AU Murakami, MS Vande Woude, GF AF Murakami, MS Vande Woude, GF TI Analysis of the early embryonic cell cycles of Xenopus; regulation of cell cycle length by Xe-wee1 and Mos SO DEVELOPMENT LA English DT Article DE Xenopus; wee1; Mos; cdc2 tyrosine phosphorylation; cell cycle ID PROTEIN-KINASE HOMOLOG; DNA-REPLICATION; EGG EXTRACTS; TYROSINE KINASE; FISSION YEAST; MAP KINASE; HUMAN WEE1; PHOSPHORYLATES P34(CDC2); NEGATIVE REGULATION; CDC25 PHOSPHATASE AB In Xenopus, cdc2 tyrosine phosphorylation is detected in the first 60-75 minute cell cycle but not in the next eleven cell cycles (cycles 2-12) which are only 30 minutes long, Here we report that the wee1/cdc25 ratio increases before the first mitotic interphase, We show that the Xe-wee1 protein is absent in stage VI oocytes and is expressed from meiosis II until gastrulation, A dominant negative form of Xe-wee1 (KM wee1) reduced the level cdc2 tyrosine phosphorylation and length of the first cycle, However, the ratio of wee1/cdc25 did not decrease after the first cycle and therefore did not explain the lack of cdc2 tyrosine phosphorylation in, nor the rapidity of, cycles 2-12, Furthermore, there was no evidence for a wee1/myt1 inhibitor in cycles 2-12, We examined the role of Mos in the first cycle because it is present during the first 20 minutes of this cycle. We arrested the rapid embryonic cell cycle (cycle 2 or 3) with Mos and restarted the cell cycle with calcium ionophore; the 30 minute cycle was converted into a 60 minute cycle, with cdc2 tyrosine phosphorylation, In addition, the injection of a non-degradable Mos (MBP-Mos) into the first cycle resulted in a dramatic elongation of this cycle (to 140 minutes), MBP-Mos did not delay DNA replication or the translation of cyclins A or B; it did, however, result in the marked accumulation of tyrosine phosphorylated cdc2, Thus, while the wee1/cdc25 ratio changes during development, these changes may not be responsible for the variety of cell cycles observed during early Xenopus embryogenesis, Our experiments indicate that Mos/MAPK can also contribute to cell cycle length. C1 NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA. RP Vande Woude, GF (reprint author), NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA. EM woude@ncifcrf.gov NR 76 TC 85 Z9 91 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 0950-1991 J9 DEVELOPMENT JI Development PD JAN PY 1998 VL 125 IS 2 BP 237 EP 248 PG 12 WC Developmental Biology SC Developmental Biology GA YX504 UT WOS:000072046900009 PM 9486797 ER PT J AU Damjanovski, S Huynh, MH Motamed, K Sage, EH Ringuette, M AF Damjanovski, S Huynh, MH Motamed, K Sage, EH Ringuette, M TI Regulation of SPARC expression during early Xenopus development: Evolutionary divergence and conservation of DNA regulatory elements between amphibians and mammals SO DEVELOPMENT GENES AND EVOLUTION LA English DT Article DE SPARC; xenopus; embryonic expression; promoter element divergence ID FIBROBLAST GROWTH-FACTOR; EXTRACELLULAR-MATRIX; MESODERM INDUCTION; SECRETED PROTEIN; EMBRYOS; GENE; SEQUENCE; BINDING; ACTIVIN; LAEVIS AB SPARC (Secreted Protein, Acidic, Rich in Cysteine/osteonectin/BM-40) is a highly conserved metal-binding extracellular matrix (ECM) glycoprotein which is first expressed by Xenopus embryos during late gastrulation/early neurulation (stage 12/13), by presumptive notochord and semitic cells. When animal cap explants of stage 9 embryos were cultured in vitro, SPARC expression was not detected until sibling embryos reached late neurula stage (stage 19). Addition of activin, a potent dorsal mesoderm inducer, to animal caps resulted in SPARC being expressed by the time sibling embryos reached stage 16. While basic fibroblast growth factor (bFGF), a ventral mesoderm inducer, had modest effects on SPARC mRNA expression, the combination of both activin and bFGF was synergistic. The appearance, however, of SPARC transcripts 11 h after the addition of activin and bFGF, indicates that unknown intermediates were likely to be involved in activating SPARC expression. In order to identify the potential intermediate regulatory factors which may activate and control SPARC expression, we examined the genomic organization of the 5' end of the Xenopus SPARC gene. No significant homology to the equivalent region that is highly conserved in the mouse, bovine and human SPARC genes was observed. Thus, while mammalian SPARC promoters lack TATA or CAAT boxes, the Xenopus gene contains a consensus TATA box. Moreover, promoter-proximal GGA-box repeats necessary for high level expression of mammalian SPARC are absent in Xenopus. When reporter constructs containing the 5' flanking region of the Xenopus gene were microinjected into two-cell embryos, 868 bp of 5' flanking DNA was sufficient to mimic the temporal and tissue-specific pattern of SPARC expression observed in whole embryos. While a bovine SPARC promoter reporter construct containing 740 bp of the 5' flanking DNA was expressed at a significant level in Xenopus embryos, significant differences in the cell-type expression of the reporter genes were obtained between the bovine and Xenopus constructs. The data indicate that zygotic activation of SPARC mRNA is mediated by regulatory factors acting downstream of major mesoderm induction events. The high DNA sequence conservation at the 5' end of mammalian SPARC genes is not conserved in Xenopus. These differences led to differences in their ability to direct tissue-specific gene expression in early Xenopus embryos. C1 Univ Toronto, Dept Zool, Toronto, ON M5S 3G5, Canada. NICHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Univ Washington, Dept Biol Struct, Seattle, WA 98195 USA. RP Ringuette, M (reprint author), Univ Toronto, Dept Zool, Toronto, ON M5S 3G5, Canada. RI Damjanovski, Sashko/N-8728-2015 FU NIGMS NIH HHS [GM40711] NR 36 TC 18 Z9 18 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0949-944X J9 DEV GENES EVOL JI Dev. Genes Evol. PD JAN PY 1998 VL 207 IS 7 BP 453 EP 461 DI 10.1007/s004270050136 PG 9 WC Cell Biology; Evolutionary Biology; Developmental Biology SC Cell Biology; Evolutionary Biology; Developmental Biology GA YZ970 UT WOS:000072313400005 PM 9510540 ER PT J AU Andrews, J Levenson, I Oliver, B AF Andrews, J Levenson, I Oliver, B TI New AUG initiation codons in a long 5 ' UTR create four dominant negative alleles of the Drosophila C2H2 zinc-finger gene ovo SO DEVELOPMENT GENES AND EVOLUTION LA English DT Article DE C2H2 zinc-finger; germ-line sex determination; dominant-negative; oogenesis ID SEX DETERMINATION; X-CHROMOSOME; MELANOGASTER; GERMLINE; INSERTIONS; SHAVENBABY; MUTATIONS; SEQUENCES; LOCUS AB Promoters active in the germline produce OVO-A and OVO-B mRNAs encoding isoforms of a putative transcription factor. The isoforms have a common C2H2 zinc-finger domain but different N-termini that include potential effector domains. Single point mutations in three dominant-negative ovo(D) mutations result in new in-frame initiation codons in OVO-B mRNAs and amino acid substitutions within charged regions of OVO-A proteins. Three lines of evidence suggest that the dominant activity is due to the new initiation codons in OVO-B mRNAs and not the amino acid substitutions in OVO-A. First, we made a fourth ovo(D) allele by inserting a new in-frame AUG. This ovo(D4) allele encodes a nearly full-length OVO-A isoform from OVO-B mRNAs. Second, engineered stop codons in ovo(D1) downstream of the new AUG abolished dominant negative activity. Third, a substantial deletion of an OVO-A region encoding a highly charged amino acid domain fully rescued loss-of-function ovo alleles. These data suggest that ovo(D) mutations result in inappropriate expression of OVO-A in the female germline. C1 NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. RP Andrews, J (reprint author), NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. NR 20 TC 17 Z9 17 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0949-944X J9 DEV GENES EVOL JI Dev. Genes Evol. PD JAN PY 1998 VL 207 IS 7 BP 482 EP 487 DI 10.1007/s004270050139 PG 6 WC Cell Biology; Evolutionary Biology; Developmental Biology SC Cell Biology; Evolutionary Biology; Developmental Biology GA YZ970 UT WOS:000072313400008 PM 9510543 ER PT J AU Melloy, PG Ewart, JL Cohen, MF Desmond, ME Kuehn, MR Lo, CW AF Melloy, PG Ewart, JL Cohen, MF Desmond, ME Kuehn, MR Lo, CW TI No turning, a mouse mutation causing left-right and axial patterning defects SO DEVELOPMENTAL BIOLOGY LA English DT Article DE notochord; floorplate; nodal; sonic hedgehog; Brachyury; HNF-3 beta; lefty; left/right patterning; laterality; heart looping; mouse embryos; cardiovascular defects ID LEFT-RIGHT ASYMMETRY; SONIC-HEDGEHOG; SITUS-INVERSUS; EXTRACELLULAR-MATRIX; HEART MALFORMATIONS; NOTOCHORD FORMATION; POLARIZING ACTIVITY; NODAL EXPRESSION; DEFICIENT MICE; NEURAL-TUBE AB Patterning along the left/right axes helps establish the orientation of visceral organ asymmetries, a process which is of fundamental importance to the viability of an organism. A Linkage between left/right and axial patterning is indicated by the finding that a number of genes involved in left/right patterning also play a role in anteroposterior and dorsoventral patterning. We have recovered a spontaneous mouse mutation causing left/right patterning defects together with defects in anteroposterior and dorsoventral patterning. This mutation is recessive lethal and was named no turning (nt) because the mutant embryos fail to undergo embryonic turning. nt embryos exhibit cranial neural tube closure defects and malformed somites and are caudally truncated. Development of the heart arrests at the looped heart tube stage, with cardiovascular defects indicated by ballooning of the pericardial sac and the pooling of blood in various regions of the embryo. Interestingly, in nt embryos, the direction of heart looping was randomized. Nodal and lefty, two genes that are normally expressed only in the left lateral plate mesoderm, show expression in the right and left lateral plate mesoderm. Lefty, which is normally also expressed in the floorplate, is not found in the prospective floorplate of nt embryos. This suggests the possibility of notochordal defects. This was confirmed by histological analysis and the examination of sonic hedgehog, Brachyury, and HNF-3 beta gene expression. These studies showed that the notochord is present in the early nt embryo, but degenerates as development progresses. Overall, these findings support the hypothesis that the notochord plays an active role in left/right patterning. Our results suggest that nt may participate in this process by modulating the notochordal expression of HNF-3 beta. (C) 1998 Academic Press. C1 Univ Penn, Dept Biol, Goddard Lab, Philadelphia, PA 19104 USA. Villanova Univ, Dept Biol, Villanova, PA 19085 USA. NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. RP Lo, CW (reprint author), Univ Penn, Dept Biol, Goddard Lab, Philadelphia, PA 19104 USA. RI Kuehn, Michael/A-4573-2014 OI Kuehn, Michael/0000-0002-7703-9160 FU NICHD NIH HHS [HD29573] NR 53 TC 80 Z9 80 U1 1 U2 4 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN 1 PY 1998 VL 193 IS 1 BP 77 EP 89 DI 10.1006/dbio.1997.8787 PG 13 WC Developmental Biology SC Developmental Biology GA YV600 UT WOS:000071843000007 PM 9466889 ER PT J AU He, HY Gao, C Vrensen, G Zelenka, P AF He, HY Gao, C Vrensen, G Zelenka, P TI Transient activation of cyclin B/Cdc2 during terminal differentiation of lens fiber cells SO DEVELOPMENTAL DYNAMICS LA English DT Article DE cyclin; cyclin-dependent kinase; differentiation; denucleation; lens ID TUMOR-SUPPRESSOR GENE; TRANSGENIC MICE; RETINOBLASTOMA PROTEIN; KINASE; EXPRESSION; APOPTOSIS; INDUCTION; P34(CDC2); INHIBITOR; COMPLEX AB Previous work has shown that postmitotic, differentiating fiber cells of the embryonic chicken lens express cyclin B and Cdc2. The present study explores the possible physiological role of these proteins in lens differentiation by examining the developmental regulation of cyclin B/Cdc2 expression and activity in lens fiber cells of embryonic and newborn rats. Cyclin B mRNA and protein were detected not only in the lens epithelium, which contains proliferating cells, but also in postmitotic, differentiating fiber cells. In contrast, cyclin A mRNA and protein were detected only in epithelial cells, Immunoprecipitation with cyclin B antibody coprecipitated Cdc2 from both epithelial and fiber cell extracts. Immunoprecipitates of cyclin B from both epithelial cells and fiber cells showed H1 kinase activity when assayed in vitro, but the developmental pattern of cyclin B-associated kinase activity in these two lens fractions was markedly different. In the epithelium, H1 kinase activity decreased gradually with developmental age in parallel with the decrease in epithelial cell proliferation, whereas, in the fiber cells, kinase activity peaked sharply at embryonic day 18 (E18) and E19. Microscopic examination of rat lenses indicated that peak cyclin B/Cdc2 activity was correlated with changes in chromatin structure and nuclear envelope breakdown in the terminally differentiating primary lens fiber cells. These findings suggest that cyclin B/Cdc2 activity may play an active role in nuclear changes leading to primary fiber cell denucleation. (C) 1998 Wiley-Liss, Inc. C1 NEI, NIH, Bethesda, MD 20892 USA. Netherlands Ophthalm Res Inst, Dept Morphol, NL-1100 AC Amsterdam, Netherlands. RP Zelenka, P (reprint author), Bldg 6,Room 214,6 Ctr Dr,MSC 2730, Bethesda, MD 20892 USA. NR 35 TC 19 Z9 19 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD JAN PY 1998 VL 211 IS 1 BP 26 EP 34 DI 10.1002/(SICI)1097-0177(199801)211:1<26::AID-AJA3>3.0.CO;2-9 PG 9 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA YN976 UT WOS:000071228900003 PM 9438421 ER PT J AU Oliver, B Pauli, D AF Oliver, B Pauli, D TI Suppression of distinct ovo phenotypes in the drosophila female germline by maleless(-) and Sex-lethal(M) SO DEVELOPMENTAL GENETICS LA English DT Article DE chromatin; C2H2 zinc finger; oogenesis; sex determination; spermatogenesis ID LINE SEX DETERMINATION; DOSAGE COMPENSATION REGULATORS; OVARIAN TUMOR GENE; X-CHROMOSOME; INDUCTIVE SIGNALS; MELANOGASTER; LETHAL; EXPRESSION; MUTATIONS; LOCUS AB Mutations in ovo result in several different phenotypes, which we show are due to the regulation of distinct developmental pathways. Two X (female) germ cells require ovo(+) activity for viability, but 1X (male) germ cells do not, in our study we observed suppression of the ovo germline-lethality phenotype in loss-of-function maleless (mle) Females indicating that ovo(+) and mle(+) have opposing effects in female germ cells, or that they are hierarchically related. Gain-of-function Sex-lethal (Sxl) alleles and male specific lethal-2 alleles did not suppress he ovo germline death phenotype. Many of the surviving germ cells in females mutant for both ovo and mle showed ovarian tumors. in contrast to the germline viability phenotype, we did observe suppression of the tumor phenotype in females heterozygous for gain-of-function alleles of Sxl. Further, females mutant for some hypomorphic ovo alleles were rendered fertile by Sxl gain-of-function alleles. Thus, ovo(+) is required For at least two distinct functions, one involving mle(+), and one mediated by Sxl(+) gene products. The existence of ovo(+) functions independent of mle(+) and Sxl(+) is likely. Dev. Genet. 23:335-346, 1998. (C) 1998 Wiley-Liss, Inc.dagger C1 NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. Univ Geneva, Dept Zool & Anim Biol, Geneva, Switzerland. RP Oliver, B (reprint author), NIDDK, Cellular & Dev Biol Lab, NIH, MSC 2715, Bethesda, MD 20892 USA. EM oliver@helix.nih.gov NR 62 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0192-253X J9 DEV GENET JI Dev. Genet. PY 1998 VL 23 IS 4 BP 335 EP 346 DI 10.1002/(SICI)1520-6408(1998)23:4<335::AID-DVG8>3.0.CO;2-M PG 12 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA 152CA UT WOS:000077756900008 PM 9883585 ER PT J AU Maixner, A Hecker, TP Phan, QN Wassarman, DA AF Maixner, A Hecker, TP Phan, QN Wassarman, DA TI A screen for mutations that prevent lethality caused by expression of activated sevenless and Ras1 in the Drosophila embryo SO DEVELOPMENTAL GENETICS LA English DT Article DE signal transduction; embryogenesis; Trithorax group; eye development; receptor tyrosine kinase ID RECEPTOR TYROSINE KINASE; RAS1-MEDIATED PHOTORECEPTOR DEVELOPMENT; SERINE THREONINE PHOSPHATASES; TRACHEAL CELL-MIGRATION; RNA-POLYMERASE-II; PROTEIN PHOSPHATASE-2A; EYE DEVELOPMENT; SACCHAROMYCES-CEREVISIAE; CAENORHABDITIS-ELEGANS; NUCLEOTIDE-SEQUENCE AB Ras1 plays a critical role in receptor tyrosine kinase (RTK) signal transduction pathways that function during Drosophila development. We demonstrate that mis-expression of constitutively active forms of Ras1 (Ras1(V12)) and the Sevenless (Sev) RTK (Sev(S11)) during embryogenesis causes lethality due to inappropriate activation of RTK/Ras1 signaling pathways. Genetic and molecular data indicate that the rate of Sev(S11)/sev-Ras1(V12) lethality is sensitive to the expression level of both transgenes. To identify genes that encode components of RTK/Ras1 signaling pathways or modulators of RNA polymerase II transcription, we took advantage of the dose-sensitivity of the system and screened for second site mutations that would dominantly suppress the lethality. The collection of identified suppressors includes the PR55 subunit of Protein Phosphatase 2A indicating that downstream of Sev and Ras 1 this subunit acts as a negative regulator of phosphatase activity. The isolation of mutations in the histone deacetylase RPD3 suggests that it functions as positive regulator of sev enhancer-driven transcription. Finally, the isolation of mutations in the Trithorax group gene devenir and the characterized allelism with the Breathless RTK encoding gene provides evidence for Ras1-mediated regulation of homeotic genes. Dev. Genet. 23:347-361, 1998. (C) 1998 Wiley-Liss, Inc.dagger C1 NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. RP Wassarman, DA (reprint author), NICHHD, Cell Biol & Metab Branch, NIH, Bldg 18T,Room 101, Bethesda, MD 20892 USA. NR 78 TC 19 Z9 19 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0192-253X J9 DEV GENET JI Dev. Genet. PY 1998 VL 23 IS 4 BP 347 EP 361 DI 10.1002/(SICI)1520-6408(1998)23:4<347::AID-DVG9>3.0.CO;2-C PG 15 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA 152CA UT WOS:000077756900009 PM 9883586 ER PT J AU Vermaak, D Wolffe, AP AF Vermaak, D Wolffe, AP TI Chromatin and chromosomal controls in development SO DEVELOPMENTAL GENETICS LA English DT Review DE histone variants; nucleosome modification; chromodomain proteins; repeat-induced silencing; heterochromatin; dosage compensation; vertebrate embryogenesis; transcriptional regulation; nuclear compartmentalization ID POSITION-EFFECT VARIEGATION; LINKER HISTONES B4; DROSOPHILA-MELANOGASTER; GENE-EXPRESSION; XENOPUS-LAEVIS; TRICHOSTATIN-A; X-CHROMOSOME; IN-VIVO; ACETYLATION; TRANSCRIPTION AB Chrominatin and chromosomes have major regulatory roles in development. Nucleosome positioning and modification, chromatin structural transitions and domain organization all contribute to the regulation of individual genes and gene families. Chromosomal position and nuclear compartmentalization represent important contributory factors in determining cell fate. These controls may explain many interesting and unexplored features of developmental systems. (C) 1998 Wiley-Liss, Inc.dagger. C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. RP Wolffe, AP (reprint author), NICHHD, Mol Embryol Lab, NIH, Bldg 18T,Rm 106, Bethesda, MD 20892 USA. NR 50 TC 30 Z9 31 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0192-253X J9 DEV GENET JI Dev. Genet. PY 1998 VL 22 IS 1 BP 1 EP 6 PG 6 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA YZ557 UT WOS:000072266000001 PM 9499575 ER PT J AU Kaneko, KJ DePamphilis, ML AF Kaneko, KJ DePamphilis, ML TI Regulation of gene expression at the beginning of mammalian development and the TEAD family of transcription factors SO DEVELOPMENTAL GENETICS LA English DT Article DE zygotic gene expression; TEA DNA binding domain genes; mouse embryo ID ENHANCER FACTOR-I; DNA-BINDING DOMAIN; M-CAT MOTIF; MOUSE DEVELOPMENT; HISTONE ACETYLATION; PROMOTER ACTIVITY; XENOPUS-LAEVIS; TRICHOSTATIN-A; SV40 ENHANCER; 1-CELL STAGE AB In mouse development, transcription is first detected in late 1-cell embryos, but translation of newly synthesized transcripts does not begin until the 2-cell stage. Thus, the onset of zygotic gene expression (ZGE) is regulated al the level of both transcription and translation. Chromatin-mediated repression is established after formation of a 2-cell embryo, concurrent with the developmental acquisition of enhancer function. The mosi effective enhancer in cleavage stage mouse embryos depends on DNA binding sites for TEF-1, the prototype for a family of transcription factors that share the same TEA DNA binding domain. Mice contain al least Four, and perhaps five, genes with the same TEA DNA binding domain (mTEAD genes). Since mTEAD-2 is the only one expressed during the first 7 days of mouse development, ii is most likely responsible for the TEAD transcription factor activity that first appears at the beginning of ZGE. All four mTEAD genes are er:pressed at later embryonic stages and in adult tissues, virtually every tissue expresses at least one family member, consistent with a critical role for TEAD proteins in either cell proliferation or differentiation. The 72-amino acid TEA DNA binding domains in mTEAD-2, 3, and 4 are similar to 99% homologous io the same domain in mTEAD-1, and ail four proteins bind specifically to the same DNA sequences in vitro with a K-d value of 16-38 nM DNA. Since TEAD proteins appear to be involved in both activation and repression of different genes and do no: appear to be functionally redundant, differential activity of TEAD proteins must result either from association with other proteins or from differential sensitivity to chromatin packaged DNA binding sites. (C) 1998 Wiley-Liss, Inc. C1 NICHHD, NIH, Bethesda, MD 20892 USA. RP NICHHD, NIH, Bldg 6,Room 416, Bethesda, MD 20892 USA. EM kjaneko@box-k.nih.gov NR 57 TC 76 Z9 80 U1 1 U2 9 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0192-253X J9 DEV GENET JI Dev. Genet. PY 1998 VL 22 IS 1 BP 43 EP 55 DI 10.1002/(SICI)1520-6408(1998)22:1<43::AID-DVG5>3.0.CO;2-7 PG 13 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA YZ557 UT WOS:000072266000005 PM 9499579 ER PT J AU Wai, AWK Ng, LJ Watanabe, H Yamada, Y Tam, PPL Cheah, KSE AF Wai, AWK Ng, LJ Watanabe, H Yamada, Y Tam, PPL Cheah, KSE TI Disrupted expression of matrix genes in the growth plate of the mouse cartilage matrix deficiency (cmd) mutant SO DEVELOPMENTAL GENETICS LA English DT Article DE aggrecan; cartilage matrix deficiency; growth plate abnormal expression of matrix molecules; mouse mutant ID PROCOLLAGEN MESSENGER-RNAS; COLLAGEN-X-GENE; IX COLLAGEN; CHONDROCYTE DIFFERENTIATION; SKELETAL DEVELOPMENT; AMINO-PROPEPTIDE; II PROCOLLAGEN; PRO-ALPHA-2(XI) COLLAGEN; TRANSGENIC MICE; EXON STRUCTURE AB Chondrodysplasia in the autosomal recessive cartilage matrix deficiency (cmd) mutant is caused by lock of the proteoglycan aggrecan arising from a mutation in the gene. Homozygous cmd/cmd mice are characterized by disorganisation of chondrocytes in the growth plate, disproportionate dwarfism, late, and perinatal lethality. We have studied the impact of the aggrecan deficiency on the expression of other matrix genes during the differentiation of chondrocytes in the growth plate of cmd/cmd 18.5 day fetuses. Compared with the wild-type, there are significant differences in the growth plates of cmd mutants in the combinations of co-expression of genes encoding the glycoprotein link protein, proteoglycan syndecan 3, collagens alpha 1 (X) [Col10a1], alpha 2 (XI) [Col11a2], and the alternative transcripts of alpha 1 (II) [Col2a1 type IIA form], and alpha 1 (IX) [Col9a1 long and short forms]. The discordance of gene expression in cmd chondrocytes may be additional factors contributing io the disrupted cellular architecture of the growth plate resulting from the primary absence of aggrecan. (C) 1998 Wiley-Liss, Inc. C1 Univ Hong Kong, Dept Biochem, Hong Kong, Peoples R China. NIDR, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA. Childrens Med Res Inst, Embryol Unit, Wentworthville, NSW, Australia. RP Cheah, KSE (reprint author), Univ Hong Kong, Dept Biochem, Sassoon Rd, Hong Kong, Peoples R China. EM hrmbdkc@hkumd1.hku.hk NR 59 TC 30 Z9 31 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0192-253X J9 DEV GENET JI Dev. Genet. PY 1998 VL 22 IS 4 BP 349 EP 358 DI 10.1002/(SICI)1520-6408(1998)22:4<349::AID-DVG5>3.0.CO;2-6 PG 10 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA ZX992 UT WOS:000074575900005 PM 9664687 ER PT J AU Montpied, P Yan, GM Paul, SM Morrow, AL AF Montpied, P Yan, GM Paul, SM Morrow, AL TI Transient increase in cerebellar transcriptional activity precedes the expression of GABA(A) receptor alpha 6 subunit mRNA during postnatal maturation SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE GABA(A) receptor alpha 6 subunit; developmental regulation; polyadenylated RNA; northern analysis; dot-blot hybridization; in situ hybridization ID MESSENGER-RNA EXPRESSION; RAT-BRAIN; DEVELOPMENTAL EXPRESSION; GRANULE CELLS; GENE-EXPRESSION; CORTEX; ACTIN; ANTAGONIST; NEURONS; PROTEIN AB The purpose of this study was to investigate the postnatal expression of GABA(A) receptor alpha 6 subunit genes in the context of cerebellar differentiation. We examined steady-state levels of GABB(A) receptor alpha 1 and alpha 6 subunit mRNAs, polyadenylated (polyA(+)) mRNA and beta-actin mRNA in 7-, 14-, 21-, 28-, 35-, 49- and 120-day-old rats. Messenger RNA expression and splicing were evaluated in parallel using Northern blot analysis and in situ hybridization histochemistry. The expression of mature GABA(A) receptor alpha 6 subunit mRNA species (2.7 kb) was found 1 week after birth in cerebellar granule cells. Prior to stable expression of the mature alpha 6 subunit gene, we detected large alpha 6 subunit premessengers (3.8 and 3.5 kb) by Northern blot analysis. These premessenger species were detected in prenatal day (PND) 15 and neonatal rat cerebellum, when the mature alpha 6 subunit mRNAs (2.7 kb) were not yet expressed. The maximal. expression of mature alpha 6 subunit mRNA species was observed at PND 21 when the peak level of cerebellar transcriptional activity was measured by polyA(+) RNA levels. In contrast, beta-actin mRNA expression was decreased at PND 21 compared to birth levels. These major transcriptional events take place during a period of about 1 week (between PND 14 and 21), immediately following the most active phase of cell division in the external granule layer and migration of granule cells to the internal granule cell layer. Comparison between the relative abundance of these genes shows that differential regulation of each gene occurs during postnatal development. The induction of GABA(A) receptor alpha 6 subunit gene expression is preceded by a reduction in beta-actin mRNA levels and a transient increase in total transcriptional activity. The expression of alpha 6 subunit mRNA is maintained at the PND 21 level through adulthood, but the alpha 1 subunit mRNA levels decrease drastically within the following week (from PND 21 to 28). These results suggest that tissue-specific expression of the GABA(A) receptor alpha 6 subunit gene is correlated with a series of developmentally regulated morphologic and transcriptional events. C1 NIMH, Clin Neurosci Branch, Mol Pharmacol Sect, Bethesda, MD 20892 USA. Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA. Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27515 USA. Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27515 USA. RP Montpied, P (reprint author), CNRS UPR 8402, INSERM U249, Expt Med Lab, F-34060 Montpellier, France. FU FIC NIH HHS [F05-TWO-4591-01] NR 42 TC 4 Z9 4 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PD JAN-FEB PY 1998 VL 20 IS 1 BP 74 EP 82 DI 10.1159/000017301 PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA ZF143 UT WOS:000072867200008 PM 9600393 ER PT J AU Westergaard, GC Byrne, G Suomi, SJ AF Westergaard, GC Byrne, G Suomi, SJ TI Early lateral bias in tufted capuchins (Cebus apella) SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Article DE capuchin, Cebus; development; handedness; laterality ID CHIMPANZEES PAN-TROGLODYTES; HAND PREFERENCE; CEREBRAL LATERALIZATION; BIOLOGICAL MECHANISMS; HEAD-ORIENTATION; RIGHT-HANDEDNESS; TOOL-USE; MONKEYS; INFANT; ASSOCIATIONS AB We investigated the development of lateral bias in infant tufted capuchins (Cebus apella) by recording head orientation during the first 2 postnatal weeks and hand preference during Weeks 23 to 24 and 47 to 48. We found that lateral bias for head orientation at I to 2 weeks was negatively related to hand preference at 23 to 24 weeks. Further, we found population-level left-hand preferences at both 23 to 24 and 47 to 48 weeks, and that hand preference at 23 to 24 weeks is positively correlated with hand preference at 47 to 48 weeks. We also noted a trend toward a sex difference in the direction of neonatal head orientation, with males exhibiting a left-side preference and females exhibiting a lack of preference toward either side. Our findings differ from those obtained in studies with developing humans and chimpanzees in two important ways. First, the trend for head orientation and hand preference in infant capuchins Mns to the left rather than to the right. Second, we found a negative relation between direction of early head orientation and subsequent hand preference. It seems likely that research examining cerebral development in capuchins will help us to better understand the occurrence of left-handedness and the development of cerebral dominance in humans. (C) 1998 John Wiley & Sons, Inc. C1 NICHHD, Comparat Ethol Lab, Poolesville, MD 20837 USA. RP Westergaard, GC (reprint author), NICHHD, Comparat Ethol Lab, Poolesville, MD 20837 USA. NR 40 TC 12 Z9 13 U1 0 U2 4 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0012-1630 J9 DEV PSYCHOBIOL JI Dev. Psychobiol. PD JAN PY 1998 VL 32 IS 1 BP 45 EP 50 DI 10.1002/(SICI)1098-2302(199801)32:1<45::AID-DEV5>3.0.CO;2-T PG 6 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA YQ497 UT WOS:000071393700005 PM 9452907 ER PT J AU Tamis-LeMonda, CS Chen, LA Bornstein, MH AF Tamis-LeMonda, CS Chen, LA Bornstein, MH TI Mothers' knowledge about children's play and language development: Short-term stability and interrelations SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID SYMBOLIC PLAY; COGNITIVE-DEVELOPMENT; BELIEFS; OBJECTS; INFANTS AB Sixty-four mothers of children ranging in age from 6 to 58 months were asked to determine, for pairings of play and language items, which item was more advanced developmentally. This procedure was repeated within 2 weeks. In general, mothers' orderings of play and language items matched those established in the developmental Literature and were stable over the short term. Mothers' knowledge about language development was stronger than and unrelated to their knowledge about play, suggesting that maternal knowledge about developmental domains is differentiated and specific. Finally, mothers' judgments about the developmental milestones depended on their children's current developmental stage: Mothers were less accurate at estimating the timing of milestones that their children had mastered many months earlier, supporting the view that mothers' knowledge is informed by their children's recent rather than past achievements in specific areas. C1 NYU, Dept Appl Psychol, New York, NY 10003 USA. NICHHD, Rockville, MD USA. RP Tamis-LeMonda, CS (reprint author), NYU, Dept Appl Psychol, 239 Greene St,5th Floor, New York, NY 10003 USA. EM cst@xp.psych.nyu.edu FU NICHD NIH HHS [HD20807, HD20559]; NIMH NIH HHS [MH48915] NR 57 TC 21 Z9 21 U1 0 U2 2 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0012-1649 J9 DEV PSYCHOL JI Dev. Psychol. PD JAN PY 1998 VL 34 IS 1 BP 115 EP 124 DI 10.1037/0012-1649.34.1.115 PG 10 WC Psychology, Developmental SC Psychology GA YR371 UT WOS:000071488700010 PM 9471009 ER PT J AU Nagi, DK Knowler, WC Mohamed-Ali, V Bennett, PH Yudkin, JS AF Nagi, DK Knowler, WC Mohamed-Ali, V Bennett, PH Yudkin, JS TI Intact proinsulin, des 31,32 proinsulin, and specific insulin concentrations among nondiabetic and diabetic subjects in populations at varying risk of type 2 diabetes SO DIABETES CARE LA English DT Article ID ACTIVATOR INHIBITOR PAI-1; PIMA-INDIANS; SPLIT PROINSULIN; GLUCOSE-TOLERANCE; GLYCEMIC CONTROL; C-PEPTIDE; MELLITUS; RESISTANCE; SECRETION; NIDDM AB OBJECTIVE - To examine hyperinsulinemia, insulin secretion, and beta-cell function in Pima Indians, South Asians, and whites, populations at varying risk of diabetes. RESEARCH DESIGN AND METHODS-We investigated 136 Pima Indian, 98 Asian, and 80 white nondiabetic and 172 Pima Indian, 40 Asian, and 49 white diabetic subjects. Highly specific assays for insulin, intact proinsulin, and des 31,32 proinsulin were used. Insulin secretion was assessed using ratio of increment (0 to 30 min) in insulin to glucose concentrations during an oral glucose tolerance test (OGTT). RESULTS-Nondiabetic Pima Indians were significantly more obese than Asians and whites. Pima Indian subjects had significantly higher (P < 0.01) fasting insulin concentrations (median 109 pmol/l, range 40-250) than Asian (37 pmol/l, range 17-91) and white (30 pmol/l, range 10-82) subjects. These differences remained significant when controlled for obesity Nondiabetic Pima Indians also had higher fasting C-peptide concentrations and higher early insulin secretion during an OGTT Fasting concentrations of intact proinsulin and des 31,32 proinsulin were also significantly higher in Pima Indians (P < 0.01). However, the proportion of proinsulin-like molecules was significantly lower (P < 0.01) in Pima Indians (median 7.9% vs. 12.7% for South Asians and 12.2% for whites). Subjects with diabetes from the three ethnic groups showed significantly higher fasting insulin concentrations but lower 30-min insulin and lower ratios of increment (0-30 min) in insulin to glucose concentrations than did nondiabetic subjects, The proportion of proinsulin-like molecules was not significantly different in diabetic subjects from the three ethnic groups. CONCLUSIONS - These specific assays for insulin indicate that after adjusting for obesity, nondiabetic Pima Indians are truly hyperinsulinemic, which is consistent with their insulin resistance as measured by other methods. Hyperinsulinemia in this population with a high risk of diabetes is likely to be due to enhanced insulin secretion. Furthermore, in Pima Indians, the predominant beta-cell secretory product is insulin and not its precursors. We conclude that the differences in the risk of diabetes among these three groups are not due to differences in insulin secretion or insulin processing. Subjects with type 2 diabetes have defective early insulin secretion during OGTTs but show fasting hyperinsulinemia even when specific assays for insulin are used. C1 NIDDKD, NIH, Phoenix, AZ USA. UCL, Whittington Hosp, Sch Med, Dept Med, London, England. RP Nagi, DK (reprint author), Pinderfields Hosp Trust, Edna Coates Ctr, Aberford Rd, Wakefield WF1 4DG, England. RI Yudkin, John/C-1988-2008 NR 41 TC 17 Z9 23 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JAN PY 1998 VL 21 IS 1 BP 127 EP 133 DI 10.2337/diacare.21.1.127 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN892 UT WOS:000071219200024 PM 9538983 ER PT J AU Pahor, M Kritchevsky, SB Zuccala, G Guralnik, JM AF Pahor, M Kritchevsky, SB Zuccala, G Guralnik, JM TI Diabetes and risk of adverse events with calcium antagonists SO DIABETES CARE LA English DT Letter ID INCREASE; CANCER C1 Univ Tennessee, Dept Prevent Med, Memphis, TN 38105 USA. Catholic Univ Rome, Dept Internal Med & Geriatr, Rome, Italy. NIA, Epidemiol Demog & Biometry Program, Bethesda, MD 20892 USA. RP Pahor, M (reprint author), Univ Tennessee, Dept Prevent Med, 66 N Pauline,Suite 633, Memphis, TN 38105 USA. NR 11 TC 28 Z9 28 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JAN PY 1998 VL 21 IS 1 BP 193 EP 194 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN892 UT WOS:000071219200036 PM 9538995 ER PT J AU Narayan, KMV Hoskin, M Kozak, D Kriska, AM Hanson, RL Pettitt, DJ Nagi, DK Bennett, PH Knowler, WC AF Narayan, KMV Hoskin, M Kozak, D Kriska, AM Hanson, RL Pettitt, DJ Nagi, DK Bennett, PH Knowler, WC TI Randomized clinical trial of lifestyle interventions in Pima Indians: A pilot study SO DIABETIC MEDICINE LA English DT Article DE NIDDM; obesity; prevention; diet; exercise; clinical trial ID WEIGHT-LOSS; PREFERENCES; PROGRAM; NIDDM AB A pilot trial was conducted to test adherence to specific lifestyle interventions among Pima Indians of Arizona, and to compare them for changes in risk factors for diabetes mellitus, Ninety-five obese, normoglycaemic men and women, aged 25-54 years, were randomized to treatments named 'Pima Action' (Action) and 'Pima Pride' (Pride), which were tested Sea; 12 months. Action involved structured activity and nutrition interventions, and Pride included unstructured activities emphasizing Pima history and culture, Adherence to interventions, changes in self-reported activity and diet, and changes in weight, glucose concentrations, and other risk factors were assessed regularly. Thirty-five eligible subjects who had declined randomization were also followed as an 'observational' group and 22 members of this group were examined once at a median of 25 months for changes in weight and glucose concentration. After 12 months of intervention, members of both intervention groups reported increased levels of physical activity (median: Action 7.3 h month(-1), Pride 6.3 h month(-1), p < 0.001 for each), and Pride members reported decreased starch intake (28 g, p = 0.008). Body mass index, systolic and diastolic blood pressures, weight, 2-h glucose and 2-h insulin had all increased in Action members (p < 0.003 for each), and waist circumference had decreased in Pride members (p = 0.05). Action members gained more weight than Pride members (2.5 kg vs 0.8 kg, p = 0.06), and had a greater increase in 2-h glucose than Pride members (1.33 mM vs 0.03 mM, p = 0.007). Members of the observational group gained an average of 1.9 kg year(-1) in weight and had an increase of 0.36 mM year(-1) in 2-h glucose. Sustaining adherence in behavioural interventions over a long term was challenging. Pimas may find a less direct, less structured, and more participative intervention more acceptable than a direct and highly structured approach, (C) 1998 John Wiley & Sons, Ltd. C1 NIDDKD, Diabet & Arthrit Epidemiol Sect, Phoenix Epidemiol & Clin Res Branch, Phoenix, AZ USA. RP Narayan, KMV (reprint author), Ctr Dis Control & Prevent, DDT, NCCDPHP, 4770 Buford Highway NE,Mailstop K-10, Atlanta, GA 30341 USA. RI Narayan, K.M. Venkat /J-9819-2012; Hanson, Robert/O-3238-2015 OI Narayan, K.M. Venkat /0000-0001-8621-5405; Hanson, Robert/0000-0002-4252-7068 NR 27 TC 58 Z9 58 U1 2 U2 7 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 0742-3071 J9 DIABETIC MED JI Diabetic Med. PD JAN PY 1998 VL 15 IS 1 BP 66 EP 72 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YT689 UT WOS:000071632700010 PM 9472866 ER PT J AU Sherman, ME Schiffman, MH Strickler, H Hildesheim, A AF Sherman, ME Schiffman, MH Strickler, H Hildesheim, A TI Prospects for a prophylactic HPV vaccine: Rationale and future implications for cervical cancer screening SO DIAGNOSTIC CYTOPATHOLOGY LA English DT Article; Proceedings Paper CT IAP Symposium CY OCT, 1996 CL BUDAPEST, HUNGARY DE papillomavirus; vaccine; VLP; cervix; cytology ID VIRUS-LIKE PARTICLES; COTTONTAIL RABBIT PAPILLOMAVIRUS; THERAPEUTIC VACCINATION; MUCOSAL PAPILLOMAVIRUS; L1 PROTEIN; IMMUNIZATION; PROTECTION; INFECTION; RISK AB Cytologic screening in combination with ablative therapy has helped reduce cervical cancer mortality in the developed world. Despite the success of this approach, cervical cancer remains a major cause of death, especially among women with limited access to health care. Recognition that human papillomaviruses (HPVs) are the main etiologic agent in cervical cancer suggests that a prophylactic vaccine could reduce the incidence of HPV infection and, therefore, achieve cancer central with reduced reliance on costly screening programs. rn this review, the rationale for developing a prophylactic HPV vaccine and the potential impact that vaccination would have on cervical cancer screening are discussed. (C) 1998 Wiley-Liss, Inc. C1 George Washington Univ, Med Ctr, Dept Pathol, Washington, DC 20037 USA. RP Sherman, ME (reprint author), NCI, NIH, Environm Epidemiol Branch, Execut Plaza N443,6130 Execut Blvd, Rockville, MD 20852 USA. NR 25 TC 22 Z9 25 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 8755-1039 J9 DIAGN CYTOPATHOL JI Diagn. Cytopathol. PD JAN PY 1998 VL 18 IS 1 BP 5 EP 9 DI 10.1002/(SICI)1097-0339(199801)18:1<5::AID-DC2>3.0.CO;2-G PG 5 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA YP899 UT WOS:000071327200002 PM 9451552 ER PT J AU von Agoston, D Santha, E Shieh, G Lala, R Dobi, A AF von Agoston, D Santha, E Shieh, G Lala, R Dobi, A TI Isolation and structural and genetic analysis of the mouse enkephalin gene and its d(AC/TG)(n) repeats SO DNA SEQUENCE LA English DT Article DE gene; opioid; repetitive DNA; sequence ID PREPROENKEPHALIN MESSENGER-RNA; GALACTOSIDASE FUSION GENE; TRANSGENIC MICE; HUMAN PROENKEPHALIN; TRANSCRIPTION FACTORS; OPIOID-PEPTIDES; NERVOUS-SYSTEM; Z-DNA; EXPRESSION; BRAIN AB Enkephalins, the endogenous opioids, mediate a wide variety of intercellular communications through ontogeny and their involvement has been suggested in drug addiction and alcohol abuse as well as in various neuropsychiatric disorders. In order to generate a genetic model, we have isolated the mouse enkephalin (mENK) gene, analyzed its regulatory region and compared its structure to the well characterized rat ENK (rENK) gene. We analyzed 2600 bp and found 3 highly homologous regions: The highest level (98%) of positional and sequence homology between mice and rats was in the TATA/proximal regulatory region. This region contains all the inducible regulatory elements (enkCRE1, NF1, AP-2, NFkB, etc.) and also an octamer-like element at -543 bp. This high homology is interrupted in both mice and rats by the typically polymorphic d(AC/TG)(n) and d(TC/GA)(n) dinucleotide repeats positioned between nucleotides -670 and -950. The position and orientation of these repetitive elements differ substantially in the two species. Genomic PCR analysis of the d(AC/TG)(n) repeat in various mouse strains, including aberrant behavioral or neurological phenotypes, showed lack of polymorphism at this repeat. The positional and sequence homologies between the rat and the mouse ENK genes decrease in more upstream regions due to the presence of nonhomologues repetitive DNA sequences. C1 NICHD, LDN, NIH, Bethesda, MD 20892 USA. RP von Agoston, D (reprint author), Uniformed Serv Univ Hlth Sci, Dept Anat & Cell Biol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA. NR 46 TC 3 Z9 3 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-5179 J9 DNA SEQUENCE JI DNA Seq. PY 1998 VL 9 IS 4 BP 217 EP 226 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 194AF UT WOS:000080169400003 ER PT J AU Stratakis, CA Taymans, SE AF Stratakis, CA Taymans, SE TI Structure of the gene coding for calcineurin B (PPP3R1) and mapping to D2S358-D2S1778 (chromosomal region 2p15) SO DNA SEQUENCE LA English DT Article DE calcineurin B; PPP3R1 gene; chromosome 2p15; radiation hybrid mapping; intron-exon structure ID PROTEIN PHOSPHATASE; SEQUENCE AB Calcineurin is a protein phosphatase with an important role in signal transduction; its calcium-binding regulatory subunit, calcineurin B, is widely present in the brain and is coded by the PPP3R1 gene which was mapped recently to human chromosome 2. Calcineurin has long been considered a candidate for psychiatric and/or monogenic brain disorders. The present study reports the intron-exon structure of the PPP3R1 gene with the proximal intronic sequences, its genetic mapping to D25358-D251778 on chromosome 2p15, and its exclusion in a genetic disorder mapped proximal to this locus. C1 NICHD, UGEN, SPE, DEB,NIH, Bethesda, MD 20892 USA. RP Stratakis, CA (reprint author), NICHD, UGEN, SPE, DEB,NIH, Bldg 10,Room 10 N 262,10 Ctr Dr MSC 1862, Bethesda, MD 20892 USA. NR 14 TC 3 Z9 3 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-5179 J9 DNA SEQUENCE JI DNA Seq. PY 1998 VL 9 IS 4 BP 227 EP 230 DI 10.3109/10425179809105209 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 194AF UT WOS:000080169400004 PM 10520753 ER PT J AU Gorelick, DA Montoya, ID Johnson, EO AF Gorelick, DA Montoya, ID Johnson, EO TI Sociodemographic representation in published studies of cocaine abuse pharmacotherapy SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article; Proceedings Paper CT 147th Annual Meeting of the American-Psychiatric-Association CY MAY 21-26, 1994 CL PHILADELPHIA, PENNSYLVANIA SP Amer Psychiat Assoc, NIMH, Dept Vet Affairs, Cooperat Studies Program, Med Res Serv DE cocaine; pharmacotherapy; sociodemographic ID NATIONAL-COMORBIDITY-SURVEY; UNITED-STATES; PREVALENCE AB This study evaluated: (1) the reporting of sociodemographic characteristics of research subjects in published outpatient studies of cocaine abuse pharmacotherapy; (2) the association of study characteristics with such reporting and with the distribution of characteristics; and (3) the comparison of sociodemographic characteristics in the research subjects with those of a community-based sample of cocaine abusers who had sought treatment. Medline search identified 68 articles on cocaine abuse outpatient pharmacotherapy published from 1983 to 1993 in an English language, peer-reviewed journal. Sociodemographic characteristics of research subjects (n = 1802) were compared with those of respondents (weighted n = 135) to the National Comorbidity Survey (1990-1992), who reported at least one cocaine-related problem and had sought substance abuse treatment. Only three (4.4%) articles reported all six of the following sociodemographic characteristics of their subjects: 82.4%, reported mean age; 58.8%, race/ethnicity; 85.3%, sex; 22.1%, employment status; 13.2%, educational status; and 5.9%, socioeconomic status/income. Compared to survey respondents, research subjects were significantly more likely to be African-American and live in the Northeast region of the US and marginally more likely to be male and currently unemployed. These findings indicate that many published articles do not follow currently recommended guidelines for describing sociodemographic characteristics of research subjects and that, aside from race/ethnicity and geographic location, research subjects are fairly comparable in basic sociodemographic characteristics to the larger population of treatment-seeking individuals with cocaine-related problems. (C) 1998 Elsevier Science Ireland Ltd. C1 NIDA, Div Intramural Res, NIH, Baltimore, MD 21224 USA. RP Gorelick, DA (reprint author), NIDA, Div Intramural Res, NIH, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 11 TC 10 Z9 10 U1 1 U2 1 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 JAN 1 PY 1998 VL 49 IS 2 BP 89 EP 93 DI 10.1016/S0376-8716(97)00143-9 PG 5 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA ZC149 UT WOS:000072544800002 PM 9543645 ER PT J AU Stadtman, ER Berlett, BS AF Stadtman, ER Berlett, BS TI Reactive oxygen-mediated protein oxidation in aging and disease SO DRUG METABOLISM REVIEWS LA English DT Review ID METAL-CATALYZED OXIDATION; MIXED-FUNCTION OXIDATION; COLI GLUTAMINE-SYNTHETASE; COVALENT MODIFICATION; CARBONYL CONTENT; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; MULTICATALYTIC PROTEASE; SUPEROXIDE-DISMUTASE; PLASMA-PROTEINS; FREE-RADICALS C1 NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Stadtman, ER (reprint author), NHLBI, Biochem Lab, NIH, Bldg 3,Room 222, Bethesda, MD 20892 USA. NR 87 TC 352 Z9 363 U1 7 U2 27 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1998 VL 30 IS 2 BP 225 EP 243 DI 10.3109/03602539808996310 PG 19 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA ZN147 UT WOS:000073614600002 PM 9606602 ER PT J AU Hrycyna, CA Gottesman, MM AF Hrycyna, CA Gottesman, MM TI Multidrug ABC transporters from bacteria to man: an emerging hypothesis for the universality of molecular mechanism and function SO DRUG RESISTANCE UPDATES LA English DT Review ID PEROXISOMAL MEMBRANE-PROTEIN; RESISTANCE P-GLYCOPROTEIN; DROSOPHILA-MELANOGASTER; CYSTIC-FIBROSIS; GENE ABCR; SEQUENCE; HOMOLOG; ENCODES; CLONING; YEAST C1 NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. RP Gottesman, MM (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37,Room IA-09,37 Convent Dv,MSC 4255, Bethesda, MD 20892 USA. NR 32 TC 18 Z9 18 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 1368-7646 J9 DRUG RESIST UPDATE JI Drug Resist. Update PY 1998 VL 1 IS 2 BP 81 EP 83 DI 10.1016/S1368-7646(98)80019-8 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 127PP UT WOS:000076360000001 PM 16904390 ER PT J AU Barry, CE Slayden, RA Mludli, K AF Barry, CE Slayden, RA Mludli, K TI Mechanisms of isoniazid resistance in Mycobacterium tuberculosis SO DRUG RESISTANCE UPDATES LA English DT Review ID CATALASE-PEROXIDASE GENE; MOLECULAR MECHANISMS; OXIDATIVE-STRESS; DRUG-RESISTANCE; KATG MUTATIONS; INHA; AHPC; STRAINS; TARGET; SENSITIVITY AB Isoniazid (INH) is a widely used front-line antituberculous agent with bacteriocidal activity at concentrations as low as 150 nM against Mycobacterium tuberculosis. INH is a prodrug and requires activation by an endogenous mycobacterial enzyme, the catalase-peroxidase KatG, before exerting toxic effects on cellular targets. Resistance to INH develops primarily through failure to activate the prodrug due to point mutations in the katG gene. In addition to mutations in katG, mutations in several other loci, such as the alkylhydroperoxidase AhpC and the enoylreductase InhA, may contribute to INH resistance. Although these markers can be used to accurately predict clinical INH resistance in a large number of cases, the molecular mechanisms involved remain largely speculative and incomplete. C1 NIAID, TB Res Unit, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. RP Barry, CE (reprint author), NIAID, TB Res Unit, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. RI Barry, III, Clifton/H-3839-2012; Slayden, Richard/O-8626-2016 OI Slayden, Richard/0000-0001-6857-7277 FU Intramural NIH HHS [Z01 AI000783-11] NR 49 TC 19 Z9 19 U1 4 U2 9 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 1368-7646 J9 DRUG RESIST UPDATE JI Drug Resist. Update PY 1998 VL 1 IS 2 BP 128 EP 134 DI 10.1016/S1368-7646(98)80028-9 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 127PP UT WOS:000076360000010 PM 16904399 ER PT J AU Sandor, V Fojo, T Bates, SE AF Sandor, V Fojo, T Bates, SE TI Future perspectives for the development of P-glycoprotein modulators SO DRUG RESISTANCE UPDATES LA English DT Review ID MULTIDRUG-RESISTANCE GENE; HUMAN-LUNG-CANCER; POTENT CYCLOPROPYLDIBENZOSUBERANE MODULATOR; ACUTE LYMPHOBLASTIC-LEUKEMIA; REDUCED DRUG ACCUMULATION; FLOW CYTOMETRIC ANALYSIS; ADVANCED BREAST-CANCER; CARCINOMA CELL-LINES; PHASE-I; IMMUNOHISTOCHEMICAL DETECTION AB Resistance to chemotherapeutic agents constitutes one of the major obstacles to the successful treatment of cancer. While several mechanisms underlying drug resistance have been elucidated, the most widely studied mechanism involves the efflux of antineoplastic drugs from cancer cells by P-glycoprotein, the 170 kD glycoprotein product of the MDR-I gene. The observation that several compounds are able to inhibit P-glycoprotein in vitro created optimism that the problem of multidrug resistance in cancer could be quickly resolved by moving these compounds into the clinic. However, despite a large number of clinical trials with several different putative Pgp modulators, the value of Pgp modulation in clinical oncologic practice remains unresolved. While these initial trials have not answered the question of whether Pgp is an important mechanism of resistance in human cancers, or whether modulation of Pgp is likely to positively impact on the treatment of cancer, they have provided insights regarding the problems inherent in conducting trials of this nature. These clinical insights, along with knowledge gained from continued basic research on drug resistance mediated by Pgp and related transporters, will form a strong foundation for future research into the role of Pgp and Pgp modulation in the treatment of cancer. The ubiquitous nature of transporters and the high prevalence of transporter substrates among antineoplastic drugs, compel the development of modulators that can be used to prevent or reverse drug resistance. C1 NCI, Med Branch, NIH, Bethesda, MD 20892 USA. RP Bates, SE (reprint author), NCI, Med Branch, NIH, Bldg 10,Room 12N226, Bethesda, MD 20892 USA. EM sebates@helix.nih.gov NR 131 TC 52 Z9 53 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 1368-7646 J9 DRUG RESIST UPDATE JI Drug Resist. Update PY 1998 VL 1 IS 3 BP 190 EP 200 DI 10.1016/S1368-7646(98)80039-3 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 127PQ UT WOS:000076360100007 PM 17092805 ER PT J AU Chase, TN AF Chase, TN TI The significance of continuous dopaminergic stimulation in the treatment of Parkinson's disease SO DRUGS LA English DT Article; Proceedings Paper CT XIIth International Symposium on Parkinsons Disease CY MAR 23-26, 1997 CL LONDON, ENGLAND ID CENTRAL PATHOPHYSIOLOGICAL MECHANISMS; MOTOR RESPONSE ALTERATIONS; NMDA RECEPTOR BLOCKADE; OXIDATIVE STRESS; LEVODOPA THERAPY; FLUCTUATIONS; AGONISTS; DYSKINESIAS; MONKEYS; NEURONS AB Levodopa continues to be the most effective agent for the symptomatic treatment of Parkinson's disease. No other drug marches its ability to suppress par kinsonian symptoms, especially in patients with advanced disease. But over time, initial benefits begin to wane, not so much because of a decline in efficacy against core symptoms, but rather because of a rise in adverse effects. Most common are the motor response complications that appear within a few years of treatment initiation and ultimately affect most parkinsonian patients. These progressively disabling complications include response fluctuations and abnormal involuntary movements. Current evidence indicates that 'wearing-off' fluctuations, typically the first motor complication to become clinically evident, initially reflect the loss of buffering normally provided by striatal dopaminergic terminals. Thus, with increasing degeneration of the nigrostriatal system, swings in plasma levodopa concentrations associated with standard dosage regimens produce nonphysiological fluctuations in intrasynaptic dopamine. As a result of long term discontinuous stimulation, secondary changes occur at sires downstream from the dopamine system and now appear to underlie the progressive worsening of 'wearing-off' phenomena as well as the eventual appearance of other response complications. Chronic intermittent stimulation of normally tonically active dopaminergic receptors activates specific signalling cascades in striatal dopaminoceptive medium spiny neurons, and this evidently results in long term potentiation of the synaptic efficacy of glutamate receptors of the N-methyl-D-aspartate (NMDA) subtype on these GABAergic efferents. As a consequence of their increasing sensitivity to excitation by cortical glutamatergic projections, it would, however, appear that medium spiny neuron function changes to favour the appearance of response fluctuations of the 'on-off' type and peak dose dyskinesias. The inability of standard levodopa treatment to restore striatal dopaminergic function in a more physiological manner clearly contributes to the appearance of motor complications. Continuous dopaminergic replacement not only reverses these complications in parkinsonian patients but also prevents their development in animal models of Parkinson's disease. Thus, pharmaceutical approaches that provide relatively continuous dopamine receptor stimulation might confer both prophylactic and palliative benefit to parkinsonian patients. Several such strategies are currently under development, and include various methods to prolong the duration of action of levodopa as well as the use of transdermally administered or very long acting dopamine agonists. C1 NINDS, Expt Therapeut Branch, NIH, Bethesda, MD 20892 USA. RP Chase, TN (reprint author), NINDS, Expt Therapeut Branch, NIH, Bldg 10,Room 5C103,10 Ctr Dr,MSC 1406, Bethesda, MD 20892 USA. NR 46 TC 121 Z9 125 U1 0 U2 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 0012-6667 J9 DRUGS JI Drugs PY 1998 VL 55 SU 1 BP 1 EP 9 DI 10.2165/00003495-199855001-00001 PG 9 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA YW308 UT WOS:000071920900002 PM 9483164 ER PT J AU La Paro, KM Sexton, D Snyder, P AF La Paro, KM Sexton, D Snyder, P TI Program quality characteristics in segregated and inclusive early childhood settings SO EARLY CHILDHOOD RESEARCH QUARTERLY LA English DT Article ID DEVELOPMENTALLY APPROPRIATE PRACTICES; TEACHERS BELIEFS; YOUNG-CHILDREN; CARE; DISABILITIES; EDUCATION AB Program quality characteristics in 58 community-based early childhood settings which were currently serving at least one child with disabilities were examined. Observations of the environment and classrooms practices were conducted in the classrooms and teachers completed questionnaires related to beliefs in and implementation of Developmentally Appropriate Practices (DAP). Results indicated that segregated and inclusive settings were generally similar across measures of program quality and levels of quality were moderately good in both types of settings. Teacher demographic variables were not related to the selected program quality indicators. The similarity in selected quality characteristics may reflect ongoing convergence in practice and quality in early childhood and early childhood special education settings. C1 Univ Virginia, Charlottesville, VA 22903 USA. Univ Alabama, Birmingham, AL USA. Louisiana State Univ, Med Ctr, Baton Rouge, LA 70803 USA. RP La Paro, KM (reprint author), NICHD, Study Early Child Care, POB 9051, Charlottesville, VA 22906 USA. NR 33 TC 19 Z9 19 U1 0 U2 2 PU ABLEX PUBL CORP PI STAMFORD PA 100 PROSPECT ST, PO BOX 811, STAMFORD, CT 06904-0811 USA SN 0885-2006 J9 EARLY CHILD RES Q JI Early Childhood Res. Q. PY 1998 VL 13 IS 1 BP 151 EP 167 DI 10.1016/S0885-2006(99)80030-1 PG 17 WC Education & Educational Research; Psychology, Developmental SC Education & Educational Research; Psychology GA ZX530 UT WOS:000074526000009 ER PT B AU Leapman, RD AF Leapman, RD BE Benavides, HAC Yacaman, MJ TI Biological microanalysis and compositional mapping by electron energy-loss spectroscopy SO ELECTRON MICROSCOPY 1998, VOL 1: GENERAL INTEREST AND INSTRUMENTATION LA English DT Proceedings Paper CT 14th International Congress on Electron Microscopy CY AUG 31-SEP 04, 1998 CL CANCUN, MEXICO SP Mexican Soc Microscopy, Consejo Nacl Ciencia & Tecnol, Inst Nacl Invest Nucl, Univ Autonoma Estado Mexico, Univ Veracruzana, Ctr Invest & Estudios Avanzados, Univ Nacl Autonoma Mexico, Ctr Invest Mat Avanzados, Inst Politecn Nacl, Univ Autonoma Nuevo Leon C1 NIH, Biomed Engn & Instrumentat Program, DIRS, Bethesda, MD 20892 USA. RP Leapman, RD (reprint author), NIH, Biomed Engn & Instrumentat Program, DIRS, Bldg 10, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND BN 0-7503-0564-9 PY 1998 BP 317 EP 318 PG 2 WC Materials Science, Multidisciplinary; Microscopy SC Materials Science; Microscopy GA BL87G UT WOS:000077017600147 ER PT B AU Leapman, RD Jarnik, M Steven, AC AF Leapman, RD Jarnik, M Steven, AC BE Benavides, HAC Yacaman, MJ TI Mapping sulfur-rich proteins in cornifying epithelia by energy-filtering and EELS SO ELECTRON MICROSCOPY 1998, VOL 1: GENERAL INTEREST AND INSTRUMENTATION LA English DT Proceedings Paper CT 14th International Congress on Electron Microscopy CY AUG 31-SEP 04, 1998 CL CANCUN, MEXICO SP Mexican Soc Microscopy, Consejo Nacl Ciencia & Tecnol, Inst Nacl Invest Nucl, Univ Autonoma Estado Mexico, Univ Veracruzana, Ctr Invest & Estudios Avanzados, Univ Nacl Autonoma Mexico, Ctr Invest Mat Avanzados, Inst Politecn Nacl, Univ Autonoma Nuevo Leon C1 NIH, Biomed Engn & Instrumentat Program, DIRS, Bethesda, MD 20892 USA. RP Leapman, RD (reprint author), NIH, Biomed Engn & Instrumentat Program, DIRS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND BN 0-7503-0564-9 PY 1998 BP 689 EP 690 PG 2 WC Materials Science, Multidisciplinary; Microscopy SC Materials Science; Microscopy GA BL87G UT WOS:000077017600322 ER PT B AU Steven, AC Conway, JF Cheng, N Zlotnick, A Stahl, SJ Wingfield, PT AF Steven, AC Conway, JF Cheng, N Zlotnick, A Stahl, SJ Wingfield, PT BE Benavides, HAC Yacaman, MJ TI Mapping protein folds in "single particle" density maps from cryo-electron microscopy at 8 - 10 angstrom resolution. SO ELECTRON MICROSCOPY 1998, VOL 1: GENERAL INTEREST AND INSTRUMENTATION LA English DT Proceedings Paper CT 14th International Congress on Electron Microscopy CY AUG 31-SEP 04, 1998 CL CANCUN, MEXICO SP Mexican Soc Microscopy, Consejo Nacl Ciencia & Tecnol, Inst Nacl Invest Nucl, Univ Autonoma Estado Mexico, Univ Veracruzana, Ctr Invest & Estudios Avanzados, Univ Nacl Autonoma Mexico, Ctr Invest Mat Avanzados, Inst Politecn Nacl, Univ Autonoma Nuevo Leon C1 NIAMS, NIH, Bethesda, MD 20892 USA. RP Steven, AC (reprint author), NIAMS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND BN 0-7503-0564-9 PY 1998 BP 727 EP 728 PG 2 WC Materials Science, Multidisciplinary; Microscopy SC Materials Science; Microscopy GA BL87G UT WOS:000077017600339 ER PT B AU Trus, BL Gibson, W Cheng, N Steven, AC AF Trus, BL Gibson, W Cheng, N Steven, AC BE Benavides, HAC Yacaman, MJ TI Cytomegalovirus capsid structure and tegument binding SO ELECTRON MICROSCOPY 1998, VOL 4: BIOLOGICAL SCIENCES LA English DT Proceedings Paper CT 14th International Congress on Electron Microscopy CY AUG 31-SEP 04, 1998 CL CANCUN, MEXICO SP Mexican Soc Microscopy, Consejo Nacl Ciencia & Tecnol, Inst Nacl Invest Nucl, Univ Autonoma Estado Mexico, Univ Veracruzana, Ctr Invest & Estudios Avanzados, Univ Nacl Autonoma Mexico, Ctr Invest Mat Avanzados, Inst Politecn Nacl, Univ Autonoma Nuevo Leon C1 NIAMS, Struct Biol Lab, NIH, Bethesda, MD 20892 USA. RP Trus, BL (reprint author), NIAMS, Struct Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND BN 0-7503-0567-3 PY 1998 BP 295 EP 296 PG 2 WC Biology; Microscopy SC Life Sciences & Biomedicine - Other Topics; Microscopy GA BL87K UT WOS:000077020500144 ER PT B AU Lins, U Farina, M Kurc, M Kachar, B AF Lins, U Farina, M Kurc, M Kachar, B BE Benavides, HAC Yacaman, MJ TI Freeze-etching of otoliths and extracellular matrix of the vestibular sensory epithelium of frog and guinea pig. SO ELECTRON MICROSCOPY 1998, VOL 4: BIOLOGICAL SCIENCES LA English DT Proceedings Paper CT 14th International Congress on Electron Microscopy CY AUG 31-SEP 04, 1998 CL CANCUN, MEXICO SP Mexican Soc Microscopy, Consejo Nacl Ciencia & Tecnol, Inst Nacl Invest Nucl, Univ Autonoma Estado Mexico, Univ Veracruzana, Ctr Invest & Estudios Avanzados, Univ Nacl Autonoma Mexico, Ctr Invest Mat Avanzados, Inst Politecn Nacl, Univ Autonoma Nuevo Leon C1 NIDOCD, NIH, Bethesda, MD 20892 USA. RP Kachar, B (reprint author), NIDOCD, NIH, Bethesda, MD 20892 USA. RI Lins, Ulysses/N-7282-2015 OI Lins, Ulysses/0000-0002-1786-1144 NR 0 TC 0 Z9 0 U1 0 U2 1 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND BN 0-7503-0567-3 PY 1998 BP 307 EP 308 PG 2 WC Biology; Microscopy SC Life Sciences & Biomedicine - Other Topics; Microscopy GA BL87K UT WOS:000077020500150 ER PT J AU Lurie, IS Hays, PA Casale, JF Moore, JM Castell, DM Chan, KC Issaq, HJ AF Lurie, IS Hays, PA Casale, JF Moore, JM Castell, DM Chan, KC Issaq, HJ TI Capillary electrophoresis analysis of isomeric truxillines and other high molecular weight impurities in illicit cocaine SO ELECTROPHORESIS LA English DT Article DE capillary electrophoresis; truxillines; cocaine; cyclodextrins ID SEPARATION AB The analysis of by-products and impurities in illicit cocaine, including the isomeric truxillines, is important for derivation of both strategic and tactical intelligence. In the present study, various capillary electrophoresis techniques were investigated for this purpose. The use of the anionic beta-cyclodextrin sulfobutyl ether IV as a run buffer additive at pH 8.6 gave a good separation of the truxillines and similar high molecular weight impurities in less than eight minutes. These impurities were first isolated from the bulk cocaine matrix using liquid-liquid extraction and size-exclusion high performance liquid chromatography. There was a red shift in the UV spectra obtained for the truxillines using photodiode array (PDA) UV detection during CE analysis. This anomalous behavior is attributed to photo-degradation of the truxillines during the PDA-UV irradiation process. Laser-induced fluorescence detection using a UV krypton/fluoride laser provided greater selectivity and sensitivity versus UV detection for certain uncharacterized high molecular weight impurities. C1 US Drug Enforcement Adm, Special Testing & Res Lab, Mclean, VA 22102 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Frederick, MD USA. RP Lurie, IS (reprint author), US Drug Enforcement Adm, Special Testing & Res Lab, 7704 Old Springhouse Rd, Mclean, VA 22102 USA. OI Lurie, Ira/0000-0003-3844-5120 NR 9 TC 15 Z9 15 U1 0 U2 1 PU WILEY-V C H VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD JAN PY 1998 VL 19 IS 1 BP 51 EP 56 DI 10.1002/elps.1150190110 PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA YZ041 UT WOS:000072214200009 PM 9511862 ER PT J AU McSweegan, E AF McSweegan, E TI Infectious diseases and mental illness: Is there a link? SO EMERGING INFECTIOUS DISEASES LA English DT Letter ID LYME C1 NIAID, Bethesda, MD 20892 USA. RP McSweegan, E (reprint author), NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 8 TC 5 Z9 5 U1 2 U2 2 PU CENTER DISEASE CONTROL PI ATLANTA PA ATLANTA, GA 30333 USA SN 1080-6040 J9 EMERG INFECT DIS JI Emerg. Infect. Dis PD JAN-MAR PY 1998 VL 4 IS 1 BP 123 EP 124 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YX165 UT WOS:000072012900018 PM 9452407 ER PT J AU Ascoli, GA Pergami, P Luu, KX Alkon, DL Bramanti, E Bertucci, C Di Bari, L Salvadori, P AF Ascoli, GA Pergami, P Luu, KX Alkon, DL Bramanti, E Bertucci, C Di Bari, L Salvadori, P TI Use of CD and FT-IR to determine the secondary structure of purified proteins in the low-microgram range SO ENANTIOMER LA English DT Article DE circular dichroism; Fourier transform infrared spectroscopy; protein conformation; cp20; calexcitin; prion ID CIRCULAR-DICHROISM; PRION PROTEIN; CALEXCITIN; CALCIUM AB The spectroscopic characterization of protein secondary structure is often partially unreliable when samples are not extremely pure and abundant. This problem may be overcome by the combination of circular dichroism (CD) and Fourier transform infrared spectroscopy (FT-IR). We used these methods to characterize the secondary structure of two proteins of neurobiological interest, calexcitin (CE) and the cellular isoform of prion protein (PrPC). Both proteins were purified with multiple chromatographic steps and were obtained in buffer with high purity (> 95%) and in low amount (similar to 2 mu g). The samples were analyzed by circular dichroism (down to 184 or 182 nm), recovered, and deposited on films for infrared analysis. The spectral deconvolution from the two methods yielded secondary structures in good agreement with each other as well as with theoretical predictions based on amino acid sequence. The conformation of CE was found to be dependent on its concentration and on calcium binding. The secondary structure of cellular native PrP varied dramatically with the detergent used. In conclusion, the combination of CD and FT-IR analysis is suitable for the characterization of the conformational changes induced by ligand binding and/or by different solvent conditions when the protein of interest is only scarcely available. The methods used here provide valuable insights into the putative correlation between protein structure and activity. C1 Univ Pisa, Dipartimento Chim & Chim Ind, CNR, Ctr Studio Macromol Stereordinate Otticamente Att, I-56126 Pisa, Italy. George Mason Univ, Krasnow Inst Adv Study, Fairfax, VA 22030 USA. Univ Pavia, Neurol Inst C Mondino, I-27100 Pavia, Italy. NINDS, Lab Adapt Syst, NIH, Bethesda, MD 20892 USA. Univ Pisa, Ist Chim Analit Strumentale, CNR, Dipartimento Chim & Chim Ind, Pisa, Italy. RP Salvadori, P (reprint author), Univ Pisa, Dipartimento Chim & Chim Ind, CNR, Ctr Studio Macromol Stereordinate Otticamente Att, Via Risorgimento 35, I-56126 Pisa, Italy. RI Di Bari, Lorenzo/H-4804-2015; Bramanti, Emilia/E-1114-2011 OI Di Bari, Lorenzo/0000-0003-2347-2150; Bramanti, Emilia/0000-0001-8478-7370 NR 16 TC 3 Z9 3 U1 0 U2 4 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD, PO BOX 90, READING RG1 8JL, BERKS, ENGLAND SN 1024-2430 J9 ENANTIOMER JI Enantiomer PY 1998 VL 3 IS 4-5 BP 371 EP 381 PG 11 WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA 148BG UT WOS:000077531900011 PM 9861703 ER PT J AU Balla, T Varnai, P Tian, Y Smith, RD AF Balla, T Varnai, P Tian, Y Smith, RD TI Signaling events activated by angiotensin II receptors: What goes before and after the calcium signals SO ENDOCRINE RESEARCH LA English DT Article; Proceedings Paper CT 8th Conference on the Adrenal Cortex CY JUN 13-16, 1998 CL ORFORD, CANADA SP Univ Laval, Univ Montreal, McGill Univ, Univ Sherbrooke, Univ Toronto, Univ Sherbrooke, Ctr Res, Univ Montreal, Ctr Res, Univ Laval, Ctr Res, Duglas Hosp Res Ctr, Med Res Council Canada, Merck Frosst, Bayer, BiochemPharma ID PLECKSTRIN HOMOLOGY DOMAIN; ADRENAL GLOMERULOSA CELLS; KINASE; PROTEIN; STIMULATION AB Angiotensin II (Ang II) receptors of the AT(1) subtype are coupled to heterotrimeric G nucleotide-binding proteins, G(q/11), to activate phospholipase C-P isoforms with production of inositol 1,4,5-trisphosphate (InsP(3)) and diacylglycerol. The resultant release of intracellular Ca2+ and increased Ca2+ influx are major determinants of several acute cellular responses initiated by Ang II, including secretion of aldosterone from the adrenal cortex and smooth muscle contraction. However, cellular events related to more prolonged effects of Ang II, such as hypertrophic and hyperplastic responses, are triggered by intracellular signaling cascades that are less dependent on Ca2+ signals. The Ang II-induced activation of Raf-1 kinase, p42 MAP-kinase and c-fos expression in response to Ang II in adrenal glomerulosa cells does not require Ca2+ influx. Moreover, the dose-response relationships for Raf-1 activation, MAP-kinase activation and mitogenesis show significantly higher sensitivity to Ang II than the InsP(3), Ca2+-release and aldosterone secretory responses. The sensitivities of both Raf-1 kinase and MAP-kinase stimulation by Ang II to the inhibitors of phosphoinositide kinases, wortmannin and LY 294002, suggest that inositol phospholipids may play a role in these activation events unrelated to their role in Ca2+ signaling. To investigate the changes of various inositides after stimulation at the single cell level, fluorescent probes were developed in which pleckstrin homology domains with distinct binding specificities to inositol phospholipids were fused to the green fluorescent protein and expressed in NIH 3T3 cells. The use of these probes revealed heterogeneity of the inositol lipid pools and their complex relationship to Ca2+ signals. The use of these tools will help to further clarify the complex role of these lipids in initiating Ca2+-dependent and -independent signaling responses. C1 NIH, Endocrinol & Reprod Res Branch, Bethesda, MD 20892 USA. RP Balla, T (reprint author), NIH, Endocrinol & Reprod Res Branch, Bldg 10, Bethesda, MD 20892 USA. OI Balla, Tamas/0000-0002-9077-3335 NR 11 TC 22 Z9 23 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 1998 VL 24 IS 3-4 BP 335 EP 344 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150ZW UT WOS:000077697300007 PM 9888505 ER PT J AU Kruse, M Bornstein, SR Uhlmann, K Paeth, G Scherbaum, WA AF Kruse, M Bornstein, SR Uhlmann, K Paeth, G Scherbaum, WA TI Leptin down-regulates the steroid producing system in the adrenal SO ENDOCRINE RESEARCH LA English DT Article; Proceedings Paper CT 8th Conference on the Adrenal Cortex CY JUN 13-16, 1998 CL ORFORD, CANADA SP Univ Laval, Univ Montreal, McGill Univ, Univ Sherbrooke, Univ Toronto, Univ Sherbrooke, Ctr Res, Univ Montreal, Ctr Res, Univ Laval, Ctr Res, Duglas Hosp Res Ctr, Med Res Council Canada, Merck Frosst, Bayer, BiochemPharma ID RAT AB OB protein leptin inhibits the secretion of cortisol in primary cultures of bovine adrenocortical cells and down-regulates 17 alpha-hydroxylase cytochrome P450 mRNA expression. To analyze if leptin regulates other major enzymes involved in adrenal steroidogenesis we tested its effect on mRNA expression for two further key enzymes, C21-hydroxylase (P450C21) and side-chain cleavage enzyme (P450SCC). Cultured bovine cortical cells were stimulated for 24 hours with 10 nM ACTH, with 10 nM ACTH plus 100 ng/ml leptin or left unstimulated as controls. Stimulation with ACTH led to a 1.75-fold increase of P450C21 mRNA and a 3.31-fold increase of P450SCC mRNA compared to unstimulated controls. Addition of leptin led to a reduction of ACTH-stimulated mRNA accumulation of 73% for P450C21 and of 45% for P450SCC. We therefore suggest that leptin reduces cortisol synthesis in the adrenal by down-regulating the steroid producing enzyme cascade in the cortical cell. C1 Univ Dusseldorf, Diabet Res Inst, Clin Dept, D-4000 Dusseldorf, Germany. NICHHD, Bethesda, MD 20892 USA. Univ Leipzig, Dept Internal Med 3, Leipzig, Germany. RP Kruse, M (reprint author), Univ Dusseldorf, Diabet Res Inst, Clin Dept, D-4000 Dusseldorf, Germany. NR 10 TC 51 Z9 53 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 1998 VL 24 IS 3-4 BP 587 EP 590 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150ZW UT WOS:000077697300044 PM 9888542 ER PT J AU Wolkersdorfer, GW Marx, C Lohmann, T Brauer, S Schroder, S Brown, J Mitsiades, N Chrousos, GP Bornstein, SR AF Wolkersdorfer, GW Marx, C Lohmann, T Brauer, S Schroder, S Brown, J Mitsiades, N Chrousos, GP Bornstein, SR TI The mercy of adrenocortical tumor cells on lymphocytes SO ENDOCRINE RESEARCH LA English DT Article; Proceedings Paper CT 8th Conference on the Adrenal Cortex CY JUN 13-16, 1998 CL ORFORD, CANADA SP Univ Laval, Univ Montreal, McGill Univ, Univ Sherbrooke, Univ Toronto, Univ Sherbrooke, Ctr Res, Univ Montreal, Ctr Res, Univ Laval, Ctr Res, Duglas Hosp Res Ctr, Med Res Council Canada, Merck Frosst, Bayer, BiochemPharma ID HUMAN ADRENAL-GLAND; FAS LIGAND; EXPRESSION AB Immunologic escape includes the loss of Fas-receptor and the gain of Fas-ligand expression. Normal adrenal glands express the Fas-receptor and MHC class II molecules in inner cortical zones. A distinctive feature of adrenocortical tumors is the loss of MHC class II expression. Here we demonstrate loss of Fas and gain of Fas-ligand expression in the adrenocortical carcinoma cell line NCI-H295 by immunohistochemistry and RT-PCR. In a co-culture system of tumor cells and HLA-matched leukocytes, CD 8-positive or CD 4-positive lymphocytes, we examined the immunologic escape and the ability to induce apoptosis in the immune cells. The direct co-culture with either leukocytes, CD 8-positive or CD 4-positive lymphocytes reduced spontaneous apoptosis in immune cells from 49.9% to 13.0%, 8.6% and 15.3%, respectively, as determined by FAGS analysis of Annexin V binding and LDH release in the medium. In co-culture, cortisol secretion increased up to 200%. Cellular communication does not induce apoptosis in immune cells, but promotes their survival. This may be due to partial HLA class I mismatches contributing to immunologic activity. The viability of the tumor cells was not affected, and these cells were stimulated to secrete cortisol. In summary, immune escape of adrenocortical carcinomas may occur because of altered Fas/Fas-L system expression and loss of MHC class H expression. C1 Univ Leipzig, Dept Internal Med, D-7010 Leipzig, Germany. Univ Leipzig, Inst Clin Immunol, D-7010 Leipzig, Germany. Univ Miami, Div Appl Marine Phys, Coral Gables, FL 33124 USA. NICHHD, Bethesda, MD 20892 USA. NCI, Bethesda, MD 20892 USA. RP Wolkersdorfer, GW (reprint author), Univ Leipzig, Dept Internal Med, D-7010 Leipzig, Germany. NR 12 TC 1 Z9 1 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 1998 VL 24 IS 3-4 BP 711 EP 716 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150ZW UT WOS:000077697300066 PM 9888563 ER PT J AU Uhlmann, K Bottner, A Haidan, A Kino, T Wiznerowicz, M Trzeciak, H Ehrhart-Bornstein, M Bornstein, SR AF Uhlmann, K Bottner, A Haidan, A Kino, T Wiznerowicz, M Trzeciak, H Ehrhart-Bornstein, M Bornstein, SR TI Basal catecholamine and cortisol secretion in primary chromaffin cell cultures before and after purification and retroviral transfection SO ENDOCRINE RESEARCH LA English DT Article; Proceedings Paper CT 8th Conference on the Adrenal Cortex CY JUN 13-16, 1998 CL ORFORD, CANADA SP Univ Laval, Univ Montreal, McGill Univ, Univ Sherbrooke, Univ Toronto, Univ Sherbrooke, Ctr Res, Univ Montreal, Ctr Res, Univ Laval, Ctr Res, Duglas Hosp Res Ctr, Med Res Council Canada, Merck Frosst, Bayer, BiochemPharma AB We have investigated the effects of supraphysiological concentrations of catecholamines on glucocorticoid secretion in vitro. These effects were analyzed in adrenocortical cells shown to be present in chromaffin cell cultures as well as in cortical cells cocultured with transfected chromaffin cells that overproduce catecholamines. Cortisol release from residual cortical cells in chromaffin cell cultures was found to be 2.5 times higher than from isolated adrenocortical cells. Removal of the adrenocortical cells from the chromaffin cells resulted in an almost complete cessation of cortisol secretion. Catecholamine overproduction was achieved by transfecting chromaffin cells with the blank retroviral vector pSAM-EN. Coculture of adrenocortical cells with these transfected chromaffin cells further enhanced the stimulating effect of chromaffin cells on cortisol 2.3-fold compared to normal cocultures. In conclusion, cortical cells in chromaffin cell cultures secrete significant amounts of cortisol, which should be considered when evaluating the endocrine function of these cell cultures and which can be abolished by purification. The hormonal activity of adrenocortical cells is highly increased in an environment of catecholamine overproduction, which is of both basic and clinical importance. C1 Univ Leipzig, Leipzig, Germany. Dept Physiol Chem, Poznan, Poland. NICHD, NIH, Bethesda, MD USA. RP Uhlmann, K (reprint author), Univ Leipzig, Leipzig, Germany. RI Korner, Antje/B-3988-2015 OI Korner, Antje/0000-0001-6001-0356 NR 10 TC 1 Z9 1 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 1998 VL 24 IS 3-4 BP 753 EP 757 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150ZW UT WOS:000077697300075 PM 9888572 ER PT J AU Glasow, A Haidan, A Gillespie, J Kelly, PA Chrousos, GP Bornstein, SR AF Glasow, A Haidan, A Gillespie, J Kelly, PA Chrousos, GP Bornstein, SR TI Differential expression of prolactin receptor (PRLR) in normal and tumorous adrenal tissues: Separation of cellular endocrine compartments by laser capture microdissection (LCM) SO ENDOCRINE RESEARCH LA English DT Article; Proceedings Paper CT 8th Conference on the Adrenal Cortex CY JUN 13-16, 1998 CL ORFORD, CANADA SP Univ Laval, Univ Montreal, McGill Univ, Univ Sherbrooke, Univ Toronto, Univ Sherbrooke, Ctr Res, Univ Montreal, Ctr Res, Univ Laval, Ctr Res, Duglas Hosp Res Ctr, Med Res Council Canada, Merck Frosst, Bayer, BiochemPharma AB PRL stimulates adrenal steroidogenesis. In this study, we compared the PRLR expression in normal and tumorous adrenal tissues and investigated a potential proliferative effect of PRL, in adrenal cells. mRNA expression of long and intermediate forms of PRLR was detected in both normal adrenal cortex as well as benign and malignant adrenal tumors and in the human adrenocortical carcinoma cell line NCI-H295. Molecular analysis of cells procured by LCM clearly demonstrated that PRLR mRNA is expressed in the adrenal cortex but not in the medulla. Immunostaining revealed PRLR protein in all three zones of the normal adrenal cortex. Furthermore, adrenal carcinomas and adenomas stained positive for the PRLR, while in phaeochromocytomas as in the normal adrenal medulla, no specific staining was observed. By WST-1 test, we could show that PRL (10(-7) M) decreased proliferation and viability of adrenal cells in primary cell culture suggesting that PRL is not a mitogenic factor of adrenocortical cells. C1 Univ Leipzig, Dept Internal Med 3, Leipzig, Germany. INSERM, Paris, France. NCI, Dept Pathol, NIH, Bethesda, MD 20892 USA. NICHD, Dev Endocrinol Branch, NIH, Bethesda, MD USA. RP Glasow, A (reprint author), Univ Leipzig, Dept Internal Med 3, Leipzig, Germany. RI Kelly, Paul/A-7951-2008 NR 11 TC 21 Z9 21 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 1998 VL 24 IS 3-4 BP 857 EP 862 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150ZW UT WOS:000077697300090 PM 9888587 ER PT J AU Kirschner, LS Taymans, SE Stratakis, CA AF Kirschner, LS Taymans, SE Stratakis, CA TI Characterization of the adrenal gland pathology of Carney complex, and molecular genetics of the disease. SO ENDOCRINE RESEARCH LA English DT Article; Proceedings Paper CT 8th Conference on the Adrenal Cortex CY JUN 13-16, 1998 CL ORFORD, CANADA SP Univ Laval, Univ Montreal, McGill Univ, Univ Sherbrooke, Univ Toronto, Univ Sherbrooke, Ctr Res, Univ Montreal, Ctr Res, Univ Laval, Ctr Res, Duglas Hosp Res Ctr, Med Res Council Canada, Merck Frosst, Bayer, BiochemPharma C1 NICHD, Unit Genet & Endocrinol, DEB, SPE,NIH, Bethesda, MD 20892 USA. RP Kirschner, LS (reprint author), NICHD, Unit Genet & Endocrinol, DEB, SPE,NIH, 10 Ctr Dr MSC 1862, Bethesda, MD 20892 USA. NR 0 TC 8 Z9 10 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 1998 VL 24 IS 3-4 BP 863 EP 864 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150ZW UT WOS:000077697300091 PM 9888588 ER PT J AU Willenberg, HS Bornstein, SR Dumser, T Ehrhart-Bornstein, M Barocka, A Chrousos, GP Scherbaum, WA AF Willenberg, HS Bornstein, SR Dumser, T Ehrhart-Bornstein, M Barocka, A Chrousos, GP Scherbaum, WA TI Morphological changes in adrenals from victims of suicide in relation to altered apoptosis SO ENDOCRINE RESEARCH LA English DT Article; Proceedings Paper CT 8th Conference on the Adrenal Cortex CY JUN 13-16, 1998 CL ORFORD, CANADA SP Univ Laval, Univ Montreal, McGill Univ, Univ Sherbrooke, Univ Toronto, Univ Sherbrooke, Ctr Res, Univ Montreal, Ctr Res, Univ Laval, Ctr Res, Duglas Hosp Res Ctr, Med Res Council Canada, Merck Frosst, Bayer, BiochemPharma ID MAJOR DEPRESSION; GLAND VOLUME; WEIGHT AB Endocrine dysfunction may cause psychiatric symptoms and, vice versa, psychiatric diseases may lead to endocrine alterations. The adrenal as the end organ of both the hypothalamic-pituitary-adrenocortical and sympatho-adrenal axes is subject to the functional changes of the stress system. Thus, increased adrenal gland weight was observed previously in victims of violent suicide. This study was designed to analyze the morphological and morphodynamic changes of adrenals from suicide victims. We investigated 30 adrenals obtained from 15 suicide victims using immunohistochemistry and a computerized video system. In addition, apoptosis and cell proliferation were analyzed. We found a significant enlargement of the adrenal cortex to 158.8 % (SD = 29.8 %, p < 0.01) that was restricted to the two inner zones only (zona reticularis, 161.6 +/- 35.3 %; zona fasciculata, 186.4 +/- 34.4 %). This increase in adrenocortical size correlated with a decrease in the number of apoptotic cells within the zona fasciculata. In conclusion, these results clearly demonstrate chronic structural adrenal changes in suicide victims. The adrenal gland mirrors the functional changes of the stress system which leaves an imprint on the morphology of the gland. C1 Univ Dusseldorf, Diabet Res Inst, D-4000 Dusseldorf, Germany. NICHHD, Bethesda, MD 20892 USA. Inst Aviat Med AF, Dept Forens Med, Fuerstenfeldbrueck, Germany. Univ Erlangen Nurnberg, Psychiat Clin, D-8520 Erlangen, Germany. NIMH, Bethesda, MD 20892 USA. RP Willenberg, HS (reprint author), Univ Dusseldorf, Diabet Res Inst, D-4000 Dusseldorf, Germany. NR 9 TC 14 Z9 14 U1 1 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 1998 VL 24 IS 3-4 BP 963 EP 967 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150ZW UT WOS:000077697300110 PM 9888607 ER PT J AU Korach, KS AF Korach, KS TI Another five years SO ENDOCRINOLOGY LA English DT Editorial Material C1 NIEHS, NIH, LRDT Receptor Bio Sect, Res Triangle Pk, NC 27709 USA. RP Korach, KS (reprint author), NIEHS, NIH, LRDT Receptor Bio Sect, POB 12233,111 Alexander Dr, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1998 VL 139 IS 1 BP 3 EP 4 DI 10.1210/en.139.1.3 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN232 UT WOS:000071146300002 PM 28200312 ER PT J AU Jacot, TA Clemmons, DR AF Jacot, TA Clemmons, DR TI Effect of glucose on insulin-like growth factor binding protein-4 proteolysis SO ENDOCRINOLOGY LA English DT Article ID SMOOTH-MUSCLE-CELLS; EXPERIMENTAL DIABETES-MELLITUS; FACTOR-I; HUMAN-FIBROBLASTS; MESANGIAL CELLS; RAT; GENE; EXPRESSION; IDENTIFICATION; TRANSCRIPTION AB The role of hyperglycemia in diabetic changes of the insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) has not been clearly established. We therefore determined whether glucose modulates IGFBP synthesis and stability in vitro. Porcine vascular smooth muscle cells (pSMC) cultured in low glucose (pSMC-L) had 2.1-fold more IGFBP-4 in the conditioned medium compared with pSMC cultured in high glucose (pSMC-H) (P < 0.01). In contrast, IGFBP-2 levels remained constant. Although pSMC-H and pSMC-L cultures expressed similar levels of IGFBP-4 messenger RNA, in vitro protease assays demonstrated an increase in IGFBP-4 proteolysis in pSMC-H conditioned medium compared with pSMC-L conditioned medium (P < 0.01). The protease had properties similar to a previously characterized IGFBP-4 protease. The addition of 20 mM mannitol to pSMC-L cultures did not decrease IGFBP-4 levels, suggesting that the difference in IGFBP-4 proteolysis was not osmotically induced. The change was not due to selection bias, because cultures that were initially isolated from aortic explants in high and low glucose still exhibited the glucose-dependent difference in IGFBP-4 proteolytic activity. The results suggest that high glucose acts on pSMC to induce a change in IGFBP-4 proteolytic activity, which results in increased IGF-I availability to its receptors thereby enhancing the SMC proliferative response. C1 Univ N Carolina, Sch Med, Dept Med, Div Endocrinol & Metab, Chapel Hill, NC 27599 USA. NIDDKD, Renal Cell Biol Sect, NIH, Bethesda, MD 20892 USA. RP Clemmons, DR (reprint author), Univ N Carolina, Sch Med, Dept Med, Div Endocrinol & Metab, Campus Box 7170,6111 Thurston Bowles Bldg, Chapel Hill, NC 27599 USA. FU NHLBI NIH HHS [HL-56580] NR 39 TC 9 Z9 9 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1998 VL 139 IS 1 BP 44 EP 50 DI 10.1210/en.139.1.44 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN232 UT WOS:000071146300008 PM 9421396 ER PT J AU Wijkander, J Landstrom, TR Manganiello, V Belfrage, P Degerman, E AF Wijkander, J Landstrom, TR Manganiello, V Belfrage, P Degerman, E TI Insulin-induced phosphorylation and activation of phosphodiesterase 3B in rat adipocytes: Possible role for protein kinase B but not mitogen-activated protein kinase or p70 S6 kinase SO ENDOCRINOLOGY LA English DT Article ID INHIBITED CAMP-PHOSPHODIESTERASE; GLYCOGEN-SYNTHASE KINASE-3; EPIDIDYMAL FAT-CELLS; PHOSPHATIDYLINOSITOL 3-KINASE; GLUCOSE-TRANSPORT; GLUCOSE-TRANSPORTER-4 TRANSLOCATION; SIGNAL-TRANSDUCTION; SKELETAL-MUSCLE; SER/THR KINASE; ADIPOSE-TISSUE AB Insulin stimulation of adipocytes results in serine phosphorylation/ activation of phosphodiesterase 3E (PDE 3B) and activation of a kinase that phosphorylates PDE 3B in vitro, key events in the anti lipolytic action of this hormone. We have investigated the role for p70 S6 kinase, mitogen-activated protein kinases (MAP kinases), and protein kinase B (PKB) in the insulin signaling pathway leading to phosphorylation/activation of PDE 3B in adipocytes. Insulin stimulation of adipocytes resulted in increased activity of p70 S6 kinase, which was completely blocked by pretreatment with rapamycin. However, rapamycin had no effect on the insulin-induced phosphorylation/ activation of PDE 3B or the activation of the kinase that phosphorylates PDE 3B. Stimulation of adipocytes with insulin or phorbol myristate acetate induced activation of MAP kinases. Pretreatment of adipocytes with the MAP kinase kinase inhibitor PD 98059 was without effect on the insulin-induced activation of PDE 3B. Furthermore, phorbol myristate acetate stimulation did not result in phosphorylation/activation of PDE, 3B or activation of the kinase that phosphorylates PDE 3B. Using Mono Q and Superdex chromatography, the kinase that phosphorylates PDE 3B was found to co-elute with PKB, but not with p70 S6 kinase or MAP kinases. Furthermore, both PKB and the kinase that phosphorylates PDE 3B were