FN Thomson Reuters Web of Science™ VR 1.0 PT S AU EGWUAGU, CE SZTEIN, J CHAN, CC MAHDI, R NUSSENBLATT, RB CHEPELINSKY, AB AF EGWUAGU, CE SZTEIN, J CHAN, CC MAHDI, R NUSSENBLATT, RB CHEPELINSKY, AB BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI TRANSGENIC RAT AND MOUSE MODELS FOR STUDYING THE ROLE OF GAMMA INTERFERON AND MHC CLASS-II IN INTRAOCULAR DISEASES AND AUTOIMMUNITY SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LABS,VET RES & RESOURCES SECT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 131 EP 134 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00033 ER PT S AU LAI, JC WAWROUSEK, EF LEE, RS CHAN, CC WHITCUP, SM GERY, I AF LAI, JC WAWROUSEK, EF LEE, RS CHAN, CC WHITCUP, SM GERY, I BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI ANALYSIS OF PERIPHERAL TOLERANCE TO AUTOLOGOUS ANTIGENS EXPRESSED IN AN IMMUNOLOGICALLY PRIVILEGED SITE SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LABS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 139 EP 142 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00035 ER PT S AU WAWROUSEK, EF LAI, JC GERY, I CHAN, CC AF WAWROUSEK, EF LAI, JC GERY, I CHAN, CC BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI PROGRESSIVE INFLAMMATORY DISEASE AND NEOVASCULARIZATION IN THE EYES OF INTERLEUKIN-1 beta TRANSGENIC MICE SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NAT EYE INST,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 8 Z9 8 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 143 EP 146 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00036 ER PT S AU ESUMI, N JENDOUBI, M AF ESUMI, N JENDOUBI, M BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI ISOLATION AND CHARACTERIZATION OF THE MOUSE ORNITHINE AMINOTRANSFERASE GENE FOR GENE TARGETING BY HOMOLOGOUS RECOMBINATION SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 151 EP 154 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00038 ER PT S AU JENDOUBI, M AF JENDOUBI, M BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI RETINAL SURVIVAL IN TRANSGENIC MICE EXPRESSING HUMAN ORNITHINE partial derivative AMINOTRANSFERASE SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 155 EP 158 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00039 ER PT S AU LACORAZZA, HD JENDOUBI, M AF LACORAZZA, HD JENDOUBI, M BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI ORNITHINE-delta-AMINOTRANSFERASE GENE TRANSFER TO CHO DEFICIENT CELLS BY RETROVIRUS TRANSDUCTION SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 159 EP 162 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00040 ER PT S AU RIVERO, JL JENDOUBI, M AF RIVERO, JL JENDOUBI, M BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI GENE TARGETING OF INVARIANT CHAIN GENE BY HOMOLOGOUS RECOMBINATION AS A TOOL TO STUDY IMMUNOREGULATION IN AUTOIMMUNE DISEASES SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 163 EP 166 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00041 ER PT S AU CHANAUD, NP FELIX, NJ SILVER, PB RIZZO, LV CASPI, RR NUSSENBLATT, RB GERY, I AF CHANAUD, NP FELIX, NJ SILVER, PB RIZZO, LV CASPI, RR NUSSENBLATT, RB GERY, I BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI INDUCTION OF ORAL TOLERANCE IN CD8 CELL DEFICIENT MICE SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,BETHESDA,MD. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 2 Z9 2 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 213 EP 216 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00052 ER PT S AU KOZHICH, AT NUSSENBLATT, RB GERY, I AF KOZHICH, AT NUSSENBLATT, RB GERY, I BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI ENHANCEMENT OF ORAL TOLERANCE BY BACTERIAL PRODUCTS SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,BETHESDA,MD. NR 0 TC 1 Z9 1 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 217 EP 220 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00053 ER PT S AU RIZZO, LV MILLERRIVERO, NE CHAN, CC WIGGERT, B NUSSENBLATT, RB CASPI, RR AF RIZZO, LV MILLERRIVERO, NE CHAN, CC WIGGERT, B NUSSENBLATT, RB CASPI, RR BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI EFFECT OF INTERLEUKIN-2 ON THE INDUCTION OF ORAL TOLERANCE IN EXPERIMENTAL AUTOIMMUNE UVEORETINITIS SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 1 Z9 1 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 221 EP 224 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00054 ER PT S AU GUEXCROSIER, Y PITTET, N HERBORT, CP AF GUEXCROSIER, Y PITTET, N HERBORT, CP BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI THALIDOMIDE AND SUPIDIMIDE DOWNREGULATE THE INFLAMMATION IN ENDOTOXIN-INDUCED UVEITIS SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 237 EP 240 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00057 ER PT S AU PENG, B LI, Q LUYO, D WHITCUP, SM ROBERGE, FG CHAN, CC AF PENG, B LI, Q LUYO, D WHITCUP, SM ROBERGE, FG CHAN, CC BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI TREATMENT OF ALLERGIC CONJUNCTIVITIS IN MURINE MODEL SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,BETHESDA,MD. NR 0 TC 4 Z9 4 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 249 EP 252 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00060 ER PT S AU HOOKS, JJ WANG, Y KOMURASAKI, Y PERCOPO, C NAGINENI, CN DETRICK, B AF HOOKS, JJ WANG, Y KOMURASAKI, Y PERCOPO, C NAGINENI, CN DETRICK, B BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI MOLECULAR AND IMMUNOLOGIC MECHANISMS INVOLVED IN CORONAVIRUS INDUCED RETINOPATHY SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,IMMUNOL LAB,IMMUNOL & VIROL SECT,BETHESDA,MD. NR 0 TC 1 Z9 1 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 273 EP 276 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00065 ER PT S AU WANG, Y PERCOPO, CM BURNIER, MN DETRICK, B HOOKS, JJ AF WANG, Y PERCOPO, CM BURNIER, MN DETRICK, B HOOKS, JJ BE Nussenblatt, RB Whitcup, SM Caspi, RR Gery, I TI GENETICS OF THE VIRUS DETERMINES RETINAL TISSUE DAMAGE INDUCED BY CORONAVIRUSES SO ADVANCES IN OCULAR IMMUNOLOGY SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th International Symposium on the Immunology and Immunopathology of the Eye (IIPE) CY JUN 22-24, 1994 CL NIH CAMPUS, BETHESDA, MD HO NIH CAMPUS C1 NEI,LAB IMMUNOL,IMMUNOL & VIROL SECT,BETHESDA,MD. NR 0 TC 1 Z9 1 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 0-444-81742-5 J9 INT CONGR SER PY 1994 VL 1068 BP 297 EP 300 PG 4 WC Immunology; Ophthalmology SC Immunology; Ophthalmology GA BC27A UT WOS:A1994BC27A00071 ER PT S AU SHINOHARA, T KIKUCHI, T RAJU, K BRETIMAN, M AF SHINOHARA, T KIKUCHI, T RAJU, K BRETIMAN, M BE Moller, M Pevet, P TI PROMOTERS OF RETINAL S-ANTIGEN (ARRESTIN) GENES CONTAIN SEQUENCE MOTIF COMMON TO OTHER PHOTORECEPTOR SPECIFIC PROMOTERS, INTERACT WITH RETINAL NUCLEAR FACTORS AND DIRECT CELL TYPE SPECIFIC EXPRESSION SO ADVANCES IN PINEAL RESEARCH: 8 SE ADVANCES IN PINEAL RESEARCH LA English DT Proceedings Paper CT VIth Colloquium of the European Pineal Society (EPS 1993) CY JUL 23-27, 1993 CL COPENHAGEN, DENMARK SP EUROPEAN PINEAL SOC C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN LIBBEY & CO PI LONDON PA 13 SMITHS YARD, SUMMERLEY ST, LONDON, ENGLAND SW18 4HR SN 0269-0071 BN 0-86196-426-8 J9 ADV PINEAL PY 1994 VL 8 BP 239 EP 248 PG 10 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA BC73E UT WOS:A1994BC73E00025 ER PT J AU ZOCCHI, A CABIB, S PUGLISIALLEGRA, S AF ZOCCHI, A CABIB, S PUGLISIALLEGRA, S TI OPPOSITE STRAIN-DEPENDENT DIFFERENCES FOR INTERMALE AGGRESSIVE-BEHAVIOR ELICITED BY INDIVIDUAL HOUSING AND HOUSING WITH A FEMALE IN THE MOUSE SO AGGRESSIVE BEHAVIOR LA English DT Article DE AGGRESSIVE BEHAVIOR; INDIVIDUAL HOUSING; HOUSING WITH A FEMALE; INBRED MICE ID INBRED STRAINS; ISOLATED MICE; BRAIN-AREAS; GENOTYPE; TESTS AB Male mice of the C57BL/6 strain show a significant increase in aggression toward a nonaggressive mate conspecific following 72 hr of individual housing. However, this increase was no longer evident following 2 weeks of individual housing. When housed with a female, C57BL/6 mice show significantly more aggression than singly housed mice of the same strain after 72 hr as well as 2, 4, 8 weeks of differential housing. Male C57BL/6 mice housed with a female also show significantly higher levels of aggression than DBA/2 mice living in the same housing condition after 4 or 8 weeks of differential housing. Finally, male DBA/2 mice individually housed for 8 weeks are significantly more aggressive than mice of the same strain housed with a female for the same time. These results indicate that the increase in aggressive behavior observed following isolation and cohabitation with a female in the mouse is not the same phenomenon. (C) 1994 Wiley-Liss, Inc. C1 UNIV ROMA LA SAPIENZA,DIPARTIMENTO PSICOL,I-00185 ROME,ITALY. RP ZOCCHI, A (reprint author), NIMH,BEHAV PHARMACOL BRANCH,BLDG 10,ROOM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 30 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 0096-140X J9 AGGRESSIVE BEHAV JI Aggressive Behav. PY 1994 VL 20 IS 4 BP 305 EP 314 DI 10.1002/1098-2337(1994)20:4<305::AID-AB2480200404>3.0.CO;2-2 PG 10 WC Behavioral Sciences; Psychology, Multidisciplinary SC Behavioral Sciences; Psychology GA NX130 UT WOS:A1994NX13000003 ER PT S AU ROTH, GS JOSEPH, JA AF ROTH, GS JOSEPH, JA BE Pierpaoli, W Regelson, W Fabris, N TI CELLULAR AND MOLECULAR MECHANISMS OF IMPAIRED DOPAMINERGIC FUNCTION DURING AGING SO AGING CLOCK: THE PINEAL GLAND AND OTHER PACEMAKERS IN THE PROGRESSION OF AGING AND CARCINOGENESIS - THIRD STROMBOLI CONFERENCE ON AGING AND CANCER SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on The Aging Clock: The Pineal Gland and Other Pacemakers in the Progression of Aging and Carcinogenesis/3rd Stromboli Conference on Aging and Cancer (NATO Advanced Research Workshop) CY JUN 04-09, 1993 CL STROMBOLI, ITALY SP NATO ID MOTOR BEHAVIORAL DEFICITS; RECEPTOR SUPER-SENSITIVITY; AGE-RELATED-CHANGES; DIETARY RESTRICTION; CHRONIC PROLACTIN; ESTROGEN-TREATMENT; SENESCENT ANIMALS; MESSENGER-RNA; RAT STRIATUM; REDUCTION RP ROTH, GS (reprint author), NIA,FRANCIS SCOTT KEY MED CTR,GERONTOL RES CTR,MOLEC PHYSIOL & GENET SECT,CELLULAR & MOLEC BIOL,BALTIMORE,MD 21224, USA. NR 49 TC 66 Z9 67 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 0-89766-860-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 719 BP 129 EP 135 DI 10.1111/j.1749-6632.1994.tb56824.x PG 7 WC Oncology; Endocrinology & Metabolism; Immunology; Multidisciplinary Sciences; Physiology SC Oncology; Endocrinology & Metabolism; Immunology; Science & Technology - Other Topics; Physiology GA BA43X UT WOS:A1994BA43X00008 PM 8010587 ER PT S AU JUCKER, M INGRAM, DK AF JUCKER, M INGRAM, DK BE Pierpaoli, W Regelson, W Fabris, N TI AGE-RELATED FIBRILLAR MATERIAL IN MOUSE-BRAIN - ASSESSING ITS POTENTIAL AS A BIOMARKER OF AGING AND AS A MODEL OF HUMAN NEURODEGENERATIVE DISEASE SO AGING CLOCK: THE PINEAL GLAND AND OTHER PACEMAKERS IN THE PROGRESSION OF AGING AND CARCINOGENESIS - THIRD STROMBOLI CONFERENCE ON AGING AND CANCER SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on The Aging Clock: The Pineal Gland and Other Pacemakers in the Progression of Aging and Carcinogenesis/3rd Stromboli Conference on Aging and Cancer (NATO Advanced Research Workshop) CY JUN 04-09, 1993 CL STROMBOLI, ITALY SP NATO ID HEPARAN-SULFATE PROTEOGLYCANS; ALZHEIMERS-DISEASE; CORPORA-AMYLACEA; ALEXANDERS DISEASE; PRECURSOR PROTEIN; HIGH-AFFINITY; BINDS; ASTROCYTES; LAMININ; MICE C1 ETH ZURICH,DEPT NEUROBIOL,CH-8093 ZURICH,SWITZERLAND. RP JUCKER, M (reprint author), NIA,GERONTOL RES CTR,CELLULAR & MOLEC BIOL LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 54 TC 14 Z9 14 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 0-89766-860-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 719 BP 238 EP 247 DI 10.1111/j.1749-6632.1994.tb56832.x PG 10 WC Oncology; Endocrinology & Metabolism; Immunology; Multidisciplinary Sciences; Physiology SC Oncology; Endocrinology & Metabolism; Immunology; Science & Technology - Other Topics; Physiology GA BA43X UT WOS:A1994BA43X00016 PM 8010596 ER PT B AU ADLER, WH SONG, LJ CHOPRA, RK WINCHURCH, RA WAGGIE, KS NAGEL, JE AF ADLER, WH SONG, LJ CHOPRA, RK WINCHURCH, RA WAGGIE, KS NAGEL, JE BE Powers, DC Morley, JE Coe, RM TI IMMUNE DEFICIENCY OF AGING SO AGING, IMMUNITY, AND INFECTION LA English DT Proceedings Paper CT Aging, Immunity, and Infection Symposium CY SEP, 1992 CL ST LOUIS, MO C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 6 Z9 6 U1 0 U2 0 PU SPRINGER PUBL CO PI NEW YORK PA 536 BROADWAY, NEW YORK, NY 10012 BN 0-8261-8180-5 PY 1994 BP 66 EP 81 PG 16 WC Geriatrics & Gerontology; Immunology SC Geriatrics & Gerontology; Immunology GA BB77C UT WOS:A1994BB77C00006 ER PT J AU DECKER, CF MASUR, H AF DECKER, CF MASUR, H TI CURRENT STATUS OF PROPHYLAXIS FOR OPPORTUNISTIC INFECTIONS IN HIV-INFECTED PATIENTS SO AIDS LA English DT Review DE OPPORTUNISTIC INFECTIONS; PROPHYLAXIS; HIV; AIDS; PNEUMOCYSTIS; TOXOPLASMOSIS; MYCOBACTERIUM AVIUM COMPLEX; CYTOMEGALOVIRUS; MYCOBACTERIUM TUBERCULOSIS ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PNEUMOCYSTIS-CARINII PNEUMONIA; MYCOBACTERIUM-AVIUM COMPLEX; TRIMETHOPRIM-SULFAMETHOXAZOLE; TOXOPLASMIC ENCEPHALITIS; AEROSOLIZED PENTAMIDINE; CONTROLLED TRIAL; SECONDARY PROPHYLAXIS; VIRUS INFECTION; CLINICAL-FEATURES C1 NIH, CTR CLIN, DEPT CRIT CARE MED, BETHESDA, MD 20892 USA. NATL NAVAL MED CTR, DIV INFECT DIS, BETHESDA, MD USA. NR 86 TC 24 Z9 24 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD JAN PY 1994 VL 8 IS 1 BP 11 EP 20 DI 10.1097/00002030-199401000-00003 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NA432 UT WOS:A1994NA43200002 PM 8011221 ER PT J AU NUSSENBLATT, RB DESMET, M PODGOR, M LANE, C POLIS, M PIZZO, P PERRY, C BELFORT, R AF NUSSENBLATT, RB DESMET, M PODGOR, M LANE, C POLIS, M PIZZO, P PERRY, C BELFORT, R TI THE USE OF THE FLAREPHOTOMETRY IN THE DETECTION OF CYTOMEGALIC VIRUS RETINITIS IN AIDS PATIENTS SO AIDS LA English DT Letter ID IMMUNODEFICIENCY C1 NIAID,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. ESCOLA PAULISTA MED HOSP SAO PAULO,BR-04034 SAO PAULO,BRAZIL. RP NUSSENBLATT, RB (reprint author), NEI,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Belfort Jr, Rubens/E-2252-2012 OI Belfort Jr, Rubens/0000-0002-8422-3898 NR 5 TC 7 Z9 8 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD JAN PY 1994 VL 8 IS 1 BP 135 EP 136 DI 10.1097/00002030-199401000-00026 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NA432 UT WOS:A1994NA43200025 PM 8011230 ER PT J AU TAMASHIRO, H KAGAN, J LANDAY, A NICHOLSON, JKA HEARN, T DENNY, T THOMPSON, P THOMAS, M RUSSELL, T BRANDES, W JACKSON, B MEISNER, P GELB, W CORBET, D DELETOILLE, P PAU, B MANDY, F WONG, W JENSEN, B CEKORIC, T QUINN, T FRANCIS, S HOFF, R LISSE, I OSHAUGHNESSY, M KATAAHA, P DEPEREZ, GE KARAM, M WEISSENBACHER, M ZACARIAS, F AF TAMASHIRO, H KAGAN, J LANDAY, A NICHOLSON, JKA HEARN, T DENNY, T THOMPSON, P THOMAS, M RUSSELL, T BRANDES, W JACKSON, B MEISNER, P GELB, W CORBET, D DELETOILLE, P PAU, B MANDY, F WONG, W JENSEN, B CEKORIC, T QUINN, T FRANCIS, S HOFF, R LISSE, I OSHAUGHNESSY, M KATAAHA, P DEPEREZ, GE KARAM, M WEISSENBACHER, M ZACARIAS, F TI REPORT OF A WHO WORKSHOP ON FLOW-CYTOMETRY AND ALTERNATIVE METHODOLOGIES FOR CD4 LYMPHOCYTE DETERMINATIONS - APPLICATIONS FOR DEVELOPING-COUNTRIES WASHINGTON, DC, 16 APRIL 1992 SO AIDS LA English DT Editorial Material C1 NIH,BETHESDA,MD. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL. CTR DIS CONTROL,ATLANTA,GA 30333. UNIV MED & DENT NEW JERSEY,NEWARK,NJ 07103. BECTON DICKINSON IMMUNOCYTOMETRY SYST,SAN JOSE,CA 95131. COULTER CYTOMETRY,HIALEAH,FL. CASE WESTERN RESERVE UNIV,SCH MED,CLEVELAND,OH. T CELL DIAGNOST INC,CAMBRIDGE,MA. SANOFI DIAGNOST PASTEUR,MONTREAL,PQ,CANADA. UNIV MONTPELLIER,FAC PHARM,F-34059 MONTPELLIER,FRANCE. FED CTR AIDS,OTTAWA,ON,CANADA. ZYNAXIS CELL SCI INC,MALVERN,PA. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. NIAID,DIV AIDS,VACCINE TRIALS SECT,ROCKVILLE,MD. HVIDOVRE UNIV HOSP,DEPT PATHOL,HVIDOVRE,DENMARK. ST PAULS HOSP,BC CTR EXCELLENCE HIV AIDS,VANCOUVER,BC,CANADA. NAKASERO BLOOD BANK,KAMPALA,UGANDA. INST IMMUNOL,CLIN IMMUNOL NALT CTR,RETROVIRAL INFECT PROGRAMME,CARACAS,VENEZUELA. WHO,PAN AMER HLTH ORG,REG OFF AMER,WASHINGTON,DC. RP TAMASHIRO, H (reprint author), WHO,GLOBAL PROGRAMME AIDS,RES OFF,CH-1211 GENEVA 27,SWITZERLAND. RI Tamashiro, Hidehiko/B-2403-2013 NR 4 TC 1 Z9 1 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD JAN PY 1994 VL 8 IS 1 BP WHO1 EP WHO4 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NA432 UT WOS:A1994NA43200030 ER PT J AU BENSON, J TSCHACHLER, E GESSAIN, A YANAGIHARA, R GALLO, RC FRANCHINI, G AF BENSON, J TSCHACHLER, E GESSAIN, A YANAGIHARA, R GALLO, RC FRANCHINI, G TI CROSS-NEUTRALIZING ANTIBODIES AGAINST COSMOPOLITAN AND MELANESIAN STRAINS OF HUMAN T-CELL LEUKEMIA/LYMPHOTROPIC VIRUS TYPE-I IN SERA FROM INHABITANTS OF AFRICA AND THE SOLOMON-ISLANDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID PAPUA-NEW-GUINEA; TROPICAL SPASTIC PARAPARESIS; HTLV-I; CHILD TRANSMISSION; LYMPHOMA-LEUKEMIA; HUMAN RETROVIRUS; LYMPHOCYTES; VARIANT; GP46; GLYCOPROTEINS AB The so-called cosmopolitan strains of human T cell leukemia/lymphotropic virus type I (HTLV-I) from Japan, Africa, the West Indies, and the Americas differ only slightly (<3%) in their genomic sequence. On the other hand, the Melanesian strains of HTLV-I are somewhat more divergent, exhibiting only 93% sequence similarity with the cosmopolitan strains. Despite this difference, sera from individuals infected with Melanesian strains cross-react with T cells infected with cosmopolitan strains of HTLV-I, indicating an overall conservation of the B cell immunoprevalent epitopes. Neutralizing antibodies against HTLV-I in sera from virus-infected Africans and Melanesians were assayed by determining their ability to block the formation of syncytia in cocultures of 8166 and T cell lines harboring either, cosmopolitan or Melanesian HTLV-I isolates. All six African sera blocked the formation of syncytia with cells infected with HTLV-I-C91-PL, a viral isolate from the United States. Similarly, ail six Melanesian sera inhibited syncytium formation with cells infected with HTLV-I-MEL3, a virus isolate from the Solomon Islands. Although most of these sera inhibited syncytium formation in cell cultures carrying the cosmopolitan as well as the Melanesian HTLV-I strains, neutralizing antibody titers tended to be higher against the homologous virus. All sera failed to inhibit syncytium formation when cells were infected with HTLV-II. These data indicate the involvement of one or more epitopes in syncytial formation, some of which are conserved in all strains of HTLV-I. If antigenic determinants for neutralization play an important role in protection against HTLV-I infection, as suggested by studies in infected rabbits and humans, vaccines for worldwide application should include the envelope proteins from a Melanesian strain of HTLV-I. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV VIENNA,SCH MED,A-1090 VIENNA,AUSTRIA. NATL INST NEUROL DISORDERS & STROKE,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. NR 44 TC 12 Z9 12 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JAN PY 1994 VL 10 IS 1 BP 91 EP 96 DI 10.1089/aid.1994.10.91 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA MV293 UT WOS:A1994MV29300011 PM 8179967 ER PT J AU GESSAIN, A KORALNIK, IJ FULLEN, J BOERI, E MORA, C BLANK, A SALAZARGRUESO, EF KAPLAN, J SAXINGER, WC DAVIDSON, M LAIRMORE, MD LEVINE, P FRANCHINI, G AF GESSAIN, A KORALNIK, IJ FULLEN, J BOERI, E MORA, C BLANK, A SALAZARGRUESO, EF KAPLAN, J SAXINGER, WC DAVIDSON, M LAIRMORE, MD LEVINE, P FRANCHINI, G TI PHYLOGENETIC STUDY OF 10 NEW HTLV-I STRAINS FROM THE AMERICA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Note ID T-CELL LEUKEMIA; VIRUS TYPE-I; NUCLEOTIDE-SEQUENCE ANALYSIS; TROPICAL SPASTIC PARAPARESIS; NATURAL ANTIBODIES; MOLECULAR-CLONING; HUMAN RETROVIRUS; LYMPHOMA; PROVIRUS; PATIENT C1 NINCDS,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. HOSP UNIV VALLE,CALI,COLOMBIA. UNIV CHICAGO,CANC RES CTR,DEPT NEUROL,CHICAGO,IL 60637. CTR DIS CONTROL,RETROVIRUS DIS BRANCH,ATLANTA,GA 30333. ALASKA NATIVE MED CTR,DEPT MED,ANCHORAGE,AK 99501. OHIO STATE UNIV,DEPT VET PATHOBIOL,COLUMBUS,OH 43210. NCI,VIRAL EPIDEMIOL BRANCH,ROCKVILLE,MD 20852. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 36 TC 20 Z9 22 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JAN PY 1994 VL 10 IS 1 BP 103 EP 106 DI 10.1089/aid.1994.10.103 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA MV293 UT WOS:A1994MV29300013 PM 7514013 ER PT J AU ARTHUR, LO BESS, JW BENVENISTE, RE HENDERSON, LE AF ARTHUR, LO BESS, JW BENVENISTE, RE HENDERSON, LE TI IMMUNIZATION OF MACAQUES WITH CELLULAR ANTIGENS ASSOCIATED WITH SIMIAN IMMUNODEFICIENCY VIRUS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. RI Bess, Jr., Julian/B-5343-2012 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S135 EP S135 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800060 ER PT J AU BERZOFSKY, JA AHLERS, JD SHIRAI, M PENDLETON, CD TAKESHITA, T DUNLOP, N MINASSIAN, A NEWMAN, M NARA, PL AF BERZOFSKY, JA AHLERS, JD SHIRAI, M PENDLETON, CD TAKESHITA, T DUNLOP, N MINASSIAN, A NEWMAN, M NARA, PL TI CONSTRUCTION OF CANDIDATE SYNTHETIC PEPTIDE VACCINES FOR HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract ID RESPONSES; MICE C1 NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S115 EP S115 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800054 ER PT J AU BIBERFELD, G PUTKONEN, P ANDERSSON, S MAKITALO, B THORSTENSSON, R FRANCHINI, G TARTAGLIA, J PAOLETTI, E AF BIBERFELD, G PUTKONEN, P ANDERSSON, S MAKITALO, B THORSTENSSON, R FRANCHINI, G TARTAGLIA, J PAOLETTI, E TI VACCINATION OF CYNOMOLGUS MONKEYS WITH A CANARY POX HIV-2 VACCINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 KAROLINSKA INST,S-10521 STOCKHOLM,SWEDEN. SWEDISH INST INFECT DIS CONTROL,S-10521 STOCKHOLM,SWEDEN. NCI,BETHESDA,MD. VIROGENET CORP,TROY,NY. NR 0 TC 1 Z9 1 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S136 EP S136 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800065 ER PT J AU BRIDBORD, K AF BRIDBORD, K TI PREPARATIONS FOR AIDS VACCINE EVALUATIONS - AIDS INTERNATIONAL TRAINING AND RESEARCH-PROGRAM SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS RP BRIDBORD, K (reprint author), NIH,FOGARTY INT CTR,INT STUDIES BRANCH,31 CTR DR,MSC 2220,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S227 EP S229 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800110 PM 7865307 ER PT J AU CLEGHORN, F JACK, N EDWARDS, J MURPHY, J PAUL, R MAHABIR, B BARTHOLOMEW, C BLATTNER, W AF CLEGHORN, F JACK, N EDWARDS, J MURPHY, J PAUL, R MAHABIR, B BARTHOLOMEW, C BLATTNER, W TI PREPARATIONS FOR AIDS VACCINE EVALUATIONS - RISK-FACTORS FOR HIV-1 AMONG STD CLINIC ATTENDERS IN TRINIDAD SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI, VIRAL EPIDEMIOL BRANCH, ROCKVILLE, MD 20852 USA. NCI, BETHESDA, MD USA. UNIV W INDIES, CAREC, ST AUGUSTINE, TRINID & TOBAGO. MINIST HLTH, ST JOSEPH, TRINID & TOBAGO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0889-2229 EI 1931-8405 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S248 EP S248 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800121 ER PT J AU CLEGHORN, F JACK, N GREENBERG, M WEINHOLD, K EDWARDS, J MURPHY, J PAUL, R MAHABIR, B BARTHOLOMEW, C BLATTNER, W AF CLEGHORN, F JACK, N GREENBERG, M WEINHOLD, K EDWARDS, J MURPHY, J PAUL, R MAHABIR, B BARTHOLOMEW, C BLATTNER, W TI PREPARATIONS FOR AIDS VACCINE EVALUATIONS - PRIMARY HIV-1 INFECTION IN A HIGH PREVALENCE POPULATION IN TRINIDAD SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI, VIRAL EPIDEMIOL BRANCH, ROCKVILLE, MD 20852 USA. NCI, BETHESDA, MD USA. DUKE UNIV, DURHAM, NC USA. UNIV W INDIES, CAREC, ST AUGUSTINE, TRINID & TOBAGO. MINIST HLTH, ST JOSEPH, TRINID & TOBAGO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0889-2229 EI 1931-8405 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S248 EP S248 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800120 ER PT J AU CLEGHORN, F JACK, N EDWARDS, J MURPHY, J PAUL, R MAHABIR, B BARTHOLOMEW, C BLATTNER, W AF CLEGHORN, F JACK, N EDWARDS, J MURPHY, J PAUL, R MAHABIR, B BARTHOLOMEW, C BLATTNER, W TI PREPARATION FOR AIDS VACCINE EVALUATION IN TRINIDAD/TOBAGO - A REVIEW OF ACTIVITY TO DATE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI, VIRAL EPIDEMIOL BRANCH, ROCKVILLE, MD 20852 USA. NCI, BETHESDA, MD USA. UNIV W INDIES, CAREC, ST AUGUSTINE, TRINID & TOBAGO. MINIST HLTH, ST JOSEPH, TRINID & TOBAGO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0889-2229 EI 1931-8405 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S248 EP S248 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800119 ER PT J AU GARTNER, S LIU, YL LEWIS, MG POLONIS, V ELKINS, WR ZACK, PM MIAO, J HUNTER, EA GREENHOUSE, J EDDY, GA AF GARTNER, S LIU, YL LEWIS, MG POLONIS, V ELKINS, WR ZACK, PM MIAO, J HUNTER, EA GREENHOUSE, J EDDY, GA TI HIV-1 INFECTION IN PIGTAILED MACAQUES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS ID HUMAN-IMMUNODEFICIENCY-VIRUS; GLYCOPROTEIN GP120; MACACA-NEMESTRINA; CHIMPANZEES; TYPE-1; IMMUNIZATION; RECOMBINANT; CHALLENGE; MODEL; AIDS AB Four pigtailed macaques were inoculated with autologous cells expressing low levels of human immunodeficiency virus type 1 (HIV-1). During the first 10 weeks, infectious virus was recovered from peripheral blood mononuclear cells (PBMCs) and lymph nodes from three of the animals. Subsequently, HIV-1 DNA was frequently detected in uncultured PBMCs from all three animals, and virus was isolated from one of them at weeks 38 and 61. The fourth animal, which was rechallenged at week 10 with cell-free virus isolated from one of the others, never became virus isolation positive, but harbored HIV-1 proviral genomes. These virus infections were accompanied by the development of varied HIV-1-specific humoral immune responses. Antibodies to gp160 were first apparent at week 8 in the three initially infected animals and persisted. The animal from whom virus was isolated at late times also developed persisting antibodies to HIV-1 p24 and gp120. Antibodies to gp120 and gp160 became apparent in the rechallenged animal at 1 week following reinoculation, but they waned with time. In vivo passage of the virus was attempted at week 6. One recipient pigtailed macaque and one recipient cynomolgus monkey failed to become detectably infected following transfusion of virus-positive blood and lymph node cells. The long-term presence of HIV-1-specific antibodies and proviral genomes in these animals, and the recovery of infectious virus more than 1 year following inoculation, are indicative of persistent infection, and confirm previous reports that pigtailed macaques are susceptible to HIV-1. C1 WALTER REED ARMY INST RES,DIV RETROVIROL,DEPT RETROVIRAL RES,ROCKVILLE,MD 20850. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. RP GARTNER, S (reprint author), HENRY M JACKSON FDN RES LAB,1600 E GUDE DR,ROCKVILLE,MD 20850, USA. NR 12 TC 12 Z9 12 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S129 EP S133 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800058 PM 7865287 ER PT J AU HARRER, E HARRER, T BUCHBINDER, S MANN, DL FEINBERG, M YILMA, T JOHNSON, RP WALKER, BD AF HARRER, E HARRER, T BUCHBINDER, S MANN, DL FEINBERG, M YILMA, T JOHNSON, RP WALKER, BD TI HIV-1-SPECIFIC CYTOTOXIC T-LYMPHOCYTE RESPONSE IN HEALTHY, LONG-TERM NONPROGRESSING SEROPOSITIVE PERSONS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INFECT DIS UNIT,BOSTON,MA 02114. DEPT PUBL HLTH,SAN FRANCISCO,CA 94102. NCI,FREDERICK,MD 21702. UNIV CALIF SAN FRANCISCO,GLADSTONE INST VIROL & IMMUNOL,SAN FRANCISCO,CA 94141. UNIV CALIF DAVIS,DAVIS,CA 95616. NR 0 TC 42 Z9 42 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S77 EP S78 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800037 PM 7532426 ER PT J AU HOFF, R AF HOFF, R TI PREPARATIONS FOR HIV VACCINE TRIALS - MOVING FROM BASE-LINE STUDIES TO EFFICACY TRIALS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS RP HOFF, R (reprint author), NIAID,DIV AIDS,6003 EXECUT BLVD 2B12,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S191 EP S193 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800096 PM 7865298 ER PT J AU JACK, N CLEGHORN, F EDWARDS, J PAUL, R MAHABIR, B MURPHY, J BARTHOLOMEW, C BLATTNER, W AF JACK, N CLEGHORN, F EDWARDS, J PAUL, R MAHABIR, B MURPHY, J BARTHOLOMEW, C BLATTNER, W TI PREPARATIONS FOR AIDS VACCINE EVALUATIONS - HIV-1 SEROPREVALENCE AND SEROINCIDENCE IN AN STD CLINIC IN TRINIDAD SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CARIBBEAN EPIDEMIOL CTR,PORT OF SPAIN,TRINID & TOBAGO. NCI,BETHESDA,MD 20892. MINIST HLTH,ST JOSEPH,TRINID & TOBAGO. UNIV W INDIES,CAREC,ST AUGUSTINE,TRINID & TOBAGO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S248 EP S248 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800122 ER PT J AU JOHNSTON, MI NOE, JS KILLEN, JY AF JOHNSTON, MI NOE, JS KILLEN, JY TI RECENT ADVANCES IN AIDS VACCINE RESEARCH-AND-DEVELOPMENT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS ID INFECTION; COHORT; HIV-1 AB There is an urgent need for a prophylactic vaccine to protect individuals from AIDS and to help abate the growing epidemic. In October 1993, the Conference on Advances in AIDS Vaccine Development reviewed the state-of-the-art in vaccine research and confirmed both the progress that has been made and the challenges that remain. Approximately 12 candidate vaccines are now in phase I/II clinical trials. To date, these products appear to be safe and capable of eliciting immune responses in vaccinees. Other vaccine strategies in development include the use of new formulations and the design of vaccine products capable of inducing a mucosal immune response. Progress has also been made in the establishment of domestic and international sites at which efficacy trials can be conducted when appropriate vaccine candidates are identified, and preparatory activities at these sites are ongoing. The possibility that one or more candidates may enter efficacy trials within the next 2 years underscores numerous issues that must be considered in preparation for these trials. These include the importance of ease of vaccine administration and cost, and an array of social, legal, and ethical issues of concern to those individuals who will be asked to participate in efficacy trials. The purpose of this article is to highlight recent advances in vaccine research and development and to define the complex factors that will impact the NIAID's position on advancing candidates into phase III trials. RP JOHNSTON, MI (reprint author), NIAID,DIV AIDS,SOLAR BLDG,ROOM 2A16,6003 EXECUT BLVD MSC 76,BETHESDA,MD 20892, USA. NR 71 TC 4 Z9 4 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S317 EP S323 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800157 PM 7865330 ER PT J AU KEEFER, MC BELSHE, R GRAHAM, B MCELRATH, J CLEMENTS, ML SPOSTO, R FAST, P AF KEEFER, MC BELSHE, R GRAHAM, B MCELRATH, J CLEMENTS, ML SPOSTO, R FAST, P TI SAFETY PROFILE OF HIV VACCINATION - FIRST 1000 VOLUNTEERS OF AIDS VACCINE EVALUATION GROUP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS C1 ST LOUIS UNIV,ST LOUIS,MO. VANDERBILT UNIV,SCH MED,NASHVILLE,TN 37212. UNIV WASHINGTON,SCH MED,SEATTLE,WA. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD. EMMES CORP,POTOMAC,MD. NIAID,DIV AIDS,VACCINE RES & DEV BRANCH,BETHESDA,MD 20892. RP KEEFER, MC (reprint author), UNIV ROCHESTER,MED CTR,SCH MED & DENT,DEPT MED,INFECT DIS UNIT,601 ELMWOOD AVE,BOX 689,ROCHESTER,NY 14642, USA. NR 3 TC 10 Z9 10 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S139 EP S140 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800068 PM 7865288 ER PT J AU LAWRENCE, DN AF LAWRENCE, DN TI HIV VACCINE DEVELOPMENT TO MEET US AND INTERNATIONAL NEEDS - OVERVIEW OF A PANEL DISCUSSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS RP LAWRENCE, DN (reprint author), NIAID,DIADS,6003 EXECUT BLVD 2A11,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S315 EP S316 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800156 ER PT J AU LAWRENCE, DN GLASS, MJ SCHULTZ, AM AF LAWRENCE, DN GLASS, MJ SCHULTZ, AM TI CONFERENCE ON ADVANCES IN AIDS VACCINE DEVELOPMENT 1993 - EPILOGUE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material RP LAWRENCE, DN (reprint author), NIAID,DIV AIDS,SOLAR BLDG,RM 2B09,6003 EXECUT BLVD,ROCKVILLE,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S325 EP S325 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800158 ER PT J AU MATTHEWS, T MCDANAL, C GREENWELL, T STREILEIN, A DAVISON, D RULAND, M BOLOGNESI, D BRADAC, J WALKER, MC AF MATTHEWS, T MCDANAL, C GREENWELL, T STREILEIN, A DAVISON, D RULAND, M BOLOGNESI, D BRADAC, J WALKER, MC TI SEROLOGICAL REACTIVITY FROM HIV-1 VACCINE RECIPIENTS PARTICIPATING IN THE AIDS VACCINE CLINICAL-TRIALS NETWORK SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. NIAID,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S55 EP S55 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800024 ER PT J AU MAYS, TD MAUREY, K AF MAYS, TD MAUREY, K TI PREPARATIONS FOR AIDS VACCINE TRIALS - INTELLECTUAL PROPERTY ISSUES RELATED TO AIDS VACCINE DEVELOPMENT FROM A FEDERAL LABORATORY PERSPECTIVE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS RP MAYS, TD (reprint author), NCI,OFF TECHNOL DEV,ROOM 4A51,BLDG 31,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S301 EP S301 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800151 PM 7865325 ER PT J AU MCNAMARA, JG ROGERS, M GOLDENTHAL, K JACKSON, JB ROSSI, P FENTON, T FAST, PE AF MCNAMARA, JG ROGERS, M GOLDENTHAL, K JACKSON, JB ROSSI, P FENTON, T FAST, PE TI CONFERENCE ON ADVANCES IN AIDS VACCINE DEVELOPMENT - 1993 REPORT OF PERINATAL INTERVENTION WORKING GROUP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS C1 NIAID,DIV AIDS,BETHESDA,MD 20852. CTR DIS CONTROL,DIV HIV AIDS,ATLANTA,GA 30333. US FDA,CTR BIOL EVALUAT & RES,ROCKVILLE,MD 20857. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. UNIV ROME,ROME,ITALY. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RI rossi, paolo/D-6504-2012 NR 1 TC 1 Z9 1 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S161 EP S164 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800090 PM 7865292 ER PT J AU MESTECKY, J WALKER, MC MATHIESON, BJ WALKER, BD AF MESTECKY, J WALKER, MC MATHIESON, BJ WALKER, BD TI CONFERENCE ON ADVANCES IN AIDS VACCINE DEVELOPMENT - 1993 - SUMMARY - MUCOSAL IMMUNITY WORKSHOP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS ID HUMAN-IMMUNODEFICIENCY-VIRUS; ANTIBODY-PRODUCING CELLS; EXTERNAL SECRETIONS; PERIPHERAL-BLOOD; PAROTID-SALIVA; HIV-1; INDUCTION; RESPONSES; ANTIGEN; SYSTEM C1 NIAID,DIV AIDS,VACCINE RES & DEV BRANCH,BASIC RES & DEV PROGRAM,BETHESDA,MD 20892. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. NR 56 TC 1 Z9 1 U1 1 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S165 EP S170 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800091 PM 7865293 ER PT J AU MILLER, CJ MARTHAS, M MCCHESNEY, M LOHMAN, B TORTEN, J TELM, S ALEXANDER, NJ AF MILLER, CJ MARTHAS, M MCCHESNEY, M LOHMAN, B TORTEN, J TELM, S ALEXANDER, NJ TI EFFECT OF SEMINAL PLASMA ON VAGINAL TRANSMISSION OF CELL-FREE SIV AND DISSEMINATION OF SIV FOLLOWING VAGINAL INOCULATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. UNIV CALIF DAVIS,CALIF REG PRIMATE RES CTR,DAVIS,CA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S68 EP S68 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800034 ER PT J AU MONTEFIORI, DC CORNELL, RJ ZHOU, JY ZHOU, JT HIRSCH, VM JOHNSON, PR AF MONTEFIORI, DC CORNELL, RJ ZHOU, JY ZHOU, JT HIRSCH, VM JOHNSON, PR TI MECHANISM OF RESISTANCE OF HIV-1 AND SIV TO COMPLEMENT LYSIS - THE ROLE OF ANTI-CELL ANTIBODIES IN VACCINE PROTECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. NIAID,INFECT DIS LAB,ROCKVILLE,MD 20852. OHIO STATE UNIV,CHILDRENS HOSP,DEPT PEDIAT,COLUMBUS,OH 43205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S135 EP S135 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800062 ER PT J AU MURPHEYCORB, M OHKAWA, S MARTIN, L WILSON, L BOHM, R BLANCHARD, J DETRICK, B VOGEL, F SCHULTZ, A AF MURPHEYCORB, M OHKAWA, S MARTIN, L WILSON, L BOHM, R BLANCHARD, J DETRICK, B VOGEL, F SCHULTZ, A TI COMPARATIVE EFFICACY OF A WHOLE KILLED SIV VACCINE IN COMBINATION WITH VARIOUS ADJUVANTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,DAIDS,BETHESDA,MD. GEORGE WASHINGTON UNIV,WASHINGTON,DC. TULANE UNIV,CTR PRIMATE,COVINGTON,LA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S115 EP S115 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800052 ER PT J AU PAUL, R CLEGHORN, F JACK, N EDWARDS, J MAHABIR, B MURPHY, J BLATTNER, W BARTHOLOMEW, C AF PAUL, R CLEGHORN, F JACK, N EDWARDS, J MAHABIR, B MURPHY, J BLATTNER, W BARTHOLOMEW, C TI SUITABILITY OF TRINIDAD/TOBAGO AS A POTENTIAL SITE FOR PHASE-III EFFICACY STUDIES OF HIV-1 VACCINES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS C1 MINIST HLTH,UWI,BARATARIA,TRINID & TOBAGO. NCI,VEB,BETHESDA,MD. RP PAUL, R (reprint author), MINIST HLTH,CAREC,ROUNDABOUT PLAZA,BARATARIA,TRINID & TOBAGO. NR 0 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S9 EP S9 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800004 PM 7865340 ER PT J AU POUND, M FRANKERUTA, G LANE, R KVOCHAK, P AF POUND, M FRANKERUTA, G LANE, R KVOCHAK, P TI EFFICACY TRIALS PREPARATIONS COLLOQUIUM IV (A) - DISCUSSANTS COMMENTS ON HIV VACCINE ACCEPTABILITY IN THE US - IMPLICATIONS FOR EDUCATION AND INFORMED CONSENT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 ACT UP,TREATMENT ACT GRP,NEW YORK,NY. MAN ALIVE METHADONE MAINTENANCE PROGRAM,BALTIMORE,MD. NIH,BETHESDA,MD 20892. RP POUND, M (reprint author), US HLTH RESOURCES & SERV ADM,ROCKVILLE,MD 20857, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S271 EP S271 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800140 ER PT J AU SALMON, D EXCLER, JL PLOTKIN, S PIALOUX, G RIVIERE, Y AUTRAN, B GLUCKMAN, JC MATTHEWS, T AF SALMON, D EXCLER, JL PLOTKIN, S PIALOUX, G RIVIERE, Y AUTRAN, B GLUCKMAN, JC MATTHEWS, T TI A PRIME-BOOST APPROACH TO HIV PREVENTIVE VACCINES USING A MN-GP160 RECOMBINANT CANARYPOX VIRUS AND ENVELOPE SUBUNITS (RGP160, V3 PEPTIDE) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 PASTEUR MERIEUX S&V,F-92430 MARNES COQUETTE,FRANCE. ANRS,PARIS,FRANCE. DUKE UNIV,DURHAM,NC 27706. NCI,BETHESDA,MD 20892. VIROGENET CORP,TROY,NY 12180. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S156 EP S156 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800077 ER PT J AU SHEON, AR AF SHEON, AR TI OVERVIEW - HIV VACCINE FEASIBILITY STUDIES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS RP SHEON, AR (reprint author), NIAID,DIV AIDS,VACCINE TRIALS & EPIDEMIOL BRANCH,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 1 TC 11 Z9 11 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S195 EP S196 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800097 PM 7865299 ER PT J AU SHEPPARD, H BRIDGES, SH MATHIESON, BJ WALKER, MC WEINHOLD, K AF SHEPPARD, H BRIDGES, SH MATHIESON, BJ WALKER, MC WEINHOLD, K TI CONFERENCE ON ADVANCES IN AIDS VACCINE DEVELOPMENT - 1993 - SUMMARY - CORRELATES OF HIV IMMUNITY WORKING GROUP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS ID HUMAN-IMMUNODEFICIENCY-VIRUS; TOXIC LYMPHOCYTES-T; PBL-SCID MICE; SEROPOSITIVE INDIVIDUALS; REVERSE-TRANSCRIPTASE; STAGING CLASSIFICATION; PASSIVE-IMMUNIZATION; MONOCLONAL-ANTIBODY; SUBUNIT VACCINES; CELL DYSFUNCTION C1 NIAID,DIV AIDS,VACCINE RES & DEV BRANCH,BASIC RES & DEV PROGRAM,BETHESDA,MD 20892. CALIF DEPT HLTH SERV,VIRAL & RICKETTSIAL DIS LAB,BERKELEY,CA 94704. NIAID,DIV AIDS,DEV THERAPEUT BRANCH,BASIC RES & DEV PROGRAM,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. NR 69 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S171 EP S176 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800092 PM 7865294 ER PT J AU TURNER, CF SHEON, AR AF TURNER, CF SHEON, AR TI BEHAVIORAL-STUDIES RELEVANT TO VACCINE TRIAL PREPARATION - AN INTRODUCTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS ID HIV AB Preparations for large-scale trials to test the efficacy of candidate HIV vaccines can benefit in several crucial ways from a targeted program of behavioral and social research. Randomized field experiments testing alternative procedures for the recruitment and retention of subjects can help identify research procedures that will ensure adequate sample sizes while minimizing sample attrition over time. Similarly, assuring that subjects accurately comprehend the potential risks of participation will require more than simply presenting scientifically accurate information. Ensuring both the adequacy and appropriateness of risk communications as well as the accuracy of subject perception of risks (across the social and cultural milieux in which vaccine trials will be undertaken) is a critical task. Ethnographic and behavioral studies can help to ensure that our obligation to obtain truly informed consent from our research subjects is fully met and documented. Monitoring risk behaviors over the course of the vaccine trials could also benefit from strategic investments in new technologies developed by social researchers to permit the collection of sensitive personal data while affording complete privacy to subjects. These new measurement technologies include procedures that permit private data collection (without a human interviewer) in any spoken language and without requiring that subjects be literate. C1 NIAID,DIV AIDS,BETHESDA,MD 20892. RP TURNER, CF (reprint author), RES TRIANGLE INST,PROGRAM HLTH & BEHAV MEASUREMENT,6101 EXECUT BLVD,ROCKVILLE,MD 20852, USA. NR 16 TC 14 Z9 14 U1 1 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S273 EP S276 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800141 PM 7865317 ER PT J AU VERMUND, SH AF VERMUND, SH TI THE ROLE OF PREVENTION RESEARCH IN HIV VACCINE TRIALS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS AB The National Institute of Allergy and Infectious Diseases has prepared for HIV vaccine efficacy trials with the hope of having a product which is deemed worthy of testing. This has entailed development of new field research infrastructure and training, in collaboration with many partners. Notably, experts in observational research and experts in field HIV prevention research have joined together in efforts to share their mutually reinforcing experiences. In crafting these potential trial sites, it has become evident that the same criteria that apply in vaccine site suitability should also apply to other prevention clinical trials. These criteria include novel approaches to barriers to sexual transmission, including topical microbicides/spermicides, treatment of sexually transmitted infections, reduction in intrapartum blood contamination, and various strategies to ensure clean needle use. Like vaccines, most of these interventions are theoretically plausible, but remain untested. With or without large scale vaccine trials, these other prevention technologies remain high priorities for HIV research. C1 NIAID,DIV AIDS,BETHESDA,MD. NR 0 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S303 EP S305 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800152 PM 7865326 ER PT J AU WALKER, MC WALKER, BD MESTECKY, J MATHIESON, BJ AF WALKER, MC WALKER, BD MESTECKY, J MATHIESON, BJ TI CONFERENCE ON ADVANCES IN AIDS VACCINE DEVELOPMENT - 1993 - SUMMARY - CYTOTOXIC T-CELL IMMUNITY WORKSHOP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Advances in AIDS Vaccine Development - 6th Annual Meeting of the National-Cooperative-Vaccine-Development-Group-for-AIDS CY OCT 30-NOV 04, 1993 CL ALEXANDRIA, VA SP NATL COOPERAT VACCINE DEV GRP AIDS, NIAID, DIV AIDS, VACCINE TEAM, FOGARTY INT CTR, AIDS INT TRAINING RES PROGRAM, CTR DIS CONTROL & PREVENT, FDA, NIDA, US AGCY INT DEV, NIAID, OFF TROP MED & INT RES, WHO, GLOBAL PROGRAMME AIDS ID IMMUNODEFICIENCY-VIRUS TYPE-1; GP160 SUBUNIT VACCINE; LYMPHOCYTE RESPONSES; ENVELOPE PROTEIN; CD4+; ELICITS C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. RP WALKER, MC (reprint author), NIAID,DIV AIDS,VACCINE RES & DEV BRANCH,6003 EXECUT BLVD,SOLAR BLDG, ROOM 2A29,BETHESDA,MD 20892, USA. NR 34 TC 3 Z9 4 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1994 VL 10 SU 2 BP S177 EP S179 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA PT118 UT WOS:A1994PT11800093 PM 7865295 ER PT J AU GREENBERG, SS XIE, JM WANG, Y MALINSKI, T SUMMER, WR MCDONOUGH, K AF GREENBERG, SS XIE, JM WANG, Y MALINSKI, T SUMMER, WR MCDONOUGH, K TI ESCHERICHIA-COLI INDUCED-INHIBITION OF ENDOTHELIUM-DEPENDENT RELAXATION AND GENE-EXPRESSION AND RELEASE OF NITRIC-OXIDE IS ATTENUATED BY CHRONIC ALCOHOL INGESTION SO ALCOHOL LA English DT Article DE NITRIC OXIDE; ETHANOL; ESCHERICHIA COLI; NITROGLYCERIN; AORTA; ADRENAL ID ETHANOL-INDUCED CONTRACTION; RAT THORACIC AORTA; TOLERANCE; CELLS; ENDOTOXIN; SYNTHASE; EDRF AB We examined the effect of chronic administration of ETOH on Escherichia coli-mediated suppression of relaxation and nitric oxide (NO) production by the rat thoracic aorta (RTA) and gene expression for constitutive NO synthase (cNOS) by the adrenal gland. Chronic alcoholic rats (''alcoholic'') were fed a diet containing ETOH as 36% of the caloric intake for 8-10 weeks. Nonalcoholic control rats (''control'') were fed an isocaloric equivalent diet containing 36% dextrin. Alcoholic rats were given an injection of similar to similar to 10(10) live E. coli through a dorsal SC catheter 24 and 19 h before experimentation (''alcoholic-septic''), and control rats were treated in an identical manner (''septic''). The next day the rats were anesthetized with ketamine-xylazine (0.1 ml/100 g rat) and rings of RTA were mounted is muscle chambers for isometric recording of force development. Rings of RTA were precontracted with an EC(50) concentration of phenylephrine, and relaxation to acetylcholine (ACh), A23187, and nitroglycerin were obtained. A23187- and ACh-induced relaxation were attenuated in RTA obtained from septic rats, whereas the relaxation to nitroglycerin was slightly enhanced. Chronic administration of ETOH attenuated the effects of E. coli on endothelium-dependent relaxation in alcoholic-septic rats. NO was measured with ozone chemiluminescence. Basal and simulated NO production was attenuated in RTA obtained from septic rats and unaffected in TRA obtained from alcoholic or alcoholic-septic rats. cNOS was unmeasurable in adrenals from septic rats. ETOH increased mRNA and cNOS, an effect amplified in alcoholic-septic rats. Thus E. coli inhibits endothelium-dependent relaxation and NO production, and ETOH attenuates these effects of E. coli on the endothelium-NO system, possibly by upregulating gene expression for cNOS. C1 LOUISIANA STATE UNIV,MED CTR,DEPT PHYSIOL,PULM & CRIT CARE MED SECT,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,DEPT PHARMACOL,PULM & CRIT CARE MED SECT,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,NIH,ALCOHOL RES CTR,NEW ORLEANS,LA 70112. OAKLAND UNIV,DEPT CHEM,ROCHESTER,MI 48309. RP GREENBERG, SS (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT MED,PULM & CRIT CARE MED SECT,SUITE 3205,1901 PERDIDO ST,NEW ORLEANS,LA 70112, USA. FU NIAAA NIH HHS [NIAAA AA07747] NR 36 TC 31 Z9 31 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0741-8329 J9 ALCOHOL JI Alcohol PD JAN-FEB PY 1994 VL 11 IS 1 BP 53 EP 60 DI 10.1016/0741-8329(94)90012-4 PG 8 WC Substance Abuse; Pharmacology & Pharmacy; Toxicology SC Substance Abuse; Pharmacology & Pharmacy; Toxicology GA MV745 UT WOS:A1994MV74500010 PM 7511391 ER PT J AU DEITZ, D ROHDE, F BERTOLUCCI, D DUFOUR, M AF DEITZ, D ROHDE, F BERTOLUCCI, D DUFOUR, M TI PREVALENCE OF SCREENING FOR ALCOHOL-USE BY PHYSICIANS DURING ROUTINE PHYSICAL-EXAMINATIONS SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article ID DRINKING; DRINKERS AB In the survey presented here, primary care patients were asked whether physicians inquired about their alcohol consumption during routine office visits. Results show that both demographics and the patient's health status affect how often the physician asked about alcohol use. In addition, the majority of survey respondents, who were seen for a checkup within the last 2 years, were not asked about their alcohol consumption. C1 NIAAA,DIV BIOMETRY & EPIDEMIOL,EPIDEMIOL BRANCH,ROCKVILLE,MD 20852. RP DEITZ, D (reprint author), CYGNUS CORP,WASHINGTON,DC, USA. NR 15 TC 22 Z9 22 U1 0 U2 0 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1994 VL 18 IS 2 BP 162 EP 168 PG 7 WC Substance Abuse SC Substance Abuse GA QA079 UT WOS:A1994QA07900013 ER PT J AU SVIKIS, DS VELEZ, ML PICKENS, RW AF SVIKIS, DS VELEZ, ML PICKENS, RW TI GENETIC-ASPECTS OF ALCOHOL-USE AND ALCOHOLISM IN WOMEN SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article ID DOPAMINE-D2 RECEPTOR GENE; CROSS-FOSTERING ANALYSIS; POPULATION TWIN SAMPLE; CONSUMPTION PATTERNS; INHERITANCE; RISK; ASSOCIATION; ABUSE; PERSONALITY; FREQUENCY AB The factors influencing alcohol use and alcoholism are not the same in women as in men. Genetic factors may contribute to these differences. C1 NIDA,INTRAMURAL RES PROGRAM,ROCKVILLE,MD. RP SVIKIS, DS (reprint author), JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205, USA. NR 41 TC 8 Z9 8 U1 3 U2 4 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1994 VL 18 IS 3 BP 192 EP 196 PG 5 WC Substance Abuse SC Substance Abuse GA QN297 UT WOS:A1994QN29700005 ER PT J AU GRANT, BF HARFORD, TC DAWSON, DA CHOU, P DUFOUR, M PICKERING, R AF GRANT, BF HARFORD, TC DAWSON, DA CHOU, P DUFOUR, M PICKERING, R TI PREVALENCE OF DSM-IV ALCOHOL-ABUSE AND DEPENDENCE - UNITED-STATES, 1992 SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article AB For the first time, results are presented on the prevalence of alcohol abuse and dependence in the United States in 1992, according to the most recent psychiatric classification of alcohol-related disorders from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV). More than 7 percent of adults surveyed met DSM-IV criteria for 1-year alcohol abuse, alcohol dependence, or both. Males were almost three times more likely than females to meet the criteria for alcohol abuse and/or dependence; however, the male-to-female ratio was lowest in the youngest age group among nonblack respondents, suggesting that the rates of these disorders in nonblack females may be catching up. RP GRANT, BF (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,BIOMETRY BRANCH,BETHESDA,MD 20892, USA. NR 8 TC 239 Z9 241 U1 0 U2 3 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1994 VL 18 IS 3 BP 243 EP 248 PG 6 WC Substance Abuse SC Substance Abuse GA QN297 UT WOS:A1994QN29700013 ER PT J AU MATTSON, ME AF MATTSON, ME TI PATIENT TREATMENT MATCHING - RATIONALE AND RESULTS SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article ID ALCOHOLISM-TREATMENT; DRINKERS; THERAPY AB Because most treatment experts now agree that no single therapy produces the best outcomes for all patients with alcohol problems, researchers are becoming interested in matching patients to certain types of treatments based on the characteristics that each patient possesses. RP MATTSON, ME (reprint author), NIAAA,PROJECT MATCH,BETHESDA,MD, USA. NR 41 TC 16 Z9 16 U1 0 U2 0 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1994 VL 18 IS 4 BP 287 EP 295 PG 9 WC Substance Abuse SC Substance Abuse GA QV244 UT WOS:A1994QV24400006 ER PT J AU BUCKHOLTZ, NS RADEBAUGH, TS AF BUCKHOLTZ, NS RADEBAUGH, TS TI NATIONAL INSTITUTE ON AGING COLLABORATIVE STUDIES IN THE STANDARDIZATION OF COGNITIVE MEASURES SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Editorial Material ID ALZHEIMERS-DISEASE CERAD; NEUROPSYCHOLOGICAL MEASURES; CONSORTIUM; ESTABLISH; REGISTRY RP BUCKHOLTZ, NS (reprint author), NIA,NEUROSCI & NEUROPSYCHOL AGING PROGRAM,GATEWAY BLDG,SUITE 3C307,7201 WISCONSIN AVE,BETHESDA,MD 20892, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PY 1994 VL 8 SU 1 BP S214 EP S216 PG 3 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA NL737 UT WOS:A1994NL73700022 PM 8068262 ER PT J AU HOLMES, D SPLAINE, M TERESI, J ORY, M BARRETT, V MONACO, C RAMIREZ, M AF HOLMES, D SPLAINE, M TERESI, J ORY, M BARRETT, V MONACO, C RAMIREZ, M TI WHAT MAKES SPECIAL CARE SPECIAL - CONCEPT MAPPING AS A DEFINITIONAL TOOL SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article ID PATTERN-MATCHING APPROACH; CONSTRUCT-VALIDITY; NURSING-HOMES; UNITS C1 COMMUNITY RES APPLICAT INC,NEW YORK,NY. COLUMBIA UNIV,CTR GERIATR & GERONTOL,NEW YORK,NY. NEW YORK STATE DEPT MENTAL HLTH,NEW YORK,NY. ALZHEIMERS ASSOCIAT,DIV PUBL POLICY,BETHESDA,MD. NIA,BETHESDA,MD 20892. RP HOLMES, D (reprint author), HEBREW HOME AGED,5901 PALISADE AVE,RIVERDALE,NY 10471, USA. NR 21 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PY 1994 VL 8 SU 1 BP S41 EP S53 PG 13 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA NL737 UT WOS:A1994NL73700005 PM 8068288 ER PT J AU HOLMES, D LINDEMAN, D ORY, M TERESI, J AF HOLMES, D LINDEMAN, D ORY, M TERESI, J TI MEASUREMENT OF SERVICE UNITS AND COSTS OF CARE FOR PERSONS WITH DEMENTIA IN SPECIAL CARE UNITS SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article C1 RUSH PRESBYTERIAN ST LUKES MED CTR,RUSH INST AGING,CHICAGO,IL 60612. RUSH PRESBYTERIAN ST LUKES MED CTR,RUSH ALZHEIMERS DIS CTR,CHICAGO,IL 60612. RUSH UNIV,CHICAGO,IL 60612. NIA,BETHESDA,MD 20892. COLUMBIA UNIV,CTR GERIATR & GERONTOL,NEW YORK,NY. COMMUNITY RES APPLICAT INC,CHICAGO,IL. RP HOLMES, D (reprint author), HEBREW HOME AGED,5901 PALISADE AVE,RIVERDALE,NY 10471, USA. NR 32 TC 1 Z9 1 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PY 1994 VL 8 SU 1 BP S328 EP S340 PG 13 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA NL737 UT WOS:A1994NL73700036 PM 8068276 ER PT J AU HOLMES, D ORY, MG TERESI, J AF HOLMES, D ORY, MG TERESI, J TI DEMENTIA SPECIAL CARE - OVERVIEW OF RESEARCH POLICY AND PRACTICE SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article C1 COMMUNITY RES APPLICAT,BETHESDA,MD. NIA,BETHESDA,MD 20892. COLUMBIA UNIV,CTR GERIATR & GERONTOL,NEW YORK,NY. NEW YORK STATE DEPT MENTAL HLTH,NEW YORK,NY. RP HOLMES, D (reprint author), HEBREW HOME AGED,5901 PALISADE AVE,RIVERDALE,NY 10471, USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PY 1994 VL 8 SU 1 BP S5 EP S13 PG 9 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA NL737 UT WOS:A1994NL73700003 PM 8068293 ER PT J AU MAAS, ML SWANSON, EA SPECHT, JP BUCKWALTER, KC AF MAAS, ML SWANSON, EA SPECHT, JP BUCKWALTER, KC TI A NURSING PERSPECTIVE ON SCUS SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article ID LONG-TERM CARE; ALZHEIMERS-DISEASE; UNITS C1 NIA,BETHESDA,MD 20892. NR 37 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PY 1994 VL 8 SU 1 BP S417 EP S424 PG 8 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA NL737 UT WOS:A1994NL73700049 PM 8068290 ER PT J AU MONJAN, AA AF MONJAN, AA TI SLEEP AND DEMENTIA - MEASUREMENT ISSUES SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Editorial Material ID HUMAN CIRCADIAN PACEMAKER; OLDER-PEOPLE; LIGHT RP MONJAN, AA (reprint author), NIA,BETHESDA,MD 20892, USA. NR 20 TC 2 Z9 2 U1 2 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PY 1994 VL 8 SU 1 BP S223 EP S226 PG 4 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA NL737 UT WOS:A1994NL73700024 PM 8068264 ER PT J AU ORY, MG AF ORY, MG TI DEMENTIA SPECIAL CARE - THE DEVELOPMENT OF A NATIONAL RESEARCH INITIATIVE SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Editorial Material RP ORY, MG (reprint author), NIA,SOCIAL SCI RES AGING BEHAV & SOCIAL RES PROGRAM,GATEWAY BLDG ROOM 533,BETHESDA,MD 20892, USA. NR 6 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PY 1994 VL 8 SU 1 BP S389 EP S394 PG 6 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA NL737 UT WOS:A1994NL73700044 PM 8068284 ER PT J AU TERESI, J LAWTON, MP ORY, M HOLMES, D AF TERESI, J LAWTON, MP ORY, M HOLMES, D TI MEASUREMENT ISSUES IN CHRONIC CARE POPULATIONS - DEMENTIA SPECIAL CARE SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Review ID EVALUATION INTERVIEW SCHEDULE; ALZHEIMERS-DISEASE PATIENTS; VISUAL EVOKED-POTENTIALS; NURSING-HOME RESIDENTS; MINI-MENTAL STATE; COMPREHENSIVE ASSESSMENT; INDICATOR-SCALES; COGNITIVE DYSFUNCTION; GERIATRIC DEPRESSION; PSYCHIATRIC-ILLNESS C1 COLUMBIA UNIV,CTR GERIATR & GERONTOL,NEW YORK,NY. NEW YORK DEPT MENTAL HLTH,NEW YORK,NY. PHILADELPHIA GERIATR CTR,PHILADELPHIA,PA. NIA,BETHESDA,MD 20892. RP TERESI, J (reprint author), HEBREW HOME AGED,5901 PALISADE AVE,RIVERDALE,NY 10471, USA. NR 274 TC 25 Z9 25 U1 3 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PY 1994 VL 8 SU 1 BP S144 EP S183 PG 40 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA NL737 UT WOS:A1994NL73700017 PM 8068256 ER PT J AU MORRISON, AR AF MORRISON, AR TI ANIMALS IN EDUCATION SO AMERICAN BIOLOGY TEACHER LA English DT Letter RP MORRISON, AR (reprint author), NIMH,PROGRAM ANIM RES ISSUES,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU NATL ASSOC BIOLOGY TEACHERS INC PI RESTON PA 11250 ROGER BACON DR #19, RESTON, VA 22090 SN 0002-7685 J9 AM BIOL TEACH JI Am. Biol. Teach. PD JAN PY 1994 VL 56 IS 1 BP 7 EP 8 PG 2 WC Biology; Education, Scientific Disciplines SC Life Sciences & Biomedicine - Other Topics; Education & Educational Research GA MP891 UT WOS:A1994MP89100005 ER PT J AU THOTAKURA, NR MORRILL, T AF THOTAKURA, NR MORRILL, T TI GLYCAN MAPPING AND SEQUENCING OF RECOMBINANT HUMAN TSH SO AMERICAN BIOTECHNOLOGY LABORATORY LA English DT Article C1 OXFORD GLYCOSYST,ROSEDALE,NY 11422. RP THOTAKURA, NR (reprint author), NIDDKD,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD, USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU INT SCIENTIFIC COMMUN INC PI SHELTON PA PO BOX 870, 30 CONTROLS DRIVE, SHELTON, CT 06484-0870 SN 0749-3223 J9 AM BIOTECHNOL LAB JI Am. Biotechnol. Lab. PD JAN PY 1994 VL 12 IS 1 BP 42 EP 42 PG 1 WC Biotechnology & Applied Microbiology; Medical Laboratory Technology SC Biotechnology & Applied Microbiology; Medical Laboratory Technology GA MX716 UT WOS:A1994MX71600007 PM 7764412 ER PT J AU SHIRANI, J BEREZOWSKI, K ROBERTS, WC AF SHIRANI, J BEREZOWSKI, K ROBERTS, WC TI OUT-OF-HOSPITAL SUDDEN-DEATH FROM LEFT-VENTRICULAR FREE-WALL RUPTURE DURING ACUTE MYOCARDIAL-INFARCTION AS THE FIRST AND ONLY MANIFESTATION OF ATHEROSCLEROTIC CORONARY-ARTERY DISEASE SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Note ID FREQUENCY; NECROPSY; MODE C1 NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. NR 5 TC 13 Z9 14 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD JAN 1 PY 1994 VL 73 IS 1 BP 88 EP 92 DI 10.1016/0002-9149(94)90733-1 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA MP703 UT WOS:A1994MP70300017 PM 8279385 ER PT J AU BLOCK, G SINHA, R GRIDLEY, G AF BLOCK, G SINHA, R GRIDLEY, G TI COLLECTION OF DIETARY-SUPPLEMENT DATA AND IMPLICATIONS FOR ANALYSIS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE VITAMIN-C; VITAMIN-E; BETA-CAROTENE; VITAMINS; DIETARY SUPPLEMENTS; EPIDEMIOLOGIC METHODS; MISCLASSIFICATION ID UNITED-STATES POPULATION; NHANES-II SURVEY; EPIDEMIOLOGIC EVIDENCE; PHARYNGEAL CANCER; QUANTITATIVE DATA; NUTRIENT SOURCES; AMERICAN DIET; FOOD SOURCES; VITAMIN-A; QUESTIONNAIRE AB The role of nutrient intake in disease outcome is often examined in epidemiologic studies. Most such studies conducted in the United States, however, have not included fortified foods or vitamin supplements. In the United States, these are important sources of vitamins C and E, but not of beta-carotene. In addition, the importance of these nutrient sources varies by race, sex, and age. Failure to include these sources produces errors in nutrient estimates, notable misclassification of individuals with regard to their total intake, and rankings of intake that bear little or no relationship to blood concentrations of those nutrients. Implications for statistical analysis are also considered. Risk analyses in which nutrients from supplements are handled as control variables or are analyzed separately may impair the ability to detect associations between total nutrient intake and disease risk. The additional source of misclassification of nutrient status for vitamins C and E and other nutrients derived from fortified foods or supplements would make it more difficult to obtain significant and consistent results in etiologic studies of these nutrients; this has not been a factor for beta-carotene, which is derived almost exclusively from fruits and vegetables. C1 NCI, DIV CANC ETIOL, BETHESDA, MD 20892 USA. RP BLOCK, G (reprint author), UNIV CALIF BERKELEY, DEPT NUTR, 419 WARREN HALL, BERKELEY, CA 94720 USA. RI Block, Gladys/E-3304-2010; Sinha, Rashmi/G-7446-2015 OI Sinha, Rashmi/0000-0002-2466-7462 NR 31 TC 84 Z9 84 U1 2 U2 3 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1994 VL 59 IS 1 SU S BP 232S EP 239S PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MQ079 UT WOS:A1994MQ07900021 PM 8279432 ER PT J AU KREBSSMITH, SM HEIMENDINGER, J SUBAR, AF PATTERSON, BH PIVONKA, E AF KREBSSMITH, SM HEIMENDINGER, J SUBAR, AF PATTERSON, BH PIVONKA, E TI ESTIMATING FRUIT AND VEGETABLE INTAKE USING FOOD FREQUENCY QUESTIONNAIRES - A COMPARISON OF INSTRUMENTS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract DE DIETARY ASSESSMENT; FOOD FREQUENCIES C1 NCI, BETHESDA, MD 20892 USA. PRODUCE BETTER HLTH FDN, NEWARK, DE USA. NR 0 TC 10 Z9 10 U1 0 U2 1 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1994 VL 59 IS 1 SU S BP 283S EP 283S PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MQ079 UT WOS:A1994MQ07900032 ER PT J AU LONGNECKER, MP LISSNER, L HOLDEN, JM FLACK, VF TAYLOR, PR STAMPFER, MJ WILLETT, WC AF LONGNECKER, MP LISSNER, L HOLDEN, JM FLACK, VF TAYLOR, PR STAMPFER, MJ WILLETT, WC TI THE VALIDITY OF A SELF-ADMINISTERED SEMIQUANTITATIVE FOOD FREQUENCY QUESTIONNAIRE IN A POPULATION-CROSS-SECTION SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract DE DIETARY ASSESSMENT; FOOD FREQUENCY; VALIDITY C1 UNIV CALIF LOS ANGELES, SCH PUBL HLTH, DEPT EPIDEMIOL, LOS ANGELES, CA 90024 USA. GOTHENBURG UNIV, S-41124 GOTHENBURG, SWEDEN. USDA, NUTRIENT COMPOSIT LAB, BELTSVILLE, MD 20705 USA. UNIV CALIF LOS ANGELES, SPH, LOS ANGELES, CA 90024 USA. NCI, DCPC, CPSB, BETHESDA, MD 20892 USA. HARVARD UNIV, CAMBRIDGE, MA 02138 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1994 VL 59 IS 1 SU S BP 283S EP 283S PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MQ079 UT WOS:A1994MQ07900033 ER PT J AU HARTMAN, AM BLOCK, G CHAN, W WILLIAMS, J MCADAMS, M AF HARTMAN, AM BLOCK, G CHAN, W WILLIAMS, J MCADAMS, M TI REPRODUCIBILITY OF A SELF-ADMINISTERED DIET HISTORY QUESTIONNAIRE OVER DIFFERENT SEASONS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract DE DIETARY ASSESSMENT; FOOD FREQUENCY; SEASONALITY; RELIABILITY C1 NCI, BETHESDA, MD 20892 USA. UNIV CALIF BERKELEY, BERKELEY, CA 94720 USA. MED COLL WISCONSIN, MILWAUKEE, WI 53226 USA. IMS, SILVER SPRING, MD USA. RI Block, Gladys/E-3304-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1994 VL 59 IS 1 SU S BP 285S EP 285S PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MQ079 UT WOS:A1994MQ07900040 ER PT J AU NICKLAS, TA TRENKNER, L MONTGOMERY, D ZIVE, M EBZERY, MK EVANS, M AF NICKLAS, TA TRENKNER, L MONTGOMERY, D ZIVE, M EBZERY, MK EVANS, M TI USE OF A FOOD RECORD ASSISTED 24-HOUR DIETARY RECALL ON 3RD GRADE STUDENTS IN A MULTICENTER TRIAL SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract DE DIETARY ASSESSMENT; FOOD RECORD RECALL; SCHOOLCHILDREN C1 NHLBI, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1994 VL 59 IS 1 SU S BP 293S EP 293S PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MQ079 UT WOS:A1994MQ07900069 ER PT J AU CRAWFORD, PAB OBARZANEK, E BARTON, B MORRISON, J AF CRAWFORD, PAB OBARZANEK, E BARTON, B MORRISON, J TI VALIDATION OF DIETARY METHODOLOGY WITH 9-YEAR-OLD AND 10-YEAR-OLD GIRLS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract DE DIETARY ASSESSMENT; EVALUATION OF METHODS; SCHOOL-AGE GIRLS C1 UNIV CALIF BERKELEY, SCH PUBL HLTH, BERKELEY, CA 94720 USA. NHLBI, BETHESDA, MD 20892 USA. MARYLAND MED RES INST, BALTIMORE, MD USA. CHILDRENS HOSP MED CTR, CINCINNATI, OH 45229 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1994 VL 59 IS 1 SU S BP 294S EP 294S PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MQ079 UT WOS:A1994MQ07900071 ER PT J AU HOLDEN, JM MANGELS, AR CHUGAHUJA, JK BEECHER, GR FORMAN, M LANZA, E AF HOLDEN, JM MANGELS, AR CHUGAHUJA, JK BEECHER, GR FORMAN, M LANZA, E TI THE DEVELOPMENT OF A CAROTENOIDS DATABASE FOR THE ASSESSMENT OF CAROTENOID INTAKE BY DIVERSE POPULATIONS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract DE DIETARY ASSESSMENT; CAROTENOIDS DATABASE C1 USDA, NUTRIENT COMPOSIT LAB, WASHINGTON, DC 20250 USA. GEORGETOWN UNIV, DEPT MED, WASHINGTON, DC USA. UNIV MARYLAND, DEPT CHEM, COLL PK, MD 20742 USA. NCI, DIV CANC PREVENT & CONTROL, BETHESDA, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1994 VL 59 IS 1 SU S BP 298S EP 298S PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MQ079 UT WOS:A1994MQ07900085 ER PT J AU SUBAR, AF FREY, CM HARLAN, LC AF SUBAR, AF FREY, CM HARLAN, LC TI DIFFERENCES IN REPORTED FOOD FREQUENCY BY SEASON OF QUESTIONNAIRE ADMINISTRATION - THE 1987 NATIONAL-HEALTH INTERVIEW SURVEY (NHIS) SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract DE DIETARY ASSESSMENT; FOOD FREQUENCY; SEASONALITY C1 NCI, APPL RES BRANCH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1994 VL 59 IS 1 SU S BP 303S EP 303S PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA MQ079 UT WOS:A1994MQ07900100 ER PT J AU BRIGGS, NC JEFFERSON, JW AF BRIGGS, NC JEFFERSON, JW TI UNTITLED SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Letter ID MONOAMINE-OXIDASE INHIBITOR; WITHDRAWAL PHENOMENA C1 DEAN FDN,MADISON,WI 53717. RP BRIGGS, NC (reprint author), NIMH,CLIN SCI LAB,CLIN NEUROPHARMACOL SECT,10-3D41,BETHESDA,MD 20892, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1994 VL 20 IS 1 BP 125 EP 125 DI 10.3109/00952999409084062 PG 1 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA MY615 UT WOS:A1994MY61500010 PM 8192131 ER PT J AU KOLAR, AF BROWN, BS HAERTZEN, CA MICHAELSON, BS AF KOLAR, AF BROWN, BS HAERTZEN, CA MICHAELSON, BS TI CHILDREN OF SUBSTANCE-ABUSERS - THE LIFE EXPERIENCES OF CHILDREN OF OPIATE ADDICTS IN METHADONE-MAINTENANCE SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID PARENTS AB We interviewed 70 substance abusers in methadone maintenance treatment regarding the life experiences of their 188 children. Sixty-four percent of the mothers reported using psychoactive drugs during their pregnancies. Eighty percent of parents reported an arrest during the time the child was growing up, 34% reported receiving treatment for an emotional disorder, and 14% were hospitalized. Four percent of the parents reported that their children had been placed in adoptive care, 9% in foster care, and 1% had a child in a group home. Forty-one percent of the parents reported that at least one of their children repeated a grade in school, 19% were involved in truancy, and 30% had been suspended from school. Twenty percent of parents reported their children's involvement with the law, and 17% reported drug or alcohol use. Problems with the law correlated highly with 1) being held back a grade, 2) truancy, 3) suspension from school, 4) expulsion from school, and 5) treatment for alcohol or drug abuse. C1 NATL INST DRUG ABUSE,ADDICT RES CTR,BALTIMORE,MD 21224. NR 23 TC 43 Z9 43 U1 1 U2 3 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1994 VL 20 IS 2 BP 159 EP 171 DI 10.3109/00952999409106780 PG 13 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA NJ038 UT WOS:A1994NJ03800002 PM 8042601 ER PT J AU CHU, KC BROWN, CC AF CHU, KC BROWN, CC TI ARSENIC INGESTION AND INTERNAL CANCERS - A REVIEW SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter ID MULTISTAGE THEORY; EXPOSURE RP CHU, KC (reprint author), NCI,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI 张, 楠/B-1010-2010 NR 8 TC 1 Z9 1 U1 0 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JAN 1 PY 1994 VL 139 IS 1 BP 115 EP 116 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MT968 UT WOS:A1994MT96800011 PM 8296769 ER PT J AU BABLER, WJ MEIER, RJ PLATO, CC AF BABLER, WJ MEIER, RJ PLATO, CC TI DERMATOGLYPHICS - TODAY AND TOMORROW SO AMERICAN JOURNAL OF HUMAN BIOLOGY LA English DT Meeting Abstract C1 BAYLOR COLL DENT,DALLAS,TX 75266. INDIANA UNIV,DEPT ANTHROPOL,BLOOMINGTON,IN 47405. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 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 1042-0533 J9 AM J HUM BIOL JI Am. J. Hum. Biol. PY 1994 VL 6 IS 1 BP 115 EP 115 PG 1 WC Anthropology; Biology SC Anthropology; Life Sciences & Biomedicine - Other Topics GA NA672 UT WOS:A1994NA67200019 ER PT J AU GARRUTO, RM LITTLE, MA AF GARRUTO, RM LITTLE, MA TI THE MAN AND THE BIOSPHERE (MAB) PROGRAM AND BIOLOGY RESEARCH SO AMERICAN JOURNAL OF HUMAN BIOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. SUNY BINGHAMTON,BINGHAMTON,NY 13901. NR 0 TC 0 Z9 0 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 1042-0533 J9 AM J HUM BIOL JI Am. J. Hum. Biol. PY 1994 VL 6 IS 1 BP 122 EP 122 PG 1 WC Anthropology; Biology SC Anthropology; Life Sciences & Biomedicine - Other Topics GA NA672 UT WOS:A1994NA67200037 ER PT J AU RUSSELL, CM WILLIAMSON, DF BARTKO, JJ BRADLEY, EL AF RUSSELL, CM WILLIAMSON, DF BARTKO, JJ BRADLEY, EL TI SIMULATION STUDY OF A PANEL OF RELIABILITY INDICATORS APPLIED TO PAIRED MEASUREMENTS SO AMERICAN JOURNAL OF HUMAN BIOLOGY LA English DT Article ID ANTHROPOMETRIC MEASUREMENTS; AGREEMENT; HEALTH AB Reliability is a subject of continuing discussion in biomedial specialty areas, including physical anthropology and nutritional epidemiology. The purpose of this study was to explore techniques of detecting differences between two evaluators or methods. A field study in which anthropometric dimensions would be taken by two independent evaluators on each participant in a study group was simulated. A panel of reliability indicators was applied across a broad range of parameters using simulation, and then the panel was applied to field anthropometric data. The panel consisted of the intraclass correlation coefficient (ICC), paired t-test, a simultaneous test of evaluator means and variances, technical error of measurement, mean absolute difference, and mean difference. The simultaneous test for equal evaluator means and variances uses regression to model paired differences versus paired sums. The simulation demonstrated general properties of the reliability indicators across many conditions of population variance, measurer bias, and measurer error variance. High values of ICC often exist in cases in which the measurers are different. The simultaneous test is thus a powerful method for detecting measurer differences, especially when combined with the paired t-test. However, a single reliability indicator that is sufficient to determine all measurer inconsistencies was not identified. The field study and the simulation permitted the development of a logical approach to determining the source and magnitude of measurer differences using the panel of reliability indicators. (C) 1994 Wiley-Liss, Inc. C1 CTR DIS CONTROL & PREVENT,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,DIV NUTR,ATLANTA,GA 30341. UNIV ALABAMA,SCH PUBL HLTH,DEPT BIOSTAT,BIRMINGHAM,AL 35294. UNIV ALABAMA,SCH MED,DEPT BIOSTAT,BIRMINGHAM,AL 35294. UNIV ALABAMA,SCH DENT,DEPT BIOSTAT,BIRMINGHAM,AL 35294. MED COLL GEORGIA,DEPT ORAL DIAG,AUGUSTA,GA 30912. MED COLL GEORGIA,PATIENT SERV,AUGUSTA,GA 30912. NIMH,DRUG ALCOHOL ABUSE & MENT HLTH ADM,DIV APPL SERV RES,BETHESDA,MD 20892. RP RUSSELL, CM (reprint author), MED COLL GEORGIA,OFF BIOSTAT,AUGUSTA,GA 30912, USA. NR 18 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 1042-0533 J9 AM J HUM BIOL JI Am. J. Hum. Biol. PY 1994 VL 6 IS 3 BP 311 EP 320 DI 10.1002/ajhb.1310060306 PG 10 WC Anthropology; Biology SC Anthropology; Life Sciences & Biomedicine - Other Topics GA NN261 UT WOS:A1994NN26100005 ER PT J AU JUENGST, ET AF JUENGST, ET TI HUMAN GENOME RESEARCH AND THE PUBLIC-INTEREST - PROGRESS NOTES FROM AN AMERICAN SCIENCE POLICY EXPERIMENT SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID PROJECT; DISEASE AB This essay reviews the efforts of the U.S. Human Genome Project to anticipate and address the ethical, legal, and social implications of new advances in human genetics. Since 1990, approximately $10 million has been awarded by the National Institutes of Health and the Department of Energy, in support of 65 research, education, and public discussion projects. These projects address four major areas of need: (1) the need for both client-centered assessments of new genetic services and for improved knowledge of the psychosocial and ethnocultural factors that shape clients' clinical genetic experiences; (2) the need for clear professional policies regarding human-subject research, clinical practice standards, and public health goals in human genetics; (3) the need for social policy protection against unfair access to and use of personal genetic information; and (4) the need for improved public and professional understanding and discussion of these issues. The Human Genome Project's goal is to have defined, by 1995, policy options and programs capable of addressing these needs. RP JUENGST, ET (reprint author), NATL CTR HUMAN GENOME RES,ETHICAL LEGAL & SOCIAL IMPLICATIONS BRANCH,BLDG 38A,ROOM 617,BETHESDA,MD 20892, USA. OI Juengst, Eric/0000-0002-8374-5774 NR 46 TC 17 Z9 17 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JAN PY 1994 VL 54 IS 1 BP 121 EP 128 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA MQ700 UT WOS:A1994MQ70000016 PM 8279462 ER PT J AU GOLOMB, E HILL, MR BROWN, RG KEISER, HR AF GOLOMB, E HILL, MR BROWN, RG KEISER, HR TI OUABAIN ENHANCES THE MITOGENIC EFFECT OF SERUM IN VASCULAR SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article DE OUABAIN; C-FOS; C-MYC; VASCULAR SMOOTH MUSCLE CELLS; HYPERTENSION; POLYMERASE CHAIN REACTION AB Recently ouabain has been shown to induce transcription of proto-oncogenes in different cell types. In the present study, we examined the effect of ouabain on the proliferation of cultured vascular smooth muscle cells (VSMCs). Primary aortic VSMCs of spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats, and the rat VSMC cell line A10, were used. Different concentrations of ouabain (10(-9) to 10(-5) mol/L) were added to either quiescent or proliferating cells, and the cell number, the rate of thymidine incorporation into DNA, and the transcription of c-fos and c-myc were examined. The addition of ouabain to proliferating VSMC increased the rate of thymidine incorporation into DNA in a dose-dependent manner, and induced the transcription of the proto-oncogenes within 1 h. This latter response disappeared after 24 h. The number of cells significantly increased in response to low concentrations of ouabain (10(-8) to 10(-7) mol/L), but gradually decreased in response to higher concentrations of the agent, probably due to a toxic effect. Addition of ouabain to quiescent cells, in medium without serum, did not promote cell growth by any of the parameters examined. According to a current theory, endogenous digitalis-like substances possess natriuretic and hypertensive properties, and provide the link between an excessive intake of salt and high blood pressure. The mitogenic effect of ouabain on VSMCs may be a component of this hypertensive action. RP GOLOMB, E (reprint author), NHLBI,HYPERTENS ENDOCRINE BRANCH,9000 ROCKVILLE PIKE,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 31 Z9 31 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD JAN PY 1994 VL 7 IS 1 BP 69 EP 74 PG 6 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MQ684 UT WOS:A1994MQ68400010 PM 8136113 ER PT J AU LOCKSHIN, MD AF LOCKSHIN, MD TI LUPUS AND ANTIPHOSPHOLIPID ANTIBODY SYNDROME - EITHER, NEITHER, OR BOTH SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material ID ANTICARDIOLIPIN ANTIBODIES; CLINICAL IMPORTANCE; ERYTHEMATOSUS; INDUCTION; FEATURES RP LOCKSHIN, MD (reprint author), NIAMSD,EXTRAMURAL PROGRAM,BLDG 31, ROOM 4C-32,BETHESDA,MD 20892, USA. NR 15 TC 10 Z9 10 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD JAN PY 1994 VL 96 IS 1 BP 1 EP 2 DI 10.1016/0002-9343(94)90107-4 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA MU313 UT WOS:A1994MU31300001 PM 8304355 ER PT J AU BERCHUCK, A KOHLER, MF MARKS, JR WISEMAN, R BOYD, J BAST, RC AF BERCHUCK, A KOHLER, MF MARKS, JR WISEMAN, R BOYD, J BAST, RC TI THE P53 TUMOR-SUPPRESSOR GENE FREQUENTLY IS ALTERED IN GYNECOLOGIC CANCERS SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE P53; GYNECOLOGIC CANCER; TUMOR SUPPRESSOR GENE; MUTATION ID EPITHELIAL OVARIAN-CARCINOMA; HUMAN PAPILLOMAVIRUS TYPE-16; CERVICAL-CARCINOMA; ENDOMETRIAL CARCINOMA; PROTO-ONCOGENE; LUNG-CANCER; CELL-LINES; MUTATIONS; OVEREXPRESSION; ACCUMULATION AB Mutation of the p53 tumor suppressor gene, often accompanied by overexpression of mutant p53 protein, is the most frequent molecular genetic event described thus far in human cancers. In adenocarcinomas of the ovary and endometrium, p53 overexpression is seen in approximately 10% to 15% of early and 40% to 50% of advanced cancers. Similar to many other types of human cancers, ovarian and endometrial cancers that overexpress p53 protein contain mutations in conserved regions of the p53 gene. These mutations are predominantly transitions, which suggests that they arise spontaneously rather than being caused by carcinogen exposure. Alteration of the p53 gene does not appear to be a feature of endometrial hyperplasias or benign or borderline ovarian tumors. Although mutation and overexpression of p53 rarely occur in cancers of the cervix, vulva, and vagina, it has been shown that human papillomavirus E6 oncoproteins bind to and inactivate p53 protein. Studies of the p53 gene have begun to provide insight into the molecular pathogenesis of gynecologic cancers. C1 DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. DUKE UNIV,DEPT MED & IMMUNOL,DURHAM,NC. DUKE COMPREHENS CANC CTR,DURHAM,NC. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. RP BERCHUCK, A (reprint author), DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,BOX 3079,DURHAM,NC 27710, USA. RI Bast, Robert/E-6585-2011 OI Bast, Robert/0000-0003-4621-8462 FU NCI NIH HHS [CA 55640] NR 58 TC 159 Z9 164 U1 0 U2 3 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD JAN PY 1994 VL 170 IS 1 BP 246 EP 252 PN 1 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA MT975 UT WOS:A1994MT97500042 PM 8296829 ER PT J AU DVORAK, AM SEDER, RA PAUL, WE MORGAN, ES GALLI, SJ AF DVORAK, AM SEDER, RA PAUL, WE MORGAN, ES GALLI, SJ TI EFFECTS OF INTERLEUKIN-3 WITH OR WITHOUT THE C-KIT LIGAND, STEM-CELL FACTOR, ON THE SURVIVAL AND CYTOPLASMIC GRANULE FORMATION OF MOUSE BASOPHILS AND MAST-CELLS IN-VITRO SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID GROWTH-FACTOR; MOLECULAR-CLONING; SI-LOCUS; T-CELLS; RECEPTOR; IGE; IDENTIFICATION; RAT; CDNA AB We assessed the ultrastructure and the cell-surface expression of receptors for immunoglobulin E (Fc epsilon R), and c-kit, the receptor for stem cell factor (SCF), in mouse basophils and mast cells present in short-term cultures of mouse bone marrow cells in interleukin-3 (IL-3) with or without SCF. Basophils did not develop increased numbers of cytoplasmic granules and underwent apoptosis in cultures containing IL-3 and SCF, whereas mast cells thrived and developed increased numbers of granules. Basophils were nearly all Fc epsilon R(+) c-kit(-) when sorted after culture in IL-3 and SCF; most mast cells were Fc epsilon R(+) c-kit(+). However, a second population of Fc epsilon R(+) c-kit(-) mast cells was present after culture in IL-3 and SCF. These c-kit receptor-negative mast cells were less mature than c-kit(+) mast cells and contained significantly fewer cytoplasmic granules than the c-kit(+) mast cells present in the same cultures (P<0.0010). Thus, mouse basophils express little or no c-kit receptor on their surface, nor can the survive for long periods in SCF-supplemented cultures. By contrast, mouse mast cells seem to express the Fc epsilon R early in their development, even before they express detectable c-kit receptors on their surface. IL-3 promotes cytoplasmic granule formation in immature mast cells, but even more granules are formed when c-kit receptor-positive immature mast cells are cultured in both SCF and IL-3. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. BETH ISRAEL HOSP,CHARLES A DANA RES INST,BOSTON,MA 02215. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RP DVORAK, AM (reprint author), BETH ISRAEL HOSP,DEPT PATHOL,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NIAID NIH HHS [AI-33372, AI-22674, AI-23990] NR 30 TC 55 Z9 55 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JAN PY 1994 VL 144 IS 1 BP 160 EP 170 PG 11 WC Pathology SC Pathology GA MR310 UT WOS:A1994MR31000017 PM 7507298 ER PT J AU BURGENERKAIRUZ, P CORTHESYTHEULAZ, I MERILLAT, AM GOOD, P GEERING, K ROSSIER, BC AF BURGENERKAIRUZ, P CORTHESYTHEULAZ, I MERILLAT, AM GOOD, P GEERING, K ROSSIER, BC TI POLYADENYLATION OF NA+-K+-ATPASE BETA(1)-SUBUNIT DURING EARLY DEVELOPMENT OF XENOPUS-LAEVIS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CYTOPLASMIC POLYADENYLATION ELEMENT; MESSENGER RIBONUCLEIC ACID; STAGE VI OOCYTE ID AMPHIBIAN EMBRYONIC NEURONS; MATERNAL MESSENGER-RNA; BETA-SUBUNIT; INTRACELLULAR-TRANSPORT; ALPHA-SUBUNITS; MEIOTIC MATURATION; OOCYTE MATURATION; POLY(A) ADDITION; NERVOUS-SYSTEM; SODIUM-PUMP AB In fully grown Xenopus oocytes, the synthesis of beta-subunits is limiting for the formation of functional Na+-K+-adenosinetriphosphatase aip-complexes (Geering, K. FEBS Lett. 285: 189-193, 1991). In the present study, we show that during oocyte growth (from stage I to stage VI) alpha(1)-, but not beta(1)- or beta(3)-isoform, mRNAs accumulate. In addition, beta-mRNAs are apparently sequestered in an untranslated pool in fully grown oocytes (stage VI). From fertilization to morulation, the total pools of alpha(1)-, beta(1)-, or beta(3)-mRNAs vary little. Whereas polyadenylated [poly(A)(+)] alpha(1)- and beta(3)-isoform mRNAs did not change significantly, poly(A)(+) beta(1)-mRNA abundance increased three- to fourfold at morulation, accompanied by a parallel increase in beta(1)-protein synthesis. After midblastula transition (i.e., at early gastrula) and during neurulation, poly(A)(+) alpha(1)- and beta(3)-mRNAs accumulated rapidly, whereas poly(A)(+) beta(1)-mRNA accumulation was delayed by similar to 2 h, beginning only at early neurula. Our results indicate that 1) the abundance of poly(A)(+) beta(1)-mRNA is rate limiting during embryonic development for the assembly of alpha(1)/beta(1)-heterodimers, shown to be involved in the vectorial transport of sodium in kidney cells, and 2) the polyadenylation of beta(1)-mRNA is a rate-limiting factor during morulation for the synthesis and assembly of new sodium pumps at the time of blastocoel fluid formation. The 3'-untranslated region of beta(1)-mRNA (but not of alpha(1)-mRNA) expresses cytoplasmic polyadenylation elements (CPEs) with the consensus sequence AXXAUUUU(A/U)(A/U)(A/U). A role of CPE in the differential polyadenylation of alpha(1)- and beta(1)-mRNA is proposed. C1 NICHHD,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892. RP BURGENERKAIRUZ, P (reprint author), UNIV LAUSANNE,INST PHARMACOL & TOXICOL,CH-1005 LAUSANNE,SWITZERLAND. NR 46 TC 7 Z9 7 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP C157 EP C164 PN 1 PG 8 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100018 PM 8304412 ER PT J AU HARRIS, PJ CHATTON, JY TRAN, PH BUNGAY, PM SPRING, KR AF HARRIS, PJ CHATTON, JY TRAN, PH BUNGAY, PM SPRING, KR TI PH, MORPHOLOGY, AND DIFFUSION IN LATERAL INTERCELLULAR SPACES OF EPITHELIAL-CELL MONOLAYERS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE FLUORESCENCE MICROSCOPY; FLUORESCENCE RECOVERY AFTER PHOTOBLEACHING; FLUID TRANSPORT; MADIN-DARBY CANINE KIDNEY CELLS; LLC-PK1 CELLS ID LEAKY EPITHELIA; WATER TRANSPORT; KIDNEY; IDENTIFICATION; MICROSCOPY; PLAQUES; MODELS; FLOW; SALT AB The lateral intercellular spaces (LIS) of reabsorptive epithelia are the site ofthe proposed local osmotic gradient responsible for transepithelial transport. We developed techniques for loading the LIS of living cultured renal cells (MDCK and LLC-PK1) with the fluorescent dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF), visualizing LIS geometry, measuring pH, and determining the BCECF diffusion coefficient within the LIS. The LIS pH was remarkably constant and differed substantially from that of the superfusate in both the presence and absence of HCO3 or CO2. The LIS of MDCK cells had a pH of 7.66 +/- 0.04 in bicarbonate-free solutions of pH 7.0, 7.4, or 7.8. In bicarbonate-containing solutions, MDCK LTS pH was acidic to the superfusate by 0.3-0.4 units. In the absence of bicarbonate, the LIS of LLC-PK1 cells was markedly acidic (6.83 +/- 0.05), becoming alkaline by similar to 0.25 units in the presence of bicarbonate. Gradients in pH or dye concentration were not detected within the LIS. The diffusion coefficient of BCECF within the LIS was approximately equal to that seen in free solution. C1 NIH,NATL CTR RES SERV,BETHESDA,MD 20892. RP HARRIS, PJ (reprint author), NHLBI,BETHESDA,MD 20892, USA. NR 23 TC 44 Z9 44 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP C73 EP C80 PN 1 PG 8 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100009 PM 8304432 ER PT J AU SILVERMAN, HS DILISA, F HUI, RC MIYATA, H SOLLOTT, SJ HANSFORD, RG LAKATTA, EG STERN, MD AF SILVERMAN, HS DILISA, F HUI, RC MIYATA, H SOLLOTT, SJ HANSFORD, RG LAKATTA, EG STERN, MD TI REGULATION OF INTRACELLULAR FREE MG2+ AND CONTRACTION IN SINGLE ADULT MAMMALIAN CARDIAC MYOCYTES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MAGNESIUM; HYPOXIA; ENERGETICS ID CYTOSOLIC FREE MAGNESIUM; CHICKEN HEART-CELLS; ISCHEMIC RAT-HEART; SKELETAL-MUSCLE; VENTRICULAR MYOCYTES; CALCIUM; ATP; PH; REOXYGENATION; MITOCHONDRIA AB Studies in isolated cardiac myocytes have increased our understanding of intracellular Ca2+ regulation. Because less is known about Mg2+ regulation, adult rat ventricular myocytes were loaded with the Mg2+-sensitive fluorescent probe mag-indo 1, and changes in intracellular Mg2+ concentration ([Mg2+](i)) and cell length were examined under a variety of conditions. The fluorescent signal was calibrated intracellularly and found to differ slightly from that for the probe in solution. Roughly 40% of the signal was intramitochondrial; the remainder was localized in the cytosol. Basal [Mg2+](i) averaged 1.02 +/- 0.03 mM (n = 53 cells). No change in [Mg2+](i) was observed during a single electrically stimulated contraction, and only a minor increase was seen during rapid electrical stimulation, which was expected to raise intracellular Ca2+ concentration ([Ca2+](i)) to similar to 1 mu M. An acid shift in intracellular pH of similar to 1 pH unit was accompanied by a small change in [Mg2+](i) (0.34 +/- 0.03 mM, n = 6, P < 0.05). No change in [Mg2+](i) was observed when cells were superfused with 15 mM Mg2+, despite marked changes in contraction. [Mg2+](i) more than doubled when cells were depleted of ATP by exposure to hypoxia or metabolic inhibitors. The increase in [Mg2+](i) was abrupt and occurred at the time of the failure of contraction, plateauing as rigor contracture developed. Reoxygenation was accompanied by a gradual fall in [Mg2+](i) in cells that recovered mechanical function, and in a subset of cells that underwent hypercontracture. Studies in cell suspensions confirmed that rapid cellular energy depletion was accompanied by increases in [Mg2+](i) and parallel decreases in ATP. Thus [Mg2+](i) was largely insensitive to changes in [Ca2+](i) or pH(i) and extracellular [Mg2+] but was rapidly altered by changes in energy state in a manner that was related to specific changes in cell morphology and contractile function. C1 JOHNS HOPKINS MED INST,DIV CARDIOL,BALTIMORE,MD 21205. RP SILVERMAN, HS (reprint author), NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224, USA. FU NHLBI NIH HHS [K08-HL-02539, R01-HL-42050, P50-HL-17655] NR 36 TC 99 Z9 99 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP C222 EP C233 PN 1 PG 12 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100026 PM 8304418 ER PT J AU GIUSTINA, A LICINI, M SCHETTINO, M DOGA, M PIZZOCOLO, G NEGROVILAR, A AF GIUSTINA, A LICINI, M SCHETTINO, M DOGA, M PIZZOCOLO, G NEGROVILAR, A TI PHYSIOLOGICAL-ROLE OF GALANIN IN THE REGULATION OF ANTERIOR-PITUITARY FUNCTION IN HUMANS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ADRENOCORTICOTROPIC HORMONE; CORTISOL; GROWTH HORMONE ID GROWTH-HORMONE SECRETION; PROLACTIN SECRETION; MEDIAN-EMINENCE; RAT GALANIN; NEURONS; THYROTROPIN; INVOLVEMENT; MECHANISMS; PORCINE AB The aim of our study was to elucidate the physiological role of the neuropeptide galanin in the regulation of anterior pituitary function in human subjects. Six healthy men (age range 26-35 yr, body mass index range 20-24 kg/m(2)) underwent in random order 1) an intravenous bolus injection of growth hormone-releasing hormone (GHRH)-(1-29)-NH2 (100 mu g) + thyrotropin-releasing hormone (TRH, 200 mu g) + luteinizing hormone-releasing hormone (LHRH, 100 mu g) + corticotropin-releasing hormone (CRH, 100 mu g), and 2) intravenous saline (100 ml) at time 0 plus either human galanin (500 mu g) in saline (100 mo or saline (100 mi) from -15 to +30 min. Human galanin determined a significant increase in serum GH (GH peak: 11.3 +/- 2.2 mu g/l) from both baseline and placebo levels. No significant differences were observed between GH values after galanin and those after GHRH alone (24.3 +/- 5.2 mu g/l). Human galanin significantly enhanced the GH response to GHRH (peak 49.5 +/- 10 mu g/l) with respect to either GHRH or galanin alone. Human galanin caused a slight decrease in baseline serum adrenocorticotropic hormone (ACTH; 16.3 +/- 2.4 pg/ml) and cortisol levels (8 +/- 1.5 mu g/dl). Galanin also determined a slight reduction in both the ACTH (peak 27 +/- 8 pg/ml) and cortisol (peak 13.8 +/- 1.3 mu g/dl) responses to CRH. Baseline and releasing hormone-stimulated secretions of prolactin, thyroid-stimulating hormone, LK, and follicle-stimulating hormone were not altered by galanin. Our data suggest a physiological role for the neuropeptide galanin in the regulation of GH secretion in humans. A minor inhibitory role seems to be played by galanin in regulating ACTH and cortisol levels. C1 UNIV BRESCIA,CATTEDRA CLIN MED & CHIM,I-25125 BRESCIA,ITALY. NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. NR 30 TC 27 Z9 27 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP E57 EP E61 PN 1 PG 5 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100043 PM 7508194 ER PT J AU QUON, MJ AF QUON, MJ TI ADVANCES IN KINETIC-ANALYSIS OF INSULIN-STIMULATED GLUT-4 TRANSLOCATION IN ADIPOSE-CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GLUCOSE TRANSPORTER; MATHEMATICAL MODELING; COMPUTER SIMULATION ID GLUCOSE-TRANSPORT; PLASMA-MEMBRANE; EXPRESSION; SURFACE AB Advances in kinetic analysis of insulin-stimulated GLUT-4 translocation in adipose cells. Am. J. Physiol. 266 (Endocrinol. Metab. 29): E144-E150, 1994.-GLUT-4 is the major insulin-sensitive glucose transporter in muscle and adipose tissue. Regulation of GLUT-4 is an important component of whole body glucose homeostasis. Abnormalities in the regulation of insulin-stimulated reversible translocation of glucose transporters have been observed in various pathological states, including diabetes. Recently, the development of specific photolabels for glucose transporters and the availability of antibodies against the various transporter isoforms have presented the opportunity for detailed kinetic analysis of GLUT-4 regulation. A kinetic analysis of some of the most recent data is presented to demonstrate how this approach can advance the understanding of GLUT-4 regulation. Some areas in which the currently available data limit the ability to resolve certain mechanistic questions are noted. Using a two-compartment model, we show that the mechanism of insulin-stimulated GLUT-4 translocation is likely to involve a large increase in the exocytosis rate of GLUT-4 with a minimal decrease in the endocytosis rate. Mathematical models based on these kinetic analyses are helpful for testing hypotheses and designing experiments to elucidate the molecular and cellular mechanisms of GLUT-4 regulation under normal and pathological conditions. This type of approach may be useful for evaluating the contribution of GLUT-4 regulation to the pathogenesis of diabetes. RP QUON, MJ (reprint author), NIDDKD,DIABET BRANCH,BLDG 10,RM 8S-239,BETHESDA,MD 20892, USA. RI Quon, Michael/B-1970-2008 NR 21 TC 10 Z9 10 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP E144 EP E150 PN 1 PG 7 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100054 PM 8304439 ER PT J AU HAN, JS MAEDA, Y ECELBARGER, C KNEPPER, MA AF HAN, JS MAEDA, Y ECELBARGER, C KNEPPER, MA TI VASOPRESSIN-INDEPENDENT REGULATION OF COLLECTING DUCT WATER PERMEABILITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CARBACHOL; INTRACELLULAR CALCIUM; MUSCARINIC RECEPTORS; PHOSPHOINOSITIDE PATHWAY ID STIMULATED PHOSPHOINOSITIDE HYDROLYSIS; PROTEIN KINASE-C; CELLS; CALCIUM; TUBULE; HORMONE; CAMP; ACTIVATION; RECEPTOR; RISES AB Studies were conducted in microdissected rat terminal inner medullary collecting duct (IMCD) segments to determine whether agents that activate the phosphoinositide signaling pathway regulate osmotic water permeability independent of the action of vasopressin. Water was withheld from the rats for 24 h before the experiments, a procedure that yields a stably high osmotic water permeability in isolated perfused terminal IMCDs in the absence of vasopressin. In the present studies, the vasopressin-independent osmotic water permeability was sustained at similar to 300 mu m/s for at least 90 min. We used the cholinergic agent carbachol (10-100 mu M) to activate the phosphoinositide pathway. This agent has previously been reported to increase the hydrolysis of inositol phospholipids in IMCD cells without altering adenosine 3',5'-cyclic monophosphate production. In preliminary studies, we demonstrated (using fura 2) that carbachol transiently increases intracellular calcium and that this response was blocked by atropine, confirming that muscarinic receptors are coupled to activation of the phosphoinositide signaling pathway in these cells. In the absence of vasopressin, both carbachol (10 mu M) and phorbol myristate acetate (1 nM) inhibited osmotic water permeability by 40-50% within 10 min. These effects were partially blocked by calphostin C, an inhibitor of protein kinase C. These results demonstrate that activation of phosphatidylinositol hydrolysis and/or activation of protein kinase C markedly inhibits osmotic water permeability in isolated perfused IMCD segments, even in the absence of prior stimulation by vasopressin. C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. NR 30 TC 29 Z9 29 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP F139 EP F146 PN 2 PG 8 WC Physiology SC Physiology GA NA598 UT WOS:A1994NA59800102 PM 7905713 ER PT J AU JAFFA, AA LEROITH, D ROBERTS, CT RUST, PF MAYFIELD, RK AF JAFFA, AA LEROITH, D ROBERTS, CT RUST, PF MAYFIELD, RK TI INSULIN-LIKE GROWTH-FACTOR-I PRODUCES RENAL HYPERFILTRATION BY A KININ-MEDIATED MECHANISM SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE RENAL KALLIKREIN; KININ RECEPTOR ANTAGONIST; RENAL VASODILATION ID GLOMERULAR MESANGIAL CELLS; DIETARY-PROTEIN; FILTRATION RATE; PLASMA-FLOW; KIDNEY; KALLIKREIN; EXPRESSION; BINDING; RNA AB Insulin-like growth factor-I (IGF-I) infusion into rats and humans reduces renal vascular resistance and raises glomerular filtration rate (GFR) and renal plasma flow (RPF). To investigate whether kinins mediate the renal vasodilatory effects of IGF-I, we infused rats with IGF-I alone or in the presence of a B-2 kinin receptor antagonist. Left kidney GFR, RPF, and kinin excretion were measured during infusion of vehicle and subsequently during 60-min infusion ofIGF-I or IGF-I plus kinin antagonist. IGF-I was given as a bolus (150 mu g/kg body wt), followed by infusion at a rate of 8.3 mu g.kg(-1).min(-1) for 60 min. The kinin antagonist was infused at a dose of 1 mu g.kg(-1).min(-1) for 60 min before the start of IGF-I infusion. GFR and RPF increased significantly after IGF-I infusion was begun, from baseline levels of 1.70 +/- 0.12 and 6.21 +/- 0.34 to 2.12 +/- 0.11 and 7.91 +/-: 0.29 ml/min, respectively, at 20 min (P < 0.001). This effect was maintained throughout 60 min of infusion. The increase in GFR and RPF was associated with a marked rise in urinary kinin excretion, from a baseline of 8.51 +/- 6.7 to 24.7 +/- 6.7 pg/min at 20 min and 40.3 +/- 10.4 pg/min at 40 min (P < 0.001). Pretreatment with the kinin receptor antagonist blocked the rise in GFR and RPF in response to IGF-I. These data suggest that the renal vasodilatory effect of IGF-I is mediated by kinins. C1 MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT BIOMETRY,CHARLESTON,SC 29425. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29425. NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. RP JAFFA, AA (reprint author), MED UNIV S CAROLINA,DEPT MED,DIV ENDOCRINOL DIABET & METAB,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 27 TC 26 Z9 26 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP F102 EP F107 PN 2 PG 6 WC Physiology SC Physiology GA NA598 UT WOS:A1994NA59800096 PM 8304475 ER PT J AU MASSARO, GD SINGH, G MASON, R PLOPPER, CG MALKINSON, AM GAIL, DB AF MASSARO, GD SINGH, G MASON, R PLOPPER, CG MALKINSON, AM GAIL, DB TI BIOLOGY OF THE CLARA CELL SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Discussion ID LUNG; LOCALIZATION; PROTEINS; AIRWAYS; MICE C1 NHLBI,DIV LUNG DIS,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20007. DEPT VET AFFAIRS MED CTR,PITTSBURGH,PA 15240. NATL JEWISH CTR IMMUNOL & RESP MED,DENVER,CO 80206. UNIV CALIF DAVIS,SCH VET MED,DAVIS,CA 95616. UNIV COLORADO,DEPT PHARMACOL,BOULDER,CO 80309. NR 18 TC 48 Z9 49 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP L101 EP L106 PN 1 PG 6 WC Physiology SC Physiology GA NA591 UT WOS:A1994NA59100089 PM 7905712 ER PT J AU ZATZ, M LANGE, GD ROLLAG, MD AF ZATZ, M LANGE, GD ROLLAG, MD TI WHAT DOES CHANGING THE TEMPERATURE DO TO THE MELATONIN RHYTHM IN CULTURED CHICK PINEAL CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CIRCADIAN RHYTHMS; ENTRAINMENT; HEAT SPECK ID N-ACETYLTRANSFERASE ACTIVITY; HEAT-SHOCK RESPONSE; PHOTOENDOCRINE TRANSDUCTION; CIRCADIAN PACEMAKER; DARK PULSES; LIGHT; MIMICS; OSCILLATOR; DEPENDENCE; AMPLITUDE AB Chick pineal cells in static culture display a persistent, photosensitive circadian rhythm of melatonin production and release. We previously described the effects of light, the major physiological regulator of circadian rhythms, on the amplitude, period, and phase of the melatonin rhythm. Here we describe the effects of temperature, another physiological regulator of circadian rhythms, on the amplitude, period, and phase of this rhythm. Maintaining cells at 40.0-43.3 degrees C (104-11O degrees F) instead of 36.7 degrees C (98 degrees F) doubled the amplitude of the melatonin rhythm. In contrast, amplitude was reduced by about half at 33.3 degrees C (92 degrees F), and at 46.7 degrees C (116 degrees F) melatonin production was stopped within a few hours. Although temperatures of 40.0-43.3 degrees C raised melatonin output (unlike light, which suppresses it), they lengthened the period of the rhythm (as does constant light). Exposure of cells to 8-h pulses of these temperatures (40.0-43.3 degrees C) induced both phase delays and phase advances of the rhythm in subsequent cycles, with a phase dependence similar to that for the phase shifts induced by light pulses. Pulses of 40.0-43.3 degrees C were, however, weaker in their phase-shifting effects than light pulses. Pulses at still higher temperatures (46.7 degrees C) markedly inhibited melatonin output and delayed or disrupted the rhythm. The relationships (physiological and mechanistic) between the effects of temperature and light on the melatonin rhythm remain to be determined. C1 NINCDS,INSTRUMENT & COMP SECT,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT ANAT & CELL BIOL,BETHESDA,MD 20814. RP ZATZ, M (reprint author), NIMH,LCB,BIOCHEM PHARMAOL SECT,BLDG 36,RM 2A-17,BETHESDA,MD 20892, USA. NR 34 TC 10 Z9 10 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD JAN PY 1994 VL 266 IS 1 BP R50 EP R58 PN 2 PG 9 WC Physiology SC Physiology GA NA598 UT WOS:A1994NA59800052 PM 8304555 ER PT J AU MAIMAN, LA GREENLAND, P HILDRETH, NG COX, C AF MAIMAN, LA GREENLAND, P HILDRETH, NG COX, C TI PUBLIC CHOLESTEROL SCREENING IN THE PREVIOUSLY DIAGNOSED - MISUSE OF RESOURCES OR BENEFICIAL FUNCTION SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE LA English DT Article AB The attendance of individuals with a previous diagnosis of hyperlipidemia at public cholesterol screenings is often criticized as a misuse of such programs. This study explored the post-screening actions of 811 participants in a cholesterol screening program who had previously been diagnosed with cholesterol elevations and whose blood levels at this screening required further medical referral. We also studied the responses of physicians from whom these subjects sought care. Within five months, 559 of 753 participants completing the survey (74.0%) sought medical follow-up. Physicians retested the blood cholesterol levels of 75.0% of these 559; high-risk screenees were more likely to be retested and to be informed that their levels were elevated than moderate-risk subjects (P < .0001). Physicians increased cholesterol-lowering dietary advice for high-risk subjects (P < .0001) and medication prescriptions for both risk groups (P < .0001). Participants seeking medical care after the screening program had better cholesterol-lowering dietary practices and reported increased regimen compliance (moderate-risk: P = .01; high-risk: P < .0001) than those individuals not obtaining medical follow-up. One year after screening, blood cholesterol levels were 4.5% lower (P = .001) in those complying with referral but were virtually unchanged in noncompliers. Screening program confirmation of high blood cholesterol levels combined with referral appeared to have a positive impact on previously diagnosed screenees. We conclude that there may be merit in including previously diagnosed individuals in cholesterol screening programs. RP MAIMAN, LA (reprint author), NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,6100 EXECUT BLVD,ROOM 7B05,BETHESDA,MD 20892, USA. FU NHLBI NIH HHS [HL00982, HL34895]; NICHD NIH HHS [HD00538] NR 0 TC 2 Z9 2 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0749-3797 J9 AM J PREV MED JI Am. J. Prev. Med. PD JAN-FEB PY 1994 VL 10 IS 1 BP 20 EP 25 PG 6 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA MY873 UT WOS:A1994MY87300005 PM 8172727 ER PT J AU GIBSON, DC AF GIBSON, DC TI REGIONAL PRIMATE RESEARCH CENTERS PROGRAM SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article RP GIBSON, DC (reprint author), NIH,NATL CTR RES RESOURCES,COMPARAT MED PROGRAM,REG PRIMATE RES CTR PROGRAM,WESTWOOD BLDG,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 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 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1994 VL 34 IS 1 BP 97 EP 100 DI 10.1002/ajp.1350340115 PG 4 WC Zoology SC Zoology GA PE987 UT WOS:A1994PE98700013 ER PT J AU BOINSKI, S MITCHELL, CL AF BOINSKI, S MITCHELL, CL TI MALE RESIDENCE AND ASSOCIATION PATTERNS IN COSTA-RICAN SQUIRREL-MONKEYS (SAIMIRI-OERSTEDI) SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article DE SAIMIRI; SQUIRREL MONKEY; MALE AFFILIATION; DISPERSAL; PHILOPATRY; SPATIAL ASSOCIATION; NEAREST NEIGHBORS ID INBREEDING AVOIDANCE; FEMALE TRANSFER; MATING SYSTEMS; BEHAVIOR; DISPERSAL; MAMMALS; PRIMATES; ECOLOGY; CEBIDAE; FOREST AB A model is developed to interpret the evolution of the unusual pattern of male residence and social structure in the Costa Rican squirrel monkey (Saimiri oerstedi). Observations of a wild population document that males 1) maintain close spatial and social associations with other males, especially other males in their birth cohort, but not females and infants; 2) exhibit negligible within-troop male-male aggression, high levels of antipredator vigilance, and frequent predator deterrence; 3) cooperate in aggressive olfactory investigation of females; and 4) maintain residence in their natal troop with their male birth cohort, eventually succeeding to reproductive positions in their natal troop. Less commonly, male age-cohorts leave the troop well past reproductive maturity and usurp the reproductive male cohort in another troop. We suggest that this divergence from the social structure typical of male squirrel monkeys in Peru (males transient between troops, weak male-male bonds, high within-troop male aggression, little investment in anti-predator behavior) arose because female S. oerstedi in Costa Rica ape not philopatric. In Costa Rica, long term reproductive cooperation is likely advantageous to males, because of the frequent movement of female S. oerstedi between troops; the potential costs of inbreeding are reduced. Male S. oerstedi of all ages residing in the same troop, but especially those of the same age cohort, are predicted to have a much higher degree of genetic relatedness than adult females. (C) 1994 Wiley-Liss, Inc. C1 NIH,CTR ANIM,COMPARAT ETHOL LAB,POOLESVILLE,MD. AMAZONIAN BIODIVERS PROJECT,CUZCO,PERU. RP BOINSKI, S (reprint author), UNIV FLORIDA,DEPT ANTHROPOL,1350 TURLINGTON,GAINESVILLE,FL 32611, USA. NR 51 TC 29 Z9 29 U1 0 U2 10 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1994 VL 34 IS 2 BP 157 EP 169 DI 10.1002/ajp.1350340207 PG 13 WC Zoology SC Zoology GA PH345 UT WOS:A1994PH34500005 ER PT J AU NORCROSS, JL NEWMAN, JD FITCH, W AF NORCROSS, JL NEWMAN, JD FITCH, W TI RESPONSES TO NATURAL AND SYNTHETIC PHEE CALLS BY COMMON MARMOSETS (CALLITHRIX-JACCHUS) SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article DE MARMOSETS; CALLITHRIX JACCHUS; VOCALIZATIONS; PLAYBACK ID SAGUINUS-OEDIPUS-OEDIPUS; COTTON-TOP TAMARINS; LONG CALLS; PAIR-BOND; BEHAVIOR; VOCALIZATIONS; REPERTOIRE; INTRUDERS AB Captive adult common marmosets (Callithrix jacchus) produce whistle-like ''phee'' calls in two contexts: in the home cage, where phee calls may function as part of territorial marking behavior, and when separated from social companions, where phee calls may function to reunite conspecifics. Natural and synthesized calls representing the acoustic structure of male and female calls in each context were presented to adult marmosets in a playback paradigm. Marmosets demonstrated discriminative abilities according to the context of the call and the caller's sex. Vocal and behavioral responses indicated increased vigilance and territorial behavior, following playbacks of naturally produced calls as well as synthetic calls. All animals scanned more frequently following produced calls as well as synthetic calls. All animals scanned more frequently following natural home cage as well as isolation calls, but only increased contact behavior (trills) in response to home cage calls. The responses were dimorphic according to the sex of the caller, where adult males scanned more following male calls, and adult females were more aggressive following male and female calls. The differential behavioral responses to playbacks of marmoset phee calls suggest a biological relevance to subtle differences found in the acoustic parameters of the phee call. (C) 1994 Wiley-Liss, Inc. C1 NICHHD,COMPARAT ETHOL LAB,POOLESVILLE,MD 20837. NR 35 TC 18 Z9 18 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1994 VL 33 IS 1 BP 15 EP 29 DI 10.1002/ajp.1350330103 PG 15 WC Zoology SC Zoology GA NH800 UT WOS:A1994NH80000002 ER PT J AU WESTERGAARD, GC SUOMI, SJ AF WESTERGAARD, GC SUOMI, SJ TI HIERARCHICAL COMPLEXITY OF COMBINATORIAL MANIPULATION IN CAPUCHIN MONKEYS (CEBUS-APELLA) SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article DE CAPUCHINS; CEBUS; COMBINATORIAL MANIPULATION; TOOL-USE ID TOOL USE; MANUFACTURE; CUPS AB The purpose of this study was to examine the hierarchical complexity of combinatorial manipulation in capuchin monkeys (Cebus apella). Two experiments were conducted. In Experiment 1 capuchins were presented with an apparatus designed to accommodate the use of probing tools. In Experiment 2 the same capuchins were presented with sets of nesting containers. Five of the ten subjects used probing tools and seven subjects placed objects in the containers. The capuchins' behavior reflected three hierarchically organized combinatorial patterns displayed by chimpanzees and human infants. Although the capuchins sometimes displayed the two more complex patterns (''pot'' and ''subassembly''), their combinatorial behavior was dominated by the simplest pattern (''pairing''). In this regard capuchins may not attain the same grammar of manipulative action that has been reported for chimpanzees and young human children. (C) 1994 Wiley-Liss, Inc.* RP WESTERGAARD, GC (reprint author), NICHHD,COMPARAT ETHOL LAB,POB 529,POOLESVILLE,MD 20837, USA. NR 18 TC 30 Z9 30 U1 2 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1994 VL 32 IS 3 BP 171 EP 176 DI 10.1002/ajp.1350320303 PG 6 WC Zoology SC Zoology GA MY360 UT WOS:A1994MY36000002 ER PT J AU BREIER, A BUCHANAN, RW KIRKPATRICK, B DAVIS, OR IRISH, D SUMMERFELT, A CARPENTER, WT AF BREIER, A BUCHANAN, RW KIRKPATRICK, B DAVIS, OR IRISH, D SUMMERFELT, A CARPENTER, WT TI EFFECTS OF CLOZAPINE ON POSITIVE AND NEGATIVE SYMPTOMS IN OUTPATIENTS WITH SCHIZOPHRENIA SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DEFICIT SYNDROME; NONDEFICIT FORMS; CHLORPROMAZINE; TRIAL AB Objective: Clozapine is an atypical neuroleptic with superior efficacy in severely ill, treatment-resistant inpatients with schizophrenia. To determine if clozapine's differential efficacy generalizes to less ill, outpatient populations, the authors examined the effects of clozapine on positive and negative symptoms in outpatients with schizophrenia. Method: Outpatients with schizophrenia who had histories of partial response to conventional neuroleptics and who had not responded to a prospective 6-week trial of fluphenazine participated in a 10-week, double-blind, parallel-groups comparison of clozapine and haloperidol. Thirteen men and six women were given clozapine, and 15 men and five women were given haloperidol. Clinical response rates were determined and effects on primary versus secondary negative symptoms were addressed. Doses of clozapine and haloperidol at the end of the 10-week trial were 410.5 mg/day (SD=45.8) and 24.8 mg/day (SD=5.5), respectively. Results: Clozapine was superior to haloperidol for treating positive symptoms. In addition, eight of the patients given clozapine and only one of the patients given haloperidol fulfilled clinical responder criteria. Clozapine was also superior to haloperidol for treating negative symptoms, although these effects were relatively minor. Negative symptoms were significantly affected in the subgroup of patients with nondeficit schizophrenia but not in the subgroup with deficit schizophrenia. Overall, clozapine was well tolerated. Conclusions: Clozapine has superior efficacy for treating positive symptoms in partially responsive outpatients with chronic schizophrenia, suggesting that it has utility for a broad spectrum of patients with schizophrenia beyond the most severely ill. C1 UNIV MARYLAND,SCH MED,MARYLAND PSYCHIAT RES CTR,DEPT PSYCHIAT,BALTIMORE,MD 21201. RP BREIER, A (reprint author), NIMH,EXPTL THERAPEUT BRANCH,BLDG 10,RM 4N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Louza, Mario/H-8540-2013 OI Louza, Mario/0000-0003-1359-4111 FU NIMH NIH HHS [NIMH MH-40279, NIMH MH-45074] NR 34 TC 319 Z9 322 U1 3 U2 7 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JAN PY 1994 VL 151 IS 1 BP 20 EP 26 PG 7 WC Psychiatry SC Psychiatry GA MN949 UT WOS:A1994MN94900006 PM 8267129 ER PT J AU DIAL, TH GRIMES, PE LEIBENLUFT, E PINCUS, HA AF DIAL, TH GRIMES, PE LEIBENLUFT, E PINCUS, HA TI SEX-DIFFERENCES IN PSYCHIATRISTS PRACTICE PATTERNS AND INCOMES SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article AB Objective and Method: Using data from the APA's 1988-1989 Professional Activities Survey, the authors compared male and female psychiatrists on demographic characteristics, training, practice patterns, and income. Results: In keeping with previous studies' findings, female respondents on the average were younger than male respondents and more likely to have taken a residency or fellowship in child or adolescent psychiatry, worked fewer hours per week, allocated their working hours differently among types of activities, saw fewer patients per week, and worked in somewhat different settings. Multiple regression analysis showed that women had significantly lower mean net annual income than men after the effects of those predictors were statistically controlled. Conclusions: Differences in age, training, hours worked in specific settings, and numbers of patients do not completely account for the gender gap in psychiatrists' annual incomes. C1 HLTH INSURANCE ASSOC AMR,DEPT POLICY DEV & RES,WASHINGTON,DC. AMER PSYCHIAT ASSOC,OFF RES,WASHINGTON,DC 20009. NIMH,CLIN PSYCHOBIOL BRANCH,ROCKVILLE,MD 20857. NR 9 TC 24 Z9 24 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JAN PY 1994 VL 151 IS 1 BP 96 EP 101 PG 6 WC Psychiatry SC Psychiatry GA MN949 UT WOS:A1994MN94900017 PM 8267142 ER PT J AU BREEN, N KESSLER, L AF BREEN, N KESSLER, L TI CHANGES IN THE USE OF SCREENING MAMMOGRAPHY - EVIDENCE FROM THE 1987 AND 1990 NATIONAL-HEALTH INTERVIEW SURVEYS SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID BREAST-CANCER; SOCIOECONOMIC-STATUS; LOW-COST; WOMEN; AGE; PHYSICIANS; MORTALITY; KNOWLEDGE; COMMUNITY; BARRIERS AB Objectives. Mammography rates reported by women in the National Health Interview Surveys of 1990 and 1987 are examined. Why this screening modality is not more frequently used is explored. Methods. Data from the 1987 and 1990 National Health Interview Surveys, conducted by the National Center for Health Statistics, are cross-tabulated and compared. Results. In 1987, approximately 17% of women over 40 years of age reported having had a screening mammogram in the previous year. In 1990, the rate doubled. Race declined in importance; income and education remained strong, positive predictors of screening. Conclusions. Despite this dramatic increase, two thirds of women, are not having screening mammograms. Use was not higher primarily because women did not realize that screening mammography tests for breast cancer in asymptomatic, women. Primary care physicians are the main source of health education for screening mammography. The data suggest that public health programs to promote screening mammography should especially target primary care physicians and women with low incomes and education. Likewise, health care providers should ensure that their patients are referred to facilities that deliver high-quality mammography at low cost to make the procedure more accessible. RP BREEN, N (reprint author), NCI, APPL RES BRANCH, EPN 313, BETHESDA, MD 20892 USA. NR 55 TC 264 Z9 264 U1 1 U2 2 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA SN 0090-0036 EI 1541-0048 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 1994 VL 84 IS 1 BP 62 EP 67 DI 10.2105/AJPH.84.1.62 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NB627 UT WOS:A1994NB62700012 PM 8279613 ER PT J AU RODGERS, AB KESSLER, LG PORTNOY, B POTOSKY, AL PATTERSON, B TENNEY, J THOMPSON, FE KREBSSMITH, SM BREEN, N MATHEWS, O KAHLE, LL AF RODGERS, AB KESSLER, LG PORTNOY, B POTOSKY, AL PATTERSON, B TENNEY, J THOMPSON, FE KREBSSMITH, SM BREEN, N MATHEWS, O KAHLE, LL TI EAT FOR HEALTH - A SUPERMARKET INTERVENTION FOR NUTRITION AND CANCER RISK REDUCTION SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID INFORMATION; PROGRAM; EDUCATION; POINT; FOODS AB Objectives. The results of an evaluation of ''Eat for Health,'' a supermarket nutrition intervention, are presented. The study tested whether such a program could be successfully carried out and whether it could effect changes in knowledge, attitudes, and food purchasing behavior in line with nutrition and cancer risk reduction guidelines. Methods. The evaluation consisted of an in-store monitoring element, an in-store and telephone consumer survey, and an analysis of sales data on selected foods. A matched-pair design, using a total of 40 stores in the intervention and comparison groups, was used. Results. The intervention was successfully implemented and had limited success in changing some. food purchasing behaviors. There appeared to be no effect on knowledge and attitudes except for increased awareness of a link between diet and cancer and of the program itself. Conclusions. Despite the intervention's success, limitations of the consumer survey and sales data analyses and the continuing diffusion ot nutrition messages throughout society make it difficult to specify the impact of this program on consumer nutrition knowledge and behaviors. C1 PROSPECT ASSOCIATES, ROCKVILLE, MD USA. NCI, DIV CANC PREVENT & CONTROL, BETHESDA, MD 20892 USA. GIANT FUND INC, DEPT CONSUMER AFFAIRS, WASHINGTON, DC USA. INFORMAT MANAGEMENT SERV INC, SILVER SPRING, MD USA. OI Rodgers, Anthony/0000-0003-1282-1896 NR 22 TC 34 Z9 35 U1 2 U2 2 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA SN 0090-0036 EI 1541-0048 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 1994 VL 84 IS 1 BP 72 EP 76 DI 10.2105/AJPH.84.1.72 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NB627 UT WOS:A1994NB62700014 PM 8279615 ER PT J AU WELLS, BL BROWN, CC HORM, JW CARLETON, RA LASATER, TM AF WELLS, BL BROWN, CC HORM, JW CARLETON, RA LASATER, TM TI WHO PARTICIPATES IN CARDIOVASCULAR-DISEASE RISK FACTOR SCREENINGS - EXPERIENCE WITH A RELIGIOUS ORGANIZATION BASED PROGRAM SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note ID CHURCHES AB Adult members who declined participation in cardiovascular disease risk factor screenings offered at religious organizations were randomly selected and asked to participate in screenings at their homes. Relationships between screening participation and sociodemographic, behavioral, and physiological measures were examined. Age, knowledge of cardiovascular disease risk factors, body mass index, current smoking status, previous report of elevated blood pressure, current diastolic blood pressure measurement, frequency of worship service attendance, and residential distance from the religious organization screening site were important predictors of screening response. Those with conspicuous risk factors appeared less likely to initially respond to religious organization site screening invitations. C1 NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. NATL CTR HLTH STAT,DIV HLTH INTERVIEW STAT,HYATTSVILLE,MD 20782. MEM HOSP RHODE ISL,DIV CARDIOL,PAWTUCKET,RI. BROWN UNIV,DEPT MED,PROVIDENCE,RI 02912. MEM HOSP RHODE ISL,DIV HLTH EDUC,PAWTUCKET,RI. BROWN UNIV,DEPT COMMUNITY HLTH,PROVIDENCE,RI 02912. RP WELLS, BL (reprint author), HLTH RESOURCES & SERV ADM,BUR PRIMARY HLTH CARE,OFF EVALUAT ANAL & RES,ROOM 7-3A2,E-W TOWERS,ROCKVILLE,MD 20857, USA. FU NHLBI NIH HHS [HL28919] NR 20 TC 7 Z9 7 U1 0 U2 3 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 1994 VL 84 IS 1 BP 113 EP 115 DI 10.2105/AJPH.84.1.113 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NB627 UT WOS:A1994NB62700023 PM 8279596 ER PT J AU KNEBEL, AR JANSONBJERKLIE, SL MALLEY, JD WILSON, AG MARINI, JJ AF KNEBEL, AR JANSONBJERKLIE, SL MALLEY, JD WILSON, AG MARINI, JJ TI COMPARISON OF BREATHING COMFORT DURING WEANING WITH 2 VENTILATORY MODES SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID OBSTRUCTIVE PULMONARY-DISEASE; POSITIVE AIRWAY PRESSURE; MECHANICAL VENTILATION; DYSPNEA; SCALES; WORK AB In twenty-one patients ventilated for greater than or equal to 3 days, we compared similar levels of partial support provided by synchronized intermittent mandatory ventilation (SIMV) and pressure support ventilation (PSV) in terms of breathing comfort. On a single day, eligible subjects experienced, in random order, both SIMV and PSV weaning protocols (sequential 20% reductions in support at timed intervals) separated by a 1 to 3 h rest. Breathing comfort was defined by subjective ratings of dyspnea and anxiety. Subjects reported significant levels of preweaning dyspnea and anxiety despite resting for at least 6 h. Dyspnea and anxiety were not significantly different between the two methods at any level of support. Our findings suggest that dyspnea and anxiety are higher than expected on ''full'' ventilator support, and that comfort may not differ between PSV and SIMV during active withdrawal of machine support. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD. UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL NURSING,SAN FRANCISCO,CA 94143. UNIV MINNESOTA,ST PAUL RAMSEY MED CTR,PULM & CRIT CARE MED SECT,ST PAUL,MN 55101. OI Wilson, Alyson/0000-0003-1461-6212 NR 24 TC 43 Z9 46 U1 0 U2 3 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD JAN PY 1994 VL 149 IS 1 BP 14 EP 18 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NP717 UT WOS:A1994NP71700004 PM 8111572 ER PT J AU KELLEY, MJ BECKER, KL RUSHIN, JM VENZON, D PHELPS, R IHDE, DC BLISS, DP MELBY, K SNIDER, RH JOHNSON, BE AF KELLEY, MJ BECKER, KL RUSHIN, JM VENZON, D PHELPS, R IHDE, DC BLISS, DP MELBY, K SNIDER, RH JOHNSON, BE TI CALCITONIN ELEVATION IN SMALL-CELL LUNG-CANCER WITHOUT ECTOPIC PRODUCTION SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID GENE-RELATED PEPTIDE; ASYMPTOMATIC CIGARETTE SMOKERS; BOMBESIN-LIKE PEPTIDES; PULMONARY-DISEASE; MULTIPLE MARKERS; TUMOR-MARKERS; LINES; EXPRESSION; CARCINOMA; SERUM AB To determine the relative contribution of ectopic calcitonin (CT) production versus nonectopic secretion of CT in patients with small cell lung cancer (SCLC), serum and urine immunoreactive CT (iCT) levels of 86 different subjects were measured by radioimmunoassay (RIA) using two polyclonal antisera (Ab3b and Ab4). The subjects included 49 previously untreated patients with SCLC, 17 smokers, and 20 nonsmokers. Serum and urine iCT values were highest in the patients with SCLC, intermediate in the smokers, and lowest in the nonsmokers (p < 0.0003). Sixteen of the 49 patients with SCLC had tumor cell lines available for determination of CT mRNA expression by RNase protection assay (RPA) and iCT production by RIA. CT mRNA was detected in nine of 16 subjects and iCT in eight of 16. The tumor cell lines of seven patients had undetectable CT by both RPA and RIA, and of these, five had elevated urine or serum iCT values compared with those of nonsmokers, and two had levels above all values in the smoker group. Immunohistochemical staining of formalin-fixed, paraffin-embedded tumor samples detected iCT in two of four tumors from patients whose tumor cell lines had CT mRNA by RPA and iCT by RIA, but in none of six whose tumor cell lines had undetectable CT mRNA. Thus, increased iCT values in some patients with SCLC are likely due to sources other than CT production by tumor cells. C1 NCI, BIOSTAT & DATA MANAGEMENT SECT, BETHESDA, MD USA. VET ADM MED CTR, DIV ENDOCRINOL, WASHINGTON, DC 20422 USA. GEORGE WASHINGTON UNIV, WASHINGTON, DC USA. ST JOSEPHS HOSP, ATLANTA, GA USA. NATL NAVAL MED CTR, LAB DEPT, BETHESDA, MD USA. RP KELLEY, MJ (reprint author), NATL NAVAL MED CTR, NCI, NAVY MED ONCOL BRANCH, BLDG 8, ROOM 5101, BETHESDA, MD 20889 USA. RI Venzon, David/B-3078-2008; OI Kelley, Michael/0000-0001-9523-6080 NR 39 TC 11 Z9 11 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD JAN PY 1994 VL 149 IS 1 BP 183 EP 190 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA NP717 UT WOS:A1994NP71700032 PM 8111580 ER PT J AU COZENS, AL YEZZI, MJ KUNZELMANN, K OHRUI, T CHIN, L ENG, K FINKBEINER, WE WIDDICOMBE, JH GRUENERT, DC AF COZENS, AL YEZZI, MJ KUNZELMANN, K OHRUI, T CHIN, L ENG, K FINKBEINER, WE WIDDICOMBE, JH GRUENERT, DC TI CFTR EXPRESSION AND CHLORIDE SECRETION IN POLARIZED IMMORTAL HUMAN BRONCHIAL EPITHELIAL-CELLS SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID CYSTIC-FIBROSIS GENE; CONDUCTANCE REGULATOR GENE; TRACHEAL EPITHELIUM; SIMIAN VIRUS-40; MAMMALIAN-CELLS; MESSENGER-RNA; CL; TRANSPORT; CHANNEL; IDENTIFICATION AB A major limitation in the study of vectorial ion transport, secretion, and differentiated function in the human airway epithelium has been the lack of suitable cell culture systems. Progress in this direction has been made through the transformation of primary cultured epithelial cells. However, these transformants tend to lose differentiated properties with increasing serial passage, particularly following crisis. The successful establishment of a postcrisis SV40 large T-antigen transformed epithelial cell line derived from human bronchial epithelium is described. This cell line, 16HBE14o-, retains differentiated epithelial morphology and functions. Cell cultures show the presence of tight junctions and cilia, and monolayers generate transepithelial resistance, as measured in Ussing chambers, and retain beta-adrenergic stimulation of cAMP-dependent chloride ion transport, measured either by Cl-36- efflux or as short-circuit current in Ussing chambers. The cells also increase chloride transport in response to bradykinin or calcium ionophore. In addition, 16HBE14o- cells express levels of both the cystic fibrosis transmembrane conductance regulator (CFTR) mRNA and protein readily detectable by Northern and Western hybridization analysis, respectively. These cells provide a valuable resource for studying the modulation of CFTR and its role in regulation of chloride ion transport in human airway epithelium as well as other aspects of human airway cell biology. C1 UNIV CALIF SAN FRANCISCO,NIH,CYST FIBROSIS RES CTR,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,DEPT PATHOL,SU203 BOX 0911,SAN FRANCISCO,CA 94143. OI Kunzelmann, Karl/0000-0002-4583-7037 FU NHLBI NIH HHS [HL41928]; NIDDK NIH HHS [DK46002, DK39619] NR 50 TC 595 Z9 605 U1 3 U2 21 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD JAN PY 1994 VL 10 IS 1 BP 38 EP 47 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA MT982 UT WOS:A1994MT98200006 PM 7507342 ER PT J AU KINGMA, DW MEDEIROS, LJ BARLETTA, J RAFFELD, M MANN, RB AMBINDER, RF JAFFE, ES AF KINGMA, DW MEDEIROS, LJ BARLETTA, J RAFFELD, M MANN, RB AMBINDER, RF JAFFE, ES TI EPSTEIN-BARR-VIRUS IS INFREQUENTLY IDENTIFIED IN NON-HODGKINS-LYMPHOMAS ASSOCIATED WITH HODGKINS-DISEASE SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE HODGKINS DISEASE; NON-HODGKINS LYMPHOMA; COMPOSITE LYMPHOMA; EPSTEIN-BARR VIRUS (EBV); RNA IN-SITU HYBRIDIZATION; EBER; IMMUNODEFICIENCY ID POLYMERASE CHAIN-REACTION; REED-STERNBERG CELLS; IMMUNOGLOBULIN GENE REARRANGEMENTS; CHRONIC LYMPHOCYTIC-LEUKEMIA; SMALL NUCLEAR-RNA; INSITU HYBRIDIZATION; B-CELL; BIOTINYLATED PROBES; FREQUENT DETECTION; EXPRESSION AB Epstein-Barr virus (EBV) was identified in a subset of cases of Hodgkin's disease (HD) and in some non-Hodgkin's lymphomas (NHLs), particularly those associated with immunodeficiency. Because patients with HD have associated immune system defects, we hypothesized that EBV might be involved in NHLs associated with HD. Using fixed paraffin sections and in situ hybridization for EBV EBERI RNA, we studied 12 cases of composite NHL + HD, two patients with NHL who simultaneously also had HD involving a different site (simultaneous HD and NHL), 14 NHLs arising in patients who previously had HD, and seven NHLs from patients who subsequently developed HD. Epstein-Barr virus was identified most frequently in composite NHL + HD. Five (42%) cases of composite NHL + HD contained EBV in Reed-Sternberg and Hodgkin cells, four of which also had EBV-positive NHLs, diffuse mixed or large-cell type, with 10 to more than 50 EBV-positive cells per x 400 microscopic field. These results suggest that in this subset of four cases, both the NHL and HD components may have arisen from the same EBV-infected progenitor cell. We did not find EBV in two cases of simultaneous NHL and HD or in seven NHLs preceding development of HD. We identified EBV in only two of 14 NHLs following HD, one small noncleaved cell lymphoma and one plasmacytoma, both containing more than 50 EBV-positive cells per x 400 microscopic field. These results suggest that EBV plays a minimal role in NHLs associated with HD, with the exception of composite NHL + HD. Hodgkin's disease-associated immune defects may be involved in the pathogenesis of a subset of NHLs following HD, but the exact pathogenesis of most NHLs associated with HD remains uncertain. Parallels with the high-grade Burkitt-like lymphomas associated with human immunodeficiency virus infection are noted. C1 NCI,DIV CANC BIOL DIAG & CTR,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,BETHESDA,MD 20892. RHODE ISL HOSP,DEPT PATHOL,PROVIDENCE,RI 02902. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NR 45 TC 80 Z9 80 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD JAN PY 1994 VL 18 IS 1 BP 48 EP 61 DI 10.1097/00000478-199401000-00005 PG 14 WC Pathology; Surgery SC Pathology; Surgery GA MN376 UT WOS:A1994MN37600005 PM 8279628 ER PT J AU RAVDIN, JI KELSALL, BL AF RAVDIN, JI KELSALL, BL TI ROLE OF MUCOSAL SECRETORY IMMUNITY IN THE DEVELOPMENT OF AN AMEBIASIS VACCINE SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article; Proceedings Paper CT Symposium on Mucosal Immunity: Protection Against Pathogens, at the Annual Meeting of the American-Society-of-Tropical-Medicine-and-Hygiene CY NOV 19, 1992 CL SEATTLE, WA SP AMER SOC TROP MED & HYGIENE ID PATHOGENIC ENTAMOEBA-HISTOLYTICA; IGA ANTIBODY DETECTION; ADHERENCE LECTIN; INVASIVE AMEBIASIS; ASYMPTOMATIC INFECTION; IMMUNOGLOBULIN-A; BINDING LECTIN; GALACTOSE; INVITRO; SERA AB Invasive colonic infection by the enteric protozoan Entamoeba histolytica elicits a mucosal anti-amebic IgA antibody response. The E. histolytica galactose-inhibitable adherence protein (GIAP) mediates parasitic binding to colonic mucins and epithelial cells. Anti-GIAP secretory IgA antibodies are found during invasive amebiasis and can be elicited by immunization of rats with the native protein. Entamoeba histolytica contains potent IgA degradative activities due to its cysteine-specific proteases. Research is needed to further understand the role of secretory antibodies in natural or vaccine-induced immunity to E. histolytica. C1 CLEVELAND VET AFFAIRS MED CTR,CLEVELAND,OH 44106. NIH,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. RP RAVDIN, JI (reprint author), CASE WESTERN RESERVE UNIV,DEPT MED,10701 E BLVD,CLEVELAND,OH 44106, USA. FU NIAID NIH HHS [AI-07046, AI-18841] NR 35 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PY 1994 VL 50 IS 5 SU S BP 36 EP 41 PG 6 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA NT291 UT WOS:A1994NT29100006 PM 8203722 ER PT J AU GWADZ, RW AF GWADZ, RW TI GENETIC APPROACHES TO MALARIA CONTROL - HOW LONG THE ROAD SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article; Proceedings Paper CT Symposium on Prevention of Tropical Diseases: Status of New and Emerging Vector Control Strategies, at the 40th Annual Meeting of the American-Society-of-Tropical-Medicine-and-Hygiene CY DEC 02, 1991 CL BOSTON, MA SP AMER SOC TROP MED & HYGIENE, AMER COMM MED ENTOMOL ID MOSQUITO ANOPHELES-GAMBIAE; AEDES-AEGYPTI; PLASMODIUM-GALLINACEUM; CUTICULAR COMPONENTS; ARABIENSIS DIPTERA; DNA-PROBE; CULICIDAE; COMPLEX; VECTOR; DIFFERENTIATION AB Malaria control schemes based on the yet untested concept of replacing vector populations with mosquitoes of the same species unable to transmit the parasite offer one more means of attacking this important public health problem. Research is underway in several laboratories aimed at defining factors that can act to interrupt the development of the malaria parasite in the mosquito host, the genetic basis for such refractory mechanisms, methods for introducing genes coding for refractory mechanisms into the mosquito genome, and methods for replacing vector populations in the field. The complexities of such an undertaking are many and varied, but the potential impact of a successful replacement strategy on the epidemiology of malaria in the target area could be significant. RP GWADZ, RW (reprint author), NIAID,MALARIA RES LAB,BETHESDA,MD 20892, USA. NR 53 TC 24 Z9 24 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PY 1994 VL 50 IS 6 SU S BP 116 EP 125 PG 10 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA NX799 UT WOS:A1994NX79900012 PM 7912907 ER PT J AU PETRI, HL MISHKIN, M AF PETRI, HL MISHKIN, M TI BEHAVIORISM, COGNITIVISM AND THE NEUROPSYCHOLOGY OF MEMORY SO AMERICAN SCIENTIST LA English DT Article ID CAUDATE-NUCLEUS; HIPPOCAMPAL-FORMATION; LESIONS; MONKEYS; RECOGNITION; IMPAIRMENT; AMYGDALA; DISSOCIATION; ACQUISITION; AMNESIA C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. RP PETRI, HL (reprint author), TOWSON STATE UNIV,DEPT PSYCHOL,BALTIMORE,MD 21204, USA. NR 37 TC 61 Z9 62 U1 0 U2 2 PU SIGMA XI-SCI RES SOC PI RES TRIANGLE PK PA PO BOX 13975, RES TRIANGLE PK, NC 27709 SN 0003-0996 J9 AM SCI JI Am. Scientist PD JAN-FEB PY 1994 VL 82 IS 1 BP 30 EP 37 PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA MQ201 UT WOS:A1994MQ20100013 ER PT B AU KORN, EL GRAUBARD, BI AF KORN, EL GRAUBARD, BI GP AMER STAT ASSOC TI Variance estimation for superpopulation parameters: Should one use with-replacement estimators? SO AMERICAN STATISTICAL ASSOCIATION 1994 PROCEEDINGS OF THE SECTION ON SURVEY RESEARCH METHODS, VOLS I AND II LA English DT Proceedings Paper CT 49th Annual Meeting of the American-Association-for-Public-Opinion-Research CY MAY 11-15, 1994 CL DANVERS, MA SP Amer Assoc Public Opin Res DE FINITE-POPULATION; CLUSTER SAMPLING; PROBABILITY-PROPORTIONAL-TO-SIZE SAMPLING C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 BN 1-883276-10-1 PY 1994 BP 124 EP 132 PG 9 WC Social Sciences, Mathematical Methods; Statistics & Probability SC Mathematical Methods In Social Sciences; Mathematics GA BD50X UT WOS:A1994BD50X00017 ER PT B AU HUGHES, AL BRODSKY, MD AF HUGHES, AL BRODSKY, MD GP AMER STAT ASSOC TI Variance estimation of drug abuse episodes using the bootstrap SO AMERICAN STATISTICAL ASSOCIATION 1994 PROCEEDINGS OF THE SECTION ON SURVEY RESEARCH METHODS, VOLS I AND II LA English DT Proceedings Paper CT 49th Annual Meeting of the American-Association-for-Public-Opinion-Research CY MAY 11-15, 1994 CL DANVERS, MA SP Amer Assoc Public Opin Res DE VARIANCE ESTIMATION; BOOTSTRAP; DRUG-RELATED EMERGENCY ROOM EPISODES; ESTABLISHMENT SURVEYS C1 NIDA,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 BN 1-883276-10-1 PY 1994 BP 212 EP 217 PG 6 WC Social Sciences, Mathematical Methods; Statistics & Probability SC Mathematical Methods In Social Sciences; Mathematics GA BD50X UT WOS:A1994BD50X00030 ER PT B AU GREENBLATT, JC BERTOLUCCI, D AF GREENBLATT, JC BERTOLUCCI, D GP AMER STAT ASSOC TI Characteristics of persons who reported driving under the influence of alcohol or other drugs SO AMERICAN STATISTICAL ASSOCIATION 1994 PROCEEDINGS OF THE SECTION ON SURVEY RESEARCH METHODS, VOLS I AND II LA English DT Proceedings Paper CT 49th Annual Meeting of the American-Association-for-Public-Opinion-Research CY MAY 11-15, 1994 CL DANVERS, MA SP Amer Assoc Public Opin Res DE SURVEY; DRIVING UNDER THE INFLUENCE; DRUG ABUSE C1 NIAAA,SUBST ABUSE & MENTAL HLTH SERV ADM,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 BN 1-883276-10-1 PY 1994 BP 547 EP 552 PG 6 WC Social Sciences, Mathematical Methods; Statistics & Probability SC Mathematical Methods In Social Sciences; Mathematics GA BD50X UT WOS:A1994BD50X00091 ER PT B AU COLLIVER, JD GFROERER, JC AF COLLIVER, JD GFROERER, JC GP AMER STAT ASSOC TI Predictors of drug abuse treatment utilization among frequent cocaine users SO AMERICAN STATISTICAL ASSOCIATION 1994 PROCEEDINGS OF THE SECTION ON SURVEY RESEARCH METHODS, VOLS I AND II LA English DT Proceedings Paper CT 49th Annual Meeting of the American-Association-for-Public-Opinion-Research CY MAY 11-15, 1994 CL DANVERS, MA SP Amer Assoc Public Opin Res DE HOUSEHOLD SURVEYS; DRUG ABUSE DATA; COCAINE ABUSE; TREATMENT UTILIZATION; LOGISTIC REGRESSION C1 NIDA,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 BN 1-883276-10-1 PY 1994 BP 553 EP 558 PG 6 WC Social Sciences, Mathematical Methods; Statistics & Probability SC Mathematical Methods In Social Sciences; Mathematics GA BD50X UT WOS:A1994BD50X00092 ER PT J AU SALVADORI, S GUERRINI, R FORLANI, V BRYANT, SD ATTILA, M LAZARUS, LH AF SALVADORI, S GUERRINI, R FORLANI, V BRYANT, SD ATTILA, M LAZARUS, LH TI PREREQUISITE FOR HIS(4) IN DELTORPHIN-A FOR HIGH DELTA-OPIOID RECEPTOR SELECTIVITY SO AMINO ACIDS LA English DT Article DE AMINO ACIDS; DELTORPHINS; PEPTIDE SYNTHESIS; OPIOID RECEPTORS; MOLECULAR DYNAMICS SIMULATIONS ID AMPHIBIAN SKIN; HIGH-AFFINITY; RAT-BRAIN; TOPOGRAPHICAL REQUIREMENTS; FUNCTIONAL EXPRESSION; DERMORPHIN; PEPTIDES; ANALOGS; ACID; DERMENKEPHALIN AB Analysis of deltorphin A position 4 analogues included: backbone constrained N(alpha)MeHis, spinacine (Spi), N(alpha)MePhe and the tetrahydroisoquinoline-3-carboxylic acid (Tic); spatially confined side-chain (Phg); and imidazole alkylation of L- and D-His(4) enantiomers. High delta selectivity was lost with the following replacements: N(alpha)MeHis(4), N alpha MePhe(4) and Phg(4) reduced delta binding and the constrained residues also increased mu binding; ring closure between the side-chain and amino group to yield Spi(4) or Tic(4) increased mu affinity. Imidazole methylation of His(4) marginally affected opioid binding and doubled delta selectivity; alkylated D-His(4)-derivatives generally maintained delta selectivity in spite of decreased delta affinities. Thus, His(4) imidazole preserves delta selectivity by facilitating high delta binding and by repulsion at the mu receptor. Several low energy conformers of deltorphin A indicated that the His(4) imidazole preferred a spatial orientation parallel to the phenolic side-chain of Tyr(1) suggestive that this conformation might contribute to high delta affinity and selectivity. C1 NIEHS,ENVIRONM NEUROSCI LAB,PEPTIDE NEUROCHEM SECT,RES TRIANGLE PK,NC 27709. UNIV FERRARA,DEPT PHARMACEUT SCI,FERRARA,ITALY. UNIV HELSINKI,DEPT PHARMACOL,DIV PHARM & TOXICOL,HELSINKI,FINLAND. OI Guerrini, Remo/0000-0002-7619-0918; SALVADORI, Severo/0000-0002-8224-2358 NR 45 TC 13 Z9 13 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0939-4451 J9 AMINO ACIDS JI Amino Acids PY 1994 VL 7 IS 3 BP 291 EP 304 DI 10.1007/BF00807704 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PV525 UT WOS:A1994PV52500006 PM 24186126 ER PT J AU CESSAC, JW RAO, PN KIM, HK AF CESSAC, JW RAO, PN KIM, HK TI CHIROSPECIFIC SYNTHESIS OF D-P-CHLOROHOMOPHENYLALANINE AND L-P-CHLOROHOMOPHENYLALANINE N-T-BOC DCHA SALTS SO AMINO ACIDS LA English DT Article DE AMINO ACIDS; CHIROSPECIFIC; D-GLUCOSAMINE HYDROCHLORIDE; D-MANNOSAMINE HYDROCHLORIDE; L-N-T-BUTYLOXYCARBONYLSERINAL; D-N-T-BUTYLOXYCARBONYLSERINAL; D-P-CHLOROHOMOPHENYLALANINE N-T-BOC DCHA SALT; L-P-CHLOROHOMOPHENYLALANINE N-T-BOC DCHA SALT ID LIQUID-CHROMATOGRAPHIC RESOLUTION; 2,3,4,6-TETRA-O-ACETYL-BETA-D-GLUCOPYRANOSYL ISOTHIOCYANATE; AMINO-ACIDS; ANTAGONISTS; DERIVATIZATION; HORMONE AB The chirospecific conversions of D-glucosamine hydrochloride and D-mannosamine hydrochloride to the configurationally stable L and D isomers of N-t-butyloxycarbonylserinal were carried out by t-butylcarbonylation followed by sodium borohydride reduction and sodium meta-periodate oxidation. Reaction of the L and D aldehydes with the Wittig reagent prepared from 4-chlorobenzyltriphenylphosphonium chloride and butyl lithium followed by catalytic hydrogenation, Jones oxidation and salt formation with dicyclohexylamine gave the DCHA salts of the D and L isomers of p-chlorohomophenylalanine N-t-Boc in high enatiomeric excess. The optical purity of the title compounds was established by hydrolysis to the respective free amino acids, followed by chiral derivatization and HPLC analysis. C1 SW FDN BIOMED RES,DEPT ORGAN CHEM,SAN ANTONIO,TX 78228. NICHHD,CONTRACEPT DEV BRANCH,BETHESDA,MD 20892. NR 11 TC 2 Z9 2 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0939-4451 J9 AMINO ACIDS JI Amino Acids PY 1994 VL 6 IS 1 BP 97 EP 105 DI 10.1007/BF00808125 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF753 UT WOS:A1994NF75300008 PM 24190745 ER PT J AU MILLER, SPF DONKERSLOOT, JA THOMPSON, J AF MILLER, SPF DONKERSLOOT, JA THOMPSON, J TI ENZYMATIC-SYNTHESIS AND CHARACTERIZATION OF N-5-(CARBOXYMETHYL)-L-ORNITHINE AND N-6-(CARBOXYMETHYL)-L-LYSINE SO AMINO ACIDS LA English DT Article DE AMINO ACIDS; N-(CARBOXYALKYL)AMINO ACIDS; N-6-(CARBOXYMETHYL)LYSINE; N-5-(CARBOXYMETHYL)ORNITHINE; LACTOCOCCUS LACTIS ID N-EPSILON-CARBOXYMETHYLLYSINE; STREPTOCOCCUS-LACTIS; NADP+ OXIDOREDUCTASE; LACTOCOCCUS-LACTIS; IDENTIFICATION; N5-(L-1-CARBOXYETHYL)-L-ORNITHINE; PURIFICATION; ACIDS; N-5-(1-CARBOXYETHYL)ORNITHINE; COMPLICATIONS AB This report describes the enzyme-catalyzed synthesis, characterization, and chromatographic separation of N-6-(carboxymethyl)-L-lysine and N-5 -(carboxymethyl)-L-ornithine. The two N omega-(carboxyalkyl)amino acids are formed via a reductive condensation between glyoxylate and the epsilon- or delta-amino groups of lysine and ornithine, respectively. Both reactions are catalyzed by the NADPH-dependent enzyme, N-5-(carboxyethyl)ornithine synthase [EC 1.5.1.24], found in some strains of the lactic acid bacterium Lactococcus lactis subsp. lactis. C1 NIDR, MICROBIAL ECOL LAB, BETHESDA, MD 20892 USA. NINCDS, DEV & METAB NEUROL BRANCH, BETHESDA, MD 20892 USA. NR 32 TC 2 Z9 2 U1 0 U2 2 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0939-4451 EI 1438-2199 J9 AMINO ACIDS JI Amino Acids PY 1994 VL 6 IS 2 BP 189 EP 198 DI 10.1007/BF00805846 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NG877 UT WOS:A1994NG87700007 PM 24190788 ER PT J AU LLOYD, RA GENTLEMAN, S CHADER, GJ AF LLOYD, RA GENTLEMAN, S CHADER, GJ TI ASSAY OF TUBULIN ACETYLTRANSFERASE ACTIVITY IN SUBCELLULAR TISSUE FRACTIONS SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID ACETYLATED ALPHA-TUBULIN; MICROTUBULES; PROTEINS; STABILITY; FLAGELLA; CILIA RP LLOYD, RA (reprint author), NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 23 TC 7 Z9 7 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 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD JAN PY 1994 VL 216 IS 1 BP 42 EP 46 DI 10.1006/abio.1994.1005 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA MP888 UT WOS:A1994MP88800005 PM 8135364 ER PT J AU SUPKO, JG MALSPEIS, L AF SUPKO, JG MALSPEIS, L TI DETERMINATION OF MICHELLAMINE-B IN BIOLOGICAL-FLUIDS BY HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY WITH FLUORESCENCE DETECTION SO ANALYTICAL BIOCHEMISTRY LA English DT Article RP SUPKO, JG (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,PHARMACEUT CHEM LAB,FREDERICK,MD 21702, USA. NR 6 TC 8 Z9 8 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 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD JAN PY 1994 VL 216 IS 1 BP 52 EP 60 DI 10.1006/abio.1994.1007 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA MP888 UT WOS:A1994MP88800007 PM 8135366 ER PT J AU DEUTSCH, J HEGEDUS, L GREIG, NH RAPOPORT, SI SONCRANT, TT AF DEUTSCH, J HEGEDUS, L GREIG, NH RAPOPORT, SI SONCRANT, TT TI EVIDENCE OF TRANSACYLATION OF SCOPOLAMINE IN THE GAS-CHROMATOGRAPH INLET SO ANALYTICAL LETTERS LA English DT Article DE SCOPOLAMINE; ATROPINE; GAS CHROMATOGRAPHY; MASS SPECTROMETRY; TRANSACYLATION ID PLASMA; PHASE; IONS AB Scopolamine, a muscarinic receptor antagonist, was derivatized with heptafluorobutyric anhydride (HFBA), separated on a capillary GC column and characterized by electron impact mass spectrometry. The highest ion (m/z 351) in the mass spectrum of HFBA derivatized scopolamine (MW 499) corresponded to the molecular ion of HFB scopoline (M(+), m/z 351). fragmentation pattern in this mass spectrum was different from that obtained for HFB scopoline reported in the literature and used as reference material. In an attempt to explain the differences we suggest that HFB scopolamine undergoes a transacylation in the GC-MS inlet system. This results in an unexpected isomer of HFB scopoline. GC-MS studies of HFB scopolamine, its deuterium-labelled analogues and of HFB atropine support this transacylation hypothesis. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. RP DEUTSCH, J (reprint author), HEBREW UNIV JERUSALEM,SCH PHARM,IL-91120 JERUSALEM,ISRAEL. NR 9 TC 1 Z9 1 U1 1 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0003-2719 J9 ANAL LETT JI Anal. Lett. PY 1994 VL 27 IS 4 BP 671 EP 679 PG 9 WC Chemistry, Analytical SC Chemistry GA NA891 UT WOS:A1994NA89100002 ER PT J AU YAMAZAKI, S DEGEORGE, JJ BELL, JM RAPOPORT, SI AF YAMAZAKI, S DEGEORGE, JJ BELL, JM RAPOPORT, SI TI EFFECTS OF PENTOBARBITAL ON INCORPORATION OF PLASMA PALMITATE INTO RAT-BRAIN SO ANESTHESIOLOGY LA English DT Article DE BRAIN, BLOOD FLOW, FATTY ACIDS, PHOSPHOLIPIDS; CARBON DIOXIDE, HYPERCAPNIA; HYPNOTICS, BARBITURATES, PENTOBARBITAL; METABOLISM LIPIDS ID CEREBRAL GLUCOSE-UTILIZATION; FATTY-ACID; UNANESTHETIZED RATS; BLOOD-FLOW; ISCHEMIA; ANESTHESIA; LIBERATION; RESPONSES; PROTEIN; CORTEX AB Background: Barbiturates are reported to reduce brain oxidative metabolism and brain free fatty acid release during ischemia by mechanisms that are as yet unclear. To elucidate their action on brain lipid metabolism, an in vivo method was used to quantify the effect of pentobarbital on the incorporation of radiolabeled palmitic acid from blood into lipids of the rat brain. Methods: [9,10-H-3]-Palmitate was infused intravenously in an awake rat or in a rat lightly anesthetized or made comatose by pentobarbital. Twenty minutes after infusion was begun, the rat was killed and non-(H2O)-H-3 radioactivity in individual brain lipid compartments was determined. Incorporation coefficients (k*) were calculated by dividing the lipid compartment radioactivities by the integrated plasma radioactivity to 20 min. Results: Net brain k* for [9,10-H-3]-palmitate was reduced by 36-40% in pentobarbital-anesthetized rats. This reduction was unrelated to depth of anesthesia or to the presence of hypercapnia and acidosis, because breathing 7.5% CO2 had no effect on k* in awake rats. Anesthesia reduced radiolabel incorporation into phospholipids by 46-53% and into neutral lipids by 20-26% but did not change the distribution of radiolabel among phospholipid or neutral lipid classes. Conclusions: Pentobarbital has a profound effect on brain lipid metabolism. It reduces incorporation of plasma palmitate into brain, more so into phospholipids than into neutral lipids, independently of changes in cerebral blood flow. Reduced incorporation likely reflects reduced turnover of palmitate within brain lipids (mainly phosphatidylcholine), consistent with evidence that barbiturates also reduce release of free fatty acids during brain ischemia. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 39 TC 20 Z9 20 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD JAN PY 1994 VL 80 IS 1 BP 151 EP 158 DI 10.1097/00000542-199401000-00022 PG 8 WC Anesthesiology SC Anesthesiology GA MR300 UT WOS:A1994MR30000022 PM 8291704 ER PT B AU DUBNER, R AF DUBNER, R BE Stanley, TH Ashburn, MA TI SPINAL-CORD NEURONAL PLASTICITY - MECHANISMS OF PERSISTENT PAIN FOLLOWING TISSUE-DAMAGE AND NERVE INJURY SO ANESTHESIOLOGY AND PAIN MANAGEMENT SE DEVELOPMENTS IN CRITICAL CARE MEDICINE AND ANESTHESIOLOGY LA English DT Proceedings Paper CT 39th Annual Postgraduate Course in Anesthesiology CY FEB 18-22, 1994 CL SNOWBIRD, UT C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,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 0-7923-2662-8 J9 DEV C C MED PY 1994 VL 29 BP 19 EP 34 PG 16 WC Anesthesiology SC Anesthesiology GA BA26U UT WOS:A1994BA26U00002 ER PT J AU REMADI, S ISMAIL, A KARPUZ, V FINCI, V ZACHARIE, S VASSILAKOS, P AF REMADI, S ISMAIL, A KARPUZ, V FINCI, V ZACHARIE, S VASSILAKOS, P TI CELLULAR (JUVENILE) FIBROADENOMA OF THE BREAST - A CLINICOPATHOLOGICAL AND IMMUNOHISTOCHEMICAL STUDY OF 7 CASES SO ANNALES DE PATHOLOGIE LA French DT Article ID FINE NEEDLE ASPIRATION; CYSTOSARCOMA PHYLLODES; GIANT FIBROADENOMA; PROLIFERATIONS; BENIGN AB A review of 82 fibroadenomas, collected over a period of 18 years, from female patients aged below 20 years, revealed 7 cases of cellular (juvenile) variant. The tumors are solitary, with an average diameter of 4 cm, these are characterized by a rich cellular stroma and a prominent glandular epithelium. Cellular fibroadenomas often pose to the pathologist serious problems of differential diagnosis, especially with phyllodes tumors. The patient's age together with the histological criterias that we have underlined should make the diagnosis more obvious. As the cellular fibroadenoma is seen essentially during adolescence, surgeons have tendancy to preserve the maximum amount of breast tissue. The 2 cases in which we have observed recurrences were seen after incomplete resection of the primary tumor. Therefore, we are of the opinion that a security zone of mammary parenchyma is mandatory. C1 HOP CANTONAL UNIV GENEVA,DEPT CLIN PATHOL,DIV GYNECOPATHOL & CYTOL,GENEVA,SWITZERLAND. NIAID,BETHESDA,MD 20892. NR 24 TC 7 Z9 7 U1 0 U2 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0242-6498 J9 ANN PATHOL JI Ann. Pathol. PY 1994 VL 14 IS 6 BP 392 EP 397 PG 6 WC Pathology SC Pathology GA PZ412 UT WOS:A1994PZ41200005 PM 7857414 ER PT J AU GRIDLEY, G KLIPPEL, JH HOOVER, RN FRAUMENI, JF AF GRIDLEY, G KLIPPEL, JH HOOVER, RN FRAUMENI, JF TI INCIDENCE OF CANCER AMONG MEN WITH THE FELTY SYNDROME SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID RENAL-TRANSPLANT RECIPIENTS; RHEUMATOID-ARTHRITIS; MALIGNANT NEOPLASMS; HODGKINS-DISEASE; NEUTROPENIA; MORTALITY; RISK; MANIFESTATIONS; LYMPHOMA; SPLENECTOMY AB Objective: To estimate the incidence of cancer (especially lymphoproliferative malignancies) in patients with the Felty syndrome. Design: A retrospective cohort study. Setting: A computerized database of all discharge records for 1969 to 1990 from a Veterans Affairs hospital. Patients: 906 men with a discharge diagnosis of the Felty syndrome. Measurements: Standardized incidence ratios (SIR) (ratios of observed-to-expected events) estimated the risk for specific cancers. Hospital records confirmed the diagnoses of the Felty syndrome and cancer. Results: We observed a twofold increase in total cancer incidence (137 patients; SIR = 2.09; 95% CI, 1.8 to 2.5). The risk for non-Hodgkin lymphoma (19 patients; SIR = 12.8, CI, 7.7 to 20.0) was much greater than the twofold increase in risk for lymphoma generally reported for rheumatoid arthritis. The risk for leukemia was increased but only within 5 years of the first hospitalization for the Felty syndrome, (13 patients; SIR = 7.67; CI, 4.1 to 13.1). Conclusion: The increased risk for non-Hodgkin lymphoma after the Felty syndrome in our study is similar to the risk associated with the Sjogren syndrome and may reflect similar immunostimulatory mechanisms. C1 NATL INST ARTHRITIS & MUSCULOSKELETAL & SKIN DISORDERS,BETHESDA,MD 20892. RP GRIDLEY, G (reprint author), NCI,EPN 443,BETHESDA,MD 20892, USA. NR 32 TC 71 Z9 71 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JAN 1 PY 1994 VL 120 IS 1 BP 35 EP 39 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA MP280 UT WOS:A1994MP28000006 PM 8250454 ER PT J AU BENNETT, GJ AF BENNETT, GJ TI HYPOTHESES ON THE PATHOGENESIS OF HERPES ZOSTER-ASSOCIATED PAIN SO ANNALS OF NEUROLOGY LA English DT Article; Proceedings Paper CT Workshop on Varicella-Zoster Virus Infection: New Insights into Pathogenesis and Post-Herpetic Neuralgia CY MAY 13-14, 1993 CL BETHESDA, MD SP VARICELLA ZOSTER VIRUS RES FDN INC, NIAID, NIA, NIDR, NIDOCD ID MECHANICAL HYPERALGESIA; TRANSSYNAPTIC DEGENERATION; NEUROGENIC HYPERALGESIA; SECONDARY HYPERALGESIA; NERVE INJURY; SPINAL-CORD; SKIN; NEURALGIA; INPUT; NEUROPATHY RP BENNETT, GJ (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 49,ROOM 1A11,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 39 TC 43 Z9 44 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 1994 VL 35 SU S BP S38 EP S41 DI 10.1002/ana.410350712 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NM514 UT WOS:A1994NM51400011 PM 8185295 ER PT J AU MAX, MB AF MAX, MB TI TREATMENT OF POSTHERPETIC NEURALGIA - ANTIDEPRESSANTS SO ANNALS OF NEUROLOGY LA English DT Article; Proceedings Paper CT Workshop on Varicella-Zoster Virus Infection: New Insights into Pathogenesis and Post-Herpetic Neuralgia CY MAY 13-14, 1993 CL BETHESDA, MD SP VARICELLA ZOSTER VIRUS RES FDN INC, NIAID, NIA, NIDR, NIDOCD ID DIABETIC NEUROPATHY SYMPTOMS; RELIEVES POSTHERPETIC NEURALGIA; LOW-DOSE AMITRIPTYLINE; CHRONIC PAIN; DOUBLE-BLIND; PLACEBO; DESIPRAMINE; TRIAL; ANALGESIA AB Five controlled clinical trials and extensive clinical experience have shown that amitriptyline and several other antidepressants reduce the severity of post-herpetic neuralgia. Studies in post-herpetic neuralgia and in painful diabetic neuropathy suggest that blockade of norepinephrine reuptake is the most important action accounting for pain relief; selective agents such as desipramine may be useful in patients unable to tolerate amitriptyline side effects. The selective serotonin reuptake inhibitors, zimelidine and paroxetine, have shown little effectiveness in neuropathic pain, but small studies in diabetic neuropathy have shown that paroxetine and citalopram have modest effects. Studies of the latter agents in post-herpetic neuralgia, concentration-response studies of amitriptyline, and studies of drug combinations including antidepressants may lead to improved treatment. RP MAX, MB (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,CLIN TRIALS UNIT,BLDG 10,ROOM 3C-405,BETHESDA,MD 20892, USA. NR 28 TC 43 Z9 44 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 1994 VL 35 SU S BP S50 EP S53 DI 10.1002/ana.410350715 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NM514 UT WOS:A1994NM51400014 PM 8185299 ER PT J AU SPRING, SB LAUGHLIN, C ARVIN, AM HAY, J STRAUS, SE WHITLEY, RJ GERSHON, AA SILVERSTEIN, SJ AF SPRING, SB LAUGHLIN, C ARVIN, AM HAY, J STRAUS, SE WHITLEY, RJ GERSHON, AA SILVERSTEIN, SJ TI WORKSHOP SUMMARY SO ANNALS OF NEUROLOGY LA English DT Editorial Material C1 NIAID,DIV INTRAMURAL RES,BETHESDA,MD. STANFORD UNIV,DEPT PEDIAT,STANFORD,CA 94305. SUNY COLL BUFFALO,DEPT MICROBIOL,BUFFALO,NY 14222. UNIV ALABAMA,DEPT PEDIAT,BIRMINGHAM,AL. COLUMBIA UNIV,COLUMBIA PRESBYTERIAN MED CTR,DEPT PEDIAT,NEW YORK,NY 10032. COLUMBIA UNIV,COLL PHYS & SURG,DEPT MICROBIOL,NEW YORK,NY. RP SPRING, SB (reprint author), NIAID,DIV MICROBIOL & INFECT DIS,SOLAR BLDG,ROOM 3A-14,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 1994 VL 35 SU S BP S2 EP S3 DI 10.1002/ana.410350703 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NM514 UT WOS:A1994NM51400002 ER PT J AU STRAUS, SE AF STRAUS, SE TI OVERVIEW - THE BIOLOGY OF VARICELLA-ZOSTER VIRUS-INFECTION SO ANNALS OF NEUROLOGY LA English DT Article; Proceedings Paper CT Workshop on Varicella-Zoster Virus Infection: New Insights into Pathogenesis and Post-Herpetic Neuralgia CY MAY 13-14, 1993 CL BETHESDA, MD SP VARICELLA ZOSTER VIRUS RES FDN INC, NIAID, NIA, NIDR, NIDOCD ID HERPES-ZOSTER; THERAPY; GANGLIA; ACYCLOVIR; DNA AB Varicella-zoster virus infection is manifested initially as chickenpox. The virus persists for life in sensory nerve ganglia, from which it reactivates in many people to cause tester. Among the many recognized complications of these infections, post-tester neuralgia is the most frequently debilitating. The molecular events of virus replication, latency, and reactivation, and the pathogenesis of post-tester neuralgia, are incompletely understood and inadequately addressed by current therapeutic strategies. RP STRAUS, SE (reprint author), NIAID,CLIN INVEST LAB,BLDG 10,ROOM 11N228,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 17 TC 15 Z9 15 U1 1 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 1994 VL 35 SU S BP S4 EP S8 DI 10.1002/ana.410350704 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NM514 UT WOS:A1994NM51400003 PM 8185296 ER PT J AU JAFFE, ES ZARATEOSORNO, A KINGMA, DW RAFFELD, M MEDEIROS, LJ AF JAFFE, ES ZARATEOSORNO, A KINGMA, DW RAFFELD, M MEDEIROS, LJ TI THE INTERRELATIONSHIP BETWEEN HODGKINS-DISEASE AND NON-HODGKINS-LYMPHOMAS SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT 5th International Conference on Malignant Lymphoma CY JUN 09-12, 1993 CL LUGANO, SWITZERLAND DE COMPOSITE LYMPHOMA; EPSTEIN-BARR VIRUS; HODGKINS DISEASE; IMMUNODEFICIENCY; NON-HODGKINS LYMPHOMA ID CHRONIC LYMPHOCYTIC-LEUKEMIA; EPSTEIN-BARR-VIRUS; B-CELL LYMPHOMA; REED-STERNBERG CELLS; MYCOSIS-FUNGOIDES; NODULAR PARAGRANULOMA; MONOCLONAL-ANTIBODIES; COMPOSITE LYMPHOMA; PREDOMINANCE TYPE; SUBTYPE AB Background: While Hodgkin's disease (HD) and the non-Hodgkin's lymphomas (NHLs) have long been regarded as distinct disease entities, recent observations suggest a closer association. The analysis of cases in which both diseases are present in the same anatomic site (composite lymphomas), or in separate sites (simultaneous or sequential HD and NHL), indicates that this phenomenon occurs more frequently than would be expected by chance alone. Design: We reviewed our experience with composite, simultaneous, and sequential cases of HD and NHL, including both nodular lymphocyte-predominant HD (NLPHD) and the other (so-called 'usual') subtypes of HD. Cases analyzed included 43 cases of NLPHD and large-cell lymphoma (LCL); 14 cases of NHL following HD; 12 cases of composite lymphoma; 2 cases of simultaneous HD and NHL involving different sites; 8 cases of chronic lymphocytic leukemia (CLL) with Reed-Sternberg (RS) cells; and 22 cases of HD following NHL. Immunophenotypic analysis of both components (HD & NHL) was performed when possible. In addition, in situ hybridization for Epstein-Barr virus (EBV) EBER1 mRNA was performed in 35 cases of usual HD associated with NHL. Results: The most common form of composite lymphoma was coexistent NLPHD with LCL of B-cell immunophenotype. With the abnormal cells of NLPHD also being of B-cell lineage, this finding suggests the existence of a clonal relationship between the two components. The association of nodular sclerosis or mixed cellularity HD and NHL was less common but still significant. The vast majority of the NHL associated with HD were of B-cell origin, most commonly follicular lymphomas. EBV was identified more frequently in the NHL of composite NHL + HD (4/12 cases; 33%) than the other patient groups studied (2/23; 9%). Moreover, in 4/5 composite lymphomas both the HD and NHL component were EBV-positive, suggesting an origin from a common EBV-infected progenitor cell. Conclusion: These findings suggest that, at least in some cases, HD may be clonally related to an underlying B-cell malignancy, and that the Reed-Sternberg cell may be an altered B lymphocyte. A process that may have a different pathogenesis is the late occurrence of aggressive, usually EBV-negative (12/14 cases), B-cell NHL in patients successfully treated for HD. Such tumors may be related to an underlying and persistent immunodeficiency in these patients, and may be of similar pathogenesis to the Burkitt-like lymphomas associated with HIV-infection. RP JAFFE, ES (reprint author), NCI,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,ROOM 2N202,BETHESDA,MD 20892, USA. NR 52 TC 12 Z9 12 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 1994 VL 5 SU 1 BP S7 EP S11 PG 5 WC Oncology SC Oncology GA MX109 UT WOS:A1994MX10900004 ER PT J AU MAGRATH, IT AF MAGRATH, IT TI PROSPECTS FOR THE THERAPEUTIC USE OF ANTISENSE OLIGONUCLEOTIDES IN MALIGNANT-LYMPHOMAS SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT 5th International Conference on Malignant Lymphoma CY JUN 09-12, 1993 CL LUGANO, SWITZERLAND ID INHIBITION; GROWTH; DNA AB Combinations of cytotoxic drugs, based almost entirely upon the results of empirical clinical trials, are the foundation of the modem management of the non-Hodgkin's lymphomas. While highly effective in the high-grade (particularly pediatric) lymphomas, and able to cure a significant fraction of intermediate-grade lymphomas, it has yet to be proven that patients with low-grade lymphomas can be cured by chemotherapy. Yet even if 100% of patients were potentially curable by chemotherapy, the significant medical cost with respect to both immediate and late toxicity is reason enough to search for radically different approaches to therapy. Of particular appeal is the possibility that therapy might be developed that is targeted to the very genetic lesions that are responsible for the pathogenesis of lymphomas. Such therapy should, by definition, be largely specific for the lymphoma cells, and hence devoid of the major side effects presently encountered. Recent advances in the understanding of the molecular basis of lymphomagenesis have provided sufficient information to begin to develop approaches of this kind. Here, I discuss the prospects for sequence-specific therapy, focusing specifically on antisense oligonucleotides. These short stretches of DNA bind specifically to RNA molecules and prevent their translation. If the targeted RNA molecules are specific to the tumor cells, or derived from pathogenetically relevant viral genomes, such therapy has at least the theoretical possibility of inhibiting tumor cell growth, or even killing tumor cells, without causing significant damage to normal cells. RP MAGRATH, IT (reprint author), NCI,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA. NR 13 TC 4 Z9 4 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 1994 VL 5 SU 1 BP S67 EP S70 PG 4 WC Oncology SC Oncology GA MX109 UT WOS:A1994MX10900016 ER PT J AU SCHWAB, G DUROUX, I CHAVANY, C HELENE, C SAISONBEHMOARAS, E AF SCHWAB, G DUROUX, I CHAVANY, C HELENE, C SAISONBEHMOARAS, E TI AN APPROACH FOR NEW ANTICANCER DRUGS - ONCOGENE-TARGETED ANTISENSE DNA SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT Meeting on Recent Advances in the Biology and Treatment of Solid Tumours CY OCT 01-02, 1993 CL DURHAM, ENGLAND SP LILLY ONCOL DE ANTISENSE DNA; HA-RAS; HYBRID ARREST; ONCOGENES; OLIGONUCLEOTIDE CARRIER ID OLIGONUCLEOTIDES; INVIVO AB Background: Ras oncogenes owe their transforming properties to single point mutations in the sequence coding for the catalytic part of the p21 protein. These mutations lead to changes in cellular proliferation and tumorigenic properties. Point mutations represent a defined target for antisense oligonucleotides which specifically suppress translation of the targeted mRNA. However, the use of oligonucleotides in vivo has, until now, been limited by their instability in serum. New techniques: Different strategies have been developed to protect the oligonucleotides and increase their transport into the target cell. Linking intercalating agents, hydrophobic groups or polycations to oligonucleotides or encapsulating them in liposomes resulted in a higher resistance to exonucleases and increased oligonucleotide penetration into cells. The stability and cellular uptake of antisense oligonucleotides can also be improved by associating them with polyalkylcyanoacrylate nanoparticles. The polymeric nature renders these small particles more stable than liposomes in biological fluids and during storage. Method: Antisense oligonucleotides directed to the point mutation (G to T) in codon 12 of the Ha-ras mRNA were adsorbed to nanoparticles in the presence of hydrophobic cations. Results: These stabilized oligonucleotides selectively inhibited the proliferation of cells expressing this point mutation and partially reversed their tumorigenicity in nude mice. C1 MUSEUM NATL HIST NAT,BIOPHYS LAB,43 RUE CUVIER,F-75231 PARIS 05,FRANCE. AMGEN GMBH,MUNICH,GERMANY. NIH,BETHESDA,MD 20892. NR 11 TC 3 Z9 3 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 1994 VL 5 SU 4 BP S55 EP S58 PG 4 WC Oncology SC Oncology GA NP848 UT WOS:A1994NP84800010 ER PT J AU WALDMANN, TA AF WALDMANN, TA TI LYMPHOKINE RECEPTORS - A TARGET FOR IMMUNOTHERAPY OF LYMPHOMAS SO ANNALS OF ONCOLOGY LA English DT Article; Proceedings Paper CT 5th International Conference on Malignant Lymphoma CY JUN 09-12, 1993 CL LUGANO, SWITZERLAND DE ADULT T-CELL LEUKEMIA; ANTI-TAC MONOCLONAL ANTIBODY; HUMAN T-CELL LYMPHOTROPIC VIRUS-1; INTERLEUKIN-2 RECEPTORS ID T-CELL LEUKEMIA; NON-HODGKINS LYMPHOMAS; ANTI-TAC-H; INTERLEUKIN-2 RECEPTOR; MONOCLONAL-ANTIBODY; HUMANIZED ANTIBODY; PSEUDOMONAS EXOTOXIN; IL-2 RECEPTOR; LYMPHOCYTES; EXPRESSION AB Lymphoma cells often express lymphokine receptors that provide a target for therapy. For example, malignant cells of patients with HTLV-1-associated adult T-cell leukemia/lymphoma (ATL) express IL-2 receptors. In contrast, normal resting cells do not express the IL-2 receptors identified by the anti-Tac monoclonal antibody. Using the unmodified anti-Tac monoclonal antibody, one-third of die 19 patients treated with ATL have undergone a remission. However, unmodified murine monoclonal antibodies are limited by their immunogenicity and their poor effector functions. To address these issues, we used genetic engineering to produce humanized anti-Tac that contains the complementarity-determining regions from the mouse with the remainder of the antibody derived from human IgG1-kappa. Humanized anti-Tac is dramatically less immunogenic than the murine versions and, in contrast to the parent antibody, manifests antibody-dependent cellular cytotoxicity with human mononuclear cells. To enhance its effector function, anti-Tac was armed with toxins or with alpha- and beta-emitting radionuclides. In a clinical trial with Y-90-anti-Tac, 11 of the 17 patients with ATL underwent a partial or sustained complete remission. Thus, the clinical application of lymphokine-receptor-directed therapy provides a new perspective for treatment of certain lymphomas, including HTLV-1-associated ATL. RP WALDMANN, TA (reprint author), NCI,METAB BRANCH,BETHESDA,MD 20892, USA. NR 31 TC 5 Z9 5 U1 1 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 1994 VL 5 SU 1 BP S13 EP S17 PG 5 WC Oncology SC Oncology GA MX109 UT WOS:A1994MX10900005 ER PT J AU LUDLOW, CL VANPELT, F YEH, J RHEW, K COHEN, LG HALLETT, M AF LUDLOW, CL VANPELT, F YEH, J RHEW, K COHEN, LG HALLETT, M TI LIMITATIONS OF ELECTROMYOGRAPHY AND MAGNETIC STIMULATION FOR ASSESSING LARYNGEAL MUSCLE CONTROL SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE ELECTROMYOGRAPHY; LARYNGEAL MUSCLES; MAGNETIC STIMULATION ID SPASMODIC DYSPHONIA; FACIAL-NERVE; CONDUCTION; ELECTRODE; RESPONSES; DYSTONIA; BRAIN; COIL AB The development of new phonosurgical techniques has increased the level of interest in the field of neurolaryngology. This field requires valid techniques for determining if muscle activation is normal. Laryngeal electromyography is being used more frequently to assess muscle innervation and synkinesis. Further, magnetic stimulation has been introduced as a noninvasive technique for nerve stimulation. Technical limitations that affect the clinical utility of both these techniques are reviewed: 1) difficulties obtaining selective and accurate electromyographic laryngeal muscle recordings. 