FN Thomson Reuters Web of Science™ VR 1.0 PT J AU COHEN, GD AF COHEN, GD TI NUTRITION AND AGING - CURRENT ISSUES AND FUTURE IMPERATIVES NIH, BETHESDA, JUNE 15-16, 1992 - WELCOMING REMARKS SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Editorial Material RP COHEN, GD (reprint author), NIA,BLDG 31,ROOM 2C-35,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD APR PY 1993 VL 5 IS 2 SU 1 BP 1 EP 1 PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LH701 UT WOS:A1993LH70100001 ER PT J AU KORPER, SP AF KORPER, SP TI NUTRITION AND AGING - CURRENT ISSUES AND FUTURE IMPERATIVES NIH, BETHESDA, JUNE 15-16, 1992 - CONFERENCE OBJECTIVES SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Editorial Material CT INTERNATIONAL SYMP ON NUTRITION AND AGING : CURRENT ISSUES AND FUTURE IMPERATIVES CY JUN 15-16, 1992 CL NIH, BETHESDA, MD HO NIH DE ELDERLY; HEALTH POLICY; NUTRITION RP KORPER, SP (reprint author), NIA,BLDG 31,ROOM 5C05,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD APR PY 1993 VL 5 IS 2 SU 1 BP 5 EP 8 PG 4 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LH701 UT WOS:A1993LH70100003 PM 8399448 ER PT J AU MAGGI, S SORENSON, AW STEEL, K AF MAGGI, S SORENSON, AW STEEL, K TI THE NEED FOR A STRICT METHODOLOGY IN DIETARY SURVEYS - THE EXPERIENCE OF THE WHO OSTEOPOROSIS PROJECT SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON NUTRITION AND AGING : CURRENT ISSUES AND FUTURE IMPERATIVES CY JUN 15-16, 1992 CL NIH, BETHESDA, MD HO NIH DE AGING; EPIDEMIOLOGY; NUTRITION AB There are three basic dietary data collection tools: direct weighing, diet diaries and diet recalls. Each technique has inherent strengths and weaknesses. Direct weighing requires great cooperation from the participants, is expensive and time consuming; diary methods tend to distort usual intake patterns, while retrospective data collection methods are subject to respondent memory bias. Therefore, there are differences in study outcomes depending on the methodologies used; comparisons of data collected in different studies would only be possible if a standardized method were utilized. The Project on Osteoporosis of the World Health Organization is a cross-national study, designed to explore the differences in the incidence of hip fracture and to ascertain risk and protective factors for bone loss and fractures in the older populations in different countries. The objective of the diet assessment is to evaluate the role of diet on osteoporotic hip fracture, and on loss of bone mass. Major effort during the preparation of the proposal was devoted to the development of strategies for assessing the validity and reliability of the instruments selected and the comparability of the results obtained in the participating countries. Such strategies include re-interviews of the participants, proxy interviews and comparisons of data obtained by the food frequency method and those recorded in diaries. RP MAGGI, S (reprint author), NIA,WHO,PROGRAM RES AGING,BLDG 31,ROOM 2C09,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD APR PY 1993 VL 5 IS 2 SU 1 BP 23 EP 28 PG 6 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LH701 UT WOS:A1993LH70100006 PM 8399444 ER PT J AU HARRIS, T BURT, VL BRIEFEL, RR MCDOWELL, M SORENSON, A AF HARRIS, T BURT, VL BRIEFEL, RR MCDOWELL, M SORENSON, A TI THE NATIONAL-HEALTH AND NUTRITION EXAMINATION SURVEY-III - DESCRIBING THE HEALTH AND NUTRITIONAL-STATUS OF OLDER AMERICANS SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON NUTRITION AND AGING : CURRENT ISSUES AND FUTURE IMPERATIVES CY JUN 15-16, 1992 CL NIH, BETHESDA, MD HO NIH DE AGED; EPIDEMIOLOGY; GERIATRIC; NUTRITION; SURVEY AB The National Health and Nutrition Examination III will provide important data for examination of the health and nutritional status of persons in the U.S. Innovations in the study, particularly the inclusion of persons over age 74 and the focus of the survey on the major chronic diseases of old age, will enhance the value for older persons. Response rates for phase 1 (1988-1991) show that about 80% of all older subjects agreed to the interview; examination rates declined with age, but the use of a home examination increased the response rate for those aged 75 or older by about 9% to 67% for men and about 62% for women. Analytic plans include examination of the effect of nutrition on health, as well as the effect of health status on the distribution of nutritional risk factors in old age. RP HARRIS, T (reprint author), NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,GERIATR EPIDEMIOL OFF,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD APR PY 1993 VL 5 IS 2 SU 1 BP 29 EP 36 PG 8 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA LH701 UT WOS:A1993LH70100007 PM 8399445 ER PT J AU MCGOWAN, JA AF MCGOWAN, JA TI OSTEOPOROSIS - ASSESSMENT OF BONE LOSS AND REMODELING SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Review DE BIOMARKERS; DENSITOMETRY; OSTEOPOROSIS; REMODELING AB Osteoporosis, the most common metabolic bone disorder, is a major health problem in older individuals, and especially in postmenopausal women throughout the world. It is characterized by low bone mass, structural deterioration, and an increased risk of fracture. The expected growth in the percentage of the world population over 65 years of age suggests that control of the chronic diseases of the elderly must be a major international priority. In order to design and implement appropriate prevention and treatment strategies for osteoporosis, it is necessary to assess the extent of the disease or condition in populations, and in individuals in a clinical setting. This review focuses on available and emerging techniques to measure bone mass or density, and on the role of biochemical markers of bone remodeling in the prediction of future bone loss. In order to prevent a disease that progresses without any obvious symptoms, it is important to determine not only the current status of bone mass and remodeling but also to develop methods to predict future bone loss. Different information is derived from each of the assessment approaches, and a combination of measures may be necessary to develop accurate predictive models. RP MCGOWAN, JA (reprint author), NIAMSD,BONE BIOL & BONE DIS BRANCH,5333 WESTBARD AVE,WESTWOOD BLDG ROOM 403,BETHESDA,MD 20892, USA. NR 0 TC 15 Z9 15 U1 0 U2 1 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD APR PY 1993 VL 5 IS 2 BP 81 EP 93 PG 13 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA KW370 UT WOS:A1993KW37000002 PM 8324006 ER PT J AU GUEYENDIAYE, A CLARK, RJ SAMUEL, KP NDOURSARR, AN OUANGRE, A SANGARE, L MBOUP, S MARLINK, RG PAPAS, TS CHILD, RH COLLSECK, AM ESSEX, ME KANKI, PJ AF GUEYENDIAYE, A CLARK, RJ SAMUEL, KP NDOURSARR, AN OUANGRE, A SANGARE, L MBOUP, S MARLINK, RG PAPAS, TS CHILD, RH COLLSECK, AM ESSEX, ME KANKI, PJ TI COST-EFFECTIVE DIAGNOSIS OF HIV-1 AND HIV-2 BY RECOMBINANT-EXPRESSED ENV PEPTIDE (566/996) DOT-BLOT ANALYSIS SO AIDS LA English DT Article DE HIV-1; HIV-2; AIDS; SEROLOGIC ASSAYS; RETROVIRUS DIAGNOSIS; RECOMBINANT HIV ENV ANTIGENS; WEST-AFRICA ID HUMAN IMMUNODEFICIENCY VIRUS; CROSS-REACTIVITY; WEST-AFRICA; INFECTION; TYPE-1 AB Objective: To characterize the recombinant env peptides, 566 (HIV-1) and 996 (HIV-2), for their ability to serodiagnose HIV-1 and HIV-2 infection. To develop a cost-effective dot-blot format for these peptides, and to evaluate its performance in a developing country laboratory. Design: The recombinant env peptides were evaluated using a select panel of sera (n = 327) with known serostatus from geographically diverse areas. A dot-blot assay was developed and tested on a second set of immunoblotted sera (n = 331) and further evaluated in the field on a third set of sera (n = 2718) from study populations. Methods: All sera were evaluated by immunoblot with both HIV-1 and HIV-2 viral lysates. The recombinant env peptides were characterized in immunoblot assay before development of the dot-blot assay. Results: The 566 (HIV-1) peptide showed 100% sensitivity and specificity. The 996 (HIV-2) peptide performed similarly, but showed the presence of HIV-1 cross-reactive epitopes. When the two env peptides were used together, there was high specificity and sensitivity for detecting HIV-positive sera in both immunoblot and dot-blot formats. The dot-blot assay performed in the field showed slightly lower specificity and sensitivity for HIV diagnosis. The relative cost of this assay combined with non-commercial immunoblot confirmation was 10-fold lower than conventional commercial assays. Conclusions: The 566 and 996 env peptides are appropriate antigens for HIV serotype diagnosis. A dot-blot assay using these peptides may be a useful cost-effective method for HIV diagnosis applicable in developing country laboratories. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,665 HUNTINGTON AVE,BOSTON,MA 02115. UNIV CHEIKH ANTA DIOP,BACTERIOL & VIROL LAB,DAKAR,SENEGAMBIA. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21701. FANN HOSP,DEPT INFECT DIS,DAKAR,SENEGAMBIA. FU NHLBI NIH HHS [5P50 HL33774]; PHS HHS [P01 A1 26487, P01 A1 30795] NR 19 TC 9 Z9 9 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD APR PY 1993 VL 7 IS 4 BP 475 EP 481 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA KZ427 UT WOS:A1993KZ42700004 PM 8507413 ER PT J AU CHATTERJEE, P GARZINODEMO, A SWINNEY, P ARYA, SK AF CHATTERJEE, P GARZINODEMO, A SWINNEY, P ARYA, SK TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-2 MULTIPLY SPLICED TRANSCRIPTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID LONG TERMINAL REPEAT; FUNCTIONAL-ANALYSIS; TRANS-ACTIVATOR; TRANSLATION; GENES; EXPRESSION AB Viral transcripts, particularly those of the regulatory genes (e.g., rev) in lymphocytic cells chronically infected with human immunodeficiency virus type 2, consist of two types, differing in the structure of the leader sequence derived from the 5' long terminal repeat (LTR). Some transcripts undergo a specific splicing event within the 5' LTR, removing an intron consisting of a part of the R region whereas others do not. Because this spliced-out R region is a part of the trans-activation response element (TAR), it could influence trans-activator (Tat)-mediated trans-activation of viral gene expression. Moreover, this part of the R region is predicted to contain a stable secondary structure that could affect the efficiency of translation of the transcripts without this splicing. Thus, the 5' LTR splicing could have important consequences for virus replication, latency, and pathogenicity. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 20 TC 11 Z9 11 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1993 VL 9 IS 4 BP 331 EP 335 DI 10.1089/aid.1993.9.331 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA KY808 UT WOS:A1993KY80800006 PM 8512748 ER PT J AU GOLDMAN, D BROWN, GL ALBAUGH, B ROBIN, R GOODSON, S TRUNZO, M AKHTAR, L LUCASDERSE, S LONG, J LINNOILA, M DEAN, M AF GOLDMAN, D BROWN, GL ALBAUGH, B ROBIN, R GOODSON, S TRUNZO, M AKHTAR, L LUCASDERSE, S LONG, J LINNOILA, M DEAN, M TI DRD2 DOPAMINE RECEPTOR GENOTYPE, LINKAGE DISEQUILIBRIUM, AND ALCOHOLISM IN AMERICAN-INDIANS AND OTHER POPULATIONS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE DRD2; LINKAGE DISEQUILIBRIUM; ALCOHOLISM; DRUG ABUSE ID ALLELIC ASSOCIATION; GENE; METABOLITES AB We defined interpopulation differences in the frequency of the dopamine D2 receptor DRD2/Taq1 A1 allele, which has previously been associated with alcoholism. Frequencies of the Al allele in unrelated subjects were 0.18 to 0.20 (se = 0.02 to 0.03) in several Caucasian populations previously assessed, 0.38 (+/- 0.05) in American Blacks (n = 44), 0.63 (+/- 0.07) in Jemez Pueblo Indians (n = 23), and 0.80 (+/- 0.04) in Cheyenne Indians (n = 52). The existence of large interpopulation differences in the frequency of the Taq1 alleles suggests that associations to disease status could readily be generated or masked if disease and control groups were uneven in ethnic composition. To address the possibility that the 4-fold higher frequency of the Al allele in Cheyenne Indians was related to an increased vulnerability to alcoholism in that population, 47 Cheyenne Indians were psychiatrically interviewed and blind-rated. However, there was no significant difference between interviewed controls (0.73 +/- 0.06, n = 24), subjects with alcoholism and/or drug abuse (0.74 +/- 0.06, n = 23) and noninterviewed population controls (0.87 +/- 0.05, n = 20). Legitimate association of the DRD2/Taq1 allele to alcoholism would presumably require it to be in linkage disequilibrium (nonrandom association) with a functional mutation at DRD2 or elsewhere. The level of disequilibrium would vary between populations and could place an upper bound on the strength of an association. To provide a model for the extent and variation of disequilibrium at DRD2, the level of linkage disequilibrium between the Taq1 RFLP and a second DRD2 polymorphism, the SSCP variant in the immediate 3' region of the gene, was determined in three populations. The normalized disequilibrium values were 0.36 in U.S. Caucasians (n = 48), 0.34 in Finns (n = 86), and 0.78 in Cheyenne Indians (n = 34). C1 NIAAA,CLIN STUDIES LAB,BETHESDA,MD. INST BEHAV RES,CLINTON,OK. NCI,FREDERICK,MD 21701. DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD. RP GOLDMAN, D (reprint author), NIAAA,NEUROGENET LAB,DICBR,BLDG 10,ROOM 3C102,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Dean, Michael/G-8172-2012; Goldman, David/F-9772-2010 OI Dean, Michael/0000-0003-2234-0631; Goldman, David/0000-0002-1724-5405 FU NCI NIH HHS [N01-CO-74102] NR 24 TC 95 Z9 95 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD APR PY 1993 VL 17 IS 2 BP 199 EP 204 DI 10.1111/j.1530-0277.1993.tb00749.x PG 6 WC Substance Abuse SC Substance Abuse GA KZ662 UT WOS:A1993KZ66200001 PM 8488955 ER PT J AU MORRISON, AR AF MORRISON, AR TI BIOMEDICAL-RESEARCH AND THE ANIMAL RIGHTS MOVEMENT - A CONTRAST IN VALUES SO AMERICAN BIOLOGY TEACHER LA English DT Article RP MORRISON, AR (reprint author), NIMH,PROGRAM ANIM RES ISSUES,ROOM 17C-26,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU NATL ASSOC BIOLOGY TEACHERS INC PI RESTON PA 11250 ROGER BACON DR #19, RESTON, VA 22090 SN 0002-7685 J9 AM BIOL TEACH JI Am. Biol. Teach. PD APR PY 1993 VL 55 IS 4 BP 204 EP 208 PG 5 WC Biology; Education, Scientific Disciplines SC Life Sciences & Biomedicine - Other Topics; Education & Educational Research GA KW145 UT WOS:A1993KW14500006 ER PT J AU SINHA, R BLOCK, G TAYLOR, PR AF SINHA, R BLOCK, G TAYLOR, PR TI PROBLEMS WITH ESTIMATING VITAMIN-C INTAKES SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE VITAMIN-C; ASCORBIC ACID; DEHYDROASCORBIC ACID; NATIONAL HEALTH INTERVIEW SURVEY; NATIONAL HEALTH AND NUTRITION EXAMINATION SURVEY; HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY ID DEHYDROISOASCORBIC ACID; DEHYDROASCORBIC ACID; ISOASCORBIC ACID; DIETARY-INTAKE; ASCORBIC-ACID; FOOD SAMPLES; QUESTIONNAIRE; SEPARATION AB The vitamin C content of foods was examined from two national databases and new values were obtained by HPLC. HPLC values were lower in four of the five highest vitamin C contributors to the US diet (orange juice, grapefruit, tomatoes and tomato juice, and potatoes), as well as in broccoli, red peppers, and cooked collard and mustard greens, compared with values from the other databases. When HPLC values were substituted in the Health Habits and History Questionnaire, the resulting estimates of dietary intake of vitamin C in two studies were lower, Despite these lower estimates of absolute intake, in one study the correlation between dietary vitamin C and plasma ascorbic acid was similar. In conclusion, the accuracy of the vitamin C content of foods is important for estimating the absolute amount of vitamin C intake in the population but may not change the ranking of people in epidemiological studies. C1 UNIV CALIF BERKELEY,DEPT PUBL HLTH NUTR,BERKELEY,CA 94720. RP SINHA, R (reprint author), NCI,DIV CANC PREVENT & CONTROL,EPN ROOM 443,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Block, Gladys/E-3304-2010; Sinha, Rashmi/G-7446-2015 OI Sinha, Rashmi/0000-0002-2466-7462 NR 25 TC 6 Z9 6 U1 1 U2 2 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1993 VL 57 IS 4 BP 547 EP 550 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA KU629 UT WOS:A1993KU62900014 PM 8460610 ER PT J AU RAUTALAHTI, M ALBANES, D HAUKKA, J ROOS, E GREF, CG VIRTAMO, J AF RAUTALAHTI, M ALBANES, D HAUKKA, J ROOS, E GREF, CG VIRTAMO, J TI SEASONAL-VARIATION OF SERUM CONCENTRATIONS OF BETA-CAROTENE AND ALPHA-TOCOPHEROL SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE SEASONAL VARIATION; SERUM VITAMINS; BETA-CAROTENE; ALPHA-TOCOPHEROL ID GREEN-YELLOW VEGETABLES; VITAMIN-E; INTAKE FREQUENCY; DIETARY-INTAKE; PLASMA-LEVELS; DETERMINANTS; RETINOL; INHABITANTS; POPULATION; FRUITS AB We studied the seasonal variation in serum concentrations of beta-carotene and alpha-tocopherol (HPLC) in 17 247 Finnish men who smoked. Month of blood sampling was a statistically significant determinant of serum concentration of beta-carotene in a regression model including age, body mass index, alcohol and fat intakes, total serum cholesterol, and daily cigarettes as covariates. The serum concentrations were lowest in April-June and highest in October-November. The 1.5-fold increase in the serum concentration of beta-carotene during the fall reflects the seasonality of dietary sources of carotenoids in Finland. The serum concentrations of alpha-tocopherol demonstrated no seasonal variation but remained close to 27.6 mumol/L throughout the year. The results indicate that the seasonal variation of serum concentrations of beta-carotene should be taken into account in long-term studies in which comparison of groups or individuals is based on serum concentrations. C1 NCI,BETHESDA,MD 20892. RP RAUTALAHTI, M (reprint author), NATL PUBL HLTH INST,KALLIOLINNANTIE 4,SF-00140 HELSINKI,FINLAND. RI Albanes, Demetrius/B-9749-2015; Haukka, Jari/G-1484-2014 OI Haukka, Jari/0000-0003-1450-6208 FU NCI NIH HHS [N01-CN-45165] NR 29 TC 35 Z9 35 U1 0 U2 2 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1993 VL 57 IS 4 BP 551 EP 556 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA KU629 UT WOS:A1993KU62900015 PM 8460611 ER PT J AU COWIE, CC HARRIS, MI SILVERMAN, RE JOHNSON, EW RUST, KF AF COWIE, CC HARRIS, MI SILVERMAN, RE JOHNSON, EW RUST, KF TI EFFECT OF MULTIPLE RISK-FACTORS ON DIFFERENCES BETWEEN BLACKS AND WHITES IN THE PREVALENCE OF NON-INSULIN-DEPENDENT DIABETES-MELLITUS IN THE UNITED-STATES SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE CAUCASOID RACE; DIABETES-MELLITUS, NON-INSULIN-DEPENDENT; NEGROID RACE; OBESITY; RISK FACTORS ID IMPAIRED GLUCOSE-TOLERANCE; BODY-FAT DISTRIBUTION; MEXICAN-AMERICANS; PIMA-INDIANS; CHINESE MAURITIANS; MASS INDEX; FOLLOW-UP; MEN BORN; OBESITY; WEIGHT AB The higher prevalence of non-insulin-dependent diabetes mellitus (NIDDM) in US blacks as compared with whites may be due to a higher frequency of NIDDM risk factors in blacks, a higher inherent susceptibility to NIDDM among blacks, or the risk factors' having a greater effect in blacks. The authors evaluated 4,379 subjects from the Second National Health and Nutrition Examination Survey (1976-1980) for whom NIDDM was ascertained by medical history and oral glucose tolerance test, and for whom data on a number of risk factors were available. The prevalence of NIDDM was 60% higher in blacks than in whites (p < 0.001) and was highest in black women. Although most risk factors for NIDDM were more common in blacks, this higher frequency did not completely explain the racial disparity in the prevalence of NIDDM. After adjustment for all risk factors by logistic regression, an elevated risk of NIDDM was particularly evident at higher obesity levels in blacks as compared with whites; the odds were 70% higher for blacks at a percentage of desirable weight of 150 (95% confidence interval 1.1-2.8). The risk of NIDDM associated with obesity was greatest in black women: The odds in this group were sevenfold higher at a percentage of desirable weight of 150 versus 100 (95% confidence interval 2.6-18.8). The possibility of racial differences in metabolic adaptation to obesity highlights the importance of preventing this condition in blacks, particularly in black women. C1 NIDDKD,BETHESDA,MD. WESTAT CORP,ROCKVILLE,MD. RP COWIE, CC (reprint author), SOCIAL & SCI SYST INC,7101 WISCONSIN AVE,SUITE 610,BETHESDA,MD 20814, USA. NR 61 TC 107 Z9 109 U1 1 U2 2 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 1 PY 1993 VL 137 IS 7 BP 719 EP 733 PG 15 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LB812 UT WOS:A1993LB81200004 PM 8484363 ER PT J AU YANNUZZI, LA SORENSON, JA SOBEL, RS DALY, JR DEROSA, JT SEDDON, JM GRAGOUDAS, ES PULIAFITO, CA GELLES, E GONET, R BURTON, TC CULVER, J METZGER, K KALBFLEISCH, N ZARLING, D FARBER, MD BLAIR, N STELMACK, T AXELROD, A WAITR, SE CROSS, A ROLNICK, C FLOM, T HALLER, J PUSIN, S CASSEL, G APPLEGATE, CA SEIGEL, D SPERDUTO, RD HILLER, R MOWERY, R CHEW, E TAMBOLI, A MILLER, DT SOWELL, AL GUNTER, EW DUNN, M SEDDON, JM SHAMBAN, K GELLES, E LENTO, D ALEXANDER, JA PHILLIPS, DA AF YANNUZZI, LA SORENSON, JA SOBEL, RS DALY, JR DEROSA, JT SEDDON, JM GRAGOUDAS, ES PULIAFITO, CA GELLES, E GONET, R BURTON, TC CULVER, J METZGER, K KALBFLEISCH, N ZARLING, D FARBER, MD BLAIR, N STELMACK, T AXELROD, A WAITR, SE CROSS, A ROLNICK, C FLOM, T HALLER, J PUSIN, S CASSEL, G APPLEGATE, CA SEIGEL, D SPERDUTO, RD HILLER, R MOWERY, R CHEW, E TAMBOLI, A MILLER, DT SOWELL, AL GUNTER, EW DUNN, M SEDDON, JM SHAMBAN, K GELLES, E LENTO, D ALEXANDER, JA PHILLIPS, DA TI RISK-FACTORS FOR IDIOPATHIC RHEGMATOGENOUS RETINAL-DETACHMENT SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE CARDIOVASCULAR DISEASES; MYOPIA; RETINAL DETACHMENT; RISK FACTORS AB The objective of this case-control study of idiopathic retinal detachment was to evaluate previously suggested hypotheses about risk factors for retinal detachment and to investigate whether new ocular or systemic risk factors could be identified. Between 1986 and 1990, data were obtained at five US clinical centers on 253 patients with idiopathic retinal detachment and 1, 138 controls. Patients with pathologic myopia were excluded. Data were collected from interviews, clinical examinations, and laboratory analyses of blood samples. Only one clearly relevant risk factor, myopia, emerged from the analyses. An eye with a spherical equivalent refractive error of -1 to -3 diopters had a fourfold increased risk of retinal detachment compared with a nonmyopic eye; if the refractive error was greater than -3 diopters, the risk was increased 10-fold. The data suggest that almost 55% of nontraumatic detachments in eyes without previous surgery are attributable to myopia. The etiology of retinal detachment appears to be related to the architecture of the eye. The study found no evidence that systemic factors, particularly cardiovascular factors, play a role. RP YANNUZZI, LA (reprint author), NEI,BIOMETRY & EPIDEMIOL PROGRAM,BLDG 31,ROOM 6A24,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 15 TC 115 Z9 116 U1 2 U2 4 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 1 PY 1993 VL 137 IS 7 BP 749 EP 757 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA LB812 UT WOS:A1993LB81200007 ER PT J AU HERMAN, BE SWENSON, J SIEBERT, W KELLY, B HAMILTON, F AF HERMAN, BE SWENSON, J SIEBERT, W KELLY, B HAMILTON, F TI DIFFUSE CEREBRAL EDEMA FOLLOWING ENDOSCOPY SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Letter ID HYPONATREMIA C1 NATL NAVAL MED CTR, NEURO SCI INTENS CARE UNIT, BETHESDA, MD 20889 USA. NIDDKD, DEPT HLTH & HUMAN SERV, BETHESDA, MD USA. RP HERMAN, BE (reprint author), NATL NAVAL MED CTR, DEPT INTERNAL MED, DIV GASTROENTEROL, BETHESDA, MD 20889 USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD APR PY 1993 VL 88 IS 4 BP 616 EP 617 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KW463 UT WOS:A1993KW46300036 PM 8470657 ER PT J AU BRAY, GL KRONER, BL ARKIN, S ALEDORT, LW HILGARTNER, MW EYSTER, ME RAGNI, MV GOEDERT, JJ AF BRAY, GL KRONER, BL ARKIN, S ALEDORT, LW HILGARTNER, MW EYSTER, ME RAGNI, MV GOEDERT, JJ TI LOSS OF HIGH-RESPONDER INHIBITORS IN PATIENTS WITH SEVERE HEMOPHILIA-A AND HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION - A REPORT FROM THE MULTICENTER HEMOPHILIA COHORT STUDY SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE FACTOR-VIII; AIDS; INHIBITOR TITER ID FACTOR-VIII INHIBITORS; IMMUNE TOLERANCE; ANTIBODIES; AIDS; DISAPPEARANCE; INDUCTION AB To evaluate the effects of human immunodeficiency virus type 1 (HIV-1) infection on the loss of factor VIII alloantibodies, we identified 77 patients with a history of inhibitors from among a large cohort of HIV-1-infected participants enrolled in a natural history study of HIV-1 infection in hemophilia. Fifty-six patients were high responders with inhibitors titers greater than 5 Bethesda Units (BU) measured on at least one occasion. From May 1985 to December 1989, 13 of the high-responder patients were rechallenged with factor VIII concentrates after several years of treatment with other plasma products. All exhibited excellent hemostasis upon reinstitution of factor VIII. Seven of the 13 patients (11.3-46.3 years of age) were in the advanced stages of HIV-1 infection at the time of rechallenge. Inhibitor titers measured subsequent to the reinstitution of factor VIII were consistently less than 1 BU in five of these seven patients. The remaining six patients (6.1-57.5 years of age) had mild to moderate CD4+ lymphocyte depletion (absolute CD4+ cells: 262-935/mm3) at the time of factor VIII rechallenge. Follow-up inhibitor titers were negative 7-42 months after consistent factor VIII use in these six patients. The lack of anamnestic response to factor VIII in all 13 patients who were rechallenged indicates that HIV-1-infected patients who have a history of high-responder inhibitors frequently benefit from the reintroduction of factor VIII use for the control of bleeding, regardless of their stage of HIV-1 disease. C1 UNIV PITTSBURGH,PITTSBURGH,PA 15260. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. CUNY MT SINAI SCH MED,DEPT PEDIAT,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT INTERNAL MED,NEW YORK,NY 10029. CORNELL UNIV,MED CTR,NEW YORK HOSP,DEPT PEDIAT,NEW YORK,NY 10021. PENN STATE UNIV,MILTON S HERSHEY MED CTR,DEPT INTERNAL MED,HERSHEY,PA 17033. NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. RP BRAY, GL (reprint author), CHILDRENS NATL MED CTR,DIV HEMATOL ONCOL,111 MICHIGAN AVE NW,WASHINGTON,DC 20010, USA. NR 23 TC 71 Z9 71 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 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD APR PY 1993 VL 42 IS 4 BP 375 EP 379 DI 10.1002/ajh.2830420408 PG 5 WC Hematology SC Hematology GA KU623 UT WOS:A1993KU62300007 PM 8493988 ER PT J AU ZIMMERMANN, W BENDER, E ROHDE, K REIS, A WISEMAN, R FUTREAL, A KRAUSE, H PROKOPH, H WERNER, S SCHERNECK, S AF ZIMMERMANN, W BENDER, E ROHDE, K REIS, A WISEMAN, R FUTREAL, A KRAUSE, H PROKOPH, H WERNER, S SCHERNECK, S TI LINKAGE ANALYSIS IN GERMAN BREAST-CANCER FAMILIES WITH EARLY ONSET OF THE DISEASE, USING HIGHLY POLYMORPHIC MARKERS FROM THE CHROMOSOME-17Q11-Q24 REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID HORMONE; LOCUS; RISK AB Linkage analysis in German breast cancer families with early onset of the disease by using six markers on chromosome 17q11-q24 has been carried out. In the region between markers D17S250 and GH, three markers showed positive LOD scores at an estimated distance of zero. Evidence for linkage is greatest for D17S250, with a LOD score of 2.42. C1 MAX DELBRUCK CENTRUM MOLEK MED,ROBERT ROSSLE STR 10,O-1115 BERLIN,GERMANY. FREE UNIV BERLIN,INST HUMAN GENET,W-1000 BERLIN 33,GERMANY. NIEHS,RES TRIANGLE PK,NC 27709. RI Reis, Andre/D-2309-2009 OI Reis, Andre/0000-0002-6301-6363 NR 14 TC 8 Z9 8 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD APR PY 1993 VL 52 IS 4 BP 789 EP 791 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA KY059 UT WOS:A1993KY05900019 PM 8460645 ER PT J AU MOSS, N CARVER, K AF MOSS, N CARVER, K TI PREGNANT-WOMEN AT WORK - SOCIODEMOGRAPHIC PERSPECTIVES SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE PREGNANCY; EMPLOYMENT; OCCUPATION; LOW BIRTH WEIGHT; RISK FACTORS ID LOW-BIRTH-WEIGHT; MATERNAL EMPLOYMENT; PRETERM BIRTH; PREMATURITY AB The 1988 National Maternal and Infant Health Survey, a stratified random sample of 9,953 live births, shows that women who work during pregnancy are more likely to be non-Hispanic white, married, of higher income and education, to have medical insurance, and of lower parity than nonemployed pregnant women (p < .0001). They begin prenatal care earlier, are less likely to smoke, and are more likely to state that the birth was wanted (p < .0001). Similar trends are seen for full-time as compared to part-time workers. Women employed as precision production workers, operators/fabricators, or in service occupations are disadvantaged with regard to sociodemographic and behavioral risks for pregnancy outcomes relative to women in professional and managerial occupations. Black race, parity, body mass index, and smoking, but not employment, are associated with low birth weight when gestational age is controlled. The effects of stress and its buffers, paternal characteristics, physical activity, and toxic exposures, both in and out of the workplace, should be considered, as should the normative and social policy context. RP MOSS, N (reprint author), NICHHD,CTR POPULAT RES,DEMOG & BEHAV SCI BRANCH,6100 EXECUT BLVD,8B13,BETHESDA,MD 20892, USA. NR 36 TC 21 Z9 21 U1 2 U2 6 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD APR PY 1993 VL 23 IS 4 BP 541 EP 557 DI 10.1002/ajim.4700230404 PG 17 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KX380 UT WOS:A1993KX38000003 PM 8338526 ER PT J AU VETTER, R STEWART, PA DOSEMECI, M BLAIR, A AF VETTER, R STEWART, PA DOSEMECI, M BLAIR, A TI VALIDITY OF EXPOSURE IN ONE JOB AS A SURROGATE FOR EXPOSURE IN A COHORT STUDY SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE EXPOSURE ASSESSMENT; FORMALDEHYDE; OCCUPATIONAL RISK; SURROGATE ESTIMATES ID REPORTED WORK HISTORY; DEATH CERTIFICATES; INDUSTRY DATA; OCCUPATIONAL EXPOSURE; INFORMATION; INTERVIEW; FORMALDEHYDE; VALIDATION; MORTALITY; ACCURACY AB Frequently, information pertaining to only one job is available or used to evaluate risk estimates of disease in occupational epidemiologic research. The amount of misclassification that such a practice could create has not, however, been examined. We used data from a mortality study of workers employed in 10 formaldehyde-producing or -using plants to address how closely several parameters of exposure based on the first, longest, or last job held in a company compared with those based on the worker's entire employment history at the plant. The best predictor for cumulative formaldehyde exposure at the plant was the longest job at that plant, with a correlation coefficient (r) of 0.70. The correlation with average exposure over the worker's employment was 0.77 for the first job and 0.74 for the longest and last jobs. Peak exposures and highest exposure levels experienced in the plant were more closely related to the first job (r = 0.72 and r = 0. 74). The highest correlation with any of the measures was never with the last job. Variation between plants for each of these comparisons, however, was wide. These findings indicate that the use of a single job as a surrogate for exposure received at a particular worksite can result in different degrees of misclassification for different exposure measures. Even though the correlations were generally high, the associated misclassification of exposure could lead to a substantial underestimation of the relative risks in some situations. In this report two hypothetical examples show what effect the misclassification rates could have on estimates of disease risks. C1 NCI,ENVIRONM EPIDEMIOL BRANCH,OCCUPAT STUDIES SECT,BETHESDA,MD 20892. NR 25 TC 8 Z9 8 U1 1 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD APR PY 1993 VL 23 IS 4 BP 641 EP 651 DI 10.1002/ajim.4700230411 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KX380 UT WOS:A1993KX38000010 PM 8480771 ER PT J AU STRIKER, GE AF STRIKER, GE TI REDUCTION IN MORBIDITY AND MORTALITY AMONG HEMODIALYSIS-PATIENTS SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Note RP STRIKER, GE (reprint author), NIDDKD,DIV KIDNEY UROL & HEMATOL DIS,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD APR PY 1993 VL 21 IS 4 BP 452 EP 452 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA KX556 UT WOS:A1993KX55600019 ER PT J AU MARCUS, R CULVER, DH BELL, DM SRIVASTAVA, PU MENDELSON, MH ZALENSKI, RJ FARBER, B FLIGNER, D HASSETT, J QUINN, TC SCHABLE, CA SLOAN, EP TSUI, P KELEN, GD AF MARCUS, R CULVER, DH BELL, DM SRIVASTAVA, PU MENDELSON, MH ZALENSKI, RJ FARBER, B FLIGNER, D HASSETT, J QUINN, TC SCHABLE, CA SLOAN, EP TSUI, P KELEN, GD TI RISK OF HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION AMONG EMERGENCY DEPARTMENT WORKERS SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID HEPATITIS-B VIRUS; UNIVERSAL PRECAUTIONS; HIV-INFECTION; PREVALENCE; PHYSICIANS; IMMUNIZATION; PERSONNEL; EXPOSURES; MARKERS; RATES AB PURPOSE: To estimate (1) the prevalence of human immunodeficiency virus (HIV) infection in emergency department (ED) patients, (2) the frequency of blood contact (BC) in ED workers (EDWs), (3) the efficacy of gloves in preventing BC, and (4) the risk of HIV infection in EDWs due to BC. PATIENTS AND METHODS: We conducted an 8-month study in three pairs of inner-city and suburban hospital EDs in high AIDS incidence areas in the United States. At each hospital, blood specimens from approximately 3,400 ED patients were tested for HIV antibody. Observers monitored BC and glove use by EDWs. RESULTS: HIV seroprevalence was 4.1 to 8.9 per 100 patient visits in the 3 inner-city EDs, 6.1 in 1 suburban ED, and 0.2 and 0.7 in the other 2 suburban EDs. The HIV infection status of 69% of the infected patients was unknown to ED staff. Seroprevalence rates were highest among patients aged 15 to 44 years, males, blacks and Hispanics, and patients with pneumonia. BC was observed in 379 (3.9%) of 9,793 procedures; 362 (95%) of the BCs were on skin, 11 (3%) were on mucous membranes, and 6 (2%) were percutaneous. Overall procedure-adjusted skin BC rates were 11.2 BCs per 100 procedures for ungloved workers and 1.3 for gloved EDWs (relative risk = 8.8, 95 % confidence interval = 7.3 to 10.3). In the high HIV seroprevalence EDs studied, 1 in every 40 full-time ED physicians or nurses can expect an HIV-positive percutaneous BC annually; in the low HIV seroprevalence EDs studied, 1 in every 575. The annual occupational risk of HIV infection for an individual ED physician or nurse from performing procedures observed in this study is estimated as 0.008% to 0.026% (1 in 13,100 to 1 in 3,800) in a high HIV seroprevalence area and 0.0005% to 0.002% (1 in 187,000 to 1 in 55,000) in a low HIV seroprevalence area. CONCLUSIONS: In both inner-city and suburban EDs, patient HIV seroprevalence varies with patient demographics and clinical presentation; the infection status of most HIV-positive patients is unknown to ED staff. The risk to an EDW of occupationally acquiring HIV infection varies by ED location and the nature and frequency of BC; this risk can be reduced by adherence to universal precautions. C1 CORNELL UNIV,N SHORE UNIV HOSP,COLL MED,DEPT MED,DIV INFECT DIS,MANHASSET,NY 11030. CHRIST HOSP,DEPT EMERGENCY MED,OAK LAWN,IL. UNIV ILLINOIS,COLL MED,PROGRAM EMERGENCY MED,CHICAGO,IL 60680. JOHNS HOPKINS UNIV HOSP,DEPT EMERGENCY MED,BALTIMORE,MD 21205. COOK CTY HOSP,DEPT EMERGENCY MED,TRAUMA UNIT,CHICAGO,IL 60612. COOK CTY HOSP,DEPT IMMUNOL,CHICAGO,IL 60612. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV HIV AIDS CAS,ATLANTA,GA. CUNY MT SINAI SCH MED,DEPT MED,DIV CLIN IMMUNOL,NEW YORK,NY 10029. RP MARCUS, R (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,HOSP INFECT PROGRAM,HIV INFECT BRANCH,MAILSTOP A07,ATLANTA,GA 30333, USA. OI Kelen, Gabor/0000-0002-3236-8286 NR 31 TC 46 Z9 46 U1 1 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1993 VL 94 IS 4 BP 363 EP 370 DI 10.1016/0002-9343(93)90146-G PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA KX941 UT WOS:A1993KX94100004 PM 8475929 ER PT J AU JOFFE, MM LOVE, LA LEFF, RL FRASER, DD TARGOFF, IN HICKS, JE PLOTZ, PH MILLER, FW AF JOFFE, MM LOVE, LA LEFF, RL FRASER, DD TARGOFF, IN HICKS, JE PLOTZ, PH MILLER, FW TI DRUG-THERAPY OF THE IDIOPATHIC INFLAMMATORY MYOPATHIES - PREDICTORS OF RESPONSE TO PREDNISONE, AZATHIOPRINE, AND METHOTREXATE AND A COMPARISON OF THEIR EFFICACY SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID SIGNAL RECOGNITION PARTICLE; COMPUTER-ASSISTED ANALYSIS; POLYMYOSITIS; DERMATOMYOSITIS; AUTOANTIBODIES; PROGNOSIS; MYOSITIS; ONSET; DISEASES; ANTIBODY AB PURPOSE: To identify factors associated with responses to treatment with prednisone, methotrexate, or azathioprine in patients with idiopathic inflammatory myopathy, and to compare the efficacy of these drugs. PATIENTS AND METHODS: Data were collected on 113 adult patients meeting criteria for definite idiopathic inflammatory myopathy in this retrospective cohort study. Patients were categorized as responding completely, partially, or not at all to each therapeutic trial based upon clinical and laboratory criteria. RESULTS: Clinical group, presence of certain myositis-specific autoantibodies, and time from disease onset to diagnosis influenced rates of complete clinical response to these therapeutic agents. Patients with inclusion body myositis responded comparatively poorly to prednisone the other drugs: 43% had no clinical response to prednisone and none responded completely to any medication. Patients with autoantibodies to aminoacyl-tRNA synthetases or to signal recognition particle proteins were likely to respond partially, but not completely, to prednisone. No patient with a long delay to diagnosis (greater than 18 months) responded completely, compared with 34% of those with a short delay (less than 3 months). A patient's response to the first course of prednisone predicted subsequent responses to prednisone and to azathioprine better than response to methotrexate. Men responded to methotrexate better than women. Among certain subgroups of patients, responses to methotrexate were better than to either azathioprine or retreatment with prednisone. CONCLUSION: Determining the clinical group, autoantibody status, and time from disease onset to diagnosis of patients with myositis provides useful information in predicting clinical responses to therapy, and these factors should be considered in designing future therapeutic trials. Methotrexate therapy may be superior to either azathioprine or further steroid treatment alone in certain patients who do not respond completely to an initial adequate course of prednisone. C1 NIAMSD,BETHESDA,MD. NIH,DEPT REHABIL MED,BETHESDA,MD 20892. UNIV OKLAHOMA HLTH SCI CTR,HLTH SCI CTR,DEPT MED,OKLAHOMA CITY,OK 73190. OKLAHOMA MED RES FDN,IMMUNOL SECT,OKLAHOMA CITY,OK 73104. OI Miller, Frederick/0000-0003-2831-9593 FU NIAID NIH HHS [AI27181]; NIAMS NIH HHS [AR32214] NR 40 TC 154 Z9 163 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1993 VL 94 IS 4 BP 379 EP 387 DI 10.1016/0002-9343(93)90148-I PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA KX941 UT WOS:A1993KX94100006 PM 8386437 ER PT J AU NEVA, FA AF NEVA, FA TI STRONGYLOIDES HYPERINFECTION IN PATIENTS COINFECTED WITH HTLV-1 AND S-STERCORALIS - REPLY SO AMERICAN JOURNAL OF MEDICINE LA English DT Letter RP NEVA, FA (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 6 TC 1 Z9 1 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1993 VL 94 IS 4 BP 448 EP 449 DI 10.1016/0002-9343(93)90164-K PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KX941 UT WOS:A1993KX94100022 ER PT J AU GOLDENBERG, RL DAVIS, RO CLIVER, SP CUTTER, GR HOFFMAN, HJ DUBARD, MB COPPER, RL AF GOLDENBERG, RL DAVIS, RO CLIVER, SP CUTTER, GR HOFFMAN, HJ DUBARD, MB COPPER, RL TI MATERNAL RISK-FACTORS AND THEIR INFLUENCE ON FETAL ANTHROPOMETRIC MEASUREMENTS SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 11TH ANNUAL MEETING OF THE AMERICAN GYNECOLOGICAL AND OBSTETRICAL SOC CY SEP 10-12, 1992 CL HOT SPRINGS, VA SP AMER GYNECOL & OBSTETR SOC DE FETAL GROWTH RETARDATION; ULTRASONOGRAPHY; RISK FACTORS; BIRTH WEIGHT ID LOW-BIRTH-WEIGHT; GESTATIONAL-AGE; INTRAUTERINE GROWTH; BIPARIETAL DIAMETER; POPULATION; DETERMINANTS; BLACK; SIZE AB OBJECTIVE: Our purpose was to determine if and when maternal risk factors and fetal sex have an impact on specific fetal anthropometric measurements assessed by ultrasonography. STUDY DESIGN: Serial ultrasonographic examinations were performed on 1205 fetuses of indigent multiparous women who ultimately gave birth at term. Femur length, abdominal circumference, and head circumference measurements were obtained at mean gestational ages of 18, 25, 31, and 36 weeks, and an estimated fetal weight was calculated. At birth the infant was weighed and head circumference, abdominal circumference, femur length, and crown-heel length measurements were made. Regression analyses were used to determine the effect on each measurement of maternal race, height, body mass index, hypertension, weight gain, smoking, previous low birth weight, and fetal sex. RESULTS: Acting through their effect on head circumference, abdominal circumference, and fetal length, each of the risk factors and female sex were shown to have a negative effect on fetal weight. The timing of the impact, its magnitude, and the specific anthropometric measurement affected were different for each of the risk factors. CONCLUSIONS: The impact of maternal risk factors and fetal sex on estimated fetal weight has been demonstrated to occur fir$t in specific gestational age windows and is mediated through effects on specific fetal anthropometric measurements. C1 PYTHAGORAS INC,BETHESDA,MD. NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. RP GOLDENBERG, RL (reprint author), UNIV ALABAMA,DEPT OBSTET & GYNECOL,DIV MATERNAL FETAL MED,PERINATAL EPIDEMIOL UNIT,BIRMINGHAM,AL 35233, USA. FU NICHD NIH HHS [N01-HD-4-2811] NR 26 TC 36 Z9 36 U1 1 U2 4 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD APR PY 1993 VL 168 IS 4 BP 1197 EP 1205 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KY813 UT WOS:A1993KY81300017 PM 8475966 ER PT J AU ARBEIT, JM MUNGER, K HOWLEY, PM HANAHAN, D AF ARBEIT, JM MUNGER, K HOWLEY, PM HANAHAN, D TI NEUROEPITHELIAL CARCINOMAS IN MICE TRANSGENIC WITH HUMAN PAPILLOMAVIRUS TYPE-16 E6/E7 ORFS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID PRIMITIVE NEUROECTODERMAL TUMORS; LARGE-T-ANTIGEN; HUMAN KERATINOCYTES; COMPLEX-FORMATION; SUPPRESSOR GENE; CHOROID-PLEXUS; P53 MUTATIONS; BRAIN-TUMORS; CELL-LINES; TUMORIGENESIS AB The effect of the human papillomaviral (HPV) oncogenes E6 and E7 was examined in transgenic mice with a construct containing the human beta-actin promoter regulating HPV16 E6 and E7 open reading frames. In the sole line of mice that transmitted the transgene, neuroepithelial tumors appeared at 2.5 mouths of life, and by 10 mouths, 87 of 122 (71%) of the animals were dead from brain tumors. The most frequent type of tumor (74%) was an anaplastic neuroepithelial tumor associated with the ependyma of the third and fourth ventricles, which locally invaded adjacent brain tissue and spread for considerable distances along the ventricular surface. The other two types of tumors were well-differentiated choroid plexus carcinomas (26%) and rare pituitary carcinomas (8.7%). HPV16 E6 P-NA and E7 oncoprotein expression were demonstrated in tumor tissue and primary cell lines derived from the tumors. Examination of two tumor suppressor gene products, the retinoblastoma protein and p53, known to bind to HPV16 E7 and E6 oncoproteins, respectively, showed both were expressed in the primary tumor cell lines. These data support a causative role for the HPV oncoproteins in epithelial carcinogenesis. C1 UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM & BIOPHYS,SAN FRANCISCO,CA 94143. NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT SURG,SAN FRANCISCO,CA 94143. RP ARBEIT, JM (reprint author), UNIV CALIF SAN FRANCISCO,HORMONE RES INST,ROOM HSW 1090,BOX 0534,SAN FRANCISCO,CA 94143, USA. OI Munger, Karl/0000-0003-3288-9935 FU NCI NIH HHS [CA47632] NR 38 TC 67 Z9 68 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD APR PY 1993 VL 142 IS 4 BP 1187 EP 1197 PG 11 WC Pathology SC Pathology GA KY014 UT WOS:A1993KY01400025 PM 8386443 ER PT J AU FRALIX, TA MURPHY, E LONDON, RE STEENBERGEN, C AF FRALIX, TA MURPHY, E LONDON, RE STEENBERGEN, C TI PROTECTIVE EFFECTS OF ADENOSINE IN THE PERFUSED RAT-HEART - CHANGES IN METABOLISM AND INTRACELLULAR ION HOMEOSTASIS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CALCIUM; GLYCOLYSIS; ISCHEMIA; MYOCARDIUM ID CYTOSOLIC FREE CALCIUM; ISCHEMIC MYOCARDIUM; F-19 NMR; REPERFUSION; GLUCOSE; ATP; ARRHYTHMIAS; CONTRACTION; INHIBITION; GLYCOLYSIS AB Increased concentrations of intracellular H+, Na+, and Ca2+ have been observed during ischemia, and these ionic alterations have been correlated with several indexes of cell injury in a number of studies. Recently, adenosine was proposed to play a role in ischemic preconditioning, since adenosine antagonists block the protective effects of these brief intermittent periods of ischemia and reflow. In this study we evaluated the protective effects of adenosine (20 muM) on high-energy phosphate metabolism, H+ and Ca2+ accumulation, and glycolytic rate during 30 min of no-flow ischemia. Adenosine was observed to slow the onset of contracture (7.0 +/- 0.9 min) and to improve left ventricular developed pressure (62 +/-7% of initial) during reperfusion compared with untreated hearts (5.0 +/- 0.6 min and 18 +/- 5%, respectively). Intracellular Ca accumulation at the end of 30 min of ischemia was higher in the untreated (2,835 +/- 465 nM) than in the adenosine-treated (2,064 +/- 533 nM) hearts, while intracellular pH fell more in the untreated (5.85 +/- 0.17) than in the adenosine-treated hearts (6.27 +/- 0.16). Glycolytic rate and the rate of ATP decline were significantly attenuated in the adenosine-treated hearts during ischemia. Thus adenosine treatment slowed the rate of metabolism and delayed the accumulation of H+ and Ca2+ during ischemia, resulting in better recovery of function upon reflow. C1 DUKE UNIV,MED CTR,DEPT PATHOL,DURHAM,NC 27710. RP FRALIX, TA (reprint author), NIEHS,MOLEC BIOPHYS LAB,MAILDROP 4A-01,RES TRIANGLE PK,NC 27709, USA. FU NHLBI NIH HHS [R01 HL039752] NR 41 TC 79 Z9 79 U1 1 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1993 VL 264 IS 4 BP C986 EP C994 PN 1 PG 9 WC Physiology SC Physiology GA KZ603 UT WOS:A1993KZ60300028 PM 8476025 ER PT J AU KRAUS, ES CHENG, L SIKORSKI, I SPECTOR, DA AF KRAUS, ES CHENG, L SIKORSKI, I SPECTOR, DA TI EFFECT OF PHOSPHORUS RESTRICTION ON RENAL RESPONSE TO ORAL AND INTRAVENOUS PROTEIN LOADS IN RATS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE RENAL FUNCTIONAL RESERVE; HYPERFILTRATION; HYPOPHOSPHATEMIA ID MEAT MEAL; PHOSPHATE-DEPLETION; DIETARY-PROTEIN; ANGIOTENSIN-II; UREMIC RATS; FAILURE; HUMANS; HEMODYNAMICS; GLUCAGON; HYPOPHOSPHATEMIA AB Dietary phosphorus restriction ameliorates renal injury in rats. This may be due to changes in renal hemodynamics, including those factors associated with protein-induced hyperfiltration. To test this, we measured inulin clearance (C(In)), p-aminohippuric acid clearance (C(PAH), mean arterial blood pressure, and renal vascular resistance (RVR) 1 h before and 100 min after either oral gavage of 2 g bovine serum albumin or intravenous infusion of 5% glycine in female Sprague-Dawley rats previously fed for 3-8 wk a 0.5% or a 0.1% phosphorus diet. Baseline C(In), C(PAH), blood pressure, and RVR were similar. After albumin gavage, C(In) rose 20% (P < 0.01) for the 0.5% phosphorus group but did not change for rats fed the 0.1% phosphorus diet. Other measured parameters, including plasma glucagon and renin activity, were not influenced by dietary phosphorus content. In contrast, during intravenous infusion of glycine, hyperfiltration was induced in phosphorus-restricted rats. Thus dietary phosphorus restriction ablates oral protein but not intravenous amino acid-induced hyperfiltration, suggesting a gut-mediated mechanism for the former. These data highlight the potential importance of dietary phosphorus as a mediator of renal hemodynamics. C1 NIA,GERIATR RES CTR,BETHESDA,MD 20892. RP KRAUS, ES (reprint author), JOHNS HOPKINS UNIV,SCH MED,FRANCIS SCOTT KEY MED CTR,DIV RENAL MED,B2N,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 33 TC 4 Z9 4 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1993 VL 264 IS 4 BP F752 EP F759 PN 2 PG 8 WC Physiology SC Physiology GA KZ605 UT WOS:A1993KZ60500089 PM 8476079 ER PT J AU QIAN, JM ROWLEY, WH JENSEN, RT AF QIAN, JM ROWLEY, WH JENSEN, RT TI GASTRIN AND CCK ACTIVATE PHOSPHOLIPASE-C AND STIMULATE PEPSINOGEN RELEASE BY INTERACTING WITH 2 DISTINCT RECEPTORS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ENZYME SECRETION; PHOSPHOINOSITIDES; CYTOSOLIC CALCIUM; STIMULUS-SECRETION COUPLING ID DISPERSED CHIEF CELLS; GUINEA-PIG STOMACH; CHOLECYSTOKININ RECEPTORS; PANCREATIC ACINI; PARIETAL-CELLS; INOSITOL PHOSPHATES; SECRETION; CA-2+; HYDROLYSIS; BINDING AB Both gastrin and cholecystokinin (CCK) can stimulate pepsinogen release from chief cells, but controversy exists about the receptors or intracellular mediators involved. In the present study, we prepared isolated chief cells from guinea pig stomach (>90% pure) to investigate the ability of gastrin and CCK to alter cell function. The COOH-terminal octapeptide of CCK (CCK-8) caused an eightfold increase in pepsinogen release (EC50), 54 nM). Both CCK-8 and gastrin increased inositol phosphates, with CCK-8 (1 muM) and gastrin (3 muM) causing a 40- and 14-fold increase in [H-3]IP1, 10- and 6-fold for [H-3]IP2, and 8- and 4-fold for [H-3]IP3. CCK-8 caused a half-maximal increase in [H-3]IP3 at 2 nM, and the dose-response curve was monophasic, whereas with gastrin the curve was biphasic, with an EC50 of the initial component (20% maximal) at 38 nM and the second component at 10 muM. L-364,718 (0.1 muM) inhibited the secondary increase seen with gastrin concentrations > 10 nM. The CCK-A-selective agonist A-71378 was 8590% as efficacious as CCK-8 and was equally potent. With 0.1 muM L-364,718, A-71378 caused no increase in [H-3]inositol phosphates until >10 nM, whereas CCK-8 caused 15% of maximal increase at concentrations >0.3 nM. Similar results were obtained with cytosolic calcium measured using fura-2 or on CCK-8- or gastrin-stimulated pepsinogen release. These results demonstrate that gastrin and CCK-8 can alter chief cell function by interacting with either a CCK-A or CCK-B/gastrin receptor. Both receptors are coupled to phospholipase C and cause changes in inositol phosphates, cytosolic calcium, and pepsinogen release; however, the intracellular amplification differs between the two receptor subtypes. Activation by CCK-related peptides of the CCK-A receptor subtype accounts for 85-90% of the maximal changes in cellular function, and activation of the CCK-B/gastrin receptor accounts for 10-20% of maximal changes. C1 NIDDKD,DIGEST DIS BRANCH,BLDG 10,RM 93-103,BETHESDA,MD 20892. NR 33 TC 42 Z9 42 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1993 VL 264 IS 4 BP G718 EP G727 PN 1 PG 10 WC Physiology SC Physiology GA KZ603 UT WOS:A1993KZ60300086 PM 8476056 ER PT J AU GAWIN, AZ BARANIUK, JN LUNDGREN, JD KALINER, M AF GAWIN, AZ BARANIUK, JN LUNDGREN, JD KALINER, M TI EFFECTS OF GASTRIN-RELEASING PEPTIDE AND ANALOGS ON GUINEA-PIG NASAL MUCOSAL SECRETION SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE BOMBESIN; NEUROPEPTIDES; GLANDULAR SECRETION; SUBMUCOSAL GLANDS; ALBUMIN; ALKALINE PHOSPHATASE; GUINEA PIG NASAL MUCOSA ID BOMBESIN-LIKE PEPTIDES; CELL LUNG-CANCER; GROWTH-FACTORS; SUBSTANCE-P; FETAL LUNG; TACHYKININS; EXUDATION; HISTAMINE; RHINITIS; AIRWAYS AB The effects of gastrin-releasing peptide (GRP), bombesin, GRP-(1 - 16) and GRP-(21-27) on guinea pig nasal mucosal secretion were studied in vivo. GRP, bombesin, and GRP-(21-27) induced significant secretion of total protein, albumin, and alkaline phosphatase. GRP induced significant secretion at lower concentrations (10(-11) and 10(-10) M) than were required for bombesin and GRP-(21-27) (10(-7) M). GRP-(1-16) did not stimulate secretion, indicating that the COOH-terminal region of GRP contained the secretagogic principle. Capsaicin, a stimulant of nociceptive sensory nerves, stimulated GRP release into nasal secretions. These data suggest that GRP is present in guinea pig nasal mucosa and that the COOH-terminal region of GRP may regulate mucosal macromolecule secretion. C1 GEORGETOWN UNIV,MED CTR,DIV RHEUMATOL IMMUNOL & ALLERGY,3800 RESERVOIR RD NW,WASHINGTON,DC 20007. NIAID,CLIN INVEST LAB,AUERG DIS SECT,BETHESDA,MD 20892. HVIDOVRE UNIV HOSP,DEPT INFECT DIS,DK-2650 HVIDOVRE,DENMARK. NR 32 TC 4 Z9 4 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1993 VL 264 IS 4 BP L345 EP L350 PN 1 PG 6 WC Physiology SC Physiology GA KZ603 UT WOS:A1993KZ60300099 PM 8476064 ER PT J AU LEVITT, AJ JOFFE, RT MOUL, DE LAM, RW TEICHER, MH LEBEGUE, B MURRAY, MG OREN, DA SCHWARTZ, P BUCHANAN, A GLOD, CA BROWN, J AF LEVITT, AJ JOFFE, RT MOUL, DE LAM, RW TEICHER, MH LEBEGUE, B MURRAY, MG OREN, DA SCHWARTZ, P BUCHANAN, A GLOD, CA BROWN, J TI SIDE-EFFECTS OF LIGHT THERAPY IN SEASONAL AFFECTIVE-DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Note AB The authors report the frequency of side effects of light therapy in 105 patients with seasonal affective disorder treated with three intensities of light. Common symptoms to emerge during treatment were headache (19%), eyestrain (17%), and feeling ''wired'' (14%). There was no relationship between side effects and intensity of light used. C1 UNIV TORONTO,TORONTO M5S 1A1,ONTARIO,CANADA. NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. UNIV HOSP BRITISH COLUMBIA,DEPT PSYCHIAT,VANCOUVER,BC,CANADA. UNIV BRITISH COLUMBIA,VANCOUVER V6T 1W5,BC,CANADA. HARVARD UNIV,MCLEAN HOSP,SCH MED,BELMONT,MA 02178. UNIV UTAH,DEPT PSYCHIAT,SALT LAKE CITY,UT 84112. RP LEVITT, AJ (reprint author), CLARKE INST PSYCHIAT,MOOD DISORDERS PROGRAM,250 COLL ST,TORONTO M5T 1R8,ONTARIO,CANADA. RI Lam, Raymond/D-2529-2013 OI Lam, Raymond/0000-0001-7142-4669 NR 7 TC 43 Z9 43 U1 0 U2 4 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1993 VL 150 IS 4 BP 650 EP 652 PG 3 WC Psychiatry SC Psychiatry GA KW818 UT WOS:A1993KW81800019 PM 8465886 ER PT J AU DEBELLIS, MD GOLD, PW GERACIOTI, TD LISTWAK, SJ KLING, MA AF DEBELLIS, MD GOLD, PW GERACIOTI, TD LISTWAK, SJ KLING, MA TI ASSOCIATION OF FLUOXETINE TREATMENT WITH REDUCTIONS IN CSF CONCENTRATIONS OF CORTICOTROPIN-RELEASING HORMONE AND ARGININE VASOPRESSIN IN PATIENTS WITH MAJOR DEPRESSION SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Note ID CEREBROSPINAL-FLUID; ANOREXIA-NERVOSA; RAT AB The authors measured CSF concentrations of corticotropin-releasing hormone (CRH) and arginine vasopressin in nine depressed patients before and after fluoxetine treatment. They found significant decreases in CSF CRH, CSF arginine vasopressin, and Hamilton depression ratings. Thus, the therapeutic effect of this serotonin-uptake inhibitor may be related to diminution of these arousal-promoting neuropeptides. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT PSYCHIAT,NASHVILLE,TN 37232. RP DEBELLIS, MD (reprint author), NIMH,CTR CLIN,INTRAMURAL RES PROGRAM,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. RI Kling, Mitchel/F-4152-2010 OI Kling, Mitchel/0000-0002-2232-1409 NR 14 TC 208 Z9 214 U1 0 U2 5 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1993 VL 150 IS 4 BP 656 EP 657 PG 2 WC Psychiatry SC Psychiatry GA KW818 UT WOS:A1993KW81800021 PM 8465888 ER PT J AU COTE, TR DOSEMECI, M ROTHMAN, N BANKS, RB BIGGAR, RJ AF COTE, TR DOSEMECI, M ROTHMAN, N BANKS, RB BIGGAR, RJ TI NON-HODGKINS-LYMPHOMA AND OCCUPATIONAL EXPOSURE TO HAIR-DYES AMONG PEOPLE WITH AIDS SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Letter RP COTE, TR (reprint author), NCI,VIRAL EPIDEMIOL SECT,6130 EXECUT BLVD,EPN 434,ROCKVILLE,MD 20852, USA. NR 5 TC 4 Z9 4 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD APR PY 1993 VL 83 IS 4 BP 598 EP 599 DI 10.2105/AJPH.83.4.598-a PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KX086 UT WOS:A1993KX08600032 PM 8460749 ER PT J AU MULLOL, J CHOWDHURY, BA WHITE, MV OHKUBO, K RIEVES, RD BARANIUK, J HAUSFELD, JN SHELHAMER, JH KALINER, MA AF MULLOL, J CHOWDHURY, BA WHITE, MV OHKUBO, K RIEVES, RD BARANIUK, J HAUSFELD, JN SHELHAMER, JH KALINER, MA TI ENDOTHELIN IN HUMAN NASAL-MUCOSA SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID SMOOTH-MUSCLE CELLS; VASOCONSTRICTOR PEPTIDE; EPITHELIAL-CELLS; GUINEA-PIG; INVITRO; BRONCHOCONSTRICTOR; GLYCOPROTEINS; LACTOFERRIN; BINDING; RELEASE AB Endothelin (ET), a potent vasoconstrictor and bronchoconstrictor peptide synthesized by endothelial and epithelial cells, was examined for its potential functions in human inferior turbinate nasal mucosal tissue by four techniques: (1) immunoreactive ET was localized in the mucosa by immunohistochemistry; (2) receptors for ET were identified by autoradiography employing [I-125]ET; (3) ET-1 mRNA was localized by in situ hybridization; and (4) the secretory functions of ET were examined by the release of mucous and serous cell products after the addition of ET to human nasal turbinates in short-term cultures. Specific ET-1-immunoreactive material was found most extensively in small muscular arteries and in serous cells in submucosal glands. ET-1 was also found to a lower extent in the walls of venous sinusoids. [I-125]ET-1 binding sites were localized by autoradiography to submucosal glands and to venous sinusoids and small muscular arterioles. mRNA for ET-1 was found most extensively in the venous sinusoids and to a lesser extent in small muscular arteries. In mucosal explant cultures, ET-1 and ET-2 stimulated lactoferrin and mucous glycoprotein release from serous and mucous cells, but ET-3 was inactive. The observations indicate that in the human nasal mucosa, ET is present in the vascular endothelium and the serous cells in submucosal glands and acts on glandular ET receptors to induce both serous and mucous cell secretion. It is also likely that ET plays a role in the regulation of vasomotor tone. C1 NIAID,CLIN INVEST LAB,ALLERG DIS SECT,BLDG 10,ROOM 11C205,BETHESDA,MD 20892. NIH,CTR CLIN,INTENS CARE UNIT,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT MED,WASHINGTON,DC 20057. WASHINGTON HOSP CTR,DEPT FACIAL & RECONSTRUCT SURG,WASHINGTON,DC 20010. NR 35 TC 47 Z9 48 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD APR PY 1993 VL 8 IS 4 BP 393 EP 402 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA KY236 UT WOS:A1993KY23600008 PM 8476633 ER PT J AU GOLLAN, JL KALSER, SC PITT, HA STRASBERG, SM AF GOLLAN, JL KALSER, SC PITT, HA STRASBERG, SM TI GALLSTONES AND LAPAROSCOPIC CHOLECYSTECTOMY - FOREWORD SO AMERICAN JOURNAL OF SURGERY LA English DT Editorial Material C1 NIDDK,BETHESDA,MD. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. BARNES HOSP,ST LOUIS,MO 63110. RP GOLLAN, JL (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD APR PY 1993 VL 165 IS 4 BP 388 EP 389 DI 10.1016/S0002-9610(05)80928-6 PG 2 WC Surgery SC Surgery GA KY345 UT WOS:A1993KY34500001 ER PT J AU KALSER, SC AF KALSER, SC TI NATIONAL-INSTITUTES-OF-HEALTH CONSENSUS DEVELOPMENT CONFERENCE STATEMENT ON GALLSTONES AND LAPAROSCOPIC CHOLECYSTECTOMY SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT NIH CONSENSUS DEVELOPMENT CONF ON GALLSTONES AND LAPAROSCOPIC CHOLECYSTECTOMY CY SEP 14-16, 1992 CL BETHESDA, MD SP NIH, OFF MED APPL RES, NIDDKD RP KALSER, SC (reprint author), NIDDKD,DIV DIGEST DIS & NUTR,5333 WESTBARD AVE,ROOM 3A-17,BETHESDA,MD 20892, USA. NR 0 TC 108 Z9 118 U1 0 U2 2 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD APR PY 1993 VL 165 IS 4 BP 390 EP 398 PG 9 WC Surgery SC Surgery GA KY345 UT WOS:A1993KY34500002 ER PT J AU ARBER, DA WEISS, LM ALBUJAR, PF CHEN, YY JAFFE, ES AF ARBER, DA WEISS, LM ALBUJAR, PF CHEN, YY JAFFE, ES TI NASAL LYMPHOMAS IN PERU - HIGH-INCIDENCE OF T-CELL IMMUNOPHENOTYPE AND EPSTEIN-BARR-VIRUS INFECTION SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE PERU; NASAL LYMPHOMA; EPSTEIN-BARR VIRUS; MALIGNANT LYMPHOMA ID LETHAL MIDLINE GRANULOMA; NON-HODGKINS LYMPHOMAS; NATURAL-KILLER CELL; MALIGNANT-LYMPHOMAS; POLYMORPHIC RETICULOSIS; WALDEYERS RING; HONG-KONG; VIRAL-DNA; B-CELL; NOSE AB The incidence of non-Hodgkin's lymphoma of the nasal region is much higher in Peru than in the United States and is similar to the incidence of sinonasal lymphomas in Asian countries. To characterize these lymphomas, we evaluated the clinical, morphologic, and immunohistochemical features of 14 cases and also analyzed the cases for Epstein-Barr virus (EBV) RNA using a sensitive and specific in situ hybridization method. Morphologically, the cases consisted of nine large cell immunoblastic lymphomas, one diffuse mixed cell lymphoma, one diffuse small cleaved lymphoma, one small noncleaved lymphoma, and two cases unclassifiable in the Working Formulation. Eleven cases demonstrated evidence of T lineage, two were of B lineage and one of indeterminate immunophenotype. In 13 of the lymphoma cases including all of the T-cell lymphomas, EBV RNA was detected in a high percentage of cells. Double-labeling immunohistochemical and in situ hybridization studies identified CD43 positivity in the cells labeling for EBV RNA. Much smaller amounts of EBV RNA were detectable in six of eight control benign nasopharyngeal biopsy specimens, and two were completely negative. These findings are similar to the prevalence of EBV-positive T-cell lymphomas in Asian countries and differ from the findings of the more common EBV-negative B-cell nasal lymphomas in the United States. These findings suggest that EBV plays a role in the development of nasal T-cell lymphomas and that the incidence of EBV infection may explain the reported ''East-West'' difference in the incidence of nasal T-cell lymphomas. C1 UNIV TRUJILLO,TRUJILLO,PERU. NCI,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892. BELEN HOSP,TRUJIUO,PERU. RP ARBER, DA (reprint author), CITY HOPE NATL MED CTR,DIV PATHOL,1500 E DUARTE RD,DUARTE,CA 91010, USA. FU NCI NIH HHS [CA 50341] NR 52 TC 143 Z9 146 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD APR PY 1993 VL 17 IS 4 BP 392 EP 399 DI 10.1097/00000478-199304000-00010 PG 8 WC Pathology; Surgery SC Pathology; Surgery GA KT991 UT WOS:A1993KT99100010 PM 8388175 ER PT J AU CHEEVER, AW ELTOUM, IA ANDRADE, ZA COX, TM AF CHEEVER, AW ELTOUM, IA ANDRADE, ZA COX, TM TI BIOLOGY AND PATHOLOGY OF SCHISTOSOMA-MANSONI AND SCHISTOSOMA-JAPONICUM INFECTIONS IN SEVERAL STRAINS OF NUDE-MICE SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID CELL DEPRIVED MICE; GRANULOMA-FORMATION; ATHYMIC MICE; IMMUNOPATHOLOGY; MORBIDITY; SURVIVAL; SERUM AB Schistosoma mansoni and S. japonicum infections in nude mice (nu/nu) were compared with infections in nu/+ heterozygotes or intact mice. Seven to 12 weeks after exposure to S. mansoni, the responses of Swiss NCR, C3H, BALB/c and C57B1/6 nude mice did not differ substantially. Nude mice of all these strains showed minute granulomas around eggs in the liver and minimal hepatic fibrosis. Microvesicular and necrotizing changes in hepatocytes were similar in all mouse strains, and S. mansoni infections were frequently lethal to nude, but not to intact mice between the seventh and ninth weeks of infection. Nude mice that survived the ninth week of infection generally lived until the 12th week. The number of eggs per mature worm pair in the tissues of S. mansoni-infected nude mice was similar to the number in intact mice, but nude mice passed fewer eggs in the feces. Nude mice that received serum from infected intact mice excreted eggs in the stool in numbers equivalent to intact mice, but continued to form minute granulomas around S. mansoni eggs. Reconstitution with fetal thymus or with splenocytes from normal or S. mansoni-infected mice partially or completely restored hepatic granuloma size, granuloma eosinophils, hepatic fibrosis, and excretion of eggs in the feces. In contrast to S. mansoni infection, S. japonicum infections in nude mice did not cause necrosis of hepatocytes or excessive mortality, and S. japonicum eggs were passed in the feces in numbers equivalent to those passed by infected intact mice. C1 GONCALO MONIZ RES CTR FIOCRUZ,BR-91945 SALVADOR,BA,BRAZIL. RP CHEEVER, AW (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI-052590] NR 26 TC 15 Z9 18 U1 0 U2 4 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD APR PY 1993 VL 48 IS 4 BP 496 EP 503 PG 8 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA LB692 UT WOS:A1993LB69200005 PM 8480857 ER PT J AU BIRRER, P MCELVANEY, NG HUBBARD, RC RUDEBERG, A SOMMER, CW LIECHTIGALLATI, S KRAEMER, R CRYSTAL, RG AF BIRRER, P MCELVANEY, NG HUBBARD, RC RUDEBERG, A SOMMER, CW LIECHTIGALLATI, S KRAEMER, R CRYSTAL, RG TI NEUTROPHIL ELASTASE-ANTI-NEUTROPHIL ELASTASE IMBALANCE ON THE RESPIRATORY EPITHELIAL SURFACE IN CHILDREN WITH CYSTIC-FIBROSIS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV BERN,DEPT PEDIAT,CH-3010 BERN,SWITZERLAND. NHLBI,PULM BRANCH,BETHESDA,MD 20892. RI McElvaney, Noel/A-6809-2010 NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A675 EP A675 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902584 ER PT J AU BONNER, JC GOODELL, AL BADGETT, A HOFFMAN, MR AF BONNER, JC GOODELL, AL BADGETT, A HOFFMAN, MR TI ALPHA(2)-MACROGLOBULIN (ALPHA(2)M)-PROTEASE COMPLEXES INHIBIT PLATELET-DERIVED GROWTH-FACTOR (PDGF)-INDUCED LUNG FIBROBLAST PROLIFERATION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. VET ADM MED CTR,DURHAM,NC 27705. NR 1 TC 1 Z9 1 U1 1 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A277 EP A277 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901027 ER PT J AU BRODY, AR GOODELL, AL BLALOCK, LE AF BRODY, AR GOODELL, AL BLALOCK, LE TI PLATELET-DERIVED GROWTH-FACTOR (PDGF) A-CHAIN AND B-CHAIN MESSENGER-RNA LOCALIZED BY INSITU HYBRIDIZATION INVITRO IN LUNG MACROPHAGES AND INVIVO IN LUNG-TISSUE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A277 EP A277 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901026 ER PT J AU BRODY, SL METZGER, ME CRYSTAL, RG AF BRODY, SL METZGER, ME CRYSTAL, RG TI REPEAT AIRWAY ADMINISTRATION OF REPLICATION DEFICIENT RECOMBINANT ADENOVIRUS VECTORS TO NONHUMAN-PRIMATES IS SAFE AND EFFECTIVE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 6 Z9 6 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A544 EP A544 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902068 ER PT J AU COIN, PG ROGGLI, V BRODY, AR AF COIN, PG ROGGLI, V BRODY, AR TI LONG-TERM PULMONARY CLEARANCE AND FIBROGENESIS AFTER 3 CONSECUTIVE INHALATION EXPOSURES TO CHRYSOTILE ASBESTOS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A909 EP A909 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14903482 ER PT J AU DANEL, C HAY, JG CRYSTAL, RG AF DANEL, C HAY, JG CRYSTAL, RG TI BASAL CELLS EXPRESS MESSENGER-RNA TRANSCRIPTS FOR PROTEINS RESTRICTED TO DIFFERENTIATED CELLS, SUPPORTING THEIR ROLE AS PRECURSOR CELLS IN PROXIMAL HUMAN AIRWAYS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A51 EP A51 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900157 ER PT J AU DICHTER, J LUNDGREN, JD NIELSON, TL JENSEN, BN SCHATTENKERK, J LAWERENCE, M SHELHAMER, J AF DICHTER, J LUNDGREN, JD NIELSON, TL JENSEN, BN SCHATTENKERK, J LAWERENCE, M SHELHAMER, J TI SURFACTANT LIPID PHOSPHATIDYL CHOLINE IN BRONCHOALVEOLAR LAVAGE FLUID IN HIV-INFECTED PATIENTS WITH PNEUMOCYSTIS-CARINII PNEUMONIA - EFFECT OF CORTICOSTEROID-THERAPY OVER TIME SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 HVIDOVRE UNIV HOSP,DK-2650 HVIDOVRE,DENMARK. RIGSHOSP,DK-2100 COPENHAGEN,DENMARK. UNIV AMSTERDAM,ACAD MED CTR,1105 AZ AMSTERDAM,NETHERLANDS. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A34 EP A34 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900092 ER PT J AU EICHACKER, PQ WAISMAN, Y HOFFMAN, WD BANKS, SM RICHMOND, S WILSON, L NATANSON, C AF EICHACKER, PQ WAISMAN, Y HOFFMAN, WD BANKS, SM RICHMOND, S WILSON, L NATANSON, C TI EFFECTS OF PENTOTHAL ANESTHESIA, PARALYSIS, AND MECHANICAL VENTILATION ON OXYGEN DELIVERY AND CONSUMPTION DURING GRADED DECREASES IN BLOOD-FLOW IN THE CANINE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. ARMED FORCES RADIOBIOL RES INST,DEPT EXPTL HEMATOL,BETHESDA,MD 20814. CHILDRENS HOSP,NATL MED CTR,CTR EMERG MED TRAUMA,WASHINGTON,DC 20010. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A620 EP A620 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902365 ER PT J AU EISSA, NT CHU, CS CRYSTAL, RG AF EISSA, NT CHU, CS CRYSTAL, RG TI DETECTION OF ADENOVIRUS-E1A SEQUENCES IN THE RESPIRATORY EPITHELIUM OF NORMALS AND INDIVIDUALS WITH CYSTIC-FIBROSIS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A545 EP A545 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902069 ER PT J AU FLOTTE, TR AFIONE, SA SOLOW, R CONRAD, C MCGRATH, SA ZEITLIN, PL GUGGINO, WB CARTER, BJ AF FLOTTE, TR AFIONE, SA SOLOW, R CONRAD, C MCGRATH, SA ZEITLIN, PL GUGGINO, WB CARTER, BJ TI INVIVO GENE-TRANSFER WITH ADENOASSOCIATED VIRUS VECTORS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,BALTIMORE,MD 21205. NIDDK,MOLEC CELL BIOL LAB,BETHESDA,MD. TARGETED GENET CORP,SEATTLE,WA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A544 EP A544 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902067 ER PT J AU FUKUDA, Y BASSET, F FERRANS, VJ YAMANAKA, N AF FUKUDA, Y BASSET, F FERRANS, VJ YAMANAKA, N TI SIGNIFICANCE OF EARLY INTRAALVEOLAR FIBROTIC LESIONS AND FIBRONECTIN RECEPTORS IN LUNG BIOPSIES FROM PATIENTS WITH IDIOPATHIC PULMONARY FIBROSIS (IPF) SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIPPON MED COLL,DEPT PATHOL,TOKYO 113,JAPAN. FAC XAVIER BICHAT,INSERM,U82,PARIS,FRANCE. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A590 EP A590 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902247 ER PT J AU HAN, SK BRODY, SL CRYSTAL, RG AF HAN, SK BRODY, SL CRYSTAL, RG TI SUPPRESSION OF INVIVO TUMORIGENICITY OF HUMAN LUNG-CANCER CELLS BY RETROVIRUS-MEDIATED TRANSFER OF HUMAN TUMOR-NECROSIS-FACTOR-ALPHA CDNA SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A776 EP A776 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902965 ER PT J AU HAN, SK BRODY, SL CRYSTAL, RG AF HAN, SK BRODY, SL CRYSTAL, RG TI SUPPRESSION OF INVIVO TUMORIGENICITY OF HUMAN LUNG-CANCER CELLS BY RETROVIRUS-MEDIATED TRANSFER OF HUMAN TUMOR-NECROSIS-FACTOR-ALPHA CDNA SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A457 EP A457 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901737 ER PT J AU HAY, JG CHU, CS CRYSTAL, RG AF HAY, JG CHU, CS CRYSTAL, RG TI STRUCTURE, CHROMOSOMAL LOCALIZATION AND POLYMORPHISM OF THE HUMAN AIRWAY SPECIFIC GENE CODING FOR THE CLARA CELL 10 KDA PROTEIN SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A521 EP A521 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901975 ER PT J AU HERNANDEZRODRIGUEZ, NA RAMIREZ, IA BRODY, AR OSORNIOVARGAS, AR AF HERNANDEZRODRIGUEZ, NA RAMIREZ, IA BRODY, AR OSORNIOVARGAS, AR TI TIME-COURSE OF PDGF GENE-EXPRESSION AND SECRETION BY ALVEOLAR MACROPHAGES (AM) EXPOSED TO IRON PARTICLES SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 INST NACL CANCEROL,MEXICO CITY,DF,MEXICO. NIEHS,RES TRIANGLE PK,NC 27709. RI Osornio Vargas, Alvaro/D-4012-2009; Osornio Vargas, Alvaro/B-4645-2010 OI Osornio Vargas, Alvaro/0000-0001-8287-7102 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A276 EP A276 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901024 ER PT J AU KOBAYASHI, N ROSENTHAL, ER YOSHIMURA, K CRYSTAL, RG AF KOBAYASHI, N ROSENTHAL, ER YOSHIMURA, K CRYSTAL, RG TI DESIGN OF PROMOTER-CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR CDNA COMBINATIONS THAT CAN BE TRANSFERRED TO HUMAN EPITHELIAL-CELLS BUT ARE RESISTANT TO DOWN-REGULATION BY INFLAMMATORY STIMULI SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A545 EP A545 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902070 ER PT J AU LARIVEE, P LEVINE, SJ MARTINEZ, A LOGUN, C SHELHAMER, JH AF LARIVEE, P LEVINE, SJ MARTINEZ, A LOGUN, C SHELHAMER, JH TI PROTEIN-KINASE-C ZETA (ZETA) ISOZYME MEDIATES THE AIRWAY MUCIN SECRETORY EFFECT OF PLATELET-ACTIVATING-FACTOR SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A934 EP A934 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14903583 ER PT J AU LECHNER, JF BELINSKY, SA SACCOMANNO, G SAMET, JM BENNETT, WP TIERNEY, LA AF LECHNER, JF BELINSKY, SA SACCOMANNO, G SAMET, JM BENNETT, WP TIERNEY, LA TI GENE ABERRATIONS IN ALPHA-RADIATION-CAUSED LUNG-CANCER SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 INHALAT TOXICOL RES INST,ALBUQUERQUE,NM. ST MARYS HOSP,GRAND JCT,CO. UNIV NEW MEXICO,CTR CANC,ALBUQUERQUE,NM 87131. NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A331 EP A331 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901240 ER PT J AU LEMARCHAND, P JONES, M DANEL, C YAMADA, I MASTRANGELI, A CRYSTAL, RG AF LEMARCHAND, P JONES, M DANEL, C YAMADA, I MASTRANGELI, A CRYSTAL, RG TI STRATEGIES FOR ADENOVIRUS-MEDIATED GENE-THERAPY FOR CYSTIC-FIBROSIS - GENE-TRANSFER DIRECTED TO SUBMUCOSAL GLANDS INVIVO VIA THE PULMONARY-ARTERY SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NHLBI,SLAMS,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A28 EP A28 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900068 ER PT J AU LEVINE, SJ LOGUN, C LARIVEE, P SHELHAMER, JH AF LEVINE, SJ LOGUN, C LARIVEE, P SHELHAMER, JH TI IL-1-BETA INDUCES SECRETION OF RESPIRATORY MUCOUS GLYCOPROTEIN FROM HUMAN AIRWAYS INVITRO SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 9 Z9 9 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A437 EP A437 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901657 ER PT J AU LEVINE, SJ LOGUN, C LARIVEE, P SHELHAMER, JH AF LEVINE, SJ LOGUN, C LARIVEE, P SHELHAMER, JH TI TNF-ALPHA INDUCES SECRETION OF RESPIRATORY MUCOUS GLYCOPROTEIN FROM HUMAN AIRWAYS INVITRO SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,WARREN G AGNUSON CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A1011 EP A1011 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14903885 ER PT J AU LIU, JY NETTESHEIM, P RANDELL, SH AF LIU, JY NETTESHEIM, P RANDELL, SH TI BIOCHEMICAL PATHWAYS OF CELLULAR-DIFFERENTIATION DURING TRACHEAL EPITHELIAL REGENERATION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A465 EP A465 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901766 ER PT J AU LOGUN, C SHELHAMER, JH CHOPRA, DP RHIM, JS LEVINE, SJ AF LOGUN, C SHELHAMER, JH CHOPRA, DP RHIM, JS LEVINE, SJ TI RELEASE OF THE TYPE-I (P55) SOLUBLE TNF RECEPTOR FROM HUMAN AIRWAY SUBMUCOSAL GLAND MUCOUS CELLS FOLLOWING ACTIVATION OF PROTEIN-KINASE-C SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. WAYNE STATE UNIV,INST CHEM TOXICOL,DETROIT,MI 48202. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A436 EP A436 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901656 ER PT J AU MAEDA, H DANEL, C YAMAMOTO, A CRYSTAL, RG AF MAEDA, H DANEL, C YAMAMOTO, A CRYSTAL, RG TI MURINE MODEL OF NEUTROPHIL-DOMINATED LUNG INFLAMMATION INDUCED BY INVIVO ADENOVIRUS-MEDIATED GENE-TRANSFER OF THE HUMAN IL-8 CDNA SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A196 EP A196 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900726 ER PT J AU MAEDA, H DANEL, C YAMAMOTO, A CRYSTAL, RG AF MAEDA, H DANEL, C YAMAMOTO, A CRYSTAL, RG TI MURINE MODEL OF NEUTROPHIL-DOMINATED LUNG INFLAMMATION INDUCED BY INVIVO ADENOVIRUS-MEDIATED GENE-TRANSFER OF THE HUMAN IL-8 CDNA SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A243 EP A243 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900895 ER PT J AU MANZINI, S GOSO, C BLUMBERG, PM SZALLASI, A AF MANZINI, S GOSO, C BLUMBERG, PM SZALLASI, A TI PHARMACOLOGICAL CHARACTERIZATION OF VANILLOID (CAPSAICIN) RECEPTORS IN RAT AIRWAYS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 MENARINI SUD,DEPT PHARMACOL,POMEZIA,ITALY. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A812 EP A812 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14903101 ER PT J AU MARUYAMA, M YOSHIMURA, K CRYSTAL, RG AF MARUYAMA, M YOSHIMURA, K CRYSTAL, RG TI EVALUATION OF MUCOSAL SPECIFIC TRANSCRIPTIONAL REGULATORY SEQUENCES UPSTREAM FROM THE HUMAN SECRETORY LEUKOPROTEASE INHIBITOR GENE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A760 EP A760 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902916 ER PT J AU MASTRANGELI, A JAFFE, HA ROSENFELD, MA WRIGHT, SE CRYSTAL, RG AF MASTRANGELI, A JAFFE, HA ROSENFELD, MA WRIGHT, SE CRYSTAL, RG TI SOMATIC GENE-THERAPY FOR CYSTIC-FIBROSIS - CHRONIC ADMINISTRATION OF ADENOVIRAL VECTORS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 1 TC 2 Z9 2 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A545 EP A545 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902072 ER PT J AU MCELVANEY, NG DOUJAIJI, B MOAN, MJ BURNHAM, MR CRYSTAL, RG AF MCELVANEY, NG DOUJAIJI, B MOAN, MJ BURNHAM, MR CRYSTAL, RG TI AEROSOLIZATION OF RECOMBINANT SECRETORY LEUKOPROTEASE INHIBITOR TO AUGMENT THE ANTINEUTROPHIL ELASTASE DEFENSES OF THE LUNG SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. RI McElvaney, Noel/A-6809-2010 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A679 EP A679 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902599 ER PT J AU MIYASHITA, A HAY, JG CRYSTAL, RG AF MIYASHITA, A HAY, JG CRYSTAL, RG TI EXPRESSION AND REGULATION OF SECRETORY AND CYTOSOLIC PHOSPHOLIPASE-A2 IN THE HUMAN LUNG SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A664 EP A664 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902539 ER PT J AU MOAN, MJ MCELVANEY, NG DOUJAIJI, B CRYSTAL, RG AF MOAN, MJ MCELVANEY, NG DOUJAIJI, B CRYSTAL, RG TI PHARMACOKINETICS OF BIWEEKLY AUGMENTATION THERAPY OF ALPHA-1-ANTITRYPSIN DEFICIENCY WITH HUMAN PLASMA-DERIVED ALPHA-1-ANTITRYPSIN SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. RI McElvaney, Noel/A-6809-2010 NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A675 EP A675 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902583 ER PT J AU PATTERSON, M NATANSON, C HOFFMAN, W ANDRESEN, J CORREA, R KOEV, C BANKS, S RICHMOND, S WILSON, L EICHACKER, P AF PATTERSON, M NATANSON, C HOFFMAN, W ANDRESEN, J CORREA, R KOEV, C BANKS, S RICHMOND, S WILSON, L EICHACKER, P TI PULMONARY EFFECTS OF GRANULOCYTE-COLONY-STIMULATING FACTOR TREATMENT DURING OXYGEN EXPOSURE IN NON-NEUTROPENIC RATS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. CHILDRENS MED CTR,CTR EMERG MED,WASHINGTON,DC. AFPI,WASHINGTON,DC. AMGEN INC,THOUSAND OAKS,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A96 EP A96 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900332 ER PT J AU PITALE, ML LEVINE, SJ LARIVEE, P LOGUN, C KALINER, M SHELHAMER, JH AF PITALE, ML LEVINE, SJ LARIVEE, P LOGUN, C KALINER, M SHELHAMER, JH TI NEUROPEPTIDE MEDIATED CYTOKINE SECRETION IN HUMAN BRONCHIAL EPITHELIAL-CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NIH,WARREN G MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A18 EP A18 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900029 ER PT J AU PITALE, ML LEVINE, SJ LARIVEE, P LOGUN, C KALINER, M SHELHAMER, JH AF PITALE, ML LEVINE, SJ LARIVEE, P LOGUN, C KALINER, M SHELHAMER, JH TI GLUCOCORTICOID INHIBITION OF TNF-ALPHA MEDIATED GM-CSF SECRETION IN HUMAN BRONCHIAL EPITHELIAL-CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A436 EP A436 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901655 ER PT J AU PLOPPER, C WEIR, A NISHIO, S CHANG, A PHILPOT, R BUCKPITT, A AF PLOPPER, C WEIR, A NISHIO, S CHANG, A PHILPOT, R BUCKPITT, A TI CLARA CELL INJURY BY 4-IPOMEANOL DURING DIFFERENTIATION IN THE POSTNATAL RABBIT SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV CALIF DAVIS,SCH VET MED,DEPT VET ANAT & CELL BIOL,DAVIS,CA 95616. UNIV CALIF DAVIS,SCH VET MED,DEPT PHARMACOL & TOXICOL,DAVIS,CA 95616. NIEHS,MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A422 EP A422 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901600 ER PT J AU QUEZADO, ZMN NATANSON, C HOFFMAN, WD DANNER, R BANKS, S DOLAN, D HILTON, A EICHACKER, PQ AF QUEZADO, ZMN NATANSON, C HOFFMAN, WD DANNER, R BANKS, S DOLAN, D HILTON, A EICHACKER, PQ TI CARDIOPULMONARY EFFECTS OF INHALED NITRIC-OXIDE IN CANINE LOBAR AND DIFFUSE GRAM-NEGATIVE PNEUMONIA AT GRADED-LEVELS OF OXYGEN ADMINISTRATION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A720 EP A720 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902762 ER PT J AU RANDELL, SH NETTESHEIM, P AF RANDELL, SH NETTESHEIM, P TI SELECTIVE GROWTH-INHIBITION OF SUBPOPULATIONS OF RAT TRACHEAL EPITHELIAL (RTE) CELLS BY RETINOIC ACID (RA) SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A465 EP A465 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901767 ER PT J AU SETOGUCHI, Y JAFFE, HA HORIAGON, T CHU, CS CRYSTAL, RG AF SETOGUCHI, Y JAFFE, HA HORIAGON, T CHU, CS CRYSTAL, RG TI INVIVO GENE-THERAPY TARGETING THE PERITONEUM FOR ALPHA-1-ANTITRYPSIN DEFICIENCY SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A546 EP A546 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902073 ER PT J AU TRAVIS, WD TRAVIS, LB AF TRAVIS, WD TRAVIS, LB TI LUNG-CANCER INCIDENCE AND SURVIVAL BY HISTOLOGIC TYPE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A775 EP A775 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14902960 ER PT J AU VIVIANO, CJ BAKEWELL, WE HOOK, GER AF VIVIANO, CJ BAKEWELL, WE HOOK, GER TI EXTRACTS OF INFLAMMATORY CELLS FROM THE LUNGS OF RATS STIMULATE PULMONARY LEVELS OF SURFACTANT PROTEIN-A BUT NOT SURFACTANT PHOSPHOLIPID SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,CHAPEL HILL,NC 27514. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A310 EP A310 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901157 ER PT J AU WALKER, RE BOENNING, CM MURPHY, G POLIS, MA KOVACS, JA FALLOON, J DAVEY, RT SUSSMAN, HH GABEL, L CORREACORONAS, R MASUR, H LANE, HC FAUCI, AS AF WALKER, RE BOENNING, CM MURPHY, G POLIS, MA KOVACS, JA FALLOON, J DAVEY, RT SUSSMAN, HH GABEL, L CORREACORONAS, R MASUR, H LANE, HC FAUCI, AS TI THE SAFETY, PHARMACOKINETICS, AND ANTIVIRAL ACTIVITY OF N-ACETYLCYSTEINE IN HIV-INFECTED INDIVIDUALS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 STANFORD UNIV,STANFORD,CA 94305. ZAMBON CORP,E RUTHERFORD,NJ. NIH,CC,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A1004 EP A1004 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14903858 ER PT J AU WIKENHEISER, KA CLARK, JC OIE, HK WHITSETT, JA AF WIKENHEISER, KA CLARK, JC OIE, HK WHITSETT, JA TI GENERATION AND CHARACTERIZATION OF ESTABLISHED LUNG-CELL LINES FROM TRANSGENIC MICE HARBORING THE SV40 LARGE T-ANTIGEN SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,CINCINNATI,OH 45229. NCI,NATL NAVY MED CTR,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A51 EP A51 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900156 ER PT J AU WU, T LAWRENCE, M LOGUN, C SHELHAMER, J AF WU, T LAWRENCE, M LOGUN, C SHELHAMER, J TI INTERFERON-GAMMA (IFN-GAMMA) INDUCES THE EXPRESSION OF CYTOSOLIC PHOSPHOLIPASE-A2 IN HUMAN TRACHEAL EPITHELIAL-CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A19 EP A19 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900031 ER PT J AU WU, T LARIVEE, P LOGUN, C SHELHAMER, JH AF WU, T LARIVEE, P LOGUN, C SHELHAMER, JH TI THE EFFECT OF INTERLUKIN-5 ON ARACHIDONATE METABOLISM IN HUMAN TRACHEAL EPITHELIAL-CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A1011 EP A1011 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14903886 ER PT J AU WU, T LAWRENCE, M LOGUN, C SHELHAMER, J AF WU, T LAWRENCE, M LOGUN, C SHELHAMER, J TI INTERFERON-GAMMA INCREASES 15-HETE PRODUCTION IN HUMAN TRACHEAL EPITHELIAL-CELLS - INVOLVEMENT OF CYTOSOLIC PHOSPHOLIPASE-A2 ACTIVATION SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A437 EP A437 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14901658 ER PT J AU YANKASKAS, JR SUCHINDRAN, H SARKADI, B NETTESHEIM, P RANDELL, SH AF YANKASKAS, JR SUCHINDRAN, H SARKADI, B NETTESHEIM, P RANDELL, SH TI CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) PROTEIN IS SELECTIVELY EXPRESSED IN CILIATED AIRWAY EPITHELIAL-CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 UNIV N CAROLINA,CHAPEL HILL,NC 27514. NIEHS,RES TRIANGLE PK,NC 27709. RI Sarkadi, Balazs/I-5024-2013 NR 3 TC 3 Z9 3 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A26 EP A26 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900060 ER PT J AU YOO, J ERZURUM, SC HAY, JG CRYSTAL, RG AF YOO, J ERZURUM, SC HAY, JG CRYSTAL, RG TI REGULATION OF CATALASE GENE-EXPRESSION IN HUMAN BRONCHIAL EPITHELIAL-CELLS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1993 VL 147 IS 4 SU S BP A206 EP A206 PG 1 WC Respiratory System SC Respiratory System GA LB149 UT WOS:A1993LB14900763 ER PT J AU WELCH, RW ACWORTH, I LEVINE, M AF WELCH, RW ACWORTH, I LEVINE, M TI COULOMETRIC ELECTROCHEMICAL DETECTION OF HYDROXYPROLINE USING 7-CHLORO-4-NITROBENZO-2-OXA-1,3-DIAZOLE SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; CHICK TENDON COLLAGEN; FREE AMINO-ACIDS; PRECOLUMN DERIVATIZATION; SELECTIVE DETERMINATION; ASCORBIC-ACID; TRIPLE-HELIX; PROLINE; 4-CHLORO-7-NITROBENZOFURAZAN; FIBROBLASTS C1 NIDDKD,CELL BIOL & GENET LAB,BLDG 8,ROOM 415,BETHESDA,MD 20892. ESA INC,BEDFORD,MA 01730. NR 34 TC 10 Z9 10 U1 1 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD APR PY 1993 VL 210 IS 1 BP 199 EP 205 DI 10.1006/abio.1993.1173 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA KW265 UT WOS:A1993KW26500032 PM 8489018 ER PT J AU HOFFMAN, GS AF HOFFMAN, GS TI IMMUNOSUPPRESSIVE THERAPY FOR AUTOIMMUNE-DISEASES SO ANNALS OF ALLERGY LA English DT Review ID INTRAVENOUS GAMMA-GLOBULIN; INTERLEUKIN-1 RECEPTOR ANTAGONIST; CHURG-STRAUSS ANGIITIS; GIANT-CELL ARTERITIS; RHEUMATOID-ARTHRITIS; WEGENERS GRANULOMATOSIS; POLYMYALGIA RHEUMATICA; SYSTEMIC VASCULITIS; TEMPORAL ARTERITIS; POLYARTERITIS-NODOSA C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 84 TC 26 Z9 28 U1 0 U2 2 PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY PI ARLINGTON HTS PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 SN 0003-4738 J9 ANN ALLERGY JI Ann. Allergy PD APR PY 1993 VL 70 IS 4 BP 263 EP 274 PG 12 WC Allergy SC Allergy GA KX826 UT WOS:A1993KX82600002 PM 8466090 ER PT J AU CHAPNICK, EK SEPKOWITZ, DV GRADON, JD AF CHAPNICK, EK SEPKOWITZ, DV GRADON, JD TI IMMUNOSUPPRESSIVE EFFECT OF ZIDOVUDINE SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 NIH,BETHESDA,MD 20892. RP CHAPNICK, EK (reprint author), MAIMONIDES HOSP,BROOKLYN,NY 11219, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 1 PY 1993 VL 118 IS 7 BP 571 EP 571 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KU079 UT WOS:A1993KU07900022 PM 8442631 ER PT J AU SIDTIS, JJ GATSONIS, C PRICE, RW SINGER, EJ COLLIER, AC RICHMAN, DD HIRSCH, MS SCHAERF, FW FISCHL, MA KIEBURTZ, K SIMPSON, D KOCH, MA FEINBERG, J DAFNI, U AF SIDTIS, JJ GATSONIS, C PRICE, RW SINGER, EJ COLLIER, AC RICHMAN, DD HIRSCH, MS SCHAERF, FW FISCHL, MA KIEBURTZ, K SIMPSON, D KOCH, MA FEINBERG, J DAFNI, U TI ZIDOVUDINE TREATMENT OF THE AIDS DEMENTIA COMPLEX - RESULTS OF A PLACEBO-CONTROLLED TRIAL SO ANNALS OF NEUROLOGY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; VACUOLAR MYELOPATHY; HIV-1 INFECTION; AZT AB The efficacy of two doses of zidovudine was examined for the treatment of the acquired immunodeficiency syndrome (AIDS) dementia complex in a randomized, double-blinded, placebo-controlled trial conducted at nine study centers. For the initial 16 weeks, 40 subjects with mild to moderate AIDS dementia complex were randomized to one of three treatment arms: 400 mg of zidovudine five times daily, 200 mg of zidovudine five times daily, or placebo five times daily. After week 16, patients initially randomized to the placebo group were rerandomized to one of the two zidovudine treatment arms. The primary efficacy end point was improvement in performance on a battery of seven neuropsychological tests; the secondary end point was improvement on a protocol neurological evaluation directed at the cardinal features of the AIDS dementia complex. For the initial 16-week period, average z scores based on the neuropsychological test battery revealed a significant improvement in the combined treatment groups compared to the placebo group; however, when the two treatment groups were compared separately to the placebo group, only the group receiving the higher zidovudine dose exhibited significant improvement. After rerandomization of the placebo patients to one of the two treatment arms at week 16, this group also showed significant improvement in the average neuropsychological z score by week 32. These results extend previous observations that indicate a therapeutic benefit of zidovudine for the treatment of AIDS dementia complex. C1 HARVARD UNIV,SCH PUBL HLTH,AIDS CLIN TRIALS GRP STAT & DATA ANAL CTR,BOSTON,MA 02115. UNIV ROCHESTER,SCH MED,DEPT NEUROL,ROCHESTER,NY 14627. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. JOHNS HOPKINS UNIV HOSP,DIV INFECT DIS,BALTIMORE,MD 21205. UNIV MIAMI,SCH MED,DEPT MED,MIAMI,FL 33152. CUNY MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. NIAID,BETHESDA,MD 20892. MEM SLOAN KETTERING CANC CTR,DEPT NEUROL,NEW YORK,NY 10021. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. UNIV CALIF SAN DIEGO,DEPT PATHOL,SAN DIEGO,CA 92103. UNIV CALIF SAN DIEGO,DEPT MED,SAN DIEGO,CA 92103. RP SIDTIS, JJ (reprint author), UNIV MINNESOTA HOSP & CLIN,DEPT NEUROL,BOX 295,420 DELAWARE ST SE,MINNEAPOLIS,MN 55455, USA. FU NIAID NIH HHS [AI-27670]; NINDS NIH HHS [NS25701, NS26643] NR 21 TC 226 Z9 229 U1 1 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1993 VL 33 IS 4 BP 343 EP 349 DI 10.1002/ana.410330403 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA KW781 UT WOS:A1993KW78100002 PM 8489204 ER PT J AU JACOBSON, S LEHKY, T NISHIMURA, M ROBINSON, S MCFARLIN, DE DHIBJALBUT, S AF JACOBSON, S LEHKY, T NISHIMURA, M ROBINSON, S MCFARLIN, DE DHIBJALBUT, S TI ISOLATION OF HTLV-II FROM A PATIENT WITH CHRONIC, PROGRESSIVE NEUROLOGICAL DISEASE CLINICALLY INDISTINGUISHABLE FROM HTLV-I-ASSOCIATED MYELOPATHY TROPICAL SPASTIC PARAPARESIS SO ANNALS OF NEUROLOGY LA English DT Note ID VIRUS TYPE-II; CELL LEUKEMIA; HIV-1 AB An increasing spectrum of diseases has been shown to be associated with the human T-cell lymphotropic virus type I (HTLV-I), most notably a chronic, progressive myelopathy termed HTLV-I-associated myelopathy/tropical spastic paraparesis and adult T-cell leukemia. HTLV-II is a close relative of HTLV-I and is structurally similar but molecularly distinct. This virus is endemic in Amerindian populations and a high seroprevalence rate has been observed in intravenous drug abusers. Here, for the first time, we have identified a patient with a chronic, progressive neurological disease clinically indistinguishable from HTLV-I-associated myelopathy/tropical spastic paraparesis from whom we have isolated and characterized HTLV-II in the absence of any other detectable human retrovirus. Antibodies to HTLV were detected in both serum and cerebrospinal fluid, with typical HTLV-II banding patterns on Western blots. HTLV-II viral sequences were detected in high copy number from peripheral lymphocytes by polymerase chain reaction techniques, and cloning and sequencing of this virus revealed a 99.5% homology with prototype HTLV-II. These results serve to alert the medical community to the possibility that in addition to HTLV-I, HTLV-II may be associated with a neurological disorder. C1 UTANO NATL HOSP,CLIN RES CTR,KYOTO,JAPAN. VET ADM,RETROVIRUS RES CTR,BALTIMORE,MD. RP JACOBSON, S (reprint author), NIH,NEUROIMMUNOL BRANCH,BLDG 10,ROOM 5B-16,BETHESDA,MD 20892, USA. NR 18 TC 96 Z9 96 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1993 VL 33 IS 4 BP 392 EP 396 DI 10.1002/ana.410330411 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA KW781 UT WOS:A1993KW78100010 PM 8489210 ER PT J AU POGREBNIAK, HW GALLIN, JI MALECH, HL BAKER, AR MOSKALUK, CA TRAVIS, WD PASS, HI AF POGREBNIAK, HW GALLIN, JI MALECH, HL BAKER, AR MOSKALUK, CA TRAVIS, WD PASS, HI TI SURGICAL-MANAGEMENT OF PULMONARY INFECTIONS IN CHRONIC GRANULOMATOUS-DISEASE OF CHILDHOOD SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT 39TH ANNUAL MEETING OF THE SOUTHERN THORACIC SURGICAL ASSOC CY NOV 05-07, 1992 CL WESLEY CHAPEL, FL SP SO THORAC SURG ASSOC ID TRIMETHOPRIM; PHAGOCYTE; THERAPY; OXIDASE AB Chronic granulomatous disease of childhood is an inheritable disorder of phagocytic cell respiratory burst resulting in recurrent, life-threatening, catalase-positive infections. The lung is the most common site of infection, and pulmonary disease is the primary cause of death in greater than 50% of children with chronic granulomatous disease. Still, the role of surgery in management of this disease remains undefined. Between 1974 and 1990, 19 patients with chronic granulomatous disease required 31 thoracic interventions at our institution. Patients ranged in age from 2.5 to 27 years (mean age, 15 years). Seventeen of 19 patients (89%) had had previous pulmonary infections. Patients presented as toxic (temperature > 38.5-degrees-C, chest pain, and cough) in 22 instances before the 31 procedures. Aggressive surgical intervention for diagnosis and extirpation of localized infections was undertaken with lobectomy/pneumonectomy with or without other procedures (5), bisegmentectomy (2), segmentectomy with or without other procedures (5), or wedge with or without other procedures (13). In five instances, an empyema was drained; a chest tube for a sterile collection was placed in one instance. There was one intraoperative death, and 3 patients died 22 to 600 days postoperatively with overwhelming sepsis. The mean hospitalization was 101 days (range, 24 to 600 days). Wound complications occurred in 5 patients, requiring 17 separate anesthetic debridements. A change in therapy was dictated by the results of the procedure in 23 of 31 instances (74%). Thoracic surgeons must be aware of this rare cause of immunosuppression in these children and, due to the unusual nature of the pulmonary infections, should follow an aggressive approach in their diagnosis and management. C1 NCI,SURG BRANCH,THORAC ONCOL SECT,BLDG 10,RM 2B07,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NIH,CTR CLIN,SURG PATHOL LAB,BETHESDA,MD 20892. NR 20 TC 22 Z9 23 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD APR PY 1993 VL 55 IS 4 BP 844 EP 849 PG 6 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA KX854 UT WOS:A1993KX85400008 PM 8466336 ER PT J AU BICHER, A KOHN, E SAROSY, G DAVIS, P ADAMO, DO JACOB, J CHRISTIAN, M REED, E AF BICHER, A KOHN, E SAROSY, G DAVIS, P ADAMO, DO JACOB, J CHRISTIAN, M REED, E TI THE ABSENCE OF CUMULATIVE BONE-MARROW TOXICITY IN PATIENTS WITH RECURRENT ADENOCARCINOMA OF THE OVARY RECEIVING DOSE-INTENSE TAXOL AND GRANULOCYTE-COLONY STIMULATING FACTOR SO ANTI-CANCER DRUGS LA English DT Article DE CUMULATIVE TOXICITY; DOSE INTENSITY; OVARIAN CANCER; TAXOL ID CANCER; CHEMOTHERAPY; CISPLATIN; TRIALS; AGENT AB Forty-eight patients with recurrent adenocarcinoma of the ovary were treated with taxol and granulocyte colony stimulating factor (G-CSF), with a target taxol dose intensity of 250 mg/m2 every 3 weeks (83.3 mg/m2/week). We have assessed the patterns of granulocyte and platelet toxicity seen in this cohort. Individual patients received up to nine cycles of therapy. Criteria for entry onto protocol included good end organ function, good performance status and the absence of substantial co-morbid disease. Mean taxol dose intensity was 79.0 mg/m2/week for the whole cohort and did not diminish with increased duration of therapy. Granulocytopenia and thrombocytopenia were well controlled, with the average duration of platelet and neutropenic nadirs being less than 1 day for all cycles. There was no evidence of cumulative toxicity for granulocytes nor platelets, for up to eight cycles of therapy. We conclude that taxol, when given with G-CSF support, can be safely administered in a dose-intense fashion for multiple cycles of therapy, without cumulative bone marrow toxicity. C1 NCI,MED BRANCH,MED OVARIAN CANC SECT,BLDG 10,ROOM 12N226,BETHESDA,MD 20892. NR 22 TC 14 Z9 14 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4973 J9 ANTI-CANCER DRUG JI Anti-Cancer Drugs PD APR PY 1993 VL 4 IS 2 BP 141 EP 148 DI 10.1097/00001813-199304000-00003 PG 8 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA KX851 UT WOS:A1993KX85100003 PM 7683933 ER PT J AU RODRIGUEZ, G BROWN, TD BALIS, FM CRAIG, JB DENHAM, CA KUHN, JG HAVLIN, K VONHOFF, DD AF RODRIGUEZ, G BROWN, TD BALIS, FM CRAIG, JB DENHAM, CA KUHN, JG HAVLIN, K VONHOFF, DD TI A PHASE-I TRIAL OF TRIMETREXATE (NSC352122) ON A DAILY X 5 SCHEDULE IN PATIENTS WITH REFRACTORY ADULT LEUKEMIA SO ANTI-CANCER DRUGS LA English DT Article DE DOSE; HEPATOTOXICITY; LEUKEMIA; PHASE-1; TRIMETRAXATE ID FOLATE ANTAGONIST; INVITRO; CANCER; TMQ AB Seven adult patients with refractory acute leukemia were administered trimetrexate (TMTX), a non-classical folate antagonist, in a phase I trial. TMTX was administered as an intravenous bolus for five consecutive days at doses of 9-12 mg/m2 based on marrow response. The maximum tolerated dose was 12 mg/m2 . Hepatotoxicity was the dose-limiting toxicity. Initial dosage reductions in patients with liver disease and/or low protein concentrations may be necessary since TMTX is significantly protein bound and cleared primarily by hepatic metabolism. The recommended phase II dose on this dosing schedule is 9 mg/m2. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78229. CANC THERAPY & RES CTR S TEXAS,SAN ANTONIO,TX 78229. DUKE UNIV,MED CTR,DURHAM,NC. TEXAS ONCOL,PA,DALLAS,TX 75204. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. FU NCI NIH HHS [5N01CM07305-01]; NCRR NIH HHS [5M01RR01346-09] NR 19 TC 2 Z9 2 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4973 J9 ANTI-CANCER DRUG JI Anti-Cancer Drugs PD APR PY 1993 VL 4 IS 2 BP 163 EP 166 DI 10.1097/00001813-199304000-00005 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA KX851 UT WOS:A1993KX85100005 PM 8490194 ER PT J AU MCMAHON, JB GULAKOWSKI, RJ WEISLOW, OS SCHULTZ, RJ NARAYANAN, VL CLANTON, DJ PEDEMONTE, R WASSMUNDT, FW BUCKHEIT, RW DECKER, WD WHITE, EL BADER, JP BOYD, MR AF MCMAHON, JB GULAKOWSKI, RJ WEISLOW, OS SCHULTZ, RJ NARAYANAN, VL CLANTON, DJ PEDEMONTE, R WASSMUNDT, FW BUCKHEIT, RW DECKER, WD WHITE, EL BADER, JP BOYD, MR TI DIARYLSULFONES, A NEW CHEMICAL CLASS OF NONNUCLEOSIDE ANTIVIRAL INHIBITORS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REVERSE-TRANSCRIPTASE SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID HIV AB A series of variously substituted diarylsulfones and related derivatives were found to prevent human immunodeficiency virus type 1 (HIV-1) replication and HIV-1-induced cell killing in vitro. One of the more potent derivatives, 2-nitrophenyl phenyl sulfone (NPPS), completely protected human CEM-SS lymphoblastoid cells from the cytopathic effects of HIV-1 in cell culture at 1 to 5 muM concentrations. HIV-1 replication, as assessed by the production of infectious virions, viral p24 antigen, and virion reverse transcriptase (RT), was inhibited by NPPS at similar concentrations. There was no evidence of direct cytotoxicity of the drug at concentrations below 100 muM. A variety of other CD4+ T-cell lines as well as cultures of peripheral blood leukocytes and monocytes were protected from HIV-1-induced cytopathicity and/or viral replication. NPPS also inhibited several distinctly different strains of HIV-1 but was ineffective against three strains of HIV-2. Biochemical studies revealed that NPPS inhibited HIV-1 RT but not HIV-2 RT. NPPS had no direct effect on HIV-1 virions, nor did it block the initial binding of HIV-1 to target cells. Time-limited treatments of cells with NPPS found that NPPS had to be present continuously in culture to provide maximum antiviral protection. In addition, HIV-1 replication in cells in which infection was already fully established or in chronically infected cells was also unaffected by NPPS. We conclude that NPPS acts in a reversible manner as a nonnucleoside HIV-1-specific RT inhibitor. Although markedly different in structure from a larger, structurally diverse group of known HIV-1-specific nonnucleoside RT inhibitors, NPPS shares several of the biological properties that characterize this emerging new pharmacologic class. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21702. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. UNIV CONNECTICUT,DEPT CHEM,STORRS,CT 06269. SO RES INST,BIRMINGHAM,AL 35255. RP MCMAHON, JB (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES LAB,FREDERICK,MD 21702, USA. NR 16 TC 98 Z9 99 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD APR PY 1993 VL 37 IS 4 BP 754 EP 760 PG 7 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA KV991 UT WOS:A1993KV99100024 PM 7684215 ER PT J AU KAGEYAMA, S MIMOTO, T MURAKAWA, Y NOMIZU, M FORD, H SHIRASAKA, T GULNIK, S ERICKSON, J TAKADA, K HAYASHI, H BRODER, S KISO, Y MITSUYA, H AF KAGEYAMA, S MIMOTO, T MURAKAWA, Y NOMIZU, M FORD, H SHIRASAKA, T GULNIK, S ERICKSON, J TAKADA, K HAYASHI, H BRODER, S KISO, Y MITSUYA, H TI INVITRO ANTI-HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) ACTIVITIES OF TRANSITION-STATE MIMETIC HIV PROTEASE INHIBITORS CONTAINING ALLOPHENYLNORSTATINE SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID HUMAN RENIN INHIBITORS; RATIONAL DESIGN; HTLV-III; ANALOGS; AIDS; INFECTIVITY; RETROVIRUS; CLEAVAGE; ACID; SITE AB Transition state mimetic tripeptide human immunodeficiency virus (HIV) protease inhibitors containing allophenylnorstatine [(2S,3S)-3-amino-2-hydroxy-4-phenylbutyric acid] were synthesized and tested for activity against HIV in vitro. Two compounds, KNI-227 and KNI-272, which were highly potent against HIV protease with little inhibition of other aspartic proteases, showed the most potent activity against the infectivity and cytopathic effect of a wide spectrum of HIV strains. As tested in target CD4+ ATH8 cells, the 50% inhibitory concentrations of KNI-227 against HIV type 1 LAI (HIV-1LAI), HIV-1RF, HIV-1MN, and HIV-2ROD were 0.1, 0.02, 0.03, and 0.1 muM, respectively, while those of KNI-272 were 0.1, 0.02, 0.04, and 0.1 muM, respectively. Both agents completely blocked the replication of 3'-azido-2',3'-dideoxythymidine-sensitive and -insensitive clinical HIV-1 isolates at 0.08 muM as tested in target phytohemagglutinin-activated peripheral blood mononuclear cells. The ratios of 50% cytotoxic concentrations to 50% inhibitory concentrations for KNI-227 and KNI-272 were approximately 2,500 and >4,000, respectively, as assessed in peripheral blood mononuclear cells. Both compounds blocked the posttranslational cleavage of the p55 precursor protein to generate the mature p24 Gag protein in stably HIV-1-infected cells. The n-octanol-water partition coefficients of KNI-227 and KNI-272 were high, with log P(o/w) values of 3.79 and 3.56, respectively. Degradation of KNI-227 and KNI-272 in the presence of pepsin (1 mg/ml, pH 2.2) at 37-degrees-C for 24 h was negligible. Current data warrant further careful investigations toward possible clinical application of these two novel compounds. C1 NCI,MED BRANCH,BETHESDA,MD 20892. NCI,MED CHEM LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702. KYOTO PHARMACEUT UNIV,DEPT PHARMACEUT & PHARMACOKINET,KYOTO 607,JAPAN. KYOTO PHARMACEUT UNIV,DEPT MED CHEM,KYOTO 607,JAPAN. NIKKO KYODO CO LTD,PHARMACEUT & BIOTECHNOL RES LABS,SAITAMA,JAPAN. NR 43 TC 103 Z9 103 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD APR PY 1993 VL 37 IS 4 BP 810 EP 817 PG 8 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA KV991 UT WOS:A1993KV99100034 PM 8494379 ER PT J AU SHI, XL DALAL, NS KASPRZAK, KS AF SHI, XL DALAL, NS KASPRZAK, KS TI GENERATION OF FREE-RADICALS FROM HYDROGEN-PEROXIDE AND LIPID HYDROPEROXIDES IN THE PRESENCE OF CR(III) SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID DNA DAMAGE; GLUTATHIONE-REDUCTASE; HYDROXYL RADICALS; MECHANISM; CHROMIUM(VI); CHROMATE; OXYGEN; DESFERRIOXAMINE; SUPEROXIDE; ACIDS C1 W VIRGINIA UNIV,DEPT CHEM,MORGANTOWN,WV 26506. RP SHI, XL (reprint author), NCI,COMPARAT CARCINOGENESIS LAB,BLDG 538,ROOM 205,FREDERICK,MD 21702, USA. RI Shi, Xianglin/B-8588-2012 NR 42 TC 74 Z9 74 U1 2 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR PY 1993 VL 302 IS 1 BP 294 EP 299 DI 10.1006/abbi.1993.1213 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KW472 UT WOS:A1993KW47200042 PM 8385901 ER PT J AU BINDER, H CONWAY, A GERBER, LH AF BINDER, H CONWAY, A GERBER, LH TI REHABILITATION APPROACHES TO CHILDREN WITH OSTEOGENESIS IMPERFECTA - A 10-YEAR EXPERIENCE SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article DE CHILDREN; OSTEOGENESIS IMPERFECTA; REHABILITATION C1 CHILDRENS NATL MED CTR,DEPT PT OT,WASHINGTON,DC. NIH,DEPT REHABIL,BETHESDA,MD 20892. RP BINDER, H (reprint author), CHILDRENS NATL MED CTR,DEPT PHYS MED & REHABIL,111 MICHIGAN AVE NW,WASHINGTON,DC 20010, USA. NR 5 TC 19 Z9 20 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD APR PY 1993 VL 74 IS 4 BP 386 EP 390 PG 5 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA KX398 UT WOS:A1993KX39800008 PM 8466420 ER PT J AU SINDELAR, W KINSELLA, TJ CHEN, PW DELANEY, TF TEPPER, JE ROSENBERG, SA GLATSTEIN, E AF SINDELAR, W KINSELLA, TJ CHEN, PW DELANEY, TF TEPPER, JE ROSENBERG, SA GLATSTEIN, E TI INTRAOPERATIVE RADIOTHERAPY IN RETROPERITONEAL SARCOMAS - FINAL RESULTS OF A PROSPECTIVE, RANDOMIZED, CLINICAL-TRIAL SO ARCHIVES OF SURGERY LA English DT Article ID SOFT-TISSUE SARCOMAS; RADIATION-THERAPY; PERIPHERAL-NERVE; TOLERANCE; IORT AB Thirty-five patients with surgically resected sarcomas of the retroperitoneum were enrolled in a prospective, randomized, clinical trial comparing 20-Gy intraoperative radiotherapy in combination with postoperative low-dose (35- to 40-Gy) external-beam radiotherapy with postoperative high-dose (50- to 55-Gy) external-beam radiotherapy alone. Chemotherapy with doxorubicin hydrochloride, cyclophosphamide (anhydrous), and methotrexate sodium was used for a portion of the trial. Fifteen patients who received intraoperative radiotherapy and 20 control patients were followed up for a minimum of 5 years (median follow-up, 8 years). Median survival times were similar for the group that received intraoperative radiotherapy (45 months) and the control group (52 months). There were no indications of benefit from adjunctive chemotherapy. The number of locoregional recurrences was significantly lower among those who received intraoperative radiotherapy (six of 15) than control patients (16 of 20). Patients who received intraoperative radiotherapy had fewer complications of disabling radiation-related enteritis (two of 15) than control patients (10 of 20), but radiation-related peripheral neuropathy was more frequent among those who received intraoperative radiotherapy (nine of 15) than among control patients (one of 20). C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. RP SINDELAR, W (reprint author), NCI,SURG BRANCH,BETHESDA,MD 20892, USA. NR 16 TC 210 Z9 221 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD APR PY 1993 VL 128 IS 4 BP 402 EP 410 PG 9 WC Surgery SC Surgery GA KW127 UT WOS:A1993KW12700004 PM 8457152 ER PT J AU KLINMAN, DM DELLACQUA, DK CONOVER, J HUPPI, K AF KLINMAN, DM DELLACQUA, DK CONOVER, J HUPPI, K TI VH FAMILY UTILIZATION BY IGG ANTI-DNA SECRETING LYMPHOCYTES DERIVED FROM AUTOIMMUNE MRL-LPR/LPR MICE SO ARTHRITIS AND RHEUMATISM LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; FILTER-PAPER DISKS; B-CELLS; MURINE LUPUS; NZB/NZW F1-MICE; RENAL-DISEASE; GENE SEGMENTS; AUTOANTIBODIES; ANTIBODIES; STRAINS AB Objective. To evaluate the heterogeneity of the IgG anti-DNA autoantibody response of MRL/lpr mice. Methods. B cell clones were grown on nitrocellulose membranes. Those producing IgG anti-DNA antibodies were identified by a modified enzyme-linked immunospot assay, and their utilization of IgVH genes was determined by hybridization. Results. Four hundred sixty-eight IgG anti-DNA-secreting colonies were derived from 9 autoimmune MRL/lpr mice. Individual VH families contributed to anti-DNA production at a frequency roughly proportional to their representation in the expressed repertoire (except for the more frequent use of VH 7183 and less frequent use of VH 36-60). In individual mice, anti-DNA antibodies were encoded by 2-5 different IgVH families, with no single family constituting more than 27-65% of any animal's anti-DNA response. Conclusion. The IgG anti-DNA response of individual MRL/lpr mice is oligoclonal. C1 NCI,GENET LAB,BETHESDA,MD 20892. RP KLINMAN, DM (reprint author), US FDA,CTR BIOLOG EVALUAT & RES,RETROVIRUS RES LAB,BLDG 29A,ROOM 3DIO,BETHESDA,MD 20892, USA. NR 57 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD APR PY 1993 VL 36 IS 4 BP 561 EP 568 DI 10.1002/art.1780360418 PG 8 WC Rheumatology SC Rheumatology GA KW026 UT WOS:A1993KW02600017 PM 8457230 ER PT J AU FETROW, JS BRYANT, SH AF FETROW, JS BRYANT, SH TI NEW PROGRAMS FOR PROTEIN TERTIARY STRUCTURE PREDICTION SO BIO-TECHNOLOGY LA English DT Review ID KNOWLEDGE-BASED PREDICTION; SECONDARY STRUCTURE; GLOBULAR-PROTEINS; FASCICLIN-III; MEAN FORCE; PACKING; MODELS; CONFORMATIONS; SEQUENCES; ENERGY AB Prediction of protein tertiary structure remains an unsolved problem in molecular biology, but a solution to this problem is extremely important for protein engineering and rational drug design. Recent developments in motif recognition and side chain modeling present the prospect of nearly automatic model building for a large fraction of newly determined protein sequences. We review some of these new algorithms and present preliminary results of their application to the prediction of a structure for fasciclin III, a neural adhesion molecule from Drosophila. C1 NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. RP FETROW, JS (reprint author), SUNY ALBANY,DEPT BIOL SCI,1400 WASHINGTON AVE,ALBANY,NY 12222, USA. NR 56 TC 49 Z9 49 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 0733-222X J9 BIO-TECHNOL JI Bio-Technology PD APR PY 1993 VL 11 IS 4 BP 479 EP 484 DI 10.1038/nbt0493-479 PG 6 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA KV411 UT WOS:A1993KV41100030 PM 7763517 ER PT J AU SAITO, K CHEN, CY MASANA, M CROWLEY, JS MARKEY, SP HEYES, MP AF SAITO, K CHEN, CY MASANA, M CROWLEY, JS MARKEY, SP HEYES, MP TI 4-CHLORO-3-HYDROXYANTHRANILATE, 6-CHLOROTRYPTOPHAN AND NORHARMANE ATTENUATE QUINOLINIC ACID FORMATION BY INTERFERON-GAMMA-STIMULATED MONOCYTES (THP-1 CELLS) SO BIOCHEMICAL JOURNAL LA English DT Note ID 3-HYDROXYANTHRANILIC ACID; CEREBROSPINAL-FLUID; BRAIN; INDOLEAMINE-2,3-DIOXYGENASE; METABOLISM; OXIDASE; DISEASE; SERUM AB Accumulation of quinolinic acid and L-kynurenine occurs in the brain and/or blood following immune activation, and may derive from L-tryptophan following induction of indoleamine 2,3-dioxygenase and other kynurenine-pathway enzymes. In the present study a survey of various cell lines derived from either brain or systemic tissues showed that, while all cells examined reponded to interferon-gamma by increased conversion of L-[C-13(6)]tryptophan into L-kynurenine (human: B-lymphocytes, neuroblastoma, glioblastoma, lung, liver, kidney; rat brain: microglia, astrocytes and oligodendrocytes), only macrophage-derived cells (peripheral-blood mononuclear cells; THP-1, U-937) and certain liver cells (SKHep1) synthesized [C-13(6)]quinolinic acid. Tumour necrosis factor-alpha enhanced the effects of interferon-gamma in THP-1 cells. Norharmane, 6-chloro-DL-tryptophan and 4-chloro-3-hydroxyanthranilate attenuated quinolinic acid formation by THP-1 cells with IC50 values of 51 muM, 58 muM and 0.11 muM respectively. Norharmane and 6-chloro-DL-tryptophan attenuated L-kynurenine formation with IC50 values of 43 muM and 51 muM respectively, whereas 4-chloro-3-hydroxyanthranilate had no effect on L-kynurenine accumulation. The reductions in L-kynurenine and quinolinic acid formation are consistent with the reports that norharmane is an inhibitor of indoleamine 2,3-dioxygenase, 6-chloro-DL-tryptophan is metabolized through the kynurenine pathway, and 4-chloro-3-hydroxyanthranilate is an inhibitor of 3-hydroxyanthranilate 3,4-dioxygenase. These results suggest that many tissues may contribute to the production of L-kynurenine following indoleamine 2,3-dioxygenase induction and immune activation. Quinolinic acid may be directly synthesized from L-tryptophan in both macrophages and certain types of liver cells, although uptake of quinolinic acid precursors from blood may contribute to quinolinic acid synthesis in cells that cannot convert L-kynurenine into quinolinic acid. C1 NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BLDG 10,ROOM 3D40,BETHESDA,MD 20892. NIMH,EXPTL THERAPEUT BRANCH,CLIN PHARMACOL SECT,BETHESDA,MD 20892. NR 26 TC 91 Z9 92 U1 0 U2 2 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD APR 1 PY 1993 VL 291 BP 11 EP 14 PN 1 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KY085 UT WOS:A1993KY08500002 PM 8471029 ER PT J AU GAHL, WA BERNARDINI, I TIETZE, F KOHN, LD AF GAHL, WA BERNARDINI, I TIETZE, F KOHN, LD TI EFFECTS OF CYCLOHEXIMIDE AND TUNICAMYCIN ON LYSOSOMAL CYSTINE TRANSPORT IN RAT FRTL-5 CELLS SO BIOCHEMICAL MEDICINE AND METABOLIC BIOLOGY LA English DT Article ID LEUKOCYTE GRANULAR FRACTIONS; HUMAN FIBROBLAST LYSOSOMES; ENDOCYTIC MEMBRANE SYSTEM; NEUTRAL AMINO-ACIDS; THYROID-CELLS; IODIDE TRANSPORT; COUNTER-TRANSPORT; GLYCOPROTEINS; THYROTROPIN; PROTEIN C1 NICHHD,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. NIDDKD,CELL REGULAT SECT,BIOCHEM & METAB LAB,BETHESDA,MD 20892. RP GAHL, WA (reprint author), NICHHD,HUMAN BIOCHEM GENET SECT,HUMAN GENET BRANCH,BETHESDA,MD 20892, USA. NR 50 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 0885-4505 J9 BIOCHEM MED METAB B PD APR PY 1993 VL 49 IS 2 BP 243 EP 254 DI 10.1006/bmmb.1993.1026 PG 12 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA KZ097 UT WOS:A1993KZ09700013 PM 8484963 ER PT J AU JOSEPHVANDERPOOL, JR JACOBSEN, FM MURPHY, DL HILL, JL ROSENTHAL, NE AF JOSEPHVANDERPOOL, JR JACOBSEN, FM MURPHY, DL HILL, JL ROSENTHAL, NE TI SEASONAL-VARIATION IN BEHAVIORAL-RESPONSES TO M-CPP IN PATIENTS WITH SEASONAL AFFECTIVE-DISORDER AND CONTROLS SO BIOLOGICAL PSYCHIATRY LA English DT Article DE SEASONAL AFFECTIVE DISORDER; SEASONS; LIGHT; SEROTONIN; DEPRESSION; CIRCADIAN RHYTHMS ID OBSESSIVE-COMPULSIVE DISORDER; META-CHLOROPHENYLPIPERAZINE; SEROTONIN AGONIST; 5-HT1C RECEPTOR; NEURO-ENDOCRINE; HUMAN-BRAIN; LIGHT; DEPRESSION; MCPP; PHOTOTHERAPY AB This paper reports the behavioral responses to m-chlorophenylpiperazine (m-CPP), a serotonin agonist, in patients with seasonal affective disorder (SAD) and controls during the summer. Results are compared with the responses of SAD patients and controls given m-CPP in the winter. Results of the winter study were reported earlier by our group. Baseline Hamilton depression ratings in SAD patients were significantly lower in the summer than in winter (p < 0.05). Additionally, in both SAD patients and controls, there were seasonal differences on the National Institute of Mental Health (NIMH) self-rating scale items: ''depressed affect,'' ''dysphoria,'' and ''functional deficit'' at baseline. The behavioral responses to m-CPP across seasons differentiated patients from normals only in the ''activation/euphoria'' item, on which afar greater response was seen in patients than in controls during the winter. This behavioral response may be a state marker for winter depression, as it was significantly reduced after light treatment of these patients in the winter, and in the summer. SAD patients responded differently from controls on ''altered self-awareness'' and ''dysphoria'' independently of seasons, and these responses may be considered as possible trait markers for this condition. These results provide further evidence of a possible deficiency in serotonergic transmission in seasonal affective disorder. C1 NIMH,CLIN PSYCHOBIOL BRANCH,ENVIRONM PSYCHIAT SECT,BLD 10 RM 4S-239,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 58 TC 43 Z9 43 U1 1 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1993 VL 33 IS 7 BP 496 EP 504 DI 10.1016/0006-3223(93)90003-V PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA LD103 UT WOS:A1993LD10300003 PM 8390305 ER PT J AU WINKLER, JD HONG, EC BAHADOR, A KAZANIETZ, MG BLUMBER, PM AF WINKLER, JD HONG, EC BAHADOR, A KAZANIETZ, MG BLUMBER, PM TI SYNTHESIS OF INGENOL ANALOGS WITH AFFINITY FOR PROTEIN-KINASE-C SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID TUMOR PROMOTERS; CONSTRUCTION AB The synthesis and preliminary evaluation of the first biologically active analogs of ingenol are described. Both saturated and unsaturated compounds containing both the C-3 and C-20 oxygen functionalities of ingenol have substantial affinity for protein kinase C. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. RP WINKLER, JD (reprint author), UNIV PENN,DEPT CHEM,PHILADELPHIA,PA 19104, USA. NR 21 TC 24 Z9 24 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD APR PY 1993 VL 3 IS 4 BP 577 EP 580 DI 10.1016/S0960-894X(01)81232-4 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA KX347 UT WOS:A1993KX34700018 ER PT J AU BEUTLER, JA CARDELLINA, JH LIN, CM HAMEL, E CRAGG, GM BOYD, MR AF BEUTLER, JA CARDELLINA, JH LIN, CM HAMEL, E CRAGG, GM BOYD, MR TI CENTAUREIDIN, A CYTOTOXIC FLAVONE FROM POLYMNIA-FRUTICOSA, INHIBITS TUBULIN POLYMERIZATION SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article AB The characteristic pattern of differential cytotoxicity of a crude extract of the tropical plant Polymnia fruticosa was found to be similar to those of known tubulin-interactive compounds. Fractionation of the extract led to centaureidin as the major cytotoxic principle. Centaureidin inhibited tubulin polymerization, inhibited the binding of [H-3]-colchicine to tubulin, and induced mitotic figure formation in whole cells at cytotoxic concentrations. This is the first known example of a flavone with antimitotic activity. C1 NCI,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,NAT PROD BRANCH,FREDERICK,MD 21702. RP BEUTLER, JA (reprint author), UNCI,DIV CANC TREATMENT,DRUG DISCOVERY RES & DEV LAB,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702, USA. RI Beutler, John/B-1141-2009 OI Beutler, John/0000-0002-4646-1924 NR 10 TC 62 Z9 63 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD APR PY 1993 VL 3 IS 4 BP 581 EP 584 DI 10.1016/S0960-894X(01)81233-6 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA KX347 UT WOS:A1993KX34700019 ER PT J AU FUJITA, K SILVER, J AF FUJITA, K SILVER, J TI SURPRISING LABILITY OF BIOTIN-STREPTAVIDIN BOND DURING TRANSCRIPTION OF BIOTINYLATED DNA BOUND TO PARAMAGNETIC STREPTAVIDIN BEADS SO BIOTECHNIQUES LA English DT Article ID RNA-POLYMERASE TRANSCRIBES; ESCHERICHIA-COLI; T7; INITIATION; PROMOTER; ELONGATION; BINDING AB We investigated the use of immobilized DNA templates as substrates for bacterio-phage RIVA polymerases in order to develop a simple method for separating template DNA from synthesized RNA. Double-stranded DNA molecules with a T7 or T3 RNA polymerase promoter at one end and a single biotin moiety at the other end were attached to streptavidin-coated paramagnetic beads and used in transcription reactions. When the biotin was attached by a nucleotide base on the non-template strand, the DNA-bead complex was moderately stable and could be used for multiple rounds of RNA synthesis. However, when the biotin was attached through a phosphodiester bond on the template strand, the enzymatic activity of RNA polymerase reversibly dissociated up to 80% of biotinylated DNA from the streptavidin beads. Biotinylated DNA bound to streptavidin beads in this system with a binding constant on the order of 10(12) M-1. These results stress the need for careful evaluation of solid phase adaptations of standard solution reactions in molecular biology. RP FUJITA, K (reprint author), NIAID,MOLEC MICROBIOL LAB,BLDG 4,ROOM 338,BETHESDA,MD 20892, USA. NR 15 TC 27 Z9 28 U1 0 U2 5 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD APR PY 1993 VL 14 IS 4 BP 608 EP 617 PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV760 UT WOS:A1993KV76000025 PM 7682819 ER PT J AU TIBERGHIEN, P LAITHIER, V MABED, M RACADOT, E REYNOLDS, CW ANGONIN, R LOUMI, R PAVY, JJ CAHN, JY NOIR, A HERVE, P AF TIBERGHIEN, P LAITHIER, V MABED, M RACADOT, E REYNOLDS, CW ANGONIN, R LOUMI, R PAVY, JJ CAHN, JY NOIR, A HERVE, P TI INTERLEUKIN-1 ADMINISTRATION BEFORE LETHAL IRRADIATION AND ALLOGENEIC BONE-MARROW TRANSPLANTATION - EARLY TRANSIENT INCREASE OF PERIPHERAL GRANULOCYTES AND SUCCESSFUL ENGRAFTMENT WITH ACCELERATED LEUKOCYTE, ERYTHROCYTE, AND PLATELET RECOVERY SO BLOOD LA English DT Article ID COLONY-STIMULATING FACTOR; TUMOR-NECROSIS-FACTOR; MICE; IL-1; CELLS; RADIOPROTECTION; NUMBER C1 CTR REG TRANSFUS SANGUINE,UNITE GREFFE MOELLE OSSEUSE,BESANCON,FRANCE. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSES MODIFIERS PROGRAM,FREDERICK,MD 21701. NR 26 TC 19 Z9 20 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1993 VL 81 IS 7 BP 1933 EP 1939 PG 7 WC Hematology SC Hematology GA KV696 UT WOS:A1993KV69600035 PM 8461477 ER PT J AU STRONCEK, DF HOLLAND, PV BARTCH, G BIXBY, T SIMMONS, RG ANTIN, JH ANDERSON, KC ASH, RC BOLWELL, BJ HANSEN, JA HEAL, JM HENSLEEDOWNEY, PJ JAFFE, ER KLEIN, HG LAU, PM PERKINS, HA POPOVSKY, MA PRICE, TH ROWLEY, SD STEHLING, LC WEIDEN, PL WISSEL, ME MCCULLOUGH, J AF STRONCEK, DF HOLLAND, PV BARTCH, G BIXBY, T SIMMONS, RG ANTIN, JH ANDERSON, KC ASH, RC BOLWELL, BJ HANSEN, JA HEAL, JM HENSLEEDOWNEY, PJ JAFFE, ER KLEIN, HG LAU, PM PERKINS, HA POPOVSKY, MA PRICE, TH ROWLEY, SD STEHLING, LC WEIDEN, PL WISSEL, ME MCCULLOUGH, J TI EXPERIENCES OF THE 1ST 493 UNRELATED MARROW DONORS IN THE NATIONAL-MARROW-DONOR-PROGRAM SO BLOOD LA English DT Article ID SEVERE COMBINED IMMUNODEFICIENCY; BONE-MARROW; APLASTIC-ANEMIA; TRANSPLANTATION; PATIENT C1 UNIV MINNESOTA,MINNEAPOLIS,MN 55455. SACRAMENTO MED FDN,CTR BLOOD,SACRAMENTO,CA. UNIV PITTSBURGH,PITTSBURGH,PA 15260. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MED COLL WISCONSIN,MILWAUKEE,WI 53226. CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. AMER RED CROSS,REG BLOOD SERV,ROCHESTER,NY. AMER RED CROSS,REG BLOOD SERV,ST PAUL,MN. UNIV KENTUCKY,LEXINGTON,KY 40506. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. NIH,CTR CLIN,BETHESDA,MD 20892. IRWIN MEM BLOOD BANK,SAN FRANCISCO,CA. VIRGINIA MASON CLIN,SEATTLE,WA. FU NHLBI NIH HHS [N01-HB-97075] NR 17 TC 76 Z9 78 U1 2 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1993 VL 81 IS 7 BP 1940 EP 1946 PG 7 WC Hematology SC Hematology GA KV696 UT WOS:A1993KV69600036 PM 8461478 ER PT J AU WILLIAMS, CKO ALEXANDER, SS BODNER, A LEVINE, A SAXINGER, C GALLO, RC BLATTNER, WA AF WILLIAMS, CKO ALEXANDER, SS BODNER, A LEVINE, A SAXINGER, C GALLO, RC BLATTNER, WA TI FREQUENCY OF ADULT T-CELL LEUKEMIA LYMPHOMA AND HTLV-I IN IBADAN, NIGERIA SO BRITISH JOURNAL OF CANCER LA English DT Article ID WESTERN EQUATORIAL AFRICA; LEUKEMIA-LYMPHOMA; GUAYMI INDIANS; VIRUS; INFECTION; PANAMA; GABON AB Sera from a small sample of adult blood donors, healthy school children and patients with lymphoma, leukaemia, non-haematologic cancer, congenital and inflammatory disorders from Ibadan, Nigeria were screened for HTLV-I antibody by an enzyme-linked immunoabsorbent assay and confirmed by investigational Western blot. Seventy-nine of 236 positively screened samples could not be tested for confirmation. Seropositive reactivity was observed in nine of 123 blood donors, and 3 of 46 healthy school children but banding patterns on Western blot were often sparse. Among non-Burkitt's non Hodgkin's lymphoma patients six of 30 were HTLV-I positive including four of four with clinical features of adult T-cell leukaemia (ATL). Other clinical conditions had a frequency of positivity indistinguishable from healthy donors. Western blot patterns ranged from strong with multiple bands, which were uncommon, to those with only p24 and p21 envelope positive which were frequent. Given the relative paucity of clinical ATL and the unusual Western blot patterns the true rate of HTLV-I infection may be lower than estimated. It is possible that a cross-reactive HTLV-I-like virus accounts for this pattern. C1 UNIV IBADAN,COLL MED,DEPT HAEMATOL,IBADAN,NIGERIA. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,VIRAL EPIDEMIOL SECT,ROCKVILLE,MD 20892. BIOTECH RES LABS INC,ROCKVILLE,MD 20850. FU NCI NIH HHS [N01 CP 51030] NR 24 TC 12 Z9 13 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD APR PY 1993 VL 67 IS 4 BP 783 EP 786 DI 10.1038/bjc.1993.142 PG 4 WC Oncology SC Oncology GA KV247 UT WOS:A1993KV24700025 PM 8471436 ER PT J AU GOSO, C MANZINI, S BLUMBERG, PM SZALLASI, A AF GOSO, C MANZINI, S BLUMBERG, PM SZALLASI, A TI COMPETITIVE-INHIBITION BY CAPSAZEPINE OF [H-3] RESINIFERATOXIN BINDING TO THE VANILLOID RECEPTOR SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. MENARINI SUD,DEPT PHARMACOL,I-00040 POMEZIA,ITALY. NR 3 TC 3 Z9 3 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD APR PY 1993 VL 108 SU S BP P306 EP P306 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KX107 UT WOS:A1993KX10700306 ER PT J AU EGAN, MF DARGHAM, AA KIRCH, DG WYATT, RJ AF EGAN, MF DARGHAM, AA KIRCH, DG WYATT, RJ TI SERUM CREATINE-PHOSPHOKINASE ELEVATIONS IN PATIENTS WITH TARDIVE-DYSKINESIA SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Note ID DYSTONIA AB We describe a case of marked increases in serum creatine phosphokinase (CPK) associated with a dramatic exacerbation of tardive dyskinesia (TD). Chart review of eight additional patients with severe TD revealed three cases with mild CPK elevations. These cases suggest that TD, especially when accompanied by dystonia, may be associated with pathology of striated muscle. C1 CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC. DIV CLIN RES,ROCKVILLE,MD. NEUROPSYCHIAT BRANCH,WASHINGTON,DC. RP EGAN, MF (reprint author), NIMH,NEUROSCI RES CTR & ST ELIZABETHS,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032, USA. NR 11 TC 7 Z9 8 U1 1 U2 1 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD APR PY 1993 VL 162 BP 551 EP 553 DI 10.1192/bjp.162.4.551 PG 3 WC Psychiatry SC Psychiatry GA KX344 UT WOS:A1993KX34400019 PM 8097656 ER PT J AU HUMPHREYS, BL LINDBERG, DAB AF HUMPHREYS, BL LINDBERG, DAB TI THE UMLS(R) PROJECT - MAKING THE CONCEPTUAL CONNECTION BETWEEN USERS AND THE INFORMATION THEY NEED SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article ID NETWORK; MEDLINE AB Conceptual connections between users and information sources depend on an accurate representation of the content of available information sources, an accurate representation of specific user information needs, and the ability to match the two. Establishing such connections is a principal function of medical librarians. The goal of the National Library of Medicine's Unified Medical Language System(TM) (UMLS(R)) project is to facilitate the development of conceptual connections between users and relevant machine-readable information. The UMLS model involves a combination of three centrally developed Knowledge Sources (a Metathesaurus, a Semantic Network, and an Information Sources Map) and a variety of smart interface programs that make use of these Knowledge Sources to help users in different environments find machine-readable information relevant to their particular practice or research problems. The third experimental edition of the UMLS Knowledge Sources was issued in the fall of 1992. Current priorities for the UMLS project include developing applications that make use of the Knowledge Sources and using feedback from these applications to guide ongoing enhancement and expansion of the Knowledge Sources. Medical librarians are involved heavily in the direction of the UMLS project, in the development of the Knowledge Sources, and in their experimental application. The involvement of librarians in reviewing, testing, and providing feedback on UMLS products will increase the likelihood that the UMLS project will achieve its goal of improving access to machine-readable biomedical information. RP HUMPHREYS, BL (reprint author), NATL LIB MED,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. RI Winstein, Carolee/A-8375-2008 NR 41 TC 88 Z9 92 U1 0 U2 1 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD APR PY 1993 VL 81 IS 2 BP 170 EP 177 PG 8 WC Information Science & Library Science SC Information Science & Library Science GA KX031 UT WOS:A1993KX03100005 PM 8472002 ER PT J AU KINGLAND, LC HARBOURT, AM SYED, EJ SCHUYLER, PL AF KINGLAND, LC HARBOURT, AM SYED, EJ SCHUYLER, PL TI COACH(TM) - APPLYING UMLS KNOWLEDGE SOURCES IN AN EXPERT SEARCHER ENVIRONMENT SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article ID MEDLINE AB With the development of the Unified Medical Language System(TM) (UMLS(R)) Knowledge Sources, the National Library of Medicine (NLM) has produced a resource of great potential for improving the searching of MEDLINE.(R) The Coach(TM) expert searcher system, an in-house research project at NLM, is designed to help users of the GRATEFUL MED(R) front-end software improve MEDLINE search and retrieval capabilities. This paper describes the Coach program, the knowledge sources it uses, and some of the ways it applies elements of the UMLS Metathesaurus(R) to facilitate access to the biomedical literature. C1 NATL LIB MED,MESH SECT,BETHESDA,MD 20894. RP KINGLAND, LC (reprint author), NATL LIB MED,COMP SCI BRANCH,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 11 TC 24 Z9 24 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD APR PY 1993 VL 81 IS 2 BP 178 EP 183 PG 6 WC Information Science & Library Science SC Information Science & Library Science GA KX031 UT WOS:A1993KX03100006 PM 8472003 ER PT J AU MCCRAY, AT ARONSON, AR BROWNE, AC RINDFLESCH, TC RAZI, A SRINIVASAN, S AF MCCRAY, AT ARONSON, AR BROWNE, AC RINDFLESCH, TC RAZI, A SRINIVASAN, S TI UMLS(R) KNOWLEDGE FOR BIOMEDICAL LANGUAGE PROCESSING SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article AB This paper describes efforts to provide access to the free text in biomedical databases. The focus of the effort is the development of SPECIALIST, an experimental natural language processing system for the biomedical domain. The system includes a broad coverage parser supported by a large lexicon, modules that provide access to the extensive Unified Medical Language System(TM) (UMLS(R)) Knowledge Sources, and a retrieval module that permits experiments in information retrieval. The UMLS Metathesaurus(R) and Semantic Network provide a rich source of biomedical concepts and their interrelationships. Investigations have been conducted to determine the type of information required to effect a map between the language of queries and the language of relevant documents. Mappings are never straightforward and often involve multiple inferences. C1 MANAGEMENT SYST DESIGNERS INC,VIENNA,VA 22180. RP MCCRAY, AT (reprint author), NATL LIB MED,COMP SCI BRANCH,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 16 TC 41 Z9 41 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD APR PY 1993 VL 81 IS 2 BP 184 EP 194 PG 11 WC Information Science & Library Science SC Information Science & Library Science GA KX031 UT WOS:A1993KX03100007 PM 8472004 ER PT J AU SCHUYLER, PL HOLE, WT TUTTLE, MS SHERERTZ, DD AF SCHUYLER, PL HOLE, WT TUTTLE, MS SHERERTZ, DD TI THE UMLS METATHESAURUS(R) - REPRESENTING DIFFERENT VIEWS OF BIOMEDICAL CONCEPTS SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article AB The UMLS Metathesaurus(R) is a compilation of names, relationships, and associated information from a variety of biomedical naming systems representing different views of biomedical practice or research. The Metathesaurus is organized by meaning, and the fundamental unit in the Metathesaurus is the concept. Differing names for a biomedical meaning are linked in a single Metathesaurus concept. Extensive additional information describing semantic characteristics, occurrence in machine-readable information sources, and how concepts co-occur in these sources is also provided, enabling a greater comprehension of the concept in its various contexts. The Metathesaurus is not a standardized vocabulary; it is a tool for maximizing the usefulness of existing vocabularies. It serves as a knowledge source for developers of biomedical information applications and as a powerful resource for biomedical information specialists. C1 NATL LIB MED,LISTER HILL NATL CTR BIOMED COMMUN,COMP SCI BRANCH,BETHESDA,MD 20894. LEX TECHNOL INC,ALAMEDA,CA 94501. RP SCHUYLER, PL (reprint author), NATL LIB MED,MED SUBJECT HEADINGS SECT,LIB OPERAT,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 12 TC 62 Z9 62 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD APR PY 1993 VL 81 IS 2 BP 217 EP 222 PG 6 WC Information Science & Library Science SC Information Science & Library Science GA KX031 UT WOS:A1993KX03100010 PM 8472007 ER PT J AU POTTER, WZ KETTER, TA AF POTTER, WZ KETTER, TA TI PHARMACOLOGICAL ISSUES IN THE TREATMENT OF BIPOLAR DISORDER - FOCUS ON MOOD-STABILIZING COMPOUNDS SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Article; Proceedings Paper CT SATELLITE SYMP ON VALPROATE ( DIVALPROEX SODIUM ) IN THE TREATMENT OF BIPOLAR DISORDER, AT THE 42ND ANNUAL MEETING OF THE CANADIAN PSYCHIATRIC ASSOC CY SEP 18, 1992 CL MONTREAL, CANADA SP CANADIAN PSYCHIAT ASSOC ID IMPORTANT DRUG-INTERACTIONS; VALPROIC ACID; CARBAMAZEPINE; PRINCIPLES AB The acute and chronic pharmacotherapy of bipolar disorder requires an understanding of the pharmacology of very dissimilar compounds - the mood stabilizers (lithium, carbamazepine and valproate) and several classes of antidepressants. No definitive data are available on the primary mode of action of mood stabilizers, and those used show no single pharmacological property. On the other hand, the pharmacokinetics and dynamics of these compounds are well studied. C1 NIMH,W CLIN RES UNIT 3,BETHESDA,MD 20892. RP POTTER, WZ (reprint author), NIMH,EXPTL THERAPEUT BRANCH,CLIN PHARMACOL SECT,BLDG 10,ROOM 2D46,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 20 TC 11 Z9 11 U1 0 U2 0 PU CANADIAN PSYCHIATRIC ASSOC PI OTTAWA PA SUITE 200, 237 ARGYLE AVE, OTTAWA ON K2P 1B8, CANADA SN 0706-7437 J9 CAN J PSYCHIAT JI Can. J. Psychiat.-Rev. Can. Psychiat. PD APR PY 1993 VL 38 IS 3 SU 2 BP S51 EP S56 PG 6 WC Psychiatry SC Psychiatry GA LB147 UT WOS:A1993LB14700003 PM 8500079 ER PT J AU LEUNG, SW MITCHELL, JB ALNABULSI, I FRIEDMAN, N NEWSOME, J BELLDEGRUN, A KASID, U AF LEUNG, SW MITCHELL, JB ALNABULSI, I FRIEDMAN, N NEWSOME, J BELLDEGRUN, A KASID, U TI EFFECT OF L-BUTHIONINE SULFOXIMINE ON THE RADIATION RESPONSE OF HUMAN RENAL-CARCINOMA CELL-LINES SO CANCER LA English DT Article DE RENAL CELL CARCINOMA CELL LINES; RADIATION RESPONSE; GLUTATHIONE; BUTHIONINE SULFOXIMINE ID GLUTATHIONE S-TRANSFERASES; DEPLETION; CANCER; SENSITIVITY; IRRADIATION; GAMMA; INTERLEUKIN-4; INHIBITION; SURVIVAL; INVITRO AB Background. Renal cell carcinoma (RCC) is a progressive and relatively radioresistant disease. Currently, no data are available on the in vitro radiobiologic characterization of renal tumor cells to the authors' knowledge. Methods. Two RCC were cultured from specimens from previously untreated patients after either surgical resection of the primary tumor or from the malignant ascites. These two cell lines were characterized with respect to cytogenetic abnormalities, gamma radiation survival response, intracellular levels of glutathione and its related detoxification enzymes, and the effect of glutathione depletion on radiation toxicity. Results. The two RCC grew as adherent monolayer cultures with a median doubling time of 29 hours and 37 hours, respectively. Histopathologic analysis of the tumor cells grown in the renal capsule of the athymic mice confirmed their epithelial neoplastic growth. Both cell lines were aneuploid (range, 65-100 chromosomes) and had several marker chromosomes, including those derived from chromosomes 3, 7, and 11. In vitro radiation survival analysis indicated the relative radioresistance (RR; D(o), 2.35 Gy) and relative radiosensitivity (RS; D(o), 1.42 Gy), respectively, of these tumor cell lines. The levels of intracellular glutathione (GSH) were higher in the RR cells compared with the RS cells. The enzymatic activities of GSH S-transferase, GSH reductase, and the levels of GSH peroxidase and superoxide dismutase were elevated in the RS cells compared with the RR cells. L-Buthionine sulfoximine (BSO) treatment (concentration, 20 muM, applied for 17 hours) resulted in 77% and 63% GSH depletion compared with the untreated RR and RS cells, respectively. Pretreatment with higher concentration of BSO (50 muM for 17 hours) caused a modest radiosensitization of the RR cells (D(o), 1.78 Gy). Conclusions. RCC have a differential pattern of radiosensitivity. BSO treatment causes moderate radiosensitization of the relatively radioresistant renal tumor cells. C1 GEORGETOWN UNIV, LOMBARDI CANC CTR, DEPT RADIAT MED, WASHINGTON, DC 20007 USA. GEORGETOWN UNIV, RES RESOURCES FACIL, WASHINGTON, DC 20057 USA. UNIV CALIF LOS ANGELES, MED CTR DIV UROL, LOS ANGELES, CA USA. NCI, RADIAT ONCOL BRANCH, BETHESDA, MD 20892 USA. NR 40 TC 21 Z9 21 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0008-543X J9 CANCER-AM CANCER SOC JI Cancer PD APR 1 PY 1993 VL 71 IS 7 BP 2276 EP 2285 DI 10.1002/1097-0142(19930401)71:7<2276::AID-CNCR2820710718>3.0.CO;2-7 PG 10 WC Oncology SC Oncology GA KU002 UT WOS:A1993KU00200017 PM 8095848 ER PT J AU FIELDING, LP HENSON, DE AF FIELDING, LP HENSON, DE TI MULTIPLE PROGNOSTIC FACTORS AND OUTCOME ANALYSIS IN PATIENTS WITH CANCER - COMMUNICATION FROM THE AMERICAN JOINT COMMITTEE ON CANCER SO CANCER LA English DT Note DE CANCER; PROGNOSIS; STAGING; PROGNOSTIC FACTOR; OUTCOME ANALYSIS; PROGNOSTIC SYSTEMS ID BREAST-CANCER AB The authors report the establishment of a new Committee of the American Joint Committee on Cancer that has two objectives as follows: (1) to review the methods available to estimate outcome and (2) to study certain tumors to determine whether an expanded list of prognostic factors can be formulated into new prognostic systems that will have scientific value and clinical utility for treatment selection and staging. C1 NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,BETHESDA,MD 20892. RP FIELDING, LP (reprint author), ST MARYS HOSP,DEPT SURG,56 FRANKLIN ST,WATERBURY,CT 06706, USA. NR 15 TC 38 Z9 38 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1993 VL 71 IS 7 BP 2426 EP 2429 DI 10.1002/1097-0142(19930401)71:7<2426::AID-CNCR2820710742>3.0.CO;2-L PG 4 WC Oncology SC Oncology GA KU002 UT WOS:A1993KU00200040 PM 8453566 ER PT J AU CASSIDY, J AF CASSIDY, J TI THE ROLE OF THE DATA MANAGER IN CLINICAL CANCER-RESEARCH - AN OPPORTUNITY FOR NURSES SO CANCER NURSING LA English DT Article DE DATA MANAGEMENT; CLINICAL TRIALS; CLINICAL RESEARCH; AUDITS; DATA BASE; DATA MANAGER AB A clinical trial is a research study conducted in humans and designed to answer specific questions using scientifically controlled methods. These trials require considerable effort to assure that the data obtained are reliable, reproducible, and readily available. Data managers play a key role in this research effort. A nurse with a clinical background, computer knowledge, and some experience in the research environment is well suited for the role of data manager. The data manager performs a variety of tasks in this position that will enhance the quality of the data gathered in a research study. These responsibilities include designing forms, monitoring protocol accrual, abstracting data, entering data onto protocol-specific forms and/or specifically designed computerized data-entry screens, assuring the quality and the integrity of the data, and providing investigators with interim and summary reports. In addition, the data manager can be responsible for the management of a computerized clinical data base system, including the training of users and the designing of basic reports for the investigators. A nurse, functioning as a data manager, who understands research methodology, is detail oriented, and is well organized, could be a valuable asset to the clinical trials team in the successful management of any clinical study. RP CASSIDY, J (reprint author), NCI,DEPT HLTH & HUMAN SERV,CLIN ONCOL PROGRAM,BLDG 10,ROOM 12N-214,BETHESDA,MD 20892, USA. NR 6 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0162-220X J9 CANCER NURS JI Cancer Nurs. PD APR PY 1993 VL 16 IS 2 BP 131 EP 138 PG 8 WC Oncology; Nursing SC Oncology; Nursing GA KY282 UT WOS:A1993KY28200008 PM 8477401 ER PT J AU BERMAN, A CHISHOLM, L DECARVALHO, M PIEMME, JA GORRELL, CR AF BERMAN, A CHISHOLM, L DECARVALHO, M PIEMME, JA GORRELL, CR TI CANCER-CHEMOTHERAPY - INTRAVENOUS ADMINISTRATION SO CANCER NURSING LA English DT Article C1 ST LUKES ROOSEVELT HOSP,DEPT NURSING EDUC DEV & RES,NEW YORK,NY 10025. VET ADM MED CTR,MARTINSBURG,WV 25401. RP BERMAN, A (reprint author), NIH,CTR CLIN,DEPT NURSING,BETHESDA,MD 20892, USA. NR 4 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0162-220X J9 CANCER NURS JI Cancer Nurs. PD APR PY 1993 VL 16 IS 2 BP 145 EP 160 PG 16 WC Oncology; Nursing SC Oncology; Nursing GA KY282 UT WOS:A1993KY28200010 PM 8477403 ER PT J AU KADOMATSU, K ANZANO, MA SLAYTER, MV WINOKUR, TS SMITH, JM SPORN, MB AF KADOMATSU, K ANZANO, MA SLAYTER, MV WINOKUR, TS SMITH, JM SPORN, MB TI EXPRESSION OF SULFATED GLYCOPROTEIN-2 IS ASSOCIATED WITH CARCINOGENESIS INDUCED BY N-NITROSO-N-METHYLUREA IN RAT PROSTATE AND SEMINAL-VESICLE SO CANCER RESEARCH LA English DT Note ID LOBUND-WISTAR RATS; MOUSE EMBRYOGENESIS; MOLECULAR-CLONING; VENTRAL PROSTATE; MESSENGER-RNA; CDNA CLONING; CELL-DEATH; CANCER; GENE; COMPLEMENT AB To understand the molecular mechanism of carcinogenesis ill androgen-dependent tumors, we have searched for new markers which are associated with this process. In normal rat prostate and seminal vesicle, sulfated glycoprotein 2 (SGP-2) messenger RNA is barely detectable. However, we have found high levels of SGP-2 expression in the epithelial component of carcinomas of the prostate and seminal vesicle after initiation with N-nitroso-N-methylurea and promotion with testosterone propionate. We have also observed induction of SGP-2 expression in epithelial cells at early stages in carcinogenesis when cytologically malignant cells first begin to appear. SGP-2 has been reported previously to be associated with a variety of models of programmed cell death (apoptosis), including the prostate following castration. Our present findings provide a novel marker for carcinogenesis in the rat prostate and seminal vesicle. C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. RP KADOMATSU, K (reprint author), NCI,CHEMOPREVENT LAB,BLDG 41,ROOM C-629,BETHESDA,MD 20892, USA. RI Kadomatsu, Kenji/G-8083-2012 NR 18 TC 35 Z9 35 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1993 VL 53 IS 7 BP 1480 EP 1483 PG 4 WC Oncology SC Oncology GA KV615 UT WOS:A1993KV61500002 PM 8453611 ER PT J AU DANFORTH, DN SGAGIAS, MK AF DANFORTH, DN SGAGIAS, MK TI INTERLEUKIN-1-ALPHA AND INTERLEUKIN-6 ACT ADDITIVELY TO INHIBIT GROWTH OF MCF-7 BREAST-CANCER CELLS-INVITRO SO CANCER RESEARCH LA English DT Article ID TUMOR NECROSIS FACTOR; MESSENGER RIBONUCLEIC-ACID; FACTOR-BETA; DIFFERENTIAL REGULATION; ESTROGEN-RECEPTOR; EPITHELIAL-CELLS; IL-6 PRODUCTION; HEPATOMA-CELLS; PROTEIN-LEVELS; LINES AB We studied the effects of interleukin-1alpha (IL-1) and interleukin-6 (IL-6) on MCF-7 breast cancer cells to determine whether these cytokines act additively/synergistically to alter cell growth and metabolism. We found that IL-1 alone (1000 units/ml) inhibited cell growth to a greater degree (83.8%) than IL-6 alone (29.2%, P < 0.001). The combination of IL-1 + IL-6 caused greater inhibition of growth (92.9%, P < 0.02) than either cytokine alone. The additive effect was dose dependent for both IL-1 and IL-6. IL-1 and IL-6 also antagonized estradiol (10(-9) M) stimulated growth. Antagonism by the combination was greater than for either cytokine alone (P < 0.001). IL-1 or IL-6 alone each down-regulated the estrogen receptor (36.7%, P < 0.01, and 23.2%, P < 0.05, respectively), but the combination IL-1 + IL-6 did not cause a significantly greater effect than IL-1 alone. Neither IL-1 or IL-6 blocked estradiol stimulation of progesterone receptor (PR) synthesis; however, the combination IL-1 + IL-6 increased PR content by 28.4% (P < 0.01). IL-1, but not IL-6, increased secretion of transforming growth factor-beta (TGF-beta) by 2.45-fold over 72 h (P < 0.01). The increase was time dependent (detectable at 24 h) and dose dependent (maximum increase of 5.3-fold, 10,000 units/ml, P < 0.02). IL-1-induced TGF-beta secretion was blocked by estradiol (10(-9) M). Neither cytokine altered secretion of insulin-like growth factor-1. These findings indicate that IL-1 and IL-6 act additively to inhibit growth in the absence or presence of estradiol and modulate the estrogen receptor and progesterone receptor content of these cells. TGF-beta may mediate the effects of IL-1; however, other pathways appear to be required for the additive effects of these cytokines. RP DANFORTH, DN (reprint author), NCI, SURG BRANCH, BLDG 10, RM 2B38, BETHESDA, MD 20892 USA. NR 44 TC 74 Z9 74 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1993 VL 53 IS 7 BP 1538 EP 1545 PG 8 WC Oncology SC Oncology GA KV615 UT WOS:A1993KV61500014 PM 8453620 ER PT J AU LING, YH PRIEBE, W YANG, LY BURKE, TG POMMIER, Y PEREZSOLER, R AF LING, YH PRIEBE, W YANG, LY BURKE, TG POMMIER, Y PEREZSOLER, R TI INVITRO CYTOTOXICITY, CELLULAR PHARMACOLOGY, AND DNA LESIONS INDUCED BY ANNAMYCIN, AN ANTHRACYCLINE DERIVATIVE WITH HIGH-AFFINITY FOR LIPID-MEMBRANES SO CANCER RESEARCH LA English DT Article ID TOPOISOMERASE-II INHIBITORS; RESISTANT P388 LEUKEMIA; HAMSTER CELLS RESISTANT; CYTO-TOXICITY; STRAND BREAKS; ANTITUMOR ANTHRACYCLINES; MULTIDRUG RESISTANCE; SINGLE-STRAND; L1210 CELLS; ADRIAMYCIN AB Annamycin (AN) is an anthracycline antibiotic with high affinity for lipid membranes which is being developed for clinical studies formulated in liposomes. We studied the in vitro cytotoxicity, cellular pharmacology, and DNA damage induced by AN in P388 cells sensitive and resistant to doxorubicin (DOX). AN was as cytotoxic as DOX against P388-sensitive cells and about 50 times more cytotoxic than DOX against P388-resistant cells (resistance index 5 for AN versus 250 for DOX). Cellular uptake of AN by sensitive cells was 2-3-fold higher than that of DOX. In resistant cells, cellular uptake of AN and DOX was approximately 65% and 30%, respectively, of the cellular uptake in sensitive cells. As a result, cellular uptake of AN by resistant cells was higher than uptake of DOX by sensitive cells. DOX was fully retained in sensitive cells while it was effluxed rapidly from resistant cells. In contrast, efflux of AN was similar in sensitive and resistant cells, thus suggesting that it is not mediated by P-glycoprotein. AN was more effective than DOX in inducing single DNA breaks, double DNA breaks, and DNA-protein cross-links, both in sensitive and resistant cells, although DNA damage was lower in resistant cells than in sensitive cells. DNA lesions induced by AN in resistant cells were similar to or greater than those induced by DOX in sensitive cells. These studies indicate that the lack of cross-resistance between DOX and AN appears to be related, at least in part, to the relatively higher cellular uptake of AN compared with DOX and is associated with the ability of AN to induce significant DNA damage in resistant cells. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT LAB MED,HOUSTON,TX 77030. OHIO STATE UNIV,COLL PHARM,DIV PHARMACEUT,COLUMBUS,OH 43210. NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RP PEREZSOLER, R (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,DEPT MED ONCOL,DIV MED,BOX 80,HOUSTON,TX 77030, USA. FU NCI NIH HHS [CA50270] NR 47 TC 45 Z9 45 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1993 VL 53 IS 7 BP 1583 EP 1589 PG 7 WC Oncology SC Oncology GA KV615 UT WOS:A1993KV61500022 PM 8453627 ER PT J AU KIM, S KHATIBI, S HOWELL, SB MCCULLY, C BALIS, FM POPLACK, DG AF KIM, S KHATIBI, S HOWELL, SB MCCULLY, C BALIS, FM POPLACK, DG TI PROLONGATION OF DRUG EXPOSURE IN CEREBROSPINAL-FLUID BY ENCAPSULATION INTO DEPOFOAM SO CANCER RESEARCH LA English DT Article ID DEFINED SIZE-DISTRIBUTION; CYTOSINE-ARABINOSIDE; MULTIVESICULAR LIPOSOMES; 1-BETA-D-ARABINOFURANOSYLCYTOSINE; CELLS; METHOTREXATE; CHEMOTHERAPY; KINETICS; LEUKEMIA; THERAPY AB Prolonged maintenance of a therapeutic drug concentration in the cerebrospinal fluid is required for optimal treatment of leptomeningeal leukemia or carcinomatosis with cell cycle-specific antimetabolites. The pharmacokinetics of 1-beta-D-arabinofuranosylcytosine (ara-C) encapsulated into DepoFoam (Depo/Ara-C) was studied in six rhesus monkeys after intrathecal injection into the lumbar sac. Following a single 2-mg dose, the Depo/Ara-C concentration decreased biexponentially with initial and terminal half-lives of 14.6 and 156 h, respectively. The free drug concentration remained above the reported minimal cytotoxic level of 0.1 mug/ml (0.4 muM) for more than 672 h (28 days). In contrast, the half-life of ara-C following an intralumbar bolus dose of unencapsulated drug in a single animal was 0.74 h. A single intrathecal injection of Depo/Ara-C can maintain a therapeutic drug concentration in the cerebrospinal fluid for a very prolonged period. C1 NCI,DIV CANC TREATMENT,PEDIAT BRANCH,BETHESDA,MD 20892. RP KIM, S (reprint author), UNIV CALIF SAN DIEGO,CTR CANC,DEPT MED,DIV HEMATOL ONCOL,LA JOLLA,CA 92093, USA. FU NCI NIH HHS [CA 23100, CA 35309] NR 21 TC 45 Z9 46 U1 0 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1993 VL 53 IS 7 BP 1596 EP 1598 PG 3 WC Oncology SC Oncology GA KV615 UT WOS:A1993KV61500024 PM 8453629 ER PT J AU DELEO, AB BECKER, M LU, L LAW, LW AF DELEO, AB BECKER, M LU, L LAW, LW TI PROPERTIES OF A M(R) 110,000 TUMOR REJECTION ANTIGEN OF THE CHEMICALLY-INDUCED BALB/C METH A SARCOMA SO CANCER RESEARCH LA English DT Article ID ENDOPLASMIC-RETICULUM; PROTEINS; MOUSE; GLYCOPROTEIN; ASSIGNMENT; ABUNDANT; BINDING; CELLS; GP96 AB A M(r) 110,000 glycoprotein, designated gp110, isolated from the concanavalin A-Sepharose-binding protein fraction of the chemically induced BALB/c Meth A sarcoma by Mono Q fast protein liquid chromatography, has been shown to: (a) increase the resistance of these mice to growth of the Meth A sarcoma, but not the antigenically unrelated BALB/c CI-4 sarcoma, and (b) induce an antitumor cellular immune response in mice, which was detectable in cell-mediated cytotoxic assays. The immunogenicity of the concanavalin A-Sepharose-binding protein fraction of Meth A cytosol had been attributed to gp96, the major component of this fraction. The evidence presented here, however, demonstrates that Meth A gp96, when sufficiently purified, is nonimmunogenic. The results of the present analysis of gp110 strongly support the concept that gp110 represents a family of proteins expressed on a variety of chemically induced tumors, in which variations in molecular fine structure account for the antigenic diversity associated with these tumors. C1 UNIV PITTSBURGH,SCH MED,DEPT PATHOL,PITTSBURGH,PA 15213. NCI,CELL BIOL LAB,BETHESDA,MD 20892. RP DELEO, AB (reprint author), UNIV PITTSBURGH,PITTSBURGH CANC INST,DIV BASIC RES,BIOMED SCI TOWER,PITTSBURGH,PA 15213, USA. FU NCI NIH HHS [CA-44276] NR 29 TC 15 Z9 15 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1993 VL 53 IS 7 BP 1602 EP 1607 PG 6 WC Oncology SC Oncology GA KV615 UT WOS:A1993KV61500026 PM 7680955 ER PT J AU VERTINO, PM SPILLARE, EA HARRIS, CC BAYLIN, SB AF VERTINO, PM SPILLARE, EA HARRIS, CC BAYLIN, SB TI ALTERED CHROMOSOMAL METHYLATION PATTERNS ACCOMPANY ONCOGENE-INDUCED TRANSFORMATION OF HUMAN BRONCHIAL EPITHELIAL-CELLS SO CANCER RESEARCH LA English DT Article ID C-MYC PROTOONCOGENES; DNA METHYLATION; NEOPLASTIC TRANSFORMATION; DENOVO METHYLATION; TUMOR PROGRESSION; CALCITONIN GENE; LUNG-CANCER; SHORT ARM; HETEROZYGOSITY; DELETIONS AB Abnormal methylation of CpG island sequences on chromosomes 11p and 17p, and tumor phenotype-associated differential methylation of chromosome 3p loci have been described in human lung tumors (S. B. Baylin, J. W. M. Hoppener, A. de Bustros, P. H. Steenbergh, C. J. M. Lips, and B. D. Nelkin, Cancer Res., 46: 2917-2922, 1986; M. Makos, B. D. Nelkin, M. I. Lerman, F. Latif, B. Zbar, and S. B. Baylin, Proc. Natl. Acad. Sci. USA, 89: 1929-1933,1992; A. de Bustros, B. D. Nelkin, A. Silverman, G. Ehrlich, B. Poiesz, and S. B. Baylin, Proc. Natl. Acad. Sci. USA, 85: 5693-5697, 1988). Using an in vitro model of lung tumor progression, we now show that these aberrant methylation patterns occur at different stages during cellular immortalization and oncogene-induced neoplastic transformation of normal human bronchial epithelial cells (NHBE). The CALC1 CpG island locus on chromosome 11p15.4 was essentially unmethylated in NHBE and simian virus 40 T-antigen immortalized NHBE (BEAS-2B cells) but became de novo methylated in 5 of 6 BEAS-2B derived cell lines that were transfected or infected with various oncogenes and in a spontaneously neoplastically transformed subline of BEAS-2B cells. By contrast, an additional CpG island locus, pYNZ22, at 17p13.3 became fully methylated following the immortalization of NHBE and was not further changed by oncogene-induced transformation. Finally, at a non-CpG island locus pYNZ86.1 on chromosome 3p14, different tumor phenotype-associated methylation patterns became apparent only after passage of the tumorigenic oncogene-transformed bronchial epithelial cell lines in athymic nude mice. Whereas cell lines derived from tumors with a non-small cell lung carcinoma-like phenotype were significantly hypomethylated relative to their parental cell lines, a cell line derived from a tumor with a more small cell lung carcinoma-like phenotype retained the methylation status of its parental cell line. The data indicate that altered DNA methylation patterns, including the de novo methylation of normally unmethylated CpG island sequences and demethylation of nonisland sequences, arise at different stages during immortalization and oncogene-induced neoplastic transformation of bronchial epithelial cells. These findings suggest that DNA methylation abnormalities accompany, or may play a role in, the genetic changes that occur during lung tumor progression. C1 NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. RP VERTINO, PM (reprint author), JOHNS HOPKINS UNIV,CTR ONCOL,SCH MED,424 N BOND ST,BALTIMORE,MD 21231, USA. FU NCHHSTP CDC HHS [1PS0 CA58184]; NCI NIH HHS [5RO1 CA43318] NR 41 TC 36 Z9 37 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1993 VL 53 IS 7 BP 1684 EP 1689 PG 6 WC Oncology SC Oncology GA KV615 UT WOS:A1993KV61500040 PM 8453642 ER PT J AU KATO, S PETRUZZELLI, S BOWMAN, ED TURTELTAUB, KW BLOMEKE, B WESTON, A SHIELDS, PG AF KATO, S PETRUZZELLI, S BOWMAN, ED TURTELTAUB, KW BLOMEKE, B WESTON, A SHIELDS, PG TI 7-ALKYLDEOXYGUANOSINE ADDUCT DETECTION BY 2-STEP HPLC AND THE P-32 POSTLABELING ASSAY SO CARCINOGENESIS LA English DT Article ID TOBACCO-SPECIFIC NITROSAMINES; LIVER DNA; MOLECULAR EPIDEMIOLOGY; METHYLATING AGENTS; MASS-SPECTROMETRY; ETHYLATING AGENTS; NUCLEIC-ACIDS; HUMAN CANCER; RAT-LIVER; 7-METHYLGUANINE AB 7-Alkyldeoxyguanosine DNA adducts may be a marker for some N-nitroso compound exposures and subsequent human cancer risk. A sensitive and highly specific assay for the detection of 7-methyl-2'-deoxyguanosine-3'-monophosphate (7-methyldGp) and 7-ethyl-2'-deoxyguanosine-3'-monophosphate (7-ethyldGp) has been developed by combining two different HPLC purification steps with the P-32-postlabeling assay. We previously reported that ion-pair reverse-phase (IP) chromatography coupled with the P-32-postlabeling assay detects 7-methyldGp in human lung, but have found that other nucleotides and unknown adducts co-elute. Thus, weak anion exchange (AE) HPLC was added in tandem with IP HPLC prior to the P-32-postlabeling assay. 