found to translocate to membranes in response to peroxovanadate stimulation of adipocytes in a wortmannin-sensitive way. Whereas these results suggest that p70 S6 kinase and MAP kinases are not involved in the insulin-induced phosphorylation/activation of PDE 3B in rat adipocytes, they are consistent with PKB being the kinase that phosphorylates PDE 3B. C1 Lund Univ, Dept Cell & Mol Biol, Sect Mol Signalling, S-22100 Lund, Sweden. NHLBI, NIH, Bethesda, MD 20892 USA. RP Lund Univ, Dept Cell & Mol Biol, Sect Mol Signalling, POB 94, S-22100 Lund, Sweden. EM Eva.Degerman@medkem.lu.se NR 47 TC 100 Z9 101 U1 0 U2 1 PU ENDOCRINE SOC PI WASHINGTON PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1998 VL 139 IS 1 BP 219 EP 227 DI 10.1210/en.139.1.219 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN232 UT WOS:000071146300032 PM 9421418 ER PT J AU Montani, V Taniguchi, S Shong, MH Suzuki, K Ohmori, M Giuliani, C Napolitano, G Saji, M Fiorentino, B Reimold, AM Ting, JPY Kohn, LD Singer, DS AF Montani, V Taniguchi, S Shong, MH Suzuki, K Ohmori, M Giuliani, C Napolitano, G Saji, M Fiorentino, B Reimold, AM Ting, JPY Kohn, LD Singer, DS TI Major histocompatibility class II HLA-DR alpha gene expression in thyrocytes: Counter regulation by the class II transactivator and the thyroid Y box protein SO ENDOCRINOLOGY LA English DT Article ID THYROTROPIN RECEPTOR GENE; TRANSCRIPTION FACTORS; RESPONSE ELEMENT; BINDING-PROTEIN; MAMMALIAN-CELLS; MHC; COMPLEX; INTERFERON; PROMOTER; CIITA AB Aberrant expression of major histocompatibility complex (MHC) class II proteins on thyrocytes; which is associated with autoimmune thyroid disease, is mimicked by gamma-interferon (gamma-IFN). To define elements and factors that regulate class II gene expression in thyrocytes and that might be involved in aberrant expression, we have studied gamma-IFN-induced HLA-DR alpha gene expression in rat FRTL-5 thyroid cells. The present report shows that class II expression in FRTL-5 thyrocytes is positively regulated by the class II transactivator (CIITA), and that CIITA mimics the action of gamma-IFN. Thus, as is the case for gamma-IFN, several distinct and highly conserved elements on the 5'-flanking region of the HLA-DR alpha gene, the S, X-1, X-2, and Y boxes between -137 to -65 bp, are required for class II gene expression induced by pCIITA transfection in FRTL-5 thyroid cells. CIITA and gamma-IFN do not cause additive increases in HLA-DR alpha gene expression in FRTL-5 cells, consistent with the possibility that CIITA is an intermediate factor in the gamma-IFN pathway to increased class II gene expression. Additionally, gamma-IFN treatment of FRTL-5 cells induces an endogenous CIITA transcript; pCIITA transfection mimics the ability of gamma-IFN treatment of FRTL-5 thyroid cells to increase the formation of a specific and novel protein/DNA complex containing CBP, a coactivator of CRE binding proteins important for cAMP-induced gene expression; and the action of both gamma-IFN and CIITA to increase class II gene expression and increase complex formation is reduced by cotransfection of a thyroid Y box protein, which suppresses MHC class I gene expression in FRTL-5 thyroid cells and is a homolog of human YB-1, which suppresses MHC class II expression in human glioma cells. We conclude that CIITA and TSH receptor suppressor element binding protein-1 are components of the gamma-IFN-regulated transduction system which, respectively, increase or decrease class II gene expression in thyrocytes and may, therefore, be involved in aberrant class II expression associated with autoimmune thyroid disease. C1 NIDDKD, Cell Regulat Sect, Metab Dis Branch, NCI,NIH, Bethesda, MD 20892 USA. NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Dept Surg, Baltimore, MD 21287 USA. Harvard Univ, Sch Publ Hlth, Dept Canc Biol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ N Carolina, Lineberger Comprehens Canc Res Ctr, Chapel Hill, NC 27599 USA. RP Kohn, LD (reprint author), NIDDKD, Cell Regulat Sect, Metab Dis Branch, NCI,NIH, Bldg 10,Room 9C101B, Bethesda, MD 20892 USA. EM lenk@bdg10.niddk.nih.gov RI Saji, Motoyasu/E-4007-2011 NR 56 TC 24 Z9 25 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1998 VL 139 IS 1 BP 280 EP 289 DI 10.1210/en.139.1.280 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN232 UT WOS:000071146300040 PM 9421426 ER PT J AU Montani, V Shong, MH Taniguchi, S Suzuki, K Giuliani, C Napolitano, G Saito, J Saji, M Fiorentino, B Reimold, AM Singer, DS Kohn, LD AF Montani, V Shong, MH Taniguchi, S Suzuki, K Giuliani, C Napolitano, G Saito, J Saji, M Fiorentino, B Reimold, AM Singer, DS Kohn, LD TI Regulation of major histocompatibility class II gene expression in FRTL-5 thyrocytes: Opposite effects of interferon and methimazole SO ENDOCRINOLOGY LA English DT Article ID COMPLEX CLASS-I; AUTOIMMUNE THYROID-DISEASE; HUMAN THYROTROPIN RECEPTOR; HLA-DR EXPRESSION; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RNA-POLYMERASE-II; Y-BOX PROTEIN; ANTITHYROID DRUGS; GRAVES-DISEASE; EXTRACELLULAR DOMAIN AB Aberrant expression of major histocompatibility complex (MHC) class II antigens is associated with autoimmune thyroid disease; aberrant expression duplicating the autoimmune state can be induced by interferon-gamma (IFN gamma). We have studied IFN gamma-induced human leukocyte antigen (HLA)-DR alpha gene expression in rat FRTL-5 thyroid cells to identify the elements and factors important for aberrant expression. Using an HLA-DR alpha 5'-flanking region construct from -176 to +45 bp coupled to the chloramphenicol acetyltransferase reporter gene, we show that there is no basal class II gene expression in FRTL-5 thyroid cells, that IFN gamma can induce expression, and, as is the case for antigen-presenting cells from the immune system, that IFN gamma-induced expression requires several highly conserved elements on the 5'-flanking region, which, from 5' to 3', are the S, X-1, X-2, and Y boxes. Methimazole (MMI), a drug used to treat patients with Graves' disease and experimental thyroiditis in rats or mice, can suppress the IFN gamma-induced increase in HLA-DR alpha gene expression as a function of time and concentration; MMI simultaneously decreases IFN gamma-induced endogenous antigen presentation by the cell. Using gel shift assays and the HLA-DR alpha 5'-flanking region from -176 or -137 to +45 bp as radiolabeled probes, we observed the formation of a major protein-DNA complex with extracts from FRTL-5 cells untreated with IFN gamma, termed the basal or constitutive complex, and formation of an additional complex with a slightly faster mobility in extracts from cells treated with IFN gamma. MMI treatment of cells prevents IFN gamma from increasing the formation of this faster migrating complex. Formation of both complexes is specific, as evidenced in competition studies with unlabeled fragments between -137 and -38 bp from the start of transcription; nevertheless, they can be distinguished in such studies. Thus, high concentrations of double stranded oligonucleotides containing the sequence of the Y box, but not S, X-1, or X-2 box sequences, can prevent formation of the IFN gamma-increased faster migrating complex, but not the basal complex. Both complexes involve multiple proteins and can be distinguished by differences in their protein composition. Thus, using specific antisera, we show that two cAMP response element-binding proteins, activating transcription factor-1 and/or -2, are dominant proteins in the upper or basal complex. The upper or basal complex also includes c-Fos, Fra-2, Ets-2, and Oct-1. A dominant protein that distinguishes the IFN gamma-increased lower complex is CREB-binding protein (CBP), a coactivator of cAMP response element-binding proteins. We, therefore, show that aberrant expression of MHC class II in thyrocytes, induced by IFN gamma, is associated with the induction or increased formation of a novel protein-DNA complex and that its formation as well as aberrant class II expression are suppressed by MMI, a drug used to treat human and experimental autoimmune thyroid disease. Its component proteins differ from those in a major, basal, or constitutive protein-DNA complex formed with the class II 5'-flanking region in cells that are not treated with IFN gamma and that do not express the class II gene. C1 NIDDKD, Cell Regulat Sect, Metab Dis Branch, NCI,NIH, Bethesda, MD 20892 USA. NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Dept Surg, Baltimore, MD 21287 USA. Harvard Univ, Sch Publ Hlth, Dept Canc Biol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. RP Kohn, LD (reprint author), NIDDKD, Cell Regulat Sect, Metab Dis Branch, NCI,NIH, Bldg 10,Room 9C101B, Bethesda, MD 20892 USA. EM lenk@bdg10.niddk.nih.gov RI Saji, Motoyasu/E-4007-2011 FU NIAMS NIH HHS [KO8-AR-01915] NR 75 TC 33 Z9 35 U1 0 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1998 VL 139 IS 1 BP 290 EP 302 DI 10.1210/en.139.1.290 PG 13 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN232 UT WOS:000071146300041 PM 9421427 ER PT J AU Zhu, LJ Krempels, K Bardin, CW O'Carroll, AM Mezey, E AF Zhu, LJ Krempels, K Bardin, CW O'Carroll, AM Mezey, E TI The localization of messenger ribonucleic acids for somatostatin receptors 1, 2, and 3 in rat testis SO ENDOCRINOLOGY LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; RELEASE-INHIBITING HORMONE; REPRODUCTIVE-SYSTEM; GROWTH-HORMONE; FUNCTIONAL-CHARACTERIZATION; MOLECULAR-CLONING; SERTOLI-CELLS; GASTRIC-ACID; EXPRESSION; SECRETION AB Somatostatin (SRIF) exerts multiple inhibitory actions throughout the body by binding to specific SRIF receptors (sst). In recent years, five subtypes of SRIF receptors (sst1-5) have been cloned. In this study, S-35-labeled complementary RNA probes were used for in situ hybridization to localize the sst1-5 messenger RNAs (mRNAs) in the rat testis and examine the changes in their distribution during the cycle of the seminiferous epithelium. We found that sst 1-3 mRNAs were visualized in rat testes and were mainly localized within the seminiferous tubules. The signal for sst3 mRNA was also found in interstitial cells. sst4 and 5 mRNAs were not detected in rat testes with the method used in this study. In Sertoli cells, the most intense labeling for sst1 and 3 mRNAs was in stages IV-VII of the cycle of the seminiferous epithelium, which coincided with the lowest labeling intensity for sst2. In germ cells, sst1-3 mRNAs showed similar patterns of distribution. In these cells, sst1-3 mRNA was not observed at the early steps of spermatogenesis. Positive signals for sst1-3 mRNAs were first apparent in the pachytene spermatocytes at stage VII and last until stage XII and in the diplotene spermatocyte at stage XIII. Positive signals for sst1-3 were also detected in round spermatids at stages I-VIII. Labeling of spermatids dramatically decreased at stage IX, when these cells began their elongating changes. The presence of three sst in testis suggests that SRIF may play an essential role in testicular function. C1 Populat Council, Ctr Biomed Res, New York, NY 10021 USA. NINDS, Basic Neurosci Program, Bethesda, MD 20892 USA. NIMH, Lab Cellular & Mol Regulat, NIH, Bethesda, MD 20892 USA. RP Zhu, LJ (reprint author), Populat Council, Ctr Biomed Res, 1230 York Ave, New York, NY 10021 USA. EM zhu@popcbr.roekefeller.edu FU NICHD NIH HHS [HD-13541] NR 36 TC 16 Z9 16 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1998 VL 139 IS 1 BP 350 EP 357 DI 10.1210/en.139.1.350 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN232 UT WOS:000071146300047 PM 9421433 ER PT J AU Theoharides, TC Singh, LK Boucher, W Pang, XZ Letourneau, R Webster, E Chrousos, G AF Theoharides, TC Singh, LK Boucher, W Pang, XZ Letourneau, R Webster, E Chrousos, G TI Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explanation for its proinflammatory effects SO ENDOCRINOLOGY LA English DT Article ID SYMPATHETIC-NERVOUS-SYSTEM; NITRIC-OXIDE; HISTAMINE-SECRETION; IN-VITRO; GRANULOCYTE INFILTRATION; DURA-MATER; RAT; INFLAMMATION; RECEPTOR; VIVO AB Mast cells are involved in atopic disorders, often exacerbated by stress, and are located perivascularly close to sympathetic and sensory nerve endings. Mast cells are activated by electrical nerve stimulation and millimolar concentrations of neuropeptides, such as substance P (SP). Moreover, acute psychological stress induces CRH-dependent mast cell degranulation. Intradermal administration of rat/human CRH (0.1-10 mu M) in the rat induced mast cell degranulation and increased capillary permeability in a dose-dependent fashion. The effect of CRH on Evans blue extravasation was stronger than equimolar concentrations of the mast cell secretagogue compound 48/80 or SP. The free acid analog of CRH, which does not interact with its receptors (CRHR), had no biological activity. Moreover, systemic administration of antalarmin, a nonpeptide CRHR1 antagonist, prevented vascular permeability only by CRH and not by compound 48/80 or SP. CRHR1 was also identified in cultured leukemic human mast cells using RT-PCR. The stimulatory effect of CRH, like that of compound 48/80 on skin vasodilation, could not be elicited in the mast cell deficient W/W-v mice but was present in their +/+ controls, as well as in C57BL/6J mice; histamine could still induce vasodilation in the W/W-v mice. Treatment of rats neonatally with capsaicin had no effect on either Evans blue extravasation or mast cell degranulation, indicating that the effect of exogenous CRH in the skin was not secondary to or dependent on the release of neuropeptides from sensory nerve endings. The effect of CRH on Evans blue extravasation and mast cell degranulation was inhibited by the mast cell stabilizer disodium cromoglycate (cromolyn), but not by the antisecretory molecule somatostatin. To investigate which vasodilatory molecules might be involved in the increase in vascular permeability, the CRH injection site was pretreated with the H-1-receptor antagonist diphenhydramine, which largely inhibited the CRH effect, suggesting that histamine was involved in the CRH-induced vasodilation. The possibility that nitric oxide might also be involved was tested using pretreatment with a nitric oxide synthase inhibitor that, however, increased the effect of CRH. These findings indicate that CRH activates skin mast cells at least via a CRHR1-dependent mechanism leading to vasodilation and increased vascular permeability. The present results have implications for the pathophysiology and possible therapy of skin disorders, such as atopic dermatitis, eczema, psoriasis, and urticaria, which are exacerbated or precipitated by stress. C1 Tufts Univ, Sch Med, Dept Pharmacol & Expt Therapeut, Boston, MA 02111 USA. NICHHD, Sect Pediat Endocrinol, NIH, Bethesda, MD 20892 USA. RP Theoharides, TC (reprint author), Tufts Univ, Sch Med, Dept Pharmacol & Expt Therapeut, 136 Harrison Ave, Boston, MA 02111 USA. EM ttheoharides@infonet.tufts.edu RI Theoharides, Theoharis/E-5596-2010 NR 55 TC 312 Z9 320 U1 0 U2 10 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1998 VL 139 IS 1 BP 403 EP 413 DI 10.1210/en.139.1.403 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN232 UT WOS:000071146300054 PM 9421440 ER PT J AU Mezey, E Hunyady, B Mitra, S Hayes, E Liu, QS Schaeffer, J Schonbrunn, A AF Mezey, E Hunyady, B Mitra, S Hayes, E Liu, QS Schaeffer, J Schonbrunn, A TI Cell specific expression of the SST2A and SST5 somatostatin receptors in the rat anterior pituitary SO ENDOCRINOLOGY LA English DT Article ID MOLECULAR-BIOLOGY; SUBTYPES; LOCALIZATION; PHARMACOLOGY; ADENOMAS; ANTIBODY; BRAIN AB Somatostatin (SRIF), originally described as a hypothalamic hormone that inhibits the release of growth hormone was subsequently shown to inhibit the secretion of multiple pituitary hormones. Five genes encoding six different SRIF receptors (sst1,2A,2B,3,4 and 5) have been cloned and mRNAs for all five are expressed in the anterior pituitary. We used double immunostaining to determine which cells in the anterior pituitary bear sst2A and sst5 receptors. Our results show that these two receptors are widely distributed in the pituitary gland and are both present in a large percentage of GH cells. In addition, sst5 occurs in a small population of corticotrophs and a large percentage of lactotrophs whereas sst2A is found in only a few lactotrophs but a large number of corticotrophs. The sst2A receptor is also expressed in about a third of the gonadotrophs and thyrotrophs. Interestingly, sst2A and sst5 receptors colocalize in a small percentage of cells, most likely somatotrophs demonstrating that the same cells can contain multiple sst receptor subtypes. These results indicate that sst subtype specific analogs are likely to be useful for the selective regulation of individual pituitary hormones. C1 NINDS, Basic Neurosci Program, NIH, Bethesda, MD 20892 USA. Med Univ Pecs, Dept Med 1, H-7643 Pecs, Hungary. NIMH, H-7643 Pecs, Hungary. Merck Pharmaceut, Rahway, NJ USA. Univ Texas, Sch Med, Dept Integrat Biol & Pharmacol, Houston, TX 77225 USA. RP Mezey, E (reprint author), NINDS, Basic Neurosci Program, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. NR 18 TC 58 Z9 58 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1998 VL 139 IS 1 BP 414 EP 419 DI 10.1210/en.139.1.414 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN232 UT WOS:000071146300055 PM 9421441 ER PT J AU Minton, AP AF Minton, AP TI Molecular crowding: Analysis of effects of high concentrations of inert cosolutes on biochemical equilibria and rates in terms of volume exclusion SO ENERGETICS OF BIOLOGICAL MACROMOLECULES, PT B SE METHODS IN ENZYMOLOGY LA English DT Review ID POLYMER-PROTEIN INTERACTIONS; EXCLUDED-VOLUME; MACROMOLECULAR STRUCTURE; THERMODYNAMIC ACTIVITY; HEMOGLOBIN-SOLUTIONS; CONSEQUENCES; NONIDEALITY; DEPENDENCE; NETWORKS; MODEL C1 NIDDK, Chem Phys Sect, Lab Biochem & Genet, Bethesda, MD 20892 USA. RP Minton, AP (reprint author), NIDDK, Chem Phys Sect, Lab Biochem & Genet, Bethesda, MD 20892 USA. NR 29 TC 212 Z9 215 U1 1 U2 29 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1998 VL 295 BP 127 EP 149 PG 23 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BL66E UT WOS:000076213700007 PM 9750217 ER PT J AU Ferguson, LR Turner, PM Hart, DW Tindall, KR AF Ferguson, LR Turner, PM Hart, DW Tindall, KR TI Amsacrine-induced mutations in AS52 cells SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE amsacrine; AS52 cells; mutation spectrum; topoisomerase II inhibition; recombination ID SISTER-CHROMATID EXCHANGE; CHINESE-HAMSTER CELLS; TOPOISOMERASE-II; MAMMALIAN-CELLS; LARGE DELETIONS; CHO CELLS; ILLEGITIMATE RECOMBINATION; DNA TOPOISOMERASES; CHROMOSOME-DAMAGE; TK-LOCUS AB Amsacrine is an acridine-derived inhibitor of topoisomerase II that intercalates into DNA. We performed a detailed molecular analysis of 6-thioguanine (6-TG)-resistant mutant colonies arising in AS52 cells Following Amsacrine treatment. AS52 cells carry a single copy of the bacterial gpt gene, functionally expressed using the SV40 early promoter and stably integrated into the Chinese hamster ovary genome. A l-hr treatment with 0.1 to 0.5 mu M Amsacrine was both cytotoxic and mutagenic, resulting in an average mutant frequency (MF) of 143 x 10(-6) at 0.5 mu M. Fifty independent 6-TG-resistant colonies were isolated for further study. These clones were initially characterised by PCR to estimate the relative proportion of putative point mutants and deletions or rearrangements; then a subset of mutants was further characterised by Southern blotting, Northern blotting, and DNA sequence analysis. Total deletion of the gpt gene sequences was found in 1 (2%) of the mutants, and 7 (14%) of the mutant clones had altered PCR patterns, suggesting complex deletions or, rearrange ments. The remaining 42 (84%) mutants had a wildtype PCR profile. Of these, 21 mutants were Further analysed by Southern blotting. Interestingly, Southern blotting revealed genomic deletions/rearrangements in 12 of 21 mutants with a wild-type PCR profile. These deletions/rearrangements were further shown to affect gpt gene expression. The remaining nine mutants with a wild-type PCR profile were sequenced. Four of these mutants had mutations in the gpi structural gene. Overall, genomic deletions/rearrangements were observed in 12/21 independent mutants subjected to PCR and Southern blotting. Thus, deletions/rearrangements were the most common mutation observed following Amsacrine treatment of AS52 cells. Environ. Mol. Mutagen. 32.47-55, 1998. (C) 1998 Wiley-Liss, Inc. C1 Univ Auckland, Sch Med, Canc Res Lab, Auckland 1000, New Zealand. NIEHS, Lab Environm Carcinogenesis & Mutagenesis, Res Triangle Pk, NC 27709 USA. RP Ferguson, LR (reprint author), Univ Auckland, Sch Med, Canc Res Lab, Private Bag 92019, Auckland 1000, New Zealand. RI Ferguson, Lynnette/F-5989-2011 NR 35 TC 8 Z9 8 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1998 VL 32 IS 1 BP 47 EP 55 DI 10.1002/(SICI)1098-2280(1998)32:1<47::AID-EM6>3.3.CO;2-C PG 9 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 107QE UT WOS:000075219900006 PM 9707098 ER PT J AU Zeiger, E AF Zeiger, E TI The future of transgenic mutation models: Introduction to the panel discussion SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material C1 NIEHS, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA. RP Zeiger, E (reprint author), NIEHS, Environm Toxicol Program, POB 12233, Res Triangle Pk, NC 27709 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1998 VL 32 IS 2 BP 103 EP 103 DI 10.1002/(SICI)1098-2280(1998)32:2<103::AID-EM2>3.0.CO;2-N PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 125LU UT WOS:000076239700001 ER PT J AU Chen, JB Dass, SB Burkhart, JG Heflich, RH AF Chen, JB Dass, SB Burkhart, JG Heflich, RH TI Sensitivity of the phi X174 am3 allele in relation to the endogenous Hprt gene for detecting mutation in transgenic mice SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE phi X174; transgene; spleen lymphocytes; Hprt; N-ethyl-N-nitrosourea ID ETHYL-N-NITROSOUREA; ESCHERICHIA-COLI; SHUTTLE VECTORS; T-CELLS; INVIVO; MUTAGENESIS; LYMPHOCYTES; LOCUS; METHYLATION; FREQUENCY AB Transgenic mice have been developed containing multiple, chromosomally integrated copies of the Phi X174 am3 allele that serve as reporters for in vivo mutation at a single A:T basepair. In this study, we examined the relative sensitivity of the am3 transgene For detecting the in vivo mutagenicity of N-ethyl-N-nitrosourea (ENU). Three-week-old male Phi X174 mice were treated with 0, 40, and 160 mg/kg of ENU. After 1, 3, 6, and 9 weeks, animals were killed, their spleens removed, and isolated splenocytes were used to measure mutant frequencies (MFs) in both the am3 allele and the endogenous Hprt gene. For animals treated with 40 mg/kg of ENU, the Hprt assay detected an average 22-fold increase over background, while the am3 MFs averaged threefold above background. With the 160 mg/kg dose, the Hprt assay detected a 54-fold average increase, while a sixfold average increase above background was found for the transgenic locus. We conclude that the sensitivity of the am3 assay to ENU was compromised by the presence of ex vivo mutations. Adjustment of am3 MFs to exclude these ex vivo mutants could enhance the sensitivity of the assay. Environ. Mol. Mutagen. 32:229-235, 1998 (C) 1998 Wiley-Liss, Inc. C1 Natl Ctr Toxicol Res, Div Genet & Reprod Toxicol, Jefferson, AR 72079 USA. NIEHS, Res Triangle Pk, NC 27709 USA. RP Chen, JB (reprint author), Natl Ctr Toxicol Res, Div Genet & Reprod Toxicol, HFT-120, Jefferson, AR 72079 USA. EM JBChen@NCTR.FDA.GOV NR 24 TC 2 Z9 2 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1998 VL 32 IS 3 BP 229 EP 235 PG 7 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 136CF UT WOS:000076839900005 PM 9814437 ER PT J AU Zeiger, E AF Zeiger, E TI Mutation, selection, and evolution SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material C1 NIEHS, Res Triangle Pk, NC 27709 USA. RP Zeiger, E (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1998 VL 32 IS 4 BP 291 EP 291 DI 10.1002/(SICI)1098-2280(1998)32:4<291::AID-EM1>3.0.CO;2-Z PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 152PK UT WOS:000077785800001 PM 9882002 ER PT J AU Tice, RR Furedi-Machacek, M Satterfield, D Udumudi, A Vasquez, M Dunnick, JK AF Tice, RR Furedi-Machacek, M Satterfield, D Udumudi, A Vasquez, M Dunnick, JK TI Measurement of micronucleated erythrocytes and DNA damage during chronic ingestion of phenolphthalein in transgenic female mice heterozygous for the p53 gene SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE genotoxicity; p53-deficient transgenic mouse; alkaline single-cell gel electrophoresis; DNA damage; micronuclei; kinetochore; erythrocytes ID PERIPHERAL-BLOOD ERYTHROCYTES; BONE-MARROW DAMAGE; CHROMOSOME-ABERRATIONS; EXPOSURE REGIMEN; ASSAY; ANEUPLOIDY; TOXICITY; GENOTOXICITY; LYMPHOCYTES; DEFICIENT AB Phenolphthalein, a common ingredient in nonprescription laxatives and a multisex, multispecies rodent carcinogen, was evaluated under chronic exposure conditions For genotoxicity in transgenic female mice heterozygous for the p53 gene (heterozygous TSG-p53(R) mice). Phenolphthalein was administered in the diet at 200, 375, 750, 3,000, and 12,000 ppm (corresponding to a time-weighted average of 37, 71, 146, 569, and 2,074 mg/kg/day, respectively) for 6 months (183 days). On days 39, 92, 137, and 183 of treatment, peripheral blood samples were collected and evaluated For the frequency of micronucleated polychromatic and normochromatic erythrocytes (MN-PCE and MN-NCE, respectively), the percentage of PCE (%PCE) among total erythrocytes, and the extent of DNA damage (single strand breaks, alkali labile sites, DNA crosslinking) in leukocytes. In addition, the extent of DNA damage was evaluated in liver parenchymal cells sampled From mice at the end of the 6-month treatment period. DNA damage was evaluated using the alkaline (pH > 13) Single Cell Gel (SCG) assay. In addition, using a modified SCG technique, the frequencies of leukocytes and liver parenchymal cells with extremely low molecular weight DNA (indicative of apoptosis and/or necrosis) were determined. At each sample time, phenolphthalein induced a highly significant, dose-dependent increase in the Frequency of MN-PCE and MN-NCE and in %PCE. Maximal induction of MN-PCE and %PCE decreased with increasing treatment duration, most likely due to a treatment duration-dependent decrease in the relative amount of ingested phenolphthalein. A comparative analysis of the kinetochore status of MN in erythrocytes sampled from control mice and mice ingesting phenolphthalein at 12,000 ppm for 183 days indicates that the induced MN resulted predominantly but not exclusively from numerical chromosomal damage. The analysis for increased levels of DNA damage in blood leukocytes was inconclusive, with a small but statistically significant increase in DNA migration on days 39 and 137 but not on days 92 and 183. The extent of DNA migration in liver parenchymal cells sampled from mice at the end of treatment was not altered significantly. The frequencies of apoptotic and/or necrotic leukocytes and liver parenchymal cells were not increased among mice ingesting phenolphthalein. The lowest effective dose at which a significant genotoxic response (i.e., the induction of MN-NCE) was detected was 200 ppm, the lowest dose tested in this study. This dose in mice is comparable to doses (on a mg/m(2) basis) experienced by humans. (C) 1998 Wiley-Liss, Inc.* C1 Integrated Syst Lab, Res Triangle Pk, NC 27709 USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. RP Tice, RR (reprint author), Integrated Syst Lab, POB 13501, Res Triangle Pk, NC 27709 USA. EM trice@ils-inc.com FU NIEHS NIH HHS [N01-ES-15321] NR 52 TC 33 Z9 33 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1998 VL 31 IS 2 BP 113 EP 124 DI 10.1002/(SICI)1098-2280(1998)31:2<113::AID-EM3>3.0.CO;2-N PG 12 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA ZE676 UT WOS:000072818900003 PM 9544189 ER PT J AU Lowe, XR de Stoppelaar, JM Bishop, J Cassel, M Hoebee, B Moore, D Wyrobek, AJ AF Lowe, XR de Stoppelaar, JM Bishop, J Cassel, M Hoebee, B Moore, D Wyrobek, AJ TI Epididymal sperm aneuploidies in three strains of rats detected by multicolor fluorescence in situ hybridization SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE rat; epididymal sperm; aneuploidy; FISH ID PATERNAL AGE; IN-VIVO; INSITU HYBRIDIZATION; MOUSE EMBRYOS; CHROMOSOME-Y; FISH; 1,3-BUTADIENE; SPERMATOZOA; NONDISJUNCTION; TRANSLOCATION AB A multicolor fluorescence in situ hybridization (FISH) method was developed to detect aneuploidy and diploidy in epididymal sperm of rats using DNA probes specific for chromosomes 4 and Y. Fourteen healthy young-adult rats from three strains were evaluated: inbred Fisher 344/N/ehs, outbred Sprague-Dawley, and outbred WU Wistar/CPB. The hybridization efficiency of the FISH procedure was >99.9%, the sex-ratio in sperm was similar to 1 as expected, and there was no significant variation among two independent scorers. No significant variations were detected within or among strains in the frequencies of sperm disomy for chromosome 4 (1-6.5 per 10,000 cells per animal) or the Y chromosome (0-2.5 per 10,000 cells per animal). There was a trend toward increased variation among Wister rats. The frequencies of sperm-carrying hyper- and hypohaploidy for chromosome 4 were similar, suggesting a symmetrical mechanism of chromosome gain and loss during meiosis. The frequencies of Y-Y-4-4 sperm, which represent genomic meiosis II errors, did not differ significantly across strains (0.1-0.7 per 10,000 cells per strain). This FISH method for detecting aneuploidy in rat epididymal sperm provides a promising interspecies biomarker of male germ cell aneuploidy and introduces the rot as on animal model for investigating the heritable risk to offspring associated with paternal genotype, physiology, and exposure to environmental mutagens. There appear to be no significant differences among young healthy rats, mice, and men in the baseline frequencies of sperm with Y chromosomal disomy, the only chromosome for which data currently exists for all three species. (C) 1998 Wiley-Liss, Inc. C1 Univ Calif Lawrence Livermore Natl Lab, Biol & Biotech Res Program, Livermore, CA 94550 USA. Natl Inst Publ Hlth & Environm, Hlth Effects Res Lab, NL-3720 BA Bilthoven, Netherlands. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. RP Wyrobek, AJ (reprint author), Univ Calif Lawrence Livermore Natl Lab, Biol & Biotech Res Program, POB 808,L452,7000 E Ave, Livermore, CA 94550 USA. FU NIEHS NIH HHS [IAG Y01-ES-10203-00] NR 56 TC 23 Z9 25 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1998 VL 31 IS 2 BP 125 EP 132 DI 10.1002/(SICI)1098-2280(1998)31:2<125::AID-EM4>3.3.CO;2-1 PG 8 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA ZE676 UT WOS:000072818900004 PM 9544190 ER PT J AU Sata, F Araki, S Tanigawa, T Morita, Y Sakurai, S Nakata, A Katsuno, N AF Sata, F Araki, S Tanigawa, T Morita, Y Sakurai, S Nakata, A Katsuno, N TI Changes in T cell subpopulations in lead workers SO ENVIRONMENTAL RESEARCH LA English DT Article DE lymphocyte subpopulations; lead; memory T cells; CD45RO antigen; T cell differentiation ID MEMORY; LYMPHOCYTES; EXPOSURE; NAIVE; DIFFERENTIATION; CD45RO+; ANTIGEN; INDUCER; LEVEL; BLOOD AB To investigate the effects of lead on the human immune system, we analyzed T cell subpopulations and B (CD19+) cells in peripheral blood in 71 male lead workers. They were engaged in manufacturing lead stearate in a chemical factory, aged 20 to 74 (mean 48) years, Their blood lead concentrations (PbB) were between 7 and 50 (mean 19) mu g/dl. The control group consisted of 28 "healthy" male volunteers without a history of occupational exposure to lead or other hazardous substances, aged 33 to 67 (mean 55) years, In comparison with the controls, a significant reduction in the number of CD3+CD45RO+ (memory T) cells and a significant expansion in the percentage of CD8+ cells in the lead workers were found. There was a significant positive correlation between the percentage of CD3+CD45RA+ (naive T) cells and PbB in the lead workers. It is suggested that CD45RO+ memory T cells may be most susceptible to the effects of lead on T cell subpopulations. (C) 1998 Academic Press. C1 Univ Tokyo, Fac Med, Dept Publ Hlth, Bunkyo Ku, Tokyo 113, Japan. Tokyo Univ Hosp, Clin Lab, Bunkyo Ku, Tokyo 113, Japan. RP Sata, F (reprint author), NCI, NIH, Bldg 37,Room 3E24, Bethesda, MD 20892 USA. RI Nakata, Akinori/A-2399-2008 NR 17 TC 28 Z9 28 U1 1 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0013-9351 J9 ENVIRON RES JI Environ. Res. PD JAN PY 1998 VL 76 IS 1 BP 61 EP 64 DI 10.1006/enrs.1997.3790 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA YV941 UT WOS:000071879800007 PM 9466898 ER PT J AU Andrieu, N Goldstein, AM AF Andrieu, N Goldstein, AM TI Epidemiologic and genetic approaches in the study of gene-environment interaction: an overview of available methods SO EPIDEMIOLOGIC REVIEWS LA English DT Article ID NESTED CASE-CONTROL; COMPLEX SEGREGATION ANALYSIS; BREAST-CANCER; RISK-FACTORS; FAMILY HISTORY; QUANTITATIVE TRAITS; LUNG-CANCER; REPRODUCTIVE FACTORS; LOGISTIC-REGRESSION; LINKAGE ANALYSIS C1 NCI, Genet Epidemiol Branch, Bethesda, MD USA. RP Andrieu, N (reprint author), Inst Gustave Roussy, INSERM, Unite Rech Epidemiol Canc, U351, F-94805 Villejuif, France. RI ANDRIEU, Nadine/H-4255-2014 NR 61 TC 71 Z9 73 U1 0 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 USA SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1998 VL 20 IS 2 BP 137 EP 147 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 157UB UT WOS:000078079100001 PM 9919434 ER PT J AU Brownson, RC Alavanja, MCR Caporaso, N Simoes, EJ Chang, JC AF Brownson, RC Alavanja, MCR Caporaso, N Simoes, EJ Chang, JC TI Epidemiology and prevention of lung cancer in nonsmokers SO EPIDEMIOLOGIC REVIEWS LA English DT Review ID ENVIRONMENTAL TOBACCO-SMOKE; RESIDENTIAL RADON EXPOSURE; INDEPENDENT RISK FACTOR; SATURATED FAT INTAKE; TERM EX-SMOKERS; PASSIVE SMOKING; UNITED-STATES; LIFETIME NONSMOKERS; AIR-POLLUTION; BRONCHIOLOALVEOLAR CARCINOMA C1 St Louis Univ, Sch Publ Hlth, Dept Community Hlth, St Louis, MO 63108 USA. St Louis Univ, Sch Publ Hlth, Prevent Res Ctr, St Louis, MO 63108 USA. NCI, Div Canc Epidemiol & Genet, Rockville, MD USA. Missouri Dept Hlth, Div Chron Dis Prevent & Hlth Promot, Columbia, MO USA. RP Brownson, RC (reprint author), St Louis Univ, Sch Publ Hlth, Dept Community Hlth, 3663 Lindell Blvd, St Louis, MO 63108 USA. OI Simoes, Eduardo/0000-0003-4371-4305 FU NCI NIH HHS [N01-CP7-1096-01, N01-CP7-1096-02]; PHS HHS [U75/CCU710667] NR 165 TC 62 Z9 67 U1 0 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 USA SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1998 VL 20 IS 2 BP 218 EP 236 PG 19 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 157UB UT WOS:000078079100007 PM 9919440 ER PT J AU Glud, E Kjaer, SK Troisi, R Brinton, LA AF Glud, E Kjaer, SK Troisi, R Brinton, LA TI Fertility drugs and ovarian cancer SO EPIDEMIOLOGIC REVIEWS LA English DT Review ID STATES CASE-CONTROL; IN-VITRO FERTILIZATION; EUROPEAN CASE-CONTROL; GRANULOSA-CELL TUMOR; CLOMIPHENE CITRATE; UNITED-STATES; COLLABORATIVE ANALYSIS; BREAST-CANCER; INFERTILE WOMEN; GONADOTROPIN THERAPY C1 Danish Canc Soc, Div Canc Epidemiol, DK-2100 Copenhagen O, Denmark. US Dept HHS, NCI, Bethesda, MD USA. RP Glud, E (reprint author), Danish Canc Soc, Div Canc Epidemiol, Strandblvd 49,Box 939, DK-2100 Copenhagen O, Denmark. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 157 TC 37 Z9 37 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1998 VL 20 IS 2 BP 237 EP 257 PG 21 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 157UB UT WOS:000078079100008 PM 9919441 ER PT J AU Silverman, DT AF Silverman, DT TI Is diesel exhaust a human lung carcinogen? SO EPIDEMIOLOGY LA English DT Editorial Material ID OCCUPATIONAL RISK-FACTORS; SWEDISH DOCK WORKERS; RETROSPECTIVE COHORT; RAILROAD WORKERS; CASE-REFERENT; CANCER; EXPOSURE; MORTALITY; ASSOCIATIONS; INDUSTRY C1 NCI, Occupat Epidemiol Branch, Bethesda, MD 20892 USA. RP Silverman, DT (reprint author), NCI, Occupat Epidemiol Branch, EPN 418, Bethesda, MD 20892 USA. NR 35 TC 26 Z9 26 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 1998 VL 9 IS 1 BP 4 EP 6 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YM685 UT WOS:000071089500003 PM 9430259 ER PT J AU Mark, SD Wang, W Fraumeni, JF Li, JY Taylor, PR Wang, GQ Dawsey, SM Li, B Blot, WJ AF Mark, SD Wang, W Fraumeni, JF Li, JY Taylor, PR Wang, GQ Dawsey, SM Li, B Blot, WJ TI Do nutritional supplements lower the risk of stroke or hypertension? SO EPIDEMIOLOGY LA English DT Article DE antioxidants; cerebrovascular disorders; hypertension; minerals; nutrition; randomized trials; stroke; vitamins; mortality ID VITAMIN MINERAL SUPPLEMENTATION; DISEASE-SPECIFIC MORTALITY; CANCER INCIDENCE; ISCHEMIC STROKE; BLOOD-PRESSURE; FOLLOW-UP; CARDIOVASCULAR-DISEASE; ANTIOXIDANT VITAMINS; INTERVENTION TRIALS; PLASMA HOMOCYSTEINE AB Between 1986 and 1991, 29,584 persons rook Dart in a randomized nutritional intervention trial in Linxian, China, an area whose residents had chronically low intakes of several nutrients and high rates of esophageal and gastric cardia cancer as well as stroke. Using a one-half replicate of a 2(4) factorial design, we randomized individuals to one of eight groups which received combinations of four supplements: retinol and zinc (factor A); riboflavin and niacin (factor B); vitamin C and molybdenum (factor C); and beta-carotene, alpha-tocopherol (vitamin E), and selenium (factor D). Deaths that occurred during 5 years of supplementation were ascertained and classified according to cause. At the end of the supplementation period, we measured blood pressure readings and determined the prevalence of hypertension. Participants who received factor D had reductions in total mortality (9%) and total cancer mortality (13%). These individuals also had the largest reduction in stroke mortality (relative risk = 0.91; 95% confidence interval = 0.76-1.07). End-of-trial hypertension, however, was not less prevalent among those receiving factor D. Our findings contrast with the larger reductions in stroke death and hypertension found in a parallel trial of Linxian subjects with esophageal dysplasia who received a multivitamin/mineral supplement, suggesting an effect largely derived from nutrients other than those received in the present study. C1 NCI, Bethesda, MD 20892 USA. Chinese Acad Med Sci, Inst Canc, Beijing 100021, Peoples R China. Int Epidemiol Inst, Rockville, MD USA. RP Mark, SD (reprint author), NCI, Execut Plaza N,Room 403,6130 Execut Blvd,MSC 7368, Bethesda, MD 20892 USA. NR 52 TC 54 Z9 54 U1 0 U2 13 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 1998 VL 9 IS 1 BP 9 EP 15 DI 10.1097/00001648-199801000-00005 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YM685 UT WOS:000071089500006 PM 9430262 ER PT J AU Cantor, KP Lynch, CF Hildesheim, ME Dosemeci, M Lubin, J Alavanja, M Craun, G AF Cantor, KP Lynch, CF Hildesheim, ME Dosemeci, M Lubin, J Alavanja, M Craun, G TI Drinking water source and chlorination byproducts I. Risk of bladder cancer SO EPIDEMIOLOGY LA English DT Article DE bladder neoplasms; water; chlorination; case control study; gender; trihalomethane; smoking; drinking water source ID DISINFECTION BY-PRODUCTS; URINARY-TRACT; FLUID INTAKE; MORTALITY; IDENTIFICATION; ASSOCIATIONS AB We conducted a population-based case control study of bladder cancer in Iowa in 1986-1989 to evaluate the risk posed by tapwater containing chlorination byproducts. We combined information about residential history, drinking water source, beverage intake, and other factors with historical data from water utilities and measured contaminant levels to create in dices of past exposure to chlorination byproducts. The study comprised 1,123 cases and 1,983 controls who had data relat ing to at least 70% of their lifetime drinking water source. After we adjusted for potential confounders, we calculated odds ratios for duration of chlorinated surface water of 1.0 (referent), 1.0, 1.1, 1.2, and 1.5 for 0, 1-19, 20-39, 40-59, and greater than or equal to 60 years of use. We also found associations with total and average lifetime byproduct intake, as represented by trihalomethane estimates. Positive findings were restricted to men and to ever-smokers. Among men, odds ratios were 1.0 (referent), 1.1, 1.3, 1.5, and 1.9, and among ever smokers, 1.0, 1.1, 1.3, 1.0, and 2.2, after adjustment for intensity and timing of smoking. Among nonsmoking men and women, regardless of smoking habit, there was no association. Among men, smoking and exposure to chlorinated surface water mutually enhanced the risk of bladder cancer. The overall association of bladder cancer risk with duration of chlorinated surface water use that we found is consistent with the findings of other investigations, bur the differences in risk between men and women, and between smokers and nonsmokers, have not been widely observed. C1 NCI, Occupat Epidemiol Branch, DCEG, Bethesda, MD 20892 USA. Univ Iowa, Dept Prevent Med & Environm Hlth, Iowa City, IA 52242 USA. US EPA, Cincinnati, OH 45268 USA. RP Cantor, KP (reprint author), NCI, Occupat Epidemiol Branch, DCEG, Execut Plaza N,Suite 418, Bethesda, MD 20892 USA. FU NCI NIH HHS [5 KO7 CA01181, NCI NO1-CP-85614, NCI-NO1-CP-51026] NR 42 TC 217 Z9 225 U1 4 U2 34 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 1998 VL 9 IS 1 BP 21 EP 28 DI 10.1097/00001648-199801000-00007 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YM685 UT WOS:000071089500008 PM 9430264 ER PT J AU Hildesheim, ME Cantor, KP Lynch, CF Dosemeci, M Lubin, J Alavanja, M Craun, G AF Hildesheim, ME Cantor, KP Lynch, CF Dosemeci, M Lubin, J Alavanja, M Craun, G TI Drinking water source and chlorination byproducts II. Risk of colon and rectal cancers SO EPIDEMIOLOGY LA English DT Article DE colorectal neoplasms; drinking water; water source; chlorination; gender; trihalomethanes; diet; physical activity ID COLORECTAL-CANCER; PHYSICAL-ACTIVITY; MORTALITY-RATES; LOUISIANA; TRIHALOMETHANES; WISCONSIN; SITE AB We evaluated the association between chlorination byproducts and colon and rectal cancer risk in a population-based case-control study conducted in Iowa in 1986-1989. Data were gathered from 685 colon cancer cases, 655 rectal cancer cases, and 2,434 controls. We calculated odds ratios for the 560 colon cancer cases, 537 rectal cancer cases, and 1,983 controls for whom water exposure information was available for at lease 70% of their lifetime. We estimated exposure to chlorination byproducts with two types of measures: duration of lifetime at residences served by chlorinated water and estimated lifetime trihalomethane exposure. For rectal cancer, we observed an association with duration of chlorinated surface water use, with adjusted odds ratios of 1.1, 1.6, 1.6, and 2.6 for 1-19, 20-39, 40-59, and greater than or equal to 60 years of exposure, compared with no exposure. Rectal cancer risk was also associated with several different measures of estimated lifetime trihalomethane exposure. For colon cancer and subsites, we detected no important increase in risk associated with duration of chlorinated surface water, nor with trihalomethane estimates. When we evaluated chlorination byproducts jointly with other factors, we found larger relative risk estimates for rectal cancer among subjects with low dietary fiber intake. The risk related to greater than or equal to 40 years of exposure to a chlorinated surface water source was 2.4 (95% confidence interval = 1.5-4.0) for persons with low fiber intake and 0.9 (95% confidence interval = 0.4-1.8) for persons with high fiber intake, relative to the risk of persons with high-fiber diets and no exposure to chlorinated surface water. We observed a similar risk differential for low and high levels of physical activity. C1 NCI, Occupat Epidemiol Branch, DCEG, Bethesda, MD 20892 USA. Univ Iowa, Dept Prevent Med & Environm Hlth, Iowa City, IA 52242 USA. US EPA, Cincinnati, OH 45268 USA. RP Cantor, KP (reprint author), NCI, Occupat Epidemiol Branch, DCEG, Execut Plaza N,Suite 418, Bethesda, MD 20892 USA. FU NCI NIH HHS [5 KO7 CA01181, NCI NO1-CP-85614, NCI-NO1-CP-51026] NR 49 TC 107 Z9 110 U1 0 U2 10 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 1998 VL 9 IS 1 BP 29 EP 35 DI 10.1097/00001648-199801000-00008 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA YM685 UT WOS:000071089500009 PM 9430265 ER PT S AU Wolffe, AP AF Wolffe, AP BE Chadwick, DJ Cardew, G TI Epigenetics - Introduction SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID X-CHROMOSOME INACTIVATION; DEVELOPMENTAL REGULATION; DNA METHYLATION; GENE-EXPRESSION; TRANSCRIPTION; INHERITANCE; MECHANISMS; EUKARYOTES C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. RP Wolffe, AP (reprint author), NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. NR 30 TC 4 Z9 4 U1 0 U2 3 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 1 EP 5 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200001 ER PT S AU Barlow Bird Jaenisch Wolffe Gasser Horz Finnegan Allshire Fedoroff Lyon Francke Flavell AF Barlow Bird Jaenisch Wolffe Gasser Horz Finnegan Allshire Fedoroff Lyon Francke Flavell BE Chadwick, DJ Cardew, G TI Gene silencing by methyl-CpG-binding proteins - Discussion SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID EXTRACT; DNA C1 Netherlands Canc Inst, NL-1066 CX Amsterdam, Netherlands. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. MIT, Dept Biol, Whitehead Inst Biomed Res, Cambridge, MA 02142 USA. NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. Univ Munich, Inst Physiol Chem, D-80336 Munich, Germany. Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland. Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Univ Heidelberg, Zentrum Mol Biol, D-69120 Heidelberg, Germany. MRC, Mammalian Genet Unit, Didcot OX11 ORD, Oxon, England. Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Howard Hughes Med Inst, Beckman Ctr Mol & Genet Med, Stanford, CA 94305 USA. John Innes Ctr Plant Sci Res, Norwich NR4 7UH, Norfolk, England. RP Barlow (reprint author), Netherlands Canc Inst, Plesmanlaan 121, NL-1066 CX Amsterdam, Netherlands. NR 4 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 16 EP 21 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200003 ER PT S AU Kass, SU Wolffe, AP AF Kass, SU Wolffe, AP BE Chadwick, DJ Cardew, G TI DNA methylation, nucleosomes and the inheritance of chromatin structure and function SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Article; Proceedings Paper CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID TRANSCRIPTION IN-VIVO; HISTONE ACETYLATION; LINKER HISTONES; RNA GENE; PARENTAL NUCLEOSOMES; CPG SEQUENCES; POSITIVE ROLE; REPLICATION; H1; REPRESSION AB The replication of the genome during S phase is a crucial period for the establishment and maintenance of programmes of differential gene activity. Existing chromosomal structures are disrupted during replication and reassembled on both daughter chromatids. The capacity to reassemble a particular chromatin structure with defined functional properties reflects the commitment of a cell type to a particular state of determination. The core and linker histones and their modifications, enzymes that modify the histones, DNA methylation and proteins that recognize methylated DNA within chromatin may all play independent or interrelated roles in defining the functional properties of chromatin. Pre-existing protein-DNA interactions and DNA methylation in a parental chromosome will influence the structure and function of daughter chromosomes generating an epigenetic imprint. In this chapter we consider the events occurring at the eukaryotic replication fork, their consequences for pre-existing chromosomal structures and how an epigenetic imprint might be maintained. C1 Janssen Res Fdn, Dept Expt Mol Biol, B-2340 Beerse, Belgium. NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. RP Kass, SU (reprint author), Janssen Res Fdn, Dept Expt Mol Biol, Turnhoutseweg 30, B-2340 Beerse, Belgium. NR 55 TC 8 Z9 8 U1 0 U2 3 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 22 EP 35 PG 14 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200004 ER PT S AU Jaenisch Wolffe Bird Fedoroff Horz Finnegan Laird Flavell Wilkins Allshire Kooter Grosveld Pillus Meyer Gasser AF Jaenisch Wolffe Bird Fedoroff Horz Finnegan Laird Flavell Wilkins Allshire Kooter Grosveld Pillus Meyer Gasser BE Chadwick, DJ Cardew, G TI DNA methylation, nucleosomes and the inheritance of chromatin structure and function - Discussion SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID SITE-SPECIFIC ANTIBODIES; RNA GENE; HISTONE ACETYLATION; TRANSCRIPTIONAL REPRESSION; LINKER HISTONES; CPG SEQUENCES; REPLICATION; YEAST; H1; BINDING C1 MIT, Dept Biol, Whitehead Inst Biomed Res, Cambridge Ctr 9, Cambridge, MA 02139 USA. NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Univ Munich, Inst Physiol Chem, D-80336 Munich, Germany. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. Fred Hutchinson Canc Res Ctr C3168, Seattle, WA 98109 USA. John Innes Ctr Plant Sci Res, Norwich NR4 7UH, Norfolk, England. Co Biol Ltd, BioEssays, Cambridge CB4 4DL, England. Free Univ Amsterdam, Dept Genet, NL-1081 HV Amsterdam, Netherlands. Erasmus Univ, Dept Cell Biol & Genet, MGC, NL-3000 DR Rotterdam, Netherlands. Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA. Univ Leeds, Dept Biol, Leeds LS2 9JT, W Yorkshire, England. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. RP Jaenisch (reprint author), MIT, Dept Biol, Whitehead Inst Biomed Res, Cambridge Ctr 9, 77 Massachusetts Ave, Cambridge, MA 02139 USA. NR 49 TC 0 Z9 0 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 35 EP 45 PG 11 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200005 ER PT S AU Wolffe Fedoroff Bird Gasser Jaenisch Pillus Lyon Riggs Laird AF Wolffe Fedoroff Bird Gasser Jaenisch Pillus Lyon Riggs Laird BE Chadwick, DJ Cardew, G TI The methylation of CpG islands - General discussion I SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID X-CHROMOSOME INACTIVATION; DNA METHYLATION; LINKED GENES; HYPOMETHYLATION; DEMETHYLATION; SITES C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. MIT, Whitehead Inst Biomed Res, Dept Biol, Cambridge, MA 02142 USA. Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA. MRC, Mammalian Genet Unit, Didcot OX11 ORD, Oxon, England. City Hope Natl Med Ctr, Beckman Res Inst, Dept Biol, Duarte, CA 91010 USA. Fred Hutchinson Canc Res Ctr C3168, Seattle, WA 98109 USA. RP Wolffe (reprint author), NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 46 EP 50 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200006 ER PT S AU Fedoroff Paro Wolffe Horz Riggs Laird Reik Allshire Finnegan Barlow Jaenisch Francke Wilkins Grosveld Gasser AF Fedoroff Paro Wolffe Horz Riggs Laird Reik Allshire Finnegan Barlow Jaenisch Francke Wilkins Grosveld Gasser BE Chadwick, DJ Cardew, G TI Heritable chromatin states induced by the Polycomb and trithorax group genes - Discussion SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID IN-VIVO; PROTEIN C1 Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Univ Heidelberg, Zentrum Mol Biol, D-69120 Heidelberg, Germany. NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Univ Munich, Inst Physiol Chem, D-80336 Munich, Germany. City Hope Natl Med Ctr, Beckman Res Inst, Dept Biol, Duarte, CA 91010 USA. Fred Hutchinson Canc Res Ctr C3168, Seattle, WA 98109 USA. Babraham Inst, Lab Dev Genet & Imprinting, Cambridge CB2 4AT, England. Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland. CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA. Netherlands Canc Inst, NL-1066 CX Amsterdam, Netherlands. MIT, Whitehead Inst Biomed Res, Dept Biol, Cambridge, MA 02142 USA. Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Howard Hughes Med Inst, Beckman Ctr Mol & Genet Med, Stanford, CA 94305 USA. Co Biol Ltd, BioEssays, Cambridge CB4 4DL, England. Erasmus Univ, Dept Cell Biol & Genet, MGC, NL-3000 DR Rotterdam, Netherlands. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. RP Fedoroff (reprint author), Penn State Univ, Dept Biol, 208 Mueller Lab, University Pk, PA 16802 USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 61 EP 66 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200008 ER PT S AU Bird Grosveld Barlow Wolffe Jaenisch Gasser Riggs Horz Francke Finnegan Paro Laird Pillus Lyon AF Bird Grosveld Barlow Wolffe Jaenisch Gasser Riggs Horz Francke Finnegan Paro Laird Pillus Lyon BE Chadwick, DJ Cardew, G TI The dynamics of globin gene expression and position effects - Discussion SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID TRANSCRIPTION; REACTIVATION; LOCUS; MOUSE C1 Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. Erasmus Univ, Dept Cell Biol & Genet, MGC, NL-3000 DR Rotterdam, Netherlands. Netherlands Canc Inst, NL-1066 CX Amsterdam, Netherlands. NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. MIT, Whitehead Inst Biomed Res, Dept Biol, Cambridge Ctr 9, Cambridge, MA 02142 USA. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. City Hope Natl Med Ctr, Beckman Res Inst, Dept Biol, Duarte, CA 91010 USA. Univ Munich, Inst Physiol Chem, D-80336 Munich, Germany. Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Howard Hughes Med Inst, Beckman Ctr Mol & Genet Med, Stanford, CA 94305 USA. CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. Univ Heidelberg, Zentrum Mol Biol, D-69120 Heidelberg, Germany. Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA. Univ Colorado, Dept MCD Biol, Boulder, CO 80309 USA. MRC, Mammalian Genet Unit, Didcot OX11 0RD, Oxon, England. RP Bird (reprint author), Univ Edinburgh, Inst Cell & Mol Biol, Kings Bldg,Mayfield Rd, Edinburgh EH9 3JR, Midlothian, Scotland. NR 10 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 79 EP 86 PG 8 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200010 ER PT S AU Klar, AJS Ivanova, AV Dalgaard, JZ Bonaduce, MJ Grewal, SIS AF Klar, AJS Ivanova, AV Dalgaard, JZ Bonaduce, MJ Grewal, SIS BE Chadwick, DJ Cardew, G TI Multiple epigenetic events regulate mating-type switching of fission yeast SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Article; Proceedings Paper CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID SCHIZOSACCHAROMYCES-POMBE; MEIOTIC RECOMBINATION; CHROMATIN STRUCTURE; DNA STRANDS; REGION; LOCI; INHERITANCE; CASSETTES; CELLS; SWI6 AB Two epigenetic events at mat1, one of which is DNA strand specific, are required to initiate recombination during mating-type switching. The third, a chromosomally borne imprinted event at the mat2/3 internal regulates silencing and directionality of switching, and prohibits interchromosomal recombination. We speculate that the unit of inheritance in the mat2/3 interval is both DNA plus its associated chromatin structure. Such a control is likely to be essential in maintaining particular states of gene expression during development. C1 NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Gene Regulat & Chromosome Biol Lab, Frederick, MD 21702 USA. RP Klar, AJS (reprint author), NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Gene Regulat & Chromosome Biol Lab, POB B, Frederick, MD 21702 USA. NR 35 TC 18 Z9 18 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 87 EP 99 PG 13 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200011 ER PT S AU Finnegan Grewal Wolffe Allshire Riggs Paro Pillus Gasser Martienssen AF Finnegan Grewal Wolffe Allshire Riggs Paro Pillus Gasser Martienssen BE Chadwick, DJ Cardew, G TI Multiple epigenetic events regulate mating-type switching of fission yeast - Discussion SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID CHROMO DOMAIN; HUMAN GENES C1 CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Gene Regulat & Chromosome Biol Lab, Frederick, MD 21702 USA. NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland. City Hope Natl Med Ctr, Beckman Res Inst, Dept Biol, Duarte, CA 91010 USA. Univ Heidelberg, Zentrum Mol Biol, D-69120 Heidelberg, Germany. Univ Colorado, Dept MCD Biol, Boulder, CO 80309 USA. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. Univ Munich, Inst Physiol Chem, D-80336 Munich, Germany. RP Finnegan (reprint author), CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. NR 7 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 99 EP 103 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200012 ER PT S AU Allshire Wolffe Barlow Gasser Grewal Laird Riggs Jaenisch Fedoroff Horz Bird AF Allshire Wolffe Barlow Gasser Grewal Laird Riggs Jaenisch Fedoroff Horz Bird BE Chadwick, DJ Cardew, G TI Centromeres - General discussion II SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID FISSION YEAST CENTROMERES; TRANSCRIPTION; DROSOPHILA; HETEROCHROMATIN; LOCALIZATION; ACETYLATION; EXPRESSION; MUTATIONS; DOMAINS; DISRUPT C1 Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland. NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Netherlands Canc Inst, NL-1066 CX Amsterdam, Netherlands. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Gene Regulat & Chromosome Biol Lab, Frederick, MD 21702 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA. City Hope Natl Med Ctr, Beckman Res Inst, Dept Biol, Duarte, CA 91010 USA. MIT, Whitehead Inst Biomed Res, Dept Biol, Cambridge Ctr 9, Cambridge, MA 02142 USA. Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Univ Munich, Inst Physiol Chem, D-80336 Munich, Germany. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. RP Allshire (reprint author), Western Gen Hosp, MRC, Human Genet Unit, Crewe Rd, Edinburgh EH4 2XU, Midlothian, Scotland. NR 19 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 104 EP 113 PG 10 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200013 ER PT S AU Allshire Gasser Fedoroff Wolffe Pillus Horz Meyer Flavell Grewal Bird Laird Barlow AF Allshire Gasser Fedoroff Wolffe Pillus Horz Meyer Flavell Grewal Bird Laird Barlow BE Chadwick, DJ Cardew, G TI Nuclear organization and silencing: trafficking of Sir proteins - Discussion SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID CHROMOSOME C1 Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland. Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Univ Colorado, Dept MCD Biol, Boulder, CO 80309 USA. Univ Munich, Inst Physiol Chem, D-80336 Munich, Germany. Univ Leeds, Dept Biol, Leeds LS2 9JT, W Yorkshire, England. John Innes Ctr Plant Sci Res, Norwich NR4 7UH, Norfolk, England. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA. Netherlands Canc Inst, NL-1066 CX Amsterdam, Netherlands. RP Allshire (reprint author), Western Gen Hosp, MRC, Human Genet Unit, Crewe Rd, Edinburgh EH4 2XU, Midlothian, Scotland. NR 6 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 126 EP 132 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200015 ER PT S AU Wolffe Fedoroff Meyer Flavell Jaenisch Finnegan Laird Martienssen AF Wolffe Fedoroff Meyer Flavell Jaenisch Finnegan Laird Martienssen BE Chadwick, DJ Cardew, G TI Epigenetic mechanisms in the regulation of the maize Suppressor-mutator transposon - Discussion SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Univ Leeds, Dept Biol, Leeds LS2 9JT, W Yorkshire, England. John Innes Ctr Plant Sci Res, Norwich NR4 7UH, Norfolk, England. MIT, Whitehead Inst Biomed Res, Dept Biol, Cambridge Ctr 9, Cambridge, MA 02142 USA. CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA. Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. RP Wolffe (reprint author), NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 140 EP 143 PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200017 ER PT S AU Wolffe Flavell Kooter Fedoroff Reik Jaenisch Pillus Allshire Wilkins Finnegan Meyer Gasser Martienssen Matzke AF Wolffe Flavell Kooter Fedoroff Reik Jaenisch Pillus Allshire Wilkins Finnegan Meyer Gasser Martienssen Matzke BE Chadwick, DJ Cardew, G TI Transgene-promoted epigenetic switches of chalcone synthase activity in petunia plants - Discussion SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID TRANSCRIPT; ARABIDOPSIS C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. John Innes Ctr Plant Sci Res, Norwich NR4 7UH, Norfolk, England. Free Univ Amsterdam, Dept Genet, NL-1081 HV Amsterdam, Netherlands. Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Babraham Inst, Lab Dev Genet & Imprinting, Cambridge CB2 4AT, England. MIT, Whitehead Inst Biomed Res, Dept Biol, Cambridge Ctr 9, Cambridge, MA 02142 USA. Univ Colorado, Dept MCD Biol, Boulder, CO 80309 USA. Co Biol Ltd, BioEssays, Cambridge CB4 4DL, England. Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland. CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. Univ Leeds, Dept Biol, Leeds LS2 9JT, W Yorkshire, England. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. Austrian Acad Sci, Inst Mol Biol, A-5020 Salzburg, Austria. RP Wolffe (reprint author), NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 154 EP 162 PG 9 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200019 ER PT S AU Wolffe, AP AF Wolffe, AP BE Chadwick, DJ Cardew, G TI Epigenetics - Summary SO EPIGENETICS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. RP Wolffe, AP (reprint author), NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 291 EP 292 PG 2 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200037 ER PT S AU Wolffe Allshire Flavell Pillus Gasser Fedoroff Meyer Finnegan Bird Martienssen AF Wolffe Allshire Flavell Pillus Gasser Fedoroff Meyer Finnegan Bird Martienssen BE Chadwick, DJ Cardew, G TI Nucleolar organization and the silencing of endogenous sequences and transgenes - General discussion III SO EPIGENETICS-BOOK SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Epigenetics CY JUN 24-26, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID ARABIDOPSIS; DNA C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland. John Innes Ctr Plant Sci Res, Norwich NR4 7UH, Norfolk, England. Univ Colorado, Dept MCD Biol, Boulder, CO 80309 USA. Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland. Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Penn State Univ, Inst Biotechnol, University Pk, PA 16802 USA. Univ Leeds, Dept Biol, Leeds LS2 9JT, W Yorkshire, England. CSIRO, Div Plant Ind, Canberra, ACT 2601, Australia. Univ Edinburgh, Inst Cell & Mol Biol, Edinburgh EH9 3JR, Midlothian, Scotland. Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. RP Wolffe (reprint author), NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97771-3 J9 CIBA F SYMP PY 1998 VL 214 BP 163 EP 167 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; Medicine, General & Internal SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology; Genetics & Heredity; General & Internal Medicine GA BL67L UT WOS:000076284200020 ER PT J AU Bourassa, MG Yeh, W Holubkov, R Sopko, G Detre, KM AF Bourassa, MG Yeh, W Holubkov, R Sopko, G Detre, KM CA NHLBI PTCA Registry TI Long-term outcome of patients with incomplete vs complete revascularization after multivessel PTCA - A report from the NHLBI PTCA registry SO EUROPEAN HEART JOURNAL LA English DT Article DE coronary angioplasty; PTCA strategy; completeness of revascularization; prognosis ID LUMINAL CORONARY ANGIOPLASTY; MYOCARDIAL REVASCULARIZATION; BYPASS-SURGERY; ARTERY DISEASE; SURVIVAL; DETERMINANTS; METAANALYSIS; IMPROVEMENT; OPERATION; ANGINA AB Background Incomplete revascularization is frequently the goal as well as the final outcome in patients with multivessel coronary disease undergoing PTCA. However, the long-term impact of incomplete revascularization is not known and this common PTCA strategy deserves further scrutiny. Methods and results Complete revascularization was achieved in 132 of 757 patients with multivessel disease in the 1985-86 NHLBI PTCA Registry. Compared to patients in whom complete revascularization was achieved, patients with incomplete revascularization were older (P<0.05), more likely to be females (P<0.05) and to have recent myocardial infarction (P<0.05), unstable angina (P<0.001), and urgent or emergent PTCA (P<0.001). Early death, Q wave myocardial infarction and CABG rates were higher in patients with incomplete than in those with complete revascularization [significantly different (P<0.05) only for emergency and elective CABG]. At 9 years, nearly twice as many patients with incomplete revascularization experienced recurrent angina (19% vs 10% for patients with complete revascularization, P<0.05). Patients with complete revascularization were more likely to undergo repeat PTCA than those with incomplete revascularization (40% vs 30%, P<0.05). Patients with incomplete revascularization were more likely to undergo CABG than patients with complete revascularization (32% vs 14%, P<0.001; adjusted risk 2.56, 95% CI 1.60, 4.10). Among patients with incomplete revascularization, those in whom PTCA was intended but not attempted had the highest early event rates and late CABG rates. Finally, the adjusted risk of dying, having a Q wave myocardial infarction, recurrent angina or repeat PTCA was not different at 9-year follow-up among patients with and without complete revascularization. Conclusions Complete revascularization achieved by PTCA reduces late occurrence of CABG, but not adjusted rates of death, Q wave myocardial infarction, recurrent angina, and repeat PTCA in patients with multivessel coronary disease. These data tend to support the PTCA strategy of incomplete revascularization in patients with multivessel disease when complete revascularization is not feasible or not planned before the procedure. C1 Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada. Univ Pittsburgh, Pittsburgh, PA USA. NHLBI, Bethesda, MD 20892 USA. RP Bourassa, MG (reprint author), Montreal Heart Inst, 5000 Belanger St E, Montreal, PQ H1T 1C8, Canada. OI Bourassa, Martial G./0000-0002-4439-8650 NR 37 TC 51 Z9 57 U1 0 U2 2 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0195-668X J9 EUR HEART J JI Eur. Heart J. PD JAN PY 1998 VL 19 IS 1 BP 103 EP 111 DI 10.1053/euhj.1997.0574 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YU868 UT WOS:000071764100017 PM 9503182 ER PT J AU Saul, H Klausner, R AF Saul, H Klausner, R TI The first 30 months SO EUROPEAN JOURNAL OF CANCER LA English DT Editorial Material C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 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 JAN PY 1998 VL 34 IS 1 BP 3 EP 5 PG 3 WC Oncology SC Oncology GA ZA322 UT WOS:000072351900002 ER PT J AU Bakketeig, LS Butte, N de Onis, M Kramer, M O'Donnell, A Prada, JA Hoffman, HJ AF Bakketeig, LS Butte, N de Onis, M Kramer, M O'Donnell, A Prada, JA Hoffman, HJ TI Report of the IDECG Working Group on definitions, classifications, causes, mechanisms and prevention of IUGR SO EUROPEAN JOURNAL OF CLINICAL NUTRITION LA English DT Article; Proceedings Paper CT IDECG Workshop on Causes and Consequences of Intrauterine Growth Retardation CY NOV 11-15, 1996 CL BATON ROUGE, LOUISIANA SP Int Dietary Energy Consultancy Grp C1 Natl Inst Publ Hlth, Dept Populat Hlth Sci, N-0403 Oslo, Norway. Baylor Coll Med, Dept Pediat, Childrens Nutr Res Ctr, Houston, TX USA. WHO, Nutr Unit, CH-1211 Geneva 27, Switzerland. McGill Univ, Fac Med, Dept Pediat, Montreal, PQ, Canada. McGill Univ, Fac Med, Dept Epidemiol & Biostat, Montreal, PQ, Canada. Ctr Estud Nutr Infantil, Buenos Aires, DF, Argentina. Childrens Hosp, Med Ctr, Cincinnati, OH 45267 USA. Natl Inst Deafness & Commun Disorders, Epidemiol Stat & Data Syst Branch, NIH, Bethesda, MD 20892 USA. RP Bakketeig, LS (reprint author), Nestle Fdn, POB 581, CH-1001 Lausanne, Switzerland. NR 0 TC 11 Z9 11 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0954-3007 J9 EUR J CLIN NUTR JI Eur. J. Clin. Nutr. PD JAN PY 1998 VL 52 SU 1 BP S94 EP S96 PG 3 WC Nutrition & Dietetics SC Nutrition & Dietetics GA ZC415 UT WOS:000072575700015 PM 9511025 ER PT J AU Goldenberg, RL Hoffman, HJ Cliver, SP AF Goldenberg, RL Hoffman, HJ Cliver, SP TI Neurodevelopmental outcome of small-for-gestational-age infants SO EUROPEAN JOURNAL OF CLINICAL NUTRITION LA English DT Article; Proceedings Paper CT IDECG Workshop on Causes and Consequences of Intrauterine Growth Retardation CY NOV 11-15, 1996 CL BATON ROUGE, LOUISIANA SP Int Dietary Energy Consultancy Grp ID INTRAUTERINE GROWTH-RETARDATION; LOW-BIRTH-WEIGHT; LONG-TERM MORBIDITY; FOLLOW-UP; CEREBRAL-PALSY; BEHAVIORAL-DEVELOPMENT; CHILDREN BORN; PRETERM; METAANALYSIS; ASSOCIATION AB Despite many methodological difficulties, studies evaluating the relationship between being small for gestational age (SGA) at birth and various measures of adverse neurologic outcome generally show significant associations. Nevertheless, cerebral palsy is rarely found in SGA infants. Minimal neurologic dysfunction is more commonly seen in males and lower socioeconomic SGA children, and is often associated with attention deficits, hyperactivity, clumsiness, and poor school performance. Vision and hearing are generally not disturbed in SGA infants. C1 Univ Alabama, Birmingham, AL 35294 USA. Natl Inst Deafness & Commun Disorders, Epidemiol Stat & Data Syst Branch, NIH, Bethesda, MD 20892 USA. RP Goldenberg, RL (reprint author), Univ Alabama, 618 S 20th St,OHB 560, Birmingham, AL 35294 USA. NR 43 TC 52 Z9 52 U1 1 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0954-3007 J9 EUR J CLIN NUTR JI Eur. J. Clin. Nutr. PD JAN PY 1998 VL 52 SU 1 BP S54 EP S58 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA ZC415 UT WOS:000072575700009 PM 9511020 ER PT J AU Moyo, VM Makunike, R Gangaidzo, IT Gordeuk, VR McLaren, CE Khumalo, H Saungweme, T Rouault, T Kiire, CF AF Moyo, VM Makunike, R Gangaidzo, IT Gordeuk, VR McLaren, CE Khumalo, H Saungweme, T Rouault, T Kiire, CF TI African iron overload and hepatocellular carcinoma (HA-7-0-080) SO EUROPEAN JOURNAL OF HAEMATOLOGY LA English DT Article DE iron overload; hepatocellular carcinoma; Africa ID HEPATITIS-B VIRUS; ALCOHOLIC LIVER-DISEASE; BLACKS; HEMOCHROMATOSIS; HEREDITARY; INFECTION; AFLATOXIN; HEPATOMA; RISK AB Although HLA-linked hemochromatosis greatly increases the risk for hepatocellular carcinoma in people of European ancestry, iron overload in Africa is not thought to be etiologically related to this malignancy, To determine if African iron overload may be associated with hepatocellular carcinoma, we reviewed 320 consecutive diagnostic liver biopsies processed at the University of Zimbabwe from 1992 to 1994 and we selected for analysis 215 biopsies from adults that were suitable for the histological assessment of hepatocellular iron. Subjects were stratified according to hepatocellular iron grades of 0-2+ (normal levels to mild siderosis; n=183) and grades of 3+ and 4+ (distinctly elevated levels consistent with iron overload; n=32). Thirty-six subjects had hepatocellular carcinoma. Logistic regression modeling revealed a significant association between iron overload and hepatocellular carcinoma after adjustment for age, sex and and the presence of portal fibrosis or cirrhosis (p=0.041). The odds of hepatocellular carcinoma in subjects with iron overload was 3.1 (95% confidence interval of 1.05-9.4) times that of subjects without iron overload, While we could not test for exposure to viral hepatitis or to aflatoxins in this study, our findings suggest that iron overload may be a risk factor for hepatocellular carcinoma in Africa. C1 Univ Zimbabwe, Dept Med, Sch Med, Harare, Zimbabwe. Univ Zimbabwe, Dept Pathol, Sch Med, Harare, Zimbabwe. Univ Zimbabwe, Clin Epidemiol Unit, Sch Med, Harare, Zimbabwe. George Washington Univ, Med Ctr, Dept Med, Washington, DC 20037 USA. Moorhead State Univ, Dept Math, Moorhead, MN 56560 USA. NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. Ormskirk & Dist Gen Hosp, Ormskirk, Lancs, England. RP Gangaidzo, IT (reprint author), Univ Zimbabwe, Dept Med, Sch Med, POB A178, Harare, Zimbabwe. FU NICHD NIH HHS [1-HD 3-3196] NR 51 TC 32 Z9 33 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-4441 J9 EUR J HAEMATOL JI Eur. J. Haematol. PD JAN PY 1998 VL 60 IS 1 BP 28 EP 34 PG 7 WC Hematology SC Hematology GA YT118 UT WOS:000071566400005 PM 9451425 ER PT J AU Ried, T AF Ried, T TI Analysis of chromosomal aberrations by spectral karyotyping SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PY 1998 VL 6 SU 1 MA PL26 BP 26 EP 27 PG 2 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA ZX500 UT WOS:000074522800024 ER PT J AU Van Hauwe, P Everett, L Coucke, P Chen, A Ris, C Bolder, C Otten, B de Vijlder, J Smith, RJH Willems, PJ Cremers, CWRJ Green, ED Van Camp, G AF Van Hauwe, P Everett, L Coucke, P Chen, A Ris, C Bolder, C Otten, B de Vijlder, J Smith, RJH Willems, PJ Cremers, CWRJ Green, ED Van Camp, G TI Identification of 10 novel mutations in the PDS gene responsible for Pendred syndrome SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Antwerp, Dept Med Genet, B-2020 Antwerp, Belgium. Natl Human Genome Res Inst, NIH, Genome Technol Branch, Bethesda, MD 20892 USA. Univ Iowa, Dept Otolaryngol, Iowa City, IA 52242 USA. Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands. Univ Nijmegen Hosp, Dept Otolaryngol, NL-6500 HB Nijmegen, Netherlands. RI Cremers, C.W.R.J./L-4254-2015; Otten, B.J./L-4562-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PY 1998 VL 6 SU 1 MA C205 BP 35 EP 35 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA ZX500 UT WOS:000074522800060 ER PT J AU Forlino, A Porter, FD Marini, JC AF Forlino, A Porter, FD Marini, JC TI Osteogenesis imperfecta murine models: Use of the cre/lox recombination system to create the first knock-in OI mouse SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NICHD, NIH, Heritable Disorders Branch, Bethesda, MD 20892 USA. RI Forlino, Antonella/H-5385-2015 OI Forlino, Antonella/0000-0002-6385-1182 NR 0 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PY 1998 VL 6 SU 1 MA C803 BP 42 EP 42 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA ZX500 UT WOS:000074522800092 ER PT J AU Philibert, RA Horelli-Kuitunen, N Robb, AS Lee, YH Long, RT Damschroder-Williams, P Martin, BM Brennan, MB Palotie, A Ginns, EI AF Philibert, RA Horelli-Kuitunen, N Robb, AS Lee, YH Long, RT Damschroder-Williams, P Martin, BM Brennan, MB Palotie, A Ginns, EI TI The characterization and sequence analysis of thirty CTG-repeat containing genomic cosmid clones SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE trinucleotide repeat; cosmid; fluorescent in situ hybridization (FISH); sequence analysis ID FLUORESCENCE INSITU HYBRIDIZATION; TRINUCLEOTIDE REPEATS; CHROMOSOMAL ASSIGNMENT; MYOTONIC-DYSTROPHY; GENES; LIBRARIES; EXPRESSION; SELECTION; CLONING; MARKERS AB We have systematically isolated and characterized DNA containing large CTG (n>7) repeats from a human cosmid genomic DNA library. Using a CTG,, probe, more than 100 cosmid clones were identified, and 30 of these have been extensively characterized. The sequenced cosmids contain repeats that are between three and 19 perfect units (average 10 perfect repeats). The cosmids map to at least 12 different chromosomes. Sequence analysis of flanking regions suggests that more than one third of the repeats occur in exons, and many share strong sequence identity with databank sequences, including the gene involved in dentatorubral pallidoluysian atrophy (DRPLA). Genotyping of human DNA samples demonstrates that more than half of the repeats are polymorphic. This and similar collections of clones containing trinucleotide repeats should aid in the identification of genes that may contain expansions of trinucleotide repeats involved in human disease. C1 NIMH, Clin Neurosci Branch, NIH, Bethesda, MD 20892 USA. Univ Helsinki, Cent Hosp, Dept Clin Chem, Mol Genet Lab, Helsinki, Finland. RP Philibert, RA (reprint author), NIMH, Clin Neurosci Branch, NIH, Bldg 49,Room B1EE16,49 Convent Dr,MSC 4405, Bethesda, MD 20892 USA. NR 29 TC 8 Z9 8 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PD JAN PY 1998 VL 6 IS 1 BP 89 EP 94 DI 10.1038/sj.ejhg.5200157 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA ZN751 UT WOS:000073678500012 PM 9781019 ER PT J AU Slavotinek, A Rosenberg, M Knight, S Fergusson, W Gaunt, L Clayton-Smith, J Kingston, H Flint, J Biesecker, L Donnai, D AF Slavotinek, A Rosenberg, M Knight, S Fergusson, W Gaunt, L Clayton-Smith, J Kingston, H Flint, J Biesecker, L Donnai, D TI The detection of submicroscopic chromosome rearrangements in children with idiopathic mental retardation and physical differences SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 St Marys Hosp, Univ Dept Med Genet, Manchester M13 0JH, Lancs, England. St Marys Hosp, Reg Genet Serv, Manchester M13 0JH, Lancs, England. Natl Human Genome Res Inst, NIH, Bethesda, MD 20892 USA. John Radcliffe Hosp, Inst Mol Med, Oxford OX3 9DU, England. NR 0 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PY 1998 VL 6 SU 1 MA P2079 BP 91 EP 91 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA ZX500 UT WOS:000074522800359 ER PT J AU Avela, K Paavola, P Horelli-Kuitunen, N Barlund, M Kallioniemi, A de la Chapelle, A Palotie, A Lehesjoki, AE Peltonen, L AF Avela, K Paavola, P Horelli-Kuitunen, N Barlund, M Kallioniemi, A de la Chapelle, A Palotie, A Lehesjoki, AE Peltonen, L TI Construction of a physical map in the Meckel syndrome and Mulibrey Nanism critical region on chromosome 17q22 SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Helsinki, Dept Med Genet, Haartman Inst, FIN-00014 Helsinki, Finland. Natl Publ Hlth Inst, Dept Human Mol Genet, Helsinki, Finland. Folkhalsan Inst Genet, Helsinki, Finland. Univ Helsinki, Dept Clin Chem, FIN-00014 Helsinki, Finland. NIH, Dept Clin Chem, Canc Genet Lab, Bethesda, MD 20892 USA. Ohio State Univ, Ctr Comprehens Canc, Dept Clin Chem, Columbus, OH 43210 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PY 1998 VL 6 SU 1 MA P4100 BP 133 EP 133 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA ZX500 UT WOS:000074522800577 ER PT J AU Mittaz, L Roessler, E Scott, HS Rossier, C Guipponi, M Antonarakis, SE Muenke, M AF Mittaz, L Roessler, E Scott, HS Rossier, C Guipponi, M Antonarakis, SE Muenke, M TI Structure of the human lanosterol synthase gene and its analysis as a candidate for holoprosencephaly SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Ctr Med Univ Geneva, Div Med Genet, CH-1211 Geneva 4, Switzerland. NHGRI, NIH, Med Genet Branch, Bethesda, MD 20892 USA. RI Antonarakis, Stylianos/N-8866-2014 OI Antonarakis, Stylianos/0000-0001-8907-5823 NR 0 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PY 1998 VL 6 SU 1 MA P4246 BP 162 EP 162 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA ZX500 UT WOS:000074522800724 ER PT J AU Donkor, IO Abdel-Ghany, YS Kador, PF Mizoguchi, T Bartoszko-Malik, A Miller, DD AF Donkor, IO Abdel-Ghany, YS Kador, PF Mizoguchi, T Bartoszko-Malik, A Miller, DD TI Synthesis and biological activities of aldose reductase inhibitors bearing acyl benzenesulfonamides as carboxylic acid surrogates SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article DE aldose reductase inhibitor; diabetic complication; carboxylic acid surrogate; acyl benzenesulfonamide; alrestatin ID HUMAN PSOAS MUSCLE; DIABETIC COMPLICATIONS; ALDEHYDE REDUCTASE; SITE; IDENTIFICATION; ZOPOLRESTAT; DRUGS AB We have synthesized alrestatin derivatives 1 - 11 possessing acyl benzenesulfonamide groups as surrogates for the carboxylic acid moiety of alrestatin. Most of the compounds were inactive as aldose reductase inhibitors compared to alrestatin, however, some of them demonstrated selectivity towards inhibition of rat kidney aldehyde reductase compared to rat lens aldose reductase suggesting that structural differences may exist between the carboxylic acid binding domains of these closely related enzymes. The chemoreactive derivatives 9 and 10 suggested the presence of a nucleophile(s) at the carboxylic acid binding site on aldose reductase. (C) Elsevier, Paris. C1 Univ Tennessee, Ctr Hlth Sci, Dept Pharmaceut Sci, Memphis, TN 38163 USA. Ohio State Univ, Coll Pharm, Div Med Chem & Nat Prod, Columbus, OH 43210 USA. NEI, Lab Ocular Therapeut, NIH, Bethesda, MD 20892 USA. RP Miller, DD (reprint author), Univ Tennessee, Ctr Hlth Sci, Dept Pharmaceut Sci, Memphis, TN 38163 USA. NR 24 TC 10 Z9 10 U1 0 U2 1 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0223-5234 J9 EUR J MED CHEM JI Eur. J. Med. Chem. PD JAN PY 1998 VL 33 IS 1 BP 15 EP 22 DI 10.1016/S0223-5234(99)80071-3 PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA YZ908 UT WOS:000072306600002 ER PT J AU D'Olhaberriague, L Horoupian, D Wenning, GK Litvan, I AF D'Olhaberriague, L Horoupian, D Wenning, GK Litvan, I TI Limb shaking in multiple system atrophy SO EUROPEAN JOURNAL OF NEUROLOGY LA English DT Article DE limb shaking; multiple system atrophy; transient ischemic attack; orthostatic hypotension ID CEREBRAL-ISCHEMIA; HYPOTENSION; ATTACKS AB Limb shaking is a form of carotid transient ischemic attack caused by hemodynamic ischemia not usually triggered by orthostatic hypotension. We report a patient who presented with limb shaking during episodes of severe arterial hypotension in the setting of multiple system atrophy. Extreme orthostatic hypotension may result in limb shaking even in absence of relevant arterial occlusive disease. C1 NINDS, Neuroepidemiol Branch, NIH, Bethesda, MD 20892 USA. Stanford Univ, Dept Pathol Neuropathol, Stanford, CA 94305 USA. Univ Innsbruck, Dept Neurol, A-6020 Innsbruck, Austria. RP Litvan, I (reprint author), NINDS, Neuroepidemiol Branch, NIH, NIH Fed Bldg,Room 714, Bethesda, MD 20892 USA. OI Litvan, Irene/0000-0002-3485-3445 NR 26 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1351-5101 J9 EUR J NEUROL JI Eur. J. Neurol. PD JAN PY 1998 VL 5 IS 1 BP 113 EP 115 DI 10.1046/j.1468-1331.1998.510113.x PG 3 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA YU338 UT WOS:000071707300019 ER PT J AU Richmond, BJ AF Richmond, BJ TI Dynamic aspects of neuronal codes in the visual system: Clues about cortical organization SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 NIMH, Neuropsychol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 4403 BP 109 EP 109 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749400636 ER PT J AU Rohrenbeckl, AM Bettel, M Hooper, DC Nyberg, F Eiden, LE Dietzschold, B Weihel, E AF Rohrenbeckl, AM Bettel, M Hooper, DC Nyberg, F Eiden, LE Dietzschold, B Weihel, E TI Induction of COX-2 and CGRP expression in the brain of Borna disease virus infected rats; Its possible role in CNS inflammation SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 Univ Marburg, Inst Anat & Cell Biol, D-35032 Marburg, Germany. Thomas Jefferson Univ, Ctr Neurovirol, Philadelphia, PA 19107 USA. Univ Uppsala, Biomed Ctr, S-75105 Uppsala, Sweden. NIMH, Mol Neurosci Sect, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 6111 BP 166 EP 166 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749400961 ER PT J AU Eybalin, M Renard, N Lautredou-Audouv, N Safieddine, S AF Eybalin, M Renard, N Lautredou-Audouv, N Safieddine, S TI SNARE protein immunolocalization at the four types of synapse of the organ of Corti. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 INSERM, U254, F-34295 Montpellier 5, France. CRIC, F-34093 Montpellier, France. NIDCD, SNRB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 6207 BP 170 EP 170 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749400987 ER PT J AU Takemura, A Inoue, Y Kawano, K Miles, FA AF Takemura, A Inoue, Y Kawano, K Miles, FA TI Neuronal activity in medial superior temporal area of alert monkeys associated with ultra short latency disparity vergence. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 Electrotech Lab, Neurosci Sect, Ibaraki 305, Japan. NEI, Sensorimotor Res Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 6618 BP 190 EP 190 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401108 ER PT J AU Stanley, EF Sun, XP Haydon, PG Mirotznik, RR Sheng, ZH Tozer, K AF Stanley, EF Sun, XP Haydon, PG Mirotznik, RR Sheng, ZH Tozer, K TI Chick ciliary ganglion calyx synapse: A role model for vertebrate presynaptic calcium channel function. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 NINCDS, Synapt Mechanisms Sect, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 7604 BP 209 EP 209 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401216 ER PT J AU Lanuza, MA Davenport, R Snyder, E Jia, M Li, MX Kim, S Dunlap, V Nelson, PG AF Lanuza, MA Davenport, R Snyder, E Jia, M Li, MX Kim, S Dunlap, V Nelson, PG TI Mechanisms of synapse elimination at the neuromuscular function in vitro. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 NICHHD, Dev Neurobiol Lab, Bethesda, MD 20892 USA. Univ Rovira & Virgili, Fac Med & Ciencies Salut, Unitat Histol & Neurobiol, Reus 43201, Spain. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 8906 BP 219 EP 219 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401275 ER PT J AU White, IM Wise, SP AF White, IM Wise, SP TI Rule-dependent activity in the monkey prefrontal cortex. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 NIMH, Lab Sys Neurosci, Poolesville, MD 20837 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 9603 BP 249 EP 249 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401450 ER PT J AU Anlauf, M Schafer, MKH Eiden, LE Rothmund, M Eissele, R Arnold, R Weihe, E AF Anlauf, M Schafer, MKH Eiden, LE Rothmund, M Eissele, R Arnold, R Weihe, E TI Vipergic, cholinergic & monoaminergic neurotransmission in human gut: How are they related? SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 Univ Marburg, Dept Anat & Cell Biol, D-3550 Marburg, Germany. Univ Marburg, Dept Surg, D-3550 Marburg, Germany. Univ Marburg, Dept Gastroenterol, D-3550 Marburg, Germany. NIMH, Mol Neurosci Sect, Cell Biol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 11303 BP 285 EP 285 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401647 ER PT J AU Sheng, ZH AF Sheng, ZH TI Specific binding of transmitter release site-associated proteins to the calcium channel. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 NINDS, Synapt Funct Unit, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 12504 BP 320 EP 320 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401853 ER PT J AU Shen, L Pichel, JG Mayeli, T Westphal, H AF Shen, L Pichel, JG Mayeli, T Westphal, H TI GDNF mutant mice and Hirschsprung's disease SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 NICHD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 12603 BP 321 EP 321 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401854 ER PT J AU Brustle, O Jones, KN Karram, K Learish, R Duncan, I McKay, RDG AF Brustle, O Jones, KN Karram, K Learish, R Duncan, I McKay, RDG TI In vitro generation of oligodendrocytes from embryonic stem cells. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 Univ Bonn, Inst Neuropathol, Med Ctr, D-5300 Bonn, Germany. NINDS, LMB, NIH, Bethesda, MD 20892 USA. Univ Wisconsin, Sch Vet Med, Madison, WI 53706 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 13902 BP 329 EP 329 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401904 ER PT J AU Kastner, S De Weerd, P Georgopoulos, MA Desimone, R Ungerleider, LG AF Kastner, S De Weerd, P Georgopoulos, MA Desimone, R Ungerleider, LG TI Mechanisms of spatial attention in human extrastriate cortex as revealed by functional MRI. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 NIMH, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 14104 BP 331 EP 331 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749401915 ER PT J AU Serafini, R Maric, D Maric, I Ma, W Fritschy, JM Zhang, L Barker, JL AF Serafini, R Maric, D Maric, I Ma, W Fritschy, JM Zhang, L Barker, JL TI Dominant GABA(A) receptor/Cl- channel kinetics correlate with the relative expressions of alpha(2),alpha(3),alpha(5) and beta(3) subunits in embryonic rat neurones SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE FACS analysis; fluctuation analysis; in situ hybridization; immunocytochemistry ID MESSENGER-RNAS; SPINAL-CORD; POSTNATAL-DEVELOPMENT; CL CHANNELS; BRAIN; FLUCTUATIONS; SUBTYPES AB The embryonic appearance of GABAergic cells and signals in the rat nervous system coincides with the appearance of transcripts encoding some but not all of the subunits forming GABA(A) receptor/Cl- channels. Quantitative in situ hybridization studies reveal higher variabilities in alpha(2) and alpha(3) subunit transcripts relative to others examined (alpha(5), beta(2), beta(3) and gamma(2)) in six spinal and supraspinal regions. Immunocytochemistry of cells dissociated from the embryonic CNS shows that alpha(2) and alpha 3 subunits are detectable in differentiating neurones. FAGS analyses of dissociated cells immunostained with alpha(2)- -or alpha(3)-antibodies reveal immunopositive subpopulations of variable size in each region. Whole-cell recordings of acutely adherent neurones show that GABA activates Cl- currents whose fluctuations characteristically vary depending on a neurone's region of origin. Spectral analyses indicate a predominance of the low frequency (< 5 Hz) components, which vary regionally. Regression analyses reveal that (i) channel properties correlate with subunit transcript levels and (ii) dominant channel kinetics correlate with alpha(2) and alpha(3) subunit transcripts indexed as a ratio and with coexpressions of alpha(5) and beta(3). The correlations strongly suggest that alpha(3) subunits in embryonic neurones are expressed in native receptor/channel complexes with slower kinetics than those containing alpha(2) without alpha 3 subunits, Thus, GABA(A) receptor/Cl- channels in these embryonic neurones may be encoded by the six transcripts (alpha(2), alpha(3), alpha(5), and beta(2), beta(3), and gamma(2)) with proportions of alpha 2, alpha(3), alpha(5), and beta(3) subunits critical in determining their dominant kinetics. C1 NINDS, Neurophysiol Lab, NIH, Bethesda, MD 20892 USA. Univ Zurich, Inst Pharmacol, CH-8006 Zurich, Switzerland. NIMH, Biol Psychiat Branch, NIH, Bethesda, MD 20892 USA. RP Barker, JL (reprint author), NINDS, Neurophysiol Lab, NIH, Bldg 36,Room 2C-02, Bethesda, MD 20892 USA. EM jlbarker@codon.nih.gov NR 25 TC 25 Z9 25 U1 1 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PD JAN PY 1998 VL 10 IS 1 BP 334 EP 349 PG 16 WC Neurosciences SC Neurosciences & Neurology GA YR356 UT WOS:000071487200036 PM 9753142 ER PT J AU Castel, M Cohen, S Jeong, SW Zhang, BJ Fields, R Paras, P Arnheiter, H Chin, H Gainer, H AF Castel, M Cohen, S Jeong, SW Zhang, BJ Fields, R Paras, P Arnheiter, H Chin, H Gainer, H TI Immuno-localization of cat reporter protein expressed from oxytocin and vasopressin gene promoter driven-constructs in transgenic mice. SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 Hebrew Univ Jerusalem, IL-91905 Jerusalem, Israel. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1998 VL 10 SU 10 MA 17101 BP 392 EP 392 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZZ630 UT WOS:000074749402257 ER PT J AU D'Souza, RN Cavender, A Dickinson, D Roberts, A Letterio, J AF D'Souza, RN Cavender, A Dickinson, D Roberts, A Letterio, J TI TGF-beta 1 is essential for the homeostasis of the dentin-pulp complex SO EUROPEAN JOURNAL OF ORAL SCIENCES LA English DT Article; Proceedings Paper CT VIth International Conference on Tooth Morphogenesis and Differentiation CY JUN 11-15, 1997 CL GOTHENBURG, SWEDEN SP Bergstrom Instrument, Nikon, Biora, Boehringer Mannheim Biochem, City Goteborg, European COST Act B8, Odontogenesis, European J Oral Sci, Goteborg Univ, Fac Odontol, Life Technol, MedProbe, Munksgaard Forlag, Swedish Med Ref Council, Swedish Natl Board Ind & Tech Dev DE dentin; inflammation; mineralization; pulp; transforming growth factor beta ID TRANSFORMING GROWTH FACTOR-BETA-1; EXPRESSION; MOUSE; PATTERNS; INVITRO; MOLARS; PALATE AB Among the complex network of cytokines that influence odontoblast function during development and repair. TGF-beta 1 is unique in its dual abilities to function as a potent immunosuppressant and as an inducer of extracellular matrix production. These properties underscore the importance of this molecule in maintaining the homeostasis of the dentin-pulp complex after injury. The purpose of this paper is to describe new findings of our phenotypic analysis of dentition in mice in which the TGF-beta 1 gene has been disrupted. The major phenotype of TGF-beta 1(-/-) offspring is one of diffuse immune system activation with progressive inflammation; wasting and death. Our studies elf adult TGF-beta 1(-/-) dentition show widespread pulpal and periapical inflammation and necroses. In addition, the coronal surfaces of occluding molars show marked attrition. To determine whether the phenotypic changes in TGF-beta 1(-/-) dentition are directly linked to the loss of TGF-beta 1 rather than the inflammatory process itself, we studied adult dentition in TGF-beta 1(-/-) mice backcrossed into immunodeficient backgrounds. Results of our histopathologic and radiographic analyses show that teeth of TGF-beta 1(-/-) immunodeficient mice retain vitality in pulpal and periapical regions but show excessive wear of occlusal surfaces. C1 Univ Texas, Hlth Sci Ctr, Dent Branch, Dept Basic Sci, Houston, TX 77030 USA. NCI, Chemoprevent Lab, NIH, Bethesda, MD 20892 USA. RP D'Souza, RN (reprint author), Univ Texas, Hlth Sci Ctr, Dent Branch, Dept Basic Sci, 6516 John Freeman Ave,Room 4133, Houston, TX 77030 USA. OI D'Souza, Rena/0000-0002-1505-5173 FU NIDCR NIH HHS [DE 10517] NR 14 TC 40 Z9 42 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0909-8836 J9 EUR J ORAL SCI JI Eur. J. Oral Sci. PD JAN PY 1998 VL 106 SU 1 BP 185 EP 191 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZB324 UT WOS:000072459600031 PM 9541224 ER PT J AU Deutsch, D Palmon, A Dafni, L Mao, ZK Leytin, V Young, M Fisher, LW AF Deutsch, D Palmon, A Dafni, L Mao, ZK Leytin, V Young, M Fisher, LW TI Tuftelin - aspects of protein and gene structure SO EUROPEAN JOURNAL OF ORAL SCIENCES LA English DT Article; Proceedings Paper CT VIth International Conference on Tooth Morphogenesis and Differentiation CY JUN 11-15, 1997 CL GOTHENBURG, SWEDEN SP Bergstrom Instrument, Nikon, Biora, Boehringer Mannheim Biochem, City Goteborg, European COST Act B8, Odontogenesis, European J Oral Sci, Goteborg Univ, Fac Odontol, Life Technol, MedProbe, Munksgaard Forlag, Swedish Med Ref Council, Swedish Natl Board Ind & Tech Dev DE alternative splicing; protein gene structure; tuftelin ID LINKED AMELOGENESIS IMPERFECTA; PRIMARY RNA TRANSCRIPT; ENAMELIN TUFTELIN; MOUSE; HETEROGENEITY; AMELOBLASTS; MUTATION; ALBUMIN; AIH1; RAT AB The acidic enamel protein tuftelin has now been cDNA cloned, sequenced and characterized in a number of vertebrate species. Recently, the bovine tuftelin gene structure was elucidated. Cloning of the human tuftelin gene and partial sequencing of a number of exons have also been achieved. Immunologically, the protein has been shown to be conserved throughout 550 million years of vertebrate evolution. The gene has been localized to the long arm of the autosomal chromosome 1. The mapping of the human tuftelin gene to a well-defined cytogenetic region could be important in understanding the etiology of autosomally inherited amelogenesis imperfecta, the most common hereditary disease of enamel. The present paper reviews the primary structure, mRNA/cDNA structure, and gene structure of tuftelin. It describes its immunolocalization at the light microscope level and at the ultrastructural level in both the ameloblast cells and in the extracellular enamel matrix. The timing of tuftelin expression and its possible roles in enamel formation are discussed. C1 Hebrew Univ Jerusalem, Hadassah Fac Dent Med, Dept Oral Biol, Jerusalem, Israel. NIDR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA. RP Deutsch, D (reprint author), Hebrew Univ Jerusalem, Hadassah Fac Dent Med, Dept Oral Biol, POB 1172, Jerusalem, Israel. EM dddan@cc.huji.ac.il NR 46 TC 15 Z9 16 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0909-8836 J9 EUR J ORAL SCI JI Eur. J. Oral Sci. PD JAN PY 1998 VL 106 SU 1 BP 315 EP 323 PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZB324 UT WOS:000072459600049 PM 9541242 ER PT J AU Matthews, G Saklofske, DH Costa, PT Deary, IJ Zeidner, M AF Matthews, G Saklofske, DH Costa, PT Deary, IJ Zeidner, M TI Dimensional models of personality: A framework for systematic clinical assessment SO EUROPEAN JOURNAL OF PSYCHOLOGICAL ASSESSMENT LA English DT Article DE personality; traits; assessment; clinical psychology; psychotherapy ID LIFE ORIENTATION TEST; 5-FACTOR MODEL; MAJOR DEPRESSION; AXIS-I; DISORDERS; NEUROTICISM; ANXIETY; TEMPERAMENT; DIAGNOSIS; OPTIMISM AB Personality research has made considerable progress in developing dimensional models. This article reviews the application of these trait models to clinical theory and practice. Assessment of traits is useful For understanding the individual client, for diagnosis and therapy, and for tailoring the clinical interview to the needs of the patient. Dimensional models have been applied to several areas of pathology. Neuroticism and a variety of other traits are implicated in subclinical stress reactions. At the process level, the effects of traits such as neuroticism may be mediated by maladaptive coping strategies. Traits such as neuroticism may also have a causal effect on more severe mood and anxiety disorders, although ii is likely that there are reciprocal linkages between personality and pathology. As with subclinical stress, traits may influence depression and anxiety through abnormality of cognitive processes, the clinical significance of which should be assessed in the light of the individual's trait characteristics. A further area of application is personality disorder: Dimensional models capture and clarify the principal clinical features of conditions such as schizoid and antisocial disorders, it is concluded that the dimensional approach provides a framework for the systematic understanding of clinical expressions of abnormality in personality and their implications for diagnosis and treatment. C1 Univ Dundee, Dept Psychol, Dundee DD1 4HN, Scotland. Univ Saskatchewan, Saskatoon, SK S7N 0W0, Canada. NIA, Gerontol Res Ctr, NIH, Bethesda, MD 20892 USA. Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland. Univ Haifa, IL-31999 Haifa, Israel. RP Matthews, G (reprint author), Univ Dundee, Dept Psychol, Dundee DD1 4HN, Scotland. RI Deary, Ian/C-6297-2009; OI Costa, Paul/0000-0003-4375-1712 NR 93 TC 14 Z9 14 U1 2 U2 9 PU HOGREFE & HUBER PUBLISHERS PI GOTTINGEN PA ROHNSWEG 25, D-37085 GOTTINGEN, GERMANY SN 1015-5759 J9 EUR J PSYCHOL ASSESS JI Eur. J. Psychol. Assess. PY 1998 VL 14 IS 1 BP 36 EP 49 DI 10.1027/1015-5759.14.1.36 PG 14 WC Psychology, Applied SC Psychology GA ZN162 UT WOS:000073616100005 ER PT J AU Kovacik, V Patoprsty, V Havlicek, V Kovac, P AF Kovacik, V Patoprsty, V Havlicek, V Kovac, P TI Matrix-assisted laser desorption/ionization and electrospray ionization mass spectrometry: sodium-cationized oligosaccharides do not exhibit "internal-residue loss" rearrangement SO EUROPEAN MASS SPECTROMETRY LA English DT Letter DE oligosaccharides; matrix-assisted laser desorption/ionization mass spectrometry; electrospray ionization; internal residue loss; sodium cationized ions ID SPECTRA; SCAN; B/E AB A series of methylgalactotrioses, in which one or two residues were specifically deoxygenated and labeled with a fluorine atom in the C-3 position, were used as models for the study of "internal residue loss" (IRL) under the conditions of matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) and electrospray ionization (ESI) techniques. Under the conditions of measurement of MALDI-TOF post-source decay and ESI in-source decay of methyl oligosaccharides, the IRL rearrangement of [M + Na](+) ions did not take place. C1 Slovak Acad Sci, Inst Chem, Bratislava 84238, Slovakia. Acad Sci Czech Republ, Inst Microbiol, Prague 14220, Czech Republic. NIDDK, NIH, Bethesda, MD 20892 USA. RP Kovacik, V (reprint author), Slovak Acad Sci, Inst Chem, Dubravska Cesta 9, Bratislava 84238, Slovakia. RI Havlicek, Vladimir/H-2626-2014 NR 10 TC 2 Z9 2 U1 0 U2 2 PU IM PUBLICATIONS PI W SUSSEX PA 6 CHARLTON MILL, CHARLTON, CHICHESTER,, W SUSSEX, ENGLAND PO18 0HY SN 1356-1049 J9 EUR MASS SPECTROM JI Eur. Mass Spectrom. PY 1998 VL 4 IS 5 BP 417 EP 420 DI 10.1255/ejms.241 PG 4 WC Physics, Atomic, Molecular & Chemical; Spectroscopy SC Physics; Spectroscopy GA 185KQ UT WOS:000079668500017 ER PT J AU Wassermann, EM AF Wassermann, EM TI Risk and safety of repetitive transcranial magnetic stimulation: report and suggested guidelines from the international workshop on the safety of repetitive transcranial magnetic stimulation, June 5-7, 1996 SO EVOKED POTENTIALS-ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Editorial Material DE magnetics; brain stimulation; safety ID LONG-TERM POTENTIATION; DORSOLATERAL PREFRONTAL CORTEX; LOW-FREQUENCY STIMULATION; TEMPORAL-LOBE EPILEPSY; HUMAN MOTOR CORTEX; ELECTRICAL-STIMULATION; BRAIN-STIMULATION; VISUAL-CORTEX; HEARING-LOSS; NO EVIDENCE AB Single-pulse transcranial magnetic stimulation (TMS) is a safe and useful tool for investigating various aspects of human neurophysiology, particularly corticospinal function. in health and disease. Repetitive TMS (rTMS), however, is a more powerful and potentially dangerous modality, capable of regionally blocking or facilitating cortical processes. Although there is evidence that rTMS is useful for treating clinical depression, and possibly other brain disorders, it had caused 7 known seizures by 1996 and could have other undesirable effects. In June 1996 a workshop was organized to review the available data on the safety of rTMS and to develop guidelines for its safe use. This article summarizes the workshop's deliberations. In addition to issues of risk and safety, it also addresses the principles and applications of rTMS, nomenclature, and potential therapeutic effects of rTMS. The guidelines for the use of rTMS, which are summarized in an appendix, cover the ethical issues, recommended limits on stimulation parameters, monitoring of subjects (both physiologically and neuropsychologically), expertise and function of the rTMS team, medical and psychosocial management of induced seizures, and contraindications to rTMS. (C) 1998 Elsevier Science Ireland Ltd. C1 NINDS, Med Neurol Branch, NIH, Bethesda, MD 20892 USA. RP Wassermann, EM (reprint author), NINDS, Med Neurol Branch, NIH, Bldg 10,Room 5N226,10 Ctr Dr,MSC-1428, Bethesda, MD 20892 USA. EM wassermann@nih.gov NR 88 TC 1179 Z9 1222 U1 5 U2 94 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0168-5597 J9 EVOKED POTENTIAL JI Evoked Potential.-Electroencephalogr. Clin. Neurophysiol. PD JAN PY 1998 VL 108 IS 1 BP 1 EP 16 DI 10.1016/S0168-5597(97)00096-8 PG 16 WC Engineering, Biomedical; Neurosciences SC Engineering; Neurosciences & Neurology GA YW847 UT WOS:000071980000001 PM 9474057 ER PT J AU Aureli, F Smucny, D AF Aureli, F Smucny, D TI New directions in conflict resolution research SO EVOLUTIONARY ANTHROPOLOGY LA English DT News Item ID LONG-TAILED MACAQUES; WILD MOUNTAIN GORILLAS; MACACA-FASCICULARIS; RHESUS-MONKEYS; SOCIAL EVENTS; RECONCILIATION BEHAVIOR; JAPANESE MACAQUES; PIGTAIL MACAQUES; FEMALE BABOONS; VERVET MONKEYS C1 Emory Univ, Yerkes Reg Primate Res Ctr, Atlanta, GA 30322 USA. NICHD, Comparat Ethol Lab, Anim Ctr, NIH, Poolesville, MD 20837 USA. RP Aureli, F (reprint author), Emory Univ, Yerkes Reg Primate Res Ctr, Atlanta, GA 30322 USA. NR 66 TC 5 Z9 5 U1 1 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1060-1538 J9 EVOL ANTHROPOL JI Evol. Anthropol. PY 1998 VL 6 IS 4 BP 115 EP 119 DI 10.1002/(SICI)1520-6505(1998)6:4<115::AID-EVAN1>3.0.CO;2-C PG 5 WC Anthropology SC Anthropology GA ZW255 UT WOS:000074391100001 ER PT J AU O'Brien, SJ AF O'Brien, SJ TI Intersection of population genetics and species conservation - The Cheetah's dilemma SO EVOLUTIONARY BIOLOGY, VOL 30 SE EVOLUTIONARY BIOLOGY LA English DT Review ID NORTH-AMERICAN ZOOS; FREE-RANGING CHEETAHS; ACINONYX-JUBATUS; BIOLOGICAL CONSERVATION; AFRICAN CHEETAH; CONSEQUENCES; BOTTLENECKS; CONTROVERSY; RESPONSES; DIVERSITY C1 NCI, Lab Genom Divers, Frederick, MD 21702 USA. RP O'Brien, SJ (reprint author), NCI, Lab Genom Divers, Frederick, MD 21702 USA. NR 59 TC 1 Z9 1 U1 13 U2 43 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0071-3260 J9 EVOL BIOL PY 1998 VL 30 BP 79 EP 91 PG 13 WC Genetics & Heredity SC Genetics & Heredity GA BK91X UT WOS:000073863000003 ER PT J AU Breidert, M Bottner, A Moller, S Herberg, L Bornstein, S AF Breidert, M Bottner, A Moller, S Herberg, L Bornstein, S TI Apoptosis in the adrenal gland of non-obese diabetic (NOD) mice SO EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES LA English DT Article DE NOD mice; adrenal; apoptosis; immunohistochemistry; electron microscopy; infiltration ID AUTONOMIC NEUROPATHY; AUTOANTIBODIES; MEDULLARY; TYPE-1; MELLITUS; RELEASE; MOUSE; CELLS; RATS AB Apoptosis appears to play an important role in the development of diabetes in the non-obese diabetic (NOD) mouse. Since the autoimmune process leading to the manifestation of insulin dependent diabetes mellitus (IDDM) can also affect the sympathochromaffin system, we analyzed the role of apoptosis and infiltration of the adrenal medulla as features of this autoimmune process in parallel with the development of diabetes. Prediabetic and diabetic NOD mice aged 3 to 30 weeks were studied and compared with control mice. Apoptosis was assessed by in situ end-labeling method and ultrastructural analysis. Adrenals were screened for lymphocytic infiltration by conventional hematoxylin-eosin staining. Chromaffin cells were characterized by immunohistochemical staining against synaptophysin and tyrosine hydroxylase. Apoptotic nuclei were detected in all mice studied at a very low level, mainly occuring within the connective tissue between medulla and cortex. The maximum score was achieved at 3 weeks (1.91 +/- 0.48 apoptotic cells/1000 counted cells; n = 4). There was no significant difference between NOD mice and control mice. No correlation could be found between blood glucose levels and apoptosis. On the ultrastructural level, apoptotic cells presented typical features of apoptosis, i.e. condensed nuclei and cytoplasm. Neither in NOD mice nor in controls lymphocytic infiltration or fibrosis of the adrenal was detected. Even NOD mice with overt diabetes did not exhibit morphological signs of medullitis. In summary, no signs of immune destruction of the adrenal medulla in NOD mice aged 3 to 30 weeks could be detected. C1 Univ Dresden, Dept Internal Med 1, D-01307 Dresden, Germany. Univ Dusseldorf, Diabet Res Inst, D-4000 Dusseldorf, Germany. Univ Leipzig, Dept Internal Med 3, Leipzig, Germany. NICHD, Dev Endocrinol Branch, NIH, Ctr Clin, Bethesda, MD USA. RP Breidert, M (reprint author), Univ Dresden, Dept Internal Med 1, Fetscherstr 74, D-01307 Dresden, Germany. RI Korner, Antje/B-3988-2015 OI Korner, Antje/0000-0001-6001-0356 NR 17 TC 4 Z9 4 U1 0 U2 0 PU JOHANN AMBROSIUS BARTH VERLAG PI HEIDELBERG PA IM WEIHER 10, D-69121 HEIDELBERG, GERMANY SN 0947-7349 J9 EXP CLIN ENDOCR DIAB JI Exp. Clin. Endocrinol. Diabet. PY 1998 VL 106 IS 6 BP 478 EP 483 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 153GE UT WOS:000077823900008 PM 10079028 ER PT J AU Kastner, S Demmer, I Ziemann, U AF Kastner, S Demmer, I Ziemann, U TI Transient visual field defects induced by transcranial magnetic stimulation over human occipital pole SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE visual system; transcranial magnetic brain stimulation; visual field defect; phosphenes; human ID HUMAN CEREBRAL-CORTEX; HUMAN MOTOR CORTEX; STRIATE CORTEX; RETINOTOPIC ORGANIZATION; ELECTRICAL-STIMULATION; SOMATOSENSORY STIMULI; COIL STIMULATION; PERCEPTION; SUPPRESSION; EXCITATION AB Transient visual field defects (VFDs) and phosphenes were induced in normal volunteers by means of transcranial magnetic stimulation (TMS) using a circular magnetic coil of 12.5 cm diameter placed with its lower rim 2-4 cm above the inion in the midline. Subjects had to detect small, bright dots presented randomly for 14 ms in one of 60 locations on a computer screen resulting in a plot of the central 9 degrees of the visual field. In 8 of 17 subjects, transient VFDs were inducible at peak magnetic field strenghts of 1.1-1.4 T. In the central 1-3 degrees, detection of targets was impaired in both the upper and lower visual field, whereas at 4-9 degrees large parts of only the lower visual field were affected with a sharp cut-off along the horizontal meridian. Targets at 1 degrees in the lower field were affected with lower TMS intensities than corresponding locations in the upper or peripheral locations in the lower field. Detection of central targets was affected at more caudal stimulation sites than detection of peripheral targets. Phosphenes were elicitable in 14 of 17 subjects at clearly lower field strengths of 0.6-1.0 T. Many subjects perceived chromatophosphenes. From a discussion of the literature on patients with VFDs and the known topography of the human visual system, it is concluded that the transient VFDs at 1-3 degrees are probably due to stimulation of both striate cortex (V1) and extrastriate areas (V2/V3), while VFDs in the lower visual field at eccentricities 4-9 degrees are due to stimulation of V2/V3 but not V1. C1 Univ Gottingen, Dept Psychiat, D-37075 Gottingen, Germany. Univ Gottingen, Dept Clin Neurophysiol, D-37075 Gottingen, Germany. RP Kastner, S (reprint author), NIMH, Lab Brain & Cognit, Bldg 49,Room 1B80, Bethesda, MD 20892 USA. NR 39 TC 92 Z9 92 U1 1 U2 4 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PD JAN PY 1998 VL 118 IS 1 BP 19 EP 26 DI 10.1007/s002210050251 PG 8 WC Neurosciences SC Neurosciences & Neurology GA YT857 UT WOS:000071652000003 PM 9547074 ER PT J AU Peacock, J Jones, T Tock, C Lutz, R AF Peacock, J Jones, T Tock, C Lutz, R TI The onset of turbulence in physiological pulsatile flow in a straight tube SO EXPERIMENTS IN FLUIDS LA English DT Article ID OSCILLATORY PIPE-FLOW; TRANSITION AB An empirical correlation for the onset of turbulence in physiological pulsatile flow is presented. We pumped three different test fluids of kinematic viscosity 0.008-0.035 cm(2)/s through four straight tubes 0.4-3.0 cm in diameter. A Scotch yoke mechanism provided an oscillatory sine wave how component of known stroke volume and frequency. We adjusted the mean flow independently until we detected signal instabilities from hot film wall shear stress probes. The critical peak Reynolds number was found to correlate with the Womersley parameter and the Strouhal number as a power law function with a root-mean-square (rms) error of 15.2%. Experimental measurements of the laminar velocity profile are compared to theoretical predictions from Poiseuille's law and Womersley's solution. C1 NIH, Bethesda, MD 20892 USA. RP Lutz, R (reprint author), NIH, Bldg 13,Room 3N17,13 South Dr,MSC 5766, Bethesda, MD 20892 USA. NR 32 TC 31 Z9 31 U1 1 U2 7 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0723-4864 J9 EXP FLUIDS JI Exp. Fluids PD JAN PY 1998 VL 24 IS 1 BP 1 EP 9 DI 10.1007/s003480050144 PG 9 WC Engineering, Mechanical; Mechanics SC Engineering; Mechanics GA YV710 UT WOS:000071855000001 ER PT B AU Lamb, ME Leyendecker, B Scholmerich, A Fracasso, MP AF Lamb, ME Leyendecker, B Scholmerich, A Fracasso, MP BE Lewis, M Feiring, C TI Everyday experiences of infants in Euro-American and Central American immigrant families SO FAMILIES, RISK, AND COMPETENCE LA English DT Proceedings Paper CT 6th Annual Conference of the Center-for-Human-Development-and-Developmental-Disabilities on Stress and Soothing CY MAY 03-05, 1996 CL UNIV MED & DENT NEW JERSEY, R W JOHNSON MED SCH, NEW BRUNSWICK, NJ SP Univ Med Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pediat, Ctr Human Dev & Dev Disabilities, State New Jersey, Dept Human Serv, Off Prevent Mental Retardat & Dev Disabilities HO UNIV MED & DENT NEW JERSEY, R W JOHNSON MED SCH C1 NICHHD, Bethesda, MD 20892 USA. RI Schoelmerich, Axel/C-9039-2009 OI Schoelmerich, Axel/0000-0002-9844-3920 NR 0 TC 5 Z9 5 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC PUBL PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430 USA BN 0-8058-2344-1 PY 1998 BP 113 EP 131 PG 19 WC Family Studies; Psychology, Developmental SC Family Studies; Psychology GA BL27H UT WOS:000074960400006 ER PT B AU Dawud-Noursi, S Lamb, ME Sternberg, KJ AF Dawud-Noursi, S Lamb, ME Sternberg, KJ BE Lewis, M Feiring, C TI The relations among domestic violence, peer relationships, and academic performance SO FAMILIES, RISK, AND COMPETENCE LA English DT Proceedings Paper CT 6th Annual Conference of the Center-for-Human-Development-and-Developmental-Disabilities on Stress and Soothing CY MAY 03-05, 1996 CL UNIV MED & DENT NEW JERSEY, R W JOHNSON MED SCH, NEW BRUNSWICK, NJ SP Univ Med Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pediat, Ctr Human Dev & Dev Disabilities, State New Jersey, Dept Human Serv, Off Prevent Mental Retardat & Dev Disabilities HO UNIV MED & DENT NEW JERSEY, R W JOHNSON MED SCH C1 NICHHD, Bethesda, MD 20892 USA. NR 0 TC 6 Z9 6 U1 0 U2 2 PU LAWRENCE ERLBAUM ASSOC PUBL PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430 USA BN 0-8058-2344-1 PY 1998 BP 207 EP 226 PG 20 WC Family Studies; Psychology, Developmental SC Family Studies; Psychology GA BL27H UT WOS:000074960400010 ER PT J AU Akukwe, C AF Akukwe, C TI The potential impact of the 1996 welfare reforms on intimate partner violence SO FAMILY & COMMUNITY HEALTH LA English DT Article DE children; community; intimate partner violence; low income; prevention; public and private partnerships; women ID WOMEN AB Intimate partner violence harms millions of women with devastating physical and mental health consequences for them and their children. Low-income women and children are at high risk. The recent welfare legislation with strict work requirements and optional family violence provisions could make many victims choose to stay with their abusers with devastating consequences. This article argues that intimate partner violence extends beyond the current welfare debate and will require careful strategic approaches and partnerships to contain the problem. Durable public, community, and private partnerships at local, state, and national levels are critical to ending this shameful epidemic. C1 NIH, Dist Columbia Initiat Reduce Infant Mortal, Off Maternal & Child Hlth, Washington, DC USA. RP Akukwe, C (reprint author), NIH, Dist Columbia Initiat Reduce Infant Mortal, Off Maternal & Child Hlth, Washington, DC USA. NR 21 TC 1 Z9 1 U1 0 U2 2 PU ASPEN PUBL INC PI FREDERICK PA 7201 MCKINNEY CIRCLE, FREDERICK, MD 21704 USA SN 0160-6379 J9 FAM COMMUNITY HEALTH JI Fam. Community Health PD JAN PY 1998 VL 20 IS 4 BP 54 EP 62 PG 9 WC Family Studies; Public, Environmental & Occupational Health SC Family Studies; Public, Environmental & Occupational Health GA YM064 UT WOS:000071024300006 ER PT J AU Bezrukov, SM Rand, RP Vodyanoy, I Parsegian, VA AF Bezrukov, SM Rand, RP Vodyanoy, I Parsegian, VA TI Lipid packing stress and polypeptide aggregation: alamethicin channel probed by proton titration of lipid charge SO FARADAY DISCUSSIONS LA English DT Article ID LAMELLAR FORMING LIPIDS; GRAMICIDIN CHANNELS; PROTEIN FUNCTION; SURFACE-CHARGE; ION CHANNELS; MEMBRANE; CONDUCTANCE; MODEL; MODULATION; BILAYERS AB Lipid membranes are not passive, neutral scaffolds to hold membrane proteins. In order to examine the influence of lipid packing energetics on ion channel expression, we study the relative probabilities of alamethicin channel formation in dioleoylphosphatidylserine (DOPS) bilayers as a function of ph. The rationale for this strategy is our earlier finding that the higher-conductance states, corresponding to larger polypeptide aggregates, are more likely to occur in the presence of lipids prone to hexagonal H-n-phase formation (specifically DOPE), than in the presence of lamellar L-alpha-forming lipids (DOPC). In low ionic strength NaCl solutions at neutral pH, the open channel in DOPS membranes spends most of its time in states of lower conductance and resembles alamethicin channels in DOPC; at lower pH, where the lipid polar groups are neutralized, the channel probability distribution resembles that in DOPE. X-Ray diffraction studies on DOPS show a progressive decrease in the intrinsic curvature of the constituent monolayers as well as a decreased probability of H-II-phase formation when the charged Lipid fraction is increased. We explore how proton titration of DOPS affects lipid packing energetics, and how these energetics couple titration to channel formation. C1 NICHD, NIH, Bethesda, MD 20892 USA. St Petersburg Nucl Phys Inst, Gatchina 188350, Russia. Brock Univ, St Catharines, ON L2S 3A1, Canada. Off Naval Res Europe, London NW1 5TH, England. RP Bezrukov, SM (reprint author), NICHD, NIH, Bethesda, MD 20892 USA. NR 40 TC 43 Z9 44 U1 0 U2 4 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD,, CAMBRIDGE CB4 0WF, CAMBS, ENGLAND SN 0301-7249 J9 FARADAY DISCUSS JI Faraday Discuss. PY 1998 VL 111 BP 173 EP 183 PG 11 WC Chemistry, Physical SC Chemistry GA 208CD UT WOS:000080971900015 PM 10822608 ER PT J AU Gasparini, L Racchi, M Binetti, G Trabucchi, M Solerte, SB Alkon, D Etcheberrigaray, R Gibson, G Blass, J Paoletti, R Govoni, S AF Gasparini, L Racchi, M Binetti, G Trabucchi, M Solerte, SB Alkon, D Etcheberrigaray, R Gibson, G Blass, J Paoletti, R Govoni, S TI Peripheral markers in testing pathophysiological hypotheses and diagnosing Alzheimer's disease SO FASEB JOURNAL LA English DT Review DE peripheral cells; CSF; plasma; diagnosis ID AMYLOID-BETA-PROTEIN; CYTOSOLIC FREE-CALCIUM; CORTICOTROPIN-RELEASING HORMONE; APOLIPOPROTEIN-E EPSILON-4; CULTURED SKIN FIBROBLASTS; KETOGLUTARATE DEHYDROGENASE COMPLEX; CEREBROSPINAL-FLUID CONCENTRATIONS; SOMATOSTATIN-LIKE IMMUNOREACTIVITY; E ALLELE EPSILON-4; KINASE-C ACTIVITY AB Alterations in amyloid precursor protein (APP) metabolism, calcium regulation, oxidative metabolism, and transduction systems have been implicated in Alzheimer's disease (AD). Limitations to the use of postmortem brain for examining molecular mechanisms underscore the need to develop a human tissue model representative of the pathophysiological processes that characterize AD. The use of peripheral tissues, particularly of cultured skin fibroblasts derived from AD patients, could complement studies of autopsy samples and provide a useful tool with which to investigate such dynamic processes as signal transduction systems, ionic homeostasis, oxidative metabolism, and APP processing. Peripheral cells as well as body fluids (i.e., plasma and CSF) could also provide peripheral biological markers for the diagnosis of AD. The criteria required for a definite diagnosis of AD presently include clinical criteria in association with histopathologic evidence obtained from biopsy or autopsy. Thus, the use of peripheral markers as a diagnostic tool, either to predict or at least to confirm a diagnosis, may be of great importance. C1 Univ Milan, Inst Pharmacol Sci, I-20133 Milan, Italy. Alzheimers Dis Unit Sacred Heart Hosp FBF, IRCCS San Giovanni Di Dio, Brescia, Italy. Univ Rome Tor Vergata, Dept Expt Med & Biochem Sci, Rome, Italy. Univ Pavia, Geriatr Clin, Dept Internal Med, I-27100 Pavia, Italy. NINDS, Lab Adapt Syst, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Med Ctr, Inst Cognit & Computat Sci, Washington, DC 20007 USA. Cornell Univ, Coll Med, Burke Med Res Inst, New York, NY 10605 USA. RP Govoni, S (reprint author), Univ Milan, Inst Pharmacol Sci, Via Balzaretti 9, I-20133 Milan, Italy. EM govonis@ipv36.unipv.it RI Govoni, Stefano/K-2965-2015; Gasparini, Laura/G-7711-2011; Binetti, Giuliano/K-4519-2016; OI Govoni, Stefano/0000-0002-7243-6837; Gasparini, Laura/0000-0003-3894-9898; Binetti, Giuliano/0000-0003-2759-5844; Racchi, Marco/0000-0002-7185-7808 NR 210 TC 136 Z9 138 U1 1 U2 6 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN PY 1998 VL 12 IS 1 BP 17 EP 34 PG 18 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA YR723 UT WOS:000071523800003 PM 9438407 ER PT S AU Suh, E Narahari, B Simha, R AF Suh, E Narahari, B Simha, R GP IEEE COMP SOC IEEE COMP SOC TI Dynamic load balancing schemes for computing accessible surface area of protein molecules SO FIFTH INTERNATIONAL CONFERENCE ON HIGH PERFORMANCE COMPUTING, PROCEEDINGS SE PROCEEDINGS - INTERNATIONAL CONFERENCE ON HIGH PERFORMANCE COMPUTING LA English DT Proceedings Paper CT 5th International Conference on High Performance Computing CY DEC 17-20, 1998 CL CHENNAI, INDIA SP IEEE Comp Soc Tech Comm Parallel Proc, ACM SIGARCH, Indian Inst Technol, Chennai, Indian Inst Technol, Software Technol Parks India, Ctr Dev Adv Comp, India, Tata Inst Fundamental Res, India, Supercomp Educ & Res Ctr, India, CSIR Ctr Math Modeling & Comp Simulat, India AB This paper presents an experimental study of dynamic load balancing methods for a parallelized solution to a well-known problem in computational molecular biology: computing the accessible surface areas (ASA) of proteins. The main contribution is a better understanding of how certain techniques for load estimation and re-distribution must be combined carefully for effectiveness and how these combinations need to change during the course of a computation. In particular, the Shrake-Rupley ASA algorithm is implemented and three aspects of dynamic load balancing are studied: (1) how to estimate load imbalance (the estimation problem); (2) when to invoke load redistribution (the invocation problem); and (3) how to load balance (the mapping problem). The results in this paper show that a dynamically-selected mia: of algorithms in each category that adapts to changing structure within the protein works better than a static periodic application of a static mix of algorithms. C1 NIH, Ctr Informat Technol, Bethesda, MD 20892 USA. RP Suh, E (reprint author), NIH, Ctr Informat Technol, Bldg 10, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 USA SN 1094-7256 BN 0-8186-9194-8 J9 P INT C HIGH PERFORM PY 1998 BP 326 EP 333 DI 10.1109/HIPC.1998.738005 PG 8 WC Computer Science, Hardware & Architecture; Computer Science, Information Systems; Computer Science, Software Engineering; Computer Science, Theory & Methods SC Computer Science GA BM05E UT WOS:000077521400042 ER PT J AU Wang, YL Huq, HI de la Cruz, XF Lee, BK AF Wang, YL Huq, HI de la Cruz, XF Lee, BK TI A new procedure for constructing peptides into a given C alpha chain SO FOLDING & DESIGN LA English DT Article DE backbone construction; peptide construction; peptide orientation; protein folding ID PROTEIN STRUCTURES; POLYPEPTIDE BACKBONE; RECONSTRUCTION; CONFORMATIONS; REFINEMENT; RESOLUTION; ALGORITHM; PROGRAM; ENERGY; SET AB Background: In ab initio protein folding studies, it is often advantageous to build the C alpha chain first and then to construct the full structure by filling in the peptide groups and the sidechains, Many algorithms have been reported for constructing peptide groups on the C alpha chain, but most are unsuitable for use in such studies; some are too slow for screening a large number of trial C alpha chains and others use only the local geometry and ignore the effects of specific non-neighbor interactions, which can be crucial for proper folding. We needed a fast procedure for constructing the peptide groups that does not ignore the effects of long-range, specific interactions. Results: We first found rich correlations between the peptide orientation angle and both the local C alpha-chain geometry and the type of the flanking amino acid residues. These correlations can be used to greatly limit the range of possible peptide orientation angles, We devised a simple peptide construction procedure in which all orientations within this reduced range are systematically examined and the orientation is selected that minimizes a suitable energy function that includes long-range, specific interactions. When tested on known structures, the method is found to be among the fastest of known methods and attains an accuracy comparable with or better than most methods. Conclusions: The new method is fast and takes into account both the local and non-local specific interactions. It therefore appears to be suitable for use in ab initio protein folding studies, wherein a large number of C alpha chains are screened. C1 NCI, Mol Biol Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP Lee, BK (reprint author), NCI, Mol Biol Lab, Div Basic Sci, NIH, Bldg 37,Room 4B15,37 Convent Dr MSC 4255, Bethesda, MD 20892 USA. NR 23 TC 103 Z9 103 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON W1P 6LB, ENGLAND SN 1359-0278 J9 FOLD DES JI Fold. Des. PY 1998 VL 3 IS 1 BP 1 EP 10 DI 10.1016/S1359-0278(98)00003-0 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA YX374 UT WOS:000072033800003 PM 9502315 ER PT J AU Xu, D Nussinov, R AF Xu, D Nussinov, R TI Favorable domain size in proteins SO FOLDING & DESIGN LA English DT Article DE domain; entropy; free energy; protein folding; statistical analysis ID CONFORMATIONAL ENTROPY; STABILITY; BACKBONE; REGIONS AB Background: It has been observed that single-domain proteins and domains in multidomain proteins favor a chain length in the range 100-150 amino acids. To understand the origin of the favored size, we construct an empirical function for the free energy of unfolding versus the chain length, The parameters in the function are derived by fitting to the energy of hydration, entropy and enthalpy of unfolding of nine proteins. Our energy function cannot be used to calculate the energetics accurately for individual proteins because the energetics also depend on other factors, such as the composition and the conformation of the protein. Nevertheless, the energy function statistically characterizes the general relationship between the free energy of unfolding and the size of the protein. Results: The predicted optimal number of residues, which corresponds to the maximum free energy of unfolding, is 100. This is in agreement with a statistical analysis of protein domains derived from their experimental structures. When a chain is too short, our energy function indicates that the change in enthalpy of internal interactions is not favorable enough for folding because of the limited number of inter-residue contacts. A long chain is also unfavorable for a single domain because the cost of configurational entropy increases quadratically as a function of the chain length, whereas the favorable change in enthalpy of internal interactions increases linearly. Conclusions: Our study shows that the energetic balance is the dominant factor governing protein sizes and it forces a large protein to break into several domains during folding. C1 NCI, Lab Expt & Computat Biol, IRSP, SAIC Frederick,FCRDC, Frederick, MD 21702 USA. Tel Aviv Univ, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel. RP Nussinov, R (reprint author), NCI, Lab Expt & Computat Biol, IRSP, SAIC Frederick,FCRDC, Frederick, MD 21702 USA. FU NCI NIH HHS [1-CO-74102] NR 28 TC 15 Z9 15 U1 0 U2 6 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON W1P 6LB, ENGLAND SN 1359-0278 J9 FOLD DES JI Fold. Des. PY 1998 VL 3 IS 1 BP 11 EP 17 DI 10.1016/S1359-0278(98)00004-2 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA YX374 UT WOS:000072033800004 PM 9502316 ER PT J AU Chung, MS Neuwald, AF Wilbur, WJ AF Chung, MS Neuwald, AF Wilbur, WJ TI A free energy analysis by unfolding applied to 125-mers on a cubic lattice SO FOLDING & DESIGN LA English DT Article DE free energy analysis; lattice model; metropolis algorithm; protein folding problem; unfolding process ID MOLECULAR-DYNAMICS SIMULATIONS; MONTE-CARLO; MODEL PROTEINS; POLYMER-CHAINS; TRANSITION-STATES; KINETICS; THERMODYNAMICS; HETEROPOLYMERS; PRINCIPLES; RELAXATION AB Background: A common approach to the protein folding problem involves computer simulation of folding using lattice models of amino acid sequences. Key factors for good performance in such models are the correct choice of the temperature and the average interaction energy between residues. In order to push the lattice approach to its limit it is important to have a method to adjust these parameters for optimal folding that is not limited by our ability to successfully simulate folding in a reasonable time. Results: In this study, we adopt a simple cubic-lattice model and present a method for calculating the free energy of a chain as a function of the number of native contacts. This does not require that we are able to fold the sequence by simulation and it provides a method of estimating the folding transition temperature. For a given set of parameters, the free energy analysis also allows an estimate of foldability. By applying the method to sequences with 27 and 125 residues, we show that optimal folding occurs near the folding transition temperature and at either zero or small negative average interaction energy. We find ourselves able to fold only 125-mers that have significant short-range native contacts. Conclusions: A free energy analysis during unfolding is a useful tool for the study of foldability and should be applicable to a variety of folding models. In this way we are able to fold some 125-mer designed sequences and our results confirm the finding that short-range contacts contribute to foldability. C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. RP Wilbur, WJ (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. EM wilbur@ncbi.nlm.nih.gov NR 52 TC 3 Z9 3 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON W1P 6LB, ENGLAND SN 1359-0278 J9 FOLD DES JI Fold. Des. PY 1998 VL 3 IS 1 BP 51 EP 65 DI 10.1016/S1359-0278(98)00008-X PG 15 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA YX374 UT WOS:000072033800008 PM 9502320 ER PT J AU Bychkova, VE Dujsekina, AE Fantuzzi, A Ptitsyn, OB Rossi, GL AF Bychkova, VE Dujsekina, AE Fantuzzi, A Ptitsyn, OB Rossi, GL TI Release of retinol and denaturation of its plasma carrier, retinol-binding protein SO FOLDING & DESIGN LA English DT Article DE intermediate states; molten globule; protein denaturation; retinol-binding protein; retinol release ID MOLTEN-GLOBULE; DIELECTRIC-CONSTANT; BETA-LACTOGLOBULIN; ALPHA-LACTALBUMIN; CYTOCHROME-C; INTERMEDIATE; MEMBRANES; COMPLEX; STATE; CHROMATOGRAPHY AB Background: Retinol is tightly packed inside the structure of its plasma carrier (retinol-binding protein, REP). it was found that retinol release from REP to aqueous solutions is facilitated by either Very low pH or very high temperatures (i.e. by non-physiological conditions that cause protein denaturation). it was also found that alcohols induce protein conformational transitions to denatured states. On this basis, it may be suggested that retinol release in vivo is facilitated by the partial unfolding of the carrier resulting from the concerted action of the moderate local decrease of pH and the moderate local decrease of dielectric constant in proximity to the target membranes. Results: In vitro, at 37 degrees C, retinol is removed from its plasma carrier by the concerted action of the moderately low pH and the moderately low dielectric constant of solutions containing a low ionic strength buffer and methanol in variable proportions. Release of retinol is accompanied by a conformational transition of REP from the native to the molten-globule state. Conclusions: The physiological function of REP - targeted delivery of retinol is mimicked in vitro by the facilitated release of retinol (associated with a partial unfolding of the protein carrier) in solutions exhibiting pH and dielectric constant values that are within the range of Values expected in the in vivo microenvironment. C1 Univ Parma, Inst Biochem Sci, I-43100 Parma, Italy. Russian Acad Sci, Inst Prot Res, Pushchino 142292, Moscow Region, Russia. NCI, Lab Expt & Computat Biol, NIH, Bethesda, MD 20892 USA. RP Rossi, GL (reprint author), Univ Parma, Inst Biochem Sci, I-43100 Parma, Italy. NR 37 TC 25 Z9 27 U1 0 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON W1P 6LB, ENGLAND SN 1359-0278 J9 FOLD DES JI Fold. Des. PY 1998 VL 3 IS 4 BP 285 EP 291 DI 10.1016/S1359-0278(98)00039-X PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 110QD UT WOS:000075391100008 PM 9710574 ER PT J AU Tsai, CJ Xu, D Nussinov, R AF Tsai, CJ Xu, D Nussinov, R TI Protein folding via binding and vice versa SO FOLDING & DESIGN LA English DT Review ID GLOBULAR-PROTEINS; STRUCTURAL MOTIFS; SUBUNIT INTERFACES; COMPACT UNITS; FREE-ENERGY; DATA-BANK; DOMAINS; IDENTIFICATION; RECOGNITION; EQUILIBRIUM AB The terms intermolecular and intramolecular recognition are often used when referring to binding and folding, highlighting the common ground between the two processes. Most studies, however, are aimed at either one process or the other. Here, we show how knowledge from binding can aid in understanding folding and vice versa. C1 NCI, Lab Expt & Computat Biol, SAIC, FCRDC, Frederick, MD 21702 USA. Tel Aviv Univ, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel. RP Nussinov, R (reprint author), NCI, Lab Expt & Computat Biol, SAIC, FCRDC, Bldg 469,Room 151, Frederick, MD 21702 USA. EM ruthn@ncifcrf.gov FU NCI NIH HHS [1-CO-74102] NR 89 TC 49 Z9 50 U1 1 U2 5 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON W1P 6LB, ENGLAND SN 1359-0278 J9 FOLD DES JI Fold. Des. PY 1998 VL 3 IS 4 BP R71 EP R80 DI 10.1016/S1359-0278(98)00032-7 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 110QD UT WOS:000075391100001 PM 9710571 ER PT J AU Baker, PJ Hraba, T AF Baker, PJ Hraba, T TI Fifty years of immunological tolerance SO FOLIA BIOLOGICA LA English DT Editorial Material ID T-CELLS; DELETION; ANTIGEN; INVITRO; INVIVO; ANERGY; MICE C1 Acad Sci Czech Republ, Inst Mol Genet, Prague 6, Czech Republic. NIAID, NIH, Bethesda, MD 20892 USA. RP Hraba, T (reprint author), Acad Sci Czech Republ, Inst Mol Genet, Flemingovo N-2, Prague 6, Czech Republic. NR 45 TC 0 Z9 0 U1 0 U2 1 PU INST MOLECULAR GENETICS PI PRAGUE 6 PA FOLIA BIOLOGICA(PRAHA) FLEMINGOVO N.2, PRAGUE 6, CZECH REPUBLIC 166 37 SN 0015-5500 J9 FOLIA BIOL-PRAGUE JI Folia Biol.-Prague PY 1998 VL 44 IS 6 BP 189 EP 192 PG 4 WC Biochemistry & Molecular Biology; Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Oncology; Cell Biology GA 141NF UT WOS:000077149500001 PM 10730861 ER PT S AU Kidder, LH Levin, IW Lewis, EN AF Kidder, LH Levin, IW Lewis, EN BE deHaseth, JA TI Infrared spectroscopic imaging microscopy: Applications to biological systems SO FOURIER TRANSFORM SPECTROSCOPY SE AIP CONFERENCE PROCEEDINGS LA English DT Proceedings Paper CT 11th International Conference on Fourier Transform Spectroscopy (ICOFTS 11) CY AUG 10-15, 1997 CL ATHENS, GA AB The coupling of imaging modalities with spectroscopic techniques adds additional dimensions to sample analysis in both the spectroscopic and spatial domains. The particular ability of infrared (IR) imaging to explore the spatial distribution of chemically distinct species on length scales ranging from microns to kilometers demonstrates the versatility and diversity of spectroscopic Imaging. In this paper, we focus on the further development of our Fourier-transform (FT) based mid-IR spectroscopic imaging technique which combines the analytical capabilities of mid-IR spectroscopy with the morphological information obtained from optical imaging. The seamless combination of spectroscopy for molecular analysis with the power of visualization represents the future of infrared microscopy. Our spectroscopic imaging instrument integrates several infrared focal-plane arrays with a Michelson step-scan interferometer, generating high-fidelity and high spectral resolution mid-infrared spectroscopic images. The instrumentation produces multidimensional, chemically specific images, while simultaneously obtaining high resolution spectra for each detector pixel. The spatial resolution of the images approaches the diffraction Limit for mid-infrared wavelengths, while the spectral resolution is determined by the interferometer, and can be 4 cm(-1) or higher. Data derived from a variety of materials, particularly biological samples, illustrate the capabilities of the technique for readily visualizing chemical complexity and for providing statistical data on sample heterogeneity. C1 NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RP Kidder, LH (reprint author), NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER INST PHYSICS PI MELVILLE PA 2 HUNTINGTON QUADRANGLE, STE 1NO1, MELVILLE, NY 11747-4501 USA SN 0094-243X BN 1-56396-746-4 J9 AIP CONF PROC PY 1998 IS 430 BP 148 EP 158 DI 10.1063/1.55829 PG 11 WC Chemistry, Analytical; Chemistry, Physical; Instruments & Instrumentation; Polymer Science; Spectroscopy SC Chemistry; Instruments & Instrumentation; Polymer Science; Spectroscopy GA BL29A UT WOS:000075012400012 ER PT B AU Mitchell, DC Litman, BJ AF Mitchell, DC Litman, BJ BE Riemersma, RA Armstrong, R Kelly, RW Wilson, R TI Docosahexaenoic acid-containing phospholipids optimally promote rhodopsin activation SO FOURTH INTERNATIONAL CONGRESS ON ESSENTIAL FATTY ACIDS AND EICOSANOIDS LA English DT Proceedings Paper CT 4th International Congress on Essential Fatty Acids and Eicosanoids CY JUL 20-24, 1997 CL EDINBURGH, SCOTLAND SP Scotia Pharmaceut Ltd, Minist Agr Fisheries & Food, Natl Inst Alcohol & Alcoholism, Unilver, Van den Bergh Foods, Allergan, British Heart Fdn, Cancer Res Campaign, CERIN, Croda, Hewlett-Packard, Innovat Res, Int Fishmeal & Oil Mfg Assoc, Lothian & Edinburgh Enterprise, Merck Frosst, Mochida Pharmaceut Co, Nestle, Oliv Oil Council, Pharmacia-Upjohn, Pronova Biocare, Roche, Scottish Off, Topcro Pharma Res, ISSFAL ID CHAIN PHOSPHATIDYLCHOLINE VESICLES; HIGHER-ORDER ANALYSIS; FLUORESCENCE ANISOTROPY; METARHODOPSIN-I; BILAYER LIPIDS; FATTY-ACID; CHOLESTEROL; EQUILIBRIUM; DECAY; DISPERSIONS C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. RP Mitchell, DC (reprint author), NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. NR 19 TC 0 Z9 0 U1 0 U2 0 PU AMER OIL CHEMISTS SOC PI CHAMPAIGN PA 508 S 6TH ST, CHAMPAIGN, IL 61820 USA BN 0-935315-96-9 PY 1998 BP 154 EP 158 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cardiac & Cardiovascular Systems; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Biophysics; Cardiovascular System & Cardiology; Nutrition & Dietetics GA BM66D UT WOS:000079368000034 ER PT B AU Pawlosky, RJ Gupta, S Salem, N AF Pawlosky, RJ Gupta, S Salem, N BE Riemersma, RA Armstrong, R Kelly, RW Wilson, R TI Alcohol consumption in felines increases lipid peroxidation in the brain and stimulates polyunsaturated fatty acid metabolism SO FOURTH INTERNATIONAL CONGRESS ON ESSENTIAL FATTY ACIDS AND EICOSANOIDS LA English DT Proceedings Paper CT 4th International Congress on Essential Fatty Acids and Eicosanoids CY JUL 20-24, 1997 CL EDINBURGH, SCOTLAND SP Scotia Pharmaceut Ltd, Minist Agr Fisheries & Food, Natl Inst Alcohol & Alcoholism, Unilver, Van den Bergh Foods, Allergan, British Heart Fdn, Cancer Res Campaign, CERIN, Croda, Hewlett-Packard, Innovat Res, Int Fishmeal & Oil Mfg Assoc, Lothian & Edinburgh Enterprise, Merck Frosst, Mochida Pharmaceut Co, Nestle, Oliv Oil Council, Pharmacia-Upjohn, Pronova Biocare, Roche, Scottish Off, Topcro Pharma Res, ISSFAL ID ETHANOL EXPOSURE; LIVER-DISEASE; RAT-LIVER C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. RP Pawlosky, RJ (reprint author), NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. NR 22 TC 0 Z9 0 U1 0 U2 0 PU AMER OIL CHEMISTS SOC PI CHAMPAIGN PA 508 S 6TH ST, CHAMPAIGN, IL 61820 USA BN 0-935315-96-9 PY 1998 BP 317 EP 320 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cardiac & Cardiovascular Systems; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Biophysics; Cardiovascular System & Cardiology; Nutrition & Dietetics GA BM66D UT WOS:000079368000069 ER PT B AU Mitchell, DC Litman, BJ AF Mitchell, DC Litman, BJ BE Riemersma, RA Armstrong, R Kelly, RW Wilson, R TI The phospholipid bilayer mediates the effect of primary alcohols on rhodopsin activation SO FOURTH INTERNATIONAL CONGRESS ON ESSENTIAL FATTY ACIDS AND EICOSANOIDS LA English DT Proceedings Paper CT 4th International Congress on Essential Fatty Acids and Eicosanoids CY JUL 20-24, 1997 CL EDINBURGH, SCOTLAND SP Scotia Pharmaceut Ltd, Minist Agr Fisheries & Food, Natl Inst Alcohol & Alcoholism, Unilver, Van den Bergh Foods, Allergan, British Heart Fdn, Cancer Res Campaign, CERIN, Croda, Hewlett-Packard, Innovat Res, Int Fishmeal & Oil Mfg Assoc, Lothian & Edinburgh Enterprise, Merck Frosst, Mochida Pharmaceut Co, Nestle, Oliv Oil Council, Pharmacia-Upjohn, Pronova Biocare, Roche, Scottish Off, Topcro Pharma Res, ISSFAL ID METARHODOPSIN-II; ACETYLCHOLINE-RECEPTOR; RECOMBINANT MEMBRANES; GENERAL-ANESTHESIA; EQUILIBRIUM; BOVINE; PROTEIN; CHOLESTEROL; ETHANOL; BINDING C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. RP Mitchell, DC (reprint author), NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. NR 29 TC 0 Z9 0 U1 0 U2 0 PU AMER OIL CHEMISTS SOC PI CHAMPAIGN PA 508 S 6TH ST, CHAMPAIGN, IL 61820 USA BN 0-935315-96-9 PY 1998 BP 336 EP 340 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cardiac & Cardiovascular Systems; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Biophysics; Cardiovascular System & Cardiology; Nutrition & Dietetics GA BM66D UT WOS:000079368000074 ER PT J AU Bilski, P Chignell, CF AF Bilski, P Chignell, CF TI Application of singlet molecular oxygen phosphorescence measurements to assay antioxidant properties and phototoxicity of biological and environmental substances. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 294 BP S104 EP S104 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400314 ER PT J AU Bilski, P Li, MY Daub, ME Ehrenshaft, M Chignell, CF AF Bilski, P Li, MY Daub, ME Ehrenshaft, M Chignell, CF TI Antioxidant properties of pyridoxine and its derivatives: Quenching of singlet oxygen (O-1(2)). SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. N Carolina State Univ, Dept Plant Pathol, Raleigh, NC 27695 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 47 BP S28 EP S28 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400068 ER PT J AU Chen, YR Sturgeon, BE Gunther, MR Mason, RP AF Chen, YR Sturgeon, BE Gunther, MR Mason, RP TI ESR spin trapping of the cyanyl radical in cyanide cytochrome c oxidase and azidyl radical in azide cytochrome c oxidase H2O2 systems SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 8 BP S15 EP S15 DI 10.1016/S0891-5849(98)90033-8 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400029 ER PT J AU Chen, YR Gunther, MR Mason, RP AF Chen, YR Gunther, MR Mason, RP TI An ESR spin-trapping investigation of reaction of mitochondrial cytochrome c oxidase with H2O2 SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 9 BP S15 EP S15 DI 10.1016/S0891-5849(98)90033-8 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400028 ER PT J AU Colburn, N Young, M Li, JJ AF Colburn, N Young, M Li, JJ TI AP-1 transactivation required for neoplastic progression: Evidence from mouse and human keratinocytes and transgenic mice. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NCI, Gene Regulat Sect, Lab Biochem Physiol, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA P2 BP S2 EP S2 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400004 ER PT J AU Davis, DA Newcomb, FM Moskovitz, J Wingfield, PT Kaufmann, J Stahl, SJ Fales, HM Levine, RL Yarchoan, R AF Davis, DA Newcomb, FM Moskovitz, J Wingfield, PT Kaufmann, J Stahl, SJ Fales, HM Levine, RL Yarchoan, R TI Inactivation of HIV-1 and HIV-2 proteases through oxidative modification SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NCI, HAMB, NIH, Bethesda, MD 20892 USA. RI Levine, Rodney/D-9885-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 204 BP S73 EP S73 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400223 ER PT J AU Dikalov, S Viteck, M Maples, K Mason, R AF Dikalov, S Viteck, M Maples, K Mason, R TI Amyloid beta peptides enhance metal-catalyzed oxidation of hydroxylamine derivatives. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Duke Univ, Med Ctr, Durham, NC USA. Centaur Pharmaceut, Sunnyvale, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 313 BP S110 EP S110 DI 10.1016/S0891-5849(98)90338-0 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400333 ER PT J AU Dikalov, SI Viteck, M Maples, KP Mason, RP AF Dikalov, SI Viteck, M Maples, KP Mason, RP TI Amyloid beta peptides do not form radical adducts. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Duke Univ, Med Ctr, Durham, NC 27710 USA. Centaur Pharmaceut, Sunnyvale, CA 94086 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 314 BP S111 EP S111 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400334 ER PT J AU Gilbert, DL AF Gilbert, DL TI Why do so many transcription factors contain sulfur? SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NINDS, BNP, Unit ROS, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 122 BP S50 EP S50 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400142 ER PT J AU Glover, RE Ivy, ED Orringer, EP Maeda, H Mason, RP AF Glover, RE Ivy, ED Orringer, EP Maeda, H Mason, RP TI Detection of nitrosyl hemoglobin in venous blood in the treatment of sickle cell anemia with hydroxyurea SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. Univ N Carolina, Dept Med, Chapel Hill, NC 27514 USA. Kumamoto Univ Med, Dept Microbiol, Kumamoto 860, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 157 BP S60 EP S60 DI 10.1016/S0891-5849(98)90182-4 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400178 ER PT J AU Gunther, MR Mason, RP AF Gunther, MR Mason, RP TI Assignment of the "long-lived" ESR signal from metmyoglobin to a tyrosyl radical SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 12 BP S16 EP S16 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400033 ER PT J AU Han, BG Song, JH Lee, YI Chang, SH AF Han, BG Song, JH Lee, YI Chang, SH TI Mitochondrial dysfunction is involved in hydrogen peroxide-induced cell death SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIH, Lab Degenerat Dis Res, Dept Biomed Res, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 255 BP S89 EP S89 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400275 ER PT J AU Kondo, T Misik, V Riesz, P AF Kondo, T Misik, V Riesz, P TI Effect of gas-containing microspheres and echo contrast agents on free radical formation by ultrasound. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 348 BP S123 EP S123 DI 10.1016/S0891-5849(98)90373-2 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400369 ER PT J AU Kono, H Nakagami, M Connor, H Stefanovic, B Hatano, E Brenner, DA Mason, RP Thurman, RG AF Kono, H Nakagami, M Connor, H Stefanovic, B Hatano, E Brenner, DA Mason, RP Thurman, RG TI Saturated fat attenuates pathology and free radical formation in the pancreas after chronic intragastric ethanol exposure in rats SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 Univ N Carolina, Dept Pharmacol, Hepatobiol & Toxicol Lab, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Med, Chapel Hill, NC 27599 USA. NIEHS, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 270 BP S94 EP S94 DI 10.1016/S0891-5849(98)90295-7 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400290 ER PT J AU Mitchell, JB Kuppusamy, P Subramanian, S Cook, JA Devasahayam, N Afeworki, M Krishna, MC AF Mitchell, JB Kuppusamy, P Subramanian, S Cook, JA Devasahayam, N Afeworki, M Krishna, MC TI Imaging of free radicals. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NCI, Radiat Biol Branch, Bethesda, MD 20892 USA. Johns Hopkins Univ, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA P7 BP S5 EP S5 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400009 ER PT J AU Pogozelski, WK Pilskalns, BA Director-Myska, AE Hamel, C Lofts, RS Nicotera, TM Zullo, SJ Merrill, CR Blakley, WF AF Pogozelski, WK Pilskalns, BA Director-Myska, AE Hamel, C Lofts, RS Nicotera, TM Zullo, SJ Merrill, CR Blakley, WF TI Measurement of the 5-kb "common deletion" in mitochondrial DNA from Bloom syndrome lymphocytes using the fluorogenic 5 '-nuclease (TaqMan (TM)) PCR assay SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 SUNY Geneseo, Geneseo, NY 14454 USA. Armed Forces Radiobiol Res Inst, Bethesda, MD 20889 USA. Roswell Pk Canc Inst, Buffalo, NY 14214 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 301 BP S105 EP S105 DI 10.1016/S0891-5849(98)90326-4 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400321 ER PT J AU Ridnour, LA Sim, JE Wink, DA Spitz, DR AF Ridnour, LA Sim, JE Wink, DA Spitz, DR TI Isolation and partial characterization of NO-resistant cells following chronic exposure to DEA/NO SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 Washington Univ, Sect Canc Biol, St Louis, MO USA. NIH, Radiat Biol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 181 BP S66 EP S66 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400202 ER PT J AU Rota, C Chignell, CF Mason, RP AF Rota, C Chignell, CF Mason, RP TI Oxidation of 2 '-7 '-dichlorofluorescin by horseradish peroxidase. Possible implications for oxidative stress measurements SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 304 BP S106 EP S106 DI 10.1016/S0891-5849(98)90329-X PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400323 ER PT J AU Rota, C Marchesi, E Chignell, CF Mason, RP AF Rota, C Marchesi, E Chignell, CF Mason, RP TI Photoreduction of 2 '-7 '-dichlorofluorescein. An ESR study with implications for oxidative stress measurements SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Univ Bologna, Dipartimento Chim Organ A Mangini, Bologna, Italy. NR 0 TC 0 Z9 0 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 292 BP S102 EP S102 DI 10.1016/S0891-5849(98)90317-3 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400311 ER PT J AU Rusyn, I Segal, B Holland, SM Thurman, RG AF Rusyn, I Segal, B Holland, SM Thurman, RG TI NADPH oxidase is the source of oxidants for activation of NF-kappa B by the peroxisome proliferator WY-14,613 (WY) SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 Univ N Carolina, Hepatobiol & Toxicol Lab, Chapel Hill, NC USA. Univ N Carolina, Curriculum Toxicol, Chapel Hill, NC USA. NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA. RI Rusyn, Ivan/S-2426-2016 NR 0 TC 1 Z9 1 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 339 BP S118 EP S118 DI 10.1016/S0891-5849(98)90364-1 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400360 ER PT J AU Shacka, JJ Ren, RF Kim, ES Flanders, KC AF Shacka, JJ Ren, RF Kim, ES Flanders, KC TI Connection between reactive oxygen species and transforming growth factors beta in neuronal culture SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NCI, LCRC, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 322 BP S113 EP S113 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400342 ER PT J AU Stadtman, TC AF Stadtman, TC TI Selenium-dependent mammalian thioredoxin reductase SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA P18 BP S10 EP S10 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400020 ER PT J AU Szweda, PA Corrigan, K Tsai, L Oberley, T Szweda, LI AF Szweda, PA Corrigan, K Tsai, L Oberley, T Szweda, LI TI Contribution of 4-hydroxy-2-nonenal to lipofuscin formation SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 Case Western Reserve Univ, Cleveland, OH 44106 USA. Univ Wisconsin, Madison, WI USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 247 BP S86 EP S86 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400267 ER PT J AU Tsuchiya, K Corbett, J Mason, RP AF Tsuchiya, K Corbett, J Mason, RP TI Reaction mechanisms of water-soluble nitric oxide spin-trapping agent, MGD SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 191 BP S68 EP S68 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400211 ER PT J AU Velan, SS Spencer, RGS Zweier, JL Kuppusamy, P AF Velan, SS Spencer, RGS Zweier, JL Kuppusamy, P TI Electron paramagnetic resonance oximetry mapping (EPROM): A technique for in vivo measurement and visualization of oxygen gradients in tissues SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIA, Nucl Magnet Resonance Unit, NIH, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, EPR Ctr, Baltimore, MD 21205 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 305 BP S106 EP S106 DI 10.1016/S0891-5849(98)90330-6 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400325 ER PT J AU Velan, SS Kuppusamy, P Petersen, E Zweier, JL Fishbein, KW Spencer, RGS AF Velan, SS Kuppusamy, P Petersen, E Zweier, JL Fishbein, KW Spencer, RGS TI EPR oximetry mapping (EPROM) of cartilage formed in a hollow fiber bioreactor SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIA, NMR Unit, NIH, Baltimore, MD USA. Johns Hopkins Univ, Dept Med, EPR Ctr, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1998 VL 25 SU 1 MA 250 BP S86 EP S86 DI 10.1016/S0891-5849(98)90275-1 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 139VP UT WOS:000077051400270 ER PT J AU Ghio, AJ Kadiiska, MB Xiang, QH Mason, RP AF Ghio, AJ Kadiiska, MB Xiang, QH Mason, RP TI In vivo evidence of free radical formation after asbestos instillation: An ESR spin trapping investigation SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE crocidolite; POBN; lungs; radicals; rats; free radicals ID INDUCED LIPID-PEROXIDATION; RAT-LIVER MICROSOMES; CROCIDOLITE ASBESTOS; SOYBEAN LIPOXYGENASE; HYDROGEN-PEROXIDE; ADDUCTS; LUNG; IDENTIFICATION; GENERATION; DISEASES AB Tt has been postulated that the in vivo toxicity of asbestos results from its catalysis of free radical generation. We examined in vivo radical production using electron spin resonance (ESR) coupled with the spin trap alpha(4-pyridyl-1-oxide)-N-t-butylnitrone (4-POBN); 180 day-old rats were intratracheally instilled with either 500 mu g crocidolite or saline. Twenty-four hours later, histologic examination revealed a neutrophilic inflammatory response. ESR spectroscopy of the chloroform extract from lungs exposed to asbestos gave a spectrum consistent with a carbon-centered radical adduct, while those spectra from lungs instilled with saline revealed a much weaker signal. This same radical formation persisted and, even one month after instillation, could be detected in the lungs of rats exposed to asbestos. The 4-POBN adducts detected by ESR are very similar to, if not identical with, ethyl and pentyl radical adducts, providing evidence of in vivo lipid peroxidation resulting from asbestos exposure. We conclude that, after instillation of crocidolite in the rat, ESR analysis of lung tissue demonstrates in vivo free radical production. (C) 1997 Elsevier Science Inc. C1 DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. NIEHS,LAB PHARMACOL & CHEM,NIH,RES TRIANGLE PK,NC 27709. RP Ghio, AJ (reprint author), US EPA,NATL HLTH & ENVIRONM EFFECTS RES LAB,RES TRIANGLE PK,NC 27711, USA. NR 35 TC 25 Z9 27 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JAN 1 PY 1998 VL 24 IS 1 BP 11 EP 17 DI 10.1016/S0891-5849(97)00063-4 PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA YK775 UT WOS:A1998YK77500002 PM 9436609 ER PT J AU MetoshDickey, CA Mason, RP Winston, GW AF MetoshDickey, CA Mason, RP Winston, GW TI Single electron reduction of xenobiotic compounds by glucose oxidase from Aspergillus niger SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE glucose oxidase; one-electron reduction; ESR; free radical; nitro aromatic; quinone ID NITROAROMATIC COMPOUNDS; NITROBLUE TETRAZOLIUM; METABOLIC-ACTIVATION; SUPEROXIDE; MECHANISM; CYTOCHROME-P-450; FLAVOPROTEIN; QUINONES AB Various species of fungi express glucose oxidase that catalyzes formation of gluconolactone from glucose with concomitant, direct divalent reduction of molecular oxygen to hydrogen peroxide. A physiological function a ascribed to this extracellular enzyme is production of hydrogen peroxide for use in lignin degradation catalyzed by lignin peroxidases. Herein, we show that glucose oxidase can catalyze one-electron reduction of several different classes of xenobiotic compounds resulting in generation of free radical products. Electron spin resonance (ESR) spectroscopy was used to visualize the one-electron reduction products of 4-nitropyridine-N-oxide (4NPO), 1,4-naphthoquinone (1,4NQ), and dichlorophenolindolphenol (DCPIP). Hyperfine splitting constants were used to generate computer simulations of the spectra confirming the presence of free radical products. (C) 1997 Elsevier Science Inc. C1 LOUISIANA STATE UNIV, DEPT BIOCHEM, BATON ROUGE, LA 70803 USA. NIEHS, LAB PHARMACOL & CHEM, NIH, RES TRIANGLE PK, NC 27709 USA. FU NIAAA NIH HHS [AA06758] NR 30 TC 5 Z9 5 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JAN 1 PY 1998 VL 24 IS 1 BP 155 EP 160 DI 10.1016/S0891-5849(97)00207-4 PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA YK775 UT WOS:A1998YK77500018 PM 9436625 ER PT J AU Weinberg, JB Gilkeson, GS Mason, RP Chamulitrat, W AF Weinberg, JB Gilkeson, GS Mason, RP Chamulitrat, W TI Nitrosylation of blood hemoglobin and renal nonheme proteins in autoimmune MRL-lpr/lpr mice SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE nitric oxide; free radicals; rheumatoid arthritis; lupus; inflammation; glomerulonephritis; hemoglobin ID NITRIC-OXIDE PRODUCTION; MONOMETHYL-L-ARGININE; MITOCHONDRIAL RESPIRATION; RIBONUCLEOTIDE REDUCTASE; ACTIVATED MACROPHAGES; NEOPLASTIC-CELLS; RAT HEPATOCYTES; SYNOVIAL-FLUID; TREATED RATS; INHIBITION AB MRL-lpr/lpr mice spontaneously develop manifestations of autoimmunity including arthritis, vasculitis, and glomerulonephritis. The paramagnetic molecule nitric oxide has been implicated as an effector molecule in initiation and propagation of these inflammatory conditions. In this study, we utilized electron paramagnetic resonance spectroscopy to directly detect nitrosylated protein complexes as products of nitric oxide in whole blood and in kidneys of MRL-lpr/lpr mice. Electron paramagnetic resonance spectra of blood samples from MRL-lpr/lpr mice showed nitrosyl hemoglobin species. Amounts of blood nitrosyl hemoglobin in MRL-lpr/lpr mice were significantly increased as compared to age-matched control mice. Electron paramagnetic resonance spectra of MRL-lpr/lpr kidney tissue exhibited a signal characteristic of a dinitrosyl-iron-dithiolate complex at g similar to 2.04. Formation of nitrosylated nonheme protein in diseased kidneys is associated with development of glomerulonephritis in the autoimmune mice. The presence of nitrosylated nonheme protein indicates the formation of nitric oxide within the kidneys of the diseased mice signifying in situ renal nitric oxide formation. Published by Elsevier Science Inc. C1 DUKE UNIV, MED CTR, DEPT MED, DURHAM, NC 27705 USA. NIEHS, NIH, RES TRIANGLE PK, NC 27709 USA. LOUISIANA STATE UNIV, MED CTR, DEPT PHYSIOL, NEW ORLEANS, LA 70112 USA. RP Weinberg, JB (reprint author), VET ADM MED CTR, 508 FULTON ST, DURHAM, NC 27705 USA. FU NIAMS NIH HHS [AR-39162] NR 44 TC 20 Z9 21 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JAN 1 PY 1998 VL 24 IS 1 BP 191 EP 196 DI 10.1016/S0891-5849(97)00217-7 PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA YK775 UT WOS:A1998YK77500023 PM 9436630 ER PT J AU Hudson, EK Hogue, BA Souza-Pinto, NC Croteau, DL Anson, RM Bohr, VA Hansford, RG AF Hudson, EK Hogue, BA Souza-Pinto, NC Croteau, DL Anson, RM Bohr, VA Hansford, RG TI Age-associated change in mitochondrial DNA damage SO FREE RADICAL RESEARCH LA English DT Article DE mitochondrial DNA; oxidative damage; DNA repair; mitochondria; aging; liver ID OXIDATIVE DAMAGE; ESCHERICHIA-COLI; RAT; PROTEIN; ENDONUCLEASE; HEARTS; ACID AB There is an age-associated decline in the mitochondrial function of the Wistar rat heart. Previous reports from this lab have shown a decrease in mitochondrial cytochrome c oxidase (COX) activity associated with a reduction in COX gene and protein expression and a similar decrease in the rate of mitochondrial protein synthesis. Damage to mitochondrial DNA may contribute to this decline. Using the HPLC-Coularray system (ESA, USA), we measured levels of nuclear and mitochondrial 8-oxo-2'-deoxyguanosine (8-oxodG) from 6-month (young) and 23-month-old (senescent) rat liver DNA. We measured the sensitivity of the technique by damaging calf thymus DNA with photoactivated methylene blue for 30 s up to 2 h. The levels of damage were linear over the entire time course including the shorter times which showed levels comparable to those expected in liver. For the liver data, 8-oxodG was reported as a fraction of 2-deoxyguanosine (2-dG). There was no change in the levels of 8-oxodG levels in the nuclear DNA from 6 to 23-months of age. However, the levels of 8-oxodG increased 2.5-fold in the mitochondrial DNA with age. At 6 months, the level of 8-oxodG in mtDNA was 5-fold higher than nuclear and increased to approximately 12-fold higher by 23 months of age. These findings agree with other reports showing an age-associated increase in levels of mtDNA damage; however, the degree to which it increases is smaller Such damage to the mitochondrial DNA may contribute to the age-associated decline in mitochondrial function. C1 NIA, Genet Mol Lab, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. Univ Calif Berkeley, Dept Mol & Cellular Biol, Berkeley, CA 94720 USA. RP Hudson, EK (reprint author), NIA, Genet Mol Lab, Gerontol Res Ctr, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. RI Souza-Pinto, Nadja/C-3462-2013 OI Souza-Pinto, Nadja/0000-0003-4206-964X NR 25 TC 112 Z9 113 U1 0 U2 3 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 1998 VL 29 IS 6 BP 573 EP 579 DI 10.1080/10715769800300611 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 174TE UT WOS:000079050500011 PM 10098461 ER PT S AU Stadtman, ER AF Stadtman, ER BE Ozben, T TI Free radical mediated oxidation of proteins SO FREE RADICALS, OXIDATIVE STRESS, AND ANTIOXIDANTS: PATHOLOGICAL AND PHYSIOLOGICAL SIGNIFICANCE SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES A, LIFE SCIENCES LA English DT Proceedings Paper CT NATO Advanced Study Institute on Free Radicals, Oxidative Stress, and Antioxidants - Pathological and Physiological Significance CY MAY 24-JUN 04, 1997 CL ANTALYA, TURKEY SP NATO, Sci Affairs Div AB Living organisms are constantly bombarded with a battery of oxygen free radicals and other forms of reactive oxygen, leading to the modification of proteins. These modifications include: (a) fragmentation of the polypeptide chain, (b) formation of intra-and inter-molecular cross-linkages, direct oxidation of amino acid residue side chains, (c) derivatization of amino groups of lysine by reducing sugars or their oxidation products (glycation), (d) derivatization of lysine, histidine, or cysteine residues by lipid oxidation products (malondialdehyde, 2,3 unsaturated aldehydes), and (e) nitration of tyrosine residues. The generation of carbonyl derivatives (aldehydes, ketones) by some of these reactions may serve as markers of oxidative protein damage in aging and disease. The nitration of tyrosine residues can seriously compromise major mechanisms of enzyme regulation and signal transduction. And the formation of protein-protein cross linkages can lead to the accumulation of protease resistant protein polymers and inhibitors of proteases that degrade the oxidized forms of oxidatively modified proteins. C1 NHLBI, NIH, Biochem Lab, Bethesda, MD 20892 USA. RP Stadtman, ER (reprint author), NHLBI, NIH, Biochem Lab, Bldg 3,Room 222, Bethesda, MD 20892 USA. NR 0 TC 15 Z9 15 U1 0 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0258-1213 BN 0-306-45813-6 J9 NATO ADV SCI I A-LIF PY 1998 VL 296 BP 51 EP 64 PG 14 WC Biochemistry & Molecular Biology; Physiology SC Biochemistry & Molecular Biology; Physiology GA BK96C UT WOS:000073945700005 ER PT S AU Stadtman, ER AF Stadtman, ER BE Ozben, T TI The role of free radical mediation of protein oxidation in aging and disease SO FREE RADICALS, OXIDATIVE STRESS, AND ANTIOXIDANTS: PATHOLOGICAL AND PHYSIOLOGICAL SIGNIFICANCE SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES A, LIFE SCIENCES LA English DT Proceedings Paper CT NATO Advanced Study Institute on Free Radicals, Oxidative Stress, and Antioxidants - Pathological and Physiological Significance CY MAY 24-JUN 04, 1997 CL ANTALYA, TURKEY SP NATO, Sci Affairs Div AB A role of protein oxidation in aging is indicated by the following observations: The cellular level of oxidized protein increases with animal age. Age-related changes in enzyme activities can be mimicked by treatment of enzymes from young animals with reactive oxygen species (ROS) in vitro. Exposure of animals to conditions of oxidative stress leads to an increase in the intracellular level of oxidized protein. Factors that increase the life span of animals lead also to a decrease in the level of oxidized protein and vice versa. Many age-related diseases are associated with elevated levels of oxidized proteins. Some age-related changes in enzyme activities and cognitive functions can be reversed by exposing old animals to free radical spin traps. The age-related increase in oxidized proteins is a complex function of the balance between a multiplicity of prooxidants, antioxidants, and the activities of proteases that selectively degrade the oxidized forms of proteins. C1 NHLBI, NIH, Biochem Lab, Bethesda, MD 20892 USA. RP Stadtman, ER (reprint author), NHLBI, NIH, Biochem Lab, Bldg 3,Room 222, Bethesda, MD 20892 USA. NR 0 TC 11 Z9 11 U1 0 U2 3 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0258-1213 BN 0-306-45813-6 J9 NATO ADV SCI I A-LIF PY 1998 VL 296 BP 131 EP 143 PG 13 WC Biochemistry & Molecular Biology; Physiology SC Biochemistry & Molecular Biology; Physiology GA BK96C UT WOS:000073945700013 ER PT B AU Hallenbeck, JM Frerichs, KU AF Hallenbeck, JM Frerichs, KU BE Robertson, JT Nowak, TS TI Secondary ischemic neuronal damage may involve multiple factors acting as an aggregate of minor causes SO FRONTIERS IN CEREBROVASCULAR DISEASE: MECHANISMS, DIAGNOSIS, AND TREATMENT SE AMERICAN HEART ASSOCIATION MONOGRAPH SERIES LA English DT Proceedings Paper CT 20th Princeton Conference on Cerebrovascular Disease - Mechanisms, Diagnosis, and Treatment CY MAR 22-24, 1996 CL MEMPHIS, TN C1 NINDS, Stroke Branch, NIH, Bethesda, MD 20892 USA. RP Hallenbeck, JM (reprint author), NINDS, Stroke Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU FUTURA PUBL CO INC PI ARMONK PA 135 BEDFORD RD PO BOX 418, ARMONK, NY 10504-0418 USA BN 0-87993-674-6 J9 AM HEART MONOGR S PY 1998 BP 95 EP 101 PG 7 WC Cardiac & Cardiovascular Systems; Clinical Neurology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Neurosciences & Neurology GA BK07K UT WOS:000071071000007 ER PT J AU Holden, JP Stanhope, SJ AF Holden, JP Stanhope, SJ TI The effect of variation in knee center location estimates on net knee joint moments SO GAIT & POSTURE LA English DT Article DE gait; walking; kinetics; speed; knee; moment; joint center; variation ID GAIT FOLLOWING STROKE; WALKING AB To test the sensitivity of knee flexion-extension moment patterns to variation in estimates of the knee center location (KCL), inverse dynamics analysis was performed using three different KCLs for data collected from 18 healthy adult subjects who walked at five different speeds (25%, 50%, 75%, 100% and 125% of 0.785 statures.s(-1)). The KCL, which was determined using data from static subject calibration trials, was varied in software by plus or minus 10 mm in the anteroposterior direction. The effect of this KCL variation on knee moments was similar across subjects and at all five walking speeds. The relative knee center variation effect, expressed as a percentage of the mean knee moment, was progressively greater at slower walking speeds, up to 123% of the first extensor peak at the slowest speed. The implication of these results is that, while KCL variation does not affect the general shape of the moment pattern at more natural walking speeds, it can change the sign of the moment-and thus the interpretation-when the moment magnitude is small (e.g. at the very slow speeds used by some patients). When knee moments are of magnitudes less than or equal to the KCL variation effect, one cannot confidently interpret them as representing either a net flexor or extensor knee control strategy. (C) 1998 Elsevier Science B.V. C1 NIAMSD, Bethesda, MD 20892 USA. NIH, Dept Rehabil Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. NIH, Biomech Lab, Bethesda, MD 20892 USA. RP Holden, JP (reprint author), Childrens Hosp, Mot Anal Lab 5054, 3020 Childrens Way, San Diego, CA 92123 USA. NR 17 TC 51 Z9 52 U1 0 U2 5 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0966-6362 J9 GAIT POSTURE JI Gait Posture PD JAN PY 1998 VL 7 IS 1 BP 1 EP 6 DI 10.1016/S0966-6362(97)00026-X PG 6 WC Neurosciences; Orthopedics; Sport Sciences SC Neurosciences & Neurology; Orthopedics; Sport Sciences GA ZB476 UT WOS:000072475800001 ER PT J AU Kepple, TM Siegel, KL Stanhope, SJ AF Kepple, TM Siegel, KL Stanhope, SJ TI Comments on Kepple et al.: Relative contributions of the lower extremity joint moments to forward progression and support during gait - Reply SO GAIT & POSTURE LA English DT Letter C1 NIH, Dept Rehabil Med, Bethesda, MD 20892 USA. RP Kepple, TM (reprint author), NIH, Dept Rehabil Med, Bldg 10,Rm 6S 235,10 Ctr Dr,MSC-1604, Bethesda, MD 20892 USA. RI Siegel, Karen Lohmann/B-5898-2008 NR 0 TC 0 Z9 0 U1 0 U2 3 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0966-6362 J9 GAIT POSTURE JI Gait Posture PD JAN PY 1998 VL 7 IS 1 BP 75 EP 76 PG 2 WC Neurosciences; Orthopedics; Sport Sciences SC Neurosciences & Neurology; Orthopedics; Sport Sciences GA ZB476 UT WOS:000072475800011 ER PT S AU McDonald, MP Gleason, TC Robinson, JK Crawley, JN AF McDonald, MP Gleason, TC Robinson, JK Crawley, JN BE Hokfelt, T Bartfai, T Crawley, J TI Galanin inhibits performance on rodent memory tasks SO GALANIN: BASIC RESEARCH DISCOVERIES AND THERAPEUTIC IMPLICATIONS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Galanin - Basic Research Discoveries and Therapeutic Implications CY MAY 03-05, 1998 CL STOCKHOLM, SWEDEN SP Wenner Gren Fdn ID RAT VENTRAL HIPPOCAMPUS; CENTRAL NERVOUS-SYSTEM; NONMATCHING-TO-SAMPLE; BASAL FOREBRAIN; ALZHEIMERS-DISEASE; PHOSPHOINOSITIDE TURNOVER; ACETYLCHOLINE-RELEASE; PHARMACOLOGICAL CHARACTERIZATION; MOLECULAR-CLONING; NUCLEUS BASALIS AB Central administration of galanin produces performance deficits on a variety of rodent Learning and memory tasks, Galanin impairs acquisition and/or retention of the Morris water task, delayed nomnatching to position, T-maze delayed alternation, starburst radial maze, and passive avoidance in normal rats. A primary site of action is the ventral hippocampus, with an additional modulatory site in the medial septum-diagonal band. The behavioral actions of galanin at rat septohippocampal sites mediating cognitive processes are consistent with previous reports of inhibitory actions of galanin on acetylcholine release and cholinergically activated transduction at the M-1 muscarinic receptor in rat hippocampus, The peptidergic galanin receptor antagonist M40 blocks the inhibitory actions of galanin on memory tasks. Treatment combinations of M40 with an M-1 agonist, TZTP, improves performance on delayed nomnatching to position, in rats with (192)IgG-saporin induced cholinergic lesions of basal forebrain neurons. Nonpeptide, bioavailable, subtype-selective galanin receptor antagonists may provide tools to test the hypothesis that antagonism of endogenous galanin, which is overexpressed in the basal forebrain in Alzheimer's patients, can contribute to the alleviation of the cognitive deficits associated with Alzheiner's disease. C1 NIMH, Sect Behav Neuropharmacol, Expt Therapeut Branch, Bethesda, MD 20892 USA. RP Crawley, JN (reprint author), NIMH, Sect Behav Neuropharmacol, Expt Therapeut Branch, Bldg 10 Room 4D11,9000 Rockville Pike, Bethesda, MD 20892 USA. EM jncrawle@codon.nih.gov NR 59 TC 48 Z9 50 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-174-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 863 BP 305 EP 322 DI 10.1111/j.1749-6632.1998.tb10704.x PG 18 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BM29T UT WOS:000078305100026 PM 9928180 ER PT J AU Strober, W Kelsall, B AF Strober, W Kelsall, B TI To be responsive or not to be responsive, that is the mucosal question SO GASTROENTEROLOGY LA English DT Editorial Material ID RESIDENT INTESTINAL FLORA; ORAL TOLERANCE; EXPERIMENTAL COLITIS; TH2 CELLS; T-CELLS; MICE; INTERLEUKIN-12; ANTIBODIES; INDUCTION; ANERGY C1 NIAID, Clin Invest Lab, Mucosal Immun Sect, NIH, Bethesda, MD 20892 USA. RP Strober, W (reprint author), NIAID, Clin Invest Lab, Mucosal Immun Sect, NIH, 10 Ctr Dr,MSC 1890,Bldg 10,Rooms 11N 234-244, Bethesda, MD 20892 USA. NR 25 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 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 1998 VL 114 IS 1 BP 214 EP 217 DI 10.1016/S0016-5085(98)70649-3 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA YN909 UT WOS:000071220900028 PM 9428235 ER PT J AU Castillo, SO Xiao, QX Kostrouch, Z Dozin, B Nikodem, VM AF Castillo, SO Xiao, QX Kostrouch, Z Dozin, B Nikodem, VM TI A divergent role of COOH-terminal domains in Nurr1 and Nur77 transactivation SO GENE EXPRESSION LA English DT Article DE Nurr1; Nur77; transcriptional regulation; RXR; 9-cis-RA; Nurr1a; alternative splicing ID THYROID-HORMONE RECEPTOR; RETINOID-X RECEPTOR; NERVE GROWTH-FACTOR; NGFI-B NUR77; NUCLEAR RECEPTOR; ORPHAN RECEPTORS; DNA-BINDING; MEMBRANE DEPOLARIZATION; ESTROGEN-RECEPTOR; TRANSCRIPTIONAL ACTIVATION AB Orphan nuclear receptors such as Nurr1 and Nur77 have conserved amino acid sequences in the zinc finger DNA binding domains and similar COOH-terminal regions, but have no known ligands. These receptors can bind DNA sequences (response elements) as monomers and can also heterodimerize with the retinoid X receptor to activate transcription. We report here the identification and initial characterization of a novel COOH-terminal truncated isoform of Nurr1, Nurr1a. Internal splicing of Nurr1 generates a frameshift such that a stop codon is prematurely encoded resulting in a naturally occurring COOH-terminal truncation. Embryonic and postnatal mouse brain showed both Nurr1 and Nurr1a mRNAs expressed during development. To characterize essential COOH-terminal elements that may be deleted from Nurr1a and determine function in putative ligand binding, we created COOH-terminal deletion mutants. Nurr1, Nur77, and 3'-truncated mutants bind in gel mobility shift assays to the monomeric Nur77 response element (B1A-RE). However, in transient transfection assays, a truncation of as little as 15 Nurr1 COOH-terminal amino acids diminished transcriptional activation of B1A-thymidine kinase-chloramphenicol acetyltransferase reporter. This result was not seen for a similar Nur77 deletion mutant, Nur77-586. Unlike full-length Nurr1 and Nur77, transactivation by Nur77-586 was not augmented in response to the presence of retinoid-like receptor and 9-cis-retinoic acid. Thus, the interaction of putative ligand binding and transactivation for Nurr1 and Nur77 may function differently. C1 NIDDKD, NIH, Genet & Biochem Branch, Mechanisms Gene Regulat Sect, Bethesda, MD 20892 USA. RP Nikodem, VM (reprint author), NIDDKD, NIH, Genet & Biochem Branch, Mechanisms Gene Regulat Sect, 10 Ctr Dr,MSC1766, Bethesda, MD 20892 USA. NR 55 TC 11 Z9 11 U1 0 U2 1 PU COGNIZANT COMMUNICATION CORP PI ELMSFORD PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA SN 1052-2166 J9 GENE EXPRESSION JI Gene Expr. PY 1998 VL 7 IS 1 BP 1 EP 12 PG 12 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA ZH737 UT WOS:000073142600001 PM 9572393 ER PT J AU Cara, A Rybak, SM Newton, DL Crowley, R Rottschafer, SE Reitz, MS Gusella, GL AF Cara, A Rybak, SM Newton, DL Crowley, R Rottschafer, SE Reitz, MS Gusella, GL TI Inhibition of HIV-1 replication by combined expression of gag dominant negative mutant and a human ribonuclease in a tightly controlled HIV-1 inducible vector SO GENE THERAPY LA English DT Article DE gene therapy; HIV-1; ribonuclease; internal ribosome entry site; replication ID IMMUNODEFICIENCY-VIRUS TYPE-1; EOSINOPHIL-DERIVED NEUROTOXIN; CIS-ACTING SEQUENCES; RETROVIRAL VECTOR; T-LYMPHOCYTES; GENE-TRANSFER; CELL-LINES; CD4+ CELLS; VIRAL-DNA; INFECTION AB An HIV-1-based expression vector has been constructed that produces protective genes tightly regulated by HIV-1 Tat and Rev proteins. The vector contains either a single protective gene (HIV-1 gag dominant negative mutant (delta-gag)) or a combination of two different protective genes (delta-gag and eosinophil-derived neurotoxin (EDN), a human ribonuclease) which are expressed from a di-cistronic mRNA. After stable transfection of CEM T cells and following challenge with HIV-1, viral production was completely inhibited in cells transduced with the vector producing both delta-gag and EDN and delayed in cells producing delta-gag alone. In addition, cotransfection of HeLa-Tat cells with an infectious HIV-1 molecular clone and either protective vector demonstrated that the HIV-1 packaging signals present in the constructs were functional and allowed the efficient assembly of the protective RNAs into HIV-1 virions, thus potentially transmitting protection to the HIV-1 target cells. C1 NCI, Frederick Canc Res & Dev Ctr, Lab Biochem Physiol, Div Basic Sci, Frederick, MD 21702 USA. NCI, Basic Res Lab, NIH, Bethesda, MD 20892 USA. NCI, Frederick Canc Res & Dev Ctr, Intramural Res Program, SAIC Frederick, Frederick, MD 21701 USA. Inst Human Virol, Baltimore, MD USA. RP Gusella, GL (reprint author), NCI, Frederick Canc Res & Dev Ctr, Lab Biochem Physiol, Div Basic Sci, Bldg 567,Room 152, Frederick, MD 21702 USA. RI Cara, Andrea/M-4865-2015 OI Cara, Andrea/0000-0003-4967-1895 NR 34 TC 15 Z9 15 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0969-7128 J9 GENE THER JI Gene Ther. PD JAN PY 1998 VL 5 IS 1 BP 65 EP 75 DI 10.1038/sj.gt.3300545 PG 11 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 YT073 UT WOS:000071561300009 PM 9536266 ER PT S AU Walther, W Stein, U Fichtner, I Naundorf, H Alexander, M Shoemaker, RH Schlag, PM AF Walther, W Stein, U Fichtner, I Naundorf, H Alexander, M Shoemaker, RH Schlag, PM BE Walden, P Trefzer, U Sterry, W Farzaneh, F TI In vivo evaluation of a drug-inducible vector system for the combined gene- and chemotherapy of cancer SO GENE THERAPY OF CANCER SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 3rd European Conference on Gene Therapy of Cancer CY SEP 11-13, 1997 CL HUMBOLDT UNIV, CHARITE MED FAC, BERLIN, GERMANY SP German Fed Min Educ Sci Res & Technol, Bayer, Chiron, Essex Pharma, Hoechst Marion Roussel, Karl Thomae HO HUMBOLDT UNIV, CHARITE MED FAC ID COLON-CARCINOMA CELLS; MULTIDRUG-RESISTANCE; MDR1; EXPRESSION; REVERSAL; THERAPY C1 Max Delbruck Ctr Mol Med, D-13122 Berlin, Germany. NCI, Frederick Canc Res & Dev Ctr, LDDRD, Frederick, MD 21702 USA. Free Univ Berlin, Klinikum Rudolf Virchow, Robert Rossle Klin, D-13122 Berlin, Germany. RP Walther, W (reprint author), Max Delbruck Ctr Mol Med, Robert Rossle Str 10, D-13122 Berlin, Germany. NR 7 TC 2 Z9 2 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46027-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1998 VL 451 BP 139 EP 144 PG 6 WC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Research & Experimental Medicine GA BL99D UT WOS:000077389900022 PM 10026863 ER PT S AU Stein, U Walther, W Shoemaker, RH Schlag, PM AF Stein, U Walther, W Shoemaker, RH Schlag, PM BE Walden, P Trefzer, U Sterry, W Farzaneh, F TI IL-2 gene transfer for chemosensitization of multidrug-resistant human colon carcinoma cells SO GENE THERAPY OF CANCER SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 3rd European Conference on Gene Therapy of Cancer CY SEP 11-13, 1997 CL HUMBOLDT UNIV, CHARITE MED FAC, BERLIN, GERMANY SP German Fed Min Educ Sci Res & Technol, Bayer, Chiron, Essex Pharma, Hoechst Marion Roussel, Karl Thomae HO HUMBOLDT UNIV, CHARITE MED FAC ID OVEREXPRESSION; TRANSPORTER; EXPRESSION; REVERSAL C1 Max Delbruck Ctr Mol Med, D-13122 Berlin, Germany. NCI, Frederick Canc Res & Dev Ctr, LDDRD, Frederick, MD 21702 USA. Free Univ Berlin, Klinikum Rudolf Virchow, Robert Rossle Klin, D-13122 Berlin, Germany. RP Stein, U (reprint author), Max Delbruck Ctr Mol Med, Robert Rossle Str 10, D-13122 Berlin, Germany. NR 7 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46027-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1998 VL 451 BP 145 EP 149 PG 5 WC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Research & Experimental Medicine GA BL99D UT WOS:000077389900023 PM 10026864 ER PT J AU Marsh, DJ Dahia, PLM Coulon, V Zheng, ZM Dorion-Bonnet, F Call, KM Little, R Lin, AY Eeles, RA Goldstein, AM Hodgson, SV Richardson, AL Robinson, BG Weber, HC Longy, M Eng, C AF Marsh, DJ Dahia, PLM Coulon, V Zheng, ZM Dorion-Bonnet, F Call, KM Little, R Lin, AY Eeles, RA Goldstein, AM Hodgson, SV Richardson, AL Robinson, BG Weber, HC Longy, M Eng, C TI Allelic imbalance, including deletion of PTEN/MMACI, at the Cowden disease locus on 10q22-23, in hamartomas from patients with Cowden syndrome and germline PTEN mutation SO GENES CHROMOSOMES & CANCER LA English DT Article ID MOLECULAR-GENETICS; WILMS-TUMOR; RETINOBLASTOMA; INACTIVATION; FAMILY; CANCER; MAP AB Cowden disease (CD) is a rare, autosomal dominant inherited cancer syndrome characterized by multiple benign and malignant lesions in a wide spectrum of tissues. While individuals with CD have an increased risk of breast and thyroid neoplasms, the primary features of CD are hamartomas. The gene for CD has been mapped by linkage analysis to a 6 cM region on the long arm of chromosome 10 at 10q22-23. Loss of heterozygosity (LOH) studies of sporadic follicular thyroid adenomas and carcinomas, both component tumors of CD, have suggested that the putative susceptibility gene for CD is a tumor suppressor gene. Somatic missense and nonsense mutations have recently been identified in breast, prostate, and brain tumor cell lines in a gene encoding a dual specificity phosphatase, PTEN/MMACI, mapped at 10q23.3. Furthermore, germline PTEN/MMACI mutations are associated with CD. In the present study, 20 hamartomas from 11 individuals belonging to ten unrelated families with CD have been examined for LOH of markers flanking and within PTEN/MMACI. Eight of these ten families have germline PTEN/MMACI mutations. LOH involving microsatellite markers within the CD interval, and including PTEN/MMACI, was identified in two fibroadenomas of the breast, a thyroid adenoma, and a pulmonary hamartoma belonging to 3 of 11 (27%) of these patients. The wild-type allele was lost in these hamartomas. Semi-quantitative PCR performed on RNA from hamartomas from three different tissues from a CD patient suggested substantial reduction of PTEN/MMACI RNA levels in all of these tissues. The LOH identified in samples from individuals with CD and the suggestion of allelic loss and reduced transcription in hamartomas from a CD patient provide evidence that PTEN/MMACI functions as a tumor suppressor in CD. (C) 1998 Wiley-Liss, Inc. C1 Harvard Univ, Sch Med,Dept Adult Oncol, Dana Farber Canc Inst,Tradit Res Lab, Dept Med,Program Populat Sci,Human Canc Genet Uni, Boston, MA 02115 USA. Inst Bergonie, Bordeaux, France. Genome Therapeut Corp, Waltham, MA USA. NCI, Genet Epidemiol Branch, Bethesda, MD 20892 USA. Royal Marsden Hosp, Canc Res Inst, Surrey, England. Guys & St Thomas Hosp, Dept Clin Genet, London SE1 9RT, England. Royal N Shore Hosp, Kolling Inst Med Res, Mol Genet Unit, St Leonards, NSW 2065, Australia. Royal N Shore Hosp, Dept Surg, St Leonards, NSW 2065, Australia. Royal N Shore Hosp, Dept Endocrinol, St Leonards, NSW 2065, Australia. Univ Sydney, Dept Med, Sydney, NSW 2006, Australia. Univ Cambridge, Canc Res Campaign, Human Canc Genet Res Grp, Cambridge, England. RP Eng, C (reprint author), Harvard Univ, Sch Med,Dept Adult Oncol, Dana Farber Canc Inst,Tradit Res Lab, Dept Med,Program Populat Sci,Human Canc Genet Uni, SM822,44 Binney St, Boston, MA 02115 USA. RI Marsh, Deborah/I-1491-2014; Little, Randall/O-7172-2014; OI Marsh, Deborah/0000-0001-5899-4931; Eng, Charis/0000-0002-3693-5145 NR 24 TC 77 Z9 78 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD JAN PY 1998 VL 21 IS 1 BP 61 EP 69 DI 10.1002/(SICI)1098-2264(199801)21:1<61::AID-GCC8>3.0.CO;2-6 PG 9 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA YP539 UT WOS:000071288000008 PM 9443042 ER PT J AU Sellers, WR Novitch, BG Miyake, S Heith, A Otterson, GA Kaye, FJ Lassar, AB Kaelin, WG AF Sellers, WR Novitch, BG Miyake, S Heith, A Otterson, GA Kaye, FJ Lassar, AB Kaelin, WG TI Stable binding to E2F is not required for the retinoblastoma protein to activate transcription, promote differentiation, and suppress tumor cell growth SO GENES & DEVELOPMENT LA English DT Article DE retinoblastoma; transcription; E2F; tumorigenesis ID ONCOGENIC POINT MUTATIONS; SKELETAL-MUSCLE CELLS; CYCLIN-E GENE; FAMILY MEMBERS; GLUCOCORTICOID RECEPTOR; INCOMPLETE PENETRANCE; RB-1 GENE; P107; PRODUCT; PRB AB The retinoblastoma tumor suppressor protein (pRB) can inhibit cell cycle progression and promote differentiation. pRB interacts with a variety of transcription factors, including members of the E2F and C-EBP protein families and MyoD, and can either repress or activate transcription depending on the promoter under study. These biological and biochemical activities of pRB have been mapped previously to a core domain, referred to as the pRB pocket. Using a panel of synthetic pRB pocket mutants, we found that the acute induction of a G(1)/S block by pRB is linked to its ability to both bind to E2F and to repress transcription. In contrast, these functions were not required for pRB to promote differentiation, which correlated with its ability to activate transcription in concert with fate-determining proteins such as MyoD. All tumor-derived PRE mutants tested to date failed to bind to E2F and did not repress transcription. Despite an inability to bind to E2F, pRB mutants associated with a low risk of retinoblastoma, unlike high-risk mutants, retained the ability to activate transcription and promote differentiation. Thus, the pRB pocket participates in dual tumor suppressor functions, one linked to cell cycle progression and the other to differentiation control, and these functions can be genetically and mechanistically dissociated. C1 Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. NCI, USN, Med Oncol Branch, Div Clin Sci, Bethesda, MD 20889 USA. RP Kaelin, WG (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA. RI kaye, frederic/E-2437-2011; OI Novitch, Bennett/0000-0002-2696-3708 NR 59 TC 249 Z9 255 U1 1 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0890-9369 J9 GENE DEV JI Genes Dev. PD JAN 1 PY 1998 VL 12 IS 1 BP 95 EP 106 DI 10.1101/gad.12.1.95 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA YR072 UT WOS:000071455400010 PM 9420334 ER PT B AU Klein, DC Coon, SL Mazuruk, K Bernard, M Roseboom, PH Rodriguez, IR AF Klein, DC Coon, SL Mazuruk, K Bernard, M Roseboom, PH Rodriguez, IR BE Wahlstrom, J TI Biological rhythms and psychiatric disease: Focus on melatonin-related genes SO GENETIC AND PSYCHIATRIC DISORDERS SE WENNER-GREN INTERNATIONAL SERIES LA English DT Proceedings Paper CT Wenner-Gren Symposium on Genetics and Psychiatric Diseases CY JUN, 1996 CL SWEDEN SP Wenner-Gren Ctr Fdn C1 NICHHD, Dev Neurobiol Lab, Sect Neuroendocrinol, NIH, Bethesda, MD 20892 USA. RP Klein, DC (reprint author), NICHHD, Dev Neurobiol Lab, Sect Neuroendocrinol, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON PRESS LTD PI OXFORD PA THE BOULEVARD LANGFORD LANE KIDLINGTON, OXFORD OX5 1GB, ENGLAND BN 0-08-042746-4 J9 WENN GR INT PY 1998 VL 69 BP 289 EP 300 PG 12 WC Genetics & Heredity; Clinical Neurology; Neurosciences; Psychiatry SC Genetics & Heredity; Neurosciences & Neurology; Psychiatry GA BL93W UT WOS:000077224900019 ER PT J AU Hanson, RL Knowler, WC AF Hanson, RL Knowler, WC TI Analytic strategies to detect linkage to a common disorder with genetically determined age of onset: Diabetes mellitus in Pima Indians SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 4th Annual Meeting of the International-Genetic-Epidemiology-Society CY JUN 20, 1995 CL SALT LAKE CITY, UTAH SP Int Genet Epidemiol Soc DE age of onset; diabetes mellitus; non-insulin-dependent; linkage analysis; survival analysis ID AFFECTED RELATIVE PAIRS; LOD-SCORE ANALYSIS; 2-LOCUS MODELS; COMPLEX TRAITS; EXTENSIONS; LIKELIHOOD; PEDIGREES; POWER; TESTS; LOCUS AB Segregation analysis suggests that the high prevalence of non-insulin-dependent diabetes mellitus in Pima Indians may be partially due to a single locus with a major effect on age of onset. A simulation study was conducted to evaluate the power of various age-adjustment strategies in linkage analysis to detect this putative gene in 1,862 sib-pairs from 264 potentially informative nuclear families. Simulations were performed at a recombination fraction (theta) of 0.05 for values of polymorphism information content (PIC) ranging from 0.38 to 1.00. Under the codominant age-of-onset model supported by segregation analysis, power to detect linkage (at P < 0.0001) at PIC = 1.00 was 75% for the Haseman-Elston (HE) sib-pair test and 63% for the affected sib-pair test (ASP) with no age adjustment. Substantial improvements in power were possible for the HE test by defining the trait as a survival analysis "residual" (power = 91%) and for the ASP test by use of an age-of-onset threshold above which individuals are not included in the analysis (power = 90%, for age of onset < 45 yrs). The parametric method of linkage analysis was most powerful, as long as both the analysis model and the simulation model involved a genetic effect on age of onset, regardless of whether dominance at the trait locus was misspecified. Methods of age adjustment based on the probability of eventually becoming affected only improved power when the genetic effect was on susceptibility rather than age of onset. The method of age adjustment in linkage analysis may depend on whether one anticipates a genetic effect primarily on age of onset or on ultimate susceptibility, (C) 1998 Wiley-Liss, Inc.dagger. C1 NIDDKD, Diabet & Arthrit Epidemiol Sect, Phoenix, AZ 85014 USA. RP Hanson, RL (reprint author), NIDDKD, Diabet & Arthrit Epidemiol Sect, 1550 E Indian Sch Rd, Phoenix, AZ 85014 USA. RI Hanson, Robert/O-3238-2015 OI Hanson, Robert/0000-0002-4252-7068 FU NCRR NIH HHS [1 P41 RR03655] NR 42 TC 15 Z9 17 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1998 VL 15 IS 3 BP 299 EP 315 DI 10.1002/(SICI)1098-2272(1998)15:3<299::AID-GEPI7>3.0.CO;2-# PG 17 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA ZK238 UT WOS:000073299200007 PM 9593115 ER PT J AU Aitken, JF Bailey-Wilson, J Green, AC MacLennan, R Martin, NG AF Aitken, JF Bailey-Wilson, J Green, AC MacLennan, R Martin, NG TI Segregation analysis of cutaneous melanoma in Queensland SO GENETIC EPIDEMIOLOGY LA English DT Article DE skin neoplasms; genetics; family characteristics; heterogeneity ID DYSPLASTIC NEVUS SYNDROME; MALIGNANT-MELANOMA; FAMILIAL MELANOMA; GENETIC-HETEROGENEITY; LINKAGE ANALYSIS; FAMMM SYNDROME; CHROMOSOME 9P; LOCUS; KINDREDS; RISK AB To investigate whether the familial clustering of cutaneous melanoma is consistent with Mendelian inheritance of a major autosomal gene, maximum likelihood segregation analyses were performed in a population-based sample of 1,912 families ascertained through a proband with melanoma diagnosed in Queensland between 1982 and 1990. Analyses were performed with the S.A.G.E. statistical package, using the REGTL program for a binary trait with a variable age of onset. We sought medical confirmation for all family members reported to have had melanoma, and only medically verified cases among relatives were included in the analyses. The hypothesis of codominant Mendelian inheritance gave a significantly better fit to the data than either dominant or recessive Mendelian inheritance, or environmental transmission. Overall, both Mendelian inheritance of a single major gene, and purely environmental transmission were rejected (P < 0.001). In both the single major gene and environmental models, there was strong evidence of familial dependence in melanoma occurrence (P < 0.001). These results are consistent with reported genetic heterogeneity in melanoma inheritance and suggest that other familial factors, such as pigmentation, skin type, and sun exposure habits, may play an important role in the familial clustering of melanoma. Genet. Epidemiol. 