2) normal variation in movement and muscle activation patterns within and between normal individuals when producing the same speech syllables, and 3) variation in laryngeal muscle response latencies between and within normal subjects during peripheral magnetic stimulation. Given the normal variation in laryngeal electromyography and magnetic stimulation response latencies, these techniques may not yet be reliable or accurate for assessing reinnervation or synkinesis following recurrent laryngeal nerve injury. C1 NIDOCD,VOICE & SPEECH SECT,BETHESDA,MD. NINCDS,HUMAN MOTOR CONTROL SECT,BETHESDA,MD. OI Ludlow, Christy/0000-0002-2015-6171 NR 41 TC 27 Z9 27 U1 0 U2 1 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD JAN PY 1994 VL 103 IS 1 BP 16 EP 27 PG 12 WC Otorhinolaryngology SC Otorhinolaryngology GA MR290 UT WOS:A1994MR29000003 PM 8291855 ER PT J AU PASS, HI DELANEY, TF TOCHNER, Z SMITH, PE TEMECK, BK POGREBNIAK, HW KRANDA, KC RUSSO, A FRIAUF, WS COLE, JW MITCHELL, JB THOMAS, G AF PASS, HI DELANEY, TF TOCHNER, Z SMITH, PE TEMECK, BK POGREBNIAK, HW KRANDA, KC RUSSO, A FRIAUF, WS COLE, JW MITCHELL, JB THOMAS, G TI INTRAPLEURAL PHOTODYNAMIC THERAPY - RESULTS OF A PHASE-I TRIAL SO ANNALS OF SURGICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 46th Annual Cancer Symposium of the Society-of-Surgical-Oncology CY MAR 18-21, 1993 CL LOS ANGELES, CA SP SOC SURG ONCOL DE PHOTODYNAMIC THERAPY; PLEURA; MESOTHELIOMA; METASTASES; LIGHT; SENSITIZER AB Background: The management of pleural neoplasms, specifically mesothelioma, remains difficult. We performed a phase I trial in 54 patients with isolated hemithorax pleural malignancy to determine (a) the feasibility of intraoperative, intrapleural photodynamic therapy after debulking surgery; (b) the influence of light dose/sensitizer interval on postoperative morbidity in order to define the photodynamic therapy (PDT) maximal tolerated dose (MTD); and (c) whether first order dosimetry could be applied to this complex geometry. Methods: Cohorts of three patients were given escalating intraoperative light doses of 15-35 J/cm2 48 h after i.v. delivery of 2.0 mg/kg Photofrin II (Quadra Logic Technologies, Vancouver, British Columbia, Canada), and then escalating light doses of 30-32.5 J/cm2 after a 24-h sensitizer/operation interval. Twelve patients could not be debulked to the prerequisite 5 mm residual tumor thickness. The remaining 42 patients underwent 19 modified pleuropneumonectomies, five lobectomy-pleurectomies, and 18 pleurectomies. Intrapleural PDT was delivered using 630 nm light from two argon pump-dye lasers, and real-time and cumulative light doses were monitored using seven uniquely designed, computer-interfaced photodiodes. Results: There was one 30-day mortality from intraoperative hemorrhage. In the 48-h sensitizer/operation group (n = 33), possible PDT-related complications included an empyema with late hemorrhage in one of three patients at 17.5 J/cm2 and a bronchopleural fistula at 35 J/cm2. At each of these light doses, three additional patients were treated without complication. Two patients subjected to 24-h sensitizer dosing and 32.5 J/cm2 developed esophageal perforations after pleuropneumonectomy at identical sites. The MTD was declared as 30 J/cm2 light with a 24-h dosing interval when none of the six patients (three original, three repeat) at that level developed toxicity. Conclusions: These data demonstrate that resection and intrapleural PDT can be performed safely with currently available sensitizers and lasers. Phase II and III trials are now warranted at this MTD in a homogeneous population of patients with pleural malignancies. C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NCI,EXPTL PHOTOTHERAPY SECT,BETHESDA,MD 20892. NIH,NATL CTR RES RESOURCES,BETHESDA,MD 20892. RP PASS, HI (reprint author), NCI,SURG BRANCH,THORAC ONCOL SECT,BLDG 10,ROOM 2B07,BETHESDA,MD 20892, USA. NR 14 TC 63 Z9 65 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1068-9265 J9 ANN SURG ONCOL JI Ann. Surg. Oncol. PD JAN PY 1994 VL 1 IS 1 BP 28 EP 37 DI 10.1007/BF02303538 PG 10 WC Oncology; Surgery SC Oncology; Surgery GA NM328 UT WOS:A1994NM32800005 PM 7834425 ER PT J AU SIEBENLIST, U FRANZOSO, G BROWN, K AF SIEBENLIST, U FRANZOSO, G BROWN, K TI STRUCTURE, REGULATION AND FUNCTION OF NF-KAPPA-B SO ANNUAL REVIEW OF CELL BIOLOGY LA English DT Review DE I-KAPPA-B; REL; DORSAL; ANKYRIN MOTIF; GENE REGULATION; IMMUNE ACTIVATION; HIV CYTOKINES ID TUMOR-NECROSIS-FACTOR; HUMAN-IMMUNODEFICIENCY-VIRUS; DNA-BINDING ACTIVITY; PROTEIN-KINASE-C; T-CELL LEUKEMIA; CANDIDATE PROTOONCOGENE BCL-3; LONG TERMINAL REPEAT; SIGNAL-TRANSDUCTION PATHWAY; NUCLEAR-LOCALIZATION SIGNAL; DROSOPHILA MORPHOGEN DORSAL RP SIEBENLIST, U (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,BETHESDA,MD 20892, USA. NR 366 TC 1825 Z9 1901 U1 3 U2 45 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0743-4634 J9 ANNU REV CELL BIOL JI Annu. Rev. Cell Biol. PY 1994 VL 10 BP 405 EP 455 DI 10.1146/annurev.cb.10.110194.002201 PG 51 WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology GA PU882 UT WOS:A1994PU88200012 PM 7888182 ER PT J AU HOELZEL, AR AF HOELZEL, AR TI GENETICS AND ECOLOGY OF WHALES AND DOLPHINS SO ANNUAL REVIEW OF ECOLOGY AND SYSTEMATICS LA English DT Review DE MARINE MAMMALS; CETACEANS; POPULATION GENETICS; MOLECULAR GENETICS ID HUMPBACK WHALES; MITOCHONDRIAL-DNA; POPULATION-STRUCTURE; KILLER WHALES; MIGRATION; DYNAMICS; TURSIOPS AB Cetacean species are widely distributed in the world's oceans, and their populations are impacted by human activity both directly through hunting and indirectly. The determination of genetic stock boundaries and genetic diversity within stocks is essential to the conservation of genetic diversity in these as in any other species, but cetaceans present special challenges. The definition of stock boundaries based on assumptions drawn from experience with terrestrial species has proven inadequate for cetaceans. For example, genetic stock boundaries do not necessarily correspond to patterns of apparent geographic isolation. Cetaceans are capable of migrating great distances, and in some cases breeding populations mix in seasonal feeding grounds up to thousands of miles from where they breed. Among those species that breed and forage within the same geographic range, intraspecific differences in feeding ecology can lead to the genetic differentiation of local populations. This review presents a summary of the available data on genetic diversity and differentiation within cetacean species, with an emphasis on the ecological context. RP NCI, VIRAL CARCINOGENESIS LAB, BLDG 560, FREDERICK, MD 21702 USA. NR 62 TC 24 Z9 26 U1 5 U2 26 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4162 J9 ANNU REV ECOL SYST JI Annu. Rev. Ecol. Syst. PY 1994 VL 25 BP 377 EP 399 PG 23 WC Ecology; Evolutionary Biology SC Environmental Sciences & Ecology; Evolutionary Biology GA PU883 UT WOS:A1994PU88300015 ER PT J AU SCRIVER, CR EISENSMITH, RC WOO, SLC KAUFMAN, S AF SCRIVER, CR EISENSMITH, RC WOO, SLC KAUFMAN, S TI THE HYPERPHENYLALANINEMIAS OF MAN AND MOUSE SO ANNUAL REVIEW OF GENETICS LA English DT Review DE PHENYLALANINE HYDROXYLASE; PHENYLALANINE HYDROXYLATION REACTION; TETRAHYDROBIOPTERIN SYNTHESIS AND RECYCLING; PHENYLKETONURIA; PAH GENE HUMAN; PAH GENE MOUSE ID HUMAN PHENYLALANINE-HYDROXYLASE; DIHYDROPTERIDINE REDUCTASE DEFICIENCY; GTP CYCLOHYDROLASE-I; HUMAN BIOCHEMICAL GENETICS; AMINO-ACID HYDROXYLASES; MOLECULAR-BASIS; TETRAHYDROBIOPTERIN DEFICIENCY; 4A-CARBINOLAMINE DEHYDRATASE; PRENATAL-DIAGNOSIS; ESCHERICHIA-COLI C1 MONTREAL CHILDRENS HOSP,RES INST,DIV MED GENET,DEBELLE LAB,MONTREAL,PQ H3H 1P3,CANADA. BAYLOR COLL MED,HOWARD HUGHES MED INST,HOUSTON,TX 77030. NIH,NEUROCHEM LAB,BETHESDA,MD 20014. RP SCRIVER, CR (reprint author), MCGILL UNIV,DEPT HUMAN GENET & PEDIAT,MONTREAL,PQ H3H 1P3,CANADA. NR 155 TC 49 Z9 50 U1 0 U2 4 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4197 J9 ANNU REV GENET JI Annu. Rev. Genet. PY 1994 VL 28 BP 141 EP 165 PG 25 WC Genetics & Heredity SC Genetics & Heredity GA PY644 UT WOS:A1994PY64400007 PM 7893121 ER PT J AU OBRIEN, SJ AF OBRIEN, SJ TI GENETIC AND PHYLOGENETIC ANALYSES OF ENDANGERED SPECIES SO ANNUAL REVIEW OF GENETICS LA English DT Review DE POPULATION BOTTLENECK; REPRODUCTION; HOMOGENEOUS STATE OF GENES; INBREEDING; SPERM ABNORMALITIES ID NORTH-AMERICAN ZOOS; FELINE IMMUNODEFICIENCY VIRUS; CHEETAHS ACINONYX-JUBATUS; FREE-RANGING CHEETAHS; HUMAN GENOME PROJECT; MITOCHONDRIAL-DNA; HUMPBACK WHALES; AFRICAN CHEETAH; FLORIDA PANTHER; POPULATIONS RP OBRIEN, SJ (reprint author), NCI, VIRAL CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. NR 165 TC 69 Z9 74 U1 3 U2 22 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4197 EI 1545-2948 J9 ANNU REV GENET JI Annu. Rev. Genet. PY 1994 VL 28 BP 467 EP 489 PG 23 WC Genetics & Heredity SC Genetics & Heredity GA PY644 UT WOS:A1994PY64400021 PM 7893136 ER PT J AU MURPHY, PM AF MURPHY, PM TI THE MOLECULAR-BIOLOGY OF LEUKOCYTE CHEMOATTRACTANT RECEPTORS SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE CHEMOTAXIS; G PROTEIN-COUPLED RECEPTOR; INFLAMMATION; HERPESVIRUS; MALARIA ID FORMYL PEPTIDE RECEPTOR; PLATELET-ACTIVATING-FACTOR; PROTEIN-COUPLED RECEPTOR; MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; GROWTH-STIMULATORY ACTIVITY; HUMAN INTERLEUKIN-8 RECEPTOR; SIGNAL-TRANSDUCTION PATHWAYS; DIFFERENTIATED HL-60 CELLS; XENOPUS-LAEVIS OOCYTES; HUMAN C5A RECEPTOR AB Leukocytes migrate from the blood to sites of inflammation in response to locally produced chemoattractants that activate specific cell surface receptors. The primary structures of leukocyte receptors for N-formyl peptides, C5a, platelet-activating factor, and 8 of the 18 known human chemokines (interleukin-8 and related molecules) have been deduced from cloned cDNAs. All of these are seven-transmembrane-domain rhodopsin-like G protein-coupled receptors. Biochemical and molecular genetic analysis of the chemoattractant receptors indicates that the chemoattractants may have both broadly overlapping as well as specialized roles in the regulation of acute and chronic inflammation. Interestingly, the chemokine receptors have functional homologues in human cytomegalovirus and Herpesvirus saimiri. Moreover, the Duffy antigen, which mediates invasion of erythrocytes by Plasmodium vivax, a major cause of malaria, is also a chemokine binding protein. These surprising developments suggest that in addition to leukocyte-mediated inflammation, the chemokines may also be involved in erythrocyte function and, through molecular mimicry, in microbial pathogenesis. RP MURPHY, PM (reprint author), NIAID,HOST DEF LAB,BETHESDA,MD 20892, USA. NR 164 TC 1040 Z9 1059 U1 2 U2 29 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1994 VL 12 BP 593 EP 633 DI 10.1146/annurev.immunol.12.1.593 PG 41 WC Immunology SC Immunology GA NF487 UT WOS:A1994NF48700019 PM 8011292 ER PT J AU SEDER, RA PAUL, WE AF SEDER, RA PAUL, WE TI ACQUISITION OF LYMPHOKINE-PRODUCING PHENOTYPE BY CD4+ T-CELLS SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE LYMPHOKINE; IL-4; IFN-GAMMA; IL-12; T CELLS ID INTERFERON-GAMMA PRODUCTION; MIXED LEUKOCYTE REACTION; ANTIGEN-PRESENTING CELL; SPLENIC NON-B; IFN-GAMMA; STIMULATORY FACTOR; LEISHMANIA-MAJOR; IL-4 PRODUCTION; TH2 CLONES; MEDIATED-IMMUNITY AB Naive CD4(+) T cells when stimulated produce IL-2 as their major lymphokine. Upon priming, these cells develop into cells that produce either IFN gamma, TNF beta, and IL-2 or IL-4 and its congeners. The former cells are designated T-H1-like, and the latter T-H2-like. Here we review the regulation of the differentiation of naive CD4 cells into IFN gamma- or IL-4-producers. The dominant factors that determine such differentiation are lymphokines and other cytokines. IL-2 itself appears to be required for naive cells to develop into T-H1- or T-H2-like cells but is not deterministic of their differentiation fate. If IL-4 is also present during the priming period, the resultant CD4(+) T cells produce IL-4 upon restimulation; the development of IFN gamma-producing cells is strikingly inhibited by IL-4. In the absence of IL-4, priming for IFN gamma-production occurs, but this is markedly enhanced by IL-12. The role of IFN gamma in enhancing priming for IFN gamma-production is not fully resolved. In some in vitro systems, it appears to act together with IL-12 to enhance such production. Anti-IFN gamma diminishes priming for IFN gamma production in vivo. Lymphokines also exert a ''cross-regulatory'' or inhibitory effect. As noted above, IL-4 strikingly diminishes priming for IFN gamma production, although this inhibitory effect is blunted in the presence of IL-12. IFN gamma similarly diminishes priming for IL-4 production; this effect is principally observed when low concentrations of IL-4 are used in the priming culture. Although other factors may play a role in the determination of lymphokine-producing phenotype, such as antigen dose, type of antigen-presenting cell, and expression of accessory molecules and hormones, these effects appear to be secondary to the dominant role of the lymphokines and cytokines. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RI Yang, Chen/G-1379-2010 NR 107 TC 1417 Z9 1434 U1 3 U2 15 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1994 VL 12 BP 635 EP 673 DI 10.1146/annurev.immunol.12.1.635 PG 39 WC Immunology SC Immunology GA NF487 UT WOS:A1994NF48700020 PM 7912089 ER PT J AU ROBEY, E FOWLKES, BJ AF ROBEY, E FOWLKES, BJ TI SELECTIVE EVENTS IN T-CELL DEVELOPMENT SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE POSITIVE SELECTION; NEGATIVE SELECTION; LINEAGE COMMITMENT; TCR GENE REARRANGEMENT; THYMOCYTES ID MAJOR HISTOCOMPATIBILITY COMPLEX; RECEPTOR-BETA-CHAIN; ANTIGEN-PRESENTING CELLS; II-DEFICIENT MICE; POSITIVE SELECTION; TRANSGENIC MICE; THYMOCYTE DEVELOPMENT; CLONAL DELETION; LYMPHOCYTES-T; THYMIC SELECTION AB Somatic rearrangement of the genes encoding antigen receptors allows the mammalian immune system to produce receptors that can recognize virtually any foreign protein. This rearrangement process also generates nonfunctional antigen receptors as well as receptors that can recognize self-proteins. During thymic development, T cells go through a testing process which ensures that cells expressing useless or harmful antigen receptors do not mature. The selection of T cells in the thymus consists of several components driven by distinct recognition events that have distinct consequences for the cell. T cell selection appears to begin before the rearrangement process is complete. Evidence is emerging that T cells have a developmental checkpoint to make sure that the antigen receptor beta gene is successfully rearranged before development can proceed. This checkpoint also appears to be linked to the regulation of rearrangement and mechanisms to ensure that each cell expresses only one antigen receptor (allelic exclusion). After a T cell has successfully rearranged and expressed both its alpha and beta antigen receptor genes, a second phase of selection occurs. During this phase, T cells with self-reactive antigen receptors are eliminated by negative selection, and T cells that can recognize foreign peptides bound to polymorphic self-MHC molecules are selected to mature (positive selection). How these seemingly incompatible forms of selection both occur is a subject of considerable interest. Positive selection is linked also to the choice between the CD4 helper lineage and the CD8 cytotoxic T cell lineage; the mechanisms by which these two events are linked is an ongoing area of investigation. C1 NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892. RP ROBEY, E (reprint author), UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720, USA. FU NIAID NIH HHS [AI-32985-01] NR 121 TC 421 Z9 423 U1 1 U2 16 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1994 VL 12 BP 675 EP 705 DI 10.1146/annurev.immunol.12.1.675 PG 31 WC Immunology SC Immunology GA NF487 UT WOS:A1994NF48700021 PM 8011294 ER PT J AU WEINER, HL FRIEDMAN, A MILLER, A KHOURY, SJ ALSABBAGH, A SANTOS, L SAYEGH, M NUSSENBLATT, RB TRENTHAM, DE HAFLER, DA AF WEINER, HL FRIEDMAN, A MILLER, A KHOURY, SJ ALSABBAGH, A SANTOS, L SAYEGH, M NUSSENBLATT, RB TRENTHAM, DE HAFLER, DA TI ORAL TOLERANCE - IMMUNOLOGICAL MECHANISMS AND TREATMENT OF ANIMAL AND HUMAN ORGAN-SPECIFIC AUTOIMMUNE-DISEASES BY ORAL-ADMINISTRATION OF AUTOANTIGENS SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE ACTIVE SUPPRESSION; ANERGY; TGF-BETA; AUTOIMMUNITY; EAE ID MYELIN BASIC-PROTEIN; SUPPRESSOR T-CELLS; NONOBESE DIABETIC MICE; MUCOSAL IMMUNE-SYSTEM; DRIVEN BYSTANDER SUPPRESSION; GLUTAMIC-ACID DECARBOXYLASE; COLLAGEN-INDUCED ARTHRITIS; FEEDING CHOLERA-TOXIN; GROWTH-FACTOR-BETA; PEYERS PATCH AB Oral tolerance is a long recognized method to induce peripheral immune tolerance. The primary mechanisms by which orally administered antigen induces tolerance are via the generation of active suppression or clonal anergy. Low doses of orally administered antigen favor active suppression whereas higher doses favor clonal anergy. The regulatory cells that mediate active suppression act via the secretion of suppressive cytokines such as TGF beta and IL-4 after being triggered by the oral tolerogen. Furthermore, antigen that stimulates the gut-associated lymphoid tissue preferentially generates a Th2 type response. Because the regulatory cells generated following oral tolerization are triggered in an antigen-specific fashion but suppress in an antigen nonspecific fashion, they mediate ''bystander suppression'' when they encounter the fed autoantigen at the target organ. Thus it may not be necessary to identify the target autoantigen to suppress an organ-specific autoimmune disease via oral tolerance; it is necessary only to administer orally a protein capable of inducing regulatory cells that secrete suppressive cytokines. Orally administered autoantigens suppress several experimental autoimmune models in a disease- and antigen-specific fashion; the diseases include experimental autoimmune encephalomyelitis (EAE), uveitis, and myasthenia, collagen- and adjuvant-induced arthritis, and diabetes in the NOD mouse. In addition, orally administered alloantigen suppresses alloreactivity and prolongs graft survival. Initial clinical trials of oral tolerance in multiple sclerosis, rheumatoid arthritis, and uveitis have demonstrated positive clinical effects with no apparent toxicity and decreases in T cell autoreactivity. C1 BRIGHAM & WOMENS HOSP,TRANSPLANTAT LAB,BOSTON,MA 02115. BETH ISRAEL HOSP,DIV RHEUMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NEI,IMMUNOL LAB,BETHESDA,MD 20205. RP WEINER, HL (reprint author), BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,BOSTON,MA 02115, USA. RI Friedman, Aharon/C-3455-2009; OI Friedman, Aharon/0000-0002-5968-0667; khoury, samia/0000-0003-3198-6063 FU NINDS NIH HHS [NS24247, NS29352, NS23132] NR 138 TC 813 Z9 822 U1 3 U2 21 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1994 VL 12 BP 809 EP 837 DI 10.1146/annurev.immunol.12.1.809 PG 29 WC Immunology SC Immunology GA NF487 UT WOS:A1994NF48700025 PM 8011298 ER PT J AU CEASE, KB BERZOFSKY, JA AF CEASE, KB BERZOFSKY, JA TI TOWARD A VACCINE FOR AIDS - THE EMERGENCE OF IMMUNOBIOLOGY-BASED VACCINE DEVELOPMENT SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE HUMAN IMMUNODEFICIENCY VIRUS; VACCINES ID HUMAN-IMMUNODEFICIENCY-VIRUS; CYTOTOXIC LYMPHOCYTES-T; HUMAN MONOCLONAL-ANTIBODY; CLASS-II MOLECULES; CD4 BINDING-SITE; MHC CLASS-II; ENVELOPE GLYCOPROTEIN GP120; INTERFERON-GAMMA PRODUCTION; CELL-MEDIATED-IMMUNITY; NECROSIS-FACTOR-ALPHA AB Over a decade has passed since the identification of the human immunodeficiency virus (HIV) as the causative agent of AIDS. During this time, HIV has been extensively characterized, and a variety of vaccine constructs and strategies have been explored. For the most part, these have been driven by successes of the past with other pathogens, or by novel approaches enabled by technologies of the present. With the maturing of our insights into the immunopathology of HIV and basic immunological mechanisms, we are presented with unprecedented opportunities to rationally develop vaccine approaches strategically designed to counter the immunopathology of HIV. As opposed to absolute prevention of infection, the primacy goal of these strategies may be to limit infection and to assure a response to infection that prevents disease and transmission. Thus, such vaccines may fmd utility in both preventive and therapeutic roles. In this paper, we present the background and current state of immunobiology-driven vaccine development for AIDS. C1 VET ADM MED CTR,ANN ARBOR,MI 48109. NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD 20892. RP CEASE, KB (reprint author), UNIV MICHIGAN,DEPT INTERNAL MED,DIV HEMATOL ONCOL,ANN ARBOR,MI 48109, USA. FU NIAID NIH HHS [R01-AI26818] NR 477 TC 77 Z9 78 U1 0 U2 0 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1994 VL 12 BP 923 EP 989 DI 10.1146/annurev.immunol.12.1.923 PG 67 WC Immunology SC Immunology GA NF487 UT WOS:A1994NF48700028 PM 7516670 ER PT J AU MATZINGER, P AF MATZINGER, P TI TOLERANCE, DANGER, AND THE EXTENDED FAMILY SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE ANTIGEN PRESENTATION; IMMUNITY; T CELLS; DENDRITIC CELLS; VIRUSES ID T-CELL TOLERANCE; ANTIGEN-PRESENTING CELLS; TOXIC LYMPHOCYTES-T; MINOR HISTOCOMPATIBILITY ANTIGENS; CLASS-I MOLECULES; SELF-TOLERANCE; B-CELLS; TRANSGENIC MICE; IMMUNOLOGICAL-TOLERANCE; TRANSPLANTATION TOLERANCE AB For many years immunologists have been well served by the viewpoint that the immune system's primary goal is to discriminate between self and non-self. I believe that it is time to change viewpoints and, in this essay, I discuss the possibility that the immune system does not care about self and non-self, that its primary driving force is the need to detect and protect against danger, and that it does not do the job alone, but receives positive and negative communications from an extended network of other bodily tissues. RP MATZINGER, P (reprint author), NIAID,CELLULAR & MOLEC IMMUNOL LAB,BLDG 10,ROOM 111,BETHESDA,MD 20892, USA. NR 158 TC 2822 Z9 2933 U1 7 U2 83 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1994 VL 12 BP 991 EP 1045 DI 10.1146/annurev.immunol.12.1.991 PG 55 WC Immunology SC Immunology GA NF487 UT WOS:A1994NF48700029 PM 8011301 ER PT J AU SPANGRUDE, GJ AF SPANGRUDE, GJ TI BIOLOGICAL AND CLINICAL ASPECTS OF HEMATOPOIETIC STEM-CELLS SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE BONE MARROW TRANSPLANTATION; CANCER; CYTOKINE THERAPY; GENE THERAPY; STEM-CELL EXPANSION ID COLONY-STIMULATING FACTOR; BLOOD PROGENITOR CELLS; ACUTE MYELOID-LEUKEMIA; MURINE BONE-MARROW; PERIPHERAL-BLOOD; MONOCLONAL-ANTIBODY; LIMITING-DILUTION; FORMING CELLS; CFU-S; DOSE INTENSIFICATION AB Recent advances in cell isolation techniques have greatly enhanced our understanding of the phenotype and function of hematopoietic stem cells in mice and humans. Many clinical studies have established the efficacy of using peripheral blood stem cells to supplement or replace bone marrow transplantation as a therapeutic modality for several types of malignancies. This new approach to malignant disease management, perhaps in combination with posttransplantation cytokine therapy, promises to completely alter the clinical course of bone marrow transplantation. RP SPANGRUDE, GJ (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 91 TC 34 Z9 33 U1 0 U2 0 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1994 VL 45 BP 93 EP 104 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA NF168 UT WOS:A1994NF16800009 PM 7515222 ER PT J AU CHANG, LW HSIA, SMT CHAN, PC HSIEH, LL AF CHANG, LW HSIA, SMT CHAN, PC HSIEH, LL TI MACROMOLECULAR ADDUCTS - BIOMARKERS FOR TOXICITY AND CARCINOGENESIS SO ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY LA English DT Review DE BIOMONITORING AND MOLECULAR EPIDEMIOLOGY; PREDICTION OF TOXICITY AND CARCINOGENESIS; EXPOSURE INDEX OF CHEMICALS; DNA ADDUCTS ID WHITE BLOOD-CELLS; HYDROCARBON-DNA ADDUCTS; P-32 POSTLABELING ASSAY; DOSE-RESPONSE RELATIONSHIPS; AFLATOXIN-ALBUMIN ADDUCTS; HEMOGLOBIN ADDUCTS; CANCER-PATIENTS; HEPATOCELLULAR-CARCINOMA; CHEMICAL CARCINOGENESIS; MONOCLONAL-ANTIBODIES C1 UNIV ARKANSAS MED SCI HOSP,DEPT PHARMACOL & TOXICOL,LITTLE ROCK,AR 72205. MITRE CORP,MCLEAN,VA 22101. NIEHS,RES TRIANGLE PK,NC. CHANG GUNG MED COLL,DEPT PUBL HLTH,TAYUAN,TAIWAN. RP CHANG, LW (reprint author), UNIV ARKANSAS MED SCI HOSP,DEPT PATHOL,LITTLE ROCK,AR 72205, USA. NR 136 TC 30 Z9 30 U1 1 U2 2 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0362-1642 J9 ANNU REV PHARMACOL JI Annu. Rev. Pharmacol. Toxicol. PY 1994 VL 34 BP 41 EP 67 PG 27 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA NH295 UT WOS:A1994NH29500003 PM 8042856 ER PT J AU HUFF, J LUCIER, G TRITSCHER, A AF HUFF, J LUCIER, G TRITSCHER, A TI CARCINOGENICITY OF TCDD - EXPERIMENTAL, MECHANISTIC, AND EPIDEMIOLOGIC EVIDENCE SO ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY LA English DT Review DE CHEMICAL CARCINOGENESIS; LONG-TERM EXPERIMENTS; RISK ASSESSMENT; EXTRAPOLATION; RODENTS AND HUMANS ID POLYCYCLIC AROMATIC-HYDROCARBONS; DOSE-RESPONSE RELATIONSHIPS; NUCLEAR ESTROGEN-RECEPTOR; GROWTH-FACTOR RECEPTOR; BREAST-CANCER-CELLS; RAT-LIVER; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN TCDD; TUMOR PROMOTION; AH-RECEPTOR; HUMAN EXPOSURE C1 NIEHS, ENVIRONM BIOL & MED PROGRAM, RES TRIANGLE PK, NC 27709 USA. RP HUFF, J (reprint author), NIEHS, ENVIRONM CARCINOGENESIS PROGRAM, RES TRIANGLE PK, NC 27709 USA. NR 193 TC 152 Z9 155 U1 1 U2 6 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0362-1642 EI 1545-4304 J9 ANNU REV PHARMACOL JI Annu. Rev. Pharmacol. Toxicol. PY 1994 VL 34 BP 343 EP 372 PG 30 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA NH295 UT WOS:A1994NH29500014 PM 8042855 ER PT J AU MAKINO, H MANGANIELLO, VC KONO, T AF MAKINO, H MANGANIELLO, VC KONO, T TI ROLES OF ATP IN INSULIN ACTIONS SO ANNUAL REVIEW OF PHYSIOLOGY LA English DT Review DE ATP; INSULIN; PROTEIN KINASE; GLUCOSE TRANSPORT; CAMP; PHOSPHODIESTERASE ID ACETYL-COA CARBOXYLASE; SENSITIVE CAMP PHOSPHODIESTERASE; STIMULATED PROTEIN-KINASE; RAT ADIPOSE CELL; ELECTROPERMEABILIZED FAT-CELLS; EPIDERMAL GROWTH-FACTOR; RABBIT SKELETAL-MUSCLE; NUCLEAR FACTOR CREB; GLUCOSE-TRANSPORT; MAP KINASE C1 NHLBI,BETHESDA,MD 20892. VANDERBILT UNIV,SCH MED,NASHVILLE,TN 37232. RP MAKINO, H (reprint author), CHIBA UNIV,SCH MED,CHIBA 280,JAPAN. FU NIDDK NIH HHS [DK 06725, DK 19925] NR 136 TC 14 Z9 14 U1 1 U2 1 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4278 J9 ANNU REV PHYSIOL JI Annu. Rev. Physiol. PY 1994 VL 56 BP 273 EP 295 PG 23 WC Physiology SC Physiology GA NB224 UT WOS:A1994NB22400013 PM 7912059 ER PT J AU DOLJA, VV KARASEV, AV KOONIN, EV AF DOLJA, VV KARASEV, AV KOONIN, EV TI MOLECULAR-BIOLOGY AND EVOLUTION OF CLOSTEROVIRUSES - SOPHISTICATED BUILDUP OF LARGE RNA GENOMES SO ANNUAL REVIEW OF PHYTOPATHOLOGY LA English DT Review DE POSITIVE-STRAND RNA VIRUSES; ALPHAVIRUS SUPERGROUP; GENOME EXPRESSION; TAXONOMY ID BEET YELLOWS CLOSTEROVIRUS; CITRUS-TRISTEZA-VIRUS; COAT PROTEIN GENE; HEAT-SHOCK PROTEINS; PLANT-VIRUSES; NUCLEIC-ACID; NUCLEOTIDE-SEQUENCE; LEAFROLL DISEASE; CLEAVAGE SITE; KDA PROTEIN C1 UNIV CALIF RIVERSIDE,DEPT PLANT PATHOL,RIVERSIDE,CA 92521. UNIV FLORIDA,CTR AGR RES & EDUC,CTR CITRUS RES & EDUC,LAKE ALFRED,FL 33850. NIH,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. RP DOLJA, VV (reprint author), OREGON STATE UNIV,DEPT BOT & PLANT PATHOL,CORVALLIS,OR 97331, USA. NR 95 TC 130 Z9 137 U1 1 U2 5 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4286 J9 ANNU REV PHYTOPATHOL JI Annu. Rev. Phytopathol. PY 1994 VL 32 BP 261 EP 285 PG 25 WC Plant Sciences SC Plant Sciences GA PH334 UT WOS:A1994PH33400017 ER PT J AU MOON, RC KELLOFF, GJ DETRISAC, CJ STEELE, VE THOMAS, CF SIGMAN, CC AF MOON, RC KELLOFF, GJ DETRISAC, CJ STEELE, VE THOMAS, CF SIGMAN, CC TI CHEMOPREVENTION OF OH-BBN-INDUCED BLADDER-CANCER IN MICE BY OLTIPRAZ, ALONE AND IN COMBINATION WITH 4-HPR AND DFMO SO ANTICANCER RESEARCH LA English DT Article DE CHEMOPREVENTION; BLADDER; OLTIPRAZ; DFMO; 4-HPR ID ORNITHINE DECARBOXYLASE ACTIVITY; MURINE MAMMARY CARCINOGENESIS; SKIN TUMOR PROMOTION; ALPHA-DIFLUOROMETHYLORNITHINE; 5-(2-PYRAZINYL)-4-METHYL-1,2-DITHIOL-3-THIONE OLTIPRAZ; INTESTINAL CARCINOGENESIS; MOUSE SKIN; COLON CARCINOGENESIS; F344 RATS; INHIBITION AB The chemopreventive efficacy of the schistosomicidal drug oltipraz (5-(2-pyrazinyl)-4-methyl-1,2-dithiol-3-thione) was evaluated against urinary bladder transitional cell carcinoma (TCC) induced in male C57BL/6 x DBA/2FI (BDF) mice by N-butyl-N(4-hydroxybutyl)nitrosamine (OH-BBN). Oltipraz was Sed in the diet from one week prior to OH-BBN dosing until sacrifice, six months Inter: The agent at 250 mg/kg diet significantly reduced the incidence of TCC compared with that in carcinogen controls. Oltipraz also significantly reduced TCC incidence when fed at 500 mg/kg diet for 76 days, then at 125 mg/kg diet until the end of the test period. Treatment with this higher dose level of oltipraz also appeared to decrease the depth of tumor invasion. At lower close levels of 100 and 200 mg/kg diet, oltipraz alone had no effect on tumor incidence. It also was tested at these dose levels in combinations with 2-difluoromethylornithine (DFMO) and with all-trans-N-(4-hydroxphyenyl)retinamide (4-HPR). Treatment with the combination of 640 mg DFMO/kg and 100 mg oltipraz/kg diet was efficacious, although DFMO alone at 640 mg/kg diet was inactive. The combination of 1280 mg DFMO/kg and 200 mg oltipraz/kg diet reduced TCC incidence significantly compared with carcinogen controls, but the effect was no greater than that of DFMO alone at 1280 mg/kg, and weight gain was suppressed compared with carcinogen controls. The depth of tumor invasion was decreased with this combination treatment. Combinations of oltipraz at too and 200 mg/kg diet, 4-HPR at 156 and 313 mg/kg diet, and DFMO at 640 and 1280 mg/kg diet were efficacious and without apparent toxicity. Nonetheless, the three agent combinations cannot be considered more effective than DFMO alone at 1280 mg/kg diet or the lower dose combination of oltipraz and DFMO. C1 IIT,RES INST,CHICAGO,IL 60616. NCI,CHEMOPREVENT INVEST DRUG UNIT,BETHESDA,MD 20892. CCS ASSOCIATES,MENLO PK,CA 94025. FU NCI NIH HHS [N01-CN-55448-06, N01-CN-85097-02] NR 38 TC 37 Z9 37 U1 0 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDNTIOU-KALAMOU RD KAPANDRITI, POB 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD JAN-FEB PY 1994 VL 14 IS 1A BP 5 EP 11 PG 7 WC Oncology SC Oncology GA NH785 UT WOS:A1994NH78500002 PM 8166455 ER PT J AU ARRIAGADA, R PIGNON, JP IHDE, DC JOHNSON, DH PERRY, MC SOUHAMI, RL BRODIN, O JOSS, RA KIES, MS LEBEAU, B ONOSHI, T OSTERLIND, K TATTERSALL, MHN WAGNER, H AF ARRIAGADA, R PIGNON, JP IHDE, DC JOHNSON, DH PERRY, MC SOUHAMI, RL BRODIN, O JOSS, RA KIES, MS LEBEAU, B ONOSHI, T OSTERLIND, K TATTERSALL, MHN WAGNER, H TI EFFECT OF THORACIC RADIOTHERAPY ON MORTALITY IN LIMITED SMALL-CELL LUNG-CANCER - A METAANALYSIS OF 13 RANDOMIZED TRIALS AMONG 2,140 PATIENTS SO ANTICANCER RESEARCH LA English DT Article; Proceedings Paper CT 3rd International Conference on Small Cell Lung Cancer CY MAY 06-07, 1993 CL RAVENNNA, ITALY DE SMALL CELL LUNG CANCER; RANDOMIZED TRIAL; THORACIC RADIOTHERAPY; SURVIVAL METAANALYSIS ID COMBINATION CHEMOTHERAPY; RADIATION-THERAPY; CARCINOMA AB This meta-analysis was designed to evaluate the hypothesis that thoracic radiotherapy contributes to a moderate increase in overall survival in limited small-cell lung cancer. We collected individual data on all patients enrolled before December 1988 in randomized trials comparing chemotherapy alone with chemotherapy combined with thoracic radiotherapy. The study included 13 trials and 2140 patients with limited disease. A total of 433 patient with extensive disease were excluded. Overall, 1862 of 2103 patients who could be evaluated died; the median follow-up period for the surviving patients was 43 months. The relative risk of death in the combined therapy group as compared with the chemotherapy group was 0.86 (95 percent confidence interval, 0.78 to 0.94, P= 0.001), corresponding to a 14 percent reduction in the mortality rate. The benefit in terms of overall survival at three years (+/-SD) was 5.4 +/- 1.4 percent. Indirect comparison of early with late radiotherapy and of sequential with nonsequential radiotherapy did not reveal any optimal time for treatment. There was a trend toward a larger reduction in mortality among younger patients. in conclusion, thoracic radiotherapy moderately improves overall survival in patients with limited small-cell lung cancer who are treated with combination chemotherapy. C1 INST GUSTAVE ROUSSY,DEPT BIOSTAT,F-94805 VILLEJUIF,FRANCE. NCI,BETHESDA,MD 20892. VANDERBILT UNIV,DIV MED ONCOL,NASHVILLE,TN 37232. UNIV MISSOURI,HLTH SCI CTR,DEPT MED,COLUMBIA,MO 65203. COURTAULD INST BIOCHEM,DEPT ONCOL,LONDON W1P 8BT,ENGLAND. UNIV UPPSALA HOSP,DEPT ONCOL,S-75185 UPPSALA,SWEDEN. KANTONSPITAL LUZERN,MED KLIN,ONKOL ABT,LUZERN,SWITZERLAND. NORTHWESTERN UNIV,SCH MED,DIV HEMATOL ONCOL,CHICAGO,IL 60611. HOP ST ANTOINE,SERV PNEUMOL,F-75571 PARIS 12,FRANCE. OKAYAMA UNIV,SCH MED,DEPT MED,OKAYAMA 700,JAPAN. CENT SYGEHUSET HILLEROD,DEPT MED,DK-3400 HILLEROD,DENMARK. ROYAL PRINCE ALFRED HOSP,DEPT MED ONCOL,CAMPERDOWN,NSW 2050,AUSTRALIA. ALBANY MED COLL,DEPT RADIAT ONCOL,ALBANY,NY 12208. RP ARRIAGADA, R (reprint author), INST GUSTAVE ROUSSY,DEPT RADIOTHERAPY,F-94805 VILLEJUIF,FRANCE. RI Johnson, David/A-7437-2009 NR 13 TC 24 Z9 26 U1 0 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDNTIOU-KALAMOU RD KAPANDRITI, POB 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD JAN-FEB PY 1994 VL 14 IS 1B BP 333 EP 335 PG 3 WC Oncology SC Oncology GA NH786 UT WOS:A1994NH78600015 PM 8166478 ER PT J AU UHDE, TW MALLOY, LC BENSON, BB AF UHDE, TW MALLOY, LC BENSON, BB TI GROWTH-HORMONE RESPONSE TO CLONIDINE IN THE NERVOUS POINTER DOG-MODEL OF ANXIETY SO ANXIETY LA English DT Article DE ANXIETY; FEAR; GROWTH FACTORS; GROWTH HORMONE; CLONIDINE; DOGS; CANINE; NORADRENERGIC; ANIMAL MODELS; ALPHA-ADRENERGIC RECEPTORS ID ALPHA-ADRENERGIC REGULATION; PANIC DISORDER PATIENTS; NORADRENERGIC FUNCTION; BODY SIZE; I LEVELS; SECRETION; PLASMA; SENSITIVITY; PROLACTIN; RELEASE AB Blunted growth hormone responses to clonidine have been reported in most studies of humans with panic disorder but have been an inconsistent finding in the study of other anxiety syndromes. The growth hormone response to oral clonidine (100 mu g/kg) was investigated in the adult nervous pointer dog, it genetic animal model of anxiety. Compared with placebo, clonidine produced significant increases in plasma levels of growth hormone; however; there were no differences in the growth hormone (GH) responses to clonidine in the nervous compared with the normal pointer dogs. Findings in this animal model are discussed within the context of noradrenergic-hypothalamic-GH dysfunction reported in some but not all types of anxiety disorders in humans. (C) 1994 Wiley-Liss, Inc.* C1 NIMH,INTRAMURAL RES PROGRAM,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BETHESDA,MD 20892. NR 38 TC 3 Z9 3 U1 1 U2 2 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1070-9797 J9 ANXIETY JI Anxiety PY 1994 VL 1 IS 2 BP 45 EP 49 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA QC537 UT WOS:A1994QC53700001 PM 9160547 ER PT J AU GEORGE, MS MALLOY, LC SLATE, SO UHDE, TW AF GEORGE, MS MALLOY, LC SLATE, SO UHDE, TW TI PILOT MRI STUDY OF BRAIN SIZE IN NERVOUS POINTER DOGS SO ANXIETY LA English DT Note ID PANIC DISORDER PATIENTS; CLONIDINE; GLUCOSE; ANXIETY C1 NIMH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BETHESDA,MD 20892. WAYNE STATE UNIV,DEPT PSYCHIAT & BEHAV NEUROSCI,DETROIT,MI. RP GEORGE, MS (reprint author), NIMH,BIOL PSYCHIAT BRANCH,PSYCHOBIOL SECT,BLDG 10,ROOM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 30 TC 2 Z9 2 U1 6 U2 7 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1070-9797 J9 ANXIETY JI Anxiety PY 1994 VL 1 IS 3 BP 129 EP 133 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA QU581 UT WOS:A1994QU58100004 PM 9160561 ER PT J AU TANCER, ME STEIN, MB UHDE, TW AF TANCER, ME STEIN, MB UHDE, TW TI LACTIC-ACID RESPONSE TO CAFFEINE IN PANIC DISORDER - COMPARISON WITH SOCIAL PHOBICS AND NORMAL CONTROLS SO ANXIETY LA English DT Note DE PANIC DISORDER; SOCIAL PHOBIA; CAFFEINE CHALLENGE; CHEMICAL CHALLENGE ID LACTATE INFUSIONS; ANXIETY; ATTACKS C1 NIMH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BETHESDA,MD 20892. NR 12 TC 22 Z9 22 U1 0 U2 3 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1070-9797 J9 ANXIETY JI Anxiety PY 1994 VL 1 IS 3 BP 138 EP 140 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA QU581 UT WOS:A1994QU58100006 PM 9160563 ER PT J AU ALTEMUS, M SMITH, MA DIEP, V AULAKH, CS MURPHY, DL AF ALTEMUS, M SMITH, MA DIEP, V AULAKH, CS MURPHY, DL TI INCREASED MESSENGER-RNA FOR CORTICOTROPIN-RELEASING HORMONE IN THE AMYGDALA OF FAWN-HOODED RATS - A POTENTIAL ANIMAL-MODEL OF ANXIETY SO ANXIETY LA English DT Article DE AMYGDALA; HYPOTHALAMIC-PITUITARY-ADRENAL AXIS; GLUCOCORTICOID RECEPTORS; TYROSINE HYDROXYLASE; IN SITU HYBRIDIZATION ID HYDROXYLASE MESSENGER-RNA; SPRAGUE-DAWLEY RATS; PARAVENTRICULAR NUCLEUS; TYROSINE-HYDROXYLASE; THERAPEUTIC IMPLICATIONS; ALCOHOL PREFERENCE; NERVOUS-SYSTEM; CHRONIC STRESS; BRAIN; PITUITARY AB Compared to the outbred Wistar rat strain, the Fawn-hooded rat strain has several characteristics which suggest that the Fawn-hooded strain is hyperaroused. Fawn-hooded rats exhibit more freezing behavior in response to stress, have art increased preference for alcohol develop adult onset hypertension, and have elevated urinary catecholamine levels. We used quantitative in situ hybridization to investigate central components of the corticotropin releasing hormone (CRH), arginine vasopressin (AVP) and noradrenergic stress response and arousal systems in these rats. We also measured basal corticosterone levels and adrenal weights to assess tonic hypothalamic-pituitary-adrenal axis activity. Compared to Wistar rats, Fawn-hooded rats had significantly increased CRH mRNA in the central nucleus of the amygdala and reduced CRH mRNA in the paraventricular nucleus of the hypothalamus. Fawn-hooded rats also had reduced AVP mRNA expression in the parvocellular cells of the hypothalamic paraventricular nucleus. There were no differences between strains in glucocorticoid receptor mRNA in the hippocampus or the paraventricular nucleus or in mineralocorticoid receptor mRNA in the hippocampus. There was also no difference between strains in tyrosine hydroxylase mRNA in the locus ceruleus. Finally, adrenal weights were significantly reduced in the Fawn-hooded rats while basal corticosterone levels were similar in the two strains, which suggests central hypoactivity of the hypothalamic-pituitary-adrenal axis in Fawn-hooded rats compared to Wistar rats. Increased CRH mRNA in the central nucleus of the amygdala and reduced tonic hypothalamic-pituitary-adrenal axis activity may play a role in the unique behavioral and physiological characteristics of Fawn-hooded rats. (C) 1995 Wiley-Liss, Inc. C1 NIMH,DIV INTRAMURAL RES PROGRAMS,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. RP ALTEMUS, M (reprint author), NIMH,DIV INTRAMURAL RES PROGRAMS,CLIN SCI LAB,BLDG 10,ROOM 3D41,10 CTR DR MSC 1264,BETHESDA,MD 20892, USA. NR 60 TC 29 Z9 29 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1070-9797 J9 ANXIETY JI Anxiety PY 1994 VL 1 IS 6 BP 251 EP 257 PG 7 WC Psychiatry; Psychology SC Psychiatry; Psychology GA RW777 UT WOS:A1994RW77700001 PM 9160583 ER PT J AU MCCANN, UD SLATE, SO GERACI, M UHDE, TW AF MCCANN, UD SLATE, SO GERACI, M UHDE, TW TI PEPTIDES AND ANXIETY - A DOSE-RESPONSE EVALUATION OF PENTAGASTRIN IN HEALTHY-VOLUNTEERS SO ANXIETY LA English DT Article DE CCK; CHEMICAL MODELS; PANIC; SOCIAL INTERACTION; SOCIAL PHOBIA ID CHOLECYSTOKININ-TETRAPEPTIDE; PANIC DISORDER; B RECEPTOR; BEHAVIOR; CCK; ANTAGONISTS; MONKEYS; BRAIN AB A large body of data suggest that brain cholecystokinin (CCK) systems are involved in the regulation of anxiety, and numerous studies have demonstrated that CCK-4, a CCKB agonist, reliably induces panic attacks in patients with panic disorder: Recently, pentagastrin, a commercially available CCKB agonist, has been reported to have similar anxiogenic properties. To further explore the utility of pentagastrin as a challenge agent and to determine whether its effects are dose-related a dose-response study was conducted in ten healthy volunteers. Pentagastrin (0.2 mu g kg, 0.6 mu g/kg and 1.0 mu g/kg) and inactive placebo were infused over one minute on four separate challenge days in a double-blind fashion. Subjects received pentagastrin while participating in a structured social interaction task. Repeated measures of anxiety, blood pressure, pulse, ACTH, and cortisol were taken at baseline and postinfusion. Pentagastrin administration led to increases in anxiety, pulse, ACTH, cortisol and physical symptoms of panic, in a dose-related manner. Participation in the social interaction task led to increases in measures of anxiety as well as increases in pulse and blood pressure. Pew differences were found between the 0.2 mu g/kg dose of pentagastrin and placebo, or between the 0.6 mu g/kg and the 1.0 mu g/kg doses of pentagastrin. These findings support the notion that CCK systems are involved in the regulation of anxiety, and suggest that the 0.6 mu g/kg dose may be optimal for increasing symptoms of anxiety while minimizing unpleasant side effects. The powerful anxiogenic effects of the social interaction task underscore the importance of contextual variables in challenge studies. (C) 1995 Wiley-Liss, Inc.* C1 WAYNE STATE UNIV,SCH MED,DEPT PSYCHIAT & BEHAV NEUROSCI,DETROIT,MI 48202. RP MCCANN, UD (reprint author), NIMH,BIOL PSYCHIAT BRANCH,ANXIETY & AFFECT DISORDERS SECT,BLDG 10,ROOM 3N-212,BETHESDA,MD 20892, USA. NR 26 TC 7 Z9 7 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1070-9797 J9 ANXIETY JI Anxiety PY 1994 VL 1 IS 6 BP 258 EP 267 PG 10 WC Psychiatry; Psychology SC Psychiatry; Psychology GA RW777 UT WOS:A1994RW77700002 PM 9160584 ER PT J AU MARTINS, EA PIGOTT, TA BERNSTEIN, SE DOYLE, BB SUNDERLAND, B SMOLKA, VM DUBBERT, B AF MARTINS, EA PIGOTT, TA BERNSTEIN, SE DOYLE, BB SUNDERLAND, B SMOLKA, VM DUBBERT, B TI SERTRALINE IN THE TREATMENT OF PATIENTS WITH SOCIAL PHOBIA SO ANXIETY LA English DT Note DE SERTRALINE; SOCIAL PHOBIA; ANXIETY; TREATMENT ID MENTAL-DISORDERS; FLUOXETINE; PLACEBO; COMORBIDITY; CLONAZEPAM; PHENELZINE; PREVALENCE; BUSPIRONE C1 UNIV TEXAS,MED BRANCH,DEPT PSYCHIAT & BEHAV SCI,GALVESTON,TX 77550. NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. RP MARTINS, EA (reprint author), GEORGETOWN UNIV,MED CTR,DEPT PSYCHIAT,KOBER COGAN BLDG,5TH FLOOR,3750 RESERVOIR RD NW,WASHINGTON,DC 20007, USA. NR 42 TC 15 Z9 15 U1 6 U2 6 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1070-9797 J9 ANXIETY JI Anxiety PY 1994 VL 1 IS 6 BP 291 EP 297 PG 7 WC Psychiatry; Psychology SC Psychiatry; Psychology GA RW777 UT WOS:A1994RW77700008 PM 9160590 ER PT B AU PARRON, DL AF PARRON, DL BE Friedman, S TI DSM-IV - MAKING IT CULTURALLY RELEVANT SO ANXIETY DISORDERS IN AFRICAN AMERICANS LA English DT Proceedings Paper CT Symposium on Anxiety Disorders in African-Americans CY DEC 03-04, 1992 CL SUNY, HLTH SCI CTR BROOKLYN, BROOKLYN, NY HO SUNY, HLTH SCI CTR BROOKLYN C1 NIMH,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PUBL CO PI NEW YORK PA 536 BROADWAY, NEW YORK, NY 10012 BN 0-8261-8540-1 PY 1994 BP 15 EP 25 PG 11 WC Psychology, Clinical SC Psychology GA BB71N UT WOS:A1994BB71N00002 ER PT B AU VACCHIO, MS YANG, YL ASHWELL, JD AF VACCHIO, MS YANG, YL ASHWELL, JD BE Mihich, E Schimke, RT TI NUCLEAR RECEPTORS AND THYMOCYTE APOPTOSIS - SHAPING THE IMMUNE REPERTOIRE SO APOPTOSIS SE PEZCOLLER FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT 5th Pezcoller Symposium on Apoptosis CY JUN 09-11, 1993 CL TRENT, ITALY SP PEZCOLLER FDN C1 NIH,IMMUNE CELL BIOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,BETHESDA,MD 20892. 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 0-306-44733-9 J9 PEZ FDN SYM PY 1994 VL 5 BP 179 EP 200 PG 22 WC Biochemistry & Molecular Biology; Oncology; Immunology SC Biochemistry & Molecular Biology; Oncology; Immunology GA BA69H UT WOS:A1994BA69H00011 ER PT J AU RASTOGI, VK CHARY, KVR GOVIL, G HOWARD, FB MILES, HT AF RASTOGI, VK CHARY, KVR GOVIL, G HOWARD, FB MILES, HT TI INOSINE ADENOSINE BASE-PAIRING IN D-GGTACIAGTACC - DUPLEX AND HAIRPIN WITH A 2-BASE LOOP SO APPLIED MAGNETIC RESONANCE LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; DIMENSIONAL NMR-SPECTROSCOPY; DNA DUPLEX; CORRELATED SPECTROSCOPY; SOLVENT SUPPRESSION; D-GGTACGCGTACC; MISMATCH; DEOXYINOSINE; CONFORMATION; OLIGONUCLEOTIDES AB An oligonucleotide dodecamer d-GGTACIAGTACC containing two inosine-adenosine mismatched base-pairs has been studied by H-1 and P-31 NMR spectroscopy. Unique assignments of H-1 and P-31 spins have been achieved by using a recently proposed two-dimensional heteronuclear long range correlation (2D-HELCO) technique. The 2D nuclear Overhauser enhancement spectroscopy (NOESY) spectrum recorded in a mixed solvent of 90% H2O + 10% (H2O)-H-2 has been used to assign all the exchangeable imino and amino proton resonances. NMR results indicate that at concentrations above 5 mM, the molecule adopts a duplex structure where the inosine imino protons are hydrogen bonded. Cross-strand NOEs between the imino proton of I6 and H2 proton of A7 and that between H2 of I6 and H2 of A7 provide evidence for inosine-adenosine base-pairing, with both bases I6 and A7 in anti conformation. The observed NOE connectivities d1, d2 and d3 from almost the middle of the molecule to the two ends are consistent with a right handed B-DNA conformation. However, the molecule adopts a more extended conformation in the mismatch region to accommodate the bulky purine-purine (IA) base pairs. NMR experiments at lower concentrations indicate the coexistence of a monomeric hairpin with a two base loop, consisting of I6 and A7 units, in equilibrium with the duplex. 2D-ROESY experiment at such a concentration shows that the conformation of the stem of the hairpin does not deviate much from the corresponding region of the duplex and four nucleotides C5, I6, A7 and G8 undergo significant structural changes during the formation of hairpin loop. C1 TATA INST FUNDAMENTAL RES,CHEM PHYS GRP,HOMI BHABHA RD,BOMBAY 400005,INDIA. NIDDKD,BETHESDA,MD. NR 39 TC 6 Z9 6 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0937-9347 J9 APPL MAGN RESON JI Appl. Magn. Reson. PY 1994 VL 7 IS 1 BP 1 EP 19 PG 19 WC Physics, Atomic, Molecular & Chemical; Spectroscopy SC Physics; Spectroscopy GA PD295 UT WOS:A1994PD29500002 ER PT J AU CUI, XL QIN, C ZIGLER, JS AF CUI, XL QIN, C ZIGLER, JS TI RESIDUAL EDTA BOUND BY LENS CRYSTALLINS ACCOUNTS FOR THEIR REPORTED RESISTANCE TO COPPER-CATALYZED OXIDATIVE DAMAGE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID PROTEINS; EVOLUTION; CLEAVAGE C1 NEI,MECH OCULAR DIS LAB,BETHESDA,MD 20892. NR 16 TC 3 Z9 3 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 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN PY 1994 VL 308 IS 1 BP 207 EP 213 DI 10.1006/abbi.1994.1029 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MW719 UT WOS:A1994MW71900029 PM 8311454 ER PT J AU LAWTON, MP CASHMAN, JR CRESTEIL, T DOLPHIN, CT ELFARRA, AA HINES, RN HODGSON, E KIMURA, T OZOLS, J PHILLIPS, IR PHILPOT, RM POULSEN, LL RETTIE, AE SHEPHARD, EA WILLIAMS, DE ZIEGLER, DM AF LAWTON, MP CASHMAN, JR CRESTEIL, T DOLPHIN, CT ELFARRA, AA HINES, RN HODGSON, E KIMURA, T OZOLS, J PHILLIPS, IR PHILPOT, RM POULSEN, LL RETTIE, AE SHEPHARD, EA WILLIAMS, DE ZIEGLER, DM TI A NOMENCLATURE FOR THE MAMMALIAN FLAVIN-CONTAINING MONOOXYGENASE GENE FAMILY BASED ON AMINO-ACID-SEQUENCE IDENTITIES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID PIG-LIVER; COVALENT STRUCTURE; MOLECULAR-CLONING; MULTIPLE FORMS; DISTINCT; RABBIT; LUNG; MICROSOMES; FMO2; CDNA C1 NIEHS, RES TRIANGLE PK, NC 27709 USA. IGEN RES INST, SEATTLE, WA 98109 USA. CHU NECKER, INSERM, U175, F-75730 PARIS 15, FRANCE. UNIV LONDON, QUEEN MARY & WESTFIELD COLL, DEPT BIOCHEM, LONDON E1 4NS, ENGLAND. UNIV WISCONSIN, DEPT COMPARAT BIOSCI, MADISON, WI 53706 USA. UNIV WISCONSIN, CTR ENVIRONM TOXICOL, MADISON, WI 53706 USA. WAYNE STATE UNIV, SCH MED, DEPT PHARMACOL, DETROIT, MI 48201 USA. N CAROLINA STATE UNIV, DEPT TOXICOL, RALEIGH, NC 27695 USA. SANDOZ PHARMACEUT LTD, TSUKUBA RES INST, IBARAKI, OSAKA, JAPAN. UNIV CONNECTICUT, CTR HLTH, DEPT BIOCHEM, FARMINGTON, CT 06032 USA. UNIV TEXAS, CLAYTON FDN BIOCHEM INST, DEPT CHEM & BIOCHEM, AUSTIN, TX 78712 USA. UNIV WASHINGTON, DEPT MED CHEM, SEATTLE, WA 98195 USA. UCL, DEPT BIOCHEM & MOLEC BIOL, LONDON WC1E 6BT, ENGLAND. OREGON STATE UNIV, DEPT FOOD SCI & TECHNOL, CORVALLIS, OR 97331 USA. RI Phillips, Ian/A-7337-2008; OI Hines, Ronald/0000-0002-3094-4200 NR 31 TC 161 Z9 162 U1 0 U2 8 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN PY 1994 VL 308 IS 1 BP 254 EP 257 DI 10.1006/abbi.1994.1035 PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MW719 UT WOS:A1994MW71900035 PM 8311461 ER PT J AU VIRKKUNEN, M RAWLINGS, R TOKOLA, R POLAND, RE GUIDOTTI, A NEMEROFF, C BISSETTE, G KALOGERAS, K KARONEN, SL LINNOILA, M AF VIRKKUNEN, M RAWLINGS, R TOKOLA, R POLAND, RE GUIDOTTI, A NEMEROFF, C BISSETTE, G KALOGERAS, K KARONEN, SL LINNOILA, M TI CSF BIOCHEMISTRIES, GLUCOSE-METABOLISM, AND DIURNAL ACTIVITY RHYTHMS IN ALCOHOLIC, VIOLENT OFFENDERS, FIRE SETTERS, AND HEALTHY-VOLUNTEERS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID CORTICOTROPIN-RELEASING-FACTOR; CEREBROSPINAL-FLUID MONOAMINE; 5-HYDROXYINDOLEACETIC ACID; SECRETION; TESTOSTERONE; DEPRESSION; BRAIN; SCHIZOPHRENIA; NEUROPEPTIDES; SEROTONIN AB Background: There is an extensive literature describing a central serotonin deficit in alcoholic, impulsive, violent offenders and fire setters. In the present study, we investigated biochemical concomitants of impulsivity and aggressiveness, and the physiological consequences of reduced central serotonin turnover. Methods: Forty-three impulsive and 15 nonimpulsive alcoholic offenders and 21 healthy volunteers were studied in the forensic psychiatry ward of a university psychiatric department. The subjects underwent lumbar punctures and oral glucose and aspartame challenges, and their diurnal activity rhythm was measured with physical activity monitors. Discriminant function analyses were used to investigate psychophysiological and biochemical concomitants of aggressive and impulsive behaviors. Results: Alcoholic, impulsive offenders with antisocial personality disorder had low mean cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid (5-HIAA) and corticotropin levels and high mean CSF testosterone concentrations. Compared with healthy volunteers, they showed increased physical activity during the daytime. Alcoholic, impulsive offenders with intermittent explosive disorder had a low mean CSF 5-HIAA concentration and blood glucose nadir after an oral glucose challenge, and desynchronized diurnal activity rhythm. Healthy volunteers had mean CSF 5-HIAA concentrations that were intermediate between those of alcoholic, impulsive and non-impulsive offenders. Alcoholic, nonimpulsive offenders had a significantly higher mean CSF S-HIAA concentration than all the other groups, including healthy volunteers. Conclusions: In the present sample, a low CSF 5-HIAA concentration was primarily associated with impulsivity and high CSF testosterone concentration, with aggressiveness or interpersonal violence. C1 NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,BETHESDA,MD 20892. UNIV HELSINKI,DEPT PSYCHIAT,SF-00180 HELSINKI,FINLAND. UNIV HELSINKI,DEPT CLIN CHEM,SF-00100 HELSINKI,FINLAND. UCLA,HARBOR MED CTR,DIV BIOL PSYCHIAT,TORRANCE,CA 90509. EMORY UNIV,DEPT PSYCHIAT,ATLANTA,GA 30322. DUKE UNIV,MED CTR,DEPT PSYCHIAT,DURHAM,NC 27710. FIDIA GEORGETOWN NEUROSCI INST,WASHINGTON,DC. NIMH,INTRAMURAL RES PROGRAM,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. FU NIMH NIH HHS [MH 00534] NR 47 TC 416 Z9 418 U1 1 U2 19 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 1994 VL 51 IS 1 BP 20 EP 27 PG 8 WC Psychiatry SC Psychiatry GA MR516 UT WOS:A1994MR51600002 PM 7506515 ER PT J AU VIRKKUNEN, M KALLIO, E RAWLINGS, R TOKOLA, R POLAND, RE GUIDOTTI, A NEMEROFF, C BISSETTE, G KALOGERAS, K KARONEN, SL LINNOILA, M AF VIRKKUNEN, M KALLIO, E RAWLINGS, R TOKOLA, R POLAND, RE GUIDOTTI, A NEMEROFF, C BISSETTE, G KALOGERAS, K KARONEN, SL LINNOILA, M TI PERSONALITY PROFILES AND STATE AGGRESSIVENESS IN FINNISH ALCOHOLIC, VIOLENT OFFENDERS, FIRE SETTERS, AND HEALTHY-VOLUNTEERS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PLATELET MAO ACTIVITY; MONOAMINE-OXIDASE; CEREBROSPINAL-FLUID; TRAITS; BRAIN; TESTOSTERONE; DEPRESSION; BEHAVIOR AB Background: Based on clinical observations in a series of studies on Finnish alcoholic, violent offenders, we asserted that the impulsive offenders represented an extreme group of type 2 alcoholics. We also observed that these subjects were vulnerable to hypoglycemia after the administration of oral oral glucose load. Furthermore, we believe that while being hypoglycemic, the impulsive offenders are particularly irritable and aggressive. In the present study, we addressed these issues by studying psychological trait and state variables in a new group of violent offenders and fire setters, and age- and sex-matched healthy volunteers. Methods: Fifty-eight alcoholic, violent offenders and impulsive fire setters and 21 healthy volunteers were administered the Karolinska scales of personality and the Rosenzweig picture frustration test after an oral aspartame and glucose challenge. Results: The psychological test results and the criminal histories of the offenders, together with biochemical measurements, suggest that a low 5-hydroxy-indoleacetic acid concentration in cerebrospinal fluid in the alcoholic offenders is associated with irritability and impaired impulse control, and a high free testosterone concentration in cerebrospinal fluid is associated with increased aggressiveness, monotony avoidance, sensation seeking, suspiciousness, and reduced socialization. Conclusion: Finnish alcoholic, impulsive offenders have personality profiles characteristic of Scandinavian early-onset male alcoholics with antisocial traits, who have been also referred to as type 2 alcoholics. C1 NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,BETHESDA,MD 20892. UNIV HELSINKI,DEPT PSYCHIAT,SF-00180 HELSINKI,FINLAND. UNIV HELSINKI,DEPT CLIN CHEM,SF-00100 HELSINKI,FINLAND. EMORY UNIV,DEPT PSYCHIAT,ATLANTA,GA 30322. NIMH,CLIN NEUROENDOCRINOL BRANCH,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT PSYCHIAT,DURHAM,NC 27710. UCLA,HARBOR MED CTR,DEPT PSYCHIAT,DIV BIOL PSYCHIAT,TORRANCE,CA. FIDIA GEORGETOWN NEUROSCI INST,WASHINGTON,DC. FU NIMH NIH HHS [MH 00534] NR 31 TC 191 Z9 194 U1 2 U2 13 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 1994 VL 51 IS 1 BP 28 EP 33 PG 6 WC Psychiatry SC Psychiatry GA MR516 UT WOS:A1994MR51600003 PM 7506516 ER PT J AU NIELSEN, DA GOLDMAN, D VIRKKUNEN, M TOKOLA, R RAWLINGS, R LINNOILA, M AF NIELSEN, DA GOLDMAN, D VIRKKUNEN, M TOKOLA, R RAWLINGS, R LINNOILA, M TI SUICIDALITY AND 5-HYDROXYINDOLEACETIC ACID CONCENTRATION ASSOCIATED WITH A TRYPTOPHAN-HYDROXYLASE POLYMORPHISM SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID FLUID MONOAMINE METABOLITES; CROSS-FOSTERING ANALYSIS; IMPULSIVE FIRE SETTERS; CEREBROSPINAL-FLUID; SEROTONIN TRANSPORTER; DEPRESSED-PATIENTS; VIOLENT OFFENDERS; HOMOVANILLIC-ACID; BEHAVIOR; CLONING AB Background: To examine whether the tryptophan hydroxylase (TPH) gene, which codes for the rate-limiting enzyme in the biosynthesis of serotonin, may be a factor influencing serotonin turnover and behaviors controlled by serotonin. Methods: Using a polymerase chain reaction-based method, TPH genotype was determined in DNA samples from 56 impulsive and 14 nonimpulsive, alcoholic, violent offenders and 20 healthy volunteers. Results: In the behaviorally extreme impulsive group,we observed a significant association between TPH genotypeand cerebrospinal fluid 5-hydroxyindoleacetic acid (5-HIAA) concentration. No association of TPH genotype with impulsive behavior was detected. The polymorphism was also associated with a history of suicide attempts in all violent offenders, independent of impulsivity status and cerebrospinal fluid 5-HIAA concentration. Conclusion: In some individuals, a genetic variant of the TPH gene may influence 5-HIAA concentration in the cerebrospinal fluid and predisposition to suicidal behavior. C1 UNIV HELSINKI,DEPT PSYCHIAT,SF-00180 HELSINKI,FINLAND. NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,BETHESDA,MD 20892. RP NIELSEN, DA (reprint author), NIAAA,DIV INTRAMURAL CLIN & BIOL RES,NEUROGENET LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Nielsen, David/B-4655-2009; Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 38 TC 282 Z9 293 U1 1 U2 7 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 1994 VL 51 IS 1 BP 34 EP 38 PG 5 WC Psychiatry SC Psychiatry GA MR516 UT WOS:A1994MR51600004 PM 7506517 ER PT J AU HIGLEY, JD MEHLMAN, PT TAUB, D SUOMI, SJ HIGLEY, SB VICKERS, JM LINNOILA, M AF HIGLEY, JD MEHLMAN, PT TAUB, D SUOMI, SJ HIGLEY, SB VICKERS, JM LINNOILA, M TI ARE STRESS HORMONES AND SEROTONIN RELATED TO AGGRESSION IN PRIMATES - IN REPLY SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter C1 LAB ANIMAL BREEDERS & SERV,YEMASSEE,SC. US FDA,PATHOBIOL & PRIMATOL LAB,BETHESDA,MD. NIAAA,OFF SCI DIRECTOR,BETHESDA,MD. NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD 20892. RP HIGLEY, JD (reprint author), NIAAA,CLIN STUDIES LAB,ANIM CTR BLDG 112,POB 289,POOLESVILLE,MD 20837, USA. NR 4 TC 0 Z9 0 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 1994 VL 51 IS 1 BP 73 EP 73 PG 1 WC Psychiatry SC Psychiatry GA MR516 UT WOS:A1994MR51600011 ER PT J AU GIEBULTOWICZ, JM JOY, JE RIEMANN, JG RAINA, AK AF GIEBULTOWICZ, JM JOY, JE RIEMANN, JG RAINA, AK TI CHANGES IN PROTEIN-PATTERNS IN SPERM AND VAS-DEFERENS DURING THE DAILY RHYTHM OF SPERM RELEASE IN THE GYPSY-MOTH SO ARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Environmental and Endocrine Regulation of Insect Reproduction, at the XIX International Congress of Entomology CY JUL 04, 1992 CL BEIJING, PEOPLES R CHINA DE CIRCADIAN RHYTHMS; SECRETION; EPITHELIUM; SPERM BUNDLES; LYMANTRIA DISPAR ID SYSTEM CONTROLLING RELEASE; LYMANTRIA-DISPAR; LEPIDOPTERA; TESTIS; LIGHT AB In the gypsy moth, Lymantria dispar, the release of sperm bundles from the testis into the upper vas deferens (UVD) is precisely timed within each 24 h period by a circadian mechanism located in the reproductive system. in males kept under light:dark cycles of 16:8, release of sperm bundles is limited to the 3 h period that. starts before lights off. Sperm released from the testis remains in the UVD for about 12 h and then moves into the seminal vesicles, so that the UVD stays empty until the next cycle of sperm release begins. The rhythm of release appears to play a role in the terminal stages of sperm maturation and is essential for the fertility of males. Sperm bundles undergo substantial morphological changes during the release from the testis and while they are retained in the UVD. In this study, using gel electrophoresis, we compared protein patterns in sperm and in the UVD during the daily cycle of sperm release and maturation. Several protein bands evident in the sperm bundles contained in the testis were missing from the sperm bundles that had passed from the testis into the UVD. Furthermore, a number of new proteins appeared in the sperm bundles as they remained in the UVD. Some of these proteins appeared to be secreted from the UVD epithelium into the UVD lumen before being incorporated into sperm bundles. Correlations between changes in protein patterns and ultrastructural changes in sperm during the cycle of sperm release and maturation are discussed. (C) 1994 Wiley-Liss, Inc. C1 UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742. ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. USDA ARS,BIOSCI RES LAB,FARGO,ND 58105. RP GIEBULTOWICZ, JM (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,INSECT NEUROBIOL & HORMONE LAB,BARC E,BLDG 306,R 322,BELTSVILLE,MD 20705, USA. NR 20 TC 2 Z9 2 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0739-4462 J9 ARCH INSECT BIOCHEM JI Arch. Insect Biochem. Physiol. PY 1994 VL 27 IS 1 BP 65 EP 75 DI 10.1002/arch.940270108 PG 11 WC Biochemistry & Molecular Biology; Entomology; Physiology SC Biochemistry & Molecular Biology; Entomology; Physiology GA PD600 UT WOS:A1994PD60000007 ER PT J AU RUMSEY, JM ZAMETKIN, AJ ANDREASON, P HANAHAN, AP HAMBURGER, SD AQUINO, T KING, AC PIKUS, A COHEN, RM AF RUMSEY, JM ZAMETKIN, AJ ANDREASON, P HANAHAN, AP HAMBURGER, SD AQUINO, T KING, AC PIKUS, A COHEN, RM TI NORMAL ACTIVATION OF FRONTOTEMPORAL LANGUAGE CORTEX IN DYSLEXIA, AS MEASURED WITH O-15 POSITRON EMISSION TOMOGRAPHY SO ARCHIVES OF NEUROLOGY LA English DT Article ID SHORT-TERM-MEMORY; READING-DISABILITY; LEFT-HANDEDNESS; DISORDERS; CHILDREN; DEFICIENCIES; ABILITY; TASK; SPAN AB Objective: To assess the ability of dyslexic men to activate left middle to anterior language cortex normally. Design: Positron emission tomography using oxygen 15-labeled water as a tracer during rest and during a syntax task involving sentence comprehension. Setting: Research hospital. Patients or Other Participants: Fifteen right-handed, severely dyslexic men (mean [+/-SD] age, 27+/-5 years) and 20 matched controls. Interventions: None. Main Outcome Measure: Cerebral blood flow. Results: During rest, dyslexics showed reduced blood flow (relative to controls) in one left parietal region near the angular/supramarginal gyri, but otherwise normal flow. During syntactic processing, dyslexics and controls showed similar, significant activation of left middle to anterior temporal and inferior frontal cortex. Conclusions: These results, together with the previously reported failure of dyslexics to activate left temporoparietal cortex during phonologic processing, argue for dysfunction of left cortical language areas restricted to posterior language regions in dyslexia. C1 NIMH,CEREBRAL METAB LAB,CLIN BRAIN IMAGING SECT,BETHESDA,MD 20892. NIDCD,CLIN AUDIOL HEARING SECT,BETHESDA,MD. RP RUMSEY, JM (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,BETHESDA,MD 20892, USA. NR 45 TC 60 Z9 62 U1 2 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD JAN PY 1994 VL 51 IS 1 BP 27 EP 38 PG 12 WC Clinical Neurology SC Neurosciences & Neurology GA MQ506 UT WOS:A1994MQ50600005 PM 8274107 ER PT J AU ANDO, N SEN, HA BERKOWITZ, BA WILSON, CA DEJUAN, E AF ANDO, N SEN, HA BERKOWITZ, BA WILSON, CA DEJUAN, E TI LOCALIZATION AND QUANTITATION OF BLOOD-RETINAL BARRIER BREAKDOWN IN EXPERIMENTAL PROLIFERATIVE VITREORETINOPATHY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID MASSIVE PERIRETINAL PROLIFERATION; TRIAMCINOLONE ACETONIDE; INTRAVITREAL INJECTION; CELLULAR PROLIFERATION; MODEL; NEOVASCULARIZATION; SURGERY AB Objective: To determine the contribution of the breakdown of the blood-retinal barrier (BRB) as measured with magnetic resonance imaging in the development of retinal detachment in an experimental model of proliferative vitreoretinopathy. Methods: Contrast-enhanced magnetic resonance imaging was used to evaluate BRB breakdown in an intravitreal cell-injection model of proliferative vitreoretinopathy. Intravitreal injection of 2.5 X 10(5) homologous dermal fibroblasts produced specific disruption of the inner, or vascular, BRB. Results: Breakdown of the BRB was greatest in the first 3 days after injection, confirming previous work using fluorescein-based methods. Injection of 1 mg of intravitreal triamcinolone acetonide at the time of cell injection significantly reduced both BRB breakdown and the incidence of eventual traction retinal detachment. Eyes that did develop detachment had significantly greater leakage prior to its development than those that did not, regardless of steroid treatment. Conclusions: Quantitation and definitive localization of BRB leakage with magnetic resonance imaging provides a better understanding of the relationship between BRB compromise and the development of retinal detachment in this frequently used model. C1 DUKE UNIV,CTR EYE,DURHAM,NC 27706. NIEHS,RES TRIANGLE PK,NC 27709. FU NEI NIH HHS [R01 EY07576] NR 36 TC 33 Z9 34 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD JAN PY 1994 VL 112 IS 1 BP 117 EP 122 PG 6 WC Ophthalmology SC Ophthalmology GA MR521 UT WOS:A1994MR52100025 PM 8285878 ER PT J AU HIRAMATSU, Y NAGLER, RM FOX, PC BAUM, BJ AF HIRAMATSU, Y NAGLER, RM FOX, PC BAUM, BJ TI RAT SALIVARY-GLAND BLOOD-FLOW AND BLOOD-TO-TISSUE PARTITION-COEFFICIENTS FOLLOWING X-IRRADIATION SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE RADIATION; SALIVARY GLANDS; IODOANTIPYRINE; BLOOD FLOW; BLOOD-TO-TISSUE PARTITION COEFFICIENT ID RADIATION-INJURY; PAROTID-GLANDS; CELL; INVIVO AB Effects of a single high dose of X-irradiation (15 Gy) to the head and neck region in adult male rats were examined. Three days after radiation, rats were infused with [C-14]-iodoantipyrine (IAP) via the femoral vein. Animals were killed at designated times thereafter and the three major salivary glands removed. The uptake of IAP by these tissues was analysed using a pharmacokinetic model. Radiation had relatively modest effects on all measured variables when compared with results from the non-irradiated control and pair-fed groups. RP HIRAMATSU, Y (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892, USA. NR 19 TC 19 Z9 19 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0003-9969 J9 ARCH ORAL BIOL JI Arch. Oral Biol. PD JAN PY 1994 VL 39 IS 1 BP 77 EP 80 DI 10.1016/0003-9969(94)90038-8 PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA MX215 UT WOS:A1994MX21500011 PM 8179512 ER PT J AU GOTTSCHALCK, E ALEXANDERSEN, S STORGAARD, T BLOOM, ME AASTED, B AF GOTTSCHALCK, E ALEXANDERSEN, S STORGAARD, T BLOOM, ME AASTED, B TI SEQUENCE COMPARISON OF THE NONSTRUCTURAL GENES OF 4 DIFFERENT TYPES OF ALEUTIAN-MINK-DISEASE PARVOVIRUS INDICATES AN UNUSUAL DEGREE OF VARIABILITY SO ARCHIVES OF VIROLOGY LA English DT Article ID FELINE PANLEUKOPENIA VIRUS; ACUTE INTERSTITIAL PNEUMONIA; NONSTRUCTURAL PROTEIN NS2; POLYMERASE CHAIN-REACTION; AMINO-ACID SUBSTITUTIONS; CANINE HOST RANGE; MINUTE VIRUS; NUCLEOTIDE-SEQUENCE; AUTONOMOUS PARVOVIRUS; DNA-SEQUENCE AB The present work shows that at least four different sequence types of Aleutian mink disease parvovirus (ADV) are present in ADV isolates from mink. We here report the nucleotide sequences of these four types of ADV from nucleotide 123 to 2208 (map unit 3 to 46). This part of the genome encodes three non-structural (NS) proteins of ADV. Comparison of the deduced amino acid sequences of these NS proteins showed that the ADV proteins are much less conserved than the NS proteins from other members of the autonomous group of parvoviruses. In general, we found that the middle region of the ADV NS-1 protein was relatively well conserved among the types, while both the amino and carboxy-terminal ends of the protein had higher amino acid variability. Interestingly, the putative NS-3 protein from type 3 ADV is truncated in the carboxy-terminal end. The molecular evolutionary relationship among the four types of ADV was examined. This analysis, taken together with the unusually high degree of variability of the ADV types, indicates that the ADV infection in mink is likely to be an old infection compared to the other parvovirus infections or, alternatively, that ADV accumulates sequence changes much faster than other parvoviruses. C1 ROYAL VET & AGR UNIV,DEPT VET MICROBIOL,VIROL & IMMUNOL LAB,DK-1870 FREDERIKSBERG C,DENMARK. ROYAL VET & AGR UNIV,DEPT PHARMACOL & PATHOBIOL,MOLEC PATHOBIOL LAB,DK-1870 FREDERIKSBERG,DENMARK. NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 70 TC 32 Z9 33 U1 1 U2 11 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1994 VL 138 IS 3-4 BP 213 EP 231 DI 10.1007/BF01379127 PG 19 WC Virology SC Virology GA PP901 UT WOS:A1994PP90100003 PM 7998830 ER PT J AU ROSENFELD, SJ YOUNG, NS ALLING, D AYUB, J SAXINGER, C AF ROSENFELD, SJ YOUNG, NS ALLING, D AYUB, J SAXINGER, C TI SUBUNIT INTERACTION IN B19 PARVOVIRUS EMPTY CAPSIDS SO ARCHIVES OF VIROLOGY LA English DT Article ID CANINE PARVOVIRUS; IMMUNE-RESPONSE; EPITOPE; VP1; IDENTIFICATION; ANTIBODY; SYSTEM; REGION; MAP AB B19 parvovirus is a small single-stranded DNA virus with a genome that encodes only two structural proteins, designated VP1 and VP2. 60 copies of the structural proteins assemble into the viral capsid, with approximately 95% VP2 and 5% VP1. Recombinant empty capsids composed of VP2 alone or of VP2 and VP1 self-assemble into particles that are morphologically indistinguishable from full virions. Empty capsids containing both VP2 and VP1 elicit a strong neutralizing antibody response when used to immunize rabbits. Capsids containing only VP2 are similarly antigenic but elicit only weak neutralizing activity. We performed fine structure epitope mapping by measuring the reactivity of antisera raised against capsids composed of VP2 and VP1 or VP2 alone against 85 overlapping peptides spanning the sequence of the two structural proteins. A profile of the antigenic difference between empty capsids with and without VP1 was produced from the resulting data. This profile divided the sequence of the structural proteins into four regions that correlated well with expected viral structures. Thus, the addition of a small number of VP1 residues altered the antigenicity of the entire capsid. The major area of enhanced antigenicity is homologous to the spike of canine parvovirus, an area known to contain both neutralizing and host-range determinants. Our data are consistent with a model in which the unique region of VP1 is necessary for the virus to assume its mature capsid conformation. C1 NHLBI,CELLULAR HEMATOL BRANCH,BETHESDA,MD 20892. NIAID,OFF DIRECTOR,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 18 TC 16 Z9 18 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1994 VL 136 IS 1-2 BP 9 EP 18 DI 10.1007/BF01538813 PG 10 WC Virology SC Virology GA NN737 UT WOS:A1994NN73700002 PM 7516147 ER PT J AU ERICKSON, J KEMPF, D AF ERICKSON, J KEMPF, D TI STRUCTURE-BASED DESIGN OF SYMMETRICAL INHIBITORS OF HIV-1 PROTEASE SO ARCHIVES OF VIROLOGY LA English DT Article ID CRYSTAL-STRUCTURE; RENIN INHIBITORS; AIDS AB HIV-1, the causative agent of AIDS, encodes a protease that processes the viral polyproteins into the structural proteins and replicative enzymes found in mature virions. Protease activity has been shown to be essential for the proper assembly and maturation of fully infectious HIV-1. Thus, the HIV-1 protease (HIV PR) has become an important target for the design of antiviral agents for AIDS. Analysis of the three-dimensional structures of related aspartic proteinases, and later of Rous sarcoma virus protease, indicated that the active site and extended substrate binding cleft exhibits two-fold (C2) symmetry at the atomic level. We therefore set out to test whether compounds that contained a C2 axis of symmetry, and that were structurally complementary to the active site region, could be potent and selective inhibitors of HIV PR. Two novel classes of C2 or pseudo-C2 symmetric inhibitors were designed, synthesized and shown to display potent inhibitory activity towards HIV PR, and one of these, A-77003, recently entered clinical trials. The structure of the complex with A-74704 was solved using X-ray crystallographic methods and revealed a highly symmetric mode of binding, confirming our initial design principles. These studies demonstrate that relatively simple symmetry considerations can give rise to novel compound designs, allowing access to imaginative new templates for synthesis that can be translated into experimental therapeutic agents. C1 ABBOTT LABS, DIV PHARMACEUT PROD, ABBOTT PK, IL 60064 USA. RP ERICKSON, J (reprint author), NCI, FREDERICK CANC RES & DEV CTR, PROGRAM RESOURCES INC, FREDERICK BIOMED SUPERCOMP CTR, FREDERICK, MD 21702 USA. NR 16 TC 7 Z9 7 U1 1 U2 4 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0304-8608 EI 1432-8798 J9 ARCH VIROL JI Arch. Virol. PY 1994 SU 9 BP 19 EP 29 PG 11 WC Virology SC Virology GA NQ963 UT WOS:A1994NQ96300004 ER PT J AU EMERSON, SU LEWIS, M GOVINDARAJAN, S SHAPIRO, M MOSKAL, T PURCELL, RH AF EMERSON, SU LEWIS, M GOVINDARAJAN, S SHAPIRO, M MOSKAL, T PURCELL, RH TI IN-VIVO TRANSFECTION BY HEPATITIS-A VIRUS SYNTHETIC RNA SO ARCHIVES OF VIROLOGY LA English DT Article; Proceedings Paper CT 3rd International Symposium on Positive-Strand RNA Viruses CY SEP, 1992 CL CLEARWATER, FL ID COMPLETE NUCLEOTIDE-SEQUENCE; A VIRUS; CELL-CULTURE; ADAPTATION; CDNA AB Marmosets injected intrahepatically with nucleic acids (cDNA and RNA transcripts) representing the full-length genome of the wild-type HM-175 strain of hepatitis A virus experienced acute hepatitis and seroconversion to hepatitis A virus capsid proteins. The hepatitis was comparable in severity to that caused by infection with the wild-type virus. The viral cDNA and the hepatitis A virus recovered from the feces of an injected animal contained the same marker mutation. Therefore, intermediate cell culture steps can be omitted and the virulence of a hepatitis A virus encoded by a cDNA clone can be evaluated by direct transfection of marmosets. C1 RANCHO LOS AMIGOS CTR,DOWNEY,CA. BIOQUAL INC,ROCKVILLE,MD. RP EMERSON, SU (reprint author), NIH,HEPATITIS VIRUSES SECT,BLDG 7,ROOM 203,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1994 SU 9 BP 205 EP 209 PG 5 WC Virology SC Virology GA NQ963 UT WOS:A1994NQ96300021 ER PT J AU NAKHASI, HL SINGH, NK POGUE, GP CAO, XQ ROUAULT, TA AF NAKHASI, HL SINGH, NK POGUE, GP CAO, XQ ROUAULT, TA TI IDENTIFICATION AND CHARACTERIZATION OF HOST FACTOR INTERACTIONS WITH CIS-ACTING ELEMENTS OF RUBELLA-VIRUS RNA SO ARCHIVES OF VIROLOGY LA English DT Article; Proceedings Paper CT 3rd International Symposium on Positive-Strand RNA Viruses CY SEP, 1992 CL CLEARWATER, FL ID GENOME RNA; STRAND RNA; PROTEINS; TRANSLATION; BINDING; REGION AB We have analyzed the function of cis-acting elements of rubella virus RNA and the components which interact with these elements in viral RNA replication. We demonstrated that the 5'- and 3'-terminal sequences from RV RNA promote translation and negative-strand RNA synthesis of chimeric chloroamphenicol acetyltransferase (CAT) RNAs. These sequences have a potential to form stem-loop (SL) structures and bind cellular proteins specifically in RNA gel-shift and UV cross-linking assays. The 5' end binding proteins were identified to be Ro/SSA-associated antigens by virtue of being recognized in an RNA complex by an autoimmune patient serum with Ro antigen type specificity. Purification and sequence analysis of the 3' end binding protein revealed that it is a homologue of human calreticulin. The role of host proteins in RV replication is discussed. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. RP NAKHASI, HL (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL PROD,BLDG 29,RM 107,8800 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 16 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1994 SU 9 BP 255 EP 267 PG 13 WC Virology SC Virology GA NQ963 UT WOS:A1994NQ96300027 ER PT J AU LAI, CJ PETHEL, M JAN, LR KAWANO, H CAHOUR, A FALGOUT, B AF LAI, CJ PETHEL, M JAN, LR KAWANO, H CAHOUR, A FALGOUT, B TI PROCESSING OF DENGUE TYPE-4 AND OTHER FLAVIVIRUS NONSTRUCTURAL PROTEINS SO ARCHIVES OF VIROLOGY LA English DT Article; Proceedings Paper CT 3rd International Symposium on Positive-Strand RNA Viruses CY SEP, 1992 CL CLEARWATER, FL ID OCTAPEPTIDE SEQUENCE; VIRUS; PROTEASE; DOMAIN; NS2B; NS3; CLEAVAGE; PESTIVIRUSES; POLYPROTEIN; REQUIRES AB Dengue type 4 (DEN4) and other flaviviruses employ host and viral proteases for polyprotein processing. Most proteolytic cleavages in the DEN4 nonstructural protein (NS) region are mediated by the viral NS2B-NS3 protease. The N-terminal third of NS3, containing sequences homologous to serine protease active sites, is the protease domain. To determine required sequences in NS2B, deletions were introduced into DEN4 NS2B-30%NS3 cDNA and the expressed polyproteins assayed for self-cleavage. A 40 amino acid segment within NS2B was essential. Sequence analysis of NS2B predicts that this segment constitutes a hydrophilic domain surrounded by hydrophobic regions. Hydophobicity profiles of other flavivirus NS2Bs show similar patterns. Cleavage of DEN4 NS1-NS2A requires an octapeptide sequence at the NS1 C terminus and downstream NS2A. Comparison of the analogous octapeptide sequences among flaviviruses indicates a consensus cleavage sequence of (P8)/Met/Leu-Val-Xaa-Ser-Xaa-Val-Ala(P1) where Xaa are nonconserved amino acids. The effects on cleavage of amino acid substitutions in this consensus sequence were analyzed. Most substitutions of the conserved residues interfered with cleavage, whereas substitutions of non-conserved residues had little or no effect. These findings indicate that the responsible enzyme recognizes well-defined sequences at the cleavage site. RP LAI, CJ (reprint author), NIAID,INFECT DIS LAB,MOLEC VIRAL BIOL SECT,BETHESDA,MD 20892, USA. NR 12 TC 0 Z9 1 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1994 SU 9 BP 359 EP 368 PG 10 WC Virology SC Virology GA NQ963 UT WOS:A1994NQ96300037 ER PT J AU REIN, A AF REIN, A TI RETROVIRAL RNA PACKAGING - A REVIEW SO ARCHIVES OF VIROLOGY LA English DT Article ID ROUS-SARCOMA VIRUS; MURINE LEUKEMIA-VIRUS; CYS-HIS BOX; NUCLEOCAPSID PROTEIN; DIMER FORMATION; GENOMIC RNA; DEFECTIVE RETROVIRUS; ZINC FINGERS; CIS ELEMENTS; TYPE-1 AB In retroviruses, the ''Gag'' or core polyprotein is capable of assembling into virus particles and packaging the genomic RNA of the virus. How this protein recognizes viral RNA is not understood. Gag polyproteins contain a zinc-finger domain; mutants with changes in this domain assemble into virions, but a large fraction of these particles lack viral RNA. Thus, one crucial element in the RNA packaging mechanism is the zinc-finger domain. RNA sequences required for packaging (''packing signals'') have been studied both by deletion analysis and by measuring encapsidation of nonviral mRNAs containing limited insertions of viral sequence. These experiments show that all or part of the packaging signal in viral RNA is located near the 5 end of the genome. These signals appear to be quite large, i.e., hundreds of nucleotides. Each virus particle actually contains a dimer of two identical, + strand genomic RNA molecules. The nature of the dimeric linkage is not understood. In some experimental situations (including zinc-finger mutants), only a small fraction of the particles in a virus preparation contain genomic RNA. It is striking that the genomic RNA packaged in these situations is dimeric. Because of this important observation, it is speculated that only dimers are packaged, and that the dimeric structure is an element of the packaging signal. It is also suggested that the dimers undergo a conformational change (''RNA maturation'') after the virus is released from the cell, and that this change may depend upon the cleavage of the Gag polyprotein, a post-assembly event catalyzed by the virus-coded protease. RP REIN, A (reprint author), NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. NR 36 TC 11 Z9 11 U1 0 U2 0 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1994 SU 9 BP 513 EP 522 PG 10 WC Virology SC Virology GA NQ963 UT WOS:A1994NQ96300050 ER PT J AU ROME, JJ SHAYANI, V FLUGELMAN, MY NEWMAN, KD FARB, A VIRMANI, R DICHEK, DA AF ROME, JJ SHAYANI, V FLUGELMAN, MY NEWMAN, KD FARB, A VIRMANI, R DICHEK, DA TI ANATOMIC BARRIERS INFLUENCE THE DISTRIBUTION OF IN-VIVO GENE-TRANSFER INTO THE ARTERIAL-WALL - MODELING WITH MICROSCOPIC TRACER PARTICLES AND VERIFICATION WITH A RECOMBINANT ADENOVIRAL VECTOR SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Article DE GENE THERAPY; ARTERIAL CATHETERIZATION; MICROSPHERES; BETA-GALACTOSIDASE; HORSERADISH PEROXIDASE ID LOW-DENSITY-LIPOPROTEIN; ENDOTHELIAL-CELLS; BALLOON CATHETER; INVIVO; ACCUMULATION; EXPRESSION; PERMEABILITY; MICROSPHERES; CORONARY; INVITRO AB We evaluated the extent to which anatomic barriers to vector penetration might influence the distribution of successful in vivo gene transfer into the normal arterial wall. A double-balloon catheter technique with infusion pressures of 100 to 400 mm Hg was used to infuse microscopic tracer particles of the size range of liposomes and viral vectors into normal elastic arteries of sheep. Localization of the tracer particles in tissue sections by light, fluorescence, and electron microscopy suggested that vector-sized particles were delivered to the intima by direct infusion and to the adventitia via the arterial vasa vasorum. Particles were virtually absent from the arterial media. To test the predictions made from the particle studies, we repeated the infusion protocol with high-titer adenoviral vectors. Gene transfer occurred at high levels in the intima and along the adventitial vasa vasorum but again was virtually absent within the media. The ability of medial smooth muscle cells to be transduced was established in separate experiments with a high-pressure (5 atm) porous balloon infusion catheter. We conclude that (1) the anatomy of the normal elastic arterial wall imposes significant limitations on the penetration of particles in the size range of most gene-transfer vectors and (2) the distribution of in vivo gene transfer with adenoviral vectors is correctly predicted by the distribution of inert tracer particles. These findings have important implications for the design of arterial gene-transfer and gene-therapy protocols. C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,WASHINGTON,DC. CHILDRENS HOSP MED CTR,DIV CARDIOL,WASHINGTON,DC. CHILDRENS HOSP MED CTR,DIV SURG,WASHINGTON,DC. NR 46 TC 140 Z9 146 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD JAN PY 1994 VL 14 IS 1 BP 148 EP 161 PG 14 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MQ804 UT WOS:A1994MQ80400020 PM 8274471 ER PT J AU KLEIN, HG AF KLEIN, HG TI OXYGEN CARRIERS AND TRANSFUSION MEDICINE SO ARTIFICIAL CELLS BLOOD SUBSTITUTES AND IMMOBILIZATION BIOTECHNOLOGY LA English DT Article; Proceedings Paper CT Vth International Symposium on Blood Substitutes CY MAR 17-20, 1993 CL SAN DIEGO, CA ID ACQUIRED IMMUNODEFICIENCY SYNDROME; CANCER RECURRENCE; AUTOLOGOUS BLOOD; UNITED-STATES; COLLECTION; HEPATITIS; INFECTION; RISK; MECHANISMS; SURGERY AB The US blood supply is once again expanding (14 million units a year) and annual estimated whole blood and red blood cell (RBC) transfusion now exceeds 12 million units. The observed increase in total transfusions and units transfused per surgical procedure may result from more aggressive therapies, an aging population, and improved access to health care. While autologous blood collection has grown 20-fold in the past decade, autologous blood still accounts for <8% of transfusions and is unlikely to replace much more of the allogeneic transfusion needs. Although safer than ever, allogeneic blood still transmits infectious disease (HIV:1 in 225,000 units, hepatitis:1 in 3300 units, HTLV I/II:1 in 50,000 units) and poses additional immunologic and non-immunologic risks. Allogeneic RBCs are probably underutilized because of safety concerns. RP KLEIN, HG (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892, USA. NR 23 TC 30 Z9 30 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1073-1199 J9 ARTIF CELL BLOOD SUB JI Artif. Cells Blood Substit. Immobil. Biotechnol. PY 1994 VL 22 IS 2 BP 123 EP 135 DI 10.3109/10731199409117408 PG 13 WC Biotechnology & Applied Microbiology; Engineering, Biomedical; Materials Science, Biomaterials SC Biotechnology & Applied Microbiology; Engineering; Materials Science GA NQ115 UT WOS:A1994NQ11500003 PM 8087236 ER PT J AU CASSMAN, M AF CASSMAN, M TI BASIC RESEARCH AND TECHNOLOGY-TRANSFER - FEDERAL EFFORTS ARE BETTER BALANCED THAN IS APPRECIATED, BUT ECONOMIC FORCES NECESSITATE KEY ADJUSTMENTS SO ASM NEWS LA English DT Article C1 NATL INST GEN MED SCI,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0044-7897 J9 ASM NEWS JI ASM News PD JAN PY 1994 VL 60 IS 1 BP 24 EP 27 PG 4 WC Microbiology SC Microbiology GA NB933 UT WOS:A1994NB93300019 ER PT J AU STOKES, AF BELGER, A BANICH, MT BERNADINE, E AF STOKES, AF BELGER, A BANICH, MT BERNADINE, E TI EFFECTS OF ALCOHOL AND CHRONIC ASPARTAME INGESTION UPON PERFORMANCE IN AVIATION RELEVANT COGNITIVE TASKS SO AVIATION SPACE AND ENVIRONMENTAL MEDICINE LA English DT Article AB Acute dosing studies of aspartame, known commercially as ''NutraSweet,'' have failed to demonstrate any neuropsychological changes that would imply performance decrements in flight operations. Such studies may be criticized on the grounds that the administration of a single, if large, dose of aspartame is not ecologically valid. Accordingly, a double-blind chronic dosing study of aspartame was conducted using ethanol (at 0. 