FN Thomson Reuters Web of Science™ VR 1.0 PT J AU MALAWER, MM DUNHAM, W AF MALAWER, MM DUNHAM, W TI CRYOSURGERY AND ACRYLIC CEMENTATION AS SURGICAL ADJUNCTS IN THE TREATMENT OF AGGRESSIVE (BENIGN) BONE-TUMORS - ANALYSIS OF 25 PATIENTS BELOW THE AGE OF 21 SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID MAMMALIAN-CELLS AB This article reviews the clinical experience with cryosurgery (use of liquid nitrogen) and acrylic cementation (polymethylmethacrylate; PMMA) in the treatment of aggressive, benign bone sarcomas and the biologic basis of this technique. The results of 25 patients below the age of 21 treated by cryosurgery, with an average follow-up period of 60.8 months, are reported. Three approaches to surgical reconstruction were used: Group 1 (four patients) had cryosurgery with no reconstruction, Group 2 (13 patients) had bone graft reconstruction alone, and Group 3 (eight patients) had composite osteosynthesis with internal fixation, bone graft, and/or PMMA. The overall control rate was 96% (one recurrence). The tumor types were giant-cell tumor, chondroblastoma, aneurysmal bone cyst, and malignant giant-cell tumor. Nineteen lesions involved the lower extremity, and six lesions were located in the upper extremity. There were two secondary fractures (8%), one local flap necrosis, and one synovial fistula. There were no infections. Two epiphyseodeses were performed. The functional results were excellent (83%), good (13%), and fair (4%). The technique of composite osteosynthesis is recommended for all large tumors of the lower extremity. Cryosurgical results compare favorably with those obtained by en bloc resection and demonstrate the ability of cryosurgery to eradicate tumors while avoiding the need for extensive resections and reconstructive procedures. C1 NCI,SURG BRANCH,BETHESDA,MD 20892. UNIV ALABAMA,SCH MED,DEPT ORTHOPED,BIRMINGHAM,AL 35233. RP MALAWER, MM (reprint author), GEORGE WASHINGTON UNIV,CHILDRENS HOSP,MED CTR,SCH MED,111 MICHIGAN AVE NW,WASHINGTON,DC 20010, USA. NR 40 TC 55 Z9 55 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD JAN PY 1991 IS 262 BP 42 EP 57 PG 16 WC Orthopedics; Surgery SC Orthopedics; Surgery GA ET233 UT WOS:A1991ET23300007 PM 1984931 ER PT J AU MURPHY, CS PIETENPOL, JA MUNGER, K HOWLEY, PM MOSES, HL AF MURPHY, CS PIETENPOL, JA MUNGER, K HOWLEY, PM MOSES, HL TI C-MYC AND PRB - ROLE IN TGF-BETA-1 INHIBITION OF KERATINOCYTE PROLIFERATION SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID TRANSFORMING GROWTH-FACTOR; RETINOBLASTOMA GENE-PRODUCT; ADENOVIRUS E1A PROTEINS; SERUM-FREE MEDIUM; FACTOR-BETA; MESSENGER-RNA; TRANSCRIPTION FACTOR; SUSCEPTIBILITY GENE; CELLULAR PROTEINS; CANCER-CELLS C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. VANDERBILT UNIV,MED CTR,SCH MED,DEPT CELL BIOL,NASHVILLE,TN 37232. FU NCI NIH HHS [CA-09592, CA-48799, CA-42572] NR 41 TC 25 Z9 25 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 1991 VL 56 BP 129 EP 135 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800016 PM 1819482 ER PT J AU HOWLEY, PM SCHEFFNER, M HUIBREGTSE, J MUNGER, K AF HOWLEY, PM SCHEFFNER, M HUIBREGTSE, J MUNGER, K TI ONCOPROTEINS ENCODED BY THE CANCER-ASSOCIATED HUMAN PAPILLOMAVIRUSES TARGET THE PRODUCTS OF THE RETINOBLASTOMA AND P53 TUMOR-SUPPRESSOR GENES SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID CARCINOMA CELL-LINES; HPV18 REGULATORY REGION; CERVICAL-CARCINOMA; HUMAN KERATINOCYTES; ADENOVIRUS E1A; T-ANTIGEN; SV40-TRANSFORMED CELLS; BIOLOGICAL-ACTIVITIES; SUSCEPTIBILITY GENE; TRANSFORMED-CELLS C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. RI Scheffner, Martin/K-2940-2012; OI Scheffner, Martin/0000-0003-2229-0128; Munger, Karl/0000-0003-3288-9935 NR 60 TC 36 Z9 36 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 1991 VL 56 BP 149 EP 155 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800018 PM 1668080 ER PT J AU JOHNSTON, LH LOWNDES, NF JOHNSON, AL SUGINO, A AF JOHNSTON, LH LOWNDES, NF JOHNSON, AL SUGINO, A TI A CELL-CYCLE-REGULATED TRANSFACTOR, DSC1, CONTROLS EXPRESSION OF DNA-SYNTHESIS GENES IN YEAST SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID SACCHAROMYCES-CEREVISIAE; RIBONUCLEOTIDE REDUCTASE; CHROMOSOME-REPLICATION; S-PHASE; TRANSCRIPTION; PROTEIN; INITIATION; HOMOLOGY; SEQUENCE; SUBUNIT C1 NATL INST MED RES,YEAST GENET LAB,LONDON NW7 1AA,ENGLAND. NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709. OI Lowndes, Noel/0000-0002-3216-4427 NR 25 TC 19 Z9 19 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 1991 VL 56 BP 169 EP 176 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800021 PM 1819484 ER PT J AU TRUN, NJ GOTTESMAN, S LOBNEROLESEN, A AF TRUN, NJ GOTTESMAN, S LOBNEROLESEN, A TI ANALYSIS OF ESCHERICHIA-COLI MUTANTS WITH ALTERED DNA CONTENT SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID CELL-CYCLE; REPLICATION; K-12; INITIATION; DIVISION; PROTEIN; ORIGIN; EVENTS; PLOIDY; PHASE C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20982. TECH UNIV DENMARK,DEPT MICROBIOL,DK-2800 LYNGBY,DENMARK. RI Lobner-Olesen, Anders/K-4344-2014 OI Lobner-Olesen, Anders/0000-0002-0344-6417 NR 22 TC 3 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 1991 VL 56 BP 353 EP 358 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800041 PM 1819496 ER PT J AU DAAR, I ZHOU, R SHEN, RL NEBREDA, A OSKARSSON, M SANTOS, E DASILVA, PP MASUI, Y WOUDE, GFV AF DAAR, I ZHOU, R SHEN, RL NEBREDA, A OSKARSSON, M SANTOS, E DASILVA, PP MASUI, Y WOUDE, GFV TI MOS AND RAS - 2 ONCOPROTEINS THAT DISPLAY M-PHASE ACTIVITY SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID MATURATION-PROMOTING FACTOR; PROTO-ONCOGENE PRODUCT; GERMINAL-VESICLE BREAKDOWN; AMPHIBIAN EGG CYTOSOLS; MURINE SARCOMA-VIRUS; XENOPUS OOCYTES; CELL-CYCLE; SACCHAROMYCES-CEREVISIAE; CHROMOSOME CONDENSATION; PROTOONCOGENE PRODUCT C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. UNIV TORONTO,DEPT ZOOL,TORONTO M5S 1A1,ONTARIO,CANADA. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,DCBD,MATH BIOL LAB,MEMBRANE BIOL SECT,INTRAMURAL RES PROGRAM,FREDERICK,MD 21702. RI Shen, Rulong/E-4079-2011; OI Daar, Ira/0000-0003-2657-526X FU NCI NIH HHS [N01-CO-74101] NR 56 TC 1 Z9 1 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 1991 VL 56 BP 477 EP 488 PG 12 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800053 PM 1840260 ER PT J AU SIKORSKI, RS MICHAUD, WA WOOTTON, JC BOGUSKI, MS CONNELLY, C HIETER, P AF SIKORSKI, RS MICHAUD, WA WOOTTON, JC BOGUSKI, MS CONNELLY, C HIETER, P TI TPR PROTEINS AS ESSENTIAL COMPONENTS OF THE YEAST-CELL CYCLE SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID MITOTIC CHROMOSOME TRANSMISSION; SACCHAROMYCES-CEREVISIAE; GENES; MITOSIS; FAMILY; FIDELITY; MUTANTS; CDC28; MOTIF C1 NIH, NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20892 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT MOLEC BIOL & GENET, BALTIMORE, MD 21205 USA. FU NCI NIH HHS [CA-16519] NR 31 TC 70 Z9 72 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1991 VL 56 BP 663 EP 673 PG 11 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LC658 UT WOS:A1991LC65800074 PM 1819514 ER PT J AU JAIN, RB AF JAIN, RB TI ON THE ADEQUACY OF SAMPLE-SIZE DETERMINATION FORMULAS FOR 2 INDEPENDENT PROPORTIONS SO COMMUNICATIONS IN STATISTICS-SIMULATION AND COMPUTATION LA English DT Article DE STATISTICAL POWER; CONTINUITY CORRECTION; TESTS FOR 2 PROPORTIONS ID ARC SINE; APPROXIMATION AB The performance of six sample size determination formulae for two independent binomial proportions in achieving nominal levels of alpha and beta was evaluated by simulation methods. The formula given in Fleiss (1981) which is not corrected for continuity outperformed other five formulae for beta less-than-or-equal-to 10% for N > 20 and for beta > 10% for N > 100. For N less-than-or-equal-to 20, beta less-than-or-equal-to 10% and for N less-than-or-equal-to 100, beta > 10%, continuity corrected formula of Fleiss, Tytun and Ury (1980) and/or doubly continuity corrected formula of Kramer and Greenhouse (1959) may be the only satisfactory formulae to use. C1 NIDA,DIV MEDICAT DEV,ROCKVILLE,MD 20857. NR 13 TC 2 Z9 2 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0361-0918 J9 COMMUN STAT SIMULAT JI Commun. Stat.-Simul. Comput. PY 1991 VL 20 IS 2-3 BP 585 EP 617 DI 10.1080/03610919108812973 PG 33 WC Statistics & Probability SC Mathematics GA GA751 UT WOS:A1991GA75100013 ER PT J AU YU, KF AF YU, KF TI A NOTE ON THE ESTIMATION OF THE MIXING PARAMETER IN A MIXTURE OF 2 DISTRIBUTIONS SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE MIXTURE; MIXING PARAMETER; METHOD OF MOMENTS; BAYES PROCEDURE; SEQUENTIAL PROCEDURE AND MAXIMUM LIKELIHOOD ESTIMATION AB Various classical methods of estimation are compared with those proposed by From (1989) for the estimation of the mixing parameter in a mixture of two distributions. Emphasis is put on the actual implementation of the estimation methods. C1 UNIV S CAROLINA,COLUMBIA,SC 29208. NICHHD,DPR,BMSB,BETHESDA,MD 20892. NR 4 TC 5 Z9 11 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 1991 VL 20 IS 2 BP 595 EP 609 DI 10.1080/03610929108830517 PG 15 WC Statistics & Probability SC Mathematics GA FR390 UT WOS:A1991FR39000013 ER PT J AU BAKER, SG AF BAKER, SG TI EVALUATING A NEW TEST USING A REFERENCE TEST WITH ESTIMATED SENSITIVITY AND SPECIFICITY SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE DOUBLE SAMPLING; EM ALGORITHM; MISCLASSIFICATION; MISSING DATA ID LOG-LINEAR-MODELS; DIAGNOSTIC-TESTS; CATEGORICAL-DATA; EM ALGORITHM; MISCLASSIFICATION ERRORS; VARIABLES AB Methodology is proposed for evaluating a new test using a reference test. Unlike previous methodology, sensitivity and the specificity of the reference test are not assumed to be known; instead they are estimated from data comparing the reference test with a gold standard. C1 NCI,BETHESDA,MD 20892. NR 21 TC 13 Z9 13 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 1991 VL 20 IS 9 BP 2739 EP 2752 DI 10.1080/03610929108830665 PG 14 WC Statistics & Probability SC Mathematics GA GG976 UT WOS:A1991GG97600001 ER PT J AU WUN, LM AF WUN, LM TI REGRESSION-ANALYSIS OF AUTOCORRELATED POISSON-DISTRIBUTED DATA SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE AUTOCORRELATION; GENERALIZED LEAST SQUARES; HETEROSCEDASTICITY; POISSON DISTRIBUTION; REPEATED MEASUREMENT ID REPEATED MEASURES DESIGNS AB A regression model assuming Poisson-distributed data with autocorrelated errors falls into the class of regression models that have the error structure which is both heteroscedastic and autocorrelated. In general, this class of regression models are not estimable. However, due to the properties of the Poisson distribution that the variance is equal to the mean, this regression model on Poisson-distributed data with autocorrelated errors is estimable. In this note the special structure of the covariance matrix of the model with the first order autocorrelated error is derived utilizing this property. A method based on the least squares method of Frome, Kutner, and Beauchamp (1973), supplemented by steps for handling autocorrelation in studies of time series analysis, nonlinear regression, and econometrics is presented for obtaining generalized least squares estimates for the parameters of the model. C1 NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. NR 13 TC 0 Z9 0 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 1991 VL 20 IS 10 BP 3083 EP 3091 DI 10.1080/03610929108830689 PG 9 WC Statistics & Probability SC Mathematics GA GK939 UT WOS:A1991GK93900003 ER PT J AU NICHOLAS, KR COLLET, C JOSEPH, R SANKARAN, L AF NICHOLAS, KR COLLET, C JOSEPH, R SANKARAN, L TI HORMONE-RESPONSIVE SURVIVAL OF MAMMARY-GLAND EXPLANTS FROM THE PREGNANT TAMMAR WALLABY (MACROPUS-EUGENII) IN THE ABSENCE OF EXOGENOUS HORMONES AND GROWTH-FACTORS SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-PHYSIOLOGY LA English DT Article ID ALPHA-LACTALBUMIN; EPITHELIAL-CELLS; CASEIN GENE; INSULIN; PROLACTIN; ACCUMULATION; EXPRESSION; LACTATION; CLONING; BIOLOGY AB 1. The level of beta-lactoglobulin mRNA increased maximally in mammary explants from late pregnant tammars cultured for 3 days in media containing either prolactin or insulin, cortisol and prolactin. 2. The same level of accumulation occurred when explants were first cultured for 4 days in a chemically defined medium with no exogenous hormones, serum or growth factors, suggesting that the tissue remains viable and hormone-responsive during the initial incubation. 3. Mammary explants cultured for 4 days in medium with no hormones demonstrated a progressive increase in the rate of RNA and DNA synthesis suggesting that the tissue is under a positive autocrine/paracrine stimulus. C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. RP NICHOLAS, KR (reprint author), CSIRO,DIV WILDLIFE & ECOL,POB 84,LYNEHAM,ACT 2602,AUSTRALIA. RI Collet, Christopher/I-9737-2012 NR 24 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 0300-9629 J9 COMP BIOCHEM PHYS A JI Comp. Biochem. Physiol. A-Physiol. PY 1991 VL 100 IS 1 BP 163 EP 167 DI 10.1016/0300-9629(91)90201-M PG 5 WC Biochemistry & Molecular Biology; Physiology; Zoology SC Biochemistry & Molecular Biology; Physiology; Zoology GA GM017 UT WOS:A1991GM01700023 PM 1682093 ER PT J AU TULP, OL DEBOLT, SP HANSEN, CT MICHAELIS, OE AF TULP, OL DEBOLT, SP HANSEN, CT MICHAELIS, OE TI EFFECTS OF DIETARY CARBOHYDRATE AND PHENOTYPE ON ADIPOSE CELLULARITY IN FEMALE SHR/N-CP RATS SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-PHYSIOLOGY LA English DT Article ID THERMOGENESIS; TISSUE; CORPULENT; OBESITY AB 1. Adipose mass and cellularity were studied in congenic female SHR/N-cp rats fed iosenergetic diets containing 54% carbohydrate as sucrose (SU) or cooked cornstarch (CS), 20% protein, 16% mixed dietary fat plus vitamins, minerals, and non-nutritive fiber ad libitum from 5 weeks until 8.5 months of age. Measures of adipocyte lipid content, cell number per depot, and mass of principal white (WAT) and interscapular brown (IBAT) adipoe tissue depots were determined at the end of the study. 2. Final body weights (BW) of corpulent rats were more than twice those of their lean littermates, and were greater when fed the SU than the CS diet in both phenotypes. Phenotype effects (corpulent > lean) were present for fat pad weight, adipocyte number, and adipocyte lipid content in the dorsal (DOR) and retroperitoneal (RP) WAT depots. Diet effects were present for depot weight, adipocyte number, and adipocyte lipid content in both WAT depots, and were of qualitatively similar magnitude in both phenotypes. 3. IBAT weights, IBAT:BW ratios, and IBAT cell number of corpulent > lean, and were > with SU than CS diet in both phenotypes. 4. These results indicate that obesity in the corpulent phenotype of the SHR/N-cp rat occurs as the result of hypertrophy and hyperplasia of white adipose tissue, and that isoenergetic substitution of simple for complex carbohydrate resulted in greater fat accretion in both phenotypes. The greater diet and phenotype-associated adiposity occurred despite greater mass and cellularity of BAT. The results also indicate that sexual dimorphism occurs regarding effects of diet and phenotype on expression of adipose tissue development in this strain. C1 NIH,VET RESOURCES BRANCH,BETHESDA,MD 20705. USDA,ARS,BELTSVILLE HUMAN NUTR RES CTR,BELTSVILLE,MD 20507. RP TULP, OL (reprint author), DREXEL UNIV,COLL ARTS & SCI,DEPT NUTR & FOOD SCI,DIV LIFE SCI,PHILADELPHIA,PA 19104, USA. NR 38 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0300-9629 J9 COMP BIOCHEM PHYS A JI Comp. Biochem. Physiol. A-Physiol. PY 1991 VL 99 IS 1-2 BP 229 EP 234 DI 10.1016/0300-9629(91)90264-D PG 6 WC Biochemistry & Molecular Biology; Physiology; Zoology SC Biochemistry & Molecular Biology; Physiology; Zoology GA FF833 UT WOS:A1991FF83300041 PM 1675951 ER PT J AU TULP, OL HANSEN, CT MCKEE, K MICHAELIS, OE AF TULP, OL HANSEN, CT MCKEE, K MICHAELIS, OE TI EFFECTS OF DIET AND PHENOTYPE ON ADIPOSE CELLULARITY AND 5'-DEIODINASE ACTIVITY OF LIVER AND BROWN ADIPOSE-TISSUE OF DIABETIC SHR/N-CP RATS SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-PHYSIOLOGY LA English DT Article ID CORPULENT RAT; LA/N-CORPULENT; THERMOGENESIS; PARAMETERS; DISEASE; SUCROSE; OBESE; T4 AB 1. Groups of lean and obese male SHR/N-cp rats were fed isoenergetic diets containing 54% carbohydrate as cornstarch (CS) or sucrose (SU) plus other nutrients from 5 weeks of age, and measures of adiposity, thyroxine 5' deiodinase (T4-5'DI) activity, and tissue and plasma triiodothyronine (T3) content determined at 9.5 months of age. 2. Body weights (BW) of obese > lean, and were greater when fed the SU than CS diet in both phenotypes. Phenotype effects (obese > lean) were present for fat pad weights and adipose cellularity in most primary adipose tissue depots, and diet effects (SU > CS) were present for epididymal and retroperitoneal depots in both phenotypes. 3. Interscapular brown adipose tissue (IBAT) and IBAT:BW ratios of obese > lean, and diet effects (SU > CS) were present for lean but not obese rats. Liver T4-5'DI activity and plasma and tissue T3 of lean > obese, while IBAT 5'DI activity of obese > lean in the CS diet. 4. These results indicate that obesity occurs in the SHR/N-cp rat as the result of hypertrophy and hyperplasia of adipose tissue, and that isoenergetic substitution of simple for complex carbohydrate exagerates fat accretion in lean but not obese rats. Moreover, the obesity occurs in spite of greater mass, cellularity, and T4-5'DI activity of IBAT, consistent with a thermogenic defect in the obese phenotype of this strain. C1 NIH,VET RESOURCES BRANCH,BETHESDA,MD 20705. USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,BELTSVILLE,MD 20705. RP TULP, OL (reprint author), DREXEL UNIV,DEPT NUTR & FOOD SCI,PHILADELPHIA,PA 19104, USA. NR 36 TC 2 Z9 2 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0300-9629 J9 COMP BIOCHEM PHYS A JI Comp. Biochem. Physiol. A-Physiol. PY 1991 VL 99 IS 3 BP 457 EP 462 DI 10.1016/0300-9629(91)90033-9 PG 6 WC Biochemistry & Molecular Biology; Physiology; Zoology SC Biochemistry & Molecular Biology; Physiology; Zoology GA FP838 UT WOS:A1991FP83800033 PM 1678339 ER PT B AU EDDY, EM MCGEE, RS WILLIS, WD OBRIEN, DA AF EDDY, EM MCGEE, RS WILLIS, WD OBRIEN, DA BE BACCETTI, B TI IMMUNODISSECTION OF SPERM MATURATION SO COMPARATIVE SPERMATOLOGY 20 YEARS AFTER SE SERONO SYMPOSIA PUBLICATIONS FROM RAVEN PRESS LA English DT Proceedings Paper CT 6TH INTERNATIONAL CONGRESS OF SPERMATOLOGY CY AUG 30-SEP 05, 1990 CL SIENA, ITALY SP SERONO SYMPOSIA RP EDDY, EM (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,GAMETE BIOL SECT,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-654-3 J9 SERONO SYM PY 1991 VL 75 BP 643 EP 646 PG 4 WC Andrology; Biology; Obstetrics & Gynecology SC Endocrinology & Metabolism; Life Sciences & Biomedicine - Other Topics; Obstetrics & Gynecology GA BV61B UT WOS:A1991BV61B00114 ER PT J AU SPOUGE, JL AF SPOUGE, JL TI FAST OPTIMAL ALIGNMENT SO COMPUTER APPLICATIONS IN THE BIOSCIENCES LA English DT Article ID MULTIPLE SEQUENCE ALIGNMENT; ALGORITHMS; BIOLOGY; METRICS AB Algorithms often align sequences by minimizing a cost. Such algorithms usually operate by aligning successively longer subsequences until they finish the alignment. Efficient algorithms, such as those of Fickett and Ukkonen, speed the computation by ignoring bad subalignments. A general principle underlies the efficiency of these two algorithms: inequalities can direct computations to promising subalignments. Hence inequalities can be used to suggest alignment algorithms. Inequalities for unweighted end-gaps, affine and concave gap weights, etc., are discussed, and empirical results evaluating new algorithms for single indel costs and weighted end-gaps are presented. Empirical results show the new algorithms are, under certain circumstances, much faster than known algorithms. RP SPOUGE, JL (reprint author), NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,38A-8S806,BETHESDA,MD 20894, USA. NR 25 TC 7 Z9 7 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0266-7061 J9 COMPUT APPL BIOSCI JI Comput. Appl. Biosci. PD JAN PY 1991 VL 7 IS 1 BP 1 EP 7 PG 7 WC Computer Science, Interdisciplinary Applications SC Computer Science GA EW014 UT WOS:A1991EW01400001 PM 2004263 ER PT J AU LE, SY CHEN, JH MAIZEL, JV AF LE, SY CHEN, JH MAIZEL, JV TI DETECTION OF UNUSUAL RNA FOLDING REGIONS IN HIV AND SIV SEQUENCES SO COMPUTER APPLICATIONS IN THE BIOSCIENCES LA English DT Article ID MESSENGER-RNA; STATISTICAL SIGNIFICANCE; SECONDARY STRUCTURES; IMMUNODEFICIENCY; REPLICATION; STABILITY AB We have developed a method for detecting more stable and significant folding regions relative to others in the sequence. The algorithm is based on the calculation of the lowest free energy of RNA secondary structures and Monte Carlo simulation. For any given RNA segment, the stability and statistical significance of RNA folding are assessed by two measures: the stability score and the significance score. The stability score measures the degree of thermodynamic stability of the segment between all possible biological segments in the RNA sequence. The significance score characterizes the specific arrangement of the nucleotides in the segment that could imply a structural role for the sequence information. Using these two measures, we are able to detect a series of distinct folding regions where highly stable and statistically significant secondary structures occur in human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) sequences. C1 NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,ADV SCI COMP LAB,FREDERICK,MD 21701. NCI,DIV CANC BIOL & DIAG,MATH BIOL LAB,FREDERICK,MD 21701. RP LE, SY (reprint author), NATL RES COUNCIL CANADA,INST BIOL SCI,OTTAWA K1A 0R6,ONTARIO,CANADA. FU NCI NIH HHS [N01-CO-74102] NR 24 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 0266-7061 J9 COMPUT APPL BIOSCI JI Comput. Appl. Biosci. PD JAN PY 1991 VL 7 IS 1 BP 51 EP 55 PG 5 WC Computer Science, Interdisciplinary Applications SC Computer Science GA EW014 UT WOS:A1991EW01400007 PM 2004274 ER PT J AU BAXTER, S AF BAXTER, S TI AIDS EDUCATION IN THE JAIL SETTING SO CRIME & DELINQUENCY LA English DT Article RP BAXTER, S (reprint author), THE CIRCLE INC,NIDA,MCLEAN,VA, USA. NR 11 TC 20 Z9 20 U1 0 U2 0 PU SAGE SCIENCE PRESS PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0011-1287 J9 CRIME DELINQUENCY JI Crime Delinq. PD JAN PY 1991 VL 37 IS 1 BP 48 EP 63 DI 10.1177/0011128791037001005 PG 16 WC Criminology & Penology SC Criminology & Penology GA EP868 UT WOS:A1991EP86800005 ER PT J AU CHESON, BD AF CHESON, BD TI NEW MODALITIES OF THERAPY IN CHRONIC LYMPHOCYTIC-LEUKEMIA SO CRITICAL REVIEWS IN ONCOLOGY/HEMATOLOGY LA English DT Article ID HAIRY-CELL LEUKEMIA; PHASE-II TRIAL; MULTIVARIATE SURVIVAL ANALYSIS; LEUKOCYTE-A INTERFERON; TUMOR NECROSIS FACTOR; B-CLL PATIENTS; FLUDARABINE PHOSPHATE; RECOMBINANT LEUKOCYTE; CLINICAL-TRIALS; LYMPHOID MALIGNANCIES AB Chronic lymphocytic leukemia (CLL) is the most common form of leukemia in adults in Western countries. After several decades of relative inactivity, important progress has been made in our understanding of the biology and immunology of this disorder. In addition, exciting therapeutic results have been achieved with several new, unique, and effective therapies. The most interesting chemotherapeutic agent is fludarabine, a purine analogue which achieves complete remission in 13% of relapsed or refractory patients and in > 30% of previously untreated patients; the overall response rates of 60% and 75%, respectively, are superior to reports with other single agents or combination regimens. Related drugs with promising activity are 2'-deoxycoformycin, and 2-chlorodeoxyadenosine. Preliminary studies are evaluating allogenic and autologous bone marrow transplantation as potentially curative therapy. Biological approaches exploiting new insights into the immunology of CLL include the use of lymphoid growth factors. Interpretation of results of CLL studies has suffered from variability in eligibility and response criteria, especially definitions of complete remissions. Recently published standardized guidelines for CLL clinical trials will facilitate comparisons among therapies and help identify those which are most promising. Continued progress will require integration of laboratory science and clinical investigation. RP CHESON, BD (reprint author), NCI,MED SECT,CLIN INVEST BRANCH,DIV AUTOMAT CONTROL,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892, USA. NR 77 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1040-8428 J9 CRIT REV ONCOL HEMAT JI Crit. Rev. Oncol./Hematol. PY 1991 VL 11 IS 3 BP 167 EP 177 DI 10.1016/1040-8428(91)90019-9 PG 11 WC Oncology; Hematology SC Oncology; Hematology GA GF965 UT WOS:A1991GF96500001 PM 1958310 ER PT J AU VAICKUS, L BALL, ED FOON, KA AF VAICKUS, L BALL, ED FOON, KA TI IMMUNE MARKERS IN HEMATOLOGIC MALIGNANCIES SO CRITICAL REVIEWS IN ONCOLOGY/HEMATOLOGY LA English DT Review ID T-CELL RECEPTOR; ACUTE LYMPHOBLASTIC-LEUKEMIA; CHRONIC LYMPHOCYTIC-LEUKEMIA; REED-STERNBERG CELLS; ACUTE MYELOBLASTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; TERMINAL DEOXYNUCLEOTIDYL TRANSFERASE; HUMAN-BONE-MARROW; CHRONIC MYELOGENOUS LEUKEMIA; PEDIATRIC-ONCOLOGY-GROUP AB The precise delineation of biologic traits that distinguish normal hematopoietic cells from their malignant counterparts is of fundamental importance in understanding all aspects of hematologic malignancies. An increasingly sophisticated technologic battery has been utilized to dissect out these differences - primarily utilization of monoclonal antibodies, by immunoperoxidase, immunoalkaline phosphatase and flow cytometric techniques. An even more basic understanding of normal and malignant hematopoietic cells has begun to evolve as molecular biology begins to unravel gene misprogramming by Southern and Northern blot analysis and the polymerase chain reaction. These techniques not only help distinguish a normal cell from a malignant one, but characterize the malignant clone as B-lymphoid, T-lymphoid or myeloid and allow further subcategorization within these broad lineages. These distinctions are vital to the entire spectrum of basic and clinical research involving hematologic malignancies and are assuming an increasingly important role in their diagnosis, prognosis and treatment. C1 SUNY BUFFALO,DEPT MED,BUFFALO,NY 14260. DARTMOUTH COLL,HITCHCOCK MED CTR,HANOVER,NH 03756. ROSWELL PK CANC INST,DEPT MICROBIOL IMMUNOL,BUFFALO,NY. UNIV PITTSBURGH,DIV HEMATOL BONE MARROW TRANSPLANTAT,PITTSBURGH,PA 15260. UNIV PITTSBURGH,MED,PITTSBURGH,PA 15260. NCI,MONOCLONAL ANTIBODY HYBRIDOMA SECT,BALTIMORE,MD. NCI,BIOL RESPONSE MODIFIERS PROGRAM,CLIN INVEST SECT,BALTIMORE,MD. UNIV MICHIGAN,DIV HEMATOL ONCOL,ANN ARBOR,MI 48109. RP VAICKUS, L (reprint author), ROSWELL PK CANC INST,DEPT MED,DIV CLIN IMMUNOL,ELM & CARLTON ST,BUFFALO,NY 14263, USA. NR 385 TC 35 Z9 35 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1040-8428 J9 CRIT REV ONCOL HEMAT JI Crit. Rev. Oncol./Hematol. PY 1991 VL 11 IS 4 BP 267 EP 297 DI 10.1016/1040-8428(91)90029-C PG 31 WC Oncology; Hematology SC Oncology; Hematology GA GV049 UT WOS:A1991GV04900002 PM 1777090 ER PT J AU KORN, ED AF KORN, ED TI ACANTHAMOEBA MYOSIN-I - PAST, PRESENT, AND FUTURE SO CURRENT TOPICS IN MEMBRANES LA English DT Review ID HEAVY-CHAIN KINASE; ACTIVATED ATPASE ACTIVITY; AMINO-ACID-SEQUENCE; ACTIN-BINDING; DICTYOSTELIUM-DISCOIDEUM; INTESTINAL MICROVILLUS; PHOSPHORYLATION SITE; COFACTOR PROTEIN; 3RD ISOFORM; F-ACTIN C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. RI Korn, Edward/F-9929-2012 NR 61 TC 12 Z9 12 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 J9 CURR TOP MEMBR JI Curr. Top. Membr. PY 1991 VL 38 BP 13 EP 30 PG 18 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA MG417 UT WOS:A1991MG41700003 ER PT J AU OBRIEN, SJ GRAVES, JAM AF OBRIEN, SJ GRAVES, JAM TI REPORT OF THE COMMITTEE ON COMPARATIVE GENE-MAPPING SO CYTOGENETICS AND CELL GENETICS LA English DT Article C1 LA TROBE UNIV,DEPT GENET & HUMAN VARIAT,BUNDOORA,VIC 3083,AUSTRALIA. RP OBRIEN, SJ (reprint author), NCI,VIRAL CARCINOGENESIS LAB,BLDG 560,ROOM 21 105,FREDERICK,MD 21702, USA. RI Graves, Jennifer/A-1387-2008 NR 9 TC 112 Z9 114 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 1991 VL 58 IS 3-4 BP 1124 EP 1151 DI 10.1159/000133725 PG 28 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900006 ER PT J AU BONNER, TI MODI, WS SEUANEZ, HN OBRIEN, SJ AF BONNER, TI MODI, WS SEUANEZ, HN OBRIEN, SJ TI CHROMOSOMAL MAPPING OF 5 HUMAN GENES ENCODING MUSCARINIC ACETYLCHOLINE-RECEPTORS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20852. NCI,FCRDC,PROGRAM RESOURCES INC,DYNCORP,FREDERICK,MD 21701. NR 0 TC 21 Z9 22 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 1991 VL 58 IS 3-4 BP 1850 EP 1850 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900018 ER PT J AU DEAN, M LUCASDERSE, S RAMSBURG, M GOLDMAN, D WEISSMAN, A LEPPERT, M FRASER, C OBRIEN, SJ AF DEAN, M LUCASDERSE, S RAMSBURG, M GOLDMAN, D WEISSMAN, A LEPPERT, M FRASER, C OBRIEN, SJ TI GENETIC-MAPPING OF 6 HUMAN GENES SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIAAA,BETHESDA,MD. UNIV UTAH,SALT LAKE CITY,UT 84112. NIAAA,ROCKVILLE,MD 20852. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 3 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 1991 VL 58 IS 3-4 BP 1853 EP 1853 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900025 ER PT J AU GOLDSTEIN, AM BALE, SJ AF GOLDSTEIN, AM BALE, SJ TI LINKAGE ANALYSIS OF THE NEVOID BASAL-CELL CARCINOMA SYNDROME (NBCCS) SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FAMILY STUDIES SECT,BETHESDA,MD 20853. NR 7 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 1991 VL 58 IS 3-4 BP 1853 EP 1853 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900027 ER PT J AU MODI, WS OBRIEN, SJ LEVINE, MA AF MODI, WS OBRIEN, SJ LEVINE, MA TI CHROMOSOMAL ASSIGNMENT OF 2 GTP BINDING-PROTEIN SUBUNIT GENES - THE ALPHA-SUBUNIT OF ADENYLYL CYCLASE (GNAS) AND THE BETA-1 POLYPEPTIDE (GNB) SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FCRDC,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701. JOHNS HOPKINS UNIV,SCH MED,DIV ENDOCRINOL & METAB,BALTIMORE,MD 21205. NR 1 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 1991 VL 58 IS 3-4 BP 1860 EP 1860 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900041 ER PT J AU FARRER, L GRUNDFAST, K AMOS, J ARNOS, KS ASHER, J BEIGHTON, P DIEHL, S FEX, J FOY, C FRIEDMAN, T GREENBERG, J HOTH, C MILUNSKY, A MORELL, R NANCE, W NEWTON, V RAMESAR, R READ, A SKARE, J AUGUSTIN, TS STEVENS, C WAGNER, R WILCOX, E WINSHIP, I AF FARRER, L GRUNDFAST, K AMOS, J ARNOS, KS ASHER, J BEIGHTON, P DIEHL, S FEX, J FOY, C FRIEDMAN, T GREENBERG, J HOTH, C MILUNSKY, A MORELL, R NANCE, W NEWTON, V RAMESAR, R READ, A SKARE, J AUGUSTIN, TS STEVENS, C WAGNER, R WILCOX, E WINSHIP, I TI WAARDENBURG SYNDROME IS CAUSED BY DEFECTS AT MULTIPLE LOCI, ONE OF WHICH IS TIGHTLY LINKED TO ALPP ON CHROMOSOME-2 - 1ST REPORT OF THE WS CONSORTIUM SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. NIDOCD,MOLEC BIOL LAB,BETHESDA,MD 20892. BOSTON UNIV,CTR HUMAN GENET,SCH MED,BOSTON,MA 02118. GENET SERV CTR,WASHINGTON,DC 20002. MICHIGAN STATE UNIV,DEPT ZOOL,E LANSING,MI 48824. UNIV CAPE TOWN,SCH MED,CAPE TOWN 7925,SOUTH AFRICA. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PSYCHIAT,MOLEC GENET LAB,RICHMOND,VA 23298. ST MARYS HOSP,DEPT MED GENET,MANCHESTER M13 9PL,ENGLAND. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT HUMAN GENET,RICHMOND,VA 23298. UNIV OXFORD,CTR AUDIOL EDUC DEAF & SPEECH PATHOL,MANCHESTER M13 9PL,ENGLAND. RI Ramesar, Raj/I-6941-2015 OI Ramesar, Raj/0000-0001-5688-1634 NR 2 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1869 EP 1869 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900061 ER PT J AU MODI, WS POLLOCK, DD MOCK, BA BANNER, C RENAULD, JC VANSNICK, J AF MODI, WS POLLOCK, DD MOCK, BA BANNER, C RENAULD, JC VANSNICK, J TI REGIONAL LOCALIZATION OF THE HUMAN GLUTAMINASE (GLS) AND INTERLEUKIN-9 (IL9) GENES BY INSITU HYBRIDIZATION SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract ID MAPS C1 NCI,FCRDC,PROGRAM RESOURCES INC,DYNCORP,FREDERICK,MD 21701. STANFORD UNIV,DEPT BIOL SCI,STANFORD,CA 94305. NCI,BETHESDA,MD 20892. NIA,BETHESDA,MD 20892. CATHOLIC UNIV LOUVAIN,B-1348 LOUVAIN,BELGIUM. LUDWIG INST CANC RES,BRUSSELS,BELGIUM. NR 2 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1870 EP 1870 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900066 ER PT J AU POPESCU, NC SIMPSON, S FINEGAN, MM SOLINAS, S DIPAOLO, JA AF POPESCU, NC SIMPSON, S FINEGAN, MM SOLINAS, S DIPAOLO, JA TI EPSTEIN-BARR-VIRUS INTEGRATION AT A STABLE CHROMOSOME MODIFICATION-SITE IN A BURKITT-LYMPHOMA CELL-LINE SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. FED INST TECHNOL,INST ANIM PROD,ZURICH,SWITZERLAND. 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 1991 VL 58 IS 3-4 BP 1872 EP 1872 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900071 ER PT J AU DEAN, M LUCASDERSE, S OBRIEN, SJ GOLDMAN, D AF DEAN, M LUCASDERSE, S OBRIEN, SJ GOLDMAN, D TI LINKAGE MAPPING OF 6 POLYMORPHIC LYMPHOCYTE PROTEINS DETECTED BY 2-DIMENSIONAL GEL-ELECTROPHORESIS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 PROGRAM RESOURCES INC,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NIAAA,BETHESDA,MD 20892. NR 1 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 1991 VL 58 IS 3-4 BP 1875 EP 1875 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900078 ER PT J AU LERMAN, M LATIF, F TORY, K MODI, W DELISIO, J ORCUTT, ML HAMPSCH, K LINEHAN, M ZBAR, B AF LERMAN, M LATIF, F TORY, K MODI, W DELISIO, J ORCUTT, ML HAMPSCH, K LINEHAN, M ZBAR, B TI NEW RFLP MARKERS AROUND THE VONHIPPEL-LINDAU DISEASE (VHL) LOCUS SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. PROGRAM RESOURCES INC,NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 2 TC 2 Z9 2 U1 0 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1878 EP 1878 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900086 ER PT J AU MAHER, ER BENTLEY, E YATES, JR AFFARA, NA PHIPPS, M LATIF, F LERMAN, M BERTON, Z OOSTRA, BA TURNER, G CARVALHO, JG JENSEN, AM NORBY, S SORENSEN, SA GUSTAVSON, KH ENBLAD, P EEGOLOFSSON, O BENJAMIN, C HARRIS, R SAMPSON, JS WILLIAMS, A FERGUSONSMITH, MA AF MAHER, ER BENTLEY, E YATES, JR AFFARA, NA PHIPPS, M LATIF, F LERMAN, M BERTON, Z OOSTRA, BA TURNER, G CARVALHO, JG JENSEN, AM NORBY, S SORENSEN, SA GUSTAVSON, KH ENBLAD, P EEGOLOFSSON, O BENJAMIN, C HARRIS, R SAMPSON, JS WILLIAMS, A FERGUSONSMITH, MA TI GENETIC-LINKAGE ANALYSIS OF VONHIPPEL-LINDAU DISEASE SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE CB2 1QP,ENGLAND. NCI,FREDERICK,MD 21701. ERASMUS UNIV,3000 DR ROTTERDAM,NETHERLANDS. YORKSHIRE REG GENET SERV,LEEDS,ENGLAND. INST MED GENET,COPENHAGEN,DENMARK. INST FORENS GENET,COPENHAGEN,DENMARK. INST HUMAN GENET,COPENHAGEN,DENMARK. UNIV HOSP UPPSALA,S-75185 UPPSALA,SWEDEN. UNIV MANCHESTER,MANCHESTER M13 9PL,LANCS,ENGLAND. INST MED GENET WALES,CARDIFF,WALES. NR 5 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 1991 VL 58 IS 3-4 BP 1879 EP 1879 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900089 ER PT J AU TORY, K LATIF, F SCHMIDT, L WEI, MH LI, H COBLER, P ZBAR, B LERMAN, M AF TORY, K LATIF, F SCHMIDT, L WEI, MH LI, H COBLER, P ZBAR, B LERMAN, M TI A GENETIC-MAP OF CHROMOSOME-3P SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 PROGRAM RESOURCES INC,NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. NR 1 TC 1 Z9 1 U1 0 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1882 EP 1883 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900099 ER PT J AU ZBAR, B LATIF, F MODI, W HEPPELPORTAN, A DELISIO, J ORCUTT, ML HAMPSCH, K TORY, K RABBITTS, P LERMAN, M AF ZBAR, B LATIF, F MODI, W HEPPELPORTAN, A DELISIO, J ORCUTT, ML HAMPSCH, K TORY, K RABBITTS, P LERMAN, M TI 11 NEW LANDMARK RFLP LOCI ON CHROMOSOME-3P ORDERED BY FLUORESCENT INSITU HYBRIDIZATION AND GENETIC-MAPPING SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. PROGRAM RESOURCES INC,NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. MRC,CAMBRIDGE CB2 2QH,ENGLAND. NR 1 TC 0 Z9 0 U1 0 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1883 EP 1883 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900102 ER PT J AU VANDERHOUT, AH VANDERVLIES, P WIJMENGA, C OOSTERHUIS, JW LI, FP BUYS, CHCM AF VANDERHOUT, AH VANDERVLIES, P WIJMENGA, C OOSTERHUIS, JW LI, FP BUYS, CHCM TI THE REGION 3P21-P24.1, BORDERED BY D3S32 AND THRB, IDENTIFIED AS SMALLEST OVERLAPPING DELETION IN SPORADIC RENAL-CELL CARCINOMA SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV GRONINGEN,DEPT MED GENET,9700 AB GRONINGEN,NETHERLANDS. UNIV GRONINGEN,DEPT PATHOL,9700 AB GRONINGEN,NETHERLANDS. NCI,BOSTON,MA. RI Wijmenga, Cisca/D-2173-2009 NR 9 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 1991 VL 58 IS 3-4 BP 1884 EP 1884 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900103 ER PT J AU MODI, WS BONNER, TI AF MODI, WS BONNER, TI TI LOCALIZATION OF THE CANNABANOID RECEPTOR LOCUS USING NONISOTOPIC INSITU HYBRIDIZATION SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21701. NIMH,CELL BIOL 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 1991 VL 58 IS 3-4 BP 1915 EP 1915 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900179 ER PT J AU MODI, WS DEAN, M POLLOCK, DD SEUANEZ, HN CHRISTAKOS, S AF MODI, WS DEAN, M POLLOCK, DD SEUANEZ, HN CHRISTAKOS, S TI CHROMOSOMAL LOCALIZATION OF THE CALBINDIN GENE SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FCRDC,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21701. STANFORD UNIV,DEPT BIOL SCI,STANFORD,CA 94305. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT BIOCHEM & MOLEC BIOL,NEWARK,NJ 07103. NR 2 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 1991 VL 58 IS 3-4 BP 1930 EP 1930 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900220 ER PT J AU ANAGNOU, NP SEUANEZ, H MODI, WS OBRIEN, SJ PAPAMATHEAKIS, J MOSCHONAS, NK AF ANAGNOU, NP SEUANEZ, H MODI, WS OBRIEN, SJ PAPAMATHEAKIS, J MOSCHONAS, NK TI CHROMOSOMAL MAPPING OF THE HUMAN GLUTAMATE-DEHYDROGENASE (GLUD) GENES TO CHROMOSOME-10Q22.3-Q23 AND CHROMOSOME-XQ22-23 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 FDN RES & TECHNOL,INST MOLEC BIOL & BIOTECHNOL,IRAKLION 71110,GREECE. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701. NR 2 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1947 EP 1947 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900257 ER PT J AU DIONNE, CA MODI, WS CRUMLEY, G OBRIEN, SJ SCHLESSINGER, J JAYE, M AF DIONNE, CA MODI, WS CRUMLEY, G OBRIEN, SJ SCHLESSINGER, J JAYE, M TI BEK, A RECEPTOR FOR MULTIPLE MEMBERS OF THE FIBROBLAST GROWTH-FACTOR (FGF) FAMILY, MAPS TO HUMAN CHROMOSOME-10Q25.3-Q26 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 RHONE POULENC RORER CENT RES,KING OF PRUSSIA,PA 19406. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701. NYU,SCH MED,NEW YORK,NY 10016. NR 1 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 1991 VL 58 IS 3-4 BP 1948 EP 1948 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900260 ER PT J AU AMOS, CI BALE, SJ MARX, SJ AF AMOS, CI BALE, SJ MARX, SJ TI NO EVIDENCE FOR LINKAGE HETEROGENEITY IN MULTIPLE ENDOCRINE NEOPLASIA TYPE-I SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,EEB,FAMILY STUDIES SECT,BETHESDA,MD 20892. NIDDK,METAB DIS BRANCH,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 1991 VL 58 IS 3-4 BP 1954 EP 1954 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900274 ER PT J AU GAILANI, MR PETTY, EM HORSTHEMKE, B ARNOLD, A MARX, SJ BALE, AE AF GAILANI, MR PETTY, EM HORSTHEMKE, B ARNOLD, A MARX, SJ BALE, AE TI PHYSICAL MAPPING OF CHROMOSOME-11Q12-13 BY PULSED FIELD GEL-ELECTROPHORESIS (PFGE) SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. INST HUMAN GENET & ANTHROPOL,ESSEN,GERMANY. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NIH,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 1991 VL 58 IS 3-4 BP 1959 EP 1959 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900287 ER PT J AU MODI, WS LICHY, JH DEAN, M SEUANEZ, H HOWLEY, P AF MODI, WS LICHY, JH DEAN, M SEUANEZ, H HOWLEY, P TI HTS - A GENE ASSOCIATED WITH TUMOR SUPPRESSION - CHROMOSOMAL ASSIGNMENT AND RFLP IDENTIFICATION SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701. NCI,BETHESDA,MD 20892. NCI,FREDERICK,MD 21701. NR 0 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 1968 EP 1968 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900308 ER PT J AU JUST, W VETTER, U FISHER, LW KLETT, C VOGEL, W AF JUST, W VETTER, U FISHER, LW KLETT, C VOGEL, W TI INSITU LOCALIZATION OF DECORIN AND BIGLYCAN ON CHROMOSOME-12 AND CHROMOSOME-X SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract ID PROTEOGLYCAN C1 UNIV ULM,DEPT CLIN GENET,W-7900 ULM,GERMANY. NIDR,BETHESDA,MD 20892. NR 4 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 1991 VL 58 IS 3-4 BP 1977 EP 1978 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900333 ER PT J AU MODI, WS SEUANEZ, H MIETUSSNYDER, M OBRIEN, SJ KARATHANASIS, SK AF MODI, WS SEUANEZ, H MIETUSSNYDER, M OBRIEN, SJ KARATHANASIS, SK TI CHROMOSOMAL LOCALIZATION OF THE ARP-1 GENE TO 15Q26 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 DYNCORP,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK,MD 21701. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT CARDIOL,MOLEC & CELLULAR CARDIOL LAB,BOSTON,MA 02115. NR 3 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 1991 VL 58 IS 3-4 BP 1995 EP 1995 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900372 ER PT J AU MODI, WS NAPOLITANO, M CEVARIO, SJ GNARRA, JR SEUANEZ, HN LEONARD, WJ AF MODI, WS NAPOLITANO, M CEVARIO, SJ GNARRA, JR SEUANEZ, HN LEONARD, WJ TI CHROMOSOMAL LOCALIZATION OF THE ACT-2 CYTOKINE SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI,FCRDC,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21701. NICHHD,BETHESDA,MD 20892. NR 1 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 1991 VL 58 IS 3-4 BP 2008 EP 2008 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900405 ER PT J AU WHITE, JJ LEDBETTER, DH EDDY, RL SHOWS, TB STEWART, DA NUELL, MJ FRIEDMAN, V WOOD, CM OWENS, GA MCCLUNG, JK DANNER, DB MORTON, CC AF WHITE, JJ LEDBETTER, DH EDDY, RL SHOWS, TB STEWART, DA NUELL, MJ FRIEDMAN, V WOOD, CM OWENS, GA MCCLUNG, JK DANNER, DB MORTON, CC TI ASSIGNMENT OF THE HUMAN PROHIBITIN GENE (PHB) TO CHROMOSOME-17Q21 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIA,MOLEC GENET LAB,BALTIMORE,MD 21224. INST MOLEC GENET,HOUSTON,TX 77030. ROSWELL PK CANC INST,DEPT HUMAN GENET,BUFFALO,NY 14263. SR NOBLE FDN,DIV BIOMED,ARDMORE,OK 73402. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 2011 EP 2011 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900415 ER PT J AU OZCELIK, T MURPHY, PM FRANCKE, U AF OZCELIK, T MURPHY, PM FRANCKE, U TI CHROMOSOMAL ASSIGNMENT OF GENES FOR A FORMYL PEPTIDE RECEPTOR (FPR1), A STRUCTURAL HOMOLOG OF THE FORMYL PEPTIDE RECEPTOR (FPRL1) AND A LOW AFFINITY INTERLEUKIN-8 RECEPTOR (IL8RA) IN HUMAN SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 STANFORD UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT GENET,STANFORD,CA 94305. NIAID,HOST DEF LAB,BETHESDA,MD 20892. STANFORD UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT PEDIAT,STANFORD,CA 94305. NR 6 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 1991 VL 58 IS 3-4 BP 2023 EP 2024 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900444 ER PT J AU KWAN, SP LEHNER, T HAGEMANN, T TICZON, A BLAESE, M OCHS, H OTT, J ROSEN, F AF KWAN, SP LEHNER, T HAGEMANN, T TICZON, A BLAESE, M OCHS, H OTT, J ROSEN, F TI FURTHER LOCALIZATION OF THE GENE FOR WISKOTT-ALDRICH SYNDROME SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 RUSH MED COLL,DEPT IMMUNOL,CHICAGO,IL 60612. COLUMBIA UNIV,DEPT PSYCHIAT,NEW YORK,NY 10027. NCI,BETHESDA,MD 20892. UNIV WASHINGTON,DEPT PEDIAT,SEATTLE,WA 98195. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NR 4 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 1991 VL 58 IS 3-4 BP 2071 EP 2072 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900565 ER PT J AU LEGOUIS, R HARDELIN, JP LEVILLIERS, J COMPAIN, S LEPASLIER, D COHEN, D LUTFALLA, G CLAVERIE, JM BOUGUELERET, L WEISSENBACH, J PETIT, C AF LEGOUIS, R HARDELIN, JP LEVILLIERS, J COMPAIN, S LEPASLIER, D COHEN, D LUTFALLA, G CLAVERIE, JM BOUGUELERET, L WEISSENBACH, J PETIT, C TI A CANDIDATE GENE FOR THE X-LINKED KALLMANN SYNDROME SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 INST PASTEUR,F-75724 PARIS 15,FRANCE. CTR ETUD POLYMORPHISME HUMAIN,PARIS,FRANCE. CNRS,UPR 274,F-94800 VILLEJUIF,FRANCE. NIH,BETHESDA,MD 20892. RI Legouis, Renaud/G-9088-2014 NR 1 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 1991 VL 58 IS 3-4 BP 2074 EP 2074 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900571 ER PT J AU GRUBERG, L AKSENTIJEVICH, I BALOW, J DEAN, M KOVO, M PRAS, M KASTNER, DL AF GRUBERG, L AKSENTIJEVICH, I BALOW, J DEAN, M KOVO, M PRAS, M KASTNER, DL TI EXCLUSION OF CANDIDATE GENES IN FAMILIAL MEDITERRANEAN FEVER SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NCI,FCRDC,FREDERICK,MD 21702. CHAIM SHEBA MED CTR,HELLER INST MED RES,IL-52621 TEL HASHOMER,ISRAEL. NR 4 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1991 VL 58 IS 3-4 BP 2113 EP 2113 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900643 ER PT J AU KASTNER, DL AKSENTIJEVICH, I GRUBERG, L BALOW, J DEAN, M HAMPSCH, K GAZIT, E KOVO, M PRAS, M AF KASTNER, DL AKSENTIJEVICH, I GRUBERG, L BALOW, J DEAN, M HAMPSCH, K GAZIT, E KOVO, M PRAS, M TI FAMILIAL MEDITERRANEAN FEVER - A 90 MARKER EXCLUSION MAP AND EVIDENCE FOR LINKAGE TO CHROMOSOME-17 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NCI,FCRF,FREDERICK,MD 21702. CHAIM SHEBA MED CTR,TISSUE TYPING LAB,IL-52621 TEL HASHOMER,ISRAEL. CHAIM SHEBA MED CTR,HELLER INST MED RES,IL-52621 TEL HASHOMER,ISRAEL. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 NR 3 TC 4 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 1991 VL 58 IS 3-4 BP 2115 EP 2115 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900645 ER PT J AU FREDHOLM, M POLICASTRO, PF WILSON, MC AF FREDHOLM, M POLICASTRO, PF WILSON, MC TI EVIDENCE FOR THE INVOLVEMENT OF ENDOGENOUS RETROVIRAL ELEMENTS IN THE EVOLUTION OF MURINE GENOME SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract ID LEUKEMIA-VIRUS; MICE; PROVIRUSES; SEQUENCES; PROBES C1 ROYAL VET & AGR UNIV, DIV ANIM GENET, DK-1870 FREDERIKSBERG C, DENMARK. NIAID, MICROBIAL STRUCT & FUNCT LAB, HAMILTON, MT 59840 USA. Scripps Res Inst, RES INST, DEPT MOLEC BIOL & NEUROPHARMACOL, LA JOLLA, CA 92037 USA. NR 8 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 1991 VL 58 IS 3-4 BP 2135 EP 2135 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HE949 UT WOS:A1991HE94900678 ER PT J AU MODI, WS POLLOCK, DD MOCK, BA BANNER, C RENAULD, JC VANSNICK, J AF MODI, WS POLLOCK, DD MOCK, BA BANNER, C RENAULD, JC VANSNICK, J TI REGIONAL LOCALIZATION OF THE HUMAN GLUTAMINASE (GLS) AND INTERLEUKIN-9 (IL9) GENES BY INSITU HYBRIDIZATION SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID GROWTH-ENHANCING ACTIVITY; PHOSPHATE-DEPENDENT GLUTAMINASE; DISEASE RESISTANCE LOCUS; MOUSE CHROMOSOME-1; CDNA; MAPS; PURIFICATION; FACTOR-P40; EXPRESSION; COMMITTEE AB Phosphate-activated glutaminase is found in mammalian small intestine, brain, and kidney, but not in liver. The enzyme initiates the catabolism of glutamine as the principal respiratory fuel in the small intestine, may synthesize the neurotransmitter glutamate in the brain, and functions in the kidney to help maintain systemic pH homeostasis. Interleukin-9 (IL9) is a relatively new cytokine that supports the growth of helper T-cell clones, mast cells, and megakaryoblastic leukemia cells. cDNA clones have recently been obtained for each of these genes. The human loci for phosphate-activated glutaminase (GLS) and IL9 have previously been mapped to chromosomes 2 and 5, respectively, by analysis of somatic cell hybrid DNAs. By using chromosomal in situ hybridization, we have regionally mapped GLS to 2q32 --> q34 and IL9 to 5q31 --> q35. C1 CATHOLIC UNIV LOUVAIN, INT INST CELLULAR & MOLEC PATHOL, EXPTL MED UNIT, B-1348 LOUVAIN, BELGIUM. LUDWIG INST CANC RES, BRUSSELS BRANCH, BRUSSELS, BELGIUM. NCI, GENET LAB, BETHESDA, MD 20892 USA. NIA, BETHESDA, MD 20892 USA. RP DYNCORP, FREDERICK CANC RES & DEV FACIL, PROGRAM RESOURCES INC, BIOL CARCINOGENESIS & DEV PROGRAM, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N0I-CO-74102] NR 29 TC 23 Z9 23 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 1991 VL 57 IS 2-3 BP 114 EP 116 DI 10.1159/000133126 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA GG082 UT WOS:A1991GG08200010 PM 1680606 ER PT J AU LIMA, MMC SEUANEZ, HN AF LIMA, MMC SEUANEZ, HN TI CHROMOSOME-STUDIES IN THE RED HOWLER MONKEY, ALOUATTA-SENICULUS-STRAMINEUS (PLATYRRHINI, PRIMATES) - DESCRIPTION OF AN X1X2Y1Y2/X1X1X2X2 SEX-CHROMOSOME SYSTEM AND KARYOLOGICAL COMPARISONS WITH OTHER SUBSPECIES SO CYTOGENETICS AND CELL GENETICS LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL WORKSHOP ON HUMAN CHROMOSOME 17 CY MAR 15-16, 1991 CL PARK CITY, UT SP NIH, MED RES COUNCIL UK ID BELZEBUL; AOTUS AB In the red howler monkey, Alouatta seniculus stramineus (2n = 47, 48, or 49), variations in diploid chromosome number are due to different numbers of microchromosomes. Males exhibit a Y; autosome translocation involving the short arm of an individual biarmed autosome. Consequently, the sex-chromosome constitution in the male is X1X2Y1Y2, with X1 representing the original X chromosome, X2 the biarmed autosome (No. 7), Y1 the Y; 7p translocation product, and Y2 the acrocentric homolog of 7q. In the first meiotic division, a quadrivalent with a chain configuration can be observed in spermatocytes. Females have an X1X1X2X2 sex-chromosome constitution. Chromosome heteromorphisms were observed in pair 13, due to a pericentric inversion, and pair 19, due to the presence of constitutive heterochromatin. Microchromosomes, which varied in number between individuals, were also heterochromatic. NOR-staining was observed at two separate sites on a single chromosome pair (No. 10). A comparison of A.s. stramineus with A.s. macconnelli shows that these two subspecies have identical diploid chromosome numbers (47, 48, or 49), again due to a varying number of microchromosomes, and that they share a similar sex-chromosome constitution. Their karyotypes, however, are not identical, but can be derived from each other by a reciprocal translocation. Further comparisons with other A. seniculus subspecies reported in the literature indicate that this taxon is not karyologically uniform and that substantial chromosome shuffling has occurred between populations that have been considered to be subspecies by taxonomic criteria based on their morphometric attributes. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. UNIV FED PARA,DEPT GENET,BELEM,PARA,BRAZIL. NR 17 TC 41 Z9 42 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 1991 VL 57 IS 2-3 BP 151 EP 156 DI 10.1159/000133135 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA GG082 UT WOS:A1991GG08200019 PM 1914523 ER PT J AU SAVAGE, PD SHAPIRO, M LANGDON, WY VANKESSEL, ADG SEUANEZ, HN AKAO, Y CROCE, C MORSE, HC KERSEY, JH AF SAVAGE, PD SHAPIRO, M LANGDON, WY VANKESSEL, ADG SEUANEZ, HN AKAO, Y CROCE, C MORSE, HC KERSEY, JH TI RELATIONSHIP OF THE HUMAN PROTOONCOGENE CBL2 ON 11Q23 TO THE T(4-11), T(11-22), AND T(11-14) BREAKPOINTS SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID CELL RECEPTOR COMPLEX; PROTO-ONCOGENE; CHROMOSOME-11; GENE; LINE; TRANSLOCATION; REARRANGEMENT; LOCALIZATION; FRAGMENTS; LYMPHOMA AB A probe identifying CBL2, the human cellular homolog of the murine oncogene v-cbl and murine cellular protooncogene Cbl-2, and panels of rodent X human somatic cell hybrids were used to study the relationship of this protooncogene to translocations associated with acute leukemia, lymphoma, and Ewing sarcoma. CBL2 was mapped to 11 q23 and found to translocate from chromosome 11 to 4 in an acute leukemia cell line possessing a t(4;11)(q21;q23) and from chromosome 11 to 14 in a B-cell lymphoma with a t(11;14)(q23;q32). In an Ewing sarcoma cell line with a t(11;22)(q23;q12), however, CBL2 remained on chromosome 11. Additional studies of other genes in the region of 11 q23 allowed the following ordering of these genes and breakpoints: 11cen - q23 - NCAM - CD3(E-D-G) - [t(11;14), t(4;11)] - (THY1, CBL2, ETS1) - t(11;22) - 11qter. The gross structure of the CBL2 sequences examined was not altered by either of the flanking breakpoints. Given that the 5' and 3' ends of the CBL2 gene are not known and are probably not evaluated by the v-cbl probe, these results do not rule out the possibility of CBL2 involvement in the pathogenesis of a subset of acute leukemias possessing a t(4;11), B-cell lymphomas possessing a t(11;14), or Ewing sarcomas possessing a t(11;22). C1 TEMPLE UNIV,HLTH SCI CTR,SCH MED,FELS INST CANC RES & MOLEC BIOL,PHILADELPHIA,PA 19140. UNIV MINNESOTA,SCH MED,DEPT MED,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT PEDIAT,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. CATHOLIC UNIV NIJMEGEN,DEPT HUMAN GENET,NIJMEGEN,NETHERLANDS. NCI,GENET SECT,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. RI Geurts van Kessel, Ad/A-2810-2010; OI Morse, Herbert/0000-0002-9331-3705 FU NCI NIH HHS [CA-49721, CA-250917, CA-39860] NR 26 TC 43 Z9 43 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 1991 VL 56 IS 2 BP 112 EP 115 DI 10.1159/000133062 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA FF587 UT WOS:A1991FF58700012 PM 2013228 ER PT J AU JOSEPH, DR ADAMSON, MC KOZAK, CA AF JOSEPH, DR ADAMSON, MC KOZAK, CA TI GENETIC-MAPPING OF THE GENE FOR ANDROGEN-BINDING PROTEIN SEX HORMONE-BINDING GLOBULIN TO MOUSE CHROMOSOME-11 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID IDENTIFICATION; EXPRESSION; LINKAGE; MAP AB Southern blot analysis of DNAs from Chinese hamster x mouse and rat x mouse somatic cell hybrids showed that the mouse gene encoding androgen-binding protein/sex hormone-binding globulin (ABP-SHBG) is on Chromosome 11. Progeny from an intersubspecies backcross were analyzed to position this locus, termed Shbg, between Il-3 and Int-4 in the middle of this chromosome. Shbg is thus closely linked to several neurological mutations, one of which, Tr, is also associated with male sterility. The recent finding that ABP-SHBG is found throughout the rat brain raises the possibility that one of these mutations may be due to a defect in Shbg. C1 NIAID,MOLEC MICROBIOL LAB,BLDG 4,ROOM 324,BETHESDA,MD 20892. UNIV N CAROLINA,REPROD BIOL LABS,CHAPEL HILL,NC 27514. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC 27514. UNIV N CAROLINA,DEPT PHYSIOL,CHAPEL HILL,NC 27514. UNIV N CAROLINA,DEPT BIOL,CHAPEL HILL,NC 27514. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X FU NICHD NIH HHS [HD21744, 5-P30-HD-18968] NR 24 TC 16 Z9 16 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 1991 VL 56 IS 2 BP 122 EP 124 DI 10.1159/000133064 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA FF587 UT WOS:A1991FF58700014 PM 2013230 ER PT J AU DANCIGER, M KOZAK, CA ABE, T SHINOHARA, T FARBER, DB AF DANCIGER, M KOZAK, CA ABE, T SHINOHARA, T FARBER, DB TI THE GENE FOR RETINAL ROD 33-KDA PROTEIN IS ON MOUSE CHROMOSOME-1, NEAR LAMB2 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID MAMMARY-TUMOR VIRUS; CGMP-PHOSPHODIESTERASE; S-ANTIGEN; ALPHA-SUBUNIT; BETA-SUBUNIT; RD MOUSE; MAPS; TRANSDUCIN; SEQUENCES; CDNA AB A water-soluble protein (called "33-kDa protein") that exhibits light-dependent phosphorylation has been shown to be a major protein of mammalian rod photoreceptors. Although the function of this protein is unknown, it has been implicated in the biochemical cascade mediating the rod visual response. Using a retinal cDNA from the rat and somatic cell hybrids, we have mapped the gene corresponding to this protein to mouse Chromosome 1 and, by analyzing the progeny of an intersubspecific backcross, have positioned it near Lamb2 (the beta-2 chain of laminin). We have designated the gene Rpr-1 (rod photoreceptor protein-1). C1 UNIV CALIF LOS ANGELES,SCH MED,JULES STEIN EYE INST,100 STEIN PLAZA,LOS ANGELES,CA 90024. LOYOLA MARYMOUNT UNIV,LOS ANGELES,CA 90045. NIAID,BETHESDA,MD 20892. NEI,BETHESDA,MD 20892. OI Shinohara, Toshimichi/0000-0002-7197-9039 FU NEI NIH HHS [EY00331, EY02651] NR 36 TC 8 Z9 8 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 1991 VL 56 IS 3-4 BP 202 EP 205 DI 10.1159/000133089 PG 4 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA FR256 UT WOS:A1991FR25600022 PM 1675982 ER PT J AU MILLAN, FA DENHEZ, F KONDAIAH, P AKHURST, RJ AF MILLAN, FA DENHEZ, F KONDAIAH, P AKHURST, RJ TI EMBRYONIC GENE-EXPRESSION PATTERNS OF TGF BETA-1, BETA-2 AND BETA-3 SUGGEST DIFFERENT DEVELOPMENTAL FUNCTIONS INVIVO SO DEVELOPMENT LA English DT Article DE TGF-BETA; MOUSE EMBRYO; GENE EXPRESSION; CARDIOGENESIS; EPITHELIA; GROWTH FACTOR ID TRANSFORMING GROWTH-FACTOR; FACTOR-BETA; MESODERM INDUCTION; EPITHELIAL-CELLS; MESSENGER-RNAS; MOUSE; PROTEIN; TRANSITION; SEQUENCE; TISSUES AB We have compared the expression of the genes encoding transforming growth factors beta-1, beta-2 and beta-3 during mouse embryogenesis from 9.5 to 16.5 days p.c. using in situ hybridisation to cellular RNAs. Each gene has a different expression pattern, which gives some indication of possible biological function in vivo. All three genes appear to be involved in chondro-ossification, though each is expressed in a different cell type. Transcripts of each gene are also present in embryonic epithelia. Epithelial expression of TGF beta-1, beta-2 and beta-3 RNA is associated with regions of active morphogenesis involving epithelial-mesenchymal interactions. In addition, widespread epithelial expression of TGF beta-2 RNA can be correlated with epithelial differentiation per se. The localisation of TGF beta-2 RNA in neuronal tissue might also be correlated with differentiation. Finally both TGF beta-1 and beta-2 transcripts are seen in regions actively undergoing cardiac septation and valve formation, suggesting some interaction of these growth factors in this developmental process. C1 UNIV GLASGOW,DUNCAN GUTHRIE INST MED GENET,GLASGOW G3 8SJ,SCOTLAND. NIH,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 49 TC 458 Z9 466 U1 0 U2 4 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD JAN PY 1991 VL 111 IS 1 BP 131 EP 144 PG 14 WC Developmental Biology SC Developmental Biology GA EV674 UT WOS:A1991EV67400012 PM 1707784 ER PT J AU TALIAN, JC ZELENKA, PS AF TALIAN, JC ZELENKA, PS TI CALPACTIN-I IN THE DIFFERENTIATING EMBRYONIC CHICKEN LENS - MESSENGER-RNA LEVELS AND PROTEIN DISTRIBUTION SO DEVELOPMENTAL BIOLOGY LA English DT Article ID ROUS-SARCOMA VIRUS; TYROSINE KINASE SUBSTRATE; EDTA-EXTRACTABLE PROTEINS; CELLULAR SUBSTRATE; PLASMA-MEMBRANE; FIBER MEMBRANES; 36,000-DALTON SUBSTRATE; TRANSFORMING GENE; CDNA SEQUENCE; CELLS RP TALIAN, JC (reprint author), NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892, USA. NR 53 TC 14 Z9 14 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN PY 1991 VL 143 IS 1 BP 68 EP 77 DI 10.1016/0012-1606(91)90055-8 PG 10 WC Developmental Biology SC Developmental Biology GA ER174 UT WOS:A1991ER17400006 PM 1824628 ER PT J AU JAKOWLEW, SB DILLARD, PJ WINOKUR, TS FLANDERS, KC SPORN, MB ROBERTS, AB AF JAKOWLEW, SB DILLARD, PJ WINOKUR, TS FLANDERS, KC SPORN, MB ROBERTS, AB TI EXPRESSION OF TRANSFORMING GROWTH FACTOR-BETA-S 1-4 IN CHICKEN-EMBRYO CHONDROCYTES AND MYOCYTES SO DEVELOPMENTAL BIOLOGY LA English DT Article ID DEOXYRIBONUCLEIC-ACID CLONING; MESSENGER RIBONUCLEIC-ACID; NON-NEOPLASTIC TISSUES; FACTOR-TYPE-BETA; NUCLEOTIDE-SEQUENCE; COLLAGEN-SYNTHESIS; PURIFICATION; FACTOR-BETA-1; CELLS; RNA RP JAKOWLEW, SB (reprint author), NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892, USA. NR 46 TC 80 Z9 81 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN PY 1991 VL 143 IS 1 BP 135 EP 148 DI 10.1016/0012-1606(91)90061-7 PG 14 WC Developmental Biology SC Developmental Biology GA ER174 UT WOS:A1991ER17400012 PM 1985015 ER PT J AU SAXE, CL JOHNSON, R DEVREOTES, PN KIMMEL, AR AF SAXE, CL JOHNSON, R DEVREOTES, PN KIMMEL, AR TI MULTIPLE GENES FOR CELL-SURFACE CAMP RECEPTORS IN DICTYOSTELIUM-DISCOIDEUM SO DEVELOPMENTAL GENETICS LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON THE SLIME MOLDS : DICTYOSTELIUM CY NOV 02-06, 1989 CL AIRLIE, VA DE SIGNAL TRANSDUCTION; G-PROTEINS; ADENYLYL CYCLASE; GENE EXPRESSION ID SIGNAL-TRANSDUCTION PATHWAYS; G-PROTEINS; EXPRESSION; DIFFERENTIATION; SEQUENCES AB We have cloned and characterized three genes (CAR1, CAR2, CAR3) encoding potential cell surface, cyclic adenosine 3':5' monophosphate (AMP) receptors from Dictyostelium discoideum. The three proteins are predicted to be substantially similar in amino acid sequence throughout most of their transmembrane (TM) and loop domains but are distinctly different in their carboxyl terminal segments. In addition, all three genes possess an intron which interrupts an equivalent codon of TM3. CAR1 is expressed early in development when the cAMP relay system is being established. As development proceeds multiple size forms of CAR1 RNA are detected which apparently result from differences in their 5'-untranslated regions. Late in development levels of CAR1 RNA decrease. In contrast, CAR2 encodes a single sized RNA which is expressed only during postaggregative development. CAR3 expression is approximately 10% of CAR1 during early development, is maximal during tight aggregate formation but declines thereafter. Only one size class of CAR3 mRNA is detected throughout development. Because RNA for each of the three genes is present in postaggregative cells, it was of interest to determine the cell type distribution of each RNA. Gene-specific probes were hybridized to RNAs isolated from cells of Percoll gradient-enriched prespore and prestalk fractions and relative levels of hybridization compared. CAR1 and CAR3 show approximately the same pattern of accumulation; a 3-4 fold enrichment in prestalk cells. CAR2, however, is highly enriched in prestalk cells, more than 10 fold relative to prespore cells. C1 NIH,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205. NR 22 TC 72 Z9 72 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 0192-253X J9 DEV GENET JI Dev. Genet. PY 1991 VL 12 IS 1-2 BP 6 EP 13 DI 10.1002/dvg.1020120104 PG 8 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA EV913 UT WOS:A1991EV91300003 PM 2049880 ER PT J AU ARKING, R BUCK, S BERRIOS, A DWYER, S BAKER, GT AF ARKING, R BUCK, S BERRIOS, A DWYER, S BAKER, GT TI ELEVATED PARAQUAT RESISTANCE CAN BE USED AS A BIOASSAY FOR LONGEVITY IN A GENETICALLY BASED LONG-LIVED STRAIN OF DROSOPHILA SO DEVELOPMENTAL GENETICS LA English DT Article DE AGING; GENETICS OF AGING; BIOMARKERS; FREE RADICALS; CATALASE; DROSOPHILA ID AGING PROCESSES; LIFE-SPAN; MELANOGASTER; SENESCENCE; ENVIRONMENT; EXPRESSION; SELECTION; SURVIVAL AB A long-lived (L) strain of Drosophila melanogoster, derived from a normal-lived (R) strain by artificial selection, has a significantly different adult longevity. Previous work has shown that 1) the two strains age in the same manner, 2) the major genes responsible for much of the L strain's extended longevity are located on the 3rd chromosome, and 3) the extended longevity phenotype is significantly modulated by the larval environment. In this report, we investigate the resistance of the L and R strains to the lethal effects of dietary paraquat. We show that, within the limitations of our described chromosomal and environmental manipulations, the extended longevity phenotype always accompanies the phenotype of elevated paraquat resistance. In addition, reversed selection applied to the L strain results in the simultaneous decrease of both life span and paraquat resistance. Thus, the presence or absence of the latter phenotype may be used as a bioassay for the presence or absence of the extended longevity phenotype, without any necessary implication of causality. Use of this bioassay should greatly speed up the genetic analysis of this system by allowing us to identify long-lived animals at a young age. Finally, we show that the age-related loss of elevated paraquat resistance in both strains precedes all the other age-related functional decrements which we have previously noted in this system. C1 WAYNE STATE UNIV,INST GERONTOL,DETROIT,MI 48202. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP ARKING, R (reprint author), WAYNE STATE UNIV,DEPT BIOL SCI,DETROIT,MI 48202, USA. FU NCRR NIH HHS [2 SO7 RR07051-24] NR 28 TC 101 Z9 103 U1 0 U2 8 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 1991 VL 12 IS 5 BP 362 EP 370 DI 10.1002/dvg.1020120505 PG 9 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA GM924 UT WOS:A1991GM92400004 PM 1806332 ER PT J AU BERARDI, A HAXBY, JV GRADY, CL RAPOPORT, SI AF BERARDI, A HAXBY, JV GRADY, CL RAPOPORT, SI TI ASYMMETRIES OF BRAIN GLUCOSE-METABOLISM AND MEMORY IN THE HEALTHY ELDERLY SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; RECOGNITION MEMORY; NONVERBAL MEMORY; AGE-DIFFERENCES; FRONTAL-LOBE; LESIONS; PERFORMANCE; HIPPOCAMPUS; DEFICITS; AMYGDALA AB The relation of discrepancies between visual and verbal memory to right-left asymmetries of resting state brain glucose metabolism was studied in 11 healthy elderly subjects. Short- and long-term memory were measured with experimental continuous recognition tests. Regional cerebral metabolic rates for glucose were determined with positron emission tomography (PET) using 18F-fluoro-2-deoxy-D-glucose. Long-term memory discrepancy was related to parietal and hemispheric metabolic asymmetries, such that subjects with better visual than verbal memory had higher right than left brain glucose metabolic rates, whereas others showed the opposite pattern. These results show that specific visual and verbal memory abilities in the healthy elderly are related to regional differences in cerebral cortical metabolism. RP BERARDI, A (reprint author), NIH,NATL INST AGING,NEUROSCI LAB,ROOM 6C414,BLDG 10,BETHESDA,MD 20892, USA. NR 47 TC 10 Z9 10 U1 2 U2 2 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 1991 VL 7 IS 1 BP 87 EP 97 PG 11 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA FD220 UT WOS:A1991FD22000005 ER PT J AU KOSS, E HAXBY, JV DECARLI, C SCHAPIRO, MB FRIEDLAND, RP RAPOPORT, SI AF KOSS, E HAXBY, JV DECARLI, C SCHAPIRO, MB FRIEDLAND, RP RAPOPORT, SI TI PATTERNS OF PERFORMANCE PRESERVATION AND LOSS IN HEALTHY AGING SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID AGE-DIFFERENCES; MEMORY; COMPREHENSION; ADULTHOOD AB Cognitive performance was studied in 67 healthy and highly educated men, ranging in age from 21 to 92 years old. Principal component analysis yielded five independent factors: Perceptual Reasoning, Visuospatial Memory and Organization, Verbal Fund of Knowledge, Verbal Discourse Memory, and Verbal Memory and Organization. The first two factors declined significantly (p < .05) with advancing age, whereas the other factors were not significantly correlated with advancing age. Further analysis indicates that Factor 1 explains all significant age related variance in neuropsychological performance. The data suggest that decline in visuospatial performance with age occurs even in the absence of disease and that memory functions are relatively well preserved in healthy individuals. C1 NIA,NEUROSCI LAB,BALTIMORE,MD 21224. RI DeCarli, Charles/B-5541-2009; Friedland, Robert/A-2834-2010 OI Friedland, Robert/0000-0001-5721-1843 NR 64 TC 45 Z9 45 U1 0 U2 0 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 1991 VL 7 IS 1 BP 99 EP 113 PG 15 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA FD220 UT WOS:A1991FD22000006 ER PT J AU NESTOR, PG PARASURAMAN, R HAXBY, JV AF NESTOR, PG PARASURAMAN, R HAXBY, JV TI SPEED OF INFORMATION-PROCESSING AND ATTENTION IN EARLY ALZHEIMERS DEMENTIA SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID REACTION-TIME; DISEASE; MEMORY AB The speed of information processing was examined in a group of patients in the early stages of Alzheimer's disease (AD) and in a group of healthy, age-and educationally matched controls. Subjects were tested on auditory simple-reaction time (RT), visual choice-RT, and combined simple- and choice-RT tasks. The choice-RT task required elementary linguistic or visuoperceptual matching of successively presented stimuli. AD patients had normal simple RTs but had delayed RTs on the matching tasks, suggesting a slower rate of processing for the component mental operations of the matching tasks. Estimates of the attentional demands or costs of these mental operations-stimulus encoding, decision making, and response selection-were obtained by combining the matching task with the simple-RT task (probe-RT). AD patients again showed a significant slowing in choice-RT, although they exhibited normal accuracy or performance outcome. AD patients also showed increased attentional cost for letter encoding (as reflected in increased probe-RT) but not for the other constituent mental operations. The results suggest that the differential slowing of choice-RT in AD is related to the complexity and attentional demands associated with coordinating and executing the matching tasks. C1 CATHOLIC UNIV AMER,WASHINGTON,DC 20064. NIA,BETHESDA,MD 20892. NR 37 TC 34 Z9 34 U1 0 U2 1 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 1991 VL 7 IS 2 BP 243 EP 256 PG 14 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA FW527 UT WOS:A1991FW52700010 ER PT J AU CHAUHAN, DP MILLER, MS OWENS, IS ANDERSON, LM AF CHAUHAN, DP MILLER, MS OWENS, IS ANDERSON, LM TI GENE-EXPRESSION, ONTOGENY AND TRANSPLACENTAL INDUCTION OF HEPATIC UDP-GLUCURONOSYL TRANSFERASE-ACTIVITY IN MICE SO DEVELOPMENTAL PHARMACOLOGY AND THERAPEUTICS LA English DT Article DE UDP-GLUCURONOSYL TRANSFERASE; ONTOGENY; MICE; POLYCYCLIC AROMATIC HYDROCARBONS ID HUMAN-LIVER; RAT-LIVER; MOUSE-LIVER; FUNCTIONAL-HETEROGENEITY; DIFFERENTIAL INDUCTION; BETA-NAPHTHOFLAVONE; MESSENGER-RNA; 3-METHYLCHOLANTHRENE; CDNA; GLUCURONYLTRANSFERASE AB The ontogeny and transplacental inducibility of UDP-glucuronosyl transferase (UDPGT) activities potentially relevant to detoxification of polycyclic aromatic hydrocarbons were studied in (C57BL/6 X DBA/2) F1 or (DBA/2 X C57BL/6) F1 fetal mouse liver, with p-nitrophenol (PNP) and 3-hydroxybenzo[a]pyrene (3-OH-BP) as substrates. Both UDPGT activities developed during the late fetal period and reached almost 60% of the adult activity at term; PNP, but not 3-OH-BP UDPGT decreased significantly on postnatal day 1 before rising to adult levels. A single exposure to beta-naphthoflavone (beta-NF; 150 mg/kg) on day 17 of gestation induced the PNP-UDPGT activity significantly (1.5-fold) by day 19 in the B6D2 F1s but not D2B6 F1s. A single dose of 3-methylcholanthrene (MC; 100 mg/kg) or 2,3,7,8,-tetrachlorodibenzo-p-dioxin (10-mu-g/kg) did not induce, but three injections of MC also resulted in significant induction in the fetuses of C57BL/6 mothers. 3-OH-BP-UDPGT was not significantly induced by any of the chemicals in either genetic cross. In a parallel study, a gene for an inducible mouse UDPGT, designated UDPGTm-1, was shown by Northern blotting to be expressed in fetal liver by day 18 of gestation at low levels relative to adults, but was not induced transplacentally by MC, beta-NF or phenobarbital (PB). These results show that (1) at least two functionally defined UDPGT activities toward phenolic substrates are present in the late fetal mouse liver; (2) one of these is transplacentally inducible by beta-NF and MC, but only in fetuses of C57BL/6 mothers, (3) induction where achieved was relatively small in magnitude, and (4) a gene of a PB-inducible UDPGT was expressed at low levels in the fetuses but was not induced transplacentally. C1 NCI,FREDERICK CANC RES FACIL,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21701. NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. NR 44 TC 11 Z9 11 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0379-8305 J9 DEV PHARMACOL THERAP JI Dev. Pharmacol. Ther. PY 1991 VL 16 IS 3 BP 139 EP 149 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FZ825 UT WOS:A1991FZ82500004 PM 1914788 ER PT J AU SHIMOKATA, H MULLER, DC FLEG, JL SORKIN, J ZIEMBA, AW ANDRES, R AF SHIMOKATA, H MULLER, DC FLEG, JL SORKIN, J ZIEMBA, AW ANDRES, R TI AGE AS INDEPENDENT DETERMINANT OF GLUCOSE-TOLERANCE SO DIABETES LA English DT Article ID BODY-FAT DISTRIBUTION; DIABETES-MELLITUS; INSULIN SENSITIVITY; HUMAN OBESITY; METABOLISM; CARBOHYDRATE; WOMEN; MEN; DIAGNOSIS; RESPONSES C1 NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. POLISH ACAD SCI,MED RES CTR,DEPT APPL PHYSIOL,WARSAW 42,POLAND. RP SHIMOKATA, H (reprint author), NIA,GERONTOL RES CTR,CLIN PHYSIOL LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 43 TC 164 Z9 166 U1 9 U2 11 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD JAN PY 1991 VL 40 IS 1 BP 44 EP 51 DI 10.2337/diabetes.40.1.44 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EN929 UT WOS:A1991EN92900007 PM 2015973 ER PT J AU RABEN, N BARBETTI, F CAMA, A LESNIAK, MA LILLIOJA, S ZIMMET, P SERJEANTSON, SW TAYLOR, SI ROTH, J AF RABEN, N BARBETTI, F CAMA, A LESNIAK, MA LILLIOJA, S ZIMMET, P SERJEANTSON, SW TAYLOR, SI ROTH, J TI NORMAL CODING SEQUENCE OF INSULIN GENE IN PIMA-INDIANS AND NAURUANS, 2 GROUPS WITH HIGHEST PREVALENCE OF TYPE-II DIABETES SO DIABETES LA English DT Article ID STRUCTURALLY ABNORMAL INSULIN; 5' FLANKING REGION; FAMILIAL HYPERPROINSULINEMIA; PROINSULIN CONVERSION; POINT MUTATION; MELLITUS; POLYMORPHISM; IDENTIFICATION; BIOSYNTHESIS; LINKAGE C1 NIDDK,PHOENIX EPIDEMIOL & CLIN RES BRANCH,CLIN DIABET & NUTR SECT,PHOENIX,AZ. ROYAL SO MEM HOSP,LIONS INT DIABET INST,VICTORIA,AUSTRALIA. AUSTRALIAN NATL UNIV,JOHN CURTIN SCH MED RES,CANBERRA,ACT 2601,AUSTRALIA. RP RABEN, N (reprint author), NIDDKD,DIABET BRANCH,BLDG 10,ROOM 8S-243,BETHESDA,MD 20892, USA. RI Lillioja, Stephen/A-8185-2012 FU NIDDK NIH HHS [DK-25446] NR 37 TC 23 Z9 24 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD JAN PY 1991 VL 40 IS 1 BP 118 EP 122 DI 10.2337/diabetes.40.1.118 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EN929 UT WOS:A1991EN92900017 PM 2015966 ER PT J AU ZIMMET, P DOWSE, G BENNETT, P AF ZIMMET, P DOWSE, G BENNETT, P TI HYPERINSULINEMIA IS A PREDICTOR OF NON-INSULIN-DEPENDENT DIABETES-MELLITUS SO DIABETES & METABOLISM LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON NON-INSULIN DEPENDENT DIABETES TODAY CY SEP 07-08, 1990 CL HELSINGOR, DENMARK DE NON-INSULIN-DEPENDENT DIABETES-MELLITUS; HYPERINSULINEMIA; INSULIN RESISTANCE; BETA-CELL EXHAUSTION; GLUCOTOXICITY; NAURUANS; PIMAS ID IMPAIRED GLUCOSE-TOLERANCE; PIMA-INDIANS; FAT DISTRIBUTION; NATURAL-HISTORY; RISK-FACTORS; NIDDM; PREVALENCE; POPULATION; RESISTANCE; OBESITY AB Most incidence studies indicate that baseline plasma glucose, either fasting or post-glucose load, is the best predictor of progression to non-insulin-dependent diabetes mellitus (NIDDM) - the higher the level, the higher the risk. Elevated serum insulin concentrations in the presence of normal fasting plasma glucose levels reflect the presence of insulin resistance and they have also been shown to predict deterioration to NIDDM in a number of populations. Hyperinsulinaemia is a notable characteristic of populations with a high prevalence of NIDDM such as Micronesian Nauruans, American Pima Indians, Mexican-Americans and Asian Indians. In Nauruans and Pima subjects with normal glucose tolerance, those with higher postload (2-hour) serum insulin at baseline were more likely to progress to either impaired glucose tolerance (IGT) or NIDDM. Conversely, amongst subjects with IGT, progression to NIDDM was predicted by lower (but still high relative to normal) baseline insulin responsiveness. Similar results for subjects with IGT have been described in Japanese. It appears from longitudinal studies that baseline insulin and glucose levels explain much of the association of obesity with risk of NIDDM. It remains to be resolved whether obesity itself may be a manifestation of an underlying defect (such as primary hyperinsulinaemia) which leads to both obesity and NIDDM. The possible sequence of events for the development of NIDDM includes a genetic defect resulting in hyperinsulinaemia and/or insulin resistance and leading ultimately to secondary pancreatic exhaustion with an insulin secretory defect which may also be genetically determined or the result of glucotoxicity. Future studies need to determine not only whether NIDDM is preventable through lifestyle modification, but which group of individuals should be the targets for a "high risk" preventative approach. It may well be that it should be persons with relatively high insulin and glucose concentrations, rather than those who are obese but without these metabolic abnormalities. C1 NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,PHOENIX,AZ. RP ZIMMET, P (reprint author), CAULFIELD GEN MED CTR,INT DIABET INST,260 KOOYONG RD,CAULFIELD,VIC 3162,AUSTRALIA. FU NIDDK NIH HHS [DK 25446] NR 51 TC 32 Z9 32 U1 0 U2 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0338-1684 J9 DIABETES METAB JI Diabetes Metab. PY 1991 VL 17 IS 1BIS BP 101 EP 108 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FP437 UT WOS:A1991FP43700006 PM 1936464 ER PT B AU BENNETT, PH NELSON, RG AF BENNETT, PH NELSON, RG BE ANDREANI, D GUERIGUIAN, JL STRIKER, GE CONTI, FG TI THE EPIDEMIOLOGY OF KDDM IN NIDDM AND IDDM SO DIABETIC COMPLICATIONS : EPIDEMIOLOGY AND PATHOGENETIC MECHANISMS SE SERONO SYMPOSIA PUBLICATIONS FROM RAVEN PRESS LA English DT Proceedings Paper CT INTERNATIONAL SYMP ON DIABETIC COMPLICATIONS : EPIDEMIOLOGY AND PATHOGENIC MECHANISMS CY APR 17-19, 1990 CL LISBON, PORTUGAL SP ARES SERONO SYMP, INST DEV RATIONNEL AGENTS MEDICAMENTEUX RP BENNETT, PH (reprint author), NIDDK,PHOENIX EPIDEMIOL & CLIN RES BRANCH,1550 E INDIAN SCH RD,PHOENIX,AZ 85014, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-648-9 J9 SERONO SYM PY 1991 VL 69 BP 83 EP 95 PG 13 WC Endocrinology & Metabolism; Genetics & Heredity; Public, Environmental & Occupational Health; Pathology SC Endocrinology & Metabolism; Genetics & Heredity; Public, Environmental & Occupational Health; Pathology GA BU42M UT WOS:A1991BU42M00007 ER PT B AU STRIKER, LJ CONTI, FG DOI, T ELLIOT, SJ STRIKER, GE AF STRIKER, LJ CONTI, FG DOI, T ELLIOT, SJ STRIKER, GE BE ANDREANI, D GUERIGUIAN, JL STRIKER, GE CONTI, FG TI KIDNEY-DISEASE OF DIABETES-MELLITUS - THE CONTRIBUTION OF GLOMERULAR MESANGIAL CELLS TO THE GLOMERULOSCLEROSIS SO DIABETIC COMPLICATIONS : EPIDEMIOLOGY AND PATHOGENETIC MECHANISMS SE SERONO SYMPOSIA PUBLICATIONS FROM RAVEN PRESS LA English DT Proceedings Paper CT INTERNATIONAL SYMP ON DIABETIC COMPLICATIONS : EPIDEMIOLOGY AND PATHOGENIC MECHANISMS CY APR 17-19, 1990 CL LISBON, PORTUGAL SP ARES SERONO SYMP, INST DEV RATIONNEL AGENTS MEDICAMENTEUX RP STRIKER, LJ (reprint author), NIDDK,METAB DIS BRANCH,RENAL CELL BIOL UNIT,BLDG 10,ROOM 3N110,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-648-9 J9 SERONO SYM PY 1991 VL 69 BP 131 EP 143 PG 13 WC Endocrinology & Metabolism; Genetics & Heredity; Public, Environmental & Occupational Health; Pathology SC Endocrinology & Metabolism; Genetics & Heredity; Public, Environmental & Occupational Health; Pathology GA BU42M UT WOS:A1991BU42M00011 ER PT B AU ROBISON, WG AF ROBISON, WG BE ANDREANI, D GUERIGUIAN, JL STRIKER, GE CONTI, FG TI A GALACTOSEMIC RAT MODEL FOR DIABETIC-LIKE RETINAL MICROANGIOPATHIES SO DIABETIC COMPLICATIONS : EPIDEMIOLOGY AND PATHOGENETIC MECHANISMS SE SERONO SYMPOSIA PUBLICATIONS FROM RAVEN PRESS LA English DT Proceedings Paper CT INTERNATIONAL SYMP ON DIABETIC COMPLICATIONS : EPIDEMIOLOGY AND PATHOGENIC MECHANISMS CY APR 17-19, 1990 CL LISBON, PORTUGAL SP ARES SERONO SYMP, INST DEV RATIONNEL AGENTS MEDICAMENTEUX RP ROBISON, WG (reprint author), NEI,BLDG 9,RM 1E104,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-648-9 J9 SERONO SYM PY 1991 VL 69 BP 181 EP 186 PG 6 WC Endocrinology & Metabolism; Genetics & Heredity; Public, Environmental & Occupational Health; Pathology SC Endocrinology & Metabolism; Genetics & Heredity; Public, Environmental & Occupational Health; Pathology GA BU42M UT WOS:A1991BU42M00014 ER PT J AU MINOR, JR BALTZ, JK AF MINOR, JR BALTZ, JK TI FOSCARNET SODIUM SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; CYTOMEGALO-VIRUS RETINITIS; HERPES-SIMPLEX VIRUS; IMMUNE-DEFICIENCY SYNDROME; RECURRENT GENITAL HERPES; ACUTE RENAL-FAILURE; TRISODIUM PHOSPHONOFORMATE; PYROPHOSPHATE ANALOGS; INTRAVENOUS FOSCARNET; TOPICAL TREATMENT AB Cytomegalovirus (CMV), a major opportunistic viral pathogen frequently causing disease in immunocompromised patients such as organ transplant recipients and people with AIDS, may present as pneumonitis, gastrointestinal disease, or encephalitis. Its most common manifestation in patients with AIDS is retinitis which, if left untreated, invariably progresses to extensive retinal necrosis and ultimately to blindness. Ganciclovir sodium, currently the only licensed antiviral agent for the treatment of CMV retinitis, effectively controls this infection in a majority of AIDS patients, but significant granulocytopenia or thrombocytopenia related to ganciclovir therapy often limit its clinical application. Myelosuppression may be further exacerbated in AIDS patients by such other agents as zidovudine or trimethoprim/sulfamethoxazole, often necessitating dosage reductions or discontinuation of these agents in patients receiving ganciclovir. Foscarnet sodium, a pyrophosphate analog active against both cytomegalovirus and the human immunodeficiency virus type 1 (HIV), may be an effective alternative to ganciclovir in the management of CMV retinitis. Trials with intravenous foscarnet in CMV retinitis have reported favorable results using initial daily doses of 180-230 mg/kg/d given as intermittent infusions every eight hours, followed by maintenance regimens of 60-90 mg/kg/d given as single daily one- or two-hour infusions. Foscarnet therapy may result in renal impairment, and indefinite intravenous maintenance therapy may be required to prevent recurrence of CMV infection. Despite these drawbacks, foscarnet's lack of major myelosuppressive toxicity, and its activity in suppressing HIV replication, make this a potentially safe and effective alternative agent for the management of CMV infection, especially in AIDS patients. C1 NATL NAVAL MED CTR, NAVY MED ONCOL BRANCH, BETHESDA, MD 20814 USA. RP MINOR, JR (reprint author), NIH, WARREN G MAGNUSON CLIN CTR, DEPT PHARM, BLDG 10, ROOM 1-N-257, BETHESDA, MD 20892 USA. NR 59 TC 8 Z9 8 U1 0 U2 2 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD JAN PY 1991 VL 25 IS 1 BP 41 EP 47 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV669 UT WOS:A1991EV66900011 PM 1848959 ER PT J AU HOHMANN, AA LARSON, DB THOMPSON, JW BEARDSLEY, RS AF HOHMANN, AA LARSON, DB THOMPSON, JW BEARDSLEY, RS TI PSYCHOTROPIC MEDICATION PRESCRIPTION IN UNITED-STATES AMBULATORY MEDICAL-CARE SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Article ID DRUG-THERAPY; MENTAL DISORDER; BENZODIAZEPINES; PHYSICIANS; DIAGNOSIS; LONG AB Because of the pharmacologic power of psychotropic medications, the potential for adverse effects, and the changing popularity of particular psychotropic drugs, it is vital for pharmacoepidemiologists to monitor the prescribing patterns of these medications. Using data from the 1985 National Ambulatory Medical Care Survey (NAMCS), this article assesses psychotropic medication prescribing by U.S. ambulatory care physicians. Psychotropic medications are classified into three categories: minor tranquilizers (i.e., anxiolytics and sedative-hypnotics), antidepressants, and antipsychotics. The prescribing patterns of psychiatrists, primary care clinicians, and all other physicians are compared. Differences in psychotropic prescribing patterns by psychiatric diagnosis are examined as well. The excessive use of minor tranquilizers, the continuing use of first-generation psychotropic medications (particularly minor tranquilizers), and the lack of concordance between diagnoses and prescribed psychotropic medications are discussed. C1 UNIV MARYLAND,SCH PHARM,BALTIMORE,MD 21201. RP HOHMANN, AA (reprint author), NIMH,DIV APPL & SERV RES,SERV RES BRANCH,5600 FISHERS LANE,ROOM 18C-14,ROCKVILLE,MD 20857, USA. NR 25 TC 26 Z9 26 U1 2 U2 2 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD JAN PY 1991 VL 25 IS 1 BP 85 EP 89 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA EV669 UT WOS:A1991EV66900017 PM 2008789 ER PT J AU SAEED, ZA EVANS, DJ EVANS, DG CORNELIUS, MJ MATON, PN JENSEN, RT GRAHAM, DY AF SAEED, ZA EVANS, DJ EVANS, DG CORNELIUS, MJ MATON, PN JENSEN, RT GRAHAM, DY TI HELICOBACTER-PYLORI AND ZOLLINGER-ELLISON SYNDROME SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE CAMPYLOBACTER-PYLORI; HELICOBACTER-PYLORI; ZOLLINGER-ELLISON SYNDROME; PEPTIC ULCER; GASTRIC ACID SECRETION; GASTRIN ID PEPTIC-ULCER DISEASE; CAMPYLOBACTER-PYLORI; MANAGEMENT; DIAGNOSIS; INFECTION; GASTRITIS; PARIETAL AB Helicobacter pylori (previously Campylobacter pylori) is almost invariably associated with chronic duodenal ulcer disease. The relationship between H. pylori infection and duodenal ulcer in Zollinger-Ellison syndrome is unknown. We investigated the frequency of H. pylori infection in Zollinger-Ellison syndrome and also what effect H. pylori infection had on gastric function in patients with Zollinger-Ellison syndrome. H. pylori infection was diagnosed based on a specific serologic (ELISA) assay based on high-molecular-weight cell-associated proteins of H. pylori. We studied 20 patients with Zollinger-Ellison syndrome; 15 men and 5 women ranging in age from 24 to 71 years, median age 51. Six Zollinger-Ellison syndrome patients had H. pylori infection compared to 100 consecutive patients with chronic recurrent duodenal ulcer disease (P < 0.05). Pretreatment basal acid output in Zollinger-Ellison syndrome patients ranged from 7.9 to 95.0 mmol/hr, median 35.2. Pentagastrin-stimulated maximal acid output ranged from 8.5 to 132 mmol/hr, median 52.7. Acid secretion was lower in the H. pylori-infected patients than the uninfected patients (BAO 24.5 +/- 6.5 vs 45.4 +/- 6.6, and MAO 44.3 +/- 11.8 vs 67.9 +/- 10.7, for H. pylori infected vs uninfected patients, respectively). The difference in BAO was statistically significant (P < 0.05). The present results indicate that H. pylori is not a major contributing factor in duodenal ulcer associated with Zollinger-Ellison syndrome. The association of a reduced BAO with H. pylori suggests that these findings may be related. C1 BAYLOR UNIV,DEPT MED,HOUSTON,TX 77030. NIH,CTR DIGEST DIS,BETHESDA,MD 20892. RP SAEED, ZA (reprint author), VET ADM MED CTR,DEPT MED,111D,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. FU NIDDK NIH HHS [DK 39919] NR 17 TC 31 Z9 31 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD JAN PY 1991 VL 36 IS 1 BP 15 EP 18 DI 10.1007/BF01300080 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ER626 UT WOS:A1991ER62600004 PM 1984998 ER PT J AU WAXMAN, I GARDNER, JD JENSEN, RT MATON, PN AF WAXMAN, I GARDNER, JD JENSEN, RT MATON, PN TI PEPTIC-ULCER PERFORATION AS THE PRESENTATION OF ZOLLINGER-ELLISON SYNDROME SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE GASTRINOMA; PEPTIC ULCER DISEASE ID LOCALIZE GASTRINOMAS; MANAGEMENT; ANGIOGRAPHY; DIAGNOSIS; SECRETIN; THERAPY AB We examined the characteristics of patients with Zollinger-Ellison syndrome who developed a perforation prior to diagnosis to determine whether any clinical features were useful markers of the syndrome. Of 160 patients with Zollinger-Ellison syndrome, perforation occurred prior to the diagnosis being made in 11 (7%). At surgery, perforations were found in the duodenum in six cases and in the jejunum in five. In no case was tumor identified at emergency surgery, and the diagnosis of Zollinger-Ellison syndrome was made only in the postoperative period when excessive gastric secretions were noted. Neither acid output nor serum gastrin concentration were useful predictors for perforation. The patients, six men and five women, were 27-61 years old (median 48) and one had MEN-1. There patients had no symptoms prior to the perforation. The other eight had symptoms for 1-15 years, with diarrhea occurring in 45% of the cases. Following the diagnosis of Zollinger-Ellison syndrome, patients were given medication to control gastric acid hypersecretion. Eight patients remained well, but the three patients who had had a partial gastrectomy had a complicated course despite medical therapy. Although features of perforation in Zollinger-Ellison syndrome are not specific, jejunal perforation or perforation associated with a history of diarrhea is suggestive of the diagnosis. Serum gastrin should be measured in every case and a partial gastrectomy avoided. RP MATON, PN (reprint author), NIDDKD,DIGEST DIS BRANCH,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892, USA. NR 27 TC 8 Z9 8 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD JAN PY 1991 VL 36 IS 1 BP 19 EP 24 DI 10.1007/BF01300081 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ER626 UT WOS:A1991ER62600005 PM 1984999 ER PT J AU NEBERT, DW NELSON, DR COON, MJ ESTABROOK, RW FEYEREISEN, R FUJIIKURIYAMA, Y GONZALEZ, FJ GUENGERICH, FP GUNSALUS, IC JOHNSON, EF LOPER, JC SATO, R WATERMAN, MR WAXMAN, DJ AF NEBERT, DW NELSON, DR COON, MJ ESTABROOK, RW FEYEREISEN, R FUJIIKURIYAMA, Y GONZALEZ, FJ GUENGERICH, FP GUNSALUS, IC JOHNSON, EF LOPER, JC SATO, R WATERMAN, MR WAXMAN, DJ TI THE P450 SUPERFAMILY - UPDATE ON NEW SEQUENCES, GENE-MAPPING, AND RECOMMENDED NOMENCLATURE SO DNA AND CELL BIOLOGY LA English DT Article ID AMINO-ACID SEQUENCE; CDNA-DIRECTED EXPRESSION; YEAST CANDIDA-TROPICALIS; NUCLEOTIDE-SEQUENCE; MOLECULAR-CLONING; MESSENGER-RNAS; HUMAN-LIVER; CHROMOSOMAL LOCALIZATION; CYTOCHROME-P450 CDNA; RAT AB We provide here a list of 154 P450 genes and seven putative pseudogenes that have been characterized as of October 20, 1990. These genes have been described in a total of 23 eukaryotes (including nine mammalian and one plant species) and six prokaryotes. Of 27 gene families so far described, 10 exist in all mammals. These 10 families comprise 18 subfamilies, of which 16 and 14 have been mapped in the human and mouse genomes, respectively; to date, each subfamily appears to represent a cluster of tightly linked genes. We propose here a modest revision of the initially proposed (Nebert et al., DNA 6, 1-11, 1987) and updated (Nebert et al., DNA 8, 1-13, 1989) nomenclature system based on evolution of the superfamily. For the gene we recommend that the italicized root symbol CYP for human (Cyp for mouse), representing cytochrome P450, be followed by an Arabic number denoting the family, a letter designating the subfamily (when two or more exist), and an Arabic numeral representing the individual gene within the subfamily. A hyphen should precede the final number in mouse genes. We suggest that the human nomenclature system be used for other species. This system is consistent with our earlier proposed nomenclature for P450 of all eukaryotes and prokaryotes, except that we are discouraging the future use of cumbersome Roman numerals. C1 UNIV N CAROLINA,DEPT BIOCHEM & BIOPHYS,CHAPEL HILL,NC 27599. UNIV MICHIGAN,DEPT BIOL CHEM,ANN ARBOR,MI 48109. UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. OREGON STATE UNIV,DEPT ENTOMOL,CORVALLIS,OR 97331. TOHOKU UNIV,FAC SCI,DEPT CHEM,SENDAI,MIYAGI 980,JAPAN. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. VANDERBILT UNIV,MED CTR,SCH MED,DEPT BIOCHEM,NASHVILLE,TN 37232. VANDERBILT UNIV,MED CTR,SCH MED,CTR MOLEC TOXICOL,NASHVILLE,TN 37232. UNIV ILLINOIS,DEPT BIOCHEM,URBANA,IL 61801. SCRIPPS CLIN & RES FDN,DEPT BASIC & CLIN RES,LA JOLLA,CA 92037. UNIV CINCINNATI,MED CTR,DEPT MOLEC GENET BIOCHEM & MICROBIOL,CINCINNATI,OH 45267. OSAKA UNIV,INST PROT RES,OSAKA 565,JAPAN. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP NEBERT, DW (reprint author), UNIV CINCINNATI,MED CTR,DEPT ENVIRONM HLTH,CINCINNATI,OH 45267, USA. RI Feyereisen, Rene/I-3140-2012; OI Feyereisen, Rene/0000-0002-9560-571X; Nelson, David/0000-0003-0583-5421 NR 115 TC 1111 Z9 1126 U1 3 U2 40 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD JAN-FEB PY 1991 VL 10 IS 1 BP 1 EP 14 DI 10.1089/dna.1991.10.1 PG 14 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA EU671 UT WOS:A1991EU67100001 PM 1991046 ER PT J AU YEH, SY DESOUZA, EB AF YEH, SY DESOUZA, EB TI LACK OF NEUROCHEMICAL EVIDENCE FOR NEUROTOXIC EFFECTS OF REPEATED COCAINE ADMINISTRATION IN RATS ON BRAIN MONOAMINE NEURONS SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE REPEATED COCAINE ADMINISTRATION; COCAINE; NOREPINEPHRINE; DOPAMINE; DIHYDROXYPHENYLACETIC ACID; HOMOVANILLIC ACID; SEROTONIN; 5-HYDROXYINDOLEACETIC ACID ID TYROSINE-HYDROXYLASE IMMUNOREACTIVITY; SEROTONIN TERMINALS; AMINE METABOLISM; NERVE-TERMINALS; RHESUS-MONKEYS; DOPAMINE; AMPHETAMINE; SYSTEM; METHYLENEDIOXYMETHAMPHETAMINE; METHAMPHETAMINE AB Rats were injected with cocaine (20 mg/kg, s.c. or i.p. twice daily for 8 days) or saline and killed at 1, 8, 15 or 48 days after the last injection. The concentrations of norepinephrine (NE), dopamine (DA), serotonin (5-HT) and their metabolites, assayed by HPLC-EC, in frontal cortex, hippocampus, striatum, hypothalamus, midbrain, pons-medulla and spinal cord were not significantly different from those in the saline-injected controls at any of the time points examined. These data suggest that the repeated cocaine administration in rats does not produce any long-term depletion in brain catecholamine and 5-HT content suggesting no neurotoxic effects of the drug. RP YEH, SY (reprint author), NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 34 TC 54 Z9 55 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 1991 VL 27 IS 1 BP 51 EP 61 DI 10.1016/0376-8716(91)90086-E PG 11 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA EW925 UT WOS:A1991EW92500007 PM 1709403 ER PT J AU MORRISSEY, RE EUSTIS, S HASEMAN, JK HUFF, J BUCHER, JR AF MORRISSEY, RE EUSTIS, S HASEMAN, JK HUFF, J BUCHER, JR TI TOXICITY AND CARCINOGENICITY STUDIES OF NALIDIXIC-ACID IN RODENTS SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article ID STATISTICAL ISSUES; CHEMICAL MUTAGENS; DNA-REPAIR; LONG-TERM; SALMONELLA; GYRASE; WOMEN; MICE AB Toxicity and carcinogenicity studies of nalidixic acid, an antimicrobial agent used to treat bacterial infections of the urinary tract, were conducted in F344/N rats and B6C3F1 mice of each sex for 13 weeks or 2 years. In the 13-week studies, nalidixic acid was administered at dietary concentrations ranging from 1,000 to 16,000 ppm. Body weights of both rats and mice were reduced in the groups receiving diet containing 8,000 and 16,000 ppm, and feed consumption of rats in the highest treatment groups was approximately two-thirds that of controls. Degeneration of the germinal epithelium in the seminiferous tubules of the testis was observed in male rats that received 16,000 ppm; no other compound-related histopathologic effects were observed in either species. Two-year studies were conducted by feeding diets containing 0, 2,000, or 4,000 ppm nalidixic acid to groups of 50 rats and mice/sex/group. The average daily feed consumption was slightly reduced compared to control groups and resulted in approximate daily doses of 82 or 175 mg nalidixic acid/kg for low dose and high dose rats, and 220 or 475 mg/kg for low dose and high dose mice. Mean body weights of dosed rats and mice were lower than those of controls, except for groups of low dose female rats and male mice. The incidences of preputial gland neoplasms in dosed male rats and of clitoral gland neoplasms in dosed female rats were significantly increased compared to those in controls; responses in low dose groups were similar to those in high dose groups. There were decreased incidences of leukemia and mammary gland neoplasms in dosed female rats and of pituitary gland neoplasms in dosed male rats. Subcutaneous tissue fibrosarcomas were marginally increased in dosed male mice. There were no increased incidences of neoplasms in dosed female mice. Under the conditions of these studies the dietary administration of nalidixic acid was carcinogenic for rats, causing preputial gland or clitoral gland neoplasms in males and females, respectively. The association of subcutaneous neoplasms with administration of nalidixic acid to male mice was equivocal. RP MORRISSEY, RE (reprint author), NIEHS,NATL TOXICOL PROGRAM,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709, USA. NR 37 TC 10 Z9 10 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 1991 VL 14 IS 1-2 BP 45 EP 66 DI 10.3109/01480549109017868 PG 22 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA FV876 UT WOS:A1991FV87600003 PM 1889378 ER PT J AU VIG, PJS RAVI, K NATH, R AF VIG, PJS RAVI, K NATH, R TI INTERACTION OF METALS WITH BRAIN CALMODULIN PURIFIED FROM NORMAL AND CADMIUM EXPOSED RATS SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article ID MONKEY BRAIN; INHIBITION; INVITRO; METALLOTHIONEIN; TOXICITY; INVIVO AB Chronic exposure of cadmium (Cd) to rats (6 mg/kg body weight/day) led to a significant accumulation of Cd in brain and other organs. Calmodulin (CaM) isolated from brains of Cd exposed rats showed a decreased ability to stimulate CaM-dependent phosphodiesterase (PDE) as compared to that purified from unexposed animals. There was a dose dependent inhibition of CaM activity when CaM (from normal and Cd exposed rats) was incubated with different molar ratios of aluminium (Al3+), lead (Pb2+), manganese (Mn2+) and vanadium (V5+). Regression analysis of rat brain CaM activity versus varying metal ion concentration demonstrated negative slopes. However, CaM from the brains of Cd exposed rats was less sensitive to these metals in comparison to the normal rat brain CaM. These data suggest that CaM inhibition may be used as a biological marker of neurotoxicity and for elucidating the possible mechanism by which neurotoxic metals manifest toxic effects. C1 NHLBI,DEPT BIOL,BETHESDA,MD 20892. POSTGRAD INST MED EDUC & RES,DEPT BIOCHEM,CHANDIGARH 160012,INDIA. RP VIG, PJS (reprint author), UNIV MISSISSIPPI,MED CTR,DEPT NEUROL,JACKSON,MS 39216, USA. NR 26 TC 14 Z9 15 U1 0 U2 2 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 1991 VL 14 IS 1-2 BP 207 EP 218 DI 10.3109/01480549109017877 PG 12 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA FV876 UT WOS:A1991FV87600012 PM 1653697 ER PT J AU KIMES, AS RAYMON, LP MELTZER, LT HEFFNER, T LONDON, ED AF KIMES, AS RAYMON, LP MELTZER, LT HEFFNER, T LONDON, ED TI CEREBRAL METABOLIC EFFECTS OF CL-943 (8-ETHYL-7,8-DIHYDRO-1,3,5-TRIMETHYL-1H-IMIDAZO[1,2,-C]PYRAZOLO[3,4-E]-P YRIMIDINE), A POTENTIAL ANTIPSYCHOTIC DRUG SO DRUG DEVELOPMENT RESEARCH LA English DT Article DE DEOXYGLUCOSE; BRAIN METABOLISM; RAT ID PRECIPITATED MORPHINE-WITHDRAWAL; BRAIN GLUCOSE-METABOLISM; RAT-BRAIN; ENERGY-METABOLISM; CONSCIOUS RAT; SEROTONIN RECEPTORS; APOMORPHINE; AGENT; SCHIZOPHRENIA; HALOPERIDOL AB Cl-943 is a novel drug candidate that has antipsychotic-like activity in a variety of behavioral tests in rodents and primates, but has no affinity for brain dopamine (DA) receptors. In order to obtain information on the neuroanatomical substrates for its behavioral actions, we used the autoradiographic 2-deoxy-D-[1-C-14]-glucose method to map and quantify the distribution of Cl-943 effects on the regional cerebral metabolic rate(s) for glucose (rCMRglc) in the rat. The effects of Cl-943 (40 mg/kg) were assessed at 10 and at 60 min after the drug was administered intraperitoneally. In the globus pallidus and the substantia nigra pars reticulata, rCMRglc were increased at 60 min following treatment, and in the lateral habenula, rCMRglc was increased at 10 and 60 min after treatment. In contrast, the predominant effect of Cl-943 in other areas (e.g., most cortical, several thalamic, basal ganglia, limbic, and midbrain areas) was to reduce rCMRglc. The metabolic pattern produced by Cl-943 was unique and consistent with previous findings that Cl-943 resembles other antipsychotic drugs in behavioral tests but differs from those agents in tests predictive of extrapyramidal dysfunction. C1 WARNER LAMBERT PARKE DAVIS,PARKE DAVIS PHARMACEUT RES DIV,ANN ARBOR,MI. RP KIMES, AS (reprint author), NIDA,ADDICT RES CTR,NEUROSCI BRANCH,NEURPHARMACOL LAB,POB 5180,BALTIMORE,MD 21224, USA. NR 40 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 0272-4391 J9 DRUG DEVELOP RES JI Drug Dev. Res. PY 1991 VL 24 IS 1 BP 29 EP 39 DI 10.1002/ddr.430240103 PG 11 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GM921 UT WOS:A1991GM92100002 ER PT J AU LAMOUR, Y HOLLOWAY, HW RAPOPORT, SI SONCRANT, TT AF LAMOUR, Y HOLLOWAY, HW RAPOPORT, SI SONCRANT, TT TI EFFECTS OF GINKGOLIDE-B AND GINKGO BILOBA EXTRACT ON LOCAL CEREBRAL GLUCOSE-UTILIZATION IN THE AWAKE ADULT-RAT SO DRUG DEVELOPMENT RESEARCH LA English DT Article DE CEREBRAL CORTEX; CEREBRAL GLUCOSE UTILIZATION; LCGU ID BLOOD-FLOW; METABOLISM; BRAIN; AGONIST AB The effects of the extract of the leaves of Ginkgo biloba and of one of its major components, Ginkgolide B, on local cerebral glucose utilization (LCGU) have been studied in the awake adult rat. Ginkgolide B (10 mg/kg i.p.) had no significant effect on LCGU in 38 brain regions studied. In contrast, the Ginkgo biloba extract (150 mg/kg i.p. in 3 divided doses) produced significant and widespread decreases in LCGU in 21 brain regions (range 3-26% reduction). These results demonstrate that Ginkgo biloba is able to reduce brain glucose utilization, but that the substance responsible for this effect may not be Ginkgolide B. C1 NIA,NEUROSCI LAB,10-6C103,BETHESDA,MD 20892. NR 22 TC 3 Z9 3 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0272-4391 J9 DRUG DEVELOP RES JI Drug Dev. Res. PY 1991 VL 23 IS 3 BP 219 EP 225 DI 10.1002/ddr.430230303 PG 7 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FY106 UT WOS:A1991FY10600002 ER PT J AU HUBER, BE WIRTH, PJ NEWBOLD, JE AF HUBER, BE WIRTH, PJ NEWBOLD, JE TI EFFECTS OF HUMAN LYMPHOBLASTOID INTERFERON ON PROLIFERATION, GENE-EXPRESSION AND TUMORIGENICITY OF HUMAN HEPATOMA-CELL LINES SO DRUGS UNDER EXPERIMENTAL AND CLINICAL RESEARCH LA English DT Article ID B SURFACE-ANTIGEN; C-MYC EXPRESSION; HEPATOCELLULAR-CARCINOMA; DAUDI CELLS; TRANSFORMED-CELLS; RAT-LIVER; ONCOGENE; DNA; CYTOCHROME-P-450; MODULATION AB Hep G2 and Hep 3B cells, two human hepatoma cell lines, showed decreased thymidine (Thd) incorporation into intracellular acid-insoluble pools when exposed to Wellferon(R), human lymphoblastoid interferon (IFN). Inhibition was maximal after 48 h treatment with Wellferon and was reversible. Significant inhibition in Wellferon-treated Hep 3B cells was noted at concentrations of 1 IFN unit/ml, which was over 1000-fold less than that required to produce equivalent effects in Hep G2 cells. The decrease in Thd incorporation into acid-insoluble pools was due to both alterations in Thd anabolism and a small but significant decrease in incorporation into DNA with no apparent effect on nucleoside transport. The small but significant Wellferon-induced decrease in Thd incorporation into DNA was reflected in a small but significant decrease in cell proliferation in both cell lines. In addition, Wellferon induced a decrease in the steady-state level of c-myc- and P450-specific RNA transcripts but did not affect the steady-state levels of transforming growth factor-B, fos, N-Ras, or erb-B RNA transcripts. These Wellferon effects, however, did not result in any significant antitumour effects when Hep 3B or Hep G2 cells were grown in athymic nude mice treated intraperitoneally with 8 mu/kg/day Wellferon. Wellferon can induce an antiviral state in both cell lines using Semliki Forest virus and Herpes simplex virus as viral challenges. Taken collectively, these data indicate that Wellferon produces both antiviral and slight but significant antiproliferative effects in Hep G2 and Hep 3B cells, but does not produce significant antitumour effects in vivo using these cell lines in nude mice xenografts. C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. UNIV N CAROLINA CHAPEL HILL,DEPT MICROBIOL & IMMUNOL,CHAPEL HILL,NC 27715. RP HUBER, BE (reprint author), WELLCOME RES LABS,RES TRIANGLE PK,NC 27709, USA. NR 49 TC 6 Z9 6 U1 0 U2 0 PU BIOSCIENCE EDIPRINT INC PI CAROUGE PA RUE ALEXANDRE-GAVARD 16, 1227 CAROUGE, SWITZERLAND SN 0378-6501 J9 DRUG EXP CLIN RES JI Drug Exp. Clin. Res PY 1991 VL 17 IS 6 BP 281 EP 291 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GU924 UT WOS:A1991GU92400001 PM 1663028 ER PT B AU BALOW, JE AF BALOW, JE BE DAMICO, G COLASANTI, G TI CYTOTOXIC DRUGS - RATIONALE IN MANAGEMENT OF GLOMERULONEPHRITIS SO ECLAMPSIA GLOMERULONEPHRITIS UREMIA SE ISSUES IN NEPHROSCIENCES LA English DT Proceedings Paper CT 21ST COURSE ON ISSUES IN NEPHROSCIENCES CY DEC 08-11, 1989 CL MILAN, ITALY RP BALOW, JE (reprint author), NIH,KIDNEY DIS SECT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WICHTIG EDITORE SRL PI MILAN PA MILAN BN 88-85053-89-0 J9 ISS NEPHROS PY 1991 VL 191 BP 106 EP 110 PG 5 WC Medicine, Research & Experimental; Urology & Nephrology SC Research & Experimental Medicine; Urology & Nephrology GA BT15V UT WOS:A1991BT15V00015 ER PT B AU CARTWRIGHT, WS WOODWARD, AM AF CARTWRIGHT, WS WOODWARD, AM BE Cartwright, WS Kaple, JM TI HEALTH-INSURANCE COVERAGE QUESTIONS, PUBLIC-HEALTH SURVEYS, AND DRUG-ABUSE SO ECONOMIC COSTS, COST-EFFECTIVENESS, FINANCING & COMMUNITY-BASED DRUG TREATMENT SE NIDA RESEARCH MONOGRAPH SERIES LA English DT Proceedings Paper CT Technical Review Meeting on Economic Costs, Cost-Effectiveness, Financing, and Community-Based Drug Treatment CY MAY 21-22, 1990 CL ROCKVILLE, MD SP NIDA C1 NIDA,DIV APPL RES,FINANCING & SERV RES BRANCH,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST DRUG ABUSE PI ROCKVILLE PA 5600 FISHERS LANE, ROCKVILLE, MD 20857 J9 NIDA RES MG PY 1991 VL 113 BP 190 EP 204 PG 15 WC Substance Abuse; Economics; Health Policy & Services SC Substance Abuse; Business & Economics; Health Care Sciences & Services GA BA46E UT WOS:A1991BA46E00012 PM 1762640 ER PT B AU LONDON, ED AF LONDON, ED BE ADLKOFER, F THURAU, K TI GLUCOSE-METABOLISM - AN INDEX OF NICOTINE ACTION IN THE BRAIN SO EFFECTS OF NICOTINE ON BIOLOGICAL SYSTEMS SE ADVANCES IN PHARMACOLOGICAL SCIENCES LA English DT Proceedings Paper CT SATELLITE SYMP TO THE 11TH INTERNATIONAL CONGRESS OF PHARMACOLOGY : EFFECTS OF NICOTINE ON BIOLOGICAL SYSTEMS CY JUN 28-30, 1990 CL HAMBURG, FED REP GER SP GERMAN RES COUNCIL SMOKING & HLTH RP LONDON, ED (reprint author), NIDA,ADDICT RES CTR,NEUROSCI BRANCH,NEUROPHARMACOL LAB,POB 5180,BALTIMORE,MD 21224, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIRKHAUSER VERLAG PI BASEL PA BASEL BN 3-7643-2519-4 J9 ADV PHAR SC PY 1991 BP 239 EP 248 PG 10 WC Medicine, Research & Experimental; Pharmacology & Pharmacy; Physiology SC Research & Experimental Medicine; Pharmacology & Pharmacy; Physiology GA BT55S UT WOS:A1991BT55S00033 ER PT B AU COHEN, C WELZL, H BATTIG, K AF COHEN, C WELZL, H BATTIG, K BE ADLKOFER, F THURAU, K TI BEHAVIORAL INTERACTION BETWEEN NICOTINE AND CAFFEINE SO EFFECTS OF NICOTINE ON BIOLOGICAL SYSTEMS SE ADVANCES IN PHARMACOLOGICAL SCIENCES LA English DT Proceedings Paper CT SATELLITE SYMP TO THE 11TH INTERNATIONAL CONGRESS OF PHARMACOLOGY : EFFECTS OF NICOTINE ON BIOLOGICAL SYSTEMS CY JUN 28-30, 1990 CL HAMBURG, FED REP GER SP GERMAN RES COUNCIL SMOKING & HLTH RP COHEN, C (reprint author), NIDA ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIRKHAUSER VERLAG PI BASEL PA BASEL BN 3-7643-2519-4 J9 ADV PHAR SC PY 1991 BP 461 EP 464 PG 4 WC Medicine, Research & Experimental; Pharmacology & Pharmacy; Physiology SC Research & Experimental Medicine; Pharmacology & Pharmacy; Physiology GA BT55S UT WOS:A1991BT55S00059 ER PT J AU COHEN, LG BANDINELLI, S TOPKA, HR FUHR, P ROTH, BJ HALLETT, M AF COHEN, LG BANDINELLI, S TOPKA, HR FUHR, P ROTH, BJ HALLETT, M TI TOPOGRAPHIC MAPS OF HUMAN MOTOR CORTEX IN NORMAL AND PATHOLOGICAL CONDITIONS - MIRROR MOVEMENTS, AMPUTATIONS AND SPINAL-CORD INJURIES SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article; Proceedings Paper CT SYMP ON TRANSCRANIAL MAGNETIC STIMULATION AND THE MOTOR EVOKED POTENTIAL CY AUG, 1989 CL CHICAGO, IL SP E PARALYZED VET ASSOC, NATL PARALYSIS ASSOC, CHICAGO NEUROSURG CTR, FDN INVESTIGAT NEUROL DISORDERS, AMER PARALYSIS ASSOC DE MAPPING; SPINAL CORD INJURY; AMPUTATIONS; DEAFFERENTATION; PLASTICITY; MIRROR MOVEMENTS; MOTOR CORTEX ID MAGNETIC STIMULATION; PERIPHERAL-NERVE; REPRESENTATION PATTERNS; ELECTRICAL-STIMULATION; FORELIMB MUSCLES; HUMAN-BRAIN; ORGANIZATION; FACILITATION; PRIMATE; MONKEY AB We studied motor evoked potentials to transcranial magnetic stimulation in patients with unilateral upper limb amputations, complete T10-T12 spinal cord transaction, and congenital mirror movements and in controls. Different muscles in the trunk and upper and lower extremities were evaluated at rest. In controls, muscles could be activated with stimulation of regions several centimeters wide. These areas overlapped extensively when muscles studied were from the same limb and shifted positions abruptly when muscles were from different limbs. Distal muscles were easier to activate than proximal muscles and normally evidenced exclusively a contralateral representation. Congenital defects in motor control in patients with mirror movements resulted in marked dearangement of the map of outputs of distal hand muscles with enlarged and ipsilateral representations. Peripheral lesions, either acquired (amputations) or congenital (congenital absence of a limb), resulted in plastic reorganization of motor outputs targeting muscles immediately proximal to the stump. Central nervous system lesions (i.e., spinal cord injury producing paraplegia) also resulted in enlargement of the map of outputs targeting muscles proximal to the lesion. These results indicate that magnetic stimulation is a useful non-invasive tool for exploring plastic changes in human motor pathways following different types of injury. C1 NINCDS, MED NEUROL BRANCH, HUMAN MOTOR CONTROL SECT, HUMAN CORT PHYSIOL UNIT, BETHESDA, MD 20892 USA. RI Roth, Bradley/A-4920-2008 NR 64 TC 61 Z9 61 U1 0 U2 8 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PY 1991 SU 43 BP 36 EP 50 PG 15 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA HB515 UT WOS:A1991HB51500004 ER PT J AU HALLETT, M COHEN, LG BIERNER, SM AF HALLETT, M COHEN, LG BIERNER, SM TI STUDIES OF SENSORY AND MOTOR CORTEX PHYSIOLOGY - WITH OBSERVATIONS ON AKINESIA IN PARKINSONS-DISEASE SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article; Proceedings Paper CT SYMP ON TRANSCRANIAL MAGNETIC STIMULATION AND THE MOTOR EVOKED POTENTIAL CY AUG, 1989 CL CHICAGO, IL SP E PARALYZED VET ASSOC, NATL PARALYSIS ASSOC, CHICAGO NEUROSURG CTR, FDN INVESTIGAT NEUROL DISORDERS, AMER PARALYSIS ASSOC DE SENSORY CORTEX; MOTOR CORTEX; PHYSIOLOGY; MAGNETIC STIMULATION; MOTOR EVOKED POTENTIAL; ELECTROMYOGRAPHY (EMG) ID VOLUNTARY MOVEMENT; REACTION-TIME; STIMULATION; EXECUTION; POTENTIALS AB Magnetic stimulation of the brain can be used to investigate sensory and motor physiology and pathophysiology in intact humans. Although uncommon, it is possible for magnetic stimulation over sensorimotor cortex to produce paresthesis. With magnetic stimulation, it is also possible to block the conscious sensation of an electrical shock delivered to the index finger. The magnetic stimulus must be delivered in the interval from 300 mscc before to 200 mscc after the cutaneous shock and must be delivered over the contralateral hand region of the sensorimotor cortex. In a reaction time situation, the expected voluntary response may be delayed by a magnetic stimulus delivered over the sensorimotor cortex just before the movement. With the use of a relatively weak magnetic stimulus that does not produce a motor evoked potential (MEP) when the body part is at rest, but that will produce a response when the body part is activated, the reaction time can be divided into two periods. In the first period, there is no MEP and the motor cortex remains 'inexcitable'. In the second period, there is a gradual increase in MEP amplitude even though the voluntary electromyographic activity has not yet appeared. This 'excitable' period indicates the activation of motor cortex before the motor command is delivered. Application of this technique to the analysis of prolonged reaction time (akinesia) in patients with Parkinson's disease shows that the excitable period is prolonged. This describes the mechanism underlying the difficulty in the generation of a motor command in these patients. C1 NINCDS, MED NEUROL BRANCH, HUMAN MOTOR CONTROL SECT, BETHESDA, MD 20892 USA. OI Bierner, Samuel/0000-0001-9378-7209 NR 23 TC 1 Z9 1 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PY 1991 SU 43 BP 76 EP 85 PG 10 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA HB515 UT WOS:A1991HB51500006 ER PT J AU ROTH, BJ COHEN, LG HALLETT, M AF ROTH, BJ COHEN, LG HALLETT, M TI THE ELECTRIC-FIELD INDUCED DURING MAGNETIC STIMULATION SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article; Proceedings Paper CT SYMP ON TRANSCRANIAL MAGNETIC STIMULATION AND THE MOTOR EVOKED POTENTIAL CY AUG, 1989 CL CHICAGO, IL SP E PARALYZED VET ASSOC, NATL PARALYSIS ASSOC, CHICAGO NEUROSURG CTR, FDN INVESTIGAT NEUROL DISORDERS, AMER PARALYSIS ASSOC DE MAGNETIC STIMULATION; CHARGE; ELECTRIC FIELD; VECTOR POTENTIAL ID POWER DEPOSITION PATTERNS; INDUCED HYPERTHERMIA; NERVE-STIMULATION; PERIPHERAL-NERVE; SURFACE-CHARGES; COIL IMPEDANCE; MOTOR CORTEX; DISTRIBUTIONS; CURRENTS; SAMPLES AB The electric field induced in tissue during magnetic stimulation is calculated. There are two sources of the electric field: charge and a time-dependent magnetic field: both sources are important in magnetic stimulation. Charge accumulation on the tissue surface tends to shield the nerve from the stimulus. The induced electric field is generally parallel to the tissue surface. Simulations of both peripheral and central nervous system stimulation are presented. C1 NINCDS,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,HUMAN CORT PHYSIOL UNIT,MOTOR CONTROL SECT,BETHESDA,MD 20892. RI Roth, Bradley/A-4920-2008 NR 65 TC 66 Z9 66 U1 0 U2 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PY 1991 SU 43 BP 268 EP 278 PG 11 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA HB515 UT WOS:A1991HB51500023 ER PT J AU ALDROUBI, A UNSER, M TIETZ, D TRUS, B AF ALDROUBI, A UNSER, M TIETZ, D TRUS, B TI COMPUTERIZED METHODS FOR ANALYZING 2-DIMENSIONAL AGAROSE-GEL ELECTROPHEROGRAMS SO ELECTROPHORESIS LA English DT Article ID ELECTROPHORESIS AB Previous methods interpret zonal or polydisperse gel patterns of two-dimensional Serwer-type gels in terms of size and free mobility (surface net charge density). These two parameters have been determined for each component without quantitatively measuring the abundance of the components. The present study advances these previous methods by determining the relative concentration of each component by computer evaluation of densitometrically analyzed gel patterns. Suitable procedures and their underlying algorithms are presented. The mathematical routines are implemented in a user-friendly software package, called GelFit and designed for a Macintosh personal computer. The program input sonsists of digitized images of gel staining patterns exemplified by those obtained from electrophoresis of native subcellular-sized particles. The data are processed through the following steps: (i) Noise reduction and calibration. (ii) Geometrical transformation of the pattern onto a rectangular size/free mobility coordinate system using rationales of the extended Ogston model. (iii) Analysis of the transformed image to determine density maxima, density profiles along iso-free-mobility or iso-size lines, curve fitting of one-dimensional profiles or two-dimensional surfaces using Gaussian functions and curve stripping of surfaces to determine the possible number of particle populations. C1 NIH,DCRT,COMP SYST LAB,BETHESDA,MD 20892. NICHHD,THEORET & PHYS BIOL,BETHESDA,MD. NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD. RI Unser, Michael/A-1550-2008; Aldroubi, Akram/J-7186-2012 NR 9 TC 10 Z9 10 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD JAN PY 1991 VL 12 IS 1 BP 39 EP 46 DI 10.1002/elps.1150120108 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FC889 UT WOS:A1991FC88900006 PM 2050098 ER PT J AU TIETZ, D ALDROUBI, A SCHNEERSON, R UNSER, M CHRAMBACH, A AF TIETZ, D ALDROUBI, A SCHNEERSON, R UNSER, M CHRAMBACH, A TI THE DISTRIBUTION OF PARTICLES CHARACTERIZED BY SIZE AND FREE MOBILITY WITHIN POLYDISPERSE POPULATIONS OF PROTEIN-POLYSACCHARIDE CONJUGATES, DETERMINED FROM 2-DIMENSIONAL AGAROSE ELECTROPHEROGRAMS SO ELECTROPHORESIS LA English DT Article ID INFLUENZAE TYPE-B; GEL-ELECTROPHORESIS; HEMOPHILUS-INFLUENZAE; COMPUTER-SIMULATION; CHARGE AB New approaches for the characterization of polydisperse particle populations are presented*. The investigated samples contain virus-sized protein-polysaccharide conjugates which had previously been prepared as immunogens against bacterial meningitis (Hib). The analysis is based on two-dimensional agarose electrophoresis (Serwer-type). This method, like the one of O'Farrell, achieves a separation according to size and charge. It relies on a different principle, however, and is applicable to nondenatured particles which are 100 to more than 1000 times larger in mass than regular uncrosslinked proteins. Data from stained gel patterns are evaluated by the computer program ELPHOFIT, which makes it possible to standardize the gel and to construct a nomogram which defines every position on the gel in terms of particle size and free mobility (related to surface net charge density). The output of ELPHOFIT, consisting of nomogram parameters, is transferred to the image processing program GELFIT. This software is used to evaluate the computer images obtained by digitizing the stained gel patterns: (i) The nomogram is electronically superimposed on the computer image. (ii) The gel pattern is transformed from a curvilinear to a rectangular coordinate system of particle size and free mobility. The center of gravity as well as density maxima are given in coordinates of particle size and free mobility. Ranges of grey levels can be accentuated by adding 16 pseudocolors. (iii) Using surface-stripping techniques, GELFIT provides an estimate for the number of major subpopulations within each preparation. (iv) Numerical values for the distribution of particle size and free mobility are determined. Using program IMAGE, the quantitative physical assessment of a given conjugate preparation is presented in the form of a computer-generated three-dimensional plot, the shape of which serves to identify and characterize the preparation visually. The data analysis based on digitized two-dimensional gel patterns is automated to an extent that a technician can perform routine evaluations. It uses the Macintosh II personal computer. C1 NICHHD,DEV & MOLEC IMMUNOL LAB,BETHESDA,MD 20892. NICHHD,THEORET & PHYS BIOL,BETHESDA,MD 20892. NICHHD,DIV RES SERV,BIOMED ENGN & INSTRUMENT BRANCH,BETHESDA,MD 20892. RI Unser, Michael/A-1550-2008; Aldroubi, Akram/J-7186-2012 NR 22 TC 11 Z9 11 U1 1 U2 2 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD JAN PY 1991 VL 12 IS 1 BP 46 EP 54 DI 10.1002/elps.1150120109 PG 9 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FC889 UT WOS:A1991FC88900007 PM 2050099 ER PT J AU NISSIM, A JOUVIN, MH ESHHAR, Z AF NISSIM, A JOUVIN, MH ESHHAR, Z TI MAPPING OF THE HIGH-AFFINITY FC-EPSILON RECEPTOR-BINDING SITE TO THE 3RD CONSTANT REGION DOMAIN OF IGE SO EMBO JOURNAL LA English DT Article DE CHIMERIC ANTIBODIES; EXON SHUFFLING; FC-EPSILON-RI BINDING; IGE-FC-EPSILON-RI INTERACTION ID EPSILON-CHAIN FRAGMENT; BOUND IMMUNOGLOBULIN-E; RAT MAST-CELLS; ESCHERICHIA-COLI; MONOCLONAL-ANTIBODIES; NUCLEOTIDE-SEQUENCE; MEMBRANE-SURFACE; GENE-EXPRESSION; FC-RECEPTOR; INHIBITION AB Indentification of the precise region(s) on the IgE molecule that take part in the binding of IgE to its high affinity receptor (Fc-epsilon-RI) may lead to the design of IgE analogues able to block the allergic response. To localize the Fc-epsilon-RI-binding domain of mouse IgE, we attempted to confer on human IgE, which normally does not bind to the rodent receptor, the ability to bind to the rat Fc-epsilon-RI. Employing exon shuffling, we have expressed chimeric epsilon-heavy chain genes composed of a mouse (4-hydroxy-3-nitrophenyl)acetic acid (NP)-binding V(H) domain, and human C-epsilon in which various domains were replaced by their murine counterparts. This has enabled us to test the Fc-epsilon-binding of each mouse IgE domain while maintaining the overall conformation of the molecule. All of the chimeric IgE molecules which contain the murine C-epsilon-3, bound equally to both the rodent and human receptor, as well as to monoclonal antibodies recognizing a site on IgE which is identical or very close to the Fc-epsilon-RI binding site. Deletion of the second constant region domain did not impair either the binding capacity of the mutated IgE or its ability to mediate mast cell degradation. These results assign the third epsilon domain of IgE as the principal region involved in the interaction with the Fc-epsilon-RI. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. RP NISSIM, A (reprint author), WEIZMANN INST SCI,DEPT CHEM IMMUNOL,IL-76100 REHOVOT,ISRAEL. NR 38 TC 49 Z9 52 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD JAN PY 1991 VL 10 IS 1 BP 101 EP 107 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA EU787 UT WOS:A1991EU78700012 PM 1824934 ER PT J AU THOTAKURA, NR DESAI, RK BATES, LG COLE, ES PRATT, BM WEINTRAUB, BD AF THOTAKURA, NR DESAI, RK BATES, LG COLE, ES PRATT, BM WEINTRAUB, BD TI BIOLOGICAL-ACTIVITY AND METABOLIC-CLEARANCE OF A RECOMBINANT HUMAN THYROTROPIN PRODUCED IN CHINESE-HAMSTER OVARY CELLS SO ENDOCRINOLOGY LA English DT Article ID THYROID-STIMULATING HORMONE; GLYCOPROTEIN HORMONES; ALPHA-SUBUNIT; RECEPTOR-BINDING; PITUITARY; GONADOTROPIN; SERUM; OLIGOSACCHARIDES; GLYCOSYLATION; ANTIBODIES AB The presence and specific structures of the oligosaccharides on TSH have been shown to be important for its production and bioactivity. Since the carbohydrate structure of a protein reflects the glycosylation apparatus of the host cells in which the protein is expressed, we examined the biological activity and metabolic clearance of a preparation of purified recombinant human (rh) TSH derived from a stable transfectant of Chinese hamster ovary cells. Carbohydrate compositional analysis of this rTSH showed it to be more highly sialylated than a nonrecombinant, cadaver-derived pituitary hTSH. In addition, no N-acetyl galactosamine was detectable in rhTSH, which implies the absence of terminal sulfate moieties, both of which are present in pituitary-derived TSH. The immunologic activity and porcine TSH receptor-binding activity of the preparation of rhTSH were 3-to 4-fold lower than those of a standard pituitary hTSH. The rhTSH showed a maximum stimulatory activity similar to that of pituitary hTSH in two different in vitro bioassays. However, rhTSH elicited about 3-fold and 5-fold less cAMP than pituitary TSH after stimulation of adenylyl cyclase in bovine thyroid membranes and the rat FRTL-5 cell line, respectively. Removal of sialic acid did not alter the immunologic activity of rhTSH. However, the potencies of rhTSH in receptor-binding, adenylyl cyclase, and FRTL-5 assays were increased 2.4-, 2.6-, and 26.7-fold, respectively after sialic acid removal. These data suggest that the in vitro biological activity of rhTSH is influenced by its highly sialylated oligosaccharide chains. The rhTSH had a 2-fold lower metabolic clearance rate serum concentration of rhTSH at 3 h as compared to pituitary hTSH. After sialic acid removal, the rhTSH was cleared faster (7.5-fold) than pituitary hTSH, showing that its longer plasma half-life was due to its higher sialylation. Biologically active rhTSH should be of clinical value in the diagnosis and treatment of patients with thyroid cancer and as a pure hTSH reference preparation. C1 GENZYME CORP,DEPT RECOMBINANT PROT DEV,FRAMINGHAM,MA 01701. RP THOTAKURA, NR (reprint author), NIDDKD,MOLEC CELLULAR & NUTR ENDOCRINOL BRANCH,BLDG 10,RM 8D14,BETHESDA,MD 20892, USA. NR 38 TC 106 Z9 106 U1 0 U2 3 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 1991 VL 128 IS 1 BP 341 EP 348 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ492 UT WOS:A1991EQ49200044 PM 1846103 ER PT J AU STRAUS, DS OOI, GT ORLOWSKI, CC RECHLER, MM AF STRAUS, DS OOI, GT ORLOWSKI, CC RECHLER, MM TI EXPRESSION OF THE GENES FOR INSULIN-LIKE GROWTH FACTOR-I (IGF-I), IGF-II, AND IGF-BINDING PROTEINS-1 AND PROTEINS-2 IN FETAL-RAT UNDER CONDITIONS OF INTRAUTERINE GROWTH-RETARDATION CAUSED BY MATERNAL FASTING SO ENDOCRINOLOGY LA English DT Article ID MULTIPLICATION-STIMULATING ACTIVITY; E-DOMAIN PEPTIDE; MESSENGER-RNA; DEVELOPMENTAL EXPRESSION; SERUM CONCENTRATIONS; NUCLEOTIDE-SEQUENCE; RIBONUCLEIC-ACID; CHOROID-PLEXUS; SOMATOMEDIN-C; TISSUE AB Evidence suggests that insulin-like growth factors-I and -II (IGF-I and II) play a role in regulating fetal growth and development. In the fetus, IGF-I and -II are complexed with two specific binding proteins (IGFBP-1 and -2), which are thought to modulate the actions of the IGFs in target tissues. We examined regulation of the genes for IGF-I, IGF-II, IGFBP-1, and IGFBP-2 in fetal rat liver in an experimental model for intrauterine growth retardation caused by maternal fasting on days 17-21 of gestation. The mean weight of fetuses from the fasted dams was 27-32% lower than the mean weight of fetuses from the fed dams. The concentration of immunoreactive IGF-I was decreased by 71% in serum of fetuses from the fasting dams. The concentration of immunoreactive IGF-II was slightly decreased (by 12%) in serum of fetuses from the fasting dams, whereas the concentration of immunoreactive pro-IGF-II Edomain peptide was decreased by 31%. The abundance of hepatic IGF-I mRNA was decreased by 55% in fetuses from the fasting dams. In contrast, the abundance of IGF-II mRNA in fetal liver was not significantly decreased by maternal fasting. Maternal fasting caused a 2-fold increase in the abundance of IGFBP-1 mRNA in fetal liver, whereas it did not change the abundance of IGFBP-2 mRNA. The induction of IGFBP-1 mRNA in liver of the growth-retarded fetuses is similar to the induction that occurs in liver of fasting adults, while the lack of regulation of IGFBP-2 mRNA differs from the strong induction of IGFBP-2 mRNA that occurs in liver of fasting adults. In summary, these results indicate that maternal fasting causes a decrease in fetal IGF-I gene expression, a decrease in fetal serum IGF-I, and a slight decrease in fetal serum IGF-II and pro-IGF-II E-domain peptide concentrations. Maternal fasting also causes an increase in fetal IGFBP-1 gene expression. Changes in fetal insulin and glucose may be related to changes in expression of the IGF-I and IGFBP-1 genes in the growth-retarded fetuses. The decreased expression of IGF-I and -II and increased expression of the IGFBP-1 gene may contribute to the fetal growth retardation observed in this model system. C1 UNIV CALIF RIVERSIDE,DEPT BIOL,RIVERSIDE,CA 92521. NIDDKD,MOLEC CELLULAR & NUTR ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP STRAUS, DS (reprint author), UNIV CALIF RIVERSIDE,DIV BIOMED SCI,RIVERSIDE,CA 92521, USA. FU NIDDK NIH HHS [R01-DK39739] NR 56 TC 141 Z9 141 U1 0 U2 1 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 1991 VL 128 IS 1 BP 518 EP 525 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ492 UT WOS:A1991EQ49200070 PM 1846108 ER PT J AU BISWAS, R VONDERHAAR, BK AF BISWAS, R VONDERHAAR, BK TI TAMOXIFEN INHIBITION OF PROLACTIN ACTION IN THE MOUSE MAMMARY-GLAND SO ENDOCRINOLOGY LA English DT Article ID HUMAN-BREAST-CANCER; ANTIESTROGEN-BINDING-SITES; EPIDERMAL GROWTH-FACTOR; ESTROGEN-RECEPTOR; HIGH-AFFINITY; PROTEIN-SYNTHESIS; ANTI-ESTROGEN; CELL-LINE; PROLIFERATION; DISTINCT AB Binding of lactogenic hormones to particulate and solubilized microsomal membranes isolated from mammary glands of lactating mice is inhibited by direct addition of 10(-10) M or greater concentrations of triphenylethylene antiestrogens [i.e. tamoxifen (TAM), 4-hydroxy-tamoxifen, and Nafoxidine] to the binding assays. Estradiol and other antiestrogens such as BPEA (-2-(4-tert-butyl-phenoxy) ethyl diethylamine hydrochloride, LY117018, and LY 156758 do not have this effect. The triphenylethylene antiestrogens bind to the membrane-associated antiestrogen binding sites (AEBS). Effectiveness of binding to the AEBS parallels the effectiveness of inhibition of the lactogen binding. The effect is selective in that binding of epidermal growth factor and insulin to these same membranes is unaffected by the antiestrogens. Binding of PRL to membranes prepared from the livers of the lactating mice is also unaffected. Both the PRL receptor and AEBS are primarily localized to the microsomal membrane fraction of cells. Maximal inhibition of PRL binding by TAM is observed in the light microsomes that contain plasma membranes. In addition to inhibition of PRL binding, TAM also prevents the PRL-induced accumulation of caseins by cultured mouse mammary explants. Thus it appears that the triphenylethylene antiestrogens, acting through the AEBS, act as antilactogens in the normal mammary gland. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BLDG 10,ROOM 5B56,BETHESDA,MD 20892. NR 31 TC 23 Z9 23 U1 0 U2 1 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 1991 VL 128 IS 1 BP 532 EP 538 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ492 UT WOS:A1991EQ49200072 PM 1846110 ER PT J AU BENVENGA, S CAHNMANN, HJ ROBBINS, J AF BENVENGA, S CAHNMANN, HJ ROBBINS, J TI THE THYROXINE-BINDING SITE OF HUMAN APOLIPOPROTEIN-A-I - LOCATION IN THE N-TERMINAL DOMAIN SO ENDOCRINOLOGY LA English DT Article ID HIGH-DENSITY LIPOPROTEINS; AMINO-ACID SEQUENCE; STRUCTURAL DOMAINS; IDENTIFICATION; PROTEIN AB We tested the ability of nine monoclonal antibodies (MAb) against human apolipoprotein-A-I (apoA-I), the 28.3-kDa major apoprotein of high density lipoproteins (HDL), to inhibit its photoaffinity labeling with [I-125]T4. Two forms were evaluated: isolated lipid-free apoA-I(Sigma or Calbiochem) and lipid-complexed apoA-I [HDL2, (density, 1.063-1.125 g/ml) and HDL3 (density, 1.125-1.210 g/ml)]. After labeling with 0.5 nM [I-125]T4 in the presence of MAb or normal mouse IgG, the products were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and subsequent densitrometric quantitation of radioactivity associated with the 28.3-kDa band. Group IMAbs, namely those having epitopes in the N-terminal portion of apoA-I, include MAb 16 (epitopes at residues 1-16), 4 and 14 (residues 1-86), and 18 (residues 98-105); group II includes MAbs 7, 10, 15, and 17 (epitopes at residues 87-148); group III includes MAb 9 (residues 149-243). All group I MAbs inhibited [I-125]T4 binding to isolated apoA-I with this order of potency: MAb 16 (-50% to -61%) > MAb 14 (-37% to -41%) > MAb 4 (-27% to -33%) > MAb 18 (-19% to -27%). In the case of lipid-associated apoA-I, the pattern of hierarchy was variable, presumably related to the known markedly polydisperse nature of HDL, but a constant feature, in contrast to the case of isolated apoA-I, was that MAb 4 was more potent than MAb 14. Group II MAbs gave less than 3% inhibition in both isolated and lipid-complexed apoA-I. Group III MAb 9 either failed to inhibit or gave 18-27% inhibition (one preparation each of HDL2 and HDL3). We conclude that the T4 site of apoA-I is in the N-terminal domain of apoA-I, closer to the epitope for MAb 16 than to that for MAb 18, and that conformational changes occurring when apoA-I is associated with lipids in the HDL particle alter the spatial relationship between some epitopes and the T4 site. Our definition of the T4 site of apoA-I is consistent with another set of data showing that heparin failed to inhibit [I-125]T4 binding to isolated apoA-I. Heparin is known to interact with clusters of basic residues, and these residues are concentrated in the midregion of apoA-I. C1 NIDDKD,CLIN ENDOCRINOL BRANCH,BLDG 10,ROOM 8N315,BETHESDA,MD 20892. NR 23 TC 14 Z9 14 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 1991 VL 128 IS 1 BP 547 EP 552 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ492 UT WOS:A1991EQ49200074 PM 1702705 ER PT J AU DEMURA, T DRISCOLL, WJ LEE, YC STROTT, CA AF DEMURA, T DRISCOLL, WJ LEE, YC STROTT, CA TI ADRENOCORTICAL NUCLEAR PROGESTERONE-BINDING PROTEIN - IDENTIFICATION BY PHOTOAFFINITY-LABELING AND EVIDENCE FOR DEOXYRIBONUCLEIC-ACID BINDING AND STIMULATION BY ADRENOCORTICOTROPIN SO ENDOCRINOLOGY LA English DT Article ID PIG ADRENAL-CORTEX; STEROID-RECEPTORS; CHICK OVIDUCT; MESSENGER-RNA; CELLS; TRANSCRIPTION; SUBUNIT AB Nuclei of the guinea pig adrenal cortex contain a protein that specifically binds progesterone and that, biochemically, is clearly distinct from the classical progesterone receptor. The adrenocortical nuclear progesterone-binding protein has now been purified more than 2000-fold by steroid-affinity chromatography with a 75% yield. The purified protein preparation demonstrated three major bands on sodium dodecyl sulfate-polyacrylamide gel of 79K, 74K, and 50K. To determine which of the three might represent the progesterone-binding protein, steroid photoaffinity labeling was performed which resulted in the specific and exclusive labeling of a 50K band. Thus, the adrenocortical nuclear progesterone-binding protein appears to be distinct from the classical progesterone receptor not only biochemically, but also on the basis of molecular size. To test whether the adrenocortical nuclear progesterone-binding protein can be hormonally stimulated, guinea pigs were treated with ACTH. The chronic administration of ACTH caused a 4- to 6-fold increase in the specific progesterone binding capacity without a change in the binding affinity. There appeared to be no significant difference in nuclear progesterone binding between the zona fasciculata and zona reticularis. This finding suggests a mediating role for the progesterone-binding protein in ACTH action. In addition, the nuclear progesterone-binding protein bound to nonspecific DNA sequences, further suggesting a possible transcriptional regulatory role. C1 NIDDKD,ENDOCRINOL & REPROD RES BRANCH,ADRENAL CELL BIOL SECT,BLDG 10,ROOM B1-L400,BETHESDA,MD 20892. NR 21 TC 3 Z9 3 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 1991 VL 128 IS 1 BP 553 EP 558 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ492 UT WOS:A1991EQ49200075 PM 1846111 ER PT J AU CENA, V HALPERIN, JI YEANDLE, S KLEIN, DC AF CENA, V HALPERIN, JI YEANDLE, S KLEIN, DC TI NOREPINEPHRINE STIMULATES POTASSIUM EFFLUX FROM PINEALOCYTES - EVIDENCE FOR INVOLVEMENT OF BIOCHEMICAL AND GATE OPERATED BY CALCIUM AND ADENOSINE-3',5'-MONOPHOSPHATE SO ENDOCRINOLOGY LA English DT Article ID PROTEIN KINASE-C; SEROTONIN N-ACETYLTRANSFERASE; BETA-ADRENERGIC STIMULATION; PHOTONEURAL REGULATION; RAT PINEALOCYTES; SKELETAL-MUSCLE; CELL-MEMBRANE; K+ CHANNELS; PHOSPHORYLATION; RECTIFICATION AB Biochemical studies of K+ efflux from rat pinealocytes revealed for the first time that norepinephrine (NE) increases Rb-86(+) and K-42(+) efflux. The effects of NE depend upon concurrent activation of both alpha1- and beta-adrenoceptors. This effect is mediated by cAMP and Ca2+, which appear to act in conjunction to control K+ efflux; studies with charybdotoxin and tetraethylammonium indicate that a Ca2+ -sensitive K+ channel (K(ca)) appears to be involved. Patch clamp studies identified a large conductance (approximately 100 psec) K+ channel. This study also revealed for the first time that NE treatment increases the fraction of time that this channel was open. Studies of inside-out pineal membrane patches indicated that increasing Ca2+ at the cytoplasmic surface of the membrane increased the frequency of channel opening, as is typical of K(Ca) channels in this type of preparation. Outward K+ currents were almost completely blocked by tetraethylammonium (10 mM) and scorpion venom (L. quinquestriatum; 100 ng/ml). Cell-attached studies confirm that the effects of NE are mediated by intracellular second messengers. These investigations suggest that NE elevates K+ flux, probably through a large conductance K(Ca) channel, that NE acts through alpha1- and beta-adrenergic receptors, and that Ca2+ and cAMP act together through a biochemical "AND" gate to mediate the effects of receptor activation. Activation of this K(Ca) channel would have a hyperpolarizing influence and might contribute to the adrenergic hyperpolarization of pinealocytes. C1 NICHHD,NEUROENDOCRINOL SECT,DEV NEUROBIOL LAB,BLDG 36-4A07,BETHESDA,MD 20892. USN,BETHESDA NAVAL MED CTR,DEPT IMMUNOBIOL & TRANSPLANTAT,BETHESDA,MD 20814. NR 40 TC 20 Z9 20 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 1991 VL 128 IS 1 BP 559 EP 569 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ492 UT WOS:A1991EQ49200076 PM 1846112 ER PT J AU TSUTSUMI, K SAAVEDRA, JM AF TSUTSUMI, K SAAVEDRA, JM TI DIFFERENTIAL DEVELOPMENT OF ANGIOTENSIN-II RECEPTOR SUBTYPES IN THE RAT-BRAIN SO ENDOCRINOLOGY LA English DT Note ID AUTORADIOGRAPHY; BINDING AB Angiotensin II receptors in selected brain areas were characterized into two distinct subtypes by displacement with specific antagonists. The receptor subtypes had different developmental patterns. Type-1 receptors, selectively displaced by the specific angiotensin antagonist DuP-753, were predominant in adult (8-weeks-old) rats. Type-2 receptors were selectively displaced by CGP 42112 A and were expressed remarkably in young (2-weeks-old) rats. RP TSUTSUMI, K (reprint author), NIMH,PHARMACOL SECT,CLIN SCI LAB,9000 ROCKVILLE PIKE,BLDG 10,BETHESDA,MD 20892, USA. NR 12 TC 80 Z9 80 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 1991 VL 128 IS 1 BP 630 EP 632 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ492 UT WOS:A1991EQ49200084 PM 1986946 ER PT J AU MYHR, BC CASPARY, WJ AF MYHR, BC CASPARY, WJ TI CHEMICAL MUTAGENESIS AT THE THYMIDINE KINASE LOCUS IN L5178Y MOUSE LYMPHOMA-CELLS - RESULTS FOR 31 CODED COMPOUNDS IN THE NATIONAL TOXICOLOGY PROGRAM SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE TK-LOCUS; TRIFLUOROTHYMIDINE RESISTANCE; GENOTOXICITY ID MUTATION ASSAY; MUTAGENICITY; CARCINOGENICITY; MUTANTS; TK+/; S9 AB Experimental data from the testing of 31 chemicals for mutagenicity at the TK locus in L5178Y mouse lymphoma cells are presented and evaluated. If mutagenic activity was not obtained for the chemical added to suspension cultures for 4 hr, then the testing was repeated in the presence of hepatic S9 mix prepared from Aroclor 1254-induced male Fischer 344 rats. Multiple trials were performed for each chemical, and mutagenic treatments were analyzed for the induction of small and large mutant colony populations. Twelve chemicals were not detected as mutagenic one (ascorbic acid) was questionable, and 18 were evaluated as mutagenic. These results were used in the evaluations presented by Tennant et al. [Science 236:933-941, 1987] in a critical comparison of four in vitro genotoxicity assays with rodent carcinogenicity results. The mouse lymphoma assay results were in general agreement with the carcinogenicity studies. Discordant evaluations with respect to carcinogenicity (four false negatives and six false positives) were discussed from the standpoint of how the predictive performance of the in vitro mutation assay might be improved. C1 NIEHS,CELLULAR & GENET TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. RP MYHR, BC (reprint author), HAZLETON LABS AMERICA INC,DEPT GENET TOXICOL,5516 NICHOLSON LANE,KENSINGTON,MD 20895, USA. FU NIEHS NIH HHS [N01-ES-28036] NR 22 TC 56 Z9 56 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1991 VL 18 IS 1 BP 51 EP 83 DI 10.1002/em.2850180109 PG 33 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA GA206 UT WOS:A1991GA20600008 PM 1864269 ER PT J AU MCMAHON, TF CUNNINGHAM, ML AF MCMAHON, TF CUNNINGHAM, ML TI MUTAGENICITY OF METHYLAZOXYMETHANOL ACETATE IN THE PRESENCE OF ALCOHOL-DEHYDROGENASE, ALDEHYDE DEHYDROGENASE, AND RAT-LIVER MICROSOMES IN SALMONELLA-TYPHIMURIUM HIS-G46 SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE MAM; ADH; ALDH; CYCASIN; MAM ACETATE; PORCINE LIVER ESTERASE ID INHIBITION; METABOLISM; COLON; DNA; METHYLATION; CYCASIN; MUCOSA; TUMORS; INVIVO AB Methylazoxymethanol (MAM) is the short-lived toxic and carcinogenic aglycone of cycasin, a natural component of the cycad plant. In the present study, the stable acetate ester of MAM, MAM acetate, was tested in combination with porcine liver esterase and Salmonella typhimurium His G46 to study the comparative mutagenicity of this compound in the presence of rat hepatic alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and rat liver microsomes. In the presence of rat liver microsomes and an NADPH-generating system, mutagenicity of MAM acetate was not significantly altered. However, addition of rat liver 105,000g supernatant fraction and/or NAD+ significantly increased the number of his+ revertants above control. A concentration-dependent increase in mutagenicity of MAM acetate was observed for NAD+ from 50 to 200-mu-M, while NADP+ caused a decrease in mutagenicity of MAM acetate in this some concentration range. Pyrazole (100-500-mu-M) had no significant effect on mutagenicity of MAM acetate in the presence of rat liver 105,000g supernatant, while disulfiram at 500-mu-M resulted in a significant decrease in mutagenicity of MAM acetate. The results of this study implicate ALDH as essential in activation of MAM acetate to a mutagenic species in this system, while the role of ADH and microsomes appears to be minimal. C1 NIEHS,RES TRIANGLE PK,NC 27709. RP MCMAHON, TF (reprint author), US EPA,OFF PESTICIDE PROGRAMS,H7509C,401 M ST SW,WASHINGTON,DC 20460, USA. NR 16 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1991 VL 18 IS 3 BP 151 EP 156 DI 10.1002/em.2850180302 PG 6 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA GK817 UT WOS:A1991GK81700001 PM 1915309 ER PT J AU PHILLIPS, MD NASCIMBENI, B TICE, RR SHELBY, MD AF PHILLIPS, MD NASCIMBENI, B TICE, RR SHELBY, MD TI INDUCTION OF MICRONUCLEI IN MOUSE BONE-MARROW CELLS - AN EVALUATION OF NUCLEOSIDE ANALOGS USED IN THE TREATMENT OF AIDS SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE MICRONUCLEUS TEST; MOUSE BONE MARROW; NUCLEOSIDE ANALOGS; 6-THIOGUANINE; CYTARABINE HCI; 3'-AZIDO-3'-DEOXYTHYMIDINE; 2',3'-DIDEOXYCYTIDINE, 2',3'-DIDEHYDRO-3'-DEOXYTHYMIDINE; RIBAVIRIN, 2',3'-DIDEOXYADENOSINE; 2',3'-DIDEOXYCYTIDINE, 2',3'-DIDEOXYINOSINE; PENTAMIDINE ISETHIONATE ID PERIPHERAL-BLOOD ERYTHROCYTES; TOXICITY; 6-THIOGUANINE; GENOTOXICITY; PENTAMIDINE; INHIBITOR; NEOPLASIA; RIBAVIRIN; MUTAGENS; THERAPY AB Various nucleoside analogues are being used or are being considered for use as therapeutic drugs to inhibit replication of the HTLV-III/LAV virus in infected human cells. Here, the ability of seven nucleoside analogues, a combination of two analogues, and two other therapeutic compounds to induce genotoxic and cytotoxic damage in vivo was evaluated in the mouse bone marrow micronucleus test. Using o 3-consecutive-day oral treatment protocol, almost all of the test chemicals induced a significant increase in the frequency of micronucleated polychromatic erythrocytes (MN-PCE) in male B6C3F1 mice, ranked in decreasing potency as 6-thioguanine > Cytarabine HCl > 3'-azido-3'-deoxythymidine (AZT)/2',3'-dideoxycytidine combination = AZT > Ribavirin = 2',3'-didehydro-3'-deoxythymidine > 2',3'-dideoxyadenosine-2',3'-dideoxycytidine. The frequency of MN-PCE was not increased significantly by treatment with 2',3-dideoxyinosine (DDI) or pentamidine isethionate (PI). The differential ability of AZT and DDI to induce MN in mouse bone marrow was verified from peripheral blood smears prepared from subchronic (90 day) oral studies. The lack of genotoxic activity by DDI was route-specific since, when tested by intraperitoneal injection, a small but significant increase in MN-PCE was observed. A number of these chemicals induced a significant depression in erythropoiesis. However, there was not a significant correlation between the increase in MN-PCE and the depression in the percentage of PCE. This lack of a correlation suggests that factors other than DNA damage may contribute to the inhibition in the rate of erythropoiesis. The presence of increased levels of micronuclei in bone marrow PCE following treatment with various nucleoside analogues suggests that intrinsic genotoxic activity in mammalian cells should be one factor considered during drug selection for AIDS therapy. C1 INTEGRATED LAB SYST,POB 13501,RES TRIANGLE PK,NC 27709. NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [N01-ES-85209] NR 37 TC 52 Z9 53 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 1991 VL 18 IS 3 BP 168 EP 183 DI 10.1002/em.2850180305 PG 16 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA GK817 UT WOS:A1991GK81700004 PM 1915312 ER PT J AU TINDALL, KR WHITAKER, RA AF TINDALL, KR WHITAKER, RA TI RAPID LOCALIZATION OF POINT MUTATIONS IN PCR PRODUCTS BY CHEMICAL (HOT) MODIFICATION SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article; Proceedings Paper CT 22ND MEETING OF THE ENVIRONMENTAL MUTAGEN SOC CY APR 06-11, 1991 CL KISSIMMEE, FL SP ENVIRONM MUTAGEN SOC DE AS52 CELLS; GPT; PCR; CHEMICAL CLEAVAGE; HYDROXYLAMINE; OSMIUM TETROXIDE; MUTATION; HETERODUPLEX ID BASE-PAIR MISMATCHES; ESCHERICHIA-COLI; MAMMALIAN-CELLS; DNA; AMPLIFICATION; REACTIVITY; GENE; ELECTROPHORESIS; CYTOSINE; THYMINE AB Our studies of mutational mechanisms in mammalian cells use the AS52 Chinese hamster ovary cell line. AS52 mutants can be selected as 6-thioguanine resistant colonies and mutations are studied at a chromosomally integrated gpt locus. Mutant gpt sequences are amplified using the polymerase chain reaction (PCR) to distinguish deletions from putative point mutations. PCR is efficiently performed from a few thousand lysed cells or from isolated genomic DNA. Amplified mutant PCR fragments carrying putative point mutations are further characterized by localizing the site of the mutation using chemical modification. A heteroduplex molecule consisting of one wild-type and one mutant DNA strand is generated. A base mismatch will be produced at the site of the mutation. Mismatched cytosine or thymine residues are sensitive to modification by hydroxylamine or osmium tetroxide, respectively. The modified DNA heteroduplex is then sensitive to piperidine cleavage. If one strand is P-32-end labeled, then the cleavage product can be separated on a denaturing acrylamide sequencing gel and visualized using autoradiography. Thus, the site of a mutation can be localized to a specific region of the gene, thereby simplifying the DNA sequence analysis and facilitating the rapid generation of mutational sequence spectra. RP TINDALL, KR (reprint author), NIEHS,EXPTL CARCINOGENESIS & MUTAGENESIS BRANCH,E3-01,RES TRIANGLE PK,NC 27709, USA. NR 19 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 1991 VL 18 IS 4 BP 231 EP 238 DI 10.1002/em.2850180405 PG 8 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA GU244 UT WOS:A1991GU24400004 PM 1748084 ER PT J AU BELL, DA AF BELL, DA TI DETECTION OF DNA-SEQUENCE POLYMORPHISMS IN CARCINOGEN METABOLISM GENES BY POLYMERASE CHAIN-REACTION SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article; Proceedings Paper CT 22ND MEETING OF THE ENVIRONMENTAL MUTAGEN SOC CY APR 06-11, 1991 CL KISSIMMEE, FL SP ENVIRONM MUTAGEN SOC DE GLUTATHIONE TRANSFERASE MU; DEBRISOQUINE; CANCER SUSCEPTIBILITY ID DEBRISOQUINE; AMPLIFICATION; TRANSFERASE; MUTATIONS; CANCER; MU AB The glutathione transferase mu gene (GST1) and the debrisoquine hydroxylase gene (CYP2D6) are known to be polymorphic in the human population and have been associated with increased susceptibility to cancer. Smokers with low lymphocyte GST mu activity are ot higher risk for lung cancer, while low debrisoquine hydroxylase activity has been correlated with lower risk for lung and bladder cancer. Phenotypic characterization of these polymorphisms by lymphocyte enzyme activity (GST) and urine metabolite ratios (debrisoquine) is cumbersome for population studies. Recent cloning and sequencing of the mutant alleles of these genes has allowed genotyping via the polymerase chain reaction (PCR). Advantages of PCR approaches are speed, technical simplicity, and minimal sample requirements. This article reviews the PCR-based methods for detection of genetic polymorphisms in human cancer susceptibility genes. RP BELL, DA (reprint author), NIEHS,BIOCHEM RISK ANAL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 21 TC 5 Z9 6 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1991 VL 18 IS 4 BP 245 EP 248 DI 10.1002/em.2850180407 PG 4 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA GU244 UT WOS:A1991GU24400006 PM 1684153 ER PT J AU HEDDLE, JA CIMINO, MC HAYASHI, M ROMAGNA, F SHELBY, MD TUCKER, JD VANPARYS, P MACGREGOR, JT AF HEDDLE, JA CIMINO, MC HAYASHI, M ROMAGNA, F SHELBY, MD TUCKER, JD VANPARYS, P MACGREGOR, JT TI MICRONUCLEI AS AN INDEX OF CYTOGENETIC DAMAGE - PAST, PRESENT, AND FUTURE SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article; Proceedings Paper CT 22ND MEETING OF THE ENVIRONMENTAL MUTAGEN SOC CY APR 06-11, 1991 CL KISSIMMEE, FL SP ENVIRONM MUTAGEN SOC DE MICRONUCLEUS TEST; CHROMOSOME ABERRATIONS; BONE MARROW; ERYTHROCYTES; TOXICOLOGY ID ASSAY; ERYTHROCYTES; SLIDES; MICE AB The workshop was designed to present what is known about the production of micronuclei, what protocols are now accepted or proposed internationally, what new results have been obtained, and what new methods and protocols are likely to be forthcoming. This report is designed to convey the flavour of the workshop and to provide the essence of the new information. After the workshop an effort was made to determine what single protocol would satisfy the requirements set for the micronucleus test by as many regulatory agencies as possible. The result, reported here, includes the requirements of six regulatory authorities in Canada, the European Economic Community, the Organization for Economic Co-operation and Development, Japan, and the United States. C1 US EPA,OFF TOX SUBST,DIV HLTH & ENVIRONM REVIEW,WASHINGTON,DC 20460. NATL INST HYG SCI,DIV GENET & MUTAGENESIS,SETAGAYA KU,TOKYO 158,JAPAN. SANDOZ PHARMA LTD,DRUG SAFETY ASSESSMENT TOXICOL,BASEL,SWITZERLAND. NIEHS,RES TRIANGLE PK,NC 27709. UNIV CALIF LAWRENCE LIVERMORE NATL LAB,DIV BIOMED SCI,LIVERMORE,CA 94550. JANSSEN PHARMACEUT,GENET TOXICOL,B-2340 BEERSE,BELGIUM. SRI INT,MENLO PK,CA 94025. RP HEDDLE, JA (reprint author), YORK UNIV,DEPT BIOL,N YORK M3J 1P3,ONTARIO,CANADA. NR 25 TC 306 Z9 333 U1 1 U2 10 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 1991 VL 18 IS 4 BP 277 EP 291 DI 10.1002/em.2850180414 PG 15 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA GU244 UT WOS:A1991GU24400013 PM 1748091 ER PT J AU TENNANT, RW AF TENNANT, RW TI A PERSPECTIVE ON MEASUREMENT OF MUTATIONS INVIVO SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article; Proceedings Paper CT 22ND MEETING OF THE ENVIRONMENTAL MUTAGEN SOC CY APR 06-11, 1991 CL KISSIMMEE, FL SP ENVIRONM MUTAGEN SOC DE TRANSGENIC MOUSE LINES; TISSUE-SPECIFIC MUTAGENESIS; IDENTIFICATION OF MUTAGENS AB The development of transgenic mouse lines with target genes that are suitable for tissue-specific mutagenesis studies is an important contribution to the field of environmental mutagenesis. These models can accommodate many of the questions relating to metabolism, distribution and relative potency of mutagens as well as providing a more comprehensive system for the identification of mutagens. However, the lessons that the field has learned about methods, development and validation from the use of in vitro systems must be applied to the development and validation of transgenic models. RP TENNANT, RW (reprint author), NIEHS,EXPTL CARCINOGENESIS & MUTAGENESIS BRANCH,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1991 VL 18 IS 4 BP 322 EP 323 DI 10.1002/em.2850180422 PG 2 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA GU244 UT WOS:A1991GU24400021 PM 1748097 ER PT J AU LUNN, G SANSONE, EB ANDREWS, AW AF LUNN, G SANSONE, EB ANDREWS, AW TI AERIAL OXIDATION OF HYDRAZINES TO NITROSAMINES SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE SAFETY; MUTAGENICITY; N-AMINOPIPERIDINE; 1,1-DIMETHYLHYDRAZINE; N-NITROSODIMETHYLAMINE; N-NITROSOPIPERIDINE ID MUTAGENICITY AB When 1, 1-dimethylhydrazine and N-aminopiperidine were deliberately exposed to air substantial amounts of the corresponding carcinogenic nitrosamines were formed. Unoxidized samples of 1, 1-dimethylhydrazine were not mutagenic while oxidized samples (which contained much higher levels of nitrosamines) were mutagenic. Both unoxidized and oxidized samples of N-aminopiperidine were mutagenic. C1 NCI,FREDERICK CANC RES & DEV CTR,MICROBIOL MUTAGENESIS LAB,FREDERICK,MD 21702. RP LUNN, G (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,ENVIRONM CONTROL & RES PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 7 TC 8 Z9 9 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1991 VL 17 IS 1 BP 59 EP 62 DI 10.1002/em.2850170109 PG 4 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA EU288 UT WOS:A1991EU28800008 PM 1991461 ER PT J AU MCGREGOR, D BROWN, AG CATTANACH, P EDWARDS, I MCBRIDE, D RIACH, C SHEPHERD, W CASPARY, WJ AF MCGREGOR, D BROWN, AG CATTANACH, P EDWARDS, I MCBRIDE, D RIACH, C SHEPHERD, W CASPARY, WJ TI RESPONSES OF THE L5178Y MOUSE LYMPHOMA FORWARD MUTATION ASSAY .5. GASES AND VAPORS SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE PROPYLENE; 1,2-PROPYLENE OXIDE; 1,3-BUTADIENE; VINYLIDENE CHLORIDE ID TRIFLUOROTHYMIDINE-RESISTANT; VINYLIDENE-CHLORIDE; CODED CHEMICALS; MUTAGENICITY; CELLS AB A new protocol for testing vapors and gases in the L5178Y mouse lymphoma assay is presented. Four chemicals, propylene, 1,2-propylene oxide, 1,3-butadiene, and vinylidene chloride, were tested for their mutagenic potential. Cultures were exposed to the chemicals, which were delivered as vapors or gases, for 4 hr, then cultured for 2 days before plating in soft agar with or without trifluorothymidine (TFT), 3-mu-g/ml. Each chemical was tested at least twice. Significant responses were obtained with 1,2-propylene oxide and vinylidene chloride, but neither cytotoxicity nor mutagenicity was induced by 1,3-butadiene; propylene could not be classified as either mutagenic or non-mutagenic in the assay. Rat liver S9 mix was not a requirement for the mutagenic activity of 1,2-propylene oxide, whereas the liver preparation markedly enhanced both the cytotoxicity and mutagenicity of vinylidene chloride. C1 NIEHS,CANC GENET & MOLEC PATHOL SECT,POB 12233,RES TRIANGLE PK,NC 27709. INVERESK RES INT LTD,MUSSELBURGH,SCOTLAND. NR 20 TC 27 Z9 29 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1991 VL 17 IS 2 BP 122 EP 129 DI 10.1002/em.2850170209 PG 8 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA FC593 UT WOS:A1991FC59300008 PM 2009867 ER PT J AU MCGREGOR, DB BROWN, AG HOWGATE, S MCBRIDE, D RIACH, C CASPARY, WJ AF MCGREGOR, DB BROWN, AG HOWGATE, S MCBRIDE, D RIACH, C CASPARY, WJ TI RESPONSES OF THE L5178Y MOUSE LYMPHOMA CELL FORWARD MUTATION ASSAY .5. 27 CODED CHEMICALS SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE TRIFLUOROTHYMIDINE; NONMUTAGENIC COMPOUNDS; MUTAGENIC COMPOUNDS ID MUTAGENESIS ASSAY; SYSTEM; TESTS AB Twenty-seven chemicals were tested for their mutagenic potential in the L5178Y tk+/tk- mouse lymphoma cell forward mutation assay using procedures based upon those described by McGregor et al. (McGregor DB, Martin R, Cattanach P, Edwards I, McBride D, Caspary WJ (1987): Environ Mol Mutagen 9:143-160). Cultures were exposed to the chemicals for 4 hr, then cultured for 2 days before plating in soft agar with or without trifluorothymidine (TFT), 3-mu-g/ml. The chemicals were tested at least twice. Statistically significant responses were obtained with acid orange 10, aniline, benzaldehyde, o-chloroaniline, chlorodibromomethane, cytembena, 1,2-dibromo-4-(1,2-dibromomethyl) cyclohexane, dieldrin, lithocholic acid, oxytetracycline, phenazopyridine HCl, 1-phenyl-3-methyl-5-pyrazolone, sodium diethyldithiocarbamate, solvent yellow 14, tetraethylthiuram disulfide (disulfiram), 2,4-toluene diisocyanate, and 2,6-tolune diisocyanate. Apart from phenazopyridine HCl, acid orange 10, and solvent yellow 14, rat liver S9 mix was not a requirement for the mutagenic activity of these compounds. Chemicals not identified as mutagens were N-4-acetylaminofluorene, chlorpheniramine maleate, chlorpropamide, 1,4-dioxane, endrin, ethylene glycol, iron dextran, methapyrilene, sodium(2-ethylhexyl)alcohol sulfate, and 2,3,7,8-tetrachlorodibenzo-p-dioxin. C1 NIEHS,CANC GENET & MOLEC PATHOL SECT,RES TRIANGLE PK,NC 27709. INVERESK RES INT LTD,MUSSELBURGH,SCOTLAND. NR 20 TC 64 Z9 68 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 1991 VL 17 IS 3 BP 196 EP 219 DI 10.1002/em.2850170309 PG 24 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA FK100 UT WOS:A1991FK10000008 PM 1902415 ER PT J AU CAMERON, TP ROGERSBACK, AM LAWLOR, TE HARBELL, JW SEIFRIED, HE DUNKEL, VC AF CAMERON, TP ROGERSBACK, AM LAWLOR, TE HARBELL, JW SEIFRIED, HE DUNKEL, VC TI GENOTOXICITY OF MULTIFUNCTIONAL ACRYLATES IN THE SALMONELLA MAMMALIAN-MICROSOME ASSAY AND MOUSE LYMPHOMA TK+/-ASSAY SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE MUTAGENICITY TESTS; ACRYLIC ACID; S9; MFAS ID MUTAGENICITY TEST; LOCUS MUTATIONS; CELLS; CHEMICALS; CARCINOGENS AB Multifunctional acrylates are being used increasingly as replacements for solvents, and occupational and general population exposure to this structural class is expanding. Four multifunctional acrylates and acrylic acid were tested for mutagenicity in the Salmonella typhimurium and mouse lymphoma L5178Y TK +/- assays. In the Salmonella assay, two of the compounds (trimethylolpropane triacrylate) showed weakly positive results with a single tester strain (TA1535) in the presence of hamster liver S9; the other three compounds were negative. All five compounds were negative in the Salmonella assay without S9 activation. In the mouse lymphoma assay, two of the compounds (acrylic acid and ethylene glycol diacrylate) were positive in both the presence and the absence of S9, one compound was positive only in the presence of S9 (ethylene glycol dimethacrylate), and one compound was positive only in the absence of S9 (trimethylolpropane triacrylate). C1 NCI,BETHESDA,MD 20892. MICROBIOL ASSOCIATES INC,ROCKVILLE,MD. US FDA,WASHINGTON,DC 20204. NR 21 TC 9 Z9 9 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1991 VL 17 IS 4 BP 264 EP 271 DI 10.1002/em.2850170408 PG 8 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA FT157 UT WOS:A1991FT15700007 PM 2050134 ER PT J AU PRITCHARD, JB BEND, JR AF PRITCHARD, JB BEND, JR TI RELATIVE ROLES OF METABOLISM AND RENAL EXCRETORY MECHANISMS IN XENOBIOTIC ELIMINATION BY FISH SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID WINTER FLOUNDER; TELEOST AB Renal clearance techniques were used to examine the relative contributions of metabolism and renal tubular transport in determining the rates of excretion of benzo(a)pyrene (BaP) and several of its phase I metabolites by southern flounder, Paralichthys lethostigma. Each compound (H-3-labeled) was injected at a dose of 2.5-mu-mole/kg, producing plasma concentrations of 1 to 5-mu-M. Despite extensive plasma binding (> 95%), the uncorrected renal clearance of BaP-7,8-dihydrodiol exceeded the glomerular filtration rate (GFR) by more than 20-fold. Phenolic BaP metabolites also showed net secretion (1.5- to 3-fold). At times prior to 3 hr, BaP itself showed an average clearance of only 0.2 times the GFR. After 3 hr, BaP clearance increased to three times the GFR. Decreasing the dose of BaP injected also dramatically increased its clearance. Clearances of all four compounds studied were reduced by probenecid and other organic anion, including the herbicide 2,4-dichlorophenoxyacetic acid. HPLC analysis demonstrated that the bulk of the material excreted in the urine was not the parent compound, but sulfate or glucuronide conjugates of its phenolic or dihydrodiol metabolites. Excretion of sulfate conjugates predominated over the first 24 hr, whereas the glucuronide conjugates were the primary excretory products in succeeding days. In vitro, isolated renal tubules transported both glucuronide and sulfate conjugates, but sulfates were the preferred substrates. Isolated tubules were shown to be capable of catalyzing conjugation reactions, producing predominantly glucuronide conjugates. Liver slices produced both types of conjugates. Thus, the rapid excretion of BaP-7,8-dihydrodiol reflected a combination of two processes. First, this metabolite was rapidly converted to its sulfate conjugate, primarily via extrarenal tissues. Second, the sulfate conjugate was preferentially transported to the urine via secretion on the organic anion transport system. C1 UNIV FLORIDA,CV WHITNEY LAB,ST AUGUSTINE,FL 32086. UNIV WESTERN ONTARIO,FAC MED,DEPT PHARMACOL & TOXICOL,LONDON N6A 5C1,ONTARIO,CANADA. RP PRITCHARD, JB (reprint author), NIEHS,MD 19-01,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 13 TC 20 Z9 20 U1 0 U2 5 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 1991 VL 90 BP 85 EP 92 DI 10.2307/3430849 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA FD603 UT WOS:A1991FD60300012 PM 2050085 ER PT J AU HUFF, J BUCHER, J YANG, R AF HUFF, J BUCHER, J YANG, R TI CARCINOGENESIS STUDIES IN RODENTS FOR EVALUATING RISKS ASSOCIATED WITH CHEMICAL CARCINOGENS IN AQUATIC FOOD ANIMALS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID LONG-TERM CARCINOGENICITY; NATIONAL-TOXICOLOGY-PROGRAM; INDUCED BENIGN NEOPLASMS; SOLE PAROPHRYS-VETULUS; MOUSE-LIVER TUMORS; B6C3F1 MOUSE; ACTIVATED ONCOGENES; GREAT-LAKES; GROUNDWATER CONTAMINANTS; HEPATIC NEOPLASMS AB Fish and shellfish caught in polluted waters contain potentially dangerous amounts of toxic and carcinogenic chemicals. Public concern was heightened when a large percentage of winter flounder taken from Boston Harbor was found to have visible cancer of the liver; winter flounder outside the estuary area had no liver lesions. Long-term chemical carcinogenesis studies could be easily and feasibly designed using laboratory rodents offered diets containing fish caught in polluted waters. Induced cancers in rodents would corroborate field observations in fish; positive results from these studies would provide further evidence about potential human health hazards from eating substantial amounts of chemically contaminated fish. Nonetheless, fish and aquatic organisms should be viewed as environmental biological monitors of pollution or of potential human health hazards, and authorities responsible for assuring clean and safe rivers, bodies of water, and biota should give more attention to these valid biological indicators or sentinels of environmental pollution. Consequently, fish and other sea creatures alone should serve as alarms regarding whether water areas constitute public health hazards. RP HUFF, J (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 101 TC 7 Z9 7 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 1991 VL 90 BP 127 EP 132 DI 10.2307/3430856 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA FD603 UT WOS:A1991FD60300019 PM 2050050 ER PT J AU GOODRICH, MS DULAK, LH FRIEDMAN, MA LECH, JJ AF GOODRICH, MS DULAK, LH FRIEDMAN, MA LECH, JJ TI ACUTE AND LONG-TERM TOXICITY OF WATER-SOLUBLE CATIONIC POLYMERS TO RAINBOW-TROUT (ONCORHYNCHUS-MYKISS) AND THE MODIFICATION OF TOXICITY BY HUMIC-ACID SO ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY LA English DT Note DE CATIONIC POLYMERS; TOXICITY; RAINBOW TROUT; HUMIC ACID AB The toxicity of two classes of cationic polymers, epichlorhydrin/dimethylamine polyamines and quaternary amine copolymers, were investigated. Static bioassays of those polymers resulted in LC50 concentrations ranging from 271-mu-g/L to 1,733-mu-g/L. Under flow-through conditions the toxicity was 1.7 to 13.9 times greater, depending on the polymer used. Using a reference humic acid along with the polymers in toxicity studies, strong correlations were established between humic acid concentration and LC50. Even at a fairly low humic acid concentration (5 mg/L), the toxicity of the polymers was reduced 7- to 16-fold. At higher humic acid concentrations (50 mg/L), cationic polymer toxicity was reduced 33- to 75-fold. C1 NIEHS,CTR MARINE & FRESHWATER BIOMED CORE,GREAT LAKES RES FACIL,MILWAUKEE,WI 53204. AMER CYANAMID CO,DEPT TOXICOL & PROD SAFETY,WAYNE,NJ 07470. MED COLL WISCONSIN,DEPT PHARMACOL & TOXICOL,MILWAUKEE,WI 53226. NR 11 TC 46 Z9 47 U1 1 U2 6 PU SETAC PRESS PI PENSACOLA PA 1010 NORTH 12TH AVE, PENSACOLA, FL 32501-3370 SN 0730-7268 J9 ENVIRON TOXICOL CHEM JI Environ. Toxicol. Chem. PY 1991 VL 10 IS 4 BP 509 EP 515 DI 10.1897/1552-8618(1991)10[509:AALTOW]2.0.CO;2 PG 7 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA FC880 UT WOS:A1991FC88000011 ER PT J AU ANDERSON, LM FOX, SD DIXON, D BEEBE, LE ISSAQ, HJ AF ANDERSON, LM FOX, SD DIXON, D BEEBE, LE ISSAQ, HJ TI LONG-TERM PERSISTENCE OF POLYCHLORINATED BIPHENYL CONGENERS IN BLOOD AND LIVER AND ELEVATION OF LIVER AMINOPYRINE DEMETHYLASE ACTIVITY AFTER A SINGLE HIGH-DOSE OF AROCLOR-1254 TO MICE SO ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY LA English DT Article DE POLYCHLORINATED BIPHENYLS; CONGENER RETENTION; AMINOPYRINE DEMETHYLASE; MOUSE LIVER ID ENZYME-ALTERED FOCI; ADIPOSE-TISSUE MASS; POLYBROMINATED BIPHENYLS; 2,2',4,4',5,5'-HEXACHLOROBIPHENYL 6-CB; SENESCENT RODENTS; RATS; EXPOSURE; PHARMACOKINETICS; DIBENZOFURANS; INDUCTION AB Poorly metabolized polychlorinated biphenyl (PCB) congeners are bioaccumulated in the bodies of rodents and humans. Little is known about the continuing biological effects of these persistent chemicals. To determine whether a single high dose of a PCB mixture to mice would have long-term effects on liver enzymes, Aroclor 1254 was given at a single dose of 500 mg/kg to (C57BL/6 x DBA/2)F1 female mice. Paired controls received olive oil. Mice were killed at intervals of 0.5 to 55 weeks after treatment and liver assessed for aminopyrine demethylase activity. At selected time points, blood and homogenates of liver and of whole carcass were analyzed for content of PCBs by gas chromatography with electron capture detection. Hepatic aminopyrine demethylase activity was significantly elevated in Aroclor-treated mice, relative to controls, for 42 weeks after treatment. A three- to fourfold increase persisted for at least 14 weeks, with a convergence of treated and control values thereafter. Significant amounts of nine PCB congeners were detected in carcass, liver, and blood; total carcass PCB, estimated on the basis of these congeners, correlated significantly with liver aminopyrine demethylase elevation, and a similar trend was noted for liver. At 42 weeks after treatment, total PCB levels were 70 mg/kg for carcass, 2.4 mg/kg for liver and 0.28 mg/kg for blood. Congener profiles were similar in all three compartments, with the majority of the retained chemical being 2,3',4,4',5- and 2,3,3',4,4'-pentachlorobiphenyl and 2,2',4,4',5,5'- and 2,2',3,4,4',5'-hexachlorobiphenyl. These results suggest that congeners bioaccumulated after a high PCB dose retain biological activity in the body for nearly a year after treatment. C1 FREDERICK CANC RES DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21702. RP ANDERSON, LM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. NR 35 TC 18 Z9 20 U1 2 U2 4 PU SETAC PRESS PI PENSACOLA PA 1010 NORTH 12TH AVE, PENSACOLA, FL 32501-3370 SN 0730-7268 J9 ENVIRON TOXICOL CHEM JI Environ. Toxicol. Chem. PY 1991 VL 10 IS 5 BP 681 EP 690 DI 10.1897/1552-8618(1991)10[681:LPOPBC]2.0.CO;2 PG 10 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA FK302 UT WOS:A1991FK30200014 ER PT J AU ANDERSON, LM AF ANDERSON, LM TI PERSISTENT TOXICITY ASSOCIATED WITH BIOACCUMULATED POLYHALOGENATED HYDROCARBONS IN FISH, RODENTS AND PRIMATES SO ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY LA English DT Editorial Material RP ANDERSON, LM (reprint author), NCI,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21701, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SETAC PRESS PI PENSACOLA PA 1010 NORTH 12TH AVE, PENSACOLA, FL 32501-3370 SN 0730-7268 J9 ENVIRON TOXICOL CHEM JI Environ. Toxicol. Chem. PY 1991 VL 10 IS 6 BP 705 EP 706 PG 2 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA FR698 UT WOS:A1991FR69800001 ER PT J AU LUCIER, GW AF LUCIER, GW TI HUMANS ARE A SENSITIVE SPECIES TO SOME OF THE BIOCHEMICAL EFFECTS OF STRUCTURAL ANALOGS OF DIOXIN SO ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY LA English DT Article; Proceedings Paper CT SYMP AT THE 10TH ANNUAL MEETING OF THE SOC OF ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY : LONG-TERM TOXIC EFFECTS OF BIOACCUMULATED POLYCHLORINATED HYDROCARBONS CY OCT 28-NOV 02, 1989 CL TORONTO, CANADA SP SOC ENVIRONM TOXICOL & CHEM DE 2,3,7,8-TETRACHLORODIBENZODIOXIN; DIOXINS; CHLORINATED DIBENZOFURANS; CYTOCHROME P-450; EPIDERMAL GROWTH FACTOR RECEPTOR ID EPIDERMAL GROWTH-FACTOR; MONO-OXYGENASE ACTIVITY; POLYCHLORINATED-BIPHENYLS; AH-RECEPTOR; RAT-LIVER; GLUCOCORTICOID RECEPTOR; AROMATIC-HYDROCARBONS; CYTOSOLIC RECEPTOR; POTENT INDUCTION; HUMAN EXPOSURE AB In 1979, rice oil contaminated with polychlorinated dibenzofurans (PCDFs) was ingested in a widespread poisoning episode in Taiwan. The PCDFs are structural analogs of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD and the PCDFs are thought to share the same mechanism of action that involves binding to the Ah receptor. In our studies, we compared the effects of TCDD on rat liver to effects in placentas of women exposed to PCDF-contaminated rice oil. TCDD is a hepatocarcinogen in female rats. Measured parameters included concentrations of human placental PCDF congeners or rat liver TCDD and induction of cytochrome P-450 isozymes, epidermal growth factor receptor (EGFR) and glucocorticoid receptor (GCR). Placentas from PCDF-exposed women contained two PCDFs: 2,3,4,7,8-penta CDF (100 ppt) and 1,2,3,4,7,8-hexa CDF (400 ppt). The 2,3,4,7,8-penta CDF binds the Ah receptor 60% as well as TCDD, and the 1,2,4,7,8-hexa CDF binds 9% as well as TCDD. Cytochrome P1-450 was induced approximately 100-fold in exposed placentas. This induction was considered maximal. Placental PCDF concentrations associated with this induction were compared to the amount of hepatic TCDD required to maximally induce the rat liver homolog of P1-450. These comparisons, accounting for differences in Ah receptor binding, suggested that humans are more sensitive than rats to the P1-450 inductive actions of the toxic halogenated aromatics. Several assumptions are made, and their validity is discussed. As with the P1-450, humans are more sensitive to the effects of the halogenated aromatics on EGFR (EGF-stimulated autophosphorylation) and GCR (binding capacity) than are rats. Although the relationship of these biochemical changes to the carcinogenic effects of TCDD and its analogs is not clear, our data suggest that it is prudent to retain a conservative risk assessment for the toxic halogenated aromatics. RP LUCIER, GW (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 44 TC 35 Z9 36 U1 1 U2 1 PU SETAC PRESS PI PENSACOLA PA 1010 NORTH 12TH AVE, PENSACOLA, FL 32501-3370 SN 0730-7268 J9 ENVIRON TOXICOL CHEM JI Environ. Toxicol. Chem. PY 1991 VL 10 IS 6 BP 727 EP 735 DI 10.1897/1552-8618(1991)10[727:HAASST]2.0.CO;2 PG 9 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA FR698 UT WOS:A1991FR69800004 ER PT J AU BEEBE, LE FOX, SD ISSAQ, HJ ANDERSON, LM AF BEEBE, LE FOX, SD ISSAQ, HJ ANDERSON, LM TI BIOLOGICAL AND BIOCHEMICAL EFFECTS OF RETAINED POLYHALOGENATED HYDROCARBONS SO ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY LA English DT Article; Proceedings Paper CT SYMP AT THE 10TH ANNUAL MEETING OF THE SOC OF ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY : LONG-TERM TOXIC EFFECTS OF BIOACCUMULATED POLYCHLORINATED HYDROCARBONS CY OCT 28-NOV 02, 1989 CL TORONTO, CANADA SP SOC ENVIRONM TOXICOL & CHEM DE POLYHALOGENATED HYDROCARBONS; BIOACCUMULATION; TUMORIGENESIS; CYTOCHROME P-450 ID ENZYME-ALTERED FOCI; POLYCHLORINATED-BIPHENYLS; POLYBROMINATED BIPHENYLS; LIVER-TUMORS; RATS; INDUCTION; MICE; EXPOSURE; 2,2',4,4',5,5'-HEXACHLOROBIPHENYL; PHARMACOKINETICS AB The polyhalogenated aromatic hydrocarbons (PHHs), consisting of the chlorinated and brominated biphenyls, dibenzo-p-dioxins and dibenzofurans, are important environmental contaminants affecting both wildlife and humans. Although the biological effects due to acute or chronic exposure to these compounds have been extensively investigated with animal models, relatively little is known concerning the long-term ramifications of such exposure due to the persistent body burdens of some PHH congeners. This review examines the persistent effects of these contaminants for two biological end points: tumor formation and induction of cytochrome P-450-associated mixed function oxygenases in target tissues. Literature and data are presented that indicate that retained PHH congeners continue for many months to exert biological effects that contribute to tumor development in rodent livers and lungs. Effects of specific congeners, retention profiles of these congeners in target tissues and the long-term induction of cytochrome P-450 IA1-associated enzyme activity are all consistent with activation of the Ah receptor's being an integral part of the tumor promotion response. C1 NCI,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21702. NR 28 TC 5 Z9 5 U1 0 U2 2 PU SETAC PRESS PI PENSACOLA PA 1010 NORTH 12TH AVE, PENSACOLA, FL 32501-3370 SN 0730-7268 J9 ENVIRON TOXICOL CHEM JI Environ. Toxicol. Chem. PY 1991 VL 10 IS 6 BP 757 EP 763 DI 10.1897/1552-8618(1991)10[757:BABEOR]2.0.CO;2 PG 7 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA FR698 UT WOS:A1991FR69800007 ER PT J AU ALBANI, F THEODORE, WH WASHINGTON, P DEVINSKY, O BROMFIELD, E PORTER, RJ NICE, FJ AF ALBANI, F THEODORE, WH WASHINGTON, P DEVINSKY, O BROMFIELD, E PORTER, RJ NICE, FJ TI EFFECT OF FELBAMATE ON PLASMA-LEVELS OF CARBAMAZEPINE AND ITS METABOLITES SO EPILEPSIA LA English DT Article DE ANTICONVULSANTS; FELBAMATE; CARBAMAZEPINE; CARBAMAZEPINE-10,11-EPOXIDE; CARBAMAZEPINE-DIOL; DRUG INTERACTIONS ID PHENYTOIN AB Felbamate (FBM) is a novel antiepileptic drug (AED) currently undergoing clinical evaluation in the United States. During a controlled clinical trial conducted at the National Institutes of Health Clinical Center, FBM was added to constant carbamazepine (CBZ) monotherapy. CBZ total concentrations were reduced during active FBM treatment (mean reduction 25%, range 10-42%, p < 0.001). The effect was evident after the first week of treatment and reached a plateau in 2-4 weeks. To clarify the interaction mechanism, free and total concentrations of CBZ and its plasma metabolites were determined by high-performance liquid chromatography (HPLC) and ultrafiltration in four patients. In these patients, FBM treatment reduced CBZ concentrations and increased CBZ-epoxide (CBZ-E) concentrations (p < 0.01). Free fractions of all compounds were unmodified. FBM appears to be capable of inducing CBZ metabolism. CBZ-FBM interaction may be clinically relevant. C1 NINCDS,EPILEPSY BRANCH,PRECLIN PHARMACOL SECT,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,CLIN EPILEPSY SECT,BETHESDA,MD 20892. RI Nice, Frank/A-6909-2009 NR 5 TC 72 Z9 72 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD JAN-FEB PY 1991 VL 32 IS 1 BP 130 EP 132 DI 10.1111/j.1528-1157.1991.tb05624.x PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA EU284 UT WOS:A1991EU28400023 PM 1985822 ER PT J AU WEISS, SRB POST, RM AF WEISS, SRB POST, RM TI DEVELOPMENT AND REVERSAL OF CONTINGENT INEFFICACY AND TOLERANCE TO THE ANTICONVULSANT EFFECTS OF CARBAMAZEPINE SO EPILEPSIA LA English DT Article DE ANTICONVULSANT; CARBAMAZEPINE; KINDLING; SEIZURES; NEUROLOGIC MODELS ID AMYGDALA-KINDLED SEIZURES; MODEL; EPILEPSY; RAT AB The relationship of the timing of drug administration to anticonvulsant efficacy against amygdalakindled seizures was studied. During kindling development, rats received carbamazepine (CBZ, 15 mg/kg) before (CBZ-before) or after each amygdala stimulation (CBZ-after). After kindling to full seizures, when all animals were given CBZ before the stimulation, only the CBZ-after group showed a good anticonvulsant response. The rats that had received CBZ before (during development of kindled seizures) remained unresponsive to CBZ treatment (contingent inefficacy). When drug-naive or CBZ-after animals repeatedly received CBZ before electrical stimulation, they developed tolerance to its anticonvulsant effects (contingent tolerance). The tolerance could be reversed by a period of treatment with CBZ-after or by kindling the animal drug-free, but not by CBZ administration alone or by time off from both drug and seizures. These findings suggest that inefficacy and tolerance to CBZ may be affected by the temporal contingencies of drug administration and that responsiveness can be reinstated by altering these contingencies. C1 NIMH,BIOL PSYCHIAT BRANCH,ROOM 3N212,BLDG 10,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 22 TC 43 Z9 43 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD JAN-FEB PY 1991 VL 32 IS 1 BP 140 EP 145 DI 10.1111/j.1528-1157.1991.tb05626.x PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA EU284 UT WOS:A1991EU28400025 PM 1985824 ER PT J AU IADAROLA, MJ SHERWIN, AL AF IADAROLA, MJ SHERWIN, AL TI ALTERATIONS IN CHOLECYSTOKININ PEPTIDE AND MESSENGER-RNA IN ACTIVELY EPILEPTIC HUMAN TEMPORAL CORTICAL FOCI SO EPILEPSY RESEARCH LA English DT Article DE EPILEPSY; COMPLEX PARTIAL SEIZURES; CHOLECYSTOKININ; HUMAN BRAIN ID ACID-INDUCED SEIZURES; HUMAN-BRAIN; OCTAPEPTIDE; NEURONS; RAT; NEUROPEPTIDES; HIPPOCAMPUS; EXPRESSION; ENKEPHALIN; GENE AB The cholecystokinin (CCK) content of temporal cortex, obtained at neurosurgery from 22 patients with temporal lobe epilepsy, was measured by a specific radioimmunoassay. Tissue immunoreactivity was identified as authentic sulfated CCK-8 by reverse phase high performance liquid chromatography. Several samples were also analyzed by RNA blot hybridization for preproCCK mRNA. The CCK content of cortical tissue from which active epileptic spiking was recorded at the time of surgery (11 patients) was significantly decreased (20% lower) in comparison to tissue samples from a second group of 11 patients in whom the lateral temporal cortex was electrographically free of epileptiform spikes. These data suggest that the decrease may be due to continuous release of CCK as a result of abnormal neuronal firing within the focus. This hypothesis may also be consistent with our observation of a slight increase (67%) in preproCCK mRNA in the actively spiking group compared to the non-spiking cortical samples. C1 MCGILL UNIV,INST NEUROL,MONTREAL H3A 2B4,QUEBEC,CANADA. MCGILL UNIV,DEPT NEUROL & NEUROSURG,MONTREAL H3A 2B4,QUEBEC,CANADA. RP IADAROLA, MJ (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 10,RM 1A09,BETHESDA,MD 20892, USA. NR 26 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-1211 J9 EPILEPSY RES JI Epilepsy Res. PD JAN-FEB PY 1991 VL 8 IS 1 BP 58 EP 63 DI 10.1016/0920-1211(91)90036-F PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA FB515 UT WOS:A1991FB51500007 PM 2060503 ER PT J AU GOLDIN, LR MARTINEZ, MM GERSHON, ES AF GOLDIN, LR MARTINEZ, MM GERSHON, ES TI SAMPLING STRATEGIES FOR LINKAGE STUDIES SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE LA English DT Article DE LINKAGE; SAMPLING STRATEGIES; SCHIZOPHRENIA ID HETEROGENEITY; DISORDERS; DISEASES; FAMILIES; MARKERS AB Broadly there are three alternative sampling strategies for linkage studies of complex disorders such as schizophrenia. These are to select either affected sib pairs (and their parents) or small-to-medium-size pedigrees, or large pedigrees. The advantages and disadvantages of each are discussed. Our studies show that, even in the presence of heterogeneity, linkage can be found in clinically realistic sample sizes of nuclear families or medium-sized pedigrees. However, relying on affected sib pair methods in less satisfactory. RP GOLDIN, LR (reprint author), NIMH,CLIN NEUROGENET BRANCH,BLDG 10,RM 3N218,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Martinez, Maria/B-3111-2013 OI Martinez, Maria/0000-0003-2180-4537 NR 22 TC 15 Z9 15 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0940-1334 J9 EUR ARCH PSY CLIN N JI Eur. Arch. Psych. Clin. Neurosci. PY 1991 VL 240 IS 3 BP 182 EP 187 DI 10.1007/BF02190761 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA EY956 UT WOS:A1991EY95600009 PM 1827605 ER PT J AU PANZANELLI, P MULATERO, B LAZARUS, LH FASOLO, A AF PANZANELLI, P MULATERO, B LAZARUS, LH FASOLO, A TI NEUROMEDIN B-LIKE IMMUNOREACTIVITY IN THE BRAIN OF THE GREEN FROG (RANA-ESCULENTA L) SO EUROPEAN JOURNAL OF BASIC AND APPLIED HISTOCHEMISTRY LA English DT Article DE RANATENSIN SUBFAMILY; BOMBESIN; NEUROMEDIN-B-LIKE; ANTISERA; CENTRAL NERVOUS SYSTEM; FROG ID BOMBESIN-LIKE PEPTIDES; ACTIVE PEPTIDES; RAT; RANATENSIN; LOCALIZATION; GUINEA; SKIN AB Three rabbit polyclonal antisera, originally developed against neuromedin B and highly selective against ranatensin subfamily molecules, were used to study the distribution of neuromedin B-like immunoreactivity in the brain of Rana esculenta. Immunopositive cell bodies were observed in several brain regions, including medial and lateral septal nuclei, nucleus of the diagonal band of Broca, medial amygdala, ventral striatum, ventromedial and posterior thalamic nuclei, nucleus of the periventricular organ, posterior tuberculum, dorsal, lateral and ventral hypothalamic nuclei, optic tectum, mesencephalic tegmentum and central rhomboencephalic gray. A dense network of immunopositive fibers was also distributed in defined regions of the frog brain, i.e. in the medial pallium, septum, amygdala, ventral thalamus, preoptic area and posterior hypothalamus. The results of the present study, taken with available molecular biology data, indicate that the naturally occurring antigen is probably represented by a ranatensin/litorin-related antigen. C1 NIEHS,MED NUCL IMAGING LAB,PEPTIDE NEUROCHEM GRP,RES TRIANGLE PK,NC 27709. RP PANZANELLI, P (reprint author), UNIV TURIN,DIPARTMENTO BIOL ANIM,VIA ACCADEMIA ALBERTINA 17,I-10124 TURIN,ITALY. OI Panzanelli, Patrizia/0000-0002-5127-2757 NR 22 TC 6 Z9 6 U1 0 U2 0 PU LUIGI PONZIO E FIGLIO PI PAVIA PA VIA D DA CATALOGNA 1/3, 27100 PAVIA, ITALY SN 0391-7258 J9 EUR J BASIC APPL HIS PY 1991 VL 35 IS 4 BP 359 EP 370 PG 12 WC Medical Laboratory Technology SC Medical Laboratory Technology GA GU308 UT WOS:A1991GU30800003 PM 1801930 ER PT J AU ROTMENSZ, N DEPALO, G FORMELLI, F COSTA, A MARUBINI, E CAMPA, T CRIPPA, A DANESINI, GM DELLEGROTTAGLIE, M DIMAURO, MG FILIBERTI, A GALLAZZI, M GUZZON, A MAGNI, A MALONE, W MARIANI, L PALVARINI, M PERLOFF, M PIZZICHETTA, M VERONESI, U AF ROTMENSZ, N DEPALO, G FORMELLI, F COSTA, A MARUBINI, E CAMPA, T CRIPPA, A DANESINI, GM DELLEGROTTAGLIE, M DIMAURO, MG FILIBERTI, A GALLAZZI, M GUZZON, A MAGNI, A MALONE, W MARIANI, L PALVARINI, M PERLOFF, M PIZZICHETTA, M VERONESI, U TI LONG-TERM TOLERABILITY OF FENRETINIDE (4-HPR) IN BREAST-CANCER PATIENTS SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID SYNTHETIC RETINOID FENRETINIDE; BONE-DENSITY; PHASE-I; TOXICITY; THERAPY; N-(4-HYDROXYPHENYL)RETINAMIDE; PHARMACOKINETICS; PREVENTION; RATS; ACID AB A group of 53 patients initially participating in a phase I trial with the synthetic retinoid fenretinide was assessed for the long-term tolerability of this compound. The patients were evaluated after 42 months of drug intake at a dose of 200 mg/day, including a 3-day drug interruption at the end of each month, by the following examinations: a dermatological visit; an ophthalmological evaluation including an ophthalmological questionnaire and an electroretinogram (ERG); a study on blood chemistry and plasma retinol levels; a study on bone densities and on skeletal X-rays; and finally a psychological evaluation including various tests for anxiety, depression and overall mood. The results show that prolonged administration of fenretinide is well tolerated. No acute nor severe toxicity was observed and thus this compound can be considered a good candidate for chemoprevention trials in a variety of patient populations. C1 INST MED STAT & BIOMETRY,MILAN,ITALY. NEUROL INST C BESTA,MILAN,ITALY. ORTHOPED INST GAETANO PINI,MILAN,ITALY. NCI,BETHESDA,MD 20892. UNIV MILAN,DEPT DERMATOL,I-20122 MILAN,ITALY. RP ROTMENSZ, N (reprint author), IST NAZL TUMORI,VIA VENEZIAN 1,I-20133 MILAN,ITALY. RI Mariani, Luigi/C-2580-2017 OI Mariani, Luigi/0000-0001-6208-4084 FU NCI NIH HHS [2U01 CA 38567-04] NR 37 TC 96 Z9 96 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1991 VL 27 IS 9 BP 1127 EP 1131 DI 10.1016/0277-5379(91)90309-2 PG 5 WC Oncology SC Oncology GA GF193 UT WOS:A1991GF19300018 PM 1835622 ER PT J AU FARZANEH, NK WALDEN, TL HEARING, VJ GERSTEN, DM AF FARZANEH, NK WALDEN, TL HEARING, VJ GERSTEN, DM TI B700, AN ALBUMIN-LIKE MELANOMA-SPECIFIC ANTIGEN, IS A VITAMIN-D BINDING-PROTEIN SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID SERUM-ALBUMIN; TUMOR REJECTION; GENE FAMILY; PLASMA AB B700, a murine melanoma-specific antigen, is a member of the serum albumin protein family. Other members include serum albumin and vitamin D binding protein. The primary structure and biochemical functions of B700, as well as its in vivo metabolic fate, are largely unknown. We compared murine albumin, vitamin D binding protein and B700 for their ability to specifically bind [H-3]-1,25-dihydroxy-vitamin D3. Scatchard analysis revealed a single binding site for B700 with a K(a) of 51 000 mol/l and a B(max) of 4.51 x 10(-7) mol/l. There was no significant difference in the K(a) and B(max) among the albuminoid proteins. However, differences in the binding sites could be distinguished by competition experiments where vitamin D3, vitamin D2 or 7-dehydrocholesterol competed for the specific binding of 1.25-dihydroxyvitamin D3 to a greater extent by B700 than by vitamin D binding protein. The albumin binding site more closely resembles vitamin D binding protein than B700, but the data indicate that the binding function of the albuminoid proteins is conserved in B700. C1 GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20007. ARMED FORCES RADIOBIOL RES INST,DEPT RADIAT BIOCHEM,BETHESDA,MD 20814. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 23 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 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1991 VL 27 IS 9 BP 1158 EP 1162 DI 10.1016/0277-5379(91)90316-6 PG 5 WC Oncology SC Oncology GA GF193 UT WOS:A1991GF19300025 PM 1835629 ER PT J AU HU, N DAWSEY, SM WU, M TAYLOR, PR AF HU, N DAWSEY, SM WU, M TAYLOR, PR TI FAMILY HISTORY OF ESOPHAGEAL CANCER IN SHANXI-PROVINCE, CHINA SO EUROPEAN JOURNAL OF CANCER LA English DT Letter C1 CHINESE ACAD MED SCI,BEIJING,PEOPLES R CHINA. RP HU, N (reprint author), NCI,CANC PREVENT STUDIES BRANCH,EPN ROOM 211,BETHESDA,MD 20892, USA. NR 0 TC 23 Z9 24 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1991 VL 27 IS 10 BP 1336 EP 1336 DI 10.1016/0277-5379(91)90116-U PG 1 WC Oncology SC Oncology GA GN906 UT WOS:A1991GN90600037 PM 1835609 ER PT J AU PROBSTFIELD, JL RIFKIND, BM AF PROBSTFIELD, JL RIFKIND, BM TI THE LIPID-RESEARCH-CLINICS CORONARY PRIMARY PREVENTION TRIAL - DESIGN, RESULTS, AND IMPLICATIONS SO EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON LIPID LOWERING DRUGS : MECHANISMS AND ACTIONS CY SEP 21-22, 1989 CL ULM, FED REP GER SP UNIV ULM, DEPT INTERNAL MED, BOEHRINGER MANNHEIM, BRISTOL MYERS, DELALANDE ARZNEIMITTEL, FARMITALIA CARLO ERBA, HOFFMANN LA ROCHE, HOECHST, HOLPHAR ARZNEIMITTEL, KLINGE PHARMA, KNOLL DE CHOLESTEROL; LDL-CHOLESTEROL; CORONARY HEART DISEASE; ATHEROSCLEROSIS; CHOLESTYRAMINE; CLINICAL TRIAL ID MIDDLE-AGED MEN; HEART-DISEASE; ANALYTICAL PERFORMANCE; SERUM-CHOLESTEROL; COMPARABILITY; RISK AB The Coronary Primary Prevention Tiral (CPPT) was the major clinical investigation conducted in the Lipid Research Clinics (LRC) Program. There were 12 North American clinics involved in this joint double-blind protocol. The hypothesis tested was: lowering plasma cholesterol in middle-aged men with primary hyper-cholesterolemia [plasma total cholesterol greater than or equal to 265 mg/dl(6.88 mm/l)] who are otherwise healthy leads to a reduction in coronary heart disease (CHD) as manifest by a reduction in definite myocardial infarction (fatal and nonfatal) over a 7-year follow-up of all participants. The trial was conducted in 3806 male volunteers between the ages of 35 and 59, who were randomly assigned to two equal groups. The treatment group received a moderate cholesterol-lowering diet plus cholestyramine; the placebo group received an identical diet plus a placebo. The study medication was administered at 24 g daily in divided doses. The participants were followed up bimonthly for an average of 7.4 years. The diet (daily cholesterol intake of about 400 mg and a polyunsaturated fat/saturated fat ratio of 0.8) lowered plasma cholesterol by an average of 4%, as designed. The cholestyramine group experienced average plasma total cholesterol (TC) lowering and plasma low-density lipoprotein cholesterol (LDC-C) lowering 8.5% and 12.6% greater than the placebo group, respectively. This resulted in a 19% reduction in definite myocardial infarction (P < 0.05). The trial results for CHD deaths, nonfatal myocardial infarction, new positive exercise stress tests (P < 0.001) new-onset angina (P < 0.01) and coronary artery bypass surgery (P < 0.06) were consistent with and supportive of the main findings of the study. Total mortality also showed a slight decrease in the active treatment group, but the magnitude of the effect was reduced by a greater number of deaths from accidents and violence in the placebo group. The main findings of the study show that the reduction of plasma TC by lowering plasma LDL-C levels can diminish the incidence of CHD morbidity and mortality in men at high risk of CHD. A causal role for these lipids and lipoproteins in the pathogenesis of CHD is strongly suggested. The findings from this and other trials and epidemiologic studies suggest that for every 1% reduction in TC there is a 2% reduction in risk of CHD. The study cohort remains in long-term follow-up. C1 NHLBI,DIV HEART & VASC DIS,LIPID METAB & ATHEROGENESIS BRANCH,BETHESDA,MD 20892. RP PROBSTFIELD, JL (reprint author), NHLBI,DECA,CLIN TRIALS BRANCH,FED BLDG 5C-10,7550 WISCONSIN AVE,BETHESDA,MD 20892, USA. NR 42 TC 23 Z9 24 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0031-6970 J9 EUR J CLIN PHARMACOL JI Eur. J. Clin. Pharmacol. PY 1991 VL 40 SU 1 BP S69 EP S75 DI 10.1007/BF01409413 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FA469 UT WOS:A1991FA46900016 PM 2044648 ER PT J AU FOSTER, GA EIDEN, LE BRENNEMAN, DE AF FOSTER, GA EIDEN, LE BRENNEMAN, DE TI ENKEPHALIN EXPRESSION IN SPINAL-CORD NEURONS IS MODULATED BY DRUGS RELATED TO CLASSICAL AND PEPTIDERGIC TRANSMITTERS SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE ENKEPHALIN PHENOTYPIC EXPRESSION; NEURONAL CULTURE; SPINAL CORD NEURONS; EPIGENETIC REGULATION ID CENTRAL NERVOUS-SYSTEM; MESENCEPHALIC RAPHE NEURONS; RAT ADRENAL-MEDULLA; SYMPATHETIC NEURONS; TYROSINE-HYDROXYLASE; MESSENGER-RNA; MORPHOLOGICAL DEVELOPMENT; DIFFERENTIATION FACTOR; PARTIAL-PURIFICATION; EMBRYONIC MEDULLARY AB The effects of various neurotransmitter agonists and antagonists on the synthesis and release of methionine enkephalin (mENK) in neuronal cultures of mouse spinal cord and dorsal root ganglia have been measured. Blockade of electrical activity with tetrodotoxin between days 9 and 13 in culture caused a > 95% decrease in the number of mENK-immunoreactive neurons. This effect was also seen upon the blockade of glycine and beta-adrenergic receptors with strychnine and propranolol, respectively, and stimulation of GABA receptors with muscimol. Stimulation of beta-adrenergic receptors with isoproterenol, or blockade of glutamate and GABA receptors with 2-aminophosphonovalerate and strychnine, respectively, had a qualitatively opposite action on both the number of mENK-immunoreactive neurons and enkephalin peptide levels measured by radioimmunoassay. Application of substance P also enhanced the mENK cell number. These data suggest that, at lest in the spinal cord, characteristics other than the average level of impulse activity in the afferent input may be critical to the regulation of expression of mENK. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892. RP FOSTER, GA (reprint author), UNIV COLL CARDIFF,DEPT PHYSIOL,CARDIFF CF1 1XL,S GLAM,WALES. RI Foster, George/A-7521-2010; OI Eiden, Lee/0000-0001-7524-944X FU Wellcome Trust NR 52 TC 1 Z9 1 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PD JAN 1 PY 1991 VL 3 IS 1 BP 32 EP 39 DI 10.1111/j.1460-9568.1991.tb00808.x PG 8 WC Neurosciences SC Neurosciences & Neurology GA EV430 UT WOS:A1991EV43000004 PM 12106266 ER PT J AU SANDROCK, D LASTORIA, S MERINO, MJ NEUMANN, RD AF SANDROCK, D LASTORIA, S MERINO, MJ NEUMANN, RD TI POSITIVE GA-67-CITRATE SCINTIGRAPHY IN WISKOTT-ALDRICH SYNDROME WITH MALIGNANT-LYMPHOMA SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE WISKOTT-ALDRICH SYNDROME; MALIGNANT LYMPHOMA; GA-67 CITRATE SCINTIGRAPHY AB This case describes the first detection of solid lymphoma lesions by gallium-67 scintigraphy in a 12-year-old patient with Wiskott-Aldrich syndrome. Gallium 67 uptake was found in multiple sites in the patient who had developed an undifferentiated small, non-cleaved cell lymphoma. Response to chemotherapeutic treatment is correlated with findings on the gallium scintigraphy follow-up. C1 NCI,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 12 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PY 1991 VL 18 IS 11 BP 928 EP 930 DI 10.1007/BF02258459 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GN061 UT WOS:A1991GN06100009 PM 1752263 ER PT J AU KAMISGOULD, E AF KAMISGOULD, E TI A CASE-STUDY IN FRONTIER PRODUCTION ANALYSIS - ASSESSING THE EFFICIENCY AND EFFECTIVENESS OF NEW-JERSEY PARTIAL-CARE MENTAL-HEALTH-PROGRAMS SO EVALUATION AND PROGRAM PLANNING LA English DT Article C1 NIMH,DIV APPL & SERV RES,BETHESDA,MD 20892. NIMH,MENTAL HLTH STAT IMPROVEMENT PROGRAM,BETHESDA,MD 20892. RP KAMISGOULD, E (reprint author), NEW JERSEY DIV MENTAL HLTH & HOSP,13 ROSZEL RD,PRINCETON,NJ 08540, USA. NR 15 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0149-7189 J9 EVAL PROGRAM PLANN JI Eval. Program Plan. PY 1991 VL 14 IS 4 BP 385 EP 390 DI 10.1016/0149-7189(91)90022-9 PG 6 WC Social Sciences, Interdisciplinary SC Social Sciences - Other Topics GA GR780 UT WOS:A1991GR78000022 ER PT J AU AKAMIZU, T SAJI, M IKUYAMA, S KOSUGI, S TAHARA, K KOHN, LD AF AKAMIZU, T SAJI, M IKUYAMA, S KOSUGI, S TAHARA, K KOHN, LD TI THE TSH RECEPTOR IN AUTOIMMUNE BASEDOWS-DISEASE SO EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY LA English DT Article; Proceedings Paper CT INTERNATIONAL THYROID SYMP ON THE 150TH ANNIVERSARY OF BASEDOWS DISEASE CY MAY 02-06, 1990 CL HALLE, GER DEM REP ID AUTO-ANTIGEN; CLONING; EXPRESSION; CDNA; AUTOANTIBODIES; PROTEINS; CARRIER AB The cloning approaches of the past two years have opened new doors to the pursuit of our understanding Basedow's disease. The cloning of the TSH receptor is the most dramatic step; nevertheless, all the proteins mentioned in the following appear to be important molecules in the bioactivity of the thyroid cell and are implicated as autoantigens. C1 NIDDKD,BIOCHEM & METAB LAB,CELL REGULAT SECT,BETHESDA,MD 20892. NR 21 TC 0 Z9 0 U1 0 U2 0 PU JOHANN AMBROSIUS BARTH VERLAG PI HEIDELBERG PA IM WEIHER 10, D-69121 HEIDELBERG, GERMANY SN 0232-7384 J9 EXP CLIN ENDOCRINOL JI Exp. Clin. Endocrinol. PY 1991 VL 97 IS 2-3 BP 153 EP 159 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FP446 UT WOS:A1991FP44600006 PM 1915626 ER PT J AU MA, TP GRAYBIEL, AM WURTZ, RH AF MA, TP GRAYBIEL, AM WURTZ, RH TI LOCATION OF SACCADE-RELATED NEURONS IN THE MACAQUE SUPERIOR COLLICULUS SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE SUPERIOR COLLICULUS; SACCADES; ACETYLCHOLINESTERASE; EYE MOVEMENTS; PRIMATE ID EYE-MOVEMENTS; ANATOMICAL ORGANIZATION; SINGLE UNITS; MONKEY; CAT; INTERMEDIATE; LOCALIZATION; INNERVATION; AFFERENTS; RESPONSES AB The locations of saccade-related neurons were studied in the superior colliculi of two adult rhesus monkeys (Macaca mulatta) by placing marking lesions at the sites of physiologically characterized cells and comparing these histologically identified sites with the collicular laminae and acetylcholinesterase (AChE)-rich patches. Three major conclusions were drawn on the basis of 39 histologically identified sites at which saccade-related neurons were recorded. First, saccade-related neurons were distributed from the ventral half of the optic layer through the deep gray layer, and were most concentrated in the intermediate gray and white layers. Second, there was a clear relationship between the discharge characteristics of these saccade-related neurons and the depths at which they were found. Neurons having presaccadic bursts, defined as clipped and partially-clipped, tended to be encountered more dorsally, and neurons that did not have bursts (unclipped) were encountered more ventrally. Although cells having different discharge characteristics seemed to be organized along a dorsoventral axis, there was no compelling evidence that these properties were specified by their laminar locations. Third, there was no clear correlation between the locations of saccade-related neurons and the distribution of individual AChE-rich patches. Saccade-related cells were found both in the caudal superior colliculus where patches were located and in the rostral superior colliculus where patches were not found; both within and between the two tiers of AChE-rich patches in the caudal superior colliculus; and both within and between individual AChE-rich patches. However, the depth-level at which saccade-related neurons occurred generally matched the region bounded by the two tiers of AChE-rich patches in the intermediate and deep layers, and the dorsal and ventral extent of saccade-related neurons was the same as that of the AChE-rich patches. C1 NEI,SENSORIMOTOR RES LAB,BLDG 10,ROOM 10C 101,BETHESDA,MD 20892. MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. FU NEI NIH HHS [F32-EY05950, EY 5-RO1-EY02866-11] NR 49 TC 66 Z9 66 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PY 1991 VL 85 IS 1 BP 21 EP 35 PG 15 WC Neurosciences SC Neurosciences & Neurology GA FN932 UT WOS:A1991FN93200003 PM 1715825 ER PT J AU OLAH, Z KOMOLY, S NAGASHIMA, N JOO, F RAPP, UR ANDERSON, WB AF OLAH, Z KOMOLY, S NAGASHIMA, N JOO, F RAPP, UR ANDERSON, WB TI CEREBRAL-ISCHEMIA INDUCES TRANSIENT INTRACELLULAR REDISTRIBUTION AND INTRANUCLEAR TRANSLOCATION OF THE RAF PROTOONCOGENE PRODUCT IN HIPPOCAMPAL PYRAMIDAL CELLS SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE CEREBRAL ISCHEMIA; HIPPOCAMPUS; RAF PROTOONCOGENE FAMILY; RAF PROTEIN KINASE; INTRACELLULAR TRANSLOCATION; ASTROCYTE; CELL NUCLEUS; MONGOLIAN GERBIL ID GRADED BRAIN ISCHEMIA; KINASE-C; SIGNAL TRANSDUCTION; IMMUNOCYTOCHEMICAL LOCALIZATION; BIOCHEMICAL-CHANGES; ESCHERICHIA-COLI; PROTEINS; GERBILS; PHOSPHORYLATION; PROLIFERATION AB In this report we describe changes in the intracellular redistribution of raf serine/threonine protein kinase (product of the raf proto-oncogene family) in hippocampal neurons following cerebral ischemia in Mongolian gerbils. For immunohistochemical localization studies polyclonal antisera specific for each of the A, B, and Raf-1 isotypes of raf, as well as a pan-raf antisera, were employed. Of these, only sera recognizing B-raf, as well as the general v-raf (raised against the conserved C-terminal region) were positive, indicating that B-raf is the major isotype in this neuronal region. Three different ischemic models were used (repeated 3 times for two min and single 5 or 15 min occlusions, of the common carotid arteries) to demonstrate that ischemic insult causes redistribution of raf protein kinase into the cell nucleus of hippocampal neurons. Increased amounts of raf protein in the nuclei of pyramidal cells following ischemia was confirmed by Western blot analysis of isolated nuclear fractionations. Moreover, an elevation in the level of nuclear raf protein also was detected in the contralateral (i.e. non-occluded hemisphere) neurons of CA1 and CA3 subfields 4 days after the ischemic insult indicating a possible transsynaptic increase in the amount of raf protein along with redistribution. The intranuclear translocation of the immunoreactive material started from the perinucleolar rim and with time extended throughout the nucleus. Enhanced levels and altered redistribution of the raf polypeptide in the nuclei of pyramidal cells of the CA3 subfield appears to be reversible and returns to the normal level 12 days following the ischemic insult. In addition to triggering the above changes in the intracellular redistribution of raf, ischemic insult also caused an increase in the level of B-raf protein in reactive astrocytes. C1 NCI,CELLULAR ONCOL LAB,BLDG 36,ROOM ID22,BETHESDA,MD 20892. NINCDS,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. BIOL RES CTR,INST BIOPHYS,MOLEC NEUROBIOL LAB,H-6701 SZEGED,HUNGARY. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. NR 40 TC 30 Z9 30 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PY 1991 VL 84 IS 2 BP 403 EP 410 PG 8 WC Neurosciences SC Neurosciences & Neurology GA FG917 UT WOS:A1991FG91700019 PM 2065747 ER PT J AU GELLMAN, RS CARL, JR AF GELLMAN, RS CARL, JR TI MOTION PROCESSING FOR SACCADIC EYE-MOVEMENTS IN HUMANS SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE SACCADES; PURSUIT; PREDICTION; LATENCY; MOTION PROCESSING; HUMAN ID STIMULI; MONKEY AB 1. We studied the latencies and amplitudes of saccades to moving targets in normal human subjects. Targets underwent ramp or step-ramp motions. The goal was to determine how the saccadic system uses information about target velocity. 2. For simple ramp motion saccadic latency decreased as target speed increased. A threshold distance model, which assumes that the target has to move a minimum distance before saccadic processing starts, provided a good fit to the responses of all four subjects and explains discrepancies between previously published findings. 3. A double step experiment showed that target position may have some effect on saccadic amplitude when sampled almost-equal-to 70 ms before saccade onset, but it must be sampled at least 140 ms before onset for an accurate saccade to occur. 4. Saccades to simple ramp targets approximated the target position 55 ms before saccade onset. Based on our double step results, this is more compensation than possible by a simple position estimate and implies extrapolation of target motion by the saccadic system. The lack of complete compensation may be due to an underestimate of the target speed and/or of the saccadic latency. 5. A delayed-saccade paradigm resulted in saccades with a longer, constant latency and allowed longer viewing of target motion. These saccades accounted for all but almost-equal-to 20 ms of target motion, suggesting that with more processing time of target motion a better extrapolation may be generated. 6. In a step-ramp paradigm the target stepped in one direction, then moved smoothly in the opposite direction. Saccades in this paradigm could be made in either the direction of the step or in the direction of target motion: the direction and latency were determined solely by the time at which the target crossed the fixation point. This time must be calculated from target speed and position, implying that the saccadic system must use speed information to adjust latency or to cancel unnecessary saccades. C1 NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892. RP GELLMAN, RS (reprint author), UNIV CALGARY,SCH MED,DEPT CLIN NEUROSCI,CALGARY T2N 4N1,ALBERTA,CANADA. NR 18 TC 62 Z9 62 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PY 1991 VL 84 IS 3 BP 660 EP 667 PG 8 WC Neurosciences SC Neurosciences & Neurology GA FK084 UT WOS:A1991FK08400023 PM 1864336 ER PT J AU HOCHERMAN, S WISE, SP AF HOCHERMAN, S WISE, SP TI EFFECTS OF HAND MOVEMENT PATH ON MOTOR CORTICAL ACTIVITY IN AWAKE, BEHAVING RHESUS-MONKEYS SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE CEREBRAL CORTEX; MOTOR SYSTEM; MOTOR CORTEX; PREMOTOR CORTEX; SUPPLEMENTARY MOTOR CORTEX; FRONTAL LOBE; MOVEMENT TRAJECTORY; MONKEY ID INSTRUCTED-DELAY PERIOD; FREE ARM MOVEMENTS; PREMOTOR CORTEX; INTENDED MOVEMENT; 3-DIMENSIONAL SPACE; PRECENTRAL CORTEX; NEURONAL-ACTIVITY; INFERIOR AREA-6; VISUAL TARGETS; MACAQUE MONKEY AB Neuronal activity was studied in the primary (M1), supplementary (M2), dorsal premotor (PMd), and ventral premotor (PMv) cortex of awake, behaving rhesus monkeys. The animals performed forelimb movements to three targets, each approached by three different types of trajectories. With one trajectory type, the monkey moved its hand straight to the target, with another, the path curved in a clockwise direction, and with a third, the path curved in a counter-clockwise direction. We examined whether neuronal activity in these areas exclusively reflects a hand movement's net distance and direction or, alternatively, whether other factors also influence cortical activity. It was found that neuronal activity during all phases of a trial reflects aspects of movement in addition to target location. Among these aspects may be selection of an integrated motor act from memory, perhaps specifying the entirety of a path by which the hand moves to a target. C1 NIMH,NEUROPHYSIOL LAB,POB 289,POOLESVILLE,MD 20837. NR 53 TC 89 Z9 89 U1 1 U2 5 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PY 1991 VL 83 IS 2 BP 285 EP 302 PG 18 WC Neurosciences SC Neurosciences & Neurology GA EV505 UT WOS:A1991EV50500004 PM 2022240 ER PT J AU SPITZER, H RICHMOND, BJ AF SPITZER, H RICHMOND, BJ TI TASK-DIFFICULTY - IGNORING, ATTENDING TO, AND DISCRIMINATING A VISUAL STIMULUS YIELD PROGRESSIVELY MORE ACTIVITY IN INFERIOR TEMPORAL NEURONS SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE SINGLE NEURONS; INFERIOR TEMPORAL CORTEX; TASK DIFFICULTY; VISION; ATTENTION; MONKEY ID INFEROTEMPORAL CORTEX; MACAQUE; MONKEY; ATTENTION; RESPONSES AB To study the influence of task difficulty on the stimulus-elicited responses of inferior temporal (IT) neurons, the stimulus-elicited responses of 64 neurons were recorded from IT cortex of three rhesus monkeys while they performed three behavioral task - an irrelevant-stimulus task, a stimulus detection task, and a stimulus discrimination task. The monkey could ignore the stimulus entirely in the irrelevant-stimulus task, was required only to detect stimulus dimming in the stimulus detection task, and was required to attend to specific properties of the stimulus in the discrimination task. The excitatory responses in the discrimination and stimulus detection tasks were larger than those in the irrelevant-stimulus task (61 % and 33 %, respectively, of the individual differences were significant), and excitatory responses in the discrimination task were larger than those in the detection task (49 % of the individual differences reached significance). Twenty percent of the stimulus presentations elicited inhibitory responses that were followed by off-responses. The off-responses were modulated by the tasks in the same order as the excitatory on-responses. Assuming that the off-response strengths indicate the depth of the stimulus-induced inhibition, these results suggest that inhibitory responses were influenced across these tasks in a manner similar to the excitatory responses. When the neuronal responses were related to the difficulties of these task, both the response strength and errors were seen to be least during the irrelevant-stimulus task and greatest during the discrimination task. This relationship suggests that the visual responsiveness of IT neurons is related to the degree of attention the animal pays to the stimulus. Based on this and findings from several related studies, a more refined hypothesis can be formulated, namely, visual responsiveness of IT neurons is related to the degree of attention the animal pays to stimulus pattern, specifically. C1 NIMH,NEUROPSYCHOL LAB,BLDG 9,RM 1N107,BETHESDA,MD 20892. NR 27 TC 72 Z9 73 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PY 1991 VL 83 IS 2 BP 340 EP 348 PG 9 WC Neurosciences SC Neurosciences & Neurology GA EV505 UT WOS:A1991EV50500008 PM 2022243 ER PT J AU GIORDANO, T HOWARD, TH COLEMAN, J SAKAMOTO, K HOWARD, BH AF GIORDANO, T HOWARD, TH COLEMAN, J SAKAMOTO, K HOWARD, BH TI ISOLATION OF A POPULATION OF TRANSIENTLY TRANSFECTED QUIESCENT AND SENESCENT CELLS BY MAGNETIC AFFINITY CELL SORTING SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID EUKARYOTIC CELLS; MAMMALIAN-CELLS; SODIUM-BUTYRATE; EXPRESSION; DNA; EFFICIENCY; PROMOTER; GENE; FIBROBLASTS; ELECTROPORATION C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 25 TC 28 Z9 28 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 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD JAN PY 1991 VL 192 IS 1 BP 193 EP 197 DI 10.1016/0014-4827(91)90175-T PG 5 WC Oncology; Cell Biology SC Oncology; Cell Biology GA EP869 UT WOS:A1991EP86900027 PM 1845795 ER PT J AU LIN, LR REDDY, VN GIBLIN, FJ KADOR, PF KINOSHITA, JH AF LIN, LR REDDY, VN GIBLIN, FJ KADOR, PF KINOSHITA, JH TI POLYOL ACCUMULATION IN CULTURED HUMAN LENS EPITHELIAL-CELLS SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE HUMAN LENS EPITHELIUM; TISSUE CULTURE; ULTRASTRUCTURE; ALDOSE REDUCTASE; POLYOL PATHWAY; DIABETIC CATARACT; SORBINIL; AL1576 ID ALDOSE REDUCTASE; SORBITOL PATHWAY; RAT LENS; DEHYDROGENASE; INHIBITION; CATARACTS; SORBINIL C1 OAKLAND UNIV,EYE RES INST,ROCHESTER,MI 48309. NEI,BETHESDA,MD 20894. FU NEI NIH HHS [EY00484, EY02027, EY05230] NR 25 TC 33 Z9 33 U1 1 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JAN PY 1991 VL 52 IS 1 BP 93 EP 100 DI 10.1016/0014-4835(91)90132-X PG 8 WC Ophthalmology SC Ophthalmology GA EX135 UT WOS:A1991EX13500011 PM 1907924 ER PT J AU WILLIAMS, TF AF WILLIAMS, TF TI PROCEEDINGS OF A CONFERENCE ON CORRELATIONS OF AGING AND SPACE EFFECTS ON BIOSYSTEMS - OCTOBER 30 NOVEMBER 1, 1989 - FOREWORD SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material RP WILLIAMS, TF (reprint author), NIA,BLDG 31,ROOM 2C02,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 2-3 BP 121 EP 121 DI 10.1016/0531-5565(91)90001-3 PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA FR687 UT WOS:A1991FR68700001 ER PT J AU SPROTT, RL AF SPROTT, RL TI NIA PLANS AND OPPORTUNITIES SO EXPERIMENTAL GERONTOLOGY LA English DT Article RP SPROTT, RL (reprint author), NIA,BIOL AGING PROGRAM,BLDG 31,ROOM 5C15,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 2-3 BP 135 EP 136 DI 10.1016/0531-5565(91)90004-6 PG 2 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA FR687 UT WOS:A1991FR68700004 PM 1680732 ER PT J AU SPROTT, RL AF SPROTT, RL TI PROCEEDINGS OF A CONFERENCE ON CORRELATIONS OF AGING AND SPACE EFFECTS ON BIOSYSTEMS - OCTOBER 30 NOVEMBER 1, 1989 - CARDIOVASCULAR EFFECTS SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material RP SPROTT, RL (reprint author), NIA,BIOL AGING PROGRAM,BLDG 31,ROOM 5C15,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 2-3 BP 139 EP 139 PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA FR687 UT WOS:A1991FR68700006 ER PT J AU SPROTT, RL AF SPROTT, RL TI PROCEEDINGS OF A CONFERENCE ON CORRELATIONS OF AGING AND SPACE EFFECTS ON BIOSYSTEMS - OCTOBER 30 NOVEMBER 1, 1989 - BONE EFFECTS SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material RP SPROTT, RL (reprint author), NIA,BIOL AGING PROGRAM,BLDG 31,ROOM 5C15,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 2-3 BP 169 EP 169 DI 10.1016/0531-5565(91)90009-B PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA FR687 UT WOS:A1991FR68700009 ER PT J AU SPROTT, RL AF SPROTT, RL TI PROCEEDINGS OF A CONFERENCE ON CORRELATIONS OF AGING AND SPACE EFFECTS ON BIOSYSTEMS - OCTOBER 30 NOVEMBER 1, 1989 - SLEEP EFFECTS SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material RP SPROTT, RL (reprint author), NIA,BIOL AGING PROGRAM,BLDG 31,ROOM 5C15,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 2-3 BP 215 EP 215 DI 10.1016/0531-5565(91)90013-C PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA FR687 UT WOS:A1991FR68700013 ER PT J AU SPROTT, RL AF SPROTT, RL TI PROCEEDINGS OF A CONFERENCE ON CORRELATIONS OF AGING AND SPACE EFFECTS ON BIOSYSTEMS - OCTOBER 30 NOVEMBER 1, 1989 - CELLULAR EFFECTS SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material RP SPROTT, RL (reprint author), NIA,BIOL AGING PROGRAM,BLDG 31,ROOM 5C15,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 2-3 BP 245 EP 245 DI 10.1016/0531-5565(91)90016-F PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA FR687 UT WOS:A1991FR68700016 ER PT J AU SPROTT, RL AF SPROTT, RL TI PROCEEDINGS OF A CONFERENCE ON CORRELATIONS OF AGING AND SPACE EFFECTS ON BIOSYSTEMS - OCTOBER 30 NOVEMBER 1, 1989 - IMMUNOLOGICAL EFFECTS SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material RP SPROTT, RL (reprint author), NIA,BIOL AGING PROGRAM,BLDG 31,ROOM 5C15,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 2-3 BP 267 EP 267 DI 10.1016/0531-5565(91)90019-I PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA FR687 UT WOS:A1991FR68700019 ER PT J AU SPROTT, RL AF SPROTT, RL TI PROCEEDINGS OF A CONFERENCE ON CORRELATIONS OF AGING AND SPACE EFFECTS ON BIOSYSTEMS - OCTOBER 30 NOVEMBER 1, 1989 - GENETICS SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material RP SPROTT, RL (reprint author), NIA,BIOL AGING PROGRAM,BLDG 31,ROOM 5C15,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 2-3 BP 297 EP 297 DI 10.1016/0531-5565(91)90023-F PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA FR687 UT WOS:A1991FR68700023 ER PT J AU HAZZARD, DG FINCH, CE AF HAZZARD, DG FINCH, CE TI NATIONAL-INSTITUTE-ON-AGING, NIH, WORKSHOP ON ALTERNATIVE ANIMAL-MODELS FOR RESEARCH ON AGING - INTRODUCTION SO EXPERIMENTAL GERONTOLOGY LA English DT Editorial Material C1 UNIV SO CALIF,ETHEL PERCY ANDRUS GERONTOL CTR,LOS ANGELES,CA 90089. RP HAZZARD, DG (reprint author), NIA,BIOL AGING PROGRAM,BETHESDA,MD 20892, USA. NR 4 TC 6 Z9 6 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PY 1991 VL 26 IS 5 BP 411 EP 412 DI 10.1016/0531-5565(91)90028-K PG 2 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA GL102 UT WOS:A1991GL10200001 ER PT J AU MADDEN, MC ELING, TE DAILEY, LA FRIEDMAN, M AF MADDEN, MC ELING, TE DAILEY, LA FRIEDMAN, M TI THE EFFECT OF OZONE EXPOSURE ON RAT ALVEOLAR MACROPHAGE ARACHIDONIC-ACID METABOLISM SO EXPERIMENTAL LUNG RESEARCH LA English DT Article ID HYDROGEN-PEROXIDE; FATTY-ACIDS; INVITRO; INFLAMMATION; PROSTAGLANDINS; INHALATION; SEPARATION; PARTICLES; TOXICITY; RABBIT AB Rat alveolar macrophages were prelabeled with H-3-arachidonic acid (H-3-AA) and exposed to air or O3 (0.1-1.0 ppm) in vitro for 2 h. Alveolar macrophages released 3.6-fold more tritium at the 1.0 ppm exposure concentration compared with air-exposed macrophages. A significantly increased production of several H-3-AA metabolites, including 6-keto-PGF1-alpha, thromboxane B2, 12-hydroxy-5,8, 10-heptadecatrienoic acid, prostaglandins E2 and D2, leukotrienes B4 and D4, and 15-hydroxyeicosatetraenoic acid was formed by macrophages exposed to 1.0 ppm O3 compared with air-exposed macrophages as determined by high performance liquid chromatography (HPLC) analysis. O3 exposure did not alter macrophage H-3-AA metabolism in response to calcium ionophore A23187. The largest tritiated peak observed in the HPLC chromatograms of O3-exposed cells was a polar complex of products that contained various phospholipids and neutral lipids (including diacylglycerol) and possibly degradation products of H-3-AA and some of its metabolites. These changes in macrophage arachidonic acid metabolism may play an important role in the lung response to O3 exposure in vivo. C1 UNIV N CAROLINA,DEPT MED,CTR ENVIRONM MED & LUNG BIOL,CHAPEL HILL,NC 27514. NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,CURRICULUM TOXICOL,CHAPEL HILL,NC 27514. NR 39 TC 36 Z9 37 U1 1 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 1 BP 47 EP 63 DI 10.3109/01902149109063281 PG 17 WC Respiratory System SC Respiratory System GA EW339 UT WOS:A1991EW33900005 PM 1849477 ER PT J AU BOORMAN, GA DIXON, D AF BOORMAN, GA DIXON, D TI HISTOGENESIS OF MOUSE LUNG-TUMORS - AN OVERVIEW SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID CELL RP BOORMAN, GA (reprint author), NIEHS,NATL TOXICOL PROGRAM,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 14 TC 3 Z9 3 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 107 EP 109 DI 10.3109/01902149109064405 PG 3 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200002 PM 2050020 ER PT J AU DIXON, D HORTON, J HASEMAN, JK TALLEY, F GREENWELL, A NETTESHEIM, P HOOK, GE MARONPOT, RR AF DIXON, D HORTON, J HASEMAN, JK TALLEY, F GREENWELL, A NETTESHEIM, P HOOK, GE MARONPOT, RR TI HISTOMORPHOLOGY AND ULTRASTRUCTURE OF SPONTANEOUS PULMONARY NEOPLASMS IN STRAIN-A MICE SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID MOUSE LUNG; ALVEOLAR AB The microscopic and ultrastructural characteristics of spontaneous pulmonary neoplasms in strain A (strA) mice are described. Fifty-one spontaneous lung tumors were identified in 34 out of 57, 11-23-month-old male strA/Hen mice. Grossly, all tumors appeared as yellow-white, discrete nodules ranging in size from 1.0-10 mm. Tumor types were randomly distributed throughout the lung; however, the right lung lobes were most frequently involved. Histologically, tumors were classified as adenoma (34/51) or carcinoma (17/51) as defined by standard histopathologic criteria [1]. Adenomas were usually less than 4 mm in diameter and had solid (16/34), papillary (10/34), or mixed (8/34) histologic growth patterns. Carcinomas were usually greater than 4 mm in diameter and had papillary (13/17) or mixed (4/17) histologic growth patterns. Ultrastructurally, benign tumors consisted of solid or papillary areas of neoplastic type II/like cells. Cells comprising malignant tumors had varying ultrastural characteristics ranging from well-differentiated alveolar cell types to undifferentiated cells having intracytoplasmic osmiophilic dense bodies, vacuoles, or few specialized organelles commonly observed in mature nonneoplastic pulmonary epithelial cells. RP DIXON, D (reprint author), NIEHS,NATL TOXICOL PROGRAM,STAT & BIOMATH BRANCH,PULM PATHOBIOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 14 TC 25 Z9 26 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 131 EP 155 DI 10.3109/01902149109064407 PG 25 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200004 PM 1646706 ER PT J AU FOLEY, JF ANDERSON, MW STONER, GD GAUL, BW HARDISTY, JF MARONPOT, RR AF FOLEY, JF ANDERSON, MW STONER, GD GAUL, BW HARDISTY, JF MARONPOT, RR TI PROLIFERATIVE LESIONS OF THE MOUSE LUNG - PROGRESSION STUDIES IN STRAIN-A MICE SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID GROWTH-RATE; PREVALENCE; TUMOR AB The progression of pulmonary neoplasia was examined in strain A/J male mice treated with a single dose of vinyl carbamate (60 mg/kg, i.p.) 6 weeks after birth. Interim sacrifices were performed at 7, 8, 10, 12, or 14 months. Proliferative lesions of the lung were divided into four categories: hyperplasias, adenomas, carcinomas arising within adenomas, and carcinomas. Grossly visible surface tumor counts, histologic diagnoses, and morphometric measurements of histologic lesions were used to evaluate progression. Vinyl carbamate-treated mice showed increased mean surface tumor counts at all time points. Diagnostic evaluation suggested that as a function of time, the relative frequency of hyperplasias decreased and the relative frequency of adenomas increased. The relative frequency of adenomas subsequently decreased, whereas the relative frequency of carcinomas increased. At all time points, carcinomas arising within adenomas were present. As time progressed, the number of carcinomas arising within adenomas decreased, whereas the number of "pure" carcinomas increased. Morphometric analysis of lesions indicated hyperplasias to be small, that adenomas were larger than hyperplasias, and carcinomas were larger than adenomas and hyperplasias, suggesting that few adenomas or carcinomas arise de novo. Collectively, these data suggest that the majority of pulmonary tumors in A/J mice treated with vinyl carbamate arise as hyperplasias, progress to adenomas, and ultimately result in carcinomas. C1 EXPTL PATHOL LABS,RES TRIANGLE PK,NC. MED COLL OHIO,DEPT PATHOL,TOLEDO,OH 43699. RP FOLEY, JF (reprint author), NIEHS,NATL TOXICOL PROGRAM,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 18 TC 77 Z9 79 U1 0 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 157 EP 168 DI 10.3109/01902149109064408 PG 12 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200005 PM 2050022 ER PT J AU REHM, S DEVOR, DE HENNEMAN, JR WARD, JM AF REHM, S DEVOR, DE HENNEMAN, JR WARD, JM TI ORIGIN OF SPONTANEOUS AND TRANSPLACENTALLY INDUCED MOUSE LUNG-TUMORS FROM ALVEOLAR TYPE-II CELLS SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID SYRIAN GOLDEN-HAMSTERS; ULTRASTRUCTURAL FEATURES; N-NITROSODIETHYLAMINE; MICE; CARCINOGENESIS; ALLOANTIGEN; EXPRESSION; ANTIGEN; SKIN AB Mouse lung tumors were induced transplacentally in offspring by treating C3H/HeNCrMTV- and Swiss Webster [Tac:(SW)fBR] mice during different periods of gestation with a single i.p. injection of N-nitrosoethylurea (ENU) at 0.5 mmol or 0.74 mmol/kg. Quantitative and qualitative evaluation of the lung tumors in the offspring at ages ranging from 1 week to 52 weeks was carried out by light microscopic study of hematoxylin and eosin-stained (H&E) serial and step sections. By nitroblue tetrazolium enzyme histochemistry, 3-hydroxybutyrate dehydrogenase (seen predominantly in Clara cells) was localized in frozen tissue sections. By avidin-biotin peroxidase complex immunohistochemistry, various specific cellular and nuclear markers were investigated on paraffin sections (antisera against surfactant apoprotein, Clara cell antigen, lysozyme, and 5-bromo-2' deoxyuridine). Normal lung and lung tumors were also studied by electron microscopy. A histological method was developed to assess all lesions present in the entire lung. It was shown that solid and papillary tumor types arose individually and that mixed solid/papillary forms represented a progression of the benign solid adenoma to the malignant papillary carcinoma. Immunocytochemical localization of DNA synthesis with 5-bromo-2' deoxyuridine gave the highest labeling indices at early stages of tumor growth. As the size of the papillary tumors increased, fewer nuclei were labeled/mm2 of tumor section. Lack of both specific Clara cell antigen and 3-hydroxybutyrate dehydrogenase and the absence of typical nonosmiophilic Clara cell granules indicated a cell of origin other than Clara cells. Evidence for alveolar type II cell origin of both solid and papillary neoplasms in spontaneous and induced tumors was found in the expression of surfactant apoprotein, the presence of mature lamellar bodies (solid tumors) or small lamellar bodies, and immature stages of lamellar bodies (papillary tumors). Lysozyme was present in mature alveolar type II cells and solid tumors but absent in fetal lung and papillary neoplasms. Tumors induced on gestation day 14 or day 16 had all developed by 2 weeks of age and generally did not increase in multiplicity with age, whereas those induced on day 18 showed a protracted development with regard to frequency, growth (size), and progression. The multiplicity of mouse lung tumors induced at different stages of fetal development paralleled the number of alveolar type II precursor cells (i.e., followed a bell-shaped pattern peaking on day 16 of gestation). C1 PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. RP REHM, S (reprint author), NCI,DIV CANC ETIOL,COMPARAT CARCINOGENESIS LAB,TUMOR PATHOL & PATHOGENESIS SECT,FCRDC BLDG 538,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 36 TC 27 Z9 27 U1 0 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 181 EP 195 DI 10.3109/01902149109064410 PG 15 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200007 PM 2050024 ER PT J AU NETTESHEIM, P AF NETTESHEIM, P TI CELLS OF ORIGIN OF PRIMARY PULMONARY NEOPLASMS IN MICE SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO RP NETTESHEIM, P (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 215 EP 217 DI 10.3109/01902149109064412 PG 3 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200009 PM 2050026 ER PT J AU REHM, S KELLOFF, GJ AF REHM, S KELLOFF, GJ TI HISTOLOGIC CHARACTERIZATION OF MOUSE BRONCHIOLAR CELL HYPERPLASIA, METAPLASIA, AND NEOPLASIA INDUCED INTRATRACHEALLY BY 3-METHYLCHOLANTHRENE SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID RESPIRATORY-TRACT; LUNG-TUMORS; MICE; INDUCTION; ANTIGEN; LESIONS; ORIGIN AB Female B6C3F1 mice were treated intratracheally with 3-methylcholanthrene (MCA) at intervals of once every 2 weeks for a total of six doses each of 222-mu-g or 457-mu-g/mouse per dose. Animals were necropsied when found dead, moribund, or at the end of the study 43 weeks after the first treatment. Controls were treated with the vehicle (0.2% gelatin saline) only. Lungs were fixed in neutral buffered formalin and processed for light microscopic evaluation. Proliferative and metaplastic bronchiolar cell alterations were seen both within bronchioles and in the alveolar parenchyma. In both locations, changes included hyperplasia of nonciliated cells, squamous cell metaplasia, presence of ciliated cells, and mucous cell metaplasia. Mucous cells were either positive for alcian blue or the periodic-acid Schiff's reaction (PAS), or appeared eosinophilic with hematoxylin and eosin (H & E) but colorless with PAS. Tumors seemed to developed from both extra- and intrabronchiolar areas of cellular proliferation and invaded pulmonary structures. The majority were squamous cell carcinomas and adenosquamous carcinomas, accompanied by a few mucinous cell tumors and some rare tumors that were largely composed of ciliated cells. Combinations of the different metaplastic changes were frequently present in these neoplasms. In summary, it appears that tumors originating from bronchiolar cells in mice show the same morphologic variability that is observed in hyperplastic and metaplastic bronchiolar cells within airways. C1 NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT BRANCH,ROCKVILLE,MD. RP REHM, S (reprint author), NCI,DIV CANC ETIOL,COMPARAT CARCINOGENESIS LAB,TUMOR PATHOL & PATHOGENESIS SECT,FCRDC BLDG 538,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 20 TC 11 Z9 11 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 229 EP 244 DI 10.3109/01902149109064414 PG 16 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200011 PM 1646707 ER PT J AU BELINSKY, SA DEVEREUX, TR WHITE, CM FOLEY, JF MARONPOT, RR ANDERSON, MW AF BELINSKY, SA DEVEREUX, TR WHITE, CM FOLEY, JF MARONPOT, RR ANDERSON, MW TI ROLE OF CLARA CELLS AND TYPE-II CELLS IN THE DEVELOPMENT OF PULMONARY TUMORS IN RATS AND MICE FOLLOWING EXPOSURE TO A TOBACCO-SPECIFIC NITROSAMINE SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID CHEMICAL CARCINOGENESIS; LUNG-TUMORS; ACTIVATED ONCOGENES; RAS PROTOONCOGENE; DNA-POLYMERASE; N-NITROSAMINES; B6C3F1 MOUSE; F344 RATS; 4-(N-METHYL-N-NITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE; 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE AB The role of the Clara and type II cell in the development of pulmonary tumors in the A/J mouse and Fischer rat was investigated by determining the relationship of DNA methylation and repair in pulmonary cells to oncogene activation and by characterizing the morphology of pulmonary tumors induced by treatment with 4-(methynitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Marked differences in the formation of the promutagenic adduct O6-methylguanine (O6MG) were observed in pulmonary cells following treatment of rats with NNK. Concentrations of this adduct in Clara cells greatly exceeded (3- to 30-fold) those detected in type II cells and whole lung with doses of NNK ranging from 0.1 to 50 mg/kg. In addition, very low rates of repair of this adduct were detected in Clara cells, whereas efficient adduct removal occurred in type II cells. The importance of this adduct and the role of cell specificity was suggested by the fact that a strong correlation was observed between the concentration of O6MG in Clara cells and tumor incidence in the Fischer rat with doses of NNK ranging from 0.03-50 mg/kg. In contrast, no differences in adduct concentration between type II and Clara cells from A/J mice were observed under conditions resulting in pulmonary tumor formation. Activation of the K-ras gene was detected in lung tumors from A/J mice. This gene was activated by a mutation in codon 12 involving a GC to AT transition (GGT to GAT) and is consistent with base mispairing produced by the formation of O6MG. Activation of this gene was not associated with lung tumor formation in the Fischer rat. DNA from rat lung tumors did induce tumors in the nude mouse carcinogenicity assay. In addition, rat repetitive sequences were detected in DNA isolated from these nude mouse tumors. In spite of the cell selectivity for DNA methylation in Clara cells from rat and the relationship between O6MG formation and tumorigenicity, early proliferative lesions observed in both mice and rats involved the alveolar areas. Ultrastructural examination of these lesions and adenomas revealed morphologic features characteristic of the type II cell. Thus the lack of agreement between biochemical and morphological findings makes it difficult to hypothesize a cell of origin for the pulmonary neoplasms induced by NNK. However, these studies indicate that the concentration of O6MG in Clara cells is an excellent indicator of the carcinogenic potency of NNK in the rat. Moreover, the quantitation of DNA damage in target tissues over broad dose ranges should aid in the estimation of carcinogenic risk from exposure to environmental chemicals. C1 NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709. NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. NR 49 TC 46 Z9 46 U1 2 U2 2 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 263 EP 278 DI 10.3109/01902149109064417 PG 16 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200014 PM 2050030 ER PT J AU MARONPOT, RR PALMITER, RD BRINSTER, RL SANDGREN, EP AF MARONPOT, RR PALMITER, RD BRINSTER, RL SANDGREN, EP TI PULMONARY CARCINOGENESIS IN TRANSGENIC MICE SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID K-RAS PROTOONCOGENE; STRAIN-A MOUSE; TUMOR RESPONSE; LUNG-TUMORS; ACTIVATION; ONCOGENE; BIOASSAY; ENHANCER; PROMOTER; RATS AB Use of genetically engineered mice offers a unique approach to identifying and investigating factors that may influence tumor development. We have used conventional histopathologic and ultrastructural techniques to characterize lung tumors in three lines of transgenic mice bearing an albumin enhancer/promoter linked to a mutated human H-ras gene. Mice in all three lines developed multiple alveolar-bronchiolar (A/B) adenocarcinomas that are eventually lethal. The large diversity in tumor morphological features and differential tumor growth rates suggests that secondary events contribute to tumor phenotype and biological behavior. Two of the transgenic lines developed numerous A/B neoplasms within 6 to 8 weeks and thus may be useful animal models for testing potential anticancer chemotherapeutic agents. The other line lived for approximately 10 months, had fewer A/B tumors, but also developed bronchiogenic tumors. All three transgenic lines may be useful models for studying factors that affect lung tumor development. C1 UNIV WASHINGTON,HOWARD HUGHES MED INST,SEATTLE,WA 98195. UNIV PENN,SCH VET MED,REPROD PHYSIOL LAB,PHILADELPHIA,PA 19104. UNIV WASHINGTON,DEPT BIOCHEM,SEATTLE,WA 98195. RP MARONPOT, RR (reprint author), NIEHS,NATL TOXICOL PROGRAM,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 22 TC 21 Z9 23 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 305 EP 320 DI 10.3109/01902149109064420 PG 16 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200017 PM 2050033 ER PT J AU ANDERSON, MW AF ANDERSON, MW TI ONCOGENES, GROWTH-FACTORS, AND CELL SIGNALING IN MOUSE LUNG-TUMORS - AN OVERVIEW SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID DIFFERENTIAL EXPRESSION; CANCER; AMPLIFICATION; LINES; GENE; PROTOONCOGENES; ABNORMALITIES RP ANDERSON, MW (reprint author), NIEHS,MOLEC TOXICOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 23 TC 1 Z9 1 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 323 EP 325 DI 10.3109/01902149109064421 PG 3 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200018 PM 2050034 ER PT J AU YOU, M WANG, Y LINEEN, A STONER, GD YOU, L MARONPOT, RR ANDERSON, MW AF YOU, M WANG, Y LINEEN, A STONER, GD YOU, L MARONPOT, RR ANDERSON, MW TI ACTIVATION OF PROTOONCOGENES IN MOUSE LUNG-TUMORS SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID METHYL-N-NITROSOUREA; K-RAS PROTOONCOGENE; STRAIN-A MOUSE; ESCHERICHIA-COLI; B6C3F1 MOUSE; ONCOGENES; MUTATIONS; CARCINOGENESIS; RATS; SKIN AB The detection of activated protooncogenes in mouse lung tumors has led to a major advance in our understanding of carcinogenesis of the lung at the molecular level. A high frequency of activated K-ras protooncogenes has been detected in tetranitromethane (TNM)- and 1,3-butadiene-induced lung tumors in B6C3F1 mice. In the past several years, we have pursued protooncogene activation in spontaneous and chemically induced tumors of strain A mice. The strain A mouse has a high incidence of spontaneous lung tumors and is susceptible to tumor induction by chemical carcinogens. We have detected and characterized the activated protooncogenes in the DNA of both spontaneously occurring and chemically induced lung tumors of strain A mice. Activated K-ras genes were detected using the NIH/3T3 transfection assay, and the activating mutations were identified by utilizing the polymerase chain reaction (PCR) and direct sequence analysis. A strong selectivity of mutations in the K-ras genes were observed in chemically induced lung tumors, as compared to spontaneous tumors, indicating that the carcinogens directly induced point mutations in the K-ras protooncogene. These findings suggest that the strain A mouse lung tumor model appears to be a very sensitive system to identify the mechanism by which chemical carcinogens activate the K-ras gene in lung tissue in vivo. C1 NIEHS,MOLEC PATHOL LAB,RES TRIANGLE PK,NC 27709. NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709. RP YOU, M (reprint author), MED COLL OHIO,DEPT PATHOL,3000 ARLINGTON AVE,TOLEDO,OH 43699, USA. NR 42 TC 18 Z9 18 U1 0 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 389 EP 400 DI 10.3109/01902149109064426 PG 12 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200023 PM 2050038 ER PT J AU GRIESEMER, RA AF GRIESEMER, RA TI APPLICATIONS OF MOUSE LUNG-TUMOR MODELS - CARCINOGENESIS STUDIES SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO RP GRIESEMER, RA (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 6 TC 1 Z9 1 U1 0 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 403 EP 404 DI 10.3109/01902149109064427 PG 2 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200024 PM 2050039 ER PT J AU MARONPOT, RR AF MARONPOT, RR TI CORRELATION OF DATA FROM THE STRAIN-A MOUSE BIOASSAY WITH LONG-TERM BIOASSAYS SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID PULMONARY TUMOR RESPONSE; RAS PROTOONCOGENE; LUNG-TUMORS; MICE; CARCINOGENICITY; ACTIVATION AB Fifty-nine chemicals that had completed National Cancer Institute rat and mouse 2-year carcinogenicity tests were tested in the strain A mouse pulmonary tumor assay. Without knowledge of chemical identity, 53 chemicals were tested in strain A mice in one laboratory and 30 were tested in a second independent laboratory. Strain A tests on 24 of these chemicals were conducted in both laboratories. The strain A results were generally not predictive of the 2-year rat and mouse carcinogenicity test results. Furthermore, there was poor agreement of strain A results between the two laboratories. Although a variety of explanations may be invoked to explain the lack of concordance between the strain A tests and the 2-year rat and mouse tests, no one factor is sufficient to rationalize the poor concordance between strain A and 2-year carcinogenicity bioassay results. RP MARONPOT, RR (reprint author), NIEHS,NATL TOXICOL PROGRAM,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 15 TC 1 Z9 1 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 425 EP 431 DI 10.3109/01902149109064429 PG 7 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200026 PM 2050041 ER PT J AU ANDERSON, LM BEEBE, LE FOX, SD ISSAQ, HJ KOVATCH, RM AF ANDERSON, LM BEEBE, LE FOX, SD ISSAQ, HJ KOVATCH, RM TI PROMOTION OF MOUSE LUNG-TUMORS BY BIOACCUMULATED POLYCHLORINATED AROMATIC-HYDROCARBONS SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT SYMP ON MOUSE PULMONARY CARCINOGENESIS, TO HONOR THE MEMORY OF DR MICHAEL B SHIMKIN CY MAR 27-28, 1990 CL RESEARCH TRIANGLE PK, NC SP NIEHS, MED COLL OHIO ID BIPHENYL METABOLITE 4,4'-BIS(METHYLSULFONYL)-2,2',5,5'-TETRACHLOROBIPHENYL; MONOCLONAL-ANTIBODIES; BUTYLATED HYDROXYTOLUENE; N-NITROSODIMETHYLAMINE; BINDING-PROTEIN; LIVER-TUMORS; TARGET-CELLS; MICE; CYTOCHROME-P-450; RAT AB Lung tumors initiated in infant Swiss mice by N-nitrosodimethylamine (NDMA) were promoted by a single dose of a mixture of polychlorinated biphenyls (PCBs), Aroclor 1254 (250 or 500 mg/kg) given 4 days later. The tumors were typical alveologenic adenomas, and their number increased gradually over the course of 1 year to a maximum 4-fold enhancement in average tumor number compared with those given NDMA alone. The time course pattern suggested continuous tumor stimulation by the nonmetabolized PCB congeners retained in the tissues. Content of the nine major bioretained PCB congeners in carcass, liver, and lung was determined at intervals after treatment. Several showed tissue-specific retention patterns: 2,3,3',4,4'-PCB was selectively retained in lung and liver, and 2,2',3,4,4',5'-HCB in lung. In tests of the tumor-promoting ability of individual congeners, the 2,2',3,4,4',5'-HCB, an Ab receptor agonist, promoted lung tumors when given singly, whereas another prominent bioretained congener, the 2,2',4,4',5,5'-HCB, an Ab receptor antagonist, did not promote, and in fact abrogated the positive effect of the 2,2',3,4,4',5'-HCB. In a parallel examination of persistent biochemical effects, a single low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (5 nmole/kg) resulted in significant elevation of immunochemically detected protein and enzymatic activity of cytochrome P450 IA1 in lung for at least 12 weeks; these parameters were elevated for at least 30 weeks after a single dose of Aroclor 1254 (500 mg/kg). Taken together these results suggest that Ah-receptor-dependent induction of cytochrome P450 IA1 in mouse lung is correlated with and possibly causally involved in promotion of tumors by retained congeners. C1 PATHOL ASSOCIATES INC,FREDERICK CANC RES & DEV CTR,FT DETRICK,MD. RP ANDERSON, LM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701, USA. NR 37 TC 19 Z9 19 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 2 BP 455 EP 471 DI 10.3109/01902149109064432 PG 17 WC Respiratory System SC Respiratory System GA FC882 UT WOS:A1991FC88200029 PM 1904809 ER PT J AU SCHAPIRA, RM OSORNIOVARGAS, AR BRODY, AR AF SCHAPIRA, RM OSORNIOVARGAS, AR BRODY, AR TI INORGANIC PARTICLES INDUCE SECRETION OF A MACROPHAGE HOMOLOG OF PLATELET-DERIVED GROWTH-FACTOR IN A DENSITY-DEPENDENT AND TIME-DEPENDENT MANNER INVITRO SO EXPERIMENTAL LUNG RESEARCH LA English DT Article ID RAT ALVEOLAR MACROPHAGES; ASBESTOS; LUNG; INFLAMMATION; FIBROBLASTS; CHRYSOTILE; INHALATION; PDGF AB The inhalation of inorganic dust can lead to the development of interstitial pulmonary fibrosis, characterized by the accumulation of fibroblasts and connective tissue matrix in the lung interstitium. The fibrosis causes alterations in the architecture of the lung parenchyma, resulting in abnormal gas exchange and hypoxemia. In a rat model of asbestos exposure, inhaled fibers are deposited on alveolar duct bifurcations, followed by an accumulation of alveolar macrophages at the sites of dust deposition. The alveolar macrophage is though to be a major mediator of the pulmonary inflammatory response to inhaled dust. Platelet-derived growth factor (PDGF) is a cytokine that has potent chemotactic and mitogenic effects on mesenchymal cells, such as fibroblasts and smooth muscle cells. We studied the secretion of an alveolar macrophage-derived homologue of PDGF in response to carbonyl iron spheres or chrysotile asbestos fibers in vitro. We demonstrate here that rat alveolar macrophages attached to a plastic substrate produce 69 +/- 79 picograms (pg) of PDGF per 10 million macrophages. This is similar to amounts recovered from human platelets. In contrast, macrophages exposed to iron spheres secrete 429 +/- 177 pg of PDGF/10(6) macrophages after 24 h in culture. Exposure to asbestos fibers increased the PDGF production to 628 +/- 213 pg/10(6) cells. PDGF secretion was influenced by the particles in a density- and time-dependent manner. We hypothesize that PDGF and other cytokines secreted by macrophages mediate the development of dust-induced lung disease. C1 NIEHS,PULM PATHOBIOL LAB,POB 12233,RES TRIANGLE PK,NC 27709. DUKE UNIV,MED CTR,DIV ALLERGY CRIT CARE & RESP MED,DURHAM,NC 27710. RI Osornio Vargas, Alvaro/D-4012-2009; Osornio Vargas, Alvaro/B-4645-2010 OI Osornio Vargas, Alvaro/0000-0001-8287-7102 NR 29 TC 13 Z9 13 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 6 BP 1011 EP 1024 DI 10.3109/01902149109064332 PG 14 WC Respiratory System SC Respiratory System GA GR240 UT WOS:A1991GR24000003 PM 1663030 ER PT J AU WU, T LUNDGREN, JD RIEVES, RD DOERFLER, ME LOGUN, C SHELHAMER, JH AF WU, T LUNDGREN, JD RIEVES, RD DOERFLER, ME LOGUN, C SHELHAMER, JH TI PLATELET-ACTIVATING-FACTOR STIMULATES EICOSANOID PRODUCTION IN CULTURED FELINE TRACHEAL EXPLANTS SO EXPERIMENTAL LUNG RESEARCH LA English DT Article ID HUMAN AIRWAYS INVITRO; ARACHIDONIC-ACID METABOLITES; GUINEA-PIG LUNGS; EPITHELIAL-CELLS; MONOHYDROXYEICOSATETRAENOIC ACID; RESPIRATORY GLYCOCONJUGATE; RAT LUNGS; RELEASE; CYCLOOXYGENASE; GENERATION AB Eicosanoids have been shown to be major mediators of airway inflammation. Platelet-activating factor (PAF), a potent bronchoconstrictor and stimulator of respiratory mucous secretion, may mediate some of its effects via eicosanoid production. To explore eicosanoid generation by cultured feline tracheal explants, eicosanoids were measured following PAF stimulation. After labeling the explants with [H-3]arachidonic acid, supernatant from control and PAF treated explants was fractionated by reverse phase high-performance liquid chromatography (HPLC). The resulting elution pattern suggested the release of arachidonic acid (AA), 15-hydroxyeicosatetraenoic acid (HETE), leukotriene (LT)B4, C4, prostaglandin (PG) D2/E2/F2-alpha, and 6-keto-PGF1-alpha. Radioimmunoassay (RIA) following HPLC resolution confirmed that PAF induced a significantly increased release of peptido-leukotrienes, PGD2, PGE2, PGF2-alpha, LTB4, and 5-HETE, as well as thromboxane (TX) B2. The most remarkable increase was LTC4/D4/E4 (15 x control) and PGD2 (4 x control). The PAF antagonist Ro 19-3704 had an inhibitory effect on the PAF-stimulated release of peptido-leukotrienes. We conclude that PAF stimulates the production of a variety of lipoxygenase and cyclooxygenase pathway metabolites in feline airways. C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. OI Lundgren, Jens/0000-0001-8901-7850 NR 41 TC 10 Z9 10 U1 0 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PY 1991 VL 17 IS 6 BP 1079 EP 1094 DI 10.3109/01902149109064336 PG 16 WC Respiratory System SC Respiratory System GA GR240 UT WOS:A1991GR24000007 PM 1663033 ER PT B AU SOKOLOFF PORTER ROLAND WISE AF SOKOLOFF PORTER ROLAND WISE BE CHADWICK, DJ WHELAN, J TI BRAIN ENERGY-METABOLISM - CELL BODY OR SYNAPSE - GENERAL DISCUSSION SO EXPLORING BRAIN FUNCTIONAL ANATOMY WITH POSITRON TOMOGRAPHY SE CIBA FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT SYMP ON EXPLORING BRAIN FUNCTIONAL ANATOMY WITH POSITRON TOMOGRAPHY CY MAR 12-14, 1991 CL CIBA FDN, LONDON, ENGLAND HO CIBA FDN RP SOKOLOFF (reprint author), NIMH,CEREBRAL METAB LAB,BLDG 36,ROOM 1A05,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA CHICHESTER BN 0-471-92970-0 J9 CIBA F SYMP PY 1991 VL 163 BP 43 EP 51 PG 9 WC Medical Laboratory Technology; Neurosciences SC Medical Laboratory Technology; Neurosciences & Neurology GA BU85G UT WOS:A1991BU85G00004 ER PT J AU WATSON, JD COOKDEEGAN, RM AF WATSON, JD COOKDEEGAN, RM TI ORIGINS OF THE HUMAN GENOME PROJECT SO FASEB JOURNAL LA English DT Review DE GENE MAPPING; NIH; DOE; HUMAN GENOME ORGANIZATION ID GENETIC-LINKAGE MAP; BIOLOGY; YEAST; DNA AB The Human Genome Project has become a reality. Building on a debate that dates back to 1985, several genome projects are now in full stride around the world, and more are likely to form in the next several years. Italy began its genome program in 1987, and the United Kingdom and U.S.S.R in 1988. The European communities mounted several genome projects on yeast, bacteria, Drosophila, and Arabidospis thaliana (a rapidly growing plant with a small genome) in 1988, and in 1990 commenced a new 2-year program on the human genome. In the United States, we have completed the first year of operation of the National Center for Human Genome Research at the National Institutes of Health (NIH), now the largest single funding source for genome research in the world. There have been dedicated budgets focused on genome-scale research at NIH, the U.S. Department of Energy, and the Howard Hughes Medical Institute for several years, and results are beginning to accumulate. There were three annual meetings on genome mapping and sequencing at Cold Spring Harbor, New York, in the spring of 1988, 1989, and 1990; the talks have shifted from a discussion about how to approach problems to presenting results from experiments already performed. We have finally begun to work rather than merely talk. The purpose of genome projects is to assemble data on the structure of DNA in human chromosomes and those of other organisms. A second goal is to develop new technologies to perform mapping and sequencing. There have been impressive technical advances in the past 5 years since the debate about the human genome project began. We are on the verge of beginning pilot projects to test several approaches to sequencing long stretches of DNA, using both automation and manual methods. Ordered sets of yeast artificial chromosome and cosmid clones have been assembled to span more than 2 million base pairs of several human chromosomes, and a region of 10 million base pairs has been assembled for Caenorhabditis elegans by a collaboration between Washington University and the Medical Research Council laboratory in Cambridge, U.K. This project is now turning to sequencing C. elegans DNA as a logical extension of this work. These are but the first fruits of the genome project. There is much more to come. RP WATSON, JD (reprint author), NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892, USA. OI Cook-Deegan, Robert/0000-0002-8251-4237 NR 23 TC 35 Z9 37 U1 0 U2 34 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN PY 1991 VL 5 IS 1 BP 8 EP 11 PG 4 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ET609 UT WOS:A1991ET60900002 PM 1991595 ER PT J AU NAKAYAMA, H SHIBATA, M WOHLENBERG, C ROONEY, JF NOTKINS, AL AF NAKAYAMA, H SHIBATA, M WOHLENBERG, C ROONEY, JF NOTKINS, AL TI TRANSPLANTATION OF SYNGENEIC TRANSFECTED CELLS TO PROBE THE INVIVO IMMUNE-RESPONSE TO VIRAL-PROTEINS SO FASEB JOURNAL LA English DT Note DE CYTOTOXIC T-CELLS; INVIVO IMMUNE RESPONSE; TRANSPLANTATION; TRANSFECTED CELLS; VIRAL PROTEINS; HERPES SIMPLEX VIRUS; GLYCOPROTEIN-D ID SIMPLEX VIRUS TYPE-1; GLYCOPROTEIN-D; INFECTED-CELLS; HERPES; GD; TRANSFORMATION; LINES; MICE; GENE; DNA AB BALB/3T3 cells were transfected with the glycoprotein D(gD) gene of herpes simplex virus (HSV) and a cell line expressing gD on the cell surface was isolated. In vitro, Cr-51 release tests showed that the transfected cells were destroyed by anti-HSV antibody in the presence of complement. To investigate in vivo immune response, the gD-transfected cells were transplanted into the footpads of syngeneic HSV-immunized or unimmunized BALB/c mice. In unimmunized mice, transfected cells remained intact for 7 days or longer, and the site of injection showed only slight lymphocyte infiltration. In contrast, in immunized mice, transfected cells elicited massive lymphocyte infiltration and were mostly destroyed by day 4. Analysis of infiltrating cells revealed that they were mainly Thy1+ and CD8+ lymphoyctes along with small numbers of CD5+, CD4+, and B lymphocytes. These studies show that transfected murine cells expressing gD can be used to study the in vivo immune response to single viral proteins and they argue that the immune response contributes to the pathogenesis of HSV infection. C1 NIDR,ORAL MED LAB,BLDG 30,ROOM 121,BETHESDA,MD 20892. NR 21 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN PY 1991 VL 5 IS 1 BP 104 EP 108 PG 5 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ET609 UT WOS:A1991ET60900022 PM 1846831 ER PT J AU RAUB, WF AF RAUB, WF TI AGE-DISCRIMINATION IN NIH PEER-REVIEW SO FASEB JOURNAL LA English DT Letter RP RAUB, WF (reprint author), NIH,BETHESDA,MD 20814, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN PY 1991 VL 5 IS 1 BP 116 EP 116 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA ET609 UT WOS:A1991ET60900024 PM 1991579 ER PT B AU AARONSON, SA BOTTARO, DP MIKI, T RON, D FINCH, PW FLEMING, TP AHN, J TAYLOR, WG RUBIN, JS AF AARONSON, SA BOTTARO, DP MIKI, T RON, D FINCH, PW FLEMING, TP AHN, J TAYLOR, WG RUBIN, JS BE BAIRD, A KIAGSBRUN, M TI KERATINOCYTE GROWTH-FACTOR - A FIBROBLAST GROWTH-FACTOR FAMILY MEMBER WITH UNUSUAL TARGET-CELL SPECIFICITY SO FIBROBLAST GROWTH FACTOR FAMILY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON THE FIBROBLAST GROWTH FACTOR FAMILY CY JAN 16-18, 1991 CL LA JOLLA, CA SP NEW YORK ACAD SCI, AMER CYANAMID, FARMITALIA CARLO ERBA, HOFFMANN LA ROCHE, ICI PHARM GRP, JOHNSON & JOHNSON ETHICON, SCHERING PLOUGH RES, TAKEDA CHEM IND, WHITTIER INST, ALLERGAN RP AARONSON, SA (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,ROOM IE24,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Bottaro, Donald/F-8550-2010 OI Bottaro, Donald/0000-0002-5057-5334 NR 0 TC 139 Z9 145 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-690-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 638 BP 62 EP 77 DI 10.1111/j.1749-6632.1991.tb49018.x PG 16 WC Biochemistry & Molecular Biology; Developmental Biology SC Biochemistry & Molecular Biology; Developmental Biology GA BW41G UT WOS:A1991BW41G00009 PM 1664700 ER PT J AU CHAMULITRAT, W COHEN, MS MASON, RP AF CHAMULITRAT, W COHEN, MS MASON, RP TI FREE-RADICAL FORMATION FROM ORGANIC HYDROPEROXIDES IN ISOLATED HUMAN POLYMORPHONUCLEAR NEUTROPHILS SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE ORGANIC HYDROPEROXIDES; MYELOPEROXIDASE; HUMAN POLYMORPHONUCLEAR NEUTROPHILS; FREE RADICALS; SPIN TRAPPING AB We have demonstrated with electron paramagnetic resonance (EPR) that organic hydroperoxides are decomposed to free radicals by both human polymorphonuclear leukocytes (PMNs) and purified myeloperoxidase. When tert-butyl hydroperoxide was incubated with either PMNs or purified myeloperoxidase, peroxyl, alkoxyl, and alkyl radicals were trapped by the spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO). In the case of ethyl hydroperoxide, DMPO radical adducts of peroxyl and alkyl (identified as alpha-hydroxyethyl when trapped by tert-nitrosobutane) radicals were detected. Radical adduct formation was inhibited when azide was added to the incubation mixture. Myeloperoxidase-deficient PMNs produced DMPO radical adduct intensities at only about 20-30% of that of normal PMNs. Our studies suggest that myeloperoxidase in PMNs is primarily responsible for the decomposition of organic hydroperoxides to free radicals. The finding of the free radical formation derived from organic hydroperoxides by PMNs may be related to the cytotoxicity of this class of compounds. RP CHAMULITRAT, W (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU NIAID NIH HHS [AI23939] NR 0 TC 22 Z9 22 U1 0 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1991 VL 11 IS 5 BP 439 EP 445 DI 10.1016/0891-5849(91)90059-C PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA GU411 UT WOS:A1991GU41100001 PM 1663060 ER PT J AU MESSINA, MJ AF MESSINA, MJ TI OXIDATIVE STRESS STATUS AND CANCER - METHODOLOGY APPLICABLE FOR HUMAN STUDIES SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE FREE-RADICAL; OXIDATIVE STRESS STATUS; CANCER AB There is convincing evidence to suggest that oxidative stress status might be involved in the etiology of cancer, but relatively little direct human data are available. The National Cancer Institute recently sponsored a workshop evaluating methodology for measuring oxidative stress status with potential application to human studies. RP MESSINA, MJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,DIET & CANC BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 9 Z9 9 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1991 VL 10 IS 3-4 BP 175 EP 176 DI 10.1016/0891-5849(91)90072-B PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA FD464 UT WOS:A1991FD46400002 PM 1864522 ER PT J AU RUSSELL, P YAMADA, T XU, GT GARLAND, D ZIGLER, JS AF RUSSELL, P YAMADA, T XU, GT GARLAND, D ZIGLER, JS TI EFFECTS OF NAPHTHALENE METABOLITES ON CULTURED-CELLS FROM EYE LENS SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE NAPHTHALENE; DIAPHORASE; GLUTATHIONE; GLUTATHIONE REDUCTASE; LENS; FREE RADICALS AB Naphthalene is toxic to the eye and results in opacification of the lens. To investigate the metabolic events that may be occurring in the lens epithelial cells, a cell line of lens from a transgenic mouse was incubated with various metabolites of naphthalene. Naphthoquinone at 50-mu-M was toxic to most cells with a depletion of glutathione levels noted within 6 h of incubation. At 10-mu-M, naphthoquinone caused an increase in specific activity of the enzyme DT-diaphorase. This enzyme is thought to be a defense against quinones since semiquinone formation is thought to be lessened. Naphthalene-1,2-dihydrodiol at 50-mu-M also caused an increase in the specific activity of the DT-diaphorase, while at 10-mu-M no apparent change occurred in the cells. Although there was evidence of metabolic alterations in the cells with the metabolites of naphthalene, the protein profile by two-dimensional gel electrophoresis did not change and there was no indication of an increase in carbonyl formation in the soluble proteins of the cells. These experiments indicate that the metabolites of naphthalene can cause alteration in the metabolism of the lens cells but may not cause apparent changes in the major proteins within the lens epithelium. RP RUSSELL, P (reprint author), NEI,BLDG 6,RM 228,BETHESDA,MD 20892, USA. NR 0 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 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1991 VL 10 IS 5 BP 255 EP 261 DI 10.1016/0891-5849(91)90032-X PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA FG994 UT WOS:A1991FG99400001 PM 1906827 ER PT J AU SAMUNI, A KRISHNA, CM COOK, J BLACK, CDV RUSSO, A AF SAMUNI, A KRISHNA, CM COOK, J BLACK, CDV RUSSO, A TI ON RADICAL PRODUCTION BY PMA-STIMULATED NEUTROPHILS AS MONITORED BY LUMINOL-AMPLIFIED CHEMILUMINESCENCE SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE SPIN TRAPPING; SUPEROXIDE RADICAL; CYTOCHROME-C; RESPIRATORY BURST; POLYMORPHONUCLEAR LEUKOCYTES; ELECTRON SPIN RESONANCE; HYDROGEN PEROXIDE; FREE RADICALS AB The means by which neutrophils within the body ward off infectious and neoplastic processes by the activation of molecular oxygen, as well as how such mechanisms dysfunction, is the subject of extensive ongoing research. Most previous studies of neutrophil activation indicate that there is a transient production of reactive oxygen species. Luminol-amplified chemiluminescence surveillance of O2.- and H2O2 supported these general findings. Yet, recent studies showed that production of reactive oxygen species by PMA-stimulated neutrophils is not transient but persistent; however, luminol-dependent methods do not corroborate such findings. The kinetics of O2.- production by human neutrophils were studied using luminol-amplified chemiluminescence (CL), spin trapping combined with electron spin resonance detection, and ferricytochrome c reduction. The effects of pH and O2 level on luminol-amplified CL were determined using hypoxanthine/xanthine oxidase to produce O2.- and H2O2 in cell-free systems. As we have found by electron spin resonance and ferricytochrome c reduction, stimulated neutrophils continued to generate O2.- for several hours, yet when luminol-amplified CL was used to continuously follow radical production, CL was shortly lost. Similar loss of CL was observed with continuous enzymatic formation of O2.- and H2O2. The failure of the CL assay to report O2.- and H2O2 formation results from some luminol reaction product which interferes with the light reaction. Our results show that the cells are operative for long periods indicating that cell exposure to prolonged O2.- fluxes does not terminate radical production, and even when pH, [O2], and reagents are optimized, the use of luminol-amplified CL is not a valid assay for continuous monitoring of O2.- and H2O2 generated by either stimulated neutrophils or in cell-free systems. C1 NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,RADIAT ONCOL BRANCH,BLDG 10,ROOM B3-B69,9000 ROCKVILLE,BETHESDA,MD 20892. NR 0 TC 31 Z9 31 U1 1 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1991 VL 10 IS 5 BP 305 EP 313 DI 10.1016/0891-5849(91)90037-4 PG 9 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA FG994 UT WOS:A1991FG99400006 PM 1649785 ER PT J AU SINHA, BK AF SINHA, BK TI CYTOCHROME P-450-DEPENENT AND PEROXIDASE-DEPENDENT ACTIVATION OF PROCARBAZINE AND IPRONIAZID IN MAMMALIAN-CELLS SO FREE RADICAL RESEARCH COMMUNICATIONS LA English DT Article DE PROCARBAZINE; IPRONIAZID; P-450-ENZYMES ID HYDRAZINE DERIVATIVES; METABOLIC-ACTIVATION; OXIDATIVE-METABOLISM; LIVER-MICROSOMES; FREE-RADICALS; RAT-LIVER; HYDRALAZINE; BINDING RP SINHA, BK (reprint author), NCI,CLIN PHARMACOL BRANCH,BIOLCHEM & MOLEC PHARMACOL SECT,BLDG 10,ROOM 6N-119,BETHESDA,MD 20892, USA. NR 18 TC 8 Z9 8 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 8755-0199 J9 FREE RADICAL RES COM JI Free Radic. Res. Commun. PY 1991 VL 15 IS 4 BP 189 EP 195 DI 10.3109/10715769109049140 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GW778 UT WOS:A1991GW77800001 PM 1667771 ER PT J AU RESZKA, K CHIGNELL, CF AF RESZKA, K CHIGNELL, CF TI SPIN-TRAPPING OF THE SUPEROXIDE RADICAL IN APROTIC-SOLVENTS SO FREE RADICAL RESEARCH COMMUNICATIONS LA English DT Article DE EPR; SPIN TRAPPING; SUPEROXIDE RADICAL; 5,5-DIMETHYL-1-PYRROLINE-N-OXIDE ID RESONANCE SPECTROSCOPY; HYDROPEROXIDES; PEROXYL; ALKOXYL; PHOTOLYSIS; SYSTEMS; BREAKDOWN; HEMATIN C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NR 28 TC 27 Z9 27 U1 0 U2 2 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 8755-0199 J9 FREE RADICAL RES COM JI Free Radic. Res. Commun. PY 1991 VL 14 IS 2 BP 97 EP 106 DI 10.3109/10715769109094122 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FK164 UT WOS:A1991FK16400003 PM 1648022 ER PT J AU BLACK, CDV COOK, JA RUSSO, A SAMUNI, A AF BLACK, CDV COOK, JA RUSSO, A SAMUNI, A TI SUPEROXIDE PRODUCTION BY STIMULATED NEUTROPHILS - TEMPERATURE EFFECT SO FREE RADICAL RESEARCH COMMUNICATIONS LA English DT Article; Proceedings Paper CT 5TH INTERNATIONAL CONF ON SUPEROXIDE AND SUPEROXIDE DISMUTASE CY SEP 17-22, 1989 CL JERUSALEM, ISRAEL DE ELECTRON PARAMAGNETIC RESONANCE; RESPIRATORY BURST; CYTOCHROME-C; LEUKOCYTES ID SPIN-RESONANCE SPECTROSCOPY; HYDROXYL RADICAL PRODUCTION; CHEMI-LUMINESCENCE; GENERATING-SYSTEM; LEUCYL-PHENYLALANINE; TRAPPING TECHNIQUES; RESPIRATORY BURST; OXIDASE; OXYGEN; MECHANISMS C1 HEBREW UNIV JERUSALEM,SCH MED,DEPT MOLEC BIOL,IL-91010 JERUSALEM,ISRAEL. NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NR 33 TC 11 Z9 11 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 8755-0199 J9 FREE RADICAL RES COM JI Free Radic. Res. Commun. PY 1991 VL 12-3 BP 27 EP 37 DI 10.3109/10715769109145764 PN 1 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FK861 UT WOS:A1991FK86100005 PM 1649095 ER PT J AU SAMUNI, A MITCHELL, JB DEGRAFF, W KRISHNA, CM SAMUNI, U RUSSO, A AF SAMUNI, A MITCHELL, JB DEGRAFF, W KRISHNA, CM SAMUNI, U RUSSO, A TI NITROXIDE SOD-MIMICS - MODES OF ACTION SO FREE RADICAL RESEARCH COMMUNICATIONS LA English DT Article; Proceedings Paper CT 5TH INTERNATIONAL CONF ON SUPEROXIDE AND SUPEROXIDE DISMUTASE CY SEP 17-22, 1989 CL JERUSALEM, ISRAEL DE SUPEROXIDE; SUPEROXIDE DISMUTASE MIMIC; ESR; SPIN-LABELS; NITROXIDES; TERT-BUTYL HYDROPEROXIDE; CYTOTOXICITY ID CYTO-TOXICITY; SUPEROXIDE; DESFERRIOXAMINE; HYDROPEROXIDE; COMPLEXES; CELLS C1 HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. RP SAMUNI, A (reprint author), NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892, USA. NR 21 TC 91 Z9 92 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 8755-0199 J9 FREE RADICAL RES COM JI Free Radic. Res. Commun. PY 1991 VL 12-3 BP 187 EP 194 DI 10.3109/10715769109145785 PN 1 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FK861 UT WOS:A1991FK86100026 PM 1649088 ER PT J AU RIFKIND, JM ZHANG, L LEVY, A MANOHARAN, PT AF RIFKIND, JM ZHANG, L LEVY, A MANOHARAN, PT TI THE HYPOXIC STRESS ON ERYTHROCYTES ASSOCIATED WITH SUPEROXIDE FORMATION SO FREE RADICAL RESEARCH COMMUNICATIONS LA English DT Article; Proceedings Paper CT CONF ON SUPEROXIDE AND SUPEROXIDE DISMUTASE CY SEP, 1989 CL ISRAEL DE ERYTHROCYTES; SUPEROXIDE; LYSIS; HYPOXIA; OXYGEN; OXIDATION ID HEMOGLOBIN; NEUTROPHILS; MEMBRANE; BAND-3 C1 INDIAN INST TECHNOL,DEPT CHEM,MADRAS 600036,TAMIL NADU,INDIA. RP RIFKIND, JM (reprint author), NIA,GERONTOL RES CTR,CELLULAR & MOLEC BIOL LAB,BALTIMORE,MD 21224, USA. NR 23 TC 40 Z9 41 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 8755-0199 J9 FREE RADICAL RES COM JI Free Radic. Res. Commun. PY 1991 VL 12-3 BP 645 EP 652 PN 2 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FK864 UT WOS:A1991FK86400025 PM 1648015 ER PT J AU MEZEY, E PALKOVITS, M AF MEZEY, E PALKOVITS, M TI CRF-CONTAINING NEURONS IN THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS - REGULATION, ESPECIALLY BY CATECHOLAMINES SO FRONTIERS IN NEUROENDOCRINOLOGY LA English DT Review DE CRF; EPINEPHRINE; NOREPINEPHRINE; PARAVENTRICULAR NUCLEI ID CORTICOTROPIN-RELEASING-FACTOR; FACTOR MESSENGER-RNA; PARVOCELLULAR NEUROSECRETORY NEURONS; CENTRAL NERVOUS-SYSTEM; SUPRAOPTIC NUCLEI; RAT HYPOTHALAMUS; NEUROPEPTIDE-Y; IMMUNOREACTIVE NEURONS; GLUCOCORTICOID RECEPTOR; HORMONE-SECRETION AB The neurons in the paraventricular nucleus that contain corticotropin-releasing factor (CRF) are regulated by humoral and neural inputs. Considerable evidence suggests that glucocorticoids act directly on these neurons to decrease their production of CRF. The paraventricular nuclei contain many peptides in addition to CRF and many different transmitters are found in afferent neurons that converge on them. These afferents include neurons from the subfornical organ that contain angiotensin II, neurons from the septum and elsewhere that contain enkephalin and substance P, neurons from the mesencephalon that contain serotonin, and neurons from the medulla oblongata that contain norepinephrine and epinephrine. The effects of catecholamines on CRF secretion remain controversial. Unilateral section of ascending norepinephrine-containing neurons leads to an ipsilateral decrease in paraventricular CRF content. However, there is appreciable evidence that epinephrine-containing neurons inhibit CRF secretion. A reasonable working hypothesis to explain the conflicting data is that there is a dual control: norepinephrine release from ascending neurons stimulates CRF secretion whereas epinephrine release inhibits CRF secretion. C1 SEMMELWEIS UNIV MED,SCH MED,DEPT ANAT 1,H-1085 BUDAPEST 8,HUNGARY. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RI Palkovits, Miklos/F-2707-2013; OI Palkovits, Miklos/0000-0003-0578-0387 NR 107 TC 44 Z9 44 U1 0 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0091-3022 J9 FRONT NEUROENDOCRIN JI Front. Neuroendocrinol. PD JAN PY 1991 VL 12 IS 1 BP 23 EP 37 PG 15 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA FM608 UT WOS:A1991FM60800002 ER PT J AU DAHL, AR SCHLESINGER, RB HECK, HD MEDINSKY, MA LUCIER, GW AF DAHL, AR SCHLESINGER, RB HECK, HD MEDINSKY, MA LUCIER, GW TI SYMPOSIUM OVERVIEW - COMPARATIVE DOSIMETRY OF INHALED MATERIALS - DIFFERENCES AMONG ANIMAL SPECIES AND EXTRAPOLATION TO MAN SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID DNA ADDUCTS; PARTITION-COEFFICIENTS; B6C3F1 MICE; RATS; METABOLISM; BENZENE; LUNG; SENSITIVITY; DEPOSITION; AEROSOLS C1 NIEHS,RES TRIANGLE PK,NC 27709. CHEM IND INST TOXICOL,RES TRIANGLE PK,NC 27709. NYU MED CTR,INST ENVIRONM MED,NEW YORK,NY 10016. RP DAHL, AR (reprint author), LOVELACE INHALAT TOXICOL RES INST,POB 5890,ALBUQUERQUE,NM 87185, USA. NR 38 TC 16 Z9 16 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1991 VL 16 IS 1 BP 1 EP 13 DI 10.1016/0272-0590(91)90125-N PG 13 WC Toxicology SC Toxicology GA ER182 UT WOS:A1991ER18200001 PM 2019334 ER PT J AU MAHAFFEY, KR AF MAHAFFEY, KR TI BIOKINETICS OF LEAD DURING PREGNANCY SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID MOBILIZATION; CADMIUM; BLOOD RP MAHAFFEY, KR (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 10 TC 16 Z9 18 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 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1991 VL 16 IS 1 BP 15 EP 16 DI 10.1016/0272-0590(91)90127-P PG 2 WC Toxicology SC Toxicology GA ER182 UT WOS:A1991ER18200003 PM 2019340 ER PT J AU DUNNICK, JK FORBES, PD EUSTIS, SL HARDISTY, JF GOODMAN, DG AF DUNNICK, JK FORBES, PD EUSTIS, SL HARDISTY, JF GOODMAN, DG TI TUMORS OF THE SKIN IN THE HRA SKH MOUSE AFTER TREATMENT WITH 8-METHOXYPSORALEN AND UVA RADIATION SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID ULTRAVIOLET-RADIATION; HAIRLESS MICE; MUTANT MICE; PHOTOCARCINOGENESIS C1 PATHCO INC,GAITHERSBURG,MD 20879. TEMPLE UNIV,HLTH SCI CTR,PHILADELPHIA,PA 19122. EXPTL PATHOL LABS,RES TRIANGLE PK,NC 27709. RP DUNNICK, JK (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 21 TC 29 Z9 29 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1991 VL 16 IS 1 BP 92 EP 102 DI 10.1016/0272-0590(91)90138-T PG 11 WC Toxicology SC Toxicology GA ER182 UT WOS:A1991ER18200014 PM 2019354 ER PT J AU GAWORSKI, CL ARANYI, C VANA, S RAJENDRAN, N ABDO, K LEVINE, BS HALL, A AF GAWORSKI, CL ARANYI, C VANA, S RAJENDRAN, N ABDO, K LEVINE, BS HALL, A TI PRECHRONIC INHALATION TOXICITY STUDIES OF 2-MERCAPTOBENZIMIDAZOLE (2-MBI) IN F344/N RATS SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article C1 IIT,RES INST,10 W 35TH ST,CHICAGO,IL 60616. NIEHS,NATL TOXICOL PROGRAM,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. UNIV ILLINOIS,CHICAGO,IL 60612. PATHOL ASSOCIATES INC,CHICAGO,IL 60616. FU NIEHS NIH HHS [N01-ES-65135] NR 17 TC 7 Z9 8 U1 0 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD JAN PY 1991 VL 16 IS 1 BP 161 EP 171 DI 10.1016/0272-0590(91)90144-S PG 11 WC Toxicology SC Toxicology GA ER182 UT WOS:A1991ER18200020 PM 2019341 ER PT J AU WINTER, HS HENDREN, RB FOX, CH RUSSELL, GJ PEREZATAYDE, A BHAN, AK FOLKMAN, J AF WINTER, HS HENDREN, RB FOX, CH RUSSELL, GJ PEREZATAYDE, A BHAN, AK FOLKMAN, J TI HUMAN INTESTINE MATURES AS NUDE-MOUSE XENOGRAFT SO GASTROENTEROLOGY LA English DT Article ID NORMAL COLONIC MUCOSA; ATHYMIC MICE; ADENOMATOUS POLYPS; TRANSPLANTATION; DIFFERENTIATION; ADENOCARCINOMA; ANTIBODIES; RATS C1 CHILDRENS HOSP MED CTR,DEPT SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP WINTER, HS (reprint author), CHILDRENS HOSP MED CTR,DEPT PEDIAT,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI27747]; NIDDK NIH HHS [DK33506] NR 19 TC 36 Z9 37 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 1991 VL 100 IS 1 BP 89 EP 98 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA EM765 UT WOS:A1991EM76500013 PM 1983853 ER PT J AU SAXE, CL JOHNSON, RL DEVREOTES, PN KIMMEL, AR AF SAXE, CL JOHNSON, RL DEVREOTES, PN KIMMEL, AR TI EXPRESSION OF A CAMP RECEPTOR GENE OF DICTYOSTELIUM AND EVIDENCE FOR A MULTIGENE FAMILY SO GENES & DEVELOPMENT LA English DT Article DE CAMP; RECEPTORS; GENE EXPRESSION; DICTYOSTELIUM ID SIGNAL-TRANSDUCTION PATHWAYS; CYCLIC-AMP RECEPTORS; CELL-SURFACE; ADENYLATE-CYCLASE; MESSENGER-RNAS; DISCOIDEUM; MUTANTS; DIFFERENTIATION; SEQUENCES; PULSES AB We have previously reported the cloning of cDNAs for a Dictyostelium cell-surface cAMP receptor that is a member of the family of G-protein-linked receptors. Here, we report the organization and the developmental expression of this cAMP receptor gene, designated CAR1. CAR1 is a single copy gene that contains two intervening sequences. CAR1 mRNA levels are low in growing cells, rise to peak expression at 5-10 hr of development when the cAMP signaling system is maximally active, and decrease as development proceeds. At 5 hr the predominant mRNA species is approximately 1.9 kb, by 10 hr the mRNA is heterogeneous with sizes of approximately 1.9-2.1 kb, but during culmination only the 2.1 kb mRNA is detected. The variety of mRNA sizes results from differences in 5'-untranslated regions. Studies using developmental mutants with aberrant cAMP-signaling patterns indicate that pulsatile action of cAMP promotes maximal expression of CAR1 during early development. Low stringency hybridization of CAR1 probes to genomic DNA detects additional, related sequences, suggesting that there are several genes that encode a family of structurally similar receptors. Multiple functions previously attributed to the cAMP receptor instead may be fulfilled by distinct receptor subtypes encoded by specific genes. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205. RP SAXE, CL (reprint author), NIDDK,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892, USA. NR 36 TC 92 Z9 93 U1 1 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD JAN PY 1991 VL 5 IS 1 BP 1 EP 8 DI 10.1101/gad.5.1.1 PG 8 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA EV409 UT WOS:A1991EV40900001 PM 1989903 ER PT J AU SELBY, JV REED, T NEWMAN, B FABSITZ, RR CARMELLI, D AF SELBY, JV REED, T NEWMAN, B FABSITZ, RR CARMELLI, D TI EFFECTS OF SELECTIVE RETURN ON ESTIMATES OF HERITABILITY FOR BODY-MASS INDEX IN THE NATIONAL-HEART-LUNG-AND-BLOOD-INSTITUTE TWIN STUDY SO GENETIC EPIDEMIOLOGY LA English DT Article DE BIAS; LONGITUDINAL STUDIES; OBESITY; TWIN STUDIES ID RISK-FACTORS; NHLBI TWIN; DISEASE AB In the National Heart, Lung, and Blood Institute Twin Study, body mass index (BMI) was studied at military induction and at three subsequent examinations spanning five decades in a cohort of white, male World War II veterans. At military induction (1940s) and again at the first clinical examination of this study (1969-1973), there was close agreement of three commonly used estimates of heritability (range 0.72 to 0.80), and no evidence of a difference in total variance of BMI between the zygosities. However, at the last two examinations (1980s), the total variance in dizygotic (DZ) twins was significantly greater than that of monozygotic (MZ) twins (P < 0.01) and these same heritability estimates varied widely. The among-pair estimate of heritability fell to unrealistic negative values, the within-pair estimate rose to values of 1.0 or greater, and the intraclass correlation coefficient estimate was slightly lower than in the entire cohort at baseline. The cause of the unequal zygosity total variance appears to have been nonparticipation at later examinations of MZ twins with extreme values of BMI, with no evidence of a similar selection process influencing DZ twins. This selection process biased the three estimates of heritability, making it difficult to determine which estimate is the most appropriate. Despite these biases, it remains clear that genetic factors contribute substantially to BMI in this population. C1 INDIANA UNIV,SCH MED,DEPT MED GENET,INDIANAPOLIS,IN 46202. UNIV N CAROLINA,SCH PUBL HLTH,CHAPEL HILL,NC 27514. NHLBI,BETHESDA,MD 20892. SRI INT,MENLO PK,CA 94025. RP SELBY, JV (reprint author), KAISER PERMANENT,MED CARE PROGRAM,DIV RES,3451 PIEDMONT AVE,OAKLAND,CA 94611, USA. NR 13 TC 12 Z9 12 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1991 VL 8 IS 6 BP 371 EP 380 DI 10.1002/gepi.1370080603 PG 10 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA HF696 UT WOS:A1991HF69600002 PM 1806406 ER PT B AU PAVLAKIS, GN SCHWARTZ, S BENKO, DM DRYSDALE, CM SOLOMIN, L CIMINALE, V ROBINSON, R HARRISON, J CAMPBELL, M FELBER, BK AF PAVLAKIS, GN SCHWARTZ, S BENKO, DM DRYSDALE, CM SOLOMIN, L CIMINALE, V ROBINSON, R HARRISON, J CAMPBELL, M FELBER, BK BE HASELTINE, WA WONGSTAAL, F TI GENOME ORGANIZATION AND REGULATION OF HIV-1 EXPRESSION SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP PAVLAKIS, GN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BASIC RES PROGRAM,POB B,BLDG 539,ROOM 121,FREDERICK,MD 21702, USA. NR 0 TC 5 Z9 5 U1 0 U2 1 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 175 EP 192 PG 18 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00009 ER PT B AU FELBER, BK SOLOMIN, L CIMINALE, V UNGE, T BENKO, DM HARRISON, J CAMPBELL, M PAVLAKIS, GN AF FELBER, BK SOLOMIN, L CIMINALE, V UNGE, T BENKO, DM HARRISON, J CAMPBELL, M PAVLAKIS, GN BE HASELTINE, WA WONGSTAAL, F TI MECHANISM OF FUNCTION OF THE REX PROTEIN OF HTLV-1 SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP FELBER, BK (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BASIC RES PROGRAM,POB B,BLDG 539,ROOM 121,FREDERICK,MD 21702, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 193 EP 204 PG 12 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00010 ER PT B AU BERKHOUT, B JEANG, KT AF BERKHOUT, B JEANG, KT BE HASELTINE, WA WONGSTAAL, F TI TAT MEDIATED TRANSACTIVATION IS A PRE-SPLICING EVENT THAT REQUIRES A FUNCTIONAL HIV-1 TATAA ELEMENT SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP BERKHOUT, B (reprint author), NIAID,MOLEC MICROBIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 205 EP 220 PG 16 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00011 ER PT B AU DERSE, D CARROLL, R CARVALHO, M DASILVA, L MARTARANO, L AF DERSE, D CARROLL, R CARVALHO, M DASILVA, L MARTARANO, L BE HASELTINE, WA WONGSTAAL, F TI FUNCTIONAL TOPOGRAPHY OF LENTIVIRUS TAT PROTEINS DEFINED BY DOMAIN SWITCHING SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP DERSE, D (reprint author), NCI,VIRAL CARCINOGENESIS LAB,7TH ST,FREDERICK,MD 21702, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 251 EP 261 PG 11 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00014 ER PT B AU VENKATESAN, S HOLLAND, SM NEBREDA, AR MAITRA, RK AHMAD, N PARK, H WINGFIELD, P SANTOS, E AF VENKATESAN, S HOLLAND, SM NEBREDA, AR MAITRA, RK AHMAD, N PARK, H WINGFIELD, P SANTOS, E BE HASELTINE, WA WONGSTAAL, F TI REGULATION OF THE HIV GENOME - FUNCTIONAL-STUDIES OF REV, NEF AND CIS REGULATORY SEQUENCES SO GENETIC STRUCTURE AND REGULATION OF HIV SE HARVARD AIDS INSTITUTE SERIES ON GENE REGULATION OF HUMAN RETROVIRUSES LA English DT Proceedings Paper CT WORKSHOP ON GENETIC STRUCTURE AND REGULATION OF HIV CY NOV 05-07, 1990 CL BABSON COLL, WELLESLEY, MA SP HARVARD AIDS INST, ABBOTT LAB, WYETH AYERST RES, LILLY RES LAB, GLAXO RES LAB, MERCK SHARP & DOHME RES LAB HO BABSON COLL RP VENKATESAN, S (reprint author), NIAID,MOLEC MICROBIOL LAB,BLDG 4,ROOM 328,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI NEW YORK PA NEW YORK BN 0-88167-826-0 J9 HARV AIDS G PY 1991 VL 1 BP 323 EP 344 PG 22 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Medicine, Research & Experimental; Microbiology; Virology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology; Research & Experimental Medicine; Microbiology; Virology GA BT92B UT WOS:A1991BT92B00019 ER PT J AU STRATHERN, JN WEINSTOCK, KG HIGGINS, DR MCGILL, CB AF STRATHERN, JN WEINSTOCK, KG HIGGINS, DR MCGILL, CB TI A NOVEL RECOMBINATOR IN YEAST BASED ON GENE-II PROTEIN FROM BACTERIOPHAGE-F1 SO GENETICS LA English DT Article ID DOUBLE-STRAND BREAKS; RNA POLYMERASE-I; SACCHAROMYCES-CEREVISIAE; FLP RECOMBINASE; MITOTIC RECOMBINATION; FILAMENTOUS PHAGE-F1; INITIATOR PROTEIN; RIBOSOMAL DNA; S-CEREVISIAE; MAT LOCUS AB Interchromosomal mitotic recombination in yeast can be stimulated by the protein encoded by gene II of bacteriophage f1. The normal role of the gene II enzyme is to make a site-specific cleavage of a particular strand of the duplex form the bacteriophage DNA at the origin of DNA replication. The gene II protein was expressed in yeast in an attempt to determine the role of nicked DNA in the initiation of recombination. Stimulation of recombination in yeast by the gene II protein was dependent on the presence of a recognition site for gene II enzyme in the region being assayed. Recombination was stimulated in both directions from the gene II recognition site but showed a directional bias. The distribution of alleles among the recombinants indicated that the chromosome with the gene II recognition site acted as the recipient in gene conversion events. RP STRATHERN, JN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BASIC RES PROGRAM,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74101] NR 61 TC 37 Z9 37 U1 0 U2 0 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD JAN PY 1991 VL 127 IS 1 BP 61 EP 73 PG 13 WC Genetics & Heredity SC Genetics & Heredity GA EP811 UT WOS:A1991EP81100007 PM 2016047 ER PT J AU SIRACUSA, LD JENKINS, NA COPELAND, NG AF SIRACUSA, LD JENKINS, NA COPELAND, NG TI IDENTIFICATION AND APPLICATIONS OF REPETITIVE PROBES FOR GENE-MAPPING IN THE MOUSE SO GENETICS LA English DT Article ID MURINE LEUKEMIA-VIRUS; INTERSPECIFIC BACKCROSS ANALYSIS; TRIOSE PHOSPHATE ISOMERASE; BASIC-PROTEIN GENE; TRIOSEPHOSPHATE ISOMERASE; MUS-MUSCULUS; LINKAGE MAP; LOCALIZATION; CHROMOSOME-6; INTEGRATION AB Interspecific mouse hybrids that are viable and fertile provide a wealth of genetic variation that is useful for gene mapping. We are using this genetic variation to develop multilocus linkage maps of the mouse genome. As an outgrowth of this work, we have identified three repetitive probes that collectively identify 28 loci dispersed on 16 of the 19 mouse autosomes and the X chromosome. These loci establish a skeleton linkage map that can be used to detect linkage over much of the mouse genome. The molecular probes are derived from the mouse mammary tumor virus envelope gene, the ornithine decarboxylase gene, and the triose phosphate isomerase gene. The ability to scan the mouse genome quickly and efficiently in an interspecific cross using these three repetitive probes makes this system a powerful tool for identifying the chromosomal location of mutations that have yet to be cloned, mapping multigenic traits, and identifying recessive protooncogene loci associated with murine neoplastic disease. Ultimately, interspecific hybrids in conjunction with repetitive and single-copy probes will provide a rapid means to access virtually any gene of interest in the mouse genome at the molecular level. RP SIRACUSA, LD (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABI BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101]; NIGMS NIH HHS [GM12721-01] NR 55 TC 96 Z9 96 U1 0 U2 0 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD JAN PY 1991 VL 127 IS 1 BP 169 EP 179 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA EP811 UT WOS:A1991EP81100016 PM 1673105 ER PT B AU SNOW, JB AF SNOW, JB BE RUBEN, RJ VANDEWATER, TR STEEL, KP TI INTERNATIONAL-SYMPOSIUM ON THE GENETICS OF HEARING IMPAIRMENT - INTRODUCTION SO GENETICS OF HEARING IMPAIRMENT SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Editorial Material CT CONF ON GENETICS OF HEARING IMPAIRMENT CY SEP 24-26, 1990 CL NEW YORK, NY SP NEW YORK ACAD SCI, DEAFNESS RES FDN, NIH NIDCD RP SNOW, JB (reprint author), NIDCD,ROOM B2C-02,BLDG 31,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-682-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 630 BP 1 EP 2 DI 10.1111/j.1749-6632.1991.tb19569.x PG 2 WC Genetics & Heredity; Neurosciences; Otorhinolaryngology SC Genetics & Heredity; Neurosciences & Neurology; Otorhinolaryngology GA BW41A UT WOS:A1991BW41A00001 ER PT B AU PARRY, DM KAISERKUPFER, MI SHERMAN, JL PIKUS, A ELDRIDGE, R AF PARRY, DM KAISERKUPFER, MI SHERMAN, JL PIKUS, A ELDRIDGE, R BE RUBEN, RJ VANDEWATER, TR STEEL, KP TI NEUROFIBROMATOSIS-2 (BILATERAL ACOUSTIC OR CENTRAL NEUROFIBROMATOSIS), A TREATABLE CAUSE OF DEAFNESS - RECOMMENDATIONS FOR SCREENING AND FOLLOW-UP BASED ON STUDY OF ONE LARGE KINDRED SO GENETICS OF HEARING IMPAIRMENT SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON GENETICS OF HEARING IMPAIRMENT CY SEP 24-26, 1990 CL NEW YORK, NY SP NEW YORK ACAD SCI, DEAFNESS RES FDN, NIH NIDCD RP PARRY, DM (reprint author), NCI,CLIN EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 400,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-682-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 630 BP 305 EP 307 DI 10.1111/j.1749-6632.1991.tb19615.x PG 3 WC Genetics & Heredity; Neurosciences; Otorhinolaryngology SC Genetics & Heredity; Neurosciences & Neurology; Otorhinolaryngology GA BW41A UT WOS:A1991BW41A00047 PM 1952615 ER PT B AU PIKUS, A AF PIKUS, A BE RUBEN, RJ VANDEWATER, TR STEEL, KP TI AUDIOLOGICAL PROFILE IN NIEMANN-PICK-C SO GENETICS OF HEARING IMPAIRMENT SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON GENETICS OF HEARING IMPAIRMENT CY SEP 24-26, 1990 CL NEW YORK, NY SP NEW YORK ACAD SCI, DEAFNESS RES FDN, NIH NIDCD RP PIKUS, A (reprint author), NIDCD,AUDIOL CLIN,BLDG 10,ROOM 5C306,BETHESDA,MD 20892, USA. NR 0 TC 7 Z9 8 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-682-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 630 BP 313 EP 314 DI 10.1111/j.1749-6632.1991.tb19618.x PG 2 WC Genetics & Heredity; Neurosciences; Otorhinolaryngology SC Genetics & Heredity; Neurosciences & Neurology; Otorhinolaryngology GA BW41A UT WOS:A1991BW41A00050 PM 1952618 ER PT J AU COPELAND, NG SILAN, CM KINGSLEY, DM JENKINS, NA CANNIZZARO, LA CROCE, CM HUEBNER, K SIMS, JE AF COPELAND, NG SILAN, CM KINGSLEY, DM JENKINS, NA CANNIZZARO, LA CROCE, CM HUEBNER, K SIMS, JE TI CHROMOSOMAL LOCATION OF MURINE AND HUMAN IL-1 RECEPTOR GENES SO GENOMICS LA English DT Article ID LONG ARM; IMMUNOGLOBULIN SUPERFAMILY; INTERLEUKIN-1 RECEPTORS; FOLLICULAR LYMPHOMA; MOLECULAR ANALYSIS; PROTO-ONCOGENE; BETA-GENES; T-CELLS; C-FMS; MOUSE C1 TEMPLE UNIV,HLTH SCI CTR,SCH MED,FELS INST CANC RES & MOLEC BIOL,PHILADELPHIA,PA 19140. IMMUNEX CORP,SEATTLE,WA 98101. RP COPELAND, NG (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74101, CA-25875] NR 44 TC 67 Z9 67 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN PY 1991 VL 9 IS 1 BP 44 EP 50 DI 10.1016/0888-7543(91)90219-5 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA EP972 UT WOS:A1991EP97200006 PM 1672292 ER PT J AU HSIEH, WT FONG, D SLOANE, BF GOLEMBIESKI, W SMITH, DI AF HSIEH, WT FONG, D SLOANE, BF GOLEMBIESKI, W SMITH, DI TI MAPPING OF THE GENE FOR HUMAN CYSTEINE PROTEINASE-INHIBITOR STEFIN-A, STF1, TO CHROMOSOME-3CEN-Q21 SO GENOMICS LA English DT Note ID EXPRESSION; PANEL; CST3 C1 RUTGERS STATE UNIV,DEPT BIOL SCI,PISCATAWAY,NJ 08855. RUTGERS STATE UNIV,BUR BIOL RES,PISCATAWAY,NJ 08855. WAYNE STATE UNIV,SCH MED,DEPT PHARMACOL,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT MOLEC BIOL & GENET,DETROIT,MI 48201. RP HSIEH, WT (reprint author), NIMH,CLIN NEUROGENET BRANCH,BLDG 10,RM 3N218,BETHESDA,MD 20892, USA. RI Sloane, Bonnie/A-1050-2009 FU NCI NIH HHS [CA-48031, CA-48210, CA-49359] NR 11 TC 25 Z9 25 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN PY 1991 VL 9 IS 1 BP 207 EP 209 DI 10.1016/0888-7543(91)90241-6 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA EP972 UT WOS:A1991EP97200028 PM 2004763 ER PT B AU BRIGHTMAN, M AF BRIGHTMAN, M BE ABBOTT, NJ TI IMPLICATION OF ASTROGLIA IN THE BLOOD-BRAIN-BARRIER SO GLIAL-NEURONAL INTERACTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON GLIAL-NEURONAL INTERACTION CY SEP 04-07, 1990 CL UNIV CAMBRIDGE, CAMBRIDGE, ENGLAND SP NEW YORK ACAD SCI, NATL SCI FDN, ABBOTT LABS, BAYER, BRISTOL MYERS SQUIBB, FISIONS UK, GENENTECH, GLAXO RES LABS, ELSEVIER PUBL, FISONS PHARM HO UNIV CAMBRIDGE RP BRIGHTMAN, M (reprint author), NIH,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892, USA. NR 0 TC 11 Z9 11 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-680-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 633 BP 343 EP 347 PG 5 WC Neurosciences SC Neurosciences & Neurology GA BW41C UT WOS:A1991BW41C00038 ER PT J AU HELBIG, H KITTREDGE, KL COCAPRADOS, M DAVIS, J PALESTINE, AG NUSSENBLATT, RB AF HELBIG, H KITTREDGE, KL COCAPRADOS, M DAVIS, J PALESTINE, AG NUSSENBLATT, RB TI MAMMALIAN CILIARY-BODY EPITHELIAL-CELLS IN CULTURE PRODUCE TRANSFORMING GROWTH-FACTOR-BETA SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY LA English DT Article ID ENDOTHELIAL-CELLS; EYE AB Transforming growth factor-beta (TGF-beta) has recently been found in the aqueous humor. The present study was initiated to test whether the ciliary-body epithelium, the site of aqueous humor formation, is capable of producing TGF-beta. Human, rat and bovine ciliary epithelial cells were grown in tissue culture and their supernatants were tested for TGF-beta using a bioassay. After acid activation of the samples, TGF-beta activity was found in the supernatants of all three mammalian ciliary epithelial cells. Most of this activity could be blocked by a neutralizing antibody against TGF-beta type 2. Native supernatants did not contain detectable TGf-beta activity. Thus, the ciliary epithelium is capable of producing the inactive form of TGf-beta (mainly type 2) and may be a source of TGF-beta in the aqueous humor. C1 YALE UNIV,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,NEW HAVEN,CT 06510. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 13 TC 53 Z9 53 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-832X J9 GRAEF ARCH CLIN EXP JI Graefes Arch. Clin. Exp. Ophthalmol. PY 1991 VL 229 IS 1 BP 84 EP 87 DI 10.1007/BF00172268 PG 4 WC Ophthalmology SC Ophthalmology GA ET282 UT WOS:A1991ET28200016 PM 2004731 ER PT J AU ROY, MS PODGOR, MJ COLLIER, B GUNKEL, RD AF ROY, MS PODGOR, MJ COLLIER, B GUNKEL, RD TI COLOR-VISION AND AGE IN A NORMAL NORTH-AMERICAN POPULATION SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY LA English DT Article ID MUNSELL 100-HUE TEST; DESATURATED PANEL D-15; SCORES AB Color vision is known to change with age. We conducted the Farnsworth-Munsell (FM) 100-Hue and the Lanthony Desaturated Panel D-15 (DD-15) tests in 115 normal North American subjects aged 5-81 years to obtain age-specific norms for these procedures. For each test, color discrimination was best between the ages of 20 and 50 years. Both increasing age and the occurrence of lens changes were significantly associated with increasing 100-Hue error scores. Age-specific norms for the 100-Hue test were comparable with those obtained by Verriest in a European population, but such norms for the DD-15 test are problematic. Our data indicate somewhat greater variability in the DD-15 than in the 100-Hue test. C1 NEI,BETHESDA,MD 20892. NR 21 TC 33 Z9 34 U1 1 U2 4 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-832X J9 GRAEF ARCH CLIN EXP JI Graefes Arch. Clin. Exp. Ophthalmol. PY 1991 VL 229 IS 2 BP 139 EP 144 DI 10.1007/BF00170545 PG 6 WC Ophthalmology SC Ophthalmology GA FB050 UT WOS:A1991FB05000008 PM 2044973 ER PT J AU HELBIG, H KITTREDGE, KL PALESTINE, AG COCAPRADOS, M NUSSENBLATT, RB AF HELBIG, H KITTREDGE, KL PALESTINE, AG COCAPRADOS, M NUSSENBLATT, RB TI GAMMA-INTERFERON INDUCES DIFFERENTIAL EXPRESSION OF HLA-DR, HLA-DP AND HLA-DQ IN HUMAN CILIARY EPITHELIAL-CELLS SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY LA English DT Article ID HUMAN-MONOCYTES; ANTIGEN; STIMULATION; MOLECULES AB The antigen-specific activation of T-helper lymphocytes is dependent on the presentation of antigen in context with the gene products of the major histocompatibility complex class II (MHC II). Aberrant expression of MHC II on the ciliary epithelium has been observed in uveitic eyes which may enable these cells to specifically interact with lymphocytes and may play a role in ocular autoimmunity. Human MHC II consists of three subclasses termed HLA-DR, -DP and -DQ, which seem to be differentially regulated and may have different functions. The present study was initiated to investigate the dynamics of the differential MHC II expression on cultured human non-pigmented ciliary epithelial cells (NPE cells) in response to gamma-interferon (gamma-IFN) by means of immunohistochemistry. NPE cells grown in control tissue-culture medium did not express MHC class II. HLA-DR and -DP could be induced by incubation with 100 u/ml gamma-IFN for 3 days. HLA-DQ was expressed only weakly and at higher doses of gamma-IFN (greater-than-or-equal-to 500 u/ml) and longer incubation periods (greater-than-or-equal-to 5 days). After removal of the gamma-IFN stimulus, all three MHC II subclasses persisted for several days. The differential expression of HLA-DR and -DP as compared with HLA-DQ in response to gamma-IFN in the ciliary epithelium is similar to observations in other non-lymphoid ocular cells but appears to be different from the regulation of MHC II expression on lymphoid cells. Since HLA-DR and -DP seem to be linked mainly to immune-response genes, whereas a linkage to immune suppressor genes has been described for HLA-DQ, the MHC II expression on bone marrow-derived cells and non-lympoid ocular cells may serve different functions. C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. YALE UNIV,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,NEW HAVEN,CT 06510. NR 17 TC 7 Z9 7 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-832X J9 GRAEF ARCH CLIN EXP JI Graefes Arch. Clin. Exp. Ophthalmol. PY 1991 VL 229 IS 2 BP 191 EP 194 DI 10.1007/BF00170556 PG 4 WC Ophthalmology SC Ophthalmology GA FB050 UT WOS:A1991FB05000019 PM 1904385 ER PT B AU MCLACHLAN, JA NELSON, KG TAKAHASHI, T BOSSERT, NL NEWBOLD, RR KORACH, KS AF MCLACHLAN, JA NELSON, KG TAKAHASHI, T BOSSERT, NL NEWBOLD, RR KORACH, KS BE SCHOMBERG, DW TI ESTROGENS AND GROWTH-FACTORS IN THE DEVELOPMENT, GROWTH, AND FUNCTION OF THE FEMALE REPRODUCTIVE-TRACT SO GROWTH FACTORS IN REPRODUCTION SE SERONO SYMPOSIA, USA LA English DT Proceedings Paper CT SYMP ON GROWTH FACTORS IN REPRODUCTION CY APR 01-04, 1990 CL SAVANNAH, GA SP SERONO SYMP USA RP MCLACHLAN, JA (reprint author), NIEHS,REPROD & DEV TOXICOL,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 13 Z9 13 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA NEW YORK BN 0-387-97569-1 J9 SERONO SYMP PY 1991 BP 197 EP 203 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA BT32H UT WOS:A1991BT32H00014 ER PT B AU SALEM, N CARLSON, SE AF SALEM, N CARLSON, SE BE SIMOPOULOS, AP KIFER, RR MARTIN, RE BARLOW, SM TI GROWTH AND DEVELOPMENT IN INFANTS SO HEALTH EFFECTS OF OMEGA3 POLYUNSATURATED FATTY ACIDS IN SEAFOODS SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 2ND INTERNATIONAL CONF ON THE HEALTH EFFECTS OF OMEGA3 POLYUNSATURATED FATTY ACIDS IN SEAFOOD CY MAR 20-23, 1990 CL WASHINGTON, DC SP US DEPT COMMERCE, NATL OCEAN & ATMOSPER ADM, NATL MARINE FISHERIES SERV, AMER ASSOC WORLD HLTH, CTR GENET NUTRIT & HLTH, INT ASSOC FISH MEAL MANUFACTURERS, NATL FISHERIES INST, US FDA, NCI, NIAAA, NIH, NIAMSD, NICHHD RP SALEM, N (reprint author), NIAAA,CLIN STUDIES LAB,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5244-0 J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1991 VL 66 BP 20 EP 25 PG 6 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA BS88U UT WOS:A1991BS88U00005 PM 2053337 ER PT B AU BUTRUM, RR MESSINA, MJ AF BUTRUM, RR MESSINA, MJ BE SIMOPOULOS, AP KIFER, RR MARTIN, RE BARLOW, SM TI CANCER SO HEALTH EFFECTS OF OMEGA3 POLYUNSATURATED FATTY ACIDS IN SEAFOODS SE WORLD REVIEW OF NUTRITION AND DIETETICS LA English DT Proceedings Paper CT 2ND INTERNATIONAL CONF ON THE HEALTH EFFECTS OF OMEGA3 POLYUNSATURATED FATTY ACIDS IN SEAFOOD CY MAR 20-23, 1990 CL WASHINGTON, DC SP US DEPT COMMERCE, NATL OCEAN & ATMOSPER ADM, NATL MARINE FISHERIES SERV, AMER ASSOC WORLD HLTH, CTR GENET NUTRIT & HLTH, INT ASSOC FISH MEAL MANUFACTURERS, NATL FISHERIES INST, US FDA, NCI, NIAAA, NIH, NIAMSD, NICHHD RP BUTRUM, RR (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5244-0 J9 WORLD REV NUTR DIET JI World Rev.Nutr.Diet. PY 1991 VL 66 BP 48 EP 50 PG 3 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA BS88U UT WOS:A1991BS88U00011 PM 2053365 ER PT J AU WACHHOLZ, BW AF WACHHOLZ, BW TI ASSESSMENT OF TECHNIQUES TO DETERMINE PREVIOUS RADIATION EXPOSURES (EMPHASIZING EXPOSURES OCCURRING DECADES EARLIER) - INTRODUCTION SO HEALTH PHYSICS LA English DT Editorial Material RP WACHHOLZ, BW (reprint author), NCI, RADIAT EFFECTS BRANCH, BETHESDA, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PY 1991 VL 60 SU 1 BP 1 EP 2 PG 2 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA FE834 UT WOS:A1991FE83400001 ER PT J AU BENDER, MA AWA, A BROOKS, AL EVANS, HJ GROER, PG LITTLEFIELD, LG PEREIRA, C PRESTON, RJ WACHHOLZ, B AF BENDER, MA AWA, A BROOKS, AL EVANS, HJ GROER, PG LITTLEFIELD, LG PEREIRA, C PRESTON, RJ WACHHOLZ, B TI CURRENT STATUS OF CYTOGENETIC PROCEDURES TO DETECT AND QUANTIFY PREVIOUS EXPOSURES TO RADIATION - A SUMMARY SO HEALTH PHYSICS LA English DT Editorial Material AB The estimation of the magnitude of a dose of ionizing radiation to which an individual has been exposed (or of the plausibility of an alleged exposure) from chromosomal aberration frequencies determined in peripheral blood lymphocyte cultures is a well-established methodology, having first been employed over 25 y ago. The Cytogenetics Working Group has reviewed the accumulated data and the possible applicability of the technique to the determination of radiation doses to which American veterans might have been exposed as participants in nuclear weapons tests in the continental U.S. or the Pacific Atolls during the late 1940s and the 1950s or as members of the Occupational Forces entering Hiroshima or Nagasaki shortly after the nuclear detonations there. The working group believes that with prompt peripheral blood sampling, external doses to individuals of the order of about 0.1 Gy (10 rad) (or less if the exposure was to high-LET radiation) can accurately be detected and measured. It also believes that exposures of populations to doses of the order of maximum permissible occupational exposures can also be detected (but only in populations, not in an individual). Large exposures of populations can also be detected even several decades after their exposure, but only in the case of populations, and of large doses (of the order of one to several gray). The working group does not believe that cytogenetic measurements can detect internal doses from fallout radionuclides in individuals unless these are very large. The working group has approached the problem of detection of small doses (less-than-or-equal-to 0.1 Gy or less-than-or-equal-to 10 rad) sampled decades after the exposure of individuals by using a Bayesian statistical approach. Only a preliminary evaluation of this approach was possible, but it is clear that it could provide a formal statement of the likelihood that any given observation of a particular number of chromosomal aberrations in a sample of any particular number of lymphocytes actually indicates an exposure to any given dose of radiation. It is also clear that aberration frequencies (and consequently doses) would have to be quite high before much confidence could be given to either exposure or dose estimation by this method, given the approximately three decades of elapsed time between the exposures and any future blood sampling. Additional research on the problem is clearly needed, but at the moment it appears unlikely that determination of chromosomal aberration frequencies in peripheral blood lymphocytes will prove a useful method of determining ionizing radiation doses to individual veterans (though it might prove useful in showing that doses to veterans as a population were not greatly in excess of those presently estimated). C1 RADIAT EFFECTS RES FDN, MINAMI KU, HIROSHIMA 732, JAPAN. WESTERN GEN HOSP, MRC, CLIN & POPULAT CYTOGENET UNIT, EDINBURGH EH5 2XU, SCOTLAND. LOVELACE INHALAT TOXICOL RES INST, ALBUQUERQUE, NM 87185 USA. OAK RIDGE ASSOCIATED UNIV, OAK RIDGE, TN 37831 USA. UNIV SAO PAULO, SAO PAULO, BRAZIL. OAK RIDGE NATL LAB, DIV BIOL, OAK RIDGE, TN 37831 USA. NCI, RADIAT EFFECTS BRANCH, BETHESDA, MD 20892 USA. RP BENDER, MA (reprint author), ASSOCIATED UNIV INC, BROOKHAVEN NATL LAB, UPTON, NY 11973 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PY 1991 VL 60 SU 1 BP 3 EP 3 PG 1 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA FE834 UT WOS:A1991FE83400002 ER PT J AU TOOHEY, R PALMER, E ANDERSON, L BERGER, C COHEN, N EISELE, G WACHHOLZ, B BURR, W AF TOOHEY, R PALMER, E ANDERSON, L BERGER, C COHEN, N EISELE, G WACHHOLZ, B BURR, W TI CURRENT STATUS OF WHOLE-BODY COUNTING AS A MEANS TO DETECT AND QUANTIFY PREVIOUS EXPOSURES TO RADIOACTIVE MATERIALS SO HEALTH PHYSICS LA English DT Article ID INVIVO; WORKERS AB This report discusses the principles, techniques, and application of whole-body counting with respect to previous radiation exposure. Whole-body counting facilities are located nationwide and have a wide range of capabilities. A listing of these facilities is provided in Appendix A. However, only a few facilities are truly state-of-the-art and have the sophisticated capabilities required to attempt detection of low-level activity in vivo. Measurements made many years after exposure can be extremely difficult to interpret. The precision and accuracy of resulting dose estimates are functions of such factors as the assumptions made concerning intake, time since intake, radionuclide metabolism, and level of intake. The indiscriminate application of metabolic models to current body contents or minimum detectable amounts of radionuclides with relatively short effective half-lives (such as Cs-137) can lead to absurd results when used as a basis for calculating intakes 25 and 40 y ago. Skull counting for Sr-90-Y-90 and Pu-239, Pu-240 can set upper limits on possible uptakes and radiation doses, but in the case of Pu-239, Pu-240, the limits are rather high. In both cases the accuracy of the limits depends on the metabolic models used in the calculations. These models (ICRP 1979) were developed to set safety standards for the intakes of radionuclides by workers and are not intended to be used to back-calculate uptakes and radiation doses from measurements made long after the uptake. There are, therefore, large uncertainties in any conclusions derived from these calculations. The experience gained over the years with whole- and partial-body counting has consistently shown that they are of little use in determining body contents of radionuclides resulting from exposure to weapons debris decades earlier. The development of new detectors such as an array of lithium-drifted silicon devices offers some hope of lowering the minimum detectable amount (MDA) for Pu and Am, but such detectors are still several years from routine application and do not represent current state-of-the-art. Furthermore, it is doubtful that such improvements will be sufficient to meet the need of assessing radiation exposures that occurred decades earlier. C1 PACIFIC NW LAB, RICHLAND, WA 99352 USA. UNIV CALIF LAWRENCE LIVERMORE NATL LAB, LIVERMORE, CA 94550 USA. OAK RIDGE NATL LAB, OAK RIDGE, TN 37831 USA. NYU, MED CTR, TUXEDO PK, NY 10987 USA. NCI, BETHESDA, MD 20892 USA. OAK RIDGE ASSOCIATED UNIV, OAK RIDGE, TN 37831 USA. RP TOOHEY, R (reprint author), ARGONNE NATL LAB, 9700 S CASS AVE, ARGONNE, IL 60439 USA. NR 64 TC 40 Z9 40 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PY 1991 VL 60 SU 1 BP 7 EP 42 PG 36 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA FE834 UT WOS:A1991FE83400003 PM 1900815 ER PT J AU BOECKER, B HALL, R INN, K LAWRENCE, J ZIEMER, P EISELE, G WACHHOLZ, B BURR, W AF BOECKER, B HALL, R INN, K LAWRENCE, J ZIEMER, P EISELE, G WACHHOLZ, B BURR, W TI CURRENT STATUS OF BIOASSAY PROCEDURES TO DETECT AND QUANTIFY PREVIOUS EXPOSURES TO RADIOACTIVE MATERIALS SO HEALTH PHYSICS LA English DT Article ID MASS-SPECTROMETRY; FALLOUT PLUTONIUM; URINARY-EXCRETION; AUTOPSY TISSUE; SOUTHERN FINNS; SYSTEMIC PU; VARIABILITY; IONIZATION AB This report was prepared by a working group established by the Oak Ridge Associated Universities (ORAU) for the purpose of assessing the current capabilities of bioassay methods that can be used to determine the occurrence and magnitude of a previous internal deposition of one or more radionuclides. The first five sections discuss general features of the use of in-vitro bioassay samples to achieve this purpose. The remainder of the report is focused on the possible use of urine bioassay procedures to detect and quantify internal depositions of radionuclides that may have occurred in United States occupation troops in Hiroshima or Nagasaki, Japan, prior to 1 July 1946, or to personnel who participated in atmospheric nuclear weapons tests conducted between 1945 and 1962. Theoretical calculations were made to estimate the quantities of various radionuclides produced in a 20-kiloton (kt) nuclear detonation that might still be present in measurable quantities in people today if they were exposed 25 to 40 y ago. Two radionuclides that emerged as good choices for this type of bioassay analysis were Sr-90, which emits beta particles, and Pu-239, Pu-240, which emits alpha particles. The current status and future prospects of chemical procedures for analyzing in-vitro urine bioassay samples for these two radionuclides were examined to determine the minimum amounts that could be detected with current methods and how much one might expect the sensitivity of detection to improve in the near future. Most routine Pu-239, Pu-240 bioassay analyses involve detection by alpha spectrometry. The current minimum detectable amount (MDA) is about 0.74 mBq L-1 (20 fCi L-1), but this could be lowered to 74-mu-Bq L-1 (2 fCi L-1). An MDA of 0.74 mBq L-1 (20 fCi L-1) is adequate for routine bioassay analyses but is too high to detect most uptakes of Pu-239, Pu-240 that may have occurred 25 to 40 y ago. Methods under development that are or can be much more sensitive and have lower MDAs than alpha spectrometry for Pu-239 are fission track analysis and mass spectrometry. Currently, the fission track analysis method has an MDA of about 19-mu-Bq L-1 (0.5 fCi L-1), and this may eventually be lowered to 1.9-mu-Bq L-1 (0.05 fCi L-1). The current MDA for Pu-239 by mass spectrometry is about 7.4 mBq L-1 (200 fCi L-1), but the potential exists that it could be lowered to a value of about 0.37-mu-Bq L-1 (0.01 fCi L-1). For Sr-90, low-background beta counting is one of the best methods currently available. Mass spectrometry could also be used if desired. The current minimum detectable amount, MDA, for Sr-90 in a urine sample using low-background beta counting is about 7.4 mBq L-1 (200 fCi L-1) of urine. This MDA could be reduced to about 1.1 mBq L-1 (30 fCi L-1) if needed. Bioassay measurements provide only an indirect measurement of how much of a particular radionuclide is present in the body at the time of sampling. Mathematical models are used to estimate the currently retained body burden, the initial body burden when uptake occurred, and the cumulative dose equivalents received by various body organs and tissues. Models of these types for Sr-90 and Pu-39, Pu-240 have received much scientific attention over the past 40 y, and the models available for use today appear to be reasonable for interpretation of bioassay results for intakes that may have occurred 25 to 40 y ago. One of the major problems that is encountered when interpreting a particular Sr-90 or Pu-239, Pu-240 bioassay result is that, because of worldwide fallout from past atmospheric detonations, everyone contains some Sr-90 and Pu-239, Pu-240. The amount of background Sr-90 or Pu-239, Pu-240 in people is quite variable and depends on a number of factors including age, diet, and geographical location. The accuracy of bioassay for detecting a previous exposure to Sr-90 or Pu-239, Pu-240 in an individual depends, among other things, on how well the expected background level for Sr-90 or Pu-239, Pu-240 in an individual can be estimated and subtracted from the total amount present to determine whether excess Sr-90 or Pu-239, Pu-240 is present. Exposure to other radionuclides from occupational, medical, or natural background sources can also interfere with a bioassay analysis, but they can be accounted for more easily than can background levels of Sr-90 or Pu-239, Pu-240. Propagation of uncertainty values that may be representative of those encountered in an actual bioassay program indicate that the uncertainty of the dose estimated from a bioassay sample is such that the 5th and 95th percentiles can be at least four to seven times smaller or larger, respectively, than the geometric mean values. A possible strategy for implementing such a biossay program is suggested in this report. It is based on the concept of testing the usefulness of bioassay in relatively small groups of military personnel who, by virtue of their location and/or activities, may have had the highest likelihood of an internal deposition. These could be selected from situations involving exposure to descending fallout or radionuclides resuspended from various surfaces. In addition to selection of individuals based on their location or activities, individuals with high film-badge readings could also be sampled. If these efforts indicate that urine bioassay can, in fact, provide useful information on past exposures, other groups can also be sampled. When no excess Sr-90 or Pu-239, Pu-240 is detected, it is then possible to place an upper bound on the internal deposition and associated radiation dose that may have been recieved but not detected. Improving sensitivity of the analytical methods available can substantially reduce the magnitude of such undetected uptakes and radiation doses, especially for Pu-239, Pu-240. C1 DUPONT CO, SAVANNAH RIVER LAB, AIKEN, SC 29801 USA. NBS, CTR RADIAT RES, GAITHERSBURG, MD 20899 USA. UNIV CALIF LOS ALAMOS SCI LAB, LOS ALAMOS, NM 87545 USA. PURDUE UNIV, SCH HLTH SCI, W LAFAYETTE, IN 47907 USA. OAK RIDGE ASSOCIATED UNIV, OAK RIDGE, TN 37831 USA. NCI, BETHESDA, MD 20892 USA. RP BOECKER, B (reprint author), LOVELACE INHALAT TOXICOL RES INST, POB 5890, ALBUQUERQUE, NM 87185 USA. NR 99 TC 42 Z9 42 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PY 1991 VL 60 SU 1 BP 45 EP 100 PG 56 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA FE834 UT WOS:A1991FE83400004 PM 2004918 ER PT J AU LUSHBAUGH, C EISELE, G BURR, W HUBNER, K WACHHOLZ, B AF LUSHBAUGH, C EISELE, G BURR, W HUBNER, K WACHHOLZ, B TI CURRENT STATUS OF BIOLOGICAL INDICATORS TO DETECT AND QUANTIFY PREVIOUS EXPOSURES TO RADIATION SO HEALTH PHYSICS LA English DT Article AB Hematologic changes following whole-body exposure to gamma or x-ray radiation have been used to estimate dose. The usefulness of this biological indicator is limited because of the recovery of these cells with time, thus making it unsuitable for estimation of dose years after exposure. The same is true for spermatogenic indicators; recovery and restoration of sperm numbers and fertility makes this biological indicator impractical for assessing radiation dose decades after radiation exposure. As noted in the text of the report, immunological concepts are in a state of rapid development, and it is possible that improved methods for applying immunologic procedures as biological indicators of radiation may be developed in the future. However, at the present time, immunological indicators are not useful, even in an early time period, for quantitating radiation dose after total-body irradiation. A semiquantitative effect is observable in the early phase after total-body irradiation over a period of days to weeks, but there is little data available to indicate whether any of the immunological parameters can be indicative of a dose when the test is applied several years after radiation exposure. More detailed information regarding immunological indicators for estimating irradiation dose has been summarized elsewhere (Wasserman 1986). There is good agreement that ionizing radiation causes biochemical changes in the body; however, attempts to apply these changes to provide a reliable biological dosimetry system have not been particularly successful. The status of this research has been summarized by Gerber (1986). One of the difficulties has been the problem of establishing clear dose-effect relationships in humans. The lack of specificity in the response for radiation is another problem. Additional problems are due to the strict time dependency of biochemical changes and the limited duration of the changes during the postexposure period. Information on biochemical indicators is based on animal experiments; human experience is limited to a relatively few accidental human exposures and investigations involving patients undergoing radiation therapy. It appears that none of the biochemical indicators studied are currently useful for radiation dosimetry. Even if further developed, it is questionable whether or not biochemical indicators could be of use in estimating radiation dose received years and decades prior to the assay. C1 UNIV TENNESSEE, MED CTR, KNOXVILLE, TN 37920 USA. NCI, BETHESDA, MD 20892 USA. RP LUSHBAUGH, C (reprint author), OAK RIDGE ASSOCIATED UNIV, DIV MED & HLTH SCI, POB 117, OAK RIDGE, TN 37831 USA. NR 23 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PY 1991 VL 60 SU 1 BP 103 EP 109 PG 7 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA FE834 UT WOS:A1991FE83400005 PM 2004917 ER PT J AU YU, QS LIU, C BRZOSTOWSKA, M CHRISEY, L BROSSI, A GREIG, NH ATACK, JR SONCRANT, TT RAPOPORT, SI RADUNZ, HE AF YU, QS LIU, C BRZOSTOWSKA, M CHRISEY, L BROSSI, A GREIG, NH ATACK, JR SONCRANT, TT RAPOPORT, SI RADUNZ, HE TI PHYSOVENINES - EFFICIENT SYNTHESIS OF (-)-PHYSOVENINE AND (+)-PHYSOVENINE AND SYNTHESIS OF CARBAMATE ANALOGS OF (-)-PHYSOVENINE - ANTICHOLINESTERASE ACTIVITY AND ANALGESIC PROPERTIES OF OPTICALLY-ACTIVE PHYSOVENINES SO HELVETICA CHIMICA ACTA LA English DT Article ID (+/-)-PHYSOVENINE; ALKALOIDS; BINDING; SITES AB Column chromatography of easy available (+/-)-physovenine (2) on cellulose triacetate afforded (-)- and (+)-physovenine (2a and 2b, resp.). Alkaloids 2a, b required for pharmacological testing were prepared from eserolines (3a, b) by an improved procedure. Natural (-)-physovenine (2a) was equally potent in inhibiting AChE and BChE in vitro as natural physostigmine (1a), and twice as potent as the unnatural antipode 2b against AChE and 14 times as potent against BChE. Several carbamate analogs of 2a were at least as potent as the former compound in these assays. None of the compounds tested did bind to different opiate receptor or serotonine receptor preparations. Most of the compounds tested had considerable analgesic activity in the Writhing test. C1 NIDDK,NAT PROD SECT,STRUCT BIOL LAB,BETHESDA,MD 20892. CHINESE ACAD SCI,SHANGHAI INST ORGAN CHEM,SHANGHAI 200032,PEOPLES R CHINA. E MERCK AG,W-6100 DARMSTADT,GERMANY. NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 27 TC 33 Z9 36 U1 0 U2 2 PU NEW SWISS CHEMICAL SOC PI BASEL PA VERLAG HELVETICA CHIMICA ACTA, MALZGASSE 21, POSTFACH 313, CH-4010 BASEL, SWITZERLAND SN 0018-019X J9 HELV CHIM ACTA JI Helv. Chim. Acta PY 1991 VL 74 IS 4 BP 761 EP 766 DI 10.1002/hlca.19910740409 PG 6 WC Chemistry, Multidisciplinary SC Chemistry GA FU748 UT WOS:A1991FU74800008 ER PT J AU HE, XS TADIC, D BRZOSTOWSKA, M BROSSI, A BELL, M CREVELING, C AF HE, XS TADIC, D BRZOSTOWSKA, M BROSSI, A BELL, M CREVELING, C TI MAMMALIAN ALKALOIDS - SYNTHESIS AND O-METHYLATION OF (S)-3'-HYDROXYCOCLAURINE AND (R)-3'-HYDROXYCOCLAURINE AND THEIR N-METHYLATED ANALOGS WITH S-ADENOSYL-L-[METHYL-C-14]METHIONINE IN PRESENCE OF MAMMALIAN CATECHOL O-METHYLTRANSFERASE SO HELVETICA CHIMICA ACTA LA English DT Article ID ADENOSYL-L-METHIONINE; BIOSYNTHESIS; RETICULINE; PATHWAY; PLANT; (S)-RETICULINE; (R)-RETICULINE; REVISION; MORPHINE; ACID AB O-Methylation of the optically active 3'-hydroxycoclaurines 3a and 3b and of the N-methylated analogs 5a,b with S-adenosyl-L-[methyl-C-14]methionine in presence of mammalian COMT was investigated in vitro. The N-unsubstituted (1S)-and (1R)-isomers 3a and 3b, respectively, afforded almost equal amounts of the corresponding N-norreticuline 4 and N-nororientaline 19, besides two unknown by-products (see Fig. and Table 1). The N-methylated (1S)-isoquinoline 5a, on the other hand, afforded largely (S)-orientaline ((S)-19), while an almost equal mixture of (R)-reticuline (6b) and (R)-orientaline ((R)-19) was obtained from the (1R)-enantiomer 5b. The isoquinolines 3a,b and 5a,b were prepared by a Bischler-Napieralski cyclization yielding O-benzyl-protected isoquinoline 10 (Scheme 1). The optical resolution of 10 was accomplished with 2'-bromotartranilic acid. The N-methylated isoquinolines were prepared by N-formylation of 10a,b and reduction of the formamides 13a,b with diborane (--> 14a,b). Deblocking of the benzyl-ether moieties of 10a,b and 14a,b was accomplished by catalytic hydrogenation in presence of HCl, affording directly 3a,b.HCl and 5a,b.HCl, respectively. C1 NIDDK,STRUCT BIOL LAB,NAT PROD SECT,BETHESDA,MD 20892. NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 26 TC 6 Z9 6 U1 1 U2 2 PU NEW SWISS CHEMICAL SOC PI BASEL PA VERLAG HELVETICA CHIMICA ACTA, MALZGASSE 21, POSTFACH 313, CH-4010 BASEL, SWITZERLAND SN 0018-019X J9 HELV CHIM ACTA JI Helv. Chim. Acta PY 1991 VL 74 IS 7 BP 1399 EP 1411 DI 10.1002/hlca.19910740704 PG 13 WC Chemistry, Multidisciplinary SC Chemistry GA GN070 UT WOS:A1991GN07000003 ER PT B AU DIBISCEGLIE, AM NEGRO, F SMEDILE, A BERGMANN, K HOOFNAGLE, JH AF DIBISCEGLIE, AM NEGRO, F SMEDILE, A BERGMANN, K HOOFNAGLE, JH BE GERIN, JL PURCELL, RH RIZZETTO, M TI ALPHA-INTERFERON THERAPY OF CHRONIC DELTA-HEPATITIS - A PILOT-STUDY SO HEPATITIS DELTA VIRUS SE PROGRESS IN CLINICAL AND BIOLOGICAL RESEARCH LA English DT Proceedings Paper CT 3RD INTERNATIONAL SYMP ON HEPATITIS DELTA VIRUS CY OCT 26-28, 1989 CL WASHINGTON, DC SP GEORGETOWN UNIV, MED CTR, NIAID, NIH, OSPEDALE MOLINETTE, ABBOTT LAB, IMMUNO, SCHERING PLOUGH, SK&F, SORIN BIOMEDICA, WELLCOME FDN RP DIBISCEGLIE, AM (reprint author), NIDDKD,LIVER DIS SECT,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS, INC PI NEW YORK PA NEW YORK BN 0-471-56073-1 J9 PROG CLIN BIOL RES JI Prog.Clin.Biol.Res. PY 1991 VL 364 BP 393 EP 397 PG 5 WC Medicine, Research & Experimental; Virology SC Research & Experimental Medicine; Virology GA BT15R UT WOS:A1991BT15R00047 PM 2020714 ER PT J AU MIHALY, A KUHNT, U OLAH, Z RAPP, UR AF MIHALY, A KUHNT, U OLAH, Z RAPP, UR TI INDUCTION OF RAF-1 PROTEIN IMMUNOREACTIVITY IN GUINEA-PIG HIPPOCAMPAL SLICES DURING THE INVITRO MAINTENANCE SO HISTOCHEMISTRY LA English DT Article ID SIGNAL TRANSDUCTION; KINASE-ACTIVITY; INCREASE; PHOSPHORYLATION; ONCOGENE; NEURONS AB The cellular raf-1 protooncogene encodes a cytoplasmic serine/threonine protein kinase; raf-1 is expressed not only in tumour cells, but also in normal brain tissue. However, the substrate of raf-1 kinase is unknown and its function is still hypothetical. In cell cultures, mitogen stimulation may alter its properties, including its kinase activity and subcellular distribution. The aims of the present study were: (1) light- and electron microscopic immunohistochemical localization of raf-1 kinase in hippocampal slices; (2) the follow-up of the possible changes in localization and detectability during the in vitro maintenance and low-frequency stimulation. Our results suggested the induction of neuronal raf-1 kinase during the in vitro maintenance. The possibilities of increased transcription and enzyme activation are discussed. C1 MAX PLANCK INST BIOPHYS CHEM,DEPT NEUROBIOL,W-3400 GOTTINGEN,GERMANY. NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. RI Mihaly, Andras/K-5096-2012 NR 21 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-5564 J9 HISTOCHEMISTRY JI Histochemistry PY 1991 VL 96 IS 1 BP 99 EP 105 DI 10.1007/BF00266768 PG 7 WC Cell Biology SC Cell Biology GA FR014 UT WOS:A1991FR01400016 PM 1938486 ER PT J AU ROIVAINEN, R IADAROLA, M HERVONEN, A KOISTINAHO, J AF ROIVAINEN, R IADAROLA, M HERVONEN, A KOISTINAHO, J TI THE LOCALIZATION OF THE BETA-SUBTYPE OF PROTEIN-KINASE-C (PKC-BETA) IN RAT SYMPATHETIC NEURONS SO HISTOCHEMISTRY LA English DT Article ID SUPERIOR CERVICAL-GANGLION; 3 DISTINCT FORMS; IMMUNOCYTOCHEMICAL LOCALIZATION; PHORBOL ESTER; GUINEA-PIG; VESICULAR RELEASE; ENTERIC NEURONS; BRAIN; CELLS; 12-O-TETRADECANOYLPHORBOL-13-ACETATE AB The localization of PKC-beta was studied in rat sympathetic neurons using a polyclonal antibody specific for the beta-1- and beta-2-subspecies. The tissues studied included the superior cervical (SCG) and hypogastric (HGG) ganglia and the target tissues of the SCG and HGG neurons: the submandibular gland, iris, prostate and vas deferens. PKC-beta-LI was found in nerve fibers in both ganglia. A proportion of the fibers in the SCG disappeared after decentralization, suggesting that the fibers were of both pre- and postganglionic origin. The somata of the HGG and SCG neurons expressed varying amounts of PKC-beta-LI, the majority of SCG neurons being labelled only after colchicine treatment. In all target tissues there were PKC-beta-immunoreactive nerve fibers in bundles, but the most peripheral branches of the fibers were negatively labelled. The results show that PKC-beta-LI is widely present in sympathetic postganglionic neurons with mainly quantitative differences. The lack of PKC-beta in the most peripheral branches of nerve fibers might be a general feature of sympathetic postganglionic neurons, suggesting that the participation of PKC-beta in neurotransmitter release and in other functions in nerve terminals in sympathetic adrenergic neurons is unlikely. C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. RP ROIVAINEN, R (reprint author), UNIV TAMPERE,DEPT PUBL HLTH,GERONTOL LAB,POB 607,SF-33101 TAMPERE,FINLAND. NR 43 TC 11 Z9 11 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-5564 J9 HISTOCHEMISTRY JI Histochemistry PY 1991 VL 95 IS 3 BP 247 EP 253 PG 7 WC Cell Biology SC Cell Biology GA EV837 UT WOS:A1991EV83700006 PM 2050545 ER PT J AU MARTIN, JR HOLT, RK LANGSTON, C GILDEN, DH RICHARDSON, EP MANZ, HJ SINGER, DB AF MARTIN, JR HOLT, RK LANGSTON, C GILDEN, DH RICHARDSON, EP MANZ, HJ SINGER, DB TI TYPE-SPECIFIC IDENTIFICATION OF HERPES-SIMPLEX AND VARICELLA-ZOSTER VIRUS-ANTIGEN IN AUTOPSY TISSUES SO HUMAN PATHOLOGY LA English DT Article DE HERPES SIMPLEX VIRUS TYPE-1 AND TYPE-2; VARICELLA-ZOSTER VIRUS; HERPESVIRUS DIAGNOSIS AND DISEASE ID INFECTION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20057. BAYLOR UNIV,HOUSTON,TX 77030. UNIV COLORADO,SCH MED,DENVER,CO 80202. WOMEN & INFANTS HOSP RHODE ISL,PROVIDENCE,RI 02908. RP MARTIN, JR (reprint author), NIH,EXPTL NEUROPATHOL LAB,BLDG 36,ROOM 4A29,BETHESDA,MD 20892, USA. FU NIA NIH HHS [AG-06127, AG-07347] NR 13 TC 14 Z9 14 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1991 VL 22 IS 1 BP 75 EP 80 DI 10.1016/0046-8177(91)90065-W PG 6 WC Pathology SC Pathology GA ET395 UT WOS:A1991ET39500013 PM 1845866 ER PT B AU HOEG, JM AF HOEG, JM BE WILLIAMS, CL WYNDER, EL TI PHARMACOLOGICAL AND SURGICAL-TREATMENT OF DYSLIPIDEMIC CHILDREN AND ADOLESCENTS SO HYPERLIPIDEMIA IN CHILDHOOD AND THE DEVELOPMENT OF ATHEROSCLEROSIS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON HYPERLIPIDEMIA IN CHILDHOOD AND THE DEVELOPMENT OF ATHEROSCLEROSIS CY MAY 02-04, 1990 CL BETHESDA, MD SP NEW YORK ACAD SCI, BRISTOL MYERS, EASTMAN KODAK, DIV CLIN PROD, SQUIBB, BOEHRINGER MANNHEIM, CARNAT NUTRIT PROD, GERBER, PARKE DAVIS, BEST FOODS, BURROUGHS WELLCOME ID HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA; LOW-DENSITY-LIPOPROTEIN; LIVER-TRANSPLANTATION; PORTACAVAL-SHUNT; II HYPERLIPOPROTEINEMIA; CARDIOVASCULAR-DISEASE; CHOLESTYRAMINE RESIN; APOLIPOPROTEIN-B; COLESTIPOL RESIN; PLASMA-EXCHANGE RP HOEG, JM (reprint author), NHLBI,BLDG 10,ROOM 7N117,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 15 Z9 15 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-658-5 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1991 VL 623 BP 275 EP 284 DI 10.1111/j.1749-6632.1991.tb43737.x PG 10 WC Biochemistry & Molecular Biology; Cardiac & Cardiovascular Systems; Hematology; Pathology; Pediatrics SC Biochemistry & Molecular Biology; Cardiovascular System & Cardiology; Hematology; Pathology; Pediatrics GA BT59M UT WOS:A1991BT59M00026 PM 2042836 ER PT J AU CUTLER, JA FOLLMANN, D ELLIOTT, P SUH, I AF CUTLER, JA FOLLMANN, D ELLIOTT, P SUH, I TI AN OVERVIEW OF RANDOMIZED TRIALS OF SODIUM REDUCTION AND BLOOD-PRESSURE SO HYPERTENSION LA English DT Article DE BLOOD PRESSURE; SODIUM, DIETARY; CLINICAL TRIALS; RANDOM ALLOCATION; METAANALYSIS ID ESSENTIAL-HYPERTENSION; DIETARY-SODIUM; MILD HYPERTENSION; POTASSIUM SUPPLEMENTATION; SALT RESTRICTION; WEIGHT-REDUCTION; FINAL REPORT; MANAGEMENT; PREVENTION; DIURETICS AB To test for effects on systolic and diastolic blood pressure and to provide precise estimates of their magnitude, we conducted an overview of randomized clinical trials that aimed to reduce the intake of sodium in human subjects. We excluded from pooled analyses trials with confounded designs, those that compared intake levels beyond the usual range in the population, and those without published reports. Two reviewers abstracted information in duplicate and differences were reconciled. Twenty-three trials with outcome data from an aggregate of 1,536 subjects were included. Data were pooled both separately for hypertensive and normotensive subjects and for all trials combined. With the use of sample size weighting, blood pressure reductions (net of controls) were 4.9 +/- 1.3/2.6 +/- 0.8 mm Hg (systolic and diastolic, respectively, with 95% confidence limits) in hypertensive subjects and 1.7 +/- 1.0/1.0 +/- 0.7 mm Hg in normotensive subjects. The combined blood pressure reductions were 2.9 +/- 0.8/1.6 +/- 0.5 mm Hg. These changes were associated with mean reduction of urinary sodium excretion ranging from 16 to 171 mmol/24 hr for individual trials. A dose-response relation across trials was found, both in normotensive and in hypertensive subjects. These results indicate that sodium reduction lowers mean blood pressure in both hypertensive and normotensive individuals for periods of at least several months. The findings are highly consistent with results of observational epidemiological studies and have implications for preventive strategies of blood pressure control. C1 UNIV LONDON LONDON SCH HYG & TROP MED, DEPT EPIDEMIOL & POPULAT STUDIES, LONDON WC1E 7HT, ENGLAND. RP CUTLER, JA (reprint author), NHLBI, DIV EPIDEMIOL & CLIN APPLICAT, FED BLDG, ROOM 604, BETHESDA, MD 20892 USA. NR 49 TC 169 Z9 171 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1991 VL 17 IS 1 SU S BP I27 EP I33 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ET145 UT WOS:A1991ET14500007 PM 1987008 ER PT J AU CUTLER, JA AF CUTLER, JA TI PAGE,LOT,BATES 1923-1990 - IN MEMORIAM SO HYPERTENSION LA English DT Editorial Material RP CUTLER, JA (reprint author), NHLBI,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1991 VL 17 IS 1 SU S BP I2 EP I2 PG 1 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ET145 UT WOS:A1991ET14500002 ER PT J AU CUTLER, JA KOTCHEN, TA OBARZANEK, E AF CUTLER, JA KOTCHEN, TA OBARZANEK, E TI NATIONAL-HEART-LUNG-AND-BLOOD-INSTITUTE WORKSHOP ON SALT AND BLOOD-PRESSURE - INTRODUCTION SO HYPERTENSION LA English DT Editorial Material C1 W VIRGINIA UNIV,MED CTR,SCH MED,DEPT MED,MORGANTOWN,WV 26506. RP CUTLER, JA (reprint author), NHLBI,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1991 VL 17 IS 1 SU S BP I1 EP I1 PG 1 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ET145 UT WOS:A1991ET14500001 ER PT J AU ERNST, ND AF ERNST, ND TI HEALTH PROMOTION ROLES OF THE FEDERAL-GOVERNMENT AND FOOD-INDUSTRY IN NUTRITION AND BLOOD-PRESSURE SO HYPERTENSION LA English DT Article; Proceedings Paper CT WORKSHOP ON SALT AND BLOOD PRESSURE CY NOV 01-02, 1989 CL BETHESDA, MD SP NHLBI DE BLOOD PRESSURE; DIET; NUTRITION; HEALTH PROMOTION ID POLICIES AB Some principal activities of government that pertain to nutrition and blood pressure are education, information, dietary guidance, food regulatory practices, health and nutrition monitoring, biomedical research and training, and legislation. The food industry, in turn, influences the marketplace and food consumption by its response to government activities and policies. Dietary guidance recommendations call for moderation of dietary intake, improved nutrition, and greater availability in food choices in the marketplace that are consistent with dietary recommendations to reduce chronic disease risk. Health and nutrition monitoring allows measurement of the effectiveness of moderating dietary intake and controlling hypertension. Adequate support of education, nutrition and health monitoring, and biomedical research and training is necessary to control and prevent hypertension. Cooperation between government and industry can contribute to the decline in cardiovascular disease, which in 1987 cost this nation in excess of $135 billion. RP ERNST, ND (reprint author), NHLBI,7550 WISCONSIN AVE,FED BLDG,ROOM 204,BETHESDA,MD 20892, USA. NR 33 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1991 VL 17 IS 1 SU S BP I196 EP I200 PG 5 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ET145 UT WOS:A1991ET14500040 PM 1987003 ER PT J AU GRIMM, R KULLER, LH LANGFORD, HG SULLIVAN, JM MCCARRON, DA WILLIAMS, G HAMET, P TUCK, ML SCOGGINS PRINEAS, RJ ZINNER SOWERS GROBBEE, DE ELLIOTT, P TOBIAN, L AF GRIMM, R KULLER, LH LANGFORD, HG SULLIVAN, JM MCCARRON, DA WILLIAMS, G HAMET, P TUCK, ML SCOGGINS PRINEAS, RJ ZINNER SOWERS GROBBEE, DE ELLIOTT, P TOBIAN, L TI SESSION-IV - DEMOGRAPHIC MODIFIERS OF SALT BLOOD-PRESSURE RELATION - DISCUSSION SO HYPERTENSION LA English DT Discussion C1 UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT EPIDEMIOL,PITTSBURGH,PA 15213. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. UNIV TENNESSEE,CTR HLTH SCI,DIV CARDIOVASC DIS,MEMPHIS,TN 38163. OREGON HLTH SCI UNIV,NIDDKD,CLIN NUTR RES UNIT,PORTLAND,OR 97201. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV ENDOCRINE HYPERTENS,BOSTON,MA 02115. CLIN RES INST MONTREAL,MOLEC PHYSIOL LAB,MONTREAL H2W 1R7,QUEBEC,CANADA. VET ADM MED CTR,SEPULVEDA,CA 91343. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. ERASMUS UNIV,SCH MED,DEPT EPIDEMIOL & BIOSTAT,3000 DR ROTTERDAM,NETHERLANDS. UNIV LONDON LONDON SCH HYG & TROP MED,DEPT EPIDEMIOL & POPULAT SCI,LONDON WC1E 7HT,ENGLAND. UNIV MINNESOTA HOSP & CLIN,DEPT INTERNAL MED,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,MINNEAPOLIS,MN 55455. UNIV MIAMI,SCH MED,DEPT EPIDEMIOL & PUBL HLTH R669,MIAMI,FL 33136. RP GRIMM, R (reprint author), UNIV MINNESOTA,SCH PUBL HLTH,DIV MICROBIOL & PUBL HLTH,MINNEAPOLIS,MN 55455, USA. RI Grobbee, Diederick/C-7651-2014 OI Grobbee, Diederick/0000-0003-4472-4468 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1991 VL 17 IS 1 SU S BP I133 EP I134 PG 2 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ET145 UT WOS:A1991ET14500027 ER PT J AU KOTCHEN, TA LANGFORD, HG CUTLER, JA GRIMM, J STAMLER, J LUFT, EC KULLER, LH SULLIVAN, J ELLIOTT, P MCCARRON, DA STAMLER, R AF KOTCHEN, TA LANGFORD, HG CUTLER, JA GRIMM, J STAMLER, J LUFT, EC KULLER, LH SULLIVAN, J ELLIOTT, P MCCARRON, DA STAMLER, R TI SESSION-I - EPIDEMIOLOGIC OVERVIEW - INTERVENTION STUDIES - DISCUSSION SO HYPERTENSION LA English DT Discussion C1 NHLBI,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892. NORTHWESTERN UNIV,SCH MED,DEPT COMMUNITY HLTH & PREVENT MED,CHICAGO,IL 60611. UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. OREGON HLTH SCI UNIV,NIDDKD,CLIN NUTR RES UNIT,PORTLAND,OR 97201. UNIV LONDON LONDON SCH HYG & TROP MED,DEPT EPIDEMIOL & POPULAT STUDIES,LONDON WC1E 7HT,ENGLAND. UNIV TENNESSEE,CTR HLTH SCI,DIV CARDIOVASC DIS,MEMPHIS,TN 38163. UNIV PITTSBURGH,SCH PUBL HLTH,DEPT EPIDEMIOL,PITTSBURGH,PA 15213. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. RP KOTCHEN, TA (reprint author), W VIRGINIA UNIV,MED CTR,SCH MED,DEPT MED,HLTH SCI CTR N,MORGANTOWN,WV 26506, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1991 VL 17 IS 1 SU S BP I36 EP I38 PG 3 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ET145 UT WOS:A1991ET14500009 ER PT J AU MCCARRON, DA AF MCCARRON, DA TI A CONSENSUS APPROACH TO ELECTROLYTES AND BLOOD-PRESSURE - COULD WE ALL BE RIGHT SO HYPERTENSION LA English DT Article; Proceedings Paper CT WORKSHOP ON SALT AND BLOOD PRESSURE CY NOV 01-02, 1989 CL BETHESDA, MD SP NHLBI DE ELECTROLYTES; BLOOD PRESSURE; DIET; SALT INTAKE ID SALT-SENSITIVE HYPERTENSION; CALCIUM-REGULATING HORMONES; DIETARY-SODIUM RESTRICTION; DEPENDENT HYPERTENSION; PARATHYROID FUNCTION; UNITED-STATES; METABOLISM; POTASSIUM; CHLORIDE; DETERMINANT AB This commentary sets forth the hypothesis that the putative beneficial or detrimental effects of specific electrolytes on blood pressure regulation in fact reflect highly integrated responses to interactions among these cationic and anionic species. In this paradigm, the impact of any given intake of an electrolyte on arterial pressure will be influenced by the concurrent consumption of other electrolytes. Thus, the heterogeneous blood pressure response in humans to isolated manipulations of nutrients such as sodium, calcium, and potassium may be determined, in part, by the adequacy of the dietary intake of other mineral elements. If this hypothesis is validated by continued research in this area, we would have new strategies available to improve blood pressure control in humans. For example, treatment of "NaCl sensitivity" in some humans might be more effectively approached by correcting dietary deficiencies of either potassium or calcium than by restricting dietary NaCl. RP MCCARRON, DA (reprint author), OREGON HLTH SCI UNIV,NIDDK,CLIN NUTR RES UNIT,3181 SE SAM JACKSON PK RD,PORTLAND,OR 97201, USA. FU NIDDK NIH HHS [P30-DK40566] NR 38 TC 0 Z9 0 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1991 VL 17 IS 1 SU S BP I170 EP I172 PG 3 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ET145 UT WOS:A1991ET14500035 PM 1986999 ER PT J AU SULLIVAN, J LANGFORD, HG MCCARRON, D STAMLER, R HAMET, P STAMLER, J KOTCHEN, T COOPER CUTLER, J SOWERS KULLER, LH KURTZ AF SULLIVAN, J LANGFORD, HG MCCARRON, D STAMLER, R HAMET, P STAMLER, J KOTCHEN, T COOPER CUTLER, J SOWERS KULLER, LH KURTZ TI SESSION-V - ENVIRONMENTAL METABOLIC MODIFIERS OF SALT BLOOD-PRESSURE RELATION - DISCUSSION SO HYPERTENSION LA English DT Discussion C1 NHLBI,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892. W VIRGINIA UNIV,MED CTR,SCH MED,MORGANTOWN,WV 26506. NORTHWESTERN UNIV,SCH MED,DEPT COMMUNITY HLTH & PREVENT MED,CHICAGO,IL 60611. CLIN RES INST MONTREAL,MOLEC PHYSIOL LAB,MONTREAL H2W 1R7,QUEBEC,CANADA. UNIV MISSISSIPPI,MED CTR,JACKSON,MS 39216. OREGON HLTH SCI UNIV,NIDDKD,CLIN NUTR RES UNIT,PORTLAND,OR 97201. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT EPIDEMIOL,PITTSBURGH,PA 15213. RP SULLIVAN, J (reprint author), UNIV TENNESSEE,CTR HLTH SCI,DIV CARDIOVASC DIS,951 COURT AVE,MEMPHIS,TN 38163, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1991 VL 17 IS 1 SU S BP I173 EP I175 PG 3 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA ET145 UT WOS:A1991ET14500036 ER PT J AU ABE, R FOOPHILLIPS, M HODES, RJ AF ABE, R FOOPHILLIPS, M HODES, RJ TI GENETIC-ANALYSIS OF THE MLS SYSTEM - FORMAL MLS TYPING OF THE COMMONLY USED INBRED STRAINS SO IMMUNOGENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; T-CELL RECOGNITION; LYMPHOCYTE STIMULATING DETERMINANTS; IMPARTS REACTIVITY; ENCODED ANTIGENS; IMMUNE-RESPONSE; RECEPTOR; PRODUCTS; MHC; EXPRESSION AB In order to elucidate the biological role of minor lymphocyte stimulating (Mls) gene products, we have been investigating the fundamental immunogenetic characteristics of the Mls system. In this report, we describe the distribution of stimulatory Mls products, Mls(a) and Mls(c), in a panel of laboratory inbred strains based on the response pattern of H-2-compatible naive T-cell populations as well as monospecific Mls(a)- or Mls(c)-reactive T-cell clones. In addition, the expression of four different T-cell receptor (Tcr) b-V segment Tcrb-V3, -V6, -V8.1, and -V9, which were recently reported to be associated with T-cell recognition of Mls gene products in these strains, was examined. The results indicate that the majority of commonly used laboratory strains including those originally typed as Mls(a) are also expressing Mls(c) determinants and that very few independent inbred strains are non-Mls(c). Moreover, the pattern of Tcrb-V expression in spleen as well as in thymus suggests that the association between Mls expression and clonal deletion of self Mls-reactive T cells appears to be the general rule in inbred strains. Based on these results, implications for the nondetectable Mls-like gene products in other species besides the mouse are discussed. RP ABE, R (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B17,BETHESDA,MD 20892, USA. NR 44 TC 20 Z9 20 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JAN PY 1991 VL 33 IS 1 BP 62 EP 73 PG 12 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA EV728 UT WOS:A1991EV72800010 PM 1825308 ER PT J AU MURAKAMI, S MIYAKE, K KINCADE, PW HODES, RJ AF MURAKAMI, S MIYAKE, K KINCADE, PW HODES, RJ TI FUNCTIONAL-ROLE OF CD44 (PGP-1) ON ACTIVATED B-CELLS SO IMMUNOLOGIC RESEARCH LA English DT Article ID LYMPHOCYTE-HOMING RECEPTOR; CROSS-LINKING; MONOCLONAL-ANTIBODIES; INCREASED EXPRESSION; IN(LU)-RELATED P80; STROMAL CELLS; BONE-MARROW; T-CELLS; MOLECULE; ANTIGEN C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B 17,BETHESDA,MD 20892. OKLAHOMA MED RES FDN,OKLAHOMA CITY,OK 73104. FU NIAID NIH HHS [AI-19884, AI-20069] NR 45 TC 19 Z9 19 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 1 BP 15 EP 27 DI 10.1007/BF02918164 PG 13 WC Immunology SC Immunology GA FK719 UT WOS:A1991FK71900002 PM 1865129 ER PT J AU ZEITZ, M JAMES, SP STROBER, W RIECKEN, EO AF ZEITZ, M JAMES, SP STROBER, W RIECKEN, EO TI BASIC MECHANISMS IN MUCOSAL IMMUNOLOGY - PROCEEDINGS OF THE INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY AND IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL-TRACT - PREFACE SO IMMUNOLOGIC RESEARCH LA English DT Editorial Material C1 UNIV MARYLAND,DIV GASTROENTEROL,BALTIMORE,MD 21201. NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. RP ZEITZ, M (reprint author), FREE UNIV BERLIN,KLINIKUM STEGLITZ,COLL MED,DEPT GASTROENTEROL,HINDENBURGDAMM 30,W-1000 BERLIN 45,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 175 EP 176 DI 10.1007/BF02919688 PG 2 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600001 ER PT J AU ZEITZ, M SCHIEFERDECKER, HL ULLRICH, R JAHN, HU JAMES, SP RIECKEN, EO AF ZEITZ, M SCHIEFERDECKER, HL ULLRICH, R JAHN, HU JAMES, SP RIECKEN, EO TI PHENOTYPE AND FUNCTION OF LAMINA PROPRIA LYMPHOCYTES-T SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID NORMAL NONHUMAN-PRIMATES; HELPER-INDUCER; INTESTINAL LYMPHOCYTES; ADHESION MOLECULES; CELLS; ACTIVATION; SUBPOPULATIONS; EXPRESSION; MUCOSA; PREDOMINANCE C1 NIAID,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. RP ZEITZ, M (reprint author), FREE UNIV BERLIN,KLINIKUM STEGLITZ,MED CLIN,DEPT GASTROENTEROL,HINDENBURGDAMM 30,W-1000 BERLIN 45,GERMANY. NR 25 TC 39 Z9 39 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 199 EP 206 DI 10.1007/BF02919693 PG 8 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600006 PM 1955746 ER PT J AU BRAUNELWERT, L JAMES, SP AF BRAUNELWERT, L JAMES, SP TI SELECTIVE T-CELL IMMUNOREGULATORY FUNCTION AND CONTRASUPPRESSION IN THE MUCOSAL IMMUNE-SYSTEM SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID VICIA-VILLOSA LECTIN; LYMPHOCYTES-T; SURFACE GLYCOPROTEINS; BINDING; RESPONSES; LYMPHOBLASTS; SUPPRESSION; EXPRESSION; INVITRO; SUBSETS C1 NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 30 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 211 EP 217 DI 10.1007/BF02919695 PG 7 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600008 PM 1835478 ER PT J AU JAMES, SP MULLIN, GE KANOF, ME ZEITZ, M AF JAMES, SP MULLIN, GE KANOF, ME ZEITZ, M TI ROLE OF LYMPHOKINES IN IMMUNOREGULATORY FUNCTION OF MUCOSAL T-CELLS IN HUMANS AND NONHUMAN-PRIMATES SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID INTESTINAL LAMINA PROPRIA; HELPER-INDUCER; SUPPRESSOR-INDUCER; CROHNS-DISEASE; LYMPHOCYTES; EXPRESSION; ACTIVATION; INTERLEUKIN-5; PREDOMINANCE; ANTI-LEU-8 AB The findings presented above and in other studies provide substantial evidence that lymphocytes in the intestinal lamina propria differ from lymphocyte populations in the circulation or in other tissue sites in a number of ways. First, lamina propria lymphocytes are phenotypically distinct and have evidence of activation. Lymphocytes in the intestinal lamina propria are different in their potential for expression of lymphokine gene products, since activated cells from the lamina propria have high expression of mRNA for IL-2, IL-4, IL-5 and IFN-gamma-in comparison to circulating lymphocytes. Mesenteric lymph node T cells also differ from circulating lymphocytes in their high expression of IL-4 and IL-5 mRNA. A further difference between mesenteric lymph node and lamina propria T cells is that the former are capable of proliferating in response to IL-4, whereas the latter are not. These phenotypic and mRNA differences of lamina propria lymphocytes also correlate well with their high helper activity in vitro for immunoglobulin synthesis in the pokeweed mitogen system. Finally, lamina propria T cells at a site of inflammation are able to provide high helper activity in response to specific antigens. These observations are all consistent with the conclusion that T cells in the lamina propria are pleomorphic, but are highly enriched for subpopulations of activated memory cells that are geared for effector functions. These functions are likely to be critical in maintaining normal host defense in the mucosal environment. C1 NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. OI Mullin, Gerard/0000-0001-5317-6788 NR 26 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 230 EP 238 DI 10.1007/BF02919698 PG 9 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600011 PM 1955747 ER PT J AU WAHL, SM AF WAHL, SM TI THE ROLE OF TRANSFORMING GROWTH-FACTOR-BETA IN INFLAMMATORY PROCESSES SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID CELLULAR RECEPTOR; IGA PRODUCTION; LYMPHOCYTES-B; TGF-BETA; PROLIFERATION; FACTOR-BETA-1; MACROPHAGES; MODULATION; PROTEIN; CELLS RP WAHL, SM (reprint author), NIDR, IMMUNOL LAB, BETHESDA, MD 20892 USA. NR 38 TC 27 Z9 27 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 249 EP 254 DI 10.1007/BF02919701 PG 6 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600014 PM 1955749 ER PT J AU JAMES, SP MURAKAWA, Y KANOF, ME BERG, M AF JAMES, SP MURAKAWA, Y KANOF, ME BERG, M TI MULTIPLE ROLES OF LEU-8/MEL-14 IN LEUKOCYTE ADHESION AND FUNCTION SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID HIGH-ENDOTHELIAL VENULES; NODE HOMING RECEPTOR; CELL-SURFACE MOLECULE; INTESTINAL LAMINA PROPRIA; NORMAL NONHUMAN-PRIMATES; SUPPRESSOR T-CELLS; LYMPHOCYTES-T; LYMPH-NODES; MEL-14 ANTIGEN; HELPER-INDUCER AB Leu-8 and its murine homologue MEL-14 are members of a new family of adhesion molecules encoded on chromosome-1 that share common structural features, including lectin-like domains and tandem repeats homologous to complement binding proteins. The expression of Leu-8 is rapidly down-regulated during cell activation, both at the transcriptional level, and by a rapid post-translational event at the cell membrane, probably involving direct cleavage of the molecule from the cell surface. Lymphocytes that express Leu-8/MEL-14 bind selectively to HEVs in peripheral lymph nodes, and MEL-14 on neutrophils is thought to be important in the initial localization of neutrophils to sites of inflammation. In addition to its role in leukocyte adhesion, there is evidence that the Leu-8 molecule plays a role in cell function. Anti-Leu-8 monoclonal antibody increases suppressor activity of CD4+, Leu-8+ T cells for immunoglobulin synthesis, and anti-Leu-8 directly inhibits differentiation of Leu-8+ B cells. Together these findings indicate that the Leu-8 molecule in common with other cellular adhesion molecules is important not only in cellular adhesion, but also in modification of cell function. C1 NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 49 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 282 EP 292 DI 10.1007/BF02919708 PG 11 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600021 PM 1720159 ER PT J AU STROBER, W HARRIMAN, GR KUNIMOTO, DR AF STROBER, W HARRIMAN, GR KUNIMOTO, DR TI EARLY STEPS OF IGA B-CELL DIFFERENTIATION SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN AB The overall picture of IgA B cell differentiation to emerge from these studies is that sIgM-bearing 'virgin' B cells entering the Peyer's patches are subject to a microenvironment (most probably organ-specific stromal cells) which brings about initial or primary IgA switch differentiation. For reasons mentioned, this probably does not involve TGF-beta, which instead appears to operate on a cell, such as the CH12.LX B cell, which has already undergone the initial steps of IgA isotype switching. The next stage of IgA B cell differentiation involves a cell which expressed both sIgM and sIgA simultaneously and appears to produce C-mu and C-alpha-mRNA transcripts in the absence of a deletional rearrangement. Whether this involves a 'transplicing' mechanism or some other mechanism has yet to be determined. Finally, committed IgA B cells emerge from teh dual-bearing cell population which express only sIgA. These cells can migrate out of Peyer's patches and respond to various terminal differentiation factors such as IL-5, Il-6 and IFN-gamma. RP STROBER, W (reprint author), NIAID,MUCOSAL IMMUN SECT,BETHESDA,MD 20892, USA. NR 5 TC 12 Z9 12 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 386 EP 388 DI 10.1007/BF02919726 PG 3 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600039 PM 1955762 ER PT J AU LYCKE, N SEVERINSON, E STROBER, W AF LYCKE, N SEVERINSON, E STROBER, W TI MOLECULAR EFFECTS OF CHOLERA-TOXIN ON ISOTYPE DIFFERENTIATION SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID B-CELL DIFFERENTIATION; ACTIVATION; SWITCH; TRANSCRIPTS; IGG1; CAMP; INTERLEUKIN-4; PROLIFERATION; INDUCTION; IGE C1 NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. UNIV STOCKHOLM,DEPT IMMUNOL,S-10691 STOCKHOLM,SWEDEN. RP LYCKE, N (reprint author), GOTHENBURG UNIV,DEPT MED MICROBIOL & IMMUNOL,S-41346 GOTHENBURG,SWEDEN. NR 25 TC 10 Z9 10 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 407 EP 412 DI 10.1007/BF02919732 PG 6 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600045 PM 1955767 ER PT J AU HARRIMAN, GR ALLISON, KC STROBER, W AF HARRIMAN, GR ALLISON, KC STROBER, W TI EXPRESSION OF IL-5 RECEPTORS ON B-CELLS - ROLE IN MUCOSAL B-CELL RESPONSES SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID IGA; INTERLEUKIN-5; DIFFERENTIATION; MOUSE AB IL-5 plays an important role in mucosal B cell responses. An in vitro model of IgA B cell differentiation, CH12LX, has been used to demonstrate that IL-5R are expressed on both IgM+ and IgA+ B cells and that IL-5 will enhance secretion of both IgM and IgA by CH12LX B cells, depending on the surface isotype of individual cells. Further, the enhanced secretion of Ig in response to IL-5 is associated with increased steady-state levels of Ig mRNA. Finally, normal Peyer's patch B cells are also capable of expressing IL-5R in response to appropriate stimuli (i.e. anti-IgM- or anti-IgD-dextran). Thus, mucosal B cell responses to IL-5 are brought about by interaction of IL-5 with specific receptors expressed on the surface of those cells. RP HARRIMAN, GR (reprint author), NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892, USA. NR 14 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 413 EP 417 DI 10.1007/BF02919733 PG 5 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600046 PM 1955768 ER PT J AU MURAKAWA, Y STROBER, W JAMES, SP AF MURAKAWA, Y STROBER, W JAMES, SP TI CROSS-LINKING THE LEU-8 LYMPH-NODE HOMING RECEPTOR ON B-CELLS INHIBITS IMMUNOGLOBULIN-SYNTHESIS SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID HIGH-ENDOTHELIAL VENULES; HUMAN LYMPHOCYTES-B; SURFACE MOLECULE; T-CELLS; ACTIVATION; ANTI-LEU-8; LIGANDS; CR-2 AB About one half of circulating human B cells express the Leu-8 peripheral lymph node homing receptor that has been implicated in adhesion of lymphocytes and neutrophils to vascular endothelium. A novel and unique function of the Leu-8 antigen has been found in the present study: anti-Leu-8 monoclonal antibody directly inhibits B cell antibody production induced by SAC + IL-2, without affecting B cell proliferation or other early steps of B cell activation. This effect of anti-Leu-8 is unique in that other antibodies that inhibit B cell differentiation are not selective and also inhibit B cell proliferation. The inhibitory effect is not reversed by addition of T cells, monocytes, or recombinant IL-1 or IL-6 and is not blocked by anti-TGF-beta. Thus, the natural ligand(s) for Leu-8 may be capable of transducing regulatory signals that have a selective effect on B cell differentiation. RP MURAKAWA, Y (reprint author), NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892, USA. NR 26 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 441 EP 446 DI 10.1007/BF02919739 PG 6 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600052 PM 1720160 ER PT J AU SMITH, PD AF SMITH, PD TI ROLE OF CYTOKINES IN INFECTIOUS AND NONINFECTIOUS ENTEROPATHY IN PATIENTS WITH AIDS SO IMMUNOLOGIC RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON FUNDAMENTAL MECHANISMS IN MUCOSAL IMMUNOLOGY IMMUNOLOGICAL DISEASES OF THE GASTROINTESTINAL TRACT CY SEP 12-15, 1990 CL FREE UNIV BERLIN, BERLIN, FED REP GER SP NIAID, MUCOSAL IMMUN SECT, FREE UNIV BERLIN, DEPT GASTROENTEROL HO FREE UNIV BERLIN ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; INJURY RP SMITH, PD (reprint author), NIDR,CELLULAR IMMUNOL SECT,BLDG 30,RM 322,BETHESDA,MD 20892, USA. NR 20 TC 13 Z9 13 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1991 VL 10 IS 3-4 BP 447 EP 451 DI 10.1007/BF02919740 PG 5 WC Immunology SC Immunology GA GF056 UT WOS:A1991GF05600053 PM 1659606 ER PT J AU THOMPSON, HL BURBELO, PD YAMADA, Y KLEINMAN, HK METCALFE, DD AF THOMPSON, HL BURBELO, PD YAMADA, Y KLEINMAN, HK METCALFE, DD TI IDENTIFICATION OF AN AMINO-ACID-SEQUENCE IN THE LAMININ A-CHAIN MEDIATING MAST-CELL ATTACHMENT AND SPREADING SO IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; BASEMENT-MEMBRANES; SYNTHETIC PEPTIDE; GROWTH-FACTOR; INTERLEUKIN-3; FRAGMENTS; RECEPTORS; ADHESION; PROTEIN; BINDING AB PT18 mast cells and mouse bone marrow-derived mast cells have been shown to adhere and spread when in contact with a laminin substratum. Mouse bone marrow cells, however, first require activation with phorbol myristate acetate (PMA), ionophore, or antigen-specific IgE with antigen in order to exhibit these phenomena. Here, we have studied the interaction of these cells with three active synthetic peptides derived from different domains of laminin. PT18 cells and mouse bone marrow mast cells attached and spread on the 19 amino acid synthetic laminin A chain-derived peptide PA22-2, containing the active five amino acid sequence IKVAV, and this attachment did not require prior activation of the mouse bone marrow mast cells with PMA or IgE plus antigen. These cells did not adhere to the B1 chain peptide YIGSR-NH2 or the RGD-containing peptide from the A chain. PT18 cell adherence to laminin was inhibited by soluble peptide PA22-2, but not by either YIGSR-NH2, the RGD-containing, or control peptides. Antisera to the PA22-2 peptide completely abolished adherence to PA22-2, but only partially inhibited mast cell adherence to laminin. Antibody to the 67,000-32,000 MW laminin-binding protein receptor blocked cell adhesion to laminin and to the active A chain peptide. Thus, mast cell adhesion and spreading on laminin may be mediated by an interaction with the IKVAV sequence on the laminin A chain. C1 NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. RP THOMPSON, HL (reprint author), NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BLDG 10,ROOM 11C208,BETHESDA,MD 20892, USA. RI Burbelo, Peter/B-1027-2009 NR 37 TC 20 Z9 20 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD JAN PY 1991 VL 72 IS 1 BP 144 EP 149 PG 6 WC Immunology SC Immunology GA EU945 UT WOS:A1991EU94500025 PM 1997398 ER PT J AU DAX, EM ADLER, WH NAGEL, JE LANGE, WR JAFFE, JH AF DAX, EM ADLER, WH NAGEL, JE LANGE, WR JAFFE, JH TI AMYL NITRITE ALTERS HUMAN INVITRO IMMUNE FUNCTION SO IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY LA English DT Article ID VOLATILE NITRITES; KAPOSIS SARCOMA; HOMOSEXUAL MEN; ISOBUTYL NITRITE; INHALANTS; TOXICITY AB Effects on the human immune system of volatile nitrite inhalation were studied in 18 male volunteers. While nitrite inhalation decreased the absolute number of CD3+ T lymphocytes during the period of inhalation, cell numbers returned to pre-treatment levels within one week after cessation of the drug. Nitrite inhalation did not alter the percentage of CD3+, CD4+, CD8+ or CD19+ lymphocytes. Natural killer (NK) cell activity against K562 target cells was depressed by nitrite administration but returned to pre-inhalation or greater levels after nitrite discontinuation. Cell proliferation following cell activation by PHA, ConA and PWM was unaffected by amyl nitrite inhalation. We conclude that in humans inhalation of volatile nitrites causes cycles of modest immunosuppression, particularly in NK activity, followed by gradual recovery when the drug is not inhaled for several days. C1 NIA,CLIN IMMUNOL SECT,BALTIMORE,MD 21224. NIDA,CTR ADDICT RES,LEXINGTON,KY 40583. NR 26 TC 18 Z9 18 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0892-3973 J9 IMMUNOPHARM IMMUNOT JI Immunopharmacol. Immunotoxicol. PY 1991 VL 13 IS 4 BP 577 EP 587 DI 10.3109/08923979109019724 PG 11 WC Immunology; Pharmacology & Pharmacy; Toxicology SC Immunology; Pharmacology & Pharmacy; Toxicology GA GW222 UT WOS:A1991GW22200008 PM 1685501 ER PT J AU FUCHS, D KRAMER, A REIBNEGGER, G WERNER, ER DIERICH, MP GOEDERT, JJ WACHTER, H AF FUCHS, D KRAMER, A REIBNEGGER, G WERNER, ER DIERICH, MP GOEDERT, JJ WACHTER, H TI NEOPTERIN AND BETA-2-MICROGLOBULIN AS PROGNOSTIC INDEXES IN HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION SO INFECTION LA English DT Article ID IMMUNE-DEFICIENCY SYNDROME; HOMOSEXUAL MEN; HIV INFECTION; URINARY NEOPTERIN; PREDICTIVE MARKER; SYNDROME AIDS; SEROPOSITIVITY; COHORT; RISK AB The great majority of individuals with human immunodeficiency virus type 1 (HIV-1) infection presents with no signs or symptoms, or only lymphadenopathy. To initiate prophylactic measures in time it is necessary to establish risk criteria. CD4 + cell counts are significant predictors. Supplementary methods to improve the predictive information of CD4 + cell counts are still required. In addition, CD4 + cell counting is laborious, expensive, and restricted to specialized laboratories. Thus, there is also a place for more easily performed laboratory tests with similar predictive value as CD4 + cell counts. Neopterin and beta-2-microglobulin levels proved to be significant predictors of AIDS risk in HIV-1 seropositives. The predictive value of both parameters is equal to CD4 + cell counts and both markers are significant joint predictors in addition to CD4 + cell counts. Measurement of the parameters is done in serum (neopterin and beta-2-microglobulin) or urine (neopterin) specimens which reduces the risk of HIV-1 transmission compared to handling of whole-blood samples as it is required for cell counting. Although more studies are needed, especially in developing countries and in persons receiving zidovudine, it can be recommended to use neopterin and beta-2-microglobulin as additional marker to estimate AIDS risk in HIV-1 seropositive individuals. Moreover, both markers may be useful for this purpose without CD4 + cell counts if cell counting is not available. C1 LUDWIG BOLTZMANN INST AIDS FORSCH, A-6020 INNSBRUCK, AUSTRIA. UNIV TUBINGEN, INST MED BIOMETRIE, W-7400 TUBINGEN 1, GERMANY. UNIV INNSBRUCK, INST HYG, A-6020 INNSBRUCK, AUSTRIA. NCI, EPIDEMIOL & BIOSTAT PROGRAM, BETHESDA, MD 20892 USA. RP UNIV INNSBRUCK, INST MED CHEM & BIOCHEM, A-6020 INNSBRUCK, AUSTRIA. RI Reibnegger, Gilbert/H-5742-2012 OI Reibnegger, Gilbert/0000-0001-7202-2426 NR 31 TC 29 Z9 29 U1 0 U2 2 PU SPRINGER HEIDELBERG PI HEIDELBERG PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY SN 0300-8126 EI 1439-0973 J9 INFECTION JI Infection PY 1991 VL 19 SU 2 BP S98 EP S102 DI 10.1007/BF01644476 PG 5 WC Infectious Diseases SC Infectious Diseases GA FA471 UT WOS:A1991FA47100005 PM 1673120 ER PT J AU KURASHIMA, C SANDBERG, AL CISAR, JO MUDRICK, LL AF KURASHIMA, C SANDBERG, AL CISAR, JO MUDRICK, LL TI COOPERATIVE COMPLEMENT-INITIATED AND BACTERIAL LECTIN-INITIATED BACTERICIDAL ACTIVITY OF POLYMORPHONUCLEAR LEUKOCYTES SO INFECTION AND IMMUNITY LA English DT Article ID ACTINOMYCES-VISCOSUS T14V; TYPE-2 FIMBRIAL LECTIN; ESCHERICHIA-COLI; FUSOBACTERIUM-NUCLEATUM; NONOPSONIC PHAGOCYTOSIS; PSEUDOMONAS-AERUGINOSA; CHEMI-LUMINESCENCE; HUMAN-NEUTROPHILS; RECEPTORS; NAESLUNDII AB The recognition of glycoconjugate receptors on sialidase-treated polymorphonuclear leukocytes (PMNs) by the Gal/GalNAc-reactive fimbrial lectin of Actinomyces viscosus T14V has previously been shown to initiate lactose-inhibitable phagocytosis and subsequent killing of the bacteria. Although a mutant lacking fimbriae, A. viscosus 147, was not destroyed by this mechanism, the present studies demonstrate that the deposition of C3 fragments on this bacterium by anti-A. viscosus 147 immunoglobulin M (IgM) prior to incubation with either untreated or sialidase-treated PMNs correlated with a reduction in viability of approximately 2 log10. This bactericidal activity was unaffected by lactose. A similar decrease in viability was observed following the addition of untreated PMNs to A. viscosus T14V preincubated with anti-A. viscosus 147 IgM and complement, conditions favorable for C3- but not lectin-mediated bactericidal activity. Neither IgM nor complement alone was opsonic for either strain, and individually they did not alter killing of A. viscosus T14V by sialidase-treated PMNs or inhibition of this bactericidal activity by lactose. The number of viable A. viscosus T14V cells was decreased by approximately 3.5 log10 when the bacteria were incubated with IgM and complement prior to the addition of sialidase-treated PMNs, and lactose only partially inhibited this response. Thus, the PMN-dependent bactericidal activity initiated by the participation of both the actinomyces lectin and complement was significantly greater than that achieved by either ligand alone. C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. NR 49 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1991 VL 59 IS 1 BP 216 EP 221 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP751 UT WOS:A1991EP75100033 PM 1987035 ER PT J AU BARBOUR, AG CARTER, CJ BURMAN, N FREITAG, CS GARON, CF BERGSTROM, S AF BARBOUR, AG CARTER, CJ BURMAN, N FREITAG, CS GARON, CF BERGSTROM, S TI TANDEM INSERTION SEQUENCE-LIKE ELEMENTS DEFINE THE EXPRESSION SITE FOR VARIABLE ANTIGEN GENES OF BORRELIA-HERMSII SO INFECTION AND IMMUNITY LA English DT Article ID TRYPANOSOMA-BRUCEI; MAJOR PROTEINS; ESCHERICHIA-COLI; STRANDED-DNA; TRANSCRIPTION; TRANSPOSITION; BURGDORFERI; POLYMERASE; PLASMIDS; VECTORS AB The spirochete Borrelia hermsii avoids the immune response of its mammalian host through multiphasic antigenic variation. Serotype specificity is determined by variable antigens, Vmp proteins, in the outer membrane. Through nonreciprocal recombination between linear plasmids, and formerly silent vmp gene replaces another vmp gene downstream from a common expression site. To further characterize this activating site, we determined the nucleotide sequence of 6.9 kb of the common upstream expression region of strain HS1 of B. hermsii. Preceding the vmp gene promoter and a poly(dT . dA) run were three imperfectly repeated segments of 2 kb. Each of the 2-kb segments contained 1-kb elements with inverted repeats of approximately 0.2 kb each at their termini. The potential of the 1-kb elements to form stem-and-loop structures was demonstrated by heteroduplex analysis. There was no evidence of the presence of the elements elsewhere in the genome of B. hermsii. One or more of these elements may confer the unidirectionality that characterizes vmp gene switches. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UMEA UNIV,DEPT MICROBIOL,S-90187 UMEA,SWEDEN. NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840. RP BARBOUR, AG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MICROBIOL,SAN ANTONIO,TX 78284, USA. RI Barbour, Alan/B-3160-2009 OI Barbour, Alan/0000-0002-0719-5248 FU NIAID NIH HHS [AI24424] NR 46 TC 27 Z9 28 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1991 VL 59 IS 1 BP 390 EP 397 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP751 UT WOS:A1991EP75100057 PM 1987053 ER PT J AU OGATA, M PASTAN, I FITZGERALD, D AF OGATA, M PASTAN, I FITZGERALD, D TI ANALYSIS OF PSEUDOMONAS EXOTOXIN ACTIVATION AND CONFORMATIONAL-CHANGES BY USING MONOCLONAL-ANTIBODIES AS PROBES SO INFECTION AND IMMUNITY LA English DT Article ID ESCHERICHIA-COLI; DOMAIN-II; LOW PH; AERUGINOSA; TOXIN; PROTEINS; GENE AB Pseudomonas exotoxin (PE) is a protein toxin composed of three structural domains. In its native form, the toxin is a 66,000-M(r) proenzyme that must be activated to express full ADP-ribosylating activity. To study the process of activation and accompanying conformational changes, we have isolated 10 monoclonal antibodies to a 40,000-M(r) fragment of the toxin (PE40) that exhibits full enzyme activity but lacks the toxin's cell-binding domain and contains amino acids 253 to 613 (comprising domains II, Ib, and III). By using mutant PE molecules in which all of domain I and portions of domains II, Ib, and III were deleted, the locations of the epitopes for each of the antibodies were determined. Eight of these monoclonal antibodies were further characterized. Of these eight, all reacted with soluble PE40 and an interleukin-2-PE40 conjugate, but only two reacted strongly with native soluble PE. However, all eight reacted with PE after it had been immobilized on nitrocellulose or after it had been activated to express full ADP-ribosylating activity. Antibodies were also assessed for their ability to neutralize the cytotoxic activity of either PE or interleukin-2-PE40. These antibodies should be useful as probes for monitoring the activation and processing of PE that occur during endocytosis and in determining the location of epitopes that are important for toxin activity. C1 NCI,DIV CANC BIOL & DIAG,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 27 TC 32 Z9 34 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1991 VL 59 IS 1 BP 407 EP 414 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP751 UT WOS:A1991EP75100059 PM 1702764 ER PT J AU KINET, JP BLANK, U BRINI, A JOUVIN, MH KUSTER, H MEJAN, O RA, C AF KINET, JP BLANK, U BRINI, A JOUVIN, MH KUSTER, H MEJAN, O RA, C TI THE HIGH-AFFINITY RECEPTOR FOR IMMUNOGLOBULIN-E - A TARGET FOR THERAPY OF ALLERGIC DISEASES SO INTERNATIONAL ARCHIVES OF ALLERGY AND APPLIED IMMUNOLOGY LA English DT Article; Proceedings Paper CT 18TH SYMP OF THE COLLEQIUM-INTERNATIONALE-ALLERGOLOGICUM ON CELLULAR AND MOLECULAR NETWORKS IN CLINICAL IMMUNOLOGY AND ALLERGY CY SEP 22-26, 1990 CL FUNCHAL, PORTUGAL SP COLLEGIUM INT ALLERGOLOGICUM ID NATURAL-KILLER-CELLS; FC-GAMMA RECEPTOR; IGE RECEPTOR; ZETA-CHAIN; TRANSFECTED CELLS; MOLECULAR-CLONING; ALPHA-SUBUNIT; ANTIGEN RECEPTOR; MAST-CELLS; EXPRESSION AB The high-affinity receptor for IgE (Fc-epsilon-RI) on mast cells and basophils is a tetrameric complex, alpha-beta-gamma-2. Here we summarize the latest developments on the structure and function of this receptor. By genetic transfer, we have engineered a cell line secreting substantial amounts of a peptide containing exclusively the extracellular domain of the alpha-subunit. This domain by itself is sufficient to mediate high-affinity binding of IgE. Glycosylation and the presence of the other subunits are not necessary for the binding function. The gamma-subunit of Fc-epsilon-RI is part of other receptors such as Fc-gamma-RIII and the T cell receptor, and therefore is likely to play an important although still undefined functional role. A detailed knowledge of how the receptor interacts with IgE and induces cellular degranulation may lead to the design of new therapeutic approaches to allergic diseases. The potential strategies are discussed. RP KINET, JP (reprint author), NIAID,MOLEC ALLERGY & IMMUNOL SECT,TWINBROOK 2 BLDG,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. OI Brini, Anna Teresa/0000-0002-7848-8099 NR 34 TC 29 Z9 31 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0020-5915 J9 INT ARCH ALLER A IMM PY 1991 VL 94 IS 1-4 BP 51 EP 55 PG 5 WC Allergy; Immunology SC Allergy; Immunology GA GP205 UT WOS:A1991GP20500006 PM 1834584 ER PT J AU ROTTEM, M KIRSHENBAUM, AS METCALFE, DD AF ROTTEM, M KIRSHENBAUM, AS METCALFE, DD TI EARLY DEVELOPMENT OF MAST-CELLS SO INTERNATIONAL ARCHIVES OF ALLERGY AND APPLIED IMMUNOLOGY LA English DT Article; Proceedings Paper CT 18TH SYMP OF THE COLLEQIUM-INTERNATIONALE-ALLERGOLOGICUM ON CELLULAR AND MOLECULAR NETWORKS IN CLINICAL IMMUNOLOGY AND ALLERGY CY SEP 22-26, 1990 CL FUNCHAL, PORTUGAL SP COLLEGIUM INT ALLERGOLOGICUM ID COLONY-STIMULATING FACTOR; BASOPHIL-LIKE CELLS; MOUSE BONE-MARROW; GROWTH-FACTOR ACTIVITY; MONONUCLEAR PHAGOCYTES; PERIPHERAL-BLOOD; CDNA CLONE; T-CELLS; P-CELL; INTERLEUKIN-3 AB Mast cells originate from pluripotential cells in the bone marrow. Specifically, human mast cells originate from CD 34-positive progenitor cells. Mast cell proliferation requires IL-3. In the mouse, additional mast cell growth is achieved by the addition of IL-4, and GM-CSF prevents mast cell proliferation. Early bone-marrow-derived mast cells can be identified by their IgE receptors, although they may not yet have the characteristic morphology of mature mast cells. Whether these early cells may by themselves have a physiologic role, remains to be determined. Mast cells persist in culture on fibroblast monolayers, in part due to the production of soluble factor(s) from the fibroblasts themselves. Final mast cell phenotype appears dependent upon the local tissue environment. RP ROTTEM, M (reprint author), NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BLDG 10,ROOM 11C210,BETHESDA,MD 20892, USA. NR 47 TC 11 Z9 11 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0020-5915 J9 INT ARCH ALLER A IMM PY 1991 VL 94 IS 1-4 BP 104 EP 109 PG 6 WC Allergy; Immunology SC Allergy; Immunology GA GP205 UT WOS:A1991GP20500022 PM 1718881 ER PT J AU SEDER, RA PAUL, WE BENSASSON, SZ LEGROS, GS KAGEYSOBOTKA, A FINKELMAN, FD PIERCE, JH PLAUT, M AF SEDER, RA PAUL, WE BENSASSON, SZ LEGROS, GS KAGEYSOBOTKA, A FINKELMAN, FD PIERCE, JH PLAUT, M TI PRODUCTION OF INTERLEUKIN-4 AND OTHER CYTOKINES FOLLOWING STIMULATION OF MAST-CELL LINES AND INVIVO MAST-CELLS BASOPHILS SO INTERNATIONAL ARCHIVES OF ALLERGY AND APPLIED IMMUNOLOGY LA English DT Article; Proceedings Paper CT 18TH SYMP OF THE COLLEQIUM-INTERNATIONALE-ALLERGOLOGICUM ON CELLULAR AND MOLECULAR NETWORKS IN CLINICAL IMMUNOLOGY AND ALLERGY CY SEP 22-26, 1990 CL FUNCHAL, PORTUGAL SP COLLEGIUM INT ALLERGOLOGICUM ID SPLENIC NON-B; NON-T CELLS; CROSS-LINKAGE; FC-RECEPTORS; IGE; LYMPHOKINES; PATTERNS AB Interleukin-3 (IL-3)-dependent mast cell lines, upon stimulation by calcium ionophores or by Fc-epsilon-RI cross-linking, express mRNA for, and secrete, a distinct pattern of cytokines, similar to those secreted by cloned mouse T cells of the T(H2) type. The mast-cell-derived cytokines include IL-3, IL-4 IL-5, and IL-6. Not only in vitro mast cell lines, but also in vivo derived peritoneal mast cells secrete cytokines. An in vivo derived cell, in mouse spleen and bone marrow, secretes IL-4 and other cytokines upon stimulation with calcium ionophores or by Fc-epsilon-RI cross-linking or Fc-gamma-RII cross-linking. The IL-4-producing cells are highly enriched in the Fc-epsilon-R+ subset of spleen and bone marrow cells. These Fc-epsilon-R+ cells produce large amounts of IL-4, and they have characteristics similar to those of immature mast cells and/or basophils. It is possible that cytokines produced by mast cells and/or basophils participate in allergic inflammatory diseases. C1 JOHNS HOPKINS UNIV,SCH MED,JOHNS HOPKINS ASTHMA & ALLERGY CTR,DEPT MED,BALTIMORE,MD 21224. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,HADASSAH MED CTR,LAUTENBERG CTR TUMOR IMMUNOL,JERUSALEM,ISRAEL. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. FU NHLBI NIH HHS [HL37119]; NIAID NIH HHS [AI27906] NR 17 TC 84 Z9 84 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0020-5915 J9 INT ARCH ALLER A IMM PY 1991 VL 94 IS 1-4 BP 137 EP 140 PG 4 WC Allergy; Immunology SC Allergy; Immunology GA GP205 UT WOS:A1991GP20500028 PM 1834578 ER PT J AU PETRO, SJ HERRMANN, D BURROWS, D MOORE, CM AF PETRO, SJ HERRMANN, D BURROWS, D MOORE, CM TI USEFULNESS OF COMMERCIAL MEMORY AIDS AS A FUNCTION OF AGE SO INTERNATIONAL JOURNAL OF AGING & HUMAN DEVELOPMENT LA English DT Article C1 GOLDMAN SACHS & CO,NEW YORK,NY. NIMH,BETHESDA,MD 20892. SKIDMORE COLL,SARATOGA SPRINGS,NY 12866. NR 18 TC 10 Z9 10 U1 0 U2 1 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0091-4150 J9 INT J AGING HUM DEV JI Int. J. Aging Human Dev. PY 1991 VL 33 IS 4 BP 295 EP 309 DI 10.2190/0J3N-F3QB-TEDH-CUYX PG 15 WC Gerontology; Psychology, Developmental SC Geriatrics & Gerontology; Psychology GA GQ059 UT WOS:A1991GQ05900004 PM 1761318 ER PT J AU KUBICZ, A SZALEWICZ, A CHRAMBACH, A AF KUBICZ, A SZALEWICZ, A CHRAMBACH, A TI STUDIES ON THE OLIGOSACCHARIDE HETEROGENEITY OF THE ISOELECTRIC FORMS OF THE LOWER MOLECULAR-WEIGHT ACID-PHOSPHATASE OF FROG LIVER SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY LA English DT Article ID RANA-ESCULENTA; MULTIPLE FORMS; ENZYME AB 1. The lower molecular weight, heterogeneous acid phosphatase (AcPase) from the frog liver (Rana esculenta) containing AcPase I, II, III and IV was separated into enzymatically active components by isoelectric focusing in an immobilized pH gradient. 2. The blotted enzyme bands were characterized by their different binding patterns obtained with the lectins concanavalin A, wheat germ agglutinin (WGA), Lens culinaris hemagluttinin (LcH) and peanut agglutinin (PNA). 3. In situ neuraminidase treatment reduced the staining intensity of some WGA-bands and increased that of PNA-bands. 4. The finding that AcPases I, II, III and IV differ in their carbohydrate chain composition, together with previous results showing different bioactivities of AcPases III and IV, indicates a correlation between the glycosylation state of enzyme forms and their physiological action. C1 NICHHD,THEORET & PHYS BIOL LAB,BLDG 10,ROOM 6C 101,BETHESDA,MD 20892. WROCLAW B BEIRUT UNIV,INST BIOCHEM,PL-50137 WROCLAW,POLAND. NR 20 TC 5 Z9 5 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0020-711X J9 INT J BIOCHEM JI Int. J. Biochem. PY 1991 VL 23 IS 4 BP 413 EP 419 DI 10.1016/0020-711X(91)90168-M PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EW785 UT WOS:A1991EW78500005 PM 2015951 ER PT J AU FARZANEH, NK WALDEN, TL HEARING, VJ GERSTEN, DM AF FARZANEH, NK WALDEN, TL HEARING, VJ GERSTEN, DM TI COMPARISON OF THE METABOLIC-FATE AND TISSUE DISTRIBUTION OF B700, AN ALBUMIN-LIKE MELANOMA-SPECIFIC ANTIGEN WITH SERUM-ALBUMIN IN NORMAL AND TUMOR-BEARING MICE SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY LA English DT Article ID MURINE B-16 MELANOMA; MALIGNANT-MELANOMA; BINDING-PROTEIN; GROWTH; INVIVO AB 1. B700, a murine melanoma antigen, is a member of the serum albumin protein family, being closely related to murine serum albumin (MSA). 2. We have studied and compared the metabolic fate and anatomic distribution of radioiodinated B700 and MSA administered to semisyngeneic naive and tumor-bearing mice. 3. Labelled material from both proteins is excreted primarily into urine. 4. The rate of excretion of the two proteins is markedly different, with B700 having a shorter half-life in the body. 5. Despite their similar molecular weights, intact B700 represents approx. 30% of the radioactivity in the urine but only 4% of the MSA in the urine is intact. 6. These studies demonstrate that the host can readily distinguish between very similar normal (MSA) and tumor-associated (B700) molecules and process them differently. 7. Similar findings of differential fate and distribution have been reported in comparing other albuminoid molecules [Dueland S., Blomhoff R. and Pedersen J. I. (1990) Biochem. J. 267, 721-725]. C1 GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20007. USA,RADIOBIOL RES INST,DEPT RADIAT BIOCHEM,BETHESDA,MD 20814. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 25 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0020-711X J9 INT J BIOCHEM JI Int. J. Biochem. PY 1991 VL 23 IS 12 BP 1385 EP 1391 DI 10.1016/0020-711X(91)90279-V PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GP203 UT WOS:A1991GP20300006 PM 1761148 ER PT J AU LU, YY BLAIR, DG SEGAL, S SHIH, TY CLANTON, DJ AF LU, YY BLAIR, DG SEGAL, S SHIH, TY CLANTON, DJ TI TUMORIGENICITY, METASTASIS AND SUPPRESSION OF MHC CLASS-I EXPRESSION IN MURINE FIBROBLASTS TRANSFORMED BY MUTANT V-RAS DEFICIENT IN GTP BINDING SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID GUANINE-NUCLEOTIDE-BINDING; NIH 3T3 CELLS; H-RAS; BIOCHEMICAL-PROPERTIES; GENE-EXPRESSION; SARCOMA-VIRUS; P21 PROTEIN; MUTATIONS; ONCOGENE AB We have introduced point mutations in v-ras(H) to study their effects on biochemical and biological properties of the ras-encoded protein p21. Several of these mutant proteins do not bind GTP and thus lack GTPase activity, while others were shown to have their GTP binding reduced. We have introduced these ras mutants into NIH 3T3 fibroblastoid cells to study major parameters of clinical importance which are associated with neoplastic transformation, particularly MHC expression in cells, metastasis and tumorigenesis in both nude mice and immune competent mice. Our data show that certain mutations in v-ras differentially affect the expression of the transformed phenotype. Mutant ras molecules deficient in GTP binding fail to generate rapidly progressing tumors in immune competent mice, and not all morphologically transformed cells were capable of experimental metastasis. Cells transformed by certain v-ras mutants form tumors in immunocompetent mice and show reduced expression of MHC class-I antigens. Other cells are morphologically transformed and tumorigenic in athymic nude mice, but fail to form tumors in normal mice and show levels of MHC class-I antigen expression similar to non-transformed 3T3 cells. The inverse relationship between MHC class-I-antigen expression and the degree of transformation in fibroblastoid cells suggests that the ras gene product could be involved in regulating MHC expression. C1 BEN GURION UNIV NEGEV,FAC HLTH SCI,DEPT IMMUNOL & MICROBIOL,IL-84105 BEER SHEVA,ISRAEL. RP LU, YY (reprint author), NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702, USA. NR 30 TC 0 Z9 0 U1 1 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PY 1991 SU 6 BP 45 EP 53 PG 9 WC Oncology SC Oncology GA FV942 UT WOS:A1991FV94200011 ER PT J AU ADAMS, JD KLAIDMAN, LK ODUNZE, IN JOHANNESSEN, JN AF ADAMS, JD KLAIDMAN, LK ODUNZE, IN JOHANNESSEN, JN TI EFFECTS OF MPTP ON THE CEREBROVASCULATURE SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE MPTP; BRAIN MICROVASCULATURE; BLOOD BRAIN BARRIER ID INCOMPLETE CEREBRAL-ISCHEMIA; SUBSEQUENT RECIRCULATION; CORTICAL CONCENTRATIONS; REDUCED GLUTATHIONE; PEROXIDASE; RAT AB The neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, has been shown to cause pooling of blood in the brain microvasculature and decrease the permeability of the blood-brain barrier. All areas of the brain examined in this study were affected. This study points out the possibility that reduced nutrient uptake, hypoxia and ensuing free radical damage are involved in the mechanism of toxicity of this neurotoxin. C1 NIH,BETHESDA,MD 20205. RP ADAMS, JD (reprint author), UNIV SO CALIF,SCH PHARM,1985 ZONAL AVE,LOS ANGELES,CA 90033, USA. FU NINDS NIH HHS [NS-23515] NR 12 TC 10 Z9 10 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PY 1991 VL 9 IS 2 BP 155 EP 159 DI 10.1016/0736-5748(91)90006-8 PG 5 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA EZ888 UT WOS:A1991EZ88800006 PM 2058417 ER PT J AU LUSTER, MI ROSENTHAL, GJ CAO, W THOMPSON, MB MUNSON, AE PREJEAN, JD SHOPP, G FUCHS, BA GERMOLEC, DR TOMASZEWSKI, JE AF LUSTER, MI ROSENTHAL, GJ CAO, W THOMPSON, MB MUNSON, AE PREJEAN, JD SHOPP, G FUCHS, BA GERMOLEC, DR TOMASZEWSKI, JE TI EXPERIMENTAL STUDIES OF THE HEMATOLOGIC AND IMMUNE-SYSTEM TOXICITY OF NUCLEOSIDE DERIVATIVES USED AGAINST HIV-INFECTION SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article ID IMMUNODEFICIENCY VIRUS-INFECTION; PLACEBO-CONTROLLED TRIAL; AIDS-RELATED COMPLEX; BONE-MARROW; PROGENITOR CELLS; INTERFERON-ALPHA; PHASE-I; ZIDOVUDINE; INVITRO; MICE AB Adverse effects stemming from the therapeutic use of dideoxynucleoside derivatives continue to occur in patients with AIDS or AIDS-related complex. For example, the continued use of 3'-azido-3'-deoxythymidine (AZT) and 2',3'-didoxycytidine (ddC), both of which confer clinical benefits in AIDS patients, may be complicated by anemia, neutropenia and thrombocytopenia and ddC also causes peripheral neuropathy. Subsequently, the National Toxicology Program (NTP) has undertaken efforts to define and characterize the toxicities associated with currently employed and potential AIDS therapeutics in experimental animals, with particular emphasis on the hematopoietic and immune systems. In addition to AZT and ddC, 2',3'-dideoxyadenonsine (ddA), 2',3'-dideoxyinosine (ddl) and 2',3'-didehydro-dideoxythymidine (d4T) have been examined. The present studies describe: (1) the development of a poorly regenerative macrocytic anemia in mice exposed to AZT or ddC. This anemia demonstrates a rapid and progressive time course of toxicity and reversibility after cessation of treatment; (2) the selective suppression of erythroid progenitor cells in mice exposed to d4T without concomitant effects on myeloid stem cells. Myelotoxicity appears to show metabolism-dependent strain-specificity and is more evident following in vitro exposure than in vivo exposure; and (3) the immunosuppressive effects following subchronic (30-day) exposure. Of the nucleoside derivatives studied, only ddA and ddI altered immune function and these changes were confined to suppression of antibody responses. It can be concluded that the overall similarities in the hematopoietic and immune system effects between rodents and humans indicate that such animal toxicology studies provide important information relevant to the toxicity of these drugs. C1 NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. SO RES INST,BIRMINGHAM,AL 35255. LOVELACE FDN MED EDUC & RES,ALBUQUERQUE,NM 87108. NCI,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 26 TC 16 Z9 16 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PY 1991 VL 13 SU 1 BP 99 EP 107 DI 10.1016/0192-0561(91)90131-P PG 9 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA HP981 UT WOS:A1991HP98100014 PM 1668555 ER PT J AU SANDERS, VM POWELLOLIVER, FE ROSENTHAL, GJ GERMOLEC, DR LUSTER, MI AF SANDERS, VM POWELLOLIVER, FE ROSENTHAL, GJ GERMOLEC, DR LUSTER, MI TI IMMUNE-ASSOCIATED TOXICITIES INDUCED BY INVIVO AND INVITRO EXPOSURE TO INTERFERON-ALPHA ALONE OR IN COMBINATION WITH NUCLEOSIDE ANALOGS SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article ID B-CELLS; PROLIFERATION; GROWTH; BETA; AIDS; MICE AB The present studies examine whether immune-associated toxicities develop in rodents exposed to recombinant human interferon-alpha A/D (rHuIFN-alpha) alone or in combination with anti-retroviral nucleoside analogs. Four findings have emerged from these studies: (1) lymphocyte cell number and functional activity are suppressed after subchronic (1, 8 or 10 day) in vivo exposure to therapeutic doses of rHuIFN-alpha; (2) lymphocyte-associated toxicities lessen as in vivo exposure time to rHuIFN-alpha is extended; (3) T-cell-dependent antibody production is decreased after in vitro exposure of both antigen-specific T- and B-cells to rHuIFN-alpha; and (4) in vivo-induced leukocyte toxicities associated with either rHuIFN-alpha or the nucleoside analogs alone do not synergize when the therapies are combined. These data suggest that certain key immune parameters should be monitored carefully in the early stages of IFN-alpha therapy. C1 NIEHS,SYST TOX BRANCH,RES TRIANGLE PK,NC 27709. NR 19 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 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PY 1991 VL 13 SU 1 BP 109 EP 115 DI 10.1016/0192-0561(91)90132-Q PG 7 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA HP981 UT WOS:A1991HP98100015 PM 1668554 ER PT J AU LORBERBOUMGALSKI, H LAFYATIS, R CASE, JP FITZGERALD, D WILDER, RL PASTAN, I AF LORBERBOUMGALSKI, H LAFYATIS, R CASE, JP FITZGERALD, D WILDER, RL PASTAN, I TI ADMINISTRATION OF IL-2-PE40 VIA OSMOTIC PUMPS PREVENTS ADJUVANT INDUCED ARTHRITIS IN RATS - IMPROVED THERAPEUTIC INDEX OF IL-2-PE40 ADMINISTERED BY CONTINUOUS INFUSION SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article ID FUSION PROTEIN; INTERLEUKIN-2; RECEPTOR; TRANSPLANTATION; IMMUNOTHERAPY; LYMPHOCYTES; INDUCTION; TOXIN AB IL-2-PE40 is a chimeric cytotoxin composed of interleukin 2 (IL-2) fused to a truncated form of Pseudomonas exotoxin (PE) that lacks its binding domain. IL-2-PE40 has been shown to exhibit therapeutic potency in several models in vivo when administered i.p. twice a day. Here we show that the continuous administration of IL-2-PE40 by an osmotic pump specifically prevents the development of adjuvant induced arthritis in rats with an improved therapeutic efficacy as compared to daily repeated i.p. injections. Stabilization of IL-2-PE40 at 37-degrees-C for the continuous administration by pumps was achieved by adding NAD, the substrate for the enzyme portion of the chimeric toxin. C1 NIAMSD,CONNECT TISSUE DIS SECT,BETHESDA,MD 20892. RP LORBERBOUMGALSKI, H (reprint author), NCI,DIV CANC BIOL & DIAG,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 25 TC 13 Z9 14 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PY 1991 VL 13 IS 2-3 BP 305 EP 315 DI 10.1016/0192-0561(91)90112-K PG 11 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA FD820 UT WOS:A1991FD82000026 PM 2071302 ER PT J AU BEVER, CT JACOBSON, S MINGIOLI, ES MCFARLAND, HF MCFARLIN, DE LEVY, HB AF BEVER, CT JACOBSON, S MINGIOLI, ES MCFARLAND, HF MCFARLIN, DE LEVY, HB TI CHANGES IN LEUKOCYTE RECIRCULATION, NK CELL-ACTIVITY, AND HLA-DR EXPRESSION IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS OF MS PATIENTS TREATED WITH POLY ICLC SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Note ID L-LYSINE; MULTIPLE-SCLEROSIS; POLYCYTIDYLIC ACID; INTERFERON-GAMMA; CYTO-TOXICITY; CARBOXYMETHYLCELLULOSE; ENHANCEMENT; ACTIVATION; VIRUS; LYMPHOCYTES AB To investigate the cellular immune effects of the interferon inducer, Poly ICLC, in humans, peripheral blood mononuclear cells from patients with multiple sclerosis receiving Poly ICLC as part of a preliminary clinical trial were studied. Peripheral blood mononuclear cell phenotype analysis using fluoresceinated monoclonal antibodies and flow microfluorometry showed decreases in the percentages and absolute numbers of all lymphocyte subsets 24 h after infusion. These changes returned toward baseline at 48 h except the percentage of CD-4 positive cell which increased above baseline levels. The percentage of HLA-DR antigen positive cells and CD-16 (Leu 11a) positive cells were increased 24 h after infusion but returned to baseline at 48 h. NK activity as determined by chromium release from K562 target cells was decreased at 24 h but increased 48 h after drug infusion. The increases in percentages of HLA-DR antigen and CD-16 positive cells at 24 h and NK activity at 48 h are consistent with the in vitro effects of IFN while the decreases in peripheral blood mononuclear cells are suggestive of changes in cell recirculation. C1 NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. NIAID,VIRAL DIS LAB,FREDERICK,MD 21701. NR 28 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PY 1991 VL 13 IS 5 BP 613 EP 618 DI 10.1016/0192-0561(91)90084-K PG 6 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA GC881 UT WOS:A1991GC88100022 PM 1783475 ER PT J AU TRYPHONAS, H LUSTER, MI WHITE, KL NAYLOR, PH ERDOS, MR BURLESON, GR GERMOLEC, D HODGEN, M HAYWARD, S ARNOLD, DL AF TRYPHONAS, H LUSTER, MI WHITE, KL NAYLOR, PH ERDOS, MR BURLESON, GR GERMOLEC, D HODGEN, M HAYWARD, S ARNOLD, DL TI EFFECTS OF PCB (AROCLOR-1254) ON NONSPECIFIC IMMUNE PARAMETERS IN RHESUS (MACACA-MULATTA) MONKEYS SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article ID INTERLEUKIN-2 RECEPTOR EXPRESSION; TUMOR NECROSIS FACTOR; NORMAL HUMAN-LYMPHOCYTES; POLYCHLORINATED BIPHENYL; IMMUNOLOGICAL EVALUATION; THYMOSIN ALPHA-1; THYMIC HORMONES; CYTO-TOXICITY; COMPLEMENT; MODULATION AB The effects of low level, chronic polychlorinated biphenyl - Aroclor(R) 1254 - (PCB) exposure were investigated on non-specific immune parameters in female rhesus (Macaca mulatta) monkeys. Five groups of monkeys were orally administered with PCB at concentrations of 0, 5, 20, 40 or 80-mu-g/kg bw/day. Immunotoxicity testing was initiated after 55 months of exposure. The serum hemolytic complement activity in all PCB treated groups was significantly higher (P < 0.05) than that in the control group. A statistically significant dose-related increase in natural killer cell activity was evident at the 75 : 1 effector to target cell ratio. Similarly, a statistically significant dose-related increase was noted for thymosin alpha-1 levels but not for thymosin beta-4 levels. Statistically significant increased interferon levels were noted in the 20 and 80-mu-g/kg groups compared with the control group while the levels in the 40-mu-g/kg group were decreased significantly compared with the control group. The production of tumor necrosis factor by monocytes in the PCB treated groups was not different to that in the control group. The results indicated that long term exposure to PCB modulate several non-specific immune parameters. C1 GEORGE WASHINGTON UNIV,MED CTR,DEPT BIOCHEM & MOLEC BIOL,WASHINGTON,DC 20037. US EPA,HLTH EFFECTS RES LAB,RES TRIANGLE PK,NC 27711. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT TOXICOL,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT BIOSTAT,RICHMOND,VA 23298. NIEHS,IMMUNOTOXICOL GRP,RES TRIANGLE PK,NC 27709. RP TRYPHONAS, H (reprint author), HLTH & WELF CANADA,HLTH PROTECT BRANCH,BUR CHEM SAFETY,DIV TOXICOL RES,OTTAWA K1A 0L2,ONTARIO,CANADA. FU FDA HHS [5VO1-FD-01217-02, FD 226-80-0003-01]; NCI NIH HHS [5-RO1-CA24974-11] NR 45 TC 38 Z9 38 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PY 1991 VL 13 IS 6 BP 639 EP 648 DI 10.1016/0192-0561(91)90176-8 PG 10 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA GK846 UT WOS:A1991GK84600003 PM 1721612 ER PT J AU VILLA, ML ARMELLONI, S FERRARIO, E OTTAVIANI, F CLERICI, M AF VILLA, ML ARMELLONI, S FERRARIO, E OTTAVIANI, F CLERICI, M TI INTERFERENCE OF CEPHALOSPORINS WITH IMMUNE-RESPONSE - EFFECTS OF CEFONICID ON HUMAN T-HELPER CELLS SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article ID INVITRO; ERYTHROMYCIN; ANTIBIOTICS; PATHWAYS; INVIVO AB To determine the immunosuppressive effect(s) of cephalosporin cefonicid (CEFO) on human T-helper cells (Th), we exposed human peripheral blood mononuclear cells (PBMC) to various concentrations of CEFO during in vitro stimulation with a panel of T-lymphocyte stimulators that activate different Th/antigen presenting cell (APC) pathways. We evaluated the proliferation and IL-2 production induced by influenza virus (FLU), allogeneic lymphocytes (ALLO), xenogeneic mouse splenocytes (XENO) or phytohemagglutinin (PHA). The proliferative responses to FLU and XENO were much more depressed by CEFO than those to ALLO or PHA. After 7 days of culture with the highest dose of CEFO tested (200 mg/l) the stimulation index (stimulated/unstimulated culture) was near to 0 in FLU and XENO treated cultures, indicating that the response against these antigens was completely abrogated. The responses to ALLO and PHA were also impaired, but not abrogated (stimulated index > 1). Since FLU and XENO utilize the CD4 + Th/self-APC pathway our data suggested that this pathway was extremely sensitive to CEFO-induced inhibition both when the response requires memory Th cells (FLU) and virgin Th cells (XENO). The incubation with CEFO (200 mg/l) reduced the IL-2 production by XENO, FLU and ALLO to less than 20% of control cultures, while paradoxically increases to 120% the production by PHA. C1 UNIV MILAN,IST NAZ TUMORI,I-20122 MILAN,ITALY. UNIV MILAN,CATTEDRA OTORINOLARINGOIATRIA,I-20122 MILAN,ITALY. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP VILLA, ML (reprint author), UNIV MILAN,CATTEDRA IMMUNOL,I-20122 MILAN,ITALY. OI Ottaviani, Francesco/0000-0002-7862-5663 NR 11 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PY 1991 VL 13 IS 8 BP 1099 EP 1107 DI 10.1016/0192-0561(91)90161-Y PG 9 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA GV828 UT WOS:A1991GV82800007 PM 1839990 ER PT J AU PARKS, RW LONG, DL LEVINE, DS CROCKETT, DJ MCGEER, EG MCGEER, PL DALTON, IE ZEC, RF BECKER, RE COBURN, KL SILER, G NELSON, ME BOWER, JM AF PARKS, RW LONG, DL LEVINE, DS CROCKETT, DJ MCGEER, EG MCGEER, PL DALTON, IE ZEC, RF BECKER, RE COBURN, KL SILER, G NELSON, ME BOWER, JM TI PARALLEL DISTRIBUTED-PROCESSING AND NEURAL NETWORKS - ORIGINS, METHODOLOGY AND COGNITIVE FUNCTIONS SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Article DE PARALLEL DISTRIBUTED PROCESSING; NEURAL NETWORKS; ASSOCIATIONISM; POSITRON EMISSION TOMOGRAPHY; ARTIFICIAL INTELLIGENCE; NEUROPSYCHOLOGY; COGNITION ID CEREBRAL BLOOD-FLOW; ARTIFICIAL-INTELLIGENCE; VISUAL-CORTEX; BRAIN; MODEL; CONNECTIONISM; ARCHITECTURE; RECOGNITION; STIMULATION; PSYCHOLOGY C1 SO ILLINOIS UNIV,SCH MED,DEPT PSYCHIAT,SPRINGFIELD,IL 62708. MERCER UNIV,SCH MED,DEPT PSYCHIAT,MACON,GA 31207. UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616. DIGITAL SYST RESOURCES,FAIRFAX,VA. UNIV TEXAS,DEPT MATH,AUSTIN,TX 78712. UNIV BRITISH COLUMBIA,DEPT PSYCHIAT,VANCOUVER V6T 1W5,BC,CANADA. CALTECH,DEPT BIOL,PASADENA,CA 91125. RP PARKS, RW (reprint author), NIMH,PSYCHOTHERAPEUT MEDICAT DEV PROGRAM,CLIN SCI & NEUROPSYCHOL LAB,BETHESDA,MD 20892, USA. RI Bower, James/F-8343-2010 FU NIA NIH HHS [P30 AG08014]; NIMH NIH HHS [R01 MH/AG 41821-01, R01 MH/AG41821-02] NR 116 TC 9 Z9 9 U1 0 U2 1 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0020-7454 J9 INT J NEUROSCI JI Int. J. Neurosci. PY 1991 VL 60 IS 3-4 BP 195 EP 214 DI 10.3109/00207459109080640 PG 20 WC Neurosciences SC Neurosciences & Neurology GA GN108 UT WOS:A1991GN10800006 PM 1787049 ER PT J AU MCFARLIN, KE KRUESI, MJP METCALFE, DD AF MCFARLIN, KE KRUESI, MJP METCALFE, DD TI A PRELIMINARY ASSESSMENT OF BEHAVIORAL-PROBLEMS IN CHILDREN WITH MASTOCYTOSIS SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE MASTOCYTOSIS; CHILDREN; DEPRESSION; HYPERACTIVITY; HISTAMINE; AGGRESSION; INATTENTION ID PEDIATRIC MASTOCYTOSIS; SYSTEMIC MASTOCYTOSIS; HISTAMINE; HYDROXYZINE; DEPRESSION; ADJUSTMENT; DISORDERS; DISEASE AB Objective: The objectives of this study were to 1) review mastocytosis in terms of the behavioral pathology in adults, and 2) to assess a group of pediatric patients with mastocytosis to determine if similar behavioral pathology is evident. Method: Twelve children ages two to eleven referred to the NIH, a tertiary referral center for mastocytosis, were studied. Questionnaires were mailed for assessment of the child's behavior: parents completed the Childhood Behavior Checklist (CBCL) and children four years of age or more were evaluated by their teachers via the Child Behavior Checklist-Teacher Report form. Scores were compared to published normative data and to published data from other medically ill pediatric groups. Pathology was defined as present if the child scored greater than two standard deviations above published age and sex-matched norms. Results: Mean factor scores on the CBCL for children with mastocytosis did not differ significantly from published norms, but individual ratings by parents were significantly elevated in four of ten subjects. Moreover, CBCL ratings by parents were similar to those seen in other medically ill pediatric groups. None of the teacher ratings were in the pathological range. Conclusions: The results of this study indicate that no clear excess of pathology exists in children with mastocytosis. Individual children treated with antihistamines for mastocytosis seem to have a nonspecific increase in behavioral difficulties at rates similar to other medically ill groups. No unique behavioral pattern implicating histamine overproduction was identified. C1 NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N-240,9000 ROCKVILLE PK,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. NR 27 TC 1 Z9 1 U1 0 U2 0 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1991 VL 21 IS 3 BP 281 EP 289 PG 9 WC Psychiatry SC Psychiatry GA GH608 UT WOS:A1991GH60800006 PM 1955278 ER PT J AU ELMALLAKH, RS AF ELMALLAKH, RS TI MANIA IN AIDS - CLINICAL-SIGNIFICANCE AND THEORETICAL CONSIDERATIONS SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Article DE AIDS (ACQUIRED IMMUNE DEFICIENCY SYNDROME); AZT (ZIDOVUDINE); CALCIUM; INTRACELLULAR; CALCIUM CHANNEL BLOCKERS; GP-120 COAT PROTEIN; HIV (HUMAN IMMUNODEFICIENCY VIRUS-1); HYPOMANIA; MANIA; SECONDARY MANIA ID CEREBROSPINAL-FLUID; DISORDERS; MANIFESTATIONS; ILLNESS; PATIENT; ENOLASE AB Cases of mania associated with acquired immune deficiency syndrome (AIDS) are reviewed in an attempt to elucidate patterns that may be helpful in guiding treatment, determining prognosis, and understanding pathophysiology. Fourteen well-described cases in the English language literature were critically reviewed. Data was collected regarding chronological appearance of signs and symptoms, specific psychiatric symptoms, associated neurologic and cognitive function, objective testing of brain structure and function, and outcome. When mania or hypomania occur in the setting of a human immunodeficiency virus (HIV) infection, it frequently occurs once and does not recur. AIDS-associated manic states are adequately responsive to available antimanic agents, however, AIDS patients may be more prone to deleterious side effects. Although mania or hypomania may be the presenting complaints that lead to the discovery of human immunodeficiency virus (HIV) seropositive status, mania tends to occur in people exhibiting signs of immunodeficiency as is exemplified, in the sample, by death occurring within six months of the psychiatric presentation in nearly a quarter of the patients. It is hypothesized that AIDS-related mania and agitated psychosis may be related to increased intracellular free calcium. RP ELMALLAKH, RS (reprint author), NIMH,HOSP NEUROPSYCHIAT RES,NEUROPSYCHIAT BRANCH,2700 ML KING JR AVE SE,WASHINGTON,DC 20032, USA. NR 23 TC 19 Z9 20 U1 0 U2 0 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0091-2174 J9 INT J PSYCHIAT MED JI Int. J. Psychiatr. Med. PY 1991 VL 21 IS 4 BP 383 EP 391 DI 10.2190/08UJ-61E8-B2RF-0TCN PG 9 WC Psychiatry SC Psychiatry GA HB898 UT WOS:A1991HB89800006 PM 1774129 ER PT J AU BONNET, F SAILLARD, C VIGNAULT, JC GARNIER, M CARLE, P BOVE, JM ROSE, DL TULLY, JG WHITCOMB, RF AF BONNET, F SAILLARD, C VIGNAULT, JC GARNIER, M CARLE, P BOVE, JM ROSE, DL TULLY, JG WHITCOMB, RF TI ACHOLEPLASMA-SEIFFERTII SP-NOV, A MOLLICUTE FROM PLANT-SURFACES SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID MYCOPLASMA; INSECTS AB Two mollicutes (strains F7T [T = type strain] and F28) isolated from floral surfaces of plants growing in Morocco and France were capable of sustained growth in serum-free (or cholesterol-free) mycoplasma broth media. The two isolates were found to be genomically and serologically related. Morphologic examination of the organisms by electron and dark-field microscopic techniques showed that each strain consists of small, nonhelical, nonmotile, pleomorphic coccoid cells surrounded by a single cytoplasmic membrane. No evidence of cell walls was observed. Growth in serum-free or cholesterol-free medium was sustained only when the medium contained a Tween 80 fatty acid mixture (0.01 or 0.04%). The organisms grew rapidly in most conventional mycoplasma culture medium formulations containing horse or fetal bovine serum or a bovine serum fraction and under either aerobic or anaerobic environments. The optimum temperature for growth was 28-degrees-C, but multiplication occurred over a temperature range from 20 to 35-degrees-C. Both strains catabolized glucose and mannose, but did not hydrolyze arbutin, arginine, or urea. The molecular mass of the genome of strain F7T was determined to be about 886 megadaltons, while the base composition (guanine-plus-cytosine content) of the DNA was found to be 30.0 mol%. The two isolates were serologically unrelated to type strains of the 11 previously described Acholeplasma species and to 10 other unclassified sterol-nonrequiring mollicutes cultivated from various animal, plant, or insect sources. Strain F7 (= ATCC 49495) is the type strain of Acholeplasma seiffertii sp. nov. C1 INRA,BIOL CELLULAIRE & MOLEC LAB,F-33140 PONT DE LA MAYE,FRANCE. NIAID,FREDERICK CANC RES FACIL,MOLEC MICROBIOL LAB,MYCOPLASMA SECT,FREDERICK,MD 21701. USDA,INSECT PATHOL LAB,BELTSVILLE,MD 20705. NR 33 TC 5 Z9 5 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1991 VL 41 IS 1 BP 45 EP 49 PG 5 WC Microbiology SC Microbiology GA ER651 UT WOS:A1991ER65100009 ER PT J AU HICKEY, JE BROWN, BS CHUNG, AS KOLAR, AF MICHAELSON, BS AF HICKEY, JE BROWN, BS CHUNG, AS KOLAR, AF MICHAELSON, BS TI PERCEIVED RISK AND SOURCES OF INFORMATION REGARDING COCAINE SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Article DE COCAINE; RISK; PREVENTION; INFORMATION; EDUCATION ID ALCOHOL-RELATED PROBLEMS; ABUSE PREVENTION; MASS-MEDIA; PROGRAMS AB A study was made of the perceptions of risk and of the sources of information about risk regarding cocaine. Subjects were adult (N = 90) and juvenile (N = 20) cocaine abusers in seven Baltimore area treatment programs. Using structured interview, it was found that 87.8% of adults and 80.0% of youth had experienced at least one negative consequence of their cocaine use, other than addiction, prior to entry into treatment. The most common negative experience reported by both groups was the loss of reality testing. Moreover, 86.6% of adults and 65.0% of youth reported becoming addicted to cocaine before entering treatment. While juveniles sampled had entered treatment within a year of first cocaine use, adults entered treatment 7.9 years after first use and reported an average of 6.6 years of cocaine use before experiencing the first negative consequences. Television received consistently high ratings as an accessible and credible source of information about cocaine. Adolescents rated schools relatively high on the amount and accuracy of cocaine-related information provided. C1 NATL INST DRUG ABUSE,ADDICT RES CTR,CLIN PHARMACOL BRANCH,BIOL DEPENDENCE LAB,BALTIMORE,MD 21224. RP HICKEY, JE (reprint author), DEPT SERV CHILDREN YOUTH & THEIR FAMILIES,DIV CHILD MENTAL HLTH SERV,ALCOHOL & DRUG SERV,WILMINGTON,DE 19805, USA. NR 16 TC 6 Z9 6 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1991 VL 26 IS 7 BP 757 EP 767 PG 11 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA GF435 UT WOS:A1991GF43500003 PM 1959999 ER PT J AU BROWN, BS AF BROWN, BS TI RELAPSE PREVENTION IN SUBSTANCE MISUSE - INTRODUCTION SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Editorial Material RP BROWN, BS (reprint author), NIDA,COMMUNITY RES BRANCH,LEXINGTON,KY 40583, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1991 VL 25 IS 9A-10A BP 1081 EP 1083 PG 3 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA GE438 UT WOS:A1991GE43800001 ER PT J AU WEDDINGTON, WW AF WEDDINGTON, WW TI TOWARDS A REHABILITATION OF METHADONE-MAINTENANCE - INTEGRATION OF RELAPSE PREVENTION AND AFTERCARE SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Article DE ADDICTION; METHADONE; PREVENTION; REHABILITATION; RELAPSE ID TERM FOLLOW-UP; HEROIN-ADDICTS; OPIATE ADDICTS; CONDITIONED WITHDRAWAL; NARCOTIC ADDICTS; DETOXIFICATION; DEPENDENCE; PSYCHOTHERAPY; ABSTINENCE; DEPRESSION AB Methadone maintenance was originally proposed as a long-term treatment modality for opiate addiction. However, most clients leave methadone maintenance rather than take methadone indefinitely and subsequently relapse to opiate use. In this article, the author examines relapse to opiate use by clients during and after methadone maintenance treatment in the United States. He reviews models of relapse prevention and aftercare which may be applicable to clients in methadone treatment. There now exist structured and psychotherapeutic relapse prevention methods which may be integrated into methadone maintenance treatment and could serve, in addition, to revitalize methadone maintenance treatment. C1 NIDA,ADDICT RES CTR,BALTIMORE,MD. NR 77 TC 6 Z9 7 U1 1 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1991 VL 25 IS 9A-10A BP 1201 EP 1224 PG 24 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA GE438 UT WOS:A1991GE43800005 ER PT J AU BRIGHAM, J HENNINGFIELD, JE STITZER, ML AF BRIGHAM, J HENNINGFIELD, JE STITZER, ML TI SMOKING RELAPSE - A REVIEW SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Review ID TOBACCO WITHDRAWAL SYMPTOMS; SELF-EFFICACY; BODY-WEIGHT; NICOTINE REPLACEMENT; PREVENTING RELAPSE; CESSATION PROGRAMS; CIGARETTE-SMOKING; SOCIAL SUPPORT; ABSTINENCE; BEHAVIOR AB This paper reviews nicotine addiction, and discusses the difficulty of withdrawing and remaining abstinent from tobacco. Lapse and relapse are coming to be understood as part of the cessation process itself. The goals of treatment include efforts to prevent or reverse relapse by reducing the impact of relapse factors, thereby to increase the frequency and duration of remissions. Factors, reviewed that influence cessation include gender and age, health status, degree of nicotine dependence, exposure to smoking-related cues, emotional state, and use of coping strategies in high-risk situations. Successful intervention modalities include relapse prevention skills training and pharmacologic nicotine replacement. The seriousness of the health consequences of smoking supports continuation and expansion of smoking relapse research. C1 NIDA,ALCOHOL RES CTR,POB 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,BEHAV PHARMACOL RES UNIT,BALTIMORE,MD 21205. NR 58 TC 7 Z9 8 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1991 VL 25 IS 9A-10A BP 1239 EP 1255 PG 17 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA GE438 UT WOS:A1991GE43800007 ER PT J AU BROWN, BS AF BROWN, BS TI AIDS AND THE PROVISION OF DRUG-USER TREATMENT SO INTERNATIONAL JOURNAL OF THE ADDICTIONS LA English DT Article ID ABUSE TREATMENT; RISK AB The emergence of AIDS has triggered significant change in drug user treatment practices. The vast majority of programs are involved in some aspects of AIDS prevention counseling, large numbers encourage HIV testing, and an increasing number of programs offer on-site testing. Resources available to drug user treatment for AIDS prevention will likely depend on the perceived threat of AIDS to the larger community, and the public's belief in the capacity of treatment programs to reduce that threat. Programs will likely face often contradictory demands regarding service delivery. They may be asked to increase client flow while also retaining clients more effectively, providing aftercare, and working with the client's sexual partner(s). It will be the role of program administrators to provide for staff recruitment, retention, and support in an increasingly difficult environment. Alternative treatment settings will need to be explored for those intravenous drug users who cannot or will not enter existing treatment programs. RP BROWN, BS (reprint author), NIDA,COMMUNITY RES BRANCH,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 17 TC 10 Z9 10 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0020-773X J9 INT J ADDICT JI Int. J. Addict. PY 1991 VL 25 IS 12A BP 1503 EP 1514 PG 12 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA GV831 UT WOS:A1991GV83100007 ER PT B AU BROWN, DR KEITH, JM SATO, H SATO, Y AF BROWN, DR KEITH, JM SATO, H SATO, Y BE SATO, Y SATO, H TIRU, M BROWN, F TI CONSTRUCTION AND CHARACTERIZATION OF GENETICALLY INACTIVATED PERTUSSIS TOXIN SO INTERNATIONAL SYMPOSIUM ON PERTUSSIS : EVALUATION AND RESEARCH ON ACELLULAR PERTUSSIS VACCINES SE DEVELOPMENTS IN BIOLOGICAL STANDARDIZATION LA English DT Proceedings Paper CT INTERNATIONAL SYMP ON PERTUSSIS : EVALUATION AND RESEARCH ON ACELLULAR PERTUSSIS VACCINES CY SEP 14-15, 1990 CL TEIJIN INST EDUC & TRAINING, SHIZUOKA, JAPAN SP NIH, INT ASSOC BIOL STANDARDIZAT, AMVAX, BANYU PHARM, BIKEN, CHIBA SERUM INST, DENKA, KAKETSUKEN, KITASATO INST, LEDERLE PRAXIS BIOL HO TEIJIN INST EDUC & TRAINING RP BROWN, DR (reprint author), NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5457-5 J9 DEV BIOLOGICALS JI Dev. Biols PY 1991 VL 73 BP 63 EP 73 PG 11 WC Immunology; Medicine, Research & Experimental; Pathology SC Immunology; Research & Experimental Medicine; Pathology GA BU66A UT WOS:A1991BU66A00008 PM 1778335 ER PT B AU ROBBINS, JB TROLLFORS, B TARANGER, J LAGERGARD, T ZACHRISSON, G ISACSON, J AF ROBBINS, JB TROLLFORS, B TARANGER, J LAGERGARD, T ZACHRISSON, G ISACSON, J BE SATO, Y SATO, H TIRU, M BROWN, F TI IMMUNOLOGICAL EVALUATION OF A PERTUSSIS TOXOID VACCINE SO INTERNATIONAL SYMPOSIUM ON PERTUSSIS : EVALUATION AND RESEARCH ON ACELLULAR PERTUSSIS VACCINES SE DEVELOPMENTS IN BIOLOGICAL STANDARDIZATION LA English DT Proceedings Paper CT INTERNATIONAL SYMP ON PERTUSSIS : EVALUATION AND RESEARCH ON ACELLULAR PERTUSSIS VACCINES CY SEP 14-15, 1990 CL TEIJIN INST EDUC & TRAINING, SHIZUOKA, JAPAN SP NIH, INT ASSOC BIOL STANDARDIZAT, AMVAX, BANYU PHARM, BIKEN, CHIBA SERUM INST, DENKA, KAKETSUKEN, KITASATO INST, LEDERLE PRAXIS BIOL HO TEIJIN INST EDUC & TRAINING RP ROBBINS, JB (reprint author), NICHHD,DEV & MOLEC IMMUN LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5457-5 J9 DEV BIOLOGICALS JI Dev. Biols PY 1991 VL 73 BP 297 EP 303 PG 7 WC Immunology; Medicine, Research & Experimental; Pathology SC Immunology; Research & Experimental Medicine; Pathology GA BU66A UT WOS:A1991BU66A00031 PM 1778322 ER PT B AU KLEIN, DL AF KLEIN, DL BE SATO, Y SATO, H TIRU, M BROWN, F TI A PHASE-II MULTICENTER EVALUATION OF SEVERAL CANDIDATE PERTUSSIS VACCINES IN INFANTS SO INTERNATIONAL SYMPOSIUM ON PERTUSSIS : EVALUATION AND RESEARCH ON ACELLULAR PERTUSSIS VACCINES SE DEVELOPMENTS IN BIOLOGICAL STANDARDIZATION LA English DT Proceedings Paper CT INTERNATIONAL SYMP ON PERTUSSIS : EVALUATION AND RESEARCH ON ACELLULAR PERTUSSIS VACCINES CY SEP 14-15, 1990 CL TEIJIN INST EDUC & TRAINING, SHIZUOKA, JAPAN SP NIH, INT ASSOC BIOL STANDARDIZAT, AMVAX, BANYU PHARM, BIKEN, CHIBA SERUM INST, DENKA, KAKETSUKEN, KITASATO INST, LEDERLE PRAXIS BIOL HO TEIJIN INST EDUC & TRAINING RP KLEIN, DL (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5457-5 J9 DEV BIOLOGICALS JI Dev. Biols PY 1991 VL 73 BP 305 EP 309 PG 5 WC Immunology; Medicine, Research & Experimental; Pathology SC Immunology; Research & Experimental Medicine; Pathology GA BU66A UT WOS:A1991BU66A00032 PM 1778324 ER PT J AU ARESU, O NICOLO, G ALLAVENA, G MELCHIORI, A SCHMIDT, J KOPP, JB DAMORE, E CHADER, GJ ALBINI, A AF ARESU, O NICOLO, G ALLAVENA, G MELCHIORI, A SCHMIDT, J KOPP, JB DAMORE, E CHADER, GJ ALBINI, A TI INVASIVE ACTIVITY, SPREADING ON AND CHEMOTACTIC RESPONSE TO LAMININ ARE PROPERTIES OF HIGH BUT NOT LOW METASTATIC MOUSE OSTEOSARCOMA CELLS SO INVASION & METASTASIS LA English DT Article DE INVASION; BASEMENT MEMBRANE; MATRIGEL; FIBRONECTIN; LAMININ; CHEMOTAXIS; CELL SPREADING; OSTEOSARCOMA; NORMAL BONE CELLS ID BASEMENT-MEMBRANE; TUMOR INVASION; OSTEO-SARCOMA; BONE; ATTACHMENT; INVITRO; DIFFERENTIATION; MIGRATION; FIBROBLASTS; VARIANTS AB We have examined the interactions of low (Os43 and Os48) and high (Os50/K8 and Os50/K12) metastatic cell lines derived from osteosarcomas (Os) of the Balb/c mouse with fibronectin (FN) and laminin (LN). All of these cell lines formed osteogenic tumors when transplanted subcutaneously into syngeneic mice. Os43 and Os48 cells gave rise to few metastases while the Os50/K8 and Os50/K12 cells were highly metastatic. In an in vitro chemoinvasion assay only the highly metastatic cells were able to invade a reconstituted basement membrane. Although the interactions of all cell lines with FN were quite similar, their response to LN differed considerably. Within each of the cell lines, chemotactic response to and cell spreading on LN were closely correlated. Highly metastatic Os cells migrated to and spread on LN substrates to a much greater extent than low metastatic cells. Os43 and particularly Os48 showed very low migration to LN, similar to that of Balb/c 3T3 fibroblasts. They also spread poorly on LN, resembling the behavior of normal human bone cells which were used as a control. Thus, with these assays it is possible to distinguish the LN interactions associated with the metastatic phenotype of Os cells. The aquisition of LN recognition in tumor cells of bone origin may be related to their ability to invade and metastasize. This system may be valuable for the study of LN recognition molecules, their appearance, or changes with the metastatic phenotype. C1 NATL INST CANC RES,DEPT CHEM CARCINOGENESIS,VIALE BENEDETTO XV,I-16132 GENOA,ITALY. GESELL STRAHLEN & UMWELTFORSCH MBH,W-8042 NEUHERBERG,GERMANY. NIDR,BETHESDA,MD 20892. NEI,BETHESDA,MD 20892. NR 33 TC 24 Z9 24 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0251-1789 J9 INVAS METAST JI Invasion Metastasis PD JAN-FEB PY 1991 VL 11 IS 1 BP 2 EP 13 PG 12 WC Oncology SC Oncology GA FP478 UT WOS:A1991FP47800002 PM 2061001 ER PT J AU TUSA, RJ REPKA, MX SMITH, CB HERDMAN, SJ AF TUSA, RJ REPKA, MX SMITH, CB HERDMAN, SJ TI EARLY VISUAL DEPRIVATION RESULTS IN PERSISTENT STRABISMUS AND NYSTAGMUS IN MONKEYS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE STRABISMUS; NYSTAGMUS; AMBLYOPIA; VISUAL DEPRIVATION; MONKEY DEVELOPMENT ID CONGENITAL CATARACTS; EYE-MOVEMENTS; PRIMATE; CHILDREN; ACUITY; EXPERIENCE; INFANCY; COLUMNS; NUCLEUS; HEAD AB To understand to what extent visual-pattern deprivation during infancy results in strabismus and nystagmus, the authors examined the long-term consequences of this type of deprivation in monkeys during the first 50 days of life. Three cynomolgus and three rhesus monkeys had the eyelids sutured closed within 24 hr of birth. At 25 days of age, the eyelids were opened, and the eyelids of the fellow eye were sutured closed for an additional 25 days (reverse-eyelid suture). When the eyelids were opened at 50 days of age, each monkey was found to have 20-30-DELTA of exotropia and nystagmus, which persisted for the duration of the study (1 yr). The cynomolgus monkeys developed a monocular 8-10 Hz pendular nystagmus in the eye sutured first. The rhesus monkeys developed a conjugate nystagmus with both jerk and pendular components. The slow phases often had velocity-increasing profiles. The rhesus monkeys also had a superimposed latent component to the nystagmus found during monocular viewing. One additional rhesus monkey was examined after 55 days of binocular-eyelid suturing. This monkey also developed exotropia and nystagmus resembling that of the other rhesus monkeys. These findings suggest that early pattern vision in monkeys is necessary for the development of normal ocular alignment and gaze-holding ability. C1 JOHNS HOPKINS UNIV,DEPT OTOLARYNGOL,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,DEPT OPHTHALMOL,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,DEPT NEUROL,BALTIMORE,MD 21218. NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. FU NEI NIH HHS [EY01765] NR 39 TC 29 Z9 29 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1991 VL 32 IS 1 BP 134 EP 141 PG 8 WC Ophthalmology SC Ophthalmology GA EU054 UT WOS:A1991EU05400018 PM 1987095 ER PT J AU HESS, HH OKEEFE, TL KUWABARA, T WESTNEY, IV AF HESS, HH OKEEFE, TL KUWABARA, T WESTNEY, IV TI NUMBERS OF CORTICAL VITREOUS CELLS AND ONSET OF CATARACTS IN ROYAL-COLLEGE-OF-SURGEONS RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE BUTYLATED HYDROXYTOLUENE VITREOUS CELLS; MACROPHAGES; HYALOCYTES; RCS RATS; POSTERIOR SUBCAPSULAR CATARACTS; CATARACTS ID INHERITED RETINAL DYSTROPHY; RETINITIS PIGMENTOSA; SINGLET OXYGEN; RCS RATS; DAMAGE; LIGHT; MACROPHAGE; OXIDATION; STRAINS; CULTURE AB Royal College of Surgeons (RCS) rats have hereditary retinal degeneration with associated posterior subcapsular opacities. A link between light, retinal degeneration, and cataracts may consist in peroxidation of polyunsaturated fatty acids of rod outer segment lipids to yield water-soluble toxic aldehydes that can traverse the vitreous and react with bow cells and posterior lens fibers. In an immune reaction to the retinal degeneration, macrophages multiply in the retina and in the cortex of the vitreous. In dystrophics, the cortical vitreous separates readily from attachments to retina, ciliary body and lens, and from the vitreous gel. This web-like structure was stained and spread on a counting chamber. Cells were counted at 15-130 postnatal days in pink- and black-eyed RCS dystrophics and in cogenic controls to correlate numbers of cells, temporal and geographic patterns of retinal degeneration, and onset of opacities. Rats were reared in cyclic light (10-40 lux inside the cage) and fed a natural ingredient diet (NIH-07). Cortical vitreous cells increased markedly in pink- and black-eyed dystrophics at 50-53 days when slit-lamp detectable opacities occurred in both. The increase was 4.6-fold in pink- and 2.3-fold in black-eyed rats compared with controls. At 50-53 days, the dystrophy affected all quadrants of the retina severely in pink-eyed RCS but only the inferior periphery in black-eyed RCS. Consequently, severe degeneration in one quadrant may suffice to initiate an opacity. In black-eyed rats, degeneration in the rest of the retina occurs 10-35 days later, but the number of cortical vitreous cells was never as great as the number in pink-eyed rats at 50-53 days. The lower cell count in black-eyed RCS may be related to the fact that less than 3% of them ever develop mature cataracts. In contrast, one fourth of pink-eyed RCS have mature cataracts by 1 yr of age. C1 NEI,OPHTHALM PATHOL LAB,BETHESDA,MD 20892. RP HESS, HH (reprint author), NEI,OFF SCI DIRECTOR,BLDG 9,ROOM 1E-118,BETHESDA,MD 20892, USA. NR 34 TC 3 Z9 3 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1991 VL 32 IS 1 BP 200 EP 207 PG 8 WC Ophthalmology SC Ophthalmology GA EU054 UT WOS:A1991EU05400027 PM 1987101 ER PT J AU TOKUNAGA, T AF TOKUNAGA, T TI ANNUAL-REPORT ON FINDINGS OF INFECTIOUS AGENTS IN JAPAN 1990 - FOREWORD SO JAPANESE JOURNAL OF MEDICAL SCIENCE & BIOLOGY LA English DT Article C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST HEALTH PI TOKYO PA C/O JPN J MED SCI BIOL, 23-1, TOYAMA 1-CHOME, SHINJUKU-KU, TOKYO 162, JAPAN SN 0021-5112 J9 JPN J MED SCI BIOL JI Jpn. J. Med. Sci. Biol. PY 1991 VL 44 SU S BP 9 EP & PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA JN111 UT WOS:A1991JN11100001 ER PT J AU TASAKI, I BYRNE, PM AF TASAKI, I BYRNE, PM TI THERMAL AND MECHANICAL RESPONSES OF THE AMPHIBIAN SKIN TO NERVE-STIMULATION SO JAPANESE JOURNAL OF PHYSIOLOGY LA English DT Article DE AMPHIBIAN SKIN; HEAT GENERATION; MECHANICAL RESPONSES ID FROG SKIN; GLANDS; RETINA AB The isolated calf skin of the toad and bullfrog was found to generate a burst of heat in response to stimulation of the cutaneous nerve. The electric responses of the skin evoked by nerve stimulation invariably lagged behind the heat burst. The generation of a heat burst was followed by a slow mechanical response of the skin. Suppression of these responses by adrenergic blocking agents suggests that heat is produced at the junction between the gland cells and the sympathetic nerve fibers. Large mechanical changes in the skin were observed when noradrenaline was applied to the inner surface of the skin. RP TASAKI, I (reprint author), NIMH,CELL BIOL LAB,NEUROBIOL UNIT,BETHESDA,MD 20892, USA. NR 14 TC 2 Z9 2 U1 0 U2 1 PU CENTER ACAD PUBL JAPAN PI TOKYO PA C/O BUSINESS CTR ACAD SOC JPN, 16-9 HONKOMAGOME 5-CHOME BUNKYO-KU, TOKYO 113, JAPAN SN 0021-521X J9 JPN J PHYSIOL JI Jpn. J. Physiol. PY 1991 VL 41 IS 4 BP 567 EP 576 DI 10.2170/jjphysiol.41.567 PG 10 WC Physiology SC Physiology GA GP982 UT WOS:A1991GP98200003 PM 1791659 ER PT J AU LEBIHAN, D TURNER, R MOONEN, CTW PEKAR, J AF LEBIHAN, D TURNER, R MOONEN, CTW PEKAR, J TI IMAGING OF DIFFUSION AND MICROCIRCULATION WITH GRADIENT SENSITIZATION - DESIGN, STRATEGY, AND SIGNIFICANCE SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Review DE BLOOD, FLOW DYNAMICS; BLOOD VESSELS, MR STUDIES; BRAIN, MR STUDIES; BRAIN, PERFUSION; CEREBRAL BLOOD VESSELS, FLOW DYNAMICS; CEREBRAL BLOOD VESSELS, MR STUDIES; DIFFUSION IMAGING; ECHO-PLANAR IMAGING; MICROCIRCULATION IMAGING; PHYSICS; PULSE SEQUENCES; TISSUE CHARACTERIZATION; TREATMENT PLANNING AB Recent developments in the use of magnetic resonance (MR) to measure and image diffusion and blood microcirculation ("perfusion") are summarized. After a brief description of the effects of diffusion and perfusion on the MR signal, the different methods (conventional spin-echo, stimulated-echo, gradient-echo, and echo-planar imaging) that have been proposed and used to image and measure diffusion and perfusion by gradient sensitization are presented, along with their advantages and limitations. The difficulties of diffusion/perfusion imaging related to both hardware and software are then discussed. Special attention is given to specific problems encountered with in vivo studies and data analysis. Finally, the potential biologic and clinical applications are outlined, and some examples are presented. RP LEBIHAN, D (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BLDG 10,RM 1C660,BETHESDA,MD 20892, USA. RI Turner, Robert/C-1820-2008; Moonen, Chrit/K-4434-2016 OI Moonen, Chrit/0000-0001-5593-3121 NR 0 TC 150 Z9 150 U1 0 U2 7 PU SOC MAGNETIC RESONANCE IMAGING PI EASTON PA 1991 NORTHAMPTON ST, EASTON, PA 18042-3189 SN 1053-1807 J9 JMRI-J MAGN RESON IM JI JMRI-J. Magn. Reson. Imaging PD JAN-FEB PY 1991 VL 1 IS 1 BP 7 EP 28 DI 10.1002/jmri.1880010103 PG 22 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HA763 UT WOS:A1991HA76300001 PM 1802133 ER PT J AU BREZIN, AP NUSSENBLATT, RB AF BREZIN, AP NUSSENBLATT, RB TI DNA AMPLIFICATION (POLYMERASE CHAIN-REACTION) FOR THE DETECTION OF INFECTIOUS AGENTS IN OPHTHALMOLOGY SO JOURNAL FRANCAIS D OPHTALMOLOGIE LA French DT Article RP BREZIN, AP (reprint author), NIH,BLDG 10,ROOM 10N202,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0181-5512 J9 J FR OPHTALMOL JI J. Fr. Ophthamol. PY 1991 VL 14 IS 8-9 BP 488 EP 495 PG 8 WC Ophthalmology SC Ophthalmology GA GU226 UT WOS:A1991GU22600006 PM 1663961 ER PT J AU FISCHL, MA UTTAMCHANDANI, RB RESNICK, L AGARWAL, R FLETCHER, MA PATRONEREESE, J DEARMAS, L CHIDEKEL, J MCCANN, M MYERS, M AF FISCHL, MA UTTAMCHANDANI, RB RESNICK, L AGARWAL, R FLETCHER, MA PATRONEREESE, J DEARMAS, L CHIDEKEL, J MCCANN, M MYERS, M TI A PHASE-I STUDY OF RECOMBINANT HUMAN INTERFERON-ALPHA-2A OR HUMAN LYMPHOBLASTOID INTERFERON-ALPHA-N1 AND CONCOMITANT ZIDOVUDINE IN PATIENTS WITH AIDS-RELATED KAPOSIS-SARCOMA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS TYPE-1 (HIV); KAPOSIS SARCOMA (KS); INTERFERON-ALPHA; ZIDOVUDINE (AZT) ID ACQUIRED IMMUNODEFICIENCY SYNDROME; PLACEBO-CONTROLLED TRIAL; LEUKOCYTE-A INTERFERON; AZIDOTHYMIDINE AZT; ANTIGEN LEVELS; DOUBLE-BLIND; HTLV-III; THERAPY; COMPLEX; INVITRO AB To determine the safety, maximum tolerated dose, and preliminary efficacy of concomitant interferon-alpha and zidovudine therapy in AIDS-related Kaposi's sarcoma (KS), 56 patients with biopsy-proven KS and documented human immunodeficiency virus type 1 (HIV) infection were enrolled into a phase I study. Interferon-alpha was given intramuscularly at a dose of 9, 18, or 27 mu once a day and zidovudine was administered as 100 or 200 mg every 4 h for 8 weeks followed by a 48-week maintenance period. The major toxicities were anemia, neutropenia, and hepatotoxicity. Neutropenia was dose limiting with 1,200 mg of zidovudine/day and the lowest dose of interferon-alpha (9 mu/day). Hepatotoxicity was dose limiting with 27 mu of interferon and 600 mg of zidovudine/day. Cumulative dose-related anemia or neutropenia was not seen during long-term follow-up. The maximum tolerated doses for the combination were defined as 18 mu daily for interferon-alpha and 600 mg daily for ziovudine. Variable changes in CD4 lymphocytes occurred during the first 8 weeks of therapy. At higher doses of the combination, sustained increases in median CD4 lymphocyte numbers were noted (p < 0.001). In HIV antigenemic patients, progressive antigen suppression was seen with increasing doses of the combination (p < 0.005). The overall antitumor response rate was 47%. Tumor regression was associated with better survival benefits (p < 0.001) and a pretreatment CD4 cell count greater-than-or-equal-to 200 cells/mm3 (p = 0.01). In conclusion, intermediate doses of interferon-alpha and lower doses of zidovudine appear to be relatively well tolerated and associated with disease improvement, including survival benefits. C1 UNIV MIAMI,SCH MED,DEPT MED,DIV IMMUNOL,MIAMI,FL 33101. UNIV MIAMI,SCH MED,DEPT ONCOL,ANALYT PHARMACOL CORE RESOURCE,MIAMI,FL 33101. MT SINAI MED CTR,RETROVIROL LAB,MIAMI BEACH,FL 33140. NIAID,DIV AIDS,BETHESDA,MD 20892. RP FISCHL, MA (reprint author), UNIV MIAMI,SCH MED,DEPT MED,DIV GEN MED,R-60A,POB 016960,MIAMI,FL 33101, USA. FU NIAID NIH HHS [AI27675] NR 27 TC 99 Z9 99 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 1 BP 1 EP 10 PG 10 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP176 UT WOS:A1991EP17600001 PM 1670585 ER PT J AU BURNS, DN KRAMER, A YELLIN, F FUCHS, D WACHTER, H DIGIOIA, RA SANCHEZ, WC GROSSMAN, RJ GORDIN, FM BIGGAR, RJ GOEDERT, JJ AF BURNS, DN KRAMER, A YELLIN, F FUCHS, D WACHTER, H DIGIOIA, RA SANCHEZ, WC GROSSMAN, RJ GORDIN, FM BIGGAR, RJ GOEDERT, JJ TI CIGARETTE-SMOKING - A MODIFIER OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS; SMOKING; HOMOSEXUAL MEN ID T-CELL SUBSETS; SISTER-CHROMATID EXCHANGE; HELPER LYMPHOCYTES-T; HOMOSEXUAL MEN; ALVEOLAR MACROPHAGES; HIV INFECTION; LUNG-CANCER; AIDS; SMOKERS; SEROPOSITIVITY AB Two hundred and two homosexual men enrolled in a prospective cohort study of AIDS risk were assessed for differences in the occurrence and progression of human immunodeficiency virus type 1 (HIV-1) infection with respect to cigarette smoking. Among subjects who were initially seronegative, smokers were more likely than nonsmokers to become HIV-1 seropositive (p = 0.03). After seroconversion, serum beta-2-microglobulin and CD4+ lymphocyte levels were elevated in cigarette smokers relative to nonsmokers (p = 0.02 for both comparisons), but both of these differences disappeared within 2 years. There was no detectable difference in the risk of AIDS or Pneumocystis carinii pneumonia with respect to smoking. Our data suggest that cigarette smoking may alter the immune response to HIV-1 infection, but it appears to have no marked effect on clinical outcome. They also suggest that cigarette smoking may be a surrogate marker for continued high-risk sexual behavior in homosexual men. C1 NCI,VIRAL EPIDEMIOL SECT,434 EXECUT PLAZA N,BETHESDA,MD 20892. VET ADM MED CTR,DEPT MED,WASHINGTON,DC 20422. ATLANTIC RES CORP,ROCKVILLE,MD. UNIV INNSBRUCK,INST MED CHEM & BIOCHEM,A-6020 INNSBRUCK,AUSTRIA. UNIV INNSBRUCK,INST HYG,A-6020 INNSBRUCK,AUSTRIA. LUDWIG BOLTZMAN INST AIDS RES,INNSBRUCK,AUSTRIA. GEORGE WASHINGTON UNIV,MED CTR,DEPT MED,WASHINGTON,DC 20037. NR 53 TC 63 Z9 63 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 1 BP 76 EP 83 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP176 UT WOS:A1991EP17600011 PM 1670588 ER PT J AU SHIP, JA WOLFF, A SELIK, RM AF SHIP, JA WOLFF, A SELIK, RM TI EPIDEMIOLOGY OF ACQUIRED-IMMUNE-DEFICIENCY-SYNDROME IN PERSONS AGED 50 YEARS OR OLDER SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE EPIDEMIOLOGY; AGED POPULATION ID HUMAN IMMUNODEFICIENCY VIRUS; INCUBATION PERIOD; UNITED-STATES; AIDS; TRANSFUSION; INFECTION; TRANSMISSION; HEMOPHILIA; RISKS AB Acquired immune deficiency syndrome (AIDS) has afflicted persons of all ages, yet only recently has attention been devoted to AIDS in older persons. To examine the epidemiology of AIDS in persons greater-than-or-equal-to 50 years old in the United States, we analyzed cases reported to the Centers for Disease Control. The number reported annually in persons greater-than-or-equal-to 50 years old increased from 13 in 1981 to 3,562 in 1989. Through December 1989, 11,984 had been reported, representing 10% of all cases. Although male homosexual contact accounted for most cases in persons aged 50-69, blood transfusion became a more common means of exposure with increasing age, accounting for 28% of cases in persons aged 60-69 and 64% of cases in individuals aged greater-than-or-equal-to 70. The proportion of women increased from 6.1% in persons with AIDS aged 50-59 to 28.7% of those aged greater-than-or-equal-to 70. The proportion of AIDS diagnoses made in the same month as death increased from 16% in persons aged 50-59 to 37% in those aged greater-than-or-equal-to 80, suggesting either more rapid progression of disease or increasing delay in diagnosis. As the incidence in older persons continues to increase, clinicians caring for older patients must become more familiar with AIDS. C1 CTR DIS CONTROL,AIDS PROGRAM,SURVEILLANCE,ATLANTA,GA 30333. RP SHIP, JA (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,9000 ROCKVILLE PIKE,BLDG 10,BETHESDA,MD 20892, USA. NR 32 TC 91 Z9 95 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 1 BP 84 EP 88 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP176 UT WOS:A1991EP17600012 PM 1984059 ER PT J AU PARKS, WP LENES, BA TOMASULO, PA SCHIFF, ER PARKS, ES SHAW, GM LEE, H YAN, HQ LAI, SH HOLLINGSWORTH, CG NEMO, GJ MOSLEY, JW AF PARKS, WP LENES, BA TOMASULO, PA SCHIFF, ER PARKS, ES SHAW, GM LEE, H YAN, HQ LAI, SH HOLLINGSWORTH, CG NEMO, GJ MOSLEY, JW TI HUMAN T-CELL LYMPHOTROPIC VIRUS-INFECTION AMONG BLOOD-DONORS IN SOUTH FLORIDA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HTLV INFECTIONS; BLOOD DONORS; BLOOD TRANSFUSION; CROSS-SECTIONAL STUDIES ID HUMAN IMMUNODEFICIENCY VIRUS; LEUKEMIA-VIRUS; HTLV-I; UNITED-STATES; HOMOSEXUAL MEN; TRANSFUSION; TRANSMISSION; ANTIBODIES; LYMPHOMA; FAMILY AB Knowledge of the epidemiologic pattern of human T-lymphotropic virus (HTLV) in the United States is being enlarged by blood donor screening. We tested stored sera from 29,937 donations made in South Florida in 1984-1985. Twenty-three donors were confirmed as seropositive, a prevalence of 0.8 per 1,000 donations. Specificity was supported by serologic retesting and virus culture of 11 donors located for follow-up. Sex- and age-specific prevalences did not differ significantly; blacks, however, accounted for 65% of seropositive donations. Within South Florida, one section of Miami had a prevalence of 4.5 per 1,000 donations, significantly above the 0.1 to 1.1 per 1,000 rates for other parts. An epidemiologic association with known HTLV-I endemic areas could account for most infections; all seven typed isolates were characterized as HTLV-I. Exposures, however, were diverse, sometimes multiple, and had no necessary relationship to personal lifestyle. This finding suggests that sources of infection were varied. Seropositive family members emphasize familial clustering of HTLV-I infection. C1 UNIV SO CALIF,DEPT MED,1840 N SOTO ST EMB 108,LOS ANGELES,CA 90032. UNIV MIAMI,DEPT PEDIAT,MIAMI,FL 33152. UNIV MIAMI,DEPT MED,MIAMI,FL 33152. AMER RED CROSS,BLOOD SERV,S FLORIDA REG,MIAMI,FL. UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294. ABBOTT LABS,N CHICAGO,IL 60064. NHLBI,BETHESDA,MD 20892. UNIV SO CALIF,DEPT MED,LOS ANGELES,CA 90089. FU NHLBI NIH HHS [N01-HB-9-7074, N01-HB-4-7003, N01-HB-4-7002] NR 33 TC 5 Z9 5 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 1 BP 89 EP 96 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EP176 UT WOS:A1991EP17600013 PM 1670589 ER PT J AU BEHETS, FM EDIDI, B QUINN, TC ATIKALA, L BISHAGARA, K NZILA, N LAGA, M PIOT, P RYDER, RW BROWN, CC AF BEHETS, FM EDIDI, B QUINN, TC ATIKALA, L BISHAGARA, K NZILA, N LAGA, M PIOT, P RYDER, RW BROWN, CC TI DETECTION OF SALIVARY HIV-1-SPECIFIC IGG ANTIBODIES IN HIGH-RISK POPULATIONS IN ZAIRE SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE SALIVA; HIV 1-SPECIFIC IGG ANTIBODIES; ELISA; WESTERN BLOT; SEROPREVALENCE; SEROINCIDENCE; KINSHASA, ZAIRE ID HIV AB Saliva and blood samples were tested for human immunodeficiency virus-1 (HIV-1) antibodies in two high-risk populations in Kinshasa, Zaire. In a seroprevalence study of 458 sexually transmitted disease (STD) clinic attendees, 142 of 145 seropositive individuals had enzyme-linked immunosorbent assay (ELISA)-positive saliva samples (97.9% sensitivity). All saliva samples from seronegative patients were ELISA-negative (100% specificity). Of the 142 ELISA-positive saliva specimens, 137 were also Western blot-positive (94.5% sensitivity). In a subsequent seroincidence study of 315 initially seronegative female prostitutes followed during 183 woman-years of observation, 9 of 14 women who seroconverted (7.7% seroincidence) had ELISA-positive saliva samples at the time seroconversion was detected. Only three of these saliva specimens could be confirmed by Western blot. Although salivary testing for HIV-1 antibodies using conventional assays was not sensitive in detecting recent seroconversions, screening of salivary samples for HIV-1 antibody provides a convenient alternative method for conducting seroprevalence surveys in populations in whom venipuncture is not possible or convenient. C1 PROJECT SIDA,KINSHASA,ZAIRE. INST TROP MED,ANTWERP,BELGIUM. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. CTR DIS CONTROL,ATLANTA,GA 30333. NR 11 TC 49 Z9 49 U1 2 U2 5 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 2 BP 183 EP 187 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EU101 UT WOS:A1991EU10100013 PM 1987355 ER PT J AU GRAHAM, NMH ZEGER, SL KUO, V JACOBSON, LP VERMUND, SH PHAIR, JP DETELS, R RINALDO, CR SAAH, AJ AF GRAHAM, NMH ZEGER, SL KUO, V JACOBSON, LP VERMUND, SH PHAIR, JP DETELS, R RINALDO, CR SAAH, AJ TI ZIDOVUDINE USE IN AIDS-FREE HIV-1-SEROPOSITIVE HOMOSEXUAL MEN IN THE MULTICENTER AIDS COHORT STUDY (MACS), 1987-1989 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE ZIDOVUDINE; THERAPEUTIC USE; HIV-1; EPIDEMIOLOGY; HOMOSEXUALITY; INCIDENCE; PENTAMIDINE ID PLACEBO-CONTROLLED TRIAL; AZIDOTHYMIDINE AZT; SAN-FRANCISCO; BISEXUAL MEN; DOUBLE-BLIND; IMMUNODEFICIENCY; SEROCONVERSION; INFECTION; COMPLEX AB Zidovudine use data were examined in the Multicenter AIDS Cohort Study to determine (i) if the proportion of pre-AIDS participants (i.e., CD4+ cells < 200/mm3 or AIDS-related complex) taking zidovudine is high enough to explain a slower than expected rise in AIDS incidence in U.S. homosexual men since mid-1987; (ii) which factors are associated with starting zidovudine and clinical trials of zidovudine; and (iii) if pre-AIDS patients, as a group, are being undertreated. Data on zidovudine use, clinical trial participation, and sociodemographic, clinical, and hematologic variables were collected every 6 months from 1,195 AIDS-free HIV-1-seropositive homosexual men from April 1987 to September 1989. Overall prevalence of zidovudine use rose from 3.6% in mid-1987 (visit 7) to 23% in mid-1989 (visit 11). Of those with < 200 CD4+ lymphocytes/mm3, the prevalence of zidovudine use rose from 23% (24% if those taking zidovudine or placebo as part of a clinical trial are included) at visit 7 to 58% (69%) at visit 11. Of those with ARC, 20% (23%) were using zidovudine at visit 7 and 55% (65%) at visit 11. Although numbers were small, the advanced ARC participants (CD4+ cells < 200/mm3 and two or more symptoms) reported the highest treatment rates (50, 78, 80, 60, and 74% at visits 7-11, respectively). By September 1989, 42% (31%) of those with CD4+ lymphocyte levels < 200/mm3 were still not receiving zidovudine, suggesting that many high-risk, pre-AIDS individuals are being undertreated. To explore this finding further, we examined a range of sociodemographic, hematologic, and clinical variables to determine which factors best predicted initiation of zidovudine therapy outside of clinical trials. In multivariate analyses, CD4+ lymphocyte number was the most consistent predictor of initiation of therapy over all four study visits. For each 100 cells/mm3 deficit, the odds ratios were 2.3 (95% C.I. of 1.7-3.1) at visit 7 and 1.7 (95% C.I. of 1.4-2.0) at visit 11. Symptom status and education level were also associated with starting zidovudine, but not at all visits. The relatively low predictive power of the clinical variables raises the possibility that nonclinical factors not measured in the MACS (drug cost, third-party insurance restrictions, and individual preferences) may play an important role in predicting zidovudine use. Finally, comparisons were made between seropositive participants starting clinical trials of zidovudine and the rest of the study population. No important differences were found in demographic or major clinical variables between clinical trial participants and zidovudine nonusers in this study. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,CTR DATA COORDINATING,BALTIMORE,MD 21205. NIAID,DIV AIDS,BETHESDA,MD 20892. NORTHWESTERN UNIV,SCH MED,DEPT MED,HOWARD BROWN MEM CLIN,CHICAGO,IL 60611. UNIV CALIF LOS ANGELES,SCH PUBL HLTH & MED,DEPT EPIDEMIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH PUBL HLTH & MED,DEPT MED,LOS ANGELES,CA 90024. UNIV PITTSBURGH,SCH PUBL HLTH,DEPT INFECT DIS & MICROBIOL,PITTSBURGH,PA 15260. RP GRAHAM, NMH (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,624 N BROADWAY,BALTIMORE,MD 21205, USA. OI Vermund, Sten/0000-0001-7289-8698 FU PHS HHS [N01-A1-32535, N01-A1-72634, N01-A1-72676] NR 23 TC 62 Z9 62 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 267 EP 276 PG 10 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900009 PM 1671411 ER PT J AU JEANG, KT AF JEANG, KT TI MECHANISM OF ACTION OF THE HIV-1 TAT PROTEIN - INTERACTION BETWEEN TAT, CELLULAR FACTORS, AND VIRAL-DNA AND RNA TARGETS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 307 EP 307 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900023 ER PT J AU PAVLAKIS, GN FELBER, BK SCHWARTZ, S BENKO, DM SOLOMIN, L ROBINSON, R DRYSDALE, CM CIMINALE, V UNGE, T CAMPBELL, M HARRISON, J AF PAVLAKIS, GN FELBER, BK SCHWARTZ, S BENKO, DM SOLOMIN, L ROBINSON, R DRYSDALE, CM CIMINALE, V UNGE, T CAMPBELL, M HARRISON, J TI GENOME STRUCTURE AND REGULATION OF HIV-1 EXPRESSION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 308 EP 308 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900025 ER PT J AU STREBEL, K MALDARELLI, F MARTIN, MA AF STREBEL, K MALDARELLI, F MARTIN, MA TI HIV-1 VIF AND VPU GENE-PRODUCTS - STRUCTURAL AND FUNCTIONAL-ANALYSIS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 309 EP 309 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900027 ER PT J AU CHESEBRO, B AF CHESEBRO, B TI INFLUENCE OF MOUSE AND HUMAN RETROVIRAL ENVELOPE GENES ON CELL TROPISM AND PATHOGENESIS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 310 EP 310 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900029 ER PT J AU MITSUYA, H AF MITSUYA, H TI THE PAST, PRESENT, AND FUTURE OF THERAPY WITH NUCLEOSIDES ACTIVE AGAINST HIV SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 318 EP 319 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900047 ER PT J AU BITTERLICH, G RAPPAPORT, J GARTENHAUS, R LOONEY, D WONGSTAAL, F AF BITTERLICH, G RAPPAPORT, J GARTENHAUS, R LOONEY, D WONGSTAAL, F TI TRANSCELLULAR TRANSACTIVATION BY HTLV-1 TAX PROTEIN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,DEPT MED,SAN DIEGO,CA 92103. NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 320 EP 320 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900051 ER PT J AU GATIGNOL, A JEANG, KT AF GATIGNOL, A JEANG, KT TI COOPERATIVE TRANSACTIVATION OF HIV-1 LTR BY TAT AND A TAR RNA-BINDING PROTEIN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 322 EP 322 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900055 ER PT J AU KAWA, S SMITH, JS BECERRA, SP KUMAR, A WILSON, SH THOMPSON, EB AF KAWA, S SMITH, JS BECERRA, SP KUMAR, A WILSON, SH THOMPSON, EB TI EXPRESSION OF THE HIV-1 REVERSE-TRANSCRIPTASE IN SPODOPTERA-FRUGIPERDA CELLS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,MED BRANCH,DEPT HUMAN BIOL CHEM & GENET,GALVESTON,TX 77550. NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 326 EP 326 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900064 ER PT J AU MARGOLIS, DM ROBSON, AB OSTROVE, JM STRAUS, SE AF MARGOLIS, DM ROBSON, AB OSTROVE, JM STRAUS, SE TI TRANSACTIVATION OF THE HIV LONG TERMINAL REPEAT (LTR) BY HERPES-SIMPLEX VIRUS TYPE-1 (HSV-1) IMMEDIATE-EARLY GENES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. MICROBIOL ASSOCIATES INC,ROCKVILLE,MD. CTR ADV BIOTECHNOL & MED,ROBERT WOODS JOHNSON MED SCH,PISCATAWAY,NJ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 327 EP 327 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900067 ER PT J AU WATERS, DJ WILSON, C MILEY, W ARTHUR, L BLATTNER, W REITZ, M AF WATERS, DJ WILSON, C MILEY, W ARTHUR, L BLATTNER, W REITZ, M TI A SIMPLE COLORIMETRIC TRANSACTIVATION-BASED ASSAY FOR THE DETECTION AND TITRATION OF INFECTIOUS HIV-1, HIV-2, AND SIV SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,PRI DYNCORP,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 338 EP 338 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900093 ER PT J AU ANAND, R OLSON, MC RAMAKRISHNAN, S AF ANAND, R OLSON, MC RAMAKRISHNAN, S TI RIBOSOMAL INHIBITORY PROTEINS FROM PLANTS INHIBIT HIV-1 REPLICATION IN ACUTELY INFECTED PERIPHERAL-BLOOD MONONUCLEAR-CELLS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NIAID,AIDS REVIEW SECT,BETHESDA,MD 20892. UNIV MINNESOTA,DEPT PHARMACOL,MINNEAPOLIS,MN 55455. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 350 EP 351 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900120 ER PT J AU LAVIE, G MERUELO, D DAUB, M DEGAR, S LEVIN, B LAVIE, D MAZUR, Y NASR, M AF LAVIE, G MERUELO, D DAUB, M DEGAR, S LEVIN, B LAVIE, D MAZUR, Y NASR, M TI RETROVIRAL PARTICLE INACTIVATION BY ORGANIC POLYCYCLIC QUINONES - A NOVEL MECHANISM OF VIRUCIDAL ACTIVITY CHARACTERIZED BY DIMINUTION OF VIRUS PARTICLE DERIVED REVERSE-TRANSCRIPTASE ENZYMATIC-ACTIVITY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NYU MED CTR,DEPT PATHOL,NEW YORK,NY 10016. NIAID,BETHESDA,MD 20892. NYU MED CTR,KAPLAN CANC CTR,NEW YORK,NY 10016. WEIZMANN INST SCI,DEPT ORGAN CHEM,IL-76100 REHOVOT,ISRAEL. N CAROLINA STATE UNIV,DEPT PLANT PATHOL,RALEIGH,NC 27695. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 356 EP 357 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900136 ER PT J AU MCMAHO, JB CIMINALE, V PAVLAKIS, GN BADER, JP BOYD, MR AF MCMAHO, JB CIMINALE, V PAVLAKIS, GN BADER, JP BOYD, MR TI MECHANISM OF ACTION OF OXATHIIN CARBOXANILIDE - A POTENT INHIBITOR OF HIV-1 REPLICATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Meeting Abstract C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,FREDERICK,MD 21701. FREDERICK CANC RES FACIL,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 3 BP 357 EP 357 PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA EY269 UT WOS:A1991EY26900137 ER PT J AU ROSENBERG, PS GAIL, MH SCHRAGER, LK VERMUND, SH CREAGHKIRK, T ANDREWS, EB WINKELSTEIN, W MARMOR, M DESJARLAIS, DC BIGGAR, RJ GOEDERT, JJ AF ROSENBERG, PS GAIL, MH SCHRAGER, LK VERMUND, SH CREAGHKIRK, T ANDREWS, EB WINKELSTEIN, W MARMOR, M DESJARLAIS, DC BIGGAR, RJ GOEDERT, JJ TI NATIONAL AIDS INCIDENCE TRENDS AND THE EXTENT OF ZIDOVUDINE THERAPY IN SELECTED DEMOGRAPHIC AND TRANSMISSION GROUPS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE AIDS INCIDENCE; ZIDOVUDINE; ACCESS TO HEALTH CARE; HUMAN IMMUNODEFICIENCY VIRUS; BACKCALCULATION ID ACQUIRED IMMUNODEFICIENCY SYNDROME; FRANCISCO MENS HEALTH; SHORT-TERM PROJECTIONS; SAN-FRANCISCO; HIV SEROCONVERSION; UNITED-STATES; BISEXUAL MEN; INFECTION; EPIDEMIC; VIRUS AB After mid-1987 fewer than the expected number of cases of AIDS were reported in the United States in some demographic and transmission groups but not in others. Gay men (regardless of intravenous drug use), adults with hemophilia, and transfusion recipients exhibited fewer cases than expected based on previously reliable models. These favorable trends could not be explained by assuming earlier cessation of human immunodeficiency virus (HIV) infection. Favorable AIDS incidence trends were not found in heterosexual intravenous drug users or in persons infected through heterosexual contact. White gay men from New York City, Los Angeles, and San Francisco experienced markedly favorable trends, whereas little change was observed for nonwhite gay men from nonurban areas. AIDS incidence trends were quantitatively consistent with the fraction of AIDS-free persons with severe immunodeficiency who received zidovudine in three cohorts. Gay men in San Francisco used zidovudine more frequently than did adults with hemophilia, while little was used by intravenous drug users in New York City. Data describing the initial national distribution of zidovudine (March 31-September 18, 1987) indicated relatively high use by patients with severe immunodeficiency in those groups, such as urban white gay men, that subsequently experienced fewer cases of AIDS than expected. Available data suggest that zidovudine, perhaps in combination with other therapies, has been one factor contributing to favorable AIDS incidence trends in some groups. Broader application of therapy might further retard the incidence of AIDS, especially in intravenous drug users, persons infected through heterosexual contact, minorities, women, and persons diagnosed outside major metropolitan areas. C1 NIAID,DIV AIDS,EPIDEMIOL BRANCH,BETHESDA,MD 20892. BURROUGHS WELLCOME CO,DIV EPIDEMIOL INFORMAT & SURVEILLANCE,RES TRIANGLE PK,NC 27709. UNIV CALIF BERKELEY,SCH PUBL HLTH,BEHS,BERKELEY,CA 94720. NYU,SCH MED,DEPT ENVIRONM MED,NEW YORK,NY 10003. BETH ISRAEL MED CTR,INST CHEM DEPENDENCY,NEW YORK,NY 10003. NCI,ENVIRONM EPIDEMIOL BRANCH,VIRAL EPIDEMIOL SECT,ROCKVILLE,MD. RP ROSENBERG, PS (reprint author), NCI,BIOSTAT BRANCH,EPIDEMIOL METHODS SECT,6130 EXECUT BLVD,EPN 403,ROCKVILLE,MD 20892, USA. OI Marmor, Michael/0000-0001-6605-2661; Vermund, Sten/0000-0001-7289-8698 FU NCI NIH HHS [N01-CP7-1011] NR 29 TC 79 Z9 80 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 4 BP 392 EP 401 PG 10 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FC522 UT WOS:A1991FC52200006 PM 2007974 ER PT J AU BERZOFSKY, JA AF BERZOFSKY, JA TI APPROACHES AND ISSUES IN THE DEVELOPMENT OF VACCINES AGAINST HIV SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; TOXIC LYMPHOCYTES-T; MAJOR HISTOCOMPATIBILITY COMPLEX; CELL ANTIGENIC SITES; SYNTHETIC PEPTIDES; INFLUENZA NUCLEOPROTEIN; INFECTION INVITRO; ENVELOPE PROTEIN; VIRAL ENVELOPE; RECOGNITION RP BERZOFSKY, JA (reprint author), NCI, METAB BRANCH, MOLEC IMMUNOGENET & VACCINE RES SECT, BLDG 10 ROOM 6B-12, BETHESDA, MD 20892 USA. NR 92 TC 40 Z9 40 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 5 BP 451 EP 459 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FG785 UT WOS:A1991FG78500001 PM 2016682 ER PT J AU CANTOR, KP WEISS, SH GOEDERT, JJ BATTJES, RJ AF CANTOR, KP WEISS, SH GOEDERT, JJ BATTJES, RJ TI HTLV-I/II SEROPREVALENCE AND HIV HTLV COINFECTION AMONG UNITED-STATES INTRAVENOUS-DRUG-USERS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article ID CELL LEUKEMIA-VIRUS; TROPICAL SPASTIC PARAPARESIS; LOW PREVALENCE; BLOOD-DONORS; I INFECTION; TRANSMISSION; ANTIBODIES; ABUSERS; AIDS AB Data from a continuing multiyear seroprevalence survey of human T-lymphotropic virus types I or II (HTLV-I/II) among intravenous drug users in seven U.S. locations were analyzed to detect demographic patterns of seropositivity coinfection with human immunodeficiency virus type 1 (HIV-1). Seropositivity for HTLV-I/II and HIV-1 was detected by whole-virus enzyme immunoassay, with Western blot confirmation. Of 1,800 subjects recruited from methadone maintenance and detoxification clinics, 207 (11.5%) were infected with HTLV-I/II. Seropositivity for HTLV-I/II varied by racial group, age, sex, and geographic location. Blacks had a higher (age- and location-adjusted) infection rate (17.1%) than Hispanics (8.7%) or whites (5.6%), and seropositivity showed a strong gradient with increasing age. Females had a slightly higher rate (14.0%) than males (10.0%), after adjustment for age and location. Among the seven locations, the rate varied from approximately 1% (Miami and Baltimore) to 20% (Los Angeles), although the former rates were based on relatively few subjects (47 and 65, respectively). Overall, the occurrence of coinfection by HIV-1 and HTLV-I/II did not occur more frequently than expected by chance. C1 NIDA,ROCKVILLE,MD. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT PREVENT MED,NEWARK,NJ 07103. RP CANTOR, KP (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,443 EPN,BETHESDA,MD 20892, USA. NR 39 TC 29 Z9 29 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 5 BP 460 EP 467 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FG785 UT WOS:A1991FG78500002 PM 2016683 ER PT J AU DECARLI, C FUGATE, L FALLOON, J EDDY, J KATZ, DA FRIEDLAND, RP RAPOPORT, SI BROUWERS, P PIZZO, PA AF DECARLI, C FUGATE, L FALLOON, J EDDY, J KATZ, DA FRIEDLAND, RP RAPOPORT, SI BROUWERS, P PIZZO, PA TI BRAIN GROWTH AND COGNITIVE IMPROVEMENT IN CHILDREN WITH HUMAN IMMUNODEFICIENCY VIRUS-INDUCED ENCEPHALOPATHY AFTER 6 MONTHS OF CONTINUOUS INFUSION ZIDOVUDINE THERAPY SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE CHILDREN; HIV ENCEPHALOPATHY; BRAIN GROWTH; COGNITIVE IMPROVEMENT; ZIDOVUDINE THERAPY; QUANTITATIVE COMPUTERIZED TOMOGRAPHY ID AIDS ENCEPHALOPATHY; III INFECTION; TOMOGRAPHY; FEATURES; DEMENTIA; INFANTS; ATROPHY; SCANS AB The ventricular area at the level of the foramen of Monro was measured from axial x-ray computed tomography (CT) scans obtained prior to and 6 months after the initiation of continuous infusion of zidovudine (ZDV) in eight children with human immunodeficiency virus-induced encephalopathy. Evidence of moderate to severe central atrophy was present on initial CT scans (p < 0.05). Ventricular area and ventricular brain area ratio (VBR) decreased after ZDV therapy in seven of eight children (mean decrease of 21.5 and 20%, respectively, p < 0.05). The degree of decrease in VBR correlated with reductions in cerebrospinal fluid (CSF) protein concentration (r = 0.93, p < 0.01), but not lymphocyte T4 or T8 counts. Intelligence quotients (IQs) improved in all seven children tested (mean improvement of 17.7%, p < 0.01) and correlated significantly with reductions in CSF protein concentration (r = -0.85, p = 0.003). The magnitude of IQ changes was not significantly correlated with the magnitude of changes in ventricular area. We conclude that the cognitive improvement of HIV encephalopathy seen after 6 months of continuous infusion of ZDV is accompanied by reduction in brain atrophy and decreased CSF protein, suggesting an ameliorating effect of ZDV on the pathogenesis of AIDS encephalopathy in children. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,DIV CENT RES,PEDIAT BRANCH,BETHESDA,MD 20892. NINCDS,OFF CLIN DIRECTOR,BETHESDA,MD 20892. RP DECARLI, C (reprint author), NIA,NEUROSCI LAB,BLDG 10,ROOM 6C 414,BETHESDA,MD 20892, USA. RI DeCarli, Charles/B-5541-2009; Friedland, Robert/A-2834-2010 OI Friedland, Robert/0000-0001-5721-1843 NR 30 TC 59 Z9 62 U1 3 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 6 BP 585 EP 592 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FM102 UT WOS:A1991FM10200005 PM 1673712 ER PT J AU STEIN, CA NECKERS, LM NAIR, BC MUMBAUER, S HOKE, G PAL, R AF STEIN, CA NECKERS, LM NAIR, BC MUMBAUER, S HOKE, G PAL, R TI PHOSPHOROTHIOATE OLIGODEOXYCYTIDINE INTERFERES WITH BINDING OF HIV-1 GP120 TO CD4 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE PHOSPHOROTHIOATE OLIGODEOXYCYTIDINE; HIV-1; GP120; CD4 ID HUMAN IMMUNODEFICIENCY VIRUS; DEXTRAN SULFATE; SYNCYTIUM FORMATION; HTLV-III; CELLS; OLIGODEOXYNUCLEOTIDES; REPLICATION; INHIBITORS; INFECTION; RECEPTOR AB In addition to their properties as sequence-specific inhibitors of gene expression, sequence nonspecific phosphorothioate oligodeoxynucleotides have been shown to protect against the cytopathic effects of HIV-1. Although these compounds are effective inhibitors of HIV-1 reverse transcriptase in vitro, it is not certain that they exert their cytoprotective effect only in this manner. Initial binding of the HIV-1 virion to cells involves the interaction of the vira. envelope protein gp120 with CD4. In this report, we describe flow cytometric data and a solid-phase ELISA assay that document the ability of a phosphorothioate deoxycytidine 28-mer to interfere with this interaction by competing with gp120 binding to CD4. The biological importance of this interaction is demonstrated by the fact that phosphorothioate oligodeoxycytidine inhibits syncytium formation resulting from HIV-1-induced cell fusion. These data suggest that phosphorothioate oligodeoxynucleotides may exert their cytoprotective effects, perhaps at least in part, by interfering with the binding of HIV-1 to the target cells. C1 NCI,MED BRANCH,BETHESDA,MD 20892. NR 28 TC 95 Z9 95 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 7 BP 686 EP 693 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FR760 UT WOS:A1991FR76000006 PM 1711118 ER PT J AU LANG, W OSMOND, D SAMUEL, M MOSS, A SCHRAGER, L WINKELSTEIN, W AF LANG, W OSMOND, D SAMUEL, M MOSS, A SCHRAGER, L WINKELSTEIN, W TI POPULATION-BASED ESTIMATES OF ZIDOVUDINE AND AEROSOL PENTAMIDINE USE IN SAN-FRANCISCO - 1987-1989 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE ZIDOVUDINE; AEROSOL PENTAMIDINE ID HUMAN-IMMUNODEFICIENCY-VIRUS; PLACEBO-CONTROLLED TRIAL; AIDS-RELATED COMPLEX; AZIDOTHYMIDINE AZT; DOUBLE-BLIND; MENS HEALTH; RISK; HIV; SEROPOSITIVITY; INFECTION AB From the San Francisco Men's Health Study (SFMHS) and the San Francisco General Hospital Cohort we derived partially population-based estimates of zidovudine (ZDV) use in San Francisco from 1987 to 1989. Data from the SFMHS alone were used to make estimates of aerosol pentamidine (AP) use in 1989. From 1987 to 1989, zidovudine use increased from 36 to 68% in participants with AIDS. In participants with symptomatic HIV infection without AIDS and in those with less than 200 CD4 cells, ZDV use increased initially but then leveled off (from 6 to 25% and 24 to 55%, respectively). Zidovudine use with more than 500 CD4 cells increased from 0.5 to 4%. In 1989 AP use with less than 200 CD4 cells was 42% and with AIDS was 44%. Whereas 50% of participants with AIDS and < 200 CD4 were using both ZDV and AP, only 14% of those without AIDS but with < 200 CD4 cells were using both. Surprisingly few members of these cohorts are using therapies proven effective in reducing the morbidity and mortality of HIV infection. C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. UNIV CALIF BERKELEY,SCH PUBL HLTH,BERKELEY,CA 94720. NIAID,BETHESDA,MD 20892. RP LANG, W (reprint author), CHILDRENS HOSP SAN FRANCISCO,SAN FRANCISCO MENS HLTH STUDY,3700 CALIF ST,E CAMPUS,5TH FLOOR,SAN FRANCISCO,CA, USA. FU NIAID NIH HHS [N01-AI-82515] NR 12 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 7 BP 713 EP 716 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FR760 UT WOS:A1991FR76000009 PM 1675679 ER PT J AU GIBBS, DA HAMILL, DN MAGRUDERHABIB, K AF GIBBS, DA HAMILL, DN MAGRUDERHABIB, K TI POPULATIONS AT INCREASED RISK OF HIV-INFECTION - CURRENT KNOWLEDGE AND LIMITATIONS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV INFECTION; RISK GROUPS; INTRAVENOUS DRUG USERS; HOMOSEXUAL MEN; HETEROSEXUALS ID ACQUIRED IMMUNODEFICIENCY SYNDROME; CONTRACEPTIVE USE; SEXUAL-ACTIVITY; UNITED-STATES; PREGNANCY; TEENAGERS; WOMEN AB Research data describing the prevalence and patterns of behaviors that place persons at increased risk of HIV infection are extremely limited. The scarcity of data has constrained potential applications of surveillance data, research on specific high-risk behaviors, and epidemiological studies. This article critically reviews available research for four population groups: intravenous drug users, homosexual males, and sexually active adolescents and adults. The fallacies inherent in estimating risk group size underscore the need for population-based research that can provide detailed data on sexual and drug use behaviors. C1 NIMH,ROCKVILLE,MD 20857. RP GIBBS, DA (reprint author), RES TRIANGLE INST,CTR POLICY STUDIES,POB 12194,RES TRIANGLE PK,NC 27709, USA. FU PHS HHS [200-88-0615] NR 28 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 9 BP 881 EP 889 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GD597 UT WOS:A1991GD59700009 PM 1895209 ER PT J AU NEEQUAYE, AR NEEQUAYE, JE BIGGAR, RJ AF NEEQUAYE, AR NEEQUAYE, JE BIGGAR, RJ TI FACTORS THAT COULD INFLUENCE THE SPREAD OF AIDS IN GHANA, WEST AFRICA - KNOWLEDGE OF AIDS, SEXUAL-BEHAVIOR, PROSTITUTION, AND TRADITIONAL MEDICAL PRACTICES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE AFRICA; HIV; PROSTITUTES; SEXUAL BEHAVIOR; TRADITIONAL HEALERS AB Ghana is a West African nation in the early stages of the human immunodeficiency virus (HIV) epidemic. In a series of surveys done between 1987 and 1989, we examined factors related to the spread of HIV infection, including knowledge about the acquired immune deficiency syndrome (AIDS), sexual habits, use of prostitutes, traditional healer practices, and skin-piercing customs. Although a polygamous society, three-fourths of married men had only one wife. The number of sexual partners at any time was generally low. However, the divorce rate was more than 29% and 55% of married men had current sexual partners in addition to their wives. Knowledge about AIDS was widespread, yet 4% of men interviewed had had a sexual encounter with a prostitute within the last month. Use of condoms was very limited and 66% of customers of high-class prostitutes refused to use a condom even after a request to do so by the prostitute. Skin piercing, including scarification, was done by an unsterile instrument by 39% of 74 rural traditional healers, many of whom had more than one patient per day. To combat the spread of AIDS, Ghanaians will have to apply their knowledge of AIDS risk factors to their actual behavior. Many of the social customs are products of poverty and its ensuing social consequences. Funds are needed for specific AIDS prevention programs as well as improved education and health care throughout the country. C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. UNIV GHANA,SCH MED,DEPT MED,ACCRA,GHANA. UNIV GHANA,SCH MED,DEPT CHILD HLTH,ACCRA,GHANA. FU NCI NIH HHS [CP-85612-55] NR 10 TC 44 Z9 44 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 9 BP 914 EP 919 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GD597 UT WOS:A1991GD59700014 PM 1895213 ER PT J AU MILDVAN, D BUZAS, J ARMSTRONG, D ANTONISKIS, D SACKS, HS RHAME, FS MOSBACH, EW PETTINELLI, C AF MILDVAN, D BUZAS, J ARMSTRONG, D ANTONISKIS, D SACKS, HS RHAME, FS MOSBACH, EW PETTINELLI, C TI AN OPEN-LABEL, DOSE-RANGING TRIAL OF AL-721 IN PATIENTS WITH PERSISTENT GENERALIZED LYMPHADENOPATHY AND AIDS-RELATED COMPLEX SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE AL-721; HIV; PERSISTENT GENERALIZED LYMPHADENOPATHY; AIDS-RELATED COMPLEX ID AL721 AB AL 721, a lipid mixture with reported in vitro activity against human immunodeficiency virus (HIV) via cell membrane or virion cholesterol depletion, was evaluated in a multicenter, open-label, dose-ranging trial. Forty men with persistent generalized lymphadenopathy or AIDS-related complex were treated with doses of 20, 30, 40, or 50 g orally twice daily for 8 weeks, and monitored for toxicity, disease progression, and with immunologic, virologic, and serum lipid profiles. The compound was found to be well tolerated over the broad range of doses examined; adverse reactions were confined to the gastrointestinal tract, of mild to moderate severity, and self-limited in duration. Modest weight gains observed on treatment were reversed within 4 weeks following cessation of therapy. While disease progression was not observed in this short-term study, we could find no indication of an immunorestorative or antiviral effect of AL 721, as determined by T-lymphocyte subset quantitation or HIV culture. All three patients who were HIV p24 antigenemic at entry retained positive antigen levels throughout treatment. As a consequence of therapy, however, significant increases in serum lipids were observed, including elevations in both triglyceride and total cholesterol levels. In conclusion, our experience on the largest group of HIV-infected patients treated with the highest doses of AL 721 provides no support for the use of this compound as an antiretroviral agent. C1 CUNY MT SINAI SCH MED,MT SINAI MED CTR,NEW YORK,NY 10029. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. UNIV SO CALIF,LOS ANGELES,CA 90089. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NIAID,AIDS PROGRAM,BETHESDA,MD 20892. RP MILDVAN, D (reprint author), BETH ISRAEL MED CTR,1ST AVE & 16TH ST,NEW YORK,NY 10003, USA. FU NHLBI NIH HHS [HL 24061] NR 17 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 10 BP 945 EP 951 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GF673 UT WOS:A1991GF67300004 PM 1890604 ER PT J AU MARTIN, DH PEARSON, JE KUMAR, P KIRKENDOL, PL LEECH, SH GONZALEZ, FM SAXINGER, C STREICHER, HZ AF MARTIN, DH PEARSON, JE KUMAR, P KIRKENDOL, PL LEECH, SH GONZALEZ, FM SAXINGER, C STREICHER, HZ TI SEQUENTIAL MEASUREMENT OF BETA-2-MICROGLOBULIN LEVELS, P24 ANTIGEN LEVELS, AND ANTIBODY-TITERS FOLLOWING TRANSPLANTATION OF A HUMAN IMMUNODEFICIENCY VIRUS-INFECTED KIDNEY ALLOGRAFT SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE TRANSPLANT; BETA-2-MICROGLOBULIN; AIDS; P24 ANTIGEN; HIV ELISA; KIDNEY ID MICROGLOBULIN LEVELS; HOMOSEXUAL MEN; AIDS; BLOOD; BETA2-MICROGLOBULIN; LYMPHADENOPATHY; RISK AB A renal allograft recipient developed symptoms suggestive of AIDS. Serological studies revealed that the donor was positive for human immunodeficiency virus (HIV). Retrospective testing of stored sequential serum samples showed that the recipient was negative for HIV pretransplant; anti-p24 and anti-p41 antibodies appeared 10 and 49 days posttransplant, respectively. The recipient's serum beta-2-microglobulin levels were elevated 14 days posttransplant, with normal renal function, 35 days before the detection of anti-p41 antibody. p24 Antigen was detected for the first time 21 days posttransplant. In addition to p24 antigen, elevated serum beta-2-microglobulins may be a useful marker for HIV infection prior to seroconversion. C1 LOUISIANA STATE UNIV,MED CTR,DEPT PHARMACOL,NEW ORLEANS,LA 70112. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RP MARTIN, DH (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT MED,1542 TULANE AVE,NEW ORLEANS,LA 70112, USA. NR 18 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 11 BP 1118 EP 1121 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GN380 UT WOS:A1991GN38000007 PM 1753339 ER PT J AU CAMPBELL, AA BALDWIN, W AF CAMPBELL, AA BALDWIN, W TI THE RESPONSE OF AMERICAN WOMEN TO THE THREAT OF AIDS AND OTHER SEXUALLY-TRANSMITTED DISEASES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE AIDS AWARENESS; WOMEN; SEXUAL PRACTICES; CONDOMS; HETEROSEXUAL; RISK REDUCTION AB Using data from the National Survey of Family Growth, we observe that large numbers of American women say that they are responding to the rising danger of AIDS and other sexually transmitted diseases. Among the changes reported in the 1988 National Survey of Family Growth are use of condoms, sexual relations with fewer partners, reduced frequency of sexual intercourse, changes in specific sexual activities, and avoidance of sex with unknown men, bisexual men, and intravenous drug users. Interviews with a sample of the 51 million sexually active women aged 15-44 in the United States show that 28% report either that they have adopted less hazardous sexual practices or that their partners have used condoms to prevent disease. Among women exposed to higher risk of disease, the response is even greater: among unmarried women with five or more lifetime partners, 65% report modified behavior or condom use. Most of these changes occurred after the women heard of AIDS. However, there are still many women who report doing nothing to protect themselves against infection despite sexual and contraceptive behavior that appears to put them at high risk. C1 NICHHD,CTR POPULAT RES,DEMOG & BEHAV SCI BRANCH,BLDG EPN,ROOM 611,BETHESDA,MD 20892. NR 3 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 11 BP 1133 EP 1140 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GN380 UT WOS:A1991GN38000009 PM 1753341 ER PT J AU BATTJES, RJ PICKENS, RW AMSEL, Z AF BATTJES, RJ PICKENS, RW AMSEL, Z TI HIV-INFECTION AND AIDS RISK BEHAVIORS AMONG INTRAVENOUS-DRUG-USERS ENTERING METHADONE TREATMENT IN SELECTED UNITED-STATES CITIES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV; AIDS RISK BEHAVIORS; INTRAVENOUS DRUG ABUSE; TRENDS ID HUMAN-IMMUNODEFICIENCY-VIRUS; NEW-YORK-CITY; ABUSERS; ANTIBODY AB To assess trends in HIV infection and AIDS risk behaviors among intravenous drug users (IVDUs), a series of nonblinded point-prevalence surveys was conducted with admissions to methadone treatment in seven areas, including New York City; Trenton and Asbury Park, New Jersey; Baltimore; Chicago; San Antonio, Texas; and Los Angeles County between February and December 1987 (n = 713), January and June 1988 (n = 1,089), July and December 1988 (n = 932), and January and June 1989 (n = 1,110). Over the 2-year period, significant changes in HIV seropositivity levels were found in only one of the seven cities (Chicago, with levels increasing from 8.4 to 14.7%). High levels of AIDS risk behaviors (frequency of injection, needle sharing, needle cleaning, and use of shooting galleries) were found in all cities. Comparisons of trends in recent risk behaviors (past year) within cities suggest that relatively little reduction in AIDS risk behaviors had occurred during the study. C1 NIDA,ADDICT RES CTR,BALTIMORE,MD. RP BATTJES, RJ (reprint author), NIDA,5600 FISHERS LANE,RM 10A-38,ROCKVILLE,MD 20857, USA. NR 32 TC 37 Z9 37 U1 1 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 11 BP 1148 EP 1154 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GN380 UT WOS:A1991GN38000011 PM 1753342 ER PT J AU GARRIS, I RODRIGUEZ, EM DEMOYA, EA GUERRERO, E PENA, C PUELLO, E GOMEZ, E MONTERROSO, ER WEISSENBACHER, M VERMUND, SH AF GARRIS, I RODRIGUEZ, EM DEMOYA, EA GUERRERO, E PENA, C PUELLO, E GOMEZ, E MONTERROSO, ER WEISSENBACHER, M VERMUND, SH TI AIDS HETEROSEXUAL PREDOMINANCE IN THE DOMINICAN-REPUBLIC SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV; HIV SEROPREVALENCE; SEXUAL BEHAVIOR; PUBLIC HEALTH; DOMINICAN-REPUBLIC ID HIV AB AIDS surveillance data from the Dominican Republic are described for 1983-89. A positive serologic test for HIV was required, and standard clinical criteria were used for defining AIDS. There were 1,202 AIDS cases (820 men, 372 women, 10 of unknown gender) reported to the Ministry of Health, for a cumulative case rate of 17 per 100,000 persons. Rapid growth of the epidemic is noted, with 43% of the total cases reported in 1989. Heterosexual exposure accounts for 53% (593) of all cases, with a male-to-female ratio of 2.2:1, resembling a World Health Organization Pattern I/II country. Prevalence is highest in and surrounding the urbanized tourist areas of Santo Domingo and Puerto Plata and in districts with a high concentration of sugar plantation barracks, where laborers from Haiti and the Dominican Republic work and live. The distribution of AIDS cases is described by transmission exposure category, age, sex, year of diagnosis, and district. The National AIDS Surveillance Program can be improved by validation of exposure transmission categories through selected case investigation and by better reporting through training of health care providers. Surveillance data will assist in targeting future public health efforts to regions and persons at highest risk. C1 NIAID,DIV AIDS,EPIDEMIOL BRANCH,6003 EXECUT BLVD,ROOM 240P,BETHESDA,MD 20892. PAN AMER HLTH ORG,WHO,GLOBAL PROGRAM AIDS,HLTH SITUAT & TREND ASSESSMENT PROGRAM,WASHINGTON,DC. OI Vermund, Sten/0000-0001-7289-8698 FU NIAID NIH HHS [N01-AI-72649] NR 14 TC 5 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 12 BP 1173 EP 1178 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GR659 UT WOS:A1991GR65900002 PM 1941524 ER PT J AU VISCIDI, RP HILL, PM LI, SJ CERNY, EH VLAHOV, D FARZADEGAN, H HALSEY, N KELEN, GD QUINN, TC AF VISCIDI, RP HILL, PM LI, SJ CERNY, EH VLAHOV, D FARZADEGAN, H HALSEY, N KELEN, GD QUINN, TC TI DIAGNOSIS AND DIFFERENTIATION OF HTLV-I AND HTLV-II INFECTION BY ENZYME IMMUNOASSAYS USING SYNTHETIC PEPTIDES SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HTLV-I; HTLV-II; SYNTHETIC PEPTIDES; ENVELOPE PROTEINS; ENZYME IMMUNOASSAY ID CELL LEUKEMIA-VIRUS; COMPLETE NUCLEOTIDE-SEQUENCE; HUMAN MONOCLONAL-ANTIBODY; DNA; DISCRIMINATION; REACTIVITY; HYBRIDS; REGIONS; GENOME AB Synthetic peptides from the major envelope protein of HTLV-I (ENV-I, amino acid 177-213) and HTLV-II (ENV-II, amino acid 173-209) and a conserved region of the transmembrane protein (TM, amino acid 378-402) were used as antigens in microtiter plate enzyme immunoassays (EIA) to detect and discriminate antibodies to HTLV-I and II. The ENV-I and ENV-II peptide EIAs were able to correctly discriminate HTLV-I and II infections in 17 of 18 subjects whose infections were determined by a gene amplification method. Sera from 100 of 107 subjects with serologically confirmed infection with HTLV-I/II and 0 of 218 seronegative controls reacted with one or more of the peptides (sensitivity, 93.5%; specificity, 100%). Ninety-six of the 100 peptide positive sera reacted exclusively with either the ENV-I or the ENV-II peptide, thereby differentiating the two viral infections. The pattern of reactivity to the ENV peptides was distinct in different populations. Patients attending an Emergency Department, who had a history of drug abuse, and male inmate entering a correctional facility only had antibody reactivity to the ENV-II peptide. Subjects from Haiti and patients with HTLV-associated neurological disease only had antibody reactivity to the ENV-I peptide. Peptide-based enzyme immunoassays that distinguish antibodies to HTLV-I and HTLV-II will facilitate studies of the epidemiology of HTLV. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,EUDOWOOD DIV INFECT DIS,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DIV EMERGENCY MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT INT HLTH,BALTIMORE,MD 21218. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. FDN RECH MED,GENEVA,SWITZERLAND. OI Kelen, Gabor/0000-0002-3236-8286 FU NHLBI NIH HHS [HL43586]; NIAID NIH HHS [AI26521]; NIDA NIH HHS [DA04323] NR 27 TC 16 Z9 16 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PY 1991 VL 4 IS 12 BP 1190 EP 1198 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GR659 UT WOS:A1991GR65900004 PM 1941526 ER PT J AU CONE, EJ WELCH, P MITCHELL, JM PAUL, BD AF CONE, EJ WELCH, P MITCHELL, JM PAUL, BD TI FORENSIC DRUG-TESTING FOR OPIATES .1. DETECTION OF 6-ACETYLMORPHINE IN URINE AS AN INDICATOR OF RECENT HEROIN EXPOSURE - DRUG AND ASSAY CONSIDERATIONS AND DETECTION TIMES SO JOURNAL OF ANALYTICAL TOXICOLOGY LA English DT Article ID GAS-CHROMATOGRAPHY; METABOLITES; IDENTIFICATION; MORPHINE; CODEINE AB The urinary excretion pattens of 6-acetylmorphine (6-AM), free morphine, and total morphine were determined by GC/MS assay for six human subjects who received single doses of 3.0 and 6.0 mg of heroin hydrochloride. Clinical specimens were collected and combined with standardized drug urines into a 400 specimen/standard set. The urines were coded, randomized, and analyzed under blind conditions. The GC/MS assay had a limit of sensitivity of 0.81 ng/mL for 6-AM and displayed a lenear response across a concentration range of 1-100 ng/mL. Following heroin administration, 6-AM was excreted rapidly with an average half-life of 0.6 h. This resulted in a very short detection time for 6-AM with a range of 2-8 h at the most sensitive cutoff limit. This short detection time limits the usefulness of 6-AM as a marker for identification of heroin absers to a period immediately after drug use. In contrast, free morphine and total morphine were detectable up to approximately 24 h after heroin administration. The average half-life for free morphine was 3.6 h and for total morphine was 7.9 h. After morphine and codeine administration, no 6-AM was detected by GC/MS above the 0.81-ng/mL detection limit of the assay. It is concluded that the presence of 6-AM in urine can be interpreted with confidence to mean that heroin, or 6-AM, was administered within 24 h of specimen collection and that the presence of 6-AM in urine is not caused by morphine or codeine administration. C1 USN,DRUG SCREENING LAB,NORFOLK,VA 23511. RP CONE, EJ (reprint author), NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 14 TC 116 Z9 117 U1 0 U2 6 PU PRESTON PUBLICATIONS INC PI NILES PA 7800 MERRIMAC AVE PO BOX 48312, NILES, IL 60648 SN 0146-4760 J9 J ANAL TOXICOL JI J. Anal. Toxicol. PD JAN-FEB PY 1991 VL 15 IS 1 BP 1 EP 7 PG 7 WC Chemistry, Analytical; Toxicology SC Chemistry; Toxicology GA ET783 UT WOS:A1991ET78300001 PM 2046334 ER PT J AU BOYD, JH CRUMP, T AF BOYD, JH CRUMP, T TI WESTPHAL AGORAPHOBIA SO JOURNAL OF ANXIETY DISORDERS LA English DT Article C1 YALE UNIV,NEW HAVEN,CT 06520. NIH,LIB TRANSLAT UNIT,BETHESDA,MD 20892. RP BOYD, JH (reprint author), GRAND VIEW PSYCHIAT RES CTR,88 GRANDVIEW AVE,WATERBURY,CT 06708, USA. NR 19 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 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PY 1991 VL 5 IS 1 BP 77 EP 86 DI 10.1016/0887-6185(91)90018-O PG 10 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA EX250 UT WOS:A1991EX25000006 ER PT J AU RETTEW, DC CHESLOW, DL RAPOPORT, JL LEONARD, HL LENANE, MC BLACK, B SWEDO, SE AF RETTEW, DC CHESLOW, DL RAPOPORT, JL LEONARD, HL LENANE, MC BLACK, B SWEDO, SE TI NEUROPSYCHOLOGICAL TEST-PERFORMANCE IN TRICHOTILLOMANIA - A FURTHER LINK WITH OBSESSIVE-COMPULSIVE DISORDER SO JOURNAL OF ANXIETY DISORDERS LA English DT Article ID CLOMIPRAMINE; ADOLESCENTS; DESIPRAMINE; TOMOGRAPHY; FLUOXETINE; INTERVIEW C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. RP RETTEW, DC (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N-240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 40 TC 51 Z9 52 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PY 1991 VL 5 IS 3 BP 225 EP 235 DI 10.1016/0887-6185(91)90003-C PG 11 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA FY499 UT WOS:A1991FY49900003 ER PT J AU CAM, K OBERTO, J WEISBERG, RA AF CAM, K OBERTO, J WEISBERG, RA TI THE EARLY PROMOTERS OF BACTERIOPHAGE-HK022 - CONTRASTS AND SIMILARITIES TO OTHER LAMBDOID PHAGES SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; ANTITERMINATION PROTEIN; TRANSCRIPTION; REGION; REPRESSOR; GENES; RNA; RECOMBINATION; PHAGE-HK022; SPECIFICITY AB The p(L), p(R) and p(M) promoters of lambdoid phages direct the transcription of early phage genes and the prophage repressor gene. We have determined the start points of transcription for these three promoters in the lambdoid phage HK022 and have shown that the HK022 repressor represses the early promoters, p(L) and p(R), and activates the repressor promoter, p(M). HK022 resembles other phages of the lambda family in these respects, as it does in the functional organization of most of its early genes and sites. One exception is nun, the first gene of the HK022 p(L) operon, which is expressed in the presence of prophage repressor and thus differs from its lambda counterpart, gene N. We show that transcription of nun in a lysogen does not initiate at p(L) but instead starts upstream at the pM promoter. This difference in transcription fits the different roles of Nun and N proteins in the physiology of the two phages: Nun protects HK022 lysogens against superinfection with certain other lambdoid phages, while N promotes the transcription of early lambda genes. C1 NICHHD,MOLEC GENET LAB,BLDG 6,ROOM 408,BETHESDA,MD 20892. NR 34 TC 25 Z9 25 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1991 VL 173 IS 2 BP 734 EP 740 PG 7 WC Microbiology SC Microbiology GA ET446 UT WOS:A1991ET44600039 PM 1824767 ER PT J AU LI, ASW CHIGNELL, CF AF LI, ASW CHIGNELL, CF TI THE NOH VALUE IN EPR SPIN TRAPPING - A NEW PARAMETER FOR THE IDENTIFICATION OF 5,5-DIMETHYL-1-PYRROLINE-N-OXIDE SPIN ADDUCTS SO JOURNAL OF BIOCHEMICAL AND BIOPHYSICAL METHODS LA English DT Note DE SPIN TRAPPING; SPIN ADDUCT; 5,5-DIMETHYL-1-PYRROLINE-N-OXIDE AB The ratio of the nitrogen to hydrogen hyperfine splittings (alpha-N/alpha-H) of spin adducts derived from the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) has been found to be a useful parameter for adduct identification. For example, this parameter makes it possible to distinguish between the superoxide (alpha-N/alpha-H = 1.22-1.26) and peroxyl (alpha-N/alpha-H = 1.33-1.40) radical adducts of DMPO in aqueous solution. Since the alpha-N to alpha-H ratio corrects for minor differences in EPR spectrometer calibration, it is a more reproducible parameter than the alpha-N and alpha-H values themselves. C1 NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709. NR 7 TC 26 Z9 27 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-022X J9 J BIOCHEM BIOPH METH JI J. Biochem. Biophys. Methods PD JAN PY 1991 VL 22 IS 1 BP 83 EP 87 DI 10.1016/0165-022X(91)90084-A PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA EP505 UT WOS:A1991EP50500009 PM 1848570 ER PT J AU SPONSELLER, PD MALECH, HL MCCARTHY, EF HOROWITZ, SF JAFFE, G GALLIN, JI AF SPONSELLER, PD MALECH, HL MCCARTHY, EF HOROWITZ, SF JAFFE, G GALLIN, JI TI SKELETAL INVOLVEMENT IN CHILDREN WHO HAVE CHRONIC GRANULOMATOUS-DISEASE SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID ASPERGILLUS-NIDULANS; CYTOCHROME-B; OSTEOMYELITIS; INFECTIONS; CHILDHOOD AB Chronic granulomatous disease is a rare disorder of the oxidative metabolism of the white blood cells that results in immunodeficiency. In a retrospective review of the records of forty-two patients who had chronic granulomatous disease, we identified thirteen patients who had a total of twenty skeletal infections. Two types of infection were noted: Type 1, which resulted from a direct spread of the infection from an adjacent focus, usually of fungus or mycobacteria, and Type 2, which resulted from hematogenous spread, usually of Nocardia or more common bacteria. The thoracic vertebrae, ribs, and metatarsals were the most commonly involved bones. All four patients in whom the vertebrae were involved had a Type-1 fungal infection. Paresis developed in three of these patients, and two of them died. Antibiotics alone effectively eradicated the infection in only one patient. Wide operative debridement combined with administration of antibiotics was the most successful treatment. Comprehensive preoperative imaging and several cultures are necessary to locate the infection in the bone and to identify the organism. C1 NIH,DEPT PATHOL,BETHESDA,MD 20892. JOHNS HOPKINS MED INST,DEPT PATHOL,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT ORTHOPAED SURG,BALTIMORE,MD 21205. NIH,BACTERIAL DIS SECT,BETHESDA,MD 20892. NR 30 TC 44 Z9 44 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD JAN PY 1991 VL 73A IS 1 BP 37 EP 51 PG 15 WC Orthopedics; Surgery SC Orthopedics; Surgery GA EV418 UT WOS:A1991EV41800006 PM 1985993 ER PT J AU BRODER, S AF BRODER, S TI PROGRESS AND CHALLENGES IN THE GLOBAL EFFORT AGAINST CANCER SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY LA English DT Editorial Material ID TUMOR-INFILTRATING LYMPHOCYTES; ACQUIRED IMMUNODEFICIENCY SYNDROME; RETINOBLASTOMA GENE; BREAST-CANCER; LUNG-CANCER; EXPRESSION; DISEASE; CELLS; P53; INTERLEUKIN-2 AB The new decade has given birth to a large number of new concepts in our approach to cancer. The progress in molecular technology that occurred in the 1980's is being transferred in the 1990's to the bedside. The practical clinical application of basic science innovations is aimed at prevention and curative treatment of cancer in all of its forms, and is becoming a central theme of cancer therapeutics. The progress to date reflects a climate that fosters a unity of basic and clinical investigations, for example, where an understanding of tumor genetics or molecular immunoregulation can translate into an innovative clinical approach such as gene transfer therapy. The challenges that we face in this new decade arise in part from progress in certain areas, such as the discovery of natural products that have important antitumor activity but a limited source, or the increasing incidence in AIDS-related lymphomas that has come about from antiretroviral therapy-induced prolongation of survival for AIDS patients. There are critical challenges from a lack of progress in other areas, as well. The challenge of developing curative therapies is surpassed by the need to prevent those cancers before they arise. The challenge of prevention, as exemplified by the link between lung cancer and smoking, is of paramount importance. The ultimate challenge placed before the global oncology community is to ensure that the fruits of modern technology are available to all who need them. RP BRODER, S (reprint author), NCI,BETHESDA,MD 20892, USA. NR 52 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-5216 J9 J CANCER RES CLIN JI J. Cancer Res. Clin. Oncol. PY 1991 VL 117 IS 4 BP 290 EP 294 DI 10.1007/BF01630710 PG 5 WC Oncology SC Oncology GA FT385 UT WOS:A1991FT38500002 PM 2066349 ER PT J AU CHUANG, DM LIN, WW LEE, CY AF CHUANG, DM LIN, WW LEE, CY TI ENDOTHELIN-INDUCED ACTIVATION OF PHOSPHOINOSITIDE TURNOVER, CALCIUM MOBILIZATION, AND TRANSMITTER RELEASE IN CULTURED NEURONS AND NEURALLY RELATED CELL-TYPES SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL CONF ON ENDOTHELIN CY DEC 09-12, 1990 CL UNIV TSUKUBA, TSUKUBA, JAPAN SP ELECT IND ASSOC JAPAN, JAPAN AUTOMOBLIE MFG ASSOC, REG BANKS ASSOC JAPAN, FEDERAT ELECT POWER CO, JAPAN ELECT MANUFACTURERS ASSOC, JAPAN IRON & STEEL FEDERAT, LIFE INSURANCE ASSOC JAPAN, MARINE & FIRE INSURANCE ASSOC JAPAN, TOKYO BANKERS ASSOC, TRUST CO ASSOC JAPAN HO UNIV TSUKUBA DE ENDOTHELIN; PHOSPHOINOSITIDE; CALCIUM; NEURON; ASTROCYTE; GLIOMA ID CEREBELLAR GRANULE CELLS; SARAFOTOXIN; HYDROLYSIS; PEPTIDES; BINDING; BRAIN; RAT AB Endothelin (ET)-related peptides robustly stimulated [H-3]-inositol phosphate (IP) formation in cultured cerebellar granule cells, astrocytes, and C-6 glioma cells. Their agonist selectivities were ET-1 = ET-2 greater-than-or-equal-to sarafotoxin S6b > ET-3 > big ET-1 for granule cells and ET-1 greater-than-or-equal-to ET-2 greater-than-or-equal-to S6b > big ET-1 > ET-3 for cerebellar astrocytes and C-6 glioma cells. These effects were Ca2+ -dependent but insensitive to antagonists of L-type Ca2+ channels and the Na+/Ca2+ antiporter. Pretreatment of cells with ET-1 or S6b induced homologous desensitization of phosphoinositide (PI) response mediate by ET receptors. Long-term pertussis toxin (PTX) treatment at-tenuated the phosphoinositide (PI) response in astrocytes and glioma but not in granule cells. ET-1 and its related peptides increased [Ca2+]i in C-6 glioma by two distinct pathways: IP3-induced Ca2+ mobilization or receptor-operated Ca2+ influx. La3+, Mn2+, and Cd2+ inhibited the Ca2+ influx and sustained PI turnover, while Ca2+ mobilization was attenuated by phorbol ester and TMB-8. ET-induced Ca2+ influx was essential for the sustained [Ca2+]i increase and PI turnover. Homologous desensitization of [Ca2+]i increase was also noted. In cerebellar granule cells, ET evoke the release of [H-3]D-aspartate from these neurons. This action appears to be dependent on PI hydrolysis and [Ca2+]i increase and modulated by protein kinase C. RP CHUANG, DM (reprint author), NIMH,BIOL PSYCHIAT BRANCH,MOLEC NEUROBIOL SECT,BLDG 10,ROOM 3N212,BETHESDA,MD 20892, USA. NR 13 TC 25 Z9 25 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0160-2446 J9 J CARDIOVASC PHARM JI J. Cardiovasc. Pharmacol. PY 1991 VL 17 SU 7 BP S85 EP S88 PG 4 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA GU396 UT WOS:A1991GU39600023 PM 1725440 ER PT J AU VANKOOYK, Y WEDER, P HOGERVORST, F VERHOEVEN, AJ VANSEVENTER, G TEVELDE, AA BORST, J KEIZER, GD FIGDOR, CG AF VANKOOYK, Y WEDER, P HOGERVORST, F VERHOEVEN, AJ VANSEVENTER, G TEVELDE, AA BORST, J KEIZER, GD FIGDOR, CG TI ACTIVATION OF LFA-1 THROUGH A CA2+-DEPENDENT EPITOPE STIMULATES LYMPHOCYTE ADHESION SO JOURNAL OF CELL BIOLOGY LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-1; PROTEIN KINASE-C; T-CELL PROLIFERATION; PHORBOL ESTER; MONOCLONAL-ANTIBODIES; COMPLEMENT RECEPTORS; INOSITOL PHOSPHATES; SIGNAL TRANSDUCTION; MOLECULE-1 ICAM-1; ENDOTHELIAL-CELLS AB The leukocyte function-associated molecule-1 (LFA-1) plays a key role in cell adhesion processes between cells of the immune system. We investigated the mechanism that may regulate LFA-1-ligand interactions, which result in cell-cell adhesion. To this end we employed an intriguing anti-LFA-1 alpha mAB (NKI-L16), capable of inducing rather than inhibiting cell adhesion. Aggregation induced by NKI-L16 or Fab fragments thereof is not the result of signals transmitted through LFA-1. The antibody was found to recognize a unique Ca2+-dependent activation epitope of LFA-1, which is essentially absent on resting lymphocytes, but becomes induced upon in vitro culture. Expression of this epitope correlates well with the capacity of cells to rapidly aggregate upon stimulation by PMA or through the TCR/CD3 complex, indicating that expression of the NKI-L16 epitope is essential for LFA-1 to mediate adhesion. However, expression of the NKI-L16 epitope in itself is not sufficient for cell binding since cloned T lymphocytes express the NKI-L16 epitope constitutively at high levels, but do not aggregate spontaneously. Based on these observations we propose the existence of three distinct forms of LFA-1: (a) an inactive form, which does not, or only partially exposes the NKI-L16 epitope, found on resting cells; (b) an intermediate, NKI-L16+ form, expressed by mature or previously activated cells; and (c) an active (NKI-L16+) form of LFA-1, capable of high affinity ligand binding, obtained after specific triggering of a lymphocyte through the TCR/CD3 complex, by PMA, or by binding of NKI-L16 antibodies. C1 NETHERLANDS RED CROSS,BLOOD TRANSFUS SERV,CENT LAB,DEPT BLOOD CELL CHEM,AMSTERDAM,NETHERLANDS. NIH,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP VANKOOYK, Y (reprint author), NETHERLANDS CANC INST,ANTONI VANLEEUWENHOEK HUIS,DIV IMMUNOL,PLESMANLAAN 121,1066 CX AMSTERDAM,NETHERLANDS. RI Figdor, Carl/A-4232-2010; OI Figdor, Carl/0000-0002-2366-9212 NR 57 TC 189 Z9 189 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD JAN PY 1991 VL 112 IS 2 BP 345 EP 354 DI 10.1083/jcb.112.2.345 PG 10 WC Cell Biology SC Cell Biology GA ET174 UT WOS:A1991ET17400015 PM 1703161 ER PT J AU HAMMER, JA JUNG, G AF HAMMER, JA JUNG, G TI MOLECULAR-CLONING OF PROTOZOAN MYOSIN-I HEAVY-CHAIN GENES SO JOURNAL OF CELL SCIENCE LA English DT Article; Proceedings Paper CT WORKSHOP ON MOTOR PROTEINS CY SEP, 1990 CL CAMBRIDGE, ENGLAND SP EUROPEAN MOLEC BIOL ORG DE MYOSIN-I; MOLECULAR CLONING; STRUCTURE FUNCTION; GENE TARGETING; POLYMERASE CHAIN REACTION ID ACANTHAMOEBA MYOSIN; DICTYOSTELIUM-DISCOIDEUM; CELL MOTILITY; MUSCLE MYOSIN; CASTELLANII; PROTEINS; SEQUENCE; ISOFORM; DOMAINS AB Myosins I are ubiquitous, nonfilamentous, actin-based mechanoenzymes originally discovered in protozoa. The extensive in vitro biochemical studies of purified protozoan myosins I are now being complemented with in vivo studies using cloned myosin I heavy chain genes and gene targeting techniques. Here we review briefly the systems and methods being used in these efforts to dissect protozoan myosin I structure and function using molecular genetic approaches. RP HAMMER, JA (reprint author), NHLBI,CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 27 TC 0 Z9 0 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PY 1991 SU 14 BP 37 EP 40 PG 4 WC Cell Biology SC Cell Biology GA FK902 UT WOS:A1991FK90200009 ER PT J AU KELLEY, CA KAWAMOTO, S CONTI, MA ADELSTEIN, RS AF KELLEY, CA KAWAMOTO, S CONTI, MA ADELSTEIN, RS TI PHOSPHORYLATION OF VERTEBRATE SMOOTH-MUSCLE AND NONMUSCLE MYOSIN HEAVY-CHAINS INVITRO AND IN INTACT-CELLS SO JOURNAL OF CELL SCIENCE LA English DT Article; Proceedings Paper CT WORKSHOP ON MOTOR PROTEINS CY SEP, 1990 CL CAMBRIDGE, ENGLAND SP EUROPEAN MOLEC BIOL ORG DE MYOSIN; PHOSPHORYLATION; PROTEIN KINASE-C; CASEIN KINASE-II ID PROTEIN KINASE-C; LIGHT CHAIN; DNA-SEQUENCE; IDENTIFICATION; CLONING; SITES AB In this article we summarize our recent experiments studying the phosphorylation of vertebrate myosin heavy chains by protein kinase C and casein kinase II. Protein kinase C phosphorylates vertebrate nonmuscle myosin heavy chains both in vitro and in intact cells. A single serine residue near the end of the helical portion of the myosin rod is the only site phosphorylated in a variety of vertebrate nonmuscle myosin heavy chains. There does not appear to be a site for protein kinase C phosphorylation in vertebrate smooth muscle myosin heavy chains. Casein kinase II phosphorylates a single serine residue located near the carboxyl terminus of the 204 x 10(3) M(r) smooth muscle myosin heavy chain in vitro as well as in cultured smooth muscle cells. It does not phosphorylate the 200 x 10(3) M(r) smooth muscle myosin heavy chain. However, the site is present in vertebrate nonmuscle myosin heavy chains. The 204 x 10(3) M(r) myosin heavy chain of embryonic chicken gizzard smooth muscle is exceptional in not containing a site for casein kinase II phosphorylation. C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. OI Adelstein, Robert/0000-0002-8683-2144 NR 30 TC 3 Z9 3 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PY 1991 SU 14 BP 49 EP 54 PG 6 WC Cell Biology SC Cell Biology GA FK902 UT WOS:A1991FK90200011 ER PT J AU SELLERS, JR HAN, YJ KACHAR, B AF SELLERS, JR HAN, YJ KACHAR, B TI THE USE OF NATIVE THICK FILAMENTS IN INVITRO MOTILITY ASSAYS SO JOURNAL OF CELL SCIENCE LA English DT Article; Proceedings Paper CT WORKSHOP ON MOTOR PROTEINS CY SEP, 1990 CL CAMBRIDGE, ENGLAND SP EUROPEAN MOLEC BIOL ORG DE MOTILITY; MYOSIN; ACTIN; MOLLUSK; FILAMENTS ID ACTIN-FILAMENTS; SMOOTH-MUSCLE; MYOSIN HEADS; MONOCLONAL-ANTIBODIES; ELECTRON-MICROSCOPY; MOVEMENT; CABLES; FORCE; BEADS AB Native thick filaments from the clam, Mercinaria mercinaria translocate actin filaments both toward and away from the center of the thick filament in an in vitro motility assay. The thick filaments from the adductor muscle are about 10-mu-m long whereas those from the catch muscle are 30-50-mu-m long. These thick filaments should prove useful in understanding the mechanism of myosin-dependent movement of actin filaments. C1 NIDOCD,MOLEC OTOL LAB,BETHESDA,MD 20892. RP SELLERS, JR (reprint author), NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892, USA. NR 32 TC 4 Z9 4 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PY 1991 SU 14 BP 67 EP 71 PG 5 WC Cell Biology SC Cell Biology GA FK902 UT WOS:A1991FK90200015 ER PT J AU EVANS, CH AF EVANS, CH TI GROWTH AND DIFFERENTIATION - FULFILLING THE DREAM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Editorial Material RP EVANS, CH (reprint author), NCI,TUMOR BIOL SECT,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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN PY 1991 VL 45 IS 1 BP 3 EP 4 DI 10.1002/jcb.240450103 PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ET740 UT WOS:A1991ET74000001 ER PT J AU EGAN, JJ GRONOWICZ, G RODAN, GA AF EGAN, JJ GRONOWICZ, G RODAN, GA TI CELL DENSITY-DEPENDENT DECREASE IN CYTOSKELETAL ACTIN AND MYOSIN IN CULTURED OSTEOBLASTIC CELLS - CORRELATION WITH CYCLIC-AMP CHANGES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE CYTOSKELETON; OSTEOBLASTS; CELL-CELL INTERACTION ID ADENOSINE 3',5'-MONOPHOSPHATE LEVELS; LIGHT CHAIN KINASE; HEAVY-CHAIN; TRANSFORMED-CELLS; GENE-EXPRESSION; HUMAN-PLATELETS; PROTEIN-KINASE; SMOOTH-MUSCLE; BONE-CELLS; PHOSPHORYLATION AB During bone development, osteoblasts form a contiguous layer along recently deposited osteoid and their morphology changes from fibroblast-like to cuboidal. In culture, similar changes occur with increased cell density. We examined the possible role of cyclic AMP in this process since cyclic AMP was reported to increase in fibroblasts with increased cell density and similar shape changes were seen in response to parathyroid hormone, which also increases cellular cyclic AMP in osteoblastic cells. Osteoblast-enriched rat calvaria cells were seeded at increasing density. The distribution between Triton X-100 extractable and nonextractable actin and myosin was estimated by polyacrylamide gel electrophoresis. Intracellular cyclic AMP was estimated by prelabeling the cellular ATP pool with H-3-adenine, followed by extraction and separation of H-3-cAMP by high-performance liquid chromatography. We found that osteoblastic cells contain about 40 pg actin and 5.3 pg myosin per cell. Around 60% of the actin and 70% of the myosin were in the nonextractable (crosslinked) form at cell densities of 10,000 to 50,000 cells per cm2. Above 50,000 cells/cm2, there was a cell density-dependent reduction in crosslinked actin and myosin and a concomitant increase in cellular cyclic AMP. A comparable rise in cyclic AMP, produced by incubation with phosphodiesterase inhibitors, and treatment with other agents that increase cyclic AMP produced a similar decrease in the level of cytoskeletal actin and myosin. Cytochalasin B treatment, through its effect on actin polymerization, produced similar changes in cell shape and cytoskeletal actin. The findings suggest that an elevation in intracellular cyclic AMP may play a role in the density-dependent changes in cell shape and microfilament organization observed in osteoblasts. C1 UNIV CONNECTICUT,CTR HLTH,SCH MED,DEPT ORTHOPED SURG,FARMINGTON,CT 06032. MERCK SHARP & DOHME LTD,DEPT BONE BIOL & OSTEOPOROSIS RES,W POINT,PA 19486. RP EGAN, JJ (reprint author), NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892, USA. OI Gronowicz, Gloria/0000-0001-7158-3598 NR 30 TC 16 Z9 16 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN PY 1991 VL 45 IS 1 BP 93 EP 100 DI 10.1002/jcb.240450116 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ET740 UT WOS:A1991ET74000014 PM 1848564 ER PT J AU EGAN, JJ GRONOWICZ, G RODAN, GA AF EGAN, JJ GRONOWICZ, G RODAN, GA TI PARATHYROID-HORMONE PROMOTES THE DISASSEMBLY OF CYTOSKELETAL ACTIN AND MYOSIN IN CULTURED OSTEOBLASTIC CELLS - MEDIATION BY CYCLIC-AMP SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE PARATHYROID HORMONE; CYCLIC AMP; OSTEOBLASTS; ACTIN; MYOSIN; CALCIUM ID SMOOTH-MUSCLE MYOSIN; LIGHT-CHAIN KINASE; HAMSTER OVARY CELLS; ADENYLATE-CYCLASE; PROTEIN-KINASE; PLATELET MYOSIN; BINDING PROTEIN; GENE-EXPRESSION; CYTOCHALASIN-B; BONE-CELLS AB Parathyroid hormone (PTH) alters the shape of osteoblastic cells both in vivo and in vitro. In this study, we examined the effect of PTH on cytoskeletal actin and myosin, estimated by polyacrylamide gel electrophoresis of Triton X-100 (1%) nonextractable proteins. After 2-5 minutes, PTH caused a rapid and transient decrease of 50-60% in polymerized actin and myosin associated with the Triton X-100 nonextractable cytoskeleton. Polymerized actin returned to control levels by 30 min. The PTH effect was dose-dependent with an IC50 of about 1 nM, and was partially inhibited by the (3-34) PTH antagonist. PTH caused a rapid transient rise in cyclic AMP (cAMP) in these cells that peaked at 4 min, while the nadir in cytoskeletal actin and myosin was recorded around 5 min. The intracellular calcium chelator Quin-2/AM (10-mu-M) also decreased cytoskeletal actin and myosin, to the same extent as did PTH (100 nM). To distinguish between cAMP elevation and Ca++ reduction as mediators of PTH action, we measured the phosphorylation of the 20 kD (PI 4.9) myosin light chain in cells preincubated with [P-32]-orthophosphate. The phosphorylation of this protein decreased within 2-3 min after PTH addition and returned to control levels after 5 min. The calcium inophore A-23187 did not antagonize this PTH effect. Visualization of microfilaments with rhodamine-conjugated phalloidin showed that PTH altered the cytoskeleton by decreasing the number of stress fibers. These changes in the cytoskeleton paralleled changes in the shape of the cells from a spread configuration to a stellate form with retracting processes. The above findings indicate that the alteration in osteoblast shape produced by PTH involve relatively rapid and transient changes in cytoskeletal organization that appear to be mediated cAMP. C1 UNIV CONNECTICUT,CTR HLTH,SCH MED,DEPT ORTHOPED SURG,FARMINGTON,CT 06032. MERCK SHARP & DOHME LTD,W POINT,PA 19486. RP EGAN, JJ (reprint author), NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20891, USA. OI Gronowicz, Gloria/0000-0001-7158-3598 NR 45 TC 44 Z9 45 U1 1 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN PY 1991 VL 45 IS 1 BP 101 EP 111 DI 10.1002/jcb.240450117 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ET740 UT WOS:A1991ET74000015 PM 1848561 ER PT J AU EHRLICH, HP ROCKWELL, WB CORNWELL, TL RAJARATNAM, JBM AF EHRLICH, HP ROCKWELL, WB CORNWELL, TL RAJARATNAM, JBM TI DEMONSTRATION OF A DIRECT ROLE FOR MYOSIN LIGHT CHAIN KINASE IN FIBROBLAST-POPULATED COLLAGEN LATTICE CONTRACTION SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID DYSTROPHICA RECESSIVE FIBROBLASTS; INDUCED CELL CONTRACTION; SMOOTH-MUSCLE; DERMAL FIBROBLASTS; CATALYTIC SUBUNIT; PROTEIN-KINASE; CAMP; PHOSPHORYLATION; PURIFICATION; CALMODULIN AB Mixing feed fibroblasts with soluble collagen and serum-supplemented culture medium at 37-degrees-C results in the entrapment of cells within the polymerizing collagen matrix. This cellular-collagen complex is referred to as a fibroblast-populated collagen lattice (FPCL). In time, this FPCL undergoes a reduction in size called lattice contraction. The proposed mechanism for lattice contraction is cellular force produced by cytoplasmic microfilaments which organize collagen fibrils compacting the matrix. When the regulatory subunits of myosin, myosin light chains, are phosphorylated by myosin light chain kinase (MLCK), myosin ATPase activity is increased and actin-myosin dynamic filament sliding occurs. Elevated levels of myosin ATPase are required for maximal lattice contraction. Cholera toxin inhibits lattice contraction by increasing intracellular levels of cAMP. It is proposed that increased cytoplasmic concentrations of cAMP promote phosphorylation of MLCK, the enzyme important for maximizing myosin ATPase activity. Phosphorylating MLCK in vitro inhibits activity by decreasing its sensitivity to calcium-calmodulin complex. A decrease in MLCK activity would result in lower levels of myosin ATPase activity. MLCK, purified from turkey gizzard, was subjected to limited proteolytic digestion to produce calmodulin-independent-MLCK. The partially digested kinase does not require calcium-calmodulin for activation. Independent-MLCK is not subject to inhibition by phosphorylation. The electroporetic inoculation of independent-MLCK into fibroblasts before FPCL manufacture produced enhanced lattice contraction. Lattice contraction, in the presence of cholera toxin, was restored to normal levels by the prior electroporetic introduction of independent-MLCK. These findings support the hypothesis that increases in cAMP hinder lattice contraction by a mechanism involving inhibition of MLCK and myosin ATPase. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. NHLBI,BETHESDA,MD 20892. RP EHRLICH, HP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,SHRINERS BURNS INST,WOUND HEALING LAB,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [GM-32705] NR 21 TC 54 Z9 54 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 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JAN PY 1991 VL 146 IS 1 BP 1 EP 7 DI 10.1002/jcp.1041460102 PG 7 WC Cell Biology; Physiology SC Cell Biology; Physiology GA EU576 UT WOS:A1991EU57600001 PM 1846633 ER PT J AU MAHESHWARI, RK SRIKANTAN, V BHARTIYA, D KLEINMAN, HK GRANT, DS AF MAHESHWARI, RK SRIKANTAN, V BHARTIYA, D KLEINMAN, HK GRANT, DS TI DIFFERENTIAL-EFFECTS OF INTERFERON-GAMMA AND INTERFERON-ALPHA ON INVITRO MODEL OF ANGIOGENESIS SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID CAPILLARY-LIKE STRUCTURES; HUMAN-ENDOTHELIAL CELLS; BASEMENT-MEMBRANE; INHIBITION; LAMININ AB The formation of blood vessels in vivo (angiogenesis) is an important process and is usually initiated in response to injury, tumor growth, or normal tissue development. We have studied the effect of human interferon (IFN) alpha (alpha) and gamma (gamma) on the capillary-like network formation in an vitro model of angiogenesis using human umbilical vein endothelial cells (HUVEC). When HUVEC cells are plated on Matrigel (reconstituted basement membrane matrix enriched in laminin), a network of capillary like structures (endotubes) rapidly forms. IFN-alpha enhanced the tube formation in a dose-dependent manner, whereas IFN-gamma significantly inhibited the tube formation. In addition, both the enhancement and inhibition of angiogenesis by IFN-alpha and gamma was found to be greater if the cells were pretreated with IFN for 12 hr before plating on the Matrigel. These results suggest that IFN may play an important role in several vascular processes including early stages of wound healing, recanalization of thrombi, tumor growth, metastasis, normal growth, and development. C1 NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. RP MAHESHWARI, RK (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT PATHOL,BETHESDA,MD 20814, USA. NR 21 TC 76 Z9 78 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JAN PY 1991 VL 146 IS 1 BP 164 EP 169 DI 10.1002/jcp.1041460121 PG 6 WC Cell Biology; Physiology SC Cell Biology; Physiology GA EU576 UT WOS:A1991EU57600020 PM 1703547 ER PT J AU SCHMIDT, K MIES, G SOKOLOFF, L AF SCHMIDT, K MIES, G SOKOLOFF, L TI MODEL OF KINETIC-BEHAVIOR OF DEOXYGLUCOSE IN HETEROGENEOUS TISSUES IN BRAIN - A REINTERPRETATION OF THE SIGNIFICANCE OF PARAMETERS FITTED TO HOMOGENEOUS TISSUE MODELS SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE APPARENT GLUCOSE-6-PHOSPHATASE ACTIVITY; K4-STAR; MODELING; RATE CONSTANT ESTIMATION; RATE CONSTANTS ID CEREBRAL GLUCOSE-UTILIZATION; STABILITY INVIVO; METABOLIC-RATE; HUMANS AB Effects of tissue heterogeneity on regional CMR(glc) (rCMR(glc)) calculated by use of the deoxyglucose (DG) method at 45 min following the pulse of DG were evaluated in simulation studies. A theoretical model was developed to describe the kinetics of DG uptake and metabolism in heterogeneous brain tissues. Rate constants were fitted to simulation data for mixed tissue and rCMR(glc) computed on the basis of this tissue heterogeneity model. The results were compared with those obtained by use of the original model of the DG method for homogeneous tissue, both without (3K model) and with (4K model) a term to describe an apparent loss of deoxyglucose-6-phosphate (DG-6-P). As a direct consequence of tissue heterogeneity, the effective rate constant for phosphorylation of DG, k3*, declined with time. To compensate for the time-changing k3*, estimates of the dephosphorylation rate constant, k4*, were artifactually high when the 4K model was used, even though no dephosphorylation of DG-6-P actually occurred. The present study demonstrates that the finding of a significant k4*, at least within 45 min following a pulse of DG, may not represent dephosphorylation at all, but rather the consequence of measuring radioactivity in a heterogeneous tissue and applying a model designed for a homogeneous tissue. Furthermore, the high estimates of k4* resulted in significant overestimation of rCMR(glc). When rCMR(glc) was computed with the conventional single-scan or auto-radiographic method at 45 min after a pulse of DG, the 3K and tissue heterogeneity models yielded values that were within 5% of the true weighted average value for the heterogeneous tissue as a whole. We conclude that the effects of tissue heterogeneity alone can give the appearance of product loss, even when none occurs, and that the use of the 4k model with the assumption of product loss in the 45-min experimental period recommended for the DG method may lead to overestimation of the rates of glucose utilization. C1 MAX PLANCK INST NEUROL RES,DEPT EXPTL NEUROL,COLOGNE,GERMANY. RP SCHMIDT, K (reprint author), NIMH,CEREBRAL METAB LAB,BLDG 36,ROOM 1A-05,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 15 TC 46 Z9 47 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1991 VL 11 IS 1 BP 10 EP 24 PG 15 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA EP738 UT WOS:A1991EP73800002 PM 1983993 ER PT J AU DIENEL, GA CRUZ, NF MORI, K HOLDEN, JE SOKOLOFF, L AF DIENEL, GA CRUZ, NF MORI, K HOLDEN, JE SOKOLOFF, L TI DIRECT MEASUREMENT OF THE LAMBDA OF THE LUMPED CONSTANT OF THE DEOXYGLUCOSE METHOD IN RAT-BRAIN - DETERMINATION OF LAMBDA AND LUMPED CONSTANT FROM TISSUE GLUCOSE-CONCENTRATION OR EQUILIBRIUM BRAIN PLASMA DISTRIBUTION RATIO FOR METHYLGLUCOSE SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE CEREBRAL GLUCOSE UTILIZATION; HEXOSE DISTRIBUTION SPACES; HYPERGLYCEMIA; HYPOGLYCEMIA ID AUTORADIOGRAPHIC DETERMINATION; GLUCOSE-6-PHOSPHATASE ACTIVITY; CEREBRAL-CORTEX; FOCAL ISCHEMIA; BLOOD-FLOW; INVIVO; 2-DEOXY-D-GLUCOSE; PHOSPHORYLATION; 2-DEOXYGLUCOSE; METABOLISM AB Steady-state distribution spaces of 2-[C-14]deoxyglucose ([C-14]DG), glucose, and 3-O-[C-14]methylglucose at various concentrations of glucose in brain and plasma ranging from hypoglycemic to hyperglycemic levels have been determined by direct chemical analyses in the brains of conscious rats. The hexose concentrations were measured chemically in freeze-blown brain extracted with ethanol to avoid the degradation of acid-labile products of [C-14]DG back to free [C-14]DG that has been found to occur with the more commonly used perchloric acid extraction of brain. Corrections were also made for nonphophorylatable, labeled products of [C-14]DG found in the nonacidic fractions of the brain extracts, which were previously included with the assayed [C-14]DG, and for the contribution of the hexose contents in the blood in the brain, which was found to be particularly critical for the determination of the glucose distribution space, especially in hypoglycemic states. From the measured contents of the hexoses in brain and plasma, the relationships of the tissue concentrations and distribution spaces of each of the hexoses and of the lambda (i.e., ratio of tissue distribution space of DG to that of glucose) of the DG method to the tissue glucose concentration were derived. The lambda was then quantitatively related to the measured equilibrium ratio for [C-14]methylglucose over the full range of brain and plasma glucose levels. By combining these new data with the values for the lumped constant, the factor that converts rate of DG phosphorylation to glucose phosphorylation, previously determined in rats over the same range of plasma glucose levels, the phosphorylation coefficient was calculated and the lumped constant graphed as a function of the measured distribution space in brain for ]C-14[methylglucose. C1 UNIV WISCONSIN,DEPT MED PHYS,MADISON,WI 53706. RP DIENEL, GA (reprint author), NIMH,CEREBRAL METAB LAB,BLDG 36,RM 1A-05,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 42 TC 66 Z9 66 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1991 VL 11 IS 1 BP 25 EP 34 PG 10 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA EP738 UT WOS:A1991EP73800003 PM 1984002 ER PT J AU BLASBERG, RG GROOTHUIS, DR AF BLASBERG, RG GROOTHUIS, DR TI BLOOD-TUMOR BARRIER DISRUPTION CONTROVERSIES SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Letter ID BRAIN-BARRIER C1 NORTHWESTERN UNIV,DEPT NEUROL,EVANSTON,IL 60201. EVANSTON HOSP CORP,EVANSTON,IL 60201. RP BLASBERG, RG (reprint author), NIH,DEPT NUCL MED,BETHESDA,MD 20892, USA. NR 11 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1991 VL 11 IS 1 BP 165 EP 166 PG 2 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA EP738 UT WOS:A1991EP73800021 PM 1898507 ER PT J AU RAPOPORT, SI ROBINSON, PJ AF RAPOPORT, SI ROBINSON, PJ TI BLOOD-TUMOR BARRIER DISRUPTION CONTROVERSIES - REPLY SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Letter ID BRAIN-BARRIER RP RAPOPORT, SI (reprint author), NIA,NEUROSCI LAB,BETHESDA,MD 20892, USA. NR 8 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1991 VL 11 IS 1 BP 166 EP 168 PG 3 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA EP738 UT WOS:A1991EP73800022 ER PT J AU COLBY, CL AF COLBY, CL TI THE NEUROANATOMY AND NEUROPHYSIOLOGY OF ATTENTION SO JOURNAL OF CHILD NEUROLOGY LA English DT Review ID FRONTAL EYE-FIELD; MONKEY SUPERIOR COLLICULUS; NIGRA PARS RETICULATA; TEMPORAL VISUAL AREA; LATERAL GENICULATE-NUCLEUS; INFERIOR PARIETAL LOBULE; GABA-RELATED SUBSTANCES; ALERT RHESUS-MONKEY; POSTERIOR PARIETAL; FUNCTIONAL-PROPERTIES AB Attention is a distributed process. The activity of neurons in many brain structures can be modulated by the attentional state of the animal. Attention directed toward a particular external stimulus is often reflected in an enhancement of the sensory response to that stimulus. Enhancement is spatially selective for neurons in many areas and explicitly eye-movement related in most. Attention directed toward the internal representation of a stimulus may be associated with a prolongation of neural activity. These modulations of neuronal responsiveness underscore the dynamic nature of neural processing. Competition between left- and right-brain structures in the control of attention is common. While attention is perceived as a unitary process, it is subserved by many brain structures. Given the wide distribution of attentional processes, it is not surprising that children diagnosed as having attentional deficits show considerable diversity in symptoms and etiology. RP COLBY, CL (reprint author), NIH,NATL EYE INST,SENSORIMOTOR RES,BLDG 10,ROOM 10C101,BETHESDA,MD 20892, USA. NR 300 TC 55 Z9 55 U1 1 U2 2 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PY 1991 VL 6 SU S BP S90 EP S118 PG 29 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA EV301 UT WOS:A1991EV30100011 PM 1848251 ER PT J AU AUGUST, A DINGWALL, W YENJKOMSHIAN, G FEDIO, P AF AUGUST, A DINGWALL, W YENJKOMSHIAN, G FEDIO, P TI LEFT AND RIGHT BRAIN JUDGMENTS OF EMOTIONAL VERBAL STIMULI SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NIH,CLIN NEUROPSYCHOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 26 EP 26 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600047 ER PT J AU RANDOLPH, C GOLD, JM GOLDBERG, TE WEINBERGER, DR AF RANDOLPH, C GOLD, JM GOLDBERG, TE WEINBERGER, DR TI ELABORATIVE ENCODING NORMALIZES LEXICAL PRIMING DEFICITS IN SCHIZOPHRENIA SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 30 EP 31 PG 2 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600062 ER PT J AU FEDIO, P MARTIN, A DAVIDSON, R AURIELLE, E SMITH, B AF FEDIO, P MARTIN, A DAVIDSON, R AURIELLE, E SMITH, B TI ELECTRODERMAL REACTIONS AND HABITUATION BY PATIENTS WITH UNILATERAL TEMPORAL LOBECTOMY SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV WISCONSIN,DEPT PSYCHOL,MADISON,WI 53706. RI martin, alex/B-6176-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 46 EP 46 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600134 ER PT J AU HAXBY, JV RAFFAELE, KC SCHAPIRO, MB RAPOPORT, SI AF HAXBY, JV RAFFAELE, KC SCHAPIRO, MB RAPOPORT, SI TI PREDICTING FUTURE RATE OF DECLINE IN PATIENTS WITH DEMENTIA OF THE ALZHEIMER TYPE SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 51 EP 51 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600159 ER PT J AU FEIN, DA WAINWRIGHT, L MORRIS, R WATERHOUSE, L ALLEN, DA ARAM, DM WILSON, BC RAPIN, I AF FEIN, DA WAINWRIGHT, L MORRIS, R WATERHOUSE, L ALLEN, DA ARAM, DM WILSON, BC RAPIN, I TI SYMBOLIC PLAY DEVELOPMENT IN AUTISTIC AND LANGUAGE-DISORDERED CHILDREN SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NIMH,OFF AIDS PROGRAMS,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 53 EP 53 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600167 ER PT J AU GREENWOOD, PM PARASURAMAN, R HAXBY, JV AF GREENWOOD, PM PARASURAMAN, R HAXBY, JV TI SHIFTS OF VISUAL-ATTENTION IN MILD AND MODERATE ALZHEIMERS-DISEASE SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 CATHOLIC UNIV AMER,DEPT PSYCHOL,COGNIT SCI LAB,WASHINGTON,DC 20064. NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 69 EP 70 PG 2 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600242 ER PT J AU GOLD, J BERMAN, K RANDOLPH, C GOLDBERG, T WEINBERGER, D AF GOLD, J BERMAN, K RANDOLPH, C GOLDBERG, T WEINBERGER, D TI PET VALIDATION AND CLINICAL-APPLICATION OF A NOVEL PREFRONTAL TASK SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NIMH,NEUROPSYCHIAT RES HOSP,WASHINGTON,DC 20032. NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 81 EP 81 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600295 ER PT J AU WILSON, BC PEQUEGNAT, W BELMAN, A BROUWERS, P DENCKLA, M DIAMOND, A FENNELL, EB FLETCHER, JM HAGGARDY, R HITTELMAN, J HORNER, T KAIRMAN, R MATTIS, S MOSS, H STOVER, E AF WILSON, BC PEQUEGNAT, W BELMAN, A BROUWERS, P DENCKLA, M DIAMOND, A FENNELL, EB FLETCHER, JM HAGGARDY, R HITTELMAN, J HORNER, T KAIRMAN, R MATTIS, S MOSS, H STOVER, E TI NEURODEVELOPMENTAL AND NEUROLOGICAL ASSESSMENT ISSUES WITH INFANTS AND CHILDREN SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NIMH,OFF AIDS PROGRAM,ROCKVILLE,MD 20857. UNIV TEXAS,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 3 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 96 EP 97 PG 2 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600371 ER PT J AU ADAMS, KM BUTTERS, N BECKER, J BOCCELLARI, A BROUWERS, P CAMPBELL, A CHELLUNE, G HEATON, RK MARTIN, A PEQUEGNAT, W SCHMITT, F STERN, Y WILKIE, F AF ADAMS, KM BUTTERS, N BECKER, J BOCCELLARI, A BROUWERS, P CAMPBELL, A CHELLUNE, G HEATON, RK MARTIN, A PEQUEGNAT, W SCHMITT, F STERN, Y WILKIE, F TI METHODOLOGICAL AND NEUROPSYCHOLOGICAL ASSESSMENT ISSUES OF HIV-1 INFECTED ADULTS SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 UNIV MICHIGAN,MED CTR,DEPT PSYCHIAT,ANN ARBOR,MI 48109. VET ADM MED CTR,PSYCHOL SERV,LA JOLLA,CA 92161. NIMH,OFF AIDS PROGRAM,ROCKVILLE,MD 20857. NEUROL INST,NEW YORK,NY 10032. RI martin, alex/B-6176-2009 NR 0 TC 0 Z9 0 U1 0 U2 1 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 97 EP 97 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600374 ER PT J AU FLETCHER, JM FRANCIS, DJ BROUWERS, P RAUDENBUSH, SW SCHMITT, F PEQUEGNAT, W STOVER, E AF FLETCHER, JM FRANCIS, DJ BROUWERS, P RAUDENBUSH, SW SCHMITT, F PEQUEGNAT, W STOVER, E TI NEURODEVELOPMENT IN HIV-1 INFECTION AND AIDS IN INFANTS AND CHILDREN - APPLICATION OF THE PROCESS MODEL SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,HOUSTON,TX 77030. UNIV HOUSTON,DEPT PSYCHOL,HOUSTON,TX 77204. NIMH,OFF AIDS PROGRAM,ROCKVILLE,MD 20857. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 97 EP 97 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600372 ER PT J AU STERN, Y ADAMS, KM BUTTERS, N BECKER, JT BOCCELLARI, A BROUWERS, P CAMPBELL, A CHELLUNE, G HEATON, RK MARTIN, A PEQUEGNAT, W SCHMITT, F WILKIE, F AF STERN, Y ADAMS, KM BUTTERS, N BECKER, JT BOCCELLARI, A BROUWERS, P CAMPBELL, A CHELLUNE, G HEATON, RK MARTIN, A PEQUEGNAT, W SCHMITT, F WILKIE, F TI ASSESSMENT OF AIDS-RELATED COGNITIVE CHANGES - RECOMMENDATIONS OF THE NIMH WORKGROUP ON NEUROPSYCHOLOGICAL ASSESSMENT APPROACHES SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NEUROL INST,NEW YORK,NY 10032. VET ADM MED CTR,PSYCHOL SERV,LA JOLLA,CA 92161. NIMH,OFF AIDS PROGRAM,ROCKVILLE,MD 20857. UNIV MICHIGAN,MED CTR,DEPT PSYCHIAT,ANN ARBOR,MI 48109. RI martin, alex/B-6176-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 97 EP 97 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600373 ER PT J AU GOLD, J RANDOLPH, C CARPENTER, C GOLDBERG, T WEINBERGER, D AF GOLD, J RANDOLPH, C CARPENTER, C GOLDBERG, T WEINBERGER, D TI FORMS OF MEMORY FAILURE IN SCHIZOPHRENIA SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 NIMH,NEUROPSYCHIAT RES HOSP,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JAN PY 1991 VL 13 IS 1 BP 99 EP 99 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA EY986 UT WOS:A1991EY98600381 ER PT J AU USALA, SJ MENKE, JB WATSON, TL BERARD, J BRADLEY, WEC BALE, AE LASH, RW WEINTRAUB, BD AF USALA, SJ MENKE, JB WATSON, TL BERARD, J BRADLEY, WEC BALE, AE LASH, RW WEINTRAUB, BD TI A NEW POINT MUTATION IN THE 3,5,3'-TRIIODOTHYRONINE-BINDING DOMAIN OF THE C-ERBA-BETA THYROID-HORMONE RECEPTOR IS TIGHTLY LINKED TO GENERALIZED THYROID-HORMONE RESISTANCE SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID ERBA; BINDING; IDENTIFICATION; PROTEIN; LOCALIZATION; EXPRESSION; DELETION; TISSUES; LINKAGE; GENE AB Two different mutations in the C-erbA-beta thyroid hormone receptor have recently been reported as genetic abnormalities responsible for the syndrome of generalized thyroid hormone resistance (GTHR). We have now found in a third kindred, D, in which GTHR is inherited as a dominant disease, a new point mutation in the T3-binding domain of c-erbA-beta. A guanine to cytosine base substitution at nucleotide position 1305, which altered codon-335 from glutamine (CAG) to histidine (CAC), was found in one allele of 10 affected members and was not found in 6 unaffected members. This C-1305 sequence was not present in 106 random alleles, indicating that it was a mutation in c-erbA-beta, and it was tightly linked to GTHR in kindred D, with a maximum logarithm of the odds score of 4.19 at a recombination fraction of 0. The tight linkage result confirms that GTHR maps to the c-erbA-beta locus in multiple kindreds. In view of the tight linkage between the C-1305 mutation and GTHR, and that this mutation is a nonconservative alteration in a crucial region of the T3-binding domain, it is probably the genetic defect in kindred D responsible for GTHR. The kindred D receptor appears to result in a different phenotype of tissue resistance compared to the previously reported kindred A receptor with a mutation in the carboxy-terminus of c-erbA-beta. C1 INST CANC MONTREAL, MONTREAL H2L 4MI, QUEBEC, CANADA. YALE UNIV, DEPT HUMAN GENET, NEW HAVEN, CT 06510 USA. NIH, MOLEC CELLULAR & NUTR ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. RP USALA, SJ (reprint author), E CAROLINA UNIV, SCH MED, DEPT MED, GREENVILLE, NC 27858 USA. NR 29 TC 60 Z9 61 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1991 VL 72 IS 1 BP 32 EP 38 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ518 UT WOS:A1991EQ51800007 PM 1846005 ER PT J AU ESTEBAN, NV LOUGHLIN, T YERGEY, AL ZAWADZKI, JK BOOTH, JD WINTERER, JC LORIAUX, DL AF ESTEBAN, NV LOUGHLIN, T YERGEY, AL ZAWADZKI, JK BOOTH, JD WINTERER, JC LORIAUX, DL TI DAILY CORTISOL PRODUCTION-RATE IN MAN DETERMINED BY STABLE ISOTOPE-DILUTION MASS-SPECTROMETRY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HUMANS AB Growth retardation as well as the development of Cushingoid features in adrenally insufficient patients treated with the currently accepted replacement dose of cortisol (33-41-mu-mol/day.m2; 12-15 mg/m2.day) prompted us to reevaluate the cortisol production rate (FPR) in normal subjects and patients with Cushing's syndrome, using a recently developed thermospray liquid chromatography-mass spectrometry method. The stable isotope [9,12,12-H-2(3)]cortisol was infused continuously for 31 h at about 5% of the anticipated FPR. Blood samples were obtained at 20-min intervals for 24 h, spun, and pooled in 4-h groups. Tracer dilution in plasma was determined by liquid chromatography/mass spectrometry. The method was validated with controlled infusions in 6 patients with adrenal insufficiency. Results from 12 normal volunteers revealed a FPR of 27.3 +/- 7.5-mu-mol/day (9.9 +/- 2.7 mg/day) or 15.7-mu-mol/day.m2; 5.7 mg/m2. day). A previously unreported circadian variation in FPR was observed. Patients with Cushing's syndrome demonstrated unequivocal elevation of FPR (84.7 +/- 25.7-mu-mol/day) and loss of circadian rhythm. FPR and cortisol concentration correlated during each sample period in normal volunteers, indicating that cortisol secretion, rather than metabolism, is mainly responsible for changes in plasma cortisol. Our data suggest that the FPR is normal subjects may be lower than previously believed. C1 NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. MCMASTER UNIV, DEPT MED, HAMILTON L8N 3Z5, ONTARIO, CANADA. E TENNESSE CHILDRENS HOSP, KNOXVILLE, TN 37901 USA. RP ESTEBAN, NV (reprint author), NICHHD, THEORET & PHYS BIOL LAB, BLDG 10, ROOM 10C-212, BETHESDA, MD 20892 USA. NR 23 TC 251 Z9 257 U1 0 U2 8 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1991 VL 72 IS 1 BP 39 EP 45 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ518 UT WOS:A1991EQ51800008 PM 1986026 ER PT J AU PESCOVITZ, OH BARNES, KM CUTLER, GB AF PESCOVITZ, OH BARNES, KM CUTLER, GB TI EFFECT OF DESLORELIN DOSE IN THE TREATMENT OF CENTRAL PRECOCIOUS PUBERTY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HORMONE-RELEASING HORMONE; LONG-ACTING ANALOG; TERM TREATMENT; AGONIST NAFARELIN; SOMATIC GROWTH; MATURATION; INTRANASAL; CHILDREN; THERAPY; POTENT AB Central precocious puberty is effectively treated with long-acting LHRH analogs (LHRHas). Although at least six LHRHas have now been used in children, there have been no studies to determine the least effective dose of any of these analogs. We sought to determine the effect of decreasing an efficacious dose of deslorelin (D-Trp6-Pro9-NEt-LHRH) on basal and LHRH-stimulated gonadotropins, estradiol levels, and the rates of linear growth and skeletal maturation in subjects with central precocious puberty. Twenty-nine children with central precocious puberty were enrolled in a double blinded study. All subjects were treated for the initial 3 months with deslorelin at a dose (4-mu-g/kg.day, sc) known to suppress gonadotropins, linear growth velocity, and the rate of skeletal maturation. After 3 months, the subjects were randomly assigned to receive one of three daily sc doses of deslorelin: 4-mu-g/kg (n = 9), 2-mu-g/kg (n = 11), or 1-mu-g/kg (n = 9). They were treated at this dose in double blinded fashion for 15 months, after which time they resumed therapy at a dose of 4-mu-g/kg.day for an additional year. The children in the three groups did not differ in terms of chronological age, bone age, pretreatment growth rate, or Tanner stage at the onset of therapy. Similarly, there were no differences in the clinical and hormonal responses to the first 3 months of LHRHa therapy (4-mu-g/kg.day). During the 15-month period at the three different doses, the three dose groups could not be distinguished from each other in terms of pubertal stage, linear growth velocity, rate of skeletal maturation, sex steroid levels, mean LH or FSH levels, or peak FSH response to LHRH stimulation or to a dose of deslorelin. In contrast, the peak LH response to LHRH stimulation was highest in children treated with the lowest dose (1-mu-g/kg.day; P < 0.025, by multiple analysis of variance). In addition, the peak LH response to a dose of deslorelin (the LHRHa test) was higher in children treated with 1-mu-g/kg.day than in those treated with 4-mu-g/kg.day (P < 0.04). In summary, the LHRHa test is a sensitive means for detecting activation of the hypothalamic-pituitary-gonadal axis, and deslorelin at a dose of 1-mu-g/kg.day results in less gonadotropin suppression than a dose of 4-mu-g/kg.day. Based on these short term data, we hypothesize that deslorelin at a dose of 2-mu-g/kg.day has efficacy similar to that of the dose of 4-mu-g/kg.day. However, since no significant toxicity has been reported at the 4-mu-g/kg.day dose and until a longer term study can be performed in larger numbers of children, we continue to recommend that deslorelin be used at the dose of 4-mu-g/kg.day because of the more extensive data on treatment outcome that are available at this dose. In summary, the LHrha test is a sensitive means for detecting activation of the hypothalamic-pituitary-gonadal axis, and deslorelin at a dose of 1-mu-g/kg.day results in less gonadotropin suppression than a dose of 4-mu-g/kg.day. Based on these short term data, we hypothesize that deslorelin at a dose of 2-mu-g/kg.day has efficacy similar to that of the dose of 4-mu-g/kg.day. However, since no significant toxicity has been reported at the 4-mu-g/kg.day dose and until a longer term study can be performed in larger numbers of children, we continue to recommend that deslorelin be used at the dose of 4-mu-g/kg.day because of the more extensive data on treatment outcome that are available at this dose. C1 NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. INDIANA UNIV, MED CTR, DEPT PEDIAT, INDIANAPOLIS, IN 46202 USA. INDIANA UNIV, MED CTR, DEPT PHYSIOL BIOPHYS, INDIANAPOLIS, IN 46202 USA. NR 24 TC 15 Z9 15 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1991 VL 72 IS 1 BP 60 EP 64 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ518 UT WOS:A1991EQ51800011 PM 1898743 ER PT J AU BELLANTONI, MF HARMAN, SM CHO, DE BLACKMAN, MR AF BELLANTONI, MF HARMAN, SM CHO, DE BLACKMAN, MR TI EFFECTS OF PROGESTIN-OPPOSED TRANSDERMAL ESTROGEN ADMINISTRATION ON GROWTH-HORMONE AND INSULIN-LIKE GROWTH FACTOR-I IN POSTMENOPAUSAL WOMEN OF DIFFERENT AGES SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID SOMATOMEDIN-C; BODY-COMPOSITION; PLASMA ANDROSTENEDIONE; BONE LOSS; ESTRADIOL; OSTEOPOROSIS; SECRETION; RADIOIMMUNOASSAY; INDIVIDUALS; METABOLISM AB Prior studies in women have shown a positive correlation of endogenous estrogen levels with spontaneous and stimulated GH secretion and basal insulin-like growth factor-I (IGF-I levels. In postmenopausal women, estrogen replacement therapy (ERT) by the oral route increases basal and GHRH-stimulated GH secretion but decreases basal IGF-I levels. To assess the corresponding effects of transdermal ERT (tERT) on this axis, we administered four 8-week regimens of transdermal 17-beta-estradiol (Estraderm; 0, 50, 100, or 150-mu-g/day) combined with oral medroxyprogesterone acetate (10 mg each day) during weeks 3-4 and 7-8 of each 8-week regimen (except placebo) to 28 healthy nonobese postmenopausal women, aged 45.3-71.8 yr. Basal levels of estradiol (E2), GH, and IGF-I as well as GH responsivity to bolus iv administration of GH-releasing hormone-(1-44) (1-mu-g/kg), were measured before tERT and at weeks 6 and 8 of each regimen; estrone (E1) levels were measured before tERT and at week 6 of each regimen. Before tERT, age was inversely correlated with both the peak GH response to GHRH (r = -0.43; P < 0.02) and basal IGF-I levels (r = -0.37; P < 0.05), but not with basal E2, E1, or GH levels. There were progressive increases in plasma E2 and E1 levels with increasing doses of tERT (P = 0.0001), independent of age (P < 0.2) and body mass index (P > 00.2). Mean basal GH and IGF-I levels were not altered significantly by tERT or medroxyprogesterone acetate. Peak and integrated GH secretory responses to exogenous GHRH decreased with increasing tERT dose (P < 0.01) in both younger and older postmenopausal women. Our findings suggest that the known effects of tERT on bone and other tissues are not mediated via increases in circulating levels of immunoreactive GH or IGF-I, but not preclude the possibility of tERT-induced increases in the biological activity or paracrine action of IGF-I. C1 JOHNS HOPKINS UNIV, SCH MED, BALTIMORE, MD 21205 USA. FRANCIS SCOTT KEY MED CTR, DIV GERIATR MED & GERONTOL, BALTIMORE, MD USA. FRANCIS SCOTT KEY MED CTR, DIV ENDOCRINOL & METAB, BALTIMORE, MD USA. FRANCIS SCOTT KEY MED CTR, DIV GYNECOL, BALTIMORE, MD USA. RP BELLANTONI, MF (reprint author), NIA, GERONTOL RES CTR,CLIN PHYSIOL LAB,ENDOCRINOL SECT, ROOM 2B19, 4940 EASTERN AVE, BALTIMORE, MD 21224 USA. OI Bellantoni, Michele/0000-0001-8525-2247 FU NCRR NIH HHS [M01-RR-02719] NR 37 TC 107 Z9 107 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1991 VL 72 IS 1 BP 172 EP 178 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA EQ518 UT WOS:A1991EQ51800028 PM 1824707 ER PT J AU HABTEGABR, E WALLACE, RB COLSHER, PL HULBERT, JR WHITE, LR SMITH, IM AF HABTEGABR, E WALLACE, RB COLSHER, PL HULBERT, JR WHITE, LR SMITH, IM TI SLEEP PATTERNS IN RURAL ELDERS - DEMOGRAPHIC, HEALTH, AND PSYCHOBEHAVIORAL CORRELATES SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE GERIATRICS; SLEEP PATTERNS; EPIDEMIOLOGY OF AGING ID PREVALENCE; DISORDERS; APNEA; DEPRESSION; DEMENTIA; DISEASE; STATE; HOME; REM; MEN AB Altered sleep patterns, including changes in bedtime, sleep latency, total sleep time, and arising time, have been reported to occur with increasing age. We examine self-reported sleep patterns in a geographically-defined population (n = 3097) of persons aged 65 years and older. Sleep patterns were characterized according to demographic variables, clinical conditions, and physical, psychological, and social functioning. Sleep latency and total hours of sleep increased with age, and older respondents went to bed earlier. The percentage of respondents who reported feeling rested in the morning decreased with age. Women went to bed later, had longer sleep latency, and fewer hours of sleep than men, and were less likely to report feeling rested than men. Sleep patterns were also related to educational attainment, self-perceived health status, physical functional status, psychotropic drug use, alcohol use, depressive symptoms, life satisfaction, and social and recreational activity level. This population study suggests that sleep problems among the elderly are sometimes associated with treatable health conditions and modifiable behavioral and environmental characteristics. C1 NIA,BETHESDA,MD 20892. UNIV IOWA,DEPT INTERNAL MED,IOWA CITY,IA 52242. UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52242. RP HABTEGABR, E (reprint author), MICHIGAN STATE UNIV,HURLEY MED CTR,FLINT,MI 48503, USA. FU NIA NIH HHS [N01-AG-0-2106, AG-07094] NR 50 TC 78 Z9 79 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 1 BP 5 EP 13 DI 10.1016/0895-4356(91)90195-F PG 9 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA ET049 UT WOS:A1991ET04900001 PM 1986057 ER PT J AU FEUER, EJ KESSLER, LG BAKER, SG TRIOLO, HE GREEN, DT AF FEUER, EJ KESSLER, LG BAKER, SG TRIOLO, HE GREEN, DT TI THE IMPACT OF BREAKTHROUGH CLINICAL-TRIALS ON SURVIVAL IN POPULATION BASED TUMOR REGISTRIES SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE TREATMENT DISSEMINATION; JOIN POINT REGRESSION; SURVIVAL ANALYSIS; COX MODEL; WEIBULL MODEL; CURE MODEL ID DISSEMINATED TESTICULAR CANCER; ADVANCED HODGKINS-DISEASE; COMBINATION CHEMOTHERAPY; CELL TUMORS; THERAPY; VINBLASTINE; PROGRESS AB Three statistical models are developed to study the impact that two break-through clinical trials (MOPP for Hodgkin's disease and PVB for disseminated testicular cancer) had on survival in the Connecticut tumor registry and the National Cancer Institute's surveillance, Epidemiology, and End Results (SEER) registry program. A segmented regression model is used in conjunction with the Cox semi-parametric proportional hazards model, as well as the parametric Weibull and exponential cure models. These models allow us to determine approximately when survival first began to improve dramatically, indicating that improved treatments had become available, and how long it took for survival to level off again indicating that the full population survival impact had been realized. In addition, the degree to which the parametric models fit allows us to determine if the survival improvements occur within a parametric family. Results of the modelling indicate that dissemination took approximately 11 years in Hodgkin's disease while only 3 years in disseminated testicular cancer. In both disease sites survival first broke with prior trends between the time that the breakthrough trial started and its publication, indicating that earlier moderately successful 'precursor' trials with combination chemotherapy may have initiated the improved population survival trends. Reasons for the difference in dissemination time in the two cancer sites are examined in order to understand what factors may be responsible for the speed of dissemination and effective utilization of new therapies. C1 IMS INC,SILVER SPRING,MD 20904. RP FEUER, EJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,EPN ROOM 313,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 44 TC 30 Z9 30 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 2 BP 141 EP 153 DI 10.1016/0895-4356(91)90262-8 PG 13 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA EY989 UT WOS:A1991EY98900005 PM 1704907 ER PT J AU SHAW, GL FALK, RT PICKLE, LW MASON, TJ BUFFLER, PA AF SHAW, GL FALK, RT PICKLE, LW MASON, TJ BUFFLER, PA TI LUNG-CANCER RISK ASSOCIATED WITH CANCER IN RELATIVES SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE LUNG CANCER; FAMILIAL CANCER; GENETIC SUSCEPTIBILITY ID INCREASED FAMILIAL RISK; PASSIVE SMOKING; DISEASE; HISTORY; PREDISPOSITION; MARKERS AB Family history data from an incident case-control study of lung cancer conducted in the Texas Gulf Coast region between 1976 and 1980 were analyzed to evaluate the contribution of cancer in first-degree relatives to lung cancer risk. Odds ratios (OR) increased slightly as the number of relatives with any cancer increased (reaching 1.5 with 4 or more relatives with cancer). Risks were higher for tobacco-related cancers (OR = 1.5 for 2 or more relatives with these tumors) and greatest for first-degree relatives with lung cancer (OR = 2.8 for lung cancer in 2 or more relatives). For cases of squamous cell carcinoma and adenocarcinoma of the lung, risks with 3 or more relatives with any cancer were increased 2-fold (OR = 1.8 and 1.9 respectively), and a significantly elevated risk was found for having a first-degree relative with lung cancer for each histologic type (ORs from 1.7-2.1). Having a spouse with lung cancer increased lung cancer risk (OR = 2.5), and cases with lung cancer reported in a first-degree relative were diagnosed at an earlier age, as were case siblings with lung cancer. C1 UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,EPIDEMIOL RES UNIT,HOUSTON,TX 77025. RP SHAW, GL (reprint author), NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,FAMILY STUDIES SECT,BETHESDA,MD 20892, USA. FU NCI NIH HHS [N01-CP-91025-65] NR 35 TC 56 Z9 57 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 4-5 BP 429 EP 437 DI 10.1016/0895-4356(91)90082-K PG 9 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA FD427 UT WOS:A1991FD42700012 PM 2010787 ER PT J AU MANOLIO, TA SAVAGE, PJ BURKE, GL HILNER, JE LIU, K ORCHARD, TJ SIDNEY, S OBERMAN, A AF MANOLIO, TA SAVAGE, PJ BURKE, GL HILNER, JE LIU, K ORCHARD, TJ SIDNEY, S OBERMAN, A TI CORRELATES OF FASTING INSULIN LEVELS IN YOUNG-ADULTS - THE CARDIA STUDY SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE INSULIN; OBESITY; ANTHROPOMETRY; DIET; PHYSICAL ACTIVITY ID CORONARY HEART-DISEASE; BODY-FAT DISTRIBUTION; GLUCOSE-TOLERANCE; BLOOD-PRESSURE; RISK-FACTORS; CARDIOVASCULAR-DISEASE; DIABETES-MELLITUS; PLASMA-INSULIN; BEAVER-COUNTY; OBESITY AB Elevated fasting insulin is an independent risk factor for hyperlipidemia, hypertension, and cardiovascular disease, but determinants of insulin other than age and body mass remain poorly described. Potentially modifiable factors associated with insulin were identified by correlating anthropometric, dietary and physical activity data in the CARDIA cohort of 2643 black and 2472 white men and women aged 18-30 years. Insulin was positively correlated with serum glucose, body mass index (BMI), skinfold thickness, waist/hip ratio and sucrose intake, and negatively correlated with heavy physical activity score, treadmill exercise duration, and magnesium intake (each p < 0.01). After adjustment for other covariates, the positive association of insulin with waist/hip ratio, skinfold thickness, and sucrose intake remained in the group as a whole, as did the negative associations with magnesium and treadmill duration. These relationships provide insight into potentially modifiable factors affecting insulin levels, and should be considered in interpreting associations between insulin levels and cardiovascular disease. C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. UNIV ALABAMA,DEPT GEN & PREVENT MED,CARDIA COORDINATING CTR,BIRMINGHAM,AL 35205. NORTHWESTERN UNIV,SCH MED,DEPT COMMUNITY HLTH & PREVENT MED,CHICAGO,IL 60611. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT EPIDEMIOL,PITTSBURGH,PA 15261. KAISER PERMANENTE,OAKLAND,CA. UNIV ALABAMA,DEPT GEN & PREVENT MED,CARDIA FIED CTR,BIRMINGHAM,AL 35205. OI orchard, trevor/0000-0001-9552-3215 FU NHLBI NIH HHS [N01-HC-84047, N01-HC-84048, N01-HC-84049] NR 44 TC 46 Z9 46 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 6 BP 571 EP 578 DI 10.1016/0895-4356(91)90221-T PG 8 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA FP837 UT WOS:A1991FP83700014 PM 2037862 ER PT J AU CORNONIHUNTLEY, JC HARRIS, TB EVERETT, DF ALBANES, D MICOZZI, MS MILES, TP FELDMAN, JJ AF CORNONIHUNTLEY, JC HARRIS, TB EVERETT, DF ALBANES, D MICOZZI, MS MILES, TP FELDMAN, JJ TI AN OVERVIEW OF BODY-WEIGHT OF OLDER PERSONS, INCLUDING THE IMPACT ON MORTALITY - THE NATIONAL-HEALTH AND NUTRITION EXAMINATION SURVEY .1. EPIDEMIOLOGIC FOLLOW-UP-STUDY SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE BODY WEIGHT; BODY MASS INDEX; MORTALITY; FOLLOW-UP STUDY; NEVER SMOKERS ID NHANES-I; CIGARETTE-SMOKING; RELATIVE WEIGHT; UNITED-STATES; OVERWEIGHT; WOMEN; MEN; POPULATION; DISEASE; OBESITY AB The authors studied distributions of body weight for height, change in body weight with age, and the relationship between body mass index and mortality among participants in the Epidemiologic Follow-up Study of the first National Health and Nutrition Examination Survey (NHEFS) (n = 14,407), a cohort study based on an representative sample of the U.S. population. Percentiles of body weight for height according to age and sex are presented. Cross-sectional analyses of body weight suggest that mean body weight increases with age until late middle age, then plateaus and decreases for older aged persons. However, longitudinal analysis of change in weight with age shows that younger persons in the lower quintile at baseline tend to gain more than those in the higher quintile. Older persons in the higher quintile at baseline have the greatest average loss in weight. The relationship of body mass index to mortality is a U-shaped curve, with increased risks in the lowest and highest 15% of the distribution. Increased risk of mortality associated with the highest 15th percentile of the body mass index distribution, as well as the highest 15% of the joint distribution of body mass index and skinfold thickness, is statistically significant for white women. However, the risk diminishes when adjusted for the presence of disease and factors related to disease. More noteworthy is the fact that there is a statistically significant excess risk of mortality for both race and sex groups in the lowest 15% of the body mass index distribution after adjusting for smoking history, and presence of disease. Those in the lowest 15% of the joint body mass index and skinfold thickness distribution, were also at increased risk. Risk of mortality for both men and women who have lost 10% or more of their maximum lifetime weight within the last 10 years is statistically significant, even when controlling for current weight. This study has replicated previously reported relationships, while correcting for several methodological issues. C1 NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892. NATL CTR HLTH STAT,OFF ANAL & EPIDEMIOL,HYATTSVILLE,MD 20782. NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,WALTER REED MED CTR,WASHINGTON,DC 20306. UNIV ILLINOIS,SCH PUBL HLTH,CHICAGO,IL 60682. RI Albanes, Demetrius/B-9749-2015 NR 36 TC 224 Z9 225 U1 2 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 8 BP 743 EP 753 DI 10.1016/0895-4356(91)90126-T PG 11 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GL682 UT WOS:A1991GL68200006 PM 1941025 ER PT J AU REED, T QUIROGA, J SELBY, JV CARMELLI, D CHRISTIAN, JC FABSITZ, RR GRIM, CE AF REED, T QUIROGA, J SELBY, JV CARMELLI, D CHRISTIAN, JC FABSITZ, RR GRIM, CE TI CONCORDANCE OF ISCHEMIC-HEART-DISEASE IN THE NHLBI TWIN STUDY AFTER 14-18 YEARS OF FOLLOW-UP SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE HEART DISEASE; TWINS; CONCORDANCE; FAMILY HISTORY; SELECTION; CANCER ID CHOLESTEROL AB Morbidity and mortality were assessed in the NHLBI twin study at the end of 1987. Deaths were greater in DZ twins (58/520, 11.2%) than MZ twins (38/508, 7.5%). Ischemic heart disease concordances were 2.3 times higher in MZ pairs and 2.8 times higher in DZ pairs than expected based on the prevalence of ischemic heart disease in the cohort. Family history scores for heart disease, calculated 14-18 years earlier at entry to the study, were significantly higher in DZ pairs where one or both members later developed ischemic heart disease and in concordant MZ pairs than in twin-pairs without any subsequent heart disease. Concordance rates were significantly different between MZ and DZ pairs. The results agree with previous suggestions that selection at enlistment into the armed services over 40 years ago, as well as later volunteering for the NHLBI twin study, resulted in a decline in the number of concordant MZ pairs. C1 VET ADM MED CTR,LONG BEACH,CA 90822. KAISER FDN,RES INST,OAKLAND,CA. SRI INT,DEPT BEHAV MED,MENLO PK,CA 94025. NHLBI,CLIN & GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892. CHARLES R DREW POSTGRAD MED SCH,LOS ANGELES,CA 90059. RP REED, T (reprint author), INDIANA UNIV,SCH MED,DEPT MED GENET,975 W WALNUT ST,INDIANAPOLIS,IN 46202, USA. NR 26 TC 36 Z9 36 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 8 BP 797 EP 805 DI 10.1016/0895-4356(91)90132-S PG 9 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GL682 UT WOS:A1991GL68200012 PM 1941031 ER PT J AU CONNOR, RJ PROROK, PC WEED, DL AF CONNOR, RJ PROROK, PC WEED, DL TI THE CASE CONTROL DESIGN AND THE ASSESSMENT OF THE EFFICACY OF CANCER SCREENING SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE CANCER SCREENING; CASE CONTROL STUDY; RANDOMIZED TRIAL; SELF-SELECTION BIAS ID BREAST-CANCER; CERVICAL-CANCER; NIJMEGEN PROJECT; POPULATION; PROGRAM; DEFINITION; MORTALITY AB Case-control studies have been used in recent years to evaluate the efficacy of cancer screening. However, relatively little work has been done to examine the methodology itself for this purpose. In this paper, it is demonstrated that because of. self-selection bias the case-control study can yield a biased estimate of screening efficacy. Further, it is shown how this bias can be assessed using data from a randomized trial. Using data from the HIP breast cancer screening study, the magnitude of the self-selection bias is estimated and is seen to be substantial. C1 NCI,DIV CANC PREVENT & CONTROL,OFF DIRECTOR,BETHESDA,MD 20892. RP CONNOR, RJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,EXECUTIVE PLAZA N,BETHESDA,MD 20892, USA. NR 39 TC 42 Z9 42 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 IS 11 BP 1215 EP 1221 DI 10.1016/0895-4356(91)90154-2 PG 7 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GP825 UT WOS:A1991GP82500011 PM 1941016 ER PT J AU WEED, DL AF WEED, DL TI THE MERGER OF BIOETHICS AND EPIDEMIOLOGY SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT CONF ON ETHICS AND EPIDEMIOLOGY CY JUN 12-13, 1989 CL BIRMINGHAM, AL SP IND EPIDEMIOL FORUM, DUPONT DE EPIDEMIOLOGY; METHODOLOGY; ETHICS; SCIENCE; PHILOSOPHY ID CLINICAL-TRIALS; CANCER; MODELS; SYNERGISM; CAUSAL; ANTAGONISM; DIET; CARCINOGENESIS; CRITICISM; PARADIGM AB The merger of bioethics and epidemiology reflects the established idea that values are important for epidemiologic practice. It also reflects the more recent realization that standards of conduct are a timely addition to the profession. The thesis of this paper goes somewhat further and asserts that this merger represents an essential cornerstone in the foundation of a philosophy of epidemiology. Historical reflection reveals existing ontological and epistemological components to this same foundation. The union of bioethics and epidemiology suggests an important philosophical problem: selecting a method for unifying ethical and scientific reasoning. Solutions are proposed including: dialectic and critical rationalism. RP WEED, DL (reprint author), NCI,DIV CANC PREVENT & CONTROL,EXECUT PLAZA S,ROOM T-41,BETHESDA,MD 20892, USA. NR 66 TC 5 Z9 5 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PY 1991 VL 44 SU 1 BP S15 EP S22 PG 8 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA FP046 UT WOS:A1991FP04600005 PM 11649325 ER PT J AU LUNDGREN, B LIPSCHIK, GY KOVACS, JA AF LUNDGREN, B LIPSCHIK, GY KOVACS, JA TI PURIFICATION AND CHARACTERIZATION OF A MAJOR HUMAN PNEUMOCYSTIS-CARINII SURFACE-ANTIGEN SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE AIDS; IMMUNOSUPPRESSION; PNEUMOCYSTIS-CARINII PNEUMONIA; GP95; ELISA ID MONOCLONAL-ANTIBODIES; GLYCOPROTEINS; RAT; IDENTIFICATION; MACROPHAGES; INFECTION; PROTEINS; OLIGOSACCHARIDES; RESPONSES; INVITRO AB Previous studies of Pneumocystis carinii have identified the major surface antigen of rat and human isolates as proteins of 116,000 and 95,000 mol wt, respectively, that are antigenically not identical. In this study both rat and human P. carinii proteins were purified by solubilization with zymolyase followed by molecular sieve and ion exchange chromatography. The native proteins had an apparent mol wt of 290,000 or greater, based on molecular sieve studies as well as cross-linking studies. Both proteins were glycoproteins, treatment with endoglycosidase H resulted in a 9% decrease in mol wt. The carbohydrate composition of the rat P. carinii glycoprotein was distinct from the human isolate; glucose, mannose, galactose, and glucosamine occurred in approximately equimolar ratios in the human P. carinii protein, whereas glucose and mannose were the predominant sugars of the rat P. carinii protein. To evaluate humoral immune response to the human P. carinii protein, an enzyme-linked immunosorbent assay using purified protein was developed. Some, but not all, patients who subsequently developed P. carinii pneumonia demonstrated a serum antibody response to the surface antigen. Nearly all subjects without a history of P. carinii pneumonia had no detectable antibodies. Purified P. carrcini proteins will greatly facilitate the investigation of host-P. carinii interactions. C1 NIH,DEPT CRIT CARE MED,BLDG 10,ROOM 10D48,BETHESDA,MD 20892. NR 36 TC 91 Z9 91 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1991 VL 87 IS 1 BP 163 EP 170 DI 10.1172/JCI114966 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EQ976 UT WOS:A1991EQ97600022 PM 1985093 ER PT J AU COLLETTA, AA WAKEFIELD, LM HOWELL, FV DANIELPOUR, D BAUM, M SPORN, MB AF COLLETTA, AA WAKEFIELD, LM HOWELL, FV DANIELPOUR, D BAUM, M SPORN, MB TI THE GROWTH-INHIBITION OF HUMAN BREAST-CANCER CELLS BY A NOVEL SYNTHETIC PROGESTIN INVOLVES THE INDUCTION OF TRANSFORMING GROWTH-FACTOR-BETA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE AUTOCRINE; GROWTH FACTOR; BREAST CANCER; PROGESTIN ID RECEPTOR; ESTROGEN; CULTURE; CLONING; TISSUE; LINES AB Recent experimental work has identified a novel intracellular binding site for the synthetic progestin, Gestodene, that appears to be uniquely expressed in human breast cancer cells. Gestodene is shown here to inhibit the growth of human breast cancer cells in a dose-dependent fashion, but has no effect on endocrine-responsive human endometrial cancer cells. Gestodene induced a 90-gold increase in the secretion of transforming growth factor-beta (TGF-beta) by T47D human breast cancer cells. Other synthetic progestins had no effect, indicating that this induction is mediated by the novel Gestodene binding site and not by the conventional progesterone receptor. Furthermore, in four breast cancer cell lines, the extent of induction of TGF-beta correlated with intracellular levels of Gestodene binding site. No induction of TGF-beta was observed with the endometrial cancer line, HECl-B, which lacks the Gestodene binding site, but which expresses high levels of progesterone receptor. The inhibition of growth of T47D cells by Gestodene is partly reversible by a polyclonal antiserum to TGF-beta. These data indicate that the growth-inhibitory action of Gestodene may be mediated in part by an autocrine induction of TGF-beta. C1 KINGS COLL,SCH MED & DENT,RAYNE INST,DEPT SURG,TUMOR BIOL LAB,LONDON SE5 9NU,ENGLAND. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 21 TC 99 Z9 100 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1991 VL 87 IS 1 BP 277 EP 283 DI 10.1172/JCI114983 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA EQ976 UT WOS:A1991EQ97600037 PM 1985102 ER PT J AU TOLLERUD, DJ BROWN, LM CLARK, JW NEULAND, CY MANN, DL PANKIWTROST, LK BLATTNER, WA AF TOLLERUD, DJ BROWN, LM CLARK, JW NEULAND, CY MANN, DL PANKIWTROST, LK BLATTNER, WA TI CRYOPRESERVATION AND LONG-TERM LIQUID-NITROGEN STORAGE OF PERIPHERAL-BLOOD MONONUCLEAR-CELLS FOR FLOW-CYTOMETRY ANALYSIS - EFFECTS ON CELL SUBSET PROPORTIONS AND FLUORESCENCE INTENSITY SO JOURNAL OF CLINICAL LABORATORY ANALYSIS LA English DT Article DE LYMPHOCYTES; T-CELL SUBSETS; FREEZING; MONOCLONAL ANTIBODIES ID PARAFORMALDEHYDE FIXATION; MONOCLONAL-ANTIBODIES; LYMPHOCYTE SUBSETS; HEALTHY; MARKERS AB The effect of cryopreservation and long-term liquid nitrogen storage on peripheral blood mononuclear cell (PBMC) subsets was prospectively analyzed using monoclonal antibodies and flow cytometry. Brief cryopreservation did not significantly alter the proportion of positively stained cells for CD3+, CD4+, CD8+, CD14+, CD16+, and CD19 + cells. A small but statistically significant increase in the proportion of positive cells was observed for HLA-DR+ and HLe-1 + cells. Brief cryopreservation was associated with a decrease in the mean fluorescence intensity (MFI) values for CD3+, CD4+, and CD8+ cells; an increase in MFI values for CDl4+ and HLA-DR+ cells; and no change for CD16+, CD19+, and HLe-1 + cells. There was no significant change in the proportion of CD3+, CD4+, or CD16+ cells during 20 months of storage in liquid nitrogen. Small but statistically significant decreases in the proportion of CD8+ and CD19+ cells were observed over the same interval, and the proportion of CD14+ cells (monocytes) was highly variable. Chronologic changes in fluorescence intensity during long-term storage were observed for all cell subsets except CD16+ and CD19+ cells. Cryopreservation is a valuable technique for long-term storage of viable cells. For many laboratory applications, the small changes noted in the present study will have no practical importance. However, for clinical and epidemiological investigations encompassing large numbers of samples, statistical techniques to adjust for small changes during storage should be considered. C1 BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. NCI,EPIDEMIOL & BIOSTAT PROGRAM,ROCKVILLE,MD. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [YO1-CP-30500]; NHLBI NIH HHS [HL 07427] NR 17 TC 35 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 0887-8013 J9 J CLIN LAB ANAL JI J. Clin. Lab. Anal. PY 1991 VL 5 IS 4 BP 255 EP 261 PG 7 WC Medical Laboratory Technology SC Medical Laboratory Technology GA FX067 UT WOS:A1991FX06700005 PM 1890539 ER PT J AU MELCHER, GP REED, KD RINALDI, MG LEE, JW PIZZO, PA WALSH, TJ AF MELCHER, GP REED, KD RINALDI, MG LEE, JW PIZZO, PA WALSH, TJ TI DEMONSTRATION OF A CELL-WALL ANTIGEN CROSS-REACTING WITH CRYPTOCOCCAL POLYSACCHARIDE IN EXPERIMENTAL DISSEMINATED TRICHOSPORONOSIS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note ID BEIGELII; INFECTION; COLONIZATION; CUTANEUM; PATIENT AB Patients with disseminated infections caused by Trichosporon beigelii have a circulating antigen that cross-reacts with the polysaccharide capsule of Cryptococcus neoformans. We studied the localization of this antigen by immunoelectron microscopy in a rabbit model of experimental disseminated trichosporonosis. Deparaffinized lung sections were examined by using a murine monoclonal anti-cryptococcal polysaccharide antibody and colloidal gold particles coated with goat antibody to murine immunoglobulin G. Antigen that cross-reacted with the monoclonal antibody was observed in the T. beigelii cell wall and in a fibrillar matrix extending from the cell wall. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892. RP MELCHER, GP (reprint author), WILFORD HALL USAF MED CTR,DEPT MED,INFECT DIS SERV,LACKLAND AFB,TX 78236, USA. NR 17 TC 43 Z9 45 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1991 VL 29 IS 1 BP 192 EP 196 PG 5 WC Microbiology SC Microbiology GA EP044 UT WOS:A1991EP04400037 PM 1993757 ER PT J AU COHEN, LG ROTH, BJ WASSERMANN, EM TOPKA, H FUHR, P SCHULTZ, J HALLETT, M AF COHEN, LG ROTH, BJ WASSERMANN, EM TOPKA, H FUHR, P SCHULTZ, J HALLETT, M TI MAGNETIC STIMULATION OF THE HUMAN CEREBRAL-CORTEX, AN INDICATOR OF REORGANIZATION IN MOTOR PATHWAYS IN CERTAIN PATHOLOGICAL CONDITIONS SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY LA English DT Article DE MAGNETISM; MOTOR CORTEX; PLASTICITY; MAPPING ID NERVE INJURY; REPRESENTATION PATTERNS; ELECTRICAL-STIMULATION; PERIPHERAL-NERVE; COIL; ORGANIZATION; RESONANCE; RESPONSES; SAMPLES; FIELDS AB Basic principles of magnetic stimulation of biological tissues are reviewed. Noninvasive magnetic stimulation of the brain delivered over sensorimotor areas evokes movements and less commonly paresthesias in contralateral limbs. We have evaluated the maps of motor outputs in patients with (1) congenital mirror movements, which resulted in marked derangement of the map of outputs of distal hand muscles with enlarged and ipsilateral representations; (2) amputations, which resulted in plastic reorganization of motor outputs targeting muscles immediately proximal to the stump; (3) spinal cord injury, which also resulted in enlargement of the map of outputs targeting muscles proximal to the lesion level; and (4) hemispherectomy performed at an early age for intractable seizures, which resulted in the remaining hemisphere controlling ipsilateral arm muscles. These results demonstrate the potential for reorganization in motor systems following lesions in the peripheral as well as in the central nervous system. C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,HUMAN CORTICAL PHYSIOL UNIT,BETHESDA,MD 20892. NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RI Roth, Bradley/A-4920-2008 NR 56 TC 90 Z9 91 U1 1 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0736-0258 J9 J CLIN NEUROPHYSIOL JI J. Clin. Neurophysiol. PD JAN PY 1991 VL 8 IS 1 BP 56 EP 65 DI 10.1097/00004691-199101000-00007 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA EY613 UT WOS:A1991EY61300006 PM 2019651 ER PT J AU CHABNER, BA WILSON, W AF CHABNER, BA WILSON, W TI REVERSAL OF MULTIDRUG RESISTANCE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID NON-HODGKINS LYMPHOMA; DOXORUBICIN RESISTANCE; VINCRISTINE INFUSION; MULTIPLE-MYELOMA; VERAPAMIL; INVITRO RP CHABNER, BA (reprint author), NCI,BETHESDA,MD 20892, USA. NR 17 TC 51 Z9 51 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1991 VL 9 IS 1 BP 4 EP 6 PG 3 WC Oncology SC Oncology GA EP763 UT WOS:A1991EP76300002 PM 1670643 ER PT J AU LONGO, DL DEVITA, VT DUFFEY, PL WESLEY, MN IHDE, DC HUBBARD, SM GILLIOM, M JAFFE, ES COSSMAN, J FISHER, RI YOUNG, RC AF LONGO, DL DEVITA, VT DUFFEY, PL WESLEY, MN IHDE, DC HUBBARD, SM GILLIOM, M JAFFE, ES COSSMAN, J FISHER, RI YOUNG, RC TI SUPERIORITY OF PROMACE-CYTABOM OVER PROMACE-MOPP IN THE TREATMENT OF ADVANCED DIFFUSE AGGRESSIVE LYMPHOMA - RESULTS OF A PROSPECTIVE RANDOMIZED TRIAL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID NON-HODGKINS LYMPHOMA; LARGE-CELL LYMPHOMA; BONE-MARROW TRANSPLANTATION; COMBINATION CHEMOTHERAPY; HISTIOCYTIC LYMPHOMA; MALIGNANT-LYMPHOMA; AUTOLOGOUS MARROW; PREDNISONE BACOP; POOR-PROGNOSIS; CYCLOPHOSPHAMIDE C1 NCI,DIV CANC BIOL & DIAG,DIV CANC TREATMENT,BETHESDA,MD 20892. NCI,DIV CANC BIOL & DIAG,CTR CANC INFORMAT,BETHESDA,MD 20892. INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. MED BRANCH,BETHESDA,MD. NCI,DIV CANC BIOL & DIAG,DIV CANC TREATMENT,USN,MED ONCOL BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20057. LOYOLA UNIV,SCH MED,HEMATOL ONCOL SECT,MAYWOOD,IL 60153. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. NCI,DIV CANC BIOL & DIAG,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892. RP LONGO, DL (reprint author), NCI,FREDERICK CANC RES FACIL,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,BLDG 567,FREDERICK,MD 21701, USA. NR 35 TC 203 Z9 204 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1991 VL 9 IS 1 BP 25 EP 38 PG 14 WC Oncology SC Oncology GA EP763 UT WOS:A1991EP76300005 PM 1702144 ER PT J AU DURRLEMAN, S SIMON, R AF DURRLEMAN, S SIMON, R TI WHEN TO RANDOMIZE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CLINICAL-TRIALS; SAMPLE SIZES; INFORMED CONSENT C1 NCI,BIOMETR RES BRANCH,BETHESDA,MD 20892. NR 15 TC 7 Z9 7 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1991 VL 9 IS 1 BP 116 EP 122 PG 7 WC Oncology SC Oncology GA EP763 UT WOS:A1991EP76300016 PM 1985160 ER PT J AU CHUN, HG LEYLANDJONES, B CHESON, BD AF CHUN, HG LEYLANDJONES, B CHESON, BD TI FLUDARABINE PHOSPHATE - A SYNTHETIC PURINE ANTIMETABOLITE WITH SIGNIFICANT ACTIVITY AGAINST LYMPHOID MALIGNANCIES SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID CHRONIC LYMPHOCYTIC-LEUKEMIA; SOUTHWEST-ONCOLOGY-GROUP; PHASE-II TRIAL; NERVOUS-SYSTEM TOXICITY; PREVIOUSLY UNTREATED PATIENTS; RENAL-CELL CARCINOMA; F-ARA-AMP; 9-BETA-D-ARABINOFURANOSYL-2-FLUOROADENINE 5'-MONOPHOSPHATE; TUMOR-CELLS; RIBONUCLEOTIDE REDUCTASE C1 NCI,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892. NR 95 TC 96 Z9 100 U1 0 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1991 VL 9 IS 1 BP 175 EP 188 PG 14 WC Oncology SC Oncology GA EP763 UT WOS:A1991EP76300024 PM 1702143 ER PT J AU WALKER, LC RANCE, NE PRICE, DL YOUNG, WS AF WALKER, LC RANCE, NE PRICE, DL YOUNG, WS TI GALANIN MESSENGER-RNA IN THE NUCLEUS BASALIS OF MEYNERT COMPLEX OF BABOONS AND HUMANS SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE ACETYLCHOLINE; ALZHEIMERS DISEASE; INSITU HYBRIDIZATION; NUCLEUS OF THE DIAGONAL BAND OF BROCA ID CENTRAL NERVOUS-SYSTEM; ALZHEIMERS-DISEASE; SENILE DEMENTIA; CHOLINERGIC NEURONS; PARKINSONS-DISEASE; FOREBRAIN COMPLEX; IMMUNOREACTIVITY; RAT; GENE; HYPOTHALAMUS AB Galanin, a 29-amino acid peptide, has been shown by immunocytochemistry to occur in most large acetylcholinergic neurons of the complex that includes the nucleus basalis of Meynert and the nucleus of the diagonal band of Broca in nonhuman primates. In contrast, several studies have reported that most large neurons of the human nucleus basalis of Meynert complex appear to lack galanin immunoreactivity. We investigated this apparent species-difference by hybridization histochemistry for galanin messenger ribonucleic acid (mRNA) in humans and baboons. The results confirm previous immunocytochemical data; very few large neurons of the nucleus basalis of Meynert complex in humans contained detectable galanin messenger RNA, whereas most such cells in baboons were labeled by the oligodeoxynucleotide probe. The few labeled neurons in humans were primarily medial or ventral to the main body of the nucleus basalis of Meynert and corresponded in location to a minor population of relatively intensely labeled cells in baboons. These findings indicate that the indectectability of immunoreactive galanin in most cells of the nucleus basalis of Meynert complex in humans is due to a paucity or an absence of galanin messenger RNA and not to differences in posttranslational processing or transport of the peptide. Inasmuch as the probe labeled neurons in several other nuclei of both species, it is unlikely that differences in galanin messenger RNA sequences underlie the species-related disparity in hybridization in the nucleus basalis of Meynert complex. The indetectability of galanin messenger RNA in most cells of the human nucleus basalis of Meynert complex indicates that the expression of the galanin gene is regulated by as yet unidentified influences that differ in human and nonhuman primates. The varying phenotypes of galanin in primates suggest potentially important species-differences in the function of galanin in neurons of the nucleus basalis of Meynert complex. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT APPL PHYS & ELECTR,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP WALKER, LC (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,NEUROPATHOL LAB,509 PATHOL BLDG,600 N WOLFE ST,BALTIMORE,MD 21205, USA. RI Young, W Scott/A-9333-2009; Walker, L/J-6541-2015 OI Young, W Scott/0000-0001-6614-5112; Walker, L/0000-0001-9166-3261 FU NIA NIH HHS [AG 05146]; NIADDK NIH HHS [AM 14681]; NINDS NIH HHS [NS 20471] NR 35 TC 53 Z9 53 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 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JAN 1 PY 1991 VL 303 IS 1 BP 113 EP 120 DI 10.1002/cne.903030110 PG 8 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA EP664 UT WOS:A1991EP66400009 PM 1706362 ER PT J AU LEBIHAN, D MOONEN, CTW VANZIJL, PCM PEKAR, J DESPRES, D AF LEBIHAN, D MOONEN, CTW VANZIJL, PCM PEKAR, J DESPRES, D TI MEASURING RANDOM MICROSCOPIC MOTION OF WATER IN TISSUES WITH MR IMAGING - A CAT BRAIN STUDY SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE ANIMAL STUDIES; MAGNETIC RESONANCE IMAGING, PERFUSION; MAGNETIC RESONANCE IMAGING, DIFFUSION; BRAIN ID INTRAVOXEL INCOHERENT MOTIONS; DIFFUSION; PERFUSION; NMR AB Cat brain images sensitized to incoherent motion by additional gradient pulses were obtained on a 4.7 T magnetic resonance unit equipped with shielded gradient coils. The apparent diffusion coefficient of water in gray and white matter was accurately determined and imaged from the signal attenuation curve obtained as a function of gradient strength. Contrast in calculated diffusion images differed from typical T2-weighted contrast. Furthermore, in gray matter and in areas containing flowing CSF the attenuation curve was found to be biexponential. These results are interpreted in terms of a simple voxel model with microcirculation and diffusion contributions. C1 NCI,BETHESDA,MD 20892. NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,CTR INVIVO NUCL MAGNET RESONANCE,BETHESDA,MD 20892. RP LEBIHAN, D (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BLDG 10,ROOM 1C660,BETHESDA,MD 20892, USA. RI van Zijl, Peter/B-8680-2008; Moonen, Chrit/K-4434-2016 OI Moonen, Chrit/0000-0001-5593-3121 NR 16 TC 67 Z9 68 U1 1 U2 6 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD JAN-FEB PY 1991 VL 15 IS 1 BP 19 EP 25 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ET718 UT WOS:A1991ET71800002 PM 1987198 ER PT J AU HILL, SC HOEG, JM AVILA, NA AF HILL, SC HOEG, JM AVILA, NA TI NEPHROCALCINOSIS IN HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA - ULTRASOUND AND CT FINDINGS SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE DISEASES, HEREDITARY; KIDNEYS, CALCIFICATION; ULTRASOUND; COMPUTED TOMOGRAPHY; LIVER, DISEASES AB An association between homozygous familial hypercholesterolemia (FH) and nephrocalcinosis has not, to our knowledge, been previously reported. Evaluation in 10 cases of homozygous FH revealed evidence of nephrocalcinosis in 7 cases. Fine, uniform calcifications in the renal papillae were demonstrated by renal ultrasound or CT. Renal papillary necrosis was demonstrated by intravenous pyelogram in one case. No renal function impairment was noted in these seven patients. There was no evidence of hypercalcemia. These findings may have implications for the use of a potentially nephrotoxic drug for the treatment of this disease-in particular, when an immunosuppressive agent is required following liver transplantation. C1 GEORGETOWN UNIV,MED CTR,DEPT RADIOL,WASHINGTON,DC 20007. NHLBI,DIV INTRAMURAL RES,MOLEC DIS BRANCH,BETHESDA,MD 20892. RP HILL, SC (reprint author), NHLBI,WARREN G MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BLDG 10,RM 1C660,BETHESDA,MD 20892, USA. NR 10 TC 0 Z9 0 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD JAN-FEB PY 1991 VL 15 IS 1 BP 101 EP 103 DI 10.1097/00004728-199101000-00015 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ET718 UT WOS:A1991ET71800015 PM 1987176 ER PT J AU EIDELMAN, N BROWN, WE MEYER, JL AF EIDELMAN, N BROWN, WE MEYER, JL TI THE EFFECT OF PYROPHOSPHATE CONCENTRATIONS ON CALCIUM-PHOSPHATE GROWTH ON WELL-CRYSTALLIZED OCTACALCIUM PHOSPHATE AND HYDROXYAPATITE SEED CRYSTALS SO JOURNAL OF CRYSTAL GROWTH LA English DT Article ID INORGANIC PYROPHOSPHATE; BONE; CALCIFICATION; MORPHOLOGY; SOLUBILITY; CARTILAGE; TISSUES; SERUM AB The comparative effects of 0.3, 1 and 3-mu-M P2O7(4-) concentrations on the growth of calcium phosphate on octacalcium phosphate (OCP) and on "well-crystallized" hydroxyapatite (OHAp) seeds were studied. The control growth rates (without P2O7(4-) were adjusted by weight or surface area of the seed crystals. The induction periods were longer with higher P2O7(4-) concentrations and longer on OCP seeds than on the OHAp seeds. However, the final growth rates were about the same on both kinds of seeds when equal concentrations of P2O7(4-) were used, suggesting that the same phase was growing on both kinds of seeds. The growth rates were faster when higher concentrations of OHAp seeds were used. The crystal growth on both OCP and OHAp seeds was accelerated when most of the labeled P2O7(4-) disappeared from the solution. The composition of the initial phase that grew on either OCP or OHAp seed crystals appears to be OCP or partially hydrolyzed OCP. These results lead to the conclusion that apparently OCP, but not OHAp, grew on OCP and OHAp seeds in the presence of P2O7(4-). C1 NCI,BETHESDA,MD 20892. RP EIDELMAN, N (reprint author), NATL INST STAND & TECHNOL,AMER DENT ASSOC HLTH FDN,PAFFENBARGER RES CTR,GAITHERSBURG,MD 20899, USA. NR 30 TC 4 Z9 4 U1 3 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-0248 J9 J CRYST GROWTH JI J. Cryst. Growth PD JAN PY 1991 VL 108 IS 1-2 BP 385 EP 393 DI 10.1016/0022-0248(91)90386-J PG 9 WC Crystallography; Materials Science, Multidisciplinary; Physics, Applied SC Crystallography; Materials Science; Physics GA EW385 UT WOS:A1991EW38500041 ER PT J AU CAMPBELL, G LEVY, D BAILEY, JJ AF CAMPBELL, G LEVY, D BAILEY, JJ TI BOOTSTRAP COMPARISON OF FUZZY ROC CURVES FOR ECG-LVH ALGORITHMS USING DATA FROM THE FRAMINGHAM-HEART-STUDY SO JOURNAL OF ELECTROCARDIOLOGY LA English DT Article; Proceedings Paper CT 15TH ANNUAL CONF OF THE INTERNATIONAL SOC FOR COMPUTERIZED ELECTROCARDIOLOGY : COMPUTER APPLICATIONS IN ELECTROCARDIOLOGY CY APR 22-27, 1990 CL VIRGINIA BEACH, VA SP INT SOC COMP ELECTROCARDIOL ID LEFT-VENTRICULAR HYPERTROPHY; CRITERIA; RISK C1 NHLBI,FRAMINGHAM HEART STUDY,BETHESDA,MD 20892. RP CAMPBELL, G (reprint author), NIH,DIV COMP RES & TECHNOL,LSM,BLDG 12A-3045,BETHESDA,MD 20892, USA. NR 21 TC 2 Z9 2 U1 0 U2 1 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0022-0736 J9 J ELECTROCARDIOL JI J. Electrocardiol. PY 1991 VL 23 SU S BP 132 EP 137 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FB308 UT WOS:A1991FB30800024 ER PT J AU DEVINSKY, O FELDMANN, E BROMFIELD, E EMOTO, S RAUBERTAS, R AF DEVINSKY, O FELDMANN, E BROMFIELD, E EMOTO, S RAUBERTAS, R TI STRUCTURED INTERVIEW FOR PARTIAL SEIZURES - CLINICAL PHENOMENOLOGY AND DIAGNOSIS SO JOURNAL OF EPILEPSY LA English DT Article DE SEIZURES; EPILEPSY; BRAIN TUMOR ID TEMPORAL-LOBE EPILEPSY AB We administered a modified version of the Psychosensory-Psychomotor Phenomena Interview (PPPI) to 128 patients with complex partial seizures (CPS), 20 patients with generalized seizures, and 58 controls (30 normals, 28 back pain) to study the symptoms of partial seizures. The PPPI is a structured interview used by a physician to survey a spectrum of potential seizure symptoms. Use of the PPPI led to the following changes in diagnosis: 10 patients with generalized tonic-clonic seizures were found to have onset with simple partial seizures, 18 patients with complex partial seizures were found for the first time to have auras, and 4 patients with simple partial seizures were also found to have CPS. Overall, auras precede some CPS in 89% of patients. The PPPI led to recognition of more than twice the number of ictal symptoms than standard history and review of previous reports. Differences in symptom frequency (ictal and interictal) between the two seizure groups and between each seizure group and controls were studied. Although several significant associations were found, because of multiple statistical comparisons, results must be interpreted with caution. The PPPI is a valuable tool for examining paroxysmal symptoms in seizure patients, although time constraints limit its use in routine clinical practice. C1 NEW YORK SLOAN KETTERING CANC CTR,DEPT NEUROL,NEW YORK,NY. NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892. NINCDS,DIV INTRAMURAL RES,BIOMETRY BRANCH,BETHESDA,MD 20892. NEW YORK HOSP,DEPT NEUROL,NEW YORK,NY 10021. TUFTS UNIV,NEW ENGLAND MED CTR,DEPT NEUROL,BOSTON,MA 02111. NR 44 TC 18 Z9 18 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0896-6974 J9 J EPILEPSY JI J. Epilepsy PY 1991 VL 4 IS 2 BP 107 EP 116 DI 10.1016/S0896-6974(05)80069-6 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA GX789 UT WOS:A1991GX78900008 ER PT J AU DEVINSKY, O COX, C WITT, E RONSAVILLE, D FEDIO, P THEODORE, WH AF DEVINSKY, O COX, C WITT, E RONSAVILLE, D FEDIO, P THEODORE, WH TI ICTAL FEAR IN TEMPORAL-LOBE EPILEPSY - ASSOCIATION WITH INTERICTAL BEHAVIORAL-CHANGES SO JOURNAL OF EPILEPSY LA English DT Article DE SEIZURES; FEAR; BEHAVIOR ID PANIC DISORDER; PSYCHOSIS AB We studied 40 patients with temporal lobe epilepsy to determine if ictal fear was associated with changes in cognition, personality, or psychopathology. Patients with ictal fear scored higher (p < 0.10) than those without ictal fear on the Minnesota Multiphasic Personality Inventory (MMPI) Social Introversion and Psychasthenia subscales, MMPI-derived scales including depression, poor morale, and delinquency and on the Spielberger Trait Anxiety Scale. These differences were not even marginally significant with Bonferoni correction for multiple comparisons. No differences were found between these groups in the Temporal Lobe (Bear-Fedio) Questionnaire, Buss-Durkey Hostility Inventory, or history of psychiatric hospitalization. However, a history of paranoid psychosis and anxiety disorder, as well as current treatment with a neuroleptic medication, were more common in patients with ictal fear. This study provides limited support for the thesis that ictal fear is associated with behavioral changes in epilepsy, particularly symptoms of anxiety, introversion, and paranoia. C1 NINCDS,CLIN EPILEPSY SECT,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,NEUROPSYCHOL SECT,BETHESDA,MD 20892. NR 25 TC 4 Z9 4 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0896-6974 J9 J EPILEPSY JI J. Epilepsy PY 1991 VL 4 IS 4 BP 231 EP 238 DI 10.1016/0896-6974(91)90081-S PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA HK828 UT WOS:A1991HK82800007 ER PT J AU RIECKMANN, P POLI, G KEHRL, JH FAUCI, AS AF RIECKMANN, P POLI, G KEHRL, JH FAUCI, AS TI ACTIVATED LYMPHOCYTES-B FROM HUMAN IMMUNODEFICIENCY VIRUS-INFECTED INDIVIDUALS INDUCE VIRUS EXPRESSION IN INFECTED T-CELLS AND A PROMONOCYTIC CELL-LINE, U1 SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TUMOR NECROSIS FACTOR; HIV-1 AB Freshly isolated B lymphocytes from patients infected with human immunodeficiency virus (HIV), in contrast to B cells from normal controls, were shown to induce viral expression in two cell lines: ACH-2, a T cell line, and U1, a promonocytic cell line, which are chronically infected with HIV, as well as in autologous T cells. In 10 out of 10 HIV-infected individuals with hypergammaglobulinemia, spontaneous HIV-inductive capacity was found with highly purified peripheral blood B cells, whereas peripheral blood or tonsillar B cells from six healthy, HIV-negative donors did not induce HIV expression unless the cells were stimulated in vitro. The induction of HIV expression was observed in direct coculture experiments of B lymphocytes and HIV-infected cells, and could also be mediated by supernatants from cultures of B cells. Significantly higher amounts of interleukin 6 (IL-6) and tumor necrosis factor alpha-(TNF-alpha) were detected in the B cell culture supernatants from HIV-infected patients with hypergammaglobulinemia (IL-6: xbar = 536 pg/ml; TNF-alpha: xbar - 493 pg/ml), as compared with normal uninfected controls (IL-6: xbar = 18 pg/ml; TNF-alpha: xbar = 23 pg/ml). Antibodies against these cytokines abolished the HIV-inductive capacity of B cells. We conclude that in vivo activated B cells in HIV-infected individuals can upregulate the expression of virus in infected cells by secreting cytokines such as TNF-alpha and IL-6, and, therefore, may play a role in the progression of HIV infection. RP RIECKMANN, P (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B13,BETHESDA,MD 20892, USA. NR 20 TC 97 Z9 97 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1991 VL 173 IS 1 BP 1 EP 5 DI 10.1084/jem.173.1.1 PG 5 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EP659 UT WOS:A1991EP65900001 PM 1985116 ER PT J AU MARTIN, R HOWELL, MD JARAQUEMADA, D FLERLAGE, M RICHERT, J BROSTOFF, S LONG, EO MCFARLIN, DE MCFARLAND, HF AF MARTIN, R HOWELL, MD JARAQUEMADA, D FLERLAGE, M RICHERT, J BROSTOFF, S LONG, EO MCFARLIN, DE MCFARLAND, HF TI A MYELIN BASIC-PROTEIN PEPTIDE IS RECOGNIZED BY CYTOTOXIC T-CELLS IN THE CONTEXT OF 4 HLA-DR TYPES ASSOCIATED WITH MULTIPLE-SCLEROSIS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID AUTOIMMUNE ENCEPHALOMYELITIS; MOLECULES; EPITOPES; SITES AB We have examined previously the peptide specificity of the T cell response to myelin basic protein (MBP) in patients with multiple sclerosis (MS) and healthy controls, and demonstrated that an epitope spanning amino acids 87-106 was frequently recognized. Because this region is encephalitogenic in some experimental animals, it has been postulated that the response to the epitope may have relevance to MS. In this study, the fine specificity of this response is studied using four well-characterized, monospecific T cell lines from three MS patients and an identical twin of a patient. Each of the lines recognized a peptide with the same core sequence, amino acids 89-99, although the responses were affected to various degrees by truncations at the COOH- or NH-2 terminal ends of the 87-106 epitope. Importantly, the epitope was recognized in conjunction with four different HLA-DR molecules. Also, the T cell receptor beta-chain usage was heterogeneous, and each line expressed a different VDJ sequence. The four HLA-DR molecules restricting the response to this epitope have been shown to be overrepresented in MS populations in various geographic areas, suggesting that the response to this region of the MBP molecule may be relevant to the pathogenesis of MS. These findings may have important implications in designing therapeutic strategies for the disease. C1 IMMUNE RESPONSE CORP,SAN DIEGO,CA 92121. NIAID,IMMUNOGENET LAB,MOLEC IMMUNOL SECT,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT NEUROL,WASHINGTON,DC 20057. MED UNIV S CAROLINA,CHARLESTON,SC 29425. RP MARTIN, R (reprint author), NINCDS,NEUROIMMUNOL BRANCH,BLDG 10,ROOM 5B16,BETHESDA,MD 20892, USA. RI Long, Eric/G-5475-2011 OI Long, Eric/0000-0002-7793-3728 NR 24 TC 270 Z9 271 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1991 VL 173 IS 1 BP 19 EP 24 DI 10.1084/jem.173.1.19 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EP659 UT WOS:A1991EP65900003 PM 1702137 ER PT J AU WILSON, GL FOX, CH FAUCI, AS KEHRL, JH AF WILSON, GL FOX, CH FAUCI, AS KEHRL, JH TI CDNA CLONING OF THE B-CELL MEMBRANE-PROTEIN CD22 - A MEDIATOR OF B-B-CELL INTERACTIONS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID INTERCELLULAR-ADHESION MOLECULE; CARCINOEMBRYONIC ANTIGEN; IMMUNOGLOBULIN; DIFFERENTIATION; EXPRESSION; SEQUENCE; SUPERFAMILY; ACTIVATION; RECEPTOR; HOMOLOGY AB We have cloned a full-length cDNA for the B cell membrane protein CD22, which is referred to as B lymphocyte cell adhesion molecule (BL-CAM). Using subtractive hybridization techniques, several B lymphocyte-specific cDNAs were isolated. Northern blot analysis with one of the clones, clone 66, revealed expression in normal activated B cells and a variety of B cell lines, but not in normal activated T cells, T cell lines, Hela cells, or several tissues, including brain and placenta. One major transcript of approximately 3.3 kb was found in B cells although several smaller transcripts were also present in low amounts (approximately 2.6, 2.3, and 1.6 kb). Sequence analysis of a full-length cDNA clone revealed an open reading frame of 2,541 bases coding for a predicted protein of 847 amino acids with a molecular mass of 95 kD. The BL-CAM cDNA is nearly identical to a recently isolated cDNA clone for CD22, with the exception of an additional 531 bases in the coding region of BL-CAM. BL-CAM has a predicted transmembrane spanning region and a 140-amino acid intracytoplasmic domain. Search of the National Biological