2'-Deoxyguanosine-3'-monophosphate (dGp) is incorporated into the assay as an internal standard for the assessment of enzyme labeling efficiency and adduct recovery. The methodology was validated using radiolabeled DNA and liquid scintillation counting, which accounts for adduct loss from enzymatic digestion to detection. Levels of 7-ethyldGp also were correlated with accelerator mass spectrometry. The overall adduct recovery with this method was 58% for 7-methyldGp and 98% for 7-ethyldGp. The detection limit for both assays using 100 mug of DNA was one adduct in 10(8) umnodified dGp. 7-MethyldGp and 7-ethyIdGp levels were determined in ten human lung samples at levels of 1.4 - 5.4 and 0.6 - 3.1 adducts per 10(7) dGp respectively, and in five human lymphocyte samples at levels of 5.0 - 8.3 and 0.3 - 1.4 adducts per 10(7) dGp respectively. Combining the two HPLC purification steps and the P-32-postlabeling assay attains chemical specificity, retains sufficient quantitative sensitivity and should be useful in human biomonitoring studies. C1 NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. LAWRENCE LIVERMORE NATL LAB,DIV BIOL SCI,LIVERMORE,CA 94550. RI Shields, Peter/I-1644-2012 NR 56 TC 63 Z9 63 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1993 VL 14 IS 4 BP 545 EP 550 DI 10.1093/carcin/14.4.545 PG 6 WC Oncology SC Oncology GA KW704 UT WOS:A1993KW70400001 PM 8386066 ER PT J AU KAIGHN, ME KUMARI, HL SPALDING, JW BARRETT, JC IYPE, PT AF KAIGHN, ME KUMARI, HL SPALDING, JW BARRETT, JC IYPE, PT TI DIFFERENTIAL GROWTH-CONTROL OF NORMAL, PRENEOPLASTIC AND NEOPLASTIC SYRIAN-HAMSTER EMBRYO CELLS IN SERUM-FREE MEDIA SO CARCINOGENESIS LA English DT Article ID ENHANCED MORPHOLOGICAL TRANSFORMATION; REDUCED BICARBONATE CONCENTRATION; RAPID CLONAL GROWTH; DEFINED MEDIUM; EPIDERMAL-KERATINOCYTES; PRIMARY CULTURES; SERIAL PASSAGE; INDUCTION; PH; INVITRO AB The objective of this work was to develop a serum-free medium that supported the growth of secondary Syrian hamster embryo (SHE) cells suitable for use in the morphological transformation assay (MTA). The current assay employs high levels of fetal bovine serum, each lot of which must be selected for its efficacy in the assay. To circumvent the problems associated with the use of serum, two serum-free media (CGM-4 and CGM-9) were developed. The approach used was to replace serum with more defined hormones and growth factors. DME/F12 with tow NaHCO3 (pH 6.7) was chosen as a basal nutrient medium since this pH has been reported to give enhanced transformation. Both serum-free media supported the clonal high density growth of normal secondary SHE cells. These media were also found to support the growth of several established SHE cell lines exhibiting successive stages of neoplastic progression. However, significant differential responses of the individual cell lines to CGM-4 and CGM-9 were observed, whereas, in serum-supplemented medium all three tines responded similarly. These results raise the hope that CGM-4 and CGM-9 will be useful for studies of altered autocrine function during transformation and progression as well as for use in the transformation assay itself. C1 BIOL RES FAC & FACIL INC,10075-20 TYLER PL,IJAMSVILLE,MD 21754. NIEHS,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [N44-ES-02001] NR 35 TC 1 Z9 1 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1993 VL 14 IS 4 BP 579 EP 584 DI 10.1093/carcin/14.4.579 PG 6 WC Oncology SC Oncology GA KW704 UT WOS:A1993KW70400007 PM 8472318 ER PT J AU BISHOP, RE DUNN, LL PAULY, GT DOLAN, ME MOSCHEL, RC AF BISHOP, RE DUNN, LL PAULY, GT DOLAN, ME MOSCHEL, RC TI THE ROLE OF O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE IN PROTECTING RAT4 CELLS AGAINST THE MUTAGENIC EFFECTS OF O-6-SUBSTITUTED GUANINE RESIDUES INCORPORATED IN CODON-12 OF THE H-RAS GENE SO CARCINOGENESIS LA English DT Article ID METHYL-N-NITROSOUREA; ALKYLATING-AGENTS; ESCHERICHIA-COLI; MUTATIONAL SPECIFICITY; DNA-SEQUENCES; LACI GENE; REPAIR; O-6-METHYLGUANINE; ONCOGENES; OLIGONUCLEOTIDE AB The role of rat O6-alkylguanine-DNA alkyltransferase (AGT) in modulating mutagenesis by O6-substituted guanines in the rat H-ras gene was examined. Rat4 cells were transfected with vectors carrying O6-methyl-, O6-ethyl- or O6-benzylguanine residues in place of the normal guanines at either the first, second, or both the first and second positions in codon 12 (GGA) of the H-ras coding sequence. The percentage of transformed colonies was determined for cells grown in normal medium or in medium containing O6-benzylguanine to completely deplete AGT. In parallel experiments with O6-methylguanine-containing vectors, the percentage of cellular DNA harboring codon 12 mutations was determined for normal cells and cells lacking AGT. A reasonable correspondence was observed between the percentage of mutated DNA and the percentage of transformed colonies produced in both types of cells. The results indicate that the contribution of AGT to the repair of O6-substituted guanine damage decreases as the O6 substituent is changed from methyl > ethyl > benzyl. Additionally, cellular AGT appears to repair an O6-methylguanine more readily at the first position of codon 12 than the second position. However, other repair mechanisms in these mammalian cells appear to play a major role in correcting low levels of O6-substituted guanine damage including O6-methylguanine damage. C1 NCI, FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM, CHEM CARCINOGENESIS LAB,POB B, FREDERICK, MD 21702 USA. UNIV CHICAGO, MED CTR, DEPT HEMATOL ONCOL, CHICAGO, IL 60637 USA. FU NCI NIH HHS [CA-47228, N01-CO-74101] NR 45 TC 14 Z9 14 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1993 VL 14 IS 4 BP 593 EP 598 DI 10.1093/carcin/14.4.593 PG 6 WC Oncology SC Oncology GA KW704 UT WOS:A1993KW70400009 PM 8472320 ER PT J AU TSUTSUI, T WATANABE, E BARRETT, JC AF TSUTSUI, T WATANABE, E BARRETT, JC TI ABILITY OF PEROXISOME PROLIFERATORS TO INDUCE CELL-TRANSFORMATION, CHROMOSOME-ABERRATIONS AND PEROXISOME PROLIFERATION IN CULTURED SYRIAN-HAMSTER EMBRYO CELLS SO CARCINOGENESIS LA English DT Article ID <4-CHLORO-6-(2,3-XYLIDINO)-2-PYRIMIDINYLTHIO>ACETIC ACID WY-14,643; RAT-LIVER; DNA-SYNTHESIS; DI(2-ETHYLHEXYL)PHTHALATE DEHP; MORPHOLOGICAL TRANSFORMATION; MUTAGENICITY ASSAY; MAJOR METABOLITES; CLOFIBRIC ACID; OVARY CELLS; DI-(2-ETHYLHEXYL)PHTHALATE AB Di(2-ethylhexyl)phthalate (DEHP), a commonly use plasticizer, induces proliferation of peroxisomes in liver cells and causes hepatocellular carcinomas when chronically administered in the diet to rodents. To examine possible mechanisms for DEHF-associated cancer, we have measured induction of morphological transformation, chromosome aberrations and peroxisome proliferations of cultured Syrian hamster embryo (SHE) cells by DEHP and other peroxisome proliferators. Morphological transformation of SHE cells was weakly induced by treatment for 48 h with DEHP and its metabolite mono(2-ethythexyl)phthalate (MEHP). The transformation frequency by DEHP was enhanced by exogenous metabolic activation using rat liver postmitochondrial supernatants. Treatment for 24 h with DEHP resulted in chromosome aberrations of the cells only in the presence of exogenous metabolic activation. 2-(p-chlorophenoxy)-2-methylpropionic acid ethyl ester (clofibrate), a widely used hypolipidemic drug, failed to induce morphological transformation or chromosome aberrations of SHE cells. Treatment with [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio] acetic acid (WV-14,643), which is a more potent carcinogen than DEHP or clofibrate, elicited a lower frequency of morphological transformation than DEHP in the presence of exogenous metabolic activation but was more active than DEHP at inducing chromosome aberrations. Similar levels of peroxisome proliferation, as determined by an intensity of diaminobenzidine staining, were observed in cultures treated for 2 h with DEHP, MEHP, clofibrate or WY-14,643. These results suggest a possible involvement of genetic damage by DEHP metabolites in the induction of cell transformation of SHE cells by DEHP; however, no clear relationship among induction of peroxisome proliferation, carcinogenicity in vivo and cell transformation was observed. Although the ability to induce cell transformation and chromosomal mutations is not adequate to explain the carcinogenicity of this class of compounds, these biological effects may be contributory to the carcinogenic activities of peroxisome proliferators. C1 NIEHS,MOLEC CARCINOGENESIS LAB,POB 12233,RES TRIANGLE PK,NC 27709. NIPPON DENT UNIV TOKYO,SCH DENT,DEPT PHARMACOL,CHIYODA KU,TOKYO 102,JAPAN. NR 49 TC 32 Z9 34 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1993 VL 14 IS 4 BP 611 EP 618 DI 10.1093/carcin/14.4.611 PG 8 WC Oncology SC Oncology GA KW704 UT WOS:A1993KW70400013 PM 8472324 ER PT J AU KOHN, MC MELNICK, RL AF KOHN, MC MELNICK, RL TI SPECIES-DIFFERENCES IN THE PRODUCTION AND CLEARANCE OF 1,3-BUTADIENE METABOLITES - A MECHANISTIC MODEL INDICATES PREDOMINANTLY PHYSIOLOGICAL, NOT BIOCHEMICAL, CONTROL SO CARCINOGENESIS LA English DT Article ID PARTITION-COEFFICIENTS; B6C3F1 MICE; BONE-MARROW; RATS; PHARMACOKINETICS; CARCINOGENICITY; BUTADIENE; EXPOSURE AB Inhaled 1,3-butadiene, a monomer used in the production of synthetic rubber and other resins, is metabolized to mutagenic and carcinogenic epoxide intermediates. A physiologically based pharmacokinetic model of the uptake, tissue distribution, and metabolism of butadiene was constructed to determine if the biochemical kinetic constants obtained from in vitro studies are consistent with the observed in vivo uptake and metabolism. The model includes compartments for lung, blood, fat, liver, other rapidly perfused tissues ('viscera') and slowly perfused tissues. Metabolism of butadiene was assumed to occur in viscera in addition to lung and liver. Enzymatic reaction rate equations for the formation of 1,2-epoxy-3-butene, for hydrolysis of this epoxide, and for its conjugation with glutathione were also included. Physiological and biochemical parameters for the mouse, rat and human were obtained from the literature; they were not adjusted to produce a fit to experimental data. The model was used to test the hypothesis that differences in uptake and clearance of butadiene by the three species are due to differences in the activities of the metabolizing enzymes. The model reproduces whole-body observations for the mouse and rat. It predicts that inhalation uptake of butadiene and formation and retention of epoxybutene are controlled to a much greater extent by physiological parameters than by biochemical parameters and that storage in the fat represents a significant fraction of the retained butadiene. Accumulation of epoxybutene in the blood is predicted to be higher in mice than in rats or humans, but accumulation of the epoxide intermediate in the liver is predicted to be highest in humans. The epoxide tissue concentrations predicted by the model do not, by themselves, correlate with tumor incidence in mice and rats, indicating that other factors are crucial for carcinogenesis induced by butadiene. RP KOHN, MC (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 40 TC 51 Z9 52 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1993 VL 14 IS 4 BP 619 EP 628 DI 10.1093/carcin/14.4.619 PG 10 WC Oncology SC Oncology GA KW704 UT WOS:A1993KW70400014 PM 8472325 ER PT J AU HAYES, RB BI, WF ROTHMAN, N BROLY, F CAPORASO, N FENG, P YOU, XJ YIN, SN WOOSLEY, RL MEYER, UA AF HAYES, RB BI, WF ROTHMAN, N BROLY, F CAPORASO, N FENG, P YOU, XJ YIN, SN WOOSLEY, RL MEYER, UA TI N-ACETYLATION PHENOTYPE AND GENOTYPE AND RISK OF BLADDER-CANCER IN BENZIDINE-EXPOSED WORKERS SO CARCINOGENESIS LA English DT Article ID ACETYLTRANSFERASE PHENOTYPES; AROMATIC-AMINES; CARCINOGENESIS; ACTIVATION; ASSOCIATION; POPULATION; DAPSONE AB Several studies in subjects occupationally exposed to arylamine carcinogens have shown increased risks for bladder cancer associated with the slow acetylator phenotype. To follow up these reports, a case-control study of N-acetylation and bladder cancer risk was carried out among subjects occupationally exposed to benzidine, in benzidine dye production and use facilities in China. Thirty-eight bladder cancer cases and 43 controls from these factories were included for study of acetylation phenotype, by dapsone administration, and for polymorphisms in the NAT2 gene, by a polymerase chain reaction (PCR)-based test . In contrast to previous studies, no increase in bladder cancer risk was found for the slow N-acetylation phenotype (OR = 0.3; 95% CI = 0.1 - 1.3) or for slow N-acetylation-associated double mutations in NAT2 (OR = 0.5; 95% CI = 0.1-1.8). Examination of specific mutations and adjustment for age, weight, city and tobacco use did not alter the results. When examined by level of benzidine exposure in the cases, the bladder cancer risks associated with low (OR= 0.3, 95% CI = 0.0 - 2.2), medium (OR 0.7, 95% CI = 0.1 - 4.5) and high (OR = 0.6, 95% CI = 0.1-3.5) exposure showed no interaction between genotype and benzidine exposure, within the range of exposures experienced by subjects in this study. This study, which is the first to incorporate phenotypic and genotypic analyses, provides evidence that the NAT2-related slow N-acetylation polymorphism is not associated with an increased risk of bladder cancer in workers exposed to benzidine, and may have a protective effect. C1 UNIV BASEL,BIOCTR,DEPT PHARMACOL,CH-4056 BASEL,SWITZERLAND. CHINESE ACAD PREVENT MED,BEIJING,PEOPLES R CHINA. TIANJIN BUR CHEM IND,INST LABOUR HYG,TIANJIN,PEOPLES R CHINA. SHANGHAI INST OCCUPAT MED,SHANGHAI,PEOPLES R CHINA. GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20057. RP HAYES, RB (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 36 TC 128 Z9 129 U1 1 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1993 VL 14 IS 4 BP 675 EP 678 DI 10.1093/carcin/14.4.675 PG 4 WC Oncology SC Oncology GA KW704 UT WOS:A1993KW70400022 PM 8472331 ER PT J AU SINGH, J KELLOFF, G REDDY, BS AF SINGH, J KELLOFF, G REDDY, BS TI INTERMEDIATE BIOMARKERS OF COLON CANCER - MODULATION OF EXPRESSION OF RAS ONCOGENE BY CHEMOPREVENTIVE AGENTS DURING AZOXYMETHANE INDUCED COLON CARCINOGENESIS SO CARCINOGENESIS LA English DT Article ID MURINE SARCOMA-VIRUS; NONSTEROIDAL ANTIINFLAMMATORY DRUG; PROTEIN KINASE-C; MONOCLONAL-ANTIBODIES; TUMOR DEVELOPMENT; GENE-EXPRESSION; 3T3 CELLS; P21; BINDING; GROWTH AB In our attempts to evaluate the influence of chemopreventive agents on intermediate biomarkers of colon cancer, we have investigated the effect of D,L-alpha-difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase and piroxicam, a non-steroidal anti-inflammatory drug (NSAID) on the expression levels of biochemically active p21ras, the protein product of cellular ras protooncogenes during the development of azoxymethane (AOM) induced colon carcinogenesis in male F344 rats in order to explore the plausibility of using p21ras as an intermediate biochemical marker of colon cancer. Groups of male F344 rats were fed the modified AIN-76A diets containing 0 or 150 p.p.m. piroxicam or 4000 p.p.m. DFMO and administered s.c. AOM dissolved in normal saline at a dose of 15 mg/kg body wt/week, once weekly, for 4 weeks. Vehicle control groups received s.c. equal vol of normal saline. Groups of animals were then killed at 0, 4, 16, 24 and 32 weeks after the last injection of AOM or saline and their colonic mucosa and tumors analyzed for biochemically active p21ras levels. AOM treatment significantly increased the expression of biochemically active p21ras. The AOM-induced expression of biochemically active p21ras was significantly suppressed by dietary DFMO and piroxicam. DFMO exerted a more pronounced inhibitory effect on AOM-induced colon tumor development as well as the expression of biochemically active p21ras. These results indicate that the determination of biochemically active p21ras may be effectively used in clinical chemoprevention trials as an intermediate end-point to monitor the colon carcinogenesis. C1 NCI,DIV CANC CONTROL & PREVENT,CHEMOPREVENT BRANCH,BETHESDA,MD 20892. RP SINGH, J (reprint author), AMER HLTH FDN,DIV NUTR CARCINOGENESIS,1 DANA RD,VALHALLA,NY 10595, USA. FU NCI NIH HHS [CA-17613, N01-CN-85095-03] NR 52 TC 39 Z9 39 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1993 VL 14 IS 4 BP 699 EP 704 DI 10.1093/carcin/14.4.699 PG 6 WC Oncology SC Oncology GA KW704 UT WOS:A1993KW70400026 PM 8472334 ER PT J AU CHEN, LC SLY, L JONES, CS TARONE, R DE LUCA, LM AF CHEN, LC SLY, L JONES, CS TARONE, R DE LUCA, LM TI DIFFERENTIAL-EFFECTS OF DIETARY BETA-CAROTENE ON PAPILLOMA AND CARCINOMA FORMATION INDUCED BY AN INITIATION-PROMOTION PROTOCOL IN SENCAR MOUSE SKIN SO CARCINOGENESIS LA English DT Article ID VITAMIN-A; TUMORS; MICE; CANCER; CANTHAXANTHIN AB SENCAR mice were used to determine the effects of the provitamin A compound beta-carotene on papilloma formation and the conversion of papillomas to carcinomas in a two-stage protocol with one application of the initiator 7,12-dimethylbenz[a]anthracene (DMBA, 20 mug) and 20 weekly applications of the promoter 12-0-tetradecanoylphorbol-13-acetate (TPA, 2 mug). A purified vitamin A-free diet was supplemented with beta-carotene at four levels (0.6, 6, 60 and 600 mug/g of diet) for female mice and two levels (60 and 600 mug/g) for male mice. Dietary supplementations of beta-carotene did not result in significant changes in body weight and survival of female and male mice. However, papillomas developed more rapidly and papilloma incidence (% mice with papillomas) reached its maximum (100%) sooner in male mice fed 600 mug of beta-carotene/g of diet than those fed 60 mug/g. There were smaller differences in papilloma incidence among the dietary groups in female mice, but the papilloma incidence again reached 100% sooner in mice fed 600 mug of beta-carotene/g of diet. Female and male mice fed 600 mug of beta-carotene/g of diet had significantly higher papilloma yields (average number of papillomas/mouse) than other dietary groups and a very low percentage of these papillomas converted to carcinomas in these mice. Thus, beta-carotene at 600 mug/g inhibited the conversion of papillomas to carcinomas in both sexes. In addition, papilloma yields were higher in female mice and these papillomas regressed more quickly than those in the corresponding groups of male mice. In conclusion, dietary beta-carotene caused differential effects on papilloma and carcinoma yields and sex-dependent differences in papilloma formation in female and male SENCAR mice treated with DMBA and TPA in a two-stage carcinogenesis protocol. C1 NCI, CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB, BETHESDA, MD 20892 USA. NCI, BIOSTAT BRANCH, BETHESDA, MD 20892 USA. BICON INC, ROCKVILLE, MD USA. NR 24 TC 47 Z9 50 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1993 VL 14 IS 4 BP 713 EP 717 DI 10.1093/carcin/14.4.713 PG 5 WC Oncology SC Oncology GA KW704 UT WOS:A1993KW70400029 PM 8472337 ER PT J AU NEUMANN, DA WULFF, SM LEPPO, MK LOVE, LA ROSE, NR HERSKOWITZ, A AF NEUMANN, DA WULFF, SM LEPPO, MK LOVE, LA ROSE, NR HERSKOWITZ, A TI PATHOLOGICAL-CHANGES IN THE CARDIAC INTERSTITIUM OF MICE INFECTED WITH ENCEPHALOMYOCARDITIS VIRUS SO CARDIOVASCULAR PATHOLOGY LA English DT Article ID DEFINED INBRED STRAINS; DILATED CARDIOMYOPATHY; MURINE MYOCARDITIS; VIRAL MYOCARDITIS; HEART-MUSCLE; COLLAGEN; COXSACKIEVIRUS-B3; MODEL; HYPERTROPHY; FIBROSIS AB Patients with myocarditis often develop dilated cardiomyopathy and congestive heart failure. Histologically, myocarditis is manifested by rare foci of myocyte necrosis with interstitial inflammation, while cardiomyopathy is characterized by diffuse interstitial fibrosis, myocyte hypertrophy, and an absence of active interstitial inflammation. The relationship between myocardial inflammation and interstitial fibrosis is poorly understood. This relationship was examined in mice that developed a diffuse interstitial inflammation of the heart over a period of 21 days following infection with encephalomyocarditis virus. Typical early lesions (day 7) included focal zones of myocytolysis containing mononuclear and polymorphonuclear inflammatory cells that were associated with the focal loss of reticular fibers. Later pathology (days 14-21) was characterized by a sparse, diffuse interstitial myocarditis with little ongoing necrosis. Changes within the myocardial interstitium remote from healing necrotic foci were marked by reticular fiber thickening and disorganization, often associated with pleomorphic fibroblasts. Reticulin fiber deposition was quantitatively increased in sparsely inflamed regions of hearts from infected animals as compared to noninflamed regions from the same hearts (p < 0.005) or hearts of control animals (p < 0.001). Scanning electron microscopy revealed interstitial changes that were more extensive than indicated by routine staining with hematoxylin and eosin or Masson's trichrome. The progressive changes within the cardiac interstitium during the development of postmyocarditic cardiomyopathy suggest that direct viral infection of fibroblasts or an interaction between the interstitium and inflammatory cells and their secreted products may contribute to pathologic changes within the interstitial collagen matrix. C1 JOHNS HOPKINS MED INST,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT IMMUNOL & INFECT DIS,BALTIMORE,MD 21205. NIAMSD,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD. NR 54 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 1054-8807 J9 CARDIOVASC PATHOL JI Cardiovasc. Pathol. PD APR-JUN PY 1993 VL 2 IS 2 BP 117 EP 126 DI 10.1016/1054-8807(93)90023-U PG 10 WC Cardiac & Cardiovascular Systems; Pathology SC Cardiovascular System & Cardiology; Pathology GA LL960 UT WOS:A1993LL96000003 PM 25990606 ER PT J AU FRALIX, TA STEENBERGEN, C LONDON, RE MURPHY, E AF FRALIX, TA STEENBERGEN, C LONDON, RE MURPHY, E TI GLIBENCLAMIDE DOES NOT ABOLISH THE PROTECTIVE EFFECT OF PRECONDITIONING ON STUNNING IN THE ISOLATED PERFUSED RAT-HEART SO CARDIOVASCULAR RESEARCH LA English DT Article DE ATP SENSITIVE K-CHANNEL; GLIBENCLAMIDE; PRECONDITIONING PERFUSED HEART ID SENSITIVE K+ CHANNELS; CYTOSOLIC FREE CALCIUM; POTASSIUM CHANNEL; FERRET HEARTS; INFARCT SIZE; F-19 NMR; ATP; REPERFUSION; ISCHEMIA; MYOCARDIUM AB Objective: The aim was to determine if the beneficial effects of preconditioning would be affected by inhibiting ATP sensitive potassium (K(ATP)) channels in the isolated, perfused rat heart. Methods: The effects of inhibiting K(ATP) channels with glibenclamide (10 muM) were evaluated on ionic alterations and recovery of function after 30 min ischaemia in non-preconditioned hearts and in hearts that had been preconditioned with four intermittent periods of 5 min ischaemia each separated by 5 min of reflow. [Ca2+]i, pH(i), and high energy phosphate levels were measured using F-19 and P-31 nuclear magnetic resonance during the preconditioning periods of ischaemia, during 30 min of ischaemia, and during reflow, in the presence and absence of 10 muM glibenclamide. Results: High energy phosphate contents were decreased during the preconditioning period to a greater extent in glibenclamide treated hearts and the onset of contracture was hastened during the subsequent 30 min period of sustained ischaemia. However, glibenclamide (10 muM) did not abolish the protective effects of preconditioning on ion accumulation during ischaemia or on postischaemic recovery of contractile function. Recovery of left ventricular developed pressure (as % of initial value) following 30 min of ischaemia was 74(SEM 5)% in the preconditioned hearts without drug and 62(4)% in the preconditioned hearts with glibenclamide, while recovery was 25(5)% in the non-preconditioned hearts without drug and 19(2)% in the non-preconditioned hearts with drug. The alterations in [Ca2+]i and pH(i) during ischaemia were similar in the glibenclamide treated and untreated preconditioned hearts and in both cases were less marked than in the non-preconditioned untreated hearts. Conclusions: Thus, although inhibition of K(ATP) channels accelerates high energy phosphate depletion during the preconditioning period, this does not result in accentuation of the ionic derangements during a subsequent sustained period of ischaemia and does not abolish the protective effect of preconditioning on stunning in the isolated rat heart. C1 DUKE UNIV,MED CTR,DEPT PATHOL,DURHAM,NC 27710. RP FRALIX, TA (reprint author), NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709, USA. FU NHLBI NIH HHS [R01 HL039752, HL 39752] NR 38 TC 49 Z9 49 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6363 J9 CARDIOVASC RES JI Cardiovasc. Res. PD APR PY 1993 VL 27 IS 4 BP 630 EP 637 DI 10.1093/cvr/27.4.630 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KZ002 UT WOS:A1993KZ00200016 PM 8324797 ER PT J AU KITADAI, Y YAMAZAKI, H YASUI, W KYO, E YOKOZAKI, H KAJIYAMA, G JOHNSON, AC PASTAN, I TAHARA, E AF KITADAI, Y YAMAZAKI, H YASUI, W KYO, E YOKOZAKI, H KAJIYAMA, G JOHNSON, AC PASTAN, I TAHARA, E TI GC FACTOR REPRESSES TRANSCRIPTION OF SEVERAL GROWTH-FACTOR RECEPTOR GENES AND CAUSES GROWTH-INHIBITION OF HUMAN GASTRIC-CARCINOMA CELL-LINES SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID FACTOR-ALPHA; NEGATIVE REGULATION; AUTOCRINE GROWTH; PROMOTER REGION; FACTOR-II; EXPRESSION; SEQUENCE; IDENTIFICATION; PRODUCT; AMPLIFICATION AB The GC factor (GCF) binds to specific GC-rich sequences in the epidermal growth factor receptor (EGFR) gene promoter and represses its transcription. In this study, by the use of GCF transfection, we examined whether GCF represses the gene expression of several other growth factors and receptors and causes growth inhibition of cancer cells. The transfection of GCF expression vector into gastric carcinoma cell lines (TMK-1 and MKN-28) decreased the mRNA levels of transforming growth factor (TGF) alpha, insulin-like growth factor II, and c-met. The reduction of TGF-alpha expression was confirmed at the protein level by enzyme-linked immunosorbent assay. Transfection of GCF expression vector interfered with the mRNA accumulation for EGFR and TGF-beta induced by epidermal growth factor in gastric carcinoma cell lines. The carcinoma cells transfected with GCF expression vector did not grow in a serum-free medium, whereas the control cells did grow under serum-free conditions. When the growth of the gastric carcinoma cell lines was studied in nude mice, GCF-transfected carcinoma cells showed a significantly slower growth compared to the control tumor. Transient cotransfection analysis with NIH3T3 cells revealed that GCF repressed the promoter activity of TGF-alpha in addition to EGFR. These findings indicate that GCF negatively regulates gene expression of not only the EGFR but also several other growth factor and receptor genes and can inhibit the growth of gastric carcinomas in immunodeficient mice. C1 HIROSHIMA UNIV,SCH MED,DEPT PATHOL 1,1-2-3 KASUMI,MINAMI KU,HIROSHIMA 734,JAPAN. HIROSHIMA UNIV,SCH MED,DEPT INTERNAL MED 1,MINAMI KU,HIROSHIMA 734,JAPAN. NIH,MOLEC BIOL LAB,BETHESDA,MD 20892. OI Yokozaki, Hiroshi/0000-0001-5276-3331 NR 45 TC 19 Z9 19 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD APR PY 1993 VL 4 IS 4 BP 291 EP 296 PG 6 WC Cell Biology SC Cell Biology GA KX081 UT WOS:A1993KX08100006 PM 8494791 ER PT J AU CHENG, C TENNENBAUM, T DEMPSEY, PJ COFFEY, RJ YUSPA, SH DLUGOSZ, AA AF CHENG, C TENNENBAUM, T DEMPSEY, PJ COFFEY, RJ YUSPA, SH DLUGOSZ, AA TI EPIDERMAL GROWTH-FACTOR RECEPTOR LIGANDS REGULATE KERATIN-8 EXPRESSION IN KERATINOCYTES, AND TRANSFORMING GROWTH FACTOR-ALPHA MEDIATES THE INDUCTION OF KERATIN-8 BY THE V-RAS(HA) ONCOGENE SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID CYTOKERATIN ENDO-A; GENE-EXPRESSION; RAS ONCOGENE; TGF-ALPHA; MONOCLONAL-ANTIBODIES; MOUSE KERATINOCYTES; SKIN DEVELOPMENT; CARCINOMA-CELLS; CULTURED-CELLS; MESSENGER-RNAS AB Cytokeratins 8 and 18 (Endo A and B) are among the earliest expressed embryonic genes and the major components of the cytoskeleton in simple epithelia of the adult. Recent data indicate that these cytokeratins are aberrantly expressed in several epithelial tumor types and that expression in cultured mouse keratinocytes is linked to activation of the ras(Ha) oncogene. Furthermore, up-regulation of K8/K18 in keratinocytes is associated with reciprocal suppression of K1. We now show that the aberrant expression of K8 and K18 and suppression of K1 in cultured keratinocytes transduced with the v-ras(Ha) gene are mediated by a factor secreted into the culture medium. Furthermore, transforming growth factor alpha (TGF-alpha) and epidermal growth factor elicit an identical pattern of K8/K18 expression and K1 suppression in normal keratinocytes. The factor in medium from v-ras(Ha) keratinocytes is TGF-alpha, as a specific blocking antibody for rat and mouse TGF-alpha prevents the expression of K8 and restores expression of K1. The tyrosine kinase inhibitor genistein also prevents K8 induction in v-ras(Ha) keratinocytes and in normal keratinocytes treated with TGF-alpha- or v-ras(Ha)-conditioned medium. However, simply stimulating proliferation of keratinocytes by cholera toxin does not result in expression of K8 or suppression of Kl. Finally, tumor grafts from neoplastic epidermal cells overexpressing TGF-alpha via retroviral transduction of human TGF-alpha complementary DNA in vitro show coordinate expression of K8 and human TGF-alpha. These studies indicate that K8 expression in keratinocytes, and derivative neoplastic cells, in vivo and in vitro is regulated by epidermal growth factor receptor ligands. Since the expression of cytokines and K8/K18 in early embryogenesis is often coincident, cytokines may be the physiological mediators of KB/K18 expression in embryonic cells. C1 NCI,DIV CANC ETIOL,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BLDG 37,BETHESDA,MD 20892. VANDERBILT UNIV,DEPT MED & CELL BIOL,NASHVILLE,TN 37232. NR 60 TC 35 Z9 35 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD APR PY 1993 VL 4 IS 4 BP 317 EP 327 PG 11 WC Cell Biology SC Cell Biology GA KX081 UT WOS:A1993KX08100009 PM 7684248 ER PT J AU FRUGONI, P PIKE, SE TOSATO, G AF FRUGONI, P PIKE, SE TOSATO, G TI A MECHANISM OF T-CELL REGULATION OF EPSTEIN-BARR-VIRUS LATENCY SO CELLULAR IMMUNOLOGY LA English DT Article ID LYMPHOCYTES-T; GROWTH-FACTOR; B-CELLS; CYCLOSPORIN-A; VIRAL LATENCY; INVITRO; INTERLEUKIN-6; INFECTION; TRANSPLANTATION; DIFFERENTIATION RP FRUGONI, P (reprint author), NIH,CTR BIOL EVALUAT & RES,BLDG 29,ROOM 505,BETHESDA,MD 20892, USA. NR 36 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 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD APR 1 PY 1993 VL 147 IS 2 BP 256 EP 266 DI 10.1006/cimm.1993.1067 PG 11 WC Cell Biology; Immunology SC Cell Biology; Immunology GA KU302 UT WOS:A1993KU30200003 PM 8095857 ER PT J AU FREDRICKSON, DS AF FREDRICKSON, DS TI PHENOTYPING - ON REACHING BASE CAMP (1950-1975) SO CIRCULATION LA English DT Review DE LIPOPROTEINS; DYSLIPIDEMIA; HYPERLIPOPROTEINEMIA; TANGIER DISEASE; HYPERLIPIDEMIA; PHENOTYPING; APOLIPOPROTEINS; FREE FATTY ACIDS; XANTHOMAS; LIPOPROTEIN LIPASE ID LOW-DENSITY LIPOPROTEINS; CORONARY HEART-DISEASE; AMINO-ACID SEQUENCE; HUMAN PLASMA; POSTHEPARIN PLASMA; FAMILIAL HYPERCHOLESTEROLEMIA; III HYPERLIPOPROTEINEMIA; SELECTIVE MEASUREMENT; TRIGLYCERIDE LIPASE; APOLIPOPROTEIN AB The search for plasma lipoproteins began at the turn of the century. It was not until 1949 that a meeting of the Faraday Society celebrated the separation of the alpha and beta lipoproteins. At that moment, ultracentrifugists in Berkeley were already busily converting ''alpha'' to high density lipoprotein and ''beta'' to low density lipoprotein; the modern era of lipoproteins had begun. Over the succeeding 10 years, a quarrel over whether the level of S(f) 0-20 or cholesterol was the more powerful risk factor ended with an eclipse of the analytical ultracentrifuge and a surge of interest in the biological side of lipoproteins. The postheparin clearing factor became lipoprotein lipase, and free fatty acids were discovered. In 1960, abetalipoproteinemia and Tangier disease suggested that the apolipoproteins must be specific and spurred a hunt for their number and nature. The first amino acid sequences aroused speculation of ''amphipathic helices.'' By 1970, conversion of hyperlipidemia to five types of hyperlipoproteinemia led to worldwide fascination with electrophoretic patterns, ''floating beta,'' and ''the Friedewald formula'' as codes for genetic abnormalities leading to early coronary artery disease. A few years later, the appearance of ''familial combined hyperlipidemia'' confounded the phenotyping, and the discovery of the low density lipoprotein receptor heralded the coming of true genotypes. This is a Bethesda-based story of the ''climb to base camp'' preceding the joining of molecular biology with the research on lipoproteins, dyslipoproteinemia, and atherosclerosis. RP FREDRICKSON, DS (reprint author), NIH,NATL LIB MED,1W22,BETHESDA,MD 20892, USA. NR 142 TC 22 Z9 22 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR PY 1993 VL 87 IS 4 SU S BP 1 EP 15 PG 15 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA KX108 UT WOS:A1993KX10800001 ER PT J AU ZHANG, J YU, ZX HILBERT, SL YAMAGUCHI, M CHADWICK, DP HERMAN, EH FERRANS, VJ AF ZHANG, J YU, ZX HILBERT, SL YAMAGUCHI, M CHADWICK, DP HERMAN, EH FERRANS, VJ TI CARDIOTOXICITY OF HUMAN RECOMBINANT INTERLEUKIN-2 IN RATS - A MORPHOLOGICAL-STUDY SO CIRCULATION LA English DT Article DE MYOCARDITIS; MYOCARDIAL NECROSIS; LYMPHOCYTES; CELLS, ENDOTHELIAL ID HIGH-DOSE INTERLEUKIN-2; ACTIVATED KILLER CELLS; VASCULAR LEAK SYNDROME; TUMOR NECROSIS FACTOR; CYTO-TOXICITY; MONOCLONAL ANTIBODY; ENDOTHELIAL INJURY; LYMPHOCYTES; MYOCARDITIS; THERAPY AB Background. One of the side effects of interleukin 2 (IL-2) cancer immunotherapy in humans is the vascular leak syndrome, which is frequently associated with depression of myocardial function, myocarditis, and myocardial necrosis. Methods and Results. To investigate this cardiotoxicity, IL-2 (three doses of 5 x 10(5) Cetus units/day i.p.) was given to rats for 2, 3, or 5 days. Heart, lung, liver, spleen, and kidney tissues were studied by light and electron microscopy and with immunoperoxidase techniques. Cardiac changes consisted of focal lymphocytic and eosinophilic infiltration, myocyte vacuolization, myofibrillar loss, and necrosis. Ultrastructural alterations included swelling of endothelial cells, with dissociation of intercellular junctions, migration of lymphocytes into the interstitium, and interstitial hemorrhage and edema. Close contact between infiltrating lymphocytes, particularly large granular lymphocytes, and cardiac myocytes was often observed in areas of tissue damage. All lesions were more severe on day 5 than on days 2 and 3. Immunoperoxidase stains demonstrated asialo GM1 ganglioside antibody-positive, granular lymphocytes to be much more frequent in myocardium of IL-2-treated rats than in that of control rats. Conclusions. Although we cannot exclude the possibility of a direct toxic effect of IL-2 on myocytes, our observation's suggest that the myocardial damage produced by this agent is triggered by IL-2-activated lymphocytes that exert cytolytic effects, first on endothelial cells and then on cardiac myocytes, thus producing lesions that involve both the cardiac microcirculation and the muscle cells. C1 NHLBI,PATHOL BRANCH,BLDG 10,ROOM 2N240,BETHESDA,MD 20892. US FDA,DIV RES & TESTING,WASHINGTON,DC 20204. US FDA,CTR DEVICES & RADIOL HLTH,WASHINGTON,DC 20204. NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 60 TC 27 Z9 28 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR PY 1993 VL 87 IS 4 BP 1340 EP 1353 PG 14 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA KW422 UT WOS:A1993KW42200029 PM 8462156 ER PT J AU THOMPSON, HL THOMAS, L METCALFE, DD AF THOMPSON, HL THOMAS, L METCALFE, DD TI MURINE MAST-CELLS ATTACH TO AND MIGRATE ON LAMININ-COATED, FIBRONECTIN-COATED, AND MATRIGEL-COATED SURFACES IN RESPONSE TO FC-EPSILON-RI-MEDIATED SIGNALS SO CLINICAL AND EXPERIMENTAL ALLERGY LA English DT Article ID STIMULATING FACTOR; GROWTH-FACTOR; LOCOMOTION; CULTURE; FLOW AB We have examined the possibility that mouse bone marrow-derived cultured mast cells (BMCMC) have the capacity to attach to and migrate on extracellular matrix components in vitro through the use of time lapse videography. Unactivated mast cells did not display significant interaction with slide flasks coated with either 3% BSA or collagen IV, and Fc(epsilon)RI-mediated activation of BMCMC did not appreciably increase their attachment and migratory characteristics. Both activated and unactivated BMCMC adhered to surfaces coated with a synthetic IKVAV laminin polypeptide, but this association resulted in the immobilization of the cells to the substrate. BMCMC did not adhere to surfaces coated with laminin, fibronectin or matrigel until Fc(epsilon)RI-mediated activation, after which they displayed rapid, random movement on these surfaces. Cells continually interacted with laminin, fibronectin or matrigel by flattening, interspaced by periods of movement as rounded cells with small pseudopodia. The mean velocity of BMCMC on laminin, fibronectin or matrigel was similar and averaged approximately 180 mum/hr. The mean velocity of BMCMC on these three substrates was not significantly different from the mean velocity of monocytes on laminin. The movement of BMCMC on these substrates demonstrated a directional tendency. In summary, these results demonstrate that mast cells activated through Fc(epsilon)RI are capable of attachment to and motion on components of extracellular matrix, and demonstrate one mechanism by which mast cells may migrate to areas of inflammation and wound repair. C1 NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BLDG 10,ROOM 11C210,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 17 TC 26 Z9 26 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0954-7894 J9 CLIN EXP ALLERGY JI Clin. Exp. Allergy PD APR PY 1993 VL 23 IS 4 BP 270 EP 275 DI 10.1111/j.1365-2222.1993.tb00321.x PG 6 WC Allergy; Immunology SC Allergy; Immunology GA KZ746 UT WOS:A1993KZ74600006 PM 8319122 ER PT J AU GOLDBERGER, BA DARWIN, WD GRANT, TM ALLEN, AC CAPLAN, YH CONE, EJ AF GOLDBERGER, BA DARWIN, WD GRANT, TM ALLEN, AC CAPLAN, YH CONE, EJ TI MEASUREMENT OF HEROIN AND ITS METABOLITES BY ISOTOPE-DILUTION ELECTRON-IMPACT MASS-SPECTROMETRY SO CLINICAL CHEMISTRY LA English DT Note DE 6-ACETYLMORPHINE; MORPHINE; ABUSED DRUGS; METABOLISM; SOLID-PHASE EXTRACTION; GAS CHROMATOGRAPHY MASS SPECTROMETRY; SALIVA; URINE ID PERFORMANCE LIQUID-CHROMATOGRAPHY; 6-ACETYLMORPHINE; URINE; MORPHINE; IDENTIFICATION; ABUSE AB A solid-phase extraction procedure was developed for the isolation of heroin, 6-acetylmorphine, and morphine from blood, plasma, saliva, and urine with subsequent assay by gas chromatography/mass spectrometry. Aprotic solvents, mild elution conditions, and an enzyme inhibitor were used to ensure maximum analyte stability. Samples were extracted and the extract was divided into two equal portions. One portion was assayed directly for heroin; detector response was linear over a concentration range of 1.0 to 250 mug/L. The second part of the extract was reacted with N-methyl-bis-trifluoroacetamide and assayed for the trifluoroacetyl derivatives of 6-acetylmorphine and morphine; detector response was linear over a concentration range of 1.0 to 500 mug/L. The limit of sensitivity was 1.0 mug/L for each analyte. Hydrolysis of heroin to 6-acetylmorphine during extraction and analysis was <5%. The method can be used to corroborate heroin use and to study the pharmacological effects of heroin and its metabolites. C1 NATL FORENS SCI,BALTIMORE,MD 21227. NIDA,ADDICT RES CTR,BALTIMORE,MD. NR 22 TC 63 Z9 63 U1 1 U2 1 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD APR PY 1993 VL 39 IS 4 BP 670 EP 675 PG 6 WC Medical Laboratory Technology SC Medical Laboratory Technology GA KY291 UT WOS:A1993KY29100019 PM 8472364 ER PT J AU LAL, RB BUCKNER, C KHABBAZ, RF KAPLAN, JE REYES, G HADLOCK, K LIPKA, J FOUNG, SKH CHAN, L COLIGAN, JE AF LAL, RB BUCKNER, C KHABBAZ, RF KAPLAN, JE REYES, G HADLOCK, K LIPKA, J FOUNG, SKH CHAN, L COLIGAN, JE TI ISOTYPIC AND IGG SUBCLASS RESTRICTION OF THE HUMORAL IMMUNE-RESPONSES TO HUMAN T-LYMPHOTROPIC VIRUS TYPE-I SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID CELL LEUKEMIA-VIRUS; TROPICAL SPASTIC PARAPARESIS; HUMAN MONOCLONAL-ANTIBODY; HTLV-I; ENVELOPE GLYCOPROTEIN; LINEAR EPITOPES; IDENTIFICATION; GP46; IMMUNIZATION; MYELOPATHY C1 GENELABS INC,REDWOOD CITY,CA. STANFORD UNIV,DEPT PATHOL,STANFORD,CA 94305. DIAGNOST BIOTECHNOL,SINGAPORE,SINGAPORE. NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. RP LAL, RB (reprint author), CTR DIS CONTROL,RETROVIRUS DIS BRANCH,ATLANTA,GA 30333, USA. FU NHLBI NIH HHS [HL-33811]; NIDA NIH HHS [DA-06596] NR 42 TC 17 Z9 17 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 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1993 VL 67 IS 1 BP 40 EP 49 DI 10.1006/clin.1993.1043 PG 10 WC Immunology; Pathology SC Immunology; Pathology GA KT717 UT WOS:A1993KT71700006 PM 7680300 ER PT J AU MILNER, PF KRAUS, AP SEBES, JI SLEEPER, LA DUKES, KA EMBURY, SH BELLEVUE, R KOSHY, M MOOHR, JW SMITH, J AF MILNER, PF KRAUS, AP SEBES, JI SLEEPER, LA DUKES, KA EMBURY, SH BELLEVUE, R KOSHY, M MOOHR, JW SMITH, J TI OSTEONECROSIS OF THE HUMERAL HEAD IN SICKLE-CELL DISEASE SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID ALPHA-THALASSEMIA; FEMORAL-HEAD; ANEMIA; SEVERITY; GENE AB The prevalence and incidence of osteonecrosis (ON) of the humeral head in sickle cell disease was determined by a study of 2524 patients who were entered into a prospective study and followed for an average of 5.6 years. At entry, 5.6% had roentgenographic evidence of ON in one or both shoulders. There was little difference in age-adjusted prevalence among genotypes, but there were striking differences in age-specific rates. Observed at ages ranging from five to 24 years, 3.25% of sickle cell anemia (S/S) patients, but only 1.1% of sickle cell disease (S/C) patients, had ON. No S/beta+ thalassemia patients younger than 25 years of age had ON on entry. The highest age-adjusted incidence rate was found in S/S patients with concomitant alpha-thalassemia (4.85 per hundred patient-years), followed by S/beta0 thalassemia (4.84 per hundred patient-years), S/beta+ thalassemia (2.61 per hundred patient-years), S/S without alpha-thalassemia (2.54 per hundred patient-years), and S/C (1.66 per hundred patient-years). Only 20.9% of patients reported pain or had limited range of movement at the time of diagnosis. Sickle cell disease is a frequent cause of ON of the humeral head, especially in children and young adults. C1 NHLBI,SICKLE CELL DIS BRANCH,COOPERAT STUDY SICKLE CELL DIS,BETHESDA,MD 20892. UNIV TENNESSEE CTR HLTH SCI,MEMPHIS,TN 38163. NEW ENGLAND RES INST,WATERTOWN,MA. SAN FRANCISCO GEN HOSP,SAN FRANCISCO,CA 94110. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. INTERFAITH MED CTR,BROOKLYN,NY. COLUMBIA UNIV,HARLEM HOSP CTR,NEW YORK,NY 10027. UNIV ILLINOIS,CHICAGO,IL 60680. WOODHULL SUNY HSCAB,BROOKLYN,NY. RP MILNER, PF (reprint author), MED COLL GEORGIA,ADULT SICKLE CELL CLIN,BLDG FK-100,AUGUSTA,GA 30912, USA. NR 24 TC 33 Z9 34 U1 0 U2 0 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 APR PY 1993 IS 289 BP 136 EP 143 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA KY525 UT WOS:A1993KY52500018 PM 8472404 ER PT J AU FORDIS, M AF FORDIS, M TI SCIENTISTS, SOCIETIES, AND SCIENCE-EDUCATION SO CLINICAL RESEARCH LA English DT Article RP FORDIS, M (reprint author), NIH,OFF EDUC,BETHESDA,MD 20892, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP 165 EP 178 PG 14 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100002 PM 8477571 ER PT J AU ABKOWITZ, JL BROWN, KE WOOD, RW COHEN, B KOVACH, NL YOUNG, NS AF ABKOWITZ, JL BROWN, KE WOOD, RW COHEN, B KOVACH, NL YOUNG, NS TI HUMAN PARVOVIRUS-B19 (HPV-B19) IS NOT A RARE CAUSE OF ANEMIA IN HIV-SEROPOSITIVE INDIVIDUALS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV WASHINGTON,SEATTLE,WA 98195. NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. CENT PUBL HLTH LAB,LONDON NW9 5HT,ENGLAND. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A393 EP A393 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101574 ER PT J AU AMAGAI, M KLAUSKOVTUN, V UDEY, MC STANLEY, JR AF AMAGAI, M KLAUSKOVTUN, V UDEY, MC STANLEY, JR TI EXPRESSION OF THE EXTRACELLULAR (EC) REGION OF PEMPHIGUS-VULGARIS ANTIGEN (PVA) ON MOUSE FIBROBLASTS (L CELLS) CAUSES CELL-TO-CELL ADHESION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A407 EP A407 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101650 ER PT J AU AUSTIN, S WALSTON, J PERFETTI, R ROTH, J SHULDINER, AR AF AUSTIN, S WALSTON, J PERFETTI, R ROTH, J SHULDINER, AR TI RAPID SCREENING FOR MUTATIONS IN THE INSULIN-RECEPTOR GENE IN DIABETES-MELLITUS TYPE-II USING A NOVEL GEL MATRIX SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,DIV GERIATR MED & GERONTOL,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A356 EP A356 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101357 ER PT J AU BAGDADE, J RITTER, M NAGY, D KNOWLER, W AF BAGDADE, J RITTER, M NAGY, D KNOWLER, W TI IMMUNITY FROM CORONARY HEART-DISEASE (CHD) IN PIMA-INDIANS - THE ROLE OF ALTERED PLASMA TRAFFICKING OF CHOLESTERYL ESTER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 RUSH MED COLL,CHICAGO,IL 60612. NIH,PHOENIX,AZ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A285 EP A285 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100942 ER PT J AU BISWAS, P POLI, G FRANZOSO, G SIEBENLIST, U FAUCI, AS AF BISWAS, P POLI, G FRANZOSO, G SIEBENLIST, U FAUCI, AS TI THE ROLE OF ENDOGENOUS TUMOR-NECROSIS-FACTOR AND NF-KAPPA-B IN HUMAN-IMMUNODEFICIENCY-VIRUS REPLICATION IN PROMONOCYTIC U937 CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A244 EP A244 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100720 ER PT J AU BORKOWSKI, T LEE, MG UDEY, MC AF BORKOWSKI, T LEE, MG UDEY, MC TI EXPRESSION OF THE COSTIMULATORY MOLECULE-B7 BY CULTURED MURINE LANGERHANS CELLS IS REGULATED AT THE MESSENGER-RNA LEVEL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A177 EP A177 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100369 ER PT J AU BOURS, V FRANZOSO, G AZARENKO, V PARK, S KANNO, T BROWN, K SIEBENLIST, U AF BOURS, V FRANZOSO, G AZARENKO, V PARK, S KANNO, T BROWN, K SIEBENLIST, U TI THE ONCOPROTEIN BCL-3 DIRECTLY TRANSACTIVATES THROUGH KAPPA-B MOTIFS VIA ASSOCIATION WITH DNA-BINDING P50B HOMODIMERS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 3 U2 5 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A201 EP A201 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100491 ER PT J AU BRODY, SL HAN, SK CRYSTAL, RG AF BRODY, SL HAN, SK CRYSTAL, RG TI TUMOR-NECROSIS-FACTOR-ALPHA GENE-TRANSFER TO HUMAN LUNG-CANCER CELLS DOES NOT EFFECT INVITRO GROWTH BUT DOES SUPPRESS INVIVO TUMORIGENICITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A214 EP A214 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100555 ER PT J AU BROWN, K PARK, S KANNO, T FRANZOSO, G SIEBENLIST, U AF BROWN, K PARK, S KANNO, T FRANZOSO, G SIEBENLIST, U TI MUTUAL REGULATION OF THE TRANSCRIPTIONAL ACTIVATOR NF-KAPPA-B AND ITS INHIBITOR, I-KAPPA-B-ALPHA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A137 EP A137 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100134 ER PT J AU BRUGGEMAN, LA NELSON, PJ KOPP, JB GALLO, RC NOTKINS, AL KLOTMAN, PE KLOTMAN, ME AF BRUGGEMAN, LA NELSON, PJ KOPP, JB GALLO, RC NOTKINS, AL KLOTMAN, PE KLOTMAN, ME TI EVIDENCE FOR TISSUE-SPECIFIC REV ACTIVITY IN MICE TRANSGENIC FOR HIV GENES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NIDR,ORAL MED LAB,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A322 EP A322 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101163 ER PT J AU BRUGGEMAN, LA ADLER, SH KOPP, JB NOTKINS, AL RAPPAPORT, J KLOTMAN, PE AF BRUGGEMAN, LA ADLER, SH KOPP, JB NOTKINS, AL RAPPAPORT, J KLOTMAN, PE TI DIFFERENTIAL BINDING OF THE HIV-1 LTR BY THE TRANSCRIPTION FACTORS NF-KB AND SP1 IN A TRANSGENIC MOUSE MODEL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NIDR,ORAL MED LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A280 EP A280 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100916 ER PT J AU CHESTER, AC LEVINE, PH AF CHESTER, AC LEVINE, PH TI CHRONIC FATIGUE SYNDROME CRITERIA IN SICK BUILDING SYNDROME SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,DEPT MED,WASHINGTON,DC 20007. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A514 EP A514 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102288 ER PT J AU CHIPEV, CC YANG, JM STEINERT, PM COMPTON, JG AF CHIPEV, CC YANG, JM STEINERT, PM COMPTON, JG TI MUTATIONS IN THE KERATIN-10 GENE IN PATIENTS WITH EPIDERMOLYTIC HYPERKERATOSIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A475 EP A475 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102057 ER PT J AU COBB, JP NATANSON, C QUEZADO, ZMN HOFFMAN, WD KOEV, CA BANKS, S ELIN, RJ HOSSEINI, JM DANNER, RL AF COBB, JP NATANSON, C QUEZADO, ZMN HOFFMAN, WD KOEV, CA BANKS, S ELIN, RJ HOSSEINI, JM DANNER, RL TI EFFECT OF NW METHYL-L-ARGININE (NMA), A NITRIC-OXIDE SYNTHASE INHIBITOR, ON SURVIVAL IN ENDOTOXIN (LPS)-CHALLENGED CANINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A253 EP A253 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100773 ER PT J AU COHEN, OJ PANTALEO, G WALKER, R OGNIBENE, FP SHELHAMER, JH FAUCI, AS AF COHEN, OJ PANTALEO, G WALKER, R OGNIBENE, FP SHELHAMER, JH FAUCI, AS TI HIV BURDEN IN MONONUCLEAR-CELLS FROM PERIPHERAL-BLOOD VERSUS BRONCHOALVEOLAR LAVAGE OF THE SAME INDIVIDUALS - A COMPARATIVE-ANALYSIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A248 EP A248 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100742 ER PT J AU COMPTON, JG IDLER, WW AF COMPTON, JG IDLER, WW TI ORGANIZATION OF THE KERATIN GENE-CLUSTER ON HUMAN CHROMOSOME-12 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A439 EP A439 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101840 ER PT J AU CUNNION, RE KAVINSKY, CJ CUNNION, SD PARRILLO, JE AF CUNNION, RE KAVINSKY, CJ CUNNION, SD PARRILLO, JE TI PROSPECTIVE LONG-TERM SURVIVAL AMONG 123 PATIENTS WITH IDIOPATHIC DILATED CARDIOMYOPATHY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RUSH HEART INST,CHICAGO,IL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A336 EP A336 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101240 ER PT J AU DEBINSKI, W PURI, RK PASTAN, I AF DEBINSKI, W PURI, RK PASTAN, I TI CHIMERIC TOXIN COMPOSED OF HUMAN INTERLEUKIN-4 AND PSEUDOMONAS EXOTOXIN IS AN ACTIVE ANTITUMOR AGENT INVIVO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,DCBDC,LMB,BETHESDA,MD 20892. US FDA,CBER,DCB,BETHESDA,MD 20014. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A276 EP A276 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100891 ER PT J AU DEMENDEZ, I ADAMS, AG LETO, TL AF DEMENDEZ, I ADAMS, AG LETO, TL TI INVIVO RECONSTITUTION OF NADPH OXIDASE ACTIVITY IN OXIDASE DEFICIENT B-LYMPHOCYTES WITH FULL LENGTH AND DELETED FORMS OF P47 AND P67-PHOX SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A278 EP A278 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100904 ER PT J AU DENNING, MF DLUGOSZ, AA YUSPA, SH AF DENNING, MF DLUGOSZ, AA YUSPA, SH TI REDISTRIBUTION OF SPECIFIC PROTEIN-KINASE-C ISOZYMES ACCOMPANY CA2+-INDUCED KERATINOCYTE DIFFERENTIATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A446 EP A446 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101885 ER PT J AU DIGIOVANNA, JJ COMPTON, JG BALE, SJ AF DIGIOVANNA, JJ COMPTON, JG BALE, SJ TI CLINICAL HETEROGENEITY IN EPIDERMOLYTIC HYPERKERATOSIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAMS,BETHESDA,MD. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A418 EP A418 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101716 ER PT J AU DLUGOSZ, AA DHARIA, AG CHENG, C YUSPA, SH AF DLUGOSZ, AA DHARIA, AG CHENG, C YUSPA, SH TI EXPRESSION OF GRANULAR-CELL DIFFERENTIATION MARKERS IS COORDINATELY REGULATED BY PROTEIN-KINASE-C SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A476 EP A476 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102062 ER PT J AU DRUEY, KM DEGUCHI, Y KEHRL, JH AF DRUEY, KM DEGUCHI, Y KEHRL, JH TI BACTERIAL EXPRESSION OF THE HUMAN HOMEOBOX GENE HLX AND DEMONSTRATION OF SPECIFIC DNA-BINDING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A133 EP A133 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100109 ER PT J AU DUGAN, EM WASSERMANN, EM COHEN, PJ ALLEN, RH KATZ, SI HORNE, MK AF DUGAN, EM WASSERMANN, EM COHEN, PJ ALLEN, RH KATZ, SI HORNE, MK TI COBALAMIN DEFICIENCY IN DERMATITIS-HERPETIFORMIS PATIENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV COLORADO,DENVER,CO 80202. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A418 EP A418 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101717 ER PT J AU EBB, D CHIN, K RODGERS, GP AF EBB, D CHIN, K RODGERS, GP TI IDENTIFICATION OF UPSTREAM REGULATORY ELEMENTS THAT REPRESS EXPRESSION OF ADULT BETA-LIKE GLOBIN GENES IN A PRIMITIVE ERYTHROID ENVIRONMENT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,CHEM BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A206 EP A206 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100514 ER PT J AU EICHACKER, PO HAMMOND, W FARESE, A HOFFMAN, WD DANNER, RL BANKS, SM MACVITTIE, T NATANSON, C AF EICHACKER, PO HAMMOND, W FARESE, A HOFFMAN, WD DANNER, RL BANKS, SM MACVITTIE, T NATANSON, C TI SERIAL SERUM GRANULOCYTE-COLONY STIMULATING FACTOR LEVELS IN A CANINE MODEL OF BACTERIAL SEPSIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. AFRRI,BETHESDA,MD. UNIV WASHINGTON,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A240 EP A240 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100695 ER PT J AU EICHACKER, PO WAISMAN, Y NATANSON, C FARESE, A HOFFMAN, WD BANKS, SM ELIN, R HOSSEINI, I MACVITTIE, T AF EICHACKER, PO WAISMAN, Y NATANSON, C FARESE, A HOFFMAN, WD BANKS, SM ELIN, R HOSSEINI, I MACVITTIE, T TI RECOMBINANT GRANULOCYTE-COLONY STIMULATING FACTOR REDUCES ENDOTOXEMIA AND IMPROVES CARDIOVASCULAR FUNCTION AND SURVIVAL DURING BACTERIAL SEPSIS IN NON-NEUTROPENIC CANINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AFRRI,DEPT HEMATOL,BETHESDA,MD. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,DEPT EMERGENCY,WASHINGTON,DC. AMGEN INC,THOUSAND OAKS,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A240 EP A240 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100694 ER PT J AU EICHER, DM TAN, TH RICE, N OSHEA, JJ KENNEDY, ICS AF EICHER, DM TAN, TH RICE, N OSHEA, JJ KENNEDY, ICS TI EXPRESSION OF V-SRC IN T-CELLS INDUCES NUCLEAR EXPRESSION OF NF-KAPPA-B SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,FCRDC,BRMP,EXPTL IMMUNOL LAB,FREDERICK,MD 21701. NCI,FCRDC,ABL,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21701. BAYLOR COLL MED,DEPT MICROBIOL & IMMUNOL,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A210 EP A210 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100536 ER PT J AU ENK, AH KATZ, SI AF ENK, AH KATZ, SI TI HEAT-STABLE ANTIGEN - A CRITICAL COSTIMULATORY MOLECULE ON EPIDERMAL LANGERHANS CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV MAINZ,DEPT DERMATOL,W-6500 MAINZ,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A454 EP A454 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101928 ER PT J AU FISHBEIN, WN KIRSCH, IR AF FISHBEIN, WN KIRSCH, IR TI DETECTION OF CHROMOSOME-7 INVERSIONS IN PERIPHERAL-BLOOD SPECIMENS DRIED ON FILTER-PAPER AS A POPULATION SCREEN FOR POTENTIAL ONCOGENESIS AND FOR EXPOSURE TO ENVIRONMENTAL GENOTOXINS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AFIP,DIV BIOCHEM,WASHINGTON,DC. NCI,NNMC,MED ONCOL BRANCH,BETHESDA,MD 20892. NR 2 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A271 EP A271 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100863 ER PT J AU FRANZOZO, G BOURS, V AZARENKO, V PARK, S TOMITAYAMAGUCHI, M SIEBENLIST, U FAUCI, AS AF FRANZOZO, G BOURS, V AZARENKO, V PARK, S TOMITAYAMAGUCHI, M SIEBENLIST, U FAUCI, AS TI THE ONCOPROTEIN BCL-3 CAN CAUSE KAPPA-B-DEPENDENT TRANSACTIVATION BY AN INDIRECT MECHANISM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A220 EP A220 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100584 ER PT J AU FREAS, DL CORRELL, PH DOUGHERTY, SF PLUZNIK, DH KARLSSON, S AF FREAS, DL CORRELL, PH DOUGHERTY, SF PLUZNIK, DH KARLSSON, S TI EVALUATION OF RETROVIRAL VECTOR EXPRESSION IN DIFFERENTIATED MYELOID LINEAGES - EXPRESSION OF HUMAN GLUCOCEREBROSIDASE IN MURINE MACROPHAGES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEV & METAB NEUROL BRANCH,MOLEC & MED GENET SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A163 EP A163 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100284 ER PT J AU GAO, JL KUHNS, DB TIFFANY, HL MCDERMOTT, D MURPHY, PM AF GAO, JL KUHNS, DB TIFFANY, HL MCDERMOTT, D MURPHY, PM TI STRUCTURE AND FUNCTIONAL EXPRESSION OF THE HUMAN MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA(MIP-1-ALPHA) RANTES RECEPTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NCI,FCRDC,PRI DYNCORP,CLIN IMMUNOL SERV,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A208 EP A208 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100525 ER PT J AU GAUDET, SJ SLOMINSKI, A ETMINAN, M PRUSKI, D PAUS, R NAMBOODIRI, MAA AF GAUDET, SJ SLOMINSKI, A ETMINAN, M PRUSKI, D PAUS, R NAMBOODIRI, MAA TI IDENTIFICATION AND CHARACTERIZATION OF 2 ISOZYMIC FORMS OF ARYLAMINE N-ACETYLTRANSFERASE IN SYRIAN-HAMSTER SKIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. ALBANY MED COLL,DEPT MICROBIOL,ALBANY,NY 12208. ALBANY MED COLL,DEPT IMMUNOL,ALBANY,NY 12208. ALBANY MED COLL,DEPT MOLEC GENET,ALBANY,NY 12208. GEORGETOWN UNIV,DEPT BIOL,WASHINGTON,DC 20057. FREE UNIV BERLIN,UKRV,DEPT DERMATOL,W-1000 BERLIN 33,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A413 EP A413 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101685 ER PT J AU GAUDET, SJ MASTORAKOS, G PATCHEV, VK BOUZAS, EA CHADER, GJ CHROUSOS, GP AF GAUDET, SJ MASTORAKOS, G PATCHEV, VK BOUZAS, EA CHADER, GJ CHROUSOS, GP TI HIGHER SEROTONIN N-ACETYLTRANSFERASE (NAT) ACTIVITY IN INFLAMMATORY DISEASE-SUSCEPTIBLE LEWIS THAN DISEASE-RESISTANT FISCHER RATS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NICHHD,BETHESDA,MD. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A326 EP A326 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101182 ER PT J AU GLICK, AB KULKARNI, AB TENNENBAUM, T KARLSSON, S YUSPA, SH AF GLICK, AB KULKARNI, AB TENNENBAUM, T KARLSSON, S YUSPA, SH TI ANALYSIS OF TGF-BETA FUNCTION IN THE EPIDERMIS USING TGF-BETA-1 KNOCKOUT MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NINCDS,MOLEC MED GENET SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A447 EP A447 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101888 ER PT J AU HALABAN, R TYRRELL, L LONGLEY, J RUBIN, J AF HALABAN, R TYRRELL, L LONGLEY, J RUBIN, J TI UVB IRRADIATION INDUCES THE SECRETION OF GROWTH-FACTORS FROM KERATINOCYTES AND FIBROBLASTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT DERMATOL,NEW HAVEN,CT 06510. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A447 EP A447 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101891 ER PT J AU HARRIS, TB LAUNER, L AF HARRIS, TB LAUNER, L TI WEIGHT, WEIGHT CHANGE AND MOBILITY DISABILITY IN OLDER WOMEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A225 EP A225 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100605 ER PT J AU HAUSER, P WIGGS, E LEONARD, C MIXSON, AJ AN, S WEINTRAUB, BD AF HAUSER, P WIGGS, E LEONARD, C MIXSON, AJ AN, S WEINTRAUB, BD TI NEUROBIOLOGICAL CORRELATES OF GENERALIZED RESISTANCE TO THYROID-HORMONE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDKD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A274 EP A274 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100880 ER PT J AU HOCHBERG, MC LETHBRIDGECEJKU, M SCOTT, WW PLATO, CC TOBIN, JD AF HOCHBERG, MC LETHBRIDGECEJKU, M SCOTT, WW PLATO, CC TOBIN, JD TI ASSOCIATION OF BIOCHEMICAL MARKERS OF BONE AND CARTILAGE METABOLISM WITH HAND OSTEOARTHRITIS - EFFECTS OF AGE AND GENDER IN SUBJECTS FROM THE BALTIMORE LONGITUDINAL-STUDY OF AGING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. NIA,GERONTOL RES CTR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A227 EP A227 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100618 ER PT J AU HOLLAND, SM EISENSTEIN, E KUHNS, DB TURNER, ML STROBER, W GALLIN, JI AF HOLLAND, SM EISENSTEIN, E KUHNS, DB TURNER, ML STROBER, W GALLIN, JI TI DISSEMINATED MYCOBACTERIUM-AVIUM INFECTION WITHOUT HIV-INFECTION IS ASSOCIATED WITH DEFECTIVE INTERFERON-GAMMA PRODUCTION AND RESPONDS TO TREATMENT WITH INTERFERON-GAMMA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,HOST DEF LABS,BETHESDA,MD 20892. NIH,CLIN INVEST LABS,BETHESDA,MD 20892. NIH,CTR CLIN,BETHESDA,MD 20892. PRI DYN CORP,CIS,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A321 EP A321 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101155 ER PT J AU HOLLERAN, WM MENON, GK ELIAS, PM GINNS, EI SIDRANSKY, E AF HOLLERAN, WM MENON, GK ELIAS, PM GINNS, EI SIDRANSKY, E TI BETA-GLUCOCEREBROSIDASE-DEFICIENT TRANSGENIC MICE HAVE ABNORMAL STRATUM-CORNEUM LAMELLAR BILAYERS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,DEPT DERMATOL,SAN FRANCISCO,CA 94143. VET ADM MED CTR,DERMATOL SERV,SAN FRANCISCO,CA 94121. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A402 EP A402 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101617 ER PT J AU IKEWAKI, K RADER, DJ SCHAEFER, JR FAIRWELL, T ZECH, LA BREWER, HB AF IKEWAKI, K RADER, DJ SCHAEFER, JR FAIRWELL, T ZECH, LA BREWER, HB TI EVALUATION OF APOA-I KINETICS IN HUMANS USING SIMULTANEOUS ENDOGENOUS STABLE ISOTOPE AND EXOGENOUS RADIOTRACER LABELING METHODS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A155 EP A155 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100241 ER PT J AU IRONY, I HAUGHEY, M CUTLER, GB AF IRONY, I HAUGHEY, M CUTLER, GB TI THE EFFECT OF CARBENOXOLONE ON PLASMA ACTH AND 17-HYDROXYPROGESTERONE LEVELS IN CONGENITAL ADRENAL-HYPERPLASIA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A236 EP A236 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100673 ER PT J AU JACKSON, SH MALECH, HL LOMAX, KJ GALLIN, JI HOLLAND, SM AF JACKSON, SH MALECH, HL LOMAX, KJ GALLIN, JI HOLLAND, SM TI MOLECULAR-CLONING AND FUNCTIONAL EXPRESSION OF THE MURINE HOMOLOG OF P47PHOX SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A174 EP A174 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100348 ER PT J AU JACOBSON, JD NISULA, BC STEINBERG, AD AF JACOBSON, JD NISULA, BC STEINBERG, AD TI MODULATION OF EXPRESSION OF MURINE LUPUS BY GONADOTROPIN-RELEASING-HORMONE (GNRH) AGONISM AND ANTAGONISM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NIAMS,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A273 EP A273 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100879 ER PT J AU JANG, S MARKOVA, NG STEINERT, PM AF JANG, S MARKOVA, NG STEINERT, PM TI POSITIVE AND NEGATIVE ELEMENTS INVOLVED IN THE TRANSCRIPTION OF THE HUMAN PROFILAGGRIN GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A441 EP A441 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101850 ER PT J AU JAVITT, JC CHIANG, Y CANNER, JK AIELLO, LP FERRIS, FL GREENFIELD, S AF JAVITT, JC CHIANG, Y CANNER, JK AIELLO, LP FERRIS, FL GREENFIELD, S TI FEDERAL BUDGETARY SAVINGS ARE ASSOCIATED WITH IMPROVED DELIVERY OF EYE CARE FOR TYPE-II DIABETES - A REVERSAL OF CONVENTIONAL WISDOM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NEW ENGLAND MED CTR,BOSTON,MA 02111. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A569 EP A569 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102616 ER PT J AU JUSTICE, J STEVENS, LA BLITZIOTES, MM MOSS, J VAUGHAN, M AF JUSTICE, J STEVENS, LA BLITZIOTES, MM MOSS, J VAUGHAN, M TI MONOCLONAL-ANTIBODIES WHICH REQUIRE N-TERMINAL ACYLATION OF TRANSDUCIN FOR IMMUNOREACTIVITY DIFFER FUNCTIONALLY IN EFFECTS ON BETA-GAMMA-DEPENDENT REACTIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A154 EP A154 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100236 ER PT J AU KAMP, TJ MARBAN, E MITAS, M NIRENBERG, M AF KAMP, TJ MARBAN, E MITAS, M NIRENBERG, M TI TRINUCLEOTIDE REPEAT (GAT)7 REGULATES EXPRESSION OF A NEURONAL CALCIUM-CHANNEL GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 3 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A202 EP A202 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100492 ER PT J AU KARPATI, S AMAGAI, M PRUSSICK, R CEHRS, K STANLEY, JR AF KARPATI, S AMAGAI, M PRUSSICK, R CEHRS, K STANLEY, JR TI PEMPHIGUS-VULGARIS ANTIGEN (PVA) IS LOCATED WITHIN HUMAN KERATINOCYTE DESMOSOMES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A428 EP A428 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101776 ER PT J AU KELLY, JF BLACKMAN, MR SONCRANT, TT AF KELLY, JF BLACKMAN, MR SONCRANT, TT TI AGE AND GENDER INFLUENCE THE PROLACTIN RESPONSE TO INTRAVENOUS HALOPERIDOL IN HEALTHY-PERSONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NIA,GERONTOL RES CTR,BETHESDA,MD 20892. FRANCIS SCOTT KEY MED CTR,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A226 EP A226 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100609 ER PT J AU KIM, MK MCCLASKEY, JH BODENNER, DL WEINTRAUB, BD AF KIM, MK MCCLASKEY, JH BODENNER, DL WEINTRAUB, BD TI A C-FOS/C-JUN-LIKE FACTOR AND THE PITUITARY-SPECIFIC FACTOR PIT-1 ARE BOTH NECESSARY TO MEDIATE HORMONAL INDUCTION OF HUMAN THYROTROPIN-BETA (HTSH-BETA) GENE-EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A266 EP A266 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100839 ER PT J AU KIM, SY KIM, IG STEINERT, PM CHUNG, SI AF KIM, SY KIM, IG STEINERT, PM CHUNG, SI TI PROCESSING OF THE MEMBRANE-ASSOCIATED TRANSGLUTAMINASE-1 DURING EPIDERMAL DIFFERENTIATION - STRUCTURE AND FUNCTIONAL-RELATIONSHIPS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A479 EP A479 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102083 ER PT J AU KIRNBAUER, R RODEN, R LOWY, DR SCHILLER, JT AF KIRNBAUER, R RODEN, R LOWY, DR SCHILLER, JT TI PAPILLOMAVIRUS-LIKE PARTICLES PRODUCED IN INSECT CELLS - POTENTIAL APPLICATION TO VACCINE DEVELOPMENT, BASIC BIOLOGY AND SERODIAGNOSIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A508 EP A508 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102257 ER PT J AU KISS, A AGUILERA, G AF KISS, A AGUILERA, G TI INTERACTION OF DIFFERENT STRESSORS ON THE HYPOTHALAMIC PITUITARY-ADRENAL AXIS (HPA) DURING CHRONIC STRESS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A301 EP A301 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101035 ER PT J AU KOEV, CA NATANSON, C QUEZADO, ZMN MAYEUX, B HOFFMAN, WD AF KOEV, CA NATANSON, C QUEZADO, ZMN MAYEUX, B HOFFMAN, WD TI FENTANYL MAY DIRECTLY BLOCK CARDIAC BETA-AGONIST EFFECTS OF EPINEPHRINE IN DOGS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A343 EP A343 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101280 ER PT J AU KOLLIA, P FIBACH, E NOGUCHI, CT SCHECHTER, AN AF KOLLIA, P FIBACH, E NOGUCHI, CT SCHECHTER, AN TI DIFFERENTIAL RNA SPLICING IN HUMAN HEMOGLOBIN SWITCHING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,CHEM BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A207 EP A207 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100517 ER PT J AU KOST, RG HILL, EL SMITH, H STRAUS, SE AF KOST, RG HILL, EL SMITH, H STRAUS, SE TI RECURRING ACYCLOVIR-RESISTANT GENITAL HERPES IN A NORMAL HOST SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,LCI,MED VIROL SECT,BETHESDA,MD 20892. BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A173 EP A173 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100346 ER PT J AU KRASNEWICH, DM WULFSBERG, EA GAHL, WA HOLT, GD AF KRASNEWICH, DM WULFSBERG, EA GAHL, WA HOLT, GD TI ACCUMULATION OF MUCIN OLIGOSACCHARIDES IN A PATIENT WITH CLINICAL-FEATURES OF INTRACELLULAR STORAGE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. UNIV MARYLAND,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A271 EP A271 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100866 ER PT J AU KULKARNI, AB GEISER, A FRANCIS, N FLANDERS, KC ROBERTS, AB SPORN, MB WARD, JM WAHL, SM KARLSSON, S AF KULKARNI, AB GEISER, A FRANCIS, N FLANDERS, KC ROBERTS, AB SPORN, MB WARD, JM WAHL, SM KARLSSON, S TI TRANSFORMING GROWTH-FACTOR-BETA-1 NULL MUTATION IN MICE CAUSES EXCESSIVE INFLAMMATORY RESPONSE AND EARLY DEATH SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NINCDS,DEV & METAB NEUROL BRANCH,MOLEC MED GENET SECT,BETHESDA,MD 20892. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NCI,COMPARAT CARCINOGENESIS LAB,BETHESDA,MD 20892. NIDR,CELLULAR IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 2 U2 5 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A213 EP A213 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100549 ER PT J AU KWONG, CH LETO, TL AF KWONG, CH LETO, TL TI LOCALIZATION OF THE EFFECTOR DOMAIN OF RAC SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A170 EP A170 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100327 ER PT J AU LEAHEY, AM BAILEY, LC CHARNAS, LR NUSSBAUM, RL AF LEAHEY, AM BAILEY, LC CHARNAS, LR NUSSBAUM, RL TI PREMATURE TERMINATION MUTATIONS IN OCRL-1, A CANDIDATE GENE FOR LOWE SYNDROME, IN LOWE SYNDROME PATIENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV PENN,SCH MED,DEPT PEDIAT,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT GENET,PHILADELPHIA,PA 19104. HOWARD HUGHES MED INST,PHILADELPHIA,PA. NICHHD,HUMAN GENET BRANCH,NEUROGENET UNIT,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A272 EP A272 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100869 ER PT J AU LEE, MG TANG, A UDEY, MC AF LEE, MG TANG, A UDEY, MC TI A ROLE FOR E-CADHERIN (E-CAD) IN ADHESION OF MURINE EPIDERMAL GAMMA-DELTA T-CELLS (GAMMA-DELTA-TC) TO KERATINOCYTES (KC) INVITRO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A178 EP A178 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100370 ER PT J AU LEE, SC KIM, IG MAREKOV, L OKEEFE, EJ PARRY, DAD STEINERT, PM AF LEE, SC KIM, IG MAREKOV, L OKEEFE, EJ PARRY, DAD STEINERT, PM TI THE STRUCTURE OF HUMAN TRICHOHYALIN - A MULTIFUNCTIONAL EF-HAND-TYPE CALCIUM-BINDING PROTEIN, CORNIFIED CELL-ENVELOPE PRECURSOR AND KERATIN INTERMEDIATE FILAMENT ASSOCIATED PROTEIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. UNIV N CAROLINA,DEPT DERMATOL,CHAPEL HILL,NC 27514. MASSEY UNIV,PALMERSTON NORTH,NEW ZEALAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A481 EP A481 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102090 ER PT J AU LEMARCHAND, P YOO, JH ERZURUM, SC ROSENFELD, MA CRYSTAL, RG AF LEMARCHAND, P YOO, JH ERZURUM, SC ROSENFELD, MA CRYSTAL, RG TI PROTECTION OF BRONCHIAL EPITHELIAL-CELLS FROM OXIDANT INJURY BY ADENOVIRUS-MEDIATED TRANSFER OF THE HUMAN CATALASE CDNA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A224 EP A224 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100600 ER PT J AU LEMARCHAND, P JONES, M YAMADA, I CRYSTAL, RG AF LEMARCHAND, P JONES, M YAMADA, I CRYSTAL, RG TI INVIVO GENE-TRANSFER AND EXPRESSION IN NORMAL, UNINJURED BLOOD-VESSELS USING REPLICATION DEFICIENT RECOMBINANT ADENOVIRUS VECTORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NHLBI,SLAMS,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A202 EP A202 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100494 ER PT J AU LEVY, DD TANAKA, K KRAEMER, KH AF LEVY, DD TANAKA, K KRAEMER, KH TI EXPRESSION OF A TRANSFECTED DNA-REPAIR GENE (XPAC) IN XERODERMA-PIGMENTOSUM GROUP-A CELLS IMPROVES DNA-REPAIR AND MUTAGENESIS OF UV-TREATED PLASMIDS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. OSAKA UNIV,OSAKA,JAPAN. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A442 EP A442 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101856 ER PT J AU LEVYTOLEDANO, R CARO, LHP ACCILI, D TAYLOR, SI AF LEVYTOLEDANO, R CARO, LHP ACCILI, D TAYLOR, SI TI INVESTIGATION OF MECHANISM OF DOMINANT NEGATIVE EFFECT OF MUTATIONS IN TYROSINE KINASE DOMAIN OF INSULIN-RECEPTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,DIABET BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A131 EP A131 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100098 ER PT J AU LI, LW HENNINGS, H YUSPA, SH AF LI, LW HENNINGS, H YUSPA, SH TI THAPSIGARGIN AND CYCLOPIAZONIC ACID INHIBIT CA2+-INDUCED KERATINOCYTE TERMINAL DIFFERENTIATION INVITRO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A481 EP A481 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102092 ER PT J AU LICINIO, J WONG, ML ALTEMUS, M BONGIORNO, PB BERNAT, A GOLD, PW AF LICINIO, J WONG, ML ALTEMUS, M BONGIORNO, PB BERNAT, A GOLD, PW TI 24-HOUR CONCENTRATIONS OF CIRCULATING INTERLEUKIN-1-ALPHA IN HEALTHY WOMEN EXHIBIT PULSATILE PATTERNS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06510. VET ADM MED CTR,W HAVEN,CT. NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RI Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A156 EP A156 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100250 ER PT J AU MAEDA, H CRYSTAL, RG AF MAEDA, H CRYSTAL, RG TI GENE-THERAPY STRATEGY FOR THE PANCREATIC INSUFFICIENCY OF CYSTIC-FIBROSIS - ADENOVIRUS-MEDIATED TRANSFER OF THE HUMAN PANCREATIC LIPASE CDNA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A206 EP A206 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100513 ER PT J AU MAGIAKOU, MA MASTORAKOS, G GOMEZ, MT DOPPMAN, JL CUTLER, GB OLDFIELD, EH NIEMAN, LK CHROUSOS, GP AF MAGIAKOU, MA MASTORAKOS, G GOMEZ, MT DOPPMAN, JL CUTLER, GB OLDFIELD, EH NIEMAN, LK CHROUSOS, GP TI ENDOGENOUS CUSHING SYNDROME IN CHILDREN AND ADOLESCENTS - THE NIH EXPERIENCE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. NINCDS,SNB,BETHESDA,MD 20892. NIH,CC,DR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A273 EP A273 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100877 ER PT J AU MAHANTY, S MOLLIS, S RAVICHANDRAN, M JAYARAMAN, K KUMARASWAMI, V ABRAMS, JS OTTESEN, EA NUTMAN, TB AF MAHANTY, S MOLLIS, S RAVICHANDRAN, M JAYARAMAN, K KUMARASWAMI, V ABRAMS, JS OTTESEN, EA NUTMAN, TB TI EXCESS IL-10 PRODUCTION BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS IS ASSOCIATED WITH ANTIGEN-SPECIFIC HYPORESPONSIVENESS IN HUMAN LYMPHATIC FILARIASIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. DNAX RES INST MOLEC & CELLULAR BIOL INC,RES INST,PALO ALTO,CA. TB RES CTR,MADRAS,INDIA. ANNA UNIV,MADRAS,INDIA. RI Ravichandran, Manickam/A-7128-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A324 EP A324 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101171 ER PT J AU MALECH, HL HUANG, CK RENFER, L ROTROSEN, D AF MALECH, HL HUANG, CK RENFER, L ROTROSEN, D TI TYROSINE-324 OF P47(PHOX) PLAYS A FUNCTIONAL-ROLE IN CELL-FREE ACTIVATION OF PHAGOCYTE NADPH OXIDASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. UNIV CONNECTICUT,DEPT PATHOL,FARMINGTON,CT 06032. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A323 EP A323 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101166 ER PT J AU MAREKOV, L STEINERT, PM PARRY, DAD AF MAREKOV, L STEINERT, PM PARRY, DAD TI THE DETERMINATION OF THE MOLECULAR DIMENSIONS AND MODE OF ASSEMBLY OF KERATIN INTERMEDIATE FILAMENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSEY UNIV,PALMERSTON NORTH,NEW ZEALAND. NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A482 EP A482 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102097 ER PT J AU MARKOVA, NG GAN, SQ STEINERT, PM AF MARKOVA, NG GAN, SQ STEINERT, PM TI COMPLEXITY OF PROFILAGGRIN GENE-EXPRESSION IN MAMMALIAN EPIDERMIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A482 EP A482 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102098 ER PT J AU MASTRANGELI, A BAJOCCHI, G FELDMAN, S CRYSTAL, RG AF MASTRANGELI, A BAJOCCHI, G FELDMAN, S CRYSTAL, RG TI INVIVO ADENOVIRUS-MEDIATED GENE-TRANSFER TO THE CENTRAL-NERVOUS-SYSTEM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NHLBI,SLAMS,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A223 EP A223 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100596 ER PT J AU MCDONALD, LJ MOSS, J AF MCDONALD, LJ MOSS, J TI PLEIOTROPIC EFFECTS OF NITRIC-OXIDE ON ADP-RIBOSYLATION, COVALENT BINDING OF NAD, AND CATALYTIC ACTIVITY OF GLYCERALDEHYDE-3-PHOSPHATE AND ALDEHYDE DEHYDROGENASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A267 EP A267 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100842 ER PT J AU MEIER, J COREY, L BURKE, RL SAVARESE, B BARNUM, G KOST, R ADAIR, S DEKKER, C STRAUS, SE AF MEIER, J COREY, L BURKE, RL SAVARESE, B BARNUM, G KOST, R ADAIR, S DEKKER, C STRAUS, SE TI IMMUNOTHERAPY OF GENITAL HERPES WITH A RECOMBINANT HERPES-SIMPLEX VIRUS TYPE-2 GLYCOPROTEIN D (GD2) VACCINE - A PLACEBO-CONTROLLED TRIAL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LCI,BETHESDA,MD 20892. UNIV WASHINGTON,SEATTLE,WA 98195. BIOCINE INC,EMERYVILLE,CA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A199 EP A199 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100479 ER PT J AU MERENDINO, JJ THAMBI, NC SHENKER, A SPIEGEL, AM AF MERENDINO, JJ THAMBI, NC SHENKER, A SPIEGEL, AM TI DETECTION OF V2 VASOPRESSIN RECEPTOR GENE-MUTATIONS IN X-LINKED NEPHROGENIC DIABETES-INSIPIDUS BY TEMPERATURE-GRADIENT GEL-ELECTROPHORESIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD. NR 0 TC 3 Z9 3 U1 0 U2 4 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A131 EP A131 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100100 ER PT J AU MIYASHITA, A HAY, JG CRYSTAL, RG AF MIYASHITA, A HAY, JG CRYSTAL, RG TI CHARACTERIZATION OF THE HUMAN CYTOSOLIC PHOSPHOLIPASE-A2 GENE SUGGESTS THAT IT BELONGS TO AN ATYPICAL SUBCLASS OF HOUSEKEEPING GENES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A243 EP A243 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100711 ER PT J AU MOLES, JP SCHILLER, J LEIGH, I TESNIERE, A GUILHOU, JJ BASSETSEGUIN, N AF MOLES, JP SCHILLER, J LEIGH, I TESNIERE, A GUILHOU, JJ BASSETSEGUIN, N TI CORRELATION BETWEEN CK-19 EXPRESSION AND P53 ACTIVITY IN HUMAN KERATINOCYTES INVITRO AND INVIVO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 LAB DERMATOL MOLEC,MONTPELLIER,FRANCE. NIH,BETHESDA,MD 20892. ICRF,LONDON,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A482 EP A482 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102100 ER PT J AU MOLLIS, SN RAGHAVAN, N NUTMAN, TB AF MOLLIS, SN RAGHAVAN, N NUTMAN, TB TI IDENTIFICATION OF RECOMBINANT FILARIAL ANTIGENS RECOGNIZED BY IMMUNOGLOBULIN-E OF PATIENTS WITH TROPICAL PULMONARY EOSINOPHILIA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A323 EP A323 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101165 ER PT J AU NAM, MH REDA, D BOUJOUKOS, AJ MARTICH, GD AGOSTI, J SUFFREDINI, AF AF NAM, MH REDA, D BOUJOUKOS, AJ MARTICH, GD AGOSTI, J SUFFREDINI, AF TI SOLUBLE RECOMBINANT HUMAN INTERLEUKIN-1 RECEPTOR (RHIL-1R) - SAFETY AND PHARMACOKINETICS IN HUMAN VOLUNTEERS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 IMMUNEX CORP,SEATTLE,WA. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A380 EP A380 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101502 ER PT J AU NAM, MH MILLER, R BANKS, S SUFFREDINI, AF AF NAM, MH MILLER, R BANKS, S SUFFREDINI, AF TI EFFECTS OF RECOMBINANT HUMAN DIMERIC TUMOR-NECROSIS-FACTOR (TNF) RECEPTOR (TNFR-FC) ON ENDOTOXIN-INDUCED WHOLE-BLOOD CYTOKINE PRODUCTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A139 EP A139 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100148 ER PT J AU NAM, MH REDA, D BOUJOUKOS, AJ AGOSTI, J SUFFREDINI, AF AF NAM, MH REDA, D BOUJOUKOS, AJ AGOSTI, J SUFFREDINI, AF TI RECOMBINANT HUMAN DIMERIC TUMOR-NECROSIS-FACTOR (TNF) RECEPTOR (TNFR-FC) - SAFETY AND PHARMACOKINETICS IN HUMAN VOLUNTEERS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 IMMUNEX CORP,SEATTLE,WA. NIH,CTR CLIN,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 13 Z9 13 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A249 EP A249 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100748 ER PT J AU NATANSON, C REILLY, JM HOFFMAN, WD BANKS, SM DANNER, RL CUNNION, RE PARRILLO, JE AF NATANSON, C REILLY, JM HOFFMAN, WD BANKS, SM DANNER, RL CUNNION, RE PARRILLO, JE TI EFFECT OF SEPTIC SHOCK ON CARDIOVASCULAR-RESPONSES TO DOPAMINE (DA) AND NOREPINEPHRINE (NE) IN A CONSCIOUS CANINE MODEL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. DNA,AFRRI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A252 EP A252 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100767 ER PT J AU ODA, N LIU, ZY WU, YG NOGUCHI, CT AF ODA, N LIU, ZY WU, YG NOGUCHI, CT TI SELECTIVE INCREASE IN GATA-1 LEVELS IN ERYTHROLEUKEMIA-CELLS CAN TRANSACTIVATE THE HUMAN ERYTHROPOIETIN RECEPTOR (HEPOR) PROMOTER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,CHEM BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A132 EP A132 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100107 ER PT J AU OKAZAKI, IJ MOSS, J AF OKAZAKI, IJ MOSS, J TI EFFECTS ON CHOLERA TOXIN-CATALYZED AND ENDOGENOUS ADP-RIBOSYLATION OF OVEREXPRESSION OF ADP-RIBOSYLARGININE HYDROLASE, THE ENZYME RESPONSIBLE FOR CLEAVAGE OF THE ADP-RIBOSE-ARGININE BOND SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A321 EP A321 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101156 ER PT J AU PANTALEO, G GRAZIOSI, C DEMAREST, JF BUTINI, L COHEN, OJ FAUCI, AS AF PANTALEO, G GRAZIOSI, C DEMAREST, JF BUTINI, L COHEN, OJ FAUCI, AS TI EVIDENCE FOR ACTIVE HIV-INFECTION IN LYMPHOID-TISSUE DURING THE PROLONGED PERIOD OF CLINICAL LATENCY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A259 EP A259 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100805 ER PT J AU POLI, G KINTER, AL WEISSMAN, D BISWAS, P FAUCI, AS AF POLI, G KINTER, AL WEISSMAN, D BISWAS, P FAUCI, AS TI INTERACTIONS BETWEEN PRO-INFLAMMATORY AND IMMUNOREGULATORY CYTOKINES MODULATE THE EXPRESSION OF HUMAN-IMMUNODEFICIENCY-VIRUS IN MONOCYTIC CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A137 EP A137 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100133 ER PT J AU QUEZADO, ZMN NATANSON, C BANKS, SM KOEV, CA DANNER, RL ELIN, RJ HOSSEINI, JM BACHER, JD HOFFMAN, WD AF QUEZADO, ZMN NATANSON, C BANKS, SM KOEV, CA DANNER, RL ELIN, RJ HOSSEINI, JM BACHER, JD HOFFMAN, WD TI PENTOXIFYLLINE INCREASED TUMOR-NECROSIS-FACTOR LEVEL AND DECREASED SURVIVAL IN A CANINE MODEL OF GRAM-NEGATIVE SEPTIC SHOCK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A252 EP A252 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100766 ER PT J AU QUEZADO, ZMN HOFFMAN, WD YATSIV, I KOEV, CA WINKELSTEIN, JA WINKELSTEIN, BA CORK, LC BANKS, SM WILSON, L ELIN, RJ EICHACKER, PQ NATANSON, C AF QUEZADO, ZMN HOFFMAN, WD YATSIV, I KOEV, CA WINKELSTEIN, JA WINKELSTEIN, BA CORK, LC BANKS, SM WILSON, L ELIN, RJ EICHACKER, PQ NATANSON, C TI THE 3RD COMPONENT OF COMPLEMENT PROTECTS AGAINST ENDOTOXIN-INDUCED MULTIPLE ORGAN FAILURE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,DEPT CRIT CARE,WASHINGTON,DC. JOHNS HOPKINS UNIV,DEPT PEDIAT,BALTIMORE,MD 21218. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A243 EP A243 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100714 ER PT J AU QUEZADO, ZMN HOFFMAN, WD BANKS, SM ALLING, DW KOEV, CA DANNER, RL ELIN, RJ HOSSEINI, JM BACHER, JD PARKER, TS LEVINE, DM RUBIN, AL NATANSON, C AF QUEZADO, ZMN HOFFMAN, WD BANKS, SM ALLING, DW KOEV, CA DANNER, RL ELIN, RJ HOSSEINI, JM BACHER, JD PARKER, TS LEVINE, DM RUBIN, AL NATANSON, C TI THERAPEUTIC TRIAL OF RECONSTITUTED HUMAN HIGH-DENSITY-LIPOPROTEIN IN A DOG-MODEL OF GRAM-NEGATIVE SEPTIC SHOCK - PRELIMINARY-RESULTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. ROGOSIN INST,NEW YORK,NY. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A175 EP A175 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100357 ER PT J AU RADER, DJ IKEWAKI, K DUVERGER, N PRITCHARD, H FROHLICH, J CLERC, M SCHMIDT, H SANTAMARINAFOJO, S FAIRWELL, T ZECH, L BREWER, HB AF RADER, DJ IKEWAKI, K DUVERGER, N PRITCHARD, H FROHLICH, J CLERC, M SCHMIDT, H SANTAMARINAFOJO, S FAIRWELL, T ZECH, L BREWER, HB TI COMPLETE AND PARTIAL LCAT DEFICIENCY - RAPID INVIVO CATABOLISM OF LIPOPROTEINS CONTAINING BOTH APOLIPOPROTEIN-A-I AND APOLIPOPROTEIN-A-11 (LPA-1-A-11) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,MDB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A204 EP A204 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100506 ER PT J AU REDDY, SV NECKARS, L DALLAS, M WILLIAMS, R ROODMAN, GD AF REDDY, SV NECKARS, L DALLAS, M WILLIAMS, R ROODMAN, GD TI ANTISENSE CONSTRUCTS TO IL-6 MESSENGER-RNA INHIBIT BONE-RESORPTION BY OSTEOCLASTS (OCL) FROM GIANT-CELL TUMORS (GCT) OF BONE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. NIH, BETHESDA, MD 20892 USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A184 EP A184 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100403 ER PT J AU RIVA, A WILSON, GL KEHRL, JH AF RIVA, A WILSON, GL KEHRL, JH TI ANALYSIS OF THE HUMAN CD19 PROMOTER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A373 EP A373 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101461 ER PT J AU ROACH, P ZICK, Y ACCILI, D TAYLOR, SI GORDEN, P AF ROACH, P ZICK, Y ACCILI, D TAYLOR, SI GORDEN, P TI EXTREME INSULIN RESISTANCE ASSOCIATED WITH DECREASED INSULIN BINDING - MUTATION IN THE INSULIN-RECEPTOR ALPHA-SUBUNIT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DIABET BRANCH,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A274 EP A274 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100882 ER PT J AU ROCKEN, M BOULAY, JL PAUL, WE SHEVACH, EM AF ROCKEN, M BOULAY, JL PAUL, WE SHEVACH, EM TI INDUCTION OF IL-4 PRODUCTION INVIVO - A MODEL FOR THE STUDY OF ATOPY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A466 EP A466 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102003 ER PT J AU ROSENBERG, HF MORRISON, RP AF ROSENBERG, HF MORRISON, RP TI A NOVEL HEAT-SHOCK PROTEIN (HSP)-60 HOMOLOG DETECTED IN MYELOID CELL-LINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,INTRACELLULAR PARASITES LAB,HAMILTON,MT. NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A373 EP A373 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101462 ER PT J AU ROSENFELD, MA ROSENFELD, SJ DANEL, C BANKS, TC CRYSTAL, RG AF ROSENFELD, MA ROSENFELD, SJ DANEL, C BANKS, TC CRYSTAL, RG TI DISSOCIATION OF THE AMOUNT OF CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) PROTEIN AND THE RATE OF CAMP-STIMULATED CL- EFFLUX SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A185 EP A185 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100410 ER PT J AU ROTROSEN, D YEUNG, CL OSAWA, Y AF ROTROSEN, D YEUNG, CL OSAWA, Y TI P47PHOX INTERACTS WITH A HEME-BINDING DOMAIN OF CYTOCHROME-B558 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A222 EP A222 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100594 ER PT J AU RUSSO, TA LIANG, Y CROSS, AS AF RUSSO, TA LIANG, Y CROSS, AS TI THE PRESENCE OF K54 CAPSULAR POLYSACCHARIDE INCREASES THE PATHOGENICITY OF ESCHERICHIA-COLI INVIVO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. WALTER REED ARMY INST RES,WASHINGTON,DC 20307. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A248 EP A248 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100740 ER PT J AU SAVILLE, MW FOLI, A YARCHOAN, R AF SAVILLE, MW FOLI, A YARCHOAN, R TI ANTIPROLIFERATIVE ACTIVITY OF TNP-470 (AGM-1470), A NOVEL ANGIOGENESIS INHIBITOR, IN KAPOSIS-SARCOMA (KS)-RELATED SPINDLE CELL-LINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,MED BRANCH,RETROVIRAL DIS SECT,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A161 EP A161 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100276 ER PT J AU SCANDURRO, AB WANG, O GOODMAN, L LEDBETTER, S YUSPA, SH LICHTI, U AF SCANDURRO, AB WANG, O GOODMAN, L LEDBETTER, S YUSPA, SH LICHTI, U TI INTERACTION OF IMMATURE HAIR FOLLICLE BUDS WITH IMMORTALIZED DERMAL PAPILLA CELLS IN COLLAGEN MATRIX COCULTURE LEADS TO ACTIVATION OF TYPE-IV COLLAGENASES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROTECT,BETHESDA,MD 20892. NCI,BIOL CHEM LAB,BETHESDA,MD 20892. UPJOHN CO,KALAMAZOO,MI 49001. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A405 EP A405 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101638 ER PT J AU SCOTT, DC NIEMAN, LK ELLIOT, SJ OLSON, BR AF SCOTT, DC NIEMAN, LK ELLIOT, SJ OLSON, BR TI INSULIN-LIKE GROWTH FACTOR-I BINDING AND EFFECTS ON A GONADOTROPIN-RELEASING HORMONE-SECRETING NEURONAL CELL-LINE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A325 EP A325 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101177 ER PT J AU SEKHSARIA, S GALLIN, JI MALECH, HL AF SEKHSARIA, S GALLIN, JI MALECH, HL TI RETROVIRUS MEDIATED CORRECTION OF SUPEROXIDE PRODUCTION BY GENE-TRANSFER INTO PERIPHERAL-BLOOD HEMATOPOIETIC PROGENITORS (PBHP) FROM PATIENTS WITH P47(PHOX) DEFICIENT CHRONIC GRANULOMATOUS-DISEASE (CGD) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A213 EP A213 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100551 ER PT J AU SELLHEYER, K ROTHNAGEL, J BUNDMAN, D LONGLEY, M GEISER, A ROBERTS, A ROOP, D AF SELLHEYER, K ROTHNAGEL, J BUNDMAN, D LONGLEY, M GEISER, A ROBERTS, A ROOP, D TI TARGETED EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA-1 (TGF-BETA-1) TO THE EPIDERMIS LEADS TO LIVEBORN, BUT NONVIABLE TRANSGENIC MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. BAYLOR COLL MED,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A450 EP A450 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101906 ER PT J AU SETOGUCHI, Y DANEL, C CRYSTAL, RG AF SETOGUCHI, Y DANEL, C CRYSTAL, RG TI STIMULATION OF ERYTHROPOIESIS BY INVIVO GENE-THERAPY - PHYSIOLOGICAL CONSEQUENCE OF TRANSFER OF THE HUMAN ERYTHROPOIETIN GENE TO EXPERIMENTAL-ANIMALS USING AN ADENOVIRUS VECTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 3 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A259 EP A259 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100803 ER PT J AU SIERRA, ML CAMA, A KADOWAKI, T KADOWAKI, H QUON, MJ TAYLOR, SI AF SIERRA, ML CAMA, A KADOWAKI, T KADOWAKI, H QUON, MJ TAYLOR, SI TI 2 MUTANT ALLELES OF THE INSULIN-RECEPTOR GENE IN A FAMILY WITH A GENETIC FORM OF INSULIN RESISTANCE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,DIABET BRANCH,BETHESDA,MD. RI Quon, Michael/B-1970-2008 NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A131 EP A131 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100099 ER PT J AU STANLEY, SK MCCUNE, JM KANESHIMA, H JUSTEMENT, SJ SULLIVAN, M BOONE, E BASELER, M ADELSBERGER, J FOX, C ORENSTEIN, J FAUCI, AS AF STANLEY, SK MCCUNE, JM KANESHIMA, H JUSTEMENT, SJ SULLIVAN, M BOONE, E BASELER, M ADELSBERGER, J FOX, C ORENSTEIN, J FAUCI, AS TI HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) INFECTION OF THE HUMAN THYMUS IN THE SCID-HU MOUSE MODEL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. SYSTEMIX INC,PALO ALTO,CA. PRI DYN CORP,FREDERICK,MD. GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20052. AMER HISTOLABS,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A136 EP A136 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100128 ER PT J AU SUNARAKBASAK, B KISS, A AGUILERA, G AF SUNARAKBASAK, B KISS, A AGUILERA, G TI LOCALIZATION OF MESSENGER-RNA ENCODING A NOVEL ANGIOTENSIN-II (AII) RECEPTOR SUBTYPE IN THE RAT-BRAIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A154 EP A154 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100233 ER PT J AU SZALLASI, Z SMITH, CB DENNING, MF DLUGOSZ, AA YUSPA, SH PETTIT, GR BLUMBERG, PM AF SZALLASI, Z SMITH, CB DENNING, MF DLUGOSZ, AA YUSPA, SH PETTIT, GR BLUMBERG, PM TI DIFFERENTIAL REGULATION OF PROTEIN-KINASE-C ISOZYMES BY INHIBITORY 12-DEOXYPHORBOL 13-MONOESTERS, BRYOSTATIN-1 AND PHORBOL 12-MYRISTATE 13-ACETATE (PMA) IN MOUSE KERATINOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. ARIZONA STATE UNIV,CANC RES INST,TEMPE,AZ 85287. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A450 EP A450 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101909 ER PT J AU TENNENBAUM, T WILDNAUER, T BELANGER, A MROZ, A GORDON, JS AF TENNENBAUM, T WILDNAUER, T BELANGER, A MROZ, A GORDON, JS TI COMPARISON OF THE EFFECTS OF RETINOIC ACID AND AN IRRITANT, HEXADECANE, ON HAIRLESS MOUSE SKIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. JOHNSON & JOHNSON CONSUMER PROD INC,SKILLMAN,NJ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A485 EP A485 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102118 ER PT J AU THEVENIN, C KEHRL, JH AF THEVENIN, C KEHRL, JH TI ANALYSIS OF THE HUMAN CD20 PROMOTER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A169 EP A169 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100321 ER PT J AU TURNER, ML MOSHELL, A CORBETT, DW STERN, JB ROTH, MJ DIGIOVANNA, JD HORN, TD KRAEMER, KH AF TURNER, ML MOSHELL, A CORBETT, DW STERN, JB ROTH, MJ DIGIOVANNA, JD HORN, TD KRAEMER, KH TI CLEARING OF MELANOMA-INSITU WITH INTRALESIONAL ALPHA-INTERFERON IN A PATIENT WITH XERODERMA-PIGMENTOSUM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NNMC,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A425 EP A425 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101757 ER PT J AU VAMVAKOPOULOS, NC DURKIN, S CHROUSOS, GP NIERMAN, W AF VAMVAKOPOULOS, NC DURKIN, S CHROUSOS, GP NIERMAN, W TI MAPPING OF A HUMAN HEAT-SHOCK PROTEIN-90-BETA STRUCTURAL GENE WITHIN THE MAJOR HISTOCOMPATIBILITY COMPLEX (6P21) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. AMER TYPE CULTURE COLLECT,DMB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A392 EP A392 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76101570 ER PT J AU VANDERVORT, AL YAN, L MADARA, PJ COBB, JP WESLEY, RA TROPEA, MM DANNER, RL AF VANDERVORT, AL YAN, L MADARA, PJ COBB, JP WESLEY, RA TROPEA, MM DANNER, RL TI NITRIC-OXIDE (NO) INCREASES ENDOTOXIN (LPS)-INDUCED CYTOKINE PRODUCTION BY HUMAN NEUTROPHILS (PMNS) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A281 EP A281 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100918 ER PT J AU WEINBERG, WC CHAPMAN, K PELLING, J LEVINE, A YUSPA, SH AF WEINBERG, WC CHAPMAN, K PELLING, J LEVINE, A YUSPA, SH TI P53 SYNTHESIS AND P53-DEPENDENT TRANSCRIPTIONAL ACTIVITY ARE MODULATED FOLLOWING INDUCTION OF KERATINOCYTE DIFFERENTIATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. EPPLEY INST CANC RES,OMAHA,NE. PRINCETON UNIV,PRINCETON,NJ 08544. RI Weinberg, Wendy/A-8920-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A512 EP A512 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102277 ER PT J AU WEISSMAN, D POLI, G FAUCI, AS AF WEISSMAN, D POLI, G FAUCI, AS TI PERIPHERAL-BLOOD DENDRITIC CELLS PULSED WITH HIV-1 CAN INFECT UNSTIMULATED AUTOLOGOUS T-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A221 EP A221 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100588 ER PT J AU WERTHEIMER, E LU, SP BACKELJAUW, PF DAVENPORT, ML TAYLOR, SI AF WERTHEIMER, E LU, SP BACKELJAUW, PF DAVENPORT, ML TAYLOR, SI TI HOMOZYGOUS DELETION OF THE HUMAN INSULIN-RECEPTOR GENE IS COMPATIBLE WITH LIFE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DIABET BRANCH,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC 27514. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A258 EP A258 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100802 ER PT J AU WHALEN, G KATZ, P KEHRL, JH AF WHALEN, G KATZ, P KEHRL, JH TI ANALYSIS OF A NOVEL PROTEIN-KINASE PREFERENTIALLY EXPRESSED IN GERMINAL CENTER VERSUS MANTLE ZONE B-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 GEORGETOWN UNIV,WASHINGTON,DC 20007. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A208 EP A208 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100522 ER PT J AU WILMER, JL BURLESON, FG KAYAMA, F KANNO, J LUSTER, MI AF WILMER, JL BURLESON, FG KAYAMA, F KANNO, J LUSTER, MI TI RELATION OF CHEMICALLY-INDUCED INFLAMMATION IN MOUSE SKIN TO PATTERNS OF CYTOKINE PRODUCTION IN HUMAN KERATINOCYTES EXPOSED TO SKIN TOXICANTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A486 EP A486 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102122 ER PT J AU XU, LC STAHL, SK DAVE, HPG CORRELL, PH KESSLER, S DUNBAR, C KARLSSON, S AF XU, LC STAHL, SK DAVE, HPG CORRELL, PH KESSLER, S DUNBAR, C KARLSSON, S TI A CLINICALLY ACCEPTABLE PROTOCOL YIELDS HIGH-EFFICIENCY TRANSFER OF THE GLUCOCEREBROSIDASE GENE INTO CD34+ PROGENITORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NINCDS,DEV & METAB NEUROL BRANCH,BETHESDA,MD 20892. NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. USN,MED RES INST,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A194 EP A194 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100458 ER PT J AU YAN, L DANNER, RL AF YAN, L DANNER, RL TI NITRIC-OXIDE SYNTHASE (NOS) ACTIVITY IN HUMAN NEUTROPHILS (PMNS) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A247 EP A247 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76100735 ER PT J AU YANG, JM CHIPEV, CC STEINERT, PM COMPTON, JG AF YANG, JM CHIPEV, CC STEINERT, PM COMPTON, JG TI IS PALMOPLANTAR INVOLVEMENT IN EPIDERMOLYTIC HYPERKERATOSIS ASSOCIATED WITH SPECIFIC KERATIN MUTATIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A487 EP A487 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102126 ER PT J AU YONEDA, K STEINERT, PM AF YONEDA, K STEINERT, PM TI THE CORRECT EXPRESSION OF THE HUMAN LORICRIN GENE IN TRANSGENIC MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1993 VL 41 IS 2 BP A487 EP A487 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KW761 UT WOS:A1993KW76102127 ER PT J AU DELAHUNTY, MD MACK, JPG AF DELAHUNTY, MD MACK, JPG TI A GENERAL-METHOD OF CURVE FITTING AND ERROR ANALYSIS USING A SPREADSHEET - DETERMINATION OF THE BINDING CONSTANTS OF TIGHT-BINDING LIGANDS IN VARIABLE VOLUME ASSAYS SO COMPUTER APPLICATIONS IN THE BIOSCIENCES LA English DT Article ID MICHAELIS-MENTEN; REGRESSION; PROGRAMS; KINETICS AB A generalized iterative method of curve fitting and error estimation is described, using a spreadsheet with Monte Carlo simulations. The method is demonstrated on an equilibrium binding experiment with reverse transcriptase of human immunodeficiency virus-1, in which the concentration of all reactants, including enzyme, can vary arbitrarily and any number of ligands can bind tightly. C1 UNIV MARYLAND,DEPT CHEM,CATONSVILLE,MD 21228. NCI,FCRDC,MACROMOLEC STRUCT LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU PHS HHS [N01-C0-74101] NR 12 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 0266-7061 J9 COMPUT APPL BIOSCI JI Comput. Appl. Biosci. PD APR PY 1993 VL 9 IS 2 BP 127 EP 131 PG 5 WC Computer Science, Interdisciplinary Applications SC Computer Science GA KX737 UT WOS:A1993KX73700002 PM 7683246 ER PT J AU MARK, SD ROBINS, JM AF MARK, SD ROBINS, JM TI A METHOD FOR THE ANALYSIS OF RANDOMIZED TRIALS WITH COMPLIANCE INFORMATION - AN APPLICATION TO THE MULTIPLE RISK FACTOR INTERVENTION TRIAL SO CONTROLLED CLINICAL TRIALS LA English DT Article DE COMPLIANCE; RANDOMIZED CLINICAL TRIAL; ACCELERATED FAILURE TIME MODEL; LOG-RANK TEST; SMOKING CESSATION; TIME DEPENDENT COVARIATE ID CAUSAL INFERENCE; MORTALITY; SMOKING; MODELS; MRFIT AB The standard approach to analyzing randomized trials ignores information on postrandomization compliance. Application of these methods results in estimates that may lack the desired causal interpretation. We employ a new method of estimation and analyze data from the Multiple Risk Factor Intervention Trial (MRFIT) to estimate the causal effect of quitting cigarette smoking. Our procedure utilizes a method proposed by Robins and Tsiatis and allows us to take advantage of postrandomization smoking history without requiring untenable assumptions about the comparability of compliers and noncompliers. We contrast the performance of our method and the standard intent-to-treat analysis in the MRFIT data and in simulated data in which compliance rates are varied. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL & BIOSTAT,BOSTON,MA 02115. NCI,EPIDEMIOL METHODS SECT,BIOSTAT BRANCH,WASHINGTON,DC. FU NCI NIH HHS [NC15T32CA09001]; NIEHS NIH HHS [5R01ES03405, 5KO4ESOO180] NR 30 TC 94 Z9 97 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD APR PY 1993 VL 14 IS 2 BP 79 EP 97 DI 10.1016/0197-2456(93)90012-3 PG 19 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KV160 UT WOS:A1993KV16000002 PM 8500308 ER PT J AU CLEARY, PA BECK, RW ANDERSON, MM KENNY, DJ BACKLUND, J GILBERT, PR AF CLEARY, PA BECK, RW ANDERSON, MM KENNY, DJ BACKLUND, J GILBERT, PR TI DESIGN, METHODS, AND CONDUCT OF THE OPTIC NEURITIS TREATMENT TRIAL SO CONTROLLED CLINICAL TRIALS LA English DT Article DE CONTROLLED CLINICAL TRIAL; RANDOMIZED TRIAL; OPTIC NEURITIS ID CONTRAST SENSITIVITY AB The Optic Neuritis Treatment Trial (ONTT) was an investigator-initiated, multicentered, randomized, controlled clinical trial supported by cooperative agreements and grants. It was designed to evaluate the efficacy and safety of oral prednisone or intravenous methylprednisolone followed by oral prednisone as compared with oral placebo. The primary outcome measures were contrast sensitivity and visual field; secondary measures were visual acuity and color vision. Four hundred fifty-seven patients were followed for a minimum of 6 months and a maximum of 3 years. This article describes the design and the methods used to implement the ONTT. C1 UNIV S FLORIDA,COLL MED,DEPT OPHTHALMOL,TAMPA,FL 33612. DUKE UNIV,DEPT OPHTHALMOL,DURHAM,NC 27706. NIAID,BETHESDA,MD 20892. RP CLEARY, PA (reprint author), GEORGE WASHINGTON UNIV,CTR BIOSTAT,6110 EXECUT BLVD,SUITE 750,ROCKVILLE,MD 20852, USA. FU NEI NIH HHS [EY07212, EY07460, EY07461] NR 19 TC 50 Z9 52 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD APR PY 1993 VL 14 IS 2 BP 123 EP 142 DI 10.1016/0197-2456(93)90015-6 PG 20 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA KV160 UT WOS:A1993KV16000005 PM 8500302 ER PT J AU PAYTON, AJ FORSYTHE, DB DIXON, D MYERS, PH CLARK, JA SNIPE, JR AF PAYTON, AJ FORSYTHE, DB DIXON, D MYERS, PH CLARK, JA SNIPE, JR TI EVALUATION OF KETAMINE-XYLAZINE IN SYRIAN-HAMSTERS SO CORNELL VETERINARIAN LA English DT Article DE HAMSTERS; ANESTHESIA; KETAMINE; XYLAZINE ID HYDROCHLORIDE; INJECTIONS; RATS AB Few parenteral anesthetics are safe and effective in the Syrian hamster. This study evaluated the anesthetic efficacy and potential for tissue damage of ketamine-xylazine (KX). Two dosage levels were administered intraperitoneally. Ketamine at 50 mg/kg combined with 10 mg/kg xylazine did not produce a consistent, reliable level of immobilization or anesthesia. Ketamine at 150 mg/kg combined with 10 mg/kg xylazine administered IP produced an adequate level of anesthesia without tissue damage for most procedures, but supplementation with lidocaine was necessary for peritoneal incision. Careful positioning of male hamsters for IP injection is imperative to prevent inadvertent injection into the testes with subsequent tissue damage. C1 NIEHS,EXPTL TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,DIV LAB ANIM MED,CHAPEL HILL,NC 27599. RP PAYTON, AJ (reprint author), NIEHS,COMPARAT MED BRANCH,RES TRIANGLE PK,NC 27709, USA. NR 13 TC 1 Z9 1 U1 0 U2 0 PU CORNELL VETERINARIAN INC PI ITHACA PA CORNELL UNIV, ITHACA, NY 14853 SN 0010-8901 J9 CORNELL VET PD APR PY 1993 VL 83 IS 2 BP 153 EP 161 PG 9 WC Veterinary Sciences SC Veterinary Sciences GA KV484 UT WOS:A1993KV48400009 PM 8467701 ER PT J AU MASUR, H AF MASUR, H TI PARKER,MARGARET,M. SO CRITICAL CARE MEDICINE LA English DT Editorial Material RP MASUR, H (reprint author), NIH,BETHESDA,MD 20892, USA. 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 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD APR PY 1993 VL 21 IS 4 BP 486 EP 486 DI 10.1097/00003246-199304000-00004 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA KY919 UT WOS:A1993KY91900004 ER PT J AU MCGILL, CB SHAFER, BK DERR, LK STRATHERN, JN AF MCGILL, CB SHAFER, BK DERR, LK STRATHERN, JN TI RECOMBINATION INITIATED BY DOUBLE-STRAND BREAKS SO CURRENT GENETICS LA English DT Article DE RECOMBINATION; DNA REPAIR; GENE CONVERSION; YEAST ID YEAST MATING TYPE; SACCHAROMYCES-CEREVISIAE; DNA FRAGMENTS; REPAIR; SEQUENCES; MODEL; LOCUS AB The HO endonuclease was used to introduce a site-specific double-strand break (DSB) in an interval designed to monitor mitotic recombination. The interval included the trp1 and his3 genes inserted into chromosome III of S. cerevisiae between the CRY1 and MAT loci. Mitotic recombination was monitored in a diploid carrying heteroalleles of trp1 and his3. The normal recognition sites for the HO endonuclease were mutated at the MAT alleles and a synthetic recognition site for HO endonuclease was placed between trp1 and his3 on one of the chromosomes. HO-induced cleavage resulted in efficient recombination in this interval. Most of the data can be explained by double-strand gap repair in which the cut chromosome acts as the recipient. However, analysis of some of the recombinants indicates that regions of heteroduplex were generated flanking the site of the cut, and that some recombinants were the result of the cut chromosome acting as the genetic donor. RP NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, EUKARYOT GENE EXPRESS LAB, POB B, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74101] NR 38 TC 29 Z9 29 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0172-8083 EI 1432-0983 J9 CURR GENET JI Curr. Genet. PD APR PY 1993 VL 23 IS 4 BP 305 EP 314 DI 10.1007/BF00310891 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA KV174 UT WOS:A1993KV17400004 PM 8467528 ER PT J AU LIANG, LF DEAN, J AF LIANG, LF DEAN, J TI CONSERVATION OF MAMMALIAN SECONDARY SPERM RECEPTOR GENES ENABLES THE PROMOTER OF THE HUMAN GENE TO FUNCTION IN MOUSE OOCYTES SO DEVELOPMENTAL BIOLOGY LA English DT Article ID ZONA-PELLUCIDA; DEVELOPMENTAL REGULATION; GENOMIC ORGANIZATION; TRANSCRIPTION FACTOR; BINDING-PROTEIN; MESSENGER-RNAS; EXPRESSION; DNA; SEQUENCE; ZP3 RP LIANG, LF (reprint author), NIDDK,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892, USA. NR 36 TC 97 Z9 101 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 APR PY 1993 VL 156 IS 2 BP 399 EP 408 DI 10.1006/dbio.1993.1087 PG 10 WC Developmental Biology SC Developmental Biology GA KV142 UT WOS:A1993KV14200009 PM 8385033 ER PT J AU PIATIGORSKY, J AF PIATIGORSKY, J TI PUZZLE OF CRYSTALLIN DIVERSITY IN EYE LENSES SO DEVELOPMENTAL DYNAMICS LA English DT Article DE TRANSPARENT LENS; GENE SHARING; ENZYME-CRYSTALLIN; TRANSCRIPTION FACTORS; EVOLUTION ID ALPHA-B-CRYSTALLIN; DELTA-CRYSTALLIN; ARGININOSUCCINATE LYASE; DUCK LENS; STRUCTURAL PROTEIN; OCTOPUS LENS; GENE; EXPRESSION; RECRUITMENT; TISSUES AB Crystallins have evolved by various mechanisms that are associated with high expression of their genes in the eye lens. The diversity and pattern of crystallins among different species indicate that independent events have occurred at the molecular level during the evolution of the lens in different invertebrates (jellyfish, squid, and octopus) and vertebrates. Although it is possible that different crystallins are needed to fulfill the specific needs of individual species, the unexpectedly large array of proteins that function as crystallins and their abundance in the lens raise the possibility that selective pressures optimizing the function of certain transcription factors in the lens contribute to the recruitment of crystallins. (C) 1993 Wiley-Liss, Inc. RP NEI, MOLEC & DEV BIOL LAB, BLDG 6, ROOM 201, BETHESDA, MD 20892 USA. NR 46 TC 27 Z9 27 U1 0 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1058-8388 EI 1097-0177 J9 DEV DYNAM JI Dev. Dyn. PD APR PY 1993 VL 196 IS 4 BP 267 EP 272 PG 6 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA LU139 UT WOS:A1993LU13900004 PM 8219350 ER PT J AU PROCHAZKA, M LILLIOJA, S TAIT, JF KNOWLER, WC MOTT, DM SPRAUL, M BENNETT, PH BOGARDUS, C AF PROCHAZKA, M LILLIOJA, S TAIT, JF KNOWLER, WC MOTT, DM SPRAUL, M BENNETT, PH BOGARDUS, C TI LINKAGE OF CHROMOSOMAL MARKERS ON 4Q WITH A PUTATIVE GENE DETERMINING MAXIMAL INSULIN ACTION IN PIMA-INDIANS SO DIABETES LA English DT Article ID DIABETES-MELLITUS; RESISTANCE; OBESITY AB Insulin action in vivo varies widely in nondiabetic Pima Indians. Not all of this variance is attributable to individual differences in obesity, physical fitness, sex, or age, and after correcting for these co-variates, measures of insulin action aggregate in families. Insulin action at maximally stimulating insulin concentrations has a trimodal frequency distribution, particularly among obese individuals. This is consistent with the hypothesis that a codominantly inherited autosomal gene, unrelated to obesity, determines MaxM in the population. Preliminary sib-pair linkage analyses indicated the possibility of linkage between MaxM and the GYPA/B locus (encoding the MNSs red cell surface antigens) on chromosome 4q. To confirm and extend these findings, 10 additional loci on 4q were typed in 123 siblings and many of their parents from 46 nuclear families. The results indicate significant (P < 0.001) linkage of the FABP2 and ANX5 loci on 4q with MaxM, and of FABP2 with fasting insulin concentration. No linkage was found between the 4q markers and obesity. Our findings indicate that a gene on 4q, near the FABP2 and ANX5 loci, contributes to in vivo insulin action in Pima indians. C1 NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,PHOENIX,AZ 85016. NIDDKD,DIABET & ARTHRIT EPIDEMIOL SECT,PHOENIX,AZ 85016. UNIV WASHINGTON,DEPT LAB MED,SEATTLE,WA 98195. RP PROCHAZKA, M (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,PHOENIX,AZ 85016, USA. RI Lillioja, Stephen/A-8185-2012; OI Lillioja, Stephen/0000-0001-5333-5240 FU NCRR NIH HHS [1P41RR03655]; NHLBI NIH HHS [HL-40801] NR 23 TC 143 Z9 146 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 APR PY 1993 VL 42 IS 4 BP 514 EP 519 DI 10.2337/diabetes.42.4.514 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KU331 UT WOS:A1993KU33100003 PM 8454101 ER PT J AU CHARLES, MA PETTITT, DJ SAAD, MF NELSON, RG BENNETT, PH KNOWLER, WC AF CHARLES, MA PETTITT, DJ SAAD, MF NELSON, RG BENNETT, PH KNOWLER, WC TI DEVELOPMENT OF IMPAIRED GLUCOSE-TOLERANCE WITH OR WITHOUT WEIGHT-GAIN SO DIABETES CARE LA English DT Article ID PIMA-INDIANS; INSULIN ACTION AB OBJECTIVE - To evaluate whether risk factors and changes in insulin concentrations differ in subjects who develop impaired glucose tolerance with or without weight gain. Hyperinsulinemia is a risk factor for impaired glucose tolerance, and insulin concentrations increase further with the development of impaired glucose tolerance. its development, however, often is accompanied by weight gain, which, by itself, is associated with high insulin concentrations. RESEARCH DESIGN AND METHODS - Participants for this study were adult Pima Indians involved in an ongoing epidemiological study. Initially, all had normal glucose tolerance. During follow-up, 80 of 387 who did not gain weight developed impaired glucose tolerance, as did 295 of 1026 who gained weight. Risk factors for impaired glucose tolerance and the relationships between changes in weight and glucose and changes in insulin were evaluated by multivariate analyses. RESULTS - High baseline fasting insulin predicted impaired glucose tolerance regardless of weight after adjustment for age, sex, body mass index, and glucose. The development of impaired glucose tolerance was accompanied by a further increase in fasting and 2-h insulin, whether or not subjects gained weight. In both weight-change groups, impaired glucose tolerance was associated with more centralized fat distribution. CONCLUSIONS- Fasting hyperinsulinemia, a reflection of insulin resistance, is associated with the risk of developing impaired glucose tolerance. whether or not weight is gained. impaired glucose tolerance occurs when insulin resistance increases further. Weight gain is the most common precipitating factor. Aging and physical inactivity are other possible precipitating factors. C1 NATL INST DIABET & DIGEST & KIDNEY DIS,DIABET & ARTHRITIS EPIDEMIOL SECT,PHOENIX,AZ 85014. CLEVELAND CLIN FDN,DEPT BIOSTAT & EPIDEMIOL,PHOENIX,AZ. RI Nelson, Robert/B-1470-2012 FU NIDDK NIH HHS [N01-DK-7-2291] NR 8 TC 14 Z9 14 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD APR PY 1993 VL 16 IS 4 BP 593 EP 596 DI 10.2337/diacare.16.4.593 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KU330 UT WOS:A1993KU33000009 PM 8462385 ER PT J AU PETTITT, DJ MOLL, PP KNOWLER, WC MOTT, DM NELSON, RG SAAD, MF BENNETT, PH KOTTKE, BA AF PETTITT, DJ MOLL, PP KNOWLER, WC MOTT, DM NELSON, RG SAAD, MF BENNETT, PH KOTTKE, BA TI INSULINEMIA IN CHILDREN AT LOW AND HIGH-RISK OF NIDDM SO DIABETES CARE LA English DT Article ID IMPAIRED GLUCOSE-TOLERANCE; PIMA-INDIANS; DIABETES-MELLITUS; BODY-COMPOSITION; CAUCASIANS; POPULATION; PUBERTY; HYPERINSULINEMIA; RESISTANCE; AGE AB OBJECTIVE - Fasting hyperinsulinemia in the presence of normoglycemia usually indicates insulin resistance and is characteristic of populations at high risk for developing NIDDM. Hyperinsulinemia predicts the development of impaired glucose tolerance and NIDDM in Pima Indians, a population with a high incidence of NIDDM. Insulin concentrations in population-based samples of children who have different risks of developing NIDDM later in life have not been reported previously. RESEARCH DESIGN AND METHODS - We compared fasting insulin concentrations in two populations of nondiabetic children, 6-19 yr of age: Pima Indians from southern Arizona and Caucasians from Minnesota. RESULTS - Insulin concentration varied with age, sex, glucose concentration, and relative weight. Mean fasting insulin concentration was 140.3 pM in Pima Indian males, 94.4 pM in Caucasian males, 171.5 pM in Pima indian females, and 107.1 pM in Caucasian females. For each sex, the mean fasting insulin concentration, controlled for age, glucose, and relative weight, was significantly higher in the Pima Indians than in the Caucasians (P < 0.001). CONCLUSIONS - From a young age, Pima Indian children have higher fasting insulin concentrations than Caucasian children. As hyperinsulinemia predicts subsequent NIDDM, these data suggest that the susceptibility to NIDDM is manifest at a young age as fasting hyperinsulinemia. C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85014. UNIV MICHIGAN,DEPT EPIDEMIOL,ANN ARBOR,MI 48109. CLEVELAND CLIN FDN,DEPT BIOSTAT & EPIDEMIOL,PHOENIX,AZ. MAYO CLIN & MAYO FDN,DIV CARDIOVASC DIS,ROCHESTER,MN 55905. RP PETTITT, DJ (reprint author), NIDDKD,DIABET & ARTHRITIS EPIDEMIOL SECT,1550 E INDIAN SCH RD,PHOENIX,AZ 85014, USA. RI Nelson, Robert/B-1470-2012 FU NHLBI NIH HHS [HL-24489, HL-39107] NR 34 TC 48 Z9 48 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD APR PY 1993 VL 16 IS 4 BP 608 EP 615 DI 10.2337/diacare.16.4.608 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KU330 UT WOS:A1993KU33000012 PM 8462388 ER PT J AU CHERRYPEPPERS, G SHIP, JA AF CHERRYPEPPERS, G SHIP, JA TI ORAL HEALTH IN PATIENTS WITH TYPE-II DIABETES AND IMPAIRED GLUCOSE-TOLERANCE SO DIABETES CARE LA English DT Note ID MELLITUS AB OBJECTIVE - To assess the influence of type II diabetes and impaired glucose tolerance on dental, periodontal, and oral mucosal tissues. RESEARCH DESIGN AND METHODS - We examined 11 subjects with type II diabetes, 32 with impaired glucose tolerance, and 43 control subjects from the oral physiology component of the Baltimore Longitudinal Study of Aging. At the time of the study, none of the participants was taking medication nor being treated for any medical problems other than diabetes. RESULTS - Only a few statistically significant dental and periodontal changes were apparent in the group with type II diabetes, and no oral mucosal differences existed between the diabetes and control groups. Dental, periodontal, and oral mucosal parameters in patients with impaired glucose tolerance were essentially indistinguishable from the other two groups. CONCLUSIONS- These findings suggest that among well-controlled individuals with type II diabetes and impaired glucose tolerance, few appreciable differences are evident in oral health. C1 UNIV MICHIGAN,SCH DENT,DEPT ORAL MED PATHOL & SURG,ANN ARBOR,MI 48109. RP CHERRYPEPPERS, G (reprint author), NIDR,EPIDEMIOL & ORAL DIS PREVENT PROGRAM,5333 WESTBARD AVE,BETHESDA,MD 20892, USA. NR 16 TC 22 Z9 23 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD APR PY 1993 VL 16 IS 4 BP 638 EP 641 DI 10.2337/diacare.16.4.638 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KU330 UT WOS:A1993KU33000018 PM 8462394 ER PT J AU STRIKER, GE PETEN, EP CAROME, MA PESCE, CM SCHMIDT, K YANG, CW ELLIOT, SJ STRIKER, LJ AF STRIKER, GE PETEN, EP CAROME, MA PESCE, CM SCHMIDT, K YANG, CW ELLIOT, SJ STRIKER, LJ TI THE KIDNEY-DISEASE OF DIABETES-MELLITUS (KDDM) - A CELL AND MOLECULAR-BIOLOGY APPROACH SO DIABETES-METABOLISM REVIEWS LA English DT Article RP STRIKER, GE (reprint author), NIDDK,DKUHD,BLDG 31,RM 9A-17,BETHESDA,MD 20892, USA. NR 0 TC 55 Z9 55 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0742-4221 J9 DIABETES METAB REV JI Diabetes-Metab. Rev. PD APR PY 1993 VL 9 IS 1 BP 37 EP 56 PG 20 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LH539 UT WOS:A1993LH53900003 PM 8344122 ER PT J AU FRIED, MW DRAGUESKU, JO SHINDO, M SIMPSON, LH BANKS, SM HOOFNAGLE, JH DIBISCEGLIE, AM AF FRIED, MW DRAGUESKU, JO SHINDO, M SIMPSON, LH BANKS, SM HOOFNAGLE, JH DIBISCEGLIE, AM TI CLINICAL AND SEROLOGICAL DIFFERENTIATION OF AUTOIMMUNE AND HEPATITIS-C VIRUS-RELATED CHRONIC HEPATITIS SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE AUTOIMMUNE CHRONIC ACTIVE HEPATITIS; CHRONIC HEPATITIS-C; DIAGNOSIS; POLYMERASE CHAIN REACTION; SEROLOGICAL TESTING ID CHRONIC ACTIVE HEPATITIS; RECOMBINANT INTERFERON-ALFA; CONTROLLED TRIAL; ANTIBODIES; THERAPY AB Recent reports have focused on the difficulty in differentiating autoimmune hepatitis from chronic hepatitis C due to the high prevalence of anti-HCV in autoimmune hepatitis. The aim of this study was to identify clinical, biochemical, and serological variables that would help distinguish these two diseases. Pretreatment clinical and biochemical variables were compared from 1 7 patients with steroid-responsive autoimmune chronic active hepatitis and 62 patients with chronic hepatitis C. Serum samples from these patients were tested for autoantibodies and for anti-HCV by first- and second-generation ELISA, recombinant immunoblot assay, and HCV RNA by polymerase chain reaction. Patients with autoimmune hepatitis were more likely to be symptomatic (94% vs 47%, P < 0.005) and jaundiced (76% vs 0%, P < 0.005) al the time of referral. Anti-HCV was found in 53% of patients with autoimmune hepatitis, but only two were positive by immunoblot assay and only one of these had detectable HCV RNA. Antinuclear antibody (ANA) was detected in 21% of patients with chronic hepatitis C, although usually at a lower titer than in autoimmune hepatitis (geometric mean titer = 1:160 vs 1:500, P < 0.003). Patients with chronic hepatitis C who were ANA positive were older than those who were ANA negative, although there were no other differences in clinical or biochemical features between these groups. In particular, there was no difference in response rate to antiviral therapy. Thus, autoantibodies are frequently found in chronic hepatitis C, especially in older subjects, but appear to be clinically insignificant. Anti-HCV is frequently present in autoimmune hepatitis but is rarely confirmed by tests of higher specificity. These findings have important implications in selecting patients for anti-viral or immunosuppressive therapy. C1 NIAID,BETHESDA,MD 20892. UNIV SO CALIF,LIVER UNIT,DOWNEY,CA 90242. RP FRIED, MW (reprint author), NIDDKD,HEPATITIS STUDIES,SECT,BLDG 10,RM 9C-103B,BETHESDA,MD 20892, USA. NR 17 TC 80 Z9 79 U1 1 U2 1 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 APR PY 1993 VL 38 IS 4 BP 631 EP 636 DI 10.1007/BF01316792 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KW537 UT WOS:A1993KW53700008 PM 8384981 ER PT J AU DUCHMANN, R STROBER, W JAMES, SP AF DUCHMANN, R STROBER, W JAMES, SP TI QUANTITATIVE MEASUREMENT OF HUMAN T-CELL RECEPTOR-V-BETA SUBFAMILIES BY REVERSE TRANSCRIPTION-POLYMERASE CHAIN-REACTION USING SYNTHETIC INTERNAL MESSENGER-RNA STANDARDS SO DNA AND CELL BIOLOGY LA English DT Article ID RHEUMATOID-ARTHRITIS; GENE; EXPRESSION; DISEASE; USAGE; LYMPHOCYTES; PROTEIN; SINGLE; DNA AB Quantitative determination of T-cell receptor (TCR) Vbeta expression is necessary to define the changes in TCR-Vbeta subfamily expression that occur during T-cell maturation and selection and to detect alterations of the TCR-Vbeta repertoire that may be associated with human diseases. Here we describe and validate a quantitative reverse transcription-polymerase chain reaction (RT-PCR) technique to determine human TCR-Vbeta subfamily mRNA levels (as well as other mRNA species), based on the use of synthetic poly(A) mRNA internal standards that are coprocessed with native (sample) mRNA transcripts. The technique allows simultaneous reverse transcription of sample and standard mRNA and thus obviates errors arising during reverse transcription. In addition, the technique allows coamplification of several concentrations of standard mRNA (cDNA) with sample mRNA (cDNA) under conditions in which these mRNAs amplify with equal efficiency; thus, it avoids errors resulting from saturation of competition effects. Finally, the technique is sensitive to lower than 1.5-fold differences in input mRNA. To apply the technique, we also describe methods for the generation of poly(A) mRNA internal standards that can be used to quantitate TCR-Vbeta 2/6/7 and TCR-Cbeta mRNA. C1 NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. UNIV MARYLAND,DEPT MED,DIV GASTROENTEROL,BALTIMORE,MD 21201. NR 28 TC 18 Z9 19 U1 0 U2 0 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 APR PY 1993 VL 12 IS 3 BP 217 EP 225 DI 10.1089/dna.1993.12.217 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA KZ457 UT WOS:A1993KZ45700003 PM 7682080 ER PT J AU STGEORGIEV, V AF STGEORGIEV, V TI OPPORTUNISTIC INFECTIONS - TREATMENT AND DEVELOPMENTAL THERAPEUTICS OF CRYPTOSPORIDIOSIS AND ISOSPORIASIS SO DRUG DEVELOPMENT RESEARCH LA English DT Review DE CRYPTOSPORIDIOSIS; ISOSPORIASIS; MACROLIDE ANTIBIOTICS; LYTIC PEPTIDES; IMMUNOTHERAPY ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; HYPERIMMUNE BOVINE COLOSTRUM; IMMUNE-DEFICIENCY SYNDROME; NEUTRALIZATION-SENSITIVE EPITOPES; BELLI INFECTION; INTESTINAL CRYPTOSPORIDIOSIS; AIDS PATIENTS; EGG-YOLK; ROTAVIRUS GASTROENTERITIS; IMMUNOSUPPRESSED RATS AB Cryptosporidium sp. and Isospora sp. are coccidian protozoans taxonomically related to Toxoplasma gondii and Plasmodium sp. Although associated with many animal species, these pathogens are also the causative agents of cryptosporidiosis and isosporiasis, 2 invasive opportunistic infections in humans. In immunocompetent host, the infections are usually self-limited flu-like gastrointestinal disorders which resolve spontaneously. In immunocompromised patients, however, cryptosporidiosis is a severe, debilitating, and prolonged illness, with high morbidity and no known therapy effective against it. Spiramycin has been proven largely ineffective. In recent years, however, the use of immunotherapy is being actively pursued as one potentially useful approach for the treatment of cryptosporidiosis. Azithromycin, a new macrolide antibiotic, has also shown promise in preclinical studies. In the case of isosporiasis, the combination of trimethoprim and sulphamethoxazole has been found to be effective, although AIDS patients have shown a high rate of relapse and, therefore, the need for suppressive maintenance therapy. RP STGEORGIEV, V (reprint author), NIAID,SOLAR BLDG,ROOM 4C-39,BETHESDA,MD 20892, USA. NR 205 TC 5 Z9 5 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0272-4391 J9 DRUG DEVELOP RES JI Drug Dev. Res. PD APR PY 1993 VL 28 IS 4 BP 445 EP 459 DI 10.1002/ddr.430280402 PG 15 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KW508 UT WOS:A1993KW50800001 ER PT J AU HERMAN, AA YU, KF HOFFMAN, HJ KRULEWITCH, CJ BAKKETEIG, LS AF HERMAN, AA YU, KF HOFFMAN, HJ KRULEWITCH, CJ BAKKETEIG, LS TI BIRTH-WEIGHT, GESTATIONAL-AGE AND PERINATAL-MORTALITY - BIOLOGICAL HETEROGENEITY AND MEASUREMENT ERROR SO EARLY HUMAN DEVELOPMENT LA English DT Article DE FETAL GROWTH; GROWTH RETARDATION; GESTATIONAL AGE; BIRTH WEIGHT; FETAL AND NEONATAL MORTALITY ID INTRAUTERINE GROWTH-RETARDATION; RISK-FACTORS; INFANTS; MORBIDITY; SURVIVAL AB At low birth weight the variance of last menstrual period based gestational age is wide and the distribution is positively skewed toward higher values. In this study the variance of gestational age decreases rapidly as birth weight increases, skewness decreases and kurtosis increases in approaching the mean of the birth weight distribution. Some of the wider variance and positive skewness of gestational age at low birth weight appears to reflect heterogeneity of intrauterine growth, in which infants with high values of gestational age are growth retarded. We show by partitioning each birth weight group into two groups of infants with different gestational age distributions, that at low birth weight, infants with low gestational ages have higher neonatal mortality rates but lower fetal mortality rates than infants with a higher gestational age for birth weight. The differences in mortality described between small infants at different gestational ages suggest that infants with a high LMP-based gestational age have experienced a slower rate of intrauterine growth. Some authors interpret the distributional characteristics as indications of systematic error in last menstrual period based assessment of gestational age. It appears from this study that the extent of systematic error in the estimation of LMP based gestational age may have been overstated in the past. C1 NATL CTR HLTH STAT, DIV VITAL STAT, FOLLOWBACK SURVEY BRANCH, HYATTSVILLE, MD 20782 USA. NATL INST PUBL HLTH, DEPT EPIDEMIOL, OSLO 1, NORWAY. RP HERMAN, AA (reprint author), NICHHD, DIV EPIDEMIOL STAT & PREVENT RES, BETHESDA, MD 20892 USA. FU NICHD NIH HHS [N0-HD-5-2818] NR 35 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0378-3782 J9 EARLY HUM DEV JI Early Hum. Dev. PD APR PY 1993 VL 33 IS 1 BP 29 EP 44 DI 10.1016/0378-3782(93)90171-P PG 16 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA LC729 UT WOS:A1993LC72900004 PM 8319553 ER PT J AU PASCUALLEONE, A HOUSER, CM REESE, K SHOTLAND, LI GRAFMAN, J SATO, S VALLSSOLE, J BRASILNETO, JP WASSERMANN, EM COHEN, LG HALLETT, M AF PASCUALLEONE, A HOUSER, CM REESE, K SHOTLAND, LI GRAFMAN, J SATO, S VALLSSOLE, J BRASILNETO, JP WASSERMANN, EM COHEN, LG HALLETT, M TI SAFETY OF RAPID-RATE TRANSCRANIAL MAGNETIC STIMULATION IN NORMAL VOLUNTEERS SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE RAPID-RATE TRANSCRANIAL MAGNETIC STIMULATION; SAFETY; HORMONES; ELECTROENCEPHALOGRAPHY; AUDIOGRAM; SEIZURE ID MOTOR CORTEX; EPILEPSY; SPREAD; BRAIN; ACTIVATION; RELEVANCE AB In 9 normal volunteers, we studied the safety of rapid-rate transcranial magnetic stimulation (rTMS) applied to different scalp positions at various frequencies and intensities. Pure tone threshold audiometry showed temporary threshold shifts in 3 subjects. In the subject stimulated at the highest intensity, rTMS induced a focal, secondarily generalized seizure despite the absence of definite risk factors for seizures. Rapid-rate TMS did not result in any important changes in the neurological examination findings, cognitive performance, electroencephalogram, electrocardiogram, and hormone levels (prolactin, adrenocorticotropic hormone, thyroid-stimulating hormone, luteinizing hormone, and follicle-stimulating hormone). In 10 additional subjects, the electromyographic activity in several contralateral muscles showed that trains of rTMS applied to the motor cortex induced a spread of cortical excitability. The spread of excitability depended on the intensity and frequency of the stimuli and probably constituted an early epileptogenic effect of rTMS. Guidelines for preventing the undesirable side effects of rTMS are offered. C1 NINCDS,HUMAN MOTOR CONTROL SECT,HUMAN CORTICAL PHYSIOL UNIT,BLDG 10,BETHESDA,MD 20892. NINCDS,COGNIT SCI SECT,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,ELECTROENCEPHALOG LAB,BETHESDA,MD 20892. NIDOCD,HEARING SECT,BETHESDA,MD 20892. RI Pascual-Leone, Alvaro/G-6566-2011; OI Grafman, Jordan H./0000-0001-8645-4457 NR 47 TC 291 Z9 302 U1 0 U2 14 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. PD APR PY 1993 VL 89 IS 2 BP 120 EP 130 DI 10.1016/0168-5597(93)90094-6 PG 11 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA LB436 UT WOS:A1993LB43600007 PM 7683602 ER PT J AU KOMURO, I SCHALLING, M JAHN, L BODMER, R JENKINS, NA COPELAND, NG IZUMO, S AF KOMURO, I SCHALLING, M JAHN, L BODMER, R JENKINS, NA COPELAND, NG IZUMO, S TI GTX - A NOVEL MURINE HOMEOBOX-CONTAINING GENE, EXPRESSED SPECIFICALLY IN GLIAL-CELLS OF THE BRAIN AND GERM-CELLS OF TESTIS, HAS A TRANSCRIPTIONAL REPRESSOR ACTIVITY INVITRO FOR A SERUM-INDUCIBLE PROMOTER SO EMBO JOURNAL LA English DT Article DE DNA BINDING PROTEIN; HOMEOBOX; MEF-2; RSRF; TISSUE-SPECIFIC EXPRESSION ID HOMEODOMAIN-DNA INTERACTIONS; ENHANCER-BINDING-FACTOR; MESSENGER-RNAS; DROSOPHILA EMBRYOS; CRYSTAL-STRUCTURE; MAMMALIAN-CELLS; HOMEOTIC GENES; BOX GENE; MOUSE; PROTEIN AB Although it is likely that a highly complex network of transcription factors acts in concert during mammalian brain development, relatively few such genes have been characterized to date. We describe here a novel murine homeobox gene, denoted Gtx, which in adult animals is specifically expressed within glial cells of the central nervous system, including the forebrain, and in germ cells of the testis. Gtx resides on chromosome 7 and does not cosegregate with any previously mapped homeobox gene. The amino acid sequence of the predicted protein encoded by Gtx is highly divergent from that of any other known homeobox genes. The Gtx homeodomain contains unique residues at positions predicted to contact DNA bases. It did not bind to known target sites for other homeobox genes in vitro but bound with high affinity to the MEF-2 motif, a binding site for the serum response factor-related proteins. GTX efficiently competed with RSRF to bind the MEF-2 element in vitro. Co-transfection of Gtx prevented the serum-induced activation of the MEF-2-containing reporter genes. Although the true biological role of Gtx is not known, these results suggest that Gtx is a novel cell-type specific homeobox gene that has the potential to act as a transcriptional repressor for a subset of serum-inducible genes. C1 BETH ISRAEL HOSP,DIV MOLEC MED,330 BROOKLINE AVE,BOSTON,MA 02215. BETH ISRAEL HOSP,DIV CARDIOVASC,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM CELL & DEV BIOL,BOSTON,MA 02115. MIT,CTR CANC RES,CAMBRIDGE,MA 02142. MIT,DEPT BIOL,CAMBRIDGE,MA 02142. UNIV MICHIGAN,DEPT BIOL,ANN ARBOR,MI 48105. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RI Schalling, Martin/F-1518-2015 OI Schalling, Martin/0000-0001-5011-2922 FU NCI NIH HHS [N01-CO-74101] NR 81 TC 76 Z9 76 U1 0 U2 2 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 APR PY 1993 VL 12 IS 4 BP 1387 EP 1401 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KW390 UT WOS:A1993KW39000013 PM 8096811 ER PT J AU MORRISON, A JOHNSON, AL JOHNSTON, LH SUGINO, A AF MORRISON, A JOHNSON, AL JOHNSTON, LH SUGINO, A TI PATHWAY CORRECTING DNA-REPLICATION ERRORS IN SACCHAROMYCES-CEREVISIAE SO EMBO JOURNAL LA English DT Article DE 3'-]5' EXONUCLEASE; MISMATCH CORRECTION; PMS1; MUTAGENESIS; YEAST ID 5' EXONUCLEASE ACTIVITY; ESCHERICHIA-COLI; MISMATCH REPAIR; SPONTANEOUS MUTATION; POLYMERASE-DELTA; GENE CONVERSION; ARS ELEMENTS; YEAST; EXTRACTS; SEQUENCE AB Mutation of predicted 3'--> 5' exonuclease active site residues of Saccharomyces cerevisiae POL3 DNA polymerase (delta) or deletion of the PMS1 mismatch repair gene lead to relative (to wild type) spontaneous mutation rates of approximately 130 and 41, respectively, measured at a URA3 reporter gene inserted near to a defined replication origin. The POL3 exonuclease-deficient mutant pol3-01 generated most classes of single base mutation in URA3, indicating a broad specificity that generally corresponds to that of the PMS1 system. pol3-01 pms1 haploid cells ceased growth after a few divisions with no unique terminal cell morphology. A pol3-01/pol3-01 pms1/pms1 diploid was viable and displayed an estimated URA3 relative mutation rate of 2 X 10(4), which we calculate to be catastrophically high in a haploid. The relationship between the relative mutation rates of pol3-01 and pms1 was multiplicative, indicating action in series. The PMFS1 transcript showed the same cell cycle periodicity as those of a set of DNA replication genes that includes POL3, suggesting PMS1 is co-regulated with these genes. We propose that the POL3 3'--> 5' exonuclease and the PMS1 mismatch repair system act on a common pathway analogous to the dnaQ --> mutHLS pathway of DNA replication error correction in Escherichia coli. C1 NATL INST MED RES,YEAST GENET LAB,LONDON NW7 1AA,ENGLAND. RP MORRISON, A (reprint author), NIEHS,MOLEC GENET LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 33 TC 181 Z9 181 U1 1 U2 6 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 APR PY 1993 VL 12 IS 4 BP 1467 EP 1473 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KW390 UT WOS:A1993KW39000020 PM 8385605 ER PT J AU GRASSO, P REICHERT, LE SPORN, MB SANTACOLOMA, TA AF GRASSO, P REICHERT, LE SPORN, MB SANTACOLOMA, TA TI TRANSFORMING GROWTH-FACTOR-BETA-1 MODULATES CALCIUM-METABOLISM IN SERTOLI CELLS SO ENDOCRINOLOGY LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; RECEPTOR-MEDIATED UPTAKE; AKR-2B CELLS; FACTOR-BETA; 3T3 CELLS; PROTEIN; PROLIFERATION; EXPRESSION; ACTIVATION; INHIBITION AB The mechanism of signal transduction by transforming growth factor-beta1 (TGF-beta1) is largely unknown. In this study, TGF-beta1 was able to stimulate Ca-45(2+) uptake in cultured rat Sertoli cells. In contrast to the rapid stimulation of Ca-45(2+) uptake previously observed in response to FSH (<1 min), the response to TGF-beta1 required several hours and was abolished by actinomycin-D. Although TGF-beta1 had no effect on basal calcium uptake before 1 h, it completely inhibited the FSH-stimulated calcium uptake in short term incubations (2 and 20 min). These effects of TGF-beta1 on calcium metabolism may be directly related to the ability of this cytokine to regulate cell growth and differentiation in many cell systems. C1 NCI, CHEMOPREVENT LAB, BETHESDA, MD 20892 USA. ALBANY MED COLL, DEPT BIOCHEM & MOLEC BIOL, ALBANY, NY 12208 USA. NR 27 TC 12 Z9 12 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1993 VL 132 IS 4 BP 1745 EP 1749 DI 10.1210/en.132.4.1745 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KV629 UT WOS:A1993KV62900045 PM 8462475 ER PT J AU THIGPEN, K AF THIGPEN, K TI 20 YEARS OF ENVIRONMENTAL-HEALTH RESEARCH - INTRODUCTION SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material RP THIGPEN, K (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1993 VL 100 BP 3 EP 7 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400001 PM 8354164 ER PT J AU BARRETT, JC AF BARRETT, JC TI MECHANISMS OF MULTISTEP CARCINOGENESIS AND CARCINOGEN RISK ASSESSMENT SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Review ID HAMSTER EMBRYO CELLS; MOUSE SKIN CARCINOGENESIS; HUMAN-BREAST CANCER; MALIGNANT PROGRESSION; NEOPLASTIC TRANSFORMATION; ANEUPLOIDY INDUCTION; TUMOR-DEVELOPMENT; ARSENIC TRIOXIDE; MAMMALIAN-CELLS; B6C3F1 MOUSE AB Many different types of chemical exposures can increase the incidence of tumors in animals and humans, but usually a long period of time is required before the carcinogenic risk of an exposure is manisfested. Both of these observations can be explained by a multistep/multigene model of carcinogenesis. In this model, a normal cell evolves into a cancer cell as the result of heritable changes in multiple, independent genes. The two-stage model of initiation and promotion for chemical carcinogenesis has provided a paradigm by which chemicals can act by qualitatively different mechanisms, but the process of carcinogenesis is now recognized as more complex than simply initiation and promotion. Even a three-stage model of initiation, promotion. and progression, which can be operationally defined, is not adequate to describe the carcinogenic process. The number of genes altered in a cancer cell compared to a normal cell is not known- recent evidence suggests that 3-10 genetic events are involved in common adult malignancies in humans. Two distinct classes of genes, proto-oncogenes and tumor-suppressor genes, are involved in the cancer process. Multiple oncogenes may be activated in a tumor, while multiple tumor-suppressor genes may be inactivated. Identification of the genes involved in carcinogenesis and elucidation of the mechanisms of their activation or inactivation allows a better understanding of how chemical carcinogens influence the process of neoplastic evolution. The findings of multiple genetic changes (including point mutations, chromosomal translocations, deletions, gene amplification, and numerical chromosome changes) in activated proto-oncogenes and inactivated tumor-suppressor genes provide experimental support for Boveri's somatic mutation theory of carcinogenesis. In addition to mutagenic mechanisms. chemicals may heritably alter cells by epigenetic mechanisms and enhance the clonal expansion of altered cells. Most chemical carcinogens operate via a combination of mechanisms, and even their primary mechanism of action may vary depending on the target tissues. The classification of chemicals by mechanism of action or by nongenotoxic or genotoxic activity has certain inherent difficulties because no classification of chemicals is exhaustive or definitive. RP BARRETT, JC (reprint author), NIEHS,MOLEC CARCINOGENESIS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 108 TC 131 Z9 140 U1 2 U2 4 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1993 VL 100 BP 9 EP 20 DI 10.2307/3431516 PG 12 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400002 PM 8354184 ER PT J AU BRODY, AR AF BRODY, AR TI ASBESTOS-INDUCED LUNG-DISEASE SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID RAT ALVEOLAR MACROPHAGES; GROWTH-FACTOR; EPITHELIAL-CELLS; CROCIDOLITE ASBESTOS; INORGANIC PARTICLES; SIALIC-ACID; CELLULAR PROLIFERATION; CHROMOSOMAL CHANGES; PULMONARY FIBROSIS; MESOTHELIAL CELLS AB This review attempts to deal with two major questions concerning asbestos-induced lung disease: How does inhaled asbestos cause cell proliferation and fibrosis? and Will there continue to be risk from exposure to asbestos in schools and public buildings? The first is a scientific question that has spawned many interesting new experiments over the past 10 years, and there appear to be two hypothetical schemes which could explain, at least in part, the fibroproliferative effects of asbestos fibers. One supports the view that toxic oxygen radicals generated on fiber surfaces and/or intracellularly are the central mediators of disease. The second hypothesis is not mutually exclusive of the first, but, in my opinion, may be integral to it, i.e., the cellular injury induced by oxygen radicals stimulates the elaboration of multiple varieties of growth factors and cytokines that mediate the pathogenesis of asbestosis. There is increasing evidence that molecules such as platelet-derived growth factor and transforming growth factor beta, both synthesized and secreted by activated lung macrophages, are responsible, respectively, for the increased interstitial cell populations and extracellular matrix proteins that are the hallmarks of asbestos-induced fibrosis. The challenge today is to establish which combinations of the many factors released actually are playing a role in disease pathogenesis. The issue of continued risk currently is more a question of policy and perception than science because a sufficient database has not yet been established to allow full knowledge of the circumstances under which asbestos in buildings constitutes an ongoing health hazard. The litigious nature of this question does not help its resolution. In as much as public policy statements and risk assessment are not within my purview, I have focused on the state-of-the-art of asbestos as a complete carcinogen. It appears to be generally nongenotoxic, but all asbestos fiber tv pes can induce chromosomal mutations and aneuploidy, perhaps through their ability to disrupt normal chromosome segregation. RP BRODY, AR (reprint author), NIEHS,PULM PATHOBIOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 83 TC 53 Z9 55 U1 1 U2 2 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 APR PY 1993 VL 100 BP 21 EP 30 DI 10.2307/3431517 PG 10 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400003 PM 8354168 ER PT J AU DAVIS, DL BLAIR, A HOEL, DG AF DAVIS, DL BLAIR, A HOEL, DG TI AGRICULTURAL EXPOSURES AND CANCER TRENDS IN DEVELOPED-COUNTRIES SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID NON-HODGKINS-LYMPHOMA; UNITED-STATES; TRANSPLANT RECIPIENTS; PHYSICAL-FITNESS; MULTIPLE-MYELOMA; APLASTIC-ANEMIA; MORTALITY; FARMERS; RISK; LEUKEMIA AB Recent increases have been reported in industrial countries for several sites of cancer. The causes of these increases remain unknown. Efforts should proceed to identify those occupational groups with increases in the same sites, as these may indicate relevant exposures. Two analyses were undertaken: trends in cancer mortality in industrial countries were reviewed to identify recently increasing sites and summaries were compiled of studies on farmers which have shown increased risks-for these same sites of cancer. Using data provided by the World Health Organization, age-specific rates were developed for a number of sites of cancer from 1968 to 1986. Trends in the ratio of male to female cancer mortality were also assessed for several of these countries. Based on a literature review by the National Cancer Institute, patterns of cancer in farmers reported in 20 studies from 8 countries are summarized, weighting each study by its size to create combined relative risks. In industrial countries, rates of cancer mortality increased for a number of sites, including melanoma, prostate, non-Hodgkin's lymphoma, multiple myeloma, breast, brain, and kidney cancer. The ratio of male to female cancer mortality (for all sites of cancer excluding lung) has generally increased in several countries during this same time period. Many of the same sites that have increased in the general population have also been found to be increasing in farmers. Significant excesses occurred for Hodgkin's disease, multiple myeloma, leukemia, skin melanomas, and cancers of the tip, stomach, and prostate. Nonsignificant increases in risk were also noted for non-Hodgkin's lymphoma and cancers of connective tissue and brain in many surveys. These excesses occurred against a background of substantial deficits among farmers for total mortality, heart disease. and many other specific diseases. Epidemiologic studies of farmers, and other occupational groups with excess rates of these same sites of cancer, may help to identify specific causal exposures that partly account for the rising trend of certain cancers in developed countries. Despite a number of common causes, heart disease and some sites of cancer show opposite trends in the general population, with the former decreasing and the latter increasing. Thus, the causes of the increases in cancer are not likely to stem from those that are shared with heart disease, but to represent some as-yet-unrecognized risk factors. Among those that should be carefully reviewed are solvents, pesticides, engine exhausts, and animal viruses, materials to which both farmers and the general population are exposed in increasing amounts. C1 NCI,OCCUPAT STUDIES SECT,BETHESDA,MD 20892. NIEHS,RES TRIANGLE PK,NC 27709. RP DAVIS, DL (reprint author), US NATL RES COUNCIL,2101 CONSTITUT AVE NW,WASHINGTON,DC 20418, USA. NR 64 TC 13 Z9 13 U1 0 U2 2 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 APR PY 1993 VL 100 BP 39 EP 44 DI 10.2307/3431519 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400005 PM 8354180 ER PT J AU GOLDSTEIN, JA FALETTO, MB AF GOLDSTEIN, JA FALETTO, MB TI ADVANCES IN MECHANISMS OF ACTIVATION AND DEACTIVATION OF ENVIRONMENTAL CHEMICALS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID N-ACETYLTRANSFERASE PHENOTYPES; LUNG-CANCER; HUMAN-LIVER; MICROSOMAL CYTOCHROME-P-450; BLADDER CARCINOGENESIS; AROMATIC-AMINES; OXIDATION; ENZYMES; SUSCEPTIBILITY; ISOZYMES AB Environmental chemicals are both activated and detoxified by phase I and phase II enzymes. The principal enzymes involved in phase I reactions are the cytochrome P450s. The phase II enzymes include hydrolase and the conjugative enzymes such as glucuronyltransferases, glutathione transferases, N-acetyltransferase, and sulfotransferase. Although other phase I and phase II enzymes exist, the present review is limited to these enzymes. Once thought to be a single enzyme, multiple cytochrome P450 enzymes have been purified and characterized from many different species across the evolutionary tree. The application of molecular biology techniques to this field has identified more than 150 cytochrome P450 genes to date. At least 20-30 cytochrome P-450 enzymes appear to exist in each mammalian species, and many polymorphisms in these enzymes are being identified. The cytochrome P450 enzymes can now be expressed in recombinant form using cDNA expression systems. The phase II conjugative enzymes add a hydrophilic moiety such as sulfate, glucuronide, or acetate to compounds, which increases their water solubility and facilitates their excretion. However, conjugates of a number of compounds also result in more reactive electrophilic species, which appear to be the ultimate carcinogens. Many of these phase II enzymes also represent families of enzymes, and polymorphisms can affect the ability of these enzymes to metabolize chemicals. Whenever possible, we have reviewed knowledge of the human enzymes involved in particular pathways. C1 BURROUGHS WELLCOME CO,DIV EXPTL THERAPY,RES TRIANGLE PK,NC 27709. RP GOLDSTEIN, JA (reprint author), NIEHS,ENVIRONM RISK ANAL,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Goldstein, Joyce/A-6681-2012 NR 47 TC 53 Z9 55 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1993 VL 100 BP 169 EP 176 DI 10.2307/3431523 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400009 PM 8354165 ER PT J AU VANDENHEUVEL, JP LUCIER, G AF VANDENHEUVEL, JP LUCIER, G TI ENVIRONMENTAL TOXICOLOGY OF POLYCHLORINATED DIBENZO-P-DIOXINS AND POLYCHLORINATED DIBENZOFURANS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID ARYL-HYDROCARBON HYDROXYLASE; HEAT-SHOCK PROTEIN; AH-RECEPTOR; CANCER MORTALITY; IMMUNE SYSTEM; RAT-LIVER; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN; MECHANISM; TOXICITY; HEPATOCARCINOGENESIS AB Few environmental compounds have generated as much interest and controversy within the scientific community and in the lay public as polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). Their ubiquitous presence in the environment and the risk of accidental exposure has raised concern over a possible threat of PCDDs or PCDFs to human health. The most extensively studied and potent isomer is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin). Dioxin is a multisite toxicant in laboratory rodents resulting in a number of tissue-, species-, and sex-dependent responses. Much has been learned about the mechanism of dioxin's effects, especially for the induction of cytochrome P450 enzymes. Binding of PCDDs and PCDFs to a receptor protein, termed the dioxin or Ah receptor, is necessary for most biological and toxic responses. The most common toxic response used for evaluating the human health risk posed by PCDDs and PCDFs is the hepatocarcinogenic response observed primarily in rodents. Despite extensive research efforts, the effects of PCDDs and PCDFs on humans are not well characterized. However, available data indicate there is good agreement between known effects of dioxin in laboratory animals and those described in epidemiological studies for effects in humans. The sequence in events initiated by the Ah receptor interacting with dioxin-responsive genes and ending with altered patterns of differentiation and growth must be sought in order to understand tissue, species, sex. and interindividual variation in biological responses and the health risk posed by PCDDs and PCDFs. C1 NIEHS,BIOCHEM RISK ANAL LAB,POB 12233,RES TRIANGLE PK,NC 27709. NR 77 TC 70 Z9 72 U1 0 U2 8 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 APR PY 1993 VL 100 BP 189 EP 200 PG 12 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400011 PM 8394802 ER PT J AU HUFF, J AF HUFF, J TI CHEMICALS AND CANCER IN HUMANS - 1ST EVIDENCE IN EXPERIMENTAL-ANIMALS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Review ID LONG-TERM CARCINOGENESIS; IARC MONOGRAPHS PROGRAM; OCCUPATIONAL-CANCER; LUNG-CANCER; TESTICULAR CANCER; ETHYLENE-OXIDE; MORTALITY; WORKERS; EXPOSURE; RISK AB Certain human diseases have been traced to exposure to environmental and occupational chemicals. In many instances the first evidence of potential adverse effects came from experimental studies and were subsequently discovered in humans. Associations of human cancers, as a diverse group of diseases, and