1% BAL) as the positive control. No detectable cognitive performance decrements were associated with the aspartame condition. However, the alcohol results exhibited a pattern of asymmetric lateral brain impairment that closely resembles that observed in studies of depressive patients. These results have operational implications as well as theoretical importance. C1 UNIV ILLINOIS,INST AVIAT,AVIAT RES LAB,SAVOY,IL. UNIV ILLINOIS,DEPT PSYCHOL,CHAMPAIGN,IL 61820. NICHHD,NIO HUMAN GENET BRANCH,BETHESDA,MD 20892. OI Belger, Aysenil/0000-0003-2687-1966 NR 28 TC 8 Z9 8 U1 0 U2 3 PU AEROSPACE MEDICAL ASSOC PI ALEXANDRIA PA 320 S HENRY ST, ALEXANDRIA, VA 22314-3579 SN 0095-6562 J9 AVIAT SPACE ENVIR MD JI Aviat. Space Environ. Med. PD JAN PY 1994 VL 65 IS 1 BP 7 EP 15 PG 9 WC Public, Environmental & Occupational Health; Medicine, General & Internal; Sport Sciences SC Public, Environmental & Occupational Health; General & Internal Medicine; Sport Sciences GA MQ236 UT WOS:A1994MQ23600003 PM 8117231 ER PT S AU MOSS, J TSAI, SC VAUGHAN, M AF MOSS, J TSAI, SC VAUGHAN, M BE Clark, VL Bavoil, PM TI ACTIVATION OF CHOLERA-TOXIN BY ADP-RIBOSYLATION FACTORS SO BACTERIAL PATHOGENESIS, PT A: IDENTIFICATION AND REGULATION OF VIRULENCE FACTORS SE Methods in Enzymology LA English DT Review ID NUCLEOTIDE-BINDING PROTEIN; RIBOSYLTRANSFERASE ACTIVITY; ADENYLATE-CYCLASE; REGULATORY COMPONENT; HUMAN GENE; FACTOR-III; FACTOR-I; GTP; GOLGI; EXPRESSION RP NHLBI, CELLULAR METAB LAB, BETHESDA, MD 20892 USA. NR 42 TC 9 Z9 9 U1 0 U2 1 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-182136-6 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1994 VL 235 BP 640 EP 647 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88R UT WOS:A1994BA88R00051 PM 8057933 ER PT J AU STORZ, G TOLEDANO, MB AF STORZ, G TOLEDANO, MB TI REGULATION OF BACTERIAL GENE-EXPRESSION IN RESPONSE TO OXIDATIVE STRESS SO BACTERIAL PATHOGENESIS, PT B SE METHODS IN ENZYMOLOGY LA English DT Review ID REDOX-CYCLING AGENTS; ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; HEAT-SHOCK; TRANSCRIPTIONAL REGULATOR; POSITIVE REGULATOR; INDUCIBLE GENES; OXYR PROTEIN; DNA DAMAGE; REGULON RP STORZ, G (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. OI Storz, Gisela/0000-0001-6698-1241 NR 33 TC 20 Z9 21 U1 1 U2 3 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 1994 VL 236 BP 196 EP 207 PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA88S UT WOS:A1994BA88S00015 PM 7968610 ER PT S AU BOUMA, CL KEITH, JM AF BOUMA, CL KEITH, JM BE Freer, J Aitken, R Alouf, JE Boulnois, G Falmagne, P Fehrenbach, F Montecucco, C Piemont, Y Rappuoli, R Wadstrom, T Witholt, B TI REGULATION OF THE ACTINOBACILLUS-ACTINOMYCETEMCOMITANS LEUKOTOXIN PROMOTER SO BACTERIAL PROTEIN TOXINS: SIXTH EUROPEAN WORKSHOP SE ZENTRALBLATT FUR BAKTERIOLOGIE : SUPPLEMENT LA English DT Proceedings Paper CT 6th European Workshop on Bacterial Protein Toxins CY JUN 27-JUL 02, 1993 CL STIRLING, SCOTLAND SP FEDERAT EUROPEAN MICROBIOL SOC C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART 70 PA WOLLGRASWEG 49, W-7000 STUTTGART 70, GERMANY SN 0172-5629 BN 3-437-11535-9 J9 ZBL BAKT S PY 1994 VL 24 BP 100 EP 101 PG 2 WC Biochemistry & Molecular Biology; Microbiology; Toxicology SC Biochemistry & Molecular Biology; Microbiology; Toxicology GA BA51D UT WOS:A1994BA51D00016 ER PT S AU BOUMA, CL KEITH, JM AF BOUMA, CL KEITH, JM BE Freer, J Aitken, R Alouf, JE Boulnois, G Falmagne, P Fehrenbach, F Montecucco, C Piemont, Y Rappuoli, R Wadstrom, T Witholt, B TI REGULATION OF THE ACTINOBACILLUS-ACTINOMYCETEMCOMITANS LEUKOTOXIN PROMOTER SO BACTERIAL PROTEIN TOXINS: SIXTH EUROPEAN WORKSHOP SE ZENTRALBLATT FUR BAKTERIOLOGIE : SUPPLEMENT LA English DT Proceedings Paper CT 6th European Workshop on Bacterial Protein Toxins CY JUN 27-JUL 02, 1993 CL STIRLING, SCOTLAND SP FEDERAT EUROPEAN MICROBIOL SOC C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART 70 PA WOLLGRASWEG 49, W-7000 STUTTGART 70, GERMANY SN 0172-5629 BN 3-437-11535-9 J9 ZBL BAKT S PY 1994 VL 24 BP 169 EP 170 PG 2 WC Biochemistry & Molecular Biology; Microbiology; Toxicology SC Biochemistry & Molecular Biology; Microbiology; Toxicology GA BA51D UT WOS:A1994BA51D00032 ER PT S AU LEPPLA, SH KLIMPEL, KR ARORA, N AF LEPPLA, SH KLIMPEL, KR ARORA, N BE Freer, J Aitken, R Alouf, JE Boulnois, G Falmagne, P Fehrenbach, F Montecucco, C Piemont, Y Rappuoli, R Wadstrom, T Witholt, B TI ANTHRAX TOXIN LETHAL FACTOR IS A METALLOPEPTIDASE SO BACTERIAL PROTEIN TOXINS: SIXTH EUROPEAN WORKSHOP SE ZENTRALBLATT FUR BAKTERIOLOGIE : SUPPLEMENT LA English DT Proceedings Paper CT 6th European Workshop on Bacterial Protein Toxins CY JUN 27-JUL 02, 1993 CL STIRLING, SCOTLAND SP FEDERAT EUROPEAN MICROBIOL SOC DE ANTHRAX TOXIN; PROTEASE; ZINC; MACROPHAGE; THERMOLYSIN C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART 70 PA WOLLGRASWEG 49, W-7000 STUTTGART 70, GERMANY SN 0172-5629 BN 3-437-11535-9 J9 ZBL BAKT S PY 1994 VL 24 BP 386 EP 387 PG 2 WC Biochemistry & Molecular Biology; Microbiology; Toxicology SC Biochemistry & Molecular Biology; Microbiology; Toxicology GA BA51D UT WOS:A1994BA51D00078 ER PT S AU WILLIAMSON, LC NEALE, EA AF WILLIAMSON, LC NEALE, EA BE Freer, J Aitken, R Alouf, JE Boulnois, G Falmagne, P Fehrenbach, F Montecucco, C Piemont, Y Rappuoli, R Wadstrom, T Witholt, B TI TETANUS TOXIN ENTERS NEURONS THROUGH ACIDIC ENDOSOMES - STUDIES IN SPINAL-CORD CELL-CULTURES SO BACTERIAL PROTEIN TOXINS: SIXTH EUROPEAN WORKSHOP SE ZENTRALBLATT FUR BAKTERIOLOGIE : SUPPLEMENT LA English DT Proceedings Paper CT 6th European Workshop on Bacterial Protein Toxins CY JUN 27-JUL 02, 1993 CL STIRLING, SCOTLAND SP FEDERAT EUROPEAN MICROBIOL SOC C1 NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART 70 PA WOLLGRASWEG 49, W-7000 STUTTGART 70, GERMANY SN 0172-5629 BN 3-437-11535-9 J9 ZBL BAKT S PY 1994 VL 24 BP 410 EP 411 PG 2 WC Biochemistry & Molecular Biology; Microbiology; Toxicology SC Biochemistry & Molecular Biology; Microbiology; Toxicology GA BA51D UT WOS:A1994BA51D00090 ER PT S AU NEVILLE, DM SCHARFF, J RIGAUT, K SHILOACH, J SLINGERLAND, W JONKER, M AF NEVILLE, DM SCHARFF, J RIGAUT, K SHILOACH, J SLINGERLAND, W JONKER, M BE Freer, J Aitken, R Alouf, JE Boulnois, G Falmagne, P Fehrenbach, F Montecucco, C Piemont, Y Rappuoli, R Wadstrom, T Witholt, B TI IMMUNOTOXIN INDUCED T-CELL DEPLETION IN RHESUS-MONKEYS - EXPERIMENTAL AND THERAPEUTIC IMPLICATIONS SO BACTERIAL PROTEIN TOXINS: SIXTH EUROPEAN WORKSHOP SE ZENTRALBLATT FUR BAKTERIOLOGIE : SUPPLEMENT LA English DT Proceedings Paper CT 6th European Workshop on Bacterial Protein Toxins CY JUN 27-JUL 02, 1993 CL STIRLING, SCOTLAND SP FEDERAT EUROPEAN MICROBIOL SOC DE IMMUNOTOXIN; DIPHTHERIA; CRM9; CD3; FN18; TCR; RECEPTOR; ENDOCYTOSIS; TRAFFICKING; RHESUS; AUTOIMMUNE; SIV C1 NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART 70 PA WOLLGRASWEG 49, W-7000 STUTTGART 70, GERMANY SN 0172-5629 BN 3-437-11535-9 J9 ZBL BAKT S PY 1994 VL 24 BP 426 EP 430 PG 5 WC Biochemistry & Molecular Biology; Microbiology; Toxicology SC Biochemistry & Molecular Biology; Microbiology; Toxicology GA BA51D UT WOS:A1994BA51D00092 ER PT S AU LEPPLA, SH KLIMPEL, KR ARORA, N AF LEPPLA, SH KLIMPEL, KR ARORA, N BE Freer, J Aitken, R Alouf, JE Boulnois, G Falmagne, P Fehrenbach, F Montecucco, C Piemont, Y Rappuoli, R Wadstrom, T Witholt, B TI DEVELOPMENT OF ANTHRAX TOXIN BASED FUSION PROTEINS FOR TARGETING OF HIV-1-INFECTED CELLS SO BACTERIAL PROTEIN TOXINS: SIXTH EUROPEAN WORKSHOP SE ZENTRALBLATT FUR BAKTERIOLOGIE : SUPPLEMENT LA English DT Proceedings Paper CT 6th European Workshop on Bacterial Protein Toxins CY JUN 27-JUL 02, 1993 CL STIRLING, SCOTLAND SP FEDERAT EUROPEAN MICROBIOL SOC DE BACTERIAL TOXINS; ANTHRAX; PROTECTIVE ANTIGEN; HIV-1; PROTEASE; INTERLEUKIN-2; CD4; PSEUDOMONAS-EXOTOXIN; DIPHTHERIA TOXIN; CHO CELLS; FURIN; FUSION PROTEINS C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART 70 PA WOLLGRASWEG 49, W-7000 STUTTGART 70, GERMANY SN 0172-5629 BN 3-437-11535-9 J9 ZBL BAKT S PY 1994 VL 24 BP 431 EP 442 PG 12 WC Biochemistry & Molecular Biology; Microbiology; Toxicology SC Biochemistry & Molecular Biology; Microbiology; Toxicology GA BA51D UT WOS:A1994BA51D00093 ER PT S AU SHILOACH, J TSAI, A GALLO, M PETTERSON, T AF SHILOACH, J TSAI, A GALLO, M PETTERSON, T BE Freer, J Aitken, R Alouf, JE Boulnois, G Falmagne, P Fehrenbach, F Montecucco, C Piemont, Y Rappuoli, R Wadstrom, T Witholt, B TI LARGE-SCALE PRODUCTION AND PURIFICATION OF CLINICAL GRADE RECOMBINANT PSEUDOMONAS-AERUGINOSA EXOTOXIN-A FROM ESCHERICHIA-COLI SO BACTERIAL PROTEIN TOXINS: SIXTH EUROPEAN WORKSHOP SE ZENTRALBLATT FUR BAKTERIOLOGIE : SUPPLEMENT LA English DT Proceedings Paper CT 6th European Workshop on Bacterial Protein Toxins CY JUN 27-JUL 02, 1993 CL STIRLING, SCOTLAND SP FEDERAT EUROPEAN MICROBIOL SOC C1 NIDDK,BIOTECHNOL UNIT LCDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART 70 PA WOLLGRASWEG 49, W-7000 STUTTGART 70, GERMANY SN 0172-5629 BN 3-437-11535-9 J9 ZBL BAKT S PY 1994 VL 24 BP 443 EP 445 PG 3 WC Biochemistry & Molecular Biology; Microbiology; Toxicology SC Biochemistry & Molecular Biology; Microbiology; Toxicology GA BA51D UT WOS:A1994BA51D00094 ER PT S AU LEPPLA, SH KLIMPEL, KR ARORA, N AF LEPPLA, SH KLIMPEL, KR ARORA, N BE Freer, J Aitken, R Alouf, JE Boulnois, G Falmagne, P Fehrenbach, F Montecucco, C Piemont, Y Rappuoli, R Wadstrom, T Witholt, B TI MODIFIED ANTHRAX TOXIN IS A POTENTIAL ANTIVIRAL AGENT SO BACTERIAL PROTEIN TOXINS: SIXTH EUROPEAN WORKSHOP SE ZENTRALBLATT FUR BAKTERIOLOGIE : SUPPLEMENT LA English DT Proceedings Paper CT 6th European Workshop on Bacterial Protein Toxins CY JUN 27-JUL 02, 1993 CL STIRLING, SCOTLAND SP FEDERAT EUROPEAN MICROBIOL SOC DE ANTHRAX TOXIN; HIV-1; PROTEASE; MUTAGENESIS; ANTIVIRAL; FUSION TOXIN C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART 70 PA WOLLGRASWEG 49, W-7000 STUTTGART 70, GERMANY SN 0172-5629 BN 3-437-11535-9 J9 ZBL BAKT S PY 1994 VL 24 BP 448 EP 449 PG 2 WC Biochemistry & Molecular Biology; Microbiology; Toxicology SC Biochemistry & Molecular Biology; Microbiology; Toxicology GA BA51D UT WOS:A1994BA51D00096 ER PT J AU GLOWA, JR HANSEN, CT AF GLOWA, JR HANSEN, CT TI DIFFERENCES IN RESPONSE TO AN ACOUSTIC STARTLE STIMULUS AMONG 46 RAT STRAINS SO BEHAVIOR GENETICS LA English DT Article DE STARTLE RESPONSE; ACOUSTIC STIMULUS; RATS; STRAIN DIFFERENCES; BEHAVIOR ID CORTICOTROPIN-RELEASING HORMONE; FISCHER RATS; LEWIS RATS; ARTHRITIS; COCAINE AB The startle response to intense environmental stimuli is found in most, if not all, animal species. Previous studies have shown that selected rodent strains differ in startle response to an acoustic stimulus, suggesting genetic variability. The current experiment was designed to extend these differences to a wider range of rat strains. Forty-six inbred and outbred rat strains were studied. These strains exhibited differences in both the mean amplitude of the startle response and the rate of habituation to startle stimuli over repeated trials. In addition, there was a significant relationship between these measures. These results suggest that robust phenotypic differences in startle response exist among rat strains. As previous investigations have demonstrated a direct relationship between the startle response and other behavioral end points, the use of strain differences in startle response may be an effective way to determine genetic contributions to specific behavioral responses. C1 NIH,NATL CTR RES RESOURCES,VET RESOURCES BRANCH,BETHESDA,MD 20892. RP GLOWA, JR (reprint author), NIDDK,LMC,BEHAV PHARMACOL UNIT,BLDG 14D,ROOM 311,BETHESDA,MD 20892, USA. NR 21 TC 82 Z9 83 U1 0 U2 4 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD JAN PY 1994 VL 24 IS 1 BP 79 EP 84 DI 10.1007/BF01067931 PG 6 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA MY905 UT WOS:A1994MY90500008 PM 8192623 ER PT B AU GANDJBAKHCHE, AH MILLS, P SNABRE, P DUFAUX, J AF GANDJBAKHCHE, AH MILLS, P SNABRE, P DUFAUX, J BE Bonner, RF Cohn, GE Laue, TM Priezzhev, AV Katzir, A TI AGGREGATION AND DEFORMATION OF RED-BLOOD-CELLS AS PROBED BY A LASER-LIGHT SCATTERING TECHNIQUE IN A CONCENTRATED SUSPENSION .1. METHODOLOGY SO BIOCHEMICAL DIAGNOSTIC INSTRUMENTATION, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Biochemical Diagnostic Instrumentation CY JAN 24-26, 1994 CL LOS ANGELES, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS C1 NIH,PHYS SCI LAB,DCRT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1431-X J9 P SOC PHOTO-OPT INS PY 1994 VL 2136 BP 87 EP 96 DI 10.1117/12.180775 PG 10 WC Engineering, Biomedical; Medical Laboratory Technology SC Engineering; Medical Laboratory Technology GA BB03L UT WOS:A1994BB03L00010 ER PT B AU GANDJBAKHCHE, AH OTHMANE, A MILLS, P SNABRE, P DUFAUX, J AF GANDJBAKHCHE, AH OTHMANE, A MILLS, P SNABRE, P DUFAUX, J BE Bonner, RF Cohn, GE Laue, TM Priezzhev, AV Katzir, A TI AGGREGATION AND DEFORMATION OF RED-BLOOD-CELLS AS PROBED BY A LASER-LIGHT SCATTERING TECHNIQUE IN A CONCENTRATED SUSPENSION .2. COMPARISON BETWEEN NORMAL AND PATHOLOGICAL RED-BLOOD-CELLS SO BIOCHEMICAL DIAGNOSTIC INSTRUMENTATION, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Biochemical Diagnostic Instrumentation CY JAN 24-26, 1994 CL LOS ANGELES, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS C1 NIH,PHYS SCI LAB,DCRT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1431-X J9 P SOC PHOTO-OPT INS PY 1994 VL 2136 BP 97 EP 104 DI 10.1117/12.180776 PG 8 WC Engineering, Biomedical; Medical Laboratory Technology SC Engineering; Medical Laboratory Technology GA BB03L UT WOS:A1994BB03L00011 ER PT S AU SHILOACH, J BAHAR, S MILLER, B AF SHILOACH, J BAHAR, S MILLER, B BE Kelly, RM Wittrup, KD Karkare, S TI ONLINE MONITORING OF BACTERIAL MASS DURING PRODUCTION OF RECOMBINANT EXOTOXIN-A - USING AN IN-SITU STEAM STERILIZABLE SENSOR SO BIOCHEMICAL ENGINEERING VIII SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Biochemical Engineering VIII CY JUL 11-16, 1993 CL PRINCETON, NJ SP Engn Fdn, Natl Sci Fdn, New York Acad Sci ID CELL CONCENTRATION; ESCHERICHIA-COLI; CULTURES C1 CEREX CORP,IJAMSVILLE,MD 21754. RP SHILOACH, J (reprint author), NIDDKD,BIOTECHNOL UNIT,BLDG 6,ROOM B1-33,BETHESDA,MD 20892, USA. NR 8 TC 0 Z9 0 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 0-89766-914-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 745 BP 244 EP 250 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Science & Technology - Other Topics GA BD11Y UT WOS:A1994BD11Y00020 PM 7832514 ER PT J AU GOSSE, ME FLEISCHMANN, R MARSHALL, M WANG, N GARGES, S GOTTESMAN, MM AF GOSSE, ME FLEISCHMANN, R MARSHALL, M WANG, N GARGES, S GOTTESMAN, MM TI BACTERIAL EXPRESSION OF CHINESE-HAMSTER REGULATORY TYPE-I AND CATALYTIC SUBUNITS OF CYCLIC-AMP-DEPENDENT PROTEIN-KINASE AND MUTATIONAL ANALYSIS OF THE TYPE-I REGULATORY SUBUNIT SO BIOCHEMICAL JOURNAL LA English DT Article ID AMINO-ACID-SEQUENCE; ESCHERICHIA-COLI; CAMP BINDING; OVARY CELLS; CHO CELLS; SITE; RESISTANT; MUTANT; GENES; DNA AB The type-I regulatory subunit (RI) of the cyclic AMP-dependent protein kinase (PKA) from Chinese hamster ovary (CHO) cells has been cloned and expressed in a strain of BL21(DE3) Escherichia coli lacking adenylate cyclase [BL21(DE3)/Delta cya]. RI expressed in this bacterial system free of cyclic AMP is soluble and can reconstitute functional PKA. Recombinant CHO C alpha is predominantly insoluble with some active soluble protein. C beta is entirely insoluble and inactive. Soluble recombinant RI and soluble recombinant C alpha can associate in vitro and be activated by cyclic AMP. Six site-directed mutations of RI were generated to study the interaction of cyclic AMP with RI and RI-C alpha subunit interactions. Four cyclic AMP-binding-site point mutants were generated [W261R (tryptophan to arginine at position 261), a novel mutation in site A; V376G, a novel mutation in site B; G200E (site A), and Y370F (site B), previously described in bovine RI were introduced into the CHO RI for comparison purposes]. Mutants W261R, Y370F, and G200E demonstrated decreased 8-N-3-[H-3]cyclic AMP binding as well as 5-fold reduced affinity for [H-3]cyclic AMP, with threefold increased EC(50) values for cyclic AMP activation of kinase activity from reconstituted mutant holoenzymes. The mutation at V376G did not alter cyclic AMP binding or activation by cyclic AMP of mutant holoenzyme. A truncation mutant, G200Stop, which lacks both cyclic AMP-binding sites, did not bind cyclic AMP but can inhibit C alpha subunit activity. A novel mutation outside the cyclic AMP-binding regions of RI (V89A) weakened the interaction with C alpha indicated by a 7-fold lower EC(50) for mutant holoenzyme activation by cyclic AMP. C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 41 TC 3 Z9 3 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD JAN 1 PY 1994 VL 297 BP 79 EP 85 PN 1 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MQ952 UT WOS:A1994MQ95200012 PM 8280113 ER PT J AU HIPPS, DS PACKMAN, LC ALLEN, MD FULLER, C SAKAGUCHI, K APPELLA, E PERHAM, RN AF HIPPS, DS PACKMAN, LC ALLEN, MD FULLER, C SAKAGUCHI, K APPELLA, E PERHAM, RN TI THE PERIPHERAL SUBUNIT-BINDING DOMAIN OF THE DIHYDROLIPOYL ACETYLTRANSFERASE COMPONENT OF THE PYRUVATE-DEHYDROGENASE COMPLEX OF BACILLUS-STEAROTHERMOPHILUS - PREPARATION AND CHARACTERIZATION OF ITS BINDING TO THE DIHYDROLIPOYL DEHYDROGENASE COMPONENT SO BIOCHEMICAL JOURNAL LA English DT Article ID MULTIENZYME COMPLEX; ESCHERICHIA-COLI; INTERDOMAIN SEGMENT; POLYPEPTIDE-CHAIN; SEQUENCE-ANALYSIS; PROTEIN; EXPRESSION; LIPOYL; PEPTIDES; DESIGN AB The peripheral subunit-binding domain of the dihydrolipoyl acetyltransferase polypeptide chain of the pyruvate dehydrogenase multienzyme complex of Bacillus stearothermophilus was released by limited proteolysis from a di-domain (lipoyl domain plus binding domain) encoded by a subgene over-expressed in Escherichia coli. The domain was characterized by N-terminal sequence analysis, electrospray m.s. and c.d. spectroscopy. It was found to be identical in all respects to a chemically synthesized peptide of the same sequence. The association of the di-domain of the and binding domain (both natural and synthetic) with dihydrolipoyl dehydrogenase was analysed in detail and a tight binding was demonstrated. As judged by several different techniques, it was found that only one peripheral subunit-binding domain is bound to one dimer of dihydrolipoyl dehydrogenase, implying that the association is highly anti-cooperative. C1 UNIV CAMBRIDGE,CAMBRIDGE CTR MOLEC RECOGNIT,DEPT BIOCHEM,CAMBRIDGE CB2 1QW,ENGLAND. NATL CANC INST,CELL BIOL LAB,BETHESDA,MD 20892. FU Wellcome Trust NR 38 TC 25 Z9 25 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD JAN 1 PY 1994 VL 297 BP 137 EP 143 PN 1 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MQ952 UT WOS:A1994MQ95200021 PM 8280091 ER PT J AU DANA, R MALECH, HL LEVY, R AF DANA, R MALECH, HL LEVY, R TI THE REQUIREMENT FOR PHOSPHOLIPASE-A(2) FOR ACTIVATION OF THE ASSEMBLED NADPH OXIDASE IN HUMAN NEUTROPHILS SO BIOCHEMICAL JOURNAL LA English DT Article ID PROTEIN-KINASE-C; CHRONIC GRANULOMATOUS-DISEASE; UNSATURATED FATTY-ACIDS; GTP-BINDING PROTEIN; RESPIRATORY-BURST; ARACHIDONIC-ACID; 2ND MESSENGER; CYTOSOLIC PHOSPHOLIPASE-A2; INDEPENDENT ACTIVATION; GENERATING OXIDASE AB Phospholipase A(2) (PLA(2)) inhibitors suppressed simultaneously, in a dose-dependent manner, the activation of NADPH oxidase and the release of H-3-labelled arachidonic acid ([H-3]AA) stimulated by either phorbol 12-myristate 13-acetate (PMA) or opsonized zymosan (OZ) in human neutrophils. In spite of total inhibition of superoxide production in the presence of the PLA(2) inhibitors, 10 mu M bromophenacyl bromide (BPB) or 20 mu M quinacrine, a maximal phosphorylation of p47 and translocation of p47 and p67 to the neutrophil membranes induced by PMA or OZ was observed. Addition of 10 mu M free AA, which by itself did not stimulate superoxide generation, restored oxidase activity in neutrophils treated with PLA(2) inhibitors. These findings indicate that phosphorylation and translocation of the cytosolic factors to the membranes are not sufficient for generating superoxide; a functional PLA(2) is also needed to stimulate the oxidase activity. The inhibition of PLA(2) activity did not prevent the phosphorylation of p47, suggesting that the location of PLA(2) is downstream of and does not activate protein kinase C. C1 BEN GURION UNIV NEGEV,SOROKA MED CTR KUPAT HOLIM,FAC HLTH SCI,INFECT DIS LAB,IL-84105 BEER SHEVA,ISRAEL. BEN GURION UNIV NEGEV,SOROKA MED CTR KUPAT HOLIM,FAC HLTH SCI,CLIN BIOCHEM UNIT,IL-84105 BEER SHEVA,ISRAEL. NATL INST ALLERGY & INFECT DIS,HOST DEFENSE LAB,BETHESDA,MD 20892. NR 63 TC 113 Z9 114 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD JAN 1 PY 1994 VL 297 BP 217 EP 223 PN 1 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MQ952 UT WOS:A1994MQ95200032 PM 8280102 ER PT J AU COOL, DR LOH, YP AF COOL, DR LOH, YP TI IDENTIFICATION OF A SORTING SIGNAL FOR THE REGULATED SECRETORY PATHWAY AT THE N-TERMINUS OF PROOPIOMELANOCORTIN SO BIOCHIMIE LA English DT Article DE PROHORMONE; SORTING SIGNAL; CONFORMATION; REGULATED SECRETION ID TRANS-GOLGI NETWORK; MANNOSE 6-PHOSPHATE RECEPTOR; PITUITARY-TUMOR-CELLS; INTERMEDIATE LOBE; CONVERTING ENZYME; SECRETOGRANIN-I; CHROMOGRANIN-B; PROOPIOMELANOCORTIN; ADRENOCORTICOTROPIN; GRANULES AB The N-terminal 26 amino acids of the prohormone pro-opiomelanocortin (POMC) were investigated to determine whether this region has the capacity to act as a sorting signal for the regulated secretory pathway. Constructs were made using the N-terminal 101, 50, 26 or 10 amino acids of POMC fused to the chloramphenicol acetyltransferase (CAT) reporter protein and expressed in AtT20 cells to show that at least the first 26 amino acids were required to sort CAT to the regulated secretory pathway. Full length POMC was mutated by deleting amino acids 2-26 from the N-terminal region. Analysis of Neuro-2a cells expressing this mutation compared to wild type POMC indicated that these 26 amino acids contain information essential for sorting POMC to the regulated secretory pathway. The results presented here suggest the presence of a conformation-dependent signal in the N-terminal 26 amino acids of POMC responsible for sorting POMC to the regulated secretory pathway. RP COOL, DR (reprint author), NICHHD,DEV NEUROBIOL LAB,CELLULAR NEUROBIOL SECT,BLDG 49,ROOM 5A38,BETHESDA,MD 20892, USA. NR 42 TC 47 Z9 47 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0300-9084 J9 BIOCHIMIE JI Biochimie PY 1994 VL 76 IS 3-4 BP 265 EP 270 DI 10.1016/0300-9084(94)90156-2 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PF202 UT WOS:A1994PF20200011 PM 7819333 ER PT J AU PANNIERS, R AF PANNIERS, R TI HENSHAW,EDGAR,C (1929-1992) - FOREWORD SO BIOCHIMIE LA English DT Editorial Material RP PANNIERS, R (reprint author), NIH,5333 WESTBARD AVE,BETHESDA,MD 20892, USA. NR 0 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 0300-9084 J9 BIOCHIMIE JI Biochimie PY 1994 VL 76 IS 8 BP 711 EP 712 DI 10.1016/0300-9084(94)90074-4 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PX207 UT WOS:A1994PX20700002 ER PT J AU PANNIERS, R AF PANNIERS, R TI TRANSLATIONAL CONTROL DURING HEAT-SHOCK SO BIOCHIMIE LA English DT Review DE HEAT SHOCK; TRANSLATION CONTROL; INITIATION; HEAT SHOCK PROTEIN ID BINDING-PROTEIN COMPLEX; EUKARYOTIC INITIATION-FACTORS; MESSENGER-RNA TRANSLATION; POLYPEPTIDE-CHAIN INITIATION; REGULATED EIF-2-ALPHA KINASE; ASCITES TUMOR-CELLS; HELA-CELLS; DROSOPHILA-MELANOGASTER; GENE-EXPRESSION; FACTOR-II AB Regulation of translation during heat shock of Drosophila and mammalian cells is reviewed. Protein synthesis is severely inhibited by elevated temperatures but synthesis of heat shock proteins (HSPs) is resistant to this inhibition. The primary site of regulation is polypeptide chain initiation. The activities of two initiation factors, eIF-2 and eIF-4F are modulated during heat shock. A protein kinase which modulates eIF-2 activity appears to be associated with heat shock proteins (HSPs). Evidence is emerging that HSP70 acts as a heat sensor by detecting the presence of accumulating denatured proteins. In the rabbit reticulocyte lysate denatured proteins bind HSP70 releasing an eIF-2 kinase to shut down protein synthesis. It appears highly likely that a similar mechanism is acting in heat shocked cells. Cell-free protein synthesizing systems prepared from heat shocked cells are deficient in eIF-4F. Modulation of eIF-4F can explain in part the apparent preferential translation of HSP mRNAs. RP PANNIERS, R (reprint author), NIH,5333 WESTBARD AVE,BETHESDA,MD 20892, USA. NR 109 TC 63 Z9 64 U1 0 U2 4 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0300-9084 J9 BIOCHIMIE JI Biochimie PY 1994 VL 76 IS 8 BP 737 EP 747 DI 10.1016/0300-9084(94)90078-7 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA PX207 UT WOS:A1994PX20700006 PM 7893824 ER PT J AU DEBINSKI, W PASTAN, I AF DEBINSKI, W PASTAN, I TI AN IMMUNOTOXIN WITH INCREASED ACTIVITY AND HOMOGENEITY PRODUCED BY REDUCING THE NUMBER OF LYSINE RESIDUES IN RECOMBINANT PSEUDOMONAS EXOTOXIN SO BIOCONJUGATE CHEMISTRY LA English DT Article ID ESCHERICHIA-COLI; ANTITUMOR-ACTIVITY; DOMAIN-II; SEQUENCE; PROTEIN; TOXIN; AERUGINOSA; FORM; EXPRESSION; TERMINUS AB Pseudomonas exotoxin A (PE) is a protein composed of 613 amino acids arranged into three major, and one minor, domains. Immunotoxins (ITs) containing PE38, a mutant form of PE which lacks the cell binding domain (Ia, amino acids 1-252) and 16 amino acids from domain lb (amino acids 365-380), are extremely potent cytotoxic agents. which can cause a complete regression of various human carcinomas grown in nude mice. However, these ITs are a mixture of several different chemical forms since the coupling between the antibody and the toxin may occur between either the light or heavy chain of the antibody and one of the four primary amino groups present on the truncated toxin. To modify the toxin with heterobifunctional crosslinking reagents only at specific sites, we replaced lysines 590 and 606 with glutamines and lysine 613 with arginine (PE38QQR). We also added two different peptide sequences, each containing a lysine residue, at the N-terminus of PE38. In one of these the sequence is ANLAEEAFK (''Lys'' peptide), and in the other, the sequence is LQGTKLMAEE (''NLys'' peptide). The mutant toxins were coupled using a thioether linkage to monoclonal antibody B3 which recognizes an antigen present in large amounts on many human cancers. PE38QQR-containing recombinant toxins can only be linked to an antibody through the N-terminal methionine or the lysine within the peptide. B3-LysPE38QQR and B3-NLysPE38QQR were four times more cytotoxic to target cells than the corresponding B3-LysPE38 and B3-NLysPE38 ITs. Furthermore, the antitumor effect of B3-NLysPE38QQR was significantly greater than that of B3-NLysPE38. We conclude that B3-LysPE38QQR and B3-NLysPE38QQR are more active because they are more homogenous components with all the antibody coupled to the N-terminus of the toxin and not some to the C-terminus, producing ITs with very low cytotoxic activity. C1 NCI,DIV CANC BIOL,MOLEC BIOL LAB,37-4E16,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NCI,CTR DIAGNOSIS,BETHESDA,MD 20892. NR 27 TC 29 Z9 30 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD JAN-FEB PY 1994 VL 5 IS 1 BP 40 EP 46 DI 10.1021/bc00025a006 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA MW637 UT WOS:A1994MW63700006 PM 8199233 ER PT J AU SIEGALL, CB GAWLAK, SL CHACE, DF MERWIN, JR PASTAN, I AF SIEGALL, CB GAWLAK, SL CHACE, DF MERWIN, JR PASTAN, I TI IN-VIVO ACTIVITIES OF ACIDIC FIBROBLAST GROWTH FACTOR-PSEUDOMONAS EXOTOXIN FUSION PROTEINS SO BIOCONJUGATE CHEMISTRY LA English DT Article ID FACTOR-SAPORIN MITOTOXIN; CYTOTOXIC ACTIVITY; ANTITUMOR-ACTIVITY; GLUTAMIC ACID-553; ENDOTHELIAL-CELLS; ESCHERICHIA-COLI; CHIMERIC TOXINS; FACTOR RECEPTOR; FACTOR-I; HEPARIN AB Fibroblast growth factor receptors are highly expressed in a variety of cancer cells and activated vasculature. Using chimeric toxins targeted to cell-surface aFGF receptors, we have demonstrated specific cytotoxic activity to these cell types. These molecules, aFGF-PE40 and aFGF-PE4E KDEL, are fusion proteins containing acidic FGF and either a 40- or a 66-kDa binding defective form of Pseudomonas exotoxin, respectively. Both aFGF-toxin fusion proteins were able to inhibit protein synthesis in vitro in a variety of carcinoma cell lines. The half-life of aFGF-PE40 in serum was found to be 41 min when coadministered with heparin. Administration of aFGF-PE40 or aFGF-PE4E KDEL with heparin inhibits the growth of established KB and preestablished A431 epidermoid carcinoma xenografts in athymic mice. The antitumor activities of the two aFGF-toxin fusion proteins were equivalent against the KB tumor xenografts. While we were able to slow the growth of the KB tumor xenografts, we were unable to cause tumor regressions. Histochemical analysis of treated versus untreated tumor tissue revealed a difference in tumor size but not of vascularity. We conclude that aFGF-PE40 and aFGF-PE4E KDEL have in vivo antitumor activity that targets the tumor cell mass rather than vascular structures in mice xenografted with human epidermoid carcinoma. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RP SIEGALL, CB (reprint author), BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,DEPT MOLEC IMMUNOL,3005 1ST AVE,SEATTLE,WA 98121, USA. NR 40 TC 12 Z9 12 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD JAN-FEB PY 1994 VL 5 IS 1 BP 77 EP 83 DI 10.1021/bc00025a010 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA MW637 UT WOS:A1994MW63700010 PM 7515280 ER PT B AU DUNN, BB FRIEDMAN, L AF DUNN, BB FRIEDMAN, L BE Llewellyn, GC Dashek, WV ORear, CE TI DISTRIBUTION AND METABOLISM OF CITRININ - A REVIEW SO BIODETERIORATION RESEARCH 4: MYCOTOXINS, WOOD DECAY, PLANT STRESS, BIOCORROSION, AND GENERAL BIODETERIORATION LA English DT Proceedings Paper CT 4th Meeting of the Pan-American-Biodeterioration-Society CY AUG 20-25, 1991 CL ELECTR NETWORK SP PAN AMER BIODETERIORAT SOC, GEORGE WASHINGTON UNIV, SMITHSONIAN INST, CLARK ATLANTA UNIV, DEPT BIOL, USDA, RES SERV, UNIV GEORGIA, MORRIS BROWN COLL, SPELLMAN COLL, MOREHOUSE COLL, NORTH CAROLINA STATE UNIV RALEIGH, US FDA, TOXICOL STUDIES, USDA, FOREST SERV, PENN STATE UNIV, UNIV LA PLATA ARGENTINA C1 NIH,DEPT POSITRON EMISS TOMOG,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 3 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44638-3 PY 1994 BP 27 EP 40 PG 14 WC Agronomy; Microbiology; Mycology; Parasitology; Toxicology SC Agriculture; Microbiology; Mycology; Parasitology; Toxicology GA BA79F UT WOS:A1994BA79F00002 ER PT J AU KAUNE, WT DARBY, SD GARDNER, SN HRUBEC, Z IRIYE, RN LINET, MS AF KAUNE, WT DARBY, SD GARDNER, SN HRUBEC, Z IRIYE, RN LINET, MS TI DEVELOPMENT OF A PROTOCOL FOR ASSESSING TIME-WEIGHTED-AVERAGE EXPOSURES OF YOUNG-CHILDREN TO POWER-FREQUENCY MAGNETIC-FIELDS SO BIOELECTROMAGNETICS LA English DT Article DE EXPOSURE ASSESSMENT; ENVIRONMENTAL MAGNETIC FIELDS; RESIDENTIAL MAGNETIC FIELDS; EPIDEMIOLOGIC PROTOCOL; WIRE CODES ID CHILDHOOD-CANCER; LEUKEMIA; HOME AB A study was carried out in 1990 to guide the development of a protocol for assessing residential exposures of children to time-weighted-average (TWA) power-frequency magnetic fields. The principal goal of this dosimetry study was to determine whether area (i.e., spot and/or 24 h) measurements of power-frequency magnetic fields in the residences and in the schools and daycare centers of 29 children (4 months through 8 years of age) could be used to predict their measured personal 24-h exposures. TWA personal exposures, measured with AMEX-3D meters worn by subjects, were approximately log-normally distributed with both residential and nonresidential geometric means of 0.10 mu T (1.0 mG). Between-subjects variability in residential personal exposure levels (geometric standard deviation of 2.4) was substantially greater than that observed for nonresidential personal exposure levels (1.4). The correlation between log-transformed residential and total personal exposure levels was 0.97. Time-weighted averages of the magnetic fields measured in children's bedrooms, family rooms, living rooms, and kitchens were highly correlated with residential personal exposure levels (r = 0.90). In general, magnetic field levels measured in schools and daycare centers attended by subjects were smaller and less variable than measured residential fields and were only weakly correlated with measured nonresidential personal exposures. The final measurement protocol, which will be used in a large US study examining the relationship between childhood leukemia and exposure to magnetic fields, contains the following elements: normal- and low-power spot magnetic field measurements in bedrooms occupied by subjects during the 5 years prior to the date of diagnosis for cases or the corresponding date for controls; spot measurements under normal and low power-usage conditions at the centers of the kitchen and the family room; 24-h magnetic-field recordings near subjects' beds; and wire coding using the Wertheimer-Leeper method. (C) 1994 Wiley-Liss, Inc.* C1 ENERTECH CONSULTANTS,CAMPBELL,CA. WESTAT CORP,ROCKVILLE,MD. NCI,ROCKVILLE,MD. NR 23 TC 39 Z9 40 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 0197-8462 J9 BIOELECTROMAGNETICS JI Bioelectromagnetics PY 1994 VL 15 IS 1 BP 33 EP 51 DI 10.1002/bem.2250150108 PG 19 WC Biology; Biophysics SC Life Sciences & Biomedicine - Other Topics; Biophysics GA MW134 UT WOS:A1994MW13400004 PM 8155068 ER PT J AU MONROE, PJ SMITH, DL WILLIAMS, GM SMITH, DJ AF MONROE, PJ SMITH, DL WILLIAMS, GM SMITH, DJ TI BUFOTENINE HAS A PARACHLOROAMPHETAMINE-LIKE ACTION ON THE STORAGE AND RELEASE OF SEROTONIN IN RAT SPINAL-CORD SYNAPTOSOMES SO BIOGENIC AMINES LA English DT Article DE SEROTONIN; BUFOTENINE; PARACHLOROAMPHETAMINE; UPTAKE CARRIER; STORAGE; RELEASE ID PARA-CHLOROAMPHETAMINE; CHROMAFFIN GRANULES; DOPAMINE; BRAIN; 5-HYDROXYTRYPTAMINE; PHENYLBIGUANIDE; DOPAMINE; FENFLURAMINE; ACCUMULATION; TRANSPORTERS AB During a recent evaluation of the abilities of 5HT(3) agents to modulate the release of [H-3]-5HT from superfused rat spinal cord synaptosomes, bufotenine was found to be capable of increasing basal neurotransmitter efflux via a mechanism which was sensitive to blockade of the neuronal membrane transport carrier (Williams et al., 1992). The present study was undertaken to further characterize the action of bufotenine on 5HT neuronal function. Bufotenine-evoked release of [H-3]-5HT was found to be unaltered by the removal of Ca++ from the superfusion media. In addition, using reserpine pre-treated tissues, it was determined that bufotenine releases 5HT primarily from extravesicular sites. A direct interaction of bufotenine with the neuronal membrane transport carrier is suggested by the ability of bufotenine to interact with sites labelled by [H-3]-citalopram (K-i=356 +/- 31 nM). A carrier mediated mechanism of release is further suggested by a comparable potency in the drug's ability to promote release (EC(50)= 892 +/- 60 nM). Bufotenine also weakly inhibited MAO activity. These results demonstrate that bufotenine has an action on 5HT neurons comparable to p-chloroamphetamine. C1 W VIRGINIA UNIV,MED CTR,DEPT PHARMACOL & TOXICOL,MORGANTOWN,WV 26506. NIH,NIDR,NAB,BETHESDA,MD 20892. RP MONROE, PJ (reprint author), W VIRGINIA UNIV,MED CTR,DEPT ANESTHESIOL,3618 HLTH SCI S,MORGANTOWN,WV 26506, USA. NR 30 TC 3 Z9 3 U1 0 U2 0 PU VSP BV PI ZEIST PA PO BOX 346, 3700 AH ZEIST, NETHERLANDS SN 0168-8561 J9 BIOGENIC AMINES JI Biog. Amines PY 1994 VL 10 IS 3 BP 273 EP 284 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF273 UT WOS:A1994NF27300008 ER PT B AU WEHR, TA AF WEHR, TA BE Jung, EG Holick, MF TI CONSERVATION OF A PRIMORDIAL SEASONAL PHOTOPERIODIC CLOCK IN HUMAN BEINGS SO BIOLOGIC EFFECTS OF LIGHT 1993 LA English DT Proceedings Paper CT 3rd Arnold Riki Symposium on the Biologic Effects of Light CY JUN 03-05, 1993 CL RIEHEN, SWITZERLAND C1 NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WALTER DE GRUYTER PI BERLIN 30 PA GENTHINER STRASSE 13, W-1000 BERLIN 30, GERMANY BN 3-11-014096-9 PY 1994 BP 186 EP 190 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA BC73F UT WOS:A1994BC73F00021 ER PT J AU BONI, RL SIMPSON, JT NARITSIN, DB SAITO, K MARKEY, SP AF BONI, RL SIMPSON, JT NARITSIN, DB SAITO, K MARKEY, SP TI QUANTIFICATION OF L-TRYPTOPHAN AND L-KYNURENINE BY LIQUID-CHROMATOGRAPHY ELECTRON-CAPTURE NEGATIVE-ION CHEMICAL-IONIZATION MASS-SPECTROMETRY SO BIOLOGICAL MASS SPECTROMETRY LA English DT Article ID QUINOLINIC ACID; SERUM AB In a number of infectious and inflammatory diseases, stimulation of the immune system can lead to increased accumulation of tryptophan metabolites via induction of kynurenine pathway enzymes in extrahepatic tissues. We developed a liquid chromatographic/mass spectrometric (LC/MS) method suitable for tracing the disposition of C-13 isotopomers of L-tryptophan and L-kynurenine in various cultured cell, tissue slice, and whole animal model systems used to investigate tryptophan flux through the kynurenine pathway. The method employs extractive derivatization of the analytes and their H-2 infernal standards with pentafluorobenzyl bromide in order to enhance the negative ion chemical ionization (NICI) mass spectrometric response. Normal-phase liquid chromatographic separation of derivatized analytes was optimized using a silica column with organic solvents, followed by particle beam transfer and NICI-MS. Standard curves were linear over the range 1-250 ng per sample, Particle beam and mass spectrometric operating parameters were optimized with direct flow injections of 1-(methylamino) anthraquinone, which is an ideal test compound for the evaluation of LC/NICI-MS. The developed method was used to quantify the conversion of (C-13(6))L-tryptophan to (C-13(6))L-kynurenine by human monocytes (THP-1) stimulated with interferon-gamma, lung and brain tissue slices obtained from gerbils immune-stimulated with pokeweed mitogen. The effect of whole body immune stimulation on the plasma levels of engogenous L-kynurenine in mice stimulated with interferon-gamma was also quantified. C1 NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BETHESDA,MD 20892. NR 15 TC 13 Z9 14 U1 0 U2 4 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 1052-9306 J9 BIOL MASS SPECTROM JI Biol. Mass Spectrom. PD JAN PY 1994 VL 23 IS 1 BP 27 EP 32 DI 10.1002/bms.1200230106 PG 6 WC Biophysics; Spectroscopy SC Biophysics; Spectroscopy GA MP051 UT WOS:A1994MP05100005 PM 8155745 ER PT J AU ELKASHEF, AM EGAN, MF FRANK, JA HYDE, TM LEWIS, BK WYATT, RJ AF ELKASHEF, AM EGAN, MF FRANK, JA HYDE, TM LEWIS, BK WYATT, RJ TI BASAL GANGLIA IRON IN TARDIVE-DYSKINESIA - AN MRI STUDY SO BIOLOGICAL PSYCHIATRY LA English DT Article DE BASAL GANGLIA; IRON; MRI; TARDIVE DYSKINESIA ID BRAIN IRON; CHRONIC-SCHIZOPHRENIA; VITAMIN-E; ABNORMALITIES; POSTMORTEM; SYSTEM AB Alterations in brain iron could play an important role in the development of tardive dyskinesia in patients receiving neuroleptic medication. To test this hypothesis, magnetic resonance imaging scans of the brain were performed on 21 chronic schizophrenic patients. Ten patients met research diagnostic criteria for persistent tardive dyskinesia, and II were free of tardive dyskinesia. All patients had received long-term neuroleptic treatment and were on a stable neuroleptic dose for at least 3 months before scanning. The signal intensity of basal ganglia structures was obtained as a quantitative estimate of brain iron content. No difference was found in the signal intensity ratios between the two groups. This suggests that iron deposition in the basal ganglia, at least as assessed by this measure, does not play a role in the pathophysiology of tardive dyskinesia. C1 NIMH,NEUROPSYCHIAT BRANCH,WASHINGTON,DC. NIH,DIAGNOST RADIOL RES PROGRAM,WASHINGTON,DC. NIMH,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC. NR 44 TC 9 Z9 11 U1 2 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD JAN 1 PY 1994 VL 35 IS 1 BP 16 EP 21 DI 10.1016/0006-3223(94)91161-4 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA MW336 UT WOS:A1994MW33600003 PM 8167198 ER PT S AU FITZGERALD, DJ FRYLING, CM ZDANOVSKY, A SAELINGER, CB KOUNNAS, M STRICKLAND, DK LEPPLA, S AF FITZGERALD, DJ FRYLING, CM ZDANOVSKY, A SAELINGER, CB KOUNNAS, M STRICKLAND, DK LEPPLA, S BE Borth, W Feinman, RD Gonias, SL Quigley, JP Strickland, DK TI SELECTION OF PSEUDOMONAS EXOTOXIN-RESISTANT CELLS WITH ALTERED EXPRESSION OF ALPHA(2)MR LRP SO BIOLOGY OF ALPHA2-MACROGLOBULIN, ITS RECEPTOR, AND RELATED PROTEINS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Biology of Alpha-Macroglobulin, Its Receptor, and Related Proteins CY OCT 11-14, 1993 CL WOODS HOLE, MA SP NEW YORK ACAD SCI ID RECEPTOR-RELATED PROTEIN; LIPOPROTEIN RECEPTOR; ALPHA-2-MACROGLOBULIN RECEPTOR; PLASMINOGEN-ACTIVATOR; MAMMALIAN-CELLS; CHIMERIC TOXINS; CYTOSOL; GLYCOPROTEIN; COMPLEXES; SEQUENCE C1 UNIV CINCINNATI,DEPT MOLEC GENET,CINCINNATI,OH 45267. AMER RED CROSS,ROCKVILLE,MD 20855. NIH,INST DENT,BETHESDA,MD 20892. RP FITZGERALD, DJ (reprint author), NCI,DIV CANC BIOL & DIAG,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 24 TC 6 Z9 6 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 0-89766-886-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 737 BP 138 EP 144 DI 10.1111/j.1749-6632.1994.tb44307.x PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics GA BB35Z UT WOS:A1994BB35Z00011 PM 7944142 ER PT S AU BONNER, JC AF BONNER, JC BE Borth, W Feinman, RD Gonias, SL Quigley, JP Strickland, DK TI REGULATION OF PLATELET-DERIVED GROWTH-FACTOR (PDGF) AND ALVEOLAR MACROPHAGE-DERIVED PDGF BY ALPHA(2)-MACROGLOBULIN SO BIOLOGY OF ALPHA2-MACROGLOBULIN, ITS RECEPTOR, AND RELATED PROTEINS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Biology of Alpha-Macroglobulin, Its Receptor, and Related Proteins CY OCT 11-14, 1993 CL WOODS HOLE, MA SP NEW YORK ACAD SCI ID RECEPTOR-RELATED PROTEIN; IDIOPATHIC PULMONARY FIBROSIS; TUMOR-NECROSIS-FACTOR; RAT LUNG FIBROBLASTS; FACTOR-BB ISOFORMS; ALPHA-2-MACROGLOBULIN RECEPTOR; INTERFERON-GAMMA; FAST FORMS; FACTOR-AA; FACTOR-AB RP BONNER, JC (reprint author), NIEHS,PULM PATHOBIOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 51 TC 9 Z9 9 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 0-89766-886-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 737 BP 324 EP 338 DI 10.1111/j.1749-6632.1994.tb44321.x PG 15 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics GA BB35Z UT WOS:A1994BB35Z00025 PM 7524405 ER PT J AU CHAFFIN, CL ROMAN, BL PETERSON, RE HUTZ, RJ AF CHAFFIN, CL ROMAN, BL PETERSON, RE HUTZ, RJ TI PRENATAL EXPOSURE TO LOW-DOSE TCDD AUGMENTS LEVELS OF UTERINE ESTROGEN-RECEPTOR MESSENGER-RNA IN PERI-PUBERTAL RATS SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 UNIV WISCONSIN,DEPT BIOL SCI,MILWAUKEE,WI 53201. UNIV WISCONSIN,NIEHS,BIOMED CORE CTR,MILWAUKEE,WI 53201. UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1994 VL 50 SU 1 BP 76 EP 76 PG 1 WC Reproductive Biology SC Reproductive Biology GA NR591 UT WOS:A1994NR59100090 ER PT J AU ZILBERSTEIN, M GU, Y SRIVASTAVA, RK MAYO, KE PARKSARGE, OK CHOU, JY GIBORI, G AF ZILBERSTEIN, M GU, Y SRIVASTAVA, RK MAYO, KE PARKSARGE, OK CHOU, JY GIBORI, G TI ESTABLISHMENT OF A TEMPERATURE-SENSITIVE RAT DECIDUAL CELL-LINE SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 UNIV ILLINOIS,DEPT PHYSIOL & BIOPHYS,CHICAGO,IL 60680. NORTHWESTERN UNIV,DEPT BIOCHEM MOLEC & CELL BIOL,EVANSTON,IL 60201. NICHHD,HGB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1994 VL 50 SU 1 BP 94 EP 94 PG 1 WC Reproductive Biology SC Reproductive Biology GA NR591 UT WOS:A1994NR59100164 ER PT J AU BLOMBERG, LA CHEN, HW DIRAMI, G CHOU, JY DYM, M CHAN, WY AF BLOMBERG, LA CHEN, HW DIRAMI, G CHOU, JY DYM, M CHAN, WY TI CLONING AND IDENTIFICATION OF SPECIFIC CELLULAR LOCATION OF PREGNANCY-SPECIFIC BETA-1-GLYCOPROTEIN (PSG) TRANSCRIPTS IN RAT TESTIS SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD. GEORGETOWN UNIV,MED CTR,DEPT PEDIAT,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT CELL BIOL,WASHINGTON,DC 20007. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1994 VL 50 SU 1 BP 120 EP 120 PG 1 WC Reproductive Biology SC Reproductive Biology GA NR591 UT WOS:A1994NR59100266 ER PT J AU SLAYDEN, OD IZUMI, S WILSON, I VIJAYARAGHAVAN, S RUBIN, JS FINCH, P BRENNER, RM AF SLAYDEN, OD IZUMI, S WILSON, I VIJAYARAGHAVAN, S RUBIN, JS FINCH, P BRENNER, RM TI KERATINOCYTE GROWTH-FACTOR (KGF) AND KGF RECEPTOR (KGFR) MESSENGER-RNAS IN THE CERVIX, PLACENTA, AND DECIDUA OF RHESUS MACAQUES SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. RHODE ISL HOSP,PROVIDENCE,RI 02902. OREGON REG PRIMATE RES CTR,DIV REPROD SCI,BEAVERTON,OR 97006. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1994 VL 50 SU 1 BP 121 EP 121 PG 1 WC Reproductive Biology SC Reproductive Biology GA NR591 UT WOS:A1994NR59100270 ER PT J AU THOMAS, D SCHULTZ, P STEVEN, AC WALL, JS AF THOMAS, D SCHULTZ, P STEVEN, AC WALL, JS TI MASS ANALYSIS OF BIOLOGICAL MACROMOLECULAR COMPLEXES BY STEM SO BIOLOGY OF THE CELL LA English DT Article DE STEM; MOLECULAR MASS; MACROMOLECULAR COMPLEXES; MASS ANALYSIS ID TRANSMISSION ELECTRON-MICROSCOPY; IMMUNODEFICIENCY-VIRUS TYPE-1; ENERGY-LOSS SPECTROSCOPY; COATED VESICLES; MOLECULAR COMPOSITION; INELASTIC-SCATTERING; OUTER MEMBRANES; TAIL-FIBER; PROTEIN; RESOLUTION AB Scanning transmission electron microscopy (STEM) provides a superbly versatile method of measuring the masses of macromolecular complexes ranging in size from single protein subunits to large virus particles. The physical basis of the method is the elastic scattering of electrons by the component atoms of the specimen. Unstained molecules yield a dark-field signal that is proportional to their local mass density, thus allowing direct measurements of the total mass of an individual particle, as well as of the masses of its resolved domains by integrating over appropriate regions of the image. In this review, we present an introduction to the STEM method of mass analysis from a practical standpoint, stressing the essential points of specimen preparation, as well as the scope and current limitations of the method. Its potentialities are illustrated by applications to several classes of macromolecules: isolated oligomeric proteins (the envelope glycoprotein of HIV), nucleoprotein complexes (SV40 minichromosome, transcription factor TFIIIC), membranous specimens (clathrin-coated membranes, the VDAC channel), and viruses (vesicular stomatitis virus; herpes simplex virus). In the case of multicomponent complexes, STEM mass measurements of both the intact complex and of defined biochemical derivatives (for instance, after extraction of specific components), allow one to compile complete and precise molecular inventories. Finally, we briefly anticipate future advances that should allow even more precise and detailed mass mappings, the labelling of specific sites with heavy atom clusters, and elemental mapping based on weak inelastic signals acquired in parallel with the relatively intense dark-field signals that have been so successfully exploited to date. C1 CNRS,GENET MOLEC EUCARYOTES LAB,F-67085 STRASBOURG,FRANCE. NIAMS,STRUCT BIOL RES LAB,BETHESDA,MD 20892. BROOKHAVEN NATL LAB,DEPT BIOL,UPTON,NY 11973. RP THOMAS, D (reprint author), UNIV RENNES 1,CNRS,URA 256,CAMPUS BEAULIEU,F-5000 RENNES,FRANCE. NR 54 TC 42 Z9 42 U1 1 U2 4 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0248-4900 J9 BIOL CELL JI Biol. Cell PY 1994 VL 80 IS 2-3 BP 181 EP 192 DI 10.1016/0248-4900(94)90041-8 PG 12 WC Cell Biology SC Cell Biology GA PA567 UT WOS:A1994PA56700020 PM 8087068 ER PT B AU BASSER, PJ AF BASSER, PJ BE Ueno, S TI MAGNETIC STIMULATION OF PERIPHERAL AXONS - MODELS AND EXPERIMENTS SO BIOMAGNETIC STIMULATION LA English DT Proceedings Paper CT International Symposium on Biomagnetic Stimulation CY JUL 15, 1991 CL FUKUOKA, JAPAN SP KYUSHU UNIV, WORLD CONGRESS MED PHYS & BIOMED ENGN, IEEE MAGNET SOC, TOKYO CHAPTER, IEEE ENGN MED & BIOL SOC, TOKYO CHAPTER, JAPAN SOC MED ELECTR & BIOL ENGN, JAPAN BIOMAGNETISM & BIOELECTROMAGNET SOC, JAPAN SOC APPL ELECTROMAGNET, INST ELECT ENGINEERS JAPAN, MAGNET COMM, LIFE SUPPORT TECHNOL SOC, JAPANESE CONF TOPOG EEG, INST ELECT ENGINEERS JAPAN, KYUSHU CHAPTER, INST ELECTR INFORMAT & COMMUN ENGINEERS, KYUSHU CHAPTER, SOC INSTRUMENT & CONTROL ENGINEERS, KYUSHU CHAPTER, INFORMAT PROC SOC JAPAN, KYUSHU CHAPTER, JAPAN SOC MED ELECTR & BIOL ENGN, KYUSHU CHAPTER C1 NIH,BETHESDA,MD 20892. 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 0-306-44707-X PY 1994 BP 119 EP 129 PG 11 WC Engineering, Biomedical SC Engineering GA BA37X UT WOS:A1994BA37X00009 ER PT J AU CUNHA, GR SUGIMURA, Y FOSTER, B RUBIN, JS AARONSON, SA AF CUNHA, GR SUGIMURA, Y FOSTER, B RUBIN, JS AARONSON, SA TI THE ROLE OF GROWTH-FACTORS IN THE DEVELOPMENT AND GROWTH OF THE PROSTATE AND SEMINAL-VESICLE SO BIOMEDICINE & PHARMACOTHERAPY LA English DT Article DE MESENCHYMAL-EPITHELIAL INTERACTIONS; KERATINOCYTE GROWTH FACTOR; UROGENITAL SINUS MESENCHYME; DEVELOPING PROSTATE; DUCTAL BRANCHING MORPHOGENESIS; SEMINAL VESICLE; GROWTH FACTORS ID UROGENITAL SINUS MESENCHYME; ANDROGEN RECEPTOR EXPRESSION; RODENT URINARY-BLADDER; COLON CANCER-CELLS; EPITHELIAL-CELLS; TISSUE RECOMBINANTS; MOUSE PROSTATE; ORGAN-CULTURE; FACTOR-BETA; TGF BETA-1 AB Mesenchymal-epithelial interactions play a critical role in the development of the male urogenital tract in that mesenchyme induces and specifies patterns of epithelial morphogenesis, regulates epithelial proliferation, promotes epithelial cytodifferentiation, and induces and specifies epithelial functional or biochemical activity. Prostatic epithelial growth and development is dependent upon androgens. Analysis of tissue recombinants prepared with normal (wild-type) urogenital sinus mesenchyme plus Tfm (testicular feminization) epithelium has demonstrated that androgen-induced prostatic epithelial growth and ductal branching morphogenesis are elicited via paracrine influences from the androgen-receptor-positive mesenchyme. Since KGF has recently emerged as a prototypic paracrine mediator of mesenchymal-epithelial interactions, androgen-dependent prostatic development was investigated to determine the possible role of KGF using a serum-free organ culture method. For this purpose newborn rat ventral prostates (VP) were incubated in vitro in a serum basal-free medium supplemented with testosterone (T: 10(-8)M), human recombinant KGF, or a neutralizing monoclonal antibody to KGF (anti-KGF), alone or in combination. When T (10(-8) M) was added to the basal media, VPs grew and underwent extensive branching morphogenesis similar to that in situ. The anti-KGF (60 mu g/ml) inhibited T-induced VP growth (DNA content) by 33% and reduced ductal endbuds by 62% after 6 days of culture. Neonatal rat VPs grown without T exhibited reduced growth and branching morphogenesis in comparison to those grown with T. When KGF (50 ng/ml) was added to the T-deficient media, VP growth was stimulated to a level approaching that elicited by T. Ductal endbuds were elevated from 23 (without T) to 60 (without T + KGF) per explant which represents 73% of that observed in cultures grown with T. Given the facts: a) that KGF is produced by mesenchymal/fibroblastic cells and acts on epithelia; b) that androgens stimulate development and growth of the prostate via androgen-receptor-mediated processes: and c) that androgen receptors (AR) are only detected in the mesenchyme of the rat VP at birth, our data suggests that androgens regulate epithelial growth and development of the VP by acting on the AR+ mesenchymal cells to elicit the synthesis and secretion of KGF which in turn stimulates epithelial growth and development. C1 MIE UNIV,SCH MED,DEPT UROL,TSU,MIE 514,JAPAN. NCI,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. RP CUNHA, GR (reprint author), UNIV CALIF SAN FRANCISCO,DEPT ANAT,SAN FRANCISCO,CA 94143, USA. NR 80 TC 3 Z9 3 U1 0 U2 1 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0753-3322 J9 BIOMED PHARMACOTHER JI Biomed. Pharmacother. PY 1994 VL 48 SU 1 BP S9 EP S17 PG 9 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA QT879 UT WOS:A1994QT87900003 ER PT S AU DEAMER, DW AKESON, M AF DEAMER, DW AKESON, M BE Blank, M Vodyanoy, I TI ROLE OF WATER IN PROTON CONDUCTANCE ACROSS MODEL AND BIOLOGICAL-MEMBRANES SO BIOMEMBRANE ELECTROCHEMISTRY SE ADVANCES IN CHEMISTRY SERIES LA English DT Article; Proceedings Paper CT Contractors Meeting on Biomembrane Electrochemistry CY APR, 1991 CL AIRLIE, VA ID LARGE UNILAMELLAR LIPOSOMES; HYDROXYL PERMEABILITY; PHOSPHOLIPID-VESICLES; ESCHERICHIA-COLI; GRAMICIDIN-A; ATP SYNTHASE; BILAYER-MEMBRANES; LIPID-MEMBRANES; ION CHANNELS; MECHANISMS AB Proton conductance across model and biological membranes can be understood in terms of proton translocation along chains of hydrogen-bonded water molecules. This translocation mechanism accounts for the unexpectedly high permeability of lipid bilayers to proton flux, which seems to occur through rare transient defects in the bilayer barrier. The nature of the proton-conducting channel of the F1F0 adenosine 5'-triphosphate (ATP) synthase is unknown, but may use a similar translocation mechanism. We have tested the gramicidin channel as a model of such proton conductance. The channel consists of a single chain of hydrogen-bonded water molecules, and its proton conductance at saturation is near 140 pA, or 10(9) H+/s. Assuming that an adequate supply of protons is made available to the putative channel, this rate easily supports proton transport requirements of the F1F0 ATP synthase during ATP synthesis. However at neutral pH ranges diffusion of free protons probably could not maintain an adequate supply at the channel mouth. Other sources of protons must therefore be postulated. C1 NIH,MOLEC BIOL LAB,BETHESDA,MD 20892. RP DEAMER, DW (reprint author), LAWRENCE LIVERMORE NATL LAB,DEPT ZOOL,DAVIS,CA 95616, USA. NR 49 TC 1 Z9 1 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0065-2393 BN 0-8412-2524-9 J9 ADV CHEM SER PY 1994 VL 235 BP 41 EP 54 PG 14 WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary SC Biochemistry & Molecular Biology; Chemistry GA BA42T UT WOS:A1994BA42T00004 ER PT S AU PARSEGIAN, VA RAND, RP COLOMBO, M RAU, DC AF PARSEGIAN, VA RAND, RP COLOMBO, M RAU, DC BE Blank, M Vodyanoy, I TI WATER AT THE MACROMOLECULAR SURFACE - SOLVATION ENERGY AND FUNCTIONAL CONTROL SO BIOMEMBRANE ELECTROCHEMISTRY SE ADVANCES IN CHEMISTRY SERIES LA English DT Article; Proceedings Paper CT Contractors Meeting on Biomembrane Electrochemistry CY APR, 1991 CL AIRLIE, VA ID DNA DOUBLE HELICES; HYDRATION FORCES; PHOSPHOLIPID-BILAYERS; LECITHIN BILAYERS; PHASE-TRANSITION; OSMOTIC-STRESS; VOLUME CHANGES; MEMBRANES; DEFORMATION; REPULSION AB The contribution of hydration to the energetics of molecular conformation and assembly has been recognized for a long time, but has been, difficult to measure. We use osmotic stress to measure the forces and energies in molecular assemblies. The same strategy can be used to measure the contribution of water to the chemical free energy change of individually functioning molecules. We describe, as examples, the contribution of water to the gating of membrane channels to the binding of oxygen to hemoglobin; and to the forces between bilayer membranes, within nonbilayer lipid assemblies, and on macromolecular surfaces. From the magnitude of their energies we conclude that hydration-dehydration reactions play an important but neglected role in molecular function. C1 BROCK UNIV,ST CATHARINES L2S 3A1,ON,CANADA. NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. RP PARSEGIAN, VA (reprint author), NIH,DIV COMP RES & TECHNOL,STRUCT BIOL LAB,BETHESDA,MD 20892, USA. NR 44 TC 7 Z9 7 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0065-2393 BN 0-8412-2524-9 J9 ADV CHEM SER PY 1994 VL 235 BP 177 EP 196 PG 20 WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary SC Biochemistry & Molecular Biology; Chemistry GA BA42T UT WOS:A1994BA42T00010 ER PT J AU LANGE, R HEIBERLANGER, I BONFILS, C FABRE, I NEGISHI, M BALNY, C AF LANGE, R HEIBERLANGER, I BONFILS, C FABRE, I NEGISHI, M BALNY, C TI ACTIVATION VOLUME AND ENERGETIC PROPERTIES OF THE BINDING OF CO TO HEMOPROTEINS SO BIOPHYSICAL JOURNAL LA English DT Article ID SPIN-STATE EQUILIBRIUM; HIGH-PRESSURE; CARBON-MONOXIDE; CHOLESTEROL; DYNAMICS; CYTOCHROME-P-450; TEMPERATURE; CATALYSIS; PROTEINS; CHLOROPEROXIDASE AB We have investigated the CO binding to various reduced hemoproteins by stopped-flow rapid mixing as a function of pressure (from 0.1 to 200 MPa) and temperature (from 4 to 35 degrees C). In particular, we studied several varieties of cytochrome P-450: CYP11A1 (scc), CYP2B4 (LM2), CYP3A6 (LM3c), and Cyp2a (7 alpha), as well as chloroperoxidase and lactoperoxidase, and compared the results to data reported for other hemoproteins. Whereas the CO binding activation enthalpy Delta H double dagger and entropy Delta S double dagger (correlated through a compensation effect) varied greatly between the hemoproteins, with no apparent relation to structural features, the pressure effect depended on the nature of the proximal axial heme ligand: the activation volume was very small for cysteine (S-) ligand hemoproteins (Delta V double dagger = +1 to +6 mt mol(-1)), and markedly negative for histidine (N) ligand hemoproteins (Delta V double dagger = -3 to -36 ml mol(-1)). Furthermore, the transition state volume of the histidine ligand class enzymes, but not that of the cysteine ligand enzymes, depended on the solvent composition. These results suggest that the CO-binding transition state of the S-ligand class has a molecular conformation similar to the ground state. In the histidine class, however, the transition state appears to involve protein conformational changes and/or solvation processes. C1 NIEHS, REPROD & DEV TOXICOL LAB, RES TRIANGLE PK, NC 27709 USA. RP LANGE, R (reprint author), CNRS, INSERM, U128, BP 5051, F-34033 MONTPELLIER, FRANCE. NR 57 TC 32 Z9 32 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1994 VL 66 IS 1 BP 89 EP 98 PG 10 WC Biophysics SC Biophysics GA MP041 UT WOS:A1994MP04100011 PM 8130349 ER PT J AU SATIN, LS TAVALIN, SJ SMOLEN, PD AF SATIN, LS TAVALIN, SJ SMOLEN, PD TI INACTIVATION OF HIT CELL CA2+ CURRENT BY A SIMULATED BURST OF CA2+ ACTION-POTENTIALS SO BIOPHYSICAL JOURNAL LA English DT Article ID PANCREATIC BETA-CELLS; INSULIN-SECRETING CELLS; VOLTAGE-ACTIVATED CALCIUM; B-CELLS; ELECTRICAL-ACTIVITY; POTASSIUM CURRENTS; CHANNELS; MOUSE; CLAMP; GLUCOSE AB A novel voltage-clamp protocol was developed to test whether slow inactivation of Ca2+ current occurs during bursting in insulin-secreting cells. Single insulin-secreting HIT cells were patch-clamped and their Ca2+ currents were isolated pharmacologically. A computed p-cell burst was used as a voltage-clamp command and the net Ca2+ current elicited was determined as a cadmium difference current. Ca2+ current rapidly activated during the computed plateau and spike depolarizations and then slowly decayed. Integration of this Ca2+ current yielded an estimate of total Ca influx. To further analyze Ca2+ current inactivation during a burst, repetitive test pulses to +10 mV were added to the voltage command. Current elicited by these pulses was constant during the interburst, but then slowly and reversibly decreased during the depolarizing plateau. This inactivation was reduced by replacing external Ca2+ with Ba2+ as a charge carrier, and in some cells inactivation was slower in Ba2+. Experimental results were compared with the predictions of the Keizer-Smolen mathematical model of bursting, after subjecting model equations to identical voltage commands. In this model, bursting is driven by the slow, voltage-dependent inactivation of Ca current during the plateau active phase. The K-S model could account for the slope of the slow decay of spike-elicited Ca current, the waveform of individual Ca current spikes, and the suppression of test pulse-elicited Ca current during a burst command. However, the extent and rate of fast inactivation were underestimated by the model. Although there are significant differences between the data obtained and the predictions of the K-S model, the overall results show that as predicted by the model, Ca current slowly inactivates during a burst of imposed spikes, and inactivation is dependent on both Ca2+ influx and membrane depolarization. We thus show that clamping cells to their physiological voltage waveform can be readily accomplished and is a powerful approach for understanding the contribution of individual ion currents to bursting. C1 NIDDKD,BIOMATH RES BRANCH,BETHESDA,MD 20892. RP SATIN, LS (reprint author), VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOL,BOX 524,RICHMOND,VA 23298, USA. NR 27 TC 20 Z9 20 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1994 VL 66 IS 1 BP 141 EP 148 PG 8 WC Biophysics SC Biophysics GA MP041 UT WOS:A1994MP04100017 PM 8130333 ER PT J AU BASSER, PJ MATTIELLO, J LEBIHAN, D AF BASSER, PJ MATTIELLO, J LEBIHAN, D TI MR DIFFUSION TENSOR SPECTROSCOPY AND IMAGING SO BIOPHYSICAL JOURNAL LA English DT Article ID WHITE MATTER; NMR; ORIENTATION; GRADIENT; INVIVO; SYSTEM; WATER; FIELD AB This paper describes a new NMR imaging modality-MR diffusion tensor imaging. It consists of estimating an effective diffusion tensor, D-eff, within a voxel, and then displaying useful quantities derived from it. We show how the phenomenon of anisotropic diffusion of water (or metabolites) in anisotropic tissues, measured noninvasively by these NMR methods, is exploited to determine fiber tract orientation and mean particle displacements. Once D-eff is estimated from a series of NMR pulsed-gradient, spin-echo experiments, a tissue's three orthotropic axes can be determined. They coincide with the eigenvectors of D-eff while the effective diffusivities along these orthotropic directions are the eigenvalues of D-eff. Diffusion ellipsoids, constructed in each voxel from D-eff depict both these orthotropic axes and the mean diffusion distances in these directions. Moreover, the three scalar invariants of D-eff, which are independent of the tissue's orientation in the laboratory frame of reference, reveal useful information about molecular mobility reflective of local microstructure and anatomy. Inherently, tensors (like D-eff) describing transport processes in anisotropic media contain new information within a macroscopic voxel that scalars (such as the apparent diffusivity, proton density, T-1, and T-2) do not. C1 NIH, WARREN GRANT MAGNUSON CLIN CTR, DEPT DIAGNOST RADIOL, BETHESDA, MD 20892 USA. RP BASSER, PJ (reprint author), NIH, NATL CTR RES RESOURCES, BIOMED ENGN & INSTRUMENTAT PROGRAM, BETHESDA, MD 20892 USA. RI Basser, Peter/H-5477-2011 NR 29 TC 2668 Z9 2772 U1 22 U2 160 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1994 VL 66 IS 1 BP 259 EP 267 PG 9 WC Biophysics SC Biophysics GA MP041 UT WOS:A1994MP04100030 PM 8130344 ER PT J AU LUNN, G KLAUSMEYER, PJ SANSONE, EB AF LUNN, G KLAUSMEYER, PJ SANSONE, EB TI REMOVAL OF BIOLOGICAL STAINS FROM AQUEOUS-SOLUTION USING A FLOW-THROUGH DECONTAMINATION PROCEDURE SO BIOTECHNIC & HISTOCHEMISTRY LA English DT Article DE DECONTAMINATION; DISPOSAL; SAFETY; MUTAGENICITY; FLOW-THROUGH COLUMN; AMBERLITE XAD-16 ID MUTAGENICITY; WASTE; WATER AB Chromatography columns filled with Amberlite XAD-16 were used to decontaminate, using a continuous flow-through procedure, aqueous solutions of the following biological stains: acridine orange, alcian blue 8GX, alizarin red S, azure A, azure B, brilliant blue G, brilliant blue R, Congo red, cresyl violet acetate, crystal violet, eosin B, eosin Y, erythrosin B, ethidium bromide, Giemsa stain, Janus green B, methylene blue, neutral red, nigrosin, orcein, propidium iodide, rose Bengal, safranine O, toluidine blue O, and trypan blue. Adsorption was most efficient for stains of lower molecular weight (< 600). Adsorption of stain increased as the flow rate decreased; column diameter had little effect on adsorption. Adsorption of stain was greatest when finely ground resin was used, but if the resin particles were too small, column clogging occurred. Limited grinding of the resin gave increased adsorption while retaining good flow characteristics. Amberlite XAD-16 saturated with methylene blue was regenerated to its initial adsorption capacity by passing methanol through the column. The technique described provides an economical, rapid means of removing stains from aqueous solution. RP LUNN, G (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,ENVIRONM CONTROL & RES PROGRAM,FREDERICK,MD 21702, USA. NR 13 TC 4 Z9 4 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1052-0295 J9 BIOTECH HISTOCHEM JI Biotech. Histochem. PD JAN PY 1994 VL 69 IS 1 BP 45 EP 54 DI 10.3109/10520299409106260 PG 10 WC Biotechnology & Applied Microbiology; Cell Biology SC Biotechnology & Applied Microbiology; Cell Biology GA MU123 UT WOS:A1994MU12300007 PM 8148434 ER PT J AU LUEDERS, KK FEWELL, JW AF LUEDERS, KK FEWELL, JW TI HYBRIDIZATION OF DNA IN DRIED GELS PROVIDES INCREASED SENSITIVITY COMPARED WITH HYBRIDIZATION TO BLOTS SO BIOTECHNIQUES LA English DT Note ID AGAROSE GELS RP LUEDERS, KK (reprint author), NCI,BIOCHEM LAB,BLDG 37,RM 4C-03,BETHESDA,MD 20892, USA. NR 8 TC 16 Z9 16 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD JAN PY 1994 VL 16 IS 1 BP 66 EP 67 PG 2 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MQ935 UT WOS:A1994MQ93500016 PM 8136143 ER PT J AU COSTELLO, R WHEELER, D ORBAN, L CHRAMBACH, A AF COSTELLO, R WHEELER, D ORBAN, L CHRAMBACH, A TI ENHANCED ETHIDIUM FLUORESCENCE OF LARGE DNA ELECTROPHORESED IN GELS SUBMERSED IN AN IMMISCIBLE SOLVENT SO BIOTECHNIQUES LA English DT Note AB Agarose gel electrophoretic separation of a lambda/HindIII DNA marker containing detectable fragments of 23 to 2 kb was carried out in the conventional sumarine apparatus and in the horizontal gel slab apparatus of Wieme, using identical samples, agarose, gel width and procedure for ethidium bromide staining. In the Wieme apparatus, the gel on its microscope slide support is immersed in an immiscible solvent such as petroleum ether or silicone oil. Although band resolution and speed of migration are equivalent between gels run in the two systems, the relative fluorescence intensity of the ethidium bromide- stained bands is substantially more responsive to an increase in DNA length in the Wieme gels than in the submarine gels. The predicted relative fluorescence is by an average factor of 0.5 less than that observed after electrophoresis in the Wieme apparatus but is by an average factor of 3.4 more tlzan that observed on bands derived from the submarine technique. C1 NIH,BETHESDA,MD 20892. INST MOLEC GENET,GODOLLO,HUNGARY. OI Orban, Laszlo/0000-0001-5435-5948 NR 15 TC 0 Z9 0 U1 1 U2 1 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD JAN PY 1994 VL 16 IS 1 BP 108 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MQ935 UT WOS:A1994MQ93500025 PM 8136123 ER PT J AU DEFILIPPES, FM AF DEFILIPPES, FM TI A BIOLOGICAL METHOD FOR EXAMINING THE EFFECT OF CODON CHANGES IN A CONSERVED REGION OF DNA-POLYMERASE SO BIOTECHNIQUES LA English DT Article ID CELL-FREE TRANSLATION; HERPES-SIMPLEX VIRUS; VACCINIA VIRUS; MARKER RESCUE; BASE CHANGE; APHIDICOLIN; GENE; RESISTANCE; RNA AB The vaccinia virus genome encodes a DNA polymerase that is similar to other DNA polymerases. A mutation in the polymerase gene at a site that is adjacent to conserved residues allows vital replication in the presence of aphidicolin. Since wild-type virus is converted to aphidicolin-resistance by site-directed mutagenesis, it was feasible that active virus with substituted conserved residues could be detected by linking alterations to the aphidicolin-resistance mutation. Altered DNA, from a PCR, was introduced into virus by a marker transfer procedure. DNA from plaques of drug-resistant virus was amplified, and the product was sequenced to check for the conserved residue alteration. An alteration that introduced a Bg1I site was designed to facilitate the selection of drug-resistant virus containing substituted residues. One positive result was the replacement of two amino acids, tyrosine and alanine, by tryptophan and threonine. The failure to substitute aspartic acid for tyrosine indicates that drastic changes of the conserved sequence are not tolerated. Although the limitations associated with negative results apply the method provides an in vivo assay for selecting a polymerase with conserved residue changes. RP DEFILIPPES, FM (reprint author), NIAID,VIRAL DIS LAB,BETHESDA,MD 20892, USA. NR 14 TC 0 Z9 0 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD JAN PY 1994 VL 16 IS 1 BP 122 EP 127 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA MQ935 UT WOS:A1994MQ93500027 PM 8136125 ER PT B AU LEVY, H SALAZAR, A MORALES, J MORGAN, OS AF LEVY, H SALAZAR, A MORALES, J MORGAN, OS BE Gebelein, CG Carraher, CE TI THE USE OF POLYICLC IN THE TREATMENT OF AIDS SO BIOTECHNOLOGY AND BIOACTIVE POLYMERS LA English DT Proceedings Paper CT International Symposium on Biotechnology and Bioactive Polymers, at the Spring 1992 American-Chemical-Society Meeting CY APR 05-10, 1992 CL SAN FRANCISCO, CA SP AMER CHEM SOC C1 NIAID,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 0-306-44629-4 PY 1994 BP 269 EP 276 PG 8 WC Biotechnology & Applied Microbiology; Polymer Science SC Biotechnology & Applied Microbiology; Polymer Science GA BZ96B UT WOS:A1994BZ96B00026 ER PT J AU ORLIC, D ANDERSON, S BODINE, DM AF ORLIC, D ANDERSON, S BODINE, DM TI BIOLOGICAL PROPERTIES OF SUBPOPULATIONS OF PLURIPOTENT HEMATOPOIETIC STEM-CELLS ENRICHED BY ELUTRIATION AND FLOW-CYTOMETRY SO BLOOD CELLS LA English DT Article; Proceedings Paper CT Symposium on Frontiers in Stem Cell Biology CY MAY 14-16, 1993 CL SANTA FE, NM DE STEM CELLS; C-KIT RECEPTOR; GENE EXPRESSION; FLOW CYTOMETRY ID COLONY-FORMING CELLS; C-KIT; RHODAMINE-123 FLUORESCENCE; MARROW; MOUSE; SPLEEN; SEPARATION; MICE; PURIFICATION; POPULATIONS AB We have studied several features of pluripotent hematopoietic stem cells (PMSCs) and day-12 spleen colony-forming units (CFU-S) obtained from adult murine bone marrow. Single-cell suspensions of C57BL/6J mouse bone marrow were fractionated by counterflow centrifugal elutriation at flow rates (FR) of 15, 25, 30, and 35 ml/min, and with the rotor off (R/O), The fractions FR25 and FR35 contained approximately equal numbers of PHSC that could repopulate W/W-v mice. These PHSCs were further enriched by subtracting lineage-positive cells using monoclonal antibodies (MAb) and magnetic immunobeads. The resulting lineage-negative cells (Lin(-)) were then stained with a MAb for the c-kit receptor and sorted by flow cytometry. Both subsets were fractionated into cells expressing high (bright) (c-kit(BR)), low (dull) c-kit(DULL) and (negative, c-kit(NEG)) c-kit receptor. As few as 100 to 200 c-kit(BR) cells could repopulate the entire thymus and bone marrow in W/W-v mice. No PHSCs were present in the c-kit(DULL) and c-kit(NEG) fractions. We assayed fresh bone marrow and elutriation fractions FR25 and FR35 for gene expression by reverse transcriptase polymerase chain reaction. Using a semiquantitative protocol, we detected mRNA for beta-globin and flk-2, a protein tyrosine kinase receptor, in all samples except the FR25 Lin(-) c-kit(BR) subset. We consider the cells in FR25 Lin(-) c-kit(BR) to be the most primitive set of hematopoietic stem cells. C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 28 TC 19 Z9 19 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 1 BP 107 EP 120 PG 14 WC Hematology SC Hematology GA NX139 UT WOS:A1994NX13900009 PM 7527675 ER PT J AU NIENHUIS, AW AF NIENHUIS, AW TI GENE-TRANSFER INTO HEMATOPOIETIC STEM-CELLS SO BLOOD CELLS LA English DT Article; Proceedings Paper CT Symposium on Frontiers in Stem Cell Biology CY MAY 14-16, 1993 CL SANTA FE, NM DE HEMATOPOIETIC STEM CELLS; GENE TRANSFER; RECOMBINANT ADENOASSOCIATED VIRUS (RAAV); RETROVIRUS ID HUMAN ADENOSINE-DEAMINASE; BONE-MARROW CELLS; LONG-TERM EXPRESSION; HUMAN GAMMA-GLOBIN; ADENOASSOCIATED VIRUS; RETROVIRAL VECTORS; MICE; TRANSPLANTATION; TRANSDUCTION; MOUSE AB The ability to insert a gene into hematopoietic stem cells and achieve lineage specific expression of the transferred gene within hematopoeitic organs following bone marrow transplantation would create the potential to effectively treat many genetic and acquired diseases. The use of retroviral vectors to achieve this purpose has been investigated extensively in animal models and most recently, in humans. In the murine model, about 20-30% of repopulating stem cells can be genetically modified with a retroviral vector. Peripheral blood stem cells, mobilized by cytokine administration in splenectomized animals, are readily transduced and are capable of long-term reconstitution of transplant recipients with genetically modified cells. Similar protocols have been utilized to transduce highly purified stem cells from rhesus monkeys. Although long-term repopulation with cells that persistently express the transferred gene has been achieved, the frequency of cells containing the vector genome is only about 1-2%. Genetic marking of human bone marrow and peripheral blood cells has been utilized to investigate their potential for contributing to long-term reconstitution following autologous transplantation. Future work will focus on improving gene transfer efficiencies for specific therapeutic applications. C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 32 TC 20 Z9 20 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 1 BP 141 EP 148 PG 8 WC Hematology SC Hematology GA NX139 UT WOS:A1994NX13900012 PM 7994057 ER PT J AU NOGUCHI, CT AF NOGUCHI, CT TI IN-VIVO POLYMERIZATION OF SICKLE-CELL HEMOGLOBIN - A THEORETICAL-STUDY - COMMENTS SO BLOOD CELLS LA English DT Note ID S POLYMERIZATION; DISEASE PATHOPHYSIOLOGY; RHEOLOGIC PROPERTIES; CLINICAL SEVERITY; BLOOD RHEOLOGY; RED-CELLS; ANEMIA; ERYTHROCYTES; TEMPERATURE; DEFORMABILITY RP NOGUCHI, CT (reprint author), NIDDK, BIOL CHEM LAB, BETHESDA, MD 20892 USA. NR 38 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0340-4684 J9 BLOOD CELLS JI Blood Cells PY 1994 VL 20 IS 1 BP 184 EP 190 PG 7 WC Hematology SC Hematology GA NX139 UT WOS:A1994NX13900016 ER PT J AU THORP, BH JAKOWLEW, SB AF THORP, BH JAKOWLEW, SB TI ALTERED LOCALIZATION OF TRANSFORMING GROWTH FACTOR-BETA-3 DURING ENDOCHONDRAL OSSIFICATION IN RACHITIC CHICKS SO BONE LA English DT Article DE CHONDROCYTE DIFFERENTIATION; CARTILAGE; TGF-BETA; BONE; CHICKEN ID FACTOR-BETA; BONE-CELLS; CHONDROCYTES; RICKETS; PURIFICATION; REGULATOR; CARTILAGE; COLLAGEN; EMBRYO; PLATE AB Growth plates from chicks displaying hypocalcaemic rickets, hypophosphataemic rickets and dyschondroplasia were studied. Immunohistochemical staining using specific TGF-beta 3 antibodies showed disruption of TGF-beta 3 localisation in all three disorders. In hypocalcaemic rickets, transitional and hypertrophic chondrocytes showed expression of TGF-beta 3, while accumulating, proliferative chondrocytes showed little expression. In the accumulating hypertrophic chondrocytes of hypophosphataemic rickets there was a reduction in the number of chondrocytes expressing TGF-beta 3, but transitional cells stained intensely. In the accumulating transitional chondrocytes of dyschondroplastic physes there was a reduction in the number of chondrocytes containing TGF-beta 3 and, in addition, the concentration of TGF-beta 3 appeared reduced. In all three disorders, there was localisation of some TGF-beta 3 in chondrocytes that appeared to be differentiating within the areas of repair. In addition, little TGF-beta 3 was detected in osteoclasts resorbing accumulated matrix from hypocalcaemic, hypophosphataemic and dyschondroplastic growth plates. These in vivo studies show a reduction in TGF-beta 3 localisation within growth plate chondrocytes and osteoclasts in three disorders in which chondrocytes cease to differentiate. This suggests that TGF-beta 3 may be important during chondrocyte differentiation in the growth plate. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP THORP, BH (reprint author), AFRC,ROSLIN INST EDINBURGH,ROSLIN EH25 9PS,MIDLOTHIAN,SCOTLAND. NR 30 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 8756-3282 J9 BONE JI Bone PD JAN-FEB PY 1994 VL 15 IS 1 BP 59 EP 64 DI 10.1016/8756-3282(94)90892-3 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MX279 UT WOS:A1994MX27900010 PM 8024853 ER PT J AU BARRETT, J AF BARRETT, J TI THE MOLECULAR-BASIS OF GRAFT-VERSUS-LEUKEMIA IN CML SO BONE MARROW TRANSPLANTATION LA English DT Article; Proceedings Paper CT 2nd International Symposium on Autografting for Chronic Myeloid Leukaemia CY JUN 26-27, 1994 CL GENOVA, ITALY ID BONE-MARROW TRANSPLANTATION; MINOR HISTOCOMPATIBILITY ANTIGENS; CHRONIC MYELOID-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; CYTOTOXIC LYMPHOCYTES-T; IMMUNE-RESPONSES; JOINING REGION; CELL IMMUNITY; BCR-ABL; DONOR RP BARRETT, J (reprint author), NIH,NHLBI,HEMATOL BRANCH,BMT UNIT,BETHESDA,MD 20892, USA. NR 45 TC 1 Z9 1 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PY 1994 VL 14 SU 3 BP S68 EP S73 PG 6 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA QA018 UT WOS:A1994QA01800017 PM 7697013 ER PT J AU AZARI, NP HORWITZ, B PETTIGREW, KD GRADY, CL HAXBY, JV GIACOMETTI, KR SCHAPIRO, MB AF AZARI, NP HORWITZ, B PETTIGREW, KD GRADY, CL HAXBY, JV GIACOMETTI, KR SCHAPIRO, MB TI ABNORMAL PATTERN OF CEREBRAL GLUCOSE METABOLIC RATES INVOLVING LANGUAGE AREAS IN YOUNG-ADULTS WITH DOWN-SYNDROME SO BRAIN AND LANGUAGE LA English DT Article ID DOWNS-SYNDROME CHILDREN; BRAIN-REGIONS; ALZHEIMERS-DISEASE; INTERREGIONAL CORRELATIONS; TRANSMISSION MEASUREMENTS; INTERCORRELATIONS; OLD; PET; SPECIALIZATION; INDIVIDUALS C1 NIMH,DIV APPL & SERV RES,BETHESDA,MD 20892. RP AZARI, NP (reprint author), NIA,NEUROSCI LAB,BLDG 10,ROOM 6C414,BETHESDA,MD 20892, USA. NR 67 TC 28 Z9 28 U1 1 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD JAN PY 1994 VL 46 IS 1 BP 1 EP 20 DI 10.1006/brln.1994.1001 PG 20 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA MR776 UT WOS:A1994MR77600001 PM 8131038 ER PT S AU WISE, S HOUK, JC AF WISE, S HOUK, JC BE Cotterill, RMJ TI MODULAR NEURONAL ARCHITECTURE FOR PLANNING AND CONTROLLING MOTOR BEHAVIOR SO BRAIN AND MIND: SYMPOSIUM ON THE OCCASION OF THE 250TH ANNIVERSARY OF THE ROYAL DANISH ACADEMY OF SCIENCES AND LETTERS SE BIOLOGISKE SKRIFTER LA English DT Proceedings Paper CT Symposium on the Brain and Mind, on the Occasion of the 250th Anniversary of the Royal-Danish-Academy-of-Sciences-and-Letters CY AUG 17-20, 1992 CL COPENHAGEN, DENMARK C1 NIMH,NEUROPHYSIOL LAB,POOLESVILLE,MD 20837. NR 0 TC 12 Z9 12 U1 0 U2 2 PU ROYAL DANISH ACADEMY SCIENCES & LETTERS PI COPENHAGEN V PA H C ANDERSENS BLVD 35, DK-1553 COPENHAGEN V, DENMARK SN 0366-3612 BN 87-7304-255-2 J9 BIOL SKRIF PY 1994 VL 43 BP 21 EP 33 PG 13 WC Neurosciences SC Neurosciences & Neurology GA BC12V UT WOS:A1994BC12V00001 ER PT S AU DERIJK, R STERNBERG, EM AF DERIJK, R STERNBERG, EM BE deKloet, ER Azmitia, EC Landfield, PW TI CORTICOSTEROID ACTION AND NEUROENDOCRINE-IMMUNE INTERACTIONS SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci ID PITUITARY-ADRENAL AXIS; CORTICOTROPIN-RELEASING HORMONE; SUSCEPTIBLE LEWIS RATS; RHEUMATOID-ARTHRITIS; GLUCOCORTICOID RESISTANCE; INFLAMMATORY DISEASE; STRESS-RESPONSE; ACTIVATION; SECRETION; BINDING C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,NEUROENDOCRINE IMMUNOL & BEHAV UNIT,BETHESDA,MD 20892. NR 46 TC 28 Z9 28 U1 1 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 33 EP 41 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00004 PM 7825887 ER PT S AU STRATAKIS, CA KARL, M SCHULTE, HM CHROUSOS, GP AF STRATAKIS, CA KARL, M SCHULTE, HM CHROUSOS, GP BE deKloet, ER Azmitia, EC Landfield, PW TI GLUCOCORTICOSTEROID RESISTANCE IN HUMANS - ELUCIDATION OF THE MOLECULAR MECHANISMS AND IMPLICATIONS FOR PATHOPHYSIOLOGY SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci ID PRIMARY CORTISOL RESISTANCE; HORMONE-BINDING DOMAIN; RECEPTOR COMPLEX; POINT MUTATION; GENE; LOCALIZATION; FIBROBLASTS; SIGNALS; PROTEIN; FAMILY C1 UNIV HAMBURG,INST HORMONE & FERTIL RES,D-22529 HAMBURG,GERMANY. RP STRATAKIS, CA (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10 N 262,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 49 TC 25 Z9 25 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 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 362 EP 376 PG 15 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00028 PM 7825890 ER PT S AU BEAULIEU, S ROUSSE, I GRATTON, A BARDEN, N ROCHFORD, J AF BEAULIEU, S ROUSSE, I GRATTON, A BARDEN, N ROCHFORD, J BE deKloet, ER Azmitia, EC Landfield, PW TI BEHAVIORAL AND ENDOCRINE IMPACT OF IMPAIRED TYPE-II GLUCOCORTICOID RECEPTOR FUNCTION IN A TRANSGENIC MOUSE MODEL SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci ID DEPRESSION C1 MCGILL UNIV,DEPT PSYCHIAT,MONTREAL,PQ H4H 1R3,CANADA. UNIV LAVAL,DEPT PHYSIOL,QUEBEC CITY,PQ G1V 4G2,CANADA. RP BEAULIEU, S (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 4 TC 22 Z9 22 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 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 388 EP 391 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00032 PM 7825894 ER PT S AU CORODIMAS, KP LEDOUX, JE GOLD, PW SCHULKIN, J AF CORODIMAS, KP LEDOUX, JE GOLD, PW SCHULKIN, J BE deKloet, ER Azmitia, EC Landfield, PW TI CORTICOSTERONE POTENTIATION OF CONDITIONED FEAR IN RATS SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RP CORODIMAS, KP (reprint author), NYU,CTR NEURAL SCI,6 WASHINGTON PL,NEW YORK,NY 10003, USA. FU NIMH NIH HHS [MH46516, MH38774] NR 5 TC 81 Z9 82 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 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 392 EP 393 PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00033 PM 7825895 ER PT S AU KLING, MA PLUZNIK, D GLOWA, JR GOLD, PW SMITH, MA AF KLING, MA PLUZNIK, D GLOWA, JR GOLD, PW SMITH, MA BE deKloet, ER Azmitia, EC Landfield, PW TI GLUCOCORTICOID RECEPTOR (GR)-MEDIATED EFFECTS ON COCAINE KINDLING IN RATS SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. NIDDK,MED CHEM LAB,BETHESDA,MD 20892. RP KLING, MA (reprint author), NIMH,CLIN NEUROENDOCRINOL BRANCH,BLDG 10,ROOM 3S-231,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Kling, Mitchel/F-4152-2010 OI Kling, Mitchel/0000-0002-2232-1409 NR 6 TC 1 Z9 1 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 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 400 EP 402 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00036 PM 7825898 ER PT S AU THOMAS, DN POST, RM PERT, A AF THOMAS, DN POST, RM PERT, A BE deKloet, ER Azmitia, EC Landfield, PW TI CENTRAL AND SYSTEMIC CORTICOSTERONE DIFFERENTIALLY AFFECT DOPAMINE AND NOREPINEPHRINE IN THE FRONTAL-CORTEX THE AWAKE FREELY MOVING RAT SO BRAIN CORTICOSTEROID RECEPTORS: STUDIES ON THE MECHANISM, FUNCTION, AND NEUROTOXICITY OF CORTICOSTEROID ACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action CY MAR 02-05, 1994 CL ARLINGTON, VA SP New York Acad Sci ID BRAIN RP THOMAS, DN (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N 212,BETHESDA,MD 20892, USA. NR 5 TC 13 Z9 14 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 0-89766-908-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 746 BP 467 EP 469 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD11Z UT WOS:A1994BD11Z00056 PM 7825916 ER PT J AU MARTIN, WJ DECOSTA, BR WALKER, JM AF MARTIN, WJ DECOSTA, BR WALKER, JM TI EFFECTS OF SIGMA-LIGANDS ON RAT CEREBELLAR PURKINJE NEURON FIRING - AN IONTOPHORETIC STUDY SO BRAIN RESEARCH BULLETIN LA English DT Article DE SIGMA RECEPTORS; BRAIN; RAT; OPIATE; CEREBELLUM; PURKINJE NEURONS; DTG; IONTOPHORESIS ID GUINEA-PIG BRAIN; BINDING-SITES; OPIATE RECEPTORS; H-3 (+)-PENTAZOCINE; ANTIPSYCHOTIC-DRUGS; 3-PPP ENANTIOMERS; RUBRAL NEURONS; PHENCYCLIDINE; AFFINITY; HALOPERIDOL AB The electrophysiological responses of rat cerebellar Purkinje neurons to selective a ligands applied iontophoretically was examined in urethane anesthetized male Sprague-Dawley rats. 1,3-Di-o-tolylguanidine (DTG), dextrallorphan (DEX), (+)-pentazocine((+)-PENT), (+)-3-(3-Hydroxyphenyl)-N-propylpiperidine ((+)-3-PPP), and the novel diamine BD1008, were ejected from multibarrel pipettes onto individual Purkinje cells. In some neurons, cell firing was inhibited following ejections of all compounds. These inhibitory effects were dose dependent and occurred without changes in spike amplitude or duration, thus ruling out local anesthetic effects as a mechanism. (+)-3-PPP and DEX increased firing rate in 27% and 14% (n = 15, n = 14, respectively) of cells studied. The results of this study indicate that a ligands significantly alter the spontaneous firing of Purkinje neurons, consistent with previous work suggesting motor effects of a ligands via the rubro-cerebellar circuitry. C1 BROWN UNIV,DEPT PSYCHOL,SCHRIER RES LAB,PROVIDENCE,RI 02912. NIDDK,MED CHEM LAB,BETHESDA,MD 20892. OI Martin, William/0000-0002-2749-3365 FU NIDA NIH HHS [DA04988]; NIMH NIH HHS [K02MH01083, MH48869] NR 40 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 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1994 VL 35 IS 4 BP 303 EP 309 DI 10.1016/0361-9230(94)90106-6 PG 7 WC Neurosciences SC Neurosciences & Neurology GA PM278 UT WOS:A1994PM27800005 PM 7850479 ER PT J AU WOLF, SS HYDE, TM MOODY, TW SAUNDERS, RC WEINBERGER, DR KLEINMAN, JE AF WOLF, SS HYDE, TM MOODY, TW SAUNDERS, RC WEINBERGER, DR KLEINMAN, JE TI AUTORADIOGRAPHIC CHARACTERIZATION OF I-125 NEUROTENSIN BINDING-SITES IN HUMAN ENTORHINAL CORTEX SO BRAIN RESEARCH BULLETIN LA English DT Article DE NEUROTENSIN; RECEPTOR AUTORADIOGRAPHY; ENTORHINAL CORTEX; HUMAN BRAIN ID HUMAN-BRAIN; RAT-BRAIN; HIPPOCAMPAL-FORMATION; NEUROTENSIN RECEPTORS; ALZHEIMERS-DISEASE; RHESUS-MONKEY; SCHIZOPHRENIA; LOCALIZATION; REGION; ACETYLCHOLINESTERASE AB The laminar and rostro-caudal distribution of I-125-neurotensin binding sites is described in human entorhinal cortex using quantitative autoradiography. Specific binding was most prominent over the cell clusters of layer II of the entorhinal cortex throughout its rostro-caudal extent. Dense binding was also observed in the adjacent presubiculum and cortical amygdaloid transition area, whereas minimal binding was detected in the hippocampus and dentate gyrus. I-125-Neurotensin may serve as a selective probe for neurotensin receptor alterations and layer II-specific cytoarchitectural disturbances in the entorhinal cortex in neuropsychiatric diseases associated with abnormalities of the mesial temporal lobe. C1 GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT BIOCHEM,WASHINGTON,DC 20037. RP WOLF, SS (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,DIV INTRAMURAL RES PROGRAMS,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. NR 36 TC 5 Z9 5 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1994 VL 35 IS 4 BP 353 EP 358 DI 10.1016/0361-9230(94)90113-9 PG 6 WC Neurosciences SC Neurosciences & Neurology GA PM278 UT WOS:A1994PM27800012 PM 7850486 ER PT J AU BRADY, LS AF BRADY, LS TI STRESS, ANTIDEPRESSANT DRUGS, AND THE LOCUS-COERULEUS SO BRAIN RESEARCH BULLETIN LA English DT Article DE ANTIDEPRESSANTS; CORTICOTROPIN-RELEASING HORMONE; FLUOXETINE; HYPOTHALAMUS; HIPPOCAMPUS; IDAZOXAN; IMIPRAMINE; IMMOBILIZATION; LOCUS COERULEUS; NOREPINEPHRINE; PARAVENTRICULAR NUCLEUS; PHENELZINE; STRESS; TYROSINE HYDROXYLASE ID CORTICOTROPIN-RELEASING-FACTOR; TYROSINE-HYDROXYLASE ACTIVITY; FACTOR-LIKE IMMUNOREACTIVITY; BRAIN NORADRENERGIC NEURONS; CENTRAL NERVOUS-SYSTEM; INDIVIDUAL HYPOTHALAMIC NUCLEI; CHRONIC DESIPRAMINE TREATMENT; SPONTANEOUS FIRING RATE; PITUITARY-ADRENAL AXIS; MONO-AMINERGIC NEURONS AB This review presents a synthesis of a large body of seemingly inconsistent literature on the role of the locus coeruleus-norepinephrine (LC-NE) system and the corticotropin-releasing hormone (CRH)-median eminence system in mediating the CNS effects of stress and the therapeutic effects of antidepressant drugs. The clinical implications of these findings for the etiology and treatment of strsss-related psychiatric disorders such as depression will be discussed. RP BRADY, LS (reprint author), NIMH, FUNCT NEUROANAT SECT, BLDG 36, RM 2D15, BETHESDA, MD 20892 USA. NR 132 TC 68 Z9 68 U1 3 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0361-9230 EI 1873-2747 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1994 VL 35 IS 5-6 BP 545 EP 556 DI 10.1016/0361-9230(94)90168-6 PG 12 WC Neurosciences SC Neurosciences & Neurology GA PP297 UT WOS:A1994PP29700020 PM 7859112 ER PT J AU JACOBOWITZ, DM SULLIVAN, JV FITZE, PE AF JACOBOWITZ, DM SULLIVAN, JV FITZE, PE TI HUMAN BRAIN SLICER - A METHOD FOR CUTTING CORONAL SLICES OF FRESH AND FIXED HUMAN BRAINS SO BRAIN RESEARCH BULLETIN LA English DT Note DE HUMAN; BRAIN; SLICER; BRAIN SLICER ID RAT; STABILITY; REMOVAL; RNA AB A brain holder has been specially designed to make parallel thin slices of the fresh or preserved brain. Thin stainless steel plates with sharpened edges are used to cut coronal brain slices. These slices can be dissected and either frozen or preserved in a fixative. C1 NCRR,BETHESDA,MD 20892. RP JACOBOWITZ, DM (reprint author), NIMH,CLIN SCI LAB,BLDG 10,ROOM 3D-48,BETHESDA,MD 20892, USA. NR 5 TC 3 Z9 3 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1994 VL 33 IS 4 BP 461 EP 463 DI 10.1016/0361-9230(94)90290-9 PG 3 WC Neurosciences SC Neurosciences & Neurology GA MQ472 UT WOS:A1994MQ47200014 PM 8124584 ER PT J AU ARAI, R JACOBOWITZ, DM DEURA, S AF ARAI, R JACOBOWITZ, DM DEURA, S TI DISTRIBUTION OF CALRETININ, CALBINDIN-D28K, AND PARVALBUMIN IN THE RAT THALAMUS SO BRAIN RESEARCH BULLETIN LA English DT Article DE CALCIUM-BINDING PROTEIN; CALRETININ; CALBINDIN-D28K; PARVALBUMIN; THALAMUS; RAT ID CALCIUM-BINDING PROTEIN; IMMUNOHISTOCHEMICAL LOCALIZATION; DORSAL HORN; SPINAL-CORD; D28K-IMMUNOREACTIVE NEURONS; NONPYRAMIDAL NEURONS; NERVOUS-SYSTEM; IMMUNOREACTIVITY; BRAIN; HIPPOCAMPUS AB The localization of three calcium-binding proteins, calretinin, calbindin-D28k, and parvalbumin, in the rat thalamus was immunohistochemically examined. a) Some thalamic regions revealed cells almost exclusively containing one of the calcium-binding proteins. For example, almost only calretinin-stained cells were found in the central medial and paraventricular nuclei. Calbindin-D28k-stained cells were mostly found in the centrolateral, interanteromedial, anteromedial, and posterior nuclei. Only parvalbumin-positive cells were found in the central part of the reticular nucleus. b) Other regions expressed overlap between the distributions of two cell components composed of different calcium-binding proteins. For example, both calretinin-stained cells and calbindin-D28k-labeled cells were found in the lateroposterior, intermediodorsal, rhomboid, and reuniens nuclei. c) Other regions showed no cells stained for any of the calcium-binding proteins. For example, generally no calcium-binding protein was detected in neurons of the anterodorsal, anteroventral, ventrolateral, ventral posterolateral, ventral posteromedial, or gelatinosus nuclei, or of the central part of the mediodorsal nucleus. These three proteins serve as useful marker for localizing subpopulations of neurons within the thalamus. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP ARAI, R (reprint author), FUJITA HLTH UNIV,SCH MED,DEPT ANAT,TOYOAKE,AICHI 47011,JAPAN. NR 56 TC 87 Z9 88 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1994 VL 33 IS 5 BP 595 EP 614 DI 10.1016/0361-9230(94)90086-8 PG 20 WC Neurosciences SC Neurosciences & Neurology GA MY644 UT WOS:A1994MY64400017 PM 8187003 ER PT J AU NORMANNO, N CIARDIELLO, F BRANDT, R SALOMON, DS AF NORMANNO, N CIARDIELLO, F BRANDT, R SALOMON, DS TI EPIDERMAL GROWTH FACTOR-RELATED PEPTIDES IN THE PATHOGENESIS OF HUMAN BREAST-CANCER SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE AMPHIREGULIN, AUTOCRINE GROWTH REGULATION; C-ERBB-2 LIGANDS; CRIPTO; EPIDERMAL GROWTH FACTOR; EGF RECEPTOR LIGANDS; HEREGULIN; HER-2/NEU LIGANDS; JUXTACRINE GROWTH FACTORS; TRANSFORMING GROWTH FACTOR ID MAMMARY EPITHELIAL-CELLS; MESSENGER RIBONUCLEIC-ACID; FACTOR-ALPHA EXPRESSION; HA-RAS PROTOONCOGENE; FACTOR RECEPTOR; TGF-ALPHA; NEU ONCOGENE; CARCINOMA-CELLS; EGF-RECEPTOR; TRANSGENIC MICE AB A number of different epidermal growth factor (EGF)-related peptides such as EGF, transforming growth factor ct (TGF alpha), amphiregulin (AR), heregulin (HRG), and cripto-1 (CR-1), are coexpressed to varying degrees in both normal and malignant mammary epithelial cells. However, in general the frequency and level of expression of TGF alpha, AR, and CR-1 are higher in malignant breast epithelial cells than in normal mammary epithelium. In addition, several of these peptides such as TGF alpha and AR can function as autocrine and/or juxtacrine growth factors in mammary epithelial cells, and their expression is stringently regulated by mammotrophic hormones such as estrogens, activated proto-oncogenes that have been implicated in the pathogenesis of breast cancer, and other growth factors. The redundancy of expression that is observed for a number of these structurally related peptides in both normal and malignant mammary epithelial cells suggests that some of these peptides may be involved in regulating other aspects of cellular behavior such as differentiation in addition to proliferation. C1 NCI,TUMOR IMMUNOL & BIOL LAB,TUMOR GROWTH FACTOR SECT,BETHESDA,MD 20892. FDN PASCALE,IST NAZL STUDIO & CURA TUMORI,I-80131 NAPLES,ITALY. UNIV NAPOLI FEDERICO II,FAC MED & CHIRURG,CATTEDRA ONCOL MED,I-80131 NAPLES,ITALY. OI Ciardiello, Fortunato/0000-0002-3369-4841; Normanno, Nicola/0000-0002-7158-2605 NR 98 TC 93 Z9 95 U1 2 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 1994 VL 29 IS 1 BP 11 EP 27 DI 10.1007/BF00666178 PG 17 WC Oncology SC Oncology GA NB592 UT WOS:A1994NB59200003 PM 7912564 ER PT J AU MUIR, GH BUTTA, A SHEARER, RJ FISHER, C DEARNALEY, DP FLANDERS, KC SPORN, MB COLLETTA, AA AF MUIR, GH BUTTA, A SHEARER, RJ FISHER, C DEARNALEY, DP FLANDERS, KC SPORN, MB COLLETTA, AA TI INDUCTION OF TRANSFORMING GROWTH-FACTOR-BETA IN HORMONALLY TREATED HUMAN PROSTATE-CANCER SO BRITISH JOURNAL OF CANCER LA English DT Article ID RAT VENTRAL PROSTATE; CELLS; FACTOR-BETA-1; PROLIFERATION; CARCINOMA; INVIVO; DEATH; LNCAP AB Transforming growth factor beta-1 (TGF-beta 1) has been proposed as a mediator of tumour growth in a number of tumours and cell lines including prostate, and in a recent study was shown to be up-regulated in the stroma of breast cancer tissue following treatment with the anti-oestrogen tamoxifen. Immunolocalisation of the intracellular form of TGF-beta 1 confirmed that the source of the stromal TGF-beta 1 was the peritumoral fibroblasts. We present here the results of a study in which five patients with hormonally unresponsive prostatic carcinoma and seven patients responding to a luteinising hormone-releasing hormone analogue had prostate biopsies taken before and during treatment. These were stained for TGF-beta expression prior to treatment and at either relapse or 3 months later respectively. Six of seven clinically responding tumours and three of five relapsed tumours showed up-regulation of extracellular TGF-beta 1, again primarily in the stroma, with no apparent up-regulation of intracellular TGF-beta 1, TGF-beta 2 or TGF-beta 3. These data illustrate that the epithelial growth inhibitor TGF-beta 1 can be induced by hormonal manipulation in prostate cancer in vivo, and may continue to be up-regulated even after relapse. This suggests that relapse of hormonally treated prostate cancer may be associated with a failure of the epithelium to respond to stromal TGF-beta 1. C1 INST CANC RES,HARTWELL LAB,ACAD SURG SECT,LONDON SW3 6JJ,ENGLAND. ROYAL MARSDEN HOSP,LONDON SW3 6JJ,ENGLAND. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP MUIR, GH (reprint author), INST CANC RES,UROL UNIT,FULHAM RD,LONDON SW3 6JJ,ENGLAND. NR 25 TC 37 Z9 37 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD JAN PY 1994 VL 69 IS 1 BP 130 EP 134 DI 10.1038/bjc.1994.21 PG 5 WC Oncology SC Oncology GA MQ287 UT WOS:A1994MQ28700021 PM 8286194 ER PT J AU KUPFER, C AF KUPFER, C TI SETTING THE STAGE FOR ONCHOCERCIASIS SO BRITISH JOURNAL OF OPHTHALMOLOGY LA English DT Editorial Material RP KUPFER, C (reprint author), NEI,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-1161 J9 BRIT J OPHTHALMOL JI Br. J. Ophthalmol. PD JAN PY 1994 VL 78 IS 1 BP 3 EP 3 DI 10.1136/bjo.78.1.3 PG 1 WC Ophthalmology SC Ophthalmology GA MT343 UT WOS:A1994MT34300002 PM 8110694 ER PT J AU ROVATI, GE SHRAGER, R NICOSIA, S MUNSON, PJ AF ROVATI, GE SHRAGER, R NICOSIA, S MUNSON, PJ TI KINFIT-II - A NONLINEAR LEAST-SQUARES PROGRAM FOR ANALYSIS OF KINETIC BINDING DATA SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Meeting Abstract C1 UNIV MILAN,INST PHARMACOL SCI,I-20113 MILAN,ITALY. NIH,APPL STUDIES LAB,BETHESDA,MD 20892. NIH,DIV COMP RES & TECHNOL,ANALYT & BIOSTAT SECT,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD JAN PY 1994 VL 111 SU S BP P322 EP P322 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MR863 UT WOS:A1994MR86300226 ER PT J AU MADHAVI, B ANAND, CS BHARATHI, A POLASA, H AF MADHAVI, B ANAND, CS BHARATHI, A POLASA, H TI BIOTOXIC EFFECTS OF PESTICIDES ON SYMBIOTIC PROPERTIES OF RHIZOBIAL SPS SO BULLETIN OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY LA English DT Article ID PLASMIDS; GENES C1 OSMANIA UNIV,DEPT MICROBIOL,HYDERABAD 500007,ANDHRA PRADESH,INDIA. NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 16 TC 7 Z9 7 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0007-4861 J9 B ENVIRON CONTAM TOX JI Bull. Environ. Contam. Toxicol. PD JAN PY 1994 VL 52 IS 1 BP 87 EP 94 PG 8 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA MG023 UT WOS:A1994MG02300014 PM 8130422 ER PT J AU HUMPHREYS, BL MCCUTCHEON, DE AF HUMPHREYS, BL MCCUTCHEON, DE TI GROWTH-PATTERNS IN THE NATIONAL LIBRARY OF MEDICINES SERIALS COLLECTION AND IN INDEX MEDICUS(R) JOURNALS, 1966-1985 SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article AB Data from the National Library of Medicine (NLM) automated Master Serials System and its MEDLINE(R);database were used to chart the growth of NLM's serials collection and of the journals indexed in Index Medicus(R) from 1966 to 1985. The number of live serial titles in the subset of NLM's collection examined increased 30% in the twenty years. The average number of articles per Index Medicus journal increased 56%. The average number of articles in U.S. Index Medicus journals grew more rapidly than the average number in journals published elsewhere. The NLM data provide clear evidence that the years from 1966 to 1985 saw a substantial increase in the percentage of the biomedical serial literature published in English. The period from 1966 to 1985 saw substantial but uneven growth in the number of serial titles in the NLM collection and in the average number of articles in Index Medicus journals. Although data on the number of articles published in Index Medicus journals is unlikely to reflect the number of articles in other journals, the pattern of growth in the number of serials held by NLM probably reflects trends in the universe of all biomedical serials. RP HUMPHREYS, BL (reprint author), NATL LIB MED,SERIAL RECORDS SECT,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 8 TC 13 Z9 13 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD JAN PY 1994 VL 82 IS 1 BP 18 EP 24 PG 7 WC Information Science & Library Science SC Information Science & Library Science GA MR634 UT WOS:A1994MR63400003 PM 8136756 ER PT J AU FIKREE, FF BERENDES, HW AF FIKREE, FF BERENDES, HW TI RISK-FACTORS FOR TERM INTRAUTERINE GROWTH-RETARDATION - A COMMUNITY-BASED STUDY IN KARACHI SO BULLETIN OF THE WORLD HEALTH ORGANIZATION LA English DT Article ID LOW-BIRTH-WEIGHT; FETAL GROWTH; PARENTAL CONSANGUINITY; DETERMINANTS; PREMATURITY; MORTALITY; PRETERM AB Reported are the results of a community-based prospective study in four urban squatter settlements in Karachi that was carried out to assess the incidence of and risk factors for intrauterine growth retardation. The incidence of term intrauterine growth retardation was 24.4% among 738 singleton births. The socioeconomic and biological risk factors that were found to be statistically significant in a bivariate analysis were included in a logistic regression model to assess their independent effects. The major risk factors were low level of maternal education, paternal unemployment, consanguinity, short birth-to-conception intervals, short maternal stature, and low maternal weight. The population risk estimates suggest the desirability of public health interventions to improve maternal weight and birth spacing and of improvements in socioeconomic conditions, especially maternal education. Public education programmes to discourage consanguineous marriages should also be considered. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. RP FIKREE, FF (reprint author), AGA KHAN UNIV,DEPT COMMUNITY HLTH SCI,STADIUM RD,POB 3500,KARACHI 74800,PAKISTAN. NR 18 TC 23 Z9 23 U1 0 U2 0 PU WORLD HEALTH ORGANIZATION PI GENEVA 27 PA DISTRIBUTION AND SALES, CH-1211 GENEVA 27, SWITZERLAND SN 0042-9686 J9 B WORLD HEALTH ORGAN JI Bull. World Health Organ. PY 1994 VL 72 IS 4 BP 581 EP 587 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA PG585 UT WOS:A1994PG58500004 PM 7923537 ER PT S AU KHACHATURIAN, ZS AF KHACHATURIAN, ZS BE Disterhoft, JF Gispen, WH Traber, J Khachaturian, ZS TI CALCIUM HYPOTHESIS OF ALZHEIMERS-DISEASE AND BRAIN AGING SO CALCIUM HYPOTHESIS OF AGING AND DEMENTIA SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Calcium Hypothesis of Aging and Dementia CY DEC 15-17, 1993 CL NIH, BETHESDA, MD SP Alzheimers Assoc, Farbenfabriken Bayer GMBH, Fischer Fdn, French Fdn, NIA, NIH HO NIH ID PATHOGENESIS; MECHANISMS; MEMBRANES; ETIOLOGY; ALUMINUM; DEATH; GENE RP NIA, NEUROSCI & NEUROPSYCHOL AGING PROGRAM, BETHESDA, MD 20892 USA. NR 21 TC 216 Z9 224 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-879-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 747 BP 1 EP 11 PG 11 WC Cell Biology; Geriatrics & Gerontology; Multidisciplinary Sciences; Clinical Neurology; Neurosciences SC Cell Biology; Geriatrics & Gerontology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD12A UT WOS:A1994BD12A00001 PM 7847664 ER PT S AU ARISPE, N POLLARD, HB ROJAS, E AF ARISPE, N POLLARD, HB ROJAS, E BE Disterhoft, JF Gispen, WH Traber, J Khachaturian, ZS TI THE ABILITY OF AMYLOID BETA-PROTEIN [A-BETA-P(1-40)] TO FORM CA2+ CHANNELS PROVIDES A MECHANISM FOR NEURONAL DEATH IN ALZHEIMERS-DISEASE SO CALCIUM HYPOTHESIS OF AGING AND DEMENTIA SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Calcium Hypothesis of Aging and Dementia CY DEC 15-17, 1993 CL NIH, BETHESDA, MD SP Alzheimers Assoc, Farbenfabriken Bayer GMBH, Fischer Fdn, French Fdn, NIA, NIH HO NIH ID PRECURSOR PROTEIN; RAT-BRAIN; BILAYER-MEMBRANES; NEUROTOXICITY; PEPTIDES; AGGREGATION; HOMEOSTASIS; FRAGMENT; INVITRO; PATHOLOGY RP ARISPE, N (reprint author), NIDDK,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. NR 45 TC 65 Z9 67 U1 1 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-879-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 747 BP 256 EP 266 PG 11 WC Cell Biology; Geriatrics & Gerontology; Multidisciplinary Sciences; Clinical Neurology; Neurosciences SC Cell Biology; Geriatrics & Gerontology; Science & Technology - Other Topics; Neurosciences & Neurology GA BD12A UT WOS:A1994BD12A00017 PM 7847675 ER PT B AU JOHNSTON, MI FAST, PE WALKER, MC HOTH, D AF JOHNSTON, MI FAST, PE WALKER, MC HOTH, D BE Rusthoven, J Feld, R TI THE POTENTIAL OF VACCINES FOR THE CONTROL OF AIDS SO CANADIAN JOURNAL OF INFECTIOUS DISEASES, VOL 5 SUPPLEMENT A, FEBRUARY 1994: PROCEEDINGS OF THE SECOND INTERNATIONAL CONGRESS ON BIOLOGICAL RESPONSE MODIFIERS LA English DT Proceedings Paper CT 2nd International Congress on Biological Response Modifiers CY JAN 29-31, 1993 CL SAN DIEGO, CA SP INTER AMER SOC CHEMOTHERAPY DE AIDS; CLINICAL TRIALS; HUMAN IMMUNODEFICIENCY VIRUS; VACCINES C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PULSUS GROUP INC PI OAKVILLE PA 2902 S SHERIDAN WAY, OAKVILLE ON L6J 7L6, CANADA PY 1994 BP A36 EP A41 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA BC39U UT WOS:A1994BC39U00006 ER PT B AU PINCUS, SH MCCLURE, J FANG, H AF PINCUS, SH MCCLURE, J FANG, H BE Rusthoven, J Feld, R TI USE OF ANTI-HIV IMMUNOTOXINS AS PROBES OF THE BIOLOGY OF HIV-INFECTED CELLS SO CANADIAN JOURNAL OF INFECTIOUS DISEASES, VOL 5 SUPPLEMENT A, FEBRUARY 1994: PROCEEDINGS OF THE SECOND INTERNATIONAL CONGRESS ON BIOLOGICAL RESPONSE MODIFIERS LA English DT Proceedings Paper CT 2nd International Congress on Biological Response Modifiers CY JAN 29-31, 1993 CL SAN DIEGO, CA SP INTER AMER SOC CHEMOTHERAPY DE AIDS THERAPY; GP41; GP120; HUMAN IMMUNODEFICIENCY VIRUS; IMMUNOTOXIN; RICIN C1 NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PULSUS GROUP INC PI OAKVILLE PA 2902 S SHERIDAN WAY, OAKVILLE ON L6J 7L6, CANADA PY 1994 BP A23 EP A27 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA BC39U UT WOS:A1994BC39U00004 ER PT B AU SCHNITTMAN, SM AF SCHNITTMAN, SM BE Rusthoven, J Feld, R TI TREATMENT OF HIV-1 INFECTION WITH COMBINATION THERAPY - ANTIRETROVIRAL AGENTS AND BIOLOGICAL RESPONSE MODIFIERS SO CANADIAN JOURNAL OF INFECTIOUS DISEASES, VOL 5 SUPPLEMENT A, FEBRUARY 1994: PROCEEDINGS OF THE SECOND INTERNATIONAL CONGRESS ON BIOLOGICAL RESPONSE MODIFIERS LA English DT Proceedings Paper CT 2nd International Congress on Biological Response Modifiers CY JAN 29-31, 1993 CL SAN DIEGO, CA SP INTER AMER SOC CHEMOTHERAPY DE AIDS; COMBINATION THERAPY; HUMAN IMMUNODEFICIENCY VIRUS TYPE-1; INTERFERON-ALPHA; INTERLEUKIN-2 C1 NIAID,DIV AIDS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PULSUS GROUP INC PI OAKVILLE PA 2902 S SHERIDAN WAY, OAKVILLE ON L6J 7L6, CANADA PY 1994 BP A42 EP A46 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA BC39U UT WOS:A1994BC39U00007 ER PT J AU VONDERHEID, EC DIAMOND, LW VANVLOTEN, WA SCHEFFER, E MEIJER, CJLM CASHELL, AW HARDMAN, JM LAI, SM HERMANS, J MATTHEWS, MJ AF VONDERHEID, EC DIAMOND, LW VANVLOTEN, WA SCHEFFER, E MEIJER, CJLM CASHELL, AW HARDMAN, JM LAI, SM HERMANS, J MATTHEWS, MJ TI LYMPH-NODE CLASSIFICATION SYSTEMS IN CUTANEOUS T-CELL - LYMPHOMA EVIDENCE FOR THE UTILITY OF THE WORKING FORMULATION OF NON-HODGKINS-LYMPHOMAS FOR CLINICAL USAGE SO CANCER LA English DT Article DE NON-HODGKINS LYMPHOMA; PERIPHERAL T-CELL LYMPHOMA; CUTANEOUS T-CELL LYMPHOMA; MYCOSIS FUNGOIDES; SEZARY SYNDROME; DERMATOPATHIC LYMPHADENOPATHY; PROGNOSIS; CLASSIFICATION ID MYCOSIS-FUNGOIDES; SEZARY SYNDROME; DERMATOPATHIC LYMPHADENOPATHY; HISTOPATHOLOGY; TRANSFORMATION; DIAGNOSIS AB Background. This study was undertaken to compare three classification schemes used to evaluate lymph nodes (LN) obtained from patients with cutaneous T-cell lymphoma (CTCL): a modified Rappaport classification, the National Cancer Institute-Veterans Administration (NCI-VA) classification based on the relative numbers of cerebriform cells in the paracortical areas, and the Dutch classification based on the presence of cerebriform cells with large nuclei in mycosis fungoides (MF) and diffuse infiltration by cerebriform cells in Sezary syndrome. Methods. A study set of 195 LN obtained from patients with CTCL (MF, Sezary syndrome, and nonepidermotropic T-cell lymphomas) and 14 LN from patients with benign dermatoses was reviewed independently by three groups of pathologists familiar with each classification system. Results. Each classification system provided useful prognostic information. However, contrary to prior reports, no significant difference in survival was apparent in patients with uneffaced LN when classified according to the NCI-VA (LN0-2 versus LN3) or Dutch (Gr0-1 versus Gr2) ratings. In addition, all classification systems demonstrated a poor survival time associated with effaced LN. By combining results from the modified Rappaport and Dutch classifications, three prognostic groups could be identified based on cell morphology: a low-grade category with a small cell histologic subtype (median survival time, 40 months); a high-grade immunoblastic subtype (median survival time, 9 months) composed of cells with an oval nucleus containing a large, usually solitary central nucleolus; and an intermediate-grade category composed of all cases without the distinctive small cell and immunoblastic morphologies (median survival time, 26 months). Conclusions. The authors propose that clearly involved LN in CTCL can be categorized on the basis of cell morphology into prognostic groups analogous to what has been proposed for the Working Formulation for Non-Hodgkin's Lymphomas for Clinical Usage. C1 HOP HENRI MONDOR,CRETEIL,FRANCE. UNIV UTRECHT,DEPT DERMATOL,UTRECHT,NETHERLANDS. FREE UNIV AMSTERDAM,DEPT PATHOL,AMSTERDAM,NETHERLANDS. BOWMAN GRAY SCH MED,DEPT PATHOL,WINSTON SALEM,NC. ARMED FORCES INST PATHOL,WASHINGTON,DC. MED COLL PENN,DEPT NEUROL,PHILADELPHIA,PA. LEIDEN UNIV,DEPT MED STAT,2300 RA LEIDEN,NETHERLANDS. NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD. RP VONDERHEID, EC (reprint author), HAHNEMANN UNIV,DIV DERMATOL,MAILSTOP 478,BROAD & VINE ST,PHILADELPHIA,PA 19102, USA. NR 28 TC 27 Z9 28 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1994 VL 73 IS 1 BP 207 EP 218 DI 10.1002/1097-0142(19940101)73:1<207::AID-CNCR2820730136>3.0.CO;2-C PG 12 WC Oncology SC Oncology GA MP984 UT WOS:A1994MP98400035 PM 8275427 ER PT J AU JANZ, S SHACTER, E HERRMANN, A AF JANZ, S SHACTER, E HERRMANN, A TI FUSION BETWEEN ENVELOPED VIRUSES AND ERYTHROCYTE-MEMBRANES IS INDUCED BY THE ISOPREINOID ALKANE PRISTANE (2,6,10,14-TETRAMETHYLPENTADECANE) SO CANCER BIOCHEMISTRY BIOPHYSICS LA English DT Article DE MEMBRANE FUSION; VESICULAR STOMATITIS VIRUS; INFLUENZA VIRUS; FLUORESCENCE DEQUENCHING; PRISTANE; PLASMA CELL TUMORIGENESIS ID VESICULAR STOMATITIS-VIRUS; PH-DEPENDENT FUSION; INFLUENZA-VIRUS; CONFORMATIONAL CHANGE; HEMAGGLUTININ; CELLS; FLUORESCENCE; ACTIVATION; KINETICS; BILAYERS AB Pristane (2,6,10,14-tetramethylpentadecane) is an isoprenoid alkane that induces plasma cell tumors in mice. Infection with certain retroviruses accelerates tumorigenesis but the nature of the cooperation between pristane and viruses is unknown. The purpose of this study was to investigate the potential influence of pristane on the fusion between enveloped viruses and mammalian plasma membranes. Using a fluorescence dequenching assay, we found that micromolar amounts of pristane induced fusion between erythrocyte membranes and both vesicular stomatitis virus and influenza virus. Induction of fusion occurred with as little as 5 mu M pristane and reached saturation at roughly 50 mu M alkane. Control experiments revealed that induction of fluorescence dequenching was not due to extraneous phenomena such as lipid transfer or non-specific interactions with the carrier for pristane (P-cyclodextrin). Fusion was also induced by standard protocols which involve lowering the pH of the incubation medium. In the presence of pristane, low pH-triggered fusion was enhanced. The extent to which pristane induced fusion was dependent upon the orientation of the lipids in the target membrane. That is, fusion was most effective with erythrocyte ghosts which had a symmetric lipid distribution and was less effective with ghosts in which the native lipid asymmetry was maintained. Intact erythrocytes, which have an asymmetric lipid distribution, were the least effective targets. This result exactly parallels the pattern observed with acid-induced fusion. Similar patterns were also observed in the temperature dependence of fusion induced by these two protocols. The novel fusogenic activity of pristane is discussed with regard to current models of virus/membrane fusion. C1 HUMBOLDT UNIV BERLIN,FB BIOL,INST BIOPHYS,O-1040 BERLIN,GERMANY. NCI,GENET LAB,BETHESDA,MD 20892. NR 36 TC 4 Z9 4 U1 0 U2 0 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0305-7232 J9 CANCER BIOCHEM BIOPH JI Cancer Biochem. Biophys. PY 1994 VL 14 IS 1 BP 1 EP 14 PG 14 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA PM561 UT WOS:A1994PM56100001 PM 7796384 ER PT J AU DORGAN, JF REICHMAN, ME JUDD, JT BROWN, C LONGCOPE, C SCHATZKIN, A CAMPBELL, WS FRANZ, C KAHLE, L TAYLOR, PR AF DORGAN, JF REICHMAN, ME JUDD, JT BROWN, C LONGCOPE, C SCHATZKIN, A CAMPBELL, WS FRANZ, C KAHLE, L TAYLOR, PR TI THE RELATION OF REPORTED ALCOHOL INGESTION TO PLASMA-LEVELS OF ESTROGENS AND ANDROGENS IN PREMENOPAUSAL WOMEN (MARYLAND, UNITED-STATES) SO CANCER CAUSES & CONTROL LA English DT Article DE ALCOHOL; ANDROGENS; ESTROGENS; ETHYL ALCOHOL; UNITED STATES AB We undertook a cross-sectional study in 107 premenopausal women in Maryland (United States) of alcohol intake and hormonal status in order to evaluate whether plasma hormone levels might mediate the reported positive relation between alcohol ingestion and breast cancer risk. Alcohol ingestion was estimated using a drinking pattern questionnaire, a food frequency questionnaire, and seven-day food records. Fasting blood specimens were collected on days 5-7, 12-15, and 21-23 of each participant's menstrual cycle and pooled to create follicular, midcycle, and luteal phase samples, respectively, for analysis. Estrone, estrone sulfate, estradiol, androstenedione, and dehydroepiandrosterone sulfate (DHEAS) in plasma were measured by radioimmunoassay, and sex-hormone binding globulin (SHBG) was measured by an immunoradiometric assay. After adjusting for age, weight, and total energy intake, alcohol ingestion was not associated with plasma estrogens in the follicular, midcycle, or luteal phases of the menstrual cycle, nor with the level of SHBG or DHEAS in plasma averaged from the three phases of the cycle. Alcohol, however, was significantly positively associated with the average level of plasma androstenedione. Based on these cross-sectional findings among premenopausal women, the increased risk of breast cancer related to alcohol ingestion does not appear to be mediated by elevated plasma estrogen levels. Androstenedione, however, may mediate the alcohol/breast cancer-association. RP DORGAN, JF (reprint author), NCI,DIV CANC PREVENT & CONTROL,EXECUT PLAZA N,ROOM 211,BETHESDA,MD 20892, USA. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X NR 0 TC 83 Z9 85 U1 1 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD JAN PY 1994 VL 5 IS 1 BP 53 EP 60 DI 10.1007/BF01830726 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA MR717 UT WOS:A1994MR71700007 PM 8123779 ER PT J AU SUPKO, JG MALSPEIS, L AF SUPKO, JG MALSPEIS, L TI DOSE-DEPENDENT PHARMACOKINETICS OF RAPAMYCIN-28-N,N-DIMETHYLGLYCINATE IN THE MOUSE SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article ID RAPAMYCIN AY-22,989; IMMUNE-RESPONSE; ANTIFUNGAL AB Rapamycin-28-N,N-dimethylglycinate methanesulfonate salt (RG), synthesized as a potential water-soluble prodrug to facilitate parenteral administration of the antineoplastic macrolide rapamycin (RA), is active against intracranially implanted human glioma in mice. Preclinical pharmacokinetic studies to evaluate the prodrug were conducted in male CD2F1 mice treated with 10, 25, 50 and 100 mg/kg doses of RG by rapid i.v. injection. The plasma concentration of RG decayed in a distinctly triphasic manner following treatment with the 100 mg/kg dose; however, prodrug disposition was apparent biexponential at each of the lower doses. RG exhibited dose-dependent pharmacokinetics, characterized by an increase in the total plasma clearance from 12.5 to 39.3 ml.min-1 . kg-1 for dosage escalations in the range 10-50 mg/kg, while clearance values at doses of 50 and 100 mg/kg were similar. The terminal rate constants decreased linearly as the dose was increased from 10 to 100 mg/kg, eliciting an apparent prolongation of the biological half-life from 2.1 to 4.8 h. There was also a sequential increase in the steady state apparent volume of distribution from 1.73 to 8.75 1/kg. These observations are consistent with saturable binding of RG to plasma proteins while binding to tissue remains linear. Nevertheless, conversion to RA appeared to represent a prominent route of RG elimination. The molar plasma concentration of RA exceeded that of the prodrug within 30-90 min after i.v. treatment and declined very slowly thereafter, with plasma levels sustained between 0.1 and 10 mum for 48 h at each of the doses evaluated. Thus, RG effectively served as a slow release delivery system for RA, implying the possibility of maintaining therapeutic plasma levels of the drug from a more convenient dosing regimen than a continuous infusion schedule. The present findings, coupled with the demonstrated in vivo activity of RG against human brain tumor models, warrant its continued development as a much needed chemotherapeutic agent for the treatment of brain neoplasms. C1 NCI,DIV CANC TREATMENT,PHARMACEUT CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. FU NCI NIH HHS [N01-CM-97619, N01-CA-16058] NR 24 TC 13 Z9 13 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD JAN PY 1994 VL 33 IS 4 BP 325 EP 330 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA MP979 UT WOS:A1994MP97900011 PM 8281627 ER PT J AU LIEBMANN, J COOK, JA LIPSCHULTZ, C TEAGUE, D FISHER, J MITCHELL, JB AF LIEBMANN, J COOK, JA LIPSCHULTZ, C TEAGUE, D FISHER, J MITCHELL, JB TI THE INFLUENCE OF CREMOPHOR EL ON THE CELL-CYCLE EFFECTS OF PACLITAXEL (TAXOL(R)) IN HUMAN TUMOR-CELL LINES SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article ID AGENT AB We have performed DNA flow analysis, mitotic index studies, time-lapse photography, and paclitaxel uptake studies of human tumor cell lines exposed to paclitaxel. DNA flow analysis demonstrated that cells began accumulating in G2/M within 6 hrs of exposure to paclitaxel; by 12 hrs over 50% of cells accumulated in G2/M at all concentrations tested. After 24 hrs of exposure to 10 nM paclitaxel, cells underwent non-uniform mitotic division resulting in multinucleated cells. Of cells treated with 30 nM to 1000 nM paclitaxel, 75% to 85% remained blocked in G2/M for up to 72 hrs. Although a large proportion of cells treated with higher concentrations of paclitaxel (10,000 nM) was blocked in G2/M, a significant proportion (10% to 40%) of these cells was also in G1. Cells exposed to lower concentrations of paclitaxel (10 nM to 1000 nM) in medium containing 0.135% (v/v) Cremophor EL also had a relatively large proportion in G1. Mitotic index studies demonstrated that the paclitaxel-induced G2/M block was initially a mitotic block and that cells remained in mitosis for up to 24 hrs. With additional time of exposure to paclitaxel, mitotic index and time-lapse studies indicated that cells attempted to complete mitosis; however, cytokinesis was inhibited and cells became multinucleated. Time-lapse photography revealed that paclitaxel markedly prolonged the time in mitosis from 0.5 hr to 15 hr. High levels of Cremophor EL (0. 1 35% v/v) markedly reduced the number of cells in mitosis but did not alter the mitotic delay induced by paclitaxel. H-3-paclitaxel uptake studies revealed that high concentrations of Cremophor EL did reduce the rate of uptake of paclitaxel into cells but had little effect on total paclitaxel accumulation. These results confirm that paclitaxel has striking effects on the cell cycle and show that high concentrations of Cremophor EL are capable of inducing a cell cycle block distinct from the mitotic block seen with paclitaxel. These results also demonstrate that cells exposed to paclitaxel for longer than. 24 hours attempt to complete mitosis but the process of cytokinesis is inhibited. Together with cytotoxicity data, these results indicate that entry into and exit out of mitosis are prerequisites for paclitaxel cytotoxicity. RP LIEBMANN, J (reprint author), NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892, USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 18 TC 103 Z9 106 U1 0 U2 4 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD JAN PY 1994 VL 33 IS 4 BP 331 EP 339 PG 9 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA MP979 UT WOS:A1994MP97900012 PM 7904231 ER PT S AU MORGAN, RA AF MORGAN, RA BE Kimura, K Ota, K Carter, SK Friedmann, T TI PROGRESS TOWARD GENE THERAPY FOR AIDS SO CANCER CHEMOTHERAPY: CHALLENGES FOR THE FUTURE, VOL 9 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 9th Nagoya International Symposium on Cancer Treatment CY SEP 17-18, 1993 CL NAGOYA, JAPAN C1 NATL CTR HUMAN GENOME RES,CLIN GENE THERAPY BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 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 0-444-81966-5 J9 INT CONGR SER PY 1994 VL 1078 BP 199 EP 204 PG 6 WC Oncology SC Oncology GA BC31F UT WOS:A1994BC31F00019 ER PT J AU JOHNSON, ES AF JOHNSON, ES TI POULTRY ONCOGENIC RETROVIRUSES AND HUMANS SO CANCER DETECTION AND PREVENTION LA English DT Review DE AVIAN LEUKOSIS VIRUS; AVIAN SARCOMA VIRUS; CANCER; HUMANS; ONCOGENIC RETROVIRUSES; RETICULOENDOTHELIOSIS VIRUS AB Viruses of the avian leukosis/sarcoma group (ALSV) and reticuloendotheliosis viruses (REV) are highly prevalent in chickens and turkeys and naturally cause tumors in them. Commercial chickens are positive for antibodies, and a proportion actually carry infectious virus. Virus may be present in chicken products and in eggs, thus human exposure is virtually universal. The viruses show little potential for producing infectious viral particles in mammalian cells; nevertheless, they have the capacity to infect and transform mammalian cells (including human cells) in vitro, and to induce tumors in a variety of mammals, including primates. Most, but not all, of the serological studies in humans have been negative. Given the known behavior of these viruses in mammals, this was not unexpected. Moreover, there were methodological problems with most of the studies. There is some epidemiological evidence associating putative poultry exposure with cancer in humans. However, this has not been rigorously investigated. This paper is a comprehensive review of the extent of the carcinogenic potential these viruses show for humans. It is concluded, virological evidence indicates, that these viruses could conceivably have a carcinogenic potential for humans, but if so, at a level much less than in chickens. Whether this is insignificant, or translates to a real risk, is not known at the moment. Therefore, there is a need for definitive studies to completely rule out this possibility. RP JOHNSON, ES (reprint author), NIEHS, EPIDEMIOL BRANCH, ENVIRONM & MOLEC EPIDEMIOL SECT, POB 12233, RES TRIANGLE PK, NC 27709 USA. NR 0 TC 35 Z9 41 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 1994 VL 18 IS 1 BP 9 EP 30 PG 22 WC Oncology SC Oncology GA MV326 UT WOS:A1994MV32600002 PM 8162609 ER PT J AU HWU, P ROSENBERG, SA AF HWU, P ROSENBERG, SA TI THE GENETIC-MODIFICATION OF T-CELLS FOR CANCER-THERAPY - AN OVERVIEW OF LABORATORY AND CLINICAL-TRIALS SO CANCER DETECTION AND PREVENTION LA English DT Article DE TUMOR-INFILTRATING LYMPHOCYTES (TIL); IMMUNOTHERAPY; GENE THERAPY; CANCER THERAPY AB Immunotherapies using high doses of interleukin-2 and tumor-infiltrating lymphocytes (TIL) have been developed for the treatment of advanced cancer. Current efforts are aimed at enhancing the therapeutic efficacy of TIL through genetic modification. Initially, we demonstrated that retroviral-mediated gene transfer into TIL using a neomycin resistance marker gene was practical and safe for use in patient therapy. Because TIL have been shown to localize at tumor sites, we are now introducing the TNF gene into TIL in an attempt to increase the local concentrations of TNF in the tumor microenvironment without inducing systemic toxicity. Another gene being studied for insertion into TIL is a chimeric antibody/T-cell receptor gene. For many histologic types of cancer, it is relatively difficult to obtain specific TIL, but many monoclonal antibodies (mAb) exist that bind tumor-associated antigens. In order to combine the effector function of T cells with the antitumor specificity of antibodies, we have constructed chimeric receptor genes containing the Variable region domains from mAb linked to T-cell signal-transducing chains. Human TIL retrovirally transduced with a chimeric receptor gene constructed from an anti-ovarian cancer antibody were redirected to recognize and lyse ovarian cancer cell lines specifically. This approach may allow adoptive immunotherapy against histologies not previously amenable to this treatment modality. RP HWU, P (reprint author), NCI,SURG BRANCH,BLDG 10,ROOM 2B42,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 38 Z9 38 U1 1 U2 3 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 1994 VL 18 IS 1 BP 43 EP 50 PG 8 WC Oncology SC Oncology GA MV326 UT WOS:A1994MV32600004 PM 8162605 ER PT J AU HARRIS, CC AF HARRIS, CC TI SOLVING THE VIRAL-CHEMICAL PUZZLE OF HUMAN LIVER CARCINOGENESIS SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Editorial Material ID HEPATITIS-B VIRUS; HEPATOCELLULAR-CARCINOMA; AFLATOXIN EXPOSURE; RISK; HEPATOCARCINOGENESIS; ACTIVATION; DIETARY; CANCER RP HARRIS, CC (reprint author), NCI,HUMAN CARCINOGENESIS LAB,BLDG 37,ROOM 2001,BETHESDA,MD 20892, USA. NR 18 TC 49 Z9 50 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1994 VL 3 IS 1 BP 1 EP 2 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA MR391 UT WOS:A1994MR39100001 PM 8118377 ER PT J AU PALLI, D GALLI, M CAPORASO, NE CIPRIANI, F DECARLI, A SAIEVA, C FRAUMENI, JF BUIATTI, E AF PALLI, D GALLI, M CAPORASO, NE CIPRIANI, F DECARLI, A SAIEVA, C FRAUMENI, JF BUIATTI, E TI FAMILY HISTORY AND RISK OF STOMACH-CANCER IN ITALY SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID GASTRIC-CANCER; DIET; POPULATION AB One thousand sixteen gastric cancer (GC) patients and 1623 population controls, interviewed in a multicentric study in Italy, reported their family history for gastric, esophageal, and colorectal cancer. A significant association was found only with a history of GC in a sibling or in a parent [odds ratio (OR), 2.6 and 1.7, respectively], which persisted after adjusting for potential confounders including nutrient intake. Adjusted GC risk was higher for subjects having an affected mother than an affected father (OR, 2.3 and 1.3) and showed a further increase for subjects reporting both parents (OR, 3.0) or two or more siblings affected with CC (OR, 8.5). The proportion of patients with an affected first-degree relative was higher among females, in the elderly, and in high-risk areas. Among adult siblings of controls and cases, CC prevalence reported at interview was 1 and 2.7%, respectively; a further increase was shown in families with at least one parent affected (1.4 and 5.7%). GC risk associated with a positive family history was greater among residents of low-risk areas where risks were increased about two-fold. Among cases, family history of GC was not related to blood group A or to histological type according to the Lauren classification. These findings are discussed in terms of the contributions of genetic and environmental risk factors and their possible interactions. C1 IST,SEZ DISTACCATA,I-50131 FLORENCE,ITALY. UNIV MILAN,IST BIOMETRIA,I-20133 MILAN,ITALY. NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. RP PALLI, D (reprint author), CSPO,EPIDEMIOL UNIT,VA VOLTA 171,I-50131 FLORENCE,ITALY. RI Decarli, Adriano/C-3129-2017; OI Decarli, Adriano/0000-0003-1451-8292; saieva, calogero/0000-0002-0117-1608; PALLI, Domenico/0000-0002-5558-2437 FU NCI NIH HHS [N01-CP-51019] NR 18 TC 122 Z9 125 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1994 VL 3 IS 1 BP 15 EP 18 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA MR391 UT WOS:A1994MR39100004 PM 8118379 ER PT J AU INSKIP, PD EBY, NL COOKFAIR, D FREEDMAN, RS RICHARDSON, GS WACTAWSKIWENDE, J HOOVER, RN BOICE, JD AF INSKIP, PD EBY, NL COOKFAIR, D FREEDMAN, RS RICHARDSON, GS WACTAWSKIWENDE, J HOOVER, RN BOICE, JD TI SERUM ESTROGEN AND ANDROGEN LEVELS FOLLOWING TREATMENT FOR CERVICAL-CANCER SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID POST-MENOPAUSAL WOMEN; POSTMENOPAUSAL WOMEN; ENDOMETRIAL CANCER; BREAST-CANCER; CARDIOVASCULAR-DISEASE; ENDOCRINE FUNCTION; CIGARETTE-SMOKING; STEROID LEVELS; OVARIAN; RISK AB Endogenous sex hormones seem to influence the risk of several common and debilitating diseases. With a view toward better understanding the effects of surgical removal of the ovaries and high-dose pelvic radiotherapy on plasma sex hormone levels, we measured estrogen and androgen concentrations cross-sectionally among 147 women who had been treated for cervical cancer 0.3-18.5 years previously. Pelvic radiotherapy (mean dose to ovaries, 50 Gy) and bilateral ovariectomy were associated with similarly reduced hormone concentrations relative to levels among nonirradiated women with intact ovaries, most of whom had had early-stage disease and were treated by hysterectomy. There was little evidence that radiotherapy in addition to ovariectomy further lowered concentrations below levels associated with ovariectomy alone, such as might be expected if radiation was suppressing adrenal endocrine function. Among women age 50 years or older at the time of blood drawing, the removal or irradiation of the ovaries was associated with approximately 45% lower concentrations of estradiol (mean ratio [MR], 0.55; 95% confidence interval [CI], 0.32-0.95) and testosterone (MR, 0.57; 95% CI, 0.32-0.99), and 25-30% lower concentrations of estrone (MR, 0.69; 95% CI, 0.44-1.09) and androstenedione (MR, 0.76; 95% CI, 0.47-1.23), relative to the hysterectomy-only group. Among women younger than 50, ovariectomy and radiotherapy, alone or in combination, were associated with 83% lower estradiol concentrations (MR, 0.17; 95% CI, 0.09-0.31), 46% lower estrone concentrations (MR, 0.54; 95% CI, 0.37-0.81), 23% lower androstenedione concentrations (MR, 0.77; 95% CI, 0.57-1.04), and 14% lower testosterone levels (MR, 0.86; 95% CI, 0.64-1.15). A possible mechanism for the reductions among postmenopausal women involves effects on androgen-producing cells in the ovary, which retain secretory function after menopause. C1 NCI, DIV CANC ETIOL, EPIDEMIOL & BIOSTAT PROGRAM, BETHESDA, MD 20892 USA. GERMAN CANC RES CTR, INST EPIDEMIOL & BIOMETRY, W-6900 HEIDELBERG, GERMANY. SUNY BUFFALO, SCH MED, DEPT SOCIAL & PREVENT MED, BUFFALO, NY 14260 USA. SUNY BUFFALO, SCH MED, DEPT GYNECOL & OBSTET, BUFFALO, NY USA. UNIV TEXAS, MD ANDERSON CANC CTR, DEPT GYNECOL, HOUSTON, TX 77030 USA. MASSACHUSETTS GEN HOSP, VINCENT GYNECOL SERV, BOSTON, MA USA. NR 59 TC 6 Z9 6 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 EI 1538-7755 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1994 VL 3 IS 1 BP 37 EP 45 PG 9 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA MR391 UT WOS:A1994MR39100008 PM 8118384 ER PT J AU KELLOFF, GJ BOONE, CW CROWELL, JA STEELE, VE LUBET, R SIGMAN, CC AF KELLOFF, GJ BOONE, CW CROWELL, JA STEELE, VE LUBET, R SIGMAN, CC TI CHEMOPREVENTIVE DRUG DEVELOPMENT - PERSPECTIVES AND PROGRESS SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Review ID GREEN TEA POLYPHENOLS; SKIN TUMOR PROMOTION; ORNITHINE DECARBOXYLASE ACTIVITY; EPITHELIAL-CELL PROLIFERATION; OCCURRING PLANT PHENOLS; DIETARY VITAMIN-A; METHYLCHOLANTHRENE-INDUCED CARCINOGENESIS; NONSTEROIDAL ANTIINFLAMMATORY DRUG; PROSTAGLANDIN SYNTHESIS INHIBITORS; OCCURRING ORGANOSULFUR COMPOUNDS AB Chemoprevention drug development has the goal of identifying safe and effective chemopreventive agents for clinical use. Several distinctive strategies are pursued in developing chemopreventive agents: (a) identifying and validating predysplastic and early dysplastic lesions that can be used instead of cancers as endpoints for measuring chemopreventive activity; (b) identifying and testing candidate agents based on considerations of mechanisms of action; (c) evaluating combinations of agents with potential for maximizing efficacy and minimizing toxicity; and (d) applying a systematic methodology for identifying and ranking candidate agents at each stage of development to ensure discovery of the best agents and most effective use of available resources. This article discusses 22 drugs and three drug combinations which have reached an advanced stage of development as chemopreventive agents. The first generation of drugs are the most advanced, now being in Phase II and Phase III clinical trials. These drugs include several retinoids [vitamin A, 13-cis-retinoic acid, all-trans-N-(4-hydroxyphenyl)retinamide] calcium, beta-carotene, tamoxifen, and finasteride. The second generation drugs are those in Phase I clinical trials. From most to least advanced, these drugs are 2-difluoromethylornithine, sulindac, piroxicam, oltipraz, N-acetyl-l-cysteine, aspirin, ibuprofen, carbenoxolone, 18 beta-glycyrrhetinic acid, and the combination of 2-difluoromethylornithine with piroxicam. The third generation includes agents with significant evidence of chemopreventive activity in animal models. These agents are now in preclinical toxicity testing. They are S-allyl-l-cysteine, phenhexyl isothiocyanate, curcumin, ellagic acid, fumaric acid, fluasterone, and the combinations of all-trans-N-(4-hydroxyphenyl)retinamide with oltipraz and all-trans-N-(4-hydroxyphenyl) retinamide with tamoxifen. C1 CCS ASSOCIATES,PALO ALTO,CA. RP KELLOFF, GJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT INVEST STUDIES BRANCH,BETHESDA,MD 20892, USA. NR 225 TC 223 Z9 227 U1 0 U2 5 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1994 VL 3 IS 1 BP 85 EP 98 PG 14 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA MR391 UT WOS:A1994MR39100016 PM 8118391 ER PT J AU ZIMONJIC, DB POPESCU, ND DIPAOLO, JA AF ZIMONJIC, DB POPESCU, ND DIPAOLO, JA TI CHROMOSOMAL ORGANIZATION OF VIRAL INTEGRATION SITES IN HUMAN PAPILLOMAVIRUS IMMORTALIZED HUMAN KERATINOCYTE CELL-LINES SO CANCER GENETICS AND CYTOGENETICS LA English DT Article ID I-HYPERSENSITIVE SITES; FRAGILE SITES; CHROMATIN STRUCTURE; RETROVIRAL INTEGRATION; DNA-SEQUENCES; HELA-CELLS; VIRUS-DNA; EXPRESSION; INDUCTION; REGIONS AB The target specificity of viral integration is essential to determining the biologic significance of this integration to various pathologic conditions, including cancer. In this study the chromosomal features of several human papillomavirus (HPV)-16 integration sites mapped by in situ hybridization in human keratinocyte lines were visualized directly by G-banding and differential labeling with bromodeoxyuridine of later replicating domains. G-negative chromosomal bands exhibiting late replication were selectively targeted by HPV-16, suggesting that the structural and functional relationship of the state of chromatin condensation and replication is critical in accessibility to virus integration. RP ZIMONJIC, DB (reprint author), NCI,BIOL LAB,BETHESDA,MD 20892, USA. NR 40 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0165-4608 J9 CANCER GENET CYTOGEN JI Cancer Genet. Cytogenet. PD JAN PY 1994 VL 72 IS 1 BP 39 EP 43 DI 10.1016/0165-4608(94)90107-4 PG 5 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA NM230 UT WOS:A1994NM23000006 PM 8111737 ER PT J AU MERLINO, G AF MERLINO, G TI TRANSGENIC MICE AS MODELS FOR TUMORIGENESIS SO CANCER INVESTIGATION LA English DT Article ID TUMOR SUPPRESSOR GENES; E-MU-MYC; TGF-ALPHA; MAMMARY-TUMORS; T-ANTIGEN; HA-RAS; LIVER NEOPLASIA; NEU ONCOGENE; MOUSE MODEL; EXPRESSION RP MERLINO, G (reprint author), NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,37-2E24,BETHESDA,MD 20892, USA. NR 74 TC 28 Z9 28 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1994 VL 12 IS 2 BP 203 EP 213 DI 10.3109/07357909409024875 PG 11 WC Oncology SC Oncology GA NE508 UT WOS:A1994NE50800010 PM 8131095 ER PT J AU DOSIK, H GOLDSTEIN, MF POIESZ, BJ WILLIAMS, L FAHNRICH, B EHRLICH, GD DUNN, I LEVINE, PH AF DOSIK, H GOLDSTEIN, MF POIESZ, BJ WILLIAMS, L FAHNRICH, B EHRLICH, GD DUNN, I LEVINE, PH TI SEROPREVALENCE OF HUMAN T-LYMPHOTROPIC VIRUS IN BLACKS FROM A SELECTED CENTRAL BROOKLYN POPULATION SO CANCER INVESTIGATION LA English DT Article ID CELL LEUKEMIA LYMPHOMA; HTLV-II INFECTION; UNITED-STATES; C RETROVIRUS; DRUG-ABUSERS; ANTIBODIES; RISK; PATIENT; DISEASE; JAMAICA AB Human T-cell leukemia virus type I (HTLV-I) has been causally linked to adult T-cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-I-associated myelopathy. Few seroprevalence studies have been carried our in the United States. Because of the number of reports of adult T-cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-I-associated myelopathy in blacks from central Brooklyn, New York, we decided to initiate a seroprevalence study in this community. Intravenous drug users and male homosexuals were excluded. A total of 480 individuals from medical clinics and health fairs were surveyed via questionnaire, and their sera were assayed for HTLV-I/II antibody by two laboratories. An overall seroprevalence rare was 21/480 (4.4%). This is almost 200 times greater than a study of a national sample of U.S. blood donors. Rates were similar for individuals originating from the United States and the Caribbean. Nine of the 21 seropositive individuals returned for further testing. Polymerase chain reaction assays revealed that 8 were positive for HTLV-I and 1 for HTLV-II. Although this group may not be representative of the ''normal'' black population of central Brooklyn, the high seroprevalence rate-necessitates that the incidence of HTLV-I-associated illnesses be determined in this community. C1 SUNY HLTH SCI CTR,DEPT MED,BROOKLYN,NY 11203. SUNY HLTH SCI CTR,DEPT MED,DIV HEMATOL ONCOL,SYRACUSE,NY 13210. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP DOSIK, H (reprint author), INTERFAITH MED CTR,DEPT MED,555 PROSPECT PL,BROOKLYN,NY 11238, USA. FU BHP HRSA HHS [2D28PE12052-04]; NHLBI NIH HHS [R01 HL-43602-01, HB-67021] NR 33 TC 4 Z9 4 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1994 VL 12 IS 3 BP 289 EP 295 DI 10.3109/07357909409023027 PG 7 WC Oncology SC Oncology GA NM669 UT WOS:A1994NM66900003 PM 7910512 ER PT J AU POMMIER, Y LETEURTRE, F FESEN, MR FUJIMORI, A BERTRAND, R SOLARY, E KOHLHAGEN, G KOHN, KW AF POMMIER, Y LETEURTRE, F FESEN, MR FUJIMORI, A BERTRAND, R SOLARY, E KOHLHAGEN, G KOHN, KW TI CELLULAR DETERMINANTS OF SENSITIVITY AND RESISTANCE TO DNA TOPOISOMERASE INHIBITORS SO CANCER INVESTIGATION LA English DT Review ID HAMSTER OVARY CELLS; DOUBLE-STRAND BREAKS; POINT MUTATION; CYTO-TOXICITY; MAMMALIAN-CELLS; ANTITUMOR DRUGS; BIS(2,6-DIOXOPIPERAZINE) DERIVATIVES; EUKARYOTIC TOPOISOMERASE; SEQUENCE REQUIREMENTS; CAMPTOTHECIN ANALOGS RP POMMIER, Y (reprint author), NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892, USA. NR 116 TC 236 Z9 240 U1 1 U2 8 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1994 VL 12 IS 5 BP 530 EP 542 DI 10.3109/07357909409021413 PG 13 WC Oncology SC Oncology GA PH097 UT WOS:A1994PH09700012 PM 7922710 ER PT J AU KOSTAKOGLU, L DIVGI, CR HILTON, S CORDONCARDO, C SCOTT, AM KALAIGIAN, H FINN, RD SCHLOM, J LARSON, SM AF KOSTAKOGLU, L DIVGI, CR HILTON, S CORDONCARDO, C SCOTT, AM KALAIGIAN, H FINN, RD SCHLOM, J LARSON, SM TI PRESELECTION OF PATIENTS WITH HIGH TAG-72 ANTIGEN EXPRESSION LEADS TO TARGETING OF 94-PERCENT OF KNOWN METASTATIC TUMOR SITES WITH MONOCLONAL-ANTIBODY I-131 CC49 SO CANCER INVESTIGATION LA English DT Article ID COLORECTAL-CANCER PATIENTS; GLYCOPROTEIN TAG-72; ONCOFETAL ANTIGEN; B72.3; GENERATION; CARCINOMA AB We studied 18 consecutive patients with advanced colorectal cancer where primary tumors were preselected for high expression of TAG-72 antigen and who underwent a phase I radioimmunotherapy trial with an intravenously administered monoclonal antibody CC49, 20 mg, labeled with I-131 in amounts varying from 15 mCi/m(2) to 75 mCi/m(2). Whole-body images and SPECT of the abdomen obtained 1 week after infusion were compared with pretreatment CT scans. A total of 66 lesions were evaluated. SPECT revealed 2/66 lesions (3%) that were not detected by CT; 4/66 were only detected by CT: lungs (1.8 cm and <1 cm), axilla (1.5 cm), adrenal (2.5 cm). Thus, based on immunohistopathological resting in paraffin-embedded tissue blocks of primary tumors stained for TAG-72 antigen, we have selected a subset of patients (about 70% of referrals) with colorectal cancer for whom I-131-CC49 was shown to target to 62/64 CT positive lesions (97%) and 62/66 (94%) of all known positive lesions. We conclude that in patients with significant TAG-72 tumor expression there is excellent targeting of I-131-CC49 in therapeutic doses to colorectal cancer with respect to lesions detected with CT scanning. It should be noted that this study was nor designed as a comparison of the sensitivity of CT versus I-131-CC49 SPECT/planar imaging. Instead, the observed results are consistent with a biological hypothesis that in general, the primary tumor histology vis-a-vis TAG-72 expression reflects the TAG-72 expression of the metastic sites. C1 MEM SLOAN KETTERING CANC CTR,DEPT RADIOL,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,DEPT PATHOL,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,DEPT PHYS MED,NEW YORK,NY 10021. NIH,BETHESDA,MD. FU NCI NIH HHS [CM-97609] NR 23 TC 8 Z9 8 U1 1 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1994 VL 12 IS 6 BP 551 EP 558 DI 10.3109/07357909409023039 PG 8 WC Oncology SC Oncology GA PU293 UT WOS:A1994PU29300001 PM 7994589 ER PT J AU VANDENHEUVEL, JP CLARK, GC KOHN, MC TRITSCHER, AM GREENLEE, WF LUCIER, GW BELL, DA AF VANDENHEUVEL, JP CLARK, GC KOHN, MC TRITSCHER, AM GREENLEE, WF LUCIER, GW BELL, DA TI DIOXIN-RESPONSIVE GENES - EXAMINATION OF DOSE-RESPONSE RELATIONSHIPS USING QUANTITATIVE REVERSE TRANSCRIPTASE-POLYMERASE CHAIN-REACTION SO CANCER RESEARCH LA English DT Article ID UDP-GLUCURONOSYLTRANSFERASES; MESSENGER-RNA; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN; RATS; EXPRESSION; MECHANISM; TOXICITY; TCDD AB The purpose of the present experiments was to examine dose-response relationships for induction of hepatic mRNA following a single administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to rats. The induction of cytochrome P450-1A1 (CYP1A1) mRNA is compared to other ''dioxin-responsive'' genes including UDP-glucuronosyltransferase 1, plasminogen activator inhibitor 2, and transforming growth factor a using a sensitive reverse transcriptase-polymerase chain reaction-based method. Sample-to-sample variability in amplification is a concern in using polymerase chain reaction to quantitate biological responses. However, in the present study recombinant RNA templates were synthesized to use as internal standards in both the reverse transcription and the polymerase chain reaction steps. The induction of CYP1A1 mRNA was extremely sensitive to TCDD treatment with increases observed at doses as low as 1 ng/kg body weight. The induction of CYP1A1 mRNA correlated highly (R2 > 0.90) with an increase in ethoxyresorufin-o-deethylase activity, a CYP1A1-associated enzyme activity. However, induction of CYP1A1 mRNA levels was detected at lower TCDD doses than was ethoxy-resorufin-o-deethylase activity, reflecting the greater sensitivity of the reverse transcription-polymerase chain reaction approach to detect transcriptional activation of the CYP1A1 gene. UDP-glucuronosyltransferase 1 mRNA was increased over control (5-fold) but required 1000-times higher TCDD doses (1 mug/kg) to result in a significant increase than did CYP1A1. Plasminogen activator inhibitor 2 and transforming growth factor alpha mRNA, both previously shown to be induced by TCDD in human keratinocytes, were not increased in rat liver. Hence, these studies reaffirm that TCDD acts through classical receptor mechanisms with gene-to-gene differences in responsiveness. The reverse transcription-polymerase chain reaction method developed to measure mRNA for dioxin-reponsive genes in rat liver will allow for measuring multigene and tissue responses to TCDD and other xenobiotics with high sensitivity, reproducibility, and adaptability and should increase our understanding of various dose-response relationships. C1 NIEHS,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709. RP VANDENHEUVEL, JP (reprint author), PURDUE UNIV,SCH PHARMACOL & TOXICOL,DEPT PHARMACOL & TOXICOL,RE HEINE PHARM BLDG,W LAFAYETTE,IN 47907, USA. NR 25 TC 154 Z9 156 U1 0 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1994 VL 54 IS 1 BP 62 EP 68 PG 7 WC Oncology SC Oncology GA MQ280 UT WOS:A1994MQ28000016 PM 8261464 ER PT J AU MAGGI, M BALDI, E FINETTI, G FRANCESCHELLI, F BROCCHI, A LANZILLOTTI, R SERIO, M CAMBONI, MG THIELE, CJ AF MAGGI, M BALDI, E FINETTI, G FRANCESCHELLI, F BROCCHI, A LANZILLOTTI, R SERIO, M CAMBONI, MG THIELE, CJ TI IDENTIFICATION, CHARACTERIZATION, AND BIOLOGICAL-ACTIVITY OF SOMATOSTATIN RECEPTORS IN HUMAN NEUROBLASTOMA CELL-LINES SO CANCER RESEARCH LA English DT Article ID HUMAN NEURO-BLASTOMA; VASOACTIVE INTESTINAL POLYPEPTIDE; BREAST-CANCER-CELLS; RAT-BRAIN; ANALOG OCTREOTIDE; BIOCHEMICAL-CHARACTERIZATION; TYROSINE PHOSPHATASE; SMS 201-995; EXPRESSION; CLONING AB To investigate the presence of biologically active somatostatin (SS) receptors in neural crest-derived tumors, radioligand binding studies, cyclic AMP accumulation, intracellular calcium, and growth assays were performed in eight human neuroblastoma (NB) cell lines. Mathematical modeling of binding experiments strongly indicates the presence of heterogeneity of sites. The first site (SS(R1)) is present in 40% of the NB cell lines and binds with low capacity (0.5 pmol/mg protein) and high affinity (0.1-1 nM) SS14, SS28, and analogues. The second site (SS(R2)) is a high capacity site (200 pmol/mg protein), widely distributed in all of the cell lines investigated, that shows relative selectivity vet low affinity (100 nM) for SS14, SS28, and [D-Trp8]SS14 without any apparent biological activity. SS(R1) is coupled to a pertussis toxin-sensitive G protein, inhibits forskolin- or VIP-stimulated adenylate cyclase activity, decreases intracellular free calcium, and mediates inhibition (30%) of both DNA synthesis and cell growth. Analysis of cell cycle distribution in aphidicolin-synchronized SS(R1)-positive NB cells indicated that this inhibitory effect is partially mediated by a transient accumulation in G0-G1. Our data indicate high affinity binding sites for SS14, and analogues are present and biologically active in a subset of NB cells. C1 UNIV FLORENCE,SEZ MED NUCL,I-50134 FLORENCE,ITALY. UNIV FLORENCE,DIPARTIMENTO FISIOPATOL CLIN & CLIN MED 3,I-50134 FLORENCE,ITALY. SANDOZ PROD FARMACEUT,I-20135 MILAN,ITALY. NCI,PEDIAT BRANCH,MOLEC GENET SECT,BETHESDA,MD 20892. RP MAGGI, M (reprint author), UNIV FLORENCE,SEZ ENDOCRINOL,VIALE MORGAGNI 85,I-50134 FLORENCE,ITALY. NR 72 TC 43 Z9 44 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1994 VL 54 IS 1 BP 124 EP 133 PG 10 WC Oncology SC Oncology GA MQ280 UT WOS:A1994MQ28000026 PM 8261433 ER PT J AU SCHNEIDER, E HORTON, JK YANG, CH NAKAGAWA, M COWAN, KH AF SCHNEIDER, E HORTON, JK YANG, CH NAKAGAWA, M COWAN, KH TI MULTIDRUG RESISTANCE-ASSOCIATED PROTEIN GENE OVEREXPRESSION AND REDUCED DRUG-SENSITIVITY OF TOPOISOMERASE-II IN A HUMAN BREAST-CARCINOMA MCF7 CELL-LINE SELECTED FOR ETOPOSIDE RESISTANCE SO CANCER RESEARCH LA English DT Article ID STIMULATED DNA CLEAVAGE; HL-60 LEUKEMIA-CELLS; HUMAN TUMOR-CELLS; P-GLYCOPROTEIN; CANCER-CELLS; CATALYTIC ACTIVITY; CROSS-RESISTANCE; POINT MUTATION; ADRIAMYCIN; EXPRESSION AB A human breast cancer cell line (MCF7/WT) was selected for resistance to etoposide (VP-16) by stepwise exposure to 2-fold increasing concentrations of this agent. The resulting cell line (MCF7/VP) was 28-, 21-, and 9-fold resistant to VP-16, VM-26, and doxorubicin, respectively. MCF7/VP cells also exhibited low-level cross-resistance to 4'-(9-acridinylamino)-methanesulfon-m-anisidide, mitoxantrone, and vincristine and no cross-resistance to genistein and camptothecin. Furthermore, these cells were collaterally sensitive to the alkylating agents melphalan and chlorambucil. DNA topoisomerase II levels were similar in both wild-type MCF7/WT and drug-resistant MCF7/VP cells. In contrast, topoisomerase II from MCF7/VP cells appeared to be 7-fold less sensitive to drug-induced cleavable complex formation in whole cells and 3-fold less sensitive in nuclear extracts than topoisomerase II from MCF7/WT cells. Although this suggested that the resistant cells may contain a qualitatively altered topoisomerase II, no mutations were detected in either the ATP-binding nor the putative breakage/resealing regions of either DNA topoisomerase IIalpha or IIbeta. In addition, the steady-state intracellular VP-16 concentration was reduced by 2-fold in the resistant cells, in the absence of detectable mdr1/P-gp expression and without any change in drug efflux. In contrast, expression of the gene encoding the MRP was increased at least 10-fold in resistant MCF7/VP cells as compared to sensitive MCF7/WT cells. These results suggest that resistance to epipodophyllotoxins in MCF7/VP cells is multifactorial, involving a reduction in intracellular drug concentration, possibly as a consequence of MRP overexpression, and an altered DNA topoisomerase II drug sensitivity. RP SCHNEIDER, E (reprint author), NCI,MED BRANCH,BLDG 10,ROOM 12N226,900 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 58 TC 254 Z9 260 U1 3 U2 7 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1994 VL 54 IS 1 BP 152 EP 158 PG 7 WC Oncology SC Oncology GA MQ280 UT WOS:A1994MQ28000029 PM 7903202 ER PT J AU WEGHORST, CM DRAGNEV, KH BUZARD, GS THORNE, KL VANDEBORNE, GF VINCENT, KA RICE, JM AF WEGHORST, CM DRAGNEV, KH BUZARD, GS THORNE, KL VANDEBORNE, GF VINCENT, KA RICE, JM TI LOW INCIDENCE OF POINT MUTATIONS DETECTED IN THE P53 TUMOR-SUPPRESSOR GENE FROM CHEMICALLY-INDUCED RAT RENAL MESENCHYMAL TUMORS SO CANCER RESEARCH LA English DT Article ID POLYMERASE CHAIN-REACTION; CELL-CYCLE CONTROL; WILD-TYPE P53; HEPATOCELLULAR-CARCINOMA; TRANSFORMED-CELLS; BINDING-PROTEIN; MOUSE-LIVER; ANTIGEN; DNA; ONCOGENE AB Previous studies have shown renal mesenchymal tumors (RMTs) induced in rats hy a single intrarenal injection of nickel subsulfide and iron are more pleomorphic and metastatically aggressive than RMTs induced by a single ip injection of methyl(methoxymethyl)nitrosamine (DMN-OMe). While both RMT types contain high levels of K-ras activation, the specific mutational spectra within codon 12 of K-ras are quite different. Nickel subsulfide and iron-induced tumors exhibited codon 12 GGT-->GTT transversions exclusively, while DMN-OMe RMTs showed a wide array of codon 12 mutations, as well as mutations within codons 61 and 63 [K. G. Higinbotham, J. M. Rice, B. A. Diwan, K. S. Kasprzak, C. D. Reed, and A. O. Perantoni, Cancer Res., 52: 4747-4751, 1992; K. G. Higinbotham, J. M. Rice, and A. O. Perantoni, Mol. Carcinog., 5: 136-139, 1992]. In an effort to further correlate carcinogen-specific molecular events in renal tumors, we investigated the p53 tumor suppressor gene in RMTs induced by these two carcinogens for the presence of point mutations. The evolutionarily conserved portion of the coding region of the gene, including part of exon 4 through exon 10, was surveyed for point mutations utilizing single-strand conformation polymorphism and chemical cleavage of mismatches analyses. None (0 of 10) of the nickel subsulfide and iron-induced RMTs and only 1 of 10 DMN-OMe-induced tumors that were evaluated contained point mutations within this portion of the p53 gene. Direct sequencing of the one single-strand conformation polymorphism and chemical cleavage of mismatches-''positive'' DMN-OMe-induced RMT revealed a GCC-->GTC (Ala-Val) transition in codon 345 within exon 10. These results suggest that the different tumorigenic phenotypes exhibited by these two RMTs are not the result of specific mutations or patterns of mutations within the portion of the p53 gene examined and that the mutated p53 tumorigenic pathway, whereby p53 plays a major role in many human neoplasms, does not function in RMTs induced by either agent. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD 21702. RP WEGHORST, CM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC ETIOL,COMPARAT CARCINOGENESIS LAB,BLDG 538,RM 206,FREDERICK,MD 21702, USA. NR 54 TC 35 Z9 35 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1994 VL 54 IS 1 BP 215 EP 219 PG 5 WC Oncology SC Oncology GA MQ280 UT WOS:A1994MQ28000039 PM 8261441 ER PT J AU FUJIMOTO, Y HAMPTON, LL WIRTH, PJ WANG, NJ XIE, JP THORGEIRSSON, SS AF FUJIMOTO, Y HAMPTON, LL WIRTH, PJ WANG, NJ XIE, JP THORGEIRSSON, SS TI ALTERATIONS OF TUMOR-SUPPRESSOR GENES AND ALLELIC LOSSES IN HUMAN HEPATOCELLULAR CARCINOMAS IN CHINA SO CANCER RESEARCH LA English DT Article ID HEPATITIS-B VIRUS; P53 GENE; ENZYMATIC AMPLIFICATION; HETEROZYGOSITY; DNA; AFLATOXIN; MUTATIONS; CHROMOSOME-16; POLYMORPHISMS; ABERRATIONS AB Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas (HCC) from southern Africa and Qidong in China. The objective of the present work was to test the hypothesis that exposure to aflatoxin B1 either alone or coincident with other environmental carcinogens might be associated with allelic losses occurring during development of human hepatocarcinogenesis in China. The HCCs were obtained from two different areas in China: Qidong, where exposure to hepatitis B virus (HBV) and aflatoxin B1 is high; and Beijing, where exposure to HBV is high but that of aflatoxin B1 is low. We analyzed the tumors for mutations in the p53 gene and loss of heterozygosity for the p53, Rh, and APC genes and at marker loci on chromosomes 4, 13, and 16. Frequencies of mutation, loss, and aberration (mutation and loss) of the p53 gene in 25 HCCs from Qidong were 60, 58, and 80%, respectively. The frequencies in 9 HCCs from Beijing were 56, 57, and 78%. However, the frequency of a G to T transversion at codon 249 in HCCs from Qidong and Beijing were 52 and 0%, respectively. These data indicate that mutation and/or loss of heterozygosity in the p53 gene, independent of the 249 mutation, play a critical role in the development of hepatitis B virus-associated HCCs in China. Loss of the Rb and APC genes was observed in 44 and 7% of HCCs from Qidong, respectively. Allelic losses on chromosome 4 and especially on chromosome 16 were frequent in HCCs from Qidong but were not observed in HCCs from Beijing, while loss of heterozygosity on chromosome 13 occurred at similar frequency in both Qidong and Beijing. These results show a distinct difference in the pattern of allelic losses between HCCs in Qidong and Beijing and suggest that aflatoxin B1 and/or other environmental carcinogens may contribute to this difference. C1 NCI,EXPTL CARCINOGENESIS LAB,BLDG 37,ROOM 3C28,BETHESDA,MD 20892. CHINESE ACAD MED SCI,INST CANC,BEIJING,PEOPLES R CHINA. LIVER CANC INST,QIDONG,PEOPLES R CHINA. NR 37 TC 147 Z9 154 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1994 VL 54 IS 1 BP 281 EP 285 PG 5 WC Oncology SC Oncology GA MQ280 UT WOS:A1994MQ28000051 PM 7903205 ER PT J AU DOLL, R MUIR, CS FRAUMENI, JF AF DOLL, R MUIR, CS FRAUMENI, JF TI TRENDS IN CANCER INCIDENCE AND MORTALITY - INTRODUCTION SO CANCER SURVEYS LA English DT Editorial Material C1 CANC REGISTRAT SCOTLAND,DIV INFORMAT & STAT,EDINBURGH EH5 3SQ,MIDLOTHIAN,SCOTLAND. NCI,DEPT HLTH & HUMAN SERV,ROCKVILLE,MD 20852. RP DOLL, R (reprint author), RADCLIFFE INFIRM,IMPERIAL CANC RES FUND,CANC STUDIES UNIT,HARKNESS BLDG,OXFORD OX2 6HE,ENGLAND. NR 9 TC 0 Z9 0 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1994 VL 20 BP 1 EP 3 PG 3 WC Oncology SC Oncology GA PG618 UT WOS:A1994PG61800001 ER PT J AU MUIR, CS FRAUMENI, JF DOLL, R AF MUIR, CS FRAUMENI, JF DOLL, R TI THE INTERPRETATION OF TIME TRENDS SO CANCER SURVEYS LA English DT Article ID CANCER MORTALITY DATA; UNITED-STATES; PROSTATE; AUTOPSY; ENGLAND; WALES C1 NCI,DIV CANC ETIOL,ROCKVILLE,MD 20852. UNIV OXFORD,RADCLIFFE INFIRM,IMPERIAL CANC RES FUND,CANC STUDIES UNIT,OXFORD OX2 6HE,ENGLAND. RP MUIR, CS (reprint author), CANC REGISTRAT SCOTLAND,DIV INFORMAT & STAT,TRINITY PK HOUSE,S TRINITY RD,EDINBURGH EH5 3SQ,MIDLOTHIAN,SCOTLAND. NR 32 TC 17 Z9 17 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1994 VL 20 BP 5 EP 21 PG 17 WC Oncology SC Oncology GA PG618 UT WOS:A1994PG61800002 ER PT J AU BLOT, WJ DEVESA, SS MCLAUGHLIN, JK FRAUMENI, JF AF BLOT, WJ DEVESA, SS MCLAUGHLIN, JK FRAUMENI, JF TI ORAL AND PHARYNGEAL CANCERS SO CANCER SURVEYS LA English DT Article ID NASOPHARYNGEAL CARCINOMA; UNITED-STATES; CIGARETTE-SMOKING; CHANGING INCIDENCE; ESOPHAGEAL CANCER; MORTALITY; ALCOHOL; TONGUE; TRENDS; RISK RP BLOT, WJ (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892, USA. NR 56 TC 9 Z9 9 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1994 VL 20 BP 23 EP 42 PG 20 WC Oncology SC Oncology GA PG618 UT WOS:A1994PG61800003 ER PT J AU BERAL, V HERMON, C MUNOZ, N DEVESA, SS AF BERAL, V HERMON, C MUNOZ, N DEVESA, SS TI CERVICAL CANCER SO CANCER SURVEYS LA English DT Article ID MORTALITY; TRENDS; WOMEN C1 INT AGCY RES CANC,F-69372 LYON 08,FRANCE. NCI,DESCRIPT STUDIES SECT,BETHESDA,MD 20892. RP BERAL, V (reprint author), RADCLIFFE INFIRM,IMPERIAL CANC RES FUND,CANC EPIDEMIOL UNIT,GIBSON BLDG,OXFORD OX2 6HE,ENGLAND. RI Beral, Valerie/B-2979-2013 NR 23 TC 3 Z9 3 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1994 VL 20 BP 265 EP 285 PG 21 WC Oncology SC Oncology GA PG618 UT WOS:A1994PG61800015 ER PT J AU HARTGE, P DEVESA, SS FRAUMENI, JF AF HARTGE, P DEVESA, SS FRAUMENI, JF TI HODGKINS AND NON-HODGKINS-LYMPHOMAS SO CANCER SURVEYS LA English DT Review ID EPSTEIN-BARR-VIRUS; HUMAN-IMMUNODEFICIENCY-VIRUS; CHRONIC LYMPHOCYTIC-LEUKEMIA; CANCER INSTITUTE WORKSHOP; REED-STERNBERG CELLS; RHEUMATOID-ARTHRITIS; MULTIPLE-MYELOMA; RISK-FACTORS; TIME TRENDS; UNITED-STATES RP HARTGE, P (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892, USA. NR 124 TC 21 Z9 22 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1994 VL 20 BP 423 EP 453 PG 31 WC Oncology SC Oncology GA PG618 UT WOS:A1994PG61800022 PM 7534635 ER PT J AU TORRENCE, PF XIAO, W LI, GY LESIAK, K KHAMNEI, S MARAN, A MAITRA, R DONG, BH SILVERMAN, RH AF TORRENCE, PF XIAO, W LI, GY LESIAK, K KHAMNEI, S MARAN, A MAITRA, R DONG, BH SILVERMAN, RH TI 2',5'-GLIGOADENYLATE ANTISENSE CHIMERAS FOR TARGETED ABLATION OF RNA SO CARBOHYDRATE MODIFICATIONS IN ANTISENSE RESEARCH SE ACS SYMPOSIUM SERIES LA English DT Review ID DOUBLE-STRANDED-RNA; TRIPLE-HELIX FORMATION; SEQUENCE-SPECIFIC CLEAVAGE; DERIVATIZED OLIGODEOXYRIBONUCLEOSIDE METHYLPHOSPHONATES; INTERFERON-TREATED CELLS; DEPENDENT PROTEIN-KINASE; SITE-SELECTIVE CLEAVAGE; HUMAN 2-5A SYNTHETASE; MESSENGER-RNA; ENCEPHALOMYOCARDITIS VIRUS AB The unique 2',5'-phosphodiester bond-linked oligonucleotide known as 2-5A (p(n)5'A2'(p5'A2')(m)p5'A) plays a key role in mediation of the antiencephalomyocarditis virus action of interferon. 2-5A acts as a potent inhibitor of translation through the activation of a constituent latent endonuclease, the 2-5A-dependent ribonuclease (RNase), which degrades RNAs. Covalent linkage of the tetrameric p5'A2'p5'A2'p5'A2'p5'A to an antisense deoxyribonucleotide provided an adduct which was unimpaired in activation of the 2-5A-dependent RNase and which. annealed to the complementary sense DNA to give a hybrid complex with a melting temperature similar to the unmodified DNA antisense/sense duplex. Such 2-5A-antisense chimeras targeted to a modified HIV mRNA or to the dsRNA-dependent protein kinase (PKR) mRNA induced specific cleavage in their targets without affecting non-targeted mRNA species. The unaided uptake of 2-5A-antisense against the PKR mRNA in HeLa cells resulted in ablation of the PKR mRNA, with no effect on beta-actin mRNA. These findings demonstrate that 2-5A-antisense chimeras are effective and versatile reagents for the catalytic destruction of targeted RNA. C1 CLEVELAND CLIN FDN,DEPT CANC BIOL,CLEVELAND,OH 44195. RP TORRENCE, PF (reprint author), NIDDK,MED CHEM LAB,BIOMED CHEM SECT,BETHESDA,MD 20892, USA. NR 96 TC 0 Z9 0 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0097-6156 J9 ACS SYM SER PY 1994 VL 580 BP 118 EP 132 PG 15 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Chemistry, Multidisciplinary; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Chemistry; Genetics & Heredity GA BB96P UT WOS:A1994BB96P00008 ER PT J AU HOLLSTEIN, M MARION, MJ LEHMAN, T WELSH, J HARRIS, CC MARTELPLANCHE, G KUSTERS, I MONTESANO, R AF HOLLSTEIN, M MARION, MJ LEHMAN, T WELSH, J HARRIS, CC MARTELPLANCHE, G KUSTERS, I MONTESANO, R TI P53 MUTATIONS AT A-T BASE-PAIRS IN ANGIOSARCOMAS OF VINYL CHLORIDE-EXPOSED FACTORY-WORKERS SO CARCINOGENESIS LA English DT Article ID CHLOROETHYLENE OXIDE; GENE; PROTEIN; COMPLEXES; CARCINOMA; CANCERS AB Mutations in the p53 tumor suppressor gene are commonly found in the major human cancers and the mutational spectrum in some cancer types is consistent with the genotoxic effects of the associated envirommental risk factors. Thus far there is little information on p53 mutations in cancers of factory workers with a history of carcinogen exposure in the workplace. Occupational exposure to vinyl chloride causes liver angiosarcomas (ASL) and also increases the risk of several other cancers. Loss of p53 function in osteo- and fibrosarcomas can occur by two different mechanisms, p53 mutation and amplification of the MDM2 gene. We examined tumors from five vinyl chloride-exposed patients, four with ASL and one with hepatocellular carcinoma (HCC), for evidence of MDM2 proto-oncogene amplification or p53 mutation in exons 5-8. Amplification of MDM2 was not found, but in two of the angiosarcomas an A:T to T:A missense mutation was detected. p53 sequence analysis of vinyl chloride associated cancers may provide valuable information on the relationship between carcinogen exposure and DNA damage in cancer-related genes. C1 INSERM,U271,LYON,FRANCE. NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. RP HOLLSTEIN, M (reprint author), IARC,150 COURS ALBERT THOMAS,F-69372 LYON 08,FRANCE. NR 16 TC 167 Z9 171 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1994 VL 15 IS 1 BP 1 EP 3 DI 10.1093/carcin/15.1.1 PG 3 WC Oncology SC Oncology GA MR103 UT WOS:A1994MR10300001 PM 8293534 ER PT J AU TSUTSUI, T TAGUCHI, S HASEGAWA, K IDE, T KOJIMA, K MATSUMURA, M HUFF, J BARRETT, JC AF TSUTSUI, T TAGUCHI, S HASEGAWA, K IDE, T KOJIMA, K MATSUMURA, M HUFF, J BARRETT, JC TI RESERPINE-INDUCED CELL-TRANSFORMATION WITHOUT DETECTABLE GENETIC-EFFECTS IN SYRIAN-HAMSTER EMBRYO CELLS IN CULTURE SO CARCINOGENESIS LA English DT Article ID NEOPLASTIC TRANSFORMATION; ANEUPLOIDY; CHEMICALS; DIETHYLSTILBESTROL; CARCINOGENESIS; ENHANCEMENT; INDUCTION; MUTATION AB Reserpine, a naturally occurring rauwolfia alkaloid, used mainly as an antihypertensive drug, was examined for its ability to induce cell transformation and genetic effects in Syrian hamster embryo (SHE) cells in culture. Treatment of SHE cells with 2 mu g/ml of reserpine had no effect on cell growth, while 4 mu g/ml of reserpine reduced the growth rate slightly and 8 mu g/ml resulted in a significant inhibition of cell growth. Reserpine at doses of 4-8 mu g/ml for 48 h induced a dose-related increase in morphological transformation of the cells. Reserpine-transformed colonies were morphologically indistinguishable from colonies transformed with benzo[a]pyrene (B[a]P) or other chemical carcinogens. Over the dose range that resulted in cell transformation, treatment of SHE cells with reserpine failed to induce any detectable gene mutations at two genetic loci, chromosomal abnormalities including structural and numerical changes, or DNA adduct formation. These findings indicate that reserpine may have carcinogenic potential by unknown mechanisms that do not include direct induction of gene and/or chromosome mutations. C1 NIEHS,ENVIRONM CARCINOGENESIS PROGRAM,RES TRIANGLE PK,NC 27709. NIPPON DENT UNIV TOKYO,SCH DENT,DEPT PHARMACOL,CHIYODA KU,TOKYO,TOKYO 102,JAPAN. NR 34 TC 9 Z9 9 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1994 VL 15 IS 1 BP 11 EP 14 DI 10.1093/carcin/15.1.11 PG 4 WC Oncology SC Oncology GA MR103 UT WOS:A1994MR10300003 PM 8293535 ER PT J AU PARSHAD, R SANFORD, KK PRICE, FM RHIM, JS TARONE, RE FUSENIG, NE BOUKAMP, P AF PARSHAD, R SANFORD, KK PRICE, FM RHIM, JS TARONE, RE FUSENIG, NE BOUKAMP, P TI ASSOCIATION OF DEFICIENT DNA-REPAIR DURING G(2) PHASE WITH PROGRESSION FROM BENIGN TO MALIGNANT STATE IN A LINE OF HUMAN SKIN KERATINOCYTES TRANSFECTED WITH RAS ONCOGENE SO CARCINOGENESIS LA English DT Article ID MAMMARY EPITHELIAL-CELLS; NEOPLASTIC TRANSFORMATION; CHROMOSOMAL RADIOSENSITIVITY; IONIZING-RADIATION; MAMMALIAN-CELLS; X-IRRADIATION; CYCLE PERIOD; ACTIVATION; CANCER; EXPRESSION AB Human skin keratinocytes after malignant neoplastic transformation by infection with Kirsten murine sarcoma virus (KiMSV) or transfection with pSV(2) ras (containing an activated c-Ha-ras oncogene) showed a DNA repair deficiency(ies). The repair deficiency was manifest as an abnormally high frequency of chromatid breaks and gaps persisting after X-ray-induced DNA damage inflicted during the G(2) phase of the cell cycle. Non-tumorigenic control cells at that time were clearly repair-efficient. By analyzing benign and malignant tumorigenic HaCaT-ras clones, we could exclude ras p21 oncoprotein expression as the causal mechanism for repair deficiency, since both clone types expressed similar levels of the mutated protein and only the malignant tumorigenic cells showed repair deficiency. The results suggest that mutated p21 ras provided the human keratinocytes with a growth advantage in vivo (benign tumor growth), but acquisition of repair deficiency is required for progression from benign to malignant state. C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,BIOSTAT BRANCH,BETHESDA,MD 20892. HOWARD UNIV,COLL MED,DEPT PATHOL,WASHINGTON,DC. GERMAN CANC RES CTR,DIV CARCINOGENESIS & DIFFERENTIAT INVITRO,HEIDELBERG,GERMANY. NR 35 TC 9 Z9 9 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1994 VL 15 IS 1 BP 33 EP 37 DI 10.1093/carcin/15.1.33 PG 5 WC Oncology SC Oncology GA MR103 UT WOS:A1994MR10300007 PM 8293545 ER PT J AU ROMANOV, V SOBEL, ME DASILVA, PP MENARD, S CASTRONOVO, V AF ROMANOV, V SOBEL, ME DASILVA, PP MENARD, S CASTRONOVO, V TI CELL LOCALIZATION AND REDISTRIBUTION OF THE 67 KD LAMININ RECEPTOR AND ALPHA-6-BETA-1 INTEGRIN SUBUNITS IN RESPONSE TO LAMININ STIMULATION - AN IMMUNOGOLD ELECTRON-MICROSCOPY STUDY SO CELL ADHESION AND COMMUNICATION LA English DT Article DE RECEPTOR; CELL-LAMININ INTERACTIONS; INVASION AND METASTASIS ID A-GOLD TECHNIQUE; EXTRACELLULAR-MATRIX; BINDING-PROTEIN; MAMMALIAN-CELLS; TUMOR INVASION; AFFINITY; CARCINOMAS; METASTASIS; MEMBRANES; HOMOLOGY AB The 67 kDa laminin receptor (67LR), one of several cell surface laminin-binding proteins, is involved in the interactions between cancer cells and laminin during tumor invasion and metastasis. A 37 kDa polypeptide (37LRP), previously identified as the 67LR precursor, is abundantly present in the cytoplasm and has been implicated in polysome formation. To better understand the cellular localization of the 67LR and its precursor, transmission electron microscopic studies of human melanoma A2058 cells were carried out using immunogold labeling and a variety of antibodies: (a) affinity purified antibodies directed against 37LRP cDNA-derived synthetic peptides; (b) anti-67LR monoclonal antibodies raised against intact human small cell lung carcinoma cells; and (c) monoclonal antibodies against the subunits of the integrin laminin receptor, alpha 6 beta 1. Double-labeling immunocyto-chemistry revealed that anti-67LR monoclonal antibodies as well as anti-37 LRP antibodies recognized antigens that were localized in the cytoplasm in electron dense structures. As expected, cell membrane labeling was also observed. Surprisingly, alpha 6 and beta 1 integrin subunits were detected in the same cytoplasmic structures positive for the 67LR and the 37LRP. After addition of soluble laminin to A2058 cells in suspension, the number of labeled cytoplasmic structures increased especially in the vicinity of the plasma membrane, and were exported onto the cell surface. Neither fibronectin nor BSA induced such an effect. The data demonstrate that the 67 LR and the 37 LRP antibodies detect colocalized antigens that are in cytoplasmic structures with alpha 6 beta 1 integrin. These laminin binding protein rich structures could potentially form a supply of receptors that are exported to the surface upon exposure of the cells to laminin, with a consequent increase in the number of binding sites for the ligand. This system could define a mechanism through which cancer cells modulate their interaction with laminin. C1 UNIV LIEGE,METASTASIS RES LAB,B-4000 LIEGE,BELGIUM. NCI,FREDERICK CANC RES & DEV CTR,STRUCT BIOL SECT,FREDERICK,MD 21702. NCI,MOLEC PATHOL SECT,BETHESDA,MD 20892. IST NAZL TUMORI,I-20133 MILAN,ITALY. NR 28 TC 33 Z9 34 U1 0 U2 5 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1061-5385 J9 CELL ADHES COMMUN JI Cell Adhes. Commun. PY 1994 VL 2 IS 3 BP 201 EP 209 DI 10.3109/15419069409004438 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PF253 UT WOS:A1994PF25300003 PM 7827956 ER PT J AU CAHALON, L HERSHKOVIZ, R GILAT, D MILLER, A AKIYAMA, SK YAMADA, KM LIDER, O AF CAHALON, L HERSHKOVIZ, R GILAT, D MILLER, A AKIYAMA, SK YAMADA, KM LIDER, O TI FUNCTIONAL INTERACTIONS OF FIBRONECTIN AND TNF-ALPHA - A PARADIGM OF PHYSIOLOGICAL LINKAGE BETWEEN CYTOKINES AND EXTRACELLULAR-MATRIX MOIETIES SO CELL ADHESION AND COMMUNICATION LA English DT Article DE ADHESION; EXTRACELLULAR MATRIX; INTEGRINS; TNF-ALPHA ID TUMOR-NECROSIS-FACTOR; CELL-ADHESION; LYMPHOCYTE-T; BINDING; SURFACE; MACROPHAGES; HEPARIN; MODULATION; COMPONENTS; ACTIVATION C1 WEIZMANN INST SCI,DEPT CELL BIOL,IL-76100 REHOVOT,ISRAEL. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 35 TC 16 Z9 16 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 1061-5385 J9 CELL ADHES COMMUN JI Cell Adhes. Commun. PY 1994 VL 2 IS 3 BP 269 EP 273 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PF253 UT WOS:A1994PF25300012 PM 7827964 ER PT J AU SCHWEIGHOFFER, T LUCE, GEG TANAKA, Y SHAW, S AF SCHWEIGHOFFER, T LUCE, GEG TANAKA, Y SHAW, S TI DIFFERENTIAL EXPRESSION OF INTEGRINS ALPHA-6 AND ALPHA-4 DETERMINES PATHWAYS IN HUMAN PERIPHERAL CD4+ T-CELL DIFFERENTIATION SO CELL ADHESION AND COMMUNICATION LA English DT Article DE T-CELL; INTEGRIN; HOMING ID LYMPHOCYTE RECIRCULATION; REGULATED EXPRESSION; MONOCLONAL-ANTIBODY; MIGRATION PATHWAYS; HOMING RECEPTOR; ADHESION; SUBSETS; MEMORY; FIBRONECTIN; DISTINCT AB Integrins mediate leukocyte adhesion to vascular endothelium and thereby influence leukocyte recirculation. We have explored expression by peripheral blood T cells of beta 1 and beta 7 integrins, particularly alpha 4 beta 1 (VLA-4, CD49d), alpha 4 beta 7 (LPAM-1) and alpha 6 beta 1 (VLA-6, CD49f). Integrin expression differs between CD4+ cells and CD8+ cells in that CD4+ cells: 1) are more heterogeneous, particularly for alpha 4; 2) express on the average less alpha 4 and beta 7; and 3) express on the average more alpha 6 and beta 1. 2D gel electrophoretic analysis was combined with flow cytometric analysis to determine which integrin chain pairs are expressed by the CD45RO - (naive) and CD45RO+ (memory) subsets of CD4+ cells. CD45RO- (naive) cells express homogeneously at intermediate levels the three integrin pairs alpha 6 beta 1, alpha 4 beta 1 and alpha 4 beta 7. Although 2D gel analysis suggests similar average integrin chain composition for CD45RO+CD4+ (memory) cells, flow cytometric analysis demonstrates multiple subsets of CD45RO+ cells differing markedly from each other and from naive cells in levels of expression of alpha 6 and alpha 4 integrins. There are a minimum of three CD45RO+ subsets: 1) alpha 4 beta 1(hi)alpha 6 beta 1(hi)alpha 4 beta 7(neg), which comprises the majority of memory cells; 2) alpha 4 beta 7(hi)alpha 6 beta 1(low) presumptive gut-homing memory cells; and 3) alpha 6 beta 1(hi)alpha 4 beta 7(neg)alpha 4 beta 1(neg), a previously unidentified subset expected to have unique migrational-functional properties. Of particular importance in these results are: the expression by CD4+ naive cells of alpha 6 beta 1, alpha 4 beta 1 and alpha 4 beta 7, the overall prominence and regulation of alpha 6 beta 1 on CD4+ cells, and the selective decreases as well as increases in alpha 4 beta 7 and alpha 4 beta 1 during CD4+ memory specialization. Taken together, these results suggest that differential regulation of expression of alpha 4 and alpha 6 integrin chains that accompany naive-to-memory transition in CD4+ cells are instrumental in generating functional subsets of CD4+ memory cells with specialized recirculation abilities. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 36 TC 6 Z9 7 U1 1 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1061-5385 J9 CELL ADHES COMMUN JI Cell Adhes. Commun. PY 1994 VL 2 IS 5 BP 403 EP 415 DI 10.3109/15419069409004451 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PP745 UT WOS:A1994PP74500003 PM 7842255 ER PT B AU STOJILKOVIC, SS KUKULJAN, M TOMIC, M CATT, KJ AF STOJILKOVIC, SS KUKULJAN, M TOMIC, M CATT, KJ BE Dufau, ML Fabbri, A Isidori, A TI CHARACTERIZATION OF CALCIUM OSCILLATIONS IN PITUITARY GONADOTROPHS SO CELL AND MOLECULAR BIOLOGY OF THE TESTIS SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT International Symposium on Cell and Molecular Biology of the Testis CY SEP 13-14, 1993 CL MAJORCA, SPAIN SP ARES SERONO SYMP C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. RI Tomic, Melanija/C-3371-2016 NR 0 TC 1 Z9 1 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-17-1 J9 FRONT ENDOCRINOL PY 1994 VL 5 BP 39 EP 50 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA52V UT WOS:A1994BA52V00005 ER PT B AU DUFAU, ML MORRIS, CHT HU, ZZ GENG, Y XIE, X ZHUANG, L ZHANG, R BUCZKO, E AF DUFAU, ML MORRIS, CHT HU, ZZ GENG, Y XIE, X ZHUANG, L ZHANG, R BUCZKO, E BE Dufau, ML Fabbri, A Isidori, A TI THE LUTEINIZING-HORMONE RECEPTOR SO CELL AND MOLECULAR BIOLOGY OF THE TESTIS SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT International Symposium on Cell and Molecular Biology of the Testis CY SEP 13-14, 1993 CL MAJORCA, SPAIN SP ARES SERONO SYMP C1 NICHHD,MOLEC ENDOCRINOL SECT,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-17-1 J9 FRONT ENDOCRINOL PY 1994 VL 5 BP 51 EP 60 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA52V UT WOS:A1994BA52V00006 ER PT B AU NEGROVILAR, A MORETTO, M MERCHENTHALER, I LOPEZ, FJ AF NEGROVILAR, A MORETTO, M MERCHENTHALER, I LOPEZ, FJ BE Dufau, ML Fabbri, A Isidori, A TI RECENT ADVANCES IN THE CELLULAR AND MOLECULAR-BIOLOGY OF THE LUTEINIZING-HORMONE-RELEASING HORMONE (LHRH) PULSE-GENERATOR SO CELL AND MOLECULAR BIOLOGY OF THE TESTIS SE FRONTIERS IN ENDOCRINOLOGY LA English DT Proceedings Paper CT International Symposium on Cell and Molecular Biology of the Testis CY SEP 13-14, 1993 CL MAJORCA, SPAIN SP ARES SERONO SYMP C1 NIEHS,REPROD SECT,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. 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 88-85974-17-1 J9 FRONT ENDOCRINOL PY 1994 VL 5 BP 81 EP 87 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BA52V UT WOS:A1994BA52V00009 ER PT J AU USUKURA, J KHOO, W ABE, T BREITMAN, ML SHINOHARA, T AF USUKURA, J KHOO, W ABE, T BREITMAN, ML SHINOHARA, T TI CONE CELLS FAIL TO DEVELOP NORMALLY IN TRANSGENIC MICE SHOWING ABLATION OF ROD PHOTORECEPTOR CELLS SO CELL AND TISSUE RESEARCH LA English DT Article DE RETINA; TRANSGENIC ANIMALS; DIPHTHERIA TOXIN A; DIPHTHERIA-TOXIN GENE; GENES, CYTOTOXIC; OPSIN PROMOTER; CONES; RODS; INTERDEPENDENCY, DEVELOPMENTAL; MOUSE (OPSIN-DT-ALPHA, TRANSGENIC) ID CGMP-PHOSPHODIESTERASE; BETA-SUBUNIT; MOUSE RETINA; RAT RETINA; RD MOUSE; GENE; EXPRESSION; OPSIN; DEGENERATION; RHODOPSIN AB Transgenic mice were derived containing the cytotoxic dt-alpha gene driven by opsin promoter sequences. Mice expressing this construct showed progressive degeneration of rod photoreceptor cells commencing at birth, with obvious depletion of such cells by postnatal day 7. Ablation of rod photoreceptor cells in the transgenic retina was accompanied by the failure of developing cone cells to elaborate outer segments, although all other aspects of cone cell cytodifferentiation appeared normal. The results suggest that the 1.0-kb opsin promoter segment contains rod cell type specificity and that cone cells require maturation of rod cells to complete the late stages of their terminal differentiation and for their maintenance and cellular integrity. C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NAGOYA UNIV,SCH MED,DEPT ANAT,NAGOYA,AICHI 466,JAPAN. MT SINAI HOSP,SAMUEL LUNENFELD RES INST,DIV MOLEC & DEV BIOL,TORONTO M5G 1X5,ON,CANADA. UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO,ON,CANADA. OI Shinohara, Toshimichi/0000-0002-7197-9039 NR 26 TC 15 Z9 15 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0302-766X J9 CELL TISSUE RES JI Cell Tissue Res. PD JAN PY 1994 VL 275 IS 1 BP 79 EP 90 DI 10.1007/BF00305377 PG 12 WC Cell Biology SC Cell Biology GA MM222 UT WOS:A1994MM22200006 PM 8118849 ER PT J AU GOTTESMAN, MM CURRIER, S BRUGGEMANN, E LELONG, I STEIN, W PASTAN, I AF GOTTESMAN, MM CURRIER, S BRUGGEMANN, E LELONG, I STEIN, W PASTAN, I TI THE MULTIDRUG TRANSPORTER - MECHANISTIC CONSIDERATIONS SO CELL BIOLOGY AND MEMBRANE TRANSPORT PROCESSES SE CURRENT TOPICS IN MEMBRANES LA English DT Review ID RESISTANT HUMAN-CELLS; P-GLYCOPROTEIN GENE; CYSTIC-FIBROSIS GENE; MEMBRANE GLYCOPROTEIN; PHOTOACTIVE ANALOGS; ALTERED PATTERN; BINDING SITES; DRUG-BINDING; CYTOSOLIC PH; TUMOR-CELLS C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RP GOTTESMAN, MM (reprint author), NCI,CELL BIOL LAB,BLDG 37,BETHESDA,MD 20892, USA. NR 52 TC 11 Z9 11 U1 1 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 J9 CURR TOP MEMBR PY 1994 VL 41 BP 3 EP 17 DI 10.1016/S0070-2161(08)60451-7 PG 15 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA BA62Q UT WOS:A1994BA62Q00001 ER PT B AU BARRETT, JC AFSHARI, CA AF BARRETT, JC AFSHARI, CA BE Hu, VW TI CELLULAR SENESCENCE AND THE CELL-CYCLE SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 NIEHS,ENVIRONM CARCINOGENESIS PROGRAM,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. 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 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 79 EP 89 PG 11 GA BA55Y UT WOS:A1994BA55Y00009 ER PT B AU RAMPINO, NJ BOHR, VA AF RAMPINO, NJ BOHR, VA BE Hu, VW TI PREFERENTIAL REPAIR OF CISPLATIN ADDUCTS IN THE HUMAN DHFR GENE DURING G1 PHASE ASSAYED WITH T4 DNA-POLYMERASE SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 NIA,MOLEC GENET LAB,BALTIMORE,MD 21224. 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 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 167 EP 171 PG 5 GA BA55Y UT WOS:A1994BA55Y00019 ER PT B AU VANDEWOUDE, GF CHOI, TS ZHOU, RP MURAKAMI, M MATTEN, W FUKASAWA, K AF VANDEWOUDE, GF CHOI, TS ZHOU, RP MURAKAMI, M MATTEN, W FUKASAWA, K BE Hu, VW TI MOS PROTOONCOGENE AND CELL-CYCLE REGULATION SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD 21702. 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 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 247 EP 249 PG 3 GA BA55Y UT WOS:A1994BA55Y00029 ER PT B AU SANFORD, KK PARSHAD, R AF SANFORD, KK PARSHAD, R BE Hu, VW TI MONITORING AND REPAIR OF DNA-DAMAGE DURING G2 IN RELATION TO CARCINOGENESIS SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 NCI,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 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 341 EP 346 PG 6 GA BA55Y UT WOS:A1994BA55Y00040 ER PT B AU TIAN, H HARTMANN, D WAHL, L DONOGHUE, E MCGOWAN, C COSSMAN, J RUSSELL, P SAMELSON, L COHEN, DI AF TIAN, H HARTMANN, D WAHL, L DONOGHUE, E MCGOWAN, C COSSMAN, J RUSSELL, P SAMELSON, L COHEN, DI BE Hu, VW TI CELLS UNDERGOING HIV ENVELOPE-MEDIATED PROGRAMMED DEGENERATION ACCUMULATE IN G2 M PHASE SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 NIAID,IMMUNOREGULAT LAB,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 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 359 EP 366 PG 8 GA BA55Y UT WOS:A1994BA55Y00042 ER PT B AU KOHN, KW OCONNOR, PM JACKMAN, J AF KOHN, KW OCONNOR, PM JACKMAN, J BE Hu, VW TI CELL-CYCLE REGULATION AND THE CHEMOSENSITIVITY OF CANCER-CELLS SO CELL CYCLE: REGULATORS, TARGETS, AND CLINICAL APPLICATIONS SE GWUMC DEPARTMENT OF BIOCHEMISTRY ANNUAL SPRING SYMPOSIA LA English DT Proceedings Paper CT 13th Washington International Spring Symposium on Cell Cycle: Regulators, Targets, and Clinical Applications CY MAY 10-14, 1993 CL WASHINGTON, DC C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. 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 0-306-44672-3 J9 GWUMC DEPT PY 1994 BP 379 EP 388 PG 10 GA BA55Y UT WOS:A1994BA55Y00044 ER PT J AU DOMANN, FE LEVY, JP BIRRER, MJ BOWDEN, GT AF DOMANN, FE LEVY, JP BIRRER, MJ BOWDEN, GT TI STABLE EXPRESSION OF A C-JUN DELETION MUTANT IN 2 MALIGNANT MOUSE EPIDERMAL-CELL LINES BLOCKS TUMOR-FORMATION IN NUDE-MICE SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID DNA-BINDING ACTIVITY; OKADAIC ACID; PROTEIN PHOSPHATASES; FOS; TRANSFORMATION; TRANSCRIPTION; ONCOGENE; GENE; TRANSACTIVATION; PHOSPHORYLATION AB We have stably expressed a trans-activation suppressing deletion mutant of the human c-jun gene (TAM-67) in the malignant mouse epidermal cell lines 10Gy5 and PDV. Expression of the p26 mJUN protein blocked both constitutive and inducible transcriptional trans-activation of several AP-1 responsive reporter chloramphenicol acetyltransferase constructs. p26 mJUN was able to block both 12-O-tetradecanoylphorbol-13-acetate (TPA) and okadaic acid induced expression of the mouse stromelysin gene in 10Gy5 cells and TPA induced expression of the urokinase-type plasminogen activator gene in PDV cells as determined by Northern analyses. Both genes contain TPA response elements in their promoter regions and are known to be AP-1 responsive. The presence of p26 mJUN in nuclear extracts, as determined by Western blotting did not detectably alter the DNA binding activity of endogenous AP-1 as determined by gel shift analysis with an oligonucleotide containing a single high affinity AP-1 binding site. UV cross-linking studies coupled with Western analyses identified DNA bound cJUN but not mJUN in nuclear extracts of stably transfected cell lines, suggesting that the mutant JUN protein may exert some of its antioncogenic effects in malignant mouse epidermal cells by a mechanism(s) not involving DNA binding. Malignant mouse epidermal cells which stably expressed the mutant JUN protein were not only inhibited in their AP-1 trans-activation response, but also in their ability to form s.c. tumors in nude mice. These results indicate that inhibition of AP-1 mediated transcriptional trans-activation alone can be sufficient to suppress the tumorigenic phenotype in a subset of malignant mouse epidermal cells. C1 UNIV ARIZONA,ARIZONA HLTH SCI CTR,DEPT RADIAT ONCOL,1501 N CAMPBELL AVE,TUCSON,AZ 85724. NCI,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD 20850. OI Domann, Frederick/0000-0002-0489-2179 FU NCI NIH HHS [CA 42239, CA 40584]; NIEHS NIH HHS [ES 07091] NR 27 TC 121 Z9 122 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD JAN PY 1994 VL 5 IS 1 BP 9 EP 16 PG 8 WC Cell Biology SC Cell Biology GA MQ419 UT WOS:A1994MQ41900002 PM 8123597 ER PT J AU TERASAKI, M REESE, TS AF TERASAKI, M REESE, TS TI INTERACTIONS AMONG ENDOPLASMIC-RETICULUM, MICROTUBULES, AND RETROGRADE MOVEMENTS OF THE CELL-SURFACE SO CELL MOTILITY AND THE CYTOSKELETON LA English DT Article DE ENDOPLASMIC RETICULUM; DIOC(6)(3); MICROTUBULES ID GROWTH CONES; LIVING CELLS; LEADING LAMELLA; DYNAMICS; BEHAVIOR; NEURONS; ACTIN; FIBROBLASTS; TRANSPORT; INVITRO AB Relationships among the endoplasmic reticulum (ER), microtubules, and bead movements on the cell surface were investigated in the thin peripheral region of A6 cells, a frog kidney cell line. ER tubules were often aligned with microtubules, as shown by double-labeling with DiOC(6)(3) and anti-tubulin in fixed cells. In living cells stained with DiOC(6)(3) and observed in time lapse, there were frequent extensions, but few retractions, of ER tubules. In addition, there was a steady retrograde (towards the cell center) movement of all of the ER at similar to 0.3 mu m/min. Since microtubules are often aligned with the ER, microtubules must also be moving retrogradely. By simultaneous imaging, it was found that the ER moves retrogradely at the same rate as aminated latex beads on the cell surface. This indicates that the mechanisms for ER and bead movement are closely related. Cytochalasin B stopped bead and ER movement in most of the cells, providing evidence that actin is involved in both retrograde movements. The ER retracted towards the cell center in nocodazole while both ER and microtubules retracted in taxol. Time lapse observations showed that for both drugs, the retraction of the ER is the result of retrograde movement in the absence of new ER extensions. Presumably, ER extensions do not occur in nocodazole because of the absence of microtubules, and do not occur in,taxol because taxol-stabilized microtubules move retrogradely and there is no polymerization of new microtubule tracks for ER elongation. (C) 1994 Wiley-Liss, Inc. RP TERASAKI, M (reprint author), NIH,BLDG 36,ROOM 2A-29,BETHESDA,MD 20892, USA. NR 39 TC 56 Z9 58 U1 0 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0886-1544 J9 CELL MOTIL CYTOSKEL JI Cell Motil. Cytoskeleton PY 1994 VL 29 IS 4 BP 291 EP 300 DI 10.1002/cm.970290402 PG 10 WC Cell Biology SC Cell Biology GA QF996 UT WOS:A1994QF99600001 PM 7859292 ER PT B AU TANAKA, Y ADAMS, DH SHAW, S AF TANAKA, Y ADAMS, DH SHAW, S BE Metcalf, BW Dalton, BJ Poste, G Schatz, J TI PROADHESIVE CYTOKINE IMMOBILIZED ON ENDOTHELIAL PROTEOGLYCAN - A NEW PARADIGM FOR RECRUITMENT OF T-CELLS SO CELLULAR ADHESION: MOLECULAR DEFINITION TO THERAPEUTIC POTENTIAL SE NEW HORIZONS IN THERAPEUTICS : SMITH KLINE & FRENCH RESEARCH LABORATORIES SYMPOSIA SERIES LA English DT Proceedings Paper CT SmithKline-Beecham-Pharmaceuticals 7th US Research Symposium - Cellular Adhesion: Molecular Definition to Therapeutic Potential CY OCT, 1992 CL PHILADELPHIA, PA SP SMITHKLINE BEECHAM PHARM C1 NCI,EXPTL IMMUNOL BRANCH,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 0-306-44685-5 J9 N HORIZ TH PY 1994 BP 167 EP 172 PG 6 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA BA81Y UT WOS:A1994BA81Y00010 ER PT J AU WEEKS, BS HOLLOWAY, E KLOTMAN, PE AKIYAMA, SK SCHNAPER, HW KLEINMAN, HK AF WEEKS, BS HOLLOWAY, E KLOTMAN, PE AKIYAMA, SK SCHNAPER, HW KLEINMAN, HK TI 12-O-TETRADECANOYLPHORBOL 13-ACETATE STIMULATES HUMAN T-LYMPHOCYTE ADHERENCE TO THE FIBRONECTIN RGD DOMAIN AND THE LAMININ IKVAV DOMAIN SO CELLULAR IMMUNOLOGY LA English DT Article ID ENDOTHELIAL-CELL MONOLAYERS; AMINO-ACID-SEQUENCE; PLASMA FIBRONECTIN; CONNECTING SEGMENT; ADHESION SITES; BINDING DOMAIN; A-CHAIN; IDENTIFICATION; ATTACHMENT; INTEGRINS C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 44 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 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD JAN PY 1994 VL 153 IS 1 BP 94 EP 104 DI 10.1006/cimm.1994.1008 PG 11 WC Cell Biology; Immunology SC Cell Biology; Immunology GA MR994 UT WOS:A1994MR99400008 PM 8287495 ER PT S AU Iadarola, MJ Messersmith, DJ AF Iadarola, MJ Messersmith, DJ BE Urban, L TI Molecular biology of dynorphin gene expression relationship to spinal cord processing of pain SO CELLULAR MECHANISMS OF SENSORY PROCESSING: THE SOMATOSENSORY SYSTEM SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES H, CELL BIOLOGY LA English DT Proceedings Paper CT NATO Advanced Research Workshop on Cellular Mechanisms of Sensory Processing CY MAR 31-APR 03, 1993 CL WYE COLLEGE, WYE, ENGLAND SP NATO, Sci Affairs Div HO WYE COLLEGE C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 7 Z9 8 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN 33 PA HEIDELBERGER PLATZ 3, W-1000 BERLIN 33, GERMANY SN 1010-8793 BN 3-540-57625-8 J9 NATO ADV SCI INST SE PY 1994 VL 79 BP 313 EP 336 PG 4 WC Cell Biology; Neurosciences; Pharmacology & Pharmacy; Physiology SC Cell Biology; Neurosciences & Neurology; Pharmacology & Pharmacy; Physiology GA BE33Q UT WOS:A1994BE33Q00020 ER PT J AU ZHAO, J KUNG, HF AF ZHAO, J KUNG, HF TI MODULATION OF PROGESTERONE-INDUCED XENOPUS-OOCYTE MATURATION BY PROSTAGLANDINS-E1 AND E2 SO CELLULAR & MOLECULAR BIOLOGY RESEARCH LA English DT Article DE MODULATION OF OOCYTE MATURATION BY PROSTAGLANDINS ID ADENOSINE 3'-5'-CYCLIC MONOPHOSPHATE; CYCLIC-AMP; INSULIN; P21; INDUCTION; CELLS; ASSAY; RAT AB Prostaglandins E1 (PGE1) and E2 (PGE2), the general local modulators or ''local'' hormones, were able to inhibit the progesterone-induced maturation of Xenopus oocytes in vitro, but could not induce maturation by themselves. This inhibition was observed on the sensitivity of the maturation process of the oocyte responses to progesterone, but not on the maximum response or responsiveness. The decreased sensitivity of oocytes to progesterone by prostaglandin E1 or E2 was evident in both the increased concentration of progesterone and the prolonged time required for the maturation of 50% of the oocyte. PGE1 and PGE2 did not appear to affect either the basal level or the progesterone-reduced cAMP level of oocytes. Microinjection of PGE1 or PGE2 into the oocytes had no effect on progesterone-induced oocyte maturation, suggesting that other cell surface-mediated signaling events might be responsible for this modulatory effect of the progstaglandins. RP ZHAO, J (reprint author), NCI,FREDERICK CANC RES FACIL,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701, USA. NR 21 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 0968-8773 J9 CELL MOL BIOL RES JI Cell Mol. Biol. Res. PY 1994 VL 40 IS 1 BP 63 EP 68 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PF135 UT WOS:A1994PF13500007 PM 7804327 ER PT J AU LEVIN, DE BOWERS, B CHEN, CY KAMADA, Y WATANABE, M AF LEVIN, DE BOWERS, B CHEN, CY KAMADA, Y WATANABE, M TI DISSECTING THE PROTEIN-KINASE C/MAP KINASE SIGNALING PATHWAY OF SACCHAROMYCES-CEREVISIAE SO CELLULAR & MOLECULAR BIOLOGY RESEARCH LA English DT Article; Proceedings Paper CT 1994 Austin Spring Meeting on Cellular Signaling: Regulatory Phosphates and Kinases CY APR 08-10, 1994 CL AUSTIN, TX SP UNIV TEXAS AUSTIN, COLL NAT SCI, NATL SCI FDN DE YEAST; PROTEIN KINASE C; MAP KINASE; SIGNAL TRANSDUCTION ID TRANSCRIPTION FACTOR AP-2; C-MYC-GENE; MAP KINASE; CELL-CYCLE; TRANSDUCTION PATHWAY; REGULATORY DOMAIN; PHORBOL ESTERS; 2ND MESSENGERS; GROWTH-FACTOR; 3T3 CELLS AB The PKC1 gene of the budding yeast Saccharomyces cerevisiae encodes a homolog of the alpha, beta, and gamma isoforms of mammalian PKC that is essential for cell growth. Loss of PKC1 function results in a cell lysis defect that is suppressed by osmotic stabilizing agents, suggesting a defect in cell wall integrity. In this study, we show that Pkc1p-depleted cells develop holes in their cell walls positioned at their bud tips, the site to which growth is focused during polarized cell growth. This result suggests that pkc1 mutants are deficient in the process of cell wall remodeling during growth. In further support of this model, cells bearing a pkc1 Delta mutation, allowed to proliferate in the presence of osmotic stabilizing agents, possessed cell walls that were only 60% as thick as wild-type tell walls. This diminution in cell wall material affected both the beta-glucan layer and the mannoprotein layer. We have exploited the cell lysis defect of pkc1 mutants to identify genes that function within the same signalling pathway at points downstream of PKC1. These genes comprise a protein kinase cascade that culminates in the activation of the MAP kinase homolog Mpk1p. The proposed order of protein kinase function, based on genetic experiments, is Pkc1p to Bck1p to Mkk1/2p to Mpk1p. Consistent with the proposed model, Pkc1p selectively phosphorylates Bck1p in vitro and Mpk1p protein kinase activity requires a functional BCK1 gene. C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. RP LEVIN, DE (reprint author), JOHNS HOPKINS UNIV,SCH PUBL HLTH,DEPT BIOCHEM,615 N WOLFE ST,BALTIMORE,MD 21205, USA. FU NIGMS NIH HHS [R01 GM48533] NR 72 TC 100 Z9 101 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0968-8773 J9 CELL MOL BIOL RES JI Cell Mol. Biol. Res. PY 1994 VL 40 IS 3 BP 229 EP 239 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PN348 UT WOS:A1994PN34800008 PM 7874200 ER PT J AU ZHAO, J KUNG, HF MANNE, V AF ZHAO, J KUNG, HF MANNE, V TI FARNESYLATION OF P21 RAS PROTEINS IN XENOPUS OOCYTES SO CELLULAR & MOLECULAR BIOLOGY RESEARCH LA English DT Article DE RAS PROTEINS; FARNESYL PYROPHOSPHATE; FARNESYLTRANSFERASE; XENOPUS OOCYTES; MATURATION; MEVALONATE; MICROINJECTION; MEVINOLIN; CAAX BOX ID GERMINAL-VESICLE BREAKDOWN; GROWTH FACTOR-I; POSTTRANSLATIONAL MODIFICATION; ESCHERICHIA-COLI; ONCOGENIC RAS-P21; KINASE; FARNESYLTRANSFERASE; MATURATION; INSULIN; LAEVIS AB Unprocessed p21 Ras proteins microinjected into Xenopus oocytes were radiolabeled by coinjected [H-3]farnesyl pyrophosphate, a direct farnesyl donor substrate for all known mammalian farnesyl-transferases. Mevinolin, an inhibitor of HMG CoA reductase which reduces the levels of mevalonate and thus farnesyl pyrophosphate, blocked oncogenic H-Ras(va112) induced germinal vesicle breakdown in oocytes. This mevinolin caused block was completely reversed by co-injected farnesyl pyrophosphate. The putative farnesyltransferase in Xenopus oocytes was identified to be similar to those found in mammalian cells in that it requires an intact CAAX box motif in addition to the conserved cysteine residue at the fourth position from the C-terminus of Pas proteins for its farnesylating activity. Peptide inhibitors of farnesyltransferase such as CVIM and TKCVIM were shown to inhibit farnesylation of microinjected Ras proteins thereby blocking its function namely the induction of oocyte maturation. These results demonstrate that Xenopus oocytes process bacterially produced mammalian Pas proteins in a manner similar to, if not identical with that in mammalian cells, thus validating the continued use of the Xenopus oocyte system for unraveling the functions of Pas proteins. Furthermore, our results indicate that the oocyte system may be a useful in vivo model for studying the farnesylation of human Ras proteins, its regulation, and the effects of farnesyltransferase inhibitors. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOCHEM PHYSIOL LAB,FREDERICK,MD 21702. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,PRINCETON,NJ 08543. RI manne, veeraswamy/B-1954-2010 NR 55 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 0968-8773 J9 CELL MOL BIOL RES JI Cell Mol. Biol. Res. PY 1994 VL 40 IS 4 BP 313 EP 321 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PX978 UT WOS:A1994PX97800005 PM 7866432 ER PT J AU DESILVA, R ENGLEZOU, A SCHEVZOV, G GERWIN, BI HARRIS, CC GUNNING, P REDDEL, RR AF DESILVA, R ENGLEZOU, A SCHEVZOV, G GERWIN, BI HARRIS, CC GUNNING, P REDDEL, RR TI INDUCTION OF ANCHORAGE-INDEPENDENT GROWTH AND SERUM RESISTANCE IN IMMORTALIZED HUMAN BRONCHLAL EPITHELIAL-CELLS BY ALTERATION OF THE CYTOSKELETON SO CELLULAR & MOLECULAR BIOLOGY RESEARCH LA English DT Article DE CYTOSKELETON; ACTIN; MALIGNANT TRANSFORMATION; BRONCHIAL EPITHELIAL CELLS ID GAMMA-ACTIN GENES; BETA-ACTIN; NEOPLASTIC TRANSFORMATION; CULTURED-CELLS; SQUAMOUS DIFFERENTIATION; CELLULAR TUMORIGENICITY; NONCODING REGIONS; HUMAN-FIBROBLASTS; TUMOR PROMOTERS; NUDE-MICE AB Malignant transformation is frequently accompanied by obvious changes in cytoarchitecture, but the importance of these changes has been difficult to assess in view of the large number of other cellular changes that also occur. In this study, we transfected the SV40-immortalized human bronchial epithelial cell line, BEAS-2B, with human wild-type beta or gamma actin gene expression plasmids to induce cytoskeletal changes and to determine whether this was associated with altered cellular growth properties. Cells expressing the exogenous full-length actin genes underwent a fibroblastoid change in morphology which was reflected in changes in their pattern of actin cable organization, and acquired both the ability to grow under anchorage-independent conditions and resistance to the normal growth inhibitory effects of fetal bovine serum. These phenotypic changes correlated with changes in actin mRNA levels, but not with changes in actin protein levels. The phenotypically altered cells were not tumorigenic when injected subcutaneously in athymic nude mice, and they retained the ability to suppress the tumorigenic potential of a lung carcinoma cell line, HuT-292. Therefore, alteration of the cytoskeleton of immortalized human bronchial epithelial cells resulted in the acquisition of some properties commonly found in malignant cells, but did not result in tumorigenicity. C1 CHILDRENS MED RES INST,CANC RES UNIT,SYDNEY,NSW 2145,AUSTRALIA. CHILDRENS MED RES INST,CELL BIOL UNIT,SYDNEY,NSW 2145,AUSTRALIA. NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. RI Gunning, Peter/E-9058-2010; Schevzov, Galina/G-5117-2013; Reddel, Roger/A-6635-2014 OI Schevzov, Galina/0000-0002-0793-2279; Reddel, Roger/0000-0002-6302-6107 NR 42 TC 7 Z9 7 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0968-8773 J9 CELL MOL BIOL RES JI Cell Mol. Biol. Res. PY 1994 VL 40 IS 4 BP 323 EP 335 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA PX978 UT WOS:A1994PX97800006 PM 7866433 ER PT J AU WINDER, A KOBAYASHI, T TSUKAMOTO, K URABE, K AROCA, P KAMEYAMA, K HEARING, VJ AF WINDER, A KOBAYASHI, T TSUKAMOTO, K URABE, K AROCA, P KAMEYAMA, K HEARING, VJ TI THE TYROSINASE GENE FAMILY - INTERACTIONS OF MELANOGENIC PROTEINS TO REGULATE MELANOGENESIS SO CELLULAR & MOLECULAR BIOLOGY RESEARCH LA English DT Article DE TYROSINASE; TRP1; MELANIN; PIGMENTATION ID DOPACHROME TAUTOMERASE; OCULOCUTANEOUS ALBINISM; MAMMALIAN TYROSINASE; MELANIN BIOSYNTHESIS; METAL-IONS; MELANOCYTES; FIBROBLASTS; ENZYME; GLYCOPROTEIN; PIGMENTATION AB Several genes critical to the regulation of melanin production in mammals have recently been cloned and characterized. They map to the albino, brown, and slaty loci in mice, and encode proteins with similar structures and features, but with distinct catalytic capacities. The albino locus encodes tyrosinase, an enzyme with three distinct melanogenic functions, the brown locus encodes TRP1 (tyrosinase-related protein-1), and the slaty locus encodes TRP2, another tyrosinase related-protein. TRP2 functions as DOPAchrome tautomerase, an enzyme that preserves the carboxylic acid content of melanins, which would be spontaneously lost in its absence, while TRP1 is able to oxidize the DHICA produced by TRP2. In this study we have used three different systems (immune-affinity purified melanogenic enzymes, mutant melanocytes, and transfected cells) to examine the enzymatic interactions of these proteins, and their stabilization in a complex which significantly increases their physiological half-life. When extrapolated to the melanocyte,our results demonstrate the catalytic functions of these proteins and suggest how they might stably interact within a melanogenic complex in the melanosome to regulate the quantity and quality of melanin synthesized. C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,OXFORD OX1 3RE,ENGLAND. GLAXO GRP RES LTD,GREENFORD UB6 0HE,MIDDX,ENGLAND. TOCHIGI RES LABS,DEPT DERMATOL RES,HAGA,TOCHIGI 32134,JAPAN. YAMANASHI MED COLL,DEPT DERMATOL,TAMAHO,YAMANASHI 40938,JAPAN. KYUSHU UNIV,DEPT DERMATOL,HIGASHI KU,FUKUOKA 812,JAPAN. JIYUGAOKA CLIN,DEPT DERMATOL,TOKYO 152,JAPAN. NR 60 TC 77 Z9 84 U1 1 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0968-8773 J9 CELL MOL BIOL RES JI Cell Mol. Biol. Res. PY 1994 VL 40 IS 7-8 BP 613 EP 626 PG 14 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QM855 UT WOS:A1994QM85500002 PM 7787879 ER PT J AU CHUANG, LF BLACKBOURN, DJ CHUANG, AJ KILLAM, KF LIU, XM LI, Y KUNG, HF CHUANG, RY AF CHUANG, LF BLACKBOURN, DJ CHUANG, AJ KILLAM, KF LIU, XM LI, Y KUNG, HF CHUANG, RY TI EMERGENCE OF ANTIGENIC VARIANTS OF SIMIAN IMMUNODEFICIENCY VIRUS (SIVMAC) IN A SERONEGATIVE MACAQUE AFTER SIVMAC239 INFECTION SO CELLULAR & MOLECULAR BIOLOGY RESEARCH LA English DT Article DE SIMIAN AIDS; SERONEGATIVE MACAQUE; VIRAL MUTATION ID INTRAVENOUS DRUG-USERS; RHESUS-MONKEYS; PERSISTENT INFECTION; GENETIC-VARIANTS; AIDS; NEUTRALIZATION; SEQUENCE; MUTANTS AB Infection with the macaque strain of the simian immunodeficiency virus (SIVmac) induces simian immunodeficiency syndrome in rhesus macaques. This report describes the isolation and identification of antigenic variants of SIVmac in one of the infected monkeys (macaque #22803). Eight naive rhesus monkeys were inoculated with a titered viral stock of the molecularly cloned SIVmac239. Standard serological analysis revealed that all but two were seroconverted. Western blot analysis confirmed the seronegativity of macaque #22803. In addition, sera recovered from this monkey were not able to neutralize the parent SIVmac239. However, virus could be isolated from all of the infected animals, including macaque #22803. Sera recovered were reactive to the autologous virus. The results suggest that the virus from macaque #22803 may have undergone extensive antigenic shift in vivo. To test this hypothesis, a portion of the gag gene was amplified by the polymerase chain reaction (PCR), cloned, and sequenced. Sequence analysis revealed amino acid changes that were clustered between amino acids 200-245. Evaluation of the possible selective pressures contributing to the observed viral mutation revealed that in comparison with the other SIVmac239-infected monkeys, macaque #22803 produced an unusually high T cell proliferative response toward mitogen stimulation before infection, and continued to display a persistently high plasma viremia titer after infection. C1 UNIV CALIF BERKELEY,DEPT MED PHARMACOL & TOXICOL,DAVIS,CA 95616. UNIV MARYLAND,DEPT MICROBIOL & IMMUNOL,BALTIMORE,MD 21201. NCI,FREDERICK,MD 21701. FU NIDA NIH HHS [DA05901] NR 28 TC 9 Z9 9 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0968-8773 J9 CELL MOL BIOL RES JI Cell Mol. Biol. Res. PY 1994 VL 40 IS 7-8 BP 661 EP 669 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QM855 UT WOS:A1994QM85500007 PM 7787884 ER PT J AU DEGTYAREV, MY SPIEGEL, AM JONES, TLZ AF DEGTYAREV, MY SPIEGEL, AM JONES, TLZ TI THE MEMBRANE LOCALIZATION OF THE G-PROTEIN ALPHA(S) SUBUNIT IS NOT DEPENDENT ON ITS TENIR SEQUENCE OR EFFECTOR DOMAIN SO CELLULAR SIGNALLING LA English DT Article DE G PROTEIN; ADENYLYL CYCLASE; MEMBRANE ATTACHMENT; PROTEIN DOMAINS; PROTEIN TARGETING; COS CELL TRANSFECTION; SITE-DIRECTED MUTAGENESIS ID SIGNAL TRANSDUCTION; ADENYLATE-CYCLASE; BINDING-PROTEINS; BETA-SUBUNIT; COS CELLS; MYRISTOYLATION; PURIFICATION; ASSOCIATION; EXPRESSION; ACTIVATION AB The G(s) protein alpha subunit (alpha(s)) sequences conserved in non-myristoylated alpha subunits (TENIR, residues 369-373) or critical for adenylyl cyclase interaction were investigated as possible sites required for membrane localization. Substitutions were created by site-directed mutagenesis in which the TENIR residues were deleted from alpha(s) or added to the soluble, non-myristoylated alpha(i1). After transfection, COS cells were separated by centrifugation into particulate and soluble fractions. Immunoblots showed that these substitutions did not change the localization: alpha(s) +/- TENIR in the particulate fraction, non-myristoylated alpha(i1) +/- TENIR in the soluble fraction. The constitutively active alpha(i)/alpha(s) chimera (CH4A), containing four regions of alpha(s) sufficient for adenylyl cyclase activation, was mutated to prevent myristoylation (GA-CH4A). Immunoblots of transfected COS cell fractions showed CH4A in the particulate and GA-CH4A in the soluble fraction. While these regions did not lead to membrane localization, the soluble GA-CH4A could activate adenylyl cyclase in the intact cell and after reconstitution with cyc-membranes. C1 NIDDK,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892. NR 28 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 0898-6568 J9 CELL SIGNAL JI Cell. Signal. PD JAN PY 1994 VL 6 IS 1 BP 25 EP & DI 10.1016/0898-6568(94)90058-2 PG 0 WC Cell Biology SC Cell Biology GA NG007 UT WOS:A1994NG00700004 PM 8011426 ER PT J AU CASTRO, GD SIMPSON, JT CASTRO, JA AF CASTRO, GD SIMPSON, JT CASTRO, JA TI INTERACTION OF TRICHLOROMETHYL FREE-RADICALS WITH THYMINE IN A MODEL SYSTEM - A MASS-SPECTROMETRIC STUDY SO CHEMICO-BIOLOGICAL INTERACTIONS LA English DT Article DE CARBON TETRACHLORIDE; THYMINE; TRICHLOROMETHYL ID CARBON-TETRACHLORIDE; ELECTROCHEMICAL OXIDATION; METABOLIC-ACTIVATION; METHYL RADICALS; DNA ALKYLATION; INDUCED DAMAGE; LIVER; ASSAY; IDENTIFICATION; CARCINOGENS AB In previous studies from our laboratory we found that the CCl4 reactive metabolites produced during enzymatic in vitro or in vivo CCl4 biotransformation covalently bind to DNA. Further, chemically produced (CCl3)-C-. produce many adducts of unknown structure with the four DMA bases when the reaction proceeds in model systems. In the present work, we describe our attempt to elucidate by GLC/MS the structures of the adducts resulting when chemically generated (CCl3)-C-. interact with thymine. The following reaction products were identified: (i) 5-hydroxymethyl uracil; (ii) thymineglycol; (iii) 5-trichloroethyl uracil (tentative) and (iv) two isomeric 5,6-monochloro monohydroxy adducts of thymine (tentative). Reaction products found do not involve thymine positions directly participating in base-pairing processes. However, alterations in thymine structure reported if they occurred in DNA from livers of CCl4 poisoned animals, might potentially have biological significance that remains to be established. C1 NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BETHESDA,MD 20892. RP CASTRO, GD (reprint author), CITEFA CONICET ZUFRIATEGUI,CTR INVESTAGACIONES TOXICOL,4380 1603 VILLA MARTELLI,BUENOS AIRES,ARGENTINA. FU NIEHS NIH HHS [ES-05619-02] NR 47 TC 12 Z9 12 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0009-2797 J9 CHEM-BIOL INTERACT JI Chem.-Biol. Interact. PD JAN PY 1994 VL 90 IS 1 BP 13 EP 22 DI 10.1016/0009-2797(94)90107-4 PG 10 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology GA NB309 UT WOS:A1994NB30900002 PM 8131216 ER PT J AU USHER, DC SWANSON, C RADER, DJ KRAMER, J BREWER, HB AF USHER, DC SWANSON, C RADER, DJ KRAMER, J BREWER, HB TI COMPARISON OF LP(A) LEVELS IN FRESH AND FROZEN PLASMA USING ELISAS WITH EITHER ANTI-APO(A) OR ANTI-APO-B REPORTING ANTIBODIES SO CHEMISTRY AND PHYSICS OF LIPIDS LA English DT Article DE LP(A); ELISA; ATHEROSCLEROSIS ID LIPOPROTEIN AB Sandwich ELISAs with an anti-apo(a) trapping antibody and either an anti-apolipoprotein B or anti-apolipoprotein(a) reporting antibody, were used to measure the concentrations of Lp(a) in 230 plasma samples that were either freshly drawn or stored at -20 degrees C for 4-6 weeks. The assays produced significantly different results for the fresh and frozen samples, however, the magnitudes of these differences were small, about 8% higher for the frozen samples, and independent of total cholesterol, HDL cholesterol, triglyceride, apolipoprotein B or Lp(a) concentration or assay configuration. A similar difference was seen for a freshly drawn plasma sample assayed at the same time as the fresh and frozen samples, indicating the differences were due to inherent differences in the assays at the times the assays were performed. The assay configuration was an important factor in determining the Lp(a) concentrations for identically treated samples. ELISAs using the apoB reporting antibody yielded concentrations that were significantly less than those determined by ELISAs using the anti-apo(a) reporting antibody. The assay differences did not correlate with total cholesterol, HDL cholesterol, triglyceride, or apoB concentration. However, the magnitude of the difference did correlate well with Lp(a) amount. Low Lp(a) concentrations produced greater assay differences than high Lp(a) concentrations. C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. RP USHER, DC (reprint author), UNIV DELAWARE,SCH LIFE & HLTH SCI,NEWARK,DE 19716, USA. NR 6 TC 14 Z9 14 U1 1 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0009-3084 J9 CHEM PHYS LIPIDS JI Chem. Phys. Lipids PY 1994 VL 67-8 SI SI BP 243 EP 248 DI 10.1016/0009-3084(94)90143-0 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NB029 UT WOS:A1994NB02900026 PM 8187219 ER PT S AU WANK, SA PISEGNA, JR DEWEERTH, A AF WANK, SA PISEGNA, JR DEWEERTH, A BE Reeve, JR Eysselein, V Solomon, TE Go, VLW TI CHOLECYSTOKININ RECEPTOR FAMILY - MOLECULAR-CLONING, STRUCTURE, AND FUNCTIONAL EXPRESSION IN RAT, GUINEA-PIG, AND HUMAN SO CHOLECYSTOKININ SE Annals of the New York Academy of Sciences LA English DT Article ID PANCREATIC ACINAR-CELLS; GASTRIC PARIETAL-CELLS; SMOOTH-MUSCLE CELLS; BIOCHEMICAL-CHARACTERIZATION; PHARMACOLOGICAL CHARACTERIZATION; CHROMOSOMAL LOCALIZATION; DISTINCT RECEPTORS; BOVINE RHODOPSIN; PHOSPHOLIPASE-C; LIGAND-BINDING C1 NIH, BETHESDA, MD 20892 USA. RP NIDDKD, DIGEST DIS BRANCH, BETHESDA, MD 20892 USA. NR 64 TC 131 Z9 135 U1 0 U2 5 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-858-8; 0-89766-857-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 713 BP 49 EP 66 DI 10.1111/j.1749-6632.1994.tb44052.x PG 18 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Physiology SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Physiology GA BA22Q UT WOS:A1994BA22Q00007 PM 8185215 ER PT S AU JENSEN, RT QIAN, JM LIN, JT MANTEY, SA PISEGNA, JR WANK, SA AF JENSEN, RT QIAN, JM LIN, JT MANTEY, SA PISEGNA, JR WANK, SA BE Reeve, JR Eysselein, V Solomon, TE Go, VLW TI DISTINGUISHING MULTIPLE CCK RECEPTOR SUBTYPES - STUDIES WITH GUINEA-PIG CHIEF CELLS AND TRANSFECTED HUMAN CCK RECEPTORS SO CHOLECYSTOKININ SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT CCK 2993: International Symposium CY MAY 19-22, 1993 CL CHATHAM, MA SP NEW YORK ACAD SCI ID STIMULATED PEPSINOGEN SECRETION; PANCREATIC ACINAR-CELLS; GASTRIC PARIETAL-CELLS; CHOLECYSTOKININ RECEPTOR; DISTINCT RECEPTORS; FUNCTIONAL EXPRESSION; BIOLOGICAL-ACTIVITY; MOLECULAR-CLONING; HUMAN BRAIN; ANTAGONISTS RP JENSEN, RT (reprint author), NIDDKD,DIGEST DIS BRANCH,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892, USA. NR 66 TC 28 Z9 29 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 0-89766-857-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 713 BP 88 EP 106 DI 10.1111/j.1749-6632.1994.tb44055.x PG 19 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Physiology SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Physiology GA BA22Q UT WOS:A1994BA22Q00010 PM 8185217 ER PT S AU CRAWLEY, JN AF CRAWLEY, JN BE Reeve, JR Eysselein, V Solomon, TE Go, VLW TI CHOLECYSTOKININ MODULATES DOPAMINE-MEDIATED BEHAVIORS - DIFFERENTIAL ACTIONS IN MEDIAL POSTERIOR VERSUS ANTERIOR NUCLEUS-ACCUMBENS SO CHOLECYSTOKININ SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT CCK 2993: International Symposium CY MAY 19-22, 1993 CL CHATHAM, MA SP NEW YORK ACAD SCI ID HYDROXYLASE MESSENGER-RNAS; VENTRAL TEGMENTAL AREA; TYROSINE-HYDROXYLASE; INSITU HYBRIDIZATION; RAT-BRAIN; NEURONS; RECEPTORS; CCK; MESENCEPHALON; COEXISTENCE RP CRAWLEY, JN (reprint author), NIMH,EXPTL THERAPEUT BRANCH,BEHAV NEUROPHARMACOL SECT,BLDG 10,ROOM 4N214,BETHESDA,MD 20892, USA. NR 29 TC 20 Z9 20 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 0-89766-857-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 713 BP 138 EP 142 DI 10.1111/j.1749-6632.1994.tb44060.x PG 5 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Physiology SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Physiology GA BA22Q UT WOS:A1994BA22Q00015 PM 8185154 ER PT S AU PISEGNA, JR DEWEERTH, A HUPPI, K WANK, SA AF PISEGNA, JR DEWEERTH, A HUPPI, K WANK, SA BE Reeve, JR Eysselein, V Solomon, TE Go, VLW TI MOLECULAR-CLONING, FUNCTIONAL EXPRESSION, AND CHROMOSOMAL LOCALIZATION OF THE HUMAN CHOLECYSTOKININ TYPE-A RECEPTOR SO CHOLECYSTOKININ SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT CCK 2993: International Symposium CY MAY 19-22, 1993 CL CHATHAM, MA SP NEW YORK ACAD SCI ID SMOOTH-MUSCLE TUMORS; BIOCHEMICAL-CHARACTERIZATION; CCK RECEPTORS; PANCREAS; PROTEIN; CELLS; BRAIN C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. NCI,MOLEC GENET SECT,GENET LAB,BETHESDA,MD 20892. NR 18 TC 12 Z9 12 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 0-89766-857-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 713 BP 338 EP 342 DI 10.1111/j.1749-6632.1994.tb44086.x PG 5 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Physiology SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Physiology GA BA22Q UT WOS:A1994BA22Q00041 PM 8185181 ER PT S AU NILSSON, O KOLBY, L WANGBERG, B WANK, SA AHLMAN, H AF NILSSON, O KOLBY, L WANGBERG, B WANK, SA AHLMAN, H BE Reeve, JR Eysselein, V Solomon, TE Go, VLW TI EXPRESSION OF CCK-A AND CCK-B/GASTRIN RECEPTORS IN ENTEROCHROMAFFIN-LIKE CELL CARCINOIDS OF MASTOMYS-NATALENSIS SO CHOLECYSTOKININ SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT CCK 2993: International Symposium CY MAY 19-22, 1993 CL CHATHAM, MA SP NEW YORK ACAD SCI ID CHOLECYSTOKININ RECEPTOR; FUNCTIONAL EXPRESSION C1 SAHLGRENS UNIV HOSP,DEPT SURG,GOTHENBURG,SWEDEN. NIDDK,DIGEST DIS BRANCH,BETHESDA,MD 20892. RP NILSSON, O (reprint author), GOTHENBURG UNIV,SAHLGRENS HOSP,DEPT PATHOL,S-41345 GOTHENBURG,SWEDEN. NR 3 TC 7 Z9 7 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 0-89766-857-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 713 BP 435 EP 438 DI 10.1111/j.1749-6632.1994.tb44119.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Physiology SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Physiology GA BA22Q UT WOS:A1994BA22Q00074 PM 7910444 ER PT J AU LENFANT, C AF LENFANT, C TI NHLBI RESEARCH TRAINING AND CAREER-DEVELOPMENT PROGRAMS - AS YE SOW... SO CIRCULATION LA English DT Editorial Material RP LENFANT, C (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JAN PY 1994 VL 89 IS 1 BP 1 EP 2 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MQ584 UT WOS:A1994MQ58400001 PM 8281633 ER PT J AU FANANAPAZIR, L EPSTEIN, ND AF FANANAPAZIR, L EPSTEIN, ND TI GENOTYPE-PHENOTYPE CORRELATIONS IN HYPERTROPHIC CARDIOMYOPATHY - INSIGHTS PROVIDED BY COMPARISONS OF KINDREDS WITH DISTINCT AND IDENTICAL BETA-MYOSIN HEAVY-CHAIN GENE-MUTATIONS SO CIRCULATION LA English DT Article DE HYPERTROPHIC CARDIOMYOPATHY; GENETICS; SUDDEN DEATH; MISSENSE MUTATION; MYOSIN HEAVY CHAIN ID MYOCARDIAL PERFUSION ABNORMALITIES; SUDDEN-DEATH; CLINICAL MANIFESTATIONS; MISSENSE MUTATION; PATHO-PHYSIOLOGY; DNA; INTERRELATIONS; VERAPAMIL; FAMILIES; THERAPY AB Background We have previously described two distinct mutations in the beta-myosin heavy chain gene with markedly different clinical presentations and outcome: The 908(Leu-->Val) mutation was associated with a low disease penetrance and a benign prognosis. In contrast, the 403(Arg-->Gln) mutation in a Caucasian kindred was associated with a 100% disease penetrance and high incidence of sudden cardiac death. Recently, another mutation, 606(Val-->Met), has been reported to be associated with ''near normal survival'' and offered as evidence for the benign nature of neutral charge substitutions. Methods and Results We report (1) a large kindred (245 family members at risk of inheriting the disease gene) with a 256(Gly-->Glu) mutation characterized by a similar disease penetrance in adults and in children (56% and 60%, respectively) and a cumulative sudden cardiac death rate of only 2% at 50 years of age, (2) a kindred with the 606(Val-->Met) mutation with four sudden cardiac deaths in eight affected individuals, and (3) a Korean kindred with the 403(Arg-->Gln) mutation. Although the disease occurred early and was associated with a high prevalence of myocardial ischemia in both of our kindreds with the 403(Arg-->Gln) mutation, no sudden cardiac death or syncope has occurred in the Korean kindred. Furthermore, in the Caucasian kindred, all patients had nonobstructive hypertrophic cardiomyopathy, but most of the patients in the Korean kindred bed left ventricular outflow obstruction. Conclusions The conclusions are as follows: (1) Although several sudden cardiac deaths are sufficient to establish that a mutation is malignant, study of a large kindred is necessary to be certain that a mutation is benign. To date, only the 908(Leu-->Val) and the 256(Gly-->Glu) mutations satisfy this requirement. (2) The 256(Gly-->Glu) mutation demonstrates that not ail mutations that result in a charge change are malignant. (3) Conversely, the 606(Val-->Met) mutation is malignant in some kindreds; hence, despite the absence of a charge change, minor substitutions in critical regions of beta-myosin heavy chain protein may also have serious consequences. (4) The diverse ethnic origins of the two 403(Arg-->Gln) kindreds provide evidence suggesting that the identical mutation occurred independently and was associated with different genetic backgrounds. Their distinct phenotypes underline the importance of modifying genes and nongenetic factors. C1 NHLBI,CARDIOL BRANCH,INHERITED CARDIAC DIS SECT,BETHESDA,MD 20892. NR 58 TC 186 Z9 194 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JAN PY 1994 VL 89 IS 1 BP 22 EP 32 PG 11 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA MQ584 UT WOS:A1994MQ58400004 PM 8281650 ER PT J AU ZIEGELSTEIN, RC SPURGEON, HA PILI, R PASSANITI, A CHENG, L CORDA, S LAKATTA, EG CAPOGROSSI, MC AF ZIEGELSTEIN, RC SPURGEON, HA PILI, R PASSANITI, A CHENG, L CORDA, S LAKATTA, EG CAPOGROSSI, MC TI A FUNCTIONAL RYANODINE-SENSITIVE INTRACELLULAR CA2+ STORE IS PRESENT IN VASCULAR ENDOTHELIAL-CELLS SO CIRCULATION RESEARCH LA English DT Note DE ENDOTHELIUM; CA2+; RYANODINE; INDO 1 ID SARCOPLASMIC-RETICULUM; CARDIAC-MUSCLE; PROSTACYCLIN PRODUCTION; CALCIUM-CONCENTRATION; RELEASE; BRADYKININ; HISTAMINE; RAT; THROMBIN; CAFFEINE AB The presence of the ryanodine receptor was recently demonstrated in vascular and endocardial endothelium, but its function has not been established. We investigated whether functional ryanodine-sensitive Ca2+ stores are present in cultured endothelial cells from rat aorta (RAECs), human aorta (HAECs), human umbilical vein (HUVECs), and bovine pulmonary artery (BPAECs) and what role these may play in intracellular regulation. Under resting conditions, HAECs, BPAECs, and HUVECs demonstrated a slow increase in intracellular Ca2+ (indexed by indo 1 fluorescence) on exposure to 5 mu mol/L ryanodine, whereas RAECs did not. However, after an initial bradykinin exposure in RAECs, ryanodine markedly blunted the rapid increase in Ca2+ on a second exposure to bradykinin. In HUVECs, ryanodine in buffer with 1.5 mmol/L Ca2+ did not inhibit the agonist-sensitive Ca2+ increase, whereas it blunted the rapid increase in Ca2+ on histamine exposure in buffer with 5 mmol/L Ca2+ suggesting that increasing [Ca2+] enhances the binding of ryanodine to its receptor. Thus, functional ryanodine-sensitive Ca2+ stores are present in vascular endothelial cells. These appear to be involved in regulation of Ca2+ storage and release from agonist-sensitive intracellular compartments. C1 NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. NIA,GERONTOL RES CTR,BIOL CHEM LAB,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,BALTIMORE,MD. NR 34 TC 48 Z9 49 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD JAN PY 1994 VL 74 IS 1 BP 151 EP 156 PG 6 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA MW254 UT WOS:A1994MW25400017 PM 8261589 ER PT J AU MANOHAR, V HUPPI, K LIZZIO, E HOFFMAN, T AF MANOHAR, V HUPPI, K LIZZIO, E HOFFMAN, T TI MURINE SPLENIC HEMATOPOIETIC SUBPOPULATIONS - THE ENLARGED UNDIFFERENTIATED SUBSET IN NEW-ZEALAND BLACK MICE IS MULTIPOTENT STEM-CELLS SO CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY LA English DT Article ID MONOCLONAL-ANTIBODY; DIFFERENTIATION ANTIGENS; SURFACE; LYMPHOCYTES; GENES AB We recently reported that a significant population of the murine splenic non-T, non-B ''null'' cell compartment consists of non-lineage-specific, undifferentiated cells which are in the G(0) and G(1) phases of the cell cycle and that their numbers are particularly high in the spleens of New Zealand Black mice. A highly enriched population of these non-lineage-specific cells obtained by successive elimination of differentiated cells was further purified to homogeneity by fluorescence-activated cell sorting. The morphologic, phenotypic, and histochemical characteristics of this purified population suggest that these cells may be primitive hematopoietic Stem cells. The germ line configuration of the genomic DNA establishes that these are uncommitted stem cells. In vivo, these cells form day 12 colonies in the spleen and liver of lethally irradiated recipients and confer radioprotection. These cells also differentiate into T- and B-cell lineages and reconstitute the immunodeficiency in mice with severe combined immunodeficiency. In response to a combination of a very few early-acting lymphokines and/or stromal cell-conditioned medium in vitro, these tells differentiate into both myeloid and lymphoid cell types. More of these cells are obtained from the enlarged spleens of New Zealand Black mice than from those of BALB/c mice. The presence of a comparatively higher number of stem cells in the spleen than in the marrow or fetal liver provides an alternative, and possibly superior, source of uncommitted stem cells for a variety of experimental investigations or therapeutic manipulations. C1 US FDA,CTR BIOL EVALUAT & RES,DIV MONOCLONAL ANTIBODIES,CELL BIOL LAB,BETHESDA,MD 20892. NCI,GENET LAB,BETHESDA,MD 20892. NR 36 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 1071-412X J9 CLIN DIAGN LAB IMMUN JI Clin. Diagn. Lab. Immunol. PD JAN PY 1994 VL 1 IS 1 BP 99 EP 108 PG 10 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA PT561 UT WOS:A1994PT56100019 PM 7496931 ER PT J AU ABLASHI, DV AF ABLASHI, DV TI VIRAL STUDIES OF CHRONIC FATIGUE SYNDROME - SUMMARY SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material ID EPSTEIN-BARR-VIRUS; T-LYMPHOTROPIC VIRUS; HUMAN HERPESVIRUS-6; INFECTION; DYSFUNCTION; DISORDERS; FEATURES; ANTIBODY; MUSCLE; RNA C1 NCI,BETHESDA,MD. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC. NR 40 TC 22 Z9 22 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S130 EP S133 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400031 PM 8148440 ER PT J AU BRIGGS, NC LEVINE, PH AF BRIGGS, NC LEVINE, PH TI A COMPARATIVE REVIEW OF SYSTEMIC AND NEUROLOGICAL SYMPTOMATOLOGY IN 12 OUTBREAKS COLLECTIVELY DESCRIBED AS CHRONIC FATIGUE SYNDROME, EPIDEMIC NEUROMYASTHENIA, AND MYALGIC ENCEPHALOMYELITIS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID ILLNESS AB Outbreaks of illnesses of unknown etiology typified by a chronic relapsing course of constitutional symptoms and nervous system involvement have collectively been referred to as chronic fatigue syndrome, epidemic neuromyasthenia, and myalgic encephalomyelitis. To examine heterogeneity of clinical presentation, a comparative review was undertaken for 12 well-documented outbreaks reported since 1934. A systemic syndrome characterized by excessive fatigue, myalgias, headache, low-grade fever, and other constitutional symptoms was common to cases in all outbreaks. However, marked heterogeneity in the range of neurological features was apparent. On the basis of predominant neurological manifestations, outbreaks could be grouped into four levels of increasing neurological involvement: affective neuropsychological changes (level I); prominent cutaneous sensory symptoms with both affective and cognitive neuropsychological changes (level II); marked objective paresis with cutaneous sensory as well as affective and cognitive neuropsychological changes (level III); and cutaneous sensory, affective and cognitive neuropsychological, posterior column, cranial nerve, and mixed upper and lower motor neuron changes (level IV). Groups with the most prominent objective neurological findings (levels III and IV) comprised exclusively outbreaks reported between the 1930s and 1950s. All but one outbreak in groups with less prominent neurological findings (levels I and II) were reported between the 1960s and 1980s; a range of neurological features was observed for these groups. Because a complete neurological examination is not emphasized as part of the diagnostic workup in current outbreaks, it is possible that less obvious neurological findings may be overlooked. Careful evaluation of neurological features in epidemic and endemic cases of what is now called chronic fatigue syndrome may be one approach to distinguishing subtypes of what has been described in the past as a nosological entity. C1 NCI,DCE,EBP,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 32 TC 17 Z9 17 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S32 EP S42 PG 11 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400011 PM 8148451 ER PT J AU BUCHWALD, D JONES, J LEVINE, PH AF BUCHWALD, D JONES, J LEVINE, PH TI SUMMARY - CLINICAL AND MULTIDISCIPLINARY RESEARCH ON CHRONIC FATIGUE SYNDROME SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material ID PLACEBO-CONTROLLED TRIAL C1 NATL JEWISH CTR IMMUNOL & RESP MED,DEPT PEDIAT,DENVER,CO 80206. NCI,DIV CANC ETIOL,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP BUCHWALD, D (reprint author), UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98102, USA. NR 22 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S115 EP S116 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400027 ER PT J AU CHESTER, AC LEVINE, PH AF CHESTER, AC LEVINE, PH TI CONCURRENT SICK BUILDING SYNDROME AND CHRONIC FATIGUE SYNDROME - EPIDEMIC NEUROMYASTHENIA REVISITED SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID EPSTEIN-BARR VIRUS; IMMUNOLOGICAL ABNORMALITIES; INFECTION; ILLNESS; DEFINITION; DISORDERS; DISEASE AB Sick building syndrome (SBS) is usually characterized by upper respiratory complaints, headache, and mild fatigue. Chronic fatigue syndrome (CFS) is an illness with defined criteria including extreme fatigue, sore throat, headache, and neurological symptoms. We investigated three apparent outbreaks of SBS and observed another more serious illness (or illnesses), characterized predominantly by severe fatigue, that was noted by 9 (90%) of the 10 teachers who frequently used a single conference room at a high school in Truckee, California; 5 (23%) of the 22 responding teachers in the J wing of a high school in Elk Grove, California; and 9 (10%) of the 93 responding workers from an office building in Washington, D.C. In those individuals with severe fatigue, symptoms of mucous membrane irritation that are characteristic of SBS were noted but also noted were neurological complaints not typical of SBS but quite characteristic of CFS. We conclude that CFS is often associated with SBS. C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NIH,BETHESDA,MD. NR 45 TC 19 Z9 19 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S43 EP S48 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400012 PM 8148452 ER PT J AU LEVINE, PH ATHERTON, M FEARS, T HOOVER, R AF LEVINE, PH ATHERTON, M FEARS, T HOOVER, R TI AN APPROACH TO STUDIES OF CANCER SUBSEQUENT TO CLUSTERS OF CHRONIC SYNDROME - USE OF DATA FROM THE NEVADA-STATE-CANCER-REGISTRY SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID CHRONIC FATIGUE SYNDROME; NATURAL-KILLER CELLS; IMMUNOLOGICAL ABNORMALITIES; BURKITTS LYMPHOMA AB Chronic fatigue syndrome (CFS) has been increasingly associated with immune dysregulation, including depressed natural killer cell activity; this phenomenon is associated with increased susceptibility to cancer. Although anecdotal reports have suggested an association between CFS and cancer, particularly non-Hodgkin's lymphoma and brain cancer, there has been no a priori justification for evaluating such an association and no consideration of relevant parameters, such as length of latent period vs. tumor type. We reviewed data from the Nevada State Cancer Registry subsequent to a reported outbreak of a CFS-like illness in Nevada that occurred during 1984-1986. We concentrated on non-Hodgkin's lymphoma and brain/CNS tumors, with particular emphasis on persons 15-34 and 35-54 years of age. An upward trend in the incidence of brain/CNS tumors, which could be related to a national upward trend for this disease, was noted. No consistent trends were noted for non-Hodgkin's lymphoma. Because of the difficulties inherent in studies of cancer subsequent to various exposures, we evaluated the methodology for determining an association between outbreaks of CFS-like disease and cancer. We propose several approaches that should be considered in future studies for investigation of possible associations between CFS and cancer, including expected latent periods for specific tumors. C1 NEVADA CANC REGISTRY,RENO,NV. RP LEVINE, PH (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 25 TC 4 Z9 4 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S49 EP S53 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400013 PM 8148453 ER PT J AU LEVINE, PH AF LEVINE, PH TI EPIDEMIC NEUROMYASTHENIA AND CHRONIC FATIGUE SYNDROME - EPIDEMIOLOGIC IMPORTANCE OF A CLUSTER DEFINITION SO CLINICAL INFECTIOUS DISEASES LA English DT Article AB Outbreaks of illness variously identified by a number of terms, including epidemic neuromyasthenia, myalgic encephalomyelitis;,Iceland disease, and atypical poliomyelitis, have been reported from many countries during the past 45 years. Since the first well-described outbreak occurring in 1934, >60 outbreaks have been reported, but few of these have been described in considerable detail. These outbreaks are usually cited in historical reports of chronic fatigue syndrome (CFS) since each of these outbreaks appears to contain a number of cases meeting the current case definition of CFS. There has been inadequate attention given to the fact that epidemic neuromyasthenia and related clusters characterized by various complaints, including fatigue, do not have an accepted epidemiological or clinical definition, and only rarely have descriptions of these clusters included a specific case definition. When such case definitions have been applied, the occurrence of cases meeting the current case definition for CFS appears to be both variable and infrequent. This report utilizes examples of several well-documented outbreaks to emphasize specific aspects that should be considered in the investigation of future clusters. RP LEVINE, PH (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 24 TC 11 Z9 12 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S16 EP S20 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400007 PM 8148446 ER PT J AU LEVINE, PH AF LEVINE, PH TI SUMMARY AND PERSPECTIVE - EPIDEMIOLOGY OF CHRONIC FATIGUE SYNDROME SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material ID EPSTEIN-BARR VIRUS; DEFINITION; INFECTION C1 NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 38 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S57 EP S60 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400015 PM 8148454 ER PT J AU LEVINE, PH AF LEVINE, PH TI REFLECTIONS ON EPIDEMIC NEUROMYASTHENIA (CHRONIC FATIGUE SYNDROME) - DISCUSSION SO CLINICAL INFECTIOUS DISEASES LA English DT Article RP LEVINE, PH (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,VIRAL EPIDEMIOL BRACH,BETHESDA,MD 20892, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S7 EP S8 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400003 ER PT J AU LEVINE, PH AF LEVINE, PH TI CHRONIC FATIGUE SYNDROME - CURRENT CONCEPTS - ALBANY, NEW-YORK, 3-4 OCTOBER 1992 - INTRODUCTION SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material RP LEVINE, PH (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 1 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S1 EP S2 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400001 ER PT J AU SUHADOLNIK, RJ REICHENBACH, NL HITZGES, P SOBOL, RW PETERSON, DL HENRY, B ABLASHI, DV MULLER, WEG SCHRODER, HC CARTER, WA STRAYER, DR AF SUHADOLNIK, RJ REICHENBACH, NL HITZGES, P SOBOL, RW PETERSON, DL HENRY, B ABLASHI, DV MULLER, WEG SCHRODER, HC CARTER, WA STRAYER, DR TI UP-REGULATION OF THE 2-5A SYNTHETASE/RNASE L ANTIVIRAL PATHWAY ASSOCIATED WITH CHRONIC FATIGUE SYNDROME SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID DOUBLE-STRANDED-RNA; POLYADENYLIC-POLYURIDYLIC ACID; BARR VIRUS-INFECTION; WHITE BLOOD-CELLS; 2',5'-OLIGOADENYLATE SYNTHETASE; IMMUNOLOGICAL ABNORMALITIES; ENTEROVIRAL RNA; INTERFERON; ACTIVATION; AMPLIGEN AB Levels of 2',5'-oligoadenylate (2-5A) synthetase, bioactive 2-5A, and RNase L were measured in extracts of peripheral blood mononuclear cells (PBMCs) from 15 individuals with chronic fatigue syndrome (CFS) before and during therapy with the biological response modifier poly(I) poly(C,,U) and were compared with levels in healthy controls. Patients differed significantly from controls in having a lower mean basal level of latent 2-5A synthetase (P < .0001), a higher pretreatment level of bioactive 2-5A (P = .002), and a higher level of pretherapy RNase L activity (P < .0001). PBMC extracts from 10 persons with CFS had a mean basal level of activated 2-5A synthetase higher than the corresponding control value (P = .009). All seven pretherapy PBMC extracts tested were positive for the replication of human herpesvirus 6 (HHV-6). Therapy with poly(I) poly(C12U) resulted in a significant decrease in HHV-6 activity (P < .01) and in downregulation of the 2-5A synthetase/RNase L pathway in temporal association with clinical and neuropsychological improvement. The upregulated 2-5A pathway in CFS before therapy is consistent with an activated immune state and a role for persistent viral infection in the pathogenesis of CFS. The response to therapy suggests direct or indirect antiviral activity of poly(I) poly(C12U) in this situation. C1 HAHNEMANN UNIV,PHILADELPHIA,PA. CFS CLIN,INCLINE VILLAGE,NV. UNIV NEVADA,SCH MED,RENO,NV 89557. NCI,BETHESDA,MD. UNIV MAINZ,INST PHYSIOL CHEM,MAINZ,GERMANY. RP SUHADOLNIK, RJ (reprint author), TEMPLE UNIV,SCH MED,DEPT BIOCHEM,PHILADELPHIA,PA 19140, USA. RI Sobol, Robert/E-4125-2013 OI Sobol, Robert/0000-0001-7385-3563 FU NCI NIH HHS [P01 CA-29545] NR 61 TC 65 Z9 65 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1994 VL 18 SU 1 BP S96 EP S104 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA MR864 UT WOS:A1994MR86400024 PM 8148461 ER PT J AU THEODORE, WH AF THEODORE, WH TI INSIGHTS FROM FUNCTIONAL NEUROIMAGING IN THE LOCALIZATION AND DEFINITION OF FOCAL EPILEPSY SO CLINICAL NEUROSCIENCE LA English DT Article DE METABOLISM; NEUROIMAGING; EPILEPSY ID TEMPORAL-LOBE EPILEPSY; POSITRON EMISSION TOMOGRAPHY; CEREBRAL BLOOD-FLOW; COMPLEX PARTIAL SEIZURES; BENZODIAZEPINE-RECEPTOR-BINDING; BICUCULLINE-INDUCED SEIZURES; GLUCOSE-METABOLISM; COMPUTED-TOMOGRAPHY; SUBSTANTIA NIGRA; MOTOR SEIZURES AB Functional imaging techniques have become very useful for the evaluation of patients with focal epilepsy. Hypometabolism detected by FDG-PET can identify the epileptogenic temporal lobe and predict the outcome of temporal lobectomy. MR spectroscopy has also been used to delineate metabolic abnormalities in epileptic foci. The ratio of phosphocreatine to inorganic phosphate is depressed ipsilateral to seizure onset; pH may be elevated. Ictal SPECT blood-flow studies can also identify temporal lobe epileptic foci. However, interictal studies are less reliable, as are interictal PET blood flow measurements. PET functional mapping using oxygen-15 labeled water can be used to identify brain regions that are important with regard to language and memory. PET studies have suggested that benzodiazepine receptor binding may be reduced in temporal lobe epileptic foci, whereas Mu opiate receptor binding is increased. (C) 1994 Wiley-Liss, Inc.* RP THEODORE, WH (reprint author), NINCDS,CLIN EPILEPSY SECT,NIH BLDG 10,ROOM 5C-205,BETHESDA,MD 20892, USA. NR 78 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1065-6766 J9 CLIN NEUROSCI JI Clin. Neurosci. PY 1994 VL 2 IS 1 BP 89 EP 95 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA PC671 UT WOS:A1994PC67100009 ER PT J AU GONZALEZ, FJ IDLE, JR AF GONZALEZ, FJ IDLE, JR TI PHARMACOGENETIC PHENOTYPING AND GENOTYPING - PRESENT STATUS AND FUTURE POTENTIAL SO CLINICAL PHARMACOKINETICS LA English DT Review ID GENETIC-POLYMORPHISM; HUMAN-LIVER; FAMILIAL PYRIMIDINEMIA; OXIDATION POLYMORPHISM; CYTOCHROME-P-450 IIIA; S-MEPHENYTOIN; PST ACTIVITY; BREATH TEST; HYDROXYLATION; TOXICITY AB Enzymes that metabolise foreign compounds exhibit a large degree of interindividual variability in their levels of expression. In a number of instances this variability can be accounted for by null or variant alleles resulting from mutations in genes encoding these enzymes. Human variability in drug metabolism can be determined by biochemical and pharmacological assays. In cases where a genetic change has been characterised, polymerase chain reaction techniques have been developed to diagnose metabolism deficiencies. Genetic differences in certain foreign compound metabolising enzymes such as glutathione S-transferase M1, N-acetyltranferase 2 and CYP2D6 have been shown to be associated with risk for developing environmentally and occupationally based diseases such as cancer. Drug therapy can also be compromised by the existence of genetic deficiencies in a number of enzymes, including CYP2D6. It is anticipated that determination of an individual's drug metabolism capabilities by use of phenotyping and genotyping tests will allow for more rational and safe drug administration protocols. C1 UNIV NEWCASTLE UPON TYNE,SCH MED,DEPT PHARMACOL SCI,PHARMACOGENET UNIT,NEWCASTLE TYNE,TYNE & WEAR,ENGLAND. GENOTYPE LTD,NEWCASTLE TYNE,TYNE & WEAR,ENGLAND. RP GONZALEZ, FJ (reprint author), NCI,MOLEC CARCINOGENESIS LAB,BLDG 37,ROOM 3E-24,BETHESDA,MD 20892, USA. OI Idle, Jeff/0000-0002-6143-1520 NR 69 TC 178 Z9 180 U1 0 U2 6 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 0312-5963 J9 CLIN PHARMACOKINET JI Clin. Pharmacokinet. PD JAN PY 1994 VL 26 IS 1 BP 59 EP 70 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA MR435 UT WOS:A1994MR43500005 PM 8137598 ER PT J AU RYSCHON, TW AF RYSCHON, TW TI PHYSIOLOGICAL-ASPECTS OF BICYCLING SO CLINICS IN SPORTS MEDICINE LA English DT Review RP RYSCHON, TW (reprint author), NHLBI,CARDIAC ENERGET LAB,PEDIAT SCIENTIST DEV PROGRAM,BLDG 1,ROOM B3-07,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0278-5919 J9 CLIN SPORT MED JI Clin. Sports Med. PD JAN PY 1994 VL 13 IS 1 BP 15 EP 38 PG 24 WC Sport Sciences SC Sport Sciences GA MP137 UT WOS:A1994MP13700003 PM 8111849 ER PT J AU OKAMOTO, A DEMETRICK, DJ SPILLARE, EA HAGIWARA, K HUSSAIN, SP BENNETT, WP FORRESTER, K GERWIN, B GREENBLATT, MS SERRANO, M SHISEKI, M YOKOTA, J BEACH, DH HARRIS, CC AF OKAMOTO, A DEMETRICK, DJ SPILLARE, EA HAGIWARA, K HUSSAIN, SP BENNETT, WP FORRESTER, K GERWIN, B GREENBLATT, MS SERRANO, M SHISEKI, M YOKOTA, J BEACH, DH HARRIS, CC TI P16(INK4) MUTATIONS AND ALTERED EXPRESSION IN HUMAN TUMORS AND CELL-LINES SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID RETINOBLASTOMA GENE-PRODUCT; D-TYPE CYCLINS; MALIGNANT MESOTHELIOMA; BLADDER-CANCER; HOMOZYGOUS DELETIONS; CYTOGENETIC ANALYSIS; DEPENDENT REGULATION; INTERFERON GENES; SUPPRESSOR GENE; BINDING PROTEIN C1 COLD SPRING HARBOR LAB,COLD SPRING HARBOR,NY 11724. NATL CANC CTR,RES INST,CHUO KU,TOKYO 104,JAPAN. RP OKAMOTO, A (reprint author), NCI,HUMAN CARCINOGENESIS LAB,BLDG 37,BETHESDA,MD 20892, USA. RI Serrano, Manuel/H-2634-2015 OI Serrano, Manuel/0000-0001-7177-9312 NR 71 TC 20 Z9 20 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 49 EP 57 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600007 PM 7587103 ER PT J AU KIRSCH, IR ABDALLAH, JM BERTNESS, VL HALE, M LIPKOWITZ, S LISTA, F LOMBARDI, DP AF KIRSCH, IR ABDALLAH, JM BERTNESS, VL HALE, M LIPKOWITZ, S LISTA, F LOMBARDI, DP TI LYMPHOCYTE-SPECIFIC GENETIC INSTABILITY AND CANCER SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID T-CELL LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; ATAXIA-TELANGIECTASIA LYMPHOCYTES; SITE-SPECIFIC RECOMBINATION; V(D)J RECOMBINATION; 7-14 TRANSLOCATIONS; MOLECULAR ANALYSIS; PROLYMPHOCYTIC LEUKEMIA; CHROMOSOME-14 INVERSION; NONRANDOM OCCURRENCE C1 ARMED FORCES RADIOBIOL RES INST,DEPT RADIAT BIOPHYS,BETHESDA,MD 20889. CTR STUDI & RIC SANITA ESERCITO,I-00183 ROME,ITALY. RP KIRSCH, IR (reprint author), NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20889, USA. NR 77 TC 9 Z9 9 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 287 EP 295 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600032 PM 7587080 ER PT J AU KOLODNER, RD HALL, NR LIPFORD, J KANE, MF RAO, MRS MORRISON, P WIRTH, L FINAN, PJ BURN, J CHAPMAN, P EARABINO, C MERCHANT, E BISHOP, DT GARBER, J BRONNER, CE BAKER, SM WARREN, G SMITH, LG LINDBLOM, A TANNERGARD, P BOLLAG, RJ GODWIN, AR WARD, DC NORDENSKJOLD, M LISKAY, RM COPELAND, N JENKINS, N LESCOE, MK EWEL, A LEE, S GRIFFITH, J FISHEL, R AF KOLODNER, RD HALL, NR LIPFORD, J KANE, MF RAO, MRS MORRISON, P WIRTH, L FINAN, PJ BURN, J CHAPMAN, P EARABINO, C MERCHANT, E BISHOP, DT GARBER, J BRONNER, CE BAKER, SM WARREN, G SMITH, LG LINDBLOM, A TANNERGARD, P BOLLAG, RJ GODWIN, AR WARD, DC NORDENSKJOLD, M LISKAY, RM COPELAND, N JENKINS, N LESCOE, MK EWEL, A LEE, S GRIFFITH, J FISHEL, R TI HUMAN MISMATCH REPAIR GENES AND THEIR ASSOCIATION WITH HEREDITARY NONPOLYPOSIS COLON-CANCER SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID NONPOLYPOSIS COLORECTAL-CANCER; HETERODUPLEX PLASMID DNA; MUTS-ENCODED PROTEIN; SACCHAROMYCES-CEREVISIAE; ESCHERICHIA-COLI; MICROSATELLITE INSTABILITY; SOMATIC MUTATIONS; MUTATOR PHENOTYPE; NATURAL-HISTORY; CARCINOGENESIS C1 HARVARD UNIV,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA 02115. HARVARD UNIV,DANA FARBER CANC INST,MOLEC BIOL CARE FACIL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. ST JAMES UNIV HOSP,GENET EPIDEMIOL LAB,IMPERIAL CANC RES FUND,LEEDS LS9 7TF,W YORKSHIRE,ENGLAND. GEN INFIRM,DEPT SURG,LEEDS LS1 3EX,W YORKSHIRE,ENGLAND. GEN INFIRM,CTR DIGEST DIS,LEEDS LS1 3EX,W YORKSHIRE,ENGLAND. UNIV NEWCASTLE UPON TYNE,DEPT HUMAN GENET,NEWCASTLE TYNE NE2 4AA,TYNE & WEAR,ENGLAND. OREGON HLTH SCI UNIV,DEPT MOLEC & MED GENET,PORTLAND,OR 97201. YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT MOLEC BIOPHYS,NEW HAVEN,CT 06510. KAROLINSKA HOSP,DEPT MOLEC MED,S-17176 STOCKHOLM,SWEDEN. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,FREDERICK,MD 21702. UNIV VERMONT,SCH MED,DEPT MICROBIOL & MOLEC GENET,BURLINGTON,VT 05405. UNIV N CAROLINA,SCH MED,LINEBERGER CANC RES CTR,CHAPEL HILL,NC 27599. RP KOLODNER, RD (reprint author), HARVARD UNIV,DANA FARBER CANC INST,DIV CELL & MOLEC BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. OI Bishop, Tim/0000-0002-8752-8785 NR 79 TC 14 Z9 14 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 331 EP 338 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600036 PM 7587085 ER PT J AU BARRETT, JC ANNAB, LA ALCORTA, D PRESTON, G VOJTA, P YIN, Y AF BARRETT, JC ANNAB, LA ALCORTA, D PRESTON, G VOJTA, P YIN, Y TI CELLULAR SENESCENCE AND CANCER SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID HUMAN-DIPLOID FIBROBLASTS; WILD-TYPE P53; INDEFINITE DIVISION; C-MYC; POSSIBLE INVOLVEMENT; GENETIC-ANALYSIS; HUMAN-CELLS; PROTEIN; IMMORTALIZATION; CYCLE RP BARRETT, JC (reprint author), NIEHS,MOLEC CARCINOGENESIS LAB,ENVIRONM CARCINOGENESIS PROGRAM,RES TRIANGLE PK,NC 27709, USA. NR 67 TC 20 Z9 20 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 411 EP 418 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600045 PM 7587095 ER PT J AU VARMUS, HE GODLEY, LA ROY, S TAYLOR, ICA YUSCHENKOFF, L SHI, YP PINKEL, D GRAY, J PYLE, R ALDAZ, CM BRADLEY, A MEDINA, D DONEHOWER, LA AF VARMUS, HE GODLEY, LA ROY, S TAYLOR, ICA YUSCHENKOFF, L SHI, YP PINKEL, D GRAY, J PYLE, R ALDAZ, CM BRADLEY, A MEDINA, D DONEHOWER, LA TI DEFINING THE STEPS IN A MULTISTEP MOUSE MODEL FOR MAMMARY CARCINOGENESIS SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID WILD-TYPE P53; ANDROGEN RECEPTOR GENE; PROTO-ONCOGENE INT-1; HUMAN-BREAST CANCER; TRANSGENIC MICE; TUMOR VIRUS; ATAXIA-TELANGIECTASIA; CELL-LINE; PROTOONCOGENE; AMPLIFICATION C1 NCI,VARMUS LAB,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM & BIOPHYS,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT MICROBIOL & IMMUNOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,DIV MOLEC CYTOMETRY,SAN FRANCISCO,CA 94143. BAYLOR COLL MED,INST MOLEC GENET,HOUSTON,TX 77030. BAYLOR COLL MED,HOWARD HUGHES MED INST,HOUSTON,TX 77030. UNIV TEXAS,MD ANDERSON CANC CTR SCI PK,DEPT CARCINOGENESIS,SMITHVILLE,TX 78957. BAYLOR COLL MED,DEPT CELL BIOL,HOUSTON,TX 77030. RP VARMUS, HE (reprint author), NIH,OFF DIRECTOR,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA-25215, CA-54897, CA-59967] NR 56 TC 2 Z9 3 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 491 EP 499 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600053 PM 7587104 ER PT J AU WEBER, BL ABEL, KJ COUCH, FJ MERAJVER, SD CHANDRASEKHARAPPA, SC CASTILLA, L MCKINLEY, D HO, PP CALZONE, K FRANK, TS XU, J BRODY, LC COLLINS, FS AF WEBER, BL ABEL, KJ COUCH, FJ MERAJVER, SD CHANDRASEKHARAPPA, SC CASTILLA, L MCKINLEY, D HO, PP CALZONE, K FRANK, TS XU, J BRODY, LC COLLINS, FS TI PROGRESS TOWARD ISOLATION OF A BREAST-CANCER SUSCEPTIBILITY GENE, BRCA1 SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID FAMILIAL BREAST; OVARIAN-CANCER; EXON AMPLIFICATION; CHROMOSOME-17Q21; HISTORY; LINKAGE; REGION; RISK C1 UNIV PENN,DEPT GENET,PHILADELPHIA,PA 19104. UNIV MICHIGAN,DEPT GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109. NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. RP WEBER, BL (reprint author), UNIV PENN,DEPT INTERNAL MED,PHILADELPHIA,PA 19104, USA. NR 21 TC 2 Z9 2 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 531 EP 536 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600058 PM 7587109 ER PT J AU LIU, P SEIDEL, N BODINE, D SPECK, N TARLE, S COLLINS, FS AF LIU, P SEIDEL, N BODINE, D SPECK, N TARLE, S COLLINS, FS TI ACUTE MYELOID-LEUKEMIA WITH INV(16) PRODUCES A CHIMERIC TRANSCRIPTION FACTOR WITH A MYOSIN HEAVY-CHAIN TAIL SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID ACUTE MYELOMONOCYTIC LEUKEMIA; ABNORMAL EOSINOPHILS; POINT MUTATIONS; NUCLEAR FACTOR; GENE; ENHANCER; CHROMOSOME-16; PROMOTER; BINDING; AML1 C1 DARTMOUTH COLL SCH MED,DEPT BIOCHEM,HANOVER,NH 03755. UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI 48109. RP LIU, P (reprint author), NIH,NATL CTR HUMAN GENOME RES,GENE TRANSFER LAB,BETHESDA,MD 20892, USA. RI Liu, Paul/A-7976-2012 OI Liu, Paul/0000-0002-6779-025X NR 31 TC 29 Z9 29 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 547 EP 553 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600060 PM 7587111 ER PT J AU RONG, S VANDEWOUDE, GF AF RONG, S VANDEWOUDE, GF TI AUTOCRINE MECHANISM FOR MET PROTOONCOGENE TUMORIGENICITY SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID HEPATOCYTE GROWTH-FACTOR; TYROSINE KINASE-ACTIVITY; FACTOR SCATTER FACTOR; CSF-1 RECEPTOR; CELL-LINE; PROTOONCOGENE; FIBROBLASTS; EXPRESSION; ACTIVATION; CANCER RP RONG, S (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 50 TC 8 Z9 10 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 629 EP 636 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600071 PM 7587123 ER PT J AU GOTTESMAN, MM AMBUDKAR, SV NI, B ARAN, JM SUGIMOTO, Y CARDARELLI, CO PASTAN, I AF GOTTESMAN, MM AMBUDKAR, SV NI, B ARAN, JM SUGIMOTO, Y CARDARELLI, CO PASTAN, I TI EXPLOITING MULTIDRUG-RESISTANCE TO TREAT CANCER SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 59th Cold Spring Harbor Symposium on Quantitative Biology - The Molecular Genetics of Cancer CY JUN 01-08, 1994 CL COLD SPRING HARBOR, NY SP NIH, NCI, US DOE, Off Hlth & Environm Res, Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, DuPont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxo, Hoffmann LaRoche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Takeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID BACTERIAL TRANSPORT PROTEINS; P-GLYCOPROTEIN; HUMAN MDR1; INSECT CELLS; BONE-MARROW; GENE; EXPRESSION; CDNA; LOCALIZATION; MODULATION C1 NCI,MOLEC BIOL LAB,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV NEPHROL,BALTIMORE,MD 21205. RP GOTTESMAN, MM (reprint author), NCI,CELL BIOL LAB,BALTIMORE,MD 21205, USA. RI Ambudkar, Suresh/B-5964-2008 NR 35 TC 20 Z9 20 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1994 VL 59 BP 677 EP 683 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA RH966 UT WOS:A1994RH96600077 PM 7587130 ER PT J AU FOLLMANN, D WU, M GELLER, NL AF FOLLMANN, D WU, M GELLER, NL TI TESTING TREATMENT EFFICACY IN CLINICAL-TRIALS WITH REPEATED BINARY MEASUREMENTS AND MISSING OBSERVATIONS SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article; Proceedings Paper CT Workshop on Statistical Issues in Drug Testing and Drug Evaluation CY DEC 02-03, 1991 CL BETHESDA, MD SP NIDA DE BINARY REPEATED MEASURES; LONGITUDINAL DATA; LOGISTIC REGRESSION; RANDOM EFFECTS; RANK TEST ID MULTIPLE ENDPOINTS; MODELS AB This paper discusses different approaches for dealing with clinical trials with a repeated binary endpoint, where many of the binary outcomes are likely to be missing! Ad hoc tests of means and their rank analogues are discussed as well as combination tests, simple imputation, and model-based approaches. The procedures are illustrated with an example of a clinical trial in opiate-dependent individuals. C1 NHLBI,BIOSTAT RES BRANCH,BETHESDA,MD 20892. NR 12 TC 3 Z9 3 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0361-0926 J9 COMMUN STAT THEORY JI Commun. Stat.-Theory Methods PY 1994 VL 23 IS 2 BP 557 EP 574 DI 10.1080/03610929408831272 PG 18 WC Statistics & Probability SC Mathematics GA MU155 UT WOS:A1994MU15500017 ER PT J AU CHEN, TT SIMON, R AF CHEN, TT SIMON, R TI 2 MULTISTEP SELECTION PROCEDURES WITH POSSIBLE SELECTION OF 2 TREATMENTS OF EQUAL PRIOR PREFERENCE SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE DECISION PROCEDURE; SELECTION; COMBINATION DRUG; 2 BY 2 FACTORIAL; SAMPLE SIZE ID COMBINATION AB Dunnett's many-one test to compare several experimental treatment means with a control was extended in our previous paper to a decision procedure for selecting a desirable treatment when there is a strictly monotonic prior preference among the multiple treatments due to other consideration such as toxicity or cost. In this paper, we consider the case where two treatments could have equal prior preference. This formulation includes the problem of comparing a combination with its two components, or the comparison of four arms in a 2 by 2 factorial experiment. Our decision procedures will guarantee a high selection probability for the correct treatment(s) when that selection is appropriate. We establish sample size requirements for our decision procedures which can be applied to clinical trials with normal, binomial, or right censored exponential endpoints. C1 NCI,BIOMETR RES BRANCH,BETHESDA,MD 20892. NR 12 TC 2 Z9 2 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0361-0926 J9 COMMUN STAT THEORY JI Commun. Stat.-Theory Methods PY 1994 VL 23 IS 3 BP 781 EP 801 DI 10.1080/03610929408831286 PG 21 WC Statistics & Probability SC Mathematics GA MX007 UT WOS:A1994MX00700008 ER PT J AU PARK, T AF PARK, T TI MULTIVARIATE REGRESSION-MODELS FOR DISCRETE AND CONTINUOUS REPEATED MEASUREMENTS SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE ESTIMATING EQUATION; GENERALIZED LINEAR MODEL; LEAST SQUARES; LONGITUDINAL DATA; MISSING DATA; REPEATED MEASURES ANALYSIS; SEEMINGLY UNRELATED REGRESSION ID GENERALIZED LINEAR-MODELS; REPEATED MEASURES DESIGNS; LONGITUDINAL DATA; OUTCOMES AB A general class of multivariate regression models is considered for repeated measurements with discrete and continuous outcome variables. The proposed model is based on the seemingly unrelated regression model (Zellner, 1962) and an ''tension of the model of Park and Woolson (1992). The regression parameters of the model axe consistently estimated using the two-stage least squares method. When the outcome variables are multivariate normal, the two-stage estimator reduces to Zellner's two-stage estimator. As a special case, we consider the marginal distribution described by Liang and Zeger (1986). Under this distributional assumption, we show that the two-stage estimator has similar asymptotic properties and comparable small sample properties to Liang and Zeger's estimator. Since the proposed approach is based on the least squares method, however, any distributional assumption is not required for outcome variables. As a results, the proposed estimator is more robust to the marginal distribution of outcomes. C1 HANKUK UNIV FOREIGN STUDIES,DEPT STAT,KYONGGI DO 449791,SOUTH KOREA. NATL INST CHILD HLTH & HUMAN DEV,BIOMETRY & MATH STAT BRANCH,BETHESDA,MD 20892. NR 23 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0361-0926 J9 COMMUN STAT THEORY JI Commun. Stat.