15:391-401, 1998. (C) 1998 Wiley-Liss, Inc. C1 Queensland Inst Med Res, Brisbane, Qld 4029, Australia. Natl Human Genome Res Inst, NIH, Baltimore, MD USA. RP Aitken, JF (reprint author), Queensland Inst Med Res, PO Royal Brisbane Hosp, Brisbane, Qld 4029, Australia. RI Aitken, Joanne/C-5289-2009; OI Bailey-Wilson, Joan/0000-0002-9153-2920; Green, Adele/0000-0002-2753-4841; Martin, Nicholas/0000-0003-4069-8020 NR 35 TC 12 Z9 13 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1998 VL 15 IS 4 BP 391 EP 401 DI 10.1002/(SICI)1098-2272(1998)15:4<391::AID-GEPI5>3.0.CO;2-5 PG 11 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA ZX329 UT WOS:000074504600005 PM 9671988 ER PT J AU Xu, SZ Yonash, N Vallejo, RL Cheng, HH AF Xu, SZ Yonash, N Vallejo, RL Cheng, HH TI Mapping quantitative trait loci for binary traits using a heterogeneous residual variance model: an application to Marek's disease susceptibility in chickens SO GENETICA LA English DT Article DE chicken; fisher-scoring; Marek's disease; maximum likelihood; QTL; threshold trait ID ASYMPTOTIC VARIANCE; REGRESSION METHOD; EM ALGORITHM; LINE CROSSES; MARKERS AB A typical problem in mapping quantitative trait loci (QTLs) comes from missing QTL genotype. A routine method for parameter estimation involving missing data is the mixture model maximum likelihood method. We developed an alternative QTL mapping method that describes a mixture of several distributions by a single model with a heterogeneous residual variance. The two methods produce similar results, but the heterogeneous residual Variance method is computationally much faster than the mixture model approach. In addition, the new method can automatically generate sampling variances of the estimated parameters. We derive the new method in the context of QTL mapping for binary traits in a F-2 population. Using the heterogeneous residual variance model, we identified a QTL on chromosome IV that controls Marek's disease susceptibility in chickens. The QTL alone explains 7.2% of the total disease variation. C1 Univ Calif Riverside, Dept Bot & Plant Sci, Riverside, CA 92521 USA. USDA ARS, Avian Dis & Oncol Lab, E Lansing, MI 48823 USA. NIAAA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA. RP Xu, SZ (reprint author), Univ Calif Riverside, Dept Bot & Plant Sci, Riverside, CA 92521 USA. FU NIGMS NIH HHS [GM55321-01] NR 23 TC 19 Z9 22 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0016-6707 J9 GENETICA JI Genetica PY 1998 VL 104 IS 2 BP 171 EP 178 DI 10.1023/A:1003522902078 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 186GV UT WOS:000079721300006 PM 10220908 ER PT J AU Elfring, LK Daniel, C Papoulas, O Deuring, R Sarte, M Moseley, S Beek, SJ Waldrip, WR Daubresse, G DePace, A Kennison, JA Tamkun, JW AF Elfring, LK Daniel, C Papoulas, O Deuring, R Sarte, M Moseley, S Beek, SJ Waldrip, WR Daubresse, G DePace, A Kennison, JA Tamkun, JW TI Genetic analysis of brahma: The Drosophila homolog of the yeast chromatin remodeling factor SWI2/SNF2 SO GENETICS LA English DT Article ID TRANSCRIPTION IN-VIVO; POSTERIOR SEX COMBS; HOMEOTIC GENE; GLUCOCORTICOID RECEPTOR; RETINOBLASTOMA PROTEIN; MULTISUBUNIT COMPLEX; SWI/SNF COMPLEX; BINDING PROTEIN; CELL FATES; FAMILY AB The Drosophila brahma (brm) gene encodes an activator of homeotic genes related to the yeast chroma tin remodeling factor SWI2/SNF2. Here, we report the phenotype of null and dominant-negative brm mutations. Using mosaic analysis, we found that the complete loss of brm function decreases cell viability and causes defects in the peripheral nervous system of the adult. A dominant-negative brm mutation was generated by replacing a conserved lysine in the ATF-binding site of the BRM protein with an arginine. This mutation eliminates brm function in vivo but does not affect assembly of the 2-MD BRM complex. Expression of the dominant-negative BRM protein caused peripheral nervous system defects, homeotic transformations, and decreased viability. Consistent with these findings, the BRM protein is expressed at relatively high levels in nuclei throughout the developing organism. Site-directed mutagenesis was used to investigate the functions of conserved regions of the BRM protein. Domain II is essential for brm function and is required for the assembly or stability of the BRM complex. In spite of its conservation in numerous eukaryotic regulatory proteins, the deletion of die bromodomain of the BRM protein has no discernible phenotype. C1 Univ Calif Santa Cruz, Dept Biol, Sinsheimer Labs 350, Santa Cruz, CA 95064 USA. NICHHD, Genet Mol Lab, NIH, Bethesda, MD 20892 USA. RP Univ Calif Santa Cruz, Dept Biol, Sinsheimer Labs 350, Santa Cruz, CA 95064 USA. EM tamkun@biology.ucsc.edu FU NIGMS NIH HHS [GM49883] NR 85 TC 141 Z9 142 U1 0 U2 0 PU GENETICS SOCIETY AMERICA PI BETHESDA PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA SN 0016-6731 EI 1943-2631 J9 GENETICS JI Genetics PD JAN PY 1998 VL 148 IS 1 BP 251 EP 265 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA YR425 UT WOS:000071494000024 PM 9475737 ER PT J AU King, LM AF King, LM TI The role of gene conversion in determining sequence variation and divergence in the Est-5 gene family in Drosophila pseudoobscura SO GENETICS LA English DT Article ID ESTERASE-5 LOCUS; EVOLUTION; DNA; MELANOGASTER; POLYMORPHISM; DUPLICATION; ALLELES AB Nucleotide sequences of eight Est-5A and Est-5C genes corresponding to previously sequenced Est-5B members of this small gene family. The three esterase genes were also sequenced from D. persimilis and D. miranda for interspecific comparisons. The data provide evidence that gene conversion between loci contributes to polymorphism and to the homogenization of the Est-5 genes. For Est-5B which encodes one of the most highly polymorphic proteins in Drosophila, 12% of the segregating amino acid variants appear to have been introduced via gene conversion from other members of the gene family. Interlocus gene conversion can also explain high sequence similarity, especially at synonymous sites, between Est-5B and Est-5A. Tests of neutrality using interspecific comparisons show that levels of polymorphism conform to neutral expectations at each Est-5 locus. However, McDonald-Kreitman tests based on intraspecific gene comparisons indicate that positive selection on amino acids has accompanied Est-5 gene duplication and divergence in D. pseudoobscura. C1 Natl Human Genome Res Inst, Med Genet Branch, NIH, Bethesda, MD 20892 USA. Univ Miami, Dept Biol, Coral Gables, FL 33124 USA. RP King, LM (reprint author), Natl Human Genome Res Inst, Med Genet Branch, NIH, Bethesda, MD 20892 USA. FU NIGMS NIH HHS [GM-21179] NR 35 TC 28 Z9 36 U1 0 U2 0 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA SN 0016-6731 J9 GENETICS JI Genetics PD JAN PY 1998 VL 148 IS 1 BP 305 EP 315 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA YR425 UT WOS:000071494000028 PM 9475741 ER PT J AU Pruitt, KD AF Pruitt, KD TI WebWise: Guide to The Sanger Center's web site SO GENOME RESEARCH LA English DT Article C1 Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RP Pruitt, KD (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. NR 1 TC 2 Z9 2 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 1054-9803 J9 GENOME RES JI Genome Res. PD JAN PY 1998 VL 8 IS 1 BP 4 EP 8 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA YV276 UT WOS:000071807000002 PM 9445482 ER PT J AU Higgins, MJ Day, CD Smilinich, NJ Ni, L Cooper, PR Nowak, NJ Davies, C de Jong, PJ Hejtmancik, F Evans, GA Smith, RJH Shows, TB AF Higgins, MJ Day, CD Smilinich, NJ Ni, L Cooper, PR Nowak, NJ Davies, C de Jong, PJ Hejtmancik, F Evans, GA Smith, RJH Shows, TB TI Contig maps and genomic sequencing identify candidate genes in the usher 1C locus SO GENOME RESEARCH LA English DT Article ID SYNDROME TYPE-I; SULFONYLUREA RECEPTOR GENE; FAMILIAL HYPERINSULINISM; WAARDENBURG SYNDROME; MOLECULAR-CLONING; HUMAN-CHROMOSOMES; HUMAN HOMOLOG; YAC LIBRARY; MOUSE; LOCALIZATION AB Usher syndrome 1C [USH1C] is a congenital condition manifesting profound hearing loss, the absence of vestibular function, and eventual retinal degeneration. The USH1C locus has been mapped genetically to a 2- to 3-cM interval in 11p14-15.1 between D11S899 and D11S861. In an effort to identify the USH1C disease gene we have isolated the region between these markers in yeast artificial chromosomes (YACs) using a combination of STS content mapping and Alu-PCR hybridization. The YAC contig is similar to 3.5 Mb and has located several other loci within this interval, resulting in the order CEN-LDHA-SAA1-TPH-D11S1310-(D11S1888/KCNC1)-MYOD1-D11S902-D11S921-D11S1890-TEL. Subsequent haplotyping and homozygosity analysis refined the location of the disease gene to a 400-kb interval between D11S902 and D11S1890 with all affected individuals being homozygous for the internal marker D11S921. To Facilitate gene identification, the critical region has been converted into P1 artificial chromosome (PAC) clones using sequence-tagged sites (STSs) mapped to the YAC contig, Alu-PCR products generated from the YACs, and PAC end probes. A contig of >50 PAC clones has been assembled between D11S1310 and D11S1890, confirming the order of markers used in haplotyping. Three PAC clones representing nearly two-thirds of the USH1C critical region have been sequenced. PowerBLAST analysis identified six clusters of expressed sequence tags (ESTs), two known genes (BIR,SUR1) mapped previously to this region, and a previously characterized but unmapped gene NEFA (D<(N)under bar A> binding/<(EF)under bar> hand/acidic amino-acid-rich). GRAIL analysis identified 11 CpG islands and 73 exons of excellent quality. These data allowed the construction of a transcription map for the USH1C critical region, consisting of three known genes and six or more novel transcripts. Based on their map location, these loci represent candidate disease loci for USH1C. The NEFA gene was assessed as the USH1C locus by the sequencing of an amplified NEFA cDNA from an USH1C patient; however, no mutations were detected. C1 Roswell Pk Canc Inst, Dept Human Genet, Buffalo, NY 14263 USA. Univ Iowa, Dept Otolaryngol, Iowa City, IA 52242 USA. NEI, NIH, Bethesda, MD 20892 USA. Univ Texas, SW Med Ctr, McDermott Ctr Genome Res, Dallas, TX 75235 USA. RP Higgins, MJ (reprint author), Roswell Pk Canc Inst, Dept Human Genet, Buffalo, NY 14263 USA. FU NEI NIH HHS [EY10514]; NHGRI NIH HHS [HG00333]; NIDCD NIH HHS [DC02046] NR 53 TC 14 Z9 14 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 1054-9803 J9 GENOME RES JI Genome Res. PD JAN PY 1998 VL 8 IS 1 BP 57 EP 68 PG 12 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA YV276 UT WOS:000071807000008 PM 9445488 ER PT J AU Modi, WS Chen, ZQ AF Modi, WS Chen, ZQ TI Localization of the human CXC chemokine subfamily on the long arm of chromosome 4 using radiation hybrids SO GENOMICS LA English DT Article ID HUMAN GENOME; GENES; MAP; RECEPTORS; CYTOKINES; CLUSTER; BETA AB All 12 of the human CXC chemokine genes were physically mapped using gene-specific PCR primers and the GenBridge 4 radiation hybrid panel. Nine genes, PF4, PF4V1, GRO1, GCP2, PPBP, IL8, GRO2, GRO3, and SCYB5 were assigned within a 1.8-cR interval of one another on 4q. Two additional genes, MIG and INP10, map within 0.5 cR of each another and 6 cR distal to the above-mentioned group. The final gene, SDF1, is localized on 10q. Phylogenetic analyses of amino acid sequences revealed that SDF1 is the most divergent member and that the physically separated MIG-INP10 pair constitutes a distinct evolutionary lineage. (C) 1998 Academic Press. C1 NCI, Intramural Res Support Program, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. RP Modi, WS (reprint author), NCI, Intramural Res Support Program, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. NR 15 TC 39 Z9 42 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1998 VL 47 IS 1 BP 136 EP 139 DI 10.1006/geno.1997.5100 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA YU740 UT WOS:000071749500018 PM 9465307 ER PT S AU Fozard, JL Heikkinen, E AF Fozard, JL Heikkinen, E BE Graafmans, J Taipale, V Charness, N TI Maintaining movement ability in old age: Challenges for gerontechnology SO GERONTECHNOLOGY: A SUSTAINABLE INVESTMENT IN THE FUTURE SE STUDIES IN HEALTH TECHNOLOGY AND INFORMATICS LA English DT Proceedings Paper CT 2nd International Conference on Gerontechnology - A Sustainable Investment in the Future CY OCT, 1996 CL HELSINKI, FINLAND SP COST A5 Ageing & Technol, STAKES, Finnish Natl Res & Dev Ctr Welf & Hlth C1 NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. RP Fozard, JL (reprint author), NIA, Gerontol Res Ctr, 4940 Eastern Ave, Baltimore, MD 21224 USA. RI Fozard, James Leonard/B-3660-2009 NR 0 TC 5 Z9 5 U1 0 U2 0 PU I O S PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0926-9630 BN 90-5199-367-6 J9 ST HEAL T PY 1998 VL 48 BP 48 EP 61 PG 14 WC Ergonomics; Geriatrics & Gerontology; Medical Informatics SC Engineering; Geriatrics & Gerontology; Medical Informatics GA BL31D UT WOS:000075066900008 PM 10186575 ER PT J AU Streckfus, CF Baur, U Brown, LJ Bacal, C Metter, J Nick, T AF Streckfus, CF Baur, U Brown, LJ Bacal, C Metter, J Nick, T TI Effects of estrogen status and aging on salivary flow rates in healthy Caucasian women SO GERONTOLOGY LA English DT Article DE estrogen; menopause; saliva; saliva flow rates ID GLAND FUNCTION; AGE; XEROSTOMIA; SECRETION; MOUTH; SIALOCHEMISTRY; SEX AB A comparison of salivary flow rates was made between three groups of female individuals according to their menopausal status. The three groups consisted of healthy, dentate, nonmedicated women (with the exception of the use of estrogen) from the Baltimore Longitudinal Study of Aging. One group consisted of premenopausal women (n = 51), their mean age was 39 years. Another group (n = 26) was perimenopausal with a mean age of 48 years. A third group (n = 76) was postmenopausal with a mean age of 69 years, The groups were evaluated for unstimulated (U-PAR) and stimulated parotid gland flow rates (S-PAR), unstimulated (U-SUB) and stimulated submandibular/sublingual gland flow rates (S-SUB), and stimulated whole-saliva flow rates (S-WHOLE). The parotid flow rates were determined using a Carlson-Crittenden cup, while the submandibular/sublingual flow rates were determined using the National Institute of Dental Research collector. A 2% citrate solution was used for stimulation in glandular collections. Chewing a 1-cm(3) cube of paraffin was used to stimulate whole saliva. The results showed no significant differences in U-PAR, S-PAR, and S-WHOLE between the three groups. However, the premenopausal women had higher U-SUB than the postmenopausal group. The premenopausal women also had higher S-SUB than perimenopausal and postmenopausal groups. There were no differences in salivary flow rates between these taking estrogen and those that were not medicated. C1 Univ Mississippi, Med Ctr, Sch Dent, Jackson, MS 39216 USA. German Acad Exchange Serv, DAAD, Bonn, Germany. Johns Hopkins Bayview Med Ctr, Baltimore, MD USA. NIA, Gerontol Res Ctr, NIH, Bethesda, MD 20892 USA. NIDR, DEODP, NIH, Bethesda, MD 20892 USA. RP Streckfus, CF (reprint author), Univ Mississippi, Med Ctr, Sch Dent, 2500 N State St, Jackson, MS 39216 USA. NR 36 TC 42 Z9 43 U1 1 U2 5 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0304-324X J9 GERONTOLOGY JI Gerontology PD JAN-FEB PY 1998 VL 44 IS 1 BP 32 EP 39 DI 10.1159/000021980 PG 8 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA YP086 UT WOS:000071239800006 PM 9436013 ER PT S AU Rabin, O Purdon, AD Drieu, K Grange, E Chang, MCJ Deutsch, J Rapoport, SI AF Rabin, O Purdon, AD Drieu, K Grange, E Chang, MCJ Deutsch, J Rapoport, SI BE Packer, L Christen, Y TI Ginkgo biloba extract (EGb 761) may reduce neuronal death following transient cerebral ischemia by accelerating reincorporation of released arachidonic acid into brain lysophospholipids SO GINKGO BILOBA EXTRACT (EGB 761): LESSONS FROM CELL BIOLOGY SE ADVANCES IN GINKGO BILOBA EXTRACT RESEARCH LA English DT Proceedings Paper CT International Symposium on Ginkgo Biloba CY SEP 16-17, 1997 CL MONTIGNAC, FRANCE SP Ipsen Inst DE ischemia; fatty-acid metabolism; phospholipid metabolism; Ginkgo biloba extract (EGb 761); brain; gerbil; arachidonic acid; reincorporation; recovery; damage AB Ginkgo biloba extract (EGb 761) has been reported to reduce neuronal death in the hippocampus of gerbils subjected to 5 min of forebrain ischemia. One possibility is that EGb 761 acts by reducing the concentrations of unesterified fatty acids, including arachidonic acid (AA), which are released from brain phospholipids during transient ischemia and are thought to contribute to cell death. To test this hypothesis, awake gerbils that had or had not been treated with EGb 761 (150 mg/kg per os daily for 2 wk) were subjected to 5 min of bilateral occlusion of the common carotid arteries. Rates of reacylation of released AA and palmitic acid (PAM) into lysophospholipids were quantified during the following 5 min by an in vivo method that involves intravenous infusion of a radiolabeled fatty acid, followed by measurement of: 1) plasma radioactivity to time of death, 2) regional hippocampal and hindbrain radioactivity at the time of death using quantitative autoradiography, and 3) specific activity of the acyl-coenzyme A (CoA) pools (precursors for reacylation) compared with plasma specific activity (ratio defined as dilution factor;1). In untreated animals, recovery from transient ischemia was associated with a 2.6-fold increase in the rate of reincorporation of AA but no significant change in the rate of reincorporation of PAM into brain phospholipids, EGb 761 treatment significantly accelerated reincorporation of AA to 3.7 times the control mean, but had no effect on the rate of reincorporation of PAM. Thus, the reported reduction by EGb 761 of neuronal death following transient ischemia may reflect its ability to reduce neuronal exposure to high and prolonged toxic concentrations of released unesterified AA. Possible targets are the enzymes that control AA reincorporation. C1 NIA, Neurosci Lab, NIH, Bethesda, MD 20892 USA. RP Rapoport, SI (reprint author), NIA, Neurosci Lab, NIH, Bldg 10,Room 6C103,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ET MEDICALES ELSEVIER PI PARIS PA 23, RUE LINOIS, 75724 PARIS, FRANCE SN 0927-9407 BN 2-84299-023-4 J9 ADV GINKGO PY 1998 VL 7 BP 109 EP 120 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA BL66T UT WOS:000076262900009 ER PT J AU Wenthold, RJ Roche, KW AF Wenthold, RJ Roche, KW TI The organization and regulation of non-NMDA receptors in neurons SO GLUTAMATE SYNAPSE AS A THERAPEUTICAL TARGET: MOLECULAR ORGANIZATION AND PATHOLOGY OF THE GLUTAMATE SYNAPSE SE PROGRESS IN BRAIN RESEARCH LA English DT Review ID DEPENDENT PROTEIN-KINASE; LONG-TERM POTENTIATION; HIGH-AFFINITY KAINATE; SELECTIVE GLUTAMATE RECEPTORS; CULTURED HIPPOCAMPAL-NEURONS; SUBUNIT MESSENGER-RNAS; CEREBELLAR PURKINJE-CELLS; RETINAL HORIZONTAL CELLS; ACID BINDING-SITES; RAT-BRAIN C1 Natl Inst Deafness & Other Commun Disorders, Neurochem Lab, NIH, Bethesda, MD USA. RP Wenthold, RJ (reprint author), Natl Inst Deafness & Other Commun Disorders, Neurochem Lab, NIH, Bethesda, MD USA. EM went-hold@nided.nih.gov OI Roche, Katherine/0000-0001-7282-6539 NR 140 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 J9 PROG BRAIN RES PY 1998 VL 116 BP 133 EP 152 DI 10.1016/S0079-6123(08)60435-5 PG 20 WC Neurosciences SC Neurosciences & Neurology GA BM21W UT WOS:000078045300010 PM 9932375 ER PT J AU Allison, RSH Mumy, ML Wakefield, LM AF Allison, RSH Mumy, ML Wakefield, LM TI Translational control elements in the major human transforming growth factor-beta 1 mRNA SO GROWTH FACTORS LA English DT Article DE transforming growth factor-beta; translational control; polysomes; untranslated regions ID 5' NONCODING REGION; HUMAN BREAST-CANCER; BETA MESSENGER-RNA; EPITHELIAL-CELLS; 5'-UNTRANSLATED REGION; EXPRESSION PATTERNS; SECONDARY STRUCTURE; RESPONSIVE ELEMENT; GENE-EXPRESSION; TGF-BETA-1 AB Polysome analysis indicates that the major 2.4 kb transforming growth factor-beta 1 (TGF-beta 1) transcript is poorly translated, both in cultured cells, and in vivo in mouse liver. In contrast, the TGF-beta 2 transcripts are efficiently translated, The contribution of the 5'- and 3'-untranslated regions (UTRs) to the translational inhibition of the full-length TGF-beta 1 transcript was studied by deletion analysis, Despite their high G+C content, both UTRs stimulated translation in vine. However, polysome analysis of synthetic TGF-beta 1 mRNAs transfected into MCF-7 cells suggests that the cell contains a limited pool of trans-acting factors that interact with the 5'-UTR to make it inhibitory in viva, Further deletion analysis in vitro revealed multiple stimulatory and inhibitory regions in the 5'UTR, This has important implications for the translatability of the naturally occurring shorter TGF-beta 1 transcripts and provides a framework for higher resolution mapping studies. Overall, the poor translational efficiency of the major TGF-beta 1 mRNA in vivo appears to be due to a combination of poor initiation sequence context, and inhibitory interactions of limiting transacting factors with cis-inhibitory elements embedded in an otherwise stimulatory 5'UTR. C1 NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. RP Wakefield, LM (reprint author), NCI, Lab Cell Regulat & Carcinogenesis, Bldg 41,Room B1303,41 Lib Dr,MSC 5055, Bethesda, MD 20892 USA. EM wakefiel@dce41.nci.nih.gov NR 50 TC 18 Z9 19 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1998 VL 16 IS 2 BP 89 EP 100 PG 12 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA 160YJ UT WOS:000078260100001 PM 9932227 ER PT J AU Seno, M Desantis, M Kannan, S Bianco, C Tada, H Kim, N Kosaka, M Gullick, WJ Yamada, H Salomon, DS AF Seno, M Desantis, M Kannan, S Bianco, C Tada, H Kim, N Kosaka, M Gullick, WJ Yamada, H Salomon, DS TI Purification and characterization of a recombinant human cripto-1 protein SO GROWTH FACTORS LA English DT Article DE cripto; recombinant expression; refolding; 3-trimethylammoniopropyl methanethiosulfonate; beta-casein expression; Shc phosphorylation; MAPK activation; duct-like branching ID EPIDERMAL GROWTH-FACTOR; HUMAN BREAST CARCINOMAS; FACTOR FAMILY; FACTOR-ALPHA; IMMUNOHISTOCHEMICAL DETECTION; EGF FAMILY; EXPRESSION; AMPHIREGULIN; GENE; CELLS AB Cripto-1 (CR-1) is a novel protein that contains a modified EGF-like motif and that does not directly bind to any of the known erb B type-1 receptor tyrosine kinase receptors. To more clearly define the biological effects of CR-1 and to more adequately compare the structure-function relationships of CR-1 with other members of the EGF family of growth factors, we have expressed a modified, full-length recombinant human CR-1 protein (rhCR-1) in E. coli and have devised a procedure for the solubilization, refolding and purification of a biologically active form of this protein. We have generated the mature form of hCR-1 from computer assisted predictions of potential signal peptide cleavage sites. Expression of the modified rhCR-1 protein in E. coli was limited to the inclusion bodies. The rhCR-1 protein was found to be expressed at high levels in bacterial cells when fused to a histidine-tag sequence. Refolding of rhCR-1 was found to be difficult because of the large number of cysteine residues in the protein which results in protein aggregation. By chemically modifying the cysteine residues in the rhCR-1 protein with 3-trimethyl-ammoniopropyl methanethiosulfonate, additional positive charges have been introduced into the protein by this disulfiding reagent. This modification facilitates solubilization of the protein when rhCR-1 is denatured, The solubilized, denatured protein was then purified by CM cation exchange and Cs reverse phase HPLC chromatography and refolded in a redox buffer. The refolded, modified rhCR-1 protein was found to be biologically active by its ability to inhibit beta-casein expression, to stimulate the tyrosine phosphorylation of Shc and the activation of MAPK and by its capacity to facilitate branching growth of mouse mammary epithelial cells in type I collagen gels. C1 Okayama Univ, Fac Engn, Dept Biosci & Biotechnol, Okayama 7008530, Japan. NCI, Tumour Growth Factor Sect, Tumor Immunol & Biol Lab, NIH, Bethesda, MD 20892 USA. Hammersmith Hosp, ICRF, Oncol Unit, London, England. RP Seno, M (reprint author), Okayama Univ, Fac Engn, Dept Biosci & Biotechnol, 3-1-1 Tsushima Naka, Okayama 7008530, Japan. EM senom@biotech.okayama-u.ac.jp RI YAMADA, Hidenori/B-2639-2011; KOSAKA, Megumi/B-1864-2011; SENO, Masaharu /B-2092-2011 OI SENO, Masaharu /0000-0001-8547-6259 NR 45 TC 30 Z9 30 U1 0 U2 2 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1998 VL 15 IS 3 BP 215 EP 229 PG 15 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA ZH240 UT WOS:000073087400005 PM 9570042 ER PT J AU Burmester, JK Qian, SW Ohlsen, D Phan, S Sporn, MB Roberts, AB AF Burmester, JK Qian, SW Ohlsen, D Phan, S Sporn, MB Roberts, AB TI Mutational analysis of a transforming growth factor-beta receptor binding site SO GROWTH FACTORS LA English DT Article DE colon cancer; protein structure; growth inhibition; isoform ID HEMORRHAGIC TELANGIECTASIA TYPE-1; TGF-BETA; II RECEPTOR; ENDOTHELIAL-CELLS; CRYSTAL-STRUCTURE; MICROSATELLITE INSTABILITY; HIGH-AFFINITY; RAT-KIDNEY; FACTOR-BETA-1; PROTEIN AB Transforming growth factor-beta s (TGF-beta 1,beta 2,beta 3) are important regulators of cell growth and differentiation which share approximately 70% identical amino acids. Using LS513 colorectal cells, which are growth inhibited by TGF-beta 1 (ED50 of 100 pM), but are refractory to TGF-beta 2 (ED50 of 50,000 to 100,000 pM), we have determined that amino acids 92-98 of TGF-beta specify growth inhibition. The chimeric protein TGF-beta 1/beta 2(92-98), in which amino acids 92-98 of TGF-beta 1 were exchanged for the corresponding amino acids of TGF-beta 2, was indistinguishable from TGF-beta 2 at inhibiting growth of LS513 cells. In contrast, both TGF-beta 1/beta 2(92-95) and TGF-beta 1/beta 2(94-98) inhibited the growth of LS513 cells with an ED50 of approximately 1000 pM. TGF-beta 1/beta 2(95-98), in which amino acids 95-98 of TGF-beta 1 have been replaced with the corresponding amino acids of TGF-beta 2, had full activity and was indistinguishable from TGF-beta 1. Receptor cross-linking experiments demonstrated that binding of the chimeras to the type I and type Il receptors of LS513 cells was consistent with their biological activity. TGF-beta 1/beta 2(92-98), TGF-beta 1/beta 2(92-95) and TGF-beta 1/beta 2(94-98) were each similar to TGF-beta 2 in that they failed to bind to the soluble Type II receptor in a solid-phase assay. These results demonstrate that amino acids 92-98 are involved in the interaction between TGF-R and its signaling receptors and they show that modest changes within this region can substantially alter biological response. C1 Marshfield Med Res Fdn, Marshfield, WI 54449 USA. Adv Genet Technol, Gaithersburg, MD 20879 USA. Dartmouth Coll, Sch Med, Dept Pharmacol, Hanover, NH 03755 USA. NCI, Chemoprevent Lab, NIH, Bethesda, MD 20892 USA. RP Burmester, JK (reprint author), Marshfield Med Res Fdn, 1000 N Oak Ave, Marshfield, WI 54449 USA. NR 51 TC 20 Z9 20 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1998 VL 15 IS 3 BP 231 EP 242 PG 12 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA ZH240 UT WOS:000073087400006 PM 9570043 ER PT J AU Chang, AC Rick, ME Pierce, LR Weinstein, MJ AF Chang, AC Rick, ME Pierce, LR Weinstein, MJ TI Summary of a workshop on potency and dosage of von Willebrand factor concentrates SO HAEMOPHILIA LA English DT Editorial Material DE vWF concentrates; von Willebrand's disease; FVIII; surgery; ristocetin cofactor assay; haemorrhage ID VONWILLEBRAND-FACTOR; FACTOR-VIII; DISEASE; RISTOCETIN; ADHESION C1 US FDA, Ctr Biol Evaluat & Res, Div Hematol, Bethesda, MD 20892 USA. US FDA, Ctr Biol Evaluat & Res, Div Blood Applicat, Bethesda, MD 20892 USA. NIH, Hematol Serv, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA. RP Chang, AC (reprint author), US FDA, Ctr Biol Evaluat & Res, Div Hematol, 8800 Rockville Pike,HFM-340, Bethesda, MD 20892 USA. NR 20 TC 32 Z9 33 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 1351-8216 J9 HAEMOPHILIA JI Haemophilia PY 1998 VL 4 SU 3 BP 1 EP 6 PG 6 WC Hematology SC Hematology GA 156NX UT WOS:000078008600001 PM 10028311 ER PT J AU Klausner, RD Rouault, T AF Klausner, RD Rouault, T TI The molecular basis of iron metabolism SO HARVEY LECTURES, VOL 92, 1996-1997 SE HARVEY LECTURES LA English DT Review ID ELEMENT-BINDING-PROTEIN; RECEPTOR MESSENGER-RNA; HUMAN FERRITIN EXPRESSION; RESPONSIVE ELEMENT; TRANSFERRIN RECEPTOR; TRANSLATIONAL REGULATION; CYTOSOLIC ACONITASE; SULFUR CLUSTER; UNTRANSLATED REGION; K562 CELLS C1 NCI, Bethesda, MD 20892 USA. NICHHD, Bethesda, MD 20892 USA. RP Klausner, RD (reprint author), NCI, Bethesda, MD 20892 USA. NR 45 TC 3 Z9 3 U1 1 U2 2 PU WILEY-LISS, INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0073-0874 J9 HARVEY LECT PY 1998 VL 92 BP 99 EP 112 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA BL61V UT WOS:000076026600006 ER PT J AU Lenz, P Hsu, R Yee, C Yancey, K Volc-Platzer, B Stingl, G Kirnbauer, R AF Lenz, P Hsu, R Yee, C Yancey, K Volc-Platzer, B Stingl, G Kirnbauer, R TI Cicatricial pemphigoid with anti-epiligrin autoantibodies in a patient with metastatic adenocarcinoma of the endometrium SO HAUTARZT LA German DT Article DE cicatricial pemphigoid; anti-epiligrin autoantibodies; immunosuppressive therapy; paraneoplasia ID BASEMENT-MEMBRANE; SKIN-DISEASE; ANTIBODIES; IDENTIFICATION; LIGAND; TARGET; SITES AB A 71 year old female patient presented with erosions of the oral, genital and ocular mucosa, but without skin lesions. One year prior to the onset of lesions, a metastatic adenocarcinoma of the endometrium had been diagnosed. In perilesional skin, direct immunofluorescence showed linear deposits of C3 and IgG along the basement membrane zone. indirect immunofluorescence demonstrated anti-basement membrane zone antibodies which bound exclusively to the dermal side of 1M NaCl-split skin. In imm unoprecipitation studies, the autoantibodies bound a set of proteins characteristic of epiligrin/laminin-5, and they specifically immunoblotted the alpha-subunit of this protein. These results confirmed our presumed diagnosis of anti-epiligrin cicatricial pemphigoid. Combined treatment with methylprednisolone and dapsone resulted in prompt remission, despite progression of her malignancy. So far, only eight patients with anti-epiligrin cicatricial pemphigoid have been reported worldwide. Our patient represents the first case from Austria and is clinically and immunopathologically similar to previously reported cases. C1 Univ Klin Dermatol, Abt Immundermatol & Infektiose Hautkrankheiten, Allgemeines Krankenhaus Stadt Wien, A-1090 Vienna, Austria. Natl Inst Hlth, Dermatol Branch, Natl Canc Inst, Bethesda, MD USA. RP Lenz, P (reprint author), Univ Klin Dermatol, Abt Immundermatol & Infektiose Hautkrankheiten, Allgemeines Krankenhaus Stadt Wien, Wahringer Gurtel 18-20, A-1090 Vienna, Austria. NR 23 TC 20 Z9 20 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0017-8470 J9 HAUTARZT JI Hautarzt PD JAN PY 1998 VL 49 IS 1 BP 31 EP 35 DI 10.1007/s001050050697 PG 5 WC Dermatology SC Dermatology GA YX083 UT WOS:000072004700006 PM 9522190 ER PT J AU Richard, G Oosterwijk, JC AF Richard, G Oosterwijk, JC TI Keratosis follicularis spinulosa decalvans SO HAUTARZT LA German DT Letter C1 NIAMS, Genet Studies Sect, Skin Biol Lab, NIH, Bethesda, MD 20892 USA. Univ Groningen, Vakgroepe Med Genet, NL-9713 AW Groningen, Netherlands. RP Richard, G (reprint author), NIAMS, Genet Studies Sect, Skin Biol Lab, NIH, Bldg 6,Room 429,6 Ctr Dr MSC 2757, Bethesda, MD 20892 USA. RI Oosterwijk, Jan C./G-5770-2011 NR 14 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0017-8470 J9 HAUTARZT JI Hautarzt PD JAN PY 1998 VL 49 IS 1 BP 61 EP 62 DI 10.1007/s001050050703 PG 2 WC Dermatology SC Dermatology GA YX083 UT WOS:000072004700012 PM 9522196 ER PT J AU Fee, E Garofalo, ME AF Fee, E Garofalo, ME TI Life support: Three nurses on the front lines SO HEALTH AFFAIRS LA English DT Book Review C1 Natl Lib Med, Div Med, Bethesda, MD 20209 USA. Holy Cross Hosp, Silver Spring, MD USA. RP Fee, E (reprint author), Natl Lib Med, Div Med, Bethesda, MD 20209 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU PROJECT HOPE PI BETHESDA PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA SN 0278-2715 J9 HEALTH AFFAIR JI Health Aff. PD JAN-FEB PY 1998 VL 17 IS 1 BP 261 EP 262 DI 10.1377/hlthaff.17.1.261 PG 2 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA YY811 UT WOS:000072187800031 ER PT J AU Gilbert, ES AF Gilbert, ES TI Accounting for errors in dose estimates used in studies of workers exposed to external radiation SO HEALTH PHYSICS LA English DT Article DE biostatistics; dosimetry; epidemiology; radiation risk ID HANFORD SITE; MORTALITY; BIAS AB This paper discusses approaches for accounting for errors in dose estimates used in dose-response analyses of data from epidemiologic studies of workers exposed to external radiation and illustrates these approaches with analyses of data on workers at the Hanford site. In these analyses, estimates of the excess relative risk are corrected for bias in recorded doses as estimates of organ dose, and confidence intervals reflect uncertainty in the correction factors. For the Hanford data, these procedures did not greatly modify results for all cancer excluding leukemia, but the upper confidence limit for leukemia was increased by about 40%, a difference that is of some importance in comparing worker-based estimates and confidence intervals with estimates that serve as the basis of radiation protection standards. It is argued that aside from taking account of uncertainty in correction factors, no additional corrections are needed to address random errors resulting from variation in exposure energies and geometries. In addition, it is shown that because the larger cumulative doses, which are most influential in dose-response analyses, are the sums of large numbers of independent dosimeter readings, random errors resulting from variation in laboratory measurements are unlikely to be important for epidemiologic purposes. It is hoped that the approaches illustrated in this paper will be applied to future analyses of data from worker studies, especially combined analyses of data from several countries. Taking account of uncertainty in factors that correct for systematic bias will be especially important as uncertainty resulting from sampling variation decreases. C1 NCI, Radiat Epidemiol Branch, Rockville, MD 20852 USA. RP Gilbert, ES (reprint author), NCI, Radiat Epidemiol Branch, 6130 Execut Blvd,Suite 408, Rockville, MD 20852 USA. FU NIOSH CDC HHS [R01 OH03270] NR 21 TC 14 Z9 14 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PD JAN PY 1998 VL 74 IS 1 BP 22 EP 29 DI 10.1097/00004032-199801000-00003 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA YM718 UT WOS:000071093900004 PM 9415578 ER PT J AU Lerman, C Caporaso, N Main, D Audrain, J Boyd, NR Bowman, ED Shields, PG AF Lerman, C Caporaso, N Main, D Audrain, J Boyd, NR Bowman, ED Shields, PG TI Depression and self-medication with nicotine: The modifying influence of the dopamine D4 receptor gene SO HEALTH PSYCHOLOGY LA English DT Article DE smoking; genetics; depression ID FAGERSTROM TOLERANCE QUESTIONNAIRE; SMOKING CESSATION; MAJOR DEPRESSION; NOVELTY SEEKING; DEPENDENCE; POLYMORPHISM; ASSOCIATION; PERSONALITY; POPULATION; VARIANTS AB This study evaluated whether there are genetic subgroups of depressed individuals who are more or less predisposed to engage in self-medication smoking practices. Smokers (N = 231) completed self-report questionnaires of depression and smoking practices and were genotyped for the dopamine D4 receptor (DRD4) gene. A significant interaction (DRD4 Genotype x Depression) was found for stimulation smoking and negative-affect reduction smoking. Specifically, these smoking practices were significantly heightened in depressed smokers homozygous for the short alleles of DRD4 but not in those heterozygous or homozygous for the long alleles of DRD4. These preliminary results suggest that the rewarding effects of smoking and the beneficial effects of nicotine replacement therapy for depressed smokers may depend, in part, on genetic factors involved in dopamine transmission. C1 Georgetown Univ, Med Ctr, Lombardi Canc Ctr, Washington, DC 20007 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA. RP Lerman, C (reprint author), Georgetown Univ, Med Ctr, Lombardi Canc Ctr, 2233 Wisconsin Ave NW,Suite 535, Washington, DC 20007 USA. RI Shields, Peter/I-1644-2012 FU NCI NIH HHS [R01 CA63562] NR 46 TC 144 Z9 147 U1 3 U2 8 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0278-6133 J9 HEALTH PSYCHOL JI Health Psychol. PD JAN PY 1998 VL 17 IS 1 BP 56 EP 62 DI 10.1037/0278-6133.17.1.56 PG 7 WC Psychology, Clinical; Psychology SC Psychology GA YR726 UT WOS:000071524100008 PM 9459071 ER PT J AU Shi, Q Chen, K Brossi, A Verdier-Pinard, P Hamel, E McPhail, AT Lee, KH AF Shi, Q Chen, K Brossi, A Verdier-Pinard, P Hamel, E McPhail, AT Lee, KH TI Antitumor agents - Part 184 - Syntheses and antitubulin activity of compounds derived from reaction of thiocolchicone with amines: Lactams, alcohols, and ester analogs of allothiocolchicinoids SO HELVETICA CHIMICA ACTA LA English DT Article ID METHYL-ETHER; COLCHICINE AB 7-O-Substituted analogs of deaminodeoxycolchinol thiomethyl ether were synthesized and evaluated for their inhibitory effects on tubulin polymerization in vitro. Ketone 9, a key compound in this study, was derived from thiocolchicone 6 by reaction with aniline. Reaction of compound 6 with MeNH2 or BuNH2 gave tetracyclic lactams 7 and 8, respectively. Optically active alcohols 11a and 11b were obtained from racemic 11 by chemical resolution including a separation of the camphanate diastereoisomers 12a and 12b, followed by basic hydrolysis. The (aR,7R)-configuration of 12b was verified by X-ray crystallographic analysis. Almost all racemic and optically active 7-O-acyl or 7-O-aroyl compounds had strong inhibitory effects on the tubulin polymerization reaction, with IC,, values from 1.7 to 5.1 mu M. A few agents, such as the lactams 7 and 8, the camphanates 12a and 12b, the cyclohexanecarboxylates 19a and 19b, and, most notably, the (7S)-benzoate 15a, had negligible effects on polymerization, yielding IC50 values greater than 40 mu M. Ketone 9 showed strong inhibition of tubulin polymerization comparable to that of thiocolchicone (6). Optically active alcohol 11a and acyl esters 13a and 14a with a (7S)-configuration were more active than the (7R)-esters 13b and 14b. However, the esters 15a-17a with a (7S)-configuration were less active than the (7R)-isomers 15b-17b, in which the (7R)-benzoate 15b was at least 15-fold more inhibitory than the (7S)-isomer 15a. For the most part, the agents causing strongest inhibition of polymerization also caused the greatest inhibition of [H-3]colchicine binding. NMR and optical rotatory data indicate that, in polar solvents, the equilibrium in esters with a 7-O-aroyl substituent, i.e.; 15a,b, 16a,b, and 17a,b, is reversed from (aS) to (aR) or from (aR) to (aS), as compared to nonpolar solvents. C1 Univ N Carolina, Sch Pharm, Div Med Chem & Nat Prod, Nat Prod Lab, Chapel Hill, NC 27599 USA. NCI, Frederick Canc Res & Dev Ctr, Lab Drug Discovery Res & Dev,Dev Therap Program, Div Canc Treatment,Diag & Ctr, Frederick, MD 21702 USA. Duke Univ, Dept Chem, Paul M Gross Chem Lab, Durham, NC 27708 USA. RP Lee, KH (reprint author), Univ N Carolina, Sch Pharm, Div Med Chem & Nat Prod, Nat Prod Lab, Chapel Hill, NC 27599 USA. OI Verdier-Pinard, Pascal/0000-0002-6149-6578 NR 16 TC 29 Z9 30 U1 0 U2 0 PU WILEY-V C H VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0018-019X J9 HELV CHIM ACTA JI Helv. Chim. Acta PY 1998 VL 81 IS 6 BP 1023 EP 1037 DI 10.1002/hlca.19980810516 PG 15 WC Chemistry, Multidisciplinary SC Chemistry GA ZU954 UT WOS:000074253200002 ER PT J AU Messineo, C Coupland, R Bakhshi, A Raffeld, M Irving, SG Bagg, A Cossman, J AF Messineo, C Coupland, R Bakhshi, A Raffeld, M Irving, SG Bagg, A Cossman, J TI Rearrangement, hypermutation, and possible preferential use of a V(H)5 gene, V(H)32, in a Hodgkin's cell line SO HEMATOPATHOLOGY AND MOLECULAR HEMATOLOGY LA English DT Article ID HUMAN IMMUNOGLOBULIN-VH; REED-STERNBERG CELLS; INSITU HYBRIDIZATION; DISEASE; EXPRESSION; REPERTOIRE; FEATURES; LEUKEMIA; REGION; LOCUS AB Nonrandom use of immunoglobulin variable (V) gene segments is a feature of some B-cell neoplasms, possibly as a consequence of antigen selection. In Hodgkin's disease, the primary tissues, cell lines, and even single Reed-Sternberg cells can carry immunoglobulin gene rearrangements. Here, we examined the immunoglobulin heavy-chain genes of a well-characterized Hodgkin's-derived cell line, L428, and found a hypermutated V(H)32 gene involving a conventional V(N)D(N)J4-C gamma 4 rearrangement. V(H)32 is one of two rearranging members of the V(H)5 family that is also rearranged preferentially in some B-cell neoplasms and familial CLL. Unexpectedly, the closest known rearranged sequence match for the rearranged V-H gene of L428 was found in the single Reed-Sternberg cells of lymphocyte-predominance Hodgkin's disease, and is a mutated V(H)251, the only other rearranging member of the V(H)5 family. Assuming random usage of the human V-H pool, the chance of coincident V(H)5 family gene rearrangement in the two cases of Hodgkin's disease is only about 10(-3). Biased use of V-H genes suggests a B-cell target that is either selected by antigen or vulnerable to transformation at an early antigen-independent, developmental stage. These findings raise the question whether similar processes operate in Hodgkin's disease. C1 Georgetown Univ, Med Ctr, Dept Pathol, Washington, DC 20007 USA. Cross Canc Ctr, Edmonton, AB, Canada. NIH, Pathol Lab, Bethesda, MD 20892 USA. RP Cossman, J (reprint author), Georgetown Univ, Med Ctr, Dept Pathol, 3900 Reservoir Rd NW, Washington, DC 20007 USA. NR 29 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 1082-8893 J9 HEMATOPATHOL MOL HEM JI Hematopathol. Mol. Hematol. PY 1998 VL 11 IS 1 BP 19 EP 28 PG 10 WC Hematology; Pathology SC Hematology; Pathology GA YM690 UT WOS:000071090300003 ER PT J AU Chaudhary, R Kijas, J Raudsepp, T Guan, XY Zhang, H Chowdhary, BP AF Chaudhary, R Kijas, J Raudsepp, T Guan, XY Zhang, H Chowdhary, BP TI Microdissection of pig chromosomes: dissection of whole chromosomes, arms and bands for construction of paints and libraries SO HEREDITAS LA English DT Article ID RAPID GENERATION; MALIGNANT-MELANOMA; GENOMIC DNA; AMPLIFICATION; PROBES; HETEROCHROMATIN; IDENTIFICATION; MARKERS; GENES AB Chromosome microdissection is an important means to efficiently generate a large number of markers from a desired region of a genome. The present study was designed to initiate microdissection and amplification of DNA fi om whole chromosomes. arms, or bands of porcine chromosomes. The following pig (SSC) chromosomes/segments were scraped: SSC1p. SSC1q26-q2.13, SSC2q11-q14, SSC4q12-q25, SSC13, SSC13q12-q31, SSC13q32-q43, SSC13q32-q43, SSC15, and SSC16q21-q23. After amplification and PCR-labelling, the DNA from the dissected segments were painted back to normal metaphase chromosomes to test their identity. Microdissection of some of the segments (on SSC4, 13 and 15) coincides with the mapping of economically important traits. As a first step towards generation of markers, microcloning of amplified product from SSC1p and SSC15 was carried out. The libraries were screened with a (GT)(15) oligonucleotide probe. Future prospects of such a work in Farm animals are discussed. C1 Swedish Univ Agr Sci, Dept Anim Breeding & Genet, S-75007 Uppsala, Sweden. NIH, Natl Ctr Human Genome Res, Bethesda, MD 20892 USA. RP Chowdhary, BP (reprint author), Royal Vet & Agr Univ, Div Anim Genet, Gronnegards 3, DK-1870 Frederiksberg C, Denmark. RI Kijas, James/A-4656-2011; Guan, Xin-Yuan/A-3639-2009 OI Kijas, James/0000-0002-1417-8278; Guan, Xin-Yuan/0000-0002-4485-6017 NR 24 TC 7 Z9 7 U1 0 U2 1 PU HEREDITAS-DISTRIBUTION PI LANDSKRONA PA GJORLOFFSGATAN 121, 261 34 LANDSKRONA, SWEDEN SN 0018-0661 J9 HEREDITAS JI Hereditas PY 1998 VL 128 IS 3 BP 265 EP 271 DI 10.1111/j.1601-5223.1998.00265.x PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 116DZ UT WOS:000075709500012 PM 9760875 ER PT J AU Mishkin, M Vargha-Khadem, F Gadian, DG AF Mishkin, M Vargha-Khadem, F Gadian, DG TI Amnesia and the organization of the hippocampal system SO HIPPOCAMPUS LA English DT Editorial Material DE hippocampal damage; amnesia; episodic memory; semantic memory ID PARAHIPPOCAMPAL CORTICES; AREA TEO; AFFERENTS; MACAQUE; CONNECTIONS; MONKEYS; MEMORY; CORTEX; PRESTRIATE; HRP AB Early hippocampal injury in humans has been found to result in a limited form of global anterograde amnesia. At issue is whether the limitation is qualitative, with the amnesia reflecting substantially greater impairment in episodic than in semantic memory, or only quantitative, with both episodic and semantic memory being partially and equivalently impaired. Evidence from neuroanatomical and lesion studies in animals suggests that the hippocampus and subhippocampal cortices form a hierarchically organized system, such that the greatest convergence of information (and, by implication, the richest amount of association) takes place within the hippocampus, located at the top of the hierarchy. On the one hand, this evidence is consistent with the view that selective hippocampal damage produces a differential impairment in context-rich episodic memory as compared with context-free semantic memory, because only the latter can be supported by the subhippocampal cortices. On the other hand, given the system's hierarchical form of organization, this dissociation of deficits is difficult to prove, because a quantitatively limited deficit will nearly always be a viable alternative. A final choice between the alternative views is therefore likely to depend less on further evidence gathered in brain-injured patients than on which view accounts for more of the data gathered from converging approaches to the problem. (C) 1998 Wiley-Liss, Inc. C1 NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA. UCL, Inst Child Hlth, Cognit Neurosci Unit, London, England. UCL, Sch Med, Inst Child Hlth, Radiol & Phys Unit, London W1N 8AA, England. RP Mishkin, M (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 49,Room 1B80, Bethesda, MD 20892 USA. RI Gadian, David/C-4961-2008; Vargha-Khadem, Faraneh/C-2558-2008 NR 28 TC 140 Z9 141 U1 0 U2 5 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1050-9631 J9 HIPPOCAMPUS JI Hippocampus PY 1998 VL 8 IS 3 BP 212 EP 216 PG 5 WC Neurosciences SC Neurosciences & Neurology GA ZV762 UT WOS:000074338600004 PM 9662136 ER PT J AU Dore, FY Thornton, JA White, NM Murray, EA AF Dore, FY Thornton, JA White, NM Murray, EA TI Selective hippocampal lesions yield nonspatial memory impairments in rhesus monkeys SO HIPPOCAMPUS LA English DT Article DE hippocampus; primates; memory; object discrimination; macaques ID STIMULUS-STIMULUS ASSOCIATION; TEMPORAL-LOBE; AMNESIC PATIENTS; AMYGDALA; DAMAGE; SYSTEM; PERFORMANCE; RECOGNITION; OBJECTS; HUMANS AB Monkeys with removals of medial temporal lobe (MTL) structures are widely recognized as valid models of human global anterograde amnesia, a syndrome that arises consequent to damage to a finite set of brain structures situated in the medial temporal lobe and/or medial diencephalon. However, a comparison of memory deficits in human and nonhuman primates with MTL damage has presented a long-standing puzzle. Whereas amnesic patients are impaired in teaming object discrimination problems, monkeys with MTL damage are typically not. One possible explanation for this difference is that object discrimination tasks for humans and monkeys differ in that the former but not the latter requires the use of contextual information. Ii this analysis is correct, monkeys with MTL damage might be disadvantaged in learning to discriminate similar objects presented in different contexts. To test this possibility, we evaluated the effects of excitotoxic lesions of one of the MTL structures, the hippocampus, on the rate of learning of discrimination problems embedded within unique contexts. Monkeys with hippocampal lesions were impaired relative to controls in learning object discrimination problems of this type. These findings strongly support the idea that the difference in the effect on object memory of MTL damage in human and nonhuman primates is due to a difference in the opportunity to employ contextual cues rather than to a difference in the organization of memory. Hippocampus 1998, 8:323-329. (C) 1998 WiIey-Liss, Inc.dagger. C1 NIMH, Neuropsychol Lab, Bethesda, MD 20892 USA. McGill Univ, Dept Psychol, Montreal, PQ, Canada. Univ Laval, Ecole Psychol, Laval, PQ, Canada. RP Murray, EA (reprint author), NIMH, Neuropsychol Lab, 49 Convent Dr,Bldg 49,Room 1B80, Bethesda, MD 20892 USA. OI Murray, Elisabeth/0000-0003-1450-1642; White, Norman/0000-0002-4616-5252 NR 42 TC 23 Z9 23 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1050-9631 J9 HIPPOCAMPUS JI Hippocampus PY 1998 VL 8 IS 4 BP 323 EP 329 DI 10.1002/(SICI)1098-1063(1998)8:4<323::AID-HIPO2>3.0.CO;2-I PG 7 WC Neurosciences SC Neurosciences & Neurology GA 116PC UT WOS:000075732900002 PM 9744419 ER PT J AU Hoheisel, G Schauer, J Scherbaum, WA Bornstein, SR AF Hoheisel, G Schauer, J Scherbaum, WA Bornstein, SR TI The effect of corticotropin-releasing hormone (CRH) on the adrenal medulla in hypophysectomized rats SO HISTOLOGY AND HISTOPATHOLOGY LA English DT Article DE corticotropin-releasing hormone (CRH); hypophysectomy; adrenal medulla; rat (Sprague Dawley) ID SPLANCHNIC NERVE-STIMULATION; CHROMAFFIN CELLS; IMMUNOREACTIVE CORTICOTROPIN; ADRENOCORTICAL FUNCTION; CORTICAL-CELLS; GLAND; CORTEX; PHEOCHROMOCYTOMA; PITUITARY; SECRETION AB CRH occurs in the adrenal medulla of rats. We were interested to know whether CRH affects medullary chromaffin cells in the absence of ACTH. We investigated the morphological changes of the adrenal medulla in Sprague Dawley rats with light and electron microscopy in normal rats, hypophysectomized rats, and hypophysectomized rats following injections of CRH (10 mu g = 3 nmol for three days). Chromaffin cells were characterized by immunohistochemistry (anti-tyrosine hydroxylase). At light microscopy level chromaffin cells of hypophysectomized rats were reduced in number. On electron microscopy the number of granules and cell organelles were decreased. Following injections of CRH the medulla regained a more compact texture with cell organelles homogenously distributed, but with chromaffin granules still being reduced in number. Immunohistochemistry allowed the identification of chromaffin cells located within the adrenal cortex. In hypophysectomized rats these cells showed fewer signs of alterations compared to cells located within the medulla itself and had recovered better after treatment with CRH. In conclusion, CRH seems to exert a trophic effect on chromaffin cells in the absence of pituitary ACTH. This observation may provide further evidence for a close interaction of the two neuroendocrine stress systems. C1 NICHHD, Dev Endocrinol Branch, Bethesda, MD 20892 USA. Univ Leipzig, Dept Internal Med 1, Pulm Unit, Leipzig, Germany. Univ Dusseldorf, Dept Internal Med, Endocrinol Unit, D-4000 Dusseldorf, Germany. RP Bornstein, SR (reprint author), NICHHD, Dev Endocrinol Branch, Bldg 10, Bethesda, MD 20892 USA. NR 28 TC 5 Z9 5 U1 0 U2 0 PU F HERNANDEZ PI MURCIA PA PLAZA FUENSANTA 2-7 C, 30008 MURCIA, SPAIN SN 0213-3911 J9 HISTOL HISTOPATHOL JI Histol. Histopath. PD JAN PY 1998 VL 13 IS 1 BP 81 EP 87 PG 7 WC Cell Biology; Pathology SC Cell Biology; Pathology GA YN926 UT WOS:000071222600010 PM 9476637 ER PT J AU Wehr, TA AF Wehr, TA TI Effect of seasonal changes in daylength on human neuroendocrine function SO HORMONE RESEARCH LA English DT Article; Proceedings Paper CT 40th International Henri-Pierre Klotz Symposium on Clinical Endocrinology : Endocrine Rhythms - Roles of the Sleep-Wake Cycle, the Circadian Clock and Environment CY MAY 29-30, 1997 CL PARIS, FRANCE DE circadian rhythm; photoperiod; season; melatonin; prolactin; growth hormone; cortisol; light ID HUMAN MELATONIN SECRETION; SUPRACHIASMATIC NUCLEUS; CLOCK; PHOTOPERIOD; SLEEP AB The circadian pacemaker imposes stereotypic patterns of daily variation on the activity of human neuroendocrine systems. In a number of cases, these patterns exhibit waveforms that are characterized by distinct diurnal and nocturnal periods with relatively discrete transitions between them (corresponding to a biological day, a biological dusk, a biological night, and a biological dawn). In humans, for example, diurnal periods of absence of melatonin secretion, low prolactin secretion, and falling levels of cortisol alternate with nocturnal periods of active melatonin secretion, high prolactin secretion and rising levels of cortisol. In response to light, the circadian pacemaker synchronizes the timing of the biological day and night so that their timing and duration are appropriately matched with the timing and duration of the solar day and night. As the pacemaker carries out this function, it is able to adjust the duration of the biological day and night to match seasonal variation in the duration of the solar day and night. Thus, after humans have been chronically exposed to long nights (scotoperiods), the duration of nocturnal periods of active melatonin secretion, high prolactin secretion and rising levels of cortisol is longer than it is after they have been chronically exposed to short nights. Furthermore, the sleep-related peak of growth hormone secretion is half as high after exposure to long nights as it is after exposure to short nights. These responses to seasonal changes in duration of the natural scotoperiod are suppressed in most individuals - especially men - who live in modern urban environments in which they are exposed to artificial light after dark and artificial darkness during the daytime. C1 NIMH, Clin Psychobiol Branch, Bethesda, MD 20892 USA. RP Wehr, TA (reprint author), NIMH, Clin Psychobiol Branch, Bldg 10,Room 3S-231,10 Ctr Dr MSC 1390, Bethesda, MD 20892 USA. NR 17 TC 56 Z9 58 U1 1 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 1998 VL 49 IS 3-4 BP 118 EP 124 DI 10.1159/000023157 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ZE217 UT WOS:000072769800003 PM 9550111 ER PT J AU Maisog, JM Chmielowska, J AF Maisog, JM Chmielowska, J TI An efficient method for correcting the edge artifact due to smoothing SO HUMAN BRAIN MAPPING LA English DT Article DE functional neuroimaging; smoothing; convolution; artifact; correction ID PET IMAGES; ACTIVATION AB Spatial smoothing is a common pre-processing step in the analysis of functional brain imaging data. It can increase the signal to noise ratio, and specially designed smoothing filters can be used to selectively increase sensitivity to signals of specific shapes and sizes (Rosenfeld and Kak [1982]: Digital Picture Processing, vol. 2. Orlando, Fla.: Academic; Worsley et al. [1996]: Hum Brain Mapping 4:74-90). Also, some amount of spatial smoothness is required if methods from the theory of Gaussian random fields are to be used (Holmes [1994]: Statistical Issues in Functional Brain Mapping. PhD thesis, University of Glasgow). Smoothing is most often implemented as a convolution of the imaging data with a smoothing kernel, and convolution is most efficiently performed using the Convolution Theorem and the Fast Fourier Transform (Cooley and Tukey [1965]: Math Comput 19:297-301; Priestly [1981]: Spectral Analysis and Time Series. San Diego: Academic; Press et al. [1992]: Numerical Recipes in C: The Art of Scientific Computing, 2nd ed. Cambridge: Cambridge University Press). An undesirable side effect of smoothing is an artifact along the edges of the brain, where brain voxels become smoothed with non-brain voxels. This results in a dark rim which might be mistaken for hypoactivity. In this short methodological paper, we present a method for correcting functional brain images for the edge artifact due to smoothing, while retaining the use of the Convolution Theorem and the Fast Fourier Transform for efficient calculation of convolutions. (C) 1998 Wiley-Liss, Inc. C1 NIMH, Sect Funct Brian Imaging, Lab Brain & Cognit, Bethesda, MD 20892 USA. NINDS, Human Motor Control Sect, Med Neurol Branch, Bethesda, MD 20892 USA. RP Maisog, JM (reprint author), Massachusetts Gen Hosp, Dept Radiol, FND HSE 216, Boston, MA 02114 USA. NR 18 TC 5 Z9 5 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PY 1998 VL 6 IS 3 BP 128 EP 136 DI 10.1002/(SICI)1097-0193(1998)6:3<128::AID-HBM2>3.0.CO;2-5 PG 9 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA ZQ918 UT WOS:000073916100002 PM 9673668 ER PT J AU Rajapakse, JC Kruggel, F Maisog, JM von Cramon, DY AF Rajapakse, JC Kruggel, F Maisog, JM von Cramon, DY TI Modeling hemodynamic response for analysis of functional MRI time-series SO HUMAN BRAIN MAPPING LA English DT Article DE brain imaging; blood-oxygen-level-dependent contrast; functional magnetic resonance imaging; hemodynamic response function; multiple regression ID CEREBRAL BLOOD-FLOW; HUMAN VISUAL-CORTEX; HUMAN BRAIN ACTIVATION; OXIDATIVE-METABOLISM; SENSORY STIMULATION; INTRINSIC SIGNALS; 1.5 T; FMRI; ECHO; CONTRAST AB The standard Gaussian function is proposed for the hemodynamic modulation function (HDMF) of functional magnetic resonance imaging (fMRI) time-series. Unlike previously proposed parametric models, the Gaussian model accounts independently for the delay and dispersion of the hemodynamic responses and provides a more flexible and mathematically convenient model. A suboptimal noniterative scheme to estimate the hemodynamic parameters is presented. The ability of the Gaussian function to represent the HDMF of brain activation is compared with Poisson and Gamma models. The proposed model seems valid because the lag and dispersion values of hemodynamic responses rendered by the Gaussian model are in the ranges of their previously reported values in recent optical and fMR imaging studies. An extension of multiple regression analysis to incorporate the HDMF is presented. The detected activity patterns exhibit improvements with hemodynamic correction. The proposed model and efficient parameter estimation scheme facilitated the investigation of variability of hemodynamic parameters of human brain activation. The hemodynamic parameters estimated over different brain regions and across different stimuli showed significant differences. Measurement of hemodynamic parameters over the brain during sensory or cognitive stimulation may reveal vital information on physiological events accompanying neuronal activation and functional variability of the human brain, and should lead to the investigation of more accurate and complex models. Hum. Brain Mapping 6:283-300, 1998. (C) 1998 Wiley-Liss, Inc. C1 Max Planck Inst Cognit Neurosci, D-04103 Leipzig, Germany. NIMH, Sect Funct Brain Imaging, Psychol & Psychopathol Lab, Bethesda, MD 20892 USA. RP Rajapakse, JC (reprint author), Max Planck Inst Cognit Neurosci, Inselstr 22-26, D-04103 Leipzig, Germany. RI Rajapakse, Jagath/B-8485-2008; Kruggel, Frithjof/M-9201-2016 OI Rajapakse, Jagath/0000-0001-7944-1658; Kruggel, Frithjof/0000-0003-3507-5662 NR 43 TC 143 Z9 144 U1 0 U2 10 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PY 1998 VL 6 IS 4 BP 283 EP 300 DI 10.1002/(SICI)1097-0193(1998)6:4<283::AID-HBM7>3.0.CO;2-# PG 18 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 106UN UT WOS:000075169000007 PM 9704266 ER PT J AU Wassermann, EM Tormos, JM Pascual-Leone, A AF Wassermann, EM Tormos, JM Pascual-Leone, A TI Finger movements induced by transcranial magnetic stimulation change with hand posture, but not with coil position SO HUMAN BRAIN MAPPING LA English DT Article DE motor cortex; brain mapping; spinal cord; corticospinal tracts; human ID HUMAN MOTOR CORTEX; MUSCLE AB We attempted to map the representations of movements in 2 normal subjects by delivering five transcranial magnetic stimuli (TMS) with a focal coil to each of a grid of positions over the primary motor area (M1). Isometric forces were recorded from the contralateral index finger. Maps were made with the hand in a semiflexed "neutral" position, and with the thumb and index finger opposed in a "pincer" grip. The electromyogram (EMG) was monitored to ensure relaxation. The wrist was immobilized. In the neutral position, TMS at almost all positions produced abduction. Flexion was produced in the pincer position. Thus, while sensitive to changes in posture, TMS mapping may not be sensitive to the topographical organization of the M1 by movements as detected with direct cortical stimulation. (C) 1998 Wiley-Liss, Inc. C1 NINDS, Off Clin Director, NIH, Bethesda, MD 20892 USA. Univ Valencia, Dept Physiol, Valencia, Spain. Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02115 USA. RP Wassermann, EM (reprint author), 10 Ctr Dr,MSC 1428, Bethesda, MD 20892 USA. NR 11 TC 10 Z9 10 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PY 1998 VL 6 IS 5-6 BP 390 EP 393 DI 10.1002/(SICI)1097-0193(1998)6:5/6<390::AID-HBM11>3.0.CO;2-W PG 4 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 126DG UT WOS:000076277200011 PM 9788078 ER PT J AU Kopantzev, E Roschke, V Rudikoff, S AF Kopantzev, E Roschke, V Rudikoff, S TI Interleukin-2-mediated modulation of plasma cell tumor growth in a model of multiple myeloma SO HUMAN GENE THERAPY LA English DT Article ID INTERFERON-GAMMA; GENE-TRANSFER; T-CELLS; VACCINATION; IMMUNOTHERAPY; LYMPHOCYTES; IMMUNITY; CANCER AB A number of studies have demonstrated that inoculation of certain types of cancer cells engineered for expression of the interleukin-2 (IL-2) gene results in reduced tumorigenicity and/or protection from subsequent challenge with a tumorigenic dose of wild-type cells, In the current studies, we have employed murine plasma cell tumors to examine IL-2-mediated tumor rejection as a possible model for therapeutic approaches to human myeloma or plasma cell leukemia, Two murine plasma cell tumor lines, S107 and X24, were infected with a retroviral vector expressing the human IL-2 gene, and the antitumor potential of IL-2-expressing infectants was characterized in syngeneic BALB/c and BALB/c nu/nu mice. Results demonstrate that tumorigenicity of both lines correlates inversely with the amount of IL-2 produced by the tumor cells, However, there are clear differences between the two lines in terms of reduced tumorigenicity and the ability to protect against co-injected parental tumor cells that appear unrelated to IL-2 levels, More importantly, intravenous immunization of animals with irradiated, IL-2 secreting cells from either line leads to significant protection from challenge with highly metastatic parental cells, These results suggest that such an approach may warrant consideration in the treatment of human plasma cell dyscrasias. C1 NCI, Genet Lab, NIH, Bethesda, MD 20892 USA. RP Rudikoff, S (reprint author), NCI, Genet Lab, NIH, Bldg 37,Rm 2B15,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA. NR 19 TC 15 Z9 16 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD JAN 1 PY 1998 VL 9 IS 1 BP 13 EP 19 DI 10.1089/hum.1998.9.1-13 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA YR716 UT WOS:000071523100004 PM 9458238 ER PT J AU Contassot, E Ferrand, C Certoux, JM Reynolds, CW Jacob, W Chiang, YW Cahn, JY Herve, P Tiberghien, P AF Contassot, E Ferrand, C Certoux, JM Reynolds, CW Jacob, W Chiang, YW Cahn, JY Herve, P Tiberghien, P TI Retrovirus-mediated transfer of the herpes simplex type I thymidine kinase gene in alloreactive T lymphocytes SO HUMAN GENE THERAPY LA English DT Article ID BONE-MARROW TRANSPLANTATION; CELL DEPLETION; LEUKEMIA; ELIMINATION; IMMUNOTOXIN; COMBINATION; THERAPY AB We have demonstrated in previous studies that retrovirus-mediated transfer of the herpes simplex thymidine kinase (HS-tk) and neomycin phosphotransferase (neo) genes in CD3/IL-2 stimulated primary T lymphocytes followed by G418 selection resulted in T cells retaining both interleukin-2 (IL-2) and alloresponsiveness and specifically inhibited by ganciclovir (GCV). A clinical trial examining the therapeutic potential of such gene-modified donor T cells after allogeneic bone marrow transplantation is presently underway. In the present study, me have investigated the feasibility and consequences of replacing polyclonal stimulation of T cells by an allogeneic stimulation prior to retrovirus-mediated gene transfer. Exposure of allostimulated primary donor T lymphocytes to retrovirus-containing supernatant resulted in T cells resistant to G418 while maintaining a strong, GCV-sensitive, allogeneic response when subsequently restimulated with the initial allogeneic cells. Control nontransduced cells identically stimulated exhibited a weaker, GCV-insensitive, allogeneic proliferative response. The transduced T cells were also capable of GCV-sensitive alloreactivity when exposed to third-party cells with, however, a lower proliferative response than that seen with the allogeneic cells used for stimulation at the time of transduction. Importantly, this difference in the proliferative responses was not observed with control nontransduced cells identically stimulated. A similar response pattern was observed with respect to pre-cytotoxic T lymphocyte (CTL) frequencies. Overall, retrovirus-mediated gene transfer after an allogeneic stimulation can lead to efficient transduction and the pattern of alloreactivity of the HS-tk-expressing cells is consistent with the preferential transduction of alloantigen-specific dividing T cells. Such an approach could be used to generate cells both strongly alloreactive and GCV-sensitive for in vivo therapeutic use. C1 Etab Transfus Sanguine, Lab Therapeut Immunomol, F-25000 Besancon, France. NCI, Biol Resource Branch, Frederick, MD 21702 USA. Genet Therapy Inc, Gaithersburg, MD 20878 USA. CHU Besancon, Serv Hematol, F-25030 Besancon, France. RP Contassot, E (reprint author), Etab Transfus Sanguine, Lab Therapeut Immunomol, 1 Blvd Fleming, F-25000 Besancon, France. NR 17 TC 26 Z9 26 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD JAN 1 PY 1998 VL 9 IS 1 BP 73 EP 80 DI 10.1089/hum.1998.9.1-73 PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA YR716 UT WOS:000071523100010 PM 9458244 ER PT J AU Becker, A Geiger, D Schaffer, AA AF Becker, A Geiger, D Schaffer, AA TI Automatic selection of loop breakers for genetic linkage analysis SO HUMAN HEREDITY LA English DT Article DE genetics; linkage analysis; algorithms; loops; probabilistic inference; Bayesian networks ID COMPLEX PEDIGREES; COMPUTATIONS; RECOMBINATION; LIKELIHOODS; EXTENSIONS; NETWORKS; HUMANS AB Pedigree loops pose a difficult computational challenge in genetic linkage analysis. The most popular linkage analysis package, LINKAGE, uses an algorithm that converts a looped pedigree into a loopless pedigree, which is traversed many times. The conversion is controlled by user selection of individuals to act as loop breakers. The selection of loop breakers has significant impact on the running time of the subsequent linkage analysis. We have automated the process of selecting loop breakers, implemented a hybrid algorithm for it in the FASTLINK version of LINKAGE, and tested it on many real pedigrees with excellent performance. We point out that there is no need to break each loop by a distinct individual because, with minor modification to the algorithms in LINKAGE/FASTLINK, a single individual that participates in multiple marriages can serve as a loop breaker for several loops. Our algorithm for finding loop breakers, called LOOPBREAKER, is a combination of: (1) a new algorithm that is guaranteed to be optimal in the special case of pedigrees with no multiple marriages and (2) an adaptation of a known algorithm for breaking loops in general graphs. The contribution of this work is the adaptation of abstract methods from computer science to a challenging problem in genetics. C1 NHGRI, NIH, Baltimore, MD 21224 USA. Technion Israel Inst Technol, Dept Comp Sci, IL-32000 Haifa, Israel. RP Schaffer, AA (reprint author), NHGRI, NIH, Suite 2000,333 Cassell Dr, Baltimore, MD 21224 USA. EM schaffer@helix.nih.gov RI Schaffer, Alejandro/F-2902-2012 NR 39 TC 33 Z9 35 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0001-5652 J9 HUM HERED JI Hum. Hered. PD JAN-FEB PY 1998 VL 48 IS 1 BP 49 EP 60 DI 10.1159/000022781 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA YU259 UT WOS:000071698400008 PM 9463802 ER PT J AU Kawashima, I Hudson, SJ Tsai, V Southwood, S Takesako, K Appella, E Sette, A Celis, E AF Kawashima, I Hudson, SJ Tsai, V Southwood, S Takesako, K Appella, E Sette, A Celis, E TI The multi-epitope approach for immunotherapy for cancer: Identification of several CTL epitopes from various tumor-associated antigens expressed on solid epithelial tumors SO HUMAN IMMUNOLOGY LA English DT Article ID CYTOLYTIC T-LYMPHOCYTES; HUMAN GENE MAGE-3; HLA-A ALLELES; CARCINOEMBRYONIC ANTIGEN; PEPTIDE-BINDING; IMMUNODOMINANT PEPTIDE; MOLECULAR-BIOLOGY; OVARIAN-CANCER; BREAST-CANCER; CELL-LINES AB One approach to development of specific cancer immunotherapy relies on the induction of cytotoxic T lymphocytes (CTL) specific for tumor-associated antigens (TAA). Induction of TAA,specific CTL could be used towards the eradication of established rumors, or to prevent their dissemination or recurrence after primary treatment. The present study identifies a set of CTL epitopes from TAA frequently found on solid epithelial tumors such as breast, lung and gastro-intestinal tumors. Specifically, HLA-A2.1 binding peptides from the MAGE2, MAGE3, HER-2/neu and CEA antigens were rested for their capacity to elicit in vitro anti-tumor CTL using lymphocytes from normal volunteers and autologous dendritic cells as antigen-presenting cells. A total of 6 new epitopes (MAGE2[10(157)], MAGE3[9(112)],CEA[9(691)], CEA[9(24)], HER2[9(435)] and HER2[9(5)]) were identified which were capable of specifically recognizing tumor cell lines expressing HLA-A2.1 and the corresponding TAA. In one case (CEA[9(24)]), induction of vigorous anti-rumor CTL responses required epitope engineering to increase HLA-A2.1 binding affinity. Finally, most of the newly identified epitopes (5 our of 6) were found to be highly crossreactive with other common HLA alleles of the A2 supertype (A2.2, A2.3, A2.6 and A6802), thus demonstrating their potential in providing broad and non-ethnically biased population coverage. The results are discussed in the context of the development of multi-epitope-based therapies with broad applicability for patients suffering from commonly found rumors. (C) American Society for Histocompatibility and Immunogenetics, 1998. Published by Elsevier Science Inc. C1 Cytel Corp, San Diego, CA 92121 USA. Takara Shuzo Co Ltd, Biotechnol Res Labs, Shiga, Japan. NCI, Cell Biol Lab, Bethesda, MD 20892 USA. RP Celis, E (reprint author), Mayo Clin, Dept Immunol, Guggenheim 4, Rochester, MN 55905 USA. EM celis@mayo.edu FU NIAID NIH HHS [N01-AI-45241] NR 64 TC 169 Z9 177 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD JAN PY 1998 VL 59 IS 1 BP 1 EP 14 DI 10.1016/S0198-8859(97)00255-3 PG 14 WC Immunology SC Immunology GA YZ393 UT WOS:000072249900001 PM 9544234 ER PT J AU Centola, M Aksentijevich, I Kastner, DL AF Centola, M Aksentijevich, I Kastner, DL TI The hereditary periodic fever syndromes: molecular analysis of a new family of inflammatory diseases SO HUMAN MOLECULAR GENETICS LA English DT Article ID ACUTE PROMYELOCYTIC LEUKEMIA; IMMUNODEFICIENCY-VIRUS TYPE-1; FAT GLOBULE-MEMBRANE; HIGH GENE-FREQUENCY; CLASS-I REGION; MEDITERRANEAN-FEVER; HYPERIMMUNOGLOBULINEMIA-D; MULTIGENIC FAMILIES; COLCHICINE THERAPY; CLINICAL SPECTRUM AB The hereditary periodic fever syndromes are a group of Mendelian disorders characterized by episodic fever and serosal or synovial inflammation. Familial Mediterranean fever (FMF) and the hyperimmunoglobulinemia D and periodic fever syndrome are both recessively inherited, while three dominantly inherited syndromes have been described, the best-characterized of which is familial Hibernian fever (FHF). The last year has seen two major developments in this field: the FMF gene was identified an chromosome 16p by positional cloning, and a second major periodic fever locus was mapped to distal chromosome 12p. The FMF gene (MEFV) encodes a novel 781 amino acid protein; to date, eight different missense mutations and a number of polymorphisms have been described. Seven of the eight mutations occur within a region of 82 amino acids near the C-terminus, Computational analysis of the conceptual protein reveals five different domains/motifs compatible with a nuclear effector function. MEFV is expressed preferentially in granulocytes and myeloid bone marrow precursors, giving rise to speculation that the protein may serve as a transcriptional regulator of inflammation in granulocytes. The second periodic fever locus was mapped by two different groups: one studying FHF, the other studying a similar dominantly inherited syndrome designated familial periodic fever. Both genes map to the same 19 cM region on distal chromosome 12p, strongly suggesting a common locus. The molecular characterization of the periodic fever genes should provide important new insights into the regulation of inflammation in general. C1 NIAMSD, Arthritis & Rheumatism Branch, NIH, Bethesda, MD 20892 USA. RP Kastner, DL (reprint author), NIAMSD, Arthritis & Rheumatism Branch, NIH, Bldg 10,Room 9N210,9000 Rockville Pike, Bethesda, MD 20892 USA. EM kastnerd@arb.niams.nih.gov NR 81 TC 77 Z9 80 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PY 1998 VL 7 IS 10 SI SI BP 1581 EP 1588 DI 10.1093/hmg/7.10.1581 PG 8 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 128NB UT WOS:000076411900007 PM 9735379 ER PT J AU Ried, T Schrock, E Ning, Y Wienberg, J AF Ried, T Schrock, E Ning, Y Wienberg, J TI Chromosome painting: a useful art SO HUMAN MOLECULAR GENETICS LA English DT Article ID FLUORESCENCE INSITU HYBRIDIZATION; IN-SITU HYBRIDIZATION; DIGITAL IMAGING MICROSCOPY; SUPPRESSION HYBRIDIZATION; MARKER CHROMOSOMES; DNA LIBRARIES; MICRODISSECTED CHROMOSOMES; FOLLOW-UP; MOLECULAR CYTOGENETICS; GENOMIC REORGANIZATION AB Chromosome 'painting' refers to the hybridization of fluorescently labeled chromosome-specific, composite probe pools to cytological preparations. Chromosome painting allows the visualization of individual chromosomes in metaphase or interphase cells and the identification of both numerical and structural chromosomal aberrations in human pathology with high sensitivity and specificity. In addition to human chromosome-specific probe pools, painting probes have become available for an increasing range of different species, They can be applied to cross-species comparisons as well as to the study of chromosomal rearrangements in animal models of human diseases. The simultaneous hybridization of multiple chromosome painting probes, each tagged with a specific fluorochrome or fluorochrome combination, has resulted in the differential color display of human land mouse) chromosomes, i.e. color karyotyping. In this review, we will summarize recent developments of multicolor chromosome painting, describe applications in basic chromosome research and cytogenetic diagnostics, and discuss limitations and future directions. C1 Natl Human Genome Res Inst, NIH, Bethesda, MD 20892 USA. Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England. RP Ried, T (reprint author), Natl Human Genome Res Inst, NIH, Bldg 49,Room 4A28,49 Convent Dr, Bethesda, MD 20892 USA. EM tried@nhgri.nih.gov NR 90 TC 61 Z9 65 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PY 1998 VL 7 IS 10 SI SI BP 1619 EP 1626 DI 10.1093/hmg/7.10.1619 PG 8 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 128NB UT WOS:000076411900011 PM 9735383 ER PT J AU Agarwal, SK Debelenko, LV Kester, MB Guru, SC Manickam, P Olufemi, SE Skarulis, MC Heppner, C Crabtree, JS Lubensky, IA Zhuang, ZP Kim, YS Chandrasekharappa, SC Collins, FS Liotta, LA Spiegel, AM Burns, AL Emmert-Buck, MR Marx, SJ AF Agarwal, SK Debelenko, LV Kester, MB Guru, SC Manickam, P Olufemi, SE Skarulis, MC Heppner, C Crabtree, JS Lubensky, IA Zhuang, ZP Kim, YS Chandrasekharappa, SC Collins, FS Liotta, LA Spiegel, AM Burns, AL Emmert-Buck, MR Marx, SJ TI Analysis of recurrent germline mutations in the MEN1 gene encountered in apparently unrelated families SO HUMAN MUTATION LA English DT Article DE founder; haplotype; hot spot; CpG; repeats ID ENDOCRINE NEOPLASIA TYPE-1; PARATHYROID TUMORS; CPG DINUCLEOTIDES; DIRECT REPEATS; DELETIONS; CHROMOSOME-11; CANCER; METHYLATION AB Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder that manifests as varying combinations of tumors of endocrine and other tissues (parathyroids, pancreatic islets, duodenal endocrine cells, the anterior pituitary and others), The MEN1 gene is on chromosome 11q13; it was recently identified by positional cloning, We previously reported 32 different germline mutations in 47 of the 50 familial MEN1 probands studied at the NM. Eight different germline MEN1 mutations were encountered repeatedly in two or more apparently unrelated families, We analyzed the haplotypes of families with recurrent MEN1 mutations with seven polymorphic markers in the 11q13 region surrounding the MEN1 gene (from D11S1883 to D11S4908), Disease haplotypes were inferred from germline DNA and also from tumors with 11q13 loss of heterozygosity. Two different disease haplotype cores were shared by apparently unrelated families for two mutations in exon 2 (five families with 416delC and six families with 512delC). These two repeat mutations were associated with the two founder effects that we reported in a prior haplotype analysis. The disease haplotypes for each of the other six repeat mutations (seen twice each) were discordant, suggesting independent origins of these recurrent mutations. Most of the MEN1 germline mutations including all of those recurring independently occur in regions of CpG/CpNpG, short DNA repeats or single nucleotide repeat motifs. In conclusion, recurring,germline mutations account for about half of the mutations in North American MEN1 families, They result from either founder effects or independent occurrence of one mutation more than one time, Hum Mutat 12:75-82, 1998. (C) 1998 Wiley-Liss, Inc.dagger C1 NIDDK, MDB, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. NIH, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. RP Marx, SJ (reprint author), NIDDK, MDB, NIH, Bldg 10,Room 9C-101,10 Ctr Dr,MSC 1802, Bethesda, MD 20892 USA. EM stephenm@amb.niddk.nih.gov RI Agarwal, Sunita/D-1428-2016 OI Agarwal, Sunita/0000-0002-7557-3191 NR 32 TC 29 Z9 30 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1998 VL 12 IS 2 BP 75 EP 82 DI 10.1002/(SICI)1098-1004(1998)12:2<75::AID-HUMU1>3.0.CO;2-T PG 8 WC Genetics & Heredity SC Genetics & Heredity GA ZW660 UT WOS:000074433900001 PM 9671267 ER PT J AU Rogan, PK Faux, BM Schneider, TD AF Rogan, PK Faux, BM Schneider, TD TI Information analysis of human splice site mutations SO HUMAN MUTATION LA English DT Review DE information theory; mRNA splicing; donor; acceptor; cryptic; mutation; polymorphism; walker ID PRE-MESSENGER-RNA; SYNDROME TYPE-VII; DNA-BINDING SITES; CONGENITAL ADRENAL-HYPERPLASIA; MUCOPOLYSACCHARIDOSIS TYPE-II; LIPOPROTEIN-LIPASE DEFICIENCY; ACUTE INTERMITTENT PORPHYRIA; PRO-ALPHA-2(I) GENE COL1A2; BETA-THALASSEMIA GENES; CYTO-TOXIC LYMPHOCYTES AB Splice site nucleotide substitutions can be analyzed by comparing the individual information contents (R-i, bits) of the normal and variant splice junction sequences [Rogan and Schneider, 1995]. In the present study, we related splicing abnormalities to changes in R-i values of 111 previously reported splice site substitutions in 41 different genes. Mutant donor and acceptor sites have significantly less information than their normal counterparts. With one possible exception, primary mutant sites with <2.4 bits were not spliced. Sites with R-i values greater than or equal to 2.4 bits but less than the corresponding natural site usually decreased, but did not abolish splicing. Substitutions that produced small changes in R-i probably do not impair splicing and are often polymorphisms. The R-i values of activated cryptic sites were generally comparable to or greater than those of the corresponding natural splice sites. Information analysis revealed preexisting cryptic splice junctions that are used instead of the mutated natural site. Other cryptic sites were created or strengthened by sequence changes that simultaneously altered the natural site. Comparison between normal and mutant splice site R-i values distinguishes substitutions that impair splicing from those which do not, distinguishes null alleles from those that are partially functional, and detects activated cryptic splice sites. Hum Mutat 12:153-171, 1998. (C) 1998 Wiley-Liss, Inc. C1 Allegheny Univ Hlth Sci, MCP Hahnemann Sch Med, Dept Human Genet, Pittsburgh, PA 15212 USA. NCI, Frederick Canc Res & Dev Ctr, Lab Expt & Computat Biol, Frederick, MD USA. RP Rogan, PK (reprint author), Allegheny Univ Hlth Sci, MCP Hahnemann Sch Med, Dept Human Genet, 320 E North Ave, Pittsburgh, PA 15212 USA. EM progan@pgh.allegheny.edu RI Rogan, Peter/B-9845-2017; OI Rogan, Peter/0000-0003-2070-5254; Schneider, Thomas/0000-0002-9841-1531 FU NCI NIH HHS [CA74683] NR 136 TC 140 Z9 142 U1 0 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1059-7794 EI 1098-1004 J9 HUM MUTAT JI Hum. Mutat. PY 1998 VL 12 IS 3 BP 153 EP 171 DI 10.1002/(SICI)1098-1004(1998)12:3<153::AID-HUMU3>3.0.CO;2-I PG 19 WC Genetics & Heredity SC Genetics & Heredity GA 106UR UT WOS:000075169300003 PM 9711873 ER PT J AU Stolle, C Glenn, G Zbar, B Humphrey, JS Choyke, P Walther, M Pack, S Hurley, K Andrey, C Klausner, R Linehan, WM AF Stolle, C Glenn, G Zbar, B Humphrey, JS Choyke, P Walther, M Pack, S Hurley, K Andrey, C Klausner, R Linehan, WM TI Improved detection of germline mutations in the von Hippel Lindau disease tumor suppressor gene SO HUMAN MUTATION LA English DT Article DE von Hippel Lindau disease; germline mutation; pheochromocytoma; renal cell carcinoma; Southern blotting ID FIELD GEL-ELECTROPHORESIS; ENDOTHELIAL GROWTH-FACTOR; VHL GENE; IDENTIFICATION; EXPRESSION; PHENOTYPE; CARCINOMA; FAMILIES; PROTEIN; EUROPE AB von Hippel-Lindau disease (VHL) is an inherited neoplastic disorder characterized by the development of tumors in the eyes, brain, spinal cord, inner ear, adrenal gland, pancreas, kidney, and epididymis. The VHL tumor suppressor gene was identified in 1993, Initial studies reported the detection of germline mutations in the VHL gene in 39-75% of VHL families, We used tests that detect different types of mutations to improve the frequency of detection of germline mutations in VHL families, The methods included quantitative Southern blotting to detect deletions of the entire VHL gene, Southern blotting to detect gene rearrangements, fluorescence in situ hybridization (FISH) to confirm deletions, and complete sequencing of the gene, Here we report that we have detected germline mutations in the VHL gene in 100% (93/93) of VHL families tested. In addition, we describe 13 novel intragenic VHL germline mutations. With the methodology de scribed in this article, it is now possible to identify germline mutations in virtually all families with VHL. Hum Mutat 12:417-423, 1998. (C) 1998 Wiley-Liss, Inc. C1 NCI, Immunobiol Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. Univ Penn, Genet Diagnost Lab, Philadelphia, PA USA. NCI, Genet Epidemiol Branch, Bethesda, MD 20892 USA. NICHHD, Cell Biol & Metab Branch, Bethesda, MD USA. NIH, Bethesda, MD 20892 USA. NCI, Urol Oncol Branch, Bethesda, MD 20892 USA. NCI, Pathol Lab, Bethesda, MD 20892 USA. NCI, Off Director, Bethesda, MD 20892 USA. RP Zbar, B (reprint author), NCI, Immunobiol Lab, Frederick Canc Res & Dev Ctr, Bldg 560,Room 12-89,Frederick Canc Res Facil, Frederick, MD 21702 USA. EM zbar@ncifcrf.gov RI Pack, Svetlana/C-2020-2014 NR 23 TC 307 Z9 320 U1 0 U2 7 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1998 VL 12 IS 6 BP 417 EP 423 DI 10.1002/(SICI)1098-1004(1998)12:6<417::AID-HUMU8>3.0.CO;2-K PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 134ZM UT WOS:000076774100007 PM 9829911 ER PT J AU Olufemi, SE Green, JS Manickam, P Guru, SC Agarwal, SK Kester, MB Dong, QH Burns, AL Spiegel, AM Marx, SJ Collins, FS Chandrasekharappa, SC AF Olufemi, SE Green, JS Manickam, P Guru, SC Agarwal, SK Kester, MB Dong, QH Burns, AL Spiegel, AM Marx, SJ Collins, FS Chandrasekharappa, SC TI Common ancestral mutation in the MEN1 gene is likely responsible for the prolactinoma variant of MEN1 (MEN1(Burin)) in four kindreds from Newfoundland SO HUMAN MUTATION LA English DT Article DE prolactinoma; MEN1(Burin); founder effect; MEN1 gene; menin; Newfoundland ID ENDOCRINE NEOPLASIA TYPE-1; LINKAGE; LOCUS; 11Q13 AB Familiar multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder with affected individuals developing parathyroid, gastrointestinal (GI) endocrine, and anterior pituitary tumors, Four large kindreds from the Burin peninsula/Fortune Bay area of Newfoundland with prominent features of prolactinomas, carcinoids, and parathyroid tumors (referred to as MEN1(Burin)) have been described, and they show linkage to 11q13, the same locus as that of MEN1, Haplotype analysis with 16 polymorphic markers now reveals that representative affected individuals from all four families share a common haplotype over a 2.5 Mb region. A nonsense mutation in the MEN1 gene has been found to be responsible for the disease in the affected members in all four of the MEN1(Burin) families, providing convincing evidence of a common founder. (C) 1998 Wiley-Liss, Inc.(dagger). C1 NHGRI, LGT, NIH, Bethesda, MD 20892 USA. Mem Univ Newfoundland, Hlth Sci Ctr, Dept Med Genet, St Johns, NF, Canada. NIDDKD, Metab Dis Branch, NIH, Bethesda, MD 20892 USA. RP Chandrasekharappa, SC (reprint author), NHGRI, LGT, NIH, Bldg 49,Room 3E13,49 Convent Dr,MSC 4442, Bethesda, MD 20892 USA. RI Agarwal, Sunita/D-1428-2016 OI Agarwal, Sunita/0000-0002-7557-3191 NR 19 TC 80 Z9 81 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1998 VL 11 IS 4 BP 264 EP 269 DI 10.1002/(SICI)1098-1004(1998)11:4<264::AID-HUMU2>3.0.CO;2-V PG 6 WC Genetics & Heredity SC Genetics & Heredity GA ZF063 UT WOS:000072859000002 PM 9554741 ER PT J AU Sarafova, AP Choi, H Forlino, A Gajko, A Cabral, WA Tosi, L Reing, CM Marini, JC AF Sarafova, AP Choi, H Forlino, A Gajko, A Cabral, WA Tosi, L Reing, CM Marini, JC TI Three novel type I collagen mutations in osteogenesis imperfecta type IV probands are associated with discrepancies between electrophoretic migration of osteoblast and fibroblast collagen SO HUMAN MUTATION LA English DT Article DE type IV osteogenesis imperfecta; point mutations; osteoblasts ID GLYCINE SUBSTITUTIONS; ALPHA-2(I) CHAINS; BONE; PROCOLLAGEN; SKIN AB In three cases of type IV osteogenesis imperfecta (OI), we identified unique point mutations in type I collagen alpha 1(I) cDNA. In two cases, the appearance of dimers indicated the presence of cysteine substitutions in the alpha 1(I) protein chain. Cyanogen bromide digestion localized these cross links to CB8 and 3, respectively. In the third case, the overmodification pattern of the CNBr peptides was compatible with a substitution in the aa 123-402 region of either type I collagen chain. We identified a unique point mutation in each proband, which resulted in substitutions for glycine residues in a 300-aa region of the alpha 1(I) helix, specifically, Gly to Ala at codon 220 (GGT-->GCT), Gly to Cys at codon 349 (GGT-->TGT) and Gly to Cys at codon 523 (GGT-->TGT). We compared each proband's fibroblast and osteoblast collagen directly, as well as with fibroblast and osteoblast controls. For all cases, the OI osteoblast collagen was more electrophoretically delayed than OI fibroblast collagen. In the patient with G349C, OI fibroblast and osteoblast collagen synthesized in the presence of alpha,alpha'-dipyridyl co-migrated on gels, demonstrating that the electrophoretic discrepancy resulted from differences in post translational modification, Melting temperature curl es for stability of the collagen helix yielded an identical T-m for control fibroblast and osteoblast collagen (41.2 degrees C). By contrast, for collagen with the gly349-->cys substitution, the T-m of the fibroblast collagen was 1 degrees C lower than the T-m of the osteoblast collagen. These data indicate that the metabolism of mutant collagen might be cell-specific and has significant implications for understanding the phenotype/genotype correlations and the pathophysiology of OI. (C) 1998 Wiley-Liss, Inc. dagger. C1 NICHD, Sect Connect Tissue Disorders, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. Childrens Natl Med Ctr, Dept Orthoped, Washington, DC 20010 USA. Fairfax Hosp, Dept Orthoped, Fairfax, VA USA. RP Marini, JC (reprint author), NICHD, Sect Connect Tissue Disorders, Heritable Disorders Branch, NIH, Bldg 10,Room 9S241,10 Ctr Dr,MSC-1830, Bethesda, MD 20892 USA. RI Forlino, Antonella/H-5385-2015 OI Forlino, Antonella/0000-0002-6385-1182 NR 16 TC 27 Z9 31 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1998 VL 11 IS 5 BP 395 EP 403 DI 10.1002/(SICI)1098-1004(1998)11:5<395::AID-HUMU7>3.0.CO;2-4 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA ZK241 UT WOS:000073299500007 PM 9600458 ER PT J AU Pollock, PM Spurr, N Bishop, T Newton-Bishop, J Gruis, N van der Velden, PA Goldstein, AM Tucker, MA Foulkes, WD Barnhill, R Haber, D Fountain, J Hayward, NK AF Pollock, PM Spurr, N Bishop, T Newton-Bishop, J Gruis, N van der Velden, PA Goldstein, AM Tucker, MA Foulkes, WD Barnhill, R Haber, D Fountain, J Hayward, NK TI Haplotype analysis of two recurrent CDKN2A mutations in 10 melanoma families: Evidence for common founders and independent mutations SO HUMAN MUTATION LA English DT Article DE CDKN2A; melanoma; familial; mutation; founder ID KINASE-4 INHIBITOR GENE; TUMOR-SUPPRESSOR GENE; MALIGNANT-MELANOMA; PANCREATIC-CANCER; CELL-LINES; P16; LOCUS; P16(INK4A); DELETION; KINDREDS AB Germ-line mutations in CDKN2A have been shown to predispose to cutaneous malignant melanoma. We have identified 2 new melanoma kindreds which carry a duplication of a 24bp repeat present in the 5' region of CDKN2A previously identified in melanoma families fram Australia and the United States. This mutation has now been reported in 5 melanoma families from 3 continents: Europe, North America, and Australasia, The M53I mutation in exon 2 of CDKN2A has also been documented in 5 melanoma families from Australia and North America. The aim of this study was to determine whether the occurrence of the mutations in these families from geographically diverse populations represented mutation hotspots within CDKN2A or were due to common ancestors. Haplotypes of 11 microsatellite markers flanking CDKN2A were constructed in 5 families carrying the M53I mutation and 5 families carrying the 24bp duplication. There were some differences in the segregating haplotypes due primarily to recombinations and mutations within the short tandem repeat markers; however, the data provide evidence to indicate that there mere at least 3 independent 24bp duplication events and possibly only 1 original M53I mutation. This is the first study to date which indicates common founders in melanoma families from different continents. (C) 1998 Wiley-Liss, Inc. C1 Queensland Inst Med Res, Queensland Canc Fund Res Unit, Joint Expt Oncol Program, Brisbane, Qld 4006, Australia. St James Univ Hosp, Canc Mol Genet Lab, Leeds LS9 7TF, W Yorkshire, England. St James Univ Hosp, ICRF, Genet Epidemiol Lab, Leeds LS9 7TF, W Yorkshire, England. Leiden Univ, Med Ctr, MGC, Dept Human Genet, Leiden, Netherlands. Leiden Univ, Med Ctr, Dept Dermatol, Leiden, Netherlands. NCI, Genet Epidemiol Branch, Bethesda, MD 20892 USA. McGill Univ, Dept Med, Div Med Genet, Montreal, PQ, Canada. Harvard Univ, Brigham & Womens Hosp, Boston, MA 02115 USA. Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA USA. Univ So Calif, Inst Med Genet, Los Angeles, CA USA. RP Hayward, NK (reprint author), PO Royal Brisbane Hosp, Queensland Inst Med Res, Herston, Qld 4029, Australia. EM nickH@qimr.edu.au RI hayward, nicholas/C-1367-2015; OI hayward, nicholas/0000-0003-4760-1033; Gruis, Nelleke/0000-0002-5210-9150; Bishop, Tim/0000-0002-8752-8785; Newton Bishop, Julia/0000-0001-9147-6802 FU NCI NIH HHS [CA66021] NR 40 TC 50 Z9 50 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1998 VL 11 IS 6 BP 424 EP 431 DI 10.1002/(SICI)1098-1004(1998)11:6<424::AID-HUMU2>3.0.CO;2-2 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA ZK242 UT WOS:000073299600002 PM 9603434 ER PT J AU Pras, E Golomb, E Drake, C Aksentijevich, I Katz, G Kastner, DL AF Pras, E Golomb, E Drake, C Aksentijevich, I Katz, G Kastner, DL TI A splicing mutation (891+4A -> G) in SLC3A1 leads to exon 4 skipping and causes cystinuria in a Moslem Arab family SO HUMAN MUTATION LA English DT Article ID AMINO-ACID TRANSPORTER; IN-SITU HYBRIDIZATION; MOLECULAR-GENETICS; MESSENGER-RNA; IDENTIFICATION; LOCALIZATION; ASSIGNMENT; RBAT C1 NIAMSD, Arthrit & Rheumatol Branch, Bethesda, MD 20892 USA. Chaim Sheba Med Ctr, Dept Med C, IL-52621 Tel Hashomer, Israel. Chaim Sheba Med Ctr, Inst Genet, IL-52621 Tel Hashomer, Israel. Tel Aviv Univ, Sackler Sch Med, Dept Pathol, IL-69978 Tel Aviv, Israel. Univ Florida, Div Urol, Gainesville, FL 32610 USA. RP Kastner, DL (reprint author), NIAMSD, Arthrit & Rheumatol Branch, Bethesda, MD 20892 USA. NR 18 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1998 SU 1 BP S28 EP S30 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA YV593 UT WOS:000071842000010 ER PT J AU Clark, WH Tucker, MA AF Clark, WH Tucker, MA TI Problems with lesions related to the development of malignant melanoma: Common nevi, dysplastic nevi, malignant melanoma in situ, and radial growth phase malignant melanoma SO HUMAN PATHOLOGY LA English DT Article ID ULTRAVIOLET-RADIATION; MELANOCYTIC NEVI; GUINEA-PIGS; RISK-FACTOR; PROGRESSION; ANIMALS; NUMBER; CANCER; MICE; SKIN C1 Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. Beth Israel Deaconess Med Ctr, Boston, MA USA. NCI, Genet Epidemiol Branch, Bethesda, MD 20892 USA. RP Clark, WH (reprint author), Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. RI Tucker, Margaret/B-4297-2015 FU NCI NIH HHS [CA58845] NR 27 TC 21 Z9 21 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 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1998 VL 29 IS 1 BP 8 EP 14 DI 10.1016/S0046-8177(98)90384-7 PG 7 WC Pathology SC Pathology GA YT070 UT WOS:000071561000004 PM 9445128 ER PT J AU Fleming, MV Guinee, DG Chu, WS Freedman, AN Caporaso, NE Bennett, WP Colby, TV Tazelaar, H Abbondanzo, SL Jett, J Pairolero, P Trastek, V Liotta, LA Harris, CC Travis, WD AF Fleming, MV Guinee, DG Chu, WS Freedman, AN Caporaso, NE Bennett, WP Colby, TV Tazelaar, H Abbondanzo, SL Jett, J Pairolero, P Trastek, V Liotta, LA Harris, CC Travis, WD TI Bcl-2 immunohistochemistry in a surgical series of non-small cell lung cancer patients SO HUMAN PATHOLOGY LA English DT Article DE bcl-2; lung carcinoma; non-small cell; immunohistochemistry; apoptosis ID CARCINOMA-CELLS; P53; EXPRESSION; APOPTOSIS; PROTEIN; LOCALIZATION; ONCOPROTEIN; ONCOGENE; THERAPY; DEATH AB The bcl-2 gene is implicated in oncogenesis by its ability to a prolong cell survival through the inhibition of apoptosis, without increasing cell proliferation. An association between immunohistochemical staining fur bcl-2 protein and the histological type and prognosis of non-small cell carcinoma was hypothesized by Pezzella et al. (N Engl J Med 329:690-694, 1993). In a case series, we stained formalin-fixed, paraffin-embedded tumor tissue from 106 surgical non-small cell lung cancer patients with an antibody to bcl-2 protein (DAKO clone 124, Carpinteria, CA). The resulting bcl-2 staining data were evaluated for associations with demographic, histological, immunohistochemical, and genetic features, including p53 mutations. Bcl-2 staining was observed in tumors from 29 of 106 (27%) of subjects, but was significantly less frequent in subjects' adenocarcinoma histology (8 of 55, 14.6%) (P = .007). This finding persisted after adjustment for ape, gender, stage, grade, smoking history, and disease-free survival. in univariate analyses, no association was seen with age, weight, body mass index, gender, or pack-years smoking; tumor grade, stage, or patient performance status; p53 or c-erbB2 immunohistochemical staining, or p53 mutations. These data agree with earlier reports that bcl-2 staining is less common in adenocarcinomas; however, our data do not support the hypothesis that bcl-2 staining confers a better prognosis overall, in squamous cell carcinoma, or in an older patient population. Copyright (C) 1998 by W.B. Saunders Company. C1 Armed Forces Inst Pathol, Dept Pulm & Mediastinal Pathol, Washington, DC 20306 USA. NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. Armed Forces Inst Pathol, Dept Hematol & Lymphat Pathol, Washington, DC 20306 USA. NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA. Univ Utah, Dept Pathol, Salt Lake City, UT 84112 USA. RP Fleming, MV (reprint author), Armed Forces Inst Pathol, Dept Pulm & Mediastinal Pathol, 6825 16th St NW,Bldg 54,Room M003B, Washington, DC 20306 USA. NR 23 TC 33 Z9 37 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 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1998 VL 29 IS 1 BP 60 EP 64 DI 10.1016/S0046-8177(98)90391-4 PG 5 WC Pathology SC Pathology GA YT070 UT WOS:000071561000011 PM 9445135 ER PT J AU Clark, WH Hood, AF Tucker, MA Jampel, RM AF Clark, WH Hood, AF Tucker, MA Jampel, RM TI Atypical melanocytic nevi of the genital type with a discussion of reciprocal parenchymal-stromal interactions in the biology of neoplasia SO HUMAN PATHOLOGY LA English DT Article ID EXTRACELLULAR-MATRIX; MALIGNANT-MELANOMA; DIFFERENTIATION; PROGRESSION; CANCER; COMMON; ADULT; VULVA; SKIN AB Melanocytic lesions of the genital area, especially those on the vulva, may present great difficulty in histological interpretation. A histological diagnosis of malignant melanoma was made in more than one third of 56 genital area melanocytic lesions submitted in consultation to the authors. The median age of the patients with these lesions was 25 years. This article is a clinicopathological study of these lesions and distinguishes them from malignant melanoma, The stroma of the lesions of the genital area was different from the stroma seen in the dysplastic nevi and melanoma. The differences in the stromal form in the diverse lesions is useful in diagnosis and is of profound biological significance. The stroma in the reported lesions and in some lesions of melanocytic neoplasia is described in detail, and its biological significance is discussed, Three sets of cases are used in this comparative study to delineate the clinicopathological nature and the biology of the genital nevi. The 56 cases submitted in consultation constitute the primary series of our work (The Clark Cutaneous Pathology Laboratory Series). These are compared with a series of cases from the Pigmented Lesion Group of the University of Pennsylvania and Pathology Services, Inc, and another series of cases from the Genetic Epidemiology Branch of the National Cancer Institute. The two series used for comparative study contain approximately the same number of cases of dysplastic nevi and malignant melanoma as there are atypical melanocytic nevi of the genital type in the primary series. The total number of eases was studied by comparison of their attributes in a relational database, The clinical data of the primary series was acquired through the use of a questionnaire completed by the contributors. The 56 cases presented two distinctive pathological pictures, One of these is termed atypical melanocytic nevi of the genital type (AMNGT),whereas dysplastic nevi (DN) formed the second of the two pathological pictures. There were 36 AMNGT and 14 DN. The remaining six cases were common nevi without atypia or ill-defined melanocytic hyperplasias. The lesions of AMNGT are usually located on the vulva, but they are seen on the perineum and, rarely, on the mons pubis and in the axilla. Lesions similar to AMNGT have been seen uncommonly on the male genitalia. The stromal patterns were distinctive and related to specific melanocytic lesions. An unclassified (unclass) or nonspecific stromal pattern was associated with AMNGT; a pattern of regression with differentiation (diff-regress) dominated the stroma of common dermal nevi; concentric eosinophilic fibroplasia (cef) and lamellar fibroplasia (If) were present in dysplastic nevi; fibroplasia with a plaquelike lymphocytic infiltrate (fl) and diffuse eosinophilic fibroplasia (def) were noted in radial growth phase melanoma; and fibroplasia with angiogenesis (fa) or an absence of evidence for parenchymal stromal reciprocal interactions (nopsi) marked thick or deeply invasive vertical growth phase melanomas, Recommendations for management of the lesions are suggested. Conclusions: One kind of atypical melanocytic proliferation in the genital area forms a distinctive clinicopathological entity that can be distinguished from melanoma and dysplastic nevi, the AMNGT. Such lesions are more common on the labia minora or the mucosa of the clitoral region than they are on the labia majora. The other common atypical melanocytic proliferation of this area is a dysplastic nevus, which is much more common on the labia majora than on the labia minora. The reciprocal interactions between parenchyma and stroma are discussed as homeostatic processes, a continually functioning template maintaining tissue, organ, and organismal form and function. The progressive disorganization of this template in neoplasia is illustrated and is considered to be a cardinal element in the biology of neoplasia. Copyright (C) 1998 by W.B. Saunders Company. C1 NCI, Genet Epidemiol Branch, Bethesda, MD 20892 USA. Harvard Univ, Beth Israel Hosp, Sch Med, Dept Pathol, Boston, MA 02215 USA. Pathol Serv Inc, Cambridge, MA USA. Univ Penn, Sch Med, Pigmented Les Study Grp, Philadelphia, PA 19104 USA. Indiana Univ, Sch Med, Dept Dermatol, Indianapolis, IN USA. Johns Hopkins Med Inst, Dept Dermatol, Baltimore, MD 21205 USA. RP Tucker, MA (reprint author), NCI, Genet Epidemiol Branch, Execut Plaza N,Suite 439,6130 Execut Blvd,MSC 737, Bethesda, MD 20892 USA. RI Tucker, Margaret/B-4297-2015 FU NCI NIH HHS [CA58845] NR 44 TC 66 Z9 66 U1 0 U2 2 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1998 VL 29 IS 1 SU 1 BP S1 EP S24 PG 24 WC Pathology SC Pathology GA YT310 UT WOS:000071587900002 PM 9445124 ER PT J AU Kesner, JS Knecht, EA Krieg, EF Wilcox, AJ O'Connor, JF AF Kesner, JS Knecht, EA Krieg, EF Wilcox, AJ O'Connor, JF TI Detecting pre-ovulatory luteinizing hormone surges in urine SO HUMAN REPRODUCTION LA English DT Article DE creatinine; epidemiology; menstrual cycle; two-site immunofluorometric assay; women ID FOLLICLE-STIMULATING-HORMONE; RESOLVED IMMUNOFLUOROMETRIC ASSAYS; HUMAN CHORIONIC-GONADOTROPIN; PROGESTERONE METABOLITES; REPRODUCTIVE HORMONES; ENZYME-IMMUNOASSAY; IMMUNOMETRIC ASSAY; SERUM ESTRADIOL; EARLY FETAL; WOMEN AB The study objectives were to determine (i) if pre-ovulatory luteinizing hormone (LH) surges, undetected in urine by two immunoradiometric assays (IRMA), were detectable by an ultrasensitive immunofluorometric assay (IFMA) and (ii) the influence of creatinine adjustment on the detection and timing of the urinary LH surges, Daily urine specimens were contributed by healthy 25-36 year old volunteers during 14 ovulatory menstrual cycles for an epidemiological study conducted in 1983-1985, Specimens were selected as having been previously assayed by two IRMA without consistently detecting LH surges, These urine specimens were remeasured using an IFMA and adjusted for creatinine concentration, IFMA measurements revealed unambiguous LH surges in all cycles, Adjusting IRMA urinary LH values for creatinine concentrations revealed previously undetected LH surges in four of eight cycles, Creatinine adjustment also altered the timing of IRMA and IFMA LH surges by 1-5 days, These results demonstrate an IFMA that detects pre-ovulatory LH surges in unpreserved, frozen urine from cycles where such surges were previously undetectable, Further, creatinine adjustment can markedly affect detection and timing of the onset and peak of the urinary LH surge, While our analysis suggests that this adjustment improves the validity of the LH measure, this requires further investigation. C1 NIOSH, Expt Toxicol Branch, Div Biomed & Behav Sci, Cincinnati, OH 45226 USA. NIOSH, Stat Act, Div Biomed & Behav Sci, Cincinnati, OH 45226 USA. NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. Columbia Univ Coll Phys & Surg, Irving Ctr Clin Res, New York, NY 10032 USA. RP Kesner, JS (reprint author), NIOSH, Expt Toxicol Branch, Div Biomed & Behav Sci, 4676 Columbia Pkwy,MS-C23, Cincinnati, OH 45226 USA. OI Wilcox, Allen/0000-0002-3376-1311 NR 38 TC 24 Z9 25 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0268-1161 J9 HUM REPROD JI Hum. Reprod. PD JAN PY 1998 VL 13 IS 1 BP 15 EP 21 DI 10.1093/humrep/13.1.15 PG 7 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA ZA740 UT WOS:000072396100005 PM 9512221 ER PT J AU Daniels, SR McMahon, RP Obarzanek, E Waclawiw, MA Similo, SL Biro, FM Schreiber, GB Kimm, SYS Morrison, JA Barton, BA AF Daniels, SR McMahon, RP Obarzanek, E Waclawiw, MA Similo, SL Biro, FM Schreiber, GB Kimm, SYS Morrison, JA Barton, BA TI Longitudinal correlates of change in blood pressure in adolescent girls SO HYPERTENSION LA English DT Article DE blood pressure; race; obesity; adolescents ID UNITED-STATES; HYPERTENSION; CHILDREN; SEX; OBESITY; WEIGHT; BLACK; RACE; RISK; POPULATION AB The objective of this study was to assess the longitudinal changes in blood pressure in black and white adolescent girls and evaluate potential determinants of changes in blood pressure, including sexual maturation and body size. A total of 1213 black and 1166 white girls, ages 9 or 10 years at study entry, were followed up through age 14 with annual measurements of height, weight, skinfold thickness, stage of sexual maturation, systolic and diastolic blood pressures, and other cardiovascular risk factors. Average blood pressures in black girls were generally 1 to 2 mm Hg higher than in white girls of similar age over the course of the study. Age, race, stage of sexual maturation, height, and body mass index (kg/m(2)) were all significant univariate predictors of systolic and diastolic blood pressures in longitudinal regression analyses. Black girls had a significantly smaller increase in blood pressure for a given increase in body mass index compared with white girls. The predicted increases in blood pressure per unit increase in body mass index (mm Hg per kg/m(2)) were as follows: systolic, 0.65+/-0.04 in whites and 0.52+/-0.04 in blacks (P<.001); diastolic fourth Korotkoff phase, 0.31+/-0.04 in whites and 0.15+/-0.03 in blacks (P<.001); and diastolic fifth Korotkoff phase, 0.31+/-0.05 in whites and 0.16+/-0.04 in blacks (P<.001). Understanding of the determinants of the racial differences in blood pressure could provide the rationale for future interventions to reduce the excess cardiovascular mortality in black compared with white women. C1 Childrens Hosp, Med Ctr, Div Cardiol, Cincinnati, OH 45229 USA. Maryland Med Res Inst, Baltimore, MD USA. NHLBI, Bethesda, MD 20892 USA. Westat Inc, Rockville, MD USA. Univ Pittsburgh, Sch Med, Dept Clin Epidemiol & Prevent Med, Pittsburgh, PA 15260 USA. RP Daniels, SR (reprint author), Childrens Hosp, Med Ctr, Div Cardiol, 3333 Burner Ave, Cincinnati, OH 45229 USA. EM sdaniels@chmcc.org RI McMahon, Robert/C-5462-2009; OI Barton, Bruce/0000-0001-7878-8895 FU NHLBI NIH HHS [HC 55023-26] NR 29 TC 26 Z9 26 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1998 VL 31 IS 1 BP 97 EP 103 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA YU639 UT WOS:000071738900018 PM 9449398 ER PT J AU Ye, GF Park, JW Basude, R Buerk, DG Jaron, D AF Ye, GF Park, JW Basude, R Buerk, DG Jaron, D TI Incorporating O-2-Hb reaction kinetics and the Fahraeus effect into a microcirculatory O-2-CO2 transport model SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING LA English DT Article DE arteriolar role; carbon dioxide transport; compartmental model; hypoxia; microcirculation; oxygen consumption; oxygen delivery; oxygen transport ID OXYGEN-TRANSPORT; COMPARTMENTAL MODEL; GAS-TRANSPORT; BLOOD; CAPILLARIES; SIMULATION; TISSUE; NETWORKS; RELEASE; BRAIN AB The influence of O-2-Hb reaction kinetics and the Fahraeus effect on steady state O-2 and CO2 transport in cat brain microcirculation was investigated using our refined multicompartmental model, The most important model predictions include: 1) capillaries are the sites in the microcirculation where the effect of O-2-Hb kinetics is most pronounced; 2),while there is only a small difference between equilibrium and actual oxygen saturation, this effect is not negligible; 3) O-2-Hb kinetics tends to make the PO2 level at the venous entrance higher than in venules; 4) the influence of the Fahraeus effect leads to a lower tissue PO2 level than in venules and the outlet vein. The resultant decline in tissue PO2 may lead to a decrease in O-2 consumption rate and extraction ratio; 5) although the Fahraeus effect changes the ratio between arteriolar flux and capillary flux, incorporating the fahraeus effect and O-2-Hb kinetics into the simulation does not change our previous conclusion that most of the O-2 and CO2 exchange takes place at the capillary level; 6) in general, influences of O-2-Hb kinetics and Fahraeus effect are synergistic; 7) a model that excludes these two mechanisms might overestimate the tissue oxygenation level especially during severe hypoxia. C1 Respiron Inc, New Concept Dev Div, Redwood City, CA 94063 USA. Drexel Univ, Inst Biomed Engn & Sci, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Physiol, Dept Bioengn, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Inst Environm Med, Philadelphia, PA 19104 USA. NIH, Natl Ctr Res Resources, Bethesda, MD 20892 USA. RP Ye, GF (reprint author), Respiron Inc, New Concept Dev Div, 643 Bair Isl Rd,Room 212, Redwood City, CA 94063 USA. RI Buerk, Donald/F-6888-2014 FU NEI NIH HHS [EY09269] NR 29 TC 8 Z9 8 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 USA SN 0018-9294 J9 IEEE T BIO-MED ENG JI IEEE Trans. Biomed. Eng. PD JAN PY 1998 VL 45 IS 1 BP 26 EP 35 DI 10.1109/10.650348 PG 10 WC Engineering, Biomedical SC Engineering GA YM122 UT WOS:000071030900004 PM 9444837 ER PT J AU Wen, H Shah, J Balaban, RS AF Wen, H Shah, J Balaban, RS TI Hall effect imaging SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING LA English DT Article DE biomedical; characterization; conductivity; diagnostic; dielectric; electric; Hall; imaging; magnetic; tissue; ultrasound ID ULTRASOUND; CAVITATION AB This paper presents a new imaging method based on the classical Hall effect (HE), which describes the origin of a detectable voltage from a conductive object moving in a magnetic field, HE images are formed using ultrasound imaging techniques in a magnetic field, These images reflect the electrical properties of the sample, To demonstrate the feasibility of this method, images of plastic and biological samples are collected. The contrast mechanism and signal-to-noise issues are discussed. Since electrical parameters vary widely among tissue types and states, HE imaging may be a useful tool for biological research and medical diagnosis. C1 NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA. RP Wen, H (reprint author), NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA. RI Balaban, Robert/A-7459-2009; Wen, Han/G-3081-2010 OI Balaban, Robert/0000-0003-4086-0948; Wen, Han/0000-0001-6844-2997 FU Intramural NIH HHS [Z01 HL004606-12] NR 15 TC 73 Z9 76 U1 1 U2 9 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 USA SN 0018-9294 J9 IEEE T BIO-MED ENG JI IEEE Trans. Biomed. Eng. PD JAN PY 1998 VL 45 IS 1 BP 119 EP 124 DI 10.1109/10.650364 PG 6 WC Engineering, Biomedical SC Engineering GA YM122 UT WOS:000071030900013 PM 9444846 ER PT J AU Thevenaz, P Ruttimann, UE Unser, M AF Thevenaz, P Ruttimann, UE Unser, M TI A pyramid approach to subpixel registration based on intensity SO IEEE TRANSACTIONS ON IMAGE PROCESSING LA English DT Article DE affine transformation; intramodal voxel-based registration; Marquardt-Levenberg nonlinear least-squares optimization; multiresolution; spline ID IMAGE REGISTRATION; CRITERION; ALGORITHM; INTERPOLATION; MOTION AB We present an automatic subpixel registration algorithm that minimizes the mean square intensity difference between a reference and a test data set, which can be either images (two-dimensional) or volumes (three-dimensional), It uses an explicit spline representation of the images in conjunction with spline processing, and is based on a coarse-to-fine iterative strategy (pyramid approach). The minimization is performed according to a new variation (ML*) of the Marquardt-Levenberg algorithm for nonlinear least-square optimization, The geometric deformation model is a global three-dimensional (3-D) affine transformation that can be optionally restricted to rigid-body motion (rotation and translation), combined with isometric scaling, It also includes an optional adjustment of image contrast differences, We obtain excellent results for the registration of intramodality positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) data, We conclude that the multiresolution refinement strategy is more robust than a comparable single-stage method, being less likely to be trapped into a false local optimum, In addition, our improved version of the Marquardt-Levenberg algorithm is faster. C1 Swiss Fed Inst Technol, CH-1015 Lausanne, Switzerland. Natl Inst Alcohol Abuse & Alcoholism, NIH, Bethesda, MD 20892 USA. RP Swiss Fed Inst Technol, CH-1015 Lausanne, Switzerland. EM Phillippe.thevenaz@epfl.ch; ursr@nih.gov RI Unser, Michael/A-1550-2008 NR 47 TC 1025 Z9 1053 U1 4 U2 63 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA SN 1057-7149 EI 1941-0042 J9 IEEE T IMAGE PROCESS JI IEEE Trans. Image Process. PD JAN PY 1998 VL 7 IS 1 BP 27 EP 41 DI 10.1109/83.650848 PG 15 WC Computer Science, Artificial Intelligence; Engineering, Electrical & Electronic SC Computer Science; Engineering GA YM900 UT WOS:000071113100003 PM 18267377 ER PT J AU Sharma, G Trussell, HJ Vrhel, MJ AF Sharma, G Trussell, HJ Vrhel, MJ TI Optimal nonnegative color scanning filters SO IEEE TRANSACTIONS ON IMAGE PROCESSING LA English DT Letter DE color; colorimetry; color filter design; scanning AB In this correspondence, the problem of designing color scanning filters for multi-illuminant color recording is considered. The filter transmittances are determined from a minimum-mean-squared orthogonal tristimulus error criterion that minimizes the color error in estimates obtained from noisy recorded data. Nonnegativity constraints essential for physical realizability are imposed on the filter transmittances. In order to demonstrate the significant improvements obtained, the resulting filters are compared with suboptimal filters reported in earlier literature. C1 Xerox Corp, Webster, NY 14580 USA. N Carolina State Univ, Dept Elect & Comp Engn, Raleigh, NC 27695 USA. NIH, Bethesda, MD 20892 USA. RP Sharma, G (reprint author), Xerox Corp, 800 Phillips Rd, Webster, NY 14580 USA. RI Sharma, Gaurav/A-1154-2007 OI Sharma, Gaurav/0000-0001-9735-9519 NR 15 TC 40 Z9 40 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 USA SN 1057-7149 J9 IEEE T IMAGE PROCESS JI IEEE Trans. Image Process. PD JAN PY 1998 VL 7 IS 1 BP 129 EP 133 DI 10.1109/83.650859 PG 5 WC Computer Science, Artificial Intelligence; Engineering, Electrical & Electronic SC Computer Science; Engineering GA YM900 UT WOS:000071113100014 PM 18267388 ER PT J AU Kehrl, JH AF Kehrl, JH TI Heterotrimeric G protein signaling: Roles in immune function and fine-tuning by RGS proteins SO IMMUNITY LA English DT Review ID PLATELET-ACTIVATING-FACTOR; T-LYMPHOCYTE ACTIVATION; B-CELL DIFFERENTIATION; MAP KINASE ACTIVATION; BETA-GAMMA-SUBUNITS; NF-KAPPA-B; ALPHA-SUBUNITS; TYROSINE KINASES; INTRACELLULAR CALCIUM; REGULATE ACTIVATION C1 NIAID, Cell Mol Biol Sect B, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. RP Kehrl, JH (reprint author), NIAID, Cell Mol Biol Sect B, Immunoregulat Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM jkehrl@atlas.niaid.nih.gov OI Kehrl, John/0000-0002-6526-159X NR 113 TC 131 Z9 134 U1 1 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD JAN PY 1998 VL 8 IS 1 BP 1 EP 10 DI 10.1016/S1074-7613(00)80453-7 PG 10 WC Immunology SC Immunology GA YU884 UT WOS:000071765700001 PM 9462506 ER PT J AU Tolosa, E King, LB Ashwell, JD AF Tolosa, E King, LB Ashwell, JD TI Thymocyte glucocorticoid resistance alters positive selection and inhibits autoimmunity and lymphoproliferative disease in MRL-lpr/lpr mice SO IMMUNITY LA English DT Article ID T-CELL RECEPTOR; NEGATIVE SELECTION; LPR MICE; INDUCED APOPTOSIS; TRANSGENIC MICE; GENE-PRODUCTS; IPR GENE; ANTIGEN; REPERTOIRE; ACTIVATION AB Thymus-derived glucocorticoids antagonize 7 cell receptor (TCR)-induced thymocyte apoptosis, allowing the survival (positive selection) of cells bearing TCRs that recognize self antigens with low-to-moderate avidity. Here we demonstrate that expression of an antisense glucocorticoid receptor transgene in thymocytes of spontaneously autoimmune MRL-lpr/lpr mice causes the loss of specific TCR V beta-bearing T cells that are normally positively selected in this strain. These transgenic mice had lower autoantibody production and milder symptoms of autoimmune disease than MRL-/pr/lpr controls and had markedly reduced accumulation of the TCR(+)Thy-1(+)CD4(-)CD8(-)B220(+) T cells that are the hallmark of the lpr mutation. Thus, decreased glucocorticoid signaling in thymocytes alters the T cell repertoire and greatly diminishes autoimmunity in MRL-lpr/lpr autoimmune mice. C1 NCI, Lab Immune Cell Biol, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP Ashwell, JD (reprint author), NCI, Lab Immune Cell Biol, Div Basic Sci, NIH, Bethesda, MD 20892 USA. NR 60 TC 56 Z9 56 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD JAN PY 1998 VL 8 IS 1 BP 67 EP 76 DI 10.1016/S1074-7613(00)80459-8 PG 10 WC Immunology SC Immunology GA YU884 UT WOS:000071765700007 PM 9462512 ER PT J AU Mukouyama, YS Hara, T Xu, MJ Tamura, K Donovan, PJ Kim, HJ Kogo, H Tsuji, K Nakahata, T Miyajima, A AF Mukouyama, YS Hara, T Xu, MJ Tamura, K Donovan, PJ Kim, HJ Kogo, H Tsuji, K Nakahata, T Miyajima, A TI In vitro expansion of murine multipotential hematopoietic progenitors from the embryonic aorta-gonad-mesonephros region SO IMMUNITY LA English DT Article ID LEUKEMIA-INHIBITORY FACTOR; FETAL LIVER HEMATOPOIESIS; COLONY-STIMULATING FACTOR; LOW-DENSITY LIPOPROTEIN; PRIMORDIAL GERM-CELLS; ONCOSTATIN-M; STEM-CELLS; IN-VITRO; DEFINITIVE HEMATOPOIESIS; SIGNAL TRANSDUCER AB The origin of hematopoietic stem cells (HSCs) and their growth factor requirement are poorly understood. Here we describe a new in vitro culture system of the aorta-gonad-mesonephros (AGM) region, where long-term repopulating HSCs first arise. We demonstrate that oncostatin M (OSM) is expressed in the AGM and is absolutely required for the expansion of multipotential hematopoietic progenitors in vitro. In addition, OSM enhances the formation of endothelial cell clusters. Thus, OSM appears to be a key cytokine for the development of multipotential hematopoietic progenitors in the AGM, possibly acting on common precursor cells between HSCs and endothelial cells. fly using the AG M culture derived from macrophage colony-stimulating factor (M-CSF)-deficient op/op mutant embryos, we also show a pivotal role for M-CSF in fetal myelopoiesis. C1 Univ Tokyo, Inst Mol & Cellular Biosci, Bunkyo Ku, Tokyo 113, Japan. Univ Tokyo, Inst Med Sci, Minato Ku, Tokyo 108, Japan. Tokyo Univ Pharm & Life Sci, Tokyo 19203, Japan. NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA. RP Miyajima, A (reprint author), Univ Tokyo, Inst Mol & Cellular Biosci, Bunkyo Ku, 1-1-1 Yaoi, Tokyo 113, Japan. FU NCI NIH HHS [N01-CO-74101] NR 59 TC 117 Z9 119 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD JAN PY 1998 VL 8 IS 1 BP 105 EP 114 DI 10.1016/S1074-7613(00)80463-X PG 10 WC Immunology SC Immunology GA YU884 UT WOS:000071765700011 PM 9462516 ER PT J AU Martin, MP Harding, A Chadwick, R Kronick, M Cullen, M Lin, L Mignot, E Carrington, M AF Martin, MP Harding, A Chadwick, R Kronick, M Cullen, M Lin, L Mignot, E Carrington, M TI Characterization of 12 microsatellite loci of the human MHC in a panel of reference cell lines SO IMMUNOGENETICS LA English DT Article DE HLA; microsatellite loci; microsatellite typing; human; MHC ID CLASS-II REGION; POLYMORPHIC MICROSATELLITES; EVOLUTIONARY DYNAMICS; DINUCLEOTIDE REPEAT; SKELETAL REMAINS; DNA ANALYSIS; HUMAN GENOME; LINKAGE MAP; HLA-B; GENES AB The human genome contains a large number of interspersed microsatellite repeats which exhibit a high degree of polymorphism and are inherited in a Mendelian fashion, making them extremely useful genetic markers. Several microsatellites have been described in the HLA region, but allele nomenclature, a set of broadly distributed controls, and typing methods have not been standardized, which has resulted in discrepant microsatellite data between laboratories. In this report we present a detailed protocol for genotyping microsatellites using a semi-automated fluorescence-based method. Twelve microsatellites within or near the major histocompatibility complex (MHC) were typed in the 10th International Histocompatibility Workshop homozygous typing cell lines (HTCs) and alleles were designated based on size. All loci were sequenced in two HTCs providing some information on the level of complexity of the repeat sequence. A comparison of allele size obtained by genotyping versus that obtained by direct sequencing showed minor discrepancies in some cases, but these were not unexpected given the technical differences in the methodologies. Fluorescence-based typing of microsatellites in the MHC described herein is highly efficient, accurate, and reproducible, and will allow comparison of results between laboratories. C1 NCI, Intramural Res Support Program, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. Perkin Elmer Corp, Appl Biosyst Div, Foster City, CA USA. Stanford Univ, Sch Med, Dept Psychiat, Ctr Narcolepsy Res, Palo Alto, CA 94304 USA. RP Carrington, M (reprint author), NCI, Intramural Res Support Program, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. NR 29 TC 27 Z9 27 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JAN PY 1998 VL 47 IS 2 BP 131 EP 138 PG 8 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA YP988 UT WOS:000071336100004 PM 9396859 ER PT J AU Alexander, J Fikes, J Hoffman, S Franke, E Sacci, J Appella, E Chisari, FV Guidotti, LG Chesnut, RW Livingston, B Sette, A AF Alexander, J Fikes, J Hoffman, S Franke, E Sacci, J Appella, E Chisari, FV Guidotti, LG Chesnut, RW Livingston, B Sette, A TI The optimization of helper T lymphocyte (HTL) function in vaccine development SO IMMUNOLOGIC RESEARCH LA English DT Review DE PAN DR T cell helper epitopes (PADRE); peptide-based vaccines; malaria; HBV ID HEPATITIS-B VIRUS; MHC CLASS-II; COMPLEX-CLASS-II; NATURALLY PROCESSED PEPTIDES; MELANOMA ANTIGEN GP100; CELL EPITOPES; IMMUNE-RESPONSE; HLA-DR; PROMISCUOUS RECOGNITION; 3-DIMENSIONAL STRUCTURE AB Helper T lymphocyte (HTL) responses play an important role in the induction of both humoral and cellular immune responses. Therefore, HTL epitopes are likely to be a crucial component of prophylactic and immunotherapeutic vaccines. For this reason, Pan DR helper T cell epitopes (PADRE), engineered to bind most common HLA-DR molecules with high affinity and act as powerful immunogens, were developed. Short linear peptide constructs comprising PADRE and Plasmodium-derived B cell epitopes induced antibody responses comparable to more complex multiple antigen peptides (MAP) constructs in mice. These antibody responses were composed mostly of the IgG subclass, reactive against intact sporozoites, inhibitory of schizont formation in liver invasion assays, and protective against sporozoite challenge in vivo. The PADRE HTL epitope has also been shown to augment the potency of vaccines designed to stimulate a cellular immune response. Using a HBV transgenic murine model, it was found that CTL tolerance was broken by PADRE-CTL epitope Lipopeptide, but not by a similar construct containing a conventional HTL epitope. There are a number of prophylactic vaccines that are of limited efficacy, require multiple boosts, and/or confer protection to only a fraction of the immunized population. Also, in the case of virally infected or cancerous cells, new immunotherapeutic vaccines that induce strong cellular immune responses are desirable. Therefore, optimization of HTL function by use of synthetic epitopes such as PADRE or pathogen-derived, broadly crossreactive epitopes holds promise for a new generation of highly efficacious vaccines. C1 Epimmune Inc, San Diego, CA USA. USN, Med Res Inst, Rockville, MD 20852 USA. NCI, NIH, Bethesda, MD 20892 USA. Scripps Res Inst, La Jolla, CA USA. RP Sette, A (reprint author), 6555 Nancy Dr,Suite 200, San Diego, CA 92121 USA. RI Chisari, Francis/A-3086-2008; OI Guidotti, Luca G./0000-0002-0205-2678; Chisari, Francis/0000-0002-4832-1044 FU NCI NIH HHS [R37 CA 40489]; NIAID NIH HHS [N01-AI-45241, R01 AI 2001] NR 145 TC 67 Z9 79 U1 1 U2 10 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1998 VL 18 IS 2 BP 79 EP 92 DI 10.1007/BF02788751 PG 14 WC Immunology SC Immunology GA 142HD UT WOS:000077193800002 PM 9844827 ER PT S AU Allison Abbas Mason Waldmann Lenardo Mitchison Kioussis Jenkins Lechler Stockinger Hafler Shevach AF Allison Abbas Mason Waldmann Lenardo Mitchison Kioussis Jenkins Lechler Stockinger Hafler Shevach BE Bock, GR Goode, JA TI Mechanisms of peripheral T cell tolerance - Discussion SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID INDUCTION; MICE C1 Univ Calif Berkeley, Canc Res Lab, Berkeley, CA 94720 USA. Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, Boston, MA 02115 USA. Harvard Med Sch, Boston, MA 02115 USA. Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England. Sir William Dunn Sch Pathol, Oxford OX2 7QY, England. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. UCL, Sch Med, Dept Immunol, London W1P 6DB, England. Natl Inst Med Res, Div Mol Immunol, London NW7 1AA, England. Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA. Royal Postgrad Med Sch, Dept Immunol, London W12 0NN, England. Brigham & Womens Hosp, Ctr Neurol Dis, Harvard Med Sch, Boston, MA 02115 USA. RP Allison (reprint author), Univ Calif Berkeley, Canc Res Lab, Berkeley, CA 94720 USA. NR 4 TC 0 Z9 0 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 14 EP 20 PG 7 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400003 ER PT S AU Abbas Healy Hafler Lenardo Stockinger Mitchison Wraith Shevach Waldmann Cornall Jenkins Kioussis Kurts Mason AF Abbas Healy Hafler Lenardo Stockinger Mitchison Wraith Shevach Waldmann Cornall Jenkins Kioussis Kurts Mason BE Bock, GR Goode, JA TI Immunological tolerance - General discussion I SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID B-CELLS; BCL-2; MICE C1 Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, Boston, MA 02115 USA. Harvard Med Sch, Boston, MA 02115 USA. Stanford Univ, Dept Microbiol & Immunol, Howard Hughes Med Inst, Beckman Ctr,Sch Med, Stanford, CA 94305 USA. Brigham & Womens Hosp, Ctr Neurol Dis, Harvard Med Sch, Boston, MA 02115 USA. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. Natl Inst Med Res, Div Mol Immunol, London NW7 1AA, England. UCL, Sch Med, Dept Immunol, London W1P 6DB, England. Univ Bristol, Sch Med Sci, Dept Pathol & Microbiol, Bristol BS8 1TD, Avon, England. Sir William Dunn Sch Pathol, Oxford OX2 7QY, England. Univ Oxford, John Radcliffe Hosp, Nuffield Dept Med, Oxford OX3 9DU, England. Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA. Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia. Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England. RP Abbas (reprint author), Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, 75 Francis St, Boston, MA 02115 USA. NR 10 TC 0 Z9 0 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 33 EP 40 PG 8 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400006 ER PT S AU Abbas Allen Wraith Simon Allison Mitchison Jenkins Hafler Kurts Stockinger Hammerling Kioussis AF Abbas Allen Wraith Simon Allison Mitchison Jenkins Hafler Kurts Stockinger Hammerling Kioussis BE Bock, GR Goode, JA TI The study of self-tolerance using murine haemoglobin as a model self antigen - Discussion SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID T-CELLS C1 Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, Boston, MA 02115 USA. Harvard Med Sch, Boston, MA 02115 USA. Washington Univ, Sch Med, Ctr Immunol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. Univ Bristol, Sch Med Sci, Dept Pathol & Microbiol, Bristol BS8 1TD, Avon, England. Ctr Immunol Marseille Luminy, F-13288 Marseille 9, France. Univ Calif Berkeley, Canc Res Lab, Berkeley, CA 94720 USA. UCL, Sch Med, Dept Immunol, London W1P 6DB, England. Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA. Brigham & Womens Hosp, Ctr Neurol Dis, Harvard Med Sch, Boston, MA 02115 USA. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia. Natl Inst Med Res, Div Mol Immunol, London NW7 1AA, England. German Canc Res Ctr, Div Mol Immunol, Tumor Immunol Program, D-69120 Heidelberg, Germany. RP Abbas (reprint author), Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, 75 Francis St, Boston, MA 02115 USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 46 EP 53 PG 8 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400008 ER PT S AU Mitchison Schneider Allen Hammerling Shevach Abbas Mason Wraith Hafler Lechler AF Mitchison Schneider Allen Hammerling Shevach Abbas Mason Wraith Hafler Lechler BE Bock, GR Goode, JA TI Tolerance and determinant hierarchy - Discussion SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID T-CELL; LYSOZYME C1 UCL, Sch Med, Dept Immunol, London W1P 6DB, England. La Jolla Inst Allergy & Immunol, San Diego, CA 92121 USA. Washington Univ, Sch Med, Ctr Immunol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. German Canc Res Ctr, Tumor Immunol Program, Div Mol Immunol, D-69120 Heidelberg, Germany. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, Boston, MA 02115 USA. Harvard Med Sch, Boston, MA 02115 USA. Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England. Univ Bristol, Dept Pathol & Microbiol, Sch Med Sci, Bristol BS8 1TD, Avon, England. Brigham & Womens Hosp, Harvard Med Sch, Ctr Neurol Dis, Boston, MA 02115 USA. Royal Postgrad Med Sch, Dept Immunol, London W12 0NN, England. RP Mitchison (reprint author), UCL, Sch Med, Dept Immunol, Windeyer Bldg,Cleveland St, London W1P 6DB, England. NR 6 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 66 EP 72 PG 7 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400010 ER PT S AU Martin, DA Combadiere, B Hornung, F Jiang, D McFarland, H Siegel, R Trageser, C Wang, J Zheng, LX Lenardo, MJ AF Martin, DA Combadiere, B Hornung, F Jiang, D McFarland, H Siegel, R Trageser, C Wang, J Zheng, LX Lenardo, MJ BE Bock, GR Goode, JA TI Molecular genetic studies in lymphocyte apoptosis and human autoimmunity SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Article; Proceedings Paper CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID LYMPHOPROLIFERATIVE SYNDROME; FAS; DEATH; MUTATIONS; DISEASE AB Using a genetic approach, we have studied the molecular basis of human autoimmunity with special emphasis on a disease that is due to defective lymphocyte apoptosis. Recently, we and our collaborators have found that the autoimmune/ lymphoproliferative syndrome (ALPS), an inherited disease of children comprising marked lymphoid hyperplasia and autoimmune manifestations, is due to abnormalities in the CD95 gene that cause defective lymphocyte apoptosis. Our recent investigations have shown that the mutations in most families with ALPS cause either global or local changes in the structure of a cytoplasmic portion of the molecule called the 'death domain'. These death domain alterations impair binding of the adapter protein FADD/ MORT1 and result in a failure to activate apoptotic caspases after CD95 (Fas/APO-1) cross-linking. Mutations in apoptotic caspases may also contribute to the pathogenesis of ALPS in individuals that have no CD95 gene mutations. C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Martin, DA (reprint author), NIAID, Immunol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA. RI Siegel, Richard/C-7592-2009; Combadiere, Behazine/G-3881-2013 OI Siegel, Richard/0000-0001-5953-9893; NR 20 TC 5 Z9 5 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 73 EP 82 PG 10 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400011 ER PT S AU Kioussis Lenardo Cornall Mason Allen Abbas Jenkins Kurts Hammerling Simon Mitchison Waldmann Wraith AF Kioussis Lenardo Cornall Mason Allen Abbas Jenkins Kurts Hammerling Simon Mitchison Waldmann Wraith BE Bock, GR Goode, JA TI Molecular genetic studies in lymphocyte apoptosis and human autoimmunity - Discussion SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID MUTATIONS; LIGAND C1 Natl Inst Med Res, Div Mol Immunol, London NW7 1AA, England. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. Univ Oxford, John Radcliffe Hosp, Nuffield Dept Med, Oxford OX3 9DU, England. Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England. Washington Univ, Sch Med, Ctr Immunol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, Boston, MA 02115 USA. Harvard Med Sch, Boston, MA 02115 USA. Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA. Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia. German Canc Res Ctr, Div Mol Immunol, Tumor Immunol Program, D-69120 Heidelberg, Germany. Ctr Immunol Marseille Luminy, F-13288 Marseille 9, France. UCL, Sch Med, Dept Immunol, London W1P 6DB, England. Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX2 7QY, England. Univ Bristol, Sch Med, Dept Pathol & Microbiol, Bristol BS8 1TD, Avon, England. RP Kioussis (reprint author), Natl Inst Med Res, Div Mol Immunol, Mill Hill, London NW7 1AA, England. NR 8 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 82 EP 87 PG 6 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400012 ER PT S AU Mitchison Abbas Hafler Cornall Allen Mason Lechler Lenardo AF Mitchison Abbas Hafler Cornall Allen Mason Lechler Lenardo BE Bock, GR Goode, JA TI Immunological tolerance - General discussion II SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID SCREEN; LOCI C1 UCL, Sch Med, Dept Immunol, London W1P 6DB, England. Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Neurol Dis, Boston, MA 02115 USA. Univ Oxford, John Radcliffe Hosp, Nuffield Dept Med, Oxford OX3 9DU, England. Washington Univ, Sch Med, Ctr Immunol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England. Royal Postgrad Med Sch, Dept Immunol, London W12 0NN, England. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Mitchison (reprint author), UCL, Sch Med, Dept Immunol, Windeyer Bldg,Cleveland St, London W1P 6DB, England. NR 6 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 88 EP 91 PG 4 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400013 ER PT S AU Jenkins Abbas Allison Shevach Hammerling Wraith Hafler Healy Stockinger Waldmann Allen Lechler Lenardo AF Jenkins Abbas Allison Shevach Hammerling Wraith Hafler Healy Stockinger Waldmann Allen Lechler Lenardo BE Bock, GR Goode, JA TI A role for CTLA-4-mediated inhibitory signals in peripheral T cell tolerance? Discussion SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN C1 Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA. Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Univ Calif Berkeley, Canc Res Lab, Berkeley, CA 94720 USA. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. German Canc Res Ctr, Tumor Immunol Program, Div Mol Immunol, D-69120 Heidelberg, Germany. Univ Bristol, Sch Med Sci, Dept Pathol & Microbiol, Bristol BS8 1TD, Avon, England. Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Neurol Dis, Boston, MA 02115 USA. Natl Inst Med Res, Div Mol Immunol, London NW7 1AA, England. Sir William Dunn Sch Pathol, Oxford OX2 7QY, England. Royal Postgrad Med Sch, Dept Immunol, London W12 0NN, England. RP Jenkins (reprint author), Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Box 334 FUMC,420 Delaware St SE, Minneapolis, MN 55455 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 98 EP 102 PG 5 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400015 ER PT S AU Waldmann Jenkins Hafler Mitchison Shevach Abbas Kioussis Stockinger Arnold Kurts Hammerling Kamradt Mason AF Waldmann Jenkins Hafler Mitchison Shevach Abbas Kioussis Stockinger Arnold Kurts Hammerling Kamradt Mason BE Bock, GR Goode, JA TI Antigen-specific CD4(+) T cells that survive after the induction of peripheral tolerance possess an intrinsic lymphokine production defect - Discussion SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID DENDRITIC CELLS C1 Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX2 7QY, England. Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Neurol Dis, Boston, MA 02115 USA. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. UCL, Sch Med, Dept Immunol, London W1P 6DB, England. Brigham & Womens Hosp, Dept Pathol, Div Immunol Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Natl Inst Med Res, Div Mol Immunol, London NW7 1AA, England. German Canc Res Ctr, Tumor Immunol Program, Div Mol Immunol, D-69120 Heidelberg, Germany. Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia. Stanford Univ, Sch Med, Beckman Ctr, Howard Hughes Med Inst,Dept Micorobiol & Immunol, Stanford, CA 94305 USA. Charite Med Univ Klin III, D-10098 Berlin, Germany. RP Waldmann (reprint author), Univ Oxford, Sir William Dunn Sch Pathol, S Parks Rd, Oxford OX2 7QY, England. NR 5 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 113 EP 119 PG 7 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400017 ER PT S AU Shevach, EM Thornton, A Suri-Payer, E AF Shevach, EM Thornton, A Suri-Payer, E BE Bock, GR Goode, JA TI T lymphocyte-mediated control of autoimmunity SO IMMUNOLOGICAL TOLERANCE SE CIBA FOUNDATION SYMPOSIA LA English DT Article; Proceedings Paper CT Symposium on Immunological Tolerance CY JUL 08-10, 1997 CL NOVARTIS FDN, LONDON, ENGLAND HO NOVARTIS FDN ID MOLECULAR TARGETS; SELF-TOLERANCE; CELL SUBSET; DISEASE; MICE; SUPPRESSOR; THYMUS AB Autoreactive T cells can be readily identified in the peripheral lymphocyte pool of both humans and experimental animals. Peripheral tolerance may be maintained by regulatory/suppressor T cells which prevent the activation of autoantigen-specific cells. Mice thymectomized on day 3 of life (d3Tx) develop a wide spectrum of organ-specific autoimmune diseases. Reconstitution of d3Tx mice with CD4(+) CD25(+) T cells from normal mice prevents the development of disease. Similarly, CD4(+) CD25(+) T cells prevent the transfer of disease by autoantigen-specific cloned T cells derived from d3Tx mice. Thus, regulatory T cells can prevent both the induction and effector function of autoreactive T cells. In vitro, the CD4(+) CD25(+) population is anergic to stimulation through the T cell receptor (TCR) and suppresses the proliferative responses of normal CD4(+) CD25(-) cells by a contact-dependent mechanism. Suppression is not MHC-dependent, but requires activation of the CD4(+) CD25(+) population. The mechanism of suppression in vivo and the target antigen(s) of this unique regulatory population remain to be characterized. C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Shevach, EM (reprint author), NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NR 17 TC 19 Z9 21 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER PO19 1UD, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-97843-4 J9 CIBA F SYMP PY 1998 VL 215 BP 200 EP 211 PG 12 WC Immunology; Medicine, General & Internal SC Immunology; General & Internal Medicine GA BL67M UT WOS:000076284400031 PM 9760581 ER PT B AU Schooler, C Caplan, L Oates, G AF Schooler, C Caplan, L Oates, G BE Schaie, KW Schooler, C TI Aging and work: An overview SO IMPACT OF WORK ON OLDER ADULTS SE SOCIETAL IMPACT ON AGING SERIES LA English DT Proceedings Paper CT Conference on the Impact of Work on Older Adults CY OCT 16-17, 1995 CL PENN STATE UNIV, UNIVERSITY PK, PA HO PENN STATE UNIV ID OCCUPATIONAL SOCIAL-WORK; ADULT AGE-DIFFERENCES; JOB-SATISFACTION; OLDER WORKERS; PERFORMANCE; MEMORY; INFORMATION; DISEASE; SKILL C1 NIMH, Lab Socioenvironm Studies, Intramural Res Program, Bethesda, MD 20892 USA. NR 64 TC 9 Z9 9 U1 1 U2 4 PU SPRINGER PUBLISHING CO PI NEW YORK PA 11 WEST 42ND STREET, 15TH FLOOR, NEW YORK, NY 10036 USA BN 0-8261-9920-8 J9 SOCIET IMPACT AGING PY 1998 BP 1 EP 19 PG 19 WC Geriatrics & Gerontology; Industrial Relations & Labor; Psychology; Social Issues; Sociology SC Geriatrics & Gerontology; Business & Economics; Psychology; Social Issues; Sociology GA BN53M UT WOS:000082159300002 PM 11583041 ER PT B AU Riley, MW AF Riley, MW BE Schaie, KW Schooler, C TI Commentary: Psychology, sociology, and research on age SO IMPACT OF WORK ON OLDER ADULTS SE SOCIETAL IMPACT ON AGING SERIES LA English DT Proceedings Paper CT Conference on the Impact of Work on Older Adults CY OCT 16-17, 1995 CL PENN STATE UNIV, UNIVERSITY PK, PA HO PENN STATE UNIV C1 NIA, NIH, Bethesda, MD 20892 USA. NR 4 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER PUBLISHING CO PI NEW YORK PA 11 WEST 42ND STREET, 15TH FLOOR, NEW YORK, NY 10036 USA BN 0-8261-9920-8 J9 SOCIET IMPACT AGING PY 1998 BP 20 EP 27 PG 8 WC Geriatrics & Gerontology; Industrial Relations & Labor; Psychology; Social Issues; Sociology SC Geriatrics & Gerontology; Business & Economics; Psychology; Social Issues; Sociology GA BN53M UT WOS:000082159300003 ER PT B AU Schooler, C AF Schooler, C BE Schaie, KW Schooler, C TI Commentary: The institutional context of gradual retirement in Japan SO IMPACT OF WORK ON OLDER ADULTS SE SOCIETAL IMPACT ON AGING SERIES LA English DT Proceedings Paper CT Conference on the Impact of Work on Older Adults CY OCT 16-17, 1995 CL PENN STATE UNIV, UNIVERSITY PK, PA HO PENN STATE UNIV C1 NIMH, Lab Socioenvironm Studies, Intramural Res Program, Bethesda, MD 20892 USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PUBLISHING CO PI NEW YORK PA 11 WEST 42ND STREET, 15TH FLOOR, NEW YORK, NY 10036 USA BN 0-8261-9920-8 J9 SOCIET IMPACT AGING PY 1998 BP 85 EP 91 PG 7 WC Geriatrics & Gerontology; Industrial Relations & Labor; Psychology; Social Issues; Sociology SC Geriatrics & Gerontology; Business & Economics; Psychology; Social Issues; Sociology GA BN53M UT WOS:000082159300006 ER PT B AU Schooler, C AF Schooler, C BE Schaie, KW Schooler, C TI Work and the elderly: Crossing the bounds of levels and disciplines SO IMPACT OF WORK ON OLDER ADULTS SE SOCIETAL IMPACT ON AGING SERIES LA English DT Proceedings Paper CT Conference on the Impact of Work on Older Adults CY OCT 16-17, 1995 CL PENN STATE UNIV, UNIVERSITY PK, PA HO PENN STATE UNIV C1 NIMH, Lab Socioenvironm Studies, Intra Mural Res Program, Bethesda, MD 20892 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PUBLISHING CO PI NEW YORK PA 11 WEST 42ND STREET, 15TH FLOOR, NEW YORK, NY 10036 USA BN 0-8261-9920-8 J9 SOCIET IMPACT AGING PY 1998 BP 305 EP 310 PG 6 WC Geriatrics & Gerontology; Industrial Relations & Labor; Psychology; Social Issues; Sociology SC Geriatrics & Gerontology; Business & Economics; Psychology; Social Issues; Sociology GA BN53M UT WOS:000082159300019 ER PT J AU Goldman, R Shields, PG AF Goldman, R Shields, PG TI Molecular epidemiology of breast cancer SO IN VIVO LA English DT Review DE breast cancer; molecular epidemiology; p53; gene mutations; smoking ID MAMMARY EPITHELIAL-CELLS; P-32 POSTLABELING ASSAY; CARCINOGEN-DNA ADDUCTS; GENETIC POLYMORPHISMS; CIGARETTE-SMOKING; DRUG-METABOLISM; RISK; MUTATIONS; TUMORS; P53 AB Molecular epidemiology evaluates cancer risk based upon environmental exposures and genetically determined susceptibilities. Biomarkers, molecular indicators of exposure or disease state, are used to stake out the progression of a disease along plausible mechanistic pathways. Connecting biomarkers of exposure, (e.g. carcinogen DNA adducts), effect (e.g. mutations in tumor supressor genes), or disease (e.g., histological abnormalities) can clarify the etiology of cancer improve risk estimates, and lead to better preventive strategies. In this review, the following evidence is used to evaluate the possible contribution of environmental carcinogens to breast cancer: a) genetic predispositions in familial breast cancer, b) mutational spectra of the p53 tumor. supressor gene, c) chemical carcinogenesis in breast cancer models, and d) genetic polymorphisms in sporadic breast cancer. C1 NCI, Human Carcinogenesis Lab, Div Basic Res, NIH, Bethesda, MD 20892 USA. RP Shields, PG (reprint author), NCI, Human Carcinogenesis Lab, Div Basic Res, NIH, Bldg 37,Rm 2C16, Bethesda, MD 20892 USA. EM Peter_G_Shields@nih.gov RI Shields, Peter/I-1644-2012 NR 109 TC 16 Z9 16 U1 0 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE SN 0258-851X EI 1791-7549 J9 IN VIVO JI In Vivo PD JAN-FEB PY 1998 VL 12 IS 1 BP 43 EP 48 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA ZQ076 UT WOS:000073819000006 PM 9575425 ER PT J AU Gozar, MMG Price, VL Kaslow, DC AF Gozar, MMG Price, VL Kaslow, DC TI Saccharomyces cerevisiae-secreted fusion proteins Pfs25 and Pfs28 elicit potent Plasmodium falciparum transmission-blocking antibodies in mice SO INFECTION AND IMMUNITY LA English DT Article ID VACCINE CANDIDATE; SURFACE PROTEIN; MALARIA; YEAST; IMMUNITY; PURIFICATION; TARGET AB Transmission-blocking vaccines based on sexual-stage surface antigens of Plasmodium falciparum may assist in the control of this lethal form of human malaria, Two vaccine candidates, Pfs25 and Pfs28, were produced as single recombinant fusion proteins. The 39-kDa chimeric proteins, having a C-terminal His(6) tag, were secreted by Saccharomyces cerevisiae, using the prepro-alpha-factor leader sequence. Pfs25-28 fusion proteins were significantly more potent than either Pfs25 or Pfs28 alone in eliciting antibodies in mice that blocked oocyst development in Anopheles freeborni mosquitoes: complete inhibition of oocyst development in the mosquito midgut was achieved with fewer vaccinations, at a lower dose, and for a longer duration than with either Pfs25 or Pfs28 alone, Increased antigen-specific immunoglobulin G titers and highly significant lymphoproliferative stimulation by Pfs28-containing antigens suggest the presence of an immunodominant helper T-cell epitope in the Pfs28 portion of the fusion proteins, This epitope may be responsible for the enhanced humoral response to both Pfs25 and Pfs28 antigens, Protein production of the fusion protein was improved 12-fold by converting Pfs28 codons to yeast-preferred codons (TBV28), using a modified ADH(2) promoter and incorporating a (Glu-Ala)(2) repeat after the Kex2 cleavage site. C1 NIH, Malaria Vaccines Sect, Parasit Dis Lab, Bethesda, MD 20892 USA. Immunex Corp, Seattle, WA USA. RP Kaslow, DC (reprint author), NIH, Malaria Vaccines Sect, Parasit Dis Lab, Bldg 4,Room B1-31, Bethesda, MD 20892 USA. NR 20 TC 63 Z9 66 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1998 VL 66 IS 1 BP 59 EP 64 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YP559 UT WOS:000071290000009 PM 9423839 ER PT J AU Franzot, SP Mukherjee, J Cherniak, R Chen, LC Hamdan, JS Casadevall, A AF Franzot, SP Mukherjee, J Cherniak, R Chen, LC Hamdan, JS Casadevall, A TI Microevolution of a standard strain of Cryptococcus neoformans resulting in differences in virulence and other phenotypes SO INFECTION AND IMMUNITY LA English DT Article ID 2 VARIETIES; PULMONARY INFLAMMATION; PHAGOCYTOSIS; GLUCURONOXYLOMANNAN; MACROPHAGES; MENINGITIS; INFECTION; MELANIN; MICE; SUSCEPTIBILITIES AB Cryptococcus neoformans is a major fungal pathogen for patients with debilitated immune systems. However, no information is available on the stability of virulence or of phenotypes associated with virulence for C. neoformans laboratory strains. A serendipitous observation in our laboratory that one isolate of C. neoformans ATCC 24067 (strain 52D) became attenuated after continuous in vitro culture prompted us to perform a comparative study of nine strain 24067 isolates obtained from six different research laboratories. Each isolate was characterized by DNA typing, virulence for mice, proteinase production, extracellular protein synthesis, melanin synthesis, carbon assimilation pattern, antifungal drug susceptibility, colony morphology, growth rate, agglutination titers, phagocytosis by murine macrophages, capsule size, and capsular polysaccharide structure. All isolates had similar DNA typing patterns consistent with their assignment to the same strain, although minor chromosome size polymorphisms were observed in the electrophoretic karyotypes of two isolates. Several isolates had major differences in phenotypes that may be associated with virulence, including growth rate, capsule size, proteinase production, and melanization. These findings imply that C. neoformans is able to undergo rapid changes in vitro, probably as a result of adaptation to laboratory conditions, and suggest the need for careful attention to storage and maintenance conditions. In summary, our results indicate that C. neoformans (i) can become attenuated by in vitro culture and (ii) is capable of microevolution in vitro with the emergence of variants exhibiting new genotypic and phenotypic characteristics. C1 Yeshiva Univ Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Immunol & Microbiol, Div Infect Dis, Bronx, NY 10461 USA. Georgia State Univ, Dept Chem, Lab Biol & Chem Sci, Atlanta, GA 30303 USA. Univ Fed Minas Gerais, Dept Microbiol, Belo Horizonte, MG, Brazil. NICHHD, Div Intramural Res, NIH, Bethesda, MD 20892 USA. RP Casadevall, A (reprint author), Yeshiva Univ Albert Einstein Coll Med, Dept Med, Golding 701,1300 Morris Pk Ave, Bronx, NY 10461 USA. FU NIAID NIH HHS [AI13342, AI22774, AI31769] NR 50 TC 116 Z9 123 U1 0 U2 6 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1998 VL 66 IS 1 BP 89 EP 97 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YP559 UT WOS:000071290000014 PM 9423844 ER PT J AU Vazquez, N Walsh, TJ Friedman, D Chanock, SJ Lyman, CA AF Vazquez, N Walsh, TJ Friedman, D Chanock, SJ Lyman, CA TI Interleukin-15 augments superoxide production and microbicidal activity of human monocytes against Candida albicans SO INFECTION AND IMMUNITY LA English DT Article ID COLONY-STIMULATING FACTOR; TUMOR-NECROSIS-FACTOR; NATURAL-KILLER-CELLS; INTERFERON-GAMMA; IL-2 RECEPTOR; GENE-EXPRESSION; NADPH OXIDASE; GROWTH-FACTOR; BETA-CHAIN; MACROPHAGE AB Interleukin-15 (IL-15) is a newly described cytokine that shares biological activities,vith IL-2, We report here results demonstrating the ability of IL-15 to enhance superoxide production and antifungal activity of human monocytes. After 18 and 48 h of treatment with IL-15, human elutriated monocytes manifested enhanced superoxide production in response to either phorbol myristate acetate or opsonized Candida albicans blastoconidia. Similar results were obtained when monocytes were treated with IL-2, but to a lesser extent. Combination studies with IL-15 and IL-2 showed no additive or synergistic effects. Following incubation of monocytes with IL-15 for 18 h, there was no significant increase in mRNA transcripts for components of the NADPH oxidase complex, p40-phox, p47-phox, and gp91-phox, suggesting a posttranscriptional modulation of enhanced superoxide production. Antibodies against the gamma chain of the IL-2 receptor and, to a lesser extent, against the beta chain partially abrogated the IL-15-mediated enhanced superoxide production. Additionally, human monocytes showed enhanced killing activity against C. albicans after 18 h of incubation with IL-15 or IL-2, but this treatment did not enhance the ability of these cells to phagocytose the organism. In addition, the enhanced fungicidal activity seen after 18 h of treatment was no longer detectable after 48 h of cytokine treatment. Culture supernatants from the IL-15-treated monocytes were assayed for the presence of other proinflammatory cytokines. IL-15 treatment did not induce the release of detectable levels of tumor necrosis factor alpha, IL-1 beta, or IL-12. Our results indicate that IL-15 upregulates the microbicidal activity of human monocytes against C. albicans. C1 NCI, Immunocompromised Host Sect, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA. RP Chanock, SJ (reprint author), NCI, Immunocompromised Host Sect, Pediat Oncol Branch, NIH, Bldg 10,Room 13N240, Bethesda, MD 20892 USA. NR 46 TC 53 Z9 54 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1998 VL 66 IS 1 BP 145 EP 150 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YP559 UT WOS:000071290000021 PM 9423851 ER PT B AU Somogyi, R Fuhrman, S AF Somogyi, R Fuhrman, S BE Holcombe, M Paton, R TI Distributivity, a general information theoretic network measure, or why the whole is more than the sum of its parts SO INFORMATION PROCESSING IN CELLS AND TISSUES LA English DT Proceedings Paper CT 2nd International Workshop on Information Processing in Cells and Tissues (IPCAT) CY SEP 01-04, 1997 CL SHEFFIELD, ENGLAND SP SmithKline Beecham, GPT, Unilever, Hewlett Packard, Geomica, EPSRC C1 NINDS, Mol Physiol CNS Dev, LNP, NIH, Bethesda, MD 20892 USA. RP Somogyi, R (reprint author), NINDS, Mol Physiol CNS Dev, LNP, NIH, Bldg 36,Room 2C02, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA BN 0-306-45839-X PY 1998 BP 273 EP 283 PG 11 WC Biophysics; Cell Biology SC Biophysics; Cell Biology GA BL23W UT WOS:000074780100026 ER PT S AU Kidder, LH Haka, AS Faustino, PJ Lester, DS Levin, IW Lewis, EN AF Kidder, LH Haka, AS Faustino, PJ Lester, DS Levin, IW Lewis, EN BE Mantsch, HH Jackson, M Katzir, A TI Infrared spectroscopic imaging as a tool for pathology SO INFRARED SPECTROSCOPY: NEW TOOL IN MEDICINE, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Infrared Spectroscopy - New Tool in Medicine CY JAN 28-30, 1998 CL SAN JOSE, CA SP Soc Photo Opt Instrumentat Engineers, Int Biomed Opt Soc DE FTIR spectroscopy; infrared imaging; histopathology; ductal carcinoma; breast cancer AB Conventional Fourier transform infrared spectroscopy has proven to be an invaluable research and diagnostic approach for the study of a wide range of biomedical problems. In this article we describe a new biomedical imaging method which integrates high-resolution infrared spectroscopy with high-definition digital imaging. The continuing development and commercialization of long-wavelength infrared cameras or focal-plane arrays has been a key enabling technology, These imaging systems sire capable of rapidly generating chemically specific images from a variety of unstained biological tissue and cells. Image contrast is intrinsic to the sample and is determined only by its biochemical composition. In addition, data from a single experiment can be digitally manipulated to produce numerous images of the same sample, for which different spatial and biochemical properties are emphasized. We present data demonstrating the potential of the technique to generate spectroscopic signatures and images from single human breast cells. C1 NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RP Lewis, EN (reprint author), NIDDKD, Chem Phys Lab, NIH, 9000 Rockville Pike,Bldg 5,Room B1-38, Bethesda, MD 20892 USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU SPIE-INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA SN 0277-786X BN 0-8194-2696-2 J9 P SOC PHOTO-OPT INS PY 1998 VL 3257 BP 178 EP 186 DI 10.1117/12.306081 PG 9 WC Engineering, Biomedical; Medical Laboratory Technology; Optics; Pathology; Spectroscopy SC Engineering; Medical Laboratory Technology; Optics; Pathology; Spectroscopy GA BL09G UT WOS:000074239700021 ER PT J AU Yamashiro, S Takeya, M Kuratsu, J Ushio, Y Takahashi, K Yoshimura, T AF Yamashiro, S Takeya, M Kuratsu, J Ushio, Y Takahashi, K Yoshimura, T TI Intradermal injection of monocyte chemoattractant protein-1 induces emigration and differentiation of blood monocytes in rat skin SO INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY LA English DT Article DE monocyte chemoattractant protein-1; chemotactic factor; chemokine; macrophage subpopulation; lymphocyte; immunohistochemistry; ultrastructural study ID ANTIGEN-INDUCED ARTHRITIS; WHOLE KNEE-JOINT; MONOCLONAL-ANTIBODY; IMMUNOHISTOCHEMICAL ANALYSIS; MACROPHAGE POPULATIONS; CRYOSTAT SECTIONS; DENDRITIC CELLS; IN-VIVO; EXPRESSION; IDENTIFICATION AB Background: Monocyte chemoattractant protein-1 (MCP-1) is a potent chemoattractant for blood monocytes in vitro. Recent studies in MCP-1-transgenic mice revealed that the local production of MCP-1 caused monocyte infiltration. However, the kinetics of monocyte infiltration after the production of MCP-1 or the amount of MCP-1 necessary for monocyte recruitment are not known. Methods: We purified recombinant rat MCP-1 expressed in COS-7 cells, and injected it into rat skin. The infiltrating cells were examined by immunohistochemistry and ultrastructural peroxidase cytochemistry. Results: Rat recombinant MCP-1 had a molecular mass of approximately 30 kD and exhibited the peak monocyte chemotactic activity at 10(-9) M. One microgram of MCP-1 caused intra-and extravascular accumulation of mononuclear cells 3 h after injection. The cells were ED1+, indicating they were blood monocytes. The infiltration of mononuclear cells peaked at 12-24 h, and most of them were TRPM-3+ and ED3+, characteristic to exudate macrophages. None of the cells expressed ED2 or Ki-M2R antigens, markers for resident macrophages, until 3 days after injection. There was no uptake of [H-3]thymidine by the infiltrating cells. Ultrastructural peroxidase cytochemistry confirmed that the infiltrating cells were monocytes and exudate macrophages. The number of OX8+ lymphocytes also peaked at 12 h, consisting of approximately 9% of the total infiltrating cells. Conclusion: These results indicate that MCP-1 attracts blood monocytes as early as 3 h and the infiltrating monocytes differentiate into exudate macrophages in loco. However, this effect was transient and the infiltration of monocytes did not result in tissue damage. C1 NCI, Immunopathol Sect, Immunobiol Lab, FCRDC, Frederick, MD 21702 USA. Kumamoto Univ, Sch Med, Dept Pathol 2, Kumamoto 860, Japan. Kumamoto Univ, Sch Med, Dept Neurosurg, Kumamoto 860, Japan. RP Yoshimura, T (reprint author), NCI, Immunopathol Sect, Immunobiol Lab, FCRDC, Frederick, MD 21702 USA. NR 36 TC 22 Z9 25 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-2438 J9 INT ARCH ALLERGY IMM JI Int. Arch. Allergy Immunol. PD JAN PY 1998 VL 115 IS 1 BP 15 EP 23 DI 10.1159/000023825 PG 9 WC Allergy; Immunology SC Allergy; Immunology GA YP120 UT WOS:000071244700003 PM 9430491 ER PT J AU Nataraj, C Huffman, GR Kurlander, RJ AF Nataraj, C Huffman, GR Kurlander, RJ TI H2M3(wt)-restricted, Listeria monocytogenes-immune CD8 T cells respond to multiple formylated peptides and to a variety of Gram-positive and Gram-negative bacteria SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE antigen; antigen presentation; cytotoxic T lymphocyte; host immunity; MHC complex ID MHC CLASS-I; SPECIALIZED FUNCTIONS; ESCHERICHIA-COLI; LYMPHOCYTES-T; ANTIGEN; MOLECULE; PROTEIN; BINDING; IDENTIFICATION; RESIDUES AB A subset of H2M3(wt)-restricted, Listeria monocytogenes (LM)-immune CD8 effecters recognize antigen-presenting cells (APC) preincubated with heat-killed LM. The responsible product, which we have previously designated heat-killed Listeria-associated antigen (HAA), is extremely hydrophobic and resistant to proteolytic degradation. Despite the protease resistance of HAA, we now report that HAA-immune clones are uniformly responsive to fMIGWII, a formylated oligopeptide derived from the recently described LM product, lemA, While fMIGWII was by far the most potent peptide tested, over half our clones also responded to the LM-derived peptide fMIVIL and cross-reactive responses to two other unrelated formylated peptides at concentrations of <1 mu M were frequently observed, One of these peptides (fBlaZ) did not share any amino acid in common with fMIGWII except N-formyl methionine at position 1, Unformylated variants of the same peptides were inactive, HAA-immune CD8 cells also responded in an H2M3(wt)-restricted manner to APC pretreated with heat-killed or live preparations of other Gram-positive and Gram-negative bacteria such as Streptococcus pyogenes (SP) and Proteus vulgaris (PV), Unlike fMIGWII which is water soluble and protease sensitive, the native antigens extracted from SP and PV, like HAA, were very hydrophobic and proteinase K resistant, presumably reflecting in each case the association of cross-reactive polypeptides with bacterial lipid or phospholipid. Thus, HAA/lemA-immune, H2M3(wt)-restricted effecters can respond to a variety of formylated peptides and bacterial antigens in vitro. Similar cross-reactions in vivo might have physiologically significant implications. C1 Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA. RP Kurlander, RJ (reprint author), NIH, Bldg 10,Rm 2C390,10 Ctr Dr, Bethesda, MD 20892 USA. FU NIAID NIH HHS [R01-AI18073] NR 47 TC 20 Z9 20 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD JAN PY 1998 VL 10 IS 1 BP 7 EP 15 DI 10.1093/intimm/10.1.7 PG 9 WC Immunology SC Immunology GA YV987 UT WOS:000071884400002 PM 9488151 ER PT J AU Karavanov, AA Karavanova, I Perantoni, A Dawid, IB AF Karavanov, AA Karavanova, I Perantoni, A Dawid, IB TI Expression pattern of the rat Lim-1 homeobox gene suggests a dual role during kidney development SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE Lim-1; kidney; epithelial-mesenchymal transformation; tubulogenesis ID MICE LACKING GDNF; EXCRETORY SYSTEM; TYROSINE KINASE; MESENCHYME; XLIM-1; REQUIREMENT; DEFECTS; EMBRYOS; DOMAIN; BRAIN AB This study describes an in site hybridization and immunohistochemical analysis of Lim-1 homeobox gene expression during kidney development in the rat. Lim-1 is expressed at all stages of mesonephric and metanephric kidney development. In the metanephros, Lim-1 gene mRNA is first found at day 13 in the ureteric bud, but not in uninduced mesenchyme. Expression in the mesenchyme can be seen only after mesenchymal cells have condensed around the ureteric bud tips and primary vesicles have formed. Experiments with mesenchymal explants induced to differentiate in vitro by high levels of basic FGF in the absence of ureteric bud also indicate that Lim-1 expression is correlated with tubulogenesis and this experimental model faithfully reproduces its expression in vivo. During mesenchymal differentiation Lim-1 protein and mRNA were found in comma-and S-shaped bodies, proximal and distal tubules, and collecting ducts. Lim-1 mRNA and Lim-1 protein were seen transiently at early stages of glomerulus formation. In the fully differentiated kidney Lim-1 gene products disappear from mesenchymal derivatives but persist in the collecting ducts which are derived from the ureteric bud. These data suggest a dual role for the Lim-1 homeobox gene in the developing kidney, a transient developmental function in the mesenchyme and a maintenance function in the ureteric bud and its derivatives. Further we suggest that Lim-1 is not directly involved in mesenchymal induction but may participate in its epithelial transformation at later stages as its expression in mesenchyme begins only after the formation of primary vesicle. C1 NICHHD, Genet Mol Lab, NIH, Bethesda, MD 20892 USA. NCI, Comparat Carcinogenesis Lab, NIH, Frederick, MD 21701 USA. RP Dawid, IB (reprint author), NICHHD, Genet Mol Lab, NIH, Bethesda, MD 20892 USA. NR 34 TC 36 Z9 36 U1 0 U2 0 PU UNIV BASQUE COUNTRY PRESS PI BILBAO PA POST BOX 1397, E-48080 BILBAO, SPAIN SN 0214-6282 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PD JAN PY 1998 VL 42 IS 1 BP 61 EP 66 PG 6 WC Developmental Biology SC Developmental Biology GA YP557 UT WOS:000071289800007 PM 9496787 ER PT J AU Chai, Y Bringas, P Shuler, C Devaney, E Grosschedl, R Slavkin, HC AF Chai, Y Bringas, P Shuler, C Devaney, E Grosschedl, R Slavkin, HC TI A mouse mandibular culture model permits the study of neural crest cell migration and tooth development SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE mandibular morphogenesis and tooth formation; cranial neural crest cells migration; lymphoid enhancing factor 1 (Lef1) ID ALPHA-ENHANCER; MESSENGER-RNA; ENAMEL KNOT; EMBRYO; MESENCHYME; EXPRESSION; GROWTH; MORPHOGENESIS; MECHANISMS; DIVERSITY AB A major issue in developmental biology is to determine how time and position-restricted instructions are signaled and received during morphogenesis of different phenotypes, of which tooth, Meckel's cartilage and tongue formation are classical examples. It is now evident that a hierarchy of growth factors and their downstream transcription factors regulate the timing, sequence and position of cells and tissues in forming different phenotypes during embryogenesis. Here we report the development of an early mandibular organ culture model. Explants of E8 and E9 first branchial arch were cultured and produced mandibular processes with cap stage tooth formation, Meckel's cartilage and tongue development. In tandem, vital dye (Dil) labeling studies confirmed that rhombomeres 1-4 give rise to craneal neural crest (CNC) cells which emigrate from the neural fold to the forming maxillary and mandibular arches. Furthermore, we have tested the feasibility of investigating the regulation of different phenotypes within the first branchial arch by a transcription factor using this early mandibular organ culture model. Lymphoid enhancing factor 1 (Lef1), a transcription factor, has been implicated to regulate tooth formation in vivo. We have analyzed the expression of Lef1 and studied the biological effects of Lef1 on E8 embryonic mouse first branchial arch explants in organ culture. Collectively, these results demonstrate that first branchial arch explant modes is suitable for