FN Thomson Reuters Web of Science™ VR 1.0 PT J AU LENARDO, M SIEBENLIST, U AF LENARDO, M SIEBENLIST, U TI BCL-3-MEDIATED NUCLEAR-REGULATION OF THE NF-KAPPA-B TRANSACTIVATING FACTOR SO IMMUNOLOGY TODAY LA English DT Note ID BCL-3 AB The NG-KB factor governs the expression of many genes encoding immunoregulatory molecules. This activity is itself controlled. In this article, novel nuclear pathways for NF-kappaB regulation are described. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP LENARDO, M (reprint author), NIAID,IMMUNOL LAB,BETHESDA,MD 20892, USA. NR 11 TC 50 Z9 51 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD APR PY 1994 VL 15 IS 4 BP 145 EP 147 DI 10.1016/0167-5699(94)90308-5 PG 3 WC Immunology SC Immunology GA NE338 UT WOS:A1994NE33800001 PM 8198705 ER PT J AU ASHWELL, JD BERGER, NA CIDLOWSKI, JA LANE, DP KORSMEYER, SJ AF ASHWELL, JD BERGER, NA CIDLOWSKI, JA LANE, DP KORSMEYER, SJ TI COMING TO TERMS WITH DEATH - APOPTOSIS IN CANCER AND IMMUNE DEVELOPMENT SO IMMUNOLOGY TODAY LA English DT Editorial Material AB The mechanism by which cells die has received much interest in recent years, particularly with respect to its importance in the generation of tumour cells. A recent meeting* defined the progress that has been made in understanding this process. C1 CASE WESTERN RESERVE UNIV,CANC RES CTR,DEPT MED & BIOCHEM,DIV HEMATOL ONCOL,CLEVELAND,OH 44106. WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,RES LABS,ST LOUIS,MO 63110. UNIV N CAROLINA,SCH MED,DEPT PHYSIOL & BIOCHEM,CHAPEL HILL,NC 27516. UNIV DUNDEE,CANC RES CAMPAIGN LABS,DUNDEE DD1 4HN,SCOTLAND. RP ASHWELL, JD (reprint author), NIH,IMMUNE CELL BIOL LAB,BETHESDA,MD 20892, USA. RI Lane, David/C-4920-2008 NR 0 TC 61 Z9 61 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD APR PY 1994 VL 15 IS 4 BP 147 EP 151 DI 10.1016/0167-5699(94)90309-3 PG 5 WC Immunology SC Immunology GA NE338 UT WOS:A1994NE33800002 PM 7911020 ER PT J AU MOWATT, MR NGUYEN, BYT CONRAD, JT ADAM, RD NASH, TE AF MOWATT, MR NGUYEN, BYT CONRAD, JT ADAM, RD NASH, TE TI SIZE HETEROGENEITY AMONG ANTIGENICALLY RELATED GIARDIA-LAMBLIA VARIANT-SPECIFIC SURFACE-PROTEINS IS DUE TO DIFFERENCES IN TANDEM REPEAT COPY NUMBER SO INFECTION AND IMMUNITY LA English DT Article ID CYSTEINE-RICH PROTEIN; FAMILY; GENE; DNA AB Giardia lamblia undergoes antigenic variation by modulating the expression of the different genes that comprise the trophozoite's variant-specific surface protein (VSP) repertoire. We studied an epitope that is conserved among VSPs expressed by cloned trophozoite lines derived from the independent G. lamblia isolates WB, G3M, Be-2, and CAT. The epitope recognized by monoclonal antibody 6E7 lies entirely within the region of tandemly repeated 65-amino-acid units that is characteristic of these size-variant VSPs. Northern (RNA) hybridization, cDNA cloning, and DNA sequence analysis indicate that size heterogeneity among these VSPs is due to differences in the number of repetitive units. C1 UNIV ARIZONA,ARIZONA HLTH SCI CTR,DEPT INTERNAL MED,TUCSON,AZ 85724. UNIV ARIZONA,ARIZONA HLTH SCI CTR,TUCSON,AZ 85724. RP MOWATT, MR (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 26 TC 25 Z9 26 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1994 VL 62 IS 4 BP 1213 EP 1218 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NC074 UT WOS:A1994NC07400013 PM 7510666 ER PT J AU UDHAYAKUMAR, V SHI, YP KUMAR, S JUE, DL WOHLHUETER, RM LAL, AA AF UDHAYAKUMAR, V SHI, YP KUMAR, S JUE, DL WOHLHUETER, RM LAL, AA TI ANTIGENIC DIVERSITY IN THE CIRCUMSPOROZOITE PROTEIN OF PLASMODIUM-FALCIPARUM ABROGATES CYTOTOXIC-T-CELL RECOGNITION SO INFECTION AND IMMUNITY LA English DT Article ID LYMPHOCYTES-T; EPITOPES; MALARIA; POLYMORPHISM; ESCAPE AB Genetic analysis of field isolates of Plasmodium falciparum has shown selective accumulation of point mutations within the immunologically sensitive sites of the circumsporozoite (CS) protein, a vaccine candidate against malaria. This raised concern whether a vaccine containing the sequence of a selected strain of P. falciparum would be able to confer protection against other variant parasites. The answer to this question remained speculative, and in this study, we have formally tested the immunological impact of such natural variations within a known cytotoxic-T-cell (CTL) epitope, which is recognized by both human and murine CTLs. With a murine model, CTLs were generated against the 7G8 strain of P. falciparum The ability of these CTLs to lyse histocompatible targets that were pulsed with synthetic peptides corresponding to polymorphic sequences of Brazilian, Papua New Guinean, and The Gambian isolates was determined. While these CTLs were able to recognize three of the four variant CS sequences found in Brazil and Papua New Guinea, they failed to recognize four of the five variant CS sequences found in The Gambia. Among the peptides that lost their reactivity to 7G8-specific CTL, all except one had amino acid variation in more than one residue. On the other hand, only one of the four peptides that showed a positive reaction had amino acid substitutions in more than a single residue. Thus, our findings demonstrate that natural amino acid variations in the CS protein abrogate CTL recognition. Therefore, it is important to consider the implications of these results in designing CS protein-based vaccines. C1 CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,BIOTECHNOL CORE FACIL,ATLANTA,GA 30333. NIAID,MALARIA RES LAB,BETHESDA,MD 20852. RP UDHAYAKUMAR, V (reprint author), CTR DIS CONTROL & PREVENT,MALARIA BRANCH,4770 BUFORD HIGHWAY,MAIL STOP F-12,ATLANTA,GA 30341, USA. FU NIAID NIH HHS [NIAID/CDC 1-Y02-AI-00006-01] NR 16 TC 25 Z9 25 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1994 VL 62 IS 4 BP 1410 EP 1413 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NC074 UT WOS:A1994NC07400037 PM 7510668 ER PT J AU LYMAN, CA WALSH, TJ AF LYMAN, CA WALSH, TJ TI PHAGOCYTOSIS OF MEDICALLY IMPORTANT YEASTS BY POLYMORPHONUCLEAR LEUKOCYTES SO INFECTION AND IMMUNITY LA English DT Note ID CANDIDA-ALBICANS; FLOW-CYTOMETRY; DIFFERENTIATION; FLUORESCENCE; BACTERIA; ASSAY; DISTINGUISH; MECHANISM; ADHERENCE; INFECTION AB Phagocytosis is a critical function of polymorphonuclear leukocytes in the control of mycotic infections. By using a modified fluorescence quenching assay to distinguish between attached and ingested organisms, we determined the percent phagocytosis of several medically important yeasts. The percentages of phagocytosis of serum-opsonized Candida albicans, Candida tropicalis, Candida parapsilosis, and Torulopsis glabrata were all comparable at 37 degrees C. By comparison, there was significantly less phagocytosis of Cryptococcus neoformans and Trichosporon beigelii isolates (P < 0.001). Thus, phagocytosis of C. albicans by polymorphonuclear leukocytes is comparable to that of species other than C. albicans but is significantly greater than that of the basidiomycetous yeasts T. beigelii and C. neoformans. C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892. NR 32 TC 24 Z9 25 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1994 VL 62 IS 4 BP 1489 EP 1493 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NC074 UT WOS:A1994NC07400052 PM 8132358 ER PT J AU PRIOLA, SA CAUGHEY, B RAYMOND, GJ CHESEBRO, B AF PRIOLA, SA CAUGHEY, B RAYMOND, GJ CHESEBRO, B TI PRION PROTEIN AND THE SCRAPIE AGENT - IN-VITRO STUDIES IN INFECTED NEUROBLASTOMA-CELLS SO INFECTIOUS AGENTS AND DISEASE-REVIEWS ISSUES AND COMMENTARY LA English DT Article DE SCRAPIE; PRION PROTEIN; TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY; BOVINE SPONGIFORM ENCEPHALOPATHY; CREUTZFELDT-JAKOB DISEASE; NEUROBLASTOMA ID CREUTZFELDT-JAKOB DISEASE; NEURO-BLASTOMA CELLS; PRP ACCUMULATION; SULFATED GLYCOSAMINOGLYCANS; CULTURED-CELLS; MESSENGER-RNA; CONGO RED; BRAIN; INHIBITION; FIBRILS AB The mouse neuroblastoma cell line N2a was persistently infected with the Chandler strain of the mouse scrapie agent. Although the infection did not spread to infect > 1% of the cells, clones were established that had from 50 to 100% infected cells. These clones expressed the abnormal protease-resistant form of prion protein (PrP), which is believed to mediate brain degeneration in animals with scrapie and bovine spongiform encephalopathy and in humans with kuru, Creutzfeldt-Jakob disease, and Gerstmann-Straussler-Scheinker syndrome. With this in vitro system, Congo red and several sulfated polysaccharides, including heparin and pentosan polysulfate, were found to inhibit accumulation of protease-resistant PrP. These results and additional data confirming PrP binding to heparin suggested a possible role for sulfated glycosaminoglycans in the generation of protease-resistant PrP during scrapie infection. Accumulation of protease-resistant PrP was also blocked in vitro by expression of foreign PrP molecules, indicating that PrP from different species might compete for common substrates in this process. These results using scrapie infected cell lines provide new opportunities for development of drugs capable of blocking the brain degeneration caused by scrapie and other transmissible spongiform encephalopathies. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 37 TC 18 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1056-2044 J9 INFECT AGENT DIS JI Infect. Agents Dis.-Rev. Issues Comment. PD APR-JUN PY 1994 VL 3 IS 2-3 BP 54 EP 58 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA PF929 UT WOS:A1994PF92900002 PM 7812655 ER PT J AU MURPHY, PM AF MURPHY, PM TI MOLECULAR PIRACY OF CHEMOKINE RECEPTORS BY HERPESVIRUSES SO INFECTIOUS AGENTS AND DISEASE-REVIEWS ISSUES AND COMMENTARY LA English DT Review DE CHEMOKINES; INTERLEUKIN-8; CHEMOTAXIS; G PROTEIN-COUPLED RECEPTOR; INFLAMMATION; HERPESVIRUS ID GROWTH-STIMULATORY ACTIVITY; ATTRACTANT ACTIVATION PROTEIN-1; PLATELET FACTOR-IV; MACROPHAGE INFLAMMATORY PROTEIN-1; HUMAN INTERLEUKIN-8 RECEPTOR; MONOCYTE CHEMOATTRACTANT PROTEIN-1; T-CELL ADHESION; FUNCTIONAL EXPRESSION; COUPLED RECEPTORS; HUMAN-NEUTROPHILS AB To succeed as a biological entity, viruses must exploit normal cellular functions and elude the host immune system; they often do so by molecular mimicry. One way that mimicry may occur is when viruses copy and modify host genes. The best studied examples of this are the oncogenes of RNA retroviruses, but a growing number of examples are also known for DNA viruses. So far they all come from just two groups of DNA viruses, the herpesviruses and poxviruses, and the majority of examples are for genes whose products regulate immune responses, such as cytokines, cytokine receptors, and complement control proteins. This review will focus on human and herpesvirus receptors for chemokines, a family of leukocyte chemoattractant and activating factors that are thought to be important mediators of inflammation. Although the biological roles of the viral chemokine receptor homologues are currently unknown, their connection to specific sets of chemokines has suggested a number of possible functions. RP MURPHY, PM (reprint author), NIAID, HOST DEF LAB, BLDG 10, ROOM 11N113, BETHESDA, MD 20892 USA. NR 151 TC 46 Z9 48 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1056-2044 J9 INFECT AGENT DIS JI Infect. Agents Dis.-Rev. Issues Comment. PD APR-JUN PY 1994 VL 3 IS 2-3 BP 137 EP 154 PG 18 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA PF929 UT WOS:A1994PF92900012 PM 7812652 ER PT J AU KENNY, JJ GUELDE, G FISCHER, RT LONGO, DL AF KENNY, JJ GUELDE, G FISCHER, RT LONGO, DL TI INDUCTION OF PHOSPHOCHOLINE-SPECIFIC ANTIBODIES IN X-LINKED IMMUNE-DEFICIENT MICE - IN-VIVO PROTECTION AGAINST A STREPTOCOCCUS-PNEUMONIAE CHALLENGE SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE PNEUMOCOCCAL VACCINE; T-INDEPENDENT ANTIBODY RESPONSES; T15 IDIOTYPE ID ANTI-PHOSPHORYLCHOLINE ANTIBODIES; IMMUNOLOGICAL MEMORY; DEFECTIVE MICE; FATAL INFECTION; CELL SUBSET; GENE FAMILY; EXPRESSION; IMMUNODEFICIENCY; IDIOTYPE; BINDING AB X-linked immune deficient (XID) mice are susceptible to infection with Streptococcus pneumoniae because they fail to mount an immune response to the immunodominant phosphocholine (PC) epitope on the bacterial cell wall. It is difficult to induce PC-specific antibodies in XID mice because PC-specific a cells expressing the T15-, M167- and M603 idiotype (Id), which provide protection against S. pneumoniae, are deleted in these mice via an antigen-specific, receptor-mediated process. In addition, the standard PC hapten, p-diazophenylphosphocholine (DPPC), induces high affinity phenylphosphocholine (PPC)-specific antibodies in XID mice, which are not protective against S. pneumoniae. We have used a novel PC hapten, p-nitrophenyl-6-(0-phosphocholine)hydroxyhexanoate (EPC), to induce PC-specific antibodies in XID mice. The immune response to EPC-keyhole limpet hemacyanin (KLH) is dominated by IgG1, V(H)1(+), T15-Id(-), PC-inhibitable antibodies. A small IgM anti-PC response having a consistent T15-Id(+) component is also induced in XID mice, whereas normal mice produce a large IgM response dominated by T15-Id(+) antibodies. The immune response to EPC-KLH remains predominantly PC-inhibitable even after multiple immunizations, while the response to DPPC - KLH becomes dominated by PPC-specific antibodies. C.CBA/N mice immunized twice with EPC- KLH are protected against 10(4) S. pneumoniae while as few as 10 bacteria are 100% lethal for the unimmunized controls. The ability of EPC- protein to induce a long-lived, PC-specific response should make this hapten a potential TD vaccine candidate for S. pneumoniae C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP KENNY, JJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD 21702, USA. NR 45 TC 20 Z9 20 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD APR PY 1994 VL 6 IS 4 BP 561 EP 568 DI 10.1093/intimm/6.4.561 PG 8 WC Immunology SC Immunology GA NF242 UT WOS:A1994NF24200009 PM 8018596 ER PT J AU DEJONG, R VANLIER, RAW RUSCETTI, FW SCHMITT, C DEBRE, P MOSSALAYI, MD AF DEJONG, R VANLIER, RAW RUSCETTI, FW SCHMITT, C DEBRE, P MOSSALAYI, MD TI DIFFERENTIAL EFFECT OF TRANSFORMING GROWTH-FACTOR-BETA-1 ON THE ACTIVATION OF HUMAN NAIVE AND MEMORY CD4(+) T-LYMPHOCYTES SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE CD45R SUBSETS; T CELL ACTIVATION; TGF-BETA-1 ID ANTI-CD3 MONOCLONAL-ANTIBODIES; FACTOR-BETA; CELL-GROWTH; TGF-BETA; PROLIFERATION; SUBSETS; REQUIREMENTS; CD2; PHOSPHORYLATION; RESPONSIVENESS AB Transforming growth factor-beta 1 (TGF-beta 1) can have stimulatory or inhibitory effects on cell growth. For several cell types, the effect of TGF-beta 1 was found to correlate with the differentiation stage of the cells and the presence of other cytokines. We have studied here the influence of TGF-beta 1 on CD4(+) T cell activation in relation to the differentiation stage of the cells by evaluating the effect of TGF-beta 1 on the proliferative responses of purified CD4(+)CD45RA(+) (unprimed) and CD4(+)CD45RO(+) (primed) lymphocytes. Under certain conditions, TGF-beta 1 exerted a co-stimulatory effect on peripheral blood CD4(+)CD45RA(+) T cells whereas the outgrowth of CD4(+)CD45RO(+) T cells was suppressed in any activation system tested. The enhancement of proliferative responses by TGF-beta 1 in TCR/CD3 or CD2 stimulated cultures of CD45RA(+) cells involved up-regulation of CD25 expression and was dependent on the presence of exogenous IL-2 or CD28 mAbs; IL-7 driven proliferative responses were suppressed by TGF-beta 1. These observations were confirmed in experiments with purified cord blood (CB) CD4(+) T cells inasmuch as addition of TGF-beta 1 caused a 2- to 7-fold increase in IL-2 driven proliferative responses of these cells. Finally we show that, in contrast to the effect of TGF-beta 1 during primary stimulation of CB CD4(+) T cells, TGF-beta 1 suppressed T cell proliferation for similar to 40% in secondary cultures of these cells. Our findings indicate that TGF-beta 1 is a bifunctional regulator of CD4(+) T cell growth in vitro, with co-stimulatory capacities during CD45RA(+) T cell mediated primary responses and growth suppressive effects during secondary responses of CD45RO(+) T cells. C1 CHU PITIE SALPETRIERE, IMMUNOL CELLULAIRE & TISSULAIRE LAB, CNRS, URA 625, PARIS, FRANCE. UNIV AMSTERDAM, EXPTL & CLIN IMMUNOL LAB, AMSTERDAM, NETHERLANDS. NCI, LEUKOCYTE BIOL LAB, FREDERICK, MD 21702 USA. RP DEJONG, R (reprint author), NETHERLANDS RED CROSS, BLOOD TRANSFUS SERV, CENT LAB, DEPT CLIN VIROIMMUNOL, PLESMANLAAN 125, 1066 CX AMSTERDAM, NETHERLANDS. OI van Lier, Rene/0000-0002-3201-7144 NR 50 TC 52 Z9 53 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD APR PY 1994 VL 6 IS 4 BP 631 EP 638 DI 10.1093/intimm/6.4.631 PG 8 WC Immunology SC Immunology GA NF242 UT WOS:A1994NF24200016 PM 7912547 ER PT J AU CHANG, K PASTAN, I AF CHANG, K PASTAN, I TI MOLECULAR-CLONING AND EXPRESSION OF A CDNA-ENCODING A PROTEIN DETECTED BY THE K1 ANTIBODY FROM AN OVARIAN-CARCINOMA (OVCAR-3) CELL-LINE SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID MONOCLONAL-ANTIBODY; CARCINOEMBRYONIC ANTIGEN; NORMAL MESOTHELIUM; ADULT FECES; P53; ONCOGENE; CANCERS; GENES; CAK1 AB MAb KI recognizes a cell-surface glycoprotein (MW similar to 40 kDa) present in ovarian carcinomas, malignant mesotheliomas, squamous-cell carcinomas and normal mesothelial cells. In this study, expression screening was used to isolate cDNA clones encoding an antigen recognized by MAb KI from a cDNA library made from a human ovarian carcinoma cell lie (OVCAR-3). Subsequently, other clones were isolated by DNA hybridization using a cDNA probe derived from one of the initial clones. The sequence of all the clones was similar. The longest cDNA contains 2,444 base pairs, and encodes a polypeptide of 263 amino acids with a calculated molecular weight of 30,511 daltons. The nucleotide sequence and deduced amino-acid sequence of the protein show no homology to other sequences in current data bases. In vitro translation of RNA transcripts from the cDNA inserts yielded polypeptides of 29 and 30 kDa. Similar-sized proteins were obtained upon expression of the cDNA in Escherichia coli, and these proteins were reactive with MAb KI. The protein(s) expressed in E. coli were purified and used to make rabbit or mouse antisera. These antisera reacted strongly with a soluble cytosolic protein in OVCAR-3 cells, but not with the membrane-bound antigen. Soluble cytosolic proteins of a similar size, recognized with MAb KI, were found in OVCAR-3 and N87 (gastric cancer) cells but not in 10 other cancer cell lines. These data indicate that the cloned cDNA encodes a cytosolic protein that reacted with MAb KI. This soluble protein is expressed only in cells containing the CAKI surface glycoprotein, suggesting that the 2 proteins could be structurally related. (C) 1994 Wiley-Liss, Inc. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 28 TC 37 Z9 38 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 1 PY 1994 VL 57 IS 1 BP 90 EP 97 DI 10.1002/ijc.2910570117 PG 8 WC Oncology SC Oncology GA NE128 UT WOS:A1994NE12800016 PM 8150545 ER PT J AU FARMER, ME LOCKE, BZ LIU, IY MOSCICKI, EK AF FARMER, ME LOCKE, BZ LIU, IY MOSCICKI, EK TI DEPRESSIVE SYMPTOMS AND ATTRITION - THE NHANES-I EPIDEMIOLOGIC FOLLOW-UP-STUDY SO INTERNATIONAL JOURNAL OF METHODS IN PSYCHIATRIC RESEARCH LA English DT Article DE ATTRITION; DEPRESSION; EPIDEMIOLOGIC METHODS; HEALTH SURVEYS; POPULATION SURVEILLANCE; PROSPECTIVE STUDIES ID LOS-ANGELES COUNTY; GENERAL-POPULATION; NON-RESPONSE; MORTALITY; HEALTH; PREVALENCE; CANCER; SAMPLE; BIAS; RESPONDENTS AB The relation between depressive symptoms and attrition at an eight-year follow-up was investigated for 2981 subjects aged 25-77 years in the Epidemiologic Follow-Up Study (1982-1984) to the first National Health and Nutrition Examination Survey (NHANES I). Depressive symptomatology as measured by the Center for Epidemiologic Studies Depression Scale (CES-D) was examined in relation to three reasons for attrition: loss of contact, death and no personal interview but traced and presumed competent to be interviewed after controlling for age, race, sex, education, marital status, employment status, self-reported health, high blood pressure and smoking status. Subjects with scores of 16 or greater on the CES-D at baseline were 1.5 times more likely, after adjustment, to be lost to contact than were subjects scoring less than 16 on the CES-D (95% confidence interval of 1.06-2.18). There were no significant interactions with age, sex, race, education, marital status, employment status, self-reported chronic conditions, high blood pressure or smoking status. These findings suggest the utility of employing a brief scale for measuring depressive symptoms in order to predict attrition and to assess and adjust for potential selection bias in a longitudinal study. C1 UCLA,HARBOR MED CTR,TORRANCE,CA 90502. UCLA,SCH MED,TORRANCE,CA 90502. NIMH,PREVENT RES BRANCH,ROCKVILLE,MD 20857. RP FARMER, ME (reprint author), NIMH,EPIDEMIOL & PSYCHOPATHOL RES BRANCH,ROCKVILLE,MD 20857, USA. NR 49 TC 18 Z9 18 U1 1 U2 3 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 1049-8931 J9 INT J METHOD PSYCH JI Int. J. Methods Psychiatr. Res. PD APR PY 1994 VL 4 IS 1 BP 19 EP 27 PG 9 WC Psychiatry SC Psychiatry GA NF133 UT WOS:A1994NF13300004 ER PT J AU NAPOLITANO, A LOWELL, BB DAMM, D LEIBEL, RL RAVUSSIN, E JIMERSON, DC LESEM, MD VANDYKE, DC DALY, PA CHATIS, P WHITE, RT SPIEGELMAN, BM FLIER, JS AF NAPOLITANO, A LOWELL, BB DAMM, D LEIBEL, RL RAVUSSIN, E JIMERSON, DC LESEM, MD VANDYKE, DC DALY, PA CHATIS, P WHITE, RT SPIEGELMAN, BM FLIER, JS TI CONCENTRATIONS OF ADIPSIN IN BLOOD AND RATES OF ADIPSIN SECRETION BY ADIPOSE-TISSUE IN HUMANS WITH NORMAL, ELEVATED AND DIMINISHED ADIPOSE-TISSUE MASS SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE ADIPSIN; OBESITY ID COMPLEMENT FACTOR-D; GENE-EXPRESSION; MESSENGER-RNA; GLYCEROPHOSPHATE DEHYDROGENASE; OBESITY; PATHWAY; INSULIN; CELLS; MICE AB Adipsin, which is identical to complement factor D, is synthesized by fat cells, circulates in the bloodstream and is profoundly deficient in mice with genetic and hypothalamic obesity. With the recent cloning of human adipsin, a quantitative human immunoassay has been developed. In the present study, we measured adipsin blood concentrations in humans with increased and decreased adipose stores as well as adipsin secretion by adipose tissue obtained from lean and obese individuals. The results demonstrate that adipsin is released by human adipose tissue fragments as has previously been shown in mice, and that, in contrast to obese mice, blood adipsin concentrations were not reduced in the obese humans tested in this study. We also observed that blood adipsin concentrations can vary as a function of feeding or adiposity, in that they tend to be mildly elevated in obese individuals or mildly reduced in individuals with total lipo-atrophy, cachexia related to AIDS and anorexia nervosa. Thus, the circulating concentration of adipsin tends to correlate positively with degree of adiposity. Clearly, no deficiency in blood adipsin concentrations or adipsin secretion by adipose tissue was observed in the obese individuals studied. C1 BETH ISRAEL HOSP,DEPT MED,DIV ENDOCRINOL,BOSTON,MA 02215. BETH ISRAEL HOSP,DEPT MED,DIV INFECT DIS,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. SCIOS NOVA INC,MT VIEW,CA. ROCKEFELLER UNIV,HUMAN BEHAV & METAB LAB,NEW YORK,NY 10021. NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. UNIV TEXAS,SCH MED,DEPT PSYCHIAT,HOUSTON,TX. UNIV IOWA,HOSP SCH,DEPT PEDIAT,DIV DEV DISABIL,IOWA CITY,IA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 30583, 2 P30 DK 26687-12, 5 F32 DK08525-02] NR 22 TC 56 Z9 57 U1 0 U2 4 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD APR PY 1994 VL 18 IS 4 BP 213 EP 218 PG 6 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA NE982 UT WOS:A1994NE98200005 PM 8044195 ER PT J AU LEE, MS GARKOVENKO, E YUN, JS WEIJERMAN, PC PEEHL, DM CHEN, LS RHIM, JS AF LEE, MS GARKOVENKO, E YUN, JS WEIJERMAN, PC PEEHL, DM CHEN, LS RHIM, JS TI CHARACTERIZATION OF ADULT HUMAN PROSTATIC EPITHELIAL-CELLS IMMORTALIZED BY POLYBRENE-INDUCED DNA TRANSFECTION WITH A PLASMID CONTAINING AN ORIGIN-DEFECTIVE SV40-GENOME SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE PROSTATE EPITHELIAL CELLS; IMMORTALIZATION; POLYBRENE DNA TRANSFECTION; ORIGIN-DEFECTIVE SV40-GENOME ID HUMAN EPIDERMAL-KERATINOCYTES; NEOPLASTIC TRANSFORMATION; CANCER; FIBROBLASTS; INVITRO AB Normal adult human prostatic epithelial cells were infected with an adenovirus 12-SV40 virus or transfected by polybrene-induced gene transfer with a plasmid (pRSV-T) containing the SV40 early region genes or with a plasmid (pRNS-1) containing an origin-defective SV40 genome and a plasmid carrying the neomycin resistance gene. Colonies of morphologically altered cells were isolated, cultured in a serum-free medium and characterized. These cells had extended lifespan in culture compared to normal adult human prostatic epithelial cells. Both Ad12-SV40-infected and pRSV-T-transfected cultures eventually underwent senescence. pRNS-1-transfected cells (pRNS-1-1), however, have now been grown for more than 50 passages. These cells contain the SV40 genome, express SV40 T-antigen, and are not tumorigenic in nude mice. They express cytokeratins 5 and 8, like the parent cells, and are pseudodiploid. Analysis of growth regulatory processes revealed that the growth of pRNS-1-1 cells was stimulated similarly to that of normal prostatic epithelial cells by epidermal growth factor, insulin-like growth factor, and pituitary extract. The response of pRNS-1 cells to a growth-inhibitory factor, retinoic acid, was also similar to that of normal cells. However, pRNS-1-1 cells were less responsive than normal cells to growth inhibition by transforming growth factor-beta, and had lost altogether the ability of normal cells to be inhibited by tumor necrosis factor-alpha and 1,25 (OH)2 vitamin D3. Therefore transformation appeared to alter growth-inhibitory but not growth - stimulatory mechanisms. These cells should be useful in elucidating the multistep mechanism of carcinogenesis of the prostate. C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. STANFORD UNIV,MED CTR,SCH MED,DEPT UROL,STANFORD,CA 94305. JEROME H HOLLAND LAB,DEPT VIROL,ROCKVILLE,MD 20855. NR 29 TC 54 Z9 54 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD APR PY 1994 VL 4 IS 4 BP 821 EP 830 PG 10 WC Oncology SC Oncology GA ND856 UT WOS:A1994ND85600006 PM 21566988 ER PT J AU KWONCHUNG, KJ CHANG, YC AF KWONCHUNG, KJ CHANG, YC TI GENE ARRANGEMENT AND SEQUENCE OF THE 5S RIBOSOMAL-RNA IN FILOBASIDIELLA NEOFORMANS (CRYPTOCOCCUS-NEOFORMANS) AS A PHYLOGENETIC INDICATOR SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID RIBOSOMAL-RNA GENES; NUCLEOTIDE-SEQUENCES; MOLECULAR-CLONING; ADJACENT REGIONS; ORGANIZATION; DNA; TRANSCRIPTION; FUNGI; EVOLUTION; COPRINUS AB We cloned the 5S rRNA gene and determined its organization in the four genes encoding rRNAs in a ribosomal DNA repeat unit of Filobasidiella neoformans, the teleomorph of Cryptococcus neoformans. The 5S rRNA gene contained 118 nucleotides and was located 1 kb upstream from the 18S rRNA gene within the 8.6-kb fragment of the ribosomal DNA repeat unit. The sequence of the 5S rRNA gene from F. neoformans was more similar to the sequence of the 5S rRNA gene from Tremella mesenterica than to the sequences of the 5S rRNA genes from Filobasidium species. The arrangement of the rRNA genes in F. neoformans closely resembles the arrangement of the rRNA genes in mushrooms such as Schizophyllum commune,Agaricus bisporus, and Coprinus cinereus in that the 5S rRNA-coding region not only is located within the repeat unit that encodes the other rRNAs but also is transcribed in the same direction as the other rRNA genes. This is the first description of the arrangement of rRNA genes in a species belonging to the Heterobasidiomycetes. RP KWONCHUNG, KJ (reprint author), NIAID,CLIN INVEST LAB,BLDG 10,ROOM 11C304,BETHESDA,MD 20892, USA. NR 38 TC 11 Z9 11 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1994 VL 44 IS 2 BP 209 EP 213 PG 5 WC Microbiology SC Microbiology GA NE811 UT WOS:A1994NE81100004 PM 8186086 ER PT J AU WINFIELD, D SILBIGER, M BROWN, GS CLARKE, L DWYER, S YAFFE, M SHTERN, F AF WINFIELD, D SILBIGER, M BROWN, GS CLARKE, L DWYER, S YAFFE, M SHTERN, F TI TECHNOLOGY-TRANSFER IN DIGITAL MAMMOGRAPHY - REPORT OF THE JOINT NATIONAL-CANCER-INSTITUTE NATIONAL-AERONAUTICS-AND-SPACE-ADMINISTRATION WORKSHOP OF MAY 19-20 SO INVESTIGATIVE RADIOLOGY LA English DT Article DE DIGITAL IMAGING; DIGITAL MAMMOGRAPHY; TECHNOLOGY TRANSFER; IMAGE PROCESSING; COMPUTER-AIDED DIAGNOSIS AB Digital mammography is one of the most promising novel technologies for further improvement of early detection of breast cancer, offering important potential advantages: 1) improved image quality; 2) digital image processing for improved lesion contrast; 3) computer-aided diagnosis for enhanced radiologic interpretation; and 4) teleradiology for facilitated radiologic consultation. The Diagnostic Imaging Research Branch of the National Cancer Institute (NCI) recently funded an international, multidisciplinary, multi-institutional Digital Mammography Development Group for collaborations between NCI, the academic community, and industry to facilitate the integrated development and implementation of digital mammographic systems. Currently, however, digital mammography faces a number of fundamental technological roadblocks: 1) cost-effective digital detectors and displays for imaging systems; 2) the need for novel algorithms for image processing and computer-aided diagnosis; and 3) high performance, low cost digital networks to provide an ''information superhighway'' for teleradiology. To solve some of these technological problems, the Diagnostic Imaging Research Branch of NCI joined efforts with the Technology Transfer Division of the National Aeronautics and Space Administration to pursue a federal technology transfer program in digital mammography. The authors discuss the findings and recommendations of the workshop entitled ''Technology Transfer in Digital Mammography,'' which was organized and held jointly by the NCI and the National Aeronautics and Space Administration in May, 1993. Numerous innovative technologies of varying degree of promise for digital mammography were presented at the conference. In this article, specific technologies presented at the workshop by the federal and federally-supported laboratories are described, and critiques of these technologies by the leaders of the medical imaging community are presented. C1 NCI,RADIAT RES PROGRAM,DIAGNOST IMAGING RES BRANCH,ROCKVILLE,MD 20852. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. UNIV S FLORIDA,TAMPA,FL. UNIV VIRGINIA,CHARLOTTESVILLE,VA. UNIV TORONTO,TORONTO,ON,CANADA. NR 4 TC 13 Z9 13 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD APR PY 1994 VL 29 IS 4 BP 507 EP 515 DI 10.1097/00004424-199404000-00021 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NL695 UT WOS:A1994NL69500019 PM 7913457 ER PT J AU SHAO, J BRUBAKER, G LEVIN, A KIBAURI, A MASSESA, E SISO, Z KONINGS, E CLAYTON, Y KUMBY, D ALEXANDER, S WATERS, D DRUMMOND, J BIGGAR, RJ SCOTT, G MILLER, G GOEDERT, JJ BLATTNER, WA AF SHAO, J BRUBAKER, G LEVIN, A KIBAURI, A MASSESA, E SISO, Z KONINGS, E CLAYTON, Y KUMBY, D ALEXANDER, S WATERS, D DRUMMOND, J BIGGAR, RJ SCOTT, G MILLER, G GOEDERT, JJ BLATTNER, WA TI POPULATION-BASED STUDY OF HIV-1 INFECTION IN 4,086 SUBJECTS IN NORTHWEST TANZANIA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Article DE HIV-1; TANZANIA; SEROPREVALENCE ID PREVALENCE; AFRICA; EPIDEMIOLOGY; ASSOCIATION; DISEASE; UGANDA; REGION; SPREAD; AIDS AB A population-based HIV-1 seroprevalence survey of 4,086 individuals, aged 15-49 years, in the North Mara district of Tanzania from rural, periurban, and urban areas, including high-risk (prostitutes, and co-workers) individuals, was performed in 1989 and 1990. The overall seroprevalence was 7.3% (95% confidence interval, 6.5-8.1), with a gradient of seropositivity from high-risk 13.0% (9.1, 16.8), urban 8.8% (7.6, 10.0), periurban 6.5% (4.7, 8.4), to rural 2.6% (1.6, 3.7) subjects. Adjusted for population group, HIV-1 seroprevalence was significantly elevated for men over age 24 and for women 20-34 years old, while age-specific prevalence rates were similar for men and women in the rural area. Recent treponemal infection, measured by the rapid plasma reagin test, was not associated with HIV-1 seropositivity in men or women. These data suggest a growing HIV-1 epidemic paralleling rising rates in other rural areas of Africa distant from areas that have been previously recognized as having high prevalence. C1 UNIV LONDON ST BARTHOLOMEWS HOSP & MED COLL, DEPT VIROL, RES TRIANGLE INST UNIT, LONDON EC1M 6AH, ENGLAND. MUHIMBILI MED CTR, DAR ES SALAAM, TANZANIA. SHIRATI HOSP, SHIRATI, TANZANIA. DIST HOSP TARIME, TARIME, TANZANIA. REG HOSP MUSOMA, MUSOMA, TANZANIA. UNIV LONDON IMPERIAL COLL SCI & TECHNOL, LONDON, ENGLAND. GUYS HOSP, DEPT DERMATOL, LONDON, ENGLAND. UCL HOSP, DEPT MICROBIOL, LONDON, ENGLAND. MRC, EPIDEMIOL & MED CARE UNIT, HARROW, MIDDX, ENGLAND. CAMBRIDGE BIOTECH CORP, ROCKVILLE, MD USA. PRI DYNCORP, FREDERICK, MD USA. NCI, BETHESDA, MD USA. FU NCI NIH HHS [NCI-CP-EB-85603-57] NR 16 TC 23 Z9 23 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. PD APR PY 1994 VL 7 IS 4 BP 397 EP 402 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NC775 UT WOS:A1994NC77500012 PM 8133449 ER PT J AU FERRARI, G PLACE, CA AHEARNE, PM NIGIDA, SM ARTHUR, LO BOLOGNESI, DP WEINHOLD, KJ AF FERRARI, G PLACE, CA AHEARNE, PM NIGIDA, SM ARTHUR, LO BOLOGNESI, DP WEINHOLD, KJ TI COMPARISON OF ANTI-HIV-1 ADCC REACTIVITIES IN INFECTED HUMANS AND CHIMPANZEES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE ADCC; HIV; ANIMAL MODEL ID HUMAN-IMMUNODEFICIENCY-VIRUS; DEPENDENT CELLULAR CYTOTOXICITY; ENVELOPE GLYCOPROTEIN-GP120; ANTIBODIES; CELLS; SERA AB Despite its shortcomings as a disease model, the chimpanzee is still the most relevant animal model for human immunodeficiency virus type 1 (HIV-1) infection. Previous studies have revealed qualitative differences between human and chimpanzee anti-HIV-1 responses. In this study, the development of specific anti-HIV-1 antibody-dependent cellular cytotoxic (ADCC) reactivities was evaluated in chronically infected chimpanzees and compared to the human response, because anti-HIV-1 ADCC represents a major component of anti-envelope cytolytic response found in infected patients. Ten HIV-1-infected chimpanzees up to 5 years after the infection were investigated. Anti-HIV-1 ADCC-directing antibodies were detectable in only three of 10 infected chimpanzees, and in these animals, activity was apparent only several months after the HIV infection. In some of the infected animals, ADCC reactivity against infected cells preceded reactivity against gp120-coated targets. When anti-gp120 ADCC-directing antibodies were apparent, they exhibited the same broad reactivity described in humans against different HIV isolates. The pattern of ADCC reactivities in infected chimpanzees is completely different from the well-characterized anti-gp120 cytotoxic reactivities present in HIV-1-infected patients. It is a relatively rare and late-occurring event that may have an important bearing on the lack of virus-induced pathogenesis in the chimpanzee model. C1 DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. OSPED SAN RAFFAELE,VIROL LAB,MILAN,ITALY. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNACORP INC,FREDERICK,MD. RI Ferrari, Guido/A-6088-2015 FU NCI NIH HHS [2-P01-CA43447]; NIAID NIH HHS [5-R01-AI29852] NR 16 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD APR PY 1994 VL 7 IS 4 BP 325 EP 331 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA NC775 UT WOS:A1994NC77500002 PM 8133445 ER PT J AU CARUNCHO, HJ DASILVA, PP AF CARUNCHO, HJ DASILVA, PP TI ALTERATIONS IN THE INTERMEDIATE LAYER OF GOLDFISH MENINGES DURING ADAPTATION TO DARKNESS SO JOURNAL OF ANATOMY LA English DT Article DE FREEZE-FRACTURE; MEMBRANE STRUCTURE; INTERCELLULAR JUNCTIONS; TIGHT JUNCTIONS; GAP JUNCTIONS; EPENDYMIN ID CAPILLARY ENDOTHELIUM; EXTRACELLULAR FLUID; PLASMA-MEMBRANE; BRAIN; PROTEINS; ORGANIZATION; EPENDYMINS; PLASTICITY; TRANSPORT; VESICLES AB The morphological changes in the intermediate endomeningeal layer of the goldfish brain during light and dark adaptation were studied by, freeze-fracture electron microscopy. During the different stages of adaptation no significant changes were found in the density of intramembrane particles and nuclear pores in these cells. The density of plasmalemmal vesicles in the meningocyte surface increased in the groups maintained in the dark for 48 and 72 h (maximum) and then decreased in the group maintained for 96 h in the dark to a basal level. There were also morphological changes in the junctional complexes. At the upper cell membranes (in contact with the outer layer) of meningocytes in the group maintained in the dark for 48 h, we found an increase in the surface occupied by gap junctions. In addition, gap junctions were absent in the lateral membranes of meningocytes from animals maintained in the dark for 72 h. The morphology of gap junctions in the group maintained in the dark for 96 h was similar to that of the control group. These results suggest that the cells of the teleost intermediate endomeningeal layer undergo important changes in activity during adaptative experiments. C1 NCI,FREDERICK CANC RES & DEV CTR,STRUCT BIOL SECT,MATH BIOL LAB,FREDERICK,MD. NR 27 TC 4 Z9 4 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0021-8782 J9 J ANAT JI J. Anat. PD APR PY 1994 VL 184 BP 355 EP 362 PN 2 PG 8 WC Anatomy & Morphology SC Anatomy & Morphology GA NF023 UT WOS:A1994NF02300013 PM 8014126 ER PT J AU MANCHCITRON, JN LONDON, J AF MANCHCITRON, JN LONDON, J TI EXPRESSION OF THE PREVOTELLA-LOESCHEII ADHESIN GENE (PLAA) IS MEDIATED BY A PROGRAMMED FRAMESHIFTING HOP SO JOURNAL OF BACTERIOLOGY LA English DT Article ID MESSENGER-RNA; ENDOGLUCANASE GENE; ESCHERICHIA-COLI; PSEUDOKNOT; MITOCHONDRIA; SEQUENCE; CLONING; YEAST; VIRUS AB The 2.4-kb plaA gene, which encodes a Prevotella loescheii galactoside-specific adhesin, contains a programmed frameshifting hop. The frameshift region consists of two UAA termination codons, two repeats of four identical bases between the terminators, and a stem-loop structure that has the potential to form a pseudoknot located downstream from the second UAA. The stem-loop and pseudoknot are features found in a number of retroviruses where frameshifting is a more common occurrence. The terminators, sequence repeats, and secondary structures were identified in both the P. loescheii plaA gene and the mRNA transcript. An in-frame fusion of the entire plaA frameshift region between codons 9 and 10 of the lacZ gene permitted relatively efficient expression (4 to 25% of that of the control) of beta-galactosidase in Escherichia coli. C1 NIDR,MICROBIAL ECOL LAB,BLDG 30,RM 314,BETHESDA,MD 20892. FU NIDCR NIH HHS [5F32DEO5554] NR 32 TC 16 Z9 16 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD APR PY 1994 VL 176 IS 7 BP 1944 EP 1948 PG 5 WC Microbiology SC Microbiology GA ND183 UT WOS:A1994ND18300018 PM 8144461 ER PT J AU TREMPY, JE KIRBY, JE GOTTESMAN, S AF TREMPY, JE KIRBY, JE GOTTESMAN, S TI ALP SUPPRESSION OF LON - DEPENDENCE ON THE SLPA GENE SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI CHROMOSOME; LACZ OPERON FUSIONS; SATELLITE BACTERIOPHAGE-P4; PROTEIN-DEGRADATION; PROTEOLYSIS; SEQUENCES; STABILITY; MUTATION; TN10; RNA AB We have previously found that plasmids carrying the Escherichia coli alp gene (now to be called alpA) suppress two phenotypes of a DELTAlon protease mutant, overproduction of capsular polysaccharide and sensitivity to UV light. Suppression of these lon phenotypes is most likely explained by the increased degradation of the Lon substrates responsible for these phenotypes. We have called this suppressing protease activity Alp protease. The Alp protease activity is detected in cells after introduction of plasmids carrying the alpA gene, which encodes an open reading frame of 70 amino acids. Insertions which abolish Alp activity interrupt this open reading frame. We have used Tn10 and lambdaplacMu mutagenesis to identify a chromosomal locus, slpA, that is required for alpA+ suppression of DELTAlon. This locus maps at 57 min, close to the chromosomal location of alpA. The expression of beta-galactosidase from a lac transcriptional fusion to slpA is increased six- to eightfold when the alpA+ gene is present on a multicopy plasmid. Therefore, AlpA acts as a transcriptional regulator of the slpA gene(s); activation of slpA transcription is necessary to suppress the phenotypes of a DELTAlon mutation. In an accompanying paper (J. E. Kirby, J. E. Trempy, and S. Gottesman, J. Bacteriol. 176:2068-2081, 1994), we show that neither AlpA nor SlpA is a component of the protease itself but that they are part of a regulatory cascade which leads to expression of the Alp protease. C1 NCI, MOLEC BIOL LAB, BETHESDA, MD 20892 USA. NR 34 TC 24 Z9 25 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0021-9193 EI 1098-5530 J9 J BACTERIOL JI J. Bacteriol. PD APR PY 1994 VL 176 IS 7 BP 2061 EP 2067 PG 7 WC Microbiology SC Microbiology GA ND183 UT WOS:A1994ND18300032 PM 7511582 ER PT J AU KIRBY, JE TREMPY, JE GOTTESMAN, S AF KIRBY, JE TREMPY, JE GOTTESMAN, S TI EXCISION OF A P4-LIKE CRYPTIC PROPHAGE LEADS TO ALP PROTEASE EXPRESSION IN ESCHERICHIA-COLI SO JOURNAL OF BACTERIOLOGY LA English DT Article ID INTEGRATION HOST FACTOR; TRANSFER-RNA GENES; 10SA RNA; SATELLITE BACTERIOPHAGE-P4; ATTACHMENT SITE; CELL-DIVISION; PHYSICAL MAP; SEQUENCE; LOCATION; DNA AB The Escherichia coli K-12 alpA gene product, when overproduced from a multicopy plasmid, leads to suppression of the capsule overproduction and UV sensitivity phenotypes of cells mutant for the Lon ATP-dependent protease. This suppression has previously been shown to correlate with increased in vivo activity of a previously unknown energy-dependent proteolytic activity capable of degrading Lon substrates, the Alp protease. We show in an accompanying paper that alpA, which has homology to a short open reading frame in bacteriophage P4, acts as a positive transcriptional regulator of slpA, a gene linked to alpA and necessary for suppression of lon mutants (J. E. Trempy, J. E. Kirby, and S. Gottesman, J. Bacteriol. 176:2061-2067). The sequence of slpA suggests that it encodes an integrase gene closely related to P4 int and that both alpA and slpA are part of a cryptic P4-like prophage. AlpA expression increases SlpA synthesis. Increased SlpA leads, in turn, to the excision and loss of the cryptic prophage. Excision is dependent on integration host factor as well as on SlpA. Prophage excision is necessary but not sufficient for full expression of the Alp protease. A second function (named AHA) allows full protease expression; this function can be provided by the kanamycin resistance element from Tn903 when the element is present on a multicopy plasmid. Excision and loss of the cryptic prophage apparently allow expression of the Alp protease by inactivating a small stable RNA (10Sa RNA) encoded by the ssrA gene. The precursor of this RNA has its 3' end within the cryptic prophage; the mature 3' end lies within the prophage attL site. Inactivation of ssrA by insertional mutagenesis is sufficient to allow expression of the suppressing Alp protease, even in the presence of the cryptic prophage. Therefore, 10Sa RNA acts as a negative regulator of protease synthesis or activity, and prophage excision must inactivate this inhibitory function of the RNA. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. OREGON STATE UNIV,DEPT MICROBIOL,CORVALLIS,OR 97331. NR 56 TC 86 Z9 88 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD APR PY 1994 VL 176 IS 7 BP 2068 EP 2081 PG 14 WC Microbiology SC Microbiology GA ND183 UT WOS:A1994ND18300033 PM 7511583 ER PT J AU BENINATI, S SENGER, DR CORDELLAMIELE, E MUKHERJEE, AB CHACKALAPARAMPIL, I SHANMUGAM, V SINGH, K MUKHERJEE, BB AF BENINATI, S SENGER, DR CORDELLAMIELE, E MUKHERJEE, AB CHACKALAPARAMPIL, I SHANMUGAM, V SINGH, K MUKHERJEE, BB TI OSTEOPONTIN - ITS TRANSGLUTAMINASE-CATALYZED POSTTRANSLATIONAL MODIFICATIONS AND CROSS-LINKING TO FIBRONECTIN SO JOURNAL OF BIOCHEMISTRY LA English DT Article DE EXTRACELLULAR MATRIX; FIBRONECTIN; OSTEOPONTIN; TRANSGLUTAMINASE ID RAT-KIDNEY CELLS; PHYSIOLOGICAL-PROPERTIES; NONPHOSPHORYLATED FORMS; BONE SIALOPROTEIN; FACTOR-XIII; EXPRESSION; GLYCOPROTEIN; LOCALIZATION; POLYAMINES; COLLAGEN AB Osteopontin (OP) is a component of extracellular, bone, and urinary stone matrices, but the mechanism by which it is stably incorporated into such matrices remains unknown. By SDS-PAGE analysis of [I-125]OP, treated with a catalytic amount of TG, we first demonstrate both intra- and intermolecular covalent cross-linking of OP. Most importantly, the analysis of the products generated from reactions containing OF, Fn, and TG by SDS-PAGE, autoradiography, and Western blotting using either OP or Fn antibody, and quantitation of. TG-catalyzed epsilon-(gamma-glutamyl)lysine isopeptide formation between OP and Fn demonstrate, for the first time, covalent cross-linking between these two proteins. Similar reactions in the presence of polyamine substrates of TG show OP-Fn intermolecular cross-linking via N,N-bis-(gamma-glutamyl)polyamine formation. Finally, immunoprecipitation of I-125-labeled NRK cell surface proteins with anti-OF and anti-Fn antibodies, SDS-PAGE analysis, and autoradiography provides critical evidence for nonreducible OP-Fn cross-linking in vivo. These results clearly suggest that TG-mediated cross-linking between OP and Fn represents one of the most likely mechanisms by which OP becomes covalently linked to bone matrix, urinary stone matrix, and to ECM. C1 NICHHD,HUMAN GENET BRANCH,DEV GEN SECT,BETHESDA,MD 20892. BETH ISRAEL HOSP,DEPT PATHOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MCGILL UNIV,DEPT BIOL,MONTREAL,PQ,CANADA. OI Beninati, Simone/0000-0002-2704-0745 FU NCI NIH HHS [CA34025] NR 32 TC 77 Z9 78 U1 0 U2 1 PU JAPANESE BIOCHEMICAL SOC PI TOKYO PA ISHIKAWA BLDG-3F 25-16 HONGO-5-CHOME, TOKYO TOKYO 113, JAPAN SN 0021-924X J9 J BIOCHEM-TOKYO JI J. Biochem. (Tokyo) PD APR PY 1994 VL 115 IS 4 BP 675 EP 682 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NE369 UT WOS:A1994NE36900011 PM 7916341 ER PT J AU BERNSTEIN, LR FERRIS, DK COLBURN, NH SOBEL, ME AF BERNSTEIN, LR FERRIS, DK COLBURN, NH SOBEL, ME TI A FAMILY OF MITOGEN-ACTIVATED PROTEIN KINASE-RELATED PROTEINS INTERACTS IN-VIVO WITH ACTIVATOR PROTEIN-1 TRANSCRIPTION FACTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID C-JUN; TYROSINE KINASE; DNA-BINDING; MAP KINASES; FACTOR AP-1; JB6 CELLS; PHOSPHORYLATION; FOS; RESISTANT; THREONINE AB The activator protein-1 (AP-1) transcription factor modulates expression of genes involved in growth regulation, differentiation, and neoplastic transformation. Several mitogen-activated protein kinases (MAP kinases) as well as other kinases phosphorylate c-Jun and c-Fos in vitro and are postulated to control AP-1 activity. However, since many protein kinases phosphorylate substrates in vitro with which they have no association in vivo, we sought evidence for interaction in vivo between AP-1 and MAP kinase proteins. We now report detection of an association in vivo of MAP kinase-related proteins with c-Jun and AP-1 dimers by peptide mapping and two-dimensional electrophoretic analyses of proteins co-immunoprecipitated with AP-1 antigens. Extracellular signal-regulated kinase-2 and several apparently novel MAP kinase-related proteins are among the species that bind to AP-1. The large number of MAP kinase-related proteins associated with AP-1 implicates them on an important gene regulation pathway. Combinatorial association between MAP kinase-related proteins and AP-1 dimers could potentially create numerous distinct complexes that could regulate diverse genes. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS,FREDERICK,MD 21702. RP BERNSTEIN, LR (reprint author), NCI,PATHOL LAB,BLDG 10,RM 2A33,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 34 TC 71 Z9 72 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 1 PY 1994 VL 269 IS 13 BP 9401 EP 9404 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NE053 UT WOS:A1994NE05300002 PM 8144522 ER PT J AU TAKADA, T IIDA, K MOSS, J AF TAKADA, T IIDA, K MOSS, J TI EXPRESSION OF NAD GLYCOHYDROLASE ACTIVITY BY RAT MAMMARY ADENOCARCINOMA CELLS TRANSFORMED WITH RAT T-CELL ALLOANTIGEN-RT6.2 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID ESCHERICHIA-COLI; PSEUDOMONAS-AERUGINOSA; EXOTOXIN-A; ADP-RIBOSYLTRANSFERASE; NUCLEOTIDE-SEQUENCE; TOXIN; GENE; ENTEROTOXIN; CLONING; RT6 AB RT6.2 is a 26-kDa alloantigen expressed only on postthymic T cells and attached to the cell membrane through a glycosylphosphatidylinositol (GPI) anchor. It has been reported that expression of RT6.2 in animal models may correlate with lymphopenia and genetically-induced insulin-dependent diabetes mellitus. Its physiological function is unclear. Since RT6.2 has significant amino acid identity with a GPI-anchored rabbit muscle NAD:arginine ADP-ribosyltransferase, RT6.2 was expressed in rat mammary adenocarcinoma cells and the ability of the expressed protein to catalyze ADP-ribose transfer reactions was examined. Cells transformed with the RT6.2 gene expressed NAD glycohydrolase activity that was released from intact cells by phosphatidylinositol-specific phospholipase C, consistent with its presence on the cell surface. A similar activity was not detected with vector-transformed cells. RT6.2 did not ADP-ribosylate simple guanidino compounds. The molecular weight of the phosphatidylinositol-specific phospholipase C-released NAD glycohydrolase, determined by SDS-polyacrylamide gel electrophoresis, was 22,000-24,000, in good agreement with that of native RT6.2. These results strongly suggest that the rat T cell alloantigen RT6.2 is a GPI-anchored NAD glycohydrolase. RP NHLBI, CELLULAR METAB LAB, RM 5N-307, BLDG 10, BETHESDA, MD 20892 USA. NR 25 TC 70 Z9 71 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD APR 1 PY 1994 VL 269 IS 13 BP 9420 EP 9423 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NE053 UT WOS:A1994NE05300007 PM 8144525 ER PT J AU HONG, JX HAUN, RS TSAI, SC MOSS, J VAUGHAN, M AF HONG, JX HAUN, RS TSAI, SC MOSS, J VAUGHAN, M TI EFFECT OF ADP-RIBOSYLATION FACTOR AMINO-TERMINAL DELETIONS ON ITS GTP-DEPENDENT STIMULATION OF CHOLERA-TOXIN ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NUCLEOTIDE-BINDING; PROTEIN ACTIVATORS; ADENYLATE-CYCLASE; BOVINE BRAIN; EXPRESSION; MEMBRANES AB It has been proposed that the amino-terminal domain of ADP-ribosylation factor (ARF) is critical for its stimulation of cholera toxin ADP-ribosyltransferase activity. In this study, recombinant ARF1 (rARF1), rDELTA13ARF1 (recombinant ARF1 lacking the first 13 amino acids) and rPKA14ARF1 (recombinant ARF1 in which the first 14 amino acids were replaced by the first 7 amino acids of the cAMP-dependent protein kinase catalytic subunit) were used to assess the effect of the amino terminus on the ability of ARF to enhance ADP-ribosylation of agmatine by the cholera toxin A subunit. The GTP-dependent ARF activities of rDELTA13ARF1 and rPKA14ARF1 were similar to that of rARF1, whereas the GTP requirement for half-maximal activation of cholera toxin A, was somewhat higher for rARF1 than it was for rDELTA13ARF1 and rPKA14ARF1. These results are consistent with the view that the amino terminus of ARF1 is not critical for its action as a GTP-dependent activator of cholera toxin. RP HONG, JX (reprint author), NHLBI,CELLULAR METAB LAB,ROOM 5N-307,BLDG 10,BETHESDA,MD 20892, USA. NR 29 TC 48 Z9 51 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 1 PY 1994 VL 269 IS 13 BP 9743 EP 9745 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NE053 UT WOS:A1994NE05300055 PM 8144566 ER PT J AU GRZESIK, WJ ROBEY, PG AF GRZESIK, WJ ROBEY, PG TI BONE-MATRIX RGD GLYCOPROTEINS - IMMUNOLOCALIZATION AND INTERACTION WITH HUMAN PRIMARY OSTEOBLASTIC BONE-CELLS IN-VITRO SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID ARG-GLY-ASP; EXTRACELLULAR-MATRIX; VITRONECTIN RECEPTOR; SURFACE RECEPTORS; SIALOPROTEIN; FIBRONECTIN; THROMBOSPONDIN; INTEGRINS; ADHESION; DIFFERENTIATION AB The interaction of cells with extracellular matrix is essential for their anchorage, proliferation, migration, and differentiation. In bone matrix there are multiple glycoproteins that contain the integrin-binding RGD sequence: fibronectin (FN), thrombospondin (TSP), osteopontin (OPN), bone sialoprotein (BSP), type I collagen (COLL 1), and vitronectin (VN). In this study, the localization of TSP, FN, VN, and several integrins within developing human long bone using immunohistochemical methods was examined, as was the effect of all bone RGD proteins on the adhesion of human osteoblastic cells. Thrombospondin, fibronectin, and vitronectin showed distinct localization patterns within bone tissue. TSP was found mainly in osteoid and the periosteum; VN appeared to be present mainly in mature bone matrix. FN was present in the periosteum as well as within both mature and immature bone matrix. Using a panel of antiintegrin antibodies we found that bone cells in vivo and in vitro express alpha4, alpha(v), alpha5beta1, alpha(v)beta3, and beta3/beta5 integrins, and these receptors are for the most part expressed on all bone cells at different stages of maturation with quantitative rather than qualitative variations, with the exception of alpha4, which is expressed mainly by osteoblasts. Cell attachment assays were performed using primary human cells of the osteoblastic lineage under serum-free conditions. COLL 1, TSP, VN, FN, OPN, and BSP promoted bone cell attachment in a dose-dependent manner and were equivalent in action when used in equimolar concentrations. In the presence of GRGDS peptide in the medium, the adhesion to BSP, OPN, and VN was almost completely blocked (10, 10, and 15% of control, respectively), and attachment to FN, COLI. 1, and TSP was only slightly decreased (80, 75, and 55 %, respectively). These results suggest that human bone cells may use RGD-independent mechanisms for attachment to the latter glycoproteins. RP GRZESIK, WJ (reprint author), NIDR,BONE RES BRANCH,BLDG 30,ROOM 106,BETHESDA,MD 20892, USA. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 39 TC 272 Z9 277 U1 0 U2 10 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD APR PY 1994 VL 9 IS 4 BP 487 EP 496 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ND159 UT WOS:A1994ND15900007 PM 7518179 ER PT J AU WUCHERPFENNIG, AL LI, YP STETLERSTEVENSON, WG ROSENBERG, AE STASHENKO, P AF WUCHERPFENNIG, AL LI, YP STETLERSTEVENSON, WG ROSENBERG, AE STASHENKO, P TI EXPRESSION OF 92 KD TYPE-IV COLLAGENASE GELATINASE-B IN HUMAN OSTEOCLASTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID BONE-RESORBING AGENTS; CYSTEINE-PROTEINASES; CATHEPSIN-B; RESORPTION; CELLS; TISSUE; METALLOPROTEINASES; INHIBITORS; PROCOLLAGENASE; LOCALIZATION AB The digestion of type I collagen is an essential step in bone resorption. It is well established that osteoclasts solubilize the mineral phase of bone during the resorptive process, but the mechanism by which they degrade type I collagen, the major proteinaceous component of bone, is controversial. Differential screening of a human osteoclastoma cDNA library was performed to characterize genes specifically expressed in osteoclasts. A large number of cDNA clones obtained by this procedure were found to represent 92 kD type IV collagenase (gelatinase B; MMP-9, EC 3.4.24.35), as well as tartrate-resistant acid phosphatase. In situ hybridization localized mRNA for gelatinase B to multinucleated giant cells in human osteoclastomas. Gelatinase B immunoreactivity was demonstrated in giant cells from eight of eight osteoclastomas, osteoclasts in normal bone, and osteoclasts of Paget's disease by use of a polyclonal antiserum raised against a synthetic gelatinase B peptide. In contrast, no immunoreactivity for 72 kD type IV collagenase (gelatinase A; MMP-2, EC 3.4.24.24), which is the product of a separate gene, was detected in osteoclastomas or normal osteoclasts. We propose that the 92 kD type IV collagenase/gelatinase B plays an important role in the resorption of collagen during bone remodeling. C1 NCI,DEPT PATHOL,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP WUCHERPFENNIG, AL (reprint author), FORSYTH RES INST,DEPT CYTOKINE BIOL,140 FENWAY,BOSTON,MA 02115, USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NIDCR NIH HHS [DE 05590, DE 07378] NR 48 TC 109 Z9 113 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD APR PY 1994 VL 9 IS 4 BP 549 EP 556 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA ND159 UT WOS:A1994ND15900014 PM 8030443 ER PT J AU KOJI, T CHEDID, M RUBIN, JS SLAYDEN, OD CSAKY, KG AARONSON, SA BRENNER, RM AF KOJI, T CHEDID, M RUBIN, JS SLAYDEN, OD CSAKY, KG AARONSON, SA BRENNER, RM TI PROGESTERONE-DEPENDENT EXPRESSION OF KERATINOCYTE GROWTH-FACTOR MESSENGER-RNA IN STROMAL CELLS OF THE PRIMATE ENDOMETRIUM - KERATINOCYTE GROWTH-FACTOR AS A PROGESTOMEDIN SO JOURNAL OF CELL BIOLOGY LA English DT Article ID EPITHELIAL-CELLS; DECIDUOGENIC STIMULUS; BINDING-PROTEINS; RAT UTERUS; FACTOR-I; ESTROGEN; RECEPTORS; TRACT; CDNA; PROLIFERATION AB In vitro studies have shown that keratinocyte growth factor (KGF, also known as FGF-7) is secreted by fibroblasts and is mitogenic specifically for epithelial cells. Therefore, KGF may be an important paracrine mediator of epithelial cell proliferation in vivo. Because stromal cells are thought to influence glandular proliferation in the primate endometrium, we investigated the hormonal regulation and cellular localization of KGF mRNA expression in the rhesus monkey uterus. Tissues were obtained both from naturally cycling monkeys in the follicular and luteal phases of the cycle, and from spayed monkeys that were either untreated or treated with estradiol (E2) alone, E2 followed by progesterone (P), E2 PIUS P, or E2 PIUS P plus an antiprogestin (RU 486). Northern blot analysis of total RNA with P-32-labeled probes revealed that the level of KGF mRNA in the endometrium was 70-100-fold greater in the luteal phase or after P treatment than in untreated, E2-treated, or follicular phase animals. Northern analysis also showed that KGF mRNA was present in the myometrium but was unaffected by hormonal state. RU 486 treatment prevented the P-induced elevation of endometrial KGF mRNA. P-dependent elevation of endometrial KGF expression was confirmed by measurement of KGF protein in tissue extracts using a two-site enzyme-linked immunosorbent assay. In situ hybridization with nonradioactive digoxigenin-labeled cDNA probes revealed that the KGF mRNA signal, which was present only in stromal and smooth muscle cells, was-substantially increased by P primarily in the stromal cells located in the basalis region. Smooth muscle cells in the myometrium and the walls of the spiral arteries also expressed KGF mRNA, but the degree of this expression did not differ with hormonal state. P treatment led to increased proliferation in the glandular epithelium of the basalis region and to extensive growth of the spiral arteries. We conclude that the P-dependent increase in endometrial KGF resulted from a dual action of P: (a) a P-dependent induction of KGF expression in stromal cells, especially those in the basalis (zones Ill and IV), and (b) a P-dependent increase in the number of KGF-positive vascular smooth muscle cells caused by the proliferation of the spiral arteries. KGF is one of the first examples in primates of a P-induced, stromally derived growth factor that might function as a progestomedin. C1 NCI, DEPT CELLULAR & MOLEC BIOL, BETHESDA, MD 20892 USA. OREGON HLTH SCI UNIV, DEPT CELL BIOL & ANAT, PORTLAND, OR 97201 USA. FU NCRR NIH HHS [RR-00163]; NICHD NIH HHS [HD-19182, HD-18185] NR 45 TC 161 Z9 163 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1994 VL 125 IS 2 BP 393 EP 401 DI 10.1083/jcb.125.2.393 PG 9 WC Cell Biology SC Cell Biology GA NF965 UT WOS:A1994NF96500014 PM 8163555 ER PT J AU KOHN, KW JACKMAN, J OCONNOR, PM AF KOHN, KW JACKMAN, J OCONNOR, PM TI CELL-CYCLE CONTROL AND CANCER-CHEMOTHERAPY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE CELL CYCLE; CANCER CHEMOTHERAPY; CHECK POINTS; P53; CDC2; CELL DEATH; CYTOXICITY ID WILD-TYPE P53; MAMMALIAN-CELLS; DNA-REPLICATION; CDC2 KINASE; TYROSINE PHOSPHORYLATION; SACCHAROMYCES-CEREVISIAE; GENE AMPLIFICATION; NITROGEN-MUSTARD; TOPOISOMERASE-I; PROTEIN AB As detailed information accumulates about how cell cycle events are regulated, we can expect new opportunities for application to cancer therapy. The altered expression of oncogenes and tumor suppressor genes that commonly occurs in human cancers may impair the ability of the cells to respond to metabolic perturbations or stress. impaired cell cycle regulation would make cells vulnerable to pharmacologic intervention by drug regimens tailored to the defects existing in particular tumors. Recent findings that may become applicable to therapy are reviewed, and the possible form of new therapeutic stratagems is considered. (C) 1994 Wiley-Liss, Inc.* RP KOHN, KW (reprint author), NCI,DEV THERAPEUT PROGRAM,PHARMACOL LAB,BLDG 37,ROOM 5C25,BETHESDA,MD 20892, USA. NR 90 TC 82 Z9 83 U1 1 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR PY 1994 VL 54 IS 4 BP 440 EP 452 DI 10.1002/jcb.240540411 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ND155 UT WOS:A1994ND15500010 PM 8014193 ER PT J AU DALY, JW GARRAFFO, HM SPANDE, TF JARAMILLO, C RAND, AS AF DALY, JW GARRAFFO, HM SPANDE, TF JARAMILLO, C RAND, AS TI DIETARY SOURCE FOR SKIN ALKALOIDS OF POISON FROGS (DENDROBATIDAE) SO JOURNAL OF CHEMICAL ECOLOGY LA English DT Article DE ALKALOIDS; INDOLIZIDINES; PYRROLIZIDINES; HISTRIONICOTOXINS; COCCINELLINES; DENDROBATID FROGS; INSECTS; MILLIPEDES AB A wide range of alkaloids, many of which are unknown elsewhere in nature, occur in skin of frogs. Major classes of such alkaloids in dendrobatid frogs are the batrachotoxins, pumiliotoxins, histrionicotoxins, gephyrotoxins, and decahydroquinolines. Such alkaloids are absent in skin of frogs (Dendrobates auratus) raised in Panama on wingless fruit flies in indoor terraria. Raised on leaf-litter arthropods that were collected in a mainland site, such terraria-raised frogs contain tricyclic alkaloids including the beetle alkaloid precoccinelline, 1,4-disubstituted quinolizidines, pyrrolizidine oximes, the millipede alkaloid nitropolyzonamine, a decahydroquinoline, a gephyrotoxin, and histrionicotoxins. The profiles of these alkaloids in the captive-raised frogs are closer to the mainland population of Dendrobates auratus at the leaf-litter site than to the parent population of Dendrobates auratus from a nearby island site. Extracts of a seven-month sampling of leaf-litter insects contained precoccinelline, pyrrolizidine oxime 236 (major), and nitropolyzonamine (238). The results indicate a dietary origin for at least some ''dendrobatid alkaloids,'' in particular the pyrrolizidine oximes, the tricyclic coccinellines, and perhaps the histrionicotoxins and gephyrotoxins. C1 SMITHSONIAN TROP RES INST,BALBOA,PANAMA. RP DALY, JW (reprint author), NIH,BIOORGAN CHEM LAB,BETHESDA,MD 20892, USA. NR 12 TC 81 Z9 87 U1 3 U2 21 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0098-0331 J9 J CHEM ECOL JI J. Chem. Ecol. PD APR PY 1994 VL 20 IS 4 BP 943 EP 955 DI 10.1007/BF02059589 PG 13 WC Biochemistry & Molecular Biology; Ecology SC Biochemistry & Molecular Biology; Environmental Sciences & Ecology GA NG403 UT WOS:A1994NG40300010 PM 24242207 ER PT J AU WEINMANN, W MAIER, C BAUMEISTER, K PRZYBYLSKI, M PARKER, CE TOMER, KB AF WEINMANN, W MAIER, C BAUMEISTER, K PRZYBYLSKI, M PARKER, CE TOMER, KB TI ISOLATION OF HYDROPHOBIC LIPOPROTEINS IN ORGANIC-SOLVENTS BY PRESSURE-ASSISTED CAPILLARY ELECTROPHORESIS FOR SUBSEQUENT MASS-SPECTROMETRIC CHARACTERIZATION SO JOURNAL OF CHROMATOGRAPHY A LA English DT Article ID PROTEINS; PEPTIDES AB Two capillary electrophoretic (CE) separation techniques with either simultaneous solvent flow induced by hydrostatic pressure or CE followed by low pressurization with helium were developed for the analysis of extremely hydrophobic proteins, such as the lung surfactant protein SP-C. For both related procedures, buffer solutions containing up to 70% of 2-propanol were used for the capillary electrophoretic separation. This high concentration of organic co-solvent, needed to solubilize the protein, dramatically reduces the electroosmotic flow (EOF) in aminopropyltrimethoxysilane-treated fused-silica capillaries. Because the EOF was insufficient to elute the separated analytes from the capillary, two ''pressure-assisted'' CE techniques were developed. An additional flow to elute the separated analytes was produced either by raising the inlet of the capillary or by helium pressure. Using the pressurization procedure a baseline separation of the SP-C protein and its dimeric complex was obtained in a 55-minute electrophoretic run, followed by pressure elution of the analyte to the detector. The present combination of pressurization and capillary electrophoresis does not require any detergents or involatile buffer additives, which are usually needed to solubilize extremely hydrophobic lipoproteins. It is therefore applicable to on-line coupling with electrospray mass spectrometry for the direct structural characterization of hydrophobic proteins. C1 UNIV KONSTANZ,FAK CHEM,D-78434 CONSTANCE,GERMANY. NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RI Tomer, Kenneth/E-8018-2013 NR 12 TC 16 Z9 16 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 J9 J CHROMATOGR A JI J. Chromatogr. A PD APR 1 PY 1994 VL 664 IS 2 BP 271 EP 275 DI 10.1016/0021-9673(94)87015-2 PG 5 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA NF710 UT WOS:A1994NF71000015 PM 8199708 ER PT J AU LAW, WA MARTIN, A MAPOU, RL ROLLER, TL SALAZAR, AM TEMOSHOK, LR RUNDELL, JR AF LAW, WA MARTIN, A MAPOU, RL ROLLER, TL SALAZAR, AM TEMOSHOK, LR RUNDELL, JR TI WORKING-MEMORY IN INDIVIDUALS WITH HIV-INFECTION SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Article; Proceedings Paper CT 1st International Conference on the Biopsychosocial Aspects of HIV Infection CY AUG, 1991 CL AMSTERDAM, NETHERLANDS ID IMMUNODEFICIENCY-VIRUS-INFECTION; AIDS DEMENTIA COMPLEX; REACTION-TIME AB The central executive component (CE) of Baddeley's working memory model (Baddeley, 1992) was evaluated in 26 asymptomatic human immunodeficiency virus-infected individuals (HIV+) and 23 HIV-control subjects using a dual-task working memory paradigm. The HIV+ and HIV- groups showed an equivalent reduction in performance on both the primary task (visual vigilance) and the secondary task (letter span) when they were performed concurrently relative to when either task was performed alone. This result suggested normal CE functioning in these HIV+ subjects. In contrast, the HIV+ subjects had significantly longer response latencies on reaction time measures relative to the HIV- control group. These findings indicated that slowed processing in early stage HIV-infected individuals is not associated with a working memory deficit. C1 HENRY M JACKSON FDN ADV MIL MED,ROCKVILLE,MD. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT NEUROL,BETHESDA,MD 20814. WALTER REED ARMY INST RES,WASHINGTON,DC. RI martin, alex/B-6176-2009 NR 28 TC 35 Z9 38 U1 0 U2 1 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD APR PY 1994 VL 16 IS 2 BP 173 EP 182 DI 10.1080/01688639408402628 PG 10 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA NG556 UT WOS:A1994NG55600002 PM 8021304 ER PT J AU WHITE, L KATZMAN, R LOSONCZY, K SALIVE, M WALLACE, R BERKMAN, L TAYLOR, J FILLENBAUM, G HAVLIK, R AF WHITE, L KATZMAN, R LOSONCZY, K SALIVE, M WALLACE, R BERKMAN, L TAYLOR, J FILLENBAUM, G HAVLIK, R TI ASSOCIATION OF EDUCATION WITH INCIDENCE OF COGNITIVE IMPAIRMENT IN 3 ESTABLISHED POPULATIONS FOR EPIDEMIOLOGIC STUDIES OF THE ELDERLY SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE EDUCATION; INCIDENCE; COGNITIVE IMPAIRMENT; DEMENTIA; OCCUPATION; AGING ID MENTAL STATE EXAMINATION; ALZHEIMERS-DISEASE; COMMUNITY POPULATION; SYNAPSE LOSS; PREVALENCE; DEMENTIA; DISORDERS; PERFORMANCE; FRAMINGHAM; RESIDENTS AB We analyzed the association of education, occupation, and sex with incidence of cognitive impairment using data from three communities in the Established Populations for Epidemiologic Studies of the Elderly (EPESE) projects (New Haven, East Boston, and Iowa). Participants were initially interviewed in 1981-1983, with follow-up 3 and 6 years later. Incident cognitive impairment was defined on the basis of either: (1) increase in the number of errors in Short Portable Mental Status Questionnaire (SPMSQ) (i.e. from a baseline level below the cutoff value to a score above the cutoff), or (2) inability to respond to interview questions at a follow-up contact (requiring a proxy informant), or (3) death with a recorded diagnosis of a dementing illness. In multiple logistic regression models, the major factors predicting the development of cognitive impairment were advanced age, any errors on baseline SPMSQ, 8 or fewer years of education, and occupation. Education and occupation remained significant predictors after controlling for age, site, sex, stroke, and baseline SPMSQ score. C1 NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892. NR 44 TC 110 Z9 111 U1 5 U2 9 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD APR PY 1994 VL 47 IS 4 BP 363 EP 374 DI 10.1016/0895-4356(94)90157-0 PG 12 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA NG685 UT WOS:A1994NG68500006 PM 7730861 ER PT J AU SILVER, RM LUDWICKA, A HAMPTON, M OHBA, T BINGEL, SA SMITH, T HARLEY, RA MAIZE, J HEYES, MP AF SILVER, RM LUDWICKA, A HAMPTON, M OHBA, T BINGEL, SA SMITH, T HARLEY, RA MAIZE, J HEYES, MP TI A MURINE MODEL OF THE EOSINOPHILIA-MYALGIA-SYNDROME INDUCED BY 1,1'-ETHYLIDENEBIS(L-TRYPTOPHAN) SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE EMS; L-TRYPTOPHAN; EBT; FIBROSIS; MAST CELL ID TOXIC OIL SYNDROME; PROGRESSIVE SYSTEMIC-SCLEROSIS; VERSUS-HOST DISEASE; MAST-CELL DEPLETION; L-TRYPTOPHAN; PERIPHERAL NEUROPATHY; DIFFUSE FASCIITIS; GENE-EXPRESSION; PEAK-E; INGESTION AB The eosinophilia-myalgia syndrome (EMS) is a recently described disease that has been associated with the ingestion of L-tryptophan containing trace amounts of several impurities. The first such contaminant to be identified and linked epidemiologically to the EMS epidemic was 1,1'-ethylidenebis(L-tryptophan) (EBT), but its role in the etiology and pathogenesis of the syndrome has been controversial. We report the development of inflammation and fibrosis affecting the dermis and subcutis, including the fascia and perimyseal tissues, after the daily intraperitoneal administration of EBT to female C57BL/6 mice. Such changes are accompanied by increased numbers of mast cells, many of which appear to be degranulating. Plasma levels of quinolinic acid, a metabolic product of L-tryptophan via the kynurenine pathway, are reduced initially, and then become elevated when inflammation and fibrosis are more pronounced. The nature and location of the inflammatory cell infiltrate and fibrosis, as well as the presence of mast cells and alterations of L-tryptophan metabolism, are consistent with findings reported in patients with EMS. This murine model suggests that EBT may have been one of the mediators of EMS and should facilitate studies of the pathogenesis of EMS. C1 MED UNIV S CAROLINA,DEPT DERMATOL & PATHOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT LAB ANIM RESOURCES,CHARLESTON,SC 29425. NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BETHESDA,MD 20892. RP SILVER, RM (reprint author), MED UNIV S CAROLINA,DEPT MED,DIV RHEUMATOL & IMMUNOL,ROOM 912,CLIN SCI BLDG,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. OI Ludwicka-Bradley, Anna/0000-0002-3122-4678 NR 44 TC 35 Z9 36 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1994 VL 93 IS 4 BP 1473 EP 1480 DI 10.1172/JCI117125 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF562 UT WOS:A1994NF56200018 PM 8163652 ER PT J AU OSULLIVAN, MG ANDERSON, DC FIKES, JD BAIN, FT CARLSON, CS GREEN, SW YOUNG, NS BROWN, KE AF OSULLIVAN, MG ANDERSON, DC FIKES, JD BAIN, FT CARLSON, CS GREEN, SW YOUNG, NS BROWN, KE TI IDENTIFICATION OF A NOVEL SIMIAN PARVOVIRUS IN CYNOMOLGUS MONKEYS WITH SEVERE ANEMIA - A PARADIGM OF HUMAN B19 PARVOVIRUS INFECTION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PARVOVIRUS INFECTIONS; HUMAN B19 PARVOVIRUS; HAPLORHINAE; ANEMIA; CONGENITAL DYSERYTHROPOIETIC ANEMIA ID D RETROVIRUS; ACQUIRED IMMUNODEFICIENCY; RHESUS-MONKEYS; MACAQUES; GENOME; AIDS AB Although human B19 parvovirus infection has been clearly associated with a number of distinct syndromes (including severe anemia, abortion, and arthritis), detailed knowledge of its pathogenesis has been hindered by the lack of a suitable animal model. We have identified a novel simian parvovirus in cynomolgus monkeys with severe anemia. Sequencing of a 723-bp fragment of cloned viral DNA extracted from serum revealed that the simian parvovirus has 65% homology at the DNA level with the human B19 parvovirus but little homology with other known parvoviruses. Light microscopic examination of bone marrow from infected animals showed intranuclear inclusion bodies, and ultrastructural studies showed viral arrays characteristic of parvoviruses. Another striking feature was the presence of marked dyserythropoiesis in cells of the erythroid lineage, raising the possibility that B19 parvovirus infection may underlie related dyserythropoietic syndromes in human beings. Affected animals had concurrent infection with the immunosuppressive type D simian retrovirus, analogous to HIV patients who develop severe anemia because of infection with B19 parvovirus. The remarkable similarities between the simian and B19 parvoviruses suggest that experimentally infected cynomolgus monkeys may serve as a useful animal model of human B19 infection. C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. RP OSULLIVAN, MG (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,COMPARAT MED CLIN RES CTR,DEPT COMPARAT MED,MED CTR BLVD,WINSTON SALEM,NC 27157, USA. NR 24 TC 49 Z9 49 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1994 VL 93 IS 4 BP 1571 EP 1576 DI 10.1172/JCI117136 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF562 UT WOS:A1994NF56200029 PM 8163659 ER PT J AU HOLLERAN, WM GINNS, EI MENON, GK GRUNDMANN, JU FARTASCH, M MCKINNEY, CE ELIAS, PM SIDRANSKY, E AF HOLLERAN, WM GINNS, EI MENON, GK GRUNDMANN, JU FARTASCH, M MCKINNEY, CE ELIAS, PM SIDRANSKY, E TI CONSEQUENCES OF BETA-GLUCOCEREBROSIDASE DEFICIENCY IN EPIDERMIS - ULTRASTRUCTURE AND PERMEABILITY BARRIER ALTERATIONS IN GAUCHER DISEASE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE EPIDERMIS; GAUCHER DISEASE; ICHTHYOSIS; BARRIER; STRATUM CORNEUM ID X-RAY-DIFFRACTION; STRATUM-CORNEUM; SPHINGOLIPID SYNTHESIS; TARGETED DISRUPTION; MOUSE MODEL; GENE; LIPIDS; MICE; DIFFERENTIATION; CORNIFICATION AB Hydrolysis of glucosylceramide by beta-glucocerebrosidase results in ceramide, a critical component of the intercellular lamellae that mediate the epidermal permeability barrier. A subset of type 2 Gaucher patients displays ichthyosiform skin abnormalities, as do transgenic Gaucher mice homozygous for a null allele. To investigate the relationship between glucocerebrosidase deficiency and epidermal permeability barrier function, we compared the stratum corneum (SC) ultrastructure, lipid content, and barrier function of Gaucher mice to carrier and normal mice, and to hairless mice treated topically with bromoconduritol B epoxide (BrCBE), an irreversible inhibitor of glucocerebrosidase. Both Gaucher mice and BrCBE-treated mice revealed abnormal, incompletely processed, lamellar body-derived sheets throughout the SC interstices, while transgenic carrier mice displayed normal bilayers. The SC of a severely affected type 2 Gaucher's disease infant revealed similarly abnormal ultrastructure. Furthermore, the Gaucher mice demonstrated markedly elevated transepidermal water loss (4.2+/-0.6 vs < 0.10 g/m(2) per h). The electron-dense tracer, colloidal lanthanum, percolated between the incompletely processed lamellar body-derived sheets in the SC interstices of Gaucher mice only, demonstrating altered permeability barrier function. Gaucher and BrCBE-treated mice showed < 1% and < 5% of normal epidermal glucocerebrosidase activity, respectively, and the epidermis/SC of Gaucher mice demonstrated elevated glucosylceramide (5- to 10-fold), with diminished ceramide content. Thus, the skin changes observed in Gaucher mice and infants may result from the formation of incompetent intercellular lamellar bilayers due to a decreased hydrolysis of glucosylceramide to ceramide. Glucocerebrosidase therefore appears necessary for the generation of membranes of sufficient functional competence for epidermal barrier function. C1 UNIV CALIF SAN FRANCISCO, SCH MED, DEPT DERMATOL, SAN FRANCISCO, CA 94143 USA. NIMH, MOLEC NEUROGENET SECT, CLIN NEUROSCI BRANCH, BETHESDA, MD 20892 USA. RP HOLLERAN, WM (reprint author), VET AFFAIRS MED CTR, DERMATOL SERV 190, 4150 CLEMENT ST, SAN FRANCISCO, CA 94121 USA. FU NIAMS NIH HHS [AR-19098, AR-39448] NR 57 TC 178 Z9 180 U1 3 U2 5 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1994 VL 93 IS 4 BP 1756 EP 1764 DI 10.1172/JCI117160 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF562 UT WOS:A1994NF56200053 PM 8163674 ER PT J AU GAYDOS, CA ROBLIN, PM HAMMERSCHLAG, MR HYMAN, CL EIDEN, JJ SCHACHTER, J QUINN, TC AF GAYDOS, CA ROBLIN, PM HAMMERSCHLAG, MR HYMAN, CL EIDEN, JJ SCHACHTER, J QUINN, TC TI DIAGNOSTIC UTILITY OF PCR-ENZYME IMMUNOASSAY, CULTURE, AND SEROLOGY FOR DETECTION OF CHLAMYDIA-PNEUMONIAE IN SYMPTOMATIC AND ASYMPTOMATIC PATIENTS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID STRAIN TWAR; INFECTION; DISEASE; DNA AB To assess the utility of PCR-enzyme immunoassay (EIA) for diagnosis of acute infection with Chlamydia pneumoniae, we compared tissue culture, PCR-EIA, direct fluorescent-antibody (DFA) stain, and serology in studies with 56 patients with respiratory symptoms and 80 asymptomatic persons. Thirty-five patients were positive by either culture or PCR-EIA, and 101 were negative by both assays. Thirty specimens from symptomatic patients and one from an asymptomatic patient were culture positive; 23 of these were also PCR-EIA positive. Of the eight culture-positive, PCR-EIA-negative specimens, five were DFA negative and three were DFA positive. Four additional specimens were culture negative and PCR-EIA positive; of these, three were DFA positive and one was DFA negative. When we used culture- and/or DFA-positive results as a reference or ''gold standard,'' the sensitivity and specificity of PCR were 76.5 and 99.0%, respectively. When we used PCR and/or DFA-positive results as the reference, the sensitivity of culture was 87.5%. On the basis of single acute serum specimens, only 8 of these 35 patients had diagnostic antibody titers. Of the asymptomatic patients, 75% had immunoglobulin G or immunoglobulin M antibody to C. pneumoniae; 15 (18.8%) of these had antibody levels considered to be diagnostic of acute infection. This multicenter study indicates that culture and/or PCR-EIA is more reliable for prompt diagnosis of C. pneumoniae infection than single-point serology alone. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. SUNY STONY BROOK,HLTH SCI CTR,DEPT MED,STONY BROOK,NY 11794. SUNY STONY BROOK,HLTH SCI CTR,DEPT PEDIAT,STONY BROOK,NY 11794. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. RI Gaydos, Charlotte/E-9937-2010; Quinn, Thomas/A-2494-2010 NR 11 TC 107 Z9 114 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1994 VL 32 IS 4 BP 903 EP 905 PG 3 WC Microbiology SC Microbiology GA NB469 UT WOS:A1994NB46900008 PM 8027341 ER PT J AU ELLIOTT, JA TAMARKIN, L AF ELLIOTT, JA TAMARKIN, L TI COMPLEX CIRCADIAN REGULATION OF PINEAL MELATONIN AND WHEEL-RUNNING IN SYRIAN-HAMSTERS SO JOURNAL OF COMPARATIVE PHYSIOLOGY A-SENSORY NEURAL AND BEHAVIORAL PHYSIOLOGY LA English DT Article DE PINEAL; MELATONIN; CIRCADIAN RHYTHM; ACTIVITY; PHOTOPERIOD ID FUNCTIONAL-ANALYSIS; LOCOMOTOR-ACTIVITY; NOCTURNAL RODENTS; REPRODUCTIVE RESPONSE; N-ACETYLTRANSFERASE; RHYTHMS; PHOTOPERIOD; DURATION; PACEMAKERS; SECRETION AB Circadian regulation of pineal melatonin content was studied in Syrian hamsters (Mesocricetus auratus), especially melatonin peak width and the temporal correlation to wheel-running activity. Melatonin was measured by radioimmunoassay in glands removed at different circadian times with respect to activity onset (= CT 12). Pineal melatonin peak width (h; for mean greater than or equal to 125 pg/gland) and activity duration (alpha) were both 4-5 h longer after 12 or 27 weeks than after 5 or 6 days in continuous darkness (DD). Increased peak width was associated with a delay in the morning decline (M) of melatonin to baseline, correlated with a similar delay in wheel-running offset. In contrast, the evening rise (E) in melatonin occurred at approximately the same circadian phase regardless of the length of DD. Fifteen min light pulses produced similar phase-shifts in melatonin and activity. In a phase advance shift, M advanced at once, while E advanced only after several days of adjustment. Independent timing of shifts in the E and M components of the melatonin rhythm suggest that these events are controlled separately by at least two circadian oscillators whose mutual phase relationship determines melatonin peak width. This two-oscillator control of melatonin peak width is integral to the circadian mechanism of hamster photoperiodic time measurement. C1 STANFORD UNIV,HOPKINS MARINE STN,PACIFIC GROVE,CA 93950. UNIV CALIF SAN DIEGO,DEPT PSYCHIAT,LA JOLLA,CA 92093. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20205. FU NIGMS NIH HHS [GM 14516] NR 50 TC 128 Z9 130 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-7594 J9 J COMP PHYSIOL A JI J. Comp. Physiol. A-Sens. Neural Behav. Physiol. PD APR PY 1994 VL 174 IS 4 BP 469 EP 484 PG 16 WC Behavioral Sciences; Neurosciences; Physiology; Zoology SC Behavioral Sciences; Neurosciences & Neurology; Physiology; Zoology GA NF986 UT WOS:A1994NF98600008 PM 8182563 ER PT J AU DEPABLO, F DASHNER, R SHULDINER, AR ROTH, J AF DEPABLO, F DASHNER, R SHULDINER, AR ROTH, J TI XENOPUS-LAEVIS OOCYTES, EGGS AND TADPOLES CONTAIN IMMUNOACTIVE INSULIN SO JOURNAL OF ENDOCRINOLOGY LA English DT Article ID GROWTH FACTOR-I; MESODERM INDUCTION; ANTIBODIES RETARD; EMBRYOS; RECEPTOR; GENES; DIFFERENTIATION; EXPRESSION; ORGANOGENESIS; INVIVO AB Insulin is a multifunctional polypeptide hormone that regulates metabolic processes and promotes mitogenesis and differentiation in vitro in the cells and tissues of several species. Its role in vivo during embryogenesis is still poorly understood. We have previously found insulin mRNA in mature Xenopus laevis oocytes and in embryos during neurulation (before organogenesis of the pancreas takes place). We have now measured insulin immunoactivity in mature oocytes, unfertilized eggs and day-2 tadpoles. Using reversed phase high performance liquid chromatography, we found low levels of insulin in extracts of oocytes (stage VI). Both Xenopus insulin I and II were detected in unfertilized eggs. The day-2 tadpoles (stages 31-33) also contained immunoactive insulin, and in swimming tadpoles (stage 46) a few clusters of cells containing insulin immunoactivity could be identified by indirect immuno-fluorescence. Immunoblot analysis was relatively insensitive, detecting insulin only in the adult Xenopus pancreas. In summary, insulin (from maternal origin and embryonic expression) appears to be present early enough in Xenopus laevis to influence developmental processes such as neurulation. C1 NIDDK,DIABET BRANCH,BETHESDA,MD 20892. NR 33 TC 9 Z9 9 U1 0 U2 0 PU J ENDOCRINOLOGY LTD PI BRISTOL PA 17/18 THE COURTYARD, WOODLANDS, ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ SN 0022-0795 J9 J ENDOCRINOL JI J. Endocrinol. PD APR PY 1994 VL 141 IS 1 BP 123 EP 129 DI 10.1677/joe.0.1410123 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NK151 UT WOS:A1994NK15100014 PM 8014595 ER PT J AU WAKATSUKI, Y NEURATH, MF MAX, EE STROBER, W AF WAKATSUKI, Y NEURATH, MF MAX, EE STROBER, W TI THE B-CELL-SPECIFIC TRANSCRIPTION FACTOR BSAP REGULATES B-CELL PROLIFERATION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID DNA-BINDING PROTEIN; SWITCH REGIONS; LYMPHOCYTES-B; ANTISENSE RNA; GENE; DIFFERENTIATION; PROMOTER; GROWTH; ELECTROPORATION; EXPRESSION AB The B cell-specific activator protein (BSAP) is a DNA-binding transcription factor expressed in pro-B, pre-B, and mature B cells, but not in plasma cells. In this study, we explored the role of BSAP in B cell function by assessing how the content of this protein varies in cells driven by proliferative stimuli and, conversely, how artificial manipulation of BSAP activity affects cell proliferation. We found that BSAP activity of nuclear extracts increased when B cells were activated by mitogen (lipopolysaccharide [LPS]), antigen receptor-mediated signaling (surface immunoglobulin D [IgD] cross-linking) or T cell-dependent stimulation (CD40 cross-linking). We could suppress BSAP activity by exposure of B cells to phosphorothioate oligonucleotides antisense to the BSAP translation initiation start site, whereas control oligonucleotides were virtually inactive. Antisense-induced BSAP suppression was associated with a striking reduction in LPS-induced proliferation of splenic B cells and in the spontaneous proliferation of B lymphoma cells (CH12.LX), but the antisense oligonucleotide had virtually no effect on proliferation of two cell lines lacking BSAP: the T lymphoma line EL-4 and the plasma cell line MOPC-315. Overexpression of BS.AP in splenic B cells or de novo expression in MOPC-315 plasma cells induced by transfection of a BSAP expression plasmid stimulated cell proliferation. Taken together, these results suggest that BSAP activity is a rate-limiting regulator of B cell proliferation. We also found that treatment with the antisense BSAP oligonucleotide downregulated Ig class switching induced by interleukin 4 plus LPS. This effect may be secondary to reduced proliferation or could be mediated through BSAP binding sites in the IgH locus. C1 US FDA,CTR BIOL EDUC & RES,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 38 TC 130 Z9 132 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1994 VL 179 IS 4 BP 1099 EP 1108 DI 10.1084/jem.179.4.1099 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA NC777 UT WOS:A1994NC77700003 PM 7511679 ER PT J AU YOSHIMOTO, T PAUL, WE AF YOSHIMOTO, T PAUL, WE TI CD4(POS), NK1.1(POS) T-CELLS PROMPTLY PRODUCE INTERLEUKIN-4 IN RESPONSE TO IN-VIVO CHALLENGE WITH ANTI-CD3 SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID STIMULATORY FACTOR-I; MONOCLONAL-ANTIBODY; MURINE LEISHMANIASIS; INTERFERON-GAMMA; LYMPHOCYTES-T; FC-RECEPTORS; MAST-CELLS; B-CELLS; IL-4; CD4+ AB Injection of anti-CD3 antibodies causes prompt expression of interleukin (IL)-4, IL-2, and interferon gamma (IFN-gamma) mRNA among spleen cells. The optimal dose of anti-CD3 for such induction was 1.33 mug/animal; lymphokine mRNA was first observed at 30 min, peaked at 90 min, and was undetectable (for IL-4) or had declined markedly by 4 h. Cells harvested from spleens of mice injected with anti-CD3 90 min earlier secreted IL-4, IL-2, and IFN--gamma without further stimulation. By contrast, in vitro stimulation with anti-CD3 of spleen cell suspensions or splenic fragments from noninjected donors failed to cause prompt production of IL-4 and, even after 24 h of stimulation, the amount of IL-4 produced in such cells was substantially less than that secreted within 1 h by spleen cell suspensions or splenic fragments from mice injected with anti-CD3 90 min earlier. Production of IL-4 by spleen cells from anti-CD3-injected mice was not inhibited by pretreatment with anti-IL-4 antibody or with IFN-gamma or tumor growth factor beta nor enhanced by treatment with IL-4. By contrast, CTLA-4 immunoglobulin (Ig) treatment clearly diminished IL-4 production in response to in vivo anti-CD3, indicating that cellular interactions involving CD28 (or related molecules) were important in stimulation. Cell sorting analysis indicated that the cells that produced IL-4 in response to in vivo injection of anti-CD3 were highly enriched in CD4pos cells with the phenotype leukocyte cell adhesion molecule-1 (LECAM-1)dull, CD44bright, CD45RBdull, NK1.1pos. Indeed, the small population of CD4pos, NK1.1pos cells had the great majority of the IL-4-producing activity of this population. Injection with Staphylococcal enterotoxin B also caused prompt induction of IL-4 mRNA; the cells that were principally responsible for production also had the phenotype of CD4pos, NK1.1pos. These results suggest that possibility that this rare population of T cells may be capable of secreting IL-4 at the outset of immune responses and thus may act to regulate the pattern of priming of naive T cells, by providing a source of IL-4 to favor the development of T cell helper 2-like IL-4-producing cells. C1 NIAID,IMMUNOL LAB,BLDG 10,RM 11N311,FREDERICK,MD 21701. NR 61 TC 760 Z9 761 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1994 VL 179 IS 4 BP 1285 EP 1295 DI 10.1084/jem.179.4.1285 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA NC777 UT WOS:A1994NC77700022 PM 7908323 ER PT J AU GATTASS, CR KING, LB LUSTER, AD ASHWELL, JD AF GATTASS, CR KING, LB LUSTER, AD ASHWELL, JD TI CONSTITUTIVE EXPRESSION OF INTERFERON GAMMA-INDUCIBLE PROTEIN-10 IN LYMPHOID ORGANS AND INDUCIBLE EXPRESSION IN T-CELLS AND THYMOCYTES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID MONOCLONAL-ANTIBODY; IDENTIFICATION; IP-10; GENE; FAMILY; ACTIVATION; ANTIGEN; DEATH AB Interferon gamma-inducible protein 10 (IP-10), a member of a family of small proinflammatory chemotactic polypeptides, is expressed in interferon gamma-stimulated keratinocytes, macrophages, fibroblasts, and endothelial cells. Here we report that IP-10 is also expressed by activated but not resting T hybridoma cells, normal T cells, and thymocytes. Although resting lymphocytes did not synthesize IP-10, surprisingly high levels of IP-10 transcripts were found in lymphoid organs (spleen, thymus, and lymph nodes). Thymic and splenic stromal cells were found to express constitutively high levels of both IP-10 mRNA and protein, accounting for the high level of spontaneous expression in lymphoid tissue. Therefore, in addition to its role as a proinflammatory cytokine, IP-10 may participate in T cell effector function and perhaps T cell development. C1 NCI,IMMUNE CELL BIOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,ROOM 1B-40,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. FU NCI NIH HHS [F32 CA-09162] NR 33 TC 64 Z9 68 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1994 VL 179 IS 4 BP 1373 EP 1378 DI 10.1084/jem.179.4.1373 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA NC777 UT WOS:A1994NC77700033 PM 8145049 ER PT J AU ENK, AH KATZ, SI AF ENK, AH KATZ, SI TI HEAT-STABLE ANTIGEN IS AN IMPORTANT COSTIMULATORY MOLECULE ON EPIDERMAL LANGERHANS CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELLS; B-CELLS; FINE SPECIFICITY; ACTIVATION; EXPRESSION; INDUCTION; PATHWAY; GROWTH; POPULATIONS; EXPANSION AB Heat-stable antigen (HSA), expressed by activated B cells, has been described as a costimulatory molecule for CD4(+) T cells. Because epidermal Langerhans cells (LC) are known to express HSA, we determined whether LC HSA also served as a costimulator of Th cells. We have confirmed that HSA is expressed by freshly prepared (fresh) and, to a lesser extent, short-term cultured (cultured) LC and we demonstrate that costimulatory effects of HSA are prominant on fresh and 1-day cultured LC, whereas 2- to 4-day cultured LC exhibit less HSA-costimulatory activity. The anti-HSA mAb 20C9 almost completely blocked the proliferative response of Th1 or lymph node T cells induced by fresh or cultured LC. 20C9 also specifically inhibited LC-dependent IL-2 production by Th1 cells. The inhibitory effect of 20C9 was not observed when Th2 cells were substituted for Th1 cells or peripheral lymph node T cells. Furthermore, Th1 cells rescued from cocultures of T cells and 20C9-treated, Ag-pulsed LC, (but not from control-treated cocultures) were anergic to restimulation with untreated Ag-pulsed LC. These data suggest that LC HSA is an important costimulatory molecule in Th1 cell-dependent cutaneous immune reactions. C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 29 TC 55 Z9 55 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1994 VL 152 IS 7 BP 3264 EP 3270 PG 7 WC Immunology SC Immunology GA NC609 UT WOS:A1994NC60900003 PM 7908303 ER PT J AU MARINCOLA, FM ETTINGHAUSEN, S COHEN, PA CHESHIRE, LB RESTIFO, NP MULE, JJ ROSENBERG, SA AF MARINCOLA, FM ETTINGHAUSEN, S COHEN, PA CHESHIRE, LB RESTIFO, NP MULE, JJ ROSENBERG, SA TI TREATMENT OF ESTABLISHED LONG METASTASES WITH TUMOR-INFILTRATING LYMPHOCYTES DERIVED FROM A POORLY IMMUNOGENIC TUMOR ENGINEERED TO SECRETE HUMAN TNF-ALPHA SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ADHESION MOLECULE-1 ICAM-1; NECROSIS FACTOR-ALPHA; MURINE TUMOR; RECOMBINANT INTERLEUKIN-2; MONOCLONAL-ANTIBODIES; PULMONARY METASTASES; ANTITUMOR-ACTIVITY; INTERFERON-GAMMA; ANTIGEN-1 LFA-1; T-CELLS AB The growth of a poorly immunogenic methylcholanthrene (MCA)-induced murine (m) sarcoma genetically engineered to secrete human (h) TNF-alpha (MCA-102-hTNF) was studied. MCA-102-hTNF tumor cells were implanted in animals bearing three- or 7-day pulmonary metastases established with the parental line MCA-102-WT (wild type). This model approximates the clinical situation in which patients with metastatic cancer would be vaccinated with autologous tumor genetically modified to stimulate the host immune response. Reduction in the number of pulmonary metastases was occasionally seen but was not consistently reproducible. Other cytokine-producing tumors had either no effect on distant pulmonary metastases (mIL-4, IFN-gamma) or a mild, inconclusive effect similar to hTNF-alpha (mTNF-alpha). Significant growth inhibition of MCA-102-hTNF was noted in animals bearing pulmonary metastases. This inhibition was: 1)tumor specific (regression occurred only in animals bearing pulmonary metastases from the same parental line), 2) TNF specific (it was inhibited by in vivo administration of anti hTNF mAbs), 3) dependent on cellular immunity (immune-depletion with anti-CD4 or CD8 mAbs permitted growth). Tumor-infiltrating lymphocytes (TIL) could not be grown from MCA-102-WT or MCA-102-hTNF tumors nor from MCA-102-WT subcutaneous implants in mice bearing MCA-102-WT pulmonary metastases. However, TIL could be grown from hTNF-secreting tumors implanted in mice bearing MCA-102-WT metastases. These TIL were therapeutic against established lung metastases from the parental tumor in adoptive immunotherapy models. These studies suggest a strategy for using gene modified tumors for the therapy of established cancer. C1 NCI,DIV CANC BIOL DIAG & CTR,PATHOL LAB,BETHESDA,MD 20892. RP MARINCOLA, FM (reprint author), NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,SURG BRANCH,BLDG 10,ROOM 2B42,BETHESDA,MD 20892, USA. RI Restifo, Nicholas/A-5713-2008 NR 33 TC 8 Z9 8 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1994 VL 152 IS 7 BP 3501 EP 3513 PG 13 WC Immunology SC Immunology GA NC609 UT WOS:A1994NC60900028 ER PT J AU PURI, RK MEHROTRA, PT LELAND, P KREITMAN, RJ SIEGEL, JP PASTAN, I AF PURI, RK MEHROTRA, PT LELAND, P KREITMAN, RJ SIEGEL, JP PASTAN, I TI A CHIMERIC PROTEIN COMPRISED OF IL-4 AND PSEUDOMONAS EXOTOXIN IS CYTOTOXIC FOR ACTIVATED HUMAN-LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HIGH-AFFINITY; FUSION PROTEIN; TUMOR-CELLS; T-CELLS; INTERLEUKIN-4; EXPRESSION; RECEPTORS; IL-2-PE40; BINDING; GROWTH AB IL4-Pseudomonas exotoxin (IL4-PE4E) is a chimeric molecule in which human IL-4 is genetically fused to the mutated binding domain of Pseudomonas exotoxin. This molecule binds specifically to human IL-4 receptor-bearing cells. IL4-PE4E was extremely cytotoxic to highly purified anti-CD3-activated CD8(+) T lymphocytes. The cytotoxic activity of this molecule was dependent on the activation state of CD8(+) T cells: 3- and 4-day activated T cells were very susceptible to the cytotoxic activity of IL4-PE4E compared with 0- to 2-day activated cells. PHA-activated lymphocytes and PBL activated in mixed lymphocyte reaction were also highly sensitive to IL4-PE4E. CD16(+) and/or CD56(+) highly purified NK cells or highly purified, Ii-a-activated NK cells were also very sensitive to the cytotoxic effect of IL4-PE4E. IL-2-activated LAK cells had little susceptibility after 1 day but were very sensitive to IL4-PE4E after 3 days. The cytotoxic effects of IL4-PE4E were mediated through a ligand receptor interaction because excess rIL-4 abrogated these effects as did a neutralizing Ab to human IL-4. A chimeric mutant protein that can bind to IL-4 receptors but lacks the ability to inhibit protein synthesis was not cytotoxic to activated lymphocytes. The IL4-PE4E-mediated cytotoxicity of activated T cells correlated with the level of expression of IL-4 receptors on these cells. CD8+ T cells activated for 3 days expressed the highest density of IL-4 receptors compared with 1- or 2-day activated cells. Among two chimeric toxins tested only IL4-PE4E was cytotoxic to 2-day anti-CD3-activated CD8+ T lymphocytes, whereas IL6-PE4E was not active at all. These studies suggest that human IL4 toxin could be a potent agent for the elimination of activated lymphocytes in allograft rejection, some autoimmune diseases, or treatment of lymphomas and leukemias. C1 NCI, DIV CANC BIOL DIAG & CTR, MOLEC BIOL LAB, BETHESDA, MD 20892 USA. RP PURI, RK (reprint author), US FDA, NIH,CBER,DIC CELLULAR & GENE THERAPIES, MOLEC TUMOR BIOL LAB, BLDG 29A, BETHESDA, MD 20892 USA. NR 43 TC 11 Z9 13 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 APR 1 PY 1994 VL 152 IS 7 BP 3693 EP 3700 PG 8 WC Immunology SC Immunology GA NC609 UT WOS:A1994NC60900049 PM 8144944 ER PT J AU DEGRUTTOLA, V BECKETT, LA COOMBS, RW ARDUINO, JM BALFOUR, HH RASHEED, S HOLLINGER, FB FISCHL, MA VOLBERDING, P GROUP, TACT AF DEGRUTTOLA, V BECKETT, LA COOMBS, RW ARDUINO, JM BALFOUR, HH RASHEED, S HOLLINGER, FB FISCHL, MA VOLBERDING, P GROUP, TACT TI SERUM P24 ANTIGEN LEVEL AS AN INTERMEDIATE END-POINT IN CLINICAL-TRIALS OF ZIDOVUDINE IN PEOPLE INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID PLACEBO-CONTROLLED TRIAL; HIV; AIDS; AZT AB Serum p24 antigen levels were examined in subjects from three clinical trials of zidovudine to determine whether the pattern of change in serum p24 antigen during the first 8-16 weeks of therapy was associated with human immunodeficiency virus type 1 (HIV-1) disease progression or death. Among 406 patients with AIDS and a first episode of Pneumocystis carinii pneumonia, 65% had measurable pretreatment concentrations of serum p24 antigen (greater than or equal to 10 pg/mL). Changes during treatment were not associated with reduced mortality. In 637 mildly symptomatic patients, 24% had measurable concentrations, and changes were marginally associated with increased time until more advanced disease. Among 683 asymptomatic patients, 18% had measurable concentrations, and changes were not associated with increased time until progression. Despite the small number of clinical events and the low rate of serum p24 antigen positivity in the latter two studies, pretreatment serum p24 antigen levels were predictive of clinical outcome; subsequent measurements appear to be of limited use in evaluating zidovudine therapy. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,CTR STAT & DATA ANAL CTR,BOSTON,MA 02115. RUSH PRESBYTERIAN ST LUKES MED CTR,CTR RES HLTH & AGING,CHICAGO,IL 60612. UNIV WASHINGTON,DEPT LAB MED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. UNIV MINNESOTA,SCH MED,DEPT LAB MED,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT PATHOL,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT PEDIAT,MINNEAPOLIS,MN 55455. UNIV SO CALIF,SCH MED,DEPT PATHOL,LOS ANGELES,CA 90033. UNIV CALIF SAN FRANCISCO,DEPT MED ONCOL,SAN FRANCISCO,CA. BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. UNIV MIAMI,SCH MED,DEPT MED,MIAMI,FL. NIAID,BETHESDA,MD. FU NIAID NIH HHS [AI-95030, AI-82517, AI-28905] NR 13 TC 36 Z9 37 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1994 VL 169 IS 4 BP 713 EP 721 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NP111 UT WOS:A1994NP11100001 PM 8133085 ER PT J AU CUTLIP, RC MILLER, JM RACE, RE JENNY, AL KATZ, JB LEHMKUHL, HD DEBEY, BM ROBINSON, MM AF CUTLIP, RC MILLER, JM RACE, RE JENNY, AL KATZ, JB LEHMKUHL, HD DEBEY, BM ROBINSON, MM TI INTRACEREBRAL TRANSMISSION OF SCRAPIE TO CATTLE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID BOVINE SPONGIFORM ENCEPHALOPATHY; CREUTZFELDT-JAKOB DISEASE; PRION PROTEIN GENE; NEUROBLASTOMA-CELLS; SHEEP; STRAINS; KURU; HAMSTERS; ANIMALS; LINKAGE AB To determine if sheep scrapie agent(s) in the United States would induce a disease in cattle resembling bovine spongiform encephalopathy, 18 newborn calves were inoculated intracerebrally with a pooled suspension of brain from 9 sheep with scrapie. Half of the calves were euthanatized I year after inoculation. All. calves kept longer than 1 year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis, general weakness, and permanent recumbency. The incubation period was 14-18 months, and the clinical course was 1-5 months. The brain from each calf was examined for lesions and for protease-resistant prion protein. Lesions were subtle, but a disease-specific isoform of the prion protein was present in the brain of all calves. Neither signs nor lesions were characteristic of those for bovine spongiform encephalopathy. C1 USDA,ANIM & PLANT HLTH INSPECT SERV,AMES,IA. NIAID,ROCKY MT LABS,HAMILTON,MT. USDA ARS,ANIM DIS RES UNIT,PULLMAN,WA. RP CUTLIP, RC (reprint author), USDA ARS,NATL ANIM DIS CTR,POB 70,AMES,IA 50010, USA. NR 62 TC 83 Z9 85 U1 0 U2 4 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1994 VL 169 IS 4 BP 814 EP 820 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NP111 UT WOS:A1994NP11100016 PM 8133096 ER PT J AU AMAGAI, M KARPATI, S KLAUSKOVTUN, V UDEY, MC STANLEY, JR AF AMAGAI, M KARPATI, S KLAUSKOVTUN, V UDEY, MC STANLEY, JR TI EXTRACELLULAR DOMAIN OF PEMPHIGUS-VULGARIS ANTIGEN (DESMOGLEIN-3) MEDIATES WEAK HEMOPHILIC ADHESION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE DESMOSOME; CADHERIN; AUTOIMMUNE; CATENIN ID UVOMORULIN-CATENIN COMPLEX; CELL-ADHESION; E-CADHERIN; CYTOPLASMIC DOMAIN; BETA-CATENIN; MOLECULE; AUTOANTIBODIES; PLAKOGLOBIN; DISTINCT; REGION AB Pemphigus vulgaris antigen is in the cadherin supergene family. We hypothesized that the extracellular domain of pemphigus vulgaris antigen might mediate hemophilic cell adhesion because 1) the originally described cadherins (e.g., E-cadherin) mediate this type of adhesion, 2) pemphigus vulgaris antigen is localized in desmosomes that are cell adhesion junctions, and 3) autoantibodies in pemphigus vulgaris patients cause loss of cell adhesion. To test this hypothesis we used a system developed for E-cadherin that, when transfected into L cells (mouse fibroblasts), has been shown to cause aggregation. Because this aggregation requires the cytoplasmic domain of E-cadherin to bind to catenins, we made a chimeric cDNA construct that encodes the extracellular domain of pemphigus vulgaris antigen and the cytoplasmic domain of E-cadherin. Analysis by immunofluorescence and flow cytometry with pemphigus vulgaris sera indicated that the pemphigus vulgaris antigen extracellular domain of this chimeric molecule (PVEC) was expressed on the cell surface of transiently transfected cells and permanently transfected L-cell clones. Immunoprecipitation of the chimeric molecule from extracts of these clones showed that the E-cadherin cytoplasmic domain bound catenins. Surprisingly, these L-cell clones displayed only slight aggregation compared to an L-cell clone transfected with E-cadherin. This weak aggregation was, however, specific and hemophilic, as determined by cell sorting of only PVEC transfectants into aggregates from mixtures of PVEC and neomycin resistance gene transfectants, one of which was labeled with a fluorescent dye. We conclude that the extracellular domain of pemphigus vulgaris antigen mediates weak hemophilic adhesion and is not interchangeable in function with the extracellular domain of E-cadherin. C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 24 TC 73 Z9 73 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 402 EP 408 DI 10.1111/1523-1747.ep12372164 PG 7 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600003 PM 8043076 ER PT J AU DLUGOSZ, AA YUSPA, SH AF DLUGOSZ, AA YUSPA, SH TI PROTEIN-KINASE-C REGULATES KERATINOCYTE TRANSGLUTAMINASE (TG(K)) GENE-EXPRESSION IN CULTURED PRIMARY MOUSE EPIDERMAL-KERATINOCYTES INDUCED TO TERMINALLY DIFFERENTIATE BY CALCIUM SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE TRANSCRIPTION; PHORBOL ESTER; GF 109203X; BRYOSTATIN ID ESTER TUMOR PROMOTERS; RETINOIC ACID; MURINE KERATINOCYTES; PHORBOL ESTERS; ULTRASTRUCTURAL-LOCALIZATION; GENE-EXPRESSION; MESSENGER-RNA; GROWTH-FACTOR; CELLS; METABOLISM AB During the final stage of epidermal differentiation, activation of keratinocyte transglutaminase results in covalent crosslinking of a variety of proteins to form highly protective cornified cell envelopes. We have studied the regulation of keratinocyte transglutaminase (TG(K)) gene expression in murine epidermal keratinocytes induced to terminally differentiate in vitro by increasing the level of extracellular Ca++ or treatment with the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol- 13-acetate (TPA). Raising extracellular Catt induces squamous differentiation of cultured keratinocytes and elicits a concentration-dependent increase in expression of TG(K) mRNA; keratinocytes grown for 24 h in 0.12 mM Ca++ medium express similar to 12 times as much TG(K) mRNA as basal cells (grown in 0.05 mM Ca++ medium), whereas cultures exposed to 1.4 mM Ca++ express similar to 17 times as much. TPA induces squamous differentiation and TG(K) mRNA even in basal keratinocyte cultures grown in 0.05 mM Ca++ medium, suggesting that expression of this differentiation marker is regulated by the PKC signaling pathway. Induction of TG(K) mRNA in response to TPA treatment is transient, reaching a peak at 6 - 8 h and returning to baseline by 24 h. In contrast, elevation of TG(K) mRNA levels in response to Ca++ persists for at least 24 h. The increased abundance of TG(K) mRNA reflects increased transcription of the TG(K) gene, based on nuclear run-on analysis of Ca++- and TPA-treated keratinocytes. Induction of TG(K) mRNA by either TPA or Ca++ is blocked in the presence of cycloheximide, suggesting that a PKC-dependent protein factor is required for TG(K) gene expression in response to both stimuli. Furthermore, the accumulation of TG(K) mRNA in keratinocytes treated with TPA or Ca++ is blocked in cells treated with the PKC inhibitor GF 109203X or bryostatin. These results suggest that the induction of TG(K) gene expression by Ca++ is dependent on PKC, providing further support for the hypothesis that PKC plays a central role in regulating the late stages of epidermal differentiation. RP DLUGOSZ, AA (reprint author), NCI,DIV CANC ETIOL,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BLDG 37,ROOM 3B25,BETHESDA,MD 20892, USA. NR 48 TC 96 Z9 96 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 409 EP 414 DI 10.1111/1523-1747.ep12372171 PG 6 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600004 PM 7908680 ER PT J AU SETOGUCHI, Y JAFFE, HA DANEL, C CRYSTAL, RG AF SETOGUCHI, Y JAFFE, HA DANEL, C CRYSTAL, RG TI EX-VIVO AND IN-VIVO GENE-TRANSFER TO THE SKIN USING REPLICATION-DEFICIENT RECOMBINANT ADENOVIRUS VECTORS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE GENE THERAPY; ALPHA-1-ANTITRYPSIN; BETA-GALACTOSIDASE; KERATINOCYTE ID MEDIATED TRANSFER; EPIDERMAL-KERATINOCYTES; GROWTH-HORMONE; THERAPY; INVIVO; EXPRESSION; CELLS; MICE; LONG; FIBROBLASTS AB The skin has the potential for a variety of gene therapy applications. In addition to local delivery, it is the largest organ of the body, and highly vascular, and thus is an ideal site for systemic delivery of gene products. To evaluate the potential for adenovirus-mediated skin gene transfer, the replication-deficient recombinant adenovirus vectors Ad.RSV beta gal (coding for Escherichia coli beta-galactosidase) and Ad alpha 1AT (coding for human alpha 1-antitrypsin) were used in both ex vivo and in vivo approaches. Following in vitro infection with Ad.RSV beta gal, murine keratinocytes expressed beta-galactosidase. Parallel in vitro studies with Ad alpha 1AT documented de novo synthesis and secretion of human alpha 1AT as shown by [S-35]methionine labeling and immunoprecipitation. Quantification of human alpha 1AT in the culture supernatants demonstrated 0.1-0.3 mu g human alpha 1AT secreted/ml-24 h. Evaluation of the serum of mice receiving transplants (10(5) cells/ mouse) of Ad alpha 1AT-infected syngeneic keratinocytes demonstrated human alpha 1AT for at least 14 d with maximum levels of 41 ng/ml. To demonstrate the feasibility of direct adenovirus-mediated in vivo transfer of genes to the skin, Ad.RSV beta gal or Ad alpha 1AT were administered subcutaneously to mice. Histologic evaluation after 4 d demonstrated expression of beta-galactosidase in various types of skin cells. Quantification of human alpha 1AT in serum of animals infected subcutaneously with Ad alpha 1AT showed levels of 53 ng/ml at day 4, with human alpha 1AT detectable for at least 14 d. These observations support the feasibility of ex vivo and in vivo gene transfer to the skin mediated by replication-deficient adenovirus vectors. C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. CORNELL UNIV,COLL MED,DIV PULM & CRIT CARE MED,NEW YORK,NY. NR 51 TC 98 Z9 98 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 415 EP 421 DI 10.1111/1523-1747.ep12372181 PG 7 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600005 PM 8151119 ER PT J AU GLICK, AB LEE, MM KULKARNI, AB KARLSSON, S YUSPA, SH AF GLICK, AB LEE, MM KULKARNI, AB KARLSSON, S YUSPA, SH TI RAPID MALIGNANT PROGRESSION OF EPIDERMAL TUMORS DERIVED FORM TGF-BETA-1 NULL MOUSE KERATINOCYTES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 525 EP 525 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600031 ER PT J AU ROH, JY STANLEY, J AF ROH, JY STANLEY, J TI THE CYTOPLASMIC (CYT) DOMAIN OF PEMPHIGUS-VULGARIS ANTIGEN (PVA) CONFERS ADHESIVE FUNCTION ON THE EXTRACELLULAR (EC) DOMAIN OF E-CADHERIN (E-CAD) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 525 EP 525 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600030 ER PT J AU DLUGOSZ, AA CHENG, C DENNING, MF DEMPSEY, PJ COFFEY, RJ YUSPA, SH AF DLUGOSZ, AA CHENG, C DENNING, MF DEMPSEY, PJ COFFEY, RJ YUSPA, SH TI KGF INDUCES TGF-ALPHA EXPRESSION AND ACTIVATES THE EGF RECEPTOR SIGNALING PATHWAY TO ALTER KERATINOCYTE GROWTH AND DIFFERENTIATION IN-VITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. VANDERBILT UNIV,NASHVILLE,TN. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 527 EP 527 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600047 ER PT J AU LEE, MG SHARROW, SO FARR, AG SINGER, A UDEY, MC AF LEE, MG SHARROW, SO FARR, AG SINGER, A UDEY, MC TI EXPRESSION OF THE HOMOTYPIC ADHESION MOLECULE E-CADHERIN BY IMMATURE THYMOCYTES AND THYMIC EPITHELIAL-CELLS IN DEVELOPING MURINE THYMUS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. UNIV WASHINGTON,DEPT BIOL STRUCT,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 527 EP 527 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600045 ER PT J AU LEE, SC TARCSA, E MAREKOV, LN CHUNG, SI STEINERT, PM AF LEE, SC TARCSA, E MAREKOV, LN CHUNG, SI STEINERT, PM TI PROPERTIES OF BACTERIALLY EXPRESSED HUMAN TRICHOHYALIN - POST-SYNTHETIC MODIFICATIONS BY TRANSGLUTAMINASE AND PEPTIDYL ARGININE DEIMINASE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 533 EP 533 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600081 ER PT J AU HANSEN, LA TENNANT, RW AF HANSEN, LA TENNANT, RW TI EPIDERMAL PAPILLOMAS DEVELOP FROM THE FOLLICULAR EPIDERMIS IN V-HA-RAS TRANSGENIC TG.AC MICE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIEHS,ENVIRONM CARCINOGENESIS & MUTAGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 534 EP 534 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600085 ER PT J AU HOLLERAN, WM GINNS, EI FARTASCH, M ELIAS, PM SIDRANSKY, E AF HOLLERAN, WM GINNS, EI FARTASCH, M ELIAS, PM SIDRANSKY, E TI SEVERE BARRIER DYSFUNCTION IN BETA-GLUCOCEREBROSIDASE DEFICIENCY IS DUE TO MATURATIONAL BLOCKADE OF STRATUM-CORNEUM INTERCELLULAR LAMELLAE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,DEPT DERMATOL,SAN FRANCISCO,CA 94143. VET ADM MED CTR,DERMATOL SERV,SAN FRANCISCO,CA 94121. NIMH,MOLEC NEUROGENET SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 538 EP 538 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600108 ER PT J AU MORIWAKI, S TARONE, RE KRAEMER, KH AF MORIWAKI, S TARONE, RE KRAEMER, KH TI UV MUTABILITY INCREASES WITH DONOR AGE AS MEASURED WITH A SHUTTLE VECTOR PLASMID SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 539 EP 539 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600119 ER PT J AU RICHARD, G WRIGHT, A COMPTON, J BALE, S DIGIOVANNA, J AF RICHARD, G WRIGHT, A COMPTON, J BALE, S DIGIOVANNA, J TI LINKAGE OF DARIER-DISEASE TO 12Q23-24.1 IN 10 FAMILIES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 541 EP 541 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600129 ER PT J AU KIRNBAUER, R HUBBERT, NL NONNENMACHER, B LOWY, DR SCHILLER, JT ORTH, G BREITBURD, F AF KIRNBAUER, R HUBBERT, NL NONNENMACHER, B LOWY, DR SCHILLER, JT ORTH, G BREITBURD, F TI A VACCINE OF VIRUS-LIKE PARTICLES MADE IN INSECT CELLS CAN INHIBIT PAPILLOMAVIRUS INFECTION OF RABBITS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. INST PASTEUR,PAPILLOMAVIRUS LAB,PARIS,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 542 EP 542 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600137 ER PT J AU BLAUVELT, A CLERICI, M LUCEY, DR YARCHOAN, R WALKER, R SHEARER, GM KATZ, SI AF BLAUVELT, A CLERICI, M LUCEY, DR YARCHOAN, R WALKER, R SHEARER, GM KATZ, SI TI ANTIGEN PRESENTATION BY EPIDERMAL LANGERHANS CELLS IN HIV-INFECTED INDIVIDUALS IS NORMAL SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 543 EP 543 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600140 ER PT J AU NORTH, ACT STEINERT, PM PARRY, DAD AF NORTH, ACT STEINERT, PM PARRY, DAD TI MODELING OF THE KERATIN INTERMEDIATE FILAMENT MOLECULE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV LEEDS,DEPT BIOCHEM & MOLEC BIOL,LEEDS,ENGLAND. NIAMS,SKIN BIOL LAB,BETHESDA,MD. MASSEY UNIV,DEPT PHYS & BIOPHYS,PALMERSTON NORTH,NEW ZEALAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 544 EP 544 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600149 ER PT J AU KIMONIS, V DIGIOVANNA, JJ YANG, JM DOYLE, SZ BALE, SJ COMPTON, JG AF KIMONIS, V DIGIOVANNA, JJ YANG, JM DOYLE, SZ BALE, SJ COMPTON, JG TI KERATIN INTERMEDIATE FILAMENT (KIF) FUNCTION IN THE EPIDERMIS - A MUTATION IN THE V1 VARIABLE SUBDOMAIN OF KERATIN-1 CAUSES PALMOPLANTAR KERATODERMA (PPK) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 545 EP 545 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600153 ER PT J AU KOBAYASHI, T URABE, K WINDER, A JIMENEZCERVANTES, C IMOKAWA, G BREWINGTON, T SOLANO, F GARCIABORRON, JC HEARING, V AF KOBAYASHI, T URABE, K WINDER, A JIMENEZCERVANTES, C IMOKAWA, G BREWINGTON, T SOLANO, F GARCIABORRON, JC HEARING, V TI TYROSINASE-RELATED PROTEIN-1 (TRP1) FUNCTIONS AS A DHICA OXIDASE IN MELANIN BIOSYNTHESIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,OXFORD OX1 3RE,ENGLAND. UNIV MURCIA,DEPT BIOCHEM & MOLEC BIOL,MURCIA,SPAIN. RI Solano, Francisco/G-5001-2013 OI Solano, Francisco/0000-0001-9612-761X NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 552 EP 552 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600193 ER PT J AU TENNENBAUM, T MROZ, A BELANGER, A WILDNAUER, T JONES, JCR GORDON, JS AF TENNENBAUM, T MROZ, A BELANGER, A WILDNAUER, T JONES, JCR GORDON, JS TI RETINOIC ACID-INDUCED SKIN HYPERPLASIA IS ASSOCIATED WITH SPECIFIC CHANGES IN INTEGRIN EXPRESSION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,LCCTP,BETHESDA,MD 20892. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL. IL & J&J,SKILLMAN,NJ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 555 EP 555 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600214 ER PT J AU SOLLITTO, RB ABANGAN, DL STEINBERG, SM REYNOLDS, JC DIGIOVANNA, JJ AF SOLLITTO, RB ABANGAN, DL STEINBERG, SM REYNOLDS, JC DIGIOVANNA, JJ TI OSTEOPOROSIS IS ASSOCIATED WITH CHRONIC ETRETINATE THERAPY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 556 EP 556 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600216 ER PT J AU ROCKEN, M BONOMO, A LEVINE, A SHEVACH, EM RACKE, M AF ROCKEN, M BONOMO, A LEVINE, A SHEVACH, EM RACKE, M TI CYTOKINE THERAPY FOR A TH1-MEDIATED AUTOIMMUNE-DISEASE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV MUNICH,MUNICH,GERMANY. NIH,BETHESDA,MD 20892. MONSANTO CO,ST LOUIS,MO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 557 EP 557 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600224 ER PT J AU RUSSELL, LJ DIGIOVANNA, JJ HASHEM, N MARKOVA, NG COMPTON, JG BALE, SJ AF RUSSELL, LJ DIGIOVANNA, JJ HASHEM, N MARKOVA, NG COMPTON, JG BALE, SJ TI EXCLUSION MAPPING WITH CANDIDATE GENES IN LAMELLAR ICHTHYOSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. AIN SHAMS UNIV,MED GEN CLIN,CAIRO,EGYPT. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 561 EP 561 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600250 ER PT J AU HULTSCH, T KNOP, J HOHMAN, RJ AF HULTSCH, T KNOP, J HOHMAN, RJ TI CLONING, OVEREXPRESSION AND PURIFICATION OF THE PREDOMINANT MAST-CELL FK506-BINDING PROTEIN FKBP-13 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV MAINZ,DEPT DERMATOL,W-6500 MAINZ,GERMANY. NIAID,ALLERG DIS SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 564 EP 564 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600265 ER PT J AU JANG, SI STEINERT, PM MARKOVA, NG AF JANG, SI STEINERT, PM MARKOVA, NG TI DETAILED CHARACTERIZATION OF THE PROXIMAL PROMOTER REGION OF THE HUMAN PROFILAGGRIN GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 578 EP 578 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600351 ER PT J AU LEE, JH YANG, JM LEE, SC STEINERT, PM KIM, IG AF LEE, JH YANG, JM LEE, SC STEINERT, PM KIM, IG TI STRUCTURE, ORGANIZATION AND CHROMOSOMAL LOCATION OF THE HUMAN TRANSGLUTAMINASE-3 GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 578 EP 578 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600352 ER PT J AU YANG, JM LEE, JH JANG, SI MARKOVA, NG STEINERT, PM AF YANG, JM LEE, JH JANG, SI MARKOVA, NG STEINERT, PM TI LOCATION OF POSITIVE AND NEGATIVE ELEMENTS INVOLVED IN THE TRANSCRIPTION OF THE HUMAN TRANSGLUTAMINASE-3 GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 578 EP 578 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600349 ER PT J AU CAVANI, A HACKETT, C WILSON, J ROTHBARD, J KATZ, SI AF CAVANI, A HACKETT, C WILSON, J ROTHBARD, J KATZ, SI TI CHARACTERIZATION OF EPITOPES RECOGNIZED BY HAPTEN-SPECIFIC CD4+ T-CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. IMMULOG,PALO ALTO,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 584 EP 584 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600384 ER PT J AU WILMER, JL LUSTER, MI AF WILMER, JL LUSTER, MI TI CHEMICALLY-INDUCED INTERLEUKIN-8 PRODUCTION IN HUMAN EPIDERMAL KERATINOCYTE CULTURES AND ITS RELATION TO CYTOGENETIC TOXICITY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 591 EP 591 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600431 ER PT J AU KIM, SY HWANG, HK YONEDA, K MAREKOV, LN STEINERT, PM CHUNG, SI AF KIM, SY HWANG, HK YONEDA, K MAREKOV, LN STEINERT, PM CHUNG, SI TI HACAT CELLS - A NEW MODEL TO STUDY CALCIUM-INDUCED TERMINAL DIFFERENTIATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 594 EP 594 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600449 ER PT J AU YONEDA, K LEE, SC STEINERT, PM KIM, SY AF YONEDA, K LEE, SC STEINERT, PM KIM, SY TI TEMPORAL EXPRESSION OF PROTEINS IN TERMINALLY DIFFERENTIATING MAMMALIAN EPIDERMIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. KYOTO UNIV,DEPT DERMATOL,KYOTO 606,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 594 EP 594 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600446 ER PT J AU CATANI, V CANDI, E MAREKOV, LN TARCSA, E MELINO, G STEINERT, PM AF CATANI, V CANDI, E MAREKOV, LN TARCSA, E MELINO, G STEINERT, PM TI EXPRESSION AND PROPERTIES OF HUMAN LORICRIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. UNIV ROMA TOR VERGATA,DEPT EXPTL MED,ROME,ITALY. INST DERMOPAT IMMACOLATA,ROME,ITALY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 595 EP 595 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600450 ER PT J AU FINE, JD SUCHINDRAN, CM TIEN, H JOHNSON, LB MOSHELL, A AF FINE, JD SUCHINDRAN, CM TIEN, H JOHNSON, LB MOSHELL, A TI STATISTICAL CLASSIFICATION MODELS FOR INHERITED EPIDERMOLYSIS-BULLOSA (EB) COMPARISON OF THE INFLUENCE OF DIFFERENT CLINICAL-VARIABLES ON SENSITIVITY AND SPECIFICITY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV N CAROLINA,SCH PUBL HLTH,DEPT BIOSTAT,CHAPEL HILL,NC. UNIV N CAROLINA,SCH PUBL HLTH,DEPT DERMATOL,CHAPEL HILL,NC. UNIV N CAROLINA,SCH PUBL HLTH,DEPT EPIDEMIOL,CHAPEL HILL,NC. UNIV N CAROLINA,SCH MED,CHAPEL HILL,NC. NBER,SE CLIN CTR,CHAPEL HILL,NC. NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 618 EP 618 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600592 ER PT J AU TENNENBAUM, T BELANGER, AJ YUSPA, SH AF TENNENBAUM, T BELANGER, AJ YUSPA, SH TI DIFFERENTIAL REGULATION OF ALPHA-6-BETA-4 AND ALPHA-3-BETA-1 INTEGRINS IS IMPLICATED IN SPINOUS AND GRANULAR-CELL DIFFERENTIATION OF PRIMARY MOUSE KERATINOCYTES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,LCCTP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 622 EP 622 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600613 ER PT J AU HERTL, M NECKER, LM KATZ, SI AF HERTL, M NECKER, LM KATZ, SI TI ANTISENSE OLIGONUCLEOTIDES INHIBIT IFN-GAMMA INDUCED ICAM-1 EXPRESSION BY HUMAN KERATINOCYTES IN A SEQUENCE-SPECIFIC AND NON SEQUENCE-SPECIFIC MANNER SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 627 EP 627 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600647 ER PT J AU BORKOWSKI, TA FARR, AG NELSON, AJ UDEY, MC AF BORKOWSKI, TA FARR, AG NELSON, AJ UDEY, MC TI A NOVEL CELL-SURFACE PROTEIN EXPRESSED BY MURINE EPITHELIAL-CELLS, LANGERHANS CELLS (LC) AND LYMPHOID DENDRITIC CELLS (DC) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. UNIV WASHINGTON,DEPT BIOL STRUCT,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 628 EP 628 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600651 ER PT J AU HENGGE, UR CHAN, EF VOGEL, JC AF HENGGE, UR CHAN, EF VOGEL, JC TI SUCCESSFUL LONG-TERM CULTURE AND DNA TRANSFECTION OF PRIMARY PIG KERATINOCYTES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 639 EP 639 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600719 ER PT J AU LI, LW HENNINGS, H YUSPA, SH AF LI, LW HENNINGS, H YUSPA, SH TI CHELATION OF INTRACELLULAR CA2+ INHIBITS KERATINOCYTE DIFFERENTIATION IN-VITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 641 EP 641 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600727 ER PT J AU MOLES, JP SCHILLER, JT MILS, V TESNIERE, A GUILHOU, JJ BASSETSEGUIN, N AF MOLES, JP SCHILLER, JT MILS, V TESNIERE, A GUILHOU, JJ BASSETSEGUIN, N TI CHIMERIC RECONSTITUTED EPIDERMIS - A MODEL TO STUDY INTERACTIONS BETWEEN IMMORTALIZED AND NORMAL-CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 INST GENET MOLEC,MONTPELLIER,FRANCE. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1994 VL 102 IS 4 BP 642 EP 642 PG 1 WC Dermatology SC Dermatology GA NF406 UT WOS:A1994NF40600733 ER PT J AU MACPHEE, MJ WILTROUT, RH MCCORMICK, KL SAYERS, TJ PILARO, AM AF MACPHEE, MJ WILTROUT, RH MCCORMICK, KL SAYERS, TJ PILARO, AM TI A METHOD FOR OBTAINING AND CULTURING LARGE NUMBERS OF PURIFIED ORGAN-DERIVED MURINE ENDOTHELIAL-CELLS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE MURINE ENDOTHELIAL CELLS; FIBROBLAST GROWTH FACTORS ID TUMOR NECROSIS FACTOR; TISSUE-CULTURE; GROWTH-FACTOR; LYMPHOCYTES; INTERFERON; EXPRESSION; CYTOKINES; GAMMA; LINE; INTERLEUKIN-1 AB Fibroblast growth factor 1 (FGF-1)-coated collagen-gelatin sponges were affixed to various tissues to generate vascular beds, in which the vessels originated in the tissue to which the sponges were affixed. Organ-derived endothelium was obtained from vascularized sponges implanted in or on the skin, peritoneal wall, abdominal mesentery, epimysium, spleen, and liver. Collagenase digestion yielded single-cell suspensions that were analyzed by flow cytometry. Approximately 25% of the cells were positive for the endothelial cell (EC) markers MECA-32 and Sca-1 and for uptake of diIAcLDL. Similar results were obtained when sponges were implanted in several different mouse strains, although there was some evidence of heterogeneity in the degree of vascularization and EC recovery. Long-term cultures of high purity were obtained when the ECs were grown on mitomycin C-treated L929 feeder layers, in medium supplemented with cis-hydroxyproline and FGF-1. These cells have been utilized in preliminary studies of T cell-EC binding. Thus we have developed a generalized method for the recovery and culture of organ-derived murine endothelial cells. This technique should greatly improve the feasibility of studies of the interactions between murine endothelial and immune effector cells. C1 NCI,FREDERICK CANC RES & DEV CTR,EXPTL THERAPEUT SECT,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. RI Sayers, Thomas/G-4859-2015 NR 35 TC 12 Z9 12 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD APR PY 1994 VL 55 IS 4 BP 467 EP 475 PG 9 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA NE677 UT WOS:A1994NE67700007 PM 8145017 ER PT J AU PEREZSCHAEL, I BLANCO, M GARCIA, D WHITE, L ALFONZO, E CRESPO, I CUNTO, W PITTMAN, AL KAPIKIAN, AZ FLORES, J AF PEREZSCHAEL, I BLANCO, M GARCIA, D WHITE, L ALFONZO, E CRESPO, I CUNTO, W PITTMAN, AL KAPIKIAN, AZ FLORES, J TI EVALUATION OF THE ANTIGENICITY AND REACTOGENICITY OF VARYING FORMULATIONS OF THE RHESUS ROTAVIRUS-BASED QUADRIVALENT AND THE M37 ROTAVIRUS VACCINE CANDIDATES SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE RRV; IMMUNIZATION; DIARRHEA ID VENEZUELAN INFANTS; YOUNG-CHILDREN; EFFICACY; TRIAL; LIVE; DIARRHEA; RIT-4237; SEROTYPE-1; PROTECTION; MMU-18006 AB Three phase I trials of the rhesus rotavirus (RRV)-based quadrivalent vaccine [composed of serotype 3 (RRV), and serotypes 1 (D x RRV), 2 (DS1 x RRV), and 4 (ST3 x RRV) human rota-virus x RRV reassortants] and the M37 (nursery strain) rotavirus vaccine candidates were conducted in an attempt to find a safe and optimally antigenic formulation. Infants 10-20 weeks old received, in trial I, 1) the quadrivalent vaccine as two separate bivalent doses (1 X 10(4) PFU each of D x RRV and RRV, followed 4 weeks later by 1 x 10(4) PFU each of DS1 x RRV and ST3 x RRV) or 2) placebo; in trial II, 1) one dose of quadrivalent vaccine (10(4) PFU of each component), or 2) two doses of quadrivalent vaccine, or 3) a 10(4) PFU dose of M37 vaccine, or 4) M37 vaccine followed by the quadrivalent vaccine, or 5) placebo; in trial III, 1) a dose of a higher-titered quadrivalent vaccine (10(5) PFU of each component), or 2) two doses of higher titered quadrivalent vaccine, or 3) a dose of higher titered M37 vaccine (10(5) PFU) or 4) two doses of M37 vaccine (10(5) PFU), or 5) M37 vaccine (10(5) PFU) followed by the higher titered quadrivalent vaccine, or 6) placebo. A mild, transient fever during the first week post-vaccination was associated with the bivalent or quadrivalent vaccines but not with the M37 vaccine. Fourfold or greater serum IgA ELISA responses to rotavirus were observed in 48-92% of the infants receiving quadrivalent vaccine and in 32-50% of those receiving M37 vaccine. Neutralization seroresponses to human rotaviruses in infants receiving quadrivalent vaccine ranged from 9% (to serotype 3 in recipients of the first dose of bivalent vaccine in trial I) to 68% (to serotype 1 in recipients of two doses of higher titered quadrivalent vaccine in trial III). M37 vaccine induced homologous neutralization responses in 33-78% of the infants and responses to human strains sharing its VP7 (Wa) or VP4 (ST3) serotype in 13-35% of the infants. Overall, both vaccine candidates induced a greater number of antibody responses when two doses or a higher titered preparation was administered. (C) 1994 Wiley-Liss, Inc. C1 NIAID,INFECT DIS LAB,9000 ROCKVILLE PIKE,ROOM 105,BLDG 7,BETHESDA,MD 20892. MINIST SANIDAD & ASISTENCIA SOCIAL,INST BIOMED,CARACAS,VENEZUELA. IBM VENEZUELA,CTR CIENT,CARACAS,VENEZUELA. NR 27 TC 25 Z9 25 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0146-6615 J9 J MED VIROL JI J. Med. Virol. PD APR PY 1994 VL 42 IS 4 BP 330 EP 337 DI 10.1002/jmv.1890420403 PG 8 WC Virology SC Virology GA ND134 UT WOS:A1994ND13400002 PM 8046423 ER PT J AU TABOR, E AF TABOR, E TI TUMOR-SUPPRESSOR GENES, GROWTH-FACTOR GENES, AND ONCOGENES IN HEPATITIS-B VIRUS-ASSOCIATED HEPATOCELLULAR-CARCINOMA SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE CARCINOGENESIS; FOS; INSULIN-LIKE GROWTH FACTOR-II; MYC; P53; RAS; RB; TRANSFORMING GROWTH FACTOR-ALPHA ID C-FOS EXPRESSION; N-RAS ONCOGENES; P53 GENE; FACTOR-ALPHA; LIVER-TUMORS; RETINOBLASTOMA GENE; TRANSGENIC MICE; KI-RAS; POINT MUTATION; MYC ONCOGENES AB A series of changes in the genes that control hepatocyte growth, or interference with the protein products of these genes, appears to have an important role in the etiology of hepatocellular carcinoma (HCC). Mutations of the p53 tumor suppressor gene have been identified in 30-50% of HCC patients in some geographic areas. Abnormalities of the RB tumor suppressor gene have been found in 20-25% of HCCs, including 80-86% of HCCs with p53 mutations. Overexpression of transforming growth factor alpha (TGF-alpha), insulin-like growth factor II (IGF-II), and the oncogenes N-ras, c-myc, and c-fos have been found in high percentages of HCC patients. The cumulative effect of these changes may be more important than the order in which they occur. Some of these changes may explain the mechanism(s) by which the hepatitis B virus participates in the development of HCC. (C) 1994 Wiley-Liss, Inc. RP TABOR, E (reprint author), NCI,BETHESDA,MD 20892, USA. NR 86 TC 107 Z9 110 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0146-6615 J9 J MED VIROL JI J. Med. Virol. PD APR PY 1994 VL 42 IS 4 BP 357 EP 365 DI 10.1002/jmv.1890420406 PG 9 WC Virology SC Virology GA ND134 UT WOS:A1994ND13400005 PM 8046425 ER PT J AU JAEGER, MM DODANE, V KACHAR, B AF JAEGER, MM DODANE, V KACHAR, B TI MODULATION OF TIGHT JUNCTION MORPHOLOGY AND PERMEABILITY BY AN EPITHELIAL FACTOR SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE TIGHT JUNCTION; INTERCELLULAR JUNCTIONS; TRANSEPITHELIAL PERMEABILITY; TRANSEPITHELIAL ELECTRICAL RESISTANCE (TER); MDCK, A6, CACO-2 EPITHELIAL CELL CULTURES ID CULTURED TRANSPORTING EPITHELIUM; NECTURUS GALLBLADDER EPITHELIUM; CANINE KIDNEY-CELLS; OCCLUDING JUNCTIONS; MDCK CELLS; RAT-LIVER; 2 STRAINS; MONOLAYERS; RESISTANCE; MEMBRANE AB We report evidence of a factor secreted at the apical side of epithelial monolayers which modulates tight junction structure and permeability. This activity was detected within 4-7 days of conditioning of the apical medium by MDCK, A6 or Caco-2 epithelial cell lines cultured on permeable membranes in bipartite chambers. Apical conditioned medium (ACM), applied to the basolateral surface of a confluent monolayer, increased the transepithelial electrical resistance (TER), progressively reaching values 12-22% higher than the baseline within 5-10 min. After 40-60 min, the TER returned slowly to the basal value. This phenomenon was not observed either when using preheated ACM or the ACM filtrate obtained through a 30,000 MW cutoff membrane. The ACM maintained its activity even when applied to cell lines from different organs and species, as demonstrated when ACM from MDCK monolayers promoted an increase of 22% in the TER of Caco-2 cells. The increase of TER induced by the ACM treatment is accompanied by a change in the distribution of the number of tight junction strands, from an initial pattern, dominated mostly by junctions with one or two strands, to a new pattern after treatment dominated by junctions with two or three strands. Our results suggest the existence of a mechanism in epithelial cells that could signal leakage of apically secreted components to the basolateral side, thereby modulating the junction structure and permeability. C1 NATL INST DEAFNESS & OTHER COMMUN DISORDERS,CELLULAR BIOL LAB,5 RES COURT,ROOM 2A03,ROCKVILLE,MD 20850. NR 38 TC 15 Z9 15 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD APR PY 1994 VL 139 IS 1 BP 41 EP 48 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA ND266 UT WOS:A1994ND26600004 PM 8071986 ER PT J AU PHILLIP, M WERNER, H PALESE, T KOWARSKI, AA STANNARD, B BACH, LA LEROITH, D ROBERTS, CT AF PHILLIP, M WERNER, H PALESE, T KOWARSKI, AA STANNARD, B BACH, LA LEROITH, D ROBERTS, CT TI DIFFERENTIAL ACCUMULATION OF INSULIN-LIKE GROWTH-FACTOR-I IN KIDNEYS OF PREPUBERTAL AND POSTPUBERTAL STREPTOZOTOCIN-DIABETIC RATS SO JOURNAL OF MOLECULAR ENDOCRINOLOGY LA English DT Article ID GLOMERULAR MESANGIAL CELLS; INITIAL RENAL GROWTH; IGF-I; BINDING-PROTEINS; UNINEPHRECTOMIZED RATS; FILTRATION RATE; MESSENGER-RNA; SOMATOMEDIN-C; HYPERTROPHY; RECEPTOR AB Nephropathy, one of the major complications of diabetes mellitus, is characterized by an early increase in kidney size. In experimental models of diabetes, this event is preceded by a rapid and transient rise in kidney IGF-I levels, at least in adult animals. Since diabetes-associated renal changes are uncommon in young patients, we investigated the early changes in the components of the IGF system following induction of diabetes in prepubertal and postpubertal rats. The rationale for this study was the evaluation of potential differences which could lead to kidney complications only at adult stages. Unlike the situation in the postpubertal kidney, in which there was a transient accumulation of extractable IGF-I 24-48 h after streptozotocin (STZ) administration, there was a decrease of similar to 12-fold in the level of IGF-I in the prepubertal kidney over the same period of time. Paradoxically, kidney IGF-I mRNA levels were reduced by similar to 50% in the postpubertal rat 24 h after STZ treatment, whereas in the prepubertal kidney IGF-I mRNA levels were unaltered. Furthermore, the levels of IGF-I receptor mRNA and I-125-labelled IGF-I binding to kidney membranes of postpubertal diabetic rats were similar to the levels in control kidneys. On the other hand, both the levels of IGF-I receptor mRNA and I-125-labelled IGF-I binding were increased (similar to 2.5-fold (after 24 h) and similar to 3-fold (after 48 h) respectively) in prepubertal animals. In addition, increased expression of IGF-binding protein (IGFBP)-1 mRNA was seen early in diabetes in both pre- and postpubertal rats. The results of this study suggest that the transient accumulation of IGF-I in the kidney of the postpubertal diabetic rat may not be due to an increase in the local synthesis of IGF-I, but rather to an increase in IGF-I uptake from the circulation due to non-membrane-associated IGFBP-1. The lack of accumulation of IGF-I in the prepubertal kidney probably reflects the similar to 10-fold lower levels of circulating IGF-I in young as compared with adult diabetic rats. C1 NIDDK,DIABET BRANCH,BETHESDA,MD 20892. BEN GURION UNIV NEGEV,FAC HLTH SCI,DEPT PEDIAT,BEER SHEVA,ISRAEL. NIDDK,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DIV PEDIAT ENDOCRINOL,BALTIMORE,MD 21201. NR 44 TC 33 Z9 33 U1 0 U2 0 PU J ENDOCRINOLOGY LTD PI BRISTOL PA 17/18 THE COURTYARD, WOODLANDS, ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ SN 0952-5041 J9 J MOL ENDOCRINOL JI J. Mol. Endocrinol. PD APR PY 1994 VL 12 IS 2 BP 215 EP 224 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NH075 UT WOS:A1994NH07500010 PM 7520245 ER PT J AU KRAFT, T SCHNEKENBUHL, S MESSERLI, M YU, LC CHALOVICH, JM BRENNER, B AF KRAFT, T SCHNEKENBUHL, S MESSERLI, M YU, LC CHALOVICH, JM BRENNER, B TI MECHANISM OF ACTIVATION OF THE CONTRACTILE SYSTEM OF SKELETAL-MUSCLE FIBERS BY NEM-S1 COMPARED TO CALCIUM-ACTIVATION SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Meeting Abstract C1 HANNOVER MED SCH,DEPT CLIN PHYSIOL,W-3000 HANNOVER,GERMANY. ETH ZURICH,INST CELL BIOL,ZURICH,SWITZERLAND. NIH,BETHESDA,MD 20892. E CAROLINA UNIV,GREENVILLE,NC 27834. NR 0 TC 1 Z9 1 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0142-4319 J9 J MUSCLE RES CELL M JI J. Muscle Res. Cell Motil. PD APR PY 1994 VL 15 IS 2 BP 202 EP 203 PG 2 WC Cell Biology SC Cell Biology GA NH965 UT WOS:A1994NH96500109 ER PT J AU CUDA, G FANANAPAZIR, L EPSTEIN, ND SELLERS, JR AF CUDA, G FANANAPAZIR, L EPSTEIN, ND SELLERS, JR TI ABNORMAL FUNCTION OF BETA-MYOSIN IN HYPERTROPHIC CARDIOMYOPATHY SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Meeting Abstract C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. RI Cuda, Giovanni/F-5359-2012 OI Cuda, Giovanni/0000-0001-6313-1866 NR 0 TC 0 Z9 0 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0142-4319 J9 J MUSCLE RES CELL M JI J. Muscle Res. Cell Motil. PD APR PY 1994 VL 15 IS 2 BP 206 EP 206 PG 1 WC Cell Biology SC Cell Biology GA NH965 UT WOS:A1994NH96500123 ER PT J AU ESCANDON, E SOPPET, D ROSENTHAL, A MENDOZARAMIREZ, JL SZONYI, E BURTON, LE HENDERSON, CE PARADA, LF NIKOLICS, K AF ESCANDON, E SOPPET, D ROSENTHAL, A MENDOZARAMIREZ, JL SZONYI, E BURTON, LE HENDERSON, CE PARADA, LF NIKOLICS, K TI REGULATION OF NEUROTROPHIN RECEPTOR EXPRESSION DURING EMBRYONIC AND POSTNATAL-DEVELOPMENT SO JOURNAL OF NEUROSCIENCE LA English DT Article DE BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN-3; NEUROTROPHIN-4/5; NEUROTROPHINS; NEUROTROPHIN RECEPTORS; TRKB; TRKC; AFFINITY CROSS-LINKING; DEVELOPMENT ID NERVE GROWTH-FACTOR; TRK PROTOONCOGENE PRODUCT; TYROSINE PROTEIN-KINASE; AFFINITY NGF RECEPTOR; NEURAL CREST CELLS; MESSENGER-RNA; DOPAMINERGIC-NEURONS; CHOLINERGIC NEURONS; BIOLOGICAL-ACTIVITY; MOLECULAR-CLONING AB Members of the NGF family of proteins act as neurotrophic agents for defined populations of peripheral and central neurons during embryonic and postnatal development. We have studied the presence of receptors for brain-derived neurotrophic factor (BDNF) and neurotrophin-3 and -4/5 (NT-3, NT-4/5) by cross-linking radioiodinated neurotrophins to specific cell surface receptors. We have identified neurotrophin receptors representing full-length TrkB and TrkC and their truncated forms (lacking a functional cytoplasmic kinase domain) in neuronal as well as in non-neuronal tissues. During chicken embryonic and early postnatal brain development, expression of full-length TrkB and TrkC proteins preceded the onset of the truncated forms of these receptors. A similar pattern was also observed in mouse embryonic and early postnatal brain. The relative levels of neurotrophin receptors in the basal forebrain and in the hippocampus did not change significantly with age in mice. High levels of receptors for the three neurotrophins were detected in the nigrostriatal system. Full-length TrkB and TrkC receptors were found in chicken and rat embryonic ventral spinal cord, as well as on purified motoneurons. Again, truncated TrkB appeared significantly later than the full-length form on spinal motoneurons. In chicken embryonic retina and optic tectum we detected full-length TrkB and TrkC; however, the optic tectum also expressed large amounts of the truncated form of TrkB. TrkC but not TrkB was detected in chicken embryonic skeletal muscle, suggesting that NT-3 may have a novel function in this tissue. The presence of neurotrophin receptors in a wide variety of embryonic and postnatal tissues underlines the significant role of BDNF, NT-3, and NT-4/5 in embryonic and postnatal development. The regulation of the ratio of full-length versus truncated neurotrophin receptors may play an important role in the development, maturation, and maintenance of various neuronal networks. C1 GENENTECH INC, DEPT NEUROSCI, S SAN FRANCISCO, CA 94080 USA. GENENTECH INC, DEPT PROC SCI, S SAN FRANCISCO, CA 94080 USA. NCI, FREDERICK CANC RES & DEV CTR,ABL, BASIC RES PROGRAM,MOLEC EMBRYOL SECT, FREDERICK, MD 21702 USA. Univ Nacl Autonoma Mexico, FAC MED, INST FISIOL CELULAR, MEXICO CITY 04510, DF, MEXICO. Univ Nacl Autonoma Mexico, FAC MED, DEPT FISIOL, MEXICO CITY 04510, DF, MEXICO. CNRS, INSERM, F-34033 MONTPELLIER, FRANCE. RI Parada, luis/B-9400-2014; OI Henderson, Christopher/0000-0002-9936-3279 FU NCI NIH HHS [N01-CO-74101] NR 60 TC 175 Z9 177 U1 0 U2 1 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1994 VL 14 IS 4 BP 2054 EP 2068 PG 15 WC Neurosciences SC Neurosciences & Neurology GA NF026 UT WOS:A1994NF02600016 PM 8158256 ER PT J AU BACHEVALIER, J MISHKIN, M AF BACHEVALIER, J MISHKIN, M TI EFFECTS OF SELECTIVE NEONATAL TEMPORAL-LOBE LESIONS ON VISUAL RECOGNITION MEMORY IN RHESUS-MONKEYS SO JOURNAL OF NEUROSCIENCE LA English DT Article DE MEMORY; MEDIAL TEMPORAL LOBE; INFERIOR TEMPORAL CORTEX; DELAYED NONMATCHING-TO-SAMPLE TASK; INFANT MONKEY ID KLUVER-BUCY SYNDROME; INFANT MONKEYS; HIPPOCAMPAL-FORMATION; CORTEX; AGE; IMPAIRMENT; CHILDHOOD; AMYGDALA; MACAQUE; AMNESIA AB Ten-month-old infant monkeys that had received neonatal ablations of either inferior temporal cortex (area TE) or the medial temporal region were compared with age-matched normal infant monkeys in visual delayed nonmatching-to-sample with trial-unique objects. Both types of early damage caused impairment in visual recognition, but the degree of deficit after early area TE lesions differed sharply from that after early medial temporal removals. Thus, whereas early medial temporal damage yielded a marked decline in visual recognition when the delays and lists were gradually increased, early area TE damage yielded normal recognition up to a delay of 60 sec and only mild impairment at longer delays and lists. The data indicate that, unlike adult monkeys, which suffer severe and nearly equivalent losses in visual object recognition after both types of ablation, the infant monkeys' recognition ability is largely spared after early damage to area TE but not after early damage to the medial temporal lobe. Together with recent clinical reports of profound memory loss in children with early dysfunction of the medial temporal region, the present findings demonstrate that medial temporal lobe structures operate early to sustain visual recognition memory, and recovery from early damage is limited at best. Early damage to higher-order visual cortex, however, can be largely compensated, presumably by one or more of the visual cortical areas that were left intact. C1 NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. NR 60 TC 64 Z9 64 U1 0 U2 2 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1994 VL 14 IS 4 BP 2128 EP 2139 PG 12 WC Neurosciences SC Neurosciences & Neurology GA NF026 UT WOS:A1994NF02600023 PM 8158261 ER PT J AU NOGUCHI, K DUBNER, R DELEON, M SENBA, E RUDA, MA AF NOGUCHI, K DUBNER, R DELEON, M SENBA, E RUDA, MA TI AXOTOMY INDUCES PREPROTACHYKININ GENE-EXPRESSION IN A SUBPOPULATION OF DORSAL-ROOT GANGLION NEURONS SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE SUBSTANCE P; SPINAL NERVE TRANSECTION; SENSORY TRANSMISSION; REGENERATION ID PRIMARY SENSORY NEURONS; VASOACTIVE INTESTINAL POLYPEPTIDE; SCIATIC-NERVE SECTION; RAT SPINAL-CORD; SUBSTANCE-P; PERIPHERAL AXOTOMY; MESSENGER-RNAS; NEUROKININ-A; CELLS; NEUROPEPTIDES AB The distribution of dorsal root ganglion (DRG) cell sizes that show changes in preprotachykinin (PPT) gene expression and substance P (SP) levels following axotomy was examined using RNA blot analysis, in situ hybridization histochemistry, and immunocytochemistry. PPT mRNA was induced in medium-sized (1,000-2,000 mu m(2)) and large-sized (>2,000 mu m(2)) cells in the DRG after axotomy. There was a 165% increase in the number of labeled cells after sciatic transection and a 260% increase after spinal nerve transection which results in axotomy of all the cells in the ganglion. The further increase after spinal nerve transection suggests that the induction occurred in axotomized neurons. PPT mRNA label was also present in a reduced number of small (<1,000 mu m(2)) cells after axotomy. SP immunoreactivity was also induced in medium- and large-sized cells and reduced in small-sized cells. Our findings suggest that the expression of the PPT gene and SP is differentially regulated in different subpopulations of DRG neurons after axotomy and is consistent with the hypothesis that tachykinins may be important in both sensory transmission and regeneration. (C) 1994 Wiley-Liss, Inc. C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. WAKAYAMA MED COLL,DEPT ANAT 2,WAKAYAMA 640,JAPAN. RI De Leon, Marino/A-6922-2009 OI De Leon, Marino/0000-0001-6576-785X NR 43 TC 101 Z9 101 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR 1 PY 1994 VL 37 IS 5 BP 596 EP 603 DI 10.1002/jnr.490370506 PG 8 WC Neurosciences SC Neurosciences & Neurology GA NC128 UT WOS:A1994NC12800005 PM 7518007 ER PT J AU THOMPSON, BG DOPPMAN, JL OLDFIELD, EH AF THOMPSON, BG DOPPMAN, JL OLDFIELD, EH TI TREATMENT OF CRANIAL DURAL ARTERIOVENOUS-FISTULAS BY INTERRUPTION OF LEPTOMENINGEAL VENOUS DRAINAGE SO JOURNAL OF NEUROSURGERY LA English DT Article DE CRANIAL DURAL ARTERIOVENOUS MALFORMATION; DURAL ARTERIOVENOUS FISTULA; LEPTOMENINGEAL VENOUS DRAINAGE ID TRANSVENOUS EMBOLIZATION; ACQUIRED LESION; MALFORMATIONS; SINUSES; MATER; VEINS AB Cranial dural arteriovenous fistulae (AVF's) of the tentorial incisura or the dura of the middle fossa have a much higher incidence of draining via leptomeningeal veins than do AVF's of the transverse-sigmoid sinuses or the cavernous sinus. Such a drainage pattern is associated with an increased incidence of intracranial hemorrhage and progressive focal neurological deficits. Patients with cranial dural AVF's often undergo surgical excision and/or endovascular embolization for elimination of the AVF. Since these lesions are frequently large and involve the skull base or adjacent dural sinuses, extensive surgery is often required. In contrast, spinal dural AVF's with only intradural venous drainage to the medullary venous system are treated successfully by simply interrupting the vein that drains the dural AVF as it enters the subarachnoid space. The authors identified a subgroup of patients with cranial dural AVF's in whom the AVF was drained only by leptomeningeal veins, and sought to establish whether simple interruption of the vein draining the blood from the AVF into the subarachnoid space is effective and lasting treatment in this subgroup of patients, as it is in patients with spinal dural AVF's. Four adult patients with symptomatic cranial dural AVF's (two petrotentorial, one middle fossa floor, and one posterior fossa base) were identified on arteriography as having fistulae that were supplied by the internal and/or external carotid arteries and drained only via leptomeningeal veins (two entered the petrosal vein, one a cerebellar hemispheric vein, and one a mesencephalic vein). All patients underwent interruption of the vein draining the dural AVF as it penetrated the dura to enter the subarachnoid space, and experienced neurological improvement after surgery. Repeat arteriography at 1 to 2 weeks (three patients), 3 months (3 patients), 12 to 15 months (three patients), and 4 years (two patients) revealed no residual AVF and no evidence of abnormal blood now. Many cranial dural AVF's with leptomeningeal venous drainage (the type with the most aggressive behavior) are drained only by leptomeningeal veins. This subgroup of patients can be identified by selective arteriography and requires only interruption of the draining vein as it enters the subarachnoid space for successful, lasting elimination. C1 NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. NIH,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. NR 34 TC 123 Z9 127 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD APR PY 1994 VL 80 IS 4 BP 617 EP 623 DI 10.3171/jns.1994.80.4.0617 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA NC826 UT WOS:A1994NC82600003 PM 8151339 ER PT J AU BACHARACH, SL CARSON, RE AF BACHARACH, SL CARSON, RE TI WHITHER WATER SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID BLOOD-FLOW; (H2O)-O-15 RP BACHARACH, SL (reprint author), NIH,BLDG 10,RM 1C401,BETHESDA,MD 20892, USA. RI Carson, Richard/H-3250-2011 OI Carson, Richard/0000-0002-9338-7966 NR 5 TC 2 Z9 2 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD APR PY 1994 VL 35 IS 4 BP 567 EP 568 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NF262 UT WOS:A1994NF26200006 PM 8151376 ER PT J AU ANDJELKOVICH, DA MATHEW, RM LEVINE, RJ AF ANDJELKOVICH, DA MATHEW, RM LEVINE, RJ TI FOUNDRY MORTALITY REINTERPRETED - REPLY SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Letter C1 UNIV N CAROLINA,CSCC,SCH PUBL HLTH,DEPT BIOSTAT,CHAPEL HILL,NC 27599. NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP ANDJELKOVICH, DA (reprint author), CHEM IND INST TOXICOL,RES TRIANGLE PK,NC 27709, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1076-2752 J9 J OCCUP ENVIRON MED JI J. Occup. Environ. Med. PD APR PY 1994 VL 36 IS 4 BP 468 EP 468 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NE700 UT WOS:A1994NE70000014 ER PT J AU PAUL, IA NOWAK, G LAYER, RT POPIK, P SKOLNICK, P AF PAUL, IA NOWAK, G LAYER, RT POPIK, P SKOLNICK, P TI ADAPTATION OF THE N-METHYL-D-ASPARTATE RECEPTOR COMPLEX FOLLOWING CHRONIC ANTIDEPRESSANT TREATMENTS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID FORCED SWIMMING TEST; RAT CEREBRAL-CORTEX; NMDA-RECEPTOR; BINDING-SITES; D-SERINE; EXHIBIT ANTIDEPRESSANT; GLYCINE; MODULATION; INVIVO; ACID AB Chronic (14 day) but not acute (1 day) treatment of mice with clinically active antidepressants produces a significant (similar to 1.8-4.3 fold) reduction in the potency of glycine to inhibit [H-3]-5,7-dichlorkynurenic acid (5,7-DCKA) binding to strychnine-insensitive glycine receptors in neocortical membranes. Moreover, these effects were not observed following chronic treatment with a variety of nonantidepressant drugs such as D-deprenyl, chlorpromazine, salbutamol, scopolamine and chlordiazepoxide. The time course and dose-response relationships for this effect were examined after treatment with two representative antidepressant drugs (imipramine and citalopram) and electriconvulsive shock (ECS). Increases in the IC50 of glycine to inhibit [H-3]-5,7-DCKA binding were observed after treatment for 7 days with ECS, 10 days with citalopram and 14 days with imipramine, respectively, and were no longer apparent by the 10th day after cessation of treatment. These findings indicate that the antidepressant-induced reduction in the IC50 of glycine to inhibit [H-3]-5,7-DCKA binding is: 1) a slowly developing, adaptive phenomenon; 2) remarkably persistent after cessation of treatment; and 3) a significantly better predictor of antidepressant activity (22 of 23 drugs) than either beta adrenoceptor down-regulation (15 of 23 drugs) or efficacy in the forced swim test (13 of 23 drugs) [P < .01 vs. each measure, Fisher's Exact Test]. The ability of antidepressants drawn from every principal therapeutic class to effect adaptive changes in the N-methyl-D-aspartate receptor complex is consistent with the hypothesis that this ligand-gated ion channel serves as a final common pathway of antidepressant action and indicates that glutamatergic pathways may be involved in the pathophysiology of depression. C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. RI Popik, Piotr/R-5383-2016 OI Popik, Piotr/0000-0003-0722-1263 NR 53 TC 202 Z9 204 U1 0 U2 9 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1994 VL 269 IS 1 BP 95 EP 102 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NJ323 UT WOS:A1994NJ32300015 PM 8169857 ER PT J AU WELLER, M MARINI, AM MARTIN, B PAUL, SM AF WELLER, M MARINI, AM MARTIN, B PAUL, SM TI THE REDUCED UNSUBSTITUTED PTEROATE MOIETY IS REQUIRED FOR FOLATE TOXICITY OF CULTURE CEREBELLAR GRANULE NEURONS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID HIGH-DOSE METHOTREXATE; D-ASPARTATE RECEPTOR; CELLS-INVITRO; FOLIC-ACID; NEUROTOXICITY; RAT; CARBOXYPEPTIDASE-G2; LOCALIZATION; PURIFICATION; GLUTAMATE AB The proconvulsive and putative excitotoxic properties of folates led us to study folate toxicity in cultured rat cerebellar granule neurons. Exposure of these neurons to tetrahydrofolate (THF) (EC(50) = 263 +/- 12 mu M) and dihydrofolate (EC(50) = 709 +/- 29 mu M), but not to folate, formyl-THF, methyl-THF or methotrexate, resulted in a concentration-dependent neurotoxicity. THF and dihydrofolate toxicity were characterized by prominent neuronal swelling and early loss of neurite networking and could not be blocked by glutamate receptor antagonists, L-channel calcium blockers or anticonvulsants. Cleavage of THF into glutamate and tetrahydropteroate by glutamate carboxypeptidase in the presence of 1 mu M MK-801 and 5 mu M 6-cyano-7-nitroquinoxaline-2,3,dione shifted the concentration-toxicity curve to the left (EC(50) = 47 +/- 4 mu M). These results suggest (1) that the glutamate moiety is not necessary for folate toxicity, (2) that the unsubstituted reduced pteroate moiety is required for folate toxicity and (3) that unsubstituted reduced pteroates are previously unrecognized neurotoxins. Because there is no endogenous glutamate carboxypeptidase activity in cerebellar granule neuron cultures and no increase of glutamate levels in the medium of cultures exposed to THF or dihydrofolate, pteroate metabolites are unlikely to mediate the THF or dihydrofolate toxicity of cultured cerebellar granule neurons. C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 40 TC 6 Z9 6 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1994 VL 269 IS 1 BP 393 EP 401 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NJ323 UT WOS:A1994NJ32300054 PM 8169846 ER PT J AU FOLLMANN, D PROSCHAN, M AF FOLLMANN, D PROSCHAN, M TI THE EFFECT OF ESTIMATION AND BIASING STRATEGIES ON SELECTION BIAS IN CLINICAL-TRIALS WITH PERMUTED BLOCKS SO JOURNAL OF STATISTICAL PLANNING AND INFERENCE LA English DT Article DE MAXIMUM LIKELIHOOD; METHOD OF MOMENTS; RANDOM ALLOCATION; RANDOM WALK; RANDOMIZATION AB Subjects in clinical trials are frequently randomized within blocks to ensure balance between treatment groups during the accrual period. Often, the block sizes themselves are also randomly selected. If the trial is unblinded and the block size known, the treatment assignment of some subjects will be known before they are randomized. This knowledge could lead to a bias where the investigator selects healthier subjects for a particular treatment. An investigator's potential to bias a study depends on two factors: knowledge of the block distribution and the extent to which he uses this knowledge. Both factors are investigated. Knowledge of the block distribution is reflected by the variability of the estimates of the distribution. Maximum likelihood estimates (MLE) and ad hoc estimates are considered. An investigator's willingness to bias is formalized by defining a class of schemes where the decision to bias depends on the probability of correctly guessing a treatment assignment. The amount of bias these different schemes can introduce is quantified. Fixed blocks are easier to estimate and more susceptible to bias that random blocks. In general, the block distribution with least bias depends on the investigator's biasing strategy. However, block distributions with larger block sizes and uniform or increasing weights should work well in most situations. C1 NHLBI,BIOSTAT RES BRANCH,BETHESDA,MD 20892. NR 8 TC 8 Z9 8 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-3758 J9 J STAT PLAN INFER JI J. Stat. Plan. Infer. PD APR 1 PY 1994 VL 39 IS 1 BP 1 EP 17 DI 10.1016/0378-3758(94)90108-2 PG 17 WC Statistics & Probability SC Mathematics GA NB229 UT WOS:A1994NB22900001 ER PT J AU CAVANAUGH, AH SIMONS, SS AF CAVANAUGH, AH SIMONS, SS TI FACTOR-ASSISTED DNA-BINDING AS A POSSIBLE GENERAL MECHANISM FOR STEROID-RECEPTORS - FUNCTIONAL-HETEROGENEITY AMONG ACTIVATED RECEPTOR-STEROID COMPLEXES SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article ID HEPATIC GLUCOCORTICOID-RECEPTOR; TWO-DIMENSIONAL ELECTROPHORESIS; THYROID-HORMONE RECEPTORS; HEAT-SHOCK PROTEIN; RAT THYMUS-CELLS; ESTROGEN-RECEPTOR; DEXAMETHASONE 21-MESYLATE; STABILIZING FACTOR; AFFINITY; PROGESTERONE AB We previously reported that activated glucocorticoid receptor-steroid complexes from rat HTC cell cytosol exist as at least two sub-populations, one of which requires a low molecular weight (700-3000 Da) factor(s) for binding to DNA. This factor is removed by Sephadex G-50 chromatography and is found predominantly in extracts of crude HTC cell nuclei. We have now determined that factor is not limited to HTC cells since an apparently identical factor(s) was found in nuclear extracts of rat kidney and liver as well as human HeLa and MCF-7 cells. Furthermore, the DNA binding of a sub-population of human glucocorticoid receptors depends on factor. While these results were obtained with agonist (dexamethasone) bound receptors, a sub-population of HTC cell receptors covalently labeled by the antiglucocorticoid dexamethasone 21-mesylate also displayed factor-dependent DNA binding. This receptor heterogeneity was not an artifact of cell-free activation since the cell-free nuclear binding of dexamethasone mesylate labeled complexes was, as in intact cells, less than that for dexamethasone bound complexes. Earlier results suggested that the increased DNA binding with factor involved a direct interaction of receptor with factor(s). We now find that the factor-induced DNA binding is retained by amino terminal truncated (42 kDa) glucocorticoid receptors from HTC cells. Thus the ability of receptor to interact with factor(s) is encoded by the DNA and/or steroid binding domains. Two dimensional gel electrophoresis analysis of dexamethasone-mesylate labeled 98 kDa receptors revealed multiple charged isoforms for both sub-populations but no differences in the amount of the various isoforms in each sub-population. Finally, activated progesterone and estrogen receptor complexes were also found to be heterogeneous, with a similar, if not identical, small molecular weight factor(s) being required for the DNA binding of one sub-population. The observations that functional heterogeneity of receptors is not unique to glucocorticoid receptors, whether bound by an agonist or antagonist, and that the factor(s) is neither species nor tissue specific suggests that factor-assisted DNA binding may be a general mechanism for all steroid receptors. C1 NIDDK,STEROID HORMONES SECT,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. NR 65 TC 14 Z9 14 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-0760 J9 J STEROID BIOCHEM JI J. Steroid Biochem. Mol. Biol. PD APR PY 1994 VL 48 IS 5-6 BP 433 EP 446 DI 10.1016/0960-0760(94)90191-0 PG 14 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA NK697 UT WOS:A1994NK69700003 PM 8180104 ER PT J AU DIONNE, RA BERTHOLD, C AF DIONNE, RA BERTHOLD, C TI TRIAZOLAM AND DENTAL ANXIETY - REPLY SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Letter RP DIONNE, RA (reprint author), NIDR,BETHESDA,MD, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD APR PY 1994 VL 125 IS 4 BP 360 EP 360 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA NF256 UT WOS:A1994NF25600007 ER PT J AU CORBIN, SB KOHN, WG AF CORBIN, SB KOHN, WG TI THE BENEFITS AND RISKS OF DENTAL AMALGAM - CURRENT FINDINGS REVIEWED SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article ID SILVER TOOTH FILLINGS; MERCURY EXPOSURE; EXPIRED AIR AB In response to recent concern and research findings about dental amalgam, the U.S. Public Health Service conducted a comprehensive scientific review of its benefits and risks. This review would serve as a basis for examining federal policy on the use of dental amalgam as a restorative material. This article summarizes the principal findings, conclusions and recommendations from that review. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,ORAL MED PROGRAM,BETHESDA,MD. RP CORBIN, SB (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR PREVENT SERV,DIV ORAL HLTH,5600 FISHERS LANE,PKLAWN BLDG,ROCKVILLE,MD 20857, USA. NR 17 TC 37 Z9 37 U1 1 U2 2 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD APR PY 1994 VL 125 IS 4 BP 381 EP 388 PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA NF256 UT WOS:A1994NF25600009 PM 8176073 ER PT J AU ATKINSON, JC WU, AJ AF ATKINSON, JC WU, AJ TI SALIVARY-GLAND DYSFUNCTION - CAUSES, SYMPTOMS, TREATMENT SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article ID SJOGRENS-SYNDROME; DRY MOUTH; DRUG-USE; XEROSTOMIA; PREVALENCE; HYPOFUNCTION; PILOCARPINE; RADIATION; DISEASES; CANCER AB The three most common known causes of salivary gland dysfunction are medication usage, radiation therapy and Sjogren's syndrome. Current therapeutic options to treat salivary dysfunction are limited. Clinical considerations as well as the outlook for individuals experiencing salivary dysfunction ar discussed. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. NR 62 TC 86 Z9 96 U1 0 U2 2 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD APR PY 1994 VL 125 IS 4 BP 409 EP 416 PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA NF256 UT WOS:A1994NF25600012 PM 8176076 ER PT J AU SLESINSKI, MJ GLONINGER, MF COSTANTINO, JP ORENSTEIN, DM AF SLESINSKI, MJ GLONINGER, MF COSTANTINO, JP ORENSTEIN, DM TI LIPID-LEVELS IN ADULTS WITH CYSTIC-FIBROSIS SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID FATTY-ACID DEFICIENCY; LIPOPROTEIN ABNORMALITIES; PRECIPITATION PROCEDURE; CHOLESTEROL; MANAGEMENT; CHILDREN; DEFECT AB Objective To examine the hypothesis that an energy-dense, high-fat diet, which is necessary to maintain weight in adults with cystic fibrosis, does not result in high serum cholesterol levels. Design Dietary, anthropometric, and biochemical data were correlated. Setting A cystic fibrosis center in Pittsburgh, Pa. Subjects Thirty-one adults with cystic fibrosis, 50 obligate carriers of the cystic fibrosis gene, and 26 controls who did not have cystic fibrosis. Main outcome measures Adults with cystic fibrosis had a lower mean serum cholesterol level and higher mean intakes of energy and fat than controls. Statistical analyses performed Student's t test was used to determine the statistical significance between two means. Univariate correlation coefficients were determined to measure the relative intensity of association between two variables. Results Mean total serum cholesterol levels in men with cystic fibrosis was 3.1 mmol/L vs 4.7 mo\L in male controls (P<.001). Mean total serum cholesterol levels in women with cystic fibrosis was 3.2 mmol/L vs 4.3 mmol/L in female controls (P<.001). Three adults with cystic fibrosis and no signs of pancreatic insufficiency had serum cholesterol levels in the high normal range. Carriers had serum lipid levels in the same range as the controls. Conclusions/applications The findings indicate that a high-energy, high-fat diet does not raise serum lipid levels in those patients with cystic fibrosis and pancreatic insufficiency. However, those individuals with cystic fibrosis and normal pancreatic function may be at the same risk as the general population for developing high serum lipid levels. They should have their serum lipid levels monitored and be given appropriate dietary recommendations. C1 UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT EPIDEMIOL,PITTSBURGH,PA 15261. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT BIOSTAT,PITTSBURGH,PA 15261. UNIV PITTSBURGH,CTR CYST FIBROSIS,SCH MED,PITTSBURGH,PA 15213. UNIV PITTSBURGH,SCH MED,DIV PULM,PITTSBURGH,PA 15213. UNIV PITTSBURGH,SCH MED,DEPT PEDIAT,PITTSBURGH,PA 15213. RP SLESINSKI, MJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892, USA. NR 32 TC 13 Z9 13 U1 0 U2 1 PU AMER DIETETIC ASSN PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD APR PY 1994 VL 94 IS 4 BP 402 EP 408 DI 10.1016/0002-8223(94)90095-7 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA NE705 UT WOS:A1994NE70500009 PM 8144807 ER PT J AU COSTABILE, RA CHOYKE, PL FRANK, JA GIRTON, ME DIGGS, R BILLUPS, KL DESJARDINS, C AF COSTABILE, RA CHOYKE, PL FRANK, JA GIRTON, ME DIGGS, R BILLUPS, KL DESJARDINS, C TI VARIABILITY OF ISCHEMIA DURING SPERMATIC CORD TORSION IN THE RAT SO JOURNAL OF UROLOGY LA English DT Article DE INFERTILITY; BLOOD FLOW VELOCITY; PERFUSION; TESTIS ID CONTRALATERAL TESTIS; TESTICULAR TORSION AB Testicular torsion affects prepubertal males and causes testicular infarction and subfertility. Animal models of spermatic cord torsion have been used in an attempt to study the mechanism of testicular injury from torsion. Although standardized animal models of torsion have been proposed, their reliability in producing testicular ischemia has not been documented. Dynamic enhanced magnetic resonance imaging (MRI) of the testis was used in a rat model with surgically induced, unilateral, 720 degrees torsion to quantify the severity of ischemia. Intravenous dysprosium diethylenetriaminepentaacetic acid-bis methylamide (Dy-DTPA-BMA) was injected as a bolus followed by serial dynamic Turbo GRASS images. Region of interest (ROI) measurements were obtained within the testicular parenchyma during contrast enhancement and washout. Perfusion abnormalities ranging from minimal delay in contrast enhancement in the torqued testicle to complete absence of intraparenchymal blood flow were documented with dynamic enhanced MRI. Reperfusion scans 1 hour after surgical reduction of torsion showed normalization of testicular blood flow in all animals. Dynamic enhanced MRI appears to be a useful method of documenting the perfusion deficit arising from torsion of the testis. Standard animal models of torsion produce inconsistent results because they do not reliably reproduce testicular ischemia. The ability of MRI to quantify perfusion abnormalities in the testis may provide additional information in the evaluation of human patients with symptoms of testicular torsion. C1 UNIV VIRGINIA,HLTH SCI CTR,DEPT UROL,CHARLOTTESVILLE,VA. UNIV VIRGINIA,HLTH SCI CTR,DEPT PHYSIOL,CHARLOTTESVILLE,VA. NIH,DIAGNOST RADIOL RES PROGRAM,BETHESDA,MD 20892. FU NICHD NIH HHS [HD-20876]; NIDDK NIH HHS [DK-07642, DK-45179] NR 15 TC 12 Z9 12 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD APR PY 1994 VL 151 IS 4 BP 1070 EP 1072 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA NA970 UT WOS:A1994NA97000086 PM 8126796 ER PT J AU HASENKRUG, KJ SPANGRUDE, GJ NISHIO, J BROOKS, DM CHESEBRO, B AF HASENKRUG, KJ SPANGRUDE, GJ NISHIO, J BROOKS, DM CHESEBRO, B TI RECOVERY FROM FRIEND DISEASE IN MICE WITH REDUCED MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I EXPRESSION SO JOURNAL OF VIROLOGY LA English DT Article ID HOST GENETIC-CONTROL; POSITIVE SELECTION; VIRUS LEUKEMIA; CELL-SURFACE; T-CELLS; MONOCLONAL-ANTIBODIES; DIFFERENT H-2; BONE-MARROW; RFV-1 GENE; ANTIGENS AB Mice homozygous for the b allele of the MHC gene, H-2D, have a high incidence of recovery from Friend virus infections, while mice heterozygous for the b allele at H-2D have a very low incidence of recovery. Previous experiments indicated that the low recovery rates associated with heterozygosity at H-2D might be related to a gene dosage effect requiring the expression of two H-2D(b) alleles for high recovery. We investigated the effects of reduced H-2D(b) expression on recovery from Friend disease by using H-2(b) homozygous mice carrying a single beta(2)-microglobulin gene disruption. These mice had reductions in cell surface H-2D(b) expression comparable to those of H-2D(a/b) heterozygotes. Numerous cell types with various levels of H-2D(b) expression were examined, and in each case, the expression levels in the beta(2)-microglobulin mutants closely reflected those observed in the H-2D(a/b) heterozygotes. We found, however, that reduced expression did not affect recovery from Friend disease, indicating that heterozygous levels of H-2D(b) expression are sufficient for the high-recovery phenotype previously associated only with H-2D(b) homozygotes. RP HASENKRUG, KJ (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,903 S 4TH ST,HAMILTON,MT 59840, USA. NR 41 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2059 EP 2064 PG 6 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700003 PM 8138991 ER PT J AU CAUGHEY, B BROWN, K RAYMOND, GJ KATZENSTEIN, GE THRESHER, W AF CAUGHEY, B BROWN, K RAYMOND, GJ KATZENSTEIN, GE THRESHER, W TI BINDING OF THE PROTEASE-SENSITIVE FORM OF PRION PROTEIN PRP TO SULFATED GLYCOSAMINOGLYCAN AND CONGO RED SO JOURNAL OF VIROLOGY LA English DT Article ID SCRAPIE-ASSOCIATED FORM; INCUBATION PERIOD; DEXTRAN SULFATE; PHOSPHOLIPASE; POLYANIONS; PRECURSOR; INFECTION; FIBRILS; DIFFER; CELLS AB Congo red and certain sulfated glycans are potent inhibitors of protease-resistant PrP accumulation in scrapie-infected cells. One hypothesis is that these inhibitors act by blocking the association between protease-resistant PrP and sulfated glycosaminoglycans or proteoglycans (e.g., heparan sulfate proteoglycan) that is observed in amyloid plaques of scrapie-infected brain tissue. Accordingly, we have investigated whether the apparent precursor of protease-resistant PrP, protease-sensitive PrP, binds to Congo red and heparin, a highly sulfated glycosaminoglycan with an inhibitory potency like that of heparan sulfate. Protease-sensitive PrP released from the surface of mouse neuroblastoma cells bound to heparin-agarose and Congo red-glass beads. Sucrose density gradient fractionation provided evidence that at least some of the PrP capable of binding heparin-agarose was monomeric. Free Congo red blocked PrP binding to heparin and vice versa, suggesting that these ligands share a common binding site. The relative efficacies of pentosan polysulfate, Congo red, heparin, and chondroitin sulfate in blocking PrP binding to heparin-agarose corresponded with their previously demonstrated potencies in inhibiting protease-resistant PrP accumulation. These results are consistent with the idea that sulfated glycans and Congo red inhibit protease-resistant PrP accumulation by interfering with the interaction of PrP with an endogenous glycosaminoglycan or proteoglycan. C1 OREGON STATE UNIV,DEPT BIOCHEM & BIOPHYS,CORVALLIS,OR 97331. RP CAUGHEY, B (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 25 TC 187 Z9 196 U1 0 U2 7 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2135 EP 2141 PG 7 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700012 PM 7511169 ER PT J AU GOINS, WF STERNBERG, LR CROEN, KD KRAUSE, PR HENDRICKS, RL FINK, DJ STRAUS, SE LEVINE, M GLORIOSO, JC AF GOINS, WF STERNBERG, LR CROEN, KD KRAUSE, PR HENDRICKS, RL FINK, DJ STRAUS, SE LEVINE, M GLORIOSO, JC TI A NOVEL LATENCY-ACTIVE PROMOTER IS CONTAINED WITHIN THE HERPES-SIMPLEX VIRUS TYPE-1 U-L FLANKING REPEATS SO JOURNAL OF VIROLOGY LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; HUMAN TRIGEMINAL GANGLIA; TRANSCRIPT LAT PROMOTER; DNA-BINDING PROPERTIES; ZINC-FINGER PROTEIN; C-MYC PROMOTER; MESSENGER-RNA; NUCLEOTIDE-SEQUENCE; REGULATORY ELEMENTS; RESPONSE ELEMENT AB Herpes simplex virus type 1 (HSV-1) expresses a unique series of RNA molecules, the latency-associated transcripts or LATs, during latent infection of neuronal tissues. Previous studies by others have described a TATA box-containing latency-active promoter, referred to here as LAP1, located approximately 700 bp upstream of the 5' end of the major 2.0-kb LAT. In this report, transient gene expression assays mere employed to identify a second, novel latency-active promoter (LAP2) present within a region downstream of LAP1 and 5' proximal to the major 2.0-kb LAT. In contrast to LAP1, this promoter lacks a TATA box but possesses cis-acting regulatory elements and other features frequently observed within eukaryotic housekeeping gene promoters. Unlike most other HSV promoters, LAP2 was down-regulated by the viral transcriptional activators ICP4 and ICP0. The majority of LAP2-positive regulatory elements were located within sequences from -257 to -58 relative to the 5' end of the 2.0-kb LAT, and the basal promoter mapped within sequences from -14 to +28. RNase protection experiments demonstrated that chimeric LAT-chloramphenicol acetyltransferase transcripts produced in the transient assays initiated at or near the 5' end of the major 2-kb LAT. Tn5 insertional mutagenesis of the ICP4 regulatory gene determined that down-regulation of LAP2 required the ICP4 transactivating domain and targeted the minimal promoter region as the site of action by ICP4. Replicating recombinant viruses containing a LAP2-lacZ reporter gene cassette in an ectopic site (glycoprotein C locus) were shown to be active in mouse trigeminal ganglia. Taken together, these experiments suggest that the LAT region of the HSV-1 genome contains at least two latency-active promoters which may play different roles in expressing the various LATs. Alternatively, these promoters may comprise a larger promoter-regulatory complex which may influence transcription during latency. C1 UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. NIAID,CLIN INVEST LAB,MED VIROL SECT,BETHESDA,MD 20892. UNIV ILLINOIS,COLL MED,DEPT OPHTHALMOL,CHICAGO,IL 60612. UNIV ILLINOIS,COLL MED,DEPT MICROBIOL & IMMUNOL,CHICAGO,IL 60612. UNIV MICHIGAN,DEPT NEUROL,ANN ARBOR,MI 48105. UNIV MICHIGAN,VET AFFAIRS MED CTR,ANN ARBOR,MI 48105. UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48109. FU NIA NIH HHS [AG0947001]; NIAID NIH HHS [AI18228]; NIGMS NIH HHS [GM34534] NR 93 TC 142 Z9 146 U1 2 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2239 EP 2252 PG 14 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700024 PM 8139009 ER PT J AU SCHUBERT, U STREBEL, K AF SCHUBERT, U STREBEL, K TI DIFFERENTIAL ACTIVITIES OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE 1-ENCODED VPU PROTEIN ARE REGULATED BY PHOSPHORYLATION AND OCCUR IN DIFFERENT CELLULAR COMPARTMENTS SO JOURNAL OF VIROLOGY LA English DT Article ID LONG TERMINAL REPEAT; CASEIN KINASE-II; HIV-1; GENE; CD4; DNA; IDENTIFICATION; SEQUENCE; PRODUCT; CELLS AB The human immunodeficiency virus type 1 (HIV-1)-specific Vpu is an 81-amino-acid amphipathic integral membrane protein with at least two different biological functions: (i) enhancement of virus particle release from the plasma membrane of HIV-1-infected cells and (ii) degradation of the virus receptor CD4 in the endoplasmic reticulum (ER). We have previously found that Vpu is phosphorylated in infected cells at two seryl residues in positions 52 and 56 by the ubiquitous casein kinase 2. To study the role of Vpu phosphorylation on its biological activity, a mutant of the vpu gene lacking both phosphoacceptor sites was introduced into the infectious molecular clone of HIV-1, pNL4-3, as well as subgenomic Vpu expression vectors. This mutation did not affect the expression level or the stability of Vpu but had a significant effect on its biological activity in infected T cells as well as transfected HeLa cells. Despite the presence of comparable amounts of wild-type and nonphosphorylated Vpu, decay of CD4 was observed only in the presence of phosphorylated wild-type Vpu. Nonphosphorylated Vpu was unable to induce degradation of CD4 even if the proteins were artificially retained in the ER. In contrast, Vpu-mediated enhancement of virus secretion was only partially dependent on Vpu phosphorylation. Enhancement of particle release by wild-type Vpu was efficiently blocked when Vpu was artificially retained in the ER, suggesting that the two biological functions of Vpu are independent, occur at different sites within a cell, and exhibit different sensitivity to phosphorylation. RP SCHUBERT, U (reprint author), NIAID,MOLEC MICROBIOL LAB,BLDG 4,ROOM 312,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 49 TC 182 Z9 183 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2260 EP 2271 PG 12 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700026 PM 8139011 ER PT J AU KOPPE, B MENENDEZARIAS, L OROSZLAN, S AF KOPPE, B MENENDEZARIAS, L OROSZLAN, S TI EXPRESSION AND PURIFICATION OF THE MOUSE MAMMARY-TUMOR VIRUS GAG-PRO TRANSFRAME PROTEIN P-30 AND CHARACTERIZATION OF ITS DUTPASE ACTIVITY SO JOURNAL OF VIROLOGY LA English DT Article ID DEOXYURIDINE TRIPHOSPHATE NUCLEOTIDOHYDROLASE; INFECTIOUS-ANEMIA VIRUS; PFIZER MONKEY VIRUS; ESCHERICHIA-COLI; REVERSE-TRANSCRIPTASE; NUCLEOTIDE-SEQUENCE; GENE; DNA; RETROVIRUSES; ENZYME AB The mouse mammary tumor virus gag-pro transframe protein (p30) contains the nucleocapsid protein domain derived from the 3' end of gag, fused to 154 residues encoded by the 5' region of the pro open reading frame. The DNA coding for p30 was cloned into the plasmid pALTER-1, and an additional nucleotide was inserted by site-directed mutagenesis to allow the read-through from the gag into the pro open reading frame. The obtained insert was then cloned into pGEX-2T, a plasmid containing the glutathione S-transferase gene of Schistosoma japonicum and a nucleotide sequence encoding for a thrombin cleavage site. The chimeric protein (GST-p30) was isolated by affinity chromatography on a glutathione-Sepharose 4B column, and after thrombin treatment, the excised p30 was further purified on a single-stranded DNA-agarose column. This protein showed dUTPase activity, with only negligible cleavage of dATP, dGTP, dCTP, dTTP, or UTP. Its apparent K-m for dUTP was 28 mu M. The enzyme was inhibited by EDTA, but its effect could be reversed by Mg2+ and other divalent cations. dUTPase activity was also detected in purified mouse mammary tumor virus, and p30 was the only protein recognized by antibodies directed towards the carboxyl-terminal sequence of the dUTPase coding region. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. RI Menendez Arias, Luis /G-2436-2016; OI Menendez Arias, Luis/0000-0002-1251-6640 FU NCI NIH HHS [N01-CO-74101] NR 44 TC 30 Z9 31 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X EI 1098-5514 J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2313 EP 2319 PG 7 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700031 PM 8139016 ER PT J AU BELLACOSA, A DATTA, K BEAR, SE PATRIOTIS, C LAZO, PA COPELAND, NG JENKINS, NA TSICHLIS, PN AF BELLACOSA, A DATTA, K BEAR, SE PATRIOTIS, C LAZO, PA COPELAND, NG JENKINS, NA TSICHLIS, PN TI EFFECTS OF PROVIRUS INTEGRATION IN THE TPL-1/ETS-1 LOCUS IN MOLONEY MURINE LEUKEMIA VIRUS-INDUCED RAT T-CELL LYMPHOMAS - LEVELS OF EXPRESSION, POLYADENYLATION, TRANSCRIPTIONAL INITIATION, AND DIFFERENTIAL SPLICING OF THE ETS-1 MESSENGER-RNA SO JOURNAL OF VIROLOGY LA English DT Article ID THYMIC LYMPHOMAS; DNA-BINDING; ONCOGENE; GENES; PHOSPHORYLATION; PROTEINS; SEQUENCE; THYMOMAS; INVIVO; SITE AB The Tpl-1 locus was defined as a genomic DNA region which is targeted by provirus insertion during progression of Moloney murine leukemia virus-induced rat T-cell lymphomas. Using a panel of 156 (Mus musculus X Mus spretus) X Mus musculus interspecific backcross mice, we mapped Tpl-1 to mouse chromosome 9 at a distance of 1.2 +/- 0.9 centimorgans from the Ets-1 proto-oncogene (S. E. Bear, A. Bellacosa, P. A. Lazo, N. A. Jenkins, N. G. Copeland, C. Hanson, G. Levan, and P. N. Tsichlis, Proc. Natl. Acad. Sci. USA 86:7495-7499, 1989). In this report, we present evidence that all the known Tpl-1 provirus insertions occurred immediately 5' of the first exon of Ets-1 (exon A) and that the earlier detected distance between Tpl-1 and Ets-1 was due to the high frequency of meiotic recombination in the region between the site of provirus integration and exon III. Northern (RNA) blot analysis of polyadenylated RNA from normal adult rat tissues and Moloney murine leukemia virus-induced T-cell lymphomas and hybridization to a Tpl-1/Ets-1 probe derived from the 5' end of the gene revealed two lymphoid cell-specific RNA transcripts, of 5.5 and 2.2 kb. Sequence analysis of a near-full-length (4,991-bp) cDNA clone of the 5.5-kb RNA revealed a 441-amino-acid open reading frame encoding a protein identical to the human and mouse Ets-1 proteins with the exception of five and nine species-specific conservative amino acid differences, respectively. The steady-state level of the Tpl-1/Ets-1 RNA and of the Ets-1 protein was modestly elevated in tumors carrying a provirus in the Tpl-1 locus. The relative ratio of the two Ets-1 transcripts, which were shown to arise by differential polyadenylation, was not affected by provirus insertion. Moreover, the major site of transcriptional initiation, which was localized by primer extension 250 bp upstream of the 5' end of the Ets-1 cDNA clone, was shown to be identical in normal cells and tumors carrying a provirus in the Tpl-1 locus. Finally, the differential splicing of Ets-1 exon VII was shown by RNase protection to occur at a rate of 15 to 26% and to remain unaffected by provirus insertion. The subtlety of these effects, in contrast to the strong growth selection of cells with a provirus in the Tpl-1/Ets-1 locus, suggests that provirus insertion may affect the fine regulation of the gene, perhaps during cell cycle progression. C1 FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD 21702. RI Lazo, Pedro /M-6435-2014 OI Lazo, Pedro /0000-0001-8997-3025 FU NCI NIH HHS [N01-CO-74101]; NCRR NIH HHS [RR-05539] NR 34 TC 32 Z9 33 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2320 EP 2330 PG 11 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700032 PM 8139017 ER PT J AU PERERA, LP KAUSHAL, S KINCHINGTON, PR MOSCA, JD HAYWARD, GS STRAUS, SE AF PERERA, LP KAUSHAL, S KINCHINGTON, PR MOSCA, JD HAYWARD, GS STRAUS, SE TI VARICELLA-ZOSTER VIRUS OPEN READING FRAME-4 ENCODES A TRANSCRIPTIONAL ACTIVATOR THAT IS FUNCTIONALLY DISTINCT FROM THAT OF HERPES-SIMPLEX VIRUS HOMOLOG ICP27 SO JOURNAL OF VIROLOGY LA English DT Article ID IMMEDIATE-EARLY PROTEIN; LONG TERMINAL REPEAT; BETA-INTERFERON GENE; TRANS-ACTING FACTOR; REGULATORY PROTEIN; MAMMALIAN-CELLS; MESSENGER-RNA; DNA-BINDING; MACROMOLECULAR-SYNTHESIS; VIRAL POLYPEPTIDES AB Varicella-zoster virus is the etiological agent of chickenpox and tester in humans and belongs to the Alphaherpesvirinae subfamily within the family Herpesviridae. Much of the current understanding of gene regulation in alphaherpesviruses has been derived from studies of the prototype herpes simplex virus (HSV). In HSV, two virus-encoded, trans-regulatory proteins, ICP4 and ICP27, are essential for the replicative cycle of the virus. ICP4 is important in modulating HSV genes of all three kinetic classes, whereas the trans-regulatory effects of ICP27 are primarily associated with the expression of late genes. Recent evidence indicates that the trans-regulatory effects of ICP27 involve posttranscriptional processing of target gene transcripts (R. M. Sandri-Golding and G. E. Mendoza, Genes Dev. 6:848-863, 1992). The ICP27 homolog in varicella-zoster virus is a 452-amino-acid polypeptide encoded by the open reading frame 4 (ORF4) gene. Contrary to what is found with ICP27, we show that the ORF4 polypeptide is a transcriptional activator of diverse target promoters and has a critical requirement for the presence of upstream elements within these promoters to mediate its transcriptional effects. Evidence is also presented to implicate a critical role for the cysteine-rich, C-terminal region of the ORF4 polypeptide in its trans-regulatory functions. Specifically, by oligonucleotide-directed site-specific mutagenesis, we demonstrate that of 10 cysteine residues in the ORF4 polypeptide, only C-421 and C-426 are essential for transactivator function and suggest that these cysteine residues may participate in critical protein-protein interactions rather than protein-nucleic acid interactions to mediate ORF4 inducibility. C1 HENRY M JACKSON FDN,RETROVIRUS RES LAB,ROCKVILLE,MD 20850. UNIV PITTSBURGH,SCH MED,DEPT OPHTHALMOL,PITTSBURGH,PA 15213. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205. RP PERERA, LP (reprint author), NIAID,CLIN INVEST LAB,MED VIROL SECT,BLDG 10,RM 11N228,BETHESDA,MD 20892, USA. NR 60 TC 67 Z9 67 U1 2 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2468 EP 2477 PG 10 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700048 PM 8139031 ER PT J AU FREED, EO MARTIN, MA AF FREED, EO MARTIN, MA TI EVIDENCE FOR A FUNCTIONAL INTERACTION BETWEEN THE V1/V2 AND C4 DOMAINS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEIN GP120 SO JOURNAL OF VIROLOGY LA English DT Article ID PRINCIPAL NEUTRALIZING DETERMINANT; HTLV-III/LAV ENVELOPE; GENOMIC DIVERSITY; GENETIC-VARIATION; RECEPTOR-BINDING; FUSION DOMAIN; CD4 RECEPTOR; AIDS VIRUS; T-CELLS; IDENTIFICATION AB The domains of the human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein that are required for envelope function have been partially characterized. Little is known, however, about the nature of the interactions between these domains. To identify regions of the HIV-1 envelope glycoprotein that are involved in interactions necessary for proper envelope function, we constructed a series of 14 envelope recombinants between the env genes of two HIV-1 isolates. The envelope chimeras were examined for their ability to induce syncytia, to be proteolytically processed, and to function during a spreading viral infection. Our results demonstrate that the exchange between the two isolates of the first and second hypervariable regions (V1/V2) of gp120 results in defects in envelope glycoprotein processing, syncytium formation, and infectivity. Long-term passage of cultures infected with virus bearing a V1/V2 chimeric envelope glycoprotein leads to the emergence of a revertant virus with replication characteristics comparable to those of the wild type. Analysis of the revertant indicated that an Ile-->Met change in the C4 region of gp120 (between hypervariable regions V4 and V5) is responsible for the revertant phenotype. This single amino acid change restores infectivity without significantly affecting gp160 processing, CD4 binding, or the levels of virion-associated gp120. While the Ile-->Met change in C4 greatly enhances the fusogenic potential of the V1/V2 chimeric envelope glycoprotein, it has a detrimental effect on syncytium formation when analyzed in the context of the wild-type envelope. These results suggest that an interaction required for proper envelope glycoprotein function occurs between the V1/V2 and C4 regions of gp120. RP FREED, EO (reprint author), NIAID,MOLEC MICROBIOL LAB,BLDG 4,RM 307,BETHESDA,MD 20892, USA. NR 55 TC 112 Z9 112 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2503 EP 2512 PG 10 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700052 PM 8139032 ER PT J AU KABAT, D KOZAK, SL WEHRLY, K CHESEBRO, B AF KABAT, D KOZAK, SL WEHRLY, K CHESEBRO, B TI DIFFERENCES IN CD4 DEPENDENCE FOR INFECTIVITY OF LABORATORY-ADAPTED AND PRIMARY PATIENT ISOLATES OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO JOURNAL OF VIROLOGY LA English DT Article ID HERPES-SIMPLEX VIRUS; SOLUBLE CD4; ENVELOPE GLYCOPROTEIN; T-CELLS; CD4-MEDIATED FUSION; BINDING-AFFINITY; PLASMA-MEMBRANE; HIV-1 VIRIONS; SCD4 BINDING; HTLV-III AB CD4 is known to be an important receptor for human immunodeficiency virus type 1 (HIV-1) infection of T lymphocytes and macrophages. However, the limiting steps in CD4-dependent HIV-1 infections in vivo and in vitro are poorly understood. To address this issue, we produced a panel of HeLa-CD4 cell clones that express widely different amounts of CD4 and quantitatively analyzed their infection by laboratory-adapted and primary patient HIV-1 isolates. For all HIV-1 isolates, adsorption from the medium onto HeLa-CD4 cells was inefficient and appeared to be limiting for infection in the conditions of our assays. Adsorption of HIV-1 onto CD4-positive peripheral blood mononuclear cells was also inefficient. Moreover, there was a striking difference between laboratory-adapted and primary T-cell-tropic HIV-1 isolates in the infectivity titers detected on different HeLa-CD4 cells. Laboratory-adapted HIV-1 isolates infected all HeLa-CD4 cell clones with equal efficiencies regardless of the levels of CD4, whereas primary HIV-1 isolates infected these clones in direct proportion to cellular CD4 expression. Our interpretation is that for laboratory-adapted isolates, a barrier step that preceeds CD4 encounter was limiting and the subsequent CD4-dependent virus capture process was highly efficient, even at very low cell surface concentrations. In contrast, for primary HIV-1 isolates, the CD4-dependent steps appeared to be much less efficient. We conclude that primary isolates of HIV-1 infect inefficiently following contact with surfaces of CD4-positive cells, and we propose that this confers a selective disadvantage during passage in rapidly dividing leukemia cell lines. Conversely, in vivo selective pressure appears to favor HIV-1 strains that require large amounts of CD4 for infection. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. RP KABAT, D (reprint author), OREGON HLTH SCI UNIV,DEPT BIOCHEM & MOLEC BIOL L224,PORTLAND,OR 97201, USA. FU NCI NIH HHS [CA25810]; NIAID NIH HHS [AI28572] NR 54 TC 130 Z9 130 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2570 EP 2577 PG 8 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700058 PM 8139036 ER PT J AU BISWAS, P POLI, G ORENSTEIN, JM FAUCI, AS AF BISWAS, P POLI, G ORENSTEIN, JM FAUCI, AS TI CYTOKINE-MEDIATED INDUCTION OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) EXPRESSION AND CELL-DEATH IN CHRONICALLY INFECTED U1 CELLS - DO TUMOR-NECROSIS-FACTOR-ALPHA AND GAMMA-INTERFERON SELECTIVELY KILL HIV-INFECTED CELLS SO JOURNAL OF VIROLOGY LA English DT Article ID NF-KAPPA-B; MONOCLONAL-ANTIBODY; REPLICATION; PROTEIN; BINDING; FAS; MECHANISMS; ACTIVATION; CYTOLYSIS; RECEPTOR AB Infection with several DNA or RNA viruses induces a state of increased sensitivity to cell lysis mediated by tumor necrosis factor (TNF), particularly id the presence of gamma interferon (IFN-gamma). Infection of human cells with the human immunodeficiency virus (HIV) may induce a similar phenomenon. However, TNF and IFN-gamma are known upregulators of HIV replication, raising the question of the potential role of these cytokines in the selective elimination of cells infected with this virus. The present study demonstrates that chronically infected U1 cells were killed with much greater efficiency by costimulation with TNF-alpha and IFN-gamma than their uninfected parental cell line U937. However, synergistic induction of viral expression also occurred in U1 cells as a consequence of treatment with the two cytokines. Cell death in U1 cells was not caused by the massive production of virions, in that costimulation with glucocorticoid hormones and TNF-alpha or IFN-gamma resulted in high levels of virion production without cytopathicity. To investigate the nature of the selective cytotoxic effect observed in U1 cells costimulated with TNF-alpha plus IFN-gamma, a panel of uninfected cell clones was generated by limiting dilution of U937 cells and tested for response to TNF-alpha and/or IFN-gamma. In contrast to the uncloned bulk parental U937 cell line, most uninfected cell clones showed a very high susceptibility to being killed by TNF-alpha and IFN-gamma. Similar findings were obtained when both infected U1 cells and several uninfected U937 cell clones were costimulated with an anti-Fas monoclonal antibody in the presence of IFN-gamma, although, unlike cells stimulated with TNF-alpha, cells treated with anti-Fas antibody did not express virus. Therefore, the increased susceptibility to cytokine-mediated lysis observed in cell lines infected with HIV is likely due to the selection of preexisting cell clones rather than viral infection. C1 GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20037. RP BISWAS, P (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10A,ROOM 6A33,9000 ROCKVILLE PIKE,ROCKVILLE,MD 20892, USA. NR 28 TC 45 Z9 45 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2598 EP 2604 PG 7 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700061 PM 7511175 ER PT J AU HIRSCH, VM MARTIN, JE DAPOLITO, G ELKINS, WR LONDON, WT GOLDSTEIN, S JOHNSON, PR AF HIRSCH, VM MARTIN, JE DAPOLITO, G ELKINS, WR LONDON, WT GOLDSTEIN, S JOHNSON, PR TI SPONTANEOUS SUBSTITUTIONS IN THE VICINITY OF THE V3 ANALOG AFFECT CELL TROPISM AND PATHOGENICITY OF SIMIAN IMMUNODEFICIENCY VIRUS SO JOURNAL OF VIROLOGY LA English DT Article ID PRINCIPAL NEUTRALIZATION DETERMINANT; MACROPHAGE TROPISM; T-CELL; ENVELOPE GENE; TYPE-1 INVIVO; PRODUCTIVE INFECTION; VIRAL DETERMINANTS; RHESUS-MONKEYS; HTLV-III/LAV; HIV-1 AB Simian immunodeficiency virus (SIV) exists within tissues of infected macaques as a mixture of diverse genotypes. The goal of this study was to investigate the biologic significance of this variation in terms of cellular tropism and pathogenicity. PCR was used to amplify and clone 3'-half genomes from the spleen of an immunodeficient SIV-infected pig-tailed macaque (Macaca nemestrina). Eight infectious clones were generated by ligation of respective 3' clones into a related SIVsm 5' clone, and virus stocks were generated by transient transfection. Four of these viruses were infectious for macaque peripheral blood mononuclear cells (PBMC) or monocyte-derived macrophages (MDM). Three viruses with distinct tropism for macaque PBMC or MDM were tested for in vivo infectivity and pathogenicity. The ability of these three viruses to infect PBMC and macrophages correlated with differences in infectivity and pathogenicity. Thus, a virus that was infectious for both PBMC and MDM was highly infectious for macaques and induced AIDS in half of the inoculated animals. In contrast, virus that was less infectious for PBMC and not infectious for MDM induced only transient viremia. Finally, a virus that was not infectious for either primary cell type did not infect macaques. Chimeric clones exchanging portions of the envelope gene of the 62A and smH4 molecular clones and a series of point mutants were used to map the determinant of tropism to a 60-amino-acid region of gp120 encompassing the V3 analog of SIV. Naturally occurring mutations within this region were critical for determining tropism and, as a result, pathogenicity of these SIVsm clones. C1 GEORGETOWN UNIV,DEPT MICROBIOL,DIV MOLEC VIROL & IMMUNOL,ROCKVILLE,MD 20852. OHIO STATE UNIV,CHILDRENS HOSP RES FDN,DEPT PEDIAT,COLUMBUS,OH 43205. RP HIRSCH, VM (reprint author), NIAID,IMMUNODEFICIENCY VIRUSES SECT,INFECT DIS LAB,TWINBROOK FACIL,ROCKVILLE,MD 20852, USA. RI Johnson, Philip/A-6892-2009 NR 55 TC 41 Z9 41 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2649 EP 2661 PG 13 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700066 PM 8139042 ER PT J AU BUONAGURO, L BUONAGURO, FM GIRALDO, G ENSOLI, B AF BUONAGURO, L BUONAGURO, FM GIRALDO, G ENSOLI, B TI THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TAT PROTEIN TRANSACTIVATES TUMOR-NECROSIS-FACTOR BETA-GENE EXPRESSION THROUGH A TAR-LIKE STRUCTURE SO JOURNAL OF VIROLOGY LA English DT Article ID LONG TERMINAL REPEAT; TRANS-ACTIVATOR GENE; III HTLV-III; NF-KAPPA-B; CELLULAR PROTEINS; KAPOSIS-SARCOMA; LOOP SEQUENCE; HIV-1; RNA; PROMOTER AB We have previously shown that the Tat protein of human immunodeficiency virus type 1 (HIV-1) transactivates tumor necrosis factor alpha and beta (TNF alpha and TNF beta) gene expression in HIV-1-infected and in tat-transfected T-lymphocytic and monocytic cell lines. The product encoded by the first exon of the tat gene (amino acids 1 to 72) is sufficient for this transactivation. Here we show that (i) the NF-kappa B and Sp1 binding sites of the TNF beta promoter are required for Tat-mediated transactivation and (ii) a predicted stem-loop structure in the TNF beta mRNA leader region, which resembles the Tat-responsive element of the HIV-1 long terminal repeat (TAR) and which is therefore termed TAR-like, is essential for TNFP transactivation by Tat. These data suggest that similar promoter regulatory elements are necessary for Tat-mediated transactivation of both TNF beta and HIV-1 gene expression. This represents the first demonstration of a cellular gene with a regulatory element downstream of the transcriptional initiation site that, like TAR, may function as an RNA element. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. INST NAZL TUMORI FDN G PASCALE,DIV VIRAL ONCOL,I-80131 NAPLES,ITALY. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 43 TC 89 Z9 89 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2677 EP 2682 PG 6 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700069 PM 8139045 ER PT J AU KORALNIK, IJ BOERI, E SAXINGER, WC LOMONICO, A FULLEN, J GESSAIN, A GUO, HG GALLO, RC MARKHAM, P KALYANARAMAN, V HIRSCH, V ALLAN, J MURTHY, K ALFORD, P SLATTERY, JP OBRIEN, SJ FRANCHINI, G AF KORALNIK, IJ BOERI, E SAXINGER, WC LOMONICO, A FULLEN, J GESSAIN, A GUO, HG GALLO, RC MARKHAM, P KALYANARAMAN, V HIRSCH, V ALLAN, J MURTHY, K ALFORD, P SLATTERY, JP OBRIEN, SJ FRANCHINI, G TI PHYLOGENETIC ASSOCIATIONS OF HUMAN AND SIMIAN T-CELL LEUKEMIA/LYMPHOTROPIC VIRUS TYPE-I STRAINS - EVIDENCE FOR INTERSPECIES TRANSMISSION SO JOURNAL OF VIROLOGY LA English DT Article ID NON-HUMAN PRIMATES; PAPUA-NEW-GUINEA; TROPICAL SPASTIC PARAPARESIS; LEUKEMIA-LYMPHOMA VIRUS; HTLV-I; NUCLEOTIDE-SEQUENCES; MAXIMUM-LIKELIHOOD; SERUM ANTIBODIES; JAPANESE MONKEYS; SOLOMON-ISLANDS AB Homologous env sequences from 17 human T-leukemia/lymphotropic virus type I (HTLV-I) strains from throughout the world and from 25 simian T-leukemia/lymphotropic virus type I (STLV-I) strains from 12 simian species in Asia and Africa were analyzed in a phylogenetic context as an approach to resolving the natural history of these related retroviruses. STLV-I exhibited greater overall sequence variation between strains (1 to 18% compared with 0 to 9% for HTLV-I), supporting the simian origin of the modern viruses in all species. Three HTLV-I phylogenetic clusters or clades (cosmopolitan, Zaire, and Melanesia) were resolved with phenetic, parsimony, and likelihood analytical procedures. Seven phylogenetic clusters of STLV-I were resolved with the most primitive (deeply rooted) divergence involving several STLV-I strains from Asian primate species. Combined analysis of HTLV-I and STLV-I revealed that neither STLV-I clusters nor HTLV-I clusters recapitulated host species specificity; rather, multiple clades from the same species were closer to clades from other species than to each other. We interpret these evolutionary associations as support for the occurrence of multiple discrete interspecies transmissions of ancestral viruses, between primate species (including human) that led to recognizable phylogenetic clades that persist in modern species. Geographic concordance of divergent host species that harbor closely related viruses reinforces that physical feasibility for hypothesized interspecies virus transmission in the past and in the present. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD 20895. NIAID TWINBROOK,INFECT DIS LAB,ROCKVILLE,MD 20852. SW FDN BIOMED RES,SAN ANTONIO,TX 78228. UNIV TEXAS,MD ANDERSON CANC CTR,BASTROP,TX 78602. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RI Alford, Patricia/B-5559-2013 OI Alford, Patricia/0000-0003-2677-893X NR 62 TC 149 Z9 149 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1994 VL 68 IS 4 BP 2693 EP 2707 PG 15 WC Virology SC Virology GA NA307 UT WOS:A1994NA30700071 PM 7908063 ER PT J AU BACHER, JD BALIS, FM MCCULLY, CL GODWIN, KS AF BACHER, JD BALIS, FM MCCULLY, CL GODWIN, KS TI CEREBRAL SUBARACHNOID SAMPLING OF CEREBROSPINAL-FLUID IN THE RHESUS-MONKEY SO LABORATORY ANIMAL SCIENCE LA English DT Article ID CENTRAL NERVOUS-SYSTEM; PRIMATE MODEL; DRUGS; METHOTREXATE AB A previously described rhesus monkey model with two intraventricular catheter systems was expanded to provide a means of studying drug concentrations of chemotherapeutic agents such as methotrexate (MTX) in the cerebral subarachnoid cerebrospinal fluid (CSF) following intrathecal drug injection. A continuous intraventricular infusion of MTX was started through the lateral ventricular catheter 44 h before surgical placement of the cerebral subarachnoid catheter to allow for steady-state concentrations to be attained throughout the subarachnoid space. Monkeys were anesthetized intramuscularly with ketamine hydrochloride (7 mg/kg) and xylazine (6 mg/kg) to allow placement of a temporary lumbar catheter for sampling of lumbar CSF Sodium thiopental (2.5%) was given intravenously if needed for intubation and anesthesia was maintained with isoflurane (0.5 to 1.5%) and oxygen during the surgical placement and sampling of the cerebral subarachnoid catheter. A midline incision was made over the frontal bone and a 3/8-inch trephine was used to expose the dura adjacent to the lateral midline. Following puncture of the dura with an 18-gauge spinal needle, the cerebral subarachnoid catheter (0.025-inch [i.d.] x 0.047-inch [o.d] Silastic(R) tube) was passed into the subarachnoid space for approximately 10 to 17 mm. The CSF from the cerebral subarachnoid catheter was collected by gravity flow Ventricular, lumbar subarachnoid, and cerebral subarachnoid CSF were collected concurrently at 44, 46, and 48 h after the start of MTX infusion. Mean ventricular lumbar subarachnoid, and cerebral subarachnoid CSF methotrexate concentrations at steady state were 5.8, 1.0, and 1.5 mu mol/L, respectively. The animal model described demonstrates a successful means of studying drug concentrations of various drugs such as MTX throughout the CSF space during continuous intraventricular infusions. C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. RP BACHER, JD (reprint author), NIH,CTR RES RESOURCES,VET RESOURCES PROGRAM NATL,BLDG 14E,ROOM 119A,BETHESDA,MD 20892, USA. NR 9 TC 12 Z9 12 U1 1 U2 1 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI CORDOVA PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018 SN 0023-6764 J9 LAB ANIM SCI JI Lab. Anim. Sci. PD APR PY 1994 VL 44 IS 2 BP 148 EP 152 PG 5 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA NJ936 UT WOS:A1994NJ93600010 PM 8028278 ER PT J AU WEYANT, RS BURRIS, JA NICHOLS, DK WOO, E KINSEY, VS BOWER, DE BUKOWSKI, MM WEAVER, RE MOORE, TD AF WEYANT, RS BURRIS, JA NICHOLS, DK WOO, E KINSEY, VS BOWER, DE BUKOWSKI, MM WEAVER, RE MOORE, TD TI EPIZOOTIC FELINE PNEUMONIA ASSOCIATED WITH CENTERS-FOR-DISEASE-CONTROL GROUP EF-4A BACTERIA SO LABORATORY ANIMAL SCIENCE LA English DT Article ID BITE WOUNDS; PROTEINS; FLORA; DOG C1 NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,SCI SERV BRANCH,LAB SCI SECT,BETHESDA,MD 20892. SMITHSONIAN INST,NATL ZOOL PK,DEPT PATHOL,WASHINGTON,DC 20001. RP WEYANT, RS (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV BACTERIAL & MYCOT DIS,ATLANTA,GA 30333, USA. NR 22 TC 5 Z9 5 U1 0 U2 1 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI CORDOVA PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018 SN 0023-6764 J9 LAB ANIM SCI JI Lab. Anim. Sci. PD APR PY 1994 VL 44 IS 2 BP 180 EP 183 PG 4 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA NJ936 UT WOS:A1994NJ93600017 PM 8028284 ER PT J AU OVERBY, LH GARDLIK, S PHILPOT, RM SERABJITSINGH, CJ AF OVERBY, LH GARDLIK, S PHILPOT, RM SERABJITSINGH, CJ TI UNIQUE DISTRIBUTION PROFILES OF GLUTATHIONE S-TRANSFERASES IN REGIONS OF KIDNEY, URETER, AND BLADDER OF RABBIT SO LABORATORY INVESTIGATION LA English DT Article DE ALPHA-CLASS GST; PROSTAGLANDIN; PGE(2); PGD(2); PI-CLASS GST ID ARACHIDONIC-ACID METABOLISM; CORTICAL COLLECTING TUBULE; RENAL CORTEX; PROSTAGLANDINS; PURIFICATION; LOCALIZATION; ISOENZYMES; ENZYMES; LIVER; RAT AB BACKGROUND: Glutathione S-transferases detoxify a broad range of exogenous compounds, but are important also in the metabolism of endogenous compounds. Physiologically relevant substrates are the endoperoxide and hydroperoxide metabolites of arachidonic acid that play important roles in many tissues including the kidney. EXPERIMENTAL DESIGN: We used immunohistochemical and immunoblotting techniques in a systematic study of renal localization of four rabbit enzymes that represent three major mammalian cytosolic glutathione S-transferase classes, alpha, pi, and mu. RESULTS: The two alpha-class enzymes (rbGST alpha I, rbGST alpha II) were distributed discretely in kidney, ureter, and bladder, while pi and mu were widely distributed in the renal system. Immunohistochemical localization in paraffin sections with antibodies specific for rbGST alpha I or rbGST alpha II demonstrated that no compartment of the renal system contained both enzymes. Collecting ducts of the inner medulla and all epithelial cells of the kidney pelvis, ureter, and bladder contained rbGST alpha I. All cells lining proximal tubules contained rbGST alpha II. No other compartment of the renal system exhibited immunoreactivity with anti-rbGST alpha II. Antibody specific for pi reacted with cells lining nephrons, ureter, and bladder and with endothelial cells throughout the renal system. Localization of pi was most prominent in the collecting ducts of medulla and in the epithelial cells lining the kidney pelvis, ureter, and bladder. As anti-mu did not react in tissue sections, distribution of mu was determined by immunoblotting. Immunoblots of cytosolic preparations from whole kidney, cortex, medulla, and epithelia of ureter, bladder, and kidney pelvis were prepared and tested with each of the 4 antibodies. This second localization method confirmed the distribution data from tissue sections for rbGST alpha I, rb GST alpha II, and pi; also, it demonstrated that the staining observed in tissue was specifically for each enzyme. mu was detected in all the renal cytosolic preparations except those from the epithelium of the kidney pelvis. CONCLUSIONS: The discrete renal distribution of rbGST alpha I and rbGST alpha II and their distinct catalytic activities with prostaglandin substrates suggest important roles for these enzymes in prostaglandin-dependent renal functions. C1 GLAXO INC,RES INST,DEPT DRUG METAB,RES TRIANGLE PK,NC 27709. NIEHS,CELLULAR & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. NR 32 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD APR PY 1994 VL 70 IS 4 BP 468 EP 478 PG 11 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA NK099 UT WOS:A1994NK09900005 PM 8176887 ER PT J AU FUJIO, K EVARTS, RP HU, ZY MARSDEN, ER THORGEIRSSON, SS AF FUJIO, K EVARTS, RP HU, ZY MARSDEN, ER THORGEIRSSON, SS TI EXPRESSION OF STEM-CELL FACTOR AND ITS RECEPTOR, C-KIT, DURING LIVER-REGENERATION FROM PUTATIVE STEM-CELLS IN ADULT-RAT SO LABORATORY INVESTIGATION LA English DT Article DE 2-ACETYLAMINOFLUORENE; OVAL CELLS; IN SITU HYBRIDIZATION ID GROWTH-FACTOR; EPITHELIAL-CELLS; OVAL CELLS; HEPATIC DIFFERENTIATION; ALPHA-FETOPROTEIN; MOUSE DEVELOPMENT; TYROSINE KINASE; PROTEIN-KINASE; MESSENGER-RNA; SI-LOCUS AB BACKGROUND: Stem cell factor (SCF) and its receptor, c-kit, are known to play important. roles in hematopoiesis, melanogenesis, and gametogenesis. The biologic effects of the SCF/c-kit system are believed to involve survival, proliferation, and migration of early stem cell progeny. Although SCF and c-kit receptor are widely expressed during normal embryonic development, their expression in the adult is limited. EXPERIMENTAL DESIGN: The expression of SCF and c-Kit genes was examined during liver regeneration via the oval cell compartment utilizing partial hepatectomy (PH) combined with the administration of a noncarcinogenic dose of a-acetylaminofluorene (AAF) for 8 days (AAF/PH model). RESULTS: Both the ligand and the receptor genes were expressed during the early stages of oval cell proliferation after partial hepatectomy in the AAF/PH model, while neither simple partial hepatectomy nor AAF administration alone induced a noticeable expression of the SCF/c-kit system. The level of SCF mRNA increased within 12 hours after partial hepatectomy and reached a peak around day 4. Thus, the expression of SCF preceded the major expansion of the oval cell compartment. The level of c-kit transcripts gradually increased from the 12-hour time point and stayed elevated until day 11, when a large proportion of the oval cells differentiated into small basophilic hepatocytes. Separation of liver cells at day 3 in the AAF/PH model into parenchymal and nonparenchymal fractions demonstrated that the expression of both SCF and c-kit receptor genes was restricted to the nonparenchymal cells. Furthermore, in situ hybridization revealed that the c-kit transcripts were restricted to oval cells, whereas the SCF transcripts were expressed in both oval cells and Ito cells. CONCLUSIONS: The transcripts for the c-kit receptor are expressed in the early progeny of the hepatic stem cells. The SCF/c-kit system may, possibly in combination with other growth factor/receptor systems, be involved in the early activation of the hepatic stem cells as well as in the expansion and differentiation of oval cells. C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 51 TC 242 Z9 257 U1 0 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD APR PY 1994 VL 70 IS 4 BP 511 EP 516 PG 6 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA NK099 UT WOS:A1994NK09900009 PM 7513770 ER PT J AU HENDERSON, E SEAMANS, JR SOLOMON, D AF HENDERSON, E SEAMANS, JR SOLOMON, D TI ELECTRONIC CAPTURE AND CONVERSION OF MICROSCOPY IMAGES FROM CYTOLOGIC GLASS SLIDES SO LABORATORY MEDICINE LA English DT Article RP HENDERSON, E (reprint author), NATL LIB MED,LISTER HILL NATL CTR BIOMED COMMUN,BLDG 38A,ROOM 7N711,860 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLIN PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON ST, CHICAGO, IL 60612 SN 0007-5027 J9 LAB MED JI Lab. Med. PD APR PY 1994 VL 25 IS 4 BP 262 EP 263 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA NC616 UT WOS:A1994NC61600022 ER PT J AU BIBEN, M BERNHARDS, D AF BIBEN, M BERNHARDS, D TI NAIVE RECOGNITION OF CHUCK CALLS IN SQUIRREL-MONKEYS (SAIMIRI-SCIUREUS-MACRODON) SO LANGUAGE & COMMUNICATION LA English DT Article ID VOCAL BEHAVIOR; DISCRIMINATION; INDIVIDUALITY RP BIBEN, M (reprint author), NIH,BLDG 112,ROOM 205,BETHESDA,MD 20892, USA. NR 28 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0271-5309 J9 LANG COMMUN JI Lang. Commun. PD APR PY 1994 VL 14 IS 2 BP 167 EP 181 DI 10.1016/0271-5309(94)90011-6 PG 15 WC Communication; Linguistics SC Communication; Linguistics GA NF483 UT WOS:A1994NF48300003 ER PT J AU SCHLAIFER, D COOPER, MR ATTAL, M ROUSSEAU, A PRIS, J LAURENT, G MYERS, CE AF SCHLAIFER, D COOPER, MR ATTAL, M ROUSSEAU, A PRIS, J LAURENT, G MYERS, CE TI POTENTIAL STRATEGIES FOR CIRCUMVENTING MYELOPEROXIDASE-CATALYZED DEGRADATION OF VINCA ALKALOIDS SO LEUKEMIA LA English DT Note ID D-PENICILLAMINE; INHIBITION; MECHANISM; METABOLISM; NAVELBINE AB Myeloperoxidase (MPO) has recently been shown in an in vitro, cell-free system to catalyze the peroxidative degradation of vincristine (VCR). Oxidation of VCR involves a ring fission between positions 20' and 21', and is thought to be facilitated by the presence of an hydroxyl (-OH) group at position 20'. We report here two different approaches, both with potential clinical application, to decrease MPO-catalyzed vinca degradation. Firstly, we tested the hypothesis that -OH substitution at position 20' increases vinca susceptibility to peroxidation by comparing the relative extent of degradation of vinorelbine (Navelbine or NVB), which lacks a 20' hydroxyl substitution, with that of VCR. As anticipated, NVB was significantly less susceptible to MPO-catalyzed peroxidation than was VCR (p < 0.01). Secondly, we screened an array of compounds that are in current clinical use for their ability to inhibit MPO. Acetaminophen, N-acetylcysteine, propylthiouracil, D-penicillamine, mefenamic acid, dapsone, and methimazole all inhibited MPO at clinically achievable concentrations. Insofar as increased MPO activity has been observed in patients with acute myeloid leukemia, these findings suggest potential strategies for improving the activity of vinca alkaloids in this disease. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. RP SCHLAIFER, D (reprint author), HOP PURPAN,CTR HOSP REG,DIEULAFOY CLIN,DEPT HAEMATOL,PL DOCTEUR BAYLAC,F-31059 TOULOUSE,FRANCE. NR 22 TC 10 Z9 10 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 1994 VL 8 IS 4 BP 668 EP 671 PG 4 WC Oncology; Hematology SC Oncology; Hematology GA NJ517 UT WOS:A1994NJ51700022 PM 8152263 ER PT J AU BRODER, S MILLER, RW HINO, S BLATTNER, WA YOSHIDA, M ROSENBLATT, J BRADY, J FRANCHINI, G TAJIMA, K MUELLER, N TAKATSUKI, K WALDMANN, T WATANABE, T MIYOSHI, I POIESZ, B SUGAMURA, K SONODA, S JACOBSON, S BENVENISTE, R YANAGIHARA, R GALLO, R AF BRODER, S MILLER, RW HINO, S BLATTNER, WA YOSHIDA, M ROSENBLATT, J BRADY, J FRANCHINI, G TAJIMA, K MUELLER, N TAKATSUKI, K WALDMANN, T WATANABE, T MIYOSHI, I POIESZ, B SUGAMURA, K SONODA, S JACOBSON, S BENVENISTE, R YANAGIHARA, R GALLO, R TI RETROVIRUSES AND CANCER - US-JAPAN CLINICO-EPIDEMIOLOGIC EXPERIENCES HELD UNDER THE AUSPICES OF THE US-JAPAN BILATERAL AGREEMENT SO LEUKEMIA LA English DT Editorial Material C1 NCI,DEPT HLTH & HUMAN SERV,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. TOTTORI UNIV,YONAGO,TOTTORI,JAPAN. UNIV TOKYO,TOKYO,JAPAN. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. AICHI CANC CTR,RES INST,NAGOYA,JAPAN. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. KUMAMOTO UNIV,SCH MED,KUMAMOTO 860,JAPAN. KOCHI MED SCH,KOCHI,JAPAN. SUNY HLTH SCI CTR,SYRACUSE,NY 13210. TOHOKU UNIV,SENDAI,MIYAGI 982,JAPAN. KAGOSHIMA UNIV,KAGOSHIMA 890,JAPAN. NINCDS,BETHESDA,MD 20892. NCI,FREDERICK,MD 21701. NR 1 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 1994 VL 8 IS 4 BP 694 EP 704 PG 11 WC Oncology; Hematology SC Oncology; Hematology GA NJ517 UT WOS:A1994NJ51700027 ER PT J AU WELLES, SL LEVINE, PH JOSEPH, EM GOBERDHAN, LJ LEE, S MIOTTI, A CERVANTES, J BERTONI, M JAFFE, E DOSIK, H AF WELLES, SL LEVINE, PH JOSEPH, EM GOBERDHAN, LJ LEE, S MIOTTI, A CERVANTES, J BERTONI, M JAFFE, E DOSIK, H TI AN ENHANCED SURVEILLANCE PROGRAM FOR ADULT T-CELL LEUKEMIA IN CENTRAL BROOKLYN SO LEUKEMIA LA English DT Article; Proceedings Paper CT XVI Symposium of the International-Association-for-Comparative-Research-on-Leukemia-and-Relat ed-Diseases CY JUL 11-16, 1993 CL MONTREAL, CANADA SP INT ASSOC COMPARAT RES LEUKEMIA & RELATED DIS ID VIRUS TYPE-I; HTLV-I; CHILD TRANSMISSION; UNITED-STATES; LYMPHOMA; ANTIBODY; JAMAICA; RISK AB The Brooklyn Adult T-cell Leukemia/Lymphoma (ATL) study was developed to estimate the incidence of the human T-cell lymphotropic vines type I (HTLV-I)-associated ATL in the Crown Heights/Bedford Stuyvesant community. This central Brooklyn black community is an area which has already been shown in earlier reports to be endemic for HTLV-I-associated ATL. Surveillance has been conducted at seven area hospitals that serve this community, with surveillance already completed at five hospitals. Potential study subjects who are 20 years or older are identified by the review of admission records, discharge summaries, pathology and clinical chemistry reports, or physician referrals. Diagnoses of leukemia or lymphoma, or the presence of leukocytosis or hypercalcemia are used as criteria to identify the subjects. Participating subjects give a sample of blood for the determination of HTLV-V-I infection by serologic tests. At the time of enrollment, subjects provide demographic information including age, sex and birthplace. After one year of surveillance at five hospitals (39.5% of inpatient beds in the catchment), we have identified 12 cases of HTLV-I-associated ATL. The mean age of the ATL patients was 50 years, with patients being predominantly female (83.3%) and often Caribbean immigrants (83.3%). Interestingly, 42% of our cases were identified solely by findings of hypercalcemia from clinical chemistry reports. The remaining ATL cases were identified by physician referral. This enhanced surveillance program that uses both clinical and laboratory criteria for ATL case ascertainment can serve as a prototype for similar surveillance in other areas endemic for HTLV-I-associated ATL-an important effort because of the strong potential for disease prevention. C1 NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. INTERFAITH MED CTR,DEPT MED,BROOKLYN,NY. BROOKDALE HOSP,BROOKLYN,NY. BROOKLYN HOSP,BROOKLYN,NY. ST MARYS HOSP,BROOKLYN,NY. WYCKOFF HOSP,BROOKLYN,NY. RP WELLES, SL (reprint author), HARVARD UNIV,SCH PUBL HLTH,CTR STAT & DATA ANAL,DEPT BIOSTAT,ACTG,BOSTON,MA 02115, USA. NR 21 TC 1 Z9 1 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 1994 VL 8 SU 1 BP S111 EP S115 PG 5 WC Oncology; Hematology SC Oncology; Hematology GA NK665 UT WOS:A1994NK66500026 PM 8152275 ER PT J AU WILLIAMS, CKO DADA, A BLATTNER, WA AF WILLIAMS, CKO DADA, A BLATTNER, WA TI SOME EPIDEMIOLOGIC FEATURES OF THE HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I (HTLV-I) AND ATL IN NIGERIANS SO LEUKEMIA LA English DT Article; Proceedings Paper CT XVI Symposium of the International-Association-for-Comparative-Research-on-Leukemia-and-Relat ed-Diseases CY JUL 11-16, 1993 CL MONTREAL, CANADA SP INT ASSOC COMPARAT RES LEUKEMIA & RELATED DIS ID LEUKEMIA-LYMPHOMA; GUAYMI INDIANS; INFECTION; PANAMA AB With a seroprevalence rate (SPR) of 6%-10% among healthy adult blood donors (ABD), Nigeria and other African locales represent an endemic zone for HTLV-I. We studied SPR in patients with leukaemia, lymphomas, solid tumours, and chronic disorders, as well as in groups of men and women with varying sexual lifestyles. Serum specimens were screened with ELISA and then confirmed with Western blot (WB). Sexual practices were investigated among volunteers of different sexual backgrounds by means of a questionnaire. Female prostitutes (FP) (13.0%) and patients with sexually transmitted diseases (STDP) (16.7%) had the highest SPR while a low rate occurred in religious celibate males (RCM) but not in religious celibate females (RCF) (11.8%). Heterosexual activity as well as geographical location of the place of birth constituted the most important risk factors for HTLV-I. HIV antibodies were demonstrable in none of the study subjects. ATL was associated with 100% SPR (4/4) while SPR in other clinical states were not different from normal. Western blot profile was rarely of strong poly band hut more frequently of weak oligo band pattern with absent or weak pig compared to p24. Only 18% of non Hodgkin's lymphoma in Ibadan, Nigeria was seropositive compared to 50% and > 60% in Japanese and Caribbean endemic zones respectively. The high SPR and aberrant WB profiles indicate reactivity to HTLV-I and to an HTLV-II-like activity, probably a new virus in the region. Excluding the aberrant WB profile. SPR based on HTLV-I-related profile was 3.8%-4.8% in ABD, 13% in FP, 10% in STDP. 1.9% in RCM. O% in RCF, and 25% in ATL patients. The HTLV-II-related profile showed no such heterosexual association, but occurred in 75% of ATL patients. HTLV-I and probably and an HTLV-II-like virus appear to play a role in STD and lymphoma epidemiology in Nigeria. C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. RP WILLIAMS, CKO (reprint author), SASKATCHEWAN CANC FDN,ALLAN BLAIR MEM CLIN,4101 DEWDNEY AVE,REGINA S4T 7T1,SK,CANADA. FU NCI NIH HHS [N01 CP 51030] NR 12 TC 4 Z9 4 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 1994 VL 8 SU 1 BP S77 EP S82 PG 6 WC Oncology; Hematology SC Oncology; Hematology GA NK665 UT WOS:A1994NK66500018 PM 8152310 ER PT J AU WRIGHT, ND AF WRIGHT, ND TI STEALING INTO PRINT - FRAUD, PLAGIARISM, AND MISCONDUCT IN SCIENTIFIC PUBLISHING - LAFOLLETTE,MC SO LIBRARY QUARTERLY LA English DT Book Review RP WRIGHT, ND (reprint author), NATL LIB MED,DIV BIBLIOG SERV,BETHESDA,MD 20209, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0024-2519 J9 LIBR QUART JI Libr. Q. PD APR PY 1994 VL 64 IS 2 BP 221 EP 223 PG 3 WC Information Science & Library Science SC Information Science & Library Science GA NE853 UT WOS:A1994NE85300019 ER PT J AU FISK, B IOANNIDES, CG AGGARWAL, S WHARTON, JT OBRIAN, CA RESTIFO, N GLISSON, BS AF FISK, B IOANNIDES, CG AGGARWAL, S WHARTON, JT OBRIAN, CA RESTIFO, N GLISSON, BS TI ENHANCED EXPRESSION OF HLA-A,B,C AND INDUCIBILITY OF TAP-1, TAP-2, AND HLA-A,B,C BY INTERFERON-GAMMA IN A MULTIDRUG-RESISTANT SMALL-CELL LUNG-CANCER LINE SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-II REGION; DOSE MELPHALAN THERAPY; ANTIGENIC PHENOTYPE; CARCINOMA-CELLS; MOPC-315 TUMOR; GENE; PEPTIDE; TRANSPORTERS; FIBROBLAST AB Recent evidence suggests that deficient HLA Class I expression in SCLC lines may be due, in part, to down-regulation of TAP-1 and TAP-2 expression, and, thus, deficient antigen processing. Given the capability of the multidrug transporter mediating MDR, P-gp, to transport peptides, we hypothesized that P-gp may substitute for TAP-1/TAP-2 and enhance antigen processing in SCLC. To investigate this, we studied the H69 line (parent SCLC) and VPR-2 (MDR subline selected in etoposide, P-gp +). HLA-A,B,C expression was significantly increased in VPR-2 cells relative to H69, and was much more inducible with IFN-gamma. TAP-1 and TAP-2 were expressed at low levels in both lines. Differential induction of TAP-1 expression with IFN-gamma exposure was observed, with a dramatic increase in VPR-2 cells, and no change in H69. TAP-2 expression was enhanced in both lines with IFN-gamma, but to a greater degree in VPR-2. VPR-2 cells were resistant to LAK killing relative to H69, and were minimally sensitized with IFN-gamma. In contrast, IFN-gamma enhanced susceptibility of H69 to LAK killing 3-fold. The direct correlation between enhancement of HLA-A,B,C expression by IFN-gamma and the differential inducibility of TAP-1 and TAP-2 expression in P-gp-SCLC lines is novel. Relative LAK sensitivity of H69 and its increase by IFN-gamma may have clinical implications. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT GYNECOL ONCOL,HOUSTON,TX 77030. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT CELL BIOL & THORAC MED,HOUSTON,TX 77030. NCI,DIV CANC TREATMENT,SURG BRANCH,BETHESDA,MD 20892. RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z99 CA999999, Z01 BC010763-01]; NCI NIH HHS [CA16672, CA52460, CA57293] NR 36 TC 16 Z9 16 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0277-6766 J9 LYMPHOKINE CYTOK RES JI Lymphokine Cytokine Res. PD APR PY 1994 VL 13 IS 2 BP 125 EP 131 PG 7 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA NL491 UT WOS:A1994NL49100010 PM 8061113 ER PT J AU KOPPSCHNEIDER, A PORTIER, CJ AF KOPPSCHNEIDER, A PORTIER, CJ TI A STEM-CELL MODEL FOR CARCINOGENESIS SO MATHEMATICAL BIOSCIENCES LA English DT Article ID ENZYME-ALTERED FOCI; QUANTITATIVE-ANALYSIS; MULTISTAGE MODEL; DNA DAMAGE; CANCER; BIRTH; REPAIR; RATES; SKIN AB A modification to the well-known two-stage model of carcinogenesis with clonal expansion is proposed. A true stem cell is applied to the production of intermediate cells by incorporating a birth-death process with a reflecting barrier into the model. The distribution of the number of detectable intermediate cell clones is derived, and systems of differential equations are formulated for the cumulative distribution function for the appearance of malignant tumors. The model is applied to data on papilloma formation in a mouse skin painting experiment. Tests for the importance of intermediate cells in tumor incidence can be derived. C1 NIEHS,DIV BIOMETRY & RISK ASSESSMENT,RES TRIANGLE PK,NC 27709. RP KOPPSCHNEIDER, A (reprint author), DEUTSCH KREBSFORSCHUNGSZENTRUM,BIOSTAT ABT,D-69009 HEIDELBERG,GERMANY. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 25 TC 11 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0025-5564 J9 MATH BIOSCI JI Math. Biosci. PD APR PY 1994 VL 120 IS 2 BP 211 EP 232 DI 10.1016/0025-5564(94)90053-1 PG 22 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA NN423 UT WOS:A1994NN42300005 PM 8204985 ER PT J AU BURGESON, RE CHIQUET, M DEUTZMANN, R EKBLOM, P ENGEL, J KLEINMAN, H MARTIN, GR MENEGUZZI, G PAULSSON, M SANES, J TIMPL, R TRYGGVASON, K YAMADA, Y YURCHENCO, PD AF BURGESON, RE CHIQUET, M DEUTZMANN, R EKBLOM, P ENGEL, J KLEINMAN, H MARTIN, GR MENEGUZZI, G PAULSSON, M SANES, J TIMPL, R TRYGGVASON, K YAMADA, Y YURCHENCO, PD TI A NEW NOMENCLATURE FOR THE LAMININS SO MATRIX BIOLOGY LA English DT Note DE LAMININ; NOMENCLATURE AB The authors have adopted a new nomenclature for the laminins. They are numbered with arabic numeral in the order discovered. The previous A, B1 and B2 chains, and their isoforms, are alpha, beta and gamma and respectively, followed by an arabic numeral to identify the isoform. For example, the first laminin identified from the Engelbreth-Holm-Swarm tumor is laminin-1 with the chain composition alpha 1 beta 1 gamma 1.. The genes for these chains are LAMA1, LAMB1 and LAMC1, respectively. C1 MAX PLANCK INST BIOCHEM,D-82152 MARTINSRIED,GERMANY. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. UNIV BASEL,BIOCTR,CH-4056 BASEL,SWITZERLAND. UNIV REGENSBURG,DEPT BIOCHEM MICROBIOL & GENET,W-8400 REGENSBURG,GERMANY. UNIV UPPSALA,DEPT ANIM PHYSIOL,UPPSALA,SWEDEN. NIDR,BETHESDA,MD 20892. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. UNIV NICE,RECH DERMATOL LAB,NICE,FRANCE. UNIV BERN,ME MULLER INST BIOMECH,BERN,SWITZERLAND. WASHINGTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,ST LOUIS,MO 63110. UNIV OULU,BIOCTR OULU,OULU,FINLAND. UNIV OULU,DEPT BIOCHEM,OULU,FINLAND. ROBERT WOOD JOHNSON MED SCH,DEPT PATHOL,PISCATAWAY,NJ. NR 1 TC 690 Z9 696 U1 2 U2 12 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0945-053X J9 MATRIX BIOL JI Matrix Biol. PD APR PY 1994 VL 14 IS 3 BP 209 EP 211 DI 10.1016/0945-053X(94)90184-8 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NK840 UT WOS:A1994NK84000002 PM 7921537 ER PT J AU DIRKSEN, ML MORASSO, MI SARGENT, TD JAMRICH, M AF DIRKSEN, ML MORASSO, MI SARGENT, TD JAMRICH, M TI DIFFERENTIAL EXPRESSION OF A DISTAL-LESS HOMEOBOX GENE XDLL-2 IN ECTODERMAL CELL LINEAGES SO MECHANISMS OF DEVELOPMENT LA English DT Article DE ACTIVIN; DISTAL-LESS; EPIDERMIS; NEURAL INDUCTION; SKIN; XENOPUS ID MESODERM-INDUCING FACTOR; DNA-BINDING DOMAIN; XENOPUS-LAEVIS; DEVELOPING FOREBRAIN; RESTRICTED EXPRESSION; PROSPECTIVE AREAS; LIMB DEVELOPMENT; ACTIVIN-A; EMBRYOS; HOMEODOMAIN AB Neural induction in Xenopus requires the activation of new sets of genes that are necessary for cellular and regional specification of the neural tube. It has been reported earlier that members of the Distal-less homeobox gene family are specifically activated in distinct regions of the central nervous system (CNS) of Xenopus embryos (Dirksen et al., 1993; Papalopulu and Kintner, 1993). In this paper we describe in detail a-Xenopus homeobox containing gene Xdll-2, which belongs to the Distal-less gene Family. In contrast to other previously described Xenopus family members, Xdll-2 Is expressed in the embryonic ectoderm and is specifically repressed in the CNS. This repression can be mimicked in isolated animal caps by treatment with activin. Expression of Xdll-2 persists in the epidermis and some neural crest cells. Because of its spatial and temporal expression pattern this gene is a good candidate to have a regulatory function in the initial formation of the epidermis. Its high level of expression in adult skin indicates that its Function is continuously required in this tissue. C1 US FDA,CBER,DIV CELLULAR & GENE THERAPY,DEV BIOL LAB,ROCKVILLE,MD 20852. NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. NR 60 TC 53 Z9 54 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4773 J9 MECH DEVELOP JI Mech. Dev. PD APR PY 1994 VL 46 IS 1 BP 63 EP 70 DI 10.1016/0925-4773(94)90038-8 PG 8 WC Developmental Biology SC Developmental Biology GA NP827 UT WOS:A1994NP82700006 PM 7915132 ER PT J AU KASLOW, DC NUSSENZWEIG, V MILLER, L AF KASLOW, DC NUSSENZWEIG, V MILLER, L TI MEETING ON PARASITES AND THE INVERTEBRATE VECTOR - JOHN-D-AND-CATHERINE-T-MACARTHUR-FOUNDATION, NOVEMBER 18-21, 1993 SO MEMORIAS DO INSTITUTO OSWALDO CRUZ LA English DT Editorial Material C1 NYU,MED CTR,DEPT PATHOL,NEW YORK,NY 10016. RP KASLOW, DC (reprint author), NIAID,MALARIA RES LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU MEM INST OSWALDO CRUZ PI RIO DE JANEIRO PA SECRETARY CAIXA POSTAL 926, 20001 RIO DE JANEIRO, RJ, BRAZIL SN 0074-0276 J9 MEM I OSWALDO CRUZ JI Mem. Inst. Oswaldo Cruz PD APR-JUN PY 1994 VL 89 IS 2 BP 279 EP 295 PG 17 WC Parasitology; Tropical Medicine SC Parasitology; Tropical Medicine GA PQ398 UT WOS:A1994PQ39800031 PM 7885258 ER PT J AU ZURLO, F NEMETH, PM CHOKSI, RM SESODIA, S RAVUSSIN, E AF ZURLO, F NEMETH, PM CHOKSI, RM SESODIA, S RAVUSSIN, E TI WHOLE-BODY ENERGY-METABOLISM AND SKELETAL-MUSCLE BIOCHEMICAL CHARACTERISTICS SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID WEIGHT-GAIN; FIBER TYPE; EXPENDITURE; OBESITY; FAT; CARBOHYDRATE; EXERCISE; FOREARM; RATIO; RISK C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. WASHINGTON UNIV,SCH MED,DEPT NEUROL,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,ST LOUIS,MO 63110. FU NIDDK NIH HHS [DK-38375] NR 35 TC 68 Z9 70 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD APR PY 1994 VL 43 IS 4 BP 481 EP 486 DI 10.1016/0026-0495(94)90081-7 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NE553 UT WOS:A1994NE55300016 PM 8159108 ER PT J AU HENSLER, PJ ANNAB, LA BARRETT, JC PEREIRASMITH, OM AF HENSLER, PJ ANNAB, LA BARRETT, JC PEREIRASMITH, OM TI A GENE INVOLVED IN CONTROL OF HUMAN CELLULAR SENESCENCE ON HUMAN CHROMOSOME-1Q SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HUMAN-CELLS; INDEFINITE DIVISION; SUPPRESSOR ACTIVITY; LIFE-SPAN; HYBRIDS; FIBROBLASTS; LINE; IDENTIFICATION; HETEROZYGOSITY; EXPRESSION AB Normal cells in culture exhibit limited division potential and have been used as a model for cellular senescence. In contrast, tumor-derived or carcinogen- or virus-transformed cells are capable of indefinite division. Fusion of normal human diploid fibroblasts with immortal human cells yielded hybrids having limited life spans, indicating that cellular senescence was dominant. Fusions of various immortal human cell lines with each other led to the identification of four complementation groups for indefinite division. The purpose of this study was to determine whether human chromosome 1 could complement the recessive immortal defect of human cell lines assigned to one of the four complementation groups. Using microcell fusion, we introduced a single normal human chromosome 1 into immortal human cell lines representing the complementation groups and determined that it caused loss of proliferative potential of an osteosarcoma-derived cell line (TE85), a cytomegalovirus-transformed lung fibroblast cell line (CMV-Mj-HEL-1), and a Ki-ras+-transformed derivative of TE85 (143B TK-), all of which were assigned to complementation group C. This chromosome 1 caused no change in proliferative potential of cell lines representing the other complementation groups. A derivative of human chromosome 1 that had lost most of the q arm by spontaneous deletion was unable to induce senescence in any of the immortal cell lines. This finding indicates that the q arm of human chromosome 1 carries a gene or set of genes which is altered in the cell lines assigned to complementation group C and is involved in the control of cellular senescence. C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. BAYLOR COLL MED,ROY M & PHYLLIS GOUGH HUFFINGTON CTR AGING,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. RP HENSLER, PJ (reprint author), BAYLOR COLL MED,DIV MOLEC VIROL,T-236,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. FU NIA NIH HHS [T32 AGO0183, R37-AG05333] NR 33 TC 110 Z9 111 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1994 VL 14 IS 4 BP 2291 EP 2297 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NC057 UT WOS:A1994NC05700007 PM 8139534 ER PT J AU ZHAN, QM LORD, KA ALAMO, I HOLLANDER, MC CARRIER, F RON, D KOHN, KW HOFFMAN, B LIEBERMANN, DA FORNACE, AJ AF ZHAN, QM LORD, KA ALAMO, I HOLLANDER, MC CARRIER, F RON, D KOHN, KW HOFFMAN, B LIEBERMANN, DA FORNACE, AJ TI THE GADD AND MYD GENES DEFINE A NOVEL SET OF MAMMALIAN GENES ENCODING ACIDIC PROTEINS THAT SYNERGISTICALLY SUPPRESS CELL-GROWTH SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID IMMEDIATE EARLY RESPONSE; MYELOID-LEUKEMIA CELLS; TERMINAL DIFFERENTIATION; MESSENGER-RNA; EXPRESSION; P53; DNA; ARREST; FIBROBLASTS; SEQUENCE AB A remarkable overlap was observed between the gadd genes, a group of often coordinately expressed genes that are induced by genotoxic stress and certain other growth arrest signals, and the MyD genes, a set of myeloid differentiation primary response genes. The MyD116 gene was found to be the murine homolog of the hamster gadd34 gene, whereas MyD118 and gadd45 were found to represent two separate but closely related genes. Furthermore, gadd34/MyD116, gadd45, MyD118, and gadd153 encode acidic proteins with very similar and unusual charge characteristics; both this property and a similar pattern of induction are shared with mdm2, which, like gadd45, has been shown previously to be regulated by the tumor suppressor p53. Expression analysis revealed that they are distinguished from other growth arrest genes in that they are DNA damage inducible and suggests a role for these genes in growth arrest and apoptosis either coupled with or uncoupled from terminal differentiation. Evidence is also presented for coordinate induction in vivo by stress. The use of a short-term transfection assay, in which expression vectors for one or a combination of these gadd/MyD genes were transfected with a selectable marker into several different human tumor cell lines, provided direct evidence for the growth-inhibitory functions of the products of these genes and their ability to synergistically suppress growth. Taken together, these observations indicate that these genes define a novel class of mammalian genes encoding acidic proteins involved in the control of cellular growth. C1 NCI,DCT,DTP,MOLEC PHARMACOL LAB,RM 5C09,BLDG 37,BETHESDA,MD 20892. TEMPLE UNIV,HLTH SCI CTR,SCH MED,FELS INST CANC RES & MOLEC BIOL,PHILADELPHIA,PA 19140. NYU MED CTR,DEPT MED & CELL BIOL,NEW YORK,NY 10016. RI Carrier, France/C-3063-2008; Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 49 TC 450 Z9 464 U1 0 U2 10 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1994 VL 14 IS 4 BP 2361 EP 2371 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NC057 UT WOS:A1994NC05700015 PM 8139541 ER PT J AU GRANT, CM MILLER, PF HINNEBUSCH, AG AF GRANT, CM MILLER, PF HINNEBUSCH, AG TI REQUIREMENTS FOR INTERCISTRONIC DISTANCE AND LEVEL OF EUKARYOTIC INITIATION FACTOR-II ACTIVITY IN REINITIATION ON GCN4 MESSENGER-RNA VARY WITH THE DOWNSTREAM CISTRON SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID OPEN READING FRAMES; UPSTREAM AUG CODONS; SARCOMA VIRUS-RNA; TRANSLATIONAL CONTROL; SACCHAROMYCES-CEREVISIAE; FACTOR-II; PROTEIN-SYNTHESIS; GENE-EXPRESSION; ALPHA-SUBUNIT; SEQUENCE AB Translational control of the GCN4 gene in response to amino acid availability is mediated by four short open reading frames in the GCN4 mRNA leader (uORFs) and by phosphorylation of eukaryotic initiation factor 2 (eIF-2). We have proposed that reducing eIF-2 activity by phosphorylation of its alpha subunit or by a mutation in the eIF-2 recycling factor eIF-2B allows ribosomes which have translated the 5'-proximal uOPF1 to bypass uORF2 to uORF4 and reinitiate at GCN4 instead. In this report, we present two lines of evidence that all ribosomes which synthesize GCN4 have previously translated uORF1, resumed scanning, and reinitiated at the GCN4 start site. First, GCN4 expression was abolished when uORF1 was elongated to make it overlap the beginning of the GCN4 coding region. Second, GCN4 expression was reduced as uORF1 was moved progressively closer to GCN4, decreasing to only 5% of the level seen in the absence of all uORFs when only 32 nucleotides separated uORF1 from GCN4. We additionally found that inserting small synthetic uORFs between uORF4 and GCN4 inhibited GCN4 expression under derepressing conditions, confirming the idea that reinitiation at GCN4 under conditions of diminished eIF-2 activity is proportional to the distance of the reinitiation site downstream from uORF1. While uORF4 and GCN4 appear to be equally effective at capturing ribosomes scanning downstream from the 5' cap of mRNA, these two ORFs differ greatly in their ability to capture reinitiating ribosomes scanning from uORF1. When the active form of eIF-2 is present at high levels, reinitiation appears to be much more efficient at uORF4 than at GCN4 when each is located very close to uORF1. Under conditions of reduced recycling of eIF-2, reinitiation at uORF4 is substantially suppressed, which allows ribosomes to reach the GCN4 start site; in contrast, reinitiation at GCN4 in constructs lacking uORF4 is unaffected by decreasing the level of eIF-2 activity. This last finding raises the possibility that time-dependent binding to ribosomes of a second factor besides the eIF-2-GTP-Met-tRNA(i)Met ternary complex is rate limiting for reinitiation at GCN4. Moreover, our results show that the efficiency of translational reinitiation can be strongly influenced by the nature of the downstream cistron as well as the intercistronic distance. C1 NICHHD,MOLEC GENET LAB,MOLEC GENET LOWER EUKARYOTES SECT,BLDG 6B,ROOM 309,BETHESDA,MD 20892. NR 38 TC 61 Z9 62 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1994 VL 14 IS 4 BP 2616 EP 2628 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NC057 UT WOS:A1994NC05700041 PM 8139562 ER PT J AU BLANC, A RIBAS, JC WICKNER, RB SONENBERG, N AF BLANC, A RIBAS, JC WICKNER, RB SONENBERG, N TI HIS-154 IS INVOLVED IN THE LINKAGE OF THE SACCHAROMYCES-CEREVISIAE L-A DOUBLE-STRANDED-RNA VIRUS GAG PROTEIN TO THE CAP STRUCTURE OF MESSENGER-RNAS AND IS ESSENTIAL FOR M(1) SATELLITE VIRUS EXPRESSION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HELA NUCLEAR EXTRACT; YEAST KILLER TOXIN; POL FUSION PROTEIN; BINDING-PROTEINS; SPLICING INVITRO; CYTO-PATHOLOGY; COAT PROTEIN; REPLICATION; INITIATION; POLYMERASE AB The coat protein (Gag) of the double-stranded RNA virus L-A was previously shown to form a covalent bond with the cap structure of eukaryotic mRNAs. Here, we identify the linkage as a phosphoroimidazole bond between the alpha phosphate of the cap structure and a nitrogen in the Gag protein His-154 imidazole side chain. Mutations of His-154 abrogate the ability of Gag to bind to the cap structure, without affecting cap recognition, in vivo virus particle formation from an L-A cDNA clone, or in vitro specific binding and replication of plus-stranded single-stranded RNA. However, genetic analyses demonstrate that His-154 is essential for M1 satellite virus expression. C1 MCGILL UNIV,DEPT BIOCHEM,MCINTYRE MED BLDG,3655 DRUMMOND ST,ROOM 807,MONTREAL H3G 1Y6,QUEBEC,CANADA. MCGILL UNIV,MCGILL CANC CTR,MONTREAL H3G 1Y6,QUEBEC,CANADA. NIDDKD,BIOCHEM PHARMACOL LAB,GENET SIMPLE EUKARYOTES SECT,BETHESDA,MD 20892. RI Ribas, Juan/C-9864-2015 OI Ribas, Juan/0000-0001-6430-0895 NR 64 TC 35 Z9 36 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1994 VL 14 IS 4 BP 2664 EP 2674 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NC057 UT WOS:A1994NC05700045 PM 8139566 ER PT J AU CLEGG, CH KOEIMAN, NR JENKINS, NA GILBERT, DJ COPELAND, NG NEUBAUER, MG AF CLEGG, CH KOEIMAN, NR JENKINS, NA GILBERT, DJ COPELAND, NG NEUBAUER, MG TI STRUCTURAL FEATURES OF THE MURINE GENE ENCODING THE RI-BETA SUBUNIT OF CAMP-DEPENDENT PROTEIN-KINASE SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID I REGULATORY SUBUNIT; TRANSCRIPTION FACTOR AP-2; DNA-BINDING; RETINOIC ACID; POU-DOMAIN; RESPONSE ELEMENTS; OSTEOCALCIN GENE; THYROID-HORMONE; NERVOUS-SYSTEM; OVALBUMIN GENE AB The activation of cyclic AMP-dependent protein kinase is controlled by the regulatory (R) subunits of the holoenzyme. Here we present a characterization of the mouse RI beta subunit gene, which in contrast to other subunit genes of cyclic AMP-dependent protein kinase is expressed almost exclusively in neurons. It was determined that RI beta is relatively large with 11 exons spanning a minimum 75 kb. The mouse chromosomal locus (designated Prkar1b) was determined by interspecific backcross mapping and found to reside on the distal arm of chromosome 5. Previously, it was shown that 3.5 kb of DNA encompassing the RI beta promoter could direct neural-specific gene expression in transgenic mice. Analysis of this DNA suggests the presence of an unusually large number of binding sites for transcription factors ranging from tissue-specific regulators, immediate-early genes, and mediators of hormone action. In addition to 18 putative SP1 sites, we identified 27 consensus sequences for basic Helix-Loop-Helix, POU, and Pax family members, 5 AP1 sites, and over 40 half-sites for the superfamily of steroid hormone receptor. Gel mobility-shift assays employing brain nuclear extract and pure transcription factor protein established that many of these DNA sequences are functional in binding protein. The abundance and configuration of transcription factor binding sites within the promoter region of RI beta suggests that this gene is subject to complex modes of regulation in neurons. (C) 1994 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP CLEGG, CH (reprint author), BRISTOL MYERS SQUIBB PHARMACEUT RES INST,3005 1ST AVE,SEATTLE,WA 98121, USA. FU NCI NIH HHS [N01-CO-74101] NR 66 TC 13 Z9 13 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell Neurosci. PD APR PY 1994 VL 5 IS 2 BP 153 EP 164 DI 10.1006/mcne.1994.1017 PG 12 WC Neurosciences SC Neurosciences & Neurology GA NE714 UT WOS:A1994NE71400007 PM 8032683 ER PT J AU BAUMGARTNER, RA OZAWA, K CUNHAMELO, JR YAMADA, K GUSOVSKY, F BEAVEN, MA AF BAUMGARTNER, RA OZAWA, K CUNHAMELO, JR YAMADA, K GUSOVSKY, F BEAVEN, MA TI STUDIES WITH TRANSFECTED AND PERMEABILIZED RBL-2H3 CELLS REVEAL UNIQUE INHIBITORY PROPERTIES OF PROTEIN-KINASE C-GAMMA SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article ID BASOPHILIC LEUKEMIA-CELLS; HISTAMINE-RELEASE; TYROSINE PHOSPHORYLATION; HIGH-AFFINITY; 2H3 CELLS; SYNERGISTIC ACTION; CALCIUM SIGNAL; MAST-CELLS; RAT-BRAIN; IGE AB To characterize protein kinase C (PKC)gamma, an isozyme found exclusively in brain and spinal cord, its cDNA was introduced into basophilic RBL-2H3 cells that lack this isozyme. The expression of PKC gamma significantly attenuated antigen-induced responses including hydrolysis of inositol phospholipids, increase in cytosolic calcium, and secretion of granules but enhanced antigen-induced release of arachidonic acid. Instead of a sustained increase in cytosolic calcium, antigen now induced calcium oscillations; possibly as a consequence of suppression of phospholipase C activity and incomplete emptying of internal calcium stores. In addition, PKC gamma appeared to inhibit activation of other PKC isozymes because phorbol 12-myristate 13-acetate failed to act synergistically with the Ca2+ ionophore on secretion. This was confirmed in other studies where PKC gamma was shown to suppress the transduction of stimulatory signals by other isozymes of PKC on provision of these isozymes to PKC-depleted permeabilized cells. The studies in total indicated that only PKC gamma was capable of inhibiting both early and distal signals for secretion including those signals transduced by endogenous isozymes of PKC. C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RP BAUMGARTNER, RA (reprint author), NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892, USA. RI Cunha-Melo, Jose Renan/C-6262-2013 NR 38 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD APR PY 1994 VL 5 IS 4 BP 475 EP 484 PG 10 WC Cell Biology SC Cell Biology GA NL247 UT WOS:A1994NL24700008 PM 8054687 ER PT J AU PERANTONI, AO TURUSOV, VS BUZARD, GS RICE, JM AF PERANTONI, AO TURUSOV, VS BUZARD, GS RICE, JM TI INFREQUENT TRANSFORMING MUTATIONS IN THE TRANSMEMBRANE DOMAIN OF THE NEU ONCOGENE IN SPONTANEOUS RAT SCHWANNOMAS SO MOLECULAR CARCINOGENESIS LA English DT Article DE ALKYLATING AGENT; NEU ONCOGENE; SCHWANNOMA; TRANSPLACENTAL CARCINOGENESIS ID GROWTH-FACTOR RECEPTOR; HUMAN-BREAST-CANCER; TYROSINE KINASE-ACTIVITY; ETHYL-N-NITROSOUREA; C-ERBB-2 ONCOPROTEIN; POINT MUTATION; PROGNOSTIC-SIGNIFICANCE; NERVOUS-SYSTEM; DNA; ACTIVATION AB Ethylnitrosourea (ENU) given transplacentally to rats induces schwannomas of the cranial, spinal, and peripheral nerves, with a high frequency of mutations in the neu proto-oncogene. To establish the requirement for such mutations in tumorigenesis of the Schwann cell, spontaneous schwannomas from BD-Vl rats were evaluated for transforming mutations in the transmembrane domain of the protein encoded by the neu protooncogene. While all five schwannomas induced transplacentally with ENU were shown to contain T-->A transversions in base 2012 of neu by selective oligonucleotide hybridization and dideoxy sequencing of polymerase chain reaction-amplified products from paraffin sections, only one of nine spontaneous schwannomas from untreated rats had the same mutation. Examination of tumors for mutations in codon 12 of Ki-ras revealed normal alleles. Therefore, the high frequency of mutations in neu in ENU-induced tumors may be directly attributable to the carcinogen or to the period of development at which exposure occurred, and transforming mutations of the transmembrane domain of neu are not required for tumorigenesis of the Schwann Cell. (C) 1994 Wiley-Liss, Inc.* C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21701. INT AGCY RES CANC,LYON,FRANCE. RP PERANTONI, AO (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21701, USA. NR 40 TC 8 Z9 8 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD APR PY 1994 VL 9 IS 4 BP 230 EP 235 DI 10.1002/mc.2940090407 PG 6 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA NH471 UT WOS:A1994NH47100006 PM 7908527 ER PT J AU KOSUGI, S KOHN, LD AKAMIZU, T MORI, T AF KOSUGI, S KOHN, LD AKAMIZU, T MORI, T TI THE MIDDLE PORTION IN THE 2ND CYTOPLASMIC LOOP OF THE THYROTROPIN RECEPTOR PLAYS A CRUCIAL ROLE IN ADENYLATE-CYCLASE ACTIVATION SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID FRTL-5 THYROID-CELLS; SITE-DIRECTED MUTAGENESIS; ADRENERGIC-RECEPTORS; PERTUSSIS TOXIN; TSH RECEPTOR; CYCLIC-AMP; PHOSPHOLIPASE-C; LIGAND-BINDING; IODIDE EFFLUX; STIMULATION AB We have examined the role of the 2nd cytoplasmic loop of the TSH receptor (TSHR) in TSH- and TSHR autoantibody-stimulated cAMP and inositol phosphate formation using mutants created by substituting sequences from the alpha(1)- or beta(2)-adrenergic receptors (AR). Unlike similar substitution mutants involving the 3rd cytoplasmic loop that lose agonist-induced inositol phosphate but not cAMP increase after transfection into Cos-7 cells, mutants involving the 2nd loop showed significant change in generating both signals. Mutant B525, which substitutes residues 525-527 with a comparable beta(2)-AR sequence, exhibited a complete loss in TSH- or Graves' immunoglobulin G-increased cAMP signaling and a lesser loss in phosphoinositide signaling. This is a unique mutant in which cAMP response was completely lost in all those involving the 2nd or 3rd cytoplasmic loop. On the other hand, mutant B528, in which residues 528-532 are substituted with a comparable beta(2)-AR sequence, exhibited the most profound loss in phosphoinositide signaling. Mutants involving portions surrounding residues 528-532 in the 2nd cytoplasmic loop had milder losses in agonist-increased phosphoinositide signaling and much lesser losses in agonist-increased cAMP generation. The transfection efficiency of all transfectants was the same. All transfectants with mutant or wild type TSHR had a similar amount and identical profile of TSHR mRNA in Northern blots and TSHR forms on Western blots. Thus, the 2nd cytoplasmic loop is important for agonist-induced cAMP as well as for phosphoinositide signal generation, whereas the 3rd loop appears to be important only for the latter. The most important determinant for agonist-increased cAMP signal generation is in the middle of the 2nd loop, around residues 525-527. In contrast, the determinants most critical for agonist-induced phosphoinositide signaling are also located in the middle of the 2nd loop, around residues 528-532, and those with less importance are broadly distributed. C1 NIDDKD, BIOCHEM & METAB LAB, CELL REGULAT SECT, BETHESDA, MD 20892 USA. RP KOSUGI, S (reprint author), KYOTO UNIV, SCH MED,DEPT LAB MED,SAKYO KU,CLIN RES BLDG 1, ROOM 223, 54-KAWAHARA-CHO, KYOTO 60601, JAPAN. NR 52 TC 34 Z9 36 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD APR PY 1994 VL 8 IS 4 BP 498 EP 509 DI 10.1210/me.8.4.498 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NG033 UT WOS:A1994NG03300011 PM 7914349 ER PT J AU VASILE, S COLIGAN, JE YOSHIDA, M SEON, BK AF VASILE, S COLIGAN, JE YOSHIDA, M SEON, BK TI ISOLATION AND CHEMICAL CHARACTERIZATION OF THE HUMAN B29 AND MB-1 PROTEINS OF THE B-CELL ANTIGEN RECEPTOR COMPLEX SO MOLECULAR IMMUNOLOGY LA English DT Article DE B29 PROTEIN; MB-1 PROTEIN; B CELLS; ANTIGEN RECEPTOR COMPLEX; BETA-TUBULIN ID MONOCLONAL-ANTIBODY; LYMPHOCYTE-B; T-CELL; TYROSINE PHOSPHORYLATION; MOLECULAR-COMPONENTS; IGM; IMMUNOGLOBULIN; GENE; STIMULATION; EXPRESSION AB A disulfide-linked heterodimeric antigen from human B leukemia cells was detected by radioimmunoprecipitation and Western blot analysis using a monoclonal antibody (mAb). The mAb was generated against a cell membrane antigen preparation from human B prolymphocytic leukemia cells and found to define an extracellular epitope of the smaller component (beta chain) of a heterodimeric antigen on human B leukemia cells. The antigen from BALL-I, a human B leukemia cell line, and fresh (uncultured) B prolymphocytic leukemia cells was found to consist of a 44-49 kDa (alpha chain) and a 36-40 kDa (beta chain) component. An additional minor component of 34 kDa was detected in the reduced antigen from BALL-1. For chemical identification of the antigen, we isolated the antigen from a Triton X-100 lysate of BALL-I by immunoaffinity chromatography using the mAb. Determination of the amino-terminal amino acid sequences of the alpha and beta chains unequivocally identified them as the human mb-1 and B29 proteins, respectively. The sequence analyses indicate the molecular heterogeneity of the mb-1 protein and also perhaps the heterogeneity of the B29 protein. We detected three forms of the mb-1 protein which share an identical amino-terminal amino acid sequence and probably two forms of the B29 protein which share an identical amino-terminal sequence. Our sequence data allowed us to establish the authentic amino-terminal amino acid sequence of the human B29 protein which is different from those proposed by others based on cDNA sequence analyses. Comparison of the amino-terminal sequences of the human mb-1 and B29 proteins with those of the mouse mb-1 and B29 proteins showed that the majority of the conserved amino acids in the mb-1 proteins are hydrophobic amino acids. Such conservation of hydrophobic amino acids is not observed in the amino termini of the human and mouse B29 proteins. A beta-tubulin-like protein was found to be co-purified with the mb-1-B29 antigen in the present study. In addition, we found that there is a strong amino acid sequence homology between the microtubule-binding domains of certain human microtubule-associated proteins and an intracellular segment of the human mb-1 protein. C1 ROSWELL PK CANC INST,DEPT MOLEC IMMUNOL,BUFFALO,NY 14263. NIAID,MOLEC STRUCT LAB,BETHESDA,MD 20892. NR 34 TC 19 Z9 21 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD APR PY 1994 VL 31 IS 6 BP 419 EP 427 DI 10.1016/0161-5890(94)90061-2 PG 9 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA NK030 UT WOS:A1994NK03000002 PM 7514267 ER PT J AU PETERSEN, RB GOLDFARB, LG TABATON, M BROWN, P MONARI, L CORTELLI, P MONTAGNA, P AUTILIOGAMBETTI, L GAJDUSEK, DC LUGARESI, E GAMBETTI, P AF PETERSEN, RB GOLDFARB, LG TABATON, M BROWN, P MONARI, L CORTELLI, P MONTAGNA, P AUTILIOGAMBETTI, L GAJDUSEK, DC LUGARESI, E GAMBETTI, P TI A NOVEL MECHANISM OF PHENOTYPIC HETEROGENEITY DEMONSTRATED BY THE EFFECT OF A POLYMORPHISM ON A PATHOGENIC MUTATION IN THE PRNP (PRION PROTEIN GENE) SO MOLECULAR NEUROBIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Transmissible and Nontransmissible Neurodegenerative Disorders CY FEB 28-MAR 05, 1993 CL OCHO RIOS, JAMAICA SP INT BRAIN RES ORG, UNIV GOTEBORG, UNIV WEST INDIES DE FATAL FAMILIAL INSOMNIA; CREUTZFELDT-JAKOB DISEASE; DEMENTIA; PRNP; MUTATION; POLYMORPHISM; PHENOTYPE; PRION ID FATAL FAMILIAL INSOMNIA; CREUTZFELDT-JAKOB DISEASE; CODON-178; DELETIONS AB Fatal familial insomnia (FFI) is a subacute dementing illness originally described in 1986. The phenotypic characteristics of this disease include progressive untreatable insomnia, dysautonomia, endocrine and motor disorders, preferential hypometabolism in the thalamus as determined by PET scanning, and selective thalamic atrophy. These characteristics readily distinguish FFI from other previously described neurodegenerative conditions. Recently, FFI was shown to be linked to a mutation in the prion protein gene (PRNP) at codon 178, which results in the substitution of asparagine for aspartic acid. As such, FFI represents the most recent addition to the growing family of prion protein-related diseases. The mutation that results in FFI had previously been linked to a subtype of familial Creutzfeld-Jakob disease (178(Asn) CJD). The genotypic basis for the difference between FFI and 178(Asn)CJD lies in a polymorphism at codon 129 of the mutant prion protein gene: 129(Met) 178(Asn) results in FFI, 129(Val) 178(Asn) in CJD, The finding that the combination of a polymorphism and a single pathogenic mutation result in two distinct conditions represents a significant advance in our understanding of phenotypic variability. C1 NIH,BETHESDA,MD 20892. UNIV BOLOGNA,INST NEUROL,BOLOGNA,ITALY. RP PETERSEN, RB (reprint author), CASE WESTERN RESERVE UNIV,INST PATHOL,2085 ADELBERT RD,CLEVELAND,OH 44106, USA. RI Petersen, Robert/B-5075-2011; OI Petersen, Robert/0000-0002-3154-0072; Cortelli, Pietro/0000-0002-3633-8818 FU NIA NIH HHS [1RO1 AGNS08155-02, AG-08992-02] NR 15 TC 8 Z9 8 U1 3 U2 3 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD APR-JUN PY 1994 VL 8 IS 2-3 BP 99 EP 103 DI 10.1007/BF02780659 PG 5 WC Neurosciences SC Neurosciences & Neurology GA PD120 UT WOS:A1994PD12000004 PM 7999319 ER PT J AU PRIOLA, SA CAUGHEY, B AF PRIOLA, SA CAUGHEY, B TI INHIBITION OF SCRAPIE-ASSOCIATED PRP ACCUMULATION - PROBING THE ROLE OF GLYCOSAMINOGLYCANS IN AMYLOIDOGENESIS SO MOLECULAR NEUROBIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Transmissible and Nontransmissible Neurodegenerative Disorders CY FEB 28-MAR 05, 1993 CL OCHO RIOS, JAMAICA SP INT BRAIN RES ORG, UNIV GOTEBORG, UNIV WEST INDIES DE SCRAPIE; PRP; AMYLOID; CONGO RED; GLYCOSAMINOGLYCANS; ALZHEIMERS DISEASE ID NEURO-BLASTOMA CELLS; PRION PROTEIN-BIOSYNTHESIS; CREUTZFELDT-JAKOB DISEASE; INFECTED CULTURED-CELLS; PC12 CELLS; MESSENGER-RNA; SULFATED GLYCOSAMINOGLYCANS; ALZHEIMERS-DISEASE; PRECURSOR PROTEIN; AGENT REPLICATION AB Accumulation of an abnormal, protease-resistant form of an endogenous protein, PrP, is a characteristic feature of scrapie and related transmissible spongiform encephalopathies. This abnormal isoform is also present in the amyloid plaques that are often observed in these diseases. In mouse neuroblastoma cells persistently infected with scrapie, the abnormal protease-resistant isoform of PrP is derived from an operationally normal protease-sensitive precursor. Conversion of PrP to the protease-resistant state occurs either on the plasma membrane or along an endocytic pathway by an unknown mechanism. Inhibitors of protease-resistant PrP accumulation have been identified, and these include the amyloid-binding dye Congo red and certain sulfated glycans. The similarity of these compounds to sulfated glycosaminoglycans, which are components of all natural amyloids, has led to the hypothesis that the inhibitors act by competitively blocking an interaction between endogenous glycosaminoglycan(s) and PrP that is critical for amyloidogenic PrP accumulation. The proven prophylactic effect of these sulfated glycans in animal models of scrapie suggests that they represent a group of compounds that might interfere with the pathogenic formation of amyloid in a variety of diseases, such as Alzheimer's disease. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 86 TC 48 Z9 52 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD APR-JUN PY 1994 VL 8 IS 2-3 BP 113 EP 120 DI 10.1007/BF02780661 PG 8 WC Neurosciences SC Neurosciences & Neurology GA PD120 UT WOS:A1994PD12000006 PM 7999307 ER PT J AU RUBENSTEIN, R DENG, H RACE, R JU, W SCALICI, C PAPINI, M RUBENSTEIN, A KASCSAK, R CARP, R AF RUBENSTEIN, R DENG, H RACE, R JU, W SCALICI, C PAPINI, M RUBENSTEIN, A KASCSAK, R CARP, R TI SCRAPIE STRAIN INFECTION IN-VITRO INDUCES CHANGES IN NEURONAL CELLS SO MOLECULAR NEUROBIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Transmissible and Nontransmissible Neurodegenerative Disorders CY FEB 28-MAR 05, 1993 CL OCHO RIOS, JAMAICA SP INT BRAIN RES ORG, UNIV GOTEBORG, UNIV WEST INDIES DE SCRAPIE STRAINS; PC12 CELLS; NEURONAL; NEUROTRANSMITTERS; LIPID DROPLETS; PHOSPHOLIPIDS ID NERVE GROWTH-FACTOR; PHEOCHROMOCYTOMA CELLS; PRION PROTEIN; PC12 CELLS; BLASTOMA CELLS; CLONAL LINE; RELEASE; AGENT; PHOSPHATIDYLINOSITOL; METABOLISM AB PC12 cells, in the presence of nerve growth factor (NGF), support replication of the mouse-derived scrapie strains 139A and ME7, with the former yielding 100-1000-fold higher levels of infectivity. Infectivity remained cell-associated and cells did not show any gross morphological alterations, although changes were observed by electron microscopy in the form of an increased number of lipid droplets in 139A-infected cultures. Analysis of phospholipid metabolism in 139A infected cells indicated that scrapie replication did not change the inositol phosphate levels, but did not stimulate phosphoinositide synthesis. Replication was not detected in PC12 cells infected with either the hamster-derived 263K or rat-derived 139R scrapie strains.' Since scrapie-infected cultures did not exhibit cell death or any gross changes, any scrapie-induced effects would probably be manifested in nonvital cellular functions. When compared to controls, infect with the 139A scrapie strain resulted in decreased activity of the cholinergic pathway-related enzymes, as well as the GABA synthetic pathway; however, the adrenergic pathway was unaffected by scrapie infection. The effects of the 139A scrapie strain on the cholinergic system appeared to be dose-dependent and were first detected prior to the detection of scrapie strain on the cholinergic system appeared to be dose-dependent and were first detected prior to the detection of scrapie agent replication in these cells. No neurotransmitter-related enzymatic changes were detected in 263K-or 139R-infected PC12 cells. The enzymatic changes observed in ME7-infected PC12 cells and in Chandler agent-infected mouse neuroblastoma cells suggest that the significant changes in neurotransmitter levels in cultures exhibiting low infectivity titers must involve factors other than, but not excluding, replication of the agent. The role of additional factors is also suggested in studies of protein kinase C activity in 139A- and 139R-infected PC12 cells. These studies emphasize the value of the PC12 cell model system in examining the scrapie strain-host cell interaction and, in addition, supported the concept of variation among scrapie strains. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. RP RUBENSTEIN, R (reprint author), NEW YORK STATE INST BASIC RES DEV DISABIL,NEW YORK STATE OFF MENTAL RETARDAT & DEV DISA,STATEN ISL,NY 10314, USA. FU NINDS NIH HHS [R01 NS213949, R29 NS25308] NR 46 TC 9 Z9 9 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD APR-JUN PY 1994 VL 8 IS 2-3 BP 129 EP 138 DI 10.1007/BF02780663 PG 10 WC Neurosciences SC Neurosciences & Neurology GA PD120 UT WOS:A1994PD12000008 PM 7999309 ER PT J AU BROWN, P MORGAN, OC MCRAE, A RODGERSJOHNSON, P AF BROWN, P MORGAN, OC MCRAE, A RODGERSJOHNSON, P TI NEURODEGENERATIVE DISEASES - CLINICAL, EXPERIMENTAL, AND THERAPEUTIC APPROACHES .II. TRANSMISSIBLE NEURODEGENERATIVE DISORDERS - PREFACE SO MOLECULAR NEUROBIOLOGY LA English DT Editorial Material C1 UNIV W INDIES,DEPT MED,MONA,JAMAICA. GOTHENBURG UNIV,INST ANAT & CELL BIOL,GOTHENBURG,SWEDEN. UNIV W INDIES,DEPT MED,KINGSTON 7,JAMAICA. RP BROWN, P (reprint author), NIH,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD APR-JUN PY 1994 VL 8 IS 2-3 BP R5 EP R6 DI 10.1007/BF02780656 PG 2 WC Neurosciences SC Neurosciences & Neurology GA PD120 UT WOS:A1994PD12000001 ER PT J AU BADIO, B DALY, JW AF BADIO, B DALY, JW TI EPIBATIDINE, A POTENT ANALGESIC AND NICOTINIC AGONIST SO MOLECULAR PHARMACOLOGY LA English DT Article ID BINDING-SITES; RAT PHEOCHROMOCYTOMA; BRAIN; ACETYLCHOLINE; RECEPTORS; RELEASE AB Synthetic (+)- and (-)-epibatidine (an alkaloid originally characterized from frog skin) have potent analgetic activity in mice, using the hot-plate assay. The natural (+)-enantiomer, with an ED(50)of about 1.5 mu g/kg upon intraperitoneal injection, is about 2-fold more potent than the (-)-enantiomer. The analgetic activity is blocked by the nicotinic antagonist mecamylamine. Both the (+)- and (-)-enantiomers have high affinity (K-i values of 0.045 and 0.058 nM, respectively) for nicotinic sites that bind [H-3] nicotine in rat brain membranes. An analog of epibatidine with the chloro substituent of the pyridyl ring replaced with hydrogen has comparable affinity for nicotinic sites, whereas replacement with a methyl or iodo substituent lowers activity. Both (+)- and (-)-epibatidine have potent agonist activity at ganglionic-type nicotinic receptors in pheochromocytoma PC-12 cells, with EC(50) values for stimulation of sodium influx of 72 and 111 nM, respectively. (-)-Epibatidine is about 5-fold less potent as an agonist at muscle-type central nicotinic receptors of medulloblastoma TE671 cells. It would appear that the analgetic activity of epibatidine is due to activity as a nicotinic agonist. The epibatidines have little or no activity at a variety of other central receptors, including opioid receptors, muscarinic receptors, adrenergic receptors, dopamine receptors, serotonin receptors, and gamma-aminobutyric acid receptors. C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 26 TC 397 Z9 401 U1 3 U2 18 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 1994 VL 45 IS 4 BP 563 EP 569 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NH460 UT WOS:A1994NH46000001 PM 8183234 ER PT J AU STEIN, WD CARDARELLI, C PASTAN, I GOTTESMAN, MM AF STEIN, WD CARDARELLI, C PASTAN, I GOTTESMAN, MM TI KINETIC EVIDENCE SUGGESTING THAT THE MULTIDRUG TRANSPORTER DIFFERENTIALLY HANDLES INFLUX AND EFFLUX OF ITS SUBSTRATES SO MOLECULAR PHARMACOLOGY LA English DT Article ID ASCITES TUMOR-CELLS; P-GLYCOPROTEIN GENE; COMPLEMENTARY-DNA; RESISTANCE GENE; CYSTIC-FIBROSIS; ALTERED PATTERN; MDR1 CDNA; EXPRESSION; IDENTIFICATION; AMPLIFICATION AB A kinetic approach was used to analyze the mechanism by which a substitution of valine for glycine at position 185 in the multidrug transporter alters its substrate specificity so that colchicine and etoposide transport is increased, daunorubicin transport is unchanged, and vinblastine transport is decreased. Time courses for uptake and efflux of colchicine, vinblastine, etoposide, and daunorubicin for NIH/3T3 mouse cells transfected with wild-type (MDR1-G185) and mutant (MDR1-V185) strains of the human mdr1 gene were determined at room temperature in the presence and absence of an energy supply. The initial rate of vinblastine uptake was reduced approximately 5-fold by glucose feeding of ATP-depleted wild-type (MDR1-G185) cells but was only halved in MDR1-V185 transfectants. In contrast, glucose feeding decreased the initial rate of colchicine uptake approximately 4-fold in the MDR1-V185 (mutant) transfectant but not in the MDR1-G185 (wild-type) transfectant. Efflux of colchicine was accelerated >5-fold in both the MDR1-V185 (mutant) and MDR1-G185 (wild-type) transfectants when glucose was given to raise ATP levels. The effects on initial rates of colchicine uptake accounted semiquantitatively for the increased colchicine resistance of MDR1-V185 (mutant) transfectants. Similar effects were found for etoposide in the MDR-V185 transfectants. Quinidine in the external medium greatly inhibited drug entry rates but had little effect on efflux, whereas verapamil inhibited both uptake and efflux. A possible interpretation of these data is that the multidrug transporter extracts drugs from the external and internal halves of the membrane bilayer by different paths, which are distinguishable by mutation and inhibitors. C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,SILBERMAN INST LIFE SCI,DEPT BIOL CHEM,IL-91904 JERUSALEM,ISRAEL. NR 29 TC 107 Z9 108 U1 0 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 1994 VL 45 IS 4 BP 763 EP 772 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NH460 UT WOS:A1994NH46000026 PM 7910372 ER PT J AU AGBARIA, R MULLEN, CA HARTMAN, NR COONEY, DA HAO, Z BLAESE, RM JOHNS, DG AF AGBARIA, R MULLEN, CA HARTMAN, NR COONEY, DA HAO, Z BLAESE, RM JOHNS, DG TI EFFECTS OF IMP DEHYDROGENASE INHIBITORS ON THE PHOSPHORYLATION OF GANCICLOVIR IN MOLT-4 CELLS BEFORE AND AFTER HERPES-SIMPLEX VIRUS THYMIDINE KINASE GENE TRANSDUCTION SO MOLECULAR PHARMACOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; RIBAVIRIN; 9-(2-HYDROXYETHOXYMETHYL)GUANINE; 2',3'-DIDEOXYINOSINE; REPLICATION; NUCLEOSIDES; ACYCLOVIR; STIMULATE; TYPE-1; TUMORS AB We have undertaken to characterize the role of cytoplasmic 5'-nucleotidase (EC 3.1.3.5) in the phosphorylation of the antiherpes simplex virus and anti-human cytomegalovirus agent ganciclovir (GCV) in MOLT-4 cells, a human T cell line adapted to grow in suspension culture. The rate of formation of GCV triphosphate was found to be approximately doubled by preincubation of nontransfected MOLT-4 cells with agents that cause the accumulation of IMP, such as ribavirin (20 mu M) and mycophenolic acid (1 mu M), and the reaction rate was found to be unaffected by high levels of thymidine (100 mu M). With herpes simplex virus-1 thymidine kinase (HStk) gene-transduced MOLT-4 cells, the rate of GCV phosphorylation was approximately 40-fold faster than that in uninfected cells and, in marked contrast to uninfected cells, the reaction was significantly inhibited both by IMP dehydrogenase inhibitors and by thymidine. These latter effects appear to be the result of 1) the accumulation of high levels of dTTP in IMP dehydrogenase inhibitor-treated cells, with consequent feedback inhibition of HStk, and 2) direct competitive substrate inhibition by thymidine of the HStk-catalyzed phosphorylation of GCV. Thus, agents that enhance 5'-nucleotidase-catalyzed phosphorylation of GCV in uninfected cells do not play a similar role in HStk-transfected cells, a consequence of the quantitative predominance of the viral thymidine kinase-catalyzed reaction over that attributable to endogenous cytoplasmic 5'-nucleotidase. C1 NCI,DIV CANC BIOL & DIAG,METAB BRANCH,BETHESDA,MD 20892. RP AGBARIA, R (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BLDG 37,ROOM 5B22,BETHESDA,MD 20892, USA. NR 26 TC 14 Z9 15 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 1994 VL 45 IS 4 BP 777 EP 782 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NH460 UT WOS:A1994NH46000028 PM 7910373 ER PT J AU SPENCER, DL HINES, KC CASPARY, WJ AF SPENCER, DL HINES, KC CASPARY, WJ TI AN IN-SITU PROTOCOL FOR MEASURING THE EXPRESSION OF CHEMICALLY-INDUCED MUTATIONS IN MAMMALIAN-CELLS SO MUTATION RESEARCH LA English DT Article DE L5178Y MOUSE LYMPHOMA CELLS; MAMMALIAN CELL MUTAGENESIS; TRIFLUOROTHYMIDINE-RESISTANCE; TRIFLUOROTHYMIDINE; 5-AZACYTIDINE; 1-(BETA-D-ARABINOFURANOSYL)CYTOSINE (ARAC); IN-SITU PROTOCOL ID MOUSE LYMPHOMA-CELLS; SISTER-CHROMATID EXCHANGES; TRIFLUOROTHYMIDINE-RESISTANT; CHROMOSOME ANALYSIS; MUTAGENESIS ASSAY; 5-AZACYTIDINE; DNA; INDUCTION; MUTANTS; TFT AB The generation of expression curves and the evaluation of mutagenic responses of mammalian cells using standard mutagenesis assays can be inaccurate because mutant and wild-type cells are usually mixed during the expression phase. If some mutant progenitors or mutants grow more slowly than the wild-type cells during the expression period, there will be a decrease in the mutant to wild-type ratio with time and the mutant fraction will not accurately represent the number of mutational events that occurred. The mutant fraction may also inaccurately assess the number of mutations if these mutations are expressed over a number of generations during the time before selection. We previously showed that recovery of L5178Y mouse cell mutants is not complete when mutations are allowed to express in suspension because slowly growing mutants and/or mutant progenitors are diluted out during this time (Rudd et al., 1990). In order to more accurately quantitate the mutagenic response of the cells, we developed an in situ procedure which segregates and immobilizes cells during expression. Because of this immobilization, slowly growing mutant progenitors and mutants expressed at different times will have an equal probability of being scored as mutants. Thus, one mutation leads to one mutant colony and the measurement of the mutagenic response of the cells to the chemical accurately reflects the mutational events that occurred. We platcd L5178Y tk+/- mouse cells in semisolid medium immediately after treatment. As the cells grew and formed microcolonies, the selective agent TFT was added as an overlay at specified times, permitting only TFF(r) cells to survive. In this procedure, each mutation was captured as an individual colony; consequently, the measured mutation fraction accurately reflected the mutational events that occurred at the selected locus. In addition, the induced mutant colonies arising in the agar are the result of independent mutational events. We previously described the in situ protocol for L5178Y cells and showed that the spontaneous mutation rate measured was 50-fold greater than when the cells expressed the phenotype in suspension (Rudd et al., 1990). From this we concluded that the slow growth phenotype was expressed before TFT resistance. In the present paper, we evaluate the effect of chemical treatment on the mutation fraction as a function of the time to TFT addition. Using the in situ protocol, we generated expression curves for three nucleotide analogs, 5-azacytidine, TFT and AraC. The numbers of TFT(r) colonies produced at various times after treatment indicated that chemically-treated cultures had higher mutation fractions than the solvent controls. The maximal differential increase in mutation rate occurred between 30 and 60 h for 5-azacytidine and between 20 and 40 h for TFT and AraC. Our results document the feasibility of quantitating induced mutation fractions using the in situ protocol, confirm the mutagenicity of AraC and 5azacytidine and demonstrate the mutagenic activity of TFT at the tk locus. In addition to recovering mutants more accurately than the suspension protocol, the in situ protocol has the advantage of being experimentally less labor and time intensive. Therefore, we believe that this method should be considered for evaluation as an assay to measure the potential mutagenic effects of chemicals in mammalian cells in vitro. RP SPENCER, DL (reprint author), NIH,ENVIRONM CARCINOGENESIS & MUTAGENESIS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 34 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD APR PY 1994 VL 312 IS 2 BP 85 EP 97 DI 10.1016/0165-1161(94)90013-2 PG 13 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA ND831 UT WOS:A1994ND83100003 PM 7510835 ER PT J AU ROSS, HL LEE, HM HARVEY, RG DIPPLE, A AF ROSS, HL LEE, HM HARVEY, RG DIPPLE, A TI COMPARISON OF THE SITES OF REACTION OF 3 POLYCYCLIC AROMATIC-HYDROCARBONS IN THE SUPF GENE SO MUTATION RESEARCH LA English DT Article DE SUPF; SEQUENCE SPECIFICITY, BENZO[A]PYRENE; DIHYDRODIOL EPOXIDE; 5-METHYLCHRYSENE; 7-METHYLBENZ[A]ANTHRACENE ID TUMOR-INITIATING ACTIVITIES; DNA-POLYMERASE ACTION; DIOL-EPOXIDE; HUMAN-CELLS; CHEMICAL CARCINOGENESIS; DIHYDRODIOL-EPOXIDES; EXCISION REPAIR; SHUTTLE-VECTOR; MOUSE SKIN; ADDUCTS AB The distribution of hydrocarbon-DNA adducts through the supF gene in plasmid pS189 was examined using the polymerase arrest assay. For three hydrocarbon dihydrodiol epoxides, derived from 5-methylchrysene, 7-methylbenz[a]anthracene, and benzo[a]pyrene, that exhibit a preference for reaction with guanine residues in DNA, polymerase arrest spectra were similar but not identical. For each agent, guanines in different sequence contexts exhibited varying reactivities and each specific guanine did not necessarily respond to each agent in the same fashion. Thus, sequence context together with the individual dihydrodiol epoxide's chemical and physical properties all play a role in determining sites and extents of reaction within a specific gene. The polymerase arrest data were not predictive of the known sites of mutation hotspots for these dihydrodiol epoxides in the supF gene indicating that further action upon the adducted DNA by repair systems is probably necessary to determine which specific chemical adducts will ultimately give rise to mutation. C1 NCI,FREDERICK CANC RES DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,POB B,FREDERICK,MD 21702. UNIV CHICAGO,BEN MAY INST,CHICAGO,IL 60637. FU NCI NIH HHS [N01-CO-74101]; NIEHS NIH HHS [NIEHS ES04732] NR 40 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD APR 1 PY 1994 VL 306 IS 1 BP 91 EP 101 DI 10.1016/0027-5107(94)90171-6 PG 11 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA ND637 UT WOS:A1994ND63700010 PM 7512208 ER PT J AU FERRIN, LJ CAMERINIOTERO, RD AF FERRIN, LJ CAMERINIOTERO, RD TI LONG-RANGE MAPPING OF GAPS AND TELOMERES WITH RECA-ASSISTED RESTRICTION-ENDONUCLEASE (RARE) CLEAVAGE SO NATURE GENETICS LA English DT Article ID HUNTINGTON DISEASE GENE; CANDIDATE REGION; DNA; SEQUENCE; CLONES; CHROMOSOME-4; LOCATION; 4P16.3; MAPS AB RecA-assisted restriction endonuclease (RARE) cleavage is a method to perform sequence-specific cleavage of genomic DNA, and is useful in physical mapping studies. After making two modifications, we have applied this method to mapping targe regions of DNA in several cell types, including a notorious gap near the Huntington disease (HD) locus on chromosome 4. RARE cleavage fragments were analysed by pulsed field gel electrophoresis and Southern blotting and the distances between cleavage sites determined with accuracy. Using RARE cleavage, the gap measured was less than 60 kilobases in length. RARE cleavage is also a straightforward technique to map the distance from a marker to a telomere. The terminal 1.7 megabases of several HD and control cell lines were mapped with no large differences between cell lines in this region. C1 NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 25 TC 29 Z9 29 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD APR PY 1994 VL 6 IS 4 BP 379 EP 383 DI 10.1038/ng0494-379 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA ND870 UT WOS:A1994ND87000017 PM 8054978 ER PT J AU PRAS, E ARBER, N AKSENTIJEVICH, I KATZ, G SCHAPIRO, JM PROSEN, L GRUBERG, L HAREL, D LIBERMAN, U WEISSENBACH, T PRAS, M KASTNER, DL AF PRAS, E ARBER, N AKSENTIJEVICH, I KATZ, G SCHAPIRO, JM PROSEN, L GRUBERG, L HAREL, D LIBERMAN, U WEISSENBACH, T PRAS, M KASTNER, DL TI LOCALIZATION OF A GENE CAUSING CYSTINURIA TO CHROMOSOME 2P SO NATURE GENETICS LA English DT Article ID EXPRESSION CLONING; RAT-KIDNEY; LINKAGE; TRANSPORT; CDNA; MAP AB Cystinuria is an autosomal recessive disorder of amino acid transport. It is a common hereditary cause of kidney stones worldwide, and is associated with significant morbidity. in 17 affected families, we found linkage between cystinuria and three chromosome 2p markers. Maximal two-point rod scores between cystinuria and D2S119, D2S391 and D2S288 were 8.23 (theta=0.07), 3.73 (theta=0.15) and 3.03 (theta=0.12), respectively. Analysis of recombinants and multipoint linkage data indicated that the most likely order is cen-D2S391-D2S119-cystinuria-D2S177-tel. We also observed high rates of homozygosity for markers in this chromosomal region among 11 affected offspring of consanguineous marriages. Based on its map position and function, the recently cloned SLC3A1 amino acid transporter gene is a primary candidate gene for this disease. C1 NIAMSD,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD 20892. BEILINSON MED CTR,DEPT MED D,PETAH TIQWA,ISRAEL. BEILINSON MED CTR,DEPT METAB,PETAH TIQWA,ISRAEL. BEILINSON MED CTR,CLIN LABS,PETAH TIQWA,ISRAEL. HADASSAH MED CTR,DEPT UROL,JERUSALEM,ISRAEL. CHAIM SHEBA MED CTR,DEPT MED F,IL-52621 TEL HASHOMER,ISRAEL. CHAIM SHEBA MED CTR,HELLER INST MED RES,IL-52621 TEL HASHOMER,ISRAEL. INST PASTEUR,UNITE GENET MOLEC HUMAINE,CNRS,URA 1445,F-75724 PARIS 15,FRANCE. NR 33 TC 100 Z9 100 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD APR PY 1994 VL 6 IS 4 BP 415 EP 419 DI 10.1038/ng0494-415 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA ND870 UT WOS:A1994ND87000024 PM 8054985 ER PT J AU AKUNNE, HC MONN, JA THURKAUF, A JACOBSON, AE RICE, KC LINDERS, JTM JIANG, Q PORRECA, F ROTHMAN, RB AF AKUNNE, HC MONN, JA THURKAUF, A JACOBSON, AE RICE, KC LINDERS, JTM JIANG, Q PORRECA, F ROTHMAN, RB TI AN ELECTROPHILIC AFFINITY LIGAND BASED ON (+)-MK801 DISTINGUISHES PCP SITE-1 FROM PCP SITE-2 SO NEUROCHEMICAL RESEARCH LA English DT Article DE N-METHYL-D-ASPARTATE; (+)-MK801; AFFINITY LIGANDS; PCP; 1,3-DI(2-TOLYL)GUANIDINE; SIGMA RECEPTORS ID PHENCYCLIDINE BINDING-SITES; GUINEA-PIG BRAIN; AMINE REUPTAKE COMPLEX; RAT-BRAIN; PSEUDOALLOSTERIC MODULATION; EXTRACELLULAR DOPAMINE; H-3 PHENCYCLIDINE; NUCLEUS ACCUMBENS; NMDA RECEPTORS; DRUGS AB The electrophilic affinity ligand, (+)-3-isothiocyanato-5-methyl-10, 11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine hydrochloride {(+)-MK801-NCS} was characterized for its ability to acylate phencyclidine (PCP) and sigma binding sites in vivo. Initial studies, conducted with mouse brain membranes, characterized the binding sites labeled by [H-3]1-[1-(2-thienyl)cyclohexyl]piperidine ([H-3]TCP). The Kd values of [H-3]TCP for PCP site 1 (MK801-sensitive) and PCP site 2 (MK801-insensitive) were 12 nM and 68 nM, with Bmax values of 1442 and 734 fmol/mg protein, respectively. Mice were sacrificed 18-24 hours following intracerebroventricular administration of the acylator. The administration of(+)-MK801-NCS increased [H-3]TCP binding to site 2, but not to site 1. Although (+)-MK801-NCS decreased [H-3](+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b; cbcyclohepten-5,10-imine maleate ([H-3](+)-MK801) binding to site 1, it had no effect on [3(H)]TCP binding to site 1. Viewed collectively with other published data, these data support the hypothesis that PCP sites 1 and 2 are distinct binding sites, and that [H-3]TCP and [H-3](+)-MK801 label different domains of the PCP binding site associated with the NMDA receptor. C1 NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,BALTIMORE,MD 21224. NIDDK,MED CHEM LAB,BETHESDA,MD 20892. UNIV ARIZONA,DEPT PHARMACOL,TUCSON,AZ 85724. NR 41 TC 2 Z9 2 U1 0 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0364-3190 J9 NEUROCHEM RES JI Neurochem. Res. PD APR PY 1994 VL 19 IS 4 BP 385 EP 389 DI 10.1007/BF00967314 PG 5 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA NJ598 UT WOS:A1994NJ59800002 PM 8065494 ER PT J AU SPERGEL, DJ KRSMANOVIC, LZ STOJILKOVIC, SS CATT, KJ AF SPERGEL, DJ KRSMANOVIC, LZ STOJILKOVIC, SS CATT, KJ TI GLUTAMATE MODULATES [CA2+](I) AND GONADOTROPIN-RELEASING-HORMONE SECRETION IN IMMORTALIZED HYPOTHALAMIC GT1-7 NEURONS SO NEUROENDOCRINOLOGY LA English DT Article DE CALCIUM; GLUTAMATE; GONADOTROPIN-RELEASING HORMONE; HYPOTHALAMUS; NEUROSECRETION ID N-METHYL-D; AMINO-ACID NEUROTRANSMISSION; D-ASPARTATE RECEPTORS; LUTEINIZING-HORMONE; NEUROENDOCRINE REGULATION; NMDA RECEPTORS; NERVOUS-SYSTEM; CALCIUM; RAT; ACTIVATION AB Glutamate and its receptors are present in the hypothalamus and have been proposed to participate in neuroendocrine regulation, including the control of GnRH secretion. To address the mechanism of glutamate action, we measured [Ca2+]i, inositol phosphate, and secretory responses to glutamate receptor subtype agonists and antagonists in the immortalized GT1-7 cell line of GnRH-secreting hypothalamic neurons. Glutamate, N-methyl-D-aspartate (NMDA). kainate, and trans-(+/-)-1-amino-(1S,3R)-cyclopentanedicarboxylic acid increased GnRH secretion. In monolayer cultures of GT1-7 cells, L- but not D-glutamate induced a moderate, concentration-dependent rise in [Ca2+]i. The action of glutamate on [Ca2+]i was mimicked by NMDA, alpha-amino-2,3-dihydro-5-methyl-3-oxo-4-isoxazolepropanoic acid (AMPA), and kainate. Responses to NMDA were potentiated by the coagonist, glycine, and were inhibited by an antagonist of the glycine site on the NMDA receptor, 5,7-dichlorokynurenic acid (DCKA). NMDA-induced [Ca2+]i responses were also inhibited by Mg2+ and by the NMDA receptor antagonist, (5R, 10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801), but not by the AMPA/kainate antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). In contrast, responses to AMPA and kainate were inhibited by CNQX but not by Mg2+, DCKA, or MK-801. Responses to glutamate were more inhibited by MK-801 plus CNQX than by either antagonist alone. All [Ca2+]i responses were nearly abolished in Ca2+-free solution. None of the agonists stimulated inositol phosphate formation. Hence, the NMDA and AMPA/kainate subtypes, but not the metabotropic subtype, of glutamate receptor are expressed in GT1-7 cells. Activation of NMDA and AMPA/kainate receptors is followed by Ca2+ influx and subsequently by GnRH secretion. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 49,RM 6A36,BETHESDA,MD 20892. RI Spergel, David/A-4410-2011 NR 45 TC 64 Z9 65 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD APR PY 1994 VL 59 IS 4 BP 309 EP 317 DI 10.1159/000126672 PG 9 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA NB761 UT WOS:A1994NB76100001 PM 7911229 ER PT J AU VALLSSOLE, J PASCUALLEONE, A BRASILNETO, JP CAMMAROTA, A MCSHANE, L HALLETT, M AF VALLSSOLE, J PASCUALLEONE, A BRASILNETO, JP CAMMAROTA, A MCSHANE, L HALLETT, M TI ABNORMAL FACILITATION OF THE RESPONSE TO TRANSCRANIAL MAGNETIC STIMULATION IN PATIENTS WITH PARKINSONS-DISEASE SO NEUROLOGY LA English DT Article ID MOTOR-UNIT RESPONSES; CORTICAL STIMULATION; VOLUNTARY CONTRACTION; MUSCLE; CORTEX; EXCITABILITY; RIGIDITY; BRAIN; NEURONS; HEALTHY AB We studied the facilitation of the motor evoked potential (MEP) elicited with transcranial magnetic stimulation by increasing the stimulus intensity and the degree of voluntary activation of the target muscle in patients with Parkinson's disease (PD) and in normal volunteers. The threshold intensity for eliciting MEPs with the muscle at rest did not differ in PD patients and normal subjects. At rest, stimuli of similar intensity, related to the individual's threshold, elicited MEPs with amplitudes consistently larger in patients than in normal subjects, although when we compared the averaged MEP amplitude across all stimulus intensities, the differences reached only borderline statistical significance. Voluntary muscle activation elicited a smaller increase in the MEP area in PD patients than in normal subjects. Increasing the degree of voluntary muscle activation at fixed stimulus intensities elicited a smaller increase of MEP amplitude, duration, and area in PD patients than in normal subjects. These results suggest that control of the excitability of the motor system is abnormal in PD patients, with enhancement of excitability at rest and weak energization during voluntary muscle activation. C1 NINCDS,BIOMETRY & FIELD STUDIES BRANCH,MATH STAT SECT,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD. RI Pascual-Leone, Alvaro/G-6566-2011; Brasil-Neto, Joaquim/A-1171-2009 NR 29 TC 160 Z9 161 U1 5 U2 7 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1994 VL 44 IS 4 BP 735 EP 741 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA NG065 UT WOS:A1994NG06500029 PM 8164834 ER PT J AU VERDI, JM BIRREN, SJ IBANEZ, CF PERSSON, H KAPLAN, DR BENEDETTI, M CHAO, MV ANDERSON, DJ AF VERDI, JM BIRREN, SJ IBANEZ, CF PERSSON, H KAPLAN, DR BENEDETTI, M CHAO, MV ANDERSON, DJ TI P75(LNGFR) REGULATES TRK SIGNAL-TRANSDUCTION AND NGF-INDUCED NEURONAL DIFFERENTIATION IN MAH CELLS SO NEURON LA English DT Article ID NERVE GROWTH-FACTOR; TYROSINE KINASE-ACTIVITY; PROTOONCOGENE PRODUCT; FACTOR RECEPTOR; CHROMAFFIN CELLS; NEUROTROPHIN RECEPTORS; GENE-TRANSFER; PC12 CELLS; GLUCOCORTICOIDS; PHOSPHORYLATION AB We have examined NGF-induced signal transduction events and neuronal differentiation in MAH cells, a neuronal progenitor cell line, in which the expression of the two NGF receptors, p140(trk) (Trk) and p75(LNGFR) (p75), has been independently manipulated. Coexpression of a large molar excess of p75 substantially enhances the NGF-induced tyrosine autophosphorylation of Trk, compared with cells expressing Trk alone. MAH cells expressing both Trk and p75 stop dividing and acquire a mature neuronal morphology more rapidly and with greater efficiency than MAH cells expressing Trk alone. These biochemical and biological influences of p75 are not observed using a mutant form of NGF that binds Trk but not p75. These data provide evidence that p75 can modulate signal transduction through Trk in a neuronal progenitor cell context and that such modulation has functional consequences for the neuronal differentiation pathway induced by NGF. C1 CALTECH,HOWARD HUGHES MED INST,PASADENA,CA 91125. KAROLINSKA INST,STOCKHOLM,SWEDEN. NCI,FREDERICK CANC RES INST,FREDERICK,MD 21702. CORNELL UNIV,SCH MED,DEPT ANAT & CELL BIOL,NEW YORK,NY 10021. RP VERDI, JM (reprint author), CALTECH,DIV BIOL,PASADENA,CA 91125, USA. FU NINDS NIH HHS [NS23476] NR 57 TC 301 Z9 303 U1 1 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD APR PY 1994 VL 12 IS 4 BP 733 EP 745 DI 10.1016/0896-6273(94)90327-1 PG 13 WC Neurosciences SC Neurosciences & Neurology GA NH253 UT WOS:A1994NH25300003 PM 7512816 ER PT J AU MAGER, S MIN, C HENRY, DJ CHAVKIN, C HOFFMAN, BJ DAVIDSON, N LESTER, HA AF MAGER, S MIN, C HENRY, DJ CHAVKIN, C HOFFMAN, BJ DAVIDSON, N LESTER, HA TI CONDUCTING STATES OF A MAMMALIAN SEROTONIN TRANSPORTER SO NEURON LA English DT Article ID PLATELET 5-HYDROXYTRYPTAMINE TRANSPORT; NA+ GLUCOSE COTRANSPORTER; PLASMA-MEMBRANE VESICLES; GAMMA-AMINOBUTYRIC-ACID; HIGH-AFFINITY BINDING; XENOPUS-OOCYTES; ELECTROGENIC UPTAKE; ACTIVE-TRANSPORT; EXTERNAL K+; RAT-BRAIN AB We have studied permeation at a cloned rat 5-HT transporter expressed in Xenopus oocytes. [H-3]5-HT uptake and [I-125]RTI-55 binding yield a turnover rate of similar to 1/s that does not depend on membrane potential. However, in voltage-clamp experiments, three distinct currents result from 5-HT transporter expression. First, a steady-state, voltage-dependent transport-associated current is induced by 5-HT application. Second, a transient inward current is activated by voltage jumps to high negative potentials in the absence of 5-HT and is blocked by 5-HT itself. Third, a small leakage current is observed in the absence of 5-HT. All the observed currents are blocked by inhibitors of 5-HT uptake but are differentially affected by Na+, Li+, K+, Ba2+, Cs+, Cl-, and amiloride. The conducting states of the 5-HT transporter may reflect the existence of a permeation pathway similar to that of ionic channels. C1 CALTECH,DIV ENGN & APPL SCI,PASADENA,CA 91125. UNIV WASHINGTON,DEPT PHARMACOL,SEATTLE,WA 98125. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP MAGER, S (reprint author), CALTECH,DIV BIOL,PASADENA,CA 91125, USA. RI Chavkin, Charles/G-2797-2010 NR 46 TC 184 Z9 185 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD APR PY 1994 VL 12 IS 4 BP 845 EP 859 DI 10.1016/0896-6273(94)90337-9 PG 15 WC Neurosciences SC Neurosciences & Neurology GA NH253 UT WOS:A1994NH25300013 PM 8161456 ER PT J AU GROSSMAN, H CAINE, ED KETONEN, L AF GROSSMAN, H CAINE, ED KETONEN, L TI PROGRESSIVE IRRADIATION DEMENTIA AND PSYCHOSIS - CLINICAL, NEUROIMAGING, AND NEUROPSYCHOLOGICAL FEATURES SO NEUROPSYCHIATRY NEUROPSYCHOLOGY AND BEHAVIORAL NEUROLOGY LA English DT Note DE RADIOTHERAPY; NEUROPSYCHOLOGICAL TESTING; DEMENTIA ID METACHROMATIC LEUKODYSTROPHY; RADIATION-THERAPY; BRAIN METASTASES; HUMAN AUTONOMY; FRONTAL LOBES; LESIONS; BEHAVIOR; MR AB A 50-year-old woman, who survived 12 years following cranial irradiation for a frontal tumor. developed a delayed-onset, progressive neuropsychiatric disorder culminating in florid psychosis. Her symptoms and deficits fit the clinical pattern of a progressive subcortical disease and correlated with neuroimaging evidence of continuing white matter degeneration. We compare this irradiation-induced dementia to other toxic and degenerative dementias, and consider the role of cerebral white matter in the genesis of psychotic symptoms. C1 UR NIMH,CLIN RES CTR,STUDY PSYCHOPATHOL ELDERLY CRC PE,ROCHESTER,NY. UNIV ROCHESTER,MED CTR,DEPT PSYCHIAT,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT NEUROL,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT RADIOL,ROCHESTER,NY 14642. NR 30 TC 5 Z9 5 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0894-878X J9 NEUROPSY NEUROPSY BE JI Neuropsychiatr. Neuropsychol. Behav. Neurol. PD APR PY 1994 VL 7 IS 2 BP 125 EP 129 PG 5 WC Clinical Neurology; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA NJ804 UT WOS:A1994NJ80400009 ER PT J AU VOGELS, R SAUNDERS, RC ORBAN, GA AF VOGELS, R SAUNDERS, RC ORBAN, GA TI HEMISPHERIC LATERALIZATION IN RHESUS-MONKEYS CAN BE TASK-DEPENDENT SO NEUROPSYCHOLOGIA LA English DT Article ID LINE-ORIENTATION; DISCRIMINATION; CORTEX; PERCEPTION; DIRECTION; ASYMMETRY; LANGUAGE; ROTATION; DECISION; LESIONS AB Two rhesus monkeys with transection of the forebrain commissures were trained on two grating orientation-discrimination tasks. In one task, the simultaneous orientation identification task, monkeys had to decide which of two simultaneously presented gratings was horizontal. In the other task, the temporal same-different task, the monkey had to decide whether or not two successively presented gratings differed in orientation. Both monkeys showed a statistically significant individual asymmetry in the performance on the same-different task with the left hemisphere supporting superior performance compared with the right hemisphere. No such consistent lateralization was found for the identification task. These results show that the demonstration of a behavioral asymmetry depends on the type of discrimination task performed and suggest that the asymmetry is related to interhemispheric differences in higher order stimulus (cognitive) processing and not to a lateralization of early visual processes. C1 NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,WASHINGTON,DC 20032. RP VOGELS, R (reprint author), KATHOLIEKE UNIV LEUVEN,FAC GENEESKUNDE,NEURO & PSYCHOFYSIOL LAB,CAMPUS GASTHUISBERG,B-3000 LOUVAIN,BELGIUM. NR 30 TC 18 Z9 18 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PD APR PY 1994 VL 32 IS 4 BP 425 EP 438 DI 10.1016/0028-3932(94)90088-4 PG 14 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA NK984 UT WOS:A1994NK98400005 PM 8047250 ER PT J AU MCCANN, UD RIDENOUR, A SHAHAM, Y RICAURTE, GA AF MCCANN, UD RIDENOUR, A SHAHAM, Y RICAURTE, GA TI SEROTONIN NEUROTOXICITY AFTER (+/-)3,4-METHYLENEDIOXYMETHAMPHETAMINE (MDMA ECSTASY) - A CONTROLLED-STUDY IN HUMANS SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE AMPHETAMINE; SEROTONIN; PROLACTIN; NEUROTOXICITY; PERSONALITY; DRUG ABUSE ID HUMAN CEREBROSPINAL-FLUID; 5-HYDROXYINDOLEACETIC ACID; MONOAMINE METABOLITES; NONHUMAN-PRIMATES; RAT-BRAIN; 3,4-METHYLENEDIOXYMETHAMPHETAMINE ECSTASY; AMINERGIC METABOLITES; NEURONS; METHYLENEDIOXYMETHAMPHETAMINE; TERMINALS AB (+/-)3,4-Methylenedioxymethamphetamine (MDMA; ''Ecstasy''), an increasingly popular recreational drug, is known to damage brain serotonin 5-hydroxytryptamine (5-HT) neurons in experimental animals. Whether MDMA is neurotoxic in humans has not been established. Thirty MDMA users and 28 controls were admitted to a controlled inpatient setting for measurement of biologic and behavioral indexes of central 5-HT function. Outcome measures obtained after at least 2 weeks of drug abstinence included concentrations of monoamine metabolites in cerebrospinal fluid (CSF), prolactin responses to L-tryptophan, nociceptive responses to ischemic pain, and personality characteristics in which 5-HT has been implicated (i.e., impulsivity and aggression). Subjects with a history of MDMA exposure had lower levels of CSF 5-hydroxyindoleacetic acid (the major metabolite of 5-HT) than controls (p = .001). Although they resembled controls in their prolactin response to L-tryptophan and their response to ischemic pain, MDMA users had lower scores on personality measures of impulsivity (p = .004) and indirect hostility (p = .009). The CSF findings suggest that 5-HT neurotoxicity may be a potential complication of MDMA use. Further, differences in personality support the view that 5-HT systems are involved in modulating impulsive and aggressive personality traits. Additional studies of MDMA-exposed individuals are needed to confirm and extend the present findings. Such studies could help elucidate the role of 5-HT in normal brain function as well as in neuropsychiatric disease states. C1 JOHNS HOPKINS MED INST,FRANCIS SCOTT KEY MED CTR,DEPT NEUROL,BALTIMORE,MD. CONCORDIA UNIV,DEPT PSYCHOL,MONTREAL H3G 1M8,PQ,CANADA. RP MCCANN, UD (reprint author), NIMH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS UNIT,BPB,BLDG 10,ROOM 3S-239,BETHESDA,MD 20892, USA. RI shaham, yavin/G-1306-2014 FU NCRR NIH HHS [5MO1RR02719]; NIDA NIH HHS [R01DA05938] NR 48 TC 245 Z9 246 U1 1 U2 10 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD APR PY 1994 VL 10 IS 2 BP 129 EP 138 PG 10 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA NJ589 UT WOS:A1994NJ58900007 PM 7517677 ER PT J AU CHAN, AML MCGOVERN, ES CATALANO, G FLEMING, TP MIKI, T AF CHAN, AML MCGOVERN, ES CATALANO, G FLEMING, TP MIKI, T TI EXPRESSION CDNA CLONING OF A NOVEL ONCOGENE WITH SEQUENCE SIMILARITY TO REGULATORS OF SMALL GTP-BINDING PROTEINS SO ONCOGENE LA English DT Article ID SIGNAL TRANSDUCTION; VAV PROTOONCOGENE; SACCHAROMYCES-CEREVISIAE; TRANSFORMING ACTIVITY; GENE-PRODUCT; CELL-CYCLE; PROTO-DBL; CANCER; CDC24; RECEPTOR AB We generated a cDNA expression library from a human mammary epithelial cell line for detection of novel oncogenes by focus formation assay in NIH3T3 cells. A morphologically unique focus was identified and the transforming plasmid was isolated. The transforming gene, designated TIM, encoded a predicted protein species of 60 kDa containing a Dbl-Homology (DH) motif. This motif is also present in other growth regulatory molecules including Bcr, Cdc24, Vav, Ras-grf, and Ect2 which have been implicated as regulators of small GTP-binding proteins. NIH3T3 cells transfected with TIM expression plasmid showed altered growth properties in vitro and were tumorigenic when injected into nude mice. The 6.5 kilobasepair (kb) transcript of the TIM gene was mainly expressed in kidney, liver, pancreas, lung, and placenta. By analysing a panel of human-hamster somatic celt hybrids, we localized the TIM gene to human chromosome 7. RP CHAN, AML (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,1E24,BETHESDA,MD 20892, USA. NR 33 TC 48 Z9 49 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1994 VL 9 IS 4 BP 1057 EP 1063 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA NC048 UT WOS:A1994NC04800008 PM 8134109 ER PT J AU THOMPSON, J CHOUDHURY, S KASHANCHI, F DONIGER, J BERNEMAN, Z FRENKEL, N ROSENTHAL, LJ AF THOMPSON, J CHOUDHURY, S KASHANCHI, F DONIGER, J BERNEMAN, Z FRENKEL, N ROSENTHAL, LJ TI A TRANSFORMING FRAGMENT WITHIN THE DIRECT REPEAT REGION OF HUMAN HERPESVIRUS TYPE-6 THAT TRANSACTIVATES HIV-1 SO ONCOGENE LA English DT Article ID HUMAN CYTOMEGALO-VIRUS; HUMAN PAPILLOMAVIRUS TYPE-16; EPSTEIN-BARR-VIRUS; LYMPHOCYTES-T; EXANTHEM-SUBITUM; READING FRAME; STRAIN AD169; B VIRUS; DNA; IDENTIFICATION AB HHV-6 infection has been associated with several malignancies including non-Hodgkin's lymphoma and Hodgkin's disease by the presence of high antibody titer and/or the presence of HHV-6 DNA. To understand their oncogenic potential, SalI restriction fragments from HHV-6 strain U1102 were transfected into NIH3T3 cells to assess transforming ability. A 3.9-kbp SalI-L DNA fragment spanning the junction of the direct repeat left (DR(L)) and unique long segment (U(L)) regions of HHV-6 induced foci of morphologically altered cells. The SalI-L transformed NIH3T3 focal lines induced tumors in nude mice within 2 weeks. The retention of HHV-6 specific DNA observed in SalI-L transformed cells and their tumor-derived lines suggest a possible maintenance function. Since both HHV-6 infection as well as transforming fragments from other DNA viruses have been shown to transactivate the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR), SalI-L was examined for transactivation activity. SalI-L up-regulated HIV-1 LTR CAT 10-15 fold in both monkey CV-1 and human T Jurkat cells. The further study of the SalI-L transforming fragment exhibiting transactivation of HIV-1 LTR will elucidate whether these two activities are encoded by a single gene and will aid in the understanding of the interaction between HHV-6 and HIV-1 as it relates to progression of AIDS and/or AIDS-related malignancies. C1 GEORGETOWN UNIV, SCH MED, DEPT MICROBIOL, WASHINGTON, DC 20007 USA. GEORGETOWN UNIV, DEPT IMMUNOL, WASHINGTON, DC 20007 USA. TEL AVIV UNIV, DEPT CELL RES & IMMUNOL, IL-69978 TEL AVIV, ISRAEL. NCI, TUMOR CELL BIOL LAB, BETHESDA, MD 20892 USA. FU NCI NIH HHS [CA37259-07] NR 56 TC 39 Z9 42 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 EI 1476-5594 J9 ONCOGENE JI Oncogene PD APR PY 1994 VL 9 IS 4 BP 1167 EP 1175 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA NC048 UT WOS:A1994NC04800020 PM 8134119 ER PT J AU NEGGERS, Y GOLDENBERG, RL CLIVER, SP HOFFMAN, HJ COPPER, RL AF NEGGERS, Y GOLDENBERG, RL CLIVER, SP HOFFMAN, HJ COPPER, RL TI THE RELATIONSHIP BETWEEN MATERNAL SKINFOLD THICKNESS, SMOKING AND BIRTH-WEIGHT IN BLACK-AND-WHITE WOMEN SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY LA English DT Article ID PREGNANCY AB A prospective study was conducted in a sample of 1491 multiparous women to ascertain whether the relationship between maternal tricep skinfold thickness and infant birthweight is modified by smoking status and whether the relationship is different in white and black infants. Maternal tricep skinfold thickness measured at midpregnancy was a significant predictor of infant birthweight in both white and black infants after adjusting for gestational age at birth, maternal height, maternal age, parity, alcohol consumption and sex of the infant. However, maternal tricep skinfold thickness was a better predictor of birthweight in smokers compared with nonsmokers. Both white and black women with tricep skinfold thickness below the sample mean had lower infant birthweight than women with tricep skinfold at or above the mean, after adjusting for gestational age at birth, but the difference was greater in smokers (198 g for white and 221 g for black infants) than in nonsmokers (124 g for white and 120 g for black infants). These results suggest that maternal subcutaneous fat measured by tricep skinfold thickness has a greater effect on infant birthweight in smokers compared with nonsmokers, with similar effects in white and black infants. C1 UNIV ALABAMA,DEPT HUMAN NUTR,TUSCALOOSA,AL 35401. UNIV ALABAMA,DEPT OBSTET & GYNECOL,PERINATAL EPIDEMIOL UNIT,BIRMINGHAM,AL 35294. NICHHD,PREVENT RES PROGRAM,BETHESDA,MD 20892. FU NICHD NIH HHS [N01-HD-42811]; PHS HHS [282-92-0055] NR 15 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-5022 J9 PAEDIATR PERINAT EP JI Paediatr. Perinat. Epidemiol. PD APR PY 1994 VL 8 IS 2 BP 216 EP 221 DI 10.1111/j.1365-3016.1994.tb00452.x PG 6 WC Public, Environmental & Occupational Health; Obstetrics & Gynecology; Pediatrics SC Public, Environmental & Occupational Health; Obstetrics & Gynecology; Pediatrics GA NP477 UT WOS:A1994NP47700011 PM 8047489 ER PT J AU BOYCE, WT ONEILL, PL PRICE, CS HAINES, M SUOMI, SJ AF BOYCE, WT ONEILL, PL PRICE, CS HAINES, M SUOMI, SJ TI STRESS REACTIVITY AND VIOLENT INJURIES IN FREE-RANGING RHESUS-MONKEYS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A19 EP A19 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900102 ER PT J AU COLLINS, JW HERMAN, AA DAVID, RJ AF COLLINS, JW HERMAN, AA DAVID, RJ TI INCOME INCONGRUITY INCREASES THE PROPORTION OF LOW-BIRTH-WEIGHT (LESS-THAN-2500G) BIRACIAL INFANTS ONLY WHEN THE AFRICAN-AMERICAN PARENT IS THE MOTHER - A SOCIOLOGIC PHENOMENON SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NORTHWESTERN UNIV,SCH MED,DEPT PEDIAT,CHICAGO,IL 60611. NIH,BETHESDA,MD 20892. UNIV ILLINOIS,COLL MED,CHICAGO,IL 60680. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A267 EP A267 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901581 ER PT J AU DONOVAN, EF EHRENKRANZ, RA TYSON, JE VERTER, JI WRIGHT, LL BALLARD, JL AF DONOVAN, EF EHRENKRANZ, RA TYSON, JE VERTER, JI WRIGHT, LL BALLARD, JL TI A COMPARISON OF THE BALLARD AND BEST OBSTETRICAL ESTIMATES OF GESTATIONAL-AGE (OBGA) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHD NEONATAL RES NETWORK,BETHESDA,MD. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A223 EP A223 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901320 ER PT J AU ELSOHLY, MA WALLS, HC LESTER, BM BAUER, CR SHANKARAN, S BADA, H WRIGHT, L SMERIGLIO, V KRAUSESTEINRAUF, H AF ELSOHLY, MA WALLS, HC LESTER, BM BAUER, CR SHANKARAN, S BADA, H WRIGHT, L SMERIGLIO, V KRAUSESTEINRAUF, H TI ANALYSIS OF MECONIUM SPECIMENS FOR DRUGS OF ABUSE .2. INDICATIONS OF PRENATAL EXPOSURE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 EL SOHLY LABS INC,OXFORD,MS. NICHHD,NEONATAL RES NETWORK,BETHESDA,MD. NR 0 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A83 EP A83 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900484 ER PT J AU ENGLUND, JA BAKER, CJ MCKINNEY, RE RASKINO, CL SCHOENFELD, DA WARA, DW AF ENGLUND, JA BAKER, CJ MCKINNEY, RE RASKINO, CL SCHOENFELD, DA WARA, DW TI LABORATORY CHARACTERISTICS OF CHILDREN ENROLLED INTO A RANDOMIZED, DOUBLE-BLIND TRIAL OF ANTIRETROVIRAL THERAPY (ACTG-152) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD. BAYLOR COLL MED,HOUSTON,TX 77030. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A179 EP A179 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901057 ER PT J AU ENGLUND, JA BAKER, CJ MCKINNEY, RE RASKINO, CL SCHOENFELD, DA PETRIE, BL LIFSCHITZ, MC ODONNEL, K WARA, DW FOWLER, MG AF ENGLUND, JA BAKER, CJ MCKINNEY, RE RASKINO, CL SCHOENFELD, DA PETRIE, BL LIFSCHITZ, MC ODONNEL, K WARA, DW FOWLER, MG TI CLINICAL CHARACTERISTICS OF CHILDREN ENROLLED INTO A RANDOMIZED, DOUBLE-BLIND TRIAL OF ANTIRETROVIRAL THERAPY (ACTG 152) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD. BAYLOR COLL MED,HOUSTON,TX 77030. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A179 EP A179 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901056 ER PT J AU ENGLUND, JA MINK, CM BLUMBERG, DA PICHICHERO, ME EDWARDS, KM CHERRY, JD DELORIA, MA AF ENGLUND, JA MINK, CM BLUMBERG, DA PICHICHERO, ME EDWARDS, KM CHERRY, JD DELORIA, MA TI UNITED-STATES MULTICENTER EVALUATION OF ACELLULAR DTP VACCINES IN USE IN THE SWEDISH FIELD TRIAL SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOUSTON,TX 77030. NIAID,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A112 EP A112 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900657 ER PT J AU FANAROFF, AA WRIGHT, LL VERTER, J DONOVAN, EF EHRENKRANZ, RA SHANKARAN, S STEVENSON, DK AF FANAROFF, AA WRIGHT, LL VERTER, J DONOVAN, EF EHRENKRANZ, RA SHANKARAN, S STEVENSON, DK TI DELIVERIES BETWEEN 24 AND 28 WEEKS GESTATION SHOULD OCCUR AT TERTIARY CENTERS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHD NEONATAL RES NETWORK,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A224 EP A224 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901326 ER PT J AU GENEVRO, JL ANDREASSEN, CJ BAGGEROER, CE AINBINDER, AM BORNSTEIN, MH AF GENEVRO, JL ANDREASSEN, CJ BAGGEROER, CE AINBINDER, AM BORNSTEIN, MH TI WHAT HAPPENS WHEN YOU GO TO THE DOCTOR - PRESCHOOLERS KNOWLEDGE OF ROUTINE PEDIATRIC CARE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A21 EP A21 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900112 ER PT J AU GUTMAN, L MOYE, J ZIMMER, B TIAN, C AF GUTMAN, L MOYE, J ZIMMER, B TIAN, C TI TUBERCULOSIS (TBC) IN HIV-EXPOSED OR INFECTED UNITED-STATES CHILDREN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 FRONTIER SCI,AMHERST,NY. WESTAT CORP,ROCKVILLE,MD. DUKE UNIV,DURHAM,NC 27706. NICHHD,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A181 EP A181 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901068 ER PT J AU HINSON, RM SHACTER, E AF HINSON, RM SHACTER, E TI INDUCTION OF IL-6 SYNTHESIS BY CYCLOOXYGENASE AND CAMP-ASSOCIATED PATHWAYS IN MURINE PERITONEAL-MACROPHAGES SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NCI,PATHOL 1 LAB,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT PEDIAT,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A12 EP A12 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900058 ER PT J AU KALER, SG GALLO, LK PROUD, VK PERCY, AK HOLMES, CS GOLDSTEIN, DS GAHL, WA AF KALER, SG GALLO, LK PROUD, VK PERCY, AK HOLMES, CS GOLDSTEIN, DS GAHL, WA TI A-]T TRANSVERSION AT THE +3 POSITION OF A SPLICE DONOR SITE IN THE MENKES GENE ASSOCIATED WITH A DISTINCTIVE PHENOTYPE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. UNIV ALABAMA,SCH MED,DEPT PEDIAT,BIRMINGHAM,AL 35294. NINCDS,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A152 EP A152 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900897 ER PT J AU KARRON, RA WRIGHT, PF MAKHENE, MK WILSON, MH CLEMENTS, ML MURPHY, B BELSHE, RB AF KARRON, RA WRIGHT, PF MAKHENE, MK WILSON, MH CLEMENTS, ML MURPHY, B BELSHE, RB TI A LIVE ATTENUATED HUMAN PARAINFLUENZA TYPE-3 VIRUS-VACCINE IS INFECTIOUS AND IMMUNOGENIC IN INFANTS AND YOUNG-CHILDREN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. VANDERBILT UNIV,NASHVILLE,TN 37240. NIH,LID,BETHESDA,MD 20892. ST LOUIS UNIV,ST LOUIS,MO 63103. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A183 EP A183 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901082 ER PT J AU KENNEY, LB BRASSEAUX, C NICHOLSON, HS REAMAN, GH BYRNE, J AF KENNEY, LB BRASSEAUX, C NICHOLSON, HS REAMAN, GH BYRNE, J TI CANCER AND BIRTH-DEFECTS IN THE OFFSPRING OF SURVIVORS OF CHILDHOOD LEUKEMIA (ALL) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,CHILDRENS NATL MED CTR,DEPT HEMATOL ONCOL,WASHINGTON,DC 20052. CHILDRENS CANC STUDY GRP,ARCADIA,CA. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A163 EP A163 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900960 ER PT J AU KOHN, DB WEINBERG, KI LENARSKY, C CROOKS, GM HANLEY, ME LAWRENCE, K ANNETT, G BROOKS, JS WARA, D ELDER, M WILLIAMSHERMAN, D BOWEN, T HERSHFIELD, MS BERENSON, RI MOEN, RC MULLEN, CA BLAESE, RM PARKMAN, R AF KOHN, DB WEINBERG, KI LENARSKY, C CROOKS, GM HANLEY, ME LAWRENCE, K ANNETT, G BROOKS, JS WARA, D ELDER, M WILLIAMSHERMAN, D BOWEN, T HERSHFIELD, MS BERENSON, RI MOEN, RC MULLEN, CA BLAESE, RM PARKMAN, R TI GENE-THERAPY FOR NEONATES WITH ADENOSINE-DEAMINASE (ADA) DEFICIENT SCID BY RETROVIRAL-MEDIATED TRANSFER OF THE HUMAN ADA CDNA INTO UMBILICAL-CORD CD34+ CELLS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,LOS ANGELES,CA 90027. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. CALGARY CHILDRENS HOSP,CALGARY,AB,CANADA. DUKE UNIV,DURHAM,NC 27706. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A152 EP A152 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900899 ER PT J AU KUMAR, ML MURPHY, BR DESIERRA, TM KRAL, P SUBBARAO, EK AF KUMAR, ML MURPHY, BR DESIERRA, TM KRAL, P SUBBARAO, EK TI MUCOSAL RESPIRATORY SYNCYTIAL VIRUS (RSV)-SPECIFIC IGA RESPONSES IN INFANTS FOLLOWING NATURAL RSV INFECTION SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HOSP INFANTIL MEXICO DR FEDERICO GOMEZ,MEXICO CITY,DF,MEXICO. CASE WESTERN RESERVE UNIV,METROHLTH MED CTR,DEPT PEDIAT,CLEVELAND,OH 44106. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A185 EP A185 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901091 ER PT J AU LANDAU, D DOMENE, H KHER, K ROBERTS, CT LEROITH, D AF LANDAU, D DOMENE, H KHER, K ROBERTS, CT LEROITH, D TI THE EFFECT OF HYPOPHYSECTOMY ON THE EXPRESSION OF THE RENAL INSULIN-LIKE GROWTH-FACTOR (IGF) SYSTEM IN PREPUBERTAL RATS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 GWU,CHILDRENS NATL MED CTR,SCH MED,DEPT PEDIAT,WASHINGTON,DC. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD. NIDDK,DIABET BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A368 EP A368 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77902184 ER PT J AU LIVINGSTON, RA HUTTON, N HALSEY, NA KLINE, RL JOYNER, M BUTZ, A QUINN, TC AF LIVINGSTON, RA HUTTON, N HALSEY, NA KLINE, RL JOYNER, M BUTZ, A QUINN, TC TI HIV-SPECIFIC IGA IN INFANTS BORN TO HIV-SEROPOSITIVE WOMEN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,DEPT PEDIAT,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,DEPT MED,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,DEPT INT HLTH,BALTIMORE,MD 21218. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH NURSING,BALTIMORE,MD 21218. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A186 EP A186 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901099 ER PT J AU MAGIAKOU, MA MASTORAKOS, G CHROUSOS, GP AF MAGIAKOU, MA MASTORAKOS, G CHROUSOS, GP TI FINAL STATURE IN PATIENTS WITH ENDOGENOUS CUSHING SYNDROME SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A103 EP A103 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900601 ER PT J AU MALLOY, MH HOFFMAN, HJ AF MALLOY, MH HOFFMAN, HJ TI APNEA MONITORING AND SUDDEN-INFANT-DEATH-SYNDROME (SIDS) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. NIDCD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A118 EP A118 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900691 ER PT J AU MARINI, JC WANG, Q AF MARINI, JC WANG, Q TI USE OF ANTISENSE OLIGONUCLEOTIDES TO SELECTIVELY SUPPRESS PRODUCTION OF THE MUTANT ALPHA-2(I) CHAIN IN OSTEOGENESIS IMPERFECTA TYPE-IV FIBROBLASTS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A153 EP A153 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900900 ER PT J AU MCGOWAN, KA MORALES, DE KLEINMAN, HK SCHNAPER, HW AF MCGOWAN, KA MORALES, DE KLEINMAN, HK SCHNAPER, HW TI ESTROGEN-RECEPTOR BINDING STIMULATES ANGIOGENIC ACTIVITIES OF ENDOTHELIAL-CELLS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. UNIV WASHINGTON,SCH MED,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A38 EP A38 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900214 ER PT J AU MOFENSON, L PELTON, S MOYE, J NUGENT, R KORELITZ, J BETHEL, J AF MOFENSON, L PELTON, S MOYE, J NUGENT, R KORELITZ, J BETHEL, J TI SINUSITIS IN HIV-INFECTED CHILDREN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,PAMA,BETHESDA,MD. WESTAT CORP,ROCKVILLE,MD. BOSTON UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02118. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A188 EP A188 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901113 ER PT J AU NUNEZ, SB BLYE, RP BARNES, KM MALLEY, JD CUTLER, GB AF NUNEZ, SB BLYE, RP BARNES, KM MALLEY, JD CUTLER, GB TI THE EFFECT OF THE AROMATASE INHIBITOR FADROZOLE (CGS-16949A) ON SUBSEQUENT FERTILITY AND HEALTH OF OFFSPRING IN MALE AND FEMALE RATS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NICHHD,CONTRACEPT DEV BRANCH,BETHESDA,MD 20892. NICHHD,DIV COMP RES & TECHNOL,STAT & MATH METHODOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A104 EP A104 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900608 ER PT J AU PAPILE, LA KRAUSESTEINRAUF, H WRIGHT, LL STOLL, BJ DONOVAN, EF BAUER, CR TYSON, JE VERTER, J AF PAPILE, LA KRAUSESTEINRAUF, H WRIGHT, LL STOLL, BJ DONOVAN, EF BAUER, CR TYSON, JE VERTER, J TI IDENTIFICATION OF VERY-LOW-BIRTH-WEIGHT INFANTS (VLBW) AT RISK FOR CHRONIC LUNG-DISEASE (CLD) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,NEONATAL RES NETWORK,BETHESDA,MD. NR 0 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A246 EP A246 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901456 ER PT J AU PIKIS, A AKRAM, S DONKERSLOOT, JA CAMPOS, JM RODRIGUEZ, WJ AF PIKIS, A AKRAM, S DONKERSLOOT, JA CAMPOS, JM RODRIGUEZ, WJ TI PREVALENCE OF PENICILLIN-RESISTANT S-PNEUMONIA IN SIGNIFICANT PEDIATRIC INFECTIONS - A YEAR EXPERIENCE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS NATL MED CTR,WASHINGTON,DC. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A147 EP A147 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900865 ER PT J AU RAY, PE BRUGGEMAN, LA WEEKS, BE KOPP, JB BRYANT, JL OWENS, JW NOTKINS, AL KLOTMAN, PE AF RAY, PE BRUGGEMAN, LA WEEKS, BE KOPP, JB BRYANT, JL OWENS, JW NOTKINS, AL KLOTMAN, PE TI BASIC FIBROBLAST GROWTH-FACTOR AND ITS LOW-AFFINITY RECEPTORS IN THE PATHOGENESIS OF HIV-ASSOCIATED NEPHROPATHY IN TRANSGENIC MICE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,NATL MED CTR,CRI,WASHINGTON,DC 20010. NIDR,LDB,BETHESDA,MD 20892. NIDR,LOM,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A371 EP A371 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77902206 ER PT J AU RAY, PE MCCUNE, BK GEARY, KM CAREY, RM KLOTMAN, PE GOMEZ, RA AF RAY, PE MCCUNE, BK GEARY, KM CAREY, RM KLOTMAN, PE GOMEZ, RA TI COREGULATION OF TGF-BETA-2 AND RENIN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,NATL MED CTR,CRI,WASHINGTON,DC 20010. NIDR,LOM,BETHESDA,MD 20892. UNIV VIRGINIA,MED CTR,SCH MED,CHARLOTTESVILLE,VA 22901. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A371 EP A371 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77902207 ER PT J AU READ, JS TROENDLE, JF KLEBANOFF, MA AF READ, JS TROENDLE, JF KLEBANOFF, MA TI POSTNEONATAL INFECTIOUS-DISEASE MORTALITY, UNITED-STATES, 1987 SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A120 EP A120 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900705 ER PT J AU ROSS, JL FEUILLAN, P LONG, L KOWAL, K CUTLER, GB AF ROSS, JL FEUILLAN, P LONG, L KOWAL, K CUTLER, GB TI LIPID ABNORMALITIES IN TURNER SYNDROME SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. THOMAS JEFFERSON UNIV,DEPT PEDIAT,PHILADELPHIA,PA 19107. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A206 EP A206 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901219 ER PT J AU SCHNAPER, HW MAZAR, A BARNATHAN, ES KLEINMAN, HK AF SCHNAPER, HW MAZAR, A BARNATHAN, ES KLEINMAN, HK TI UROKINASE-TYPE PLASMINOGEN-ACTIVATOR (UPA) ENHANCES ENDOTHELIAL-CELL DIFFERENTIATION THROUGH A NONPROTEOLYTIC MECHANISM INVOLVING UPA-RECEPTOR (UPAR) BINDING SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 ABBOTT LABS,N CHICAGO,IL 60064. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. NR 2 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A373 EP A373 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77902214 ER PT J AU SCHOLZ, TD BALABAN, RS AF SCHOLZ, TD BALABAN, RS TI MITOCHONDRIAL F1ATPASE ACTIVITY OF CANINE MYOCARDIUM - EFFECTS OF HYPOXIA AND STIMULATION SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV IOWA,DEPT PEDIAT,IOWA CITY,IA 52242. NIH,CARDIAC ENERGET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A41 EP A41 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900229 ER PT J AU SHANDAS, R SOLOWIEJCZYK, D JONES, M MANDULEY, R YAMADA, I CAYRE, R VALDESCRUZ, L AF SHANDAS, R SOLOWIEJCZYK, D JONES, M MANDULEY, R YAMADA, I CAYRE, R VALDESCRUZ, L TI EFFECTIVE FLOW AREAS OF BILEAFLET MECHANICAL MITRAL-VALVES - STUDIES IN AN IN-VITRO PULSATILE FLOW SYSTEM AND IN A CHRONIC ANIMAL-MODEL SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MAIMONIDES HOSP,DIV PEDIAT CARDIOL,BROOKLYN,NY 11219. COLUMBIA UNIV,NEW YORK,NY 10027. NHLBI,LAMS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A41 EP A41 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900234 ER PT J AU SHANKARAN, S BAIN, R BAUER, C WRIGHT, L ZACHARY, J AF SHANKARAN, S BAIN, R BAUER, C WRIGHT, L ZACHARY, J TI A MODEL OF PRENATAL AND PERINATAL RISK-FACTORS FOR GRADE-III-IV INTRACRANIAL HEMORRHAGE (ICH) IN 4795 LESS-THAN-1500G PRETERM INFANTS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,NEONATAL RES NETWORK,BETHESDA,MD. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A287 EP A287 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901702 ER PT J AU SHANKARAN, S BAIN, R BAUER, C WRIGHT, L ZACHARY, J AF SHANKARAN, S BAIN, R BAUER, C WRIGHT, L ZACHARY, J TI ANTENATAL STEROIDS REDUCES GRADE-III-IV INTRACRANIAL HEMORRHAGE IN LESS-THAN-1500G INFANTS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,NEONATAL RES NETWORK,BETHESDA,MD. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A255 EP A255 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901509 ER PT J AU SHENKER, A VANDOP, C GEFFNER, ME RABL, W CAREL, JC MERENDINO, JI VANGALEN, PIM KOSUGI, S AF SHENKER, A VANDOP, C GEFFNER, ME RABL, W CAREL, JC MERENDINO, JI VANGALEN, PIM KOSUGI, S TI HETEROGENEITY OF LUTEINIZING-HORMONE RECEPTOR (LHR) GENE-MUTATIONS IN FAMILIAL MALE PRECOCIOUS PUBERTY (FMPP) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,MED CTR,LOS ANGELES,CA 90024. TECH UNIV MUNICH,KINDERKLIN,W-8000 MUNICH 2,GERMANY. HOP ST VINCENT DE PAUL,F-75674 PARIS 14,FRANCE. ORGANON INT BV,OSS,NETHERLANDS. KYOTO UNIV,SCH MED,KYOTO 606,JAPAN. NR 0 TC 6 Z9 6 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A106 EP A106 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900623 ER PT J AU SPECTOR, SA BLANCHARD, S CONNOR, EM SALGO, MP MCNAMARA, J AF SPECTOR, SA BLANCHARD, S CONNOR, EM SALGO, MP MCNAMARA, J TI RESULTS OF A CLINICAL-TRIAL COMPARING 2 DOSES OF 2'3'-DIDEOXYCYTIDINE (DDC) IN THE TREATMENT OF CHILDREN WITH SYMPTOMATIC HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) INFECTION WHO WERE INTOLERANT OR HAD FAILED ZIDOVUDINE (ZDV) THERAPY (ACTG-138) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,NEWARK,NJ. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. HARVARD UNIV,CAMBRIDGE,MA 02138. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. NIAID,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A197 EP A197 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901162 ER PT J AU STRATAKIS, CA MAGIAKOU, MA MASTORAKOS, G PASSARO, M OLDFIELD, EH CUTLER, GB CHROUSOS, GP AF STRATAKIS, CA MAGIAKOU, MA MASTORAKOS, G PASSARO, M OLDFIELD, EH CUTLER, GB CHROUSOS, GP TI THYROID-FUNCTION IN CHILDREN WITH CUSHING DISEASE BEFORE AND AFTER SURGICAL CURE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A107 EP A107 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77900629 ER PT J AU TYSON, J STOLL, B EHRENKRANZ, R OH, W WRIGHT, L STEVENSON, D LEMONS, J VERTER, J AF TYSON, J STOLL, B EHRENKRANZ, R OH, W WRIGHT, L STEVENSON, D LEMONS, J VERTER, J TI VITAMIN-A TO PREVENT CHRONIC LUNG-DISEASE (CLD) IN VLBW INFANTS HAS THE DOSE BEEN TOO LOW SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,NEONATAL RES NETWORK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A321 EP A321 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901908 ER PT J AU WRIGHT, LL VERTER, J YOUNES, N FANAROFF, AA STEVENSON, D STOLL, B EHRENKRANZ, RA DONOVAN, EF SHANKARAN, S AF WRIGHT, LL VERTER, J YOUNES, N FANAROFF, AA STEVENSON, D STOLL, B EHRENKRANZ, RA DONOVAN, EF SHANKARAN, S TI THE EFFECT OF ANTENATAL STEROIDS ON THE RISK OF MORTALITY AND MORBIDITY IN LOW-BIRTH-WEIGHT (BW) INFANTS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD,NEONATAL RES NETWORK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1994 VL 35 IS 4 BP A261 EP A261 PN 2 PG 1 WC Pediatrics SC Pediatrics GA NG779 UT WOS:A1994NG77901549 ER PT J AU HALL, CB GRANOFF, DM GROMISCH, DS HALSEY, NA KOHL, S MARCUSE, EK MARKS, MI NANKERVIS, GA PICKERING, LK SCOTT, GB STEELE, RW YOGEV, R PETER, G BART, KJ BROOME, C HARDEGREE, MC JACOBS, RF MACDONALD, NE ORENSTEIN, WA RABINOVICH, NR SIBER, G FINLAYSON, J WATSON, JC AF HALL, CB GRANOFF, DM GROMISCH, DS HALSEY, NA KOHL, S MARCUSE, EK MARKS, MI NANKERVIS, GA PICKERING, LK SCOTT, GB STEELE, RW YOGEV, R PETER, G BART, KJ BROOME, C HARDEGREE, MC JACOBS, RF MACDONALD, NE ORENSTEIN, WA RABINOVICH, NR SIBER, G FINLAYSON, J WATSON, JC TI RECOMMENDED TIMING OF ROUTINE MEASLES IMMUNIZATION FOR CHILDREN WHO HAVE RECENTLY RECEIVED IMMUNE GLOBULIN PREPARATIONS SO PEDIATRICS LA English DT Article ID ANTIBODY-RESPONSE; VACCINE; POLIOVIRUS; EFFICACY; INFANTS C1 CANADIAN PAEDIAT SOC,OTTAWA,ON,CANADA. AMER ACAD PEDIAT,COMM INFECT DIS,EVANSTON,IL 60204. CTR DIS CONTROL & PREVENT,ATLANTA,GA. US FDA,BETHESDA,MD 20014. AMER THORAC SOC,NEW YORK,NY. NIH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 17 TC 5 Z9 6 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD APR PY 1994 VL 93 IS 4 BP 682 EP 685 PG 4 WC Pediatrics SC Pediatrics GA ND363 UT WOS:A1994ND36300030 ER PT J AU LONDON, SJ DALY, AK THOMAS, DC CAPORASO, NE IDLE, JR AF LONDON, SJ DALY, AK THOMAS, DC CAPORASO, NE IDLE, JR TI METHODOLOGICAL ISSUES IN THE INTERPRETATION OF STUDIES OF THE CYP2D6 GENOTYPE IN RELATION TO LUNG-CANCER RISK SO PHARMACOGENETICS LA English DT Letter ID SUSCEPTIBILITY; POLYMORPHISM; POPULATION; CYP1A1 C1 UNIV NEWCASTLE UPON TYNE,SCH MED,DEPT PHARMACOL SCI,PHARMACOGENET RES UNIT,NEWCASTLE TYNE NE2 4H4,ENGLAND. NCI,DIV CANC ETIOL,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP LONDON, SJ (reprint author), UNIV SO CALIF,SCH MED,DEPT PREVENT MED,PARKVIEW MED BLDG B306,1420 SAN PABLO ST,LOS ANGELES,CA 90033, USA. RI Daly, Ann/H-3144-2011; OI Daly, Ann/0000-0002-7321-0629; Idle, Jeff/0000-0002-6143-1520; London, Stephanie/0000-0003-4911-5290 NR 6 TC 20 Z9 20 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD APR PY 1994 VL 4 IS 2 BP 107 EP 108 DI 10.1097/00008571-199404000-00009 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA NP078 UT WOS:A1994NP07800009 PM 8081412 ER PT J AU SEIDLECK, BK THURKAUF, A WITKIN, JM AF SEIDLECK, BK THURKAUF, A WITKIN, JM TI EVALUATION OF ADCI AGAINST CONVULSANT AND LOCOMOTOR STIMULANT EFFECTS OF COCAINE - COMPARISON WITH THE STRUCTURAL ANALOGS DIZOCILPINE AND CARBAMAZEPINE SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE COCAINE; ANTICONVULSANTS; DIZOCILPINE; CARBAMAZEPINE; LOCOMOTOR ACTIVITY; MICE ID RAT-BRAIN; SENSITIZATION; SEIZURES; USERS; NMDA; AMPHETAMINE; ANTAGONISTS; RECEPTORS; MK-801; MICE AB Both the antiepileptic, carbamazepine, and the N-methyl-D-aspartate receptor antagonist, dizocilpine, have shown preclinical efficacy against behavioral and toxic effects of cocaine. Nonetheless, side effects or toxicity of these compounds either alone or in conjunction with cocaine are problematic. 5-Aminocarbonyl-10,11-dihydro-5h-dibenzo[a,d]cyclohepten-5,10-imine (ADCI), a molecular hybrid of these compounds, has been shown to have a broad anticonvulsant profile with a good protective index (behavioral TD50/anticonvulsant ED(50)). In male Swiss Webster mice, ADCI and dizocilpine produced dose-dependent protection against the convulsant effects of cocaine that were insensitive to carbamazepine. However, in contrast to dizocilpine, ADCI did not produce behavioral impairment on the inverted screen test demonstrating a protective index of greater than 15; the protective index for dizocilpine was 1.2. All three compounds attenuated the locomotor stimulant effects of cocaine without significantly decreasing locomotor activity on their own, although the cocaine antagonism was not always dose dependent. Only dizocilpine increased spontaneous locomotor activity when given alone and augmented the locomotor stimulant effects of cocaine. The results confirm the novel anticonvulsant activity of ADCI and its lack of phencyclidine-like behavioral side effects. The data also suggest a modest blocking action of these compounds against the locomotor stimulatory effects of cocaine. C1 NIDA,ADDICT RES CTR,PSYCHOBIOL SECT,DRUG DEV GRP,BALTIMORE,MD 21224. NEUROGEN CORP,BRANFORD,CT. NR 35 TC 14 Z9 14 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD APR PY 1994 VL 47 IS 4 BP 839 EP 844 DI 10.1016/0091-3057(94)90285-2 PG 6 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA NB496 UT WOS:A1994NB49600010 PM 8029253 ER PT J AU DEUTSCH, SI PARK, CH HITRI, A AF DEUTSCH, SI PARK, CH HITRI, A TI ALLOSTERIC EFFECTS OF A GABA RECEPTOR-ACTIVE STEROID ARE ALTERED BY STRESS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE STRESS; GABA(A); RECEPTOR COMPLEX; STEROIDS ID ANTISEIZURE EFFICACY; CHANNEL; BRAIN AB Recently, ring A reduced metabolites of naturally occurring steroids have been shown to act as allosteric modulators of GABA-gated chloride ion conductance. Specifically, 5 alpha-pregnane-3 alpha,21-diol-20-one (allotetrahydrodeoxycorticosterone; 5 alpha THDOC) was shown to be a positive allosteric effector. For example, 5 alpha-THDOC enhances the specific binding of [H-3]flunitrazepam, a benzodiazepine receptor agonist, among other pharmacological actions. Swim stress has been shown to reduce the ability of flurazepam, a prototypic benzodiazepine agonist, to antagonize the electrical precipitation of tonic hindlimb extension in mice. This stress-induced reduction in flurazepam's antiseizure efficacy persists for up to 72 h and is associated with alterations in the specific binding of ligands to the GABA(A) receptor complex. In the current study, the potentiation of [H-3]flunitrazepam binding by 5 alpha-THDOC was greater in cerebral cortical membranes prepared from stressed mice compared with unstressed controls. Moreover, nanomolar concentrations of 5 alpha-THDOC that were ineffective in potentiating the specific binding of [S-35]TBPS in cerebral cortical membranes prepared from unstressed control mice were capable of potentiating this binding in membranes prepared from stressed animals. Specifically, 50 nM 5 alpha-THDOC caused a 23% increase in the specific binding of [S-35]TBPS in membranes from stressed mice, whereas it was without any significant effect in unstressed controls. This apparent ability of 5 alpha-THDOC to distinguish between the binding of [S-35]TBPS to crude membranes prepared from stressed and unstressed control mice was eliminated in the presence of a 5 mu M concentration of GABA. The data are consistent with an effect of stress on the ability of a GABA-positive steroid to allosterically modulate the binding of both a benzodiazepine agonist and GABA(A)-associated channel ligand. These data provide additional support for a stress-induced alteration of the GABA(A) receptor complex. C1 DEPT VET AFFAIRS MED CTR,VA NIDA RES UNIT,WASHINGTON,DC 20422. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20007. RP DEUTSCH, SI (reprint author), DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,50 IRVING ST NW,WASHINGTON,DC 20422, USA. NR 14 TC 15 Z9 15 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD APR PY 1994 VL 47 IS 4 BP 913 EP 917 DI 10.1016/0091-3057(94)90296-8 PG 5 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA NB496 UT WOS:A1994NB49600021 PM 8029262 ER PT J AU COHEN, C PICKWORTH, WB BUNKER, EB HENNINGFIELD, JE AF COHEN, C PICKWORTH, WB BUNKER, EB HENNINGFIELD, JE TI CAFFEINE ANTAGONIZES EEG EFFECTS OF TOBACCO WITHDRAWAL SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE NICOTINE; CAFFEINE; WITHDRAWAL; EEG ID CIGARETTE-SMOKING BEHAVIOR; PHYSICAL-DEPENDENCE; COFFEE-DRINKING; PERFORMANCE; NICOTINE; HUMANS; PROFILES; SYMPTOMS; BATTERY AB Six current cigarette smokers and coffee drinkers were given combinations of 0, 150, or 300 mg caffeine and 0, 2, or 4 mg nicotine polacrilex following 12-h nicotine and caffeine abstinence. On one study day, subjects were allowed to smoke cigarettes and to drink caffeinated beverages and no drugs were given. Tobacco and caffeine abstinence impaired performance on the serial addition/subtraction and digit recall tasks; decreased scores on the MBG scale and ratings of ''clear-headed'' and ''quick-witted''; and increased ratings of ''irritability,'' ''muscular tension,'' ''headache,'' ''drowsy,'' ''clumsy,'' ''feeble,'' and ''dreamy.'' The deprivation caused characteristic EEG signs of nicotine withdrawal including increased theta power and decreased alpha frequency. These EEG effects were reversed by cigarette smoking and caffeine administration, but nicotine polacrilex was less effective. Deprivation-induced performance and subjective measures were not changed by administration of nicotine and caffeine combinations. C1 NIDA,ADDICT RES CTR,CLIN PHARMACOL LAB,BALTIMORE,MD 21224. NR 38 TC 13 Z9 13 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD APR PY 1994 VL 47 IS 4 BP 919 EP 926 DI 10.1016/0091-3057(94)90297-6 PG 8 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA NB496 UT WOS:A1994NB49600022 PM 8029263 ER PT J AU AULAKH, CS HILL, JL MURPHY, DL AF AULAKH, CS HILL, JL MURPHY, DL TI LITHIUM TREATMENT RESTORES CLONIDINES EFFECT IN AN ANIMAL-MODEL OF DEPRESSION SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Note DE ALPHA(2)-ADRENERGIC HETERORECEPTORS; 5-HT1C RECEPTORS; DEPRESSION; GROWTH HORMONE; FAWN-HOODED RAT ID LONG-TERM LITHIUM; SEROTONIN RELEASE; NEURO-ENDOCRINE; GROWTH-HORMONE; RAT-BRAIN; CHLOROPHENYLPIPERAZINE; RESPONSES; DECREASES; WISTAR AB IP administration of various doses of clonidine produces significant increases in growth hormone levels in the Wistar rats but not in the Fawn-Hooded (FH) rats, a rat strain suggested to be a genetic model of depression. However, short-term lithium treatment restores clonidine's effect on growth hormone levels in the Fawn-Hooded rats. Potentiation of clonidine's effect on growth hormone levels following short-term lithium treatment appears most likely due to increased serotonergic function as a consequence of enhanced 5-HT concentrations at postsynaptic 5-HT1C receptor sites. Thus, the reversal of a deficit state in Fawn-Hooded rats by lithium treatment supports earlier studies suggesting this rat strain to represent a genetic model of depression. RP AULAKH, CS (reprint author), NIMH,CTR CLIN,CLIN SCI LAB,BLDG 10,ROOM 3D41,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 17 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD APR PY 1994 VL 47 IS 4 BP 985 EP 987 DI 10.1016/0091-3057(94)90308-5 PG 3 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA NB496 UT WOS:A1994NB49600033 PM 8029274 ER PT J AU CHAMPOUX, M SUOMI, SJ AF CHAMPOUX, M SUOMI, SJ TI BEHAVIORAL AND ADRENOCORTICAL RESPONSES OF RHESUS MACAQUE MOTHERS TO INFANT SEPARATION IN AN UNFAMILIAR ENVIRONMENT SO PRIMATES LA English DT Article DE MACACA-MULATTA; SEPARATION; BEHAVIOR; CORTISOL; MOTHER-INFANT ID MONKEYS; RESTRAINT; CORTISOL; MULTIPLE AB The behavioral and adrenocortical responses of rhesus macaque mothers to a series of four consecutive 4-day separations from their 5-month old infants in an unfamiliar environment were examined. A biphasic behavioral response to separation was observed, with passive behavior, locomotion, and vocalization highest on Day 1 of separation, and self-directed behaviors and environmental exploration peaking during Days 2 - 4. Stereotyped locomotion increased, and passive behavior decreased, across successive weeks of separation. The rhesus mothers exhibited substantial cortisol elevations one and two hours postseparation, with cortisol decreasing on the fourth day of separation. The cortisol response was strongest during the first week of separation, but robust elevations occurred in response to repeated separations. No signs of behavioral depression were observed. The results indicate that infant separation combined with removal to a novel environment can be a potent stressor for rhesus macaque mothers. C1 NICHHD,BETHESDA,MD 20892. UNIV WISCONSIN,MADISON,WI 53706. NR 35 TC 11 Z9 12 U1 0 U2 1 PU JAPAN MONKEY CENTRE PI INUYAMA AICHI PA PRIMATES, EDITORIAL OFFICE, INUYAMA AICHI 484, JAPAN SN 0032-8332 J9 PRIMATES JI Primates PD APR PY 1994 VL 35 IS 2 BP 191 EP 202 DI 10.1007/BF02382054 PG 12 WC Zoology SC Zoology GA NG484 UT WOS:A1994NG48400008 ER PT J AU STRAUSS, KI KUZNICKI, J WINSKY, L JACOBOWITZ, DM AF STRAUSS, KI KUZNICKI, J WINSKY, L JACOBOWITZ, DM TI EXPRESSION AND RAPID PURIFICATION OF RECOMBINANT RAT CALRETININ - SIMILARITY TO NATIVE RAT CALRETININ SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article ID CALCIUM-BINDING PROTEIN; IMMUNOHISTOCHEMICAL LOCALIZATION; INSITU HYBRIDIZATION; NEURONS; BRAIN AB Rat calretinin coding region was subcloned into a prokaryotic expression vector (pGEX). The glutathione-S-transferase:calretinin fusion protein produced in Escherichia coli was purified on a glutathione-Sepharose affinity column. Recombinant rat calretinin was cleaved on the column by thrombin, eluted, and purified to homogeneity using DEAE-cellulose chromatography. Recombinant and native rat calretinin performed the same on DEAE columns, denaturing polyacrylamide gel electrophoresis (SDS-PAGE), Western blots, and Ca-45 overlay on nitrocellulose blots. The recombinant calretinin migrated similarly to the more basic (pi 5.3) of two forms of native calretinin demonstrated by two-dimensional SDS-PAGE. Calcium binding equilibria revealed identical apparent binding affinity and capacity. Difference(s) between native and recombinant did not affect the binding of calcium to calretinin or antibody recognition. Thus recombinant calretinin may be useful in the elucidation of possible cellular targets of native calretinin. (C) 1994 Academic Press, Inc. RP STRAUSS, KI (reprint author), NIMH,CLIN SCI LAB,BETHESDA,MD 20892, USA. NR 16 TC 19 Z9 19 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1046-5928 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD APR PY 1994 VL 5 IS 2 BP 187 EP 191 DI 10.1006/prep.1994.1029 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA NG675 UT WOS:A1994NG67500014 PM 8054853 ER PT J AU GRIKO, YV MAKHATADZE, GI PRIVALOV, PL HARTLEY, RW AF GRIKO, YV MAKHATADZE, GI PRIVALOV, PL HARTLEY, RW TI THERMODYNAMICS OF BARNASE UNFOLDING SO PROTEIN SCIENCE LA English DT Article DE BARNASE; HYDROGEN BONDING; HYDROPHOBIC INTERACTIONS; SCANNING MICROCALORIMETRY ID BACILLUS-AMYLOLIQUEFACIENS BARNASE; MOLAR HEAT-CAPACITY; PROTEIN STABILITY; AQUEOUS-SOLUTION; PH-DEPENDENCE; RIBONUCLEASE; RESIDUES; STABILIZATION; HYDRATION; CHAIN AB The thermodynamics of barnase denaturation has been studied calorimetrically over a broad range of temperature and pH. It is shown that in acidic solutions the heat denaturation of barnase is well approximated by a 2-state transition. The heat denaturation of barnase proceeds with a significant increase of heat capacity, which determines the temperature dependencies of the enthalpy and entropy of its denaturation. The partial specific heat capacity of denatured barnase is very close to that expected for the completely unfolded protein. The specific denaturation enthalpy value extrapolated to 130 degrees C is also close to the value expected for the full unfolding. Therefore, the calorimetrically determined thermodynamic characteristics of barnase denaturation can be considered as characteristics of its complete unfolding and can be correlated with structural features - the number of hydrogen bonds, extent of van der Waals contacts, and the surface areas of polar and nonpolar groups. Using this information and thermodynamic information on transfer of protein groups into water, the contribution of various factors to the stabilization of the native structure of barnase has been estimated. The main contributors to the stabilization of the native state of barnase appear to be intramolecular hydrogen bonds. The contributions of van der Waals interactions between nonpolar groups and those of hydration effects of these groups are not as large if considered separately, but the combination of these 2 factors, known as hydrophobic interactions, is of the same order of magnitude as the contribution of hydrogen bonding. C1 JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. RUSSIAN ACAD SCI,INST PROT RES,PUSHCHINO 142292,RUSSIA. NIDDKD,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM 48036-01] NR 35 TC 70 Z9 72 U1 3 U2 6 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0961-8368 J9 PROTEIN SCI JI Protein Sci. PD APR PY 1994 VL 3 IS 4 BP 669 EP 676 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NG253 UT WOS:A1994NG25300014 PM 8003984 ER PT J AU BREWERTON, TD KRAHN, DD HARDIN, TA WEHR, TA ROSENTHAL, NE AF BREWERTON, TD KRAHN, DD HARDIN, TA WEHR, TA ROSENTHAL, NE TI FINDINGS FROM THE SEASONAL PATTERN ASSESSMENT QUESTIONNAIRE IN PATIENTS WITH EATING DISORDERS AND CONTROL SUBJECTS - EFFECTS OF DIAGNOSIS AND LOCATION SO PSYCHIATRY RESEARCH LA English DT Article DE CIRCANNUAL RHYTHMS; BULIMIA NERVOSA; ANOREXIA NERVOSA; SEASONAL AFFECTIVE DISORDER ID BULIMIA-NERVOSA; LIGHT THERAPY; DEPRESSION; SEROTONIN; MOOD AB We previously reported a high degree of seasonality as measured by the Seasonal Pattern Assessment Questionnaire (SPAQ) in 41 patients with eating disorders (ED) compared with control subjects and patients with five other affective spectrum disorders. To clarify the relationship of the specific ED diagnosis and latitude to seasonal variation in a larger sample, we administered the SPAQ to 159 women with ED as defined by DSM-III-R. Subtype diagnoses were as follows: bulimia nervosa (BN), n = 109; anorexia nervosa (AN), n = 30; BN+AN, n = 20. Patients were studied at three locations: National Institute of Mental Health (NIMH), n = 46; Medical University of South Carolina (MUSC), n = 53; University of Michigan (UM), n = 60. The control group comprised 50 female normal volunteers studied at NIMH. There was a statistically significant difference in Global Seasonality Scale (GSS) scores among the four diagnostic groups, and all ED subtypes had significantly higher GSS scores than control subjects after post hoc Bonferroni t tests. Higher GSS scores were also found in patients with BN+AN compared with patients with BN or AN alone. The patterns of change were similar to those observed in winter seasonal affective disorder (SAD). Thirteen percent of the total sample of ED patients met SPAQ criteria for winter SAD, with 2.5% each for summer SAD and subsyndromal SAD. UM BN patients (latitude 42 degrees N) had higher GSS scores and a higher prevalence of winter SAD than MUSC BN patients (latitude 33 degrees N), but this difference was not statistically significant. These data support the hypothesis that ED and SAD may involve similar pathophysiological mechanisms, possibly related to serotonin dysregulation. C1 MED UNIV S CAROLINA,EATING DISORDERS PROGRAM,CHARLESTON,SC 29425. UNIV WISCONSIN,VET ADM HOSP,DEPT PSYCHIAT,MADISON,WI. NIMH,CLIN PSYCHOBIOL BRANCH,OUTPATIENT SERV,BETHESDA,MD 20892. RP BREWERTON, TD (reprint author), MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 30 TC 32 Z9 32 U1 1 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD APR PY 1994 VL 52 IS 1 BP 71 EP 84 DI 10.1016/0165-1781(94)90121-X PG 14 WC Psychiatry SC Psychiatry GA NK809 UT WOS:A1994NK80900008 PM 8047623 ER PT J AU MILLER, DL DOPPMAN, JL AF MILLER, DL DOPPMAN, JL TI LOCALIZATION OF ENDOCRINE TUMORS WITH RADIOLABELED OCTREOTIDE SO RADIOLOGY LA English DT Letter ID SOMATOSTATIN; DIAGNOSIS C1 USN,NATL MED CTR,DEPT RADIOL,BETHESDA,MD 20889. RP MILLER, DL (reprint author), NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BLDG 10,BETHESDA,MD 20892, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 1994 VL 191 IS 1 BP 289 EP 290 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA NB685 UT WOS:A1994NB68500061 PM 8166870 ER PT J AU THORGEIRSSON, UP DALGARD, DW REEVES, J ADAMSON, RH AF THORGEIRSSON, UP DALGARD, DW REEVES, J ADAMSON, RH TI TUMOR-INCIDENCE IN A CHEMICAL CARCINOGENESIS STUDY OF NONHUMAN-PRIMATES SO REGULATORY TOXICOLOGY AND PHARMACOLOGY LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; COOKED FOOD; HEPATOCELLULAR-CARCINOMA; HETEROCYCLIC AMINES; HODGKINS-DISEASE; BLADDER-CANCER; P53 GENE; INDUCTION; RATS; CHEMOTHERAPY AB This report covers a 32-year period of an ongoing chemical carcinogenesis study in nonhuman primates, which was initiated by the National Cancer Institute in 1961. Autopsy records of 373 breeders and normal controls showed very law incidence of spontaneous malignant tumors in cynomolgus (1.5%) and rhesus (2.8%) monkeys, but considerably higher incidence in African green monkeys (8%). A large number of substances including a variety of food additives, food components, environmental contaminants, N-nitroso compounds, ''classical'' rodent carcinogens, antineoplastic agents, and immunosuppressive agents have been evaluated for long-term carcinogenic activity. Food components tested which are probably most relevant to human exposure are the artificial sweeteners, cyclamate and saccharin. After 22 years of continuous dosing, neither cyclamate nor saccharin have shown any evidence of carcinogenic effects. Similarly, the tumorigenic potential of arsenic and DDT was negligible after dosing for 15-22 years. In contrast, the fungal food contaminants, aflatoxin B-1 (AFB(1)) and sterigmatocystin (SMT), were found to be potent hepatocarcinogens. AFB, also induced adenocarcinomas of the pancreas, osteosarcomas, and other tumors. Also, the aglycone of cycasin, MAM acetate, induced a variety of tumors, but primarily hepatocellular and renal cell carcinomas. The compounds most recently introduced into the colony include three heterocyclic amines present in cooked meat. One of these compounds, 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) has proven to be one of the most potent hepatocarcinogens in the history of the monkey project, inducing malignant liver tumors in 65% of animals over a 7-year period of exposure. Of the classical rodent carcinogens studied, urethane was the only one which produced malignant tumors in the monkeys. Conversely, all except two of the N-nitroso compounds were carcinogenic. Diethylnitrosamine (DENA) was the most potent and predictable hepatocarcinogen in cynomolgus, rhesus, and African green monkeys. However, when administered intraperitoneally to galagos (a prosimian), DENA induced primarily mucoepidermoid carcinoma of the nasal cavity. N-Methyl-N-nitrosourea (MNU) was the only carcinogen persistently producing tumors in the digestive tract, mostly squamous cell carcinomas of the esophagus. Among the antineoplastic and immunosuppressive agents, procarbazine (MIH) was the only unequivocal carcinogen, with a 33% tumor incidence, causing acute nonlymphocytic leukemia in most of the cases. (C) 1994 Academic Press, Inc. C1 HAZLETON AMER INC,VIENNA,VA. RP THORGEIRSSON, UP (reprint author), NCI,DIV CANC ETIOL,BETHESDA,MD 20892, USA. NR 72 TC 101 Z9 104 U1 0 U2 16 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0273-2300 J9 REGUL TOXICOL PHARM JI Regul. Toxicol. Pharmacol. PD APR PY 1994 VL 19 IS 2 BP 130 EP 151 DI 10.1006/rtph.1994.1013 PG 22 WC Medicine, Legal; Pharmacology & Pharmacy; Toxicology SC Legal Medicine; Pharmacology & Pharmacy; Toxicology GA NH670 UT WOS:A1994NH67000001 PM 8041912 ER PT J AU LAI, DY BAETCKE, KP VU, VT COTRUVO, JA EUSTIS, SL AF LAI, DY BAETCKE, KP VU, VT COTRUVO, JA EUSTIS, SL TI EVALUATION OF REDUCED PROTOCOLS FOR CARCINOGENICITY TESTING OF CHEMICALS - REPORT OF A JOINT EPA/NIEHS WORKSHOP SO REGULATORY TOXICOLOGY AND PHARMACOLOGY LA English DT Article ID POTENCY DATABASE; ANIMAL BIOASSAYS; CHRONOLOGICAL SUPPLEMENT; RODENTS AB The current U.S. Environmental Protection Agency (EPA) and other national/international guidelines specify the use of two species and two sexes of rodents (usually the rat and the mouse) for carcinogenicity testing of chemicals. In view of the enormous number of chemicals to be tested, the high cost of testing, and the large number of animals used in the present protocol, many academic, industrial, and government authorities are examining the possibility of using a reduced protocol (less than two species and two sexes of rodents) for carcinogenicity testing of chemicals. The use of a reduced protocol offers many advantages as well as some disadvantages. To pursue further the potential implications and impacts of using a reduced protocol for carcinogenicity testing on the processes of hazard identification and risk assessment, a workshop entitled ''Evaluation of Reduced Protocols for Carcinogenicity Testing of Chemicals'' was held at the Embassy Suites Hotel in Alexandria, Virginia on September 22 and 23, 1992. It was cosponsored by EPA's Office of Prevention, Pesticides and Toxic Substances (OPPTS) and the National Toxicology Program of the National Institutes of Environmental Health Sciences (NTP/NIEHS) and attended by more than 60 participants from government, industry, academia, and the general public. The Expert Consensus Panel and most of the participants supported the use of reduced protocols in carcinogenicity testing. However, it was recognized that reduced protocols may not be appropriate for the testing of all chemicals and that additional analyses/data may be needed for selection of the most appropriate reduced protocol for certain chemicals/chemical classes. (C) 1994 Academic Press, Inc. C1 NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. RP LAI, DY (reprint author), US EPA,OFF PREVENT PESTICIDES & TOX SUBSTANCES,401 M ST,SW,WASHINGTON,DC 20460, USA. NR 18 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0273-2300 J9 REGUL TOXICOL PHARM JI Regul. Toxicol. Pharmacol. PD APR PY 1994 VL 19 IS 2 BP 183 EP 201 DI 10.1006/rtph.1994.1017 PG 19 WC Medicine, Legal; Pharmacology & Pharmacy; Toxicology SC Legal Medicine; Pharmacology & Pharmacy; Toxicology GA NH670 UT WOS:A1994NH67000005 PM 8041916 ER PT J AU HITRAK, J HUBBARD, SM FODOR, M GALLARDO, J AF HITRAK, J HUBBARD, SM FODOR, M GALLARDO, J TI CANCERFAX - NEW INFORMATION-SYSTEM FOR THE TREATMENT OF CANCER SO REVISTA MEDICA DE CHILE LA Spanish DT Article ID PDQ C1 NIH,INST NACL CANC,CTR INFORMAC INTERNACIONALES,BETHESDA,MD 20892. UNIV CHILE,HOSP J J AGUIRRE,FAC MED,DEPT MED,SECC ONCOL,SANTIAGO,CHILE. RP HITRAK, J (reprint author), UNIV CHILE,INT UNIV EXCHANGE INC,WASHINGTON,DC, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU SOC MEDICA SANTIAGO PI SANTIAGO 9 PA BERNARDA MORIN 488 PROVIDENCIA, CASILLA 168 CORREO 55, SANTIAGO 9, CHILE SN 0034-9887 J9 REV MED CHILE JI Rev. Medica Chile PD APR PY 1994 VL 122 IS 4 BP 477 EP 479 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA NR156 UT WOS:A1994NR15600018 ER PT J AU TOMANA, M SCHROHENLOHER, RE BENNETT, PH DELPUENTE, A KOOPMAN, WJ AF TOMANA, M SCHROHENLOHER, RE BENNETT, PH DELPUENTE, A KOOPMAN, WJ TI OCCURRENCE OF DEFICIENT GALACTOSYLATION OF SERUM IGG PRIOR TO THE ONSET OF RHEUMATOID-ARTHRITIS SO RHEUMATOLOGY INTERNATIONAL LA English DT Article DE GALACTOSYLATION OF IGG; RHEUMATOID ARTHRITIS; PIMA AND PAPAGO INDIANS ID GLYCOSYLATION; DISEASE AB Previous reports have shown that deficient galactosylation of serum IgG occurs in patients with rheumatoid arthritis (RA) and other autoimmune disorders. In this study, we investigated the relationship between galactosylation of serum IgG and disease status in a population of Pima and Papago Indians, who are characterized by a frequent occurrence of RA. The mean galactose levels of serum IgG collected from 11 individuals 1.5-10 years prior to onset (T1), at onset (T2), and 1.7-7 years post-onset (T3) of RA were lower than those from 25 seronegative controls without RA from the same population (P=0.01, 0.005, and less than or equal to 0.001, respectively). The mean galactose content of IgG decreased in the order T1>T2>T3, but the differences were not significant. The galactosylation of serum IgG from the RA patients did not differ from that of seropositive Pima Indian controls who did not develop RA over the course of study. The occurrence of IgG galactose deficiency in individuals with RA prior to the onset of the disease supports the contention that this phenomenon may be a risk factor for the development of RA. Furthermore, the occurrence of IgG galactose deficiency in healthy seropositive individuals suggests a relationship between diminished galactosylation and induction of rheumatoid factor (RF). C1 VET ADM MED CTR,BIRMINGHAM,AL. NIH,PHOENIX,AZ. RP TOMANA, M (reprint author), UNIV ALABAMA,DEPT MED,DIV CLIN IMMUNOL & RHEUMATOL,CH19,UAB STN,BIRMINGHAM,AL 35294, USA. NR 14 TC 11 Z9 11 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0172-8172 J9 RHEUMATOL INT JI Rheumatol. Int. PD APR PY 1994 VL 13 IS 6 BP 217 EP 220 DI 10.1007/BF00290198 PG 4 WC Rheumatology SC Rheumatology GA NJ135 UT WOS:A1994NJ13500001 ER PT J AU BRESLIN, NA SUDDATH, RL BISSETTE, G NEMEROFF, CB LOWRIMORE, P WEINBERGER, DR AF BRESLIN, NA SUDDATH, RL BISSETTE, G NEMEROFF, CB LOWRIMORE, P WEINBERGER, DR TI CSF CONCENTRATIONS OF NEUROTENSIN IN SCHIZOPHRENIA - AN INVESTIGATION OF CLINICAL AND BIOCHEMICAL CORRELATES SO SCHIZOPHRENIA RESEARCH LA English DT Article DE NEUROTENSIN; SCHIZOPHRENIA; HALOPERIDOL; CEREBROSPINAL FLUID; MONOAMINE ID NEUROLEPTIC TREATMENT; NUCLEUS-ACCUMBENS; HUMAN-BRAIN; RAT-BRAIN; NEUROPEPTIDES; DRUGS AB Neurotensin (NT), a peptide which colocalizes with dopamine in some midbrain and hypothalamic neurons, has been speculated to play a role in schizophrenic illness and in the action of antipsychotic drugs. Previous work suggested a bimodal distribution of NT in patients with schizophrenia, with a subgroup having low drug-free NT concentrations which normalize with neuroleptic treatment. We studied 15 schizophrenic patients with CSF samples collected both off and on neuroleptic medication, 12 with only drug-free (DF) samples, and 10 controls. There was no significant difference in CSF NT concentrations between patients and controls, or between patients off and on medication. However, 7 patients with DFNT CSF concentrations below the patient mean showed an increase with neuroleptic treatment. Moreover, NT was significantly lower for women. Significant correlations with NT concentrations in CSF were found with deficit symptoms in patients, and with the age of the CSF sample for all subjects. There was no correlation between CSF NT concentrations and patient age, duration of illness, or levels of amine metabolites (MHPG, 5HIAA, HVA). C1 NIMH,CTR NEUROSCI,INTRAMURAL RES PROGRAM,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. GEORGE WASHINGTON UNIV,DEPT PSYCHIAT & BEHAV SCI,WASHINGTON,DC 20037. DUKE UNIV,MED CTR,DEPT PSYCHIAT,DURHAM,NC 27710. EMORY UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,ATLANTA,GA 30322. RP BRESLIN, NA (reprint author), NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. FU NIMH NIH HHS [NIMH MH-39415] NR 22 TC 46 Z9 47 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD APR PY 1994 VL 12 IS 1 BP 35 EP 41 DI 10.1016/0920-9964(94)90082-5 PG 7 WC Psychiatry SC Psychiatry GA NE941 UT WOS:A1994NE94100005 PM 7517175 ER PT J AU COLLINS, FS AF COLLINS, FS TI COLON-CANCER SCREENING - RESPONSE SO SCIENCE LA English DT Letter RP COLLINS, FS (reprint author), NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 1 PY 1994 VL 264 IS 5155 BP 13 EP 14 DI 10.1126/science.264.5155.13-a PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND536 UT WOS:A1994ND53600003 ER PT J AU KLEIN, HG AF KLEIN, HG TI IMMUNOLOGICAL ASPECTS OF BLOOD-TRANSFUSION SO SEMINARS IN ONCOLOGY LA English DT Article; Proceedings Paper CT Symposium on New Approaches to the Treatment of Cancer-Related Anemia CY OCT 23, 1993 CL NEW YORK HOSP, CORNELL MED CTR, NEW YORK, NY SP ORTHO BIOTECH INC, R W JOHNSON PHARM RES INST HO NEW YORK HOSP, CORNELL MED CTR ID HUMAN-IMMUNODEFICIENCY-VIRUS; RECURRENT SPONTANEOUS-ABORTION; HOMOLOGOUS BLOOD; INFECTION; SURGERY; CANCER; DISEASE; CELLS; COLON; ACTIVATION RP KLEIN, HG (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892, USA. NR 35 TC 32 Z9 33 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 1994 VL 21 IS 2 SU 3 BP 16 EP 20 PG 5 WC Oncology SC Oncology GA NR594 UT WOS:A1994NR59400004 PM 8202721 ER PT J AU ADAMSON, JW SPIVAK, JL KLEIN, HG HENRY, DH DENTON, T SILVER, RT AF ADAMSON, JW SPIVAK, JL KLEIN, HG HENRY, DH DENTON, T SILVER, RT TI NEW APPROACHES TO THE TREATMENT OF CANCER-RELATED ANEMIA - A PANEL DISCUSSION SO SEMINARS IN ONCOLOGY LA English DT Discussion C1 CORNELL UNIV,MED CTR,NEW YORK HOSP,NEW YORK,NY 10021. JOHNS HOPKINS UNIV,SCH MED,DIV HEMATOL,BALTIMORE,MD 21205. NEW YORK BLOOD CTR,LINDSLEY F KIMBALL RES INST,NEW YORK,NY 10021. NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892. GRAD HOSP PHILADELPHIA,PHILADELPHIA,PA 19146. CEDARS SINAI MED CTR,DIV CARDIOTHORAC SURG,LOS ANGELES,CA 90048. NR 0 TC 1 Z9 1 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 1994 VL 21 IS 2 SU 3 BP 36 EP 41 PG 6 WC Oncology SC Oncology GA NR594 UT WOS:A1994NR59400007 ER PT J AU DRABICK, JJ MAGILL, AJ SMITH, KJ NUTMAN, TB BENSON, PM AF DRABICK, JJ MAGILL, AJ SMITH, KJ NUTMAN, TB BENSON, PM TI HYPEREOSINOPHILIC SYNDROME-ASSOCIATED WITH HIV-INFECTION SO SOUTHERN MEDICAL JOURNAL LA English DT Note ID IMMUNODEFICIENCY-VIRUS INFECTION; IMMUNE-DEFICIENCY SYNDROME; BONE-MARROW CULTURES; SELECTIVE LOSS; IGE SYNTHESIS; HOST-DISEASE; SERUM IGE; INTERLEUKIN-5; EOSINOPHILS; MANIFESTATIONS AB A hypereosinophilic syndrome associated with dermatitis has been observed rarely in association with HIV infection. We describe the case of a young man with AIDS who came to us with a diffuse cutaneous eruption, fever, angioedema, eosinophilia, and a mildly elevated serum IgE level. No allergic or infectious cause of this illness could be determined, and the patient was treated with corticosteroids and PUVA therapy, resulting in complete resolution of the dermatitis and associated findings. In this case, there were clinical and histopathologic similarities to the idiopathic hypereosinophilic syndrome and to acute graft-versus-host disease. The serum level of the cytokine interleukin-5 (IL-5), which is associated with eosinophil production, was found to be mildly elevated during the peak of the eruption, while samples drawn previously and subsequently were not. Although it appears that the syndrome we describe is associated with the measurably elevated level of IL-5, further investigation is required to determine whether there is a cause and effect relationship between IL-5 and this entity. A brief review of the literature concerning eosinophils and HIV infection is also presented in the context of this case. C1 WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. NIH,BETHESDA,MD 20892. RP DRABICK, JJ (reprint author), WALTER REED ARMY INST RES,DEPT BACTERIAL DIS,WASHINGTON,DC 20307, USA. NR 43 TC 19 Z9 20 U1 0 U2 0 PU SOUTHERN MEDICAL ASSN PI BIRMINGHAM PA 35 LAKESHORE DR PO BOX 190088, BIRMINGHAM, AL 35219 SN 0038-4348 J9 SOUTHERN MED J JI South.Med.J. PD APR PY 1994 VL 87 IS 4 BP 525 EP 529 DI 10.1097/00007611-199404000-00021 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA NG281 UT WOS:A1994NG28100022 PM 8153785 ER PT J AU ZENILMAN, ME ROSLYN, JJ AF ZENILMAN, ME ROSLYN, JJ TI SURGERY IN THE ELDERLY PATIENT .2. PREFACE SO SURGICAL CLINICS OF NORTH AMERICA LA English DT Editorial Material C1 MED COLL PENN,DEPT SURG,PHILADELPHIA,PA 19129. RP ZENILMAN, ME (reprint author), NIA,FRANCIS SCOTT KEY MED CTR,DEPT SURG,BALTIMORE,MD 21224, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0039-6109 J9 SURG CLIN N AM JI Surg. Clin.-North Am. PD APR PY 1994 VL 74 IS 2 BP R13 EP R13 PG 1 WC Surgery SC Surgery GA NH337 UT WOS:A1994NH33700001 ER PT J AU SCHEFFEL, U KIM, S CLINE, EJ KUHAR, MJ AF SCHEFFEL, U KIM, S CLINE, EJ KUHAR, MJ TI OCCUPANCY OF THE SEROTONIN TRANSPORTER BY FLUOXETINE, PAROXETINE, AND SERTRALINE - IN-VIVO STUDIES WITH [I-125] RTI-55 SO SYNAPSE LA English DT Article DE FLUOXETINE; PAROXETINE; SERTRALINE; [I-125]RTI-55; MOUSE BRAIN; SEROTONIN TRANSPORTER; ANTIDEPRESSANT ID I-125 RTI-55; DOPAMINE TRANSPORTERS; UPTAKE INHIBITOR; H-3 PAROXETINE; UPTAKE SITES; BINDING; POTENT; BRAIN; PHARMACOLOGY; REUPTAKE AB [I-125]RTI-55 was used in tracer doses to label serotonin (5-HT) transporters in vivo in the mouse brain. Fluoxetine, paroxetine, and sertraline, potent antidepressants and selective inhibitors of serotonin transporter sites, were administered in various doses and at various times. The doses and times that result in significant binding of the drugs to transporters correspond to doses and times where they are reported to have physiological effects. Estimates of occupancy rate and duration of binding to serotonin transporters were made. The rate of occupancy of the 5-HT transporter site was fastest for sertraline, intermediate for paroxetine and slowest for fluoxetine. Similarly, the duration of occupancy was significantly shorter for sertraline and paroxetine (approximately 10 h) than for fluoxetine (approximately 50 h). The results indicate that in competition studies, [I-125]RTI-55 can be used to identify doses of drugs that are physiologically effective, to determine their relative rate of occupancy, and most importantly, to measure the residency time on the central serotonin transporter in vivo. (C) 1994 Wiley-Liss, Inc. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT RADIOL,DIV NUCL MED,BALTIMORE,MD 21205. NIDA,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224. FU NIDA NIH HHS [DA 06309]; NINDS NIH HHS [NS 15080] NR 31 TC 37 Z9 37 U1 2 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-4476 J9 SYNAPSE JI Synapse PD APR PY 1994 VL 16 IS 4 BP 263 EP 268 DI 10.1002/syn.890160403 PG 6 WC Neurosciences SC Neurosciences & Neurology GA ND354 UT WOS:A1994ND35400002 PM 8059336 ER PT J AU RAMIREZ, AN MARTIN, BM GURROLA, GB POSSANI, LD AF RAMIREZ, AN MARTIN, BM GURROLA, GB POSSANI, LD TI ISOLATION AND CHARACTERIZATION OF A NOVEL TOXIN FROM THE VENOM OF THE SCORPION CENTRUROIDES LIMPIDUS LIMPIDUS KARSCH SO TOXICON LA English DT Article ID AMINO-ACID-SEQUENCE; POTASSIUM CHANNELS; BRAIN SYNAPTOSOMES; TECOMANUS HOFFMANN; TITYUS-SERRULATUS; NEUROTOXINS; NOXIUS; BINDING AB A novel peptide, toxic to mice, was purified from the venom of the Mexican scorpion Centruroides limpidus limpidus, by means of gel filtration and ion exchange chromatography, followed by high performance liquid chromatography (HPLC). The complete amino acid sequence was determined by automatic Edman degradation of reduced and alkylated toxin, and by overlapping sequences of fragments of the toxin, generated by cleavage with proteinase V8 separated by HPLC. This toxin is composed of 66 amino acid residues, contains eight half-cystine residues, and is highly similar (91%) to the amino acid sequence deduced for toxin 1 of C. limpidus tecomanus and toxin 4 from C. noxius venom (89%). This peptide displaces the binding of radiolabeled toxin 2 of C. noxius from synaptosomal membranes of rat brain with superimposable kinetics, supporting the conclusion that it belongs to the beta-scorpion toxin class. Further characterization of C. l. limpidus toxin 1, as we have named it, was performed by means of competition experiments with monoclonal antibodies and various purified scorpion toxins, using an ELISA assay. A panel of six distinct monoclonal antibodies (mAB) against toxin 2 and 3 of C. noxius was used. From these, only three clones, originally named BCF1, BCF8 and BCF9, were able to recognize toxin 1 from C. l. limpidus. C1 UNIV NACL AUTONOMA MEXICO,INST BIOTECNOL,DEPT BIOQUIM,CUERNAVACA 62270,MORELOS,MEXICO. NIMH,CLIN NEUROSCI BRANCH,MOLEC NEUROGENET SECT,BETHESDA,MD 20892. RI Possani, Lourival/J-2397-2013 NR 32 TC 21 Z9 22 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0041-0101 J9 TOXICON JI Toxicon PD APR PY 1994 VL 32 IS 4 BP 479 EP 490 DI 10.1016/0041-0101(94)90300-X PG 12 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA NK681 UT WOS:A1994NK68100010 PM 8053002 ER PT J AU PERFETTI, R EGAN, JM ZENILMAN, ME SHULDINER, AR AF PERFETTI, R EGAN, JM ZENILMAN, ME SHULDINER, AR TI EXPRESSION OF THE REGENERATING GENE IN THE PANCREAS OF AGING MICE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 4th International Congress on Pancreas and Islet Transplantation CY JUN 27-30, 1993 CL AMSTERDAM, NETHERLANDS SP BAYER NEDERLAND, BAYER AG, BOEHRINGER MANNHEIM CORP, CILAG NV SA, DU PONT PHARMA, ELI LILLY, HOECHST AG, INST RECH INT SERVIER, JOHNSON & JOHNSON, KLM ROYAL DUTCH AIRLINES, NOVO NORDISK FARMA BV, SYNTEX BV C1 JOHNS HOPKINS UNIV,SCH MED,DEPT GERONTOL & GERIATR MED,BALTIMORE,MD. RP PERFETTI, R (reprint author), NIA,GERONTOL RES CTR,DIABET UNIT,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 4 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1994 VL 26 IS 2 BP 733 EP 733 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA NH683 UT WOS:A1994NH68300196 PM 7513468 ER PT J AU KOONIN, EV AF KOONIN, EV TI YEAST PROTEIN CONTROLLING INTER-ORGANELLE COMMUNICATION IS RELATED TO BACTERIAL PHOSPHATASES CONTAINING THE HSP70-TYPE ATP BINDING DOMAIN SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Note ID ALIGNMENT RP KOONIN, EV (reprint author), NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 10 TC 29 Z9 30 U1 1 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0968-0004 J9 TRENDS BIOCHEM SCI JI Trends Biochem.Sci. PD APR PY 1994 VL 19 IS 4 BP 156 EP 157 DI 10.1016/0968-0004(94)90275-5 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NG588 UT WOS:A1994NG58800004 PM 8016863 ER PT J AU HENGEN, PN AF HENGEN, PN TI METHODS AND REAGENTS - ON THE MAGIC OF MINI-PREPS SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Software Review ID DNA; PURIFICATION AB Methods and reagents is a unique monthly column that highlights current discussions in the newsgroup bionet.molbio.methds-reagnts, available on the Internet. This month's column discusses the problems encountered by some people when switching from Promega's MagicTM mini-prep plasmid DNA isolation columns to their new WizardTM mini-prep kits. For details on how to partake in the newsgroup, see the accompanying box. RP HENGEN, PN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702, USA. NR 5 TC 5 Z9 5 U1 0 U2 3 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0968-0004 J9 TRENDS BIOCHEM SCI JI Trends Biochem.Sci. PD APR PY 1994 VL 19 IS 4 BP 182 EP 183 DI 10.1016/0968-0004(94)90283-6 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NG588 UT WOS:A1994NG58800012 PM 8016871 ER PT J AU MCMILLIAN, MK THAI, L HONG, JS OCALLAGHAN, JP PENNYPACKER, KR AF MCMILLIAN, MK THAI, L HONG, JS OCALLAGHAN, JP PENNYPACKER, KR TI BRAIN INJURY IN A DISH - A MODEL FOR REACTIVE GLIOSIS SO TRENDS IN NEUROSCIENCES LA English DT Article ID NERVE GROWTH-FACTOR; GLUTAMINE-SYNTHETASE; MESSENGER-RNA; ASTROCYTES; NEURONS; CULTURES; INVITRO; SYSTEM AB Reactive gliosis is a powerful response to brain injury and subsequent neuronal damage in vivo. Neuronal cell cultures are now well established as assays to study this process in vitro. However, equivalent studies of purified glial cell populations have only recently been achieved, following the realization that glial cells produce many of the neuropeptides, transmitters and growth factors that are produced also by neurons. There is now scope for studies in vitro that use mixed, identified populations of glial and neuronal cells to dissect the interactions between the two. Such cultures also lend themselves to assays for potential therapeutic strategies for brain injury that take account of all the different cell types found in the brain. C1 US EPA,RES TRIANGLE PK,NC 27709. RP MCMILLIAN, MK (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709, USA. RI Pennypacker, Keith/I-5092-2012; O'Callaghan, James/O-2958-2013 NR 38 TC 177 Z9 180 U1 0 U2 4 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD APR PY 1994 VL 17 IS 4 BP 138 EP 142 DI 10.1016/0166-2236(94)90086-8 PG 5 WC Neurosciences SC Neurosciences & Neurology GA ND240 UT WOS:A1994ND24000003 PM 7517589 ER PT J AU GERNA, G SEARS, J HOSHINO, Y STEELE, AD NAKAGOMI, O SARASINI, A FLORES, J AF GERNA, G SEARS, J HOSHINO, Y STEELE, AD NAKAGOMI, O SARASINI, A FLORES, J TI IDENTIFICATION OF A NEW VP4 SEROTYPE OF HUMAN ROTAVIRUSES SO VIROLOGY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; OUTER CAPSID PROTEIN-VP4; RHESUS ROTAVIRUS; UNIQUE VP4; GENE; NEUTRALIZATION; STRAINS; SPECIFICITY; INFECTIVITY; SEGMENT-4 AB A new VP4 gene allele was identified by sequencing of two rotavirus strains recovered from infants with diarrhea. Strains HAL1166 (a VP7 serotype 8 human rotavirus from Finland) and PA169 (a VP7 serotype 6 human rotavirus from Italy) present 22-43% nucleotide sequence divergence and 14-45% amino acid divergence in the VP4 gene with rotaviruses belonging to various VP4 gene alleles previously reported. Cross-neutralization analysis between PA169 and rotaviruses belonging to the other recognized VP4 (P) serotypes had previously shown that none of them was similar to PA169. Hyperimmune serum prepared against a reassortant with the VP4 gene of strain PA169 and the VP7 gene of serotype 2 strain DS1 failed to neutralize previously recognized human rotavirus VP4 serotypes, indicating that PA169 represents a new VP4 serotype specificity. In addition, one of four neutralizing monoclonal antibodies directed to the VP4 of PA169 was specific for this virus, while three others had very limited cross-reactivity with rotaviruses possessing different VP4s. (C) 1994 Academic Press, Inc. C1 NIH,INFECT DIS LAB,BETHESDA,MD 20814. AKITA UNIV,SCH MED,DEPT MICROBIOL,AKITA 010,JAPAN. RP GERNA, G (reprint author), UNIV PAVIA,IRCCS,POLICLIN S MATTEO,INST INFECT DIS,VIRUS LAB,I-27100 PAVIA,ITALY. NR 24 TC 49 Z9 50 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1994 VL 200 IS 1 BP 66 EP 71 DI 10.1006/viro.1994.1163 PG 6 WC Virology SC Virology GA NA864 UT WOS:A1994NA86400008 PM 8128639 ER PT J AU MORIUCHI, M MORIUCHI, H STRAUS, SE COHEN, JI AF MORIUCHI, M MORIUCHI, H STRAUS, SE COHEN, JI TI VARICELLA-ZOSTER VIRUS (VZV) VIRION-ASSOCIATED TRANSACTIVATOR OPEN READING FRAME-62 PROTEIN ENHANCES THE INFECTIVITY OF VZV DNA SO VIROLOGY LA English DT Note ID IMMEDIATE-EARLY PROTEIN; GENE-EXPRESSION; PROMOTER; TYPE-1; IE62 AB Varicella-zoster virus (VZV) open reading frame (ORF) 62 protein (the homolog of herpes simplex virus type 1 (HSV-1) ICP4) and ORF10 protein (the homolog of HSV-1 VP16) are virion-associated transactivators. To investigate whether these proteins function during the initial stages of VZV infection, human melanoma cells were cotransfected with purified VZV DNA, devoid of any structural proteins, along with a plasmid expressing VZV ORF62 or ORF10 under the control of the human cytomegalovirus major immediate-early promoter. Expression of ORF62 enhanced the infectivity of VZV DNA up to 70-fold. In contrast, expression of ORF10 enhanced the infectivity of VZV DNA only threefold. These results show that high-level expression of ORF62 protein increases the probability that transfected VZV DNA will result in productive infection, suggesting that this virion-associated transactivator (ORF62) has a critical role in initiating infection. (C) 1994 Academic Press, Inc. C1 NIAID,CLIN INVEST LAB,MED VIROL SECT,BETHESDA,MD 20892. NR 22 TC 61 Z9 63 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1994 VL 200 IS 1 BP 297 EP 300 DI 10.1006/viro.1994.1190 PG 4 WC Virology SC Virology GA NA864 UT WOS:A1994NA86400035 PM 8128631 ER PT J AU LEW, JF KAPIKIAN, AZ JIANG, X ESTES, MK GREEN, KY AF LEW, JF KAPIKIAN, AZ JIANG, X ESTES, MK GREEN, KY TI MOLECULAR CHARACTERIZATION AND EXPRESSION OF THE CAPSID PROTEIN OF A NORWALK-LIKE VIRUS RECOVERED FROM A DESERT SHIELD TROOP WITH GASTROENTERITIS SO VIROLOGY LA English DT Note ID IMMUNE ELECTRON-MICROSCOPY; NONBACTERIAL GASTROENTERITIS; OUTBREAKS; SEQUENCE AB Norwalk virus (NV) infection was recently found to be associated with gastroenteritis in U.S. military troops stationed in Saudi Arabia during the 1990 Desert Shield Operation. We identified a Norwalk-like virus in the stools of two military personnel with gastroenteritis by ELISA and IEM. By RT-PCR and sequence analysis, the nucleotide sequence of part of the polymerase region of each of these two ''Desert Shield'' strains (DSV275 and DSV395) was found to be 73% identical to the corresponding region of NV. In addition, one of the strains (DSV395), which underwent sequence analysis of approximately 2900 consecutive bases, had a genomic organization characteristic of the Caliciviridae. Comparison of the DSV395 amino acid sequence of the capsid region with that of three other viruses in the Norwalk group (Norwalk, Southampton, and Toronto viruses) showed amino acid identity of 47-68%. Consensus sequence analysis of these capsid proteins identified two regions of conserved amino acids that flanked an area of variable amino acids. In addition, the proteins corresponding to the capsid regions of DSV395 and NV were expressed in an in vitro translation system. Immunoprecipitation studies using the expressed capsid proteins and paired DSV395 or NV infection sera indicated the presence of shared antigenic sites between the capsid proteins of DSV395 and NV. However, hyperimmune sera specific for the self-assembled recombinant NV capsid protein did not react with DSV stool antigen in an ELISA, suggesting that there may also be unique antigenic sites not shared between DSV395 and NV. (C) 1994 Academic Press, Inc. C1 BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. RP LEW, JF (reprint author), NIAID,INFECT DIS LAB,BLDG 7,RM 129,BETHESDA,MD 20892, USA. NR 22 TC 76 Z9 77 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1994 VL 200 IS 1 BP 319 EP 325 DI 10.1006/viro.1994.1194 PG 7 WC Virology SC Virology GA NA864 UT WOS:A1994NA86400039 PM 8128635 ER PT J AU MURPHY, BR HALL, SL KULKARNI, AB CROWE, JE COLLINS, PL CONNORS, M KARRON, RA CHANOCK, RM AF MURPHY, BR HALL, SL KULKARNI, AB CROWE, JE COLLINS, PL CONNORS, M KARRON, RA CHANOCK, RM TI AN UPDATE ON APPROACHES TO THE DEVELOPMENT OF RESPIRATORY SYNCYTIAL VIRUS (RSV) AND PARAINFLUENZA VIRUS TYPE-3 (PIV3) VACCINES SO VIRUS RESEARCH LA English DT Review ID CHIMERIC FG GLYCOPROTEIN; NUCLEOTIDE-SEQUENCE ANALYSIS; SERUM ANTIBODY-RESPONSES; CELL-MEDIATED-IMMUNITY; CD4+ T-CELLS; COTTON RATS; PARA-INFLUENZA; BALB/C MICE; PULMONARY PATHOLOGY; PRIMARY INFECTION AB RSV and PIV3 are responsible for about 30% of severe viral respiratory tract disease leading to hospitilization of infants and children. For this reason, there is a need to develop vaccines effective against these viruses. Since these viruses cause severe disease in early infancy, vaccines must be effective in the presence of maternal antibody. Currently, several strategies for immunization against these viruses are being explored including peptide vaccines, subunit vaccines, vectored vaccines (e.g., vaccinia-RSV or adenovirus-RSV recombinants), and live attenuated virus vaccines. The current status of these approaches is reviewed. In addition, the immunologic basis for the disease potentiation seen in vaccinees immunized with formalin-inactivated RSV during subsequent RSV infection is reviewed. The efficacy of immunization in the presence of maternal antibody is discussed. Much progress for a RSV and PIV3 vaccine has been made and successful immunization against each of these pathogens should be achieved within this decade. C1 JOHNS HOPKINS UNIV,SCH PUBL HLTH,BALTIMORE,MD. RP MURPHY, BR (reprint author), NIAID,INFECT DIS LAB,BETHESDA,MD 20892, USA. RI Crowe, James/B-5549-2009 OI Crowe, James/0000-0002-0049-1079 NR 101 TC 107 Z9 110 U1 1 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-1702 J9 VIRUS RES JI Virus Res. PD APR PY 1994 VL 32 IS 1 BP 13 EP 36 DI 10.1016/0168-1702(94)90059-0 PG 24 WC Virology SC Virology GA NE804 UT WOS:A1994NE80400002 PM 8030364 ER PT J AU LONG, JP ANGLARD, P GNARRA, JR WALTHER, MM MERINO, MJ LIU, S LERMAN, MI ZBAR, B LINEHAN, WM AF LONG, JP ANGLARD, P GNARRA, JR WALTHER, MM MERINO, MJ LIU, S LERMAN, MI ZBAR, B LINEHAN, WM TI THE USE OF MOLECULAR-GENETIC ANALYSIS IN THE DIAGNOSIS OF RENAL-CELL CARCINOMA SO WORLD JOURNAL OF UROLOGY LA English DT Article ID COLLECTING DUCT CARCINOMA; SHORT ARM; CHROMOSOME-3; DELETION; KIDNEY; POLYMORPHISMS; SEQUENCE; TUMORS; SITE; LINE AB The most common genetic aberration seen in nonpapillary renal cell carcinoma is believed to be the loss or inactivation of allelic material on the short arm of chromosome 3 (3p). Two patients underwent nephrectomy at our institution, each initially receiving a histologic diagnosis of renal cell carcinoma. Molecular analysis of these tissues revealed no genetic deletion on 3p, prompting further histologic and immunohistochemical evaluation of the original specimens. These additional studies confirmed alternate histologies other than renal cell carcinoma in each case. These data suggest that the loss of genetic material on the short arm of chromosome 3 may be specific for nonpapillary renal cell carcinoma. Molecular analysis may prove to be a useful adjunct in establishing the diagnosis in renal neoplasms with equivocal histologies. C1 NCI,DIV CANC TREATMENT,SURG BRANCH,UROL ONCOL SECT,BETHESDA,MD 20892. NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,DIV CANC BIOL & DIAGNOSIS,FREDERICK,MD 21701. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 44 TC 8 Z9 8 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0724-4983 J9 WORLD J UROL JI World J. Urol. PD APR PY 1994 VL 12 IS 2 BP 69 EP 73 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA NL187 UT WOS:A1994NL18700003 PM 7916238 ER PT J AU OLDS, JL BHALLA, US MCPHIE, DL LESTER, DS BOWER, JM ALKON, DL AF OLDS, JL BHALLA, US MCPHIE, DL LESTER, DS BOWER, JM ALKON, DL TI LATERALIZATION OF MEMBRANE-ASSOCIATED PROTEIN-KINASE-C IN RAT PIRIFORM CORTEX - SPECIFIC TO OPERANT TRAINING CUES IN THE OLFACTORY MODALITY SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE LEARNING; MEMORY; PIRIFORM CORTEX; PROTEIN KINASE C ID PHORBOL ESTER RECEPTOR; LEARNING-SET; BRAIN; ACTIVATION; MEMORY; DISCRIMINATION; HIPPOCAMPUS; STORAGE; RABBIT; TRANSLOCATION AB Rats were trained on an olfactory and a control modality (auditory or visual) discrimination task and brain membrane-associated protein kinase C (mPKC) was subsequently assessed using quantitative autoradiography of radiolabelled phorbol ester binding. In rats which received olfactory-cued training, mPKC showed a highly significant lateralization in the piriform cortex but not in the hippocampus. Both olfactory-trained rats and control modality rats showed a significant increase in mPKC in the hippocampus when compared to naive rats. Thus, while behavioral training procedures appeared to result in a hippocampal increase in the activated state of this enzyme as has been reported elsewhere, only olfactory learning produced an piriform cortex lateralization in the activated state of the enzyme. While the functional significance of such a change in the distribution of protein kinase C is still unclear, it does suggest that the monitoring of this enzyme's activational state may prove to be a useful tool in the study of memory formation in a wide variety of behavioral contexts. C1 CALTECH,PASADENA,CA 91125. RP OLDS, JL (reprint author), NINCDS,ADAPT SYST LAB,ROOM B316A BLDG 36,BETHESDA,MD 20892, USA. RI Bower, James/F-8343-2010; Olds, James/D-2867-2011 NR 58 TC 15 Z9 15 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-4328 J9 BEHAV BRAIN RES JI Behav. Brain Res. PD MAR 31 PY 1994 VL 61 IS 1 BP 37 EP 46 DI 10.1016/0166-4328(94)90006-X PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA NE286 UT WOS:A1994NE28600005 PM 8031495 ER PT J AU HANAUSKEABEL, HM PARK, MH HANAUSKE, AR POPOWICZ, AM LALANDE, M FOLK, JE AF HANAUSKEABEL, HM PARK, MH HANAUSKE, AR POPOWICZ, AM LALANDE, M FOLK, JE TI INHIBITION OF THE G1-S TRANSITION OF THE CELL-CYCLE BY INHIBITORS OF DEOXYHYPUSINE HYDROXYLATION SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE MIMOSINE; CELL CYCLE; POSTTRANSLATIONAL MODIFICATION; HYPUSINE ID HYPUSINE-CONTAINING PROTEIN; EUKARYOTIC INITIATION FACTOR-4D; HUMAN THYMIDINE KINASE; DNA-POLYMERASE-ALPHA; H-4 HISTONE GENE; AMINO-ACID; PROLYL 4-HYDROXYLASE; HUMAN-LYMPHOCYTES; IRON CHELATOR; HUMAN P53 AB The formation of the unusual amino-acid hypusine in eIF-5A (eukaryotic initiation factor 5A) is associated with cellular proliferation. We used a panel of compounds, including mimosine, to probe the relationship between the exit from the GI phase of the cell cycle, i.e., the onset of DNA replication, and the formation of hypusine by the enzyme deoxyhypusyl hydroxylase (DOHH). These two parameters displayed the same dose dependency and structure-activity relationship. Only compounds that inhibited DOHH also suppressed proliferation. This effect was observed: (i) in spontaneously proliferating, virally transformed, and mitogen-stimulated cells; (ii) for both anchorage-dependent and anchorage-independent proliferation; and (iii) with normal and malignant cell lines. DOHH reactivation occurred rapidly after inhibitor withdrawal and correlated with synchronized entry into S. The changes in the expression of specific genes during the G1-to-S transition mimicked the physiological pattern. These findings suggest that hypusine formation in eIF-5A which occurs in a specific, invariant sequence motif acquired early in evolution, may be involved in the G1-to-S transition in the eukaryotic cells tested. C1 NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. TECH UNIV MUNICH,DEPT MED 1,DIV HEMATOL ONCOL,W-8000 MUNICH 80,GERMANY. ROCKEFELLER UNIV,COMP SERV,NEW YORK,NY 10021. HARVARD UNIV,CHILDRENS HOSP,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV GENET,BOSTON,MA 02115. RP HANAUSKEABEL, HM (reprint author), CORNELL UNIV,NEW YORK HOSP,COLL MED,DEPT PEDIAT,ROOM N-236,525 E 68TH ST,NEW YORK,NY 10021, USA. NR 75 TC 111 Z9 114 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4889 J9 BBA-MOL CELL RES JI Biochim. Biophys. Acta-Mol. Cell Res. PD MAR 31 PY 1994 VL 1221 IS 2 BP 115 EP 124 DI 10.1016/0167-4889(94)90003-5 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NE481 UT WOS:A1994NE48100003 PM 8148388 ER PT J AU KLAHR, S LEVEY, AS BECK, GJ CAGGIULA, AW HUNSICKER, L KUSEK, JW STRIKER, G BUCKALEW, V BURKART, J FURBERG, C FELTS, J MOORE, M ROCCO, H DOLECEK, T WARREN, S BEARDEN, B STARKEY, C HARVEY, J POOLE, D DAHLQUIST, S DOROSHENKO, L BRADHAM, K WEST, D AGOSTINO, J COLE, L BAKER, B HAIRSTON, K BURGOYNE, S LAZARUS, J STEINMAN, T SEIFTER, J DESMOND, M FIORENZO, M CHIAVACCI, A METALIDES, T KORZECRAMIREZ, D GOULD, S PICKETT, V PORUSH, J FAUBERT, P SPITALEWITZ, S FAUBERT, J ZIMMER, G SAUM, D BLOCK, M WOEL, J ROSE, M DENNIS, V SCHWAB, S MINDA, S CONDON, S JENKS, B ECKARD, L GEDON, G MITCH, W MARONI, B ENGLAND, B SOUCIE, J PEDERSEN, M AKPELE, L CALLAHAN, P HALL, B SHELTON, S BOSCH, J HABWE, V CULBERTSON, B STACKDUNNE, M HANKEY, M ONEILL, S WITZMANN, K GOLDMAN, C JONES, T BOYLE, D SALMON, L KOPPLE, J ADLER, S HIRSCHBERG, R DICHIRO, J SNIDER, K DEVINE, W MCKAY, S MCDONALD, J CARTER, J NELSON, W LEVEY, A COGGINS, C DWYER, J MCLAUGHLIN, M GRONICH, J KING, A STOLLAR, C RAIZMAN, D CASTALDO, L DESIMONE, D EFSTATHION, A YONKER, K FINE, J SAUL, N HUGGINS, N MARTIN, A BALDI, S MOLESKE, C SHEEHAN, K FURLONG, D HEBERT, L NAHMAN, N DRIVER, V COSIO, M HARTMAN, J LEVY, C LONDERGAN, D GILLIGAN, M BECKMAN, T SMITH, E ZACHRICH, D TISHER, C PETERSON, J WINGO, C FINLAY, R PARRIS, E IVEY, G GREGORY, P HOFFINGER, R GARCIA, D PRESTON, C BERTOLATUS, J LIM, V SNETSELAAR, L WELCH, B BROOKS, L HOLLINGER, D LICHTY, I MUELLER, D EASTIN, S TANNA, A STEELE, J RIECK, K BOURGOIGNIE, J ROTH, D GREEN, D BUTCHER, C MERRILL, D DEVELASCO, A GARCON, M ROJAS, C ZARAGOZA, M BARTON, S MASSRY, S AKMAL, M FADDA, G SMORGORZERSKI, M KIEFER, S RAUCH, S EYERMAN, M KIGAWA, L RICHARDSON, A LIFSCHITZ, M KUNAU, R NOLAN, C GOUGE, S BAKRIS, G HURA, C YOUNG, E ARMES, C WARNER, C TANSEY, A FLORES, M DELEA, C TESCHAN, P HAKIM, R BREYER, J SCHULMAN, G ROGERS, N POWERS, S MCLEROY, S FISCHER, S DEERE, M CUTLER, E KUSEK, J AGODOA, L ANDERSON, A BECK, G WILLIAMS, G GASSMAN, J GREENE, T SCHLUCHTER, M BERG, R BROWN, M CHU, L DRABIK, M FATICA, K KNUTH, T LAMBDIN, K LEATHERMAN, J MCPHERSON, J MIDCALF, V MOORE, B PARANANDI, L PEARCE, G SWINDERMAN, D WANG, S WEBB, L YANCHAR, K CAGGIULA, A MILAS, N YAMAMOTO, M AMOROSO, W AVERBACH, F COYNE, T GILLIS, B JONES, F MAURER, E MEEHAN, R NAUJELIS, J OLSON, M SCHERCH, L STANO, E STEGINK, L BRUMMEL, M LUDWIG, B VANLENTE, F WALETZKY, J ERDEI, L SOUTH, C SPAGNOLA, C OLAUGHLIN, C PROUDFIT, W UNDERWOOD, D HALL, P ROLIN, H PEXA, D JONES, E BASCH, M CHUMLEA, W DOLLIFF, G KAPLAN, R WING, R DAMICO, G DIRKS, J GRANTHAM, J HARPER, A PETERS, K STEIN, J PELLEGRINO, E VANYPERSELE, C BAIN, R GRIZZLE, J HAWKINS, C HOLLIDAY, M LUKE, R MYERS, B RUDMAN, D WHELTON, P YOUNG, D YOUNG, V AF KLAHR, S LEVEY, AS BECK, GJ CAGGIULA, AW HUNSICKER, L KUSEK, JW STRIKER, G BUCKALEW, V BURKART, J FURBERG, C FELTS, J MOORE, M ROCCO, H DOLECEK, T WARREN, S BEARDEN, B STARKEY, C HARVEY, J POOLE, D DAHLQUIST, S DOROSHENKO, L BRADHAM, K WEST, D AGOSTINO, J COLE, L BAKER, B HAIRSTON, K BURGOYNE, S LAZARUS, J STEINMAN, T SEIFTER, J DESMOND, M FIORENZO, M CHIAVACCI, A METALIDES, T KORZECRAMIREZ, D GOULD, S PICKETT, V PORUSH, J FAUBERT, P SPITALEWITZ, S FAUBERT, J ZIMMER, G SAUM, D BLOCK, M WOEL, J ROSE, M DENNIS, V SCHWAB, S MINDA, S CONDON, S JENKS, B ECKARD, L GEDON, G MITCH, W MARONI, B ENGLAND, B SOUCIE, J PEDERSEN, M AKPELE, L CALLAHAN, P HALL, B SHELTON, S BOSCH, J HABWE, V CULBERTSON, B STACKDUNNE, M HANKEY, M ONEILL, S WITZMANN, K GOLDMAN, C JONES, T BOYLE, D SALMON, L KOPPLE, J ADLER, S HIRSCHBERG, R DICHIRO, J SNIDER, K DEVINE, W MCKAY, S MCDONALD, J CARTER, J NELSON, W LEVEY, A COGGINS, C DWYER, J MCLAUGHLIN, M GRONICH, J KING, A STOLLAR, C RAIZMAN, D CASTALDO, L DESIMONE, D EFSTATHION, A YONKER, K FINE, J SAUL, N HUGGINS, N MARTIN, A BALDI, S MOLESKE, C SHEEHAN, K FURLONG, D HEBERT, L NAHMAN, N DRIVER, V COSIO, M HARTMAN, J LEVY, C LONDERGAN, D GILLIGAN, M BECKMAN, T SMITH, E ZACHRICH, D TISHER, C PETERSON, J WINGO, C FINLAY, R PARRIS, E IVEY, G GREGORY, P HOFFINGER, R GARCIA, D PRESTON, C BERTOLATUS, J LIM, V SNETSELAAR, L WELCH, B BROOKS, L HOLLINGER, D LICHTY, I MUELLER, D EASTIN, S TANNA, A STEELE, J RIECK, K BOURGOIGNIE, J ROTH, D GREEN, D BUTCHER, C MERRILL, D DEVELASCO, A GARCON, M ROJAS, C ZARAGOZA, M BARTON, S MASSRY, S AKMAL, M FADDA, G SMORGORZERSKI, M KIEFER, S RAUCH, S EYERMAN, M KIGAWA, L RICHARDSON, A LIFSCHITZ, M KUNAU, R NOLAN, C GOUGE, S BAKRIS, G HURA, C YOUNG, E ARMES, C WARNER, C TANSEY, A FLORES, M DELEA, C TESCHAN, P HAKIM, R BREYER, J SCHULMAN, G ROGERS, N POWERS, S MCLEROY, S FISCHER, S DEERE, M CUTLER, E KUSEK, J AGODOA, L ANDERSON, A BECK, G WILLIAMS, G GASSMAN, J GREENE, T SCHLUCHTER, M BERG, R BROWN, M CHU, L DRABIK, M FATICA, K KNUTH, T LAMBDIN, K LEATHERMAN, J MCPHERSON, J MIDCALF, V MOORE, B PARANANDI, L PEARCE, G SWINDERMAN, D WANG, S WEBB, L YANCHAR, K CAGGIULA, A MILAS, N YAMAMOTO, M AMOROSO, W AVERBACH, F COYNE, T GILLIS, B JONES, F MAURER, E MEEHAN, R NAUJELIS, J OLSON, M SCHERCH, L STANO, E STEGINK, L BRUMMEL, M LUDWIG, B VANLENTE, F WALETZKY, J ERDEI, L SOUTH, C SPAGNOLA, C OLAUGHLIN, C PROUDFIT, W UNDERWOOD, D HALL, P ROLIN, H PEXA, D JONES, E BASCH, M CHUMLEA, W DOLLIFF, G KAPLAN, R WING, R DAMICO, G DIRKS, J GRANTHAM, J HARPER, A PETERS, K STEIN, J PELLEGRINO, E VANYPERSELE, C BAIN, R GRIZZLE, J HAWKINS, C HOLLIDAY, M LUKE, R MYERS, B RUDMAN, D WHELTON, P YOUNG, D YOUNG, V TI THE EFFECTS OF DIETARY-PROTEIN RESTRICTION AND BLOOD-PRESSURE CONTROL ON THE PROGRESSION OF CHRONIC RENAL-DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID LONGITUDINAL DATA; INSUFFICIENCY; FAILURE; TRIAL AB Background. Restricting protein intake and controlling hypertension delay the progression of renal disease in animals. We tested these interventions in 840 patients with various chronic renal diseases. C1 NIDDKD,BETHESDA,MD 20892. WASHINGTON UNIV,MED CTR,ST LOUIS,MO. UNIV PITTSBURGH,PITTSBURGH,PA. UNIV IOWA HOSP & CLIN,IOWA CITY,IA. BOWMAN GRAY SCH MED,WINSTON SALEM,NC. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. BROOKDALE HOSP MED CTR,BROOKLYN,NY. DUKE UNIV,SCH MED,DURHAM,NC. EMORY UNIV,ATLANTA,GA 30322. GEORGE WASHINGTON UNIV,WASHINGTON,DC. HARBOR UCLA MED CTR,TORRANCE,CA. TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. OHIO STATE UNIV,COLUMBUS,OH 43210. UNIV FLORIDA,GAINESVILLE,FL. UNIV IOWA HOSP & CLIN,IOWA CITY,IA 52242. UNIV MIAMI,CORAL GABLES,FL 33124. JACKSON MEM HOSP,MED CTR,MIAMI,FL. UNIV SO CALIF,LOS ANGELES,CA. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. VANDERBILT UNIV,MED CTR,NASHVILLE,TN. HLTH CARE FINANCING ADM,SEATTLE,WA. UNIV PITTSBURGH,CTR NUTR COORDINATING,PITTSBURGH,PA. UNIV IOWA,CENT AMINO ACID LAB,IOWA CITY,IA. CLEVELAND CLIN FDN,CENT BIOCHEM LAB,CLEVELAND,OH. CLEVELAND CLIN FDN,CENT GLOMERULAR FILTRAT RATE LAB,CLEVELAND,OH. CLEVELAND CLIN FDN,CTR DRUG DISTRIBUT,CLEVELAND,OH. CLEVELAND CLIN FDN,CENT ELECTROCARDIOG LAB,CLEVELAND,OH. RP KLAHR, S (reprint author), CLEVELAND CLIN FDN,MDRD STUDY DATA COORDINATING CTR,DEPT BIOSTAT & EPIDEMIOL,P88,CLEVELAND,OH 44195, USA. NR 28 TC 1393 Z9 1424 U1 4 U2 34 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 31 PY 1994 VL 330 IS 13 BP 877 EP 884 DI 10.1056/NEJM199403313301301 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA NC608 UT WOS:A1994NC60800001 PM 8114857 ER PT J AU EDWARDS, JG BAHL, JJ FLINK, IL CHENG, SY MORKIN, E AF EDWARDS, JG BAHL, JJ FLINK, IL CHENG, SY MORKIN, E TI THYROID-HORMONE INFLUENCES BETA-MYOSIN HEAVY-CHAIN (BETA-MHC) EXPRESSION SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID RESPONSE ELEMENTS; SKELETAL-MUSCLES; GENE-EXPRESSION; ALPHA-ACTIN; RECEPTORS; BINDING; CELLS; RAT AB 3,5,3'-Triiodo-L-thyronine (T3) regulation of beta-MHC expression was studied in rat fetal heart cells using deletion mutants of both the rat and human promoter regions fused to a CAT expression vector. T3 inhibited the expression of human and rat beta-MHC constructs with an IC50 of about 1nM, which was similar to the EC50 for betaMHC-mRNA observed in cardiomyocytes. Deletion analysis of betaMHC promoter constructs suggested that a T3 response element (TRE) is located near the start of transcription. Possibly, T3-receptor binding at this site interferes with formation of the transcriptional initiation complex. (C) 1994 Academic Press, Inc. C1 UNIV ARIZONA,CTR HEART,TUCSON,AZ 85724. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. FU NHLBI NIH HHS [P01HL374123, F32HL07603]; PHS HHS [P01H120984] NR 18 TC 54 Z9 58 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 30 PY 1994 VL 199 IS 3 BP 1482 EP 1488 DI 10.1006/bbrc.1994.1398 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA ND176 UT WOS:A1994ND17600057 PM 8147894 ER PT J AU ANGLISTER, J GRZESIEK, S WANG, AC REN, H KLEE, CB BAX, A AF ANGLISTER, J GRZESIEK, S WANG, AC REN, H KLEE, CB BAX, A TI H-1, C-13, N-15 NUCLEAR-MAGNETIC-RESONANCE BACKBONE ASSIGNMENTS AND SECONDARY STRUCTURE OF HUMAN CALCINEURIN-B SO BIOCHEMISTRY LA English DT Article ID CALCIUM-BINDING PROTEINS; NMR-SPECTROSCOPY; CYCLOSPORINE-A; PEPTIDE COMPLEX; CALMODULIN; PHOSPHATASE; SPECTRA; TARGET; IDENTIFICATION; SUPPRESSION AB The calmodulin-and calcium-stimulated protein phosphatase calcineurin, PP2B, consists of two subunits: calcineurin B, which binds Ca2+, and calcineurin A, which contains the catalytic site and a calmodulin binding site. Heteronuclear 3D and 4D NMR experiments were carried out on a recombinant human calcineurin B which is a 170-residue protein of molecular mass 19.3 kDa, uniformly labeled with N-15 and C-13. The nondenaturing detergent CHAPS was used to obtain a monomeric form of calcineurin B. Three-dimensional triple resonance experiments yielded complete sequential assignment of the backbone nuclei (H-1, C-13, and N-15). This assignment was verified by a 4D HN(COCA)NH experiment carried out with 50% randomly deuteriated and uniformly N-15- and C-13-enriched calcineurin B. The secondary structure of calcineurin B has been determined on the basis of the C-13alpha and C-13beta secondary chemical shifts, J(H(N)H(alpha)) couplings, and NOE connectivities obtained from 3D N-15-separated and 4D C-13/N-15-separated NOESY spectra. Calcineurin B has eight helices distributed in four EF-hand, helix-loop-helix [Kretsinger, R. H. (1980) CRC Crit. Rev. Biochem. 8, 119-174] calcium binding domains. The secondary structure of calcineurin B is highly homologous to that of calmodulin. In comparison to calmodulin, helices B and C are shorter while helix G is considerably longer. As was observed for calmodulin in solution, calcineurin B does not have a single long central helix; rather, helices D and E are separated by a six-residue sequence in a flexible nonhelical conformation. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. WEIZMANN INST SCI,DEPT STRUCT BIOL,IL-76100 REHOVOT,ISRAEL. RP ANGLISTER, J (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 59 TC 47 Z9 48 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 29 PY 1994 VL 33 IS 12 BP 3540 EP 3547 DI 10.1021/bi00178a010 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA ND248 UT WOS:A1994ND24800010 PM 8142351 ER PT J AU ZHANG, GS MEHRINGER, JH VANDEERLIN, VMD KOZAK, CA TOLLEFSEN, DM AF ZHANG, GS MEHRINGER, JH VANDEERLIN, VMD KOZAK, CA TOLLEFSEN, DM TI MURINE HEPARIN-COFACTOR II - PURIFICATION, CDNA SEQUENCE, EXPRESSION, AND GENE STRUCTURE SO BIOCHEMISTRY LA English DT Article ID DERMATAN SULFATE; REACTIVE CENTER; MUSCLE-CELLS; THROMBIN; INHIBITOR; MOUSE; RECEPTOR; FAMILY; ALPHA-1-ANTITRYPSIN; ACTIVATION AB Heparin cofactor II (HCII) is a glycoprotein in human plasma that inhibits thrombin rapidly in the presence of dermatan sulfate or heparin. Unexpectedly, we found that HCII activity in murine plasma is present in two proteins of 68 and 72 kDa. The two proteins have the same N-terminal amino acid sequence, and both react with an antibody raised against the C-terminal nine amino acid residues of murine HCII predicted from the cDNA sequence. Treatment of the two proteins with peptide-N4-(N-acetyl-beta-glucosaminyl)asparagine amidase yields a single 54-kDa band. Thus, murine plasma contains two forms of HCII that appear to have identical amino acid sequences but differ in the composition of their N-linked oligosaccharides. HCII cDNA clones isolated from a murine liver library include a 1434 bp open reading frame following the first Met codon, a TAA stop codon, and 580 bp of 3'-untranslated sequence terminating in a poly(A) tail. The amino acid sequence deduced from the cDNA contains the N-terminal sequence of purified murine plasma HCII preceded by a 23-residue hydrophobic sequence presumed to be the signal peptide. The amino acid sequence of murine HCII is 87% identical to that of human HCII, the greatest variability occurring in the N-terminal portion of the protein. Northern blot analysis reveals a 2.3-kb HCII mRNA in murine and human liver, but no HCII mRNA is detectable in heart, brain, spleen, lung, skeletal muscle, kidney, testis, placenta, pancreas, or intestine. Southern blot analysis of restriction fragment length polymorphisms in progeny of interspecific and intersubspecific crosses indicates that mice have a single HCII gene (designated Hcf2), which maps to chromosome 16 between Prm-1 and Igl. The murine HCII gene is approximately 7.1 kb in size and consists of at least four exons and three introns. The intron/exon origanization is identical to that of the human HCII gene except at the 5' end, where the murine gene may lack a large intron in the 5'-untranslated region. Our results indicate that HCII is more highly conserved than the human and murine homologues of other serpins such as alpha1-antitrypsin and alpha1-antichymotrypsin. C1 WASHINGTON UNIV, SCH MED,DIV HEMATOL ONCOL,BOX 8125, 660 S EUCLID AVE, ST LOUIS, MO 63110 USA. NIAID, BETHESDA, MD 20892 USA. FU NHLBI NIH HHS [HL-14147] NR 58 TC 22 Z9 23 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 29 PY 1994 VL 33 IS 12 BP 3632 EP 3642 DI 10.1021/bi00178a021 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA ND248 UT WOS:A1994ND24800021 PM 7908224 ER PT J AU CAUGHEY, B AF CAUGHEY, B TI SCRAPIE-ASSOCIATED PRP ACCUMULATION AND AGENT REPLICATION - EFFECTS OF SULFATED GLYCOSAMINOGLYCAN ANALOGS SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES LA English DT Article; Proceedings Paper CT Royal-Society Discussion Meeting on Molecular Biology of Prion Diseases CY SEP 22-23, 1993 CL LONDON, ENGLAND SP ROYAL SOC ID PRION PROTEIN-BIOSYNTHESIS; CREUTZFELDT-JAKOB DISEASE; NEURO-BLASTOMA CELLS; CULTURED-CELLS; SULFATED GLYCOSAMINOGLYCANS; ALZHEIMERS-DISEASE; INCUBATION PERIOD; DEXTRAN SULFATE; AMYLOID PLAQUES; MESSENGER-RNA AB An abnormally protease-resistant and apparently neuropathogenic form of PrP accumulates in the brains of hosts with scrapie and related transmissible spongiform encephalopathies. Studies with scrapie-infected neuroblastoma cells have highlighted dramatic differences in the metabolism of the normal (protease-sensitive) and scrapie-associated (protease-resistant) isoforms of PrP. Furthermore, this model has been useful in identifying inhibitors of protease-resistant PrP accumulation and scrapie agent replication which are valuable as potential therapeutic agents and as probes of the mechanism of protease-resistant PrP formation. These inhibitors include the amyloid stain Congo red and certain sulphated glycans which are glycosaminoglycans themselves or glycosaminoglycan analogues. The relative potencies of various sulphated glycans correlate with their previously determined anti-scrapie activities in vivo, suggesting that the prophylactic effects of sulphated polyanions is due to inhibition of protease-resistant PrP accumulation. These and other observations suggest that an interaction of PrP with endogenous sulphated glycosaminoglycans or proteoglycans is important in protease-resistant PrP accumulation, and raise the possibility that therapies for transmissible spongiform encephalopathies and other amyloidoses could be based on blocking (pre)amyloid-glycosaminoglycan interactions. RP CAUGHEY, B (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 67 TC 18 Z9 18 U1 0 U2 2 PU ROYAL SOC LONDON PI LONDON PA 6 CARLTON HOUSE TERRACE, LONDON, ENGLAND SW1Y 5AG SN 0962-8436 J9 PHILOS T ROY SOC B JI Philos. Trans. R. Soc. Lond. Ser. B-Biol. Sci. PD MAR 29 PY 1994 VL 343 IS 1306 BP 399 EP 404 DI 10.1098/rstb.1994.0035 PG 6 WC Biology SC Life Sciences & Biomedicine - Other Topics GA NF689 UT WOS:A1994NF68900008 PM 7913757 ER PT J AU PURCELL, RH AF PURCELL, RH TI HEPATITIS VIRUSES - CHANGING PATTERNS OF HUMAN-DISEASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article; Proceedings Paper CT Colloquium on Changes in Human Ecology and Behavior: Effects on Infectious Diseases CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI ID NON-B-HEPATITIS; TRANSMITTED NON-A; C VIRUS; NUCLEOTIDE-SEQUENCE; DELTA VIRUS; CHIMPANZEES; ANTIGEN; TRANSMISSION; INFECTION; IMMUNITY AB Viral hepatitis is a disease of antiquity, but evidence for more than one etiologic agent has been recognized only since the 1940s, when two viruses (hepatitis A virus and hepatitis B virus) were thought to account for all disease. In the past 20 years, three additional hepatitis agents (hepatitis C virus, hepatitis D virus, and hepatitis E virus) have been discovered, and there is evidence for at least one additional virus. Each of the five recognized hepatitis viruses belongs to a different virus family, and each has a unique epidemiology. The medical impact of these viruses on society has been strongly influenced by changes in human ecology. This has resulted in some cases in diminished disease and in others in increases in the incidence of disease. RP PURCELL, RH (reprint author), NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892, USA. NR 54 TC 96 Z9 99 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2401 EP 2406 DI 10.1073/pnas.91.7.2401 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200006 PM 8146130 ER PT J AU QUINN, TC AF QUINN, TC TI POPULATION MIGRATION AND THE SPREAD OF TYPE-1 AND TYPE-2 HUMAN IMMUNODEFICIENCY VIRUSES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article; Proceedings Paper CT Colloquium on Changes in Human Ecology and Behavior: Effects on Infectious Diseases CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI DE AIDS; DEMOGRAPHY; HUMAN IMMUNODEFICIENCY VIRUS EPIDEMIOLOGY ID SEXUALLY-TRANSMITTED DISEASES; DISTANCE TRUCK-DRIVERS; HIGH-RISK GROUPS; HIV-2 INFECTION; CENTRAL-AFRICA; MIGRANT LABOR; UNITED-STATES; BELLE-GLADE; AIDS; PREVALENCE AB Over 14 million people are estimated to be infected with the human immunodeficiency viruses (HIV), with nearly three-fourths of the infected persons residing in developing countries. One factor responsible for dissemination of both HIV-1 and HIV-2 worldwide was the intense migration of individuals, from rural to urban centers with subsequent return migration and internationally due to civil wars, tourism, business purposes, and the drug trade. In sub-Saharan Africa, between 1960 and 1980, urban centers with more than 500,000 inhabitants increased from 3 to 28, and more than 75 military coups occurred in 30 countries. The result was a massive migration of rural inhabitants to urban centers concomitant with the spread of HIV-1 to large population centers. With the associated demographic, economic, and social changes, an epidemic of sexually transmitted diseases and HIV-1 was ignited. Migratory patterns were also responsible for the spread of endemic HIV-2 to neighboring West African countries and eventually to Europe, the Americas, and India. Although Southeast Asia was the last region in which HIV-1 was introduced, it has the greatest potential for rapid spread due to population density and inherent risk behaviors. Thus, the migration of poor, rural, and young sexually active individuals to urban centers coupled with large international movements of HIV-infected individuals played a prominent role in the dissemination of HIV globally. The economic recession has aggravated the transmission of HIV by directly increasing the population at risk through increased urban migration, disruption of rural families and cultural values, poverty, and prostitution and indirectly through a decrease in health care provision. Consequently, social and economic reform as well as sexual behavior education need to be intensified if HIV transmission is to be controlled. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP QUINN, TC (reprint author), JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,ROSS 1159,720 RUTLAND AVE,BALTIMORE,MD 21205, USA. RI Quinn, Thomas/A-2494-2010 NR 74 TC 124 Z9 125 U1 8 U2 26 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2407 EP 2414 DI 10.1073/pnas.91.7.2407 PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200007 PM 8146131 ER PT J AU MILLER, LH AF MILLER, LH TI IMPACT OF MALARIA ON GENETIC-POLYMORPHISM AND GENETIC-DISEASES IN AFRICANS AND AFRICAN-AMERICANS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article; Proceedings Paper CT Colloquium on Changes in Human Ecology and Behavior: Effects on Infectious Diseases CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI ID CD8+ T-CELLS; PLASMODIUM-FALCIPARUM; CIRCUMSPOROZOITE PROTEIN; RECEPTOR HETEROGENEITY; ERYTHROCYTE; PARASITES; HYPERTENSION; RESISTANCE; INVASION; SPOROZOITES AB The high mortality from malaria in sub-Sahara Africa selected multiple genes that give the population a selective advantage. Identification of the genetic basis for resistance may suggest unusual approaches to development of malarial vaccines and antimalarial drugs. Some of these genes may be deleterious, although of selective advantage within the African setting, and need to be identified for counseling for disease prevention. RP MILLER, LH (reprint author), NIAID,MALARIA RES LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. NR 53 TC 81 Z9 84 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2415 EP 2419 DI 10.1073/pnas.91.7.2415 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200008 PM 8146132 ER PT J AU LOWY, DR KIRNBAUER, R SCHILLER, JT AF LOWY, DR KIRNBAUER, R SCHILLER, JT TI GENITAL HUMAN PAPILLOMAVIRUS INFECTION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article; Proceedings Paper CT Colloquium on Changes in Human Ecology and Behavior: Effects on Infectious Diseases CY SEP 27-28, 1993 CL NATL ACAD SCI, WASHINGTON, DC HO NATL ACAD SCI ID CARCINOMA CELL-LINES; CERVICAL INTRAEPITHELIAL NEOPLASIA; HUMAN FORESKIN KERATINOCYTES; RETINOBLASTOMA GENES; TYPE-16; P53; E6; CANCER; WOMEN; RISK AB Genital human papillomavirus (HIV) infection is a common sexually transmitted disease that at the present time is not effectively controlled or treated. Many infections are inapparent and transient. However, some HPV infections result in persistent lesions that in some cases undergo carcinogenic progression. A subset of genital HPVs, designated high-risk types, are preferentially associated with high-grade dysplasias and carcinomas. About 90% of cervical cancers contain high-risk HPV DNA, most often HPV16. Development of a subunit vaccine against high-risk genital HPVs is a desirable and, it appears, an increasingly feasible long-term goal. The viral E6 and E7 oncoproteins are selectively maintained and expressed in progressed HPV tumors and could potentially be targets for therapeutic vaccines. The L1 major virion structural proteins have recently been shown to self-assemble into virus-like particles when expressed in insect cells. These particles might serve as the basis for a prophylactic vaccine to prevent genital HPV infection. RP LOWY, DR (reprint author), NCI,CELLULAR ONCOL LAB,BLDG 37,ROOM 1B-26,BETHESDA,MD 20892, USA. NR 67 TC 140 Z9 148 U1 0 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2436 EP 2440 DI 10.1073/pnas.91.7.2436 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200012 PM 8146136 ER PT J AU TOYOKUNI, S UCHIDA, K OKAMOTO, K HATTORINAKAKUKI, Y HIAI, H STADTMAN, ER AF TOYOKUNI, S UCHIDA, K OKAMOTO, K HATTORINAKAKUKI, Y HIAI, H STADTMAN, ER TI FORMATION OF 4-HYDROXY-2-NONENAL-MODIFIED PROTEINS IN THE RENAL PROXIMAL TUBULES OF RATS TREATED WITH A RENAL CARCINOGEN, FERRIC NITRILOTRIACETATE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID LOW-DENSITY-LIPOPROTEIN; INDUCED LIPID-PEROXIDATION; SEX-DIFFERENCES; CELL CARCINOMA; VITAMIN-E; NEPHROTOXICITY; KIDNEY; MICE; GLUTATHIONE; DNA AB An iron chelate, ferric nitrilotriacetate (Fe-NTA), induces proximal tubular necrosis, a consequence of lipid peroxidation, that finally leads to a high incidence of renal adenocarcinoma in rodents. Lipid peroxidation as monitored by formation of thiobarbituric acid-reactive substances and free 4-hydroxy-2-nonenal (HNE) was observed in the kidney homogenates of rats treated with Fe-NTA. Based on the fact that HNE is capable of reacting with cellular proteins, we attempted to detect the localization of HNE-modified proteins in rat kidney tissues with an immunohistochemical procedure. By means of an immunohistochemical technique using polyclonal antibody against the HNE-modified proteins, it was shown that HNE-modified proteins are formed in the target cells of this carcinogenesis model. HNE-modified proteins were detected in the renal proximal tubules 1 hr after i.p. administration of Fe-NTA (15 mg of iron per kg). Intense positivity was found in the cells with degeneration. After 6 hr, the level of HNE-protein conjugates decreased due to the subsequent necrosis. The intensity of the immunochemical reaction with HNE-modified proteins increased in parallel with an increase in the amounts of thiobartituric acid-reactive substances and free HNE that were found. Furthermore, histochemical detection of aldehydes by cold Schiff's reagent demonstrated that location of aldehydes was identical to that of the HNE-modified proteins determined by immunohistochemical procedures. It would thus appear that the production of HNE, a genotoxic and mutagenic aldehyde, and its reaction with proteins may play a role in Fe-NTA-induced renal carcinogenesis. C1 NAGOYA UNIV,SCH AGR,FOOD & BIODYNAM LAB,NAGOYA 46401,JAPAN. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RP TOYOKUNI, S (reprint author), KYOTO UNIV,FAC MED,DEPT PATHOL,SAKYO KU,KYOTO 606,JAPAN. RI Toyokuni, Shinya/C-1358-2010 OI Toyokuni, Shinya/0000-0002-5757-1109 NR 46 TC 288 Z9 291 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2616 EP 2620 DI 10.1073/pnas.91.7.2616 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200047 PM 8146163 ER PT J AU CHEN, CY OLINER, JD ZHAN, QM FORNACE, AJ VOGELSTEIN, B KASTAN, MB AF CHEN, CY OLINER, JD ZHAN, QM FORNACE, AJ VOGELSTEIN, B KASTAN, MB TI INTERACTIONS BETWEEN P53 AND MDM2 IN A MAMMALIAN-CELL CYCLE CHECKPOINT PATHWAY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HUMAN PAPILLOMAVIRUS TYPE-16; TUMOR-ANTIGEN; PROTEIN; CANCER; GENE; TRANSACTIVATION; DEGRADATION; EXPRESSION; DISTINCT; GADD45 AB Normal p53 function is required for optimal arrest of cells in the G1 phase of the cell cycle following certain types of DNA damage. Loss of this cell cycle checkpoint may contribute to tumor development by increasing the number of genetic abnormalities in daughter cells following DNA damage. The MDM2 protein is an endogenous gene product that binds to the p53 protein and is able to block p53-mediated transactivation of cotransfected reporter constructs; thus, interactions between MDM2 and p53 in this checkpoint pathway following ionizing irradiation were examined. Though increases in p53 protein by DNA damage were not abrogated by MDM2 overexpression, increased levels of MDM2, resulting either from endogenous gene amplification or from transfection of an exogenous expression vector, were associated with a reduction in the ability of cells to arrest in G1 following irradiation. In addition, expression of endogenous MDM2 was enhanced by ionizing irradiation at the level of transcription in a p53-dependent fashion. These observations demonstrate that MDM2 overexpression can inhibit p53 function in a known physiologic pathway and are consistent with the hypothesis that MDM2 may function in a ''feedback loop'' mechanism with p53, possibly acting to limit the length or severity of the p53-mediated arrest following DNA damage. C1 JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD 21287. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X FU NCI NIH HHS [CA41183, CA43460]; NIEHS NIH HHS [ES05777] NR 35 TC 305 Z9 311 U1 0 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2684 EP 2688 DI 10.1073/pnas.91.7.2684 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200061 PM 8146175 ER PT J AU NORMANNO, N SELVAM, MP QI, CF SAEKI, T JOHNSON, G KIM, N CIARDIELLO, F SHOYAB, M PLOWMAN, G BRANDT, R TODARO, G SALOMON, DS AF NORMANNO, N SELVAM, MP QI, CF SAEKI, T JOHNSON, G KIM, N CIARDIELLO, F SHOYAB, M PLOWMAN, G BRANDT, R TODARO, G SALOMON, DS TI AMPHIREGULIN AS AN AUTOCRINE GROWTH-FACTOR FOR C-HA-RAS-TRANSFORMED AND C-ERBB-2-TRANSFORMED HUMAN MAMMARY EPITHELIAL-CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HA-RAS; C-NEU; BREAST CANCER ID HUMAN-BREAST CANCER; FACTOR-ALPHA; EXPRESSION; LINE; RECEPTOR; GENE; ESTROGEN; PROTEIN AB Amphiregulin (AR), a member of the epidermal growth factor (EGF) family, was found to be as potent as EGF in stimulating the anchorage-dependent growth (ADG) of immortalized, nontransformed human mammary epithelial MCF-10A cells. MCF-10A cells transformed by either an activated human c-Ha-ras protooncogene (MCF-10A ras) or by overexpression of a nonactivated rat c-neu gene (MCF-10A neu) exhibited a 35% reduction in the response to AR in ADG when compared to MCF-10A cells, but AR was still as potent as EGF in these transformants. Exogenous AR exhibited only 15-20% of the activity of EGF in stimulating the anchorage-independent growth, a response that is normally dependent upon exogenous EGF, of the oncogene-transformed MCF-10A cells. MCF-10A cells express low levels of a 1.4-kb AR mRNA transcript, while MCF-10A ras and MCF-10A neu cells display a 15- to 30-fold increase in the levels of AR mRNA and endogenous AR protein as determined by Western blot analysis. Exogenous EGF was found to induce both AR mRNA and protein in the MCF-10A parental and transformed cells. A 20-mer phosphorothioate antisense deoxyoligonucleotide complementary to the 5' sequence of AR mRNA was able to significantly reduce the levels of endogenous AR protein and to inhibit the EGF-stimulated ADG and anchorage-independent growth of MCF-10A ras and MCF-10A neu cells. These data suggest that AR may function as an EGF-dependent autocrine growth factor in mammary epithelial cells that have been transformed by either a point-mutated c-Ha-ras or c-neu. C1 NCI,TUMOR IMMUNOL & BIOL LAB,TUMOR GROWTH FACTOR SECT,BLDG 10,BETHESDA,MD 20892. IST NAZL STUDIO & CURA TUMORI FDN PASCALE,I-80131 NAPLES,ITALY. US FDA,CTR BIOL EVALUAT & RES,DIV BLOOD APPLICAT,BETHESDA,MD 20892. US FDA,DIV CYTOKINE BIOL,BETHESDA,MD 20892. UNIV NAPOLI FEDERICO II,FAC MED & CHIRURG 2,CATTEDRA ONCOL MED,I-80131 NAPLES,ITALY. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,SEATTLE,WA 98121. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. RI PLOWMAN, Greg/E-2012-2011; OI Normanno, Nicola/0000-0002-7158-2605 NR 33 TC 97 Z9 97 U1 1 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2790 EP 2794 DI 10.1073/pnas.91.7.2790 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200083 PM 7908443 ER PT J AU SHILYANSKY, J NISHIMURA, MI YANNELLI, JR KAWAKAMI, Y JACKNIN, LS CHARMLEY, P ROSENBERG, SA AF SHILYANSKY, J NISHIMURA, MI YANNELLI, JR KAWAKAMI, Y JACKNIN, LS CHARMLEY, P ROSENBERG, SA TI T-CELL RECEPTOR USAGE BY MELANOMA-SPECIFIC CLONAL AND HIGHLY OLIGOCLONAL TUMOR-INFILTRATING LYMPHOCYTE LINES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID VARIABLE REGION GENES; INTERLEUKIN-2 RECEPTOR; SEGMENT USAGE; CHAIN; RECOGNITION; CANCER; IMMUNOTHERAPY; REPERTOIRE; ALPHA; HETEROGENEITY AB Tumor-infiltrating lymphocytes (TIL) obtained from human melanomas can specifically lyse autologous tumor in vitro and mediate tumor regression in vivo. To develop more effective therapeutic reagents and to further understand the T-cell response to tumors, the diversity of T-cell receptors (TCRs) involved in melanoma antigen recognition has been studied. The TCR variable (V) genes, joining (j) segments, and N diversity regions used by five clonal lines and one highly oligoclonal, melanoma-specific, CD8+ TIL line were examined utilizing PCR amplification with V gene subfamily-specific primers and anchor PCR. The TIL lysed multiple allogeneic melanomas expressing matched surface major histocompatibility complex class I molecules. TCR analysis confirmed the clonal nature of the TIL lines; however, the TCR repertoire was diverse. Even among the three HLA-A2 restricted TIL (TIL 1200, TIL F2-2, and TIL 5), no common V gene usage was found. Comparison of the third complementarity-determining regions of the TCRs from the HLA-A2 restricted TIL revealed no homology. Results presented here identify T-cell clonotypes that recognize epitopes on highly prevalent, shared melanoma tumor-associated antigens presented in the context of HLA-B55, HLA-A1, and HLA-A2. These T cells and the antigens they recognize represent important components for the design of new immunotherapies for patients with advanced melanoma. C1 NCI,BETHESDA,MD 20892. VIRGINIA MASON RES CTR,SEATTLE,WA 98195. RI Kawakami, Yutaka /E-7429-2013 OI Kawakami, Yutaka /0000-0003-4836-2855 NR 42 TC 68 Z9 68 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2829 EP 2833 DI 10.1073/pnas.91.7.2829 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200091 PM 7511820 ER PT J AU MONARI, L CHEN, SG BROWN, P PARCHI, P PETERSEN, RB MIKOL, J GRAY, F CORTELLI, P MONTAGNA, P GHETTI, B GOLDFARB, LG GAJDUSEK, DC LUGARESI, E GAMBETTI, P AUTILIOGAMBETTI, L AF MONARI, L CHEN, SG BROWN, P PARCHI, P PETERSEN, RB MIKOL, J GRAY, F CORTELLI, P MONTAGNA, P GHETTI, B GOLDFARB, LG GAJDUSEK, DC LUGARESI, E GAMBETTI, P AUTILIOGAMBETTI, L TI FATAL FAMILIAL INSOMNIA AND FAMILIAL CREUTZFELDT-JAKOB-DISEASE - DIFFERENT PRION PROTEINS DETERMINED BY A DNA POLYMORPHISM SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CODON-178ASN PRNP MUTATION; SPONGIFORM ENCEPHALOPATHY; ATP HYDROLYSIS; GENE; BIOLOGY; SEPARATION; REGION; AGENT AB Fatal familial insomnia and a subtype of Creutzfeldt-Jakob disease, two clinically and pathologically distinct diseases, are linked to the same mutation at codon 178 (Asp-178 --> Asn) but segregate with different genotypes determined by this mutation and the methionine-valine polymorphism at codon 129 of the prion protein gene. The abnormal isoforms of the prion protein in these two diseases were found to differ both in the relative abundance of glycosylated forms and in the size of the protease-resistant fragments. The size difference was consistent with a different protease cleavage site, suggesting a different conformation of the protease-resistant prion protein present in the two diseases. These differences are likely to be responsible for the type and location of the lesions that characterize these two diseases. Therefore, the combination of the mutation at codon 178 and the polymorphism at codon 129 determines the disease phenotype by producing two altered conformations of the prion protein. C1 CASE WESTERN RESERVE UNIV, INST PATHOL, DIV NEUROPATHOL, CLEVELAND, OH 44106 USA. NINCDS, CENT NERVOUS SYST LAB, BETHESDA, MD 44120 USA. NCI, BIOCHEM LAB, BETHESDA, MD 44120 USA. HOP LARIBOISIERE, F-75475 PARIS, FRANCE. HOP HENRI MONDOR, DEPT PATHOL, F-94010 CRETEIL, FRANCE. UNIV BOLOGNA, INST NEUROL, I-40126 BOLOGNA, ITALY. INDIANA UNIV, MED CTR, DEPT PATHOL, INDIANAPOLIS, IN 46202 USA. RI Petersen, Robert/B-5075-2011; Parchi, Piero/L-9833-2015; Chen, Shu/O-4750-2014; OI Petersen, Robert/0000-0002-3154-0072; Parchi, Piero/0000-0002-9444-9524; Chen, Shu/0000-0001-7180-3001; Cortelli, Pietro/0000-0002-3633-8818 FU NIA NIH HHS [AG-08012]; NINDS NIH HHS [NS-29822, NS-14509] NR 31 TC 228 Z9 231 U1 2 U2 16 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 29 PY 1994 VL 91 IS 7 BP 2839 EP 2842 DI 10.1073/pnas.91.7.2839 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA ND602 UT WOS:A1994ND60200093 PM 7908444 ER PT J AU MAIESE, K HOLLOWAY, HH LARSON, DM SONCRANT, TT AF MAIESE, K HOLLOWAY, HH LARSON, DM SONCRANT, TT TI EFFECT OF ACUTE AND CHRONIC ARECOLINE TREATMENT ON CEREBRAL METABOLISM AND BLOOD-FLOW IN THE CONSCIOUS RAT SO BRAIN RESEARCH LA English DT Article DE ALZHEIMERS DISEASE; ARECOLINE; CEREBRAL BLOOD FLOW; CEREBRAL GLUCOSE METABOLISM; HIPPOCAMPUS; MUSCARINIC RECEPTOR; RAT ID CHOLINERGIC AGONIST ARECOLINE; ALZHEIMERS-DISEASE; GLUCOSE-UTILIZATION; VERBAL MEMORY; RECEPTORS; BRAIN; STIMULATION; HIPPOCAMPUS; DEMENTIA; SENSITIVITY AB Treatment with the muscarinic agonist arecoline improves memory retention in patients with Alzheimer's disease (AD). In animal models, arecoline selectively increases local cerebral glucose utilization (LCGU). We examined (1) whether these focal increases in metabolism were coupled to local cerebral blood flow (LCBF) and (2) whether the effect of arecoline on LCGU and LCBF was dependent upon duration of drug administration. In groups of young Fischer-344 rats, LCGU and LCBF were determined in 59 brain regions by the [C-14]2-deoxyglucose and the [C-14]iodoantipyrine autoradiographic methods following either the acute administration of arecoline (2 mg/kg and 15 mg/kg) or the chronic three week administration of arecoline (50 mg/kg/day). In general, LCBF correlated closely with LCGU following arecoline 2 mg/kg administration, but heterogeneous regions were present. Following treatment with arecoline 15 mg/kg, the two parameters became uncoupled with LCBF increasing disproportionately in relation to LCGU. Coupling between LCBF and LCGU was preserved during chronic arecoline treatment (50 mg/kg/day) but some regions, such as the hippocampus, were uncoupled with LCGU increasing to a greater extent than LCBF. Thus, we demonstrate that acute and chronic administration of arecoline can differentially modulate LCBF and LCGU. Since clinical administration of arecoline can improve cognitive function in patients with AD, understanding the ability of arecoline to selectively alter LCBF and LCGU in regions such as the hippocampus may offer insight into the pathophysiology of AD and provide direction for the development of definitive therapy for neurodegenerative disorders. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. RP MAIESE, K (reprint author), CORNELL UNIV,MED CTR,COLL MED,DEPT NEUROL & NEUROSCI,ROOM A579,1300 YORK AVE,NEW YORK,NY 10021, USA. FU NINDS NIH HHS [NINDS KO8-NS-01599] NR 48 TC 20 Z9 21 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 28 PY 1994 VL 641 IS 1 BP 65 EP 75 DI 10.1016/0006-8993(94)91816-3 PG 11 WC Neurosciences SC Neurosciences & Neurology GA NC813 UT WOS:A1994NC81300009 PM 8019853 ER PT J AU POGUN, S BAUMANN, MH KUHAR, MJ AF POGUN, S BAUMANN, MH KUHAR, MJ TI NITRIC-OXIDE INHIBITS [H-3] DOPAMINE UPTAKE SO BRAIN RESEARCH LA English DT Article DE NITRIC OXIDE; DOPAMINE UPTAKE; DOPAMINE TRANSPORTER; GLUTAMATE ID LONG-TERM POTENTIATION; SENSITIVE DOPAMINE TRANSPORTER; SMOOTH-MUSCLE RELAXATION; D-ASPARTATE RECEPTORS; RAT STRIATUM; GLUTAMATE NEUROTOXICITY; MORPHINE-TOLERANCE; INTERCELLULAR MESSENGER; GUANYLATE-CYCLASE; N-ETHYLMALEIMIDE AB Sodium nitroprusside (SNP), a generator of nitric oxide (NO), decreased [H-3]dopamine uptake into rat striatal synaptosomal preparations in a dose-, time- and temperature-dependent fashion. Reduced hemoglobin, a substance that binds NO, prevented the SNP-induced decrease in uptake. Potassium ferri- and ferrocyanide, compounds similar to SNP that do not produce NO, were without effect on uptake. SNP inhibited [H-3]dopamine uptake in synaptosomes from nucleus accumbens and olfactory tubercle as well but with a lower potency. SNP inhibited [H-3]serotonin and [H-3]glutamate uptake but had no effect on [H-3]norepinephrine uptake. S-Nitroso-N-acetylpenicillamine (SNAP), another generator of NO, had effects similar to those of SNP. The SNP-induced decrease in [H-3]dopamine uptake was due to a V(max) decrease at 100 muM SNP and to both a V(max) and K(m) change at 300 muM SNP. Depletion of calcium by omission of calcium from buffers and addition of EGTA increased the potency of SNP in inhibiting uptake. There was no change in [H-3]WIN 35428 binding to the dopamine transporter with doses of SNP that inhibited uptake. These data indicate that NO can decrease [H-3]dopamine transporter function. C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,POB 5180,BALTIMORE,MD 21224. RI Pogun, Sakire/A-5816-2010 NR 66 TC 154 Z9 156 U1 6 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 28 PY 1994 VL 641 IS 1 BP 83 EP 91 DI 10.1016/0006-8993(94)91818-X PG 9 WC Neurosciences SC Neurosciences & Neurology GA NC813 UT WOS:A1994NC81300011 PM 7912635 ER PT J AU VAROQUI, H DIEBLER, MF MEUNIER, FM RAND, JB USDIN, TB BONNER, TI EIDEN, LE ERICKSON, JD AF VAROQUI, H DIEBLER, MF MEUNIER, FM RAND, JB USDIN, TB BONNER, TI EIDEN, LE ERICKSON, JD TI CLONING AND EXPRESSION OF THE VESAMICOL BINDING-PROTEIN FROM THE MARINE RAY TORPEDO - HOMOLOGY WITH THE PUTATIVE VESICULAR ACETYLCHOLINE TRANSPORTER UNC-17 FROM CAENORHABDITIS-ELEGANS SO FEBS LETTERS LA English DT Article DE VESICULAR ACETYLCHOLINE TRANSPORTER; VESAMICOL; TORPEDO ELECTRIC LOBE; CAENORHABDITIS ELEGANS UNC-17 ID CHOLINERGIC SYNAPTIC VESICLES; ELECTRIC ORGAN; RNA-POLYMERASE; SYSTEM; MARMORATA; RECEPTOR; FAMILY; PROTON; AH5183 AB Complementary DNA clones corresponding to a messenger RNA encoding a 56 kDa polypeptide have been obtained from Torpedo marmorata and Torpedo ocellata electric lobe libraries, by homology screening with a probe obtained from the putative acetylcholine transporter from the nematode Caenorhabditis elegans. The Torpedo proteins display approximately 50% overall identity to the C. elegans unc-17 protein and 43% identity to the two vesicle monoamine transporters (VMAT1 and VMAT2). This family of proteins is highly conserved within 12 domains which potentially span the vesicle membrane, with little similarity within the putative intraluminal glycosylated loop and at the N- and C-termini. The similar to 3.0 kb mRNA species is specifically expressed in the brain and highly enriched in the electric lobe of Torpedo. The Torpedo protein, expressed in CV-1 fibroblast cells, possesses a high-affinity binding site for vesamicol (K-d = 6 nM), a drug which blocks in vitro and in vivo acetylcholine accumulation in cholinergic vesicles. C1 OKLAHOMA MED RES FDN,PROGRAM MOLEC & CELL BIOL,OKLAHOMA CITY,OK 73104. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP VAROQUI, H (reprint author), DEPT NEUROCHIM,NEUROBIOL CELLULAIRE LAB,CNRS,F-91190 GIF SUR YVETTE,FRANCE. OI Eiden, Lee/0000-0001-7524-944X NR 37 TC 103 Z9 107 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAR 28 PY 1994 VL 342 IS 1 BP 97 EP 102 DI 10.1016/0014-5793(94)80592-X PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA ND692 UT WOS:A1994ND69200021 PM 8143858 ER PT J AU VOLKMUTH, WD DUKE, T WU, MC AUSTIN, RH SZABO, A AF VOLKMUTH, WD DUKE, T WU, MC AUSTIN, RH SZABO, A TI DNA ELECTRODIFFUSION IN A 2D ARRAY OF POSTS SO PHYSICAL REVIEW LETTERS LA English DT Article ID GEL-ELECTROPHORESIS; MOBILITY; DYNAMICS AB We consider some of the fundamental statistical mechanics of the electrodiffusion of a long polyelectrolyte, DNA, in a microlithographically constructed 2D rectangular array of cylindrical posts. The DNA polymer is shown to be free draining when not hooked on a post, and the mean time to unhook is explicitly calculated and compared to our measurements. C1 NIH,BETHESDA,MD 20892. RP VOLKMUTH, WD (reprint author), PRINCETON UNIV,DEPT PHYS,PRINCETON,NJ 08544, USA. RI Szabo, Attila/H-3867-2012 NR 26 TC 127 Z9 129 U1 2 U2 12 PU AMERICAN PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 0031-9007 J9 PHYS REV LETT JI Phys. Rev. Lett. PD MAR 28 PY 1994 VL 72 IS 13 BP 2117 EP 2120 DI 10.1103/PhysRevLett.72.2117 PG 4 WC Physics, Multidisciplinary SC Physics GA ND600 UT WOS:A1994ND60000044 ER PT J AU ROSENGARD, BR FISHBEIN, JM GIANELLO, P OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K HILL, GS SACHS, DH AF ROSENGARD, BR FISHBEIN, JM GIANELLO, P OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K HILL, GS SACHS, DH TI RETRANSPLANTATION IN MINIATURE SWINE - LACK OF A REQUIREMENT FOR GRAFT ADAPTATION FOR MAINTENANCE OF SPECIFIC RENAL-ALLOGRAFT TOLERANCE SO TRANSPLANTATION LA English DT Article; Proceedings Paper CT 19th Annual Meeting of the American-Society-of-Transplant-Surgeons CY MAY 19-21, 1993 CL HOUSTON, TX SP AMER SOC TRANSPLANT SURGEONS ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-I; KIDNEY ALLOGRAFTS; TRANSPLANTATION; REJECTION; SURVIVAL; ANTIGEN; RAT; SUPPRESSION; MECHANISM AB In miniature swine, one-haplotype class I disparate renal allografts are accepted without exogenous immunosuppression by approximately 35% of recipients. Alternatively, transplants bearing a two-haplotype class I mismatch are always rejected acutely. However, long-term acceptance in the latter animals can be achieved uniformly with a 12-day course of cyclosporine. In vitro studies of recipient cell-mediated lymphocytotoxicity responses have shown donor-specific cytotoxic T lymphocyte clones in tolerant animals, suggesting that tolerance may be a local phenomenon or a central phenomenon activated in the milieu of the graft. Six animals were retransplanted with kidneys MHC-matched to their original allograft to determine whether (1) tolerance is a central phenomenon; (2) host tolerance can be broken with a fresh challenge of donor antigen and antigen-presenting cells; and (3) graft adaptation is required for maintenance of tolerance. Four of the retransplanted animals had been spontaneous acceptors of one-haplotype class I-disparate grafts and two had been rendered tolerant to two-haplotype class I-mismatched kidneys with CsA induction. All six explanted allografts showed no histological evidence of rejection and all six retransplants were accepted without exogenous immunosuppression. These findings suggest that in miniature swine tolerance of class I-disparate kidneys is a stable, centrally mediated phenomenon that cannot be broken with a challenge of fresh donor antigen and donor-type APCs. Furthermore, successful retransplantation without immunosuppression in animals receiving CsA induction therapy for their first transplant suggests that graft adaptation is not necessary for the maintenance of tolerance. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. FU NHLBI NIH HHS [HL-18646]; NIAID NIH HHS [AI-31156] NR 26 TC 12 Z9 12 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 27 PY 1994 VL 57 IS 6 BP 794 EP 799 DI 10.1097/00007890-199403270-00003 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA ND846 UT WOS:A1994ND84600003 PM 8154022 ER PT J AU TAKAHASHI, T TANAKA, M BRANNAN, CI JENKINS, NA COPELAND, NG SUDA, T NAGATA, S AF TAKAHASHI, T TANAKA, M BRANNAN, CI JENKINS, NA COPELAND, NG SUDA, T NAGATA, S TI GENERALIZED LYMPHOPROLIFERATIVE DISEASE IN MICE, CAUSED BY A POINT MUTATION IN THE FAS LIGAND SO CELL LA English DT Article ID TUMOR-NECROSIS-FACTOR; T-CELL RECEPTOR; GENETIC-LINKAGE MAP; SYSTEMIC AUTOIMMUNITY; NEGATIVE SELECTION; CLONAL ELIMINATION; MOUSE GENOME; FACTOR-ALPHA; LPR; ANTIGEN AB Mice homozygous for lpr (lymphoproliferation) or gld (generalized lymphoproliferative disease) develop lymphadenopathy and suffer from autoimmune disease. The lpr mice have a mutation in a cell-surface protein, Fas, that mediates apoptosis. Fas ligand (FasL) is a tumor necrosis factor (TNF)-related type II membrane protein and binds to Fas. Here, mouse Fasl gene was isolated and localized to the gld region of mouse chromosome 1. Activated splenocytes from gld mice express Fasl mRNA. However, FasL in gld mice carries a point mutation in the C-terminal region, which is highly conserved among members of the TNF family. The recombinant gld FasL expressed in COS cells could not induce apoptosis in cells expressing Fas. These results indicate that lpr and gld are mutations in Fas and Fasl, respectively, and suggest important roles of the Fas system in development of T cells as well as cytotoxic T lymphocyte-mediated cytotoxicity. C1 NCI FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS,BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP TAKAHASHI, T (reprint author), OSAKA BIOSCI INST,6-2-4 FURUEDAI,SUITA,OSAKA 565,JAPAN. FU NCI NIH HHS [N01-CO-74101] NR 63 TC 1377 Z9 1396 U1 0 U2 11 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 25 PY 1994 VL 76 IS 6 BP 969 EP 976 DI 10.1016/0092-8674(94)90375-1 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ND246 UT WOS:A1994ND24600004 PM 7511063 ER PT J AU SZWEDA, LI AF SZWEDA, LI TI AGE-RELATED INCREASE IN LIVER RETINYL PALMITATE - RELATIONSHIP TO LIPOFUSCIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID VITAMIN-A; LIPID-PEROXIDATION; AGING RATS; FLUORESCENT; PRODUCTS; TISSUES; INVOLVEMENT; SUBSTANCES; STORAGE AB Lipofuscin is a general term assigned to fluorescent material that accumulates in cells as they age. It is apparent from this study that the fluorescent intensity of detergent-solubilized liver from Fisher-344 rats increased as a function of age. The fluorophore responsible for this increase was extracted with methanol and could be resolved from other cellular components when the methanol extracts were chromatographed over a re verse phase column. This compound was identified as retinyl palmitate and was found to increase throughout the entire life of the Fisher-344 rat (2-24 months), from a value of 0.26-1.77 mg/g of liver. In addition, the results presented here demonstrate that concentration, time between extraction and analysis, exposure to light, and degree of purity affect the observed fluorescent properties of retinyl palmitate. These factors affect many fluorophores and are likely to be, at least in part, responsible for the multiplicity of reported properties of lipofuscin. As has been reported for lipofuscin, retinyl palmitate accumulates in intracellular granules and exhibits fluorescence between 450 and 600 nm. Due to these similarities, the relationship between retinyl palmitate and lipofuscin warrants further investigation. RP SZWEDA, LI (reprint author), NHLBI,BIOCHEM LAB,BLDG 3,RM 221,BETHESDA,MD 20892, USA. NR 27 TC 13 Z9 13 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1994 VL 269 IS 12 BP 8712 EP 8715 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB411 UT WOS:A1994NB41100017 PM 8132600 ER PT J AU LOH, C ROMEO, C SEED, B BRUDER, JT RAPP, U RAO, A AF LOH, C ROMEO, C SEED, B BRUDER, JT RAPP, U RAO, A TI ASSOCIATION OF RAF WITH THE CD3 DELTA-CHAIN AND GAMMA-CHAIN OF THE T-CELL RECEPTOR-CD3 COMPLEX SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-TYROSINE KINASE; SERINE-THREONINE KINASE; PDGF BETA-RECEPTOR; ANTIGEN RECEPTOR; GROWTH-FACTOR; SIGNAL TRANSDUCTION; ZETA-CHAIN; PHOSPHOLIPASE-C; MONOCLONAL-ANTIBODY; BINDING-SITE AB Protein kinases and phosphatases play an important role in signal transduction. In the T cell, activation via the T cell receptor-CD3 complex results in rapid tyrosine phosphorylation of proteins, as well as subsequent increases in serine/threonine phosphorylation. The Raf serine/threonine kinase has been implicated in many receptor signaling pathways, including those of platelet-derived growth factor, epidermal growth factor, insulin, and interleukin-2 receptors. We show here that Raf is associated with the T cell receptor-CD3 complex in unstimulated murine T cells. Using a COS cell expression system, we show that a hypophosphorylated form of Raf specifically associates with the CD3 gamma and delta chains but not with the CD3 epsilon or zeta chains. These results suggest that Raf mediates signal transduction from the gamma and delta chains of the T cell receptor-CD3 complex, analogous to the role played by ZAP-70 in signal transduction mediated by the zeta chain. C1 DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. FU NIAID NIH HHS [AI27849]; NIGMS NIH HHS [GM46227] NR 62 TC 11 Z9 11 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1994 VL 269 IS 12 BP 8817 EP 8825 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB411 UT WOS:A1994NB41100033 PM 8132616 ER PT J AU LOEB, DM STEPHENS, RM COPELAND, T KAPLAN, DR GREENE, LA AF LOEB, DM STEPHENS, RM COPELAND, T KAPLAN, DR GREENE, LA TI A TRK NERVE GROWTH-FACTOR (NGF) RECEPTOR POINT MUTATION AFFECTING INTERACTION WITH PHOSPHOLIPASE C-GAMMA-1 ABOLISHES NGF-PROMOTED PERIPHERIN INDUCTION BUT NOT NEURITE OUTGROWTH SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID STIMULATES TYROSINE PHOSPHORYLATION; INTERMEDIATE FILAMENT PROTEIN; PC12 CELLS; PHEOCHROMOCYTOMA CELLS; PROTOONCOGENE PRODUCT; KINASE-ACTIVITY; HIGH-AFFINITY; MONOCLONAL-ANTIBODIES; SIGNALING COMPLEX; C-GAMMA AB We analyzed the function of Trk nerve growth factor (NGF) receptors containing a point mutation (Tyr --> Phe) in a major autophosphorylation site (Tyr-785). Tyr-785 is required for phospholipase C-gamma 1 to interact with Trk and to become tyrosine-phosphorylated in response to NGF. The altered receptors were transfected into a mutant subline of PC12 rat pheochromocytoma cells (designated PC12nnr5) that, unlike wild-type PC12 cells, lack expression of endogenous Trk and responsiveness to NGF. PC12nnr5 cells permanently transfected with Trk Y785F exhibit NGF-dependent autophosphorylation and normal NGF binding and internalization. Moreover, Trk Y785F mediates NGF-stimulated neurite outgrowth as well as a variety of additional responses including induction of immediate-early and late genes. However, in contrast to cells expressing wild-type Trk, cells expressing Trk Y785F lack NGF-promoted elevation of peripherin intermediate filament mRNA and protein. These observations indicate that phospholipase C-gamma 1 activation or other signaling pathways dependent on Tyr-785 autophosphorylation are selectively required for regulation of peripherin expression by NGF, but not for many other functional NGF responses. This supports the presence of multiple and separable signaling pathways in the NGF mechanism of action. C1 COLUMBIA UNIV COLL PHYS & SURG, DEPT PATHOL, NEW YORK, NY 10032 USA. COLUMBIA UNIV COLL PHYS & SURG, CTR NEUROBIOL & BEHAV, NEW YORK, NY 10032 USA. NCI, FREDERICK CANC RES CTR, ADV BIOSCI LABS, BASIC RES PROGRAM, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES CTR,ADV BIOSCI LABS, BASIC RES PROGRAM,PROT STRUCT GRP, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74101] NR 71 TC 109 Z9 110 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1994 VL 269 IS 12 BP 8901 EP 8910 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB411 UT WOS:A1994NB41100044 PM 7510697 ER PT J AU IWASAKI, M DARDEN, TA PARKER, CE TOMER, KB PEDERSEN, LG NEGISHI, M AF IWASAKI, M DARDEN, TA PARKER, CE TOMER, KB PEDERSEN, LG NEGISHI, M TI INHERENT VERSATILITY OF P-450 OXYGENASE - CONFERRING DEHYDROEPIANDROSTERONE HYDROXYLASE-ACTIVITY TO P-450 2A-4 BY A SINGLE AMINO-ACID MUTATION AT POSITION-117 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MOUSE; PROTEINS AB Mouse steroid 15 alpha hydroxylase P-450 2a-4 is restricted in its substrate specificity to the Delta(4), 3-ketone steroids such as androstenedione. As a result, the P-450 exhibits little hydroxylase activity toward Delta(5), 3 hydroxysteroids including dehydroepiandrosterone (DHEA). A single amino acid mutation of Ala at position 117 to Val, however, is enough to confer a high DHEA hydroxylase activity to P-450 2a-4 with 7 alpha-OH DHEA as one of the two major hydroxylated metabolites. Mouse coumarin 7-hydroxylase P-450 2a-5 contains Val at position 117, but it exhibits very low DHEA hydroxylase activity. P-450 2a-5 acquires high DHEA hydroxylase activity, however, by a mutation of Phe-209 to Asn. Moreover, the mutant P-450 2a-5 loses its activity when Val is replaced by Ala at position 117. The residue at position 117, therefore, plays the principal role in the determination of the DHEA hydroxylase activity of the P-450s. Conversely, mutations at residue 117 have little effect on the androstenedione hydroxylase activities of the P-450s. Further modeling of the DHEA binding orientation in the substrate-heme pocket of bacterial P-450cam (Iwasaki, M., Darden, T., Pedersen, L., Davis, D. G., Juvonen, R. O., Sueyoshi, T., and Negishi, M. (1993) J. Biol. Chem. 268, 759-762) provides support for the hypothesis that the type of residue at position 117 determines the steroid-substrate speci ficity of the P-450 depending on the substituent at the C3 position of steroid molecule. C1 NIEHS,REPROD & DEV TOXICOL LAB,PHARMACOGENET SECT,RES TRIANGLE PK,NC 27709. RI Pedersen, Lee/E-3405-2013; Tomer, Kenneth/E-8018-2013 OI Pedersen, Lee/0000-0003-1262-9861; NR 21 TC 24 Z9 24 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1994 VL 269 IS 12 BP 9079 EP 9083 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB411 UT WOS:A1994NB41100070 PM 8132645 ER PT J AU ACKERMANN, EJ KEMPNER, ES DENNIS, EA AF ACKERMANN, EJ KEMPNER, ES DENNIS, EA TI CA2+-INDEPENDENT CYTOSOLIC PHOSPHOLIPASE A(2) FROM MACROPHAGE-LIKE P388D(1) CELLS - ISOLATION AND CHARACTERIZATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CALCIUM-INDEPENDENT PHOSPHOLIPASE-A2; RADIATION INACTIVATION; PURIFICATION; LINE; PHOSPHOFRUCTOKINASE; MEMBRANE; LYSOPHOSPHOLIPASE; RAT; PROTEINS; BRAIN AB A novel form of an ATP-regulated, oligomeric, Ca2(+-) independent phospholipase A(2)(iPLA(2)) has been purified from the cytosol of the murine macrophage-like cell line P388D(1). The purification procedure included ammonium sulfate precipitation and sequential column chromatography on octyl-Sepharose, ATP-agarose, Mono Q fast protein liquid chromatography (FPLC), and hydroxyapatite FPLC. The resulting enzyme preparation was purified over 400,000-fold with a final specific activity of approximately 5 mu mol/min/mg using a mixed micelle assay system of Triton X-100 and dipalmitoyl phosphatidylcholine (PC). The purified enzyme was Ca2+-independent and did not show a preference for either sn-2 arachidonic acid or sn-1 alkyl-ether containing phospholipids when utilizing mixed micelles as substrate. It was found to hydrolyze dipalmitoyl-PC similar to 4-fold faster than 1-palmitoyl-2-arachidonyl-PC and similar to 15-fold faster than 1-O-hexadecyl-2-arachidonyl-PC. Triton X-100 increased the P388D(1) iPLA(2) activity with optimal activity found at a Triton/phospholipid molar ratio of 4:1. The purified enzyme was activated 2-6-fold by ATP as well as other di- and triphosphate nucleosides. This activation was sensitive to the concentration of Triton X-100 present in the assay. SDS-polyacrylamide gel electrophoresis carried out on the purified enzyme yielded a single major band at a molecular weight of about 80,000. However, radiation inactivation experiments, carried out on the cell homogenate, demonstrated a target size of 337 +/- 25 kDa, indicating that the catalytically active iPLA(2) exists as a large oligomeric complex, either through self-aggregation or association of the enzyme with other proteins. C1 UNIV CALIF SAN DIEGO, DEPT CHEM, LA JOLLA, CA 92093 USA. NIH, BETHESDA, MD 20892 USA. FU NICHD NIH HHS [HD 26171] NR 32 TC 214 Z9 214 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1994 VL 269 IS 12 BP 9227 EP 9233 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB411 UT WOS:A1994NB41100089 PM 8132660 ER PT J AU MILLER, MW HANOVER, JA AF MILLER, MW HANOVER, JA TI FUNCTIONAL NUCLEAR-PORES RECONSTITUTED WITH BETA-1-4 GALACTOSE-MODIFIED O-LINKED N-ACETYLGLUCOSAMINE GLYCOPROTEINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL-FREE-EXTRACTS; XENOPUS EGGS; PROTEIN IMPORT; DNA-REPLICATION; COMPLEX GLYCOPROTEINS; ASSEMBLY INVITRO; TRANSPORT; IDENTIFICATION; GLYCOSYLATION; ENVELOPE AB Nuclear pore proteins bearing O-linked N-acetylglucosamine (GlcNAc) are involved in nuclear transport, although a role for their glycosylation is not established. Xenopus egg extracts capable of reforming functional nuclei in vitro yielded nuclei with impaired transport and reduced nuclear pore density when depleted of wheat germ agglutinin-binding proteins. Many of the nuclear pores remaining in wheat germ agglutinin-depleted nuclei showed a striking loss of internal structure. Nuclear transport and normal nuclear pore structure were restored by the addition of nuclear pore glycoproteins from rat liver or Xenopus eggs. Glycoproteins modified by the addition of galactose to O-linked GlcNAc were also competent for assembling normal nuclear pores and restoring nuclear transport. Aphidicolin-sensitive DNA synthesis was unaffected by the removal or modification of O-linked GlcNAc glycoproteins. These data argue against a requirement for a lectin-like recognition of O-linked GlcNAc glycoproteins in nuclear pore assembly, nuclear transport, or DNA synthesis. C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 54 TC 53 Z9 53 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 25 PY 1994 VL 269 IS 12 BP 9289 EP 9297 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB411 UT WOS:A1994NB41100097 PM 8132666 ER PT J AU GERWICK, WH PROTEAU, PJ NAGLE, DG HAMEL, E BLOKHIN, A SLATE, DL AF GERWICK, WH PROTEAU, PJ NAGLE, DG HAMEL, E BLOKHIN, A SLATE, DL TI STRUCTURE OF CURACIN-A, A NOVEL ANTIMITOTIC, ANTIPROLIFERATIVE, AND BRINE SHRIMP TOXIC NATURAL PRODUCT FROM THE MARINE CYANOBACTERIUM LYNGBYA-MAJUSCULA SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Letter ID LISSOCLINUM-PATELLA; CYTOTOXICITY; TUBULIN AB Bioassay-guided fractionation of the organic extract of a Curacao collection of Lyngbya majuscula led to the isolation of a new lipid, curacin A, with exceptional brine shrimp toxic and antiproliferative activities. Its unique thiazoline-containing structure has been deduced from spectroscopic information. Pure curacin A is an antimitotic agent (IC50 values in three cell lines ranging from 7 to 200 nM) that inhibits microtubule assembly and the binding of colchicine to tubulin. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. SYNTEX DISCOVERY RES CORP,INST BIOCHEM & CELL BIOL,PALO ALTO,CA 94304. RP GERWICK, WH (reprint author), OREGON HLTH SCI UNIV,COLL PHARM,PORTLAND,OR 97201, USA. NR 12 TC 257 Z9 267 U1 3 U2 30 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD MAR 25 PY 1994 VL 59 IS 6 BP 1243 EP 1245 DI 10.1021/jo00085a006 PG 3 WC Chemistry, Organic SC Chemistry GA ND303 UT WOS:A1994ND30300006 ER PT J AU MAZUMDER, A ENGELMAN, A CRAIGIE, R FESEN, M POMMIER, Y AF MAZUMDER, A ENGELMAN, A CRAIGIE, R FESEN, M POMMIER, Y TI INTERMOLECULAR DISINTEGRATION AND INTRAMOLECULAR STRAND TRANSFER ACTIVITIES OF WILD-TYPE AND MUTANT HIV-1 INTEGRASE SO NUCLEIC ACIDS RESEARCH LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; VIRAL-DNA; PROTEIN INVITRO; CLEAVAGE; TERMINI AB We report the activities of HIV integrase protein on a novel DNA substrate, consisting of a pair of gapped duplex molecules. Integrase catalyzed an intermolecular disintegration reaction that requires positioning of a pair of the gapped duplexes in a configuration that resembles the integration intermediate. However, the major reaction resulted from an intramolecular reaction involving a single gapped duplex, giving rise to a hairpin. Surprisingly, a deletion mutant of integrase that lacks both the amino and carboxyl terminal regions still catalyzed the intermolecular disintegration reaction, but supported only a very low level of the intramolecular reaction. The central core region of integrase is therefore sufficient to both bind the gapped duplex DNA and juxtapose a pair of such molecules through protein-protein interactions. We suggest that the branched DNA structures of the previously reported disintegration substrate, and the intermolecular disintegration substrate described here, assist in stabilizing protein-protein interactions that otherwise require the amino and carboxyl terminal regions of integrase. C1 NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,ROCKVILLE,MD 20892. NIDDK,MOLEC BIOL LAB,ROCKVILLE,MD 20892. NR 29 TC 43 Z9 43 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 25 PY 1994 VL 22 IS 6 BP 1037 EP 1043 DI 10.1093/nar/22.6.1037 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA ND770 UT WOS:A1994ND77000021 PM 8152908 ER PT J AU LIU, WM MARAIA, RJ RUBIN, CM SCHMID, CW AF LIU, WM MARAIA, RJ RUBIN, CM SCHMID, CW TI ALU TRANSCRIPTS - CYTOPLASMIC LOCALIZATION AND REGULATION BY DNA METHYLATION SO NUCLEIC ACIDS RESEARCH LA English DT Article ID RNA POLYMERASE-III; SIGNAL RECOGNITION PARTICLE; HELA-CELLS; SEQUENCES; 5-AZACYTIDINE; SUBFAMILIES; REPEATS; INVITRO; SUBUNIT; GENES AB Full length Alu transcripts in HeLa cells are detected by primer extension using reverse transcriptase and are also analyzed as cloned cDNA sequences. The 5' end of these transcripts corresponds to the transcriptional start site for RNA polymerase III indicating that these RNAs are transcribed from their internal polymerase III promoters. The Alu transcripts found in cytoplasmic poly A+ RNAs appear to be organized into RNPs as assayed by sucrose gradient sedimentation. Present at about one hundred to one thousand copies per cell, the Alu transcripts are rare as compared to 7SL RNA. In agreement with previous reports that methylation inhibits Pol III-directed transcription of Alu in vitro, treatment of HeLa cells with 5-azacytidine results in Alu DNA hypomethylation and an increase in the abundance of the Alu transcript. Sequence analysis shows that many different Alu repeats including members of all subfamilies are transcribed by Pol III in vivo. cDNA sequences of the Pol III-directed transcripts exactly match the A box of the Pol III promoter element whereas in other Alu transcripts this element is not faithfully conserved. C1 UNIV CALIF DAVIS,MOLEC & CELLULAR BIOL SECT,DAVIS,CA 95616. UNIV CALIF DAVIS,DEPT CHEM,DAVIS,CA 95616. NICHHD,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM 21346] NR 33 TC 111 Z9 113 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 25 PY 1994 VL 22 IS 6 BP 1087 EP 1095 DI 10.1093/nar/22.6.1087 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA ND770 UT WOS:A1994ND77000028 PM 7512262 ER PT J AU LODI, PJ GARRETT, DS KUSZEWSKI, J TSANG, MLS WEATHERBEE, JA LEONARD, WJ GRONENBORN, AM CLORE, GM AF LODI, PJ GARRETT, DS KUSZEWSKI, J TSANG, MLS WEATHERBEE, JA LEONARD, WJ GRONENBORN, AM CLORE, GM TI HIGH-RESOLUTION SOLUTION STRUCTURE OF THE BETA-CHEMOKINE HMIP-1-BETA BY MULTIDIMENSIONAL NMR SO SCIENCE LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; RESTRAINED MOLECULAR-DYNAMICS; HUMAN INTERLEUKIN-8 RECEPTOR; MULTIPLE QUANTUM COHERENCE; 3-DIMENSIONAL STRUCTURE; DISTANCE GEOMETRY; MONOCYTE CHEMOATTRACTANT; CYTOKINE FAMILY; LARGER PROTEINS; ACT-2 CYTOKINE AB The three-dimensional structure of a member of the beta subfamily of chemokines, human macrophage inflammatory protein-1 beta (hMIP-1 beta), has been determined with the use of solution multidimensional heteronuclear magnetic resonance spectroscopy. Human MIP-1 beta is a symmetric homodimer with a relative molecular mass of similar to 16 kilodaltons. The structure of the hMIP-1 beta monomer is similar to that of the related alpha chemokine interleukin-8 (IL-8). However, the quaternary structures of the two proteins are entirely distinct, and the dimer interfaceis formed by a completely different set of residues. Whereas the IL-8 dimer is globular, the hMIP-1 beta dimer is elongated and cylindrical. This provides a rational explanation for the absence of cross-binding and reactivity between the alpha and beta chemokine subfamilies. Calculation of the solvation free energies of dimerization suggests that the formation and stabilization of the two different types of dimers arise from the burial of hydrophobic residues. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. R&D SYST INC,MINNEAPOLIS,MN 55413. NHLBI,PULM & MOLEC IMMUNOL SECT,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 60 TC 199 Z9 201 U1 0 U2 7 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 25 PY 1994 VL 263 IS 5154 BP 1762 EP 1767 DI 10.1126/science.8134838 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NC040 UT WOS:A1994NC04000036 PM 8134838 ER PT J AU BENDELAC, A KILLEEN, N LITTMAN, DR SCHWARTZ, RH AF BENDELAC, A KILLEEN, N LITTMAN, DR SCHWARTZ, RH TI A SUBSET OF CD4(+) THYMOCYTES SELECTED BY MHC CLASS-I MOLECULES SO SCIENCE LA English DT Article ID CD8+ T-CELLS; CYTOPLASMIC TAIL; BINDING-SITE; IMMATURE THYMOCYTES; THYMIC SELECTION; ALPHA-3 DOMAIN; DEFICIENT MICE; GENE FAMILY; LINEAGE; CD4+ AB To complete their maturation, most immature thymocytes depend on the simultaneous engagement of their antigen receptor [alpha beta T cell receptor (TCR)] and their CD4 or CD8 coreceptors with major histocompatibility complex class II or I ligands, respectively. However, a normal subset of mature alpha beta TCR(+) thymocytes did not follow these rules. These thymocytes expressed NK1.1 and a restricted set of alpha beta TCRs that are intrinsically class I-reactive because their positive selection was class I-dependent but CD8-independent. These cells were CD4(+) and CD4(-)8(-) but never CD8(+), because the presence of CD8 caused negative selection. Thus, neither CD4 nor CD8 contributes signals that direct their maturation into the CD4(+) and CD4(-)8(-) lineages. C1 UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT MICROBIOL & IMMUNOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT BIOCHEM & BIOPHYS,SAN FRANCISCO,CA 94143. RP BENDELAC, A (reprint author), NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892, USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 56 TC 436 Z9 436 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 25 PY 1994 VL 263 IS 5154 BP 1774 EP 1778 DI 10.1126/science.7907820 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NC040 UT WOS:A1994NC04000039 PM 7907820 ER PT J AU MILLS, JL AF MILLS, JL TI MORE ON TORTURING DATA - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP MILLS, JL (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 24 PY 1994 VL 330 IS 12 BP 862 EP 862 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA NB803 UT WOS:A1994NB80300016 ER PT J AU BIGGAR, RJ AF BIGGAR, RJ TI FURUNCULAR MYIASIS - ALTERNATIVES TO BACON THERAPY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP BIGGAR, RJ (reprint author), NCI,ROCKVILLE,MD, USA. NR 2 TC 1 Z9 2 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 23 PY 1994 VL 271 IS 12 BP 901 EP 901 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA NA743 UT WOS:A1994NA74300009 PM 8120950 ER PT J AU OBRIEN, TR AF OBRIEN, TR TI HIV-2 TRANSMISSION - IMPLICATIONS FOR SPREAD OF HIV-1 SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP OBRIEN, TR (reprint author), NCI,ROCKVILLE,MD, USA. NR 4 TC 3 Z9 3 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 23 PY 1994 VL 271 IS 12 BP 903 EP 904 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA NA743 UT WOS:A1994NA74300016 PM 8120954 ER PT J AU ROSENBERG, SA YANG, JC TOPALIAN, SL SCHWARTZENTRUBER, DJ WEBER, JS PARKINSON, DR SEIPP, CA EINHORN, JH WHITE, DE AF ROSENBERG, SA YANG, JC TOPALIAN, SL SCHWARTZENTRUBER, DJ WEBER, JS PARKINSON, DR SEIPP, CA EINHORN, JH WHITE, DE TI TREATMENT OF 283 CONSECUTIVE PATIENTS WITH METASTATIC MELANOMA OR RENAL-CELL CANCER USING HIGH-DOSE BOLUS INTERLEUKIN-2 SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID ACTIVATED KILLER CELLS; ESTABLISHED PULMONARY METASTASES; TUMOR-INFILTRATING LYMPHOCYTES; RECOMBINANT INTERLEUKIN-2; AUTOLOGOUS TUMOR; INVITRO GROWTH; IMMUNOTHERAPY; REGRESSION; RESPONSES; LYSIS AB Objective.-To determine the efficacy of treatment using high-dose bolus interleukin 2 (IL-2) in patients with metastatic melanoma or renal cell cancer. Design and Setting.-Consecutive series of all patients treated with high-dose IL-2 in the Surgery Branch of the National Cancer Institute from September 1985 through December 1992. Patients.-Two hundred eighty-three patients with metastatic melanoma or metastatic renal cell cancer who had failed standard treatment for their cancers. Interventions.-Patients received IL-2 at a dose of 720 000 IU/kg intravenously every 8 hours for a maximum of 15 doses per cycle. Two cycles constituted a treatment course, and patients with stable or responding disease received additional treatment courses. A total of 447 courses of treatment were administered. Main Outcome Measures.-Regression of measurable tumor, durability of response to treatment, and survival. Results.-Nine patients (7%) with metastatic melanoma achieved complete regression of all disease and 14 patients (10%) had partial regression. Ten patients (7%) with metastatic renal cell cancer experienced complete regression and 20 patients (13%) had partial regression. Of the 19 patients with complete regression, 15 have remained in complete remission from 7 to 91 months aftertreatment. Three treatment-related deaths (1.1%) occurred early in this series, but as experience with the administration of this IL-2 regimen increased, no treatment-related deaths occurred in 214 patients treated during the last 5 years of the study. Conclusion.-Biologic therapy with IL-2 can cause significant antitumor effects in patients with advanced metastatic melanoma or renal cell cancer. Because IL-2 does not have a direct effect on cancer cells but rather mediates its antitumor activity by altering host immune reactions, these data represent the best available evidence that immunologic therapy for cancer can be effective in selected patients. RP ROSENBERG, SA (reprint author), NCI,DIV CANC TREATMENT,SURG BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2B42,BETHESDA,MD 20892, USA. NR 47 TC 807 Z9 817 U1 2 U2 16 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 23 PY 1994 VL 271 IS 12 BP 907 EP 913 DI 10.1001/jama.271.12.907 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA NA743 UT WOS:A1994NA74300025 PM 8120958 ER PT J AU YOUNG, NS AF YOUNG, NS TI AGRANULOCYTOSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Discussion ID DRUG-INDUCED AGRANULOCYTOSIS; HEMATOPOIETIC GROWTH-FACTORS; METABOLITES; PRECURSORS; ANTIBODIES RP YOUNG, NS (reprint author), NHLBI,HEMATOL BRANCH,BLDG 10,ROOM 7C103,BETHESDA,MD 20892, USA. NR 32 TC 29 Z9 29 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 23 PY 1994 VL 271 IS 12 BP 935 EP 938 DI 10.1001/jama.271.12.935 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA NA743 UT WOS:A1994NA74300031 PM 7509883 ER PT J AU LONDON, RE GABEL, SA AF LONDON, RE GABEL, SA TI F-19 NMR-STUDIES OF FLUOROBENZENEBORONIC ACIDS .1. INTERACTION KINETICS WITH BIOLOGICALLY SIGNIFICANT LIGANDS SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; TRANSITION-STATE ANALOGS; BORONIC ACID; BORATE ESTERS; SERINE PROTEASE; BORIC-ACID; SELECTIVE INVERSION; PHENYLBORONIC ACID; LACTIC-ACID; AMINO-ACIDS AB Kinetic studies of the interaction of 4-fluorobenzeneboronic acid and the 3-chloro-4-fluoro analog with hydroxyl ions and with several biologically significant ligands have been performed using F-19 line width and magnetization transfer measurements. Analysis of pH-dependent line-width data for the boronic acid-boronate equilibrium indicates that at millimolar concentrations the boronate dissociation rates are dominated by intermolecular hydroxyl ion transfer. Dissociation rate constants for the fluorobenzeneboronates due to intermolecular hydroxyl ion transfer to the corresponding boronic acid were determined to be 2.9 X 10(6) M-1 s-s and 1 X 10(7) M-1 s-1 for 4-fluorobenzeneboronate (FBA) and 3 chloro-4-fluorobenzeneboronate (CFBA), respectively, indicating a threefold greater rate for the 3-chloro derivative. This result presumably reflects a greater tendency of CFBA toward intermolecular association. Analogously, the presence of various buffers enhanced the rate of dissociation of hydroxyl ion from 4-fluorobenzeneboronate, with values of 2 X 10(7) M-1 s-1 and 2.5 x 10(8) M-1 s-1 for the effects of phosphate and imidazole, respectively. The proton-dependent dissociation pathway in the absence of buffers is apparently not significant in the region near neutral pH. A number of bidentate boron ligands studied, including a series of carbohydrates, catechols, and alpha-hydroxy acids, form complexes with sufficient stability to result in slow exchange kinetics on the F-19 time scale. At higher pH values, multiple resonances corresponding to the various boronate complexes could often be resolved. The F-19 shifts for these adducts are typically close to that of the boronate anion, consistent with an sp3-hybridized boronate structure. However, data obtained for the FBA-sorbitol adduct at lower Ph values support the presence of a trigonal boronic acid-sorbitol adduct. Dissociation of several ligand-FBA complexes was studied using magnetization transfer techniques. As in the case of hydroxyl ion dissociation, the presence of buffers significantly accelerated the dissociation rate of boronate-ligand complexes. Results were generally in close agreement with previous stopped-flow kinetic measurements, although the dissociation rate constant from the catechols is about an order of magnitude faster than the rate extrapolated from lower pH stopped-flow measurements. RP LONDON, RE (reprint author), NIEHS,MOLEC BIOPHYS LAB,MD 17-05,BOX 12233,RES TRIANGLE PK,NC 27709, USA. NR 48 TC 31 Z9 31 U1 1 U2 10 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD MAR 23 PY 1994 VL 116 IS 6 BP 2562 EP 2569 DI 10.1021/ja00085a041 PG 8 WC Chemistry, Multidisciplinary SC Chemistry GA NE026 UT WOS:A1994NE02600041 ER PT J AU LONDON, RE GABEL, SA AF LONDON, RE GABEL, SA TI F-19 NMR-STUDIES OF FLUOROBENZENEBORONIC ACIDS .2. KINETIC CHARACTERIZATION OF THE INTERACTION WITH SUBTILISIN CARLSBERG AND MODEL LIGANDS SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID PEPTIDE BORONIC ACID; ALPHA-LYTIC PROTEASE; NUCLEAR-MAGNETIC-RESONANCE; TRANSITION-STATE ANALOGS; SERINE PROTEASE; SELECTIVE INVERSION; PHENYLBORONIC ACID; ARYLBORONIC ACIDS; CHYMOTRYPSIN; SPECTROSCOPY AB The interaction of 4-fluoro-substituted benzeneboronic acids with subtilisin Carlsberg has been studied by F-19 NMR. At a field strength of 8.5 T, the inhibitors 4-fluoro- and 3-chloro-4-fluorobenzeneboronic acids are in slow exchange with the enzyme and exhibit bound shifts typical of boronate species. Dissociation rate constants determined by magnetization transfer were found to be pH independent in the range from 6.4 to 7.4, with values of 156 s-1 (4-fluoro) and 24 s-1 (3-chloro-4-fluoro) at pH 7.4, 21-degrees-C. These values are similar to previous temperature-jump determinations of the slow component of the dissociation of analogous ligands from subtilisin BPN', demonstrating that the previously observed rates correspond to the boronate --> boronic acid transition. The interaction of 4-fluorobenzeneboronic acid (FBA) with 2-pyridylcarbinol, a model ligand for the histidine and serine groups of the active site, was also studied and demonstrated to involve chelation with both the hydroxyl oxygen and pyridyl nitrogen. Nitrogen-14 NMR studies indicate that, when complexed to the boronate, the pyridyl nitrogen exhibits a shift intermediate between the values for the protonated and unprotonated forms. This result is in close agreement with N-15 NMR studies of boronate inhibitors bound to the active site of [epsilon-N-15]histidine-labeled alpha-lytic protease. The dissociation rate constant for the 4-fluorobenzeneboronate-pyridylcarbinol complex of 22.5 s-1 is considerably slower than the dissociation rate constant for the corresponding subtilisin-boronate complex. The slower dissociation kinetics for the model complex is consistent with the conclusion that such bidentate chelation is not present for the boronate-subtilisin system under study. RP LONDON, RE (reprint author), NIEHS,MOLEC BIOPHYS LAB,MD 17-05,BOX 12233,RES TRIANGLE PK,NC 27709, USA. NR 33 TC 25 Z9 25 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD MAR 23 PY 1994 VL 116 IS 6 BP 2570 EP 2575 DI 10.1021/ja00085a042 PG 6 WC Chemistry, Multidisciplinary SC Chemistry GA NE026 UT WOS:A1994NE02600042 ER PT J AU FRECH, M DARDEN, TA PEDERSEN, LG FOLEY, CK CHARIFSON, PS ANDERSON, MW WITTINGHOFER, A AF FRECH, M DARDEN, TA PEDERSEN, LG FOLEY, CK CHARIFSON, PS ANDERSON, MW WITTINGHOFER, A TI ROLE OF GLUTAMINE-61 IN THE HYDROLYSIS OF GTP BY P21(H-RAS) - AN EXPERIMENTAL AND THEORETICAL-STUDY SO BIOCHEMISTRY LA English DT Article ID H-RAS P21; ACTIVATING PROTEIN; BIOCHEMICAL-PROPERTIES; ESCHERICHIA-COLI; MECHANISM; EXCHANGE; BINDING; GAP; CONFORMATION; SUPERFAMILY AB The active GTP-bound form of p21(ras) is converted to the biologically inactive GDP-bound form by enzymatic hydrolysis and this function serves to regulate the wild-type ras protein. The side chain of the amino acid at position 61 may play a key role in this hydrolysis of GTP by p21. Experimental studies that define properties of the Q61E mutant of p21(H-ras) are presented along with supporting molecular dynamics simulations. We find that under saturating concentrations of GTP the Q61E mutant of p21(H-ras) has a 20-fold greater rate of intrinsic hydrolysis (k(cat) = 0.57 min(-1)) than the wild type. The affinity of the Q61E variant for GTP (K-d = 115 mu M) is much lower than that of the wild type. GTPase activating protein does not activate the variant. From molecular dynamics simulations, we find that both the wild type and Q61E mutant have the residue 61 side chain in transient contact with a water molecule that is well-positioned for hydrolytic attack on the gamma phosphate. Thr-35 also is found to form a transient hydrogen bond with this critical water. These elements may define the catalytic complex for hydrolysis of the GTP [Pai et. al. (1990) EMBO J. 9, 2351]. Similarly, the G12P mutant, which also has an intrinsic hydrolysis rate similar to the wild type, is found to form the same complex in simulation. In contrast, molecular dynamics analysis of the mutants G12R, G12V, and Q61L, which have much lower intrinsic rates than the wild-type p21, do not show this complex. Thus, the experimental data for intrinsic hydrolysis rates and the molecular dynamics simulations support the view that the residue 61 side chain is involved in activating a water molecule in the GTP hydrolysis mechanism. C1 NIEHS,RES TRIANGLE PK,NC 27709. CNRS,INST PHARMACOL MOLEC & CELLULAIRE,VALBONNE,FRANCE. MAX PLANCK INST MOLEK PHYSIOL,STRUKTURELLE BIOL ABT,D-44139 DORTMUND,GERMANY. UNIV N CAROLINA,DEPT CHEM,CHAPEL HILL,NC 27514. CRAY RES INC,RES TRIANGLE PK,NC 27709. GLAXO INC,RES TRIANGLE PK,NC 27709. RI Pedersen, Lee/E-3405-2013; OI Pedersen, Lee/0000-0003-1262-9861; Foley, Charles/0000-0001-6578-9629 FU NHLBI NIH HHS [HL27995] NR 40 TC 91 Z9 92 U1 0 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 22 PY 1994 VL 33 IS 11 BP 3237 EP 3244 DI 10.1021/bi00177a014 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NC041 UT WOS:A1994NC04100014 PM 8136358 ER PT J AU MAKINO, S GOLD, PW SCHULKIN, J AF MAKINO, S GOLD, PW SCHULKIN, J TI CORTICOSTERONE EFFECTS ON CORTICOTROPIN-RELEASING HORMONE MESSENGER-RNA IN THE CENTRAL NUCLEUS OF THE AMYGDALA AND THE PARVOCELLULAR REGION OF THE PARAVENTRICULAR NUCLEUS OF THE HYPOTHALAMUS SO BRAIN RESEARCH LA English DT Article DE CORTICOSTERONE; CORTICOTROPIN-RELEASING HORMONE; AMYGDALA; PARAVENTRICULAR NUCLEUS; MESSENGER RNA ID DIFFERENTIAL REGULATION; RAT-BRAIN; BIOCHEMICAL MANIFESTATIONS; RIBONUCLEIC-ACID; ACOUSTIC STARTLE; STRESS; PITUITARY; RECEPTORS; LESIONS; IMMUNOREACTIVITIES AB Using in situ hybridization histochemistry, we report differential expression of corticotropin-releasing hormone (CRH) mRNA in the central nucleus of the amygdala (CEA) and the parvocellular region of the paraventricular nucleus of the hypothalamus (PVN) following systemic treatment with corticosterone (CORT) in adrenally-intact rats. Both injection of low (1 mg/kg/day) and high (5 mg/day) CORT reduced CRH mRNA expression in the PVN in a dose-dependent manner, although it returned to normal at the low dose by 14 days. By contrast, the high dose of CORT increased CRH mRNA transiently in the CEA at 4 days, although the low dose of CORT decreased it at 14 days. In a second experiment, we implanted a slowly-releasing CORT pellet for 2 weeks (200 mg, 60 day release) subcutaneously. This treatment produced an elevation of CRH mRNA in the CEA both at 1 and 2 weeks, whereas CRH mRNA in the PVN was decreased to a large extent as seen in the high CORT group of the first experiment. These results suggest that glucocorticoids can facilitate CRH mRNA expression in the CEA, a site implicated in anxiety and fear, while restraining the hypothalamic-pituitary-adrenal axis as indicated by the reduction in CRH mRNA in the PVN. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BEHAV NEUROSCI UNIT,BLDG 10 3S-231,BETHESDA,MD 20892. NR 38 TC 272 Z9 283 U1 1 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 21 PY 1994 VL 640 IS 1-2 BP 105 EP 112 DI 10.1016/0006-8993(94)91862-7 PG 8 WC Neurosciences SC Neurosciences & Neurology GA NB938 UT WOS:A1994NB93800013 PM 8004437 ER PT J AU SCHNEIDER, E COWAN, KH AF SCHNEIDER, E COWAN, KH TI MULTIPLE-DRUG RESISTANCE IN CANCER-THERAPY SO MEDICAL JOURNAL OF AUSTRALIA LA English DT Article ID CONFERS MULTIDRUG RESISTANCE; KB CARCINOMA-CELLS; RETROVIRAL TRANSFER; TRANSGENIC MICE; P-GLYCOPROTEIN; HUMAN MDR1; EXPRESSION; ADRIAMYCIN; GENE; CDNA RP SCHNEIDER, E (reprint author), NCI,BETHESDA,MD 20892, USA. NR 28 TC 4 Z9 4 U1 0 U2 1 PU AUSTRALASIAN MED PUBL CO LTD PI SYDNEY PA LEVEL 1, 76 BERRY ST, SYDNEY NSW 2060, AUSTRALIA SN 0025-729X J9 MED J AUSTRALIA JI Med. J. Aust. PD MAR 21 PY 1994 VL 160 IS 6 BP 371 EP 373 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA NB898 UT WOS:A1994NB89800016 PM 7907772 ER PT J AU SHIMAZAKI, K ISHIDA, A RHEE, SG TAKENAWA, T KAWAI, N AF SHIMAZAKI, K ISHIDA, A RHEE, SG TAKENAWA, T KAWAI, N TI CHANGES IN IP3 3-KINASE IMMUNOREACTIVITY FOLLOWING TRANSIENT ISCHEMIA IN GERBIL HIPPOCAMPUS SO NEUROREPORT LA English DT Article DE ISCHEMIA; GLUTAMATE RECEPTOR; GERBIL; HIPPOCAMPUS; GLUTAMATE RECEPTORS; IMMUNOHISTOCHEMISTRY; IMMUNOBLOT; 1,4,5-TRIPHOSPHATE 3-KINASE; IP3; IP4 ID INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE; RAT-BRAIN; ISCHEMIC DAMAGE; CELL-DEATH; CALCIUM; VULNERABILITY; ACCUMULATION; PROTEOLYSIS; NEURONS AB THE distribution of inositol 1,4,5-triphosphate 3-kinase (IP3 3-kinase) in the gerbil hippocampus was studied before and after transient ischaemia, by immunohistochemistry and immunoblot with monoclonal antibody to IP3 3-kinase. In control gerbils, intense IP3 3-kinase immunoreactivity was localized in the dendritic field of CA1 pyramidal neurones. However, after ischaemia for 5 min, the immunoreactivity decreased gradually, until after 24 h there was very little IP3 3-kinase detectable. Immunoblot study showed a similar decrease of IP3 3-kinase in ischaemic hippocampus. Infliction of 2 min of ischaemia prior to the 5 min of ischaemia is known to have a protective effect on the 5 min ischaemia. With the addition of the 2 min ischaemia there was no decrease in IP3 3-kinase following the 5 min ischaemia. The results suggest that IP3 3-kinase might play a critical role in inducing the delayed neuronal death following ischaemia. C1 JICHI MED SCH,DEPT PHYSIOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. NHLBI,BETHESDA,MD 20892. UNIV TOKYO,INST MED SCI,MINATO KU,TOKYO 108,JAPAN. NR 24 TC 9 Z9 9 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD MAR 21 PY 1994 VL 5 IS 7 BP 785 EP 788 DI 10.1097/00001756-199403000-00012 PG 4 WC Neurosciences SC Neurosciences & Neurology GA NE139 UT WOS:A1994NE13900012 PM 8018850 ER PT J AU GALLO, RC AF GALLO, RC TI GALLO ON MONTAGNIER SO SCIENTIST LA English DT Letter ID RETROVIRUSES HTLV-III; AIDS RP GALLO, RC (reprint author), NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 6 TC 0 Z9 0 U1 2 U2 2 PU SCIENTIST INC PI PHILADELPHIA PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104 SN 0890-3670 J9 SCIENTIST JI Scientist PD MAR 21 PY 1994 VL 8 IS 6 BP 12 EP 12 PG 1 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA NB018 UT WOS:A1994NB01800007 ER PT J AU APASOV, SG SITKOVSKY, MV AF APASOV, SG SITKOVSKY, MV TI DEVELOPMENT AND AG SPECIFICITY OF CD8+ CYTOTOXIC T-LYMPHOCYTES IN BETA-2-MICROGLOBULIN NEGATIVE, MHC CLASS I-DEFICIENT MICE IN RESPONSE TO IMMUNIZATION WITH TUMOR-CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1006 EP A1006 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702435 ER PT J AU BADIO, B DALY, JW AF BADIO, B DALY, JW TI EPIBATIDINE - A POTENT ANALGESIC AND NICOTINIC AGONIST SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A875 EP A875 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701684 ER PT J AU BALA, S KOVACS, J STEVENS, R BASELER, M WAHL, L SHER, A GAZZINELLI, RT AF BALA, S KOVACS, J STEVENS, R BASELER, M WAHL, L SHER, A GAZZINELLI, RT TI SPECIFIC AND NONSPECIFIC CYTOKINE RESPONSES TO TOXOPLASMA-GONDII OF PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM NORMAL AND HIV-INFECTED HUMANS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,CCM,CCS,BETHESDA,MD 20892. NIDR,BETHESDA,MD 20892. US FDA,DAVDP,ROCKVILLE,MD 20857. PRI DYNCORP,FREDERICK,MD 21701. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A973 EP A973 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702244 ER PT J AU BARNES, DM MILLER, DS AF BARNES, DM MILLER, DS TI GLUTATHIONE (GSH) ADDUCT FORMATION AND SECRETION IN INTACT RENAL PROXIMAL TUBULES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,CELL & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A792 EP A792 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701203 ER PT J AU BECKMAN, AL BALL, SK NEWMAN, JR MAJANE, EA YANG, HYT AF BECKMAN, AL BALL, SK NEWMAN, JR MAJANE, EA YANG, HYT TI REGIONAL CONTENT OF NEUROPEPTIDE-FF (NPFF) IN THE BRAIN OF THE GROUND-SQUIRREL (CITELLUS-LATERALIS) IN THE NON-HIBERNATING AND HIBERNATING STATES SO FASEB JOURNAL LA English DT Meeting Abstract C1 CALIF STATE UNIV LONG BEACH,DEPT PSYCHOL,LONG BEACH,CA 90840. NIMH,NEUROSCI CTR ST ELIZABETHS,WASHINGTON,DC 20032. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A626 EP A626 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700238 ER PT J AU BOYD, LF DANIELS, BF SEAMAN, WE YOKOYAMA, WM MARGULIES, DH AF BOYD, LF DANIELS, BF SEAMAN, WE YOKOYAMA, WM MARGULIES, DH TI DIRECT BINDING OF PURIFIED SOLUBLE H-2DD TO CELL-SURFACE LY-49 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. VET ADM MED CTR,SAN FRANCISCO,CA 94121. MT SINAI MED CTR,NEW YORK,NY 10029. RI Margulies, David/H-7089-2013 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A986 EP A986 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702317 ER PT J AU BRIDGMAN, CF TELFORD, IR AF BRIDGMAN, CF TELFORD, IR TI BARCODE RETRIEVAL IN HISTOLOGY - AN ANALYSIS OF STUDENT UTILIZATION OF THE TEXTBOOK INTRODUCTION-TO-FUNCTIONAL-HISTOLOGY, COMBINED WITH A VIDEO DISC SURROGATE MICROSCOPE SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIFORMED SERV UNIV HLTH SCI,NATL LIB MED,BETHESDA,MD 20814. UNIFORMED SERV UNIV HLTH SCI,DEPT ANAT,BETHESDA,MD 20814. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1017 EP A1017 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702496 ER PT J AU BROWN, ED MORRIS, VC SINHA, R RHODES, DG LEVANDER, OA AF BROWN, ED MORRIS, VC SINHA, R RHODES, DG LEVANDER, OA TI URINARY-EXCRETION OF MALONDIALDEHYDE (MDA) IN SUBJECTS FED CONTROLLED DIETS WITH MEAT COOKED AT HIGH AND LOW-TEMPERATURES SO FASEB JOURNAL LA English DT Meeting Abstract C1 USDA,BELTSVILLE HUMAN NUTR RES CTR,BELTSVILLE,MD 20705. NCI,DCE,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. RI Sinha, Rashmi/G-7446-2015 OI Sinha, Rashmi/0000-0002-2466-7462 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A719 EP A719 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700782 ER PT J AU CHRIST, M KULKARNI, A HINES, K MCCARTNEYFRANCIS, N MACKALL, C WARD, J KARLSSON, S WAHL, S AF CHRIST, M KULKARNI, A HINES, K MCCARTNEYFRANCIS, N MACKALL, C WARD, J KARLSSON, S WAHL, S TI T-LYMPHOCYTE DYSREGULATION IN MICE WITH A TGF-BETA-1 NULL MUTATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NIDDK,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NCI,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A750 EP A750 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700959 ER PT J AU COICO, RF AULAKH, CS BRODERICK, PA AF COICO, RF AULAKH, CS BRODERICK, PA TI SPLENIC T-CELL SUBSET FREQUENCIES AND MITOGEN RESPONSES IN THE FAWN-HOODED RAT SO FASEB JOURNAL LA English DT Meeting Abstract C1 CUNY,SCH MED,DEPT MICROBIOL,NEW YORK,NY 10031. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1005 EP A1005 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702429 ER PT J AU COX, JH BENNINK, JR YEWDELL, JW AF COX, JH BENNINK, JR YEWDELL, JW TI THE UBIQUITIN-DEPENDENT PROTEOLYTIC PATHWAY IS NOT INVOLVED IN PROCESSING VIRAL-ANTIGENS FOR RECOGNITION BY MHC CLASS I-RESTRICTED T-CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,VIRAL DIS LAB,BETHESDA,MD 20892. RI yewdell, jyewdell@nih.gov/A-1702-2012 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A747 EP A747 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700941 ER PT J AU DE, SK MARSH, JW AF DE, SK MARSH, JW TI HIV-I NEF DOWN-MODULATES FC-RECEPTORS IN MONOCYTE-MACROPHAGE CELL LINEAGE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A757 EP A757 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700999 ER PT J AU DENKERS, EY CASPAR, P SHER, A AF DENKERS, EY CASPAR, P SHER, A TI TOXOPLASMA-GONDII DRIVES SELECTIVE EXPANSION OF MURINE T-CELL RECEPTOR V-BETA-5-BEARING CD8 LYMPHOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A974 EP A974 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702246 ER PT J AU DEOLIVEIRA, AM CAPSONI, S HEEMSKERK, FMJ VISWANATHAN, M SAAVEDRA, JM AF DEOLIVEIRA, AM CAPSONI, S HEEMSKERK, FMJ VISWANATHAN, M SAAVEDRA, JM TI AUTORADIOGRAPHIC QUANTIFICATION OF ENDOTHELIN ET(A) RECEPTORS IN PERIPHERAL AND BRAIN ARTERIES OF THE RAT SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIMH,LCS,PHARMACOL SECT,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A616 EP A616 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700181 ER PT J AU DIBRINO, M PARKER, KC BIDDISON, WE COLIGAN, JE AF DIBRINO, M PARKER, KC BIDDISON, WE COLIGAN, JE TI ENDOGENOUS PEPTIDES BOUND TO HLA-B14 AND HLA-B44 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A777 EP A777 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701117 ER PT J AU DRUEY, K HARRISON, K DEGUCHI, Y KEHRL, JH AF DRUEY, K HARRISON, K DEGUCHI, Y KEHRL, JH TI A NOVEL HUMAN HOMEOBOX GENE DISTANTLY RELATED TO PROBOSCIPEDIA IS EXPRESSED IN LYMPHOID AND GI TISSUES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A789 EP A789 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701184 ER PT J AU EDENS, NK LONDOS, C AF EDENS, NK LONDOS, C TI 5-[I-125]IODONAPHTHYL-1-AZIDE LABELS PROTEINS IN 3T3-L1 CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MARYLAND,DEPT NUTR FOOD SCI,COLL PK,MD 20742. NIDDK,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A701 EP A701 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700676 ER PT J AU ELSON, LH SHAW, S NUTMAN, TB AF ELSON, LH SHAW, S NUTMAN, TB TI PHENOTYPES OF T-LYMPHOCYTES SUBPOPULATIONS IN HUMAN HELMINTH INFECTIONS - IDENTIFICATION OF POSSIBLE MARKERS FOR TH2 CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NIH,EXPTL IMMUNOL LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1003 EP A1003 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702416 ER PT J AU FERNANDEZBOTRAN, R HIENY, S CHILTON, PM WYNN, TA SHER, A AF FERNANDEZBOTRAN, R HIENY, S CHILTON, PM WYNN, TA SHER, A TI REGULATION OF THE SECRETION OF SOLUBLE INTERLEUKIN-4 RECEPTOR (SIL-4R) DURING MURINE SCHISTOSOMIASIS - CORRELATION WITH IL-4 PRODUCTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV LOUISVILLE,DEPT MICROBIOL & IMMUNOL,LOUISVILLE,KY 40292. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RI Wynn, Thomas/C-2797-2011; Fernandez-Botran, Rafael/J-3659-2016 OI Fernandez-Botran, Rafael/0000-0001-8138-8745 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A996 EP A996 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702377 ER PT J AU GAMBASSI, G LAKATTA, EG CARBONIN, PU CAPOGROSSI, MC AF GAMBASSI, G LAKATTA, EG CARBONIN, PU CAPOGROSSI, MC TI ACUTE EXPOSURE TO ETHANOL MODULATES CYTOSOLIC CA2+ MYOFILAMENT CA2+-SENSITIVITY AND PH OF CARDIAC MYOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA, CARDIOVASC SCI LAB, BALTIMORE, MD 21224 USA. UNIV CATTOLICA SACRO CUORE, IST CLIN MED, I-00168 ROME, ITALY. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A619 EP A619 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700201 ER PT J AU GAZZINELLI, RT WYSOKA, M DENKERS, EY HAYASHI, S HIENY, S CASPAR, P TRINCHIERI, G SHER, A AF GAZZINELLI, RT WYSOKA, M DENKERS, EY HAYASHI, S HIENY, S CASPAR, P TRINCHIERI, G SHER, A TI PARASITE-INDUCED IL-12 STIMULATES EARLY IFN-GAMMA SYNTHESIS AND RESISTANCE DURING ACUTE INFECTION WITH TOXOPLASMA-GONDII SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LPD,BETHESDA,MD 20892. NEI,LIC,BETHESDA,MD 20892. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A966 EP A966 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702206 ER PT J AU GERMOLEC, DR LUSTER, M AF GERMOLEC, DR LUSTER, M TI QUANTITATION OF METABOLIC ENZYME LEVELS IN IMMUNE CELL-POPULATIONS SO FASEB JOURNAL LA English DT Meeting Abstract C1 N CAROLINA STATE UNIV,DEPT TOXICOL,RALEIGH,NC 27695. NIEHS,BIOCHEM RISK ANAL LAB,ENVIRONM IMMUNOL GRP,RES TRIANGLE PK,NC 27709. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A646 EP A646 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700359 ER PT J AU GIARDINA, SL ANDERSON, SK YOUNG, HA SAYERS, T CHAMBERS, WH PALUMBO, G ORTALDO, JR AF GIARDINA, SL ANDERSON, SK YOUNG, HA SAYERS, T CHAMBERS, WH PALUMBO, G ORTALDO, JR TI SELECTIVE ABROGATION OF NK ACTIVITY IN RNK CELLS USING ANTISENSE NK-TR1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FCRDC,DYNCORP & BRMP,PRI,BCDP,FREDERICK,MD 21702. PCI,PITTSBURGH,PA 15213. NIAID,BETHESDA,MD 20892. RI Sayers, Thomas/G-4859-2015 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A770 EP A770 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701074 ER PT J AU GOUNNI, AS LAMKHIOUED, B KINET, JP CAPRON, A CAPRON, M AF GOUNNI, AS LAMKHIOUED, B KINET, JP CAPRON, A CAPRON, M TI EXPRESSION OF THE HIGH-AFFINITY RECEPTOR FOR IGE (FC-EPSILON-RI) BY HUMAN EOSINOPHILS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NATL INST ALLERGY & INFECT DIS,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. INST PASTEUR,CTR IMMUNOL & BIOL PARASITAIRE,F-59019 LILLE,FRANCE. NR 0 TC 2 Z9 2 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A979 EP A979 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702279 ER PT J AU HALVORSON, M COLIGAN, JE AF HALVORSON, M COLIGAN, JE TI DIFFERENTIAL REGULATION OF VLA RECEPTOR ACTIVATION AT DIFFERENT STAGES OF MOUSE T-CELL DEVELOPMENT SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,MOLEC STRUCT LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A785 EP A785 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701161 ER PT J AU HERMAN, EH ZHANG, J CHADWICK, DP FERRANS, VJ AF HERMAN, EH ZHANG, J CHADWICK, DP FERRANS, VJ TI COMPARISON OF THE CARDIOPROTECTIVE EFFECT OF DEFEROXAMINE (DFO) AND ICRF-187 ON CHRONIC DOXORUBICIN (DXR) CARDIOMYOPATHY IN SPONTANEOUSLY HYPERTENSIVE RATS (SHR) SO FASEB JOURNAL LA English DT Meeting Abstract C1 US FDA,LAUREL,MD. NIH,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A885 EP A885 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701738 ER PT J AU HINES, KL KULKAMI, AB MCCARTHY, JB TIAN, H WARD, JM CHRIST, M MCCARTNEYFRANCIS, N FURCHT, LT KARLSSON, S WAHL, SM AF HINES, KL KULKAMI, AB MCCARTHY, JB TIAN, H WARD, JM CHRIST, M MCCARTNEYFRANCIS, N FURCHT, LT KARLSSON, S WAHL, SM TI FIBRONECTIN PEPTIDES BLOCK INFLAMMATORY CELL INFILTRATION IN TGF-BETA-1 KNOCKOUT MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NINCDS,BETHESDA,MD 20892. NCI,FREDERICK,MD 21702. UNIV MINNESOTA,MED PATHOL LAB,MINNEAPOLIS,MN 55455. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A771 EP A771 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701082 ER PT J AU HONG, HL SILLS, RS GREENWELL, A BOORMAN, GA DEVEREUX, TR AF HONG, HL SILLS, RS GREENWELL, A BOORMAN, GA DEVEREUX, TR TI ACTIVATION OF THE K-RAS PROTOONCOGENE IN MOUSE LUNG-TUMORS FOLLOWING OZONE EXPOSURE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,NATL TOXICOL PROGRAM,RTP,RES TRIANGLE PK,NC 27709. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A667 EP A667 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700477 ER PT J AU HORNUNG, RL LONGO, DL KWAK, LW AF HORNUNG, RL LONGO, DL KWAK, LW TI IMMUNIZATION OF BMT DONORS AGAINST A TUMOR-SPECIFIC ANTIGEN - A STRATEGY FOR USING IMMUNE BONE-MARROW AS AN ANTITUMOR THERAPY AGAINST AN ESTABLISHED LYMPHOMA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FCRDC,BCDP,PRI DYNCORP,FREDERICK,MD 21702. NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A772 EP A772 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701087 ER PT J AU KALKWARF, HJ HEUBI, JE SPECKER, BL VIEIRA, NE YERGEY, AL AF KALKWARF, HJ HEUBI, JE SPECKER, BL VIEIRA, NE YERGEY, AL TI INTESTINAL CALCIUM-ABSORPTION DURING LACTATION AND POST-WEANING SO FASEB JOURNAL LA English DT Meeting Abstract C1 CHILDRENS HOSP,PERINATAL RES INST,CINCINNATI,OH 45229. NICHHD,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A694 EP A694 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700633 ER PT J AU KANG, C HARIHARAN, K NARA, P SODROSKI, J MOORE, J AF KANG, C HARIHARAN, K NARA, P SODROSKI, J MOORE, J TI SOLUBLE CD4-GP120 COMPLEX PREFERENTIALLY INDUCES NEUTRALIZING ANTI-GP120 ANTIBODIES DIRECTED TO THE CONFORMATIONAL DEPENDENT EPITOPES SO FASEB JOURNAL LA English DT Meeting Abstract C1 IDEC PHARMACEUT CORP,SAN DIEGO,CA 92121. NCI,VIRUS BIOL UNIT,FREDERICK,MD 21701. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. DEPT CANC BIOL,BOSTON,MA. AARON DIAMOND AIDS RES CTR,NEW YORK,NY. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A961 EP A961 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702177 ER PT J AU KASSERRA, CE TAYLOR, J BALABAN, RS AF KASSERRA, CE TAYLOR, J BALABAN, RS TI ROLE OF ADENOSINE IN CORONARY REACTIVE HYPEREMIA TO PACING AND DOBUTAMINE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CARDIAC ENERGET LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A620 EP A620 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700205 ER PT J AU KEEGAN, AD NELMS, K WANG, LM PIERCE, JH PAUL, WE AF KEEGAN, AD NELMS, K WANG, LM PIERCE, JH PAUL, WE TI Y497 OF THE HUMAN IL-4 RECEPTOR IS CRITICAL FOR IL-4-INDUCED IRS-1 PHOSPHORYLATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A744 EP A744 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700922 ER PT J AU KNUCKEY, N FINCH, P THOMPSON, N PALM, D PRIMIANO, M JOHANSON, C FLANDERS, K SPORN, M AF KNUCKEY, N FINCH, P THOMPSON, N PALM, D PRIMIANO, M JOHANSON, C FLANDERS, K SPORN, M TI THE PATTERN OF NEURONAL EXPRESSION AND THE NEUROPROTECTIVE ROLE OF TRANSFORMING GROWTH-FACTOR-BETA ISOFORMS FOLLOWING TRANSIENT CEREBRAL-ISCHEMIA SO FASEB JOURNAL LA English DT Meeting Abstract C1 RHODE ISL HOSP,DEPT CLIN NEUROSCI,PROVIDENCE,RI 02903. NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 3 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A654 EP A654 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700406 ER PT J AU LEE, L MCHUGH, L RIBAUDO, RK KOZLOWSKI, S MARGULIES, DH MAGE, MG AF LEE, L MCHUGH, L RIBAUDO, RK KOZLOWSKI, S MARGULIES, DH MAGE, MG TI FUNCTIONAL CELL-SURFACE EXPRESSION BY A RECOMBINANT SINGLE-CHAIN CLASS-I MHC MOLECULE WITH A CIS ACTIVE BETA-2-MICROGLOBULIN DOMAIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RI Margulies, David/H-7089-2013 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A777 EP A777 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701114 ER PT J AU LEMPICKI, RA TANI, Y GEIGER, S LANE, HC ZOLLAPAZNER, S COHEN, DI AF LEMPICKI, RA TANI, Y GEIGER, S LANE, HC ZOLLAPAZNER, S COHEN, DI TI EVALUATION OF T-LYMPHOCYTES EXPRESSING GENETICALLY-ENGINEERED HIV-ENV SPECIFIC RECEPTORS AS AN EFFECTIVE THERAPY FOR HIV-1 INFECTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,INST ALLERGY & INFECT DIS,BETHESDA,MD 20892. VET AFFAIRS MED CTR,RES & MED SERV LAB,NEW YORK,NY 10010. RI Lempicki, Richard/E-1844-2012 OI Lempicki, Richard/0000-0002-7059-409X 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A961 EP A961 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702178 ER PT J AU MATZ, JM BLAKE, MJ TATELMAN, H HOLBROOK, NJ AF MATZ, JM BLAKE, MJ TATELMAN, H HOLBROOK, NJ TI COLD INDUCES HEAT-SHOCK PROTEIN EXPRESSION IN BROWN ADIPOSE-TISSUE SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV N DAKOTA,DEPT PHARM & TOX,GRAND FORKS,ND 58201. NIA,MOLEC GENET LAB,BALTIMORE,MD 21224. NIA,THERMOREG LAB,BALTIMORE,MD 21224. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A960 EP A960 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702169 ER PT J AU MCKENNA, MC ZECH, L TILDON, JT ZIELKE, HR AF MCKENNA, MC ZECH, L TILDON, JT ZIELKE, HR TI USE OF COMPARTMENTAL MODELING TECHNIQUES TO ANALYZE GLUTAMATE METABOLISM IN ASTROCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MARYLAND,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21201. NCI,MATH BIOL LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A821 EP A821 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701369 ER PT J AU MILLER, DS PRITCHARD, JB AF MILLER, DS PRITCHARD, JB TI NOCODAZOLE INHIBITION OF ORGANIC ANION SECRETION IN TELEOST RENAL PROXIMAL TUBULES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,CELL & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A792 EP A792 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701201 ER PT J AU MOHANAKUMAR, KP HANBAUER, I WU, RM MURPHY, DL CHIUEH, CC AF MOHANAKUMAR, KP HANBAUER, I WU, RM MURPHY, DL CHIUEH, CC TI IN-VIVO NEUROTOXIC EFFECTS OF NO AND OH FREE-RADICALS ON THE SUBSTANTIA-NIGRA NEURONS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A656 EP A656 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700415 ER PT J AU MONGINI, P BLESSINGER, C HIGHET, P INMAN, J AF MONGINI, P BLESSINGER, C HIGHET, P INMAN, J TI EFFECT OF T-CELL CYTOKINES ON THE AFFINITY AND LIGAND VALENCY REQUIREMENTS FOR ACHIEVING FULL B-CELL ACTIVATION VIA THE MIGM SIGNALING PATHWAY SO FASEB JOURNAL LA English DT Meeting Abstract C1 HOSP JOINT DIS & MED CTR,NEW YORK,NY 10003. NIAID,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1011 EP A1011 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702464 ER PT J AU MUELLER, DL CHEN, ZM SCHWARTZ, RH GORMAN, DM KENNEDY, MK AF MUELLER, DL CHEN, ZM SCHWARTZ, RH GORMAN, DM KENNEDY, MK TI IL-3 RECEPTOR ALPHA-CHAINS ARE EXPRESSED ON A SUBSET OF CD4+ T-CELL CLONES CAPABLE OF UTILIZING IL-3 FOR GROWTH SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MINNESOTA,SCH MED,DEPT MED,MINNEAPOLIS,MN 55455. NIAID,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. IMMUNEX RES & DEV CORP,SEATTLE,WA 98101. DNAX RES INST MOLEC & CELLULAR BIOL INC,MOLEC & CELLULAR BIOL RES INST,PALO ALTO,CA 94304. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A747 EP A747 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700942 ER PT J AU NELMS, K KEEGAN, AD PAUL, WE AF NELMS, K KEEGAN, AD PAUL, WE TI MOLECULAR-INTERACTIONS IN THE IL-4 RECEPTOR SIGNALING PATHWAY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A743 EP A743 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700921 ER PT J AU OH, CK METCALFE, DD AF OH, CK METCALFE, DD TI TRANSCRIPTIONAL ACTIVATION OF THE TCA3 GENE IN MAST-CELLS FOLLOWING COCULTURE WITH ACTIVATED LYMPHOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A743 EP A743 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700917 ER PT J AU OSWALD, IP WYNN, TA CASPAR, P SHER, PA JAMES, SL AF OSWALD, IP WYNN, TA CASPAR, P SHER, PA JAMES, SL TI HUMAN MACROPHAGES AND ENDOTHELIAL-CELLS EXHIBIT CYTOTOXICITY TOWARD EXTRACELLULAR TARGETS BY A NOVEL NO AND ROI INDEPENDENT MECHANISM SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RI Wynn, Thomas/C-2797-2011; OSWALD, Isabelle/A-8497-2013 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A968 EP A968 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702216 ER PT J AU PAPCIAK, SM ADLER, WH AF PAPCIAK, SM ADLER, WH TI REGULATION OF IFN-GAMMA GENE-EXPRESSION IN ACTIVATED T-CELLS FROM YOUNG AND OLD MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A779 EP A779 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701131 ER PT J AU RAZIUDDIN HOOVER, T SARKAR, FH SMITH, M PRINCLER, G KUNG, HF AF RAZIUDDIN HOOVER, T SARKAR, FH SMITH, M PRINCLER, G KUNG, HF TI IDENTIFICATION AND CHARACTERIZATION OF A NOVEL SEQUENCE-SPECIFIC DNA-BINDING NUCLEAR MATRIX PROTEIN (NMP) FROM HUMAN BREAST-CANCER TISSUES SO FASEB JOURNAL LA English DT Meeting Abstract C1 WSU,SCH MED,DETROIT,MI 48201. NCI,FCRDC,BRMP,BLOCHEM PHYSIOL LAB,FREDERICK,MD 21702. NCI,FCRDC,DYNCORP,PRI,BCDP,BRMP,FREDERICK,MD 21702. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A671 EP A671 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700499 ER PT J AU RAZIUDIN, A LONGO, DL MASON, L BENNETT, M KUMAR, V MURPHY, WJ AF RAZIUDIN, A LONGO, DL MASON, L BENNETT, M KUMAR, V MURPHY, WJ TI NATURAL-KILLER SUBSETS IN THE REGULATION OF HEMATOPOIESIS SO FASEB JOURNAL LA English DT Meeting Abstract C1 DYNCORP INC,PRI,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. UNIV TEXAS,SW MED CTR,DALLAS,TX 75230. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A984 EP A984 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702305 ER PT J AU RHEE, H SONG, B CUSHMAN, S SHOAF, S AF RHEE, H SONG, B CUSHMAN, S SHOAF, S TI DIFFERENTIAL RESPONSES TO NOREPINEPHRINE (NE) IN ALCOHOLIC AND DIABETIC RAT AORTA SO FASEB JOURNAL LA English DT Meeting Abstract C1 US FDA,ROCKVILLE,MD 20857. NIAAA,ROCKVILLE,MD 20852. NIDDKD,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A952 EP A952 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702120 ER PT J AU RIVA, A KEHRL, JH AF RIVA, A KEHRL, JH TI A PANEL OF CD19 DEFICIENT B-CELL LINES PROVIDES INSIGHTS INTO THE MECHANISMS REGULATING CD19 GENE-TRANSCRIPTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A788 EP A788 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701179 ER PT J AU SCHRAMM, U FRICKER, G WENGER, R MILLER, DS AF SCHRAMM, U FRICKER, G WENGER, R MILLER, DS TI P-GLYCOPROTEIN-MEDIATED SECRETION OF A FLUORESCENT CYCLOSPORINE ANALOG (NBD-CSA) BY RENAL PROXIMAL TUBULES FROM A TELEOST FISH SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,CELL & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. SANDOZ PHARMA AG,CH-4002 BASEL,SWITZERLAND. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A793 EP A793 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701209 ER PT J AU SONG, L COLLINS, GD LAL, P NAGEL, JE ADLER, WH AF SONG, L COLLINS, GD LAL, P NAGEL, JE ADLER, WH TI AGE-DIFFERENCES IN TYROSINE-PHOSPHORYLATED PROTEINS IN PHORBOL-MYRISTATE ACETATE (PMA) STIMULATED PERIPHERAL-BLOOD LYMPHOCYTES (PBL) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA,GRC,CLIN IMMUNOL SECT,BALTIMORE,MD 21224. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A753 EP A753 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700975 ER PT J AU STEVENSON, MM TAM, MF OSWALD, I SHER, A AF STEVENSON, MM TAM, MF OSWALD, I SHER, A TI INTERLEUKIN-12 PROTECTS MICE AGAINST BLOOD-STAGE PLASMODIUM-CHABAUDI AS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MONTREAL GEN HOSP,RES INST,MONTREAL H3G 1A4,QUEBEC,CANADA. NIAID,BETHESDA,MD 20892. RI OSWALD, Isabelle/A-8497-2013 NR 0 TC 1 Z9 1 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A966 EP A966 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702203 ER PT J AU STRASSMANN, G NORDAN, RP AF STRASSMANN, G NORDAN, RP TI SURAMIN INTERFERES WITH INTERLEUKIN-6 RECEPTOR-BINDING IN-VITRO AND INHIBITS COLON-26-MEDIATED EXPERIMENTAL CANCER CACHEXIA IN-VIVO SO FASEB JOURNAL LA English DT Meeting Abstract C1 OTSUKA AMER PHARMACEUT INC,ROCKVILLE,MD 20850. NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20852. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A996 EP A996 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702376 ER PT J AU STROBER, W KELSALL, BL AF STROBER, W KELSALL, BL TI IN-SITU LOCALIZATION OF PEYER PATCH DENDRITIC CELLS BY IMMUNOPEROXIDASE STAINING WITH N418 MONOCLONAL-ANTIBODY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,CLIN INVEST LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1008 EP A1008 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702444 ER PT J AU TATSUMI, Y WELLS, FA INGRAM, S MATIS, LA BLUESTONE, JA AF TATSUMI, Y WELLS, FA INGRAM, S MATIS, LA BLUESTONE, JA TI MOLECULAR MECHANISM OF FUNCTIONAL-DEVELOPMENT OF TCR-GAMMA-DELTA CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CHICAGO,BEN MAY INST,CHICAGO,IL 60637. NCI,FCRDC,FREDERICK,MD 21702. ALEXION INC,NEW HAVEN,CT 06511. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A740 EP A740 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700904 ER PT J AU TAUB, DD RAGER, HC FLEMING, CL SPESSARD, AL OPPENHEIM, JJ METCALFE, D DASTYCH, J AF TAUB, DD RAGER, HC FLEMING, CL SPESSARD, AL OPPENHEIM, JJ METCALFE, D DASTYCH, J TI THE ROLE OF MAST-CELLS IN THE GENERATION OF TH1 AND TH2 CELLS IN-VITRO SO FASEB JOURNAL LA English DT Meeting Abstract C1 PRI INC,DYNCORP,CLIN SERV PROGRAM,FREDERICK,MD 21702. NCI,BRMP,MOLEC IMMUNOREGULAT,FREDERICK,MD 21702. NIAID,CLIN INVEST,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1004 EP A1004 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702421 ER PT J AU THEVENIN, C WILSON, GL KEHRL, JH AF THEVENIN, C WILSON, GL KEHRL, JH TI THE CD20 PROMOTER AS A PROTOTYPE FOR THE STUDY OF B-LINEAGE SPECIFIC GENES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A788 EP A788 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701181 ER PT J AU TUSCANO, J KEHRL, JH AF TUSCANO, J KEHRL, JH TI LYN, SYK, AND PI-3 KINASES BIND TO THE ARH1 MOTIF OF CD22 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A788 EP A788 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701183 ER PT J AU VARGAS, FF VINET, R CALVO, S AF VARGAS, FF VINET, R CALVO, S TI VOLTAGE-GATED CA++ CHANNELS IN ADRENAL-MEDULLA ENDOTHELIAL-CELLS AND THEIR LOSS DURING CELL-CULTURE SO FASEB JOURNAL LA English DT Meeting Abstract C1 US FDA,DIV CARDIORENAL DRUGS,BETHESDA,MD 20892. NIH,CELL BIOL & GENET LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A1061 EP A1061 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702753 ER PT J AU VEECH, RL GATES, D KING, MT WONDERGEM, R AF VEECH, RL GATES, D KING, MT WONDERGEM, R TI METABOLISM OF ETHANOL CAUSES HYPERPOLARIZATION OF LIVER AND ALTERATION OF DELTA-G [H+] AND [MG2+] SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,METAB LAB,ROCKVILLE,MD 20852. UNIV & TENNESSEE,SCH MED,DEPT PHYSIOL,JOHNSON CITY,TN 37614. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A952 EP A952 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702122 ER PT J AU VIGGIANO, V YOUNG, HA CIPITELLI, M SICA, A AF VIGGIANO, V YOUNG, HA CIPITELLI, M SICA, A TI NF-KAPPA-B AND A P120 INTERACT WITH THE IFN-GAMMA INTRONIC CREL BINDING-SITE C3 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FCRDC,DYNCORP,PRI,CMIS,EXPTL IMMUNOL LAB,BRMP,FREDERICK,MD 21702. NCI,FCRDC,DYNCORP,PRI,BCDP,FREDERICK,MD 21702. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A779 EP A779 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701127 ER PT J AU VILLALOBOS, AR DUNNICK, CA PRITCHARD, JB AF VILLALOBOS, AR DUNNICK, CA PRITCHARD, JB TI ACCUMULATION OF 2,4-DICHLOROPHENOXYACETIC ACID (2,4-D) BY RAT RENAL CORTICAL SLICES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A792 EP A792 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701204 ER PT J AU WADHWANI, KC CLYBUM, RE RAPOPORT, SI AF WADHWANI, KC CLYBUM, RE RAPOPORT, SI TI QUANTITATION OF THE GLUCOSE TRANSPORTER-1 GLUT1 MESSENGER-RNA LEVELS IN THE RAT BLOOD-NERVE AND BLOOD-BRAIN BARRIERS - EFFECT OF WALLERIAN DEGENERATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A653 EP A653 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700395 ER PT J AU WANG, J WALKER, H LIN, O JENKINS, NA COPELAND, N COOPER, MD AF WANG, J WALKER, H LIN, O JENKINS, NA COPELAND, N COOPER, MD TI AMINOPEPTIDASE A/BP-1 GENE ORGANIZATION, CHROMOSOMAL LOCALIZATION AND REGULATORY ELEMENTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. HOWARD HUGHES MED INST,BIRMINGHAM,AL 35294. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A964 EP A964 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702190 ER PT J AU WILLIAMS, AO KNAPTON, AD SAFFIOTTI, U AF WILLIAMS, AO KNAPTON, AD SAFFIOTTI, U TI TGF-BETA-1 IN RAT ALVEOLAR TYPE-II CELLS EXPOSED TO CRYSTALLINE SILICA IN-VIVO AND IN CULTURE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,EXPTL PATHOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A805 EP A805 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701275 ER PT J AU WISNEWSKI, AV KRESINA, TF AF WISNEWSKI, AV KRESINA, TF TI SCHISTOSOMA-JAPONICUM EGG ANTIGEN-SPECIFIC HUMAN T-CELL LINES DERIVED IN-VITRO FROM THE PERIPHERAL-BLOOD LYMPHOCYTES OF A NAIVE DONOR SO FASEB JOURNAL LA English DT Meeting Abstract C1 BROWN UNIV,INT HLTH INST,PROVIDENCE,RI 02906. NIDDK,DIV DIGEST DIS & NUTR,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A801 EP A801 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701257 ER PT J AU WYNN, TA ELTOUM, I OSWALD, IP CHEEVER, AW SHER, A AF WYNN, TA ELTOUM, I OSWALD, IP CHEEVER, AW SHER, A TI ENDOGENOUS AND EXOGENOUS REGULATION OF SCHISTOSOME EGG GRANULOMA-FORMATION BY IL-12 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. RI Wynn, Thomas/C-2797-2011; OSWALD, Isabelle/A-8497-2013 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A966 EP A966 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702204 ER PT J AU XUE, Q HALLFRISCH, J MICHAELIS, OE ROBISON, WG AF XUE, Q HALLFRISCH, J MICHAELIS, OE ROBISON, WG TI CATARACT DEVELOPMENT AND GLYCATION IN RATS FED GALACTOSE AND FRUCTOSE WITH MARGINAL COPPER SO FASEB JOURNAL LA English DT Meeting Abstract C1 USDA,BHNRC,CNL,BELTSVILLE,MD 20705. NEI,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A945 EP A945 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702078 ER PT J AU YOSHIMOTO, T PAUL, WE AF YOSHIMOTO, T PAUL, WE TI NK1.1+CD4+ T-CELLS PRODUCE IL-4 PROMPTLY IN RESPONSE TO INJECTION OF ANTI-CD3 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOL,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A997 EP A997 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19702381 ER PT J AU YOUSSEF, J CUNNINGHAM, ML BADR, M AF YOUSSEF, J CUNNINGHAM, ML BADR, M TI DOWN-REGULATION OF HEPATIC PEROXISOMAL BETA-OXIDATION DUE TO PANTOTHENIC ACID-DEFICIENCY SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MISSOURI,KANSAS CITY,MO 64108. NIEHS,CHEM BRANCH,RES TRIANGLE PK,NC 27709. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A736 EP A736 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19700878 ER PT J AU ZHANG, J HERMAN, EH YAMAMOTO, A WENTHOLD, RJ FERRANS, VJ AF ZHANG, J HERMAN, EH YAMAMOTO, A WENTHOLD, RJ FERRANS, VJ TI PULMONARY TOXICITY OF HUMAN RECOMBINANT INTERLEUKIN-2 IN RATS SO FASEB JOURNAL LA English DT Meeting Abstract C1 US FDA,LAUREL,MD 20708. NIH,BETHESDA,MD 20892. 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 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 18 PY 1994 VL 8 IS 5 BP A809 EP A809 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ND197 UT WOS:A1994ND19701302 ER PT J AU COOPER, LF UOSHIMA, K AF COOPER, LF UOSHIMA, K TI DIFFERENTIAL ESTROGENIC REGULATION OF SMALL M(R), HEAT-SHOCK PROTEIN EXPRESSION IN OSTEOBLASTS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MESSENGER-RNAS; MOLECULAR-CLONING; CELLS; BONE; OSTEOPOROSIS; ESTRADIOL; SEQUENCE; GENES; RATS; DNA AB Polymerase chain reaction amplification and sequencing of heat shock protein (HSP) 27-related transcripts present in cDNAs generated from heat-shocked osteoblast RNA revealed the expression of three related open reading frames that encode proteins of 208, 197, or 175 amino acids. Their expression as recombinant proteins in Escherichia coli demonstrated that they encode 27,000, 25,000, or 22,000 M(r) proteins. Northern blot analysis of heat shock protein 27-related transcript expression revealed that, while HSP 27 expression (850-nucleotide transcript) was induced by heat shock alone, the expression of a smaller transcript was facilitated by estrogen treatment prior to heat shock. This corresponded with the co-induction of 18,000 and 22,000 M(r) proteins by estrogen-pretreated, heat-shocked osteoblasts as revealed by fluorography. The identification of these multiple small M(r) heat shock-induced proteins demonstrated that the stress response of mammalian cells is composed of multiple, related proteins whose expression is differentially regulated. The importance of estrogen regulation of the small M(r) heat shock protein component of the stress response may be of particular significance to osteoblast physiology. C1 NIDR, CLIN INVEST & PATIENT CARE BRANCH, BETHESDA, MD 20892 USA. NR 37 TC 61 Z9 62 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 7869 EP 7873 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900009 PM 8132504 ER PT J AU LETEURTRE, F KOHLHAGEN, G FESEN, MR TANIZAWA, A KOHN, KW POMMIER, Y AF LETEURTRE, F KOHLHAGEN, G FESEN, MR TANIZAWA, A KOHN, KW POMMIER, Y TI EFFECTS OF DNA METHYLATION ON TOPOISOMERASE-I AND TOPOISOMERASE-II CLEAVAGE ACTIVITIES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID C-MYC PROTOONCOGENE; CPG BINDING-PROTEIN; HEAT-SHOCK GENES; ANTITUMOR DRUGS; CYTOSINE METHYLATION; SV40 DNA; SITES; SEQUENCE; CAMPTOTHECIN; CHROMATIN AB DNA methylation is deregulated during oncogenesis. Since several major anti-cancer drugs act on topoisomerases, we investigated the effects of cytosine methylation on topoisomerase cleavage activities. Both topoisomerase I and II cleavage patterns were modified by CpG methylation in c-myc gene DNA fragments. Topoisomerase II changes, mainly cleavage reduction, occurred for methylation sites within 7 base pairs from the topoisomerase II breaks and were different for VM-26 and azatoxin. For topoisomerase I, cleavage enhancement as well as suppression were observed. Using synthetic methylated oligonucleotides, we show that hemimethylation is sufficient to alter topoisomerase I activity. Cytosine methylation on the scissile strand within the topoisomerase I consensus sequence had strong effects. Cleavage was stimulated by methylation at position -4 and was strongly inhibited by methylation at position -3 (with position -1 being the enzyme linked nucleotide). This inhibitory effect was attributed to the presence of a methyl group in the major groove, since the transition uracil to thymine also inhibited cleavage. Altogether these results suggest an interaction of topoisomerase I with the DNA major grove at positions -3 and -4. In addition, DNA methylation may have profound effects on the activity of topoisomerases and may alter the distribution of cleavage sites produced by anticancer drugs in chromatin. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NR 66 TC 50 Z9 50 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 7893 EP 7900 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900013 PM 8132507 ER PT J AU MELILLO, G COX, GW BIRAGYN, A SHEFFLER, LA VARESIO, L AF MELILLO, G COX, GW BIRAGYN, A SHEFFLER, LA VARESIO, L TI REGULATION OF NITRIC-OXIDE SYNTHASE MESSENGER-RNA EXPRESSION BY INTERFERON-GAMMA AND PICOLINIC-ACID SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TUMOR-NECROSIS-FACTOR; MURINE PERITONEAL-MACROPHAGES; HUMAN-CELLS INVITRO; IFN-GAMMA; L-ARGININE; EFFECTOR MECHANISM; HUMAN-MONOCYTES; FACTOR-ALPHA; INDOLEAMINE 2,3-DIOXYGENASE; TRYPTOPHAN DEGRADATION AB Picolinic acid, a catabolite of L-tryptophan, is a potent co-stimulatory agent for the induction of tumoricidal activity and the production of L-arginine-dependent reactive nitrogen intermediates (RNI) in murine macrophages. We studied whether picolinic acid could affect nitric-oxide synthase (NOS) expression at the gene level in the macrophage cell line ANA-1. NOS mRNA was neither constitutively expressed nor induced by treatment with picolinic acid alone. However, low levels of NOS mRNA were induced by interferon (IFN)-gamma alone. In contrast, a major increase of NOS mRNA expression was observed after treatment with IFN-gamma plus picolinic acid. The synergism was already detectable after 5-6 h and increased up to 20 h of treatment. The ability of picolinic acid to augment IFN-gamma-dependent NOS mRNA expression was associated with a parallel increase in transcription, as demonstrated by nuclear run-on experiments. Protein synthesis was required for the induction of NOS mRNA because addition of cycloheximide dramatically reduced IFN-gamma plus picolinic acid-induced NOS mRNA expression. Finally, interleukin-4 significantly decreased IFN-gamma plus picolinic acid-induced NOS mRNA expression and NOS transcription. These data provide evidence of a molecular event connecting arginine and tryptophan metabolic pathways in the generation of RNI, and they indicate that picolinic acid can induce transcriptional activation of gene expression. C1 NCI, FREDERICK CANC RES & DEV CTR, DIV CANC TREATMENT, FREDERICK, MD 21702 USA. RP MELILLO, G (reprint author), NCI, FREDERICK CANC RES & DEV CTR, DIV CANC TREATMENT, BRMP, EXPTL IMMUNOL LAB, FREDERICK, MD 21702 USA. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 53 TC 93 Z9 93 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 8128 EP 8133 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900047 PM 7510678 ER PT J AU TORRI, AF KUNKEL, TA ENGLUND, PT AF TORRI, AF KUNKEL, TA ENGLUND, PT TI A BETA-LIKE DNA-POLYMERASE FROM THE MITOCHONDRION OF THE TRYPANOSOMATID CRITHIDIA-FASCICULATA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID KINETOPLAST DNA; DEOXYRIBONUCLEIC-ACID; CATALYTIC SUBUNIT; XENOPUS-LAEVIS; REPLICATION; GAMMA; PURIFICATION; MINICIRCLES; FIDELITY; SITES AB The mitochondrial DNA in Crithidia fasciculata, a trypanosomatid parasite, is known as kinetoplast DNA. Kinetoplast DNA has a very unusual structure, consisting of several thousand minicircles and a few dozen maxicircles, all topologically interlocked into a giant network. There is one network within each cell's single mitochondrion. We previously purified a 43-kDa DNA polymerase from C. fasciculata mitochondria (Torri, A. F., and Englund, P. T. (1992) J. Biol. Chem. 267, 4786-4792). This enzyme has properties very different from those of a DNA polymerase gamma, the conventional mitochondrial polymerase. In addition to its small size, it is nonprocessive, has no detectable exonuclease activity, and has very low fidelity. In all of these respects, the polymerase resembles a DNA polymerase beta, a gap-filling enzyme thought to function in DNA repair in the nucleus of other eukaryotes. We speculate that this enzyme may have been specially imported into the C. fasciculata mitochondrion to repair the many gaps found in minicircles following their replication. This is the first example of a beta-like polymerase from the mitochondrion of any eukaryote. C1 NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709. RP TORRI, AF (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205, USA. FU NIGMS NIH HHS [GM 27608, GM 13604] NR 28 TC 30 Z9 31 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 8165 EP 8171 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900053 PM 8132542 ER PT J AU HORI, H FENNA, RE KIMURA, S IKEDASAITO, M AF HORI, H FENNA, RE KIMURA, S IKEDASAITO, M TI AROMATIC SUBSTRATE MOLECULES BIND AT THE DISTAL HEME POCKET OF MYELOPEROXIDASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SPLEEN GREEN HEMEPROTEIN; HORSERADISH-PEROXIDASE; LIGAND-BINDING; CHLORINATING ACTIVITY; SPECTRAL PROPERTIES; PROSTHETIC GROUP; LACTOPEROXIDASE; COMPLEXES; RESONANCE; CHLORIDE AB Binding of aromatic substrate molecules to myeloperoxidase has been investigated by EPR spectroscopy and model building. Binding of aromatic substrate molecules, such as phenol, p-cresol, resorcinol, and 4-amino salicylate, replaces the original rhombic high spin EPR spectrum of the ferric enzyme (g = 6.74, 5.18, and 1.97) by another high spin signal (g = 7.04, 4.87, and 1.93) indicating that these substrate molecules bind near the heme center of the enzyme. Salicylhydroxamic acid and benzohydroxamic acid complexes of myeloperoxidase showed EPR spectra composed of high spin (g = 6.99, 4.93, and 1.95) and low spin (2.66, 2.22, and 1.81) signals. The hydroxamic side chains of these two substrates seem to interact with the heme iron. Model building based on the three-dimensional structure of the enzyme (Zeng, J., and Fenna, R. E. (1992) J. Mel. Biol. 226, 185-207) revealed the presence of a hydrophobic pocket at the entrance of the distal heme cavity where the aromatic ring of these substrates can bind. Moreover, the six-membered ring portion of salicylhydroxamic acid and benzohydroxamic acid could bind to this hydrophobic pocket with the hydroxamic side chain placed between the imidazole of the distal His and the heme iron. The EPR results on lactoperoxidase and intestinal peroxidase also suggest the presence of an aromatic substrate binding site similar to that of myeloperoxidase. C1 CASE WESTERN RESERVE UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106. OSAKA UNIV,FAC ENGN SCI,DEPT BIOPHYS ENGN,TOYONAKA,OSAKA 560,JAPAN. UNIV MIAMI,SCH MED,DEPT BIOCHEM & MOLEC BIOL,MIAMI,FL 33101. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RI Ikeda-Saito, Masao/A-5992-2008; Ikeda-Saito, Masao/K-2703-2015 FU NCRR NIH HHS [RR05695]; NIGMS NIH HHS [GM39492, GM49149] NR 35 TC 50 Z9 50 U1 1 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 8388 EP 8392 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900084 PM 8132563 ER PT J AU OKAMOTO, SI MUKAIDA, N YASUMOTO, K RICE, N ISHIKAWA, Y HORIGUCHI, H MURAKAMI, S MATSUSHIMA, K AF OKAMOTO, SI MUKAIDA, N YASUMOTO, K RICE, N ISHIKAWA, Y HORIGUCHI, H MURAKAMI, S MATSUSHIMA, K TI THE INTERLEUKIN-8 AP-1 AND KAPPA-B-LIKE SITES ARE GENETIC END TARGETS OF FK5O6-SENSITIVE PATHWAY ACCOMPANIED BY CALCIUM MOBILIZATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID T-CELL ACTIVATION; PROTEIN-KINASE-C; CYCLOSPORINE-A; LYMPHOCYTES-T; HUMAN MONOCYTES; FACTOR BINDING; EXPRESSION; ENHANCER; REL; INTERFERON AB FK506, an immunosuppressant, inhibits the production of several cytokines in T lymphocytes. We observed that FK506 suppressed the transcription of a chemotactic cytokine, interleukin-8 (IL-8) in a human T cell line, Jurkat cells, activated by phorbol 12-myristate 13-acetate (PMA) and calcium (Ca2+) ionophore (ionomycin). By deleted and mutated analysis of the IL-8 promoters, the AP-1 and kappa B-like sites were identified as the responsive elements for PMA and ionomycin. FK506 suppressed the transcriptions through the AP-1 or kappa B-like sites induced by PMA plus Ca2+-mobilizing agents, but not those induced by Ca2+-independent stimuli. In gel retardation analysis, FK506 had little effect on the binding to the AP-1 site of PMA/ionomyein-induced nuclear factors, which were recognized with anti-JunD or c-Fos antibody. In contrast, FK506 or EGTA (Ca2+ chelator) similarly affected the formation of kappa B-like site binding complexes, which were not recognized by any antibodies against the human Rel family proteins (c-Rel, p65, p50, and p49). Furthermore, we confirmed the previous report that FK506 suppressed the PMA/ionomycin-induced activation through authentic kappa B site of immunoglobulin (Ig) gene, to which NF-kappa B binding was also decreased by FK506, indicating that both IL-8 kappa B-like site and Ig kappa B Site are FK506-sensitive in spite of the difference of binding factors. Our results indicate that not only the reported IL-2 NF-AT and NFIL-2A sites and Ig kappa B site, but also the IL-8 AP-1 and kappa B-like sites are terminals of FK506-sensitive pathway involving Ca2+ mobilization. C1 KANAZAWA UNIV,CANC RES INST,DEPT PHARMACOL,KANAZAWA,ISHIKAWA 920,JAPAN. KANAZAWA UNIV,CANC RES INST,DEPT SURG,KANAZAWA,ISHIKAWA 920,JAPAN. KANAZAWA UNIV,CANC RES INST,DEPT BIOPHYS,KANAZAWA,ISHIKAWA 920,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS,BASIC RES PROGRAM,FREDERICK,MD 21702. RI Mukaida, Naofumi/D-7623-2011 OI Mukaida, Naofumi/0000-0002-4193-1851 NR 49 TC 124 Z9 125 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 8582 EP 8589 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900112 PM 7510691 ER PT J AU SIEGFRIED, JM HAN, YH DEMICHELE, MAA HUNT, JD GAITHER, AL CUTTITTA, F AF SIEGFRIED, JM HAN, YH DEMICHELE, MAA HUNT, JD GAITHER, AL CUTTITTA, F TI PRODUCTION OF GASTRIN-RELEASING PEPTIDE BY A NONSMALL CELL LUNG-CARCINOMA CELL-LINE ADAPTED TO SERUM-FREE AND GROWTH FACTOR-FREE CONDITIONS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BRONCHIAL EPITHELIAL-CELLS; BOMBESIN-LIKE PEPTIDES; TUMOR PROGRESSION; ENDOCRINE TUMORS; FACTOR RECEPTOR; FETAL LUNG; CANCER; EXPRESSION; CULTURE; ORIGIN AB Gastrin-releasing peptide is an important growth-modulating factor in developing lung epithelium. It is known to be produced by small cell carcinomas of the lung, and an autocrine loop involving gastrin-releasing peptide and its receptor has been demonstrated in many small cell lung tumors. We investigated whether such an autocrine loop could also be demonstrated in non-small cell lung carcinoma, since gastrin-releasing peptide is known to stimulate human bronchial epithelial cells, from which non-small cell tumors should emerge. We report here that gastrin-releasing peptide is produced by a bronchiolo-alveolar carcinoma cell line (A549) adapted to serum-free and growth factor-free conditions. A549 cells adapted to these conditions, termed A549-R(0) cells, display extensive membrane interdigitations, Gels apparatus, and secretory-like granules, and grow as a mixture of attached colonies and floating cells. Gastrin-releasing peptide is present in the conditioned medium produced by A549-R(0) cells. Colony formation of cells derived from a squamous cell carcinoma of the lung, 239T, was stimulated 9-fold by A549-R(0) conditioned medium or by authentic gastrin-releasing peptide, measured in serum-free conditions. The growth stimulatory activity was inhibited by a monoclonal antibody to gastrin-releasing peptide. Transcripts for receptors for the bombesin family of peptides were also demonstrated in A549-R(0) cells and 239T cells. These results demonstrate that non-small cell lung carcinomas can secrete gastrin-releasing peptide and can also respond to the peptide. C1 UNIV PITTSBURGH,PITTSBURGH CANC INST,PITTSBURGH,PA 15261. NCI,BIOMARKERS & PREVENT BRANCH,ROCKVILLE,MD 20850. RP SIEGFRIED, JM (reprint author), UNIV PITTSBURGH,DEPT PHARMACOL,E1347 BIOMED SCI TOWER,PITTSBURGH,PA 15261, USA. FU NCI NIH HHS [CA-50694, CA-09033] NR 40 TC 44 Z9 44 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 18 PY 1994 VL 269 IS 11 BP 8596 EP 8603 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB409 UT WOS:A1994NB40900114 PM 8132585 ER PT J AU ZHANG, WJ KOEHLER, KF HARRIS, B SKOLNICK, P COOK, JM AF ZHANG, WJ KOEHLER, KF HARRIS, B SKOLNICK, P COOK, JM TI SYNTHESIS OF BENZO-FUSED BENZODIAZEPINES EMPLOYED AS PROBES OF THE AGONIST PHARMACOPHORE OF BENZODIAZEPINE RECEPTORS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID BINDING-SITE; MOLECULAR YARDSTICKS; LIGANDS; STEREOCHEMISTRY; DIRECTIONALITY; ANTAGONISTS; DIMENSIONS; MECHANICS; FEATURES; DIAZEPAM AB The synthesis and in vitro evaluation of benzo-fused benzodiazepines 1-6 are described. These ''molecular yardsticks' were employed to probe the spatial dimensions of the lipophilic pocket L2 in the benzodiazepine receptor (BzR) cleft and to determine the effect of occupation of L2 with respect to agonist activity. Of the new analogs synthesized, the 7,8-benzo-fused benzodiazepine 6 displayed moderately high affinity for the BzR (IC50 = 55 nM) and exhibited both anticonvulsant (ED50 almost-equal-to 15 mg/kg) and muscle relaxant (ED50 almost-equal-to 15 mg/kg) activity. As expected, 2 and 4 interacted with the repulsive regions of interaction, S1 and S2, and exhibited low affinities for BzR. The rigid nature of these molecular yardsticks (especially 6, Figure 7) has been employed to probe the depth of L2. Moreover, in the case of 6 full occupation of L2 has resulted in an increase in the muscle relaxant effect at the expense of the anticonvulsant/anxiolytic effect. C1 UNIV WISCONSIN,DEPT CHEM,MILWAUKEE,WI 53201. IST RIC BIOL MOLEC P ANGELETTI,I-00040 POMEZIA,ITALY. NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. FU NIMH NIH HHS [NIMH MH46851] NR 61 TC 50 Z9 50 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD MAR 18 PY 1994 VL 37 IS 6 BP 745 EP 757 DI 10.1021/jm00032a007 PG 13 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ND308 UT WOS:A1994ND30800007 PM 8145224 ER PT J AU LEE, YS PEARLSTEIN, R KADOR, PF AF LEE, YS PEARLSTEIN, R KADOR, PF TI MOLECULAR MODELING STUDIES OF ALDOSE REDUCTASE INHIBITORS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID DIABETIC COMPLICATIONS; DERIVATIVES; ACIDS AB Molecular modeling studies using the AM1 quantum chemical method and a torsional fitting method have been conducted on a series of aldose reductase inhibitors (ARIs) possessing an ionizable group and/or functional group susceptible to nucleophilic attack with the aim of defining the spatial position of AR1 pharmacophores. AM1 quantum chemical calculations were conducted on ARIs possessing only an ionizable group to obtain their optimized geometries. These optimized structures were then superimposed on the model compound spirofluorene-9,5'-imidazolidine-2',4'-dione (17). This superposition study suggests that a negative charge center residing in the vicinity of the 2'-oxygen of the imidazolidine-2',4'-dione ring participates in the binding interactions. In addition, the optimized geometries of ARIs possessing both an ionizable group and an electronegative functional group were superimposed on spirofluorene-9,5'-imidazolidine-2',4'-dione(17). The latter results also suggest the presence of a region where nucleophilic substitution can occur. C1 NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. RP LEE, YS (reprint author), NEI,LOT,BLDG 10,RM 10B-13,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 21 TC 32 Z9 32 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD MAR 18 PY 1994 VL 37 IS 6 BP 787 EP 792 DI 10.1021/jm00032a011 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ND308 UT WOS:A1994ND30800011 PM 8145228 ER PT J AU MCKEE, TC CARDELLINA, JH RICCIO, R DAURIA, MV IORIZZI, M MINALE, L MORAN, RA GULAKOWSKI, RJ MCMAHON, JB BUCKHEIT, RW SNADER, KM BOYD, MR AF MCKEE, TC CARDELLINA, JH RICCIO, R DAURIA, MV IORIZZI, M MINALE, L MORAN, RA GULAKOWSKI, RJ MCMAHON, JB BUCKHEIT, RW SNADER, KM BOYD, MR TI HIV-INHIBITORY NATURAL-PRODUCTS .11. COMPARATIVE-STUDIES OF SULFATED STEROLS FROM MARINE-INVERTEBRATES SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID SPONGE; METABOLITES AB A total of 22 sulfated sterols isolated from marine sponges, ophiuroids (brittle stars), and asteroids (sea stars) were comparatively evaluated for their antiviral activity against HIV-1 and HIV-2. In general, sterols with sulfate groups at position 2, 3, or 6 were the most active, with EC50 values- of 3-13 muM against HIV-1 (RF) and 2-8 muM against HIV-2 (CBL20). Those compounds which were sulfated on the sterol D ring were completely inactive against both HIV-1 and HIV-2. Overall, sulfated sterols active against HIV-1 were also active against HIV-2. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES & DEV LAB,BLDG 1052,ROOM 121,FREDERICK,MD 21702. RI Riccio, Raffaele/A-3405-2008; Iorizzi, Maria/F-4491-2012; D'Auria, Maria Valeria/K-2586-2012; OI Riccio, Raffaele/0000-0001-5073-5513; D'Auria, Maria Valeria/0000-0003-3450-7304; Iorizzi, Maria/0000-0002-8653-6628 NR 28 TC 56 Z9 61 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD MAR 18 PY 1994 VL 37 IS 6 BP 793 EP 797 DI 10.1021/jm00032a012 PG 5 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ND308 UT WOS:A1994ND30800012 PM 8145229 ER PT J AU ROSENBERG, PS BIGGAR, RJ GOEDERT, JJ AF ROSENBERG, PS BIGGAR, RJ GOEDERT, JJ TI DECLINING AGE AT HIV-INFECTION IN THE UNITED-STATES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID AIDS RP ROSENBERG, PS (reprint author), NCI,BETHESDA,MD 20892, USA. NR 5 TC 83 Z9 83 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 17 PY 1994 VL 330 IS 11 BP 789 EP 790 DI 10.1056/NEJM199403173301114 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA NA742 UT WOS:A1994NA74200013 PM 8107749 ER PT J AU BENJAMIN, EJ LEVY, D VAZIRI, SM DAGOSTINO, RB BELANGER, AJ WOLF, PA AF BENJAMIN, EJ LEVY, D VAZIRI, SM DAGOSTINO, RB BELANGER, AJ WOLF, PA TI INDEPENDENT RISK-FACTORS FOR ATRIAL-FIBRILLATION IN A POPULATION-BASED COHORT - THE FRAMINGHAM HEART-STUDY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID EPIDEMIOLOGIC FEATURES; PREVENTION; STROKE; MORTALITY; WARFARIN; DISEASE; RHYTHM; TRIALS; TIME AB Objective.-To determine the independent risk factors for atrial fibrillation. Design.-Cohort study. Setting.-The Framingham Heart Study. Subjects.-A total of 2090 men and 2641 women members of the original cohort, free of a history of atrial fibrilltation, between the ages of 55 and 94 years. Main Outcome Measures.-Sex-specific multiple logistic regression models to identify independent risk factors for atrial fibrillation, including age, smoking, diabetes, electrocardiographic left ventricular hypertrophy, hypertension, myocardial infarction, congestive heart failure, and valve disease. Results.-During up to 38 years of follow-up, 264 men and 298 women developed atrial fibrillation, After adjusting for age and other risk factors for atrial fibrillation, men had a 1.5 times greater risk of developing atrial fibrillation than women. In the full multivariable model, the odds ratio (OR) of atrial fibrillation for each decade of advancing age was 2.1 for men and 2.2 for women (P<.0001). In addition, after multivariable adjustment, diabetes (OR, 1.4 for men and 1.6 for women), hypertension (OR, 1.5 for men and 1.4 for women), congestive heart failure (OR, 4.5 for men and 5.9 for women), and valve disease (OR, 1.8 for men and 3.4 for women) were significantly associated with risk for atrial fibrillation in both sexes. Myocardial infarction (OR, 1.4) was significantly associated with the development of atrial fibrillation in men. Women were significantly more likely than men to have valvular heart disease as a risk factor for atrial fibrillation. The multivariable models were largely unchanged after eliminating subjects with valvular heart disease. Conclusion.-In addition to intrinsic cardiac causes such as valve disease and congestive heart failure, risk factors for cardiovascular disease also predispose to atrial fibrillation. Modification of risk factors for cardiovascular disease may have the added benefit of diminishing the incidence of atrial fibrillation. C1 BOSTON UNIV,BOSTON CITY HOSP,SCH MED,CARDIOL SECT,BOSTON,MA 02118. NHLBI,BETHESDA,MD 20892. BOSTON UNIV,DEPT MATH,BOSTON,MA 02215. BOSTON UNIV,SCH MED,DEPT PREVENT MED,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. BETH ISRAEL HOSP,DIV CARDIOL,BOSTON,MA. BETH ISRAEL HOSP,DIV CLIN EPIDEMIOL,BOSTON,MA. RP BENJAMIN, EJ (reprint author), FRAMINGHAM HEART DIS EPIDEMIOL STUDY,5 THURBER ST,FRAMINGHAM,MA 01701, USA. FU NHLBI NIH HHS [N01-HC-38038]; NINDS NIH HHS [2-R01-NS-17950-11] NR 31 TC 1391 Z9 1451 U1 8 U2 32 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 16 PY 1994 VL 271 IS 11 BP 840 EP 844 DI 10.1001/jama.271.11.840 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MZ498 UT WOS:A1994MZ49800030 PM 8114238 ER PT J AU BROWN, ML NAYFIELD, SG SHIBLEY, LM AF BROWN, ML NAYFIELD, SG SHIBLEY, LM TI ADJUVANT THERAPY FOR STAGE-III COLON-CANCER - ECONOMICS RETURNS TO RESEARCH AND COST-EFFECTIVENESS OF TREATMENT SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID BREAST-CANCER; CARCINOMA; FLUOROURACIL; SURVEILLANCE; LEVAMISOLE; IMPACT AB Background: In 1989, the National Cancer Institute issued a clinical announcement advising physicians of the benefits of combined levamisole and fluorouracil as an adjuvant treatment for patients with stage III colon cancer. Purpose: We have estimated the cost-effectiveness of the combined treatment and estimated the social return on the National Institutes of Health (NIH) research investment that led to this innovative cancer treatment. Methods: A computer simulation model, CAN*TROL, was used to estimate costs and benefits for a population cross-section receiving the adjuvant treatment. A method similar to ''Q-TWiST'' was used to assess the impact of quality-of-life adjustments. Results: For a typical base-line case, the calculated cost-effectiveness is a very favorable $2094 per year of life saved. Using a variety of less favorable assumptions, cost-effectiveness is still less than $5000 per year of life saved, again a favorable value. Quality-of-life adjustments have a negligible effect on the cost-effectiveness outcome. The net present value of the return to the NIH research investment is estimated to be $1.66 billion. Conclusions: Under a wide range of reasonable assumptions, adjuvant therapy for stage III colon cancer appears to be a very cost-effective procedure. The investment in the research that resulted in this therapy promises to yield a high return. C1 NCI,DIV CANC PREVENT & CONTROL,COMMUNITY & CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NCI,OFF PROGRAM OPERAT & PLANNING,BETHESDA,MD 20892. RP BROWN, ML (reprint author), NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,SURVEILLANCE PROGRAM,EPN,RM 313,BETHESDA,MD 20892, USA. NR 34 TC 57 Z9 57 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 16 PY 1994 VL 86 IS 6 BP 424 EP 430 DI 10.1093/jnci/86.6.424 PG 7 WC Oncology SC Oncology GA NA031 UT WOS:A1994NA03100012 PM 8120916 ER PT J AU LIEBMANN, J COOK, JA FISHER, J TEAGUE, D MITCHELL, JB AF LIEBMANN, J COOK, JA FISHER, J TEAGUE, D MITCHELL, JB TI IN-VITRO STUDIES OF TAXOL AS A RADIATION SENSITIZER IN HUMAN TUMOR-CELLS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article AB Background: Cells exposed to paclitaxel (Taxol) develop a cell cycle arrest in G(2)/M. It has long been recognized that late G(2) and M are the most radiosensitive phases of the cell cycle. Purpose: These studies were performed to assess the in vitro radiosensitization properties of paclitaxel in human tumor cell lines. Methods: The effect of paclitaxel at concentrations ranging from 0 to 10000 nM on the radiation sensitivity (from 0 to as much as 10 Gy in certain experiments) of human breast (MCF-7), lung (A549), ovary (OVG-1), and pancreas (PC-Sh) adenocarcinoma cells was determined using clonogenic assays. DNA flow cytometry studies were performed to define the cell cycle characteristics of populations of cells that had been treated for 6-72 hours with 0, 100, 1000, or 10000 nM paclitaxel. Results: All cell lines developed a G(2)/M block after exposure to 100-10000 nM paclitaxel for 24 hours. However, the degree of radiosensitization produced by paclitaxel varied among the cell lines. The sensitizer enhancement ratio (SER) of paclitaxel at 10% survival was 1.8 in MCF-7 cells and 1.6 in OVG-1 cells. However, paclitaxel at any concentration was unable to enhance the radiation sensitivity of A549 cells. PC-Sh cells demonstrated a complex and inconsistent radiosensitization response to paclitaxel. At 10% survival, an SER of 1.5 was observed in PC-Sh cells. However, at 1% survival, no radiosensitization was observed in PC-Sh cells. Maneuvers that prevented paclitaxel from producing a G(2)/M block, including coincident treatment with cycloheximide or treatment of cells in plateau phase of growth, completely abrogated the radiosensitization afforded by paclitaxel in MCF-7 cells. Conclusions: Paclitaxel is a modest radiosensitizer in some, but not all, humor tumor cells. The degree of radiosensitization that we have observed with paclitaxel is similar to what has been found with other chemotherapeutic agents. The absence of radiosensitization by paclitaxel in MCF-7 cells grown to plateau phase or treated with cycloheximide implies that the development of a G(2)/M block is a necessary condition for paclitaxel radiosensitization. However, the inability of paclitaxel to radiosensitize A549 cells despite the presence of a G(2)/M block in those cells demonstrates that a G(2)/M block is not a sufficient condition for paclitaxel radiosensitization. Implications: Paclitaxel can radiosensitize to a modest degree some, but not all, human cell lines by a mechanism that requires the production of a G(2)/M cell cycle block. Additional studies are needed to define more clearly the mechanism by which paclitaxel radiosensitizes cells. RP LIEBMANN, J (reprint author), NCI,DIV CANC TREATMENT,RADIAT BIOL BRANCH,BLDG 10,RM B3B69,BETHESDA,MD 20892, USA. NR 21 TC 249 Z9 257 U1 0 U2 5 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 16 PY 1994 VL 86 IS 6 BP 441 EP 446 DI 10.1093/jnci/86.6.441 PG 6 WC Oncology SC Oncology GA NA031 UT WOS:A1994NA03100015 PM 7907149 ER PT J AU BERG, S BALIS, FM MCCULLY, CL POPLACK, DC AF BERG, S BALIS, FM MCCULLY, CL POPLACK, DC TI TOXICITY OF INTRATHECAL MELPHALAN SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter ID HIGH-DOSE MELPHALAN; PHARMACOKINETICS; CHILDREN; THERAPY; BRAIN; RAT C1 BAYLOR COLL MED,TEXAS CHILDRENS HOSP,HOUSTON,TX. RP BERG, S (reprint author), NCI,DIV CANC TREATMENT,PEDIAT BRANCH,BLDG 10,RM 13N240,BETHESDA,MD 20892, USA. NR 6 TC 1 Z9 1 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 16 PY 1994 VL 86 IS 6 BP 463 EP 463 DI 10.1093/jnci/86.6.463 PG 1 WC Oncology SC Oncology GA NA031 UT WOS:A1994NA03100019 PM 8120922 ER PT J AU CANNON, RO TRIPODI, D DILSIZIAN, V PANZA, JA FANANAPAZIR, L AF CANNON, RO TRIPODI, D DILSIZIAN, V PANZA, JA FANANAPAZIR, L TI RESULTS OF PERMANENT DUAL-CHAMBER PACING IN SYMPTOMATIC NONOBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID MYOCARDIAL PERFUSION ABNORMALITIES; SUBAORTIC STENOSIS; CLINICAL MANIFESTATIONS; OUTFLOW OBSTRUCTION; PATHO-PHYSIOLOGY; VERAPAMIL; THERAPY; INTERRELATIONS; EXERCISE; IMPACT AB Because dual-chamber (DDD) pacing has been shown to be of benefit regarding symptoms, rest and pacing hemodynamics, and exercise duration in patients with obstructive hypertrophic cardiomyopathy (HC), the effect of DDD pacing was assessed in patients with nonobstructive HC who were significantly symptomatic despite medical management. Echocardiography, treadmill exercise testing, thallium-201 scintigraphy, radionuclide angiography, and invasive measurement of rest and semi-erect bicycle exercise hemodynamics were performed in 12 patients before and approximately 4 months after permanent DDD pacing. One patient died 3 months after pacemaker implantation, because of worsening diastolic heart failure. Of the remaining 11 patients, 10 improved regarding symptoms, and treadmill exercise duration was longer during DDD pacing than during the baseline study in sinus rhythm (6.8 +/- 2.8 to 8.5 +/- 2.8 minutes; p <0.01), with a significant increase in the peak double product achieved (28.9 +/- 6.1 to 31.0 +/- 6.8 x 10(3); p <0.05). However, there were significant reductions in cardiac (3.7 +/- 0.9 to 3.1 +/-0.5 ml/min/m2; p <0.01) and stroke volume (47.4 +/- 11.4 to 38.7 +/- 6.5 ml/beat/m2; p <0.01) indexes, and a trend toward reduction in submaximal stroke volume index during DDD pacing as compared with the baseline study in sinus rhythm (44.7 +/- 13.5 to 40.9 +/- 10.9 ml/beat/m2; p = 0.097). No change in peak heart rate, cardiac or stroke volume index, mean blood pressure, or pulmonary artery or pulmonary capillary wedge pressure occurred with peak exercise during DDD pacing as compared with the initial exercise study in sinus rhythm. Furthermore, repeat exercise thallium-201 scintigraphy during DDD pacing in 9 patients showed no consistent change due to pacing. Of 10 patients >1 year after pacemaker implantation, cardiac medications have been reinitiated in 6, and DDD pacing was discontinued in 1, because of persistent or worsening symptoms. Thus, although DDD pacing in patients with nonobstructive HC was associated with improvement in symptoms and effort tolerance, there was absence of objective evidence of hemodynamic benefit, and a common need for reinitiation of medical therapy. Currently, chronic DDD pacing cannot be recommended for routine use in the management of patients with nonobstructive HC who are symptomatic despite medical management. RP CANNON, RO (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 19 TC 35 Z9 36 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAR 15 PY 1994 VL 73 IS 8 BP 571 EP 576 DI 10.1016/0002-9149(94)90336-0 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NB935 UT WOS:A1994NB93500010 PM 8147303 ER PT J AU DOMANSKI, MJ EICHHORN, EJ AF DOMANSKI, MJ EICHHORN, EJ TI BETA-BLOCKADE IN CONGESTIVE-HEART-FAILURE - THE NEED FOR A DEFINITIVE STUDY SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Editorial Material ID IDIOPATHIC DILATED CARDIOMYOPATHY; HUMAN VENTRICULAR MYOCARDIUM; ADRENERGIC-RECEPTOR DENSITY; FAILING HUMAN-HEART; METOPROLOL TREATMENT; VASODILATOR THERAPY; DOWN-REGULATION; DOUBLE-BLIND; BUCINDOLOL; PLACEBO C1 UNIV TEXAS,SW MED CTR,DIV CARDIOL,DALLAS,TX 75230. UNIV TEXAS,VET ADM MED CTR,DALLAS,TX 75230. RP DOMANSKI, MJ (reprint author), NHLBI,CLIN TRIALS BRANCH,BETHESDA,MD 20892, USA. NR 42 TC 4 Z9 4 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAR 15 PY 1994 VL 73 IS 8 BP 597 EP 599 DI 10.1016/0002-9149(94)90341-7 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NB935 UT WOS:A1994NB93500015 PM 7908497 ER PT J AU COON, H SOBELL, J HESTON, L SOMMER, S HOFF, M HOLIK, J UMAR, F ROBERTSON, M REIMHERR, F WENDER, P VEST, K MYLESWORSLEY, M GERSHON, ES DELISI, LE SHIELDS, G DALE, PW POLLOI, A WALDO, M LEONARD, S SIKELA, J FREEDMAN, R BYERLEY, W AF COON, H SOBELL, J HESTON, L SOMMER, S HOFF, M HOLIK, J UMAR, F ROBERTSON, M REIMHERR, F WENDER, P VEST, K MYLESWORSLEY, M GERSHON, ES DELISI, LE SHIELDS, G DALE, PW POLLOI, A WALDO, M LEONARD, S SIKELA, J FREEDMAN, R BYERLEY, W TI SEARCH FOR MUTATIONS IN THE BETA-1 GABA(A) RECEPTOR SUBUNIT GENE IN PATIENTS WITH SCHIZOPHRENIA SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE SCHIZOPHRENIA; GABA(A) RECEPTOR; SSCP; DNA SEQUENCE VARIANTS ID DEPENDENT DIABETES-MELLITUS; POLYMERASE CHAIN-REACTION; POINT MUTATIONS; CHROMOSOMAL LOCALIZATION; ENZYMATIC AMPLIFICATION; FUNCTIONAL EXPRESSION; COMPLEX DISEASES; HUMAN GENOME; A RECEPTORS; DNA AB As alterations in GABAergic neurotransmission have been indirectly implicated in the pathogenetics of schizophrenia, GABA(A) receptor subunit genes are plausible candidate genes for the illness. We undertook a search for sequence variations in the coding region of beta(1) subunit gene by designing intron-based primers to amplify its 9 exons. Using single strand conformation polymorphism (SSCP) analysis, we found an exon 9 variant present in 3 of 86 unrelated schizophrenic cases derived from families having at least 2 first-degree relatives with schizophrenia. Direct sequencing of the SSCP variant revealed a C-->G nucleotide transversion at codon 396 predicting a histidine to glutamine substitution in the beta(1) peptide. The predicted amino acid substitution occurs at a highly conserved site, 9 residues from a cAMP-dependent serine phosphorylation consensus sequence. All known GABA(A) beta(1) subunit genes including human, bovine, and rat, code for histidine at position 396. Although the variant cosegregated with disease in a family with 2 affected sibs, it was only transmitted to 2 of 3 affected sibs in a multiplex family, The variant was not found in an additional sample comprising 155 unrelated schizophrenics and the sequence variant was present at a low frequency (similar to 1.1%) in control groups. Although these results indicate that the sequence variant is likely to be a natural polymorphism, it is possible that the variant may be a predisposing allele in rare instances. It is also possible that the variant may change the function or regulation of the GABA(A) receptor complex and it may be of pharmacogenetic relevance. (C) 1994 Wiley-Liss, Inc. C1 UNIV UTAH,MED CTR,DEPT PSYCHIAT,SALT LAKE CITY,UT 84132. UNIV UTAH,MED CTR,DEPT HUMAN GENET,SALT LAKE CITY,UT 84132. MAYO CLIN & MAYO FDN,DEPT BIOCHEM & MOLEC BIOL,ROCHESTER,MN 55905. UNIV WASHINGTON,DEPT PSYCHIAT,SEATTLE,WA 98195. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. SUNY STONY BROOK,DEPT PSYCHIAT,STONY BROOK,NY 11794. UNIV HAWAII,STUDENT HLTH SERV,HONOLULU,HI 96822. MINIST HLTH,KOROR,PALAU. UNIV COLORADO,HLTH SCI CTR,DEPT PSYCHIAT,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT PHARMACOL,DENVER,CO 80262. OI Coon, Hilary/0000-0002-8877-5446 FU NIMH NIH HHS [MH-10168-F32, MH-42643, MH-44245] NR 64 TC 12 Z9 13 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAR 15 PY 1994 VL 54 IS 1 BP 12 EP 20 DI 10.1002/ajmg.1320540105 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA NA254 UT WOS:A1994NA25400004 PM 8178835 ER PT J AU PULVER, AE KARAYIORGOU, M WOLYNIEC, PS LASSETER, VK KASCH, L NESTADT, G ANTONARAKIS, S HOUSMAN, D KAZAZIAN, HH MEYERS, D OTT, J LAMACZ, M LIANG, KY HANFELT, J ULLRICH, G DEMARCHI, N RAMU, E MCHUGH, PR ADLER, L THOMAS, M CARPENTER, WT MANSCHRECK, T GORDON, CT KIMBERLAND, M BABB, R PUCK, J CHILDS, B AF PULVER, AE KARAYIORGOU, M WOLYNIEC, PS LASSETER, VK KASCH, L NESTADT, G ANTONARAKIS, S HOUSMAN, D KAZAZIAN, HH MEYERS, D OTT, J LAMACZ, M LIANG, KY HANFELT, J ULLRICH, G DEMARCHI, N RAMU, E MCHUGH, PR ADLER, L THOMAS, M CARPENTER, WT MANSCHRECK, T GORDON, CT KIMBERLAND, M BABB, R PUCK, J CHILDS, B TI SEQUENTIAL STRATEGY TO IDENTIFY A SUSCEPTIBILITY GENE FOR SCHIZOPHRENIA - REPORT OF POTENTIAL LINKAGE ON CHROMOSOME 22Q12-Q13.1 .1. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE GENETIC LINKAGE ANALYSIS; SCHIZOPHRENIA; HUMAN CHROMOSOME 22; HETEROGENEITY; RANDOM SEARCH ID MINOR PHYSICAL ANOMALIES; CARDIO-FACIAL SYNDROME; COMPLEX DISEASES; PSEUDOAUTOSOMAL LOCUS; FAMILIAL RISK; INTERLEUKIN-2 RECEPTORS; DIAGNOSTIC INTERVIEW; NO EVIDENCE; MARKERS; EPIDEMIOLOGY AB To identify genes responsible for the susceptibility for schizophrenia, and to test the hypothesis that schizophrenia is etiologically heterogeneous, we have studied 39 multiplex families from a systematic sample of schizophrenic patients. Using a complex autosomal dominant model, which considers only those with a diagnosis of schizophrenia or schizoaffective disorder as affected, a random search of the genome for detection of Linkage was undertaken. Pairwise linkage analyses suggest a potential linkage (LRH = 34.7 or maximum lod score = 1.54) for one region (22q12-q13.1). Reanalyses, varying parameters in the dominant model, maximized the LRH at 660.7 (maximum lod score 2.82). This finding is of sufficient interest to warrant further investigation through collaborative studies. (C) 1994 Wiley-Liss, Inc. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,DEPT BIOSTAT,BALTIMORE,MD. UNIV MARYLAND,NIMH,DEPT PSYCHIAT,BETHESDA,MD. COLUMBIA UNIV,DEPT GENET & DEV,NEW YORK,NY. COLUMBIA UNIV,DEPT PSYCHIAT,NEW YORK,NY. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. DARTMOUTH COLL,DEPT PSYCHIAT,HANOVER,NH 03755. CHILDRENS HOSP,PHILADELPHIA,PA 19104. RP PULVER, AE (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,SUITE 205,1615 THAMES ST,BALTIMORE,MD 21231, USA. RI Liang, Kung-Yee/F-8299-2011; Elango, Ramu/C-7684-2014; Elango, Ramu/I-7812-2013; Antonarakis, Stylianos/N-8866-2014 OI Elango, Ramu/0000-0003-4264-2135; Antonarakis, Stylianos/0000-0001-8907-5823 FU NCRR NIH HHS [5MO1 RR00722]; NIMH NIH HHS [NIMH RO1 MH35712, NIMH RO1 MH45588] NR 72 TC 286 Z9 295 U1 4 U2 15 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAR 15 PY 1994 VL 54 IS 1 BP 36 EP 43 DI 10.1002/ajmg.1320540108 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA NA254 UT WOS:A1994NA25400007 PM 8178837 ER PT J AU NISTICO, A YOUNG, NS AF NISTICO, A YOUNG, NS TI GAMMA-INTERFERON GENE-EXPRESSION IN THE BONE-MARROW OF PATIENTS WITH APLASTIC-ANEMIA SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE ANEMIA, APLASTIC; INTERFERON TYPE II; BONE MARROW; GENE EXPRESSION; LYMPHOKINES ID CHRONIC MYELOGENOUS LEUKEMIA; LYMPHOCYTES-T; PROGENITOR CELLS; VIRUS-INFECTIONS; TRANSGENIC MICE; SUPPRESSION; DISEASES; INVITRO; HEMATOPOIESIS; PROLIFERATION AB Objective: To determine gamma-interferon gene expression in the bone marrow of patients with aplastic anemia and controls. Most patients with acquired aplastic anemia respond to immunosuppressive therapy, implicating an immune pathophysiologic origin for this disease. RP NISTICO, A (reprint author), NHLBI,HEMATOL BRANCH,BLDG 10,ROOM 7C103,BETHESDA,MD 20892, USA. NR 40 TC 95 Z9 103 U1 0 U2 2 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 15 PY 1994 VL 120 IS 6 BP 463 EP 469 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA NB625 UT WOS:A1994NB62500003 PM 8311369 ER PT J AU HOFMANN, J OCONNOR, PM JACKMAN, J SCHUBERT, C UEBERALL, F KOHN, KW GRUNICKE, H AF HOFMANN, J OCONNOR, PM JACKMAN, J SCHUBERT, C UEBERALL, F KOHN, KW GRUNICKE, H TI THE PROTEIN-KINASE-C INHIBITOR ILMOFOSINE (BM-41-440) ARRESTS CELLS IN G2 PHASE AND SUPPRESSES CDC2 KINASE ACTIVATION THROUGH A MECHANISM DIFFERENT FROM THAT OF DNA-DAMAGING AGENTS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID ANTIPROLIFERATIVE ACTIVITY; ALKYL-LYSOPHOSPHOLIPIDS; STAUROSPORINE; LIPIDS; CYCLE AB The thioether phospholipid derivative ilmofosine (BM41440), a selective inhibitor of protein kinase C, is a new anticancer drug presently undergoing Phase II clinical trials. We have examined the influence of the compound on cell cycle progression. Ilmofosine was found to induce a dose-dependent accumulation of CA46 cells in G(2)-phase of the cell cycle. G(2)-arrest correlated with suppression of cdc2 kinase activation. Ilmofosine did not affect cdc2 kinase activity in vitro, consistent with an indirect locus of action. Ilmofosine treated CA46 cells failed to accumulate hyperphosphorylated-cdc2/cyclin B1 complexes that are observed when G(2)-arrest is induced by either nitrogen mustard or ionizing radiation, Indeed, cdc2 became dephosphorylated and cyclin B1 protein levels decreased as ilmofosine treated cells became arrested in G(2). Our findings suggest that ilmofosine down-regulates cdc2 kinase activation through a mechanism that affects the formation of cdc2/cyclin B1 complexes. (C) 1994 Academic Press, Inc. C1 NCI, DIV CANC TREATMENT, DEV THERAPEUT PROGRAM, MOLEC PHARMACOL LAB, BETHESDA, MD 20892 USA. RP HOFMANN, J (reprint author), UNIV INNSBRUCK, INST MED CHEM & BIOCHEM, FRITZ PREGL STR 3, A-6020 INNSBRUCK, AUSTRIA. NR 18 TC 33 Z9 33 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 15 PY 1994 VL 199 IS 2 BP 937 EP 943 DI 10.1006/bbrc.1994.1319 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NA914 UT WOS:A1994NA91400074 PM 8135843 ER PT J AU UVERSKY, VN PTITSYN, OB AF UVERSKY, VN PTITSYN, OB TI PARTLY FOLDED STATE, A NEW EQUILIBRIUM STATE OF PROTEIN MOLECULES - 4-STATE GUANIDINIUM CHLORIDE-INDUCED UNFOLDING OF BETA-LACTAMASE AT LOW-TEMPERATURE SO BIOCHEMISTRY LA English DT Article ID MOLTEN-GLOBULE STATE; CARBONIC-ANHYDRASE-B; HUMAN ALPHA-LACTALBUMIN; FOLDING PATHWAY; CYTOCHROME-C; STRUCTURAL CHARACTERIZATION; CONFORMATIONAL TRANSITIONS; CIRCULAR-DICHROISM; RIBONUCLEASE-A; COMPACT STATE AB Guanidinium chloride- (GdmCl-) induced unfolding of P-lactamase has been investigated by a combination of size-exclusion chromatography (SEC-FPLC) and usual optical methods. It has been shown that at low temperatures this protein unfolds through two equilibrium intermediates. The first of these intermediates is the molten globule state, while the other (which we have called a ''partly folded'' state) is less compact than the molten globule but much more compact than the unfolded state. It also preserves a substantial part of secondary structure of the native or molten globule state. We suggest that this new ''partly folded'' state of a protein molecule can be the equilibrium counterpart of the first kinetic intermediate of protein folding, formed within a few milliseconds, i.e., after the ''burst'' stage of folding. C1 NCI,MATH BIOL LAB,BETHESDA,MD 20892. RP UVERSKY, VN (reprint author), RUSSIAN ACAD SCI,INST PROT RES,PUSHCHINO 142292,RUSSIA. RI Uversky, Vladimir/F-4515-2011 OI Uversky, Vladimir/0000-0002-4037-5857 NR 67 TC 174 Z9 177 U1 0 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 15 PY 1994 VL 33 IS 10 BP 2782 EP 2791 DI 10.1021/bi00176a006 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA886 UT WOS:A1994NA88600006 PM 8130190 ER PT J AU GARRETT, DS LODI, PJ SHAMOO, Y WILLIAMS, KR CLORE, GM GRONENBORN, AM AF GARRETT, DS LODI, PJ SHAMOO, Y WILLIAMS, KR CLORE, GM GRONENBORN, AM TI DETERMINATION OF THE SECONDARY STRUCTURE AND FOLDING TOPOLOGY OF AN RNA-BINDING DOMAIN OF MAMMALIAN HNRNP A1 PROTEIN USING 3-DIMENSIONAL HETERONUCLEAR MAGNETIC-RESONANCE SPECTROSCOPY SO BIOCHEMISTRY LA English DT Article ID SMALL NUCLEAR RIBONUCLEOPROTEIN; NMR-SPECTROSCOPY; LARGER PROTEINS; C-PROTEINS; N-15 NMR; IDENTIFICATION; SPECTRA; C-13; ASSIGNMENT; SEQUENCE AB The secondary structure and folding topology of the first RNA binding domain of the human hnRNP A1 protein was determined by multidimensional heteronuclear NMR spectroscopy. The 92 amino acid long domain exhibits a beta alpha beta beta alpha beta folding pattern, arranged in a four-stranded antiparallel beta-sheet flanked by two alpha-helices, which is very similar to that found for other members of this family. Regions of marked variation between the structurally characterized RNA binding proteins of this class to date are mainly localized in the loops connecting the secondary structure elements. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. YALE UNIV,SCH MED,DEPT MOLEC BIOPHYS & BIOCHEM,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,HOWARD HUGHES MED INST,NEW HAVEN,CT 06510. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 FU NIGMS NIH HHS [GM31539] NR 47 TC 45 Z9 45 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 15 PY 1994 VL 33 IS 10 BP 2852 EP 2858 DI 10.1021/bi00176a015 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA886 UT WOS:A1994NA88600015 PM 8130198 ER PT J AU PARK, JW ELBENNA, J SCOTT, KE CHRISTENSEN, BL CHANOCK, SJ BABIOR, BM AF PARK, JW ELBENNA, J SCOTT, KE CHRISTENSEN, BL CHANOCK, SJ BABIOR, BM TI ISOLATION OF A COMPLEX OF RESPIRATORY BURST OXIDASE COMPONENTS FROM RESTING NEUTROPHIL CYTOSOL SO BIOCHEMISTRY LA English DT Article ID CELL-FREE SYSTEM; CHRONIC GRANULOMATOUS-DISEASE; NADPH OXIDASE; SUBCELLULAR-LOCALIZATION; PLASMA-MEMBRANE; ACTIVATION; PURIFICATION; PROTEINS; ENZYME AB The respiratory burst oxidase of neutrophils is a multicomponent enzyme, dormant in resting cells, that catalyzes the reduction of oxygen to O2(-) at the expense of NADPH. In the resting neutrophil, some of the components of the oxidase, including proteins p47(phox) and p67(phox) are in the cytosol, while the rest are in a fraction that usually copurifies with plasma membrane. Recent evidence has suggested that at least some of the cytosolic oxidase components exist as a complex. We have now purified such a complex from the cytoplasm of resting neutrophils using an affinity column prepared with an antibody that recognizes the C-terminal decapeptide of p47(phox). Immunoblotting showed that the complex contained both p47(phox) and p67(phox). When supplemented with recombinant p67(phox), the complex displayed considerable activity in a cell-free oxidase-activating system, and even without added p67(phox), the complex could more than double O(2)(-)production in an oxidase-activating system supplemented with suboptimal amounts of cytosol. Isolation of the complex was blocked by preincubating the affinity column with CFSTKRKLASAV, the peptide against which the antibody was raised. On gel filtration, the complex migrated with a molecular weight of 240-300K, similar to that observed with whole neutrophil cytosol. The p47(phox)/p67(phox) ratio in the gel-filtered complex was approximately 1 to 1. These results indicate that in resting neutrophil cytosol, p47(phox) and p67(phox) exist as a complex. C1 SCRIPPS RES INST, DEPT MOLEC & EXPTL MED, LA JOLLA, CA 92037 USA. NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA. FU NIAID NIH HHS [AI-28479, AI-24227, AI-30742] NR 28 TC 83 Z9 84 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 15 PY 1994 VL 33 IS 10 BP 2907 EP 2911 DI 10.1021/bi00176a021 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA886 UT WOS:A1994NA88600021 PM 8130204 ER PT J AU GILLETTE, JR DARBYSHIRE, JF SUGIYAMA, K AF GILLETTE, JR DARBYSHIRE, JF SUGIYAMA, K TI THEORY FOR THE OBSERVED ISOTOPE EFFECTS ON THE FORMATION OF MULTIPLE PRODUCTS BY DIFFERENT KINETIC MECHANISMS OF CYTOCHROME-P450 ENZYMES SO BIOCHEMISTRY LA English DT Article ID LIVER MICROSOMAL CYTOCHROME-P-450; HYDROXYLATION; INTERMEDIATE; SYSTEMS; PROBES; STEP AB Cytochrome P450 systems are unusual in that many of them can convert a substrate to a number of different metabolites. Several kinetic mechanisms may be envisioned by which the metabolites may be formed. In each of the mechanisms, the substrate combines with the enzyme in different orientations to form a set of (ES) complexes that then are activated to a set of (EOS) complexes. The fate of these (EOS) complexes determines the kinetic mechanism. In the ''parallel pathway'' mechanism, the (EOS) complexes are so stable and rigid they cannot be converted either directly or indirectly to complexes with different orientations; the orientation of the (ES) complexes thus determines which metabolite will be formed. In the ''nondissociative'' mechanisms, the complexes are not rigid; instead they undergo interconversion while the substrate remains in the active site of the enzyme. In the ''dissociative'' mechanisms, the (EOS) complexes dissociate to (EO) and (S), but recombine to form (EOS) complexes with either the same or different orientations. Steady-state equations describing the deuterium isotope effects for these kinetic mechanisms have been derived and solved for competitive experiments, in which equal concentrations of both deuterated and nondeuterated substrates are present in incubation mixtures, and for noncompetitive experiments, in which only one of the substrates is present. The equations reveal that comparisons of the isotope effects on the formation of a metabolite by a pathway that does not involve the abstraction of a deuterium from a deuterated substrate (the non-deuterium abstraction pathway) in both experiments can differentiate between the kinetic mechanisms. A value of 1.0 for (nu)(H)/(nu)(D) in the competitive experiment, but <1.0 to >1.0 for the value of (V-max/K-m)(H)/(V-max/K-m)(D) in the noncompetitive experiment, is diagnostic for the ''dissociative'' mechanisms. Values of 1.0 in both kinds of experiments are diagnostic for the ''parallel pathway'' mechanism. Values of <1.0 in both types of experiments are diagnostic for the ''nondissociative mechanisms. The equations also predict possible unusual substrate-inhibitor interactions when the ''dissociative'' mechanism is operative. RP GILLETTE, JR (reprint author), NHLBI,CHEM PHARMACOL LAB,BLDG 10,ROOM 8N-117,BETHESDA,MD 20892, USA. NR 20 TC 26 Z9 26 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 15 PY 1994 VL 33 IS 10 BP 2927 EP 2937 DI 10.1021/bi00176a024 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA886 UT WOS:A1994NA88600024 PM 8130206 ER PT J AU DARBYSHIRE, JF GILLETTE, JR NAGATA, K SUGIYAMA, K AF DARBYSHIRE, JF GILLETTE, JR NAGATA, K SUGIYAMA, K TI DEUTERIUM-ISOTOPE EFFECTS ON A-RING AND D-RING METABOLISM OF TESTOSTERONE BY CYP2C11 - EVIDENCE FOR DISSOCIATION OF ACTIVATED ENZYME-SUBSTRATE COMPLEXES SO BIOCHEMISTRY LA English DT Article ID LIVER MICROSOMAL CYTOCHROME-P-450; RAT-LIVER; ISOZYMES; PURIFICATION AB Cytochrome P450 systems are unusual in that many of them can convert a substrate to a number of different metabolites by several possible kinetic mechanisms. Steady-state equations describing the deuterium isotope effects for mechanisms in which different orientations of the substrate relative to the perferryl oxygen in the active site of the enzyme are achieved before a hydrogen (or possibly an electron) is abstracted have been derived and solved (Gillette et al., 1994). These equations have been used to elucidate the kinetic mechanisms by which CYP2C11 converts testosterone to 2 alpha-hydroxytestosterone on the one hand and 16 alpha-hydroxytestosterone and androstenedione on the other. We have synthesized testosterone-2,2,4,6,6-H-2(5) and compared its metabolism by CYP2C11 with that of nondeuterated testosterone. In this system, deuterated 2 alpha-hydroxytestosterone would be formed by a deuterium abstraction pathway via the active oxygen intermediate (EOS(w)) and the D-ring metabolites would be formed by non-deuterium abstraction pathways from active oxygen intermediates represented by (EOS(x)). The results revealed that testosterone in the activated enzyme-substrate complexes, (EOS(w)) and (EOS(x)), does not change orientations while it is in the active site of CYP2C11. Instead, two of the noncompetitive experiments indicated that testosterone is able to dissociate from the (EOS) complexes and reassociate in either the same or different orientations. A third noncompetitive experiment suggested that testosterone in the (EOS) complexes does not change orientations while it is in the active site of CYP2C11, nor does it dissociate from the (EOS) complexes; instead, the pattern of metabolite formation is governed almost solely by the orientation of testosterone in the (ES(w)) and (ES(x)) complexes. C1 NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 11 TC 18 Z9 18 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 15 PY 1994 VL 33 IS 10 BP 2938 EP 2944 DI 10.1021/bi00176a025 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA886 UT WOS:A1994NA88600025 PM 8130207 ER PT J AU BOGUSLAVSKY, V REBECCHI, M MORRIS, AJ JHON, DY RHEE, SG MCLAUGHLIN, S AF BOGUSLAVSKY, V REBECCHI, M MORRIS, AJ JHON, DY RHEE, SG MCLAUGHLIN, S TI EFFECT OF MONOLAYER SURFACE PRESSURE ON THE ACTIVITIES OF PHOSPHOINOSITIDE-SPECIFIC PHOSPHOLIPASE-C-BETA-1, PHOSPHOLIPASE-C-GAMMA-1, AND PHOSPHOLIPASE-C-DELTA-1 SO BIOCHEMISTRY LA English DT Article ID AIR-WATER-INTERFACE; ALPHA-SUBUNITS; PHOSPHATIDYLINOSITOL 4,5-BISPHOSPHATE; SIGNAL TRANSDUCTION; BASIC PEPTIDES; ACIDIC LIPIDS; G-PROTEINS; ACTIVATION; MEMBRANES; BINDING AB Three isoforms of phospholipase C, either PLC-beta(1), PLC-gamma(1), or PLC-delta(1), were added to the aqueous subphase beneath phospholipid monolayers formed at an air-solution interface, and the initial rate of hydrolysis of phosphatidylinositol 4,5-bisphosphate was measured after addition of 10 mu M free Ca2+. The monolayers were formed from mixtures of phosphatidylcholine (65% PC), phosphatidylserine (33% PS), and phosphatidylinositol 4,5-bisphosphate (2% PIP2). Increasing the surface pressure of the monolayer, pi, from 15 to 25 mN/m decreases the rate of hydrolysis 16-, 13-, and 5-fold for PLC-beta(1), PLC-gamma(1), and PLC-delta(1), respectively. The simplest interpretation of these results is that a portion of each of the enzymes of area A(p) must insert into the monolayer, doing work pi A(p), prior to hydrolysis of PIP2; binding studies with simple model compounds of known cross-sectional area are consistent with this interpretation. Removing the monovalent acidic lipid PS from the monolayer decreases the initial rates of hydrolysis of PIP2 about 3-fold for each PLC isoform, which suggests that negative electrostatic surface potentials increase the PLC activity. C1 SUNY STONY BROOK,HLTH SCI CTR,STONY BROOK,NY 11794. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RI Morris, Andrew/B-7869-2010 FU NIGMS NIH HHS [GM-43422] NR 51 TC 115 Z9 115 U1 4 U2 7 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 15 PY 1994 VL 33 IS 10 BP 3032 EP 3037 DI 10.1021/bi00176a036 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NA886 UT WOS:A1994NA88600036 PM 8130216 ER PT J AU BROWN, TM BLACK, B UHDE, TW AF BROWN, TM BLACK, B UHDE, TW TI THE SLEEP ARCHITECTURE OF SOCIAL PHOBIA SO BIOLOGICAL PSYCHIATRY LA English DT Note DE SOCIAL PHOBIA; SLEEP; ANXIETY; EEG; POLYSOMNOGRAPHY ID PANIC ATTACKS; DISORDER C1 NIH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BETHESDA,MD 20892. NR 16 TC 24 Z9 24 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1994 VL 35 IS 6 BP 420 EP 421 DI 10.1016/0006-3223(94)90009-4 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NF092 UT WOS:A1994NF09200009 PM 8018789 ER PT J AU GLOVINSKY, D AF GLOVINSKY, D TI EARLY ANTIPSYCHOTIC RESPONSE TO RESUMPTION OF NEUROLEPTICS IN DRUG-FREE CHRONIC-SCHIZOPHRENIC PATIENTS - REPLY SO BIOLOGICAL PSYCHIATRY LA English DT Letter RP GLOVINSKY, D (reprint author), NATL INST MENTAL HLTH,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAR 15 PY 1994 VL 35 IS 6 BP 429 EP 430 DI 10.1016/0006-3223(94)90016-7 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NF092 UT WOS:A1994NF09200016 ER PT J AU INSKIP, PD BOICE, JD AF INSKIP, PD BOICE, JD TI RADIOTHERAPY-INDUCED LUNG-CANCER AMONG WOMEN WHO SMOKE SO CANCER LA English DT Editorial Material ID CONTRALATERAL BREAST; HODGKINS-DISEASE; MORTALITY; LYMPHOMA; RISK RP INSKIP, PD (reprint author), NCI,RADIAT EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 408,6130 EXECUT BLVD,ROCKVILLE,MD 20852, USA. NR 16 TC 17 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 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1994 VL 73 IS 6 BP 1541 EP 1543 DI 10.1002/1097-0142(19940315)73:6<1541::AID-CNCR2820730603>3.0.CO;2-G PG 3 WC Oncology SC Oncology GA NA319 UT WOS:A1994NA31900002 PM 8156480 ER PT J AU POCKAJ, BA SHERRY, RM WEI, JP YANNELLI, JR CARTER, CS LEITMAN, SF CARASQUILLO, JA STEINBERG, SM ROSENBERG, SA YANG, JC AF POCKAJ, BA SHERRY, RM WEI, JP YANNELLI, JR CARTER, CS LEITMAN, SF CARASQUILLO, JA STEINBERG, SM ROSENBERG, SA YANG, JC TI LOCALIZATION OF INDIUM-111-LABELED TUMOR-INFILTRATING LYMPHOCYTES TO TUMOR IN PATIENTS RECEIVING ADOPTIVE IMMUNOTHERAPY SO CANCER LA English DT Article DE TUMOR INFILTRATING LYMPHOCYTES; RADIO IMAGING; CYCLOPHOSPHAMIDE; IMMUNOTHERAPY; MELANOMA ID INVIVO ANTITUMOR-ACTIVITY; HIGH-DOSE INTERLEUKIN-2; ACTIVATED KILLER-CELLS; METASTATIC MELANOMA; ENDOTHELIAL-CELL; T-CELLS; RECOMBINANT INTERLEUKIN-2; ADHESION MOLECULE; AUTOLOGOUS TUMOR; NECROSIS-FACTOR AB Background. The adoptive transfer of interleukin-2 (IL-2)-cultured tumor infiltrating lymphocytes (TIL) can cause tumor regression in patients with metastatic melanoma. Methods. Thirty-eight patients with metastatic melanoma receiving high dose IL-2 and TIL were studied for the ability of autologous In-111-labeled TIL to localize to metastatic tumor deposits by gamma camera imaging and biopsy. Single bolus cyclophosphamide was administered 24-36 hours before TIL infusion in 27 treatment courses. Results. Tumor localization by In-111-labeled TIL was seen by gamma camera imaging in 26 (68.4%) treatment courses. In a univariate analysis of factors influencing TIL traffic, cyclophosphamide administration was significantly associated with the ability to localize tumor by radionuclide imaging (P2 = 0.026). Twenty-one of 26 (80.8%) treatment courses given with cyclophosphamide demonstrated tumor localization, compared with only 5 of 12 (41.7%) treatment courses without cyclophosphamide. In addition, patients whose In-111-labeled TIL imaged their tumor received significantly more TIL than did those that did not (P2 = 0.0052). Biopsies revealed a greater accumulation of In-111 in cutaneous tumors than in normal skin biopsy specimens (0.0021 and 0.0004% injectate/gram of tissue, respectively; P2 = <0.001). The median tumor-to-normal-skin ratio of simultaneous biopsies was 5.0. Finally, 10 of 26 (38.5%) patients who had tumor localization by scan had a clinical response, whereas no responses were noted in 12 patients whose tumors were not imaged (P2 = 0.022). Conclusions. Localization in tumor may be important in the mechanism of TIL antitumor activity because no clinical responses were seen in patients who did not have their tumors imaged with In-111-TIL. Cyclophosphamide administration before TIL and IL-2 therapy and the administration of large numbers of TIL appear to improve the frequency of TIL localization to tumor. C1 NCI,SURG BRANCH,BETHESDA,MD 20892. UNIV HOSP CLEVELAND,DEPT SURG,CLEVELAND,OH. MED COLL GEORGIA,DEPT SURG,AUGUSTA,GA 30912. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NIH,WARREN G MAGNUSEN CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD. NIH,WARREN G MAGNUSEN CLIN CTR,DEPT NUCL MED,BETHESDA,MD. NR 31 TC 134 Z9 135 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1994 VL 73 IS 6 BP 1731 EP 1737 DI 10.1002/1097-0142(19940315)73:6<1731::AID-CNCR2820730630>3.0.CO;2-H PG 7 WC Oncology SC Oncology GA NA319 UT WOS:A1994NA31900029 PM 8156501 ER PT J AU SRIVASTAVA, S AF SRIVASTAVA, S TI COMPUTER-APPLICATIONS FOR EARLY DETECTION AND STAGING OF CANCER - INTRODUCTION SO CANCER LETTERS LA English DT Editorial Material RP SRIVASTAVA, S (reprint author), NATL CANC INST,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,BETHESDA,MD, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD MAR 15 PY 1994 VL 77 IS 2-3 BP 67 EP 68 DI 10.1016/0304-3835(94)90087-6 PG 2 WC Oncology SC Oncology GA NG274 UT WOS:A1994NG27400001 ER PT J AU GOPAL, R SRIVASTAVA, S AF GOPAL, R SRIVASTAVA, S TI HIGH-PERFORMANCE COMPUTING AND COMMUNICATIONS - POTENTIAL APPLICATIONS IN CANCER-RESEARCH SO CANCER LETTERS LA English DT Article DE HIGH PERFORMANCE COMPUTING IN CANCER; CANCER DATABASE LINKAGE; IMAGE TRANSMISSION AND ANALYSIS; COMPUTER-AIDED DIAGNOSIS; CANCER PATIENT MANAGEMENT AB Application of high performance computing and communications (HPCC) in the health care system has begun to unfold. Computers are increasingly being used in data information flow, patient management, diagnosis and in estimating prognosis, treatment, drug design, and the education, and training of health professionals. The fast gigabit network, three-dimensional displays of medical images, automation of laboratory testings, linkage of large databases, computer-aided diagnosis, and interpretation have revolutionized medical care. These achievements have been possible in large part due to rapidly advancing fields of software algorithms, computational science, and communication technologies that have enabled the user to remotely access and share information in consistent and cost-effective way regardless of their geographical location. The present article introduces several facets of 'HPCC grand challenges' and discusses the role of HPCC in cancer prevention and control through accurate diagnosis and prognosis, image analysis and interpretation, and faster database linkage for evaluating outcome of the cancer-related health services research. C1 NCI,EARLY DETECT BRANCH,ROCKVILLE,MD 20852. SOFTGEN CORP,GERMANTOWN,MD. NR 18 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD MAR 15 PY 1994 VL 77 IS 2-3 BP 69 EP 77 DI 10.1016/0304-3835(94)90088-4 PG 9 WC Oncology SC Oncology GA NG274 UT WOS:A1994NG27400002 PM 8168068 ER PT J AU ZAVRAZHINA, I YAROSLAVSKY, LP AF ZAVRAZHINA, I YAROSLAVSKY, LP TI COMPUTER-ASSISTED TECHNOLOGIES IN LUNG-CANCER DIAGNOSIS AND STAGING SO CANCER LETTERS LA English DT Article DE COMPUTER-ASSISTED RADIOLOGY; LUNG CANCER STAGING; IMAGE PROCESSING; DATA FUSION AB A paradigm for digital image processing in radiological diagnosis and an appropriate algorithmic instrumentation toolset for the implementation of image processing methods on inexpensive computers and workstations are outlined briefly. Examples of computer-assisted technologies for lung cancer differential diagnosis are given that exhibit considerable increase in diagnostic accuracy. Multimodal image processing and data fusion in lung cancer diagnosis are discussed and a 'road map' for examining lung cancer patients is suggested on the basis of clinical experience in the use of different modalities for lung cancer staging. C1 NCI,BETHESDA,MD 20892. NCRR,BEIP,BETHESDA,MD 20892. NR 18 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD MAR 15 PY 1994 VL 77 IS 2-3 BP 191 EP 200 DI 10.1016/0304-3835(94)90102-3 PG 10 WC Oncology SC Oncology GA NG274 UT WOS:A1994NG27400016 PM 8168066 ER PT J AU SLAYTER, MV ANZANO, MA KADOMATSU, K SMITH, JM SPORN, MB AF SLAYTER, MV ANZANO, MA KADOMATSU, K SMITH, JM SPORN, MB TI HISTOGENESIS OF INDUCED PROSTATE AND SEMINAL-VESICLE CARCINOMA IN LOBUND-WISTAR RATS - A SYSTEM FOR HISTOLOGICAL SCORING AND GRADING SO CANCER RESEARCH LA English DT Article ID CANCER; ADENOCARCINOMAS; INDUCTION; NEOPLASIA AB We have developed a grading system for the evaluation of the histogenesis of neoplastic lesions of the prostate and seminal vesicle of the laboratory rat. Prostatic and seminal vesicle carcinomas were induced in Lobund-Wistar rats by initiation with 30 mg/kg N-nitroso-N-methylurea i.v., followed by promotion with 40 mg testosterone propionate implants 1 week later and at 3-month intervals thereafter. Experimental and control groups were sacrificed at various time points between 5 and 11 months after dosing with N-nitroso-N-methylurea in order to visualize progressive stages of carcinogenesis of the dorsolateral prostate, the anterior prostate, and the seminal vesicle. A system of staging was created which allows three different categories (in situ change, invasion, desmoplasia) of tumor development to be ranked progressively in a manner conducive to nonparametric analysis. Each category was then further subdivided to create a total of six stages. This system can be used to evaluate agents which modify tumor induction or suppression. The application of this staging system to the measurement of the effects of the synthetic retinoid, 4-hydroxyphenyl retinamide, on prostatic carcinogenesis in the Lobund-Wistar rat is described. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP SLAYTER, MV (reprint author), ARMED FORCES INST PATHOL,DEPT VET PATHOL,WASHINGTON,DC 20306, USA. RI Kadomatsu, Kenji/G-8083-2012 NR 19 TC 36 Z9 36 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1440 EP 1445 PG 6 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700011 PM 8137245 ER PT J AU MULLEN, CA COALE, MM LOWE, R BLAESE, RM AF MULLEN, CA COALE, MM LOWE, R BLAESE, RM TI TUMORS EXPRESSING THE CYTOSINE DEAMINASE SUICIDE GENE CAN BE ELIMINATED IN-VIVO WITH 5-FLUOROCYTOSINE AND INDUCE PROTECTIVE IMMUNITY TO WILD-TYPE TUMOR SO CANCER RESEARCH LA English DT Article ID ESCHERICHIA-COLI; CELLS; STRATEGY; PURINE; MOUSE AB Successful expression of the cytosine deaminase (CD) suicide gene in vivo is demonstrated in three weakly immunogenic murine tumor models: the 102 and 205 fibrosarcomas and the 38 adenocarcinoma. Normal mammalian cells do not contain cytosine deaminase, but tumor cells transduced with retroviral vectors containing the CD gene metabolize the relatively nontoxic prodrug 5-fluorocytosine to the highly toxic 5-fluorouracil. In vitro cells expressing the CD gene are killed by 5-fluorocytosine while unmodified cells are not. When injected into syngeneic mice, CD+ tumors can also be eliminated in vivo by systemic treatment with 5-fluorocytosine without significant toxicity to the host. Animals whose CD+ tumors were eliminated with prodrug treatment resist subsequent rechallenge with unmodified wild type tumor. This posttreatment immunity appears to be tumor specific. Applications of the CD system in gene therapy models are discussed. RP MULLEN, CA (reprint author), NCI,DIV CANC BIOL DIAG & CTR,METAB BRANCH,BLDG 10,ROOM 4N115,BETHESDA,MD 20892, USA. NR 20 TC 219 Z9 223 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1994 VL 54 IS 6 BP 1503 EP 1506 PG 4 WC Oncology SC Oncology GA NA887 UT WOS:A1994NA88700021 PM 8137255 ER PT J AU ITO, Y SETO, Y BRANNAN, CI COPELAND, NG JENKINS, NA FUKUNAGA, R NAGATA, S AF ITO, Y SETO, Y BRANNAN, CI COPELAND, NG JENKINS, NA FUKUNAGA, R NAGATA, S TI STRUCTURAL-ANALYSIS OF THE FUNCTIONAL GENE AND PSEUDOGENE ENCODING THE MURINE GRANULOCYTE COLONY-STIMULATING-FACTOR RECEPTOR SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article ID HUMAN ERYTHROPOIETIN RECEPTOR; CHROMOSOMAL LOCALIZATION; GENOMIC ORGANIZATION; PROMOTER REGION; RAS GENE; TRANSCRIPTION; EXPRESSION; SEQUENCES; CLONING; RNA AB Granulocyte colony-stimulating factor is a cytokine which specifically regulates the production of neutrophilic granulocytes. The granulocyte colony-stimulating-factor receptor (GCSFR) is mainly expressed in neutrophils and their precursor cells. In this study, we isolated the chromosomal gene for murine GCSFR and determined its structure. Like the human GCSFR gene homolog, it consists of 17 exons. The exon-intron organization of the murine and human GCSFR-encoding genes are very similar, except that exon 14 and exon 15 in the murine gene are interrupted by a larger intron (greater than 10 kbp) than that found in the human gene (128 bp). This GCSFR-encoding functional gene (Csfgr) was localized to the distal region of murine chromosome 4 by interspecific backcross mapping. A comparison of the 5' flanking sequence of murine and human Csfgr revealed that a sequence of approximately 300 bp upstream from the cap site is highly conserved. Within this region, an 18-nucleotide element conserved in the promoter of the genes for neutrophil-specific enzymes, was found approximately 140 bp upstream from the cap site, suggesting an involvement of this element in the specific expression of GCSFR in neutrophilic granulocytes. In addition to the functional GCSFR-encoding gene, we isolated a pseudogene for GCSFR, which is flanked by a 15-bp direct repeat at the 5' and 3' ends, and lacks all introns, exons 1-3 and exons 7-8 of the functional gene. The processed pseudogene has, in its most 5' region, a sequence of approximately 200 bp that is highly related to the DNA sequence approximately 1.2 kbp upstream of the cap site of the functional gene. C1 OSAKA BIOSCI INST,SUITA,OSAKA 565,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,BETHESDA,MD 20892. FU NCI NIH HHS [N0-CO-74101] NR 45 TC 23 Z9 23 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD MAR 15 PY 1994 VL 220 IS 3 BP 881 EP 891 DI 10.1111/j.1432-1033.1994.tb18691.x PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NB530 UT WOS:A1994NB53000026 PM 8143742 ER PT J AU KLUG, CA GERETY, SJ SHAH, PC CHEN, YY RICE, NR ROSENBERG, N SINGH, H AF KLUG, CA GERETY, SJ SHAH, PC CHEN, YY RICE, NR ROSENBERG, N SINGH, H TI THE V-ABL TYROSINE KINASE NEGATIVELY REGULATES NF-KAPPA-B REL FACTORS AND BLOCKS KAPPA-GENE TRANSCRIPTION IN PRE-B-LYMPHOCYTES SO GENES & DEVELOPMENT LA English DT Article DE TYROSINE KINASE; NF-KAPPA-B REL ACTIVITY; KAPPA-GENE; TRANSCRIPTION; ABELSON MURINE LEUKEMIA VIRUS ID ENHANCER-BINDING-PROTEIN; MURINE LEUKEMIA-VIRUS; IMMUNOGLOBULIN GENES; CONSTANT REGION; LYMPHOID-CELLS; BONE-MARROW; REARRANGEMENT; ACTIVATION; LOCUS; MOUSE AB Transformation of B-lineage precursors by the Abelson murine leukemia virus appears to arrest development at the pre-B stage. Abelson-transformed pre-B cell lines generally retain transcriptionally inactive, unrearranged immunoglobulin kappa alleles. We demonstrate that nontransformed pre-B cells expanded from the mouse bone marrow efficiently transcribe unrearranged kappa alleles. In addition, they contain activated complexes of the NF-kappaB/Rel transcription factor family, in contrast with their Abelson-transformed counterparts. Using conditionally transformed pre-B cell lines, we show that the v-abl viral transforming protein, a tyrosine kinase, blocks germ-line kappa gene transcription and negatively regulates NF-kappaB/Rel activity. An active v-abl kinase specifically inhibits the NF-kappaB/Rel-dependent kappaK intron enhancer, which is implicated in promoting both transcription and rearrangement of the kappa locus. v-abl inhibits the activated state of NF-kappaB/Rel complexes in a pre-B cell via a post-translational mechanism that results in increased stability of the inhibitory subunit IkappaBalpha. This analysis suggests a molecular pathway by which v-abl inhibits kappa locus transcription and rearrangement. C1 UNIV CHICAGO,HOWARD HUGHES MED INST,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MOLEC GENET & CELL BIOL,CHICAGO,IL 60637. TUFTS UNIV,SCH MED,GRAD PROGRAM IMMUNOL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,DEPT MOLEC BIOL & MICROBIOL,BOSTON,MA 02111. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. FU NCI NIH HHS [CA 24220]; NIGMS NIH HHS [5T32GM08369, GM07183] NR 44 TC 78 Z9 78 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR 15 PY 1994 VL 8 IS 6 BP 678 EP 687 DI 10.1101/gad.8.6.678 PG 10 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA ND121 UT WOS:A1994ND12100004 PM 7926758 ER PT J AU WYMORE, RS KORENBERG, JR KINOSHITA, KD AIYAR, J COYNE, C CHEN, XN HUSTAD, CM COPELAND, NG GUTMAN, GA JENKINS, NA CHANDY, KG AF WYMORE, RS KORENBERG, JR KINOSHITA, KD AIYAR, J COYNE, C CHEN, XN HUSTAD, CM COPELAND, NG GUTMAN, GA JENKINS, NA CHANDY, KG TI GENOMIC ORGANIZATION, NUCLEOTIDE-SEQUENCE, BIOPHYSICAL PROPERTIES, AND LOCALIZATION OF THE VOLTAGE-GATED K+ CHANNEL GENE KCNA4/KV1.4 TO MOUSE CHROMOSOME-2 HUMAN-11P14 AND MAPPING OF KCNC1 KV3.1 TO MOUSE-7 HUMAN-11P14.3-P15.2 AND KCNA1 KV1.1 TO HUMAN-12P13 SO GENOMICS LA English DT Article ID INACTIVATING POTASSIUM CHANNEL; LONG-QT SYNDROME; FUNCTIONAL EXPRESSION; INSITU HYBRIDIZATION; MOLECULAR-CLONING; SKELETAL-MUSCLE; LINKAGE MAP; SHORT ARM; CELLS; REGION AB A genomic clone encoding the Shaker-related potassium channel gene, Kcna4/mKv1.4, was isolated from mice. Its coding region is contained in a single exon, encodes a protein of 654 amino acids, and shares approximately 91% nucleotide sequence identity with human KCNA4/hKv1.4. We show that 0.8 kb of the 5' noncoding region (NCR), the entire protein coding region (approximately 2.0 kb), and all of the known 3' NCR (approximately 1.1 kb) are contained within a single exon; the remaining 0.5 kb of the 5' NCR is separated from this exon by a 3.4-kb intron. The sequenced genomic region thus accounts for essentially all of the longest known transcript (4.5 kb), although the precise ends of this transcript have not been defined. The 3' NCR contains several ATTTA and ATTTG motifs that are thought to destabilize mRNAs, and these are also present in rat, bovine, and human KcnA4/Kv1.4 cDNAs. It also contains three conserved polyadenylation signals, alternate utilization of which could generate mRNAs of differing stabilities. The 5' NCR of Kcna4/mKv1.4 may also serve to regulate channel expression. This region is approximately 85% identical to KCNA4/hKv1.4 and contains eight consensus translation start sites [(G, A)NNATG] that, based on the 5'-3' scanning model, would lead to a lowering of translational efficiency. The shortest Kcna4/Kv1.4 transcript (2.4 kb) can contain at most 400 bp of NCR and should lack the 3' ATTTAs and most of the 5' ATGs; this transcript might therefore exhibit increased stability and translational efficiency. The Kcna4/mKv1.4 channel exhibited biophysical and pharmacological properties indistinguishable from its rat and human homologues. Kcna4/mKv1.4 lies on mouse chromosome 2, near the Fshb locus, and in humans on the proximal half of chromosome 11p14 near human FSHB. Another K+, channel gene, Kcnc1/mKv3.1, lies approximately 1.8 cM from the Myod-1 gene on mouse chromosome 7, and in situ hybridization localizes KCNC1/hKv3.1 to the homologous region on human chromosome 11p14.3-p15.2. A third gene, KCNA1/hKv1.1, was mapped to human 12p13. (C) 1994 Academic Press, Inc. C1 UNIV CALIF IRVINE,DEPT MICROBIOL & MOLEC GENET,IRVINE,CA 92717. CEDARS SINAI MED CTR,DIV MED GENET,LOS ANGELES,CA 90048. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP WYMORE, RS (reprint author), UNIV CALIF IRVINE,DEPT PHYSIOL & BIOPHYS,MED SCI I,IRVINE,CA 92717, USA. FU NCI NIH HHS [NCI NO1-CO-74101]; NHGRI NIH HHS [HG00037-03]; NIAID NIH HHS [AI24783] NR 60 TC 34 Z9 35 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR 15 PY 1994 VL 20 IS 2 BP 191 EP 202 DI 10.1006/geno.1994.1153 PG 12 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NB820 UT WOS:A1994NB82000005 PM 8020965 ER PT J AU PERFETTI, R HAWKINS, AL GRIFFIN, CA EGAN, JM ZENILMAN, ME SHULDINER, AR AF PERFETTI, R HAWKINS, AL GRIFFIN, CA EGAN, JM ZENILMAN, ME SHULDINER, AR TI ASSIGNMENT OF THE HUMAN PANCREATIC REGENERATING (REG) GENE TO CHROMOSOME-2P12 SO GENOMICS LA English DT Note ID STONE PROTEIN; EXPRESSION; SEQUENCE; INSULIN; ISLETS AB A cDNA termed reg (for regenerating gene) has been isolated and characterized from a rat pancreatic library. Expression of reg is markedly increased in regenerating islets and decreased when insulin gene expression is inhibited. These findings have led to the hypothesis that reg may be involved in the expansion of beta-cell mass during regeneration as well as in the maintenance of normal beta-cell function. The human reg gene has a high degree of similarity to the rat reg gene. To determine the chromosomal location of the human reg gene, we analyzed two panels of mouse- or hamster-human hybrid cell lines containing a single human chromosome or several different human chromosomes. DNA extracts from these cell lines were analyzed for the presence of the human reg gene by polymerase chain reaction. In addition, human metaphase chromosomes were used for fluorescence in situ hybridization to further confirm the chromosomal assignment and to determine the subchromosomal localization. With these approaches, we show that the human reg gene is located on the short arm of chromosome 2 near the centromere at band 2p12. (C) 1994 Academic Press, Inc. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT SURG,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT GERIATR MED & GERONTOL,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD 21287. RP PERFETTI, R (reprint author), NIA,CLIN PHYSIOL LAB,DIABET UNIT,ROOM 2B02,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 17 TC 9 Z9 10 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR 15 PY 1994 VL 20 IS 2 BP 305 EP 307 DI 10.1006/geno.1994.1173 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NB820 UT WOS:A1994NB82000025 PM 8020983 ER PT J AU ZABAROVSKY, ER ALLIKMETS, R KHOLODNYUK, I ZABAROVSKA, VI PAULSSON, N BANNIKOV, VM KASHUBA, VI DEAN, M KISSELEV, LL KLEIN, G AF ZABAROVSKY, ER ALLIKMETS, R KHOLODNYUK, I ZABAROVSKA, VI PAULSSON, N BANNIKOV, VM KASHUBA, VI DEAN, M KISSELEV, LL KLEIN, G TI CONSTRUCTION OF REPRESENTATIVE NOTL LINKING LIBRARIES SPECIFIC FOR THE TOTAL HUMAN GENOME AND FOR HUMAN CHROMOSOME-3 SO GENOMICS LA English DT Note ID GENE MARKERS; CPG ISLANDS; CLONING AB NotI linking clones represent valuable tools for both physical and genetic mapping. Using procedures that we have previously described, several chromosome 3-specific NotI linking libraries have been constructed. Here, we describe the construction of six independent NotI linking libraries specific for the total human genome. These libraries were made using three different vectors and two combinations of restriction enzymes. Altogether, these six libraries contain more than 1 million recombinant phages. Considering that the human genome contains about 3000-5000 NotI sites, it is likely that all clonable NotI sites are present in these libraries. Two of the six libraries were transferred into plasmid form. At the same time, a chromosome 3-specific EcoRI-NotI library (NRL1) was constructed. This library considerably increases the representation of cloned NotI sites in combination with previously constructed libraries that were made using BamHI-NotI digestion. All libraries are available on request. (C) 1994 Academic Press, Inc. C1 ENGELHARDT MOLEC BIOL INST,MOSCOW 117984,RUSSIA. NCI,FREDERICK,MD 21702. UKRAINIAN ACAD SCI,INST MOLEC BIOL,KIEV 252627,UKRAINE. RP ZABAROVSKY, ER (reprint author), KAROLINSKA INST,DEPT TUMOR BIOL,BOX 60400,S-10401 STOCKHOLM 60,SWEDEN. RI Zabarovsky, Eugene/A-6645-2010; Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 FU NCI NIH HHS [5 RO1 CA14054-15] NR 18 TC 29 Z9 29 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR 15 PY 1994 VL 20 IS 2 BP 312 EP 316 DI 10.1006/geno.1994.1175 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NB820 UT WOS:A1994NB82000027 PM 8020985 ER PT J AU POPESCU, N ZIMONJIC, D HATCH, C BONNER, W AF POPESCU, N ZIMONJIC, D HATCH, C BONNER, W TI CHROMOSOMAL MAPPING OF THE HUMAN HISTONE GENE-H2AZ TO 4Q24 BY FLUORESCENCE IN-SITU HYBRIDIZATION SO GENOMICS LA English DT Note ID SEQUENCE; VARIANT; H2A.Z; GENE C1 NCI,DCT,DTP,MOLEC PHARMACOL LAB,BLDG 37,ROOM 5D17,BETHESDA,MD 20892. NCI,DCE,CPCP,BIOL LAB,BETHESDA,MD 20892. NR 7 TC 36 Z9 36 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR 15 PY 1994 VL 20 IS 2 BP 333 EP 335 DI 10.1006/geno.1994.1182 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NB820 UT WOS:A1994NB82000034 PM 8020992 ER PT J AU VAMVAKOPOULOS, NC KUNZ, J OLBERDING, U SCHERER, SW SIOUTOPOULOU, TO SCHNEIDER, V DURKIN, AS NIERMAN, WC AF VAMVAKOPOULOS, NC KUNZ, J OLBERDING, U SCHERER, SW SIOUTOPOULOU, TO SCHNEIDER, V DURKIN, AS NIERMAN, WC TI MAPPING THE HUMAN GROWTH HORMONE-RELEASING HORMONE-RECEPTOR (GHRHR) GENE TO THE SHORT ARM OF CHROMOSOME-7 (7P13-P21) NEAR THE EPIDERMAL GROWTH-FACTOR RECEPTOR (EGFR) GENE SO GENOMICS LA English DT Note ID PITUITARY; DWARF C1 AMER TYPE CULTURE COLLECT,DEPT MOLEC BIOL,ROCKVILLE,MD 20852. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. UNIV MARBURG,MED ZENTRUM HUMANGENET,D-35037 MARBURG,GERMANY. HOSP SICK CHILDREN,RES INST,DEPT GENET,TORONTO M5G 1X8,ONTARIO,CANADA. UNIV ATHENS,SCH MED,ATHENS,GREECE. AMER TYPE CULTURE COLLECT,DEPT MOLEC BIOL,ROCKVILLE,MD 20852. RI Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013 OI Scherer, Stephen /0000-0002-8326-1999 NR 11 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR 15 PY 1994 VL 20 IS 2 BP 338 EP 340 DI 10.1006/geno.1994.1185 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NB820 UT WOS:A1994NB82000037 PM 8020995 ER PT J AU PALLI, D CIPRIANI, F DECARLI, A GALLI, M SAIEVA, C FRAUMENI, JF BLOT, WJ BUIATTI, E AF PALLI, D CIPRIANI, F DECARLI, A GALLI, M SAIEVA, C FRAUMENI, JF BLOT, WJ BUIATTI, E TI REPRODUCTIVE HISTORY AND GASTRIC-CANCER AMONG POSTMENOPAUSAL WOMEN SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID PROGESTERONE RECEPTORS; ESTROGEN; POPULATION; ESTRADIOL; PARITY; DIET AB A total of 339 post-menopausal women with gastric cancer (GC) and 515 population controls were interviewed in a multicenter study in Italy for information on reproductive history, dietary habits and other socio-demographic variables. After adjusting for these factors, GC risk was significantly higher among women reporting menopause below age 45, while no effect was shown for age at menarche, parity, age at first livebirth, and number of abortions. When age at menopause was considered together with age at menarche for an index of fertility years, GC risk showed a significant inverse relation to duration of fertility. These results suggest a protective role for endocrine or other factors related to late age at menopause or to length of fertility. These findings may be relevant to explain the fact that rates of GC reported among females are lower than among males around the world, and suggest the need for further research into hormonal and other related risk factors. (C) 1994 Wiley-Liss, Inc. C1 UNIV MILAN,IST STAT MED & BIOMETRIA,I-20122 MILAN,ITALY. IST NAZL TUMORI,I-20133 MILAN,ITALY. GENOA CTR STUDIO & PREVENZ ONCOL,IST TUMORI,SEZ DISTACCATA,FLORENCE,ITALY. NCI,BETHESDA,MD 20892. RP PALLI, D (reprint author), CTR STUDIO & PREVENZ ONCOL,EPIDEMIOL UNIT,VIALE A VOLTA 171,I-50131 FLORENCE,ITALY. RI Decarli, Adriano/C-3129-2017; OI Decarli, Adriano/0000-0003-1451-8292; saieva, calogero/0000-0002-0117-1608; PALLI, Domenico/0000-0002-5558-2437 FU NCI NIH HHS [N01-CP-51019] NR 23 TC 47 Z9 47 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD MAR 15 PY 1994 VL 56 IS 6 BP 812 EP 815 DI 10.1002/ijc.2910560609 PG 4 WC Oncology SC Oncology GA NB110 UT WOS:A1994NB11000008 PM 8119771 ER PT J AU GHAREHBAGHI, K PAULL, KD KELLEY, JA BARCHI, JJ MARQUEZ, VE COONEY, DA MONKS, A SCUDIERO, D KROHN, K JAYARAM, HN AF GHAREHBAGHI, K PAULL, KD KELLEY, JA BARCHI, JJ MARQUEZ, VE COONEY, DA MONKS, A SCUDIERO, D KROHN, K JAYARAM, HN TI CYTOTOXICITY AND CHARACTERIZATION OF AN ACTIVE METABOLITE OF BENZAMIDE RIBOSIDE, A NOVEL INHIBITOR OF IMP DEHYDROGENASE SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID 2-BETA-D-RIBOFURANOSYLTHIAZOLE-4-CARBOXAMIDE NSC 286193; ADENINE-DINUCLEOTIDE TAD; TIAZOFURIN; LEUKEMIA; MECHANISM; ANALOGS; DRUG; CELLS; LEVEL AB Benzamide riboside exhibits significant cytotoxicity against a variety of human tumor cells in culture. On the basis of metabolic studies, the primary target of this drug's action appears to be IMP dehydrogenase (IMPDH). Incubation of human myelogenous leukemia K562 cells with an IC50 concentration of benzamide riboside resulted in an expansion of IMP pools (5.9-fold), with a parallel reduction in the concentration of GMP (90%), GDP (63%), GTP (55%) and dGTP (40%). On kinetic grounds, it was deduced that benzamide riboside (whose K-i versus IMPDH is 6.4 mM, while that of its 5'-monophosphate is 3.9 mM) or its 5'-monophosphate were unlikely to be responsible for inhibition of this target enzyme, IMPDH, since only micromolar concentrations of benzamide riboside were needed to exert potent inhibition of tumor-cell growth. Studies on the metabolism of this C-nucleoside have revealed the presence of a new peak eluting in the nucleoside diphosphate area on HPLC. Treatment of this peak with venom phosphodiesterase degraded it and concurrently nullified its inhibitory activity verses IMPDH; alkaline phosphatase, on the other hand, totally failed to digest the anabolite. These results suggest that the metabolite in question is the phosphodiester, benzamide adenine dinucleotide (BAD). Evidence that the inhibitor was an analog of NAD, wherein the nicotinamide moiety has been replaced by benzamide, was provided by both NMR and mass spectrometric analysis and confirmed by enzymatic synthesis. Further insight into the nature of the active principle was obtained from kinetic studies, which established that BAD competitively inhibited NAD utilization by partially purified IMPDH from K562 cells with a K-i of 0.118 mu M. In concert, these studies establish that benzamide riboside exhibits potent antiproliferative activity by inhibiting IMPDH through BAD. (C) 1994 Wiley-Liss, Inc. C1 INDIANA UNIV,SCH MED,EXPTL ONCOL LAB,INDIANAPOLIS,IN 46202. NCI,INFORMAT TECHNOL BRANCH,BETHESDA,MD 20892. NCI,MED CHEM LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD 21702. UNIV GESAMTHSCH PADERBORN,DIV ORGAN CHEM,W-4790 PADERBORN,GERMANY. RI Barchi Jr., Joseph/N-3784-2014 FU NCI NIH HHS [NCI CA 51770, NCI NO1CO-23910] NR 22 TC 51 Z9 52 U1 0 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD MAR 15 PY 1994 VL 56 IS 6 BP 892 EP 899 DI 10.1002/ijc.2910560623 PG 8 WC Oncology SC Oncology GA NB110 UT WOS:A1994NB11000022 PM 7907081 ER PT J AU ANDERSON, W CHAN, CC NUSSENBLATT, RB WHITCUP, SM AF ANDERSON, W CHAN, CC NUSSENBLATT, RB WHITCUP, SM TI TOPICAL HEPARIN INHIBITS COMPOUND-48/80 INDUCED ALLERGIC CONJUNCTIVITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NATL NAVAL MED CTR, DEPT OPHTHALMOL, BETHESDA, MD 20814 USA. NEI, BETHESDA, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1291 EP 1291 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500181 ER PT J AU PENG, B LI, Q ROBERGE, F WHITCUP, SM LUYO, D CHAN, CC AF PENG, B LI, Q ROBERGE, F WHITCUP, SM LUYO, D CHAN, CC TI TOPICAL RAPAMYCIN INHIBITS ALLERGIC CONJUNCTIVITIS IN A MURINE MODEL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1292 EP 1292 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500182 ER PT J AU MATURI, RK NUSSENBLATT, RB DESMET, MD AF MATURI, RK NUSSENBLATT, RB DESMET, MD TI PREVALENCE OF TEAR HYPOSECRETION AND VITAMIN-A-DEFICIENCY IN PATIENTS WITH AIDS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1308 EP 1308 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500253 ER PT J AU REDMOND, TM JENKINS, NA GILBERT, DJ COPELAND, NG HAMEL, CP AF REDMOND, TM JENKINS, NA GILBERT, DJ COPELAND, NG HAMEL, CP TI THE GENE FOR THE RETINAL-PIGMENT EPITHELIUM-SPECIFIC PROTEIN RPE65 IS LOCALIZED TO HUMAN 1P31 AND MOUSE-3 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1312 EP 1312 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500274 ER PT J AU TOMBRANTINK, J RODRIGUEZ, IR MAZURUK, K SHIVARAM, S LI, A CHADER, G AF TOMBRANTINK, J RODRIGUEZ, IR MAZURUK, K SHIVARAM, S LI, A CHADER, G TI STRUCTURAL-ANALYSIS OF THE GENE FOR PIGMENT-EPITHELIUM DIFFERENTIATION (PEDF) FACTOR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1312 EP 1312 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500275 ER PT J AU SRIVASTAVA, OP SRIVASTAVA, K HEJTMANCIK, JF HOPE, J AF SRIVASTAVA, OP SRIVASTAVA, K HEJTMANCIK, JF HOPE, J TI AGE-RELATED DEGRADATIVE PATHWAYS OF HUMAN LENS BETA-A3/A1-CRYSTALLINS AND DELTA-D-CRYSTALLINS ARE PROGRAMMED SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV ALABAMA,SCH OPTOMETRY,DEPT PHYSIOL OPT,BIRMINGHAM,AL 35294. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1314 EP 1314 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500280 ER PT J AU HACKETT, S HENDERER, J VINORES, S CSAKY, C LAROCHELLE, W CAMPOCHIARO, P AF HACKETT, S HENDERER, J VINORES, S CSAKY, C LAROCHELLE, W CAMPOCHIARO, P TI PLATELET-DERIVED GROWTH-FACTORS (PDGFS) ARE AUTOCRINE GROWTH STIMULATORS IN RPE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV HOSP,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1385 EP 1385 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500608 ER PT J AU KUTTY, RK KUTTY, G WIGGERT, B CHADER, GJ DARROW, RM ORGANISCIAK, DT AF KUTTY, RK KUTTY, G WIGGERT, B CHADER, GJ DARROW, RM ORGANISCIAK, DT TI LIGHT DAMAGE INCREASES THE EXPRESSION OF HEME OXYGENASE-1 (HO-1) IN THE RETINA - PROTECTION BY THE ANTIOXIDANT DIMETHYLTHIOUREA (DMTU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. WRIGHT STATE UNIV,DEPT BIOCHEM & MOLEC BIOL,DAYTON,OH 45435. NR 1 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1391 EP 1391 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500637 ER PT J AU BRAUN, CI FREIDLIN, V SPERDUTO, RD STRAHLMAN, ER AF BRAUN, CI FREIDLIN, V SPERDUTO, RD STRAHLMAN, ER TI MYOPIC PROGRESSION OF SCHOOLCHILDREN IN COLUMBIA, MARYLAND SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. MERCK SHARP & DOHME LTD,BLUE BELL,PA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1394 EP 1394 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500648 ER PT J AU CONNOLLY, WES DESCHENES, J GOLDSTEIN, D RIZZO, L BURNIER, MN AF CONNOLLY, WES DESCHENES, J GOLDSTEIN, D RIZZO, L BURNIER, MN TI MHC CLASS-1 EXPRESSION IN PATIENTS WITH MYOPIA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MCGILL UNIV,DEPT OPHTHALMOL,MONTREAL H3A 2T5,QUEBEC,CANADA. NEI,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1415 EP 1415 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500734 ER PT J AU SOUKIASIAN, SH LINDSEY, P KINGMA, D NAVARROROMAN, L JAFFE, ES AF SOUKIASIAN, SH LINDSEY, P KINGMA, D NAVARROROMAN, L JAFFE, ES TI IMMUNOSUPPRESSION ASSOCIATED ANGIOCENTRIC IMMUNOPROLIFERATIVE LESION (AIL) WITH ORBITAL INVOLVEMENT - CONJUNCTIVAL HISTOPATHOLOGY AND THE IMPLICATION OF EPSTEIN-BARR-VIRUS IN PATHOGENESIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 LAHEY CLIN FDN,MED CTR,DEPT OPHTHALMOL,BURLINGTON,MA. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1448 EP 1448 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500900 ER PT J AU GENTLEMAN, S CHADER, GJ AF GENTLEMAN, S CHADER, GJ TI INTERACTION OF MICROTUBULE-ASSOCIATED PROTEIN ACETYLTRANSFERASE WITH ARRESTIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1462 EP 1462 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500966 ER PT J AU HAZARD, ES LIN, ZY NICKERSON, JM WIGGERT, B CHADER, G CROUCH, RK AF HAZARD, ES LIN, ZY NICKERSON, JM WIGGERT, B CHADER, G CROUCH, RK TI A CIRCULAR-DICHROISM (CD) ANALYSIS OF IRBP SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. EMORY UNIV,ATLANTA,GA 30322. MED UNIV S CAROLINA,DEPT OPHTHALMOL,CHARLESTON,SC 29425. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1464 EP 1464 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500980 ER PT J AU OKAJIMA, TIL WIGGERT, B CHADER, GJ PEPPERBERG, DR AF OKAJIMA, TIL WIGGERT, B CHADER, GJ PEPPERBERG, DR TI IRBP-STIMULATED PROCESSING OF RETINOIDS IN THE RETINAL-PIGMENT EPITHELIUM (RPE) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV ILLINOIS,DEPT OPHTHALMOL & VISUAL SCI,CHICAGO,IL 60680. NEI,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1464 EP 1464 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500979 ER PT J AU WU, YQ CHADER, GJ BECERRA, SP AF WU, YQ CHADER, GJ BECERRA, SP TI PURIFICATION AND CHARACTERIZATION OF PIGMENT EPITHELIUM-DERIVED FACTOR FROM BOVINE INTERPHOTORECEPTOR MATRIX SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1465 EP 1465 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58500986 ER PT J AU WHITCUP, SM HAYASHI, S RIZZO, L LAI, JC GAZZINELLI, R NUSSENBLATT, RB CHAN, CC AF WHITCUP, SM HAYASHI, S RIZZO, L LAI, JC GAZZINELLI, R NUSSENBLATT, RB CHAN, CC TI SYSTEMIC ANTI-IL-12 ANTIBODY EXACERBATES ENDOTOXIN-INDUCED UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIAID,HOWARD HUGHES MED INST,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1481 EP 1481 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501048 ER PT J AU IWATA, T VACAPACHECO, G RODRIGUEZ, IR CARPER, DA AF IWATA, T VACAPACHECO, G RODRIGUEZ, IR CARPER, DA TI HUMAN SORBITOL DEHYDROGENASE - CANDIDATE GENE FOR CONGENITAL CATARACT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. INST MEXICANO SEGURO SOCIAL,GUADALAJARA,MEXICO. NR 1 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1493 EP 1493 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501095 ER PT J AU CARUSO, RC MULLER, SF REUTER, LM KAISERKUPFER, MI AF CARUSO, RC MULLER, SF REUTER, LM KAISERKUPFER, MI TI MEASUREMENT OF SPATIAL SUMMATION WITH AUTOMATED STATIC PERIMETRY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1509 EP 1509 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501175 ER PT J AU BOUZAS, EA WHITCUP, SM SRAN, P NUSSENBLATT, RB VALLE, D GERY, I KAISERKUPFER, MI AF BOUZAS, EA WHITCUP, SM SRAN, P NUSSENBLATT, RB VALLE, D GERY, I KAISERKUPFER, MI TI THYROID-DISEASE IN PATIENTS WITH RETINAL DEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1526 EP 1526 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501260 ER PT J AU HIKITA, N DASTGHEIB, K MOCHIZUKI, M NUSSENBLATT, RB CHAN, CC AF HIKITA, N DASTGHEIB, K MOCHIZUKI, M NUSSENBLATT, RB CHAN, CC TI EFFECT OF TOPICAL FK506 ON EXPERIMENTAL MELANIN-PROTEIN INDUCED UVEITIS (EMIU) IN RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. KURUME UNIV,DEPT OPHTHALMOL,KURUME,FUKUOKA 830,JAPAN. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1540 EP 1540 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501334 ER PT J AU DASTGHEIB, K HIKITA, N WALTON, RC HAYASHI, S CHAN, CC AF DASTGHEIB, K HIKITA, N WALTON, RC HAYASHI, S CHAN, CC TI EXPERIMENTAL MELANIN-PROTEIN INDUCED UVEITIS (EMIU) - SUSCEPTIBILITY AND RECURRENCE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1541 EP 1541 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501336 ER PT J AU KOZHICH, AT BRAUN, E WIGGERT, B GERY, I AF KOZHICH, AT BRAUN, E WIGGERT, B GERY, I TI UVEITOGENICITY AND IMMUNOGENICITY OF IRBP PEPTIDES IN DIFFERENT RAT STRAINS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1561 EP 1561 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501429 ER PT J AU MAHDI, RM CASPI, RR KOZHICH, AT KOZHICH, OA SILVER, PB NUSSENBLATT, RB EGWUAGU, CE AF MAHDI, RM CASPI, RR KOZHICH, AT KOZHICH, OA SILVER, PB NUSSENBLATT, RB EGWUAGU, CE TI CYTOKINE MESSENGER-RNA EXPRESSION FOLLOWING ADOPTIVE TRANSFER OF UVEITOGENIC T-CELLS INTO ATHYMIC AND EUTHYMIC LEWIS RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1561 EP 1561 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501428 ER PT J AU PRENDERGAST, RA COSKUNCAN, NM LUTTY, GA MCLEOD, DS CASPI, RR AF PRENDERGAST, RA COSKUNCAN, NM LUTTY, GA MCLEOD, DS CASPI, RR TI INDUCTION OF ADOPTIVE T-CELL-MEDIATED EAU - TEMPORAL APPEARANCE OF SPECIFIC AND CONTROL ACTIVATED T-CELLS IN RETINAL TISSUE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,WILMER INST,BALTIMORE,MD 21218. NEI,BETHESDA,MD 20892. JHU,APPL PHYS LAB,LAUREL,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1561 EP 1561 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501427 ER PT J AU SINGH, DP SINGH, VK SHINOHARA, T AF SINGH, DP SINGH, VK SHINOHARA, T TI A SINGLE AMINO-ACID SUBSTITUTION OF CORE RESIDUES OF S-ANTIGEN PEPTIDES CONFERS THE CAPACITY TO PREVENT EXPERIMENTAL AUTOIMMUNE UVEITIS (EAU) IN LEWIS RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. SGPGIMS,DEPT IMMUNOL,LUCKNOW,INDIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1561 EP 1561 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501430 ER PT J AU QIN, C RAO, PV ZIGLER, JS AF QIN, C RAO, PV ZIGLER, JS TI ARE NUCLEOTIDE-BINDING ENZYME/CRYSTALLINS PART OF A DEFENSE SYSTEM AGAINST OXIDATIVE DAMAGE IN THE LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MECH OCULAR DIS LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1569 EP 1569 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501458 ER PT J AU BOATRIGHT, JH BORST, DE NAGPAL, S RAM, H NICKERSON, JM AF BOATRIGHT, JH BORST, DE NAGPAL, S RAM, H NICKERSON, JM TI CHARACTERIZATION OF TRANS-ACTING FACTORS AND CIS-ACTING ELEMENTS IN THE IRBP GENE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 EMORY UNIV,SCH MED,ATLANTA,GA 30322. NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1578 EP 1578 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501493 ER PT J AU KIKUCHI, T SHINOHARA, T AF KIKUCHI, T SHINOHARA, T TI PHOTORECEPTOR CONSERVED ELEMENT (PCE 1) ASSOCIATED WITH PHOTORECEPTOR-SPECIFIC PROMOTER ACTIVITY WERE FOUND IN ARRESTIN GENES OF -12 TO -24 OF THE MOUSE AND THE 1ST INTRON OF BOVINE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1578 EP 1578 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501492 ER PT J AU ROBISON, WG LAVER, NM AF ROBISON, WG LAVER, NM TI SORBINIL PREVENTION OF CATARACTS AND RETINOPATHY IN THE GALACTOSE-FED RAT MODEL OF DIABETIC COMPLICATIONS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20057. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1586 EP 1586 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501526 ER PT J AU GREENTREE, W TAKAHASHI, Y WYMAN, M KADOR, PF AF GREENTREE, W TAKAHASHI, Y WYMAN, M KADOR, PF TI QUANTITATIVE-ANALYSES OF RETINAL VESSEL CHANGES IN GALACTOSE-FED DOGS - INTERVENTION STUDIES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1589 EP 1589 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501541 ER PT J AU SECCHI, EF LISAK, MJ SATO, S KADOR, PF AF SECCHI, EF LISAK, MJ SATO, S KADOR, PF TI PRESENCE OF POLYOL PATHWAY IN FIBROBLAST SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1589 EP 1589 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501540 ER PT J AU BLAKE, DA VOGEL, T ROBERTS, DD CALDWELL, DR WHIKEHART, DR AF BLAKE, DA VOGEL, T ROBERTS, DD CALDWELL, DR WHIKEHART, DR TI CRYOPRESERVATION OF CORNEAL ENDOTHELIAL-CELLS DEPLETES PLASMA-MEMBRANE NA,K-ATPASE ACTIVITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TULANE UNIV,SCH MED,DEPT OPHTHALMOL,NEW ORLEANS,LA 70112. NCI,PATHOL LAB,BETHESDA,MD 20892. UNIV ALABAMA,VISION SCI RES CTR,BIRMINGHAM,AL 35294. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1600 EP 1600 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501598 ER PT J AU NEUENSCHWANDER, H JULIA, C WYMAN, M KADOR, PF AF NEUENSCHWANDER, H JULIA, C WYMAN, M KADOR, PF TI CORNEAL ENDOTHELIAL CHANGES IN GALACTOSE-FED DOGS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1601 EP 1601 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501603 ER PT J AU LEE, J JIAO, X HEJTMANCIK, F KAISERKUPFER, M CHADER, GJ AF LEE, J JIAO, X HEJTMANCIK, F KAISERKUPFER, M CHADER, GJ TI THE DISTRIBUTION OF FATTY-ACID-BINDING PROTEINS IN HUMAN BIETTIS CRYSTALLINE DYSTROPHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1608 EP 1608 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501641 ER PT J AU PUTILINA, T WONG, P SAMUDRALA, S GENTLEMAN, S CHADER, G AF PUTILINA, T WONG, P SAMUDRALA, S GENTLEMAN, S CHADER, G TI IDENTIFICATION OF HUMAN GENES USING PROBES BASED ON GENES FROM C-ELEGANS INVOLVED IN NEURODEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1609 EP 1609 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501642 ER PT J AU JIAO, X LEE, J DETURCO, EBR BAZAN, NG CHADER, GJ AF JIAO, X LEE, J DETURCO, EBR BAZAN, NG CHADER, GJ TI TISSUE DISTRIBUTION OF DOCOSAHEXAENOIC ACID-BINDING PROTEINS IN POODLES WITH PROGRESSIVE ROD-CONE DEGENERATION (PRCD) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. LOUISIANA STATE UNIV,MED CTR,DEPT OPHTHALMOL,NEW ORLEANS,LA 70112. NR 0 TC 3 Z9 3 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1611 EP 1611 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501653 ER PT J AU ZELENKA, PS AF ZELENKA, PS TI PERIODIC GENE-EXPRESSION IN THE LENS EPITHELIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1640 EP 1640 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501793 ER PT J AU LASA, SM DATILES, MB FREIDLIN, V AF LASA, SM DATILES, MB FREIDLIN, V TI POTENTIAL VISION TESTS IN PATIENTS WITH CATARACTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPTHALMOL GENET & CLIN SERV BRANCH,BETHESDA,MD 20892. NEI,DIV BIOMETRY & EPIDEMIOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1655 EP 1655 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501851 ER PT J AU COURTNEY, SM FINKEL, LH BUCHSBAUM, G AF COURTNEY, SM FINKEL, LH BUCHSBAUM, G TI THE EFFECT OF OPPONENT PROCESSING AND SPATIAL INTEGRATION ON EQUIVALENT SURROUNDS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract ID CONTRAST C1 NIMH,PHILADELPHIA,PA. UNIV PENN,DEPT BIOENGN,PHILADELPHIA,PA 19104. NR 5 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1657 EP 1657 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501861 ER PT J AU JOSEPH, JS OPTICAN, LM AF JOSEPH, JS OPTICAN, LM TI SCALING EFFECTS IN RAPID FORM PERCEPTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1664 EP 1664 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501888 ER PT J AU CHEUNG, MK DASTGHEIB, K CHAN, CC ROBERGE, FG AF CHEUNG, MK DASTGHEIB, K CHAN, CC ROBERGE, FG TI INHIBITION OF PMN LEUKOCYTE RECRUITMENT BY NPC-15669 PREVENTS ENDOTOXIN-INDUCED UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1684 EP 1684 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501984 ER PT J AU HAYASHI, S GAZZINELLI, R CHAN, CC PHAM, N ROBERGE, FG AF HAYASHI, S GAZZINELLI, R CHAN, CC PHAM, N ROBERGE, FG TI IN-VIVO INHIBITION OF NITRIC-OXIDE ENHANCES OCULAR AND CNS INFLAMMATION IN MURINE TOXOPLASMOSIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1685 EP 1685 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501989 ER PT J AU JANG, S LI, Q WHITCUP, SM PENG, B NUSSENBLATT, RB CHAN, CC AF JANG, S LI, Q WHITCUP, SM PENG, B NUSSENBLATT, RB CHAN, CC TI SUSCEPTIBILITY TO ENDOTOXIN-INDUCED UVEITIS VARIES IN DIFFERENT MURINE STRAINS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH ART & SCI,ANN ARBOR,MI 48109. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1685 EP 1685 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501987 ER PT J AU PARKS, DJ CHEUNG, MK CHAN, CC ROBERGE, FG AF PARKS, DJ CHEUNG, MK CHAN, CC ROBERGE, FG TI THE ROLE OF NITRIC-OXIDE IN ENDOTOXIN-INDUCED UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1685 EP 1685 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501988 ER PT J AU ROBERGE, FG HAYASHI, S AF ROBERGE, FG HAYASHI, S TI NITRIC-OXIDE IS RESPONSIBLE FOR THE INHIBITION OF LYMPHOCYTE-PROLIFERATION IN TOXOPLASMA-GONDII INFECTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1685 EP 1685 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58501992 ER PT J AU ABE, T KIKUCHI, T TAMAI, M SHINOHARA, T AF ABE, T KIKUCHI, T TAMAI, M SHINOHARA, T TI CHARACTERIZATION OF MOUSE AND HUMAN PHOSDUCIN PROMOTERS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. TOHOKU UNIV,DEPT OPHTHALMOL,SENDAI,MIYAGI 980,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1702 EP 1702 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502078 ER PT J AU BERNSTEIN, SL KUTTY, G WIGGERT, B ALBERT, DM NICKERSON, JM AF BERNSTEIN, SL KUTTY, G WIGGERT, B ALBERT, DM NICKERSON, JM TI THE EXPRESSION OF RETINA-SPECIFIC GENES BY MOUSE RETINOBLASTOMA CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV WISCONSIN,DEPT OPHTHALMOL & VISUAL SCI,MADISON,WI 53706. EMORY UNIV,DEPT OPHTHALMOL,ATLANTA,GA 30322. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1702 EP 1702 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502077 ER PT J AU BORST, DE AF BORST, DE TI DNA METHYLATION OF THE IRBP PROMOTER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1703 EP 1703 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502086 ER PT J AU NOONAN, DM MANCUSO, T CHADER, GJ BOBOLA, N RAVAZZOLO, R ALBINI, A AF NOONAN, DM MANCUSO, T CHADER, GJ BOBOLA, N RAVAZZOLO, R ALBINI, A TI A SINGLE CIS-ACTING ELEMENT CONFERS TISSUE-SPECIFIC EXPRESSION OF THE IRBP GENE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract ID BINDING PROTEIN IRBP C1 IST NAZL RIC CANC,GENOA,ITALY. NEI,BETHESDA,MD 20892. IST BIOL GENET,GENOA,ITALY. NR 4 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1704 EP 1704 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502087 ER PT J AU HAYNES, JI FREDERIKSE, P PIATIGORSKY, J AF HAYNES, JI FREDERIKSE, P PIATIGORSKY, J TI IDENTIFICATION OF DNA ELEMENTS CONTROLLING ALPHA-B-CRYSTALLIN GENE-EXPRESSION IN THE MLG LUNG-CELL LINE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1705 EP 1705 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502097 ER PT J AU ILAGAN, JG SAX, CM CVEKL, A KANTOROW, M PIATIGORSKY, J AF ILAGAN, JG SAX, CM CVEKL, A KANTOROW, M PIATIGORSKY, J TI FUNCTIONAL AND PROTEIN-BINDING ANALYSIS OF THE PE-2 REGULATORY REGION IN THE MOUSE ALPHA-A-CRYSTALLIN PROMOTER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1705 EP 1705 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502098 ER PT J AU LACORAZZA, HD RIVERO, JL JENDOUBI, M AF LACORAZZA, HD RIVERO, JL JENDOUBI, M TI CORRECTION OF GENETIC AND ENZYMATIC-ACTIVITY OF ORNITHINE ALPHA-AMINOTRANSFERASE INTO CHO DEFICIENT CELL-LINE USING RETROVIRAL-MEDIATED GENE-TRANSFER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1705 EP 1705 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502094 ER PT J AU GOPALSRIVASTAVA, R PIATIGORSKY, J AF GOPALSRIVASTAVA, R PIATIGORSKY, J TI REGULATION OF THE MURINE ALPHA-B-CRYSTALLIN PROMOTER IN TRANSGENIC MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1706 EP 1706 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502100 ER PT J AU JAWORSKI, CJ WISTOW, GJ AF JAWORSKI, CJ WISTOW, GJ TI LP2 - A MEMBER OF THE LIPID RETINOID-BINDING PROTEIN SUPERFAMILY IN BOVINE LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LMOB,MOLEC STRUCT & FUNCT SECT,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1706 EP 1706 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502101 ER PT J AU LI, X WISTOW, GJ PIATIGORSKY, J AF LI, X WISTOW, GJ PIATIGORSKY, J TI LINKAGE AND INTERGENIC SPACER OF THE DUCK DELTA-CRYSTALLIN GENES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1706 EP 1706 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502099 ER PT J AU SAX, CM KANTOROW, M CVEKL, A GOPALSRIVASTAVA, R ILAGAN, JG PIATIGORSKY, J AF SAX, CM KANTOROW, M CVEKL, A GOPALSRIVASTAVA, R ILAGAN, JG PIATIGORSKY, J TI FUNCTIONAL AND PROTEIN-BINDING ANALYSIS OF THE MOUSE ALPHA-A-CRYSTALLIN PE1 REGULATORY REGION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1706 EP 1706 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502104 ER PT J AU SINGH, AK KUMAR, G SHINOHARA, T SHICHI, H AF SINGH, AK KUMAR, G SHINOHARA, T SHICHI, H TI PORCINE S-ANTIGEN (S-AG) - MOLECULAR-STRUCTURE AND OCULAR DISTRIBUTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 WAYNE STATE UNIV,SCH MED,DEPT OPHTHALMOL,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT MOLEC BIOL GENET,DETROIT,MI 48201. NEI,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1709 EP 1709 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502111 ER PT J AU CHANG, M ABE, T KIKUCHI, T SHINOHARA, T AF CHANG, M ABE, T KIKUCHI, T SHINOHARA, T TI THE SEQUENCE OF THE HUMAN PHOSDUCIN GENE AND ITS 5'-FLANKING REGION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV PENN,SCHEIE EYE INST,DEPT OPHTHALMOL,PHILADELPHIA,PA 19104. NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1718 EP 1718 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502161 ER PT J AU FARR, EA BORST, DE CHADER, GJ BRADLEY, DJ AF FARR, EA BORST, DE CHADER, GJ BRADLEY, DJ TI DEVELOPMENTAL REGULATION OF THE MOUSE INTERPHOTO-RECEPTOR RETINOL-BINDING PROTEIN GENE IN THE FETAL AND POSTNATAL EYE AND PINEAL-GLAND SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,RETINAL CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. HOWARD HUGHES MED INST,BETHESDA,MD. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1727 EP 1727 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502195 ER PT J AU LAVER, NM ROBISON, WG HANSEN, BC AF LAVER, NM ROBISON, WG HANSEN, BC TI SPONTANEOUSLY DIABETIC MONKEYS AS A MODEL FOR DIABETIC-RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20057. NEI,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. RI Hansen, Barbara/J-8723-2012 OI Hansen, Barbara/0000-0001-9646-3525 NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1733 EP 1733 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502219 ER PT J AU TAKAHASHI, Y WYMAN, M KADOR, PF AF TAKAHASHI, Y WYMAN, M KADOR, PF TI RETINAL NEOVASCULARIZATION IN GALACTOSE-FED DOGS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1734 EP 1734 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502222 ER PT J AU ANGLADE, E CHANAUD, NP GERY, I AF ANGLADE, E CHANAUD, NP GERY, I TI RECOVERIN IS A POTENT UVEITOGEN IN RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1738 EP 1738 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502240 ER PT J AU VISTICA, BP ANGLADE, E GERY, I AF VISTICA, BP ANGLADE, E GERY, I TI UVEITOGENICITY, IMMUNOGENICITY AND ANTIGENICITY OF NEUROCALCIN AND CHIMERIC MOLECULES OF NEUROCALCIN AND RECOVERIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1738 EP 1738 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502241 ER PT J AU FONG, DS FERRIS, FL DAVIS, MD CHEW, EY AF FONG, DS FERRIS, FL DAVIS, MD CHEW, EY TI A POORLY RECOGNIZED CAUSE OF SEVERE VISUAL-LOSS IN DIABETICS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,CLIN TRIALS BRANCH,BETHESDA,MD 20892. UNIV WISCONSIN,FUNDUS PHOTOG READING CTR,MADISON,WI 53706. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1749 EP 1749 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502284 ER PT J AU KUTTY, G KUTTY, RK NAGINENI, CN HOOKS, JJ CHADER, GJ WIGGERT, B AF KUTTY, G KUTTY, RK NAGINENI, CN HOOKS, JJ CHADER, GJ WIGGERT, B TI REVERSE TRANSCRIPTION-PCR (RT-PCR) ANALYSIS OF INDUCIBLE FORMS OF NITRIC-OXIDE SYNTHASE AND HEME OXYGENASE - DIFFERENTIAL EXPRESSION IN HUMAN RETINAL-PIGMENT EPITHELIAL (RPE) CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1758 EP 1758 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502323 ER PT J AU DETRICK, B RHAME, J NAGINENI, C WANG, Y HOOKS, JJ AF DETRICK, B RHAME, J NAGINENI, C WANG, Y HOOKS, JJ TI MODULATION OF RPE CELLULAR PROTEINS DURING CMV INFECTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1762 EP 1762 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502350 ER PT J AU PEREZ, J WORKMAN, H REDMOND, M SINGH, DP SHINOHARA, T AF PEREZ, J WORKMAN, H REDMOND, M SINGH, DP SHINOHARA, T TI PHYSIOLOGICAL AND MORPHOLOGICAL ALTERATIONS OF THE RPE AND RETINA FOLLOWING IMMUNOLOGICAL ABLATION OF THE RPE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,MIAMI,FL 33152. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1764 EP 1764 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502360 ER PT J AU DEREVJANIK, NL VINORES, SA MAHLOW, J HENDERER, JD FRIEDMAN, Z JOHNSON, M CSAKY, C LAROCHELLE, W CAMPOCHIARO, PA AF DEREVJANIK, NL VINORES, SA MAHLOW, J HENDERER, JD FRIEDMAN, Z JOHNSON, M CSAKY, C LAROCHELLE, W CAMPOCHIARO, PA TI UP-REGULATION OF EXPRESSION OF PDGFS AND THEIR RECEPTORS IN RPE CELLS IN WOUND REPAIR MODELS AND EPIRETINAL MEMBRANES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205. NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1770 EP 1770 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502386 ER PT J AU LI, Q DASTGHEIB, K HIKITA, N EGWUAGU, C NUSSENBLATT, RB CHAN, CC AF LI, Q DASTGHEIB, K HIKITA, N EGWUAGU, C NUSSENBLATT, RB CHAN, CC TI TGF-BETA-1 MESSENGER-RNA EXPRESSION IN EXPERIMENTAL MELANIN-PROTEIN INDUCED UVEITIS (EMIU) AND IN EXPERIMENTAL AUTOIMMUNE UVEITIS (EAU) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1807 EP 1807 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502571 ER PT J AU ZIERHUT, M CHAN, CC DUIJVESTIJN, A NUSSENBLATT, RB WHITCUP, SM AF ZIERHUT, M CHAN, CC DUIJVESTIJN, A NUSSENBLATT, RB WHITCUP, SM TI HIGH ENDOTHELIAL VENULES IN IRBP-INDUCED EXPERIMENTAL AUTOIMMUNE UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV TUBINGEN,DEPT OPHTHALMOL,W-7400 TUBINGEN 1,GERMANY. NEI,IMMUNOL LAB,BETHESDA,MD 20892. UNIV LIMBURG,DEPT IMMUNOL,6200 MD MAASTRICHT,NETHERLANDS. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1807 EP 1807 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502569 ER PT J AU MARTINS, MC HOOKS, JJ GAZZINELLI, R NUSSENBLATT, R BURNIER, MNN AF MARTINS, MC HOOKS, JJ GAZZINELLI, R NUSSENBLATT, R BURNIER, MNN TI EVALUATION OF THE EFFECT OF DRUGS (ATOVAQUONE AND SULFADIAZINE) IN THE EXPERIMENTAL-MODEL OF ACQUIRED OCULAR TOXOPLASMOSIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. MCGILL UNIV,DEPT OPHTHALMOL,MONTREAL H3A 2T5,QUEBEC,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1808 EP 1808 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502575 ER PT J AU BETTELHEIM, FA ZIGLER, JS AF BETTELHEIM, FA ZIGLER, JS TI CALCIUM CATARACT AS A MODEL TO STUDY ORIENTATION FLUCTUATIONS CAUSED BY CHANGE IN INTRINSIC BIREFRINGENCE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract ID LENS C1 ADELPHI UNIV,DEPT CHEM,GARDEN CITY,NY 11530. NEI,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1809 EP 1809 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502578 ER PT J AU KUSZAK, JR PETERSON, KL HERBERT, KL SIVAK, JG AF KUSZAK, JR PETERSON, KL HERBERT, KL SIVAK, JG TI THE INTERRELATIONSHIP OF LENS SUTURAL ANATOMY AND OPTICAL-QUALITY AS A FUNCTION OF AGE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT PATHOL,CHICAGO,IL 60612. RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT OPHTHALMOL,CHICAGO,IL 60612. UNIV WATERLOO,SCH OPTOMETRY,WATERLOO N2L 3G1,ONTARIO,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1809 EP 1809 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502576 ER PT J AU HAXBY, JV UNGERLEIDER, LG HORWITZ, B MAISOG, JM GRADY, CL AF HAXBY, JV UNGERLEIDER, LG HORWITZ, B MAISOG, JM GRADY, CL TI NEURAL SYSTEMS FOR ENCODING AND RETRIEVING NEW LONG-TERM VISUAL MEMORIES - A PET-RCBF STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIMH,LPP,FUNCT BRAIN IMAGING,BETHESDA,MD 20892. NIMH,NEUROPHYSIOL LAB,BETHESDA,MD 20892. NIA,NEUROL SCI LAB,BETHESDA,MD 20892. NR 0 TC 9 Z9 9 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1813 EP 1813 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502591 ER PT J AU WURTZ, RH AF WURTZ, RH TI NEUROPHYSIOLOGY OF MOTION AND DISPARITY IN THE VISUAL-CORTEX OF THE MONKEY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1815 EP 1815 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502598 ER PT J AU WONG, P VANVEEN, T KUTTY, K BERNSTEIN, S BORST, D RODRIGUEZ, I PFEFFER, B WIGGERT, B TENNISWOOD, M CHADER, G AF WONG, P VANVEEN, T KUTTY, K BERNSTEIN, S BORST, D RODRIGUEZ, I PFEFFER, B WIGGERT, B TENNISWOOD, M CHADER, G TI MOLECULAR CHARACTERIZATION OF AN APOPTOSIS INDUCIBLE GENE, TRPM-2 CLUSTERIN, AND ITS EXPRESSION IN THE MAMMALIAN EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD. GOTHENBURG UNIV,DEPT ZOOL,S-41124 GOTHENBURG,SWEDEN. UNIV OTTAWA,DEPT BIOCHEM,OTTAWA K1N 6N5,ONTARIO,CANADA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1820 EP 1820 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502614 ER PT J AU BOWESRICKMAN, C RAPOPORT, A DANCIGER, M CAVALLO, C KOZAK, C FARBER, DB AF BOWESRICKMAN, C RAPOPORT, A DANCIGER, M CAVALLO, C KOZAK, C FARBER, DB TI CLONING AND CHARACTERIZATION OF NOVEL PHOTORECEPTOR-SPECIFIC CDNAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,JSEI,LOS ANGELES,CA 90024. ST LOUIS UNIV,DEPT OPHTHALMOL,ABEI,ST LOUIS,MO 63103. LOYOLA MARYMOUNT UNIV,LOS ANGELES,CA 90045. NIAID,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1833 EP 1833 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502667 ER PT J AU RIZZO, LV SILVER, PB GAZZINELLI, RT CHAN, CC WIGGERT, B CASPI, RR AF RIZZO, LV SILVER, PB GAZZINELLI, RT CHAN, CC WIGGERT, B CASPI, RR TI EXPRESSION OF CYTOKINE GENES WITHIN THE EYE IN MURINE EAU SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1862 EP 1862 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502810 ER PT J AU SARTANI, G SILVER, PB STRASSMANN, G CHAN, CC CASPI, RR AF SARTANI, G SILVER, PB STRASSMANN, G CHAN, CC CASPI, RR TI EFFECT OF SURAMIN TREATMENT ON INDUCTION OF EAU SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. OTSUKA AMER PHARMACEUT,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1862 EP 1862 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502808 ER PT J AU GURU, SC USUKURA, J KIKUCHI, T SINGH, VK REDMOND, TM SHINOHARA, T AF GURU, SC USUKURA, J KIKUCHI, T SINGH, VK REDMOND, TM SHINOHARA, T TI IMMUNOGENIC ABLATION OF OCULAR-TISSUES BY THE ADMINISTRATION OF SPECIFIC ANTIGENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,LRCMB,BETHESDA,MD 20892. NAGOYA UNIV,SCH MED,DEPT ANAT,NAGOYA,AICHI 466,JAPAN. SGPGIMS,DEPT IMMUNOL,LUCKNOW,INDIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1863 EP 1863 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502816 ER PT J AU CHANAUD, NP SHILOACH, J HAFLER, DA EGWUAGU, CE NUSSENBLATT, RB GERY, I AF CHANAUD, NP SHILOACH, J HAFLER, DA EGWUAGU, CE NUSSENBLATT, RB GERY, I TI RECOMBINANT HUMAN S-ANTIGEN (R-HSAG) - UVEITOGENICITY AND ANTIGENICITY IN THE RAT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NIDDK,BETHESDA,MD. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1864 EP 1864 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502818 ER PT J AU RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B AF RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B TI AFFINITY OF HSP 70 FROM EBV TRANSFORMED HUMAN B-CELLS FOR BOVINE AND HUMAN IRBP PEPTIDES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1864 EP 1864 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502817 ER PT J AU DESMET, MD RENGARAJAN, K CHADER, GJ WIGGERT, B AF DESMET, MD RENGARAJAN, K CHADER, GJ WIGGERT, B TI CHARACTERIZATION OF B-CELL PROTEINS BINDING SPECIFICALLY TO UVEITOPATHOGENIC PEPTIDE 1169-1191 OF BOVINE IRBP SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1865 EP 1865 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502824 ER PT J AU MILLERRIVERO, NE RIZZO, LV CHAN, CC WIGGERT, B NUSSENBLATT, RB CASPI, RR AF MILLERRIVERO, NE RIZZO, LV CHAN, CC WIGGERT, B NUSSENBLATT, RB CASPI, RR TI SUPPRESSION OF IRBP-INDUCED EAU IN MICE BY FEEDING IRBP, AND ITS POTENTIATION BY INTERLEUKIN-2 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1865 EP 1865 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502823 ER PT J AU WALTON, RC LAI, JC CHANAUD, NP CHAN, CC GERY, I WHITCUP, SM AF WALTON, RC LAI, JC CHANAUD, NP CHAN, CC GERY, I WHITCUP, SM TI INHIBITION OF EXPERIMENTAL AUTOIMMUNE UVEITIS BY MDL 28,842 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1865 EP 1865 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502826 ER PT J AU MARTIN, DF PARKS, DJ MELLOW, SD FERRIS, FL CHEW, EY WALTON, RC ANAND, R ASHTON, P DAVIS, MD NUSSENBLATT, RB AF MARTIN, DF PARKS, DJ MELLOW, SD FERRIS, FL CHEW, EY WALTON, RC ANAND, R ASHTON, P DAVIS, MD NUSSENBLATT, RB TI THE GANCICLOVIR IMPLANT FOR CYTOMEGALOVIRUS RETINITIS - A RANDOMIZED, CONTROLLED CLINICAL-TRIAL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV TEXAS SW,DALLAS,TX. NEI,BETHESDA,MD 20892. EMORY UNIV,ATLANTA,GA 30322. UNIV KENTUCKY,LEXINGTON,KY 40506. UNIV WISCONSIN,MADISON,WI 53706. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1893 EP 1893 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58502954 ER PT J AU GARLAND, D DATILES, MB ZIGLER, JS DUGLASTABOR, Y AF GARLAND, D DATILES, MB ZIGLER, JS DUGLASTABOR, Y TI POSTTRANSLATIONAL MODIFICATION OF HUMAN CRYSTALLINS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1904 EP 1904 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503003 ER PT J AU KANTOROW, M PIATIGORSKY, J AF KANTOROW, M PIATIGORSKY, J TI ALPHA-CRYSTALLIN SMALL HEAT-SHOCK PROTEIN HAS AUTOKINASE ACTIVITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1904 EP 1904 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503001 ER PT J AU OBROSOVA, I INOUE, J GREENTREE, W SATO, S RODRIGUEZ, L KADOR, PF AF OBROSOVA, I INOUE, J GREENTREE, W SATO, S RODRIGUEZ, L KADOR, PF TI EVALUATION OF S-88-0773 ON SUGAR CATARACT FORMATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1931 EP 1931 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503116 ER PT J AU MORI, K TAKAHASHI, Y TSUDUKI, S KADOR, PF AKAGI, Y AF MORI, K TAKAHASHI, Y TSUDUKI, S KADOR, PF AKAGI, Y TI SIGNIFICANCE OF ALDOSE REDUCTASE TO EXPERIMENTAL CORNEAL EPITHELIOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 FUKUI MED SCH,DEPT OPHTHALMOL,FUKUI 91011,JAPAN. NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1946 EP 1946 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503192 ER PT J AU VIVINO, MA MAHURKAR, A TRUS, B LOPEZ, ML DATILES, MB AF VIVINO, MA MAHURKAR, A TRUS, B LOPEZ, ML DATILES, MB TI QUANTITATIVE-ANALYSIS OF RETROILLUMINATION IMAGES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. NEI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1947 EP 1947 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503201 ER PT J AU LIZAK, MJ MORI, K CECKLER, TL KADOR, PF BALABAN, RS AF LIZAK, MJ MORI, K CECKLER, TL KADOR, PF BALABAN, RS TI MAGNETIC-RESONANCE-IMAGING OF THE GALACTOSEMIC DOG EYE USING MAGNETIZATION-TRANSFER CONTRAST ENHANCEMENT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1948 EP 1948 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503204 ER PT J AU LOPEZ, ML DATILES, MB PODGOR, M VIVINO, MA MAHURKAR, A LASA, SM AF LOPEZ, ML DATILES, MB PODGOR, M VIVINO, MA MAHURKAR, A LASA, SM TI REPRODUCIBILITY STUDY ON THE NEI RETROILLUMINATION IMAGE-ANALYSIS SYSTEM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1962 EP 1962 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503272 ER PT J AU MAGNO, BV FREIDLIN, V LASA, SM DATILES, MB AF MAGNO, BV FREIDLIN, V LASA, SM DATILES, MB TI COMPARISON OF LINEAR, MULTILINEAR AND MASK MICRODENSITOMETRIC ANALYSES OF SCHEIMPFLUG IMAGES OF THE LENS NUCLEUS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,OPHTHALM GENET & CLIN SERV BRANCH,BETHESDA,MD 20892. NEI,DIV BIOMETRY & EPIDEMIOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1962 EP 1962 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503273 ER PT J AU HOF, PR UNGERLEIDER, LG WEBSTER, MJ ADAMS, M MORRISON, JH AF HOF, PR UNGERLEIDER, LG WEBSTER, MJ ADAMS, M MORRISON, JH TI NEUROFILAMENT PROTEIN AND GLUTAMATE-RECEPTOR SUBUNIT PROTEINS DEFINE SUBSETS OF CORTICOCORTICAL PROJECTIONS IN THE MONKEY VISUAL-CORTEX SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 CUNY MT SINAI SCH MED,DEPT NEUROBIOL,NEW YORK,NY 10029. NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1971 EP 1971 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503315 ER PT J AU GAWNE, TJ KJAER, TW RICHMOND, BJ AF GAWNE, TJ KJAER, TW RICHMOND, BJ TI STRIATE CORTICAL-NEURONS SHOW SIMILAR RESPONSES TO ISOLUMINANT TEXTURED AS TO BLACK OR WHITE BARS, BUT WITH A 35 MS DELAY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1976 EP 1976 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503341 ER PT J AU INANA, G HOTTA, Y MASHIMA, Y AKAKI, Y CHAMBERS, C MURAKAMI, A WELEBER, RG KENNAWAY, NG SHIONO, T AF INANA, G HOTTA, Y MASHIMA, Y AKAKI, Y CHAMBERS, C MURAKAMI, A WELEBER, RG KENNAWAY, NG SHIONO, T TI MOLECULAR-GENETIC BASIS OF GYRATE ATROPHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 BASCOM PALMER EYE INST,MIAMI,FL. JUNTENDO UNIV,TOKYO 113,JAPAN. KEIO UNIV,TOKYO 108,JAPAN. OSAKA UNIV,OSAKA,JAPAN. NEI,BETHESDA,MD 20892. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. TOHOKU UNIV,SENDAI,MIYAGI 980,JAPAN. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1984 EP 1984 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503376 ER PT J AU EGWUAGU, CE SZTEIN, J CHAN, CC MAHDI, R NUSSENBLATT, RB CHEPELINSKY, AB AF EGWUAGU, CE SZTEIN, J CHAN, CC MAHDI, R NUSSENBLATT, RB CHEPELINSKY, AB TI TRANSGENIC RAT AND MOUSE MODELS FOR THE STUDY OF INTRAOCULAR EFFECTS OF GAMMA-IFN AND AUTOIMMUNITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. RI Sztein, Jorge/B-7165-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1987 EP 1987 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503386 ER PT J AU CHAN, CC GERY, I NUSSENBLATT, RB MOZES, E SINGER, DS AF CHAN, CC GERY, I NUSSENBLATT, RB MOZES, E SINGER, DS TI PERIOCULAR INFLAMMATION IN MICE WITH EXPERIMENTAL SYSTEMIC LUPUS-ERYTHEMATOSUS (SLE) - A NEW EXPERIMENTAL EYE DISEASE AND ITS MODULATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1994 VL 35 IS 4 BP 1988 EP 1988 PG 1 WC Ophthalmology SC Ophthalmology GA MZ585 UT WOS:A1994MZ58503392 ER EF