Research Foundation protein database revealed that this protein is a member of the immunoglobulin super family and that it had significant homology with three homotypic cell adhesion proteins: carcinoembryonic antigen (29% identity over 460 amino acids), myelin-associated glycoprotein (27% identity over 425 amino acids), and neural cell adhesion molecule (21.5% over 274 amino acids). Northern blot analysis revealed low-level BL-CAM mRNA expression in unactivated tonsillar B cells, which was rapidly increased after B cell activation with Staphylococcus aureus Cowan strain 1 and phorbol myristate acetate, but not by various cytokines, including interleukin 4(IL-4), IL-6, and gamma-interferon. In situ hybridization with an antisense BL-CAM RNA probe revealed expression in B cell-rich areas in tonsil and lymph node, although the most striking hybridization was in the germinal centers. COS cells transfected with a BL-CAM expression vector were immunofluorescently stained positively with two different CD22 antibodies, each of which recognizes a different epitope. Additionally, both normal tonsil cells and a B cell line were found to adhere to COS transfected with BL-CAM in the sense but not the antisense direction. Based on the similarity of BL-CAM to other homotypic cell adhesion molecules together with our transfection data, we conclude that BL-CAM may be an important mediator of B-B cell interactions and may play a role in the localization of B lymphocytes in lymphoid tissues. C1 NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B13,BETHESDA,MD 20892. OI Kehrl, John/0000-0002-6526-159X NR 34 TC 146 Z9 148 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1991 VL 173 IS 1 BP 137 EP 146 DI 10.1084/jem.173.1.137 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EP659 UT WOS:A1991EP65900015 PM 1985119 ER PT J AU PEARCE, EJ CASPAR, P GRZYCH, JM LEWIS, FA SHER, A AF PEARCE, EJ CASPAR, P GRZYCH, JM LEWIS, FA SHER, A TI DOWN-REGULATION OF TH1 CYTOKINE PRODUCTION ACCOMPANIES INDUCTION OF TH2 RESPONSES BY A PARASITIC HELMINTH, SCHISTOSOMA-MANSONI SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID T-CELL CLONE; PROTECTIVE IMMUNITY; MONOCLONAL-ANTIBODIES; MICE; RESISTANCE; INFECTIONS; MOUSE; EGGS; INVITRO; ASSAY AB In the mouse, infection with Schistosoma mansoni results in an egg-producing infection and associated disease, whereas vaccination with attenuated larval stages produces a substantial and specific immunity in the absence of egg-induced pathology. Preliminary data showing enhanced interleukin-5 (IL-5) production by T cells from infected mice and interferon-gamma (IFN-gamma) synthesis by cells from vaccinated animals (7), suggested differential CD4+ subset stimulation by the different parasite stimuli. To confirm this hypothesis, lymphocytes from vaccinated or infected animals were compared for their ability to produce IFN-gamma and IL-2 (secreted by Th1 cells) as compared with IL-4 and IL-5 (characteristic Th2 cytokines). After stimulation with specific antigen or mitogen, T cells from vaccinated mice or prepatently infected animals responded primarily with Th1 lymphokines, whereas lymphocytes from patently infected mice instead produced Th2 cytokines. The Th2 response in infected animals was shown to be induced by schistosome eggs and directed largely against egg antigens, whereas the TH1 reactivity in vaccinated mice was triggered primarily by larval antigens. Interestingly, Th1 responses in mice carrying egg-producing infections were found to be profoundly downregulated. Moreover, the injection of eggs into vaccinated mice resulted in a reduction of antigen and mitogen-stimulated Th1 function accompanied by a coincident expression of Th2 responses. Together, the data suggest that coincident with the induction of Th2 responses, murine schistosome infection results in an inhibition of potentially protective Th1 function. This previously unrecognized downregulation of Th1 cytokine production may be an important immunological consequence of helminth infection related to host adaptation. C1 BIOMED RES INST,ROCKVILLE,MD 20852. RP PEARCE, EJ (reprint author), NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU Intramural NIH HHS [ZIA AI000579-24]; NIAID NIH HHS [AI-16006] NR 38 TC 693 Z9 710 U1 2 U2 17 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1991 VL 173 IS 1 BP 159 EP 166 DI 10.1084/jem.173.1.159 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EP659 UT WOS:A1991EP65900017 PM 1824635 ER PT J AU ROBERTS, K YOKOYAMA, WM KEHN, PJ SHEVACH, EM AF ROBERTS, K YOKOYAMA, WM KEHN, PJ SHEVACH, EM TI THE VITRONECTIN RECEPTOR SERVES AS AN ACCESSORY MOLECULE FOR THE ACTIVATION OF A SUBSET OF GAMMA/DELTA-T-CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID EXTRACELLULAR-MATRIX PROTEINS; GAMMA-DELTA; LYMPHOCYTES-T; MONOCLONAL-ANTIBODIES; FIBRONECTIN RECEPTOR; MYCOBACTERIUM-TUBERCULOSIS; STAPHYLOCOCCUS-AUREUS; PLASMA FIBRONECTIN; ANTIGEN RECEPTOR; SYNOVIAL-FLUID AB Constitutive production of cytokines was observed in 3 of 12 gamma/delta T-cell lines derived from murine epidermis and correlated with the expression of the C-gamma-4, V-delta-6 T cell receptor (TCR). After adaptation of one of the lines (T195/BW) to serum-free culture conditions, cessation of the "spontaneous" production of interleukin 4 (IL-4) was observed and IL-4 production could then be induced by the addition of RGD-containing extracellular matrix (ECM) proteins to the culture. The response to the ECM proteins could be completely inhibited by an mAb to the murine vitronectin receptor (VNR). However, the induction of IL-4 production could also be inhibited by anti-CD3 and by an anti-clonotypic mAb to the TCR-gamma/delta of T195/BW. As TCR-gamma/delta loss mutants of T195/BW also failed to respond to ECM proteins, these data demonstrate that engagement of the VNR by its ligand is necessary, but not sufficient, for the induction of IL-4 production. Furthermore, the VNR is expressed by many other T cell clones (both gamma/delta and alpha/beta), none of which produce lymphokines constitutively. Taken together, these observations strongly favor the view that not only is coexpression of the VNR and TCR required for the induction of IL-4 production, but that the TCR must also be engaged by its ligand, most likely a cell surface antigen expressed by the hybridoma itself. RP ROBERTS, K (reprint author), NIAID,IMMUNOL LAB,BETHESDA,MD 20892, USA. NR 59 TC 113 Z9 113 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1991 VL 173 IS 1 BP 231 EP 240 DI 10.1084/jem.173.1.231 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA EP659 UT WOS:A1991EP65900024 PM 1702138 ER PT J AU FEINSTONE, SM AF FEINSTONE, SM TI THE VIROLOGY OF HEPATITIS-C SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY LA English DT Article; Proceedings Paper CT SATELLITE MEETING OF THE INTERNATIONAL ASSOC FOR THE STUDY OF THE LIVER : TREATMENT OF VIRAL HEPATITIS CY SEP 03-05, 1990 CL GOLD COAST, AUSTRALIA SP SCHERING PLOUGH ID VIRUS GENOME; NON-A C1 NIH,FOOD & DRUG ADM,CTR BIOL EVALUAT & RES,DIV VIROL,BETHESDA,MD 20892. NR 5 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON VICTORIA 3053, AUSTRALIA SN 0815-9319 J9 J GASTROEN HEPATOL JI J. Gastroenterol. Hepatol. PY 1991 VL 6 SU 1 BP 26 EP 28 DI 10.1111/j.1440-1746.1991.tb01163.x PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GQ304 UT WOS:A1991GQ30400008 PM 1661191 ER PT J AU EMERSON, SU TSAREV, SA PURCELL, RH AF EMERSON, SU TSAREV, SA PURCELL, RH TI BIOLOGICAL AND MOLECULAR COMPARISONS OF HUMAN (HM-175) AND SIMIAN (AGM-27) HEPATITIS-A VIRUSES SO JOURNAL OF HEPATOLOGY LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON GENETIC HETEROGENEITY OF HEPATITIS VIRUSES : CLINICAL IMPLICATIONS CY APR 05-07, 1991 CL SESTRIERE, ITALY ID COMPLETE NUCLEOTIDE-SEQUENCE; WILD-TYPE; HAV AB Comparisons of HM-175, the prototype human strain of hepatitis A virus, and AGM-27, a simian isolate, indicate that the two HAV viruses differ substantially in sequence and in biological characteristics. The extent of the differences suggests that hepatitis A viruses have a greater potential for diversity than previously assumed. RP EMERSON, SU (reprint author), NIAID,HEPATITIS VIRUSES SECT,INFECT DIS LAB,BLDG 7,ROOM 203,BETHESDA,MD 20892, USA. NR 10 TC 2 Z9 2 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0168-8278 J9 J HEPATOL JI J. Hepatol. PY 1991 VL 13 SU 4 BP S144 EP S145 DI 10.1016/0168-8278(91)90047-F PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HH596 UT WOS:A1991HH59600035 PM 1668325 ER PT J AU PURCELL, RH MILLER, RH AF PURCELL, RH MILLER, RH TI THE NATURE OF GENETIC-VARIATION AMONG VIRUSES SO JOURNAL OF HEPATOLOGY LA English DT Article; Proceedings Paper CT INTERNATIONAL MEETING ON GENETIC HETEROGENEITY OF HEPATITIS VIRUSES : CLINICAL IMPLICATIONS CY APR 05-07, 1991 CL SESTRIERE, ITALY ID HEPATITIS-B VIRUS; NUCLEOTIDE-SEQUENCE; A VIRUS; RNA; RETROVIRUSES; REPLICATION; EVOLUTION; ORIGIN; GENOME AB Genetic variation among viruses may seem unimportant and academic - related only to pedagogical classification of things - but accurate determination of genetic relationships can have important implications, from characterizing the molecular basis of attenuation of viral vaccines to furthering knowledge about origins of viruses and even of life itself. It can even help to establish priority in the discovery of viruses when properly applied (1). The purpose of this brief review is to demonstrate how viruses change and what implications these changes can have on the delicate balance between the viral parasite and its host. Examples will be drawn from the hepatitis viruses when possible. RP PURCELL, RH (reprint author), NIAID,HEPATITIS VIRUSES SECT,INFECT DIS LAB,BLDG 7,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 26 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0168-8278 J9 J HEPATOL JI J. Hepatol. PY 1991 VL 13 SU 4 BP S2 EP S5 DI 10.1016/0168-8278(91)90014-3 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HH596 UT WOS:A1991HH59600002 PM 1822512 ER PT J AU PURCELL, RH AF PURCELL, RH TI GENETIC-HETEROGENEITY OF HEPATITIS VIRUSES - CLINICAL IMPLICATIONS - CONCLUDING REMARKS SO JOURNAL OF HEPATOLOGY LA English DT Editorial Material RP PURCELL, RH (reprint author), NIAID,HEPATITIS VIRUSES SECT,INFECT DIS LAB,BLDG 7,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0168-8278 J9 J HEPATOL JI J. Hepatol. PY 1991 VL 13 SU 4 BP S162 EP S162 DI 10.1016/0168-8278(91)90051-C PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HH596 UT WOS:A1991HH59600039 ER PT J AU SHAW, RF AF SHAW, RF TI THE QUESTION OF NATURAL-SELECTION AGAINST MUTABLE-TO-TERMINATOR CODONS SO JOURNAL OF HEREDITY LA English DT Note ID NUCLEOTIDE SUBSTITUTIONS; GENETIC-CODE; MUTATION; HEMOGLOBIN; USAGE AB Codons that differ from a terminator triplet by only a single base are sometimes thought, because of their greater risk of undergoing a harmful mutation, to be kept at a reduced frequency by natural selection. The present study on human genes shows that these codons are infrequent, but their low frequency is not directly related to their risk of mutation to terminator. Rather, it is a consequence of their ending in A or G; comparable A-ending and G-ending codons that are not mutable to terminator are also infrequent. Natural selection does not appear to have depressed the frequency of mutable-to-terminator codons by directly eliminating some of them individually. It may have depressed their frequency indirectly by adjusting mutation rates in the population so that most of the purine-ending codons - and consequently most of the mutable-to-terminator ones as well - are infrequent. RP SHAW, RF (reprint author), NIH,BLDG 12A,RM3045,BETHESDA,MD 20892, USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0022-1503 J9 J HERED JI J. Hered. PD JAN-FEB PY 1991 VL 82 IS 1 BP 77 EP 80 PG 4 WC Evolutionary Biology; Genetics & Heredity SC Evolutionary Biology; Genetics & Heredity GA FU868 UT WOS:A1991FU86800017 PM 1997593 ER PT J AU SHIMIZU, T NETTESHEIM, P MAHLER, JF RANDELL, SH AF SHIMIZU, T NETTESHEIM, P MAHLER, JF RANDELL, SH TI CELL TYPE-SPECIFIC LECTIN STAINING OF THE TRACHEOBRONCHIAL EPITHELIUM OF THE RAT - QUANTITATIVE STUDIES WITH GRIFFONIA-SIMPLICIFOLIA-I ISOLECTIN-B4 SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article ID TRACHEO-BRONCHIAL EPITHELIUM; BASAL CELLS; CLARA CELLS; DIFFERENTIATION; SURFACE; BINDING; GLYCOCONJUGATE; GALACTOSE; LIGHT; HISTOCHEMISTRY C1 NIEHS,PULM PATHOBIOL LAB,POB 12233,RES TRIANGLE PK,NC 27709. NR 35 TC 31 Z9 31 U1 0 U2 0 PU HISTOCHEMICAL SOC INC PI NEW YORK PA MT SINAI MEDICAL CENTER 19 EAST 98TH ST SUTIE 9G, NEW YORK, NY 10029 SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD JAN PY 1991 VL 39 IS 1 BP 7 EP 14 PG 8 WC Cell Biology SC Cell Biology GA EM802 UT WOS:A1991EM80200002 PM 1701188 ER PT J AU BROWN, JD NEWCOMER, SF AF BROWN, JD NEWCOMER, SF TI TELEVISION VIEWING AND ADOLESCENTS SEXUAL-BEHAVIOR SO JOURNAL OF HOMOSEXUALITY LA English DT Article ID SOAP OPERAS; INTIMACY; TV C1 NICHHD,DOMOG & BEHAV SCI BRANCH,WASHINGTON,DC. RP BROWN, JD (reprint author), UNIV N CAROLINA,JOURNALISM,204B HOWELL HALL CB 3365,CHAPEL HILL,NC 27599, USA. FU PHS HHS [APR-000914A] NR 26 TC 76 Z9 77 U1 2 U2 10 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0091-8369 J9 J HOMOSEXUAL JI J. Homosex. PY 1991 VL 21 IS 1-2 BP 77 EP 91 DI 10.1300/J082v21n01_07 PG 15 WC Psychology, Multidisciplinary; Social Sciences, Interdisciplinary SC Psychology; Social Sciences - Other Topics GA GB425 UT WOS:A1991GB42500005 PM 1856474 ER PT J AU MURAKAWA, Y STROBER, W JAMES, SP AF MURAKAWA, Y STROBER, W JAMES, SP TI MONOCLONAL-ANTIBODY AGAINST THE HUMAN PERIPHERAL LYMPH-NODE HOMING RECEPTOR HOMOLOG (LEU-8) INHIBITS B-CELL DIFFERENTIATION BUT NOT B-CELL PROLIFERATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INDUCER T-CELLS; INTESTINAL LAMINA PROPRIA; HUMAN LYMPHOCYTES-B; HELPER-INDUCER; COGNATE INTERACTIONS; SUPPRESSOR-INDUCER; ADHESION MOLECULES; SURFACE MOLECULE; SUB-POPULATIONS; GROWTH-FACTOR AB Previous studies have shown that a subpopulation of circulating human B cells expresses the Leu 8 peripheral lymph node homing receptor homologue and that these B cells are capable of producing Ig in response to staphylococcus A Cowan I (SAC). In the present study the effect of a signal delivered via the Leu 8 molecule (using anti-Leu 8 mAb) on B cells was examined. Initially, it was shown that immobilized anti-Leu 8 suppressed IgM and IgG secretion of B cells activated by SAC + IL-2 but not that by PWM-prestimulated B cells or B cells stimulated with PWM in the presence of CD4+, Leu 8- T cells (a source of helper cells). It was also shown that anti-Leu 8 did not suppress SAC + IL-2-stimulated B cell proliferation or expression of IL-2R alpha-chain or c-myc mRNA in B cells. The addition of T cells, monocytes, purified IL-2, rIL-1, rIL-6, or human B cell growth factor did not overcome the inhibitory effect of anti-Leu 8 on SAC-stimulated B cell Ig production, and the inhibitory effect of anti-Leu 8 was not blocked by anti-TGF-beta. Finally, inhibition of B cell differentiation occurred even when anti-Leu 8 was added up to 72 hours after initiation of cell culture. Thus, anti-Leu 8 is unique among inhibitors of B cell function in that it can down-regulate immunoglobulin synthesis without affecting B cell proliferation. These findings suggest that a natural ligand for Leu 8 could affect not only homing of B cells, but also B cell differentiation. RP MURAKAWA, Y (reprint author), NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BLDG 10,ROOM 11N 250,BETHESDA,MD 20892, USA. NR 49 TC 18 Z9 18 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1991 VL 146 IS 1 BP 40 EP 46 PG 7 WC Immunology SC Immunology GA EQ340 UT WOS:A1991EQ34000007 PM 1701799 ER PT J AU WAHL, SM ALLEN, JB OHURA, K CHENOWETH, DE HAND, AR AF WAHL, SM ALLEN, JB OHURA, K CHENOWETH, DE HAND, AR TI IFN-GAMMA INHIBITS INFLAMMATORY CELL RECRUITMENT AND THE EVOLUTION OF BACTERIAL-CELL WALL-INDUCED ARTHRITIS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID RECOMBINANT INTERFERON-GAMMA; LOW AFFINITY RECEPTOR; RHEUMATOID-ARTHRITIS; STIMULATED PRODUCTION; PERIPHERAL-BLOOD; DOWN-REGULATION; MACROPHAGE; EXPRESSION; ACTIVATION; MONOCYTES AB Localization of streptococcal cell wall Ag(SCW) in the synovial tissue of treated rats induces an influx of leukocytes and a cell-mediated immune response leading to arthritis and joint destruction. Systemic administration of the T cell product, IFN-gamma (10(6) U/kg/day), suppresses the recruitment of leukocytes into the synovium and effectively inhibits the inflammation and pathology characteristic of SCW-induced arthritis (articular index 10.4 +/- 0.6 for SCW vs 2.0 +/- 0.7 for SCW with IFN-gamma, p < 0.005). Monocyte-macrophages from animals treated with IFN-gamma exhibited defective chemotactic responses when tested in vitro and furthermore, monocytes cultured with IFN-gamma (25 to 500 U/ml) in vitro had significantly suppressed chemotactic responses to the complement fragment C5a (p < 0.005). The decreased ability to migrate to C5a was associated with decreased binding of fluorochrome-conjugated C5a indicative of reduced expression of C5a receptors. Based on these data, IFN-gamma that induces monocyte maturation as reflected by increased Ia expression conversely inhibits C5a receptor expression. Although locally elevated IFN-gamma levels may serve to inhibit recruitment away from an inflammatory site, systemic exposure to IFN-gamma appears to inhibit leukocyte recruitment to the inflammatory site by its ability to induce premature maturation and concomitant inability to respond to certain chemotactic ligands. Inasmuch as monocyte recruitment to the synovium is pivotal in the development of SCW-induced polyarthritis, the ability of IFN-gamma to inhibit this event effectively inhibits the synovial pathology. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. BAXTER HLTH CARE,SANTA ANA,CA 92705. RP WAHL, SM (reprint author), NIDR,CELLULAR IMMUNOL SECT,BLDG 30,RM 326,BETHESDA,MD 20892, USA. NR 47 TC 50 Z9 50 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1991 VL 146 IS 1 BP 95 EP 100 PG 6 WC Immunology SC Immunology GA EQ340 UT WOS:A1991EQ34000017 PM 1898608 ER PT J AU CHEUNG, SC CHATTOPADHYAY, SK HARTLEY, JW MORSE, HC PITHA, PM AF CHEUNG, SC CHATTOPADHYAY, SK HARTLEY, JW MORSE, HC PITHA, PM TI ABERRANT EXPRESSION OF CYTOKINE GENES IN PERITONEAL-MACROPHAGES FROM MICE INFECTED WITH LP-BM5 MULV, A MURINE MODEL OF AIDS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INDUCED IMMUNODEFICIENCY SYNDROME; TUMOR NECROSIS FACTOR; IFN-BETA; HUMAN THYMOCYTES; LEUKEMIA-VIRUS; LYMPHOCYTES-T; C57BL/6 MICE; CELL-GROWTH; RETROVIRUS; INDUCTION AB Mice infected with LP-BM5 murine leukemia virus (MuLV) develop a syndrome denoted as murine AIDS. Macrophages harvested from the peritoneal cavities of these mice at 4 or 9 wk postinoculation with LP-BM5 MuLV were analyzed by Northern hybridization for the presence of the defective LP-BM5 virus and their ability to synthesize various cytokines upon induction with Newcastle disease virus (NDV) or (LPS). Neither IFN-alpha or IFN-beta was found to be constitutively expressed in LP-BM5-infected macrophages and in NDV induction studies, and the levels of biologically active IFN-alpha and its mRNA were found to be lower in LP-BM5 MuLV-infected macrophages than in the macrophages from uninfected controls. Similarly, after NDV or LPS induction, the levels of TNF mRNA and TNF protein were significantly lower in LP-BM5-infected macrophages than in macrophages from uninfected mice. The LP-BM5 MuLV-infected macrophages constitutively expressed low levels of IL-1-beta, and when induced with LPS, the relative levels of IL-1-beta were significantly higher in infected than in uninfected macrophages. Although no constitutive expression of IL-6 was detected, the levels of IL-6 mRNA induced with NDV were higher in LP-BM5 MuLV-infected macrophages than in controls. Thus, we found alterations in the expression of selected cytokines in macrophages from mice inoculated with LP-BM5 MuLV rather than a general deregulation of all cytokine expression. These results show that macrophages infected with the defective LP-BM5 virus respond differently to NDV- or LPS-stimulation and suggest that aberrant expression of certain cytokine genes may play a role in the immunopathologic condition in mice with murine AIDS. C1 JOHNS HOPKINS UNIV,CTR ONCOL,418 N BOND ST,BALTIMORE,MD 21231. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. OI Morse, Herbert/0000-0002-9331-3705 FU NCI NIH HHS [CA50158, 5T32CA09243]; NIAID NIH HHS [AI19737] NR 40 TC 70 Z9 71 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1991 VL 146 IS 1 BP 121 EP 127 PG 7 WC Immunology SC Immunology GA EQ340 UT WOS:A1991EQ34000021 PM 1701789 ER PT J AU STOTTER, H CUSTER, MC BOLTON, ES GUEDEZ, L LOTZE, MT AF STOTTER, H CUSTER, MC BOLTON, ES GUEDEZ, L LOTZE, MT TI IL-7 INDUCES HUMAN LYMPHOKINE-ACTIVATED KILLER-CELL ACTIVITY AND IS REGULATED BY IL-4 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN PERIPHERAL-BLOOD; GROWTH-FACTOR; T-CELL; INTERLEUKIN-7; LYMPHOCYTES; TUMOR; PRECURSOR; INDUCTION; RECEPTOR; BETA AB Induction of lymphokine-activated killer (LAK) activity by IL-2 has been described and characterized as broadly cytolytic activity against both fresh and cultured tumors. rIL-7 in the absence of IL-2 also induces LAK activity in human cells. This activity is unique for IL-7, because it is not shared by other cytokines including IL-1, IL-4, IL-6, and TNF-alpha. IL-7 also induces either de novo or increased expression of the surface markers CD25 (Tac, IL-2R alpha-chain), CD54 (ICAM-1), Mic-beta-1 (IL-2R beta-chain) and CD69 (early T cell activation Ag). IL-7-induced LAK activity is independent of IL-2 secretion, because it is not abrogated by IL-2 antisera. The LAK precursor responding to IL-7 stimulation is enriched in the null cell fraction as has been demonstrated for IL-2-induced LAK cells. TGF-beta and IL-4 interfere with generation of LAK activity by IL-7. Anti-IL-4 antiserum enhances IL-7 induced LAK activity and augments induction of surface marker expression by IL-7. This may be indirect evidence that IL-7 stimulation leads to induction of IL-4 activity. Our results describe the activation of mature lymphoid cells by IL-7. This and the previously described role of IL-7 in lymphohemopoiesis makes it a cytokine of potential therapeutic value for treatment of immunodeficiency states and possibly the immunotherapy of cancer. C1 NCI,SURG BRANCH,TUMOR IMMUNOL SECT,BETHESDA,MD 20892. RI Guedez, Liliana/H-4951-2012 NR 41 TC 91 Z9 91 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1991 VL 146 IS 1 BP 150 EP 155 PG 6 WC Immunology SC Immunology GA EQ340 UT WOS:A1991EQ34000025 PM 1670602 ER PT J AU SEI, Y YOSHIMOTO, K MCINTYRE, T SKOLNICK, P ARORA, PK AF SEI, Y YOSHIMOTO, K MCINTYRE, T SKOLNICK, P ARORA, PK TI MORPHINE-INDUCED THYMIC HYPOPLASIA IS GLUCOCORTICOID-DEPENDENT SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LYMPHOCYTES-T; INDUCED IMMUNOMODULATION; THYMOCYTES; ADDICTS; INVIVO; CELLS; DIFFERENTIATION; ENDONUCLEASE; ACTIVATION; BLOOD AB Mice administered morphine as a s.c. pellet implant exhibit a marked and sustained thymic hypoplasia as well as suppression of T lymphocyte functions. In the present study, the effects of morphine on thymocyte differentiation were characterized. Morphine produced a significant decrease in both the number and proportion of CD4+/CD8+ double positive (DP) cells. The percentage of the CD4+/CD8-, CD4-/CD8+, and CD4-/CD8- double negative subsets in these mice was proportionally increased. Morphine also increased the proportion of cells expressing either the epsilon-chain of the CD3 complex or the IL-2R. The initial reduction in the proportion of DP thymocytes appeared fully recovered by 10 days post-implantation, although the number of DP thymocytes gradually returned to normal over a 3-wk period. Morphine administration resulted in a marked increase in serum corticosterone levels, and a single injection of dexamethasone mimicked the effects of morphine on thymus differentiation. Furthermore, adrenalectomy abolished the morphine-induced decrease in CD4+/CD8+ thymocytes relative to a sham-operated group. The present findings are consistent with the hypothesis that morphine-induced thymic hypoplasia may be mediated by an increase in the circulating levels of corticosterone. C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 30 TC 77 Z9 78 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1991 VL 146 IS 1 BP 194 EP 198 PG 5 WC Immunology SC Immunology GA EQ340 UT WOS:A1991EQ34000032 PM 1824589 ER PT J AU GAZZINELLI, RT HAKIM, FT HIENY, S SHEARER, GM SHER, A AF GAZZINELLI, RT HAKIM, FT HIENY, S SHEARER, GM SHER, A TI SYNERGISTIC ROLE OF CD4+ AND CD8+ LYMPHOCYTES-T IN IFN-GAMMA PRODUCTION AND PROTECTIVE IMMUNITY INDUCED BY AN ATTENUATED TOXOPLASMA-GONDII VACCINE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INTERFERON-GAMMA; MONOCLONAL-ANTIBODIES; CYTOKINE PRODUCTION; DEFICIENCY SYNDROME; CELL CLONE; LYMPHOKINE; MICE; ENCEPHALITIS; LYT-2+; RESISTANCE AB BALB/c mice vaccinated with a temperature-sensitive mutant (TS-4) of Toxoplasma gondii develop complete resistance to lethal challenge with a highly virulent toxoplasma strain (RH). This immunity is known to be dependent on IFN-gamma synthesis. In vitro and in vivo T cell depletions were performed in order to identify the subsets responsible for both protective immunity and IFN-gamma production. When stimulated with crude tachyzoite Ag in vitro, CD4+ cells from vaccinated mice produced high levels of TH1 cytokines (IL-2 and IFN-gamma) but not TH2 cytokines (IL-4 and IL-5). CD8+ cells, in contrast, produced less IFN-gamma and no detectable IL-2. Nevertheless, they could be induced to synthesize IFN-gamma when exposed in culture to exogenous IL-2. In vivo treatment with anti-CD4 plus anti-CD8 or anti-IFN-gamma antibodies during challenge infection completely abrogated resistance to T. gondii. In contrast, treatment with anti-CD4 alone failed to reduce immunity, whereas anti-CD8 treatment partially decreased vaccine-induced resistance. These results suggest that although IFN-gamma and IL-2-producing CD4+ lymphocytes are induced by vaccination, IFN-gamma-producing CD8+ T cells are the major effectors of immunity in vivo. Nevertheless, CD4+ lymphocytes appear to play a synergistic role in vaccine-induced immunity, probably through the augmentation of IFN-gamma synthesis by the CD8+ effector cells. This hypothesis is supported by the observation that when giving during vaccination, as opposed to after challenge, anti-CD4 antibodies are capable of blocking protective immunity. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP GAZZINELLI, RT (reprint author), NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BLDG 4,RM 126,9000 ROCKVILLE,BETHESDA,MD 20892, USA. NR 36 TC 461 Z9 474 U1 0 U2 12 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1991 VL 146 IS 1 BP 286 EP 292 PG 7 WC Immunology SC Immunology GA EQ340 UT WOS:A1991EQ34000046 PM 1670604 ER PT J AU CROEN, KD OSTROVE, JM DRAGOVIC, L STRAUS, SE AF CROEN, KD OSTROVE, JM DRAGOVIC, L STRAUS, SE TI CHARACTERIZATION OF HERPES-SIMPLEX VIRUS TYPE-2 LATENCY-ASSOCIATED TRANSCRIPTION IN HUMAN SACRAL GANGLIA AND IN CELL-CULTURE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HUMAN TRIGEMINAL GANGLIA; HUMAN SENSORY GANGLIA; INSITU HYBRIDIZATION; RNA COMPLEMENTARY; INFECTED NEURONS; GENITAL HERPES; GENE; DELETION; MICE; ESTABLISHMENT AB The ability of herpes simplex virus type 2 (HSV-2) to establish latency in and reactivate from sacral dorsal root sensory ganglia is the basis for recurrent genital hepes. The expression of HSV-2 genes in latently infected human sacral ganglia was investigated by in situ hybridization. Hybridizations with a probe from the long repeat region of HSV-2 revealed strong nuclear signals overlying neurons in sacral ganglia from five of nine individuals. The RNA detected overlaps with the transcript for infected cell protein O but in the opposite, or "anti-sense," orientation. These observations mimic those made previously with HSV-1 in human trigeminal ganglia and confirm the recent findings during latency in HSV-2-infected mice and guinea pigs. Northern hybridization of RNA from infected Vero cells showed that an HSV-2 latency-associated transcript was similar in size to the larger (1.85 kb) latency transcript of HSV-1. Thus, HSV-1 and HSV-2 latency in human sensory ganglia are similar, if not identical, in terms of their cellular localization and pattern of transcription. C1 NIAID,CLIN INVEST LAB,MED VIROL SECT,9000 ROCKVILLE PIKE,BLDG 10,RM 11N113,BETHESDA,MD 20892. OFF MED EXAMINER WAYNE CTY,DETROIT,MI. NR 39 TC 38 Z9 41 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1991 VL 163 IS 1 BP 23 EP 28 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA EP678 UT WOS:A1991EP67800005 PM 1845807 ER PT J AU BALACHANDRAN, N TIRAWATNAPONG, S PFEIFFER, B ABLASHI, DV SALAHUDDIN, SZ AF BALACHANDRAN, N TIRAWATNAPONG, S PFEIFFER, B ABLASHI, DV SALAHUDDIN, SZ TI ELECTROPHORETIC ANALYSIS OF HUMAN HERPESVIRUS-6 POLYPEPTIDES IMMUNOPRECIPITATED FROM INFECTED-CELLS WITH HUMAN SERA SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HBLV HUMAN HERPESVIRUS-6; SIMPLEX VIRUS TYPE-1; EXANTHEM SUBITUM; LYMPHOPROLIFERATIVE DISORDERS; ANTIBODY; HHV-6; IDENTIFICATION; PREVALENCE; ADULTS; RASH AB Proteins of human herpesvirus 6 (HHV-6) eliciting human antibody responses were examined in serum from healthy adults and patients with AIDS, chronic fatigue syndrome, Hodgkin's disease, and Sjogren's syndrome. HHV-6 IgG antibody titers measured by immunofluorescence (IF) ranged from 1:10 to 1:1280. Lysates of HHV-6-infected and uninfected cells labeled with [S-35]methionine, [H-3]glucosamine, and I-125 were immunoprecipitated with sera and analyzed electophoretically. Sera with IF titers greater-than-or-equal-to 1:20 immunoprecipitated > [S-35]methionine-labeled HHV-6 polypeptides of approximately 26-180 kDa. At least 10 HHV-6 glycoproteins and 8 HHV-6 polypeptides associated with the surfaces of infected cells were recognized by human sera. The approximate molecular masses of glycoproteins immunoprecipitated by human sera were similar to those immunoprecipitated by monoclonal antibodies. The labeling intensity of HHV-6 protein bands increased with increasing IF titer, and the effect was most prominent for HHV-6 glycopolypeptides. No reactivities with specific HHV-6 polypeptide(s) were characteristic of a given patient group. These findings suggest that HHV-6 glycoproteins are good targets for human antibody responses. C1 NCI,DIV CANC ETIOL,BETHESDA,MD 20892. RP BALACHANDRAN, N (reprint author), UNIV KANSAS,MED CTR,DEPT MICROBIOL MOLEC GENET & IMMUNOL,KANSAS CITY,KS 66103, USA. FU NCRR NIH HHS [RR-05373]; NIAID NIH HHS [AI-24224] NR 40 TC 18 Z9 18 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1991 VL 163 IS 1 BP 29 EP 34 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA EP678 UT WOS:A1991EP67800006 PM 1845808 ER PT J AU LAL, RB RUDOLPH, DL LAIRMORE, MD KHABBAZ, RF GARFIELD, M COLIGAN, JE FOLKS, TM AF LAL, RB RUDOLPH, DL LAIRMORE, MD KHABBAZ, RF GARFIELD, M COLIGAN, JE FOLKS, TM TI SEROLOGIC DISCRIMINATION OF HUMAN T-CELL LYMPHOTROPIC VIRUS-INFECTION BY USING A SYNTHETIC PEPTIDE-BASED ENZYME-IMMUNOASSAY SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HTLV-I INFECTION; MONOCLONAL-ANTIBODY; ENVELOPE PROTEIN; LEUKEMIA; BLOOD; HIV; IDENTIFICATION; POLYMERASE; PREDICTION; SEQUENCE AB Synthetic peptides corresponding with unique regions of the envelope glycoproteins (gp46) of human T cell lymphotropic viruses (HTLVs) were used in an enzyme immunoassay to determine if HTLV-I and -II infections could be discriminated. Two synthetic HTLV-I sequence-derived peptides, Env-1 (amino acids 191-215) and Env-5 (amino acids 242-257), reacted with 92% and 100% of the serum specimens (n = 52) from HTLV-I-infected persons, respectively. Although a small percentage (8.6%) of serum specimens from persons infected with HTLV-II cross-reacted with Env-1, none of these specimens reacted with Env-5. Peptide Env-2 encoded by the envelope region of HTLV-II (amino acids 187-210) reacted with serum speciments from both HTLV-I (94%)- and HTLV-II (74%)-infected patients, whereas Env-6, another HTLV-II peptide (amino acids 238-254), reacted with < 6% of the specimens. Therefore, the Env-5 peptide with amino acid sequence SerProAsnValSerValProSerSerSerSerThuProLeuLeuTyr represents an immunodominant domain of HTLV-I that is recognized by serum antibodies from all HTLV-I-infected persons. Moreover, the Env-5-based ELISA allows a categorical distinction between the closely related HTLV-I and -II infections. C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. RP LAL, RB (reprint author), CTR DIS CONTROL,DIV VIRAL & RICKETTSIAL DIS,RETROVIRUS DIS BRANCH,MAIL STOP G19,ATLANTA,GA 30333, USA. NR 35 TC 55 Z9 55 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1991 VL 163 IS 1 BP 41 EP 46 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA EP678 UT WOS:A1991EP67800008 PM 1984475 ER PT J AU BIGGAR, RJ BUSKELLBALES, Z YAKSHE, PN CAUSSY, D GRIDLEY, G SEEFF, L AF BIGGAR, RJ BUSKELLBALES, Z YAKSHE, PN CAUSSY, D GRIDLEY, G SEEFF, L TI ANTIBODY TO HUMAN RETROVIRUSES AMONG DRUG-USERS IN 3 EAST-COAST AMERICAN CITIES, 1972-1976 SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID PNEUMOCYSTIS-CARINII PNEUMONIA; NEW-YORK-CITY; VIRUS TYPE-I; IMMUNODEFICIENCY; INFECTION; ABUSERS AB Between 1972 and 1976, 585 persons attending methadone maintenance clinics at East Coast veterans hospitals were enrolled in a survey of hepatitis antibody prevalence. Sera were tested for human immunodeficiency virus (HIV) and human T lymphotropic virus (HTLV) using both HTLV-I and HTLV-II immunoblots. Clinical and death records were also reviewed. None of the sera and HIV antibodies (upper 95% confidence limit, 0.5%); however, 103 (18%) had reactivity to HTLV. The profile of reactivity suggested that these subjects had been exposed to HTLV-II rather than to HTLV-I. Prevalence was as high in the early 1970s as today and correlated with duration of drug use rather than age. Neither cancers, specific neurologic diseases, nor excess death from any cause (overall 14%) could be ascribed to seropositivity. Therefore, HTLV (probably HTLV-II) has been a common infection of drug users for many years but adverse outcomes following infection were not demonstrated. C1 VET ADM MED CTR,WASHINGTON,DC. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20007. RP BIGGAR, RJ (reprint author), NCI,VIRAL EPIDEMIOL SECT,EXECUT PLAZA N,RM 434,6130 EXECUT BLVD,ROCKVILLE,MD 20852, USA. NR 24 TC 34 Z9 34 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1991 VL 163 IS 1 BP 57 EP 63 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA EP678 UT WOS:A1991EP67800011 PM 1670608 ER PT J AU CHESEBRO, B WEHRLY, K METCALF, J GRIFFIN, DE AF CHESEBRO, B WEHRLY, K METCALF, J GRIFFIN, DE TI USE OF A NEW CD4-POSITIVE HELA-CELL CLONE FOR DIRECT QUANTITATION OF INFECTIOUS HUMAN-IMMUNODEFICIENCY-VIRUS FROM BLOOD-CELLS OF AIDS PATIENTS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID POLYMERASE CHAIN-REACTION; PERIPHERAL-BLOOD; MONONUCLEAR-CELLS; T-CELL; HUMAN RETROVIRUS; VISNA VIRUS; RFV-3 GENE; INDIVIDUALS; AMPLIFICATION; EXPRESSION AB A new CD4-positive HeLa cell line (clone 1022) with increased sensitivity for human immunodeficiency virus (HIV) isolated derived from AIDS patients could titer infectivity of HIV from most isolates at a level equal to that observed using normal human phytohemagglutinin (PHA)-stimulated lymphocyte cultures. By use of this clone with a focal immunoassay (FIA), peripheral blood mononuclear cells (PBMC) producing HIV were detected in 15% of seropositive asymptomatic patients and 23% of AIDS patients at a frequency of 1 in 2 X 10(4) to 3 X 10(6) PBMC. HIV detection by primary FIA correlated with low CD4-positive cells counts. HIV activation in cocultures with PHA blasts resulted in increasing numbers of cells releasing HIV starting 3-4 days after cocultivation. The low incidence of HIV detection by direct FIA compared with the high incidence if HIV isolation after cocultivation with PHA blasts provided quantiative infectivity data suggesting that HIV was in a state of latency or low expression in most PBMC of AIDS patients. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. RP CHESEBRO, B (reprint author), NIAID,ROCKY MT LABS,PERSISTANT VIRAL DIS,903 S 4TH ST,HAMILTON,MT 59840, USA. NR 31 TC 66 Z9 67 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1991 VL 163 IS 1 BP 64 EP 70 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA EP678 UT WOS:A1991EP67800012 PM 1984477 ER PT J AU BLOM, HJ BOERS, GHJ TANGERMAN, A GAHL, WA TRIJBELS, JMF AF BLOM, HJ BOERS, GHJ TANGERMAN, A GAHL, WA TRIJBELS, JMF TI ALTERNATIVE METHIONINE DEGRADATION VIA THE TRANSAMINATION PATHWAY - AN OPTION FOR THERAPY FOR HOMOCYSTINURIA DUE TO CYSTATHIONINE SYNTHASE DEFICIENCY SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article; Proceedings Paper CT SYMP AT THE 28TH ANNUAL MEETING OF THE SOC FOR THE STUDY OF INBORN ERRORS OF METABOLISM : LIVER AND INHERITED METABOLIC DISORDERS CY SEP 04-07, 1990 CL BIRMINGHAM, ENGLAND SP SOC STUDY INBORN ERRORS METAB ID DEHYDROGENASE C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. UNIV HOSP NIJMEGEN,DIV GASTROENTEROL,6500 HB NIJMEGEN,NETHERLANDS. UNIV HOSP NIJMEGEN,DIV ENDOCRINOL,6500 HB NIJMEGEN,NETHERLANDS. RP BLOM, HJ (reprint author), UNIV HOSP NIJMEGEN,DEPT PAEDIAT,POB 9101,6500 HB NIJMEGEN,NETHERLANDS. NR 7 TC 4 Z9 4 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1991 VL 14 IS 3 BP 375 EP 378 DI 10.1007/BF01811707 PG 4 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA FW414 UT WOS:A1991FW41400028 PM 1770796 ER PT J AU BIRRER, P MCELVANEY, NG CHANGSTROMAN, LM CRYSTAL, RG AF BIRRER, P MCELVANEY, NG CHANGSTROMAN, LM CRYSTAL, RG TI ALPHA-1-ANTITRYPSIN DEFICIENCY AND LIVER-DISEASE SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article ID HUMAN ALPHA-1-PROTEINASE INHIBITOR; HEPATIC ENDOPLASMIC-RETICULUM; ALPHA-ANTITRYPSIN DEFICIENCY; GLUCOSE-REGULATED PROTEINS; MOLECULAR-BASIS; HEAT-SHOCK; PIZ-ALPHA-1-ANTITRYPSIN VARIANT; ALPHA1-ANTITRYPSIN DEFICIENCY; PIZ ALPHA-1-ANTITRYPSIN; TRANSGENIC MICE AB Alpha-1-antitrypsin (alpha-1-AT) deficiency, one of the most common lethal hereditary disorders among Caucasians, is associated with emphysema in adults, while in children it is associated with liver disease. Produced in the liver and released into the plasma, alpha-1-AT serves as the body's major inhibitor of neutrophil elastase, a powerful proteolytic enzyme capable of degrading extracellular structural proteins. The pathogenesis of the liver disease associated with alpha-1-AT deficiency is not as well understood, but is clearly linked to specific mutations in coding exons of the alpha-1-AT gene, and the resulting accumulation of alpha-1-AT within hepatocytes. At present, therapy for the liver disease associated with alpha-1-AT deficiency is sympotomatic, with liver transplantation as a last resort. New strategies are being developed to suppress the accumulation of alpha-1-AT by transferring the normal gene into the liver. RP BIRRER, P (reprint author), NHLBI,PULM BRANCH,BETHESDA,MD 20892, USA. RI McElvaney, Noel/A-6809-2010 NR 67 TC 26 Z9 27 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1991 VL 14 IS 4 BP 512 EP 525 DI 10.1007/BF01797921 PG 14 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA FY969 UT WOS:A1991FY96900009 PM 1749216 ER PT J AU DECOSTA, BR MATTSON, MV AF DECOSTA, BR MATTSON, MV TI SYNTHESIS AND EVALUATION OF [H-3] 4-FLUORO-1-[1-(3-HYDROXYPHENYL)CYCLOHEXYL]PIPERIDINE, A POTENTIAL TOOL FOR AUTORADIOGRAPHIC STUDY OF THE PHENCYCLIDINE RECEPTOR SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE TRITIUM LABELED 4-FLUORO-1-[1-(3-HYDROXYPHENYL)CYCLOHEXYL]PIPERIDINE; AUTORADIOGRAPHIC; PHENCYCLIDINE (PCP) RECEPTOR; PET SCANNING LIGAND ID ASPARTATE; BINDING; LIGANDS AB The synthesis and in vitro binding of high specific activity tritium labelled 4-fluoro-1-[1-(3-hydroxphenyl)cyclohexyl] piperidine ([H-3]FOH-PCP), a potential probe for autoradiographic study of the phencyclidine (PCP) receptor is described. [H-3]FOH-PCP will allow evaluation of [F-18]FOH-PCP as a PET scanning ligand for PCP receptors. RP DECOSTA, BR (reprint author), NIDDKD,MED CHEM LAB,BETHESDA,MD 20892, USA. NR 22 TC 2 Z9 2 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0362-4803 J9 J LABELLED COMPD RAD JI J. Label. Compd. Radiopharm. PD JAN PY 1991 VL 29 IS 1 BP 63 EP 74 DI 10.1002/jlcr.2580290109 PG 12 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA EU019 UT WOS:A1991EU01900008 ER PT J AU ALAUPOVIC, P KNIGHTGIBSON, C WANG, CS DOWNS, D KOREN, E BREWER, HB GREGG, RE AF ALAUPOVIC, P KNIGHTGIBSON, C WANG, CS DOWNS, D KOREN, E BREWER, HB GREGG, RE TI ISOLATION AND CHARACTERIZATION OF AN APOA-II-CONTAINING LIPOPROTEIN (LP-A-II-B COMPLEX) FROM PLASMA VERY LOW-DENSITY LIPOPROTEINS OF PATIENTS WITH TANGIER DISEASE AND TYPE-V HYPERLIPOPROTEINEMIA SO JOURNAL OF LIPID RESEARCH LA English DT Article DE APO-B-CONTAINING LIPOPROTEINS; APOLIPOPROTEINS; NEUTRAL LIPIDS; PHOSPHOLIPIDS; HUMAN MILK LIPOPROTEIN LIPASE; IMMUNOAFFINITY CHROMATOGRAPHY; MONOCLONAL ANTIBODIES; ELECTROIMMUNOASSAY ID APOLIPOPROTEIN-B; MONOCLONAL-ANTIBODY; HUMAN-SERUM; QUANTITATIVE-DETERMINATION; IMMUNOAFFINITY CHROMATOGRAPHY; SEPARATE ELECTROIMMUNOASSAYS; METABOLIC HETEROGENEITY; RADIAL IMMUNODIFFUSION; ELECTRO-IMMUNOASSAY; PARTICLES AB Previous studies have shown that very low density lipoproteins (VLDL) from patients with Tangier disease are less effective as a substrate for human milk lipoprotein lipase (LPL) than VLDL from normal controls as assessed by measuring the first order rate constant (k1) of triglyceride hydrolysis. Tangier VLDL also has a higher content of apolipoprotein (apo) A-II than normal VLDL. To explore the possible relationship between the relatively high concentration of apoA-II in VLDL and low k1 values, Tangier VLDL were fractionated on an anti-apoA-II immunosorber. The retained fraction contained a newly identified triglyceride-rich lipoprotein characterized by the presence of apolipoproteins A-II, B, C-I, C-II, C-III, D, and E (LP-A-II:B:C:D:E: or LP-A-II:B complex), wherease the unretained fraction consisted of previously identified triglyceriderich apoB-containing lipoproteins free of apoA-II. In VLDL from patients with Tangier disease or type V hyperlipoproteinemia, the LP-A-II:B complex accounted for 70-90% and 25-70% of the total apoB content, respectively. The LP-A-II:B complexes had similar lipid and apolipoprotein composition; they were poor substrates for LPL as indicated by their low k1 values (0.014-0.016 min-1). In contrast, the apoA-II-free lipoproteins present in unretained fractions were effective substrates for LPL with k1 values equal to or greater than 0.0313 min-1. These results indicate that triglyceride-rich lipoproteins consist of several apoB-containing lipoproteins, including the LP-A-II:B complex, and that lipoprotein particles of similar size and density but distinct apolipoprotein composition also possess distinct metabolic properties. C1 UNIV OKLAHOMA,HLTH SCI CTR,DEPT BIOCHEM & MOLEC BIOL,OKLAHOMA CITY,OK 73104. NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. RP ALAUPOVIC, P (reprint author), OKLAHOMA MED RES FDN,LIPOPROT & ATHEROSCLEROSIS RES PROGRAM,OKLAHOMA CITY,OK 73104, USA. FU NHLBI NIH HHS [HL-23181] NR 70 TC 58 Z9 58 U1 0 U2 0 PU LIPID RESEARCH INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD JAN PY 1991 VL 32 IS 1 BP 9 EP 19 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA EW565 UT WOS:A1991EW56500002 PM 1901345 ER PT J AU ATAMNA, IZ JANINI, GM MUSCHIK, GM ISSAQ, HJ AF ATAMNA, IZ JANINI, GM MUSCHIK, GM ISSAQ, HJ TI SEPARATION OF XANTHINES AND URIC ACIDS BY CAPILLARY ZONE ELECTROPHORESIS AND MICELLAR ELECTROKINETIC CAPILLARY ELECTROPHORESIS SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; CAFFEINE METABOLISM; THEOPHYLLINE; RESOLUTION AB A CZE method was developed for the separation of xanthines and uric acid derivatives which are normally present in human plasma and urine as metabolites of caffeine. The methyl-substituted uric acids were separated using a 0.05 M sodium phosphate buffer (pH 7.0) at an applied voltage of 10 kV. In contrast, the separation of the methyl-substituted xanthines was only possible in the MECE mode, where SDS (0.15 M) was added to the buffer system. When both types of compounds were present in the same sample, optimum resolution (12 peaks for 13 standard solutes) was realized in the MECE mode with 0.15 M SDS added to the 0.05 M, pH 7 phosphate buffer at an applied voltage of 15 kV. RP ATAMNA, IZ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,POB B,FREDERICK,MD 21702, USA. NR 12 TC 24 Z9 24 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 3 BP 427 EP 435 DI 10.1080/01483919108049262 PG 9 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FK418 UT WOS:A1991FK41800002 ER PT J AU CARDELLINA, JH AF CARDELLINA, JH TI HPLC SEPARATION OF TAXOL AND CEPHALOMANNINE SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID INSECTICIDAL DITERPENES; BRIAREUM-POLYANTHES; TAXUS-BREVIFOLIA; AGENT AB Taxol [1], a highly functionalized antimitotic diterpene which occurs as a minor component of extracts of the bark from trees of the genus Taxus, is required in increasingly larger quantities for clinical trials. Final purification of taxol requires separation from cephalomannine [2]. An efficient separation of those closely related analogs has been achieved by normal phase HPLC on a cyanopropyl column. RP CARDELLINA, JH (reprint author), NCI,DRUG DISCOVERY RES & DEV LAB,BLDG 1052,ROOM 121,FREDERICK,MD 21701, USA. NR 12 TC 87 Z9 89 U1 0 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 4 BP 659 EP 665 DI 10.1080/01483919108049278 PG 7 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FK419 UT WOS:A1991FK41900005 ER PT J AU ISSAQ, HJ JANINI, GM ATAMNA, IZ MUSCHIK, GM AF ISSAQ, HJ JANINI, GM ATAMNA, IZ MUSCHIK, GM TI SEPARATIONS BY HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY AND CAPILLARY ZONE ELECTROPHORESIS - A COMPARATIVE-STUDY SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID ION-EXCHANGE CHROMATOGRAPHY; GEL-ELECTROPHORESIS; MICELLAR SOLUTIONS; INFLUENCE MOBILITY; PROTEINS; RESOLUTION; PEPTIDES; OLIGONUCLEOTIDES; SELECTIVITY; RETENTION AB In this comparative study we attempt to examine the similarities and differences between analytical high-pressure liquid chromatography and capillary zone electrophoresis with regards to mechanism of separation, instrumentation and fields of application. Based on careful reading of the recent literature it is safe to conclude that the two techniques are complimentary, especially for the separation and analysis of biomolecules. Both have points of strength and weakness. Capillary zone electrophoresis is superior whenever high peak capacity is required such as in the analysis of DNA fragments, while high pressure liquid chromatography is superior for small and neutral molecules and in its quantitative capabilities. C1 NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. RP ISSAQ, HJ (reprint author), DYNCORP,PROGRAM RESOURCES INC,POB B,FREDERICK,MD 21702, USA. NR 82 TC 28 Z9 28 U1 1 U2 5 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 5 BP 817 EP 845 DI 10.1080/01483919108049290 PG 29 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FL642 UT WOS:A1991FL64200001 ER PT J AU ISSAQ, HJ SEBURN, KE HIGHTOWER, JR AF ISSAQ, HJ SEBURN, KE HIGHTOWER, JR TI THIN-LAYER CHROMATOGRAPHIC SEPARATIONS BY CONVENTIONAL GLASS BACKED PLATES AND EMPORE SHEETS - A COMPARATIVE-STUDY SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article AB A comparison of separations using conventional TLC plates and Empore sheets is presented. The results show that in certain cases the Empore sheets failed to reproduce the separations obtained using silica gel plates, however, the retention times were comparable. The reversed phase C-18 Empore sheets were found to: (a) require much longer development times than C-18 TLC plates; (b) small increases in water content in the mobile phase (2%) contributed to considerable increase in development time; and (c) the maximum recommended percent water (v/v) in the mobile phase for meaningful and acceptable experimental time should not exceed 20%. It was observed that the Empore sheets were easier to spot than the TLC plates but harder to write on. Day-to-day and experiment to experiment R(f) reproductibility of Empore sheets was better than 5%. RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,DYN CORP,POB B,FREDERICK,MD 21701, USA. NR 8 TC 5 Z9 5 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 8 BP 1511 EP 1517 DI 10.1080/01483919108049632 PG 7 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FW392 UT WOS:A1991FW39200008 ER PT J AU SHIBUSAWA, Y ITO, Y AF SHIBUSAWA, Y ITO, Y TI HIGH-SPEED COUNTERCURRENT CHROMATOGRAPHY OF DIPEPTIDES ON A POLAR 2-PHASE SOLVENT SYSTEM SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID COLUMNS AB The performance of the high-speed countercurrent chomatograph was evaluated by separating dipeptide samples on a polar biphasic solvent composed of n-butanol-acetic acid-water (4:1:5, v/v/v). Best results were obtained with a set of multilayer coils of small helical diameter by eluting with the upper nonaqueous phase in a head to tail direction at a flow rate of 1 or 2 ml/min. Four components were completely resolved in 5 to 11 hours. Other types of coiled column such as a multilayer coil with large helical diameter (in a commercial model) and eccentric dual-layer coil assemblies mounted on a horizontal coil planet centrifuge also yielded satisfactory separations. RP SHIBUSAWA, Y (reprint author), NHLBI,BIOPHYS CHEM LAB,BLDG 10,ROOM 7N322,BETHESDA,MD 20892, USA. NR 8 TC 1 Z9 1 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 8 BP 1575 EP 1586 DI 10.1080/01483919108049636 PG 12 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FW392 UT WOS:A1991FW39200012 ER PT J AU SUPKO, JG MALSPEIS, L AF SUPKO, JG MALSPEIS, L TI A REVERSED-PHASE HPLC METHOD FOR DETERMINING CAMPTOTHECIN IN PLASMA WITH SPECIFICITY FOR THE INTACT LACTONE FORM OF THE DRUG SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID PLANT ANTITUMOR AGENTS; DNA TOPOISOMERASE-I; ANTILEUKEMIC ACTIVITY; BIOLOGICAL-ACTIVITY; ANALOGS; NSC-100880; PHARMACOKINETICS; CPT-11; CELLS AB Camptothecin is a pentacyclic indole alkaloid with a terminal alpha-hydroxy-delta-lactone ring, which in aqueous media at physiological pH, exists in equilibrium with the dissociated open-lactone carboxylate. The rate of equilibration between the two components is slow enough to permit their separation by reversed-phase HPLC. Selective determination of the intact lactone form of the drug was achieved by direct analysis of plasma samples immediately upon deproteinization with a solution of the internal standard in methanol chilled to -70-degrees-C. Acidification of the sample to pH 2 with perchloric acid prior to protein precipitation effected complete lactonization of the carboxylate and, therefore, provided a measure of total drug levels. Plasma concentrations of the carboxylate may be calculated from the difference between total drug and intact lactone determinations. Chromatography was performed on a 5-mu-m Ultrasphere ODS column (4.6 mm x 25 cm) preceded by a 1.5 cm RP-18 Brownlee Guard column with an eluent composed of acetonitrile-0.1 M ammonium acetate buffer, pH 5.5 (28:72, v/v) with 1 mM sodium dodecyl sulfate at a flow rate of 1.0 ml/min. The drug was monitored by fluorescence detection with excitation at 347 nm and a 418 nm emission cutoff filter. Approximately 3.0 hr was required to assay an 8 point standard curve and a drug-free plasma sample. Employing 50-mu-l of plasma, the lowest concentration on the camptothecin lactone and total drug standard curves, 2.82 nM (0.49 ng/ml), was quantified with 3.79 and 5.58% coefficients of variation, respectively. The method has been shown to be specific and reproducible. C1 NCI,FREDERICK CANC RES FACIL,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21701. RP SUPKO, JG (reprint author), OHIO STATE UNIV,COLL PHARM,COLUMBUS,OH 43210, USA. NR 35 TC 35 Z9 35 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 9 BP 1779 EP 1803 DI 10.1080/01483919108049653 PG 25 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FX103 UT WOS:A1991FX10300012 ER PT J AU SUPKO, JG MALSPEIS, L AF SUPKO, JG MALSPEIS, L TI CONCURRENT DETERMINATION OF MERBARONE AND ITS URINARY METABOLITES BY REVERSED-PHASE HPLC WITH PRECOLUMN PHENOLIC ACETYLATION SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID ANTITUMOR AGENT; NSC 336628 AB Three prominent oxidative metabolites, 2-oxo-desthiomerbarone, 4'-hydroxymerbarone and 4'-hydroxy-2-oxo-desthiomerbarone are excreted in the urine of patients treated with merbarone (NSC 336628), an investigational anticancer agent. The highly polar phenolic metabolites were readily acylated using acetic anhydride in the presence of potassium carbonate without structurally altering the parent drug or 2-oxodesthiomerbarone. Capacity factors of the derivatives were sufficiently enhanced to effect their separation from interfering endogenous urinary constituents under isocratic reversed-phase conditions. Chromatography was performed on a 4-mu-m Nova-Pak C18 column (3.9 mm x 15 cm) utilizing methanol-water (25:75, v/v) containing ammonium acetate (67 mM), acetic acid (33 mM), magnesium sulfate (40 mM) and sodium dodecyl sulfate (1 mM) as the mobile phase with UV detection at 293 nm. This method permitted the concurrent determination of merbarone and its three metabolites in a single urine sample. without preliminary isolation or purification procedures, by HPLC directly after an essentially quantitative, very rapid and phenol specific derivatization. Employing 100-mu-l of urine, calibration curves were constructed with analyte concentrations in the range 0.25-10.0-mu-g/ml, the lower limit being sufficient for quantitation in 24 hour pooled urines acquired during 7 days from cancer patients treated with the drug according to 5 day continuous intravenous infusion dosing regimens. RP SUPKO, JG (reprint author), NCI,FREDERICK CANC RES FACIL,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702, USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 11 BP 2169 EP 2188 DI 10.1080/01483919108049682 PG 20 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA GC457 UT WOS:A1991GC45700011 ER PT J AU ISSAQ, HJ AF ISSAQ, HJ TI HPLC 91, BASEL, SWITZERLAND, JUNE 3-7, 1991 SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Editorial Material RP ISSAQ, HJ (reprint author), FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 15 BP 2999 EP 3000 PG 2 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA GK478 UT WOS:A1991GK47800012 ER PT J AU FORD, H MERSKI, CL KELLEY, JA AF FORD, H MERSKI, CL KELLEY, JA TI A RAPID MICROSCALE METHOD FOR THE DETERMINATION OF PARTITION-COEFFICIENTS BY HPLC SO JOURNAL OF LIQUID CHROMATOGRAPHY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; NUCLEOSIDE ANALOGS; LIPOPHILICITY; CONSTANTS; HIV AB A rapid, reliable and simple microscale method for the determination of octanol-water partition coefficients has been developed and evaluated. Rapid solute partitioning and facile octanol-water phase separation is accomplished in a commercially available mixer-separator device. The relative concentration of solute in each phase is then measured directly by computer-based reverse phase HPLC. The procedure requires only 10-mu-g of sample, which need not be pure, and uses 1 ml or less of both n-octanol and pH 7.0 phosphate buffer. Log P values of 26 compounds, mainly nucleoside analogues with anti-HIV and antitumor activity, have been determined in the range 0.7 to -2.4 with a precision better than +/- 0.04 log units. For compounds with literature data available, measured log P values are in good agreement (better than +/- 0.2 log units) with those values obtained by traditional "shake-flask" methodology. The described method is applicable to both single compound analysis and simultaneous multiple compound determinations through use of isocratic or gradient HPLC techniques. RP FORD, H (reprint author), NCI,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892, USA. NR 21 TC 37 Z9 37 U1 0 U2 5 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0148-3919 J9 J LIQ CHROMATOGR JI J. Liq. Chromatogr. PY 1991 VL 14 IS 18 BP 3365 EP 3386 DI 10.1080/01483919108049396 PG 22 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA GP788 UT WOS:A1991GP78800010 ER PT J AU KAY, LE IKURA, M BAX, A AF KAY, LE IKURA, M BAX, A TI THE DESIGN AND OPTIMIZATION OF COMPLEX NMR EXPERIMENTS APPLICATION TO A TRIPLE-RESONANCE PULSE SCHHEME CORRELATING H-ALPHA, NH, AND N-15 CHEMICAL-SHIFTS IN N-15-C-13-LABELED PROTEINS SO JOURNAL OF MAGNETIC RESONANCE LA English DT Article ID TWO-DIMENSIONAL NMR; RELAYED COHERENCE TRANSFER; SPECTROSCOPY; SIGNALS; SPECTRA RP KAY, LE (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 2,BETHESDA,MD 20892, USA. NR 26 TC 110 Z9 110 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-2364 J9 J MAGN RESON PD JAN PY 1991 VL 91 IS 1 BP 84 EP 92 DI 10.1016/0022-2364(91)90410-U PG 9 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA ET221 UT WOS:A1991ET22100009 ER PT J AU BERKOWITZ, BA AF BERKOWITZ, BA TI SELECTIVE SUPPRESSION OF THE ATP ALPHA-PHOSPHATE AND GAMMA-PHOSPHATE RESONANCES IN P-31 NMR SO JOURNAL OF MAGNETIC RESONANCE LA English DT Note ID DECOUPLER RP BERKOWITZ, BA (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 9 TC 1 Z9 1 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-2364 J9 J MAGN RESON PD JAN PY 1991 VL 91 IS 1 BP 170 EP 173 PG 4 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA ET221 UT WOS:A1991ET22100020 ER PT J AU BAX, A IKURA, M KAY, LE ZHU, G AF BAX, A IKURA, M KAY, LE ZHU, G TI REMOVAL OF F1-BASE-LINE DISTORTION AND OPTIMIZATION OF FOLDING IN MULTIDIMENSIONAL NMR-SPECTRA SO JOURNAL OF MAGNETIC RESONANCE LA English DT Note ID CORRELATION SPECTROSCOPY; PRACTICAL ASPECTS; PROTEINS; PHASE; SENSITIVITY RP BAX, A (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 12 TC 145 Z9 145 U1 1 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-2364 J9 J MAGN RESON PD JAN PY 1991 VL 91 IS 1 BP 174 EP 178 DI 10.1016/0022-2364(91)90422-P PG 5 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA ET221 UT WOS:A1991ET22100021 ER PT J AU SZALMA, S PELCZER, I BORER, PN LEVY, GC AF SZALMA, S PELCZER, I BORER, PN LEVY, GC TI SELECTIVE DISCRETE FOURIER TRANSFORMATION, AN ALTERNATIVE APPROACH FOR MULTIDIMENSIONAL NMR DATA-PROCESSING SO JOURNAL OF MAGNETIC RESONANCE LA English DT Note ID SPECTRA; SPECTROSCOPY; HOMONUCLEAR; ASSIGNMENT; H-1-NMR C1 SYRACUSE UNIV,DEPT CHEM,NIH,RESOURCE NUCL MAGNET RESONANCE & DATA PROC,SYRACUSE,NY 13244. NR 16 TC 4 Z9 4 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 0022-2364 J9 J MAGN RESON PD JAN PY 1991 VL 91 IS 1 BP 194 EP 198 DI 10.1016/0022-2364(91)90426-T PG 5 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA ET221 UT WOS:A1991ET22100025 ER PT J AU ROMANS, P SEELEY, DC KEW, Y GWADZ, RW AF ROMANS, P SEELEY, DC KEW, Y GWADZ, RW TI USE OF A RESTRICTION-FRAGMENT-LENGTH-POLYMORPHISM (RFLP) AS A GENETIC-MARKER IN CROSSES OF ANOPHELES-GAMBIAE (DIPTERA, CULICIDAE) - INDEPENDENT ASSORTMENT OF A DIPHENOL OXIDASE RFLP AND AN ESTERASE LOCUS SO JOURNAL OF MEDICAL ENTOMOLOGY LA English DT Article DE INSECTA; ANOPHELES-GAMBIAE; MALARIA REFRACTORINESS; RESTRICTION FRAGMENT LENGTH POLYMORPHISM ID CYSTIC-FIBROSIS GENE; DROSOPHILA-MELANOGASTER; PLASMODIUM-CYNOMOLGI; REFRACTORY STRAIN; LINKAGE MAP; IDENTIFICATION; LOCALIZATION; ASSOCIATION; EXPRESSION; WALKING AB Analysis of restriction fragment length polymorphism (RFLP) is a powerful tool for analyzing linkage relationships in species where few genetic markers have been described and where conduct of crosses is difficult. It also permits integration of genetic and physical (cytogenetic) data when the probes have been mapped by in situ hybridization. To illustrate the utility of the method, and because some mutations of a diphenol oxidase gene might conceivably produce the malaria refractoriness phenotype of ookinete-oocyst encapsulation, backcrosses between two inbred lines of Anopheles gambiac Giles were carried out to determine the linkage relationship between the diphenol oxidase A2 (Dox) gene and the esterase locus associated with refractoriness to Plasmodium cynomolgi NIH. The Dox alleles were a Sal I restriction fragment length polymorphism visualized by probing Southern blotted DNA from portions of individual mosquitoes with a cloned Dox gene probe. The two genes were shown to segregate independently. C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 23 TC 14 Z9 15 U1 0 U2 1 PU ENTOMOL SOC AMER PI LANHAM PA 9301 ANNAPOLIS RD, LANHAM, MD 20706 SN 0022-2585 J9 J MED ENTOMOL JI J. Med. Entomol. PD JAN PY 1991 VL 28 IS 1 BP 147 EP 151 PG 5 WC Entomology; Veterinary Sciences SC Entomology; Veterinary Sciences GA EQ856 UT WOS:A1991EQ85600024 PM 1674545 ER PT J AU COPP, RR MARQUEZ, VE AF COPP, RR MARQUEZ, VE TI SYNTHESIS OF 2 CYCLOPENTENYL-3-DEAZAPYRIMIDINE CARBOCYCLIC NUCLEOSIDES RELATED TO CYTIDINE AND URIDINE SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID TUMOR-CELLS; 3-DEAZAURIDINE; ANTITUMOR; ANALOG; CYCLOPENTENYLCYTOSINE; 3-DEAZAPYRIMIDINES; 3-DEAZACYTIDINE; TRIPHOSPHATE; SYNTHETASE; INHIBITION AB The cytosine analogue of neplanocin A, cyclopentenylcytosine (CPE-C, 3), has significant antitumor and antiviral activity commensurate with the drug's ability to produce a significant depletion of cytidine triphosphate (CTP) levels that result from the potent inhibition of cytidine triphosphate synthetase. Another important antitumor agent, previously identified as a potent inhibitor of the same enzyme, is 3-deazauridine (2). The synthesis of the cyclopentenyl nucleosides 3-deaza-CPE-C (5) and 3-deaza-CPE-U (6) was undertaken in order to investigate the effects of a modified 3-deaza pyrimidine aglycon moiety on the biological activity of the parent CPE-C. These compounds were synthesized via an S(N)2 displacement reaction on cyclopenten-1-ol methanesulfonate (10) by the sodium salt of the corresponding aglycon. In each case, separation and characterization of the corresponding N- and O-alkylated products was necessary before final removal of the blocking groups. The target compounds were devoid of in vitro antiviral activity against the HSV-1 and human influenza viruses. Although 3-deaza-CPE-C was nontoxic to L1210 cells in culture, 3-deaza-CPE-U displayed significant cytotoxicity against murine L1210 leukemia in vitro. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NR 24 TC 28 Z9 28 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD JAN PY 1991 VL 34 IS 1 BP 208 EP 212 DI 10.1021/jm00105a032 PG 5 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ET545 UT WOS:A1991ET54500032 PM 1992119 ER PT J AU TSENG, CKH MARQUEZ, VE MILNE, GWA WYSOCKI, RJ MITSUYA, H SHIRASAKI, T DRISCOLL, JS AF TSENG, CKH MARQUEZ, VE MILNE, GWA WYSOCKI, RJ MITSUYA, H SHIRASAKI, T DRISCOLL, JS TI A RING-ENLARGED OXETANOCIN-A ANALOG AS AN INHIBITOR OF HIV INFECTIVITY SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; NUCLEOSIDE ANALOGS; ACID; CONFORMATION; DERIVATIVES AB Two ring-expanded analogues (compounds 2 and 3) of the anti-HIV fermentation product oxetanocin A (1) were synthesized from commercially available diacetone D-glucose. Antiviral testing against HIV in ATH8 cells revealed that the ring-expanded analogue 2 possessed a similar activity profile as oxetanocin A. Neither compound, however, was capable of providing full protection to the cells against HIV infection. The isomeric ring-expanded analogue 3 was totally devoid of anti-HIV activity. Molecular modeling suggested that while oxetanocin A and compounds 2 and 3 share a large common substructure with the potent anti-HIV drug, dideoxyadenosine (ddA), the extra hydroxymethyl substituent may contribute negatively to the binding of these molecules to a critical enzyme. The negative contribution may be less important in oxetanocin and isomer 2 than in isomer 3. From these studies it would appear that both oxetane and tetrahydrofuran rings are equivalent templates to support the adenine base in terms of anti-HIV activity. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NR 32 TC 72 Z9 72 U1 1 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD JAN PY 1991 VL 34 IS 1 BP 343 EP 349 DI 10.1021/jm00105a054 PG 7 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ET545 UT WOS:A1991ET54500054 PM 1992135 ER PT J AU SPRUCE, LW GALE, JB BERLIN, KD VERMA, AK BREITMAN, TR JI, XH VANDERHELM, D AF SPRUCE, LW GALE, JB BERLIN, KD VERMA, AK BREITMAN, TR JI, XH VANDERHELM, D TI NOVEL HETEROAROTINOIDS - SYNTHESIS AND BIOLOGICAL-ACTIVITY SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ORNITHINE DECARBOXYLASE ACTIVITY; THERAPEUTIC ANTICANCER AGENTS; RETINOIC ACID ANALOGS; VITAMIN-A; PHARMACOLOGICAL ACTIVITY; TERMINAL DIFFERENTIATION; 13-CIS-RETINOIC ACID; DERMATOLOGY; CELLS; CARCINOGENESIS AB In this study, 13 heteroarotinoids were synthesized. The key step in each preparation was the condensation of the appropriate chroman-, thiochroman-, or benzothienyl-substituted phosphorus ylide, obtained from the independent synthesis of the corresponding phosphonium salts, with selected polyene-substituted aldehyde esters. Nine of these heterocycles contained a thiochroman group, two had a chroman group, and two others had a benzothienyl system. Screening of the compounds was with one of two assays. One assay measured the ability of a retinoid to inhibit the phorbol ester induced increase of mouse epidermal ornithine decarboxylase (ODC) activity. The other assay measured retinoid-induced differentiation of the human myoloid leukemia cell line HL-60. In the ODC assay, all thirteen compounds were screened. The most active heteroarotinoids were ester 10 [methyl (E)-4-[2-(2,2,4,4-tetramethylthiochroman-6-yl)-1-propenyl]benzoate] and acid 11 [(E)-4-[2-(2,2,4,4-tetramethyl-3,4-dihydro-2H-1-benzothiopyran-6-yl)-1-propenyl]benzoic acid]. Both of these retinoids had ID50 values (dose required for half-maximal inhibition of phorbol ester induced ODC activity) of about 0.3 nmol. In comparison, the ID50 value for trans-retinoic acid (1) was 0.12 nmol while the ID50 values for acids 7 and 9, namely (2Z,4E,6E)-3,7-dimethyl-7-(4,4-dimethylthiochroman-6-yl)-2,2,4,6-heptatienoic acid and (2E,4E,6E)-3,7-dimethyl-7-(2,2,4,4-tetramethylthiochroman-6-yl)-2,4,6-heptatrienoic acid, respectively, were about 3.5 nmol. Heteroarotinoids 8 and 12-17 had ID50 values of 35 nmol or greater. With a thiochroman unit, the most active acids in decreasing order of activity in the ODC assay were 7 > 9 > 8. Thus, simple replacement of the terminal propenyl system [C(16,17,18)] in 7 with a cyclopropyl group produced acid 8 [(2E,4E,6E)-7-methyl-7-(4,4-dimethylthiochroman-6-yl)-2,3-methylene-4,6-hepatadienoic acid with markedly reduced activity. With a benzoic acid group as part of the structure attached to the thiochroman unit, the ODC activity was enhanced as shown in 10 and 11. The combination of the 2,2,4,4-tetramethylthiochroman group and the benzoic acid (or ester) terminal group seemed to enhance the biological action which resembles that found with (E)-4-[2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl]benzoic acid (TTNPB, 6b), a well-known model system. Replacing the protons with fluorine in the C(12) methyl group in the side chain and altering the orientation of the aryl groups around the double bond from anti to syn lowered ODC activity in both the thiochroman- and chroman-containing systems. Esters 12 and 14 [methyl (E)-4-[2-(trifluoromethyl)-2-(2,2,4,4-tetramethylthiochroman-6-yl)ethenyl]benzoate and methyl (E)-4-[2-(trifluoromethyl)-2-(4,4-dimethylthiochroman-6-yl)ethenyl]benzoate, respectively] and acid 13 [(E)-4-[2-(trifluoromethyl)-2-(2,2,4,4-tetramethylthiochroman-6-yl)ethenyl]benzoic acid] were essentially inactive while acid 15 [(E)-4-[2-(trifluoromethyl)-2-(4,4-dimethylthiochroman-6-yl)ethenyl]benzoic acid] exhibited moderate activity in the ODC assay. In the chroman family, both ester 16 [methyl (E)-4-[2-(trifluoromethyl)-2-(4,4-dimethylchroman-6-yl)ethenyl]benzoate] and acid 17 [(E)-4-[2-(trifluoromethyl)-2-(4,4-dimethylchroman-6-yl)ethenyl]benzoic acid] had unfavorable ID50 values. An observation is that since acid 13 differs only slightly from acid 15 [the latter is devoid of the geminal dimethyl group at C(2)] and acid 15 differs only slightly from acid 17 (the latter has an oxygen atom and the former a sulfur atom), possibly the nature of the hetroatom and the stereochemistry of the alpha-position may play important roles in regulating activity, but more examples are required to establish a trend. Changing the ring size from a fused six-six system to a five-six system led to ester 6c [methyl(E)-4-[2-(2,3-dihydro-3,3-dimethylbenzo[b]thien-5-yl)-1-propenyl]benzoate] and acid 6d [(E)-4-[2-(2,3-dihydro-3,3-dimethylbenzo[b]thienyl-5-yl)-1-propenyl]benzoic acid], respectively. In separate experiments from those with 2-17, both 6c and 6d exhibited similar inhibition of ODC activity to that of trans-retinoic acid (1) at the 34 nmol level. The ID50 values of topically administered 6c and 6d were, however, 10 and 200 times greater than that of 1, respectively. Of eight heteroarotinoids examined in the HL-60 assay system, only acid 7 [(2Z,4E,6E)-3,7-dimethyl-7-(4,4-dimethylthiochroman-6-yl)-2,4,6-heptatrienoic acid] displayed modest activity. This acid had an ED50 value (dose required for half-maximal effect) of 500 nM. In comparison, the ED50 for trans-retinoic acid (1) was 50 nM. All of the other heteroarotinoids had ED50 values which were greater than 1000 nM. C1 OKLAHOMA STATE UNIV,DEPT CHEM,STILLWATER,OK 74078. UNIV WISCONSIN,WISCONSIN CLIN CANC CTR,DEPT HUMAN ONCOL,MADISON,WI 53792. NCI,BIOL CHEM LAB,BETHESDA,MD 20892. UNIV OKLAHOMA,DEPT CHEM,NORMAN,OK 73019. RI Ji, Xinhua/C-9664-2012 OI Ji, Xinhua/0000-0001-6942-1514 NR 74 TC 30 Z9 30 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD JAN PY 1991 VL 34 IS 1 BP 430 EP 439 DI 10.1021/jm00105a065 PG 10 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA ET545 UT WOS:A1991ET54500065 PM 1992144 ER PT J AU GARCIAPEREZ, A BURG, MB AF GARCIAPEREZ, A BURG, MB TI ROLE OF ORGANIC OSMOLYTES IN ADAPTATION OF RENAL-CELLS TO HIGH OSMOLALITY SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Review DE OSMOREGULATION; SORBITOL; BETAINE; INOSITOL; GLYCEROPHOSPHORYLCHOLINE; ALDOSE REDUCTASE ID HIGH EXTRACELLULAR NACL; ALDOSE REDUCTASE; MEDULLARY CELLS; OSMOREGULATORY PROTEIN; MAGNETIC-RESONANCE; INNER MEDULLA; RAT; MYOINOSITOL; SORBITOL; ACCUMULATION RP GARCIAPEREZ, A (reprint author), NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892, USA. NR 69 TC 119 Z9 119 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD JAN PY 1991 VL 119 IS 1 BP 1 EP 13 DI 10.1007/BF01868535 PG 13 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA EQ973 UT WOS:A1991EQ97300001 PM 1901090 ER PT J AU GINSBERG, L GILBERT, DL GERSHFELD, NL AF GINSBERG, L GILBERT, DL GERSHFELD, NL TI MEMBRANE BILAYER ASSEMBLY IN NEURAL TISSUE OF RAT AND SQUID AS A CRITICAL PHENOMENON - INFLUENCE OF TEMPERATURE AND MEMBRANE-PROTEINS SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE BILAYER ASSEMBLY; NEURAL MEMBRANES; CRITICAL TEMPERATURE ID PHOSPHOLIPID SURFACE BILAYERS; AIR-WATER-INTERFACE; BICINCHONINIC ACID; ISOLATED MYELIN; PERMEABILITY; DEPENDENCE; LIPIDS; BRAIN AB Cell membrane bilayers have been reconstructed in vitro utilizing total lipid extracts from rat neural tissue (forebrain, cerebellum, brainstem and spinal cord) and from the optic lobe and fin nerve of the squid Loligo pealei. In agreement with the critical state theory of bilayer assembly (Gershfeld, N.L. 1986. Biophys. J. 50:457-461: Gershfeld, N.L. 1989. J. Phys. Chem. 93:5256-5261), these lipid extracts spontaneously formed purely unilamellar structures in aqueous dispersion, but only at a critical temperature, T*, which was species dependent. For all the rat tissues T* = 37 +/- 1-degrees-C: for squid neural extracts T* = 15.5 +/- 1.4-degrees-C. These values correspond to 'physiological' temperatures for both organisms, implying that their lipid metabolism is geared to permit spontaneous assembly of unilamellar membranes at the ambient temperature in the tissues. Membrane protein composition had little or no effect on critical bilayer formation. C1 NINCDS,BIOPHYS LAB,BETHESDA,MD 20892. RP GINSBERG, L (reprint author), NIAMSK,PHYS BIOL LAB,BETHESDA,MD 20892, USA. RI Ginsberg, Lionel/C-8704-2009 NR 40 TC 14 Z9 14 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD JAN PY 1991 VL 119 IS 1 BP 65 EP 73 DI 10.1007/BF01868541 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA EQ973 UT WOS:A1991EQ97300007 PM 2008012 ER PT J AU ENOMOTO, KI FURUYA, K MAENO, T EDWARDS, C OKA, T AF ENOMOTO, KI FURUYA, K MAENO, T EDWARDS, C OKA, T TI OSCILLATING ACTIVITY OF A CALCIUM-ACTIVATED K+ CHANNEL IN NORMAL AND CANCEROUS MAMMARY CELLS IN CULTURE SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE CA-2+-ACTIVATED K+ CHANNEL; CA-2+ OSCILLATION; INWARD RECTIFICATION; CHARYBDOTOXIN; APAMIN ID EPIDERMAL GROWTH-FACTOR; EPITHELIAL-CELLS; POTASSIUM CHANNELS; SMALL CONDUCTANCE; SKELETAL-MUSCLE; COLLAGEN GELS; RESPONSES; CHARYBDOTOXIN; NEURONS; APAMIN AB Calcium-activated potassium channels were the channels most frequently observed in primary cultured normal mammary cell and in the established mammary tumor cell, MMT060562. In both cells, single-channel and whole-cell clamp recordings sometimes showed slow oscillations of the Ca2+-gated K+ current. The characteristics of the Ca2+-activated K+ channels in normal and cancerous mammary cells were quite similar. The slope conductances changed from 8 to 70 pS depending on the mode of recording and the ionic composition in the patch electrode. The open probability of this channel increased between 0.1 to 1 mu-M of the intracellular Ca2+, but it was independent of the membrane potential. Charybdotoxin reduced the activity of the Ca2+-activated K+ channel and the oscillation of the membrane current, but apamin had no apparent effect. The application of tetraethylammonium (TEA) from outside and BaCl2 from inside of the cell diminished the activity of the channel. The properties of this channel were different from those of both the large conductance (BK or MAXI K) and small conductance (SK) type Ca2+-activated K+ channels. C1 NIDDKD,MOLEC & CELL BIOL,BETHESDA,MD 20892. NATL INST PHYSIOL SCI,DEPT CELLULAR PHYSIOL,OKAZAKI,AICHI 444,JAPAN. UNIV S FLORIDA,COLL MED,TAMPA,FL 33612. RP ENOMOTO, KI (reprint author), SHIMANE MED UNIV,DEPT PHYSIOL,IZUMO,SHIMANE 693,JAPAN. NR 32 TC 24 Z9 25 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD JAN PY 1991 VL 119 IS 2 BP 133 EP 139 DI 10.1007/BF01871412 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA EU215 UT WOS:A1991EU21500003 PM 1710671 ER PT J AU KUKULJAN, M GONCALVES, AA ATWATER, I AF KUKULJAN, M GONCALVES, AA ATWATER, I TI CHARYBDOTOXIN-SENSITIVE-K(CA) CHANNEL IS NOT INVOLVED IN GLUCOSE-INDUCED ELECTRICAL-ACTIVITY IN PANCREATIC BETA-CELLS SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE CALCIUM-ACTIVATED POTASSIUM CHANNELS; CHARYBDOTOXIN; PANCREATIC BETA-CELL ID CA-2+-ACTIVATED K+-CHANNEL; SINGLE POTASSIUM CHANNELS; INSULIN-SECRETING CELLS; ISLET B-CELLS; HIGH-CONDUCTANCE; CALCIUM; MOUSE; PERMEABILITY; CURRENTS; DEPOLARIZATION AB The effects of charybdotoxin (CTX) on single [Ca2+]i-activated potassium channel (K(Ca)) activity and whole-cell K+ currents were examined in rat and mouse pancreatic beta-cells in culture using the patch-clamp method. The effects of CTX on glucose-induced electrical activity from both cultured beta-cells and beta-cells in intact islets were compared. K(Ca) activity was very infrequent at negative patch potentials (-70 < V(m) < 0 mV), channel activity appearing at highly depolarized V(m). K(Ca) open probability at these depolarized V(m) values was insensitive to glucose (10 and 20 mM) and the metabolic uncoupler 2,4 dinitrophenol (DNP). However, DNP blocked glucose-evoked action potential firing and reversed glucose-induced inhibition of the activity of K+ channels of smaller conductance. The venom from Leiurus quinquestriatus hebreus (LQV) and highly purified CTX inhibited K(Ca) channel activity when applied to the outer aspect of the excised membrane patch. CTX (5.8 and 18 nM) inhibited channel activity by 50 and 100%, respectively. Whole-cell outward K+ currents exhibited an early transient component which was blocked by CTX, and a delayed component which was insensitive to the toxin. The individual spikes evoked by glucose, recorded in the perforated-patch modality, were not affected by CTX (20 nM). Moreover, the frequency of slow oscillations in membrane potential, the frequency of action potentials and the rate of repolarization of the action potentials recorded from pancreatic islet beta-cells in the presence of glucose were not affected by CTX. We conclude that the K(Ca) does not participate in the steady-state glucose-induced electrical activity in rodent pancreatic islets. RP KUKULJAN, M (reprint author), NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. NR 40 TC 58 Z9 59 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD JAN PY 1991 VL 119 IS 2 BP 187 EP 195 DI 10.1007/BF01871418 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA EU215 UT WOS:A1991EU21500009 PM 1710672 ER PT J AU MCCUNE, SK VOIGT, MM AF MCCUNE, SK VOIGT, MM TI REGIONAL BRAIN DISTRIBUTION AND TISSUE ONTOGENIC EXPRESSION OF A FAMILY OF ALPHA-ADRENERGIC RECEPTOR MESSENGER-RNAS IN THE RAT SO JOURNAL OF MOLECULAR NEUROSCIENCE LA English DT Article ID ALPHA-2-ADRENERGIC RECEPTOR; ADRENOCEPTOR HETEROGENEITY; H-3 RAUWOLSCINE; MESSENGER-RNA; BINDING-SITES; CLONING; CDNA; SUBTYPE; CHROMATOGRAPHY; METHYLMERCURY AB Probes derived from three unique alpha-adrenergic receptor cDNA clones were used to examine the mRNA distribution of these receptor subtypes in the brain and peripheral tissues through development. The clones for the three subtypes have been isolated from a rat brain cDNA library and are the rat equivalent of the hamster alpha-1B, the rat homolog of the human alpha-2C10 (platelet), and the rat equivalent of the human alpha-2C4 (kidney). Transcripts for all three receptors are present diffusely throughout the adult rat brain, but there are regional variations that are subtype specific. The brain ontogeny of mRNA expression for the alpha-1B and alpha-2C4 subtypes exhibits an almost linear increase from the neonate to the adult, while the alpha-2C10 mRNA transcript remains constant through postnatal day 8 and then declines into adulthood. Peripheral tissues also demonstrate selective expression of these three receptor subtypes. The alpha-1B receptor is expressed in detectable amounts in all tissues examined except adult kidney, while the alpha-2C10 and alpha-2C4 receptors are more selectively localized; the alpha-2C10 receptor RNA is more prevalent in embryonic tissues. Thus, it appears that receptor subtypes of the same family are expressed differentially throughout the brain and peripheral tissues and that this expression is developmentally regulated in an independent manner. C1 NINCDS,MOLEC BIOL LAB,BETHESDA,MD 20892. RP MCCUNE, SK (reprint author), NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892, USA. NR 42 TC 12 Z9 12 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0895-8696 J9 J MOL NEUROSCI JI J. Mol. Neurosci. PY 1991 VL 3 IS 1 BP 29 EP 37 DI 10.1007/BF02896846 PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA FR810 UT WOS:A1991FR81000004 PM 1653001 ER PT J AU TAN, GT PEZZUTO, JM KINGHORN, AD HUGHES, SH AF TAN, GT PEZZUTO, JM KINGHORN, AD HUGHES, SH TI EVALUATION OF NATURAL-PRODUCTS AS INHIBITORS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 (HIV-1) REVERSE-TRANSCRIPTASE SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID ALKALOIDS; AIDS; POLYMERASES; FAGARONINE; AGENTS AB Inhibition of human immunodeficiency virus reverse transcriptase is currently considered a useful approach in the prophylaxis and intervention of acquired immunodeficiency syndrome (AIDS), and natural products have not been extensively explored as inhibitors of this enzyme. We currently report that the reverse transcriptase assay developed for the detection of the enzyme in virions involving polyadenylic acid.oligodeoxythymidylic acid (poly rA.oligo dT) and radiolabeled thymidine 5'-triphosphate (TTP), can be applied as a simple method for screening the human immunodeficiency virus type 1 reverse transcriptase (HIV-1 RT) inhibitory potential of natural products. As reported herein, 156 pure natural products have been examined in this system. Benzophenanthridine alkaloids such as fagaronine chloride [1] and nitidine chloride, which are known inhibitors of avian myeloblastosis virus reverse transcriptase, demonstrated potent activity in the HIV-1 RT system, and 1 (IC50 10-mu-g/ml) was adopted as a positive-control substance. Additional inhibitors found were columbamine iodide [2] and other protoberberine alkaloids, the isoquinoline alkaloid O-methylpsychotrine sulfate [3], and the iridoid fulvoplumierin [4]. A number of indolizidine, pyrrolizidine, quinolizidine, indole, and other alkaloids, as well as compounds of many other structural classes, were tested and found to be inactive. A total of 100 plant extracts have also been evaluated, and 15 of these extracts showed significant inhibitory activity. Because tannins and other polyphenolic compounds are potent reverse transcriptase inhibitors, methods were evaluated for the removal of these from plant extracts prior to testing. Polyphenolic compounds were found to be responsible for the activity demonstrated by the majority of plant extracts. After appropriate tannin removal procedures were established, the bioassay system was shown to be generally applicable to both pure natural products and plant extracts. The method also proved useful in directing an isolation procedure with Plumeria rubra to yield fulvoplumierin [4] as an active compound (IC50 45-mu-g/ml). C1 UNIV ILLINOIS,COLL PHARM,PROGRAM COLLABORAT RES PHARMACEUT SCI,CHICAGO,IL 60612. UNIV ILLINOIS,COLL PHARM,DEPT MED CHEM & PHARMACOGNOSY,CHICAGO,IL 60612. UNIV ILLINOIS,COLL MED,DIV SURG ONCOL,CHICAGO,IL 60612. NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LABS INC,BASIC RES PROGRAM,FREDERICK,MD 21701. OI Kinghorn, A. Douglas/0000-0002-6647-8707 FU NCI NIH HHS [N01-CO-74101] NR 29 TC 213 Z9 218 U1 2 U2 12 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD JAN-FEB PY 1991 VL 54 IS 1 BP 143 EP 154 DI 10.1021/np50073a012 PG 12 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA FD076 UT WOS:A1991FD07600012 PM 1710653 ER PT J AU MURATA, Y YEH, HJC PANNELL, LK JONES, TH FALES, HM MASON, RT AF MURATA, Y YEH, HJC PANNELL, LK JONES, TH FALES, HM MASON, RT TI NEW KETODIENES FROM THE INTEGUMENTAL LIPIDS OF THE GUAM BROWN TREE SNAKE, BOIGA-IRREGULARIS SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; MASS-SPECTROMETRY; GARTER SNAKES; SPECTROSCOPY; SEX AB A mixture of six new long chain ketodienes, (6Z,26Z)-pentatriacontadien-2-one [1], (8Z,26Z)-pentatriacontadien-2-one [2], (6Z,27Z)-hexatriacontadien-2-one [3], (8Z,27Z)-hexatriacontadien-2-one [4], (6Z,28Z)-heptatriacontadien-2-one [5], and (8Z,28Z)-heptatriacontadien-2-one [6], has been separated from the cuticular lipids of the Guam brown tree snake Boiga irregularis. Their structures were determined by chemical and spectral means. C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. NR 18 TC 15 Z9 16 U1 0 U2 1 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD JAN-FEB PY 1991 VL 54 IS 1 BP 233 EP 240 DI 10.1021/np50073a024 PG 8 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA FD076 UT WOS:A1991FD07600024 PM 2045818 ER PT J AU LESCH, KP LERER, B AF LESCH, KP LERER, B TI THE 5-HT RECEPTOR G-PROTEIN EFFECTOR SYSTEM COMPLEX IN DEPRESSION .1. EFFECT OF GLUCOCORTICOIDS SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Article DE GLUCOCORTICOIDS; 5-HT RECEPTORS; GTP-BINDING PROTEINS; DEPRESSION ID NEURO-ENDOCRINE RESPONSES; CORTICOTROPIN-RELEASING-FACTOR; FAWN-HOODED RATS; CORTICOSTERONE SECRETION; PARAVENTRICULAR NUCLEUS; REPEATED IMMOBILIZATION; SEROTONIN RECEPTORS; ADENYLATE-CYCLASE; SUICIDE VICTIMS; FRONTAL-CORTEX AB Hormonal modulation of neurotransmission emerged as a concept from the recognition that adrenocortical steroids exert profound effects at the level of receptors, G-proteins and effector units. G-proteins, a family of guanine nucleotide binding regulatory components that couple neurotransmitter receptors to various types of intracellular effector systems, appear to be a key target of glucocorticoid (GC) action in the CNS. It is thought that G(s)/G(i) mediates stimulation/inhibition of adenylate cyclase (AC system), which forms cyclic AMP as second messenger, while receptors stimulating phospholipase C do so through G(o) to produce two second messengers, inositol 1,4,5-triphosphate and diacylglycerol (PI system). Recent evidence suggests that GC increase G(s-alpha)-and decrease G(i-alpha)-protein subunit expression without affecting G(o-alpha). Activation of central pre- and postsynaptic 5-HT1A receptors which are linked to the G(i) - AC complex, induces hypothermia and ACTH/cortisol release in rodents and humans. Compared with controls, patients with a major depressive disorder exhibit increased basal cortisol secretion associated with decreased hypothermic and ACTH/cortisol responses. The attenuated neuroendocrine and thermoregulatory response to 5-HT1A receptor activation may reflect a GC-dependent feedback inhibition of the hypothalamic-pituitary-adrenal (HPA) system and subsensitivity of the presynaptic 5-HT1A - G(i) - AC complex function. Differential regulation of 5-HT1A and 5-HT2 function leading to a relative 5-HT2 - G(o) - PI complex supersensitivity may maintain HPA hyperactivity during the course of depression. These findings corroborate recent reports that GC, via GC - GC receptor (GR) complex activated promotion of gene transcription, modify the expression 5-HT1A-coupled G(i) (but not 5-HT2-coupled G(o) resulting in altered sensitivity of 5-HT1A-mediated signal transduction and further support the hypothesis of a differential regulation of 5-HT1A and 5-HT2 receptor function and a GC - GR/5-HT1A - G-protein - effector system-related abnormality in depression. C1 UNIV WURZBURG,DEPT PSYCHIAT,W-8700 WURZBURG,GERMANY. YAACOV HERZOG CTR BRAIN & PSYCHIAT RES ERATH NASHIM,JERUSALEM,ISRAEL. RP LESCH, KP (reprint author), NIMH,CTR CLIN,CLIN SCI LAB,10-3D41,BETHESDA,MD 20892, USA. RI Lesch, Klaus-Peter/J-4906-2013 OI Lesch, Klaus-Peter/0000-0001-8348-153X NR 89 TC 55 Z9 57 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1991 VL 84 IS 1-2 BP 3 EP 18 DI 10.1007/BF01249105 PG 16 WC Neurosciences SC Neurosciences & Neurology GA FE172 UT WOS:A1991FE17200001 PM 1647169 ER PT J AU MURPHY, DL SIMS, KB KAROUM, F GARRICK, NA DELACHAPELLE, A SANKILA, EM NORIO, R BREAKEFIELD, XO AF MURPHY, DL SIMS, KB KAROUM, F GARRICK, NA DELACHAPELLE, A SANKILA, EM NORIO, R BREAKEFIELD, XO TI PLASMA AMINE OXIDASE ACTIVITIES IN NORRIE DISEASE PATIENTS WITH AN X-CHROMOSOMAL DELETION AFFECTING MONOAMINE-OXIDASE SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Article DE BENZYLAMINE; DOPAMINE; SEROTONIN; GENETICS ID INHIBITOR-RELATED CHARACTERISTICS; VASCULAR SMOOTH-MUSCLE; BENZYLAMINE OXIDASE; CEREBROSPINAL-FLUID; RAT-BRAIN; CLORGYLINE; METABOLITES; SUBSTRATE; GENE; CATECHOLAMINES AB Two individuals with an X-chromosomal deletion were recently found to lack the genes encoding monoamine oxidase type A (MAO-A) and MAO-B. This abnormality was associated with almost total (90%) reductions in the oxidatively deaminated urinary metabolites of the MAO-A substrate, norepinephrine, and with marked (100-fold) increases in an MAO-B substrate, phenylethylamine, confirming systemic functional consequences of the genetic enzyme deficiency. However, urinary concentrations of the deaminated metabolites of dopamine and serotonin (5-HT) were essentially normal. To investigate other deaminating systems besides MAO-A and MAO-B that might produce these metabolites of dopamine and 5-HT, we examined plasma amine oxidase (AO) activity in these two patients and two additional patients with the same X-chromosomal deletion. Normal plasma AO activity was found in all four Norrie disease-deletion patients, in four patients with classic Norrie disease without a chromosomal deletion, and in family members of patients from both groups. Marked plasma amine metabolite abnormalities and essentially absent platelet MAO-B activity were found in all four Norrie disease-deletion patients, but in none of the other subjects in the two comparison groups. These results indicate that plasma AO is encoded by gene(s) independent of those for MAO-A and MAO-B, and raise the possibility that plasma AO, and perhaps the closely related tissue AO, benzylamine oxidase, as well as other atypical AOs or MAOs encoded independently from MAO-A and MAO-B may contribute to the oxidative deamination of dopamine and 5-HT in humans. C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MOLEC NEUROGENET,WALTHAM,MA. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT NEUROL,BOSTON,MA 02114. NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,WASHINGTON,DC 20032. UNIV HELSINKI,DEPT MED GENET,SF-00100 HELSINKI 10,FINLAND. VAESTOELIITTO,DEPT MED GENET,HELSINKI,FINLAND. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. RP MURPHY, DL (reprint author), NIMH,CLIN SCI LAB,CTR CLIN,10-3D41,BETHESDA,MD 20892, USA. FU NICHD NIH HHS [HD00824]; NINDS NIH HHS [NS21921] NR 57 TC 29 Z9 32 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1991 VL 83 IS 1-2 BP 1 EP 12 DI 10.1007/BF01244447 PG 12 WC Neurosciences SC Neurosciences & Neurology GA ER309 UT WOS:A1991ER30900001 PM 2018626 ER PT J AU OREN, DA AF OREN, DA TI RETINAL MELATONIN AND DOPAMINE IN SEASONAL AFFECTIVE-DISORDER SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Article DE WINTER; DEPRESSION; EYE; LIGHT; PHOTOTHERAPY ID SEROTONIN N-ACETYLTRANSFERASE; TYROSINE-HYDROXYLASE ACTIVITY; LIGHT THERAPY; PHOTOTHERAPY; EYE; ANTIDEPRESSANT; INHIBITION; HYPOTHESIS; SECRETION; TIME AB The author describes how phototherapy may treat seasonal affective disorder (SAD) by stimulating the production of retinal dopamine and suppressing the production of retinal melatonin. This hypothesis offers a framework in which winter-induced retinal dopamine deficiency or retinal melatonin overactivity may cause SAD and by which light reverses this syndrome. This hypothesis is consistent with recent data indicating that phototherapy in SAD acts specifically through the eyes. RP OREN, DA (reprint author), NIMH,CLIN PSYCHOL,BLDG 10,ROOM 45239,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 69 TC 25 Z9 25 U1 0 U2 1 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1991 VL 83 IS 1-2 BP 85 EP 95 DI 10.1007/BF01244455 PG 11 WC Neurosciences SC Neurosciences & Neurology GA ER309 UT WOS:A1991ER30900009 PM 2018631 ER PT J AU DECKERT, J JORGENSEN, MB AF DECKERT, J JORGENSEN, MB TI POSTSYNAPTIC AND PRESYNAPTIC LESIONS IN THE CA1 REGION OF HIPPOCAMPUS - EFFECT ON [H-3] FORSKOLIN AND [H-3] PHORBOLDIBUTYRATE ESTER BINDING SO JOURNAL OF NEURAL TRANSMISSION-GENERAL SECTION LA English DT Article DE LOCALIZATION; ADENYLATE CYCLASE; PROTEIN KINASE-C; HIPPOCAMPUS; CA1 PYRAMIDAL CELLS ID PROTEIN KINASE-C; RAT-BRAIN; CYCLIC-AMP; CEREBRAL-ISCHEMIA; AUTORADIOGRAPHIC ANALYSIS; RECEPTOR; SLICES; 12,13-DIBUTYRATE; ACCUMULATION; LOCALIZATION AB The effect of transient cerebral ischemia and intraventricular injection of kainic acid on adenylate cyclase and protein kinase C as labeled by [H-3]forskolin ([H-3]FOR) and [H-3]phorboldibutyrate ester ([H-3]PDBU) in several rat brain microregions was investigated in a quantitative autoradiographic study. Four days after transient four vessel occlusion a 80% loss of [H-3]FOR and a 35% loss of [H-3]PDBU binding could be measured in the CA1 stratum radiatum of operated Wistar rats as compared to control rats. Four days after intraventricular injection of kainic acid only a marginal loss of [H-3]FOR and a 30% increase of [H-3]PDBU binding was seen in the CA1 stratum radiatum while in the CA3 stratum lucidum and radiatum respectively a 30% loss of [H-3]FOR and no significant change in [H-3]PDBU binding was observed. As transient cerebral ischemia and intraventricular kainic acid injection are depleting the hippocampal CA1 region of CA1 pyramidal cells and axons of CA3 pyramidal cells respectively in rat brain, these findings strongly suggest that both adenylate cyclase and protein kinase C are localized in CA1 pyramidal cells of rat hippocampus. C1 NIMH,BPB,NEUROCHEM UNIT,BETHESDA,MD 20892. UNIV COPENHAGEN,INST NEUROPATHOL,PHARMABIOTEC RES CTR,DK-1168 COPENHAGEN,DENMARK. RP DECKERT, J (reprint author), UNIV WURZBURG,NERVEN KLIN,FUCHSLEINSTR 15,W-8700 WURZBURG,GERMANY. RI Jorgensen, Martin Balslev/K-5758-2012 OI Jorgensen, Martin Balslev/0000-0002-1321-8901 NR 27 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM-GEN JI J. Neural Transm.-Gen. Sect. PY 1991 VL 83 IS 3 BP 205 EP 214 DI 10.1007/BF01253390 PG 10 WC Neurosciences SC Neurosciences & Neurology GA EZ537 UT WOS:A1991EZ53700005 PM 2031710 ER PT J AU PRELL, GD KHANDELWAL, JK BURNS, RS BLANDINA, P MORRISHOW, AM GREEN, JP AF PRELL, GD KHANDELWAL, JK BURNS, RS BLANDINA, P MORRISHOW, AM GREEN, JP TI LEVELS OF PROS-METHYLIMIDAZOLEACETIC ACID - CORRELATION WITH SEVERITY OF PARKINSONS-DISEASE IN CSF OF PATIENTS AND WITH THE DEPLETION OF STRIATAL DOPAMINE AND ITS METABOLITES IN MPTP-TREATED MICE SO JOURNAL OF NEURAL TRANSMISSION-PARKINSONS DISEASE AND DEMENTIA SECTION LA English DT Article DE PARKINSONS DISEASE; PROS-METHYLIMIDAZOLEACETIC ACID; MPTP; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; DOPAMINE; DOPAMINE METABOLITES; HOMOVANILLIC ACID; DOPAC; NOREPINEPHRINE ID PERFORMANCE LIQUID-CHROMATOGRAPHY; PRIMARY OLFACTORY PATHWAY; RAT-BRAIN; REGIONAL DISTRIBUTION; CEREBROSPINAL-FLUID; 3-METHYLHISTIDINE EXCRETION; HISTAMINE TURNOVER; AMINO-ACIDS; CELL LOSS; CARNOSINE AB The cerebrospinal fluid (CSF) levels of pros-methylimidazoleacetic acid (p-MIAA) in thirteen medication-free patients with mild to moderate Parkinson's disease were highly correlated (Spearman's rho = 0.749, p < 0.005) with the severity of signs of the disease as scored on the Columbia University Rating Scale. Levels of p-MIAA in males (n = 8) and females (n = 5) were each significantly correlated with scores of severity (rho = 0.78, p < 0.05 and rho = 1.0, p < 0.05, respectively). In C57BL/6 mice treated with 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP), levels of p-MIAA were significantly correlated with the depleted levels of dopamine (r = 0.85, p < 0.01), homovanillic acid (r = 0.79, p < 0.02), 3,4-dihydroxyphenylacetic acid (r = 0.84, p < 0.01) and norepinephrine (r = 0.91, p < 0.002) in striatum, but not in cortex of the same mice. No such correlations were observed in either striatum or cortex of saline-treated control mice. Mean levels of p-MIAA in CSF did not differ significantly between patients and age-matched controls; and mean levels of p-MIAA in striatum did not differ between MPTP-treated mice and controls. The simplest hypothesis to account for these strong correlations in the absence of differences in mean levels of p-MIAA is that accumulation of p-MIAA [or process(es) that govern its accumulation] influences a failing nigrostriatal system. It is also possible (in analogy with findings in other diseases and with other drugs) that measurements of the putative metabolite(s) of p-MIAA may distinguish the patients and the MPTP-treated mice from their respective controls. Elucidation of the processes that regulate formation and disposition of p-MIAA in brain and information on the neural effects of p-MIAA, its precursors and its putative metabolites may yield insight into factors that regulate the progression of Parkinson's disease, and may shed additional light on the cause(s) of this disease. C1 CUNY MT SINAI SCH MED,DEPT PHARMACOL,BOX 1215,NEW YORK,NY 10029. NIMH,EXPTL THERAPEUT SECT,BETHESDA,MD 20892. FU NIMH NIH HHS [MH-31805]; NINDS NIH HHS [NS-28012] NR 93 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0936-3076 J9 J NEURAL TRANSM-PARK JI J. Neural Transm.