-Theory Methods PY 1994 VL 23 IS 6 BP 1547 EP 1564 DI 10.1080/03610929408831339 PG 18 WC Statistics & Probability SC Mathematics GA NJ738 UT WOS:A1994NJ73800001 ER PT J AU TULP, OL MICHAELIS, OE SERVETNICK, DA HANSEN, CT BLACK, DE AF TULP, OL MICHAELIS, OE SERVETNICK, DA HANSEN, CT BLACK, DE TI NONSHIVERING THERMOGENESIS AND OBESITY IN THE DIABETIC WKY/N-CP RAT SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-PHYSIOLOGY LA English DT Article DE WKY/N-CP RATS; ISOENERGETIC DIETS; ADIPOCYTE SIZE; FAT PAD; IBAT; RMR; T4; T4-T3 RATIOS ID BROWN ADIPOSE-TISSUE; CELLULARITY AB Groups of lean and obese WKY/N-cp rats were fed a diet containing 54% carbohydrate, 20% protein, and 16% fat plus other essential nutrients from 1 until 8 months of age. Final body weights of obese were 1.7-fold > lean littermates. The greater BW were associated with marked increases in adipocyte size, number/depot, and fat pad mass in all major white adipose tissue depots. Interscapular brown adipose tissue (IBAT) mass of obese was 3-fold > lean, and represented a greater proportion of final body weight in obese than lean. The greater IBAT obese was due to greater lipid accretion and increased non-fat residue than occurred in lean rats. Resting thermogenesis (RMR) of lean > obese. The thermic response to norepinephrine was proportionately similar in both phenotypes, but the thermic response to cold (4 degrees C) of lean much greater than obese. Serum T4 concentrations and T4:T3 ratios of lean > obese, while serum T3 concentrations were similar in the two phenotypes. These results are consistent with a decreased capacity for NST in the obese phenotype of this stain, and suggest that the decreased NST may be due in part to alterations in BAT-mediated thermoregulation, in combination with impairments in other neuroendocrine or hormonal mediators of thermogenesis. C1 US AGR RES SERV,BELTSVILLE,MD 20705. NIH,VET RESOURCES BRANCH,BETHESDA,MD 20507. RP TULP, OL (reprint author), DREXEL UNIV,COLL ARTS & SCI,DEPT NUTR & FOOD SCI,PHILADELPHIA,PA 19104, USA. NR 20 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 0300-9629 J9 COMP BIOCHEM PHYS A JI Comp. Biochem. Physiol. A-Physiol. PD JAN PY 1994 VL 107 IS 1 BP 195 EP 201 DI 10.1016/0300-9629(94)90293-3 PG 7 WC Biochemistry & Molecular Biology; Physiology; Zoology SC Biochemistry & Molecular Biology; Physiology; Zoology GA MV328 UT WOS:A1994MV32800031 ER PT B AU GOLOMB, D RINZEL, J AF GOLOMB, D RINZEL, J BE Eeckman, FH TI SYNCHRONIZATION AMONG HETEROGENEOUS INHIBITORY RTN NEURONS GLOBALLY COUPLED SO COMPUTATION IN NEURONS AND NEURAL SYSTEMS LA English DT Proceedings Paper CT 2nd Annual Computation and Neural Systems Meeting CY JUL 31-AUG 07, 1993 CL WASHINGTON, DC C1 NIDDK,MATH RES BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC PUBLISHERS PI NORWELL PA 101 PHILIP DRIVE, ASSINIPPI PARK, NORWELL, MA 02061 BN 0-7923-9465-8 PY 1994 BP 27 EP 32 PG 6 WC Computer Science, Artificial Intelligence; Neurosciences SC Computer Science; Neurosciences & Neurology GA BC03V UT WOS:A1994BC03V00005 ER PT S AU CRAGG, GM BOYD, MR GREVER, MR MAYS, TD NEWMAN, DJ SCHEPARTZ, SA AF CRAGG, GM BOYD, MR GREVER, MR MAYS, TD NEWMAN, DJ SCHEPARTZ, SA BE Adams, RP Miller, JS Golenberg, EM Adams, JE TI NATURAL PRODUCT DRUG DISCOVERY AND DEVELOPMENT AT THE NATIONAL-CANCER-INSTITUTE - POLICIES FOR INTERNATIONAL COLLABORATION AND COMPENSATION SO CONSERVATION OF PLANT GENES II: UTILIZATION OF ANCIENT AND MODERN DNA SE MONOGRAPHS IN SYSTEMATIC BOTANY FROM THE MISSOURI BOTANICAL GARDEN LA English DT Proceedings Paper CT 2nd Meeting of the DNA Bank-Net - Conservation of Plant Genes II: Utilization of Ancient and Modern DNA CY APR 05-07, 1993 CL ST LOUIS, MO SP DNA BANK NET C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MISSOURI BOTANICAL GARDEN PI ST LOUIS PA BO BOX 299, ST LOUIS, MO 63166 SN 0161-1542 BN 0-915279-20-7 J9 MONOG SYST BOTAN PY 1994 VL 48 BP 221 EP 232 PG 12 WC Biotechnology & Applied Microbiology; Plant Sciences; Genetics & Heredity SC Biotechnology & Applied Microbiology; Plant Sciences; Genetics & Heredity GA BB95G UT WOS:A1994BB95G00019 ER PT B AU OPTICAN, LM AF OPTICAN, LM BE Fuchs, AF Brandt, T Buttner, U Zee, D TI Control of saccade trajectory by the superior colliculus SO CONTEMPORARY OCULAR MOTOR AND VESTIBULAR RESEARCH: A TRIBUTE TO DAVID A. ROBINSON LA English DT Proceedings Paper CT International Meeting on Contemporary Ocular Motor and Vestibular Research - A Tribute to David A Robinson CY 1993 CL EIBSEE, GERMANY C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. NR 0 TC 33 Z9 33 U1 0 U2 1 PU GEORG THIEME VERLAG PI STUTTGART 30 PA RUDIGERSTR 14, W-7000 STUTTGART 30, GERMANY BN 3-13-100421-5 PY 1994 BP 98 EP 105 PG 8 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA BD64D UT WOS:A1994BD64D00013 ER PT B AU ROBINSON, DL COWIE, RJ AF ROBINSON, DL COWIE, RJ BE Fuchs, AF Brandt, T Buttner, U Zee, D TI Subcortical contributions to head movements in macaques SO CONTEMPORARY OCULAR MOTOR AND VESTIBULAR RESEARCH: A TRIBUTE TO DAVID A. ROBINSON LA English DT Proceedings Paper CT International Meeting on Contemporary Ocular Motor and Vestibular Research - A Tribute to David A Robinson CY 1993 CL EIBSEE, GERMANY C1 NEI,SENSORIMOTOR RES LAB,VISUAL BEHAV SECT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART 30 PA RUDIGERSTR 14, W-7000 STUTTGART 30, GERMANY BN 3-13-100421-5 PY 1994 BP 291 EP 294 PG 4 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA BD64D UT WOS:A1994BD64D00058 ER PT B AU BUSETTINI, C KRAUZLIS, RJ MILES, FA AF BUSETTINI, C KRAUZLIS, RJ MILES, FA BE Fuchs, AF Brandt, T Buttner, U Zee, D TI Short-latency vergence responses SO CONTEMPORARY OCULAR MOTOR AND VESTIBULAR RESEARCH: A TRIBUTE TO DAVID A. ROBINSON LA English DT Proceedings Paper CT International Meeting on Contemporary Ocular Motor and Vestibular Research - A Tribute to David A Robinson CY 1993 CL EIBSEE, GERMANY C1 NEI,BETHESDA,MD 20892. NR 0 TC 5 Z9 5 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART 30 PA RUDIGERSTR 14, W-7000 STUTTGART 30, GERMANY BN 3-13-100421-5 PY 1994 BP 312 EP 319 PG 8 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA BD64D UT WOS:A1994BD64D00061 ER PT B AU KRAUZLIS, RJ LISBERGER, SG AF KRAUZLIS, RJ LISBERGER, SG BE Fuchs, AF Brandt, T Buttner, U Zee, D TI A model of eye velocity memory for pursuit SO CONTEMPORARY OCULAR MOTOR AND VESTIBULAR RESEARCH: A TRIBUTE TO DAVID A. ROBINSON LA English DT Proceedings Paper CT International Meeting on Contemporary Ocular Motor and Vestibular Research - A Tribute to David A Robinson CY 1993 CL EIBSEE, GERMANY C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART 30 PA RUDIGERSTR 14, W-7000 STUTTGART 30, GERMANY BN 3-13-100421-5 PY 1994 BP 418 EP 420 PG 3 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA BD64D UT WOS:A1994BD64D00091 ER PT B AU WALKER, MF FITZGIBBON, EJ GOLDBERG, EE AF WALKER, MF FITZGIBBON, EJ GOLDBERG, EE BE Fuchs, AF Brandt, T Buttner, U Zee, D TI Predictive visual responses in monkey superior Colliculus SO CONTEMPORARY OCULAR MOTOR AND VESTIBULAR RESEARCH: A TRIBUTE TO DAVID A. ROBINSON LA English DT Proceedings Paper CT International Meeting on Contemporary Ocular Motor and Vestibular Research - A Tribute to David A Robinson CY 1993 CL EIBSEE, GERMANY C1 NEI,LAB SENSORIMOTOR,BETHESDA,MD. NR 0 TC 5 Z9 5 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART 30 PA RUDIGERSTR 14, W-7000 STUTTGART 30, GERMANY BN 3-13-100421-5 PY 1994 BP 512 EP 519 PG 8 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA BD64D UT WOS:A1994BD64D00105 ER PT B AU WURTZ, RH MUNOZ, DP AF WURTZ, RH MUNOZ, DP BE Fuchs, AF Brandt, T Buttner, U Zee, D TI Organization of saccade related neurons in monkey superior colliculus SO CONTEMPORARY OCULAR MOTOR AND VESTIBULAR RESEARCH: A TRIBUTE TO DAVID A. ROBINSON LA English DT Proceedings Paper CT International Meeting on Contemporary Ocular Motor and Vestibular Research - A Tribute to David A Robinson CY 1993 CL EIBSEE, GERMANY C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD. NR 0 TC 6 Z9 6 U1 2 U2 2 PU GEORG THIEME VERLAG PI STUTTGART 30 PA RUDIGERSTR 14, W-7000 STUTTGART 30, GERMANY BN 3-13-100421-5 PY 1994 BP 520 EP 527 PG 8 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA BD64D UT WOS:A1994BD64D00106 ER PT J AU SCHOOLER, C AF SCHOOLER, C TI JAPANESE SENSE OF SELF - ROSENBERGER,NR SO CONTEMPORARY SOCIOLOGY-A JOURNAL OF REVIEWS LA English DT Book Review RP SCHOOLER, C (reprint author), NIH,LAB SOCIO ENV STUDIES,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU AMER SOCIOLOGICAL ASSOC PI WASHINGTON PA 1722 N ST NW, WASHINGTON, DC 20036-2981 SN 0094-3061 J9 CONTEMP SOCIOL JI Contemp. Sociol.-J. Rev. PD JAN PY 1994 VL 23 IS 1 BP 24 EP 26 DI 10.2307/2074840 PG 3 WC Sociology SC Sociology GA NE084 UT WOS:A1994NE08400019 ER PT J AU SCHOOLER, C AF SCHOOLER, C TI RE-MADE IN JAPAN - EVERYDAY LIFE AND CONSUMER TASTE IN A CHANGING SOCIETY - TOBIN,JJ SO CONTEMPORARY SOCIOLOGY-A JOURNAL OF REVIEWS LA English DT Book Review RP SCHOOLER, C (reprint author), NIH,LAB SOCIO ENV STUDIES,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU AMER SOCIOLOGICAL ASSOC PI WASHINGTON PA 1722 N ST NW, WASHINGTON, DC 20036-2981 SN 0094-3061 J9 CONTEMP SOCIOL JI Contemp. Sociol.-J. Rev. PD JAN PY 1994 VL 23 IS 1 BP 24 EP 26 DI 10.2307/2074840 PG 3 WC Sociology SC Sociology GA NE084 UT WOS:A1994NE08400020 ER PT J AU GAJDUSEK, DC AF GAJDUSEK, DC TI EARLY INSPIRATION SO CREATIVITY RESEARCH JOURNAL LA English DT Editorial Material RP GAJDUSEK, DC (reprint author), NIH,CENT NERVOUS SYST STUDIES LAB,BLDG 36,ROOM 5B21,BETHESDA,MD 20892, USA. NR 38 TC 0 Z9 0 U1 0 U2 0 PU ABLEX PUBL CORP PI NORWOOD PA 355 CHESTNUT ST, NORWOOD, NJ 07648 SN 1040-0419 J9 CREATIVITY RES J JI Creativ. Res. J. PY 1994 VL 7 IS 3-4 BP 341 EP 349 PG 9 WC Psychology, Educational; Psychology, Multidisciplinary SC Psychology GA QC855 UT WOS:A1994QC85500010 ER PT J AU RUTTIMANN, UE AF RUTTIMANN, UE TI STATISTICAL APPROACHES TO DEVELOPMENT AND VALIDATION OF PREDICTIVE INSTRUMENTS SO CRITICAL CARE CLINICS LA English DT Article RP RUTTIMANN, UE (reprint author), NIAAA,CLIN STUDIES LAB,9000 ROCKVILLE PIKE,BLDG 10,ROOM 3C102,BETHESDA,MD 20892, USA. NR 0 TC 73 Z9 76 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0749-0704 J9 CRIT CARE CLIN JI Crit. Care Clin. PD JAN PY 1994 VL 10 IS 1 BP 19 EP 35 PG 17 WC Critical Care Medicine SC General & Internal Medicine GA MW343 UT WOS:A1994MW34300004 PM 8118728 ER PT J AU PARKER, MM OGNIBENE, FP ROGERS, P SHELHAMER, JH MASUR, H PARRILLO, JE AF PARKER, MM OGNIBENE, FP ROGERS, P SHELHAMER, JH MASUR, H PARRILLO, JE TI SEVERE PNEUMOCYSTIS-CARINII PNEUMONIA PRODUCES A HYPERDYNAMIC PROFILE SIMILAR TO BACTERIAL PNEUMONIA WITH SEPSIS SO CRITICAL CARE MEDICINE LA English DT Article DE PNEUMOCYSTIS CARINII PNEUMONIA; HEMODYNAMICS; BACTERIAL INFECTION; SEPSIS; INFECTION; PNEUMONIA; CARDIAC OUTPUT; HYPOTENSION; HYPOXEMIA; RESPIRATORY FAILURE ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; MYOCARDIAL DEPRESSION; CLINICAL-FEATURES; CONTROLLED TRIAL; SEPTIC SHOCK; CORTICOSTEROIDS AB Objectives: To investigate the effects of Pneumocystis carinii on the cardiovascular system. To compare the hemodynamic data from patients with P. carinii pneumonia with those data from patients with bacterial pneumonia with sepsis. Design: Retrospective, descriptive study of prospectively gathered hemodynamic and clinical data. Setting: Tertiary referral hospital, medical intensive care unit. Patients: Forty-one consecutive patients with severe P. carinii pneumonia and 31 patients with bacterial pneumonia who had invasive hemodynamic monitoring for management of hypotension and/or hypoxemia. Measurements and Main Results: On initial presentation, both groups had a hyperdynamic hemodynamic profile that included tachycardia, an increased cardiac index, and a low systemic vascular resistance index. The mean heart rate of the P. carinii pneumonia patients (113 +/- 3 beats/min) was significantly lower than that of the patients with bacterial pneumonia (126 +/- 4 beats/min). The cardiac index, systemic vascular resistance index, pulmonary vascular resistance index, and pulmonary artery pressures did not differ significantly between the two groups. The patients with bacterial pneumonia had a significantly lower mean left ventricular stroke volume index and stroke work index than the patients with P. carinii pneumonia Conclusion: P. carinii can produce a hyperdynamic hemodynamic profile similar to that seen in patients with bacterial pneumonia with sepsis. C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 15 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1994 VL 22 IS 1 BP 50 EP 54 PG 5 WC Critical Care Medicine SC General & Internal Medicine GA RJ947 UT WOS:A1994RJ94700012 PM 8124974 ER PT B AU CAREY, MA AF CAREY, MA BE Morse, JM TI THE GROUP EFFECT IN FOCUS GROUPS - PLANNING, IMPLEMENTING, AND INTERPRETING FOCUS GROUP RESEARCH SO CRITICAL ISSUES IN QUALITATIVE RESEARCH METHODS LA English DT Proceedings Paper CT Think Tank Symposium on Critical Issues in Qualitative Research Methods CY NOV, 1992 CL SAMUEL MERRITT COLL, OAKLAND, CA HO SAMUEL MERRITT COLL C1 NIH,NATL CTR NURSING RES,BETHESDA,MD 20892. NR 0 TC 122 Z9 127 U1 1 U2 4 PU SAGE PUBLICATIONS INC PI NEWBURY PK PA 2455 TELLER RD, NEWBURY PK, CA 91320 BN 0-8039-5043-8 PY 1994 BP 225 EP 243 PG 19 WC Nursing SC Nursing GA BA86M UT WOS:A1994BA86M00012 ER PT B AU SUNDERLAND, T LITTLE, J CANTILLON, M BAHRO, M MOLCHAN, S AF SUNDERLAND, T LITTLE, J CANTILLON, M BAHRO, M MOLCHAN, S BE Langer, SZ Brunello, N Racagni, G Mendlewicz, J TI Pharmacologic treatment of depression in elderly neuropsychiatric patients SO CRITICAL ISSUES IN THE TREATMENT OF AFFECTIVE DISORDERS SE INTERNATIONAL ACADEMY FOR BIOMEDICAL AND DRUG RESEARCH LA English DT Proceedings Paper CT Collegium-Internationale-Neuro-Psychopharmacologicum Regional Workshop CY MAR 12-14, 1994 CL PARIS, FRANCE SP COLLEGIUM INT NEURO PSYCHOPHARMACOLOGICUM RP NIMH,LCS,GERIATR PSYCHIAT SECT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 3-8055-6032-X J9 INT ACAD B JI Int.Acad.Biomed.Drug Res. PY 1994 VL 9 BP 52 EP 57 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA BC89L UT WOS:A1994BC89L00008 ER PT B AU POTTER, WZ MANJI, HK AF POTTER, WZ MANJI, HK BE Langer, SZ Brunello, N Racagni, G Mendlewicz, J TI Clinical onset of antidepressant action: Implications for new drug development SO CRITICAL ISSUES IN THE TREATMENT OF AFFECTIVE DISORDERS SE INTERNATIONAL ACADEMY FOR BIOMEDICAL AND DRUG RESEARCH LA English DT Proceedings Paper CT Collegium-Internationale-Neuro-Psychopharmacologicum Regional Workshop CY MAR 12-14, 1994 CL PARIS, FRANCE SP COLLEGIUM INT NEURO PSYCHOPHARMACOLOGICUM RP NIMH,EXPTL THERAPEUT BRANCH,CLIN PHARMACOL SECT,BETHESDA,MD 20892, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 3-8055-6032-X J9 INT ACAD B JI Int.Acad.Biomed.Drug Res. PY 1994 VL 9 BP 118 EP 126 PG 9 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA BC89L UT WOS:A1994BC89L00016 ER PT J AU ROTH, BJ AF ROTH, BJ TI MECHANISMS FOR ELECTRICAL-STIMULATION OF EXCITABLE TISSUE SO CRITICAL REVIEWS IN BIOMEDICAL ENGINEERING LA English DT Review DE EXCITATION; ELECTRIC FIELD; ANODE-MAKE; ANODE-BREAK; CATHODE-MAKE; CATHODE-BREAK; ACTIVATING FUNCTION; VIRTUAL ANODE; VIRTUAL CATHODE; MAGNETIC STIMULATION; BIDOMAIN; CRITICAL POINT; DEFIBRILLATION ID OPEN-CHEST DOGS; DIMENSIONAL CARDIAC MODEL; VARYING MAGNETIC-FIELDS; SPINAL-CORD STIMULATION; PERIPHERAL-NERVE; VENTRICULAR-FIBRILLATION; OPTICAL RECORDINGS; ACTION-POTENTIALS; ELECTROMAGNETIC INDUCTION; BUNDLE STIMULATION AB Electric fields excite electrically active tissue by several mechanisms. A long, straight, uniform fiber is polarized by an activating function, proportional to the axial gradient of the axial electric field. During unipolar anodal stimulation, the activating function results in two areas of depolarization (virtual cathodes) that are responsible for anode-make stimulation. During unipolar cathodal stimulation, the virtual anodes can be exploited to produce unidirectional propagation and physiological recruitment of axons. Anode-break stimulation of nerves arises from the intrinsic properties of the sodium channel kinetics; cathode-break stimulation in nerves is anode-break stimulation at a virtual anode. The activating function applies to magnetic stimulation as well as to electric stimulation. Other important mechanisms of stimulation arise if the fiber is terminated, nonuniform, or curved. In the brain, cortical neurons are excited when the electric field is directed from the dendrites toward the axon. Possible mechanisms for cortical excitation are the impedance mismatch between the axon and dendritic tree, and the axon bending as it enters the white matter. Transcranial magnetic stimulation differs from transcranial electric stimulation because during magnetic stimulation the electric field is parallel to the brain surface, whereas during electric stimulation the electric field has components both parallel and perpendicular to the brain surface. Cardiac tissue can be represented by use of the bidomain model. This model predicts that a point-source stimulus results in adjacent areas of depolarized and hyperpolarized tissue. The presence of virtual anodes during cathodal stimulation is analogous to the creation of virtual anodes along a one-dimensional fiber by the activating function. Anode- and cathode-break stimulation both occur in cardiac tissue, but the mechanism may be different than for nerve and may depend on diffusion of depolarization into a previously hyperpolarized region. Electrical stimulation of cardiac tissue can cause reentry through a critical point mechanism. Two mechanisms for defibrillation have been hypothesized: (1) the relatively high junctional resistance between cardiac cells causes each cell to be depolarized on one side and hyperpolarized on the other; and (2) the fiber tracts within the heart behave like individual fibers, with fiber curvature providing a mechanism for polarization. Similarities among nerve, brain, and cardiac stimulation are emphasized. RP ROTH, BJ (reprint author), NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13,ROOM 3W13,BETHESDA,MD 20892, USA. RI Roth, Bradley/A-4920-2008 NR 194 TC 106 Z9 106 U1 2 U2 20 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, STE 1202, NEW YORK, NY 10016-7892 SN 0278-940X J9 CRIT REV BIOMED ENG JI Crit. Rev. Biomed. Eng. PY 1994 VL 22 IS 3-4 BP 253 EP 305 PG 53 WC Engineering, Biomedical SC Engineering GA TF628 UT WOS:A1994TF62800002 PM 8598130 ER PT J AU FERRIOLA, PC NETTESHEIM, P AF FERRIOLA, PC NETTESHEIM, P TI REGULATION OF NORMAL AND TRANSFORMED TRACHEOBRONCHIAL EPITHELIAL-CELL PROLIFERATION BY AUTOCRINE GROWTH-FACTORS SO CRITICAL REVIEWS IN ONCOGENESIS LA English DT Review DE NEOPLASTIC PROGRESSION; LUNG; CARCINOGENESIS; AUTOCRINE GROWTH FACTORS ID LUNG-CANCER; FACTOR-BETA; FACTOR RECEPTOR; FACTOR-ALPHA; TGF-ALPHA; FACTOR-I; NEOPLASTIC PROGRESSION; DIFFERENTIAL EXPRESSION; SIGNAL TRANSDUCTION; FACTOR DEPENDENCE AB Several peptide growth factors have been identified as autocrine regulators of normal tracheobronchial epithelial cells, including the transforming growth factors alpha and beta. Using in vitro tissue culture models of multistep neoplastic transformation as well as cell lines derived from human bronchogenic tumors, a significant number of growth factors have been found to function as autocrine factors for neoplastic tracheobronchial cells as well. In several instances, the regulation of the autocrine pathway is disrupted in neoplastic tracheobroncial cells compared with their normal counterparts. These results indicate that there are multiple aberrations in growth factor pathways occurring in tracheobronchial epithelial cells during progression to the neoplastic phenotype. C1 NIEHS,PULM PATHOBIOL LAB,EPITHELIAL CARCINOGENESIS GRP,RES TRIANGLE PK,NC 27709. NR 81 TC 4 Z9 4 U1 0 U2 0 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 SN 0893-9675 J9 CRIT REV ONCOGENESIS JI Crit. Rev. Oncog. PY 1994 VL 5 IS 2-3 BP 107 EP 120 PG 14 WC Biochemistry & Molecular Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Oncology; Cell Biology GA PT407 UT WOS:A1994PT40700001 PM 7849083 ER PT J AU POPESCU, NC AF POPESCU, NC TI CHROMOSOME FRAGILITY AND INSTABILITY IN HUMAN CANCER SO CRITICAL REVIEWS IN ONCOGENESIS LA English DT Review DE FRAGILE SITE; TRANSLOCATION; DELETION; PROTOONCOGENE; TUMOR SUPPRESSOR GENE; VIRUS INTEGRATION; CHEMICAL CARCINOGENS ID ACUTE PROMYELOCYTIC LEUKEMIA; RETINOIC ACID RECEPTOR; RENAL-CELL CARCINOMA; FLUORESCENCE INSITU HYBRIDIZATION; CHRONIC MYELOGENOUS LEUKEMIA; SISTER CHROMATID EXCHANGES; BREAKPOINT CLUSTER REGION; POLYMERASE CHAIN-REACTION; I-HYPERSENSITIVE SITES; HEPATITIS-B VIRUS AB The development of cancer is a multistep process triggered by physical, chemical, or biological carcinogenic factors, with the progression to an invasive phenotype requiring cumulative genetic alterations. Not all cellular genomic sequences are equally susceptible to carcinogenic factors or involved in pathologically relevant genetic alterations. Because of structural chromatin organization and DNA replication, certain genomic regions exhibit an increased fragility and tendency to recombination. At these regions, called fragile sites, there is a convergence of specific deletions, translocations, chemically induced lesions, and virus integrations. Isolation and cloning of sequences at fragile sites are important to a better understanding of the carcinogenesis process and to development of preventive measures. RP POPESCU, NC (reprint author), NCI,BIOL LAB,BETHESDA,MD 20892, USA. NR 181 TC 37 Z9 38 U1 0 U2 0 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 SN 0893-9675 J9 CRIT REV ONCOGENESIS JI Crit. Rev. Oncog. PY 1994 VL 5 IS 2-3 BP 121 EP 140 PG 20 WC Biochemistry & Molecular Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Oncology; Cell Biology GA PT407 UT WOS:A1994PT40700002 PM 7849084 ER PT J AU FUCHS, BA SANDERS, VM AF FUCHS, BA SANDERS, VM TI THE ROLE OF BRAIN-IMMUNE INTERACTIONS IN IMMUNOTOXICOLOGY SO CRITICAL REVIEWS IN TOXICOLOGY LA English DT Review DE IMMUNOTOXICOLOGY; INDIRECT IMMUNOTOXICITY; PSYCHONEUROIMMUNOLOGY; NEUROIMMUNOMODULATION; BRAIN-IMMUNE INTERACTIONS; SYMPATHETIC NERVOUS SYSTEM; HYPOTHALAMIC-PITUITARY-ADRENAL AXIS ID CORTICOTROPIN-RELEASING-FACTOR; BETA-ADRENERGIC RECEPTORS; SYMPATHETIC NERVOUS-SYSTEM; ANTIBODY-RESPONSE INVITRO; PITUITARY-ADRENAL AXIS; B-CELL ACTIVATION; NATURAL-KILLER CYTOTOXICITY; BLOOD MONONUCLEAR-CELLS; SPLENIC WHITE PULP; CYCLIC-AMP AB Certain xenobiotics (or the metabolites) can damage immunocompetence by directly interacting with one or more of the cells of the immune system and adversely affecting its function. It has also been proposed that xenobiotics may indirectly affect immune function by affecting other organ systems that will in turn affect immunocompetence. This review surveys evidence that supports the existence of a functional link between the brain and the immune system. In addition, we review data that support the concept that a xenobiotic-induced dysfunction in the neuroendocrine system may be associated with an immune dysfunction as well. Such chemicals do not necessarily interact directly with immunocompetent cells but would instead act to disrupt regulatory brain-immune interactions. This class of indirectly acting immunotoxic xenobiotics would not be detected in the typical in vitro screening assays. C1 NIEHS,RES TRIANGLE PK,NC 27709. RP FUCHS, BA (reprint author), VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOL,BOX 980613 MCV STN,RICHMOND,VA 23298, USA. NR 201 TC 27 Z9 27 U1 2 U2 2 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, JOURNALS CUSTOMER SERVICE, BOCA RATON, FL 33431 SN 1040-8444 J9 CRIT REV TOXICOL JI Crit. Rev. Toxicol. PY 1994 VL 24 IS 2 BP 151 EP 176 DI 10.3109/10408449409049309 PG 26 WC Toxicology SC Toxicology GA NJ749 UT WOS:A1994NJ74900002 PM 8037843 ER PT J AU WOLFFE, AP AF WOLFFE, AP TI INSULATING CHROMATIN SO CURRENT BIOLOGY LA English DT Note ID HAIRY-WING PROTEIN; DROSOPHILA-MELANOGASTER; GENE; TRANSCRIPTION; EXPRESSION; BOUNDARIES; REPRESSION; SUPPRESSOR; ENHANCER; ASSAY RP WOLFFE, AP (reprint author), NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892, USA. NR 17 TC 36 Z9 36 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD JAN 1 PY 1994 VL 4 IS 1 BP 85 EP 87 DI 10.1016/S0960-9822(00)00022-1 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MY541 UT WOS:A1994MY54100021 PM 7922323 ER PT J AU VARMA, A KWONCHUNG, KJ AF VARMA, A KWONCHUNG, KJ TI FORMATION OF A MINICHROMOSOME IN CRYPTOCOCCUS-NEOFORMANS AS A RESULT OF ELECTROPORATIVE TRANSFORMATION SO CURRENT GENETICS LA English DT Article DE TRANSFORMATION; MINICHROMOSOME; YEAST; CRYPTOCOCCUS NEOFORMANS ID SCHIZOSACCHAROMYCES-POMBE; SACCHAROMYCES-CEREVISIAE; ARTIFICIAL CHROMOSOMES; GENETIC-ANALYSIS; HIGH-FREQUENCY; DNA FRAGMENTS; YEAST; CONSTRUCTION; URA5; MUTANTS AB A minichromosome of approximately 270 kilobases was generated following complementation of a ura5 mutant strain of C. neoformans with the plasmid pURA5g2. This is the first report of the in-vivo generation of a minichromosome by the method of electroporative transformation. The minichromosome occurred at a relatively high (>20%) frequency in transformants that were stable for uracil protoprophy. The minichromosome was maintained in linear form as a large extrachromosomal element of the normal karyotype. Gel-purified DNA from the minichromosome readily transformed the ura5 mutant of C. neoformans. Southern-blot analysis of the minichromosome revealed the presence of multiple copies of the URA5 gene and ribosomal DNA sequences in addition to containing telomere-like sequence rep eats. The minichromosome was transmitted through mitosis and meiosis with extremely-high fidelity. RP VARMA, A (reprint author), NIAID,CLIN INVEST LAB,CLIN MYCOL SECT,BLDG 10,BETHESDA,MD 20892, USA. NR 32 TC 18 Z9 18 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0172-8083 J9 CURR GENET JI Curr. Genet. PY 1994 VL 26 IS 1 BP 54 EP 61 DI 10.1007/BF00326305 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA NT717 UT WOS:A1994NT71700009 PM 7954897 ER PT B AU DAYTON, DH AF DAYTON, DH BE Cosmi, EV DiRenzo, GC TI NEW TECHNOLOGIES FOR BIRTH DEFECTS AND GENETIC DISEASES SO CURRENT PROGRESS IN PERINATAL MEDICINE LA English DT Proceedings Paper CT 2nd World Congress of Perinatal Medicine CY SEP 19-24, 1993 CL ROME, ITALY SP CNR, UNIV LA SAPIENZA ROMW, ITALIAN MINIST UNIV SCI & TECHNOL RES, ITALIAN MINIST HLTH, WHO, INT FEDERAT OBSTET & GYNECOL, INT CONFEDERAT MIDWIVES, MOTHER & CHILD INT, MARCH DIMES DEFECTS FDN, INT FDN FRATEBENEFRATELLI, ROME, EUROPEAN COMMUNITY CONCERTED ACT PROJECTS, LAZIO DIST HLTH AUTHORITY C1 NICHHD,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 BN 1-85070-560-7 PY 1994 BP 187 EP 192 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA BC49F UT WOS:A1994BC49F00028 ER PT B AU YAFFE, SJ WILLINGER, M AF YAFFE, SJ WILLINGER, M BE Cosmi, EV DiRenzo, GC TI SUDDEN INFANT DEATH SYNDROME PROGRAM AT THE NATIONAL-INSTITUTE-OF-CHILD-HEALTH-AND-HUMAN-DEVELOPMENT SO CURRENT PROGRESS IN PERINATAL MEDICINE LA English DT Proceedings Paper CT 2nd World Congress of Perinatal Medicine CY SEP 19-24, 1993 CL ROME, ITALY SP CNR, UNIV LA SAPIENZA ROMW, ITALIAN MINIST UNIV SCI & TECHNOL RES, ITALIAN MINIST HLTH, WHO, INT FEDERAT OBSTET & GYNECOL, INT CONFEDERAT MIDWIVES, MOTHER & CHILD INT, MARCH DIMES DEFECTS FDN, INT FDN FRATEBENEFRATELLI, ROME, EUROPEAN COMMUNITY CONCERTED ACT PROJECTS, LAZIO DIST HLTH AUTHORITY 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 BN 1-85070-560-7 PY 1994 BP 723 EP 730 PG 8 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA BC49F UT WOS:A1994BC49F00103 ER PT B AU CATZ, C WILLINGER, M AF CATZ, C WILLINGER, M BE Cosmi, EV DiRenzo, GC TI EVALUATION OF HOME MONITORING FOR INFANTS AT HIGH RISK FOR SIDS SO CURRENT PROGRESS IN PERINATAL MEDICINE LA English DT Proceedings Paper CT 2nd World Congress of Perinatal Medicine CY SEP 19-24, 1993 CL ROME, ITALY SP CNR, UNIV LA SAPIENZA ROMW, ITALIAN MINIST UNIV SCI & TECHNOL RES, ITALIAN MINIST HLTH, WHO, INT FEDERAT OBSTET & GYNECOL, INT CONFEDERAT MIDWIVES, MOTHER & CHILD INT, MARCH DIMES DEFECTS FDN, INT FDN FRATEBENEFRATELLI, ROME, EUROPEAN COMMUNITY CONCERTED ACT PROJECTS, LAZIO DIST HLTH AUTHORITY 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 BN 1-85070-560-7 PY 1994 BP 731 EP 736 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA BC49F UT WOS:A1994BC49F00104 ER PT J AU DONOVAN, PJ AF DONOVAN, PJ TI GROWTH-FACTOR REGULATION OF MOUSE PRIMORDIAL GERM-CELL DEVELOPMENT SO CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY, VOL 29 SE CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY LA English DT Review ID LEUKEMIA-INHIBITORY FACTOR; EMBRYONIC STEM-CELLS; TYROSINE KINASE RECEPTOR; IL-6 SIGNAL TRANSDUCER; KIT-LIGAND EXPRESSION; C-KIT; CARCINOMA-CELLS; W-LOCUS; OLIGODENDROCYTE DEVELOPMENT; BLASTOCYST IMPLANTATION RP DONOVAN, PJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 119 TC 90 Z9 96 U1 1 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0070-2153 J9 CURR TOP DEV BIOL PY 1994 VL 29 BP 189 EP 225 DI 10.1016/S0070-2153(08)60551-7 PG 37 WC Biochemistry & Molecular Biology; Developmental Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Developmental Biology; Genetics & Heredity GA BD99G UT WOS:A1994BD99G00006 PM 7530182 ER PT S AU WAKATSUKI, Y NEURATH, MF STROBER, W AF WAKATSUKI, Y NEURATH, MF STROBER, W BE Tsuchiya, M Yodoi, J Hibi, T Miura, S TI CROSS-LINKING CD40 BY RECOMBINANT MURINE LIGANDS INDUCES B-CELL PROLIFERATION AND DIRECTS ISOTYPE DIFFERENTIATION SO CURRENT TOPICS IN MUCOSAL IMMUNOLOGY 1993 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT Tokyo International Symposium on Mucosal Immunology 1993 CY AUG 25-27, 1993 CL TOKYO, JAPAN C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0-444-81586-4 J9 INT CONGR SER PY 1994 VL 1047 BP 75 EP 81 PG 7 WC Immunology SC Immunology GA BA04H UT WOS:A1994BA04H00009 ER PT S AU KITANI, A STROBER, W AF KITANI, A STROBER, W BE Tsuchiya, M Yodoi, J Hibi, T Miura, S TI DIFFERENTIAL REGULATION OF GERM-LINE AND MATURE TRANSCRIPTS IN HUMAN-IGA SUBCLASS DIFFERENTIATION SO CURRENT TOPICS IN MUCOSAL IMMUNOLOGY 1993 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT Tokyo International Symposium on Mucosal Immunology 1993 CY AUG 25-27, 1993 CL TOKYO, JAPAN C1 NIAID,MUCOSAL IMMUN SECT,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0-444-81586-4 J9 INT CONGR SER PY 1994 VL 1047 BP 237 EP 240 PG 4 WC Immunology SC Immunology GA BA04H UT WOS:A1994BA04H00036 ER PT B AU LEE, YH GONZALEZ, FJ AF LEE, YH GONZALEZ, FJ BE Lechner, MC TI MECHANISMS OF LIVER-SPECIFIC EXPRESSION OF THE CYP2D5 GENE SO CYTOCHROME P450: BIOCHEMISTRY, BIOPHYSICS AND MOLECULAR BIOLOGY LA English DT Proceedings Paper CT 8th International Conference on Cytochrome P450: Biochemistry, Biophysics and Molecular Biology CY OCT 24-28, 1993 CL CALOUSTE GULBENKIAN FDN, LISBON, PORTUGAL SP INT UNION BIOCHEM & MOLEC BIOL, JUNTA NACL INVESTIGAC CIENT & TECNOL HO CALOUSTE GULBENKIAN FDN RP LEE, YH (reprint author), NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN LIBBEY EUROTEXT LTD PI MONTROUGE PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE BN 2-7420-0050-X PY 1994 BP 59 EP 65 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA BA85R UT WOS:A1994BA85R00008 ER PT B AU NEGISHI, M IWASAKI, M SUEYOSHI, T DARDEN, TA PEDERSEN, LG AF NEGISHI, M IWASAKI, M SUEYOSHI, T DARDEN, TA PEDERSEN, LG BE Lechner, MC TI MOLECULAR ENGINEERING STEROID HYDROXYLASE-ACTIVITY OF MAMMALIAN P450S SO CYTOCHROME P450: BIOCHEMISTRY, BIOPHYSICS AND MOLECULAR BIOLOGY LA English DT Proceedings Paper CT 8th International Conference on Cytochrome P450: Biochemistry, Biophysics and Molecular Biology CY OCT 24-28, 1993 CL CALOUSTE GULBENKIAN FDN, LISBON, PORTUGAL SP INT UNION BIOCHEM & MOLEC BIOL, JUNTA NACL INVESTIGAC CIENT & TECNOL HO CALOUSTE GULBENKIAN FDN RP NEGISHI, M (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN LIBBEY EUROTEXT LTD PI MONTROUGE PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE BN 2-7420-0050-X PY 1994 BP 225 EP 232 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA BA85R UT WOS:A1994BA85R00036 ER PT B AU OSAWA, Y DAVILA, JC MEYER, CA NAKATSUKA, M AF OSAWA, Y DAVILA, JC MEYER, CA NAKATSUKA, M BE Lechner, MC TI MECHANISM-BASED INACTIVATION OF NITRIC-OXIDE SYNTHASE, A P450 LIKE ENZYME, BY XENOBIOTICS SO CYTOCHROME P450: BIOCHEMISTRY, BIOPHYSICS AND MOLECULAR BIOLOGY LA English DT Proceedings Paper CT 8th International Conference on Cytochrome P450: Biochemistry, Biophysics and Molecular Biology CY OCT 24-28, 1993 CL CALOUSTE GULBENKIAN FDN, LISBON, PORTUGAL SP INT UNION BIOCHEM & MOLEC BIOL, JUNTA NACL INVESTIGAC CIENT & TECNOL HO CALOUSTE GULBENKIAN FDN RP OSAWA, Y (reprint author), NHLBI,CHEM PHARMACOL LAB,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU JOHN LIBBEY EUROTEXT LTD PI MONTROUGE PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE BN 2-7420-0050-X PY 1994 BP 459 EP 462 PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA BA85R UT WOS:A1994BA85R00074 ER PT J AU ROBINSON, WP CHRISTIAN, SL LEDBETTER, DH SCHINZEL, AA AF ROBINSON, WP CHRISTIAN, SL LEDBETTER, DH SCHINZEL, AA TI RECOMBINATION IN THE PERICENTROMERIC REGION OF CHROMOSOME 15Q SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 INST MED GENET,ZURICH,SWITZERLAND. NATL CTR HUMAN GENOME RES,BETHESDA,MD. RI Robinson, Wendy/I-9590-2014 OI Robinson, Wendy/0000-0002-2010-6174 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 1 BP 18 EP 18 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NQ631 UT WOS:A1994NQ63100012 ER PT J AU SUTCLIFFE, JS NAKAO, M MUTIRANGURA, A CHRISTIAN, S LEDBETTER, DH BEAUDET, AL AF SUTCLIFFE, JS NAKAO, M MUTIRANGURA, A CHRISTIAN, S LEDBETTER, DH BEAUDET, AL TI PHYSICAL MAPPING AND ISOLATION OF EXPRESSED SEQUENCES IN THE PRADER-WILLI ANGELMAN CRITICAL REGION OF CHROMOSOME 15Q11-]Q13 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOWARD HUGHES MED INST,HOUSTON,TX. NATL CTR HUMAN GENOME RES,BETHESDA,MD. RI Mutirangura, Apiwat /C-8197-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 1 BP 19 EP 19 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NQ631 UT WOS:A1994NQ63100015 ER PT J AU CHRISTIAN, SL ROBINSON, WP MUTIRANGURA, A NAKAO, M BEAUDET, AL LEDBETTER, DH AF CHRISTIAN, SL ROBINSON, WP MUTIRANGURA, A NAKAO, M BEAUDET, AL LEDBETTER, DH TI FINE MAPPING OF 8 ADDITIONAL SHORT TANDEM REPEATS (STRS) AND EXPANSION OF THE YAC CONTIG WITHIN THE PRADER-WILLI-ANGELMAN-SYNDROME CRITICAL REGION ON CHROMOSOME-15Q11.2-]Q12 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NATL CTR HUMAN GENOME RES,BETHESDA,MD. UNIV ZURICH,INST MED GENET,ZURICH,SWITZERLAND. CHULALONGKORN UNIV,FAC MED,DEPT ANAT,BANGKOK 10330,THAILAND. BAYLOR COLL MED,INST MOLEC GENET,HOUSTON,TX 77030. BAYLOR COLL MED,HOWARD HUGHES MED INST,HOUSTON,TX 77030. RI Mutirangura, Apiwat /C-8197-2009; Robinson, Wendy/I-9590-2014 OI Robinson, Wendy/0000-0002-2010-6174 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 1 BP 21 EP 21 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NQ631 UT WOS:A1994NQ63100021 ER PT J AU RICHARD, I BROUX, O CHIANNIKULCHAI, N FOUGEROUSSE, F ALLAMAND, V BOURG, N BRENGUIER, L DEVAUD, C PASTURAUD, P ROUDAUT, C POLYMEROPOULOS, M SCHULTZ, R COHEN, D BECKMANN, JS AF RICHARD, I BROUX, O CHIANNIKULCHAI, N FOUGEROUSSE, F ALLAMAND, V BOURG, N BRENGUIER, L DEVAUD, C PASTURAUD, P ROUDAUT, C POLYMEROPOULOS, M SCHULTZ, R COHEN, D BECKMANN, JS TI REGIONAL LOCALIZATION OF HUMAN-CHROMOSOME-15 LOCI SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 GENETHON,F-91000 EVRY,FRANCE. CTR ETUD POLYMORPHISME HUMAIN,F-75010 PARIS,FRANCE. ST ELIZABETH HOSP,NIH,WASHINGTON,DC. UNIV TEXAS,SOUTHWESTERN MED CTR,DALLAS,TX 75235. RI Richard, isabelle/J-8298-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 1 BP 22 EP 22 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NQ631 UT WOS:A1994NQ63100022 ER PT J AU WANG, MG YI, H HILFIKER, H CARAFOLI, E STREHLER, EE MCBRIDE, OW AF WANG, MG YI, H HILFIKER, H CARAFOLI, E STREHLER, EE MCBRIDE, OW TI LOCALIZATION OF 2 GENES ENCODING PLASMA-MEMBRANE CA2+ ATPASES ISOFORM-2 (ATP2B2) AND ISOFORM-3 (ATP2B3) TO HUMAN-CHROMOSOME-3P26-]P25 AND HUMAN-CHROMOSOME-XQ28, RESPECTIVELY SO CYTOGENETICS AND CELL GENETICS LA English DT Article; Proceedings Paper CT 2nd International Workshop on Human Chromosome 15 Mapping 1994 CY FEB 18-20, 1994 CL EYNSHAM HALL, EYNSHAM, ENGLAND HO EYNSHAM HALL ID ION MOTIVE ATPASES; HUMAN X-CHROMOSOME; CALCIUM-PUMP; REGION; IDENTIFICATION; SEQUENCE; CLONING; GENOME; DXS15; MAP AB The plasma membrane Ca2+ ATPases (PMCA) represent a highly conserved, widely dispersed, multigene family in eukaryotes consisting of at least four functional genes. The genes for PMCA isoforms 1 and 4 (ATP2B1 and ATP2B4) have been previously localized to human chromosomes 12q21 --> q23 and 1q25 --> q32, respectively. Based upon results of fluorescence in situ hybridization (FISH), analysis of somatic cell hybrids, and genetic linkage analyses, we now report localization of ATP2B3 (PMCA isoform 3) to human chromosome Xq28, and confirm the recent localization of ATP2B2 (PMCA isoform 2) to chromosome 3p26 --> p25. In contrast to ATP2B1 and ATP2B4, recent studies have suggested tissue specific regulation of expression of both ATP2B2 and ATP2B3 particularly in the nervous system. The genes for several neurological and neuromuscular diseases have been assigned to the distal portion of Xq, and ATP2B3 is a candidate gene for these diseases. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. ETH ZURICH,BIOCHEM LAB,ZURICH,SWITZERLAND. RI Carafoli, Ernesto/K-5192-2016 OI Carafoli, Ernesto/0000-0002-7826-0094 NR 33 TC 34 Z9 37 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 1 BP 41 EP 45 DI 10.1159/000133794 PG 5 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NQ631 UT WOS:A1994NQ63100028 PM 8187550 ER PT J AU WANG, MG ZAKUT, R YI, H ROSENBERG, S MCBRIDE, OW AF WANG, MG ZAKUT, R YI, H ROSENBERG, S MCBRIDE, OW TI LOCALIZATION OF THE MAGE1 GENE ENCODING A HUMAN-MELANOMA ANTIGEN TO CHROMOSOME XQ28 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID FAMILIAL MELANOMA; LOCUS AB MAGE1 encodes a tumor specific antigen MZ2-E that elicited a cytotoxic T lymphocytic response (CTL) in the patient from whom it was derived. In this study, cDNA and genomic probes have been used to localize this gene by Southern analysis of a human-rodent somatic cell hybrid panel. The probes detect a small multigene family, and both MAGE1 and several other members of this family are located on the long arm of the human X chromosome. A cosmid with a 12-kb insert including the entire MAGE1 gene was biotinylated and used to further localize the gene to Xq28 by in situ hybridization of metaphase spreads. The function of this antigen in normal cells and tumor cells currently remains unclear. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 18 TC 16 Z9 16 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 2 BP 116 EP 119 DI 10.1159/000133810 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NX883 UT WOS:A1994NX88300008 PM 8039421 ER PT J AU DRACOPOLI, NC BRUNS, GAP BRODEUR, GM LANDES, GM MATISE, TC SELDIN, MF VANCE, JM WEITH, A AF DRACOPOLI, NC BRUNS, GAP BRODEUR, GM LANDES, GM MATISE, TC SELDIN, MF VANCE, JM WEITH, A TI REPORT OF THE FIRST INTERNATIONAL WORKSHOP ON HUMAN-CHROMOSOME-1 MAPPING 1994 - HELD ON MARCH 25-27, 1994 AT BETHESDA, MD (USA) SO CYTOGENETICS AND CELL GENETICS LA English DT Review ID CELL LUNG-CANCER; MOUSE CHROMOSOME-3; GENETIC-LINKAGE; ENDOCRINE NEOPLASIA; TYROSINE KINASE; BREAST-CANCER; RECEPTOR GENE; PHYSICAL MAP; SHORT ARM; PRE-B C1 CHILDRENS HOSP,MED CTR,DIV GENET,BOSTON,MA 02115. CHILDRENS HOSP PHILADELPHIA,DEPT ONCOL,PHILADELPHIA,PA. INTEGRATED GENET INC,FRAMINGHAM,MA 01701. UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710. IMP,VIENNA,AUSTRIA. RP DRACOPOLI, NC (reprint author), NIH,NATL CTR HUMAN GENOME RES,49-4A82,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 132 TC 10 Z9 10 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 3 BP 143 EP 165 DI 10.1159/000133816 PG 23 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PD868 UT WOS:A1994PD86800002 ER PT J AU HOUSEAL, TW LEVERONE, B DRACOPOLI, N KLINGER, KW LANDES, GM AF HOUSEAL, TW LEVERONE, B DRACOPOLI, N KLINGER, KW LANDES, GM TI INTEGRATING THE GENETIC AND PHYSICAL MAP OF CHROMOSOME 1P SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 INTEGRATED GENET INC,VIVIGEN,FRAMINGHAM,MA 01701. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 3 BP 168 EP 169 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PD868 UT WOS:A1994PD86800012 ER PT J AU HUSSUSSIAN, C ENGELSTEIN, M JOHNSON, D DRACOPOLI, NC AF HUSSUSSIAN, C ENGELSTEIN, M JOHNSON, D DRACOPOLI, NC TI DEVELOPMENT OF STSS FROM A 1P36-]P35 MICRODISSECTION LIBRARY SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. UNIV MIAMI,DEPT BIOCHEM & MOLEC BIOL,MIAMI,FL 33136. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 3 BP 169 EP 169 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PD868 UT WOS:A1994PD86800014 ER PT J AU MOCK, BA KRALL, M DOSIK, J HOLIDAY, D POTTER, M AF MOCK, BA KRALL, M DOSIK, J HOLIDAY, D POTTER, M TI GENETIC-MAPPING OF TUMOR SUSCEPTIBILITY GENES INVOLVED IN MOUSE PLASMACYTOMAGENESIS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 3 BP 171 EP 171 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PD868 UT WOS:A1994PD86800020 ER PT J AU REINER, O BARAM, I SAPIR, T CARROZZO, R LINDSAY, EA BALDINI, A LEDBETTER, DH CASKEY, CT GALGERBER, O AF REINER, O BARAM, I SAPIR, T CARROZZO, R LINDSAY, EA BALDINI, A LEDBETTER, DH CASKEY, CT GALGERBER, O TI LIS2 GENE AND PSEUDOGENE, LOCATED ON THE SHORT AND LONG ARM OF CHROMOSOME-2 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 WEIZMANN INST SCI,DEPT MOLEC GENET & VIROL,IL-76100 REHOVOT,ISRAEL. TEL AVIV UNIV,SACKLER SCH MED,DEPT HUMAN GENET,TEL AVIV,ISRAEL. INST G GASLINI,MED LAB 3,I-16145 GENOA,ITALY. BAYLOR COLL MED,INST MOLEC GENET,HOUSTON,TX 77030. NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 243 EP 243 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500015 ER PT J AU BEIER, DR ELLIOT, R TAYLOR, BA MOCK, B NADEAU, JH AF BEIER, DR ELLIOT, R TAYLOR, BA MOCK, B NADEAU, JH TI CONSERVATION OF LINKAGE RELATIONSHIPS BETWEEN SUBCHROMOSOMAL REGIONS OF HUMAN-CHROMOSOME-12 AND MOUSE CHROMOSOME-6, CHROMOSOME-10 AND CHROMOSOME-15 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. ROSWELL PK CANC INST,BUFFALO,NY. JACKSON LAB,BAR HARBOR,ME 04609. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 267 EP 267 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500025 ER PT J AU ELKAHLOUN, A SU, YA KRIZMAN, D DEJONG, P MELTZER, PS AF ELKAHLOUN, A SU, YA KRIZMAN, D DEJONG, P MELTZER, PS TI PHYSICAL AND EXPRESSION MAP FOR THE 12Q13-]Q15 REGION AMPLIFIED IN MESENCHYMAL TUMORS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,BETHESDA,MD 20892. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 268 EP 268 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500028 ER PT J AU FORUS, A SCHMITT, JM PEDEUTOUR, F TURCCAREL, C MELTZER, P FODSTAD, O MYKLEBOST, O AF FORUS, A SCHMITT, JM PEDEUTOUR, F TURCCAREL, C MELTZER, P FODSTAD, O MYKLEBOST, O TI AMPLIFICATION OF 12Q13-]Q14 IN HUMAN SARCOMA - IS THERE A COMMON SELECTIVE GENE, OR ARE DIFFERENT MECHANISMS IMPORTANT IN DIFFERENT SETS OF TUMORS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract ID MDM2; CHROMOSOME-12; REGION C1 NORWEGIAN RADIUM HOSP,INST CANC RES,DEPT TUMOR BIOL,N-0310 OSLO,NORWAY. FAC MED NICE,CNRS,URA 1462,CANC CYTOGENET LAB,F-06034 NICE,FRANCE. NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,MOLEC CYTOGENET SECT,BETHESDA,MD 20892. RI Myklebost, Ola/E-9335-2010 OI Myklebost, Ola/0000-0002-2866-3223 NR 8 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 269 EP 269 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500031 ER PT J AU POLYMEROPOULOUS, MH AF POLYMEROPOULOUS, MH TI 32 EXPRESSED SEQUENCE TAGS ON CHROMOSOME-12 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 273 EP 273 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500043 ER PT J AU HULSEBOS, TJM MARCHUK, D CUMMINGS, LM COPELAND, NG THOMAS, G AF HULSEBOS, TJM MARCHUK, D CUMMINGS, LM COPELAND, NG THOMAS, G TI NF1-CRYSTALLIN AND BETA-CRYSTALLIN RELATED GENES ON HUMAN-CHROMOSOME-22 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV AMSTERDAM,ACAD MED CTR,INST HUMAN GENET,1105 AZ AMSTERDAM,NETHERLANDS. UNIV MICHIGAN,SCH MED,DEPT RADIAT ONCOL,ANN ARBOR,MI. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,FREDERICK,MD 21702. INST CURIE,TUMOR GENET LAB,PARIS,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 287 EP 287 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500057 ER PT J AU KRIZMAN, DB HOFMANN, TA AF KRIZMAN, DB HOFMANN, TA TI IDENTIFICATION OF GENES USING 3' TERMINAL EXON TRAPPING SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 67 IS 4 BP 396 EP 397 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA PM375 UT WOS:A1994PM37500206 ER PT J AU JANNE, PA DUTRA, AS DRACOPOLI, NC CHARNAS, LR PUCK, JM NUSSBAUM, RL AF JANNE, PA DUTRA, AS DRACOPOLI, NC CHARNAS, LR PUCK, JM NUSSBAUM, RL TI LOCALIZATION OF THE 75-KDA INOSITOL POLYPHOSPHATE-5-PHOSPHATASE (INPP5B) TO HUMAN-CHROMOSOME BAND-1P34 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID HUMAN-PLATELETS; EXPRESSION AB The 75-kDa (type II) inositol polyphosphate-5-phosphatase, originally described in platelets, is one of at least three known enzymes capable of dephosphorylating inositol-1,4,5-trisphosphate (IP3) to inositol-1,4-bisphosphate (IP2). To further characterize these enzymatic forms, we have mapped the gene (INPP5B) coding for the 75-kDa type II enzyme, Using a combination of human x rodent somatic cell hybrids and fluorescence in situ hybridization, we have determined that this gene maps to human chromosome band 1p34. C1 NIH,NATL CTR HUMAN GENOME RES,GENET DIS RES LAB,BLDG 49-4A72,BETHESDA,MD 20892. NICHHD,BETHESDA,MD. UNIV PENN,SCH MED,DEPT GENET,PHILADELPHIA,PA 19104. FU NHGRI NIH HHS [R01-HG00233]; NICHD NIH HHS [R01-HD23245]; NIGMS NIH HHS [T32-GM07170] NR 13 TC 6 Z9 6 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 66 IS 3 BP 164 EP 166 DI 10.1159/000133691 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NC702 UT WOS:A1994NC70200005 PM 8125013 ER PT J AU GREENBAUM, IF GUNN, SJ SMITH, SA MCALLISTER, BF HALE, DW BAKER, RJ ENGSTROM, MD HAMILTON, MJ MODI, WS ROBBINS, LW ROGERS, DS WARD, OG DAWSON, WD ELDER, FFB LEE, MR PATHAK, S STANGL, FB AF GREENBAUM, IF GUNN, SJ SMITH, SA MCALLISTER, BF HALE, DW BAKER, RJ ENGSTROM, MD HAMILTON, MJ MODI, WS ROBBINS, LW ROGERS, DS WARD, OG DAWSON, WD ELDER, FFB LEE, MR PATHAK, S STANGL, FB TI CYTOGENETIC NOMENCLATURE OF DEER MICE, PEROMYSCUS (RODENTIA) - REVISION AND REVIEW OF THE STANDARDIZED KARYOTYPE - REPORT OF THE COMMITTEE-FOR-THE-STANDARDIZATION-OF-CHROMOSOMES-OF-PEROMYSCUS SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID EVOLUTIONARY RELATIONSHIPS; SYSTEMATIC IMPLICATIONS; PERICENTRIC-INVERSION; PRIMITIVE KARYOTYPE; PACIFIC-NORTHWEST; SEX-CHROMOSOMES; CRICETIDAE; MOUSE; HETEROCHROMATIN; BOYLII AB A revision of the standardized karyotype of deer mice (Peromyscus) is presented. This revision addresses short-comings of the original standardization, contains a substantial increase in the number of G-band markers and provides a nomenclature for the G-bands of each autosome and the X chromosome. Using the revised standardized karyotype, we specify the particular G-bands or patterns that identify each chromosome and catalog the more problematic chromosome identifications and likely misidentifications. For each chromosome, we present an overview of previously reported variation in euchromatic arrangement and heterochromatic constitution. We then review previous applications of the standardized karyotype and summarize the predominant findings from cytogenetic and cytosystematic studies of Peromyscus and related taxa. C1 PAN AMER UNIV,DEPT BIOL,EDINBURG,TX 78539. TEXAS A&M UNIV,DEPT BIOL,KINGSVILLE,TX. UNIV ROCHESTER,DEPT BIOL,ROCHESTER,NY 14627. YALE UNIV,DEPT BIOL,NEW HAVEN,CT 06520. TEXAS TECH UNIV,DEPT BIOL,LUBBOCK,TX 79409. TEXAS TECH UNIV MUSEUM,LUBBOCK,TX 79409. ROYAL ONTARIO MUSEUM,DEPT MAMMOL,TORONTO M5S 2C6,ONTARIO,CANADA. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD. SW MISSOURI STATE UNIV,DEPT BIOL,SPRINGFIELD,MO 65802. BRIGHAM YOUNG UNIV,DEPT ZOOL,PROVO,UT 84602. UNIV ARIZONA,DEPT ECOL & EVOLUT BIOL,TUCSON,AZ 85721. UNIV S CAROLINA,DEPT BIOL,COLUMBIA,SC 29208. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,HOUSTON,TX 77225. UNIV TEXAS,MD ANDERSON HOSP & TUMOR INST,DEPT CELL BIOL,HOUSTON,TX 77030. MIDWESTERN STATE UNIV,DEPT BIOL,WICHITA FALLS,TX 76308. RP GREENBAUM, IF (reprint author), TEXAS A&M UNIV,DEPT BIOL,COLLEGE STN,TX 77843, USA. RI McAllister, Bryant/A-3015-2008 FU NIGMS NIH HHS [GM-27014] NR 70 TC 27 Z9 28 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 66 IS 3 BP 181 EP 195 DI 10.1159/000133696 PG 15 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NC702 UT WOS:A1994NC70200010 PM 8125018 ER PT J AU MATHERN, P GOLDMUNTZ, EA DU, Y ZHA, H CASH, JM CROFFORD, LJ WILDER, RL REMMERS, EF AF MATHERN, P GOLDMUNTZ, EA DU, Y ZHA, H CASH, JM CROFFORD, LJ WILDER, RL REMMERS, EF TI 9 POLYMORPHIC MARKERS CHARACTERIZED BY POLYMERASE CHAIN-REACTION TECHNIQUES FORM 2 LINKAGE GROUPS ON RAT CHROMOSOME-8 SO CYTOGENETICS AND CELL GENETICS LA English DT Article AB Five genes and four anonymous polymorphic markers, forming two linkage groups, were mapped in Fz intercross progeny of F344/N x LEW/N rats using polymerase chain reaction (PCR) techniques. Both linkage groups were assigned to rat chromosome 8 because they contained genetic loci previously mapped to this chromosome. The first group was comprised of markers for three anonymous loci and two gene loci, thymus cell antigen-1 (Thy1) and tropoelastin (Eln). The second group was comprised of markers for one anonymous locus and three gene loci, cellular retinol binding protein II (Rbp2), matrin F/G (Matr1), and acyl-peptide hydrolase (Apeh). Seven markers (identified by simple sequence repeat associated length polymorphisms) were characterized in an additional 13 inbred rat strains (ACI/N, BN/SsN, BUF/N, LER/N, LOU/ MN, MNR/N, MR/N, SHR/N, SR/Jr, SS/Jr, WBB1/N, WBB2/N, and WKY/N). Two to six alleles were detected for each marker. The reported markers should facilitate genetic mapping and monitoring of inbred rat strains. C1 NIAMS,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD 20892. RI Crofford, Leslie/J-8010-2013 NR 7 TC 10 Z9 10 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 66 IS 4 BP 283 EP 286 DI 10.1159/000133713 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA NK379 UT WOS:A1994NK37900033 PM 7909284 ER PT J AU ALLIKMETS, R KASHUBA, V ZAKHARYEV, V PETROV, N PETTERSSON, B MODI, W DEAN, M KISSELEV, L KLEIN, G ZABAROVSKY, E AF ALLIKMETS, R KASHUBA, V ZAKHARYEV, V PETROV, N PETTERSSON, B MODI, W DEAN, M KISSELEV, L KLEIN, G ZABAROVSKY, E TI MAPPING OF NOTI LINKING CLONES ON CHROMOSOME-3 - TOOLS TO JOIN PHYSICAL AND GENETIC MAPS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. KAROLINSKA INST,S-10401 STOCKHOLM 60,SWEDEN. ROYAL INST TECHNOL,S-10044 STOCKHOLM 70,SWEDEN. NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21701. MOSCOW MOLEC BIOL INST,MOSCOW,RUSSIA. RI Zabarovsky, Eugene/A-6645-2010 NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 35 EP 35 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400002 ER PT J AU CROSSEY, PA RICHARDS, FM LATIF, F JONES, MH PHIPPS, ME FOSTER, K TORY, K LINEHAN, WM AFFARA, NA LERMAN, M ZBAR, B FERGUSONSMITH, MA MAHER, ER AF CROSSEY, PA RICHARDS, FM LATIF, F JONES, MH PHIPPS, ME FOSTER, K TORY, K LINEHAN, WM AFFARA, NA LERMAN, M ZBAR, B FERGUSONSMITH, MA MAHER, ER TI GENETIC-LINKAGE BETWEEN VONHIPPEL-LINDAU (VHL) DISEASE AND 3 MICROSATELLITE POLYMORPHISMS REFINES THE LOCALIZATION OF THE VHL LOCUS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE,ENGLAND. JAPANESE FDN CANC RES,INST CANC,TOKYO 170,JAPAN. NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,FREDERICK,MD 21701. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 35 EP 36 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400004 ER PT J AU HEPPELLPARTON, AC NACHEVA, E LATIF, F LERMAN, MI OGILVIE, D CARTER, N RABBITTS, PH AF HEPPELLPARTON, AC NACHEVA, E LATIF, F LERMAN, MI OGILVIE, D CARTER, N RABBITTS, PH TI THE U2020 PARADOX SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MRC,CLIN ONCOL & RADIOTHERAPEUT UNIT,CAMBRIDGE CB2 2QH,ENGLAND. UNIV CAMBRIDGE,MRC CTR,DEPT HAEMATOL,CAMBRIDGE CB2 2QH,ENGLAND. NCI,IMMUNOBIOL LAB,FREDERICK,MD 21701. ICI PLC,PHARMACEUT,MACCLESFIELD SK10 4TG,CHESHIRE,ENGLAND. UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE CB2 1QP,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 37 EP 38 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400009 ER PT J AU LAFORGIA, S LASOTA, J MODI, W LATIF, F TORY, K ZBAR, B LERMAN, M HUEBNER, K AF LAFORGIA, S LASOTA, J MODI, W LATIF, F TORY, K ZBAR, B LERMAN, M HUEBNER, K TI PHYSICAL AND GENETIC-MAPPING OF OVER 100 3P MARKERS SURROUNDING THE T(3 8) BREAKPOINT SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 JEFFERSON CANC INST,PHILADELPHIA,PA. NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 40 EP 40 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400015 ER PT J AU LERMAN, MI LATIF, F TORY, K GNARRA, J YAO, M DUH, FM ORCUTT, ML STACKHOUSE, T KUZMIN, I MODI, WS GEIL, L SCHMIDT, L ZHOU, FW LI, H WEI, MH GLENN, G RICHARDS, F FERGUSONSMITH, M LEPASLIER, D CHUMAKOV, I COHEN, D CHINAULT, C MAHER, ER LINEHAN, WM ZBAR, B AF LERMAN, MI LATIF, F TORY, K GNARRA, J YAO, M DUH, FM ORCUTT, ML STACKHOUSE, T KUZMIN, I MODI, WS GEIL, L SCHMIDT, L ZHOU, FW LI, H WEI, MH GLENN, G RICHARDS, F FERGUSONSMITH, M LEPASLIER, D CHUMAKOV, I COHEN, D CHINAULT, C MAHER, ER LINEHAN, WM ZBAR, B TI MOLECULAR-CLONING OF THE VONHIPPEL-LINDAU TUMOR-SUPPRESSOR GENE SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702. CTR ETUD POLYMORPHISME HUMAIN,F-75010 PARIS,FRANCE. NCI,SURG BRANCH,BETHESDA,MD 20892. UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE CB2 1QP,ENGLAND. BAYLOR COLL MED,INST MOLEC GENET,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 5 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 41 EP 41 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400018 ER PT J AU PHIPPS, ME RICHARDS, FM AFFARA, NA LATIF, F LEVERSHA, MA FERGUSONSMITH, ME NAKAMURA, Y LERMAN, M ZBAR, B FERGUSONSMITH, MA MAHER, ER AF PHIPPS, ME RICHARDS, FM AFFARA, NA LATIF, F LEVERSHA, MA FERGUSONSMITH, ME NAKAMURA, Y LERMAN, M ZBAR, B FERGUSONSMITH, MA MAHER, ER TI PHYSICAL MAPPING OF CHROMOSOME-3P25-P26 BY FLUORESCENCE IN-SITU HYBRIDIZATION (FISH) SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE,ENGLAND. NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,FREDERICK,MD 21701. JAPANESE FDN CANC RES,INST CANC,TOKYO 170,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 44 EP 44 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400025 ER PT J AU RABBITTS, PH DOUGLAS, J LATIF, F LERMAN, MI JAMES, L GRUNDY, C OGILVIE, D AF RABBITTS, PH DOUGLAS, J LATIF, F LERMAN, MI JAMES, L GRUNDY, C OGILVIE, D TI YAC CONTIG MAPPING OF THE U2020 DELETION SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 MRC,CLIN ONCOL & RADIOTHERAPEUT UNIT,CAMBRIDGE CB2 2QH,ENGLAND. NCI,IMMUNOBIOL LAB,FREDERICK,MD 21701. ICI PLC,APPL PSYCHOL,MACCLESFIELD SK10 4TG,CHESHIRE,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 44 EP 44 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400026 ER PT J AU TORY, K SCHMIDT, L LI, H WEI, MH GEIL, L HUSTAD, T LATIF, F LERMAN, M ZBAR, B AF TORY, K SCHMIDT, L LI, H WEI, MH GEIL, L HUSTAD, T LATIF, F LERMAN, M ZBAR, B TI LINKAGE MAPPING OF 175 LOCI ON HUMAN CHROMOSOME-3 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21701. NCI,FCRDC,IMMUNOBIOL LAB,FREDERICK,MD 21701. NR 0 TC 1 Z9 1 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 47 EP 47 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400033 ER PT J AU LYU, MS ADAMSON, MC ZIMMERMAN, KL KOZAK, CA AF LYU, MS ADAMSON, MC ZIMMERMAN, KL KOZAK, CA TI LINKAGE AND SYNTENY HOMOLOGIES BETWEEN HUMAN CHROMOSOME-7 AND MOUSE CHROMOSOME-2, CHROMOSOME-5, CHROMOSOME-6, CHROMOSOME-10, CHROMOSOME-11, CHROMOSOME-12, AND CHROMOSOME-13 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 71 EP 72 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400066 ER PT J AU DURKIN, AS NIERMAN, WC ZOGHBI, H JONES, C KOZAK, CA MAGLOTT, DR AF DURKIN, AS NIERMAN, WC ZOGHBI, H JONES, C KOZAK, CA MAGLOTT, DR TI CHROMOSOME ASSIGNMENT OF HUMAN BRAIN EXPRESSED SEQUENCE TAGS (ESTS) BY ANALYZING FLUORESCENTLY LABELED PCR PRODUCTS FROM HYBRID CELL PANELS SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID POLYMERASE CHAIN-REACTION; ENDOPLASMIC-RETICULUM; MOUSE CHROMOSOME-4; RAPID ISOLATION; HUMAN GENOME; PROTEIN; GENE; IDENTIFICATION; LOCUS; SUBUNIT AB Sixty-three human brain cDNA sequences were newly assigned to individual human chromosomes. Ten of these were subregionally localized, and one was also mapped in the mouse genome. Four previously reported assignments were refined. PCR primers were designed from expressed sequence tags (ESTs) and tested for specific amplification from human genomic DNA. DNA was then amplified, often in multiplexed PCR reactions, using DNA from somatic cell hybrid mapping panels as templates. The amplification products were identified using an automated fluorescence detection system. Chromosomal assignments were made by discordancy analysis. Thirteen newly localized cDNAs exhibited homology to previously reported sequences. EST01471 was shown to correspond to human microtubule-associated protein 1B (MAP1B), confirming the previous mapping of this gene to human chromosome 5. Other genes tentatively assigned to chromosomes based on these results were a component of the signal peptide receptor of the endoplasmic reticulum (EST00745) and a cyclic AMP-regulated phosphoprotein (EST01041) on chromosome 1, a protein phosphatase 2A 55-kDa regulatory subunit (EST01650) on chromosome 4, an NAD(P) transhydrogenase (EST01744) on chromosome 5, ribosomal proteins L1a or L1b (EST01627) and L18a (EST01583), a brain transcription factor (BF-1, EST00795) on chromosome 14, a milk fat globule membrane-related protein (EST01678) on chromosome 15, a putative peptide initiation factor (EST00675) on chromosome 17, thiosulfate sulfurtransferase (TST) on chromosome 22, and moesin (MSN) (EST00896) and a human equivalent of rat spot 14 (S14) (EST00887) on Xp11 --> cen and Xpter --> p21.3, respectively. C1 AMER TYPE CULTURE COLLECT,DEPT MOLEC BIOL,12301 PARKLAWN DR,ROCKVILLE,MD 20852. ELEANOR ROOSEVELT INST CANC RES,DENVER,CO. AMER TYPE CULTURE COLLECT,DEPT BIOINFORMAT,ROCKVILLE,MD 20852. BAYLOR COLL MED,DEPT PEDIAT,HOUSTON,TX 77030. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 41 TC 22 Z9 25 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 86 EP 91 DI 10.1159/000133606 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400073 PM 8404072 ER PT J AU SATOH, H EBERT, R WISEMAN, RW BARRETT, JC AF SATOH, H EBERT, R WISEMAN, RW BARRETT, JC TI THE RB GENE LOCATES ON CHROMOSOME-15 AT BAND-15Q13 IN THE SYRIAN-HAMSTER SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID MOUSE CHROMOSOMES; CHINESE-HAMSTER; INSITU HYBRIDIZATION; HIGH-RESOLUTION; LOCALIZATION; NOMENCLATURE; CONSERVATION; ASSIGNMENT; CELLS AB The retinoblastoma susceptibility gene, which encodes a nuclear phosphoprotein (Rb), plays an important role in cell-cycle progression in both normal development and tumorigenesis. Using a Syrian hamster cDNA probe homologous to the human retinoblastoma gene (RB), we have localized the gene to chromosome band 15q13 by conventional in situ hybridization. C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. UNIV WURZBURG,INST PHARMACOL & TOXICOL,W-8700 WURZBURG,GERMANY. RP SATOH, H (reprint author), UNIV TOKYO,INST MED SCI,DEPT PATHOL,4-6-1 SHIROKANEDAI,MINATO KU,TOKYO 108,JAPAN. NR 24 TC 5 Z9 5 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 1-2 BP 127 EP 129 DI 10.1159/000133617 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA ME404 UT WOS:A1994ME40400084 PM 8404065 ER PT J AU SHARON, G GARFINKEL, D AF SHARON, G GARFINKEL, D TI DEVELOPMENT OF A TRANSPOSON TAGGING SYSTEM FOR MANIPULATING RECOMBINANT YACS IN SACCHAROMYCES-CEREVISIAE SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FCRDC,MOVABLE GENET ELEMENTS SECT,EUKARYOT GENE EXPRESS LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 3 BP 159 EP 159 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA MJ491 UT WOS:A1994MJ49100004 ER PT J AU BERRETTINI, W FERRARO, T GOLDIN, L DETERAWADLEIGH, S CHOI, H MUNIEC, D NURNBERGER, J GERSHON, E AF BERRETTINI, W FERRARO, T GOLDIN, L DETERAWADLEIGH, S CHOI, H MUNIEC, D NURNBERGER, J GERSHON, E TI A LINKAGE MAP OF CHROMOSOME-18 - EVIDENCE FOR LINKAGE OF MANIC-DEPRESSIVE ILLNESS TO 18P11 MARKERS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,DEPT PSYCHIAT,PHILADELPHIA,PA 19107. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. INDIANA UNIV,INST PSYCHIAT RES,INDIANAPOLIS,IN 46204. NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 3 BP 160 EP 161 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA MJ491 UT WOS:A1994MJ49100007 ER PT J AU ZIMONJIC, DB POPESCU, NC MATSUI, T ITO, M CHIHARA, K AF ZIMONJIC, DB POPESCU, NC MATSUI, T ITO, M CHIHARA, K TI LOCALIZATION OF THE HUMAN CHOLECYSTOKININ-B GASTRIN RECEPTOR GENE (CCKBR) TO CHROMOSOME 11P15.5-]P15.4 BY FLUORESCENCE IN-SITU HYBRIDIZATION SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID CANCER CELLS; CLONING; BINDING; GROWTH; TUMOR; LINES AB A human cholecystokinin-B/gastrin receptor cDNA (CCKBR) has been recently cloned and its transcriptional product has been characterized. The cDNA probe was mapped by fluorescence in situ hybridization to chromosome 11 at bands p15.5 --> p15.4. The localization of this receptor gene provides a useful marker for this region of chromosome 11 permitting the identification of diseases involving the gene and interactions with other genes. C1 KOBE UNIV,SCH MED,DEPT MED,DIV 3,KOBE 650,JAPAN. NCI,BIOL LAB,BETHESDA,MD 20892. RI Matsui, Toshimitsu/E-8065-2010 NR 12 TC 43 Z9 44 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 3 BP 184 EP 185 DI 10.1159/000133628 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA MJ491 UT WOS:A1994MJ49100030 PM 8222757 ER PT J AU DU, Y REMMERS, EF GOLDMUNTZ, EA ZHA, H MATHERN, P CROFFORD, LJ WILDER, RL AF DU, Y REMMERS, EF GOLDMUNTZ, EA ZHA, H MATHERN, P CROFFORD, LJ WILDER, RL TI SIMPLE SEQUENCE REPEAT LENGTH POLYMORPHISMS MAPPED TO RAT CHROMOSOME-11 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID WALL-INDUCED ARTHRITIS; LEWIS RATS; F344 RATS; MOUSE; NORVEGICUS; FRAGMENTS AB Two genes and two anonymous DNA loci were mapped to rat chromosome 11 using F2 intercross progeny of Fischer (F344/N) and Lewis (LEW/N) inbred rats. These four loci formed a single linkage group covering 21.5 cM with the following map order: somatostatin (SST)-D11N161-D11N18-cell surface protein (MOX2). These four loci were typed by PCR-based simple sequence repeat (SSR) length polymorphism detection. For each marker four to seven different alleles were detected using a panel of 13 inbred rat strains (F344/N, LEW/N, BN/SsN, BUF/N, LER/N, MR/N, MNR/N, LOU/MN, ACI/N, WBB1/N, WBB2/N, SHR/N, WKY/N). Comparative gene mapping analysis suggests syntenic conservation between rat chromosome 11 and mouse Chromosome 16. RP DU, Y (reprint author), NIAMSD,ARTHRIT & RHEUMATISM BRANCH,BLDG 10,ROOM 9N228,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013 NR 18 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1994 VL 65 IS 3 BP 186 EP 189 DI 10.1159/000133629 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA MJ491 UT WOS:A1994MJ49100031 PM 8222758 ER PT J AU ANDERSON, PM HANSON, DC HASZ, DE HALET, MR BLAZAR, BR OCHOA, AC AF ANDERSON, PM HANSON, DC HASZ, DE HALET, MR BLAZAR, BR OCHOA, AC TI CYTOKINES IN LIPOSOMES - PRELIMINARY STUDIES WITH IL-1, IL-2, IL-6, GM-CSF AND INTERFERON-GAMMA SO CYTOKINE LA English DT Article DE CYTOKINES; LIPOSOMES; INTERLEUKINS; GM-CSF; INTERFERON ID COLONY-STIMULATING FACTOR; INTERLEUKIN-2 LIPOSOMES; PRIMARY AMINES; FLUOROMETRIC ASSAY; FUNGAL-INFECTIONS; AMPHOTERICIN-B; PROTEINS; MICE; FLUORESCAMINE; TOXICITY C1 UNIV MINNESOTA,DEPT PEDIAT,DIV HEMATOL ONCOL,MINNEAPOLIS,MN. UNIV MINNESOTA,DEPT PEDIAT,DIV BONE MARROW TRANSPLANT,MINNEAPOLIS,MN. NCI,FREDERICK CANC RES CTR,BETHESDA,MD. FU NCI NIH HHS [NCI CA53517] NR 44 TC 65 Z9 65 U1 0 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4666 J9 CYTOKINE JI Cytokine PD JAN PY 1994 VL 6 IS 1 BP 92 EP 101 DI 10.1016/1043-4666(94)90014-0 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA MZ191 UT WOS:A1994MZ19100014 PM 8003640 ER PT B AU NOGUCHI, M RUSSEL, SM LEONARD, WJ AF NOGUCHI, M RUSSEL, SM LEONARD, WJ BE Romagnani, S DelPrete, G Abbas, AK TI COMMON GAMMA-CHAIN (GAMMA-C) - MOLECULAR-BASIS FOR X-LINKED SEVERE COMBINED IMMUNODEFICIENCY SO CYTOKINES: BASIC PRINCIPLES AND PRACTICAL APPLICATIONS SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT 3rd International Conference on Cytokines: Basic Principle and Practical Applications CY MAR 28-30, 1994 CL FLORENCE, ITALY SP ARES SERONO SYMPOSIA RP NOGUCHI, M (reprint author), NHLBI,PULM & MOLEC IMMUNOL SECT,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 88-85974-25-3 J9 CHALL MOD MED PY 1994 VL 8 BP 65 EP 77 PG 13 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BB62K UT WOS:A1994BB62K00010 ER PT B AU SHER, A WYNN, TA DENKERS, EY OSWALD, IP JANKOVIC, D STEVENSON, M SEDER, R CHEEVER, AW GAZZINELLI, RT AF SHER, A WYNN, TA DENKERS, EY OSWALD, IP JANKOVIC, D STEVENSON, M SEDER, R CHEEVER, AW GAZZINELLI, RT BE Romagnani, S DelPrete, G Abbas, AK TI IL-12 DEPENDENT IFN-GAMMA SYNTHESIS - A MAJOR PATHWAY OF INNATE RESISTANCE AND IMMUNOREGULATION IN PARASITIC DISEASE SO CYTOKINES: BASIC PRINCIPLES AND PRACTICAL APPLICATIONS SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT 3rd International Conference on Cytokines: Basic Principle and Practical Applications CY MAR 28-30, 1994 CL FLORENCE, ITALY SP ARES SERONO SYMPOSIA RP SHER, A (reprint author), NIAID,IMMUNOL & CELL BIOL SECT,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-25-3 J9 CHALL MOD MED PY 1994 VL 8 BP 117 EP 126 PG 10 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BB62K UT WOS:A1994BB62K00016 ER PT B AU SHEARER, GM CLERICI, M AF SHEARER, GM CLERICI, M BE Romagnani, S DelPrete, G Abbas, AK TI CELLULAR-IMMUNITY AND A TYPE-1 CYTOKINE PROFILE IN PROTECTION AGAINST HIV AND AIDS SO CYTOKINES: BASIC PRINCIPLES AND PRACTICAL APPLICATIONS SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT 3rd International Conference on Cytokines: Basic Principle and Practical Applications CY MAR 28-30, 1994 CL FLORENCE, ITALY SP ARES SERONO SYMPOSIA RP SHEARER, GM (reprint author), NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ARES-SERONO SYMPOSIA PUBLICATIONS PI ROME PA VIA RAVENNA 8, 00161 ROME, ITALY BN 88-85974-25-3 J9 CHALL MOD MED PY 1994 VL 8 BP 139 EP 145 PG 7 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BB62K UT WOS:A1994BB62K00018 ER PT B AU GRAZIOSI, C GANTT, KR PANTALEO, G FAUCI, AS AF GRAZIOSI, C GANTT, KR PANTALEO, G FAUCI, AS BE Romagnani, S DelPrete, G Abbas, AK TI ANALYSIS OF CYTOKINE EXPRESSION IN PERIPHERAL IN BLOOD AND LYMPH-NODE DURING HIV-INFECTION SO CYTOKINES: BASIC PRINCIPLES AND PRACTICAL APPLICATIONS SE CHALLENGES OF MODERN MEDICINE LA English DT Proceedings Paper CT 3rd International Conference on Cytokines: Basic Principle and Practical Applications CY MAR 28-30, 1994 CL FLORENCE, ITALY SP ARES SERONO SYMPOSIA C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 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 88-85974-25-3 J9 CHALL MOD MED PY 1994 VL 8 BP 147 EP 156 PG 10 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BB62K UT WOS:A1994BB62K00019 ER PT B AU MULLEN, CA AF MULLEN, CA BE Bergmann, L Mitrou, PS TI DEVELOPMENT OF LIVE TUMOR VACCINES USING RETROVIRAL VECTORS FOR TRANSFER OF SUICIDE GENES AND CYTOKINES SO CYTOKINES IN CANCER THERAPY SE CONTRIBUTIONS TO ONCOLOGY LA English DT Proceedings Paper CT 2nd Frankfurt International Cytokine Symposium CY JUN 25-27, 1992 CL FRANKFURT, GERMANY RP MULLEN, CA (reprint author), NCI,DIV CANC BIOLDIAG & CTR,METAB BRANCH,BLDG 10,ROOM GB05,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 3-8055-5809-0 J9 CONTR ONCOL PY 1994 VL 46 BP 260 EP 268 PG 9 WC Oncology SC Oncology GA BA40Z UT WOS:A1994BA40Z00029 ER PT J AU PEPE, S RUGGIERO, A TORTORA, G CIARDIELLO, F GARBI, C YOKOZAKI, H CHOCHUNG, YS CLAIR, T SKALHEGG, BS BIANCO, AR AF PEPE, S RUGGIERO, A TORTORA, G CIARDIELLO, F GARBI, C YOKOZAKI, H CHOCHUNG, YS CLAIR, T SKALHEGG, BS BIANCO, AR TI FLOW-CYTOMETRIC DETECTION OF THE RI-ALPHA SUBUNIT OF TYPE-I CAMP-DEPENDENT PROTEIN-KINASE IN HUMAN-CELLS SO CYTOMETRY LA English DT Note DE IMMUNOFLUORESCENCE; CAMP-DEPENDENT PROTEIN KINASE; CELL CYCLE; HUMAN LYMPHOCYTES; HUMAN MAMMARY CELLS ID MAMMARY EPITHELIAL-CELLS; CYCLIC-AMP ANALOGS; REGULATORY SUBUNIT; GROWTH-CONTROL; MOLECULAR-CLONING; RAT FIBROBLASTS; DIFFERENTIATION; TRANSFORMATION; EXPRESSION; RECEPTOR AB cAMP-dependent protein kinase (PKA) is composed of two genetically distinct catalytic (C) and regulatory (R) subunits. There are two different classes of PKA, designated as type I and type II, which contain distinct R subunits (RI or RII, respectively) but share a common C subunit. Enhanced expression of type I PKA has been correlated with cell proliferation and neoplastic transformation. Detection of the different PKA subunits is usually performed by photoaffinity labeling with 8-N-3-P-32-cAMP or by radioimmunolabeling techniques. Both techniques are time consuming and require a high number of cells and the use of radioactive reagents. Using the MCF-10A normal human mammary cell line infected with a recombinant retroviral vector containing the human RI alpha gene (MCF-10A RI alpha), we have developed a flow-cytometric assay to detect the intracellular content of RI alpha protein in human cells. MCF-10A and MCF-10A RI alpha cells were fixed in 1.5% paraformaldehyde at 37 degrees C for 15 min and permeabilized by methanol and acetone (1:1) at -20 degrees C for 5 min before staining with a specific IgG2a MoAb followed by a FITC-conjugate rabbit-anti mouse IgG. This procedure was also successfully utilized to recognize RI alpha protein content in human peripheral blood lymphocytes. Flow-cytometric detection of the RI alpha subunit in human cells is feasible and allows the study of the role of type I PKA in cell growth and neoplastic transformation. (C) 1994 Wiley-Liss, Inc. C1 FAC MED & CHIRURG 2 NAPOLI,DIPARTIMENTO BIOL & PATOL CELLULARE & MOLEC L CALIFANO,NAPLES,ITALY. NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NATL HOSP NORWAY,INST IMMUNOL & RHEUMATOL,N-0027 OSLO 1,NORWAY. RP PEPE, S (reprint author), FAC MED & CHIRURG 2 NAPOLI,CATTEDRA ONCOL MED,VIA S PANSINI 5,I-80131 NAPLES,ITALY. NR 33 TC 18 Z9 18 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0196-4763 J9 CYTOMETRY JI Cytometry PD JAN 1 PY 1994 VL 15 IS 1 BP 73 EP 79 DI 10.1002/cyto.990150112 PG 7 WC Biochemical Research Methods; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA MT920 UT WOS:A1994MT92000011 PM 8162827 ER PT B AU HENNIGHAUSEN, L AF HENNIGHAUSEN, L BE Rios, MS Sastre, A Juezz, MAP Estrala, A DeBastian, C TI THE MILK GLAND AS BIOREACTOR FOR THERAPEUTIC AND NUTRITIONAL PROTEINS SO DAIRY PRODUCTS IN HUMAN HEALTH AND NUTRITION LA English DT Proceedings Paper CT 1st World Congress of Dairy Products in Human Health and Nutrition CY JUN 07-10, 1993 CL MADRID, SPAIN SP EUROPEAN COMMUNITY C1 NIH,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU A A BALKEMA PI ROTTERDAM PA PO BOX 1675, 3000 BR ROTTERDAM, NETHERLANDS BN 90-5410-359-0 PY 1994 BP 25 EP 29 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA BA67W UT WOS:A1994BA67W00003 ER PT J AU ISHIKAWA, K TAKAGI, S CHOW, LC ISHIKAWA, Y EANES, ED ASAOKA, K AF ISHIKAWA, K TAKAGI, S CHOW, LC ISHIKAWA, Y EANES, ED ASAOKA, K TI BEHAVIOR OF A CALCIUM-PHOSPHATE CEMENT IN SIMULATED BLOOD-PLASMA IN-VITRO SO DENTAL MATERIALS LA English DT Article ID CANAL SEALER-FILLER; P-RICH LAYER; HYDROXYAPATITE CEMENT; GLASS-CERAMICS; APATITE; BONE; CA AB Objectives. The purpose of this study was to gain a better understanding of the integration of calcium phosphate cement (CPC) implants in biological tissue Methods. An in vitro continuous flow system was employed to examine the protracted behavior of disc-shaped specimens of this bioactive material under sustained physiological-like solution conditions. Weight measurement, diametral tensile strength measurement (DTS), scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FTIR), and powder x-ray diffraction (XRD) were used to characterize the CPC samples as a function of immersion time. Results. When CPC was immersed in simulated blood plasma in which the Ca (2.5 mmol/L) and inorganic phosphate (1.0 mmol/L) levels were kept constant, both the weight and DTS of the specimens steadily increased to about 1.5 times their original values over a period of 20 wk. SEM observations showed new precipitate formations in intimate contact with the original CPC surface. FTIR and XRD analyses revealed that the precipitate was a B-type carbonate hydroxyapatite (OHAp), the type of OHAp observed in bone and dentin. On the other hand, the interior of CPC discs did not show an increase in either bulk density or OHAp content. Thus, the increases in weight and DTS are attributal to the OHAp precipitation on the CPC surface. Significance. The results suggest that under in vivo conditions, CPC implants would not dissolve in physiological fluids. OHAp coatings may form on the implants, which may enhance bonding of implants to bone by mechanically strengthening the interface between them. C1 NIST,PAFFENBARGER RES CTR,AM DENT ASSOC HLTH FDN,GAITHERSBURG,MD 20899. UNIV TOKUSHIMA,SCH DENT,DEPT DENT ENGN,TOKUSHIMA 770,JAPAN. NIST,NIDR,BONE RES BRANCH,RES ASSOCIATE PROGRAM,GAITHERSBURG,MD. FU NIDCR NIH HHS [DE05030] NR 25 TC 60 Z9 62 U1 3 U2 11 PU ACAD DENTAL MATERIALS PI DALLAS PA BAYLOR COLLEGE DENTISTRY, 3302 GASTON AVE, DALLAS, TX 75266-0677 SN 0109-5641 J9 DENT MATER JI Dent. Mater. PD JAN PY 1994 VL 10 IS 1 BP 26 EP 32 DI 10.1016/0109-5641(94)90018-3 PG 7 WC Dentistry, Oral Surgery & Medicine; Materials Science, Biomaterials SC Dentistry, Oral Surgery & Medicine; Materials Science GA PG946 UT WOS:A1994PG94600005 PM 7995472 ER PT J AU KARPATI, S AMAGAI, M PRUSSICK, R STANLEY, JR AF KARPATI, S AMAGAI, M PRUSSICK, R STANLEY, JR TI PEMPHIGUS-VULGARIS ANTIGEN IS A DESMOSOMAL DESMOGLEIN SO DERMATOLOGY LA English DT Article; Proceedings Paper CT Tricontinental Symposium on Autoimmune Skin Diseases CY NOV 01, 1993 CL KYOTO, JAPAN SP GLAXO PHARM CO LTD, BAYER YAKUHIN LTD, DAIICHI PHARM CO LTD, DAINIPPON PHARM CO LTD, EISAI PHARM CO LTD, JAPAN BOEHRINGER INGELHEIM CO LTD, JAPAN SHERRING PHARM CO LTD, JAPAN UPJOHN PHARM CO LTD, JAPAN WELLCOME PHARM CO LTD, KAKEN PHARM CO LTD, KISSEI PHARM CO LTD, KOWA PHARM CO LTD, KYOWA HAKKO KOGYO CO LTD, MARUHO CO LTD, MOCHIDA PHARM CO LTD, NIPPON ROCHE KK, NIPPON ZOKI PHARM CO LTD, NOV CO LTD, SAN DOZ PHARM CO LTD, SANKYO PHARM CO LTD, SHISEIDO COSMET CO LTD, SHIONOGI PHARM CO LTD, SS PHARM CO LTD, SUMITOMO PHARM CO LTD, TAKEDA CHEM IND LTD, TANABE PHARM CO LTD, TEIKOKU HORMONE MFG CO LTD, YAMANOUCHI PHARM CO LTD DE PEMPHIGUS VULGARIS ANTIGEN; DESMOSOMES; DESMOGLEIN; CADHERINS ID CELL-ADHESION; ULTRASTRUCTURAL-LOCALIZATION; AUTOANTIBODIES; CADHERIN AB Because pemphigus vulgaris antigen (PVA) is homologous to desmogleins which are in desmosomes, we asked whether PVA is also localized to desmosomes. Immunogold electron microscopy was used to localize binding of PV antibodies. Rabbit antibodies raised against fusion proteins containing the extracellular portion of PVA bound to desmosomes of cultured keratinocytes. PV patient serum affinity-purified on one of these fusion proteins and injected into neonatal mice localized to separating desmosomes. These results show that PVA belongs to the desmoglein subfamily of cadherins according to sequence, localization and, presumably, function. C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. RI Amagai, Masayuki/K-5325-2013 OI Amagai, Masayuki/0000-0003-3314-7052 NR 13 TC 13 Z9 13 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1994 VL 189 SU 1 BP 24 EP 26 PG 3 WC Dermatology SC Dermatology GA NN206 UT WOS:A1994NN20600007 PM 8049558 ER PT S AU LEAPMAN, RD SUN, S HUNT, JA ANDREWS, SB AF LEAPMAN, RD SUN, S HUNT, JA ANDREWS, SB BE Sarikaya, M Wickramasinghe, HK Isaacson, M TI EELS IMAGING OF BIOLOGICAL MATERIALS SO DETERMINING NANOSCALE PHYSICAL PROPERTIES OF MATERIALS BY MICROSCOPY AND SPECTROSCOPY SE MATERIALS RESEARCH SOCIETY SYMPOSIUM PROCEEDINGS LA English DT Proceedings Paper CT Symposium on Determining Nanoscale Physical Properties of Materials by Microscopy and Spectroscopy CY NOV 29-DEC 03, 1993 CL BOSTON, MA SP MAT RES SOC C1 NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MATERIALS RESEARCH SOC PI PITTSBURGH PA 9800 MCKNIGHT RD, SUITE 327, PITTSBURGH, PA 15237 SN 0272-9172 BN 1-55899-231-6 J9 MATER RES SOC SYMP P PY 1994 VL 332 BP 351 EP 359 PG 9 WC Materials Science, Characterization & Testing SC Materials Science GA BC22T UT WOS:A1994BC22T00047 ER PT B AU WEINBERGER, DR BERMAN, KF GOLD, J GOLDBERG, T AF WEINBERGER, DR BERMAN, KF GOLD, J GOLDBERG, T BE Haith, MM Benson, JB Roberts, RJ Pennington, BF TI NEURAL MECHANISMS OF FUTURE-ORIENTED PROCESSES - INVIVO PHYSIOLOGICAL STUDIES OF HUMANS SO DEVELOPMENT OF FUTURE-ORIENTED PROCESSES SE JOHN D AND CATHERINE T MACARTHUR FOUNDATION SERIES ON MENTAL HEALTH AND DEVELOPMENT LA English DT Proceedings Paper CT Conference of the MacArthur Foundation on Development of Future-Oriented Processes CY APR, 1992 CL BRECKENRIDGE, CO SP MACARTHUR FDN C1 ST ELIZABETH HOSP,NIMH,WASHINGTON,DC 20032. NR 0 TC 7 Z9 7 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5801 S ELLIS AVE, CHICAGO, IL 60637 BN 0-226-31306-9 J9 MAC FDN MEN PY 1994 BP 221 EP 242 PG 22 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA BC79N UT WOS:A1994BC79N00009 ER PT J AU SHI, YB HAYES, WP AF SHI, YB HAYES, WP TI THYROID HORMONE-DEPENDENT REGULATION OF THE INTESTINAL FATTY-ACID-BINDING PROTEIN GENE DURING AMPHIBIAN METAMORPHOSIS SO DEVELOPMENTAL BIOLOGY LA English DT Article ID XENOPUS-LAEVIS; NUCLEOTIDE-SEQUENCE; EXPRESSION; LARVAL; VILLIN C1 NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892. RP SHI, YB (reprint author), NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892, USA. NR 30 TC 106 Z9 110 U1 2 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN PY 1994 VL 161 IS 1 BP 48 EP 58 DI 10.1006/dbio.1994.1006 PG 11 WC Developmental Biology SC Developmental Biology GA MQ974 UT WOS:A1994MQ97400006 PM 8293885 ER PT J AU FUJII, T PICHEL, JG TAIRA, M TOYAMA, R DAWID, IB WESTPHAL, H AF FUJII, T PICHEL, JG TAIRA, M TOYAMA, R DAWID, IB WESTPHAL, H TI EXPRESSION PATTERNS OF THE MURINE LIM CLASS HOMEOBOX GENE LIM1 IN THE DEVELOPING BRAIN AND EXCRETORY SYSTEM SO DEVELOPMENTAL DYNAMICS LA English DT Article DE LIM1; HOMEODOMAIN PROTEINS; LIM CLASS HOMEOBOX GENES; XLIM1 ID PAIRED BOX GENE; RESTRICTED EXPRESSION; MOUSE DEVELOPMENT; DNA-POLYMERASE; PROTEIN ISL-1; HOMEODOMAIN; DOMAIN; MORPHOGENESIS; NEUROGENESIS; DROSOPHILA AB We report the cloning, sequence analysis, and developmental expression pattern of lim1, a member of the LIM class homeobox gene family in the mouse. lim1 cDNA encodes a predicted 406 amino acid protein that is 93% identical with the product of the Xenopus LIM class homeobox gene Xlim1. We have characterized lim1 expression from day 8.5 post coitum onward. Northern blot analysis of RNA transcripts indicates that lim1 is expressed both during embryogenesis and in the adult brain. Analysis by wholemount and section in situ hybridization shows lim1 expression in the central nervous system from the telencephalon through the spinal cord and in the developing excretory system including pronephric region, mesonephros, nephric duct, and metanephros. In the metanephros, lim1 is strongly expressed in renal vesicles and S-shaped bodies, and transcripts are also detected in the ureteric branches. (C) 1994 Wiley-Liss, Inc.* C1 NICHHD,MAMMALIAN GENES & DEV LAB,BETHESDA,MD 20892. NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. NR 55 TC 147 Z9 148 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 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD JAN PY 1994 VL 199 IS 1 BP 73 EP 83 PG 11 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA MU900 UT WOS:A1994MU90000007 PM 7909459 ER PT J AU WOLFFE, AP AF WOLFFE, AP TI INHERITANCE OF CHROMATIN STATES SO DEVELOPMENTAL GENETICS LA English DT Review DE TRANSCRIPTION FACTOR; HISTONE; NUCLEOSOME; HETEROCHROMATIN; REPLICATION; CHROMODOMAIN PROTEIN; TRANSCRIPTION; METHYLATION ID POSITION-EFFECT VARIEGATION; GENE-TRANSCRIPTION INVITRO; NEWLY REPLICATED CHROMATIN; CPG BINDING-PROTEIN; RIBOSOMAL-RNA GENES; DNA-REPLICATION; X-CHROMOSOME; DEVELOPMENTAL REGULATION; PARENTAL NUCLEOSOMES; HISTONE ACETYLATION RP WOLFFE, AP (reprint author), NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892, USA. NR 63 TC 47 Z9 49 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 0192-253X J9 DEV GENET JI Dev. Genet. PY 1994 VL 15 IS 6 BP 463 EP 470 DI 10.1002/dvg.1020150604 PG 8 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA QF984 UT WOS:A1994QF98400003 PM 7834905 ER PT J AU CASEY, BJ VAUSS, YC SWEDO, SE AF CASEY, BJ VAUSS, YC SWEDO, SE TI COGNITIVE-FUNCTIONING IN SYDENHAMS CHOREA .1. ATTENTIONAL PROCESSES SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article AB Ten patients with Sydenham's chorea, ages 7 to 15 years, were tested on a computerized battery of tasks assessing attentional processing. Relative to controls, the patients with Sydenham's chorea showed decrements in performance on tasks assessing response inhibition and divided attention. However, normal attentional functioning was observed on tasks assessing spatial attention, sustained attention, and shifts in attentional set. These results are discussed in relation to deficits observed in patients of other basal ganglia disorders. RP CASEY, BJ (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 20 TC 14 Z9 14 U1 1 U2 4 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 8756-5641 J9 DEV NEUROPSYCHOL JI Dev. Neuropsychol. PY 1994 VL 10 IS 2 BP 75 EP 88 PG 14 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA NN285 UT WOS:A1994NN28500001 ER PT J AU CASEY, BJ VAUSS, YC CHUSED, A SWEDO, SE AF CASEY, BJ VAUSS, YC CHUSED, A SWEDO, SE TI COGNITIVE-FUNCTIONING IN SYDENHAMS CHOREA .2. EXECUTIVE FUNCTIONING SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID SYMPTOMS; CHILDREN AB Ten patients with Sydenham's chorea, ages 7 to 15 years, were tested on two executive functioning tasks-the Tower of Hanoi and the Wisconsin Card Sorting Task (WCST). Both tasks have demonstrated deficits in performance by other basal ganglia disorders (e.g., Huntington's chorea, Parkinson's disease). Deficits were observed during performance of the Tower of Hanoi, but not the WCST, relative to age- and sex-matched controls. The results are discussed in terms of frontostriatal circuits involved in maintaining and sequencing of spatially controlled motor moves and thought to be affected in Sydenham's chorea. RP CASEY, BJ (reprint author), NIMH, CHILD PSYCHIAT BRANCH, BLDG 10, ROOM 6N240, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 28 TC 13 Z9 13 U1 1 U2 3 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 8756-5641 J9 DEV NEUROPSYCHOL JI Dev. Neuropsychol. PY 1994 VL 10 IS 2 BP 89 EP 96 PG 8 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA NN285 UT WOS:A1994NN28500002 ER PT J AU ZAHNWAXLER, C AF ZAHNWAXLER, C TI UNTITLED SO DEVELOPMENTAL PSYCHOLOGY LA English DT Editorial Material RP ZAHNWAXLER, C (reprint author), NIMH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0012-1649 J9 DEV PSYCHOL JI Dev. Psychol. PD JAN PY 1994 VL 30 IS 1 BP 3 EP 3 PG 1 WC Psychology, Developmental SC Psychology GA MR407 UT WOS:A1994MR40700001 ER PT J AU ABATI, A CAJIGAS, A HIJAZI, YM AF ABATI, A CAJIGAS, A HIJAZI, YM TI METASTATIC EPITHELIOID HEMANGIOENDOTHELIOMA IN A PLEURAL EFFUSION - DIAGNOSIS BY CYTOLOGY SO DIAGNOSTIC CYTOPATHOLOGY LA English DT Note DE EPITHELIOID HEMANGIOENDOTHELIOMA; PLEURAL EFFUSION; METASTASES AB Epithelioid hemangioendothelioma (EH) is a vascular neoplasm of uncertain malignant potential. We report a 22-yr-old female with a primary malignant EH of the iliac bone with adjacent soft tissue involvement which, during its metastatic course, presented as a pleural effusion. The effusion was cellular with tumor cells present both singly and in clusters. Distinguishing cytologic features included cytoplasmic vacuolization consistent with primitive intracytoplasmic lumen formation, variability in cell size, biphasic cytoplasmic staining with Diff-Quik stain, multinucleation, cell in cell engulfment, and multiple prominent nucleoli. Differential diagnosis based on morphology included malignant mesothelioma and adenocarcinoma Immunocytochemical stains on the neoplastic cells were positive for Ulex Europaeus, Factor VIII-related antigen, and CD34, reflecting vascular differentiation and confirming the diagnosis of metastatic EH to the pleural cavity. (C) 1994 Wiley-Liss, Inc.