FN Thomson Reuters Web of Science™ VR 1.0 PT J AU MOODY, GB FELDMAN, CL BAILEY, JJ AF MOODY, GB FELDMAN, CL BAILEY, JJ TI STANDARDS AND APPLICABLE DATABASES FOR LONG-TERM ECG MONITORING SO JOURNAL OF ELECTROCARDIOLOGY LA English DT Article C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NIH,BETHESDA,MD 20892. RP MOODY, GB (reprint author), MIT,DIV HLTH SCI & TECHNOL,MIT ROOM 20A-113,CAMBRIDGE,MA 02139, USA. NR 9 TC 7 Z9 7 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0022-0736 J9 J ELECTROCARDIOL JI J. Electrocardiol. PY 1993 VL 26 SU S BP 151 EP 155 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NE170 UT WOS:A1993NE17000036 PM 8189117 ER PT J AU MCAREAVEY, D FANANAPAZIR, L AF MCAREAVEY, D FANANAPAZIR, L TI ALTERED CARDIAC HEMODYNAMIC AND ELECTRICAL STATES IN NORMAL SINUS RHYTHM FOLLOWING CHRONIC DUAL-CHAMBER PACING IN OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY SO JOURNAL OF ELECTROCARDIOLOGY LA English DT Article; Proceedings Paper CT 17TH ANNUAL CONF OF THE INTERNATIONAL SOC FOR COMPUTERIZED ELECTROCARDIOLOGY : RESEARCH AND APPLICATIONS IN COMPUTERIZED ELECTROCARDIOLOGY CY MAY 02-07, 1992 CL KEYSTONE, CO SP INT SOC COMP ELECTROCARDIOL RP MCAREAVEY, D (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 714,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0022-0736 J9 J ELECTROCARDIOL JI J. Electrocardiol. PY 1993 VL 25 SU S BP 29 EP 29 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KT884 UT WOS:A1993KT88400010 ER PT J AU FRANKEL, RA POTTALA, EW BAILEY, JJ AF FRANKEL, RA POTTALA, EW BAILEY, JJ TI AN IMPROVED FILTER FOR ECG BASE-LINE WANDER IN REAL-TIME ISCHEMIA MONITORING SO JOURNAL OF ELECTROCARDIOLOGY LA English DT Article; Proceedings Paper CT 17TH ANNUAL CONF OF THE INTERNATIONAL SOC FOR COMPUTERIZED ELECTROCARDIOLOGY : RESEARCH AND APPLICATIONS IN COMPUTERIZED ELECTROCARDIOLOGY CY MAY 02-07, 1992 CL KEYSTONE, CO SP INT SOC COMP ELECTROCARDIOL C1 NIH,DIV COMP RES & TECHNOL,APPL STUDIES LAB,BLDG 12A ROOM 2041,BETHESDA,MD 20892. MED COLL OHIO,DEPT PHYSIOL & BIOPHYS,TOLEDO,OH 43699. NR 2 TC 0 Z9 0 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0022-0736 J9 J ELECTROCARDIOL JI J. Electrocardiol. PY 1993 VL 25 SU S BP 156 EP 156 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KT884 UT WOS:A1993KT88400041 ER PT J AU ROCHA, EMM HOLLINGDALE, MR GWADZ, R KRETTLI, AU AF ROCHA, EMM HOLLINGDALE, MR GWADZ, R KRETTLI, AU TI EXOERYTHROCYTIC DEVELOPMENT OF PLASMODIUM-GALLINACEUM SPOROZOITES IN A CHICKEN FIBROBLAST CELL-LINE AND INHIBITION OF THE CELL INVASION BY SPECIFIC ANTISPOROZOITE MONOCLONAL-ANTIBODIES SO JOURNAL OF EUKARYOTIC MICROBIOLOGY LA English DT Article DE SL-29 CELLS; SPOROZOITE INFECTIVITY; ANTIBODY INHIBITION; EXOERYTHROCYTIC FORMS ID INVITRO DEVELOPMENT; HUMAN HEPATOCYTES; HEPATIC STAGES; CULTIVATION; FALCIPARUM; FORMS; VIVAX AB Cultivation of the Plasmodium gallinaceum exoerythrocytic forms from sporozoites was attempted in three different cell lines: HEPG2-A16 (from a human hepatoma), VERO (monkey kidney epithelial cells) and SL-29 (chicken embryo fibroblast cells). The sporozoites invaded all three cell types but their development into exoerythrocytic forms ocurred only in the SL-29 cells. In the presence of specific monoclonal antibodies against the major circumsporozoite protein, there were varying degrees of inhibition of parasite invasion of the SL-29 cells. Of seven monoclonal antibodies tested, two completely inhibited cell invasion at high concentrations and caused intense inhibition at concentrations as low as 2.5 mug/ml, four caused intense inhibition at these various concentrations, and one had no effect on sporozoite invasion. C1 FED UNIV MINAS GERAIS,ICB,DEPT PARASITOL,BR-30190 BELO HORIZON,MG,BRAZIL. FIOCRUZ MS,RENE RACHOU RES CTR,BR-30190 BELO HORIZON,MG,BRAZIL. BIOMED RES INST,ROCKVILLE,MD. NIAID,BETHESDA,MD 20892. NR 19 TC 7 Z9 7 U1 0 U2 0 PU SOC PROTOZOOLOGISTS PI LAWRENCE PA 810 E 10TH ST, LAWRENCE, KS 66044 SN 1066-5234 J9 J EUKARYOT MICROBIOL JI J. Eukaryot. Microbiol. PD JAN-FEB PY 1993 VL 40 IS 1 BP 64 EP 66 DI 10.1111/j.1550-7408.1993.tb04883.x PG 3 WC Microbiology SC Microbiology GA KQ688 UT WOS:A1993KQ68800011 PM 8457801 ER PT J AU SLATTERY, JP LUTZ, RA VRIJENHOEK, RC AF SLATTERY, JP LUTZ, RA VRIJENHOEK, RC TI REPEATABILITY OF CORRELATIONS BETWEEN HETEROZYGOSITY, GROWTH AND SURVIVAL IN A NATURAL-POPULATION OF THE HARD CLAM MERCENARIA-MERCENARIA L SO JOURNAL OF EXPERIMENTAL MARINE BIOLOGY AND ECOLOGY LA English DT Article DE BIVALVE; GROWTH; HARD CLAM; HETEROZYGOSITY; MERCENARIA; SURVIVAL ID MYTILUS-EDULIS-L; GENETIC HETEROZYGOSITY; POSSIBLE EXPLANATIONS; CRASSOSTREA-VIRGINICA; ENZYME HETEROZYGOSITY; ALLOZYME HOMOZYGOSITY; MULINIA-LATERALIS; STRESS RESPONSE; MARINE BIVALVES; COOT CLAM AB A single population of the hard clam Mercenaria mercenaria was examined for repeatability of correlations between multilocus heterozygosity and fitness-related traits. Clams were collected in June 1986, October 1987, and June 1988 from a site at Shark River Inlet, New Jersey. A large sample taken in 1988 gave the best representation of all age classes, particularly new recruits. Genetic variation was estimated using nine protein-encoding gene loci. All three samples were deficient in heterozygotes; however, deficiencies were heterogeneous across loci, providing no evidence for systematic inbreeding. Although multilocus heterozygosity was not associated with growth rate in any of the three samples, the large 1988 sample revealed a significant association with age. A resampling analysis of the 1988 data set revealed that detection of weak heterozygosity-age correlations was profoundly influenced by sample size and dependent upon adequate representation of young age classes in the population. C1 RUTGERS STATE UNIV, CTR THEORET & APPL GENET, POB 231, NEW BRUNSWICK, NJ 08903 USA. NCI, GENET SECT, VIRAL CARCINOGENESIS LAB, FREDERICK, MD 21701 USA. RUTGERS STATE UNIV, DEPT MARINE & COASTAL STUDIES, NEW BRUNSWICK, NJ 08903 USA. NR 55 TC 14 Z9 14 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-0981 J9 J EXP MAR BIOL ECOL JI J. Exp. Mar. Biol. Ecol. PY 1993 VL 165 IS 2 BP 209 EP 224 DI 10.1016/0022-0981(93)90106-X PG 16 WC Ecology; Marine & Freshwater Biology SC Environmental Sciences & Ecology; Marine & Freshwater Biology GA KH759 UT WOS:A1993KH75900006 ER PT J AU WAHL, SM ALLEN, JB COSTA, GL WONG, HL DASCH, JR AF WAHL, SM ALLEN, JB COSTA, GL WONG, HL DASCH, JR TI REVERSAL OF ACUTE AND CHRONIC SYNOVIAL INFLAMMATION BY ANTITRANSFORMING GROWTH-FACTOR-BETA SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID FACTOR-BETA-1; HYPERPLASIA; CHEMOTAXIS; RECEPTORS AB Transforming growth factor beta (TGF-beta) induces leukocyte recruitment and activation, events central to an inflammatory response. In this study, we demonstrate that antagonism of TGF-beta with a neutralizing antibody not only blocks inflammatory cell accumulation, but also tissue pathology in an experimental model of chronic erosive polyarthritis. Intraarticular injection of monoclonal antibody 1D11.16, which inhibits both TGF-beta1 and TGF-beta2 bioactivity, into animals receiving an arthropathic dose of bacterial cell walls significantly inhibits arthritis. Inhibition was observed with a single injection of 50 mug antibody, and a 1-mg injection blocked acute inflammation >75% compared with the contralateral joints injected with an irrelevant isotype control antibody (MOPC21) as quantitated by an articular index (Al = 0.93 +/- 0.23 for 1D11.16, and AI = 4.0 +/- 0 on day 4; p <0.001). Moreover, suppression of the acute arthritis achieved with a single injection of antibody was sustained into the chronic, destructive phase of the disease (on day 18, AI = 0.93 +/- 0.07 vs. AI = 2.6 +/- 0.5; p <0.01). The decreased inflammatory index associated with anti-TGF-beta treatment was consistent with histopathologic and radiologic evidence of a therapeutic response. These data implicate TGF-beta as a profound agonist not only in the early events responsible for synovial inflammation, but also in the chronicity of streptococcal cell wall fragment-induced inflammation culminating in destructive pathology. Interrupting the cycle of leukocyte recruitment and activation with TGF-beta antagonists may provide a mechanism for resolution of chronic destructive lesions. C1 CELTRIX PHARMACEUT INC, SANTA CLARA, CA 95052 USA. RP WAHL, SM (reprint author), NIDR, CELLULAR IMMUNOL SECT, IMMUNOL LAB, BLDG 30, ROOM 331, BETHESDA, MD 20892 USA. NR 28 TC 127 Z9 128 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1993 VL 177 IS 1 BP 225 EP 230 DI 10.1084/jem.177.1.225 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KE652 UT WOS:A1993KE65200026 PM 8418203 ER PT J AU FISHER, DL HOLLAND, MM MITCHELL, L SLEDZIK, PS WILCOX, AW WADHAMS, M WEEDN, VW AF FISHER, DL HOLLAND, MM MITCHELL, L SLEDZIK, PS WILCOX, AW WADHAMS, M WEEDN, VW TI EXTRACTION, EVALUATION, AND AMPLIFICATION OF DNA FROM DECALCIFIED AND UNDECALCIFIED UNITED-STATES CIVIL-WAR BONE SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PHYSICAL ANTHROPOLOGY; DEOXYRIBONUCLEIC ACID (DNA); HUMAN BONE DNA; HISTORICAL SKELETAL REMAINS; FORENSIC DNA TYPING; MITOCHONDRIAL DNA (MTDNA) ID HUMAN MITOCHONDRIAL-DNA; SKELETAL REMAINS; SEQUENCE; FRAGMENTS; REGION AB Deoxyribonucleic acid (DNA) was extracted from documented skeletal specimens of U.S. Civil War soldiers to determine the need for decalcification prior to extraction, The polymerase chain reaction (PCR) was performed to determine if the calcification state had an effect on the ability to amplify the extracts and to determine how successful amplification would be with these aged specimens. Bone samples were pulverized to a fine powder and divided into two sets. One set of samples was decalcified and the other set left undecalcified. Both sets were extracted using an organic procedure. The results demonstrate that decalcification is not a necessary step in the extraction process and that the yield of DNA is generally two times greater when decalcification is omitted. Furthermore, the calcification state had no effect on the ability to perform the PCR. Although the extracted DNA was very degraded, a 410 base pair (bp) segment of the mitochondrial DNA (mtDNA) control region was amplified. These results suggest that DNA can be extracted and amplified from 125 year old bone without decalcification, which may assist in the identity of modern and historic forensic specimens. C1 NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. ARMED FORCES INST PATHOL,NATL MUSEUM HLTH & MED,WASHINGTON,DC 20306. CELLMARK DIAGNOST,GERMANTOWN,MD. RP FISHER, DL (reprint author), ARMED FORCES INST PATHOL,ARMED FORCES DNA IDENTIFICAT LAB,OFF ARMED FORCES MED EXAMINER,WASHINGTON,DC 20306, USA. NR 26 TC 62 Z9 65 U1 0 U2 6 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD JAN PY 1993 VL 38 IS 1 BP 60 EP 68 PG 9 WC Medicine, Legal SC Legal Medicine GA KH541 UT WOS:A1993KH54100012 PM 8426158 ER PT J AU KLEIN, HG AF KLEIN, HG TI TRANSFUSION IN TRANSPLANT PATIENTS - THE GOOD, THE BAD, AND THE UGLY SO JOURNAL OF HEART AND LUNG TRANSPLANTATION LA English DT Article; Proceedings Paper CT 1992 ANNUAL MEETING OF THE INTERNATIONAL SOC FOR HEART AND LUNG TRANSPLANTATION CY APR 01, 1992 CL SAN DIEGO, CA SP INT SOC HEART & LUNG TRANSPLANTAT AB Several transfusion-related complications have particular relevance to the transplant setting. Transfusions reportedly improve solid organ graft survival, especially when the donor and recipient share at least one HLA-DR antigen. Whereas the mechanism for this effect is unclear, less favorable ''immunomodulating'' effects of transfusion may increase postoperative infections and shorten survival time and disease-free intervals in patients with a variety of malignancies who are undergoing surgery. The contribution of the different components of the blood transfusion to these outcomes remains speculative. Directed donations, especially from relatives and in the setting of a recipient who is immunosuppressed, may give rise to a severe but under-appreciated immunologic consequence of transfusion: graft-versus-host disease. Although still rarely reported, transfusional graft-versus-host disease is almost invariably fatal. This complication is entirely avoidable if the transfused blood product is appropriately gamma-irradiated. Infectious complications remain the most feared consequence of transfusion; the cytomegalovirus, the human immunodeficiency virus, and hepatitis B and C may run a more fulminant course in transplant patients who are immunosuppressed. Red cell substitutes, hematopoietic growth factors, and autologous transfusion are among the strategies for preventing complications of blood transfusion. With the advent of cyclosporine and more potent and specific immunosuppressive therapies, the desirability of preoperative transfusion for organ grafts warrants reevaluation. RP KLEIN, HG (reprint author), NIH,CTR CLIN,BLDG 10,RM IC 711,BETHESDA,MD 20892, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1053-2498 J9 J HEART LUNG TRANSPL JI J. Heart Lung Transplant. PD JAN-FEB PY 1993 VL 12 IS 1 BP S7 EP S12 PN 1 PG 6 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery; Transplantation SC Cardiovascular System & Cardiology; Respiratory System; Surgery; Transplantation GA KN545 UT WOS:A1993KN54500031 PM 8443186 ER PT J AU PURCELL, RH AF PURCELL, RH TI CONTROL OF HEPATITIS-A BY INACTIVATED VACCINES - UNANSWERED QUESTIONS AND UNRESOLVED ISSUES SO JOURNAL OF HEPATOLOGY LA English DT Article; Proceedings Paper CT International Symposium on Hepatitis A Vaccine CY JUN 10, 1992 CL RHODES, GREECE DE NORMAL IMMUNE GLOBULIN; COMBINED VACCINES; LIVE VACCINES ID A VACCINE; VIRUS; ANTIBODY; CHILDREN; TRIAL AB The recent development of safe and effective inactivated hepatitis A virus vaccines provides for the first time the opportunity to control hepatitis A, However, control will depend upon the intelligent use of the vaccines. How and when hepatitis A vaccines should be used will be determined from the results of studies of the levels and duration of protective antibody, determination of optimum immunization schedules, estimations of the continuing need for normal immune globulin and discussions of how hepatitis A vaccine can be incorporated into national and international vaccination programs. Cost and feasibility will determine whether live attenuated hepatitis A vaccines will become useful adjuncts or replacements for inactivated hepatitis A vaccines. RP PURCELL, RH (reprint author), NIAID,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892, USA. NR 22 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0168-8278 J9 J HEPATOL JI J. Hepatol. PY 1993 VL 18 SU 2 BP S61 EP S64 DI 10.1016/S0168-8278(05)80381-2 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA MU464 UT WOS:A1993MU46400014 PM 8182277 ER PT J AU HOOFNAGLE, JH DIBISCEGLIE, AM SHINDO, M AF HOOFNAGLE, JH DIBISCEGLIE, AM SHINDO, M TI ANTIVIRAL THERAPY OF HEPATITIS-C - PRESENT AND FUTURE SO JOURNAL OF HEPATOLOGY LA English DT Article; Proceedings Paper CT 5TH INTERNATIONAL SYMP ON VIRAL HEPATITIS CY JAN 30-FEB 01, 1992 CL MADRID, SPAIN DE CHRONIC HEPATITIS; CIRRHOSIS; HEPATITIS-C VIRUS; CONTROLLED TRIALS; ANTIVIRAL THERAPY; INTERFERON; RIBAVIRIN; POLYMERASE CHAIN REACTION ID NON-B-HEPATITIS; CHRONIC NON-A; RANDOMIZED CONTROLLED TRIAL; RECOMBINANT ALPHA-INTERFERON; CHRONIC ACTIVE HEPATITIS; VIRUS-INFECTION; TRANSPLANTATION; ANTIBODIES; ALFA AB The current recommendations for therapy of chronic hepatitis C are a 6-month course of alpha-interferon in doses of 3 million units 3 times weekly. Patients should have compensated chronic liver disease with elevations in serum aminotransferases, serologic evidence of hepatitis C virus (HCV) infection and chronic hepatitis by liver biopsy. At present, a long-term beneficial response to alpha-interferon occurs in only 10-25% of patients. The modest long-term response rate and the restricted recommendations for use of interferon leave several unresolved issues regarding therapy of this disease. Do patients with atypical, severe or advanced disease warrant therapy? What is the optimal dose and duration of treatment? How can one increase the response rate to interferon? How can one predict which patients are likely to benefit from therapy? Which patients are likely to relapse if therapy is stopped? Ultimately, what is needed to answer these issues are better techniques to assess HCV infection and monitor therapy as well as more effective and better-tolerated agents that can be used alone or in combination with alpha-interferon. RP HOOFNAGLE, JH (reprint author), NIDDKD,DIGEST DIS BRANCH,LIVER DIS SECT,BLDG 31,ROOM 9A23,BETHESDA,MD 20892, USA. NR 31 TC 32 Z9 32 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0168-8278 J9 J HEPATOL JI J. Hepatol. PY 1993 VL 17 SU 3 BP S130 EP S136 DI 10.1016/S0168-8278(05)80438-6 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX958 UT WOS:A1993KX95800025 PM 8509628 ER PT J AU GIMBLE, JM DORHEIM, MA YOUKHANA, K HUDSON, J NEAD, M GILLY, M WOOD, WJ HERMANSON, GG KUEHL, M WALL, R KINCADE, PW AF GIMBLE, JM DORHEIM, MA YOUKHANA, K HUDSON, J NEAD, M GILLY, M WOOD, WJ HERMANSON, GG KUEHL, M WALL, R KINCADE, PW TI ALTERNATIVELY SPLICED PP52 MESSENGER-RNA IN NONLYMPHOID STROMAL CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SEQUENCE-ANALYSIS; GENE; EXPRESSION; EXTINCTION; HYBRIDS; FRAGMENTS; PROTEIN; MYELOMA; LINES; LSP1 AB The 52-kDa phosphoprotein, also reported as lymphocyte-specific gene 1 and WP34, is transcribed as a 1.6-kb mRNA in B lymphocytes, B cell lines, and untransformed T cells. This gene encodes a cytoplasmic and plasma membrane-associated protein that is phosphorylated at a casein kinase II site and reportedly binds calcium. Based on these properties, it has been hypothesized that lymphoid form of the 52-kDa phosphoprotein protein may play a role in lymphocyte signal transduction. We show that alternatively spliced mRNA are expressed from this gene in nonlymphoid cell lines (myocytes, stromal cells, fibroblasts). These cell lines do not express the 1.6-kb lymphoid cell-specific transcript. Instead, mRNA of 2.0 and 2.8 kb are detected in varying abundance. A full-length 2.0-kb cDNA has been cloned and sequenced from the BMS2 stromal cell line by conventional screening and polymerase chain reaction-based methods. This cDNA clone, designated S37, has a single open reading frame encoding a 328 amino acid peptide. The nucleotide sequence of the S37 stromal cell cDNA is identical to that of the lymphocyte derived pp52 cDNA from the 3' poly(A) tail to the codon encoding the amino acid at residue 24. This region of the S37 cDNA clone encodes a protein that is identical to that encoded by the lymphoid pp52 cDNA and includes a casein kinase II phosphorylation site. However, the two clones differ in their 5' nucleotide sequence and their NH3 terminal amino acid sequence. This organization is consistent with alternative exon utilization. These results suggest that tissue-specific control mechanisms are used to generate different forms of lymphoid form of the 52-kDa phosphoprotein mRNA in lymphoid cells versus mesoderm-derived, nonlymphoid cell lineages. C1 MOLEC BIOL INST, LOS ANGELES, CA 90024 USA. NCI, NAVY MED ONCOL BRANCH, BETHESDA, MD 20892 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MICROBIOL & IMMUNOL, LOS ANGELES, CA 90024 USA. RP GIMBLE, JM (reprint author), OKLAHOMA MED RES FDN, IMMUNOBIOL & CANC PROGRAM, 825 NE 13TH ST, OKLAHOMA CITY, OK 73104 USA. FU NCI NIH HHS [CA12800, CA50898]; NIGMS NIH HHS [GM40185] NR 26 TC 22 Z9 23 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1993 VL 150 IS 1 BP 115 EP 121 PG 7 WC Immunology SC Immunology GA KE757 UT WOS:A1993KE75700013 PM 8417117 ER PT J AU JENSEN, JP CENCIARELLI, C HOU, DM RELLAHAN, BL DEAN, M WEISSMAN, AM AF JENSEN, JP CENCIARELLI, C HOU, DM RELLAHAN, BL DEAN, M WEISSMAN, AM TI T-CELL ANTIGEN RECEPTOR-ETA SUBUNIT - LOW-LEVELS OF EXPRESSION AND LIMITED CROSS-SPECIES CONSERVATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ZETA-CHAIN; MOLECULAR-CLONING; COMPLEX; ACTIVATION; IDENTIFICATION; CD3-ZETA; GENE; LINE AB The eta-subunit of the TCR is derived from an alternative splice product of the TCR-zeta gene. The eta-subunit has been extensively characterized in murine T cells, where up to 10% of TCR bear zeta-eta heterodimers rather than zeta-homodimers. In contrast to the significant levels of eta found in murine T cells, in human PBL an eta-like region is expressed spliced to upstream exons of the zeta-gene at no more than 0.25% the level of zeta-mRNA. Analysis of genomic DNA from five additional mammalian species demonstrated that eta-like sequences are highly conserved at a nucleic acid level. The protein sequences encoded in the eta-regions from various species ranged from 28 to 92 amino acids in length, with the first seven deduced amino acids of eta-being common to all species. Within three to five amino acids of this region, all species have five consecutive charged amino acids. Beyond this point, due to translation in different reading frames, there is no significant amino acid homology. The findings of low level of expression of eta-RNA, limited cross-species conservation on a protein level, and the lack of an established functional role for this alternative splice product raise questions as to the potential roles that this subunit may play in TCR function. C1 NCI,DIV CANC BIOL DIAG & CTR,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4817,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NIH,HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,FREDERICK,MD 21702. OI Dean, Michael/0000-0003-2234-0631 NR 35 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 JAN 1 PY 1993 VL 150 IS 1 BP 122 EP 130 PG 9 WC Immunology SC Immunology GA KE757 UT WOS:A1993KE75700014 PM 8417118 ER PT J AU PUNTURIERI, A SHIRAKATA, Y BOVOLENTA, C KIKUCHI, G COLIGAN, JE AF PUNTURIERI, A SHIRAKATA, Y BOVOLENTA, C KIKUCHI, G COLIGAN, JE TI MULTIPLE CIS-ACTING ELEMENTS ARE REQUIRED FOR PROPER TRANSCRIPTION OF THE MOUSE V-DELTA-1 T-CELL RECEPTOR PROMOTER SO JOURNAL OF IMMUNOLOGY LA English DT Article ID DNA-BINDING PROTEINS; LOOP-HELIX PROTEIN; GAMMA-DELTA; REGULATORY ELEMENTS; MAMMALIAN-CELLS; CD3-DELTA GENE; BOX-BINDING; ALPHA LOCUS; 3' END; ENHANCER AB To gain insight into the developmentally regulated expression of the mouse TCR Vdelta-gene segments, we have investigated the role of the 5' promoter region of the Vdelta1 -gene. Transient transfection assays showed that a construct encompassing 267 nucleotides upstream from the mapped transcriptional start site was capable of driving promoter activity when transfected into Vdelta1+ T cells. The inclusion of an additional 459-bp 5' segment to this construct did not affect promoter activity. However, a deletion of 222 5' nucleotides from the same construct dramatically decreased promoter activity. In vivo genomic footprinting localized several protein-DNA interactions to the stretch of DNA shown to have transcriptional activity. A computer analysis revealed that the segments of DNA participating in these protein-DNA interactions were identical to the previously described cyclic AMP response element (CRE), E box, and leukemia virus E26 cis-acting elements. Transient transfection assays performed with -267 bp constructs containing mutations at each of the localized cis-acting elements revealed that the CRE, E box, and Ets elements work together in driving promoter activity and that the CRE and Ets elements are the most important for driving transcription. Gel mobility shift analyses showed that each of these cis-acting elements is capable of binding specific nuclear factors present in Vdelta1-expressing cells. These data indicate that multiple transcription factors acting in concert are responsible for Vdelta1 gene expression. C1 NIAID,BIOL RESOURCES BRANCH,BLDG 4,ROOM 413,BETHESDA,MD 20892. NR 69 TC 8 Z9 8 U1 1 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1993 VL 150 IS 1 BP 139 EP 150 PG 12 WC Immunology SC Immunology GA KE757 UT WOS:A1993KE75700016 PM 8417120 ER PT J AU SYKES, M ABRAHAM, VS HARTY, MW PEARSON, DA AF SYKES, M ABRAHAM, VS HARTY, MW PEARSON, DA TI IL-2 REDUCES GRAFT-VERSUS-HOST DISEASE AND PRESERVES A GRAFT-VERSUS-LEUKEMIA EFFECT BY SELECTIVELY INHIBITING CD4+ T-CELL ACTIVITY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; II H-2 DIFFERENCES; MAJOR HISTOCOMPATIBILITY BARRIERS; CHRONIC MYELOGENOUS LEUKEMIA; SYNGENEIC LYMPHOMA; LYMPHOCYTES-T; INTERLEUKIN-2; MICE; DEPLETION; INVIVO AB We have recently demonstrated, in a fully MHC-mismatched murine bone marrow transplantation model, that administration of a short course of high dose IL-2 markedly diminishes graft-vs-host disease (GVHD) without compromising alloengraftment or the graft-vs-leukemia (GVL) effect of allogeneic T cells. We have now evaluated the mechanism of the dissociation of GVL and GVHD observed in this model. We demonstrate that CD4+ T cells were required to produce severe, acute GVHD in the fully MHC-mismatched plus minor histocompatibility Ag-mismatched A/J-->B10 strain combination. The GVHD-producing activity of A/J CD4+ T cells administered without CD8+ T cells was inhibited by IL-2 treatment. In contrast, CD8+ T cells alone mediated the GVL effect observed in the EL4 leukemia/lymphoma model, and CD4+ cells did not contribute to this effect. This CD8-mediated GVL activity was not inhibited by IL-2 treatment. Because naive A/J CD8+ T cells administered without CD4+ T cells did not produce acute GVHD, we were unable to evaluate the effect of IL-2 in this model. However, when A/J donors were presensitized with B10 skin grafts, CD4-depleted A/J spleen cells were capable of causing acute GVHD in B10 recipients. This CD8-mediated GVHD was not inhibited by treatment with IL-2. However, IL-2 did partially inhibit the GVHD produced by nondepleted presensitized A/J spleen cells, probably due to selective inhibition of the function of presensitized A/J CD4+ T cells. The dissociation of GVHD and GVL against the EL4 leukemia/lymphoma in IL-2-treated mice can therefore be explained by selective inhibition by IL-2 of CD4 activity. C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,CTR TRANSPLANTAT RES BIOL,BOSTON,MA 02129. FU NCI NIH HHS [R01CA55290] NR 46 TC 114 Z9 116 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 JAN 1 PY 1993 VL 150 IS 1 BP 197 EP 205 PG 9 WC Immunology SC Immunology GA KE757 UT WOS:A1993KE75700023 PM 8093257 ER PT J AU BOSCO, MC MUSSO, T GUSELLA, GL GIOVARELLI, M FORNI, M SOLETI, A MASUELLI, L MODESTI, A FORNI, G VARESIO, L AF BOSCO, MC MUSSO, T GUSELLA, GL GIOVARELLI, M FORNI, M SOLETI, A MASUELLI, L MODESTI, A FORNI, G VARESIO, L TI SELECTIVE TRANSFORMATION OF HOST LYMPHOCYTES INVIVO BY RETROVIRUS-PRODUCING MACROPHAGES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID RECOMBINANT MURINE RETROVIRUS; FRESH BONE-MARROW; V-MYC ONCOGENES; CELL-LINE; MONONUCLEAR PHAGOCYTES; MONOCLONAL ANTIBODY; GENE-EXPRESSION; NEWBORN MICE; FETAL LIVER; B-CELLS AB Macrophage-mediated retroviral transformation of host cells was studied in vivo utilizing the cloned murine macrophage-line GG2EE, generated by in vitro infection of bone marrow cells from C3H/HeJ mice (H-2k) with the acute transforming retrovirus J2 bearing the v-myc and v-raf oncogenes. Because GG2EE macrophages produce the J2 retrovirus, the development of secondary, J2 virus-induced tumors after the injection of the cell line into several strains of mice was evaluated. GG2EE cells proliferated and gave rise to histiocytic tumors in syngeneic mice and in allogeneic athymic Swiss mice. The inoculum of GG2EE cells in allogeneic DBA/2 mice (H-2d) and, to a lesser extent, in BALB/c (H-2d) and BALB/k (H-2k) mice gave rise to a small, solid mass at the injection site. Although the initial tumor was slowly rejected, secondary lymphomas belonging to the B or T cell lineage developed, leading to mouse death. Extensive phenotypic, functional, and chromosomal analyses proved that lymphomas were derived from host T and B cell transformation. Southern and Northern blot studies showed that J2 virus was integrated and expressed in lymphoma cells, demonstrating that the virus was transmitted to the host lymphocytes and suggesting that it was causal in lymphoma development. The existence of close and protracted interactions between GG2EE macrophages and allogeneic host lymphocytes and the presence of viral particles in the area of macrophage-lymphocyte contact were demonstrated by histologic and ultrastructural analysis. Rejection of J2 virus-infected lymphocytes in allogeneic mice suggested that host lymphocyte transformation was dependent upon the macrophage cell type. These results demonstrate that macrophage-derived J2 retrovirus transforms host lymphocytes in vivo in allogeneic mice and that a condition of host alloreactivity is critical for such event. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV,FREDERICK,MD 21702. UNIV TURIN,INST MICROBIOL,I-10124 TURIN,ITALY. CNR,CTR IMMUNOGENET & HISTOCOMPATIBIL,TURIN,ITALY. REGINA MARGHERITA CHILDRENS HOSP,DEPT PATHOL,TURIN,ITALY. UNIV ROME,DEPT EXPTL MED,I-00100 ROME,ITALY. UNIV CHIETI,CHIETI,ITALY. RP BOSCO, MC (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702, USA. RI Bosco, Maria Carla/J-7928-2016; varesio, luigi/J-8261-2016; OI Bosco, Maria Carla/0000-0003-1857-7193; varesio, luigi/0000-0001-5659-2218; Giovarelli, Mirella/0000-0002-7397-3466 FU NCI NIH HHS [N01-CO-74102] NR 54 TC 3 Z9 3 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 JAN 1 PY 1993 VL 150 IS 1 BP 278 EP 289 PG 12 WC Immunology SC Immunology GA KE757 UT WOS:A1993KE75700031 PM 8417128 ER PT J AU HOM, SS SCHWARTZENTRUBER, DJ ROSENBERG, SA TOPALIAN, SL AF HOM, SS SCHWARTZENTRUBER, DJ ROSENBERG, SA TOPALIAN, SL TI SPECIFIC RELEASE OF CYTOKINES BY LYMPHOCYTES INFILTRATING HUMAN MELANOMAS IN RESPONSE TO SHARED MELANOMA ANTIGENS SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE CYTOKINE SECRETION; MELANOMA ANTIGENS; TUMOR-INFILTRATING LYMPHOCYTES ID TUMOR-NECROSIS-FACTOR; RECOMBINANT INTERFERON-GAMMA; T-CELL CLONES; COLONY-STIMULATING FACTORS; PHASE-I TRIAL; FACTOR-ALPHA; AUTOLOGOUS MELANOMA; CANCER-PATIENTS; METASTATIC MELANOMA; SURFACE-ANTIGENS AB Lysis of autologous and human leucocyte antigen (HLA)-matched allogeneic melanomas by cultured human tumor-infiltrating leukocytes (TIL) suggests that shared melanoma antigens (Ag) exist and are recognized by TIL in the context of self major histocompatibility complex (MHC) molecules. We have recently shown that cytokine release by TIL is another indicator of the specific interaction with autologous tumor. To determine if recognition of shared melanoma Ag can also induce cytokine release, seven melanoma TIL, which lysed autologous tumor, were co-cultured with autologous tumor or with 7-12 HLA-matched or unmatched melanoma stimulators for 6-24 h. Supernatants were collected and assayed by ELISA for the presence of granulocyte/macrophage colony stimulating factor (GM-CSF), interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-4, and IL-6. Among five of six melanoma TIL for which autologous tumor was available, autologous melanoma cells stimulated specific release of at least one of three cytokines: GM-CSF, IFN-gamma, and TNF-alpha. Neither IL-4 nor IL-6 secretion by three TIL cultures tested was enhanced upon contact with tumor. For six of seven TIL cultures, HLA-matched allogeneic melanomas also stimulated significant cytokine release; HLA-Al, -A2, -A24, -B8, and Cw7 were identified as possible restriction elements. The cytokine secretion induced by both autologous and allogeneic HLA-matched melanomas could be blocked by an anti-MHC I antibody. These data suggest that cytokines can be specifically released by TIL recognizing a shared melanoma antigen in the context of self MHC molecules. C1 NCI,SURG BRANCH,DIV CANC TREATMENT,BLDG 10,ROOM 2B42,BETHESDA,MD 20892. NR 33 TC 65 Z9 65 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1993 VL 13 IS 1 BP 18 EP 30 DI 10.1097/00002371-199301000-00003 PG 13 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA KD649 UT WOS:A1993KD64900003 PM 8435428 ER PT J AU SPRIGGS, DR GUERRANT, RL AF SPRIGGS, DR GUERRANT, RL TI SUMMARY OF THE 27TH UNITED-STATES - JAPAN JOINT CONFERENCE ON CHOLERA AND RELATED DIARRHEAL DISEASES SO JOURNAL OF INFECTIOUS DISEASES LA English DT Editorial Material ID ESCHERICHIA-COLI; VIBRIO-CHOLERAE; ENTEROTOXIN; VIRULENCE; TOXIN C1 UNIV VIRGINIA HOSP, DIV GEOG MED, CHARLOTTESVILLE, VA 22908 USA. RP NIAID, DIV MICROBIOL & INFECT DIS, ENTER DIS BRANCH, SOLAR BLDG, ROOM 3A-06, BETHESDA, MD 20892 USA. NR 17 TC 2 Z9 2 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0022-1899 EI 1537-6613 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1993 VL 167 IS 1 BP 1 EP 6 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KE846 UT WOS:A1993KE84600001 PM 8093361 ER PT J AU BROWNE, MJ MAYER, KH CHAFEE, SBD DUDLEY, MN POSNER, MR STEINBERG, SM GRAHAM, KK GELETKO, SM ZINNER, SH DENMAN, SL DUNKLE, LM KAUL, S MCLAREN, C SKOWRON, G KOUTTAB, NM KENNEDY, TA WEITBERG, AB CURT, GA AF BROWNE, MJ MAYER, KH CHAFEE, SBD DUDLEY, MN POSNER, MR STEINBERG, SM GRAHAM, KK GELETKO, SM ZINNER, SH DENMAN, SL DUNKLE, LM KAUL, S MCLAREN, C SKOWRON, G KOUTTAB, NM KENNEDY, TA WEITBERG, AB CURT, GA TI 2',3'-DIDEHYDRO-3'-DEOXYTHYMIDINE (D4T) IN PATIENTS WITH AIDS OR AIDS-RELATED COMPLEX - A PHASE-I TRIAL SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; PLACEBO-CONTROLLED TRIAL; ANTI-HIV AGENT; 2',3'-DIDEOXYINOSINE DDI; AZIDOTHYMIDINE AZT; DOUBLE-BLIND; ZIDOVUDINE; INVITRO; POTENT; 3'-AZIDO-2',3'-DIDEOXYTHYMIDINE AB 2',3'-didehydro-3'-deoxythymidine (d4T) is a pyrimidine analogue and inhibitor of reverse transcriptase with potent in vitro activity against human immunodeficiency virus (HIV). A phase I trial of d4T was conducted in 41 HIV-infected patients, 12 with AIDS and 29 with AIDS-related complex (ARC). Thirty-six patients were evaluatable. The maximum tolerated dose was 2 mg/kg/day. The dose-limiting toxicity was sensory peripheral neuropathy, which occurred in 20 patients (55%). Four patients (11%) developed hepatotoxicity. Five (14%) developed anemia requiring a transfusion but not discontinuation of drug. The mean +/- SE plasma elimination half-life at all dose levels was 1.2 +/- 0.09 h. Increased or stable absolute CD4 counts were seen in most patients. The majority of patients with detectable serum p24 antigen levels had a persistent decrease by 6 months. d4T is a promising drug for patients with AIDS or ARC. This clinical trial is continuing to determine the minimal effective dose. C1 BROWN UNIV,AIDS PROGRAM,PROVIDENCE,RI 02912. UNIV RHODE ISL,COLL PHARM,ANTIINFECT PHARMACOL RES UNIT,KINGSTON,RI 02881. NCI,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB CO,WALLINGFORD,CT. BRISTOL MYERS CO LABS,SYRACUSE,NY 13221. RP BROWNE, MJ (reprint author), ROGER WILLIAMS GEN HOSP,DEPT MED,825 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. NR 34 TC 152 Z9 154 U1 0 U2 2 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 JAN PY 1993 VL 167 IS 1 BP 21 EP 29 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KE846 UT WOS:A1993KE84600004 PM 8093363 ER PT J AU KALER, SG GAHL, WA BERRY, SA HOLMES, CS GOLDSTEIN, DS AF KALER, SG GAHL, WA BERRY, SA HOLMES, CS GOLDSTEIN, DS TI PREDICTIVE VALUE OF PLASMA-CATECHOLAMINE LEVELS IN NEONATAL DETECTION OF MENKES DISEASE SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Note C1 NINCDS,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. UNIV MINNESOTA,DEPT PEDIAT,MINNEAPOLIS,MN 55455. RP KALER, SG (reprint author), NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892, USA. OI Berry, Susan/0000-0001-7970-688X NR 4 TC 21 Z9 21 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1993 VL 16 IS 5 BP 907 EP 908 DI 10.1007/BF00714295 PG 2 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA MC266 UT WOS:A1993MC26600024 PM 8295415 ER PT J AU MILSTIEN, S KAUFMAN, S SAKAI, N AF MILSTIEN, S KAUFMAN, S SAKAI, N TI TETRAHYDROBIOPTERIN BIOSYNTHESIS DEFECTS EXAMINED IN CYTOKINE-STIMULATED FIBROBLASTS SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article ID DIHYDROPTERIDINE REDUCTASE; DEFICIENCY; HYPERPHENYLALANINEMIA; PHENYLKETONURIA; METABOLISM; BIOPTERIN; NEOPTERIN AB Incubation of primary skin fibroblast cultures with the cytokines interferon-gamma and tumour necrosis factor-alpha stimulates the de novo pathway of tetrahydrobiopterin biosynthesis. Fibroblasts from patients with the two most common types of genetic defects of tetrahydrobiopterin metabolism that cause hyperphenylalaninaemia show characteristic pterin responses predicted by the nature of the defect. Cells from a child with 6-pyruvoyl-tetrahydropterin synthase deficiency produce higher than normal levels of neopterin and no biopterin. Fibroblasts from dihydropteridine reductase-deficient children produce normal levels of tetrahydrobiopterin, which gradually becomes partially oxidized, and higher than normal levels of neopterin. As a model for cells with the rarest form of tetrahydrobiopterin deficiency, lack of GTP cyclohydrolase activity, normal fibro blasts were treated with 2,4-diamino-6-hydroxypyrimidine to inhibit GTP cyclohydrolase activity by >90%, the level expected in patients with a GTP cyclohydrolase deficiency. Neopterin and biopterin synthesis rates of <10% of normal levels were readily detectable. Therefore, analysis of the patterns of the pterins synthesized by fibroblasts can aid in the diagnosis of the hyperphenylalaninaemias as caused by disorders of tetrahydrobiopterin metabolism. RP NIMH, NEUROCHEM LAB, BLDG 36, ROOM 3D-30, BETHESDA, MD 20892 USA. NR 16 TC 10 Z9 10 U1 0 U2 1 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0141-8955 EI 1573-2665 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1993 VL 16 IS 6 BP 975 EP 981 DI 10.1007/BF00711513 PG 7 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA ML990 UT WOS:A1993ML99000008 PM 8127073 ER PT J AU SCHATZKIN, A FREEDMAN, L SCHIFFMAN, M AF SCHATZKIN, A FREEDMAN, L SCHIFFMAN, M TI AN EPIDEMIOLOGIC PERSPECTIVE ON BIOMARKERS SO JOURNAL OF INTERNAL MEDICINE LA English DT Article DE BIOMARKER; CERVIX DYSPLASIA; COLONIC POLYPS; DIET; EPIDEMIOLOGY; MALIGNANT NEOPLASM ID CELL-PROLIFERATION; CANCER; MUCOSA; CONSUMPTION; ANTIGEN; WOMEN AB The authors discuss biological markers from an epidemiologic perspective, emphasizing the importance of integrating biomarkers into large-scale observational and intervention studies. Whereas any biologic phenomenon can be considered a biomarker, an intermediate end-point is defined as being on the causal pathway between exposure and disease. An intermediate end-point is a valid surrogate for a disease in relation to a given exposure if, and only if, that exposure causes a similar change in the occurrence of both the intermediate end-point and the disease. Cancer studies using surrogate end-points may be shorter, smaller and cheaper than those using malignancy per se as an outcome. Three types of studies may be carried out to determine whether a given biomarker is an intermediate end-point and whether it can serve as a surrogate: (i) exposure-marker studies, (ii) marker-disease studies, and (iii) studies comprising all three elements, exposure, marker, and disease. The authors discuss statistical aspects of these three types of studies and provide examples from investigations of alcohol-hormones-breast cancer, diet-epithelial proliferation markers-large bowel adenomatous polyps, and reproductive risk factors-human papillomavirus infection-cervical cancer. RP SCHATZKIN, A (reprint author), NCI,CANC PREVENT STUDIES BRANCH,6130 EXECUT BLVD,RM 211,ROCKVILLE,MD 20852, USA. NR 16 TC 14 Z9 14 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0954-6820 J9 J INTERN MED JI J. Intern. Med. PD JAN PY 1993 VL 233 IS 1 BP 75 EP 79 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA KM376 UT WOS:A1993KM37600015 PM 8429292 ER PT J AU SOPKO, G AF SOPKO, G TI OVERVIEW OF PERCUTANEOUS CORONARY CATHETER-BASED REVASCULARIZATION - PAST AND PRESENT AND THE ROLE OF FEDERAL-FUNDING SO JOURNAL OF INVASIVE CARDIOLOGY LA English DT Review RP SOPKO, G (reprint author), NHLBI,DHVD,CARDIAC DIS BRANCH,FED BLDG,ROOM 3C06,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HEALTH MANAGEMENT PUBLICATIONSINC PI WAYNE PA 950 WEST VALLEY RD, STE 2800, WAYNE, PA 19087 SN 1042-3931 J9 J INVASIVE CARDIOL JI J. Invasive Cardiol. PD JAN-FEB PY 1993 VL 5 IS 1 BP 28 EP 34 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KL146 UT WOS:A1993KL14600005 PM 10148299 ER PT J AU LEE, SC WANG, M MCBRIDE, OW OKEEFE, EJ KIM, IG STEINERT, PM AF LEE, SC WANG, M MCBRIDE, OW OKEEFE, EJ KIM, IG STEINERT, PM TI HUMAN TRICHOHYALIN GENE IS CLUSTERED WITH THE GENES FOR OTHER EPIDERMAL STRUCTURAL PROTEINS AND CALCIUM-BINDING PROTEINS AT CHROMOSOMAL LOCUS 1Q21 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID HUMAN INVOLUCRIN GENE; HAIR FOLLICLE; CITRULLINE; REGION AB Trichohyalin is a major differentiation product of hard keratinizing tissues such as the inner root sheath and medullary cells of the hair follicle and the filiform papillae of the tongue, as well as terminally differentiating epidermal cells. It consists largely of quasi-repeating peptide repeats and functions primarily as an intermediate filament-associated protein in these tissues. By mapping with human-rodent somatic cell hybrids and fluorescent in situ hybridization, we demonstrate that its gene maps to chromosomal region 1q21. Interestingly, genes encoding several other structural proteins expressed during terminal differentiation in the epidermis map to this region, as do also several members of the S-100 class of small calcium-binding proteins. C1 NIAMS,SKIN BIOL BRANCH,BLDG 6,ROOM 425,BETHESDA,MD 20892. NCI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT DERMATOL,CHAPEL HILL,NC 27514. NR 26 TC 26 Z9 26 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 JAN PY 1993 VL 100 IS 1 BP 65 EP 68 DI 10.1111/1523-1747.ep12354504 PG 4 WC Dermatology SC Dermatology GA KJ497 UT WOS:A1993KJ49700010 PM 8423399 ER PT J AU RAYNAUD, F GERBAUD, P BOULOC, A GORIN, I ANDERSON, WB EVAINBRION, D AF RAYNAUD, F GERBAUD, P BOULOC, A GORIN, I ANDERSON, WB EVAINBRION, D TI RAPID EFFECT OF TREATMENT OF PSORIATIC ERYTHROCYTES WITH THE SYNTHETIC RETINOID ACITRETIN TO INCREASE 8-AZIDO CYCLIC-AMP BINDING TO THE RI REGULATORY SUBUNIT SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID DEPENDENT PROTEIN-KINASE; MELANOMA-CELLS; ACID; IDENTIFICATION; RECEPTOR; RETINOYLATION; HL-60-CELLS AB We have recently demonstrated a deficiency in the cyclic adenosine monophosphate (cAMP)-dependent protein kinases (PKA), the intracellular mediator of AMP, in psoriasis. This enzyme defect is expressed in fibroblasts and in red blood cells isolated from psoriatic patients. In these cells, the abnormality noted in cAMP binding to PKA correlates well with the severity of the disease and is corrected by long-term treatment with etretinate. In this study, we determined the effect of oral administration of acitretin in four psoriatic patients on the altered cAMP binding observed with the RI regulatory subunit of PKA in erythrocytes prepared from these patients. Acitretin (30 mg/day) induced a rapid (within 1 h) increase in the ability of the RI regulatory subunit of erythrocytes to bind the 8-azido[P-32]cAMP photoaffinity analogue of cAMP. The maximal plateau for this effect of acitretin was observed within 24 h of treatment and preceded the clinical improvement of the disease. The effect of acitretin was dose-dependent, with the maximal response observed at 40 mg acitretin/d. In addition, the rapid exposure (15 min) of erythrocytes isolated from untreated patients exhibiting severe psoriasis to acitretin also promoted an increase in binding of 8-azido[P-32]CAMp to the RI cAMP binding protein. Retinoic acid and 13-cis-retinoic acid were as efficient as acitretin in inducing the increase in binding of 8-azido[P-32]CAMp to the RI regulatory subunit, whereas arotinoid was without effect. These results suggest that acitretin may act to modify PKA (the RI regulatory subunit) at the post-transcriptional level, and this may reflect, in part, on the mechanism of action of this synthetic retinoid. Further, monitoring this biochemical event may be helpful in determining the choice of retinoid therapy and in the management of its pharmacology. C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. HOSP TARNIER,DEPT DERMATOL,PARIS,FRANCE. RP RAYNAUD, F (reprint author), ECOLE NORM SUPER,CNRS,PHYSIOPATHOL DEV LAB,8EME ETAGE,46 RUE ULM,F-75230 PARIS 05,FRANCE. NR 28 TC 10 Z9 10 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 JAN PY 1993 VL 100 IS 1 BP 77 EP 81 DI 10.1111/1523-1747.ep12354923 PG 5 WC Dermatology SC Dermatology GA KJ497 UT WOS:A1993KJ49700012 PM 8380830 ER PT J AU ADELSTEIN, S NOGUCHI, M YI, HF ROSENBLATT, HM FILIPOVICH, AH MODI, WS MCBRIDE, OW LEONARD, WJ AF ADELSTEIN, S NOGUCHI, M YI, HF ROSENBLATT, HM FILIPOVICH, AH MODI, WS MCBRIDE, OW LEONARD, WJ TI INTERLEUKIN-2 RECEPTOR GAMMA-CHAIN MUTATION RESULTS IN X-LINKED SEVERE COMBINED IMMUNODEFICIENCY IN HUMANS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NIH,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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 39 EP 39 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500039 ER PT J AU STRASSMANN, G NORDAN, RP AF STRASSMANN, G NORDAN, RP TI INHIBITION OF IL-6 RECEPTOR-BINDING AND BIOLOGICAL RESPONSE IN-VITRO AND OF COLON-26 MEDIATED EXPERIMENTAL CANCER CACHEXIA IN-VIVO BY SURAMIN SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 OTSUKA AMER PHARMACEUT INC,DEPT IMMUNOL,ROCKVILLE,MD 20850. NCI,CLIN PHARMACOL BRANCH,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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 40 EP 40 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500040 ER PT J AU LLOYD, A BIRAGYN, A JOHNSTON, J TAUB, D SPRENGER, H OPPENHEIM, J KELVIN, D AF LLOYD, A BIRAGYN, A JOHNSTON, J TAUB, D SPRENGER, H OPPENHEIM, J KELVIN, D TI IL-8 RECEPTOR REGULATION IN POLYMORPHONUCLEAR LEUKOCYTES BY G-CSF AND LPS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. PRINCE HENRY HOSP,LITTLE BAY,NSW 2036,AUSTRALIA. RI Lloyd, Andrew/E-7334-2017 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 48 EP 48 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500087 ER PT J AU CHAUDHRI, G PASS, H AF CHAUDHRI, G PASS, H TI DIFFERENTIAL REGULATION OF CELL-SURFACE AND SECRETED TNF BIOSYNTHESIS IN LPS-STIMULATED MACROPHAGES SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI,SURG BRANCH,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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 51 EP 51 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500105 ER PT J AU DEBELL, KE HODES, R GRAHAM, L YUAN, D HOFFMAN, T BONVINI, E AF DEBELL, KE HODES, R GRAHAM, L YUAN, D HOFFMAN, T BONVINI, E TI SIGNALING PATHWAYS IN MURINE TH1 AND TH2 CLONES SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NIH,CBER,DMA,CELL BIOL LAB,BETHESDA,MD 20892. NIA,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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 57 EP 57 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500146 ER PT J AU DOUKAS, M CHAVAN, A JACOBSON, S KELLER, J GASS, C BOONE, T HALEY, B AF DOUKAS, M CHAVAN, A JACOBSON, S KELLER, J GASS, C BOONE, T HALEY, B TI OCCUPANCY OF THE NUCLEOTIDE-BINDING SITE OF GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR (GM-CSF) INTERFERES WITH RECEPTOR-LIGAND INTERACTION SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 VET ADM MED CTR,LEXINGTON,KY 40511. UNIV KENTUCKY,LUCILLE P MARKEY CANC CTR,LEXINGTON,KY 40536. NCI,FREDERICK,MD 21701. AMGEN INC,THOUSAND OAKS,CA. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 65 EP 65 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500193 ER PT J AU COLDITZ, I SEOW, HF YOSHIMURA, T CLARKE, R BEH, K AF COLDITZ, I SEOW, HF YOSHIMURA, T CLARKE, R BEH, K TI LEUKOCYTE RECRUITMENT IN-VIVO BY IL-8 IN AN AUTOLOGOUS MODEL SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 CSIRO,DIV ANIM HLTH,ARMIDALE,NSW 2350,AUSTRALIA. CSIRO,DIV ANIM HLTH,PARKVILLE,VIC 3052,AUSTRALIA. CSIRO,DIV ANIM HLTH,GLEBE,NSW 2037,AUSTRALIA. NCI,FCRDC,FREDERICK,MD 21702. RI Colditz, Ian/A-1289-2008 OI Colditz, Ian/0000-0001-9497-5148 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 68 EP 68 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500205 ER PT J AU HORUK, R HENZEL, W GRIMLEY, C DARBONNE, W CHITNIS, C MILLER, L HADLEY, T COLBY, T AF HORUK, R HENZEL, W GRIMLEY, C DARBONNE, W CHITNIS, C MILLER, L HADLEY, T COLBY, T TI THE HUMAN ERYTHROCYTE CHEMOKINE RECEPTOR IS A RECEPTOR FOR THE MALARIAL PARASITE PLASMODIUM-VIVAX SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 GENENTECH INC,S SAN FRANCISCO,CA 94080. NIH,MALARIA RES LAB,BETHESDA,MD 20892. JG BROWN CANC CTR,DIV MED ONCOL HEMATOL,LOUISVILLE,KY 40292. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 68 EP 68 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500206 ER PT J AU YOSHIMURA, T AF YOSHIMURA, T TI MONOCYTE CHEMOATTRACTANT PROTEIN-1 (MCP-1) - STUDY OF MCP-1 MESSENGER-RNA EXPRESSION IN ANIMAL-MODELS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,IMMUNOBIOL LAB,IMMUNOPATHOL SECT,FREDERICK,MD 21702. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 68 EP 68 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500208 ER PT J AU SAMELSON, LE AF SAMELSON, LE TI THE T-CELL ANTIGEN RECEPTOR - PHOSPHORYLATION EVENTS ACCOMPANYING ACTIVATION SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 71 EP 71 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500228 ER PT J AU WAHL, SM HINES, KL CHRIST, M MCCARTNEYFRANCIS, N KULKARNI, A KARLSSON, S FURCHT, L MCCARTHY, JB AF WAHL, SM HINES, KL CHRIST, M MCCARTNEYFRANCIS, N KULKARNI, A KARLSSON, S FURCHT, L MCCARTHY, JB TI ADHESION, RECRUITMENT, AND ACTIVATION OF MONONUCLEAR PHAGOCYTES IN INFLAMMATION SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NINCDS,BETHESDA,MD 20892. UNIV MINNESOTA,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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 74 EP 74 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500242 ER PT J AU RUSSELL, SM HARADA, N NAKAMURA, Y NOGUCHI, M LELAND, P MIYAJIMA, A PURI, RK LEONARD, WJ AF RUSSELL, SM HARADA, N NAKAMURA, Y NOGUCHI, M LELAND, P MIYAJIMA, A PURI, RK LEONARD, WJ TI THE INTERLEUKIN-2 RECEPTOR-GAMMA CHAIN IS A COMPONENT OF THE INTERLEUKIN-4 RECEPTOR SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NHLBI,PULM & MOLEC IMMUNOL SECT,BETHESDA,MD 20892. DNAX RES INST MOLEC & CELLULAR BIOL INC,PALO ALTO,CA 94304. US FDA,CBER,DIV CELLULAR & GENE THERAPY,BETHESDA,MD 20014. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 107 EP 107 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500443 ER PT J AU LLOYD, A TAUB, D WANG, JM JOHNSTON, J OPPENHEIM, J KELVIN, D AF LLOYD, A TAUB, D WANG, JM JOHNSTON, J OPPENHEIM, J KELVIN, D TI FUNCTIONAL AND PROMISCUOUS CHEMOKINE RECEPTORS ENCODED BY HUMAN CYTOMEGALOVIRUS SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. PRINCE HENRY HOSP,DEPT IMMUNOPATHOL,LITTLE BAY,NSW 2036,AUSTRALIA. RI Lloyd, Andrew/E-7334-2017 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 131 EP 131 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500586 ER PT J AU WILTROUT, RH USUI, N MORI, M CARLINO, JA LONGO, DL KELLER, J RUSCETTI, FW GRZEGORZEWSKI, K AF WILTROUT, RH USUI, N MORI, M CARLINO, JA LONGO, DL KELLER, J RUSCETTI, FW GRZEGORZEWSKI, K TI HEMATOPOIETIC AND CHEMOPROTECTIVE EFFECTS OF RHTGF-BETA IN MICE SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,DCT,BRMP,FREDERICK,MD 21702. NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21702. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1993 SU S BP 133 EP 133 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA ME185 UT WOS:A1993ME18500593 ER PT J AU KLEIN, HG LOHSE, P DUVERGER, N ALBERS, JJ RADER, DJ ZECH, LA SANTAMARINAFOJO, S BREWER, HB AF KLEIN, HG LOHSE, P DUVERGER, N ALBERS, JJ RADER, DJ ZECH, LA SANTAMARINAFOJO, S BREWER, HB TI 2 DIFFERENT ALLELIC MUTATIONS IN THE LECITHIN - CHOLESTEROL ACYLTRANSFERASE (LCAT) GENE RESULTING IN CLASSIC LCAT DEFICIENCY - LCAT (TYR(83)-]STOP) AND LCAT (TYR(156)-]ASN) SO JOURNAL OF LIPID RESEARCH LA English DT Article DE HYPOALPHALIPOPROTEINEMIA; CORNEAL OPACITIES; DNA SEQUENCE ANALYSIS; LCAT ACTIVITY; LCAT MASS; RESTRICTION FRAGMENT LENGTH POLYMORPHISM; SITE-DIRECTED MUTAGENESIS ID FISH-EYE DISEASE; MASSIVE CORNEAL OPACITIES; HIGH-DENSITY LIPOPROTEIN; APOLIPOPROTEIN-A-I; FAMILIAL LECITHIN; SECONDARY STRUCTURE; NUCLEOTIDE-SEQUENCE; GENOMIC SEQUENCES; GLOBULAR-PROTEINS; CHAIN-REACTION AB The molecular defects in the lecithin:cholesterol acyltransferase (LCAT) gene have been identified in a 52-year-old patient with classic LCAT deficiency, presenting with corneal clouding and proteinuria. Plasma total cholesterol was normal, triglycerides were elevated, whereas high density lipoprotein (HDL) cholesterol (8 mg/dl) and plasma cholesteryl esters (6% of total cholesterol) were markedly reduced. Plasma cholesterol esterification rate (pCER) was zero, alpha-LCAT activity, assayed using an HDL-like proteoliposome substrate was reduced to 1.6% of control, and LCAT mass was 3.7% of normal plasma levels. DNA sequence analysis of the proband's LCAT gene identified a C to A substitution, converting tyr83 to a stop codon, and a T to A transition, replacing tyr156 by asn. Restriction analysis of PCR-amplified DNA from the proband, a control and his four children using the enzymes Acc I and Rsa I established that the patient is a compound heterozygote for both mutations. The two children, heterozygous for the stop codon defect, were phenotypically indistinguishable from the two with the tyr156 defect. In vitro expression of LCAT (tyr156-->asn) in human embryonic kidney-293 cells established the functional significance of this mutation. The secreted translation product had only 6% of control mass and no detectable CER; however, the residual LCAT mass of the in vitro expressed LCAT (tyr156-->asn) demonstrated a specific alpha-LCAT activity of 30% of control, suggesting that this amino acid substitution results in a mutant enzyme that retains some enzymic activity, but may be rapidly catabolized. In summary, we have identified two unique defects in the LCAT gene that lead to the expression of classic LCAT deficiency in this kindred. C1 UNIV WASHINGTON, HARBORVIEW MED CTR,SCH MED,DEPT MED, NW LIPID RES CLIN, SEATTLE, WA 98104 USA. RP NHLBI, MOLEC DIS BRANCH, BLDG 10, ROOM 7N117, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 59 TC 47 Z9 47 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0022-2275 EI 1539-7262 J9 J LIPID RES JI J. Lipid Res. PD JAN PY 1993 VL 34 IS 1 BP 49 EP 58 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KF525 UT WOS:A1993KF52500005 PM 8445342 ER PT J AU TISCHLER, M CARDELLINA, JH AF TISCHLER, M CARDELLINA, JH TI A SIMPLE METHOD FOR THE SEPARATION OF TRITERPENE CARBOXYLIC-ACIDS SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article AB A polybutadiene-coated alumina column has been found to resolve a closely related mixture of naturally occurring triterpene carboxylic acids much more efficiently than conventional octadecylsilyl-bonded (C18) silica columns. Further, this separation could be achieved without ion-pairing, ion-suppression or other buffering techniques. RP TISCHLER, M (reprint author), NCI,DIV CANC TREATMENT,DRUG DISCOVERY RES & DEV LAB,DEV THERAPEUT PROGRAM,BLDG 1052,ROOM 121,FREDERICK,MD 21702, USA. NR 5 TC 4 Z9 4 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1993 VL 16 IS 1 BP 15 EP 19 DI 10.1080/10826079308020893 PG 5 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA KE872 UT WOS:A1993KE87200002 ER PT J AU FOX, SD SHAW, GL CAPORASO, NE WELSH, SE MELLINI, DW FALK, R ISSAQ, HJ AF FOX, SD SHAW, GL CAPORASO, NE WELSH, SE MELLINI, DW FALK, R ISSAQ, HJ TI THE DETERMINATION OF DEBRISOQUINE AND ITS 4-HYDROXY METABOLITE IN URINE BY CAPILLARY GAS-CHROMATOGRAPHY AND HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID LUNG-CANCER; 4-HYDROXYDEBRISOQUINE AB A comparative evaluation of capillary gas chromatography and high performance liquid chromatography for the determination of debrisoquine (D) and 4-hydroxydebrisoquine (4HOD) in human urine was undertaken to determine which is the better method to use for routine analysis with emphasis on reproducibility, selectivity and sensitivity. The results show that although GC is more sensitive than HPLC with UV detection it is comparable to HPLC with fluorescence detection. HPLC is simpler and requires very little sample clean-up, while GC requires sample clean-up, derivatization and extraction which is tedious and time consuming. The chromatographic HPLC analysis is completed in less than 10 minutes while the GC procedure takes about twice that time. Overall, the HPLC procedure using fluorescence detection, is selective, simple, fast and gives reproducible results. The HPLC sensitivity for both D and 4HOD, using fluorescence detection is 25 mug/L which is adequate for studies involving phenotyping of human populations. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,POB B,FREDERICK,MD 21702. NCI,BETHESDA,MD 20892. NR 19 TC 7 Z9 7 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1993 VL 16 IS 6 BP 1315 EP 1327 DI 10.1080/10826079308020955 PG 13 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA KU931 UT WOS:A1993KU93100007 ER PT J AU MELLINI, DW CAPORASO, NE ISSAQ, HJ AF MELLINI, DW CAPORASO, NE ISSAQ, HJ TI DETERMINATION OF THE CAFFEINE METABOLITE AFMU IN HUMAN URINE BY COLUMN SWITCHING HPLC SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID ACETYLATION; VARIABILITY; PHENOTYPE AB A column switching HPLC procedure is described for the quantification of the caffeine metabolite AFMU (5-acetylamino-6-formylamino-3-methyluracil) from other metabolites in human urine. The procedure is simple, easy to use and allows the reliable quantification of AFMU without interference from other metabolites. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,POB B,FREDERICK,MD 21702. NCI,BETHESDA,MD 20892. NR 12 TC 5 Z9 5 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1993 VL 16 IS 6 BP 1419 EP 1426 DI 10.1080/10826079308020961 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA KU931 UT WOS:A1993KU93100013 ER PT J AU CHAN, KC JANINI, GM MUSCHIK, GM ISSAQ, HJ AF CHAN, KC JANINI, GM MUSCHIK, GM ISSAQ, HJ TI PULSED UV LASER-INDUCED FLUORESCENCE DETECTION OF NATIVE PEPTIDES AND PROTEINS IN CAPILLARY ELECTROPHORESIS SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article; Proceedings Paper CT 3RD ANNUAL FREDERICK CONF ON CAPILLARY ELECTROPHORESIS CY OCT 20-21, 1992 CL FREDERICK, MD AB A pulsed UV laser operating at 248 nm was used for the laser-induced fluorescence (LIF) detection of native tryptophan-containing compounds in capillary electrophoresis. The limit of detection (LOD) of tryptophan was found to be 3.3x10(-9) M (S/N=2). The LODs of the model proteins conalbumin and bovine serum albumin were found to be 1.3x10(-9) and 4x10(-9) M (S/N=2), respectively. These results were at least two orders of magnitude more sensitive when compared to UV absorption at 214 nm. RP CHAN, KC (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES,POB B,FREDERICK,MD 21702, USA. NR 14 TC 55 Z9 56 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1993 VL 16 IS 9-10 BP 1877 EP 1890 DI 10.1080/10826079308019903 PG 14 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA LD281 UT WOS:A1993LD28100002 ER PT J AU HEEGAARD, NHH ROBEY, FA AF HEEGAARD, NHH ROBEY, FA TI USE OF CAPILLARY ZONE ELECTROPHORESIS FOR THE ANALYSIS OF DNA-BINDING TO A PEPTIDE DERIVED FROM AMYLOID P COMPONENT SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article; Proceedings Paper CT 3RD ANNUAL FREDERICK CONF ON CAPILLARY ELECTROPHORESIS CY OCT 20-21, 1992 CL FREDERICK, MD ID AFFINITY ELECTROPHORESIS; PROTEIN; SERUM AB Capillary zone electrophoresis was used to characterize the binding interactions between oligonucleotides and synthetic peptides derived from human serum amyloid P component. From a solution containing free and peptide-bound oligonucleotides, free nucleotide was separated from the complex by means of electrophoresis. In this way, both qualitative and quantitative aspects of the binding could be assessed rapidly using minute amounts of unlabelled samples. Minimal structures and sequence specificity of binding of nucleotides and peptides could be characterized and, based on the quantitative output of the electrophoretic analysis, binding constants were estimated. In theory, the approach is applicable for any molecular interaction where the charge/mass ratio of complexes differ from the free molecules and where at least one of the interacting components is quantitatively recoverable and detectable in the capillary electrophoresis system. As such, it is the only method available for simple and fast estimates of binding parameters for unlabelled low molecular weight compounds in solution. RP HEEGAARD, NHH (reprint author), NIDR,CELLULAR DEV & ONCOL LAB,PEPTIDE & IMMUNOCHEM UNIT,BLDG 30,RM 211,BETHESDA,MD 20892, USA. NR 14 TC 46 Z9 47 U1 2 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1993 VL 16 IS 9-10 BP 1923 EP 1939 DI 10.1080/10826079308019906 PG 17 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA LD281 UT WOS:A1993LD28100005 ER PT J AU ELISSA, BD JANINI, GM AF ELISSA, BD JANINI, GM TI HYPERCHEM FOR PC - WINDOWS VERSION SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article RP ELISSA, BD (reprint author), NCI,FREDERICK CANC RES CTR,FREDERICK,MD 21701, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1993 VL 16 IS 11 BP 2425 EP 2426 PG 2 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA LH231 UT WOS:A1993LH23100017 ER PT J AU JANINI, GM CHAN, KC MUSCHIK, GM ISSAQ, HJ AF JANINI, GM CHAN, KC MUSCHIK, GM ISSAQ, HJ TI OPTIMIZATION OF RESOLUTION IN CAPILLARY ZONE ELECTROPHORESIS - EFFECT OF SOLUTE MOBILITY AND BUFFER PH SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID SILICA CAPILLARIES; ELECTRIC-FIELD; SEPARATION; CHROMATOGRAPHY; EFFICIENCY; PARAMETERS; PROTEINS; VOLTAGE AB A reformulated version of the resolution equation in CZE that explicitly relates resolution to migration time is presented. Selectivity and resolution are enhanced with increasing migration time if the increase in time is a result of independent manipulation of electroosmotic flow. If the increase in migration time is a result of simultaneous changes in electroosmotic flow and electrophoretic mobility, selectivity and resolution deteriorate with increasing migration time. Optimum resolution for organic acid isomers is attained at a pH value that is about 0.3 units lower than the average pK of the two acids, even though selectivity continuously increases with decreasing pH. Both selectivity and resolution deteriorate with increasing electroosmotic flow in the same direction as electrophoretic mobility, however, selectivity is more sensitive than resolution to such changes. RP JANINI, GM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,POBB,FREDERICK,MD 21702, USA. NR 28 TC 15 Z9 15 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1993 VL 16 IS 17 BP 3591 EP 3607 DI 10.1080/10826079308019655 PG 17 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA MK145 UT WOS:A1993MK14500001 ER PT J AU ISSAQ, HJ AF ISSAQ, HJ TI THE 3RD ANNUAL FREDERICK CONFERENCE ON CAPILLARY ELECTROPHORESIS - OCTOBER 20-21, 1992 FREDERICK, MARYLAND SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Editorial Material RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1993 VL 16 IS 9-10 BP R13 EP R14 PG 2 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA LD281 UT WOS:A1993LD28100001 ER PT J AU MCNELLIS, D AF MCNELLIS, D TI A VIEW FROM BETHESDA - THE 4TH ANNUAL NICHD ASPEN CONFERENCE SO JOURNAL OF MATERNAL-FETAL INVESTIGATION LA English DT Editorial Material RP MCNELLIS, D (reprint author), NICHHD,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0939-6322 J9 J MATERN-FETAL INVES JI J. Matern.-Fetal Invest. PY 1993 VL 3 IS 1 BP 3 EP 3 PG 1 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KW481 UT WOS:A1993KW48100001 ER PT J AU SCHWAN, TG AF SCHWAN, TG TI SEX-RATIO AND PHORETIC MITES OF FLEAS (SIPHONAPTERA, PULICIDAE AND HYSTRICHOPSYLLIDAE) ON THE NILE GRASS RAT (ARVICANTHIS-NILOTICUS) IN KENYA SO JOURNAL OF MEDICAL ENTOMOLOGY LA English DT Article DE FLEAS; MITES; PHORESY ID SP-N ACARI; ASTIGMATA; HYPOPUS AB The sex ratio of fleas and their phoretic mites associated with the Nile grass rat, Arvicanthis niloticus (Desmarest), were studied during 14 mo in a grassland community of Lake Nakuru National Park, Kenya. Females of the fleas Dinopsyllus lypusus Jordan & Rothschild, Ctenophthalmus calceatus cabirus Jordan & Rothschild, and Xenopsylla cheopis bantorum Jordan infested more grass rats and in greater numbers than did males. Phoretic hypopi (heteromorphic deutonymphs) of two species of mites, Psylloglyphus uilenbergi Fain and Paraceroglyphus xenopsylla Fain & Schwan, varied seasonally in their abundance on fleas and utilized female fleas over male fleas for their major source of transport. Additionally, the mites were very host specific with nearly 100% of those identified on D. lypusus and C. calceatus cabirus being P. uilenbergi and 89% of the mites identified on X. cheopis bantorum being P. xenopsylla. This level of specificity suggests that these mite-flea associations are highly evolved. The importance of female fleas as hosts for transporting mites also suggests that female-biased sex ratios of fleas on their hosts may be caused, in part, by females being more important as dispersers within flea populations. RP SCHWAN, TG (reprint author), US PHS,NIAID,ARTHROPOD BORNE DIS SECT,VECTORS & PATHOGENS LAB,ROCKY MT LABS,HAMILTON,MT 59840, USA. NR 60 TC 9 Z9 9 U1 0 U2 2 PU ENTOMOL SOC AMER PI LANHAM PA 9301 ANNAPOLIS RD, LANHAM, MD 20706 SN 0022-2585 J9 J MED ENTOMOL JI J. Med. Entomol. PD JAN PY 1993 VL 30 IS 1 BP 122 EP 135 PG 14 WC Entomology; Veterinary Sciences SC Entomology; Veterinary Sciences GA KJ315 UT WOS:A1993KJ31500016 PM 8433319 ER PT J AU THOMAS, RE KARSTENS, RH SCHWAN, TG AF THOMAS, RE KARSTENS, RH SCHWAN, TG TI EFFECT OF YERSINIA-PESTIS INFECTION ON TEMPERATURE PREFERENCE AND MOVEMENT OF THE ORIENTAL RAT FLEA (XENOPSYLLA-CHEOPIS) (SIPHONAPTERA, PULICIDAE) SO JOURNAL OF MEDICAL ENTOMOLOGY LA English DT Article DE XENOPSYLLA-CHEOPIS; YERSINIA-PESTIS; BEHAVIORAL FEVER ID BEHAVIORAL FEVER; PLAGUE AB Previous laboratory studies have shown that inoculation of bacterial endotoxin into the hemocoel of some arthropods, or natural infection by a number of pathogens, causes them to seek out a higher ambient temperature. This phenomenon has been called behavioral fever. Yersinia pestis is an endotoxin-producing bacterium that relies on infection of fleas for transmission. Behavioral fever in fleas might enhance the transmission of plague if infected fleas were induced to seek out a warm-bodied host after the death of an infected host. Our study indicates that in thermal gradients Y. pestis infected Oriental rat fleas (Xenopsylla cheopis) do not exhibit behavioral fever and in one experiment sought out a significantly lower temperature. C1 US PHS,NIAID,ROCKY MT LABS,ARTHROPOD BORNE INFECT DIS SECT,VECTORS & PATHOGENS LAB,903 S 4TH ST,HAMILTON,MT 59840. NR 12 TC 5 Z9 5 U1 2 U2 7 PU ENTOMOL SOC AMER PI LANHAM PA 9301 ANNAPOLIS RD, LANHAM, MD 20706 SN 0022-2585 J9 J MED ENTOMOL JI J. Med. Entomol. PD JAN PY 1993 VL 30 IS 1 BP 209 EP 213 PG 5 WC Entomology; Veterinary Sciences SC Entomology; Veterinary Sciences GA KJ315 UT WOS:A1993KJ31500025 PM 8433328 ER PT J AU TEDESCHI, V PURCELL, RH EMERSON, SU AF TEDESCHI, V PURCELL, RH EMERSON, SU TI PARTIAL CHARACTERIZATION OF HEPATITIS-A VIRUSES FROM 3 INTERMEDIATE PASSAGE LEVELS OF A SERIES RESULTING IN ADAPTATION TO GROWTH IN CELL-CULTURE AND ATTENUATION OF VIRULENCE SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE PCR SEQUENCE; PATHOGENICITY; HM-175; 5' REGION; 2BC REGION ID COMPLETE NUCLEOTIDE-SEQUENCE; WILD-TYPE VIRUS; VIRAL-RNA; REPLICATION; PROTEINS; VACCINES; STRAINS; REGION; HM175 AB Viruses from passages 9/10, 21, and 32 of a serially passaged human isolate of hepatitis A virus, strain HM-175, were partially sequenced and compared for their abilities to grow in cell cultures and to cause disease in primates. Viruses from all passages grew more efficiently in cell culture than did the wild-type virulent virus from which they were derived, and all displayed some degree of attenuation of virulence for primates. Within the 5' noncoding region and the 2B2C region of the HAV genome, passage 9/10 virus differed in sequence from wild-type at a single and novel position in the 2C gene, while the sequence of the passage 32 virus was almost identical to that of a fully attenuated passage 35 virus. Passage 21 viruses were found to consist of a mixture of viruses which included all but two of the 13 mutations present in the sequenced regions of the virus from passage 32. C1 NIAID,LID,HEPATITIS VIRUSES SECT,BLDG 7,ROOM 203,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. FIOCRUZ MS,INST OSWALDO CRUZ,DEPT VIROL,RIO JANEIRO,BRAZIL. NR 18 TC 11 Z9 11 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 JAN PY 1993 VL 39 IS 1 BP 16 EP 22 DI 10.1002/jmv.1890390105 PG 7 WC Virology SC Virology GA KG413 UT WOS:A1993KG41300004 PM 8380839 ER PT J AU PASCALE, E LIU, C VALLE, E USDIN, K FURANO, AV AF PASCALE, E LIU, C VALLE, E USDIN, K FURANO, AV TI THE EVOLUTION OF LONG INTERSPERSED REPEATED DNA (L1, LINE 1) AS REVEALED BY THE ANALYSIS OF AN ANCIENT RODENT L1 DNA FAMILY SO JOURNAL OF MOLECULAR EVOLUTION LA English DT Article DE L1 FAMILY EVOLUTION; LINE FAMILY; LONG INTERSPERSED REPEATED DNA; ANCIENT L1 FAMILY; L1 FAMILY AMPLIFICATION ID ESTIMATING SEQUENCE DIVERGENCE; HUMAN TRANSPOSABLE ELEMENT; NUCLEOTIDE-SEQUENCE; STATISTICAL-METHODS; MOUSE; RAT; END; PSEUDOGENES; PROTEIN; AMPLIFICATION AB All modern mammals contain a distinctive, highly repeated (greater-than-or-equal-to 50,000 members) family of long interspersed repeated DNA called the L1 (LINE 1) family. While the modern L1 families were derived from a common ancestor that predated the mammalian radiation approximately 80 million years ago, most of the members of these families were generated within the last 5 million years. However, recently we demonstrated that modern murine (Old World rats and mice) genomes share an older long interspersed repeated DNA family that we called Lx. Here we report our analysis of the DNA sequence of Lx family members and the relationship of this family to the modern L1 families in mouse and rat. The extent of DNA sequence divergence between Lx members indicates that the Lx amplification occurred about 12 million years ago, around the time of the murine radiation. Parsimony analysis revealed that Lx elements were ancestral to both the modern rat and mouse L1 families. However, we found that few if any of the evolutionary intermediates between the Lx and the modern L1 families were extensively amplified. Because the modern L1 families have evolved under selective pressure, the evolutionary intermediates must have been capable of replication. Therefore, replication-competent L1 elements can reside in genomes without undergoing extensive amplification. We discuss the bearing of our findings on the evolution of L1 DNA elements and the mammalian genome. C1 NIDDKD,BIOCHEM PHARMACOL LAB,GENOM STRUCT & FUNCT SECT,BLDG 8,ROOM 203,BETHESDA,MD 20892. NR 51 TC 61 Z9 62 U1 0 U2 4 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2844 J9 J MOL EVOL JI J. Mol. Evol. PD JAN PY 1993 VL 36 IS 1 BP 9 EP 20 DI 10.1007/BF02407302 PG 12 WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity GA KC508 UT WOS:A1993KC50800002 PM 8433380 ER PT J AU LESCH, KP GROSS, J WOLOZIN, BL MURPHY, DL RIEDERER, P AF LESCH, KP GROSS, J WOLOZIN, BL MURPHY, DL RIEDERER, P TI EXTENSIVE SEQUENCE DIVERGENCE BETWEEN THE HUMAN AND RAT-BRAIN VESICULAR MONOAMINE TRANSPORTER - POSSIBLE MOLECULAR-BASIS FOR SPECIES-DIFFERENCES IN THE SUSCEPTIBILITY TO MPP+ SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Note DE HUMAN; RAT; VESICULAR MONOAMINE TRANSPORTER; CDNA; BRAIN; PLATELETS; MPP+ ID PARKINSONS-DISEASE; AMINE TRANSPORTER; TOXICITY AB A cDNA encoding the human brain vesicular monoamine transporter (VMT) was isolated and sequenced using PCR. The cDNA contains an open reading frame encoding a hydrophobic polypeptide of 514 amino acids with twelve membrane spanning segments, a calculated molecular weight of 55,709 Da, and an estimated isoelectrical point of 5.62. A structurally identical transporter is expressed in human platelets. Two intraplasmatic consensus phosphorylation sites of cAMP-dependent protein kinase recognition and two potential protein kinase C phosphorylation sites may be central to the regulation of the VMT. Although the human brain VMT is 90.7% homologous to the rat protein, an extensive sequence divergence occurs in the large luminal loop located between the first two transmembrane domains. This loop displays a remarkably reduced homology of 64.0% with several deletions and insertions, although four putative glycosylation sites are conserved. Since functional vesicular monoamine transport supresses MPP+ toxicity and sequence divergence in the large luminal loop of the VMT expressed in rat brain and adrenal medulla may play a role in differential neurotoxic effects of MPP+, our findings indicate one possible molecular basis for the substantial species differences in the suceptibility to MPP+ demonstrated among humans, non-human primates, and rodents. They are also likely to facilitate molecular pharmacologic and genetic investigations of the human VMT in neurodegenerative disorders. C1 NIMH,CTR CLIN,LCS,CLIN NEUROPHARMACOL SECT,BETHESDA,MD 20892. RP LESCH, KP (reprint author), UNIV WURZBURG,DEPT PSYCHIAT,FUCHSLEINSTR 15,D-97080 WURZBURG,GERMANY. RI Lesch, Klaus-Peter/J-4906-2013 OI Lesch, Klaus-Peter/0000-0001-8348-153X NR 12 TC 18 Z9 19 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1993 VL 93 IS 1 BP 75 EP 82 DI 10.1007/BF01244941 PG 8 WC Neurosciences SC Neurosciences & Neurology GA LN861 UT WOS:A1993LN86100009 PM 8373557 ER PT J AU LESCH, KP WOLOZIN, BL ESTLER, HC MURPHY, DL RIEDERER, P AF LESCH, KP WOLOZIN, BL ESTLER, HC MURPHY, DL RIEDERER, P TI ISOLATION OF A CDNA-ENCODING THE HUMAN BRAIN-SEROTONIN TRANSPORTER SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Note DE HUMAN; SEROTONIN TRANSPORTER; CDNA SEQUENCE; POLYMERASE CHAIN REACTION ID ANTIDEPRESSANTS; EXPRESSION; CLONING; BINDING AB A cDNA encoding a serotonin transporter (5-HTT) in the human dorsal raphe nucleus was isolated and sequenced using cross-species amplification of human 5-HTT partial cDNA by the polymerase chain reaction (PCR) and the RACE-PCR procedure, designed for rapid amplification of 3' and 5' cDNA ends. The cDNA contains an open reading frame encoding a hydrophobic polypeptide of 630 amino acids with a calculated molecular weight of approximately 70kDa. The human 5-HTT is approximately 92% homologous to the rat protein but contains an additional consensus phosphorylation site for cAMP-dependent protein kinase recognition located in the cytoplasmic N-terminal region, while a potential protein kinase C phosphorylation site identified in the rat homolog is not conserved in the human 5-HTT. Hydropathicity analysis revealed twelve membrane spanning segments, a topology proposed for other cloned sodium-dependent transporters. C1 NIMH,CTR CLIN,LCS,NEUROPHARMACOL SECT,BETHESDA,MD 20892. RP LESCH, KP (reprint author), UNIV WURZBURG,DEPT PSYCHIAT,FUCHSLEINSTR 15,W-8700 WURZBURG,GERMANY. RI Lesch, Klaus-Peter/J-4906-2013 OI Lesch, Klaus-Peter/0000-0001-8348-153X NR 10 TC 176 Z9 179 U1 0 U2 3 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1993 VL 91 IS 1 BP 67 EP 72 DI 10.1007/BF01244919 PG 6 WC Neurosciences SC Neurosciences & Neurology GA KM728 UT WOS:A1993KM72800006 PM 8452685 ER PT J AU DOUDET, DJ WYATT, RJ CANNONSPOOR, E SUDDATH, R MCLELLAN, CA COHEN, RM AF DOUDET, DJ WYATT, RJ CANNONSPOOR, E SUDDATH, R MCLELLAN, CA COHEN, RM TI 6-[F-18]FLUORO-L-DOPA AND CEREBRAL BLOOD-FLOW IN UNILATERALLY MPTP-TREATED MONKEYS SO JOURNAL OF NEURAL TRANSPLANTATION & PLASTICITY LA English DT Article DE BLOOD FLOW; F-18-DOPA; POSITRON EMISSION TOMOGRAPHY; MPTP; PARKINSONS DISEASE ID POSITRON EMISSION TOMOGRAPHY; BRAIN TRANSFER CONSTANTS; TIME UPTAKE DATA; DOPAMINERGIC-NEURONS; CHRONIC PARKINSONISM; GRAPHICAL EVALUATION; PET SCANS; METABOLISM; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; HEMIPARKINSONISM AB Intravenous administration of O-15-labeled water and 6-[F-18]-L-fluorodopa were used to assess abnormal striatal activity in monkeys after long-term recovery of unilateral lesions of the dopaminergic nigro-striatal system induced by the neurotoxin MPTP. PET data were examined in relation to behavioral and biological parameters. Cerebral blood flow and 6-[F-18]-L-DOPA uptake were found to be significantly reduced in the lesioned striatum, compared to the unaffected side and to normal controls. There was no correlation between cerebral blood flow and any of the behavioral parameters. The uptake rate constant of F-18-DOPA from blood to striatum and the ratios of striatum to occipital areas were highly correlated to the concentrations of homovanillic acid in the cerebrospinal fluid of the same animals but not to the rotational behavior. This MPTP-induced model of striatal dopamine deficiency in primates presents similarities with idiopathic Parkinson's disease and may be used to evaluate the effects of dopaminergic lesions and transplants on brain function. C1 NIMH,IRP,NEUROPSYCHIAT BRANCH,BETHESDA,MD 20892. RP DOUDET, DJ (reprint author), NIMH,LCM,IRP,CLIN BRAIN IMAGING SECT,BLDG 10-4N317,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 30 TC 8 Z9 9 U1 0 U2 0 PU FREUND PUBLISHING HOUSE PI LONDON PA STE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA SN 0792-8483 J9 J NEURAL TRANSP PLAS JI J. Neural Transplant. Plast. PD JAN-MAR PY 1993 VL 4 IS 1 BP 27 EP 38 PG 12 WC Neurosciences; Transplantation SC Neurosciences & Neurology; Transplantation GA MG887 UT WOS:A1993MG88700003 PM 7509198 ER PT J AU DEMEDINACELI, L WYATT, RJ AF DEMEDINACELI, L WYATT, RJ TI A METHOD FOR SHORTENING OF THE RAT SPINE AND ITS NEUROLOGIC CONSEQUENCES SO JOURNAL OF NEURAL TRANSPLANTATION & PLASTICITY LA English DT Article DE RAT; SPONDYLECTOMY; SPINAL CORD INJURY; THORACIC SPINE ID CORD AB Large laboratory animals are the usual choice for complex surgical procedures on the spine and spinal cord, such as shortening of the spine. It would, however, be advantageous to be able to use a small inexpensive mammal like the rat. We describe a procedure which allows thoracic spondylectomy (T8-T9) to be performed in the rat with a satisfactory survival rate (69%). Functional consequences of the procedure on animals with uninjured spinal cord were monitored over a period of six months, at which time histologic examination was performed. There was a good correlation between operative trauma, consisting of mechanical injury to the cord assessed from the surgical notes, and the duration of postoperative spinal shock. Animals for which the cord appeared laminated or deformed at the time of sacrifice tended to show incomplete functional recovery. Cord cavitation developed in most surviving animals (78%) but did not have a measurable adverse effect on functional outcome. In the present study, the cord was not intentionally injured; however, availability of this procedure may facilitate the future development of methods to implement recovery of function following spinal cord injury. RP DEMEDINACELI, L (reprint author), NIMH,CTR NEUROSCI,WAW BLDG,ST ELIZABETHS,WASHINGTON,DC 20032, USA. NR 32 TC 4 Z9 4 U1 0 U2 0 PU FREUND PUBLISHING HOUSE PI LONDON PA STE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA SN 0792-8483 J9 J NEURAL TRANSP PLAS JI J. Neural Transplant. Plast. PD JAN-MAR PY 1993 VL 4 IS 1 BP 39 EP 52 PG 14 WC Neurosciences; Transplantation SC Neurosciences & Neurology; Transplantation GA MG887 UT WOS:A1993MG88700004 PM 8110862 ER PT J AU DEEN, DF CHIARODO, A GRIMM, EA FIKE, JR ISRAEL, MA KUN, LE LEVIN, VA MARTON, LJ PACKER, RJ PEGG, AE ROSENBLUM, ML SUIT, HD WALKER, MD WIKSTRAND, CJ WILSON, CB WONG, AJ YUNG, WKA AF DEEN, DF CHIARODO, A GRIMM, EA FIKE, JR ISRAEL, MA KUN, LE LEVIN, VA MARTON, LJ PACKER, RJ PEGG, AE ROSENBLUM, ML SUIT, HD WALKER, MD WIKSTRAND, CJ WILSON, CB WONG, AJ YUNG, WKA TI BRAIN-TUMOR WORKING GROUP-REPORT ON THE 9TH INTERNATIONAL-CONFERENCE ON BRAIN-TUMOR RESEARCH AND THERAPY SO JOURNAL OF NEURO-ONCOLOGY LA English DT Review DE BRAIN TUMOR RESEARCH; BRAIN TUMOR THERAPY; POLYAMINES CELL KINETICS; RADIATION NECROSIS ID CENTRAL NERVOUS-SYSTEM; HYPERFRACTIONATED RADIATION-THERAPY; GROWTH-FACTOR RECEPTOR; PHASE-I-II; MALIGNANT GLIOMAS; GLIOBLASTOMA-MULTIFORME; MONOCLONAL-ANTIBODY; RECURRENT GLIOMAS; ALPHA-DIFLUOROMETHYLORNITHINE; PROGNOSTIC IMPORTANCE AB Proceedings of the 9th International Conference on Brain Tumor Research and Therapy: 1. Introduction; 2. Surgery; 3. Radiation therapy; 4. Chemotherapy; 5. Immunotherapy; 6. Growth-regulatory alterations; 7. Molecular genetics; 8. Brain tumor invasion; 9. Normal tissue damage; 10. Polyamines. C1 UNIV CALIF SAN FRANCISCO, SAN FRANCISCO, CA 94143 USA. NCI, BETHESDA, MD 20892 USA. UNIV TEXAS, MD ANDERSON CANC CTR, HOUSTON, TX USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN USA. CHILDRENS NATL MED CTR, WASHINGTON, DC USA. PENN STATE UNIV, MILTON S HERSHEY MED CTR, HERSHEY, PA 17033 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA USA. NINCDS, BETHESDA, MD USA. DUKE UNIV, DURHAM, NC USA. FOX CHASE CANC CTR, PHILADELPHIA, PA 19111 USA. NR 149 TC 46 Z9 46 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PY 1993 VL 16 IS 3 BP 243 EP 272 DI 10.1007/BF01057041 PG 30 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA ME927 UT WOS:A1993ME92700010 PM 7905510 ER PT J AU ALTSCHULER, RA KURIYAMA, H WENTHOLD, RJ AF ALTSCHULER, RA KURIYAMA, H WENTHOLD, RJ TI COCHLEAR NEUROTRANSMITTERS - RECEPTORS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 UNIV MICHIGAN,KRESGE HEARING RES INST,ANN ARBOR,MI 48109. NIDCD,NEUROCHEM 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S234 EP S234 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500925 ER PT J AU BRENNEMAN, DE AVIDOR, R GOZES, I AF BRENNEMAN, DE AVIDOR, R GOZES, I TI INTERLEUKIN-1 AND VASOACTIVE-INTESTINAL-PEPTIDE - PARTNERS IN CNS NEUROTROPHISM SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892. TEL AVIV UNIV,DEPT CHEM PATHOL,IL-69978 TEL AVIV,ISRAEL. 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S188 EP S188 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500742 ER PT J AU BUONANNO, A WONG, L PARTIN, K WINTERS, C MAYER, ML AF BUONANNO, A WONG, L PARTIN, K WINTERS, C MAYER, ML TI MOLECULAR COMPOSITION OF GLUTAMATE RECEPTORS CONFERS UNIQUE ELECTROPHYSIOLOGICAL PROPERTIES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,LDN,MOLEC NEUROBIOL UNIT,BETHESDA,MD 20892. NIH,CELLULAR & MOLEC NEUROPHYSIOL,BETHESDA,MD 20892. RI Mayer, Mark/H-5500-2013; Partin, Kathryn/A-8706-2015 OI Partin, Kathryn/0000-0003-3801-3299 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S260 EP S260 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56501023 ER PT J AU CERRUTI, C PILOTTE, N UHL, G KUHAR, MJ AF CERRUTI, C PILOTTE, N UHL, G KUHAR, MJ TI WITHDRAWAL OF COCAINE REDUCES THE DOPAMINE TRANSPORTER MESSENGER-RNA EXPRESSION IN 2 VENTRAL TEGMENTAL AREA SUBNUCLEI SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIDA,ARC,MOL PHARMACOL LABS,BALTIMORE,MD 21224. NIDA,ARC,MOL NEUROBIOL LABS,BALTIMORE,MD 21224. 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S69 EP S69 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500268 ER PT J AU DEGEORGE, J CHANG, M NARIAI, T RAPOPORT, SI AF DEGEORGE, J CHANG, M NARIAI, T RAPOPORT, SI TI USE OF REGIONAL IN-VIVO INCORPORATION OF FATTY-ACIDS TO ASSESS BRAIN STRUCTURE AND FUNCTION SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,LNS,BETHESDA,MD 20014. 