-Park. Dis. Dement. Sect. PY 1991 VL 3 IS 2 BP 109 EP 125 DI 10.1007/BF02260886 PG 17 WC Clinical Neurology SC Neurosciences & Neurology GA GB306 UT WOS:A1991GB30600004 PM 1910485 ER PT J AU MCINTYRE, T SKOLNICK, P AF MCINTYRE, T SKOLNICK, P TI TERT-[S-35]BUTYLBICYCLOPHOSPHOROTHIONATE BINDING UNDER EQUILIBRIUM AND NONEQUILIBRIUM CONDITIONS - DIFFERENTIAL-EFFECTS OF BARBITURATES AND GAMMA-AMINOBUTYRIC-ACID IN THE LONG-SLEEP AND SHORT-SLEEP SELECTED MOUSE LINES SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE PHENOBARBITAL; PENTOBARBITAL; ETHANOL; GAMMA-AMINOBUTYRIC ACID; TERT-BUTYLBICYCLOPHOSPHOROTHIONATE; CHLORIDE CHANNELS; SELECTED LINES ID RECEPTOR-IONOPHORE COMPLEX; CHLORIDE CHANNEL COMPLEX; SELECTIVELY-BRED MICE; BENZODIAZEPINE RECEPTORS; ETHANOL; DEPRESSANT; ALCOHOL; SITES; RAT; TERT-BUTYLBICYCLOPHOSPHOROTHIONATE AB Significant differences were demonstrated between the long-sleep (LS) and short-sleep (SS) selected mouse lines in the abilities of barbiturates and gamma-aminobutyric acid (GABA) to inhibit t-[S-35]butylbicyclophosphorothionate ([S-35]TBPS) binding to well-washed cerebral cortical membranes. Thus, using phenobarbital to initiate the dissociation of [S-35]TBPS, the extent of inhibition was significantly greater in LS mice (but not SS mice) than would be predicted using equilibrium conditions. Pentobarbital had the opposite effect, causing ]S-35[TBPS to dissociate to a greater extent in SS than LS membranes. [S-35]TBPS binding was dissociated from LS and SS membranes by GABA to a greater and lesser extent, respectively, than would be predicted from equilibrium studies. Because no line differences in the potencies of these drugs to inhibit [S-35]TBPS binding were found using equilibrium conditions, these results indicate that the association rates of barbiturates and GABA may be different between these lines. These findings are consistent with neurochemical studies indicating differences in the benzodiazepine/GABA receptor-chloride channel complex in these selected lines and may explain their differential sensitivities to certain agents acting through this supramolecular complex. RP MCINTYRE, T (reprint author), NIDDK,NEUROSCI LAB,BLDG 8,ROOM 105,BETHESDA,MD 20892, USA. NR 38 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1991 VL 56 IS 1 BP 287 EP 293 DI 10.1111/j.1471-4159.1991.tb02594.x PG 7 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA EP043 UT WOS:A1991EP04300040 PM 1846173 ER PT J AU TSUTSUMI, K SAAVEDRA, JM AF TSUTSUMI, K SAAVEDRA, JM TI QUANTITATIVE AUTORADIOGRAPHY REVEALS DIFFERENT ANGIOTENSIN-II RECEPTOR SUBTYPES IN SELECTED RAT-BRAIN NUCLEI SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE ANGIOTENSIN ANTAGONIST; SUBFORNICAL ORGAN; PARAVENTRICULAR NUCLEUS; INFERIOR OLIVE; RECEPTOR CLASSIFICATION ID BINDING-SITES; PARAVENTRICULAR NUCLEUS; SUBFORNICAL ORGAN; HYPERTENSIVE RATS AB Heterogeneity of rat brain angiotensin II receptors was revealed by quantitative autoradiography after incubation with I-125-Sar1-angiotensin II and displacement with the angiotensin II antagonists CGP 42112 A and DuP-753 and by receptor sensitivity to dithiothreitol. Receptors in areas involved in cardiovascular and fluid control-the subfornical organ, nucleus of the solitary tract, paraventricular nucleus, and area postrema-are displaced by DuP-753 with an IC50 of 1 x 10(-7) M, are sensitive to 5 mM dithiothreitol, and thus are angiotensin II type-1. Receptors in the inferior olive are displaced by CGP 42112 A (IC50, 1 x 10(-9)) but not by DuP-753 in concentrations up to 10(-4) M, are insensitive to 5 mM dithiothreitol, and thus are angiotensin II type-2. C1 NIMH,CLIN SCI LAB,PHARMACOL SECT,BLDG 10,ROOM 2D-45,BETHESDA,MD 20892. NR 16 TC 142 Z9 143 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1991 VL 56 IS 1 BP 348 EP 351 DI 10.1111/j.1471-4159.1991.tb02602.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA EP043 UT WOS:A1991EP04300048 PM 1987323 ER PT J AU DEGEORGE, JJ NARIAI, T YAMAZAKI, S WILLIAMS, WM RAPOPORT, SI AF DEGEORGE, JJ NARIAI, T YAMAZAKI, S WILLIAMS, WM RAPOPORT, SI TI ARECOLINE-STIMULATED BRAIN INCORPORATION OF INTRAVENOUSLY ADMINISTERED FATTY-ACIDS IN UNANESTHETIZED RATS SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE ARACHIDONATE; FATTY ACIDS; CHOLINERGIC STIMULATION; BRAIN; METABOLISM; ARECOLINE ID CENTRAL NERVOUS-SYSTEM; C62B GLIOMA-CELLS; ARACHIDONIC-ACID; PHOSPHOINOSITIDE HYDROLYSIS; CHOLINERGIC STIMULATION; PHOSPHATIDIC-ACID; METABOLISM; MOBILIZATION; ACTIVATION; PHOSPHOLIPASE-A2 AB Brain incorporation of [1-C-14]arachidonate ([C-14]AA; 170 mu-Ci/kg), [1-C-14]docosahexaenoate ([C-14]DA; 100 mu-Ci/kg), or [9,10-H-3]palmitate ([H-3]PA; 6.4 mCi/kg) infused intravenously for 5 min was examined in the awake rat following systemic administration of the cholinomimetic arecoline (15 mg/kg i.p.). The rat was killed 15 min after infusion, and the brain was removed, frozen, and prepared for biochemical analysis and autoradiography. Brain radioactivity, normalized for plasma exposure, was increased by 41 and 45% in arecoline-treated rats given [C-14]AA and [C-14]DA, respectively. Pretreatment with atropine prevented the increase in fatty acid incorporation. Arecoline treatment had no effect on brain incorporation of [H-3]PA. Quantitative autoradiography indicated regionally selective increases in brain [C-14]AA and [C-14]DA incorporation in response to arecoline. The results suggest that intravenously administered radiolabeled fatty acids can be used to study neurotransmitter-stimulated brain lipid metabolism in vivo. RP NIA, NEUROSCI LAB, BLDG 10, ROOM 6C103, BETHESDA, MD 20892 USA. NR 25 TC 109 Z9 110 U1 0 U2 1 PU WILEY PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0022-3042 EI 1471-4159 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1991 VL 56 IS 1 BP 352 EP 355 DI 10.1111/j.1471-4159.1991.tb02603.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA EP043 UT WOS:A1991EP04300049 PM 1824784 ER PT J AU WITT, DM CARTER, CS INSEL, TR AF WITT, DM CARTER, CS INSEL, TR TI OXYTOCIN RECEPTOR-BINDING IN FEMALE PRAIRIE VOLES - ENDOGENOUS AND EXOGENOUS ESTRADIOL STIMULATION SO JOURNAL OF NEUROENDOCRINOLOGY LA English DT Article DE OXYTOCIN RECEPTORS; ANTERIOR OLFACTORY NUCLEUS; INVITRO AUTORADIOGRAPHY; PRAIRIE VOLE; RAT ID VENTROMEDIAL HYPOTHALAMIC NUCLEUS; MICROTUS-OCHROGASTER; LORDOSIS BEHAVIOR; POSTPARTUM ESTRUS; OVARIAN HORMONES; SEXUAL-BEHAVIOR; ESTROUS-CYCLE; RAT-BRAIN; VASOPRESSIN; PROGESTERONE AB Previous studies have demonstrated that oxytocin receptors in specific nuclei of rat forebrain are regulated by gonadal steroids. The current study used in vitro receptor autoradiography to investigate the distribution and regulation of oxytocin receptors in the forebrain of the female prairie vole (Microtus ochrogaster). In contrast to rats, in female prairie voles gonadal steroid secretion and oestrus behaviour result from male chemosignal stimulation and ovulation is induced by mating. Thus, the prairie vole brain provides an opportunity for investigating links between environmental stimuli, gonadal steroids and oxytocin receptors. Using a selective oxytocin receptor ligand [I-125]d(CH2)5[Tyr(Me)2,Tyr-NH2(9)]ornithine vasotocin I-125]OTA), specific binding was found in several regions including the anterior olfactory nucleus, the ventromedial nucleus of the hypothalamus, the bed nucleus of the stria terminalis, the amygdala and several cortical areas. Following ovariectomy, oestradiol benzoate (10-mu-g) administration increased oxytocin receptor binding 100% in the anterior olfactory nucleus, but did not affect receptors in other regions. Gonadally-intact females, exposed to male chemosignals, had significant increases in both endogenous oestradiol levels and anterior olfactory nucleus oxytocin receptor binding relative to gonadally-intact females unexposed to male chemosignals. Following prolonged exposure to males with ad libitum mating, [I-125]OTA receptor binding decreased to the levels found in unstimulated females. These results demonstrate that increases in oestrogen levels, of either exogenous or endogenous origin, can modulate oxytocin receptors in the brains of female prairie voles. In contrast to rats, oestrogen in female prairie voles appears to affect receptors in the anterior olfactory nucleus rather than the hypothalamus. We suggest that the species differences in oxytocin receptor distribution and gonadal steroid responsiveness reflect variations in reproductive physiology and possibly behaviour. C1 UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742. RP WITT, DM (reprint author), NIMH,CLIN SCI LAB,COMPARAT STUDIES BRAIN & BEHAV SECT,POB 289,POOLESVILLE,MD 20837, USA. NR 28 TC 65 Z9 65 U1 1 U2 6 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0953-8194 J9 J NEUROENDOCRINOL JI J. Neuroendocrinol. PY 1991 VL 3 IS 2 BP 155 EP 161 DI 10.1111/j.1365-2826.1991.tb00258.x PG 7 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA FL131 UT WOS:A1991FL13100009 PM 19215517 ER PT J AU VERBALIS, JG HOFFMAN, GE ROSENBAUM, LC NILAVER, G LOH, YP AF VERBALIS, JG HOFFMAN, GE ROSENBAUM, LC NILAVER, G LOH, YP TI GENERATION AND CHARACTERIZATION OF AN ANTISERUM DIRECTED AGAINST NEUROHYPOPHYSEAL PROHORMONES SO JOURNAL OF NEUROENDOCRINOLOGY LA English DT Article DE NEUROHYPOPHYSIS; NEUROPHYSIN; PROHORMONES; OXYTOCIN; VASOPRESSIN ID MAGNOCELLULAR NEUROSECRETORY-SYSTEM; SMALL CELL-CARCINOMA; ARGININE VASOPRESSIN; LUTEINIZING-HORMONE; TUMOR-MARKERS; NEUROPHYSIN; PRECURSOR; NEURONS; LUNG; RAT AB An antiserum to neurohypophyseal prohormones was generated by immunization of rabbits with a synthetic peptide fragment bridging the prohormone cleavage site between the vasopressin (AVP) and human AVP-neurophysin sequences of pro-pressophysin. Polyclonal antibodies directed against this peptide cross-reacted with intact human pro-pressophysin (ED50 of 260 fmol), but not with either of the final products of enzymatic processing, AVP and human AVP-neurophysin. Gel electrophoresis and Western immunoblotting of pituitary or hypothalamic extracts from multiple species including mouse, cow and man identified a protein band of molecular weight consistent with intact pro-pressophysin; in hypothalamic extracts from normally-hydrated rats no protein bands were stained, but in extracts from Brattleboro rats a faint band in the area of pro-oxyphysin was identified. Immunohistochemical studies using the antiserum demonstrated the presence of only very small amounts of immunoreactive prohormone in a few widely scattered cells in the hypothalami of normally-hydrated rats. However, after 5 days of solute loading with 2% NaCl as drinking solution, staining for intact prohormone was prominent in the supraoptic and paraventricular nuclei of the hypothalamus. Combined immunoperoxidase-immunofluorescence labeling for prohormone and either AVP-neurophysin or oxytocin-neurophysin revealed prohormone staining in both types of magnocellular neurons in rat hypothalami. These studies suggest that during states of accelerated synthesis and secretion of neurohypophyseal hormones some accumulation of intact prohormone occurs in both AVP and oxytocin magnocellular neurons. C1 UNIV PITTSBURGH,DEPT PHYSIOL,PITTSBURGH,PA 15261. OREGON HLTH SCI UNIV,DEPT BIOCHEM,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DIV NEUROSURG,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT CELL BIOL & ANAT,PORTLAND,OR 97201. NICHHD,DEV BIOL LAB,CELLULAR NEUROBIOL SECT,BETHESDA,MD 20892. RP VERBALIS, JG (reprint author), UNIV PITTSBURGH,DEPT MED,930 SCAIFE HALL,PITTSBURGH,PA 15261, USA. NR 35 TC 5 Z9 5 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0953-8194 J9 J NEUROENDOCRINOL JI J. Neuroendocrinol. PY 1991 VL 3 IS 3 BP 267 EP 272 DI 10.1111/j.1365-2826.1991.tb00274.x PG 6 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA FX400 UT WOS:A1991FX40000007 PM 19215463 ER PT J AU MERCHENTHALER, I CULLER, MD NEGROVILAR, A AF MERCHENTHALER, I CULLER, MD NEGROVILAR, A TI LOCALIZATION OF INHIBIN ALPHA-SUBUNIT IMMUNOREACTIVITY IN THE RAT ADRENAL-CORTEX SO JOURNAL OF NEUROENDOCRINOLOGY LA English DT Article DE INHIBIN; IMMUNOCYTOCHEMISTRY; ADRENAL CORTEX ID PORCINE FOLLICULAR-FLUID; SEQUENCE-ANALYSIS; OVARIAN INHIBINS; HUMAN-PLACENTA; BETA-A; EXPRESSION; SECRETION; PROTEIN; CLONING; TISSUES AB Inhibin, a water soluble, non-steroidal glycoprotein hormone that inhibits follicle-stimulating hormone secretion, is produced by the gonads and several non-gonadal tissues (placenta, pituitary and brain). This study describes the presence of inhibin alpha-chain-immunoreactive cells in the adrenal cortex of intact adult male rats and the effects of hypophysectomy and adrenocorticotropin treatment on the expression of inhibin in that gland. In intact rats, the majority of the immunoreactive cells were found scattered in the zona glomerulosa and reticularis. The zona fasciculata contained only a few cells immunopositive for the inhibin alpha-chain. No immunoreactive cells were found in the medulla. Hypophysectomy resulted in a dramatic reduction in alpha-subunit immunoreactivity with only scattered cells observed in the zona glomerulosa and reticularis (0 to 2 cells/section). No immunoreactive cells were found in the zona fasciculata or the medulla. Following supraphysiologic adrenocorticotropin administration to hypophysectomized animals, the number of inhibin alpha-chain-immunoreactive cells significantly increased in each zone of the adrenal cortex. The most prominent changes were seen in the zona reticularis. Interestingly, in the adrenocorticotropin-treated animals scattered immunopositive cells were also present in the medulla. Our results suggest that inhibin-related peptide(s) exist within the adrenal gland and that the expression of these peptides is regulated by adrenocorticotropin. Inhibin-related peptide(s) may, therefore, play a paracrine and/or endocrine role in the adrenal function. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,REPROD NEUROENDOCRINOL SECT,RES TRIANGLE PK,NC 27709. RP MERCHENTHALER, I (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,FUNCT MORPHOL SECT,MAIL DROP C4-07,RES TRIANGLE PK,NC 27709, USA. NR 27 TC 2 Z9 2 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0953-8194 J9 J NEUROENDOCRINOL JI J. Neuroendocrinol. PY 1991 VL 3 IS 4 BP 425 EP 428 DI 10.1111/j.1365-2826.1991.tb00298.x PG 4 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA GE768 UT WOS:A1991GE76800013 PM 19215487 ER PT J AU LITVAN, I MOHR, E WILLIAMS, J GOMEZ, C CHASE, TN AF LITVAN, I MOHR, E WILLIAMS, J GOMEZ, C CHASE, TN TI DIFFERENTIAL MEMORY AND EXECUTIVE FUNCTIONS IN DEMENTED PATIENTS WITH PARKINSONS AND ALZHEIMERS-DISEASE SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID CLINICOPATHOLOGICAL CORRELATIONS; SUBCORTICAL DEMENTIA; COGNITIVE IMPAIRMENT; DYSFUNCTION; DEFICITS AB Selected aspects of verbal memory and executive function were compared in 11 demented Parkinson's disease (PD) patients and 11 Alzheimer's disease (AD) patients with equally severe dementia, with 11 healthy controls matched for age and education. Semantic and episodic memory were impared in all patients compared with controls, but to a relatively greater degree in AD patients than in those with PD. In contrast, demented PD patients were relatively more compromised on executive tasks. These findings, taken in the context of the neuropathological and neurochemical overlap between demented PD and AD patients, suggest that differences in neurobehavioural patterns in patients with these diseases are relative, rather than absolute. C1 NINCDS,EXPTL THERAPEUT BRANCH,BLDG 10,ROOM 5C103,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892. OI Litvan, Irene/0000-0002-3485-3445 NR 52 TC 83 Z9 84 U1 2 U2 7 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD JAN PY 1991 VL 54 IS 1 BP 25 EP 29 DI 10.1136/jnnp.54.1.25 PG 5 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA ET337 UT WOS:A1991ET33700005 PM 2010755 ER PT J AU FIELDS, RD YU, C NELSON, PG AF FIELDS, RD YU, C NELSON, PG TI CALCIUM, NETWORK ACTIVITY, AND THE ROLE OF NMDA CHANNELS IN SYNAPTIC PLASTICITY INVITRO SO JOURNAL OF NEUROSCIENCE LA English DT Article ID LONG-TERM POTENTIATION; D-ASPARTATE RECEPTORS; INOSITOL PHOSPHOLIPID-METABOLISM; HIPPOCAMPAL SLICE PREPARATION; OCULAR DOMINANCE COLUMNS; EXCITATORY AMINO-ACIDS; CENTRAL NERVOUS-SYSTEM; MOUSE CENTRAL NEURONS; KITTEN VISUAL-CORTEX; CULTURED SPINAL-CORD AB Functionally effective neuronal circuits are constructed through a competitive process that requires patterned neuronal activity elicited by structured input from the environment. To explore the mechanisms of this activity-dependent synaptic restructuring, we have developed an in vitro preparation of mouse spinal cord neurons maintained in a 3-chambered cell-culture system. Sensory afferents that received chronic electrical stimulation for 3-5 d developed stronger synaptic connections than unstimulated afferents converging onto the same postsynaptic spinal cord neuron. Exposure to 100-mu-M DL-2-amino-5-phosphonovaleric acid (APV), an antagonist of the NMDA channel, during the stimulation period prevented the competitive advantage associated with electric stimulation. However, when APV was applied with a higher concentration of calcium (3 mM), activity-dependent synaptic plasticity was no longer inhibited by the NMDA receptor antagonist. This reversal of APV block of the plasticity was not impaired by reducing transmitter release with 3 mM magnesium (in addition to 3 mM calcium and APV). A suppressant effect of APV on spontaneous activity was observed, which was attributed to loss of the NMDA component of the EPSP. Activity-dependent plasticity was also blocked if spontaneous activity was suppressed with dilute tetrodotoxin (TTX; 5-10 nM), a dosage that reduces excitability of neurons but is insufficient to block sodium-dependent action potentials. These experiments bring into question how NMDA channel activation is involved in the processes of synaptic remodeling during development. The data suggest that postsynaptic activity is required for synaptic remodeling, but this activity need not involve NMDA receptor activation specifically for activity-evoked synaptic plasticity. Instead, the mechanism for plasticity appears to operate through calcium-dependent processes in general. RP FIELDS, RD (reprint author), NICHHD, DEV NEUROBIOL LAB, BLDG 36, ROOM 2A21, BETHESDA, MD 20892 USA. NR 93 TC 63 Z9 63 U1 2 U2 2 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JAN PY 1991 VL 11 IS 1 BP 134 EP 146 PG 13 WC Neurosciences SC Neurosciences & Neurology GA ER417 UT WOS:A1991ER41700011 PM 1702460 ER PT J AU BAIZER, JS UNGERLEIDER, LG DESIMONE, R AF BAIZER, JS UNGERLEIDER, LG DESIMONE, R TI ORGANIZATION OF VISUAL INPUTS TO THE INFERIOR TEMPORAL AND POSTERIOR PARIETAL CORTEX IN MACAQUES SO JOURNAL OF NEUROSCIENCE LA English DT Article ID MARMOSET CALLITHRIX-JACCHUS; STRIATE PROJECTION ZONE; SQUIRREL-MONKEY SAIMIRI; FRONTAL EYE FIELDS; CORTICAL AREA V4; RHESUS-MONKEY; FUNCTIONAL-PROPERTIES; TOPOGRAPHIC ORGANIZATION; VISUOTOPIC ORGANIZATION; PRELUNATE GYRUS AB It has been proposed that visual information in the extrastriate cortex is conveyed along 2 major processing pathways, a "dorsal" pathway directed to the posterior parietal cortex, underlying spatial vision, and a "ventral" pathway directed to the inferior temporal cortex, underlying object vision. To determine the relative distributions of cells projecting to the 2 pathways, we injected the posterior parietal and inferior temporal cortex with different fluorescent tracers in 5 rhesus monkeys. The parietal injections included the ventral intraparietal (VIP) and lateral intraparietal (LIP) areas, and the temporal injections included the lateral portions of cytoarchitectonic areas TE and TEO. There was a remarkable segregation of cells projecting to the 2 systems. Inputs to the parietal cortex tended to arise either from areas that have been implicated in spatial or motion analysis or from peripheral field representations in the prestriate cortex. By contrast, inputs to the temporal cortex tended to arise from areas that have been implicated in form and color analysis or from central field representations. Cells projecting to the parietal cortex were found in visual area 2 (V2), but only in the far peripheral representations of both the upper and lower visual field. Likewise, labeled cells found in visual areas 3 (V3) and 4 (V4) were densest in their peripheral representations. Heavy accumulations of labeled cells were found in the dorsal parieto-occipital cortex, including the parieto-occipital (PO) area, part A of V3 (V3A), and the dorsal prelunate area (DP). In the superior temporal sulcus, cells were found within several motion-sensitive areas, including the middle temporal area (MT), the medical superior temporal area (MST), the fundus of the superior temporal area (FST), and the superior temporal polysensory area (STP), as well as within anterior portions of the sulcus whose organization is as yet poorly defined. Cells projecting to areas TE and TEO in the temporal cortex were located within cytoarchitectonic area TG at the temporal pole and cytoarchitectonic areas TF and TH on the parahippocampal gyrus, as well as in noninjected portions of area TE buried within the superior temporal sulcus. In the prestriate cortex, labeled cells were found in V2, V3, and V4, but, in contrast to the loci labeled after parietal injections, those labeled after temporal injections were concentrated in the foveal or central field representations. Although few double-labeled cells were seen, 2 regions containing inter-mingles parietal- and temporal-projection cells were area V4 and the cortex at the bottom of the anterior superior temporal sulcus. Based on the results of injections of anterograde tracers in one additional case, the latter region also appears to receive converging inputs from the 2 visual pathways and may therefore be a site of integration of spatial and object information. C1 NIMH,NEUROPSYCHOL LAB,BLDG 9,ROOM 1N107,BETHESDA,MD 20892. FU NIMH NIH HHS [MH42130] NR 121 TC 420 Z9 422 U1 1 U2 22 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JAN PY 1991 VL 11 IS 1 BP 168 EP 190 PG 23 WC Neurosciences SC Neurosciences & Neurology GA ER417 UT WOS:A1991ER41700014 PM 1702462 ER PT J AU CLEMENTS, JD BUZY, JM AF CLEMENTS, JD BUZY, JM TI AUTOMATED IMAGE-ANALYSIS FOR COUNTING UNSTAINED CULTURED NEURONS SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE IMAGE ANALYSIS; CELL CULTURE; NEURONAL DEATH; HUMAN IMMUNODEFICIENCY VIRUS; GLYCOPROTEIN-120 ID SPINAL-CORD CULTURES; QUANTITATIVE-ANALYSIS; ENVELOPE PROTEIN; CELLS; PROCESSOR; PEPTIDE; DEATH AB A fully automated image analysis technique was developed for counting the number of live or fixed, unstained neurones present in a representative region of a cell culture dish. A dish containing cultured mouse hippocampal neurones was placed on the motorized stage of an inverted microscope, and the neurones were visualized using Hoffman modulation contrast optics. The resulting image was digitized, and processed by subtracting the background illumination, low pass filtering, thresholding, then deleting objects whose areas fell outside a specified range. Two threshold levels were used, each with its own area range, and the two resulting binary images were combined. The number of objects in the combined image was counted. The number of cells in each field was also counted manually, and the processing was repeated on a series of 100 fields covering a representative region of the dish. The automated counts were highly correlated with the manual counts for each of the 12 culture dishes examined in this study. The correlation coefficient was calculated for the manual and automated counts from each dish, and the values ranged from 0.91 to 0.97. Six of the dishes were treated with the envelope protein of the human immunodeficiency virus (gp120), which reduces survival of neurones in this system. The six treated dishes were found to have significantly fewer neurones than the six control dishes, using either manual or automated counting techniques. C1 NIH,NEUROPHYSIOL LAB,BETHESDA,MD 20892. NIH,DEV NEUROBIOL LAB,BETHESDA,MD 20892. NR 17 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 J9 J NEUROSCI METH JI J. Neurosci. Methods PD JAN PY 1991 VL 36 IS 1 BP 1 EP 8 DI 10.1016/0165-0270(91)90131-I PG 8 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA EZ940 UT WOS:A1991EZ94000001 PM 1712054 ER PT J AU MASCAGNI, M AF MASCAGNI, M TI A PARALLELIZING ALGORITHM FOR COMPUTING SOLUTIONS TO ARBITRARILY BRANCHED CABLE NEURON MODELS SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE NEURON; BRANCHING; NUMERICAL ALGORITHM; CABLE MODEL; COMPARTMENTAL MODEL AB An algorithm for the solution of branching one-dimensional cable neuron models is presented. The algorithm is based on solving the finite-difference approximations to a cable or compartmental model of a neuron with a time implicit integration scheme. The algorithm solves the linear system of equations that must be solved at each time step with implicit algorithms via an "exact domain decomposition". This domain decomposition allows the solution of the unbranched and branching regions of the neuron to be done separately and permits a wide variety of possible implementations on parallel computers. Similarly, the separation of the straight and branched regions allows the solution of these two problems to be accomplished with linear system algorithms optimized for each class of problems. In contrast to other widely used methods (Hines, M. (1984) Int. J. Biomed. Comput., 15: 69-75), this algorithm can be used with arbitrary branching geometries, even those which contain closed loops. C1 INST DEF ANAL,SUPERCOMP RES CTR,APPLICAT RES GRP,BOWIE,MD 20715. RP MASCAGNI, M (reprint author), NIDDK,MATH RES BRANCH,BLDG 31,ROOM 4B-54,BETHESDA,MD 20892, USA. NR 15 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 J9 J NEUROSCI METH JI J. Neurosci. Methods PD JAN PY 1991 VL 36 IS 1 BP 105 EP 114 DI 10.1016/0165-0270(91)90143-N PG 10 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA EZ940 UT WOS:A1991EZ94000013 PM 2062108 ER PT J AU AGOSTON, DV EIDEN, LE BRENNEMAN, DE AF AGOSTON, DV EIDEN, LE BRENNEMAN, DE TI CALCIUM-DEPENDENT REGULATION OF THE ENKEPHALIN PHENOTYPE BY NEURONAL-ACTIVITY DURING EARLY ONTOGENY SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Note DE ENKEPHALIN; SPINAL CORD; DEVELOPMENT; NEURONAL ACTIVITY; CALCIUM ID MOUSE SPINAL-CORD; PREPROENKEPHALIN MESSENGER-RNA; RAT ADRENAL-MEDULLA; BOVINE CHROMAFFIN CELLS; A GENE-EXPRESSION; PROTEIN KINASE-C; ELECTRICAL-ACTIVITY; NERVOUS-SYSTEM; MEMBRANE DEPOLARIZATION; SYMPATHETIC NEURONS AB Genetic components of the neuronal phenotype are regulated by epigenetic factors-trophic molecules and neuronal activity-during neurodifferentiation. Developing neurons in dissociated cultures of embryonic mouse spinal cord show spontaneous electrical activity for two days with tetrodotoxin (TTX) causes virtually complete down-regulation of preproenkephalin A gene transcripts in embryonic spinal cord cultures. This TTX-induced down-regulation is fully reversed upon reinitiation of neuronal activity (removal of TTX from cultures). This reversible, tetrodotoxin-induced down-regulation of enkephalin mRNA is confined to a restricted period of early neurodevelopment (days 7 to 21 in culture). Since depolarization triggers calcium entry through voltage-activated calcium channels, we have investigated the involvement of calcium in the mechanism of this activity- and age-dependent regulation of preproenkephalin A expression. The selective activation of the L-type of voltage-sensitive calcium channels by a dihydropyridine derivative [(+) 202-791] prevented this TTX-induced down-regulation without reducing methionine enkephalin secretion. This effect was observed only when the drug was applied to electrically active cultures, prior to the addition of TTX. Simultaneous application of (+) 202-791 and TTX, or pretreatment with TTX, failed to prevent TTX-induced down-regulation. Thus, activity-dependent phenotypic plasticity of met-enkephalinergic neurons in spinal cord is: 1) maximum at an early age of neuronal development (< 10 days in culture) and becomes less apparent in old cultures (> 30 days); 2) reversible throughout; and 3) mediated by calcium entry through L-type channels. C1 NICHHD,DEV NEUROBIOL LAB,BLDG 36,RM 2A21,BETHESDA,MD 20892. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. OI Eiden, Lee/0000-0001-7524-944X NR 57 TC 34 Z9 35 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD JAN PY 1991 VL 28 IS 1 BP 140 EP 148 DI 10.1002/jnr.490280115 PG 9 WC Neurosciences SC Neurosciences & Neurology GA EU579 UT WOS:A1991EU57900014 PM 1645773 ER PT J AU BANKIEWICZ, KS PLUNKETT, RJ JACOBOWITZ, DM KOPIN, IJ OLDFIELD, EH AF BANKIEWICZ, KS PLUNKETT, RJ JACOBOWITZ, DM KOPIN, IJ OLDFIELD, EH TI FETAL NONDOPAMINERGIC NEURAL IMPLANTS IN PARKINSONIAN PRIMATES - HISTOCHEMICAL AND BEHAVIORAL-STUDIES SO JOURNAL OF NEUROSURGERY LA English DT Article DE PARKINSONS DISEASE; NEURAL IMPLANTATION; MPTP; DOPAMINE; RHESUS MONKEY ID NERVE GROWTH-FACTOR; FIMBRIA-FORNIX TRANSECTION; ADRENAL-MEDULLA GRAFTS; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE MPTP; ASTROGLIAL PROLIFERATION; DOPAMINERGIC-NEURONS; ROTATIONAL BEHAVIOR; BASAL FOREBRAIN; CELLS-INVITRO; BRAIN INJURY AB Implantation of fetal dopamine-containing tissue into performed cavities in the caudate nucleus of 1-methyl-4-phenyl-1,2,3 6-tetrahydropyridine (MPTP)-induced parkinsonian monkeys leads to behavioral recovery. Recovery may be related to two sources of dopamine: the grafted cells and/or the sprouted fibers from host dopaminergic neurons. The authors undertook this study to determine whether behavioral recovery requires release of dopamine by the implanted tissue, and to establish if nondopaminergic fetal central nervous system implants can induce sprouting of dopamine fibers in the primate brain and cause behavioral recovery. Rhesus monkeys with MPTP-induced hemiparkinsonism or full parkinsonism and a stable neurological deficit were used for this study. Cavities were created in the caudate nuclei anterior to the foramen of Monro via an open microsurgical approach. Fetal cerebellum or spinal cord was implanted into the preformed cavities of three monkeys. Control parkinsonian monkeys showed no recovery. However, implant-induced improvement was stable for up to 6 months after implantation. Sprouted dopaminergic fibers oriented from the ventral striatum and nucleus accumbens were found in the area of the tissue implant in the animals that received fetal grafts but were not present in the control monkeys. It is concluded that brain implants do not need to contain dopamine to induce functional recovery in MPTP-induced parkinsonian primates. Implant-induced and trophic factor-mediated dopaminergic sprouting by the host brain plays a role in the behavioral recovery and may well be responsible for the clinical improvement seen in parkinsonian patients after brain implants. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP BANKIEWICZ, KS (reprint author), NINCDS,CLIN NEUROSCI BRANCH,SURG NEUROL BRANCH,BETHESDA,MD 20892, USA. NR 46 TC 74 Z9 75 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD JAN PY 1991 VL 74 IS 1 BP 97 EP 104 DI 10.3171/jns.1991.74.1.0097 PG 8 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA EP617 UT WOS:A1991EP61700016 PM 1670609 ER PT J AU OTUAMA, LA PHILLIPS, PC SMITH, QR UNO, Y DANNALS, RF WILSON, AA RAVERT, HT LOATS, S LOATS, HA WAGNER, HN AF OTUAMA, LA PHILLIPS, PC SMITH, QR UNO, Y DANNALS, RF WILSON, AA RAVERT, HT LOATS, S LOATS, HA WAGNER, HN TI L-METHIONINE UPTAKE BY HUMAN CEREBRAL-CORTEX - MATURATION FROM INFANCY TO OLD-AGE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID AMINO-ACID TRANSPORT; POSITRON EMISSION TOMOGRAPHY; BLOOD-BRAIN-BARRIER; PROTEIN; INHIBITION; PHENYLKETONURIA; ANALOGS; SYSTEM; INVIVO; PLASMA AB Age-associated changes in amino acid transport from blood to normal frontal cortex were studied using positron emission tomography (PET). Seventeen patients, 1.8-71 yr, were injected intravenously with tracer dosed of [C-11]L-methionine and baseline PET scan was obtained. To assess competitive inhibition of [C-11]L-methionine uptake, patients received wither oral L-phenylalanine or an i.v. infusion of amino acids 1 hr before a second PET study. Uptake of [C-11]L-methionine by frontal cortex decreased seven-fold between 1.8 and 71 yr (r = -0.71; p < 0.05). Blood-to-brain transfer of [C-11]L-methionine, at 4.5 yr, exceeded mean adult values by more than five-fold. Competitive inhibition reduced L-methionine uptake in all patients older than 4.6 yr. These developmental changes parallel findings in animals. The neutral amino acid transport system may modulate human brain amino acid levels to meet changing developmental metabolic needs. C1 JOHNS HOPKINS UNIV HOSP,DEPT RADIOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV HOSP,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV HOSP,DEPT ONCOL,BALTIMORE,MD 21205. NIA,NEUROSCI LAB,BETHESDA,MD 20892. LOATS ASSOCIATES,WESTMINSTER,MD. RI Wilson, Alan/A-1788-2011 FU NCI NIH HHS [CA 32846]; NINDS NIH HHS [NS 15080] NR 33 TC 33 Z9 33 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JAN PY 1991 VL 32 IS 1 BP 16 EP 22 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ER809 UT WOS:A1991ER80900008 PM 1988624 ER PT J AU GOLDSTEIN, DS CHANG, PC SMITH, CB HERSCOVITCH, P AUSTIN, SM EISENHOFER, G KOPIN, IJ AF GOLDSTEIN, DS CHANG, PC SMITH, CB HERSCOVITCH, P AUSTIN, SM EISENHOFER, G KOPIN, IJ TI DOSIMETRIC ESTIMATES FOR CLINICAL POSITRON EMISSION TOMOGRAPHIC SCANNING AFTER INJECTION OF [F-18] 6-FLUORODOPAMINE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID NERVOUS-SYSTEM; ORTHOSTATIC HYPOTENSION; CIRCULATORY CONTROL; NEURONAL UPTAKE; PLASMA; NOREPINEPHRINE; CATECHOLAMINES; NEUROTRANSMITTERS; NORADRENALINE; ISOPRENALINE AB Positron emission tomographic (PET) scanning after systemic i.v. injection of fluorine-18-6-fluorodopamine ([F-18]-6F-DA) is a method for visualizing and measuring regional sympathetic nervous system innervation and function. Based on results of preclinical studies of rats and dogs and on previous literature about the fate of injected tracer-labeled catecholamines, dosimetric estimates for clinical studies are presented here. After injection of 1 mCi of [F-18]-F-DA, the radiation dose would be highest to the wall of the urinary bladder (1.40 rem/mCi), due to accumulation of radioactive metabolites of [F-18]-F-DA in urine. Radioactivity also would accumulate in bile. Organs receiving the next highest dose would be the kidneys (0.9 rem/mCi) and small intestine (0.2 rem/mCi). The parenchymal radiation dose would be lowest in the brain, since there is an effective blood-brain barrier for circulating catecholamines. Radiation doses to all organs after administration of 1 mCi of [F-18]-F-DA to humans would be less than 3 rem and, therefore, within current FDA guidelines. C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,PET SECT,OFF DIRECTOR,BETHESDA,MD 20892. NINCDS,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. BAKER MED RES INST,PRAHRAN,VIC 3181,AUSTRALIA. NR 47 TC 8 Z9 8 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JAN PY 1991 VL 32 IS 1 BP 102 EP 110 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA ER809 UT WOS:A1991ER80900023 PM 1988612 ER PT J AU VAUPEL, DB CONE, EJ AF VAUPEL, DB CONE, EJ TI PHARMACODYNAMIC AND PHARMACOKINETIC ACTIONS OF KETOCYCLAZOCINE ENANTIOMERS IN THE DOG - ABSENCE OF SIGMA-LIKE OR PHENCYCLIDINE-LIKE ACTIVITY SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID CHRONIC SPINAL DOG; DISCRIMINATIVE STIMULUS PROPERTIES; SCHEDULE-CONTROLLED BEHAVIOR; NALORPHINE-LIKE DRUGS; GUINEA-PIG BRAIN; BINDING-SITES; MORPHINE-LIKE; PHARMACOLOGICAL ANALYSIS; N-ALLYLNORMETAZOCINE; OPIATE RECEPTORS AB The effects of the optical isomers and the racemic form of ketocyclazocine (KC) were compared with morphine and U-50,488H in the chronic spinal dog. l-KC and dl-KC produced depression of nociceptive reflexes, miosis, relaxation of the nictitating membrane and sedation, whereas d-KC lacked pharmacological activity. Peak plasma levels and distribution phase half-lives for dl-, l- and d-KC were similar, indicating no major dispositional differences between the isomers of KC despite a trend for d-KC to have a longer elimination half-life, slower plasma clearance and a greater apparent volume of distribution than l-KC. Although a relatively low dose of naltrexone (0.01 mg/kg) was sufficient to shift morphine dose-effect curves to the right, this dose of naltrexone was not sufficient to shift the dose-effect curves of dl-KC to the right. A dose of 1 mg/kg of naltrexone was required, consistent with the view that the effects were mediated by kappa opioid receptors. The overall pharmacological profile of l-KC differed from that of the more selective kappa opioid agonist U-50,488H, which produced both stimulatory and sedative effects. Neither l-KC nor U-50,488H produced pharmacological profiles typical of the sigma agonist d-N-allylnormetazocine or phencyclidine. The data suggest that the pharmacological activity of KC resides in the l-enantiomer, that the effects are kappa opioid receptor-mediated and that the binding of d-KC to haloperidol-sensitive sigma receptors does not produce N-allylnormetazocine- or phencyclidine-like actions in the dog. C1 NIDA,ADDICT RES CTR,CHEM & DRUG METAB LAB,BALTIMORE,MD 21224. RP VAUPEL, DB (reprint author), NIDA,ADDICT RES CTR,NEUROPHARMACOL,POB 5180,BALTIMORE,MD 21224, USA. NR 47 TC 4 Z9 4 U1 2 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD JAN PY 1991 VL 256 IS 1 BP 211 EP 221 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA ET542 UT WOS:A1991ET54200031 PM 1846414 ER PT J AU COHEN, LG ZEFFIRO, T BOOKHEIMER, S WASSERMANN, EM FUHR, P MATSUMOTO, J TORO, C HALLETT, M AF COHEN, LG ZEFFIRO, T BOOKHEIMER, S WASSERMANN, EM FUHR, P MATSUMOTO, J TORO, C HALLETT, M TI REORGANIZATION IN MOTOR PATHWAYS FOLLOWING A LARGE CONGENITAL HEMISPHERIC LESION IN MAN - DIFFERENT IPSILATERAL MOTOR REPRESENTATION AREAS FOR IPSILATERAL AND CONTRALATERAL MUSCLES SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Meeting Abstract C1 NIH,HUMAN CORT PHYSIOL UNIT,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NR 0 TC 16 Z9 16 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PY 1991 VL 438 BP P33 EP P33 PG 1 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA FY486 UT WOS:A1991FY48600031 ER PT J AU LAIRD, JMA BENNETT, GJ AF LAIRD, JMA BENNETT, GJ TI ANESTHETIZED RATS WITH AN EXPERIMENTAL PERIPHERAL MONONEUROPATHY HAVE DECREASED DORSAL-ROOT POTENTIALS (DRPS) AND COMPOUND ACTION-POTENTIALS (CAPS) SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Meeting Abstract C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. NR 2 TC 1 Z9 1 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PY 1991 VL 438 BP P305 EP P305 PG 1 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA FY486 UT WOS:A1991FY48600294 ER PT J AU HARDIN, TA WEHR, TA BREWERTON, T KASPER, S BERRETTINI, W RABKIN, J ROSENTHAL, NE AF HARDIN, TA WEHR, TA BREWERTON, T KASPER, S BERRETTINI, W RABKIN, J ROSENTHAL, NE TI EVALUATION OF SEASONALITY IN 6 CLINICAL POPULATIONS AND 2 NORMAL-POPULATIONS SO JOURNAL OF PSYCHIATRIC RESEARCH LA English DT Article ID AFFECTIVE-DISORDER; LIGHT; MOOD AB The Seasonal Pattern Assessment Questionnaire (SPAQ) was used to evaluate retrospectively self-reported seasonal changes in mood and behavior (seasonality) of two normal and six clinical populations: patients with winter-seasonal affective disorder (SAD), summer-SAD, eating disorders, bipolar affective disorder, major depressive disorder and subsyndromal winter-SAD. The SPAQ successfully discriminated between groups expected to have high seasonality scores, such as winter-SAD, summer-SAD and subsyndromal winter-SAD, and normal controls. Bipolars and major depressives had normal seasonality scores. Patients with eating disorders had unexpectedly high scores. There was a general tendency for all groups to eat and sleep more and to gain weight in the winter. The implications of these findings are discussed. C1 MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC 29425. UNIV BONN,DEPT PSYCHIAT,W-5300 BONN,GERMANY. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. NEW YORK STATE PSYCHIAT INST & HOSP,NEW YORK,NY 10032. RP HARDIN, TA (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,BLDG 10,ROOM 4S 239,9000 ROCKSVILLE PIKE,BETHESDA,MD 20892, USA. NR 23 TC 113 Z9 113 U1 0 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0022-3956 J9 J PSYCHIAT RES JI J. Psychiatr. Res. PY 1991 VL 25 IS 3 BP 75 EP 87 DI 10.1016/0022-3956(91)90001-Q PG 13 WC Psychiatry SC Psychiatry GA GJ464 UT WOS:A1991GJ46400001 PM 1941711 ER PT J AU LUTZ, RA STEINER, FP BENKE, D MERTENS, S MINDER, E VONDERSCHMITT, D AF LUTZ, RA STEINER, FP BENKE, D MERTENS, S MINDER, E VONDERSCHMITT, D TI A COMPUTER-CONTROLLED DEVICE TO FACILITATE STUDIES OF THE KINETICS OF LIGAND-BINDING - BINDING OF DIAZEPAM TO BOVINE BRAIN MEMBRANES SO JOURNAL OF RECEPTOR RESEARCH LA English DT Article; Proceedings Paper CT 4TH SWISS WORKSHOP OF METHODOLOGY IN RECEPTOR RESEARCH CY MAY 06-10, 1990 CL LUCERNE, SWITZERLAND SP CIBA GEIGY, SANDOZ, GIVAUDAN, SCHERING PLOUGH, ICI, PHARM GRP ID BOUND ACETYLCHOLINE-RECEPTOR; TORPEDO-MARMORATA; FLUORESCENCE; AGONIST AB A device to facilitate kinetic receptor filtration assays is described. The receptor containing membranes and the labeled ligand are placed in two separate syringes and are rapidly mixed into a collecting syringe using a pneumatic ram. Shortly after the start of mixing, a pneumatically controlled valve switches the collecting syringe containing the receptor-ligand mixture to the filtration unit. Filtration is performed on glass/microfiber filters or equivalent by pushing the plunger of the collecting syringe by a stepper motor. A valve positioner controlling several valves allows the filtered membranes to be washed and dried by pressure in any user programmable sequence. Further filtration of the receptor-ligand mixture can be programmed at selected time points. The entire system is controlled by an IBM-PC. With this system, the association and dissociation of diazepam from crude bovine-brain membranes has been studied at 4-degrees-C. The dissociation shows a biphasic pattern with half lifes of 1.3 and more than 23 minutes respectively. Association appears to be into a single compartment. C1 NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. UNIV ZURICH,INST PHARMAKOL,CH-8091 ZURICH,SWITZERLAND. RP LUTZ, RA (reprint author), UNIV HOSP ZURICH,INST KLIN CHEM,CH-8091 ZURICH,SWITZERLAND. NR 11 TC 1 Z9 1 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0197-5110 J9 J RECEPTOR RES JI J. Recept. Res. PY 1991 VL 11 IS 1-4 BP 79 EP 89 DI 10.3109/10799899109066390 PG 11 WC Cell Biology SC Cell Biology GA FK030 UT WOS:A1991FK03000006 PM 1886086 ER PT J AU BROWN, JL BUSH, M PACKER, C PUSEY, AE MONFORT, SL OBRIEN, SJ JANSSEN, DL WILDT, DE AF BROWN, JL BUSH, M PACKER, C PUSEY, AE MONFORT, SL OBRIEN, SJ JANSSEN, DL WILDT, DE TI DEVELOPMENTAL-CHANGES IN PITUITARY-GONADAL FUNCTION IN FREE-RANGING LIONS (PANTHERA-LEO-LEO) OF THE SERENGETI PLAINS AND NGORONGORO CRATER SO JOURNAL OF REPRODUCTION AND FERTILITY LA English DT Article DE LION; GNRH; LH; TESTOSTERONE; RECEPTORS; TESTIS; SPERMATOZOA ID TESTICULAR GONADOTROPIN RECEPTORS; HORMONE LH-RH; SEMEN CHARACTERISTICS; MALE-RATS; TESTOSTERONE; PUBERTY; CHEETAH; BULLS; EJACULATE; SECRETION AB Pituitary-gonadal function was examined in male lions free-ranging in the Serengeti Plains or geographically isolated in the Ngorongoro Crater of Tanzania. Lions were classified by age as adult (6.1-9.8 years), young adult (3.3-4.5 years) or prepubertal (1.4-1.6 years, Serengeti Plains only). Each animal was anaesthetized and then bled at 5-min intervals for 100 min before and 140 min after i.v. administration of saline or GnRH (1-mu-g/kg body weight). Basal serum LH and FSH concentrations were similar (P > 0.05) among age classes and between locations. In Serengeti Plains lions, net LH peak concentrations after GnRH were approximately 35% greater (P < 0.05) in prepubertal than in either adult or young adult animals. GnRH-stimulated LH release was similar (P > 0.05) between adult and young adult lions, and these responses were similar (P > 0.05) to those measured in Ngorongoro Crater lions. Basal and GnRH-stimulated testosterone secretion was higher (P < 0.05) in adult than in young adult lions and lowest (P < 0.05) in prepubertal lions. Age-class differences in testosterone production were related directly to the concentrations of LH receptors in the testis (P < 0.05). Basal and GnRH-stimulated testosterone secretion and gonadotrophin receptor concentrations within age classes were similar (P > 0.05) between lions of the Serengeti Plains and Ngorongoro Crater. Lower motility and higher percentages of structurally abnormal spermatozoa were observed in electroejaculates of young adult compared to adult Serengeti Plains males (P < 0.05) and were associated with decreased steroidogenic activity. In contrast, there were no age-related differences in ejaculate characteristics of Ngorongoro Crater lions. Seminal quality in the Crater population was poor in adult and young adult animals and was unrelated to alterations in pituitary or testicular function. In summary, only seminal quality in adult male lions was affected by location, whereas age significantly affected both basal and GnRH-stimulated testosterone secretion and seminal quality (Serengeti Plains only) in sexually mature males. The striking seminal/endocrine differences among pride (breeding) males of different ages raises questions about the impact of age on individual reproductive performance in this species. C1 SMITHSONIAN INST,NATL ZOOL PK,WASHINGTON,DC 20008. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. SAN DIEGO ZOOL SOC,DEPT VET SERV,SAN DIEGO,CA 92112. RP BROWN, JL (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT OBSTET & GYNECOL,BETHESDA,MD 20814, USA. NR 39 TC 22 Z9 22 U1 1 U2 11 PU J REPROD FERTIL INC PI CAMBRIDGE PA 22 NEWMARKET RD, CAMBRIDGE, ENGLAND CB5 8DT SN 0022-4251 J9 J REPROD FERTIL JI J. Reprod. Fertil. PD JAN PY 1991 VL 91 IS 1 BP 29 EP 40 PG 12 WC Reproductive Biology SC Reproductive Biology GA EV278 UT WOS:A1991EV27800004 PM 1899889 ER PT J AU PLATTO, MJ OCONNELL, PG HICKS, JE GERBER, LH AF PLATTO, MJ OCONNELL, PG HICKS, JE GERBER, LH TI THE RELATIONSHIP OF PAIN AND DEFORMITY OF THE RHEUMATOID FOOT TO GAIT AND AN INDEX OF FUNCTIONAL AMBULATION SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE RHEUMATOID ARTHRITIS; FOOT; GAIT; PAIN; FUNCTIONAL ASSESSMENT ID ARTHRITIS; DISEASE; MOTION; KNEE AB We evaluated the relationships among pain, structural deformity of the foot, 4 variables of gait, and an index of functional ambulation in 31 patients with rheumatoid arthritis. We saw significant correlations between the ambulation index and all gait variables (p < 0.005). For the group as a whole, pain in the foot did not correlate with structural deformity. However, when patients were grouped according to the relative preponderance preponderance of pain or deformity and duration of disease, we found correlations between the sites of pain and deformity. Pain in the lower extremity, and the knee or hindfoot separately, showed correlations with functional ambulation. Foot deformity did not correlate with functional ambulation at all. Foot pain correlated well with velocity and especially stride length (p < 0.005), and not as well with cadence and double stance time. Fewer correlations were seen between foot deformity and gait. In general, hindfoot disease was associated with greater impairment of gait and mobility than forefoot disease. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT REHABIL MED,BLDG 10,65235,BETHESDA,MD 20892. UNIV PITTSBURGH,DIV REHABIL MED,PITTSBURGH,PA 15260. NR 23 TC 86 Z9 87 U1 1 U2 2 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD JAN PY 1991 VL 18 IS 1 BP 38 EP 43 PG 6 WC Rheumatology SC Rheumatology GA EW175 UT WOS:A1991EW17500008 PM 2023197 ER PT J AU ATKINSON, JC AF ATKINSON, JC TI LYSOZYME CONCENTRATION IN SALIVA OF PATIENTS WITH SJOGRENS-SYNDROME - REPLY SO JOURNAL OF RHEUMATOLOGY LA English DT Letter ID SECRETORY IMMUNOGLOBULIN; GLANDS RP ATKINSON, JC (reprint author), NIH,BLDG 10,RM IU-14,BETHESDA,MD 20892, USA. NR 4 TC 1 Z9 1 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD JAN PY 1991 VL 18 IS 1 BP 150 EP 151 PG 2 WC Rheumatology SC Rheumatology GA EW175 UT WOS:A1991EW17500042 ER PT J AU GOLD, RS PARCEL, GS WALBERG, HJ LUEPKER, RV PORTNOY, B STONE, EJ AF GOLD, RS PARCEL, GS WALBERG, HJ LUEPKER, RV PORTNOY, B STONE, EJ TI SUMMARY AND CONCLUSIONS OF THE THTM EVALUATION - THE EXPERT WORK GROUP PERSPECTIVE SO JOURNAL OF SCHOOL HEALTH LA English DT Article ID HEALTH PROMOTION; EDUCATION; PREVENTION; DIFFUSION; PROGRAMS; SCHOOLS C1 UNIV TEXAS,HLTH SCI CTR,CTR HLTH PROMOT RES & DEV,HOUSTON,TX 77030. UNIV ILLINOIS,COLL EDUC,CHICAGO,IL 60680. UNIV MINNESOTA,DEPT PUBL HLTH,MINNEAPOLIS,MN 55455. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. RP GOLD, RS (reprint author), UNIV MARYLAND,DEPT HLTH EDUC,HPER BLDG,ROOM 2387,COLLEGE PK,MD 20742, USA. NR 9 TC 13 Z9 14 U1 0 U2 0 PU AMER SCHOOL HEALTH ASSOC PI KENT PA PO BOX 708, KENT, OH 44240 SN 0022-4391 J9 J SCHOOL HEALTH JI J. Sch. Health PD JAN PY 1991 VL 61 IS 1 BP 39 EP 42 PG 4 WC Education & Educational Research; Education, Scientific Disciplines; Health Care Sciences & Services; Public, Environmental & Occupational Health SC Education & Educational Research; Health Care Sciences & Services; Public, Environmental & Occupational Health GA EX414 UT WOS:A1991EX41400009 ER PT J AU CHAE, K JOHNSTON, SH KORACH, KS AF CHAE, K JOHNSTON, SH KORACH, KS TI MULTIPLE ESTROGEN BINDING-SITES IN THE UTERUS - STEREOCHEMISTRY OF RECEPTOR AND NONRECEPTOR BINDING OF DIETHYLSTILBESTROL AND ITS METABOLITES SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article ID RAT UTERUS; ANALOGS; HETEROGENEITY; ENANTIOMERS; SEPARATION; CYTOSOL; PROBES AB Indenestrol A (IA), an oxidative metabolite of the synthetic estrogen diethylstilbestrol (DES), has high binding affinity for estrogen receptor in mouse uterine cytosol but possesses weak biological activity. Racemic mixture of optically active [H-3]indenestrol A (IA-Rac) was separated and purified into individual enantiomers on a semi-preparative scale by HPLC with a Chiralpak OP(+) column. The structure-activity relationship was investigated among the [H-3]IA enantiomers (IA-R and IA-S) and [H-3]DES through direct saturation binding assays using mouse uterine cytosol. Specific binding curves and Scatchard plots were obtained for each [H-3]ligand; DES, IA-Rac, IA-R and IA-S. IA-S enantiomer (K(d) = 0.67) binds to the estrogen receptor with the same affinity as DES (K(d) = 0.71) and four times higher affinity than IA-R (K(d) = 2.56). The number of binding sites for IA-S is approximately the same as estradiol, DES and IA-Rac while IA-R binds far fewer sites than the other ligands. Saturation binding assays indicated that [H-3]DES and [H-3]IA enantiomers exhibited a higher level of non-specific binding to the cytosol receptor compared to estradiol which has a low level of non-specific binding. These binding studies led to the detection of an additional binding component for the stilbestrol compounds in estrogen target tissue cytosol preparations. Sucrose density gradient separation assays under low salt conditions showed that both [H-3]DES and [H-3]IA compounds bound to the 8S form of the receptor, the same as E2. But, in addition both DES and IA bound to another binding component in 4S region. The binding to the 4S component were partially displaced by the addition of excess unlabeled E2 and DES. Further characterization of the 4S component is described. RP CHAE, K (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,RECEPTOR BIOL SECT,POB 12233,RES TRIANGLE PK,NC 27709, USA. OI Korach, Kenneth/0000-0002-7765-418X NR 18 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 0960-0760 J9 J STEROID BIOCHEM JI J. Steroid Biochem. Mol. Biol. PD JAN PY 1991 VL 38 IS 1 BP 35 EP 42 DI 10.1016/0960-0760(91)90398-O PG 8 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA EZ946 UT WOS:A1991EZ94600004 PM 1997122 ER PT J AU HAVERKOS, HW AF HAVERKOS, HW TI INFECTIOUS-DISEASES AND DRUG-ABUSE - PREVENTION AND TREATMENT IN THE DRUG-ABUSE TREATMENT SYSTEM SO JOURNAL OF SUBSTANCE ABUSE TREATMENT LA English DT Article; Proceedings Paper CT EUROPEAN SYMP ON AIDS AND DRUG ABUSE : PROVIDING CARE FOR HIV-INFECTED DRUG USERS CY AUG 28-30, 1990 CL VIENNA, AUSTRIA SP WHO DE INFECTIOUS DISEASES AND DRUG ABUSE; AIDS; HEPATITIS-B VIRUS; SEXUALLY TRANSMITTED DISEASES; TUBERCULOSIS ID HUMAN-IMMUNODEFICIENCY-VIRUS; PLACEBO-CONTROLLED TRIAL; AIDS-RELATED COMPLEX; HIV INFECTION; AZIDOTHYMIDINE AZT; UNITED-STATES; DOUBLE-BLIND; METHADONE; EPIDEMIOLOGY; OUTBREAK AB Several communicable infectious diseases, including AIDS, hepatitis B infection, gonorrhea, syphilis, and tuberculosis, are increasing among drug abusers. Drug abuse treatment programs may be ideal sites to identify those infections and initiate and maintain appropriate medical management. This paper reviews the epidemiology of those infections among drug abusers in the USA, presents rudimentary aspects of medical management of selected infectious diseases, and discusses the need to integrate infectious diseases, drug abuse treatment, and public health approaches if we are to reverse, or at least stabilize, the trends of those diseases. RP HAVERKOS, HW (reprint author), NIDA,DIV CLIN RES,ROOM 10A-38,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 35 TC 32 Z9 32 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0740-5472 J9 J SUBST ABUSE TREAT JI J. Subst. Abus. Treat. PY 1991 VL 8 IS 4 BP 269 EP 275 DI 10.1016/0740-5472(91)90050-K PG 7 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA GX175 UT WOS:A1991GX17500012 PM 1787552 ER PT J AU GREINER, JW SMALLEY, RV BORDEN, EC MARTIN, EW GUADAGNI, F ROSELLI, M SCHLOM, J AF GREINER, JW SMALLEY, RV BORDEN, EC MARTIN, EW GUADAGNI, F ROSELLI, M SCHLOM, J TI APPLICATIONS OF MONOCLONAL-ANTIBODIES AND RECOMBINANT CYTOKINES FOR THE TREATMENT OF HUMAN COLORECTAL AND OTHER CARCINOMAS SO JOURNAL OF SURGICAL ONCOLOGY LA English DT Article DE INTERFERON-GAMMA; TAG-72; RADIOIMMUNOGUIDED SURGERY ID CA-72-4 RADIOIMMUNOASSAY; TUMOR-CELLS; ANTIGEN; B72.3; GENERATION; SPECTRUM; LESIONS; TAG-72; CANCER; GAMMA AB Monoclonal antibodies (MAbs) which recognize a human tumor antigen, termed tumor-associated glycoprotein-72 (TAG-72), have successfully been used to localize primary as well as metastatic colorectal tumor lesions in patients. The localization of the anti-TAG-72 MAbs has also been exploited intraoperatively using a hand-held gamma probe. That procedure, termed radioimmunoguided surgery (RIGS), has identified occult tumors which were not detected using standard external imaging techniques. In another clinical trial, interferon-gamma (IFN-gamma) was administered intraperitoneally to patients diagnosed with either gastrointestinal or ovarian carcinoma with secondary ascites. Analysis of the tumor cells isolated from the malignant ascites revealed a substantial increase in TAG-72 expression on the surface of tumor cells isolated from seven of eight patients. The results provide evidence that the combination of an anti-carcinoma MAb with the administration of a cytokine, such as IFN-gamma, may be an effective approach for the detection and subsequent treatment, of colorectal carcinoma. C1 UNIV WISCONSIN,CTR CLIN CANC,DEPT HUMAN ONCOL,MADISON,WI 53706. OHIO STATE UNIV,COLL MED,DEPT SURG,COLUMBUS,OH 43210. RP GREINER, JW (reprint author), NCI,TUMOR IMMUNOL BIOL LAB,BLDG 10,ROOM 8B07,BETHESDA,MD 20892, USA. RI Martin Jr, Edward/E-3604-2011 NR 15 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 0022-4790 J9 J SURG ONCOL JI J. Surg. Oncol. PY 1991 SU 2 BP 9 EP 13 PG 5 WC Oncology; Surgery SC Oncology; Surgery GA GG967 UT WOS:A1991GG96700003 ER PT J AU GUADAGNI, F ROSELLI, M AMATO, T COSIMELLI, M MANNELLA, E TEDESCO, M GRASSI, A CASALE, V CAVALIERE, F GREINER, JW SCHLOM, J AF GUADAGNI, F ROSELLI, M AMATO, T COSIMELLI, M MANNELLA, E TEDESCO, M GRASSI, A CASALE, V CAVALIERE, F GREINER, JW SCHLOM, J TI CLINICAL-EVALUATION OF SERUM TUMOR-ASSOCIATED GLYCOPROTEIN-72 AS A NOVEL TUMOR-MARKER FOR COLORECTAL-CANCER PATIENTS SO JOURNAL OF SURGICAL ONCOLOGY LA English DT Article DE MONOCLONAL ANTIBODIES; CA72-4 ASSAY; COLORECTAL CANCER; TUMOR MARKER ID MONOCLONAL-ANTIBODY B72.3; CARCINOEMBRYONIC ANTIGEN; TAG-72; CARCINOMA; RADIOIMMUNOASSAY; GENERATION; CELLS; CEA AB A novel tumor marker, tumor-associated glycoprotein-72 (TAG-72), has been identified using monoclonal antibody (MAb) B72.3. Using immunohistochemical techniques, TAG-72 has been found in carcinomas of various origin including colon, stomach, breast, lung, prostate, and ovary, as well as in body fluids. The presence of TAG-72 in serum samples from 260 patients with colorectal disease (malignant or benign) has been evaluated using the CA72-4 assay. Approximately 40% of patients with colorectal cancer exhibit elevated levels of this marker; moreover, the presence of positive levels of TAG-72 significantly correlates with advanced stages of disease, suggesting that TAG-72 may be a good marker of advanced colorectal cancer. Only 2% of the patients diagnosed with colorectal disease had elevated TAG-72 serum levels indicating the high specificity of this marker. A comparative study with carcinoembryonic antigen (CEA) serum levels showed a complementarity of the two tumor markers; in fact, 49.6% of CEA negative cases scored positive for TAG-72. A longitudinal evaluation of TAG-72 serum levels in 31 patients with malignant disease was performed. The results indicate that patients with increasing TAG-72 serum levels postoperatively may be indicative of recurrent disease. In 60% of patients in which significant changes of CEA levels could not be detected, TAG-72 showed rising positive levels prior to clinical evidence of recurrent disease. These results suggest that the simultaneous use of TAG-72 and CEA serum markers may be useful in the diagnosis of recurrent disease and therefore play an important role in the clinical management of cancer patients. C1 REGINA ELENA INST CANC RES,DEPT SURG,I-00161 ROME,ITALY. REGINA ELENA INST CANC RES,DEPT DIGEST ENDOSCOPY,I-00161 ROME,ITALY. UNIV ROME 2,SCH MED,DEPT SURG,ROME,ITALY. NCI,TUMOR IMMUNOL & BIOL,BETHESDA,MD 20892. RP GUADAGNI, F (reprint author), REGINA ELENA INST CANC RES,CLIN PATHOL LAB,VIALE REGINA ELENA 291,I-00161 ROME,ITALY. RI Cavaliere, Francesco/J-7635-2016 OI Cavaliere, Francesco/0000-0001-6501-8648 NR 24 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0022-4790 J9 J SURG ONCOL JI J. Surg. Oncol. PY 1991 SU 2 BP 16 EP 20 PG 5 WC Oncology; Surgery SC Oncology; Surgery GA GG967 UT WOS:A1991GG96700005 ER PT J AU LEFOR, AT ROSENBERG, SA AF LEFOR, AT ROSENBERG, SA TI THE SPECIFICITY OF LYMPHOKINE-ACTIVATED KILLER (LAK) CELLS-INVITRO - FRESH NORMAL MURINE TISSUES ARE RESISTANT TO LAK-MEDIATED LYSIS SO JOURNAL OF SURGICAL RESEARCH LA English DT Article ID PERIPHERAL-BLOOD LYMPHOCYTES; RECOMBINANT INTERLEUKIN-2; ADOPTIVE IMMUNOTHERAPY; TUMOR-CELLS; CANCER; METASTASES; SARCOMAS; GROWTH; LINES RP LEFOR, AT (reprint author), NCI,SURG BRANCH,BETHESDA,MD 20892, USA. RI Lefor, Alan/E-9979-2012 OI Lefor, Alan/0000-0001-6673-5630 NR 28 TC 11 Z9 11 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD JAN PY 1991 VL 50 IS 1 BP 15 EP 23 DI 10.1016/0022-4804(91)90004-6 PG 9 WC Surgery SC Surgery GA EQ968 UT WOS:A1991EQ96800003 PM 1987427 ER PT J AU BROCK, MA AF BROCK, MA TI CHRONOBIOLOGY AND AGING SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Review ID AGE-RELATED-CHANGES; RUNNING-WHEEL ACTIVITY; OLD MALE-RATS; LYMPHOCYTE BLASTOGENIC RESPONSES; CONSTANT LIGHTING CONDITIONS; MICRODISSECTED BRAIN-AREAS; HAMSTERS PHODOPUS-SUNGORUS; RUNWHEEL ACTIVITY PATTERNS; VASOPRESSIN MESSENGER-RNA; GROWTH-HORMONE SECRETION RP BROCK, MA (reprint author), NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 199 TC 147 Z9 148 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1991 VL 39 IS 1 BP 74 EP 91 PG 18 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA EU218 UT WOS:A1991EU21800013 PM 1898956 ER PT J AU HARMAN, D AF HARMAN, D TI HOW EFFECTIVE IS SUFFIXING SO JOURNAL OF THE AMERICAN SOCIETY FOR INFORMATION SCIENCE LA English DT Article ID STEMMING ALGORITHM; RETRIEVAL AB The interaction of suffixing algorithms and ranking techniques in retrieval performance, particularly in an online environment, was investigated. Three general purpose suffixing algorithms were used for retrieval on the Cranfield 1400, Medlars, and CACM test collections, with no significant improvement in performance shown for any of the algorithms. A failure analysis suggested three modifications to ranking techniques: variable weighting of term variants, selective stemming depending on query length, and selective stemming depending on term importance. None of these modifications improved performance. Recommendations are made regarding the uses of suffixing in an online environment. C1 NATL LIB MED,LISTER HILL CTR BIOMED COMMUN,BETHESDA,MD 20209. NR 17 TC 112 Z9 113 U1 2 U2 5 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0002-8231 J9 J AM SOC INFORM SCI JI J. Am. Soc. Inf. Sci. PD JAN PY 1991 VL 42 IS 1 BP 7 EP 15 DI 10.1002/(SICI)1097-4571(199101)42:1<7::AID-ASI2>3.0.CO;2-P PG 9 WC Computer Science, Information Systems; Information Science & Library Science SC Computer Science; Information Science & Library Science GA EP960 UT WOS:A1991EP96000002 ER PT J AU DIETER, MP JAMESON, CW ELWELL, MR LODGE, JW HEJTMANCIK, M GRUMBEIN, SL RYAN, M PETERS, AC AF DIETER, MP JAMESON, CW ELWELL, MR LODGE, JW HEJTMANCIK, M GRUMBEIN, SL RYAN, M PETERS, AC TI COMPARATIVE TOXICITY AND TISSUE DISTRIBUTION OF ANTIMONY POTASSIUM TARTRATE IN RATS AND MICE DOSED BY DRINKING-WATER OR INTRAPERITONEAL INJECTION SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH LA English DT Article AB Antimony potassium tartrate (APT) is a complex salt that until recently was used worldwide as an antischistosomal drug. Treatment was efficacious only if APT was administered intravenously to humans at a near lethal total dose of 36 mg/kg. Because unconfirmed epidemiologic studies suggested there might be an association between APT treatment and bladder cancer, we initiated prechronic toxicity studies with the drug to select a route of administration and doses in the event that chronic studies of APT were needed. The toxicity and concentration of tissue antimony levels were compared in 14-d studies with F344 rats and B6C3F1 mice administered APT in the drinking water or by ip injection to determine the most appropriate route for longer term studies. Drinking water doses estiamted by water consumption were 0, 16, 28, 59, 94, and 168 mg/kg in rats and 0, 59, 98, 174, 273, and 407 mg/kg in mice, and ip doses were 0, 1.5, 3.6, 11, and 22 mg/kg in rats and 0, 6, 13, 25, 50, and 100 mg/kg in mice. APT was poorly absorbed and relatively nontoxic orally, whereas ip administration of the drug caused mortality, body weight decrements, and lesions in the liver and kidney at doses about one order of magnitude below those in drinking water. Because of these data and the dose-related accumulation of antimony in the target organs, an ip dose regimen was selected for subsequent studies. Both sexes of F344 rats and B6C3F1 mice were given 0, 1.5, 3, 6, 12, and 24 mg/kg doses of APT every other day for 90 d by ip injection. There were no clinical signs of toxicity nor gross or microscopic lesions in mice that could be attributed to toxicity of APT, although elevated concentrations of antimony were detected in the liver and spleen of mice. Rats were more sensitive than mice to the toxic effects of APT, exhibiting dose-related mortality, body weight decrements, and hepatotoxicity. The concentrations of antimony measured in liver, blood, kidney, spleen, and heart of rats were proportional to dose, but there were no biochemical changes indicative of toxicity except in the liver. Hepatocellular degeneration and necrosis occurred in association with dose-related elevations in activities of the liver-specific serum enzymes sorbitol dehydrogenase and alanine aminotransferase. By alternating the site of abdominal injection and the days of treatment, mesenteric inflammation at the site of administration was minimized in the rats and mice, indicating that the ip route would be suitable for chronic studies. Since hepatotoxicity in rats occurred in dose groups where there was little evidence of renal toxicity and no cardiac toxicity, serial measurement of liver-specific serum enzyme activities may be useful to monitor the presence and progression of hepatocellular degeneration in longer-term exposures. C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. BATTELLE MEM INST,COLUMBUS DIV,COLUMBUS,OH 43201. RP DIETER, MP (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 48 TC 20 Z9 23 U1 0 U2 3 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0098-4108 J9 J TOXICOL ENV HEALTH JI J. Toxicol. Environ. Health PY 1991 VL 34 IS 1 BP 51 EP 82 PG 32 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA GF658 UT WOS:A1991GF65800005 PM 1890693 ER PT J AU BURKA, LT WASHBURN, KD IRWIN, RD AF BURKA, LT WASHBURN, KD IRWIN, RD TI DISPOSITION OF [C-14] FURAN IN THE MALE F344 RAT SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH LA English DT Article ID METABOLITES; EXCRETION; INVIVO AB In a recently completed 2-yr bioassay, furan was found to induce cholangiocarcinomas at high incidence in rats. The disposition of single and multiple gavage doses of [2,5-C-14]furan has been determined in male F344 rats to aid in interpretation of that study. In the 24 h after dosing about 80% of the furan-derived radioactivity was eliminated, primarily via urine and expired air. [C-14]Carbon dioxide was a major metabolite, indicating that furan ring opening followed by complete oxidation of at least one of the labeled carbons was a major part of the overall metabolism of furan. Liver contained more furan-derived radioactivity by far than other tissues after 24 h. Approximately 80% of the radioactivity in liver was not extracted by organic solvents and was associated with protein. There was either no binding to DNA or the furan-DNA adduct was not stable to the isolation procedure. Repeated daily administration of [C-14]furan resulted in a more or less linear increase in covalent binding through four doses; at this point the amount of nonextractable radioactivity plateaus. Urine contained at least 10 metabolites, again indicating extensive metabolism of the furan ring. From the data obtained in this study it is clear that furan is metabolized to reactive species, apparently primarily in liver, and these intermediates react with protein. The hepatotoxicity resulting from furan exposure may be due to the reaction of furan metabolites with liver macromolecules; the presence of some of these reactive metabolites following chronic exposure to furan may result in cholangiocarcinomas. RP BURKA, LT (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 22 TC 69 Z9 71 U1 1 U2 10 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0098-4108 J9 J TOXICOL ENV HEALTH JI J. Toxicol. Environ. Health PY 1991 VL 34 IS 2 BP 245 EP 257 PG 13 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA GL483 UT WOS:A1991GL48300008 PM 1920528 ER PT J AU TAYLOR, PR REILLY, AA STELMA, JM LAWRENCE, CE AF TAYLOR, PR REILLY, AA STELMA, JM LAWRENCE, CE TI ESTIMATING SERUM POLYCHLORINATED BIPHENYL LEVELS IN HIGHLY EXPOSED WORKERS - AN EMPIRICAL-MODEL SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH LA English DT Article AB A regression model estimating high-homolog polychlorinated biphenyl (PCB) serum concentration on the basis of job exposure categorizations was developed. The model assumes first-order kinetics with a half-life determined empirically and uses variables that incorporate both intensity and duration of exposure over a 30-yr period. In order to compare the efficiency of these regression-based exposure estimates relative to often-used epidemiological parameters, models with dichotomized, ordinal, and continuous exposure surrogates were also investigated. Among the alternative exposure categorizations the most straightforward measure, ever versus never direct, was a particularly poor predictor of serum PCB level (r2 = .01). Nearly all of the candidate exposure measures we tried predicted serum levels poorly. The best of these after the fact was with total months employed in direct-exposure jobs (r2 = .43). None of the logical deductive models approached the predictability of the empirical model developed here (r2 = .69). C1 NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,STAT & COMP SCI LAB,ALBANY,NY 12201. RP TAYLOR, PR (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892, USA. FU NCI NIH HHS [5T32-CA-09001]; PHS HHS [210-81-5102] NR 7 TC 7 Z9 7 U1 0 U2 0 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0098-4108 J9 J TOXICOL ENV HEALTH JI J. Toxicol. Environ. Health PY 1991 VL 34 IS 4 BP 413 EP 422 PG 10 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA GV302 UT WOS:A1991GV30200001 PM 1960759 ER PT J AU SHIEH, YSC BARIC, RS SOBSEY, MD TICEHURST, J MIELE, TA DELEON, R WALTER, R AF SHIEH, YSC BARIC, RS SOBSEY, MD TICEHURST, J MIELE, TA DELEON, R WALTER, R TI DETECTION OF HEPATITIS-A VIRUS AND OTHER ENTEROVIRUSES IN WATER BY SSRNA PROBES SO JOURNAL OF VIROLOGICAL METHODS LA English DT Article DE HEPATITIS-A VIRUS; ENTEROVIRUS; RIBOPROBE; GENE PROBE; DETECTION; WATER ID COMPLETE NUCLEOTIDE-SEQUENCE; MOLECULAR HYBRIDIZATION; STRAINS; ASSAY; RNA; PICORNAVIRUSES; GENOME; CDNA; B3 AB Sensitive and specific methods are needed to detect hepatitis A virus (HAV) and other human enteroviruses in environmental samples such as drinking water and foods. Clones of cDNA encoding the 5'-most 1 kb of the HAV and coxsackievirus B3 (CB3) genomes were subcloned into T7/SP6 RNA transcription vectors. In vitro transcribed RNA from the T7 promoter detected their respective HAV or CB3 genomic RNA. Conversely, SP6 transcripts detected viral negative-stranded RNA but not the genome. When both ssRNA probes were tested at high temperature (65-degrees-C), they did not hybridize with intracellular RNAs from 6 primate cell cultures used for isolation of HAV and other enteroviruses. The HAV probe did not hybridize with 13 different enteroviruses but detected as little as 500-1000 infectious units of the 7 strains of HAV tested. Conversely, the CB3 probe showed strong homology with all 13 enteroviruses tested but not HAV. The probes were used to detect HAV and other enteroviruses in water samples after virus amplification in cell culture. HAV was detected in water samples obtained during a waterborne hepatitis outbreak using the ssRNA probe. These samples were negative for HAV by direct solid phase radioimmunoassay and were not positive by immunoassays of inoculated cell cultures until several weeks of propagation. The CB3 ssRNA probe detected enteroviruses in samples of surface water and drinking water that were negative for cytopathic effects in inoculated cell cultures. C1 UNIV N CAROLINA,SCH PUBL HLTH,CHAPEL HILL,NC 27599. NIAID,HEPATITIS VIRUSES SECT,INFECT DIS LAB,BETHESDA,MD 20892. DEPT CARDIOVASC PATHOL,WASHINGTON,DC. AGR UNIV VIENNA,A-1180 VIENNA,AUSTRIA. RI Ticehurst, John/I-7532-2012 NR 43 TC 22 Z9 22 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-0934 J9 J VIROL METHODS JI J. Virol. Methods PD JAN PY 1991 VL 31 IS 1 BP 119 EP 136 PG 18 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Virology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Virology GA EY235 UT WOS:A1991EY23500011 PM 1849914 ER PT J AU BERGERON, D POLIQUIN, L KOZAK, CA RASSART, E AF BERGERON, D POLIQUIN, L KOZAK, CA RASSART, E TI IDENTIFICATION OF A COMMON VIRAL INTEGRATION REGION IN CAS-BR-E MURINE LEUKEMIA VIRUS-INDUCED NON-T-CELL, NON-B-CELL LYMPHOMAS SO JOURNAL OF VIROLOGY LA English DT Article ID MAMMARY-TUMOR VIRUS; I-HYPERSENSITIVE SITES; PROVIRAL INSERTION; MYELOBLASTIC LEUKEMIAS; C-MYB; RETROVIRUS INTEGRATION; RECOMBINANT GENOMES; MOLECULAR-CLONING; PUTATIVE ONCOGENE; PROTO-ONCOGENE C1 UNIV QUEBEC,DEPT SCI BIOL,CP 8888,SUCCURSALE A,MONTREAL H3C 3P8,QUEBEC,CANADA. NIH,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 66 TC 46 Z9 48 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1991 VL 65 IS 1 BP 7 EP 15 PG 9 WC Virology SC Virology GA EM926 UT WOS:A1991EM92600002 PM 1845910 ER PT J AU EARL, PL KOENIG, S MOSS, B AF EARL, PL KOENIG, S MOSS, B TI BIOLOGICAL AND IMMUNOLOGICAL PROPERTIES OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEIN - ANALYSIS OF PROTEINS WITH TRUNCATIONS AND DELETIONS EXPRESSED BY RECOMBINANT VACCINIA VIRUSES SO JOURNAL OF VIROLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; MONOCLONAL-ANTIBODIES; AIDS VIRUS; HTLV-III; TRANSMEMBRANE PROTEIN; RECEPTOR-BINDING; ENV-PROTEIN; SEROPOSITIVE INDIVIDUALS; NEUTRALIZING ANTIBODIES; IMMUNODOMINANT EPITOPE C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP EARL, PL (reprint author), NIAID,VIRAL DIS LAB,BETHESDA,MD 20892, USA. NR 50 TC 237 Z9 237 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1991 VL 65 IS 1 BP 31 EP 41 PG 11 WC Virology SC Virology GA EM926 UT WOS:A1991EM92600005 PM 1985202 ER PT J AU WICKNER, RB ICHO, T FUJIMURA, T WIDNER, WR AF WICKNER, RB ICHO, T FUJIMURA, T WIDNER, WR TI EXPRESSION OF YEAST L-A DOUBLE-STRANDED-RNA VIRUS PROTEINS PRODUCES DEREPRESSED REPLICATION - A SKI- PHENOCOPY SO JOURNAL OF VIROLOGY LA English DT Article ID SACCHAROMYCES-CEREVISIAE; CHROMOSOMAL GENES; SUPERKILLER MUTATIONS; KILLER SYSTEMS; CYTO-PATHOLOGY; COAT PROTEIN; PLASMID; M1; PARTICLES; INVITRO RP WICKNER, RB (reprint author), NIDDKD,BIOCHEM PHARMACOL LAB,GENET SIMPLE EUKARYOTES SECT,BETHESDA,MD 20892, USA. RI Fujimura, Tsutomu/K-5807-2014 OI Fujimura, Tsutomu/0000-0002-9457-6769 NR 42 TC 43 Z9 43 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1991 VL 65 IS 1 BP 155 EP 161 PG 7 WC Virology SC Virology GA EM926 UT WOS:A1991EM92600019 PM 1985195 ER PT J AU BARBOSA, MS VASS, WC LOWY, DR SCHILLER, JT AF BARBOSA, MS VASS, WC LOWY, DR SCHILLER, JT TI INVITRO BIOLOGICAL-ACTIVITIES OF THE E6 AND E7 GENES VARY AMONG HUMAN PAPILLOMAVIRUSES OF DIFFERENT ONCOGENIC POTENTIAL SO JOURNAL OF VIROLOGY LA English DT Article ID HUMAN FORESKIN KERATINOCYTES; CERVICAL-CARCINOMA; TYPE-16 DNA; EPITHELIAL-CELLS; ACTIVATED RAS; TRANSFORMATION; IMMORTALIZATION; IDENTIFICATION; SUFFICIENT; TRANSCRIPTION C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [5T32CA 09030] NR 38 TC 127 Z9 130 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1991 VL 65 IS 1 BP 292 EP 298 PG 7 WC Virology SC Virology GA EM926 UT WOS:A1991EM92600035 PM 1845889 ER PT J AU REMINGTON, KM CHESEBRO, B WEHRLY, K PEDERSEN, NC NORTH, TW AF REMINGTON, KM CHESEBRO, B WEHRLY, K PEDERSEN, NC NORTH, TW TI MUTANTS OF FELINE IMMUNODEFICIENCY VIRUS RESISTANT TO 3'-AZIDO-3'-DEOXYTHYMIDINE SO JOURNAL OF VIROLOGY LA English DT Article ID REVERSE-TRANSCRIPTASE; ZIDOVUDINE AZT; AIDS; AZIDOTHYMIDINE; INFECTIVITY; SENSITIVITY; CATS C1 UNIV MONTANA,DIV BIOL SCI,MISSOULA,MT 59812. NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. UNIV CALIF DAVIS,SCH VET MED,DEPT MED,DAVIS,CA 95616. FU NIAID NIH HHS [AI28189] NR 16 TC 82 Z9 82 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1991 VL 65 IS 1 BP 308 EP 312 PG 5 WC Virology SC Virology GA EM926 UT WOS:A1991EM92600037 PM 1845891 ER PT J AU FEDERSPIEL, MJ CRITTENDEN, LB PROVENCHER, LP HUGHES, SH AF FEDERSPIEL, MJ CRITTENDEN, LB PROVENCHER, LP HUGHES, SH TI EXPERIMENTALLY INTRODUCED DEFECTIVE ENDOGENOUS PROVIRUSES ARE HIGHLY EXPRESSED IN CHICKENS SO JOURNAL OF VIROLOGY LA English DT Article ID AVIAN-LEUKOSIS VIRUS; MOLONEY LEUKEMIA-VIRUS; GERM LINE; CHROMOSOMAL POSITION; RETROVIRAL GENOMES; MICE; INSERTION; GENES; ACTIVATION; INFECTION C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,POB B,FREDERICK,MD 21702. MICHIGAN STATE UNIV,DEPT MICROBIOL & PUBL HLTH,E LANSING,MI 48824. USDA ARS,REG POULTRY RES LAB,E LANSING,MI 48823. FU NCI NIH HHS [N01-CO-74101] NR 23 TC 28 Z9 28 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1991 VL 65 IS 1 BP 313 EP 319 PG 7 WC Virology SC Virology GA EM926 UT WOS:A1991EM92600038 PM 1845892 ER PT J AU ANTONI, BA RABSON, AB MILLER, IL TREMPE, JP CHEJANOVSKY, N CARTER, BJ AF ANTONI, BA RABSON, AB MILLER, IL TREMPE, JP CHEJANOVSKY, N CARTER, BJ TI ADENOASSOCIATED VIRUS REP PROTEIN INHIBITS HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PRODUCTION IN HUMAN-CELLS SO JOURNAL OF VIROLOGY LA English DT Article ID TRANS-ACTIVATOR GENE; LONG TERMINAL REPEAT; MAMMALIAN-CELLS; MESSENGER-RNA; CELLULAR-TRANSFORMATION; HTLV-III; EXPRESSION; DNA; REPLICATION; VECTOR C1 NIDDKD,MOLEC & CELLULAR BIOL LAB,ROOM 304,BLDG 8,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 61 TC 88 Z9 90 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1991 VL 65 IS 1 BP 396 EP 404 PG 9 WC Virology SC Virology GA EM926 UT WOS:A1991EM92600049 PM 1845899 ER PT J AU PAUL, R SCHUETZE, S KOZAK, SL KOZAK, CA KABAT, D AF PAUL, R SCHUETZE, S KOZAK, SL KOZAK, CA KABAT, D TI THE SFPI-1 PROVIRAL INTEGRATION SITE OF FRIEND-ERYTHROLEUKEMIA ENCODES THE ETS-RELATED TRANSCRIPTION FACTOR-PU.1 SO JOURNAL OF VIROLOGY LA English DT Note ID PROTEINS; COMMON; CELLS; ACID; DNA C1 OREGON HLTH SCI UNIV,SCH MED,DEPT BIOCHEM & MOLEC BIOL,PORTLAND,OR 97201. NIAID,VIRAL GENET LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA25810] NR 22 TC 110 Z9 113 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1991 VL 65 IS 1 BP 464 EP 467 PG 4 WC Virology SC Virology GA EM926 UT WOS:A1991EM92600058 PM 1985210 ER PT J AU ADELMAN, RC GIBSON, DC AF ADELMAN, RC GIBSON, DC TI COHEN,BENNETT,J. - IN MEMORIAM SO JOURNALS OF GERONTOLOGY LA English DT Item About an Individual C1 NIH,NATL CTR RES RESOURCES,ANIM RESOURCES PROGRAM,BETHESDA,MD 20892. RP ADELMAN, RC (reprint author), UNIV MICHIGAN,INST GERONTOL,ANN ARBOR,MI 48109, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0022-1422 J9 J GERONTOL JI J. Gerontol. PD JAN PY 1991 VL 46 IS 1 BP B1 EP B1 PG 1 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA FJ109 UT WOS:A1991FJ10900017 ER PT J AU SHIP, JA PATTON, LL TYLENDA, CA AF SHIP, JA PATTON, LL TYLENDA, CA TI AN ASSESSMENT OF SALIVARY FUNCTION IN HEALTHY PREMENOPAUSAL AND POSTMENOPAUSAL FEMALES SO JOURNALS OF GERONTOLOGY LA English DT Article ID BURNING MOUTH SYNDROME; FLOW-RATE; YEAST CONCENTRATIONS; ESTROGEN USE; MENOPAUSE; LACTOBACILLUS; DEPRESSION; XEROSTOMIA; SECRETION; SYMPTOM AB The elderly represent the most rapidly growing segment of the U.S. population, and the majority of this group are females. The average woman can anticipate living about a third of her life beyond menopause, and many U.S. women undergo hormonal replacement in an attempt to relieve menopausal symptoms. Little is understood about the relationship between menopause, hormonal replacement therapy, and the oral structures, although oral discomfort, xerostomia, and salivary hypofunction have been associated with postmenopausal women. The effects of menopausal status and estrogen therapy on subjective reports of oral dryness and discomfort and objective measurements of major salivary gland output were assessed in 43 healthy premenopausal and postmenopausal females. No complaints of xerostomia or burning mouth and no alterations in the quantity of saliva occurred in this population. This study suggests that among healthy women salivary gland function is not significantly influenced by menopause or hormonal replacement therapy. RP SHIP, JA (reprint author), NIDR,9000 ROCKVILLE PIKE,BLDG 10,ROOM 1N-113,BETHESDA,MD 20892, USA. NR 45 TC 15 Z9 15 U1 0 U2 2 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0022-1422 J9 J GERONTOL JI J. Gerontol. PD JAN PY 1991 VL 46 IS 1 BP M11 EP M15 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA FJ109 UT WOS:A1991FJ10900003 PM 1986036 ER PT J AU SPRING, KR JACOBSON, KA AF SPRING, KR JACOBSON, KA TI SYMPOSIUM ON OPTICAL METHODS APPLICABLE TO RENAL RESEARCH - SUMMARY SO KIDNEY INTERNATIONAL LA English DT Editorial Material RP SPRING, KR (reprint author), NIH,BLDG 10-6N307,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1991 VL 39 IS 1 BP 1 EP 8 DI 10.1038/ki.1991.1 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA EN616 UT WOS:A1991EN61600001 PM 2002623 ER PT J AU HORIKOSHI, S KUBOTA, S MARTIN, GR YAMADA, Y KLOTMAN, PE AF HORIKOSHI, S KUBOTA, S MARTIN, GR YAMADA, Y KLOTMAN, PE TI EPIDERMAL GROWTH-FACTOR (EGF) EXPRESSION IN THE CONGENITAL POLYCYSTIC MOUSE KIDNEY SO KIDNEY INTERNATIONAL LA English DT Article ID RENAL CYSTIC-DISEASE; METANEPHRIC ORGAN-CULTURE; BASEMENT-MEMBRANE; EPITHELIAL-CELLS; HUMAN-FIBROBLASTS; FLUID SECRETION; MESSENGER-RNA; MURINE MODEL; INVITRO; NA+ C1 NIDR,DEV BIOL & ANOMALIES LAB,MOLEC MED SECT,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 37 TC 62 Z9 62 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1991 VL 39 IS 1 BP 57 EP 62 DI 10.1038/ki.1991.7 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA EN616 UT WOS:A1991EN61600007 PM 2002633 ER PT J AU SIAMOPOULOS, KC DROSOS, A SOTSIOU, F STRIKER, L PSIHOS, D ELISAF, M MOUTSOPOULOS, HM AF SIAMOPOULOS, KC DROSOS, A SOTSIOU, F STRIKER, L PSIHOS, D ELISAF, M MOUTSOPOULOS, HM TI THE CLINICAL PICTURE AND EVOLUTION OF LUPUS NEPHRITIS SO KIDNEY INTERNATIONAL LA English DT Meeting Abstract C1 UNIV IOANNINA,DEPT INTERNAL MED,IOANNINA,GREECE. EVANGELISMOS MED CTR,DEPT PATHOL,GR-140 ATHENS,GREECE. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1991 VL 39 IS 1 BP 185 EP 185 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA EN616 UT WOS:A1991EN61600029 ER PT J AU MCCARRON, DA LUFT, FC AF MCCARRON, DA LUFT, FC TI HETEROGENEITY OF HYPERTENSION - THE DIFFERENCES IN EFFECT OF DIETARY ELECTROLYTES SO KLINISCHE WOCHENSCHRIFT LA German DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON SODIUM RESTRICTION AS A PUBLIC HEALTH MEASURE FOR THE GENERAL POPULATION CY OCT 05, 1990 CL BONN, FED REP GER DE HYPERTENSION; BLOOD PRESSURE; SODIUM; CALCIUM; MAGNESIUM; CHLORIDE; DIET; FEEDING ID SALT-SENSITIVE HYPERTENSION; CALCIUM-REGULATING HORMONES; BLOOD-PRESSURE RESPONSE; SODIUM RESTRICTION; DEPENDENT HYPERTENSION; PARATHYROID FUNCTION; MILD HYPERTENSION; CONTROLLED TRIAL; UNITED-STATES; METABOLISM AB Nonpharmacologic approaches to patients with hypertension are a worthwhile avenue to treatment as well as a laudable public health goal. Reduced salt intake has been the primary dietary measure. However, recently attention has also been directed at potassium, calcium, magnesium, and the anions accompanying these cations. Further, the importance of total caloric intake and confounding dietary variables such as alcohol consumption have been appreciated. It is important to recognize that nutrients are not ingested in isolation, but rather as interactive constituents of a total diet. This principle may account for some of the heterogeneity of the human blood pressure response to variations of individual electrolyte intake. Moreover, failure to appreciate this heterogeneity and interactive effects may result in other than the desired effect in the population at risk. C1 UNIV ERLANGEN NURNBERG,LEHRSTUHL INNERE MED NEPHROL,W-8520 ERLANGEN,GERMANY. RP MCCARRON, DA (reprint author), OREGON HLTH SCI UNIV,DIV NEPHROL & HYPERTENS,NIDDK,CLIN NUTR RES UNIT,NDB,PORTLAND,OR 97201, USA. NR 60 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0023-2173 J9 KLIN WOCHENSCHR PY 1991 VL 69 SU 25 BP 97 EP 102 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA FZ050 UT WOS:A1991FZ05000016 PM 1921257 ER PT J AU MASON, RT HOYT, RF PANNELL, LK WELLNER, EF DEMETER, B AF MASON, RT HOYT, RF PANNELL, LK WELLNER, EF DEMETER, B TI CAGE DESIGN AND CONFIGURATION FOR ARBOREAL REPTILES SO LABORATORY ANIMAL SCIENCE LA English DT Note C1 NHLBI,LAB ANIM MED & SURG SECT,BETHESDA,MD 20892. NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,BETHESDA,MD 20892. SMITHSONIAN INST,NATL ZOOL PK,DEPT REPTILES,WASHINGTON,DC 20008. NR 13 TC 6 Z9 6 U1 0 U2 1 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI CORDOVA PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018 SN 0023-6764 J9 LAB ANIM SCI JI Lab. Anim. Sci. PD JAN PY 1991 VL 41 IS 1 BP 84 EP 86 PG 3 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA EY638 UT WOS:A1991EY63800019 PM 1849598 ER PT J AU AXIOTIS, C PEREZ, M CAMPO, E MERINO, MJ CHARONIS, A NEUMANN, R AF AXIOTIS, C PEREZ, M CAMPO, E MERINO, MJ CHARONIS, A NEUMANN, R TI LAMININ IN THYROID-TUMORS REFLECTS DIFFERENTIATION AND NOT METASTATIC POTENTIAL SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A31 EP A31 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600191 ER PT J AU AXIOTIS, C MERINO, MJ CAMPO, E LAPORTE, N NEUMANN, R AF AXIOTIS, C MERINO, MJ CAMPO, E LAPORTE, N NEUMANN, R TI P-GLYCOPROTEIN IS EXPRESSED IN THYROID CARCINOMAS BUT NOT IN BENIGN CONDITIONS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A31 EP A31 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600192 ER PT J AU CAMPO, E MERINO, MJ NEUMANN, R LIOTTA, L STETTLERSTEVENSON, W AF CAMPO, E MERINO, MJ NEUMANN, R LIOTTA, L STETTLERSTEVENSON, W TI ANTI-COLLAGENASE-IV ANTIBODIES DEMONSTRATE ENZYME PHENOTYPES OF NORMAL AND MALIGNANT THYROID FOLLICULAR CELLS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A32 EP A32 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600196 ER PT J AU GILBERT, L MASOOD, S BARNES, R ELWOOD, L MERINO, M LAZAROUS, D COWAN, KH AF GILBERT, L MASOOD, S BARNES, R ELWOOD, L MERINO, M LAZAROUS, D COWAN, KH TI THE RELATIONSHIP BETWEEN GLUTATHIONE-S-TRANSFERASE EXPRESSION AND ESTROGEN AND PROGESTERONE-RECEPTOR STATUS IN BREAST-CANCER BY IMMUNOCYTOCHEMICAL ASSAY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BREAST CANC SECT,BETHESDA,MD 20892. UNIV FLORIDA,HLTH SCI CTR,JACKSONVILLE,FL. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A11 EP A11 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600073 ER PT J AU GRAMLICH, TL CRAWFORD, LJ RADER, JI STERNBERG, EM DESCHRYVERKECSKEMETI, K AF GRAMLICH, TL CRAWFORD, LJ RADER, JI STERNBERG, EM DESCHRYVERKECSKEMETI, K TI GASTROINTESTINAL (GI) LESIONS IN LEWIS RATS AFTER EXPOSURE TO IMPLICATED L-TRYPTOPHAN (L-TRP) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 CASE WESTERN RESERVE UNIV,INST SMALL ANIM MED & SURG,CLEVELAND,OH 44106. NIH,BETHESDA,MD 20892. NIMH,BETHESDA,MD 20892. US FDA,WASHINGTON,DC 20204. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A36 EP A36 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600222 ER PT J AU HIJAZI, Y TSOKOS, M NAVARRO, S HOROWITZ, M AXIOTIS, C AF HIJAZI, Y TSOKOS, M NAVARRO, S HOROWITZ, M AXIOTIS, C TI IMMUNOHISTOCHEMICAL DETECTION OF P-GLYCOPROTEIN IN EWINGS-SARCOMA AND PERIPHERAL NEUROECTODERMAL TUMORS (PNET) BEFORE AND AFTER CHEMOTHERAPY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A5 EP A5 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600037 ER PT J AU HOLLINGSWORTH, HC PEIPER, SC JAFFE, ES AF HOLLINGSWORTH, HC PEIPER, SC JAFFE, ES TI KIKUCHI-FUJIMOTO DISEASE (KFD) - DETECTION OF EPSTEIN-BARR-VIRUS GENOMES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. NCI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A74 EP A74 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600447 ER PT J AU JONES, RT PFEIFER, AMA KLEINSZANTO, AJP HARRIS, CC TRUMP, BF AF JONES, RT PFEIFER, AMA KLEINSZANTO, AJP HARRIS, CC TRUMP, BF TI MORPHOLOGICAL-STUDIES OF A MODEL FOR SMALL-CELL LUNG-CANCER SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A116 EP A116 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600701 ER PT J AU KOVACS, G AF KOVACS, G TI MOLECULAR DIFFERENTIAL PATHOLOGY OF RENAL-CELL TUMORS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BALTIMORE CANC RES CTR,BALTIMORE,MD 21211. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A49 EP A49 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600297 ER PT J AU MCCUNE, BK CHANDRA, R PATTERSON, K SPORN, MB TSOKOS, M AF MCCUNE, BK CHANDRA, R PATTERSON, K SPORN, MB TSOKOS, M TI DIFFERENTIAL EXPRESSION OF TRANSFORMING GROWTH FACTOR-BETA-1 IN SMALL ROUND CELL TUMORS OF CHILDHOOD SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. CHILDRENS HOSP,NATL MED CTR,MED CTR,WASHINGTON,DC 20010. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A110 EP A110 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600664 ER PT J AU MCCUNE, BK MULLIN, BR FLANDERS, KC JAFFURS, WJ SPORN, MB AF MCCUNE, BK MULLIN, BR FLANDERS, KC JAFFURS, WJ SPORN, MB TI IMMUNOLOCALIZATION OF TGF-BETA ISOTYPES IN LESIONS OF THE HUMAN BREAST SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. COLUMBIA HOSP WOMEN,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A12 EP A12 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600080 ER PT J AU MEDEIROS, LJ PEIPER, SC YANO, T ELWOOD, L RAFFELD, M JAFFE, ES AF MEDEIROS, LJ PEIPER, SC YANO, T ELWOOD, L RAFFELD, M JAFFE, ES TI ANGIOCENTRIC IMMUNOPROLIFERATIVE LESIONS (AILS) - A MOLECULAR ANALYSIS OF 8 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV ALABAMA,BIRMINGHAM,AL 35294. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A78 EP A78 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600475 ER PT J AU MERINO, MJ CAMPO, E NEUMANN, R CHARONIS, A LIOTTA, L STETLERSTEVENSON, W TAVASSOLI, FT AF MERINO, MJ CAMPO, E NEUMANN, R CHARONIS, A LIOTTA, L STETLERSTEVENSON, W TAVASSOLI, FT TI EARLY INVASIVE OVARIAN SEROUS TUMORS - DO ANTIBODIES FACILITATE THE RECOGNITION OF INVASION SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A59 EP A59 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600358 ER PT J AU MERINO, MJ SPENCER, WF LINEHAN, M ROSENBERG, SA AF MERINO, MJ SPENCER, WF LINEHAN, M ROSENBERG, SA TI HISTOLOGIC-CHANGES IN RENAL-CELL CARCINOMA FOLLOWING IL-2-BASED IMMUNOTHERAPY SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A49 EP A49 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600300 ER PT J AU NELSON, AM FIRPO, A KAMENGA, M BROWN, C EDIDI, B ANGRITT, P MULLICK, FG AF NELSON, AM FIRPO, A KAMENGA, M BROWN, C EDIDI, B ANGRITT, P MULLICK, FG TI HIV-1 INFECTION AND CHORTOAMNIONITIS - A CASE-CONTROL STUDY, KINSHASA, ZAIRE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 PROJET SIDA,KINSHASA,ZAIRE. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A88 EP A88 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600535 ER PT J AU NOGUERA, R NAVARRO, S TSOKOS, M TRICHE, T LLOMBARTBOSCH, A AF NOGUERA, R NAVARRO, S TSOKOS, M TRICHE, T LLOMBARTBOSCH, A TI MODULATION OF ONCOGENE EXPRESSION IN EWINGS-SARCOMA CELL-LINES WITH DIFFERENTIATION SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV VALENCIA,VALENCIA,SPAIN. NIH,BETHESDA,MD 20892. CHILDRENS HOSP,LOS ANGELES,CA 90027. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A7 EP A7 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600050 ER PT J AU PEIPER, SC ELROD, JP PARKHURST, JB JAFFE, ES AF PEIPER, SC ELROD, JP PARKHURST, JB JAFFE, ES TI DETECTION OF EPSTEIN-BARR-VIRUS (EBV) IN ANGIOCENTRIC IMMUNOPROLIFERATIVE LESION BY PCR SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. UNIV OKLAHOMA,OKLAHOMA CITY,OK. NCI,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A81 EP A81 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600490 ER PT J AU ROSENGARD, AM FORRESTER, KF REDDEL, R PFEIFER, A STAHL, J HARRIS, CC LIOTTA, LA STEEG, PS AF ROSENGARD, AM FORRESTER, KF REDDEL, R PFEIFER, A STAHL, J HARRIS, CC LIOTTA, LA STEEG, PS TI INTERACTION OF THE RAS ONCOGENE AND THE NM23 CANDIDATE SUPPRESSOR GENE IN HUMAN LUNG-CANCER SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A118 EP A118 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600715 ER PT J AU SILVERMAN, T JACOB, W COHEN, R SAFER, B AF SILVERMAN, T JACOB, W COHEN, R SAFER, B TI IDENTIFICATION AND CHARACTERIZATION OF A NOVEL TRANSCRIPTION FACTOR PARTICIPATING IN THE EXPRESSION OF ELF2 ALPHA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A106 EP A106 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600642 ER PT J AU TOKI, T KURMAN, R SCHIFFMAN, M WACHOLDER, S SHAH, K AF TOKI, T KURMAN, R SCHIFFMAN, M WACHOLDER, S SHAH, K TI BASALOID AND WARTY CARCINOMA OF THE VULVA - DISTINCTIVE TYPES OF SQUAMOUS CARCINOMA ASSOCIATED WITH HUMAN PAPILLOMAVIRUS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP A62 EP A62 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600378 ER PT J AU AXIOTIS, C HIJAZI, Y JEFFERSON, J TSOKOS, M AF AXIOTIS, C HIJAZI, Y JEFFERSON, J TSOKOS, M TI EXPRESSION OF P-GLYCOPROTEIN IN SMALL ROUND CELL TUMORS OF CHILDHOOD SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1991 VL 64 IS 1 BP P1 EP P1 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA EV366 UT WOS:A1991EV36600766 ER PT B AU GREENWALD, P SONDIK, E AF GREENWALD, P SONDIK, E BE ROZEN, P REICH, CB WINAWER, SJ TI NATIONAL-CANCER-INSTITUTES STRATEGY FOR COLORECTAL-CANCER SO LARGE BOWEL CANCER : POLICY, PREVENTION, RESEARCH AND TREATMENT SE FRONTIERS OF GASTROINTESTINAL RESEARCH LA English DT Proceedings Paper CT 2ND INTERNATIONAL CONF ON GASTROINTESTINAL CANCER CY 1989 CL JERUSALEM, ISRAEL RP GREENWALD, P (reprint author), NCI,DIV CANC PREVENT & CONTROL,BLDG 31,ROOM 10A52,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5269-6 J9 FRONT GASTR RES JI Front.Gastrointest.Res. PY 1991 VL 18 BP 13 EP 24 PG 12 WC Oncology; Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Oncology; Gastroenterology & Hepatology; Pharmacology & Pharmacy GA BT41M UT WOS:A1991BT41M00003 ER PT B AU GREENWALD, P WITKIN, KM AF GREENWALD, P WITKIN, KM BE ROZEN, P REICH, CB WINAWER, SJ TI PRIMARY PREVENTION OF COLON CANCER SO LARGE BOWEL CANCER : POLICY, PREVENTION, RESEARCH AND TREATMENT SE FRONTIERS OF GASTROINTESTINAL RESEARCH LA English DT Proceedings Paper CT 2ND INTERNATIONAL CONF ON GASTROINTESTINAL CANCER CY 1989 CL JERUSALEM, ISRAEL RP GREENWALD, P (reprint author), NCI,DIV CANC PREVENT & CONTROL,BLDG 31,ROOM 10A52,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5269-6 J9 FRONT GASTR RES JI Front.Gastrointest.Res. PY 1991 VL 18 BP 25 EP 37 PG 13 WC Oncology; Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Oncology; Gastroenterology & Hepatology; Pharmacology & Pharmacy GA BT41M UT WOS:A1991BT41M00004 ER EF