studies of rhombencephalic crest cell fate during mandibular morphogenesis and can be used as a model with direct access to investigate the molecular mechanism in regulating first branchial arch morphogenesis. C1 Univ So Calif, Ctr Craniofacial Mol Biol, Sch Dent, Los Angeles, CA 90033 USA. Univ Calif San Francisco, Dept Microbiol, San Francisco, CA 94143 USA. NIAMSD, Craniofacial Dev Sect, NIH, Bethesda, MD 20892 USA. RP Chai, Y (reprint author), Univ So Calif, Ctr Craniofacial Mol Biol, Sch Dent, 2250 Alcazar St, Los Angeles, CA 90033 USA. FU NIDCR NIH HHS [DE-09165] NR 37 TC 33 Z9 36 U1 1 U2 2 PU UNIV BASQUE COUNTRY PRESS PI BILBAO PA POST BOX 1397, E-48080 BILBAO, SPAIN SN 0214-6282 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PD JAN PY 1998 VL 42 IS 1 BP 87 EP 94 PG 8 WC Developmental Biology SC Developmental Biology GA YP557 UT WOS:000071289800010 PM 9496790 ER PT J AU Grabel, L Becker, S Lock, L Maye, P Zanders, T AF Grabel, L Becker, S Lock, L Maye, P Zanders, T TI Using EC and ES cell culture to study early development: recent observations on Indian hedgehog and Bmps SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE ES cells; EC cells; Indian hedgehog; Bmps; extraembryonic endoderm ID TERATOCARCINOMA STEM-CELLS; BONE MORPHOGENETIC PROTEIN-4; MOTOR-NEURON INDUCTION; MURINE YOLK-SAC; SONIC-HEDGEHOG; VISCERAL ENDODERM; PARIETAL ENDODERM; MOUSE EMBRYOS; IN-VITRO; AUTOPROTEOLYTIC CLEAVAGE AB Despite great technological advances in the study of mammalian development in the past two decades, certain problems in early development, such as how the extraembryonic lineages are established, have remained intractable. We suggest that teratocarcinoma (EC) and embryonic stem cells (ES) remain useful in vitro tools for studying some of these problems. We present a continuation of our studies on the role of IHH-based signaling in early development and demonstrate that the IHH N-peptide is expressed in the outer visceral endoderm cells of both the EC and ES-derived embryoid body. We also show that Bmp2 is upregulated and Bmp4 downregulated during the differentiation of F9 EC cells into embryoid bodies, whereas both genes are upregulated when J7 ES cells differentiate into embryoid bodies. We also examine the spatial localization of Ihh, Bmp2, and Bmp4 in day 6.5-7.0 and 7.5-8.0 embryos by in situ hybridization analysis. These data support the EC temporal expression data in that all 3 genes are expressed in visceral endoderm. Bmp4 expression appears to be limited to extraembryonic regions, where mesoderm as well as visceral endoderm are stained. Ihh and Bmp2 are expressed in extraembryonic tissues and the embryo proper. Functional roles for the observed expression patterns are discussed. C1 Wesleyan Univ, Dept Biol, Middletown, CT 06459 USA. NCI, Cryopreservat Special Program, ABL Basic Res Program, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. RP Grabel, L (reprint author), Wesleyan Univ, Dept Biol, Middletown, CT 06459 USA. EM lgrabel@wesleyan.edu NR 75 TC 33 Z9 33 U1 0 U2 0 PU UNIV BASQUE COUNTRY PRESS PI BILBAO PA POST BOX 1397, E-48080 BILBAO, SPAIN SN 0214-6282 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PY 1998 VL 42 IS 7 SI SI BP 917 EP 925 PG 9 WC Developmental Biology SC Developmental Biology GA 135HK UT WOS:000076795600012 PM 9853822 ER PT J AU Donovan, PJ AF Donovan, PJ TI The germ cell - the mother of all stem cells SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE PGC; mouse; embryo; EG cells; teratoma ID LEUKEMIA INHIBITORY FACTOR; TYROSINE KINASE RECEPTOR; EMBRYONIC ANTIGEN SSEA-1; ONCOGENE C-KIT; MOUSE EMBRYOS; GROWTH-FACTOR; PROTO-ONCOGENE; TARGETED DISRUPTION; DEFICIENT GCD; IN-VITRO AB The germline, uniquely amongst the lineages of the embryo, carries the genome from generation to generation and is therefore the only lineage which retains true developmental totipotency. Paradoxically, when mouse primordial germ cells (PGCs) are introduced into a host blastocyst, they do not contribute to either the germline or the soma, suggesting that they are restricted in developmental potency. Conversely, in vivo PGCs give rise to embryonal carcinoma (EC) cells, the pluripotent stem cells of teratomas, benign tumors containing derivatives of the three primary germ layers. Similarly, PGCs can be converted in vitro into embryonic germ (EG) cells, pluripotent stem cells capable of giving rise to somatic and germline chimeras. The ability of PGCs to form EC cells in vivo and EG cells in vitro suggests that developmental potency of PGCs is regulateable. The molecular mechanisms controlling PGC growth and differentiation are gradually being elucidated through the characterization of sterile mutants and through the use of in vitro culture systems. Understanding how a PGC can give rise to a pluripotent stem cell could give significant insights into the regulation of developmental totipotency as well as having important implications for male fertility and the etiology of testicular cancer. C1 NCI, Cell Biol Dev & Differentiat Grp, ABL Basic Res Program, FCRDC, Frederick, MD USA. RP Donovan, PJ (reprint author), Thomas Jefferson Univ, Kimmel Canc Ctr, 233 S 10th St,BLSB 706, Philadelphia, PA 19107 USA. EM pdonovan@lac.jci.tju.edu NR 76 TC 45 Z9 49 U1 2 U2 2 PU UNIV BASQUE COUNTRY PRESS PI BILBAO PA POST BOX 1397, E-48080 BILBAO, SPAIN SN 0214-6282 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PY 1998 VL 42 IS 7 SI SI BP 1043 EP 1050 PG 8 WC Developmental Biology SC Developmental Biology GA 135HK UT WOS:000076795600026 PM 9853836 ER PT J AU Silva, EG Tornos, C Zhuang, ZP Merino, MJ Gershenson, DM AF Silva, EG Tornos, C Zhuang, ZP Merino, MJ Gershenson, DM TI Tumor recurrence in stage I ovarian serous neoplasms of low malignant potential SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE ovary; tumor recurrence; serous; low malignant potential ID BORDERLINE EPITHELIAL TUMORS; PERITONEAL IMPLANTS; MICROINVASION; FEATURES; BEHAVIOR AB Eleven patients treated at the University of Texas M. D. Anderson Cancer Center for recurrent disease after resection of a stage I ovarian serous neoplasm of low malignant potential (SNLMP) are reported. At the time of diagnosis, the age of the patients ranged from 26 to 43 years (mean 33). Seven patients had stage IB tumors and 4 had stage IA tumors. All patients were treated with a total abdominal hysterectomy and bilateral salpingo-oophorectomy. The size of the ovarian tumors ranged from 4 to 15 cm in maximum dimension. Stromal microinvasion was seen in 2 cases, and foci of endosalpingiosis were seen in the peritoneum in 8 cases. Nine patients were treated with radiotherapy and 2 with chemotherapy, The time to recurrent disease ranged from 7 to 39 years (mean 16). Eight tumors recurred in the pelvis or abdomen, 2 in the neck with subsequent abdominal involvement, and 1 in the pleura without abdominal or pelvic involvement. In 10 cases, the recurrent tumors were serous carcinoma, and in 1 case it was a SNLMP. Recurrences were treated with chemotherapy in 10 cases and with hormones in 1 case. Seven patients died of progressive serous carcinoma 2 to 5 years after the recurrence. One patient died of leukemia with recurrent ovarian tumor 10 years after the recurrence was detected. Two patients are alive with progressive disease 1 and 7 years after the recurrence, and 1 patient whose disease recurred as a SNLMP is alive with no evidence of disease 9 years after the recurrence. These 11 patients were compared with 16 patients who had stage I ovarian SNLMPs that did not recur after a minimum follow-up of 15 years. There was no difference in the age of the patients, gravidity, size of the tumors, or several microscopic parameters, including degree of epithelial proliferation, number of mitoses, and nuclear atypia, Microinvasion was found in one case. The only significant difference between the two groups was the low frequency of endosalpingiosis in the cases that had no disease recurrences (12.5% versus 72.7%), In summary, we found no clinical or pathologic features that can unequivocally predict the recurrence of stage I ovarian SNLMPs. Because of the long interval to recurrence, the fact that the recurrent tumors in 10 of II patients were serous carcinomas, and the result of the X-chromosome inactivation in one case, the recurrent tumors could represent independent primaries or a slow progression of one clone present in the SNLMPs. C1 Univ Texas, MD Anderson Cancer Ctr, Dept Pathol, Houston, TX 77030 USA. NIH, Bethesda, MD 20892 USA. RP Silva, EG (reprint author), Univ Texas, MD Anderson Cancer Ctr, Dept Pathol, Box 85,1515 Holcombe St, Houston, TX 77030 USA. NR 22 TC 40 Z9 40 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 JAN PY 1998 VL 17 IS 1 BP 1 EP 6 DI 10.1097/00004347-199801000-00001 PG 6 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA YU405 UT WOS:000071713800001 PM 9475184 ER PT J AU Yamanaka, R Lekstrom-Himes, J Barlow, C Wynshaw-Boris, A Xanthopoulos, KG AF Yamanaka, R Lekstrom-Himes, J Barlow, C Wynshaw-Boris, A Xanthopoulos, KG TI CCAAT enhancer binding proteins are critical components of the transcriptional regulation of hematopoiesis (Review) SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE LA English DT Review DE CCAAT enhancer binding protein; C/EBP-deficient mice; hematopoiesis; myeloid leukemia; transcriptional factors ID FACTOR-RECEPTOR PROMOTER; ACUTE MYELOID-LEUKEMIA; C/EBP FAMILY MEMBERS; B-CELL DEVELOPMENT; ZINC FINGER GENE; NF-KAPPA-B; LEUCINE-ZIPPER; DNA-BINDING; C-MYB; TARGETED DISRUPTION AB The coordinated expression of four different CCAAT/enhancer binding proteins (C/EBPs), C/EBP alpha, C/EBP beta, C/EBP delta, and C/EBP epsilon constitutes a critical component of the myeloid differentiation program. C/EBPs are modular proteins, consisting of an activation domain, DNA binding domain and leucine zipper dimerization region. Recent studies including the analysis of mice deficient in several C/EBP proteins emphasize the effects of these molecules in hematopoiesis. C/EBP alpha is a master regulator of myeloid progenitors, C/EBP beta plays an important role in macrophage and B-cell development, C/EBP gamma is involved in B-cell development, and C/EBP delta is upregulated during myelopoiesis. Furthermore, C/EBP epsilon is a regulator of terminal differentiation of eosinophils and functional maturation of neutrophils. The formation of alternative combinations of tissue-specific and cell-stage specific C/EBP dimers may allow differential regulation of target genes in hematopoietic cells and commitment to distinctive hematopoietic lineages. C1 NIH, Clin Gene Therapy Branch, Bethesda, MD 20892 USA. NIH, Lab Genet Dis Res, Bethesda, MD 20892 USA. NIH, Nalt Human Genome Res Inst, Bethesda, MD 20892 USA. RP Xanthopoulos, KG (reprint author), Aurora Biosci Corp, 11010 Torreyana Rd, San Diego, CA 92121 USA. NR 106 TC 75 Z9 76 U1 1 U2 3 PU PROFESSOR D A SPANDIDOS PI ATHENS PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE SN 1107-3756 J9 INT J MOL MED JI Int. J. Mol. Med. PD JAN PY 1998 VL 1 IS 1 BP 213 EP 221 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 117DT UT WOS:000075765900031 PM 9852222 ER PT J AU Dadras, SS Thorgeirsson, SS Rao, MS Reddy, JK AF Dadras, SS Thorgeirsson, SS Rao, MS Reddy, JK TI Implication of hydrogen peroxide generation and apoptosis in the neoplastic transformation of mouse fibroblasts overexpressing peroxisomal fatty acyl-CoA oxidase SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE peroxisome; fatty acyl-CoA oxidase; H2O2; apoptosis; transformation; oxidative damage ID RAT-LIVER; TRANSGENIC MICE; PROLIFERATOR; CELLS; GENE; ACID; DNA; HEPATOCARCINOGENESIS; DEHYDROGENASE; TUMORIGENESIS AB Receptor-mediated overexpression of H2O2-generating peroxisomal fatty acyl-CoA oxidase (AOX) has been implicated in peroxisome proliferator-induced hepatocarcinogenesis. To investigate the role of rat AOX generated H2O2 in transformation, we overexpressed this enzyme in a non-tumorigenic mouse fibroblast cell line (LM tk(-)) under control of mouse urinary protein promoter. The clones overexpressing rat peroxisomal AOX, when exposed to a fatty acid substrate (100 mu M linoleic acid) for 6 to 96 h, demonstrated >10-fold increase of intracellular H2O2. This increase in H2O2 concentration was associated with increased apoptosis as evidenced by DNA fragmentation, in situ terminal deoxynucleotide transferase dUTP nick end-labeling (TUNEL). These cell lines stably expressing AOX formed colonies in soft agar in proportion to the duration (1-7 weeks) of exposure to a fatty acid substrate (100 mu M linoleic acid, erucic acid or nervonic acid) and these transformants developed into fibrosarcomas when injected in athymic nude mice. These results suggest that H2O2 generated by AOX overexpression in immortalized fibroblasts leads to apoptosis, and the extent and duration of H2O2 and possibly other DNA damaging reactive oxygen species generated by the overexpression of peroxisomal AOX can influence apoptosis and neoplastic transformation. C1 Northwestern Univ, Sch Med, Dept Pathol, Chicago, IL 60611 USA. NCI, NIH, Bethesda, MD 20892 USA. RP Reddy, JK (reprint author), Northwestern Univ, Sch Med, Dept Pathol, 303 E Chicago Ave, Chicago, IL 60611 USA. FU NIGMS NIH HHS [GM23750, T32-GM08152] NR 36 TC 11 Z9 11 U1 0 U2 2 PU PROFESSOR D A SPANDIDOS PI ATHENS PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1998 VL 12 IS 1 BP 37 EP 44 PG 8 WC Oncology SC Oncology GA YN388 UT WOS:000071163600003 PM 9454884 ER PT J AU Barendswaard, EC Scott, AM Divgi, CR Williams, C Coplan, K Riedel, E Yao, TJ Gansow, OA Finn, RD Larson, SM Old, LJ Welt, S AF Barendswaard, EC Scott, AM Divgi, CR Williams, C Coplan, K Riedel, E Yao, TJ Gansow, OA Finn, RD Larson, SM Old, LJ Welt, S TI Rapid and specific targeting of monoclonal antibody A33 to a colon cancer xenograft in nude mice SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE mAb A33; targeting; colon cancer xenograft ID SINGLE-CHAIN FV; INTRACELLULAR CATABOLISM; SOLID TUMORS; PHASE I/II; CELLS; CARCINOMA; SURFACE; RADIOIMMUNOTHERAPY; LOCALIZATION; FRAGMENTS AB Monoclonal antibody (mAb) A33 detects a glycoprotein homogeneously expressed by >95% of human colon cancers and by normal colon cells. The A33 antigen is not secreted or shed and after mAb A33 binds to antigen on the cell membrane, a fraction of membrane-bound mAb A33 is internalized into endosomes. Phase I I-131-mAb A33 biodistribution studies have shown consistent, specific tumor-targeting, and phase I radioimmunotherapy trials with I-131- Or I-125-mAb A33 have demonstrated antitumor effects. Here we describe a nude mouse model that was established using a human colon cancer cell line, SW1222, which grows as a relatively hypovascular, invasive heterotransplant when injected i.m. Peak uptake of I-131-labeled or In-111-chelated mAb A33 was observed at 48-96 h, with a mean of 34% (SE +/- 5.0) and 46.7% (SE +/- 1.7) injected dose per gram of tumor tissue, respectively. In-111-mAb A33 was retained in tumor tissue longer than halide radioimmunoconjugates. The specificity of antibody localization was assessed using a control antibody (tumor uptake and pharmacokinetics), a control tumor, corrections for vascular antibody blood-pooling in tumor tissue, and blocking of radiolabeled mAb A33 localization by pretreating mice with excess unlabeled mAb A33. These experiments demonstrate that mAb A33 localization in tumor was specific, and they emphasize the unexpected rapidity with which the antibody localizes. Our conclusions were confirmed by immunohistochemical techniques which allowed direct visualization of localization and distribution of the humanized version of mAb A33 in tumor tissue. Furthermore, antibody doses approximating tumor-saturating doses demonstrated that a homogeneous distribution of antibody in tumor is possible. This model will be valuable for studies focusing on general physiologic aspects of antibody-to-tumor cell localization and critical as a guide to the evaluation of various A33 antibody constructs and combinations with other therapies for the treatment of colon cancer. C1 Mem Sloan Kettering Canc Ctr, Lab Hematopoiet Canc Immunochem, Ludwig Inst Canc Res, New York, NY 10021 USA. Mem Sloan Kettering Canc Ctr, Nucl Med Serv, New York, NY 10021 USA. Mem Sloan Kettering Canc Ctr, Dept Biostat & Epidemiol, New York, NY 10021 USA. Mem Sloan Kettering Canc Ctr, Dept Med Phys, New York, NY 10021 USA. NCI, Bethesda, MD 20892 USA. RP Barendswaard, EC (reprint author), Mem Sloan Kettering Canc Ctr, Lab Hematopoiet Canc Immunochem, Ludwig Inst Canc Res, 1275 York Ave, New York, NY 10021 USA. FU NCI NIH HHS [CA-08748, CA-33049] NR 41 TC 21 Z9 23 U1 0 U2 1 PU PROFESSOR D A SPANDIDOS PI ATHENS PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1998 VL 12 IS 1 BP 45 EP 53 PG 9 WC Oncology SC Oncology GA YN388 UT WOS:000071163600004 PM 9454885 ER PT J AU Lamberts, H Magruder, K Kathol, RG Pincus, HA Okkes, I AF Lamberts, H Magruder, K Kathol, RG Pincus, HA Okkes, I TI The classification of mental disorders in primary care: A guide through a difficult terrain SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE classification; diagnosis; mental disorders; mental health; primary care; psychiatry; conversion; compatibility ID HEALTH-CARE AB Background: Primary care physicians traditionally have a strong interest in the mental health of their patients. Three classification systems are available for them to diagnose, label, and classify mental disorders: 1) The ICD-10 approach with three options, 2) The DSM-IV approach with two options, and 3) the ICPC approach with two options. This article lists important similarities and differences between the systems to help potential users choose the option that best meets their needs. Methods: Definitions for depressive disorder, anxiety disorder, and somatization disorder are compared on five characteristics of classification: 1. the domain, 2. the scope, 3. the nature of the definitions, 4. focus on episodes of care, and 5. clinical guidelines. Results: Primary care physicians and psychiatrists have different perspectives, reflected in different classifications. Each system has specific possibilities and limitations with regard to the diagnosis of mental disorders. For common mental disorders it is possible, however, to choose codes from one system while maintaining compatibility with the other two. Comparability as to the diagnostic content of the different classes, however, is more difficult to establish. The available classification systems give both primary care physicians and psychiatrists options to diagnose, label, and to classify mental disorders from their own perspective, but once a system has been chosen the clinical comparability of a patient with the same diagnosis in other systems is limited. Conclusion: Compatibility among systems can be optimized by strictly following a number of rules. The conversion between ICPC and ICD-10 land consequently DSM-IV) allows simultaneous use of ICPC and ICD-10 as a classification and DSM-IV as the standard nomenclature. This is of particular interest for computer based patient records in primary care. The clinical comparability of the same diagnosis in different systems however is limited by the characteristics of the different system. C1 Univ Amsterdam, Acad Med Ctr, Dept Family Med, NL-1105 AZ Amsterdam, Netherlands. NIMH, Rockville, MD 20857 USA. Univ Iowa Hosp & Clin, Iowa City, IA 52242 USA. Amer Psychiat Assoc, Washington, DC USA. RP Lamberts, H (reprint author), Univ Amsterdam, Acad Med Ctr, Dept Family Med, Meibergdreef 15, NL-1105 AZ Amsterdam, Netherlands. NR 26 TC 8 Z9 8 U1 0 U2 0 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 USA SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1998 VL 28 IS 2 BP 159 EP 176 PG 18 WC Psychiatry SC Psychiatry GA 111FD UT WOS:000075425900001 PM 9724886 ER PT J AU Lebowitz, BD AF Lebowitz, BD TI Editorial: Priorities for agenda building: Mental health and primary care SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Editorial Material C1 NIMH, Rockville, MD 20857 USA. RP Lebowitz, BD (reprint author), NIMH, 5600 Fishers Lane,Room 10-75, Rockville, MD 20857 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 USA SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1998 VL 28 IS 4 BP 375 EP 378 PG 4 WC Psychiatry SC Psychiatry GA 178YX UT WOS:000079297700003 PM 10207739 ER PT J AU Brawley, OW AF Brawley, OW TI The study of untreated syphilis in the Negro male SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE syphilis; minorities; Blacks; clinical trials AB Purpose: The participation of minorities in clinical studies is the subject of much discussion and has even become the subject of Federal law. The project known as the Tuskegee Syphilis Study and officially titled "The Tuskegee Study of Untreated Syphilis in the Negro Male," is one of the great debacles of American medicine and a national shame, Despite the fact that its existence is,yell known, many do not know the historical facts of the study nor the context of the study, My purpose here is to recount the facts of the study and its historical context, Methods: The history recounted here Is taken from documents gathered during a U.S. Senate investigation of the study, original papers located in National Library of Medicine, and books about the trial. Results: The trial began in 1931 as a survey of the natural history of untreated tertiary syphilis in Black men. This study enrolled 399 men with syphilis and 201 uninfected men to serve as controls, All were at least 25 years old at enrollment. The men were told they were in a study, but never educated about the implications. Later, men were not informed that there was a treatment for effective treatment for their disease-a treatment that was being withheld from them, This trial continued till 1972. Conclusion: Many of the issues that led to the study and caused it to continue for 40 years still exist, The lessons of the Public Health Study of Untreated Syphilis in the Untreated Negro include the dangers of paternalism, arrogance, blind loyalty, and misuse of science, "Those who do not appreciate history are condemned to repeat it" (Alfred North Whitehead). (C) 1998 Elsevier Science Inc. C1 NCI, Off Special Populat Res, Bethesda, MD 20892 USA. RP Brawley, OW (reprint author), NCI, Off Special Populat Res, Fed Bldg Suite 312,7550 Wisconsin Ave, Bethesda, MD 20892 USA. NR 3 TC 34 Z9 35 U1 2 U2 7 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 1 PY 1998 VL 40 IS 1 BP 5 EP 8 DI 10.1016/S0360-3016(97)00835-3 PG 4 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA YN393 UT WOS:000071164200003 PM 9422551 ER PT J AU Wang, X Ding, I Xie, HC Wu, T Wersto, N Huang, K Okunieff, P AF Wang, X Ding, I Xie, HC Wu, T Wersto, N Huang, K Okunieff, P TI Hyperbaric oxygen and basic fibroblast growth factor promote growth of irradiated bone SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE cytokine; FGF; toxicity; angiogenesis; prevention ID COLONY-STIMULATING FACTOR; TUMOR NECROSIS FACTOR; SUPEROXIDE-DISMUTASE; ENDOTHELIAL-CELLS; PROGENITOR CELLS; CLINICAL-TRIAL; FACTOR-BETA; BLOOD-FLOW; TGF-BETA; RADIATION AB Purpose: The goal of the current experiment is to test for protective effect of hyperbaric oxygen (HBO) and basic fibroblast growth factor (bFGF) on bone growth. Methods and Materials: Control C3H mice received hind leg irradiation at 0, 10, 20, or 30 Gy. HBO-treated groups received radiation 1, 5, or 9 weeks before beginning HBO. The remaining groups began bFGF +/- HBO 1 or 5 weeks after 30 Gy. HBO treatments were given 5 days per week for 4 weeks at 2 ATA for 3 h/day. bFGF was given intravenously at 6 mu g twice a week for 4 weeks. Results: HBO improved bone growth after radiation in the 10 and 20 Gy groups. At 18 weeks control tibia length discrepancy is 0.0, 4.2, 8.2, and 10.7% after 0, 10, 20, and 30 Gy, respectively. HBO beginning in week 1, 5, or 9 following 10 Gy decreased these discrepancies to 2.0% (p < 0.05), 1.8% (p < 0.05), and 2.4% (p < 0.05), respectively. After 20 Gy, HBO decreased these discrepancies to 7.0% (p = ns), 4.9% (p < 0.05), and 3.6% (p < 0.05), respectively. At 30 Gy, HBO alone had no effect on bone shortening. bFGF improved tibia length discrepancy with or without HBO. At 18 weeks length discrepancies were 6.5% (p < 0.05) and 7.3 (p < 0.05), and after bFGF alone were 6.8% (p < 0.05) and 7.3% (p < 0.05) for treatment beginning in week 1 or 5, respectively. Tibial growth at 18 and 33 weeks following radiation were similar. Conclusion: Radiation effects on bone growth can be significant reduced by HBO after 10 or 20 Gy, but not after 30 Gy. At 30 Gy bFGF still significantly reduced the degree of bone shortening, but HBO provided no added benefit to bFGF therapy. (C) 1998 Elsevier Science Inc. C1 NCI, Radiat Oncol Branch, Bethesda, MD 20892 USA. RP Okunieff, P (reprint author), NCI, Radiat Oncol Branch, Bldg 10,B3B69,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 54 TC 16 Z9 16 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JAN 1 PY 1998 VL 40 IS 1 BP 189 EP 196 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA YN393 UT WOS:000071164200028 PM 9422576 ER PT J AU McCutchen, CW AF McCutchen, CW TI Consolidation theory derived without invoking porosity SO INTERNATIONAL JOURNAL OF SOLIDS AND STRUCTURES LA English DT Article ID ARTICULAR-CARTILAGE AB Blot and Willis wrote that consolidation theory could be derived without reference to porosity. I do so in this article. The coefficients in the consolidation equation that results are easier to understand than Biot's. In special cases the theory leads to three-dimensional diffusion equations. One such is when all constituents of the material are intrinsically incompressible, a good approximation for articular cartilage. In one dimension the conditions leading to a diffusion equation are much broader. Published by Elsevier Science Ltd. RP McCutchen, CW (reprint author), NIDDKD,NIH,BETHESDA,MD 20892, USA. NR 12 TC 3 Z9 4 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0020-7683 J9 INT J SOLIDS STRUCT JI Int. J. Solids Struct. PD JAN PY 1998 VL 35 IS 1-2 BP 69 EP 81 DI 10.1016/S0020-7683(97)00056-5 PG 13 WC Mechanics SC Mechanics GA YJ567 UT WOS:A1998YJ56700005 ER PT J AU Quinn, TC AF Quinn, TC TI Molecular variants of HIV-1 and their impact on vaccine development SO INTERNATIONAL JOURNAL OF STD & AIDS LA English DT Article C1 NIAID, Immunoregulat Lab, Bethesda, MD 20892 USA. RP Quinn, TC (reprint author), NIAID, Immunoregulat Lab, Bldg 10, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ROYAL SOC MEDICINE PRESS LTD PI LONDON PA 1 WIMPOLE STREET, LONDON W1M 8AE, ENGLAND SN 0956-4624 J9 INT J STD AIDS JI Int. J. STD AIDS PY 1998 VL 9 SU 1 BP 2 EP 2 DI 10.1258/0956462981921567 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 147QN UT WOS:000077577700002 PM 9874106 ER PT J AU Williamson, DL Whitcomb, RF Tully, JG Gasparich, GE Rose, DL Carle, P Bove, JM Hackett, KJ Adams, JR Henegar, RB Konai, M Chastel, C French, FE AF Williamson, DL Whitcomb, RF Tully, JG Gasparich, GE Rose, DL Carle, P Bove, JM Hackett, KJ Adams, JR Henegar, RB Konai, M Chastel, C French, FE TI Revised group classification of the genus Spiroplasma SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article DE Spiroplasma; Mollicutes ID WASP MONOBIA-QUADRIDENS; SP-NOV; CLASS MOLLICUTES; SEROLOGICAL CLASSIFICATION; BEETLE COLEOPTERA; GROUP-I; TAXONOMY; DEFORMATION; SUBGROUPS; CLUSTER AB Significant changes have been made in the systematics of the genus Spiroplasma (class Mollicutes) since it was expanded by revision in 1987 to include 23 groups and eight sub-groups. Since that time, two additional spiroplasmas have been assigned group numbers and species names. More recently, specific epithets have been assigned to nine previously designated groups and three sub-groups. Also, taxonomic descriptions and species names have been published for six previously ungrouped spiroplasmas. These six new organisms are: Spiroplasma alleghenense (strain PLHS-1(T)) (group XXVI), Spiroplasma lineolae (strain TALS-2(T) (group XXVII), Spiroplasma platyhelix (strain PALS-1(T)) (group XXVIII), Spiroplasma montanense (strain HYOS-1(T) (group XXXI). Spiroplasma helicoides (strain TABS-2(T) (group XXXII) and Spiroplasma tabanidicola (strain TAUS-1(T)) (group XXXIII). Also, group XVII, which became vacant when strain DF-1(T) (Spiroplasma chrysopicola) was transferred to group VIII, has been filled with strain Tab 4c. The discovery of Laboratory, US these strains reflects continuing primary search in insect reservoirs, Department of particularly horse flies and deer flies (Diptera :Tabanidae). In the current revision, new group designations for 10 spiroplasma strains, including six recently named organisms, are proposed. Three unnamed but newly grouped spiroplasmas are strain TIUS-1 (group XXIX; ATCC 51751) from a typhiid wasp (Hymenoptera: Tiphiidae), strain BIUS-1 (group XXX; ATCC 51750) from floral surfaces of the tickseed sunflower (Bidens sp.) and strain BARC 1901 (group XXXIV; ATCC 700283). Strain BARC 2649 (ATCC 700284) from Tabanus lineola has been proposed as a new sub-group of group VIII. Strains TIUS-1 and BIUS-1 have unusual morphologies, appearing as helices at only certain stages in culture. In this revision, potentially important intergroup serological relationships observed between strain DW-1 (group II) from a neotropical Drosophila species and certain sub-group representatives of group I spiroplasmas are also reported. C1 SUNY Stony Brook, Dept Anat Sci, Stony Brook, NY 11794 USA. USDA, Vegetable Lab, Beltsville, MD 20705 USA. NIAID, Frederick Canc Res Facil, Mol Microbiol Lab, Mycoplasma Sect, Frederick, MD 21701 USA. USDA, Insect Biocontrol Lab, Beltsville, MD 20705 USA. INRA, Biol Cellulaire & Mol Lab, F-33883 Villenave Dornon, France. Fac Med, Dept Microbiol & Sante Publ, F-29285 Brest, France. Georgia So Univ, Dept Biol, Statesboro, GA 30460 USA. RP Williamson, DL (reprint author), SUNY Stony Brook, Dept Anat Sci, Stony Brook, NY 11794 USA. EM dwmson@mail.som.sunysb.edu NR 71 TC 58 Z9 58 U1 2 U2 10 PU SOC GENERAL MICROBIOLOGY PI READING PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING, BERKS, ENGLAND RG7 1AE SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1998 VL 48 BP 1 EP 12 PN 1 PG 12 WC Microbiology SC Microbiology GA ZD676 UT WOS:000072711200001 PM 9542070 ER PT J AU Heldtander, M Pettersson, B Tully, JG Johansson, KE AF Heldtander, M Pettersson, B Tully, JG Johansson, KE TI Sequences of the 16S rRNA genes and phylogeny of the goat mycoplasmas Mycoplasma adleri, Mycoplasma auris, Mycoplasma cottewii and Mycoplasma yeatsii SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article DE goat mycoplasmas; Mycoplasma adleri; Mycoplasma auris; Mycoplasma cottewii; Mycoplasma yeatsii ID RIBOSOMAL-RNA GENES; SP-NOV; PLASMID DNA; DEFINITION; CLUSTER AB The nucleotide sequences of the 16S rRNA genes from the type strains of four goat mycoplasmas, Mycoplasma adleri, Mycoplasma auris, Mycoplasma cottewii and Mycoplasma yeatsii, were determined by direct solid-phase DNA sequencing, Polymorphisms were found in two of the 16S rRNA gene sequences, showing the existence of two different rRNA operons. Three polymorphisms were found in M. adleri, and one was found in M. yeatsii. The sequence information was used for the construction of phylogenetic trees. M. adleri was included in the Mycoplasma lipophilum cluster within the hominis group. M. auris was comprised in the Mycoplasma hominis cluster of the hominis group, M. cottewii and M. yeatsii were found to be very closely related with only four nucleotide differences, and they grouped with Mycoplasma putrefaciens in the Mycoplasma mycoides cluster within the spiroplasma group, Sequencing of two field isolates of M. cottewii and M. yeatsii, geographically distant from the type strains, showed that the 16S rRNA gene from the field isolate of M. cottewii was identical to the one from the type strain. The field isolate of M. yeatsii had only two nucleotide differences to the type strain and these were present in only one of the two rRNA operons. Sequencing of the 16S rRNA genes from two unidentified mycoplasma isolates from Nepal indicated that they should both be regarded as M. auris strains. C1 Natl Vet Inst, Dept Bacteriol, S-75007 Uppsala, Sweden. Royal Inst Technol, Dept Biochem & Biotechnol, S-10044 Stockholm, Sweden. NIAID, Frederick Canc Res & Dev Ctr, Mycoplasma Sect, Frederick, MD 21702 USA. RP Johansson, KE (reprint author), Natl Vet Inst, Dept Bacteriol, POB 7073, S-75007 Uppsala, Sweden. EM Kaggen@sva.se NR 29 TC 25 Z9 25 U1 0 U2 0 PU SOC GENERAL MICROBIOLOGY PI READING PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG, BERKS, ENGLAND SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1998 VL 48 BP 263 EP 268 PN 1 PG 6 WC Microbiology SC Microbiology GA ZD676 UT WOS:000072711200028 PM 9542096 ER PT J AU Haseman, JK AF Haseman, JK TI National Toxicology Program experience with dietary restriction: Does the manner in which reduced body weight is achieved affect tumor incidence? SO INTERNATIONAL JOURNAL OF TOXICOLOGY LA English DT Article; Proceedings Paper CT 17th Annual Meeting of the American-College-of-Toxicology CY NOV, 1996 CL VALLEY FORGE, PENNSYLVANIA SP Amer Coll Toxicol DE dietary restriction; national toxicology program; rodent carcinogenicity studies; tumor incidence; body weight ID F344/N RATS; SURVIVAL; MICE AB The increasing body weights and the associated increased tumor incidences observed in recent long-term rodent bioassays may adversely affect study sensitivity for detecting rodent carcinogenicity. For example, increasing body weights may result in reduced survival and fewer animals at risk for tumor development. Moreover, the increased control tumor incidences observed in the more recent studies make it more difficult to establish firm baseline values and to use historical control data in the overall evaluation of experimental results. Finally, if dosed animals are significantly lighter than, controls within a given study, then it may be more difficult to detect carcinogenic effects for those tumor sites sensitive to body weight changes. One approach to deal with this problem is food restriction, and the recently completed NTP Dietary Restriction. Study confirmed that reducing food intake can reduce background tumor rates in control animals. There was also a slight increase in survival (approximately 2 wh on average) in the food restricted animals. However, the experimental protocol that restricted food consumption in both dosed and control groups appeared to have reduced sensitivity for detecting carcinogenic effects relative to the standard NTP protocol. One important, but often overlooked, issue when considering dietary restriction is that tumor incidence profiles may differ for animals of equivalent body weight, depending upon how the reduced body weights were achieved. An evaluation of data from NTP long-term rodent studies and from the NTP Dietary Restriction Study indicates that food restricted animals show a significant reduction in a number ofsite-specific tumors relative to equivalently sized ad libitum-fed animals. These results suggest that a dietary restriction strategy that focuses on achieving similar body weights in dosed and control groups may produce false positive outcomes if substantially more food restriction is required for control groups than for dosed animals (e.g., if control animals must receive a moderate (15-20%) degree of food restriction to achieve body weights equivalent to those observed in ad libitum-fed dosed animals). Results from the NTP Dietary Restriction Study also demonstrate that a moderate (15-20%) food restriction protocol applied equally to dosed and control animals may produce false negative outcomes if the resulting body weights are substantially different in dosed and control groups. Alternative strategies for reducing body weights are briefly discussed, but at present it is unclear which strategy or combination. of strategies will ultimately prove to be most effective for dealing with the problem of increasing body weights. C1 NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. RP Haseman, JK (reprint author), NIEHS, Biostat Branch, POB 12233, Res Triangle Pk, NC 27709 USA. NR 22 TC 6 Z9 6 U1 1 U2 2 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNPOWDER SQUARE, LONDON EC4A 3DE, ENGLAND SN 1091-5818 J9 INT J TOXICOL JI Int. J. Toxicol. PY 1998 VL 17 SU 2 BP 119 EP 134 PG 16 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 110AY UT WOS:000075358100006 ER PT B AU Brown, P AF Brown, P BE Goebel, K TI Modern medical technology and iatrogenic Creutzfeldt-Jakob disease SO INTERNATIONAL SEMINAR ON NUCLEAR WAR AND PLANETARY EMERGENCIES - 22ND SESSION: NUCLEAR SUBMARINE DECONTAMINATION, CHEMICAL STOCKPILED WEAPONS, NEW EPIDEMICS, CLONING OF GENES, NEW MILITARY THREATS, GLOBAL PLANETARY CHANGES: OZONE HOLE & CLIMATE IMPACT, DESERTIFICATION, WATER, FORESTRY & URBANISM, AND COSMIC OBJECTS & ENERGY SE SCIENCE AND CULTURE SERIES: NUCLEAR STRATEGY AND PEACE TECHNOLOGY LA English DT Proceedings Paper CT International Seminar on Nuclear War and Planetary Emergencies : 22nd Session - Nuclear Submarine Decontamination, Chemical Stockpiled Weapons, New Epidemics, Cloning CY AUG 19-24, 1997 CL E MAJORANA CTR SCI CULTURE, ERICE, ITALY HO E MAJORANA CTR SCI CULTURE C1 NIH, Bethesda, MD 20892 USA. RP Brown, P (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 981-02-3526-7 J9 SCI CULT NUCL STRAT PY 1998 BP 95 EP 96 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA BL97Z UT WOS:000077341100008 ER PT S AU Strober, W AF Strober, W BE Wiedenmann, B Rosewicz, S Zeitz, M Riecken, EO TI Interactions between epithelial cells and immune cells in the intestine SO INTESTINAL PLASTICITY IN HEALTH AND DISEASE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Intestinal Plasticity in Health and Disease CY OCT 15-18, 1997 CL BERLIN, GERMANY SP New York Acad Sci, Ipsen Pharma GmbH, Falk Fdn e V, Astra GmbH, Aussenamt Freien Univ Berlin, Bayer AG, BYK Gulden, Essex Pharma Gmbh, Pharmacia & Upjohn GmbH, Hoffmann La Roche AG, Schebo Tech GmbH, Thiemann Arzeimittel GmbH ID INTERCELLULAR-ADHESION MOLECULE-1; PROINFLAMMATORY CYTOKINES; REGULATED EXPRESSION; INVASIVE BACTERIA; INFECTION; NEUTROPHILS; INTERLEUKIN-8; ATTACHMENT; MONOLAYERS; RECEPTORS AB Not merely a passive barrier as previously assumed, epithelial cells act as sensitive indicators of infection that initiate defense responses. Noninvasive as well as invasive organisms have been demonstrated to elicit production of chemoattractants. That noninvasive organisms have this capacity suggests that receptor-mediated signaling pathways may be involved. Epithelial cells have been found to release both chemokines and cytokines in a precise mixture that varies according to the origin or maturity of the cell. Different microorganisms also elicit different response patterns. The information presented provides a basis for a new view of epithelial cell function in relation to host defense. C1 NIAID, Mucosal Immun Sect, Clin Invest Lab, NIH, Bethesda, MD 20892 USA. RP Strober, W (reprint author), NIAID, Mucosal Immun Sect, Clin Invest Lab, NIH, Bethesda, MD 20892 USA. NR 19 TC 37 Z9 37 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-152-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 859 BP 37 EP 45 DI 10.1111/j.1749-6632.1998.tb11109.x PG 9 WC Multidisciplinary Sciences; Physiology SC Science & Technology - Other Topics; Physiology GA BM18X UT WOS:000077943500003 PM 9928368 ER PT S AU Neurath, MF Fuss, I Schurmann, G Pettersson, S Arnold, K Muller-Lobeck, H Strober, W Herfarth, C Meyer, KH Buschenfelde, Z AF Neurath, MF Fuss, I Schurmann, G Pettersson, S Arnold, K Muller-Lobeck, H Strober, W Herfarth, C Meyer, KH Buschenfelde, Z BE Wiedenmann, B Rosewicz, S Zeitz, M Riecken, EO TI Cytokine gene transcription by NF-kappa B family members in patients with inflammatory bowel disease SO INTESTINAL PLASTICITY IN HEALTH AND DISEASE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Intestinal Plasticity in Health and Disease CY OCT 15-18, 1997 CL BERLIN, GERMANY SP New York Acad Sci, Ipsen Pharma GmbH, Falk Fdn e V, Astra GmbH, Aussenamt Freien Univ Berlin, Bayer AG, BYK Gulden, Essex Pharma Gmbh, Pharmacia & Upjohn GmbH, Hoffmann La Roche AG, Schebo Tech GmbH, Thiemann Arzeimittel GmbH ID T-CELLS; TARGETED DISRUPTION; IMMUNE-RESPONSES; PATHOGENIC ROLES; EXHIBIT DEFECTS; ACTIVATION; ALPHA; MICE; INHIBITION; IMMUNOSUPPRESSION AB We examined the expression of the transcription factor NF-kappa B, a nuclear trans-acting factor known to play a key role in cytokine gene regulation, in patients with inflammatory bowel disease (IBD). It was found that LP macrophages in Crohn's disease (CD) and ulcerative colitis (UC) display high levels of NF-kappa B DNA-binding activity accompanied by an increased production of interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)alpha. Western blot studies showed an increased expression of the p50 and c-rel subunits of NF-kappa B; however, the most striking finding was an increased expression level of NF-kappa B p65 in patients with CD and UC. Selective downregulation of p65 in IBD macrophages by a specific antisense phosphorothioate oligonucleotide was sufficient to considerably reduce production of proinflammatory cytokines. These results demonstrate a characteristic increase of NF-kappa B binding levels in patients with IBD. The data suggest that antisense DNA targeting NF-kappa B p65 can be used as a novel molecular approach for the treatment of patients with IBD. C1 Univ Mainz, Lab Immunol 1, Med Clin, D-55101 Mainz, Germany. NIAID, Mucosal Immun Sect, LCI, MIS,NIH, Bethesda, MD 20892 USA. Univ Heidelberg, Dept Surg, D-6900 Heidelberg, Germany. Karolinska Inst, Ctr Biotechnol, Huddinge, Sweden. Josefshosp, Wiesbaden, Germany. Deutsch Klin Diagnost, D-6200 Wiesbaden, Germany. RP Neurath, MF (reprint author), Univ Mainz, Lab Immunol 1, Med Clin, Langenbecksr, D-55101 Mainz, Germany. RI Pettersson, Sven/F-9511-2015 NR 29 TC 144 Z9 155 U1 0 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-152-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 859 BP 149 EP 159 DI 10.1111/j.1749-6632.1998.tb11119.x PG 11 WC Multidisciplinary Sciences; Physiology SC Science & Technology - Other Topics; Physiology GA BM18X UT WOS:000077943500013 PM 9928378 ER PT S AU Marth, T Zeitz, M Ludviksson, B Strober, W Kelsall, B AF Marth, T Zeitz, M Ludviksson, B Strober, W Kelsall, B BE Wiedenmann, B Rosewicz, S Zeitz, M Riecken, EO TI Murine model of oral tolerance - Induction of fas-mediated apoptosis by blockade of interleukin-12 SO INTESTINAL PLASTICITY IN HEALTH AND DISEASE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Intestinal Plasticity in Health and Disease CY OCT 15-18, 1997 CL BERLIN, GERMANY SP New York Acad Sci, Ipsen Pharma GmbH, Falk Fdn e V, Astra GmbH, Aussenamt Freien Univ Berlin, Bayer AG, BYK Gulden, Essex Pharma Gmbh, Pharmacia & Upjohn GmbH, Hoffmann La Roche AG, Schebo Tech GmbH, Thiemann Arzeimittel GmbH C1 Univ Saarlandes Kliniken, D-66421 Homburg, Germany. NIH, Mucosal Immun Sect, Bethesda, MD 20892 USA. RP Marth, T (reprint author), Univ Saarlandes Kliniken, D-66421 Homburg, Germany. OI Ludviksson, Bjorn/0000-0002-6445-148X NR 5 TC 21 Z9 21 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-152-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1998 VL 859 BP 290 EP 294 DI 10.1111/j.1749-6632.1998.tb11148.x PG 5 WC Multidisciplinary Sciences; Physiology SC Science & Technology - Other Topics; Physiology GA BM18X UT WOS:000077943500042 PM 9928407 ER PT B AU Blanchette-Mackie, EJ Pentchev, PG AF Blanchette-Mackie, EJ Pentchev, PG BE Chang, TY Freeman, DA TI Cholesterol distribution in Golgi, lysosomes and endoplasmic reticulum SO INTRACELLULAR CHOLESTEROL TRAFFICKING LA English DT Proceedings Paper CT Meeting on Intracellular Cholesterol Trafficking CY APR, 1997 CL ST LOUIS, MO SP Bristol Myers Squibb, Merck & Co, Parke Davis DE Golgi; trans Golgi cisternae; lysosomes; endoplasmic reticulum; intracellular cholesterol ID NIEMANN-PICK DISEASE; DENSITY LIPOPROTEIN UPTAKE; INTRACELLULAR CHOLESTEROL; HUMAN-FIBROBLASTS; FREEZE-FRACTURE; CERAMIDE ANALOG; C FIBROBLASTS; APPARATUS; ACCUMULATION; MACROPHAGES AB Insight into the effect of exogeneously derived lipoprotein cholesterol on distribution of intracellular membrane cholesterol has been gained from structural studies on normal and Niemann Pick Type C human fibroblasts. Endocytic uptake of LDL enriches Golgi cholesterol in both normal and NPC cells. However, the NPC mutation and treatment of normal cells with progesterone during LDL uptake produces abnormal accumulation of cholesterol in lysosomes and trans Golgi cisternae. This lysosomal/Golgi block in cholesterol trafficking results in the inability of endocytosed cholesterol to induce cellular homestatic responses. In addition to lysosomes and Golgi the endoplasmic reticulum can also be a site along the intracellular cholesterol transport pathway that becomes a temporary depot for cholesterol. Specific inhibition of acyl CoA:cholesterol acyltransferase with S-58035 during endocytic uptake results in a reversable accumulation of cholesterol in membranes of ER. Thus the ER, normally low in intracellular cholesterol, has the capacity to act as a sink for endocytosed cholesterol when esterification is blocked. In contrast to the lysosomal/Golgi cholesterol sequestration, ER accumulation of cholesterol does not compromise but appears to enhance the induction of cellular homeostatic responses. C1 NIDDKD, NIH, Bethesda, MD 20892 USA. NINDS, NIH, Bethesda, MD 20892 USA. RP Blanchette-Mackie, EJ (reprint author), NIDDKD, NIH, Bethesda, MD 20892 USA. NR 31 TC 10 Z9 10 U1 0 U2 0 PU KLUWER ACADEMIC PUBLISHERS PI NORWELL PA 101 PHILIP DRIVE, ASSINIPPI PARK, NORWELL, MA 02061 USA BN 0-7923-8365-6 PY 1998 BP 53 EP 73 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA BM64Z UT WOS:000079335300006 ER PT B AU Neufeld, EB AF Neufeld, EB BE Chang, TY Freeman, DA TI What the Niemann-Pick type C gene has taught us about cholesterol transport SO INTRACELLULAR CHOLESTEROL TRAFFICKING LA English DT Proceedings Paper CT Meeting on Intracellular Cholesterol Trafficking CY APR, 1997 CL ST LOUIS, MO SP Bristol Myers Squibb, Merck & Co, Parke Davis DE Niemann-Pick type C disease; NPC1; npc1; lysosomes; Golgi complex; cyclodextrin; brefeldin A; endocytosed cholesterol ID LOW-DENSITY LIPOPROTEIN; LDL-DERIVED CHOLESTEROL; ACYL-COENZYME-A; DISEASE TYPE-C; PLASMA-MEMBRANE; ENDOPLASMIC-RETICULUM; CULTURED FIBROBLASTS; INTRACELLULAR-TRANSPORT; LYSOSOMAL CHOLESTEROL; GM2 GANGLIOSIDE AB Niemann-Pick Type C disease (NP-C) is characterized by abnormal accumulation of endocytosed cholesterol in lysosomes and the Golgi complex and by delayed induction of cellular homeostatic responses to cholesterol. Positional and complementation cloning has recently identified both the human NPC1 and the syntenic mouse Npc1 genes. Complementation analysis has shown that a second mutant human gene, designated NPC2, produces an identical phenotype. The notable cellular defect in NP-C disease involves impaired trafficking of lysosomally-derived cholesterol to the plasma membrane and endoplasmic reticulum. Defective enrichment of regulatory sterol pools in the endoplasmic reticulum delays induction of homeostatic responses. Current evidence suggests that the two NPC proteins may: (i) mediate transport of endocytically-derived cholesterol from lysosomes to the Golgi complex and (ii) be linked to regulation of anterograde and retrograde Golgi cholesterol transport. In addition to the disruptions in cholesterol metabolism, impaired trafficking of endocytosed glycolipids along the NPC protein-mediated pathway may play a role in the neuropathology associated with NP-C disease. Future studies of the NPC genes and their products will provide insight into the relationship between cholesterol and glycolipid trafficking. C1 NIDDKD, Lipid Cell Biol Sect, Lab Cell Biochem & Biol, NIH, Bethesda, MD 20892 USA. RP Neufeld, EB (reprint author), NIDDKD, Lipid Cell Biol Sect, Lab Cell Biochem & Biol, NIH, Bethesda, MD 20892 USA. NR 53 TC 10 Z9 10 U1 0 U2 0 PU KLUWER ACADEMIC PUBLISHERS PI NORWELL PA 101 PHILIP DRIVE, ASSINIPPI PARK, NORWELL, MA 02061 USA BN 0-7923-8365-6 PY 1998 BP 93 EP 107 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA BM64Z UT WOS:000079335300008 ER PT J AU Cheung, AP Hallock, YF Vishnuvajjala, BR Nguyenle, T Wang, E AF Cheung, AP Hallock, YF Vishnuvajjala, BR Nguyenle, T Wang, E TI Compatibility and stability of bryostatin 1 in infusion devices SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE bryostatin; polyvinyl chloride; polypropylene; infusion; diethylhexylphthalate ID PROTEIN-KINASE-C; ACTIVATION; PROGENITORS; RECEPTOR; CELLS; AGENT AB Bryostatin I is currently in phase II clinical trial sponsored by the National Cancer Institute as an anticancer chemotherapeutic agent. Bryostatin 1 for injection was supplied in a dual pack containing a drug vial and a diluent vial and was manufactured by Ben Venue Laboratories, Inc (Bedford, OH). The stability and compatibility of the bryostatin 1-PET formulation, diluted to 1 and 10 mu g/mL in saline and benzyl alcohol preserved saline, with polypropylene(PP) and polyvinyl chloride (PVC) bags at room temperature (27 degrees C) were studied. All experiments were conducted in triplicate and analyses were performed using a validated, stability-indicating, high performance liquid chromatography (HPLC) assay. Bryostatin 1 solutions were compatible with PP bags. At both concentrations and with both salines, the bryostatin content remained unchanged during the 28-day storage period, benzyl alcohol concentration in the preserved saline solutions also remained relatively constant. In PVC bags, however, a decrease in bryostatin 1 concentrations without generation of decomposition products was observed at both dilutions and with both salines during the 28-day storage. A decrease in benzyl alcohol concentration in the preserved saline was also observed. While no diethylhexylphthalate (DEHP) leakage into the solution was observed in PP bags, DEHP leakage in PVC infusion bags was observed on day 2 of storage which increased with storage time and leveled off on day 6. The amount of DEHP leached into drug solution is dependent on the drug concentration. This study suggests bryostatin-PET formulation diluted with preserved saline can be used for long-term (4 week) intravenous administration using PP infusion bags, but not with PVC bags. C1 NCI, Dev Therapeut Program, Pharmaceut Resources Branch, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. SRI Int, Div Life Sci, Pharmaceut Analyt Lab, Menlo Park, CA 94025 USA. RP Hallock, YF (reprint author), NCI, Dev Therapeut Program, Pharmaceut Resources Branch, Div Canc Treatment & Diag, 6130 Execut Blvd,Suite 841, Bethesda, MD 20892 USA. FU NCI NIH HHS [N01-CM-27750] NR 14 TC 7 Z9 7 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1998 VL 16 IS 3 BP 227 EP 236 DI 10.1023/A:1006187710029 PG 10 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 195ZB UT WOS:000080282100004 PM 10360602 ER PT J AU Nelson, TJ Gusev, PA Alkon, DL AF Nelson, TJ Gusev, PA Alkon, DL TI Identification of ion channel regulating proteins by patch-clamp analysis SO ION CHANNELS, PT B SE METHODS IN ENZYMOLOGY LA English DT Review ID POTASSIUM CHANNELS; FIBROBLASTS; CURRENTS; CALCIUM C1 NINDS, Lab Adapt Syst, NIH, Bethesda, MD 20892 USA. RP Nelson, TJ (reprint author), NINDS, Lab Adapt Syst, NIH, Bethesda, MD 20892 USA. NR 18 TC 1 Z9 1 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1998 VL 293 BP 194 EP 201 PN B PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BL52B UT WOS:000075762300012 PM 9711610 ER PT B AU Ackerman, MJ AF Ackerman, MJ BE Laxminarayan, S MicheliTzanakou, E TI Telemedicine: Information can help cure SO ITAB 98: 1998 IEEE INTERNATIONAL CONFERENCE ON INFORMATION TECHNOLOGY APPLICATIONS IN BIOMEDICINE LA English DT Meeting Abstract CT 1998 IEEE International Conference on Information Technology Applications in Biomedicine (ITAB 98) CY MAY 16-17, 1998 CL WASHINGTON, D.C. SP IEEE CS Tech Comm Digital Lib C1 Natl Lib Med, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA BN 0-7803-4973-3 PY 1998 BP 14 EP 14 PG 1 WC Computer Science, Interdisciplinary Applications; Engineering, Biomedical; Medical Informatics SC Computer Science; Engineering; Medical Informatics GA BL12G UT WOS:000074369100003 ER PT B AU Martino, RL Kempner, KM Johnson, CA AF Martino, RL Kempner, KM Johnson, CA BE Laxminarayan, S MicheliTzanakou, E TI Information technology applications in biomedical research SO ITAB 98: 1998 IEEE INTERNATIONAL CONFERENCE ON INFORMATION TECHNOLOGY APPLICATIONS IN BIOMEDICINE LA English DT Proceedings Paper CT 1998 IEEE International Conference on Information Technology Applications in Biomedicine (ITAB 98) CY MAY 16-17, 1998 CL WASHINGTON, D.C. SP IEEE CS Tech Comm Digital Lib AB High end computer systems, high speed networks, and other advanced information technologies provide the performance needed in today's biomedical research computing environment. NIH participates in the national Computing, Information, and Communications Research and Development (CIC R&D) program by applying these new technologies to problems in biomedicine. We describe a high speed networking example, the Radiology Consultation WorkStation, and a high end computing example, Positron Emission Tomographic (PET) image reconstruction. The NIH Cancer Genome Anatomy Project (CGAP) provides an example of a major biomedical research effort that will require the creative use of information technology in the future. We end with conclusions concerning the impact new technologies have had on biomedical research and a discussion of plans for the future. C1 NIH, Computat Biosci & Engn Lab, Div Comp Res & Technol, Bethesda, MD 20892 USA. RP Martino, RL (reprint author), NIH, Computat Biosci & Engn Lab, Div Comp Res & Technol, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA BN 0-7803-4973-3 PY 1998 BP 28 EP 34 DI 10.1109/ITAB.1998.674667 PG 7 WC Computer Science, Interdisciplinary Applications; Engineering, Biomedical; Medical Informatics SC Computer Science; Engineering; Medical Informatics GA BL12G UT WOS:000074369100008 ER PT J AU Small, PLC AF Small, PLC TI Shigella and Escherichia coli strategies for survival at low pH SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article; Proceedings Paper CT International Symposium Celebrating the Centennary of the Discovery of the Shigas Bacillus CY FEB 26-27, 1998 CL JAPAN SP Kitasato Inst, Japanese Soc Bacteriol, Japanese Assoc Infect Dis, Japan Soc Chemotherapy ID ACID-RESISTANCE PHENOTYPE; DECARBOXYLASE; MICROORGANISMS; TOLERANCE; BACTERIA; FLEXNERI; GENES; RPOS C1 NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. RP Small, PLC (reprint author), NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. NR 22 TC 3 Z9 3 U1 0 U2 2 PU NATL INST INFECTIOUS DISEASES PI TOKYO PA C/O JPN J MED SCI BIOL, TOYAMA 1-23-1, SHINJUKU-KU, TOKYO, 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PY 1998 VL 51 SU 1 BP S81 EP S89 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 150QC UT WOS:000077675500009 PM 10211439 ER PT J AU Madio, DP van Gelderen, P Olson, AW de Zwart, JA Fawcett, TW Holbrook, NJ Mandel, M Moonen, CTW AF Madio, DP van Gelderen, P Olson, AW de Zwart, JA Fawcett, TW Holbrook, NJ Mandel, M Moonen, CTW TI On the feasibility of MRI-guided focused ultrasound for local induction of gene expression SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE MRI; focused ultrasound; gene therapy; gene expression; proton resonance frequency (PRF) temperature mapping; heat shock protein (hsp70) ID TEMPERATURE AB Gene therapy is a promising approach to the treatment of many forms of disease, including cancer. Of critical concern in its implementation is the ability to control the location, duration, and level of expression of the therapeutic gene. Here, we propose the use of local heat in combination with a heat-sensitive promoter to help accomplish this. Certain members of the family of heat shock protein (hsp) promoters display a regulation that depends strongly on temperature. We present a study of natural hsp70 induction in rat leg by MRI-guided focused ultrasound to investigate the hsp70 promoter as a possible candidate for use in control of gene expression with local heat. A temperature increase of 5-8 degrees C in the focal region for 45 minutes led to a differential expression of the hsp70 mRNA between the focal region and the surrounding tissue ranging from a factor of 3 to 67. C1 NIH, In Vivo NMR Res Ctr, BEIP, NCRR, Bethesda, MD 20892 USA. RP Madio, DP (reprint author), Schlumberger Doll Res Ctr, Old Quarry Rd, Ridgefield, CT 06877 USA. RI Moonen, Chrit/K-4434-2016 OI Moonen, Chrit/0000-0001-5593-3121 NR 9 TC 75 Z9 77 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1053-1807 J9 JMRI-J MAGN RESON IM JI JMRI-J. Magn. Reson. Imaging PD JAN-FEB PY 1998 VL 8 IS 1 BP 101 EP 104 DI 10.1002/jmri.1880080120 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 193NN UT WOS:000080143000017 PM 9500267 ER PT J AU Brown, JA Howcroft, TK Singer, DS AF Brown, JA Howcroft, TK Singer, DS TI HIV Tat protein requirements for transactivation and repression of transcription are separable SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV; Tat protein; repression; transactivation; transcription ID IMMUNODEFICIENCY-VIRUS TYPE-1; LONG TERMINAL REPEAT; CLASS-I; MUTATIONAL ANALYSIS; ACTIVATING REGION; TRANS-ACTIVATOR; DOWN-MODULATION; CELL-LINE; EXPRESSION; GENE AB The HIV Tat protein, primarily characterized as a transcriptional activator of the viral long terminal repeat (LTR), is also a potent repressor of major histocompatibility complex (MHC) class I transcription. In the present study, we demonstrate that these two functional activities are distinct and mediated by discrete, but overlapping, structural domains of Tat. Tat repressor activity depends on C-terminal sequences, whereas transactivation depends on N-terminal sequences; both functions require core sequences. The repressor activity requires a domain encompassing the region encoded by the second exon of the Tat gene, beginning at amino acid 73, with a C-terminal limit between amino acids 80 and 83. Tat repressor function also depends on the presence of a lysine at position 41, located within the core of the protein. Tat repressor activity is independent of two N-terminal domains essential for transactivation: the acidic segment and the cysteine-rich region. Conversely, Tat transactivation is independent of the second exon-encoded region of Tat. As further support for this novel model of separable Tat functions, we show that in murine fibroblasts, Tat represses class I promoter activity, but does not transactivate the HIV LTR. We propose that distinct structural domains mediate the two functionally distinct activities associated with the Tat protein. C1 NCI, Mol Regulat Sect, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. RP Singer, DS (reprint author), NCI, Mol Regulat Sect, Expt Immunol Branch, NIH, Bldg 10,Room 4B-17, Bethesda, MD 20892 USA. NR 39 TC 21 Z9 21 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN 1 PY 1998 VL 17 IS 1 BP 9 EP 16 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YR043 UT WOS:000071451900002 PM 9436753 ER PT J AU Yang, G D'Souza, MP Vyas, GN AF Yang, G D'Souza, MP Vyas, GN TI Neutralizing antibodies against HIV determined by amplification of viral long terminal repeat sequences from cells infected in vitro by nonneutralized virions SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1; PCR; HIV-neutralizing antibodies; vaccines; laboratory assays ID IMMUNODEFICIENCY-VIRUS TYPE-1; MONOCLONAL-ANTIBODIES; ANTIGEN-DETECTION; PROVIRAL DNA; CHIMPANZEES; REPLICATION; ISOLATE; PLASMA; ASSAYS; PCR AB Based on the earliest intracellular synthesis of nascent HIV-1 long terminal repeat (LTR) fragments, we have established a heminested polymerase chain reaction (HNPCR) amplification of the 5' LTR sequences (LTR-HNPCR) for molecular assay of virus-neutralizing antibodies (VNAb). We incubated HIV antibodies with virus isolates for an hour, followed by addition of lymphoid cells (H-9, or peripheral blood mononuclear cells [PBMC]) and further incubation for an hour. After washing the cells three times for thorough removal of free virions and antibodies, LTR-HNPCR consistently revealed HIV DNA in H-9 cells after 15 minutes, in PBMC after 4 hours, and corresponding virion expression after 7 days in culture. Replication-competent HIV detected by LTR-HNPCR following overnight culture of infected PBMC for 16 to 18 hours was comparable with tissue culture infectivity measured by p24 antigen expression at 7 days. After establishing a molecular assay for in vitro HIV neutralization by HIV Ig, a panel of five HIV isolates tested with 6 monoclonal antibodies and HIV Ig revealed that LTR-HNPCR was comparable with other VNAb assays. These preliminary data indicate that the molecular assay for HIV neutralization has a clear-cut end point, is specific, reliable, and more rapid than other VNAb assays. Therefore, it offers potential utility in evaluating immune response to candidate vaccines. C1 Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA. NIAID, Div Aids, Bethesda, MD 20892 USA. RP Vyas, GN (reprint author), Univ Calif San Francisco, Dept Lab Med, UCSF Box 0134,513 Parnassus Ave,Room S-555, San Francisco, CA 94143 USA. EM vyas@pangloss.ucsf.edu FU NHLBI NIH HHS [HB-6-7020, R01-HL-53384] NR 27 TC 5 Z9 6 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN 1 PY 1998 VL 17 IS 1 BP 27 EP 34 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA YR043 UT WOS:000071451900004 PM 9436755 ER PT J AU Peterson, KP Bowers, C Peterson, CM AF Peterson, KP Bowers, C Peterson, CM TI Prevalence of ethanol consumption may be higher in women than men in a university health service population as determined by a biochemical marker: Whole blood-associated acetaldehyde above the 99th percentile for teetotalers SO JOURNAL OF ADDICTIVE DISEASES LA English DT Article ID HEMOGLOBIN-ASSOCIATED ACETALDEHYDE; ALCOHOLISM SCREENING-TEST; DEPRESSIVE SYMPTOMS; DIABETES-MELLITUS; MOOD DISORDERS; MICE; VOLUNTEERS; DRINKING; ADDUCTS; GENDER AB To estimate ethanol consumption by university students attending a student health facility, a biochemical marker of alcohol intake [whole blood associated acetaldehyde (WBAA)] was quantified by fluorimetric HPLC. Over a two year period we studied blood samples, coded by date and sex, from 645 females and 332 males, and compared the results to previously established reference ranges for teetotalers by sex. Men had higher absolute values for WBAA than women (9.9 versus 9.5 mu M in the present study). However, significantly greater numbers of women (74%) than men (44%) had WBAA levels above the 99th percentile for teetotalers. Variations occurred during the academic year, with significant elevations occurring in the late fall and winter months. Testing of WBAA levels in a student health service may be important especially for women to facilitate counseling on the dangers of alcohol abuse. C1 Sansum Med Res Fdn, Santa Barbara, CA 93105 USA. Univ Calif Santa Barbara, Student Hlth Serv, Santa Barbara, CA 93106 USA. RP Peterson, CM (reprint author), NIH, DBDR, 6701 Rockledge Dr,MSC 7950, Bethesda, MD 20892 USA. RI Peterson, Karen/E-8084-2015 OI Peterson, Karen/0000-0001-6737-8698 FU NIAAA NIH HHS [AA07614] NR 36 TC 3 Z9 3 U1 0 U2 1 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1055-0887 EI 1545-0848 J9 J ADDICT DIS JI J. Addict. Dis. PY 1998 VL 17 IS 3 BP 13 EP 23 DI 10.1300/J069v17n03_02 PG 11 WC Substance Abuse SC Substance Abuse GA 136NZ UT WOS:000076867100002 PM 9789156 ER PT J AU Haverkos, HW AF Haverkos, HW TI HIV/AIDS and drug abuse: Epidemiology and prevention SO JOURNAL OF ADDICTIVE DISEASES LA English DT Article ID OUT-OF-TREATMENT; HIV-INFECTION; COCAINE USE; METHADONE; AIDS; SEROCONVERSION AB In the United States, the AIDS epidemic is a dynamic process with increasing rates of AIDS reported among women, minority populations, heterosexual men, and users of drugs by routes other than injection. The 1993 CDC AIDS definition change has created some difficulties in interpreting trends in the United States. Drug use continues to represent a significant problem among HIV-infected persons. Several strategies have been advanced to decrease transmission of HIV among drug, users, their sexual partners and children. However, more effective and comprehensive prevention and treatment strategies are needed. C1 Natl Inst Drug Abuse, Intramural Res Program, NIH, Rockville, MD USA. RP Haverkos, HW (reprint author), US FDA, HFD 530,5600 Fishers Lane, Rockville, MD 20857 USA. NR 37 TC 14 Z9 14 U1 2 U2 2 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1998 VL 17 IS 4 BP 91 EP 103 PG 13 WC Substance Abuse SC Substance Abuse GA 142FP UT WOS:000077189700008 PM 9848034 ER PT J AU Brody, DT Kojima, D Metcalfe, DD AF Brody, DT Kojima, D Metcalfe, DD TI Mast cell IL-4 release is related to the initial expression of VCAM-1 and the development of pulmonary eosinophilia in a mouse asthma model. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 221 BP S51 EP S51 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800222 ER PT J AU Hizawa, N Freidhoff, LR Chiu, YF Ehrlich, E Luehr, CA Weber, JL Huang, SK Barnes, KC Marsh, DG Beaty, TH AF Hizawa, N Freidhoff, LR Chiu, YF Ehrlich, E Luehr, CA Weber, JL Huang, SK Barnes, KC Marsh, DG Beaty, TH CA Collaborative Study Genetics Asthma TI A genome-wide screening for genes influencing dermatophagoides pteronyssinus (Der p)-specific IgE responsiveness. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Johns Hopkins Asthma & Allergy Ctr, Baltimore, MD USA. Johns Hopkins Sch Hyg, Baltimore, MD USA. Beckman Instruments Inc, Chaska, MN USA. Marshfield Clin, Marshfield, WI USA. NHLBI, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 772 BP S188 EP S188 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800771 ER PT J AU Jones, JC DeKruyff, RH Potter, M Barsh, GS Umetsu, DT AF Jones, JC DeKruyff, RH Potter, M Barsh, GS Umetsu, DT TI Mapping a gene on murine chromosome 11 associated with high IL-4 responsiveness. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Stanford Univ, Stanford, CA 94305 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 716 BP S174 EP S174 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800716 ER PT J AU Kimura, T Zhang, J Sagawa, K Sakaguchi, K Appella, E Siraganian, RP AF Kimura, T Zhang, J Sagawa, K Sakaguchi, K Appella, E Siraganian, RP TI SHP-1 and SHP-2 associate with high affinity IgE receptor. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 440 BP S106 EP S106 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800440 ER PT J AU Mekori, YA Drucker, I Bhattacharyya, SP Kirshenbaum, AS Metcalfe, DD AF Mekori, YA Drucker, I Bhattacharyya, SP Kirshenbaum, AS Metcalfe, DD TI Activated T lymphocytes induce degranulation and cytokine production by human mast cells following cell-to-cell contact. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Meir Gen Hosp, Kfar Saba, Israel. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 671 BP S162 EP S163 PN 2 PG 2 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800671 ER PT J AU Nakano, T Adachi, S Metcalfe, DD AF Nakano, T Adachi, S Metcalfe, DD TI Antiproliferative effect of alpha-melanocyte-stimulating hormone (alpha-MSH) on proliferation of human mast cell leukemia (HMC-1) cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 894 BP S215 EP S215 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800892 ER PT J AU Oh, CK Vliagoftis, H Rumsaeng, V Metcalfe, DD Cho, JJ AF Oh, CK Vliagoftis, H Rumsaeng, V Metcalfe, DD Cho, JJ TI Identification and categorization of inducible mast cell genes in a subtraction library. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Harbor Med Ctr, Torrance, CA 90509 USA. NIAID, NIH, Bethesda, MD 20892 USA. RI Vliagoftis, Harissios/C-6480-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 159 BP S36 EP S36 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800160 ER PT J AU Pauls, JD Brems, J Pockros, PJ Saven, A Wagner, RL Weber, R Metcalfe, DD Christiansen, SC AF Pauls, JD Brems, J Pockros, PJ Saven, A Wagner, RL Weber, R Metcalfe, DD Christiansen, SC TI Mastocytosis: Diverse presentations and outcomes. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID, NIH, Bethesda, MD 20892 USA. Scripps Clin, La Jolla, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 892 BP S215 EP S215 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800890 ER PT J AU Prussin, C Foster, B Ludy, LM Metcalfe, DD AF Prussin, C Foster, B Ludy, LM Metcalfe, DD TI Basophils are the predominant IL-4 producing peripheral blood cells both in vivo and in vitro SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 177 BP S40 EP S41 PN 2 PG 2 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800178 ER PT J AU Rumsaeng, V Garala, MH Foster, B Vliagoftis, H Metcalfe, DD AF Rumsaeng, V Garala, MH Foster, B Vliagoftis, H Metcalfe, DD TI Interferon-gamma induces C-X-C chemokines, IFN-inducible protein-10 (IP-10) and mig gene expression in human mast cell line, HMC-1. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Chulalongkorn Univ, Bangkok, Thailand. NIH, Bethesda, MD 20892 USA. RI Vliagoftis, Harissios/C-6480-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 69 BP S16 EP S16 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800070 ER PT J AU Worobec, AS Foster, BA Semere, T Longley, BJ Metcalfe, DD AF Worobec, AS Foster, BA Semere, T Longley, BJ Metcalfe, DD TI Identification of the mutation Asp816Tyr in the c-kit receptor in an adult patient with urticaria pigmentosa from birth. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. Columbia Univ Coll Phys & Surg, New York, NY 10032 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1998 VL 101 IS 1 MA 893 BP S215 EP S215 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA YW339 UT WOS:000071924800891 ER PT J AU Joseph, RE Oyler, JM Wstadik, AT Ohuoha, C Cone, EJ AF Joseph, RE Oyler, JM Wstadik, AT Ohuoha, C Cone, EJ TI Drug testing with alternative matrices I. Pharmacological effects and disposition of cocaine and codeine in plasma, sebum, and stratum corneum SO JOURNAL OF ANALYTICAL TOXICOLOGY LA English DT Article ID VELLUS HAIR FOLLICLE; INTRAVENOUS COCAINE; GAS-CHROMATOGRAPHY; ORAL COCAINE; BREAST-MILK; EXCRETION; METABOLITES; HUMANS; URINE; HEROIN C1 NIDA, Addict Res Ctr, Div Intramural Res, Baltimore, MD 21224 USA. RP Cone, EJ (reprint author), NIDA, Addict Res Ctr, Div Intramural Res, POB 5180, Baltimore, MD 21224 USA. NR 61 TC 24 Z9 26 U1 3 U2 6 PU PRESTON PUBLICATIONS INC PI NILES PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 USA SN 0146-4760 J9 J ANAL TOXICOL JI J. Anal. Toxicol. PD JAN-FEB PY 1998 VL 22 IS 1 BP 6 EP 17 PG 12 WC Chemistry, Analytical; Toxicology SC Chemistry; Toxicology GA YW033 UT WOS:000071888900002 PM 9491963 ER PT J AU Quezado, ZMN Natanson, C Karzai, W Danner, RL Koev, CA Fitz, Y Dolan, DP Richmond, S Banks, SM Wilson, L Eichacker, PQ AF Quezado, ZMN Natanson, C Karzai, W Danner, RL Koev, CA Fitz, Y Dolan, DP Richmond, S Banks, SM Wilson, L Eichacker, PQ TI Cardiopulmonary effects of inhaled nitric oxide in normal dogs and during E-coli pneumonia and sepsis SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE Escherichia coli; hypoxemia; fractional inspired oxygen; pulmonary artery pressure ID HYPOXIC PULMONARY VASOCONSTRICTION; RESPIRATORY-DISTRESS-SYNDROME; VENTILATION-PERFUSION DISTRIBUTIONS; BLOOD-FLOW DISTRIBUTION; GAS-EXCHANGE; DOSE-RESPONSE; LUNG INJURY; PSEUDOMONAS PNEUMONIA; VASCULAR-RESISTANCE; ENDOTOXIN-SHOCK AB We investigated the effect of inhaled nitric oxide (NO) at increasing fractional inspired O-2 concentrations (FIO2) on hemodynamic and pulmonary function during Escherichia coli pneumonia. Thirty-eight conscious, spontaneously breathing, tracheotomized 2-yr-old beagles had intrabronchial inoculation with either 0.75 or 1.5 x 10(10) colony-forming units/kg of E. coli 0111:B4 (infected) or 0.9% saline (noninfected) in one or four pulmonary lobes. We found that neither the severity nor distribution (lobar vs. diffuse) of bacterial pneumonia altered the effects of NO. However, in infected animals, with increasing FIO2 (0.08, 0.21, 0.50, and 0.85), NO (80 parts/million) progressively increased arterial PO2 [-0.3 +/- 0.6, 3 +/- 1, 13 +/- 4, 10 +/- 9 (mean +/- SE) Torr, respectively] and decreased the mean arterial-alveolar O-2 gradient (0.5 +/- 0.3, 4 +/- 2, -8 +/- 7, -10 +/- 9 Torr, respectively). In contrast, in noninfected animals, the effect of NO was significantly different and opposite; NO progressively decreased mean PO2 with increasing FIO2 (2 +/- 1, -5 +/- 3, -2 +/- 3, and -12 +/- 5 Torr, respectively; P < 0.05 compared with infected animals) and increased mean arterial-alveolar O-2 gradient (0.3 +/- 0.04, 2 +/- 2, 1 +/- 3, 11 +/- 5 Torr; P < 0.05 compared with infected animals). In normal and infected animals alike, only at FIO2 less than or equal to 0.21 did NO significantly lower mean pulmonary artery pressure, pulmonary artery occlusion pressure, and pulmonary vascular resistance index (all P < 0.01). However, inhaled NO had no significant effect on increases in mean pulmonay artery pressure associated with bacterial pneumonia. Thus, during bacterial pneumonia, inhaled NO had only modest effects on oxygenation dependent on high FIO2 and did not affect sepsis-induced pulmonary hypertension. These data do not support a role for inhaled NO in bacterial pneumonia. Further studies are necessary to determine whether, in combination with ventilatory support, NO may have more pronounced effects. C1 NIH, Dept Crit Care Med, Bethesda, MD 20892 USA. RP Eichacker, PQ (reprint author), NIH, Dept Crit Care Med, Bldg 10,Rm 7D43,9000 Rockville Pike, Bethesda, MD 20892 USA. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 61 TC 22 Z9 22 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JAN PY 1998 VL 84 IS 1 BP 107 EP 115 PG 9 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA YR127 UT WOS:000071461000014 PM 9451624 ER PT J AU Holden, HE Stoll, RE Spalding, JW Tennant, RW AF Holden, HE Stoll, RE Spalding, JW Tennant, RW TI Hemizygous Tg center dot AC transgenic mouse as a potential alternative to the two-year mouse carcinogenicity bioassay: Evaluation of husbandry and housing factors SO JOURNAL OF APPLIED TOXICOLOGY LA English DT Article DE benzene; carcinogenicity; papillomas; phorbol ester; Tg.AC; transgenic mouse ID HA-RAS GENE; RODENT CARCINOGENICITY; MICE; TUMORS; SKIN; MODELS; RISK AB The dermal Tg.AC transgenic mouse model has been proposed as a potential alternative to the conventional (e.g. oral, dermal, parenteral, inhalation, etc.) 2-year rodent bioassay for detecting chemical carcinogenicity. The present study was designed to address a number of technical aspects of this model as well as to augment the database being developed with the Tg.AC system at the NIEHS. Hemizygous Tg.AC mice were implanted s.c. with microchips for identification and housed individually in polycarbonate (i.e. 'plastic') or suspended stainless-steel wire-bottom (i.e. 'metal') cages. Treatment consisted of dermal application of the test or control material in treatment volumes of 200 mu l of acetone. Groups of 10 males and 10 females were treated as follows: G1-shaved, no treatment; G2-acetone control seven times a week; G3-100 mu l of benzene three times a week; G4-150 mu l of benzene three times a week; G5-1.25 mu g of phorbol ester (PMA) twice a week. The G1-G5 mice were housed in plastic caging with Alpha-dri(R) bedding. Three additional groups were housed in stainless-steel wire-bottom caging: G6-shaved, no treatment; G7-acetone control seven times a week; G8-1.25 mu g of PMA twice a week. The PMA-treated mice (G5 and G8) served as the positive controls. Mice were treated for 20 weeks followed by a 6-week recovery period prior to necropsy. The incidence of dermal papillomas in the shaved area was recorded weekly. There were no spontaneous papillomas in the target area of any of the untreated (G1) or vehicle control (G2) animals in the polycarbonate cages. One papilloma was observed in the untreated mice (G6) and one in the vehicle control group (G7) in the steel cages. This suggests that the type of caging, the shaving process, microchip implantation and daily acetone treatment for 20 weeks are all consistent with a very low background incidence of papillomas in this model. Papillomas were observed in the positive control groups as early as 4 weeks of treatment and increased both in number per mouse and number of mice affected up to a maximum average of 3.5 papillomas per mouse and 55% (11/20) mice with papillomas in G5 and 2.7 and 80% (16/20) in G8. A plateau was reached at about week 13 and the numbers of papillomas remained stable through the rest of the treatment and recovery phases. The low dose of benzene (100 mu l) showed no significant effect, whereas the higher dose (150 mu l) produced a moderate number of papillomas beginning at about week 11. The results of this study are comparable with earlier studies at the NIEHS and indicate reproducibility between laboratories and that the Tg.AC transgenic mouse model is suitable for use in an industrial pre-clinical safety evaluation context, (C) 1998 John Wiley & Sons, Ltd. C1 Boehringer Ingelheim Pharmaceut Inc, Dept Toxicol & Safety Assessment, Ridgefield, CT 06877 USA. NIEHS, Lab Environm Carcinogenesis & Mutagenesis, Res Triangle Pk, NC 27709 USA. RP Holden, HE (reprint author), Boehringer Ingelheim Pharmaceut Inc, Dept Toxicol & Safety Assessment, 900 Ridgebury Rd, Ridgefield, CT 06877 USA. NR 22 TC 17 Z9 19 U1 1 U2 4 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 0260-437X J9 J APPL TOXICOL JI J. Appl. Toxicol. PD JAN-FEB PY 1998 VL 18 IS 1 BP 19 EP 24 DI 10.1002/(SICI)1099-1263(199801/02)18:1<19::AID-JAT464>3.3.CO;2-H PG 8 WC Toxicology SC Toxicology GA YZ295 UT WOS:000072240100003 PM 9526830 ER PT J AU Kolenbrander, PE Andersen, RN Baker, RA Jenkinson, HF AF Kolenbrander, PE Andersen, RN Baker, RA Jenkinson, HF TI The adhesion-associated sca operon in Streptococcus gordonii encodes an inducible high-affinity ABC transporter for Mn2+ uptake SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; OLIGOPEPTIDE TRANSPORT; SUPEROXIDE-DISMUTASE; ORAL STREPTOCOCCI; BINDING; PROTEIN; SYSTEM; GENE; MANGANESE AB ScaA lipoprotein in Streptococcus gordonii is a member of the LraI family of homologous polypeptides found among streptococci, pneumococci, and enterococci. It is the product of the third gene within the scaCBA operon encoding the components of an ATP-binding cassette (ABC) transporter system. Inactivation of scaC (ATP-binding protein) or scaA (substrate-binding protein) genes resulted in both impaired growth of cells and >70% inhibition of Mn-54(2+) uptake in media containing <0.5 mu M Mn2+. In wild-type and scaC mutant cells, production of ScaA was induced at low concentrations of extracellular Mn2+ (<0.5 mu M) and by the addition of greater than or equal to 20 mu M Zn2+. Sea permease-mediated uptake of Mn-54(2+) was inhibited by Zn2+ but not by Ca2+, Mg2+, Fe2+, or Cu2+. Reduced uptake of Mn-54(2+) by sea mutants and by wild-type cells in the presence of Zn2+ was abrogated by the uncoupler carbonylcyanide m-chlorophenylhydrazone, suggesting that Mn2+ uptake under these conditions was proton motive force dependent. The frequency of DNA-mediated transformation was reduced >20-fold in sea mutants. The addition of 0.1 mM Mn2+ to the transformation medium restored only partly the transformability of mutant cells, implying an alternate role for Sea proteins in the transformation process. Cells of sea mutants were unaffected in other binding properties tested and were unaffected in sensitivity to oxidants. The results show that Sea permease is a high-affinity mechanism for the acquisition of Mn2+ and is essential for growth of streptococci under Mn2+-limiting conditions. C1 NIDR, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA. Univ Otago, Dept Oral Biol & Oral Pathol, Mol Oral Biol Lab, Dunedin, New Zealand. RP Kolenbrander, PE (reprint author), NIDR, Oral Infect & Immun Branch, NIH, Bldg 30,Room 310,30 Convent Dr MSC 4350, Bethesda, MD 20892 USA. OI Jenkinson, Howard/0000-0002-9195-7945 NR 38 TC 96 Z9 101 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1998 VL 180 IS 2 BP 290 EP 295 PG 6 WC Microbiology SC Microbiology GA YR216 UT WOS:000071472600014 PM 9440518 ER PT J AU Honkakoski, P Negishi, M AF Honkakoski, Paavo Negishi, Masahiko TI Regulatory DNA Elements of Phenobarbital-Responsive Cytochrome P450 CYP2B Genes SO JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY LA English DT Review AB This article reviews recent progress in characterizing cis-acting DNA elements of the phenobarbital-inducible CYP2B genes. Whereas proximal DNA elements such as the C/EBP binding site regulate basal transcription activity, phenobarbital-responsive enhancer activity is governed by the distal element (designated phenobarbital-responsive enhancer module, PBREM) residing about -2.3 kbp upstream from the transcription start site. Proximal elements are not required to enhance the phenobarbital-inducible transcription, since the PBREM can confer the inducibility to several heterologous promoters. Repression of the basal transcription by a negative element upstream of the -0.8 kbp region, however, may be necessary for the proper regulation of the CYP2B genes. (C) 1997 John Wiley & Sons, Inc. J Biochem Toxicol 12: 3-9, 1998 C1 [Honkakoski, Paavo; Negishi, Masahiko] NIEHS, Pharmacogenet Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Negishi, M (reprint author), NIEHS, Pharmacogenet Sect, Reprod & Dev Toxicol Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. EM negishi@niehs.nih.gov OI Honkakoski, Paavo/0000-0002-4332-3577 NR 48 TC 61 Z9 62 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1095-6670 J9 J BIOCHEM MOL TOXIC JI J. Biochem. Mol. Toxicol. PY 1998 VL 12 IS 1 BP 3 EP 9 PG 7 WC Biochemistry & Molecular Biology; Toxicology SC Biochemistry & Molecular Biology; Toxicology GA V27VX UT WOS:000208641800002 PM 9414482 ER PT J AU Cherrington, NJ Falls, JG Rose, RL Clements, KM Philpot, RM Levi, PE Hodgson, E AF Cherrington, Nathan J. Falls, J. Greg Rose, Randy L. Clements, Kieran M. Philpot, Richard M. Levi, Patricia E. Hodgson, Ernest TI Molecular Cloning, Sequence, and Expression of Mouse Flavin-Containing Monooxygenases 1 and 5 (FMO1 and FMO5) SO JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY LA English DT Article DE Flavin-Containing Monooxygenase; FMO1; FMO5; Sequence; Expression; Phorate AB Full-length cDNA clones encoding FMO1 and FMO5 have been isolated from a library constructed with mRNA from the liver of a female CD-1 mouse. The derived sequence of FMO1 contains 2310 bases: 1596 in the coding region, 301 in the 5'-flanking region, and 413 in the 3'-flanking region. The sequence for FMO5 consists of 3168 bases; 1599 in the coding region, 812 in the 5'-flanking region, and 757 in the 30'-flanking region. The sequence of FMO1 encodes a protein of 532 amino acids with a predicted molecular weight of 59.9 kDa and shows 83.3% identity to human FMO1 and 83-94% identity to other FMO1 homologs. FMO5 encodes a protein of 533 amino acids with a predicted molecular weight of 60.0 kDa and 84.1% identity to human FMO5 and 83-84% identity to other FMO5 orthologs. Two GxGxxG putative pyrophosphate binding domains exist beginning at positions 9 and 191 for FMO1, and 10 and 192 for FMO5. Mouse FMO1 and FMO5 were expressed in E. coli and show similar mobility to the native proteins as determined by SDSPAGE. The expressed FMO1 protein showed activity. toward methimazole, and FMO5 was active toward noctylamine. In addition, FMO1 was shown to metabolize radiolabeled phorate, whereas FMO5 showed no activity toward phorate. (C) 1998 John Wiley & Sons, Inc. J Biochem Toxicol 12: 205-212, 1998 C1 [Cherrington, Nathan J.; Falls, J. Greg; Rose, Randy L.; Levi, Patricia E.; Hodgson, Ernest] N Carolina State Univ, Dept Toxicol, Raleigh, NC 27695 USA. [Falls, J. Greg] Duke Univ, Dept Radiat Oncol, Med Ctr, Durham, NC 27710 USA. [Clements, Kieran M.] N Carolina State Univ, Deparemtnt Entomol, Raleigh, NC 27695 USA. [Philpot, Richard M.] NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA. RP Hodgson, E (reprint author), N Carolina State Univ, Dept Toxicol, Box 7633, Raleigh, NC 27695 USA. NR 44 TC 17 Z9 19 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1095-6670 J9 J BIOCHEM MOL TOXIC JI J. Biochem. Mol. Toxicol. PY 1998 VL 12 IS 4 BP 205 EP 212 PG 8 WC Biochemistry & Molecular Biology; Toxicology SC Biochemistry & Molecular Biology; Toxicology GA V27WA UT WOS:000208642100002 PM 9580872 ER PT J AU Kepple, TM Sommer, HJ Siegel, KL Stanhope, SJ AF Kepple, TM Sommer, HJ Siegel, KL Stanhope, SJ TI A three-dimensional musculoskeletal database for the lower extremities SO JOURNAL OF BIOMECHANICS LA English DT Article DE bones; muscles; landmarks; scaling ID ANTHROPOMETRIC SCALING METHOD; MUSCLE ATTACHMENTS; MODEL; VARIABILITY; KNEE; HIP AB A three-dimensional musculoskeletal database of the lower extremities has been developed for use in human musculoskeletal models. The locations of idealized muscle attachments on the pelvis, both femurs, both tibias and fibulas, and both feet were accurately digitized for 52 dried skeletal specimens. The mean specimen heights were 177.5 cm (male) and 166.2 cm (female) and the mean specimen age at the time of death was 48.8 yr. Statistical accumulation and scaling techniques were used to generate highly representative normative models, which were divided into groups and tested for differences based on gender and race. From the test results, the pelvis was divided into a male model(RMS = 8.6 mm), a black female model(RMS = 7.0 mm) and a white female model (RMS = 7.3 mm). The foot was separated into black (RMS = 3.7 mm) and white models (RMS = 3.6 mm). Single models were used for the femur (RMS = 6.5 mm) and the tibia/fibula (RMS = 3.7). Containing over 12000 anatomical landmarks digitized from 52 dried skeletons, this study represents an improvement over previous databases by an order of magnitude. Published by Elsevier Science Ltd. C1 NIH, Biomech Lab, Bethesda, MD 20892 USA. Penn State Univ, Dept Mech Engn, University Pk, PA 16802 USA. RP Kepple, TM (reprint author), NIH, Biomech Lab, Bldg 10,Room 6S 235,10 Ctr Dr,MSC 1604, Bethesda, MD 20892 USA. NR 17 TC 37 Z9 37 U1 1 U2 9 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0021-9290 J9 J BIOMECH JI J. Biomech. PD JAN PY 1998 VL 31 IS 1 BP 77 EP 80 PG 4 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA ZR428 UT WOS:000073974600010 PM 9596541 ER PT J AU Jeang, KT AF Jeang, KT TI Tat, Tat-associated kinase, and transcription SO JOURNAL OF BIOMEDICAL SCIENCE LA English DT Review DE human immunodeficiency virus; Tat; transcription; Sp1; RNA polymerase II; protein kinase ID HUMAN-IMMUNODEFICIENCY-VIRUS; RNA-POLYMERASE-II; LONG TERMINAL REPEAT; CELLULAR PROTEIN-KINASE; TRANS-ACTIVATOR GENE; IN-VITRO; PREINITIATION COMPLEX; BINDING PROTEIN; HIV-1; ELONGATION AB The HIV-1 Tat protein is an RNA-binding transcriptional transactivator. Recent findings suggest that Tat associates with a cellular kinase that phosphorylates the carboxyl-terminal domain of the largest subunit of RNA polymerase II. Here we review, in brief, the role of Tat-associated kinase in Tat-activated transcription. We discuss evidence that suggests involvement of TFIIH and/or P-TEFb. C1 NIAID, Mol Microbiol Lab, Mol Virol Sect, NIH, Bethesda, MD 20892 USA. RP Jeang, KT (reprint author), NIAID, Mol Microbiol Lab, Mol Virol Sect, NIH, Bethesda, MD 20892 USA. RI Jeang, Kuan-Teh/A-2424-2008 NR 57 TC 22 Z9 22 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1021-7770 J9 J BIOMED SCI JI J. Biomed. Sci. PD JAN-FEB PY 1998 VL 5 IS 1 BP 24 EP 27 PG 4 WC Cell Biology; Medicine, Research & Experimental SC Cell Biology; Research & Experimental Medicine GA ZF206 UT WOS:000072874300003 PM 9570510 ER PT J AU Cai, ML Huang, Y Sakaguchi, K Clore, GM Gronenborn, AM Craigie, R AF Cai, ML Huang, Y Sakaguchi, K Clore, GM Gronenborn, AM Craigie, R TI An efficient and cost-effective isotope labeling protocol for proteins expressed in Escherichia coli SO JOURNAL OF BIOMOLECULAR NMR LA English DT Article DE heteronuclear NMR; isotope labeling; protein expression ID HETERONUCLEAR NMR-SPECTROSCOPY AB A cost-effective protocol for uniform N-15 and/or C-13 isotope labeling of bacterially expressed proteins is presented. Unlike most standard protocols, cells are initially grown in a medium containing nutrients at natural abundance and isotopically labeled nutrients are only supplied at the later stages of growth and during protein expression. This permits the accumulation of a large cell mass without the need to employ expensive isotopically labeled nutrients. The abrupt decrease in oxygen consumption that occurs upon complete exhaustion of essential nutrients is used to precisely time the switch between unlabeled and labeled nutrients. Application of the protocol is demonstrated for wild-type and a mutant of the N-terminal zinc-binding domain of HIV-1 integrase. C1 NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. NIDDKD, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. RP Clore, GM (reprint author), NIDDKD, Chem Phys Lab, NIH, Bldg 5, Bethesda, MD 20892 USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 8 TC 129 Z9 132 U1 0 U2 14 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0925-2738 J9 J BIOMOL NMR JI J. Biomol. NMR PD JAN PY 1998 VL 11 IS 1 BP 97 EP 102 DI 10.1023/A:1008222131470 PG 6 WC Biochemistry & Molecular Biology; Spectroscopy SC Biochemistry & Molecular Biology; Spectroscopy GA ZF207 UT WOS:000072874400007 PM 9566315 ER PT J AU Wakisaka, A Tanaka, H Barnes, J Liang, CT AF Wakisaka, A Tanaka, H Barnes, J Liang, CT TI Effect of locally infused IGF-I on femoral gene expression and bone turnover activity in old rats SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID GROWTH-FACTOR-I; OVARIECTOMIZED RATS; CORTICAL BONE; ADULT; AGE AB Previously, we showed that the age-dependent deficit in bone formation activity can be attributed in part to a decline in local expression of insulin-like growth factor I (IGF-I) and altered mitogenic response of old osteoprogenitor cells to IGF-I. To establish the cellular basis for using IGF-I as a possible therapeutic agent for osteoporosis, we examined the effect of locally infused (50 ng/day for 14 days) on the expression of osteoblast-related genes in femurs of old rats. Northern and dot blot analyses showed that the expression of procollagen (I), osteopontin, alkaline phosphatase, and osteocalcin was increased 0.4- to 1.5-fold in IGF-1-treated femurs as compared with control femurs. Histomorphometric analyses were carried out in parallel experiments to assess the changes in bone remodelling activity. Trabecular bone volume, trabecular number, and trabecular thickness were increased 56%, 29%, and 23%, respectively, whereas trabecular separation was reduced 26% by IGF-1 treatment. IGF-I treatment increased significantly the osteoid volume, osteoid surface, osteoblast number, and osteoblast surface. Mineralizing surface and mineral apposition rate, kinetic indices of bone formation, were also stimulated by IGF-I treatment. The bone formation rate was stimulated 81% in IGF-I-treated femurs as compared with control femurs. In contrast, eroded surface and osteoclast surface, parameters associated with bone resorption, were not affected by IGF-I treatment. These findings suggest that local administration of IGF-I into femurs of old rats can stimulate the expression of matrix proteins and improve trabecular bone status by stimulating bone formation without any appreciable effect on bone resorption. C1 NIA, Ctr Gerontol Res, NIH, Baltimore, MD 21224 USA. RP Liang, CT (reprint author), NIA, Ctr Gerontol Res, NIH, 4940 Eastern Ave, Baltimore, MD 21224 USA. NR 29 TC 32 Z9 34 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD JAN PY 1998 VL 13 IS 1 BP 13 EP 19 DI 10.1359/jbmr.1998.13.1.13 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YN807 UT WOS:000071209800003 PM 9443785 ER PT J AU Arguello, F Alexander, MA Greene, JF Stinson, SF Jorden, JL Smith, EM Kalavar, NT Alvord, WG Klabansky, RL Sausville, EA AF Arguello, F Alexander, MA Greene, JF Stinson, SF Jorden, JL Smith, EM Kalavar, NT Alvord, WG Klabansky, RL Sausville, EA TI Preclinical evaluation of 9-chloro-2-methylellipticinium acetate alone and in combination with conventional anticancer drugs for the treatment of human brain tumor xenografts SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY LA English DT Article DE brain tumor; glioma; preclinical evaluation; human tumor xenograft; ellipticinium ID 2-METHYL-9-HYDROXYELLIPTICINIUM ACETATE; ELLIPTICINIUM SALTS; CELL LINES; IN-VITRO; CHEMOTHERAPY; CYTOTOXICITY; CISPLATIN; ETOPOSIDE; DELIVERY; DESIGN AB Some ellipticine derivative salts, including 9-chloro-2-methylellipticinium (CME), have been found to have a marked selectivity against all eight brain tumor cell lines of the U.S. National Cancer Institute's disease-oriented in vitro screen. We initiated in vivo antitumor studies to explore the feasibility for further development of this class of compounds. We found that CME was extremely toxic to nude mice when given i.p. at a dose of 25 mg/kg for 3 consecutive days. Animals treated by this route experienced an increase in hepatic transaminases and histopathological changes in the liver, compatible with mitochondrial damage. In contrast, when the portal circulation was bypassed and the same dose of CME was given i.v., animals tolerated daily bolus injections for 5 consecutive days. This 5-day i.v. bolus schedule had consistent antitumor activity, with 28.1% growth delay on s.c. implanted human U251 gliomas. When the potentially high peaks of CME in the portal circulation were avoided by using a 3-day continuous infusion with osmotic minipumps implanted i.p. to release 3.4 mg kg(-1) h(-1) or 6.6 mg kg(-1) h(-1) CME, there were only modest increases in liver enzymes and leukopenia, but no meaningful antitumor activity was observed. In contrast, continuous infusion in the s.c. space was well tolerated and was accompanied by a demonstrable growth delay in s.c. U251 human gliomas of 37.8%. When CME was used in conjunction with carmustine, etoposide or cisplatin, no synergistic activities were observed, but additive effects were demonstrated. Our pharmacokinetic and disposition studies with CME argue against the notion that large and invasive tumors in the brain lack blood-brain barrier features. When CME was used in animals bearing orthotopically implanted U251 gliomas in the brain of nude mice, the survival of the treated animals was not better than vehicle controls, and the addition of CME to carmustine therapy did not improve the survival of those animals treated with carmustine alone. We conclude that, in spite of its marked cytotoxicity in vitro on a variety of human brain tumor cell lines, including U251 glioma cells, CME has a modest antitumor effect on extracranially implanted U251 glioma tumors, and no beneficial effect in animals bearing the same U251 tumor in the brain, owing to a poor penetration into the brain parenchyma. C1 NCI, Frederick Canc Res & Dev Ctr, Div Canc Treatment, Dev Therapeut Program,Lab Drug Discovery,NIH, Frederick, MD 21702 USA. Scott & White Clin, Dept Pathol, Temple, TX 76508 USA. NCI, Frederick Canc Res & Dev Ctr, Data Management Serv Inc, Frederick, MD 21702 USA. RP Arguello, F (reprint author), 1416 Crescent Spot Lane, Frederick, MD 21703 USA. NR 26 TC 13 Z9 14 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0171-5216 J9 J CANCER RES CLIN JI J. Cancer Res. Clin. Oncol. PD JAN PY 1998 VL 124 IS 1 BP 19 EP 26 DI 10.1007/s004320050128 PG 8 WC Oncology SC Oncology GA YX713 UT WOS:000072069800004 PM 9498830 ER PT J AU Zhang, J Kovac, P AF Zhang, J Kovac, P TI Synthesis of some analogs of the methyl alpha-glycoside of the presumed antigenic determinant of the O-specific polysaccharide of Vibrio cholerae O : 1, serotype Ogawa SO JOURNAL OF CARBOHYDRATE CHEMISTRY LA English DT Article ID REPEATING UNIT; CRYSTAL-STRUCTURE; BINDING; O/1; LIPOPOLYSACCHARIDE; TRISACCHARIDE; DISACCHARIDE; ANTIBODIES; MIMICKING; TERMINUS AB The following analogs of the title determinant, methyl 4,6-dideoxy-4-(3 -deoxy-L-glycero-tetronamido)-2-O-methyl-alpha-D-mannopyranoside, have been prepared: methyl 3,4,6,-trideoxy-4-(3-deoxy-L-glycero-tetronamido)-2-O-methyl-alpha-D-mannopyranoside, methyl 4,6-dideoxy-4-(4-hydroxybutyramido)-2-O-methyl-alpha-D-mannopyranoside, methyl 4,6-dideoxy-4-(3,4-dideoxy-L-glycero-tetronamido)-2-O-methyl-alpha-D-mannopyranoside, methyl 4,6-dideoxy-4-(3-deoxy-D-glycero-tetronamido)-2-O-methyl-alpha-D-mannopyranoside, methyl 4,6-dideoxy-4-(2-deoxy-L-glycero-tetronamido)2-O-methyl-alpha-D-mannopyranoside, methyl 4-acetamido-4,6-dideoxy-2-O-methyl-alpha-D-mannopyranoside, methyl 4,6-dideoxy-4-(3 -deoxy-L-glycero-tetronamido)-2-O-ethyl-alpha-D-mannopyranoside, and methyl 4,6-dideoxy-4-(3-deoxy-L-glycero-tetronamido)-2-O-propyl-alpha-D-mannopyranoside. C1 NIDDK, NIH, Bethesda, MD 20892 USA. RP Zhang, J (reprint author), NIDDK, NIH, 8 Ctr Dr, Bethesda, MD 20892 USA. NR 22 TC 5 Z9 5 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0732-8303 J9 J CARBOHYD CHEM JI J. Carbohydr. Chem. PY 1998 VL 17 IS 3 BP 341 EP 357 DI 10.1080/07328309808002896 PG 17 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA ZM320 UT WOS:000073526700002 ER PT J AU Hodosi, G Kovac, P AF Hodosi, G Kovac, P TI Epimerization of carbohydrates via stannylene acetals. A practical synthesis of D-talose SO JOURNAL OF CARBOHYDRATE CHEMISTRY LA English DT Article ID MOLYBDATE IONS; ALDOSES AB When treated with Bu2SnO in a suitable solvent, reducing sugars preferentially form 1,2-O-stannylene acetals and, on prolonged treatment with a slight excess of the reagent at reflux temperature, they undergo epimerization. This allows simple preparation of rare monosaccharides from readily available, unprotected starting materials. The process is equilibrium driven, and the equilibrium is shifted largely in favor of structures having an axial hydroxyl group at position 2. C1 NIDDK, NIH, Bethesda, MD 20892 USA. RP Kovac, P (reprint author), NIDDK, NIH, Bethesda, MD 20892 USA. NR 15 TC 6 Z9 6 U1 0 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0732-8303 J9 J CARBOHYD CHEM JI J. Carbohydr. Chem. PY 1998 VL 17 IS 4-5 BP 557 EP 565 DI 10.1080/07328309808002337 PG 9 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA ZY834 UT WOS:000074666000006 ER PT J AU DePamphilis, ML AF DePamphilis, ML TI Initiation of DNA replication in eukaryotic chromosomes SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE eukaryote; DNA replication; replication origin; pre-replication complex; initiation proteins; origin recognition complex; DNA unwinding; nuclear structure; chromatin structure; DNA methylation; animal development; metazoa; mammal; frog; fly; yeast; Xenopus; Drosophila; Sciara ID XENOPUS EGG EXTRACTS; ORIGIN; CHROMATIN; BINDING; COMPLEX; REGION; LOCUS; SITE AB Our understanding of the process by which eukaryotes regulate initiation of DNA replication has made remarkable advances in the past few years, thanks in large part to the explosion of genetic and biochemical information on the budding yeast, Saccharomyces cerevisiae. At least three major concepts have emerged: 1) The sequence of molecular events that determines when replication begins and how frequently each replication site is used are conserved among most, if not all, eukaryotes; 2) specific replication origins are used in most, if not all, eukaryotes that consist of a flexible modular anatomy; and 3) epigenetic factors such as chromatin structure and nuclear organization determine which of many potential replication origins are used at different stages in animal development. Thus, the current state of our knowledge suggests a simple unifying concept-all eukaryotes utilize the same basic proteins and DNA sequences to initiate replication, but the metazoa can change both the number and locations of replication origins In response to the demands of animal development. J. Cell. Biochem. Suppls. 