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S57 EP S57 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500223 ER PT J AU ERICKSON, JD EIDEN, LE AF ERICKSON, JD EIDEN, LE TI MOLECULAR-CLONING AND EXPRESSION OF A HUMAN VESICULAR H+/ MONOAMINE ANTIPORTER SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CELL BIOL LAB,MOLEC NEUROSCI SECT,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S24 EP S24 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500094 ER PT J AU GALLO, V PATNEAU, D MAYER, M VACCARINO, F CURTIS, J RUSSELL, J AF GALLO, V PATNEAU, D MAYER, M VACCARINO, F CURTIS, J RUSSELL, J TI GLUTAMATE RECEPTORS IN GLIAL PROGENITOR CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,CELL & MOLEC NEUROPHYSIOL,BETHESDA,MD. YALE UNIV,YALE CHILD STUDY CTR,NEW HAVEN,CT 06520. RI Mayer, Mark/H-5500-2013 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S259 EP S259 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56501021 ER PT J AU GALLO, V PATNEAU, D MAYER, M CURTIS, J RUSSELL, J AF GALLO, V PATNEAU, D MAYER, M CURTIS, J RUSSELL, J TI GLUTAMATE RECEPTORS IN GLIAL PROGENITOR CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,CELL & MOL NEUROPHYSIOL LAB,BETHESDA,MD 20892. RI Mayer, Mark/H-5500-2013 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S61 EP S61 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500235 ER PT J AU GOZES, I GLOWA, J BRENNEMAN, DE MCCUNE, SK LEE, E WESTPHAL, H AF GOZES, I GLOWA, J BRENNEMAN, DE MCCUNE, SK LEE, E WESTPHAL, H TI VIP FUNCTION ASSESSED BY MOLECULAR-GENETIC TECHNIQUES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 TEL AVIV UNIV,SACKLER SCH MED,TEL AVIV,ISRAEL. NIMH,BETHESDA,MD 20892. NICHHD,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S86 EP S86 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500334 ER PT J AU KAUFMAN, E DRISCOLL, B AF KAUFMAN, E DRISCOLL, B TI EVIDENCE FOR COOPERATIVITY BETWEEN NEURONS AND ASTROGLIA IN THE REGULATION OF CO2 FIXATION IN-VITRO SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S243 EP S243 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500956 ER PT J AU KONIG, N PARIAT, M DRIAN, MJ SERRANO, P WENTHOLD, RJ AF KONIG, N PARIAT, M DRIAN, MJ SERRANO, P WENTHOLD, RJ TI AMPA RECEPTOR PROTEINS ARE DETECTABLE VERY EARLY ALONG LONGITUDINAL BOUNDARIES IN THE EMBRYONIC HINDBRAIN AND UPPER SPINAL-CORD SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 EPHE,INSERM,U336,F-34095 MONTPELLIER,FRANCE. NIDCD,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S9 EP S9 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500033 ER PT J AU LESTER, DS OLDS, JL SCHREURS, BG ALKON, DL AF LESTER, DS OLDS, JL SCHREURS, BG ALKON, DL TI INCORPORATION AND METABOLISM OF A FLUORESCENT PHOSPHOLIPASE SUBSTRATE INTO LIVING BRAIN-SLICES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,NEURAL SYST SECT,BETHESDA,MD 20892. RI Olds, James/D-2867-2011 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S57 EP S57 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500224 ER PT J AU MADELIAN, V LAVIGNE, E MANGANIELLO, V GUSOVSKY, F AF MADELIAN, V LAVIGNE, E MANGANIELLO, V GUSOVSKY, F TI DIFFERENT PKCS REGULATE DIFFERENT CYCLIC-NUCLEOTIDE PHOSPHODIESTERASES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,ALBANY,NY 12201. NIH,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S219 EP S219 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500868 ER PT J AU MCBAIN, CJ DINGLEDINE, R AF MCBAIN, CJ DINGLEDINE, R TI AMPA RECEPTOR-MEDIATED SPONTANEOUS EPSCS IN CA3 HIPPOCAMPAL INTERNEURONS - MULTIPLE RECEPTOR SUBTYPES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,LCMN,BETHESDA,MD 20892. EMORY UNIV,SCH MED,DEPT PHARMACOL,ATLANTA,GA 30322. RI dingledine, Ray/F-5173-2011 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S262 EP S262 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56501033 ER PT J AU MCKENNA, MC ZECH, L TILDON, JT ZIELKE, HR AF MCKENNA, MC ZECH, L TILDON, JT ZIELKE, HR TI A COMPUTER-MODEL OF C-14 GLUTAMATE METABOLISM IN PRIMARY CULTURES OF RAT-BRAIN ASTROCYTES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. NIH,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S228 EP S228 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500902 ER PT J AU MURPHY, DL CHIUEH, CC ANDREWS, AM GRADY, TA BROOCKS, A PIGOTT, TA AF MURPHY, DL CHIUEH, CC ANDREWS, AM GRADY, TA BROOCKS, A PIGOTT, TA TI SEROTONERGIC-DOPAMINERGIC INTERACTIONS IN NEUROTOXICITY AND NEUROPROTECTION SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Andrews, Anne/B-4442-2011 OI Andrews, Anne/0000-0002-1961-4833 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S116 EP S116 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500457 ER PT J AU NOWAK, G LAYER, RT SKOLNICK, P PAUL, IA AF NOWAK, G LAYER, RT SKOLNICK, P PAUL, IA TI ADAPTATION OF THE N-METHYL-D-ASPARTATE RECEPTOR FOLLOWING CHRONIC ANTIDEPRESSANTS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. NR 2 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S51 EP S51 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500200 ER PT J AU PARADA, LF AF PARADA, LF TI TRK NEUROTROPHIN RECEPTORS - IMPORTANT REGULATORS OF VERTEBRATE DEVELOPMENT SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. RI Parada, luis/B-9400-2014 NR 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S58 EP S58 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500225 ER PT J AU RAYMOND, J MONIOT, B DEMEMES, D WENTHOLD, RJ DECHESNE, CJ AF RAYMOND, J MONIOT, B DEMEMES, D WENTHOLD, RJ DECHESNE, CJ TI IMMUNOCYTOCHEMICAL LOCALIZATION OF AMPA SELECTIVE GLUTAMATE-RECEPTOR SUBUNITS IN THE VESTIBULAR NUCLEI OF THE RAT SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 USTL,INSERM,U254,F-34095 MONTPELLIER,FRANCE. NIDCD,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S262 EP S262 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56501032 ER PT J AU SOKOLOFF, L AF SOKOLOFF, L TI SITES AND MECHANISMS OF CHANGES IN LOCAL ENERGY-METABOLISM IN NEURAL TISSUES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S241 EP S241 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500949 ER PT J AU STEPHENS, R RABIN, S GREENE, L THIELE, C KAPLAN, DR AF STEPHENS, R RABIN, S GREENE, L THIELE, C KAPLAN, DR TI NEURONAL SIGNAL-TRANSDUCTION BY TRK/NGF RECEPTORS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. COLUMBIA UNIV,NEW YORK,NY 10027. NCI,FCRDC,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S120 EP S120 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500471 ER PT J AU TRULLAS, R FAIMAN, CP VIU, EP SKOLNICK, P AF TRULLAS, R FAIMAN, CP VIU, EP SKOLNICK, P TI ANTIDEPRESSANT PROPERTIES OF FUNCTIONAL ANTAGONISTS AT THE NMDA RECEPTOR COMPLEX SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 CSIC,CID,DEPT NEUROCHEM,E-08034 BARCELONA,SPAIN. NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. RI Trullas, Ramon/D-2197-2016 OI Trullas, Ramon/0000-0001-7951-9881 NR 0 TC 0 Z9 0 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S50 EP S50 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500199 ER PT J AU WASCHEK, JA AGOSTON, D AF WASCHEK, JA AGOSTON, D TI TRANSCRIPTIONAL CONTROL OF THE HUMAN AND MOUSE VASOACTIVE-INTESTINAL-PEPTIDE GENES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. NICHHD,DEV NEUROBIOL 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S67 EP S67 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500259 ER PT J AU WENTHOLD, RJ PETRALIA, RS ZHU, WS AF WENTHOLD, RJ PETRALIA, RS ZHU, WS TI BIOCHEMICAL-PROPERTIES OF GLUTAMATE RECEPTORS DETERMINED WITH SUBUNIT-SPECIFIC ANTIBODIES SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIDCD,NEUROCHEM 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S259 EP S259 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56501020 ER PT J AU WENTHOLD, RJ PETRALIA, RS ZHU, WS AF WENTHOLD, RJ PETRALIA, RS ZHU, WS TI SUBUNIT-SPECIFIC ANTIBODIES TO STUDY THE STRUCTURE AND DISTRIBUTION OF GLUTAMATE RECEPTORS SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIDCD,NEUROCHEM 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 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1993 VL 61 SU S BP S123 EP S123 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA LM565 UT WOS:A1993LM56500484 ER PT J AU SAITO, K NOWAK, TS MARKEY, SP HEYES, MP AF SAITO, K NOWAK, TS MARKEY, SP HEYES, MP TI MECHANISM OF DELAYED INCREASES IN KYNURENINE PATHWAY METABOLISM IN DAMAGED BRAIN-REGIONS FOLLOWING TRANSIENT CEREBRAL-ISCHEMIA SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE INDOLEAMINE-2,3-DIOXYGENASE; KYNURENINASE; KYNURENINE 3-HYDROXYLASE; 3-HYDROXYANTHRANILATE-3,4-DIOXYGENASE; KYNURENINE TRANSAMINASE; QUINOLINIC ACID; CEREBRAL ISCHEMIA; INFLAMMATION; MACROPHAGES; GERBIL; BRAIN ID CENTRAL NERVOUS-SYSTEM; QUINOLINIC ACID CONCENTRATIONS; CEREBROSPINAL-FLUID; HUNTINGTONS-DISEASE; RAT-BRAIN; INDOLEAMINE 2,3-DIOXYGENASE; FOREBRAIN ISCHEMIA; GERBIL BRAIN; NEURONAL DEGENERATION; CELL-PROLIFERATION AB Delayed increases in the levels of an endogenous N-methyl-D-aspartate receptor agonist, quinolinic acid (QUIN), have been demonstrated following transient ischemia in the gerbil and were postulated to be secondary to induction of indoleamine-2,3-dioxygenase (IDO) and other enzymes of the L-tryptophan-kynurenine pathway. In the present study, proportional increases in IDO activity and QUIN concentrations were found 4 days after 10 min of cerebral ischemia, with both responses in hippocampus > striatum > cerebral cortex > thalamus. These increases paralleled the severity of local brain injury and inflammation. IDO activity and QUIN concentrations were unchanged in the cerebellum of postischemic gerbils, which is consistent with the preservation of blood flow and resultant absence of pathology in this region. Blood QUIN and L-kynurenine concentrations were not affected by ischemia. Brain tissue QUIN levels at 4 days postischemia exceeded blood concentrations, minimizing a role for breakdown of the blood-brain barrier. Marked increases in the activity of kynureninase, kynurenine 3-hydroxylase, and 3-hydroxyanthranilate-3,4-dioxygenase were also detected in hippocampus but not in cerebellum on day 4 of recirculation. In vivo synthesis of [C-13(6)]QUIN was demonstrated, using mass spectrometry, in hippocampus but not in cerebellum of 4-day postischemic animals 1 h after intracisternal administration Of L-[C-13(6)]tryptophan. However, accumulation of QUIN was demonstrated in both cerebellum and hippocampus of control gerbils following an intracisternal injection of 3-hydroxyanthranilic acid, which verifies the availability of precursor to both regions when administered intracisternally. Notably, although IDO activity and QUIN concentrations were unchanged in the cerebellum of ischemic gerbils, both IDO activity and QUIN content were increased in cerebellum to approximately the same degree as in hippocampus, striatum, cerebral cortex, and thalamus 24 h after immune stimulation by systemic pokeweed mitogen administration, demonstrating that the cerebellum can increase IDO activity and QUIN content in response to immune activation. No changes in kynurenic acid concentrations in either hippocampus, cerebellum, or cerebrospinal fluid were observed in the postischemic gerbils compared with controls, in accordance with the unaffected activity of kynurenine aminotransferase activity. Collectively, these results support roles for IDO, kynureninase, kynurenine 3-hydroxylase, and 3-hydroxyanthranilate-3,4-dioxygenase in accelerating the conversion Of L-tryptophan and other substrates to QUIN in damaged brain regions following transient cerebral ischemia. Immunocytochemical results demonstrated the presence of macrophage infiltrates in hippocampus and other brain regions that parallel the extent of these biochemical changes. We hypothesize that increased kynurenine pathway metabolism after ischemia reflects the presence of macrophages and other reactive cell populations at sites of brain injury. C1 NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BLDG 10,ROOM 3D40,BETHESDA,MD 20892. NINCDS,STROKE BRANCH,BETHESDA,MD 20892. NR 65 TC 145 Z9 147 U1 1 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1993 VL 60 IS 1 BP 180 EP 192 DI 10.1111/j.1471-4159.1993.tb05836.x PG 13 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KD041 UT WOS:A1993KD04100021 PM 8417138 ER PT J AU PENNYPACKER, KR WALCZAK, D THAI, L FANNIN, R MASON, E DOUGLASS, J HONG, JS AF PENNYPACKER, KR WALCZAK, D THAI, L FANNIN, R MASON, E DOUGLASS, J HONG, JS TI KAINATE-INDUCED CHANGES IN OPIOID PEPTIDE GENES AND AP-1 PROTEIN EXPRESSION IN THE RAT HIPPOCAMPUS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE GENE REGULATION; HIPPOCAMPUS; KAINATE; OPIOID PEPTIDES; SEIZURES; TRANSCRIPTION FACTORS ID ENKEPHALIN-LIKE IMMUNOREACTIVITY; TRANSCRIPTION FACTOR AP-1; ACID-INDUCED SEIZURES; IMMEDIATE-EARLY GENES; C-FOS; MESSENGER-RNA; JUN ENCODES; CYCLIC AMP; PROENKEPHALIN; BRAIN AB In the rat hippocampus, jun, c-fos, and fos-related antigen immunoreactivity, AP-1 DNA binding, and opioid peptide gene expression were examined after kainate treatment to determine whether the induction and DNA binding of AP-1 transcription factors are correlated with the expression of the opioid peptide genes. One and one-half hours after kainate administration, fos-related antigen and jun immunoreactivity and AP-1 DNA binding were induced; maximal elevation was observed after 4.5 h. Transcription factor expression and DNA binding increased in a dose-dependent manner. Preprodynorphin and preproenkephalin mRNA induction was also dose dependent. The anticonvulsants, pentobarbital and diazepam, effectively blocked electroencephalographic seizure activity caused by kainate treatment, whereas valproic acid was approximately 50% effective. Opioid peptide gene expression, fos-related antigen and jun immunoreactivity, and AP-1 DNA binding all reflected similar reductions after anticonvulsant treatment. Therefore, expression and DNA binding activity of the AP-1 transcription factors are correlated with opioid peptide gene expression in the rat hippocampus. C1 SOLVAY PHARMACEUT,MARIETTA,GA. OREGON HLTH SCI UNIV,VOLLUM INST,PORTLAND,OR 97201. RP PENNYPACKER, KR (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,MD 14-06,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Pennypacker, Keith/I-5092-2012 NR 34 TC 63 Z9 63 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1993 VL 60 IS 1 BP 204 EP 211 DI 10.1111/j.1471-4159.1993.tb05839.x PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KD041 UT WOS:A1993KD04100024 PM 8417141 ER PT J AU DACUNHA, A JEFFERSON, JA JACKSON, RW VITKOVIC, L AF DACUNHA, A JEFFERSON, JA JACKSON, RW VITKOVIC, L TI GLIAL CELL-SPECIFIC MECHANISMS OF TGF-BETA-1 INDUCTION BY IL-1 IN CEREBRAL-CORTEX SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE PATHOGENESIS; ASTROCYTES; OLIGODENDROCYTES; MICROGLIA; CYTOKINES ID GROWTH-FACTOR-BETA; IMMUNE-DEFICIENCY-SYNDROME; CENTRAL-NERVOUS-SYSTEM; FACTOR MESSENGER-RNA; RAT SCHWANN-CELLS; CULTURED ASTROCYTES; INTERLEUKIN-1; BRAIN; LOCALIZATION; FACTOR-BETA-1 AB Transforming growth factor beta-1 (TGF-beta1) immunoreactive product (IRP) has recently been detected in autopsied brains of individuals who died with central nervous system diseases and/or fever but not in normal individuals or in normal rodent brain. However, the mechanism(s) of induction of TGF-beta1 in brain and the identity of cells expressing TGF-beta1 need to be understood before a role, if any, for this potent pleiotropic cytokine in neuropathogenesis can be discerned. Towards this end we determined that IL-1 stimulated the production of TGF-beta1 IRP in cells and TGF-beta1 activity in culture fluids of all glial cells, astrocytes, microglial cells, and oligodendrocytes, derived from neonatal rat cortex and grown in cell type-enriched cultures. TGF-beta1 production in vitro varied with the cell type and isoform of IL-1. Oligodendrocytes produced the most and astrocytes the least amount of TGF-beta1. IL-1alpha stimulated TGF-beta1 production in all glial cell types, whereas IL-1beta did not. In vivo, TGF-beta1 IRP was detected in human tissues from cerebral frontal cortex and subcortical white matter only when interleukin-1 (IL-1) was elevated in the same tissues. Moreover, the amount of detectable TGF-beta1 was positively correlated with the amount of detectable IL-1 (rho = 0.605; P = 0.003), as determined by morphometry. Double-labelling of cells for their phenotypic markers and expression of TGF-beta1 indicated that all glial cells, but not neurons, expressed TGF-beta1. IL-1alpha and IL-1beta IRPs were also detected in all three glial cell types, most frequently in astrocytes and least frequently in microglial cells. The cells containing both cytokine IRPs were also detected. These results indicate that TGF-beta1 may be induced by IL-1 in all glial cells of the frontal cortex, by both autocrine and paracrine mechanisms. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 62 TC 130 Z9 133 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD JAN PY 1993 VL 42 IS 1 BP 71 EP 86 DI 10.1016/0165-5728(93)90214-J PG 16 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA KJ766 UT WOS:A1993KJ76600009 PM 8423208 ER PT J AU BELCHEVA, M BARG, J ROWINSKI, J CLARK, WG GLOECKNER, CA HO, A GAO, XM CHUANG, DM COSCIA, C AF BELCHEVA, M BARG, J ROWINSKI, J CLARK, WG GLOECKNER, CA HO, A GAO, XM CHUANG, DM COSCIA, C TI NOVEL OPIOID BINDING-SITES ASSOCIATED WITH NUCLEI OF NG108-15 NEUROHYBRID CELLS SO JOURNAL OF NEUROSCIENCE LA English DT Article DE OPIOID RECEPTOR; NUCLEUS; NEUROHYBRID CELLS; SUBCELLULAR FRACTIONATION; OPIOID PEPTIDE; IMMUNOHISTOCHEMISTRY ID EPIDERMAL GROWTH-FACTOR; OPIATE RECEPTOR-BINDING; RAT-BRAIN; HYBRID-CELLS; PERTUSSIS TOXIN; MEMBRANE; TRANSPORT; LOCALIZATION; SYSTEMS; IDENTIFICATION AB Nuclear opioid binding sites have been discovered in NG108-15 neurohybrid cells. Marker enzyme analyses as well as electron and fluorescence microscopy studies attested to the high degree of purity of the nuclear preparations. Immunohistochemical studies on cryostat sections of NG108-15 cells with an antibody to the opioid receptor corroborated a nuclear localization. H-3-[D-Pen2,D-Pen5]enkephalin (H-3-DPDPE), H-3-[D-Ala2,D-Leu5]enkephalin (H-3-DADLE), and H-3-diprenorphine binding parameters, K(d) and B(max) values, and heterologous competition binding and stereospecificity data satisfied criteria for the presence of delta-opioid sites in purified nuclear preparations. Neither mu-([D-Ala2,mephe4,gly-ol5] enkephalin), dihydromorphine, nor K-(U69593) specific binding was detectable in purified nuclear preparations. Rates of association and dissociation of H-3-[D-Ser2,L-Leu5]enkephalyl-Thr were comparable to values obtained previously for opioid receptors. Opioid binding was also shown in subnuclear preparations from NG108-15 cell cultures. Agonists, H-3-DADLE and H-3-DPDPE, bind with high affinity to nuclear membranes and with lower affinity to chromatin. In contrast, partial agonist H-3-diprenorphine high-affinity binding sites were predominant in chromatin, while low-affinity binding was found in the nuclear membrane. Accordingly, 5'-guanylylimidodiphosphate sensitivity of H-3-DADLE binding was detected in nuclear membranes but not in chromatin. Both agonist and partial agonist opioid binding to nuclear membrane and chromatin were abolished upon cycloheximide treatment of NG108-15 cells. Taken together, the results suggest that NG108-15 cells contain newly synthesized GTP binding regulatory protein (G-protein)-coupled delta-opioid receptors in nuclear membranes and uncoupled opioid binding sites in chromatin. C1 ST LOUIS UNIV,SCH MED,EA DOISY DEPT BIOCHEM & MOLEC BIOL,ST LOUIS,MO 63104. NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. NR 60 TC 41 Z9 42 U1 0 U2 0 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 JAN PY 1993 VL 13 IS 1 BP 104 EP 114 PG 11 WC Neurosciences SC Neurosciences & Neurology GA KG659 UT WOS:A1993KG65900009 PM 8423466 ER PT J AU NEALE, EA BOWERS, LM SMITH, TG AF NEALE, EA BOWERS, LM SMITH, TG TI EARLY DENDRITE DEVELOPMENT IN SPINAL-CORD CELL-CULTURES - A QUANTITATIVE STUDY SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE FRACTAL DIMENSION; DEVELOPMENT; NEURONAL CULTURES; SHOLL ANALYSIS; MORPHOLOGIC COMPLEXITY; DENDRITE BRANCHING ID UNDERLYING NEURITE OUTGROWTH; FRACTAL ANALYSIS; VERTEX ANALYSIS; NEURONAL SHAPE; EDGE-DETECTION; RAT; CEREBELLUM; GROWTH; IMAGES; TREES AB Neurons in dissociated cell culture provide a favorable system for the quantitative analysis of structural changes and the examination of structure-function relationships during development. Fragment C of tetanus toxin was used to label neurons in murine spinal cord cell cultures and dendrite outgrowth was monitored by a number of measures. The dissociated neurons increased in morphologic complexity from approximate spheres to highly branched structures during the first week in culture. Much of the structural complexity of the dendrite arbor, as quantified by fractal dimension, was established within 48 hr after plating, i.e., prior to the development of interneuronal contacts. During the first few days in culture, dendrite branching complexity increased more rapidly than dendrite size, whereas after 4 days, fractal dimension remained relatively constant while dendrites continued to grow. Fractal analysis has provided data which suggest that the early development of dendrite branching complexity is determined intrinsically. Fractal dimension, as an effective index of morphologic complexity, should be a useful tool for the further study of extrinsic signals which might modify the generation or stabilization of dendrite form. C1 NINCDS,NEUROPHYSIOL LAB,BETHESDA,MD 20892. RP NEALE, EA (reprint author), NICHHD,DEV NEUROBIOL LAB,BLDG 36,ROOM 2A21,BETHESDA,MD 20892, USA. NR 45 TC 62 Z9 64 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 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD JAN 1 PY 1993 VL 34 IS 1 BP 54 EP 66 DI 10.1002/jnr.490340107 PG 13 WC Neurosciences SC Neurosciences & Neurology GA KF232 UT WOS:A1993KF23200006 PM 8423636 ER PT J AU SANDROCK, D MERINO, MJ NORTON, JA NEUMANN, RD AF SANDROCK, D MERINO, MJ NORTON, JA NEUMANN, RD TI ULTRASTRUCTURAL HISTOLOGY CORRELATES WITH RESULTS OF THALLIUM-201/TECHNETIUM-99M PARATHYROID SUBTRACTION SCINTIGRAPHY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID OXYPHIL CELL ADENOMAS; LOCALIZATION; HYPERPARATHYROIDISM; TL-201; ANTIBODIES; GLANDS; LESIONS; SCAN AB Specimens from 15 scintigraphically true-positive adenomas (golden standard: histology), 15 false-negative adenomas, 15 true-positive hyperplasias, 15 false-negative hyperplasias, 15 true-negative normal glands from patients with hyperparathyroidism, and 15 normal glands from patients without hyperparathyroidism, all selected randomly, were studied. After fixation, sectioning and H and E staining, in all 90 tissues the number of oxyphil, chief, and clear cells was counted in five randomly selected squares (103 x 103 mum). In 30 tissues, the number of mitochondria per cell was counted in five randomly selected cells from each lesion in transmission electron photomicrographs. Total cell counts in each group and number of chief cells showed no correlation with lesion detectability by scintigraphy. However, true-positive lesions had a significantly higher number of oxyphil cells than false-negative or normal glands. Twenty-one of 30 true-positive lesions had a oxyphil-to-clear cell ratio > 1; in contrast to only two of 30 false-negative lesions and 0 of 30 normal glands (p < 0.0005). The number of mitochondria per cell was higher in oxyphil cells in true-positive lesions (adenomas: 155 +/- 58, hyperplasias: 55 +/- 18) than in chief or clear cells in false-negative or normal lesions (30 +/- 15, p < 0.001). Our data suggest that the detectability of abnormal parathyroid glands by Tl-201/Tc-99m subtraction scintigraphy is in part dependent upon the presence of mitochondria-rich oxyphil cells. C1 NCI,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,PATHOL LAB,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 34 TC 53 Z9 53 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 JAN PY 1993 VL 34 IS 1 BP 24 EP 29 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KE715 UT WOS:A1993KE71500009 PM 8418265 ER PT J AU BHATHENA, SJ BERLIN, E JUDD, JT LAW, JS CASTRO, JS BHAGAVAN, HN BALLARDBARBASH, R NAIR, PP AF BHATHENA, SJ BERLIN, E JUDD, JT LAW, JS CASTRO, JS BHAGAVAN, HN BALLARDBARBASH, R NAIR, PP TI PLASMA OPIOID-PEPTIDES AND ACTH RESPONSES TO FISH OIL AND VITAMIN-E SUPPLEMENTATION IN MALE-SUBJECTS SO JOURNAL OF NUTRITIONAL BIOCHEMISTRY LA English DT Note DE FISH OIL FEEDING; OMEGA-3 FATTY ACIDS; VITAMIN-E; BETA-ENDORPHIN; ENKEPHALINS; ACTH ID REGIONAL BLOOD-FLOW; BETA-ENDORPHIN; DIABETES-MELLITUS; FATTY-ACIDS; CARDIOVASCULAR-DISEASE; GLUCOSE-HOMEOSTASIS; LIPOLYTIC-ACTIVITY; INSULIN; RAT; ENKEPHALINS AB Fish oils, high in omega-3 fatty acids, affect lipid and carbohydrate metabolism partly through their effects on the levels of hormones involved in their metabolism. Recently, a role for opiates in glucose homeostasis and lipid metabolism has been reported. It is possible that some of the effects of fish oils on carbohydrate and lipid metabolism may be, in part, mediated through changes in opiates. We therefore studied the effects of fish od and fish oil plus vitamin E, a potent antioxidant, on plasma opiates and adrenocorticotrophic hormone (ACTH) in normal subjects. Forty healthy men consumed diets providing 40% of energy from fat and a minimum of 25 mg vitamin E for 28 weeks. During the first 10 weeks, diets were supplemented with placebo, 15 g mixed fat/day. During the second 10 weeks, placebo was replaced by 15 g/day of fish oil concentrate. During the last 8 weeks, 200 U/day of vitamin E was added to fish oil. Plasma opioid peptides were measured by radioimmunoassay after eluting from C18 Sep-Pak cartridges. Fish oil feeding significantly decreased plasma beta-endorphin compared with placebo, but had no significant effects on plasma ACTH, met-, and leu-enkephalins. Fish oil plus vitamin E appeared to further decrease beta-endorphin and significantly increased both enkephalins. Thus, it is possible that in addition to hormonal changes, alterations in opiate tone may also partly explain the effect of fish oil and vitamin E on plasma glucose, triglyceride, and other metabolic and physiologic processes. C1 USDA,BELTSVILLE HUMAN NUTR RES CTR,LIPID NUTR LAB,BELTSVILLE,MD. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. RP BHATHENA, SJ (reprint author), USDA,BHNRC,CARBOHYDRATE NUTR LAB,BLDG 307 E,ROOM 311,BELTSVILLE,MD 20705, USA. NR 30 TC 0 Z9 0 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0955-2863 J9 J NUTR BIOCHEM JI J. Nutr. Biochem. PD JAN PY 1993 VL 4 IS 1 BP 45 EP 48 DI 10.1016/0955-2863(93)90019-S PG 4 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA KF875 UT WOS:A1993KF87500007 ER PT J AU SHIELDS, PG AF SHIELDS, PG TI INHERITED FACTORS AND ENVIRONMENTAL EXPOSURES IN CANCER RISK SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Article ID N-ACETYLTRANSFERASE PHENOTYPES; FRAGMENT-LENGTH-POLYMORPHISM; ACID-DEPENDENT ACYLTRANSFERASES; URINARY-BLADDER CARCINOGENESIS; L-MYC GENE; LUNG-CANCER; P53 GENE; ACETYLATION PHENOTYPE; CIGARETTE-SMOKING; HUMAN-LIVER AB Carcinogenesis is a multistage process that results from the interaction of carcinogenic exposures, cellular macromolecules (eg, DNA), and endogenous mutational mechanisms. Involved in these processes are metabolic activation and detoxification of chemical carcinogens, genetic sequences of protooncogenes and tumor suppressor genes, and DNA repair, among others. Each of these vary widely among individuals and can be associated with increased cancer risk. Cytochrome P4501A1, P4502E1 and N-acetyl transferase 2 are examples of enzymes involved in the metabolic activation of potential environmental carcinogens such as polycyclic aromatic hydrocarbons, benzene, and aromatic amines, respectively. Germ-line mutations in these genes are common and associated with abnormal enzymatic function that are mechanistically related to quantitative changes in binding of carcinogens to DNA. Allelic frequencies for these mutations vary among different racial and ethnic populations and may explain, in part, differences in cancer rates. Risk assessments attempt to predict cancer rates in humans using mathematical models that are often based upon limited experimental data. They do not generally incorporate the numerous stages of carcinogenesis or interindividual variation. Thus, sensitive and resistant populations are not sufficiently considered. This limits the accuracy of currently applied risk assessment models. RP SHIELDS, PG (reprint author), NCI,DIV CANC ETIOL,HUMAN CARCINOGENESIS LAB,BLDG 37,ROOM 2C16,BETHESDA,MD 20892, USA. RI Shields, Peter/I-1644-2012 NR 97 TC 20 Z9 20 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 JAN PY 1993 VL 35 IS 1 BP 34 EP 41 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KF929 UT WOS:A1993KF92900010 PM 8423501 ER PT J AU ROTTEM, M FAUCI, AS HALLAHAN, CW KERR, GS LEBOVICS, R LEAVITT, RY HOFFMAN, GS AF ROTTEM, M FAUCI, AS HALLAHAN, CW KERR, GS LEBOVICS, R LEAVITT, RY HOFFMAN, GS TI WEGENER GRANULOMATOSIS IN CHILDREN AND ADOLESCENTS - CLINICAL PRESENTATION AND OUTCOME SO JOURNAL OF PEDIATRICS LA English DT Article AB We prospectively studied and compared clinical features, treatment, course of illness, and long-term morbidity and mortality rates for Wegener granulomatosis in 23 childhood-onset patients with those of 135 adult-onset patients who were studied concurrently. Treatment was usually provided with glucocorticoids and cyclophosphamide. The mean follow-up period was 8.7 years for childhood-onset and 7.6 years for adult-onset Wegener granulomatosis. Most aspects of Wegener granulomatosis were similar in childhood-onset and adult-onset patients. Permanent morbidity from disease occurred in 86% of both groups. However, some features were significantly different. Wegener granulomatosis in childhood-onset patients was complicated five times more often by subglottic stenosis and twice as often by nasal deformity. Treatment-related permanent morbidity occurred in 22% of childhood-onset patients and 45% of adult-onset patients. After similar periods of cyclophosphamide therapy and follow-up, cyclophosphamide-related malignancies were less likely (0% vs 11%) to have developed in childhood-onset patients. Although 89% of patients treated with glucocorticoids and cyclophosphamide had remission, prolonged delay in achieving remission and relapses led in both patient groups to freedom from active disease for approximately 50% of the total patient-years. As a result, morbidity was substantial and has led to comparative studies of alternative therapies. C1 NIAID, CLIN INVEST LAB, BETHESDA, MD 20892 USA. NIAID, IMMUNOREGULAT, BETHESDA, MD 20892 USA. NIDCD, BETHESDA, MD USA. NR 17 TC 135 Z9 144 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD JAN PY 1993 VL 122 IS 1 BP 26 EP 31 DI 10.1016/S0022-3476(05)83482-1 PG 6 WC Pediatrics SC Pediatrics GA KG341 UT WOS:A1993KG34100005 PM 8419611 ER PT J AU KALER, SG WESTMAN, JA BERNES, SM ELSAYED, AM BOWE, CM FREEMAN, KLB WU, CD WALLACH, MT AF KALER, SG WESTMAN, JA BERNES, SM ELSAYED, AM BOWE, CM FREEMAN, KLB WU, CD WALLACH, MT TI GASTROINTESTINAL HEMORRHAGE ASSOCIATED WITH GASTRIC POLYPS IN MENKES DISEASE SO JOURNAL OF PEDIATRICS LA English DT Note AB We describe two infants with Menkes disease who had serious gastrointestinal bleeding from solitary gastric polyps. Hemorrhage in one patient was acute and proved fatal. Histopathologic examinations showed submucosal vascular ectasia with mucosal hyperplasia, edema, and ulceration. Gastric polyps may represent an underappreciated clinical abnormality in Menkes disease. C1 CHILDRENS HOSP, DEPT PEDIAT, COLUMBUS, OH 43205 USA. PHOENIX CHILDRENS HOSP, DEPT NEUROL, PHOENIX, AZ USA. ARMED FORCES RADIOBIOL RES INST, DEPT HEPAT & GASTROINTESTINAL PATHOL, BETHESDA, MD 20814 USA. RHODE ISL HOSP, DIV PEDIAT NEUROL, PROVIDENCE, RI 02902 USA. RHODE ISL HOSP, DIV GASTROENTEROL, PROVIDENCE, RI 02902 USA. RHODE ISL HOSP, DEPT PATHOL, PROVIDENCE, RI 02902 USA. RHODE ISL HOSP, DEPT DIAGNOST IMAGING, PROVIDENCE, RI 02902 USA. RP KALER, SG (reprint author), NICHHD, HUMAN GENET BRANCH, 9S-242, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. RI Westman, Judith/E-4294-2011 NR 7 TC 28 Z9 28 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD JAN PY 1993 VL 122 IS 1 BP 93 EP 95 DI 10.1016/S0022-3476(05)83496-1 PG 3 WC Pediatrics SC Pediatrics GA KG341 UT WOS:A1993KG34100018 PM 8419622 ER PT J AU BOUCHER, FD MODLIN, JF WELLER, S RUFF, A MIROCHNICK, M PELTON, S WILFERT, C MCKINNEY, R CRAIN, MJ ELKINS, MM BLUM, MR PROBER, CG AF BOUCHER, FD MODLIN, JF WELLER, S RUFF, A MIROCHNICK, M PELTON, S WILFERT, C MCKINNEY, R CRAIN, MJ ELKINS, MM BLUM, MR PROBER, CG TI PHASE-1 EVALUATION OF ZIDOVUDINE ADMINISTERED TO INFANTS EXPOSED AT BIRTH TO THE HUMAN-IMMUNODEFICIENCY-VIRUS SO JOURNAL OF PEDIATRICS LA English DT Article ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; CONTINUOUS-INFUSION; HIV INFECTION; DOUBLE-BLIND; 3'-AZIDO-3'-DEOXYTHYMIDINE; PHARMACOKINETICS; CHILDREN; AZT; METABOLITE AB This study evaluated the safety, tolerability, and pharmacokinetics of zidovudine administered intravenously and orally to infants born to women infected with the human immunodeficiency virus. Thirty-two symptom-free infants were enrolled before 3 months of age. The pharmacokinetics of zidovudine were evaluated in each infant after single intravenously and orally administered doses of zidovudine on consecutive days, and during long-term oral administration of the drug for 4 to 6 weeks. As new patients were enrolled, doses of zidovudine were progressively increased from 2 to 4 mg/kg. Therapy was continued for up to 12 months in 7 of the infants proved to be infected with human immunodeficiency virus. Zidovudine was generally well tolerated; 20 children (62.5%) hod anemia (hemoglobin level <10.0 gm/dl) during therapy and 9 (28.1%) had neutropenia (neutrophil count less-than-or-equal-to 5750 cells/mm3); these hematologic abnormalities usually resolved spontaneously. The total body clearance of zidovudine increased significantly with age, from an average of 10.9 ml/min per kilogram in infants less-than-or-equal-to 14 days of age to 19.0 ml/min per kilogrom in older infants (p < 0.0001). Concurrently, there was a significant decrease in serum half-life from 3.12 hours in infants less-than-or-equal-to 14 days to 1.87 hours in older infants (p = 0.0002). Oral absorption was satisfactory and bioavailability decreased significantly with age, from 89% in infants less-than-or-equal-to 14 days to 61% in those >14 days of age (p = 0.0002). Plasma concentrations of zidovudine were calculated to be in excess of 1 mumol/L (0.267 mug/ml) for 4.12 +/- 1.86 hours and 2.25 +/- 0.78 hours after oral doses of 2 mg/kg in infants younger than 2 weeks ond 3 mg/kg in older infants, respectively. We conclude that zidovudine administered at oral doses of 2 mg/kg every 6 hours to infants aged less than 2 weeks and 3 mg/kg every 6 hours to infants older than 2 weeks resulted in plasma concentrations that are considered virustatic against human immunodeficiency virus. Zidovudine was well tolerated by infants at these doses. C1 STANFORD UNIV, MED CTR, SCH MED, DEPT PEDIAT, STANFORD, CA 94305 USA. JOHNS HOPKINS UNIV, DEPT PEDIAT, BALTIMORE, MD 21218 USA. BOSTON CITY HOSP, DEPT PEDIAT, BOSTON, MA 02118 USA. DUKE UNIV, MED CTR, DEPT PEDIAT, DURHAM, NC 27710 USA. UNIV ALABAMA, DEPT PEDIAT, BIRMINGHAM, AL 35294 USA. BURROUGHS WELLCOME CO, DEPT PEDIAT, RES TRIANGLE PK, NC 27709 USA. NIAID, DEPT PEDIAT, AIDS CLIN TRIALS GRP, BETHESDA, MD 20892 USA. OI Boucher, Francois/0000-0003-0051-854X FU NCRR NIH HHS [M01 RR 00533]; NIAID NIH HHS [AI27541, AI27865] NR 20 TC 79 Z9 81 U1 0 U2 5 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD JAN PY 1993 VL 122 IS 1 BP 137 EP 144 DI 10.1016/S0022-3476(05)83507-3 PG 8 WC Pediatrics SC Pediatrics GA KG341 UT WOS:A1993KG34100029 PM 8419601 ER PT J AU MUELLER, BU STEINBERG, S PIZZO, PA AF MUELLER, BU STEINBERG, S PIZZO, PA TI FAILURE OF INTRAVENOUS PENTAMIDINE PROPHYLAXIS FOR PNEUMOCYSTIS-CARINII PNEUMONIA - REPLY SO JOURNAL OF PEDIATRICS LA English DT Letter C1 NCI, BIOSTAT & DATA MANAGEMENT SECT, BETHESDA, MD 20892 USA. NCI, INFECT DIS SECT, BETHESDA, MD 20892 USA. RP MUELLER, BU (reprint author), NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA. NR 6 TC 6 Z9 6 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD JAN PY 1993 VL 122 IS 1 BP 163 EP 164 DI 10.1016/S0022-3476(05)83514-0 PG 2 WC Pediatrics SC Pediatrics GA KG341 UT WOS:A1993KG34100034 ER PT J AU MOORE, LVH MOORE, WEC RILEY, C BROOKS, CN BURMEISTER, JA SMIBERT, RM AF MOORE, LVH MOORE, WEC RILEY, C BROOKS, CN BURMEISTER, JA SMIBERT, RM TI PERIODONTAL MICROFLORA OF HIV POSITIVE SUBJECTS WITH GINGIVITIS OR ADULT PERIODONTITIS SO JOURNAL OF PERIODONTOLOGY LA English DT Article DE GINGIVITIS MICROBIOLOGY; PERIODONTITIS MICROBIOLOGY; HIV ID SP-NOV; BACTERIOLOGY; HUMANS AB The subgingival microflora of 39 HIV + subjects with gingivitis or adult periodontitis was cultured quantitatively anaerobically for bacteria, spirochetes, and mycoplasma and aerobically for yeasts. Isolates were characterized by conventional biochemical tests, polyacrylamide gel electrophoresis of soluble proteins, cellular fatty acid profiles, immunofluorescence, and immunodiffusion. In general, the same types of bacteria were isolated from the subgingival crevice of HIV + subjects as we previously had isolated from the subgingival crevice of non-HIV subjects. A statistically significant difference was found between the composition of the flora of HIV + subjects with adult periodontitis (AP) and concurrent studies of a non-HIV + AP population. Mycoplasma salivarium was significantly elevated in the HIV+ subjects examined. Yeasts were isolated from only 10% of the samples and from 13% of the HIV-positive subjects at 0.05 to 0.0002% of the total cultivable count when present. C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. VIRGINIA COMMONWEALTH UNIV,DEPT PERIODONT,RICHMOND,VA 23284. RP MOORE, LVH (reprint author), VIRGINIA POLYTECH INST & STATE UNIV,DEPT ANAEROB MICROBIOL,BLACKSBURG,VA 24061, USA. FU NIDCR NIH HHS [N01-DE-02577] NR 23 TC 57 Z9 63 U1 0 U2 0 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD JAN PY 1993 VL 64 IS 1 BP 48 EP 56 PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KJ144 UT WOS:A1993KJ14400007 PM 8426289 ER PT J AU KATZ, JL GRIFFITHS, JW SHARPE, LG DESOUZA, EB WITKIN, JM AF KATZ, JL GRIFFITHS, JW SHARPE, LG DESOUZA, EB WITKIN, JM TI COCAINE TOLERANCE AND CROSS-TOLERANCE SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID D2 DOPAMINE-RECEPTORS; RAT NUCLEUS-ACCUMBENS; LOCAL-ANESTHETICS; D-AMPHETAMINE; H-3 DOPAMINE; BRAIN; BINDING; INJECTIONS; MICE; DISPOSITION AB Pharmacological mechanisms by which tolerance develops to the behavioral effects of cocaine were assessed by examining cross-tolerance to specific drugs. Daily experimental sessions were conducted in which rats were trained to press a key under a fixed-ratio 30-response schedule of food reinforcement (each 30th response produced food). Each of the drugs studied decreased rates of responding before initiating daily (10 mg/kg, i.p.) treatment with cocaine. Treatment with cocaine produced a small, significant shift to the right in the cocaine dose-effect curve; the ED50 values changed from 13.3 to 21.7 mg/kg. Cross-tolerance was not conferred to the indirect agonist, d-amphetamine, the direct agonist apomorphine, the D1-selective agonists SKF 38393 or fenoldopam, or the D2-selective agonists quinpirole or (-)-NPA. Cross-tolerance was conferred to the close structural analog of cocaine, WIN 35,428, but not to another dopamine uptake inhibitor, GBR 12909. Tolerant rats showed no change in specific binding of [H-3]SCH 23390 to D1 receptors, [H-3]spiperone to D2 receptors, [H-3]GBR 12935 to dopamine uptake sites in striatum, [H-3]paroxetine to serotonin uptake sites or [H-3]mazindol to norepinephrine uptake sites in cortex or hippocampus. In addition, there were no changes in transmitter levels indicative of neurotoxicity. Serum levels of cocaine were not appreciably different in groups of cocaine- and saline-treated rats. The present results suggest that the modest tolerance that can develop to the behavioral effects of cocaine does not confer significant functional or metabolic changes in the effects of drugs acting on dopaminergic systems. Importantly, the tolerance produced by repeated administration of cocaine does not produce a cross-tolerance to GBR 12909, suggesting differences in mechanism among different structural forms of dopamine uptake inhibitors. C1 NIDA,ADDICT RES CTR,PSYCHOBIOL LAB,BALTIMORE,MD. NIDA,ADDICT RES CTR,NEUROBIOL LAB,BALTIMORE,MD. OI Katz, Jonathan/0000-0002-1068-1159 NR 46 TC 34 Z9 34 U1 1 U2 1 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 JAN PY 1993 VL 264 IS 1 BP 183 EP 192 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KG484 UT WOS:A1993KG48400028 PM 8093724 ER PT J AU SUNAGA, K CHUANG, DM ISHITANI, R AF SUNAGA, K CHUANG, DM ISHITANI, R TI TETRAHYDROAMINOACRIDINE IS NEUROTROPHIC AND PROMOTES THE EXPRESSION OF MUSCARINIC RECEPTOR-COUPLED PHOSPHOINOSITIDE TURNOVER IN DIFFERENTIATING CEREBELLAR GRANULE CELLS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID PRIMARY CULTURES; RAT-BRAIN; SURVIVAL; NEURONS; PHOSPHATIDYLINOSITOL; GLUTAMATE; LITHIUM; TACRINE; RELEASE; M2 AB We have investigated whether 9-amino-1,2,3,4-tetrahydroacridine (THA), a drug with potential antidementia activity, has a trophic action on differentiating cerebellar granule cells by using the method of [H-3]inositol incorporation into inositol-containing phospholipid. Addition of THA (30-50 muM) prevented the extensive neuronal degeneration which occurred in the growth medium containing ''low'' K+ (15 mM). These effects were similar to the neuroprotective action caused by the presence of 100 muM N-methyl-D-aspartate (NMDA). Neurotrophic effects of THA and NMDA on cells grown in low K+ were also demonstrated by direct microscopic examination of cellular morphology. Measurement of phosphoinositide (PI) response in the rescued cells indicated that NMDA modestly promoted the PI response to carbachol and norepinephrine but markedly stimulated the activity induced by glutamate. In contrast, although THA had little or no influence on the maturation of the norepinephrine- and glutamate-induced PI response, it selectively enhanced the activity stimulated by carbachol. Furthermore, the THA treatment drastically increased the V(max) value of carbachol-induced PI turnover with no significant alteration in the EC50 value. Scatchard analysis of the binding of N-[H-3]methylscopolamine to intact granule cells indicated a selective increase in the maximum binding value in cells grown in THA-supplementing medium. These observations suggest that THA seems to selectively up-regulate muscarinic cholinergic receptors. C1 JOSAI UNIV,NEUROPHARMACOL GRP,SAKADO,SAITAMA 35002,JAPAN. NIMH,BIOL PSYCHIAT BRANCH,MOLEC NEUROBIOL SECT,BETHESDA,MD 20892. NR 31 TC 17 Z9 17 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 JAN PY 1993 VL 264 IS 1 BP 463 EP 468 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KG484 UT WOS:A1993KG48400065 PM 8380869 ER PT J AU BALSKUBIK, R ABLEITNER, A HERZ, A SHIPPENBERG, TS AF BALSKUBIK, R ABLEITNER, A HERZ, A SHIPPENBERG, TS TI NEUROANATOMICAL SITES MEDIATING THE MOTIVATIONAL EFFECTS OF OPIOIDS AS MAPPED BY THE CONDITIONED PLACE PREFERENCE PARADIGM IN RATS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID VENTRAL TEGMENTAL AREA; GUINEA-PIG BRAIN; LATERAL HYPOTHALAMUS; NUCLEUS ACCUMBENS; BETA-ENDORPHIN; OPIATE REWARD; BINDING-SITES; KAPPA; RECEPTORS; DYNORPHIN AB An unbiased conditioned place preference paradigm was used to examine the neuroanatomical substrates mediating the reinforcing and aversive effects of mu and kappa opioid agonists. Unilateral microinjection of the selective mu agonist DAMGO into the ventral tegmental area (VTA), the origin of the mesolimbic and mesocortical dopamine (DA) systems, resulted in dose-dependent preferences for the drug-associated place. Intracranial injections of DAMGO into terminal projection sites of VTA DA neurons, the nucleus accumbens and the medial prefrontal cortex, however, as well as into the lateral hypothalamus, were without effect. In contrast, microinjections of the kappa agonist U50,488H and the dynorphin derivative E-2078 into the VTA produced place aversions. Place aversions were also observed after microinjections of U50,488H and E-2078 into the nucleus accumbens, medial prefrontal cortex and lateral hypothalamus. However, microinjections of mu and kappa agonists into either the origin of the mesostriatal DA system, the substantia nigra or into its major terminal field, the nucleus caudatus-putamen, was without effect. Autoradiographic studies revealed that the substances remained within a restricted area around the injection site, confirming that the effects observed were mediated therein. Thus, these data suggest an important role for the A10 neurons in the VTA in the regulation of both mu and kappa opioid-induced motivational states. The rewarding effects are associated with the activation of mu receptors in the VTA, whereas aversive effects are associated with the activation Of kappa receptors in the VTA and its limbic-cortical terminal regions. C1 NIDA,ADDICT RES CTR,PRECLIN PHARMACOL BRANCH,POB 51801,BALTIMORE,MD 21224. MAX PLANCK INST PSYCHIAT,DEPT NEUROPHARMACOL,W-8033 MARTINSRIED,GERMANY. UNIV MUNICH,SCH TOXICOL & PHARM VET,DEPT PHARMACOL,W-8000 MUNICH 2,GERMANY. NR 36 TC 313 Z9 317 U1 0 U2 1 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 JAN PY 1993 VL 264 IS 1 BP 489 EP 495 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KG484 UT WOS:A1993KG48400069 PM 8093731 ER PT J AU BETAGERI, GV BLACK, CDV SZEBENI, J WAHL, LM WEINSTEIN, JN AF BETAGERI, GV BLACK, CDV SZEBENI, J WAHL, LM WEINSTEIN, JN TI FC-RECEPTOR-MEDIATED TARGETING OF ANTIBODY-BEARING LIPOSOMES CONTAINING DIDEOXYCYTIDINE TRIPHOSPHATE TO HUMAN MONOCYTE MACROPHAGES SO JOURNAL OF PHARMACY AND PHARMACOLOGY LA English DT Article ID CENTRIFUGAL ELUTRIATION CCE; MONONUCLEAR CELL SUBSETS; LYMPHOCYTE-T; TUMORICIDAL PROPERTIES; FLUORESCENT LIPOSOMES; COVALENT ATTACHMENT; MONOCLONAL-ANTIBODY; ENRICHED FRACTIONS; MURAMYL DIPEPTIDE; HTLV-III AB Liposomes bearing surface-attached antibody (L-Ab) molecules can be used for various purposes including the immunospecific delivery of drugs or other materials to antigenic target cells. In this study, L-Ab were prepared to deliver an anti-human immunodeficiency virus (HIV) drug, dideoxycytidine triphosphate (ddCTP) to human monocyte/macrophages. Cells of the monocyte/macrophage lineage are an important reservoir of HIV-1. A mouse monoclonal antibody IgG2a was labelled with I-125 and modified using N succinimidyl-3-(2-pyridyldithio)propionate (SPDP) as a heterobifunctional reagent in order to conjugate with liposomes to produce a covalent bond (thioether). SPDP-modified antibody was incubated with liposomes containing 5 mol% of maleimido phenyl butyrate phosphatidylethanolamine (MPB-PE) at room temperature (21-degrees-C) for 24 h. L-Ab were separated from free and aggregated antibodies by centrifugation. L-Ab were characterized by measuring particle size and binding to anti-mouse IgG-sepharose. Ninety five per cent of the liposomal (L-Ab) lipid label was bound to anti-mouse IgG-sepharose, whereas only 7% of plain liposomes were bound, indicating non-specific binding. Uptake of L-Ab was measured in human monocyte/macrophages as a function of time and compared with that of plain liposomes. The uptake increased with time and it was 4-6 times greater than that of plain liposomes although part of that effect may have been due to unreacted MPB groups. C1 NIDR,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 37 TC 26 Z9 27 U1 0 U2 2 PU ROYAL PHARMACEUTICAL SOC GREAT BRITAIN PI LONDON PA 1 LAMBETH HIGH ST, LONDON, ENGLAND SE1 7JN SN 0022-3573 J9 J PHARM PHARMACOL JI J. Pharm. Pharmacol. PD JAN PY 1993 VL 45 IS 1 BP 48 EP 53 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KH170 UT WOS:A1993KH17000011 PM 8094446 ER PT J AU LAVORI, PW WARSHAW, M KLERMAN, G MUELLER, TI LEON, A RICE, J AKISKAL, H AF LAVORI, PW WARSHAW, M KLERMAN, G MUELLER, TI LEON, A RICE, J AKISKAL, H TI SECULAR TRENDS IN LIFETIME ONSET OF MDD STRATIFIED BY SELECTED SOCIODEMOGRAPHIC RISK-FACTORS SO JOURNAL OF PSYCHIATRIC RESEARCH LA English DT Article ID MAJOR DEPRESSIVE DISORDER; RATES AB We used multivariate proportional hazards (Cox) models to investigate the effects of cohort of birth on age of first onset of major depression measured independently at two occasions, about six years apart, in the first degree relatives of probands with major affective illnesses. We estimated the cohort trends in strata defined by sociodemographic and other measures, to see if the cohort trends are the same across strata. Graphical summaries of the trends reveal a generally consistent pattern of increasing rates and earlier age of onset with successive birth cohorts, across all strata examined. The relatives with a divorced parent had a somewhat delayed secular increase, suggesting either a ceiling effect or an interaction of the two risk factors (recent cohort of birth and divorced parents) such that the combined effect is less than the sum of the individual effects. Otherwise, the cohort effect is persistent and ubiquitous in this sample. C1 NIMH,MOOD ANXIETY & PERSONAL DISORDERS BRANCH,ROCKVILLE,MD 20857. BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021. WASHINGTON UNIV,SCH MED,DEPT PSYCHIAT,ST LOUIS,MO 63110. NR 16 TC 19 Z9 19 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0022-3956 J9 J PSYCHIAT RES JI J. Psychiatr. Res. PD JAN-MAR PY 1993 VL 27 IS 1 BP 95 EP 109 DI 10.1016/0022-3956(93)90054-6 PG 15 WC Psychiatry SC Psychiatry GA LF141 UT WOS:A1993LF14100011 PM 8515394 ER PT J AU JUDD, LL AF JUDD, LL TI THE NIMH RESEARCH-PROGRAM IN PANIC DISORDER - THE PRESENT AND FUTURE SO JOURNAL OF PSYCHIATRIC RESEARCH LA English DT Article; Proceedings Paper CT Conference on Panic and Anxiety: A Decade of Progress CY JUN, 1990 CL GENEVA, SWITZERLAND C1 NIMH,BETHESDA,MD 20892. RP JUDD, LL (reprint author), UNIV CALIF SAN DIEGO,DEPT PSYCHIAT,LA JOLLA,CA 92093, USA. NR 9 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0022-3956 J9 J PSYCHIAT RES JI J. Psychiatr. Res. PY 1993 VL 27 SU 1 BP 221 EP 228 DI 10.1016/0022-3956(93)90030-6 PG 8 WC Psychiatry SC Psychiatry GA MT326 UT WOS:A1993MT32600019 PM 8145179 ER PT J AU HOAGWOOD, K AF HOAGWOOD, K TI POSTSTRUCTURALIST HISTORICISM AND THE PSYCHOLOGICAL CONSTRUCTION OF ANXIETY DISORDERS SO JOURNAL OF PSYCHOLOGY LA English DT Article AB When applied to the construction of anxiety disorders, theories of poststructuralist historicism emphasize acts of interpretation that constitute and construct the disorders and problematize the processes by which meaning is constructed. An examination of the historical formulations of anxiety disorders, and in particular, agoraphobia, provides the opportunity for reanalyzing traditional approaches to the classifications of disorders. Psychological issues of paradox, attachment, and personal identity, which are crucial to current conceptualizations of agoraphobia, are acutely problematized within a poststructuralist historicist hermeneutic. A rethinking of disorder construction from within this hermeneutic suggests replacing individualistic conceptualizations of personal identity with a broader view that recognizes and celebrates multiplicity and that displays formulations of the self in a contextualized and historicized status, thus enabling a fuller engagement with the social world. RP HOAGWOOD, K (reprint author), NIMH,DIV EPIDEMIOL & SERV RES,ROCKVILLE,MD 20857, USA. NR 70 TC 0 Z9 0 U1 0 U2 1 PU HELDREF PUBLICATIONS PI WASHINGTON PA 1319 EIGHTEENTH ST NW, WASHINGTON, DC 20036-1802 SN 0022-3980 J9 J PSYCHOL JI J. Psychol. PD JAN PY 1993 VL 127 IS 1 BP 105 EP 122 PG 18 WC Psychology, Multidisciplinary SC Psychology GA LB813 UT WOS:A1993LB81300011 PM 8510049 ER PT J AU GROSSMAN, F MANJI, HK POTTER, WZ AF GROSSMAN, F MANJI, HK POTTER, WZ TI PLATELET ALPHA-2-ADRENOCEPTORS IN DEPRESSION - A CRITICAL-EXAMINATION SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Review DE ALPHA-ADRENOCEPTORS; PLATELETS; DEPRESSION; RADIOLIGAND STUDIES; REVIEW ID CLONIDINE-DISPLACING-SUBSTANCE; ADRENERGIC-RECEPTOR SUBTYPES; GROWTH-HORMONE RESPONSE; LOCUS COERULEUS NEURONS; H-3 YOHIMBINE BINDING; RAT VAS-DEFERENS; HUMAN BRAIN-STEM; ALPHA-2-ADRENERGIC RECEPTORS; ADENYLATE-CYCLASE; DRUG-TREATMENT AB During the past decade, results from radioligand studies comparing platelet alpha2-adrenoreceptors in depressed patients and healthy volunteers have been inconsistent, especially when related to the known functional characteristics of these receptors. Despite the availability of radioligands for alpha2-adrenoreceptors, inherent methodological problems exist which make data from these studies difficult to interpret. The authors review the overall data from radioligand studies using [H-3] clonidine and [H-3] yohimbine of platelet alpha2-adrenoreceptors in depressed patients and healthy volunteers. Theoretical and methodological issues are critically examined in the light of recent findings. Finally, alternative strategies for studying alpha2-adrenoreceptors in clinical populations are considered. C1 NIMH, CLIN PHARMACOL SECT, EXPTL THERAPEUT BRANCH, BETHESDA, MD 20892 USA. NR 108 TC 19 Z9 19 U1 0 U2 1 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0269-8811 EI 1461-7285 J9 J PSYCHOPHARMACOL JI J. Psychopharmacol. PY 1993 VL 7 IS 1 BP 4 EP 18 PG 15 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KV534 UT WOS:A1993KV53400002 PM 22290365 ER PT J AU WEINGARTNER, HJ JOYCE, EM SIROCCO, KY ADAMS, CM ECKARDT, MJ GEORGE, T LISTER, RG AF WEINGARTNER, HJ JOYCE, EM SIROCCO, KY ADAMS, CM ECKARDT, MJ GEORGE, T LISTER, RG TI SPECIFIC MEMORY AND SEDATIVE EFFECTS OF THE BENZODIAZEPINE TRIAZOLAM SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Article DE TRIAZOLAM; MEMORY; SEDATION ID LORAZEPAM-INDUCED AMNESIA; ALZHEIMERS-DISEASE; IMPLICIT MEMORY; EXPLICIT MEMORY; SYSTEMS; DIAZEPAM; IMPAIRMENT; RECOGNITION; SCOPOLAMINE; FLUMAZENIL AB Fifteen normal volunteers were administered placebo, 0.250, 0.375 and 0.500 mg of triazolam in a double-blind cross-over design. Triazolam induced robust dose-dependent impairments in explicit memory of information presented after drug administration. Subjects were unaware of their memory deficit (an impairment in meta-cognition). In contrast, memory for information presented prior to the administration of triazolam was facilitated following the administration of low doses of triazolam. Implicit memory and access to knowledge memory was unaltered by this benzodiazepine, An analysis of these results controlling for concurrent sedation as measured subjectively, through the use of self rating scales and objectively, based upon psychomotor performance, demonstrated that the amnestic effects of triazolam are largely independent of sedative effects. The pattern of memory changes induced by benzodiazepines, such as triazolam, is similar to the memory inpairment expressed in amnestic patients but unlike the pattern of impaired memory evident in dementia such as Alzheimer's disease. C1 CHARING CROSS & WESTMINSTER MED SCH,ACAD DEPT PSYCHIAT,LONDON W6 8RP,ENGLAND. RP WEINGARTNER, HJ (reprint author), NIAAA,DICBR,CLIN STUDIES LAB,COGNIT NEUROSCI SECT,BLDG 10,ROOM 3B19,BETHESDA,MD 20892, USA. NR 60 TC 31 Z9 31 U1 6 U2 6 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-8811 J9 J PSYCHOPHARMACOL JI J. Psychopharmacol. PY 1993 VL 7 IS 4 BP 305 EP 315 DI 10.1177/026988119300700401 PG 11 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA MN600 UT WOS:A1993MN60000001 PM 22290993 ER PT J AU DANION, JM WEINGARTNER, H FILE, SE JAFFARD, R SUNDERLAND, T TULVING, E WARBURTON, DM AF DANION, JM WEINGARTNER, H FILE, SE JAFFARD, R SUNDERLAND, T TULVING, E WARBURTON, DM TI PHARMACOLOGY OF HUMAN-MEMORY AND COGNITION - ILLUSTRATIONS FROM THE EFFECTS OF BENZODIAZEPINES AND CHOLINERGIC DRUGS SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Article DE MEMORY; COGNITION; BENZODIAZEPINES; CHOLINERGIC DRUGS; HUMAN; ALZHEIMERS DISEASE ID LORAZEPAM-INDUCED AMNESIA; HEALTHY-YOUNG VOLUNTEERS; PROTEIN-KINASE-C; IMPLICIT MEMORY; EXPLICIT MEMORY; WORKING MEMORY; DIAZEPAM; NICOTINE; SYSTEMS; FACILITATION AB The current research methods, findings and questions that are being addressed in studies of the pharmacology of human memory and cognition are reviewed. Memory is not a unitary function. Neuropsychological studies of brain-damaged memory-impaired patients, as well as neuroimaging and drug studies in normal individuals indicate that different forms of learning and memory are subserved by different brain systems. Animal drug studies have also provided evidence that, while distinct, memory systems are not independent, but operate in close interaction with one another. Recent human studies of benzodiazepines and of cholinergic drugs demonstrate the value of the psychological models and of the experimental paradigms that are available from cognitive sciences for exploring how drugs alter cognitive and memory functions. They also show how drugs can be used as tools for analyzing the distinct neurochemical mechanisms underlying independent cognitive processes, and so find effective drugs rationally from a knowledge of the neurochemical bases of cognition. This research leads to specific recommendations concerning treatments that may improve memory functioning, for instance in Alzheimer's disease. C1 NIMH, BETHESDA, MD 20892 USA. UMDS, GUYS HOSP, DIV PHARMACOL SCI, PSYCHOPHARMACOL RES UNIT, LONDON SE1 9RT, ENGLAND. LAB NEUROSCI COMPORTEMENTALES & COGNIT, F-33405 TALENCE, FRANCE. BAYCREST CTR GERIATR CARE, ROTMAN RES INST, N YORK M6A 2E1, ON, CANADA. RP DANION, JM (reprint author), HOP UNIV STRASBOURG, SERV PSYCHIAT 1, DEPT PSYCHIAT ADULTES, 1 PL HOP, BP 426, F-67091 STRASBOURG, FRANCE. NR 58 TC 23 Z9 23 U1 2 U2 4 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0269-8811 EI 1461-7285 J9 J PSYCHOPHARMACOL JI J. Psychopharmacol. PY 1993 VL 7 IS 4 BP 371 EP 377 DI 10.1177/026988119300700409 PG 7 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA MN600 UT WOS:A1993MN60000009 PM 22291001 ER PT J AU PORRELLI, RN MUNSON, PJ RODBARD, D AF PORRELLI, RN MUNSON, PJ RODBARD, D TI A MODEL FOR THE EFFECT OF ESTROGEN ANTAGONISTS ON COOPERATIVE ESTRADIOL BINDING SO JOURNAL OF RECEPTOR RESEARCH LA English DT Article ID RECEPTOR ACTIVATION; POSITIVE COOPERATIVITY; INDUCED INHIBITION; TRANSFORMATION; ESTRIOL; TEMPERATURE; KINETICS; AFFINITY; STATE AB Partial agonists such as estriol and estrone have been reported to diminish or even eliminate the upward convexity of the Scatchard plot of the binding of labeled estradiol to estrogen receptor. This has been interpreted as agonist interference with the receptor dimerization induced by estradiol. In order to investigate how a partial agonist or antagonist might interfere with dimerization we have developed a theoretical mass-action law model, where soluble receptors can dimerize and bind to two different ligands. Special attention was devoted to manifestations of positive cooperativity to determine whether they could be modified by competition with a second ligand. This was done using a computer program that evaluated a large set of combinations of affinity constants in an effort to explore all possible situations. The model could reproduce the effect of a second ligand on the cooperative binding of estradiol to the estrogen receptor but only if the second ligand was anticooperative, which is not the case of estriol, estrone and tamoxifen. Furthermore, even when the Scatchard plot was linear, the model still required dimerization of the receptor in most of the cases, showing that the addition of an antagonist may eliminate the upward curvature of the Scatchard without truly eliminating dimerization or cooperativity. We conclude that the effect of a second ligand on the binding of labeled estradiol to estrogen receptor is not necessarily due to interference with dimerization and/or cooperativity. The inability of this model to fully explain the published data for estriol. estrone, clomiphene, and tamoxifen suggests that a more complex mechanism is involved. C1 NIH,DIV COMP RES & TECHNOL,OFF DIRECTOR,BETHESDA,MD 20892. RP PORRELLI, RN (reprint author), NIH,ANALYT BIOSTAT SECT,BETHESDA,MD 20892, USA. NR 27 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0197-5110 J9 J RECEPTOR RES JI J. Recept. Res. PY 1993 VL 13 IS 7 BP 1055 EP 1081 DI 10.3109/10799899309063264 PG 27 WC Cell Biology SC Cell Biology GA LM741 UT WOS:A1993LM74100004 PM 8366504 ER PT J AU BROWN, JL BUSH, M PACKER, C PUSEY, AE MONFORT, SL OBRIEN, SJ JANSSEN, DL WILDT, DE AF BROWN, JL BUSH, M PACKER, C PUSEY, AE MONFORT, SL OBRIEN, SJ JANSSEN, DL WILDT, DE TI HORMONAL CHARACTERISTICS OF FREE-RANGING FEMALE LIONS (PANTHERA-LEO) OF THE SERENGETI PLAINS AND NGORONGORO CRATER SO JOURNAL OF REPRODUCTION AND FERTILITY LA English DT Article ID PUMA FELIS-CONCOLOR; LUTEINIZING-HORMONE; REPRODUCTIVE PHYSIOLOGY; INVITRO FERTILIZATION; PLASMA-CONCENTRATIONS; OVARIECTOMIZED EWES; EMBRYO DEVELOPMENT; GENETIC-VARIATION; GONADAL RESPONSE; CLOUDED LEOPARD AB Pituitary responses to gonadotrophin-releasing hormone (GnRH) and prolactin and steroid secretory profiles were examined in two populations of adult, female lions in the Serengeti (one outbred in the Serengeti Plains and one inbred in the Ngorongoro Crater) to determine whether reductions in genetic variability adversely affected endocrine function. GnRH-induced gonadotrophin secretion was also examined after adrenocorticotrophic hormone (ACTH) treatment to determine whether acute increases in serum cortisol altered pituitary function. Anaesthetized lions were administered (i) saline i.v. after 10 and 100 min of blood sampling; (ii) saline at 10 min and GnRH (1 mug kg-1 body weight) after 100 min; or (iii) ACTH (3 mug kg-1) at 10 min and GnRH after 100 min of sampling. Basal serum cortisol and basal and GnRH-induced gonadotrophin secretion were similar (P > 0.05) between females of the Ngorongoro Crater and Serengeti Plains. After ACTH, serum cortisol increased two- to threefold over baseline values and the response was unaffected (P > 0.05) by location. ACTH-induced increases in serum cortisol had no effect on subsequent basal or GnRH-stimulated luteinizing hormone (LH) or follicle-stimulating hormone (FSH) secretion. Overall mean serum progesterone concentrations ranged from 0.2 to 5.4 ng ml-1 with the exception of four females (two in the Serengeti and two in the Crater, progesterone range, 18.4-46.5 ng ml-1) that were presumed pregnant (three of these females were observed nursing cubs several weeks later). There were no differences (P > 0.05) between Serengeti and Crater lions in mean serum progesterone, oestradiol or prolactin concentrations, and hormone secretion was not influenced (P > 0.05) by GnRH or ACTH treatment. Although Ngorongoro Crater lions have decreased genetic variability, the reproductive-endocrine system of females appears functionally normal compared with outbred counterparts living in the Serengeti Plains. Furthermore, the acute rise in serum cortisol after ACTH administration in lions fails to alter subsequent GnRH-induced gonadotrophin release, suggesting that short-term changes in adrenal activity do not markedly affect pituitary responsiveness in this species. C1 CONSERVAT & RES CTR,FRONT ROYAL,VA 22630. UNIV MINNESOTA,DEPT ECOL EVOLUT & BEH,MINNEAPOLIS,MN 55455. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. ZOOL SOC SAN DIEGO,DEPT VET SCI,SAN DIEGO,CA 92112. RP BROWN, JL (reprint author), SMITHSONIAN INST,NATL ZOOL PK,DEPT ANIM HLTH,WASHINGTON,DC 20008, USA. NR 44 TC 9 Z9 10 U1 1 U2 11 PU J REPROD FERTIL INC PI CAMBRIDGE PA 22 NEWMARKET RD, CAMBRIDGE, ENGLAND CB5 8DT SN 0022-4251 J9 J REPROD FERTIL JI J. Reprod. Fertil. PD JAN PY 1993 VL 97 IS 1 BP 107 EP 114 PG 8 WC Reproductive Biology SC Reproductive Biology GA KK741 UT WOS:A1993KK74100016 PM 8385220 ER PT J AU GILAD, GM LI, R WYATT, RJ TIZABI, Y AF GILAD, GM LI, R WYATT, RJ TIZABI, Y TI EFFECTS OF GENOTYPE ON AGE-RELATED ALTERATIONS IN THE CONCENTRATIONS OF STRESS HORMONES IN PLASMA AND HYPOTHALAMIC MONOAMINES IN RATS SO JOURNAL OF REPRODUCTION AND FERTILITY LA English DT Article; Proceedings Paper CT 1ST INTERNATIONAL SYMP ON NEUROBIOLOGY AND NEUROENDOCRINOLOGY OF AGEING CY JUL 19-24, 1992 CL BREGENZ, AUSTRIA SP LAND VORARLBERG, SO ILLINOIS UNIV CARBONDALE, PRESIDENTS OFF, SO ILLINOIS UNIV CARBONDALE, GRAD SCH, SO ILLINOIS UNIV SPRINGFIELD, SCH MED, SIGMA TAU PHARM DE AGING; RESTRAINT STRESS; RAT; STRESS HORMONES; MONOAMINES ID CORTICOTROPIN-RELEASING FACTOR; DOPAMINERGIC NEURONAL FUNCTION; SYMPATHO-ADRENAL SYSTEM; OLD MALE-RATS; ADRENOCORTICOTROPIN SECRETION; CORTICOSTERONE RESPONSES; BIOSYNTHETIC-ENZYMES; HYDROXYLASE ACTIVITY; STRAIN DIFFERENCES; PROLACTIN-RELEASE AB The adaptive response of the neuroendocrine system to stress is known to be impaired during ageing, and this impairment may be genetically determined. To elucidate further the effect of genotype, inbred male rats of the Wistar-Kyoto (WKY) strain, characterized by their hyper-reactivity to stressors and shorter life span, were compared with Brown-Norway (BN) rats. In young BN rats, resting prolactin concentrations were lower than in WKY animals and were reduced with age, while in WKY rats they remained unchanged with age. In young rats of both strains prolactin concentrations were highest after subjecting them to stressful stimuli for 15 min. After 2 h of restraint stress (during which the animals were confined to a narrow space that restricted movement) prolactin concentrations in young rats returned to pre-stress values, while remaining high in aged rats of both strains. Concentrations of corticotrophin (or adrenocorticotrophic hormone, ACTH) were lower in BN than in WKY rats and did not change with age in either strain. After 2 h of stress, ACTH concentrations were still slightly higher than normal in both young and aged BN rats, but not in WKY rats. Corticosterone concentrations were similar in young WKY and BN rats and were reduced in aged rats of both strains. After 2 h of stress, corticosterone concentrations were still high in aged, but not in young rats of both strains. However, this stress-induced increase was larger (3.7 times as much) in the BN strain than in the WKY strain (in which the increase was 1.7 times as much). The concentrations of hypothalamic monoamines were similar in young rats of both strains, although stress resulted in reduced noradrenaline concentrations, as previously documented, and in minor increases in 3,4-dihydroxyphenylacetic acid in both strains. During ageing, basal noradrenaline concentrations were reduced only in WKY rats, while the amount of 5-HT increased selectively in BN rats. Concentrations of 5-hydroxyindoleacetic acid were increased after stress in aged WKY rats only. The results demonstrate that resting plasma concentrations of the stress hormones ACTH and corticosterone and of prolactin are lower in BN than in WKY rats. In ageing, however, the stress-induced increases in the concentrations of these hormones are relatively higher in the BN strain, which is characterized by a longer life span. Taken together with previous findings, this study indicates that higher basal activity and increased stress-induced activation of the neuronal and endocrine systems are directly associated with the behavioural hyper-reactivity to stressors. However, the study implies that a robust neuroendocrine response to stressors during ageing may be directly correlate with longevity. C1 ST ELIZABETH HOSP,NIMH,NEUROSCI RES CTR,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. HOWARD UNIV,COLL MED,DEPT PHARMACOL,WASHINGTON,DC 20059. NR 72 TC 0 Z9 0 U1 0 U2 0 PU J REPROD FERTIL INC PI CAMBRIDGE PA 22 NEWMARKET RD, CAMBRIDGE, ENGLAND CB5 8DT SN 0022-4251 J9 J REPROD FERTIL JI J. Reprod. Fertil. PY 1993 SU 46 BP 119 EP 130 PG 12 WC Reproductive Biology SC Reproductive Biology GA KQ829 UT WOS:A1993KQ82900012 ER PT J AU WEISS, GH GITTERMAN, M AF WEISS, GH GITTERMAN, M TI MOTION IN A PERIODIC POTENTIAL DRIVEN BY RECTANGULAR PULSES SO JOURNAL OF STATISTICAL PHYSICS LA English DT Article; Proceedings Paper CT NATO ADVANCED RESEARCH WORKSHOP : STOCHASTIC RESONANCE IN PHYSICS AND BIOLOGY CY MAR 30-APR 03, 1992 CL SAN DIEGO, CA SP NATO, USN, LAB NCCOSC DE NONLINEAR DYNAMICS; JOSEPHSON JUNCTIONS; STOCHASTIC PROCESSES ID NOISE AB Exact solutions are found for the averaged velocity of an overdamped pendulum driven by a series of square pulses. The formalism developed can be applied to either periodic or random switching as well as cases intermediate between the two. The phenomenon known as phase locking can be shown to exist when periodic switching is used. C1 BAR ILAN UNIV,DEPT PHYS,IL-52100 RAMAT GAN,ISRAEL. RP WEISS, GH (reprint author), NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892, USA. NR 14 TC 11 Z9 11 U1 0 U2 2 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0022-4715 J9 J STAT PHYS JI J. Stat. Phys. PD JAN PY 1993 VL 70 IS 1-2 BP 93 EP 105 DI 10.1007/BF01053956 PG 13 WC Physics, Mathematical SC Physics GA KJ465 UT WOS:A1993KJ46500008 ER PT J AU GITTERMAN, M WEISS, GH AF GITTERMAN, M WEISS, GH TI ESCAPE OF A PERIODICALLY DRIVEN PARTICLE FROM A METASTABLE STATE IN A NOISY SYSTEM SO JOURNAL OF STATISTICAL PHYSICS LA English DT Article; Proceedings Paper CT NATO ADVANCED RESEARCH WORKSHOP : STOCHASTIC RESONANCE IN PHYSICS AND BIOLOGY CY MAR 30-APR 03, 1992 CL SAN DIEGO, CA SP NATO, USN, LAB NCCOSC DE DYNAMIC SYSTEMS; METASTABLE STATES; 1ST PASSAGE TIMES ID ELECTRON-PARAMAGNETIC-RESONANCE; STOCHASTIC RESONANCE AB We consider the statistical properties of the escape time of a particle initially sitting in a potential well subject to a combination of white noise and a periodic forcing term. As one finds in the case of the much-studied bistable potential, different kinds of resonant effects can occur, as measured by the survival probability and the average residence time. When this time is considered as a function of the noise strength, then we show that for small amplitudes of the forcing term there are no resonant effects, while for large amplitudes such effects can appear. We also show that a resonant phenomenon is possible in terms of the amplitude of a periodic forcing term. C1 BAR ILAN UNIV,DEPT PHYS,IL-52100 RAMAT GAN,ISRAEL. RP GITTERMAN, M (reprint author), NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892, USA. NR 9 TC 25 Z9 25 U1 0 U2 3 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0022-4715 J9 J STAT PHYS JI J. Stat. Phys. PD JAN PY 1993 VL 70 IS 1-2 BP 107 EP 123 DI 10.1007/BF01053957 PG 17 WC Physics, Mathematical SC Physics GA KJ465 UT WOS:A1993KJ46500009 ER PT J AU SHIRANI, J ROBERTS, WC AF SHIRANI, J ROBERTS, WC TI SOLITARY CORONARY OSTIUM IN THE AORTA IN THE ABSENCE OF OTHER MAJOR CONGENITAL CARDIOVASCULAR ANOMALIES SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID MYOCARDIAL-INFARCTION; CLINICAL SIGNIFICANCE; ARTERY; ORIGIN; SINUS; VALSALVA; CIRCUMFLEX; ANEURYSM; PATIENT; ANGINA AB Objectives. This study examines the distribution patterns and the clinical significance of the ''solitary coronary ostium'' in the aorta in the absence of other major congenital cardiovascular anomalies. Background. Ogden in 1970 classified ''single coronary artery'' into 14 basic distribution patterns. Since then, other patterns of distribution of single coronary artery have been recognized. Distinction has also been made between the cases with and without other major congenital cardiovascular anomalies or coronary artery atresia and those without these additional abnormalities. Single coronary artery has been generally considered to be a benign clinical entity. Methods. This study describes 10 cases of single coronary artery at necropsy and reviews 87 previously reported cases, 35 diagnosed at necropsy and 52 by coronary angiography. Results. We classified single coronary artery into 20 categories on the basis of the location of the solitary coronary ostium, the presence or absence of an aberrant-coursing coronary artery and the course taken by the aberrant-coursing coronary artery. When atherosclerotic coronary artery disease was absent, 15% (8 of 53) of the patients reviewed with single coronary artery had myocardial ischemia as a direct consequence of the coronary anomaly. Conclusions. The anatomic classification presented is useful from both clinical and surgical viewpoints. This comprehensive classification of this rare anomaly facilitates description of the various distribution patterns of single coronary artery and their clinical significance. RP SHIRANI, J (reprint author), NHLBI,PATHOL BRANCH,BLDG 10,ROOM 2N258,BETHESDA,MD 20892, USA. NR 63 TC 87 Z9 94 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JAN PY 1993 VL 21 IS 1 BP 137 EP 143 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KG398 UT WOS:A1993KG39800019 PM 8417054 ER PT J AU GIFT, HC NEWMAN, JF AF GIFT, HC NEWMAN, JF TI HOW OLDER ADULTS USE ORAL HEALTH-CARE SERVICES - RESULTS OF A NATIONAL-HEALTH INTERVIEW SURVEY SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article AB This report describes the dental visit patterns of adults aged 65 and older. The analyses compare dental visit patterns by socioeconomic factors, perceived health status and dentate status. C1 GEORGIA STATE UNIV,ATLANTA,GA 30303. RP GIFT, HC (reprint author), NIDR,DIS & PREVENT HLTH PROMOT BRANCH,EPIDEMIOL & ORAL DIS PROGRAM,BETHESDA,MD 20892, USA. NR 10 TC 52 Z9 53 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 JAN PY 1993 VL 124 IS 1 BP 89 EP 93 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KF876 UT WOS:A1993KF87600016 PM 8445149 ER PT J AU CONWELL, Y FORBES, NT COX, C CAINE, ED AF CONWELL, Y FORBES, NT COX, C CAINE, ED TI VALIDATION OF A MEASURE OF PHYSICAL ILLNESS BURDEN AT AUTOPSY - THE CUMULATIVE ILLNESS RATING-SCALE SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article AB Objective: To further validate an objective measure of physical illness burden, the Cumulative Illness Rating Scale (CIRS). Design: Survey with correlation of CIRS ratings made from physician interviews and review of medical records with postmortem ratings made independently at tissue autopsy. Subjects: Victims of completed suicide investigated by both psychological and tissue autopsy (n = 72). Results: CIRS ratings made by examination of tissue at autopsy were highly predictive of analogous ratings based on historical data, accounting for 75% of the variance in CIRS scores. Taking autopsy findings as the gold standard of objective health assessment, historical ratings tend to under-estimate physical illness at high levels of tissue pathology and to overestimate burden at lower levels. Conclusions: The CIRS score, when derived from all available sources of medical information, is a valid objective measure of physical illness burden and has broad applicability to research in geriatrics. C1 UNIV ROCHESTER,NIMH,CLIN RES CTR STUDY PSYCHOPATHOL ELDERLY,ROCHESTER,NY 14627. OFF MED EXAMINER,MONROE CTY,NY. UNIV ROCHESTER,MED CTR,SCH MED,DEPT BIOSTAT,ROCHESTER,NY 14642. RP CONWELL, Y (reprint author), UNIV ROCHESTER,MED CTR,SCH MED,DEPT PSYCHIAT,300 CRITTENDEN BLVD,ROCHESTER,NY 14642, USA. FU NIMH NIH HHS [K07MH00748, MH40381] NR 10 TC 224 Z9 225 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1993 VL 41 IS 1 BP 38 EP 41 PG 4 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA KF886 UT WOS:A1993KF88600008 PM 8418120 ER PT J AU JONES, BP AF JONES, BP TI REPRESSION - THE EVOLUTION OF A PSYCHOANALYTIC CONCEPT FROM THE 1890S TO THE 1990S SO JOURNAL OF THE AMERICAN PSYCHOANALYTIC ASSOCIATION LA English DT Article ID IMPLICIT MEMORY; EMOTION; DISCRIMINATION AB The author presents a summary of Freud's concept of repression, including modifications of the concept from 1894 to 1932. Several more recent treatments are examined, including those of Piaget; Rosenblatt and Thickstun; Galin; Kissin; Shapiro and Perry; Schwartz; the cognitive and experimental psychologists, including Kihlstrom and Erdelyi; the ''connectionists''; and Edelman. Finally, the author delineates several different types of repression, outlining how the different models might apply to the different types of repression. C1 NIMH,PSYCHOL & PSYCHOPATHOL LAB,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,SCH MED,WASHINGTON,DC 20052. GEORGE WASHINGTON UNIV,SCH MED,WASHINGTON,DC 20052. NR 67 TC 9 Z9 9 U1 0 U2 0 PU INT UNIV PRESS INC PI MADISON PA 59 BOSTON POST RD PO BOX 1524, MADISON, CT 06443-1524 SN 0003-0651 J9 J AM PSYCHOANAL ASS JI J. Am. Psychoanal. Assoc. PY 1993 VL 41 IS 1 BP 63 EP 93 PG 31 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA KJ164 UT WOS:A1993KJ16400003 PM 8426058 ER PT J AU HALLETT, M DUBINSKY, RM AF HALLETT, M DUBINSKY, RM TI GLUCOSE-METABOLISM IN THE BRAIN OF PATIENTS WITH ESSENTIAL TREMOR SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE ESSENTIAL TREMOR; POSITRON EMISSION TOMOGRAPHY; GLUCOSE METABOLISM; CEREBELLUM; INFERIOR OLIVARY NUCLEUS; THALAMUS ID VIM THALAMOTOMY; SPINAL-CORD; STIMULATION; CEREBELLUM; NUCLEUS; ROOT; RAT AB Using positron emission tomography with [F-18]fluoro-2-deoxyglucose, we determined the regional cerebral metabolic rate of glucose utilization at rest in 8 medication-free patients with essential tremor and in 10 normal subjects. Taking the metabolic values of regions of interest as ratios to the mean hemispheric metabolism, the patients showed significant glucose hypermetabolism of the medulla and thalami, but not of the cerebellar cortex. This study lends support to earlier suggestions that circuits involving the inferior olivary nuclei in the medulla and the thalmus are involved in the generation of essential tremor. RP HALLETT, M (reprint author), NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BLDG 10,ROOM 5N226,BETHESDA,MD 20892, USA. NR 17 TC 97 Z9 103 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD JAN PY 1993 VL 114 IS 1 BP 45 EP 48 DI 10.1016/0022-510X(93)90047-3 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA KG672 UT WOS:A1993KG67200008 PM 8433096 ER PT J AU WALTHER, MM LINEHAN, WM AF WALTHER, MM LINEHAN, WM TI SURGERY FOLLOWING RESPONSE TO INTERFERON-ALPHA-BASED THERAPY FOR RESIDUAL RENAL-CELL CARCINOMA - COMMENT SO JOURNAL OF UROLOGY LA English DT Editorial Material RP WALTHER, MM (reprint author), NCI,SURG BRANCH,UROL ONCOL SECT,BETHESDA,MD 20892, USA. NR 9 TC 0 Z9 0 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 JAN PY 1993 VL 149 IS 1 BP 21 EP 22 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA KE259 UT WOS:A1993KE25900007 ER PT J AU MICKISCH, GH PAI, LH SIEGSMUND, M CAMPAIN, J GOTTESMAN, MM PASTAN, I AF MICKISCH, GH PAI, LH SIEGSMUND, M CAMPAIN, J GOTTESMAN, MM PASTAN, I TI PSEUDOMONAS EXOTOXIN CONJUGATED TO MONOCLONAL-ANTIBODY MRK16 SPECIFICALLY KILLS MULTIDRUG RESISTANT CELLS IN CULTURED RENAL CARCINOMAS AND IN MDR-TRANSGENIC MICE SO JOURNAL OF UROLOGY LA English DT Article DE ANTIBODIES, MONOCLONAL; CARCINOMA, RENAL CELL; PROSTATIC NEOPLASMS; EXOTOXINS; MICE, TRANSGENIC ID INTRINSIC DRUG-RESISTANCE; GROWTH-FACTOR; BONE-MARROW; EXPRESSION; CANCER; GENE; PROTEIN; KIDNEY; RNA AB Using renal carcinoma and prostate carcinoma cell lines, we investigated the concept of targeting and killing multidrug resistant cells in urogenital cancers. Renal carcinoma lines HTB44, 45, 46, and 47 expressed a relatively low, but detectable level of multidrug resistance (MDR)1 mRNA as indicated by Northern blot analysis, whereas prostate lines LNCaP and DU145 were found to be MDR1-negative. Anti-P-glycoprotein monoclonal antibody MRK16 was conjugated to Pseudomonas exotoxin (PE) by a stable thioether bond. Treatment with MRK16-PE resulted in a dose-dependent killing of multidrug resistant renal carcinoma cells, while non-MDR expressing prostate carcinoma cells were not affected. Addition of excess MRK16 blocked the effect of MRK16-PE. Furthermore, MOPC-PE, a non-MDR associated monoclonal antibody control conjugate, did not target and kill multidrug resistant renal carcinoma cells. Having established that MRK16-PE was active against and specific for multidrug resistant cells in culture, we also tested bioactivity in MDR-transgenic mice, whose bone marrow cells express the human MDR1 gene at a level approximately equal to that found in many human cancers. Again, MRK16-PE killed multidrug resistant bone marrow cells with high efficiency in an intact animal, and killing was blocked by unconjugated MRK16. C1 NCI,DCBDC,MOLEC BIOL LAB,BLDG 37,RM 4E16,BETHESDA,MD 20892. NCI,DCBDC,CELL BIOL LAB,BETHESDA,MD 20892. NR 26 TC 25 Z9 26 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 JAN PY 1993 VL 149 IS 1 BP 174 EP 178 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA KE259 UT WOS:A1993KE25900056 PM 8417204 ER PT J AU TSUNETSUGUYOKOTA, Y OHSHIMA, M NAITO, A CHERMANN, JC SHIH, J YOSHIKURA, H AF TSUNETSUGUYOKOTA, Y OHSHIMA, M NAITO, A CHERMANN, JC SHIH, J YOSHIKURA, H TI NEW HIV PLAQUE TITRATION - APPLICATION TO THE ASSAY OF NEUTRALIZING ANTIBODY SO JOURNAL OF VIROLOGICAL METHODS LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS; PLAQUE ASSAY; NEUTRALIZING ANTIBODY ID HUMAN-IMMUNODEFICIENCY-VIRUS; T-LYMPHOTROPIC RETROVIRUS; MURINE LEUKEMIA-VIRUS; MONOCLONAL-ANTIBODIES; SERUM NEUTRALIZATION; CARRYING CELLS; AIDS; CHIMPANZEES; INFECTIVITY; PROTECTION AB A simple, sensitive and accurate plaque assay was developed using HPB-Ma, a variant of the human T-cell line HPB-ALL, which becomes adherent to the substratum after infection with an amphotropic murine sarcoma virus (MSVa). The simplicity of this novel plaque assay allowed us to. examine a large number of serum samples from patients with HIV infection for neutralizing antibody activity against two human immunodeficiency virus type-1 (HIV-1) strains. During the progression of clinical disease, the neutralizing activity in the sera from two individual patients remained unchanged or increased. A patient with a known time of HIV infection produced cross-neutralizing antibody at 25-34 weeks. The neutralizing activity in the sera from 17 asymptomatic carriers, four patients with AIDS-related complex and four AIDS patients was also examined and was found to be unrelated to the clinical stage. C1 UNIV TOKYO,FAC MED,DEPT BACTERIOL,BUNKYO KU,TOKYO 106,JAPAN. INSERM,U322,UNITE RECH RETROVIRUS & MALAD ASSOCIEES,F-13258 MARSEILLE 09,FRANCE. NIH,CTR CLIN,DEPT TRANSFUS MED,BETHESDA,MD 20892. RP TSUNETSUGUYOKOTA, Y (reprint author), NATL INST HLTH,DEPT IMMUNOL,2-10-35 KAMI OSAKI,SHINAGAWA KU,TOKYO 141,JAPAN. NR 37 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-0934 J9 J VIROL METHODS JI J. Virol. Methods PD JAN PY 1993 VL 41 IS 1 BP 47 EP 57 DI 10.1016/0166-0934(93)90162-K PG 11 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Virology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Virology GA KK262 UT WOS:A1993KK26200006 PM 8432763 ER PT J AU PRINCE, GA PORTER, DD JENSON, AB HORSWOOD, RL CHANOCK, RM GINSBERG, HS AF PRINCE, GA PORTER, DD JENSON, AB HORSWOOD, RL CHANOCK, RM GINSBERG, HS TI PATHOGENESIS OF ADENOVIRUS TYPE-5 PNEUMONIA IN COTTON RATS (SIGMODON-HISPIDUS) SO JOURNAL OF VIROLOGY LA English DT Article ID ANTIGENS; DISEASE; MODEL AB Cotton rats (Sigmodon hispidus) were inoculated intranasally with 10(2.0) to 10(10.0) PFU of human adenovirus type 5. The virus replicated to a high titer in pulmonary tissues, with the peak titer being proportional to the input dose. The 50% lethal dose was 10(9.4) PFU. Histopathologic changes were proportional to the infecting inoculum and included the infiltration of interstitial and intra-alveolar areas, moderate damage to bronchiolar epithelium, and cellular infiltration of peribronchiolar and perivascular regions. These changes could be divided into two phases: an early phase (affecting alveoli, bronchiolar epithelium, and peribronchiolar regions) with an infiltrate consisting primarily of monocytes-macrophages and neutrophils, with occasional lymphocytes, and a later phase (affecting peribronchiolar and perivascular regions) with an infiltrate consisting almost exclusively of lymphocytes. In both phases, the predominant process was the response of the host to infection, rather than direct viral damage to infected cells. An infecting inoculum of 10(8.0) PFU or larger caused severe damage to type II alveolar cells, which were swollen, showed a loss of lamellar bodies, and were surrounded by polymorphonuclear leukocytes and macrophages. No evidence of complete viral replication was found in type II alveolar cells. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PATHOL & LAB MED,LOS ANGELES,CA 90024. VIRION SYST INC,ROCKVILLE,MD 20850. GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20007. NIH,INFECT DIS LAB,BETHESDA,MD 20892. COLUMBIA UNIV COLL PHYS & SURG,DEPT MED,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT MICROBIOL,NEW YORK,NY 10032. NR 33 TC 140 Z9 142 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 JAN PY 1993 VL 67 IS 1 BP 101 EP 111 PG 11 WC Virology SC Virology GA KB970 UT WOS:A1993KB97000012 PM 8380066 ER PT J AU NAM, SH COPELAND, TD HATANAKA, M OROSZLAN, S AF NAM, SH COPELAND, TD HATANAKA, M OROSZLAN, S TI CHARACTERIZATION OF RIBOSOMAL FRAMESHIFTING FOR EXPRESSION OF POL GENE-PRODUCTS OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE-I SO JOURNAL OF VIROLOGY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; MAMMARY-TUMOR VIRUS; ROUS-SARCOMA VIRUS; PRO-GENE; GAG; RETROVIRUS; DNA; TRANSLATION; SUPPRESSION; PROTEASE AB For study of the pol gene expression of human T-cell leukemia virus type I (HTLV-1), RNA was transcribed in vitro from proviral DNA and translated in rabbit reticulocyte lysates. This cell-free translation resulted in two major translation products representing the Gag and Gag-Pro polyproteins. By contrast, the Gag-Pro-Pol polyprotein could be readily observed only when translation was performed with mutant mRNA in which the protease (pro) reading frame was aligned to gag to eliminate the frameshifting event in the gag-pro overlap. The results indicated that two independent ribosomal frameshifting events are required for expression of the HTLV-1 pol gene product. Studies with mutant DNAs facilitated the characterization of the primary structure of the HTLV-1 mRNA responsible for the ribosomal frameshift in the pro-pol overlap and demonstrated that the frameshift occurs at the signal sequence UUUAAAC. Direct amino acid sequencing of the transframe protein localized the site of the frameshift to the asparagine codon AAC. C1 NCI, FREDERICK CANC RES & DEV CTR, MOLEC VIROL & CARCINOGENESIS LAB, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA. KYOTO UNIV, INST VIRUS RES, KYOTO 606, JAPAN. FU NCI NIH HHS [N01-CO-74101] NR 40 TC 50 Z9 55 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 JAN PY 1993 VL 67 IS 1 BP 196 EP 203 PG 8 WC Virology SC Virology GA KB970 UT WOS:A1993KB97000022 PM 8416368 ER PT J AU OWSIANKA, AM HART, G MURPHY, M GOTTLIEB, J BOEHME, R CHALLBERG, M MARSDEN, HS AF OWSIANKA, AM HART, G MURPHY, M GOTTLIEB, J BOEHME, R CHALLBERG, M MARSDEN, HS TI INHIBITION OF HERPES-SIMPLEX VIRUS TYPE-1 DNA-POLYMERASE-ACTIVITY BY PEPTIDES FROM THE UL42 ACCESSORY PROTEIN IS LARGELY NONSPECIFIC SO JOURNAL OF VIROLOGY LA English DT Article ID BINDING PROTEIN; RIBONUCLEOTIDE REDUCTASE; GENE-PRODUCT; ORIGIN; IDENTIFICATION; REPLICATION; REGION; GENOME; SUBUNIT-2; TERMINUS AB To identify regions in the ULA2 protein of herpes simplex virus type 1 which affect viral DNA polymerase activity, a series of 96 overlapping pentadecapeptides spanning the entire 488 amino acids of the UL42 protein were synthesized and tested for their ability to inhibit polymerase activity on a primed single-stranded M13 DNA template. Two assays were used: formation of full-length double-stranded M13 molecules and rate of incorporation of deoxyribonucleoside triphosphates. Peptides from five noncontiguous regions of the UL42 protein were found to inhibit herpes simplex virus type 1 polymerase activity in both the presence and absence of UL42 protein. The most active peptides from each region correspond to amino acids 23 to 38 (peptide 6), 64 to 78 (peptide 14), 89 to 102 (peptide 19), 229 to 243 (peptide 47), and 279 to 293 (peptide 57). By two different methods (DNA mobility shift and DNA precipitation), peptides 14, 19, 47, and 57 were found to bind DNA; they most probably inhibit enzyme activity by this mechanism. Peptide 6 did not bind DNA and must act by some mechanism other than competing for DNA. The inhibitory peptides were also tested for activity against mammalian polymerase ci and the Klenow fragment of Escherichia coli polymerase. Although some limited specificity was demonstrated (up to 10-fold for peptide 6), all the peptides showed significant activity against both polymerase alpha and E. coli polymerase. C1 MRC,VIROL UNIT,CHURCH ST,GLASGOW G11 5JR,SCOTLAND. GLAXO GRP RES LTD,GREENFORD UB6 0HE,MIDDX,ENGLAND. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 31 TC 12 Z9 12 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 JAN PY 1993 VL 67 IS 1 BP 258 EP 264 PG 7 WC Virology SC Virology GA KB970 UT WOS:A1993KB97000029 PM 8380075 ER PT J AU ENSOLI, B BUONAGURO, L BARILLARI, G FIORELLI, V GENDELMAN, R MORGAN, RA WINGFIELD, P GALLO, RC AF ENSOLI, B BUONAGURO, L BARILLARI, G FIORELLI, V GENDELMAN, R MORGAN, RA WINGFIELD, P GALLO, RC TI RELEASE, UPTAKE, AND EFFECTS OF EXTRACELLULAR HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TAT PROTEIN ON CELL-GROWTH AND VIRAL TRANSACTIVATION SO JOURNAL OF VIROLOGY LA English DT Article ID TRANS-ACTIVATOR GENE; LONG-TERM CULTURE; KAPOSIS-SARCOMA; HTLV-III; T-CELLS; AIDS; EXPRESSION; HIV-1; REPLICATION; RECEPTOR AB During acute human immunodeficiency virus type 1 (HIV-1) infection or after transfection of the tat gene, Tat protein is released into the cell culture supernatant. In this extracellular form, Tat stimulates both HIV-1 gene expression and the growth of cells derived from Kaposi's sarcoma (KS) lesions of HIV-1-infected individuals (AIDS-KS cells). Tat protein and its biological activities appear in the cell supernatants at the peak of Tat expression, when the rate of cell death is low (infection) or cell death is undetectable (transfection) and increased levels of cytoplasmic Tat are present. Tat-containing supernatants stimulate maximal AIDS-KS cell growth but only low to moderate levels of HIV-1 gene expression. This is due to the different concentrations of exogenous Tat required for the two effects. The cell growth-promoting effects of Tat peak at between 0.1 and 1 ng of purified recombinant protein per ml in the cell growth medium and do not increase with concentration. In contrast, both the detection of nuclear-localized Tat taken up by cells and the induction of HIV-1 gene expression or replication require higher Tat concentrations (greater-than-or-equal-to 100 ng/ml), and all increase linearly with increasing amounts of the exogenous protein. These data suggest that Tat can be released by a mechanism(s) other than cell death and that the cell growth-promoting activity and the virus-transactivating effect of extracellular Tat are mediated by different pathways. C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NIADDKD,PROT EXPRESS LAB,BETHESDA,MD 20892. RP ENSOLI, B (reprint author), NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892, USA. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 52 TC 694 Z9 705 U1 1 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 JAN PY 1993 VL 67 IS 1 BP 277 EP 287 PG 11 WC Virology SC Virology GA KB970 UT WOS:A1993KB97000031 PM 8416373 ER PT J AU BRESSLER, P BROWN, K TIMMER, W BOURS, V SIEBENLIST, U FAUCI, AS AF BRESSLER, P BROWN, K TIMMER, W BOURS, V SIEBENLIST, U FAUCI, AS TI MUTATIONAL ANALYSIS OF THE P50-SUBUNIT OF NF-KAPPA-B AND INHIBITION OF NF-KAPPA-B ACTIVITY BY TRANSDOMINANT P50 MUTANTS SO JOURNAL OF VIROLOGY LA English DT Article ID DNA-BINDING SUBUNIT; REL-ASSOCIATED PP40; P65 SUBUNIT; C-REL; TRANSCRIPTION FACTORS; V-REL; PROTEIN; ONCOGENE; CLONING; DORSAL AB The NF-kappaB family of DNA-binding proteins regulates the expression of many cellular and viral genes. Each of these proteins has an N-terminal region that is homologous to the c-Rel proto-oncogene product, and this Rel homology region defines both DNA binding and protein dimerization properties of the individual proteins. Most of the NF-kappaB family members have been shown to associate with themselves or with each other to form homodimers or heterodimers, and previous studies have shown that dimerization of NF-kappaB factors is necessary to provide a functional DNA binding domain. We have used site-directed mutagenesis to identify regions in the Rel homology domain of the p50/NF-kappaB protein that are important for DNA binding and protein dimerization. Our studies have identified mutations of p50 that interfere with DNA binding only and those that interfere with protein dimerization. Mutations of p50 which disrupt only DNA binding were still able to associate with other members of the NF-kappaB protein family. We demonstrate that such heterodimeric complexes inhibit transcriptional activation mediated in trans through a cis-acting kappaB motif; therefore, we have identified trans-dominant negative mutants of p50. RP BRESSLER, P (reprint author), NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892, USA. NR 32 TC 55 Z9 55 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 JAN PY 1993 VL 67 IS 1 BP 288 EP 293 PG 6 WC Virology SC Virology GA KB970 UT WOS:A1993KB97000032 PM 8416374 ER PT J AU LAUTENBERGER, JA PAPAS, TS AF LAUTENBERGER, JA PAPAS, TS TI INVERSION OF A CHICKEN ETS-1 PROTOONCOGENE SEGMENT IN AVIAN LEUKEMIA VIRUS-E26 SO JOURNAL OF VIROLOGY LA English DT Note ID HOST RANGE; NUCLEOTIDE-SEQUENCE; TRANSFORMING GENE; V-ETS; RETROVIRUSES; LOCUS AB The segment of the avian leukemia virus E26 genome near the termination of the p135gag-myb-ets open reading frame contains an inversion of the chicken ets-1 sequence. The inversion contains at least 41 bp and may be as large as 46 bp. This results in the replacement of 13 amino acids of chicken ets-1, with 16 amino acids derived from reverse complement of the normal ets-1 coding strand or read-through into E26 env sequences. At least 13 of these codons are specified by the inverted ets sequences. This represents the first reported occurrence of inverted oncogene sequences in a natural retrovirus. The inverted ets sequences are immediately followed by sequences homologous to the Rous sarcoma virus Prague B env gene. Since the E26 env sequence is more closely related to subgroup B avian retroviruses than to avian retroviruses from subgroups A, C, D, or E, the progenitor of E26 was a virus belonging to avian retrovirus subgroup B. RP LAUTENBERGER, JA (reprint author), NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702, USA. NR 18 TC 9 Z9 9 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 JAN PY 1993 VL 67 IS 1 BP 610 EP 612 PG 3 WC Virology SC Virology GA KB970 UT WOS:A1993KB97000075 PM 8380097 ER PT J AU LI, BG LARRALDE, G GORZIGLIA, M AF LI, BG LARRALDE, G GORZIGLIA, M TI HUMAN ROTAVIRUS-K8 STRAIN REPRESENTS A NEW VP4 SEROTYPE SO JOURNAL OF VIROLOGY LA English DT Note ID OUTER CAPSID PROTEIN; AMINO-ACID-SEQUENCE; NEUTRALIZATION EPITOPES; UNIQUE VP4; BACULOVIRUS RECOMBINANT; IDENTIFICATION; ANTIBODIES; SPECIFICITIES; INFECTIVITY; CHALLENGE AB The complete VP4 gene of the human rotavirus (HRV) K8 strain (G1 serotype) was cloned and inserted into the baculovirus transfer vector pVL941 under the control of the polyhedrin promoter. A K8VP4 recombinant baculovirus was obtained by cotransfection of Spodoptera frugiperda (Sf9) cells with transfer vector DNA containing the K8VP4 gene and wild-type baculovirus DNA. Infection of Sf9 cells with this VP4 recombinant baculovirus resulted in the production of a protein that is similar in size and antigenic activity to the authentic VP4 of the K8 strain. Guinea pigs immunized with the expressed VP4 developed antibodies that neutralized the infectivity of the K8 strain. This antiserum neutralized HRV strains belonging to VP4 serotypes 1A, 1B, and 2 with efficiency eightfold or lower than that of the homologous virus, indicating that the human rotavirus K8 strain represents a distinct VP4 serotype (P3). In addition, low levels of cross-immunoprecipitation of the K8VP4 and its VP5 and VP8 subunits with hyperimmune antisera to HRV strains representing different VP4 serotype specificities also suggested that the K8 strain possesses a unique VP4 with few epitopes in common with other P-serotype strains. C1 NIAID,INFECT DIS LAB,BETHESDA,MD 20892. NR 24 TC 12 Z9 12 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 JAN PY 1993 VL 67 IS 1 BP 617 EP 620 PG 4 WC Virology SC Virology GA KB970 UT WOS:A1993KB97000077 PM 8380098 ER PT J AU SHIP, JA WEIFFENBACH, JM AF SHIP, JA WEIFFENBACH, JM TI AGE, GENDER, MEDICAL-TREATMENT, AND MEDICATION EFFECTS ON SMELL IDENTIFICATION SO JOURNALS OF GERONTOLOGY LA English DT Article ID OF-PENNSYLVANIA SMELL; OLFACTORY FUNCTION; ODOR IDENTIFICATION; NASAL PUNGENCY; UNIVERSITY; PERCEPTION; ABILITY; TASTE AB Olfactory function diminishes with increasing age, which may impact on the safety and quality of life of older persons. This study examined the influence of age, gender, medical treatment, and medications on smell identification in a group of generally healthy individuals. Males (n = 221) and females (n = 166) between the ages Of 19 and 95 years, from the oral physiology component of the Baltimore Longitudinal Study of Aging, were administered the University of Pennsylvania Smell Identification Test [UPSIT; (1)]. Older subjects had lower UPSIT scores, were more likely to be anosmic, and more often complained about their sense of smell and taste compared to younger subjects. Females had higher UPSIT scores compared to males. Although these age and gender effects are comparable to previous findings, performance among all subjects was superior to other studies; this is attributable, in part, to the overall healthy status of the population. Subjects being treated for medical problems and taking prescription medications had slightly lower UPSIT scores and more smell and taste complaints compared to other subjects, but these findings did not achieve statistical significance. Results suggest that age-related declines in olfaction occur as a part of the normal physiological aging process. C1 NIDR, CLIN INVEST & PATIENT CARE BRANCH, BETHESDA, MD 20892 USA. NR 54 TC 61 Z9 64 U1 3 U2 3 PU GERONTOLOGICAL SOC AMER PI WASHINGTON PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA SN 0022-1422 J9 J GERONTOL JI J. Gerontol. PD JAN PY 1993 VL 48 IS 1 BP M26 EP M32 PG 7 WC Gerontology SC Geriatrics & Gerontology GA KF930 UT WOS:A1993KF93000006 PM 8418141 ER PT J AU SCHNAPER, HW KLEINMAN, HK GRANT, DS AF SCHNAPER, HW KLEINMAN, HK GRANT, DS TI ROLE OF LAMININ IN ENDOTHELIAL-CELL RECOGNITION AND DIFFERENTIATION SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT SYMP ON CELL AND MOLECULAR BIOLOGY OF BASEMENT MEMBRANES IN HEALTH AND DISEASE : FOREFRONTS IN NEPHROLOGY CY SEP 20-22, 1991 CL AIRLIE, VA SP INT SOC NEPHROL ID FIBROBLAST GROWTH-FACTOR; EXTRACELLULAR-MATRIX INTERACTIONS; CAPILLARY-LIKE STRUCTURES; BASEMENT-MEMBRANE; ANGIOGENESIS INVITRO; COMPONENTS; RAT; MORPHOGENESIS; ORGANIZATION; CHEMOTAXIS AB The vascular endothelium normally is maintained in a quiescent state, but under certain conditions it is induced to undergo marked changes in behavior and form new vascular structures. A complex interaction among various growth and differentiation factors and the extracellular milieu regulates this behavior. One series of signals affecting endothelial behavior is provided by laminin, a major structural protein of basement membrane. These signals have been studied using Matrigel, a reconstituted basement membrane preparation from the murine Englebreth-Holm-Swarm sarcoma, in an in vitro assay of endothelial cell differentiation. Three biologically-active sequences from the laminin molecule have been evaluated. Synthetic peptides that include the sequences -RGD-, -YIGSR-, and -SIKVAV- mediate, respectively, cell binding to Matrigel, alterations in cell morphology, and induction of migration and collagenase activity. Preliminary data indicate that observations made with this system may be relevant to endothelial function in vivo. Endothelial cell differentiation on Matrigel may thus be a useful in vitro model for the study of certain steps in angiogenesis. C1 CHILDRENS HOSP,NATL MED CTR,DEPT NEPHROL,WASHINGTON,DC 20010. RP SCHNAPER, HW (reprint author), NIDR,DEV BIOL LAB,BLDG 30,ROOM 407,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 47 TC 42 Z9 42 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1993 VL 43 IS 1 BP 20 EP 25 DI 10.1038/ki.1993.5 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA KC891 UT WOS:A1993KC89100005 PM 8433560 ER PT J AU CIOCE, V MARGULIES, IMK SOBEL, ME CASTRONOVO, V AF CIOCE, V MARGULIES, IMK SOBEL, ME CASTRONOVO, V TI INTERACTION BETWEEN THE 67 KILODALTON METASTASIS-ASSOCIATED LAMININ RECEPTOR AND LAMININ SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT SYMP ON CELL AND MOLECULAR BIOLOGY OF BASEMENT MEMBRANES IN HEALTH AND DISEASE : FOREFRONTS IN NEPHROLOGY CY SEP 20-22, 1991 CL AIRLIE, VA SP INT SOC NEPHROL ID CELL-ADHESION; EXTRACELLULAR-MATRIX; BINDING-PROTEIN; CARCINOMA-CELLS; HEPARIN-BINDING; MESSENGER-RNA; CANCER-CELLS; IV COLLAGEN; HUMAN COLON; FIBRONECTIN AB Normal and neoplastic cells interact with laminin via a variety of cell surface proteins. The specific binding sites on laminin for each particular cell surface laminin-binding protein have not yet been identified. In this study, the interaction between laminin and the high affinity metastasis-associated 67 kD laminin receptor (67 LR) was investigated by electron microscopy using the rotary shadowing technique. Laminin receptor that was purified from human colon carcinoma metastases appeared as a globular structure with a diameter of 5.2 +/- 0.8 nm. The 67 LR specifically bound to laminin on its long arm close to the intersection of the long and the short arms. There was no specific interaction of bovine serum albumin with laminin. Biochemical confirmation of the rotary shadowing experiments included slot blot solid phase assays in which [I-125]-labeled 67 LR bound in a dose dependent manner to laminin as well as to the chymotrypsin resistant (C1) fragment of laminin that contains a short piece of the long arm. [I-125]-labeled 67 LR did not bind to the pepsin resistant (P1) fragment of laminin that did not contain that segment on the long arm. This study therefore identifies the binding site on laminin for the 67 kD metastasis-associated laminin receptor as a region on the long arm of laminin close to the intersection of the four arms. C1 NCI,PATHOL LAB,TUMOR INVAS & METASTASIS SECT,BLDG 10,ROOM 2A33,BETHESDA,MD 20892. NR 39 TC 15 Z9 16 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1993 VL 43 IS 1 BP 30 EP 37 DI 10.1038/ki.1993.7 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA KC891 UT WOS:A1993KC89100007 PM 8433567 ER PT J AU STRACKE, ML SOROUSH, M LIOTTA, LA SCHIFFMANN, E AF STRACKE, ML SOROUSH, M LIOTTA, LA SCHIFFMANN, E TI CYTOSKELETAL AGENTS INHIBIT MOTILITY AND ADHERENCE OF HUMAN TUMOR-CELLS SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT SYMP ON CELL AND MOLECULAR BIOLOGY OF BASEMENT MEMBRANES IN HEALTH AND DISEASE : FOREFRONTS IN NEPHROLOGY CY SEP 20-22, 1991 CL AIRLIE, VA SP INT SOC NEPHROL ID HUMAN-MELANOMA CELLS; CHEMOTAXIS; MICROTUBULES; FIBROBLASTS; LOCOMOTION; MIGRATION; INVASION; LAMININ; MATRIX AB Cytoskeletal agents have been demonstrated to inhibit stimulated motility and substrate adherence by the human tumor cell line, A2058. cis-tubulozole, taxol, and cytochalasin D were tested for their effects on chemotaxis in response to a tumor cytokine, autocrine motility factor, and on adherence to several substrata: laminin- and gelatin-coated dishes as well as tissue culture plastic. Cytochalasin D, which inhibits microfilament polymerization, abolished stimulated motility. Taxol, which stabilizes microtubules, decreased stimulated motility to a greater degree than cis-tubulozole, which inhibits microtubular polymerization. In contrast, cis-tubulozole had the greatest inhibitory effect on adherence with a gelatin substratum more affected (100% inhibition) than tissue culture plastic (90%) or laminin substratum (52%). Taxol affected adherence in the same order but less than cis-tubulozole. Cytochalasin D had no significant effect on adherence to laminin with moderate inhibition of adherence to tissue culture plastic or gelatin. These data suggest that, in these tumor cells, microfilaments are more crucial for motility than adherence, but the dynamic polymerization and depolymerization of microtubules are required for both types of cellular activities. RP STRACKE, ML (reprint author), NCI,PATHOL LAB,BLDG 10,ROOM 2A33,BETHESDA,MD 20892, USA. NR 28 TC 37 Z9 39 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1993 VL 43 IS 1 BP 151 EP 157 DI 10.1038/ki.1993.25 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA KC891 UT WOS:A1993KC89100025 PM 8094471 ER PT J AU BROWN, PD KLEINER, DE UNSWORTH, EJ STETLERSTEVENSON, WG AF BROWN, PD KLEINER, DE UNSWORTH, EJ STETLERSTEVENSON, WG TI CELLULAR ACTIVATION OF THE 72 KDA TYPE-IV PROCOLLAGENASE/TIMP-2 COMPLEX SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT SYMP ON CELL AND MOLECULAR BIOLOGY OF BASEMENT MEMBRANES IN HEALTH AND DISEASE : FOREFRONTS IN NEPHROLOGY CY SEP 20-22, 1991 CL AIRLIE, VA SP INT SOC NEPHROL ID TISSUE INHIBITOR; INTERSTITIAL COLLAGENASE; FIBROBLAST COLLAGENASE; ENDOGENOUS ACTIVATION; 72-KDA PROGELATINASE; LATENT COLLAGENASE; METALLOPROTEINASES-2; IDENTIFICATION; PURIFICATION; METASTASIS AB Members of the collagenase family of enzymes have been implicated as central mediators of a number of both physiologic and pathologic processes. The 72-kDa type IV collagenase is secreted as a latent proenzyme, complexed with tissue inhibitor of metalloproteinase-2 (TIMP-2). Like other members of the collagenase family, this enzyme complex must be converted to a catalytically active form for proteolytic remodeling of extracellular matrix to occur. In the current study we demonstrate an inducible cell-mediated activation of the 72-kDa type IV procollagenase/TIMP-2 complex. Isolation of the 62 kDa activated enzyme/TIMP-2 complex from conditioned media of concanavalin A treated WI-38 fibroblasts demonstrated that the cell activated species was proteolytically active and amino terminal sequencing gave the sequence YNFF. This is identical to that of the 62 kDa species generated following organomercurial activation of purified 72-kDa type IV procollagenase/TIMP-2 complex. We have also isolated biosynthetically S-35-labeled 72-kDa type IV procollagenase/TIMP-2 complex and used this to further study the cellular activation process. In cell lines tested the activator was retained in the residual cell fraction following lysis in the presence of 0.2% (wt/vol) Brij-35. Inhibitor studies demonstrated that processing and activation of 72-kDa type IV procollagenase/TIMP-2 complex by the residual fraction was inhibited by 5 mM ethylenediaminetetraacetic acid and 0.5 mM 1,10-phenanthroline demonstrating a metal atom dependence. The species responsible for activation could be partially recovered in soluble form with 0.5% (vol/vol) Triton X-100 and 0.25% (wt/vol) CHAPS but was not salt extractable. This cellular activation process differs from that demonstrated for interstitial collagenase in that it is not mediated by soluble factors and is not plasminogen activator/plasmin dependent. C1 NCI,PATHOL LAB,ROOM 2A33,BLDG 10,BETHESDA,MD 20892. RI Stetler-Stevenson, William/H-6956-2012; OI Stetler-Stevenson, William/0000-0002-5500-5808; Kleiner, David/0000-0003-3442-4453 NR 24 TC 125 Z9 125 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1993 VL 43 IS 1 BP 163 EP 170 DI 10.1038/ki.1993.27 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA KC891 UT WOS:A1993KC89100027 PM 8433556 ER PT J AU ABBOUD, HE SCHENA, FP COHEN, JJ STERZEL, RB STRIKER, G GESUALDO, L FINE, LG STRIKER, L PETEN, E THOMSON, N CAMERON, S BORSATTI, A RUBINKELLY, VE REMUZZI, G AF ABBOUD, HE SCHENA, FP COHEN, JJ STERZEL, RB STRIKER, G GESUALDO, L FINE, LG STRIKER, L PETEN, E THOMSON, N CAMERON, S BORSATTI, A RUBINKELLY, VE REMUZZI, G TI GROWTH-FACTORS IN GLOMERULONEPHRITIS SO KIDNEY INTERNATIONAL LA English DT Discussion ID TUMOR-NECROSIS-FACTOR; GLOMERULAR MESANGIAL CELLS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MEMBRANE ATTACK COMPLEX; FACTOR-I; FACTOR-BETA; GENE-EXPRESSION; PDGF RECEPTOR; ENDOTHELIAL-CELLS; MESSENGER-RNA C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. UNIV BARI, DIV NEPHROL, I-70124 BARI, ITALY. SUNY STONY BROOK, STONY BROOK, NY 11794 USA. UNIV ERLANGEN NURNBERG, W-8520 ERLANGEN, GERMANY. NIH, DIV KIDNEY UROL & HEMATOL DIS, BETHESDA, MD 20892 USA. UNIV COLL & MIDDLESEX SCH MED, DEPT MED, LONDON, ENGLAND. NIDDKD, BETHESDA, MD USA. UNIV HOSP PADOVA, DIV NEPHROL, PADUA, ITALY. MONASH UNIV, QUEEN VICTORIA MED CTR, MELBOURNE, VIC 3004, AUSTRALIA. GUYS HOSP, LONDON SE1 9RT, ENGLAND. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. MARIO NEGRI INST PHARMACOL RES, KIDNEY DIS LAB, I-20157 MILAN, ITALY. RP ABBOUD, HE (reprint author), UNIV TEXAS, HLTH SCI CTR, DIV NEPHROL, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. RI Schena, Francesco /K-6982-2016 OI Schena, Francesco /0000-0001-7927-5207 FU NIDDK NIH HHS [DK 43988, DK 33665] NR 156 TC 198 Z9 200 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1993 VL 43 IS 1 BP 252 EP 267 DI 10.1038/ki.1993.39 PG 16 WC Urology & Nephrology SC Urology & Nephrology GA KC891 UT WOS:A1993KC89100039 PM 8433565 ER PT J AU PETEN, EP STRIKER, LJ GARCIAPEREZ, A STRIKER, GE AF PETEN, EP STRIKER, LJ GARCIAPEREZ, A STRIKER, GE TI STUDIES BY COMPETITIVE PCR OF GLOMERULOSCLEROSIS IN GROWTH-HORMONE TRANSGENIC MICE SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON MOLECULAR APPROACHES TO NEPHROLOGY CY MAR 19-21, 1992 CL BARI, ITALY SP FRESENIUS SISTEMI TERAPEUTICI ID POLYMERASE CHAIN-REACTION; MESSENGER-RNA LEVELS; EXTRACELLULAR-MATRIX; PROGRESSIVE GLOMERULOSCLEROSIS; IV COLLAGEN; NEPHRITIS; EXPRESSION; GLOMERULI; LAMININ; KIDNEY AB We have shown that the glomerulosclerotic lesions of mice transgenic for bovine growth hormone (bGH mice) consisted of a change in the phenotype of glomerular collagens and an elevation of the mRNAs for these collagens in whole kidney. The purpose of this study was to determine whether these phenotypic and quantitative changes were present in the glomeruli. We used the increased sensitivity afforded by reverse transcription followed by the polymerase chain reaction (RT-PCR) to detect type I collagen mRNA and a quantitative PCR assay to quantitate type IV collagen mRNA in microdissected glomeruli. There was a six- to eightfold increase in alpha1IV collagen mRNA in the glomeruli of bGh mice. alpha1(I) collagen mRNA was present in glomeruli of bGH mice, which is consistent with our previous findings that the sclerotic mesangium contained type I collagen peptides by immunofluorescence microscopy. Normal glomeruli did not contain detectable amounts of all collagen mRNA. In summary, we found a phenotypic change in glomeruli of mice transgenic for bGH consisting of increased type IV collagen mRNA levels and the appearance of type I collagen mRNA. Thus, the development of glomerulosclerosis appeared to be at least partially regulated at a pretranslational level. C1 NIDDK,METAB DIS BRANCH,RENAL CELL BIOL SECT,BLDG 10,ROOM 3N110,BETHESDA,MD 20892. NHLBI,KIDNEY & ELECTROLYTE METAB,BETHESDA,MD 20892. NR 22 TC 24 Z9 24 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1993 VL 43 SU 39 BP S55 EP S58 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA KD536 UT WOS:A1993KD53600011 PM 8468927 ER PT J AU YANG, CW STRIKER, LJ KOPCHICK, JJ CHEN, WY PESCE, CM PETEN, EP STRIKER, GE AF YANG, CW STRIKER, LJ KOPCHICK, JJ CHEN, WY PESCE, CM PETEN, EP STRIKER, GE TI GLOMERULOSCLEROSIS IN MICE TRANSGENIC FOR NATIVE OR MUTATED BOVINE GROWTH-HORMONE GENE SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON MOLECULAR APPROACHES TO NEPHROLOGY CY MAR 19-21, 1992 CL BARI, ITALY SP FRESENIUS SISTEMI TERAPEUTICI ID POLYMERASE CHAIN-REACTION; FACTOR-I; PROGRESSIVE GLOMERULOSCLEROSIS; MESANGIAL CELLS; EXPRESSION; SCLEROSIS; TURNOVER; LESIONS AB Mice transgenic for bovine growth hormone (bGH) develop an increase in body weight and glomerular lesions characterized by a disproportionate increment in glomerular volume and progressive mesangial sclerosis. The relationship between glomerular size and body growth in bGH mice was further investigated by examining mice transgenic for a mutated GH gene (bGH-m11) which failed to enhance body growth. The glomeruli in bGH-m11 mice exhibited an increase in size and glomerulosclerosis comparable to those found in bGH mice. The levels of al type IV collagen mRNA, as measured by the competitive polymerase chain reaction in isolated microdissected glomeruli, were markedly elevated in mice transgenic for both bGH and bGH-m11 genes. These data suggest that body growth on one hand, and glomerular hypertrophy and sclerosis on the other hand, are mediated by different portions of GH or different second messenger signaling systems. C1 NIDDKD,RENAL CELL BIOL SECT,METAB DIS BRANCH,BLDG 10,ROOM 3N110,BETHESDA,MD 20892. OHIO UNIV,DEPT ZOOL,MOLEC & CELLULAR BIOL PROGRAM,ATHENS,OH 45701. OHIO UNIV,EDISON ANIM BIOTECHNOL CTR,ATHENS,OH 45701. NR 26 TC 13 Z9 13 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1993 VL 43 SU 39 BP S90 EP S94 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA KD536 UT WOS:A1993KD53600018 ER PT J AU ABATI, A SOLOMON, D AF ABATI, A SOLOMON, D TI DIAGNOSIS OF PULMONARY MICROVASCULAR METASTATIC TUMOR BY CYTOLOGIC EVALUATION OF SWAN-GANZ DERIVED BLOOD SPECIMENS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A27 EP A27 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200152 ER PT J AU ABRUZZO, L JAFFE, ES CAMPO, E STETLERSTEVENSON, MA SANDER, C BAUER, F DOW, N MEDEIROS, LJ AF ABRUZZO, L JAFFE, ES CAMPO, E STETLERSTEVENSON, MA SANDER, C BAUER, F DOW, N MEDEIROS, LJ TI IMMATURE HEMATOPOIETIC-CELL NEOPLASMS WITH POTENTIAL FOR DIFFERENTIATION ALONG T-LYMPHOID AND MYELOID LINES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV BARCELONA,BARCELONA 7,SPAIN. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. RHODE ISL HOSP,PROVIDENCE,RI 02902. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A84 EP A84 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200492 ER PT J AU ARBER, DA WEISS, LM ALBUJAR, PE JAFFE, ES AF ARBER, DA WEISS, LM ALBUJAR, PE JAFFE, ES TI NASAL LYMPHOMAS IN PERU - HIGH-INCIDENCE OF T-CELL IMMUNOPHENOTYPE AND EPSTEIN-BARR-VIRUS INFECTION SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV TRUJILLO,TRUJILLO,PERU. CITY HOPE NATL MED CTR,DUARTE,CA 91010. BELAN HOSP,TRUJILLO,PERU. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A84 EP A84 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200496 ER PT J AU BENNETT, WP BORKOWSKI, A COLBY, TV JONES, RT LANE, DP METCALF, RA SAMET, JM TAKESHIMA, Y TRAVIS, WD TRUMP, BF VAHAKANGAS, KH WELSH, JA HARRIS, CC AF BENNETT, WP BORKOWSKI, A COLBY, TV JONES, RT LANE, DP METCALF, RA SAMET, JM TAKESHIMA, Y TRAVIS, WD TRUMP, BF VAHAKANGAS, KH WELSH, JA HARRIS, CC TI P53 MUTATION AND IMMUNOPOSITIVITY IN THE PATHOGENESIS OF HUMAN BRONCHOGENIC-CARCINOMA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV MARYLAND,BALTIMORE,MD 21201. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. UNIV DUNDEE,DUNDEE DD1 4HN,SCOTLAND. UNIV NEW MEXICO,ALBUQUERQUE,NM 87131. UNIV OULU,SF-90100 OULU 10,FINLAND. RI Lane, David/C-4920-2008 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A129 EP A129 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200759 ER PT J AU CAMPO, E MUNOZ, J MIQUEL, R PALACIN, A SLOAN, BF LIOTTA, LA CARDESA, A BUCK, MR AF CAMPO, E MUNOZ, J MIQUEL, R PALACIN, A SLOAN, BF LIOTTA, LA CARDESA, A BUCK, MR TI CATHEPSIN-B EXPRESSION IN COLORECTAL CARCINOMAS CORRELATES WITH TUMOR PROGRESSION SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV BARCELONA,HOSP CLIN,BARCELONA 7,SPAIN. WAYNE STATE UNIV,DETROIT,MI 48202. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A44 EP A44 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200254 ER PT J AU CASTIGLIONI, T MERINO, MJ ELSNER, B BUCK, M AF CASTIGLIONI, T MERINO, MJ ELSNER, B BUCK, M TI ARE CATHEPSINS-B, CATHEPSINS-D OR CATHEPSINS-L OF PROGNOSTIC VALUE IN THE DIAGNOSIS OF BREAST-CANCER SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CEMIC,BUENOS AIRES,ARGENTINA. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A13 EP A13 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200069 ER PT J AU DEAVERS, M GUINEE, D KOSS, M TRAVIS, W AF DEAVERS, M GUINEE, D KOSS, M TRAVIS, W TI GRANULAR-CELL TUMORS (GCT) OF THE LUNG - CLINICOPATHOLOGICAL STUDY OF 15 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 WRAMC,DEPT PATHOL,WASHINGTON,DC. AFIP,DEPT PATHOL,WASHINGTON,DC. NCI,PATHOL 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A129 EP A129 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200764 ER PT J AU FEMANDEZ, PL MERINO, MJ GOMEZMORALES, M CASTRONOVO, V LIU, FT SOBEL, ME AF FEMANDEZ, PL MERINO, MJ GOMEZMORALES, M CASTRONOVO, V LIU, FT SOBEL, ME TI IMMUNOHISTOCHEMICAL STUDY OF THE 31KD LAMININ BINDING-PROTEIN AND LAMININ IN THYROID CARCINOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. FAC MED GRANADA,GRANADA,SPAIN. SCRIPPS CLIN & RES FDN,LA JOLLA,CA 92037. HOSP CLIN BARCELONA,BARCELONA,SPAIN. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A38 EP A38 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200218 ER PT J AU GAFFEY, MJ FRIERSON, HF MEDEIROS, LJ WEISS, LM AF GAFFEY, MJ FRIERSON, HF MEDEIROS, LJ WEISS, LM TI THE RELATIONSHIP OF EPSTEIN-BARR-VIRUS TO INFECTION-RELATED AND FAMILIAL HEMOPHAGOCYTIC SYNDROME AND SECONDARY HEMOPHAGOCYTOSIS - AN INSITU HYBRIDIZATION STUDY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV VIRGINIA,HLTH SCI CTR,CHARLOTTESVILLE,VA 22903. NCI,BETHESDA,MD 20892. CITY HOPE NATL MED CTR,DUARTE,CA 91010. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A90 EP A90 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200528 ER PT J AU GIORDANO, TJ MEDEIROS, LJ MONTERROSO, V LINEHAN, WM MERINO, MJ AF GIORDANO, TJ MEDEIROS, LJ MONTERROSO, V LINEHAN, WM MERINO, MJ TI IMMUNOHISTOCHEMICAL DETECTION OF PREALBUMIN IN RENAL-CELL CARCINOMA AND OTHER TISSUES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A60 EP A60 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200348 ER PT J AU GREINER, TC JAFFE, ES AF GREINER, TC JAFFE, ES TI ANALYSIS OF CLONAL TCR-GAMMA GENE REARRANGEMENTS IN PARAFFIN EMBEDDED T-CELL LYMPHOID NEOPLASMS BY DENATURING GRADIENT GEL-ELECTROPHORESIS OF GC-CLAMPED PCR PRODUCTS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A91 EP A91 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200535 ER PT J AU GUINEE, D KOSS, M TRAVIS, W AF GUINEE, D KOSS, M TRAVIS, W TI IMMUNOHISTOCHEMISTRY (IHC) OF SMALL-CELL LUNG-CARCINOMA (SCLC) IN TRANSBRONCHIAL BIOPSIES (TBB) AND OPEN LUNG BIOPSIES (OLB) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 AFIP,DEPT PULM & MEDIASTINAL PATHOL,WASHINGTON,DC. NCI,PATHOL 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A131 EP A131 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200772 ER PT J AU HIJAZI, Y WORTHY, E STEINBERG, S HOROWITZ, M TSOKOS, M AF HIJAZI, Y WORTHY, E STEINBERG, S HOROWITZ, M TSOKOS, M TI EWING SARCOMA (ES) VS PRIMITIVE NEUROECTODERMAL TUMOR (PNET) - DOES HISTOLOGY PLAY A ROLE IN PROGNOSIS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A126 EP A126 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200745 ER PT J AU JHANWAR, SC CHEN, Q LI, FP PARRY, D BRENNAN, ME AF JHANWAR, SC CHEN, Q LI, FP PARRY, D BRENNAN, ME TI CYTOGENETIC ABERRATIONS IN MALIGNANT PERIPHERAL-NERVE SHEATH TUMORS (MPNST) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A7 EP A7 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200033 ER PT J AU KARAMERIS, A QUEZADO, M TSOKOS, M AF KARAMERIS, A QUEZADO, M TSOKOS, M TI P-53 MUTATIONS IN RHABDOMYOSARCOMA DETECTED BY A NONRADIOISOTOPIC METHOD ON PARAFFIN SECTIONS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A127 EP A127 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200748 ER PT J AU KARAMERIS, A MISER, J MISER, A TSOKOS, M AF KARAMERIS, A MISER, J MISER, A TSOKOS, M TI PROLIFERATING CELL NUCLEAR ANTIGEN (PCNA) IN CHILDHOOD RHABDOMYOSARCOMA (RMS) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 CHILDRENS HOSP,MED CTR,SEATTLE,WA. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A7 EP A7 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200034 ER PT J AU KINGMA, DW MEDIEROS, LJ ROMAN, LN JAFFE, ES AF KINGMA, DW MEDIEROS, LJ ROMAN, LN JAFFE, ES TI EXPRESSION OF EPSTEIN-BARR VIRAL(EBV) EBERI RNA IN MULTIFOCAL AIL OF DISCORDANT HISTOLOGIC GRADES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. RHODE ISL HOSP,PROVIDENCE,RI 02902. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A94 EP A94 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200552 ER PT J AU KINGMA, DW MEDEIROS, LJ AMBINDER, RF JAFFE, ES AF KINGMA, DW MEDEIROS, LJ AMBINDER, RF JAFFE, ES TI EPSTEIN-BARR-VIRUS IN COMPOSITE NON-HODGKINS-LYMPHOMA AND HODGKINS-DISEASE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A94 EP A94 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200551 ER PT J AU KINGMA, DW MEDEIROS, LJ ZARATEOSORNO, A LONGO, DL AMBINDER, RF JAFFE, ES AF KINGMA, DW MEDEIROS, LJ ZARATEOSORNO, A LONGO, DL AMBINDER, RF JAFFE, ES TI HODGKINS-DISEASE (HD) FOLLOWING NON-HODGKINS-LYMPHOMA (NHL) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A93 EP A93 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200550 ER PT J AU LINNOILA, RI BECKER, RL STEINBERG, SM KAISER, HR LACK, EE AF LINNOILA, RI BECKER, RL STEINBERG, SM KAISER, HR LACK, EE TI THE ROLE OF S100 PROTEIN CONTAINING CELLS IN THE PROGNOSIS OF SYMPATHOADRENAL PARAGANGLIOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. GEORGETOWN UNIV,DEPT PATHOL,WASHINGTON,DC 20057. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A39 EP A39 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200224 ER PT J AU LUBENSKY, IA YANG, JC MERINO, MJ AF LUBENSKY, IA YANG, JC MERINO, MJ TI SARCOMAS OF THE BREAST - THE NCI EXPERIENCE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A17 EP A17 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200092 ER PT J AU MEDEIROS, LJ KINGMA, DW MARTIN, AW BARKER, RL JAFFE, ES PEIPER, SC AF MEDEIROS, LJ KINGMA, DW MARTIN, AW BARKER, RL JAFFE, ES PEIPER, SC TI EPSTEIN-BARR-VIRUS (EBV)-INDUCED LYMPHOPROLIFERATIVE DISORDERS (LPD) MANIFESTING AS PLASMACYTOMAS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 JG BROWN CANC CTR,LOUISVILLE,KY. RHODE ISL HOSP,PROVIDENCE,RI 02902. NCI,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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A96 EP A96 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200565 ER PT J AU MERINO, MJ ROTH, M LUBENSKY, IA AF MERINO, MJ ROTH, M LUBENSKY, IA TI METASTATIC OVARIAN-CANCER PRESENTING AS PRIMARY-CARCINOMA OF THE BREAST SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A76 EP A76 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200446 ER PT J AU MERINO, MJ FERNANDEZ, PL DONNE, C LUNA, MA AF MERINO, MJ FERNANDEZ, PL DONNE, C LUNA, MA TI MALIGNANT MIXED TUMORS OF THE BREAST SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. MD ANDERSON HOSP,HOUSTON,TX. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A17 EP A17 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200094 ER PT J AU MONTERROSO, V MERINO, MJ JAFFE, ES MEDEIROS, LJ AF MONTERROSO, V MERINO, MJ JAFFE, ES MEDEIROS, LJ TI NON-HODGKIN LYMPHOMA (NHL) INVOLVING THE OVARY - A CLINICOPATHOLOGICAL ANALYSIS OF 39 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A76 EP A76 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200448 ER PT J AU MOSKALUK, C COWAN, K MERINO, M AF MOSKALUK, C COWAN, K MERINO, M TI EXPRESSION OF GSTPI IN BENIGN AND MALIGNANT PROSTATE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A65 EP A65 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200379 ER PT J AU SANDER, CA JAFFE, ES YANO, T ABRUZZO, LV MEDEIROS, LJ AF SANDER, CA JAFFE, ES YANO, T ABRUZZO, LV MEDEIROS, LJ TI LYMPHOBLASTIC LYMPHOMA OF B-CELL LINEAGE (B-LBL) INVOLVING SKIN SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,HEMATOPATHOL SECT,BETHESDA,MD 20892. RHODE ISL HOSP,DEPT PATHOL,PROVIDENCE,RI 02902. NR 0 TC 1 Z9 1 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A99 EP A99 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200585 ER PT J AU SCOPA, CD MASTORAKOS, G MERINO, MJ CHROUSOS, GP AF SCOPA, CD MASTORAKOS, G MERINO, MJ CHROUSOS, GP TI IMMUNOREACTIVE CORTICOTROPIN RELEASING HORMONE IN THE HUMAN OVARY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,PATHOL LAB,BETHESDA,MD 20892. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A41 EP A41 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200237 ER PT J AU STETLERSTEVENSON, M WANG, J LEVY, A STETLERSTEVENSON, WG AF STETLERSTEVENSON, M WANG, J LEVY, A STETLERSTEVENSON, WG TI DIFFERENTIAL EXPRESSION OF TISSUE INHIBITORS OF MATRIX METALLOPROTEINASES (TIMPS) AND MATRIX METALLOPROTEINASES (MM9-2, MMP-9) IN CELLS OF B-CELL AND T-CELL ORIGIN SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,PATHOL LAB,BETHESDA,MD 20892. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A100 EP A100 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200591 ER PT J AU ZARATEOSORNO, A MEDEIROS, LJ KINGMA, DW BARLETTA, J LONGO, DL AMBINDER, RF JAFFE, ES AF ZARATEOSORNO, A MEDEIROS, LJ KINGMA, DW BARLETTA, J LONGO, DL AMBINDER, RF JAFFE, ES TI NON-HODGKINS-LYMPHOMA (NHL) FOLLOWING HODGKINS-DISEASE (HD) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1993 VL 68 IS 1 BP A104 EP A104 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA KJ102 UT WOS:A1993KJ10200611 ER PT J AU TSAO, YH EVANS, DF RAND, RP PARSEGIAN, VA AF TSAO, YH EVANS, DF RAND, RP PARSEGIAN, VA TI OSMOTIC-STRESS MEASUREMENTS OF DIHEXADECYLDIMETHYLAMMONIUM ACETATE BILAYERS AS A FUNCTION OF TEMPERATURE AND ADDED SALT SO LANGMUIR LA English DT Article ID INTERFERENCE CONTRAST MICROSCOPY; AQUEOUS-ELECTROLYTE SOLUTIONS; 2 MICA SURFACES; RANGE 0-100 NM; MYELIN FIGURES; LECITHIN BILAYERS; HYDRATION FORCES; AMMONIUM ACETATE; SURFACTANTS; MEMBRANES AB Interaction forces between dihexadecyldimethylammonium acetate (DHDAA) bilayers were measured using osmotic stress (OS) and surface forces apparatus (SFA) techniques as a function of temperature and sodium acetate concentration (5-500 mM). Below T(c), the hydrocarbon chain melting temperature, the two techniques gave identical force curves. Above T(c), the OS-derived repulsive forces were slightly higher and more slowly decaying than the SFA-derived curves. The difference is consistent with a contribution from thermal-mechanical undulations allowed to occur in the multilayers used in the OS preparation but suppressed in the SFA by immobilization of the bilayers onto mica surfaces. The OS measurements at surface separations of 0-8 angstrom showed strong hydration form identical above and below T(c). This observation would suggest that neither thermal-mechanical undulations nor molecular protrusions contribute significantly to DHDAA hydration forces. Above T(c) and below a critical osmotic stress, P(c), DHDAA bilayers unbind from multilayers to form myelin structures. Visualization by video-enhanced microscopy (VEM) shows that the myelin structures coexist with a gradually disappearing and progressively dehydrated multilayer phase. Comparison of P(c) for different salt concentrations with the direct electrostatic P(e) and mechanical undulatory P(f) components suggests that unbinding occurs at a constant value of P(e) which is independent of salt concentration and bilayer separation. C1 UNIV MINNESOTA,DEPT CHEM ENGN & MAT SCI,MINNEAPOLIS,MN 55455. BROCK UNIV,ST CATHARINES L2S 3A1,ONTARIO,CANADA. NIH,BETHESDA,MD 20892. NR 35 TC 47 Z9 47 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0743-7463 J9 LANGMUIR JI Langmuir PD JAN PY 1993 VL 9 IS 1 BP 233 EP 241 DI 10.1021/la00025a045 PG 9 WC Chemistry, Multidisciplinary; Chemistry, Physical; Materials Science, Multidisciplinary SC Chemistry; Materials Science GA KJ101 UT WOS:A1993KJ10100045 ER PT J AU DELANEY, TF SINDELAR, WF THOMAS, GF DELUCA, AM TAUBENBERGER, JK AF DELANEY, TF SINDELAR, WF THOMAS, GF DELUCA, AM TAUBENBERGER, JK TI TOLERANCE OF SMALL-BOWEL ANASTOMOSES IN RABBITS TO PHOTODYNAMIC THERAPY WITH DIHEMATOPORPHYRIN ETHERS AND 630 NM RED-LIGHT SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE ABDOMINAL SURGERY; INTESTINES; LASER; PHOTOTHERAPY; TOLERANCE ID NORMAL TISSUE; INTRAPERITONEAL; RATS AB Photodynamic therapy (PDT) is being evaluated in experimental clinical trials in patients with peritoneal malignancies. Some patients require partial small bowel resection with re-anastomosis prior to PDT because of bulky tumor or focal involvement of the small bowel by tumor. To assess the safety of PDT in this setting, the tolerance of small bowel anastomoses in New Zealand white rabbits to PDT with dihematoporphyrin ethers (DHE) and 630 nm light was studied. With conventional DHE doses of 1.5-2.5 mg/kg given 24 hours prior to surgery and light doses of 0-20 J/cm(2) of 630 nm light, no adverse effects were seen on the healing of small bowel anastomoses. Higher photosensitizer doses of 10 mg/kg and 20 mg/kg in conjunction with 20 J/cm(2), however, induced failure and breakdown of fresh anastomoses in 2/3 and 4/4 animals, respectively. (C) 1993 Wiley-Liss, Inc.* C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 17 TC 3 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1993 VL 13 IS 6 BP 664 EP 671 DI 10.1002/lsm.1900130611 PG 8 WC Dermatology; Surgery SC Dermatology; Surgery GA MK723 UT WOS:A1993MK72300010 PM 8295476 ER PT B AU JUENGST, ET AF JUENGST, ET GP SUFFOLK UNIVERSITY LAW SCHOOL TI THE HUMAN GENOME PROJECT - SOCIETY RESPONSIBILITY FOR THE ETHICAL, LEGAL, AND SOCIAL IMPLICATIONS SO LAW AND SCIENCE AT THE CROSSROADS: BIOMEDICAL TECHNOLOGY, ETHICS, PUBLIC POLICY AND THE LAW LA English DT Proceedings Paper CT Conference on Law and Science at the Crossroads: Biomedical Technology, Ethics, Public Policy and the Law CY OCT 21-22, 1993 CL BOSTON, MA SP SUFFOLK UNIV LAW SCH, UNIV MASSACHUSETTS MED CTR, OFF CONTINUING EDUC C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SUFFOLK UNIV LAW SCHOOL PI BOSTON PA ADVANCED LEGAL STUDIES, 41 TEMPLE STREET, BOSTON, MA 02114 PY 1993 BP 275 EP 275 PG 1 WC Law; Social Sciences, Biomedical SC Government & Law; Biomedical Social Sciences GA BZ93T UT WOS:A1993BZ93T00035 ER PT B AU JUENGST, ET WATSON, JD AF JUENGST, ET WATSON, JD GP SUFFOLK UNIVERSITY LAW SCHOOL TI HUMAN GENOME RESEARCH AND THE RESPONSIBLE USE OF NEW GENETIC KNOWLEDGE SO LAW AND SCIENCE AT THE CROSSROADS: BIOMEDICAL TECHNOLOGY, ETHICS, PUBLIC POLICY AND THE LAW LA English DT Proceedings Paper CT Conference on Law and Science at the Crossroads: Biomedical Technology, Ethics, Public Policy and the Law CY OCT 21-22, 1993 CL BOSTON, MA SP SUFFOLK UNIV LAW SCH, UNIV MASSACHUSETTS MED CTR, OFF CONTINUING EDUC DE HUMAN GENOME; NATIONAL-CENTER-FOR-HUMAN-GENOME-RESEARCH; ETHICAL; LEGAL AND SOCIAL IMPLICATIONS; GENETIC TESTS; COUNSELING; ACCESS TO GENETIC INFORMATION C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SUFFOLK UNIV LAW SCHOOL PI BOSTON PA ADVANCED LEGAL STUDIES, 41 TEMPLE STREET, BOSTON, MA 02114 PY 1993 BP 277 EP 280 PG 4 WC Law; Social Sciences, Biomedical SC Government & Law; Biomedical Social Sciences GA BZ93T UT WOS:A1993BZ93T00036 ER PT B AU JUENGST, ET AF JUENGST, ET GP SUFFOLK UNIVERSITY LAW SCHOOL TI PRIORITIES IN PROFESSIONAL ETHICS AND SOCIAL-POLICY FOR HUMAN-GENETICS SO LAW AND SCIENCE AT THE CROSSROADS: BIOMEDICAL TECHNOLOGY, ETHICS, PUBLIC POLICY AND THE LAW LA English DT Proceedings Paper CT Conference on Law and Science at the Crossroads: Biomedical Technology, Ethics, Public Policy and the Law CY OCT 21-22, 1993 CL BOSTON, MA SP SUFFOLK UNIV LAW SCH, UNIV MASSACHUSETTS MED CTR, OFF CONTINUING EDUC C1 NIH,NATL CTR HUMAN GENOME RES,PROGRAM ETHICAL LEGAL & SOCIAL IMPLICAT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SUFFOLK UNIV LAW SCHOOL PI BOSTON PA ADVANCED LEGAL STUDIES, 41 TEMPLE STREET, BOSTON, MA 02114 PY 1993 BP 281 EP 282 PG 2 WC Law; Social Sciences, Biomedical SC Government & Law; Biomedical Social Sciences GA BZ93T UT WOS:A1993BZ93T00037 ER PT B AU LEROITH, D WERNER, H BONDY, C ROBERTS, CT AF LEROITH, D WERNER, H BONDY, C ROBERTS, CT BE Laron, Z Parks, JS TI ONTOGENY OF THE INSULIN-LIKE GROWTH-FACTOR RECEPTORS SO LESSONS FROM LARON SYNDROME ( LS ) 1966-1992: A MODEL OF GH AND IGF-1 ACTION AND INTERACTION SE PEDIATRIC AND ADOLESCENT ENDOCRINOLOGY LA English DT Proceedings Paper CT ARES-SERONO SYMP ON LESSONS FROM LARON SYNDROME ( LS ) 1966-1992 : A MODEL OF GH AND IGF-1 ACTION AND INTERACTION CY MAY 25-26, 1992 CL LISBON, PORTUGAL SP ARES SERONO SYMP RP LEROITH, D (reprint author), NIDDK,DIABET BRANCH,BLDG 10,ROOM 85239,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5671-3 J9 PEDIAT AD E PY 1993 VL 24 BP 192 EP 201 PG 10 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pediatrics SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pediatrics GA BY26G UT WOS:A1993BY26G00026 ER PT B AU LEROITH, D ADAMO, M KATO, H ROBERTS, CT AF LEROITH, D ADAMO, M KATO, H ROBERTS, CT BE Laron, Z Parks, JS TI DIVERGENCE OF INSULIN AND INSULIN-LIKE GROWTH FACTOR-I SIGNALING PATHWAYS SO LESSONS FROM LARON SYNDROME ( LS ) 1966-1992: A MODEL OF GH AND IGF-1 ACTION AND INTERACTION SE PEDIATRIC AND ADOLESCENT ENDOCRINOLOGY LA English DT Proceedings Paper CT ARES-SERONO SYMP ON LESSONS FROM LARON SYNDROME ( LS ) 1966-1992 : A MODEL OF GH AND IGF-1 ACTION AND INTERACTION CY MAY 25-26, 1992 CL LISBON, PORTUGAL SP ARES SERONO SYMP RP LEROITH, D (reprint author), NIDDK,DIABET BRANCH,BLDG 10,ROOM 85239,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 6 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5671-3 J9 PEDIAT AD E PY 1993 VL 24 BP 346 EP 358 PG 13 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pediatrics SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pediatrics GA BY26G UT WOS:A1993BY26G00045 ER PT J AU CHESON, BD AF CHESON, BD TI PURINE ANALOGS IN LYMPHOPROLIFERATIVE DISORDERS SO LEUKEMIA & LYMPHOMA LA English DT Article; Proceedings Paper CT Meeting on Leukemia...The Next Question CY MAR 24-27, 1993 CL HOUSTON, TX DE HAIRY CELL LEUKEMIA; PURINE ANALOGS; CLL; PROLYMPHOCYTIC LEUKEMIA; NON-HODGKINS LYMPHOMA RP CHESON, BD (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,CLIN INVEST BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-8194 J9 LEUKEMIA LYMPHOMA JI Leuk. Lymphoma PY 1993 VL 11 SU 2 BP 153 EP 159 DI 10.3109/10428199309064276 PG 7 WC Oncology; Hematology SC Oncology; Hematology GA MQ775 UT WOS:A1993MQ77500024 PM 7907252 ER PT J AU LAMBERT, GW EISENHOFER, G JENNINGS, GL ESLER, MD AF LAMBERT, GW EISENHOFER, G JENNINGS, GL ESLER, MD TI REGIONAL HOMOVANILLIC-ACID PRODUCTION IN HUMANS SO LIFE SCIENCES LA English DT Article ID CENTRAL DOPAMINERGIC ACTIVITY; PLASMA DIHYDROXYPHENYLALANINE; NOREPINEPHRINE TURNOVER; SCHIZOPHRENIC-PATIENTS; METABOLITES; SYSTEM; RAT; NORADRENALINE; DEBRISOQUIN; HYPOTENSION AB Peripheral plasma levels of homovanillic acid (HVA), the deaminated and o-methylated metabolite of dopamine, are often used as an indicator of central nervous system dopaminergic activity. Using percutaneously placed catheters, we studied the regional inputs into the plasma HVA pool in 60 healthy volunteers. Veno-arterial differences and organ plasma flows were used to quantify the relative amounts of HVA contributed by various sites into the peripheral circulation. Positive arterio-venous HVA gradients were found in the pulmonary, hepatosplanchnic, skeletal muscle and jugular vessels of the normal volunteers. No HVA increment was found in the coronary sinus. The renal circulation was determined to be the principal site of HVA clearance, extracting 27 nmol/min. The regional contributions of HVA were as follows: lungs 21 nmol/min, hepatosplanchnic organs 3 nmol/min, skeletal muscle 3 nmol/min and the brain 4 nmol/min. The pattern of regional HVA production contrasted with that of the deaminated dopamine metabolite, dihydroxyphenylacetic acid, for which the heart was the principal site of production identified. Sixteen patients with chronic congestive heart failure (CHF) and 6 patients with pure autonomic failure (PAF) were also studied to investigate possible effects of sympathetic nervous system overactivity and underactivity on peripheral HVA production and plasma HVA concentration. The resting arterial plasma HVA concentration in CHF was increased approximately 3-fold. Unexpectedly, this was attributable to reduced HVA plasma clearance, not increased HVA production. Total HVA production in PAF was diminished by 40 %. PAF patients had normal resting arterial HVA levels, this being accounted for by a 57 % fall in the renal plasma clearance of HVA. Acute sympathetic nervous system activation in response to bicycle riding was accompanied by a 34 % increase in the arterial concentration of HVA. It can be concluded that HVA is produced at a number of sites throughout the body not renowned for their dopaminergic innervation. Regional HVA production is associated, in part, with the metabolism of precursor dopamine in sympathetic nerves and at a rate which appears to be influenced by sympathetic nervous activity. To obtain an accurate indication of central dopaminergic activity the confounding influences of HVA plasma clearance and peripheral HVA production must be excluded. C1 BAKER MED RES INST,ALFRED BAKER MED UNIT,PRAHRAN,VIC 3181,AUSTRALIA. NIH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP LAMBERT, GW (reprint author), BAKER MED RES INST,HUMAN AUTONOM FUNCT LAB,COMMERCIAL RD,PRAHRAN,VIC 3181,AUSTRALIA. RI Jennings, Garry/B-3914-2009; Lambert, Gavin/E-7384-2010 OI Lambert, Gavin/0000-0003-0315-645X NR 38 TC 25 Z9 25 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 1 BP 63 EP 75 DI 10.1016/0024-3205(93)90612-7 PG 13 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LE505 UT WOS:A1993LE50500007 PM 8515683 ER PT J AU CIZZA, G KVETNANSKY, R TARTAGLIA, ME BLACKMAN, MR CHROUSOS, GP GOLD, PW AF CIZZA, G KVETNANSKY, R TARTAGLIA, ME BLACKMAN, MR CHROUSOS, GP GOLD, PW TI IMMOBILIZATION STRESS RAPIDLY DECREASES HYPOTHALAMIC CORTICOTROPIN-RELEASING HORMONE-SECRETION INVITRO IN THE MALE 344/N FISCHER RAT SO LIFE SCIENCES LA English DT Article ID PITUITARY-ADRENAL AXIS; GROWTH-HORMONE; PARAVENTRICULAR NUCLEUS; LEWIS RATS; GLUCOCORTICOIDS; HEMORRHAGE; MECHANISM; ARTHRITIS; BASAL AB Corticotropin-Releasing-Hormone (CRH) is the principal secretagogue for plasma ACTH and corticosterone secretion and plays an important role in coordinating a variety of physiological and behavioral responses to stress. To explore whether there is a rapid change in the secretory response of the hypothalamic CRH neuron during acute stress, we report here a study of the effects of KCl and norepinephrine (NE) on CRH release in vitro from rat hypothalami explanted after 5, 30, 60, and 120 minutes of immobilization. We also measured the plasma levels of ACTH, beta-endorphin, corticosterone, prolactin, GH, and TSH at these intervals. As the duration of immobilization increased, KCl and NE-induced CRH release in vitro progressively fell. After reaching a maximal rise after 30 minutes of immobilization, plasma ACTH, beta-endorphin, and prolactin progressively fell in plasma, whereas corticosterone remained elevated up to 120 minutes; TSH and GH secretion rapidly declined and remained suppressed. Taken together, these data suggest that during immobilization stress, the responsiveness of the hypothalamic CRH neuron rapidly falls, owing either to CRH depletion and/or desensitization to NE, and this is paralleled by a concomitant decrease in pituitary-adrenal responsiveness. C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NINCDS,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NIA,GERONTOL RECH INST,BALTIMORE,MD 21224. RP CIZZA, G (reprint author), NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. NR 31 TC 20 Z9 20 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 3 BP 233 EP 240 DI 10.1016/0024-3205(93)90674-R PG 8 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LG814 UT WOS:A1993LG81400007 PM 8391619 ER PT J AU FARRIS, FF DEDRICK, RL AF FARRIS, FF DEDRICK, RL TI ABSORPTION OF METHYLMERCURY FROM HAIR INGESTED BY RATS SO LIFE SCIENCES LA English DT Article ID MAMMALIAN PREY DIGESTIBILITY; INORGANIC MERCURY; TRANSPORT AB Hair taken from rats dosed with Hg-203-labeled methylmercury was fed to previously untreated rats in order to determine if the organo-mercurial was available for release from the hair matrix within the gut lumen and for subsequent systemic absorption. Cumulative fecal excretion data were consistent with an absorption of about 80% of the ingested methylmercury. The relative amounts of methylmercury and of its metabolite, inorganic mercury, in the feces indicated that the percentage of the parent compound released from hair within the intestine equaled or exceeded the estimated bioavailability. Radioactivity in tissues of animals killed 42 hr following hair consumption confirmed that mercury absorption had occurred. C1 NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RP FARRIS, FF (reprint author), US FDA,CTR DRUG EVALUAT & RES,DIV CLIN PHARMACOL,4 RES COURT,ROOM 314,ROCKVILLE,MD 20850, USA. NR 30 TC 2 Z9 2 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 12 BP 1023 EP 1029 DI 10.1016/0024-3205(93)90125-M PG 7 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LT666 UT WOS:A1993LT66600007 PM 8361326 ER PT J AU BERGASA, NV THOMAS, DA VERGALLA, J TURNER, ML JONES, EA AF BERGASA, NV THOMAS, DA VERGALLA, J TURNER, ML JONES, EA TI PLASMA FROM PATIENTS WITH THE PRURITUS OF CHOLESTASIS INDUCES OPIOID RECEPTOR-MEDIATED SCRATCHING IN MONKEYS SO LIFE SCIENCES LA English DT Article ID RAT MODEL AB The medullary dorsal horn is a site of action of opiates in producing facial scratching. Extracts of plasma (0.4 mul) from 4 patients with the pruritus of cholestasis induced facial scratching when microinjected into the medullary dorsal horn of monkeys. This extract-induced scratching could be abolished or prevented by administering the opioid receptor antagonist, naloxone. Neither saline nor an extract of plasma from a nonpruritic cholestatic patient induced scratching when similarly administered. We infer that plasma of patients with the pruritus of cholestasis contains a factor which induces pruritus by a central opioid receptor-mediated mechanism. C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. NIDDKD,LIVER DIS SECT,BETHESDA,MD. NCI,DERMATOL SECT,BETHESDA,MD 20892. NR 10 TC 50 Z9 51 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 16 BP 1253 EP 1257 PG 5 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LW976 UT WOS:A1993LW97600001 PM 8412484 ER PT J AU WESS, J AF WESS, J TI MUTATIONAL ANALYSIS OF MUSCARINIC ACETYLCHOLINE-RECEPTORS - STRUCTURAL BASIS OF LIGAND-RECEPTOR G-PROTEIN INTERACTIONS SO LIFE SCIENCES LA English DT Review ID SITE-DIRECTED MUTAGENESIS; BETA-ADRENERGIC-RECEPTOR; 3RD CYTOPLASMIC LOOP; ANTAGONIST BINDING; COUPLED RECEPTORS; ALPHA-2-ADRENERGIC RECEPTORS; CHOLINERGIC RECEPTOR; ADENYLATE-CYCLASE; TYROSINE RESIDUES; BOVINE RHODOPSIN AB Molecular cloning studies have revealed the existence of five molecularly distinct muscarinic acetylcholine receptors (m1-m5), which differ in their tissue distribution, ligand binding properties, and functional profiles. Structurally (and functionally), the muscarinic receptors are members of the superfamily of G protein-coupled receptors. A variety of different mutagenesis techniques have been used to study the molecular basis of muscarinic receptor function. This approach has led to the identification of distinct receptor domains (or individual amino acids) predicted to play key roles in ligand binding, agonist-dependent receptor activation, and G protein coupling. Since all G protein-linked receptors share a similar molecular architecture, the information gained from the mutational analysis of muscarinic receptors should help delineate functionally important regions of other members of this receptor family. RP WESS, J (reprint author), NIDDKD,BIOORGAN CHEM LAB,BLDG 8A,ROOM B1A-09,BETHESDA,MD 20892, USA. NR 80 TC 82 Z9 83 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 19 BP 1447 EP 1463 DI 10.1016/0024-3205(93)90618-D PG 17 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MA451 UT WOS:A1993MA45100001 PM 8412508 ER PT J AU BAGDY, G SZEMEREDI, K LISTWAK, SJ KEISER, HR GOLDSTEIN, DS AF BAGDY, G SZEMEREDI, K LISTWAK, SJ KEISER, HR GOLDSTEIN, DS TI PLASMA-CATECHOLAMINE, RENIN-ACTIVITY, AND ACTH RESPONSES TO THE SEROTONIN RECEPTOR AGONIST DOI IN JUVENILE SPONTANEOUSLY HYPERTENSIVE RATS SO LIFE SCIENCES LA English DT Article ID SYMPATHETIC-NERVE ACTIVITY; BLOOD-PRESSURE; CONSCIOUS RATS; HEART-RATE; CORTICOSTERONE SECRETION; M-CHLOROPHENYLPIPERAZINE; ARTERIAL-PRESSURE; MENTAL STRESS; INCREASES; ACTIVATION AB Mean arterial blood pressure (MAP), heart rate (HR) and arterial plasma levels of corticotropin (ACTH), renin activity (PRA) and catechols [norepinephrine (NE), epinephrine (EPI), and the intraneuronal NE metabolite dihydroxyphenylglycol (DHPG)] at baseline and in response to the serotonin-1C/2 (5-HT1C/ 5-HT2) agonist 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane (DOI, 1.0 mg/kg i.a.) in conscious, freely-moving,juvenile (4 week old) spontaneously hypertensive rats (SHR's) and age-matched Wistar-Kyoto (WKY) normotensive control rats were measured simultaneously. Baseline levels of MAP, NE, DHPG, and EPI all were significantly higher in the SHR's. There was a similar trend for PRA, but ACTH did not differ between the two strains. DOI produced marked increases in levels of MAP, ACTH, EPI, and also PRA but did not affect NE or DHPG concentrations. HR decreased only in the WKY group after administration of DOI. The magnitudes of the EPI and ACTH responses did not differ between the rat strains. Responses of MAP and PRA were significantly larger in SHR's. These results suggest that there is a selective hyperresponsiveness of PRA and blood pressure to 5-HT2 receptor stimulation parallel to a deficient baroreceptor reflex in juvenile SHR's. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. NHLBI,HYPERTENS ENDOCRINE BRANCH,BETHESDA,MD 20892. RP BAGDY, G (reprint author), NATL INST PSYCHIAT & NEUROL,EXPTL MED LAB,POB 1,H-1281 BUDAPEST 27,HUNGARY. OI Bagdy, Gyorgy/0000-0001-8141-3410 NR 43 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 21 BP 1573 EP 1582 DI 10.1016/0024-3205(93)90180-B PG 10 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MD198 UT WOS:A1993MD19800001 PM 8231634 ER PT J AU GALA, RR SHEVACH, EM AF GALA, RR SHEVACH, EM TI INFLUENCE OF BROMOCRIPTINE ADMINISTRATION TO MOTHERS ON THE DEVELOPMENT OF PUP THYMOCYTE AND SPLENOCYTE SUBSETS AND ON MITOGEN-INDUCED PROLIFERATION IN THE MOUSE SO LIFE SCIENCES LA English DT Article ID GROWTH-HORMONE; MILK PROLACTIN; MICE; RATS; LYMPHOCYTES; DEFICIENCY; FEMALE; SERUM AB The influence of prolactin (PRL) on the development of the immune system in the mouse was studied by injecting mothers with bromocriptine (CB-154) to produce hypoprolactinemic milk. Alterations in pup thymocyte and splenocyte cell subsets were observed to graded doses of CB-154 administered to mothers. There was an increase in the relative percentages of neonate thymic CD4 and CD8 cells at 5 days of age when mothers were injected with 100 mug of CB-1 54 2 x daily from day 1 to 5 of lactation, however, there was no alteration in absolute thymic subset cell numbers. The relative percentage of pup spleen CD4, CD8 and B cells were increased when mothers were administered 50 or 100 mug of CB-154 and the 50 mug dose resulted in a significant increase in the absolute number of CD4 cells while the 100 mug dose induced a significant decrease in the three splenic cell subsets examined. Graded doses of CB-154 administered to mothers resulted in decreases in the PRL concentration of stomach milk as measured by the Nb2 cell proliferation assay. The serum PRL level of the pups, however, was not altered by any dose of CB-154 injected to the mothers. The administration of PRL to pups nursing mothers given the 100 mug dose of CB-154 did not alter the pup thymocyte and splenocyte subset population from that of litter-mate controls. The administration of mouse PRL and mouse growth hormone antisera to pups nursing saline-injected mothers did not alter thymocyte and splenocyte subsets from that of saline-injected litter mate controls. The proliferation of neonatal thymocytes by Con-A stimulation was not altered by CB-154 injection to mothers and PRL administration to pups. However, since the percentage of thymic CD4 and CD8 cells in the thymus was increased 2 to 3 fold, the apparent lack of effect was in fact a decrease in the responsiveness of the thymocytes. Con-A stimulation of neonatal splenocytes resulted in a significant increase in proliferation for mothers administered CB-154 in keeping with the increase relative percentage of CD4 and CD8 cells observed. Prolactin administration to the pups did not alter the response. LPS stimulation of neonatal splenocytes increased the proliferation of B cells taken from pup nursing mothers administered CB-154 and PRL administration appeared to partially block this proliferation. The data suggest that the changes observed in thymocyte and splenocyte subsets of pups nursing mothers receiving CB-154 was not due to the hypoprolactinemic milk but may be due to other factors such as undernutrition. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RP GALA, RR (reprint author), WAYNE STATE UNIV,SCH MED,DEPT PHYSIOL,DETROIT,MI 48201, USA. FU PHS HHS [IPA 2-8325806] NR 24 TC 11 Z9 11 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 26 BP 1981 EP 1994 DI 10.1016/0024-3205(93)90020-4 PG 14 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MH902 UT WOS:A1993MH90200007 PM 8255161 ER PT J AU MALIN, DH LAKE, JR ARCANGELI, KAR DESHOTEL, KD HAUSAM, DD WITHERSPOON, WE CARTER, VA YANG, HYT PAL, B BURGESS, K AF MALIN, DH LAKE, JR ARCANGELI, KAR DESHOTEL, KD HAUSAM, DD WITHERSPOON, WE CARTER, VA YANG, HYT PAL, B BURGESS, K TI SUBCUTANEOUS INJECTION OF AN ANALOG OF NEUROPEPTIDE-FF PRECIPITATES MORPHINE ABSTINENCE SYNDROME SO LIFE SCIENCES LA English DT Letter ID PHASE PEPTIDE-SYNTHESIS; RAT SPINAL-CORD; MODULATING PEPTIDE; RECEPTORS; FLFQPQRFAMIDE; TOLERANCE AB Neuropeptide FF (NPFF) has been shown to exert various antiopiate actions, including precipitation of opiate abstinence syndrome by third ventricle injection in morphine dependent rats. In the present study, dansyl-Pro-Gln-Arg-Phe-amide, a lipophilic analog of NPFF, was injected into morphine dependent rats and appropriate sham controls at a dose of 9 mg/kg s.c. Comparison groups were injected with ethanol/water vehicle alone. The NPFF analog precipitated a vigorous opiate abstinence syndrome in morphine dependent rats. but not in sham controls. C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. TEXAS A&M UNIV SYST,DEPT CHEM,COLL STN,TX 77843. RP MALIN, DH (reprint author), UNIV HOUSTON CLEAR LAKE,BOX 237,HOUSTON,TX 77058, USA. RI Burgess, Kevin/B-5372-2015 OI Burgess, Kevin/0000-0001-6597-1842 NR 20 TC 10 Z9 11 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 17 BP PL261 EP PL266 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LX473 UT WOS:A1993LX47300010 ER PT J AU ROTHMAN, RB BECKETTS, KM RADESCA, LR DECOSTA, BR RICE, KC CARROLL, FI DERSCH, CM AF ROTHMAN, RB BECKETTS, KM RADESCA, LR DECOSTA, BR RICE, KC CARROLL, FI DERSCH, CM TI STUDIES OF THE BIOGENIC-AMINE TRANSPORTERS .2. A BRIEF STUDY ON THE USE OF [H-3] DA-UPTAKE-INHIBITION TO TRANSPORTER-BINDING-INHIBITION RATIOS FOR THE IN-VITRO EVALUATION OF PUTATIVE COCAINE ANTAGONISTS SO LIFE SCIENCES LA English DT Letter ID DOPAMINE TRANSPORTERS; RECEPTORS; LIGAND; SITE AB The cocaine receptor on the dopamine transporter is a logical target binding site for the design and synthesis of novel agents for evaluation as possible cocaine antagonists. Although there is no widely accepted and validated assay for detecting a cocaine antagonist, one commonly accepted strategy is to compare the IC50 value of a test agent for inhibition of [H-3]dopamine uptake and its IC50 value for inhibition of the binding of a transporter ligand such as [I-1251]RTI-55. The goal of such a comparison is to guide the synthesis of agents which have high ''uptake-to-binding ratios'', i.e. agents which are much more potent in the binding assay than they are in the uptake assay. In the present study we tested the hypothesis that ratios different from unity can result from the fact that the two assays are conducted under markedly different conditions. The results showed that conducting the uptake and binding assays under identical conditions reduced the GBR12935 uptake-to-binding ratio of 6.20 (under standard assay conditions) to 0.36. These data indicate that uptake-to-binding ratios must be interpreted with caution, and emphasizes the need for simpler and less expensive methods than cocaine self-administration paradigms to screen compounds as modulators of cocaine reinforcement. C1 LAB MED CHEM,BETHESDA,MD 20892. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. RP ROTHMAN, RB (reprint author), NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,POB 5180,BALTIMORE,MD 21224, USA. NR 16 TC 24 Z9 24 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 17 BP PL267 EP PL272 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LX473 UT WOS:A1993LX47300011 ER PT J AU WITKIN, JM AF WITKIN, JM TI BLOCKADE OF THE LOCOMOTOR STIMULANT EFFECTS OF COCAINE AND METHAMPHETAMINE BY GLUTAMATE ANTAGONISTS SO LIFE SCIENCES LA English DT Letter ID RECEPTOR ANTAGONIST; ASPARTATE AB The AMPA antagonist, NBQX, produced dose-dependent blockade of the locomotor stimulant effects of cocaine and methamphetamine in male, Swiss-Webster mice at doses which did not alter spontaneous locomotion. A similar finding was obtained with the competitive NMDA antagonist, NPC 12626, although blockade was only observed at the highest dose studied. The NMDA antagonists, (+)-HA-966 and 7-chlorokynurenic acid (7-CKA), which act at the strychnine-insensitive modulatory site of the NMDA receptor, only blocked the stimulatory effects of methamphetamine and with (+)-HA-966, blockade was only achieved at a dose that decreased spontaneous locomotor activity. These results provide evidence for the involvement of glutamatergic input in the control of behavior involving mesolimbic dopamine. Along with other findings these results suggest that glutamate receptors may be a target for the development of pharmacological therapies for the treatment of psychomotor stimulant abuse and for other disorders involving hyperfunction of the mesolimbic dopamine system (eg. schizophrenia). RP WITKIN, JM (reprint author), NIDA ADDICT RES CTR,POB 5180,DRUG DEV GRP,BALTIMORE,MD 21224, USA. NR 20 TC 24 Z9 24 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 53 IS 24 BP PL405 EP PL410 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA MG810 UT WOS:A1993MG81000011 PM 7902523 ER PT J AU MOODY, TW CUTTITTA, F AF MOODY, TW CUTTITTA, F TI GROWTH-FACTOR AND PEPTIDE RECEPTORS IN SMALL-CELL LUNG-CANCER SO LIFE SCIENCES LA English DT Review ID GASTRIN-RELEASING PEPTIDE; SWISS 3T3 CELLS; HIGH-AFFINITY RECEPTORS; BOMBESIN-LIKE PEPTIDES; GRP-LIKE PEPTIDES; MONOCLONAL-ANTIBODY; GENE-EXPRESSION; CLONAL GROWTH; FACTOR-I; ANTIMITOTIC ACTIVITY AB In the past decade, over 1000 continuous human cell lines have been established from lung cancer biopsy specimens. Numerous growth factors and receptors have been identified in the small cell lung cancer (SCLC) cell lines. SCLC is a neuroendocrine tumor which contains numerous peptides, including bombesin/gastrin releasing peptide (BN/GRP), and receptors. High levels of GRP mRNA and immunoreactivity are present in SCLC cells. The secretion rate of GRP from SCLC cells is increased by vasoactive intestinal peptide (VIP), which elevates the intracellular cAMP. GRP binds to cell surface receptors, elevates cytosolic calcium and stimulates the growth of SCLC cells. Additional SCLG growth factors include insulin-like growth factor I (IGF-I) and transferrin. IGF-I mRNA and protein is present in SCLC. IGF-I binds with high affinity to SCLC cells and stimulates tyrosine kinase activity and growth. Transferrin is also present in SCLC cells. Transferrin binds with high affinity to SCLC cells and stimulates iron transport and growth. Synthetic peptide antagonists and monoclonal antibodies have been identified which disrupt autocrine growth pathways and inhibit SCLC growth. C1 NCI,BIOMARKERS & PREVENT RES BRANCH,DIV CANC PREVENT & CONTROL,KENSINGTON,MD 20895. RP MOODY, TW (reprint author), GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT BIOCHEM & MOLEC BIOL,WASHINGTON,DC 20037, USA. FU NCI NIH HHS [CA-48071, CA-53477] NR 90 TC 89 Z9 89 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 14 BP 1161 EP 1173 DI 10.1016/0024-3205(93)90098-N PG 13 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KP469 UT WOS:A1993KP46900001 PM 8383784 ER PT J AU BUTLER, JD LEVIN, SW FACCHIANO, A MIELE, L MUKHERJEE, AB AF BUTLER, JD LEVIN, SW FACCHIANO, A MIELE, L MUKHERJEE, AB TI AMINO-ACID-COMPOSITION AND N-TERMINAL SEQUENCE OF PURIFIED CYSTINE BINDING-PROTEIN OF ESCHERICHIA-COLI SO LIFE SCIENCES LA English DT Article ID TRANSPORT AB Cystine Binding Protein (CBP), a commercially available crude protein extract obtained by osmotic shock of Escherichia coli (E. coli) , was studied to characterize further its cystine binding properties and to elucidate its cystine transport activity. We report here the amino acid composition, the N-terminal amino acid sequence analysis and some binding characteristics of the purified cystine binding component of CBP. A search of the Swiss-Prot version 20 data base revealed that this sequence is unique. C1 WALTER REED ARMY MED CTR,DEPT PEDIAT,EXCEPT FAMILY MEMBER PROGRAM,WASHINGTON,DC 20307. NICHHD,HUMAN GENET BRANCH,DEV GENET SECT,BETHESDA,MD 20892. RP BUTLER, JD (reprint author), NICHHD,GENET DIS INVOLVING SULPHUR METAB,BLDG 10,RM 10N308,BETHESDA,MD 20892, USA. RI Facchiano, Antonio/J-4744-2012; Facchiano, Antonio/K-5984-2016 OI Facchiano, Antonio/0000-0002-4243-2392 NR 11 TC 18 Z9 19 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 14 BP 1209 EP 1215 DI 10.1016/0024-3205(93)90103-A PG 7 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KP469 UT WOS:A1993KP46900006 PM 8450713 ER PT J AU DAS, PC DAS, KP BAGCHI, K DEY, CD AF DAS, PC DAS, KP BAGCHI, K DEY, CD TI EVALUATION OF TISSUE ASCORBIC-ACID STATUS IN DIFFERENT HORMONAL STATES OF FEMALE RAT SO LIFE SCIENCES LA English DT Article ID ORAL-CONTRACEPTIVES; RELEASE AB The distribution pattern of ascorbic acid in the endocrine organs and/or tissues was investigated during various sexual states of female rats to demonstrate a correlation between ascorbic acid concentration and sex hormone activity. The concentration of ascorbic acid was estimated in the plasma, liver, pancreas, thyroid, ovary, adrenal and pituitary of contraceptive steroid treated, bilatarally ovariectomized, sham-operated and normal control animals at four different phases of estrous cycle to delineate a relationship between the level of ascorbic acid in different organs/tissues at various sex hormonal states. Statistically significant changes were observed in the concentration of ascorbic acid in different endocrine organs/tissues following contraceptive steroid treatment, ovariectomy and during the estrous phases. our results suggest that the concentration of ascorbic acid in the endocrine organs and/or tissues varies during different sexual states of rat. C1 UNIV CALCUTTA,COLL SCI & TECHNOL,DEPT PHYSIOL,CALCUTTA 700009,W BENGAL,INDIA. HOWARD UNIV,COLL MED,DEPT MICROBIOL,WASHINGTON,DC 20059. RP DAS, PC (reprint author), NIEHS,MOLEC CARCINOGENESIS LAB,C2-14,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 25 TC 15 Z9 15 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 18 BP 1493 EP 1498 DI 10.1016/0024-3205(93)90111-F PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KW215 UT WOS:A1993KW21500004 PM 8483380 ER PT J AU SAINI, A SEI, Y AF SAINI, A SEI, Y TI MORPHINE INHIBITS SIGNAL TRANSDUCTION SUBSEQUENT TO ACTIVATION OF PROTEIN-KINASE-C IN MOUSE SPLENOCYTES SO LIFE SCIENCES LA English DT Article ID OPIATE-INDUCED IMMUNOSUPPRESSION; LYMPHOCYTES-T; ADDICTS; INVIVO; RECEPTORS; BLOOD; MICE AB Morphine administered as a subcutaneous implant was previously reported to inhibit the mitogen-induced initial increases in cytoplasmic free calcium concentrations ([Ca2+]i) in mouse splenocytes. The present studies were initiated to determine whether morphine affects signal transduction subsequent to activation of protein kinase C (PKC) in immune cells. Administration of morphine significantly inhibited the phorbol myristate acetate (PMA)-stimulated increase in interleukin-2 receptor (IL-2R) expression in both CD4+ and CD8+ mouse T cells. In contrast. morphine treatment had no effect on PMA/calcium ionophore (A23187)-induced increase in IL-2 secretion, suggesting a selective inhibition of IL-2R expression. Simultaneous administration of morphine and the opiate antagonist naltrexone blocked the effect of morphine on CD4+ cells. The inhibition of PMA-stimulated IL-2R expression was not reproduced by incubating splenocytes with morphine (10(-8)-10(-5)M). These results suggest that this effect of morphine was mediated through opiate-receptors. but not directly via opiate receptors located on T cells. Moreover. adrenalectomy abolished this effect of morphine in CD4+ but not CD8+ T cells. suggesting that the inhibitory effect of morphine on IL-2R expression in CD4+ T cells may be mediated through a morphine-induced increase in corticosteroid levels. Thus. opiate-induced immunosuppression may involve an inhibition of post-PKC events, especially IL-2R expression. as well as impairment of earlier events in the activation of immune cells such as the increase in [Ca2+]i. RP SAINI, A (reprint author), NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892, USA. NR 24 TC 6 Z9 6 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 22 BP 1751 EP 1758 DI 10.1016/0024-3205(93)90463-D PG 8 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KY757 UT WOS:A1993KY75700002 PM 8098501 ER PT J AU SAINI, A SEI, Y AF SAINI, A SEI, Y TI AGE-RELATED IMPAIRMENT OF EARLY AND LATE EVENTS OF SIGNAL TRANSDUCTION IN MOUSE IMMUNE CELLS SO LIFE SCIENCES LA English DT Article ID LYMPHOCYTES-T; ACTIVATION; MITOGENS; FLUO-3; MICE AB The effects of aging were studied on both early and late [subsequent to activation of protein kinase C (PKC)] events of signal transduction in mouse T cell subsets. Aged C57Bl/6 mice showed significant suppression of Con A-stimulated Ca2+ mobilization in both CD4+ and CD8+T cells compared to young mice. When early signaling was bypassed by stimulating cells with the combination of a calcium ionophore and a phorbol ester. [H-3]thymidine incorporation was comparable between young and aged mice while Con A-stimulated [H-3]thymidine uptake remained depressed in aged mice. These results suggest that impairment of early (but not late) events may be responsible for the suppression of T cell proliferation in aged animals. Further, aged mice exhibited a significant increase in spontaneous proliferation resulting in a robust reduction of the stimulation index of both Con A and PMA/A23187-induced proliferation. Similarly. aged mice exhibited a significant increase in spontaneous IL-2R expression in both CD4+ and CD8+ T cells. No differences in IL-2 secretion were found between young and aged mice. The change in IL-2R expression was positively correlated with increased spontaneous proliferation. Overall these results suggest that: 1) impaired early (pre-PKC) rather than later (post-PKC) events of signaling may be responsible for poor proliferation of T cells. and 2) endogeneous activation of cells related to increased level of IL-2R expression may play an important role in aging-associated immunosuppression. RP SAINI, A (reprint author), NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892, USA. NR 14 TC 29 Z9 29 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 22 BP 1759 EP 1765 DI 10.1016/0024-3205(93)90464-E PG 7 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KY757 UT WOS:A1993KY75700003 PM 8492638 ER PT J AU FOLEY, TD LINNOILA, M AF FOLEY, TD LINNOILA, M TI IDENTIFICATION OF A 3RD ISOFORM OF NA+, K+-ATPASE ACTIVITY IN RAT-BRAIN SYNAPTOSOMES SO LIFE SCIENCES LA English DT Letter ID ENZYMATIC-PROPERTIES; HIGH-AFFINITY; OUABAIN; NA,K-ATPASE; EXPRESSION; ISOZYMES; PUMP AB H-3-ouabain binding and ouabain-inhibitable Rb-86+ (K+) uptake were investigated as a means to identify a third isoform of Na+, K+-ATPase in crude synaptosome preparations. The specific binding of low concentrations (10 nM and 1 uM) of H-3-ouabain, in crude synaptosome preparations, was markedly inhibited by K+ (0.5-5 mM). Accordingly, Rb-86+ (K+) uptake, in the presence of 5 mM K+ was not sensitive to inhibition by low concentrations (10(-11)-10(-7) M) of ouabain. Higher concentrations (10(-6)-10(-2.6) M) of ouabain resulted in a biphasic inhibition of K+ uptake, which distinguished the activities of the presumed alpha 2 and alpha 1 isozymes of Na+, K+-ATPase. Reduction of K+ (1.25 mM and 0.5 mM) in the incubation, resulted in the observation of a third component of ouabain-sensitive K+ uptake. This Na+, K+-ATPase activity, which was defined, pharmacologically, as very sensitive (VS) to ouabain, exhibited IC50s of 3.6 nM and 92 nM at 1.25 mM K+ and 0.5 mM K+, respectively. Inhibition of ouabain binding and VS-dependent K+ uptake, at a high, physiological concentration (5 mM) of K+, suggests that VS may be an inactive isoform of brain Na+, K+-ATPase under resting conditions. RP FOLEY, TD (reprint author), NIAAA,DICBR,CLIN STUDIES LAB,12501 WASHINGTON AVE,ROCKVILLE,MD 20852, USA. NR 17 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 24 BP PL273 EP PL278 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA LB474 UT WOS:A1993LB47400012 ER PT J AU SZALLASI, A CONTE, B GOSO, C BLUMBERG, PM MANZINI, S AF SZALLASI, A CONTE, B GOSO, C BLUMBERG, PM MANZINI, S TI CHARACTERIZATION OF A PERIPHERAL VANILLOID (CAPSAICIN) RECEPTOR IN THE URINARY-BLADDER OF THE RAT SO LIFE SCIENCES LA English DT Letter ID PRIMARY SENSORY NEURONS; RESINIFERATOXIN; ANALOGS; BINDING AB Specific binding of [H-3]resiniferatoxin (RTX) is thought to represent the vanilloid (capsaicin) receptor. In the present study, we have used this binding assay to identify for the first time a vanilloid receptor in the periphery and to compare it to central vanilloid receptors present in dorsal root ganglia (DRG) as well as in spinal cord of the rat. Rat urinary bladder membranes bound [H-3]RTX with a K(d) of 30 +/- 4 pM and a B(max) of 65 +/- 14 fmol/mg protein; the corresponding values were 19 +/- 3 pM and 104 +/- 14 fmol/mg protein in DRG, and 16 +/- 3 pM and 50 +/- 9 fmol/mg protein in spinal cord. Capsaicin inhibited [H-3]RTX binding to membranes from urinary bladder, spinal cord, and DRG with similar potency (K(i) values were 0.5 +/- 0.1 muM, 0.3 +/- 0.1, and 0.6 +/- 0.1 muM, respectively). Interestingly, [H-3]RTX bound to urinary bladder in a non-cooperative fashion in contrast with the apparent positive cooperativity of [H-3]RTX binding in both DRG and spinal cord (cooperativity index = 1.8 and 1.7, respectively). This finding suggests heterogeneity in the properties of the vanilloid receptors in the rat. C1 NCI,BETHESDA,MD 20892. RP SZALLASI, A (reprint author), MENARINI SUD,DEPT PHARMACOL,VIA TITO SPERI 10,I-00040 POMEZIA,ITALY. NR 19 TC 24 Z9 24 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1993 VL 52 IS 20 BP PL221 EP PL226 PG 6 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KX649 UT WOS:A1993KX64900012 PM 8483387 ER PT B AU ALEXANDER, NJ AF ALEXANDER, NJ BE Griffin, PD Johnson, PM TI ADVERSE-EFFECTS OF IMMUNIZATION OF MALES WITH SPERM ANTIGENS SO LOCAL IMMUNITY IN REPRODUCTIVE TRACT TISSUES SE SCIENTIFIC BASIS OF FERTILITY REGULATION LA English DT Proceedings Paper CT Symposium on Local Immunity in Tract Tissues CY NOV 26-30, 1990 CL NATL INST IMMUNOL, NEW DELHI, INDIA SP WHO, SPECIAL PROGRAMME RES DEV & RES TRAINING HUMAN REPROD HO NATL INST IMMUNOL C1 NICHHD,CTR POPULAT RES,CONTRACEPT DEV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS DELHI PI NEW DELHI PA 2/11 ANSARI RD, DARYAGANJ, NEW DELHI 110002, INDIA BN 0-19-563148-X J9 SCI BAS FER PY 1993 BP 391 EP 398 PG 8 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA BA82N UT WOS:A1993BA82N00025 ER PT B AU SULLIVAN, F HAHN, S GLATSTEIN, E AF SULLIVAN, F HAHN, S GLATSTEIN, E BE Hansen, HH TI FUTURE-DEVELOPMENTS IN RADIATION ONCOLOGY FOR THE MANAGEMENT OF CARCINOMA OF THE LUNG SO LUNG CANCER, VOL 9 NOS 1-6 MARCH 1993: PROCEEDINGS OF THE SIXTH WORLD CONFERENCE ON LUNG CANCER LA English DT Proceedings Paper CT 6th World Conference on Lung Cancer CY NOV 10-14, 1991 CL MELBOURNE, AUSTRALIA DE RADIATION ONCOLOGY; LUNG CANCER; FUTURE DEVELOPMENTS C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENTIFIC PUBLISHERS IRELAND LTD PI LIMERICK PA PO BOX 85, LIMERICK, IRELAND PY 1993 BP 81 EP 87 PG 7 WC Oncology; Respiratory System SC Oncology; Respiratory System GA BZ61U UT WOS:A1993BZ61U00009 ER PT B AU MULSHINE, JL CUTTITTA, F SCOTT, F QUINN, KA SHAW, G AVIS, I TRESTON, AM AF MULSHINE, JL CUTTITTA, F SCOTT, F QUINN, KA SHAW, G AVIS, I TRESTON, AM BE Hansen, HH TI STRATEGIES FOR LUNG-CANCER CHEMOPREVENTION SO LUNG CANCER, VOL 9 NOS 1-6 MARCH 1993: PROCEEDINGS OF THE SIXTH WORLD CONFERENCE ON LUNG CANCER LA English DT Proceedings Paper CT 6th World Conference on Lung Cancer CY NOV 10-14, 1991 CL MELBOURNE, AUSTRALIA C1 NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENTIFIC PUBLISHERS IRELAND LTD PI LIMERICK PA PO BOX 85, LIMERICK, IRELAND PY 1993 BP 357 EP 360 PG 4 WC Oncology; Respiratory System SC Oncology; Respiratory System GA BZ61U UT WOS:A1993BZ61U00043 ER PT B AU IHDE, DC AF IHDE, DC BE Hansen, HH TI PROPHYLACTIC CRANIAL IRRADIATION - CURRENT CONTROVERSIES SO LUNG CANCER, VOL 9 SUPPL NO 1 (1993) LA English DT Proceedings Paper CT Satellite Symposium on Current Perspectives in the Treatment of Small Cell Lung Cancer CY NOV 10, 1991 CL MELBOURNE, AUSTRALIA DE SMALL CELL LUNG CANCER; CENTRAL NERVOUS SYSTEM METASTASES; PROPHYLACTIC CRANIAL IRRADIATION C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENTIFIC PUBLISHERS IRELAND LTD PI LIMERICK PA PO BOX 85, LIMERICK, IRELAND PY 1993 BP S69 EP S74 PG 6 WC Oncology; Respiratory System SC Oncology; Respiratory System GA BZ83P UT WOS:A1993BZ83P00006 ER PT B AU JOHNSON, BE SALEM, C NESBITT, J GAZDAR, AF LESAR, M PHELPS, R EDISON, M LINNOILA, RI PHARES, J PASS, H MULSHINE, JL MINNA, JD GLATSTEIN, E IHDE, DC AF JOHNSON, BE SALEM, C NESBITT, J GAZDAR, AF LESAR, M PHELPS, R EDISON, M LINNOILA, RI PHARES, J PASS, H MULSHINE, JL MINNA, JD GLATSTEIN, E IHDE, DC BE Hansen, HH TI LIMITED STAGE SMALL-CELL LUNG-CANCER TREATED WITH CONCURRENT HYPERFRACTIONATED CHEST RADIOTHERAPY AND ETOPOSIDE CISPLATIN SO LUNG CANCER, VOL 9 SUPPL NO 1 (1993) LA English DT Proceedings Paper CT Satellite Symposium on Current Perspectives in the Treatment of Small Cell Lung Cancer CY NOV 10, 1991 CL MELBOURNE, AUSTRALIA DE HYPERFRACTIONATION; CONCURRENT; SMALL CELL LUNG CANCER C1 NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20889. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENTIFIC PUBLISHERS IRELAND LTD PI LIMERICK PA PO BOX 85, LIMERICK, IRELAND PY 1993 BP S21 EP S26 PG 6 WC Oncology; Respiratory System SC Oncology; Respiratory System GA BZ83P UT WOS:A1993BZ83P00002 ER PT J AU HELPERN, JA DERESKI, MO KNIGHT, RA ORDIDGE, RJ CHOPP, M QING, ZX AF HELPERN, JA DERESKI, MO KNIGHT, RA ORDIDGE, RJ CHOPP, M QING, ZX TI HISTOPATHOLOGICAL CORRELATIONS OF NUCLEAR-MAGNETIC-RESONANCE IMAGING PARAMETERS IN EXPERIMENTAL CEREBRAL-ISCHEMIA SO MAGNETIC RESONANCE IMAGING LA English DT Article DE NMR; MRI; DIFFUSION; HISTOPATHOLOGY; CEREBRAL ISCHEMIA; STROKE AB Changes in the nuclear magnetic resonance (NMR) parameters of spin-lattice relaxation (T1), spin-spin relaxation (T2), proton density (rho), and water diffusion (D(NMR)) were measured over time together with the histopathological status in three regions of rat brain cortex after permanent middle cerebral artery occlusion (MCA-O). Histological response ranged from severe irreversible damage (necrosis and cavitation) to relatively mild and apparently reversible damage. D(NMR) was the only NMR parameter which demonstrated a statistically significant change in all three regions of brain studied. Additionally, rho was significantly increased only in the region of brain studied which eventually progressed to necrosis and cavitation. Finally, data are presented which indicate that changes in T2, D(NMR), and rho can occur independently of one another. RP HELPERN, JA (reprint author), HENRY FORD HLTH SCI CTR,DEPT NEUROL,NIH,CTR CEREBROVASC DIS RES,2799 W GRAND BLVD,DETROIT,MI 48202, USA. RI Ordidge, Roger/F-2755-2010; OI Ordidge, Roger/0000-0002-1005-3654 FU NINDS NIH HHS [NS23393] NR 0 TC 76 Z9 77 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0730-725X J9 MAGN RESON IMAGING JI Magn. Reson. Imaging PY 1993 VL 11 IS 2 BP 241 EP 246 DI 10.1016/0730-725X(93)90028-C PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KR563 UT WOS:A1993KR56300010 PM 8455433 ER PT J AU TURNER, R AF TURNER, R TI GRADIENT COIL DESIGN - A REVIEW OF METHODS SO MAGNETIC RESONANCE IMAGING LA English DT Review DE GRADIENT COILS; MRI GRADIENTS; COIL DESIGN; COILS AB Methods of coil design for MRI gradient coils and other purposes are discussed. The conflicting requirements for satisfactory gradient coil performance are described and analyzed. Design methods are classified into discrete wire techniques and current density techniques. The advantages and disadvantages of each group of methods are described, and optimization methods are summarized. These include the target field approach, and constrained inductance and power minimization. Design for low fringe fields is described, including active shielding. RP TURNER, R (reprint author), NHLBI,CARDIAC ENERGET LAB,BETHESDA,MD 20892, USA. RI Turner, Robert/C-1820-2008 NR 0 TC 217 Z9 223 U1 12 U2 57 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0730-725X J9 MAGN RESON IMAGING JI Magn. Reson. Imaging PY 1993 VL 11 IS 7 BP 903 EP 920 DI 10.1016/0730-725X(93)90209-V PG 18 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA MB034 UT WOS:A1993MB03400001 PM 8231676 ER PT B AU DEJONG, WW LEUNISSEN, JAM WISTOW, GJ AF DEJONG, WW LEUNISSEN, JAM WISTOW, GJ BE Szalay, FS Novacek, MJ Mckenna, MC TI EYE LENS CRYSTALLINS AND THE PHYLOGENY OF PLACENTAL ORDERS - EVIDENCE FOR A MACROSCELID-PAENUNGULATE CLADE SO MAMMAL PHYLOGENY : PLACENTALS LA English DT Proceedings Paper CT MAMMAL CONF CY MAY 28-JUN 01, 1990 CL AMER MUSEUM NAT HIST, NEW YORK, NY HO AMER MUSEUM NAT HIST RP WISTOW, GJ (reprint author), NEI,MOLEC & DEV BIOL LAB,ROOM 222,BLDG 6,BETHESDA,MD 20892, USA. NR 0 TC 46 Z9 46 U1 0 U2 0 PU SPRINGER-VERLAG PI NEW YORK PA NEW YORK BN 0-387-97853-4 PY 1993 BP 5 EP 12 PG 8 WC Anatomy & Morphology; Zoology SC Anatomy & Morphology; Zoology GA BY45Y UT WOS:A1993BY45Y00002 ER PT J AU CASH, JM REMMERS, EF GOLDMUNTZ, EA CROFFORD, LJ ZHA, HB HANSEN, CT WILDER, RL AF CASH, JM REMMERS, EF GOLDMUNTZ, EA CROFFORD, LJ ZHA, HB HANSEN, CT WILDER, RL TI GENETIC-MAPPING OF THE ATHYMIC NUDE (RNU) LOCUS IN THE RAT TO A REGION CHROMOSOME-10 SO MAMMALIAN GENOME LA English DT Article ID EXPRESSION; ARTHRITIS; SYNOVIUM; INSITU AB The nude trait in the rat is transmitted in an autosomal recessive manner and is associated with thymic aplasia, T-cell deficiency, and hairlessness. Congenic rats homozygous for the RNU (Rowett nude) locus are important models in the study of inflammatory disease, tumor growth, and transplant rejection. The RNU locus has not been previously mapped, and the nature of the gene product is unknown. To determine the map location of this gene, a single F344.rnu/rnu (athymic nude congenic Fischer rat) male congenic rat was bred with 3 LEW/N (NIH stock Lewis rat) female rats to produce F1 progeny. Twelve F1 brother-sister breeding pairs were established. Forty-nine phenotypically nude F2 offspring (198 total) were obtained. Linkage analysis done on F2 DNA revealed highly significant cosegregation between the nude phenotype and eight polymorphic markers located on Chromosome (Chr) 10. The tightest linkages were with: MYH3 (embryonic, skeletal myosin heavy chain) and SHBG (sex hormone-binding globulin), giving 2 point lod scores of 20.2, and 20.0, respectively. The map order and map distances, determined by multipoint linkage calculations, were: RR24-(16.1 cM)-MYH3-(3.5 cM)-SHBG-(4.7 cM)-RNU-(11.9 cM)-F16F2-(24.1 cM)-CLATP (citrate lyase ATPase)-(2.4 cM)-ACE (angiotensin converting enzyme)/PPY (pancreatic polypeptide)-(14.1 cM)-RR1023. The position of the RNU locus in the rat corresponds closely with that of the recently reported nu locus in the mouse. This finding suggests that the nude phenotype in the rat and the mouse arise from defects in homologous genes. C1 NATL INST ARTHRITIS & MUSCULOSKELETAL & SKIN DIS,ARTHRITIS & RHEUMATISM BRANCH,BLDG 10,BETHESDA,MD 20892. NIH,GENET RESOURCES SECT,VET RESOURCES BRANCH,BETHESDA,MD 20892. RI Perez , Claudio Alejandro/F-8310-2010; Crofford, Leslie/J-8010-2013 OI Perez , Claudio Alejandro/0000-0001-9688-184X; NR 24 TC 22 Z9 22 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 1 BP 37 EP 42 DI 10.1007/BF00364661 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA KG322 UT WOS:A1993KG32200006 PM 8422500 ER PT J AU LUEDERS, KK FRANKEL, WN MIETZ, JA KUFF, EL AF LUEDERS, KK FRANKEL, WN MIETZ, JA KUFF, EL TI GENOMIC MAPPING OF INTRACISTERNAL A-PARTICLE PROVIRAL ELEMENTS SO MAMMALIAN GENOME LA English DT Article ID RECOMBINANT INBRED STRAINS; MURINE LEUKEMIA PROVIRUSES; OLIGONUCLEOTIDE PROBES; MOUSE CHROMOSOME-17; LINKAGE MAP; GENE; DNA; IDENTIFICATION; HYBRIDIZATION; LOCALIZATION AB Intracisternal A-particle (IAP) proviral elements are moderately reiterated and widely dispersed in the mouse genome. Oligonucleotide probes have been derived from three distinctive IAP element subfamilies (LS elements) that are transcriptionally active in normal mouse B- and T-cells. In HindIII digests, LS element-specific oligonucleotides each react with a limited number of restriction fragments that represent junctions between proviral and flanking DNA. These fragments have characteristic strain distribution patterns (SDPs) which are polymorphic in the DNAs of different mouse strains. We have established chromosomal assignments for 44 LS proviral loci by comparing their SDPs with those of known genetic markers in the BXD set of RI mouse strains. Some of the loci have also been scored in the CXB RI set. The IAP LS loci can provide a significant number of markers with a recognized genetic organization to the mouse genome map. C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. JACKSON LAB,BAR HARBOR,ME 04609. RP LUEDERS, KK (reprint author), NCI,BIOCHEM LAB,BLDG 37,ROOM 4C-03,BETHESDA,MD 20892, USA. NR 46 TC 34 Z9 34 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 2 BP 69 EP 77 DI 10.1007/BF00290429 PG 9 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA KH459 UT WOS:A1993KH45900001 PM 8431640 ER PT J AU JOHNSON, KR COOK, SA WARDBAILEY, P BUSTIN, M DAVISSON, MT AF JOHNSON, KR COOK, SA WARDBAILEY, P BUSTIN, M DAVISSON, MT TI IDENTIFICATION AND GENETIC-MAPPING OF THE MURINE GENE AND 20 RELATED SEQUENCES ENCODING CHROMOSOMAL PROTEIN HMG-17 SO MAMMALIAN GENOME LA English DT Article ID PROCESSED PSEUDOGENES; LEUKEMIA PROVIRUSES; MULTIGENE FAMILY; CDNA SEQUENCE; MUS-MUSCULUS; LINKAGE MAP; MOUSE; LOCALIZATION; LOCUS; REGION AB HMG-17 is an abundant, nonhistone chromosomal protein that binds preferentially to nucleosomal core particles of mammalian chromatin. The human gene for HMG-17 has been localized to Chromosome (Chr) 1p, but the murine gene has not been previously mapped. Here we identify the murine functional gene, Hmg17, from among more than 25 related sequences (probably processed pseudogenes) and show that it is located on mouse Chr 4, in a region known to have conserved linkage relationships with human Chr 1p. We also report the map locations of 20 additional Hmg17-related sequences on mouse Chrs 1, 2, 3, 5, 7, 8, 9, 13, 15, 16, 17, 18, and X. The multiple, dispersed members of the Hmg17 multigene family can be detected efficiently with a single cDNA probe and provide useful markers for genetic mapping studies in mice. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP JOHNSON, KR (reprint author), JACKSON LAB,600 MAIN ST,BAR HARBOR,ME 04609, USA. RI Bustin, Michael/G-6155-2015 FU NCI NIH HHS [CA34196]; NCRR NIH HHS [RR01183]; NIGMS NIH HHS [GM46697] NR 38 TC 25 Z9 25 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 2 BP 83 EP 89 DI 10.1007/BF00290431 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA KH459 UT WOS:A1993KH45900003 PM 8094303 ER PT J AU REMMERS, EF GOLDMUNTZ, EA CASH, JM ZHA, HB CROFFORD, LJ MISIEWICZPOLTORAK, B MATHERN, P WILDER, RL AF REMMERS, EF GOLDMUNTZ, EA CASH, JM ZHA, HB CROFFORD, LJ MISIEWICZPOLTORAK, B MATHERN, P WILDER, RL TI MAP OF 7 POLYMORPHIC MARKERS ON RAT CHROMOSOME-14 - LINKAGE CONSERVATION WITH HUMAN CHROMOSOME-4 SO MAMMALIAN GENOME LA English DT Article ID STRAIN DIFFERENCES; ALPHA-FETOPROTEIN; F344 RATS; INFECTION; MOUSE; LEW; SUSCEPTIBILITY; HYBRIDIZATION; ARTHRITIS; ANTIBODY AB Seven polymorphic markers identified by polymerase chain reaction (PCR) amplification, including markers for six genes-DRD1L (dopamine receptor, D1-like-2), GLUKA (glucokinase), PF4 (platelet factor 4), ALB (albumin), AFP (alpha-fetoprotein), and BSP (bone sialoprotein)-and one anonymous locus (D14N52), were mapped to a single 67-cM linkage group with F2 intercross progeny of F344/N and LEW/N inbred rat strains. Two of these markers, ALB and AFP, have previously been assigned to rat Chromosome (Chr) 14, allowing assignment of this entire linkage group. Five of the markers-DRD1L, PF4, ALB, AFP, and BSP-have been physically mapped to a large region of human Chr 4 encompassing the p arm and the q arm to band q28. Homologs of two of the markers, ALB and AFP, have been mapped to Chr 5 in the mouse. Comparison of human Chr 4 with the homologous regions on Chr 14 of the rat and Chr 5 of the mouse indicated that linkage conservation with human Chr 4 extends over a greater region in the rat than in the mouse. The markers described here were found to be highly polymorphic in twelve inbred strains (F344/N, LEW/N, ACI/N, BUF/N, BN/SsN, LOU/MN, MNR/N, MR/N, SHR/N, WBB1/N, WBB2/N, and WKY/N). These polymorphic markers should be useful in genetic linkage studies of important phenotypes in rats. RP REMMERS, EF (reprint author), NIAMSD,ARTHRIT & RHEUMATISM BRANCH,BLDG 10 ROOM 9N240,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013 NR 27 TC 20 Z9 20 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 2 BP 90 EP 94 DI 10.1007/BF00290432 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA KH459 UT WOS:A1993KH45900004 PM 8431642 ER PT J AU CHAKRABORTI, A LIPPMAN, DL LOH, HH KOZAK, CA LEE, NM AF CHAKRABORTI, A LIPPMAN, DL LOH, HH KOZAK, CA LEE, NM TI GENETIC-MAPPING OF OPIOID BINDING-PROTEIN GENE(S) TO MOUSE CHROMOSOME-9 SO MAMMALIAN GENOME LA English DT Note ID RAT-BRAIN; RECEPTOR; CELLS C1 UNIV MINNESOTA,DEPT PHARMACOL,MINNEAPOLIS,MN 55455. RP CHAKRABORTI, A (reprint author), NIAID,BETHESDA,MD 20892, USA. FU NIDA NIH HHS [DA-00564, DA-01583, DA-05695] NR 18 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 3 BP 179 EP 182 DI 10.1007/BF00352235 PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA KP760 UT WOS:A1993KP76000008 PM 8439730 ER PT J AU WADA, K ZIMMERMAN, KL ADAMSON, MC YOKOTANI, N WENTHOLD, RJ KOZAK, CA AF WADA, K ZIMMERMAN, KL ADAMSON, MC YOKOTANI, N WENTHOLD, RJ KOZAK, CA TI GENETIC-MAPPING OF THE MOUSE GENE ENCODING DIPEPTIDYL AMINOPEPTIDASE-LIKE PROTEINS SO MAMMALIAN GENOME LA English DT Note ID IDENTIFICATION; SEQUENCE; CDNA; IV C1 NIAID,MOLEC MICROBIOL LAB,BLDG 4,ROOM 329,BETHESDA,MD 20892. NIDOCD,NEUROCHEM LAB,BETHESDA,MD 20892. NR 17 TC 11 Z9 11 U1 1 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 4 BP 234 EP 237 DI 10.1007/BF00417570 PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA KX214 UT WOS:A1993KX21400010 PM 8499659 ER PT J AU REMMERS, EF GOLDMUNTZ, EA ZHA, HB CROFFORD, LJ CASH, JM MATHERN, P DU, Y WILDER, RL AF REMMERS, EF GOLDMUNTZ, EA ZHA, HB CROFFORD, LJ CASH, JM MATHERN, P DU, Y WILDER, RL TI LINKAGE MAP OF 7 POLYMORPHIC MARKERS ON RAT CHROMOSOME-18 SO MAMMALIAN GENOME LA English DT Article ID MULTIPLE GENE-CONTROL; STRAIN DIFFERENCES; INDUCED ARTHRITIS; F344 RATS; INFECTION; LEWIS; SUSCEPTIBILITY; ANTIBODY; PRIMERS; MODEL AB A genetic linkage map of seven polymorphic markers was created with F2 intercross progeny of F344/N and LEW/N rats and assigned to rat Chromosome (Chr) 18. Five of the markers described were defined by simple sequence length polymorphisms (SSLPs) associated with five genes: transthyretin (TTR), trypsin inhibitor-like protein (TILP), beta2 adrenergic receptor (ADRB2), olfactory neuron-specific G protein (OLF), and gap junction protein (GJA1). One marker was defined by a restriction fragment length polymorphism (RFLP) detected with a probe for the human colony stimulating factor 1 receptor (CSF1R) gene. The D18N1R locus was defined by an anonymous DNA fragment amplified by the randomly amplified polymorphic DNA (RAPD) technique with a single short primer. These seven DNA loci formed a single genetic linkage group 30.4 cM in length with the following order: TTR-6.8 cM-D18N1R-9.1 cM-TILP-4.3 cM-CSF1R-0 cM-ADRB2-10.2 cM-OLF-0 cM-GJA1. The five SSLP markers were highly polymorphic. In a total of 13 inbred rat strains analyzed (F344/N, LEW/N, LOU/MN, WBB1/N, WBB2/N, MR/N, MNR/N, ACI/N, SHR/N, WKY/N, BN/SsN, BUF/N, and LER/N), three to six alleles were detected for each marker. Remarkable linkage conservation was detected between the region of rat Chr 18 mapped and a region of mouse Chr 18. However, genes associated with these markers have been mapped to three different human chromosomes (Chrs 5, 6, and 18). The markers described here should be useful for genetic mapping studies and genetic monitoring of inbred rat strains. RP REMMERS, EF (reprint author), NIAMSD,ARTHRITIS & RHEUMAT BRANCH,BLDG 10,ROOM 9N228,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013 NR 35 TC 24 Z9 30 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 5 BP 265 EP 270 DI 10.1007/BF00417433 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA LA328 UT WOS:A1993LA32800006 PM 8099512 ER PT J AU GREGOR, P PATEL, A SHIMADA, S LIN, CL ROCHELLE, JM KITAYAMA, S SELDIN, MF UHL, GR AF GREGOR, P PATEL, A SHIMADA, S LIN, CL ROCHELLE, JM KITAYAMA, S SELDIN, MF UHL, GR TI MURINE SEROTONIN TRANSPORTER - SEQUENCE AND LOCALIZATION TO CHROMOSOME-11 SO MAMMALIAN GENOME LA English DT Note ID RAT-BRAIN; CLONING; EXPRESSION; MOUSE C1 DUKE UNIV,DEPT MED,DURHAM,NC 27710. DUKE UNIV,DEPT MICROBIOL,DURHAM,NC 27710. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. RP GREGOR, P (reprint author), NIDA,MOLEC PHARMACOL ADDICT RES CTR,BOX 5180,BALTIMORE,MD 21224, USA. RI Lin, Chien-liang/E-3513-2011 FU NHGRI NIH HHS [HG00101] NR 17 TC 25 Z9 26 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 5 BP 283 EP 284 DI 10.1007/BF00417438 PG 2 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA LA328 UT WOS:A1993LA32800011 PM 8507984 ER PT J AU MOCK, BA KRALL, MM PADLAN, C DOSIK, JK SCHUBART, UK AF MOCK, BA KRALL, MM PADLAN, C DOSIK, JK SCHUBART, UK TI THE GENE FOR LAP18, LEUKEMIA-ASSOCIATED PHOSPHOPROTEIN-P18 (METABLASTIN), MAPS TO DISTAL MOUSE CHROMOSOME-4 SO MAMMALIAN GENOME LA English DT Note ID DIFFERENTIATION; CELLS; ENCODES; PROTEIN; P19 C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10461. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DIV MOLEC PHARMACOL,BRONX,NY 10461. RP MOCK, BA (reprint author), NCI,GENET LAB,BLDG 37,ROOM 2B-08,BETHESDA,MD 20892, USA. FU NINDS NIH HHS [R01-NS 26333] NR 14 TC 20 Z9 21 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 8 BP 461 EP 462 DI 10.1007/BF00296823 PG 2 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA LP892 UT WOS:A1993LP89200009 PM 8104060 ER PT J AU PILON, AL KOZAK, CA NEBERT, DW PUGA, A AF PILON, AL KOZAK, CA NEBERT, DW PUGA, A TI LOCALIZATION OF THE MURINE HMG1 GENE, ENCODING AN HMG-BOX PROTEIN, TO MOUSE CHROMOSOME-2 SO MAMMALIAN GENOME LA English DT Note ID BINDING-PROTEIN; DNA; RECEPTOR; DOMAIN; RECOGNITION; CLONING; BENDS C1 NICHHD,DEV PHARMACOL LAB,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RI Puga, Alvaro/B-7676-2008 FU NIEHS NIH HHS [P30 ES06096] NR 29 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 IS 10 BP 612 EP 614 DI 10.1007/BF00361395 PG 3 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA MA813 UT WOS:A1993MA81300013 PM 8268661 ER PT J AU ABBOTT, CM BLANK, R EPPIG, JT FIEDOREK, FT FRANKEL, W FRIEDMAN, JM HUPPI, KE JACKSON, I STEEL, K MOCK, BA STOYE, J SEMAN, RW AF ABBOTT, CM BLANK, R EPPIG, JT FIEDOREK, FT FRANKEL, W FRIEDMAN, JM HUPPI, KE JACKSON, I STEEL, K MOCK, BA STOYE, J SEMAN, RW TI MOUSE CHROMOSOME-4 SO MAMMALIAN GENOME LA English DT Article C1 ROCKEFELLER UNIV,HOWARD HUGHES MED INST,NEW YORK,NY 10021. JACKSON LAB,BAR HARBOR,ME 04609. UNIV N CAROLINA,DEPT MED,DIV ENDOCRINE,CHAPEL HILL,NC 27599. NCI,GENET LAB,BETHESDA,MD 20892. WESTERN GEN HOSP,MRC,HUMAN GENET UNIT,EDINBURGH EH4 2XU,MIDLOTHIAN,SCOTLAND. UNIV NOTTINGHAM,MRC,INST HEARING RES,NOTTINGHAM NG7 2RD,ENGLAND. NATL INST MED RES,LONDON NW7 1AA,ENGLAND. NIEHS,RES TRIANGLE PK,NC 27709. RP ABBOTT, CM (reprint author), UCL,DEPT GENET & BIOCHEM,WOLFSON HOUSE,4 STEPHENSON WAY,LONDON NW1 2HE,ENGLAND. RI Abbott, Catherine/C-7306-2013 FU NHGRI NIH HHS [HG00316] NR 0 TC 19 Z9 19 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 SI SI BP S58 EP S71 DI 10.1007/BF00360830 PG 14 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA MB819 UT WOS:A1993MB81900006 PM 8268685 ER PT J AU BROWN, SDM AVNER, P BOYD, Y CHAPMAN, V RASTAN, S SEFTON, L THOMAS, JD HERMAN, GE AF BROWN, SDM AVNER, P BOYD, Y CHAPMAN, V RASTAN, S SEFTON, L THOMAS, JD HERMAN, GE TI MOUSE X-CHROMOSOME SO MAMMALIAN GENOME LA English DT Article C1 INST PASTEUR,UNITE GENET MOLEC MURINE,F-75724 PARIS 15,FRANCE. MRC,RADIOBIOL UNIT,DIDCOT OX11 ORD,OXON,ENGLAND. DEPT MOLEC & CELLULAR BIOL,BUFFALO,NY 14263. CLIN RES CTR,COMPARAT BIOL SECT,HARROW HA1 3UJ,MIDDX,ENGLAND. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. INST MOLEC GENET,HOUSTON,TX 77030. RP BROWN, SDM (reprint author), ST MARYS HOSP,IMPERIAL COLL SCI TECHNOL & MED,SCH MED,DEPT BIOCHEM & MOLEC GENET,LONDON W2 1PG,ENGLAND. NR 0 TC 16 Z9 16 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 SI SI BP S269 EP S281 DI 10.1007/BF00360846 PG 13 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA MB819 UT WOS:A1993MB81900022 PM 8268681 ER PT J AU CECI, JD AF CECI, JD TI MOUSE CHROMOSOME-8 SO MAMMALIAN GENOME LA English DT Article RP CECI, JD (reprint author), NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL,BASIC RES PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 0 TC 12 Z9 12 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 SI SI BP S121 EP S135 DI 10.1007/BF00360834 PG 15 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA MB819 UT WOS:A1993MB81900010 PM 8268668 ER PT J AU KOZAK, CA STEPHENSON, DA AF KOZAK, CA STEPHENSON, DA TI MOUSE CHROMOSOME-5 SO MAMMALIAN GENOME LA English DT Article C1 UNIV LONDON UNIV COLL,DEPT GENET & BIOMETRY,LONDON NW1 2HE,ENGLAND. RP KOZAK, CA (reprint author), NIAID,MOLEC MICROBIOL LAB,BLDG 4,ROOM 329,BETHESDA,MD 20892, USA. FU NHGRI NIH HHS [HG00170-1] NR 0 TC 25 Z9 25 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 SI SI BP S72 EP S87 DI 10.1007/BF00360831 PG 16 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA MB819 UT WOS:A1993MB81900007 PM 8268686 ER PT J AU MOCK, BA NEUMANN, PE EPPIG, JT DUNCAN, RC HUPPI, KE AF MOCK, BA NEUMANN, PE EPPIG, JT DUNCAN, RC HUPPI, KE TI MOUSE CHROMOSOME-15 SO MAMMALIAN GENOME LA English DT Article C1 NCI,PATHOL LAB,BETHESDA,MD 20892. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. JACKSON LAB,BAR HARBOR,ME 04609. RP MOCK, BA (reprint author), NCI,GENET LAB,BETHESDA,MD 20892, USA. NR 0 TC 7 Z9 7 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 SI SI BP S211 EP S222 DI 10.1007/BF00360841 PG 12 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA MB819 UT WOS:A1993MB81900017 PM 8268676 ER PT J AU MOORE, KJ ELLIOTT, RW AF MOORE, KJ ELLIOTT, RW TI MOUSE CHROMOSOME-6 SO MAMMALIAN GENOME LA English DT Article C1 ROSWELL PK CANC INST,DEPT MOLEC & CELLULAR BIOL,BUFFALO,NY 14263. RP MOORE, KJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL,BASIC RES PROGRAM,POB 8,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101]; NICHD NIH HHS [HD28623] NR 0 TC 12 Z9 12 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1993 VL 4 SI SI BP S88 EP S109 DI 10.1007/BF00360832 PG 22 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA MB819 UT WOS:A1993MB81900008 PM 8268687 ER PT S AU JUCKER, M BIALOBOK, P KLEINMAN, HK WALKER, LC HAGG, T INGRAM, DK AF JUCKER, M BIALOBOK, P KLEINMAN, HK WALKER, LC HAGG, T INGRAM, DK BE Johnnessen, JN TI LAMININ-LIKE AND LAMININ-BINDING PROTEIN-LIKE IMMUNOREACTIVE ASTROCYTES IN RAT HIPPOCAMPUS AFTER TRANSIENT ISCHEMIA - ANTIBODY TO LAMININ-BINDING PROTEIN IS A SENSITIVE MARKER OF NEURAL INJURY AND DEGENERATION SO MARKERS OF NEURONAL INJURY AND DEGENERATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MARKERS OF NEURONAL INJURY AND DEGENERATION CY APR 22-24, 1992 CL BETHESDA, MD SP SIGMA XI, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, FDA, NIOSH, NIH, US EPA RP JUCKER, M (reprint author), NIA,GERONTOL RES CTR,BALTIMORE,MD 21224, USA. OI Walker, Lary/0000-0001-9166-3261 NR 0 TC 13 Z9 13 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-795-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 679 BP 245 EP 252 DI 10.1111/j.1749-6632.1993.tb18304.x PG 8 WC Neurosciences SC Neurosciences & Neurology GA BY50G UT WOS:A1993BY50G00021 PM 8512187 ER PT S AU MARINI, AM PAUL, SM AF MARINI, AM PAUL, SM BE Johnnessen, JN TI INDUCTION OF A NEUROPROTECTIVE STATE IN CEREBELLAR GRANULE CELLS FOLLOWING ACTIVATION OF N-METHYL-D-ASPARTATE RECEPTORS SO MARKERS OF NEURONAL INJURY AND DEGENERATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MARKERS OF NEURONAL INJURY AND DEGENERATION CY APR 22-24, 1992 CL BETHESDA, MD SP SIGMA XI, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, FDA, NIOSH, NIH, US EPA RP MARINI, AM (reprint author), NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BETHESDA,MD 20892, USA. NR 0 TC 14 Z9 14 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-795-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 679 BP 253 EP 259 DI 10.1111/j.1749-6632.1993.tb18305.x PG 7 WC Neurosciences SC Neurosciences & Neurology GA BY50G UT WOS:A1993BY50G00022 PM 8099772 ER PT S AU POLLARD, HB ADEYEMO, M DHARIWAL, K LEVINE, M CAOHUY, H MARKEY, S MARKEY, CJ YOUDIM, MBH AF POLLARD, HB ADEYEMO, M DHARIWAL, K LEVINE, M CAOHUY, H MARKEY, S MARKEY, CJ YOUDIM, MBH BE Johnnessen, JN TI THE GOLDFISH AS A DRUG DISCOVERY VEHICLE FOR PARKINSONS-DISEASE AND OTHER NEURODEGENERATIVE DISORDERS SO MARKERS OF NEURONAL INJURY AND DEGENERATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MARKERS OF NEURONAL INJURY AND DEGENERATION CY APR 22-24, 1992 CL BETHESDA, MD SP SIGMA XI, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, FDA, NIOSH, NIH, US EPA RP POLLARD, HB (reprint author), NIDDKD,CELL BIOL & GENET,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 1 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-795-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 679 BP 317 EP 320 DI 10.1111/j.1749-6632.1993.tb18314.x PG 4 WC Neurosciences SC Neurosciences & Neurology GA BY50G UT WOS:A1993BY50G00031 PM 8512193 ER PT S AU MARKEY, SP MARKEY, CJ WANG, TCL AF MARKEY, SP MARKEY, CJ WANG, TCL BE Johnnessen, JN TI OXIDATIVE DAMAGE IN DOUBLE-STRANDED GENOMIC DNA AS MEASURED BY GC MS ASSAY OF A THYMINE GLYCOL DERIVATIVE SO MARKERS OF NEURONAL INJURY AND DEGENERATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MARKERS OF NEURONAL INJURY AND DEGENERATION CY APR 22-24, 1992 CL BETHESDA, MD SP SIGMA XI, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, FDA, NIOSH, NIH, US EPA RP MARKEY, SP (reprint author), NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-795-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 679 BP 352 EP 357 DI 10.1111/j.1749-6632.1993.tb18321.x PG 6 WC Neurosciences SC Neurosciences & Neurology GA BY50G UT WOS:A1993BY50G00038 PM 8512198 ER PT S AU CHIUEH, CC MURPHY, DL MIYAKE, H LANG, K TULSI, PK HUANG, SJ AF CHIUEH, CC MURPHY, DL MIYAKE, H LANG, K TULSI, PK HUANG, SJ BE Johnnessen, JN TI HYDROXYL FREE-RADICAL (.OH) FORMATION REFLECTED BY SALICYLATE HYDROXYLATION AND NEUROMELANIN - IN-VIVO MARKERS FOR OXIDANT INJURY OF NIGRAL NEURONS SO MARKERS OF NEURONAL INJURY AND DEGENERATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MARKERS OF NEURONAL INJURY AND DEGENERATION CY APR 22-24, 1992 CL BETHESDA, MD SP SIGMA XI, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, FDA, NIOSH, NIH, US EPA RP CHIUEH, CC (reprint author), NIMH,CLIN SCI LAB,NIH CLIN CTR 10 ROOM 3D-41,BETHESDA,MD 20892, USA. NR 0 TC 41 Z9 41 U1 1 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-795-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 679 BP 370 EP 375 DI 10.1111/j.1749-6632.1993.tb18324.x PG 6 WC Neurosciences SC Neurosciences & Neurology GA BY50G UT WOS:A1993BY50G00041 PM 8390147 ER PT S AU LEE, WH BONDY, C AF LEE, WH BONDY, C BE Johnnessen, JN TI INSULIN-LIKE GROWTH-FACTORS AND CEREBRAL-ISCHEMIA SO MARKERS OF NEURONAL INJURY AND DEGENERATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MARKERS OF NEURONAL INJURY AND DEGENERATION CY APR 22-24, 1992 CL BETHESDA, MD SP SIGMA XI, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, FDA, NIOSH, NIH, US EPA RP LEE, WH (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 25 Z9 26 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-795-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 679 BP 418 EP 422 DI 10.1111/j.1749-6632.1993.tb18332.x PG 5 WC Neurosciences SC Neurosciences & Neurology GA BY50G UT WOS:A1993BY50G00049 PM 7685573 ER PT S AU QUACH, TT SCHRIER, BK DUCHEMIN, AM AF QUACH, TT SCHRIER, BK DUCHEMIN, AM BE Johnnessen, JN TI GENE-EXPRESSION IN BRAIN INJURY - IDENTIFICATION OF A NEW CDNA STRUCTURALLY RELATED TO ADHESIVE AND TROPHIC AGENTS SO MARKERS OF NEURONAL INJURY AND DEGENERATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MARKERS OF NEURONAL INJURY AND DEGENERATION CY APR 22-24, 1992 CL BETHESDA, MD SP SIGMA XI, ALCOHOL DRUG ABUSE & MENTAL HLTH ADM, FDA, NIOSH, NIH, US EPA RP QUACH, TT (reprint author), NICHHD,DEV NEUROBIOL LAB,MOLEC NEUROBIOL UNIT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-795-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 679 BP 423 EP 430 DI 10.1111/j.1749-6632.1993.tb18333.x PG 8 WC Neurosciences SC Neurosciences & Neurology GA BY50G UT WOS:A1993BY50G00050 PM 8512207 ER PT S AU MILLS, JL RAYMOND, E AF MILLS, JL RAYMOND, E BE Keen, CL Bendich, A Willhite, CC TI EFFECTS OF RECENT RESEARCH ON RECOMMENDATIONS FOR PERICONCEPTIONAL FOLATE SUPPLEMENT USE SO MATERNAL NUTRITION AND PREGNANCY OUTCOME SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON MATERNAL NUTRITION AND PREGNANCY OUTCOME CY MAY 17-20, 1992 CL SAN DIEGO, CA SP NEW YORK ACAD SCI, HOFFMANN LA ROCHE, MARCH DIMES BIRTH DEFECTS, NICHHD, NIH, NIDDKD, BASF, BURROUGHS WELLCOME, R W JOHNSON PHARM RES INST, LEDERLE CONSUMER RP MILLS, JL (reprint author), NICHHD,DESPR,EPIDEMIOL BRANCH,PEDIATR EPIDEMIOL SECT,BLDG 6100,ROOM 7B03,BETHESDA,MD 20892, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-753-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 678 BP 137 EP 145 PG 9 WC Endocrinology & Metabolism; Nutrition & Dietetics; Obstetrics & Gynecology SC Endocrinology & Metabolism; Nutrition & Dietetics; Obstetrics & Gynecology GA BX95R UT WOS:A1993BX95R00012 ER PT J AU CAVDAR, AO GOZDASOGLU, S YAVUZ, G BABACAN, E UNAL, E ULUOGLU, O YUCESAN, S MAGRATH, IT AKAR, N AF CAVDAR, AO GOZDASOGLU, S YAVUZ, G BABACAN, E UNAL, E ULUOGLU, O YUCESAN, S MAGRATH, IT AKAR, N TI BURKITTS-LYMPHOMA BETWEEN AFRICAN AND AMERICAN TYPES IN TURKISH CHILDREN - CLINICAL, VIRAL (EBV), AND MOLECULAR STUDIES SO MEDICAL AND PEDIATRIC ONCOLOGY LA English DT Article DE LYMPHOMA; BURKITT; CHILDREN; TURKEY ID CHEMOTHERAPY; EXPERIENCE AB Seventy-two Turkish children with Burkitt's lymphoma (BL) observed during a period of 22 years (1968-1990) have been analysed retrospectively. The diagnosis was established histologically according to WHO criteria. BL represented 50% of NHL in this series. The patients were staged according to Ziegler's system. The median age of patients was 5.5 years with a sex (M/F) ratio of 2.1/1. The most common primary site of tumor involvement was the abdomen (69.4%), which was followed by facial tumors, in particular the jaw and orbit (49.9%). There were 21 cases with jaw (29.1%) and 15 cases with orbital involvement (20.8%) at initial presentation. The majority of the patients (84.4%) were in advanced stages (C and D) at initial diagnosis. Facial tumors observed in Turkish children with BL were more similar to African Burkitt's lymphoma than American or European cases. High titers of antibodies against VCA and EA of EBV were also seen in our recent cases of BL. Two main treatment regimens, namely, single agent chemotherapy with cyclophosphamide (CYX) (1968-1974) and three drug (COM) combination chemotherapy, were used consecutively (1974-1988). COM has been shown to produce better results than single agent therapy. The clinical presentation, mean age, and high antibodies (IgG) to EBV and preliminary molecular studies revealed that BL appears to be in between African and non-African types in Turkish children. This will be further elucidated by direct examination of tumor cells for EBV and investigation of the molecular characteristics of Turkish tumors. Such studies are presently under way. C1 UNIV ANKARA,PEDIAT HEMATOL & ONCOL RES CTR,ANKARA,TURKEY. UNIV ANKARA,DEPT PEDIAT SURG,ANKARA,TURKEY. GAZI UNIV,DEPT PATHOL,ANKARA,TURKEY. NCI,LEUKEMIA BRANCH,BETHESDA,MD 20892. NR 30 TC 22 Z9 22 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 0098-1532 J9 MED PEDIATR ONCOL JI Med. Pediatr. Oncol. PY 1993 VL 21 IS 1 BP 36 EP 42 DI 10.1002/mpo.2950210108 PG 7 WC Oncology; Pediatrics SC Oncology; Pediatrics GA KD835 UT WOS:A1993KD83500007 PM 8381202 ER PT J AU PETRILLI, AS BIANCHI, A KUSANO, E MELARAGNO, R NASPITZ, C MENDONCA, JD PIZZO, PA AF PETRILLI, AS BIANCHI, A KUSANO, E MELARAGNO, R NASPITZ, C MENDONCA, JD PIZZO, PA TI FEVER AND GRANULOCYTOPENIA IN CHILDREN WITH CANCER - A STUDY OF 299 EPISODES WITH 2 TREATMENT PROTOCOLS IN BRAZIL SO MEDICAL AND PEDIATRIC ONCOLOGY LA English DT Article DE INFECTION; FEVER; CANCER; GRANULOCYTOPENIA; CHILDREN; FUNGAL INFECTION; BACTERIAL INFECTION; ANTIBIOTICS ID EMPIRIC ANTIBIOTIC-THERAPY; TICARCILLIN PLUS AMIKACIN; NEUTROPENIC PATIENTS; COMBINATION; INFECTIONS; MALIGNANCIES; PIPERACILLIN AB In Brazil, 226 children with cancer presenting 299 episodes of fever and neutropenia (greater-than-or-equal-to 500/mm3) were treated with two consecutive empirical regimens. Regimen I-Cefoxitin Amikacin-Carbenicillin; and Regimen II Ceftriaxone-Amikacin. 67.0% of the patients had leukemias or lymphomas, documented infections occurred in 47.2%, superinfections occurred in 18.7% (Reg. I) and 17.8% (Reg. II) of the episodes. The most common agents identified in Reg. I and Reg. II were, respectively, Gram negative rods (55.0%) and Gram positive cocci (52.6%). The overall rate of success with modifications (Amphotericin B, Vancomycin, Clindamycin, Metronidazole) was higher in Reg. II (93.0%) than in Reg. I (84.0%). This study shows that the appropriate formula to maximize the successful treatment of children with cancer, fever and neutropenia in developing nations includes adherence to established principles of supportive care, utilizing the optimal antibiotic agents available in the country. It is important to promote the necessary modifications along the treatment having in mind the high index of resistent agents. C1 AC CAMARGO HOSP,DEPT PEDIAT ONCOL,BACTERIOL SECT,SAO PAULO,BRAZIL. HOSP SERV PUBL ESTADUAL SAO PAULO,SAO PAULO,BRAZIL. NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892. AC CAMARGO HOSP,IMMUNOL SECT,SAO PAULO,BRAZIL. RP PETRILLI, AS (reprint author), PAULISTA MED SCH,DEPT PEDIAT,PEDIAT ONCOL SECT,R BOTUCATU 743,BR-04023 SAO PAULO,BRAZIL. RI Petrilli, Antonio/B-7906-2012 NR 22 TC 11 Z9 12 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0098-1532 J9 MED PEDIATR ONCOL JI Med. Pediatr. Oncol. PY 1993 VL 21 IS 5 BP 356 EP 361 DI 10.1002/mpo.2950210509 PG 6 WC Oncology; Pediatrics SC Oncology; Pediatrics GA LB938 UT WOS:A1993LB93800008 PM 8492751 ER PT B AU WU, TC LICHTEN, M AF WU, TC LICHTEN, M BE Haseltine, FP Heyner, S TI POSITION EFFECTS IN MEIOTIC RECOMBINATION SO MEIOSIS II: CONTEMPORARY APPROACHES TO THE STUDY OF MEIOSIS LA English DT Proceedings Paper CT Conference on Meiosis II - Contemporary Approaches to the Study of Meiosis CY OCT, 1991 CL UNIV PENN, PHILADELPHIA, PA SP UNIV PENN, NIH, NICHHD HO UNIV PENN C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1333 H STREET NW, WASHINGTON, DC 20005 BN 0-87168-524-8 PY 1993 BP 19 EP 36 PG 18 WC Genetics & Heredity SC Genetics & Heredity GA BC10H UT WOS:A1993BC10H00003 ER PT B AU HASELTINE, FP HEYNER, S AF HASELTINE, FP HEYNER, S BE Haseltine, FP Heyner, S TI MEIOSIS-II - CONTEMPORARY APPROACHES TO THE STUDY OF MEIOSIS SO MEIOSIS II: CONTEMPORARY APPROACHES TO THE STUDY OF MEIOSIS LA English DT Proceedings Paper CT Conference on Meiosis II - Contemporary Approaches to the Study of Meiosis CY OCT, 1991 CL UNIV PENN, PHILADELPHIA, PA SP UNIV PENN, NIH, NICHHD HO UNIV PENN C1 NICHHD,CTR POPULAT RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1333 H STREET NW, WASHINGTON, DC 20005 BN 0-87168-524-8 PY 1993 BP R11 EP R19 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA BC10H UT WOS:A1993BC10H00001 ER PT J AU HERRMANN, A CLAGUE, MJ BLUMENTHAL, R AF HERRMANN, A CLAGUE, MJ BLUMENTHAL, R TI ROLE OF TARGET MEMBRANE-STRUCTURE IN FUSION WITH INFLUENZA-VIRUS - EFFECT OF MODULATING ERYTHROCYTE TRANSBILAYER PHOSPHOLIPID DISTRIBUTION SO MEMBRANE BIOCHEMISTRY LA English DT Article DE INFLUENZA VIRUS; FUSION; ERYTHROCYTE; LIPID DISTRIBUTION ID VESICULAR STOMATITIS-VIRUS; PH-DEPENDENT FUSION; RED-BLOOD-CELLS; PLASMA-MEMBRANE; ASYMMETRIC DISTRIBUTION; HEMAGGLUTININ; FLUORESCENCE; SPECTRIN; VESICLES; KINETICS AB To study the role of the target membrane in influenza virus fusion we chose erythrocyte membranes whose phospholipid arrangement can readily be modified. The phospholipids of normal erythrocytes are arranged asymmetrically across the plasma membrane, phosphatidylcholine (PC) and sphingomyelin are predominantly on the outer surface, whereas others such as phosphatidylserine (PS) and phosphatidylethanolamine (PE) are predominantly restricted to the inner leaflet. However, erythrocytes can be lyzed and resealed under conditions where the asymmetric distribution of phospholipids is lost or retained. Low pH-induced fusion of the A/PR 8 strain of influenza virus, monitored spectrofluorometrically by the octadecylrhodamine dequenching assay, was more rapid with lipid-symmetric erythrocyte ghosts than with lipid-asymmetric ghosts or intact erythrocytes. Neither conversion of PS in the lipid-symmetric ghost membrane to PE by means of the enzyme PS decarboxylaze, nor incorporation of spin-labeled phospholipid analogs with PS, PC or PE headgroups into the outer leaflet of lipid-asymmetric erythrocytes altered rates or extents of fusion of A/PR 8 with the modified target. These results indicate that effects on influenza virus fusion are not associated with any particular phospholipid headgroup, but rather related to the packing characteristics of the target membrane. C1 NCI,LMMB,MEMBRANE STRUCT & FUNCT,BLDG 10,ROOM 4A01,BETHESDA,MD 20892. OI Clague, Michael/0000-0003-3355-9479 NR 45 TC 13 Z9 13 U1 0 U2 1 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0149-046X J9 MEMBRANE BIOCHEM PD JAN-MAR PY 1993 VL 10 IS 1 BP 3 EP 15 DI 10.3109/09687689309150248 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LA232 UT WOS:A1993LA23200001 PM 8510561 ER PT B AU WAALKES, MP AF WAALKES, MP BE SUZUKI, KT Imura, N Kimura, M TI MEDICAL IMPLICATIONS OF METALLOTHIONEIN SO METALLOTHIONEIN III: BIOLOGICAL ROLES AND MEDICAL IMPLICATIONS SE ADVANCES IN LIFE SCIENCES LA English DT Proceedings Paper CT 3rd International Conference on Metallothionein CY DEC, 1992 CL TSUKUBA, JAPAN SP JAPAN SOC BIOMED RES TRACE ELEMENTS, JAPANESE SOC TOXICOL SCI, RES FDN PHARM SCI, JAPANESE CANC ASSOC, JAPANESE SOC AGR CHEM, JAPANESE BIOCHEM SOC, JAPANESE SOC HYGIENE, MOLEC BIOL SOC JAPAN, PHARM SOC JAPAN RP WAALKES, MP (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BLDG 538,RM 205-E,FREDERICK,MD 21701, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIRKHAUSER VERLAG PI BASEL PA PO BOX 133, CH-4010 BASEL, SWITZERLAND BN 3-7643-2769-3 J9 ADV LIF SCI PY 1993 BP 243 EP 253 PG 11 WC Biochemistry & Molecular Biology; Biology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Research & Experimental Medicine; Microbiology GA BZ44B UT WOS:A1993BZ44B00014 ER PT B AU WAALKES, MP DIWAN, BA COOGAN, TP WEGHORST, CM WARD, JM RICE, JM CHERIAN, MG GOYER, RA AF WAALKES, MP DIWAN, BA COOGAN, TP WEGHORST, CM WARD, JM RICE, JM CHERIAN, MG GOYER, RA BE SUZUKI, KT Imura, N Kimura, M TI THE TUMOR SUPPRESSIVE ACTIVITY OF CADMIUM SO METALLOTHIONEIN III: BIOLOGICAL ROLES AND MEDICAL IMPLICATIONS SE ADVANCES IN LIFE SCIENCES LA English DT Proceedings Paper CT 3rd International Conference on Metallothionein CY DEC, 1992 CL TSUKUBA, JAPAN SP JAPAN SOC BIOMED RES TRACE ELEMENTS, JAPANESE SOC TOXICOL SCI, RES FDN PHARM SCI, JAPANESE CANC ASSOC, JAPANESE SOC AGR CHEM, JAPANESE BIOCHEM SOC, JAPANESE SOC HYGIENE, MOLEC BIOL SOC JAPAN, PHARM SOC JAPAN RP WAALKES, MP (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BLDG 538,RM 205-E,FREDERICK,MD 21701, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIRKHAUSER VERLAG PI BASEL PA PO BOX 133, CH-4010 BASEL, SWITZERLAND BN 3-7643-2769-3 J9 ADV LIF SCI PY 1993 BP 303 EP 314 PG 12 WC Biochemistry & Molecular Biology; Biology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Research & Experimental Medicine; Microbiology GA BZ44B UT WOS:A1993BZ44B00019 ER PT B AU HAMER, DH AF HAMER, DH BE SUZUKI, KT Imura, N Kimura, M TI MOLECULAR-GENETICS OF METALLOTHIONEIN - AN OVERVIEW SO METALLOTHIONEIN III: BIOLOGICAL ROLES AND MEDICAL IMPLICATIONS SE ADVANCES IN LIFE SCIENCES LA English DT Proceedings Paper CT 3rd International Conference on Metallothionein CY DEC, 1992 CL TSUKUBA, JAPAN SP JAPAN SOC BIOMED RES TRACE ELEMENTS, JAPANESE SOC TOXICOL SCI, RES FDN PHARM SCI, JAPANESE CANC ASSOC, JAPANESE SOC AGR CHEM, JAPANESE BIOCHEM SOC, JAPANESE SOC HYGIENE, MOLEC BIOL SOC JAPAN, PHARM SOC JAPAN RP HAMER, DH (reprint author), NCI,BIOCHEM LAB,CELL REGULAT SECT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIRKHAUSER VERLAG PI BASEL PA PO BOX 133, CH-4010 BASEL, SWITZERLAND BN 3-7643-2769-3 J9 ADV LIF SCI PY 1993 BP 347 EP 350 PG 4 WC Biochemistry & Molecular Biology; Biology; Medicine, Research & Experimental; Microbiology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Research & Experimental Medicine; Microbiology GA BZ44B UT WOS:A1993BZ44B00022 ER PT S AU SELLERS, JR CUDA, G WANG, F HOMSHER, E AF SELLERS, JR CUDA, G WANG, F HOMSHER, E BE Scholey, JM TI MYOSIN-SPECIFIC ADAPTATIONS OF THE MOTILITY ASSAY SO METHODS IN CELL BIOLOGY, VOL 39: MOTILITY ASSAYS FOR MOTOR PROTEINS SE Methods in Cell Biology LA English DT Review ID SINGLE ACTIN-FILAMENTS; SMOOTH-MUSCLE MYOSIN; SLIDING MOVEMENT; INVITRO MOTILITY; SKELETAL-MUSCLE; HEAVY-MEROMYOSIN; THICK FILAMENTS; STEP SIZE; VELOCITY; PARAMYOSIN C1 UNIV CALIF LOS ANGELES, CTR HLTH SCI, SCH MED, DEPT PHYSIOL, LOS ANGELES, CA 90024 USA. RP NHLBI, MOLEC CARDIOL LAB, BETHESDA, MD 20892 USA. RI Cuda, Giovanni/F-5359-2012 OI Cuda, Giovanni/0000-0001-6313-1866 NR 36 TC 64 Z9 65 U1 0 U2 4 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X BN 0-12-638920-4; 0-12-564139-7 J9 METHOD CELL BIOL JI Methods Cell Biol. PY 1993 VL 39 BP 23 EP 49 DI 10.1016/S0091-679X(08)60159-4 PG 27 GA BZ58U UT WOS:A1993BZ58U00002 PM 8246800 ER PT J AU KACHAR, B URRUTIA, R RIVOLTA, MN MCNIVEN, MA AF KACHAR, B URRUTIA, R RIVOLTA, MN MCNIVEN, MA TI MYOSIN-MEDIATED VESICULAR TRANSPORT IN THE EXTRUDED CYTOPLASM OF CHARACEAN ALGAE CELLS SO METHODS IN CELL BIOLOGY, VOL 39 SE METHODS IN CELL BIOLOGY LA English DT Review ID ACTIN-FILAMENTS; ACANTHAMOEBA; NITELLA C1 MAYO CLIN & MAYO FDN,CTR BASIC RES DIGEST DISORDERS,ROCHESTER,MN 55905. RP KACHAR, B (reprint author), NIDOCD,CELLULAR BIOL LAB,BETHESDA,MD 20892, USA. NR 16 TC 5 Z9 5 U1 0 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-679X J9 METHOD CELL BIOL PY 1993 VL 39 BP 179 EP 190 DI 10.1016/S0091-679X(08)60170-3 PG 12 GA BZ58U UT WOS:A1993BZ58U00013 PM 8246797 ER PT J AU URRUTIA, R MURPHY, DB KACHAR, B MCNIVEN, MA AF URRUTIA, R MURPHY, DB KACHAR, B MCNIVEN, MA TI KINESIN-MEDIATED VESICULAR TRANSPORT IN A BIOCHEMICALLY DEFINED ASSAY SO METHODS IN CELL BIOLOGY, VOL 39 SE METHODS IN CELL BIOLOGY LA English DT Review ID MICROTUBULE-ACTIVATED ATPASE; BOVINE ADRENAL-MEDULLA; ACANTHAMOEBA-CASTELLANII; ACTOMYOSIN ATPASE; ACTIN; PURIFICATION; MYOSIN; MOTILITY; MUSCLE C1 JOHNS HOPKINS UNIV,SCH MED,DEPT CELL BIOL & ANAT,BALTIMORE,MD 21205. MAYO CLIN & MAYO FDN,CTR DIGEST DIS,ROCHESTER,MN 55905. RP URRUTIA, R (reprint author), NIDOCD,CELLULAR BIOL LAB,BETHESDA,MD, USA. NR 25 TC 4 Z9 4 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-679X J9 METHOD CELL BIOL PY 1993 VL 39 BP 253 EP 266 DI 10.1016/S0091-679X(08)60175-2 PG 14 GA BZ58U UT WOS:A1993BZ58U00018 PM 8246802 ER PT J AU ASHORN, P BERGER, EA MOSS, B AF ASHORN, P BERGER, EA MOSS, B TI VACCINIA VIRUS VECTORS FOR STUDY OF MEMBRANE-FUSION MEDIATED BY HUMAN-IMMUNODEFICIENCY-VIRUS ENVELOPE GLYCOPROTEIN AND CD4 SO METHODS IN ENZYMOLOGY LA English DT Review ID SYNCYTIUM FORMATION; HTLV-III; EXPRESSION; CELLS; AIDS; INDUCTION; INFECTION; PROTEIN; SYSTEM; GENES C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RP ASHORN, P (reprint author), UNIV TAMPERE,DEPT BIOCHEM SCI,IMMUNOPATHOL LAB,TAMPERE,FINLAND. NR 22 TC 7 Z9 7 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 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 221 BP 12 EP 18 DI 10.1016/0076-6879(93)21004-R PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU443 UT WOS:A1993LU44300003 PM 8361369 ER PT J AU MORRIS, SJ ZIMMERBERG, J SARKAR, DP BLUMENTHAL, R AF MORRIS, SJ ZIMMERBERG, J SARKAR, DP BLUMENTHAL, R TI KINETICS OF CELL-FUSION MEDIATED BY VIRAL SPIKE GLYCOPROTEINS SO METHODS IN ENZYMOLOGY LA English DT Review ID INFLUENZA-VIRUS HEMAGGLUTININ; MEMBRANE-FUSION; FLUORESCENCE MICROSCOPY; ERYTHROCYTE-GHOSTS; EVENTS; MACROMOLECULES; MECHANISM; MOLECULES; PROTEIN; PROBES C1 NICHHD, THEORET & PHYS BIOL LAB, BETHESDA, MD 20892 USA. NCI, MEMBRANE STRUCT & FUNCT SECT, MATH BIOL LAB, BETHESDA, MD 20892 USA. UNIV DELHI, DEPT BIOCHEM, NEW DELHI 110021, INDIA. RP MORRIS, SJ (reprint author), UNIV MISSOURI, SCH BIOL SCI, DEPT MOLEC BIOL & BIOCHEM, KANSAS CITY, MO 64110 USA. NR 32 TC 12 Z9 12 U1 0 U2 3 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1993 VL 221 BP 42 EP 58 DI 10.1016/0076-6879(93)21006-T PG 17 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU443 UT WOS:A1993LU44300005 PM 8361385 ER PT J AU ZIMMERBERG, J AF ZIMMERBERG, J TI SIMULTANEOUS ELECTRICAL AND OPTICAL MEASUREMENTS OF INDIVIDUAL MEMBRANE-FUSION EVENTS DURING EXOCYTOSIS SO METHODS IN ENZYMOLOGY LA English DT Review ID PHOSPHOLIPID-BILAYER MEMBRANES; CAPACITANCE MEASUREMENTS; SECRETORY VESICLE; MAST-CELLS; FORMS; PORE RP ZIMMERBERG, J (reprint author), NICHHD,THEORET & PHYS BIOL,BETHESDA,MD 20892, USA. NR 19 TC 5 Z9 5 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 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 221 BP 99 EP 112 DI 10.1016/0076-6879(93)21010-6 PG 14 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU443 UT WOS:A1993LU44300009 PM 8361389 ER PT J AU LENNARZ, WJ RUIZBRAVO, N AF LENNARZ, WJ RUIZBRAVO, N TI IDENTIFICATION OF MOLECULES INVOLVED IN SPERM-EGG FUSION SO METHODS IN ENZYMOLOGY LA English DT Review ID SEA-URCHIN EGGS; ZONA-PELLUCIDA; ACROSOME REACTION; INOSITOL 1,4,5-TRISPHOSPHATE; METALLOENDOPROTEASE ACTIVITY; ADHESIVE PROTEIN; MOUSE SPERM; FERTILIZATION; BINDING; RECEPTOR C1 NATL INST GEN MED SCI,GENET PROGRAM,BETHESDA,MD 20892. RP LENNARZ, WJ (reprint author), SUNY,DEPT BIOCHEM & CELL BIOL,STONY BROOK,NY 11794, USA. FU NICHD NIH HHS [HD 18590] NR 38 TC 1 Z9 1 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 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 221 BP 261 EP 272 DI 10.1016/0076-6879(93)21023-2 PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU443 UT WOS:A1993LU44300022 PM 8395635 ER PT J AU CHERNOMORDIK, LV AF CHERNOMORDIK, LV TI FUSION OF SEMISPHERICAL MEMBRANES SO METHODS IN ENZYMOLOGY LA English DT Review ID PLANAR BILAYER-MEMBRANES; PHOSPHOLIPID-VESICLES; MOLECULAR MECHANISMS; AQUEOUS CONTENTS; LIPID-MEMBRANES; FORCES; LIPOSOMES; ADHESION; MODEL; EXOCYTOSIS RP CHERNOMORDIK, LV (reprint author), NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892, USA. NR 58 TC 1 Z9 1 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 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 220 BP 100 EP 111 DI 10.1016/0076-6879(93)20077-G PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU442 UT WOS:A1993LU44200009 PM 8350748 ER PT J AU PURI, A CLAGUE, MJ SCHOCH, C BLUMENTHAL, R AF PURI, A CLAGUE, MJ SCHOCH, C BLUMENTHAL, R TI KINETICS OF FUSION OF ENVELOPED VIRUSES WITH CELLS SO METHODS IN ENZYMOLOGY LA English DT Review ID VESICULAR STOMATITIS-VIRUS; PH-DEPENDENT FUSION; INFLUENZA-VIRUS; MEMBRANE-FUSION; CULTURED-CELLS; SENDAI VIRUS; VERO CELLS; FLUORESCENCE; PRETREATMENT; ERYTHROCYTES RP PURI, A (reprint author), NCI,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892, USA. OI Clague, Michael/0000-0003-3355-9479 NR 37 TC 8 Z9 8 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 220 BP 277 EP 287 DI 10.1016/0076-6879(93)20089-L PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU442 UT WOS:A1993LU44200021 PM 8394493 ER PT J AU CHUNG, CT MILLER, RH AF CHUNG, CT MILLER, RH TI PREPARATION AND STORAGE OF COMPETENT ESCHERICHIA-COLI-CELLS SO METHODS IN ENZYMOLOGY LA English DT Review ID TRANSFORMATION RP CHUNG, CT (reprint author), NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892, USA. NR 5 TC 36 Z9 41 U1 1 U2 7 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 218 BP 621 EP 627 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU441 UT WOS:A1993LU44100043 PM 8510550 ER PT J AU PADMANABHAN, R PADMANABHAN, R HOWARD, T GOTTESMAN, MM HOWARD, BH AF PADMANABHAN, R PADMANABHAN, R HOWARD, T GOTTESMAN, MM HOWARD, BH TI MAGNETIC AFFINITY CELL SORTING TO ISOLATE TRANSIENTLY TRANSFECTED CELLS, MULTIDRUG-RESISTANT CELLS, SOMATIC-CELL HYBRIDS, AND VIRALLY INFECTED-CELLS SO METHODS IN ENZYMOLOGY LA English DT Review ID MAMMALIAN-CELLS; EUKARYOTIC CELLS; DNA; EXPRESSION; EFFICIENCY; PROTEIN; GENE; ELECTROPORATION; TRANSFORMATION; PURIFICATION C1 UNIV KANSAS, MED CTR, DEPT BIOCHEM & MOLEC BIOL, KANSAS CITY, KS 66103 USA. NCI, CELL BIOL LAB, BETHESDA, MD 20892 USA. NICHHD, MOLEC GROWTH REGULAT LAB, BETHESDA, MD 20892 USA. RP PADMANABHAN, R (reprint author), NIH, BETHESDA, MD 20892 USA. NR 35 TC 11 Z9 11 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 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1993 VL 218 BP 637 EP 651 PG 15 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LU441 UT WOS:A1993LU44100045 PM 7685471 ER PT J AU KANE, SE GOTTESMAN, MM AF KANE, SE GOTTESMAN, MM TI USE OF MULTIDRUG-RESISTANCE GENE IN MAMMALIAN EXPRESSION VECTORS SO METHODS IN ENZYMOLOGY LA English DT Review ID BACTERIAL TRANSPORT PROTEINS; P-GLYCOPROTEIN; COMPLEMENTARY-DNA; EUKARYOTIC CELLS; TRANSGENIC MICE; DRUG-RESISTANCE; TUMOR-CELLS; BONE-MARROW; MDR1 GENE; CDNA C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. RP KANE, SE (reprint author), CITY HOPE NATL MED CTR,DUARTE,CA 91010, USA. NR 34 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 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 217 BP 34 EP 47 PG 14 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LE024 UT WOS:A1993LE02400005 PM 8097271 ER PT J AU KASLOW, DC RAWLINGS, DJ AF KASLOW, DC RAWLINGS, DJ TI INTRODUCING RESTRICTION SITES INTO DOUBLE-STRANDED PLASMID DNA SO METHODS IN ENZYMOLOGY LA English DT Review C1 UNIV CALIF LOS ANGELES,HOWARD HUGHES MED INST,LOS ANGELES,CA 90024. RP KASLOW, DC (reprint author), NIAID,MOLEC VACCINE SECT,MALARIA RES LAB,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 217 BP 295 EP 301 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LE024 UT WOS:A1993LE02400021 PM 8386292 ER PT J AU CLEVIDENCE, BA BIERI, JG AF CLEVIDENCE, BA BIERI, JG TI ASSOCIATION OF CAROTENOIDS WITH HUMAN PLASMA-LIPOPROTEINS SO METHODS IN ENZYMOLOGY LA English DT Review ID HIGH-DENSITY LIPOPROTEINS; AFFINITY-CHROMATOGRAPHY; ALPHA-TOCOPHEROL; PRECIPITATION PROCEDURE; INDIVIDUAL CAROTENOIDS; BETA-CAROTENE; CHOLESTEROL; SEPARATION; TRANSPORT C1 NIDDKD,BETHESDA,MD 20892. RP CLEVIDENCE, BA (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,LIPID NUTR LAB,BELTSVILLE,MD 20705, USA. NR 30 TC 120 Z9 122 U1 0 U2 7 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1993 VL 214 BP 33 EP 46 PG 14 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LE023 UT WOS:A1993LE02300004 PM 8469147 ER PT J AU PARK, E SHINOHARA, N ARN, JS SHARROW, SO WANECK, GL SACKS, DH AF PARK, E SHINOHARA, N ARN, JS SHARROW, SO WANECK, GL SACKS, DH TI ANTIGENIC HETEROGENEITY OF QA-2 ANTIGENS IN C57BL/6 SO MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE QA-2; MHC CLASS-I ANTIGEN; PI LINKAGE; HETEROGENEITY; MULTIGENE ID MAJOR HISTOCOMPATIBILITY COMPLEX; N-ACETYLGLUCOSAMINIDASE-F; FUNCTIONAL LYMPHOCYTES-T; CLASS-I GENES; MONOCLONAL-ANTIBODIES; TRANSPLANTATION ANTIGENS; EXPRESSION; MOUSE; REGION; IDENTIFICATION AB The Qa-2 antigens are class I-like molecules encoded by genes mapped telomeric to the H-2D region on chromosome 17 in the mouse. A panel of 8 new monoclonal anti-Qa-2 antibodies derived from a C3H.KBR anti-C3H. SW immunization was studied. Immunoprecipitation of I-125-labeled C57BL/6 splenocyte antigens showed that all of these antibodies precipitated 40 kDa molecules which could be completely precleared by the monoclonal antibody 20-8-4, which had previously been shown to crossreact with Qa-2. One of the monoclonal antibodies (1-12-1), however, was found not to completely preclear Qa-2 antigens precipitable by the other 7 antibodies or by 20-8-4, suggesting the existence of at least two different species of Qa-2 molecules. Cell lines transfected with Q7 or Q9 genes were reactive with all 9 antibodies and the Qa-2 antigens expressed on surface membranes of these cells were completely precleared by both 20-8-4 and 1-12-1. Therefore, the observed heterogeneity of these molecules cannot be explained by an antigenic difference between the Q7 and Q9 gene products. 2D gel analyses showed identical pI spectra between Qa-2 molecules precipitated with 20-8-4 and 1-12-1. In addition, all of the monoclonal antibodies reacted with labeled antigen preparations following treatment with Endo F or neuraminidase, indicating that carbohydrate moieties are probably not responsible for the antigenic difference between the two species of Qa-2 antigen. C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 43 TC 1 Z9 1 U1 0 U2 0 PU CENTER ACADEMIC PUBL JAPAN PI TOKYO PA 4-16 YAYOI 2-CHOME, BUNKYO-KU, TOKYO 113, JAPAN SN 0385-5600 J9 MICROBIOL IMMUNOL JI Microbiol. Immunol. PY 1993 VL 37 IS 9 BP 743 EP 752 PG 10 WC Immunology; Microbiology SC Immunology; Microbiology GA LX329 UT WOS:A1993LX32900010 PM 8271976 ER PT J AU NAKAGOMI, O ISEGAWA, Y UEDA, S FLORES, J AF NAKAGOMI, O ISEGAWA, Y UEDA, S FLORES, J TI 2 DISTINCT CLUSTERINGS OF THE VP8-ASTERISK GENE OF ROTAVIRUSES POSSESSING THE AU-1 GENE-4 ALLELE SO MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE ROTAVIRUS; VP4 GENE; REASSORTMENT; GENOGROUP ID OUTER CAPSID PROTEIN-VP4; ACID-SEQUENCE ANALYSIS; UNIQUE VP4; GENOGROUPS; STRAINS; NEUTRALIZATION; REASSORTMENT; EPITOPES; MEMBERS; BOVINE AB A phylogenetic tree constructed by the unweighted pair group method with arithmetic means (UPGMA) for the VP8* gene from 13 human and two feline rotavirus strains possessing the AU-1 gene 4 allele revealed that these strains could be classified into two clusters which did not correspond with the year of isolation or the host species from which they originated. Nine of 10 human strains and one feline strain isolated. In Japan formed one cluster, whereas three human strains from Italy and one feline strain from Australia formed the other. Human strain K8 from Japan was distantly related to the Australo-European clustering. C1 OSAKA UNIV,MICROBIAL DIS RES INST,DEPT PREVENT MED,SUITA,OSAKA 560,JAPAN. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. RP NAKAGOMI, O (reprint author), AKITA UNIV,SCH MED,DEPT MICROBIOL,1-1-1 HONDO,AKITA 010,JAPAN. NR 16 TC 7 Z9 7 U1 0 U2 0 PU CENTER ACADEMIC PUBL JAPAN PI TOKYO PA 4-16 YAYOI 2-CHOME, BUNKYO-KU, TOKYO 113, JAPAN SN 0385-5600 J9 MICROBIOL IMMUNOL JI Microbiol. Immunol. PY 1993 VL 37 IS 10 BP 817 EP 820 PG 4 WC Immunology; Microbiology SC Immunology; Microbiology GA MC074 UT WOS:A1993MC07400011 PM 8289689 ER PT J AU GOYON, C LICHTEN, M AF GOYON, C LICHTEN, M TI TIMING OF MOLECULAR EVENTS IN MEIOSIS IN SACCHAROMYCES-CEREVISIAE - STABLE HETERODUPLEX DNA IS FORMED LATE IN MEIOTIC PROPHASE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DOUBLE-STRAND BREAKS; GENE CONVERSION; INITIATION SITE; HOMOLOGOUS SEQUENCES; CHROMOSOME SYNAPSIS; ESCHERICHIA-COLI; 3-STRANDED DNA; RECA-PROTEIN; WILD-TYPE; RECOMBINATION AB To better understand the means by which chromosomes pair and recombine during meiosis, we have determined the time of appearance of heteroduplex DNA relative to the times of appearance of double-strand DNA breaks and of mature recombined molecules. Site-specific double-strand breaks appeared early in meiosis and were formed and repaired with a timing consistent with a role for breaks as initiators of recombination. Heteroduplex-containing molecules appeared about 1 h after double-strand breaks and were followed shortly by crossover products and the first meiotic nuclear division. We conclude that parental chromosomes are stably joined in heteroduplex-containing structures late in meiotic prophase and that these structures are rapidly resolved to yield mature crossover products. If the chromosome pairing and synapsis observed earlier in meiotic prophase is mediated by formation of biparental DNA structures, these structures most likely either contain regions of non-Watson-Crick base pairs or contain regions of heteroduplex DNA that either are very short or dissociate during DNA purification. Two loci were examined in this study: the normal ARG4 locus, and an artificial locus consisting of an arg4-containing plasmid inserted at MAT. Remarkably, sequences in the ARG4 promoter that suffered double-strand cleavage at the normal ARG4 locus were not cut at significant levels when present at MAT::arg4. These results indicate that the formation of double-strand breaks during meiosis does not simply involve the specific recognition and cleavage of a short nucleotide sequence. C1 NCI,BIOCHEM LAB,BLDG 37,ROOM 4D14,BETHESDA,MD 20892. RI Lichten, Michael/C-5795-2013 OI Lichten, Michael/0000-0001-9707-2956 NR 48 TC 116 Z9 116 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 JAN PY 1993 VL 13 IS 1 BP 373 EP 382 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KD785 UT WOS:A1993KD78500040 PM 8417336 ER PT J AU HANNIG, EM CIGAN, AM FREEMAN, BA KINZY, TG AF HANNIG, EM CIGAN, AM FREEMAN, BA KINZY, TG TI GCD11, A NEGATIVE REGULATOR OF GCN4 EXPRESSION, ENCODES THE GAMMA SUBUNIT OF EIF-2 IN SACCHAROMYCES-CEREVISIAE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID INITIATION FACTOR-II; AMINO-ACID-SEQUENCE; MESSENGER-RNA TRANSLATION; OPEN READING FRAMES; ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; BIOSYNTHETIC GENES; STRUCTURAL GENES; DNA-SEQUENCES; HOST STRAINS AB The eukaryotic translation initiation factor eIF-2 plays a critical role in regulating the expression of the yeast transcriptional activator GCN4. Mutations in genes encoding the alpha and beta subunits of eIF-2 alter translational efficiency at the GCN4 AUG codon and constitutively elevate GCN4 translation. Mutations in the yeast GCD11 gene have been shown to confer a similar phenotype. The nucleotide sequence of the cloned GCD11 gene predicts a 527-amino-acid polypeptide that is similar to the prokaryotic translation elongation factor EF-Tu. Relative to EF-Tu, the deduced GCD11 amino acid sequence contains a 90-amino-acid N-terminal extension and an internal cysteine-rich sequence that contains a potential metal-binding finger motif. We have identified the GCD11 gene product as the gamma subunit of eIF-2 by the following criteria: (i) sequence identities with mammalian eIF-2gamma peptides; (ii) increased eIF-2 activity in extracts prepared from cells cooverexpressing GCD11, eIF-2alpha, and eIF-2beta; and (iii) cross-reactivity of antibodies directed against the GCD11 protein with the 58-kDa polypeptide present in purified yeast eIF-2. The predicted GCD11 polypeptide contains all of the consensus elements known to be required for guanine nucleotide binding, suggesting that, in Saccharomyces cerevisiae, the gamma subunit of eIF-2 is responsible for GDP-GTP binding. C1 NICHHD,MOLEC GENET LOWER EUKARYOTES SECT,MOLEC GENET LAB,BETHESDA,MD 20892. CASE WESTERN RESERVE UNIV,SCH MED,DEPT BIOCHEM,CLEVELAND,OH 44106. RP HANNIG, EM (reprint author), UNIV TEXAS,MOLEC & CELL BIOL,POB 830688,RICHARDSON,TX 75083, USA. FU NIGMS NIH HHS [GM26796] NR 75 TC 72 Z9 74 U1 0 U2 2 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 JAN PY 1993 VL 13 IS 1 BP 506 EP 520 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KD785 UT WOS:A1993KD78500053 PM 8417348 ER PT J AU CARTY, MP HAUSER, J LEVINE, AS DIXON, K AF CARTY, MP HAUSER, J LEVINE, AS DIXON, K TI REPLICATION AND MUTAGENESIS OF UV-DAMAGED DNA TEMPLATES IN HUMAN AND MONKEY CELL-EXTRACTS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SIMIAN VIRUS-40 DNA; SHUTTLE VECTOR PLASMID; PYRIMIDINE DIMERS; ESCHERICHIA-COLI; MAMMALIAN-CELLS; ULTRAVIOLET-LIGHT; POINT MUTATIONS; INVITRO; PHOTOPRODUCT; SPECIFICITY AB We have used in vitro DNA replication systems from human HeLa cells and monkey CV-1 cells to replicate a UV-damaged simian virus 40-based shuttle vector plasmid, pZ189. We found that replication of the plasmid was inhibited in a UV fluence-dependent manner, but even at UV fluences which caused damage to essentially all of the plasmid molecules some molecules became completely replicated. This replication was accompanied by an increase (up to 15-fold) in the frequency of mutations detected in the supF gene of the plasmid. These mutations were predominantly G:C-A:T transitions similar to those observed in vivo. Treatment of the UV-irradiated plasmid DNA with Escherichia coli photolyase to reverse pyrimidine cyclobutane dimers (the predominant UV-induced photoproduct) before replication prevented the UV-induced inhibition of replication and reduced the frequency of mutations in supF to background levels. Therefore, the presence of pyrimidine cyclobutane dimers in the plasmid template appears to be responsible for both inhibition of replication and mutation induction. Further analysis of the replication of the UV-damaged plasmid revealed that closed circular replication products were sensitive to T4 endonuclease V (a pyrimidine cyclobutane dimer-specific endonuclease) and that this sensitivity was abolished by treatment of the replicated DNA with E. coli photolyase after replication but before T4 endonuclease treatment. These results demonstrate that these closed circular replication products contain pyrimidine cyclobutane dimers. Density labeling experiments revealed that the majority of plasmid DNA synthesized in vitro in the presence of bromodeoxyuridine triphosphate was hybrid density whether or not the plasmid was treated with UV radiation before replication; therefore, replication of UV-damaged templates appears to occur by the normal semiconservative mechanism. All of these data suggest that replication of UV-damaged templates occurs in vitro as it does in vivo and that this replication results in mutation fixation. C1 NICHHD,VIRUSES & CELLULAR BIOL SECT,BETHESDA,MD 20892. RP CARTY, MP (reprint author), UNIV CINCINNATI,DEPT ENVIRONM HLTH,CINCINNATI,OH 45267, USA. FU NIEHS NIH HHS [ES05400, 1 P30 ES06096] NR 29 TC 61 Z9 61 U1 1 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 JAN PY 1993 VL 13 IS 1 BP 533 EP 542 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KD785 UT WOS:A1993KD78500055 PM 8417349 ER PT J AU NELSON, N MARKS, MS DRIGGERS, PH OZATO, K AF NELSON, N MARKS, MS DRIGGERS, PH OZATO, K TI INTERFERON CONSENSUS SEQUENCE-BINDING PROTEIN, A MEMBER OF THE INTERFERON REGULATORY FACTOR FAMILY, SUPPRESSES INTERFERON-INDUCED GENE-TRANSCRIPTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CLASS-I GENE; INDUCIBLE ENHANCER ELEMENT; LONG TERMINAL REPEAT; IFN-BETA GENES; ALPHA-INTERFERON; GAMMA-INTERFERON; NUCLEAR FACTORS; STIMULATED TRANSCRIPTION; CYTOPLASMIC ACTIVATION; TERATOCARCINOMA CELLS AB We previously isolated a cDNA clone encoding interferon consensus sequence-binding protein (ICSBP), a member of the interferon regulatory factor (IRF) family, that binds to the interferon (IFN)-stimulated response element (ISRE) of many IFN-regulated genes. In this investigation, we studied the functional role of ICSBP by transient cotransfection of ICSBP cDNA with IFN-responsive reporter genes into the human embryonal carcinoma cell line N-Tera2. These cells were shown not to express ICSBP or IRF-2, thus allowing functional analysis of transfected cDNAs. Cotransfection of ICSBP into cells treated with retinoic acid or any of the IFNs (alpha, beta, or gamma) repressed expression of a chloramphenicol acetyltransferase reporter driven by the major histocompatibility complex class I gene promoter. Similarly, ICSBP repressed expression of chloramphenicol acetyltransferase reporters driven by the ISREs of the 2'-5' oligoadenylate synthetase, guanylate-binding protein, and ISG-15 genes in IFN-treated cells. The repression was dependent on the presence of the ISRE in the reporter. Deletion analysis showed that the putative N-terminal DNA binding domain of ICSBP by itself is capable of mediating the repression. Using the same cotransfection conditions as for ICSBP, a similar repression of these reporters was observed with IRF-2. Finally, ICSBP repressed the IRF-1-mediated induction of major histocompatibility complex class I and IFN-beta reporters in the absence of IFN or retinoic acid. Taken together, these results suggest that ICSBP is a negative regulatory factor capable of repressing transcription of target genes induced by IFN, retinoic acid, or IRF-1. C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. OI Marks, Michael/0000-0001-7435-7262 NR 83 TC 177 Z9 177 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 JAN PY 1993 VL 13 IS 1 BP 588 EP 599 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KD785 UT WOS:A1993KD78500061 PM 7678054 ER PT J AU MARKOVA, NG MAREKOV, LN CHIPEV, CC GAN, SQ IDLER, WW STEINERT, PM AF MARKOVA, NG MAREKOV, LN CHIPEV, CC GAN, SQ IDLER, WW STEINERT, PM TI PROFILAGGRIN IS A MAJOR EPIDERMAL CALCIUM-BINDING PROTEIN SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CORNEUM BASIC-PROTEIN; STRATUM-CORNEUM; INTERMEDIATE FILAMENTS; HUMAN LORICRIN; GENE; FILAGGRIN; SEQUENCE; TRANSCRIPTION; EXPRESSION; DIFFERENTIATION AB Profilaggrin is a major highly phosphorylated protein component of the keratohyalin granules of mammalian epidermis. It contains 10 to '12 tandemly repeated filaggrin units and is processed into the intermediate filament-associated protein filaggrin by specific dephosphorylation and proteolysis during terminal differentiation of the epidermal cells. Later, filaggrin itself is degraded to free amino acids that participate in maintenance of epidermal flexibility. The present paper describes the structural organization of the 5' region of the human profilaggrin gene as well as the amino terminus of the profilaggrin protein. The primary profilaggrin transcript consists of three exons and two introns. The first exon (exon I) is only 54 bp and is untranslated. The coding sequences are distributed between exon II (159 bp) and exon III, which contains the information for 10 to 12 filaggrin repeats (972 bp each) and the 3' noncoding sequences. A very large intron separates exons I and II. The combination of a very short exon I with an unusually long intron 1 makes the structure of the profilaggrin gene unique among the epidermally expressed genes investigated so far. Comparison of the expression patterns revealed by primer extension and RNase protection analysis of foreskin epidermal and cultured keratinocyte RNAs suggests that alternately spliced messages, which are different from profilaggrin mRNA, are transcribed from the profilaggrin gene system at earlier stages of epidermal differentiation. The amino terminus of profilaggrin exhibits a significant homology to the small calcium-binding S100-like proteins. It contains two alpha-helical regions, termed EF-hands, that bind calcium in vitro. This is the first example of functional calcium-binding domains fused to a structural protein. We suggest that in addition to its role in filament aggregation and the maintenance of epidermal flexibility, profilaggrin may play an important role in the differentiation of the epidermis by autoregulating its own processing in a calcium-dependent manner or by participating in the transduction of calcium signal in epidermal cells. C1 NIAMSD,SKIN BIOL BRANCH,BLDG 10,ROOM 9N228,BETHESDA,MD 20892. NR 67 TC 110 Z9 110 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 JAN PY 1993 VL 13 IS 1 BP 613 EP 625 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KD785 UT WOS:A1993KD78500063 PM 8417356 ER PT J AU WIESE, RJ GOTO, H PRAHL, JM MARX, SJ THOMAS, M ALAQEEL, A DELUCA, HF AF WIESE, RJ GOTO, H PRAHL, JM MARX, SJ THOMAS, M ALAQEEL, A DELUCA, HF TI VITAMIN D-DEPENDENCY RICKETS TYPE-II - TRUNCATED VITAMIN-D RECEPTOR IN 3 KINDREDS SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Article DE CALCIUM; BONE; 1,25-DIHYDROXYVITAMIN-D; HEREDITARY RICKETS; VITAMIN-D RESISTANCE ID 1,25-DIHYDROXYVITAMIN-D3 RECEPTOR; HEREDITARY RESISTANCE; OSTEOCALCIN GENE; DNA; EXPRESSION; MUTATION; QUANTITATION; FAMILIES; BINDING; ASSAY AB Fibroblasts from three patients with vitamin D-dependency rickets type II were used to study mutations in the 1,25-dihydroxyvitamin D3 receptor responsible for this hereditary disease. Normal human fibroblasts contain 43 +/- 13 fmol receptor/mg protein as determined by immunoradiometric assay and 22 +/- 3 fmol/mg by ligand binding assay. The fibroblasts from the rachitic patients contained no receptor detectable by either method. The 1,25-(OH)2D receptor cDNA for cells from each kindred was produced from total RNA using reverse transcription and polymerase chain reaction amplification. When these cDNAs were sequenced, it was found that each cell line contained a nucleotide substitution resulting in a stop codon in the coding sequence. The predicted resultant receptor protein is 69 amino acids long in one family, and 148 and 291 amino acids long in two other families. These truncated proteins have little or no 1,25-dihydroxyvitamin D3-binding domain accounting for 1,25-dihydroxyvitamin D resistance. C1 UNIV WISCONSIN,DEPT BIOCHEM,420 HENRY MALL,MADISON,WI 53706. NATL INST DIABET DIGEST & KIDNEY DIS,BETHESDA,MD 20205. RIYADH ARMED FORCES HOSP,DEPT PAEDIAT,RIYADH 11159,SAUDI ARABIA. FU NIDDK NIH HHS [DK14881] NR 33 TC 44 Z9 44 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0303-7207 J9 MOL CELL ENDOCRINOL JI Mol. Cell. Endocrinol. PD JAN PY 1993 VL 90 IS 2 BP 197 EP 201 DI 10.1016/0303-7207(93)90152-A PG 5 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA KG535 UT WOS:A1993KG53500007 PM 8388340 ER PT J AU GILAD, GM CASERO, RA BUSTO, R GLOBUS, MYT AF GILAD, GM CASERO, RA BUSTO, R GLOBUS, MYT TI POLYAMINES IN RAT-BRAIN EXTRACELLULAR-SPACE AFTER ISCHEMIA SO MOLECULAR AND CHEMICAL NEUROPATHOLOGY LA English DT Article DE POLYAMINES, EXTRACELLULAR PUTRESCINE, SPERMIDINE AND SPERMINE; ISCHEMIA, TRANSIENT GLOBAL ISCHEMIA; BRAIN, DORSOLATERAL REGION OF THE RAT CORPUS STRIATUM; MICRODIALYSIS, EXTRACELLULAR FLUID COLLECTION BY MICRODIALYSIS PROBE; HIGH PERFORMANCE LIQUID CHROMATOGRAPHY (HPLC), POLYAMINE MEASUREMENTS BY HPLC ID DERIVATIVES; SPERMINE; RECEPTOR; SEPARATION; MODULATION; BINDING; TISSUE; URINE AB This article reports measurements of extracellular polyamines in rat brain. Microdialysis probes were implanted in the striatum and microperfusion samples were collected before, during, and after transient (20 min) global ischemia. Polyamine levels in microperfusates were measured by reverse-phase high-performance liquid chromatography after precolumn derivatization. No significant changes in extracellular polyamines were detected for up to 3 h following ischemia. We conclude that extracellular levels of polyamines (1) are comparable to the low levels in other extracellular compartments, and (2) do not change during the initial period of reperfusion, the period most critical for neuron survival after ischemia. C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSURG,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. JOHNS HOPKINS UNIV,SCH MED,JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD 21231. UNIV MIAMI,SCH CHEM,DEPT NEUROL D4-5,CEREBRAL VASC DIS RES CTR,MIAMI,FL 33101. NR 30 TC 12 Z9 12 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 1044-7393 J9 MOL CHEM NEUROPATHOL JI Mol. Chem. Neuropathol. PD JAN-FEB PY 1993 VL 18 IS 1-2 BP 27 EP 33 PG 7 WC Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA KQ791 UT WOS:A1993KQ79100003 PM 8466594 ER PT J AU GILAD, GM GILAD, VH WYATT, RJ AF GILAD, GM GILAD, VH WYATT, RJ TI ACCUMULATION OF EXOGENOUS POLYAMINES IN GERBIL BRAIN AFTER ISCHEMIA SO MOLECULAR AND CHEMICAL NEUROPATHOLOGY LA English DT Article ID ORNITHINE DECARBOXYLASE; RAT-BRAIN; REGIONAL DISTRIBUTION; SYMPATHETIC NEURONS; NERVOUS-SYSTEM; MONKEY BRAIN; SPERMINE; BINDING; RECEPTOR; MODULATION AB Regionally selective delayed neuronal degeneration is a characteristic sequel of cerebral ischemia. Recent evidence indicates that changes in brain polyamine metabolism may be critical for nerve cell survival after ischemia. Within hours after ischemia, intracellular putrescine levels are greatly increased and remain elevated for days, whereas only minor changes are noted in the levels of the polyamines spermine and spermidine. In contrast, the extracellular levels of all polyamines are low after ischemia. Injections of polyamines following ischemia, however, can protect neurons in the gerbil brain from delayed cell death, with spermine being the most potent of the polyamines. In the present study, therefore, we sought to determine if increased polyamine uptake occurs in the brain after ischemia. In the hippocampal slice preparation, temperature-dependent uptake was unique for spermine, but not for spermidine or putrescine. Uptake of [C-14]spermine was transiently increased after ischemia, peaking at 150% of control by 12-13 h and subsiding by 24 h. Intravenous injections of [H-3]spermidine resulted in a postischemic accumulation of this polyamine throughout the forebrain parenchyma. We conclude that: 1. Active cellular uptake of spermine is transiently increased early after ischemia; 2. A nonspecific accumulation of exogenous polyamines occurs early after ischemia probably owing to a compromised blood-brain barrier, and 3. The findings indicate that exogenous polyamines can exert their effect directly in the brain after ischemia. C1 ST ELIZABETH HOSP,NIMH,NEUROSCI RES CTR,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. NR 37 TC 14 Z9 14 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 1044-7393 J9 MOL CHEM NEUROPATHOL JI Mol. Chem. Neuropathol. PD JAN-FEB PY 1993 VL 18 IS 1-2 BP 197 EP 210 PG 14 WC Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA KQ791 UT WOS:A1993KQ79100017 PM 8466593 ER PT S AU MCENERY, MW SNOWMAN, AM SEAGAR, MJ COPELAND, TD TAKAHASHI, M AF MCENERY, MW SNOWMAN, AM SEAGAR, MJ COPELAND, TD TAKAHASHI, M BE Higashida, H Yoshioka, T Mikoshiba, K TI IMMUNOLOGICAL CHARACTERIZATION OF PROTEINS ASSOCIATED WITH THE PURIFIED OMEGA-CONOTOXIN GVIA RECEPTOR SO MOLECULAR BASIS OF ION CHANNELS AND RECEPTORS INVOLVED IN NERVE EXCITATION, SYNAPTIC TRANSMISSION AND MUSCLE CONTRACTION: IN MEMORY OF PROFESSOR SHOSAKU NUMA SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Molecular Basis of Ion Channels and Receptors Involved in Nerve Excitation Synaptic Transmission and Muscle Contraction (In Memory of Professor Shosaku Numa) CY JAN 12-15, 1993 CL TOKYO, JAPAN SP NEW YORK ACAD SCI ID SENSITIVE CALCIUM CHANNELS; SYNAPTIC VESICLES; SUBUNIT STRUCTURE; SKELETAL-MUSCLE; BRAIN; SYNAPTOTAGMIN C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. FAC MED NORD,INSERUM,U374,MARSEILLE,FRANCE. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. MITSUBISHI KASEI INST LIFE SCI,MACHIDA 194,TOKYO,JAPAN. RP MCENERY, MW (reprint author), CASE WESTERN RESERVE UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,E521 10900 EUCLID AVE,CLEVELAND,OH 44106, USA. RI Mikoshiba, Katsuhiko/N-7943-2015 NR 14 TC 5 Z9 5 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-823-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 707 BP 386 EP 391 DI 10.1111/j.1749-6632.1993.tb38078.x PG 6 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences; Physiology SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology; Physiology GA BZ86C UT WOS:A1993BZ86C00042 PM 9137576 ER PT S AU USUKURA, J KHOO, W ABE, T SHINOHARA, BT BREITMAN, M AF USUKURA, J KHOO, W ABE, T SHINOHARA, BT BREITMAN, M BE Higashida, H Yoshioka, T Mikoshiba, K TI ABNORMAL-DEVELOPMENT OF CONE CELLS IN TRANSGENIC MICE ABLATED OF ROD PHOTORECEPTOR CELLS SO MOLECULAR BASIS OF ION CHANNELS AND RECEPTORS INVOLVED IN NERVE EXCITATION, SYNAPTIC TRANSMISSION AND MUSCLE CONTRACTION: IN MEMORY OF PROFESSOR SHOSAKU NUMA SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Molecular Basis of Ion Channels and Receptors Involved in Nerve Excitation Synaptic Transmission and Muscle Contraction (In Memory of Professor Shosaku Numa) CY JAN 12-15, 1993 CL TOKYO, JAPAN SP NEW YORK ACAD SCI ID RHODOPSIN; RETINA C1 MT SINAI HOSP,TORONTO M5G 1X5,ON,CANADA. NIH,BETHESDA,MD 20895. RP USUKURA, J (reprint author), NAGOYA UNIV,SCH MED,DEPT ANAT,SHOWA KU,65 TSURUMAI,NAGOYA 466,JAPAN. RI Mikoshiba, Katsuhiko/N-7943-2015; OI Shinohara, Toshimichi/0000-0002-7197-9039 NR 9 TC 2 Z9 2 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-823-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 707 BP 550 EP 553 DI 10.1111/j.1749-6632.1993.tb38123.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences; Physiology SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology; Physiology GA BZ86C UT WOS:A1993BZ86C00087 PM 9137618 ER PT J AU KLAUSNER, RD ROUAULT, TA AF KLAUSNER, RD ROUAULT, TA TI A DOUBLE LIFE - CYTOSOLIC ACONITASE AS A REGULATORY RNA-BINDING PROTEIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article ID IRON-RESPONSIVE ELEMENT; FERRITIN MESSENGER-RNA; AFFINITY PURIFICATION; IRE-BP; IDENTIFICATION; MECHANISM; SYNTHASE; CLUSTER RP KLAUSNER, RD (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 31 TC 79 Z9 78 U1 0 U2 2 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 JAN PY 1993 VL 4 IS 1 BP 1 EP 5 PG 5 WC Cell Biology SC Cell Biology GA KM253 UT WOS:A1993KM25300001 PM 8443405 ER PT J AU FUKUYAMA, R CHANDRASEKARAN, K RAPOPORT, SI AF FUKUYAMA, R CHANDRASEKARAN, K RAPOPORT, SI TI NERVE GROWTH FACTOR-INDUCED NEURONAL DIFFERENTIATION IS ACCOMPANIED BY DIFFERENTIAL INDUCTION AND LOCALIZATION OF THE AMYLOID PRECURSOR PROTEIN (APP) IN PC12-CELLS AND VARIANT PC12S-CELLS SO MOLECULAR BRAIN RESEARCH LA English DT Article DE AMYLOID PRECURSOR PROTEIN; NERVE GROWTH FACTOR; PC12-CELL; IMMUNOPRECIPITATION; ALTERNATIVE SPLICING; ALZHEIMER DISEASE; SYNAPSE; WESTERN BLOT ID ALZHEIMERS-DISEASE; MESSENGER-RNAS; HUMAN-BRAIN; PHEOCHROMOCYTOMA CELLS; CORE PROTEIN; BETA; EXPRESSION; GENE; IDENTIFICATION; CLEAVAGE AB PC12 cells and the morphological variant PC12S cells in culture were examined by immunochemical methods for the presence of the amyloid precursor protein (APP), before and after treatment with the nerve growth factor (NGF). In untreated PC12, untreated PC12S and in NGF-treated PC12 cells, APP was localized in the cytoplasm, whereas in NGF-treated PC12S cells, APP was localized at growth cones, processes and cytoplasm. In PC12 cells, three major forms of APP (695 and 751/770) were detected by Western blot. After NGF treatment, only the level of APP 695 was increased. Immunoprecipitation studies in PC12 cells revealed six protein species, corresponding to immature and mature forms of each of the three APP 695, 751 and 770 proteins. Addition of NGF increased the synthesis of the immature and mature forms of APP695. In PC12S cells, only the higher molecular weight forms of AP-P (751/770) were detected by both Western blot and immunoprecipitation. Addition of NGF had no effect on their levels. In both cell types, the level of the secreted form of APP showed a significant transient increase after NGF treatment. These results suggest that NGF can differentially regulate the molecular forms of APP and the localization of APP within the cell. RP FUKUYAMA, R (reprint author), NIA,NEUROSCI LAB,BLDG 10,RM 6C 103,BETHESDA,MD 20892, USA. NR 36 TC 48 Z9 48 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD JAN PY 1993 VL 17 IS 1-2 BP 17 EP 22 DI 10.1016/0169-328X(93)90067-Y PG 6 WC Neurosciences SC Neurosciences & Neurology GA KJ352 UT WOS:A1993KJ35200003 ER PT J AU LESCH, KP AULAKH, CS WOLOZIN, BL TOLLIVER, TJ HILL, JL MURPHY, DL AF LESCH, KP AULAKH, CS WOLOZIN, BL TOLLIVER, TJ HILL, JL MURPHY, DL TI REGIONAL BRAIN EXPRESSION OF SEROTONIN TRANSPORTER MESSENGER-RNA AND ITS REGULATION BY REUPTAKE INHIBITING ANTIDEPRESSANTS SO MOLECULAR BRAIN RESEARCH LA English DT Article DE SEROTONIN TRANSPORTER MESSENGER RNA; POLYMERASE CHAIN REACTION; REGIONAL BRAIN EXPRESSION; ANTIDEPRESSANT DRUG ID RAT-BRAIN; BINDING-SITES; HIGH-AFFINITY; H-3 PAROXETINE; CLONING; 5-HYDROXYTRYPTAMINE; IMIPRAMINE; RELEASE; MICRODIALYSIS; LOCALIZATION AB Regional expression and antidepressant drug-induced regulation of mRNA encoding the serotonin (5-HT) transporter were studied in rat brain. While 5-HT transporter mRNA is abundantly expressed in the midbrain raphe complex, lower concentrations were also found in frontal cortex, hippocampus, and neostriatum using a combination of reverse transcriptase-polymerase chain reaction (RT-PCR), Southern hybridization, and sequence analysis. Long-term administration of antidepressants which inhibit 5-HT reuptake, but not monoamine oxidase inhibitors or 5-HT receptor agonists, decrease 5-HT transporter mRNA steady-state concentrations. Based on these observations, we conclude that (1) mRNA coding for the 5-HT transporter is present in several brain areas associated with ascending HT pathways, and (2) chronic treatment with reuptake inhibiting antidepressants may be associated with regulation of the 5-HT transporter at the level of gene expression which may contribute to the neuroadaptive mechanisms that likely underlie their therapeutic efficacy. C1 NIMH,CTR CLIN,CLIN SCI LAB,NEUROPHARMACOL SECT,BETHESDA,MD 20892. RI Lesch, Klaus-Peter/J-4906-2013 OI Lesch, Klaus-Peter/0000-0001-8348-153X NR 26 TC 198 Z9 201 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD JAN PY 1993 VL 17 IS 1-2 BP 31 EP 35 DI 10.1016/0169-328X(93)90069-2 PG 5 WC Neurosciences SC Neurosciences & Neurology GA KJ352 UT WOS:A1993KJ35200005 ER PT J AU MORI, N TAJIMA, Y SAKAGUCHI, H VANDENBERGH, DJ NAWA, H SALVATERRA, PM AF MORI, N TAJIMA, Y SAKAGUCHI, H VANDENBERGH, DJ NAWA, H SALVATERRA, PM TI PARTIAL CLONING OF THE RAT CHOLINE-ACETYLTRANSFERASE GENE AND INSITU LOCALIZATION OF ITS TRANSCRIPTS IN THE CELL BODY OF CHOLINERGIC NEURONS IN THE BRAIN-STEM AND SPINAL-CORD SO MOLECULAR BRAIN RESEARCH LA English DT Article DE GENE EXPRESSION; INSITU HYBRIDIZATION; EXON; INTRON; MESSENGER RNA; RNASE PROTECTION ID NERVE GROWTH-FACTOR; ALZHEIMERS-DISEASE; REGULATORY ELEMENTS; DIFFERENTIATION FACTOR; MESSENGER-RNAS; 1ST INTRON; EXPRESSION; FOREBRAIN; HYBRIDIZATION; ORGANIZATION AB We have isolated recombinant lambda (A) phages which contain a part of the rat choline acetyltransferase (ChAT) gene. Restriction and Southern blot analyses using synthetic oligonucleotides indicate that these clones overlap one another and contain at least four exons which reside in 16.4 kb of sequence encoding from the middle to the 3' end, but not the 5'-region, of the rat ChAT gene. Partial sequence analyses revealed that the clones contain an exon whose nucleotide sequence corresponds to a highly conserved region of ChAT during evolution. RNase protection mapping experiments show that sequences represented by this exon are expressed at high levels in the spinal cord of adult rats and at low but detectable levels in PC12 cells. By using the genomic sequences, including the exon, as a hybridization probe, we have detected ChAT mRNAs in situ in rat tissues. In situ hybridization experiments using radioactive and non-radioactive probes revealed that cholinergic motoneurons in the spinal cord, the laterodorsal tegmental nucleus as well as the hypoglossal nucleus in the brain stem were labeled, suggesting that the genomic sequence can be used as a probe to measure the ChAT mRNA levels in those cholinergic neurons. The results also indicate that the non-radioactive method gives a better resolution in localizing the expression of ChAT transcripts in the cytoplasm of cholinergic neurons. C1 CITY HOPE NATL MED CTR,BECKMAN RES INT,DIV NEUROSCI,DUARTE,CA 91010. BECKMAN NEUROSCI CTR,COLD SPRING HARBOR LAB,COLD SPRING HARBOR,NY 11724. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. RP MORI, N (reprint author), UNIV SO CALIF,ETHEL PERCY ANDRUS GERONTOL CTR,DIV NEUROGERONTOL,MC-0191,LOS ANGELES,CA 90089, USA. NR 58 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD JAN PY 1993 VL 17 IS 1-2 BP 101 EP 111 DI 10.1016/0169-328X(93)90078-4 PG 11 WC Neurosciences SC Neurosciences & Neurology GA KJ352 UT WOS:A1993KJ35200014 PM 8381893 ER PT J AU WALTHER, D TAKEMURA, M UHL, G AF WALTHER, D TAKEMURA, M UHL, G TI FOS FAMILY MEMBER CHANGES IN NUCLEUS CAUDALIS NEURONS AFTER PRIMARY AFFERENT STIMULATION - ENHANCEMENT OF FOS-B AND C-FOS SO MOLECULAR BRAIN RESEARCH LA English DT Article DE FOS-B; C-FOS IN RNA; PROENKEPHALIN; NUCLEUS CAUDALIS; TRIGEMINAL GANGLIA ID RAT SPINAL-CORD; MESSENGER-RNAS; GENE-EXPRESSION; JUN PROTEINS; PREPROENKEPHALIN; PREPRODYNORPHIN; PROENKEPHALIN; TRANSCRIPTION; INDUCTION; ELEMENTS AB In situ hybridization using cDNAs complementary to specific regions of the mRNAs encoding four members of the FOS transcription factor gene family reveals modest levels of hybridization over superficial lamina of the nucleus caudalis of the spinal tract of the trigeminal in sections taken from unstimulated brains. Fos B expression is markedly and rapidly enhanced ipsilateral to electrical stimulation of the trigeminal ganglia. c-fos mRNA also changes; these differences contrast with the lack of significant changes in the low basal levels of expression of fra-1 and fra-2 mRNAs. The prominent change in fos B mRNA is mediated largely by an increase in the number of neurons that express hybridization densities above background after stimulation. This result, taken together with data on stimulation-induced changes in expression of preproenkephalin and other AP-1 transcription factors in wild-type animals and stimulation-induced changes in CAT activity in transgenic mice expressing portions of the proenkephalin promoter, is consistent with a role for the enhanced fos B expression in upregulation of expression of preproenkephalin in these neurons. C1 NIDA, MOLEC NEUROBIOL LAB, ADDICT RES CTR, POB 5180, BALTIMORE, MD 21224 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROSCI, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROL, BALTIMORE, MD 21205 USA. NR 29 TC 17 Z9 18 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD JAN PY 1993 VL 17 IS 1-2 BP 155 EP 159 DI 10.1016/0169-328X(93)90084-3 PG 5 WC Neurosciences SC Neurosciences & Neurology GA KJ352 UT WOS:A1993KJ35200020 ER PT J AU MESCO, ER CARLSON, SG JOSEPH, JA ROTH, GS AF MESCO, ER CARLSON, SG JOSEPH, JA ROTH, GS TI DECREASED STRIATAL D2-DOPAMINE RECEPTOR MESSENGER-RNA SYNTHESIS DURING AGING SO MOLECULAR BRAIN RESEARCH LA English DT Note DE DOPAMINE; AGING; STRIATUM; MESSENGER RNA SYNTHESIS; DOPAMINE-D2 RECEPTOR ID DOPAMINE-RECEPTORS; MESSENGER-RNA; RAT STRIATUM; DNA DAMAGE; AGE; BINDING; RECOVERY; BLOCKADE; BRAIN; GENE AB Decreases in striatal dopamine receptors during aging are related to deficits in motor functions, and are highly correlated with the D2 receptor subtype. Some receptor loss is attributed to cell death, while the remainder is thought to be related to synthetic capacity. We discuss here our findings, for isolated rat striatal nuclei, which indicate a 50% overall decrease in the synthesis of the dopamine D2 mRNA in aged nuclei. C1 FRANCIS SCOTT KEY MED CTR,NIA,GERONTOL RES CTR,NATHAN W SHOCK LABS,MOLEC GENET LAB,BALTIMORE,MD 21224. FRANCIS SCOTT KEY MED CTR,NIA,MOLEC & CELLULAR BIOL LAB,MOLEC PHYSIOL & GENET SECT,BALTIMORE,MD 21224. NR 25 TC 33 Z9 33 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD JAN PY 1993 VL 17 IS 1-2 BP 160 EP 162 DI 10.1016/0169-328X(93)90085-4 PG 3 WC Neurosciences SC Neurosciences & Neurology GA KJ352 UT WOS:A1993KJ35200021 PM 8381899 ER PT J AU SORSCHER, DH BARRETT, JC CORDEIROSTONE, M AF SORSCHER, DH BARRETT, JC CORDEIROSTONE, M TI TIMING OF REPLICATION OF DIFFERENTIALLY TRANSCRIBED GENES IN SYRIAN-HAMSTER EMBRYO FIBROBLASTS SO MOLECULAR CARCINOGENESIS LA English DT Article DE DNA REPLICATION; GENE DUPLICATION; TRANSCRIPTION; NEOPLASTIC TRANSFORMATION; TUMOR SUPPRESSOR GENE ID BETA-GLOBIN GENE; TUMOR-SUPPRESSOR GENE; C3H 10T1/2 CELLS; DNA-REPLICATION; H19 GENE; S-PHASE; EXPRESSION; DETERMINANT; APHIDICOLIN; ACTIVATION AB Syrian hamster embryo cell lines have been used as models of neoplastic progression in vitro. Changes in phenotype and biological properties have been observed in these cell lines in association with modulation of gene transcription. We explored this natural evolution of cells in culture to investigate the reported relationship between transcriptional activity and replication in early S phase. In this study we used two nontumorigenic cell lines that had either retained (supB+) or lost (supB-) the ability to suppress tumorigenicity of malignantly transformed hamster fibroblasts (BP6T). In association with the loss of suppressor gene function, supB cells have downregulated the expression of the H19 and tropomyosin-I (TM-I) genes, which are actively transcribed in supB+ cells. Synchronous populations of supB+ and supB- cells were pulse-labeled with [H-3]thymidine and bromodeoxyuridine at 1-h intervals during S phase; the replicating DNA was isolated by centrifugation in cesium chloride gradients and hybridized to P-32 labeled gene probes. No correlation was found between the timing of gene replication and the status of expression of these two genes. TM-I replicated during the first hour and H19 replicated between the second and third hours of the s phase in the expressing and nonexpressing cell lines. Immunoglobulin gene sequences, known to be late-replicating infibroblasts, replicated at the end of the S phase. These results suggest that downregulation of transcription is not always accompanied by a concomitant change in time of gene replication from early to late S phase. (C) 1993 Wiley-Liss, Inc. C1 UNIV N CAROLINA,SCH MED,LINEBERGER COMPREHENS CANC CTR,CHAPEL HILL,NC 27514. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. FU NCI NIH HHS [P01-CA42765] NR 29 TC 5 Z9 5 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. PY 1993 VL 8 IS 1 BP 28 EP 33 DI 10.1002/mc.2940080108 PG 6 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA LT201 UT WOS:A1993LT20100006 PM 8352888 ER PT J AU SUN, Y NAKAMURA, K HEGAMYER, G DONG, ZG COLBURN, N AF SUN, Y NAKAMURA, K HEGAMYER, G DONG, ZG COLBURN, N TI NO POINT MUTATION OF HA-RAS OR P53 GENES EXPRESSED IN PRENEOPLASTIC-TO-NEOPLASTIC PROGRESSION AS MODELED IN MOUSE JB6 CELL VARIANTS SO MOLECULAR CARCINOGENESIS LA English DT Article DE TUMOR PROMOTION PROGRESSION; POINT MUTATION; P53 EXPRESSION; MESSENGER RNA TRANSCRIPTS; TPA REGULATION ID WILD-TYPE P53; TUMOR SUPPRESSOR GENE; HUMAN-BREAST-CANCER; DNA DAMAGE; TRANSFORMATION; PROMOTER; RESISTANT; PROTEIN; APOPTOSIS; ONCOGENE AB Alterations of the p53 gene have been found in many human and animal tumors, and ras mutations have been seen somewhat less frequently. Loss of p53 tumor suppressor activity has been implicated in multistage tumor promotion/progression after initiation by Ha-ras or Ki-ras activation. Whether p53 or ras alterations occur during promotion of neoplastic transformation in JB6 cells has not been reported. Using a series of mouse JB6 variants representing different stages of progression toward the tumor-cell phenotype, we investigated whether mutational activation of Ha-ras and mutational inactivation and altered expression of the p53 gene occurred during progression. We report here that neither point mutations of the Ha-ras or p53 genes nor p53 structural alterations were involved in this process. Although there was no significant difference in steady-state levels of p53 mRNA, an elevated level of immunoprecipitable p53 protein was observed in a subset of transformed cells. We also report the detection of a second 2.2-kb p53-hybridizing transcript. This transcript was not translated into p53 protein and may be a nuclear precursor of the mature message. Both p53-hybridizing transcripts were downregulated by prolonged 12-0-tetradecanoylphorbol-13-acetate (TPA) treatment (24 h) regardless of the stage of progression. We conclude from this study that in JB6 variants (1) mutational activation of Ha-ras and inactivation of p53 are unlikely to be involved in preneoplastic progression; (2) increased amounts of p53 protein may be involved in a subset of transformed cells, possibly reflecting a longer half-life, as demonstrated in other systems; and (3) late downregulation of p53 mRNA but not protein expression may be a secondary response in the TPA-mediated signal transduction pathway. (C) 1993 Wiley-Liss, Inc.