chemicals have been made since the middle 1700s. Since then, nearly 100 chemicals, mixtures of chemicals, or exposure circumstances are now recognized as being or strongly implicated as being carcinogenic to humans. Of the less than 1000 agents evaluated adequately for carcinogenicity in laboratory animals, a varying spectrum of data from studies on humans are available for only about 20-25%. So far, more than 60 agents are linked unequivocally as causing cancer in humans, and another 50 or so are strongly suspected of being carcinogenic to humans. Not all of these have been or can be evaluated in animals because some are industrial processes or ''occupations,'' some are environmental and cultural risk factors, and some are mixtures of agents. For those that can be studied experimentally, the qualitative concordance between humans and animals approaches unity, and in every case there is at least one common organ site of cancer in both species. The evidence of carcinogenicity in experimental animals preceded that observed in humans for nearly 30 agents and is the subject of this paper. RP HUFF, J (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 147 TC 63 Z9 63 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1993 VL 100 BP 201 EP 210 DI 10.2307/3431526 PG 10 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400012 PM 8354167 ER PT J AU LUSTER, MI ROSENTHAL, GJ AF LUSTER, MI ROSENTHAL, GJ TI CHEMICAL-AGENTS AND THE IMMUNE-RESPONSE SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID IMMUNODEFICIENCY VIRUS-INFECTION; NATURAL-KILLER ACTIVITY; CONTACT HYPERSENSITIVITY; SUPPRESSOR CELLS; TOXICITY; MICE; PENTAMIDINE; INHIBITION; AZT; INTERLEUKIN-1 AB Our desire to understand the potential adverse human health effects of environmental chemical exposure has coincided with an increased understanding of the immune system and an appreciation of its complex regulatory network. This has spawned a broad interest in the area of immnunotoxicology within the scientific community as well as certain concerns in the public sector regarding chemical-induced hypersensitivity and immunosuppression. The incidence of alleged human sensitization to chemicals has increased, in part, due to the fact that chemical companies are moving to larger and/or different markets. It has been estimated that 35 million Americans suffer from allergic disease, of which 2-5% are from occupational exposure. Although there is not yet a clear understanding of dose-response relationships or disease predisposition, there are many well-defined examples (isocyanates, anhydrides) of chemical sensitizers in humans and experimental animals. Evidence that chemicals suppress immune responses in humans is considerably less well established, although there is a public perception that chemicals generally cause immunosuppression. This perception has been fueled by highly publicized legal cases and scientific controversies within the academic and industrial communities. As a consequence of these public and scientific concerns, many of the regulatory agencies are developing immunotoxicity testing guidelines. At the present, however, there are limitations on adequate human methodology and data that allow the extrapolation of animal data to assess human risk. The potential for human immunosuppression remains of concern, however, because of a large database generated from animal studies that demonstrates immunosuppression as well as reports of immunosuppression in humans inadvertently (e.g., halogenated aromatic hydrocarbons) or occupationally (asbestos, benzene) exposed to xenobiotics. This concern is exacerbated by current knowledge regarding the long-term consequences of immunosuppression that may be associated with pathologic conditions (e.g., cancer, increased infections). Likewise, exposure to immunotoxic xenobiotics may represent additional risk to individuals with already fragile immune systems (e.g., malnutrition, infancy, old age). In another light, there has been considerable public concern regarding ''chemical hypersensitivity syndrome'' (also referred to as ''multiple chemical sensitivities syndrome'') and its relationship to hypersensitivity as well as immunosuppression. Although there exists- a substantial population who claim to have this disorder, the syndrome is not well understood. Several mediators- have been proposed including disorders of immune regulation as well as conditioned responses to odors involving pharmacologic and/or psychologic mechanisms. At present, them is no definitive evidence that these syndromes are immunologically mediated. RP LUSTER, MI (reprint author), NIEHS,NATL TOXICOL PROGRAM,POB 12233 C1-04,RES TRIANGLE PK,NC 27709, USA. NR 48 TC 73 Z9 76 U1 1 U2 7 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 APR PY 1993 VL 100 BP 219 EP 236 DI 10.2307/3431528 PG 18 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400014 PM 8354170 ER PT J AU MELNICK, RL SHACKELFORD, CC HUFF, J AF MELNICK, RL SHACKELFORD, CC HUFF, J TI CARCINOGENICITY OF 1,3-BUTADIENE SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID INHALATION PHARMACOKINETICS; SPECIES-DIFFERENCES; B6C3F1 MICE; GAS UPTAKE; BUTADIENE; RATS; MORTALITY; EXPOSURE; WORKERS; ACTIVATION AB 1,3-Butadiene, a high-production volume chemical used largely in the manufacture of synthetic rubber, is a multiple organ carcinogen in rats and mice. In inhalation studies conducted in mice by the National Toxicology Program, high rates of early lethal lymphomas occurring at exposure levels of 625 ppm or higher reduced the development and expression of later developing tumors at other sites. Use of survival-adjusted tumor rates to account for competing risk factors provided a clearer indication of the dose responses for 1,3-butadiene-induced neoplasms. An increase in lung tumors in female mice was observed at exposure concentrations as low as 6.25 ppm, the lowest concentration ever used in a long-term carcinogenicity study of this gas. Human exposures to 1,3-butadiene by workers employed at facilities that produce this chemical and at facilities that produce styrene-butadiene rubber have been measured at levels higher than those that cause cancer in animals. Furthermore, epidemiology studies have consistently revealed associations between occupational exposure to 1,3-butadiene and excess mortality due to lymphatic and hematopoietic cancers. In response to the carcinogenicity findings for 1,3-butadiene in animals and in humans, the occupational Safety and Health Administration has proposed lowering the occupational exposure standard for this chemical from 1000 ppm to 2 ppm. Future work is needed to understand the mechanisms of tumor induction by 1,3-butadiene: however, the pursuit of this research should not delay the reduction of human exposure to this chemical. RP MELNICK, RL (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 50 TC 23 Z9 23 U1 0 U2 2 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 APR PY 1993 VL 100 BP 227 EP 236 DI 10.2307/3431529 PG 10 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400015 PM 8354171 ER PT J AU PIVER, WT AF PIVER, WT TI CONTAMINATION AND RESTORATION OF GROUNDWATER AQUIFERS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Review ID NON-HODGKINS-LYMPHOMA; SOFT-TISSUE SARCOMA; METHANOGENIC CONDITIONS; INSITU BIODEGRADATION; MALIGNANT-LYMPHOMA; ORGANIC-CHEMICALS; NEW-ZEALAND; AGRICULTURAL PRACTICES; PESTICIDE APPLICATORS; CHLORINATED ETHENES AB Humans are exposed to chemicals in contaminated groundwaters that are used as sources of drinking water. Chemicals contaminate groundwater resources as a result of waste disposal methods for toxic chemicals, overuse of agricultural chemicals, and leakage of chemicals into the subsurface from buried tanks used to hold fluid chemicals and fuels. In the process, both the solid portions of the subsurface and the groundwaters that now through these porous structures have become contaminated. Restoring these aquifers and minimizing human exposure to the parent chemicals and their degradation products will require the identification of suitable biomarkers of human exposure; better understandings of how exposure can be related to disease outcome; better understandings of mechanisms of transport of pollutants, in the heterogeneous structures of the subsurface; and field testing and evaluation of methods proposed to restore and cleanup contaminated aquifers. In this review, progress in these many different but related activities is presented. RP NIEHS, POB 12233, RES TRIANGLE PK, NC 27709 USA. NR 115 TC 2 Z9 2 U1 0 U2 4 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1993 VL 100 BP 237 EP 247 DI 10.2307/3431530 PG 11 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400016 PM 8354172 ER PT J AU PRITCHARD, JB AF PRITCHARD, JB TI AQUATIC TOXICOLOGY - PAST, PRESENT, AND PROSPECTS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID SEA-SURFACE MICROLAYER; ORGANIC POLLUTANTS; MARINE ORGANISMS; UNITED-STATES; FISH; TOXICITY; CARCINOGEN; METABOLISM; CHEMICALS; DISPOSITION AB Aquatic organisms have played important roles as early warning and monitoring systems for pollutant burdens in our environment. However, they have significant potential to do even more, just as they have in basic biology where preparations like the squid axon have been essential tools in establishing physiological and biochemical mechanisms. This review provides a brief summary of the history of aquatic toxicology, focusing on the nature of aquatic contaminants, the levels of contamination in our waters, and the origins of these agents. It considers the features of the aquatic environment that determine the availability of xenobiotics to aquatic life and the fate of foreign chemicals within the organism. Finally, toxic effects are considered with primary emphasis on the potential of aquatic models to facilitate identification of the underlying mechanisms of toxicity. RP PRITCHARD, JB (reprint author), NIEHS, CELLULAR & MOLEC PHARMACOL LAB, RES TRIANGLE PK, NC 27709 USA. NR 97 TC 16 Z9 20 U1 1 U2 9 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1993 VL 100 BP 249 EP 257 DI 10.2307/3431531 PG 9 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400017 PM 8354173 ER PT J AU SCHWETZ, BA HARRIS, MW AF SCHWETZ, BA HARRIS, MW TI DEVELOPMENTAL TOXICOLOGY - STATUS OF THE FIELD AND CONTRIBUTION OF THE NATIONAL TOXICOLOGY PROGRAM SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID GLYCOL DIMETHYL ETHER; TOXICITY EVALUATION; C57BL/6N MICE; CD RATS AB The NTP has conducted developmental toxicity studies on more than 50 chemicals, often in multiple species. Several chemicals caused developmental toxicity in the absence of any toxicity to the mother. Although hazard to humans is determined by the level of exposure to the chemical and its inherent toxicity, those agents that selectively disturb the development of the conceptus are of particular concern because other manifestations of toxicity would not warn the mother of overexposure. Whether the LOAEL (lowest-observed adverse effect level) for maternal toxicity was high or low did not correlate with the potential of chemicals to cause developmental toxicity. The form of developmental toxicity that determined the LOAEL most frequently was decreased body weight in mice and rats, but not rabbits, where the LOAEL was determined more often by an increase in resorptions. Several in vitro and short-term tests appear promising as screens to predict the outcome of developmental toxicity studies in mammals. However, the only screens that have undergone formal validation studies are those evaluated by the NTP. Improvements in our ability to predict risk to humans have been limited by our knowledge of the mechanisms by which agents cause developmental toxicity. Thus, future growth is dependent on a better understanding of the biological processes that regulate normal development. therein providing the necessary framework for understanding mechanisms of abnormal development. RP SCHWETZ, BA (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 32 TC 28 Z9 28 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1993 VL 100 BP 269 EP 282 DI 10.2307/3431533 PG 14 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400019 PM 8354175 ER PT J AU SHELBY, MD BISHOP, JB MASON, JM TINDALL, KR AF SHELBY, MD BISHOP, JB MASON, JM TINDALL, KR TI FERTILITY, REPRODUCTION, AND GENETIC-DISEASE - STUDIES ON THE MUTAGENIC EFFECTS OF ENVIRONMENTAL AGENTS ON MAMMALIAN GERM-CELLS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID DOMINANT-LETHAL MUTATIONS; ETHYLENE-OXIDE; LOCUS TEST; MALE-MICE; HERITABLE TRANSLOCATIONS; MENDELIAN DISEASE; FETAL ANOMALIES; TRANSGENIC MICE; IMPAIRED LIFE; HUMAN GENOME AB Because genetically based diseases have a major impact on human health, the National Institute of Environmental Health Sciences (NIEHS) has conducted a research and testing program for more than a decade to address chemical induction of heritable genetic damage in the germ cells of mammals. Although most genetic disease results from preexisting mutations, a portion is due to the occurrence of new mutations. The supposition that exposure to mutagenic chemicals contributes to the occurrence of new mutations in the human population is strongly supported by the results from animal models. Such studies clearly demonstrate the potential of environmental chemicals to induce mutations in both somatic and reproductive cells of mammals. This NIEHS program has become a leader in the identification of genetic hazards in the environment and in the acquisition of animal model data used by regulatory agencies in assessing genetic risks to human health. RP SHELBY, MD (reprint author), NIEHS,ENVIRONM CARCINOGENESIS & MUTAGENESIS BRANCH,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU NIEHS NIH HHS [N01-ES-95273, NIEHS YO1-ES-10067, NIEHS YO1-ES-20085] NR 66 TC 55 Z9 57 U1 0 U2 2 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 APR PY 1993 VL 100 BP 283 EP 291 DI 10.2307/3431534 PG 9 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400020 PM 8354176 ER PT J AU TENNANT, RW ZEIGER, E AF TENNANT, RW ZEIGER, E TI GENETIC TOXICOLOGY - CURRENT STATUS OF METHODS OF CARCINOGEN IDENTIFICATION SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID MICRONUCLEATED POLYCHROMATIC ERYTHROCYTES; MOUSE LYMPHOMA CELL; HAMSTER OVARY CELLS; CHEMICAL-STRUCTURE; BONE-MARROW; SALMONELLA-TYPHIMURIUM; RODENT CARCINOGENICITY; STATISTICAL-ANALYSIS; PERIPHERAL-BLOOD; TOXICITY ASSAYS AB A critical aspect of the efforts to relate the results of short-term genetic toxicity tests with those from long-term rodent tests for carcinogens is the quality and consistency of the studies conducted by the National Toxicology Program. Analysis of the results in relationship to chemical structure has shown that mutagenic potential is a primary risk factor for carcinogen identification. Chemicals positive in the Salmonella assay generally possess ''structural alerts'' for electrophilic interactions, am predominantly represented among chemicals producing trans-species carcinogenic effects in rodents, and among those identified as carcinogenic to humans. Current efforts are aimed at defining toxicological, structural, and mechanistic properties of nonmutagens that are carcinogenic in rodents. RP TENNANT, RW (reprint author), NIEHS,EXPTL CARCINOGENESIS & MUTAGENESIS BRANCH,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 47 TC 32 Z9 32 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1993 VL 100 BP 307 EP 315 DI 10.2307/3431536 PG 9 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA LF734 UT WOS:A1993LF73400022 PM 8354178 ER PT J AU BECKING, GC BOYES, WK DAMSTRA, T MACPHAIL, RC AF BECKING, GC BOYES, WK DAMSTRA, T MACPHAIL, RC TI ASSESSING THE NEUROTOXIC POTENTIAL OF CHEMICALS - A MULTIDISCIPLINARY APPROACH SO ENVIRONMENTAL RESEARCH LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL SYMP ON NEUROBEHAVIORAL METHODS AND EFFECTS IN OCCUPATIONAL AND ENVIRONMENTAL HEALTH CY JUL 08-11, 1991 CL TOKYO, JAPAN ID EVOKED-POTENTIALS; TRIMETHYLTIN; TOXICOLOGY; CHLORDIMEFORM; RAT C1 US EPA,HLTH EFFECTS RES LAB,RES TRIANGLE PK,NC 27711. NIEHS,RES TRIANGLE PK,NC 27709. RP BECKING, GC (reprint author), WHO,INT PROGRAMME CHEM SAFETY,RES TRIANGLE PK,NC 27709, USA. NR 35 TC 3 Z9 3 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0013-9351 J9 ENVIRON RES JI Environ. Res. PD APR PY 1993 VL 61 IS 1 BP 164 EP 175 DI 10.1006/enrs.1993.1061 PG 12 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA KY556 UT WOS:A1993KY55600018 PM 8472671 ER PT J AU BOUSSAOUD, D BARTH, TM WISE, SP AF BOUSSAOUD, D BARTH, TM WISE, SP TI EFFECTS OF GAZE ON APPARENT VISUAL RESPONSES OF FRONTAL-CORTEX NEURONS SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE FRONTAL CORTEX; GAZE; PREMOTOR CORTEX; SPATIAL CODING; MONKEY ID POSTERIOR PARIETAL CORTEX; MACAQUE MONKEY; RHESUS-MONKEY; CORTICAL CONNECTIONS; INFERIOR AREA-6; POSITION; MOVEMENT; STIMULI; PROJECTIONS; DIRECTION AB Previous reports have argued that single neurons in the ventral premotor cortex of rhesus monkeys (PMv, the ventrolateral part of Brodmann's area 6) typically show spatial response fields that are independent of gaze angle. We reinvestigated this issue for PMv and also explored the adjacent prearcuate cortex (PAv, areas 12 and 45). Two rhesus monkeys were operantly conditioned to press a switch and maintain fixation on a small visual stimulus (0.2-degrees x 0.2-degrees) while a second visual stimulus (1-degrees x 1-degrees or 2-degrees x 2-degrees) appeared at one of several possible locations on a video screen. When the second stimulus dimmed, after an unpredictable period of 0.4-1.2 s, the monkey had to quickly release the switch to receive liquid reinforcement. By presenting stimuli at fixed screen locations and varying the location of the fixation point, we could determine whether single neurons encode stimulus location in ''absolute space'' or any other coordinate system independent of gaze. For the vast majority of neurons in both PMv (90%) and PAv (94%), the apparent response to a stimulus at a given screen location varied significantly and dramatically with gaze angle. Thus, we found little evidence for gaze-independent activity in either PMv or PAv neurons. The present result in frontal cortex resembles that in posterior parietal cortex, where both retinal image location and eye position affect responsiveness to visual stimuli. C1 NIMH,NEUROPHYSIOL LAB,POB 289,POOLESVILLE,MD 20837. RI Boussaoud, Driss/B-6932-2008 NR 50 TC 92 Z9 93 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. PD APR PY 1993 VL 93 IS 3 BP 423 EP 434 PG 12 WC Neurosciences SC Neurosciences & Neurology GA KY579 UT WOS:A1993KY57900006 PM 8519333 ER PT J AU ONG, RC MAENO, M KUNG, HF AF ONG, RC MAENO, M KUNG, HF TI MURINE STEM-CELL FACTOR STIMULATES ERYTHROPOIETIC DIFFERENTIATION OF VENTRAL MESODERM IN XENOPUS GASTRULA EMBRYO SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID GROWTH-FACTOR; BLOOD ISLAND; HEMATOPOIETIC-CELLS; YOLK-SAC; LAEVIS; EXPRESSION; CHIMERAS; ONTOGENY; RECEPTOR; LARVAL C1 NCI,FCRDC,BIOCHEM PHYSIOL LAB,POB B,BLDG 560,ROOM 31-76,FREDERICK,MD 21702. NR 22 TC 8 Z9 8 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 APR PY 1993 VL 205 IS 2 BP 326 EP 330 DI 10.1006/excr.1993.1093 PG 5 WC Oncology; Cell Biology SC Oncology; Cell Biology GA KZ288 UT WOS:A1993KZ28800017 PM 7683272 ER PT J AU CASSEL, A COTTLERFOX, M DOREN, S DUNBAR, CE AF CASSEL, A COTTLERFOX, M DOREN, S DUNBAR, CE TI RETROVIRAL-MEDIATED GENE-TRANSFER INTO CD34-ENRICHED HUMAN PERIPHERAL-BLOOD STEM-CELLS SO EXPERIMENTAL HEMATOLOGY LA English DT Note DE RETROVIRUS; GENE TRANSFER; STEM CELLS ID HEMATOPOIETIC PROGENITOR CELLS; COLONY-STIMULATING FACTOR; TERM MARROW CULTURE; TRANSPLANTATION; INVITRO; RECONSTITUTION; TRANSDUCTION; EXPRESSION; EFFICIENCY; INFECTION AB Retroviral-mediated gene transfer has been shown to be a feasible method for the introduction of new genes into bone marrow hematopoietic stem cells. We have investigated the application of this technology to primitive CD34-enriched human peripheral blood cells as a potential alternative stem cell source. Bone marrow (BM) and peripheral blood (PB) CD34-enriched cells from normal volunteers and patients with multiple myeloma were exposed to retroviral vectors containing the neomycin-resistance gene and gene transfer efficiency into colony-forming unit colonies (CFU-C) and CD34(+) cells was assessed by polymerase chain reaction (PCR). Peripheral blood was a target equally efficient to BM, and PB cells mobilized with chemotherapy and growth factors were also shown to take up retroviral vectors readily. Conditions favoring gene transfer were investigated, and exposure of cells to interleukin-3 (IL-3), interleukin-6 (IL-6), and stem cell factor (SCF) during a 72-hour transduction was found to be most effective. The use of PB stem cells as targets for gene transfer could allow repeated collections and transductions, with obvious advantages over a single BM collection. C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NIH,CTR CLIN,DEPT TRANSFUS MED,BETHESDA,MD 20892. NR 37 TC 156 Z9 157 U1 1 U2 1 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD APR PY 1993 VL 21 IS 4 BP 585 EP 591 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA MW609 UT WOS:A1993MW60900017 PM 7681785 ER PT J AU SCHAMBRA, PE AF SCHAMBRA, PE TI KINYOUN LEGACY - THE INTERNATIONAL DIMENSIONS OF THE NATIONAL-INSTITUTES-OF-HEALTH SO FASEB JOURNAL LA English DT Article RP SCHAMBRA, PE (reprint author), NIH,FOGARTY INT CTR,BLDG 31,RM B2C39,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 1 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 APR 1 PY 1993 VL 7 IS 6 BP 503 EP 504 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA KY009 UT WOS:A1993KY00900002 PM 8472889 ER PT J AU THOMSON, EJ ROTHENBERG, K AF THOMSON, EJ ROTHENBERG, K TI REPRODUCTIVE GENETIC TESTING - IMPACT UPON WOMEN - INTRODUCTION SO FETAL DIAGNOSIS AND THERAPY LA English DT Editorial Material RP THOMSON, EJ (reprint author), NATL CTR HUMAN GENOME RES,BLDG 38A,ROOM 604,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-3837 J9 FETAL DIAGN THER JI Fetal Diagn. Ther. PD APR PY 1993 VL 8 SU 1 BP 2 EP 5 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA LC666 UT WOS:A1993LC66600002 ER PT J AU THOMSON, EJ AF THOMSON, EJ TI REPRODUCTIVE GENETIC TESTING - IMPLICATIONS FOR NURSING-EDUCATION SO FETAL DIAGNOSIS AND THERAPY LA English DT Article; Proceedings Paper CT WORKSHOP ON REPRODUCTIVE GENETIC TESTING : IMPACT UPON WOMEN CY NOV 21-23, 1991 CL BETHESDA, MD SP NIH, NICHD, NATL CTR HUMAN GENOME RES, NATL CTR NURSING RES, OFF WOMENS HLTH DE GENETICS; NURSING EDUCATION AB Reproductive genetic testing technologies are expanding at an exponential rate. Nurses are increasingly being called upon to provide these services to women. This paper discusses the status of nursing education in genetics and identifies immediate needs for nurses in order to be adequately prepared to respond to these increased demands. The future role of nurses in providing genetic services is delineated. RP THOMSON, EJ (reprint author), NATL CTR HUMAN GENOME RES,BLDG 38A,ROOM 604,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-3837 J9 FETAL DIAGN THER JI Fetal Diagn. Ther. PD APR PY 1993 VL 8 SU 1 BP 232 EP 235 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA LC666 UT WOS:A1993LC66600027 PM 8512650 ER PT J AU MORGAN, DL MAHLER, JF OCONNOR, RW PRICE, HC ADKINS, B AF MORGAN, DL MAHLER, JF OCONNOR, RW PRICE, HC ADKINS, B TI STYRENE INHALATION TOXICITY STUDIES IN MICE .1. HEPATOTOXICITY IN B6C3F1 MICE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID LIVER; EXPOSURE; HEPATOCYTES; INDUSTRY; OXIDE; RESISTANCE C1 MANTECH ENVIRONM TECHNOL INC,RES TRIANGLE PK,NC 27709. RP MORGAN, DL (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 26 TC 47 Z9 47 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 APR PY 1993 VL 20 IS 3 BP 325 EP 335 DI 10.1006/faat.1993.1042 PG 11 WC Toxicology SC Toxicology GA KZ304 UT WOS:A1993KZ30400008 PM 8504906 ER PT J AU HEBERT, CD ELWELL, MR TRAVLOS, GS ZEIGER, E FRENCH, JE BUCHER, JR AF HEBERT, CD ELWELL, MR TRAVLOS, GS ZEIGER, E FRENCH, JE BUCHER, JR TI INHALATION TOXICITY OF 1,6-HEXANEDIAMINE DIHYDROCHLORIDE IN F344/N RATS AND B6C3F(1) MICE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID ZERO DOSE CONTROL; RD50 CONCENTRATION; VIRAL-INFECTIONS; TUMOR PREVALENCE; BODY-WEIGHT; HEXAMETHYLENEDIAMINE; CHEMICALS; SURVIVAL; LESIONS; DIAMINE C1 NIEHS,EXPTL CARCINOGENESIS BRANCH,RES TRIANGLE PK,NC 27709. RP HEBERT, CD (reprint author), NIEHS,EXPTL TOXICOL BRANCH,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 43 TC 1 Z9 1 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 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1993 VL 20 IS 3 BP 348 EP 359 DI 10.1006/faat.1993.1045 PG 12 WC Toxicology SC Toxicology GA KZ304 UT WOS:A1993KZ30400011 PM 8504909 ER PT J AU PURCELL, RH AF PURCELL, RH TI THE DISCOVERY OF THE HEPATITIS VIRUSES SO GASTROENTEROLOGY LA English DT Article RP PURCELL, RH (reprint author), NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892, USA. NR 1 TC 86 Z9 94 U1 1 U2 6 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 APR PY 1993 VL 104 IS 4 BP 955 EP 963 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LM684 UT WOS:A1993LM68400001 PM 8385046 ER PT J AU HOOFNAGLE, JH DIBISCEGLIE, AM WAGGONER, JG PARK, Y AF HOOFNAGLE, JH DIBISCEGLIE, AM WAGGONER, JG PARK, Y TI INTERFERON-ALFA FOR PATIENTS WITH CLINICALLY APPARENT CIRRHOSIS DUE TO CHRONIC HEPATITIS-B SO GASTROENTEROLOGY LA English DT Article ID HUMAN ALPHA-INTERFERON; CONTROLLED TRIAL; LIVER-TRANSPLANTATION; THERAPY; IMMUNOPROPHYLAXIS; RECIPIENTS RP HOOFNAGLE, JH (reprint author), NIDDKD,DIGEST DIS BRANCH,LIVER DIS SECT,BLDG 10,ROOM 9C103,BETHESDA,MD 20892, USA. NR 19 TC 165 Z9 171 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 APR PY 1993 VL 104 IS 4 BP 1116 EP 1121 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA LM684 UT WOS:A1993LM68400021 PM 8462800 ER PT J AU BENYA, RV SHIKADO, F FATHI, Z BATTEY, JB MANTEY, S JENSEN, RT AF BENYA, RV SHIKADO, F FATHI, Z BATTEY, JB MANTEY, S JENSEN, RT TI HOMOLOGOUS DESENSITIZATION TO NEUROMEDIN-B (NMB) BY PROGRESSIVE DOWN-REGULATION OF THE NMB RECEPTOR (NMBR) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIDDK,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 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 APR PY 1993 VL 104 IS 4 SU S BP A812 EP A812 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703225 ER PT J AU BENYA, RV FATHI, Z BATTEY, JB JENSEN, RT AF BENYA, RV FATHI, Z BATTEY, JB JENSEN, RT TI GASTRIN-RELEASING PEPTIDE RECEPTOR (GRPR) STIMULATED INCREASES IN CAMP ARE NOT INVOLVED IN RECEPTOR INTERNALIZATION OR DESENSITIZATION BUT MAY BE IMPORTANT FOR C-FOS ACTIVATION AND CELL-PROLIFERATION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NIDDK,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 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 APR PY 1993 VL 104 IS 4 SU S BP A812 EP A812 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703223 ER PT J AU BENYA, RV METZ, DC FISHBEYN, VA STRADER, DB ORBUCH, M JENSEN, RT AF BENYA, RV METZ, DC FISHBEYN, VA STRADER, DB ORBUCH, M JENSEN, RT TI GASTRINOMA CAN BE THE INITIAL PRESENTATION FOR PATIENTS WITH MULTIPLE ENDOCRINE NEOPLASIA TYPE-I (MEN-I) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A42 EP A42 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95700162 ER PT J AU BERGASA, NV NEWMAN, W ROTHLEIN, R JONES, EA ADAMS, DH AF BERGASA, NV NEWMAN, W ROTHLEIN, R JONES, EA ADAMS, DH TI SERUM LEVELS OF SOLUBLE ADHESION MOLECULES (I-CAM-1, V-CAM-1 AND E-SELECTIN ARE MARKEDLY ELEVATED IN PRIMARY BILIARY-CIRRHOSIS (PBC) AND UNAFFECTED BY LOW-DOSE ORAL METHOTREXATE TREATMENT SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,LIVER DIS SECT,BETHESDA,MD. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 2 TC 10 Z9 10 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 APR PY 1993 VL 104 IS 4 SU S BP A877 EP A877 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703479 ER PT J AU BOIRIVANT, M FIOCCHI, C DUCHMANN, R STROBER, W AF BOIRIVANT, M FIOCCHI, C DUCHMANN, R STROBER, W TI DIFFERENTIAL IMPAIRMENT OF LAMINA PROPRIA T-CELLS RESPONSES IN INFLAMMATORY BOWEL-DISEASE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. RI BOIRIVANT, MONICA/B-9977-2016 NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A672 EP A672 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95702670 ER PT J AU BOIRIVANT, M MURAKAWA, Y FIOCCHI, C STROBER, W AF BOIRIVANT, M MURAKAWA, Y FIOCCHI, C STROBER, W TI LAMINA PROPRIA T-CELLS ARE ANERGIC SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. CLEVELAND CLIN EDUC FDN,CLEVELAND,OH 44106. RI BOIRIVANT, MONICA/B-9977-2016 NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A672 EP A672 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95702669 ER PT J AU COHEN, ME KHURANA, S MONTGOMERY, JL KREYDIYYEH, S RHEE, SG DONOWITZ, M AF COHEN, ME KHURANA, S MONTGOMERY, JL KREYDIYYEH, S RHEE, SG DONOWITZ, M TI CARBACHOL ELEVATES RABBIT ILEAL BRUSH-BORDER PHOSPHOLIPASE-C ACTIVITY, AN EFFECT ASSOCIATED WITH AN INCREASE IN AMOUNT AND TYROSINE (TYR) PHOSPHORYLATION OF PHOSPHATIDLYINOSITOL SPECIFIC PHOSPHOLIPASE C-GAMMA SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,GI UNIT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,GI UNIT,BALTIMORE,MD 21205. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A240 EP A240 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95700951 ER PT J AU COLLEN, MJ JENSEN, RT AF COLLEN, MJ JENSEN, RT TI COMPARISON OF IDIOPATHIC GASTRIC-ACID HYPERSECRETION WITH ZOLLINGER-ELLISON SYNDROME SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. LOMA LINDA UNIV,MED CTR,DIV GASTROENTEROL,LOMA LINDA,CA 92350. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A58 EP A58 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95700228 ER PT J AU COLLEN, MJ ABDULIAN, JD CHEN, YK BRANSON, MM WIRSHUP, JF JENSEN, RT AF COLLEN, MJ ABDULIAN, JD CHEN, YK BRANSON, MM WIRSHUP, JF JENSEN, RT TI IDIOPATHIC GASTRIC-ACID HYPERSECRETION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 LOMA LINDA UNIV,MED CTR,DIV GASTROENTEROL,LOMA LINDA,CA 92350. NIDDK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A58 EP A58 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95700226 ER PT J AU DEWEERTH, A PISEGNA, JR WANK, SA AF DEWEERTH, A PISEGNA, JR WANK, SA TI CLONING AND FUNCTIONAL EXPRESSION OF A CCKB RECEPTOR FROM GUINEA-PIG GALLBLADDER SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 10 Z9 10 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 APR PY 1993 VL 104 IS 4 SU S BP A497 EP A497 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95701974 ER PT J AU FELLEY, CP MANTEY, SA SUTLIFF, VE PRADHAN, TK JENSEN, RT AF FELLEY, CP MANTEY, SA SUTLIFF, VE PRADHAN, TK JENSEN, RT TI GASTRIC CHIEF CELLS POSSESS HIGH-AFFINITY SOMATOSTATIN RECEPTORS REGULATED BY SECRETAGOGUES ACTING THROUGH EITHER THE CALCIUM OR THE CAMP PATHWAY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A823 EP A823 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703268 ER PT J AU FELLEY, CP MANTEY, SA PRADHAN, TK JENSEN, RT AF FELLEY, CP MANTEY, SA PRADHAN, TK JENSEN, RT TI GASTRIC CHIEF CELLS POSSESS BOMBESIN RECEPTORS OF THE GASTRIN-RELEASING PEPTIDE (GRP)-PREFERRING SUBTYPE WHICH DO NOT MEDIATE PEPSINOGEN SECRETION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A77 EP A77 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95700303 ER PT J AU FERRAZ, MLG SILVA, AEB CAMPBELL, DA DIBISCEGLIE, AM LUCEY, MR AF FERRAZ, MLG SILVA, AEB CAMPBELL, DA DIBISCEGLIE, AM LUCEY, MR TI FULMINANT HEPATIC-FAILURE IN PATIENTS UNDERGOING LIVER-TRANSPLANTATION - EVIDENCE OF A NON-A,B,C,D,E SYNDROME SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI 48109. NIH,HEPATITIS STUDIES SECT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A901 EP A901 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703575 ER PT J AU FISHBEYN, VA COY, DH JIANG, NZ JENSEN, RT AF FISHBEYN, VA COY, DH JIANG, NZ JENSEN, RT TI A CHIMERIC VIP-PACAP ANALOG BUT NOT VIP PSEUDOPEPTIDES FUNCTION AS VIP RECEPTOR ANTAGONISTS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 TULANE UNIV,NEW ORLEANS,LA 70118. NIDDK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A303 EP A303 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95701204 ER PT J AU FISHBEYN, VA NORTON, JA FRAKER, DL BENYA, RV STRADER, DB ORBUCH, M PISEGNA, JR METZ, DC JENSEN, RT AF FISHBEYN, VA NORTON, JA FRAKER, DL BENYA, RV STRADER, DB ORBUCH, M PISEGNA, JR METZ, DC JENSEN, RT TI PROSPECTIVE-STUDY OF THE BEST METHOD TO FIND DUODENAL GASTRINOMAS IN PATIENTS WITH ZOLLINGER-ELLISON SYNDROME (ZES) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NR 0 TC 3 Z9 3 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 APR PY 1993 VL 104 IS 4 SU S BP A304 EP A304 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95701205 ER PT J AU GU, ZF PRADHAN, TK COY, DH JENSEN, RT AF GU, ZF PRADHAN, TK COY, DH JENSEN, RT TI ACTIONS OF GALANIN FRAGMENTS ON GASTRIC SMOOTH-MUSCLE CELLS IN GUINEA-PIGS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. NIDDK,DIGEST DIS BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A828 EP A828 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703285 ER PT J AU GU, ZF ROSSOWSKI, WJ COY, DH PRADHAM, TK JENSEN, RT AF GU, ZF ROSSOWSKI, WJ COY, DH PRADHAM, TK JENSEN, RT TI PUTATIVE GALANIN CHIMERIC RECEPTOR ANTAGONISTS FUNCTIONS AS FULL AGONISTS IN GASTROINTESTINAL SMOOTH-MUSCLE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD. NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A515 EP A515 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95702048 ER PT J AU GU, ZF PRADHAN, TK JENSEN, RT AF GU, ZF PRADHAN, TK JENSEN, RT TI GALANIN-INDUCED RELAXATION IN GASTRIC SMOOTH-MUSCLE CELLS IS MEDIATED ONLY BY CYCLIC-AMP SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD. NR 1 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A515 EP A515 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95702046 ER PT J AU HOOFNAGLE, JH LOMBARDERO, M AF HOOFNAGLE, JH LOMBARDERO, M TI LIVER-DONOR AGE AND OUTCOME OF LIVER-TRANSPLANTATION - NIDDK LIVER-TRANSPLANTATION DATABASE (LTD) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DDDN,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT EPIDEMIOL,PITTSBURGH,PA 15260. NR 0 TC 5 Z9 5 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 APR PY 1993 VL 104 IS 4 SU S BP A917 EP A917 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703641 ER PT J AU KAWAHITO, Y SANO, H CHROUSOS, GP WILDER, RL YURI, K KAWATA, M KATO, H KONDO, M AF KAWAHITO, Y SANO, H CHROUSOS, GP WILDER, RL YURI, K KAWATA, M KATO, H KONDO, M TI THE PRODUCTION OF COTICOTROPIN-RELEASING HORMONE IN NORMAL HUMAN COLONIC MUCOSAL CELLS(ENTEROCHROMAFFIN CELLS) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 KYOTO PREFECTURAL UNIV MED,DEPT INTERNAL MED 1,KYOTO 602,JAPAN. KYOTO PREFECTURAL UNIV MED,DEPT ANAT,KYOTO 602,JAPAN. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD. NIAMS,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD. NR 0 TC 3 Z9 3 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 APR PY 1993 VL 104 IS 4 SU S BP A1044 EP A1044 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95704142 ER PT J AU KITSUKAWA, Y FELLEY, C METZ, DC JENSEN, RT AF KITSUKAWA, Y FELLEY, C METZ, DC JENSEN, RT TI THAPSIGARGIN (TG) REVEALS DISTINCT ROLES FOR CA2+ INFLUX, CYTOPLASMIC CA2+([CA2+]I) AND INTRACELLULAR CA2+ STORES IN MEDIATING SECRETAGOGUE-INDUCED PEPSINOGEN RELEASE FROM CHIEF CELLS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DDB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A119 EP A119 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95700469 ER PT J AU KIYASU, P DIBISCEGLIE, A LOVELL, M GAFFEY, M LOBO, P ISHITANI, M STEVENSON, W PRUETT, T CALDWELL, S AF KIYASU, P DIBISCEGLIE, A LOVELL, M GAFFEY, M LOBO, P ISHITANI, M STEVENSON, W PRUETT, T CALDWELL, S TI HEPATITIS-C VIRUS RECURRENCE AFTER ORTHOTOPIC LIVER-TRANSPLANTATION - CLINICAL-FEATURES DURING THE 1ST YEAR SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV VIRGINIA,CHARLOTTESVILLE,VA 22903. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A928 EP A928 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703686 ER PT J AU LATHAM, PS PILARO, AM PHONTANGTHAM, P VARESIO, L AF LATHAM, PS PILARO, AM PHONTANGTHAM, P VARESIO, L TI CHARACTERIZATION OF A RAT KUPFFER CELL-LINE - ENDOTOXIN INDUCES TNF-ALPHA AND DOWN-REGULATES CSF-1 RECEPTOR SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20052. NCI,FC DC,BIOL RESPONSE MODIFIERS PROGRAM,LMI,LEI,FREDERICK,MD 21701. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A934 EP A934 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703710 ER PT J AU MASON, A SALLIE, R DOHNER, D DEHNER, M WHITE, H GELB, L WILLIAMS, R PERRILLO, R AF MASON, A SALLIE, R DOHNER, D DEHNER, M WHITE, H GELB, L WILLIAMS, R PERRILLO, R TI PREVALENCE OF HERPES-VIRIDAE DNA IN THE LIVER OF PATIENTS WITH FULMINANT HEPATIC-FAILURE NON-A NON-B SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 WASHINGTON UNIV,VAMC,SCH MED,ST LOUIS,MO 63130. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. NIH,BETHESDA,MD 20892. UNIV LONDON KINGS COLL HOSP,INST LIVER STUDIES,LONDON SE5 8RX,ENGLAND. OI Mason, Andrew/0000-0002-0470-9522 NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A950 EP A950 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703774 ER PT J AU METZ, DC KUCHNIO, M FRAKER, DL VENZON, DJ JAFFE, G STETLERSTEVENSON, M JENSEN, RT AF METZ, DC KUCHNIO, M FRAKER, DL VENZON, DJ JAFFE, G STETLERSTEVENSON, M JENSEN, RT TI FLOW-CYTOMETRY AND ZOLLINGER-ELLISON SYNDROME (ZES) - CORRELATION WITH DISEASE EXTENT AND SURVIVAL SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NCI,BETHESDA,MD 20892. NIH,DEPT PATHOL,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A428 EP A428 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95701699 ER PT J AU MOHAN, P KALER, SG MORGAN, RO ARTHURSMITH, A KERZNER, B AF MOHAN, P KALER, SG MORGAN, RO ARTHURSMITH, A KERZNER, B TI DETECTION OF COPPER-BINDING LIGANDS IN RAT BILE BY COPPER AFFINITY-CHROMATOGRAPHY AND COPPER BLOTTING SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 CHILDRENS NATL MED CTR,DEPT GASTROENTEROL,WASHINGTON,DC. NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A957 EP A957 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703801 ER PT J AU MROZINSKI, J COY, D NEYA, M MANTEY, S JENSEN, R AF MROZINSKI, J COY, D NEYA, M MANTEY, S JENSEN, R TI SIDE-CHAIN RESTRICTED ANALOGS - A NEW CLASS OF BOMBESIN RECEPTOR ANTAGONISTS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. TULANE UNIV,NEW ORLEANS,LA 70118. NR 0 TC 1 Z9 1 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A323 EP A323 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95701281 ER PT J AU MULLIN, GE VEZZA, FR SAMPAT, A MAYCON, Z KATZ, R EISENSTIEN, E KATZ, S WEISSMAN, G MCKINLEY, M FISHER, SE AF MULLIN, GE VEZZA, FR SAMPAT, A MAYCON, Z KATZ, R EISENSTIEN, E KATZ, S WEISSMAN, G MCKINLEY, M FISHER, SE TI ABNORMAL IL-10 MESSENGER-RNA PRODUCTION IN THE INTESTINAL MUCOSAL LESIONS OF INFLAMMATORY BOWEL-DISEASE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 CORNELL UNIV,N SHORE UNIV HOSP,COLL MED,DEPT MED,MANHASSET,NY 11030. CORNELL UNIV,N SHORE UNIV HOSP,COLL MED,DEPT PEDIAT,MANHASSET,NY 11030. NIAID,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 0 TC 29 Z9 29 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 APR PY 1993 VL 104 IS 4 SU S BP A751 EP A751 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95702981 ER PT J AU ORBUCH, M COY, DH MROZINSKI, JE MANTEY, SA TAYLOR, JE MOREAU, JP JENSEN, RT AF ORBUCH, M COY, DH MROZINSKI, JE MANTEY, SA TAYLOR, JE MOREAU, JP JENSEN, RT TI DISCOVERY OF A NOVEL CLASS OF NEUROMEDIN-B RECEPTOR (NMB-R) ANTAGONISTS - SUBSTITUTED SOMATOSTATIN ANALOGS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. TULANE UNIV,NEW ORLEANS,LA 70118. BIOMEASURE INC,HOPKINTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A845 EP A845 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703353 ER PT J AU PISEGNA, JR WANK, SA AF PISEGNA, JR WANK, SA TI MOLECULAR-CLONING AND FUNCTIONAL EXPRESSION OF THE PITUITARY ADENYLATE-CYCLASE ACTIVATING POLYPEPTIDE (PACAP) TYPE-1 RECEPTOR SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD. NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A847 EP A847 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703361 ER PT J AU SARTOR, RB BENDER, DE ALLEN, JB ZIMMERMANN, EM HOLT, LC PARDO, MS LUND, PK WAHL, SM AF SARTOR, RB BENDER, DE ALLEN, JB ZIMMERMANN, EM HOLT, LC PARDO, MS LUND, PK WAHL, SM TI CHRONIC EXPERIMENTAL ENTEROCOLITIS AND EXTRAINTESTINAL INFLAMMATION ARE T-LYMPHOCYTE DEPENDENT SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV N CAROLINA,CTR GI BIOL & DIS,CHAPEL HILL,NC 27514. NIDR,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 18 Z9 18 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 APR PY 1993 VL 104 IS 4 SU S BP A775 EP A775 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703079 ER PT J AU SCHMIDT, HHJ DIEKSTAHL, F IKEWAKI, K RADER, D KLEIN, HG LOHSE, P BOJANOVSKI, D BREWER, HB MANNS, M AF SCHMIDT, HHJ DIEKSTAHL, F IKEWAKI, K RADER, D KLEIN, HG LOHSE, P BOJANOVSKI, D BREWER, HB MANNS, M TI MOLECULAR GENETIC AND INVIVO KINETIC FINDINGS IN A PATIENT WITH FISH EYE DISEASE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HANNOVER MED SCH,GASTROENTEROL & HEPATOL ABT,W-3000 HANNOVER 61,GERMANY. NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A986 EP A986 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703918 ER PT J AU SILVA, AE HOSEIN, B WISNIEWOLSKI, R FANG, C SHINDO, M WAGGONER, JG DIBISCEGLIE, AM AF SILVA, AE HOSEIN, B WISNIEWOLSKI, R FANG, C SHINDO, M WAGGONER, JG DIBISCEGLIE, AM TI DIAGNOSIS OF CHRONIC HEPATITIS-C - COMPARISON OF IMMUNOASSAYS AND THE POLYMERASE CHAIN-REACTION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,HEPATITIS STUDIES SECT,BETHESDA,MD 20892. UBI,LAKE SUCCESS,NY. AMER RED CROSS,BLOOD SERV,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A995 EP A995 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703952 ER PT J AU SJOGREN, MH INNIS, B REDFIELD, R PERINE, P TICEHURST, J MUSHAHWAR, I DAWSON, G MALIK, I AHMED, A DUNCAN, F LEGTERS, L PURCELL, RH AF SJOGREN, MH INNIS, B REDFIELD, R PERINE, P TICEHURST, J MUSHAHWAR, I DAWSON, G MALIK, I AHMED, A DUNCAN, F LEGTERS, L PURCELL, RH TI ASSESSMENT OF SEROLOGICAL RESPONSES DURING ACUTE AND CONVALESCENT STAGES OF HEPATITIS-E VIRUS-INFECTION USING A NEW IMMUNOASSAY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 WALTER REED ARMY INST RES,WASHINGTON,DC 20307. ABBOTT LABS,N CHICAGO,IL 60064. NIH,BETHESDA,MD 20892. UNIV HLTH SCI,UNIFORMED SERV,BETHESDA,MD. PAKISTAN UNITED STATES LAB SEROEPIDEMIOL,RAWALPINDI,PAKISTAN. RI Ticehurst, John/I-7532-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A997 EP A997 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95703961 ER PT J AU STRADER, DB ORBUCH, M FISHBEYN, VA BENYA, RV BENJAMIN, SB LUBENSKY, I JENSEN, RT METZ, DC AF STRADER, DB ORBUCH, M FISHBEYN, VA BENYA, RV BENJAMIN, SB LUBENSKY, I JENSEN, RT METZ, DC TI ENDOSCOPY, MANOMETRY AND HISTOPATHOLOGY OF THE ESOPHAGUS IN ZOLLINGER-ELLISON SYNDROME (ZES) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DDB,BETHESDA,MD. NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A199 EP A199 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95700786 ER PT J AU YURDAYDIN, C ENGLER, H LI, Y WALSH, TJ BASILE, AS JONES, EA AF YURDAYDIN, C ENGLER, H LI, Y WALSH, TJ BASILE, AS JONES, EA TI THE ROLE OF GUT BACTERIA IN THE ACCUMULATION OF BENZODIAZEPINE RECEPTOR (BZR) LIGANDS IN HEPATIC-ENCEPHALOPATHY (HE) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,NEUROSCI LAB,BETHESDA,MD. NIDDK,LIVER DIS SECT,BETHESDA,MD. NIH,PATHOL CLIN,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 APR PY 1993 VL 104 IS 4 SU S BP A1022 EP A1022 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95704062 ER PT J AU ZENILMAN, ME PERFETTI, R SHULDINER, AR AF ZENILMAN, ME PERFETTI, R SHULDINER, AR TI PANCREATIC REGENERATION GENE (REG) EXPRESSION DURING ISLET GROWTH INTHE RAT SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,DEPT SURG,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,DEPT MED,BALTIMORE,MD 21218. NIA,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1993 VL 104 IS 4 SU S BP A655 EP A655 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95702602 ER PT J AU ZSCHABITZ, A NEURATH, M GABIUS, HJ SCHMIDT, W STOFFT, E AF ZSCHABITZ, A NEURATH, M GABIUS, HJ SCHMIDT, W STOFFT, E TI CHARACTERIZATION OF EXTRACELLULAR-MATRIX COMPONENTS IN THE HUMAN PANCREAS DURING FETAL DEVELOPMENT SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 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 APR PY 1993 VL 104 IS 4 SU S BP A657 EP A657 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KX957 UT WOS:A1993KX95702609 ER PT J AU BEHAN, DP POTTER, E LEWIS, KA JENKINS, NA COPELAND, N LOWRY, PJ VALE, WW AF BEHAN, DP POTTER, E LEWIS, KA JENKINS, NA COPELAND, N LOWRY, PJ VALE, WW TI CLONING AND STRUCTURE OF THE HUMAN CORTICOTROPIN RELEASING FACTOR-BINDING PROTEIN GENE (CRHBP) SO GENOMICS LA English DT Article ID INDUCIBLE ENHANCER; DNA-SEQUENCES; HUMAN-PLASMA; HORMONE; ELEMENTS C1 FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. UNIV READING,DEPT BIOCHEM & PHYSIOL,READING RG6 2AJ,BERKS,ENGLAND. RP BEHAN, DP (reprint author), SALK INST BIOL STUDIES,CLAYTON FDN LABS PEPTIDE BIOL,LA JOLLA,CA 92037, USA. FU NIDDK NIH HHS [DK 26741, DK 07044]; PHS HHS [N01-74101]; Wellcome Trust NR 26 TC 54 Z9 56 U1 1 U2 2 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 APR PY 1993 VL 16 IS 1 BP 63 EP 68 DI 10.1006/geno.1993.1141 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA KW205 UT WOS:A1993KW20500009 PM 8198617 ER PT J AU HUNT, CR GASSER, DL CHAPLIN, DD PIERCE, JC KOZAK, CA AF HUNT, CR GASSER, DL CHAPLIN, DD PIERCE, JC KOZAK, CA TI CHROMOSOMAL LOCALIZATION OF 5 MURINE HSP70 GENE FAMILY MEMBERS - HSP70-1, HSP70-2, HSP70-3, HSC70T, AND GRP78 SO GENOMICS LA English DT Article ID HEAT-SHOCK PROTEIN; GLUCOSE-REGULATED PROTEIN; EXPRESSION; SEQUENCE; CONSERVATION; DROSOPHILA; CLONING; REGION C1 WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63108. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. DUPONT MERCK PHARMACEUT CO,WILMINGTON,DE 19880. NIAID,BETHESDA,MD 20892. FU NCI NIH HHS [R29 CA50503]; NIAID NIH HHS [AI15322]; NIDCR NIH HHS [DEO9164] NR 31 TC 74 Z9 75 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 APR PY 1993 VL 16 IS 1 BP 193 EP 198 DI 10.1006/geno.1993.1158 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA KW205 UT WOS:A1993KW20500026 PM 8486356 ER PT J AU PORTER, BE JUSTICE, MJ COPELAND, NG JENKINS, NA HUNTER, DD MERLIE, JP SANES, JR AF PORTER, BE JUSTICE, MJ COPELAND, NG JENKINS, NA HUNTER, DD MERLIE, JP SANES, JR TI S-LAMININ - MAPPING TO MOUSE CHROMOSOME-9 AND EXPRESSION IN THE LINKED MUTANTS TIPPY AND DUCKY SO GENOMICS LA English DT Note ID GENETIC-LINKAGE MAP; PROTEIN; CHAIN; VARIANTS; MEROSIN; MURINE; LOCUS C1 WASHINGTON UNIV,MED CTR,DEPT ANAT & NEUROBIOL,660 S EUCLID,ST LOUIS,MO 63110. WASHINGTON UNIV,MED CTR,DEPT MOLEC BIOL & PHARMACOL,ST LOUIS,MO 63110. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 25 TC 9 Z9 9 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 APR PY 1993 VL 16 IS 1 BP 278 EP 281 DI 10.1006/geno.1993.1178 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA KW205 UT WOS:A1993KW20500046 PM 8486374 ER PT J AU POZSGAY, V AF POZSGAY, V TI A METHOD FOR GLYCOCONJUGATE SYNTHESIS SO GLYCOCONJUGATE JOURNAL LA English DT Article DE GLYCOCONJUGATE SYNTHESIS; REDUCTIVE AMINATION; OMEGA-ALDEHYDOALKYL AGLYCON; IMMUNOADSORBENT; DISACCHARIDE ID REDUCTIVELY AMINATED DISACCHARIDES; B STREPTOCOCCAL POLYSACCHARIDES; IMMUNOCHEMICAL CHARACTERIZATION; OLIGOSACCHARIDES; PROTEINS; GLYCOPROTEINS; GLYCOSIDES; ANTIGEN; NEOGLYCOPROTEINS; DERIVATIVES AB 7-Formylheptyl glycosides of 2-acetamido-2-deoxy-beta-D-glucopyranose and O-alpha-L-rhamnopyranosyl-(1 --> 3)-O-alpha-L-rhamnopyranose were synthesized and were coupled by reductive amination to bovine serum albumin and aminopropyl glass, respectively. C1 UNIV GEORGIA,DEPT BIOCHEM,ATHENS,GA 30602. UNIV GEORGIA,COMPLEX CARBOHYDRATE RES CTR,ATHENS,GA 30602. NIDDKD,MED CHEM LAB,BETHESDA,MD 20892. RP POZSGAY, V (reprint author), NICHHD,MOLEC & DEV IMMUN LAB,BLDG 6,RM 145,BETHESDA,MD 20892, USA. NR 29 TC 15 Z9 16 U1 0 U2 2 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0282-0080 J9 GLYCOCONJUGATE J JI Glycoconjugate J. PD APR PY 1993 VL 10 IS 2 BP 133 EP 141 DI 10.1007/BF00737710 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA LQ218 UT WOS:A1993LQ21800002 PM 8400822 ER PT J AU HENDERSON, CE ELIA, G GARFINKEL, D POIRIER, MC SHAMKHANI, H RUNOWICZ, CD AF HENDERSON, CE ELIA, G GARFINKEL, D POIRIER, MC SHAMKHANI, H RUNOWICZ, CD TI PLATINUM CHEMOTHERAPY DURING PREGNANCY FOR SEROUS CYSTADENOCARCINOMA OF THE OVARY SO GYNECOLOGIC ONCOLOGY LA English DT Article ID CIS-DIAMMINEDICHLOROPLATINUM; CARCINOMA; CISPLATIN C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. YESHIVA UNIV ALBERT EINSTEIN COLL MED,JACK D WEILER HOSP,MONTEFIORE MED CTR,BRONX,NY 10461. NR 9 TC 53 Z9 53 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 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD APR PY 1993 VL 49 IS 1 BP 92 EP 94 DI 10.1006/gyno.1993.1092 PG 3 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA LB923 UT WOS:A1993LB92300018 PM 8482567 ER PT J AU MAHAFFEY, JA PARKHURST, MA JAMES, AC CROSS, FT ALAVANJA, MCR BOICE, JD EZRINE, S HENDERSON, P BROWNSON, RC AF MAHAFFEY, JA PARKHURST, MA JAMES, AC CROSS, FT ALAVANJA, MCR BOICE, JD EZRINE, S HENDERSON, P BROWNSON, RC TI ESTIMATING PAST EXPOSURE TO INDOOR RADON FROM HOUSEHOLD GLASS SO HEALTH PHYSICS LA English DT Article DE RADIOACTIVITY, RESIDUAL; RADON DECAY PRODUCTS; EXPOSURE, RADIATION; EPIDEMIOLOGY AB CR-39 plastic was attached to household glass objects to learn whether residual radioactivity from radon decay products could be measured and correlated with cumulative radon exposures over defined time periods. Such an approach could be used to increase the completeness of exposure data collected in epidemiologic studies of residential radon. Inability to estimate radon concentrations for all residences adversely effects statistical power and thus the ability to detect an effect of radon exposure on lung cancer risk. A feasibility study was performed to determine if affixing CR-39 surface monitors to selected glass, ceramic, or enameled objects provided comparable estimates of past residential radon exposure to those obtained from year-long ambient alpha track-etch measurements. The CR-39 measurements of alpha activity in the surface of selected objects correlated with ambient radon measurements (R2 = 0.48) provided that reliable information was obtained on the history and age of the objects. This technique has now been incorporated into an epidemiologic study of radon and lung cancer to more fully estimate past exposure to indoor radon. C1 SURVEY RES ASSOCIATES, BALTIMORE, MD 21209 USA. MISSOURI DEPT HLTH, COLUMBIA, MO 65203 USA. NCI, BETHESDA, MD 20814 USA. SURVEY RES ASSOCIATES, ST LOUIS, MO 63124 USA. RP MAHAFFEY, JA (reprint author), PACIFIC NW LAB, BATTELLE BLVD,POB 999, RICHLAND, WA 99352 USA. FU NCI NIH HHS [Y01-CP0-0054] NR 13 TC 45 Z9 45 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PD APR PY 1993 VL 64 IS 4 BP 381 EP 391 DI 10.1097/00004032-199304000-00005 PG 11 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 LN111 UT WOS:A1993LN11100005 PM 8449720 ER PT J AU TUCKER, MA AF TUCKER, MA TI SOLID 2ND CANCERS FOLLOWING HODGKIN DISEASE SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID MALIGNANT-MELANOMA; DYSPLASTIC NAEVI; LUNG-CANCER; LYMPHOMA; RISK; RADIOTHERAPY; ASSOCIATION C1 NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892. RI Tucker, Margaret/B-4297-2015 NR 29 TC 31 Z9 33 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1993 VL 7 IS 2 BP 389 EP 400 PG 12 WC Oncology; Hematology SC Oncology; Hematology GA KV656 UT WOS:A1993KV65600006 PM 8468272 ER PT J AU SEO, HC WILLEMS, PJ KRETZ, KA MARTIN, BM OBRIEN, JS AF SEO, HC WILLEMS, PJ KRETZ, KA MARTIN, BM OBRIEN, JS TI FUCOSIDOSIS - 4 NEW MUTATIONS AND A NEW POLYMORPHISM SO HUMAN MOLECULAR GENETICS LA English DT Article ID GENE AB Fucosidosis is a rare lysosomal storage disease due to a nearly complete deficiency of alpha-L-fucosidase (EC 3.2.1.51). In this study, all 8 exons of the alpha-L-fucosidase structural gene (FUCA-1) were amplified by PCR methods, and the amplified products were subcloned and sequenced. Five patient groups with fucosidosis were selected according to their ethnic backgrounds and haplotypes for RFLPs in FUCA-1. Four presumptive disease causing mutations were detected: 1) A major deletion of DNA containing the last two exons of FUCA-1 in two Algerian siblings. 