30/31:8-17, 1998. Published 1998 Wiley-Liss, Inc.dagger. C1 NICHHD, NIH, Bethesda, MD 20892 USA. RP DePamphilis, ML (reprint author), NICHHD, NIH, Bldg 6,Room 416, Bethesda, MD 20892 USA. NR 37 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1998 SU 30-31 BP 8 EP + PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 154ZV UT WOS:000077921800003 ER PT J AU Jones, TH Garraffo, HM Blum, MS Everett, DM Hastings, H Ware, AB AF Jones, TH Garraffo, HM Blum, MS Everett, DM Hastings, H Ware, AB TI Elucidation of dimethylalkylpyrazines from the ant Streblognathus aethiopicus by GC-FTIR SO JOURNAL OF CHEMICAL ECOLOGY LA English DT Article DE pyrazines; GC-FTIR; Streblognathus; gamergate ID PYRAZINES; HYMENOPTERA; FORMICIDAE; PONERINAE AB The presumed mandibular gland secretions from the workers and gamergates of two colonies of Streblognathus aethiopicus have been found to contain a homologous series of 3,5-dimethyl-2-alkylpyrazines (3,5-dimethyl-2-butylpyrazine, 1; 3,5-dimethyl-2-pentylpyrazine, 2; and 3,5-dimethyl-2-hexylpyrazine, 3). The structures of these compounds were determined from their mass spectra along with a comparison of their GC-FTIR spectra with those of all the isomers of a lower homolog. This is the first time that this combination of techniques has been applied to the study of insect pyrazines. The relative amounts and proportions of these compounds were different for gamergates and workers, with the latter containing 2-10 times more total pyrazines and having a higher proportion of 2 and 3. The possible significance of this finding is discussed. C1 Virginia Mil Inst, Dept Chem, Lexington, VA 24450 USA. NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA. Univ Georgia, Dept Entomol, Athens, GA 30602 USA. Univ Georgia, Dept Comp Sci, Athens, GA 30602 USA. Rhodes Univ, Dept Zool & Entomol, ZA-6140 Grahamstown, South Africa. RP Jones, TH (reprint author), Virginia Mil Inst, Dept Chem, Lexington, VA 24450 USA. NR 14 TC 5 Z9 5 U1 1 U2 2 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0098-0331 EI 1573-1561 J9 J CHEM ECOL JI J. Chem. Ecol. PD JAN PY 1998 VL 24 IS 1 BP 125 EP 134 DI 10.1023/A:1022345114057 PG 10 WC Biochemistry & Molecular Biology; Ecology SC Biochemistry & Molecular Biology; Environmental Sciences & Ecology GA YR564 UT WOS:000071507900010 ER PT J AU Jacobsen, LK Rapoport, JL AF Jacobsen, LK Rapoport, JL TI Research update: Childhood-onset schizophrenia: Implications of clinical and neurobiological research SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Review DE schizophrenia; diagnosis; genetics; risk factors; pharmacology; neuro-development ID EMISSION COMPUTED-TOMOGRAPHY; MONOZYGOTIC TWINS DISCORDANT; CEREBRAL BLOOD-FLOW; GRAY-MATTER VOLUME; AGE-OF-ONSET; BRAIN MORPHOLOGY; ADOLESCENT SCHIZOPHRENIA; ADULT SCHIZOPHRENIA; GLUCOSE-METABOLISM; NEUROLEPTIC-NAIVE AB Childhood-onset schizophrenia is a rare, clinically severe form of schizophrenia, which is associated with disrupted cognitive, linguistic, and social development well before the appearance of frank psychotic symptoms. This disruption of multiple developmental domains signals the important opportunity these patients present for examining neurodevelopmental and other etiologic hypotheses of schizophrenia. The present research update reviews studies of the phenomenology and neurobiology of childhood-onset schizophrenia conducted since 1994. Findings from these studies indicate that children can be diagnosed with schizophrenia using unmodified DSM-III, -IIIR, and -IV criteria, and that the atypical neuroleptic clozapine is an effective medication for this treatment refractory group. Neuropsychologic and neurobiologic studies generally support continuity with adult-onset schizophrenia, with evidence of more severe premorbid impairment. Longitudinal studies show preliminary evidence of progressive ventricular enlargment and more prolonged deterioration in intellectual function than is seen in the adult-onset disorder. If replicated, these observations, together with the insidious onset of this disorder, would suggest that the pathologic underpinning of childhood-onset schizophrenia is not a single static lesion or event but may be a continuous or multi-event process. C1 NIMH, Child Psychiat Branch, Child Pschol Branch, Bethesda, MD 20892 USA. RP Jacobsen, LK (reprint author), NIMH, Child Psychiat Branch, Child Pschol Branch, Bldg 10,Rm 6N240,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 127 TC 101 Z9 102 U1 9 U2 10 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD JAN PY 1998 VL 39 IS 1 BP 101 EP 113 DI 10.1017/S002196309700173X PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA YX510 UT WOS:000072047800006 PM 9534088 ER PT J AU Evenson, DA Perry, E Kloster, B Hurley, R Stroncek, DF AF Evenson, DA Perry, E Kloster, B Hurley, R Stroncek, DF TI Therapeutic apheresis for babesiosis SO JOURNAL OF CLINICAL APHERESIS LA English DT Article DE Babesia; RBC transfusion; plasmapheresis ID TRANSFUSION-TRANSMITTED BABESIOSIS; INFECTION AB Infection with the tick-borne protozoa Babesia is becoming more common. Babesiosis is usually successfully treated with antibiotics but, in some cases, apheresis may also be indicated. We report two patients with babesiosis and hemolysis treated by apheresis and antibiotics. One case had traditional indications for red blood cell (RBC) exchange, and a second patient was treated with RBC exchange, and plasmapheresis for hemolysis, probably secondary to Babesia parasitemia. Case 1 involved a 44-year-old man with chronic relapsing pancreatitis who had become infected with Babesia from a unit of RBCs transfused during surgery. At 5 weeks after surgery, fever and severe hemolysis developed, along with a hemoglobin of 69 g/L; 30% of his RBCs were found to be infected with Babesia. This patient had several postoperative complications; the babesiosis was treated with clindamycin, quinine, and three RBC exchanges. Parasitemia fell to less then 1% of RBCs, but the patient died of pancreatitis. Case 2 was a 47-year-old man with a renal transplant who had been receiving immunosuppressive therapy for 8 years. He had a history of tick bites, fever, and hemolytic anemia. Analysis of a peripheral blood smear detected Babesia. He was initially treated with antibiotic therapy and two RBC exchanges. Hemolysis improved transiently but worsening parasitemia developed later, as well as an IgG RBC autoantibody. He was then treated by plasmapheresis and RBC exchange. Although his condition improved, he had a third hemolytic episode, which was treated with plasmapheresis and RBC exchange before the parasitemia and autoimmune hemolytic anemia disappeared. In conclusion, immunosuppressed or severely ill people who become infected with Babesia may benefit from RBC exchange or plasmapheresis, or both. (C) 1998 Wiley-Liss, Inc. C1 Univ Minnesota, Sch Med, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Dept Med, Minneapolis, MN 55455 USA. Mem Blood Ctr Minnesota, Minneapolis, MN USA. Amer Red Cross, N Cent Blood Serv, St Paul, MN USA. RP Stroncek, DF (reprint author), NIH, Dept Transfus Med, 10 Ctr Dr,MSC-1184,Bldg 10,Room 10711, Bethesda, MD 20892 USA. NR 18 TC 39 Z9 40 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0733-2459 J9 J CLIN APHERESIS JI J. Clin. Apheresis PY 1998 VL 13 IS 1 BP 32 EP 36 DI 10.1002/(SICI)1098-1101(1998)13:1<32::AID-JCA7>3.0.CO;2-A PG 5 WC Hematology SC Hematology GA ZJ926 UT WOS:000073267600007 PM 9590496 ER PT J AU Alvero, R Kimzey, L Sebring, N Reynolds, J Loughran, M Nieman, L Olson, BR AF Alvero, R Kimzey, L Sebring, N Reynolds, J Loughran, M Nieman, L Olson, BR TI Effects of fasting on neuroendocrine function and follicle development in lean women SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GONADOTROPIN-RELEASING-HORMONE; PULSATILE LUTEINIZING-HORMONE; ENDOCRINE PEAK DETECTION; ANOREXIA-NERVOSA; BIOLOGICAL VALIDATION; REPRODUCTIVE FUNCTION; SERUM THYROTROPIN; POSITIVE ACCURACY; PULSE AMPLITUDE; MACACA-MULATTA AB A 72-h fast in normal weight women during the follicular phase results in transient alterations in neuroendocrine function, but follicle development and follicular phase length remain unaltered. In this study we evaluated neuroendocrine and ovulatory function in lean women (body fat, less than or equal to 20%) undergoing a similar 72-h fast. Compared to fed controls, fasted lean women experienced significant weight loss, blunting of the diurnal variation of cortisol, suppression of the nocturnal TSH rise, and a decrease in T-3 levels after a 72-h fast. In contrast to similarly fasted, normal weight women, lean women have significantly higher evening cortisol levels and do not exhibit a normal nocturnal TSH rise after the fast. Lean fasted women exhibited a 19% decrease in the number of LH pulses over 24 h compared to fed women (12.9 +/- 1.3 vs. 16.0 +/- 1.9; P < 0.05). Fasting did not result in significant differences in mean LH, LH amplitude, LH area under the curve, and mean FSH levels in these lean women. Of the seven fasted cycles, two were anovulatory. In the five women studied in fed and fasted cycles, one had interrupted lead follicle development with anovulation, and four had significant lengthening of the follicular phase compared to those during their fed cycles (14.4 +/- 1.2 vs. 13.2 +/- 1.0 days; P = 0.01). The clinical observations made in this small sample of lean women showing more profound changes in neuroendocrine function, anovulation, and lengthened follicular phase after fasting suggest that lean women may be more vulnerable to fasting stress than normal weight women. C1 William Beaumont Army Med Ctr, Dept Obstet & Gynecol, El Paso, TX 79922 USA. NICHHD, Warren G Magnuson Clin Ctr, Dept Nursing, NIH, Bethesda, MD 20892 USA. NICHHD, Dept Diet & Nutr, NIH, Bethesda, MD 20892 USA. NICHHD, Dept Nucl Med, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. Waterbury Hosp & Hlth Ctr, Waterbury, CT 06702 USA. RP Alvero, R (reprint author), William Beaumont Army Med Ctr, Dept Obstet & Gynecol, 5005 N Piedras, El Paso, TX 79922 USA. NR 23 TC 17 Z9 17 U1 1 U2 2 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 JAN PY 1998 VL 83 IS 1 BP 76 EP 80 DI 10.1210/jc.83.1.76 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YP375 UT WOS:000071270600014 PM 9435419 ER PT J AU Merke, DP Tajima, T Chhabra, A Barnes, K Mancilla, E Baron, J Cutler, GB AF Merke, DP Tajima, T Chhabra, A Barnes, K Mancilla, E Baron, J Cutler, GB TI Novel CYP11B1 mutations in congenital adrenal hyperplasia due to steroid 11 beta-hydroxylase deficiency SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Editorial Material ID SPLICE-SITE MUTATION; DONOR SITE; GENE; DISEASE; IDENTIFICATION; SUBSTITUTIONS; EXON-7 AB The second most common cause of congenital adrenal hyperplasia is 11 beta-hydroxylase deficiency, an autosomal recessive disorder. We performed genetic analysis of CYP11B1, the gene encoding steroid 11 beta-hydroxylase, in three patients with classic 11 beta-hydroxylase deficiency. Herein we describe the first splice donor site mutation, a new nonsense mutation, and a new missense mutation in this disorder. An African-American patient was found to be a compound heterozygote for a codon 318+1G-->A substitution at the 5'-splice donor site of intron 5, in combination with Q356X, a nonsense mutation previously reported in an African-American patient. A Caucasian patient was found to be a compound heterozygote with a novel missense mutation, T318R, in combination with a previously reported 28-bp deletion in exon 2. A different mutation at codon 318 (T318M) has been described previously. A Caucasian patient was heterozygous for a novel nonsense mutation (Q19X) in exon 2. The second mutation was not identified in this patient. Multiple apparent polymorphisms were also observed. Two of these polymorphisms in CYP11B1 represent sequences from CYP11B2, suggesting that gene conversion may have occurred. In summary, we have identified three novel mutations and two previously reported mutations in CYP11B1 patients with 11 beta-hydroxylase deficiency. Our data suggest the presence of a mutational hot spot at codon 318 of CYP11B1, and the possibility of a founder effect in frequently identified mutations. C1 NIH, Dev Endocrinol Branch, NICHHD, Bethesda, MD 20892 USA. RP Merke, DP (reprint author), NIH, Dev Endocrinol Branch, NICHHD, Bldg 10,Room 10N262,10 Ctr Dr,MSC 1862, Bethesda, MD 20892 USA. RI Toshihiro, Tajima/A-5720-2012 NR 23 TC 56 Z9 60 U1 1 U2 1 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 JAN PY 1998 VL 83 IS 1 BP 270 EP 273 DI 10.1210/jc.83.1.270 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YP375 UT WOS:000071270600050 PM 9435454 ER PT J AU Bornstein, SR Licinio, J Tauchnitz, R Engelmann, L Negrao, AB Gold, P Chrousos, GP AF Bornstein, SR Licinio, J Tauchnitz, R Engelmann, L Negrao, AB Gold, P Chrousos, GP TI Plasma leptin levels are increased in survivors of acute sepsis: Associated loss of diurnal rhythm in cortisol and leptin secretion SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID TUMOR-NECROSIS-FACTOR; CRITICALLY-ILL PATIENTS; NOCTURNAL RISE; POTENTIAL ROLE; ADRENAL-GLAND; SEPTIC SHOCK; WEIGHT-LOSS; EXPRESSION; HUMANS; INTERLEUKIN-6 AB Recent animal and human studies have suggested that leptin secretion is closely linked to the functions of the hypothalamic-pituitary-adrenal (HPA) axis and the immune system, both of which are crucial in influencing the course and outcome of critical illness. Therefore, we measured basal plasma leptin levels and examined the circadian secretion of leptin, in parallel with the hormones of the HPA axis and a key cytokine, interleukin-6, in critically ill patients with acute sepsis. Sixteen critically ill patients from the University of Leipzig Intensive Care Unit were recruited for this study. All of these patients fulfilled the standard diagnostic criteria for sepsis. Plasma leptin levels were measured in all patients and controls at 09:00. In addition, in a subgroup of eight critically ill patients and all of the nine controls plasma leptin, cortisol, ACTH and interleukin-6 concentrations were measured every 4 hours for 24 hours. Mean plasma leptin levels were three-fold higher (18.9 +/- 4.5 ng/ml) in critically ill patients than controls (3.8 +/- 1.0 ng/ml, p<0.05). Similarly, ACTH levels were lower (7.8 +/- 3.4 pmol/l) in patients than in controls (17.1 +/- 1.5 pmol/l, p<.001), while plasma cortisol levels were increased (947.6 +/- 144 nmol/l) in patients compared to controls (361.1+/-29, p<0.001). Morning plasma interleukin-6 levels were markedly elevated in all patients with sepsis (1238.0+/-543.1 pg/ml) versus controls (6.4 +/- 1.7, p<0.001). The controls exhibited a nyctohemeral fluctuation in plasma leptin levels with peak levels at 23:00; in contrast septic patients, had no nocturnal rise of leptin. In healthy controls, plasma leptin and cortisol had reciprocal circadian rhythms with high nocturnal leptin levels and low nocturnal cortisol concentrations; in critically ill patients, this relation was abolished. Mean leptin levels were three-fold higher in patients who survived the septic episode (25.5+/-6.2, n=10) than in non-survivors (8.0+/-3.7, n=6, p<0.01). We conclude that in addition to its function as an anti-obesity factor, leptin may play a role in a severe stress state such as acute sepsis. C1 NICHD, Dev Endocrinol Branch, Bethesda, MD 20892 USA. NIMH, Clin Neuroendocrinol Branch, Bethesda, MD 20892 USA. Univ Leipzig, Dept Internal Med 1, D-04103 Leipzig, Germany. Univ Leipzig, Dept Internal Med 3, D-04103 Leipzig, Germany. RP Bornstein, SR (reprint author), NICHD, Dev Endocrinol Branch, Bethesda, MD 20892 USA. RI Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 39 TC 255 Z9 265 U1 0 U2 7 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 JAN PY 1998 VL 83 IS 1 BP 280 EP 283 DI 10.1210/jc.83.1.280 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YP375 UT WOS:000071270600052 PM 9435456 ER PT J AU Tsai-Morris, CH Geng, Y Buczko, E Dufau, ML AF Tsai-Morris, CH Geng, Y Buczko, E Dufau, ML TI A novel human luteinizing hormone receptor gene SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID CHORIOGONADOTROPIN RECEPTOR; LH RECEPTOR; RAT; PROMOTER; FAMILY AB A novel human luteinizing hormone receptor (LHR) gene was isolated from a human placental genomic library. This gene (Gene II) differs from that previously isolated from a lymphocyte library (Gene I) by several base changes in the 5' flanking region and the deletion of 6 nucleotides in the coding region (+55 to +60). The sequence of the exon 1 coding region of gene II conforms to the sequence of the human ovarian LHR cDNA. Furthermore, primer extension and reporter gene analyses indicate that both the Gene II promoter and the human ovarian LHR mRNA transcriptional start sites are located within the -176 bp TATA-less 5' flanking domain. Additional upstream transcriptional start sites (>-176 bp) were identified in human testicular mRNA and the human choriocarcinoma JAR cell. Restriction enzyme analysis verifies that both LHR genes are present in the human genome, and gene dosing reveals four copies of the human LHR in contrast to a single copy in the rat genome. Chromosomal mapping localizes all copies of the human LHR to the chromosome 2p16-21 loci. These studies suggest that tissue-specific LHR promoter utilization and LHR gene expression may be correlated with gene diversity. C1 NIH, Sect Mol Endocrinol Endocrinol & Reprod Res Bran, NICHHD, Bethesda, MD 20892 USA. RP Dufau, ML (reprint author), NIH, Sect Mol Endocrinol Endocrinol & Reprod Res Bran, NICHHD, Bldg 49, Bethesda, MD 20892 USA. NR 11 TC 28 Z9 29 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 JAN PY 1998 VL 83 IS 1 BP 288 EP 291 DI 10.1210/jc.83.1.288 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA YP375 UT WOS:000071270600054 PM 9435458 ER PT J AU Strober, W Kelsall, B Marth, T AF Strober, W Kelsall, B Marth, T TI Oral tolerance SO JOURNAL OF CLINICAL IMMUNOLOGY LA English DT Review DE oral tolerance; tolerance; Peyer's patch; lamina propria; T cell; macrophage; B cell; cytokines; TGF-beta; IL-12; IL-4; IFN-gamma; clonal deletion; anergy; suppression; suppressor cell; IgA; immunoglobulin ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; SUPPRESSOR T-CELLS; GROWTH-FACTOR-BETA; DELAYED-TYPE HYPERSENSITIVITY; SYSTEMIC IMMUNE-RESPONSES; ESTABLISHED EXPERIMENTAL COLITIS; CHRONIC INTESTINAL INFLAMMATION; DRIVEN BYSTANDER SUPPRESSION; COLLAGEN-INDUCED ARTHRITIS AB Oral tolerance is the immunologic mechanism by which the mucosal immune system maintains unresponsiveness to the myriad of antigens in the mucosal environment which might otherwise induce untoward immune responses. Recent studies have shown that it is mediated by several distinct, yet interacting mechanisms including the generation of suppressive T cells producing antigen nonspecific cytokines and the induction of clonal deletion and/or anergy. In this review of oral tolerance, we discuss these mechanisms in detail and show how oral tolerance or lack therof may explain the occurrence of mucosal inflammation. In addition, we discuss how induction of oral tolerance can be used to treat autoimmune states. C1 NIAID, Mucosal Immun Sect, Clin Invest Lab, NIH, Bethesda, MD 20892 USA. Univ Saarland, Homburg, Germany. RP Strober, W (reprint author), Bldg 10,11N238,10 Ctr Dr, Bethesda, MD 20892 USA. NR 134 TC 112 Z9 116 U1 0 U2 2 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0271-9142 J9 J CLIN IMMUNOL JI J. Clin. Immunol. PD JAN PY 1998 VL 18 IS 1 BP 1 EP 30 DI 10.1023/A:1023222003039 PG 30 WC Immunology SC Immunology GA YT982 UT WOS:000071667600001 PM 9475350 ER PT J AU Sloand, EM Maciejewski, JP Sato, T Bruny, J Kumar, P Kim, S Weichold, FF Young, NS AF Sloand, EM Maciejewski, JP Sato, T Bruny, J Kumar, P Kim, S Weichold, FF Young, NS TI The role of interleukin-converting enzyme in Fas-mediated apoptosis in HIV-1 infection SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE interleukin-converting enzyme; Fas; apoptosis; HIV; AIDS ID ICE-LIKE PROTEASE; T-LYMPHOCYTES; CELL-DEATH; ICE/CED-3 PROTEASE; MOLECULAR-CLONING; INTERFERON-GAMMA; ACTIVATION; IDENTIFICATION; INDIVIDUALS; INVOLVEMENT AB Apoptosis of CD4(+) lymphocytes is partially responsible for the depletion of these cells in HIV-infected individuals, CD4(+) lymphocytes from HIV-l-infected patients express higher membrane levels of the Fas receptor, and are particularly susceptible to apoptosis after Fas triggering, IL-1 beta-converting enzyme (ICE) is a key enzyme of the apoptotic machinery involved in Fas-mediated apoptosis of normal lymphocytes, The role of ICE in mediating the increased susceptibility of CD4(+) lymphocytes from HIV-l-infected patients to apoptosis has not been examined, In this study, we found that ICE mRNA was present in T cells from both HIV-l-infected patients and controls, Active ICE proteins, p10 and p20, were demonstrated by immunoblot in lymphocytes from HIV-l-infected patients and in normal lymphocytes after treatment with Fas agonist, CH11 mAb. Cocultivation of lymphocytes from HIV-l-infected persons with Fas antagonist, antibody ZB4, resulted in decreased expression of ICE protein in lymphocytes from HIV-infected patients, and decreased apoptosis, Similar effects were obtained when cells were treated with synthetic ICE inhibitors, which blocked apoptosis in response to Fas triggering, When CD4(+) and CD8(+) cells were sorted by flow cytometry and analyzed by reverse transcriptase PCR, ICE mRNA was present in both CD8(+) and CD4(+) cells, However, flow cytometric analysis of lymphocytes with intracellular staining for ICE demonstrated ICE protein in the CD4(+) but not the CD8(+) cell fraction derived from blood of HIV-1-infected patients, These data suggest that activation of ICE occurs in vivo in CD4(+) lymphocytes from HIV-l-infected individuals, and may account for the increased susceptibility of CD4(+) cells to apoptosis. C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Med Ctr, Washington, DC 20007 USA. Univ Nevada, Sch Med, Dept Internal Med, Reno, NV 89557 USA. Univ Maryland, Inst Human Virol, Baltimore, MD 21201 USA. RP Sloand, EM (reprint author), NHLBI, Hematol Branch, NIH, Bldg 31,Room 4A11,31 Ctr Dr MSC 2490, Bethesda, MD 20892 USA. EM sloande@gwgate.nhlbi.nih.gov NR 34 TC 24 Z9 24 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN 1 PY 1998 VL 101 IS 1 BP 195 EP 201 DI 10.1172/JCI530 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA YQ513 UT WOS:000071395300024 PM 9421482 ER PT J AU Tanaka, E Tacke, M Kobayashi, M Nakatsuji, Y Kiyosawa, K Schmolke, S Engel, AM Hess, G Alter, HJ AF Tanaka, E Tacke, M Kobayashi, M Nakatsuji, Y Kiyosawa, K Schmolke, S Engel, AM Hess, G Alter, HJ TI Past and present hepatitis G virus infections in areas where hepatitis C is highly endemic and those where it is not endemic SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID NON-B-HEPATITIS; NON-A; POSTTRANSFUSION HEPATITIS; DISEASE ASSOCIATION; LONG-TERM; TRANSFUSION; ANTIBODY; CLONING; JAPAN AB We reported previously on an area in Japan where over 30% of the inhabitants were positive for hepatitis C virus (HCV) antibody, In the present study, clinical features of hepatitis G virus (HGV) infection in this area of high endemicity were compared to those in an area where HCV is not endemic. A total of 400 individuals were selected randomly from those who were medically screened for liver disease in 1993; 200 were from the high-endemicity area, and the other 200 were from the no-endemicity area, HGV RNA was measured by reverse transcription and PCR with primers in the 5' noncoding region, Antibody to HGV envelope protein E2 was measured by an enzyme-linked immunosorbent assay, Prevalence of any HGV marker in the high endemicity area (32%) was significantly (P < 0.0001) higher than that in the no-endemicity area (6%); similar differences, 32% versus 3% (P < 0.0001), had been observed for HCV markers (HCV RNA and HCV antibody), In areas of both high and no endemicity, HCV markers were significantly more prevalent in individuals with any HGV marker than in those without HGV markers, and age-specific prevalence of HGV markers was distributed similarly to that of any HCV marker. Among possible routes of HGV transmission that were analyzed, folk medicine was significant in the high-endemicity area, but blood transfusion was the major route in the no-endemicity area. The rate of accompanying viremia in HGV infection (15%) nas significantly lower than that in HCV infection (78%) (P < 0.0001), In conclusion, HGV infection was highly prevalent in the area of high HCV endemicity and was closely associated with HCV infection, HGV seemed to be transmitted via the practice of folk medicine as well as blood transfusion, HGV resulted in a chronic carrier state less frequently than did HCV. C1 Shinshu Univ, Sch Med, Dept Internal Med 2, Matsumoto, Nagano 390, Japan. NIH, Dept Transfus Med, Bethesda, MD 20892 USA. RP Tanaka, E (reprint author), Shinshu Univ, Sch Med, Dept Internal Med 2, 3-1-1 Asahi, Matsumoto, Nagano 390, Japan. NR 24 TC 24 Z9 25 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1998 VL 36 IS 1 BP 110 EP 114 PG 5 WC Microbiology SC Microbiology GA YM068 UT WOS:000071024700023 PM 9431931 ER PT J AU Brambilla, D Leung, S Lew, J Todd, J Herman, S Cronin, M Shapiro, DE Bremer, J Hanson, C Hillyer, GV McSherry, GD Sperling, RS Coombs, RW Reichelderfer, PS AF Brambilla, D Leung, S Lew, J Todd, J Herman, S Cronin, M Shapiro, DE Bremer, J Hanson, C Hillyer, GV McSherry, GD Sperling, RS Coombs, RW Reichelderfer, PS TI Absolute copy number and relative change in determinations of human immunodeficiency virus type 1 RNA in plasma: Effect of an external standard on kit comparisons SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID AMPLICOR-HIV MONITOR; ZIDOVUDINE TREATMENT; QUANTIFICATION; INFECTION; ASSAY; TRANSMISSION; QUANTITATION; THERAPY; INFANT; AIDS AB Use of a common set of human immunodeficiency virus type 1 (HIV-1) RNA standards eliminated differences among absolute HIV-1 RNA copy number estimates made with three commercially available assays. The relative changes in the viral RNA levels determined by the commercial assays were similar and were unaffected by the use of a common set of standards. C1 New England Res Inst, Watertown, MA 02172 USA. NIAID, Bethesda, MD 20892 USA. Chiron Corp, Emeryville, CA 94608 USA. Roche Mol Syst, Branchburg, NJ 08876 USA. Organon Teknika Corp, Durham, NC 27712 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Rush Presbyterian St Lukes Med Ctr, Chicago, IL 60612 USA. Baylor Coll Med, Houston, TX 77030 USA. Univ Puerto Rico, Sch Med, San Juan, PR 00936 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA. Mt Sinai Med Ctr, New York, NY 10029 USA. Univ Washington, Seattle, WA 98195 USA. RP Reichelderfer, PS (reprint author), NIAID, NIH, DAIDS, 6003 Execut Blvd, Rockville, MD 20776 USA. FU NIAID NIH HHS [N0-AI-35172, N01-AI-95030, U01 AI025883, U01 AI034858, U01 AI027664, P01 AI030731, N01-AI-35161] NR 20 TC 36 Z9 37 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1998 VL 36 IS 1 BP 311 EP 314 PG 4 WC Microbiology SC Microbiology GA YM068 UT WOS:000071024700069 PM 9431977 ER PT J AU Varterasian, ML Mohammad, RM Eilender, DS Hulburd, K Rodriguez, DH Pemberton, PA Pluda, JM Dan, MD Pettit, GR Chen, BDM Al-Katib, AM AF Varterasian, ML Mohammad, RM Eilender, DS Hulburd, K Rodriguez, DH Pemberton, PA Pluda, JM Dan, MD Pettit, GR Chen, BDM Al-Katib, AM TI Phase I study of bryostatin 1 in patients with relapsed non-Hodgkin's lymphoma and chronic lymphocytic leukemia SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LARGE-CELL LYMPHOMA; INVIVO ACTIVITY; DIFFERENTIATION; CHEMOTHERAPY; INVITRO; AGENTS; GROWTH; CANCER; GRADE; LINES AB Purpose: To define, in a phase I study in relapsed non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukemia (CLL), the maximum-tolerated dose (MTD), major toxicities, and possible antitumor activity of bryostatin 1, a macrocyclic lactone. Patients and Methods: Bryostatin 1 was delivered by 72-hour continuous infusion every 2 weeks to patients with relapsed NHL or CLL, at doses that ranged from 12 mu g/m(2) to 180 mu g/m(2) per course. Correlative investigations included evaluations of total protein kinase C (PKC) in peripheral blood and lymphoid differentiation in patient tumor tissue. Results: Twenty-nine patients were treated, including three patients with CLL and 26 with NHL. Generalized myalgia was the dose-limiting toxicity (DLT) and occurred in two of three patients treated with bryostatin 1 at 180 mu g/m(2) per course. Myalgias were dose-related and cumulative, and often started in the thighs and calves, improved with activity, were somewhat responsive to analgesics, and often took weeks to resolve once taken off study Six patients were treated at the MTD of 120 mu g/m(2) pel course. Myalgia, headache, and fatigue were common, Hematologic toxicity was uncommon. Total cumulative doses of bryostatin 1 up to 1,134 mu g/m(2) have been administered without untoward toxicity. Eleven patients achieved stable disease for 2 to 19 months. An in vitro assay for total PKC evaluation in patient peripheral-blood samples demonstrated activation within the first 2 hours with subsequent down-regulation by 24 hours, which was maintained throughout the duration of the 72-hour infusion. Conclusion: This phase 1 study defined the MTD and recommended phase II dose of bryostatin 1, when administered over 72 hours every 2 weeks, to be 120 mu g/m(2) (40 mu g/m(2)/d for 3 days). Generalized myalgia was the DLT. Future studies will define the precise activity of bryostatin 1 in subsets elf patients with lymphoproliferative malignancies and its efficacy in combination with other agents. (C) 1998 by American Society of Clinical Oncology. C1 Karmanos Canc Inst, Detroit, MI USA. NCI, Invest Drug Branch, Canc Therapy Evaluat Program, Div Canc Treatment & Diagnosis, Rockville, MD USA. Arizona State Univ, Dept Chem, Tempe, AZ 85287 USA. RP Varterasian, ML (reprint author), Wayne State Univ, Harper Hosp, Div Hematol & Oncol, 3990 John R,4 Brush S, Detroit, MI 48201 USA. FU NCI NIH HHS [CA 22453-19, U01 CA62487-03] NR 25 TC 89 Z9 91 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1998 VL 16 IS 1 BP 56 EP 62 PG 7 WC Oncology SC Oncology GA YQ270 UT WOS:000071368500010 PM 9440723 ER PT J AU Berg, SL Blaney, SM Adamson, PC O'Brien, M Poplack, DG Arndt, C Blatt, J Balis, FM AF Berg, SL Blaney, SM Adamson, PC O'Brien, M Poplack, DG Arndt, C Blatt, J Balis, FM TI Phase I trial and pharmacokinetic study of pyrazoloacridine in children and young adults with refractory cancers SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ANTICANCER AGENTS; NSC-366140; PD115934 AB Purpose: To define the maximum-tolerated dose (MTD), quantitative and qualitative toxicities, recommended phase II dose, and pharmacokinetics of pyrazoloacridine (PZA) administered as a 1- or 24-hour infusion in children and young adults with refractory cancers. Patients and Methods: Twenty-two patients received PZA as a 1-hour infusion at doses of 380 mg/m(2) (n = 3), 495 mg/m(2) (n = 6), 640 mg/m(2) (n = 6), and 835 mg/m(2) (n = 7). An additional four patients received PZA as a 24-hour infusion at the MTD (640 mg/m(2)) for the 1-hour infusion schedule. Plasma samples were obtained for pharmacokinetic analysis in 17 patients. PZA concentration in plasma was measured by reverse-phase highperformance liquid chromatography (HPLC). A two-compartment pharmacokinetic model was fit to the PZA plasma concentration data. Results: On the 1-hour infusion schedule, dose-limiting myelosuppression (neutropenia more than thrombocytopenia) was observed in two of seven patients at the 835-mg/m(2) dose level. Myelosuppression did not appear to be ameliorated by prolonging the infusion to 24 hours. Nonhematologic toxicities were minor. Significant neurotoxicity, which was dose-limiting in adults treated with a 1-hour infusion of PZA, was observed in one patient treated at 640 mg/m(2), but was not dose-limiting. There was marked interpatient variability in plasma PZA concentrations at all dose levels. The pharmacokinetic profile of PZA was characterized by an initial rapid decline (alpha half-life [t(1/2)alpha], 0.5 hours) followed by a prolonged elimination phase (t(1/2)beta, 30 hours). The volume of distribution at steady-state (Vd(ss)) was 700 L/m(2) and the clearance was 300 ml/min/m(2). There was no evidence of dose-dependent clearance. The area under the PZA concentration-time curve (AUC) correlated poorly with dose and was more predictive of the degree of myelosuppression than was PZA dose. Conclusion: PZA administered as 1- or 24-hour infusion is well tolerated by children and young adults. The dose-limiting toxicity (DLT) is myelosuppression. Neurotoxicity is not prominent in this age group. There was marked interpatient variation in plasma concentrations of PZA. The recommended dose for phase II studies is 640 mg/m(2). (C) 1998 by American Society of Clinical Oncology. C1 Baylor Coll Med, Texas Childrens Canc Ctr, Houston, TX 77030 USA. Texas Childrens Hosp, Texas Childrens Canc Ctr, Houston, TX 77030 USA. NCI, Pediat Branch, Bethesda, MD 20892 USA. Mayo Clin, Rochester, MN USA. Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA. RP Berg, SL (reprint author), Baylor Coll Med, Texas Childrens Canc Ctr, 6621 Fannin St,MC 3-3320, Houston, TX 77030 USA. NR 17 TC 13 Z9 13 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 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1998 VL 16 IS 1 BP 181 EP 186 PG 6 WC Oncology SC Oncology GA YQ270 UT WOS:000071368500028 PM 9440741 ER PT J AU Yang, JC Chang, AE Baker, AR Sindelar, WF Danforth, DN Topalian, SL Delaney, T Glatstein, E Steinberg, SM Merino, MJ Rosenberg, SA AF Yang, JC Chang, AE Baker, AR Sindelar, WF Danforth, DN Topalian, SL Delaney, T Glatstein, E Steinberg, SM Merino, MJ Rosenberg, SA TI Randomized prospective study of the benefit of adjuvant radiation therapy in the treatment of soft tissue sarcomas of the extremity SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LOCAL RECURRENCE; SUPERFICIAL TRUNK; CHEMOTHERAPY; TRIAL; BRACHYTHERAPY; METASTASES; MANAGEMENT; SURVIVAL; SURGERY; ADULTS AB Purpose: This randomized, prospective study assesses the impact of postoperative external-beam radiation therapy on local recurrence (LR), overall survival (OS), and quality of life after limb-sparing resection of extremity sarcomas. Patients and Methods: Patients with extremity tumors and a limb-sparing surgical option were randomized to receive or not receive postoperative adjuvant external-beam radiotherapy. Patients with high-grade sarcomas received postoperative adjuvant chemotherapy whereas patients with low-grade sarcomas or locally aggressive nonmalignant tumors were randomized after surgery alone, Results: Ninety-one patients with high-grade lesions were randomized; 47 to receive radiotherapy (XRT) and 44 to not receive XRT. With a median follow-up of 9.6 years, a highly significant decrease (P-2 = .0028) in the probability of LR was seen with radiation, but no difference in OS was shown, Of 50 patients with low-grade lesions (24 randomized to resection alone and 26 to resection and postoperative XRT), there was also a lower probability of LR (P-2 = .016) in patients receiving XRT, again, without a difference in OS. A concurrent quality-of-life study showed that extremity radiotherapy resulted in significantly worse limb strength, edema, and range of motion, but these deficits were often transient and had few measurable effects on activities of daily life or global quality of life, Conclusion: This study indicates that although postoperative external-beam radiotherapy is highly effective in preventing LRs, selected patients with extremity soft tissue sarcoma who have a low risk of LR may not require adjuvant XRT after limb-sparing surgery (LSS). (C) 1998 by American Society of Clinical Oncology. C1 NCI, Surg Branch, Bethesda, MD 20892 USA. NCI, Radiat Oncol Branch, Biostat & Data Management Sect, Bethesda, MD 20892 USA. NCI, Lab Surg Pathol, Bethesda, MD 20892 USA. RP Yang, JC (reprint author), NCI, Surg Branch, Bldg 10,Room 2B37, Bethesda, MD 20892 USA. EM jcyang@NCI.NIH.gov NR 31 TC 651 Z9 678 U1 1 U2 10 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1998 VL 16 IS 1 BP 197 EP 203 PG 7 WC Oncology SC Oncology GA YQ270 UT WOS:000071368500030 PM 9440743 ER PT J AU Smith, MA Ungerleider, RS Korn, EL Rubinstein, L Simon, R AF Smith, MA Ungerleider, RS Korn, EL Rubinstein, L Simon, R TI Secrecy for Data Monitoring Committees: Inferior ethics, bad policy - Reply SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter C1 NCI, Bethesda, MD 20892 USA. RP Smith, MA (reprint author), NCI, Bethesda, MD 20892 USA. NR 2 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 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1998 VL 16 IS 1 BP 391 EP 391 PG 1 WC Oncology SC Oncology GA YQ270 UT WOS:000071368500061 ER PT J AU Meltzer, HY Casey, DE Garver, DL Marder, SR Masand, PS Miller, D Pickar, D Tandon, R AF Meltzer, HY Casey, DE Garver, DL Marder, SR Masand, PS Miller, D Pickar, D Tandon, R CA Collaborative Working Grp Clinical Trial Evalua TI Measuring outcome in schizophrenia: Differences among the atypical antipsychotics SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Symposium Clinical Trial Evaluations and Outcome Measures in Psychiatry CY NOV 21, 1997 CL CHICAGO, ILLINOIS ID DOUBLE-BLIND; OLANZAPINE TRIAL; RISPERIDONE; PLACEBO; HALOPERIDOL; CLOZAPINE; QUALITY; SCALE; LIFE; MULTICENTER AB The advent of the atypical antipsychotics marked a new era in the history of the treatment of psychotic disorders. To evaluate the published literature about the available atypical antipsychotics-clozapine, risperidone, olanzapine, and quetiapine-and select the most appropriate treatment for specific patients, physicians need to understand the outcome measures used in clinical studies, the pharmacologic differences that explain varying side effect profiles, and pharmacoeconomic assessments that are used in the decision-making process. While the atypical antipsychotics have established efficacy in the overall treatment of schizophrenia, they may differ in their effects on factors such as cognitive function, overall quality of life, adverse events, and hospitalization status. Each of these factors should be considered when weighing treatment options for an individual patient. C1 Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, Nashville, TN 37212 USA. Vet Affairs Med Ctr, Psychiat Serv, Portland, OR USA. Vet Affairs N Texas Med Ctr, Dallas, TX USA. Tufts Univ, Boston, MA 02111 USA. W Los Angeles Vet Affairs Med Ctr, Psychiat Serv, Los Angeles, CA 90073 USA. SUNY Hlth Sci Ctr, Dept Psychiat, Syracuse, NY 13210 USA. Univ Iowa Hosp & Clin, Dept Psychiat, Iowa City, IA 52242 USA. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. Univ Michigan, Med Ctr, Ann Arbor, MI USA. RP Meltzer, HY (reprint author), Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, 1601 23rd Ave S,Suite 306, Nashville, TN 37212 USA. RI Meltzer, Herbert/E-8131-2013 NR 40 TC 35 Z9 36 U1 1 U2 4 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 12 BP 3 EP 9 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120FD UT WOS:000075943700001 ER PT J AU Murphy, DL Andrews, AM Wichems, CH Li, Q Tohda, M Greenberg, B AF Murphy, DL Andrews, AM Wichems, CH Li, Q Tohda, M Greenberg, B TI Brain serotonin neurotransmission: An overview and update with an emphasis on serotonin subsystem heterogeneity, multiple receptors, interactions with other neurotransmitter systems, and consequent implications for understanding the actions of serotonergic drugs SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Roundtable Symposium on Optimizing Clinical Use of SSRIs - Theory and Practice CY DEC 06, 1997 CL SAN FRANCISCO, CALIFORNIA ID CHRONIC ANTIDEPRESSANT TREATMENT; PRIMARY PULMONARY-HYPERTENSION; MEDIAN RAPHE NUCLEI; A-DEFICIENT MICE; REUPTAKE INHIBITORS; 5-HT2C RECEPTOR; ACETYLCHOLINE-RELEASE; AGGRESSIVE-BEHAVIOR; MESSENGER-RNAS; IN-VIVO AB Knowledge about serotonergic neurotransmission has been expanding rapidly. Recent research has delineated 15 molecularly different serotonin receptors and multiple, discrete neuronal and nonneuronal (including endocrine) pathways and mechanisms that mediate the many functions of serotonin. Nonetheless, gaps remain regarding aspects of the anatomy and physiology of serotonin in its roles as a neurotransmitter, a neuromodulator, and a hormone. Few serotonin receptor-selective drugs are available for clinical use. A group of selective serotonin reuptake inhibitors (SSRIs) remain the agents with greatest therapeutic utility, although the mechanisms underlying their delayed efficacy, which clearly result from adaptive consequences following repeated administration rather than early uptake inhibition of serotonin by itself, are incompletely understood and appear to involve changes in signal transduction and gene expression in serotonergic and other neurotransmitter systems. C1 NIMH, Clin Sci Lab, Intramural Res Program, Clin Ctr,NIH, Bethesda, MD 20892 USA. RP Murphy, DL (reprint author), NIMH, Clin Sci Lab, Intramural Res Program, Clin Ctr,NIH, 10-3D41, Bethesda, MD 20892 USA. RI Andrews, Anne/B-4442-2011 OI Andrews, Anne/0000-0002-1961-4833 NR 118 TC 90 Z9 92 U1 3 U2 15 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 15 BP 4 EP 12 PG 9 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 126ZP UT WOS:000076325500002 PM 9786305 ER PT J AU Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R AF Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R CA Collaborative Working Grp Clinical Trial Evalua TI Clinical development of atypical antipsychotics: Research design and evaluation SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Symposium Clinical Trial Evaluations and Outcome Measures in Psychiatry CY NOV 21, 1997 CL CHICAGO, ILLINOIS ID BLIND OLANZAPINE TRIAL; SCHIZOPHRENIC-PATIENTS; PARALLEL-GROUP; HALOPERIDOL; PLACEBO; RISPERIDONE; MULTICENTER; QUETIAPINE; CHLORPROMAZINE; CLOZAPINE AB Clinical trials support the efficacy and safety of new drugs on the market. They provide the United States Food and Drug Administration with the information needed to approve an Investigational New Drug application and are the basis for package inserts provided by the manufacturers that guide clinicians in the use of a new drug. Because clinical trials are vital to the effective and safe use of new drugs, it is important to understand who participates in them, what questions are answered by clinical trials, and what questions are raised. The reader who asks the proper questions about issues such as methodology, affiliations of the investigators, statistical analyses performed, location of study centers, and study populations will derive the most information from the report of a clinical trial. C1 Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, Nashville, TN 37212 USA. Vet Affairs Med Ctr, Psychiat Serv, Portland, OR USA. Vet Affairs N Texas Med Ctr, Dallas, TX USA. Tufts Univ, Boston, MA 02111 USA. W Los Angeles Vet Affairs Med Ctr, Psychiat Serv, Los Angeles, CA 90073 USA. SUNY Hlth Sci Ctr, Dept Psychiat, Syracuse, NY 13210 USA. Univ Iowa Hosp & Clin, Dept Psychiat, Iowa City, IA 52242 USA. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. Univ Michigan, Med Ctr, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Meltzer, HY (reprint author), Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, 1601 23rd Ave S,Suite 306, Nashville, TN 37212 USA. RI Meltzer, Herbert/E-8131-2013 NR 25 TC 0 Z9 0 U1 2 U2 2 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 12 BP 10 EP 16 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120FD UT WOS:000075943700002 ER PT J AU Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R AF Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R CA Collaborative Working Grp Clinical Trial Evalua TI Adverse effects of the atypical antipsychotics SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Symposium Clinical Trial Evaluations and Outcome Measures in Psychiatry CY NOV 21, 1997 CL CHICAGO, ILLINOIS ID BLIND OLANZAPINE TRIAL; SCHIZOPHRENIC PATIENTS; CLOZAPINE; HALOPERIDOL; RISPERIDONE; PLACEBO; DRUGS; SERTINDOLE; DOPAMINE; MULTICENTER AB Adverse effects of antipsychotics often lead to noncompliance. Thus, clinicians should address patients' concerns about adverse effects and attempt to choose medications that will improve their patients' quality of life as well as overall health. The side effect profiles of the atypical antipsychotics are more advantageous than those of the conventional neuroleptics. Conventional agents are associated with unwanted central nervous system effects, including extrapyramidal symptoms (EPS), tardive dyskinesia, sedation, and possible impairment of some cognitive measures, as well as cardiac effects, orthostatic hypotension, hepatic changes, anticholinergic side effects, sexual dysfunction, and weight gain. The newer atypical agents have a lower risk of EPS, but are associated in varying degrees with sedation, cardiovascular effects, anticholinergic effects, weight gain, sexual dysfunction, hepatic effects, lowered seizure threshold (primarily clozapine), and agranulocytosis (clozapine only). Since the incidence and severity of specific adverse effects differ among the various atypicals, the clinician should carefully consider which side effects are most likely-to lead to the individual's dissatisfaction and noncompliance before choosing an antipsychotic for a particular patient. C1 Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, Nashville, TN 37212 USA. Vet Affairs Med Ctr, Psychiat Serv, Portland, OR USA. Vet Affairs N Texas Med Ctr, Dallas, TX USA. Tufts Univ, Boston, MA 02111 USA. W Los Angeles Vet Affairs Med Ctr, Psychiat Serv, Los Angeles, CA 90073 USA. SUNY Hlth Sci Ctr, Dept Psychiat, Syracuse, NY 13210 USA. Univ Iowa Hosp & Clin, Dept Psychiat, Iowa City, IA 52242 USA. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. Univ Michigan, Med Ctr, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Meltzer, HY (reprint author), Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, 1601 23rd Ave S,Suite 306, Nashville, TN 37212 USA. RI Meltzer, Herbert/E-8131-2013 NR 57 TC 5 Z9 8 U1 2 U2 3 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 12 BP 17 EP 22 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120FD UT WOS:000075943700003 ER PT J AU Zametkin, AJ Liotta, W AF Zametkin, AJ Liotta, W TI The neurobiology of attention-deficit/hyperactivity disorder SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on Current Issues in Attention Deficit Disorders CY NOV 13, 1996 CL BLOOMINGDALE, ILLINOIS SP Inst Med Studies, Wyeth Ayerst Labs ID DEFICIT-HYPERACTIVITY DISORDER; CEREBRAL GLUCOSE-METABOLISM; QUANTITATIVE MORPHOLOGY; DOPAMINE TRANSPORTER; BRAIN METABOLISM; CORPUS-CALLOSUM; CAUDATE-NUCLEUS; THYROID-HORMONE; ADULTS; CHILDREN AB We provide a comprehensive review of the neurobiological basis of attention-deficit/hyperactivity disorder. This summary was accomplished by a review of research in three areas: neuroimaging, genetics, and neurochemistry. Additionally, we also discuss a newer conceptualization of the disorder. Although none of the current findings present a unified picture of the pathophysiology of the disorder, the vast array of studies reviewed do highlight CNS abnormalities that, when taken together, present a convincing argument that the cause clearly resides within the realm of developing brain. C1 NIMH, Bethesda, MD 20892 USA. RP Zametkin, AJ (reprint author), NIMH, Bethesda, MD 20892 USA. NR 43 TC 66 Z9 69 U1 6 U2 11 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 7 BP 17 EP 23 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA ZY498 UT WOS:000074627800003 PM 9680049 ER PT J AU Meltzer, HY Casey, DE Garver, DL Lasagna, S Marder, SR Masand, PS Miller, D Pickar, D Tandon, R AF Meltzer, HY Casey, DE Garver, DL Lasagna, S Marder, SR Masand, PS Miller, D Pickar, D Tandon, R CA Collaborative Working Grp Clinical Trial Evalua TI Assessment of EPS and tardive dyskinesia in clinical trials SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Symposium Clinical Trial Evaluations and Outcome Measures in Psychiatry CY NOV 21, 1997 CL CHICAGO, ILLINOIS ID DOUBLE-BLIND; ANTIPSYCHOTIC-DRUGS; OLANZAPINE TRIAL; SCHIZOPHRENIA; HALOPERIDOL; RISPERIDONE; PLACEBO; CLOZAPINE; SYMPTOMS; MULTICENTER AB The incidence of acute extrapyramidal symptoms (EPS)-akathisia, dystonia, and parkinsonism-associated with traditional antipsychotics varies, but most researchers agree that neuroleptic-induced EPS occur in 50% to 75% of patients who take conventional antipsychotics. Atypical antipsychotics were developed to widen the therapeutic index and to reduce EPS. Although the mechanisms are unclear, the risk of EPS is less with the novel antipsychotics than with conventional drugs, and agents that produce low levels of acute EPS are likely to produce less tardive dyskinesia. Nevertheless; clinicians should exercise caution when comparing data from investigations of the novel antipsychotics and, until long-term data become available, should administer the new drugs at doses below the EPS-producing level. C1 Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, Nashville, TN 37212 USA. Vet Affairs Med Ctr, Psychiat Serv, Portland, OR USA. Vet Affairs N Texas Med Ctr, Dallas, TX USA. Tufts Univ, Boston, MA 02111 USA. W Los Angeles Vet Affairs Med Ctr, Psychiat Serv, Los Angeles, CA 90073 USA. Univ Iowa Hosp & Clin, Dept Psychiat, Iowa City, IA 52242 USA. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. Univ Michigan, Med Ctr, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Meltzer, HY (reprint author), Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, 1601 23rd Ave S,Suite 306, Nashville, TN 37212 USA. RI Meltzer, Herbert/E-8131-2013 NR 27 TC 0 Z9 0 U1 2 U2 2 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 12 BP 23 EP 27 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120FD UT WOS:000075943700004 ER PT J AU Meltzer, HY Casey, DE Garver, DL Marder, SR Masand, PS Miller, D Pickar, D Tandon, R AF Meltzer, HY Casey, DE Garver, DL Marder, SR Masand, PS Miller, D Pickar, D Tandon, R CA Collaborative Working Grp Clinical Trial Evalua TI Assessing the effects of atypical antipsychotics on negative symptoms SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Symposium Clinical Trial Evaluations and Outcome Measures in Psychiatry CY NOV 21, 1997 CL CHICAGO, ILLINOIS ID DOUBLE-BLIND; SCHIZOPHRENIC-PATIENTS; REFRACTORY SCHIZOPHRENIA; NEUROLEPTIC TREATMENT; RISPERIDONE; HALOPERIDOL; PLACEBO; OLANZAPINE; CLOZAPINE; TRIAL AB Attempts to clarify the domains of schizophrenia gained importance when the atypical antipsychotics joined the armamentarium of schizophrenia treatments because of evidence that these agents art: superior to conventional antipsychotics for the treatment of negative symptoms. Negative symptoms can be divided into 3 components: (1) deficit or primary enduring negative symptoms that may or may not respond to treatment, (2) primary nonenduring negative symptoms, and (3) secondary negative symptoms that are associated with positive symptoms, extrapyramidal symptoms, depression, and environmental deprivation. The atypical antipsychotics have generally been found to be more effective than conventional antipsychotics against the totality of negative symptoms, but their effects on specific components are still under study. Sophisticated statistical tools such as path analysis have been used in investigations of the direct and indirect effects of atypical antipsychotics on negative symptoms, but these tools have limitations. Future study is needed to identify specific components of negative symptoms that may respond preferentially to one or another of the atypical antipsychotics. C1 Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, Nashville, TN 37212 USA. Vet Affairs Med Ctr, Psychiat Serv, Portland, OR USA. Vet Affairs N Texas Med Ctr, Dallas, TX USA. Tufts Univ, Boston, MA 02111 USA. W Los Angeles Vet Affairs Med Ctr, Psychiat Serv, Los Angeles, CA 90073 USA. SUNY Hlth Sci Ctr, Dept Psychiat, Syracuse, NY 13210 USA. Univ Iowa Hosp & Clin, Dept Psychiat, Iowa City, IA 52242 USA. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. Univ Michigan, Med Ctr, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Meltzer, HY (reprint author), Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, 1601 23rd Ave S,Suite 306, Nashville, TN 37212 USA. RI Meltzer, Herbert/E-8131-2013 NR 47 TC 7 Z9 7 U1 4 U2 8 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 12 BP 28 EP 34 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120FD UT WOS:000075943700005 ER PT J AU Tune, LE Sunderland, T AF Tune, LE Sunderland, T TI New cholinergic therapies: Treatment tools for the psychiatrist SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on Alzheimer's Disease Management - Algorithmic Strategies for Diagnosis and Treatment CY MAY 17, 1997 CL SAN DIEGO, CALIFORNIA SP Amer Psychiat Assoc ID ESTROGEN REPLACEMENT THERAPY; ALZHEIMERS-DISEASE; CONTROLLED TRIAL; DEMENTIA; TACRINE; RISK AB This article reviews the current status of therapy with acetylcholine-enhancing compounds in the management of patients with Alzheimer's disease. The focus is on pivotal articles investigating the role of cholinergic augmentation strategies, including precursor loading and acetylcholinesterase (AChE) inhibitors, in the management of cognitive and noncognitive symptoms of Alzheimer's disease. Precursor loading strategies have been for the most part unimpressive. By contrast, studies with AChE inhibitors-tacrine and donepezil-have been promising. For patients in whom hepatotoxicity and gastrointestinal side effects were not problematic, tacrine improves cognitive performance and selected secondary psychiatric symptoms and significantly delays nursing home placement. Donepezil, recently approved for use in mild to moderate Alzheimer's disease, appears to be less toxic and better tolerated than tacrine. It improves performance on cognitive testing and, in one preliminary investigation, demonstrated a sustained drug effect over several years. Therapy with AChE inhibitors provides modest significant symptomatic improvement in patients with mild to moderate Alzheimer's disease. C1 Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Wesley Woods Ctr Aging, Atlanta, GA 30329 USA. NIMH, Geriatr Psychiat Branch, NIH, Bethesda, MD 20892 USA. RP Tune, LE (reprint author), Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Wesley Woods Ctr Aging, 1841 Clifton Rd NE, Atlanta, GA 30329 USA. NR 21 TC 11 Z9 11 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 13 BP 31 EP 35 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120VJ UT WOS:000075977800005 PM 9771828 ER PT J AU Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R AF Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R CA Collaborative Working Grp Clinical Trial Evalua TI Evaluating the effects of antipsychotics on cognition in schizophrenia SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Symposium Clinical Trial Evaluations and Outcome Measures in Psychiatry CY NOV 21, 1997 CL CHICAGO, ILLINOIS ID NEGATIVE SYMPTOMS; CLOZAPINE; DYSFUNCTION; RISPERIDONE; IMPROVEMENT; DEFICITS; DECLINE; AGENTS; MEMORY AB Cognitive deficits are an integral feature of schizophrenia and have a deleterious effect on the ability of schizophrenic patients to work and function in a social environment. Drugs that bring about substantial cognitive improvement represent a major contribution in improving the quality of life in schizophrenia. Recent studies have suggested that the atypical antipsychotics may be more useful than conventional agents for improving cognition. There is evidence that scores on neuropsychological assessments have improved after treatment with clozapine, risperidone, and quetiapine. Future research is needed to characterize and quantify the cognitive effects of the atypical antipsychotics. C1 Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, Nashville, TN 37212 USA. Vet Affairs Med Ctr, Psychiat Serv, Portland, OR USA. Vet Affairs N Texas Med Ctr, Dallas, TX USA. Tufts Univ, Boston, MA 02111 USA. W Los Angeles Vet Affairs Med Ctr, Psychiat Serv, Los Angeles, CA 90073 USA. SUNY Hlth Sci Ctr, Dept Psychiat, Syracuse, NY 13210 USA. Univ Iowa Hosp & Clin, Dept Psychiat, Iowa City, IA 52242 USA. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. Univ Michigan, Med Ctr, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Meltzer, HY (reprint author), Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, 1601 23rd Ave S,Suite 306, Nashville, TN 37212 USA. RI Meltzer, Herbert/E-8131-2013 NR 22 TC 2 Z9 2 U1 1 U2 3 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 12 BP 35 EP 40 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120FD UT WOS:000075943700006 ER PT J AU Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R AF Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R CA Collaborative Working Grp Clinical Trial Evalua TI Atypical antipsychotics for treatment of depression in schizophrenia and affective disorders SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Symposium Clinical Trial Evaluations and Outcome Measures in Psychiatry CY NOV 21, 1997 CL CHICAGO, ILLINOIS ID PSYCHOTIC MOOD DISORDERS; SCHIZOAFFECTIVE DISORDER; NEGATIVE SYMPTOMS; RISPERIDONE; CLOZAPINE; HALOPERIDOL; OLANZAPINE; SCALE; MANIA AB Depression in schizophrenia may be partially responsible for the increased suicide rate in schizophrenic patients, which is more than 20 times higher than that found in the general population. Affective disorders in patients with schizophrenia are associated with a poor outcome, an increased risk of relapse, and a high rate of suicide. There is evidence that atypical antipsychotics may contribute to a reduction in suicidality, and although the new drugs are marketed for the treatment of schizophrenia, their novel psychopharmacologic effects suggest the possibility of other therapeutic applications. Recent studies of the efficacy of the novel antipsychotics found that these agents may produce an antidepressant effect in schizophrenia and may be used as either an adjunctive medication or an alternative to mood stabilizers in patients with affective disorders. C1 Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, Nashville, TN 37212 USA. Vet Affairs Med Ctr, Psychiat Serv, Portland, OR USA. Tufts Univ, Boston, MA 02111 USA. W Los Angeles Vet Affairs Med Ctr, Psychiat Serv, Los Angeles, CA 90073 USA. Vet Affairs N Texas Med Ctr, Dallas, TX USA. SUNY Hlth Sci Ctr, Dept Psychiat, Syracuse, NY 13210 USA. Univ Iowa Hosp & Clin, Dept Psychiat, Iowa City, IA 52242 USA. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. Univ Michigan, Med Ctr, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Meltzer, HY (reprint author), Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, 1601 23rd Ave S,Suite 306, Nashville, TN 37212 USA. RI Meltzer, Herbert/E-8131-2013 NR 28 TC 1 Z9 1 U1 4 U2 5 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 12 BP 41 EP 45 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120FD UT WOS:000075943700007 ER PT J AU Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R AF Meltzer, HY Casey, DE Garver, DL Lasagna, L Marder, SR Masand, PS Miller, D Pickar, D Tandon, R CA Collaborative Working Grp Clinical Trial Evalua TI Treatment of special populations with the atypical antipsychotics SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Closed Symposium Clinical Trial Evaluations and Outcome Measures in Psychiatry CY NOV 21, 1997 CL CHICAGO, ILLINOIS ID RISPERIDONE; SCHIZOPHRENIA; CLOZAPINE; DISORDERS; PSYCHOSIS; SYMPTOMS; EFFICACY AB Atypical antipsychotics have become the treatment of choice for patients experiencing a first episode of schizophrenia. In addition, they are often prescribed for conditions such as bipolar disorder and dementia. While clinical trials have not yet established the efficacy of the atypical antipsychotics for these uses, a number of reports offer preliminary evidence that the atypical antipsychotics may be beneficial for affective disorders, substance abuse disorder, senile dementia, and pathologic aggression. Atypical agents may be particularly effective and tolerable in elderly patients who are especially susceptible to the adverse effects of conventional antipsychotic medication. Lower dosages are more necessary for the elderly than for younger adults. Current evidence suggests that clozapine is the most effective atypical antipsychotic for neuroleptic-resistant patients. Risperidone, olanzapine, and quetiapine may also be effective in a subset of these patients. C1 Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, Nashville, TN 37212 USA. Vet Affairs Med Ctr, Psychiat Serv, Portland, OR USA. Vet Affairs N Texas Med Ctr, Dallas, TX USA. Tufts Univ, Boston, MA 02111 USA. W Los Angeles Vet Affairs Med Ctr, Psychiat Serv, Los Angeles, CA 90073 USA. SUNY Hlth Sci Ctr, Dept Psychiat, Syracuse, NY 13210 USA. Univ Iowa Hosp & Clin, Dept Psychiat, Iowa City, IA 52242 USA. NIMH, Intramural Res Program, Bethesda, MD 20892 USA. Univ Michigan, Med Ctr, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Meltzer, HY (reprint author), Vanderbilt Univ, Sch Med, Dept Psychiat, Div Psychopharmacol, 1601 23rd Ave S,Suite 306, Nashville, TN 37212 USA. RI Meltzer, Herbert/E-8131-2013 NR 35 TC 1 Z9 1 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1998 VL 59 SU 12 BP 46 EP 52 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120FD UT WOS:000075943700008 ER PT J AU Moody, SL Zipser, D AF Moody, SL Zipser, D TI A model of reaching dynamics in primary motor cortex SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID NEURONAL POPULATION VECTOR; FREE ARM MOVEMENTS; CORTICAL ACTIVITY; 3-DIMENSIONAL SPACE; VISUAL TARGETS; RHESUS-MONKEYS; NEURAL-NETWORK; DIRECTION; REPRESENTATION; TRAJECTORIES AB Features of virtually all voluntary movements are represented in the primary motor cortex. The movements can be ongoing, imminent, delayed, or imagined. Our goal was to investigate the dynamics of movement representation in the motor cortex. To do this we trained a fully recurrent neural network to continually output the direction and magnitude of movements required to reach randomly changing targets. Model neurons developed preferred directions and other properties similar to real motor cortical neurons. The key finding is that when the target for a reaching movement changes location, the ensemble representation of the movement changes nearly monotonically, and the individual neurons comprising the representation exhibit strong, nonmonotonic transients. These transients serve as internal recurrent signals that force the ensemble representation to change more rapidly than if it were limited by the time constants of individual neurons. These transients, if they exist, could be observed in experiments that require only slight modifications of the standard paradigm used to investigate movement representation in the motor cortex. C1 NIMH, Lab Syst Neurosci, Poolesville, MD 20837 USA. Univ Calif San Diego, San Diego, CA 92103 USA. RP Moody, SL (reprint author), NIMH, Lab Syst Neurosci, POB 608, Poolesville, MD 20837 USA. FU NIMH NIH HHS [5R01MH45271] NR 35 TC 12 Z9 12 U1 0 U2 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD JAN PY 1998 VL 10 IS 1 BP 35 EP 45 DI 10.1162/089892998563761 PG 11 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA YV645 UT WOS:000071848500002 PM 9526081 ER PT J AU Stager, SV Ludlow, SL AF Stager, SV Ludlow, SL TI The effects of fluency-evoking conditions on voicing onset types in persons who do and do not stutter SO JOURNAL OF COMMUNICATION DISORDERS LA English DT Article DE dysfluency; hard onset; breathy onset; fluency-evoking conditions ID SYLLABIC STRESS; PATTERN; EVENTS AB Voicing onset changes between control conditions and three fluency-evoking conditions (choral reading [CHORAL], delayed auditory feedback [DAF], and noise [NOISE]) were studied in 12 persons who do not stutter and 10 who do stutter. Voicing onsets were distinguished physiologically using airflow prior to voicing, with zero airflow prevoicing categorized as hard and the rest as breathy. Persons who stutter were more fluent under all fluency-evoking conditions than control conditions. Speaking under fluency-evoking conditions did not significantly increase the overall proportion of breathy onsets from control conditions for either group. However, looking only at hard onsets in the control condition, we found that both groups changed significantly more to breathy (p = 0.001) under CHORAL and NOISE. In persons who stutter, onset type was not associated with whether a word was produced fluently or dysfluently in the control condition. Also, no relationship was found between onsets changing to breathy under fluency-evoking conditions and onsets changing to fluent. The results suggest that although fluency-evoking conditions can modify some voicing onset behaviors, these modifications do not relate to improvements in fluency. Published by Elsevier Science Inc. C1 NATL INST DEAFNESS & OTHER COMMUN DISORDERS, VOICE & SPEECH SECT, BETHESDA, MD USA. OI Stager, Sheila/0000-0002-4294-2114; Ludlow, Christy/0000-0002-2015-6171 NR 41 TC 6 Z9 7 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0021-9924 J9 J COMMUN DISORD JI J. Commun. Disord. PD JAN-FEB PY 1998 VL 31 IS 1 BP 33 EP 52 DI 10.1016/S0021-9924(97)00049-X PG 20 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA YL169 UT WOS:A1998YL16900002 PM 9421766 ER PT J AU Mccrae, RR Costa, PT del Pilar, GH Rolland, JP Parker, WD AF Mccrae, RR Costa, PT del Pilar, GH Rolland, JP Parker, WD TI Cross-cultural assessment of the five-factor model - The revised NEO personality inventory SO JOURNAL OF CROSS-CULTURAL PSYCHOLOGY LA English DT Article ID 5-FACTOR MODEL; DIMENSIONS; TRAITS; GENERALIZABILITY; PERCEPTION; JAPANESE; LANGUAGE; TAXONOMY; RATINGS AB The five-factor model (FFM) is a representation of the patterns of covariation of personality traits in terms of five broad factors. The Revised NEO Personality Inventory, a questionnaire measure of the FFM, has recently been translated into a number of different languages, permitting tests of its cross-cultural replicability. Data from Filipino and French translations are presented, showing clear and detailed replication of the American normative factor structure when targeted rotation is used. Results from these and other cross-cultural and behavior genetic studies suggest that the FFM is a biologically based human universal. Applications of trait psychology in clinical, educational, and organizational settings may prove generalizable across cultures, and cross-cultural psychologists can profitably explore the expression of the same personality traits in different cultural contexts. C1 NIA, Gerontol Res Ctr, Personal Stress & Coping Sect, NIH, Baltimore, MD 21224 USA. Univ Paris 10, Nanterre, France. Johns Hopkins Univ, Baltimore, MD 21218 USA. RP Mccrae, RR (reprint author), NIA, Gerontol Res Ctr, Personal Stress & Coping Sect, NIH, 4940 Eastern Ave, Baltimore, MD 21224 USA. EM jeffm@mvx.grc.nia.nih.gov OI Costa, Paul/0000-0003-4375-1712 NR 56 TC 119 Z9 125 U1 19 U2 63 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0022-0221 J9 J CROSS CULT PSYCHOL JI J. Cross-Cult. Psychol. PD JAN PY 1998 VL 29 IS 1 BP 171 EP 188 DI 10.1177/0022022198291009 PG 18 WC Psychology, Social SC Psychology GA YQ324 UT WOS:000071373900009 ER PT J AU Eanes, ED AF Eanes, ED TI Untitled SO JOURNAL OF DENTAL RESEARCH LA English DT Letter C1 NIDR, Mineral Chem & Struct Sect, Craniofacial & Skeletal Dis Branch, Bethesda, MD 20892 USA. RP Eanes, ED (reprint author), NIDR, Mineral Chem & Struct Sect, Craniofacial & Skeletal Dis Branch, Bethesda, MD 20892 USA. NR 5 TC 3 Z9 3 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD JAN PY 1998 VL 77 IS 1 BP 6 EP 6 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YQ665 UT WOS:000071411000003 PM 9437394 ER PT J AU Keller, J Reed, M Slavkin, H AF Keller, J Reed, M Slavkin, H TI Symposium: Celebrating our past, envisioning our future. A half century of oral health. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1 BP 106 EP 106 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800002 ER PT J AU D'Souza, RN Slavkin, HC AF D'Souza, RN Slavkin, HC TI Symposium: Genetic pathways of patterning and differentiation in craniofacial development. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Texas, Hlth Sci Ctr, Houston, TX 77225 USA. NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 68 BP 114 EP 114 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800071 ER PT J AU Kingman, A Brunelle, JA Winn, DM Drury, TF Kleinman, DV AF Kingman, A Brunelle, JA Winn, DM Drury, TF Kleinman, DV TI Evaluation NHANES III examiners' ability to assess oral health conditions. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 76 BP 115 EP 115 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800079 ER PT J AU Forrest, JL Horowitz, AM Shmuely, Y AF Forrest, JL Horowitz, AM Shmuely, Y TI Dental hygienists caries prevention knowledge and practices. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Thomas Jefferson Univ, Philadelphia, PA 19107 USA. NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 143 BP 123 EP 123 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800141 ER PT J AU Jackson, R Kelly, S Isaacs, R Brizendine, E Stookey, G Brunelle, J AF Jackson, R Kelly, S Isaacs, R Brizendine, E Stookey, G Brunelle, J TI Comparison of caries experience and level of fluorosis. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. Indiana Univ, Sch Dent, Indianapolis, IN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 302 BP 143 EP 143 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800303 ER PT J AU Nonaka, K Shum, L Takahashi, K Takahashi, I Nuckolls, GH Semba, I Slavkin, HC AF Nonaka, K Shum, L Takahashi, K Takahashi, I Nuckolls, GH Semba, I Slavkin, HC TI Bmp4 induced chondrogenesis by upregulation of an activator Sox9 and a repressor Msx2. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIAMS, Craniofacial Dev Sect, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 376 BP 152 EP 152 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800376 ER PT J AU Brunelle, JA Redford, M Doherty, I Nelson, K Mulligan, RA Greenspan, JS Komaroff, E AF Brunelle, JA Redford, M Doherty, I Nelson, K Mulligan, RA Greenspan, JS Komaroff, E TI Women's interagency HIV study oral protocol: Design, methods and sample characteristics. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NERI, Boston, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 397 BP 155 EP 155 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800395 ER PT J AU Macphail, LA Komaroff, E Navazesh, M Phelan, J Redford, M AF Macphail, LA Komaroff, E Navazesh, M Phelan, J Redford, M TI Oral candidiasis in women: HIV, covariates, viral load, and CD4. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NERI, Boston, MA USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ So Calif, Los Angeles, CA 90089 USA. NIDR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 399 BP 155 EP 155 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800396 ER PT J AU Mulligan, R Navazesh, M Komaroff, E Redford, M Greenspan, D AF Mulligan, R Navazesh, M Komaroff, E Redford, M Greenspan, D TI Prevalence of salivary gland enlargement in HIV+ women. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NERI, Boston, MA USA. Univ So Calif, Los Angeles, CA 90089 USA. NIDR, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 400 BP 155 EP 155 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800400 ER PT J AU D'Souza, RN Cavender, A Sood, R Tarnuzzer, R Roberts, A Letterio, J AF D'Souza, RN Cavender, A Sood, R Tarnuzzer, R Roberts, A Letterio, J TI Dental abnormalities in TGF-beta 1(-/-) mice: A role for TGF-beta 1 in biomineralization? SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Texas, Hlth Sci Ctr, Houston, TX USA. Univ Florida, Gainesville, FL USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 412 BP 157 EP 157 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800414 ER PT J AU Sobiski, C Denucci, D AF Sobiski, C Denucci, D TI The effect of cognitive behavioral therapy on TMD pain perception. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 539 BP 173 EP 173 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800538 ER PT J AU O'Loughlin, P Miller, GA Wang, YF D'Alesandro, M Ferry, L Diehl, SR AF O'Loughlin, P Miller, GA Wang, YF D'Alesandro, M Ferry, L Diehl, SR TI Effect of smoking cessation on total serum IgG2. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 USN, Sch Dent, Bethesda, MD 20814 USA. Geocenters Inc, Bethesda, MD USA. NIDR, NIH, Bethesda, MD 20892 USA. Loma Linda VA Med Ctr, Loma Linda, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 693 BP 192 EP 192 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800690 ER PT J AU Albandar, JM Kingman, A AF Albandar, JM Kingman, A TI Periodontal status of United States adults, 1988-1994. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 712 BP 194 EP 194 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800711 ER PT J AU Diehl, SR Wang, YF Beck, H Gao, Y Khanna, A Gu, X Burmeister, JA Schenkein, HA AF Diehl, SR Wang, YF Beck, H Gao, Y Khanna, A Gu, X Burmeister, JA Schenkein, HA TI Interleukin-1 genotypes and risk of early onset periodontitis - A family based study of linkage disequilibrium. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. Geocenters Inc, Bethesda, MD USA. VCU, Clin Res Ctr Periodontal Dis, Richmond, CA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 717 BP 195 EP 195 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800714 ER PT J AU Chin, K Dionne, RA AF Chin, K Dionne, RA TI Retrospective evaluation of gender and race on acute pain. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Pain & Neurosensory Mechanisms Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 729 BP 197 EP 197 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800728 ER PT J AU Mangan, D Lipton, J Jackson, L AF Mangan, D Lipton, J Jackson, L TI Grantsmanship 1998. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Duv Extramural Res, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 749 BP 199 EP 199 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800746 ER PT J AU Garcia, I Drury, TF AF Garcia, I Drury, TF TI Oral health of adult Mexican-Americans in South/West US SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 810 BP 207 EP 207 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800812 ER PT J AU Selwitz, RH Eklund, SA Oldakowski, RJ AF Selwitz, RH Eklund, SA Oldakowski, RJ TI Dental caries patterns: Implications for pit and fissure sealants. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. Univ Michigan, Sch Publ Hlth, Ann Arbor, MI 48109 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 836 BP 210 EP 210 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800836 ER PT J AU Takeyama, H Yamaguchi, S Kiyomura, H Birkedal-Hansen, H AF Takeyama, H Yamaguchi, S Kiyomura, H Birkedal-Hansen, H TI Collagenase and TIMP-1 mRNA in midpalatal cartilage following mechanical expansion. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Meikai Univ, Sch Dent, Dept Orthodont, Sakado, Saitama, Japan. NIDR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 924 BP 221 EP 221 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800923 ER PT J AU Drury, TF AF Drury, TF TI Place, poverty, and oral health among US children and youth. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 944 BP 223 EP 223 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800940 ER PT J AU Hargreaves, KM Dionne, RA Holland, GR Goodis, HE Flores, CM AF Hargreaves, KM Dionne, RA Holland, GR Goodis, HE Flores, CM TI Mediators and mechanisms of inflammatory pain. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Michigan, Ann Arbor, MI 48109 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NIDR, PANS, Bethesda, MD 20892 USA. Univ Texas, Hlth Sci Ctr, Dept Endocrinol, San Antonio, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 940 BP 223 EP 223 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684800938 ER PT J AU Wang, SL O'Connell, BC Kagami, H Baum, BJ Atkinson, JC AF Wang, SL O'Connell, BC Kagami, H Baum, BJ Atkinson, JC TI Clodronate treatment does not increase salivary gland transgene expression. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, GTTB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1011 BP 232 EP 232 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801006 ER PT J AU Tomar, SL Winn, DM AF Tomar, SL Winn, DM TI Coronal and root caries among US adult users of chewing tobacco. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Calif San Francisco, NIDR, Sch Dent, Bethesda, MD USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1205 BP 256 EP 256 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801197 ER PT J AU Zavras, A Jones, JE Wang, YF Douglas, CW Diehl, SR AF Zavras, A Jones, JE Wang, YF Douglas, CW Diehl, SR TI Molecular epidemiological investigation of the etiology of oral cancer. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Harvard Univ, Sch Dent Med, Boston, MA 02115 USA. Geocenters Inc, Bethesda, MD USA. NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1208 BP 256 EP 256 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801202 ER PT J AU Antonucci, JM Fowler, BO Stansbury, JW AF Antonucci, JM Fowler, BO Stansbury, JW TI Facile synthesis of silanated derivatives of Bis-GMA. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. NIST, Gaithersburg, MD 20899 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1233 BP 260 EP 260 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801235 ER PT J AU Brennan, M Fox, PC AF Brennan, M Fox, PC TI Matrix metalloproteinases in serum and parotid saliva of primary Sjogren's syndrome patients. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, GTTB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1283 BP 266 EP 266 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801277 ER PT J AU Navazesh, M Mulligan, R Komaroff, E Redford, M Greenspan, D Phelan, J AF Navazesh, M Mulligan, R Komaroff, E Redford, M Greenspan, D Phelan, J TI Prevalence of xerostomia and salivary gland hypofunction in HIV+ women. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ So Calif, Los Angeles, CA 90089 USA. NERI, Boston, MA USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. N Port VA, LI, NY USA. NIDR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1281 BP 266 EP 266 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801276 ER PT J AU Weiffenbach, JM Adesanya, MR Morrell, CH Metter, EJ Winn, DM AF Weiffenbach, JM Adesanya, MR Morrell, CH Metter, EJ Winn, DM TI Differential effects of age on major salivary gland flow rates. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. NIA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1397 BP 280 EP 280 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801390 ER PT J AU Palmer, RJ Park, J Pedraza, AJ Suci, P Geesey, G Kolenbrander, PE White, DC AF Palmer, RJ Park, J Pedraza, AJ Suci, P Geesey, G Kolenbrander, PE White, DC TI Flowcell for combined FTIR spectroscopy confocal microscopy applied to oral biofilm research. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Tennessee, Ctr Environm Biotechnol, Knoxville, TN 37932 USA. Univ Tennessee, Dept Mat Sci Engn, Knoxville, TN 37932 USA. Montana State Univ, Ctr Biofilm Engn, Bozeman, MT 59717 USA. NIDR, NIH, Bethesda, MD 20892 USA. Oak Ridge Natl Lab, Div Environm Sci, Oak Ridge, TN 37831 USA. NR 0 TC 0 Z9 0 U1 3 U2 3 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1455 BP 287 EP 287 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801447 ER PT J AU Watson, II Hodges, JS Helgeson, M Smith, B AF Watson, II Hodges, JS Helgeson, M Smith, B TI Access to dental care for an institutionalized elderly population. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. Univ Minnesota, Apple Tree Dent Inc, Minneapolis, MN 55455 USA. Univ Michigan, Ann Arbor, MI 48109 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI A MA 1558 BP 300 EP 300 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA YU125 UT WOS:000071684801554 ER PT J AU Caterina, J Shi, J Krakora, S Bartlett, J Engler, J Birkedal-Hansen, H AF Caterina, J Shi, J Krakora, S Bartlett, J Engler, J Birkedal-Hansen, H TI Isolation and characterization of the murine enamelysin gene. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. Univ Alabama, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 20 BP 634 EP 634 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400023 ER PT J AU Tsutsui, T Tamura, Y Yagi, E Hasegawa, K Barrett, JC AF Tsutsui, T Tamura, Y Yagi, E Hasegawa, K Barrett, JC TI Cell-transforming and genotoxic activities of bisphenol-A. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Nippon Dent Univ, Tokyo, Japan. NIEHS, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 66 BP 640 EP 640 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400069 ER PT J AU Shi, S Satomura, K Kuznetsov, S Mankani, M Robey, PG AF Shi, S Satomura, K Kuznetsov, S Mankani, M Robey, PG TI Transplantation of human marrow stromal cells involves in biphasic osteogenesis in vivo. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 92 BP 643 EP 643 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400094 ER PT J AU Albandar, JM Kingman, A Lamster, IB AF Albandar, JM Kingman, A Lamster, IB TI beta-Glucuronidase activity and level of subgingival bacteria as markers of severity of early-onset periodontitis. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. Columbia Univ, Div Periodont, New York, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 118 BP 646 EP 646 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400118 ER PT J AU Gordon, SM Chin, K Brahim, JS Dionne, RA AF Gordon, SM Chin, K Brahim, JS Dionne, RA TI Evaluation of the influence of gender on report of acute postsurgical pain. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Pain & Neurosurg Mech Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 290 BP 668 EP 668 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400291 ER PT J AU Gordon, SM Brahim, JS Jaber, L Kent, AA Dionne, RA AF Gordon, SM Brahim, JS Jaber, L Kent, AA Dionne, RA TI Additive analgesic effect of an NMDA receptor blocker-opioid combination in the oral surgery model. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 289 BP 668 EP 668 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400287 ER PT J AU Hoffman, MP Jung, DW Roque, E Rahemtulla, B Kleinman, HK AF Hoffman, MP Jung, DW Roque, E Rahemtulla, B Kleinman, HK TI Laminin peptides bind syndecans and are important for acinar formation of salivary gland (HSG) cells. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 312 BP 670 EP 670 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400310 ER PT J AU Drury, TF Horowitz, AM AF Drury, TF Horowitz, AM TI The oral health benefits of postsecondary education. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 588 BP 705 EP 705 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400587 ER PT J AU Yamagishi, H Walsh, TJ Sein, T O'Connell, BC AF Yamagishi, H Walsh, TJ Sein, T O'Connell, BC TI Anticandidal activity of histatins-3, -5, -9 against azole susceptible and azole resistant C-albicans. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, GTTB, NIH, Bethesda, MD 20892 USA. NCI, Pediat Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 767 BP 727 EP 727 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400760 ER PT J AU Jaber, L Swaim, WD Brahim, JS Dionne, RA AF Jaber, L Swaim, WD Brahim, JS Dionne, RA TI Immunohistochemical localization of mu-opioid receptors in human dental pulp. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 922 BP 747 EP 747 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400921 ER PT J AU Eliav, E Herzberg, U Gracely, R Benoliel, R Caudle, R Nahlieli, O Kenshalo, D AF Eliav, E Herzberg, U Gracely, R Benoliel, R Caudle, R Nahlieli, O Kenshalo, D TI A novel method to assess orofacial pain in the rat SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NAB, NIH, Bethesda, MD 20892 USA. Hadassah Sch Dent Med, Dept Oral Diag, Jerusalem, Israel. Barzilai Med Ctr, Dept Maxillofacial Surg, Oral Med Serv, Ashqelon, Israel. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 948 BP 750 EP 750 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400946 ER PT J AU Pallante, M Sodhi, A Zchar, M Gutkind, JS AF Pallante, M Sodhi, A Zchar, M Gutkind, JS TI Angiogenic pathways regulated by oncogenic Kaposi's sarcoma associated herpesvirus genes. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA. RI Gutkind, J. Silvio/A-1053-2009 NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 992 BP 755 EP 755 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335400988 ER PT J AU Wallace, J Luan, X Feng, J Dixon, M Shi, S Yamada, Y Macdougall, M Young, M AF Wallace, J Luan, X Feng, J Dixon, M Shi, S Yamada, Y Macdougall, M Young, M TI Isolation and characterization of bovine and rat dentin sialophosphoprotein cDNAs. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. Univ Manchester, Manchester M13 9PL, Lancs, England. Univ Texas, Hlth Sci Ctr, San Antonio, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 1117 BP 771 EP 771 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335401109 ER PT J AU Birkedal-Hansen, B Parker, M Gluckman, JL Stambrook, P Li, YQ Pavelic, ZP Stetler-Stevenson, WG AF Birkedal-Hansen, B Parker, M Gluckman, JL Stambrook, P Li, YQ Pavelic, ZP Stetler-Stevenson, WG TI TIMP gene expression in head and neck SCC and adjacent tissues. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NCI, Bethesda, MD 20892 USA. Univ Cincinnati, Cincinnati, OH 45221 USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 1285 BP 792 EP 792 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335401276 ER PT J AU Canto, MT Horowitz, AM Goodman, HS Watson, MR Cohen, LA Fedele, DJ AF Canto, MT Horowitz, AM Goodman, HS Watson, MR Cohen, LA Fedele, DJ TI Veterans oral cancer knowledge, risky behaviors and dental services utilization SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 VAMHCS, Perry Point, MD 20892 USA. NIDR, NIH, Bethesda, MD USA. DHMH, Baltimore, MD 20742 USA. Univ Maryland Baltimore Cty, Coll Dent Surg, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 1560 BP 826 EP 826 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335401553 ER PT J AU Forrest, JL Horowitz, AM Shmuely, Y AF Forrest, JL Horowitz, AM Shmuely, Y TI Dental hygienists knowledge, opinions and practices related to oral cancer SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Thomas Jefferson Univ, Philadelphia, PA 19107 USA. NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 1559 BP 826 EP 826 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335401549 ER PT J AU Horowitz, AM Goodman, HS Yellowitz, JA Drury, TF AF Horowitz, AM Goodman, HS Yellowitz, JA Drury, TF TI Dentists' practices regarding oral cancer prevention and early detection SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Maryland, Sch Dent, Baltimore, MD 21201 USA. NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 1556 BP 826 EP 826 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335401551 ER PT J AU Yellowitz, JA Horowitz, AM Goodman, HS Drury, TF AF Yellowitz, JA Horowitz, AM Goodman, HS Drury, TF TI A survey of US dentists' knowledge of oral cancer SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Maryland, Sch Dent, DHMH, Baltimore, MD 21201 USA. NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 1555 BP 826 EP 826 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335401547 ER PT J AU Zavras, AI Douglass, CW Diehl, SR AF Zavras, AI Douglass, CW Diehl, SR TI Lifestyle risk factors of oral cancer in a low incidence county SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 1563 BP 827 EP 827 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335401555 ER PT J AU Tomar, SL Marcus, SE AF Tomar, SL Marcus, SE TI Cigarette smoking and periodontitis among US adults SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 1585 BP 830 EP 830 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335401578 ER PT J AU Yamada, Y Lee, SK Yamada, KM AF Yamada, Y Lee, SK Yamada, KM TI Oral and craniofacial genome project. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2022 BP 884 EP 884 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402016 ER PT J AU Macphail, L Komaroff, E Alves, M Navazesh, M Phelan, J Redford, M AF Macphail, L Komaroff, E Alves, M Navazesh, M Phelan, J Redford, M TI Oral candidiasis, oral hygiene and HIV serostatus in WIHS women. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. NERI, Boston, MA USA. Univ Illinois, Chicago, IL USA. Univ So Calif, Los Angeles, CA USA. NIDR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2104 BP 894 EP 894 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402097 ER PT J AU Greenspan, D Komaroff, E Kamrath, H Redford, M Phelan, J Navazesh, M Alves, M Greenspan, JS Barr, C Mulligan, R AF Greenspan, D Komaroff, E Kamrath, H Redford, M Phelan, J Navazesh, M Alves, M Greenspan, JS Barr, C Mulligan, R TI Prevalence and associations of oral mucosal lesions in HIV+ women: The WIHS study. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. NERI, Boston, MA USA. NIDR, Washington, DC USA. Univ So Calif, Los Angeles, CA 90089 USA. Univ Illinois, Chicago, IL 60680 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2105 BP 895 EP 895 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402098 ER PT J AU Selwitz, RH Albandar, JM Harris, MJ AF Selwitz, RH Albandar, JM Harris, MJ TI Periodontal disease in diagnosed diabetes: US population, 1988-94. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, NIH, Bethesda, MD 20892 USA. NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2139 BP 899 EP 899 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402131 ER PT J AU Gannot, G Grisius, MM Fox, PC AF Gannot, G Grisius, MM Fox, PC TI The role of IL-6 and its receptor in Sjogren's syndrome SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, GTTB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2183 BP 904 EP 904 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402173 ER PT J AU Sommer, B Kuznetsov, SA Majolagbe, A Satomura, K Young, MF AF Sommer, B Kuznetsov, SA Majolagbe, A Satomura, K Young, MF TI Multiple factors potentially control human bone sialoprotein expression. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, CSDB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2177 BP 904 EP 904 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402170 ER PT J AU Chai, Y Zhao, J Warburton, D Slavkin, HC AF Chai, Y Zhao, J Warburton, D Slavkin, HC TI TGF-beta type II receptor regulates mandibular morphogenesis. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ So Calif, Sch Dent, CCMB, Los Angeles, CA 90089 USA. NIDR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2221 BP 909 EP 909 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402211 ER PT J AU Derouen, T Martin, M Woods, J Townes, B Leroux, B Sarnat, H Leitao, J Caldas, C Braveman, N AF Derouen, T Martin, M Woods, J Townes, B Leroux, B Sarnat, H Leitao, J Caldas, C Braveman, N TI Casa Pia study of the health effects of dental amalgam. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 Univ Washington, Seattle, WA 98195 USA. Univ Lisbon, P-1699 Lisbon, Portugal. NIDR, Bethesda, MD 20892 USA. RI Leroux, Brian/H-2254-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2594 BP 956 EP 956 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402587 ER PT J AU Grisius, MM Fox, PC AF Grisius, MM Fox, PC TI Salivary cytokines in Sjogren's syndrome. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, GTTB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2792 BP 980 EP 980 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402781 ER PT J AU Caterina, N Caterina, J Yamada, S Longenecker, G Yermovsky, A Shi, J Netzel-Arnett, S Windsor, J Holmback, K Novas, N Mann, M Engler, J Birkedal-Hansen, H AF Caterina, N Caterina, J Yamada, S Longenecker, G Yermovsky, A Shi, J Netzel-Arnett, S Windsor, J Holmback, K Novas, N Mann, M Engler, J Birkedal-Hansen, H TI Targeted mutation of murine TIMP-2 gene. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR, Bethesda, MD 20892 USA. Univ Alabama, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1998 VL 77 SI B MA 2905 BP 995 EP 995 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA ZK546 UT WOS:000073335402893 ER PT J AU Domanski, MJ Exner, DV AF Domanski, MJ Exner, DV TI Prevention of sudden cardiac death - A current perspective SO JOURNAL OF ELECTROCARDIOLOGY LA English DT Article; Proceedings Paper CT 23rd Annual ISCE Conference on Research and Technology Transfer in Computerized Electrocardiology CY APR 18-23, 1998 CL KEYSTONE, COLORADO ID LEFT-VENTRICULAR DYSFUNCTION; ACUTE MYOCARDIAL-INFARCTION; CONGESTIVE-HEART-FAILURE; TERM FOLLOW-UP; RANDOMIZED TRIAL; CLINICAL-TRIAL; DRUG-THERAPY; HIGH-RISK; MORTALITY; ARRHYTHMIAS C1 NHLBI, Clin Trails Grp, Rockledge Ctr 2, Bethesda, MD 20892 USA. RP Domanski, MJ (reprint author), NHLBI, Clin Trails Grp, Rockledge Ctr 2, 6701 Rockledge Dr,Rm 8146, Bethesda, MD 20892 USA. NR 45 TC 2 Z9 2 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI PHILADELPHIA PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA SN 0022-0736 J9 J ELECTROCARDIOL JI J. Electrocardiol. PY 1998 VL 31 SU S BP 47 EP 53 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 165EL UT WOS:000078507200009 PM 9988005 ER PT J AU Dosemeci, M Benichou, J AF Dosemeci, M Benichou, J TI An alternative test for trend in exposure-response analysis SO JOURNAL OF EXPOSURE ANALYSIS AND ENVIRONMENTAL EPIDEMIOLOGY LA English DT Article DE epidemiologic methods; exposure scoring; Mantel-extension test; test for monotonic dose-response; test for trend AB The Mantel-extension chi-square test for overall trend is commonly used in evaluating dose-response relationships in epidemiologic studies. As illustrated by others, it is not an optimal test for a monotonic dose-response. In addition, the result of this test depends heavily upon the scores assigned to the exposure categories. The selection of the score may have a substantial impact on the test statistic and consequently on the interpretation of the study results. A monotonic dose-response relationship exists when risk increases (or decreases) with increasing exposure. Although the Mantel-extension test is one of the most cited test for trend, it is not a sensitive test to reflect the incremental risk change of a dose-response relationship which may potentially generate misleading results. We propose an alternative test for the evaluation of a monotonic dose-response, which reconfigurates the Mantel-Haenszel chi square test for dichotomous exposure series into a polychotomous exposure series. The proposed test generates chi values that are sensitive to incremental increase (or decrease) in risk at each exposure category and does not require exposure scores. The test is a simple summation of Mantel-Haenszel chi statistics obtained in for 2 X 2 tables over adjacent exposure categories (i.e., the sum of Mantel-Haenszel chi values between categories 1 and 2, 2 and 3, 3 and 4 and 1-1 and 1). Several examples are presented to illustrate that the proposed test generates more realistic chi values than those obtained by the Mantel-extension test for trend. C1 NCI, Epidemiol & Biostat Program, Rockville, MD 20892 USA. RP Dosemeci, M (reprint author), NCI, Epidemiol & Biostat Program, Execut Plaza N,Room 418, Rockville, MD 20892 USA. NR 9 TC 10 Z9 10 U1 0 U2 3 PU PRINCETON SCIENTIFIC PUBL INC PI PRINCETON PA PO BOX 2155, PRINCETON, NJ 08543 USA SN 1053-4245 J9 J EXPO ANAL ENV EPID JI J. Expo. Anal. Environ. Epidemiol. PD JAN-MAR PY 1998 VL 8 IS 1 BP 9 EP 15 PG 7 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA YT398 UT WOS:000071598900003 PM 9470101 ER PT J AU Sneiderman, CA AF Sneiderman, CA TI University of Nebraska's 25th Annual Family Practice Review, 1996. SO JOURNAL OF FAMILY PRACTICE LA English DT Software Review C1 Natl Lib Med, Bethesda, MD USA. RP Sneiderman, CA (reprint author), Natl Lib Med, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 USA SN 0094-3509 J9 J FAM PRACTICE JI J. Fam. Pract. PD JAN PY 1998 VL 46 IS 1 BP 92 EP 93 PG 2 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA YT180 UT WOS:000071573500015 ER PT J AU Thomsen, CA Ter Maat, J AF Thomsen, CA Ter Maat, J TI Evaluating the cancer information service: A model for health communications. Part 1 SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article ID CARE AB The Cancer Information Service (CIS) was established in 1975 by the National Cancer Institute (NCI) to meet the information needs of cancer patients, their families, health professionals, and the public. As the nation's foremost source for cancer information, the CIS applies a unique health communications model to bring the latest research findings on cancer prevention, detection, treatment, and supportive care to the nation. It does this through two main program components: a toll-free telephone service (1-800-4-CANCER) and an outreach program that focuses on providing technical assistance, specifically to partners reaching minority and underserved audiences. During its 22-year history, more than 7.5 million callers have reached the CIS telephone service. In addition, 100,000 requests are received each year fr om 4,500 organizations nationwide seeking cancer-related outreach expertise. This overview describes the CIS model for health communications, describes the program's impact in broad terms, and defines the critical role evaluation plays in each program component. The overview describes two customer satisfaction and impact surveys performed by an independent survey research film in 1996 to evaluate the CIS model: (a) the telephone service user survey, a random sample of 2,489 persons representing major caller groups who were interviewed 3 to 6 weeks after their initial call to the CIS; and (b) the outreach partner survey, a random sample of 867 partner organizations, the majority of which reach minority and underserved audiences with information and programs, surveyed within a few months after a contact with the CIS outreach program. Impact data for both program areas were favorable: Approximately 8 out of IO CIS callers reported that the information they received had a positive Impact (either in eliciting a positive action [56%] or in reassurance of decisions made [22%]) and two-thirds of CIS partners said the CIS has an important impact on their programs. C1 NCI, Canc Informat Serv Branch, Off Canc Commun, Bethesda, MD 20892 USA. CODA Res Inc, Silver Spring, MD USA. RP Thomsen, CA (reprint author), NCI, Canc Informat Serv Branch, Off Canc Commun, 31 Ctr Dr,MSC 2580,Bldg 31,Rom 10A16, Bethesda, MD 20892 USA. NR 37 TC 27 Z9 27 U1 2 U2 2 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PY 1998 VL 3 SU S BP 1 EP 13 DI 10.1080/108107398127210 PG 13 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 118BY UT WOS:000075818900004 PM 10977265 ER PT J AU Thomsen, CA Ter Maat, J AF Thomsen, CA Ter Maat, J TI Description of survey methods for the CIS telephone service user survey and CIS outreach partner survey SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article AB Both the CIS telephone service user survey and CIS outreach partner survey were statistically based surveys conducted in accordance with standard research practices and techniques. Following are descriptions of the research designs for each survey, the sample selection techniques employed, and the response rate statistics. C1 NCI, Canc Informat Serv Branch, Off Canc Commun, Bethesda, MD 20892 USA. CODA Res Inc, Silver Spring, MD USA. RP Thomsen, CA (reprint author), NCI, Canc Informat Serv Branch, Off Canc Commun, 31 Ctr Dr MSC 2580,Bldg 31,Rm 10A16, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PY 1998 VL 3 SU S BP 14 EP 20 DI 10.1080/108107398127229 PG 7 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 118BY UT WOS:000075818900005 PM 10977267 ER PT J AU Fleisher, L Kornfeld, J Ter Maat, J Davis, SW Laepke, K Bradley, A AF Fleisher, L Kornfeld, J Ter Maat, J Davis, SW Laepke, K Bradley, A TI Building effective partnerships: A national evaluation of the Cancer Information Service outreach program. Part 2 SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article ID COALITIONS AB The Cancer Information Service's (CIS) nationally coordinated, regionally focused outreach program establishes partnerships with government, nonprofit, and private organizations to reach underserved and minority populations. A national random sample telephone survey, conducted with 867 partner organizations who had contact with the CIS in early 1996, assessed the types of CIS assistance used, satisfaction with and usefulness of these services, organizational characteristics,and the overall impact on partners' cancer-related programs. CIS partners provide programs for the medically underserved (79%) and specific racial and ethnic groups (72%) and address a range of cancer control issues. Partners use a,ld highly value an array of CIS assistance. Over 90% are satisfied with the CIS services. Diffusion of accurate and science-based information, materials and resources is a key element of the outreach assistance. Two out of three partners are receiving late-breaking news and scientific information from the CIS and 86% are disseminating it to their constituents. The majority of those partners surveyed reported that they rely on the CIS to assist with their most important cancer programs. Sixty-eight percent of the partners rated the CIS assistance as important or very important to their cancer-related programs. These survey results indicate that the CIS outreach program provides key support to partners' cancer programs and has an impact on their efforts. The results support the effectiveness of a regionally based outreach program working in partnership with existing organizations at the state, county, a,ld local level who are addressing the needs of underserved populations. C1 Fox Chase Canc Ctr, Canc Informat Serv, Cheltenham, PA 19012 USA. Univ Miami, Sch Med, Canc Informat Serv, Miami, FL USA. CODA Res Inc, Silver Spring, MD USA. No Calif Canc Ctr, Canc Informat Serv, Union City, CA USA. NCI, Bethesda, MD 20892 USA. Penrose St Francis Hlth Serv, Canc Informat Serv, Colorado Springs, CO USA. RP Fleisher, L (reprint author), Fox Chase Canc Ctr, Canc Informat Serv, 510 Township Line Rd, Cheltenham, PA 19012 USA. FU NCI NIH HHS [N01-CO-33033] NR 16 TC 11 Z9 11 U1 0 U2 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PY 1998 VL 3 SU S BP 21 EP 35 DI 10.1080/108107398127238 PG 15 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 118BY UT WOS:000075818900006 PM 10977268 ER PT J AU Kornfeld, J Fleisher, L Ter Maat, J Vanchieri, C Hohenemser, L Stevens, N AF Kornfeld, J Fleisher, L Ter Maat, J Vanchieri, C Hohenemser, L Stevens, N TI Reaching minority and underserved populations: The impact of the Cancer Information Service's outreach program. Part 3 SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article ID PARTNERSHIP AB Through its regional outreach program, the Cancer Information Service (CIS) develops partnership with organizations that reach minority and underserved populations and connects them,vith accurate cancer information and art array of support services and resources. To evaluate the usefulness, satisfaction, and impact of the CIS outreach program on partner organizations, a national random sample survey was conducted by an independent research Jinn in 1996. This paper focuses on the survey results of 359 special population partner organizations that identified their main audience as a specific racial or ethnic group and/or the underserved. Almost all (84% to 93%) rated the services provided by the CIS outreach program to be very important or important to meeting the goals of their projects. A large majority of these special population partners stated that the CIS provided them with the latest cancer information (67%) and National Cancer Institute (NCI) resources (83%), and more than half (57%) utilized CIS expertise to develop and plan programs. Special populations partners were more likely to use an array of CIS assistance than other CIS partners. Furthermore, they,cere more likely to be heavy users of CIS assistance and more likely than other CIS partners to indicate that the CIS had an important impact on their programs. The results indicate that the CIS's nationally coordinated, regionally focused outreach program provides critical support and has an important impact on the cancer-related programs of partner organizations that reach minority and underserved audiences. C1 Sylvester Comprehens Canc Ctr, Canc Informat Serv, Miami, FL 33136 USA. Fox Chase Canc Ctr, Canc Informat Serv, Cheltenham, PA USA. CODA Res Inc, Silver Spring, MD USA. Vanchieri Commun, Bethesda, MD USA. NCI, Canc Informat Serv, Bethesda, MD 20892 USA. RP Kornfeld, J (reprint author), Sylvester Comprehens Canc Ctr, Canc Informat Serv, 1150 NW 14th Ave,Suite 207, Miami, FL 33136 USA. FU NCI NIH HHS [N01-CO-33033] NR 21 TC 5 Z9 5 U1 0 U2 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PY 1998 VL 3 SU S BP 36 EP 49 DI 10.1080/108107398127247 PG 14 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 118BY UT WOS:000075818900007 PM 10977269 ER PT J AU Ward, JAD Baum, S Ter Maat, J Thomsen, CA Maibach, EW AF Ward, JAD Baum, S Ter Maat, J Thomsen, CA Maibach, EW TI Value and impact of the Cancer Information Service telephone service. Part 4 SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article ID LIBRARIES; EDUCATION; NEEDS AB The Cancer Information Service (CIS) of the National Cancer Institute (NCI) is a health communications program that disseminates information through two channels: to individuals through a toll-free telephone service a,td to organizations (serving primarily underserved populations) through an outreach program. People call the 1-800-4-CANCER line to meet a variety of information needs. The information specialists who respond to these calls are prepared to answer questions ranging from cancer prevention to early detection, treatment, and survivorship. In a 1996 random sample survey, 2,489 callers were asked why they called, how they valued the information, and what health-related actions they took or decisions they made since their call. Results show the CIS is highly valued by its users, with satisfaction high across gender, age, education, and racial/ethnic groups. While differences in satisfaction were observed by caller type and,subject of inquiry, nearly all respondents reported that contact with the CIS increased knowledge, provided reassurance, and influenced decisionmaking and health behavior. Overall, 95% were satisfied with CIS information, 98% trusted the information, 92% reported an increase in knowledge, 69% felt reassured, and 73% said the information helped them to better cope with their concerns. Eight out of 10 callers reported the information they received had a positive impact, with 56% reporting taking a positive health action. Results demonstrate that health communications programs like the CIS can fill information gaps consumers must bridge to make informed health care decisions and can play an important public health role in motivating people to take actions to reduce risks and/or make decisions that lead to improved health status. C1 Univ Texas, Md Anderson Canc Ctr, Canc Informat Serv, Houston, TX 77030 USA. UAB, Ctr Comprehens Canc, Canc Informat Serv, Birmingham, AL USA. CODA Res Inc, Silver Spring, MD USA. NCI, Canc Informat Serv Branch, Bethesda, MD 20892 USA. Porter Novelli, Washington, DC USA. RP Ward, JAD (reprint author), Univ Texas, Md Anderson Canc Ctr, Canc Informat Serv, 1515 Holcombe Blvd, Houston, TX 77030 USA. FU PHS HHS [N01-C0-33030] NR 37 TC 32 Z9 32 U1 1 U2 4 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PY 1998 VL 3 SU S BP 50 EP 70 DI 10.1080/108107398127256 PG 21 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 118BY UT WOS:000075818900008 PM 10977270 ER PT J AU Davis, SW Fleisher, L Ter Maat, J Muha, C Laepke, K AF Davis, SW Fleisher, L Ter Maat, J Muha, C Laepke, K TI Treatment and clinical trials decisionmaking: The impact of the Cancer Information Service. Part 5 SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article ID CHRONIC ILLNESS AB The Cancer Information Service (CIS) provides accurate, up-to-date information to cancer patients, their families, the general public, and health professionals. In 1996, the CIS telephone service received 208,971 calls from people with questions about cancer treatments and clinical trials (total calls = 500,000). Cancer information specialists are trained and certified to access the PDQ database of treatment options and clinical trials, to translate medical information into understandable terms in order to help callers make treatment decisions, and to discuss clinical trials proactively. A telephone service user survey was conducted to assess the satisfaction and impact of the assistance and information provided to CIS callers. Almost half of the callers (46% of those calling for treatment information:, 50% calling for clinical trial information) discussed the CIS information with a physician. Over half (55% treatment, 54% clinical trial) said the information helped them make a treatment decision. Twenty-four percent of treatment and 64% bf clinical trial callers had enrolled in or had considered a clinical trial. Almost all (95%) were satisfied with information received from the CIS. The authors find thai the CIS is fulfilling its role in disseminating information on cancer treatment and clinical trials through its telephone service. The CIS proactively educates treatment callers about clinical trials. However, the CIS needs to apply other strategies to reach medically underserved populations. Although most callers were able to understand the information, clinical trial callers found the information more difficult than did treatment callers. The CIS is working to simplify written clinical trial information. C1 No Calif Canc Ctr, Canc Informat Serv, Union City, CA 94587 USA. Fox Chase Canc Ctr, Canc Informat Serv, Cheltenham, PA USA. CODA Res Inc, Silver Spring, MD USA. NCI, Canc Informat Serv, Bethesda, MD 20892 USA. RP Davis, SW (reprint author), No Calif Canc Ctr, Canc Informat Serv, 32960 Alvarado Niles Rd, Union City, CA 94587 USA. FU NCI NIH HHS [N01-CO-33033] NR 26 TC 14 Z9 14 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PY 1998 VL 3 SU S BP 71 EP 85 DI 10.1080/108107398127265 PG 15 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 118BY UT WOS:000075818900009 PM 10977271 ER PT J AU Maibach, EW Davis, SW Ter Maat, J Rivera, N AF Maibach, EW Davis, SW Ter Maat, J Rivera, N TI Promoting cancer prevention and screening: The impact of the Cancer Information Service. Part 7 SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article ID SMOKING CESSATION; HEALTH PROMOTION; MAMMOGRAPHY; INTERVENTION; PROGRAM; MEDIA; COMMUNICATION; CAMPAIGN; HABITS; WOMEN AB Cancer Information Service (CIS) inquiries about cancer prevention and screening are an important opportunity to educate callers about primary or secondary cancer prevention, facilitate their decision-making, and, where appropriate, encourage action. An evaluation was conducted to assess whether these callers' information needs are being satisfied and to determine if the information provided facilitates decisionmaking and subsequent risk reduction actions. A random sample of 2,489 callers was surveyed during a 5-week period, 3 to 6 weeks after their initial call to CIS; prevention or screening was stated as the main reason for calling by 331 respondents. A series of questions was asked regarding level of satisfaction with CIS's performance and how helpful the information provided was in terms of feeling more knowledgeable, making decisions, and taking action. The vast majority of respondents were satisfied with the information received, found it to be helpful, felt more knowledgeable as a result, and would call CIS again with subsequent questions. Although demand characteristics are a possible soul ce of bias, nearly three-quarters of the respondents reported subsequently disc:ussing the information provided with someone else, and almost half sought additional information recommended by CIS. Nearly two-thirds of primary prevention respondents and about half of secondary prevention respondents indicated that they had taken some risk-reducing action subsequent to their interaction with CIS. The CIS is effectively satisfying the information needs of prevention and screening callers; information it is providing is effectively facilitating decisionmaking and stimulating callers to take action. C1 Porter Novelli, Washington, DC 20036 USA. No Calif Canc Ctr, Canc Informat Serv, Union City, CA USA. CODA Res Inc, Silver Spring, MD USA. NCI, Canc Informat Serv, Bethesda, MD 20892 USA. RP Maibach, EW (reprint author), Porter Novelli, 1120 Connecticut Ave, Washington, DC 20036 USA. OI Maibach, Edward/0000-0003-3409-9187 FU NCI NIH HHS [NCI-CO-50507-50] NR 44 TC 11 Z9 11 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PY 1998 VL 3 SU S BP 97 EP 108 DI 10.1080/108107398127283 PG 12 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 118BY UT WOS:000075818900011 PM 10977273 ER PT J AU Muha, C Smith, KS Baum, S Ter Maat, J Ward, JA AF Muha, C Smith, KS Baum, S Ter Maat, J Ward, JA TI The use and selection of sources in information seeking: The Cancer Information Service experience. Part 8 SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article ID BEHAVIOR; WOMEN AB The Cancer Information Service (CIS), the voice of the National Cancer Institute (NCI) for more than 20 years, disseminates information through two channels: a toll-free, telephone service (1-800-4-CANCER) and an outreach program which develops partnerships with organizations that reach underserved populations. In 1996, the telephone service handled approximately 500,000 calls on a range of topics, including cancer treatment, clinical trials, coping issues, referrals to services, prevention, causes, and symptoms of cancer. As part of a national telephone service user survey, conducted in 1996, that examined the impact of the CIS program, callers were asked what additional sources they went to for the same information that they requested from the CIS. The survey revealed that the CIS plays a critical role for information seekers. Almost 59% of surveyed callers contacted no other sources to address the topic they discussed with the CIS. Almost half of the callers who contacted other sources made all of those contacts before calling the CIS. Younger callers (under 40), those with a higher level of education, and those seeking information about treatment and causes of cancer were more likely to contact other sources for the same information. Health professionals, libraries, and bookstores were the most commonly used non-CIS sources. This variety in information seeking highlights the need for services, like the CIS, that can meet the diverse information needs of callers. C1 NCI, Off Canc Commun, Canc Informat Serv, Bethesda, MD 20892 USA. Univ Alabama, Ctr Comprehens Canc, Birmingham, AL USA. CODA Res Inst, Silver Spring, MD USA. Univ Texas, Md Anderson Canc Ctr, Houston, TX USA. RP Muha, C (reprint author), NCI, Off Canc Commun, Canc Informat Serv, 31 Ctr Dr,MSC 2580,Bldg 31,Room 10A16, Bethesda, MD 20892 USA. NR 15 TC 38 Z9 38 U1 2 U2 6 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PY 1998 VL 3 SU S BP 109 EP 120 DI 10.1080/108107398127292 PG 12 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 118BY UT WOS:000075818900012 PM 10977266 ER PT J AU Chikada, M Shiota, T Aida, S Yamada, I Sahn, DJ Jones, M AF Chikada, M Shiota, T Aida, S Yamada, I Sahn, DJ Jones, M TI A method for estimating aortic regurgitant effective orifice area by digital Doppler color flow mapping SO JOURNAL OF HEART VALVE DISEASE LA English DT Article ID VALVE-REPLACEMENT; QUANTITATIVE ASSESSMENT; CONTINUOUS-WAVE; LATE SURVIVAL; INSUFFICIENCY; ACCELERATION; SHEEP AB Background and aims of the study: Although non-invasive assessment of the severity of aortic regurgitation (AR) is important, quantitative evaluation of AR can be difficult in clinical settings. Most Doppler echocardiographic methods have been compared with angiographic grading of AR severity. However, while aortic angiography is used widely for grading AR severity, the method is only semi-quantitative. A computed semi-automatic digital color Doppler method has recently been described fur calculating stroke volume and cardiac output. The study aim was to develop a method of evaluating AR severity by using a digital automated color Doppler method (ACM) along with continuous wave (CW) Doppler for estimating aortic regurgitant effective orifice area. Methods: A total of 22 different hemodynamic conditions were studied in six sheep. Regurgitant volumes (RV) were determined by electromagnetic flowmetry (EM) and by ACM. AR effective orifice areas (EOAs) were determined by dividing each of the RVs by the time integrals of the AR continuous wave velocities. AR EOAs by ACM were compared with those obtained by EM and with other EM indices of regurgitant severity. ACM was accurate for quantifying AR EOAs (r = 0.96). Results and conclusions: Calculated AR EOA correlated well with peak AR flow and regurgitant fraction by EM. The combined ACM/CW Doppler method can be useful for estimating non-invasively the aortic regurgitant EOA and for evaluating the severity of AR. C1 NHLBI, NIH, Lab Anim Med & Surg, Bethesda, MD 20892 USA. Oregon Hlth Sci Univ, Clin Care Ctr Congenital Heart Dis, Portland, OR 97201 USA. RP Jones, M (reprint author), NHLBI, NIH, Lab Anim Med & Surg, Bldg 14E 107A, Bethesda, MD 20892 USA. NR 30 TC 2 Z9 2 U1 0 U2 0 PU I C R PUBLISHERS PI NORTHWOOD PA CRISPIN HOUSE, 12/A SOUTH APPROACH, MOOR PARK, NORTHWOOD, ENGLAND HA6 2ET SN 0966-8519 J9 J HEART VALVE DIS JI J. Heart Valve Dis. PD JAN PY 1998 VL 7 IS 1 BP 102 EP 107 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA YU967 UT WOS:000071774600017 PM 9502147 ER PT J AU Saito, M Matsumine, H Tanaka, H Ishikawa, A Shimoda-Matsubayashi, S Schaffer, AA Mizuno, Y Tsuji, S AF Saito, M Matsumine, H Tanaka, H Ishikawa, A Shimoda-Matsubayashi, S Schaffer, AA Mizuno, Y Tsuji, S TI Refinement of the gene locus for autosomal recessive juvenile parkinsonism (AR-JP) on chromosome 6q25.2-27 and identification of markers exhibiting linkage disequilibrium SO JOURNAL OF HUMAN GENETICS LA English DT Article DE autosomal recessive juvenile parkinsonism (AR-JP); Parkinson's disease (PD); chromosome 6q25.2-27; linkage disequilibrium ID FAMILIES; MAP; DNA AB Autosomal recessive juvenile parkinsonism (AR-JP) (MIM 600116) is a hereditary neurodegenerative disorder characterized by levodopa-responsive parkinsonism with a mean age at onset of 23.2 years. We recently mapped the AR-JP gene locus to a 17-cM interval on chromosome 6q25.2-27. To further narrow the candidate region of the AR-JP gene, we performed detailed linkage analysis using densely placed genetic markers in this region (D6S437, D6S1581, D6S1579, D6S305, D6S411, SOD2, D6S253, D6S1599, D6S1719 and D6S264). Pairwise linkage analysis revealed the highest cumulative maximal lod score of 9.13 at D6S1579 (theta = 0.05), and multipoint linkage analysis revealed the highest cumulative lod score of 12.4 at the locus 3 cM telomeric to D6S1599. Observation of obligate recombination events narrowed the candidate region to a 13-cM region between D6S1579 and D6S264. Furthermore, we identified two marker loci, D6S1579 and D6S1599, which exhibit strong linkage disequilibrium with the AR-JP locus: chi(2) (2 x n table) = 84.22; P < 0.0001, chi(2) [likelihood-ratio test (LRT)] = 20.66; P < 0.0001, lambda = 0.40 and chi(2) (2 x n table) = 63.37; P < 0.0001, chi(2) (LRT) = 10.32; P < 0.0001, lambda = 0.30, respectively. These results suggest that the candidate region for the AR-JP gene is most likely located near the 4-cM region encompassing D6S1579 and D6S1599. C1 Niigata Univ, Brain Res Inst, Dept Neurol, Niigata 951, Japan. Juntendo Univ, Sch Med, Dept Neurol, Tokyo 113, Japan. Nishiojiya Natl Hosp, Dept Neurol, Niigata, Japan. NIH, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. RP Tsuji, S (reprint author), Niigata Univ, Brain Res Inst, Dept Neurol, 1-757 Asahimachi Dori, Niigata 951, Japan. EM tsuji@cc.niigata-u.ac.jp RI Schaffer, Alejandro/F-2902-2012 NR 26 TC 8 Z9 8 U1 0 U2 4 PU SPRINGER-VERLAG TOKYO PI TOKYO PA 3-3-13, HONGO, BUNKYO-KU, TOKYO, 113, JAPAN SN 1434-5161 J9 J HUM GENET JI J. Hum. Genet. PY 1998 VL 43 IS 1 BP 22 EP 31 DI 10.1007/s100380050032 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA ZT831 UT WOS:000074132100005 PM 9609994 ER PT J AU Pericle, F Pinto, LA Hicks, S Kirken, RA Sconocchia, G Rusnak, J Dolan, MJ Shearer, GM Segal, DM AF Pericle, F Pinto, LA Hicks, S Kirken, RA Sconocchia, G Rusnak, J Dolan, MJ Shearer, GM Segal, DM TI Cutting edge: HIV-1 infection induces a selective reduction in STAT5 protein expression SO JOURNAL OF IMMUNOLOGY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; TYROSINE PHOSPHORYLATION; SIGNAL-TRANSDUCTION; CELLS; TAT AB HIV-1 infection is accompanied by qualitative and quantitative defects in CD4(+) T lymphocytes, Loss of immune function in HIV patients is usually associated with a profound dysregulation of cytokine production. To investigate whether cytokine signaling defects occur during HIV infection, PHA blasts from healthy human donors were infected with two strains of HIV-1 and screened for the expression of STAT proteins used in cytokine signaling, A selective decrease in STAT5B was seen 8 days after infection with the BZ167 dual-tropic HIV isolate, but not with the Ba-L, M-tropic strain, Based on these findings, purified T cells from HIV-infected patients in different stages of disease were also tested for STAT expression; decreases in STAT5A, STAT5B, and STAT1 alpha were observed in all patients, The reduction in STATs seen in vivo and in vitro after HIV infection may contribute to the loss of T cell function in HIV disease. C1 NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. NCI, Intramural Res Support Program, Sci Applicat Int Corp,Lab Mol Immunoregulat, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. Wilford Hall USAF Med Ctr, HIV Unit, Lackland AFB, TX 78236 USA. RP Segal, DM (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10,Room 4B17, Bethesda, MD 20892 USA. NR 31 TC 52 Z9 53 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1998 VL 160 IS 1 BP 28 EP 31 PG 4 WC Immunology SC Immunology GA YW266 UT WOS:000071915100007 PM 9551952 ER PT J AU Raziuddin, A Longo, DL Mason, L Ortaldo, JR Bennett, M Murphy, WJ AF Raziuddin, A Longo, DL Mason, L Ortaldo, JR Bennett, M Murphy, WJ TI Differential effects of the rejection of bone marrow allografts by the depletion of activating versus inhibiting Ly-49 natural killer cell subsets SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HYBRID RESISTANCE; MULTIGENE FAMILY; NK CELLS; T-CELLS; MOLECULES; RECEPTOR; MICE; BIOLOGY; CLONING; GRAFTS AB Natural killer cells mediate the specific rejection of bone marrow cell (BMC) allografts in lethally irradiated mice. The Ly-49 family of molecules present on subsets of murine NK cells appears capable of binding class I MHC molecules, resulting in transmission of an inhibitory signal to the NK cell, These Ly-49 family members have been shown to have an immunoreceptor tyrosine-based inhibitory motif that is responsible for the inhibitory signal. However, a new Ly-49 family member was found that lacks this motif, Ly-49D, and evidence suggests that this may be an activating receptor, We therefore compared the role of the activating Ly-49 member with NK cells bearing inhibitory Ly-49 receptors in BMC rejection, Depletion of Ly-49D(+) NK cells in H-2(b) mice abrogated their ability to reject H-2(d) BMC allografts. Similarly, Ly-49C(+) NK cells also were shown to mediate the specific rejection of H-2(d) BMC, When both subsets were depleted, an additive enhancement of BMC engraftment was observed, indicating that both subsets play a role in the rejection of allogeneic H-2-homozygous H-2(d) BMC, However, rejection of H-2(b x d) or D8 (H-2(b), D-d transgene) BMC allografts was unaffected by Ly-49C(+) NK cell depletion in H-2(b) mice, In marked contrast, depletion of Ly-49D(+) NK cells in H-2(b) mice totally abrogated the rejection of H-2(b x d) heterozygous BMC in support of in vitro data suggesting that Ly-49D(+) NK cells receive activating signals, Therefore, NK subsets demonstrate a differential ability to reject H-2 homozygous and heterozygous BMC. C1 NCI, Intramural Res Support Program, SAIC Frederich, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. NCI, Expt Immunol Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. NIA, Baltimore, MD 21224 USA. Univ Texas, SW Med Ctr, Dallas, TX 75235 USA. RP Murphy, WJ (reprint author), NCI, Intramural Res Support Program, SAIC Frederich, Frederick Canc Res & Dev Ctr, Bldg 567,Room 210, Frederick, MD 21702 USA. NR 30 TC 68 Z9 69 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1998 VL 160 IS 1 BP 87 EP 94 PG 8 WC Immunology SC Immunology GA YW266 UT WOS:000071915100014 PM 9551959 ER PT J AU van Oers, NSC Love, PE Shores, EW Weiss, A AF van Oers, NSC Love, PE Shores, EW Weiss, A TI Regulation of TCR signal transduction in murine thymocytes by multiple TCR zeta-chain signaling motifs SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL-RECEPTOR; IMMATURE CD4+CD8+ THYMOCYTES; PROTEIN-TYROSINE KINASES; ANTIGEN-RECEPTOR; MICE LACKING; ACTIVATION; COMPLEX; ZAP-70; PHOSPHORYLATION; CD3-EPSILON AB The alpha beta TCR is a multimeric protein complex comprising ligand-binding and signal-transducing subunits. The signal transduction processes are mediated by the immunoreceptor tyrosine-based activation motifs (ITAMs), and up to 10 ITAMs are present within a single TCR complex, This multiplicity may allow for signal amplification and/or the formation of qualitatively distinct intracellular signals, Notably, the TCR-zeta subunit contains three ITAMs, and exists as a disulfide-linked homodimer in the TCR complex, In normal murine thymocytes and peripheral T cells, a proportion of TCR-zeta molecules is constitutively tyrosine phosphorylated and associated with the ZAP-70 protein tyrosine kinase, We examined the contribution of the different TCR-zeta ITAMs in regulating the constitutive phosphorylation of the TCR-zeta subunit in thymocytes by analyzing TCR-zeta-deficient mice that had been reconstituted with either full-length or single ITAM-containing TCR-zeta subunits, We report in this work that in the absence of a full-length TCR-zeta subunit, there is no apparent constitutive phosphorylation of the remaining TCR/CD3 ITAMs. Following TCR ligation, all of the CD3 ITAMs become inducibly phosphorylated and associate with the ZAP-70 protein tyrosine kinase, Regardless of the number of TCR-zeta ITAMs present in the TCR complex, we report that a number of molecules involved in downstream signaling events, such as ZAP-70, SLP-76, and pp36, are all inducibly tyrosine phosphorylated following TCR ligation, These results support the notion that the different TCR ITAMs function in a quantitative rather than qualitative manner. C1 Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Immunol & Microbiol, San Francisco, CA 94143 USA. NICHHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD 20892 USA. RP Weiss, A (reprint author), Univ Calif San Francisco, Howard Hughes Med Inst, U-330,3rd & Parnassus Ave, San Francisco, CA 94143 USA. FU NIGMS NIH HHS [GM-39553] NR 40 TC 65 Z9 65 U1 1 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1998 VL 160 IS 1 BP 163 EP 170 PG 8 WC Immunology SC Immunology GA YW266 UT WOS:000071915100023 PM 9551968 ER PT J AU Epstein, SL Lo, CY Misplon, JA Bennink, JR AF Epstein, SL Lo, CY Misplon, JA Bennink, JR TI Mechanism of protective immunity against influenza virus infection in mice without antibodies SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CYTOTOXIC T-LYMPHOCYTES; A VIRUSES; EPITHELIAL-CELLS; INTERFERON-GAMMA; RSV CHALLENGE; B-CELLS; NUCLEOPROTEIN; HEMAGGLUTININ; PROTEIN; RECOMBINANTS AB There is considerable interest in developing viral vaccines intended to induce T cell immunity, especially cytotoxic CD8(+) T lymphocytes, when Abs are not protective or are too narrow in viral strain specificity. We have studied protective immunity in doubly inactivated (DI) mice devoid of Abs and mature B cells. When infected with influenza B virus, these mice cleared the virus in a process dependent upon CD8(+) T lymphocytes. Cytotoxic activity was detected in lung lymphocytes of DI mice after primary or secondary infection, and was abrogated by depletion of CD8(+) cells in vivo. Challenge experiments showed that DI mice could be protected by immunization against reinfection 1 mo later, and protection was virus specific. Depletion of CD4(+) or CD8(+) T cells in vivo during the challenge period partially abrogated, and depletion of both subsets completely abrogated, the protection. This indicates that both CD4(+) and CD8(+) T cells are required effecters in the optimal control of virus replication. Thus, when Abs fail to protect against varying challenge viruses, as is the case with variant strains of influenza and HIV, there is hope that T cells might be able to act alone. C1 NIAID, Viral Dis Lab, Viral Immunol Sect, NIH, Bethesda, MD 20892 USA. US FDA, Ctr Biol Evaluat & Res, Div Cellular & Gene Therapies, Mol Immunol Lab, Bethesda, MD 20892 USA. RP Epstein, SL (reprint author), US FDA, CBER, OTRR, DCGT, 1401 Rockville Pike,HFM-521, Rockville, MD 20852 USA. NR 45 TC 125 Z9 130 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1998 VL 160 IS 1 BP 322 EP 327 PG 6 WC Immunology SC Immunology GA YW266 UT WOS:000071915100042 PM 9551987 ER PT J AU Steel, C Nutman, TB AF Steel, C Nutman, TB TI Helminth antigens selectively differentiate unsensitized CD45RA(+)CD4(+) human T cells in vitro SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INTERFERON-GAMMA PRODUCTION; HUMAN LYMPHATIC FILARIASIS; RECEPTOR TRANSGENIC MICE; PARASITE-SPECIFIC ANERGY; IN-VITRO; IFN-GAMMA; SUBSET DIFFERENTIATION; IMMUNE RESPONSIVENESS; LYMPHOKINE PRODUCTION; CYTOKINE PRODUCTION AB Human filarial helminth infections are characterized by type 2 immune responses to parasite Ag that can persist for the life of the individual; one possible cause for this may be prenatal exposure to the blood-borne microfilarial (Mf) stage of the parasite. To examine the relationship between early exposure to filarial Ag and subsequent immune responsiveness, CD45RA(+)CD4(+) cells from normal unsensitized donors were stimulated in vitro with soluble microfilarial Ag (MfAg) from the filarial parasite Brugia malayi in the presence of APCs. MfAg alone induced proliferation and IFN-gamma and IL-5 production in unsensitized CD45RA(+)CD4(+) cells, demonstrating the ability of filarial Ags to prime naive T cells in the absence of exogenous cytokines and dendritic cells. Adding exogenous cytokine(s) (particularly IL-12 and IL-4) during priming was able to alter the MfAg-specific responses of CD45RA(+)CD4(+) cells as well as subsequent responses to Ag. Interestingly, priming solely with MfAg led to enhanced IL-5 production following Ag restimulation, suggesting that MfAg preferentially primes for type 2 responses. These data demonstrate that filarial Ags by themselves can specifically prime CD45RA(+)CD4(+) cells in vitro and do so in such a way as to deviate the immune response. C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. RP Steel, C (reprint author), NIAID, Parasit Dis Lab, NIH, Bldg 4,Room 126, Bethesda, MD 20892 USA. EM cathy_steel@nih.gov NR 60 TC 14 Z9 14 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1998 VL 160 IS 1 BP 351 EP 360 PG 10 WC Immunology SC Immunology GA YW266 UT WOS:000071915100046 PM 9551991 ER PT J AU Biddison, WE Cruikshank, WW Center, DM Pelfrey, CM Taub, DD Turner, RV AF Biddison, WE Cruikshank, WW Center, DM Pelfrey, CM Taub, DD Turner, RV TI CD8(+) myelin peptide-specific T cells can chemoattract CD4(+) myelin peptide-specific T cells: Importance of IFN-inducible protein 10 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PERIPHERAL-BLOOD LYMPHOCYTES; MULTIPLE-SCLEROSIS; BASIC-PROTEIN; PROTEOLIPID PROTEIN; INFLUENZA-VIRUS; VIRAL PEPTIDES; EXPRESSION; CD4+; IDENTIFICATION; RESPONSES AB The demyelination process that occurs in the central nervous system (CNS) of patients with multiple sclerosis (MS) is due, in part, to an inflammatory response in which CD4(+) and CD8(+) T cells and macrophages infiltrate white matter, While it is thought that the inflammatory and demyelination process in MS is the product of Th1-associated cytokines secreted by CD4(+) myelin protein-specific T cells present in the CNS, the mechanisms that are responsible for the recruitment and maintenance of these myelin-reactive CD4(+) T cells in the CNS have not been elucidated, We have shown previously that CD8(+)CTL that recognize peptides derived from sequences of the myelin proteolipid protein (PLP) presented by HLA class I molecules can be generated in vitro, and that these PLP-specific CD8(+)CTL secrete the proinflammatory chemokines macrophage-inflammatory protein-1 alpha and -1 beta, IL-16, and IP-10. In this study, we demonstrate that soluble products of these PLP-specific CD8(+)CTL can chemoattract CD4(+) T cells that are specific for a myelin basic protein peptide and a PLP peptide, and that the majority of this chemotactic activity is mediated by IFN-inducible protein 10. These results demonstrate that PLP-specific CD8(+) T cells can play a role in the recruitment and retention of myelin-derived peptide-specific CD4(+) T cells, and indicate that they may play a proinflammatory role in the pathogenesis of MS. C1 NINDS, Mol Immunol Sect, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA. Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02115 USA. Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Frederick, MD 21702 USA. RP Biddison, WE (reprint author), NINDS, Mol Immunol Sect, Neuroimmunol Branch, NIH, Bldg 10,Room 5B-16, Bethesda, MD 20892 USA. OI Pelfrey, Clara/0000-0002-6108-7555 NR 33 TC 55 Z9 56 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1998 VL 160 IS 1 BP 444 EP 448 PG 5 WC Immunology SC Immunology GA YW266 UT WOS:000071915100057 PM 9552002 ER PT J AU Kim, CJ Parkinson, DR Marincola, F AF Kim, CJ Parkinson, DR Marincola, F TI Immunodominance across HLA polymorphism: Implications for cancer immunotherapy SO JOURNAL OF IMMUNOTHERAPY LA English DT Review DE immunodominance; HLA; polymorphism; CTL ID TUMOR-INFILTRATING LYMPHOCYTES; CYTOLYTIC T-LYMPHOCYTES; MELANOMA ANTIGEN GP100; CLASS-I MOLECULES; MHC CLASS-I; PEPTIDE-BINDING MOTIF; HUMAN GENE MAGE-3; CELL-LINES; PERIPHERAL-BLOOD; METASTATIC MELANOMA AB Recent advances in the understanding of the mechanisms leading to tumor recognition by the immune system have shown that, at least in the case of human melanoma, the majority of cytotoxic T lymphocytes (CTL) identified in association with in vivo tumor regression after interleukin-2 therapy recognize nonmutated molecules expressed by most melanoma cells. For this reason, peptide-based or whole protein vaccination protocols against melanoma-associated antigens (MAA) are ongoing in several institutions, with the goal of inducing tumor regression by enhancing in vivo specific antitumor CTL reactivity. The rationale for the use of such vaccines is supported by: (a) preclinical evidence that vaccination with major histocompatibility complex class I restricted epitopes can enhance effectively cellular immunity, (b) evidence that potent antimelanoma CTL reactivity can be generated by repetitive in vitro stimulation of peripheral blood monocytes with MAA, and (c) evidence that the systemic administration of the same MAA can elicit antitumor CTL reactivity in vivo. As strategies are being developed for the development of sound vaccines, two basic approaches are investigated: one vaccination strategy is based on the administration of the specific amino acid sequence recognized by the CTL in association with a particular human leukocyte antigen (HLA) restriction element, and the other is based on the administration of the whole antigenic molecule, which relies on the organism's antigen-processing capabilities to render suitable the antigen for induction of HLA class I restricted CTL reactivity in vivo. Among the various factors complicating T-cell-based vaccination approaches stands the polymorphism of the HLA molecules. HLA are the most polymorphic of human genes, and because such polymorphism is clustered in the functional peptide-binding region, the binding of antigenic peptides is necessarily restricted to specific HLA alleles. This limits the interactions between CTL and antigen to specific sequences for each HLA allele. For this reason, the ability of an individual antigen to function as a T-cell immunogen in the context of different HLA allele restriction elements is an open question. It seems logical that whole-molecule vaccines have the potential advantage of broader use across patient populations. In particular, large antigenic molecules may contain multiple peptide sequences with putative binding properties for different HLA alleles, which in turn may elicit T-cell reactivity across the polymorphism of HLA. Such a concept, however, relies on the assumption that the same antigen may function with similar efficiency as an immunogen in association with different HLA alleles, independently from the epitopic sequence recognized in the various situations. This concept has been challenged recently by several practical observations and remains, in our opinion, an open question. This review will address the practical question of immunogenicity of molecules across the HLA polymorphism. We postulate that the complexity and success of the development of peptide-based vaccination strategies depend on the severity of this restriction, which is currently only incompletely studied and understood. Although no solutions are offered to the problem, emphasis is placed on the importance of this question, hopefully to stimulate the interest of other researchers, particularly in clinical settings, toward the investigation of this type of problem. C1 NCI, Surg Branch, Div Clin Sci, NIH, Bethesda, MD 20892 USA. NIH, HLA Lab, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA. Novartis AG, Oncol Therapeut, E Hanover, NJ USA. RP Marincola, F (reprint author), NCI, Surg Branch, Div Clin Sci, NIH, Bldg 10,Room 2B56, Bethesda, MD 20892 USA. NR 130 TC 23 Z9 24 U1 2 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1998 VL 21 IS 1 BP 1 EP 16 PG 16 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA YQ041 UT WOS:000071341500001 PM 9456431 ER PT J AU Cormier, JN Abati, A Fetsch, P Hijazi, YM Rosenberg, SA Marincola, FM Topalian, SL AF Cormier, JN Abati, A Fetsch, P Hijazi, YM Rosenberg, SA Marincola, FM Topalian, SL TI Comparative analysis of the in vivo expression of tyrosinase, MART-1/Melan-A, and gp100 in metastatic melanoma lesions: Implications for immunotherapy SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE melanoma; immunotherapy; tyrosinase; MART-1; gp100 ID CYTOLYTIC T-LYMPHOCYTES; TUMOR-INFILTRATING LYMPHOCYTES; POLYMERASE CHAIN-REACTION; HLA-A2 MELANOMAS; IN-VIVO; CELLS; ANTIGENS; GENE; RECOGNIZE; EPITOPES AB A variety of human melanoma-associated antigens (MAA) have been identified that can be recognized by T lymphocytes in a major histocompatibility complex-restricted fashion. Among them, tyrosinase, MART-1/Melan- A, and gp100 are derived from nonmutated melanocyte lineage-specific antigens (Ag). These Ag can be recognized by CD8(+) and, in the case of tyrosinase, CD4(+) T cells. The in situ expression of MAA may be a significant cofactor in determining the recognition of melanoma targets by Ag-specific T cells. In this study, we examined the patterns of expression of these MAA using immunohistochemical methods on 30 metastatic tumor deposits derived from 25 patients. MAA expression was heterogeneous among the 30 specimens and also within individual lesions. Of note, 23% of the samples examined failed to express the gp100 protein, and 17% of samples had no detectable expression of MART-1. In contrast, all lesions demonstrated some degree of tyrosinase expression even in cases where both gp100 and MART-1 were not detectable. In addition, 60% of samples (18 of 30) showed strong positivity for tyrosinase (>75% of cells staining) compared with 40% for gp100 and 36% for MART-1. Currently, a number of experimental immunotherapies for melanoma are directed against the MAA tyrosinase, MART-1, and gp100. Although threshold levels of Ag required for T-cell recognition have not yet been defined, tumor-associated Ag expressed in high density, such as tyrosinase, may be better targets for future immunotherapy trials. C1 NCI, Surg Branch, NIH 102B47, Bethesda, MD 20892 USA. NCI, Pathol Lab, Div Clin Sci, NIH, Bethesda, MD 20892 USA. RP Topalian, SL (reprint author), NCI, Surg Branch, NIH 102B47, Bethesda, MD 20892 USA. NR 21 TC 79 Z9 80 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1998 VL 21 IS 1 BP 27 EP 31 DI 10.1097/00002371-199801000-00003 PG 5 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA YQ041 UT WOS:000071341500003 PM 9456433 ER PT J AU Mahmoud, AAF La Montagne, J Takeda, Y AF Mahmoud, AAF La Montagne, J Takeda, Y TI Summary of the International Conference on Emerging Infectious Diseases US-Japan Cooperative Medical Science Program, Bangkok, 1997 SO JOURNAL OF INFECTIOUS DISEASES LA English DT Editorial Material C1 Case Western Reserve Univ Hosp, Dept Med, Cleveland, OH 44106 USA. NIAID, Div Microbiol & Infect Dis, Bethesda, MD 20892 USA. Int Med Ctr Japan, Res Inst, Tokyo, Japan. RP Mahmoud, AAF (reprint author), Case Western Reserve Univ Hosp, Dept Med, 11100 Euclid Ave, Cleveland, OH 44106 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1998 VL 177 IS 1 BP 3 EP 4 DI 10.1086/513828 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA YM597 UT WOS:000071080700002 PM 9419162 ER PT J AU Feinberg, JE Hurwitz, S Cooper, D Sattler, FR MacGregor, RR Powderly, W Holland, GN Griffiths, PD Pollard, RB Youle, M Gill, MJ Holland, FJ Power, ME Owens, S Coakley, D Fry, J Jacobson, MA AF Feinberg, JE Hurwitz, S Cooper, D Sattler, FR MacGregor, RR Powderly, W Holland, GN Griffiths, PD Pollard, RB Youle, M Gill, MJ Holland, FJ Power, ME Owens, S Coakley, D Fry, J Jacobson, MA TI A randomized, double-blind trial of valaciclovir prophylaxis for cytomegalovirus disease in patients with advanced human immunodeficiency virus infection SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT XIth International Conference on AIDS CY JUL 07-13, 1996 CL VANCOUVER, CANADA ID DOSE ORAL ACYCLOVIR; ZIDOVUDINE; AIDS; GANCICLOVIR; PREVENTION; SURVIVAL; ASSOCIATION; RECIPIENTS; CMV AB Cytomegalovirus (CMV) disease is a common complication of advanced human immunodeficiency virus (HIV) infection, Administration of oral valaciclovir, a valine ester of acyclovir, achieves sufficient plasma acyclovir levels to inhibit many clinical isolates, Acyclovir has been associated with enhanced survival in AIDS but not with CMV disease prevention, CMV-seropositive patients (1227) with CD4 cell counts <100/mm(3) were enrolled in a randomized, double-blind trial, Valaciclovir, 8 g/day, was compared with acyclovir, 3.2 or 0.8 g/day, for CMV prevention; all three arms were compared for survival, The confirmed CMV disease rate was 11.7% among valaciclovir recipients and 17.5% in the pooled acyclovir arms, a 33% reduction in risk, Time to confirmed CMV disease was significantly longer for the valaciclovir group (P = .03), A trend toward earlier mortality for valaciclovir recipients was seen (P = .06), Toxicity and earlier medication discontinuation were more common in this group, Valaciclovir significantly reduces the risk of CMV disease, Further exploration of a better-tolerated dose is warranted. C1 Univ Cincinnati, Dept Med, Cincinnati, OH 45267 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Natl Ctr HIV Epidemiol & Clin Res, Sydney, NSW, Australia. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Univ So Calif, Los Angeles, CA 90089 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Penn, Philadelphia, PA 19104 USA. Washington Univ, St Louis, MO 63130 USA. Royal Free Hosp, Sch Med, London, England. Kobler Ctr, London, England. Univ Texas, Galveston, TX USA. Univ Calgary, Calgary, AB T2N 1N4, Canada. NIAID, Div Aids, NIH, Bethesda, MD 20892 USA. Glaxo Wellcome, Antiviral Clin Res, Res Triangle Pk, NC USA. Glaxo Wellcome, Antiviral Clin Res, Beckenham, Kent, England. RP Feinberg, JE (reprint author), Univ Cincinnati, Holmes Hosp, Eden & Bethesda Aves, Cincinnati, OH 45267 USA. RI Gill, John/G-7083-2016 OI Gill, John/0000-0002-8546-8790 NR 32 TC 73 Z9 77 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1998 VL 177 IS 1 BP 48 EP 56 DI 10.1086/513804 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA YM597 UT WOS:000071080700009 PM 9419169 ER PT J AU Shirai, M Arichi, T Nakazawa, T Berzofsky, JA AF Shirai, M Arichi, T Nakazawa, T Berzofsky, JA TI Persistent infection by Helicobacter pylori down-modulates virus-specific CD8(+) cytotoxic T cell response and prolongs viral infection SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID RECOMBINANT VACCINIA VIRUS; TOXIC LYMPHOCYTES-T; IMMUNE-RESPONSES; LEISHMANIA-MAJOR; HIV-INFECTION; MONOCLONAL-ANTIBODIES; SCHISTOSOMA-MANSONI; INTERFERON-GAMMA; HELPER ACTIVITY; TH2 SUBSETS AB To determine whether Helicobacter pylori infection affects clearance of a concomitant viral infection and cytotoxic T lymphocyte (CTL) and cytokine response to that infection, H. pylori-infected BALB/c mice were challenged with a recombinant vaccinia virus expressing human immunodeficiency virus type 1 gp160, Two H. pylori strains, a colonizing clinical isolate (KS612) and an established standard noncolonizing strain (NCTC11637), were compared, Clearance of recombinant vaccinia virus was reduced in KS612-infected mice compared with NCTC11637-infected and control mice, As a potential mechanism, in contrast to control or NCTC11637-infected mice, the H, pylori clinical isolate KS612 diminished gp160-specific and vaccinia virus-specific CTL activity, even in the presence of exogenous interleukin-2, Furthermore, KS612-infected mice had reduced Th1 cytokine responses to gp120 in vitro compared with control or NCTC11637-infected mice, These results have implications for possible effects of prevalent H. pylori infection on other human diseases. C1 NCI, Mol Immunogenet & Vaccine Res Sect, Metab Branch, NIH, Bethesda, MD 20892 USA. Yamaguchi Univ, Sch Med, Dept Microbiol, Yamaguchi, Japan. Kagawa Med Sch, Dept Internal Med 3, Kagawa, Japan. RP Berzofsky, JA (reprint author), NCI, Mol Immunogenet & Vaccine Res Sect, Metab Branch, NIH, Bldg 10,Room 6B-12, Bethesda, MD 20892 USA. NR 72 TC 28 Z9 29 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1998 VL 177 IS 1 BP 72 EP 80 DI 10.1086/513827 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA YM597 UT WOS:000071080700012 PM 9419172 ER PT J AU Corriveau, CC Madara, PJ Van Dervort, AL Tropea, MM Wesley, RA Danner, RL AF Corriveau, CC Madara, PJ Van Dervort, AL Tropea, MM Wesley, RA Danner, RL TI Effects of nitric oxide on chemotaxis and endotoxin-induced interleukin-8 production in human neutrophils SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; SYNTHASE MESSENGER-RNA; MONOMETHYL-L-ARGININE; CYCLIC-GMP; MONOCYTE CHEMOTAXIS; ENDOTHELIAL-CELLS; DIFFERENTIAL REGULATION; MONONUCLEAR-CELLS; GENE-EXPRESSION; IL-8 EXPRESSION AB The effects of nitric oxide (NO) on human neutrophil chemotactic responses and release of interleukin (IL)-8 was studied. Neutrophils exposed to chemoattractants (IL-8, FMLP, leukotriene B-4, and C5a) failed to show increases in intracellular guanosine 3',5'-cyclic monophosphate (cGMP), an indicator of NO production, Although NO increased cGMP in neutrophils, neither of two NO donors (sodium nitroprusside and 3-morpholino-sydonimine) nor a NO synthase inhibitor (N-omega-nitro-L-arginine) altered FMLP-or IL-8-elicited neutrophil chemotaxis (P > .25 for all). However, lipopolysaccharide-induced IL-8 production was increased in a dose-dependent manner by a combination of sodium nitroprusside and N-acetylcysteine (P = .03) or by S-nitrosoglutathione (P = .004), NO-augmented IL-8 release was not reproduced by treating neutrophils with dibutyryl-cGMP, Upregulation of IL-8 release by NO was associated with increased IL-8 mRNA levels (P = .009). These data suggest that NO does not directly affect neutrophil chemotaxis but may indirectly alter chemotactic responses by increasing IL-8 production via a cGMP-independent pathway. C1 NIH, Dept Crit Care Med, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA. Childrens Natl Med Ctr, Washington, DC 20010 USA. RP Danner, RL (reprint author), NIH, Dept Crit Care Med, Warren Grant Magnuson Clin Ctr, Bldg 10,Room 7D43, Bethesda, MD 20892 USA. NR 61 TC 36 Z9 36 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1998 VL 177 IS 1 BP 116 EP 126 DI 10.1086/513829 PG 11 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA YM597 UT WOS:000071080700018 PM 9419178 ER PT J AU Ramachandran, S Thompson, RW Gam, AA Neva, FA AF Ramachandran, S Thompson, RW Gam, AA Neva, FA TI Recombinant cDNA clones for immunodiagnosis of strongyloidiasis SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 45th Annual Meeting of the American-Society-of-Tropical-Medicine-and-Hygiene CY DEC 01-05, 1996 CL BALTIMORE, MARYLAND SP Amer Soc Trop Med & Hyg ID LINKED-IMMUNOSORBENT-ASSAY; FAR-EAST PRISONERS; STERCORALIS INFECTION; DIAGNOSIS; VIRUS; WAR; HYPERINFECTION; ANTIBODIES; PROTEINS; FAMILY AB Because diagnosis of strongyloidiasis by stool examination is unreliable and because of the potential for serious disease in Strongyloides infections, there is need for improved diagnostic aids to facilitate recognition and treatment of this parasitic infection. Serologic testing, when available, requires antigen preparation from infected primates or dogs that can be difficult to maintain, Several recombinant clones from a cDNA library prepared from the infective stage of Strongyloides stercoralis were characterized. Serologic results indicate that the recombinant proteins were equally or more reactive than the larval somatic antigen, No cross-reactivity with recombinant antigen 5a was found with sera from patients with filarial or intestinal nematode infections, Recombinant antigens 5a and 12a detected parasite-specific IgE and IgG4 antibodies in Strongyloides-infected patients. Sequence analysis showed these antigens to be rich in proline and charged amino acids, Lack of homology from database searches suggests that the antigens are unique, These recombinant antigens should be useful in diagnostic and epidemiologic studies of strongyloidiasis. C1 NIH, Parasit Dis Lab, Bethesda, MD 20892 USA. US FDA, Ctr Biol Evaluat, Bethesda, MD 20892 USA. RP Ramachandran, S (reprint author), NIH, Parasit Dis Lab, 9000 Rockville Pike,Bldg 4,Room 126, Bethesda, MD 20892 USA. NR 25 TC 24 Z9 24 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVENUE, CHICAGO, IL 60637 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1998 VL 177 IS 1 BP 196 EP 203 DI 10.1086/513817 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA YM597 UT WOS:000071080700028 PM 9419188 ER PT J AU Duhe, RJ Farrar, WL AF Duhe, RJ Farrar, WL TI Structural and mechanistic aspects of Janus kinases: How the two-faced god wields a double-edged sword SO JOURNAL OF INTERFERON AND CYTOKINE RESEARCH LA English DT Review ID PROTEIN-TYROSINE KINASE; GROWTH-HORMONE RECEPTOR; GAMMA SIGNAL-TRANSDUCTION; COLONY-STIMULATING FACTOR; MEMBRANE-PROXIMAL REGION; MICE LACKING JAK3; INTERFERON-GAMMA; ERYTHROPOIETIN RECEPTOR; MOLECULAR-CLONING; CRYSTAL-STRUCTURE AB The Janus family of protein-tyrosine kinases has long been known to function in signal transduction pathways initiated by a host of cytokines, A brief overview of the role of Janus kinases (Jaks) in both cytokine and noncytokine signaling pathways highlights the broad physiologic importance of this kinase family, New insights into the structural and mechanistic regulatory aspects of Janus kinases are rapidly emerging, Recent mutational analyses allow the dissection of Jaks into three distinct structural domains governing receptor affiliation, autoregulation, and catalysis, A fourth domain determining substrate specificity is as yet poorly defined and is, therefore, discussed in the context of known substrates and inhibitors, a collection of molecules that have been expanded recently to include Stam and Jab, The proposed mechanism of the interconversion of Janus kinases from inactive to fully active enzymes involves three states of enzymatic activity, Additional layers of regulation can be independently superimposed on this multistate model, providing a simplified description of the behavior of Janus kinases under normal and pathologic circumstances. C1 NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, SAIC, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Cytokine Mol Mechanisms Sect, Mol Immunoregulat Lab, Frederick, MD 21702 USA. RP Duhe, RJ (reprint author), NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, SAIC, POB B, Frederick, MD 21702 USA. NR 129 TC 23 Z9 23 U1 0 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1079-9907 J9 J INTERF CYTOK RES JI J. Interferon Cytokine Res. PD JAN PY 1998 VL 18 IS 1 BP 1 EP 15 DI 10.1089/jir.1998.18.1 PG 15 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA YU337 UT WOS:000071707200001 PM 9475661 ER PT J AU Rossi, A Jang, SI Ceci, R Steinert, PM Markova, NG AF Rossi, A Jang, SI Ceci, R Steinert, PM Markova, NG TI Effect of AP1 transcription factors on the regulation of transcription in normal human epidermal keratinocytes SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE differentiation; gene transcription ID DIFFERENTIATION-SPECIFIC EXPRESSION; HUMAN LORICRIN GENE; C-FOS; PROXIMAL PROMOTER; RETINOIC ACID; PROTOONCOGENE EXPRESSION; AP-1 ELEMENT; BINDING; JUN; CELLS AB The conversion of basal keratinocytes to spinous and granular cells is accompanied by the synthesis of a series of epidermal proteins in a differentiation-specific pattern. The transcription of several of these epidermal marker genes is regulated by activator protein 1 (AP1) interactions at their promoter regions. In the epidermis the various AP1 transcription factors are not present uniformly but appear to have a differentiation-specific distribution. We have explored whether the AP1 regulated expression of the keratin 5, transglutaminase 1, involucrin, and loricrin genes reflects the distribution of the AP1 factors in the epidermis. We have found that c-jun and junD activate and junB downregulates the transcription of both basal and suprabasal genes. The effect of c-jun is exerted through interactions with c-fos at the AP1 motifs in the target promoters, whereas both junB and junD act independently of the binding at the AP1 sites. Thus c-jun and junD act as general positive regulators whereas junB acts as a general suppressor of epidermal-specific genes. Therefore, the differentiation specificity of the API regulation must be determined not only by the formation of distinct DNA/AP1 complexes but also by interactions involving other transcriptional regulators and/or distal regulatory elements. C1 NIAMSD, Skin Biol Lab, NIH, Bethesda, MD 20892 USA. Univ Rome Tor Vergata, Dept Expt Med, I-00173 Rome, Italy. RP Steinert, PM (reprint author), NIAMSD, Skin Biol Lab, NIH, Bldg 6,Room 425,Mail Stop 20892-2752, Bethesda, MD 20892 USA. OI Ceci, Roberta/0000-0002-8900-8839 NR 40 TC 79 Z9 79 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JAN PY 1998 VL 110 IS 1 BP 34 EP 40 DI 10.1046/j.1523-1747.1998.00071.x PG 7 WC Dermatology SC Dermatology GA YN002 UT WOS:000071123200008 PM 9424084 ER PT J AU Hertl, M Amagai, M Sundaram, H Stanley, J Ishii, K Katz, SI AF Hertl, M Amagai, M Sundaram, H Stanley, J Ishii, K Katz, SI TI Recognition of desmoglein 3 by autoreactive T cells in pemphigus vulgaris patients and normals SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE autoimmunity; peptides; T lymphocytes ID MAJOR HISTOCOMPATIBILITY COMPLEX; MYELIN BASIC-PROTEIN; CLASS-II GENES; AUTOIMMUNE-DISEASES; ACETYLCHOLINE-RECEPTOR; EXTRACELLULAR DOMAIN; MULTIPLE-SCLEROSIS; JEWISH PATIENTS; SELF-PEPTIDES; AUTOANTIBODIES AB Pemphigus vulgaris (PV) is an autoimmune blistering disease of the skin and is caused by autoantibodies against desmoglein 3 (Dsg3) on epidermal keratinocytes. Because the production of autoantibodies is presumably T cell dependent, Dsg3-specific T cell reactivity was investigated in 14 PV patients and 12 healthy donors. Peripheral blood mononuclear cells from seven PV patients with active disease showed a primary in vitro response to a recombinant protein containing the extracellular portion (EC1-5) of Dsg3, whereas two of seven PV patients in remission or under immunosuppressive treatment exhibited only secondary (2 degrees) or tertiary (3 degrees) T cell responses to Dsg3. T cell responses to Dsg3 were also observed in four of 12 healthy individuals upon 2 degrees or 3 degrees stimulation with Dsg3. Both PV patients and healthy responders were either positive for DR beta 1*0402 - which is highly prevalent in PV - or positive for DR11 alleles homologous to DR beta 1*0402. Two CD4+ Dsg3-specific T cell lines and 12 T cell clones from two PV patients and two CD4+ T cell lines and eight T cell clones from two normals were also stimulated by a Dsg3 protein devoid of the EC2-3 (Delta N1), suggesting that epitopes were located in the EC1, EC4, and/or EC5. Using Dsg3 peptides, one immunodominant peptide (residues 161-177) was also identified in the EC2. These observations demonstrate that T cell responses to Dsg3 can be detected in PV patients and in healthy donors carrying major histocompatibility class II alleles identical or similar to those highly prevalent in PV. C1 NCI, Dermatol Branch, Bethesda, MD 20892 USA. Keio Univ, Dept Dermatol, Tokyo, Japan. Univ Penn, Sch Med, Dept Dermatol, Philadelphia, PA 19104 USA. RP Hertl, M (reprint author), Rhein Westfal TH Aachen, Hautklin, Pauwelsstr 30, D-52074 Aachen, Germany. RI Amagai, Masayuki/K-5325-2013 OI Amagai, Masayuki/0000-0003-3314-7052 NR 28 TC 77 Z9 84 U1 0 U2 3 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JAN PY 1998 VL 110 IS 1 BP 62 EP 66 DI 10.1046/j.1523-1747.1998.00086.x PG 5 WC Dermatology SC Dermatology GA YN002 UT WOS:000071123200013 PM 9424089 ER PT J AU Lagasse, GW Bailey-Wilson, JE Borrouso, LB Rothschild, H AF Lagasse, GW Bailey-Wilson, JE Borrouso, LB Rothschild, H TI The use of the computer simulation program SIMLINK to identify families from southern Louisiana that were useful for linkage studies of lung cancer. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 Natl Human Genome Res Inst, NIH, Baltimore, MD USA. Louisiana State Univ, Med Ctr, New Orleans, LA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 9A EP 9A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700045 ER PT J AU Goebel, J Franks, A Robey, F Mikovits, J Lowry, RP AF Goebel, J Franks, A Robey, F Mikovits, J Lowry, RP TI Attenuation of IL-2 signaling by CD4 ligand involves the cytoskeleton but does not require P56LCK. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 Univ S Alabama, Transplantat Immunol Lab, Mobile, AL 36688 USA. Tulane Hosp Children, New Orleans, LA USA. NIH, Bethesda, MD 20892 USA. NIH, Frederick, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 23A EP 23A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700120 ER PT J AU Seidner, SR Jobe, AH Ikegami, M Segura, L Mendelson, CR AF Seidner, SR Jobe, AH Ikegami, M Segura, L Mendelson, CR TI Postnatal dexamethasone and surfactant regulation in preterm baboons of borderline viability. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 Univ Texas, Hlth Sci Ctr, Dept Pediat, San Antonio, TX 78284 USA. Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA. Univ Texas, Dept Biochem, Dallas, TX 75230 USA. NIH, BPD Resource Ctr, San Antonio, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 41A EP 41A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700214 ER PT J AU Shinar, RZ Natarajan, K Margulies, DH AF Shinar, RZ Natarajan, K Margulies, DH TI In vitro refolding and characterization of bacterially-expressed D-d-peptide complexes. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 Univ Calif San Diego, Sch Med, La Jolla, CA 92093 USA. NIAID, NIH, Bethesda, MD 20892 USA. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 78A EP 78A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700411 ER PT J AU Jones, JC Umetsu, DT Potter, M DeKruyff, RH AF Jones, JC Umetsu, DT Potter, M DeKruyff, RH TI Mapping a gene on murine chromosome 11 associated with high IL-4 responsiveness and Th2 development. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 Stanford Univ, Stanford, CA 94305 USA. Natl Canc Inst, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 113A EP 113A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700599 ER PT J AU Gabriele, L Phung, JP Thornton, AM Giannakakou, P Ozato, K Morse, HC AF Gabriele, L Phung, JP Thornton, AM Giannakakou, P Ozato, K Morse, HC TI Apoptosis of myeloid cells is regulated by interferon consensus sequence binding protein: Implications for malignant transformation of myeloid cells. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 NIAID, Immunopathol Lab, NIH, Bethesda, MD 20892 USA. NICHHD, Lab Mol Growth Regulat, NIH, Bethesda, MD 20892 USA. NCI, Div Clin Sci, Med Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 117A EP 117A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700620 ER PT J AU Bird, LM Ma, M Rosenberg, M Biesecker, LG AF Bird, LM Ma, M Rosenberg, M Biesecker, LG TI An "unknown syndrome" due to occult chromosomal deletion. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 Childrens Hosp, Div Dysmorphol, San Diego, CA USA. NHGRI, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 119A EP 119A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700635 ER PT J AU Wong, A Gutkind, JS AF Wong, A Gutkind, JS TI A novel signaling pathway links the small GTP-binding protein Rho to nuclear responses mediated by CREB and CBP/P300. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 NIDR, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA. RI Gutkind, J. Silvio/A-1053-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 127A EP 127A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700676 ER PT J AU Currey, KM Shapiro, BA Tracy, SA Chapman, NM AF Currey, KM Shapiro, BA Tracy, SA Chapman, NM TI RNA structure determinants of cardiovirulence in coxsackievirus B3. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 Univ Nebraska, Dept Pathol & Microbiol, Omaha, NE 68182 USA. NCI, IPS, DBS, NIH, Frederick, MD 21701 USA. Univ Maryland, Dept Pediat, Baltimore, MD 21201 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 1998 VL 46 IS 1 BP 173A EP 173A PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA YU124 UT WOS:000071684700921 ER PT J AU Vodovotz, Y Kopp, JB Takeguchi, H Shrivastav, S Coffin, D Lucia, MS Mitchell, JB Webber, R Letterio, J Wink, D Roberts, AB AF Vodovotz, Y Kopp, JB Takeguchi, H Shrivastav, S Coffin, D Lucia, MS Mitchell, JB Webber, R Letterio, J Wink, D Roberts, AB TI Increased mortality, blunted production of nitric oxide, and increased production of TNF-alpha in endotoxemic TGF-beta 1 transgenic mice SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE NOS2; septic shock ID TRANSFORMING GROWTH-FACTOR; INFLAMMATORY RESPONSE SYNDROME; SYNTHASE MESSENGER-RNA; SMOOTH-MUSCLE CELLS; FACTOR-BETA; SEPTIC SHOCK; MOUSE MACROPHAGES; BREAST-CANCER; IN-VIVO; PERITONEAL-MACROPHAGES AB The expression of the inducible isoform of nitric oxide synthase (NOS2, iNOS) is increased in patients undergoing sepsis as well as in animal models in which septic shock is induced by injection of bacterial lipopolysaccharide (LPS). Transforming growth factor-beta 1 (TGF-beta 1) potently suppresses NO production both in vitro and in vivo., After intraperitoneal injection of LPS, mice over-expressing a cDNA coding for active TGF-beta 1 in the liver (Alb/TGF-beta 1) exhibited reduced serum levels of the NO reaction products NO2- + NO3- compared,vith controls, Paradoxically, while endotoxemic. Alb/TGF-beta 1 mice expressed much less NOS2 protein in peritoneal exudate cells than did endotoxemic wild-type mice, Alb/TGF-beta 1 mice expressed more NOS2 mRNA and protein in both liver and kidney. Alb/TGF-beta 1 mice treated with LPS had eightfold higher serum tumor necrosis factor alpha (TNF-alpha) levels and experienced increased mortality compared with wildtype mice, which was associated with renal insufficiency, These results suggest that renal dysfunction, decreased production of NO, and/or increased production of TNF-alpha are associated with increased mortality of endotoxemic Alb/TGF-beta 1 mice. C1 NIDDKD, Kidney Dis Sect, Metab Dis Branch, NIH, Bethesda, MD 20892 USA. NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA. NCI, Chemoprevent Lab, NIH, Bethesda, MD 20892 USA. Res & Diagnost Antibodies, Richmond, CA USA. RP Vodovotz, Y (reprint author), Cardiol Res Fdn, 110 Irving St NW,Suite 4B-1, Washington, DC 20010 USA. EM yxv1@mhg.edu NR 65 TC 22 Z9 25 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JAN PY 1998 VL 63 IS 1 BP 31 EP 39 PG 9 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YR625 UT WOS:000071514000004 PM 9469470 ER PT J AU Marincola, FM Panelli, MC Wunderlich, J Rosenberg, SA AF Marincola, FM Panelli, MC Wunderlich, J Rosenberg, SA TI Phase I study in patients with metastatic melanoma of immunization with dendritic cells presenting epitopes derived from the melanoma associated antigens MART-1 and gp-100. SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1998 SU 2 MA S18 BP 15 EP 15 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA 126TN UT WOS:000076309900020 ER PT J AU Cox, D Zhang, Q Lee, D Dondaldson, JG Greenberg, S AF Cox, D Zhang, Q Lee, D Dondaldson, JG Greenberg, S TI Distinct signaling requirements for actin assembly and pseudopod extension during phagocytosis SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 Columbia Univ, Dept Med, New York, NY USA. Columbia Univ, Dept Pharmacol, New York, NY USA. NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1998 SU 1 MA 65 BP 20 EP 20 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA 117YP UT WOS:000075810700066 ER PT J AU Akiyama, Y Komschlies, K Finch, LR Young, HA Wiltrout, RH Ruscetti, FW AF Akiyama, Y Komschlies, K Finch, LR Young, HA Wiltrout, RH Ruscetti, FW TI Transforming growth factor (TGF)-beta 1 promotes the development of dendritic cell (DC) from mouse bone marrow cells by upregulation of bcl-2 SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, LEI, Frederick, MD 21702 USA. SAIC, IRSP, Frederick, MD 21702 USA. SAIC, CSP, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1998 SU 2 MA A19 BP 21 EP 21 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA 126TN UT WOS:000076309900040 ER PT J AU Yamada, N Katz, SI AF Yamada, N Katz, SI TI Generation of fully mature dendritic cells from the CD14+ cell line XS52 using cytokines and agonistic anti-CD40 monoclonal antibody SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI, Dermatol Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1998 SU 2 MA A23 BP 22 EP 22 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA 126TN UT WOS:000076309900044 ER PT J AU Danilkovitch, A Leonard, EJ AF Danilkovitch, A Leonard, EJ TI Kinases involved in MSP/RON signaling SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI, Frederick, MD 21702 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1998 SU 1 MA 141 BP 32 EP 32 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA 117YP UT WOS:000075810700140 ER PT J AU Jakob, T Walker, PS Krieg, AM Udey, MC Vogel, J AF Jakob, T Walker, PS Krieg, AM Udey, MC Vogel, J TI Activation of cutaneous dendritic cells by bacterial DNA and CpG-oligodeoxynucleotides: Implications for the induction of Th1 responses by immunostimulatory DNA. SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 Univ Iowa, Dept Med, Iowa City, IA 52246 USA. NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA. RI Jakob, Thilo/J-1621-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1998 SU 2 MA B31 BP 36 EP 36 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA 126TN UT WOS:000076309900098 ER EF