* C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYN CORP,BCDP,FREDERICK,MD 21701. RP SUN, Y (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,CELL BIOL SECT,FREDERICK,MD 21702, USA. NR 46 TC 52 Z9 53 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1993 VL 8 IS 1 BP 49 EP 57 DI 10.1002/mc.2940080111 PG 9 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA LT201 UT WOS:A1993LT20100009 PM 8352891 ER PT J AU OLIVERO, OA POIRIER, MC AF OLIVERO, OA POIRIER, MC TI PREFERENTIAL INCORPORATION OF 3'-AZIDO-2',3'-DIDEOXYTHYMIDINE INTO TELOMERIC DNA AND Z-DNA-CONTAINING REGIONS OF CHINESE-HAMSTER OVARY CELLS SO MOLECULAR CARCINOGENESIS LA English DT Article DE 3'-AZIDO-2',3'-DIDEOXYTHYMIDINE; TELOMERE; Z-DNA; IMMUNOHISTOCHEMISTRY; METAPHASE CHROMOSOME ID VIRUS REVERSE-TRANSCRIPTASE; TERMINAL TRANSFERASE-ACTIVITY; 3'-AZIDO-3'-DEOXYTHYMIDINE; CHROMOSOMES; RIBONUCLEOPROTEIN; PHARMACOLOGY; TETRAHYMENA; REPEATS; ENZYME; LINE AB 3'-Azido-2',3'-dideoxythymidine (azidothymidine; AZT) induces bone marrow toxicity in patients chronically given therapeutic doses of drug and is tumorigenic in rodents, inducing squamous cell tumors in vaginal tissues of mice and rats. In the study reported here, we explored the incorporation of AZT into specific regions of mammalian chromosomal DNA. CHO cells were exposed to AZT for 4 h, allowed to complete at least one cell cycle, and then arrested in metaphase with colchicine. Regions of concentrated AZT incorporation were identified in individual metaphase chromosomes by immunohistochemistry using antiserum specific for AZT and a secondary antiserum with a streptavidin-Texas red end point. These studies demonstrated that most of the intensely staining regions were chromosomal ends or telomeres. When 18 metaphases were examined, all telomeres but one (39 of 40) were positive at least once. Using an anti-Z-DNA antibody, chromosomal regions containing DNA in Z conformation were also localized by immunohistochemistry using a rhodamine-conjugated secondary antibody. When metaphase chromosome spreads were stained for either AZT or Z-DNA, ideograms showing localization of AZT (18 metaphases) and DNA in Z configuration (26 metaphases) were drawn for every chromosome of each metaphase examined. These ideograms demonstrated that 60% of the regions that stained positive for AZT were also positive for Z-DNA. Furthermore, slides incubated with both antibodies, using streptavidin-Texas red to identify AZT and fluorescein to identify Z-DNA, confirmed colocalization of the two markers. Additional experiments exploring the induction of chromatin bridges in AZT-treated cells suggest that the analogue may be able to bind to and disrupt the normal functioning of telomeric DNA. (C) 1993 Wiley-Liss, Inc.* RP OLIVERO, OA (reprint author), NCI,CELLULAR CARCINOGENIS & TUMOR PROMOT LAB,BLDG 37,ROOM 3B12,BETHESDA,MD 20892, USA. NR 24 TC 28 Z9 29 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1993 VL 8 IS 2 BP 81 EP 88 DI 10.1002/mc.2940080204 PG 8 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA MA385 UT WOS:A1993MA38500003 PM 8397798 ER PT J AU JIAO, JL GUTTENPLAN, JB GLICKMAN, BW ANDERSON, MW XIN, LY ZIELENSKA, M AF JIAO, JL GUTTENPLAN, JB GLICKMAN, BW ANDERSON, MW XIN, LY ZIELENSKA, M TI MUTATIONAL SPECIFICITIES OF ENVIRONMENTAL CARCINOGENS IN THE LACL GENE OF ESCHERICHIA-COLI .7. THE HOST-MEDIATED ASSAY AND ITS COMPARISON WITH IN-VITRO MUTAGENESIS INDUCED BY 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE SO MOLECULAR CARCINOGENESIS LA English DT Note DE MUTATIONAL SPECIFICITY; HOST-MEDIATED ASSAY; ALKYLATING AGENTS ID TOBACCO-SPECIFIC NITROSAMINES; LIVER-MICROSOMES; CANCER; LUNG; METABOLISM; EXPOSURE; INVIVO; SMOKE; RATS; DNA AB To investigate the influence of different types of metabolic activation (9,000 x g supernatant (S9) activation vs. a host-mediated approach) on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced mutational specificity, we determined by DNA sequencing the distribution of forward mutations recovered in the N-terminal region of the lacI gene of Escherichia coli. After activation with the 59 liver fraction from rats treated with Aroclor 1254, a diverse spectrum of mutations was recovered, with 55% of the events being G:C-->A:T transitions. In contrast, after the host-mediated assay in mice, G:C-->A:T transitions accounted for over 94% of the mutations recovered. Generally, NNK metabolism can proceed through two distinct pathways, involving either alpha-methyl or methylene hydroxylation. These two pathways produce different distributions of DNA damage. The difference in the mutational spectra we observed thus likely reflects the difference in the contributions of each pathway under the two different treatment conditions. (C) 1993 Wiley-Liss, Inc. C1 CTR ENVIRONM HLTH,DEPT BIOL,9865 W SAANICH RD,SIDNEY V8L 3S1,BC,CANADA. UNIV VICTORIA,VICTORIA V8W 2Y2,BC,CANADA. NYU,DEPT BIOCHEM,NEW YORK,NY 10003. NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709. NR 27 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1993 VL 8 IS 3 BP 127 EP 131 DI 10.1002/mc.2940080302 PG 5 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA MH443 UT WOS:A1993MH44300001 PM 8216731 ER PT J AU TOPOL, LZ KISSELJOVA, NP GUTIERREZ, ML DEICHMAN, GI MUSATKINA, EA SHTUTMAN, MS ZAKAMALDINA, TZ BLAIR, DG TATOSYAN, AG AF TOPOL, LZ KISSELJOVA, NP GUTIERREZ, ML DEICHMAN, GI MUSATKINA, EA SHTUTMAN, MS ZAKAMALDINA, TZ BLAIR, DG TATOSYAN, AG TI MODULATION OF PP60(V-SRC) AND PP60(C-SRC) EXPRESSION IN ROUS-SARCOMA VIRUS - TRANSFORMED HAMSTER FIBROBLASTS TRANSFECTED WITH ACTIVATED N-RAS SO MOLECULAR CARCINOGENESIS LA English DT Article DE ONCOGENES; DNA TRANSFECTION; GENE EXPRESSION; HAMSTER CELLS; TUMORIGENICITY ID CELLULAR SRC KINASES; ONCOGENE EXPRESSION; TYROSINE PHOSPHORYLATION; DEPENDENT TRANSCRIPTION; MONOCLONAL-ANTIBODIES; PROTEIN INTERACTIONS; SH2 DOMAINS; C-SRC; GTPASE; GAP AB Three phenotypically different hamster cell lines transformed with Rous sarcoma virus (RSV) were transfected with plasmid DNA containing an activated N-ras oncogene, and nine clones expressing various levels of p21N-ras were characterized. We examined the effects of p21N-ras on expression and kinase activity of resident src proteins by using a variety of assays that allowed us to discriminate between viral and cellular src proteins. In eight clones with a 10- to 20-fold increase in p21N-ras levels relative to the endogenous protein, we observed a marked reduction in the synthesis and kinase activity of p60v-src. This decrease correlated with transcriptional downregulation of RSV genomic and v-src subgenomic mRNAs. In the same cells, we found a concomitant accumulation of p60c-src and, accordingly, an increase in its protein kinase activity without an apparent increase in c-src mRNA levels. Therefore, modulation of viral and cellular src proteins in cells overexpressing p21 N-ras appeared to result from two distinct effects: a downregulation of long terminal repeat-driven transcription and a more complex interaction with cellular effectors that control the stability of p60c-src. Such modulation also seemed to depend on the levels of p21N-ras and, possibly, on host-cell factors, since it was not observed in the third cell line, in which the relative increase in p21N-ras was only 2.5-fold to fivefold. (C) 1993 Wiley-Liss, Inc.* C1 MOSCOW CANC RES CTR,ONCOGENE REGULAT LABS,MOSCOW,RUSSIA. MOSCOW CANC RES CTR,ANTI TUMOR IMMUN LABS,MOSCOW,RUSSIA. RP TOPOL, LZ (reprint author), NCI,FCRDC,MOLEC ONCOL LAB,POB B,FREDERICK,MD 21702, USA. NR 53 TC 14 Z9 14 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. PY 1993 VL 8 IS 3 BP 167 EP 176 DI 10.1002/mc.2940080307 PG 10 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA MH443 UT WOS:A1993MH44300006 PM 8216735 ER PT J AU DEVEREUX, TR BELINSKY, SA MARONPOT, RR WHITE, CM HEGI, ME PATEL, AC FOLEY, JF GREENWELL, A ANDERSON, MW AF DEVEREUX, TR BELINSKY, SA MARONPOT, RR WHITE, CM HEGI, ME PATEL, AC FOLEY, JF GREENWELL, A ANDERSON, MW TI COMPARISON OF PULMONARY O-6-METHYLGUANINE DNA ADDUCT LEVELS AND KI-RAS ACTIVATION IN LUNG-TUMORS FROM RESISTANT AND SUSCEPTIBLE MOUSE STRAINS SO MOLECULAR CARCINOGENESIS LA English DT Article DE DNA ADDUCTS; KI-RAS ONCOGENE; MURINE LUNG CARCINOGENESIS ID TOBACCO-SPECIFIC CARCINOGEN; POLYMERASE CHAIN-REACTION; CHEMICAL CARCINOGENESIS; A/J MICE; P53 MUTATIONS; CELL ORIGIN; II CELLS; 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE; PROTOONCOGENE; METABOLISM AB The role of O6-methylguanine (O6MG) DNA adduct formation and persistence in the formation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK)-induced lung tumors from resistant C57BL/6 and susceptible A/J mice was investigated. In addition, the frequencies of pulmonary tumor formation and Ki-ras activation were defined in C57BL/6 mice treated with NNK or vinyl carbamate(VC), and the role of the p53 gene in pulmonary carcinogenesis in these resistant mice was examined. One day after treatment with 100 mg/kg NNK, O6MG adduct concentrations were twofold to eightfold higher in Clara cells and type II cells than in small cells or whole lungs from both mouse strains. The concentrations of O6MG in isolated cells decreased at a similar rate in the two strains of mice. Lung tumors were detected by 27 mo of age in 18% of the C57BL/6 mice after a single 100 mg/kg dose of NNK and in 46% of these mice after a single 60 mg/kg dose of VC. In contrast, the tumor incidence in untreated C57BL/6 mice was 4%. Only one of 22 lung tumors from C57BL/6 mice treated with NNK contained an activated Ki-ras gene that was associated with an O6MG DNA adduct, whereas previous studies detected activated Ki-ras oncogenes in most of the NNK-induced lung tumors analyzed from susceptible A/J and resistant C3H mice. The small differences in formation and persistence of the O6MG adduct in whole lung or isolated lung cells from A/J and C57BL/6 strains do not account for the differences in either susceptibility for tumor formation or activation of the Ki-ras gene between these strains. In contrast to the low number of NNK-induced tumors with Ki-ras mutations in the resistant mice, 11 of 20 lung tumors from VC-treated mice contained activated Ki-ras genes. Neither p53 tumor suppressor gene mutations nor overexpression of the p53 protein were detected in spontaneous or chemically induced lung tumors in C57BL/6 mice. Thus, although Ki-ras activation was detected in some tumors, pathways independent of ras activation and p53 inactivation also appear to be involved in lung tumorigenesis in this resistant mouse strain. (C) 1993 Wiley-Liss, Inc.* C1 NIEHS,CHEM PATHOL BRANCH,RES TRIANGLE PK,NC 27709. INHALAT TOXICOL RES INST,MOLEC & CELLULAR TOXICOL GRP,ALBUQUERQUE,NM. RP DEVEREUX, TR (reprint author), NIEHS,MOLEC TOXICOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Hegi, Monika/O-4796-2015 OI Hegi, Monika/0000-0003-0855-6495 NR 45 TC 84 Z9 84 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1993 VL 8 IS 3 BP 177 EP 185 DI 10.1002/mc.2940080308 PG 9 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA MH443 UT WOS:A1993MH44300007 PM 8216736 ER PT J AU HERZOG, CR SCHUT, HAJ MARONPOT, RR YOU, M AF HERZOG, CR SCHUT, HAJ MARONPOT, RR YOU, M TI RAS MUTATIONS IN 2-AMINO-3-METHYLIMIDAZO-[4,5-F]QUINOLINE INDUCED-TUMORS IN THE CDF1 MOUSE SO MOLECULAR CARCINOGENESIS LA English DT Article DE ONCOGENE; TUMOR INDUCTION; HETEROCYCLIC AMINE; GENE ACTIVATION ID HETEROCYCLIC AMINES; N-ACETYLBENZIDINE; BROILED SARDINE; BEEF EXTRACT; FOOD MUTAGEN; COOKED-FOOD; DNA ADDUCTS; 2-AMINO-3-METHYLIMIDAZO<4,5-F>QUINOLINE; CARCINOGENICITY; ACTIVATION AB 2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) is a very potent mutagen that is carcinogenic in rodents and nonhuman primates. IQ-induced CDF1 mouse lung and liver tumors were examined for activated Ki-ras and Ha-ras genes, respectively. Polymerase chain reaction (PCR)-amplified target DNAs were analyzed for mutations of codons 12, 13, and 61 by single-strand conformation polymorphism (SSCP) and direct sequencing methods. All mutations were localized to codon 61 of the ras genes. Forty-nine of 54 lung tumors induced by IQ possessed activating Ki-ras mutations, as did 20 of 26 lung tumors from the vehicle-treated animals; 80% and 75% of these mutations, respectively, were A-->T transversions of the second nucleotide redundant. One lung adenoma from the IQ-treated group contained a tandem duplication of the sequence corresponding to codons 50-57 of the Ki-ras gene (unpublished observations). In addition, seven of 34 IQ-induced liver tumors harbored activating Ha-ras mutations: five were C-->A (G-->T) transversions at the first nucleotide, and two were A-->T transversions at the second nucleotide of codon 61. None of the 15 liver tumors collected from the vehicle-treated mice possessed Ha-ras mutations in codon 12, 13, or 61. These data indicate that IQ induces Ha-ras gene activation in CDF1 mouse liver tumors. The mechanism of lung tumor induction by IQ, however, is obscured by the high frequency of Ki-ras A-->T mutations observed in both the IQ-induced and spontaneous lung tumors. The different ras mutational spectra in lung and liver tumors may suggest either that two different pathways of IQ metabolism exist in these organs or that IQ contributes to CDF1 lung tumorigenesis by a mechanism other than its direct interaction with the Ki-ras gene. (C) 1993 Wiley-Liss, Inc. C1 MED COLL OHIO,DEPT PATHOL,3000 ARLINGTON AVE,POB 10008 HEB 263,TOLEDO,OH 43699. NIEHS,RES TRIANGLE PK,NC 27709. FU NCI NIH HHS [CA47484, CA58554] NR 34 TC 11 Z9 11 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. PY 1993 VL 8 IS 3 BP 202 EP 207 DI 10.1002/mc.2940080311 PG 6 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA MH443 UT WOS:A1993MH44300010 PM 8216739 ER PT J AU AVIS, I JETT, M KASPRZYK, PG CUTTITTA, F TRESTON, AM MANECKJEE, R MULSHINE, JL AF AVIS, I JETT, M KASPRZYK, PG CUTTITTA, F TRESTON, AM MANECKJEE, R MULSHINE, JL TI EFFECT OF GASTRIN-RELEASING PEPTIDE ON THE PANCREATIC TUMOR-CELL LINE (CAPAN) SO MOLECULAR CARCINOGENESIS LA English DT Note DE PANCREATIC CANCER; GROWTH FACTORS; GASTRIN-RELEASING PEPTIDE RECEPTORS ID LUNG-CANCER; INOSITOL PHOSPHATES; AUTOCRINE GROWTH; CALCIUM SIGNAL; 2H3 CELLS; BOMBESIN; RECEPTORS; EXPRESSION; ANTAGONIST; RAT AB TheGastrin-releasing peptide (GRP) has previously been shown to be an autocrine growth factor for small cell lung cancer, and our objective in the study presented here was to determine whether GRP has a similar role in pancreatic cancer. Using I-125-GRP, We demonstrated binding to specific, saturable, high-affinity sites (K-d = 1 nM; B-max = 245 fmol/mg protein) in membrane preparations from the pancreatic tumor cell line Capan. The receptors were found to be biologically active. In whole cells, a GRP analogue bound to these receptors and stimulated rapid transfer of tritium from the tritiated lipid inositol pool to inositol triphosphates. Exogenous GRP addition stimulated incorporation of [H-3]thymidine into DNA 20-60%. This stimulatory effect was blocked by the addition of a monoclonal antibody that complexed specifically with the receptor-binding portion of the peptide. In addition, the monoclonal antibody inhibited the growth of Capan cells in an in vitro growth assay without exogenous peptide. Bombesin receptor-specific antagonists also inhibited growth in a similar fashion. These data suggest that paracrine production of GRP may be important in pancreatic tumor growth, or that low-levels of a GRP-like peptide may play an autocrine role in this tumor. (C) 1993 Wiley-Liss, Inc. C1 NCI,DIV CANC PREVENT & CANC CONTROL,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD 20850. WALTER REED ARMY RES CTR,DIV PATHOL,WASHINGTON,DC. ONCOLOGIX INC,GAITHERSBURG,MD. BAYLOR UNIV,SIMMONS CANC CTR,DALLAS,TX. NR 35 TC 18 Z9 18 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1993 VL 8 IS 4 BP 214 EP 220 DI 10.1002/mc.2940080403 PG 7 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA MP108 UT WOS:A1993MP10800002 PM 8280369 ER PT J AU BERGEL, M BHATIA, K SIWARSKI, D GUTIERREZ, M HOCHMAN, J HUPPI, K AF BERGEL, M BHATIA, K SIWARSKI, D GUTIERREZ, M HOCHMAN, J HUPPI, K TI ASSOCIATION OF TUMORIGENIC AND NONTUMORIGENIC (IMMUNOGENIC) VARIANTS IN A MOUSE T-CELL LYMPHOMA WITH 2 DISTINCT P53 MUTATIONS SO MOLECULAR CARCINOGENESIS LA English DT Note DE P53 MUTATION; SINGLE-STRAND CONFORMATION POLYMORPHISM ID TUMOR SUPPRESSOR GENE; PROGRESSION; CARCINOMAS; ONCOGENE; OCCUR AB An in vitro model system for xenogenization has been developed in which an immunogenic, nonmalignant phenotype was selected from a highly malignant T-cell line (S49). We showed by single-strand conformation polymorphism and DNA sequence analysis that specific point mutations in the p53tumor suppressor gene correlated with a change from a tumorigenic a nontumorigenic (immunogenic) phenotype. Specifically, we found that the highly malignant S49 cell line T-60 contains an Arg-->Gln substitution at residue 246 in exon 7 of p53. In contrast, nontumorigenic (immunogenic) variants (T-25-Adh and Rev-1) exhibited a Gly-->Ser substitution at residue 242 of p53. In two subsequent tumorigenic revertants derived from Rev-1, we again found the Arg-->Gln substitution at residue 246 that was found initially in the T-60 cells. Thus, mutation at residue 246 of p53 was associated with a highly malignant phenotype, whereas a novel mutation at residue 242 of p53 appeared to be associated with a nonmalignant phenotype and may have actually protected the host through immunization. We conclude that mutation of residue 242 may represent a new class of permissive (nonmalignant) mutations in the mouse that are analogous to the Li-Fraumeni mutation in humans. (C) 1993 Wiley-Liss, Inc. C1 NCI,MOLEC GENET SECT,GENET LAB,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,DEPT CELL & ANIM BIOL,JERUSALEM,ISRAEL. NCI,PEDIAT BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD. NR 25 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1993 VL 8 IS 4 BP 221 EP 227 DI 10.1002/mc.2940080404 PG 7 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA MP108 UT WOS:A1993MP10800003 PM 8280370 ER PT J AU ESTEVE, A LEHMAN, T JIANG, W WEINSTEIN, IB HARRIS, CC RUOL, A PERACCHIA, A MONTESANO, R HOLLSTEIN, M AF ESTEVE, A LEHMAN, T JIANG, W WEINSTEIN, IB HARRIS, CC RUOL, A PERACCHIA, A MONTESANO, R HOLLSTEIN, M TI CORRELATION OF P53 MUTATIONS WITH EPIDERMAL GROWTH-FACTOR RECEPTOR OVEREXPRESSION AND ABSENCE OF MDM2 AMPLIFICATION IN HUMAN ESOPHAGEAL CARCINOMAS SO MOLECULAR CARCINOGENESIS LA English DT Article DE TUMOR SUPPRESSOR GENES; ONCOGENE; GENE AMPLIFICATION ID C-MYC; GENE-MUTATIONS; EGF RECEPTOR; HUMAN-TUMORS; WILD-TYPE; CANCER; PROTEIN; RAS; EXPRESSION; PRODUCT AB Esophageal carcinomas from 24 patients, most of whom were smokers and consumed alcoholic beverages daily, were analyzed for mutations in exons 5-8 of the p53 tumor suppressor gene. Mutations were identified by polymerase chain reaction amplification and direct sequencing in 12 of 24 (50%) of the samples; almost half of the mutations were at A:T base pairs. Nuclear accumulation of p53 protein, determined by immunohistochemistry with the CM-1 polyclonal antibody, was observed in all cases in which a missense mutation in the p53 gene was detected. None of the 24 carcinomas had amplification of the mdm2 gene, an alternate pathway to p53 loss of function. Alterations involving three other cancer-related genes associated with human esophageal carcinogenesis, c-erbB-1/epidermal growth factor receptor (EGFR), c-myc, and retinoblastoma (Rb), were examined by Southern blot or immunohistochemical analysis in the same sample set to explore the possibility of a link between oncogene activation and loss of tumor suppressor function. While no associations were observed between amplification of the c-myc or EGFR genes and p53 abnormalities, a significant correlation (P < 0.01) was seen between the presence of p53 mutation and EGFR overexpression. Absence of Rb protein, measured immunohistochemically, was observed in four tumors, none of which had aberrations of the p53 gene. (C) 1993 Wiley-Liss, Inc. C1 INT AGCY RES CANC,F-69372 LYON 08,FRANCE. NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY. UNIV PADUA,INST GEN SURG,PADUA,ITALY. NR 36 TC 49 Z9 49 U1 0 U2 3 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. PY 1993 VL 8 IS 4 BP 306 EP 311 DI 10.1002/mc.2940080414 PG 6 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA MP108 UT WOS:A1993MP10800013 PM 8280379 ER PT J AU BARRETT, JC ANDERSON, M AF BARRETT, JC ANDERSON, M TI MOLECULAR MECHANISMS OF CARCINOGENESIS IN HUMANS AND RODENTS SO MOLECULAR CARCINOGENESIS LA English DT Editorial Material RP BARRETT, JC (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 19 Z9 20 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1993 VL 7 IS 1 BP 1 EP 13 DI 10.1002/mc.2940070102 PG 13 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA KN407 UT WOS:A1993KN40700001 PM 8094618 ER PT J AU BRISSETTE, JL MISSERO, C YUSPA, SH DOTTO, GP AF BRISSETTE, JL MISSERO, C YUSPA, SH DOTTO, GP TI DIFFERENT LEVELS OF V-HA-RAS P21 EXPRESSION IN PRIMARY KERATINOCYTES TRANSFORMED WITH HARVEY SARCOMA-VIRUS CORRELATE WITH BENIGN VERSUS MALIGNANT BEHAVIOR SO MOLECULAR CARCINOGENESIS LA English DT Note DE ONCOGENE; PAPILLOMA CARCINOMA; EPIDERMIS; RETROVIRAL INFECTION ID MOUSE SKIN CARCINOGENESIS; POINT MUTATION; HUMAN ONCOGENE; GENE FAMILY; PROGRESSION; ACTIVATION; CARCINOMA; CELLS; PAPILLOMAS; TUMORS AB Primary mouse keratinocytes transformed with an activated ras oncogene transduced by helper-free Harvey sarcoma virus (HaSV) form predominantly benign tumors. In contrast, keratinocytes transformed with helper-associated HaSV form malignant tumors. We report here that this different tumorigenic behavior correlated with a much higher level of v-Ha-ras p21 protein in cells transformed with the helper-associated virus. The high level of v-ras expression in these cells was due to viral spread beyond the initial infection. The low level of v-ras p21 expression that resulted from single-hit infection with helper-free virus, together with the intrinsic heterogeneity of primary keratinocytes, explains, at least in part, the different tumorigenic behavior of keratinocytes transformed by the two types of viruses. C1 YALE UNIV,SCH MED,DEPT PATHOL,NEW HAVEN,CT 06510. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. FU NCI NIH HHS [P01 CA 16038-19]; NIAMS NIH HHS [R01 AR 39190-01] NR 25 TC 15 Z9 15 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. PY 1993 VL 7 IS 1 BP 21 EP 25 DI 10.1002/mc.2940070105 PG 5 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA KN407 UT WOS:A1993KN40700004 PM 8435106 ER PT J AU BISGAARD, HC PARMELEE, DC DUNSFORD, HA SECHI, S THORGEIRSSON, SS AF BISGAARD, HC PARMELEE, DC DUNSFORD, HA SECHI, S THORGEIRSSON, SS TI KERATIN-14 PROTEIN IN CULTURED NONPARENCHYMAL RAT HEPATIC EPITHELIAL-CELLS - CHARACTERIZATION OF KERATIN-14 AND KERATIN-19 AS ANTIGENS FOR THE COMMONLY USED MOUSE MONOCLONAL-ANTIBODY OV-6 SO MOLECULAR CARCINOGENESIS LA English DT Article DE KERATIN-14; LIVER; OV-6; NONPARENCHYMAL CELLS ID OVAL CELLS; HEPATOCELLULAR-CARCINOMA; LIVER; EXPRESSION; DIFFERENTIATION; HEPATOCYTES; LINEAGES; ORIGIN; TRANSFORMATION; PROLIFERATION AB We have recently reported that cell lines of nonparenchymal origin isolated from rat liver and pancreas, which have been suggested to be the progeny of a facultative stem cell compartment in vivo, express an unusual combination of keratins (K). These cell lines express K8 and K14 but not K18 and K5, their normal partners in filament formation (Bisgaard HC, Thorgeirsson SS, J Cell Physiol 147:333-343, 1991). However, upon spontaneous transformation and differentiation toward a hepatoblastlike progeny, K14 expression is abrogated and replaced by expression of K18 (Wirth et al., Electrophoresis 13:305-332, 1992). In the study presented here, we confirmed by protein sequence analysis that K14 was a major component of the intermediate filaments in a nonparenchymal cell line of hepatic origin. Immunocytochemical analysis of the cells in monolayer demonstrated that K8 as well as K14 were incorporated in the cellular cytoskeleton. Further analysis by immunoprecipitation showed that filament complexes were formed between K8 and K14 as atypical partners. Thus, we concluded that in some nonparenchymal cell lines isolated from rat liver, K8 and K14 form a major intermediate filament network. Finally, we showed that an antibody widely used in studies of the cell lineages of hepatic and pancreatic tissues and their neoplasms, the mouse monoclonal antibody OV-6, recognizes a common epitope in K14 and K19. C1 NCI,EXPTL CARCINOGENESIS LAB,BLDG 37,3C28,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 27 TC 65 Z9 66 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. PY 1993 VL 7 IS 1 BP 60 EP 66 DI 10.1002/mc.2940070110 PG 7 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA KN407 UT WOS:A1993KN40700009 PM 7679578 ER PT J AU TENNANT, RW HARRIS, CC KAUFMAN, DG NESNOW, S SLAGA, TJ STEVENSON, DE TRUMP, BF AF TENNANT, RW HARRIS, CC KAUFMAN, DG NESNOW, S SLAGA, TJ STEVENSON, DE TRUMP, BF TI 6TH ASPEN CANCER CONFERENCE - MOLECULAR MECHANISMS OF GENETIC DEREGULATION IN TOXICITY AND CARCINOGENESIS SO MOLECULAR CARCINOGENESIS LA English DT Editorial Material C1 UNIV N CAROLINA,SCH MED,DEPT PATHOL,CHAPEL HILL,NC 27599. SHELL OIL CO,WESTHOLLOW RES CTR,HOUSTON,TX 77210. NCI,DIV CANC ETIOL,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. US EPA,HLTH EFFECTS RES LAB,CARCINOGENESIS & METAB BRANCH,RES TRIANGLE PK,NC 27711. UNIV TEXAS,M D ANDERSON CANC CTR,DIV SCI PK RES,SMITHVILLE,TX 78957. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. RP TENNANT, RW (reprint author), NIEHS,EXPTL CARCINOGENESIS & MUTAGENESIS BRANCH,POB 12233,MD E4-02,RES TRIANGLE PK,NC 27705, USA. NR 0 TC 3 Z9 3 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. PY 1993 VL 7 IS 2 BP 67 EP 72 PG 6 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA KV562 UT WOS:A1993KV56200001 PM 8096139 ER PT J AU NOUSO, K BOHR, VA SCHUT, HAJ SNYDERWINE, EG AF NOUSO, K BOHR, VA SCHUT, HAJ SNYDERWINE, EG TI QUANTITATION OF 2-AMINO-3-METHYLIMIDAZO[4,5-F]QUINOLINE AND 2-AMINO-3,8-DIMETHYLIMIDAZO[4,5-F]QUINOXALINE DNA ADDUCTS IN SPECIFIC SEQUENCES USING ALKALI OR UVRABC EXCINUCLEASE SO MOLECULAR CARCINOGENESIS LA English DT Article DE HETEROCYCLIC AMINE FOOD MUTAGENS; DNA ADDUCTS; SOUTHERN HYBRIDIZATION; P-32-POSTLABELING METHOD; DHFR GENE ID HAMSTER OVARY CELLS; DIHYDROFOLATE-REDUCTASE GENE; DEOXYRIBONUCLEIC-ACID; HETEROCYCLIC AMINES; COOKED FOOD; REPAIR; MUTAGENICITY; DAMAGE; 2-HYDROXYAMINO-3-METHYLIMIDAZOLO<4,5-F>QUINOLINE; IDENTIFICATION AB 2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) are carcinogens found in cooked meats that form DNA adducts upon metabolic activation. Purified DNA from Chinese hamster ovary (CHO) cells was reacted in vitro with the active metabolites N-acetoxy-IQ or N-acetoxy-MeIQx, and the adduct levels in the 5' dihydrofolate reductase (DHFR) gene and downstream region were quantitated by Southern hybridization. Adducted and restricted DNA was treated with Escherichia coli uvrABC excinuclease or alkali (0.1 N NaOH, 37-degrees-C, 60 min) to incise DNA at IQ and MeIQx adduct sites. The DNA was then denatured with formamide, electrophoresed on a neutral agarose gel, transferred to a support membrane, and hybridized with sequence-specific DNA probes. Both uvrABC and alkali reduced the intensity of Southern hybridization in proportion to the number of IQ or MeIQx adducts in DNA, indicating that these adducts are substrates for uvrABC and that they form alkali-labile lesions in DNA. IQ and MeIQx adduct levels were the same in the 5' DHFR gene and in the downstream region. Southern hybridization analysis of pBR322 containing known levels of IQ or MelQx adducts showed that the efficiency of cutting IQ or MeIQx adducts by uvrABC excinuclease and alkali was approximately 30% and 15%, respectively. P-32-postlabeling studies examining adduct level in bulk DNA further showed that the adduct profiles were identical in pBR322, CHO DNA, and cultured CHO cells exposed to the reactive metabolites of IQ or MeIQx. The results indicate that IQ and MelQx adducts can be quantitated in specific genomic sequences and that this method should be directly applicable to studies of gene-specific repair of these adducts in cultured cells. C1 NCI,DIV CANC ETIOL,BLDG 37,ROOM 3C28,BETHESDA,MD 20892. NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. MED COLL OHIO,DEPT PATHOL,TOLEDO,OH 43699. NR 40 TC 7 Z9 7 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. PY 1993 VL 7 IS 2 BP 126 EP 134 DI 10.1002/mc.2940070211 PG 9 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA KV562 UT WOS:A1993KV56200010 PM 8457290 ER PT J AU MELNICK, RL HUFF, J BARRET, JC MARONPOT, RR LUCIER, G PORTIER, CJ AF MELNICK, RL HUFF, J BARRET, JC MARONPOT, RR LUCIER, G PORTIER, CJ TI CELL-PROLIFERATION AND CHEMICAL CARCINOGENESIS - A SYMPOSIUM OVERVIEW SO MOLECULAR CARCINOGENESIS LA English DT Editorial Material RP MELNICK, RL (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 32 TC 18 Z9 18 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. PY 1993 VL 7 IS 3 BP 135 EP 138 DI 10.1002/mc.2940070302 PG 4 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA LC376 UT WOS:A1993LC37600001 PM 8489710 ER PT J AU SATOH, H LAMB, PW DONG, JT EVERITT, J BOREIKO, C OSHIMURA, M BARRETT, JC AF SATOH, H LAMB, PW DONG, JT EVERITT, J BOREIKO, C OSHIMURA, M BARRETT, JC TI SUPPRESSION OF TUMORIGENICITY OF A549 LUNG ADENOCARCINOMA CELLS BY HUMAN CHROMOSOME-3 AND CHROMOSOME-11 INTRODUCED VIA MICROCELL-MEDIATED CHROMOSOME TRANSFER SO MOLECULAR CARCINOGENESIS LA English DT Article DE TUMOR SUPPRESSOR GENES; LUNG CANCER; NON-SMALL-CELL LUNG CANCER ID SHORT ARM; DNA-SEQUENCE; WILMS-TUMOR; REGION 3P21; CARCINOMA; CANCER; GENES; LINES AB To map tumor suppressor genes for lung adenocarcinomas, we introduced normal human chromosomes 3, 7, and 11 into the A549 tumor cell line by microcell-mediated chromosome transfer to test which chromosomes had the ability to suppress tumorigenicity. These human chromosomes, which contain the neomycin gene as a selectable marker, were transferred into A549 lung adenocarcinoma cells at frequencies of 0.3-1.8 x 10(-6). Two microcell hybrid clones with an introduced chromosome 3, two with an introduced chromosome 7, and six with an introduced chromosome 11 were isolated and examined for their growth properties and tumorigenicity in nude mice. Whereas parental A549 cells formed tumors with an average latency of 68 d, both microcell hybrids with an introduced chromosome 3 failed to form tumors for over 360 d. Similar tumorigenicity results were obtained when the clones were implanted into denuded tracheas, a more orthotopic transplantation site. The two clones with an introduced chromosome 7 were still tumorigenic; they formed tumors within 100-123 d after injection and grew progressively, although the tumors grew slightly slower than the parental cells did. Among the six clones with an introduced chromosome 11, one clone was still highly tumorigenic but did not contain an extra copy of an intact introduced chromosome 11. Three clones with a single intact copy of introduced chromosome 11 formed tumors with latency periods significantly longer than those of the parental cells. Two clones had two copies of the introduced chromosome 11, and both failed to form tumors within 1 yr of injection. These results indicate that chromosomes 3 and 11 can suppress the tumorigenicity of A549 lung adenocarcinoma cells. C1 NIEHS,MOLEC CARCINOGENESIS LAB,POB 12233,RES TRIANGLE PK,NC 27709. TOTTORI UNIV,SCH LIFE SCI,DEPT MOLEC & CELL GENET,TOTTORI 680,JAPAN. CHEM IND INST TOXICOL,RES TRIANGLE PK,NC 27709. NR 27 TC 56 Z9 57 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1993 VL 7 IS 3 BP 157 EP 164 DI 10.1002/mc.2940070306 PG 8 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA LC376 UT WOS:A1993LC37600005 PM 8098218 ER PT J AU AFSHARI, CA BARRETT, JC AF AFSHARI, CA BARRETT, JC TI NEGATIVE REGULATION OF MITOGEN-STIMULATED, ANCHORAGE-INDEPENDENT CELL-GROWTH BY A TUMOR-SUPPRESSOR GENE-FUNCTION SO MOLECULAR CARCINOGENESIS LA English DT Article DE GROWTH REGULATION; PLATELET-DERIVED GROWTH FACTOR; EPIDERMAL GROWTH FACTOR; TUMOR SUPPRESSION; SIGNAL TRANSDUCTION ID KINASE-C ACTIVATION; PROTEIN-KINASE; RB GENE; FACTOR-ALPHA; RETINOBLASTOMA; EXPRESSION; PRODUCT; CYCLE; PHOSPHORYLATION; FIBROBLASTS AB Immortal, nontumorigenic cell lines of Syrian hamster embryo (SHE) cells with different tumor-suppressing activity were isolated. Subclones from the parental cells were isolated that either had retained (supB+) or lost (supB-) the ability to suppress tumorigenicity after hybridization with tumor cells. The growth properties of these cells were studied to determine how this tumor-suppressor gene function influences cell growth. When the cells were grown on plastic, their growth properties were similar, and neither cell type grew in soft agar containing 10% serum, which supported the growth of tumorigenic cells. However, in agar supplemented with growth factors and 10% serum, supB- cells formed colonies whereas supB+ cells did not. Efficient growth (colony-forming efficiencies greater than 20%) of supB- cells was obtained in agar supplemented with serum and a combination of epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and insulin (EPI) or with serum and basic fibroblast growth factor (bFGF). The effect of EPI and bFGF together was additive. supB+ cells failed to grow under any of these conditions, suggesting that the suppressor gene function blocked the growth response of the cells to multiple growth factors when the cells were suspended in agar. In SupB- cells, transforming growth factor-beta1 and retinoic acid inhibited anchorage-independent growth response to EPI but not the growth response to bFGF. These observations are consistent with the hypothesis that bFGF stimulates the growth of supB- cells by a signal transduction pathway that differs from the pathway stimulated by EGF or PDGF. Thus, this suppressor gene function may regulate anchorage-independent growth at some common point in signal transduction for multiple mitogens. (C) 1993 Wiley-Liss, Inc.* C1 NIEHS,MOLEC CARCINOGENESIS LAB,MD C2-15,POB 12233,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,CHAPEL HILL,NC 27514. NR 48 TC 6 Z9 6 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. PY 1993 VL 7 IS 4 BP 249 EP 256 DI 10.1002/mc.2940070407 PG 8 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA LK596 UT WOS:A1993LK59600006 PM 8394717 ER PT J AU KOSUGI, S BAN, T KOHN, LD AF KOSUGI, S BAN, T KOHN, LD TI IDENTIFICATION OF THYROID-STIMULATING ANTIBODY-SPECIFIC INTERACTION SITES IN THE N-TERMINAL REGION OF THE THYROTROPIN RECEPTOR SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID IDIOPATHIC MYXEDEMA PATIENTS; GRAVES-DISEASE; TSH RECEPTOR; LIGAND-BINDING; BETA-2-ADRENERGIC RECEPTOR; GONADOTROPIN RECEPTORS; FUNCTIONAL EXPRESSION; BLOCKING ANTIBODIES; MOLECULAR-CLONING; AUTOANTIBODIES AB Using mutants of the N-terminal region (residues 30-76) of the rat TSH receptor (TSHR), which substitute corresponding segments of rat gonadotropin receptors or hydrophilic (serine) and hydrophobic (alanine) amino acids as appropriate, we show that residues 30-33, 34-37, 42-45, 52-56, and 58-61, in addition to threonine-40, are determinants for the interaction of thyroid-stimulating autoantibodies (stimulating TSHRAbs) with the TSHR. The most important, residues 34-37,42-45, and 52-56, whose mutants lose stimulating TSHRAb activity with at least 11 of 12 (>90%) of the Graves' immunoglobulins G tested, are, like threonine-40, in regions of the TSHR that are nonhomologous with gonadotropin receptors. These data establish at least in part, therefore, the basis for the thyroid-specific effects of stimulating TSHRAbs. In no case do the same mutants lose their reactivity with TSH or blocking-type TSHR autoantibodies (blocking TSHRAbs) from hypothyroid patients with idiopathic myxedema. Since the latter have been shown to interact with high affinity TSH-binding sites on the C-terminal portion of the external domain of the TSHR, stimulating TSHRAbs and blocking TSHRAbs react with different receptor determinants, which can be presumed to have different roles in receptor function. This can explain the hyper- or hypothyroidism of different thyroid autoimmune diseases with receptor antibodies. Residues 30-33, 42-45, and threonine-40 appear to be related to the agonist action of TSH, since in each case mutation results in low affinity TSH binding, but normal TSH-increased cAMP activity, similar, for example, to a beta-adrenergic agonist. Using a receptor antibody to identify different receptor forms in the membrane, we can also identify determinants in this N-terminal region (residues 30-76) whose mutation results in a loss of all activities without apparently altering receptor synthesis, processing, or integration within the bilayer. These are residues 38 and 39, cysteine-41, residues 46-51, leucine-57, threonine-62, and, within residues 66-76, serine-69, alanine-71, phenylalanine-72, serine-74, leucine-75, and proline-76. We suggest that these residues are at the very least important in the conformational array of receptor determinants necessary for interactions with TSH and stimulating TSHRAbs. C1 NIDDKD, BIOCHEM & METAB LAB,CELL REGULAT SECT,BLDG 10, ROOM 9B-L3, BETHESDA, MD 20892 USA. NR 46 TC 84 Z9 85 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 JAN PY 1993 VL 7 IS 1 BP 114 EP 130 DI 10.1210/me.7.1.114 PG 17 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KK295 UT WOS:A1993KK29500013 PM 8095322 ER PT S AU GOLDMAN, D OBRIEN, SJ AF GOLDMAN, D OBRIEN, SJ BE Zimmer, EA White, TJ Cann, RL Wilson, AC TI 2-DIMENSIONAL PROTEIN ELECTROPHORESIS IN PHYLOGENETIC STUDIES SO MOLECULAR EVOLUTION: PRODUCING THE BIOCHEMICAL DATA SE Methods in Enzymology LA English DT Review ID 2-DIMENSIONAL GEL-ELECTROPHORESIS; GENETIC-DISTANCE; RESOLUTION C1 NCI, VIRAL CARCINOGENESIS LAB, FREDERICK, MD 21701 USA. RP GOLDMAN, D (reprint author), NIAAA, NEUROGENET LAB, BETHESDA, MD 20892 USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 18 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-182125-0 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1993 VL 224 BP 113 EP 121 DI 10.1016/0076-6879(93)24009-J PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ58X UT WOS:A1993BZ58X00008 PM 8264382 ER PT J AU KAMMORGAN, LNW LAVOIE, TB SMITHGILL, SJ KIRSCH, JF AF KAMMORGAN, LNW LAVOIE, TB SMITHGILL, SJ KIRSCH, JF TI SITE-DIRECTED MUTAGENESIS IN ANALYSIS OF PROTEIN-PROTEIN INTERACTIONS SO MOLECULAR EVOLUTION: PRODUCING THE BIOCHEMICAL DATA SE METHODS IN ENZYMOLOGY LA English DT Review ID AMINO-ACID SEQUENCE; EGG-WHITE LYSOZYME; ANTIBODY-ANTIGEN COMPLEX; 3-DIMENSIONAL STRUCTURE; ENZYME C1 BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,PRINCETON,NJ 08544. NCI,GENET LAB,BETHESDA,MD 20892. RP KAMMORGAN, LNW (reprint author), UNIV CALIF BERKELEY,DIV BIOCHEM & MOLEC BIOL,BERKELEY,CA 94720, USA. FU NIAID NIH HHS [AIO7989]; NIGMS NIH HHS [GM35393] NR 38 TC 5 Z9 5 U1 0 U2 4 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1993 VL 224 BP 503 EP 516 DI 10.1016/0076-6879(93)24037-U PG 14 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ58X UT WOS:A1993BZ58X00036 PM 8264405 ER PT S AU WISTOW, G AF WISTOW, G BE Zimmer, EA White, TJ Cann, RL Wilson, AC TI IDENTIFICATION OF LENS CRYSTALLINS - A MODEL SYSTEM FOR GENE RECRUITMENT SO MOLECULAR EVOLUTION: PRODUCING THE BIOCHEMICAL DATA SE Methods in Enzymology LA English DT Review ID ARGININOSUCCINATE LYASE GENE; ALPHA-ENOLASE; STRUCTURAL PROTEINS; ENZYME-CRYSTALLINS; SEQUENCE-ANALYSIS; TAU-CRYSTALLIN; AVIAN LENSES; DUCK LENS; EVOLUTION; SUPERFAMILY RP WISTOW, G (reprint author), NEI, MOLEC STRUCT & FUNCT SECT, BETHESDA, MD 20892 USA. NR 48 TC 10 Z9 10 U1 2 U2 4 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-182125-0 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1993 VL 224 BP 563 EP 575 DI 10.1016/0076-6879(93)24042-S PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ58X UT WOS:A1993BZ58X00041 PM 8264411 ER PT J AU CONRAD, DH KOZAK, CA VERNACHIO, J SQUIRE, CM RAO, M EICHER, EM AF CONRAD, DH KOZAK, CA VERNACHIO, J SQUIRE, CM RAO, M EICHER, EM TI CHROMOSOMAL LOCATION AND ISOFORM ANALYSIS OF MOUSE FC-EPSILON-RII/CD23 SO MOLECULAR IMMUNOLOGY LA English DT Article ID LOW-AFFINITY RECEPTOR; FC-EPSILON RECEPTOR; CHRONIC LYMPHOCYTIC-LEUKEMIA; DNA POLYMERASE-BETA; IGE-BINDING FACTORS; SOLUBLE CD23; B-CELLS; MESSENGER-RNA; LINKAGE MAP; EXPRESSION AB The gene for the mouse low affinity receptor for IgE (Fc(epsilon)RII, also known as CD23) was mapped on Chromosome (Chr) 8 proximal to Plat. This gene, symbolized Fcer2 (formerly Fce2) resides in a region of Chr 8 with linkage homology with human chromosomes 8 and 19. The mouse Fc(epsilon)RII was examined for the presence of alternate N-terminal forms such as seen in humans. An antisense RNA probe was prepared from the 5' end of the cDNA through the first 660 bp of the cDNA and was used to analyze message from Fc(epsilon)RII+ B cells and B cell hybridomas both before and after treatment with interleukin 4 (IL-4). Using RNase protection analysis, a major 640 bp band corresponding to the full length probe was seen, even after activation of the cells with LPS in the presence of IL-4, which is known to give high expression levels of the Fc(epsilon)RII. This result suggests that the mouse does not produce significant levels of an alternate IL-4 inducible Fc(epsilon)RII, as seen in man, and this may explain the more restricted cell lineage expression of the Fc(epsilon)RII in the mouse. C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. JACKSON LAB,BAR HARBOR,ME 04609. JOHNS HOPKINS UNIV,DEPT MOLEC BIOL,BALTIMORE,MD 21239. RP CONRAD, DH (reprint author), VIRGINIA COMMONWEALTH UNIV,DEPT MICROBIOL & IMMUNOL,BOX 678,MCV STN,RICHMOND,VA 23298, USA. FU NIAID NIH HHS [R01 AI018697, AI18697]; NIGMS NIH HHS [GM20919] NR 53 TC 25 Z9 26 U1 0 U2 0 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 JAN PY 1993 VL 30 IS 1 BP 27 EP 33 DI 10.1016/0161-5890(93)90423-9 PG 7 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA KA986 UT WOS:A1993KA98600004 PM 8417372 ER PT J AU HARINDRANATH, N DONADEL, G SIGOUNAS, G NOTKINS, AL AF HARINDRANATH, N DONADEL, G SIGOUNAS, G NOTKINS, AL TI COMPARISON OF COMPLETE NUCLEOTIDE-SEQUENCE OF THE HUMAN-IGM HEAVY-CHAIN CONSTANT REGION OF POLYREACTIVE AND MONOREACTIVE ANTIBODIES SO MOLECULAR IMMUNOLOGY LA English DT Note ID CD5+ B-CELLS; RHEUMATOID-ARTHRITIS; HIGH-AFFINITY; GENES; VH RP HARINDRANATH, N (reprint author), NIDR,ORAL MED LAB,BLDG 30,RM 121,BETHESDA,MD 20892, USA. NR 11 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 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD JAN PY 1993 VL 30 IS 1 BP 111 EP 112 PG 2 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA KA986 UT WOS:A1993KA98600015 PM 8417370 ER PT J AU SAKAI, N KAUFMAN, S MILSTIEN, S AF SAKAI, N KAUFMAN, S MILSTIEN, S TI TETRAHYDROBIOPTERIN IS REQUIRED FOR CYTOKINE-INDUCED NITRIC-OXIDE PRODUCTION IN A MURINE MACROPHAGE CELL-LINE (RAW-264) SO MOLECULAR PHARMACOLOGY LA English DT Note ID GUANOSINE TRIPHOSPHATE CYCLOHYDROLASE; TUMOR-NECROSIS-FACTOR; L-ARGININE; INTERFERON-GAMMA; NITROGEN-OXIDES; RAT-BRAIN; SYNTHASE; NITRATE; BIOSYNTHESIS; INDUCTION AB The murine macrophage cell line RAW 264 constitutively synthesizes tetrahydrobiopterin (BH4), the cofactor required for the hydroxylation of the aromatic amino acids and for the production of nitric oxide. Stimulation of the cells with interferon-gamma and lipopolysaccharide induced the production of nitric oxide and increased BH4 levels further. When the cells were stimulated in the presence of 2,4-diamino-6-hydroxypyrimidine (DAHP), an inhibitor of BH4 biosynthesis, biopterin levels decreased by 90% within 6 hr, whereas nitrite production was essentially unaffected. Pretreatment of the cells for 12 hr with DAHP decreased intracellular BH4 concentrations by >95% yet inhibited the cytokine-stimulated production of nitric oxide by only 50%. However, pretreatment with DAHP plus N-acetylserotonin, an inhibitor of sepiapterin reductase, the terminal enzyme of the BH4 biosynthetic pathway, decreased biopterin levels by >99% and inhibited nitric oxide synthesis by 90%. This inhibition could be reversed by loading the cells with dihydrobiopterin, a precursor of BH4 via the dihydrofolate reductase salvage pathway. In addition, these studies revealed that N-acetylserotonin has a direct inhibitory effect on nitric oxide synthesis, acting in a BH4-independent manner. The results presented here support previous suggestions, based on experiments with isolated enzymes, that BH4 is absolutely required for cytokine-stimulated nitric oxide production in macrophages and they suggest that only a small fraction of the total intracellular BH4 pool in macrophages is utilized in the production of fully active nitric oxide synthase. C1 NIMH,NEUROCHEM LAB,BLDG 36,ROOM 3D-30,BETHESDA,MD 20892. NR 33 TC 87 Z9 87 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 JAN PY 1993 VL 43 IS 1 BP 6 EP 10 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KH565 UT WOS:A1993KH56500002 PM 7678692 ER PT J AU BEBENEK, K THOMAS, DC ROBERTS, JD ECKSTEIN, F KUNKEL, TA AF BEBENEK, K THOMAS, DC ROBERTS, JD ECKSTEIN, F KUNKEL, TA TI EFFECTS OF 3'-AZIDO-3'-DEOXYTHYMIDINE METABOLITES ON SIMIAN VIRUS-40 ORIGIN-DEPENDENT REPLICATION AND HETERODUPLEX REPAIR IN HELA-CELL EXTRACTS SO MOLECULAR PHARMACOLOGY LA English DT Article ID BONE-MARROW-CELLS; DNA-REPLICATION; REVERSE-TRANSCRIPTASE; INVITRO REPLICATION; MUTATIONAL SPECIFICITY; MISMATCH CORRECTION; POLYMERASE-GAMMA; ESCHERICHIA-COLI; INHIBITION; MECHANISM AB Although the capacity of 3'-azido-3'-deoxythymidine (AZT) triphosphate, an active metabolite of the antiviral agent zidovudine (AZT), to inhibit polymerization by a variety of purified DNA polymerases has been described, it is important to understand its effect on replication by the more complex protein assemblies responsible for DNA replication in human cells. In the present study, we have determined the effects of AZT metabolites on the efficiency of simian virus 40 origin-dependent bidirectional replication of double-stranded DNA in extracts of human HeLa cells. Replication was inhibited by AZT diphosphate and AZT triphosphate, but only at concentrations exceeding those thought to be present in vivo. However, replication was inhibited by AZT monophosphate at concentrations previously reported to accumulate in human cells cultured in the presence of AZT, suggesting that AZT monophosphate may contribute to cytotoxicity by inhibiting chromosomal replication. In an attempt to determine whether AZT treatment could have longer term mutagenic effects on cells, we also determined the effects of these AZT derivatives on replication fidelity and on the efficiency of repair of DNA substrates containing single-base mismatches. Despite the ability of a normal deoxynucleoside monophosphate to reduce the fidelity of DNA replication, presumably by reducing exonucleolytic proofreading of errors, neither the mono-, di-, nor triphosphate form of AZT reduced base substitution fidelity when present in replication reactions. Similarly, the efficiency of repair of DNA substrates containing single-base mismatches was unaffected by these compounds. However, replication fidelity was affected by perturbations in relative and absolute concentrations of deoxynucleoside triphosphate substrates similar to those reported to occur in AZT-treated cells. Thus, AZT treatment could potentially be mutagenic in vivo via reduced replication fidelity resulting from alterations in deoxynucleoside triphosphate pools. C1 NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709. MAX PLANCK INST EXPTL MED,CHEM ABT,W-3400 GOTTINGEN,GERMANY. NR 45 TC 11 Z9 11 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JAN PY 1993 VL 43 IS 1 BP 57 EP 63 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KH565 UT WOS:A1993KH56500010 PM 8380884 ER PT J AU MCCRAE, RR AF MCCRAE, RR TI AGREEMENT OF PERSONALITY PROFILES ACROSS OBSERVERS SO MULTIVARIATE BEHAVIORAL RESEARCH LA English DT Article ID 5-FACTOR MODEL; SPOUSE RATINGS; SELF-REPORTS; INVENTORY AB To assess cross-observer agreement on personality profiles, an Index of Profile Agreement and an associated coefficient, r(pa),are proposed which take into account both the difference between the ratings and the extremeness of their mean. Using data from the Revised NEO Personality Inventory (NEO-PI-R), this coefficient is shown to be superior to Cattell's (1949) r(p) in identifying matched versus mismatched pairs of peer ratings/self-reports (N = 250) and spouse ratings/self-reports (N = 68). Suggestions are made for the interpretation and use of the two measures of profile agreement for group comparisons and for the interpretation of individual cases. Limitations of the coefficients are also discussed. RP MCCRAE, RR (reprint author), NIA,GERONTOL RES CTR,PERSONAL STRESS & COPING SECT,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 24 TC 37 Z9 37 U1 1 U2 7 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0027-3171 J9 MULTIVAR BEHAV RES JI Multivariate Behav. Res. PY 1993 VL 28 IS 1 BP 25 EP 40 DI 10.1207/s15327906mbr2801_2 PG 16 WC Mathematics, Interdisciplinary Applications; Social Sciences, Mathematical Methods; Psychology, Experimental; Statistics & Probability SC Mathematics; Mathematical Methods In Social Sciences; Psychology GA LL870 UT WOS:A1993LL87000002 PM 26824993 ER PT B AU HADLEY, EC AF HADLEY, EC BE Buckwalter, JA Goldberg, VM Woo, SLY TI MORBID CONSEQUENCES OF AGING PROCESSES - METHODOLOGIC ISSUES SO MUSCULOSKELETAL SOFT-TISSUE AGING: IMPACT ON MOBILITY LA English DT Proceedings Paper CT Workshop on Age-Related Changes in the Musculoskeletal Soft Tissues CY NOV 14-17, 1992 CL COLORADO SPRINGS, CO SP AMER ACAD ORTHOPAED SURGEONS, NIAMSD, NIA C1 NIA,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ACAD ORTHOPAEDIC SURGEONS PI ROSEMONT PA 6300 NORTH RIVER RD, ROSEMONT, IL 60018 BN 0-89203-086-0 PY 1993 BP 35 EP 47 PG 13 WC Endocrinology & Metabolism; Geriatrics & Gerontology SC Endocrinology & Metabolism; Geriatrics & Gerontology GA BA08K UT WOS:A1993BA08K00004 ER PT J AU JIAO, JL GLICKMAN, BW ANDERSON, MW ZIELINSKA, M AF JIAO, JL GLICKMAN, BW ANDERSON, MW ZIELINSKA, M TI MUTATIONAL SPECIFICITY OF N-NITROSODIMETHYLAMINE - COMPARISON BETWEEN INVIVO AND INVITRO ASSAYS SO MUTATION RESEARCH LA English DT Article DE HOST-MEDIATED ASSAY; SPECIFICITY, MUTATIONAL; NDMA; S9; N-NITROSODIMETHYLAMINE ID ESCHERICHIA-COLI; LACI GENE; FORMALDEHYDE; MUTAGENESIS; REPRESSOR; NITROSAMINES; REPAIR; CELLS AB We have determined the DNA alterations recovered after treatment with Aroclor 1254-treated rat S9-activated N-nitrosodimethylamine (NDMA) in the N-terminal region of the lacI gene of E. coli. A total of 125 independent LaCI(-d) mutants of E. coli were characterized by DNA sequencing. Consistent with the known methylating ability of this compound, the predominant mutation was the G : C --> A : T transition, which accounted for 90% of all the mutations recovered. Non G : C --> A : T events include 2 G : C --> T : A, 2 G : C --> C : G, 2 A : T --> G : C, 3 A : T --> T : A and 3 frameshifts. Contingency analysis reveals that NDMA-induced mutations recovered after in vitro activation (S9) have a spectrum very similar to that previously obtained after in vivo activation employing a mouse host-mediated assay. In both systems, G : C --> A: T events clearly dominate and their distribution reveals similar site-specificity. Moreover, the proportion and kind of non-G : C --> A : T events are also similar. C1 YORK UNIV,DEPT BIOL,N YORK M3J 1P3,ONTARIO,CANADA. NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709. NR 25 TC 12 Z9 12 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 JAN PY 1993 VL 301 IS 1 BP 27 EP 31 DI 10.1016/0165-7992(93)90052-W PG 5 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA KF086 UT WOS:A1993KF08600005 PM 7677940 ER PT J AU MARAGOS, CM ANDREWS, AW KEEFER, LK ELESPURU, RK AF MARAGOS, CM ANDREWS, AW KEEFER, LK ELESPURU, RK TI MUTAGENICITY OF GLYCERYL TRINITRATE (NITROGLYCERIN) IN SALMONELLA-TYPHIMURIUM SO MUTATION RESEARCH LA English DT Article DE GLYCERYL TRINITRATE; NITROGLYCERIN; NITRIC OXIDE; SEQUENCE ANALYSIS; SALMONELLA-TYPHIMURIUM ID NITRIC-OXIDE; TARGET SEQUENCES; RATS; DNA; NITROARENES; INDUCTION; MUTATIONS; NITRATE; STRAINS; AGENTS AB The recent finding that the clinical nitrovasodilator, glyceryl trinitrate (GTN), is mutagenic in Salmonella typhimurium strain TA1535 has been examined in closer detail, with emphasis on its mechanism of action. GTN increased the number of His+ revertants to a maximum of 4 times over background at a GTN dose of 5 mumol/plate. Hamster liver S9 depressed the toxicity of high GTN doses and increased the maximum number of revertants to 5 times over background at 10 mumol/plate. GTN did not cause significant reversion in any of the six other S. typhimurium strains tested (TA1975, TA102, TA1538, TA100, TA100NR, YG1026), although signs of toxicity were observed. Therefore, the mutagenicity of GTN was manifest only in the repair-deficient (uvrB and lacking in pKM101) strain which is responsive to single base changes. Oligonucleotide probe hybridization of TA1535 revertants showed that virtually all of the GTN-induced mutants contained C --> T transitions in either the first or second base of the hisG46 (CCC) target codon, with a preference for the latter. A similar mutational spectrum was seen previously with a complex of spermine and nitric oxide (NO) which releases nitric oxide. This suggests that NO, which can be derived from GTN via metabolic reduction, may be responsible for GTN's mutagenic action. The known NO scavenger oxymyoglobin did not substantially alter the dose response of GTN, indicating that extracellular NO was not mediating reversion. The data are consistent with the hypothesis that intracellular nitric oxide is responsible for the observed mutations. C1 NCI,FREDERICK CANC RES & DEV CTR,CHEM SECT,COMPARAT CARCINOGENESIS LAB,BLDG 538,ROOM 205E,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PRI DYN CORP,FREDERICK,MD 21702. US FDA,ROCKVILLE,MD 20857. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 FU NCI NIH HHS [N01-CO-74102] NR 23 TC 26 Z9 28 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD JAN PY 1993 VL 298 IS 3 BP 187 EP 195 DI 10.1016/0165-1218(93)90040-K PG 9 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA KG888 UT WOS:A1993KG88800006 PM 7678153 ER PT J AU DABHOLKAR, M BOSTICKBRUTON, F WEBER, C EGWUAGU, C BOHR, VA REED, E AF DABHOLKAR, M BOSTICKBRUTON, F WEBER, C EGWUAGU, C BOHR, VA REED, E TI EXPRESSION OF EXCISION REPAIR GENES IN NONMALIGNANT BONE-MARROW FROM CANCER-PATIENTS SO MUTATION RESEARCH LA English DT Article DE EXCISION REPAIR GENES; BONE MARROW, NONMALIGNANT; CANCER PATIENTS; DNA-REPAIR GENES; ERCC GENES ID DNA-REPAIR; MOLECULAR-CLONING; BIOLOGICAL CHARACTERIZATION; CDNA CLONING; ERCC-1; TRANSFECTION; HOMOLOGY; CORRECTS; DEFECT AB The patterns of expression of 3 human DNA-repair genes (ERCC1, ERCC2, ERCC6) were assessed in 52 bone-marrow specimens obtained from cancer patients prepared for autologous bone-marrow transplantation. Marrow was collected prior to the initiation of treatment in patients with sarcoma or testicular cancer; marrow was collected after initial cytoreductive therapy for patients with non-Hodgkin's lymphoma, Hodgkin's disease, and other tumors. Slot-blot analysis of marrow RNA showed a bimodal pattern of ERCC1, ERCC2 and ERCC6 gene expression with relative expression values ranging more than 200-fold. This pattern was seen in all patient groups and appeared to be independent of whether or not patients had received prior chemotherapy. In all patient groups, when expression was low for ERCC1, expression was also low for ERCC2 and ERCC6, suggesting that expression of these genes may be coordinated within an individual although they are located on two different chromosomes. Southern blot analyses of Pst I digests of DNA from 6 bone-marrow samples indicate no differences in ERCC1 gene copy number between high expressors and low expressors. There is absence of restriction fragment length polymorphism for ERCC1 suggesting that the different levels of expression in high and low expressors were not due to major deletions or rearrangements of the ERCC1 gene. We conclude that expression of these ERCC genes may vary widely between individuals, and that within an individual, their expression may be linked and coordinated by a common regulatory mechanism. C1 NCI,9000 ROCKVILLE PIKE,BLDG 10,RM 12N226,BETHESDA,MD 20892. LAWRENCE LIVERMORE NATL LAB,DIV BIOMED SCI,LIVERMORE,CA 94550. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NR 27 TC 38 Z9 39 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 JAN PY 1993 VL 293 IS 2 BP 151 EP 160 DI 10.1016/0921-8777(93)90066-P PG 10 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA KH370 UT WOS:A1993KH37000006 PM 7678143 ER PT J AU JANZ, S SHACTER, E AF JANZ, S SHACTER, E TI ACTIVATED MURINE NEUTROPHILS INDUCE UNSCHEDULED DNA-SYNTHESIS IN LYMPHOCYTES-B SO MUTATION RESEARCH LA English DT Article DE NEUTROPHILS; OXIDANTS; DNA DAMAGE; DNA REPAIR; UNSCHEDULED DNA SYNTHESIS; LYMPHOCYTES-B ID SISTER-CHROMATID EXCHANGES; HYDROGEN-PEROXIDE; TUMOR PROMOTER; OXIDATIVE STRESS; POLYMORPHONUCLEAR LEUKOCYTES; SUPEROXIDE ANION; SOS CHROMOTEST; REPAIR ENZYMES; BASE DAMAGE; CELLS AB Activated neutrophils induce DNA damage in neighboring cells by secreting reactive oxygen, compounds into the extracellular milieu. Repair of this damage is required to prevent mutagenesis and neoplastic transformation. Conditions were established to detect the activation of excision-repair pathways (unscheduled DNA synthesis) by measuring stimulated thymidine uptake in target B lymphocytes exposed to activated neutrophils. Murine neutrophils were cocultured in serum-free medium with splenic B cells or with murine plasmacytoma cells for 2 h. Unscheduled DNA synthesis in the B cells was detected at neutrophil:target cell ratios of 1:1 to 4:1 when the neutrophils were activated with phorbol myristate acetate. Reagent H2O2 alone (greater-than-or-equal-to 6 muM) also induced UDS whereas HOCl (up to 4 mM) did not. No repair synthesis was observed within the neutrophils themselves. Control experiments indicated that the induction of UDS by neutrophils and H2O2 was not due to formation of a stable genotoxic compound from HU. On the contrary, scavenging of free H2O2 by HU probably lowered the levels of UDS that could be detected by these agents. Induction of unscheduled DNA synthesis by neutrophils and H2O2 occurred under conditions of less cytostasis than was found with other DNA-damaging agents such as 4-nitroquinoline 1-oxide or gamma-irradiation. This may reflect a heightened responsiveness of the cells to repair of damage from physiological oxidants. The results demonstrate that DNA damage induced by reactive oxygen intermediates can be repaired by nucleotide excision-repair pathways. C1 NCI, GENET LAB, BLDG 37, RM 2B03, BETHESDA, MD 20892 USA. NR 63 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES JI Mutat. Res. PD JAN PY 1993 VL 293 IS 2 BP 173 EP 186 DI 10.1016/0921-8777(93)90068-R PG 14 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA KH370 UT WOS:A1993KH37000008 PM 7678145 ER PT J AU HAMER, DH AF HAMER, DH TI KINKY HAIR DISEASE SHEDS LIGHT ON COPPER-METABOLISM SO NATURE GENETICS LA English DT Editorial Material RP HAMER, DH (reprint author), NCI,BETHESDA,MD 20892, USA. NR 6 TC 8 Z9 8 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 JAN PY 1993 VL 3 IS 1 BP 3 EP 4 DI 10.1038/ng0193-3 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA KF372 UT WOS:A1993KF37200002 PM 8490649 ER PT J AU SZALLASI, A BLUMBERG, PM AF SZALLASI, A BLUMBERG, PM TI [H-3] RESINIFERATOXIN BINDING BY THE VANILLOID RECEPTOR - SPECIES-RELATED DIFFERENCES, EFFECTS OF TEMPERATURE AND SULFHYDRYL-REAGENTS SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY LA English DT Article DE [H-3]RESINIFERATOXIN BINDING; VANILLOID RECEPTOR; POSITIVE COOPERATIVITY; SPECIES-RELATED DIFFERENCES ID P-LIKE IMMUNOREACTIVITY; ROOT GANGLION NEURONS; GENE-RELATED PEPTIDE; SUBSTANCE-P; TOPICAL CAPSAICIN; EFFERENT FUNCTION; SENSORY NEURONS; INDUCED RELEASE; GUINEA-PIG; RESINIFERATOXIN AB Specific binding of [H-3]resiniferatoxin (RTX) is thought to represent the vanilloid (capsaicin) receptor. In the present study, we have used this binding assay to elucidate the contribution of differential receptor expression to the capsaicin-resistance of hamsters and rabbits; binding parameters were compared to those of species (rats, mice) regarded as capsaicin-sensitive. Whereas the 5-fold lower affinity for [H-3]RTX binding in the hamster (100 pM) as compared to the rat (20 pM) is unlikely to account for the 100-fold difference in the in vivo responses of RTX-induced inflammation and hypothermia, the lack of detectable specific [H-3]RTX binding sites in the rabbit might represent the predominant mechanism of capsaicin-resistance in this species. Regulation of the vanilloid receptor was further characterized in the rat. In accord with the temperature dependence of both in vivo and in vitro capsaicin actions, we found a marked temperature dependence for association rates. Dissociation turned out to have complex kinetics dependent on time and receptor occupancy. Low pH (5.5 - 7.0) did not affect receptor binding. Preincubation with heavy metal cations and other sulfhydryl-reactive agents inhibited specific [H-3]RTX binding indicating that the vanilloid receptor is a thiol-protein, and that free sulfhydryl groups play an essential role in agonist binding activity. Preliminary characterization suggested noncompetitive inhibition. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NR 51 TC 64 Z9 64 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0028-1298 J9 N-S ARCH PHARMACOL JI Naunyn-Schmiedebergs Arch. Pharmacol. PD JAN PY 1993 VL 347 IS 1 BP 84 EP 91 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KH726 UT WOS:A1993KH72600014 PM 8446186 ER PT S AU YOUNG, NS BROWN, KE AF YOUNG, NS BROWN, KE BE Guigon, M Lemoine, FM Dainiak, N Schechter, A Najman, A TI THE B19 PARVOVIRUS RECEPTOR - IMPLICATIONS FOR DISEASE PATHOGENESIS SO NEGATIVE REGULATION OF HEMATOPOIESIS: FROM FUNDAMENTAL ASPECTS TO CLINICAL APPLICATIONS SE COLLOQUE INSERM LA English DT Proceedings Paper CT 3rd International Conference on Negative Regulation of Hematopoiesis CY APR 18-22, 1993 CL PARIS, FRANCE SP UNIV PIERRE & MARIE CURIE, FAC MED ST ANTOINE, DEPT HEMATOL, INSERM, NIH, ASSISTANCE PUBLIQUE HOPITAUX PARIS C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS INSERM PI PARIS PA 101 RUE DE TOLBIAC, 75645 PARIS, FRANCE SN 0768-3154 BN 2-7420-0015-1 J9 COLLOQ INSE PY 1993 VL 229 BP 375 EP 380 PG 6 WC Hematology SC Hematology GA BZ85R UT WOS:A1993BZ85R00070 ER PT S AU SCHWARTZ, GN KESSLER, SW FRANCIS, ML HOOVER, DL ROTHWELL, SW BURRELL, LM MELTZER, MS AF SCHWARTZ, GN KESSLER, SW FRANCIS, ML HOOVER, DL ROTHWELL, SW BURRELL, LM MELTZER, MS BE Guigon, M Lemoine, FM Dainiak, N Schechter, A Najman, A TI NEGATIVE REGULATORS MAY MEDIATE HEMATOPOIETIC SUPPRESSION IN HIV-INFECTED BONE-MARROW LONG-TERM CULTURES SO NEGATIVE REGULATION OF HEMATOPOIESIS: FROM FUNDAMENTAL ASPECTS TO CLINICAL APPLICATIONS SE COLLOQUE INSERM LA English DT Proceedings Paper CT 3rd International Conference on Negative Regulation of Hematopoiesis CY APR 18-22, 1993 CL PARIS, FRANCE SP UNIV PIERRE & MARIE CURIE, FAC MED ST ANTOINE, DEPT HEMATOL, INSERM, NIH, ASSISTANCE PUBLIQUE HOPITAUX PARIS C1 NCI,TRANSPLANTAT THERAPY SECT,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU EDITIONS INSERM PI PARIS PA 101 RUE DE TOLBIAC, 75645 PARIS, FRANCE SN 0768-3154 BN 2-7420-0015-1 J9 COLLOQ INSE PY 1993 VL 229 BP 403 EP 405 PG 3 WC Hematology SC Hematology GA BZ85R UT WOS:A1993BZ85R00076 ER PT B AU CUMMINGS, NB EGGERS, PW AF CUMMINGS, NB EGGERS, PW BE Oreopoulos, DG Michelis, MF Herschorn, S TI DECISION TO FORGO ESRD TREATMENT SO NEPHROLOGY AND UROLOGY IN THE AGED PATIENT SE DEVELOPMENTS IN NEPHROLOGY LA English DT Proceedings Paper CT 3rd International Conference on Geriatric Nephrology and Urology CY APR 03-05, 1992 CL TORONTO, CANADA SP CONGRESS CANADA C1 NIDDKD,SCH MED,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-2019-0 J9 DEV NEPHROL PY 1993 VL 34 BP 585 EP 595 PG 11 WC Geriatrics & Gerontology; Urology & Nephrology SC Geriatrics & Gerontology; Urology & Nephrology GA BA07W UT WOS:A1993BA07W00063 ER PT B AU CUMMINGS, NB AF CUMMINGS, NB BE Oreopoulos, DG Michelis, MF Herschorn, S TI ALLOCATION OF SCARCE RESOURCES - JUSTICE AND RATIONING OF HEALTH-CARE SO NEPHROLOGY AND UROLOGY IN THE AGED PATIENT SE DEVELOPMENTS IN NEPHROLOGY LA English DT Proceedings Paper CT 3rd International Conference on Geriatric Nephrology and Urology CY APR 03-05, 1992 CL TORONTO, CANADA SP CONGRESS CANADA C1 NIDDKD,SCH MED,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-2019-0 J9 DEV NEPHROL PY 1993 VL 34 BP 597 EP 603 PG 7 WC Geriatrics & Gerontology; Urology & Nephrology SC Geriatrics & Gerontology; Urology & Nephrology GA BA07W UT WOS:A1993BA07W00064 ER PT J AU GRADY, CL HAXBY, JV HORWITZ, B GILLETTE, J SALERNO, JA GONZALEZAVILES, A CARSON, RE HERSCOVITCH, P SCHAPIRO, MB RAPOPORT, SI AF GRADY, CL HAXBY, JV HORWITZ, B GILLETTE, J SALERNO, JA GONZALEZAVILES, A CARSON, RE HERSCOVITCH, P SCHAPIRO, MB RAPOPORT, SI TI ACTIVATION OF CEREBRAL BLOOD-FLOW DURING A VISUOPERCEPTUAL TASK IN PATIENTS WITH ALZHEIMER-TYPE DEMENTIA SO NEUROBIOLOGY OF AGING LA English DT Article DE POSITRON EMISSION TOMOGRAPHY; BRAIN; ALZHEIMERS DISEASE; COGNITION; FACE PERCEPTION; EXTRASTRIATE CORTEX ID POSITRON EMISSION TOMOGRAPHY; POSTERIOR PARIETAL CORTEX; BALINTS SYNDROME; BEHAVIORAL ENHANCEMENT; METABOLIC ASYMMETRIES; VISUAL DISTURBANCES; DISEASE; ATTENTION; DYSFUNCTION; PATTERNS AB Changes in regional cerebral blood flow (rCBF) associated with a face-matching task were examined using positron emission tomography (PET) and (H2O)-O-15 in 7 patients with mild-moderate dementia of the Alzheimer type (DAT) and in 8 healthy age-matched controls. rCBF was normalized to whole brain flow and pixel-by-pixel difference images were computed by contrasting flow during a control task to flow during face matching. Both patients and controls showed bilateral rCBF increases in occipitotemporal extrastriate cortex during face matching. The magnitude of these increases was not significantly different between the groups. In addition, the patients showed greater rCBF activation in regions of occipital and frontal cortex. These results show that early in the course of DAT, patients utilize extrastriate cortex to perform a visuoperceptual task, as do control subjects but also show rCBF increases in additional cortical areas. Activation of these additional areas of cortex in the patients may reflect an increased attentional load during face matching due to their reduced cognitive capacity. C1 NIH,DEPT POSITRON EMISS TOMOG,CTR CLIN,BETHESDA,MD 20892. RP GRADY, CL (reprint author), NIA,NEUROSCI LAB,BRAIN AGING & DEMENTIA SECT,BLDG 10,ROOM 6C414,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Carson, Richard/H-3250-2011 OI Carson, Richard/0000-0002-9338-7966 NR 60 TC 87 Z9 88 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD JAN-FEB PY 1993 VL 14 IS 1 BP 35 EP 44 DI 10.1016/0197-4580(93)90018-7 PG 10 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA KK329 UT WOS:A1993KK32900004 PM 8450930 ER PT S AU RITZ, MC KUHAR, MJ AF RITZ, MC KUHAR, MJ BE Wonnacott, S Lunt, GG TI PSYCHOSTIMULANT DRUGS AND A DOPAMINE HYPOTHESIS REGARDING ADDICTION - UPDATE ON RECENT RESEARCH SO NEUROCHEMISTRY OF DRUG DEPENDENCE SE BIOCHEMICAL SOCIETY SYMPOSIUM LA English DT Article; Proceedings Paper CT Biochemical-Society Symposium no. 59 CY DEC, 1992 CL ROYAL FREE HOSP SCH MED, LONDON, ENGLAND SP BIOCHEM SOC HO ROYAL FREE HOSP SCH MED ID COCAINE BINDING-SITES; METHADONE-MAINTAINED PATIENTS; MEDIAL PREFRONTAL CORTEX; VENTRAL TEGMENTAL AREA; RAT NUCLEUS-ACCUMBENS; FREELY MOVING RATS; INTRAVENOUS COCAINE; RHESUS-MONKEYS; 6-HYDROXYDOPAMINE LESIONS; BENZODIAZEPINE RECEPTORS AB Evidence that psychostimulant drugs interact principally with monoamines, and in particular with the mesolimbic pathway that utilizes dopamine as the neurotransmitter, has prompted the dopamine hypothesis of psychostimulant addiction. This hypothesis proposes that enhancement of dopamine neurotransmission in the mesolimbic pathway is fundamental to the reinforcing properties of many drugs of abuse. Cocaine, the best characterized psychostimulant, is seen to fulfil this hypothesis by blocking dopamine transporters, thereby preventing re-uptake of the neurotransmitter and enhancing its synaptic concentration (Fig. 1). This biochemical mechanism is supported by behavioural data. For example, concordance between binding to the transporter and changes in locomotor activity has been demonstrated for a large series of cocaine analogues. The dopamine hypothesis suggests possible pharmacotherapeutic strategies to combat psychostimulant use, and these approaches, including available human data and future directions of pharmacological treatments are discussed in this paper. The limitations of the dopamine hypothesis with respect to psychostimulant dependence and abuse liability are also summarized, to provide a broad perspective of the current status of this hypothesis. C1 UNIV NEW MEXICO,CTR ALCOHOLISM SUBST ABUSE & ADDICT,ALBUQUERQUE,NM 87131. NIDA,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224. RP RITZ, MC (reprint author), UNIV NEW MEXICO,DEPT PSYCHIAT,ALBUQUERQUE,NM 87131, USA. NR 114 TC 32 Z9 34 U1 3 U2 5 PU PORTLAND PRESS LTD PI LONDON PA 59 PORTLAND PL, LONDON, ENGLAND W1N 3AJ SN 0067-8694 BN 1-85578-034-8 J9 BIOCHEM SOC SYMP PY 1993 VL 59 IS 59 BP 51 EP 64 PG 14 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BZ96Q UT WOS:A1993BZ96Q00004 PM 7910741 ER PT S AU MARLEY, RJ SHIMOSATO, K ELMER, GI MINER, LL AF MARLEY, RJ SHIMOSATO, K ELMER, GI MINER, LL BE Wonnacott, S Lunt, GG TI PHARMACOGENETIC APPROACHES TO DRUG-DEPENDENCE SO NEUROCHEMISTRY OF DRUG DEPENDENCE SE BIOCHEMICAL SOCIETY SYMPOSIUM LA English DT Article; Proceedings Paper CT Biochemical-Society Symposium no. 59 CY DEC, 1992 CL ROYAL FREE HOSP SCH MED, LONDON, ENGLAND SP BIOCHEM SOC HO ROYAL FREE HOSP SCH MED ID SHORT-SLEEP MICE; LONG-SLEEP; CONVULSANT PROPERTIES; MOUSE LINES; COCAINE; SENSITIVITY; SEIZURES; BINDING; SYSTEM; GABA AB The aim of this volume is to bring together information about both the neurochemical mechanisms associated with the actions of drugs of abuse and the psychopharmacological and behavioural effects of these drugs. One approach that is proving to be quite useful for bringing together these two very diverse fields is the use of classical pharmacogenetic techniques. Pharmacogenetics is defined as the study of genetic and environmental factors underlying individual differences in response to pharmacological or toxicological agents. Much of the early work in this field dealt with genetic differences in drug metabolism and other pharmacokinetic parameters [1]. More recently, however, attention has been directed towards understanding the implications of genetic differences associated with pharmacodynamic parameters mediating the actions of drugs. This paper discusses the use of pharmacogenetic techniques in drug abuse research. It presents an overview of some of the more common genetic techniques available for use in drug research and provides some examples from research projects that have employed these approaches. RP MARLEY, RJ (reprint author), NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 42 TC 1 Z9 1 U1 0 U2 0 PU PORTLAND PRESS LTD PI LONDON PA 59 PORTLAND PL, LONDON, ENGLAND W1N 3AJ SN 0067-8694 BN 1-85578-034-8 J9 BIOCHEM SOC SYMP PY 1993 VL 59 IS 59 BP 153 EP 172 PG 20 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy GA BZ96Q UT WOS:A1993BZ96Q00011 PM 8192684 ER PT J AU KLING, MA RUBINOW, DR DORAN, AR ROY, A DAVIS, CL CALABRESE, JR NIEMAN, LK POST, RM CHROUSOS, GP GOLD, PW AF KLING, MA RUBINOW, DR DORAN, AR ROY, A DAVIS, CL CALABRESE, JR NIEMAN, LK POST, RM CHROUSOS, GP GOLD, PW TI CEREBROSPINAL-FLUID IMMUNOREACTIVE SOMATOSTATIN CONCENTRATIONS IN PATIENTS WITH CUSHINGS-DISEASE AND MAJOR DEPRESSION - RELATIONSHIP TO INDEXES OF CORTICOTROPIN-RELEASING HORMONE AND CORTISOL SECRETION SO NEUROENDOCRINOLOGY LA English DT Article DE SOMATOSTATIN; CORTICOTROPIN-RELEASING HORMONE; CORTISOL; CEREBROSPINAL FLUID; CUSHINGS DISEASE; MAJOR DEPRESSION ID AFFECTIVE-ILLNESS; CSF SOMATOSTATIN; GROWTH-HORMONE; BIOCHEMICAL MANIFESTATIONS; SENILE DEMENTIA; CEREBRAL-CORTEX; ALZHEIMER TYPE; RHESUS-MONKEY; RESPONSES; STRESS AB To further explore the differential effects of peripherally and centrally derived hypercortisolism on neurohormonal systems implicated in the pathophysiology of mood and cognitive disturbances, we examined the cerebrospinal fluid (CSF) concentrations of immunoreactive somatostatin (IR-SRIF) in patients with Cushing's disease and major depression and the relationship of these levels to CSF immunoreactive corticotropin-releasing hormone (CRH) concentrations and urinary free cortisol excretion. In particular, since CSF SRIF levels consistently have been shown to be reduced in depression, we wished to assess whether decreased centrally directed SRIF was more likely a primary or a secondary factor in the hypercortisolism of major depression. CSF SRIF levels were significantly reduced in 11 patients with documented Cushing's disease and in 1 patient with ectopic adrenocorticotropic hormone secretion as compared with both 41 healthy volunteers (19.4 +/- 2.9 vs. 37.4 +/- 1.5 pmol/l; p < 0.01) and 28 patients with major depression (30.2 +/- 2.4 pmol/l; p < 0.05), whose CSF SRIF levels were also significantly reduced as compared with controls (p < 0.05). CSF SRIF levels in the Cushing's disease patients correlated positively with CSF CRH (r = 0.64; p < 0.025), suggesting that either the sustained hypercortisolism in these patients and/or its suppression of central CRH secretion contributed to the reduction in SRIF. A more modest but significant correlation between CSF SRIF and CSF CRH was observed in the healthy volunteers (r = 0.37; d.f = 37; p < 0.02); in the depressed patients, no linear relationship, but rather an inverted U-shaped relationship was found which significantly fit by a quadratic function (r2 = 0.90; d.f. = 22; p < 0.001). In the depressed patients, the CSF SRIF levels also showed an inverted quadratic relationship with urinary free cortisol excretion (r2 = 0.87; d.f. = 16; p < 0.001). These findings, together with those from recent preclinical and human volunteer studies, suggest that CRH is a positive modulator of central SRIF release under physiological conditions, while glucocorticoid excess tends to suppress SRIF. These data are of interest in the light of evidence suggesting an involvement of SRIF in functions such as mood regulation, learning, and memory which are disturbed in both Cushing's disease and major depression. C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP KLING, MA (reprint author), NIMH,IRP,CTR CLIN,CLIN NEUROENDOCRINOL BRANCH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Kling, Mitchel/F-4152-2010 OI Kling, Mitchel/0000-0002-2232-1409 NR 69 TC 28 Z9 28 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD JAN PY 1993 VL 57 IS 1 BP 79 EP 88 DI 10.1159/000126345 PG 10 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA KU368 UT WOS:A1993KU36800012 PM 8097579 ER PT J AU PATTERSON, MC DIBISCEGLIE, AM HIGGINS, JJ ABEL, RB SCHIFFMANN, R PARKER, CC ARGOFF, CE GREWAL, RP YU, K PENTCHEV, PG BRADY, RO BARTON, NW AF PATTERSON, MC DIBISCEGLIE, AM HIGGINS, JJ ABEL, RB SCHIFFMANN, R PARKER, CC ARGOFF, CE GREWAL, RP YU, K PENTCHEV, PG BRADY, RO BARTON, NW TI THE EFFECT OF CHOLESTEROL-LOWERING AGENTS ON HEPATIC AND PLASMA-CHOLESTEROL IN NIEMANN-PICK DISEASE TYPE-C SO NEUROLOGY LA English DT Article ID STORAGE DISORDER; ESTERIFICATION; ACCUMULATION AB Niemann-Pick disease type C (NP-C) is a neurovisceral lipidosis characterized by defective intracellular trafficking of cholesterol and lysosomal accumulation of unesterified cholesterol, believed to be an offending metabolite. We studied the effect of cholesterol-lowering agents on hepatic and plasma cholesterol levels in NP-C by randomly assigning 25 patients with NP-C to one of five treatment regimens containing different combinations of cholestyramine, lovastatin, nicotinic acid, or dimethyl sulfoxide (DMSO). Unesterified cholesterol content was measured in liver biopsies before and after 4 months' treatment. All drug regimens except DMSO alone reduced hepatic and plasma cholesterol levels. Toxicity was limited and did not prevent any patient from completing the study. The combination of cholestyramine, lovastatin, and nicotinic acid lowered cholesterol levels in liver and blood with minimal side effects. A controlled clinical study will be necessary to determine if this regimen influences the rate of neurologic progression. C1 NINCDS,DEV & METAB NEUROL BRANCH,BLDG 10,ROOM 3D03,BETHESDA,MD 20892. NINCDS,BIOMETRY & FIELD STUDIES BRANCH,BETHESDA,MD 20892. NATL INST DIABET & DIGEST & KIDNEY DIS,LIVER DIS SECT,BETHESDA,MD. NATL INST DIABET & DIGEST & KIDNEY DIS,DIGEST DIS BRANCH,BETHESDA,MD. OI Patterson, Marc/0000-0002-1116-126X NR 16 TC 68 Z9 70 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1993 VL 43 IS 1 BP 61 EP 64 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA KJ189 UT WOS:A1993KJ18900011 PM 8423912 ER PT J AU POST, RM KETTER, TA PAZZAGLIA, PJ GEORGE, MS MARANGELL, L DENICOFF, K AF POST, RM KETTER, TA PAZZAGLIA, PJ GEORGE, MS MARANGELL, L DENICOFF, K TI NEW DEVELOPMENTS IN THE USE OF ANTICONVULSANTS AS MOOD STABILIZERS SO NEUROPSYCHOBIOLOGY LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON ANTIEPILEPTIC DRUGS IN PSYCHIATRY CY JAN 29-30, 1993 CL FREIBURG, GERMANY SP DESITIN PHARMA, DEUT FORSCHUNGSGEMEINSCH DE LITHIUM; CARBAMAZEPINE; VALPROATE; NIMODIPINE; VERAPAMIL; RAPID CYCLING; BIPOLAR ILLNESS; TOLERANCE; PROPHYLAXIS; KINDLING ID BIPOLAR DISORDER; CONTINGENT TOLERANCE; CALCIUM-ANTAGONISTS; ACUTE MANIA; CARBAMAZEPINE; VALPROATE; LITHIUM; PROPHYLAXIS; PREVENTION; SPECTRUM AB There is increasing recognition that lithium is inadequate in the treatment of up to 50% of bipolar patients. In addition to subgroups that are nonresponsive from the outset, loss of efficacy (tolerance) and discontinuation-induced refractoriness have recently been observed. The anticonvulsants carbamazepine and valproate are effective alternative or adjunctive treatments, but tolerance can also occur during their long-term prophylactic use. New treatment algorithms for this loss ef efficacy, including combination therapies, require further systematic study. Preliminary data suggesting that some patients with extremely rapid and chaotic mood fluctuations may respond to the L-type calcium channel blocker nimodipine are presented, and the theoretical implications discussed. RP POST, RM (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 38 TC 26 Z9 26 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0302-282X J9 NEUROPSYCHOBIOLOGY JI Neuropsychobiology PY 1993 VL 27 IS 3 BP 132 EP 137 DI 10.1159/000118968 PG 6 WC Neurosciences; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA LU185 UT WOS:A1993LU18500004 PM 8232827 ER PT J AU WOLKOWITZ, OM COPPOLA, R BREIER, A DORAN, AR RUBINOW, DR BERRETTINI, WH KLING, MA PICKAR, D AF WOLKOWITZ, OM COPPOLA, R BREIER, A DORAN, AR RUBINOW, DR BERRETTINI, WH KLING, MA PICKAR, D TI QUANTITATIVE ELECTROENCEPHALOGRAPHIC CORRELATES OF STEROID-ADMINISTRATION IN MAN SO NEUROPSYCHOBIOLOGY LA English DT Article DE QUANTITATIVE ELECTROENCEPHALOGRAPHY; EEG; STEROIDS; PREDNISONE; BEHAVIOR; MOOD; SOMATOSTATIN; BETA-ENDORPHIN; NOREPINEPHRINE ID SOMATOSTATIN SRIF; ALPHA-RHYTHM; EEG; CORTISOL; BEHAVIOR AB Elevated levels of circulating corticosteroids are frequently associated with behavioral alterations in man, although the mechanisms by which corticosteroids may affect behavior are poorly understood. To evaluate possible effects of exogenous corticosteroids on brain electrophysiological functioning and the relationship of such effects to behavioral and biochemical changes, we administered prednisone (80 mg p.o. daily for 5 days) in a double-blind manner to 11 medically healthy volunteers. Quantitative electroencephalogram analysis was performed following 4 days of prednisone administration and during the preceding and ensuing placebo administration periods. Central theta wave brain electrical activity significantly increased following prednisone administration and returned to baseline following prednisone withdrawal. This effect was directly correlated with prednisone-induced increases in subjective sadness ratings and with decreases in self-rated energy and well-being. Prednisone-induced reductions in peak alpha wave activity were also directly correlated with increases in subjective sadness and Symptom Checklist-90 ratings and with decreases in self-rated 'hypomanic' symptoms. Further, prednisone-induced increases in theta activity were significantly correlated with prednisone-induced decreases in CSF levels of somatostatin-like immunoreactivity, and prednisone-induced decreases in peak alpha activity were significantly correlated with decreases in CSF levels of norepinephrine and with relative increases (or lesser decreases) in CSF levels of beta-endorphin and beta-lipotropic hormone. This preliminary report of the concomitant development of prednisone-induced changes in brain electrical activity, neurochemistry and behavior highlights areas for future exploration in the study of corticosteroid effects on behavior in man. C1 NIMH,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,MARYLAND PSYCHIAT RES CTR,BALTIMORE,MD 21201. CANYON SPRINGS HOSP,CATHEDRAL CITY,CA. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT PSYCHIAT,PHILADELPHIA,PA 19107. RP WOLKOWITZ, OM (reprint author), UNIV CALIF SAN FRANCISCO,DEPT PSYCHIAT,401 PARNASSUS AVE,SAN FRANCISCO,CA 94143, USA. RI Kling, Mitchel/F-4152-2010 OI Kling, Mitchel/0000-0002-2232-1409 NR 34 TC 9 Z9 9 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0302-282X J9 NEUROPSYCHOBIOLOGY JI Neuropsychobiology PY 1993 VL 27 IS 4 BP 224 EP 230 DI 10.1159/000118985 PG 7 WC Neurosciences; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA LW117 UT WOS:A1993LW11700006 PM 8232843 ER PT J AU PERSICO, AM SCHINDLER, CW BRANNOCK, MT GONZALEZ, AM SURRATT, CK UHL, GR AF PERSICO, AM SCHINDLER, CW BRANNOCK, MT GONZALEZ, AM SURRATT, CK UHL, GR TI DOPAMINERGIC GENE-EXPRESSION DURING AMPHETAMINE WITHDRAWAL SO NEUROREPORT LA English DT Article DE DOPAMINE TRANSPORTER; TYROSINE HYDROXYLASE; SYNAPTIC VESICULAR AMINE TRANSPORTER; AMPHETAMINE; PSYCHOSTIMULANT; WITHDRAWAL; GENE EXPRESSION ID RAT-BRAIN SYNAPTOSOMES; TYROSINE-HYDROXYLASE; COMPLEMENTARY-DNA; H-3 AMPHETAMINE; COCAINE; INCREASE; SEQUENCE; REGIONS; SYSTEM; REWARD AB ANIMALs and humans display a constellation of behavioral and neurochemical signs after termination of psychostimulant administration. Amphetamine withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of kev genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (TH), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT). Withdrawal from 7.5 mg kg-1 i.p. amphetamine (b.i.d. for a two week duration) yields no significant changes in rat DAT mRNA. TH mRNA levels are modestly enhanced over the same week of withdrawal, during which dopamine levels and behavioral novelty responses are both depressed. SVAT expression is significantly blunted following chronic amphetamine treatment. Altered TH and/or SVAT gene expression might contribute to restoring normal function to neurons ''withdrawing'' from amphetamine treatments. C1 NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. NR 25 TC 22 Z9 22 U1 0 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD JAN PY 1993 VL 4 IS 1 BP 41 EP 44 DI 10.1097/00001756-199301000-00010 PG 4 WC Neurosciences SC Neurosciences & Neurology GA KN461 UT WOS:A1993KN46100010 PM 8095821 ER PT J AU BACHEVALIER, J BRICKSON, M HAGGER, C AF BACHEVALIER, J BRICKSON, M HAGGER, C TI LIMBIC-DEPENDENT RECOGNITION MEMORY IN MONKEYS DEVELOPS EARLY IN INFANCY SO NEUROREPORT LA English DT Article DE DEVELOPMENT; RECOGNITION MEMORY; LIMBIC SYSTEM; NONHUMAN PRIMATE AB INFANTILE amnesia, the absence of memories from infancy and early childhood, has been attributed to an immaturity of the limbic system in infancy. Contrary to this view, we now report that limbic-dependent recognition memory is present as early as one month of age in monkeys. Memory measured by the paired-comparison preferential looking task, normally present in infant monkeys within the first month of life, is absent after damage to the amygdaloid complex and hippocampal formation, suggesting that limbic structures make a critical contribution to visual recognition memory even at this early age. The findings reopen the question of the locus of the neural immaturity that underlies infantile amnesia. C1 UNIV TEXAS,SCH MED,DEPT NEUROBIOL & ANAT,HOUSTON,TX 77030. RP BACHEVALIER, J (reprint author), NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892, USA. NR 16 TC 133 Z9 134 U1 0 U2 9 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD JAN PY 1993 VL 4 IS 1 BP 77 EP 80 DI 10.1097/00001756-199301000-00020 PG 4 WC Neurosciences SC Neurosciences & Neurology GA KN461 UT WOS:A1993KN46100020 PM 8453042 ER PT J AU MILLER, EK DESIMONE, R AF MILLER, EK DESIMONE, R TI SCOPOLAMINE AFFECTS SHORT-TERM-MEMORY BUT NOT INFERIOR TEMPORAL NEURONS SO NEUROREPORT LA English DT Article DE SCOPOLAMINE; MEMORY; MACAQUE MONKEY; INFERIOR TEMPORAL CORTEX ID RECOGNITION MEMORY; HIPPOCAMPAL-FORMATION; CORTEX; MONKEYS AB EFFECTS of scopolamine on performance of a delayed matching-to-sample task and on the properties of neurons in anterior-ventral inferior temporal (IT) cortex were examined in two monkeys. Both monkeys were impaired on the task after systemic administration of scopolamine, suggesting that scopolamine disrupts recency memory. Despite the behavioral deficit, neurons in IT cortex, a region having an important role in visual memory and neuronal properties consistent with that role, were largely unaffected by scopolamine. This dissociation between the behavioral and neuronal effects of scopolamine indicates that the drug either acts at a different site or disrupts unobserved mechanisms at the IT site. RP MILLER, EK (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 9,ROOM 1E104,BETHESDA,MD 20892, USA. NR 13 TC 48 Z9 48 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 JAN PY 1993 VL 4 IS 1 BP 81 EP 84 DI 10.1097/00001756-199301000-00021 PG 4 WC Neurosciences SC Neurosciences & Neurology GA KN461 UT WOS:A1993KN46100021 PM 8453043 ER PT J AU HEEMSKERK, FMJ ZORAD, S SELTZER, A SAAVEDRA, JM AF HEEMSKERK, FMJ ZORAD, S SELTZER, A SAAVEDRA, JM TI CHARACTERIZATION OF BRAIN ANGIOTENSIN-II AT2-RECEPTOR SUBTYPE USING [I-125] CGP-42112A SO NEUROREPORT LA English DT Article DE RENIN-ANGIOTENSIN; BRAIN DEVELOPMENT; BRAIN ANGIOTENSIN SYSTEM; ANGIOTENSIN RECEPTORS; CGP-42112A; QUANTITATIVE AUTORADIOGRAPHY ID SELECTIVE NONPEPTIDE ANTAGONISTS; RAT-BRAIN; RECEPTOR SUBTYPES AB RECENTLY two subtypes of angiotensin receptors have been described, AT1 and AT2. Currently used radiolabeled agonists and antagonists are not able to discriminate between these receptor subtypes. Here we characterize the use of [I-125] CGP 42112A, a novel, specific ligand for AT2 receptors, in a membrane binding assay and in autoradiography of brain sections of 2 week old rats. [I-125] CGP 42112A bound with high affinity and autoradiography revealed binding selectively localized to areas known to express the AT2 receptor subtype only. CGP 42112A, angiotensin II, angiotensin Ill and PD 123177 competed for [I-125] CGP 42112A binding, with potencies consistent with high affinity and specific binding to AT2 receptors. Thus [I-125] CGP 42112A will be a useful new tool to study AT2 receptors. RP HEEMSKERK, FMJ (reprint author), NIMH,CLIN SCI LAB,PHARMACOL SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2D-45,BETHESDA,MD 20892, USA. NR 16 TC 28 Z9 28 U1 1 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD JAN PY 1993 VL 4 IS 1 BP 103 EP 105 DI 10.1097/00001756-199301000-00027 PG 3 WC Neurosciences SC Neurosciences & Neurology GA KN461 UT WOS:A1993KN46100027 PM 8453029 ER PT S AU POST, RM AF POST, RM BE Mendlewicz, J Brunello, N Langer, SZ Racagni, G TI EVALUATION OF LONG-TERM PROPHYLACTIC TREATMENTS OF DEPRESSIVE-DISORDERS SO NEW PHARMACOLOGICAL APPROACHES TO THE THERAPY OF DEPRESSIVE DISORDERS SE INTERNATIONAL ACADEMY FOR BIOMEDICAL AND DRUG RESEARCH LA English DT Proceedings Paper CT Inaugural Workshop and Inaugural Session of the European Decade of Brain Research CY SEP 21-23, 1992 CL BRUSSELS, BELGIUM RP POST, RM (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N212,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA BASEL SN 1019-2029 BN 3-8055-5746-9 J9 INT ACAD B JI Int.Acad.Biomed.Drug Res. PY 1993 VL 5 BP 101 EP 113 PG 13 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA BZ35N UT WOS:A1993BZ35N00010 ER PT S AU HANBAUER, I AF HANBAUER, I BE Moncada, S Nistico, G Higgs, EA TI THE ROLE OF NITRIC-OXIDE IN NEUROTRANSMITTER RELEASE SO NITRIC OXIDE: BRAIN AND IMMUNE SYSTEM SE PORTLAND PRESS PROCEEDINGS LA English DT Proceedings Paper CT 1st International Meeting on Nitric Oxide: Brain and Immune System CY SEP 16-18, 1992 CL PARAELIOS, ITALY SP SOC ITALIANA NEUROIMMUNOMODULAZIONE C1 NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PORTLAND PRESS LTD PI LONDON PA 59 PORTLAND PL, LONDON, ENGLAND W1N 3AJ SN 0966-4068 BN 1-85578-046-1 J9 PORTL PR P PY 1993 BP 135 EP 141 PG 7 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA BZ76W UT WOS:A1993BZ76W00013 ER PT S AU BEZRUKOV, SM KASIANOWICZ, JJ AF BEZRUKOV, SM KASIANOWICZ, JJ BE Handel, PH Chung, AL TI NOISE-ANALYSIS OF IONIZATION KINETICS IN A PROTEIN ION-CHANNEL SO NOISE IN PHYSICAL SYSTEMS AND 1/F FLUCTUATIONS SE AIP Conference Proceedings LA English DT Proceedings Paper CT INTERNATIONAL CONF ON NOISE IN PHYSICAL SYSTEMS AND 1/F FLUCTUATION ( ICNF 93 ) CY 1993 CL UNIV MISSOURI, ST LOUIS, MO HO UNIV MISSOURI C1 NIDDK, LBM, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER INST PHYSICS PI MELVILLE PA 2 HUNTINGTON QUADRANGLE, STE 1NO1, MELVILLE, NY 11747-4501 USA SN 0094-243X BN 1-56396-270-5 J9 AIP CONF PROC PY 1993 IS 285 BP 677 EP 680 PG 4 WC Physics, Applied; Physics, Condensed Matter SC Physics GA BZ02N UT WOS:A1993BZ02N00143 ER PT S AU ALLEGRA, CJ VOELLER, D AF ALLEGRA, CJ VOELLER, D BE Rustum, YM TI CLINICAL USE OF LEUCOVORIN - INTRACELLULAR METABOLISM SO NOVEL APPROACHES TO SELECTIVE TREATMENTS OF HUMAN SOLID TUMORS: LABORATORY AND CLINICAL CORRELATION SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT International Symposium on Novel Approaches to Selective Treatments of Human Tumors: Laboratory and Clinical Correlation CY SEP 10-12, 1992 CL BUFFALO, NY RP ALLEGRA, CJ (reprint author), NCI,NAY MED ONCOL BRANCH,BETHESDA,MD 20889, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44592-1 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1993 VL 339 BP 43 EP 49 PG 7 WC Oncology; Medicine, General & Internal; Pharmacology & Pharmacy SC Oncology; General & Internal Medicine; Pharmacology & Pharmacy GA BZ51M UT WOS:A1993BZ51M00005 PM 8178727 ER PT S AU GREM, JL MCATEE, N DRAKE, JC STEINBERG, S ALLEGRA, CJ AF GREM, JL MCATEE, N DRAKE, JC STEINBERG, S ALLEGRA, CJ BE Rustum, YM TI DOSE-DEPENDENT INHIBITION OF ASPARTATE CARBAMOYLTRANSFERASE IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS IN PATIENTS RECEIVING N-(PHOSPHONACETYL)-L-ASPARTATE SO NOVEL APPROACHES TO SELECTIVE TREATMENTS OF HUMAN SOLID TUMORS: LABORATORY AND CLINICAL CORRELATION SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT International Symposium on Novel Approaches to Selective Treatments of Human Tumors: Laboratory and Clinical Correlation CY SEP 10-12, 1992 CL BUFFALO, NY C1 NCI,DIV CANC TREATMENT,CLIN CTR,CANC NURSING SERV,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,BIOSTAT BRANCH,BETHESDA,MD 20892. RP GREM, JL (reprint author), USN,MED CTR,NCI,NAVY MED ONCOL BRANC,BLDG 8,ROOM 5101,BETHESDA,MD 20889, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44592-1 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1993 VL 339 BP 119 EP 123 PG 5 WC Oncology; Medicine, General & Internal; Pharmacology & Pharmacy SC Oncology; General & Internal Medicine; Pharmacology & Pharmacy GA BZ51M UT WOS:A1993BZ51M00013 PM 8178710 ER PT S AU CHU, E ALLEGRA, CJ AF CHU, E ALLEGRA, CJ BE Rustum, YM TI REGULATION OF THYMIDYLATE SYNTHASE IN HUMAN COLON-CANCER CELLS TREATED WITH 5-FLUOROURACIL AND INTERFERON-GAMMA SO NOVEL APPROACHES TO SELECTIVE TREATMENTS OF HUMAN SOLID TUMORS: LABORATORY AND CLINICAL CORRELATION SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT International Symposium on Novel Approaches to Selective Treatments of Human Tumors: Laboratory and Clinical Correlation CY SEP 10-12, 1992 CL BUFFALO, NY RP CHU, E (reprint author), USN HOSP,NCI,NAVY MED ONCOL BRANCH,NMOB 8-5101,BETHESDA,MD 20889, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44592-1 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1993 VL 339 BP 143 EP 151 PG 9 WC Oncology; Medicine, General & Internal; Pharmacology & Pharmacy SC Oncology; General & Internal Medicine; Pharmacology & Pharmacy GA BZ51M UT WOS:A1993BZ51M00016 PM 8178713 ER PT J AU JOHN, CS SAGA, T KINUYA, S LE, N JEONG, JM PAIK, CH REBA, RC VARMA, VM MCAFEE, JG AF JOHN, CS SAGA, T KINUYA, S LE, N JEONG, JM PAIK, CH REBA, RC VARMA, VM MCAFEE, JG TI AN IMPROVED SYNTHESIS OF [I-125] N-(DIETHYLAMINOETHYL)-4-IODOBENZAMIDE - A POTENTIAL LIGAND FOR IMAGING MALIGNANT-MELANOMA SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article ID I-123 AB To improve the radiolabeling yield and the specific activity of [I-125]N-(2-diethylaminoethyl)-4-iodobenzamide (DAB), the aryltributyltin precursor was synthesized from the N-(2-diethylaminoethyl)-4-bromobenzamide derivative by palladium catalyzed stannylation using bis(tributyltin). The radiolabeled product, [I-125]DAB, was obtained by an iododestannylation reaction in high radiochemical yields (85-94%, radiochemical purity, > 98%) using chloramine-T as an oxidizing agent. The specific activity was greater than 1600 Ci/mmol. The biodistribution studies in nude mice implanted with human malignant melanoma xenograft showed a good tumor uptake (6.14% ID/g at 1 h, 2.81% ID/g at 6h and 0.42% ID/g at 24h) of [I-125]DAB. Unfortunately, a high uptake in the non-target organs, such as liver and lung, was found. At 1 h post-injection the activity level in liver and lung was 11.76 and 7.58% ID/g, respectively. A slow clearance of activity from liver and lung was observed at 6 h (3.43 and 0.49% ID/g). These results demonstrate that iodinated IDAB is a potential radiopharmaceutical for the management of patients with malignant melanoma. C1 NIH,BETHESDA,MD 20892. RI Jeong, Jae Min/E-2102-2012 OI Jeong, Jae Min/0000-0003-2611-6020 NR 10 TC 26 Z9 26 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD JAN PY 1993 VL 20 IS 1 BP 75 EP 79 DI 10.1016/0969-8051(93)90138-K PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KC913 UT WOS:A1993KC91300009 PM 8461882 ER PT J AU ZIMMET, J JARLEBARK, L HAMMARBERG, T VANGALEN, PJM JACOBSON, KA HEILBRONN, E AF ZIMMET, J JARLEBARK, L HAMMARBERG, T VANGALEN, PJM JACOBSON, KA HEILBRONN, E TI SYNTHESIS AND BIOLOGICAL-ACTIVITY OF NOVEL 2-THIO DERIVATIVES OF ATP SO NUCLEOSIDES & NUCLEOTIDES LA English DT Article ID CULTURED CHICK MYOTUBES; ADENINE-NUCLEOTIDES; PHOSPHOLIPASE-C; SMOOTH-MUSCLE; ADENOSINE; AGONIST; CALCIUM; CELLS; MOBILIZATION; INHIBITORS AB 2-Alkylthio analogues of adenosine 5'-triphosphate were synthesized and evaluated as P2y purinocepter agonists. ATP and analogues transiently increased intracellular Ca2+ levels in C6 glioma cells and in skeletal muscle derived myotubes in culture. Most derivatives were resistant to stepwise dephosphorylation by ecto-ATPases. C1 UNIV STOCKHOLM,NEUROCHEM & NEUROTOXICOL UNIT,S-10691 STOCKHOLM,SWEDEN. NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031116-20, Z99 DK999999] NR 32 TC 23 Z9 23 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0732-8311 J9 NUCLEOS NUCLEOT JI Nucleosides Nucleotides PY 1993 VL 12 IS 1 BP 1 EP 20 DI 10.1080/07328319308016190 PG 20 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KK476 UT WOS:A1993KK47600001 PM 25181577 ER PT J AU PERLMAN, ME AF PERLMAN, ME TI SYNTHESIS OF 2'-DEUTERIO TUBERCIDIN AND ADENOSINE AND THE CORRESPONDING ARABINO ANALOGS SO NUCLEOSIDES & NUCLEOTIDES LA English DT Article ID ACID RELATED-COMPOUNDS; SECONDARY ALCOHOLS; MASS-SPECTROMETRY; NUCLEOSIDES; OXIDATION; 3'-KETONUCLEOSIDES; 2'-KETONUCLEOSIDES; RIBONUCLEOSIDES; BIOSYNTHESIS; SUBSTITUTION AB The 2'-deuterio arabino analogs of tubercidin and adenosine have been prepared by Swern oxidation of the 3',5'-TPDS derivatives of tubercidin and adenosine and reduction with NaBD4. Subsequent inversion of stereochemistry at C-2' yielded [2'-H-2]tubercidin and [2'-H-2]adenosine with 98% deuterium incorporation. RP PERLMAN, ME (reprint author), NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709, USA. NR 23 TC 8 Z9 8 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0732-8311 J9 NUCLEOS NUCLEOT JI Nucleosides Nucleotides PY 1993 VL 12 IS 1 BP 73 EP 82 DI 10.1080/07328319308016195 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KK476 UT WOS:A1993KK47600006 ER PT J AU ALDROUBI, A UNSER, M AF ALDROUBI, A UNSER, M TI FAMILIES OF MULTIRESOLUTION AND WAVELET SPACES WITH OPTIMAL PROPERTIES SO NUMERICAL FUNCTIONAL ANALYSIS AND OPTIMIZATION LA English DT Article ID ORTHONORMAL BASES; SAMPLING THEOREM; CONVERGENCE; REPRESENTATION; ONDELETTES AB Under suitable conditions, if the scaling functions phi1 and phi2 generate the multiresolutions V(j)(phi1) and V(j)(phi2), then their convolution phi1 * phi2 also generates a multiresolution V(j)(phi1 * phi2). Moreover, if p is an appropriate convolution operator from 1, into itself and if phi is a scaling function generating the multiresolution V(j)(phi), then p * phi is a scaling function generating the same multiresolution V(j)(phi) = V(j)(p * phi). Using these two properties, we group the scaling and wavelet functions into equivalent classes and consider various equivalent basis functions of the associated function spaces. We use the n-fold convolution product to construct sequences of multiresolution and wavelet spaces V(j)(phi(n)) and W(j)(phi(n)) with increasing regularity. We discuss the link between multiresolution analysis and Shannon's sampling theory. We then show that the interpolating and orthogonal pre- and post-filters associated with the multiresolution sequence V(0)(phi(n)) asymptotically converge to the ideal lowpass filter of Shannon. We also prove that the filters associated with the sequence of wavelet spaces W(0)(phi(n)) converge to the ideal bandpass filter. Finally, we construct the basic wavelet sequences psi(b)n and show that they tend to Gabor functions. This provides wavelets that are nearly time-frequency optimal. The theory is illustrated with the example of polynomial splines. C1 NIH, BIOMED ENGN & INSTRUMENTAT PROGRAM, BETHESDA, MD 20892 USA. RI Unser, Michael/A-1550-2008; Aldroubi, Akram/J-7186-2012 NR 59 TC 77 Z9 81 U1 0 U2 2 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA SN 0163-0563 EI 1532-2467 J9 NUMER FUNC ANAL OPT JI Numer. Funct. Anal. Optim. PY 1993 VL 14 IS 5-6 BP 417 EP 446 DI 10.1080/01630569308816532 PG 30 WC Mathematics, Applied SC Mathematics GA ML365 UT WOS:A1993ML36500001 ER PT J AU LUCAS, MD ATWOOD, JR HAGAMAN, R AF LUCAS, MD ATWOOD, JR HAGAMAN, R TI REPLICATION AND VALIDATION OF ANTICIPATED TURNOVER MODEL FOR URBAN REGISTERED NURSES SO NURSING RESEARCH LA English DT Article; Proceedings Paper CT 23RD ANNUAL COMMUNICATING NURSING RESEARCH CONF CY MAY 02-05, 1990 CL DENVER, CO ID JOB-SATISFACTION; HOSPITAL NURSES AB Replication of the Anticipated Turnover Model Among Nurses for urban registered nurses provided substantial support for the stability and generalizability of the theoretical model In both the original and replication studies, causal modeling was used to test the theoretical model predicting job satisfaction, anticipated turnover, and actual turnover. The replication study included 385 full-time nurses in two public and two private urban hospitals. The replication validated, with younger, more educated staff, the major findings from the original study. Group cohesion and job satisfaction effectively predicted anticipated turnover in the replication and the original study. Anticipated turnover was a good predictor of actual turnover, with discriminant analysis yielding 73.2% successful predictions in the replication study and 76.2% in the original study. Job satisfaction effectively buffered job stress. The replication also substantiated the position that job satisfaction strategies need to be targeted specifically to the types of clinical services. C1 UNIV S CAROLINA,COLL NURSING,COLUMBIA,SC 29208. UNIV N CAROLINA,SCH PUBL HLTH,DEPT HLTH BEHAV & HLTH EDUC,CHAPEL HILL,NC 27514. RP LUCAS, MD (reprint author), NATL CTR NURSING RES,ACUTE & CHRON ILLNESS BRANCH,BETHESDA,MD, USA. FU BHP HRSA HHS [NU00908]; NINR NIH HHS [KO7NR00008] NR 28 TC 62 Z9 62 U1 0 U2 3 PU AMER J NURSING CO PI NEW YORK PA 555 W 57TH ST, NEW YORK, NY 10019-2961 SN 0029-6562 J9 NURS RES JI Nurs. Res. PD JAN-FEB PY 1993 VL 42 IS 1 BP 29 EP 35 PG 7 WC Nursing SC Nursing GA KQ376 UT WOS:A1993KQ37600006 PM 8424064 ER PT J AU GUO, WD ZHENG, W LI, JY CHEN, JS BLOT, WJ AF GUO, WD ZHENG, W LI, JY CHEN, JS BLOT, WJ TI CORRELATIONS OF COLON-CANCER MORTALITY WITH DIETARY FACTORS, SERUM MARKERS, AND SCHISTOSOMIASIS IN CHINA SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL LA English DT Article ID LARGE-BOWEL CANCER; REPUBLIC-OF-CHINA; ESOPHAGEAL CANCER; COLORECTAL-CANCER; RISK-FACTORS; CHOLESTEROL LEVELS; STOMACH-CANCER; VEGETABLES; POLYPS; FRUIT AB To determine correlates of the geographic variation in colon cancer mortality within China, dietary variables, biochemical markers, and other factors from an ecological survey in 49 Chinese rural counties were examined. High consumption of animal foods, salt-preserved vegetables, and beer was associated with increased mortality of colon cancer, whereas the rates were significantly inversely related with intake of green vegetables. Serum levels of total cholesterol, urea nitrogen, and lipid peroxide were positively correlated with colon cancer mortality, after adjustment for each other and for other blood nutrients. No appreciable associations, however, were found between colon cancer and serum levels of beta-carotene, alpha-tocopherol, vitamin C, and selenium. In addition, prevalence of schistosomiasis was significantly correlated with increased colon cancer mortality. This ecological study indicates that observations from earlier analytic investigations in Western societies may apply to a Chinese rural population and suggests that schistosomiasis and dietary factors may contribute to the remarkable geographic variation of colon cancer in China. C1 CHINESE ACAD MED SCI,INST CANC,BEIJING,PEOPLES R CHINA. CHINESE ACAD PREVENT MED,INST NUTR & FOOD HYG,BEIJING,PEOPLES R CHINA. RP GUO, WD (reprint author), NCI,EXECUT PLAZA N,RM 431,BETHESDA,MD 20892, USA. NR 35 TC 22 Z9 22 U1 1 U2 1 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0163-5581 J9 NUTR CANCER JI Nutr. Cancer PY 1993 VL 20 IS 1 BP 13 EP 20 PG 8 WC Oncology; Nutrition & Dietetics SC Oncology; Nutrition & Dietetics GA LQ540 UT WOS:A1993LQ54000002 PM 8415126 ER PT J AU DAUSCH, JG FULLERTON, FR AF DAUSCH, JG FULLERTON, FR TI INCREASED LEVELS OF S-ADENOSYLMETHIONINE IN THE LIVERS OF RATS FED VARIOUS FORMS OF SELENIUM SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL LA English DT Article ID AZO-DYE HEPATOCARCINOGENESIS; DNA METHYLATION; CANCER; 2-ACETYLAMINOFLUORENE; PROTECTION; METHIONINE; TOXICITY AB The levels of S-adenosylmethionine (SAM) were determined in the livers of male weanling rats fed six different forms of selenium for five weeks. The following forms of selenium were administrated in the diet in logarithmic doses: sodium selenite, sodium selenate, sodium selenide, selenomethionine, selenocystine, and selenium sulfide. An overall increase in hepatic SAM was observed, and all compounds resulted in at least one observation where SAM was significantly, elevated (p < 0.01). No dose-response relationship was found to exist, however. A comparison of the relative toxicity of each of the selenicals was based on a dose of 10 ppm dietary selenium for each chemical form. The elevation of SAM resulting from the subchronic administration of selenium may be one mechanism involved in the well-known chemopreventive effects in experimental models. C1 CTR DIS CONTROL,NATL CTR HLTH STAT,HYATTSVILLE,MD. US FDA,NATL CTR TOXICOL RES,JEFFERSON,AR 72079. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 34 TC 3 Z9 3 U1 1 U2 2 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0163-5581 J9 NUTR CANCER JI Nutr. Cancer PY 1993 VL 20 IS 1 BP 31 EP 39 PG 9 WC Oncology; Nutrition & Dietetics SC Oncology; Nutrition & Dietetics GA LQ540 UT WOS:A1993LQ54000004 PM 8415128 ER PT J AU SWANSON, CA GRIDLEY, G GREENBERG, RS SCHOENBERG, JB SWANSON, GM BROWN, LM HAYES, R SILVERMAN, D POTTERN, L AF SWANSON, CA GRIDLEY, G GREENBERG, RS SCHOENBERG, JB SWANSON, GM BROWN, LM HAYES, R SILVERMAN, D POTTERN, L TI A COMPARISON OF DIETS OF BLACKS AND WHITES IN 3 AREAS OF THE UNITED-STATES SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL LA English DT Article ID HEALTH INTERVIEW SURVEY; ESOPHAGEAL CANCER; NUTRIENT INTAKE; LUNG-CANCER; GASTRIC-CANCER; RISK; FOOD; FAT; MEN; QUESTIONNAIRE AB Dietary factors may contribute to the increased cancer risk of blacks. As a first step to explore this hypothesis, we examined food frequency data obtained by interview with 1,976 adults (881 blacks and 1,095 whites) randomly selected from three areas of the United States. The a priori hypothesis was that blacks were more likely to consume diets low in fruits and vegetables and/or high in fat, particularly saturated fat. Contrary to expectation, blacks were more frequent consumers of fruits and vegetables considered to be protective against cancer (e.g., citrus fruits, cruciferous vegetables, and vegetables rich in vitamins A and C). Intake of both total and saturated fat was slightly lower among blacks than whites. This analysis does not rule out a role for these dietary factors in the etiology of cancer but indicates that ascribing the excess cancer risk among blacks to their frequency of fruit and vegetable consumption or intake of fat per se is inadequate. This suggests that alternative dietary explanations for the racial disparity in cancer risk should be pursued in future studies. C1 EMORY UNIV,SCH PUBL HLTH,ATLANTA,GA 30329. NEW JERSEY STATE DEPT HLTH,SPECIAL EPIDEMIOL PROGRAM,TRENTON,NJ 08625. MICHIGAN STATE UNIV,CTR CANC,E LANSING,MI 48824. RP SWANSON, CA (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,6130 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 39 TC 38 Z9 38 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0163-5581 J9 NUTR CANCER JI Nutr. Cancer PY 1993 VL 20 IS 2 BP 153 EP 165 PG 13 WC Oncology; Nutrition & Dietetics SC Oncology; Nutrition & Dietetics GA LW485 UT WOS:A1993LW48500007 PM 8233981 ER PT J AU RAO, GN HASEMAN, JK AF RAO, GN HASEMAN, JK TI INFLUENCE OF CORN-OIL AND DIET ON BODY-WEIGHT, SURVIVAL, AND TUMOR INCIDENCES IN F344/N RATS SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL LA English DT Article ID NATIONAL-CANCER-INSTITUTE; ESSENTIAL FATTY-ACID; B6C3F1 MICE; CARCINOGENESIS; GROWTH; RESTRICTION; PANCREAS; LESIONS; HISTORY; PROGRAM AB Amount and type of fat and energy density of diets may influence tumor incidences. The purpose of this report is to summarize the influence of com oil gavage and different nonpurified diets on spontaneous tumor incidences in 64 diet and 59 corn oil gavage control groups in two-year studies involving approximately 6, 100 control Fischer 344 rats of each sex. The maximum mean body weight attained during the course of the study, survival at 106 weeks of age, and spontaneous tumor incidences of groups fed different nonpurified diets with or without corn oil gavage were summarized and evaluated for differences. Male rats fed NIH-07 open-formula diet with or without corn oil gavage had significantly higher body weight, lower survival, and higher incidence of pancreatic acinar cell tumors than rats fed commercial proprietary diets with or without corn oil gavage. Female rats fed NIH-07 diet with or without corn oil gavage had significantly higher body weights and pancreatic tumor incidences than groups fed commercial diets. Time-related trends could account for other apparent differences in tumor incidences between the groups fed commercial and NIH-07 diets. Corn oil gavage significantly increased the body weight and pancreatic tumor incidences but decreased the incidence of leukemia, a lethal tumor, which resulted in higher survival in male rats. Corn oil gavage significantly lowered the body weight and anterior pituitary tumor incidence in female rats. The pancreatic acinar cell tumor incidence appears to be due to a combination of fat intake and body weight. C1 NIEHS,DIV BIOMETRY & RISK ASSESSMENT,RES TRIANGLE PK,NC 27709. RP RAO, GN (reprint author), NIEHS,NATL TOXICOL PROGRAM,DIV TOXICOL RES & TESTING,MD OA-01,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 27 TC 18 Z9 18 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0163-5581 J9 NUTR CANCER JI Nutr. Cancer PY 1993 VL 19 IS 1 BP 21 EP 30 PG 10 WC Oncology; Nutrition & Dietetics SC Oncology; Nutrition & Dietetics GA KU904 UT WOS:A1993KU90400003 PM 8446512 ER PT S AU LEVINE, M CANTILENA, CC DHARIWAL, KR AF LEVINE, M CANTILENA, CC DHARIWAL, KR BE Simopoulos, AP TI INSITU KINETICS AND ASCORBIC-ACID REQUIREMENTS SO NUTRITION AND FITNESS IN HEALTH AND DISEASE SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 2ND INTERNATIONAL CONF ON NUTRITION AND FITNESS CY MAY 23-25, 1992 CL ATHENS, GREECE SP INT OLYMP ACAD, MINIST CULTURE, FAO, WHO, GEN SECRETARIAT ATHLETICS GREECE, PRESIDENTS COUNCIL PHYS FITNESS & SPORTS, PAN AMER HLTH ORG, NICHHD, HELLENIC PHARM ASSOC, INT UNION NUTR SCI, AMER ASSOC WORLD HLTH RP LEVINE, M (reprint author), NIDDKD,CELL BIOL & GENET LAB,BLDG 8,ROOM 415,BETHESDA,MD 20892, USA. NR 0 TC 19 Z9 20 U1 0 U2 0 PU KARGER PI BASEL PA BASEL SN 0084-2230 BN 3-8055-5706-X J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1993 VL 72 BP 114 EP 127 PG 14 WC Cardiac & Cardiovascular Systems; Nutrition & Dietetics; Physiology SC Cardiovascular System & Cardiology; Nutrition & Dietetics; Physiology GA BY28Y UT WOS:A1993BY28Y00011 PM 8506699 ER PT S AU SALEM, N WARD, GR AF SALEM, N WARD, GR BE Simopoulos, AP TI ARE OMEGA-3-FATTY-ACIDS ESSENTIAL NUTRIENTS FOR MAMMALS SO NUTRITION AND FITNESS IN HEALTH AND DISEASE SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 2ND INTERNATIONAL CONF ON NUTRITION AND FITNESS CY MAY 23-25, 1992 CL ATHENS, GREECE SP INT OLYMP ACAD, MINIST CULTURE, FAO, WHO, GEN SECRETARIAT ATHLETICS GREECE, PRESIDENTS COUNCIL PHYS FITNESS & SPORTS, PAN AMER HLTH ORG, NICHHD, HELLENIC PHARM ASSOC, INT UNION NUTR SCI, AMER ASSOC WORLD HLTH RP SALEM, N (reprint author), NIAAA,ADAMHA,DICBR,MEMBRANE BIOCHEM & BIOPHYS LAB,10-3C103,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 44 Z9 45 U1 0 U2 2 PU KARGER PI BASEL PA BASEL SN 0084-2230 BN 3-8055-5706-X J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1993 VL 72 BP 128 EP 147 PG 20 WC Cardiac & Cardiovascular Systems; Nutrition & Dietetics; Physiology SC Cardiovascular System & Cardiology; Nutrition & Dietetics; Physiology GA BY28Y UT WOS:A1993BY28Y00012 PM 8506700 ER PT J AU DEBRITTON, RC HILDESHEIM, A DELAO, SL BRINTON, LA SATHYA, P REEVES, WC AF DEBRITTON, RC HILDESHEIM, A DELAO, SL BRINTON, LA SATHYA, P REEVES, WC TI HUMAN PAPILLOMAVIRUSES AND OTHER INFLUENCES ON SURVIVAL FROM CERVICAL-CANCER IN PANAMA SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID PROGNOSTIC-SIGNIFICANCE; DNA; ASSOCIATION; CARCINOMA; P53; EPIDEMIOLOGY; TYPE-16 AB Objective: To determine the influence on survival from cervical cancer of human papillomaviruses (HPVs) and other factors including age, herpes simplex virus type 2 (HSV-2) antibody status, and number of pregnancies. Methods: We followed 196 women diagnosed with invasive cervical cancer in Panama for an average of 32 months. Clinical and risk-factor information was obtained from these women through an interview and review of medical records. We assessed HPV DNA status by testing tumor specimens using polymerase chain reaction, Southern blot, and slot blot techniques. Kaplan-Meier survival curves and Cox proportional hazards model were used to assess the risk of mortality associated with selected variables. Results: Eighty-one percent (N = 144) of the women tested for HPV were positive. Absence of HPV DNA was associated with a 1.9-fold excess risk of mortality (95% confidence interval [CI] 1.1-3.3) after controlling for age, clinical stage at diagnosis, number of pregnancies, and HSV-2 seropositivity. Women diagnosed with cervical cancer before the age of 30 had a ninefold excess risk of dying compared with those diagnosed at age 50 or older (relative risk [RR] 9.3, 95% CI 3.4-25.5). Parity was also an independent prognostic factor. Women with six or more pregnancies had a 2.5-fold excess risk of dying compared with women with three or fewer (95% CI 1.2-5.3). Years of education, presence of HSV-2 antibodies, age at first intercourse, number of sexual partners, oral contraceptive use, and cigarette smoking were not significantly associated with prognosis. Conclusion: These findings suggest that women negative for HPV DNA, those who are diagnosed at an early age, and those who have multiple pregnancies might have more aggressive tumors. C1 NCI,ENVIRONM EPIDEMIOL BRANCH,6130 EXECUT BLVD,EPN ROOM 443,BETHESDA,MD 20892. MCMASTER UNIV,DEPT PATHOL,MOLEC VIROL & IMMUNOL PROGRAM,HAMILTON L8S 4L8,ONTARIO,CANADA. NATL ONCOL INST,PANAMA CITY,PANAMA. SMITHSONIAN INST,PANAMA CITY,PANAMA. NATL CTR DIS CONTROL,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIAL DIS,ATLANTA,GA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 FU NCI NIH HHS [1R01-CA-42042] NR 22 TC 40 Z9 40 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD JAN PY 1993 VL 81 IS 1 BP 19 EP 24 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KE011 UT WOS:A1993KE01100004 PM 8380103 ER PT J AU STEPHENS, EV KALINEC, G BRANN, MR GUTKIND, JS AF STEPHENS, EV KALINEC, G BRANN, MR GUTKIND, JS TI TRANSFORMING G-PROTEIN-COUPLED RECEPTORS TRANSDUCE POTENT MITOGENIC SIGNALS IN NIH 3T3 CELLS INDEPENDENT ON CAMP INHIBITION OR CONVENTIONAL PROTEIN-KINASE-C SO ONCOGENE LA English DT Article ID MUSCARINIC ACETYLCHOLINE-RECEPTORS; STIMULATES DNA-SYNTHESIS; GROWTH-FACTOR RECEPTOR; S PHASE PROGRESSION; A9 L-CELLS; PERSISTENT ACTIVATION; HAMSTER FIBROBLASTS; CARBACHOL ACTION; PHORBOL ESTERS; EXPRESSION AB We have used the expression of human acetylcholine muscarinic receptor (mAChR) genes in NIH 3T3 cells as a model for dissecting the molecular basis of cellular transformation induced by G protein-coupled receptors. Those mAChR subtypes efficiently coupled to PIP, hydrolysis (m1, m3 and m5) induced agonist-dependent celt transformation whereas those inhibiting adenylyl cyclase (m2, m4) lack transforming activity. In the present study, we demonstrate that in cells expressing ml but not m2 mAChRs the cholinergic agonist (carbachol) is alone as potent a stimulant for DNA synthesis as platelet-derived growth factor (PDGF) or serum. Furthermore, induction of DNA synthesis is shown to correlate with activation of PIP, hydrolysis but not with inhibition of adenylyl cyclase. We also examined the rote of protein kinase C (PKC) in mitogenic signalling through ml mAChRs, and found that NIH 3T3 cells express PKC-alpha and PCK-zeta as the only conventional or Ca2+-independent PKC isozyme, respectively. Prolonged treatment with TPA depleted cells of PKC-alpha but not of PKC-zeta. In TPA-treated NIH 3T3 celts, the mitogenic response to a subsequent stimulation with TPA was absolutely abolished, but the response to PDGF or serum was not. Moreover, PKC depletion did not decrease DNA synthesis induced by carbachol. We conclude that carbachol potently induces reinitiation of DNA synthesis through the activation of transforming mAChR subtypes, independently of inhibition of adenylyl cyclase and conventional PKCs. C1 NIDR,MOLEC SIGNALING GRP,CELLULAR REV & ONCOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. UNIV VERMONT,COLL MED,DEPT PSYCHIAT,NEUROSCI RES UNIT,BURLINGTON,VT 05405. RI Gutkind, J. Silvio/A-1053-2009 NR 46 TC 37 Z9 37 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN PY 1993 VL 8 IS 1 BP 19 EP 26 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN005 UT WOS:A1993KN00500003 PM 8380916 ER PT J AU SUN, Y COLBURN, NH OBERLEY, LW AF SUN, Y COLBURN, NH OBERLEY, LW TI DECREASED EXPRESSION OF MANGANESE SUPEROXIDE-DISMUTASE MESSENGER-RNA AND PROTEIN AFTER IMMORTALIZATION AND TRANSFORMATION OF MOUSE-LIVER CELLS SO ONCOLOGY RESEARCH LA English DT Article ID GENE; FIBROBLASTS; CARCINOMA; SEQUENCE; MYC AB Altered levels of superoxide dismutase (SOD), the enzyme that scavenges toxic superoxide anion produced during normal metabolism or after oxidative insult, have been implicated in multistage carcinogenesis of both rodents and humans. Using a mouse liver cell model, we report here that after cellular immortalization, both copper- and zinc-containing superoxide dismutase (Cu,ZnSOD) and manganese superoxide dismutase (MnSOD) activities decreased dramatically and that cellular transformation further decreased MnSOD but not Cu,ZnSOD activity. Decreased enzyme activities seen in transformed cells (Tx) were due to decreased amounts of immunoreactive enzyme protein that results from decreased superoxide dismutase mRNA expression. This downregulation of gene expression may occur at the transcriptional level, as suggested by results with cycloheximide (Chx) and actinomycin D (AcD) treatments. C1 UNIV IOWA,RADIAT RES LAB,IOWA CITY,IA 52242. RP SUN, Y (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701, USA. FU NCI NIH HHS [CA-41267] NR 32 TC 19 Z9 22 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0965-0407 J9 ONCOL RES JI Oncol. Res. PY 1993 VL 5 IS 3 BP 127 EP 132 PG 6 WC Oncology SC Oncology GA MB031 UT WOS:A1993MB03100003 PM 8260749 ER PT J AU AUGUST, EM DUNCAN, KLK MALINOWSKI, NM CYSYK, RL AF AUGUST, EM DUNCAN, KLK MALINOWSKI, NM CYSYK, RL TI INHIBITION OF FIBROBLAST HYALURONIC-ACID PRODUCTION BY SURAMIN SO ONCOLOGY RESEARCH LA English DT Article ID FACTOR RECEPTOR-BINDING; HTLV-III/LAV INFECTION; PROTEIN KINASE-C; GROWTH-FACTOR; PROSTATE-CANCER; REVERSE-TRANSCRIPTASE; POTENT INHIBITOR; TUMOR INVASION; CELLS; INVIVO AB Hyaluronic acid (HA) is an extracellular matrix glycosaminoglycan localized in the stroma of solid tumors, where it facilitates cell movement and thus tumor invasion and metastasis. This localization of HA is due to its synthesis by stromal fibroblasts in response to paracrine factors produced by the tumor. Such tumor-stromal interactions have been shown to be crucial to the development and progression of prostate cancer. Suramin is an effective antitumor agent in hormone-refractory prostate cancer, but its mechanism(s) of action is not well understood. However, the properties of suramin as an agent which disrupts growth factor action, and the importance of tumor-stroma interactions in prostate tumor development and in HA synthesis led us to study the effect of suramin on HA synthesis. Suramin inhibited HA synthesis by calf serum-stimulated Swiss 3T3 fibroblasts at clinically relevant concentrations (IC50 = 183 mu g/mL). Increasing the serum concentration from 10 to 20% did not change the IC50 for HA synthesis, but increased the IC50 for [H-3]thymidine incorporation from 206 to 342 mu g/mL, indicating that the antiproliferative effect of suramin can be dissociated from its effect on HA synthesis. Suramin did not alter the cellular concentrations of the two precursors for HA synthesis (UDP-glucuronic acid and UDP-N-acetylglucosamine) at early time points and did not inhibit the HA synthetase activity of isolated membranes at concentrations up to 800 mu g/mL. However, suramin treatment abolished the rise in HA synthetase activity that follows the serum stimulation of quiescent 3T3 fibroblasts in a concentration-dependent fashion, indicating an effect of suramin on the signal transduction pathways involved in the regulation of HA synthesis. These data suggest that one mechanism responsible for suramin's antitumor effect is to block tumor-associated HA synthesis, which is a component of tumor progression. RP AUGUST, EM (reprint author), NCI,DIV CANC TREATMENT,MED CHEM LAB,DEV THERAPEUT PROGRAM,9000 ROCKVILLE PIKE,BLDG 37,ROOM 5E10,BETHESDA,MD 20892, USA. RI Duncan, Kimberly /C-3655-2013 NR 38 TC 6 Z9 6 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0965-0407 J9 ONCOL RES JI Oncol. Res. PY 1993 VL 5 IS 10-11 BP 415 EP 422 PG 8 WC Oncology SC Oncology GA NL501 UT WOS:A1993NL50100003 PM 8054702 ER PT J AU HEYSE, SP AF HEYSE, SP TI EPIDEMIOLOGY OF HIP-FRACTURES IN THE ELDERLY - A CROSS-NATIONAL ANALYSIS OF MORTALITY-RATES FOR FEMORAL-NECK FRACTURES SO OSTEOPOROSIS INTERNATIONAL LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON OSTEOPOROSIS CY NOV 05-07, 1991 CL KOBE, JAPAN RP HEYSE, SP (reprint author), NIAMSD,OFF PREVENT EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD, USA. NR 6 TC 2 Z9 2 U1 0 U2 0 PU SPRINGER-VERLAG LONDON LTD PI GODALMING PA SWEETAPPLE HOUSE CATTESHALL ROAD, GODALMING, SURREY, ENGLAND GU7 3DJ SN 0937-941X J9 OSTEOPOROSIS INT JI Osteoporosis Int. PY 1993 VL 3 SU 1 BP S16 EP S19 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KP881 UT WOS:A1993KP88100004 ER PT J AU OPARA, EC GO, VLW AF OPARA, EC GO, VLW TI DUAL EFFECTS OF GASTRIC-INHIBITORY POLYPEPTIDE ON INSULIN-SECRETION SO PANCREAS LA English DT Article DE INCRETIN; PANCREATIC HORMONE RELEASE; STIMULATION; SUPPRESSION ID GLUCAGON; GLUCOSE; GIP; CHOLECYSTOKININ; INCRETIN; RELEASE; CELLS; ACIDS AB The role of gastric inhibitory polypeptide (GIP) on insulin secretion in the presence of different glucose concentrations has been studied in perifused microdissected murine islets. Insulin secretion was concentration dependent in the presence of glucose alone: Switching the perifusion buffer from 5.5 to 11.1 and 22.2 mM glucose caused an increase in insulin response assessed as the total integrated area under the curve over a 20-min period (6.4 +/- 0.48 and 12.1 +/- 0.58 ng, respectively; p < 0.01, n = 6). If 11.1 mM glucose perifusion in the presence of GIP was preceded by 5.5 mM glucose alone, the integrated insulin secretion/20 min above basal level was attenuated (1.46 +/- 0.10 vs. 0.37 +/- 0.03 ng; p < 0.01, n = 6), and withdrawal of GIP from the perifusion buffer resulted in the restoration of 11.1 mM glucose-stimulated insulin secretion (1.46 +/- 0.10 vs. 1.98 +/- 0.12 ng). If islets were continuously perifused with 11.1 mM glucose, the addition of GIP did not alter insulin secretion. In contrast, the addition of GIP to 22.2 mM glucose perifusion buffer further enhanced the high glucose-induced insulin secretion above basal (12.1 +/- 0.58 vs. 14.5 +/- 0.84 ng; p < 0.05, n = 6). These observations are consistent with a hypothesis that during a low glucose condition, GIP prevents the risk of hypoglycemia by suppressing insulin secretion, while during a high glucose load, glucose-induced insulin stimulation is potentiated by GIP, presumably to prevent hyperglycemia. C1 NIDKD, CELL BIOL & GENET LAB, BETHESDA, MD USA. UNIV CALIF LOS ANGELES, DEPT MED, LOS ANGELES, CA USA. NR 22 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0885-3177 J9 PANCREAS JI Pancreas PD JAN PY 1993 VL 8 IS 1 BP 39 EP 43 DI 10.1097/00006676-199301000-00009 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KH837 UT WOS:A1993KH83700008 PM 8419907 ER PT J AU BOSCHERO, AC TOMBACCINI, D CARNEIRO, EM ATWATER, IJ AF BOSCHERO, AC TOMBACCINI, D CARNEIRO, EM ATWATER, IJ TI DIFFERENCES IN K+ PERMEABILITY BETWEEN CULTURED ADULT AND NEONATAL RAT ISLETS OF LANGERHANS IN RESPONSE TO GLUCOSE, TOLBUTAMIDE, DIAZOXIDE, AND THEOPHYLLINE SO PANCREAS LA English DT Article DE ADULT AND NEONATAL CULTURED RAT ISLETS; GLUCOSE; K+ PERMEABILITY; RB-86 EFFLUX; SULFONYLUREAS; THEOPHYLLINE ID PANCREATIC BETA-CELLS; INDUCED INSULIN RELEASE; PROTEIN KINASE-C; B-CELLS; SECRETORY RESPONSE; NET UPTAKE; CHANNELS; ATP; STIMULATION; EFFLUX AB The effects of glucose, tolbutamide, and diazoxide on K+ permeability in neonatal and adult rat pancreatic islets, maintained in culture 1 week, were investigated by measuring the Rb-86 outflow rate from prelabeled islets. In the absence of glucose, the Rb-86 efflux was significantly lower in neonatal than adult islets. Raising the glucose concentration to 2.8, 5.6, 8.3, and 11.1 mM produced a marked reduction in the Rb-86 efflux in adult islets but only a minor reduction in neonatal islets. The effect of tolbutamide to reduce, and diazoxide to increase, the Rb-86 efflux was also less in neonatal islets. These results are discussed with respect to previously reported differences in insulin secretion from neonatal and adult islets in culture. C1 NIDDK,CELL BIOL & GENET LAB,BLDG 8,RM 326,BETHESDA,MD. UNICAMP,DEPT FISIOL & BIOFIS 1,CAMPINAS,BRAZIL. RI Carneiro, Everardo /D-4758-2012; Boschero, Antonio/O-7525-2014 OI Boschero, Antonio/0000-0003-3829-8570 NR 32 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0885-3177 J9 PANCREAS JI Pancreas PD JAN PY 1993 VL 8 IS 1 BP 44 EP 49 DI 10.1097/00006676-199301000-00010 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KH837 UT WOS:A1993KH83700009 PM 8419908 ER PT J AU ZIERDT, CH AF ZIERDT, CH TI TAXONOMIC STATUS OF BLASTOCYSTIS-HOMINIS - REPLY SO PARASITOLOGY TODAY LA English DT Letter RP ZIERDT, CH (reprint author), NIH,DEPT CLIN PATHOL,MICROBIOL SERV,BLDG 10,ROOM 2C-343,BETHESDA,MD 20892, USA. NR 4 TC 6 Z9 7 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0169-4758 J9 PARASITOL TODAY JI Parasitol. Today PD JAN PY 1993 VL 9 IS 1 BP 18 EP 18 DI 10.1016/0169-4758(93)90157-B PG 1 WC Parasitology SC Parasitology GA KE322 UT WOS:A1993KE32200008 PM 15463657 ER PT B AU CHIUEH, CC MIYAKE, H PENG, MT AF CHIUEH, CC MIYAKE, H PENG, MT BE Narabayashi, H Nagatsu, T Yanagisawa, N Mizuno, Y TI ROLE OF DOPAMINE AUTOXIDATION, HYDROXYL RADICAL GENERATION, AND CALCIUM OVERLOAD IN UNDERLYING MECHANISMS INVOLVED IN MPTP-INDUCED PARKINSONISM SO PARKINSONS DISEASE : FROM BASIC RESEARCH TO TREATMENT SE ADVANCES IN NEUROLOGY LA English DT Proceedings Paper CT 10TH INTERNATIONAL SYMP ON PARKINSONS DISEASE CY OCT 27-30, 1991 CL TOKYO, JAPAN SP WORLD FEDERAT NEUROL, RES COMM EXTRAPYRAMIDAL DIS, JAPAN INTRACTABLE DIS RES FDN RP CHIUEH, CC (reprint author), NIMH,BLDG 10,RM 3D-41,BETHESDA,MD 20892, USA. NR 0 TC 165 Z9 165 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-967-4 J9 ADV NEUROL JI Adv.Neurol. PY 1993 VL 60 BP 251 EP 258 PG 8 WC Biochemistry & Molecular Biology; Clinical Neurology; Pathology; Physiology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pathology; Physiology GA BX37W UT WOS:A1993BX37W00037 PM 8380519 ER PT B AU UHL, GR KITAYAMA, S AF UHL, GR KITAYAMA, S BE Narabayashi, H Nagatsu, T Yanagisawa, N Mizuno, Y TI A CLONED DOPAMINE TRANSPORTER - POTENTIAL INSIGHTS INTO PARKINSONS-DISEASE PATHOGENESIS SO PARKINSONS DISEASE : FROM BASIC RESEARCH TO TREATMENT SE ADVANCES IN NEUROLOGY LA English DT Proceedings Paper CT 10TH INTERNATIONAL SYMP ON PARKINSONS DISEASE CY OCT 27-30, 1991 CL TOKYO, JAPAN SP WORLD FEDERAT NEUROL, RES COMM EXTRAPYRAMIDAL DIS, JAPAN INTRACTABLE DIS RES FDN RP UHL, GR (reprint author), NIDA,ADDICT RES CTR,MOLEC NEUROBIOL LAB,BOX 5180,BALTIMORE,MD 21224, USA. NR 0 TC 27 Z9 27 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-967-4 J9 ADV NEUROL JI Adv.Neurol. PY 1993 VL 60 BP 321 EP 324 PG 4 WC Biochemistry & Molecular Biology; Clinical Neurology; Pathology; Physiology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pathology; Physiology GA BX37W UT WOS:A1993BX37W00048 PM 8380524 ER PT S AU SHEARER, WT ROSENBLATT, HM SCHLUCHTER, MD MOFENSON, LM DENNY, TN WILLOUGHBY, A NUGENT, R MOYE, J BERENDES, HW RIGAPEREZ, JG DURAKO, S JORDAN, C HIRSCHHORN, R BETHEL, J SHAH, K CHOW, J EDELSON, P SANDERS, D BONAGURA, V VALACER, D HENLEY, W BAMJI, M GUPTA, A LI, KI ABRAMS, EJ FIKRIG, S BAKSHI, SS PAHWA, S KRASINSKI, K PITT, J BERNSTEIN, L RUBINSTEIN, A JOHNSON, G COOPER, ER FRENKEL, L LISCHNER, HW RAPHAEL, SA JOHNSON, JP RAKUSAN, T NESHEIM, S NAHMIAS, A KEYSERLING, H YOGEV, R CHADWICK, E RICH, K GUERRAHANSON, IC PETRU, A DIAZ, C SANTINI, JLC JIMENEZ, E GARCIATRIAS, E ACANTILADO, C SCHWARTZ, R PEAVY, HH KALICA, A KASTENSPORTES, C VRIEM, C WEINSTEIN, C WU, MC BOYETT, J MOODIE, D BECK, G BAETZGREENWALT, B EASLEY, K GOLDFARB, J GRAGG, L MCHUGH, M MEHTA, A MEZIANE, M STERBA, R HOUSER, H MARTIN, R AYERS, N BAKER, C BRICKER, T DEMMLER, G DOYLE, M DYSON, M GARSON, A GONIK, B HAMMILL, H HANSEN, TN HANSON, IC HIATT, P HOOTS, K JACOBSON, R KEARNEY, D KLINE, MW KOZINETZ, C LANGSTON, C LAPIN, C LUDOMIRSKY, A MOORE, W PICKERING, L SINGLETON, E TABER, L LIPSHULTZ, S CLEVELAND, R COLAN, S COLIN, A COOPER, E CRANLEY, W MCINTOSH, K ORAV, EJ PEREZATAYDE, A PELTON, S SANDERS, S STEINBACH, S TREVES, ST TUOMALA, R WOHL, MEB KATTAN, M DISCHE, R FYFE, B HEATON, S ROSEN, J SPERLING, R BIERMAN, F MELLINS, R ALDERSON, P BERDON, WE FLEISHMAN, W GERSONY, W KOUMBOURLIS, AC LARUSSA, P MARBOE, C MILLER, R QUITTELL, LM STARC, T KAPLAN, S ALKHATIB, Y BOECHAT, I BOYER, P BRYSON, Y CHEN, D DOROSHOW, R ELASHOFF, R GARG, M HAWKINS, R HOHN, A KOVACS, A PLATZKER, A SETTLAGE, R WILLIAMS, R WOO, M WOOD, BP SUMAYA, CV JENSON, H AF SHEARER, WT ROSENBLATT, HM SCHLUCHTER, MD MOFENSON, LM DENNY, TN WILLOUGHBY, A NUGENT, R MOYE, J BERENDES, HW RIGAPEREZ, JG DURAKO, S JORDAN, C HIRSCHHORN, R BETHEL, J SHAH, K CHOW, J EDELSON, P SANDERS, D BONAGURA, V VALACER, D HENLEY, W BAMJI, M GUPTA, A LI, KI ABRAMS, EJ FIKRIG, S BAKSHI, SS PAHWA, S KRASINSKI, K PITT, J BERNSTEIN, L RUBINSTEIN, A JOHNSON, G COOPER, ER FRENKEL, L LISCHNER, HW RAPHAEL, SA JOHNSON, JP RAKUSAN, T NESHEIM, S NAHMIAS, A KEYSERLING, H YOGEV, R CHADWICK, E RICH, K GUERRAHANSON, IC PETRU, A DIAZ, C SANTINI, JLC JIMENEZ, E GARCIATRIAS, E ACANTILADO, C SCHWARTZ, R PEAVY, HH KALICA, A KASTENSPORTES, C VRIEM, C WEINSTEIN, C WU, MC BOYETT, J MOODIE, D BECK, G BAETZGREENWALT, B EASLEY, K GOLDFARB, J GRAGG, L MCHUGH, M MEHTA, A MEZIANE, M STERBA, R HOUSER, H MARTIN, R AYERS, N BAKER, C BRICKER, T DEMMLER, G DOYLE, M DYSON, M GARSON, A GONIK, B HAMMILL, H HANSEN, TN HANSON, IC HIATT, P HOOTS, K JACOBSON, R KEARNEY, D KLINE, MW KOZINETZ, C LANGSTON, C LAPIN, C LUDOMIRSKY, A MOORE, W PICKERING, L SINGLETON, E TABER, L LIPSHULTZ, S CLEVELAND, R COLAN, S COLIN, A COOPER, E CRANLEY, W MCINTOSH, K ORAV, EJ PEREZATAYDE, A PELTON, S SANDERS, S STEINBACH, S TREVES, ST TUOMALA, R WOHL, MEB KATTAN, M DISCHE, R FYFE, B HEATON, S ROSEN, J SPERLING, R BIERMAN, F MELLINS, R ALDERSON, P BERDON, WE FLEISHMAN, W GERSONY, W KOUMBOURLIS, AC LARUSSA, P MARBOE, C MILLER, R QUITTELL, LM STARC, T KAPLAN, S ALKHATIB, Y BOECHAT, I BOYER, P BRYSON, Y CHEN, D DOROSHOW, R ELASHOFF, R GARG, M HAWKINS, R HOHN, A KOVACS, A PLATZKER, A SETTLAGE, R WILLIAMS, R WOO, M WOOD, BP SUMAYA, CV JENSON, H BE Lyman, WD Rubinstein, A TI IMMUNOLOGICAL TARGETS OF HIV-INFECTION - T-CELLS SO PEDIATRIC AIDS: CLINICAL, PATHOLOGIC, AND BASIC SCIENCE PERSPECTIVES SE Annals of the New York Academy of Sciences LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; LYMPHOCYTE SUBSETS; MONOCLONAL-ANTIBODIES; HEALTHY-CHILDREN; IMMUNOGLOBULIN; TYPE-1; DEATH; RISK C1 UNIV TEXAS, BAYLOR COLL MED, SCH MED, DEPT PEDIAT, HOUSTON, TX 77030 USA. BAYLOR COLL MED, DEPT MICROBIOL, HOUSTON, TX 77030 USA. BAYLOR COLL MED, DEPT IMMUNOL, HOUSTON, TX 77030 USA. CLEVELAND CLIN FDN, DEPT BIOSTAT EPIDEMIOL, CLEVELAND, OH 44195 USA. NICHHD, ROCKVILLE, MD 20892 USA. UNIV MED & DENT NEW JERSEY, DEPT PEDIAT, NEWARK, NJ 07103 USA. CHILDRENS HOSP NEW JERSEY, NEWARK, NJ 07103 USA. NICHHD, PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH, BETHESDA, MD USA. NICHHD, DIV PREVENT RES, BETHESDA, MD 20892 USA. WESTAT CORP, ROCKVILLE, MD USA. LINCOLN HOSP CTR, BRONX, NY USA. NEW YORK HOSP, CORNELL MED CTR, NEW YORK, NY USA. SCHNEIDER CHILDRENS HOSP, LONG ISL JEWISH MED CTR, QUEENS HOSP CTR, NEW HYDE PK, NY 11042 USA. BETH ISRAEL MED CTR, NEW YORK, NY USA. METROPOLITAN HOSP CTR, NEW YORK, NY USA. NEW YORK MED COLL, VALHALLA, NY USA. HARLEM HOSP MED CTR, NEW YORK, NY USA. SUNY HLTH SCI CTR, BROOKLYN, NY USA. ST LUKES ROOSEVELT HOSP, NEW YORK, NY USA. N SHORE UNIV HOSP, MANHASSET, NY USA. NYU, BELLEVUE HOSP CTR, MED CTR, NEW YORK, NY 10016 USA. BABIES HOSP, NEW YORK, NY USA. ALBERT EINSTEIN COLL MED, BRONX, NY USA. UNIV CONNECTICUT, CTR HLTH, HARTFORD, CT USA. BOSTON CITY HOSP, BOSTON, MA USA. UNIV MED & DENT NEW JERSEY, ROBERT WOOD JOHNSON MED SCH, NEW BRUNSWICK, NJ USA. ST CHRISTOPHERS HOSP, PHILADELPHIA, PA USA. UNIV MARYLAND, BALTIMORE, MD USA. CHILDRENS HOSP, NATL MED CTR, WASHINGTON, DC 20010 USA. EMORY UNIV, SCH MED, ATLANTA, GA USA. CHILDRENS MEM HOSP, CHICAGO, IL USA. UNIV ILLINOIS, COLL MED, CHICAGO, IL USA. CHILDRENS HOSP, MED CTR, OAKLAND, CA USA. UNIV PUERTO RICO, SAN JUAN, PR USA. SAN JUAN CITY HOSP, SAN JUAN, PR USA. RAMON RUIZ ARNAU UNIV HOSP, BAYAMON, PR USA. MILES INC, CUTTER BIOL, BERKELEY, CA 94701 USA. NHLBI, BETHESDA, MD USA. CASE WESTERN RESERVE UNIV, CLEVELAND, OH USA. HARVARD UNIV, CHILDRENS HOSP, SCH MED, BOSTON, MA 02115 USA. MT SINAI SCH MED, NEW YORK, NY USA. COLUMBIA UNIV, PRESBYTERIAN HOSP CITY NEW YORK, NEW YORK, NY USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. UNIV TEXAS, HLTH SCI CTR, SAN ANTONIO, TX USA. RP SHEARER, WT (reprint author), TEXAS CHILDRENS HOSP, DEPT ALLERGY & IMMUNOL, 6221 FANNIN, MS 1-3291, HOUSTON, TX 77030 USA. OI Denny, Thomas/0000-0002-7364-8276 FU NHLBI NIH HHS [HR-96040]; NIAID NIH HHS [AI-27551]; NICHD NIH HHS [HD-26603] NR 34 TC 11 Z9 11 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-792-1; 0-89766-791-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 693 BP 35 EP 51 DI 10.1111/j.1749-6632.1993.tb26255.x PG 17 WC Immunology; Multidisciplinary Sciences; Pathology; Pediatrics; Virology SC Immunology; Science & Technology - Other Topics; Pathology; Pediatrics; Virology GA BZ45X UT WOS:A1993BZ45X00006 PM 7903519 ER PT S AU KAIRAM, R KLINE, J LEVIN, B BRAMBILLA, D COULTER, D KUBAN, K LANSKY, L MARSHALL, P VELEZBORRAS, J RODRIGUEZ, E AF KAIRAM, R KLINE, J LEVIN, B BRAMBILLA, D COULTER, D KUBAN, K LANSKY, L MARSHALL, P VELEZBORRAS, J RODRIGUEZ, E BE Lyman, WD Rubinstein, A TI RELIABILITY OF NEUROLOGIC ASSESSMENT IN A COLLABORATIVE STUDY OF HIV-INFECTION IN CHILDREN SO PEDIATRIC AIDS: CLINICAL, PATHOLOGIC, AND BASIC SCIENCE PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Pediatric Aids: Clinical, Pathologic, and Basic Science Perspectives CY NOV 18-21, 1992 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID AGREEMENT C1 COLUMBIA UNIV,NEW YORK,NY 10025. NEW YORK STATE PSYCHIAT INST & HOSP,NEW YORK,NY. NEW ENGLAND RES INST,WATERTOWN,MA. BOSTON UNIV,SCH MED,BOSTON,MA 02118. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. CHILDRENS MEM HOSP,CHICAGO,IL. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA. UNIV PUERTO RICO,SAN JUAN,PR. NIAID,BETHESDA,MD. RP KAIRAM, R (reprint author), ST LUKES ROOSEVELT HOSP,NEW YORK,NY 10025, USA. FU NIAID NIH HHS [N0I-AI-8507, N0I-AI-82506, N0I-AI-05072] NR 17 TC 3 Z9 3 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-791-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 693 BP 123 EP 140 DI 10.1111/j.1749-6632.1993.tb26261.x PG 18 WC Immunology; Multidisciplinary Sciences; Pathology; Pediatrics; Virology SC Immunology; Science & Technology - Other Topics; Pathology; Pediatrics; Virology GA BZ45X UT WOS:A1993BZ45X00012 PM 8267257 ER PT S AU EIDEN, LE RAUSCH, DM DACUNHA, A MURRAY, EA HEYES, M SHARER, L NOHR, D WEIHE, E AF EIDEN, LE RAUSCH, DM DACUNHA, A MURRAY, EA HEYES, M SHARER, L NOHR, D WEIHE, E BE Lyman, WD Rubinstein, A TI AIDS AND THE CENTRAL-NERVOUS-SYSTEM - EXAMINING PATHOBIOLOGY AND TESTING THERAPEUTIC STRATEGIES IN THE SIV-INFECTED RHESUS-MONKEY SO PEDIATRIC AIDS: CLINICAL, PATHOLOGIC, AND BASIC SCIENCE PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Pediatric Aids: Clinical, Pathologic, and Basic Science Perspectives CY NOV 18-21, 1992 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-DEFICIENCY SYNDROME; FLUID QUINOLINIC ACID; BLOOD-BRAIN-BARRIER; CEREBROSPINAL-FLUID; HIV-INFECTION; HTLV-III; NEUROLOGIC SYNDROMES; NEOCORTICAL DAMAGE; DEMENTIA COMPLEX C1 NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. UMD,NEW JERSEY MED SCH,DEPT LAB MED & PATHOL,NEWARK,NJ 07103. JOHANNES GUTENBERG UNIV,DEPT ANAT,MAINZ,GERMANY. RP EIDEN, LE (reprint author), NIMH,CELL BIOL LAB,MOLEC NEUROSCI SECT,BLDG 36,ROOM 3A-17,BETHESDA,MD 20892, USA. NR 62 TC 5 Z9 5 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-791-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 693 BP 229 EP 244 DI 10.1111/j.1749-6632.1993.tb26271.x PG 16 WC Immunology; Multidisciplinary Sciences; Pathology; Pediatrics; Virology SC Immunology; Science & Technology - Other Topics; Pathology; Pediatrics; Virology GA BZ45X UT WOS:A1993BZ45X00022 PM 8267267 ER PT S AU RODRIGUEZ, EM MENDEZ, H RICH, K SHEON, A FOX, H GREEN, K DIAZ, C BRAMBILLA, D MOFENSON, L AF RODRIGUEZ, EM MENDEZ, H RICH, K SHEON, A FOX, H GREEN, K DIAZ, C BRAMBILLA, D MOFENSON, L BE Lyman, WD Rubinstein, A TI MATERNAL DRUG-USE IN PERINATAL HIV STUDIES - THE WOMEN AND INFANTS TRANSMISSION STUDY SO PEDIATRIC AIDS: CLINICAL, PATHOLOGIC, AND BASIC SCIENCE PERSPECTIVES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Pediatric Aids: Clinical, Pathologic, and Basic Science Perspectives CY NOV 18-21, 1992 CL WASHINGTON, DC SP NEW YORK ACAD SCI ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYPE-1; BORN C1 SUNY HLTH SCI CTR,BROOKLYN,NY 11203. UNIV ILLINOIS,DEPT PEDIAT,CHICAGO,IL 60612. COLUMBIA UNIV,COLL PHYSICIANS & SURGEONS,DEPT OBSTET & GYNECOL,NEW YORK,NY 10032. UNIV MASSACHUSETTS,SCH MED,DEPT OBSTET & GYNECOL,WORCESTER,MA 01605. UNIV PUERTO RICO,DEPT PEDIAT,SAN JUAN,PR 00936. NEW ENGLAND RES INST,WATERTOWN,MA 02172. NICHHD,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,ROCKVILLE,MD 20852. RP RODRIGUEZ, EM (reprint author), NIAID,DIV AIDS,BETHESDA,MD 20892, USA. NR 9 TC 15 Z9 15 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-791-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 693 BP 245 EP 248 DI 10.1111/j.1749-6632.1993.tb26272.x PG 4 WC Immunology; Multidisciplinary Sciences; Pathology; Pediatrics; Virology SC Immunology; Science & Technology - Other Topics; Pathology; Pediatrics; Virology GA BZ45X UT WOS:A1993BZ45X00023 PM 8267268 ER PT J AU SHOEMAKER, L WELCH, TR BERGSTROM, W ABRAMS, SA YERGEY, AL VIEIRA, N AF SHOEMAKER, L WELCH, TR BERGSTROM, W ABRAMS, SA YERGEY, AL VIEIRA, N TI CALCIUM KINETICS IN THE HYPERPROSTAGLANDIN-E SYNDROME SO PEDIATRIC RESEARCH LA English DT Article ID BARTTERS-SYNDROME; PARATHYROID-HORMONE; HYPERCALCIURIA; PROSTAGLANDINS; INDOMETHACIN; NEPHROCALCINOSIS; HYPOPHOSPHATEMIA; HYPERRENINEMIA; HYPERPLASIA; METABOLISM AB Metabolic investigations, including the use of stable isotopes of calcium, were used to study calcium kinetics in three children with the hyperprostaglandin E syndrome. The studies were performed both during indomethacin treatment and in the absence of therapy. Off therapy, each child had hypercalciuria (mean urinary calcium excretion 0.478 mM/kg/d), hyperprostaglandinuria, and elevated serum calcitriol concentration. All had diminished bone density and were euparathyroid. Indomethacin treatment was associated with a marked reduction in serum calcitriol concentration, as well as decreased prostaglandin E excretion. Mean urinary calcium excretion fell to 0.135 mM/kg/d. The stable isotope studies defined two components to the hypercalciuria of this disease: an indomethacin-sensitive dietary contribution and a relatively indomethacin-resistant bone resorptive element. Bone densitometry confirmed the presence of the resorptive element by demonstrating skeletal demineralization. C1 UNIV CINCINNATI,COLL MED,DEPT PEDIAT,CINCINNATI,OH 45229. BAYLOR COLL MED,HOUSTON,TX 77030. SUNY HLTH SCI CTR,SYRACUSE,NY 13210. CHILDRENS HOSP RES FDN,DIV NEPHROL,CINCINNATI,OH 45229. NIH,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. OI Abrams, Steven/0000-0003-4972-9233 FU PHS HHS [123] NR 45 TC 32 Z9 32 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 JAN PY 1993 VL 33 IS 1 BP 92 EP 96 DI 10.1203/00006450-199301000-00019 PG 5 WC Pediatrics SC Pediatrics GA KE705 UT WOS:A1993KE70500019 PM 8433868 ER PT J AU BLAESE, RM AF BLAESE, RM TI DEVELOPMENT OF GENE-THERAPY FOR IMMUNODEFICIENCY - ADENOSINE-DEAMINASE DEFICIENCY SO PEDIATRIC RESEARCH LA English DT Article; Proceedings Paper CT CONF ON RECENT ADVANCES IN PATHOPHYSIOLOGY OF PRIMARY IMMUNE DEFICIENCIES AND IMMUNOGLOBULIN INFLAMMATORY NEUROLOGICAL DISORDERS CY JAN 24-25, 1992 CL INDIAN WELLS, CA ID BONE-MARROW TRANSPLANTATION; EXPRESSION; SEQUENCES; DISEASES; CELLS AB Deficiency of adenosine deaminase (ADA) results in severe combined immunodeficiency. Clinical cure has been observed in several ADA-severe combined immunodeficiency patients after bone marrow transplantation in which only donor T cells were engrafted, suggesting that T-cell correction alone is sufficient for full immune reconstitution. Children without an HLA-matched donor have been treated with polyethylene glycol-ADA as enzyme replacement therapy, resulting in varying degrees of immunologic and clinical improvement. In September 1990, we began treating a 4-y-old girl with periodic infusions of autologous culture-expanded T cells genetically corrected by insertion of a normal ADA gene using retroviral-mediated gene transfer with the LASN vector. After 2 y of polyethylene glycol-ADA treatment and before gene therapy, sbe continued to experience recurrent infections, was anergic and lymphopenic, and was deficient in isohemagglutinins. After seven infusions totaling 7 x 10(10) T cells, she has demonstrated a substantial increase in the number of circulating T cells (571/muL pre-gene therapy versus a mean of 1995/muL with gene therapy infusions every 6-8 wk) and the ADA activity in her peripheral blood T cells has increased > 10-fold. The increase in T-cell numbers and ADA activity has been associated with the development of positive delayed-type hypersensitivity skin tests, a significant increase in the level of isohemagglutinins, the regrowth of tonsils, and a decreased number of infectious illnesses. This improvement has persisted during suspension of treatment for more than 6 mo. A second patient treated since February 1991 has shown similar improvement in immune status. Both patients have tolerated the treatments without complication and are able to participate fully in school and social activities. These findings demonstrate that infusions of polyclonal autologous T cells metabolically corrected by ADA gene transfer can be an effective treatment for some children with ADA-severe combined immunodeficiency. C1 NCI,CELLULAR IMMUNOL SECT,METAB BRANCH,BETHESDA,MD 20892. NR 27 TC 68 Z9 69 U1 0 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD JAN PY 1993 VL 33 IS 1 SU S BP S49 EP S55 DI 10.1203/00006450-199304001-00010 PG 7 WC Pediatrics SC Pediatrics GA KF285 UT WOS:A1993KF28500010 PM 8433875 ER PT J AU JAFFE, JS EISENSTEIN, E SNELLER, MC STROBER, W AF JAFFE, JS EISENSTEIN, E SNELLER, MC STROBER, W TI T-CELL ABNORMALITIES IN COMMON VARIABLE IMMUNODEFICIENCY SO PEDIATRIC RESEARCH LA English DT Article; Proceedings Paper CT CONF ON RECENT ADVANCES IN PATHOPHYSIOLOGY OF PRIMARY IMMUNE DEFICIENCIES AND IMMUNOGLOBULIN INFLAMMATORY NEUROLOGICAL DISORDERS CY JAN 24-25, 1992 CL INDIAN WELLS, CA ID PERIPHERAL-BLOOD LYMPHOCYTES; INTERFERON-GAMMA; DIFFERENTIATION; INTERLEUKIN-2; SUPPRESSOR; EXPRESSION; ACTIVATION; SUBSETS; HELPER AB Common variable immunodeficiency (CVI) is a heterogeneous condition marked by a number of different immunologic defects. One group of patients, perhaps 60% of the CVI group as a whole, is characterized by T cells that produce reduced amounts of IL-2 (mRNA and protein product), IL-4, and IL-5 (mRNA) when stimulated with phytohemagglutinin. This defect does not extend to all lymphokines, however, because the cells produce normal amounts of interferon-gamma (mRNA and protein product) when exogenous IL-2 is present. Recently, we have reexamined the T cell lymphokine production defect using a panoply of T-cell activation stimuli and have shown that the defect is a subtle one that depends on activation of the cell via the CD3-T-cell receptor complex. Because T cells proliferate normally when stimulated via this receptor, this finding suggests the presence of a ''downstream'' defect, perhaps one involving the factors that are necessary for activation of lymphokine genes. A second form of CVI, in this case involving approximately 30% of the CVI group as a whole, is characterized by a reduced CD4/CD8 ratio and elevated numbers of CD8+ T cells bearing the CD57 marker. Although the CD4+ T cells in this patient group elaborate normal amounts of IL-2 under various activation conditions, their CD8+ T cells produce increased amounts of interferon-gamma. Furthermore, the CD8+ T cells in this case act as ''suppressor'' T cells, which suppress IgG production but not IgM production of purified (normal) SAC+, IL-2-induced B cells. These ''CD8hi'' CVI patients display lymphocyte phenotype markers that are similar to those of patients with chronic viral infection; thus, it is possible that they have an immunodeficiency resulting from a subtle infection that results in the development of T cells capable of down-regulating B-cell responses. Overall, these studies allow a better definition of CVI and suggest potential lymphokine-based therapies of selected patients. C1 NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 21 TC 30 Z9 30 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 JAN PY 1993 VL 33 IS 1 SU S BP S24 EP S28 PG 5 WC Pediatrics SC Pediatrics GA KF285 UT WOS:A1993KF28500006 PM 7679486 ER PT J AU MOFENSON, LM MOYE, J AF MOFENSON, LM MOYE, J TI INTRAVENOUS IMMUNE GLOBULIN FOR THE PREVENTION OF INFECTIONS IN CHILDREN WITH SYMPTOMATIC HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO PEDIATRIC RESEARCH LA English DT Article ID PNEUMOCYSTIS-CARINII PNEUMONIA; AIDS-RELATED COMPLEX; B DEFECTS INVITRO; HIV-INFECTION; DEFICIENCY SYNDROME; PNEUMOCOCCAL BACTEREMIA; BACTERIAL-INFECTIONS; GAMMA-GLOBULIN; IMMUNOGLOBULIN; RESPONSES AB Infection with human immunodeficiency virus (HIV) causes a progressive immunodeficiency, often manifested in adults by the development of infections with relatively rare, opportunistic organisms. However, in HIV-infected children, recurrent serious infections with common encapsulated bacteria, as well as recurrent minor bacterial and viral infections, may be early and frequent manifestations of HIV disease. The use of i.v. immune globulin (IVIG) has been shown to prevent infections in patients with primary immunodeficiency and in uncontrolled studies of HIV-infected children. This article reviews the problem of and immunologic predisposition for recurrent infections in pediatric HIV infection and reports on the use of IVIG for prophylaxis. Updated analysis from the National Institute of Child Health and Human Development IVIG Clinical Trial, a multicenter, double-blind, placebo-controlled trial of the safety and efficacy of IVIG for the prevention of infections in children with symptomatic HIV infection, is presented. Between March 1988 and January 1991, 376 children with clinical or immunologic evidence of HIV disease who were randomized to receive IVIG or albumin placebo were enrolled in this trial. In children with an entry CD4+ count of 200/mm3 or higher, IVIG significantly increased the time free from serious bacterial infections and significantly decreased the rates of minor bacterial infections and viral infections. RP MOFENSON, LM (reprint author), NICHHD, PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH, 6100 EXECUT BLVD, BETHESDA, MD 20892 USA. NR 49 TC 15 Z9 15 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0031-3998 EI 1530-0447 J9 PEDIATR RES JI Pediatr. Res. PD JAN PY 1993 VL 33 IS 1 SU S BP S80 EP S89 PG 10 WC Pediatrics SC Pediatrics GA KF285 UT WOS:A1993KF28500015 PM 8433880 ER PT J AU SHEARER, GM CLERICI, M AF SHEARER, GM CLERICI, M TI ABNORMALITIES OF IMMUNE REGULATION IN HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO PEDIATRIC RESEARCH LA English DT Article; Proceedings Paper CT CONF ON RECENT ADVANCES IN PATHOPHYSIOLOGY OF PRIMARY IMMUNE DEFICIENCIES AND IMMUNOGLOBULIN INFLAMMATORY NEUROLOGICAL DISORDERS CY JAN 24-25, 1992 CL INDIAN WELLS, CA ID AIDS-RELATED COMPLEX; T-CELL CLONES; PHASE-I TRIAL; HIV-INFECTION; 2',3'-DIDEOXYINOSINE DDI; ENVELOPE GLYCOPROTEIN; SUPPRESSOR FACTORS; GAMMA PRODUCTION; LYMPHOCYTES-T; ANTIGEN AB The severe depletion of CD4+ T cells is the most obvious and dramatic immunologic event that occurs in individuals infected with the human immunodeficiency virus (HIV) type 1 during development to AIDS. Nevertheless, a complex and sequential pattern of loss of T-helper cell (TH) function can occur years before development of AIDS symptoms. Such suppression could be due to immunosuppressive factors that are either products of HIV, such as gp120 and tat, or HIV-induced immunoregulatory cytokines such as transforming growth factor-beta and IL-10. Recent data suggest that multiple and independent immunosuppressive factors, including gp120-induced suppression and IL-10, are responsible for the loss of TH function seen in HIV-infected individuals before development of symptoms. The same TH functional abnormalities observed in adult patients are also seen in pediatric cases. Pediatric cases of HIV infection present some unique problems, however, in that one needs to be able to distinguish between HIV-induced suppression of TH function and the absence of TH function that is due to lack of maturation or immunologic priming. RP SHEARER, GM (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B17,BETHESDA,MD 20892, USA. NR 48 TC 22 Z9 22 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 JAN PY 1993 VL 33 IS 1 SU S BP S71 EP S75 PG 5 WC Pediatrics SC Pediatrics GA KF285 UT WOS:A1993KF28500013 PM 8433878 ER PT J AU ROTHMAN, RB XU, H CHAR, GU KIM, A DECOSTA, BR RICE, KC ZIMMERMAN, DM AF ROTHMAN, RB XU, H CHAR, GU KIM, A DECOSTA, BR RICE, KC ZIMMERMAN, DM TI PHENYLPIPERIDINE OPIOID ANTAGONISTS THAT PROMOTE WEIGHT-LOSS IN RATS HAVE HIGH-AFFINITY FOR THE KAPPA-2B (ENKEPHALIN-SENSITIVE) BINDING-SITE SO PEPTIDES LA English DT Article DE OPIOID RECEPTORS; KAPPA-RECEPTORS; LY255582; NALTREXONE; NALOXONE; APPETITE ID BOVINE ADRENAL-MEDULLA; GUINEA-PIG BRAIN; OBESE ZUCKER RAT; OPIATE RECEPTOR; SPINAL-CORD; SUBTYPE; PEPTIDES; APPETITE; AGONIST; DRUGS AB Certain opioid antagonists of the phenylpiperidine series (PPAs), such as LY255582, seem unique efficacious at producing weight loss in lean and meal-fed obese Zucker rats. Comparison of the pharmacological and receptor binding profile of PPAs that promote marked weight loss with those that do not has failed to find any obvious differences between these two groups of narcotic antagonists, which might explain the differences in their biological activities. The potent stimulatory effect of dynorphin, and other kappa agonists, on feeding behavior suggests that the antagonists that promote weight loss might have high affinity for kappa receptors. The recent demonstration by several laboratories Of kappa receptor heterogeneity prompted us to test the hypothesis that the antagonists that promote weight loss might have high affinity for a subtype of kappa binding sites. In the present study, therefore, we determined the K(i) values of five PPAs, naloxone, and naltrexone at mu, delta, kappa1, kappa2a, and kappa2b binding sites. The data indicate that antagonists having subnanomolar K(i) values and high selectivity for the kappa2b binding site (relative to the kappa2a binding site) are efficacious at promoting weight loss. C1 NIDDK,MED CHEM LAB,BETHESDA,MD 20892. ELI LILLY CORP,LILLY RES LABS,INDIANAPOLIS,IN 46285. RP ROTHMAN, RB (reprint author), NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,POB 5180,BALTIMORE,MD 21224, USA. NR 25 TC 18 Z9 19 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0196-9781 J9 PEPTIDES JI Peptides PD JAN-FEB PY 1993 VL 14 IS 1 BP 17 EP 20 DI 10.1016/0196-9781(93)90005-2 PG 4 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA KK582 UT WOS:A1993KK58200003 PM 8382809 ER PT J AU LAZARUS, LH SALVADORI, S ATTILA, M GRIECO, P BUNDY, DM WILSON, WE TOMATIS, R AF LAZARUS, LH SALVADORI, S ATTILA, M GRIECO, P BUNDY, DM WILSON, WE TOMATIS, R TI INTERACTION OF DELTORPHIN WITH OPIOID RECEPTORS - MOLECULAR DETERMINANTS FOR AFFINITY AND SELECTIVITY SO PEPTIDES LA English DT Article DE DELTORPHIN; OPIOID RECEPTORS; PEPTIDE SYNTHESIS; RAT BRAIN RECEPTORS ID SOLID-PHASE SYNTHESIS; PROTECTED PEPTIDE-FRAGMENTS; DELTA-RECEPTOR; ENKEPHALIN ANALOGS; CONFORMATIONAL PROPERTIES; DIFFERENTIAL ANTAGONISM; CHEMOTACTIC PEPTIDES; BIOLOGICAL-ACTIVITY; OPIATE RECEPTORS; LIGAND-BINDING AB Opioid receptor analyses of deltorphin A (H-Tyr-D-Met-Phe-His-Leu-Met-Asp-NH2) analogues indicated the following: (a) increased negativity differentially affected affinities (K(i)) and selectivity (K(i)mu/K(i)delta); (b) shifted sequence heptapeptides, [Asp5,Leu6,Met-NH27] and [Asp4,His5,Leu6,Met-NH27], reversed selectivity (delta --> mu); (c) substitutions at positions 4, 5, and 6 diminished selectivity, with changes in residue 5 being the most detrimental; (d) C-terminal deletions differentially effected K(i). These are the first data to demonstrate a reversal of delta selectivity in heptapeptides containing a negative charge and indicate that modifications in affinity occur through changes in both anionic and hydrophobic properties of residues at specific positions in the peptide. Deltorphin analogues might also be applied to differentiate between opioid receptor subsites. C1 UNIV FERRARA,DEPT PHARMACEUT SCI,I-44100 FERRARA,ITALY. UNIV NAPLES,DEPT PHARMACEUT SCI,I-80138 NAPLES,ITALY. RP LAZARUS, LH (reprint author), NIEHS,INTEGRAT BIOL LAB,PEPTIDE NEUROCHEM SECT,POB 12233,RES TRIANGLE PK,NC 27709, USA. OI SALVADORI, Severo/0000-0002-8224-2358 NR 57 TC 42 Z9 42 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0196-9781 J9 PEPTIDES JI Peptides PD JAN-FEB PY 1993 VL 14 IS 1 BP 21 EP 28 DI 10.1016/0196-9781(93)90006-3 PG 8 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA KK582 UT WOS:A1993KK58200004 PM 8382810 ER PT J AU MALIN, DH PAYZA, K LAKE, JR CORRIERE, LS BENSON, TM SMITH, DA KELLEY, RS HO, KK BURGESS, K AF MALIN, DH PAYZA, K LAKE, JR CORRIERE, LS BENSON, TM SMITH, DA KELLEY, RS HO, KK BURGESS, K TI ENHANCED ANTIOPIATE ACTIVITY IN PEPTIDOMIMETICS OF FMRFAMIDE CONTAINING Z-2,3-METHANOMETHIONINE SO PEPTIDES LA English DT Article DE FMRFA; NPFF; NPFF RECEPTORS; NEUROPEPTIDE FF; F8FAMIDE; ANTIOPIATE PEPTIDES; CYCLOPROPYLOGS; PEPTIDOMIMETICS; RAT; OPIATE DEPENDENCE; OPIATE ABSTINENCE SYNDROME ID ENDOGENOUS OPIATE ANTAGONIST; DEFEAT-INDUCED ANALGESIA; INDUCED OPIOID ANALGESIA; INHIBITORY INFLUENCES; SPINAL-CORD; NEUROPEPTIDE; PEPTIDE; MORPHINE; RAT; IMMUNOREACTIVITY AB FMRFa is a molluscan peptide that has shown antiopiate activity in a number of mammalian test systems. The current study determined the antiopiate potency of FMRFa and two conformationally constrained peptidomimetics of FMRFa containing stereoisomers of Z-2,3-methanomethionine. Morphine abstinence sips were observed after varying doses (0.25-25.0 mug) of these substances were injected into the third ventricle of morphine-dependent rats. Although both peptidomimetics were far more potent than FMRFa itself, they bound with lower affinity than FMRFa to rat spinal cord receptors for the mammalian FMRFa-like peptide, NPFF. C1 NIMH, WASHINGTON, DC 20032 USA. RICE UNIV, HOUSTON, TX 77251 USA. RP MALIN, DH (reprint author), UNIV HOUSTON CLEAR LAKE, BOX 237, HOUSTON, TX 77058 USA. RI Burgess, Kevin/B-5372-2015 OI Burgess, Kevin/0000-0001-6597-1842 FU NIDA NIH HHS [DAO6554] NR 37 TC 37 Z9 37 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0196-9781 J9 PEPTIDES JI Peptides PD JAN-FEB PY 1993 VL 14 IS 1 BP 47 EP 51 DI 10.1016/0196-9781(93)90009-6 PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA KK582 UT WOS:A1993KK58200007 PM 8382812 ER PT J AU WEINHOLD, LL SHARPE, LG JAFFE, JH AF WEINHOLD, LL SHARPE, LG JAFFE, JH TI HOUSING CONDITIONS INFLUENCE ACQUISITION OF SUFENTANIL AEROSOL SELF-ADMINISTRATION IN RATS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE HOUSING CONDITIONS; SUFENTANIL AEROSOL; SELF-ADMINISTRATION; ENVIRONMENT ID FOOD-DEPRIVATION; SOCIAL-ISOLATION; COCAINE; AMPHETAMINE AB At weaning, rats were housed either individually or in pairs and as adults were trained to poke their nose in and out of a port that dispensed a 2-s exposure of sufentanil aerosol (50-mug/ml solution). During the acquisition phase, which consisted of five nightly sessions lasting 14-16 h, individually caged rats responded for more sufentanil aerosol than did pair-caged animals when the fixed ratio (FR) requirement was gradually increased from FR 1 to FR 5 over the rive sessions. During the maintenance phase, which consisted of daytime 2-h sessions at an FR 5 schedule of reinforcement, there were no differences between individually and pair-caged animals responding for sufentanil or for water vapor. Both groups responded significantly more for sufentanil than for water vapor. Based upon present evidence, it is suggested that environmental and biologic determinants may change psychomotor behavior in a way that could influence the rate by which animals acquire drug-seeking behavior. RP WEINHOLD, LL (reprint author), NATL INST DRUG ABUSE,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 15 TC 5 Z9 5 U1 0 U2 2 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 JAN PY 1993 VL 44 IS 1 BP 141 EP 144 DI 10.1016/0091-3057(93)90291-Z PG 4 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA KG426 UT WOS:A1993KG42600018 PM 8381544 ER PT J AU CHOCHUNG, YS CLAIR, T AF CHOCHUNG, YS CLAIR, T TI THE REGULATORY SUBUNIT OF CAMP-DEPENDENT PROTEIN-KINASE AS A TARGET FOR CHEMOTHERAPY OF CANCER AND OTHER CELLULAR DYSFUNCTIONAL-RELATED DISEASES SO PHARMACOLOGY & THERAPEUTICS LA English DT Article; Proceedings Paper CT 4th International Symposium on Molecular Aspects of Chemotherapy CY JUN 23-25, 1993 CL GDANSK, POLAND SP INT SOC CHEMOTHERAPY, MINIST NATL EDUC WARSZAWA, TU GDANSK, FAC CHEM, POLISH ACAD SCI, INST BIOCHEM & BIOPHYS, UNESCO, GLOBAL NETWORK MOLEC & CELL BIOL, F HOFFMAN LAROCHE & CO, STERLING WINTHROP PHARM, RES DIV, WELLCOME RES LABS BECKENHAM DE CYCLIC AMP; PROTEIN KINASE; CANCER; CHEMOTHERAPY; ANTISENSE OLIGONUCLEOTIDE; HYPERTENSION ID CYCLIC-AMP-BINDING; HL-60 LEUKEMIA-CELLS; AMINO-ACID-SEQUENCE; ADENOSINE 3'-5'-CYCLIC MONOPHOSPHATE; FRIEND-ERYTHROLEUKEMIC CELLS; RI-ALPHA-SUBUNIT; MAMMARY EPITHELIAL-CELLS; HORMONE-SENSITIVE LIPASE; GROWTH-CONTROL; RAT-LIVER AB Three separate experimental approaches, using site-selective cAMP analogs, antisense strategy and retroviral vector-mediated gene transfer, have provided evidence that two isoforms, the RI- and RII-regulatory subunits of cAMP-dependent protein kinase, have opposite roles in cell growth and differentiation; RI being growth stimulatory while RII is a growth-inhibitory and differentiation-inducing protein. As RI expression is enhanced during chemical or viral carcinogenesis, in human cancer cell lines and in primary human tumors, it is a target for cancer diagnosis and therapy. 8-Cl-cAMP and RI antisense oligodeoxynucleotide, those that effectively down-regulate RI, and up-regulate RII(beta), provide new approaches toward the treatment of cancer. This approach to modulation of RI vs RII cAMP transducers may also be beneficial toward therapy of endocrine or cellular dysfunction-related diseases where abnormal signal transduction of cAMP is critically involved. RP CHOCHUNG, YS (reprint author), NCI,TUMOR IMMUNOL & BIOL LAB,CELLULAR BIOCHEM SECT,BETHESDA,MD 20892, USA. NR 172 TC 74 Z9 74 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0163-7258 J9 PHARMACOL THERAPEUT JI Pharmacol. Ther. PY 1993 VL 60 IS 2 BP 265 EP 288 DI 10.1016/0163-7258(93)90010-B PG 24 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NG264 UT WOS:A1993NG26400008 PM 8022860 ER PT J AU SMITH, MR MATTHEWS, NT JONES, KA KUNG, HF AF SMITH, MR MATTHEWS, NT JONES, KA KUNG, HF TI BIOLOGICAL ACTIONS OF ONCOGENES SO PHARMACOLOGY & THERAPEUTICS LA English DT Review ID RETINOBLASTOMA SUSCEPTIBILITY GENE; PROTEIN-KINASE-C; TUMOR SUPPRESSOR GENES; ERYTHROLEUKEMIA CELL-DIFFERENTIATION; NEUROFIBROMATOSIS TYPE-1 GENE; AVIAN ERYTHROBLASTOSIS VIRUS; SIGNAL TRANSDUCTION PATHWAYS; NUCLEOTIDE EXCHANGE-REACTION; GTPASE-ACTIVATING PROTEIN; GROWTH-FACTOR STIMULATION AB Cancer, in many cases, results from multistep genetic mutation. Certain genes can have a predisposed susceptibility to mutations that lead to cancer because of chromosome location or their importance in the control of cell cycles. Mutations that deregulate the expression or activity of enzymes involved in the biochemical pathways of growth and differentiation or that suppress the expression of negative cell cycle control factors result in activation of oncogenesis. The study of oncogenes and tumor suppressor genes has greatly influenced our understanding of the molecular origins of cancer. We focus here on the normal biological action of proto-oncogenes compared with the transforming activities of oncogenes and tumor suppressor genes, and we discuss possible mechanisms of oncogenic transformation. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,BIOCHEM PHYSIOL LAB,FREDERICK,MD 21702. RP SMITH, MR (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,PROGRAM RESOURCES INC,DYNCORP,FREDERICK,MD 21702, USA. NR 231 TC 8 Z9 8 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0163-7258 J9 PHARMACOL THERAPEUT JI Pharmacol. Ther. PY 1993 VL 58 IS 2 BP 211 EP 236 DI 10.1016/0163-7258(93)90050-N PG 26 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA LT512 UT WOS:A1993LT51200004 PM 8415879 ER PT J AU ANDERSEN, O AUTRUP, H DAYAN, AD FENGER, J FORSLUND, J GRANDJEAN, P GRON, P JENSEN, FP KEIDING, L KJAERGAARD, S LARSEN, JC LEWTAS, J LYNGE, E MOLLER, H MOLLER, L NIELSEN, PA OSTENFELDT, N PILSGAARD, H PORTIER, C POULSEN, E RASTOGI, SC SKOV, T THOMSEN, AS ULBAK, K OSTERLIND, A AF ANDERSEN, O AUTRUP, H DAYAN, AD FENGER, J FORSLUND, J GRANDJEAN, P GRON, P JENSEN, FP KEIDING, L KJAERGAARD, S LARSEN, JC LEWTAS, J LYNGE, E MOLLER, H MOLLER, L NIELSEN, PA OSTENFELDT, N PILSGAARD, H PORTIER, C POULSEN, E RASTOGI, SC SKOV, T THOMSEN, AS ULBAK, K OSTERLIND, A TI REPORT FROM THE WORKING-GROUP-ON-CANCER-AND-THE-NON-OCCUPATIONAL-ENVIRONMENT SO PHARMACOLOGY & TOXICOLOGY LA English DT Editorial Material C1 ST BARTHOLOMEWS HOSP,COLL MED,DH DEPT TOXICOL,DOMINION HOUSE,59 BARTHOLOMEW CLOSE,LONDON EC1 7ED,ENGLAND. US EPA,HLTH EFFECTS RES LAB,RES TRIANGLE PK,NC 27711. NATL BOARD HLTH,DIV PREVENT & GEN HYG,DK-1012 COPENHAGEN K,DENMARK. INT AGCY RES CANC,F-69372 LYON,FRANCE. NATL FOOD AGCY,INST TOXICOL,DK-2860 SOBORG,DENMARK. NIEHS,STAT & BIOMATH BRANCH,RISK METHODOL SECT,RES TRIANGLE PK,NC 27709. DANISH CANC SOC,DANISH CANC REGISTRY,DK-2100 COPENHAGEN 0,DENMARK. NATL INST RADIAT HYG,DK-2700 BRONSHOJ,DENMARK. BISPEBJERG HOSP,DEPT DERMATOL,DK-2400 COPENHAGEN,DENMARK. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0901-9928 J9 PHARMACOL TOXICOL JI Pharmacol. Toxicol. PY 1993 VL 72 SU 1 BP S167 EP S171 PG 5 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA KR800 UT WOS:A1993KR80000025 ER PT J AU HUFF, J AF HUFF, J TI ISSUES AND CONTROVERSIES SURROUNDING QUALITATIVE STRATEGIES FOR IDENTIFYING AND FORECASTING CANCER-CAUSING AGENTS IN THE HUMAN ENVIRONMENT SO PHARMACOLOGY & TOXICOLOGY LA English DT Article AB Certain chemicals, mixtures of chemicals, exposure circumstances, life-styles and personal or cultural habits, occupations, viruses, living conditions, and physical agents have been causally associated with cancers in humans. Most however are not considered potentially carcinogenic, and the proportion of 'agents' eventually identified to cause cancer is projected to be relatively low. Current methods to identify carcinogenic potential of chemicals rely largely on short-term in vitro and in vivo tests, mid- & long-term in vivo assays, molecular mechanisms, epidemiological investigations, and structural-activity-effect-relationships. Thus, the scientific and public health communities must continue to utilize available means and concomitantly strive to develop newer methods and tools to more easily, quickly, cheaply, and reliably identify carcinogens in the human milieu. Since adequate human studies are typically absent, the most useful method for identifying potential human carcinogens continues to be long-term carcinogenesis experiments. Agents identified as causing cancers in humans have been shown to cause cancer in animals, and this knowledge, together with similarities in mechanisms of carcinogenesis across species, led to the scientific logic and public health strategy that chemicals shown clearly to be carcinogenic in animals should be considered as being likely and anticipated to present cancer risks to humans. The quest of hazard identification efforts is cancer prevention, largely by reducing or eliminating exposures to chemicals that cause cancer and other diseases. RP HUFF, J (reprint author), NIEHS, POB 12233, RES TRIANGLE PK, NC 27709 USA. NR 126 TC 1 Z9 1 U1 1 U2 1 PU BLACKWELL MUNKSGAARD PI FREDERIKSBERG C PA 1 ROSENORNS ALLE, DK-1970 FREDERIKSBERG C, DENMARK SN 0901-9928 J9 PHARMACOL TOXICOL JI Pharmacol. Toxicol. PY 1993 VL 72 SU 1 BP S12 EP S27 PG 16 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA KR800 UT WOS:A1993KR80000003 ER PT J AU PORTIER, CJ AF PORTIER, CJ TI MECHANISTIC MODELING AND RISK ASSESSMENT SO PHARMACOLOGY & TOXICOLOGY LA English DT Article; Proceedings Paper CT CONF ON ENVIRONMENT AND CANCER CY MAY 10-13, 1992 CL AARHUS, DENMARK SP DANISH CANC SOC ID METHYLENE-CHLORIDE; CARCINOGENESIS AB Risk Assessment in the United States has been rapidly changing over the last few years. The historical methods and endpoints by which risk estimates were derived are gradually being replaced by newer methods and a broader spectrum of endpoints. For carcinogenic risk assessment, there is movement from the routinely used ''linearized multistage model'' for low dose risk estimation to methodology which is more deeply rooted in carcinogenic mechanisms and which allows the incorporation of additional data into the estimation of risks in a direct, quantitative fashion. There is also a determined effort under way to develop methods for assessing risks from exposure based on other endpoints such as effects on the immune system and the reproductive system. This paper briefly discusses some of the statistical and mathematical issues which will play important roles in determining the utility and precision of these new methods for estimating risks from environmental exposures. RP PORTIER, CJ (reprint author), NIEHS,STAT & BIOMATH BRANCH,RISK METHODOL SECT,RES TRIANGLE PK,NC 27709, USA. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 24 TC 1 Z9 1 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0901-9928 J9 PHARMACOL TOXICOL JI Pharmacol. Toxicol. PY 1993 VL 72 SU 1 BP S28 EP S32 PG 5 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA KR800 UT WOS:A1993KR80000004 ER PT J AU MITCHELL, CL BARNES, MI AF MITCHELL, CL BARNES, MI TI EFFECT OF DESTRUCTION OF DENTATE GRANULE CELLS ON KINDLING INDUCED BY STIMULATION OF THE PERFORANT PATH SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE HIPPOCAMPUS; DENTATE GRANULE CELLS; KINDLING; SEIZURES; AFTERDISCHARGE; EPILEPSY ID SEIZURES AB Bilateral destruction of dentate granule cells in both the dorsal and ventral hippocampal formation had no effect on the threshold for hippocampal afterdischarge before or after kindling. Neither did it affect the number of stimulations required to attain kindling. However, the duration of afterdischarge was significantly longer in colchicine-lesioned animals compared to those receiving artificial cerebrospinal fluid. This was true for the threshold for afterdischarge as well as at the first and last kindling trials. These results suggest that dentate granule cells may inhibit the duration of afterdischarge induced by perforant path stimulation or that other postlesion changes occur which result in a prolongation of hippocampal afterdischarge. RP MITCHELL, CL (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 8 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 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD JAN PY 1993 VL 53 IS 1 BP 45 EP 49 DI 10.1016/0031-9384(93)90009-5 PG 5 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA KH493 UT WOS:A1993KH49300008 PM 8434068 ER PT J AU RIPAMONTI, U MA, SS CUNNINGHAM, NS YEATES, L REDDI, AH AF RIPAMONTI, U MA, SS CUNNINGHAM, NS YEATES, L REDDI, AH TI RECONSTRUCTION OF THE BONE-BONE MARROW ORGAN BY OSTEOGENIN, A BONE MORPHOGENETIC PROTEIN, AND DEMINERALIZED BONE-MATRIX IN CALVARIAL DEFECTS OF ADULT PRIMATES SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID EXTRACELLULAR-MATRIX; INDUCTIVE PROTEIN; DIFFERENTIATION; REPAIR AB Information concerning the efficacy of osteogenin, a bone morphogenetic protein, and demineralized bone matrix in orthotopic sites in nonhuman primates is a prerequisite for potential clinical application in humans. After exposure of the calvaria, 84 cranial defects, 25 mm in diameter, were prepared in 26 adult male baboons (Papio ursinus). Defects were implanted with insoluble collagenous bone matrix (ICBM, the inactive collagenous residue after dissociative extraction of bone matrix with 4 M guanidine hydrochloride) reconstituted with osteogenin fractions isolated from baboon bone matrix by chromatography on heparin-Sepharose and hydroxy-apatite-Ultrogel (Og Hep-HA) or osteogenin further purified using Sephacryl S-200 gel filtration chromatography (Og S-200). Baboon osteogenin with the highest biologic activity in a rodent bioassay, as determined by alkaline phosphatase activity, calcium content, and histologic analysis, was used for orthotopic implantation in baboons. Additional defects were implanted with baboon demineralized bone matrix (DBM) or ICBM without osteogenin as control. Defects also were grafted with corticocancellous bone harvested from the iliac crest or left ungrafted to monitor the spontaneous regeneration potential of the adult baboon calvaria. Undecalcified bone sections at 7 mum were prepared from the harvested specimens 30 and 90 days after surgery. Histomorphometry demonstrated that Og S-200 induced copious amounts of bone and osteoid as early as day 30 (P < 0.01 versus ICBM, autogenous grafts and untreated defects). At day 90, in implants of Og S-200, Og Hep-HA, and DBM, bone and marrow formation was extensive, culminating in complete regeneration of the craniotomies. In implants of DBM, bone formed with an intervening phase of cartilage development. This provides the phenotypic evidence of endochondral bone differentiation by induction in defects of membranous calvarial bone in adult primates. These results establish the potential therapeutic application of osteogenin and demineralized bone matrix for the architectural reconstruction of the bone-bone marrow organ in humans. C1 NIDR,BONE CELL BIOL SECT,BETHESDA,MD 20892. RP RIPAMONTI, U (reprint author), UNIV WITWATERSRAND,MRC,DENT RES INST,PO WITS,JOHANNESBURG 2050,SOUTH AFRICA. RI Roden, Laura/D-1364-2010 OI Roden, Laura/0000-0002-1941-898X NR 26 TC 60 Z9 62 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JAN PY 1993 VL 91 IS 1 BP 27 EP 36 DI 10.1097/00006534-199301000-00005 PG 10 WC Surgery SC Surgery GA KE189 UT WOS:A1993KE18900005 PM 8416537 ER PT B AU SCHEFFNER, M MUNGER, K HUIBREGTSE, JM MIETZE, JA HOWLEY, PM AF SCHEFFNER, M MUNGER, K HUIBREGTSE, JM MIETZE, JA HOWLEY, PM BE Marks, PA Turler, H Weil, R TI INTERACTION OF THE HPV-E6 AND HPV-E7 ONCOPROTEINS WITH THE TUMOR-SUPPRESSOR PROTEIN-P53 AND PROTEIN-PRB SO PRECANCEROUS LESIONS: A MULTIDISCIPLINARY APPROACH SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT Workshop on Precancerous Lesions: A Multidisciplinary Approach CY MAR 29-31, 1992 CL MONTREUX, SWITZERLAND SP AERS SERONO SYMPOSIA RP SCHEFFNER, M (reprint author), NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892, USA. RI Scheffner, Martin/K-2940-2012 OI Scheffner, Martin/0000-0003-2229-0128 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-10-4 J9 CHALL MOD MED PY 1993 VL 1 BP 177 EP 189 PG 13 WC Oncology; Medicine, Research & Experimental SC Oncology; Research & Experimental Medicine GA BZ61B UT WOS:A1993BZ61B00016 ER PT B AU HARRIS, CC AF HARRIS, CC BE Marks, PA Turler, H Weil, R TI P53 TUMOR-SUPPRESSOR GENE - MUTATIONAL SPECTRUM SO PRECANCEROUS LESIONS: A MULTIDISCIPLINARY APPROACH SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT Workshop on Precancerous Lesions: A Multidisciplinary Approach CY MAR 29-31, 1992 CL MONTREUX, SWITZERLAND SP AERS SERONO SYMPOSIA RP HARRIS, CC (reprint author), NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-10-4 J9 CHALL MOD MED PY 1993 VL 1 BP 209 EP 220 PG 12 WC Oncology; Medicine, Research & Experimental SC Oncology; Research & Experimental Medicine GA BZ61B UT WOS:A1993BZ61B00020 ER PT B AU OCONNELL, ML HUARTE, J BELIN, D VASSALLI, JD STRICKLAND, S AF OCONNELL, ML HUARTE, J BELIN, D VASSALLI, JD STRICKLAND, S BE Bavister, BD TI TRANSLATION CONTROL IN OOCYTES - A CRITICAL ROLE FOR THE POLY(A) TAIL OF MATERNAL MESSENGER-RNAS SO PREIMPLANTATION EMBRYO DEVELOPMENT SE SERONO SYMPOSIA, USA LA English DT Proceedings Paper CT Symposium on Preimplantation Embryo Development CY AUG 15-18, 1991 CL NEWTON, MA SP SERONO SYMP C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 BN 0-387-97934-4 J9 SERONO SYMP PY 1993 BP 38 EP 42 PG 5 WC Developmental Biology SC Developmental Biology GA BZ95X UT WOS:A1993BZ95X00003 ER PT S AU HARLAN, WR AF HARLAN, WR BE Williams, CL Kimm, SYS TI EPIDEMIOLOGY OF CHILDHOOD OBESITY - A NATIONAL PERSPECTIVE SO PREVENTION AND TREATMENT OF CHILDHOOD OBESITY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Prevention and Treatment of Childhood Obesity CY MAR 09-11, 1993 CL BETHESDA, MD SP NEW YORK ACAD SCI, NIH, NIDDKD, NHLBI, NICHHD, WYETH AYERST LABS ID SECULAR TRENDS; UNITED-STATES; BODY-MASS; OVERWEIGHT; POPULATIONS RP HARLAN, WR (reprint author), NIH,BLDG 1,ROOM 260,BETHESDA,MD 20892, USA. NR 18 TC 26 Z9 26 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-831-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 699 BP 1 EP 5 DI 10.1111/j.1749-6632.1993.tb18831.x PG 5 WC Endocrinology & Metabolism; Multidisciplinary Sciences; Nutrition & Dietetics; Pediatrics SC Endocrinology & Metabolism; Science & Technology - Other Topics; Nutrition & Dietetics; Pediatrics GA BZ46T UT WOS:A1993BZ46T00002 PM 8267299 ER PT S AU OBARZANEK, E AF OBARZANEK, E BE Williams, CL Kimm, SYS TI METHODOLOGICAL ISSUES IN ESTIMATING THE PREVALENCE OF OBESITY IN CHILDHOOD SO PREVENTION AND TREATMENT OF CHILDHOOD OBESITY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Prevention and Treatment of Childhood Obesity CY MAR 09-11, 1993 CL BETHESDA, MD SP NEW YORK ACAD SCI, NIH, NIDDKD, NHLBI, NICHHD, WYETH AYERST LABS RP OBARZANEK, E (reprint author), NHLBI,FED BLDG,ROOM 604,BETHESDA,MD 20892, USA. NR 4 TC 13 Z9 13 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-831-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 699 BP 278 EP 279 DI 10.1111/j.1749-6632.1993.tb18866.x PG 2 WC Endocrinology & Metabolism; Multidisciplinary Sciences; Nutrition & Dietetics; Pediatrics SC Endocrinology & Metabolism; Science & Technology - Other Topics; Nutrition & Dietetics; Pediatrics GA BZ46T UT WOS:A1993BZ46T00037 PM 8267327 ER PT J AU GARRISON, RJ GOLD, RS WILSON, PWF KANNEL, WB AF GARRISON, RJ GOLD, RS WILSON, PWF KANNEL, WB TI EDUCATIONAL-ATTAINMENT AND CORONARY HEART-DISEASE RISK - THE FRAMINGHAM OFFSPRING STUDY SO PREVENTIVE MEDICINE LA English DT Article ID CIGARETTE-SMOKING; PHYSICAL-ACTIVITY; YOUNG-ADULTS; CARDIA; MORTALITY; TRENDS; LEVEL C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,EPIDEMIOL & BIOMETRY PROGRAM,FIELD STUDIES & BIOMETRY BRANCH,FRAMINGHAM,MA 01701. BOSTON UNIV,SCH MED,PREVENT MED & EPIDEMIOL SECT,FRAMINGHAM,MA 01701. RP GARRISON, RJ (reprint author), NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,EPIDEMIOL & BIOMETRY PROGRAM,BETHESDA,MD 20892, USA. NR 26 TC 67 Z9 70 U1 1 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0091-7435 J9 PREV MED JI Prev. Med. PD JAN PY 1993 VL 22 IS 1 BP 54 EP 64 DI 10.1006/pmed.1993.1004 PG 11 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA KH602 UT WOS:A1993KH60200004 PM 8475012 ER PT B AU SCHMITT, JM KNUTTEL, A GANDJBAKHCHE, A BONNER, RF AF SCHMITT, JM KNUTTEL, A GANDJBAKHCHE, A BONNER, RF BE Podbielska, H Katzir, A TI OPTICAL CHARACTERIZATION OF DENSE TISSUES USING LOW-COHERENCE INTERFEROMETRY SO PROCEEDINGS OF HOLOGRAPHY, INTERFEROMETRY, AND OPTICAL PATTERN RECOGNITION IN BIOMEDICINE III SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT 3rd Meeting on Holography, Interferometry, and Optical Pattern Recognition in Biomedicine CY JAN 19-20, 1993 CL LOS ANGELES, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS, BIOMED OPT SOC C1 NCRR,NATL INST HLTH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RI Bonner, Robert/C-6783-2015; Podbielska, Halina/A-7311-2012 OI Podbielska, Halina/0000-0001-7162-8530 NR 0 TC 55 Z9 55 U1 0 U2 5 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1116-7 J9 P SOC PHOTO-OPT INS PY 1993 VL 1889 BP 197 EP 211 DI 10.1117/12.155715 PG 15 WC Engineering, Biomedical; Optics SC Engineering; Optics GA BZ41F UT WOS:A1993BZ41F00022 ER PT B AU LINDBERG, DAB AF LINDBERG, DAB BE Reichert, A Sadan, BA Bengtsson, S Bryant, J Piccolo, U TI HIGH-PERFORMANCE COMPUTING AND COMMUNICATIONS - THE MEDICAL CONNECTION SO PROCEEDINGS OF MIE 93: ELEVENTH INTERNATIONAL CONGRESS OF THE EUROPEAN FEDERATION FOR MEDICAL INFORMATICS LA English DT Proceedings Paper CT 11th International Congress of the European-Federation-for-Medical-Informatics - MIE 93 CY APR 18-22, 1993 CL JERUSALEM, ISRAEL SP EUROPEAN FEDERAT MED INFORMAT, ISRAEL ASSOC MED INFORMAT C1 US NATL LIB MED,BETHESDA,MD 20894. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FREUND PUBL HOUSE LTD PI LONDON PA SUITE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA BN 965-294-091-7 PY 1993 BP 19 EP 23 PG 5 WC Computer Science, Information Systems; Information Science & Library Science SC Computer Science; Information Science & Library Science GA BZ59J UT WOS:A1993BZ59J00004 ER PT J AU RYU, S KIM, J ADHYA, S GARGES, S AF RYU, S KIM, J ADHYA, S GARGES, S TI PIVOTAL ROLE OF AMINO-ACID AT POSITION-138 IN THE ALLOSTERIC HINGE REORIENTATION OF CAMP RECEPTOR PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID GENE ACTIVATOR PROTEIN; ESCHERICHIA-COLI; CYCLIC-AMP; CONFORMATIONAL TRANSITIONS; RAMAN-SPECTROSCOPY; DNA; BINDING; CAP; RESOLUTION; COMPLEX AB The cAMP receptor protein (CRP) of Escherichia coli needs cAMP for an allosteric change to regulate gene expression by binding to specific DNA sites. The hinge region connecting the DNA-binding domain to the cAMP-binding domain has been proposed to participate in the cAMP-induced allosteric change necessary to adjust C and D alpha-helices for movement of the DNA-binding F alpha-helix away from the protein surface. The role of the hinge region for a conformation change in CRP was tested by studying the effects of single amino acid substitutions at residue 138 located within the hinge. Physiological studies of wild-type and mutant cells and biochemical analysis of purified wild-type and mutant CRP revealed at least three groups of altered CRPs: (i) CRP that behaves like wild type (CRP+); (ii) CRP that binds cAMP but does not complete the structural changes required for specific DNA binding, proteolytic cleavage, and transcription activation (CRP(allo)); and (iii) CRP that shows some or all; of these conformational changes without cAMP (CRP*). These results show a pivotal role of position 138 from which change emanates and provide further evidence that a hinge reorientation involving residue 138 is involved in the interhelical adjustments. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 27 TC 59 Z9 60 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 JAN 1 PY 1993 VL 90 IS 1 BP 75 EP 79 DI 10.1073/pnas.90.1.75 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KF407 UT WOS:A1993KF40700016 PM 8380500 ER PT J AU PINCUS, SH MCCLURE, J AF PINCUS, SH MCCLURE, J TI SOLUBLE CD4 ENHANCES THE EFFICACY OF IMMUNOTOXINS DIRECTED AGAINST GP41 OF THE HUMAN-IMMUNODEFICIENCY-VIRUS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE COMBINATION THERAPY; AIDS; ANTIBODY; IMMUNOGLOBULIN ID RICIN-A-CHAIN; ENVELOPE GLYCOPROTEIN; MONOCLONAL-ANTIBODIES; NONHUMAN-PRIMATES; INFECTED-CELLS; T-CELLS; HIV; REGION; DISSOCIATION; BINDING AB Monoclonal antibodies specific for the gp120) or gp41 portions of the human immunodeficiency virus (HIV) envelope protein gp160 were conjugated to ricin A chain, and their immunotoxic activities against HIV-infected cells were evaluated in the presence or absence of soluble CD4 (sCD4). Immunotoxin activity was measured in vitro as cytotoxicity and inhibition of secretion of infectious HIV. The efficacy of anti-gp41 immunotoxins was enhanced at least 30-fold in the presence of sCD4. This effect was specific for HIV-infected cells, but not for uninfected cells, and was seen at concentrations of sCD4 as low as 0.1 mug/ml. Anti-gp120 immunotoxins were marginally inhibited at higher concentrations of sCD4. Flow cytometry analyses showed that sCD4 increased the expression of gp41 on the surface of infected cells and increased internalization of gp120 and gp41. These data suggest that sCD4 alters the cellular trafficking of HIV envelope proteins. These findings also have important implications for the therapeutic use of anti-HIV immunotoxins and may be generalizable to other immunotoxins as well. C1 BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,SEATTLE,WA 98121. RP PINCUS, SH (reprint author), NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840, USA. NR 28 TC 25 Z9 25 U1 0 U2 0 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 JAN 1 PY 1993 VL 90 IS 1 BP 332 EP 336 DI 10.1073/pnas.90.1.332 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KF407 UT WOS:A1993KF40700068 PM 8419938 ER PT J AU HENNINGS, H GLICK, AB GREENHALGH, DA MORGAN, DL STRICKLAND, JE TENNENBAUM, T YUSPA, SH AF HENNINGS, H GLICK, AB GREENHALGH, DA MORGAN, DL STRICKLAND, JE TENNENBAUM, T YUSPA, SH TI CRITICAL ASPECTS OF INITIATION, PROMOTION, AND PROGRESSION IN MULTISTAGE EPIDERMAL CARCINOGENESIS SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID MOUSE SKIN TUMORS; HARVEY-RAS GENE; MALIGNANT CONVERSION; HA-RAS; BENIGN-TUMORS; FOS ONCOGENE; CELL-LINES; V-RAS; PAPILLOMAS; URETHANE AB Carcinogenesis in mouse skin can be divided into three distinct stages: initiation, promotion, and progression (malignant conversion). Initiation, induced by a single exposure to a genotoxic carcinogen, can result from a mutation in a single critical gene (e.g., ras(Ha)), apparently in only a few epidermal cells. The change is irreversible. Promotion, resulting in the development of numerous benign tumors (papillomas), is accomplished by the repeated application of a nonmutagenic tumor promoter. The effects of single applications of tumor promoters are reversible since papillomas do not develop after insufficient exposure of initiated skin to promoters or when the interval between individual promoter applications is increased sufficiently. The reversibility of promotion suggests an epigenetic mechanism. Promoter treatment provides an environment that allows the selective clonal expansion of foci of initiated cells. The conversion of squamous papillomas to carcinomas (termed progression or malignant conversion) occurs spontaneously at a low frequency. The rate of progression to malignancy can be significantly increased by treatment of papilloma-bearing mice with certain genotoxic agents. These progressor agents or converting agents are likely to act via a second genetic change in papillomas already bearing the initiating mutation. Progression in the skin is characterized by genetic changes that result in several distinct changes in the levels or activity of structural proteins, growth factors, and proteases. The mechanisms involved in progression are being studied in epidermal cell culture. In order to determine the in vivo phenotype of cultured cells, a grafting system was developed in which the cells were transferred from culture to a prepared skin bed in athymic mice. Introduction of an activated v-fos oncogene into initiated cells bearing an activated ras(Ha) gene produced cells with a carcinoma phenotype, i.e., carcinomas formed when the cells were grafted as part of reconstituted skin. Grafted keratinocytes containing the ras(Ha) gene alone produced papillomas; with v-fos alone, normal skin formed when grafted. The ras(Ha)/fos carcinomas showed changes in differentiation markers characteristic of chemically induced carcinomas. A cell culture assay utilizing cells initiated by the introduction of an activated ras(Ha) oncogene was developed to study progression. After exposure of initiated cells to progressor agents under conditions in which the proliferation of the ras(Ha)-initiated cells was suppressed, proliferating foci developed, with a good correlation of activity in the assay with activity in the progression stage in vivo. The cell culture assay provides a quantitative model to study chemically induced neoplastic progression and may be useful to identify potential progressor agents. RP HENNINGS, H (reprint author), NCI,DIV CANC ETIOL,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BLDG 37,BETHESDA,MD 20892, USA. NR 54 TC 94 Z9 95 U1 1 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD JAN PY 1993 VL 202 IS 1 BP 1 EP 18 PG 18 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KE687 UT WOS:A1993KE68700001 PM 8424089 ER PT J AU BARRETT, JC AF BARRETT, JC TI NEOPLASTIC PROGRESSION OF SYRIAN-HAMSTER EMBRYO CELLS IN CULTURE SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID POSSIBLE INVOLVEMENT; SENESCENT CELLS; CHROMOSOME; INVITRO; CYCLE; LINE; IMMORTALIZATION; TRANSFORMATION; PHOSPHORYLATE; SUPPRESSION RP BARRETT, JC (reprint author), NIEHS,MOLEC CARCINOGENESIS LAB,MD D2-04,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 35 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD JAN PY 1993 VL 202 IS 1 BP 30 EP 36 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KE687 UT WOS:A1993KE68700005 PM 8424093 ER PT J AU DAVIS, CD ZECH, L GREGER, JL AF DAVIS, CD ZECH, L GREGER, JL TI MANGANESE METABOLISM IN RATS - AN IMPROVED METHODOLOGY FOR ASSESSING GUT ENDOGENOUS LOSSES SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID DIETARY MANGANESE; TRUE ABSORPTION; GROWING-RATS; COPPER; BALANCE; PHOSPHORUS; TRANSPORT; PROTEIN AB Manganese homeostasis is believed to be maintained by excretion of excess absorbed manganese through the gut, but the extent of endogenous gut losses of manganese has not been quantitated. We developed a model with rats to quantitate endogenous gut losses of manganese in which the parenterally administered isotope was distributed like fed isotope. Intraportally injected Mn-54 complexed to albumin distributed in tissues like the fed isotope, but carrier-free Mn-54 injected intraperitoneally, intravenously, or intraportally, or Mn-54 complexed to transferrin and injected intraportally did not. Thus, manganese appears to be complexed to albumin or an albumin-like protein when it leaves the intestine. A mathematical model of manganese metabolism in rats fed Mn-54 was developed using the SAAM and CONSAM computer programs. It was determined that the liver, not the pancreas, was the major source of endogenous gut losses of manganese. Young, growing rats fed 45 mug of Mn/g diet were calculated to absorb 8.2% of their manganese intake and then to lose 37% of the absorbed manganese through gut endogenous losses. C1 NCI,BETHESDA,MD 20892. RP DAVIS, CD (reprint author), UNIV WISCONSIN,DEPT NUTR SCI,1415 LINDEN DR,MADISON,WI 53706, USA. FU NIDDK NIH HHS [R01-DK41940]; PHS HHS [5T32CS09451] NR 27 TC 60 Z9 62 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD JAN PY 1993 VL 202 IS 1 BP 103 EP 108 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KE687 UT WOS:A1993KE68700014 PM 8424090 ER PT B AU UNSER, M ALDROUBI, A AF UNSER, M ALDROUBI, A GP JOHNS HOPKINS UNIV TI GENERALIZED SAMPLING WITH APPLICATION TO THE WAVELET TRANSFORM SO PROCEEDINGS OF THE TWENTY-SEVENTH ANNUAL CONFERENCE ON INFORMATION SCIENCES AND SYSTEMS LA English DT Proceedings Paper CT 27th Annual Conference on Information Sciences and Systems CY MAR 24-26, 1993 CL JOHNS HOPKINS UNIV, BALTIMORE, MD SP JOHNS HOPKINS UNIV, DEPT ELECT & COMP ENGN HO JOHNS HOPKINS UNIV C1 NIH,NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHNS HOPKINS UNIV DEPT ELECTRICA & COMPUTER ENGINEERING PI BALTIMORE PA BALTIMORE, MD 21218 PY 1993 BP 40 EP 45 PG 6 WC Computer Science, Information Systems; Engineering, Electrical & Electronic; Optics SC Computer Science; Engineering; Optics GA BB64Q UT WOS:A1993BB64Q00008 ER PT J AU WILLIAMS, LR RYLETT, RJ INGRAM, DK JOSEPH, JA MOISES, HC TANG, AH MERVIS, RF AF WILLIAMS, LR RYLETT, RJ INGRAM, DK JOSEPH, JA MOISES, HC TANG, AH MERVIS, RF TI NERVE GROWTH-FACTOR AFFECTS THE CHOLINERGIC NEUROCHEMISTRY AND BEHAVIOR OF AGED RATS SO PROGRESS IN BRAIN RESEARCH LA English DT Review ID MESENCEPHALIC LOCOMOTOR REGION; ACETYLTRANSFERASE ACTIVITY; ALZHEIMERS-DISEASE; BASAL FOREBRAIN; ACETYLCHOLINE; PERFORMANCE; IMPAIRMENT; ANTAGONISM; NEURONS; SYSTEM C1 UNIV WESTERN ONTARIO,DEPT PHYSIOL,LONDON N6A 3K7,ONTARIO,CANADA. UNIV WESTERN ONTARIO,ROBARTS RES INST,LONDON N6A 3K7,ONTARIO,CANADA. NIA,GERONTOL RES CTR,MOLEC PHYSIOL & GENET SECT,BALTIMORE,MD 21224. UNIV MICHIGAN,DEPT PHYSIOL,ANN ARBOR,MI 48109. NEUROMETRIX IMAGING RES INC,COLUMBUS,OH. RP WILLIAMS, LR (reprint author), UPJOHN CO,CNS DIS RES,KALAMAZOO,MI 49001, USA. RI Rylett, Rebecca Jane/K-3597-2013 OI Rylett, Rebecca Jane/0000-0002-9158-9599 NR 25 TC 14 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 J9 PROG BRAIN RES JI Prog. Brain Res. PY 1993 VL 98 BP 251 EP 256 PG 6 WC Neurosciences SC Neurosciences & Neurology GA MA269 UT WOS:A1993MA26900032 PM 8248514 ER PT J AU COLBY, CL DUHAMEL, JR GOLDBERG, ME AF COLBY, CL DUHAMEL, JR GOLDBERG, ME TI THE ANALYSIS OF VISUAL SPACE BY THE LATERAL INTRAPARIETAL AREA OF THE MONKEY - THE ROLE OF EXTRARETINAL SIGNALS SO PROGRESS IN BRAIN RESEARCH LA English DT Review ID PARIETAL ASSOCIATION CORTEX; SACCADE-RELATED ACTIVITY; FRONTAL EYE FIELDS; SUPERIOR COLLICULUS; MACAQUE; RESPONSES; NEURONS; PRIMATE; MEMORY; MECHANISMS RP COLBY, CL (reprint author), NEI,SENSORIMOTOR RES LAB,BLDG 10,ROOM 10C-101,BETHESDA,MD 20892, USA. NR 31 TC 46 Z9 46 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 J9 PROG BRAIN RES JI Prog. Brain Res. PY 1993 VL 95 BP 307 EP 316 DI 10.1016/S0079-6123(08)60378-7 PG 10 WC Neurosciences SC Neurosciences & Neurology GA LD817 UT WOS:A1993LD81700027 PM 8493341 ER PT J AU ROBINSON, DL AF ROBINSON, DL TI FUNCTIONAL CONTRIBUTIONS OF THE PRIMATE PULVINAR SO PROGRESS IN BRAIN RESEARCH LA English DT Review ID VISUAL SPATIAL ATTENTION; MONKEY SUPERIOR COLLICULUS; INDUCED STIMULUS MOVEMENT; BEHAVING RHESUS-MONKEY; INFERIOR PULVINAR; MACACA-MULATTA; CORTICAL PROJECTIONS; LATERAL PULVINAR; RECEPTIVE-FIELDS; PARIETAL CORTEX RP ROBINSON, DL (reprint author), NEI,SENSORIMOTOR RES LAB,VISUAL BEHAV SECT,BETHESDA,MD 20892, USA. NR 47 TC 56 Z9 56 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 J9 PROG BRAIN RES JI Prog. Brain Res. PY 1993 VL 95 BP 371 EP 380 DI 10.1016/S0079-6123(08)60382-9 PG 10 WC Neurosciences SC Neurosciences & Neurology GA LD817 UT WOS:A1993LD81700031 PM 8493346 ER PT S AU DOPPMAN, JL AF DOPPMAN, JL BE Mornex, R Jaffiol, C Leclere, J TI THE VALUE OF LOCAL HORMONE SAMPLING IN THE EVALUATION OF THE HYPOTHALAMOPITUITARY AXIS SO PROGRESS IN ENDOCRINOLOGY SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES LA English DT Proceedings Paper CT 9th International Congress of Endocrinology: Progress in Endocrinology CY SEP, 1992 CL NICE, FRANCE C1 NIH,WARREN & MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA SN 0969-2622 BN 1-85070-469-4 J9 I C S S PY 1993 VL 3 BP 106 EP 110 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA12S UT WOS:A1993BA12S00023 ER PT S AU LOPEZ, FJ MERCHENTHALER, I LIPOSITS, Z MORETTO, M MEADE, EH NEGROVILAR, A AF LOPEZ, FJ MERCHENTHALER, I LIPOSITS, Z MORETTO, M MEADE, EH NEGROVILAR, A BE Mornex, R Jaffiol, C Leclere, J TI GALANIN - A HYPOTHALAMIC HYPOPHYSIOTROPIC HORMONE SO PROGRESS IN ENDOCRINOLOGY SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES LA English DT Proceedings Paper CT 9th International Congress of Endocrinology: Progress in Endocrinology CY SEP, 1992 CL NICE, FRANCE C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,REPROD MORPHOL SECT,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA SN 0969-2622 BN 1-85070-469-4 J9 I C S S PY 1993 VL 3 BP 143 EP 146 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA12S UT WOS:A1993BA12S00031 ER PT S AU NEGROVILAR, A LOPEZ, F MERCHENTHALER, I WETSEL, W AF NEGROVILAR, A LOPEZ, F MERCHENTHALER, I WETSEL, W BE Mornex, R Jaffiol, C Leclere, J TI STEROID EFFECTS ON LHRH CELLS SO PROGRESS IN ENDOCRINOLOGY SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES LA English DT Proceedings Paper CT 9th International Congress of Endocrinology: Progress in Endocrinology CY SEP, 1992 CL NICE, FRANCE C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA SN 0969-2622 BN 1-85070-469-4 J9 I C S S PY 1993 VL 3 BP 152 EP 154 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA12S UT WOS:A1993BA12S00033 ER PT S AU WEINTRAUB, BD AF WEINTRAUB, BD BE Mornex, R Jaffiol, C Leclere, J TI GENERALIZED THYROID-HORMONE RESISTANCE SO PROGRESS IN ENDOCRINOLOGY SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES LA English DT Proceedings Paper CT 9th International Congress of Endocrinology: Progress in Endocrinology CY SEP, 1992 CL NICE, FRANCE C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA SN 0969-2622 BN 1-85070-469-4 J9 I C S S PY 1993 VL 3 BP 326 EP 330 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA12S UT WOS:A1993BA12S00075 ER PT S AU AGUILERA, G AF AGUILERA, G BE Mornex, R Jaffiol, C Leclere, J TI ANGIOTENSIN-II RECEPTOR SUBTYPES AND REGULATION OF ALDOSTERONE SECRETION IN THE ADRENAL GLOMERULOSA ZONE IN THE RAT SO PROGRESS IN ENDOCRINOLOGY SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES LA English DT Proceedings Paper CT 9th International Congress of Endocrinology: Progress in Endocrinology CY SEP, 1992 CL NICE, FRANCE C1 NICHHD,ENDOCRINE PHYSIOL SECT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA SN 0969-2622 BN 1-85070-469-4 J9 I C S S PY 1993 VL 3 BP 541 EP 544 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA12S UT WOS:A1993BA12S00124 ER PT S AU TAYLOR, SI ACCILI, D CAMA, A KOLLER, E LEVYTOLEDANO, R QUON, MJ SIERRA, MD WERTHEIMER, E AF TAYLOR, SI ACCILI, D CAMA, A KOLLER, E LEVYTOLEDANO, R QUON, MJ SIERRA, MD WERTHEIMER, E BE Mornex, R Jaffiol, C Leclere, J TI MUTATIONS IN THE INSULIN-RECEPTOR GENE IN INSULIN-RESISTANT PATIENTS SO PROGRESS IN ENDOCRINOLOGY SE INTERNATIONAL CONGRESS, SYMPOSIUM AND SEMINAR SERIES LA English DT Proceedings Paper CT 9th International Congress of Endocrinology: Progress in Endocrinology CY SEP, 1992 CL NICE, FRANCE C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP LTD PI LANCASTER PA CASTERTON HALL, CARNFORTH, LANCASTER, ENGLAND LA6 2LA SN 0969-2622 BN 1-85070-469-4 J9 I C S S PY 1993 VL 3 BP 811 EP 813 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA12S UT WOS:A1993BA12S00185 ER PT J AU KIM, HY SALEM, N AF KIM, HY SALEM, N TI LIQUID-CHROMATOGRAPHY MASS-SPECTROMETRY OF LIPIDS SO PROGRESS IN LIPID RESEARCH LA English DT Review ID HIGH-PERFORMANCE LIQUID; MOLECULAR-SPECIES ANALYSIS; FATTY-ACID COMPOSITION; PHOSPHOLIPIDS; IONIZATION; INTERFACE; SEPARATION; PHOSPHATIDYLCHOLINE; QUANTITATION; CAPILLARY RP KIM, HY (reprint author), NIAAA,DICBR,MEMBRANE BIOCHEM & BIOPHYS LAB,MASS SPECTROMETRY SECT,BLDG 10,ROOM 3C-212,BETHESDA,MD 20892, USA. NR 56 TC 31 Z9 34 U1 0 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0163-7827 J9 PROG LIPID RES JI Prog. Lipid. Res. PY 1993 VL 32 IS 3 BP 221 EP 245 DI 10.1016/0163-7827(93)90008-K PG 25 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA MP686 UT WOS:A1993MP68600001 PM 8140113 ER PT J AU ROBINSON, JK CRAWLEY, JN AF ROBINSON, JK CRAWLEY, JN TI THE ROLE OF GALANIN IN CHOLINERGICALLY-MEDIATED MEMORY PROCESSES SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE ACETYLCHOLINE; ALZHEIMERS DISEASE; GALANIN; HIPPOCAMPUS; MEMORY; NEUROPEPTIDES; NUCLEUS BASALIS OF MEYNERT ID CENTRAL NERVOUS-SYSTEM; BASAL FOREBRAIN COMPLEX; RAT VENTRAL HIPPOCAMPUS; ALZHEIMERS-DISEASE; CEREBRAL-CORTEX; PARKINSONS-DISEASE; NUCLEUS BASALIS; MESSENGER-RNA; BINDING-SITES; PHOSPHOINOSITIDE TURNOVER AB 1. Galanin, a 29 amino-acid neuroactive peptide, has been shown to affect diverse processes throughout the nervous system and to coexist with several ''classical'' neurotransmitters, including norepinephrine, serotonin, and acetylcholine. 2. Galanin coexists with acetylcholine in neurons of the medial septum, diagonal band, and nucleus basalis of Meynert, cells which degenerate during the course of Alzheimer's disease. 3. In the ventral hippocampus, galanin inhibits the release of acetylcholine and inhibits carbachol stimulated phosphatidyl inositol hydrolysis. 4. Galanin impairs choice accuracy in learning and memory paradigms in rats, and is therefore hypothesized to be a contributory factor in the memory and cognitive disabilities found in Alzheimer's patients. 5. Newly developed galanin antagonists, by eliminating putative inhibitory effects of endogenous galanin on cholinergic function, may serve as useful therapies for memory disorders. RP ROBINSON, JK (reprint author), NIMH,EXPTL THERAPEUT BRANCH,UNIT BEHAV NEUROPHARMACOL,BLDG 10,ROOM 4N214,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 90 TC 19 Z9 19 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0278-5846 J9 PROG NEURO-PSYCHOPH JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry PD JAN PY 1993 VL 17 IS 1 BP 71 EP 85 DI 10.1016/0278-5846(93)90033-O PG 15 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA JZ938 UT WOS:A1993JZ93800003 PM 7677976 ER PT J AU PETERKOFSKY, A REIZER, A REIZER, J GOLLOP, N ZHU, PP AMIN, N AF PETERKOFSKY, A REIZER, A REIZER, J GOLLOP, N ZHU, PP AMIN, N TI BACTERIAL ADENYLYL CYCLASES SO PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL 44 SE PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY LA English DT Review ID SUGAR PHOSPHOTRANSFERASE SYSTEM; SITE-DIRECTED MUTAGENESIS; ESCHERICHIA-COLI F1-ATPASE; NUCLEOTIDE-BINDING DOMAIN; ELONGATION-FACTOR TU; BORDETELLA-PERTUSSIS; BACILLUS-ANTHRACIS; CYCLIC-AMP; SALMONELLA-TYPHIMURIUM; RHIZOBIUM-MELILOTI C1 UNIV CALIF SAN DIEGO,DEPT BIOL,LA JOLLA,CA 92093. RP PETERKOFSKY, A (reprint author), NHLBI,BIOCHEM GENET LAB,BLDG 10,BETHESDA,MD 20892, USA. NR 116 TC 43 Z9 44 U1 3 U2 4 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0278-5846 J9 PROG NUCLEIC ACID RE PY 1993 VL 44 BP 31 EP 65 DI 10.1016/S0079-6603(08)60216-0 PG 35 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ69K UT WOS:A1993BZ69K00002 PM 8434125 ER PT J AU MOSS, J VAUGHAN, M AF MOSS, J VAUGHAN, M TI ADP-RIBOSYLATION FACTORS - PROTEIN ACTIVATORS OF CHOLERA-TOXIN SO PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL 45 SE PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY LA English DT Review ID LABILE ENTERO-TOXIN; NUCLEOTIDE-BINDING-PROTEINS; ADENOSINE-DIPHOSPHATE-RIBOSYLATION; AMINO-ACID-SEQUENCE; ADENYLATE-CYCLASE; ESCHERICHIA-COLI; RIBOSYLTRANSFERASE ACTIVITY; REGULATORY COMPONENT; SIGNAL TRANSDUCTION; GUANYL NUCLEOTIDES RP MOSS, J (reprint author), NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892, USA. NR 81 TC 2 Z9 2 U1 1 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0278-5846 J9 PROG NUCLEIC ACID RE PY 1993 VL 45 BP 47 EP 65 DI 10.1016/S0079-6603(08)60866-1 PG 19 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ69L UT WOS:A1993BZ69L00003 PM 8341803 ER PT J AU OPPENHEIM, AB KORNITZER, D ALTUVIA, S COURT, DL AF OPPENHEIM, AB KORNITZER, D ALTUVIA, S COURT, DL TI POSTTRANSCRIPTIONAL CONTROL OF THE LYSOGENIC PATHWAY IN BACTERIOPHAGE-LAMBDA SO PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL 46 SE PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY LA English DT Review ID INTEGRATION HOST FACTOR; CII GENE-EXPRESSION; OOP ANTISENSE RNA; ESCHERICHIA-COLI; PHAGE-LAMBDA; COLIPHAGE-LAMBDA; MESSENGER-RNA; TRANSLATION INITIATION; INT GENE; PROTEIN C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHROMOSOME BIOL LAB,FREDERICK,MD 21702. RP OPPENHEIM, AB (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT MOLEC GENET,IL-91910 JERUSALEM,ISRAEL. FU NIGMS NIH HHS [GM38694] NR 61 TC 16 Z9 17 U1 1 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0278-5846 J9 PROG NUCLEIC ACID RE PY 1993 VL 46 BP 37 EP 49 DI 10.1016/S0079-6603(08)61017-X PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ69M UT WOS:A1993BZ69M00002 PM 8234786 ER PT J AU MORRISON, A SUGINO, A AF MORRISON, A SUGINO, A TI DNA-POLYMERASE-II, THE EPSILON-POLYMERASE OF SACCHAROMYCES-CEREVISIAE SO PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL 46 SE PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY LA English DT Review ID CELL NUCLEAR ANTIGEN; EXONUCLEASE ACTIVE-SITE; DEOXYRIBONUCLEIC-ACID POLYMERASES; HIGHLY CONSERVED REGION; REPLICATION FACTOR-C; STIMULATORY FACTOR-I; ESCHERICHIA-COLI; 3'-5' EXONUCLEASE; AMINO-ACID; NUCLEOTIDE-SEQUENCE C1 NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709. NR 124 TC 21 Z9 21 U1 2 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0278-5846 J9 PROG NUCLEIC ACID RE PY 1993 VL 46 BP 93 EP 120 DI 10.1016/S0079-6603(08)61019-3 PG 28 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ69M UT WOS:A1993BZ69M00004 PM 8234788 ER PT J AU YAMAZAKI, H DILWORTH, A MYERS, CE SINHA, BK AF YAMAZAKI, H DILWORTH, A MYERS, CE SINHA, BK TI SURAMIN INHIBITS DNA-DAMAGE IN HUMAN PROSTATE-CANCER CELLS TREATED WITH TOPOISOMERASE INHIBITORS IN-VITRO SO PROSTATE LA English DT Article DE ETOPOSIDE; CAMPTOTHECINS; COMBINATION CHEMOTHERAPY ID TUMOR-NECROSIS-FACTOR; ANTICANCER DRUG; GROWTH-FACTOR; STRAND BREAKS; FREE-RADICALS; MECHANISM; ETOPOSIDE; POLYMERASES; XENOGRAFTS; LINES AB Suramin, a highly sulfonated drug, has been reported to be effective against several human malignancies in vitro and in vivo, and currently is undergoing clinical trials against prostate tumors. The biochemical and molecular mechanisms for suramin's antiproliferative activity are not clear. In order to define the biochemical basis for its antitumor activity and to enhance suramin's chemotherapeutic potential while decreasing its toxicity, we have examined interactions of suramin with topoisomerase I and II and several clinically active anticancer drugs against the human prostate (PC3 and LNCaP) cancer cell line. While etoposide, m-AMSA, camptothecin, and SN-38 (the active metabolite of CPT-11) were active in killing prostate cells as single agents, combinations of suramin and these agents were antagonistic against these cells. We found that suramin inhibited activities of purified topoisomerase I and II in vitro as measured by relaxation and cleavage assays. Further studies indicated that suramin also inhibited the drug-induced DNA damage in vitro and in isolated nuclei. These findings indicate that combinations of suramin with topoisomerase inhibitors, for example, VP-16, m-AMSA, or CPT, may not be beneficial to patients receiving suramin-containing chemotherapy. (C) 1993 Wiley-Liss, Inc. C1 NCI,CLIN PHARMACOL BRANCH,BIOCHEM & MOLEC PHARMACOL SECT,BLDG 10,ROOM 6N-119,BETHESDA,MD 20892. NR 33 TC 16 Z9 16 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 0270-4137 J9 PROSTATE JI Prostate PY 1993 VL 23 IS 1 BP 25 EP 36 DI 10.1002/pros.2990230104 PG 12 WC Endocrinology & Metabolism; Urology & Nephrology SC Endocrinology & Metabolism; Urology & Nephrology GA LQ794 UT WOS:A1993LQ79400003 PM 8393191 ER PT J AU PARDA, DS THRAVES, PJ KUETTEL, MR LEE, MS ARNSTEIN, P KAIGHN, ME RHIM, JS DRITSCHILO, A AF PARDA, DS THRAVES, PJ KUETTEL, MR LEE, MS ARNSTEIN, P KAIGHN, ME RHIM, JS DRITSCHILO, A TI NEOPLASTIC TRANSFORMATION OF A HUMAN PROSTATE EPITHELIAL-CELL LINE BY THE V-KI-RAS ONCOGENE SO PROSTATE LA English DT Article DE PROSTATE CARCINOGENESIS; 267B1 CELL LINE; IN-VITRO TRANSFORMATION ID EXPRESSION; CARCINOMA; CANCER; ADENOCARCINOMA; CARCINOGENESIS; ACTIVATION; P21 AB Investigations of mechanisms of human prostate carcinogenesis are limited by the unavailability of a suitable in vitro model system. We have demonstrated that an immortal, but nontumorigenic, human epithelial cell line (267B1) established from fetal prostate tissue can be malignantly transformed by a biological carcinogen, and can serve as a useful model for investigations of the progression steps of carcinogenesis. Activated Ki-ras was introduced into 267B1 cells by infection with the Kirsten murine sarcoma virus. Morphological alterations and anchorage-independent growth were observed; when cells were injected into nude mice, poorly differentiated adenocarcinomas developed. These findings represent the first evidence of malignant transformation of human prostate epithelial cells in culture, and support a role for Ki-ras activation in a multistep process for prostate neoplastic transformation. (C) 1993 Wiley-Liss, Inc. C1 GEORGETOWN UNIV,SCH MED,VINCENT T LOMBARDI CANC RES CTR,DEPT RADIAT MED,WASHINGTON,DC 20007. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. BIOL RES FAC & FACIL,IJAMSVILLE,MD. FU NCI NIH HHS [P01-CA52066, CA52954, CA52945] NR 19 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 0270-4137 J9 PROSTATE JI Prostate PY 1993 VL 23 IS 2 BP 91 EP 98 DI 10.1002/pros.2990230202 PG 8 WC Endocrinology & Metabolism; Urology & Nephrology SC Endocrinology & Metabolism; Urology & Nephrology GA LY671 UT WOS:A1993LY67100001 PM 8378190 ER PT J AU FISHER, RJ FIVASH, MJ BAXEVANIS, AD MAVROTHALASSITIS, G BLADEN, SV MOUDRIANAKIS, EN PAPAS, TS AF FISHER, RJ FIVASH, MJ BAXEVANIS, AD MAVROTHALASSITIS, G BLADEN, SV MOUDRIANAKIS, EN PAPAS, TS TI REAL-TIME MEASUREMENT OF THE ETSI PROTEIN AND ETSI BASIC DOMAIN INTERACTION WITH MATRIX-BOUND SPECIFIC AND MUTANT-DNA SO PROTEIN ENGINEERING LA English DT Meeting Abstract C1 DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD. DATA MANAGEMENT SERV,FREDERICK,MD. JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. RI Fisher, Robert/B-1431-2009 NR 1 TC 3 Z9 3 U1 1 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PY 1993 VL 6 SU S BP 13 EP 13 PG 1 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KT952 UT WOS:A1993KT95200018 ER PT J AU HODGE, DR PANAYIOTAKIS, A ROBINSON, L WATSON, DK SETH, A AF HODGE, DR PANAYIOTAKIS, A ROBINSON, L WATSON, DK SETH, A TI EXPRESSION OF ETS1 TRANSCRIPTION FACTOR USING BACULOVIRAL SYSTEM IN SF9 INSECT CELLS AND ITS SEQUENCE-SPECIFIC BINDING WITH HIV-2 LTR SO PROTEIN ENGINEERING LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. NCI,FCRDC,DYNCORP INC,PROGRAM RESOURCES,FREDERICK,MD 21702. NR 4 TC 0 Z9 0 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PY 1993 VL 6 SU S BP 32 EP 32 PG 1 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KT952 UT WOS:A1993KT95200048 ER PT J AU PASTAN, IH AF PASTAN, IH TI RECOMBINANT TOXINS - NEW AND THERAPEUTIC AGENTS FOR CANCER SO PROTEIN ENGINEERING LA English DT Meeting Abstract C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PY 1993 VL 6 SU S BP 60 EP 60 PG 1 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KT952 UT WOS:A1993KT95200088 ER PT J AU BHAT, NK DERSE, D ADACHI, Y SUZUKI, H ROMANOSPICA, V PAPAS, TS AF BHAT, NK DERSE, D ADACHI, Y SUZUKI, H ROMANOSPICA, V PAPAS, TS TI CHARACTERIZATION OF VIRAL REGULATORY MUTANT PROTEINS FROM HUMAN T-CELL LEUKEMIA-VIRUS INFECTED CELL-LINES SO PROTEIN ENGINEERING LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. DYNCORP INC,PROGRAM RESOURCES,FREDERICK,MD 21702. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. ADV BIOSCI LABS INC,FREDERICK CANC RES & DEV CTR,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 3 TC 0 Z9 0 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PY 1993 VL 6 SU S BP 62 EP 62 PG 1 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KT952 UT WOS:A1993KT95200091 ER PT J AU MESRI, EA FU, YM KREITMAN, RJ EPSTEIN, SE PASTAN, I AF MESRI, EA FU, YM KREITMAN, RJ EPSTEIN, SE PASTAN, I TI ADDITION OF A HEPARIN BINDING-SITE TO A CHIMERIC TOXIN CONFERS HEPARIN MODULATION AND IMPROVES ITS CYTOTOXICITY TO TUMOR AND PROLIFERATING VASCULAR SMOOTH-MUSCLE CELLS SO PROTEIN ENGINEERING LA English DT Meeting Abstract C1 NCI,DCBDC,MOLEC BIOL LAB,BETHESDA,MD 20892. NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 4 TC 0 Z9 0 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PY 1993 VL 6 SU S BP 67 EP 67 PG 1 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KT952 UT WOS:A1993KT95200102 ER PT J AU QASBA, PK MASIBAY, AS BOEGGEMAN, EE BALAJI, PV AF QASBA, PK MASIBAY, AS BOEGGEMAN, EE BALAJI, PV TI STUDY OF THE FUNCTIONAL DOMAINS OF BETA-1-4GALACTOSYLTRANSFERASE THROUGH THE EXPRESSION OF THE DELETION CONSTRUCTS OF CDNA IN ESCHERICHIA-COLI AND MAMMALIAN-CELLS - DISULFIDE BOND BETWEEN CYS134 AND CYS247 IS REQUIRED FOR FOLDING AND ENZYME-ACTIVITY WHILE THE TRANSMEMBRANE DOMAIN IS ESSENTIAL FOR STABLE EXPRESSION IN MAMMALIAN-CELLS SO PROTEIN ENGINEERING LA English DT Meeting Abstract C1 NIH,DIV CANC INST,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PY 1993 VL 6 SU S BP 99 EP 99 PG 1 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KT952 UT WOS:A1993KT95200151 ER PT J AU SAMUDZI, CT NGUYEN, NY RUBIN, JR AF SAMUDZI, CT NGUYEN, NY RUBIN, JR TI CRYSTALLIZATION AND PRELIMINARY-X-RAY DIFFRACTION STUDIES OF DOGFISH C-REACTIVE PROTEIN SO PROTEINS-STRUCTURE FUNCTION AND GENETICS LA English DT Article DE DOGFISH C-REACTIVE PROTEIN; VAPOR PHASE EQUILIBRATION; AMMONIUM SULFATE; SITTING DROP TECHNIQUE; HEXAMERS ID POLYSACCHARIDE AB Crystals of dogfish (Mustelus canis) C-reactive protein were obtained through vapor phase equilibration using the sitting drop rod technique with ammonium sulfate as the precipitating agent. The space group was determined to be P1 (triclinic lattice) with unit cell dimensions of a = 82.91, b = 92.25 and c = 103.40 angstrom; alpha = 83.36-degrees, beta = 89.76-degrees, and gamma = 81.30-degrees. These crystals diffract to about 2.6 angstrom resolution and contain two hexamers in the asymmetric unit. C1 US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,BETHESDA,MD 20892. RP SAMUDZI, CT (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 20 TC 1 Z9 1 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-3585 J9 PROTEINS JI Proteins PD JAN PY 1993 VL 15 IS 1 BP 100 EP 102 DI 10.1002/prot.340150112 PG 3 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KC061 UT WOS:A1993KC06100011 PM 8451236 ER PT S AU MAURIZI, MR AF MAURIZI, MR BE Bond, JS Barrett, AJ TI ATP-DEPENDENT PROTEASES SO PROTEOLYSIS AND PROTEIN TURNOVER SE PORTLAND PRESS PROCEEDINGS LA English DT Proceedings Paper CT 9th International-Committee-on-Proteolysis Meeting: Proteolysis and Protein Turnover CY OCT, 1992 CL WILLIAMSBURG, VA SP INT COMM PROTEOLYSIS C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PORTLAND PRESS LTD PI LONDON PA 59 PORTLAND PL, LONDON, ENGLAND W1N 3AJ SN 0966-4068 BN 1-85578-041-0 J9 PORTL PR P PY 1993 BP 65 EP 71 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ95S UT WOS:A1993BZ95S00010 ER PT S AU GOTTESMAN, MM AF GOTTESMAN, MM BE Bond, JS Barrett, AJ TI CATHEPSIN-L AND CANCER SO PROTEOLYSIS AND PROTEIN TURNOVER SE PORTLAND PRESS PROCEEDINGS LA English DT Proceedings Paper CT 9th International-Committee-on-Proteolysis Meeting: Proteolysis and Protein Turnover CY OCT, 1992 CL WILLIAMSBURG, VA SP INT COMM PROTEOLYSIS C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU PORTLAND PRESS LTD PI LONDON PA 59 PORTLAND PL, LONDON, ENGLAND W1N 3AJ SN 0966-4068 BN 1-85578-041-0 J9 PORTL PR P PY 1993 BP 247 EP 251 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BZ95S UT WOS:A1993BZ95S00036 ER PT J AU RUDORFER, MV SKWERER, RG ROSENTHAL, NE AF RUDORFER, MV SKWERER, RG ROSENTHAL, NE TI BIOGENIC-AMINES IN SEASONAL AFFECTIVE-DISORDER - EFFECTS OF LIGHT THERAPY SO PSYCHIATRY RESEARCH LA English DT Article DE SEASONAL DEPRESSION; PHOTOTHERAPY; CEREBROSPINAL FLUID MONOAMINE METABOLITES; PLASMA NOREPINEPHRINE; ORTHOSTATIC CHALLENGE ID PLASMA NOREPINEPHRINE; CEREBROSPINAL-FLUID; HOMOVANILLIC-ACID; 5-HYDROXYINDOLEACETIC ACID; ELECTROCHEMICAL DETECTION; WINTER DEPRESSION; CSF; METABOLITES; 3-METHOXY-4-HYDROXYPHENYLGLYCOL; ANTIDEPRESSANTS AB Wintertime measures of central and peripheral monoamine neurotransmitter system activity in 17 medication-free depressed patients with seasonal affective disorder (SAD) were compared with those in eight healthy volunteers. Mean cerebrospinal fluid (CSF) concentrations of the principal metabolites of norepinephrine (NE), serotonin, and dopamine did not differ between the two groups, nor did mean basal or orthostatically stimulated plasma NE levels. Patients' pretreatment depression ratings were inversely correlated with resting plasma NE concentrations. Fourteen SAD patients were clear responders to 2 weeks of full-spectrum bright light treatment. Neither the transmitter measures nor their interrelatedness was affected significantly by phototherapy. C1 NIMH,EXPTL THERAPEUT BRANCH,CLIN STUDIES UNIT,CLIN PHARMACOL SECT,BETHESDA,MD 20892. SARCOSTA PALMS HOSP,ADULT SERV,SARCOSTA,FL. NIMH,CLIN PSYCHOBIOL BRANCH,ENVIRONM PSYCHIAT SECT,BETHESDA,MD 20892. RP RUDORFER, MV (reprint author), NIMH,DCTR,CLIN TREATMENT RES BRANCH,5600 FISHERS LN,RM 18-105,ROCKVILLE,MD 20857, USA. NR 39 TC 32 Z9 32 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD JAN PY 1993 VL 46 IS 1 BP 19 EP 28 DI 10.1016/0165-1781(93)90004-Z PG 10 WC Psychiatry SC Psychiatry GA KQ095 UT WOS:A1993KQ09500003 PM 7681996 ER PT J AU JOFFE, RT MOUL, DE LAM, RW LEVITT, AJ TEICHER, MH LEBEGUE, B OREN, DA BUCHANAN, A GLOD, CA MURRAY, MG BROWN, J SCHWARTZ, P AF JOFFE, RT MOUL, DE LAM, RW LEVITT, AJ TEICHER, MH LEBEGUE, B OREN, DA BUCHANAN, A GLOD, CA MURRAY, MG BROWN, J SCHWARTZ, P TI LIGHT VISOR TREATMENT FOR SEASONAL AFFECTIVE-DISORDER - A MULTICENTER STUDY SO PSYCHIATRY RESEARCH LA English DT Article DE DEPRESSION; PHOTOTHERAPY; CIRCANNUAL RHYTHM ID THERAPY AB The effectiveness of light therapy in seasonal affective disorder (SAD) was evaluated in 105 subjects across five centers. Three intensities of light (60 lux, 600 lux, and 3500 lux) were used in a 2-week randomized, parallel design. There was no significant difference in antidepressant efficacy of the three intensities of light. All three intensities produced a similar frequency of antidepressant response to each other and to that reported in previous studies. There were site differences in the severity of depression during light treatment, but diagnosis and medication status did not affect antidepressant response. These findings suggest that light therapy has an antidepressant action by a nonspecific effect or that light is biologically active in the treatment of SAD across a wide range of intensities. C1 UNIV HOSP BRITISH COLUMBIA,MOOD DISORDERS PROGRAM,VANCOUVER,BC,CANADA. UNIV BRITISH COLUMBIA,VANCOUVER V6T 1W5,BC,CANADA. UNIV TORONTO,MOOD DISORDERS PROGRAM,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV TORONTO,DEPT PSYCHIAT,TORONTO M5S 1A1,ONTARIO,CANADA. NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. MCLEAN HOSP,BELMONT,MA 02178. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV UTAH,DEPT PSYCHIAT,SALT LAKE CITY,UT 84112. RI Lam, Raymond/D-2529-2013 OI Lam, Raymond/0000-0001-7142-4669 NR 15 TC 43 Z9 43 U1 0 U2 0 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 JAN PY 1993 VL 46 IS 1 BP 29 EP 39 DI 10.1016/0165-1781(93)90005-2 PG 11 WC Psychiatry SC Psychiatry GA KQ095 UT WOS:A1993KQ09500004 PM 8464953 ER PT J AU DORN, LD SUSMAN, EJ PETERSEN, AC AF DORN, LD SUSMAN, EJ PETERSEN, AC TI CORTISOL REACTIVITY AND ANXIETY AND DEPRESSION IN PREGNANT ADOLESCENTS - A LONGITUDINAL PERSPECTIVE SO PSYCHONEUROENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; POSTPARTUM BLUES; BIOCHEMICAL MANIFESTATIONS; SALIVARY CORTISOL; YOUNG ADOLESCENTS; NEGATIVE AFFECT; BETA-ENDORPHIN; STRESS; MOOD; PERSONALITY AB The purpose of this investigation was to examine: (1) the relations among cortisol reactivity (short term changes in cortisol concentration) and anxiety and depression symptoms in adolescents during pregnancy and early postpartum, and (2) cortisol reactivity and psychosocial variables as predictors of anxiety and depression symptoms in pregnancy and early postpartum. Cortisol reactivity, an index of hypothalamic-pituitary-adrenal activity, was hypothesized to be a vulnerability factor for poor physical and mental health outcomes in adolescents. Forty adolescents aged 14 to 19 years (M = 17.3, SD = 1.3) were enrolled in the study and were seen at < 20 weeks gestation (T1), 34-36 weeks gestation (T2), and 2-3 weeks postpartum (T3). Blood was drawn for cortisol at T1 and T3. Psychological assessments of anxiety and depression symptoms, life optimism, and self-worth were administered at T1, T2, and T3. There were significant correlations among cortisol reactivity and anxiety and depression symptoms at T1 and T3, but the correlations were the reverse of the hypothesized direction. Pregnant adolescents with increased cortisol reactivity (cortisol concentrations that increased across a 40-min period) had fewer symptoms of anxiety and depression than other adolescents. Longitudinal analyses showed that anxiety and depression symptoms at T1 were a stronger predictor of postpartum anxiety and depression than was cortisol reactivity, life optimism, self-worth, or age at pregnancy. C1 PENN STATE UNIV,UNIV PK,PA 16802. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. RP DORN, LD (reprint author), NIMH,BLDG 10,3 SOUTH 231,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU NINR NIH HHS [F31 NR05965] NR 77 TC 31 Z9 31 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4530 J9 PSYCHONEUROENDOCRINO JI Psychoneuroendocrinology PY 1993 VL 18 IS 3 BP 219 EP 239 DI 10.1016/0306-4530(93)90006-7 PG 21 WC Endocrinology & Metabolism; Neurosciences; Psychiatry SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry GA KW576 UT WOS:A1993KW57600006 PM 8516425 ER PT J AU MOLCHAN, SE HILL, JL MARTINEZ, RA LAWLOR, BA MELLOW, AM RUBINOW, DR BISSETTE, G NEMEROFF, CB SUNDERLAND, T AF MOLCHAN, SE HILL, JL MARTINEZ, RA LAWLOR, BA MELLOW, AM RUBINOW, DR BISSETTE, G NEMEROFF, CB SUNDERLAND, T TI CSF SOMATOSTATIN IN ALZHEIMERS-DISEASE AND MAJOR DEPRESSION - RELATIONSHIP TO HYPOTHALAMIC-PITUITARY-ADRENAL AXIS AND CLINICAL MEASURES SO PSYCHONEUROENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING FACTOR; DEXAMETHASONE SUPPRESSION TEST; PRIMARY DEGENERATIVE DEMENTIA; CEREBROSPINAL-FLUID CONCENTRATIONS; FACTOR-LIKE IMMUNOREACTIVITY; URINARY-FREE CORTISOL; ADRENOCORTICOTROPIN SECRETION; MONOAMINE METABOLITES; SENILE DEMENTIA; HORMONE AB Patients with Alzheimer's disease (AD) and major depression have been shown to have overlapping clinical symptoms and biological markers, including decreased concentrations of cerebrospinal fluid (CSF) somatostatin-like immunoreactivity (SLI), which may be related to alterations in the hypothalamic-pituitary-adrenal axis activity. As in prior studies, we found that CSF SLI was significantly decreased in a group of AD patients (N = 49) and a group of elderly patients with major depression (N = 18), as compared with 13 age-matched controls (F[2, 77] = 12.9, p < .001). In the present study, CSF SLI and CSF corticotropin-releasing factor correlated significantly within the group of AD patients (r = 0.49, p < .0004) and almost attained significance in the depressed patients (r = 0.47, p < .07). CSF SLI correlated significantly with urinary free cortisol within each patient group (r = -0.51, p < .03). Clinical measures of dementia severity and depression did not consistently correlate with CSF SLI in either patient group. C1 NIMH,GERIATR PSYCHOPHARMACOL SECT,BETHESDA,MD 20892. NIMH,CLIN SCI LAB,BIOSTAT UNIT,BETHESDA,MD 20892. NIMH,BEHAV ENDOCRINOL SECT,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. UNIV DUBLIN,DEPT PSYCHIAT,DUBLIN 2,IRELAND. UNIV MICHIGAN,DEPT PSYCHIAT,ANN ARBOR,MI 48109. DUKE UNIV,DEPT PSYCHIAT,DURHAM,NC 27706. EMORY UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,ATLANTA,GA 30322. FU NIMH NIH HHS [NIMH MN-42088, NIMH MN-40524] NR 80 TC 46 Z9 46 U1 2 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4530 J9 PSYCHONEUROENDOCRINO JI Psychoneuroendocrinology PY 1993 VL 18 IS 7 BP 509 EP 519 DI 10.1016/0306-4530(93)90044-L PG 11 WC Endocrinology & Metabolism; Neurosciences; Psychiatry SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry GA LW897 UT WOS:A1993LW89700006 PM 7903467 ER PT J AU HSIAO, JK POTTER, WZ AGREN, H OWEN, RR PICKAR, D AF HSIAO, JK POTTER, WZ AGREN, H OWEN, RR PICKAR, D TI CLINICAL INVESTIGATION OF MONOAMINE NEUROTRANSMITTER INTERACTIONS SO PSYCHOPHARMACOLOGY LA English DT Article DE MONOAMINE NEUROTRANSMITTER SYSTEMS; SCHIZOPHRENIA; CLOZAPINE; NEUROLEPTICS ID BETA-ADRENERGIC RECEPTORS; RAT CEREBRAL-CORTEX; CEREBROSPINAL-FLUID; DORSAL RAPHE; DEPRESSED-PATIENTS; HOMOVANILLIC-ACID; NORADRENERGIC INNERVATION; METABOLITE CONCENTRATIONS; ELECTROCONVULSIVE SHOCK; DESIPRAMINE TREATMENT AB Monoamine neurotransmitter systems are widely thought to be involved in the pathophysiology of affective disorders and schizophrenia and the mechanism of action of antidepressant and antipsychotic drugs. Previous clinical studies have focused on individual monoamine function in isolation, even though a large number of preclinical studies have demonstrated that monoamine neurotransmitter systems interact with one another. In the present paper, preclinical data on monoamine neurotransmitter interactions are reviewed, and two methods for examining monoamine neurotransmitter system interactions in clinical data are presented. One of the best replicated findings in biological psychiatry is that monoamine metabolites in CSF correlate with one another. The degree of correlation may be in part a measure of the degree of interaction between the parent monoamine neurotransmitter systems. Another approach to studying interactions is the use of HVA/5HIAA and HVA/MHPG ratios as an index of interactions between 5HT-DA and NE-DA. When these methods are applied in schizophrenia, patients are found to have decreased monoamine metabolite correlations compared to normal controls. Metabolite correlations increase significantly after antipsychotic treatment, and the HVA/5HIAA and HVA/MHPG ratios also increase, suggesting that neuroleptics may act in part by strengthening interactions between monoamines. BPRS ratings are negatively correlated with HVA/5HIAA and HVA/MHPG so that patients with higher ratios have fewer symptoms, particularly after treatment. These results provide direct experimental support for hypotheses suggesting that interactions between monoamine neurotransmitters are important in schizophrenia. Some of the effects of the atypical neuroleptic, clozapine, on metabolite correlations and ratios are also discussed. C1 UNIV HOSP UPPSALA,DEPT PSYCHIAT,UPPSALA,SWEDEN. UNIV ARKANSAS,VET ADM HOSP,DEPT PSYCHIAT,FAYETTEVILLE,AR 72701. RP HSIAO, JK (reprint author), NIMH,EXPTL THERAPEUT BRANCH,CLIN PHARMACOL SECT,BLDG 10,ROOM 4N214,BETHESDA,MD 20892, USA. NR 84 TC 20 Z9 20 U1 1 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PY 1993 VL 112 IS 1 SU S BP S76 EP S84 DI 10.1007/BF02245010 PG 9 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV406 UT WOS:A1993LV40600009 PM 7831444 ER PT J AU OHUOHA, DC HYDE, TM KLEINMAN, JE AF OHUOHA, DC HYDE, TM KLEINMAN, JE TI THE ROLE OF SEROTONIN IN SCHIZOPHRENIA - AN OVERVIEW OF THE NOMENCLATURE, DISTRIBUTION AND ALTERATIONS OF SEROTONIN RECEPTORS IN THE CENTRAL-NERVOUS-SYSTEM SO PSYCHOPHARMACOLOGY LA English DT Article DE 5-HT RECEPTORS; CLASSIFICATION; NOMENCLATURE; POSTMORTEM STUDIES; SCHIZOPHRENIA ID CSF 5-HYDROXYINDOLEACETIC ACID; PLATELET MONOAMINE-OXIDASE; 5-HT3 RECOGNITION SITES; RAT-BRAIN; CEREBROSPINAL-FLUID; FRONTAL-CORTEX; AUTORADIOGRAPHIC LOCALIZATION; ATYPICAL NEUROLEPTICS; DOPAMINE-D2 RECEPTORS; TRYPTOPHAN-METABOLISM AB Serotonin is a neurotransmitter that is widely distributed throughout the central nervous system. The role of serotonin in schizophrenia is still unclear. Postmortem studies of serotonin receptor subtypes in schizophrenia have been inconclusive for the most part. The most promising findings involve a reduction in 5-HT2 receptors and 5-HT reuptake sites in the prefrontal cortex of schizophrenic patients. In this paper we review the function, distribution and pharmacological characteristics of serotonin receptors. Postmortem studies are also reviewed, focusing upon the role of these receptors in schizophrenia. C1 ST ELIZABETH HOSP,DEPT PSYCHIAT,WASHINGTON,DC 20032. RP OHUOHA, DC (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,IRP,CLIN BRAIN DISORDERS BRANCH,NEUROPATHOL SECT,WASHINGTON,DC 20032, USA. NR 177 TC 43 Z9 44 U1 2 U2 5 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PY 1993 VL 112 IS 1 SU S BP S5 EP S15 DI 10.1007/BF02245003 PG 11 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA LV406 UT WOS:A1993LV40600002 PM 7831440 ER PT J AU SCHINDLER, CW GOLDBERG, SR KATZ, JL AF SCHINDLER, CW GOLDBERG, SR KATZ, JL TI PHARMACOLOGICAL SPECIFICITY OF ENHANCED SENSITIVITY TO NALTREXONE IN RATS SO PSYCHOPHARMACOLOGY LA English DT Article DE OPIOID ANTAGONISTS; OPIOID AGONISTS; ENHANCED SENSITIVITY; AMPHETAMINE; CHLORDIAZEPOXIDE; SCHEDULE-CONTROLLED BEHAVIOR; RATS ID QUATERNARY NARCOTIC-ANTAGONISTS; VENTRAL TEGMENTAL AREA; RECEPTOR UP-REGULATION; SQUIRREL-MONKEYS; KAPPA-OPIOIDS; MORPHINE; NALOXONE; SUPERSENSITIVITY; INCREASES; SITES AB Rats treated weekly with cumulative doses (1-100 mg/kg, IP) of naltrexone develop an enhanced sensitivity to the operant response-rate decreasing effect of naltrexone. In the present experiment the pharmacological specificity of that enhanced sensitivity was determined by testing a variety of drugs for cross-sensitivity to naltrexone. Cross-sensitivity was evaluated with two procedures. In one, dose-effect functions were determined for each of the test compounds before and after the development of enhanced sensitivity to naltrexone in a single group of rats. In the second procedure, one group of rats was made sensitive to naltrexone, while a second was not. Test compounds were then evaluated in both groups. For both procedures, a shift to the left in the dose-effect functions similar to naltrexone was considered evidence of cross-sensitivity. Of the opioid antagonists tested, only naloxone showed clear cross-sensitivity to naltrexone, although MR 2266 and diprenorphine also showed evidence of cross-sensitivity. The opioid antagonist quadazocine did not show cross-sensitivity to naltrexone on the day of testing, although some evidence of cross-sensitivity was evident 24 h later. In addition, the dose-effect function for d-amphetamine was significantly changed following naltrexone treatment. No evidence of cross-sensitivity was observed for the optical isomer of naloxone, d-naloxone, or for naloxone's quaternary derivative, naloxone methiodide. None of the opioid agonists or agonist-antagonists tested showed cross-sensitivity to naltrexone (i.e. morphine, U-50, 488H, ethylketocyclazocine, N-allylnormetazocine and pentazocine). The non-opioid drugs chlordiazepoxide and phencyclidine also failed to show evidence of cross-sensitivity. However, the dose-effect curves for chlordiazepoxide were shifted significantly to the right following naltrexone treatment. The results of the present experiment indicate that the enhanced sensitivity which develops to naltrexone in rats is stereospecific and centrally mediated. The effect is specific, in that it does not appear to confer changes in the behavioral effects of non-opioids or even opioid agonists. C1 UNIV MARYLAND,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201. RP SCHINDLER, CW (reprint author), NIDA,ADDICT RES CTR,PRECLIN PHARMACOL LAB,POB 5180,BALTIMORE,MD 21224, USA. OI Katz, Jonathan/0000-0002-1068-1159 NR 39 TC 10 Z9 10 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD JAN PY 1993 VL 110 IS 1-2 BP 60 EP 68 DI 10.1007/BF02246951 PG 9 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KG315 UT WOS:A1993KG31500009 PM 7870900 ER PT J AU TIRELLI, E TERRY, P AF TIRELLI, E TERRY, P TI BIPHASIC LOCOMOTOR EFFECTS OF THE DOPAMINE D1-AGONIST SKF-38393 AND THEIR ATTENUATION IN NONHABITUATED MICE SO PSYCHOPHARMACOLOGY LA English DT Article DE D1 RECEPTOR; D1 AGONIST; D1 ANTAGONIST; LOCOMOTION; BIPHASIC; HYPERACTIVITY; SKF 38393; SCH 39166; C57B1/6J MICE ID D1 ANTAGONIST SCH-23390; NUCLEUS-ACCUMBENS; SELECTIVE D-1; RECEPTOR AGONISTS; STEREOTYPED BEHAVIOR; D2-DOPAMINE AGONISTS; D2 RECEPTORS; SCH 23390; RATS; RESPONSES AB The locomotor stimulatory effects of the dopamine D1 receptor partial agonist SKF 38393 were examined in male C57B1/6J mice. Non-habituated mice showed marked dose-related (3-300 mg/kg, SC) locomotor stimulation. The time-course effect was biphasic at very high doses (100-300 mg/kg), with dose-related locomotor depression followed by dose-related long-term hyperlocomotion. For all doses, locomotor effects were detectable throughout the 4-h test period. To determine whether these effects were mediated by D1 receptor stimulation, effects of SKF 38393 were assessed in combination with behaviorally inactive and active doses (0.1 and 0.2 mg/kg, respectively) of the selective D1 receptor antagonist SCH 39166. Both doses of SCH 39166 attenuated the hyperlocomotion induced by 30 mg/kg of the agonist to a similar degree. However, neither dose was able to reverse either the depressant or the stimulatory effects of 300 mg/kg SKF 38393. These results demonstrate effects of the prototypical D1 agonist previously unobserved, and raise questions concerning the nature of agonist/antagonist interactions at the D1 receptor subtype. RP TIRELLI, E (reprint author), NIDA,ADDICT RES CTR,PSYCHOBIOL SECT,POB 5180,BALTIMORE,MD 21224, USA. NR 58 TC 15 Z9 15 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD JAN PY 1993 VL 110 IS 1-2 BP 69 EP 75 DI 10.1007/BF02246952 PG 7 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KG315 UT WOS:A1993KG31500010 PM 7870901 ER PT J AU ARNOLD, LE AF ARNOLD, LE TI NURTURING A VIGOROUS METHODOLOGY FOR CHILD AND ADOLESCENT TREATMENT RESEARCH SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 26-29, 1992 CL BOCA RATON, FL SP NEW CLIN DRUG EVALUAT UNIT, NIMH, DIV CLIN & TREATMENT RES RP ARNOLD, LE (reprint author), NIMH,ROCKVILLE,MD 20857, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 3 EP 4 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300001 ER PT J AU ARNOLD, LE AF ARNOLD, LE TI A COMPARATIVE OVERVIEW OF TREATMENT RESEARCH METHODOLOGY - ADULT VS CHILD AND ADOLESCENT, PSYCHOPHARMACOLOGICAL VS PSYCHOSOCIAL TREATMENTS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 26-29, 1992 CL BOCA RATON, FL SP NEW CLIN DRUG EVALUAT UNIT, NIMH, DIV CLIN & TREATMENT RES AB This article provides a broad overview in a comparison format of some general methodological issues relevant to treatment research with children and adolescents. Two sets of comparisons are required to develop vigorous child and adolescent treatment research methodology: differences in methodology between adult and child/adolescent treatment studies, and similarities and differences between psychopharmacological and psychosocial treatment research in children and adolescents. This article discusses these issues and organizes them into tabular comparisons. Adult and child/adolescent methodologies differ in many ways, including ethics, recruitment, compliance, nature of variables and confounds, development and maturation, physiology, assessment, contextual factors, and background assumptions. Future treatment studies must increasingly assess interactions and additive or synergistic effects of pharmacological and psychosocial treatments. Integration of both treatment modalities into the same study requires knowledge of similarities and differences in their respective methodologies. This article compares and contrasts pharmacological and psychosocial research methodologies on 11 issues: diagnostic assessment, subject selection, design, controls, length of study, sample size, developmental issues, nature and frequency of contacts with subjects, compliance facilitation, outcome assessment, and data analysis and interpretation. C1 OHIO STATE UNIV,COLUMBUS,OH 43210. RP ARNOLD, LE (reprint author), NIMH,DIV CLIN & TREATMENT RES,CHILD & ADOLESCENT DISORDERS RES BRANCH,ROCKVILLE,MD 20857, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 5 EP 17 PG 13 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300002 PM 8378511 ER PT J AU JENSEN, PS AF JENSEN, PS TI DEVELOPMENT AND IMPLEMENTATION OF MULTIMODAL AND COMBINED TREATMENT STUDIES IN CHILDREN AND ADOLESCENTS - NIMH PERSPECTIVES SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 26-29, 1992 CL BOCA RATON, FL SP NEW CLIN DRUG EVALUAT UNIT, NIMH, DIV CLIN & TREATMENT RES ID OUTCOME RESEARCH; PSYCHOTHERAPY; DEPRESSION; THERAPY AB Over the last decade, combined psychosocial and pharmacologic treatment studies have been marked by increasing methodologic sophistication and complexity. While the design and implementation of such studies with adults is difficult, even more levels of complexity must be faced by investigators who develop such studies with children. This paper reviews the rationale, background, and design considerations related to the development and implementation of such studies. In particular, issues related to the choice of particular treatment combinations, subject selection strategies, and assessment approaches are discussed. Because most childhood conditions have complex roots lying both in biological and psychosocial phenomena, greater use of multimodal treatment research approaches will be critical to advance the field of child and adolescent treatment research. Recommendations are outlined for future study designs for child and adolescent treatment trials. RP JENSEN, PS (reprint author), NIMH,DIV CLIN & TREATMENT RES,CHILD & ADOLESCENT DISORDERS RES BRANCH,ROCKVILLE,MD 20857, USA. OI Jensen, Peter/0000-0003-2387-0650 NR 11 TC 14 Z9 14 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 19 EP 26 PG 8 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300003 PM 8378508 ER PT J AU HIBBS, ED AF HIBBS, ED TI PSYCHOSOCIAL TREATMENT RESEARCH WITH CHILDREN AND ADOLESCENTS - METHODOLOGICAL ISSUES SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 26-29, 1992 CL BOCA RATON, FL SP NEW CLIN DRUG EVALUAT UNIT, NIMH, DIV CLIN & TREATMENT RES ID PSYCHOTHERAPY-RESEARCH AB Psychotherapy research with children is based mainly on adult methodologies. Common issues include blas in recruitment of subjects, demographics, developmental concerns, and control group considerations. The advantages and drawbacks of various types of control groups, such as walt-list controls, and placebo conditions are discussed along with ethical issues. Instrument choice, validity and reliability, and standardization of procedures in conducting research are addressed. Finally, the therapist as a variable is reviewed, including selection and assignment of therapists, and therapist blas. RP HIBBS, ED (reprint author), NIMH,DIV CLIN & TREATMENT RES,CHILD & ADOLESCENT DISORDERS RES BRANCH,ROCKVILLE,MD 20857, USA. NR 28 TC 7 Z9 7 U1 1 U2 2 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 27 EP 33 PG 7 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300004 PM 8378509 ER PT J AU RUDORFER, MV AF RUDORFER, MV TI CHALLENGES IN MEDICATION CLINICAL-TRIALS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article ID MAJOR DEPRESSIVE DISORDER; DESIGNED DOUBLE-BLIND; ADOLESCENT DEPRESSION; PREPUBERTAL CHILDREN; PLASMA-LEVEL; CO-MORBIDITY; SERUM LEVELS; FOLLOW-UP; PLACEBO; NORTRIPTYLINE AB The keystone of pharmacological therapy is the medication clinical trial. Beyond the straightforward administration of an adequate amount of medication for a sufficient duration of time, attention to a variety of methodologic issues is necessary to ensure a successful study. These include diagnostic and severity criteria for entry into the trial and a host of potentially confounding biological and psychosocial factors. Adequacy of treatment must be insured, aided by continued refinement of plasma drug concentration monitoring and understanding of the role of active metabolites. Outcome measures must be valid and reliable. These principles are being applied to the still-new field of child and adolescent psychopharmacology. Results thus far have indicated the importance of placebo control in young populations. The equivocal efficacy demonstrated to date for pharmacotherapy in controlled antidepressant trials in children and adolescents has limited understanding of dose (or plasma level)/response relationships which could serve to optimize further studies. RP RUDORFER, MV (reprint author), NIMH, DIV CLIN & TREATMENT RES, CLIN TREATMENT RES BRANCH, ROOM 18-105, ROCKVILLE, MD 20857 USA. NR 63 TC 9 Z9 9 U1 2 U2 2 PU MEDWORKS MEDIA GLOBAL, LLC PI HERMOS BEACH PA 670 FIFTH STREET, STE A, HERMOS BEACH, CA 90254 USA SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 35 EP 44 PG 10 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300005 PM 8378510 ER PT J AU KANE, JM DAUPHINAIS, D BARNES, TRE ADLER, LA RIFKIN, A AF KANE, JM DAUPHINAIS, D BARNES, TRE ADLER, LA RIFKIN, A TI ASSESSING NEGATIVE SYMPTOMS AND EXTRAPYRAMIDAL SYMPTOMS IN SCHIZOPHRENIA - WORKSHOP REPORT SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 26-29, 1992 CL BOCA RATON, FL SP NEW CLIN DRUG EVALUAT UNIT, NIMH, DIV CLIN & TREATMENT RES ID RATING-SCALE; INDUCED AKATHISIA; HALOPERIDOL C1 NIMH,DIV CLIN & TREATMENT RES,CLIN TREATMENT RES BRANCH,ROCKVILLE,MD 20857. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. CHARING CROSS & WESTMINSTER MED SCH,ACAD DEPT PSYCHIAT,LONDON,ENGLAND. NEW YORK DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,NEW YORK,NY. NYU,SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10003. QUEENS HOSP CTR,GLEN OAKS,NY. LONG ISL JEWISH MED CTR,HILLSIDE HOSP,DEPT PSYCHIAT,GLEN OAKS,NY 11004. NR 35 TC 6 Z9 6 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 45 EP 49 PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300006 PM 8104351 ER PT J AU REYNOLDS, CF LEBOWITZ, BD SCHNEIDER, LS AF REYNOLDS, CF LEBOWITZ, BD SCHNEIDER, LS TI THE NIH CONSENSUS DEVELOPMENT CONFERENCE ON THE DIAGNOSIS AND TREATMENT OF DEPRESSION IN LATE-LIFE - AN OVERVIEW SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 26-29, 1992 CL BOCA RATON, FL SP NEW CLIN DRUG EVALUAT UNIT, NIMH, DIV CLIN & TREATMENT RES AB The National Institutes of Health (NIH) Consensus Development Conference on the Diagnosis and Treatment of Depression in Late Life took place on November 4-6, 1991. The full statement of the Consensus Panel, chaired by Arnold J. Friedhoff, M.D., was published in a Consensus Statement and in the Journal of the American Medical Association. The purpose of this article is to provide a brief overview of the planning for the Consensus Development Conference, with particular emphasis on the questions posed by the National Institute of Mental Health (NIMH) Planning Committee to members of the panel. This is followed by a brief synopsis of the panel's opinions on issues raised by the NIMH Planning Committee, as well as their opinions on the most promising issues for future research in late-life depression. The main purposes of the NIH Consensus Development Conference were first, to translate research findings into guidelines for clinical practice, so far as this is possible, and second, to suggest promising directions for the Nation's research agenda in late-life depression. C1 NIMH,DIV CLIN & TREATMENT RES,MENT DISORDERS AGING RES BRANCH,ROCKVILLE,MD 20857. UNIV SO CALIF,DEPT PSYCHIAT,LOS ANGELES,CA 90089. RP REYNOLDS, CF (reprint author), WESTERN PSYCHIAT INST & CLIN,DEPT PSYCHIAT,3811 OHARA ST,PITTSBURGH,PA 15213, USA. FU NIMH NIH HHS [MH-37869, MH-00295, MH-43832] NR 0 TC 21 Z9 21 U1 0 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 83 EP 85 PG 3 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300011 PM 8378516 ER PT J AU GWIRTSMAN, HE AF GWIRTSMAN, HE TI OVERVIEW OF THE DEFINITION, PREVALENCE, AND COMORBIDITY OF BULIMIC DISORDERS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 32ND ANNUAL MEETING OF THE NEW CLINICAL DRUG EVALUATION UNIT CY MAY 26-29, 1992 CL BOCA RATON, FL SP NEW CLIN DRUG EVALUAT UNIT, NIMH, DIV CLIN & TREATMENT RES ID BINGE EATING DISORDER; CULTURAL EXPECTATIONS; DIAGNOSTIC-CRITERIA; NERVOSA; WOMEN; THINNESS RP GWIRTSMAN, HE (reprint author), NIMH,DIV CLIN & TREATMENT RES,ROCKVILLE,MD 20857, USA. NR 21 TC 3 Z9 3 U1 2 U2 2 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 1 BP 109 EP 114 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA LN223 UT WOS:A1993LN22300014 PM 8378503 ER PT J AU HAIGLER, HJ COTT, JM RUDORFER, MV SCHOENFELD, RE POTTER, WZ VITIELLO, B EVERIST, HD AF HAIGLER, HJ COTT, JM RUDORFER, MV SCHOENFELD, RE POTTER, WZ VITIELLO, B EVERIST, HD TI PSYCHOTHERAPEUTIC MEDICATIONS DEVELOPMENT PROGRAM (PMDP) SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article AB The Psychotherapeutic Medications Development Program (PMDP) of the National Institute of Mental Health was established in 1990. The purpose of the PMDP is to improve, enhance, and speed the development of new medications and improve the therapeutic usefulness of existing medications for the treatment of mental illness. The PMDP will fulfill this mission by implementing four initiatives. In the drug discovery and development initiative, the PMDP will aid in the development of promising new drugs. This initiative will also include improving the therapeutic usefulness of existing medications. In the technology transfer initiative, PMDP will improve the technology transfer from academic and government researchers to the pharmaceutical industry; improve the dissemination of information concerning technology transfer opportunities as it pertains to psychotherapeutic medications; and enhance technology transfer by acting as a broker to bring interested parties together. For the third initiative, the PMDP will develop and maintain a capability to clinically evaluate psychotherapeutic medications. The PMDP will also act to facilitate the development and testing of new concepts and models of mental illness. There is a detailed description of the steps that are involved in developing a new chemical entity (NCE) from the conceptual stage to a medication that is approved for the treatment of a particular illness. The pharmaceutical industry estimates that this medication development process costs $238 million. RP HAIGLER, HJ (reprint author), NIMH,ROOM 17C-26,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 2 TC 2 Z9 2 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 2 BP 241 EP 247 PG 7 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA MC720 UT WOS:A1993MC72000016 PM 8290672 ER PT J AU WEIDEN, P SCHOOLER, NR SEVERE, JB LEE, JH SCHULZ, SC AF WEIDEN, P SCHOOLER, NR SEVERE, JB LEE, JH SCHULZ, SC TI STABILIZATION AND DEPOT NEUROLEPTIC DOSAGES SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article ID CONTROLLED TRIAL; SCHIZOPHRENIA; DEFINITIONS; RELAPSE AB Little is known about the stabilization phase of schizophrenia. To address this deficiency, we studied the prescribing patterns of fluphenazine decanoate (FZD) for a cohort of schizophrenic patients recovering from an acute psychotic episode who were being followed in the Treatment Strategies in Schizophrenia (TSS) multi-site maintenance study. Dosage data from the first 208 successfully-stabilized TSS subjects were examined. We hypothesized five groups on the basis of dosage prescribed and dosage stability over time: (1) STABLE HIGH, (2) STABLE INTERMEDIATE, (3) STABLE LOW, (4) UNSTABLE RAISING, and (5) UNSTABLE LOWERING. The dosage patterns were rated and analyzed against predictive and outcome variables. Most of the subjects (n = 168, or 82%) fit one of the five hypothesized dosage pattern groups. Our preliminary findings are as follows: (1) all groups improved during stabilization; (2) baseline symptom severity did not distinguish among dosage pattern groups; (3) STABLE dose groups needed less time to stabilize than did the UNSTABLE groups, but the STABLE groups did not have a better medication response; (4) many of the UNSTABLE LOWERING subjects apparently received a ''loading dose'' strategy (e.g., initial FZD dose greater-than-or-equal-to 25 mg), which was paradoxically associated with a longer stabilization time. C1 WESTERN PSYCHIAT INST & CLIN,PITTSBURGH,PA 15261. US FDA,ROCKVILLE,MD 20857. NIMH,ROCKVILLE,MD 20857. UNIV HOSP CLEVELAND,CLEVELAND,OH 44106. RP WEIDEN, P (reprint author), ST LUKES ROOSEVELT HOSP,PSYCHIAT T8,428 W 59TH ST,NEW YORK,NY 10012, USA. FU NIMH NIH HHS [UO1 MH40007, UO1 MH39992, UO1 MH39998] NR 20 TC 10 Z9 10 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 2 BP 269 EP 275 PG 7 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA MC720 UT WOS:A1993MC72000020 PM 8290676 ER PT J AU MITCHELL, P AF MITCHELL, P TI CHLORPROMAZINE TURNS 40 SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Editorial Material C1 UNIV NEW S WALES,SCH PSYCHIAT,KENSINGTON,NSW 2033,AUSTRALIA. NIMH,CLIN PHARMACOL SECT,BETHESDA,MD. OI Mitchell, Philip/0000-0002-7954-5235 NR 19 TC 3 Z9 3 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 3 BP 341 EP 344 PG 4 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA MM925 UT WOS:A1993MM92500001 ER PT J AU ALTEMUS, M GLOWA, JR MURPHY, DL AF ALTEMUS, M GLOWA, JR MURPHY, DL TI ATTENUATION OF FOOD-RESTRICTION-INDUCED RUNNING BY CHRONIC FLUOXETINE TREATMENT SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 31st Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 14-18, 1992 CL SAN JUAN, PR SP Amer Coll Neuropsychopharm ID OBSESSIVE-COMPULSIVE DISORDER; ANOREXIA-NERVOSA; TRIAL AB In rats, 90-minute daily access to food is sufficient to maintain or even increase body weight. However, when rats are provided with access to a running wheel for the remaining portion of the day, progressive increases in activity and decreases in weight reach life-threatening proportions within 1-2 weeks. To investigate this phenomenon as a possible animal model of obsessive-compulsive disorder (OCD), rats were treated i.p. daily for 5 weeks with fluoxetine, an antidepressant that relieves OCD symptoms; imipramine, an antidepressant that does not affect OCD symptoms; or saline prior to exposure to food restriction and the running wheel. Compared with saline-treated controls, rats treated with fluoxetine showed significant attenuation of wheel running, anorexia, and weight loss. However, rats treated with imipramine did not differ from saline-treated controls on any measures. These results indicate that food-restriction-induced compulsive running and the associated anorexia are selectively prevented by treatment with an antidepressant that blocks serotonin reuptake. This raises the possibility that this repetitive, maladaptive behavior may be a valid animal model for OCD. C1 NIDDKD,DIV INTRAMURAL RES PROGRAMS,MED CHEM LAB,BETHESDA,MD. RP ALTEMUS, M (reprint author), NIMH,DIV INTRAMURAL RES PROGRAMS,CLIN SCI LAB,BLDG 10,ROOM 3D41,BETHESDA,MD 20892, USA. NR 12 TC 34 Z9 35 U1 0 U2 2 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 3 BP 397 EP 400 PG 4 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA MM925 UT WOS:A1993MM92500010 PM 8121967 ER PT J AU WINSLOW, JT SHAPIRO, L CARTER, CS INSEL, TR AF WINSLOW, JT SHAPIRO, L CARTER, CS INSEL, TR TI OXYTOCIN AND COMPLEX SOCIAL-BEHAVIOR - SPECIES COMPARISONS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 31st Annual Meeting of the American-College-of-Neuropsychopharmacology CY DEC 14-18, 1992 CL SAN JUAN, PR SP Amer Coll Neuropsychopharm ID MICROTUS-OCHROGASTER; AFFILIATIVE BEHAVIOR; RATS; VOLES; ORGANIZATION; TESTOSTERONE; PRAIRIE; BINDING AB The neurohypophyseal peptide hormone oxytocin functions as a neuropeptide in several brain areas in addition to its role as a posterior pituitary hormone. Several studies have determined significant differences in patterns of oxytocin receptor binding in the brains of two closely related species of vole. One of the defining features of these two species is remarkably different reproductive behavior strategies. The prairie vole forms long-term monogamous relationships; the montane vole is polygamous. One potential measure of the formation of a pair bond in prairie voles is the development of intense aggressive behavior directed at male conspecifics following a mating bout. Oxytocin had little effect on aggressive behavior when administered before mating but had profound effects on the aggression of male prairie voles when administered after mating. Oxytocin had relatively modest effects on the behavior of montane voles, and neither the behavior nor the peptide effects were affected by mating experience. The data indicate that differences in peptide binding in these two species of vole may be functionally related to differences in social behavior. C1 NIH,NEUROPHYSIOL LAB,DEV BIOPSYCHOL UNIT,POOLESVILLE,MD. RP WINSLOW, JT (reprint author), HOECHST ROUSSEL PHARMACEUT PROPRIETARY LTD,RT 202-204,POB 2500,SOMERVILLE,NJ 08876, USA. NR 24 TC 52 Z9 52 U1 1 U2 7 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 3 BP 409 EP 414 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA MM925 UT WOS:A1993MM92500012 PM 8121969 ER PT J AU KEITH, SJ MATTHEWS, SM AF KEITH, SJ MATTHEWS, SM TI THE VALUE OF PSYCHIATRIC-TREATMENT - ITS EFFICACY IN SEVERE MENTAL-DISORDERS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Editorial Material C1 NIMH,DIV CLIN & TREATMENT RES,ROCKVILLE,MD. RP KEITH, SJ (reprint author), UNIV NEW MEXICO,DEPT PSYCHIAT,ALBUQUERQUE,NM 87131, USA. NR 3 TC 20 Z9 20 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 4 BP 427 EP 430 PG 4 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA NV126 UT WOS:A1993NV12600001 PM 8084976 ER PT J AU SCHOOLER, NR KEITH, SJ AF SCHOOLER, NR KEITH, SJ TI THE CLINICAL RESEARCH BASE FOR THE TREATMENT OF SCHIZOPHRENIA SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article ID INTERMITTENT NEUROLEPTIC PROPHYLAXIS; INPATIENT FAMILY INTERVENTION; MAINTENANCE CHEMOTHERAPY; AFTERCARE TREATMENT; EXPRESSED EMOTION; CONTROLLED TRIAL; RELAPSE RATES; FOLLOW-UP; FLUPHENAZINE; HALOPERIDOL C1 NIMH,DIV CLIN TREATMENT RES,ROCKVILLE,MD 20857. RP SCHOOLER, NR (reprint author), UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,DEPT PSYCHIAT,PSYCHOSIS RES PROGRAM,3811 O HARA ST,PITTSBURGH,PA 15213, USA. NR 78 TC 38 Z9 38 U1 6 U2 7 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1993 VL 29 IS 4 BP 431 EP 446 PG 16 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA NV126 UT WOS:A1993NV12600002 PM 7916158 ER PT J AU MARCUS, SE GIOVINO, GA PIERCE, JP HAREL, Y AF MARCUS, SE GIOVINO, GA PIERCE, JP HAREL, Y TI MEASURING TOBACCO USE AMONG ADOLESCENTS SO PUBLIC HEALTH REPORTS LA English DT Article ID SMOKING C1 CTR DIS CONTROL & PREVENT,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,OFF SMOKING & HLTH,ATLANTA,GA. UNIV CALIF SAN DIEGO,CTR CANC,DEPT CANC PREVENT & CONTROL,LA JOLLA,CA 92093. BAR ILAN UNIV,DEPT SOCIOL,RAMAT GAN,ISRAEL. RP MARCUS, SE (reprint author), NIDR,EPIDEMIOL & ORAL DIS PREVENT PROGRAM,BETHESDA,MD 20892, USA. NR 25 TC 11 Z9 11 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PY 1993 VL 108 SU 1 BP 20 EP 24 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MB812 UT WOS:A1993MB81200005 PM 8210270 ER PT J AU BLANKEN, AJ AF BLANKEN, AJ TI MEASURING USE OF ALCOHOL AND OTHER DRUGS AMONG ADOLESCENTS SO PUBLIC HEALTH REPORTS LA English DT Article ID SUBSTANCE ABUSE; COCAINE ABUSE; DISEASE; DISORDERS; MARIJUANA; PATTERNS; ETHANOL; SMOKERS; TOBACCO; LIVER RP BLANKEN, AJ (reprint author), NIDA,DIV EPIDEMIOL & PREVENT RES,LEXINGTON,KY 40583, USA. NR 46 TC 12 Z9 12 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PY 1993 VL 108 SU 1 BP 25 EP 30 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MB812 UT WOS:A1993MB81200006 PM 8210271 ER PT J AU MEISSNER, HI AF MEISSNER, HI TI SHOULD MAMMOGRAPHY SCREENING BE PROMOTED IF QUALITY ASSURANCE IS LACKING - REPLY SO PUBLIC HEALTH REPORTS LA English DT Letter RP MEISSNER, HI (reprint author), NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD JAN-FEB PY 1993 VL 108 IS 1 BP 135 EP 135 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KL046 UT WOS:A1993KL04600022 ER PT S AU CARSON, RE AF CARSON, RE BE Uemura, K Lassen, NA Jones, T Kanno, I Hatazawa, J Miura, S Murakami, M Iida, H Fujita, H Inugami, A TI PET PARAMETER-ESTIMATION USING LINEAR INTEGRATION METHODS - BIAS AND VARIABILITY CONSIDERATIONS SO QUANTIFICATION OF BRAIN FUNCTION: TRACER KINETICS AND IMAGE ANALYSIS IN BRAIN PET SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT International Symposium on Quantification of Brain Function (Brain PET 93 Akita) CY MAY 29-31, 1993 CL AKITA, JAPAN SP JAPANESE SOC CEREBRAL BLOOD FLOW & METAB, JAPANESE SOC NUCL MED, JAPAN BRAIN FDN, AKITA PREFECTURE, AKITA CITY, AKITA PREFECTURE CEREBROVASC MED FDN, AKITA RES INST BRAIN & BLOOD VESSELS, KEITOKUKAI FIJIWARA MEM HOSP, SEIRANKAI HONJOH DAIICHI HOSP ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL BLOOD-FLOW; COMPUTED-TOMOGRAPHY; HUMAN BRAIN; KINETICS; BINDING; MAPS RP CARSON, RE (reprint author), NCI,DEPT PET,BETHESDA,MD 20892, USA. RI Carson, Richard/H-3250-2011 OI Carson, Richard/0000-0002-9338-7966 NR 20 TC 28 Z9 28 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-89859-X J9 INT CONGR SER PY 1993 VL 1030 BP 499 EP 509 PG 11 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Neurosciences; Physiology SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ68P UT WOS:A1993BZ68P00057 ER PT S AU HORWITZ, B MCINTOSH, AR AF HORWITZ, B MCINTOSH, AR BE Uemura, K Lassen, NA Jones, T Kanno, I Hatazawa, J Miura, S Murakami, M Iida, H Fujita, H Inugami, A TI NETWORK MODELING AND FUNCTIONAL NEUROIMAGING FOR MAPPING BRAIN COGNITIVE FUNCTION SO QUANTIFICATION OF BRAIN FUNCTION: TRACER KINETICS AND IMAGE ANALYSIS IN BRAIN PET SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT International Symposium on Quantification of Brain Function (Brain PET 93 Akita) CY MAY 29-31, 1993 CL AKITA, JAPAN SP JAPANESE SOC CEREBRAL BLOOD FLOW & METAB, JAPANESE SOC NUCL MED, JAPAN BRAIN FDN, AKITA PREFECTURE, AKITA CITY, AKITA PREFECTURE CEREBROVASC MED FDN, AKITA RES INST BRAIN & BLOOD VESSELS, KEITOKUKAI FIJIWARA MEM HOSP, SEIRANKAI HONJOH DAIICHI HOSP ID PATHWAYS; OBJECT RP HORWITZ, B (reprint author), NIA,NEUROSCI LAB,BLDG 10,ROOM 6C414,BETHESDA,MD 20892, USA. RI McIntosh, Anthony/G-4955-2011 NR 18 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-89859-X J9 INT CONGR SER PY 1993 VL 1030 BP 589 EP 596 PG 8 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Neurosciences; Physiology SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ68P UT WOS:A1993BZ68P00066 ER PT J AU QU, T WU, YH WANG, XY LIU, YF YE, YH WU, CC AF QU, T WU, YH WANG, XY LIU, YF YE, YH WU, CC TI TC-99M LABELING ON MONOCLONAL-ANTIBODIES VIA N,N'-ETHYLENE-BIS-L-CYSTEINE SO RADIOCHIMICA ACTA LA English DT Article; Proceedings Paper CT Topical Symposium on the Behavior and Utilization of Technetium CY MAR 18-20, 1993 CL SENDAI, JAPAN SP TOHOKU UNIV SENDAI, CHEM DEPT DE TC-99M; MONOCLONAL ANTIBODY; RADIOLABELING ID CHELATING AGENT; TC-99M; COMPLEXES AB A new developed excellent kidney imaging agent, N,N'-ethylene-bis-L-cysteine (EC) has been used as a bifunctional chelating agent (BFCA) for Tc-99m labeling of monoclonal antibodies (MoAb). A new conjugation agent N-hydroxyl-1,4-epoxyl-cyclohex-5-ene-2,3-di-carboxyl-imide (HONCE) and a watersoluble dehydrating agent 1-ethyl-3-(3-dimethylaminopropyl)-carbo-diimide (EDC) were used to accomplish the conjugation of EC with antibodies. A conjugation yield of 30-40% was obtained. The experimental conditions were optimized for the best conjugation performance. Tc-99m labeling was then completed after conjugation. More than 80% of the immunoreactivity was retained after monoclonal antibodies conjugated with EC. More than 70% of the radioactivity was retained in the labeled complex Tc-99m-EC-Ab after incubation in fresh EC and cysteine solutions for 16-20 h. The biodistributions of labeled antibody in mice were also determined. C1 BEIJING UNIV,DEPT CHEM,BEIJING 100871,PEOPLES R CHINA. NIH,BETHESDA,MD 20892. RP QU, T (reprint author), BEIJING UNIV,DEPT TECH PHYS,BEIJING 100871,PEOPLES R CHINA. NR 16 TC 3 Z9 3 U1 0 U2 1 PU R OLDENBOURG VERLAG PI MUNICH 80 PA ROSENHEIMER STR 145 POSTFACH 801360, W-8000 MUNICH 80, GERMANY SN 0033-8230 J9 RADIOCHIM ACTA JI Radiochim. Acta PY 1993 VL 63 SI SI BP 209 EP 212 PG 4 WC Chemistry, Inorganic & Nuclear; Nuclear Science & Technology SC Chemistry; Nuclear Science & Technology GA MT324 UT WOS:A1993MT32400040 ER PT J AU MIRZADEH, S KUMAR, K GANSOW, OA AF MIRZADEH, S KUMAR, K GANSOW, OA TI THE CHEMICAL FATE OF BI-212-DOTA FORMED BY BETA- DECAY OF PB-212(DOTA)2- SO RADIOCHIMICA ACTA LA English DT Article DE PB-212-BI-212; RADIOIMMUNOTHERAPY; MULTIDENTATE LIGANDS; DOTA; EXCHANGE REACTION; HOT-ATOM CHEMISTRY; RADIOCHEMISTRY ID N-ACETIC ACIDS; MONOCLONAL-ANTIBODY; RADIOIMMUNOTHERAPY; GENERATOR; PB-212 AB The increasing use of inert metal complexes in radioimmunotherapy prompted us to explore the potential use of Pb-212 chelates. Herein, we report a study of the chemical fate of the Bi-212-DOTA complex formed by beta- decay of Pb-212(DOTA)2-(H-4DOTA = 1,4,7,10-tetraazacyclododecanetetraacetic acid). To assure that both parent and daughter complexes were thermally stable, kinetic studies were performed with Pb-203(II) and Bi-206(III) which showed that both lead and bismuth complexes with DOTA undergo chemical exchange only very slowly in aqueous solution at pH 4-10. To investigate whether the complex ion which results from decay of Pb-212(DOTA)2- was intact and also stable, solutions initially containing only this ion were analyzed for amounts of DOTA-complexed and uncomplexed Bi-212 after attaining transient equilibrium with Bi-212. The fraction of Bi-212 radioactivity not complexed to DOTA, vide infra, was found to be 36+/-2%. This value represents the fraction of breakup of Bi-212(DOTA)- formed from beta- decay of the parent complex. By considering the various extranuclear processes responsible for kinetic and electronic excitation of the Bi-212 daughter, break-up of the Bi-212-DOTA complex is ascribed to the internal conversion of gamma-rays emitted by the excited Bi-212 nuclide. C1 NCI,RADIAT ONCOL BRANCH,CHEM SECT,BETHESDA,MD 20892. NR 49 TC 58 Z9 58 U1 1 U2 4 PU R OLDENBOURG VERLAG PI MUNICH 80 PA ROSENHEIMER STR 145 POSTFACH 801360, W-8000 MUNICH 80, GERMANY SN 0033-8230 J9 RADIOCHIM ACTA JI Radiochim. Acta PY 1993 VL 60 IS 1 BP 1 EP 10 PG 10 WC Chemistry, Inorganic & Nuclear; Nuclear Science & Technology SC Chemistry; Nuclear Science & Technology GA KJ309 UT WOS:A1993KJ30900001 ER PT B AU TULLY, JG AF TULLY, JG BE Kahane, I Adoni, A TI BIOLOGY OF MOLLICUTES SO RAPID DIAGNOSIS OF MYCOPLASMAS SE FEMS SYMPOSIUM LA English DT Proceedings Paper CT FEMS Workshop on Rapid Diagnosis of Mycoplasmas CY AUG 11-23, 1991 CL JERUSALEM, ISRAEL SP FEDERAT EUROPEAN MICROBIOL SOC C1 NIAID,MYCOPLASMA SECT,FREDERICK,MD 21701. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44621-9 J9 FEMS SYMP PY 1993 IS 62 BP 3 EP 14 PG 12 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA BZ71Z UT WOS:A1993BZ71Z00002 ER PT B AU TULLY, JG AF TULLY, JG BE Kahane, I Adoni, A TI SEROLOGICAL IDENTIFICATION OF MOLLICUTES SO RAPID DIAGNOSIS OF MYCOPLASMAS SE FEMS SYMPOSIUM LA English DT Proceedings Paper CT FEMS Workshop on Rapid Diagnosis of Mycoplasmas CY AUG 11-23, 1991 CL JERUSALEM, ISRAEL SP FEDERAT EUROPEAN MICROBIOL SOC C1 NIAID,MYCOPLASMA SECT,FREDERICK,MD 21701. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44621-9 J9 FEMS SYMP PY 1993 IS 62 BP 121 EP 130 PG 10 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA BZ71Z UT WOS:A1993BZ71Z00009 ER PT B AU MAGGI, S AF MAGGI, S BE Beregi, E Gergely, IA Rajczi, K TI WORLD-HEALTH-ORGANIZATION - PROGRAM FOR RESEARCH ON AGING SO RECENT ADVANCES IN AGING SCIENCE, VOLS I AND II LA English DT Proceedings Paper CT XVth Congress of the International-Association-of-Gerontology: Recent Advances in Aging Science CY JUL 04-09, 1993 CL BUDAPEST, HUNGARY SP INT ASSOC GERONTOL C1 NIA,OFF RES AGING,HLTH ELDERLY PROGRAMME,WHO,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MONDUZZI EDITORE PI 40128 BOLOGNA PA VIA FERRARESE 119/2, 40128 BOLOGNA, ITALY BN 88-323-0704-9 PY 1993 BP 31 EP 33 PG 3 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA BA08F UT WOS:A1993BA08F00006 ER PT J AU LAMB, JC CHAPIN, RE AF LAMB, JC CHAPIN, RE TI TESTICULAR AND GERM-CELL TOXICITY - IN-VITRO APPROACHES SO REPRODUCTIVE TOXICOLOGY LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON IN VITRO METHODS IN REPRODUCTIVE TOXICOLOGY CY MAY 19-20, 1992 CL NATL ARTS CTR, OTTAWA, CANADA SP ORG ECON COOPERAT & DEV, INT PROGRAMME CHEM SAFETY HO NATL ARTS CTR DE TESTIS; TESTICULAR TOXICITY; LEYDIG CELL; SERTOLI CELL; IN-VITRO MODEL SYSTEMS ID PRIMARY CULTURES; SERTOLI; MODULATION; PHTHALATE AB Research on testicular toxicology has been advanced significantly by the introduction of in vitro testing systems. In vivo systems, however, are still essential parts of the risk assessment process, and they are unlikely to be eliminated by in vitro model systems. While in vivo systems are needed to study the integrated male reproductive system, in vitro systems are uniquely suited to investigate specific mechanisms of action in the testis. In vitro systems substantially improve the interpretation and use of in vivo systems. In vitro models can be used alone or in combination with each other to test hypotheses about testicular toxicity. Numerous systems are described in the literature, including Sertoli-germ cell cocultures, Sertoli cell-enriched cultures, germ cell-enriched cultures, Leydig cell cultures, and Leydig-Sertoli cell cocultures. These systems have been used to test relative toxicologic activity of selected chemicals in a class, to investigate the cellular response to certain toxicants, to study the metabolic capability of cells, and to describe the interaction of adjacent cell types. C1 NIEHS,RES TRIANGLE PK,NC 27709. RP LAMB, JC (reprint author), JELLINEK SCHWARTZ & CONNOLLY INC,1015 15TH ST NW,SUITE 500,WASHINGTON,DC 20005, USA. OI Chapin, Robert/0000-0002-5997-1261 NR 24 TC 8 Z9 8 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0890-6238 J9 REPROD TOXICOL JI Reprod. Toxicol. PY 1993 VL 7 SU 1 BP 17 EP 22 DI 10.1016/0890-6238(93)90065-F PG 6 WC Reproductive Biology; Toxicology SC Reproductive Biology; Toxicology GA LU305 UT WOS:A1993LU30500003 PM 8400636 ER PT J AU BURKA, LT CHAPIN, RE AF BURKA, LT CHAPIN, RE TI TOXICOKINETICS OF [C-14] SALIGENIN CYCLIC-O-TOLYL PHOSPHATE IN ANESTHETIZED MALE F344 RATS SO REPRODUCTIVE TOXICOLOGY LA English DT Article DE SALIGENIN CYCLIC O-TOLYL PHOSPHATE; TESTIS; ORGANOPHOSPHATE; TOXICOKINETICS; NEUROTOXIC; REPRODUCTIVE TOXICITY; LIVER; KIDNEY ID ORTHO-CRESYL PHOSPHATE; METABOLISM AB Saligenin cyclic o-tolyl phosphate (SCOTP) has been proposed as the active metabolite of tri-o-cresyl phosphate (TOCP), a neurotoxic organophosphate. TOCP is also toxic to the testis and SCOTP mimics some of this toxicity. The stability of SCOTP in vivo and its uptake by selected tissues has been measured. Total radioactivity and SCOTP-associated radioactivity were determined in male F-344 rats treated i.v. with 1 mg of [C-14]-SCOTP/kg. The half-life of SCOTP in blood was 8.0 +/- 1.1 min. Testes, brain, and muscle had lower concentrations of [C-14]-SCOTP-derived radioactivity than blood. Liver and kidney had higher concentrations of radioactivity than blood. HPLC analysis of liver, kidney, testes, and blood extracts showed that 2.8, 48, 11, and 180/o, respectively, of the radioactivity present at 5 min was SCOTP. The amount of SCOTP declined rapidly, and at 30 min SCOTP could be detected only in kidney. It appears that SCOTP, although reactive, has sufficient stability to be transported from organ to organ. There is no evidence, however, of active uptake of SCOTP from blood by the testes. Evidence was obtained that SCOTP may act as an alkylating agent. RP BURKA, LT (reprint author), NIEHS,NATL TOXICOL PROGRAM,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 8 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 0890-6238 J9 REPROD TOXICOL JI Reprod. Toxicol. PY 1993 VL 7 IS 1 BP 81 EP 86 DI 10.1016/0890-6238(93)90013-W PG 6 WC Reproductive Biology; Toxicology SC Reproductive Biology; Toxicology GA KK822 UT WOS:A1993KK82200011 PM 8448420 ER PT J AU SCHWETZ, BA AF SCHWETZ, BA TI IN-VITRO APPROACHES IN DEVELOPMENTAL TOXICOLOGY SO REPRODUCTIVE TOXICOLOGY LA English DT Editorial Material CT INTERNATIONAL WORKSHOP ON IN VITRO METHODS IN REPRODUCTIVE TOXICOLOGY CY MAY 19-20, 1992 CL NATL ARTS CTR, OTTAWA, CANADA SP ORG ECON COOPERAT & DEV, INT PROGRAMME CHEM SAFETY HO NATL ARTS CTR DE DEVELOPMENTAL TOXICOLOGY; IN-VITRO; TERATOLOGY; DEVELOPMENTAL BIOLOGY; MALFORMATIONS; EMBRYO; FETUS; SCREENS RP SCHWETZ, BA (reprint author), NIEHS,POB 12233,MD D4-02,RES TRIANGLE PK,NC 27709, USA. NR 5 TC 2 Z9 2 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0890-6238 J9 REPROD TOXICOL JI Reprod. Toxicol. PY 1993 VL 7 SU 1 BP 125 EP 127 DI 10.1016/0890-6238(93)90078-L PG 3 WC Reproductive Biology; Toxicology SC Reproductive Biology; Toxicology GA LU305 UT WOS:A1993LU30500016 PM 8400631 ER PT J AU SCHWETZ, BA AF SCHWETZ, BA TI UTILITY OF IN-VITRO ASSAYS - SUMMARY OF INTERNATIONAL WORKSHOP ON IN-VITRO METHODS IN REPRODUCTIVE TOXICOLOGY SO REPRODUCTIVE TOXICOLOGY LA English DT Editorial Material RP SCHWETZ, BA (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0890-6238 J9 REPROD TOXICOL JI Reprod. Toxicol. PY 1993 VL 7 SU 1 BP 171 EP 173 DI 10.1016/0890-6238(93)90083-J PG 3 WC Reproductive Biology; Toxicology SC Reproductive Biology; Toxicology GA LU305 UT WOS:A1993LU30500021 ER PT J AU KU, WW CHAPIN, RE WINE, RN GLADEN, BC AF KU, WW CHAPIN, RE WINE, RN GLADEN, BC TI TESTICULAR TOXICITY OF BORIC-ACID (BA) - RELATIONSHIP OF DOSE TO LESION DEVELOPMENT AND RECOVERY IN THE F344 RAT SO REPRODUCTIVE TOXICOLOGY LA English DT Article DE BORIC ACID; BORON; TESTIS; TOXICITY; RATS ID MALE REPRODUCTIVE-SYSTEM; TESTIS; 2,5-HEXANEDIONE; EXPOSURE; SPERMATOGENESIS; MORPHOGENESIS; MAINTENANCE; ANDROGEN; ATROPHY; BORON AB High-dose boric acid (BA) produces testicular lesions in adult rats, characterized by inhibited spermiation followed by atrophy. The present study addressed whether inhibited spermiation can be separated from atrophy based on dose, compared testis boron (B) dosimetry to lesion development, determined how inhibited spermiation was reflected by common reproductive endpoints, and examined reversibility of the testicular lesions. Rats were fed 3000, 4500, 6000, or 9000 ppm BA for up to 9 weeks and examined. Recovery was assessed for up to 32 weeks post treatment. Inhibited spermiation could be separated from atrophy based on dose (inhibited spermiation: 3000/4500 ppm; atrophy: 6000/9000 ppm), with each lesion aspect expressed at different threshold testis B concentrations (inhibited spermiation: 5.6 mug B/g and atrophy: 11.9 mug B/g) with no B accumulation during the 9-week exposure. These data suggest that separate mechanisms may be operating for these lesion aspects based on testis B concentration and that B dose rate was important for testicular toxicity. Inhibited spermiation was most reliably reflected by informed testicular histology, with the more severe cases decreasing epididymal sperm count to levels that could affect fertility. After treatment, serum and testis B levels in all dose groups rapidly fell to background levels at the earliest time points evaluated (7 days and 8 weeks posttreatment, respectively). The severely inhibited spermiation at 4500 ppm was resolved by 16 weeks posttreatment, but areas of focal atrophy were detected that did not recover posttreatment. Also, no signs of recovery from atrophy were observed (6000 and 9000 ppm). Atrophic tubules contained a normal complement of spermatogonia (2.6 to 2.9 germ cells/100 Sertoli cells), with occasional dividing and degenerating germ cells. Elevations in serum FSH and LH levels suggested an intact hormonal response to the atrophy. In summary, 1) the different aspects of the BA-induced testicular lesion can be separated using different doses, 2) inhibited spermiation does not necessarily proceed to atrophy, and 3) there is no recovery from the atrophy despite the absence of testis B after treatment. The ability to separate inhibited spermiation from atrophy based on dose and testis B dosimetry will be useful in evaluating possible mechanisms. Furthermore, the presence of dividing spermatogonia during long-term BA-induced atrophy suggests that this model should be useful for identifying critical components involved in the reinitiation of spermatogenesis. C1 NIEHS,NATL TOXICOL PROGRAM,DEV & REPROD TOXICOL GRP,RES TRIANGLE PK,NC 27709. RP KU, WW (reprint author), NIEHS,STAT & BIOMATH BRANCH,POB 12233,MD A2-02,RES TRIANGLE PK,NC 27709, USA. OI Chapin, Robert/0000-0002-5997-1261 FU NIEHS NIH HHS [N01-ES-15307] NR 42 TC 87 Z9 96 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0890-6238 J9 REPROD TOXICOL JI Reprod. Toxicol. PY 1993 VL 7 IS 4 BP 305 EP 319 DI 10.1016/0890-6238(93)90020-8 PG 15 WC Reproductive Biology; Toxicology SC Reproductive Biology; Toxicology GA LU573 UT WOS:A1993LU57300003 PM 8400621 ER PT J AU KU, WW SHIH, LM CHAPIN, RE AF KU, WW SHIH, LM CHAPIN, RE TI THE EFFECTS OF BORIC-ACID (BA) ON TESTICULAR CELLS IN CULTURE SO REPRODUCTIVE TOXICOLOGY LA English DT Article DE BORIC ACID; BORON; TOXICITY; RATS; TESTIS; CULTURED CELLS ID PLASMINOGEN-ACTIVATOR; SERTOLI CELLS; HORMONAL-STIMULATION; SPERMATOGENIC CELLS; DNA-SYNTHESIS; LEYDIG-CELLS; RAT TESTIS; MAINTENANCE; PHTHALATE; TOXICITY AB High-dose boric acid (BA) exposure produces testicular lesions in adult rats characterized by inhibited spermiation that may progress to nonrecoverable atrophy. The mechanism for the testicular toxicity of BA is unknown. To examine possible direct effects, the present study evaluated selected aspects of various testicular cell culture systems after in vitro BA exposure. Specifically, the hallmarks of the BA testicular toxicity were addressed: the mild hormone effect, the initial inhibition of spermiation, and atrophy. No effect of BA on the steroidogenic function of isolated Leydig cells was observed, supporting the contention of a CNS-mediated rather than a direct hormone effect. Since increased testicular cyclic AMP (cAMP) produces inhibited spermiation, and a role for the serine proteases plasminogen activators (PAs) in spermiation has been proposed, we evaluated both Sertoli cell cAMP accumulation in Sertoli-germ cell cocultures and the stage-specific secretion of PA activity in cultured seminiferous tubules after in vitro BA exposure, respectively. The results showed that the inhibited spermiation is not due to BA effects on either process. To address the atrophy, we evaluated BA effects in Sertoli-germ cell cocultures on t) morphology/germ cell attachment, which might identify a target cell; 2) Sertoli cell energy metabolism, because lactate, secreted by Sertoli cells, is a preferred energy source for germ cells; and 3) DNA/RNA synthesis, because germ cells synthesize DNA/RNA and BA impairs nucleic acid synthesis in liver and may do so in testis. Despite the absence of overt morphologic changes and germ cell loss, the most sensitive in vitro endpoint was DNA synthesis of mitotic/meiotic germ cells, with energy metabolism in Sertoli or germ cells affected to a lesser extent. A re-evaluation of testis sections from rats exposed to BA revealed a decrease in the early germ cell/Sertoli cell ratio prior to atrophy. Thus, although the mechanism for the inhibited spermiation is still undefined and is the subject of future work, these combined studies revealed some changes offering a plausible explanation for the atrophy aspect of the BA testicular lesion. RP KU, WW (reprint author), NIEHS,NATL TOXICOL PROGRAM,DEV & REPROD TOXICOL GRP,POB 12233,MD E1-02,RES TRIANGLE PK,NC 27709, USA. OI Chapin, Robert/0000-0002-5997-1261 NR 41 TC 22 Z9 23 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0890-6238 J9 REPROD TOXICOL JI Reprod. Toxicol. PY 1993 VL 7 IS 4 BP 321 EP 331 DI 10.1016/0890-6238(93)90021-X PG 11 WC Reproductive Biology; Toxicology SC Reproductive Biology; Toxicology GA LU573 UT WOS:A1993LU57300004 PM 7691281 ER PT J AU CESBRON, MF DUBREMETZ, JF SHER, A AF CESBRON, MF DUBREMETZ, JF SHER, A TI THE IMMUNOBIOLOGY OF TOXOPLASMOSIS - INTRODUCTION SO RESEARCH IN IMMUNOLOGY LA English DT Editorial Material C1 INSERM,U42,F-59651 VILLENEUVE DASCQ,FRANCE. NIH,PARASIT DIS LAB,BETHESDA,MD 20892. RP CESBRON, MF (reprint author), INST PASTEUR,CNRS,INSERM,U167,CIBP,F-59019 LILLE,FRANCE. RI cesbron delauw, marie france/M-6076-2014 NR 0 TC 6 Z9 6 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD JAN PY 1993 VL 144 IS 1 BP 7 EP 8 DI 10.1016/S0923-2494(05)80088-4 PG 2 WC Immunology SC Immunology GA KK613 UT WOS:A1993KK61300001 PM 8451523 ER PT J AU DENKERS, EY SHER, A GAZZINELLI, RT AF DENKERS, EY SHER, A GAZZINELLI, RT TI CD8+ T-CELL INTERACTIONS WITH TOXOPLASMA-GONDII - IMPLICATIONS FOR PROCESSING OF ANTIGEN FOR CLASS-I-RESTRICTED RECOGNITION SO RESEARCH IN IMMUNOLOGY LA English DT Article ID LYMPHOCYTES-T; INFECTED CELLS; HOST-CELLS; MICE; RESISTANCE; INTERFERON; ANTIBODY; LYT-2+; GENES; P-30 RP DENKERS, EY (reprint author), NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BETHESDA,MD 20892, USA. NR 28 TC 43 Z9 44 U1 0 U2 1 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD JAN PY 1993 VL 144 IS 1 BP 51 EP 57 DI 10.1016/S0923-2494(05)80099-9 PG 7 WC Immunology SC Immunology GA KK613 UT WOS:A1993KK61300012 PM 8095730 ER PT J AU MOULIN, AM DARCY, F SIBLEY, LD KRAHENBUHL, JL HERION, P SAAVEDRA, R SHER, A DENKERS, E GAZZINELLI, R MCLEOD, R BROWN, C MACK, D SUZUKI, Y AF MOULIN, AM DARCY, F SIBLEY, LD KRAHENBUHL, JL HERION, P SAAVEDRA, R SHER, A DENKERS, E GAZZINELLI, R MCLEOD, R BROWN, C MACK, D SUZUKI, Y TI THE IMMUNOBIOLOGY OF TOXOPLASMOSIS - DISCUSSION SO RESEARCH IN IMMUNOLOGY LA English DT Discussion DE TOXOPLASMOSIS, TOXOPLASMA-GONDII; IMMUNOBIOLOGY, PATHOGENESIS; FORUM ID NUCLEOSIDE TRIPHOSPHATE HYDROLASE; MAJOR SURFACE-ANTIGEN; PARASITOPHOROUS VACUOLE; MONOCLONAL-ANTIBODIES; DENSE GRANULES; HOST-CELL; GONDII; PROTEINS; MEMBRANE; CLONING C1 HOP LAENNEC,DEPT MICROBIOL PARASITOL,F-75015 PARIS,FRANCE. INST PASTEUR,CTR IMMUNOL & BIOL PARASITAIRE,CNRS,UNITE 624,INSERM,U167,F-59019 LILLE,FRANCE. WASHINGTON UNIV,SCH MED,DEPT MOLEC MICROBIOL,ST LOUIS,MO 63110. LOUISIANA STATE UNIV,LAB RES BRANCH,GWL HANSENS DIS CTR,DEPT IMMUNOL,BATON ROUGE,LA 70894. INNOGENET NV,B-9052 GHENT,BELGIUM. NATL AUTONOMOUS UNIV MEXICO,INST INVEST BIOMED,DEPT INMUNOL,MEXICO CITY 04510,DF,MEXICO. NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BETHESDA,MD 20892. MICHAEL REESE HOSP & MED CTR,DEPT MED,CHICAGO,IL 60616. JIKEI UNIV,DEPT PARASITOL,TOKYO 105,JAPAN. RP MOULIN, AM (reprint author), CNRS,INSERM,U158,F-75005 PARIS,FRANCE. NR 38 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD JAN PY 1993 VL 144 IS 1 BP 68 EP 79 PG 12 WC Immunology SC Immunology GA KK613 UT WOS:A1993KK61300016 ER PT B AU AYYAGARI, R SMITH, RJH LEE, EC KIMBERLING, WJ JAY, M BIRD, A HEJTMANCIK, JF AF AYYAGARI, R SMITH, RJH LEE, EC KIMBERLING, WJ JAY, M BIRD, A HEJTMANCIK, JF BE Hollyfield, JG Anderson, RE LaVail, MM TI HETEROGENEITY OF USHER SYNDROME TYPE-I SO RETINAL DEGENERATION: CLINICAL AND LABORATORY APPLICATIONS LA English DT Proceedings Paper CT International Symposium on Retinal Degeneration CY SEP 15-20, 1992 CL SARDINIA, ITALY C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44570-0 PY 1993 BP 127 EP 133 PG 7 WC Medical Laboratory Technology; Ophthalmology SC Medical Laboratory Technology; Ophthalmology GA BZ55M UT WOS:A1993BZ55M00012 ER PT J AU SAFFIOTTI, U DANIEL, LN MAO, Y WILLIAMS, AO KAIGHN, ME AHMED, N KNAPTON, AD AF SAFFIOTTI, U DANIEL, LN MAO, Y WILLIAMS, AO KAIGHN, ME AHMED, N KNAPTON, AD TI BIOLOGICAL STUDIES ON THE CARCINOGENIC MECHANISMS OF QUARTZ SO REVIEWS IN MINERALOGY LA English DT Review ID INDUCED TRANSFORMATION; EPITHELIAL-CELLS; MAMMALIAN-CELLS; POTENTIAL ROLE; SILICA; RAT; PROLIFERATION; INDUCTION; FIBER; DUST RP SAFFIOTTI, U (reprint author), NCI, EXPTL PATHOL LAB, BETHESDA, MD 20892 USA. NR 53 TC 1 Z9 1 U1 0 U2 0 PU MINERALOGICAL SOC AMER PI CHANTILLY PA 3635 CONCORDE PKWY STE 500, CHANTILLY, VA 20151-1125 USA SN 0275-0279 J9 REV MINERAL JI Rev. Mineral. PY 1993 VL 28 BP 523 EP 544 PG 22 WC Mineralogy SC Mineralogy GA MJ529 UT WOS:A1993MJ52900018 ER PT S AU LEROITH, D ROBERTS, CT AF LEROITH, D ROBERTS, CT BE Raizada, MK Leroith, D TI INSULIN-LIKE GROWTH-FACTORS SO ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEMS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON THE ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEM CY NOV 04-07, 1992 CL ARLINGTON, VA SP NEW YORK ACAD SCI, GENETECH, ABBOTT LABS, PHARM PROD DIV, BURROUGHS WELLCOME, LILLY RES LABS, NIA, NIDDKD, NIMH, NINDS, SMITHKLINE BEECHAM PHARM RP ROBERTS, CT (reprint author), NIDDKD,DIABET BRANCH,MOLEC & CELLULAR PHYSIOL SECT,BLDG 10,ROOM 8S-239,BETHESDA,MD 20892, USA. NR 0 TC 56 Z9 56 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-789-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 692 BP 1 EP 9 PG 9 WC Endocrinology & Metabolism; Neurosciences; Physiology SC Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ06R UT WOS:A1993BZ06R00001 ER PT S AU LEROITH, D WERNER, H FARIA, TN KATO, H ADAMO, M ROBERTS, CT AF LEROITH, D WERNER, H FARIA, TN KATO, H ADAMO, M ROBERTS, CT BE Raizada, MK Leroith, D TI INSULIN-LIKE GROWTH-FACTOR RECEPTORS - IMPLICATIONS FOR NERVOUS-SYSTEM FUNCTION SO ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEMS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON THE ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEM CY NOV 04-07, 1992 CL ARLINGTON, VA SP NEW YORK ACAD SCI, GENETECH, ABBOTT LABS, PHARM PROD DIV, BURROUGHS WELLCOME, LILLY RES LABS, NIA, NIDDKD, NIMH, NINDS, SMITHKLINE BEECHAM PHARM RP LEROITH, D (reprint author), NIDDKD,DIABET BRANCH,BLDG 10,ROOM 8S239,BETHESDA,MD 20892, USA. NR 0 TC 36 Z9 36 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-789-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 692 BP 22 EP 32 PG 11 WC Endocrinology & Metabolism; Neurosciences; Physiology SC Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ06R UT WOS:A1993BZ06R00003 ER PT S AU BONDY, CA LEE, WH AF BONDY, CA LEE, WH BE Raizada, MK Leroith, D TI PATTERNS OF INSULIN-LIKE GROWTH-FACTOR AND IGF RECEPTOR GENE-EXPRESSION IN THE BRAIN - FUNCTIONAL IMPLICATIONS SO ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEMS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON THE ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEM CY NOV 04-07, 1992 CL ARLINGTON, VA SP NEW YORK ACAD SCI, GENETECH, ABBOTT LABS, PHARM PROD DIV, BURROUGHS WELLCOME, LILLY RES LABS, NIA, NIDDKD, NIMH, NINDS, SMITHKLINE BEECHAM PHARM RP BONDY, CA (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N262,BETHESDA,MD 20892, USA. NR 0 TC 44 Z9 45 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-789-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 692 BP 33 EP 43 PG 11 WC Endocrinology & Metabolism; Neurosciences; Physiology SC Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ06R UT WOS:A1993BZ06R00004 ER PT S AU GUROFF, G AF GUROFF, G BE Raizada, MK Leroith, D TI NERVE GROWTH-FACTOR AS A NEUROTROPHIC AGENT SO ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEMS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON THE ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEM CY NOV 04-07, 1992 CL ARLINGTON, VA SP NEW YORK ACAD SCI, GENETECH, ABBOTT LABS, PHARM PROD DIV, BURROUGHS WELLCOME, LILLY RES LABS, NIA, NIDDKD, NIMH, NINDS, SMITHKLINE BEECHAM PHARM RP GUROFF, G (reprint author), NICHHD,GROWTH FACTORS SECT,BLDG 49,ROOM 5A64,BETHESDA,MD 20892, USA. NR 0 TC 10 Z9 10 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-789-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 692 BP 51 EP 59 PG 9 WC Endocrinology & Metabolism; Neurosciences; Physiology SC Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ06R UT WOS:A1993BZ06R00006 ER PT S AU BEITNERJOHNSON, D NESTLER, EJ AF BEITNERJOHNSON, D NESTLER, EJ BE Raizada, MK Leroith, D TI CHRONIC MORPHINE DECREASES INSULIN-LIKE GROWTH FACTOR-I LEVELS IN THE VENTRAL TEGMENTAL AREA OF THE RAT-BRAIN SO ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEMS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON THE ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEM CY NOV 04-07, 1992 CL ARLINGTON, VA SP NEW YORK ACAD SCI, GENETECH, ABBOTT LABS, PHARM PROD DIV, BURROUGHS WELLCOME, LILLY RES LABS, NIA, NIDDKD, NIMH, NINDS, SMITHKLINE BEECHAM PHARM RP BEITNERJOHNSON, D (reprint author), NIDDK,DIABET BRANCH,BLDG 10,RM 8S-239,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-789-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 692 BP 246 EP 248 PG 3 WC Endocrinology & Metabolism; Neurosciences; Physiology SC Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ06R UT WOS:A1993BZ06R00024 ER PT S AU PERFETTI, R SHULDINER, AR AF PERFETTI, R SHULDINER, AR BE Raizada, MK Leroith, D TI INSULIN, BUT NOT INSULIN-LIKE GROWTH FACTOR-I, IS EXPRESSED DURING EARLY NERVOUS-SYSTEM DEVELOPMENT IN PREPANCREATIC XENOPUS-EMBRYOS SO ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEMS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON THE ROLE OF INSULIN-LIKE GROWTH FACTORS IN THE NERVOUS SYSTEM CY NOV 04-07, 1992 CL ARLINGTON, VA SP NEW YORK ACAD SCI, GENETECH, ABBOTT LABS, PHARM PROD DIV, BURROUGHS WELLCOME, LILLY RES LABS, NIA, NIDDKD, NIMH, NINDS, SMITHKLINE BEECHAM PHARM RP PERFETTI, R (reprint author), NIA,DIABET UNIT,ROOM 2B02,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-789-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 692 BP 268 EP 269 PG 2 WC Endocrinology & Metabolism; Neurosciences; Physiology SC Endocrinology & Metabolism; Neurosciences & Neurology; Physiology GA BZ06R UT WOS:A1993BZ06R00031 ER PT S AU BAUM, BJ AF BAUM, BJ BE Malamud, D Tabak, L TI PRINCIPLES OF SALIVA SECRETION SO SALIVA AS A DIAGNOSTIC FLUID SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SALIVA AS A DIAGNOSTIC FLUID CY OCT 22-25, 1992 CL PANAMA CITY BEACH, FL SP NEW YORK ACAD SCI, BLOCK DRUG, COLGATE PALMOLIVE, EPITOPE, NASA, NIDR, SALIVA DIAGNOST SYST, ABBOTT LABS, ENZYMATICS, HOFFMANN LA ROCHE RP BAUM, BJ (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 113 Z9 116 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-787-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 694 BP 17 EP 23 PG 7 WC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology SC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology GA BZ06S UT WOS:A1993BZ06S00003 ER PT S AU TURNER, RJ AF TURNER, RJ BE Malamud, D Tabak, L TI MECHANISMS OF FLUID SECRETION BY SALIVARY-GLANDS SO SALIVA AS A DIAGNOSTIC FLUID SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SALIVA AS A DIAGNOSTIC FLUID CY OCT 22-25, 1992 CL PANAMA CITY BEACH, FL SP NEW YORK ACAD SCI, BLOCK DRUG, COLGATE PALMOLIVE, EPITOPE, NASA, NIDR, SALIVA DIAGNOST SYST, ABBOTT LABS, ENZYMATICS, HOFFMANN LA ROCHE RP TURNER, RJ (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 50 Z9 51 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-787-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 694 BP 24 EP 35 DI 10.1111/j.1749-6632.1993.tb18339.x PG 12 WC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology SC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology GA BZ06S UT WOS:A1993BZ06S00004 PM 8215060 ER PT S AU CONE, EJ AF CONE, EJ BE Malamud, D Tabak, L TI SALIVA TESTING FOR DRUGS OF ABUSE SO SALIVA AS A DIAGNOSTIC FLUID SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SALIVA AS A DIAGNOSTIC FLUID CY OCT 22-25, 1992 CL PANAMA CITY BEACH, FL SP NEW YORK ACAD SCI, BLOCK DRUG, COLGATE PALMOLIVE, EPITOPE, NASA, NIDR, SALIVA DIAGNOST SYST, ABBOTT LABS, ENZYMATICS, HOFFMANN LA ROCHE RP CONE, EJ (reprint author), NIDA,ADDICT RES CTR,BALTIMORE,MD 21224, USA. NR 0 TC 107 Z9 110 U1 0 U2 6 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-787-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 694 BP 91 EP 127 DI 10.1111/j.1749-6632.1993.tb18346.x PG 37 WC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology SC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology GA BZ06S UT WOS:A1993BZ06S00011 PM 8215090 ER PT S AU FOX, PC AF FOX, PC BE Malamud, D Tabak, L TI SALIVARY MONITORING IN ORAL-DISEASES SO SALIVA AS A DIAGNOSTIC FLUID SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SALIVA AS A DIAGNOSTIC FLUID CY OCT 22-25, 1992 CL PANAMA CITY BEACH, FL SP NEW YORK ACAD SCI, BLOCK DRUG, COLGATE PALMOLIVE, EPITOPE, NASA, NIDR, SALIVA DIAGNOST SYST, ABBOTT LABS, ENZYMATICS, HOFFMANN LA ROCHE RP FOX, PC (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,CLIN INVEST SECT,BETHESDA,MD 20892, USA. NR 0 TC 15 Z9 15 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-787-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 694 BP 234 EP 237 DI 10.1111/j.1749-6632.1993.tb18356.x PG 4 WC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology SC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology GA BZ06S UT WOS:A1993BZ06S00021 PM 8215058 ER PT S AU ATKINSON, JC AF ATKINSON, JC BE Malamud, D Tabak, L TI THE ROLE OF SALIVARY MEASUREMENTS IN THE DIAGNOSIS OF SALIVARY AUTOIMMUNE-DISEASES SO SALIVA AS A DIAGNOSTIC FLUID SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SALIVA AS A DIAGNOSTIC FLUID CY OCT 22-25, 1992 CL PANAMA CITY BEACH, FL SP NEW YORK ACAD SCI, BLOCK DRUG, COLGATE PALMOLIVE, EPITOPE, NASA, NIDR, SALIVA DIAGNOST SYST, ABBOTT LABS, ENZYMATICS, HOFFMANN LA ROCHE RP ATKINSON, JC (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 22 Z9 22 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-787-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 694 BP 238 EP 251 DI 10.1111/j.1749-6632.1993.tb18357.x PG 14 WC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology SC Dentistry, Oral Surgery & Medicine; Endocrinology & Metabolism; Immunology; Physiology GA BZ06S UT WOS:A1993BZ06S00022 PM 8215059 ER PT J AU NISULA, BC AF NISULA, BC TI MEASUREMENT OF HUMAN CHORION GONADOTROPIN BY BIOLOGICAL METHODS SO SCANDINAVIAN JOURNAL OF CLINICAL & LABORATORY INVESTIGATION LA English DT Article DE BIOASSAYS OF HCG; BIOLOGICAL ACTIVITIES OF HCG; INTERSTITIAL CELL-STIMULATING; THYROID-STIMULATING; THYROTROPIC ID HUMAN LUTEINIZING-HORMONE; INVITRO BIOASSAY; LH; EXPRESSION; SECRETION; RECEPTOR; ASSAY; SERUM; RAT AB The clinically significant biological activities of hCG result from its interaction with LH and TSH receptors. In vivo bioassays for measurement of these hCG activities have many disadvantages including complexity, expense, labor-intensity, and insensitivity. In vitro bioassays based on animal Leydig cell responses are widely used in research studies, but since they are based on animal receptors, their relevance to human biology remains uncertain. Visible on the horizon are in vitro bioassays constructed with human receptor genes transfected into cell systems by modem molecular techniques. RP NISULA, BC (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. NR 11 TC 2 Z9 2 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5513 J9 SCAND J CLIN LAB INV JI Scand. J. Clin. Lab. Invest. PY 1993 VL 53 SU 216 BP 114 EP 117 DI 10.3109/00365519309086912 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA LP528 UT WOS:A1993LP52800007 ER PT J AU LUNDGREN, B KOVACS, JA MATHIESEN, L NIELSEN, JO LUNDGREN, JD AF LUNDGREN, B KOVACS, JA MATHIESEN, L NIELSEN, JO LUNDGREN, JD TI IGM RESPONSE TO A HUMAN PNEUMOCYSTIS-CARINII SURFACE-ANTIGEN IN HIV-INFECTED PATIENTS WITH PULMONARY SYMPTOMS SO SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; ANTIBODIES; PNEUMONIA; DIAGNOSIS; PROTEINS AB We have developed an ELISA to detect IgM antibodies to a major human Pneumocystis carinii surface antigen (gp95), and investigated the IgM response in 128 HIV-infected patients who underwent bronchoscopy for evaluation of pulmonary symptoms. Only 5 (4%) patients had IgM antibodies to P. carinii gp95. Four of the 5 patients with IgM antibodies also had IgG antibodies to gp95 and microbiologically proven P. carinii pneumonia (PCP). In 76/128 patients for whom serial samples were available, changes in antibody response were determined. In 3 patients we demonstrated an increase in IgM antibody response to gp95. These patients also showed an increase in IgG antibodies to gp95 and had microbiologically proven PCP. Prior to the development of the IgM response, IgG antibodies to gp95 were detectable in all 3 patients. Thus, HIV-infected patients with PCP seldom produce IgM antibodies to the major human P. carinii surface antigen. The increase in IgM response during the course of PCP observed in 3 patients suggests either reinfection with a new strain, or antigenic drift of an already acquired strain of P. carinii. C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RP LUNDGREN, B (reprint author), UNIV COPENHAGEN,HVIDOVRE HOSP,DEPT INFECT DIS 144,DK-2650 HVIDOVRE,DENMARK. OI Lundgren, Jens/0000-0001-8901-7850 NR 19 TC 12 Z9 12 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5548 J9 SCAND J INFECT DIS JI Scand. J. Infect. Dis. PY 1993 VL 25 IS 4 BP 515 EP 520 DI 10.3109/00365549309008535 PG 6 WC Infectious Diseases SC Infectious Diseases GA LX848 UT WOS:A1993LX84800017 PM 8248753 ER PT J AU KIRCH, DG AF KIRCH, DG TI INFECTION AND AUTOIMMUNITY AS ETIOLOGIC FACTORS IN SCHIZOPHRENIA - A REVIEW AND REAPPRAISAL SO SCHIZOPHRENIA BULLETIN LA English DT Review ID ACUTE PSYCHIATRIC-DISORDERS; LYMPHOCYTE SUB-POPULATIONS; HERPES-SIMPLEX VIRUS; CEREBROSPINAL-FLUID; CYTOMEGALO-VIRUS; VIRAL HYPOTHESIS; SERUM INTERFERON; NEUROLOGICAL DISORDERS; PRENATAL EXPOSURE; ANTIBODY-TITERS AB The focus of schizophrenia research has been turning from studies of structural and functional brain abnormalities to an increasing emphasis on possible etiologic factors. One etiologic hypothesis is that schizophrenia is the result of an infection (especially by a virus) or of an autoimmune reaction (perhaps following an infection) against central nervous system (CNS) tissue. Indirect evidence supporting this hypothesis includes possible geographic variance in the prevalence of schizophrenia, a season-of-birth effect, and observed associations between schizophrenia and prenatal exposure to viral epidemics. Several studies of cell-based and humoral immunity, as well as studies of cytokines, have indicated abnormalities in the immune function of schizophrenia patients, but many of these findings have not been replicated consistently. In addition, most observed alterations in immune function have been modest in degree and nonspecific. Attempts to identify a specific infectious agent or an antibody directed against CNS tissue have not produced a consistently replicable finding. In summary, no research evidence to date irrefutably indicates an infectious or autoimmune etiologic process in schizophrenia. It is probably unreasonable, however, to view schizophrenia as having a single cause. It is much more likely to be a heterogeneous disorder resulting from interactions between multiple factors, including the person's genetic endowment and various environmental influences. Infectious agents or CNS auto-antibodies may well be among these environmental variables. A major current emphasis is on studying potential interactions between exposure to an infection or an autoimmune response and key early phases of brain development. A corresponding priority in the research agenda will be the development of animal models of CNS development that might elucidate the pathogenic mechanisms of such an interaction. RP KIRCH, DG (reprint author), NIMH,BLDG 10,RM 4N-224,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 137 TC 134 Z9 139 U1 2 U2 4 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1993 VL 19 IS 2 BP 355 EP 370 PG 16 WC Psychiatry SC Psychiatry GA LH084 UT WOS:A1993LH08400009 PM 8322038 ER PT J AU TORREY, EF BOWLER, AE RAWLINGS, R TERRAZAS, A AF TORREY, EF BOWLER, AE RAWLINGS, R TERRAZAS, A TI SEASONALITY OF SCHIZOPHRENIA AND STILLBIRTHS SO SCHIZOPHRENIA BULLETIN LA English DT Article ID PRENATAL EXPOSURE; INFLUENZA EPIDEMICS; ADULT SCHIZOPHRENIA; MENTAL-DISORDERS; BIRTH; ETIOLOGY; DEATHS; FETAL; AGE AB A study of the birth pattern of 30,467 patients with schizophrenia and 428,406 stillbirths in New York State showed a significant winter-month excess in both schizophrenia births (p = 0.0000) and stillbirths (p = 0.0000). Excess births of individuals with schizophrenia in November and December provided additional evidence to refute the age-incidence explanation for the observed seasonality. Time series spectral analysis showed coherence in the pattern of schizophrenia births and stillbirths of 0.898 (p < 0.003) with schizophrenia births preceding stillbirths by 13 days. These results suggest that a common etiological seasonal factor affects a subgroup of births of individuals who later develop schizophrenia and a subgroup of stillbirths. Nutritional factors, temperature, and infectious agents known to cause both central nervous system disease and stillbirths are possible candidates. C1 NIAAA,INTRAMURAL RES PROGRAM,CLIN STUDIES LAB,BETHESDA,MD. RP TORREY, EF (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,TWIN STUDY UNIT,WASHINGTON,DC 20032, USA. NR 37 TC 30 Z9 30 U1 1 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1993 VL 19 IS 3 BP 557 EP 562 PG 6 WC Psychiatry SC Psychiatry GA LX603 UT WOS:A1993LX60300006 PM 8235458 ER PT J AU GOLDBERG, TE HYDE, TM KLEINMAN, JE WEINBERGER, DR AF GOLDBERG, TE HYDE, TM KLEINMAN, JE WEINBERGER, DR TI COURSE OF SCHIZOPHRENIA - NEUROPSYCHOLOGICAL EVIDENCE FOR A STATIC ENCEPHALOPATHY SO SCHIZOPHRENIA BULLETIN LA English DT Article ID 1ST EPISODE SCHIZOPHRENIA; FOLLOW-UP; NEUROLEPTICS; BRAIN; STABILITY; DEFICITS; RISK AB The course of cognitive function in schizophrenia has often been debated. In one view, it is thought to be akin to that of a progressive dementia with relentless cognitive decline. In another view, the deficits are thought to remain relatively stable, analogous to those of a static encephalopathy. Review of longitudinal and cross-sectional studies strongly supports the latter interpretation. In particular, we present data from a recent cross-sectional study in which cohorts of patients in their third, fourth, fifth, sixth, and seventh decades of life were administered a battery of tests known to be sensitive to progressive dementing diseases. All patients were carefully screened to exclude those with neurologic, systemic, or psychiatric comorbid conditions, and cohorts were matched on estimated premorbid intellectual capacity. Although scores on most tests were impaired, no evidence of decline across groups was observed. These results are also consistent with neuroimaging and neuropathological studies in that no evidence for an active degenerative process has been discovered. C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,NEUROL CLIN,WASHINGTON,DC 20032. RP GOLDBERG, TE (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,NEUROPSYCHOL BRANCH,WASHINGTON,DC 20032, USA. NR 64 TC 141 Z9 143 U1 6 U2 12 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1993 VL 19 IS 4 BP 797 EP 804 PG 8 WC Psychiatry SC Psychiatry GA MH200 UT WOS:A1993MH20000013 PM 8303228 ER PT J AU LOCHMAN, JE DUNN, SE KLIMESDOUGAN, B AF LOCHMAN, JE DUNN, SE KLIMESDOUGAN, B TI AN INTERVENTION AND CONSULTATION MODEL FROM A SOCIAL COGNITIVE PERSPECTIVE - A DESCRIPTION OF THE ANGER COPING PROGRAM SO SCHOOL PSYCHOLOGY REVIEW LA English DT Article ID AGGRESSIVE BOYS; NONAGGRESSIVE BOYS; BEHAVIORAL INTERVENTIONS; ATTRIBUTIONAL BIASES; SCHOOL CONSULTATION; PEER REJECTION; SELF; TEACHERS; CHILDREN; PSYCHOLOGISTS AB This article provides a rationale and description of a school-based anger coping program for aggressive children. The need for school-based, preventive interventions with this population is discussed. The conceptual model for this intervention is outlined and relevant findings on social cognitive-process are briefly overviewed. Based on this conceptual model, the cognitive-behavioral intervention framework is described, and relevant outcome research findings are reviewed. The article advocates that universal interventions and teacher consultation can be used to augment secondary prevention programs such as the Anger Coping Program. The article concludes by advocating for comprehensive social-cognitive interventions which also provide programming for parents. C1 NIMH,DEV PSYCHOL LAB,BETHESDA,MD 20892. CHILDRENS PSYCHIAT INST,BUTNER,NC. DUKE UNIV,MED CTR,DEPT PSYCHOL SOCIAL & HLTH SCI,DURHAM,NC 27710. RP LOCHMAN, JE (reprint author), DUKE UNIV,MED CTR,DEPT PSYCHIAT,BOX 2906,DURHAM,NC 27710, USA. NR 82 TC 27 Z9 27 U1 1 U2 4 PU NATL ASSN SCHOOL PSYCHOL PI HARRISONBURG PA JAMES MADISON UNIV DEPT PSYCHOL, HARRISONBURG, VA 22807 SN 0279-6015 J9 SCHOOL PSYCHOL REV JI Sch. Psychol. Rev. PY 1993 VL 22 IS 3 BP 458 EP 471 PG 14 WC Psychology, Educational SC Psychology GA MF346 UT WOS:A1993MF34600008 ER PT J AU CULVER, KW AF CULVER, KW TI SPLICE OF LIFE - GENETIC THERAPY COMES OF AGE SO SCIENCES-NEW YORK LA English DT Article C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0036-861X J9 SCIENCES JI Sci.-New York PD JAN-FEB PY 1993 VL 33 IS 1 BP 18 EP 24 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MP754 UT WOS:A1993MP75400010 PM 11651523 ER PT J AU CAMPAGNE, MMV VILLALBADIAZ, F MEACCI, E MANGANIELLO, C KESSIN, RH AF CAMPAGNE, MMV VILLALBADIAZ, F MEACCI, E MANGANIELLO, C KESSIN, RH TI SELECTION OF CDNAS FOR PHOSPHODIESTERASES THAT HYDROLYZE GUANOSINE 3'5'-MONOPHOSPHATE IN ESCHERICHIA-COLI SO SECOND MESSENGERS AND PHOSPHOPROTEINS LA English DT Article ID CYCLIC-NUCLEOTIDE PHOSPHODIESTERASES; AFFINITY CAMP PHOSPHODIESTERASE; ENCODING GMP SYNTHETASE; MOLECULAR-CLONING; DICTYOSTELIUM-DISCOIDEUM; SACCHAROMYCES-CEREVISIAE; IMP DEHYDROGENASE; AMP PHOSPHODIESTERASE; SEQUENCE; GENE AB A genetic selection procedure has been developed which makes the growth of E. coli dependent on expression of a cGMP phosphodiesterase cDNA. E. coli does not contain a cGMP phosphodiesterase, and guanine auxotrophs cannot extract the guanine from cGMP. If a functional cGMP phosphodiesterase is introduced, then guaA auxotrophs will grow on cGMP as a guanine source. The method also selects GMP synthetase cDNAs, which complement the guanine auxotrophy directly. Expression of a Dictyostelium discoideum or human heart cyclic nucleotide phosphodiesterase cDNA permits growth of the E. coli guaA auxotroph in the presence of cGMP. Several commercial cDNA libraries were corrupt and contained phosphodiesterase and/or GMP synthetase sequences that were from a contaminating DNA source. C1 COLUMBIA UNIV,DEPT ANAT & CELL BIOL,NEW YORK,NY 10032. NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 32 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0895-7479 J9 SEC MESS PHOSPHOPROT JI Second Messeng. Phosphoprot. PY 1993 VL 14 IS 3 BP 127 EP 137 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NE278 UT WOS:A1993NE27800003 ER PT B AU HOFFMAN, BJ AF HOFFMAN, BJ BE Vanhoutte, PM Saxena, PR Paoletti, R Brunello, N TI MOLECULAR-BIOLOGY OF SEROTONIN UPTAKE SITES SO SEROTONIN: FROM CELL BIOLOGY TO PHARMACOLOGY AND THERAPEUTICS SE MEDICAL SCIENCE SYMPOSIA SERIES LA English DT Proceedings Paper CT 2nd International Symposium on Serotonin from Cell Biology to Pharmacology and Therapeutics CY SEP 15-18, 1992 CL HOUSTON, TX SP SEROTONIN CLUB, GIOVANNI LORENZINI MED FDN, FONDAZIONE GIOVANNI LORENZINI C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 5 Z9 5 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-2518-4 J9 MED SCI SYMP SER PY 1993 VL 5 BP 9 EP 19 PG 11 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy; Physiology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy; Physiology GA BZ51T UT WOS:A1993BZ51T00002 ER PT B AU MURPHY, DL BROOCKS, A AULAKH, C PIGOTT, TA AF MURPHY, DL BROOCKS, A AULAKH, C PIGOTT, TA BE Vanhoutte, PM Saxena, PR Paoletti, R Brunello, N TI ANXIOLYTIC EFFECTS OF DRUGS ACTING ON 5-HT RECEPTOR SUBTYPES SO SEROTONIN: FROM CELL BIOLOGY TO PHARMACOLOGY AND THERAPEUTICS SE MEDICAL SCIENCE SYMPOSIA SERIES LA English DT Proceedings Paper CT 2nd International Symposium on Serotonin from Cell Biology to Pharmacology and Therapeutics CY SEP 15-18, 1992 CL HOUSTON, TX SP SEROTONIN CLUB, GIOVANNI LORENZINI MED FDN, FONDAZIONE GIOVANNI LORENZINI C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-2518-4 J9 MED SCI SYMP SER PY 1993 VL 5 BP 223 EP 230 PG 8 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy; Physiology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy; Physiology GA BZ51T UT WOS:A1993BZ51T00026 ER PT B AU LINNOILA, M VIRKKUNEN, M TOKOLA, R NIELSEN, D GOLDMAN, D AF LINNOILA, M VIRKKUNEN, M TOKOLA, R NIELSEN, D GOLDMAN, D BE Vanhoutte, PM Saxena, PR Paoletti, R Brunello, N TI ALCOHOLIC VIOLENT OFFENDERS - BEHAVIORAL, ENDOCRINE, DIURNAL RHYTHM, AND GENETIC CORRELATES OF LOW CSF 5-HIAA CONCENTRATIONS SO SEROTONIN: FROM CELL BIOLOGY TO PHARMACOLOGY AND THERAPEUTICS SE MEDICAL SCIENCE SYMPOSIA SERIES LA English DT Proceedings Paper CT 2nd International Symposium on Serotonin from Cell Biology to Pharmacology and Therapeutics CY SEP 15-18, 1992 CL HOUSTON, TX SP SEROTONIN CLUB, GIOVANNI LORENZINI MED FDN, FONDAZIONE GIOVANNI LORENZINI C1 NIAAA,DIV INTRAMURAL CLIN & BIOL RES,BETHESDA,MD 20893. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-2518-4 J9 MED SCI SYMP SER PY 1993 VL 5 BP 255 EP 261 PG 7 WC Biochemistry & Molecular Biology; Neurosciences; Pharmacology & Pharmacy; Physiology SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Pharmacology & Pharmacy; Physiology GA BZ51T UT WOS:A1993BZ51T00030 ER PT B AU CUTLER, GB AF CUTLER, GB BE Grave, GD Cutler, GB TI OVERVIEW OF PREMATURE SEXUAL DEVELOPMENT SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP CUTLER, GB (reprint author), NICHHD,DEV ENDOCRINOL SECT,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 1 EP 10 PG 10 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00001 ER PT B AU OERTER, KE MANASCO, PK BARNES, KM JONES, J HILL, SC CUTLER, GB AF OERTER, KE MANASCO, PK BARNES, KM JONES, J HILL, SC CUTLER, GB BE Grave, GD Cutler, GB TI ADULT HEIGHT IN PRECOCIOUS PUBERTY AFTER LONG-TERM TREATMENT WITH DESLORELIN SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP OERTER, KE (reprint author), NICHHD,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 45 EP 54 PG 10 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00005 ER PT B AU LAUE, L CUTLER, GB AF LAUE, L CUTLER, GB BE Grave, GD Cutler, GB TI CURRENT TREATMENT OF FAMILIAL MALE PRECOCIOUS PUBERTY SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP LAUE, L (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 193 EP 205 PG 13 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00018 ER PT B AU MANASCO, PK GIRTON, ME DIGGS, RL DOPPMAN, JL GEUILLAN, PP BARNES, KM CUTLER, GB LORIAUX, DL ALBERTSON, BD AF MANASCO, PK GIRTON, ME DIGGS, RL DOPPMAN, JL GEUILLAN, PP BARNES, KM CUTLER, GB LORIAUX, DL ALBERTSON, BD BE Grave, GD Cutler, GB TI INSIGHT INTO THE ETIOLOGY OF FAMILIAL MALE PRECOCIOUS PUBERTY SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP MANASCO, PK (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 229 EP 234 PG 6 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00021 ER PT B AU WEINSTEIN, LS SHENKER, A AF WEINSTEIN, LS SHENKER, A BE Grave, GD Cutler, GB TI ACTIVATING MUTATIONS OF THE STIMULATORY-G PROTEIN-G(S) IN THE MCCUNE-ALBRIGHT SYNDROME - INSIGHT INTO GONADOTROPIN-INDEPENDENT SEXUAL PRECOCITY SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP WEINSTEIN, LS (reprint author), NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 235 EP 251 PG 17 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00022 ER PT B AU FEUILLAN, PP AF FEUILLAN, PP BE Grave, GD Cutler, GB TI TREATMENT OF SEXUAL PRECOCITY IN GIRLS WITH THE MCCUNE-ALBRIGHT SYNDROME SO SEXUAL PRECOCITY: ETIOLOGY, DIAGNOSIS, AND MANAGEMENT LA English DT Proceedings Paper CT CONF ON SEXUAL PRECOCITY CY OCT 28-31, 1990 CL AIRLIE, VA SP NICHD RP FEUILLAN, PP (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-7817-0078-7 PY 1993 BP 243 EP 251 PG 9 WC Endocrinology & Metabolism; Pediatrics SC Endocrinology & Metabolism; Pediatrics GA BZ01H UT WOS:A1993BZ01H00023 ER PT J AU UNSER, M ALDROUBI, A EDEN, M AF UNSER, M ALDROUBI, A EDEN, M TI A FAMILY OF POLYNOMIAL SPLINE WAVELET TRANSFORMS SO SIGNAL PROCESSING LA English DT Article DE WAVELET TRANSFORM; BETA-SPLINES; POLYNOMIAL SPLINES; INTERPOLATION; BINOMIAL FILTERS; QUADRATURE MIRROR FILTERS (QMF); BIORTHOGONALITY; MULTIRESOLUTION SIGNAL ANALYSIS AB This paper presents an extension of the family of orthogonal Battle/Lemarie spline wavelet transforms with emphasis on filter bank implementation. Spline wavelets that are not necessarily orthogonal within the same resoluton level, are constructed by linear combination of polynomial spline wavelets of compact support, the natural counterpart of classical B-spline functions. Mallat's fast wavelet transform algorithm is extended to deal with these non-orthogonal basis functions. The impulse and frequency responses of the corresponding analysis and synthesis filters are derived explicitly for polynomial splines of any order n (n odd). The link with the general framework of biorthogonal wavelet transforms is also made explicit. The special cases of orthogonal, B-spline, cardinal and dual wavelets are considered in greater detail. The B-spline (respectively dual) representation is associated with simple FIR binomial synthesis (respectively analysis) filters and recursive analysis (respectively synthesis) filters. The cardinal representation provides a sampled representation of the underlying continuous functions (interpolation property). The distinction between cardinal and orthogonal representation vanishes as the order of the spline is increased; both wavelets tend asymptotically to the bandlimited sinc-wavelet. The distinctive features of these various representations are discussed and illustrated with a texture analysis example. RP UNSER, M (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13,BETHESDA,MD 20892, USA. RI Unser, Michael/A-1550-2008; Aldroubi, Akram/J-7186-2012 NR 0 TC 130 Z9 133 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-1684 J9 SIGNAL PROCESS JI Signal Process. PD JAN PY 1993 VL 30 IS 2 BP 141 EP 162 DI 10.1016/0165-1684(93)90144-Y PG 22 WC Engineering, Electrical & Electronic SC Engineering GA KJ019 UT WOS:A1993KJ01900001 ER PT J AU WIENER, LS SPENCER, ED DAVIDSON, R FAIR, C AF WIENER, LS SPENCER, ED DAVIDSON, R FAIR, C TI NATIONAL TELEPHONE SUPPORT GROUPS - A NEW AVENUE TOWARD PSYCHOSOCIAL SUPPORT FOR HIV-INFECTED CHILDREN AND THEIR FAMILIES SO SOCIAL WORK WITH GROUPS LA English DT Article ID DISABLED ADULTS; THERAPY; AIDS AB The complexity of psychosocial needs that HIV-infected children and their families confront makes innovative approaches for group support a necessity. In response, National Telephone Support Groups were developed for children, non-infected siblings, infected and noninfected mothers, infected and non-infected fathers, foster parents and grandparents. As each group was recorded and transcribed this article is a preliminary step towards identifying and reporting the psychosocial challenges of living with HIV and die impact of the group on individual members. The initial organization of the groups, the format, content, structure and practical considerations, such as cost and accessibility are described. The results of pre and post test questionnaires examining isolation and group usefulness are also presented in this article. C1 INST BEHAV & HLTH INC,ROCKVILLE,MD. NIH,BETHESDA,MD 20892. RP WIENER, LS (reprint author), NCI,PEDIAT HIV PSYCHOSOCIAL SUPPORT PROGRAM,BETHESDA,MD 20892, USA. NR 19 TC 16 Z9 17 U1 1 U2 1 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0160-9513 J9 SOC WORK GROUPS PY 1993 VL 16 IS 3 BP 55 EP 71 DI 10.1300/J009v16n03_05 PG 17 WC Social Work SC Social Work GA MD876 UT WOS:A1993MD87600004 ER PT J AU HERMANN, HR BLUM, MS FALES, HM AF HERMANN, HR BLUM, MS FALES, HM TI VENOM SPRAYING BY A TROPICAL POLISTINE WASP (HYMENOPTERA, VESPIDAE, POLISTINAE) SO SOCIOBIOLOGY LA English DT Article DE PAPER WASPS; DEFENSIVE MECHANISM; PHENYLACETALDEHYDE; PARACHARTERGUS-AZTECUS ID PLANT AB Parachartergus aztecus demonstrates venom spraying as one of its defensive mechanisms. Venom spraying has been reported in only a few vespids, and among the wasps it appears to be restricted to that family. Phenylacetaldehyde, a previously undetected glandular product of hymenopterans, is released during venom spraying and appears to have a purely defensive function. C1 NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. RP HERMANN, HR (reprint author), UNIV GEORGIA,DEPT ENTOMOL,ATHENS,GA 30602, USA. NR 9 TC 3 Z9 3 U1 0 U2 1 PU CALIF STATE UNIV PI CHICO PA DEPT BIOL SCI, CHICO, CA 95929 SN 0361-6525 J9 SOCIOBIOLOGY JI Sociobiology PY 1993 VL 23 IS 1 BP 95 EP 99 PG 5 WC Entomology SC Entomology GA LY232 UT WOS:A1993LY23200009 ER PT J AU DIPELLEGRINO, G WISE, SP AF DIPELLEGRINO, G WISE, SP TI EFFECTS OF ATTENTION ON VISUOMOTOR ACTIVITY IN THE PREMOTOR AND PREFRONTAL CORTEX OF A PRIMATE SO SOMATOSENSORY AND MOTOR RESEARCH LA English DT Article DE PREMOTOR CORTEX; ATTENTION; FRONTAL LOBE; PREFRONTAL CORTEX ID FRONTAL EYE FIELDS; DELAYED-RESPONSE PERFORMANCE; PARIETAL ASSOCIATION CORTEX; MONKEY CEREBRAL-CORTEX; VISUALLY GUIDED ARM; RHESUS-MONKEY; UNIT-ACTIVITY; NEURONAL-ACTIVITY; FUNCTIONAL-ORGANIZATION; BEHAVIORAL ENHANCEMENT AB We examined neuronal activity in the primate premotor (PM) and pre-frontal (PF) areas during a demanding spatial matching task. On each behavioral trial, a rhesus monkey moved its forelimb when a visual stimulus, called the ''prime stimulus,'' reappeared at a previously cued location. Because it triggered a movement, the part of space cued by the prime stimulus had to be either remembered or attended during the time between prime stimulus presentations. Between the first and second appearances of the prime stimulus, behaviorally irrelevant visual stimuli could appear at one or several locations other than that of the prime stimulus. We could thereby examine the activity that followed a stimulus when it was attended versus when it was irrelevant and presumably unattended. We found that visuospatial attention affected neuronal activity in both the motor and ''nonmotor'' parts of the frontal cortex. The magnitude of attention effects exceeded that previously reported-a finding that probably resulted from the intensive attentional demands of the present task. C1 NIMH,CTR ANIM,NEUROPHYSIOL LAB,POB 608,POOLESVILLE,MD 20837. NR 73 TC 53 Z9 53 U1 0 U2 2 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0899-0220 J9 SOMATOSENS MOT RES JI Somatosens. Mot. Res. PY 1993 VL 10 IS 3 BP 245 EP 262 PG 18 WC Neurosciences SC Neurosciences & Neurology GA LW953 UT WOS:A1993LW95300002 PM 8237213 ER PT S AU BERZOFSKY, JA AF BERZOFSKY, JA BE Bystryn, JC Ferrone, S Livingston, P TI EPITOPE SELECTION AND DESIGN OF SYNTHETIC VACCINES - MOLECULAR APPROACHES TO ENHANCING IMMUNOGENICITY AND CROSS-REACTIVITY OF ENGINEERED VACCINES SO SPECIFIC IMMUNOTHERAPY OF CANCER WITH VACCINES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SPECIFIC IMMUNOTHERAPY OF CANCER WITH VACCINES CY JAN 21-24, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI, NCI, BIOMIRA INC, CAMBRIDGE BIOTECH, AMER CYANAMID, BRISTOL MYERS SQUIBB, PHARM RES INST, CYTOGEN CORP, GENENTECH, GENETICS INST, HOFFMANN LA ROCHE RP BERZOFSKY, JA (reprint author), NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BLDG 10,ROOM 6B12,BETHESDA,MD 20892, USA. NR 0 TC 30 Z9 30 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-825-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 690 BP 256 EP 264 PG 9 WC Oncology; Immunology; Pharmacology & Pharmacy SC Oncology; Immunology; Pharmacology & Pharmacy GA BY95C UT WOS:A1993BY95C00027 ER PT S AU GRUBER, J COLE, JS AF GRUBER, J COLE, JS BE Bystryn, JC Ferrone, S Livingston, P TI VACCINES FOR HUMAN CANCERS OF VIRAL ETIOLOGY SO SPECIFIC IMMUNOTHERAPY OF CANCER WITH VACCINES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SPECIFIC IMMUNOTHERAPY OF CANCER WITH VACCINES CY JAN 21-24, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI, NCI, BIOMIRA INC, CAMBRIDGE BIOTECH, AMER CYANAMID, BRISTOL MYERS SQUIBB, PHARM RES INST, CYTOGEN CORP, GENENTECH, GENETICS INST, HOFFMANN LA ROCHE RP GRUBER, J (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-825-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 690 BP 311 EP 321 PG 11 WC Oncology; Immunology; Pharmacology & Pharmacy SC Oncology; Immunology; Pharmacology & Pharmacy GA BY95C UT WOS:A1993BY95C00032 ER PT S AU SOGN, JA FINERTY, JF HEATH, AK SHEN, GLC AUSTIN, FC AF SOGN, JA FINERTY, JF HEATH, AK SHEN, GLC AUSTIN, FC BE Bystryn, JC Ferrone, S Livingston, P TI CANCER VACCINES - THE PERSPECTIVE OF THE CANCER IMMUNOLOGY BRANCH, NCI SO SPECIFIC IMMUNOTHERAPY OF CANCER WITH VACCINES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SPECIFIC IMMUNOTHERAPY OF CANCER WITH VACCINES CY JAN 21-24, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI, NCI, BIOMIRA INC, CAMBRIDGE BIOTECH, AMER CYANAMID, BRISTOL MYERS SQUIBB, PHARM RES INST, CYTOGEN CORP, GENENTECH, GENETICS INST, HOFFMANN LA ROCHE RP SOGN, JA (reprint author), NCI,DIV CANC BIOL DIAGNOSIS & CTR,CANC IMMUNOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-825-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 690 BP 322 EP 330 PG 9 WC Oncology; Immunology; Pharmacology & Pharmacy SC Oncology; Immunology; Pharmacology & Pharmacy GA BY95C UT WOS:A1993BY95C00033 ER PT S AU KANTOR, J ABRAMS, S IRVINE, K SNOY, P KAUFMAN, H SCHLOM, J AF KANTOR, J ABRAMS, S IRVINE, K SNOY, P KAUFMAN, H SCHLOM, J BE Bystryn, JC Ferrone, S Livingston, P TI SPECIFIC IMMUNOTHERAPY USING A RECOMBINANT VACCINIA VIRUS EXPRESSING HUMAN CARCINOEMBRYONIC ANTIGEN SO SPECIFIC IMMUNOTHERAPY OF CANCER WITH VACCINES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SPECIFIC IMMUNOTHERAPY OF CANCER WITH VACCINES CY JAN 21-24, 1993 CL WASHINGTON, DC SP NEW YORK ACAD SCI, NCI, BIOMIRA INC, CAMBRIDGE BIOTECH, AMER CYANAMID, BRISTOL MYERS SQUIBB, PHARM RES INST, CYTOGEN CORP, GENENTECH, GENETICS INST, HOFFMANN LA ROCHE RP KANTOR, J (reprint author), NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892, USA. NR 0 TC 12 Z9 12 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-825-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 690 BP 370 EP 373 PG 4 WC Oncology; Immunology; Pharmacology & Pharmacy SC Oncology; Immunology; Pharmacology & Pharmacy GA BY95C UT WOS:A1993BY95C00047 ER PT J AU BRODER, S AF BRODER, S TI THE CHALLENGE OF CANCER-RESEARCH SO STEM CELLS LA English DT Review DE CANCER RESEARCH CHALLENGES; MOLECULAR MEDICINE; BREAST CANCER; VACCINES; PREVENTION; TUMOR DIAGNOSIS; THERAPY AB The challenge of cancer research can be summarized by simple statistics. In 1992, more than 1.1 million Americans are expected to develop cancer, and roughly 520,000 are expected to die from cancer. The National Cancer Institute's (NCI's) mission is to eradicate the death and suffering from cancer, to cure cancer once it starts and ultimately to prevent cancer. To this end, initiatives that promote continued development of sophisticated molecular technologies and clinical application of those technologies to the prevention, diagnosis and treatment of cancer are of surpassingly high priority. Epidemiological studies tell us that at least 30-50% of cancer is directly related to smoking, diet and environmental factors. Treatment studies indicate that significant gains in survival are possible and have already been achieved in some cancers, with promise from new drugs and other modalities (including genetic engineering) for still other cancers. Prevention strategies such as smoking reduction, diet, environmental measures, chemoprevention and vaccine development have the potential to achieve a substantial reduction in cancer mortality. This reduction, realized over two decades, would result in at least 100,000 lives saved per year in this country, and a large number can be saved just by applying what we already know. RP BRODER, S (reprint author), NCI,BLDG 31,RM 11A-48,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 8 TC 2 Z9 2 U1 0 U2 1 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 1066-5099 J9 STEM CELLS JI Stem Cells PD JAN PY 1993 VL 11 IS 1 BP 3 EP 8 PG 6 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA KM168 UT WOS:A1993KM16800001 PM 8457778 ER PT J AU POGREBNIAK, HW MATTHEWS, W BLACK, C RUSSO, A MITCHELL, JB SMITH, P ROTH, JA PASS, HI AF POGREBNIAK, HW MATTHEWS, W BLACK, C RUSSO, A MITCHELL, JB SMITH, P ROTH, JA PASS, HI TI TARGETED PHOTOTHERAPY WITH SENSITIZER-MONOCLONAL ANTIBODY CONJUGATE AND LIGHT SO SURGICAL ONCOLOGY-OXFORD LA English DT Article DE ANIMAL MODEL; HEMATOPORPHYRIN; LASER; MONOCLONAL ANTIBODY; PHOTOFRIN-II; PHOTOTHERAPY AB Photodynamic therapy (PDT) was performed in vitro and in vivo using monoclonal antibody conjugated to hematoporphyrin (HP). The antibody (45-2D9) recognized a cell surface glycoprotein on cells derived from NIH 3T3 cells which were transformed with the ras oncogene (45-342). Radionuclide imaging with either In-111 or I-125 chelated to 45-2D9 or the isotype identical (IgG1) antibody MOPPC-21 revealed selectivity of 45-2D9 for 45-342 flank tumours in nude mice, and minimal targetting for a 45-342 clone which did not express the cell surface glycoprotein. The 45-2D9-HP conjugate resulted in selective killing of the 45-342 line compared with the parent line in vitro. At HP concentrations of 76 mug ml-1, the 45-2D9-HP conjugate resulted in significantly more long-term cures of PDT treated flank tumours compared with free HP at the same concentration. 45-2D9 alone had no effect on tumour growth. The antibody-HP conjugate resulted in significantly less local toxicity compared with standard Photofrin II PDT, and also achieved a greater number of long-term cures. This 'photoimmunotherapy' demonstrates the ability to treat established tumours with greater efficacy and decreased morbidity, probably due to specific sensitizer targetting which allows normal surrounding tissue to be spared upon illumination. RP POGREBNIAK, HW (reprint author), NCI,THORAC ONCOL SECT,BETHESDA,MD 20892, USA. NR 0 TC 15 Z9 16 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0960-7404 J9 SURG ONCOL JI Surg. Oncol.-Oxf. PY 1993 VL 2 IS 1 BP 31 EP 42 DI 10.1016/0960-7404(93)90042-W PG 12 WC Oncology; Surgery SC Oncology; Surgery GA KW241 UT WOS:A1993KW24100005 PM 8252191 ER PT J AU PIEGORSCH, WW HASEMAN, JK AF PIEGORSCH, WW HASEMAN, JK TI STATISTICAL-METHODS FOR ANALYZING DEVELOPMENTAL TOXICITY DATA - REPLY SO TERATOGENESIS CARCINOGENESIS AND MUTAGENESIS LA English DT Letter RP PIEGORSCH, WW (reprint author), NIEHS,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709, USA. NR 8 TC 0 Z9 0 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 0270-3211 J9 TERATOGEN CARCIN MUT JI Teratogenesis Carcinog. Mutagen. PY 1993 VL 13 IS 4 BP 195 EP 197 DI 10.1002/tcm.1770130406 PG 3 WC Oncology; Genetics & Heredity; Toxicology SC Oncology; Genetics & Heredity; Toxicology GA LY250 UT WOS:A1993LY25000005 ER PT J AU RODRIGUEZ, JB MARKEY, SP ZIFFER, H AF RODRIGUEZ, JB MARKEY, SP ZIFFER, H TI PREPARATION OF 2(R) AND 2(S) METHYL-2-METHYLGLYCERATES SO TETRAHEDRON-ASYMMETRY LA English DT Article ID DNA-POLYMERASE-I; THYMINE GLYCOL; THYMIDINE GLYCOL; ACID; RESIDUES; INVITRO; LIGANDS; DAMAGE; ASSAY AB Optically pure samples of both enantiomers of methyl 2,3-dihydroxy-2-methylpropanoate were prepared by a chromatographic separation of their (-)-menthyl esters followed by hydrolysis and methylation. Their absolute stereochemistries were established by conversion into their 3-0-acetyl derivatives, compounds of established configuration. NMR and CG-MS methods of determining the optical purities of the diols are described. C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. RP RODRIGUEZ, JB (reprint author), NIMH,CLIN SCI LAB,BETHESDA,MD 20892, USA. OI Rodriguez, Juan Bautista/0000-0002-5180-096X NR 20 TC 5 Z9 5 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0957-4166 J9 TETRAHEDRON-ASYMMETR JI Tetrahedron: Asymmetry PD JAN PY 1993 VL 4 IS 1 BP 101 EP 108 DI 10.1016/S0957-4166(00)86020-6 PG 8 WC Chemistry, Inorganic & Nuclear; Chemistry, Organic; Chemistry, Physical SC Chemistry GA KL276 UT WOS:A1993KL27600019 ER PT B AU ASANUMA, C AF ASANUMA, C BE Minciacchi, D Molinari, M Macchi, G Jones, EG TI SPECIFIC DISTRIBUTION OF SOME NONSPECIFIC AFFERENTS UPON INDIVIDUAL THALAMIC RETICULAR NUCLEUS NEURONS SO THALAMIC NETWORKS FOR RELAY AND MODULATION SE PERGAMON STUDIES IN NEUROSCIENCE LA English DT Proceedings Paper CT Symposium on Thalamic Networks for Relay and Modulation, as a Satellite to the 15th Annual Meeting of the European-Neuroscience-Association CY SEP, 1992 CL CATHOLIC UNIV, ROME, ITALY HO CATHOLIC UNIV C1 NIMH,NIH ANIM CTR,NEUROPHYSIOL LAB,POOLESVILLE,MD. RI Molinari, Marco/A-9624-2010 OI Molinari, Marco/0000-0001-9808-9688 NR 0 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON PRESS LTD PI OXFORD PA THE BOULEVARD LANGFORD LANE KIDLINGTON, OXFORD, ENGLAND OX5 1GB BN 0-08-042274-8 J9 PERG S NEUR PY 1993 IS 9 BP 323 EP 336 PG 14 WC Neurosciences SC Neurosciences & Neurology GA BC12X UT WOS:A1993BC12X00027 ER PT S AU LANDS, WEM AF LANDS, WEM BE Lee, KT Oike, Y Kanazawa, T TI EICOSANOIDS AND HEALTH SO THIRD INTERNATIONAL CONFERENCE ON NUTRITION IN CARDIO-CEREBROVASCULAR DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT 3RD INTERNATIONAL CONF ON NUTRITION IN CARDIO-CEREBROVASCULAR DISEASES CY APR 22-25, 1992 CL AOMORI CITY, JAPAN SP HIROSAKI UNIV SCH MED, 2ND DEPT INTERNAL MED, REIMEIKYO REHAB HOSP RP LANDS, WEM (reprint author), NIAAA,DIV BASIC RES,PARKLAWN BLDG,RM 16C-06,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 0 TC 19 Z9 19 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-775-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 676 BP 46 EP 59 PG 14 WC Cardiac & Cardiovascular Systems; Endocrinology & Metabolism; Neurosciences; Nutrition & Dietetics; Pathology SC Cardiovascular System & Cardiology; Endocrinology & Metabolism; Neurosciences & Neurology; Nutrition & Dietetics; Pathology GA BX95Q UT WOS:A1993BX95Q00006 ER PT J AU AIME, C BRISTOL, L COHENKAMINSKY, S BERRIH-AKNIN, S DURUM, S TAKACS, L AF AIME, C BRISTOL, L COHENKAMINSKY, S BERRIH-AKNIN, S DURUM, S TAKACS, L TI IL-1 MESSENGER-RNA EXPRESSION DETECTED BY IN-SITU HYBRIDIZATION AND POLYMERASE CHAIN-REACTION IN HUMAN THYMUS AND THYMOMA - CORRELATION WITH LATE T-CELL MATURATION IN NORMAL VERSUS NEOPLASTIC THYMUS SO THYMUS LA English DT Article DE IN-SITU HYBRIDIZATION; INTERLEUKIN-1; THYMOMAS; THYMUS ID CORTICAL THYMOCYTE; GENE-EXPRESSION; INTERLEUKIN-1; INDUCTION; RECEPTOR; DELETION; DIFFERENTIATION; LYMPHOCYTE; ANTIBODIES; PHENOTYPE AB Interleukin-1 has long been suggested to participate in the development of T-cells in the thymus. To determine whether IL-1 was produced in the human thymus, we used the technique of in situ hybridization and PCR amplification of mRNA, High levels of IL-1 mRNA were detected in cells at the cortico-medullary border, which separates immature from mature T-cells, suggesting a role for IL-1 in a late stage in T-cell maturation. IL-1 transcripts were detectable by a single step PCR reaction in these samples. We examined a series thymomas (human thymic epithelial tumors) that induce partial T-cell maturation: In this group of thymomas T-cells develop to the cortical stage but not beyond. We failed to detect high levels of IL-1 mRNA expression in these tumors by in-situ hybridization, IL-1 mRNA was detected only in one of these samples by a single step PCR amplification. However, alt of the samples were positive, when analyzed with a more sensitive, two step amplification of IL-1 mRNA by the use of nested primers. These results are consistent with the hypothesis that higher level of IL-1 expression is either the consequence of, or required for late T-cell maturation. C1 FAC MED PARIS SUD, DEPT HUMAN PHYSIOL,CELLULAR IMMUNOL LAB,CNRS, URA D1159, F-92350 LE PLESSIS ROBINSON, FRANCE. NIAAA, SPECIAL PROJECTS UNIT, PHYSIOL & PHARMACOL STUDIES LAB, ROCKVILLE, MD 20852 USA. NCI, BIOL RESPONSE MODIFIERS PROGRAM, MOLEC IMMUNOREGULAT LAB, FREDERICK, MD 21701 USA. RI Berrih-Aknin, Sonia/F-8025-2013 NR 34 TC 3 Z9 3 U1 0 U2 1 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0165-6090 J9 THYMUS JI Thymus PY 1993 VL 22 IS 1 BP 45 EP 54 PG 10 WC Immunology SC Immunology GA MF424 UT WOS:A1993MF42400004 PM 8303777 ER PT S AU SUBAR, AF HARLAN, LC WYNDER, E RIMM, E HALEY, N BOLTONSMITH, C DIANA, J RENAUD, S HOFFMANN AF SUBAR, AF HARLAN, LC WYNDER, E RIMM, E HALEY, N BOLTONSMITH, C DIANA, J RENAUD, S HOFFMANN BE Diana, JN Pryor, WA TI NUTRIENT AND FOOD GROUP INTAKE BY TOBACCO USE STATUS - THE 1987 NATIONAL-HEALTH INTERVIEW SURVEY SO TOBACCO SMOKING AND NUTRITION: INFLUENCE OF NUTRITION ON TOBACCO-ASSOCIATED HEALTH RISKS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON TOBACCO SMOKING AND NUTRITION : INFLUENCE OF NUTRITION ON TOBACCO-ASSOCIATED HEALTH RISKS CY SEP 14-16, 1992 CL LEXINGTON, KY SP UNIV KENTUCKY, TOBACCO & HLTH RES INST RP SUBAR, AF (reprint author), NCI,APPL RES BRANCH,EXECUT PLAZA N,ROOM 313,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 38 Z9 39 U1 1 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-807-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 686 BP 310 EP 322 DI 10.1111/j.1749-6632.1993.tb39193.x PG 13 WC Substance Abuse; Public, Environmental & Occupational Health; Nutrition & Dietetics SC Substance Abuse; Public, Environmental & Occupational Health; Nutrition & Dietetics GA BY39Z UT WOS:A1993BY39Z00027 PM 8512257 ER PT J AU WILLIAMS, AO BANKS, PM LIEBELT, AG STEWART, HL SAFFIOTTI, U AF WILLIAMS, AO BANKS, PM LIEBELT, AG STEWART, HL SAFFIOTTI, U TI ANGIOFOLLICULAR LYMPHOID HYPERPLASIA (CASTLEMANS DISEASE) IN 2 MICE TREATED WITH POLYOMA-VIRUS OR URETHANE SO TOXICOLOGIC PATHOLOGY LA English DT Article DE INTERLEUKIN-6; RETROVIRUS; KAPOSIS SARCOMA; ANGIOGENESIS; PLASMACYTOSIS AB Localized angiofollicular hyperplasia, otherwise known as Castleman's disease, is described in the lymph nodes of 2 mice of different strains, one inoculated with polyoma virus at birth and the other given urethane within 24 hr of birth. A plasma cell component in the lesion, suggestive of bone marrow stem cell involvement, was present in the mouse treated with polyoma virus but absent in the mouse given intraperitoneal urethane. Dysregulated interleukin 6 has recently been reported to produce the systemic variety of angiofollicular hyperplasia in mice, but the role of this cytokine in the localized variety described in this report is not known. This lesion appears to be rare in mice, but when present it could easily be missed or overlooked because the typical layering of follicle cells and the relatively large germinal centers seen in humans do not appear prominent in mice. Although there is, obviously, no proof of a causal relationship between the lesion and polyoma virus or urethane, it is suggested that this lesion be searched for in order to estimate its frequency and possible etiologic associations. RP WILLIAMS, AO (reprint author), NCI,DIV CANC ETIOL,EXPTL PATHOL LAB,BLDG 41,ROOM C-105,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PY 1993 VL 21 IS 1 BP 26 EP 34 PG 9 WC Pathology; Toxicology SC Pathology; Toxicology GA LR665 UT WOS:A1993LR66500004 PM 8397437 ER PT J AU KURATA, Y DIWAN, BA UNO, H RICE, JM WARD, JM AF KURATA, Y DIWAN, BA UNO, H RICE, JM WARD, JM TI PATHOLOGY OF PRENEOPLASTIC AND NEOPLASTIC RENAL TUBULAR LESIONS INDUCED IN F344 RATS BY SODIUM BARBITAL, A NONGENOTOXIC RENAL CARCINOGEN AND NEPHROTOXIN SO TOXICOLOGIC PATHOLOGY LA English DT Article DE KIDNEY; RENAL CELL TUMOR; ATYPICAL HYPERPLASIA; DYSPLASIA; IMMUNOHISTOCHEMISTRY; ENZYME; VIMENTIN; ULTRASTRUCTURE AB Sodium barbital (NaBB), a long-duration sedative/hypnotic barbiturate, is a nongenotoxic nephrotoxin and induces chronic persistent increases in rates of cell proliferation in renal cortical tubules of male F-344/NCr rats. In 5 of our 2-stage carcinogenesis experiments with NaBB at doses of 500, 1,000, or 4,000 ppm for periods of up to 106 wk of age, renal tubular cell tumors were found in incidences of up to 25% in rats receiving only NaBB while fewer than 1% of controls had renal epithelial tumors. We reviewed renal tubular proliferative lesions found in these studies and classified the lesions based on morphology, histogenesis, and immunohistochemical findings. Renal dysplastic tubules (DTs; atypical hyperplasia), putative preneoplastic lesions rarely seen in controls, were found in the renal cortex of more than 50% of the NaBB-exposed rats. DTs were classified into grades 1-3, based on lesion size and growth patterns. All renal adenomas were usually of the basophilic phenotype, and 70% of basophilic adenomas displayed solid patterns, while tumors with papillary, cystic, or tubular patterns were seen less commonly. By serial or step sectioning of the DTs and tumors, evidence was found indicating that the high grades (grade 2 or 3) of DTs, some of which arose in the P1 or P2 segment of the proximal tubules, were sometimes connected to the adenomas. Vimentin expression was demonstrated immunohistochemically in NaBB-induced renal tubular adenomas but not in normal tubules. Tumors were usually not immunoreactive for glutathione S-transferase, placental form, but heterogeneous immunoreactivity was also seen in some tumors. Lysozyme was absent in preneoplastic and neoplastic lesions induced by NaBB, while some intact normal proximal convoluted tubules were immunoreactive. The common tumor phenotype induced by NaBB, the basophilic solid adenoma, was similar to the most common type of spontaneous renal tumor found in untreated aging F-344 rats. NaBB may promote naturally occurring renal preneoplastic or neoplastic tubular lesions of this unique phenotype, but it is also possible that it may induce these lesions de novo. C1 NCI,DIV CANC ETIOL,COMPARAT CARCINOGENESIS LAB,TUMOR PATHOL & PATHOGENESIS SECT,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74102] NR 0 TC 3 Z9 3 U1 0 U2 0 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PY 1993 VL 21 IS 1 BP 35 EP 45 PG 11 WC Pathology; Toxicology SC Pathology; Toxicology GA LR665 UT WOS:A1993LR66500005 PM 8378705 ER PT J AU WARD, JM UNO, H FRITH, CH AF WARD, JM UNO, H FRITH, CH TI IMMUNOHISTOCHEMISTRY AND MORPHOLOGY OF REACTIVE LESIONS IN LYMPH-NODES AND SPLEEN FROM RATS AND MICE SO TOXICOLOGIC PATHOLOGY LA English DT Article DE HEMATOPOIETIC SYSTEM; LYMPHOCYTE ANTIGENS; AGING AB The use of immunohistochemistry with anatomical and systematized classifications of nonneoplastic lesions in hematopoietic pathology of lymph nodes and spleens from rats and mice is described. Polyclonal antisera and monoclonal antibodies to leukocyte and other antigens can be used with frozen or fixed tissue sections to identify changes in cell populations in these tissues in response to tissue injury and aging. A classification for reactive lesions of lymph nodes and spleen is proposed that can be utilized for computerized pathology and toxicology data systems. These classifications are based on a systematized anatomic distribution of the lesions with the aid of immunohistochemistry. The association of some lesions with early leukemia or lymphoma of rats and mice is also discussed. RP WARD, JM (reprint author), NCI,FCRDC,OFF LAB ANIM SCI,VET & TUMOR PATHOL SECT,FAIRVIEW 201,FREDERICK,MD 21702, USA. NR 0 TC 19 Z9 19 U1 0 U2 3 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PY 1993 VL 21 IS 2 BP 199 EP 205 PG 7 WC Pathology; Toxicology SC Pathology; Toxicology GA LR953 UT WOS:A1993LR95300011 PM 8210942 ER PT J AU FREDRICKSON, TN TANG, Y CHATTOPADHYAY, SK MORSE, HC HARTLEY, JW AF FREDRICKSON, TN TANG, Y CHATTOPADHYAY, SK MORSE, HC HARTLEY, JW TI RETROVIRUS-INDUCED LYMPHOPROLIFERATION AS A MODEL FOR DEVELOPING DIAGNOSTIC-CRITERIA FOR MALIGNANT-LYMPHOMA IN MICE SO TOXICOLOGIC PATHOLOGY LA English DT Article DE MULV; MOUSE LYMPHOMAS; HISTOLOGY; CLONALITY; SCID MICE AB Several methods for evaluating lymphoproliferative lesions in mice were compared. The model systems included spontaneous lymphomas arising in CWD mice and NFS mice congenic for ecotropic murine leukemia virus (MuLV) induction loci and a series of transplants in mice with severe combined immunodeficiency disease mutation of cells derived from mice infected with LP-BM5 MuLV. Primary lymphomas and donor tissues and transplants were examined using histopathology, flow cytometry, and Southern blot analysis of DNA for rearrangements of immunoglobulin and T-cell receptor genes and for viral integrations. The use of flow cytometric analysis, to establish cell lineage and define population size, and DNA analysis, for cell lineage and clonality determination, allowed the identification of malignant lymphoproliferations. Histologic evaluation did not define clonal populations of particular lineage but did provide other indications of malignancy such as invasiveness and presence of a dominant morphologic cell type. Thus, the precision of diagnosis of mouse lymphomas can be considerably enhanced by augmenting histopathologic examination with antigenic and molecular characterizations that can define malignant populations. RP FREDRICKSON, TN (reprint author), NCI,REGISTRY EXPTL CANC,BLDG 41,ROOM D311,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI Morse, Herbert/0000-0002-9331-3705 FU NIAID NIH HHS [N01-AI-72622] NR 0 TC 5 Z9 5 U1 0 U2 0 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PY 1993 VL 21 IS 2 BP 219 EP 228 PG 10 WC Pathology; Toxicology SC Pathology; Toxicology GA LR953 UT WOS:A1993LR95300013 PM 8210944 ER PT J AU DEVOR, DE WAALKES, MP GOERING, P REHM, S AF DEVOR, DE WAALKES, MP GOERING, P REHM, S TI DEVELOPMENT OF AN ANIMAL-MODEL FOR TESTING HUMAN BREAST IMPLANTATION MATERIALS SO TOXICOLOGIC PATHOLOGY LA English DT Article DE POLYURETHANE FOAM; MAMMARY TISSUE RESPONSE; MOUSE; COMPARISON AB Although breast implant materials have been tested in laboratory species since the early 1950s, a standardized evaluation system does not currently exist in which human-made polymers are exposed directly to the mammary milieu of female animals. The present study evaluated such a model as the basis for future experiments on long-term tissue effects. Polyesterurethane disks, 6 mm in diameter x 3 mm thick, were inserted bilaterally beneath the axillobrachial and inguinal mammary/fat pads of 50 9-wk-old female B6D2F1 mice (4 implants each). Implant sites were examined histologically at time points 24 hr to 47 wk after surgery. An acute inflammatory reaction at the implant edges began within 24 hr, and macrophages were found lining the smooth polyurethane fiber surfaces at the periphery by day 2. Multinucleated foreign body giant cells formed by day 4, and by week 4 giant cells contained polyurethane fragments within the cytoplasm, implying degradation of the material. Implant sites showed declining subacute inflammatory responses and increasing fibrosis by week 5. By 13 wk, the polyurethane disks appeared to be integrated into the growing adipose and mammary tissues. Although not apparent on gross inspection, microscopic examination showed that polyurethane fibers moved progressively into adjacent tissues and were always associated with chronic granulomatous inflammation. Histologic findings in the present study are strikingly similar to the human response to polyurethane-coated breast implants. These results suggest the applicability of this model to appropriately test mammaplasty materials in mammary tissues. RP DEVOR, DE (reprint author), NCI,FCRDC,COMPARAT CARCINOGENESIS LAB,TUMOR PATHOL SECT,BLDG 538,ROOM 220,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 0 TC 8 Z9 8 U1 0 U2 0 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PY 1993 VL 21 IS 3 BP 261 EP 273 PG 13 WC Pathology; Toxicology SC Pathology; Toxicology GA MA732 UT WOS:A1993MA73200001 PM 8248715 ER PT J AU RAO, GN EDMONDSON, J ELWELL, MR AF RAO, GN EDMONDSON, J ELWELL, MR TI INFLUENCE OF DIETARY-PROTEIN CONCENTRATION ON SEVERITY OF NEPHROPATHY IN FISCHER-344 (F-344/N) RATS SO TOXICOLOGIC PATHOLOGY LA English DT Article DE BODY WEIGHT; WATER CONSUMPTION; URINE VOLUME; URINARY PROTEIN; NONPURIFIED DIETS; OPEN FORMULA DIETS AB Nephropathy is an age-related spontaneous disease of most rat strains, and protein content of diet may affect the severity. The purpose of this study was to determine the effect of a 15% protein nonpurified diet on body weight and severity of nephropathy in comparison to a 23% protein NIH-07 diet. Groups of 25 male and 25 female Fischer-344 (F-344) rats, 6 wk of age, were fed the 23 or 15% protein diet ad libitum for 2 yr. Rats were weighed at 1-4-wk intervals, and mean body weights were determined. Water consumption measurements and urinalysis were done at approximately 3-mo intervals during the second year of the study. At the end of the 2-yr study, kidneys from all rats, including those that died or were euthanatized after the eightieth week of the study, were examined by light microscopy and graded for severity of nephropathy as grades 1-4 (minimal, mild, moderate, marked). Growth patterns and the maximum body weights attained by each sex fed the 23 or 15% protein diet were not significantly different. The severity of nephropathy in male rats was significantly higher when fed the 23% protein diet (2.8 moderate to marked) compared to the 15% protein diet (1.3 minimal to mild). The severity of nephropathy in female rats increased slightly when fed the 23% protein diet (1.5 minimal to mild) compared to the 15% protein diet (1.0 minimal). When the 23% protein diet group was compared to the 15% protein diet group, the 24-hr urine volume, proteinuria, and water consumption values were increased, especially during the last 3 mo of the study. Reduction of protein concentration in the diet from 23 to 15% decreased the protein consumption by similar to 30% and markedly decreased the severity of nephropathy, especially in male F-344 rats, without substantial changes in growth patterns and body weight gains. RP RAO, GN (reprint author), NIEHS,NATL TOXICOL PROGRAM,MD A0-01,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 31 Z9 31 U1 0 U2 0 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PY 1993 VL 21 IS 4 BP 353 EP 361 PG 9 WC Pathology; Toxicology SC Pathology; Toxicology GA MH204 UT WOS:A1993MH20400002 PM 8290866 ER PT J AU TREINEN, KA SNEEDEN, JL HEINDEL, JJ AF TREINEN, KA SNEEDEN, JL HEINDEL, JJ TI SPECIFIC-INHIBITION OF FSH-STIMULATED CAMP ACCUMULATION BY DELTA-9-TETRAHYDROCANNABINOL IN CULTURED RAT GRANULOSA-CELLS SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID DELTA-1-TETRAHYDROCANNABINOL; CANNABINOIDS; SERTOLI RP TREINEN, KA (reprint author), NIEHS,NATL TOXICOL PROGRAM,DEV & REPROD TOXICOL GRP,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 20 TC 11 Z9 11 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 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD JAN PY 1993 VL 118 IS 1 BP 53 EP 57 DI 10.1006/taap.1993.1008 PG 5 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA KG763 UT WOS:A1993KG76300008 PM 8381567 ER PT J AU SHIRAISHI, N BARTER, RA UNO, H WAALKES, MP AF SHIRAISHI, N BARTER, RA UNO, H WAALKES, MP TI EFFECT OF PROGESTERONE PRETREATMENT ON CADMIUM TOXICITY IN THE MALE FISCHER (F344/NCR) RAT SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID BINDING PROTEINS; METALLOTHIONEIN; RESISTANCE; TESTES; INJURY; MICE; RNA C1 NCI,FREDERICK CANC RES & DEV CTR,INORGAN CARCINOGENESIS SECT,BLDG 538,ROOM 205E,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,TUMOR PATHOL & PATHOGENESIS SECT,FREDERICK,MD 21702. NR 23 TC 27 Z9 30 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 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD JAN PY 1993 VL 118 IS 1 BP 113 EP 118 DI 10.1006/taap.1993.1016 PG 6 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA KG763 UT WOS:A1993KG76300016 PM 8430418 ER PT J AU WARNER, HR AF WARNER, HR TI MECHANISMS OF ANTIOXIDANT ACTION ON LIFE-SPAN - OVERVIEW SO TOXICOLOGY AND INDUSTRIAL HEALTH LA English DT Article ID ZINC SUPEROXIDE-DISMUTASE; LIPID-PEROXIDATION; HYDROGEN-PEROXIDE; DROSOPHILA-MELANOGASTER; RADICAL PRODUCTION; OXIDATIVE STRESS; LONGEVITY; DNA; INCREASE; PARAQUAT RP WARNER, HR (reprint author), NIA,BIOL AGING PROGRAM,GATEWAY BLDG,SUITE 2C231,BETHESDA,MD 20892, USA. NR 46 TC 3 Z9 3 U1 0 U2 0 PU PRINCETON SCIENTIFIC PUBL INC PI PRINCETON PA PO BOX 2155, PRINCETON, NJ 08543 SN 0748-2337 J9 TOXICOL IND HEALTH JI Toxicol. Ind. Health PD JAN-APR PY 1993 VL 9 IS 1-2 BP 151 EP 161 PG 11 WC Public, Environmental & Occupational Health; Toxicology SC Public, Environmental & Occupational Health; Toxicology GA KD769 UT WOS:A1993KD76900010 PM 8418510 ER PT J AU BAKER, GT AF BAKER, GT TI EFFECTS OF VARIOUS ANTIOXIDANTS ON AGING IN DROSOPHILA SO TOXICOLOGY AND INDUSTRIAL HEALTH LA English DT Article DE DROSOPHILA; CENTROPHENOXINE; VITAMIN-E; LIFE-SPAN; PHYSIOLOGICAL FITNESS; DNA REPAIR DEFICIENT MUTANT (MEI-41D5) ID LIFE-SPAN; MELANOGASTER; LONGEVITY; REPAIR; STRAINS C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP BAKER, GT (reprint author), SHOCK AGING RES FDN,14628 CARONA DR,SILVER SPRING,MD 20905, USA. FU PHS HHS [2T32A00034-04-08] NR 49 TC 5 Z9 5 U1 0 U2 2 PU PRINCETON SCIENTIFIC PUBL INC PI PRINCETON PA PO BOX 2155, PRINCETON, NJ 08543 SN 0748-2337 J9 TOXICOL IND HEALTH JI Toxicol. Ind. Health PD JAN-APR PY 1993 VL 9 IS 1-2 BP 163 EP 186 PG 24 WC Public, Environmental & Occupational Health; Toxicology SC Public, Environmental & Occupational Health; Toxicology GA KD769 UT WOS:A1993KD76900011 PM 8418511 ER PT J AU STADTMAN, ER OLIVER, CN STARKEREED, PE RHEE, SG AF STADTMAN, ER OLIVER, CN STARKEREED, PE RHEE, SG TI AGE-RELATED OXIDATION REACTION IN PROTEINS SO TOXICOLOGY AND INDUSTRIAL HEALTH LA English DT Article ID GLUTAMINE-SYNTHETASE; DENATURED PROTEINS; ESCHERICHIA-COLI; DEGRADATION; ENZYME; PURIFICATION; PROTEOLYSIS; TURNOVER; PROTEASE; SYSTEM RP STADTMAN, ER (reprint author), NHLBI,BIOCHEM LAB,9000 ROCKVILLE PIKE,BLDG 3,ROOM 222,BETHESDA,MD 20892, USA. NR 22 TC 22 Z9 23 U1 0 U2 2 PU PRINCETON SCIENTIFIC PUBL INC PI PRINCETON PA PO BOX 2155, PRINCETON, NJ 08543 SN 0748-2337 J9 TOXICOL IND HEALTH JI Toxicol. Ind. Health PD JAN-APR PY 1993 VL 9 IS 1-2 BP 187 EP 196 PG 10 WC Public, Environmental & Occupational Health; Toxicology SC Public, Environmental & Occupational Health; Toxicology GA KD769 UT WOS:A1993KD76900012 PM 8093419 ER PT J AU CADET, JL AF CADET, JL TI MOVEMENT-DISORDERS - THERAPEUTIC ROLE OF VITAMIN-E SO TOXICOLOGY AND INDUSTRIAL HEALTH LA English DT Article ID PARKINSONS-DISEASE; TARDIVE-DYSKINESIA; LIPID-PEROXIDATION; SUBSTANTIA NIGRA; FREE-RADICALS; RAT-BRAIN; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE MPTP; DOPAMINERGIC NEUROTOXICITY; 6-HYDROXYDOPAMINE 6-OHDA; SUPEROXIDE FORMATION RP NIDA, ARC, CLIN PSYCHOPHARMACOL SECT, CELLULAR & MOLEC NEUROTOXICOL UNIT, POB 5180, BALTIMORE, MD 21224 USA. NR 74 TC 3 Z9 3 U1 0 U2 1 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0748-2337 EI 1477-0393 J9 TOXICOL IND HEALTH JI Toxicol. Ind. Health PD JAN-APR PY 1993 VL 9 IS 1-2 BP 337 EP 347 PG 11 WC Public, Environmental & Occupational Health; Toxicology SC Public, Environmental & Occupational Health; Toxicology GA KD769 UT WOS:A1993KD76900024 PM 8093421 ER PT B AU KIM, MK MCCLASKEY, JH BODENNER, DL WEINTRAUB, BD AF KIM, MK MCCLASKEY, JH BODENNER, DL WEINTRAUB, BD GP ASSOC AMER PHYSICIANS TI A C-FOS/C-JUN-LIKE FACTOR AND THE PITUITARY-SPECIFIC FACTOR PIT-1 ARE BOTH NECESSARY TO MEDIATE INDUCTION OF THE HUMAN THYROTROPIN BETA-PROMOTER SO TRANSACTIONS OF THE ASSOCIATION OF AMERICAN PHYSICIANS, VOL 106 SE TRANSACTIONS OF THE ASSOCIATION OF AMERICAN PHYSICIANS LA English DT Proceedings Paper CT 106th Session of the Association-of-American-Physicians CY APR 30-MAY 03, 1993 CL WASHINGTON, DC SP ASSOC AMER PHYSICIANS C1 NIDDKD,MOLEC CELLULAR & ENDOCRINOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSOC AMER PHYSICIANS PI ST LOUIS PA WASHINGTON UNIV MED SCHOOL, DEPT MEDICINE, BOX 8125, 660 S EUCLID AVE, ST LOUIS, MO 63110 J9 T ASSOC AM PHYSICIAN PY 1993 VL 106 BP 62 EP 68 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA BA07V UT WOS:A1993BA07V00006 PM 8036746 ER PT B AU MCDONALD, LJ MOSS, J AF MCDONALD, LJ MOSS, J GP ASSOC AMER PHYSICIANS TI PLEIOTROPIC EFFECTS OF NITRIC-OXIDE ON ADP-RIBOSYLATION, COVALENT BINDING OF NAD, AND CATALYTIC ACTIVITY OF GLYCERALDEHYDE-3-PHOSPHATE AND ALDEHYDE DEHYDROGENASES SO TRANSACTIONS OF THE ASSOCIATION OF AMERICAN PHYSICIANS, VOL 106 SE TRANSACTIONS OF THE ASSOCIATION OF AMERICAN PHYSICIANS LA English DT Proceedings Paper CT 106th Session of the Association-of-American-Physicians CY APR 30-MAY 03, 1993 CL WASHINGTON, DC SP ASSOC AMER PHYSICIANS C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ASSOC AMER PHYSICIANS PI ST LOUIS PA WASHINGTON UNIV MED SCHOOL, DEPT MEDICINE, BOX 8125, 660 S EUCLID AVE, ST LOUIS, MO 63110 J9 T ASSOC AM PHYSICIAN PY 1993 VL 106 BP 155 EP 161 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA BA07V UT WOS:A1993BA07V00018 PM 8036738 ER PT J AU LEVINE, PH MANNS, A AF LEVINE, PH MANNS, A TI TRANSFUSION TRANSMISSION OF HUMAN T-LYMPHOTROPIC VIRUS TYPE-I AND TYPE-II - LESSONS TO BE LEARNED FROM LOOK-BACK INVESTIGATIONS AND IMPLICATIONS FOR PATIENT COUNSELING SO TRANSFUSION LA English DT Editorial Material ID CELL LEUKEMIA-LYMPHOMA; HTLV-II; BLOOD-TRANSFUSION; GUAYMI INDIANS; UNITED-STATES; INFECTION; RISK; COMPONENTS; RECIPIENTS; MYELOPATHY RP LEVINE, PH (reprint author), NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 38 TC 4 Z9 4 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD JAN PY 1993 VL 33 IS 1 BP 4 EP 6 DI 10.1046/j.1537-2995.1993.33193142308.x PG 3 WC Hematology SC Hematology GA KL697 UT WOS:A1993KL69700002 PM 8379967 ER PT S AU CHESEBRO, B WEHRLY, K CAUGHEY, B NISHIO, J ERNST, D RACE, R AF CHESEBRO, B WEHRLY, K CAUGHEY, B NISHIO, J ERNST, D RACE, R GP INT ASSOC BIOL STAND TI FOREIGN PRP EXPRESSION AND SCRAPIE INFECTION IN TISSUE-CULTURE CELL-LINES SO TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES - IMPACT ON ANIMAL AND HUMAN HEALTH SE DEVELOPMENTS IN BIOLOGICAL STANDARDIZATION LA English DT Proceedings Paper CT INTERNATIONAL MEETING ON TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES - IMPACT ON ANIMAL AND HUMAN HEALTH CY JUN 23-24, 1992 CL HEIDELBERG, GERMANY SP ARES SERONO SYMPOSIA, FIDIA RES FDN RP CHESEBRO, B (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 0 TC 42 Z9 43 U1 0 U2 0 PU KARGER PI BASEL PA BASEL SN 0301-5149 BN 3-8055-5831-7 J9 DEV BIOL STAND JI Dev. Biols PY 1993 VL 80 BP 131 EP 140 PG 10 WC Biology; Pathology SC Life Sciences & Biomedicine - Other Topics; Pathology GA BY91M UT WOS:A1993BY91M00018 PM 8270103 ER EF