* RP ABATI, A (reprint author), NCI,PATHOL LAB,CYTOPATHOL SERV,BLDG 10,ROOM 2A19,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 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 8755-1039 J9 DIAGN CYTOPATHOL JI Diagn. Cytopathol. PY 1994 VL 11 IS 1 BP 64 EP 67 DI 10.1002/dc.2840110115 PG 4 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA PC251 UT WOS:A1994PC25100014 PM 7956664 ER PT S AU FREEDMAN, LS CLIFFORD, CK AF FREEDMAN, LS CLIFFORD, CK BE Weisburger, EK TI Meta-analysis of animal experiments: Elucidating relationships between dietary fat and mammary tumor development in rodents SO DIET AND BREAST CANCER SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 4th Annual Conference of the American-Institute-for-Cancer-Research on Diet and Cancer - Diet and Breast Cancer CY SEP 02-03, 1993 CL WASHINGTON, DC SP AMER INST CANC RES C1 NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,BETHESDA,MD 20892. NR 0 TC 9 Z9 10 U1 0 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44895-5 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1994 VL 364 BP 93 EP 100 PG 8 WC Oncology; Medicine, Research & Experimental; Nutrition & Dietetics; Obstetrics & Gynecology SC Oncology; Research & Experimental Medicine; Nutrition & Dietetics; Obstetrics & Gynecology GA BB96T UT WOS:A1994BB96T00009 PM 7725963 ER PT S AU DIPPLE, A PELTONEN, K CHENG, SC ROSS, H BIGGER, CAH AF DIPPLE, A PELTONEN, K CHENG, SC ROSS, H BIGGER, CAH BE Jacobs, MM TI CHEMICAL AND MUTAGENIC SPECIFICITIES OF POLYCYCLIC AROMATIC HYDROCARBON CARCINOGENS SO DIET AND CANCER: MARKERS, PREVENTION, AND TREATMENT SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 3rd Annual Conference on Diet and Cancer: Markers, Prevention, and Treatment CY OCT 29-30, 1992 CL MCLEAN, VA SP AMER INST CANC RES C1 NCI,FREDERICK CANC RES P DEV CTR,ABL BAS RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 0 TC 9 Z9 9 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 0-306-44723-1 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1994 VL 354 BP 101 EP 116 PG 16 WC Oncology; Nutrition & Dietetics SC Oncology; Nutrition & Dietetics GA BA42R UT WOS:A1994BA42R00007 PM 8067279 ER PT J AU JAKOWLEW, SB CIMENT, G TUAN, RS SPORN, MB ROBERTS, AB AF JAKOWLEW, SB CIMENT, G TUAN, RS SPORN, MB ROBERTS, AB TI EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA-2 AND BETA-3 MESSENGER-RNAS AND PROTEINS IN THE DEVELOPING CHICKEN-EMBRYO SO DIFFERENTIATION LA English DT Article ID DEOXYRIBONUCLEIC-ACID CLONING; MESSENGER RIBONUCLEIC-ACID; NON-NEOPLASTIC TISSUES; TGF-BETA; DIFFERENTIAL EXPRESSION; MOUSE DEVELOPMENT; RNA EXPRESSION; ADULT TISSUES; PURIFICATION; CELLS AB Specific cDNA probes and antibodies for chicken transforming growth factor (TGF)-beta 2 and beta 3 were used to study expression of TGF-beta 2 and beta 3 mRNAs and proteins in the developing chicken embryo. Expression of the mRNAs for both TGF-beta isoforms was detected by day 1.5 of incubation (Hamburger and Hamilton stage 10) by RNA Northern blot analysis and increased with developmental age. Expression of TGF-beta 2 and beta 3 mRNAs was detected in every embryonic tissue examined, with the level of expression of both isoforms being high in heart, brain and muscle and low in kidney and liver. Coordinate unidirectional upregulation of expression of TGF-beta 2 and beta 3 mRNAs occurred in most embryonic tissues with development except the heart, where the steady-state level of expression of TGF-beta 2 mRNA decreased with age, while that of TGF-beta 3 mRNA increased. In situ hybridization analysis detected TGF-beta 2 and beta 3 mRNAs as early as the definitive primitive streak stage (stage 4). During neurulation (stage 10), TGF-beta 2 and beta 3 mRNAs were detected in cells of all three germ layers; TGF-beta 3 mRNA was detected in neurectoderm as well. Following neurulation, TGF-beta 3 mRNA was detected in the neural tube, notochord, ectoderm, endoderm, sclerotome and dermomyotome at stage 16; expression of TGF-beta 2 mRNA was not as prominent as TGF-beta 3 mRNA in these structures. By stage 29, both TGF-beta 2 and beta 3 mRNAs were localized in several tissues including heart, lung, gizzard and feathers. Immunohistochemical staining analysis detected immunoreactive TGF-beta 2 and beta 3 proteins in all three germ layers of stage 4 embryos. Staining for TGF-beta 2 and beta 3 proteins was detected in several cell types and tissues in the early developing embryo frequently in the same locations as TGF-beta 2 and beta 3 mRNAs, with staining for TGF-beta 2 being less intense than TGF-beta 3. However, in some cases, localization of TGF-beta 2 and beta 3 proteins was different from that of the mRNAs, indicating that a complex mechanism of transcription, translation and secretion exits during chicken embryogenesis. These and other results suggest that TGF-beta 2 and beta 3 may play important roles and act through both autocrine and paracrine mechanisms in the development of many tissues in the chicken. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. OREGON HLTH SCI UNIV,DEPT CELL BIOL & ANAT,PORTLAND,OR 97201. THOMAS JEFFERSON UNIV,DEPT ORTHOPAED SURG,PHILADELPHIA,PA 19107. FU NICHD NIH HHS [HD 15822, HD 29937]; NINDS NIH HHS [NS 23883] NR 63 TC 80 Z9 80 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD JAN PY 1994 VL 55 IS 2 BP 105 EP 118 DI 10.1046/j.1432-0436.1994.5520105.x PG 14 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA MW354 UT WOS:A1994MW35400002 PM 8143928 ER PT B AU JAFFE, ES AF JAFFE, ES BE Harris, NL Banks, PM Jaffe, ES TI Angiofollicular lymph node hyperplasia, localized (true Castleman's disease), hyaline-vascular type SO DISORDERS OF THE LYMPH NODES AND RELATED ORGANS LA English DT Proceedings Paper CT 58th Annual Anatomic Pathology Slide Seminar of the American-Society-of-Clinical-Pathologists CY OCT 15-16, 1992 CL LAS VEGAS, NV SP Amer Soc Clin Pathologists C1 NCI,HEMATOPATHOL SECT,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLINICAL PATHOLOGISTS PI CHICAGO PA 2100 W HARRISON, CHICAGO, IL 60612 BN 0-89189-365-2 PY 1994 BP 115 EP 120 PG 6 WC Pathology SC Pathology GA BE22G UT WOS:A1994BE22G00018 ER PT S AU WOOD, RD AF WOOD, RD BE Wallace, SS VanHouten, B Kow, YW TI STUDYING NUCLEOTIDE EXCISION-REPAIR OF MAMMALIAN DNA IN A CELL-FREE SYSTEM SO DNA DAMAGE: EFFECTS ON DNA STRUCTURE AND PROTEIN RECOGNITION SE Annals of the New York Academy of Sciences LA English DT Article ID COMPLEMENTATION GROUP-E; PIGMENTOSUM GROUP-G; DAMAGED DNA; BINDING-PROTEIN; POLYMERASE-DELTA; NUCLEAR ANTIGEN; ESCHERICHIA-COLI; CALF THYMUS; EXTRACTS; GENE C1 NIH, BETHESDA, MD USA. UNIV VERMONT, BURLINGTON, VT USA. RP WOOD, RD (reprint author), IMPERIAL CANC RES FUND, CLARE HALL LABS, S MIMMS EN6 3LD, HERTS, ENGLAND. RI Wood, Richard/E-7855-2011 OI Wood, Richard/0000-0002-9495-6892 NR 59 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 USA SN 0077-8923 BN 0-89766-885-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 726 BP 274 EP 280 DI 10.1111/j.1749-6632.1994.tb52827.x PG 7 WC Biochemistry & Molecular Biology; Genetics & Heredity; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Genetics & Heredity; Science & Technology - Other Topics GA BB02U UT WOS:A1994BB02U00022 PM 8092683 ER PT S AU PROTIC, M AF PROTIC, M BE Wallace, SS VanHouten, B Kow, YW TI EUKARYOTIC DAMAGED DNA-BINDING PROTEINS - DNA-REPAIR PROTEINS OR TRANSCRIPTION FACTORS SO DNA DAMAGE: EFFECTS ON DNA STRUCTURE AND PROTEIN RECOGNITION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on DNA Damage: Effects on DNA Structure and Protein Recognition CY JUL 31-AUG 04, 1993 CL BURLINGTON, VT SP NEW YORK ACAD SCI RP PROTIC, M (reprint author), NICHHD,DNA REPLICAT REPAIR & MUTAGENESIS SECT,BLDG 6,ROOM 1A-15,BETHESDA,MD 20892, USA. NR 4 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 0-89766-884-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1994 VL 726 BP 333 EP 335 DI 10.1111/j.1749-6632.1994.tb52843.x PG 3 WC Biochemistry & Molecular Biology; Genetics & Heredity; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Genetics & Heredity; Science & Technology - Other Topics GA BB02U UT WOS:A1994BB02U00037 PM 8092697 ER PT J AU SENA, M BRAVO, DT VONAGOSTON, D WASCHEK, JA AF SENA, M BRAVO, DT VONAGOSTON, D WASCHEK, JA TI HIGH CONSERVATION OF UPSTREAM REGULATORY SEQUENCES ON THE HUMAN AND MOUSE VASOACTIVE-INTESTINAL-PEPTIDE (VIP) GENES SO DNA SEQUENCE LA English DT Article DE AP-2; CONSENSUS; CREB; TRANSCRIPTION; VIP; Z-DNA ID TRANSCRIPTIONAL ACTIVATION; RAT; EXPRESSION; ENHANCER; CELLS AB The neuropeptide vasoactive intestinal peptide (VIP) gene is subject to complex transcriptional regulation resulting in expression of the encoded peptides in distinct subpopulations of neurons in most structures of the nervous system, and tissue-specific changes in expression in response to a variety of hormone and environmental factors. This diverse regulation allows the encoded peptides to carry out putative neurotransmitter, neuromodulator, trophic, neuroendocrine, and immune functions. Despite the potential significance of the processes governing its expression, only the human gene has been studied in any depth, and only a single regulatory element has been identified, a cAMP-responsive sequence less than 100 bp upstream from the transcriptional start site. Because tissue-specific patterns of VIP expression are remarkably well conserved between rodents and humans, we isolated the mouse VIP gene and compared 5' flanking sequences with that of the human gene to identify homologous regions which might be involved in regulation common to both species. Of significant interest is a 210 bp region located more than 1.1 kb upstream from the transcription start site that is 91% conserved between the two species. Of addi- tional interest is a 34 bp perfect dCA.dTC repeat present only on the mouse gene which may be capable of forming Z-DNA. C1 UNIV CALIF LOS ANGELES, LOS ANGELES, CA 90024 USA. NICHHD, DEV NEUROBIOL LAB, BETHESDA, MD 20892 USA. FU NICHD NIH HHS [HD04612, HD06576] NR 19 TC 17 Z9 18 U1 0 U2 0 PU INFORMA HEALTHCARE PI NEW YORK PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA SN 1042-5179 J9 DNA SEQUENCE JI DNA Seq. PY 1994 VL 5 IS 1 BP 25 EP 29 DI 10.3109/10425179409039701 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA PY447 UT WOS:A1994PY44700004 PM 7894056 ER PT J AU UHL, GR PERSICO, A AF UHL, GR PERSICO, A TI MEETING REPORT - COLLABORATIVE APPROACHES IN DRUG-ABUSE GENETICS SO DRUG AND ALCOHOL DEPENDENCE LA English DT Editorial Material DE ASSOCIATION; ADDICTION; TWIN; COCAINE; HEROIN C1 JOHNS HOPKINS SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21224. NIDA,ADDICT RES CTR,MOLEC NEUROBIOL BRANCH,BALTIMORE,MD 21224. RP UHL, GR (reprint author), JOHNS HOPKINS SCH MED,DEPT NEUROL,BALTIMORE,MD 21224, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD JAN PY 1994 VL 34 IS 2 BP 161 EP 162 DI 10.1016/0376-8716(94)90137-6 PG 2 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA MY752 UT WOS:A1994MY75200010 ER PT J AU BRADLEY, SG MUNSON, AE MCCAY, JA BROWN, RD MUSGROVE, DL WILSON, S STERN, M LUSTER, MI WHITE, KL AF BRADLEY, SG MUNSON, AE MCCAY, JA BROWN, RD MUSGROVE, DL WILSON, S STERN, M LUSTER, MI WHITE, KL TI SUBCHRONIC 10 DAY IMMUNOTOXICITY OF POLYDIMETHYLSILOXANE (SILICONE) FLUID, GEL AND ELASTOMER AND POLYURETHANE DISKS IN FEMALE B6C3F1 MICE SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article ID GALLIUM-ARSENIDE; IMMUNOGENICITY; INVITRO; CELLS AB Millions of people have been exposed to silicones because of the widespread use in consumer products such as cosmetics and toiletries, food products, household products and paints. Silicones have wide use in medical practice, including lubricants in tubing and syringes, and as implantable devices. The most prevalent silicone in medical use is polydimethylsiloxane. This study was undertaken to determine the subchronic immunotoxicologic potential of the principal constituents of breast implants: silicone fluid, silicone gel and silicone elastomer. An alternative covering for devices containing silicons gels, polyurethane, was also included in the study. Silicone fluid and gel were injected subcutaneously into female B6C3F1 mice (1 ml/mouse) and 6 mm disks of silicons elastomer or polyurethane were implanted subcutaneously. There were no treatment-related deaths or overt signs of toxicity. None of the tested materials had notable effects on body or organ weights, erythrocytes or leukocytes in the blood, blood chemistries such as alanine aminotransferase, urea nitrogen, glucose, albumin or total protein The cellularity of the bone marrow and responses to CSF-GM and CSF-M were normal. The tested silcones did not alter the distribution of B cells and T cells in the spleen, but polyurethane perturbed the distribution of CD4(+)CD8(+) and CD4(-)CD8(-) T cells. The antibody response to sheep erythrocytes was not markedly altered, nor were proliferative responses to concanavalin A, phytohemagglutinin, lipopolysaccharide or allogeneic cells. Reticuloendothelial function was normal, but polyurethane evoked an enhanced phagocytosis of Covaspheres by adherent peritoneal cells. Natural killer cell activity and serum complement were not altered. All silicone materials afforded modest protection to a challenge with Listeria monocytogenes that killed 40 to 58% of control mice. Host resistance to Streptococcus pneumoniae or the B16F10 tumor was not affected by any of the treatments. There is a pattern indicative of some perturbation of T cell differentiation in mice implanted with a polyurethane disk. C1 VIRGINIA COMMONWEALTH UNIV,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOSTAT,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOMED ENGN,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT MICROBIOL & IMMUNOL,RICHMOND,VA 23298. NIEHS,NATL TOXICOL PROGRAM,SYST TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [ES 55094] NR 31 TC 25 Z9 25 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-0545 J9 DRUG CHEM TOXICOL JI Drug Chem. Toxicol. PY 1994 VL 17 IS 3 BP 175 EP 220 DI 10.3109/01480549409017860 PG 46 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA PD438 UT WOS:A1994PD43800001 PM 7988383 ER PT J AU BRADLEY, SG WHITE, KL MCCAY, JA BROWN, RD MUSGROVE, DL WILSON, S STERN, M LUSTER, MI MUNSON, AE AF BRADLEY, SG WHITE, KL MCCAY, JA BROWN, RD MUSGROVE, DL WILSON, S STERN, M LUSTER, MI MUNSON, AE TI IMMUNOTOXICITY OF 180 DAY EXPOSURE TO POLYDIMETHYLSILOXANE (SILICONE) FLUID, GEL AND ELASTOMER AND POLYURETHANE DISKS IN FEMALE B6C3F1 MICE SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article ID BREAST IMPLANTS; DIETHYLSTILBESTROL; DISEASE; CELLS AB Millions of people have been exposed to silicones which are present in consumer goods such as cosmetics and toiletries, processed foods and household products. In addition, silicones have been used extensively in medical practice as a lubricant in tubing and syringes, and as implantable devices. A silicone widely used in medical practice is polydimethylsiloxane. This study was undertaken to determine the immunotoxicologic potential of long term exposure to the principal constituents of breast implants: silicone fluid, silicone gel and silicone elastomer. An alternative covering for devices containing silicone gels, polyurethane, was also included in the study. Silicone fluid and gel were injected subcutaneously into female B6C3F1 mice (1 ml/mouse) and 6 mm disks of silicone elastomer or polyurethane were implanted subcutaneously. There were no treatment-related deaths or overt signs of toxicity during the 180 day exposure. None of the tested materials had notable effects on body or organ weights, erythrocytes or leukocytes in the blood, blood chemistries such as alanine aminotransferase, urea nitrogen, glucose, albumin or total protein, or serum CH 50 or C3 levels. The cellularity of the bone marrow and responses to CSF-GM and CSF-M were normal. The tested silcones and polyurethane marginally reduced the level of Ig(+) cells in the spleen but did not consistently alter the distribution of T cell surface markers. The antibody response to sheep erythrocytes was not markedly altered, nor were proliferative responses to concanavalin A, phytohemagglutinin, lipopolysaccharide or allogeneic cells. Reticuloendothelial function was normal, as was phagocytosis of chicken erythrocytes and Covaspheres by adherent peritoneal cells. Natural killer cell activity was depressed in all silicone treatment groups and in mice implanted with polyurethane. No silicone or polyurethane treatment group displayed altered susceptibility to a challenge with Listeria monocytogenes, Streptococcus pneumoniae or the B16F10 tumor. The only consistent effect of 180 day exposure to silicone materials or polyurethane was a modest depression of natural killer cell activity. C1 VIRGINIA COMMONWEALTH UNIV,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOSTAT,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOMED ENGN,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT MICROBIOL & IMMUNOL,RICHMOND,VA 23298. NIEHS,NATL TOXICOL PROGRAM,SYST TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [ES55094] NR 38 TC 12 Z9 12 U1 1 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-0545 J9 DRUG CHEM TOXICOL JI Drug Chem. Toxicol. PY 1994 VL 17 IS 3 BP 221 EP 269 DI 10.3109/01480549409017861 PG 49 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA PD438 UT WOS:A1994PD43800002 PM 7988384 ER PT J AU BURNS, LA BRADLEY, SG WHITE, KL MCCAY, JA FUCHS, BA STERN, M BROWN, RD MUSGROVE, DL HOLSAPPLE, MP LUSTER, MI MUNSON, AE AF BURNS, LA BRADLEY, SG WHITE, KL MCCAY, JA FUCHS, BA STERN, M BROWN, RD MUSGROVE, DL HOLSAPPLE, MP LUSTER, MI MUNSON, AE TI IMMUNOTOXICITY OF NITROBENZENE IN FEMALE B6C3F1 MICE SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article ID N-NITROSODIMETHYLAMINE; HOST-RESISTANCE; TOXICITY; EXPOSURE; IMMUNITY; INVITRO AB Nitrobenzene (NBZ) is primarily employed as an oxidizing agent in the synthesis of analine and benzene compounds. It produces myelotoxic effects and effects on erythrocytes in both animal models and man. Reported hepatosplenomegaly and effects on the bone marrow are indicators that NBZ may be immunotoxic. In these studies, female B6C3F1 mice were exposed to 30, 100 and 300 mg/kg of NBZ in corn oil by gavage for 14 consecutive days. To assess the immunotoxic potential of NBZ, body and organ weights were determined and selected immunologic and host resistance responses were studied. In these studies, the liver and spleen appeared to be the primary target organs. Both liver and spleen weights were dose dependently increased. Gross histopathologic examinations revealed significant changes in the spleen, consisting of severe congestion of the red pulp areas with erythrocytes and reticulocytes. Serum chemistry profiles showed increases in alanine aminotransferase and aspartate aminotransferase activities, indicating liver toxicity. Hematologic studies showed a decrease in erythrocyte number and a concomitant increase in mean corpuscular hemoglobin and mean corpuscular volume. A dose-dependent increase in peripheral reticulocytes was also seen. DNA synthesis was enhanced, as was the number of formed elements and the number of monocyte/granulocyte stem cells in the bone marrow of treated mice. IgM responses were decreased and the phagocytic activity of macrophages in the liver was dose dependently increased with a concomitant decrease in the activities in the spleen and lung. Other immunological parameters examined were unchanged. Host resistance to microbial or viral infection was not markedly altered by NBZ; however, there were trends towards increased susceptibility where T-cell function contributes to host defense. These data indicate that NBZ-induced hemolysis and liver injury are linked to the observed alterations in bone marrow activity. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT BIOSTAT,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MICROBIOL & IMMUNOL,RICHMOND,VA 23298. NIEHS,NATL TOXICOL PROGRAM,SYST TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [ES 05288, ES 07087] NR 34 TC 4 Z9 4 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-0545 J9 DRUG CHEM TOXICOL JI Drug Chem. Toxicol. PY 1994 VL 17 IS 3 BP 271 EP 315 DI 10.3109/01480549409017862 PG 45 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA PD438 UT WOS:A1994PD43800003 PM 7988385 ER PT J AU BURNS, LA BRADLEY, SG WHITE, KL MCCAY, JA FUCHS, BA STERN, M BROWN, RD MUSGROVE, DL HOLSAPPLE, MP LUSTER, MI MUNSON, AE AF BURNS, LA BRADLEY, SG WHITE, KL MCCAY, JA FUCHS, BA STERN, M BROWN, RD MUSGROVE, DL HOLSAPPLE, MP LUSTER, MI MUNSON, AE TI IMMUNOTOXICITY OF MONO-NITROTOLUENES IN FEMALE B6C3F1 MICE .1. PARA-NITROTOLUENE SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article ID GALLIUM-ARSENIDE; SUPPRESSION; MUTAGENICITY; TARGETS; RATS AB para-Nitrotoluene (p-nitrotoluene) is used primarily as an intermediate in the production of various dyes, explosives, pharmaceuticals, and in the production of rubber and agricultural products. Previous investigations indicated that p-nitrotoluene was mutagenic in the Ames Test and that other mono-substituted nitrotoluenes bound covalently to hepatic macromolecules. The objective of these studies was to evaluate the potential immunotoxicity of p-nitrotoluene in mice exposed by the oral route. Mice exposed to p-nitrotoluene (200-600 mg/kg) daily for 14 days showed modest dose-dependent increases in liver and spleen weights. The livers of mice exposed subchronically to 400 and 600 mg/kg showed a mild to moderate swelling of the hepatocytes adjacent to the central veins; this swelling appeared to be reversible and there was no evidence of necrosis. The proportion of monocytes in blood was decreased in mice treated with p-nitrotoluene or toluene. Serum chemistries, bone marrow cellularity and the number of CFU-M and CFU-GM were unaffected. Immunologic investigations showed p-nitrotoluene suppressed the IgM response to sRBC and the DHR response to KLH. There was a 24% decrease in the percentage of CD4+ T lymphocytes in the spleen. There was no dose-dependent alteration of peritoneal macrophage numbers or differential count, unstimulated natural killer cell activity, response to B cell mitogen LPS, C3 activity or interferon levels. Exposure of mice to p-nitrotoluene decreased resistance to Listeria monocytogenes but not to Streptococcus pneumoniae, Plasmodium yoelii or the B16F10 melanoma, and increased resistance to the PYB6 tumor. These studies indicated that the immune system is an important target for toxicity of p-nitrotoluene. The decreased host resistance to L. monocytogenes can be attributed to the decrease in T lymphocytes and to a decreased delayed hypersensitivity response to KLH. C1 VIRGINIA COMMONWEALTH UNIV,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOSTAT,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOMED ENGN,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT MICROBIOL & IMMUNOL,RICHMOND,VA 23298. NIEHS,NATL TOXICOL PROGRAM,SYST TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [ES 55094] NR 29 TC 8 Z9 8 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-0545 J9 DRUG CHEM TOXICOL JI Drug Chem. Toxicol. PY 1994 VL 17 IS 3 BP 317 EP 358 DI 10.3109/01480549409017863 PG 42 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA PD438 UT WOS:A1994PD43800004 PM 7988386 ER PT J AU BURNS, LA WHITE, KL MCCAY, JA FUCHS, BA STEM, M BROWN, RD MUSGROVE, DL HOLSAPPLE, MP LUSTER, MI BRADLEY, SG MUNSON, AE AF BURNS, LA WHITE, KL MCCAY, JA FUCHS, BA STEM, M BROWN, RD MUSGROVE, DL HOLSAPPLE, MP LUSTER, MI BRADLEY, SG MUNSON, AE TI IMMUNOTOXICITY OF MONO-NITROTOLUENES IN FEMALE B6C3F1 MICE .2. META-NITROTOLUENE SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article AB The nitrotoluenes are chemicals used in dyes, agricultural products, pharmaceuticals and explosives. In the present studies, the toxicology and immunotoxicity of meta-nitrotoluene (m-nitrotoluene) were evaluated. Mice, exposed to m-nitrotoluene at dose levels of 200, 400 and 600 mg/kg/body weight for 2 weeks by gastric gavage, gained body weight over the treatment period to a slightly greater extent than the control groups. Of the selected organs weighed, the liver and kidney of mice exposed to m-nitrotoluene were increased in weight while the thymus weight was decreased. The liver of mice exposed to m-nitfotoluene, but not ortho-nitrotoluene, showed slight to moderate swelling of the hepatocytes adjacent to the central veins. The hepatocyte swelling appeared to be reversible and there was no evidence of necrosis. The hematology and serum chemistries examined were unaffected by m-nitrotoluene exposure although there were modest decreases in the percentage of polymorphonuclear leukocytes and eosinophils in differential blood counts. Bone marrow cellularity and the number of CFU/M and CFU/GM were unaffected by m-nitrotoluene exposure. m-Nitrotoluene suppressed the IgM response to sRBC and the DHR response to KLH. There was a slight (8%) decrease in the percentage of B lymphocytes in the spleen. The response to the T cell mitogens was suppressed by as much as 39%. Fc-mediated adherence and phagocytosis of chicken erythrocytes and Mt cell activity were increased dose dependently in mice exposed to m-nitrotoluene. Several immune parameters were unaffected by exposure to m-nitrotoluene, including the IgG response to sRBC, responses to the B cell mitogen LPS and to allogeneic cells, and serum interferon levels. Resistance to Streptococcus pneumoniae and Plasmodium yoelii were unaffected also. Resistance to the tumor model PYB6 was increased. Exposure of mice to m-nitrotoluene decreased resistance to Listeria monocytogenes. The decreased resistance to L. monocytogenes may be related to an effect on T cells, evidenced by a decrease in T cell numbers and in the DHR. C1 VIRGINIA COMMONWEALTH UNIV,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOSTAT,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOMED ENGN,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT MICROBIOL & IMMUNOL,RICHMOND,VA 23298. NIEHS,NATL TOXICOL PROGRAM,SYST TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [ES 55094] NR 23 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-0545 J9 DRUG CHEM TOXICOL JI Drug Chem. Toxicol. PY 1994 VL 17 IS 3 BP 359 EP 399 DI 10.3109/01480549409017864 PG 41 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA PD438 UT WOS:A1994PD43800005 PM 7988387 ER PT J AU BURNS, LA BRADLEY, SG WHITE, KL MCCAY, JA FUCHS, BA STERN, M BROWN, RD MUSGROVE, DL HOLSAPPLE, MP LUSTER, MI MUNSON, AE AF BURNS, LA BRADLEY, SG WHITE, KL MCCAY, JA FUCHS, BA STERN, M BROWN, RD MUSGROVE, DL HOLSAPPLE, MP LUSTER, MI MUNSON, AE TI IMMUNOTOXICITY OF 2,4-DIAMINOTOLUENE IN FEMALE B6C3F1 MICE SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article ID AROMATIC AMINE 2,4-DIAMINOTOLUENE; RAT; EXPOSURE; INVITRO AB 2,4-Diaminotoluene (DAT) has been demonstrated to be a potent carcinogen. The present studies were carried our to determine the toxic and immunotoxic potential of DAT. Mice exposed to DAT at 25-100 mg/kg per day for 14 days by gavage showed a 42% increase in liver weight and a slight decrease in spleen weight, Histopathologic evaluation of selected organs showed the liver to be the major target with morphological changes which were dose dependent. The high dose (100 mg/kg) was associated with moderate centrilobular necrosis. No abnormal structure was noted in the spleen, lungs, thymus, kidney or mesenteric lymph nodes. The liver toxicity was associated with an elevation in alanine aminotransferase activity. The only change noted in selected hematologic parameters was a 64% increase in peripheral blood leukocytes. Mice exposed to DAT showed a decreased IgM and IgG response to sheep erythrocytes. The decrease was not a function of a decreased number of B cells because the number of B cells increased dose dependently. Proliferative capacity of immunocompetent cells was not impaired by exposure to DAT as measured by the response to several mitogens. The delayed hypersensitivity response to keyhole limpet hemocyanin in mice exposed to DAT was increased, Natural killer cell activity was decreased dose dependently and may represent a spleen cell pool shift because the number of B cells increased in the presence of a decreasing spleen size. Serum C3 was suppressed at the high dose of DAT. Phagocytosis by splenic macrophages, but not peritoneal macrophages, was inhibited by DAT exposure. DAT exposure for 14 days decreased host resistance to the bacteria, Streptococcus pneumoniae and Listeria monocytogenes, while host resistance to the pulmonary tumor model, B16F10, and the PYB6 fibrosarcoma was unaffected by DAT exposure. These data indicate that DAT is hepatotoxic and perturbs the differentiation and maturation of leukocytes. C1 VIRGINIA COMMONWEALTH UNIV,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOSTAT,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT BIOMED ENGN,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,DEPT MICROBIOL & IMMUNOL,RICHMOND,VA 23298. NIEHS,NATL TOXICOL PROGRAM,SYST TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [ES 55094] NR 33 TC 5 Z9 5 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-0545 J9 DRUG CHEM TOXICOL JI Drug Chem. Toxicol. PY 1994 VL 17 IS 3 BP 401 EP 436 PG 36 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA PD438 UT WOS:A1994PD43800006 PM 7988388 ER PT J AU YUAN, JH DUNNICK, JK BARNES, ER FINDLAY, JWA AF YUAN, JH DUNNICK, JK BARNES, ER FINDLAY, JWA TI CODEINE TOXICOKINETICS IN RATS DURING A 2-YEAR DOSED FEED STUDY SO DRUG METABOLISM AND DISPOSITION LA English DT Article ID PHARMACOKINETICS; RADIOIMMUNOASSAY; PHOSPHATE; MORPHINE; PLASMA AB Codeine toxicokinetics in F344 rats of both sexes were determined during a 2-year chronic toxicology study using dosed feed as the exposure route with a 12 hr light/dark cycle starting at 7:00 a.m. Rats were allowed to access to dosed feed formulations ad libitum with codeine concentrations at 0, 400, 800, and 1600 ppm. Blood samples were collected from individual rat on days 7, 21, and 90 at 7:00 p.m., 11:00 p.m., 3:00 a.m., and 7:00 a.m. Additional samples were collected at 16 and 24 months between 6:00-8:00 a.m. Plasma concentrations of codeine and morphine were determined directly by radioimmunoassay. Concentrations of their conjugates were determined indirectly by measuring the total amount of free codeine and morphine released after samples were treated with beta-glucuronidase. Results indicated that plasma concentrations of both codeine and morphine steadily decreased from day 7 to 16 months and then rebounded at 24 months. Results also indicated that plasma concentrations of both codeine and morphine correlated well with the amounts of codeine added to the feed. Bioavailability of codeine using the dosed feed route increased with dose, varying from 10% to 25%, which was somewhat higher than the previously reported similar to 8% bioavailability using the gavage route. Concentrations of conjugated codeine were very low, whereas concentrations of conjugated morphine were very high. These results suggested that demethylation of codeine to morphine in rats is the main metabolic pathway and was maintained over the course of the study. C1 NIEHS,RES TRIANGLE PK,NC. BURROUGHS WELLCOME CO,DIV PHARMACOKINET & DRUG METAB,DURHAM,NC. NR 18 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-9556 J9 DRUG METAB DISPOS JI Drug Metab. Dispos. PD JAN-FEB PY 1994 VL 22 IS 1 BP 14 EP 20 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NA670 UT WOS:A1994NA67000003 PM 8149873 ER PT J AU ANDERSON, LM KOSENIAUSKAS, R BURAK, ES LOGSDON, DL CARTER, JP DRIVER, CL GOMBAR, CT MAGEE, PN HARRINGTON, GW AF ANDERSON, LM KOSENIAUSKAS, R BURAK, ES LOGSDON, DL CARTER, JP DRIVER, CL GOMBAR, CT MAGEE, PN HARRINGTON, GW TI SUPPRESSION OF IN-VIVO CLEARANCE OF N-NITROSODIMETHYLAMINE IN MICE BY COTREATMENT WITH ETHANOL SO DRUG METABOLISM AND DISPOSITION LA English DT Article ID HUMAN CANCER; METABOLISM; DIMETHYLNITROSAMINE; NITROSAMINES; ALCOHOL; BLOOD; RAT; DEMETHYLASE; DISPOSITION; INHIBITORS AB Oral cotreatment of mice with ethanol results in increased tumors in extrahepatic organs caused by some nitrosamines. This action, attributed in part to inhibition of hepatic first-pass carcinogen metabolism by ethanol, has possible relevance to the enhancing effect of alcoholic beverage consumption on human cancer risk. In this study, the effects of ethanol on clearance of N-nitrosodimethylamine (NDMA) were quantified in Swiss female and strain A male mice. In Swiss mice, a 1.6 g/kg ig ethanol dose preceding 1 or 5 mg/kg iv NDMA resulted in 20- to 30-fold increases in area-under-the-blood-concentration-vs.-time curves, mean residence times, and clearance half-times, and similar decreases in clearance. For a 0.5 mg/kg ig NDMA dose, the pharmacokinetic parameters were altered 30-fold and 450-fold by simultaneous ethanol doses of 0.08 and 0.8 g/kg, respectively. With 5 mg NDMA/kg ig, 0.4, 0.8, and 1.6 g/kg ethanol resulted in 6-, 10-, and 20-fold changes in clearance parameters. Comparison of the data with results obtained previously with patas monkeys indicated comparable effects of ethanol on tissue exposure to NDMA in the two species, confirming potential human applicability. In experiments with strain A mice, NDMA concentrations were also monitored in lung and liver. NDMA amounts in lung paralleled those in blood, and were more than sufficient to account for the previously reported increases in DNA adducts and tumors in lungs of similarly treated strain A mice. C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD. TEMPLE UNIV,DEPT CHEM,PHILADELPHIA,PA 19122. TEMPLE UNIV,FELS RES INST,PHILADELPHIA,PA. SMITH KLINE BEECHAM CORP,KING OF PRUSSIA,PA. RP ANDERSON, LM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,BLDG 538,FREDERICK,MD 21702, USA. NR 34 TC 18 Z9 18 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-9556 J9 DRUG METAB DISPOS JI Drug Metab. Dispos. PD JAN-FEB PY 1994 VL 22 IS 1 BP 43 EP 49 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NA670 UT WOS:A1994NA67000008 PM 8149888 ER PT J AU POIRIER, MC AF POIRIER, MC TI HUMAN EXPOSURE MONITORING, DOSIMETRY, AMD CANCER RISK ASSESSMENT - THE USE OF ANTISERA SPECIFIC FOR CARCINOGEN-DNA ADDUCTS AND CARCINOGEN-MODIFIED DNA SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium, Honoring the Research Contributions of Dr Elizabeth C Miller and Dr James A Miller CY DEC 10-11, 1992 CL LITTLE ROCK, AR SP IMOV ARKANSAS MED SCI, DEPT PHARM & TOXICOL, DIV TOXICOL ID WHITE BLOOD-CELLS; COKE-OVEN WORKERS; BENZOPYRENE DIOL EPOXIDE; SISTER CHROMATID EXCHANGE; PERFORMANCE LIQUID-CHROMATOGRAPHY; POLYCYCLIC AROMATIC-HYDROCARBONS; HAMSTER OVARY CELLS; MOLECULAR DOSIMETRY; HUMAN-TISSUES; IMMUNOLOGICAL DETECTION RP POIRIER, MC (reprint author), NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BLDG 37,RM 3B25,BETHESDA,MD 20892, USA. NR 75 TC 18 Z9 19 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1994 VL 26 IS 1-2 BP 87 EP 109 DI 10.3109/03602539409029786 PG 23 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NK834 UT WOS:A1994NK83400006 PM 8082583 ER PT J AU CONNEY, AH CHANG, RL JERINA, DM WEI, SJC AF CONNEY, AH CHANG, RL JERINA, DM WEI, SJC TI STUDIES ON THE METABOLISM OF BENZO[A]PYRENE AND DOSE-DEPENDENT DIFFERENCES IN THE MUTAGENIC PROFILE OF ITS ULTIMATE CARCINOGENIC METABOLITE SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium, Honoring the Research Contributions of Dr Elizabeth C Miller and Dr James A Miller CY DEC 10-11, 1992 CL LITTLE ROCK, AR SP IMOV ARKANSAS MED SCI, DEPT PHARM & TOXICOL, DIV TOXICOL ID HUMAN-LIVER; OPTICAL ENANTIOMERS; LUNG-CANCER; RISK-FACTORS; DEBRISOQUINE; ACTIVATION; 7,8-DIOL-9,10-EPOXIDES; BENZO(A)PYRENE; OXIDATION; PHENOTYPE C1 NIDDKD,BIOORGAN CHEM LAB,OXIDAT MECH SECT,BETHESDA,MD 20892. RP CONNEY, AH (reprint author), RUTGERS STATE UNIV,COLL PHARM,DEPT CHEM BIOL & PHARMACOGNOSY,CANC RES LAB,PISCATAWAY,NJ 08855, USA. FU NCI NIH HHS [CA 49756] NR 63 TC 115 Z9 120 U1 1 U2 9 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1994 VL 26 IS 1-2 BP 125 EP 163 DI 10.3109/03602539409029788 PG 39 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NK834 UT WOS:A1994NK83400008 PM 8082562 ER PT J AU GONZALEZ, FJ GELBOIN, HV AF GONZALEZ, FJ GELBOIN, HV TI ROLE OF HUMAN CYTOCHROMES P450 IN THE METABOLIC-ACTIVATION OF CHEMICAL CARCINOGENS AND TOXINS SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium, Honoring the Research Contributions of Dr Elizabeth C Miller and Dr James A Miller CY DEC 10-11, 1992 CL LITTLE ROCK, AR SP IMOV ARKANSAS MED SCI, DEPT PHARM & TOXICOL, DIV TOXICOL ID HUMAN-LIVER-MICROSOMES; CDNA-DIRECTED EXPRESSION; ERYTHROMYCIN BREATH TEST; AMINO-ACID SEQUENCE; SACCHAROMYCES-CEREVISIAE; LUNG-CANCER; OXIDATION POLYMORPHISM; GENETIC-POLYMORPHISM; INDUCIBLE EXPRESSION; HYDROXYLASE-ACTIVITY RP GONZALEZ, FJ (reprint author), NCI,BLDG 37,ROOM 3E24,BETHESDA,MD 20892, USA. NR 121 TC 390 Z9 400 U1 1 U2 8 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1994 VL 26 IS 1-2 BP 165 EP 183 DI 10.3109/03602539409029789 PG 19 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NK834 UT WOS:A1994NK83400009 PM 8082563 ER PT J AU LEHMAN, TA GREENBLATT, M BENNETT, WP HARRIS, CC AF LEHMAN, TA GREENBLATT, M BENNETT, WP HARRIS, CC TI MUTATIONAL SPECTRUM OF THE P53 TUMOR-SUPPRESSOR GENE - CLUES TO CANCER ETIOLOGY AND MOLECULAR PATHOGENESIS SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium, Honoring the Research Contributions of Dr Elizabeth C Miller and Dr James A Miller CY DEC 10-11, 1992 CL LITTLE ROCK, AR SP IMOV ARKANSAS MED SCI, DEPT PHARM & TOXICOL, DIV TOXICOL ID HUMAN HEPATOCELLULAR CARCINOMAS; HEPATITIS-B VIRUS; K-RAS ONCOGENE; MAMMALIAN-CELLS; AFLATOXIN EXPOSURE; SEQUENCE SPECIFICITY; SHUTTLE VECTOR; POINT MUTATION; LUNG-TUMORS; DNA-REPAIR RP LEHMAN, TA (reprint author), NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 66 TC 10 Z9 10 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1994 VL 26 IS 1-2 BP 221 EP 235 DI 10.3109/03602539409029793 PG 15 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NK834 UT WOS:A1994NK83400013 PM 8082567 ER PT J AU BIGGER, CAH CHEH, A LATIF, F FISHEL, R CANELLA, KA STAFFORD, GA YAGI, H JERINA, DM DIPPLE, A AF BIGGER, CAH CHEH, A LATIF, F FISHEL, R CANELLA, KA STAFFORD, GA YAGI, H JERINA, DM DIPPLE, A TI DNA STRAND BREAKS INDUCED BY CONFIGURATIONALLY ISOMERIC HYDROCARBON DIOL EPOXIDES SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Arkansas Toxicology Symposium, Honoring the Research Contributions of Dr Elizabeth C Miller and Dr James A Miller CY DEC 10-11, 1992 CL LITTLE ROCK, AR SP IMOV ARKANSAS MED SCI, DEPT PHARM & TOXICOL, DIV TOXICOL ID 3,4-DIOL-1,2-EPOXIDES; BINDING; BASES C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHROMOSOME BIOL LAB,FREDERICK,MD 21702. AMERICAN UNIV,DEPT CHEM,WASHINGTON,DC 20016. NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. FU NCI NIH HHS [NQ1-CO-74101] NR 22 TC 7 Z9 7 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1994 VL 26 IS 1-2 BP 287 EP 299 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NK834 UT WOS:A1994NK83400017 PM 8082571 ER PT J AU RUDORFER, MV MANJI, HK POTTER, WZ AF RUDORFER, MV MANJI, HK POTTER, WZ TI COMPARATIVE TOLERABILITY PROFILES OF THE NEWER VERSUS OLDER ANTIDEPRESSANTS SO DRUG SAFETY LA English DT Review AB Although the standard tricyclic antidepressants (TCAs) are generally effective in the treatment of depression, they can cause several troublesome adverse effects. Chief among these are their anticholinergic actions, which range from annoying dryness of the mouth and constipation to potentially dangerous urinary retention and confusion or delirium in the ill and elderly. Cardiovascular effects of TCAs include orthostatic hypotension, tachycardia and cardiac conduction slowing. Many TCAs are sedating and promote weight gain. Also problematic is the potential lethality of TCAs in overdose. The continual introduction of a host of new antidepressants over the past 15 years has provided an opportunity to improve the benefit-risk ratio for many patients by reducing medication-related toxicity. Selective serotonin reuptake inhibitors (SSRIs) and amfebutamone (bupropion), among others, are examples of effective antidepressants free of tricyclic-like anticholinergic, cardiovascular, sedating and appetite/weight-increasing effects. However, the new-generation drugs also present adverse effects of their own, including gastrointestinal distress, agitation and drug-drug interactions in the case of the SSRIs, and the risk of seizures or psychosis in amfebutamone recipients. Monoamine oxidase (MAO) inhibitors have also been refined; reversible inhibitors of MAO-type A afford protection against the usually feared hypertensive reaction to indirect sympathomimetic substances. The availability of new-generation antidepressants thus increases the likelihood of clinical response with a reduction in unwanted toxicity. C1 NIMH,DIV CLIN & TREATMENT RES,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892. NR 0 TC 84 Z9 86 U1 0 U2 1 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 0114-5916 J9 DRUG SAFETY JI Drug Saf. PD JAN PY 1994 VL 10 IS 1 BP 18 EP 46 PG 29 WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology GA MT053 UT WOS:A1994MT05300003 PM 8136085 ER PT B AU SWANGO, PA KLEINMAN, DV AF SWANGO, PA KLEINMAN, DV BE Squier, CA Hill, MW TI ORAL SOFT TISSUE DISEASES IN GERIATRIC POPULATIONS - AN EPIDEMIOLOGIC OVERVIEW SO EFFECT OF AGING IN ORAL MUCOSA AND SKIN LA English DT Proceedings Paper CT Symposium on the Effect of Aging in Oral Mucosa and Skin CY MAY 07-08, 1993 CL UNIV IOWA, COLL DENISTRY, IOWA CITY, IA SP CLIN CORE CTR ORAL HLTH RES HO UNIV IOWA, COLL DENISTRY C1 NIDR,FIELD STUDIES SECT,EPIDEMIOL & ORAL DIS PREVENT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 1 U1 0 U2 0 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-8493-9403-1 PY 1994 BP 1 EP 7 PG 7 WC Dentistry, Oral Surgery & Medicine; Dermatology; Physiology SC Dentistry, Oral Surgery & Medicine; Dermatology; Physiology GA BC21K UT WOS:A1994BC21K00001 ER PT B AU EDEN, HS AF EDEN, HS GP IEEE TI Biomedical engineering at the Biomedical Engineering and Instrumentation Program, NIH SO ELECTRO '94 LA English DT Proceedings Paper CT Electro 94 International CY MAY 10-12, 1994 CL BOSTON, MA C1 NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU I E E E PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 BN 0-7803-2630-X PY 1994 BP 643 EP 648 PG 6 WC Business; Computer Science, Information Systems; Computer Science, Software Engineering; Engineering, Biomedical; Engineering, Manufacturing; Engineering, Electrical & Electronic SC Business & Economics; Computer Science; Engineering GA BD92Y UT WOS:A1994BD92Y00062 ER PT B AU BOOY, FP TRUS, BL NEWCOMB, WW BROWN, JC CONWAY, JF STEVEN, AC AF BOOY, FP TRUS, BL NEWCOMB, WW BROWN, JC CONWAY, JF STEVEN, AC BE Jouffrey, B Colliex, C TI Localisation of the 12kDa protein, VP26, in the capsid of herpes simplex virus type 1 SO ELECTRON MICROSCOPY 1994, VOL 1: INTERDISCIPLINARY DEVELOPMENTS AND TOOLS LA English DT Proceedings Paper CT 13th International Congress on Electron Microscopy CY JUL 17-22, 1994 CL PARIS, FRANCE SP Int Federat Soc Electron Microscopy, Minist Enseignement Super & Recher, Acad Sci, Minist Affaires Etrangeres, European Union, CNRS, INSERM, CEA C1 NIAMS,STRUCT BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS PHYSIQUE PI LES ULIS PA AVENUE DU HOGGAR, ZONE INDUSTRIELLE COURTABOEUF, BP112 91944 LES ULIS, FRANCE BN 2-86883-225-3 PY 1994 BP 27 EP 28 PG 2 WC Instruments & Instrumentation; Microscopy; Optics SC Instruments & Instrumentation; Microscopy; Optics GA BE09X UT WOS:A1994BE09X00009 ER PT B AU TRUS, BL HOMA, FL THOMSEN, DR NEWCOMB, WW BOOY, FP BROWN, JC STEVEN, AC AF TRUS, BL HOMA, FL THOMSEN, DR NEWCOMB, WW BOOY, FP BROWN, JC STEVEN, AC BE Jouffrey, B Colliex, C TI Visualization of herpesvirus capsids assembled in a recombinant baculovirus system by cryo-electron microscopy SO ELECTRON MICROSCOPY 1994, VOLS 3A AND 3B: APPLICATIONS IN BIOLOGICAL SCIENCES LA English DT Proceedings Paper CT 13th International Congress on Electron Microscopy CY JUL 17-22, 1994 CL PARIS, FRANCE SP Int Federat Soc Electron Microscopy, Minist Enseignement Super & Recher, Acad Sci, Minist Affaires Etrangeres, European Union, CNRS, INSERM, CEA C1 NIH,STRUCT BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS PHYSIQUE PI LES ULIS PA AVENUE DU HOGGAR, ZONE INDUSTRIELLE COURTABOEUF, BP112 91944 LES ULIS, FRANCE BN 2-86883-228-8 PY 1994 BP 527 EP 528 PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE09Z UT WOS:A1994BE09Z00245 ER PT B AU KOCSIS, E KESSEL, M STEVEN, AC AF KOCSIS, E KESSEL, M STEVEN, AC BE Jouffrey, B Colliex, C TI Micropolymorphism of phage T4 capsid surface lattice when expansion is induced without prior cleavage: Multivariate statistical analysis shows different sub-states SO ELECTRON MICROSCOPY 1994, VOLS 3A AND 3B: APPLICATIONS IN BIOLOGICAL SCIENCES LA English DT Proceedings Paper CT 13th International Congress on Electron Microscopy CY JUL 17-22, 1994 CL PARIS, FRANCE SP Int Federat Soc Electron Microscopy, Minist Enseignement Super & Recher, Acad Sci, Minist Affaires Etrangeres, European Union, CNRS, INSERM, CEA C1 NIAMSD,STRUCT BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS PHYSIQUE PI LES ULIS PA AVENUE DU HOGGAR, ZONE INDUSTRIELLE COURTABOEUF, BP112 91944 LES ULIS, FRANCE BN 2-86883-228-8 PY 1994 BP 531 EP 532 PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE09Z UT WOS:A1994BE09Z00247 ER PT B AU CERRITELLI, ME SIMON, MN VACA, M CONWAY, JF STEVEN, AC AF CERRITELLI, ME SIMON, MN VACA, M CONWAY, JF STEVEN, AC BE Jouffrey, B Colliex, C TI The long tail-fibers of bacteriophage T4: Determination of stoichiometry and domainal structure by dark-field STEM SO ELECTRON MICROSCOPY 1994, VOLS 3A AND 3B: APPLICATIONS IN BIOLOGICAL SCIENCES LA English DT Proceedings Paper CT 13th International Congress on Electron Microscopy CY JUL 17-22, 1994 CL PARIS, FRANCE SP Int Federat Soc Electron Microscopy, Minist Enseignement Super & Recher, Acad Sci, Minist Affaires Etrangeres, European Union, CNRS, INSERM, CEA C1 NIAMS,STRUCT BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS PHYSIQUE PI LES ULIS PA AVENUE DU HOGGAR, ZONE INDUSTRIELLE COURTABOEUF, BP112 91944 LES ULIS, FRANCE BN 2-86883-228-8 PY 1994 BP 539 EP 540 PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE09Z UT WOS:A1994BE09Z00251 ER PT B AU LEAPMAN, RD SUN, SQ SHI, SL GALLANT, PE REESE, TS ANDREWS, SB AF LEAPMAN, RD SUN, SQ SHI, SL GALLANT, PE REESE, TS ANDREWS, SB BE Jouffrey, B Colliex, C TI Biological electron energy loss spectroscopy and mapping in the field-emission STEM (invited) SO ELECTRON MICROSCOPY 1994, VOLS 3A AND 3B: APPLICATIONS IN BIOLOGICAL SCIENCES LA English DT Proceedings Paper CT 13th International Congress on Electron Microscopy CY JUL 17-22, 1994 CL PARIS, FRANCE SP Int Federat Soc Electron Microscopy, Minist Enseignement Super & Recher, Acad Sci, Minist Affaires Etrangeres, European Union, CNRS, INSERM, CEA C1 NIH,NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS PHYSIQUE PI LES ULIS PA AVENUE DU HOGGAR, ZONE INDUSTRIELLE COURTABOEUF, BP112 91944 LES ULIS, FRANCE BN 2-86883-228-8 PY 1994 BP 801 EP 804 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE09Z UT WOS:A1994BE09Z00375 ER PT B AU RULONG, S DASILVA, PP WOUDE, GFV AF RULONG, S DASILVA, PP WOUDE, GFV BE Jouffrey, B Colliex, C TI Immunogold electron microscopy study of oncogenic proteins SO ELECTRON MICROSCOPY 1994, VOLS 3A AND 3B: APPLICATIONS IN BIOLOGICAL SCIENCES LA English DT Proceedings Paper CT 13th International Congress on Electron Microscopy CY JUL 17-22, 1994 CL PARIS, FRANCE SP Int Federat Soc Electron Microscopy, Minist Enseignement Super & Recher, Acad Sci, Minist Affaires Etrangeres, European Union, CNRS, INSERM, CEA C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. RI Shen, Rulong/E-4079-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS PHYSIQUE PI LES ULIS PA AVENUE DU HOGGAR, ZONE INDUSTRIELLE COURTABOEUF, BP112 91944 LES ULIS, FRANCE BN 2-86883-228-8 PY 1994 BP 1083 EP 1084 PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE09Z UT WOS:A1994BE09Z00506 ER PT B AU PIMENTA, P TOURAY, M MILLER, L AF PIMENTA, P TOURAY, M MILLER, L BE Jouffrey, B Colliex, C TI An ultrastructural study of the malaria parasite in the salivary gland of mosquito vectors SO ELECTRON MICROSCOPY 1994, VOLS 3A AND 3B: APPLICATIONS IN BIOLOGICAL SCIENCES LA English DT Proceedings Paper CT 13th International Congress on Electron Microscopy CY JUL 17-22, 1994 CL PARIS, FRANCE SP Int Federat Soc Electron Microscopy, Minist Enseignement Super & Recher, Acad Sci, Minist Affaires Etrangeres, European Union, CNRS, INSERM, CEA C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS PHYSIQUE PI LES ULIS PA AVENUE DU HOGGAR, ZONE INDUSTRIELLE COURTABOEUF, BP112 91944 LES ULIS, FRANCE BN 2-86883-228-8 PY 1994 BP 1417 EP 1418 PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE09Z UT WOS:A1994BE09Z00670 ER PT J AU CERESINI, G MERCHENTHALER, A NEGROVILAR, A MERCHENTHALER, I AF CERESINI, G MERCHENTHALER, A NEGROVILAR, A MERCHENTHALER, I TI AGING IMPAIRS GALANIN EXPRESSION IN LUTEINIZING-HORMONE-RELEASING HORMONE NEURONS - EFFECT OF OVARIECTOMY AND/OR ESTRADIOL TREATMENT SO ENDOCRINOLOGY LA English DT Article ID MEDIAL PREOPTIC AREA; MALE-RAT; HYPOTHALAMUS; TRANSITION; EXHAUSTION; SYSTEM; BRAIN; AXONS; AGE AB In the medial preoptic area and the diagonal band of Broca, a subset of LHRH neurons coexpresses galanin at a 4- to B-fold higher rate in female than male rats, suggesting that estradiol (E(2)) plays a key role in galanin gene expression within LHRH neurons. In the present studies we investigated the incidence of colocalization of these peptides in different age groups, i.e. 2-, 10-, 18-, and 24-month-old intact female Fisher rats; 24-month-old El-treated rats; 24-month-old ovariectomized (OVX) rats; and 24-month-old OVX E(2)-treated rats with single or double labeling immunocytochemistry. For cell counting, we took advantage of the typical fusiform morphology of galanin-immunoreactive neurons that colocalize LHRH. The presence of both peptides in the same perikaryon was substantiated by double staining representative sections from each brain. Our observations indicate that the number of galanin/LHRH-coexpressing perikarya dramatically decreased with age. Although in 18-month-old rats a moderate decline was observed, in 24-month-old female rats no, or only a few, faintly stained, fusiform galanin-immunopositive perikarya were present. Although galanin was absent from LHRH neurons of aged rats, their LHRH content was not altered. E(2) treatment of intact 24-month-old rats had no effect on the low incidence of colocalization. However, when OVX 24-month-old rats were E(2) treated, the incidence of colocalization increased to the level seen in 2- or 10-month-old estrous animals. Our observations on the presence of colocalizing perikarya in intact and E(2)-treated aged animals provide further evidence for the key role of E(2) in galanin gene expression within LHRH neurons and emphasize that some ovarian factor(s) may blunt this effect. C1 NIEHS,FUNCT MORPHOL SECT,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC 27516. NR 49 TC 16 Z9 16 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1994 VL 134 IS 1 BP 324 EP 330 DI 10.1210/en.134.1.324 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA MQ621 UT WOS:A1994MQ62100047 PM 7506207 ER PT B AU YOSHINAGA, K AF YOSHINAGA, K BE Glasser, SR Mulholland, J Psychoyos, A TI FUTURE PROSPECT OF RESEARCH ON ENDOCRINOLOGY OF EMBRYO ENDOMETRIAL INTERACTIONS SO ENDOCRINOLOGY OF EMBRYO-ENDOMETRIUM INTERACTIONS SE REPRODUCTIVE BIOLOGY LA English DT Proceedings Paper CT Satellite Symposium of the 9th International Congress of Endocrinology on Endocrinology of Embryo-Endometrial Interactions CY SEP 06-10, 1992 CL BORDEAUX, FRANCE C1 NICHHD,CTR POPULAT RES,REPROD SCI BRANCH,BETHESDA,MD 20892. NR 0 TC 8 Z9 9 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44809-2 J9 REPROD BIOL PY 1994 BP 391 EP 400 PG 10 WC Developmental Biology; Endocrinology & Metabolism; Obstetrics & Gynecology; Reproductive Biology SC Developmental Biology; Endocrinology & Metabolism; Obstetrics & Gynecology; Reproductive Biology GA BB96G UT WOS:A1994BB96G00032 ER PT J AU ZEIGER, E AF ZEIGER, E TI OLD PROTOCOLS, AS DO OLD HABITS, DIE HARD SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material ID SALMONELLA TESTER STRAIN; MUTAGENICITY TEST; CARCINOGENS; ASSAY RP ZEIGER, E (reprint author), NIEHS,ENVIRONM TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709, USA. NR 18 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 24 IS 1 BP 1 EP 2 DI 10.1002/em.2850240102 PG 2 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA NZ310 UT WOS:A1994NZ31000001 PM 8050412 ER PT J AU SHELBY, MD AF SHELBY, MD TI THE CYTOGENETIC EFFECTS OF AZT SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Letter ID AIDS RP SHELBY, MD (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 8 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 24 IS 2 BP 148 EP 149 DI 10.1002/em.2850240211 PG 2 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA PH323 UT WOS:A1994PH32300010 PM 7925329 ER PT J AU ZEIGER, E AF ZEIGER, E TI EVERYBODY KNOWS ABOUT DNA SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material RP ZEIGER, E (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 24 IS 3 BP 155 EP 155 DI 10.1002/em.2850240302 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA QF993 UT WOS:A1994QF99300001 PM 7957117 ER PT J AU KUSSER, WC MIAO, XL GLICKMAN, BW FRIEDLAND, JM ROTHMAN, N HEMSTREET, GP MELLOT, J SWAN, DC SCHULTE, PA HAYES, RB AF KUSSER, WC MIAO, XL GLICKMAN, BW FRIEDLAND, JM ROTHMAN, N HEMSTREET, GP MELLOT, J SWAN, DC SCHULTE, PA HAYES, RB TI P53 MUTATIONS IN HUMAN BLADDER-CANCER SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE PCR; SSCP; TUMOR SUPPRESSOR GENE P53; BLADDER CANCER ID GENE; DNA; AMPLIFICATION; POLYMORPHISM AB Mutations in the tumor suppressor gene p53 play an important role in carcinogenesis and tumor progression. To assess the status of p53 from genomic DNA from bladder cancer samples a two stage polymerase chain reaction was employed. The technique provided material for subsequent detection of mutations by Single Strand Conformation Polymorphism (SSCP) analysis followed by DNA sequence analysis. SSCP analysis of exons 5 to 9 of p53 was performed using fragments from PCR end-labeled with P-32 followed by autoradiography using an electrophoresis system with temperature control. This SSCP method improved resolution of mutations in exons 5, 7, and 8 and the sharpness of bands in exons 6 and 9. Bonds with altered migration patterns were excised from the dried SSCP gels, reamplified by PCR, and sequenced. Mutations in conserved exons 5, 6, 7, 8, and 9 of the p53 gene were analyzed from bladder tumor biopsies. Our results are consistent with the literature in that mutations in p53 are predominantly found in high grade bladder cancer (Odds Ratio = 4.05, Fisher Exact P = 0.104); however, the results were not statistically significant due to small numbers. Eight of 35 (23%) tumor samples examined showed mutations in p53 (including two double mutations). Six of 13 (46%) grade III and IV tumors had p53 mutations vs. 2 of 17 (12%) grade I and II tumors. Normal individuals carried no p53 mutations. We found no correlation between pock years of smoking and mutation in p53. The spectrum of mutations confirmed a high proportion of G:C C:G transversions as well as the occurrence of double mutations. (C) 1994 Wiley-Liss, Inc. C1 NCI,ROCKVILLE,MD. UNIV OKLAHOMA,OKLAHOMA CITY,OK. CTR DIS CONTROL,NATL CTR INFECT DIS,ATLANTA,GA 30333. CDC,NIOSH,CINCINNATI,OH. RP KUSSER, WC (reprint author), UNIV VICTORIA,CTR ENVIRONM HLTH,DEPT BIOL,VICTORIA,BC V8W 2Y2,CANADA. FU PHS HHS [211-91-0007] NR 19 TC 27 Z9 27 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 24 IS 3 BP 156 EP 160 DI 10.1002/em.2850240303 PG 5 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA QF993 UT WOS:A1994QF99300002 PM 7957118 ER PT J AU KLIGERMAN, AD BISHOP, JB EREXSON, GL PRICE, HC OCONNOR, RW MORGAN, DL ZEIGER, E AF KLIGERMAN, AD BISHOP, JB EREXSON, GL PRICE, HC OCONNOR, RW MORGAN, DL ZEIGER, E TI CYTOGENETIC AND GERM-CELL EFFECTS OF PHOSPHINE INHALATION BY RODENTS .2. SUBACUTE EXPOSURES TO RATS AND MICE SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE PHOSPHINE; LYMPHOCYTES; RODENTS; CHROMOSOME ABERRATIONS; SISTER CHROMATID EXCHANGES; MICRONUCLEUS ID PERIPHERAL-BLOOD; MICRONUCLEI; LYMPHOCYTES AB Phosphine (PH3) is a highly toxic grain fumigant to which there is significant human workplace exposure. To determine the in vivo cytogenetic effects of inhalation of PH3, male F344/N rats and B6C3F1 mice were exposed to target concentrations of 0, 1.25, 2.5, or 5 ppm PH3 for 6 hr/day for 9 days over an 11-day period. Approximately 20 hr after the termination of exposures, blood was removed from the mice and rats by cardiac puncture and the lymphocytes cultured for analyses of sister chromatid exchanges and chromosome aberrations in rats and mice, and micronuclei (MN) in cytochalasin B-induced binucleated lymphocytes from mice. In addition, bone marrow (rats) and peripheral blood (mice) smears were made for the analysis of MN in polychromatic and normochromatic erythrocytes. No significant increase in any of the cytogenetic endpoints was found at any of the concentrations examined. These results indicate that concentrations of PH3 up to 5 ppm are not genotoxic to rodents when administered by inhalation for 9 days during an 11-day period as measured by several cytogenetic assays. To evaluate the effects of PH3 on male germ cells, a dominant lethal test was conducted in male mice exposed to 5 ppm PH3 for 10 days over a 12-day period and mated to groups of untreated females (2 females/male) on each of 6 consecutive 4-day mating intervals. None of the 6 groups of females exhibited a significant increase in percent resorptions. These results indicate that exposure to 5 ppm PH3 by inhalation does not induce dominant lethality in male mouse germ cells at steps in spermatogenesis ranging from late differentiating spermatogonia/early primary spermatocytes through mature sperm. (C) 1994 Wiley-Liss, Inc.* C1 NIEHS,ENVIRONM TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. ENVIRONM HLTH RES & TESTING INC,RES TRIANGLE PK,NC 27709. MANTECH ENVIRONM TECHNOL INC,RES TRIANGLE PK,NC 27709. RP KLIGERMAN, AD (reprint author), US EPA,DIV GENET TOXICOL,MUTAGENESIS & CELLULAR TOXICOL BRANCH,MAIL DROP-68,RES TRIANGLE PK,NC 27711, USA. NR 25 TC 8 Z9 8 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 24 IS 4 BP 301 EP 306 DI 10.1002/em.2850240407 PG 6 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA QL156 UT WOS:A1994QL15600006 PM 7851342 ER PT J AU DRAKE, JW AF DRAKE, JW TI LOOKING BACKWARD ON CT CENTURY OF MUTATION RESEARCH SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE MUTATION RESEARCH; HISTORY; MUTAGENESIS; MECHANISMS ID MUTAGENESIS; DELETION; DNA AB Our understanding of the mutation process and how it impacts target populations has deepened steadily during the hundred years since 1919. Recent advances in engineering genetically determined social traits points towards the logical culmination of this knowledge. (C) 1994 Wiley-Liss, Inc. RP DRAKE, JW (reprint author), NIEHS,MOLEC GENET LAB E301,RES TRIANGLE PK,NC 27709, USA. NR 30 TC 3 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 23 SU 24 BP 11 EP 14 DI 10.1002/em.2850230605 PG 4 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA NJ844 UT WOS:A1994NJ84400004 PM 8162900 ER PT J AU PIEGORSCH, WW LOCKHART, AMC MARGOLIN, BH TINDALL, KR GORELICK, NJ SHORT, JM CARR, GJ THOMPSON, ED SHELBY, MD AF PIEGORSCH, WW LOCKHART, AMC MARGOLIN, BH TINDALL, KR GORELICK, NJ SHORT, JM CARR, GJ THOMPSON, ED SHELBY, MD TI SOURCES OF VARIABILITY IN DATA FROM A LACI TRANSGENIC MOUSE MUTATION ASSAY SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE DNA STORAGE; EXTRABINOMIAL VARIABILITY; HIERARCHICAL SAMPLING; MUTAGENICITY; STATISTICAL METHODS; TRANSGENE; TRANSGENIC MOUSE ID SHUTTLE VECTOR; INVIVO; MICE; MODEL AB Experimental features of a transgenic mouse mutation assay based on a lad target transgene from Escherichia coli are considered in detail. Sources of variability in the experimental protocol that can affect the statistical nature of the observations are examined with the goal of identifying sources of excess variation in the observed mutant fractions. The sources include plate-to-plate (within packages), package-to-package (within animals), and animal-to-animal (within study) variability. Data from two laboratories are evaluated, using various statistical methods to identify excess variability. Results suggest only scattered patterns of excess variability, except possibly in those cases where genomic DNA from test animals is stored for extended periods (e.g., > 90 days) after isolation from tissues. Further study is encouraged to examine the validity and implications of this time/storage-related effect; (C) 1994 Wiley-Liss, Inc.* C1 UNIV N CAROLINA, CHAPEL HILL, NC USA. PROCTER & GAMBLE CO, CINCINNATI, OH USA. STRATAGENE INC, LA JOLLA, CA USA. NIEHS, RES TRIANGLE PK, NC USA. COMP SCI CORP, RES TRIANGLE PK, NC USA. RP PIEGORSCH, WW (reprint author), UNIV S CAROLINA, DEPT STAT, COLUMBIA, SC 29208 USA. OI Piegorsch, Walter/0000-0003-2725-5604 NR 22 TC 63 Z9 63 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0893-6692 EI 1098-2280 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 23 IS 1 BP 17 EP 31 DI 10.1002/em.2850230105 PG 15 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA MT842 UT WOS:A1994MT84200003 PM 8125080 ER PT J AU SHELBY, MD AF SHELBY, MD TI HUMAN GERM-CELL MUTAGENS SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE GENETIC RISK; GENETIC DISEASE; MUTATION EPIDEMIOLOGY; RISK ESTIMATION ID HUMAN-SPERM; CANCER; RADIOTHERAPY; ABERRATIONS; RADIATION; CHILDREN; MUTATION AB Human genetic disorders constitute a major public health burden in this country and around the world. The possibility that exposures to mutagenic environmental agents may result in induced genetic damage in human germ cells and thereby increase the incidence of genetic disease has been investigated in research laboratories and in epidemiology studies for decades. The capacity of ionizing radiation and some chemicals to induce transmissible genetic damage in the germ cells of laboratory mammals has been clearly demonstrated and extensively investigated. To date, no clear evidence of such effects in humans has been reported although increased frequencies of chromosomal aberrations have been detected in human sperm following exposures to radiation or chemotherapeutic agents. Evolving methods to detect molecular changes in DNA offer to improve our abilities to detect induced genetic changes. The integration of these methods into mutation epidemiology studies promises to help resolve some of the questions regarding human genetic risk. (C) 1994 Wiley-Liss, Inc. RP SHELBY, MD (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 34 TC 25 Z9 25 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 23 SU 24 BP 30 EP 34 DI 10.1002/em.2850230609 PG 5 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA NJ844 UT WOS:A1994NJ84400008 PM 8162905 ER PT J AU FOUREMAN, P MASON, JM VALENCIA, R ZIMMERING, S AF FOUREMAN, P MASON, JM VALENCIA, R ZIMMERING, S TI CHEMICAL MUTAGENESIS TESTING IN DROSOPHILA .9. RESULTS OF 50 CODED COMPOUNDS TESTED FOR THE NATIONAL-TOXICOLOGY-PROGRAM SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE SEX-LINKED RECESSIVE LETHAL; TRANSLOCATION; DROSOPHILA MELANOGASTER; MUTAGEN AB Fifty chemicals were tested for mutagenic activity in post-meiotic and meiotic germ cells of male Drosophila melanogaster using the sex-linked recessive lethal (SLRL) assay. As in the previous studies in this series, feeding was chosen as the first route of administration. If the compound failed to induce mutations by this route, injection exposure was used. One gaseous chemical (l,3-butadiene) was tested only by inhalation. Those chemicals that were mutagenic in the sex-linked recessive lethal assay were further tested for the ability to induce reciprocal translocations. Eleven of the 50 chemicals tested were mutagenic in the SLRL assay. These included bis(2-chloroethyl) ether, 1,4-butanediol diglycidyl ether, 1-chloro-2-propanol, dimethyl methylphosphonate, dimethyl morpholinophosphoramidate, dimethyloldihydroxyethylene urea, 2,2-dimethyl vinyl chloride, hexamethylphosphoramide, isatin-5-sulfonic acid (Na salt), isopropyl glycidyl ether, and urethane. Five of these, including 1,4-butanediol diglycidyl ether, 2,2-dimethyl vinyl chloride, hexamethylphosphoramide, isopropyl glycidyl ether, and urethane, also induced reciprocal (C) 1994 Wiley-Liss, Inc. C1 NIEHS,CELLULAR & GENET TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. BROWN UNIV,DIV BIOL & MED,PROVIDENCE,RI. UNIV WISCONSIN,DEPT ZOOL,MADISON,WI. FU NIEHS NIH HHS [N01-ES-3-5027, N01-ES-3-5028, N01-ES-7-5182] NR 20 TC 26 Z9 27 U1 0 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 23 IS 1 BP 51 EP 63 DI 10.1002/em.2850230109 PG 13 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA MT842 UT WOS:A1994MT84200007 PM 8125083 ER PT J AU FOUREMAN, P MASON, JM VALENCIA, R ZIMMERING, S AF FOUREMAN, P MASON, JM VALENCIA, R ZIMMERING, S TI CHEMICAL MUTAGENESIS TESTING IN DROSOPHILA .10. RESULTS OF 70 CODED CHEMICALS TESTED FOR THE NATIONAL-TOXICOLOGY-PROGRAM SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE SEX-LINKED RECESSIVE LETHAL; TRANSLOCATION; DROSOPHILA MELANOGASTER; MUTAGEN ID HAMSTER OVARY CELLS; CHROMATID EXCHANGE TESTS; SALMONELLA MUTAGENICITY; CHROMOSOME ABERRATION; MUTATION FREQUENCIES; INVITRO; CARCINOGENICITY; RODENTS; LABORATORIES; RESPONSES AB Seventy chemicals were tested for the ability to induce sex-linked recessive lethal (SLRL) mutations in postmeiotic and meiotic germ cells of male Drosophila melanogaster. As in the previous studies in this series, adult feeding was chosen as the first route of administration. If the compound failed to induce mutations by this route, injection exposure was used. Two chemicals, n-butane and propylene, were gaseous and therefore tested only by inhalation. One chemical (dimethylcarbamoyl chloride) was tested only by injection. Those chemicals that were mutagenic in the SLRL assay were further tested for the ability to induce reciprocal translocations. Sixteen of the 70 chemicals tested were mutagenic in the SLRL assay: 3-chloro-2-methylpropene, 3-(chloromethyl)pyridine HCl, dimethylcarbamoyl chloride, HC blue 1,3-iodo-1,2-propanediol, malaoxon, N,N'-methylene-bisacrylamide, 4,4'-methylenedianiline 2HCl, ziram, cis-dichlorodiaminoplatinum II, 1,2-dibromoethane, dibromomannitol, 1,2-epoxypropane, glycidol, myleran, and toluene diisocyanate. The last seven also induced reciprocal translocations. A comparison of the results from the SLRL assay with other assays for mutagens and carcinogens suggests that the SLRL assay is highly specific, but poorly sensitive, both for mutagens and potential carcinogens. (C) 1994 Wiley-Liss, Inc.* C1 NIEHS,GENET LAB,RES TRIANGLE PK,NC 27709. UNIV WISCONSIN,DEPT ZOOL,MADISON,WI 53706. BROWN UNIV,DIV BIOL & MED,PROVIDENCE,RI 02912. FU NIEHS NIH HHS [N01-ES-7-5182, N01-ES-3-5027, N01-ES-3-5028] NR 47 TC 34 Z9 35 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1994 VL 23 IS 3 BP 208 EP 227 DI 10.1002/em.2850230310 PG 20 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA NG628 UT WOS:A1994NG62800009 PM 8162896 ER PT J AU PORTIER, CJ AF PORTIER, CJ TI BIOSTATISTICAL ISSUES IN THE DESIGN AND ANALYSIS OF ANIMAL CARCINOGENICITY EXPERIMENTS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID MULTISTAGE MODEL; 2-STAGE MODELS; DNA DAMAGE; CANCER; AGENTS; REPAIR AB Two-year animal carcinogenicity experiments are used to evaluate the potential carcinogenicity from exposure to chemicals. The choice of exposure levels, the allocation of animals to doses, the length of exposure, and the choice of interim sacrifice times all affect the power of statistical tests for carcinogenic effects and the variance of interpolated estimates of carcinogenic risk. In this paper, one aspect of this problems is considered: the ability of tumor incidence data to provide information on carcinogenic mechanism and the optimal choice of design parameters with which to achieve this purpose. The direct application of biochemical data to the estimation of carcinogenic risk is also discussed in detail. RP PORTIER, CJ (reprint author), NIEHS, POB 12233, RES TRIANGLE PK, NC 27709 USA. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 17 TC 17 Z9 18 U1 0 U2 1 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 5 EP 8 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000002 PM 8187725 ER PT J AU PIEGORSCH, WW AF PIEGORSCH, WW TI STATISTICAL-MODELS FOR GENETIC SUSCEPTIBILITY IN TOXICOLOGICAL AND EPIDEMIOLOGIC INVESTIGATIONS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT International Biostatistics Conference in the Study of Toxicology CY MAY 23-25, 1991 CL UNIV TOKYO, TOKYO, JAPAN SP BIOMETR SOC, JAPANESE REG, ENVIRONM MUTAGEN SOC JAPAN, JAPANESE SOC BIOPHARM STAT, NATL INST HYGIEN SCI JAPAN, NATL INST ENVIRONM HLTH SCI US HO UNIV TOKYO ID DEBRISOQUINE METABOLIC PHENOTYPE; LUNG-CANCER; MOLECULAR-GENETICS; SIGNIFICANCE TESTS; BLADDER-CANCER; POLYMORPHISM; TABLES; LOCUS; MICE; RISK AB Models are presented for use in assessing genetic susceptibility to cancer (or other diseases) with animal or human data. Observations are assumed to be in the form of proportions, hence a binomial sampling distribution is considered. Generalized linear models are employed to model the response as a function of the genetic component; these include logistic and complementary log forms. Susceptibility is measured via odds ratios of response, relative to a background genetic group. Significance tests and confidence intervals for these odds ratios are based on maximum Likelihood estimates of the regression parameters. Additional consideration is given to the problem of gene-environment interactions and to testing whether certain genetic identifiers/categories may be collapsed into a smaller set of categories. The collapsibility hypothesis provides an example of a mechanistic context wherein nonhierarchical models for the linear predictor can sometimes make sense. C1 NIEHS,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709. OI Piegorsch, Walter/0000-0003-2725-5604 NR 47 TC 1 Z9 1 U1 1 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 77 EP 82 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000013 PM 8187729 ER PT J AU MARGOLIN, BH KIM, BS SMITH, MG FETTERMAN, BA PIEGORSCH, WW ZEIGER, E AF MARGOLIN, BH KIM, BS SMITH, MG FETTERMAN, BA PIEGORSCH, WW ZEIGER, E TI SOME COMMENTS ON POTENCY MEASURES IN MUTAGENICITY RESEARCH SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID PREDICTING RODENT CARCINOGENICITY; GENETIC TOXICITY ASSAYS; STATISTICAL-ANALYSIS; CHEMICALS AB In this article, the measurement of the potency of a chemical or mixture from its dose response in a particular assay is addressed. Attention is focused on data from the Ames Salmonella assay. Three measures of potency are explored and shown to be highly correlated. The presentation then discusses specific areas of research that might benefit from a study of potency. C1 YONSEI UNIV, DEPT APPL STAT, SEOUL 120749, SOUTH KOREA. NIEHS, STAT & BIOMATH BRANCH, RES TRIANGLE PK, NC 27709 USA. NIEHS, EXPTL TOXICOL BRANCH, RES TRIANGLE PK, NC 27709 USA. RP MARGOLIN, BH (reprint author), UNIV N CAROLINA, SCH PUBL HLTH, DEPT BIOSTAT, CHAPEL HILL, NC 27599 USA. OI Piegorsch, Walter/0000-0003-2725-5604 FU NIEHS NIH HHS [5 T32 ES07018]; PHS HHS [293-90-1-0005] NR 12 TC 6 Z9 6 U1 0 U2 0 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 91 EP 94 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000015 PM 8187732 ER PT J AU HOEL, DG PORTIER, CJ AF HOEL, DG PORTIER, CJ TI NONLINEARITY OF DOSE-RESPONSE FUNCTIONS FOR CARCINOGENICITY SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT International Biostatistics Conference in the Study of Toxicology CY MAY 23-25, 1991 CL UNIV TOKYO, TOKYO, JAPAN SP BIOMETR SOC, JAPANESE REG, ENVIRONM MUTAGEN SOC JAPAN, JAPANESE SOC BIOPHARM STAT, NATL INST HYGIEN SCI JAPAN, NATL INST ENVIRONM HLTH SCI US HO UNIV TOKYO ID RISK ASSESSMENT; CANCER; MODEL; PROMOTION; EXPOSURE; POLICY; DNA AB Carcinogenesis data for 315 chemicals were obtained from the National Cancer Institute-National Toxicology Program (NCI-NTP) bioassay programs and were analyzed to examine the shape of carcinogenesis dose-response curves. Tumor site data were more often consistent with a quadratic response than with a linear response, suggesting that the routine use of linear dose-response models will often overestimate risk. Information from in vivo short-term mutagenicity and genotoxicity assays was also obtained for most of these rodent bioassays. It was found that there were no clear relationships between the shape of the carcinogenesis dose-response curve and the result of the short-term test. These observations argue against the concept that carcinogens that are positive in a short-term assay be regulated using a Linear dose-response curve and those that are negative be regulated using a sublinear dose-response curve or a safety factor approach. C1 NIEHS,RES TRIANGLE PK,NC 27709. RI Portier, Christopher/A-3160-2010 OI Portier, Christopher/0000-0002-0954-0279 NR 78 TC 32 Z9 32 U1 0 U2 4 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 109 EP 113 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000018 PM 8187698 ER PT J AU SUK, WA AF SUK, WA TI SUPERFUND BASIC RESEARCH-PROGRAM MEETING REPORTS - INTRODUCTION SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material RP SUK, WA (reprint author), NIEHS,DIV EXTRAMURAL RES & TRAINING,SUPER BASIC RES PROGRAM,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 219 EP 220 PG 2 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000031 ER PT J AU KAMRIN, MA FISCHER, LJ SUK, WA FOUTS, JR PELLIZZARI, E THORNTON, K AF KAMRIN, MA FISCHER, LJ SUK, WA FOUTS, JR PELLIZZARI, E THORNTON, K TI ASSESSMENT OF HUMAN EXPOSURE TO CHEMICALS FROM SUPERFUND SITES SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID POLYCHLORINATED-BIPHENYLS; ORGANIC-CHEMICALS; TRANSPORT; MODEL; PHARMACOKINETICS; CONTAMINANTS; SOIL; ZONE; FISH C1 NIEHS, DIV EXTRAMURAL RES & TRAINING, SUPERFUND BASIC RES PROGRAM, RES TRIANGLE PK, NC 27709 USA. RES TRIANGLE INST, RES TRIANGLE PK, NC 27709 USA. FTN ASSOCIATES, LITTLE ROCK, AR 72211 USA. RP KAMRIN, MA (reprint author), MICHIGAN STATE UNIV, INST ENVIRONM TOXICOL, C-231 HOLDEN HALL, E LANSING, MI 48824 USA. NR 57 TC 6 Z9 6 U1 0 U2 2 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 221 EP 228 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000032 PM 8187712 ER PT J AU SMITH, MT SUK, WA AF SMITH, MT SUK, WA TI APPLICATION OF MOLECULAR BIOMARKERS IN EPIDEMIOLOGY SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT International Biostatistics Conference in the Study of Toxicology CY MAY 23-25, 1991 CL UNIV TOKYO, TOKYO, JAPAN SP BIOMETR SOC, JAPANESE REG, ENVIRONM MUTAGEN SOC JAPAN, JAPANESE SOC BIOPHARM STAT, NATL INST HYGIEN SCI JAPAN, NATL INST ENVIRONM HLTH SCI US HO UNIV TOKYO C1 NIEHS,DIV EXTRAMURAL RES & TRAINING,SUPERFUND BASIC RES PROGRAM,RES TRIANGLE PK,NC 27709. UNIV CALIF BERKELEY,SCH PUBL HLTH,DEPT BIOMED & ENVIRONM HLTH SCI,BERKELEY,CA 94720. NR 5 TC 5 Z9 5 U1 0 U2 0 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 229 EP 235 PG 7 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000033 PM 8187713 ER PT J AU SAROFIM, AF SUK, WA AF SAROFIM, AF SUK, WA TI HEALTH-EFFECTS OF COMBUSTION BY-PRODUCTS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID TOXICITY; MODEL C1 NIEHS,DIV EXTRAMURAL RES & TRAINING,SUPERFUND BASIC RES PROGRAM,RES TRIANGLE PK,NC 27709. MIT,BOSTON,MA. NR 21 TC 6 Z9 6 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 237 EP 244 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000034 PM 8187714 ER PT J AU AUST, SD BOURQUIN, A LOPER, JC SALANITRO, JP SUK, WA TIEDJE, J AF AUST, SD BOURQUIN, A LOPER, JC SALANITRO, JP SUK, WA TIEDJE, J TI BIODEGRADATION OF HAZARDOUS WASTES SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT International Biostatistics Conference in the Study of Toxicology CY MAY 23-25, 1991 CL UNIV TOKYO, TOKYO, JAPAN SP BIOMETR SOC, JAPANESE REG, ENVIRONM MUTAGEN SOC JAPAN, JAPANESE SOC BIOPHARM STAT, NATL INST HYGIEN SCI JAPAN, NATL INST ENVIRONM HLTH SCI US HO UNIV TOKYO ID TRICHLOROETHYLENE; MINERALIZATION; AQUIFER; SAND C1 NIEHS,RES TRIANGLE PK,NC 27709. UTAH STATE UNIV,CTR BIOTECHNOL,LOGAN,UT 84322. ECOVA,CORPORATE OFF,REDMOND,WA 98052. UNIV CINCINNATI,DEPT MOLEC GENET BIOCHEM & MICROBIOL,CINCINNATI,OH 45267. SHELL DEV CO,WESTHOLLOW RES CTR,HOUSTON,TX 77251. MICHIGAN STATE UNIV,E LANSING,MI 48824. NR 14 TC 2 Z9 2 U1 0 U2 0 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 1994 VL 102 SU 1 BP 245 EP 252 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NB330 UT WOS:A1994NB33000035 PM 8187715 ER PT J AU SECHI, S PARMELEE, D ROLLER, PP JENNINGS, GT AF SECHI, S PARMELEE, D ROLLER, PP JENNINGS, GT TI STRUCTURAL CHARACTERIZATION OF CYTOSOLIC NADP(+)-DEPENDENT ISOCITRATE DEHYDROGENASE FROM RAT OVARY SO ENZYME & PROTEIN LA English DT Article DE ISOCITRATE DEHYDROGENASE; NADP; CIRCULAR DICHROISM; AMINO ACID SEQUENCE; RAT; OVARY; UNFOLDING ID MITOCHONDRIAL; PURIFICATION; SEQUENCE; HEART; LIVER; ISOENZYMES; GENE; PIG AB Cytosolic NADP(+)-dependent isocitrate dehydrogenase was purified to homogeneity from superovulated rat ovaries. Amino acid sequence information was obtained by analyzing peptides generated by digestion with either cyanogen bromide or trypsin. Eleven peptides were sequenced and a total of 146 amino acids were identified. Nine of these peptides were found to be 60-100% identical with sequences from mitochondrial NADP(+)-dependent isocitrate dehydrogenase. Conservation of amino acids was observed for residues that were previously identified as potentially binding isocitrate-Mg2+. Circular dichroism measurements showed that the structure is composed of approximately 35% alpha-helix and 21% beta-sheet segments. Temperature denaturation studies indicated that the enzyme is more stable in the presence of isocitrate. C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. NIH,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NR 25 TC 0 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1019-6773 J9 ENZYME PROTEIN JI Enzyme Protein PY 1994 VL 48 IS 1 BP 27 EP 36 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QQ547 UT WOS:A1994QQ54700004 PM 7787968 ER PT J AU GERMOLEC, DR LUSTER, MI AF GERMOLEC, DR LUSTER, MI TI HYPERSENSITIVITY AND OCCUPATIONAL EXPOSURE SO EOS-RIVISTA DI IMMUNOLOGIA ED IMMUNOFARMACOLOGIA LA English DT Article ID CROSS-SECTIONAL SURVEY; PLATINUM REFINERY; RESPIRATORY ALLERGY; NICKEL DERMATITIS; ASTHMA; WORKERS; SENSITIZATION; FORMALDEHYDE; PESTICIDES; CHEMICALS C1 NIEHS,ENVIRONM IMMUNOL & NEUROBIOL GRP,RES TRIANGLE PK,NC 27709. NR 58 TC 0 Z9 0 U1 0 U2 1 PU SIGMA-TAU PI ROME PA VIALE SHAKESPEARE 47, 00144 ROME, ITALY SN 0392-6699 J9 EOS-RIV IMMUNOL PY 1994 VL 14 IS 3-4 BP 107 EP 113 PG 7 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA RH836 UT WOS:A1994RH83600004 ER PT J AU COUGHLIN, SS BENICHOU, J WEED, DL AF COUGHLIN, SS BENICHOU, J WEED, DL TI ATTRIBUTABLE RISK-ESTIMATION IN CASE-CONTROL STUDIES SO EPIDEMIOLOGIC REVIEWS LA English DT Article ID BREAST-CANCER; CONFIDENCE-INTERVALS; LOGISTIC-REGRESSION; LARGE-STRATA; SPARSE DATA; MODELS; FRACTION; CONSUMPTION; PROBABILITY; ADJUSTMENT C1 NCI,DIV CANC PREVENT & CONTROL,PREVENT ONCOL BRANCH,BETHESDA,MD 20892. NCI,DIV CANC ETIOL,BIOSTAT BRANCH,BETHESDA,MD 20892. RP COUGHLIN, SS (reprint author), TULANE UNIV,SCH PUBL HLTH & TROP MED,DEPT BIOSTAT & EPIDEMIOL,1430 TULANE AVE,NEW ORLEANS,LA 70112, USA. RI Osborne, Nicholas/N-4915-2015 OI Osborne, Nicholas/0000-0002-6700-2284 FU NCI NIH HHS [1P30-CA51008, 1P50-CA58185]; NHLBI NIH HHS [R29 HL44904] NR 52 TC 110 Z9 111 U1 2 U2 7 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1994 VL 16 IS 1 BP 51 EP 64 PG 14 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NW918 UT WOS:A1994NW91800005 PM 7925727 ER PT J AU DWYER, DM STRICKLER, H GOODMAN, RA ARMENIAN, HK AF DWYER, DM STRICKLER, H GOODMAN, RA ARMENIAN, HK TI USE OF CASE-CONTROL STUDIES IN OUTBREAK INVESTIGATIONS SO EPIDEMIOLOGIC REVIEWS LA English DT Article ID TOXIC-SHOCK SYNDROME; EOSINOPHILIA-MYALGIA SYNDROME; PUBLIC-HEALTH-SERVICE; RISK-FACTORS; LEGIONNAIRES-DISEASE; MULTISTATE OUTBREAK; WOUND INFECTIONS; REYES-SYNDROME; CONSUMPTION; EPIDEMIOLOGY C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. CTR DIS CONTROL & PREVENT,EPIDEMIOL PROGRAM OFF,ATLANTA,GA 30341. RP DWYER, DM (reprint author), MARYLAND DEPT HLTH & MENTAL HYG,CTR CLIN EPIDEMIOL,EPIDEMIOL & DIS CONTROL PROGRAM,BALTIMORE,MD 21201, USA. NR 56 TC 20 Z9 20 U1 3 U2 3 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1994 VL 16 IS 1 BP 109 EP 123 PG 15 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NW918 UT WOS:A1994NW91800010 PM 7925720 ER PT J AU RON, E CARTER, R JABLON, S MABUCHI, K AF RON, E CARTER, R JABLON, S MABUCHI, K TI AGREEMENT BETWEEN DEATH CERTIFICATE AND AUTOPSY DIAGNOSES AMONG ATOMIC-BOMB SURVIVORS SO EPIDEMIOLOGY LA English DT Article DE AUTOPSY; DEATH CERTIFICATES; MORTALITY; CAUSE OF DEATH; VALIDATION STUDY; SENSITIVITY; SPECIFICITY; RADIATION EXPOSURE; NEOPLASMS; CARDIOVASCULAR DISEASES; INFECTIOUS DISEASES AB Based on the Atomic Bomb Casualty Commission/Radiation Effects Research Foundation series of over 5,000 autopsies, we examined death certificate accuracy for 12 disease categories and assessed the effect of potential modifying factors on agreement and accuracy. The overall percentage agree ment between death certificate and autopsy diagnoses was only 52.5%. Although neoplasms had the highest detection rate, almost 25% of cancers diagnosed at autopsy were nevertheless missed on death certificates. Confirmation and detection rates were above 70% for neoplasms and external causes of death only. Confirmation rates were between 50 and 70% for infectious diseases and heart and other vascular diseases. Detection rates reached a similar level for infectious, cerebrovascular, and digestive diseases. Specificity rates were above 90% for all except the cerebrovascular disease category. Overall agreement decreased with increasing age at death and was worse for deaths occurring outside of hospital. There was some suggestion that agreement improved over time, bur no indication that radiation dose, sex, city of residence, or inclusion in a biennial clinical examination program influenced agreement. Since the inaccuracy of death certificate diagnoses can have major implications for health research and planning, it is important to be aware that their accuracy is low and that it can vary widely depending on cause, age, and place of death. RP RON, E (reprint author), NCI,RADIAT EPIDEMIOL BRANCH,EPN-408,BETHESDA,MD 20892, USA. NR 0 TC 51 Z9 54 U1 0 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 1994 VL 5 IS 1 BP 48 EP 56 DI 10.1097/00001648-199401000-00009 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MQ008 UT WOS:A1994MQ00800009 PM 8117782 ER PT J AU DOSEMECI, M COCCO, P GOMEZ, M STEWART, PA HEINEMAN, EF AF DOSEMECI, M COCCO, P GOMEZ, M STEWART, PA HEINEMAN, EF TI EFFECTS OF 3 FEATURES OF A JOB-EXPOSURE MATRIX ON RISK ESTIMATES SO EPIDEMIOLOGY LA English DT Note DE MISCLASSIFICATION; EXPOSURE ASSESSMENT; EXPOSURE CATEGORIZATION; JOB-EXPOSURE MATRICES; OCCUPATIONAL EXPOSURES; EPIDEMIOLOGIC METHODS; DATA COLLECTION; BIAS AB We tested the impact of three features of a job-exposure matrix on risk estimates in a case-control study that evaluated the association of methylene chloride and astrocytic brain cancer. These features were probability of use of the agent; the consideration of decade of predominant use of methylene chloride within each occupation; and the use of a more specific industrial occupational coding system. We compared the risk estimates obtained with and without these features. The introduction of each feature had a striking effect on the estimate of relative risk. The odds ratio ranged from 1.47 with none of these features, to 2.47 with high probability of exposure within industry and occupation, to 4.15 with high probability of exposure and specific industrial-occupational coding, to 6.08 with the three features together. These results indicate that the degree of exposure misclassification can be reduced by the introduction of these features into the job-exposure matrix. RP DOSEMECI, M (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,OCCUPAT STUDIES SECT,EBP,EXECUT PLAZA N,ROOM 418,ROCKVILLE,MD 20892, USA. NR 0 TC 55 Z9 55 U1 1 U2 7 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 1994 VL 5 IS 1 BP 124 EP 127 DI 10.1097/00001648-199401000-00019 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA MQ008 UT WOS:A1994MQ00800019 PM 8117771 ER EF