2) A G to T mutation in exon 6 resulting in an in-frame termination codon (E375X) in eight Hispanic patients from Colorado and New Mexico. 3) A G to A mutation (G60D) in exon 1 in four Italian patients and in three related French-American (Cajun) patients. This G60D mutation creates a unique site for AflIII. 4) A frameshift mutation resulted from a two-base deletion in exon 2 (K151fs) in an Italian patient. This deletion obliterates a unique BstXI site and creates a new BpmI site, and was found in only this patient and in only one allele. The rationale for proposing these defects as disease causing mutations includes pedigree analysis and the predicted consequences of each defect upon the activity and the concentration of the enzyme. An A to G transition (Q281R) in exon 5 was found to be present in homozygous form in affected patients and also in normal subjects; it appears to be a newly identified polymorphism. It causes a charge change and may be responsible for the electrophoretic variant phenotype of fucosidosis. This polymorphism is inherited concordant with the RFLP PvuII-BgII haplotype 2-2, 2-2. The 4 new mutations identified here comprise 70% of alleles of the 25 fucosidosis patients in our study. C1 UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,CTR MOLEC GENET,LA JOLLA,CA 92093. UNIV INSTELLING ANTWERP,DEPT MED GENET,B-2610 WILRIJK,BELGIUM. STRATAGENE CLONING SYST,LA JOLLA,CA 92037. NIMH,CLIN NEUROSCI BRANCH,MOLEC NEUROGENET SECT,BETHESDA,MD 20892. FU NIDDK NIH HHS [DK07318]; NINDS NIH HHS [NS08682-23A] NR 19 TC 25 Z9 26 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1993 VL 2 IS 4 BP 423 EP 429 DI 10.1093/hmg/2.4.423 PG 7 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA KW632 UT WOS:A1993KW63200014 PM 8504303 ER PT J AU LEAHEY, AM CHARNAS, LR NUSSBAUM, RL AF LEAHEY, AM CHARNAS, LR NUSSBAUM, RL TI NONSENSE MUTATIONS IN THE OCRL-1 GENE IN PATIENTS WITH THE OCULOCEREBRORENAL SYNDROME OF LOWE SO HUMAN MOLECULAR GENETICS LA English DT Note ID POINT MUTATIONS; TRANSLOCATION; POLYMORPHISMS AB A candidate gene, OCRL-1, for the oculocerebrorenal syndrome of Lowe (OCRL) has been identified via positional cloning strategies. We have now developed RT-PCR techniques which allow amplification of nearly all of the open reading frame from total RNA and have used the PCR products for mutational analysis. Single strand conformational polymorphism analysis detected aberrant migration in two unrelated patients, both of whom were shown to have the same nonsense mutation at base 2746 on direct sequencing. An additional patient was found to be missing a segment from his RNA that corresponds to an entire exon. The identification of mutations in the OCRL-1 gene provides strong genetic evidence for its being the gene involved in Lowe syndrome. C1 UNIV PENN,SCH MED,DEPT GENET,PHILADELPHIA,PA 19104. CHILDRENS HOSP PHILADELPHIA,DEPT PEDIAT,DIV HEMATOL & ONCOL,PHILADELPHIA,PA. HOWARD HUGHES MED INST,PHILADELPHIA,PA 19104. NICHHD,HUMAN GENET BRANCH,NEUROGENET UNIT,BETHESDA,MD 20892. FU NCI NIH HHS [T32CA09615]; NICHD NIH HHS [5-R01-HD23245-04] NR 13 TC 51 Z9 52 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1993 VL 2 IS 4 BP 461 EP 463 DI 10.1093/hmg/2.4.461 PG 3 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA KW632 UT WOS:A1993KW63200020 PM 8504307 ER PT J AU POLYMEROPOULOS, MH HONG, XA IDE, SE MERRIL, CR AF POLYMEROPOULOS, MH HONG, XA IDE, SE MERRIL, CR TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE D14S99E LOCUS SO HUMAN MOLECULAR GENETICS LA English DT Article RP POLYMEROPOULOS, MH (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,ROOM 131,2700 MARTIN LUTHER KING AVE,WASHINGTON,DC 20032, USA. NR 2 TC 5 Z9 5 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1993 VL 2 IS 4 BP 490 EP 490 DI 10.1093/hmg/2.4.490 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA KW632 UT WOS:A1993KW63200032 PM 8504315 ER PT J AU WHITE, WB BERSON, AS ROBBINS, C JAMIESON, MJ PRISANT, LM ROCCELLA, E SHEPS, SG AF WHITE, WB BERSON, AS ROBBINS, C JAMIESON, MJ PRISANT, LM ROCCELLA, E SHEPS, SG TI NATIONAL STANDARD FOR MEASUREMENT OF RESTING AND AMBULATORY BLOOD PRESSURES WITH AUTOMATED SPHYGMOMANOMETERS SO HYPERTENSION LA English DT Article DE BLOOD PRESSURE DETERMINATION; BLOOD PRESSURE MONITORS ID EXERCISE AB The Association for the Advancement of Medical Instrumentation develops voluntary standards for medical devices so that manufacturers might provide information on their product and basic safety and performance criteria that should be considered in qualifying the instrument for clinical use. American national standards are generated through a consensus process by committees consisting of experts in research, development, and design from user, industry, and government communities. Draft standards are made available for public review and may become American national standards after review by the American National Standards Institute. The first American national standard for electronic and automated sphygmomanometers was published in monograph form in 1987. The objective of the revised 1992 standard for electronic and automated sphygmomanometers is to provide updated labeling, safety, and performance requirements that help ensure that consumers and health care professionals are supplied with safe, accurate devices for the indirect measurement of blood pressure, including ambulatory blood pressure recorders. This standard permits validation of the automatic or electronic device by comparison with either direct, intra-arterial blood pressure measurements or the noninvasive cuff/stethoscope technique, based on Korotkoff sounds identified by individuals trained in auscultation. This summary report of the 1992 American national standard for automatic sphygmomanometers provides recommendations for the methods of comparison, statistical analysis of the data, presentation of the results, and criteria for acceptability. Users, researchers, and instrument designers should refer to the American national standard monograph for detailed requirements. C1 TYCOS INSTRUMENTS,RES & DEV,ARDEN,NC. NHLBI,NATL HIGH BLOOD PRESSURE EDUC PROGRAM,BETHESDA,MD 20892. MAYO CLIN & MAYO GRAD SCH MED,DIV HYPERTENS,ROCHESTER,MN. NHLBI,DEVICES & TECH BRANCH,BETHESDA,MD 20892. MED COLL GEORGIA,CARDIOL SECT,AUGUSTA,GA 30912. MED COLL GEORGIA,HYPERTENS SECT,AUGUSTA,GA 30912. UNIV TEXAS,HLTH SCI CTR,DIV CLIN PHARMACOL,SAN ANTONIO,TX 78284. MAYO CLIN & MAYO GRAD SCH MED,DIV CARDIOVASC DIS,ROCHESTER,MN. RP WHITE, WB (reprint author), UNIV CONNECTICUT,CTR HLTH,HYPERTENS & VASC DIS SECT,FARMINGTON,CT 06032, USA. NR 14 TC 219 Z9 229 U1 0 U2 10 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD APR PY 1993 VL 21 IS 4 BP 504 EP 509 PG 6 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA KW069 UT WOS:A1993KW06900017 PM 8458649 ER PT J AU SANDBERG, K JI, H CATT, KJ AF SANDBERG, K JI, H CATT, KJ TI DIFFERENTIAL REGULATION OF ANGIOTENSIN-II RECEPTOR SUBTYPES IN THE RAT-BRAIN DURING DIETARY-SODIUM CHANGES SO HYPERTENSION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD APR PY 1993 VL 21 IS 4 BP 530 EP 530 PG 1 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA KW069 UT WOS:A1993KW06900031 ER PT J AU UNSER, M ALDROUBI, A EDEN, M AF UNSER, M ALDROUBI, A EDEN, M TI THE L(2) POLYNOMIAL SPLINE PYRAMID SO IEEE TRANSACTIONS ON PATTERN ANALYSIS AND MACHINE INTELLIGENCE LA English DT Article DE BINOMIAL FILTERS; B-SPLINES; DECIMATION; INTERPOLATION; MULTIGRID METHODS; MULTIRESOLUTION; POLYNOMIAL SPLINES; PYRAMID; RECURSIVE FILTERS; SCALE SPACE; SIGNAL APPROXIMATION; SPLINE FILTERS; WAVELET TRANSFORM ID SCALE-SPACE; INTERPOLATION; ALGORITHMS; REPRESENTATION; SIGNALS; IMAGES AB The first part of this paper is concerned with the derivation of general methods for the L2 approximation of signals by polynomial splines. Such approximations can be represented in a variety of ways using different sets of shift-invariant basis functions (e.g., cardinal, dual, orthogonal or standard B-splines). The main result is that the expansion coefficients of the approximation are obtained by linear filtering and sampling. The second part applies those results to construct a L2 polynomial spline pyramid that is a parametric multiresolution representation of a signal. This hierarchical data structure is generated by repeated application of a REDUCE function (prefilter and down-sampler). A complementary EXPAND function (up-sampler and post-filter) allows a finer resolution mapping of any coarser level of the pyramid. Four equivalent representations of this pyramid are considered, and the corresponding REDUCE and EXPAND filters are determined explicitly for polynomial splines of any order n (odd). Some image processing examples are presented. The present formulation provides a number of interesting links with several other multiresolution techniques including the wavelet transform, scale-space filtering, and Burt's Gaussian and Laplacian pyramids. In particular, we demonstrate that the performance of the Laplacian pyramid can be improved significantly by using a modified EXPAND function associated with the dual representation of a cubic spline pyramid. RP UNSER, M (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892, USA. RI Unser, Michael/A-1550-2008; Aldroubi, Akram/J-7186-2012 NR 44 TC 99 Z9 105 U1 1 U2 5 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 SN 0162-8828 J9 IEEE T PATTERN ANAL JI IEEE Trans. Pattern Anal. Mach. Intell. PD APR PY 1993 VL 15 IS 4 BP 364 EP 379 DI 10.1109/34.206956 PG 16 WC Computer Science, Artificial Intelligence; Engineering, Electrical & Electronic SC Computer Science; Engineering GA KU543 UT WOS:A1993KU54300004 ER PT J AU BAKER, PJ AF BAKER, PJ TI EFFECT OF ENDOTOXIN ON SUPPRESSOR T-CELL FUNCTION SO IMMUNOBIOLOGY LA English DT Article ID III PNEUMOCOCCAL POLYSACCHARIDE; MONOPHOSPHORYL LIPID-A; LOW-DOSE PARALYSIS; ANTIBODY-RESPONSE; B-CELLS; MICE; LIPOPOLYSACCHARIDE; INACTIVATION; LYMPHOCYTES; EXPRESSION RP BAKER, PJ (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK II RES FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 35 TC 8 Z9 8 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0171-2985 J9 IMMUNOBIOLOGY JI Immunobiology PD APR PY 1993 VL 187 IS 3-5 BP 372 EP 381 PG 10 WC Immunology SC Immunology GA LB467 UT WOS:A1993LB46700015 PM 8101179 ER PT J AU MARTICH, GD BOUJOUKOS, AJ SUFFREDINI, AF AF MARTICH, GD BOUJOUKOS, AJ SUFFREDINI, AF TI RESPONSE OF MAN TO ENDOTOXIN SO IMMUNOBIOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; HUMAN SEPTIC SHOCK; INTRAVENOUS ENDOTOXIN; METABOLIC RESPONSE; CARDIOVASCULAR DYSFUNCTION; ACTIVATES NEUTROPHILS; ESCHERICHIA-COLI; FACTOR-ALPHA; LUNG INJURY; INTERLEUKIN-1 AB Endotoxin, a cell wall component of Gram-negative bacteria, plays a central role in the pathogenesis of septic shock. By administering small doses of intravenous endotoxin to humans, a variety of acute inflammatory responses are induced which are qualitatively similar to those that occur during the early stages of septic shock. Within hours of the administration of intravenous endotoxin to human volunteers, changes occur in systemic hemodynamics, ventricular function, pulmonary gas exchange and permeability. In conjunction with these changes in organ function, a wide variety of inflammatory mediators are released which appear to contribute to these responses. These include the release of proinflammatory cytokines (e.g. tumor necrosis factor-alpha, IL-1beta, IL-6, IL-8), activation of the fibrinolytic system, kallikrein-kinin generation and phospholipase A2 release. Phagocytic leukocytes are primed for enhanced inflammatory responses following endotoxin administration. Counter-regulatory responses are initiated in parallel and may serve to limit some of the end-organ responses by the inflammatory mediators. This human model provides a unique opportunity to extend previous concepts of acute inflammation and to evaluate the earliest responses activated after exposure to an important bacterial component. Defining the pathways and responses initiated during acute human endotoxemia may allow a better understanding of host responses that are critical to the development of organ dysfunction and shock due to severe infections. C1 NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,WARREN G MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BLDG 10,BETHESDA,MD 20892. NR 61 TC 209 Z9 214 U1 3 U2 4 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0171-2985 J9 IMMUNOBIOLOGY JI Immunobiology PD APR PY 1993 VL 187 IS 3-5 BP 403 EP 416 PG 14 WC Immunology SC Immunology GA LB467 UT WOS:A1993LB46700017 PM 8330905 ER PT J AU ZHOU, DH CHREST, FJ ADLER, W MUNSTER, A WINCHURCH, RA AF ZHOU, DH CHREST, FJ ADLER, W MUNSTER, A WINCHURCH, RA TI INCREASED PRODUCTION OF TGF-BETA AND IL-6 BY AGED SPLEEN-CELLS SO IMMUNOLOGY LETTERS LA English DT Article DE IMMUNITY; IMMUNOSENESCENCE; CYTOKINE; INTERLEUKIN ID GROWTH FACTOR-BETA; KILLER CELLS; INTERLEUKIN-6; LYMPHOCYTES; PROLIFERATION; INTERFERON AB Aging is accompanied by a progressive decline in immunity in every species that has been studied. Despite its ubiquity, the causes of immunosenescence are unknown. Transforming growth factor beta (TGF-beta) is a cytokine with potent, immunosuppressive properties. Cells from aged mice produce increased levels of TGF-beta in vitro along with similar increases in interleukin 6 (Il-6), a cytokine which is immunosuppressive at elevated concentrations. Il-6 does not upregulate TGF-beta production, but high concentrations of Il-6 increase the percentage of cells expressing the TGF-beta receptor. Increased TGF-beta production and Il-6-induced upregulation of the TGF-beta receptor may be factors contributing to age-associated immunosuppression. C1 JOHNS HOPKINS UNIV,CTR ASTHMA & ALLERGY,SCH MED,5501 HOPKINS BAYVIEW CIRCLE,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,FRANCIS SCOTT KEY MED CTR,SCH MED,BALTIMORE,MD 21218. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 18 TC 31 Z9 32 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD APR PY 1993 VL 36 IS 1 BP 7 EP 12 DI 10.1016/0165-2478(93)90061-6 PG 6 WC Immunology SC Immunology GA LF433 UT WOS:A1993LF43300002 PM 8393837 ER PT J AU FUCHS, E MATZINGER, P AF FUCHS, E MATZINGER, P TI B-CELLS DRIVE DIVERSIFICATION - BUT NOT DIRECTLY SO IMMUNOLOGY TODAY LA English DT Note C1 NIH,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. RP FUCHS, E (reprint author), JOHNS HOPKINS UNIV,CTR ONCOL,RM 3-127,600 N WOLFE ST,BALTIMORE,MD 21287, USA. NR 0 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD APR PY 1993 VL 14 IS 4 BP 153 EP 153 DI 10.1016/0167-5699(93)90275-P PG 1 WC Immunology SC Immunology GA KY243 UT WOS:A1993KY24300004 ER PT J AU METZGER, H AF METZGER, H TI INTERNATIONAL IMMUNOLOGY SO IMMUNOLOGY TODAY LA English DT Editorial Material RP METZGER, H (reprint author), NIAMS,RM 9N-228,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD APR PY 1993 VL 14 IS 4 BP 188 EP 189 PG 2 WC Immunology SC Immunology GA KY243 UT WOS:A1993KY24300013 ER PT J AU DELCARMEN, R PEDERSEN, FA HUFFMAN, LC BRYAN, YE AF DELCARMEN, R PEDERSEN, FA HUFFMAN, LC BRYAN, YE TI DYADIC DISTRESS MANAGEMENT PREDICTS SUBSEQUENT SECURITY OF ATTACHMENT SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE ATTACHMENT; DISTRESS MANAGEMENT; PRENATAL ANXIETY ID INFANT-MOTHER ATTACHMENT; INDIVIDUAL-DIFFERENCES; FAMILY DEVELOPMENT; 1ST YEAR; TEMPERAMENT; CHILDREN; BEHAVIOR; LIFE; RESPONSIVENESS; ASSOCIATIONS AB The purpose of this study was to examine methodologically independent infant, maternal, and dyadic variables to predict security of attachment. The subjects were 52 mothers and their firstborn infants from middle- to upper-middle-class backgrounds. Prenatal assessment of maternal characteristics included measures of depression, anxiety, and self-efficacy. Infant characteristics were assessed via a standardized laboratory procedure at 3 months of age. Dyadic behaviors were observed in the home also at 3 months of age. At 12 months of age, security of attachment was assessed in the Strange Situation procedure. Results indicate that prenatal maternal anxiety and dyadic behaviors involving distress management were the best predictors of security of attachment. This study provides support for the role of maternal characteristics measured in the prenatal period as well as mother-infant dyadic patterns involving distress management in determining subsequent security of attachment. C1 UNIV DELAWARE,NEWARK,DE 19718. PURDUE UNIV,W LAFAYETTE,IN 47907. RP DELCARMEN, R (reprint author), NIMH,CHILD & ADOLESCENT DISORDERS RES BRANCH,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 60 TC 40 Z9 40 U1 1 U2 7 PU ABLEX PUBL CORP PI NORWOOD PA 355 CHESTNUT ST, NORWOOD, NJ 07648 SN 0163-6383 J9 INFANT BEHAV DEV JI Infant Behav. Dev. PD APR-JUN PY 1993 VL 16 IS 2 BP 131 EP 147 DI 10.1016/0163-6383(93)80014-Y PG 17 WC Psychology, Developmental SC Psychology GA LQ452 UT WOS:A1993LQ45200001 ER PT J AU ROILIDES, E UHLIG, K VENZON, D PIZZO, PA WALSH, TJ AF ROILIDES, E UHLIG, K VENZON, D PIZZO, PA WALSH, TJ TI ENHANCEMENT OF OXIDATIVE RESPONSE AND DAMAGE CAUSED BY HUMAN NEUTROPHILS TO ASPERGILLUS-FUMIGATUS HYPHAE BY GRANULOCYTE COLONY-STIMULATING FACTOR AND GAMMA INTERFERON SO INFECTION AND IMMUNITY LA English DT Article ID TUMOR-NECROSIS-FACTOR; CHRONIC GRANULOMATOUS-DISEASE; BONE-MARROW TRANSPLANTATION; RAPID COLORIMETRIC ASSAY; CANDIDA-ALBICANS; POLYMORPHONUCLEAR NEUTROPHILS; FUNGICIDAL ACTIVITY; INVIVO ACTIVATION; RESPIRATORY BURST; HUMAN MACROPHAGES AB Invasive aspergillosis is a serious fungal infection caused by the proliferation and invasion of Aspergillus hyphae in tissue. Neutrophils (PMNs) are the most important line of defense against Aspergillus hyphae. To investigate the role of granulocyte colony-stimulating factor (G-CSF) and gamma interferon (IFN-gamma) against Aspergillus fumigatus, we studied the effects of the two cytokines on the oxidative burst and the capacity of normal human PMNs to damage hyphae of the organism. G-CSF enhanced PMN oxidative burst measured as superoxide anion (O2-) production in response to N-formylmethionyl leucyl phenylalanine, serum opsonized hyphae, and nonopsonized hyphae by 75, 37, and 24%, respectively, compared with control PMNs (P < 0.015). IFN-gamma also induced increases of 52, 71, and 96%, respectively, in response to the same stimuli (P < 0.006). In addition, the capacity of PMNs to damage hyphae as measured by the 3-4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MMT) colorimetric metabolic assay was significantly enhanced by G-CSF and IFN-gamma (P < 0.01 and < 0.05, respectively). The enhancement was achieved irrespective of serum opsonization of the hyphae, suggesting upregulatory actions of the two cytokines on signal pathways specific for opsonized and nonopsonized hyphae. The combination of the two cytokines exhibited an additive effect at the higher concentrations compared with the effects of the cytokines alone (P < 0.05). Pretreatment of PMNs with protein synthesis inhibitors showed that IFN-gamma activates PMN function through transcriptional regulation, whereas the effect of G-CSF does not require new proteins. These in vitro effects suggest modulatory roles for G-CSF and IFN-gamma in the host defense against Aspergillus hyphae irrespective of serum opsonization and a potential utility of the cytokines as adjuncts for the prevention and possible treatment of invasive aspergillosis. C1 NCI,INFECT DIS SECT,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 49 TC 163 Z9 167 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 APR PY 1993 VL 61 IS 4 BP 1185 EP 1193 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KU320 UT WOS:A1993KU32000004 PM 7681040 ER PT J AU CHEEVER, AW XU, YH SHER, A FINKELMAN, FD COX, TM MACEDONIA, JG AF CHEEVER, AW XU, YH SHER, A FINKELMAN, FD COX, TM MACEDONIA, JG TI SCHISTOSOMA-JAPONICUM-INFECTED MICE SHOW REDUCED HEPATIC-FIBROSIS AND EOSINOPHILIA AND SELECTIVE-INHIBITION OF INTERLEUKIN-5 SECRETION BY CD4+- CELLS AFTER TREATMENT WITH ANTI-INTERLEUKIN-2 ANTIBODIES SO INFECTION AND IMMUNITY LA English DT Article ID SOLUBLE EGG ANTIGEN; GRANULOMA-FORMATION; IL-2; MANSONI; INVIVO; DEFICIENCY; PATTERNS; CULTURES AB Schistosoma japonicum-infected mice were injected with antibodies to interleukin-2 (IL-2) and/or IL-2 receptor to clarify the role of IL-2 on the granulomatous reaction around schistosome eggs in the liver. Granulomas were of normal or slightly increased size in animals subjected to IL-2 blockade, but hepatic fibrosis was markedly decreased in treated animals 10 weeks after infection. Anti-IL-2 treatment significantly decreased the in vitro secretion of IL-5 by antigen-stimulated spleen cells, and peripheral eosinophilia and tissue eosinophilia were diminished. Secretion of IL-2, IL-4, and gamma interferon was unaffected. Our results indicate that IL-2 is not an essential determinant of granuloma size in S. japonicum-infected mice but that, as in Schistosoma mansoni infection, the development of hepatic fibrosis is critically dependent on IL-2 levels and granuloma size and hepatic fibrosis are differentially regulated. C1 UNIFORMED SERV UNIV HLTH SCI,F EDWARD HEBERT SCH MED,DEPT MED,BETHESDA,MD 20814. RP CHEEVER, AW (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI 052590] NR 24 TC 12 Z9 12 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1993 VL 61 IS 4 BP 1288 EP 1292 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KU320 UT WOS:A1993KU32000017 PM 8095922 ER PT J AU WHITMIRE, WM GARON, CF AF WHITMIRE, WM GARON, CF TI SPECIFIC AND NONSPECIFIC RESPONSES OF MURINE B-CELLS TO MEMBRANE BLEBS OF BORRELIA-BURGDORFERI SO INFECTION AND IMMUNITY LA English DT Article ID LYME-DISEASE SPIROCHETE; CHROMOSOMAL GENE; SURFACE PROTEIN; T-CELL; ARTHRITIS; ANTIGEN; LIPOPOLYSACCHARIDE; INTERLEUKIN-1; MICE; IGM AB Lymphocyte blastogenesis assays and immunoblotting were used to investigate and compare murine B-cell responses to preparations of extracellular membrane blebs (BAg) and spirochetes (Ag) of Borrelia burgdorferi. Immunoblotting BAg, Ag, and medium control preparations with serum from naive and infected C57BL/10 mice revealed that BAg and Ag had similar specific reactivity profiles except that major antigens of 83, 60, and 41 kDa were detected in Ag but not in BAg. It was determined that 1 mug (dry weight) of Ag contained 0.0051 and 0.0063 mug of outer surface proteins A (OspA) and OspB, respectively, whereas 1 mug (dry weight) of BAg contained 0.0024 mug of OspA and 0.0015 mug of OspB. Both BAg and Ag caused blastogenesis in cultures of spleen cells from both groups of mice, but BAg-stimulated lymphocytes exhibited significantly greater (P less-than-or-equal-to 0.05) blastogenesis after 2 or 6 days of culture than did lymphocytes stimulated by Ag or medium control. Flow cytometry and antibody capture enzyme-linked immunosorbent assays identified responding lymphocytes as B cells which secreted polyclonal immunoglobulin M (IgM) but not IgG or IgA. Treatment of BAg and lipopolysaccharide controls with polymyxin B resulted in as much as 20.7 and 54.3% mean decreases in blastogenesis, respectively. Fractionation of BAg or Ag by ultracentrifugation before culture with spleen cells from naive mice indicated that B-cell blastogenesis was probably associated with spirochetal membranes. The results of this study demonstrate that specific humoral responses are directed towards extracellular membrane blebs which lack the 83-, 60-, and 41-kDa antigens of intact spirochetes and that blebs also possess significant nonspecific mitogenic activity for murine B cells. This activity was not due entirely to typical lipopolysaccharide or OspA and OspB lipoproteins. RP WHITMIRE, WM (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA. NR 40 TC 68 Z9 68 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1993 VL 61 IS 4 BP 1460 EP 1467 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KU320 UT WOS:A1993KU32000043 PM 8454350 ER PT J AU BEEKMANN, SE OSTERHOLM, MT HENDERSON, DK AF BEEKMANN, SE OSTERHOLM, MT HENDERSON, DK TI TUBERCULOSIS IN THE HEALTH-CARE SETTING IN THE 1990S - FROM BIRD ISLAND TO THE BRONX SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article C1 MINNESOTA DEPT HLTH,ACUTE DIS EPIDEMIOL SECT,MINNEAPOLIS,MN. NIH,HOSP EPIDEMIOL SERV,BETHESDA,MD 20892. NIH,OFF DIRECTOR,BETHESDA,MD 20892. RP BEEKMANN, SE (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,BLDG 10,ROOM 4A-21,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 12 TC 9 Z9 9 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD APR PY 1993 VL 14 IS 4 BP 228 EP 232 PG 5 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA KW584 UT WOS:A1993KW58400016 PM 8478546 ER PT J AU KING, CL NUTMAN, TB AF KING, CL NUTMAN, TB TI CYTOKINES AND IMMEDIATE HYPERSENSITIVITY IN PROTECTIVE IMMUNITY TO HELMINTH INFECTIONS SO INFECTIOUS AGENTS AND DISEASE-REVIEWS ISSUES AND COMMENTARY LA English DT Article DE CYTOKINES; HELMINTHS; IMMEDIATE HYPERSENSITIVITY; EOSINOPHILIA; IGE; MAST CELL ID SCHISTOSOMA-MANSONI INFECTION; HUMAN FILARIASIS; IGE RESPONSES; IMMUNOLOGICAL RESPONSES; PARASITE ANTIGEN; MAST-CELLS; RESISTANCE; EOSINOPHIL; REINFECTION; RESPONSIVENESS AB Infection with tissue-invasive helminth infections characteristically induces immunological responses associated with immediate hypersensitivity such as IgE elevations, tissue and peripheral blood eosinophilia, and mast cell hyperplasia. Specific sets of cytokines appear to regulate these responses; the resulting responses reflect the balance of upregulatory and inhibitory signals these cytokines provide. The nature of these cytokines and their role in both protective immunity and pathogenesis in helminth infections of humans is the subject of this review. C1 NIH,PARASIT DIS LAB,BLDG 4 ROOM 126,BETHESDA,MD 20892. CASE WESTERN RESERVE UNIV,SCH MED,DIV GEOG MED,CLEVELAND,OH 44106. NR 47 TC 8 Z9 8 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1056-2044 J9 INFECT AGENT DIS JI Infect. Agents Dis.-Rev. Issues Comment. PD APR PY 1993 VL 2 IS 2 BP 103 EP 108 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA LH704 UT WOS:A1993LH70400005 PM 8162355 ER PT J AU NUSSINOV, R AF NUSSINOV, R TI STRONG SEQUENCE PATTERNS IN EUKARYOTIC PROMOTER REGIONS - POTENTIAL IMPLICATIONS FOR DNA-STRUCTURE SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY LA English DT Article ID HOMOOLIGOMER TRACTS; BASE SEQUENCE; B-DNA; CONFORMATION; DEPENDENCE; CHROMATIN; SIGNALS; ORIGIN; SITES AB 1. Analysis of eukaryotic sequences reveals recurring trends in upstream regions. Oligomers composed of (G/C)n and (A/T)m blocks are preferentially flanked by (G/C)2 doublets on their 3' rather than on their 5' ends, that is (G/C)n(A/T)m(G/C)2 > (G/C)n+2(A/T)m. 2. These trends are stronger for larger n and smaller m. Additional trends are outlined below. 3. The trends are correlated with DNA structural parameters, in particular with twist and roll angles. 4. Generally, the trends hold if the base pair step joining the 5' (G/C)2 doublet to the (G/C)n (A/T)m oligomer is not undertwisted and is not strongly rolled into the major groove. 5. Other DNA parameters crucial for DNA-protein interactions are discussed as well. C1 TEL AVIV UNIV,SACKLER FAC MED,SACKLER INST MOLEC MED,IL-69978 TEL AVIV,ISRAEL. RP NUSSINOV, R (reprint author), DYNCORP,PRI,NCI,FREDERICK CANC RES & DEV CTR,MATH BIOL LAB,POB B,BLDG 469,RM 151,FREDERICK,MD 21702, USA. FU NCI NIH HHS [1-CO-74102] NR 22 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 0020-711X J9 INT J BIOCHEM JI Int. J. Biochem. PD APR PY 1993 VL 25 IS 4 BP 597 EP 607 DI 10.1016/0020-711X(93)90669-6 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KV208 UT WOS:A1993KV20800019 PM 8467958 ER PT J AU ROBBINS, PF EGGENSPERGER, D QI, CF SCHLOM, J AF ROBBINS, PF EGGENSPERGER, D QI, CF SCHLOM, J TI DEFINITION OF THE EXPRESSION OF THE HUMAN CARCINOEMBRYONIC ANTIGEN AND NONSPECIFIC CROSS-REACTING ANTIGEN IN HUMAN BREAST AND LUNG CARCINOMAS SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID MONOCLONAL-ANTIBODIES; IMMUNOHISTOCHEMICAL EVALUATION; PULMONARY ADENOCARCINOMA; DIFFERENTIAL EXPRESSION; PLEURAL MESOTHELIOMA; HUMAN MAMMARY; GENE FAMILY; CEA; TUMORS; EPITOPES AB Mouse cell lines transfected with carcinoembryonic antigen (CEA) and with 2 other members of the human CEA gene family, non-specific cross-reacting antigen (NCA) and biliary glycoprotein (BGP), were used to analyze the specificity of several monoclonal antibodies (MAbs). MAbs COL-1 and COL-6 were shown to react with the transfected CEA gene product but not with NCA, confirming previous results. Cells expressing the transfected BGP gene product also failed to react with COL-1 and COL-6. The MAb B6.2 reacted with cells expressing the NCA gene product but not with those expressing CEA or BGP. The MAb B1.1 reacted strongly with the transfected CEA and BGP gene products but only weakly with the NCA gene product. These antibodies were then utilized in the histochemical analysis of a number of primary and secondary breast and lung tumors. The results indicate that a majority of breast and lung tumors express CEA, and nearly all breast and lung tumors express NCA. Fairly homogeneous expression of CEA and NCA was seen in the majority of both breast and lung tumors. Our results indicate that CEA may be an important target for immunotherapy in a large number of patients with breast and lung tumors. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BLDG 10,ROOM 8B07,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 34 TC 41 Z9 41 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 1 PY 1993 VL 53 IS 6 BP 892 EP 897 PG 6 WC Oncology SC Oncology GA KW597 UT WOS:A1993KW59700003 PM 8386136 ER PT J AU KOHN, EC HOLLISTER, GH DIPERSIO, JD WAHL, S LIOTTA, LA SCHIFFMANN, E AF KOHN, EC HOLLISTER, GH DIPERSIO, JD WAHL, S LIOTTA, LA SCHIFFMANN, E TI GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR INDUCES HUMAN MELANOMA-CELL MIGRATION SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID GM-CSF RECEPTORS; ENDOTHELIAL-CELLS; METASTATIC CELLS; TUMOR-CELLS; PROTEINS; NEUTROPHILS; PURIFICATION; CLONING AB Tumor metastasis is the primary cause of death for cancer patients. The metastatic cascade requires successful tumor cell invasion into and through vascular and parenchymal barriers. We have shown that autocrine motility factor (AMF, autotaxin) and the insulin-like growth factors (IGFs) induce tumor-cell migration. Since granulocyte-macrophage colony-stimulating factor (GM-CSF) has been shown to prime neutrophils for chemotaxis, we have therefore studied the influence of GM-CSF upon tumor cells and report that GM-CSF stimulates migration of these cells in a dose-dependent fashion. The ED50 for A2058 human melanoma cell line chemotaxis to GM-CSF is approx. 60 pM. The motile response to GM-CSF was additive to that of IGF-I and AMF, both of which are potent attractants for tumor cells. Pre-treatment of cells for 2 hr with non-toxic concentrations of pertussis toxin (PT) or amiloride resulted in a 50% inhibition of chemotaxis to GM-CSF. Therefore, GM-CSF, through PT- and amiloride-sensitive signal pathways, is a potent attractant for melanoma cells, the response to which is additive to that of other attractants. The presence of the GM-CSF receptor in A2058 melanoma cells was indicated by Northern-blot analysis which identified message transcripts of 2.1 and 3.0 kb. These data emphasize the versatility of the melanoma cell migration response to an array of cytokines, including GM-CSF. C1 NIDR,BETHESDA,MD 20892. UNIV ROCHESTER,SCH MED,SAMUEL E DURAND BONE MARROW TRANSPLANT CTR,ROCHESTER,NY 14627. NCI,PATHOL LAB,BETHESDA,MD 20892. RP KOHN, EC (reprint author), NCI,MED BRANCH,BLDG 10,RM 2A33,BETHESDA,MD 20892, USA. NR 24 TC 27 Z9 27 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 1 PY 1993 VL 53 IS 6 BP 968 EP 972 PG 5 WC Oncology SC Oncology GA KW597 UT WOS:A1993KW59700017 PM 8473054 ER PT J AU WU, J SHIVER, J HARGROVE, ME TING, CC AF WU, J SHIVER, J HARGROVE, ME TING, CC TI ROLE OF PROTEIN-KINASE-C AND CYTOKINES ON THE FUNCTION AND PRODUCTION OF CYTOLYTIC GRANULES IN ALPHA-CD3-ACTIVATED KILLER-CELL-MEDIATED KILLING OF TUMOR-CELLS SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID TOXIC LYMPHOCYTES-T; STIMULATORY FACTOR; CYTOPLASMIC GRANULES; CYTO-TOXICITY; TARGET-CELLS; ANTIBODY; ACTIVATION; INHIBITOR AB The effects of PMA and staurosporine (PKC depletor/antagonist) and IL-2/IL4 were used to determine the role of PKC and cytokine on alphaCD3-induced activated killer cells (CD3-AK). The present study examines their effects on the production of BLT-esterase and on the effector function of CD3-AK cells as well as the cytolytic granules. The production of BLT-esterase generally correlated with the cytolytic activity of CD3-AK cells and was reduced by PKC depletor/inhibitor but increased by IL4. In studying the effector function of CD3-AK cells, we found that adding PMA or SSP at the effector phase inhibited the PKC-dependent slow lysis. PMA, but not SSP, also reduced fast lysis, which was shown to be a PKC-independent event. Additional experiments were performed to determine the effect of PKC on the lytic granules and to ascertain whether PMA has other effects on the effector-to-target relationship unrelated to PKC. It was found that neither PMA nor SSP affects the function of cytolytic granules, as measured by hemolytic assay against anucleated target (SRBC). These findings indicate that PKC has no direct effect on the granules. During testing against the nucleated tumor target through a novel approach using non-cytolytic surrogate killers, the lytic activity of the granules was inhibited by PMA, suggesting that exocytosis or delivery of granules to nucleated target cells may require mobilization of intracellular Ca2+ in the killer cells, and this process is inhibited by PMA. Our findings indicate that PKC and cytokines regulate the production but not the lytic activity of cytolytic granules. Nonetheless, delivery of cytolytic granules from killer cells to the nucleated tumor target appears to be a Ca2+-dependent event unrelated to PKC. C1 NCI,OFF DIRECTOR,BLDG 10,ROOM 4B17,BETHESDA,MD 20892. NCI,DIV CELL BIOL DIAGNOSIS & CTR,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 22 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 1 PY 1993 VL 53 IS 6 BP 973 EP 977 PG 5 WC Oncology SC Oncology GA KW597 UT WOS:A1993KW59700018 PM 8473055 ER PT J AU ANDRADE, ZA CHEEVER, AW AF ANDRADE, ZA CHEEVER, AW TI CHARACTERIZATION OF THE MURINE MODEL OF SCHISTOSOMAL HEPATIC PERIPORTAL FIBROSIS (PIPESTEM FIBROSIS) SO INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY LA English DT Article DE PIPESTEM FIBROSIS; EXPERIMENTAL SCHISTOSOMIASIS; SCHISTOSOMAL GRANULOMA; SCHISTOSOMA-MANSONI; SCHISTOSOMA-JAPONICUM AB During mild (one to two pairs of worms) and prolonged (23 weeks or more) mouse infections with Schistosoma mansoni, but not with S. japonicum, periovular granulomas and fibrosis were seen to be preferentially located along periportal tissues. This caused fibrotic expansion of the portal spaces on a background of normal-looking hepatic parenchyma, a picture mimicking 'clay pipestem fibrosis' seen in human patients with advanced schistosomiasis. The model was reproduced in outbred and in several strains of inbred mice, and their main characteristics were studied and compared to the human counterpart. A balanced consideration of the similarities and differences between the murine model and human pipestem fibrosis is needed for the adequate utilization of this simple, reproducible and inexpensive experimental model. C1 NIAID, PARASIT DIS LAB, BETHESDA, MD 20892 USA. FIOCRUZ MS, GONCALO MONIZ RES CTR, BR-41945 SALVADOR, BRAZIL. NR 23 TC 26 Z9 26 U1 0 U2 1 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0959-9673 EI 1365-2613 J9 INT J EXP PATHOL JI Int. J. Exp. Pathol. PD APR PY 1993 VL 74 IS 2 BP 195 EP 202 PG 8 WC Pathology SC Pathology GA KW707 UT WOS:A1993KW70700010 PM 8499320 ER PT J AU WHITCOMB, RF TULLY, JG ROSE, DL CARLE, P BOVE, JM HENEGAR, RB HACKETT, KJ CLARK, TB KONAI, M ADAMS, J WILLIAMSON, DL AF WHITCOMB, RF TULLY, JG ROSE, DL CARLE, P BOVE, JM HENEGAR, RB HACKETT, KJ CLARK, TB KONAI, M ADAMS, J WILLIAMSON, DL TI SPIROPLASMA-MONOBIAE SP-NOV FROM THE VESPID WASP MONOBIA-QUADRIDENS (HYMENOPTERA, VESPIDAE) SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID CLASSIFICATION; MYCOPLASMAS; DEFORMATION; TAXONOMY; FLOWERS; DISEASE AB Spiroplasma strain MQ-1T (T = type strain) from the hemolymph of the vespid wasp Monobia quadridens differed serologically from other spiroplasma species, groups, and subgroups. Cells of strain MQ-1T were helical and motile and possessed a single cytoplasmic membrane, with no evidence of a cell wall. The organism grew in conventional mycoplasma medium, in serum fraction, SM-1, MID, and SP-4 liquid media, and on SP-4 solid medium in either aerobic or anaerobic environments. The optimum temperature for growth was 32-degrees-C, but multiplication occurred over a wide temperature range (10 to 37-degrees-C). The doubling time at 32-degrees-C in M1D medium was 1.9 h. Strain MQ-1T catabolized glucose but hydrolyzed neither arginine nor urea. Previous work showed that strain MQ-1T has a unique methylase, previously known only in eucaryotes. Also, strain MQ-1T induces production of tumor necrosis factor in bone marrow macrophages. The guanine-plus-cytosine content of the DNA was 28 +/- 1 mol%. The genome size of strain MQ-1T was 940 kb (627 MDa); a similar strain, MQ-8, had a genome size of 985 kb (657 MDa). Strain MQ-1T and its allies have the smallest genomes known in the genus Spiroplasma. Strain MQ-1 (= ATCC 33825) is designated the type strain of a new species, Spiroplasma monobiae. C1 SUNY STONY BROOK,DEPT ANAT SCI,STONY BROOK,NY 11794. NIAID,FREDERICK CANC RES FACIL,MOLEC MICROBIOL LAB,MYCOPLASMA SECT,FREDERICK,MD 21702. INRA,BIOL CELLULAIRE & MOLEC LAB,F-33883 VILLENAVE DORNON,FRANCE. RP WHITCOMB, RF (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705, USA. NR 37 TC 4 Z9 5 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1993 VL 43 IS 2 BP 256 EP 260 PG 5 WC Microbiology SC Microbiology GA KX917 UT WOS:A1993KX91700010 ER PT J AU WHITCOMB, RF VIGNAULT, JC TULLY, JG ROSE, DL CARLE, P BOVE, JM HACKETT, KJ HENEGAR, RB KONAI, M WILLIAMSON, DL AF WHITCOMB, RF VIGNAULT, JC TULLY, JG ROSE, DL CARLE, P BOVE, JM HACKETT, KJ HENEGAR, RB KONAI, M WILLIAMSON, DL TI SPIROPLASMA-CLARKII SP-NOV FROM THE GREEN JUNE BEETLE (COLEOPTERA, SCARABAEIDAE) SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID CLASSIFICATION; TAXONOMY AB Spiroplasma strain CN-5T (T = type strain), isolated from the gut of the cetoniine scarabaeid beetle Cotinus nitida, was serologically distinct from other spiroplasma species, groups, and subgroups. Cells of strain CN-5T were shown by light microscopy to be helical, motile filaments. Cells in early passages exhibited strong translational motility that tended to be lost in later passages. Electron microscopy showed that the cells were bounded by a single cytoplasmic membrane with no evidence of a cell wall. The organism was not susceptible to penicillin. Strain CN-5T grew well in SM-1, M1D, and SP-4 liquid media and on solid SP4 medium under aerobic or anaerobic conditions. The doubling time at 30-degrees-C, the optimum temperature, was 4.3 h. The strain also grew in 1% serum fraction medium. Strain CN-5T produced acid from glucose and catabolized arginine, but did not hydrolyze urea. The guanine-plus-cytosine content of the DNA was 29 +/- 1 mol%. The genome size was 1,770 kb (1,186 MDa). Other uncloned isolates obtained from C. nitida or the cetoniine hermit flower beetle Osmoderma eremicola exhibited similar or identical serological patterns. Since no other hosts were discovered in extensive studies, strain CN-5T (previously designated group IX) appears to represent a cluster of relatively host-specific cetoniine beetle-associated strains. Strain CN-5 (= ATCC 33827) is designated the type strain of a new species, Spiroplasma clarkii. C1 SUNY STONY BROOK,DEPT ANAT SCI,STONY BROOK,NY 11794. INRA,BIOL CELLULAIRE & MOLEC LAB,F-33883 VILLENAVE DORNON,FRANCE. NIAID,FREDERICK CANC RES FACIL,MOLEC MICROBIOL LAB,MYCOPLASMA SECT,FREDERICK,MD 21702. RP WHITCOMB, RF (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705, USA. NR 33 TC 3 Z9 3 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1993 VL 43 IS 2 BP 261 EP 265 PG 5 WC Microbiology SC Microbiology GA KX917 UT WOS:A1993KX91700011 ER PT J AU HACKETT, KJ WHITCOMB, RF TULLY, JG ROSE, DL CARLE, P BOVE, JM HENEGAR, RB CLARK, TB CLARK, EA KONAI, M ADAMS, JR WILLIAMSON, DL AF HACKETT, KJ WHITCOMB, RF TULLY, JG ROSE, DL CARLE, P BOVE, JM HENEGAR, RB CLARK, TB CLARK, EA KONAI, M ADAMS, JR WILLIAMSON, DL TI SPIROPLASMA-INSOLITUM SP-NOV, A NEW SPECIES OF GROUP-I SPIROPLASMA WITH AN UNUSUAL DNA-BASE COMPOSITION SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID HOST-PARASITE RELATIONSHIPS; CLASSIFICATION; MYCOPLASMAS; DEFORMATION; METABOLISM; DIVERSITY; TAXONOMY; DISEASE AB Spiroplasma strain M55, isolated from a fall flower in Maryland, showed patterns of partial serological cross-reactivity with the other seven group I spiroplasma subgroups but was not serologically related to other spiroplasma groups. Strain M55 had less than 70% DNA-DNA homology with group I subgroups previously assigned binomial names and was unique among the group I subgroups in possessing a higher guanine-plus-cytosine content in its DNA (28 +/- 1 mol%, versus 26 +/- 1 mol% for other group I subgroups). The genome size was 1,850 kb (1,233 MDa). Extensive data on the metabolism of strain M55 and the community ecology of this and similar strains have been reported. These circumstances fulfill criteria proposed by the Subcommittee on the Taxonomy of Mollicutes for elevation of mollicute subgroups to species status. Accordingly, strain M55 was characterized according to proposed minimal standards for species descriptions. Cells of strain M55 were shown by light microscopy to be helical, motile filaments. Electron microscopy showed that the cells possessed no cell wall and were bounded by a single membrane; they were insensitive to penicillin (1,000 U/ml). Strain M55 was culturable in MlD and SP-4 liquid media under aerobic (with or without enhanced carbon dioxide) or anaerobic environments. Optimal growth occurred at 30-degrees-C, with a doubling time of 7.2 h. Growth occurred from 15 to 37-degrees-C but not at 10 or 42-degrees-C. Strain M55 did not utilize urea or hydrolyze arginine but did produce acid from glucose. As a consequence of these studies, strain M55 is designated the type strain (M55T;ATCC 33502T) of a new species, Spiroplasma insolitum. C1 NIAID,FREDERICK CANC RES FACIL,MOLEC MICROBIOL LAB,MYCOPLASMA SECT,FREDERICK,MD 21702. INRA,BIOL CELLULAIRE & MOLEC LAB,F-33883 VILLENAVE DORNON,FRANCE. SUNY STONY BROOK,DEPT ANAT SCI,STONY BROOK,NY 11794. RP HACKETT, KJ (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705, USA. NR 44 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1993 VL 43 IS 2 BP 272 EP 277 PG 6 WC Microbiology SC Microbiology GA KX917 UT WOS:A1993KX91700013 ER PT J AU GASPARICH, GE SAILLARD, C CLARK, EA KONAI, M FRENCH, FE TULLY, JG HACKETT, KJ WHITCOMB, RF AF GASPARICH, GE SAILLARD, C CLARK, EA KONAI, M FRENCH, FE TULLY, JG HACKETT, KJ WHITCOMB, RF TI SEROLOGIC AND GENOMIC RELATEDNESS OF GROUP-VIII AND GROUP-XVII SPIROPLASMAS AND SUBDIVISION OF SPIROPLASMA GROUP-VIII INTO SUBGROUPS SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID CLASS MOLLICUTES; GENUS; CLASSIFICATION; MOSQUITOS; TABANIDAE AB Spiroplasmas are currently classified in a group system. Criteria for separation of the twenty-four currently designated groups include serologic relatedness, polyacrylamide gel electrophoretic patterns of proteins, guanine-plus-cytosine base ratios, and, in some cases, DNA-DNA homology. The analysis of DNA-DNA homology and serologic data from a large array of strains recently discovered in dipteran insects reveals that group VIII strain EA-1 from a syrphid fly, strain TAAS-1 from a horse fly, and group XVII strain DF-1 from a deer fly belong to a large complex (supergroup) of strains with various degrees of interrelatedness. Strains DF-1 and EA-1 share DNA-DNA homology of 33 to 48% (high-stringency conditions), while strain TAAS-1 shares 42 to 67% homology with DF-I and EA-1. The strains had temperature optima of 30 to 37-degrees-C, but the temperature minima and maxima reflected the geographic region of strain origin. These three strains also share G+C values of about 30 mol%, utilize arginine, and tend to grow in culture to very high titers (10(11) cells per ml). The helical cells of these strains are smaller than those of other spiroplasmas and readily pass through filter pores of 220 nm. These data support the taxonomic placement of the biotypes represented by strains EA-1, DF-1, and TAAS-1 into one supergroup, group VIII, with subgroups designated as VIII-1, VIII-2, and VIII-3, respectively. It is proposed that group XVII remain vacant. C1 NIAID,FREDERICK CANC RES CTR,MYCOPLASMA SECT,FREDERICK,MD 21702. INRA,CELLULAIRE & MOLEC BIOL LAB,F-33883 VILLENAVE DORNON,FRANCE. GEORGIA SO UNIV,DEPT BIOL,STATESBORO,GA 30460. RP GASPARICH, GE (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,INST PLANT SCI,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705, USA. NR 27 TC 19 Z9 19 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1993 VL 43 IS 2 BP 338 EP 341 PG 4 WC Microbiology SC Microbiology GA KX917 UT WOS:A1993KX91700023 ER PT J AU ABALAINCOLLOC, ML WILLIAMSON, DL CARLE, P ABALAIN, JH BONNET, F TULLY, JG KONAI, M WHITCOMB, RF BOVE, JM CHASTEL, C AF ABALAINCOLLOC, ML WILLIAMSON, DL CARLE, P ABALAIN, JH BONNET, F TULLY, JG KONAI, M WHITCOMB, RF BOVE, JM CHASTEL, C TI DIVISION OF GROUP-XVI SPIROPLASMAS INTO SUBGROUPS SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID CLASS MOLLICUTES; CLASSIFICATION; FRANCE; GENUS; MOSQUITOS; DISEASE AB Some group XVI spiroplasmas, such as strains CC-1 (Spiroplasma cantharicola) and CB-1, are associated with cantharid beetles. Fifteen related but heterogeneous strains have been isolated from mosquitoes, other insects, and a flower in France and the United States. In the present study, these seventeen strains have been compared by deformation and metabolism inhibition serological tests, by one-dimensional protein sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and by determination of the guanine-plus-cytosine content of their DNA. Five of the 17 strains were further compared by DNA-DNA hybridization and by restriction enzyme (EcoRI and HindIII) analysis of their DNA. On the basis of the resulting data, we propose that group XVI be subdivided into three subgroups. Subgroup XVI-I is represented by strain CC-1 (ATCC 43207) from a cantharid beetle in the United States, and strain MQ-6 from a wasp; subgroup XVI-2 is represented by strain CB-1 (ATCC 43208) from a cantharid beetle and two strains from mosquitoes, all in the United States; and subgroup XVI-3 is represented by strain Ar-1357 (ATCC 51126) and contains 11 strains from mosquitoes and 1 strain from a flower, all from the Savoy region of France. C1 USDA ARS,BELTSVILLE AGR RES CTR,INST PLANT PROTECT,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705. FAC MED BREST,BIOCHIM LAB,F-29285 BREST,FRANCE. INRA,BIOL CELLULAIRE & MOLEC LAB,F-33883 VILLENAVE DORNON,FRANCE. UNIV BORDEAUX 2,F-33883 VILLENAVE DORNON,FRANCE. SUNY HLTH SCI CTR STONY BROOK,DEPT ANAT SCI,STONY BROOK,NY 11794. NIAID,FREDERICK CANC RES CTR,MOLEC MICROBIOL LAB,MYCOPLASMA SECT,FREDERICK,MD 21701. RP ABALAINCOLLOC, ML (reprint author), FAC MED BREST,BACTERIOL LAB,22 AVE CAMILLE DESMOULINS,F-29285 BREST,FRANCE. NR 26 TC 19 Z9 19 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1993 VL 43 IS 2 BP 342 EP 346 PG 5 WC Microbiology SC Microbiology GA KX917 UT WOS:A1993KX91700024 ER PT J AU TULLY, JG BOVE, JM LAIGRET, F WHITCOMB, RF AF TULLY, JG BOVE, JM LAIGRET, F WHITCOMB, RF TI REVISED TAXONOMY OF THE CLASS MOLLICUTES - PROPOSED ELEVATION OF A MONOPHYLETIC CLUSTER OF ARTHROPOD-ASSOCIATED MOLLICUTES TO ORDINAL RANK (ENTOMOPLASMATALES ORD NOV), WITH PROVISION FOR FAMILIAL RANK TO SEPARATE SPECIES WITH NONHELICAL MORPHOLOGY (ENTOMOPLASMATACEAE FAM NOV) FROM HELICAL SPECIES (SPIROPLASMATACEAE), AND EMENDED DESCRIPTIONS OF THE ORDER MYCOPLASMATALES, FAMILY MYCOPLASMATACEAE SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Note ID STEROL-REQUIRING MOLLICUTE; FIELD ELECTROPHORESIS; ACHOLEPLASMA; CLASSIFICATION; TRYPTOPHAN; DISEASE; PLANTS; GOATS; UGA AB On the basis of recent phylogenetic studies of 47 species within the class Mollicutes and recent molecular and physiologic findings that distinguish a new group of non-sterol-requiring insect and plant mollicutes from Achokplasma species, we propose a revised taxonomy of the class Mollicutes. Order I (Mycoplasmataks) is retained as described earlier (S. Razin and E. A. Freundt, p. 740-742, in N. R. Krieg and J. G. Holt, ed., Bergey's Manual of Systematic Bacteriology, vol. 1, 1984), with provision for a single family (Mycoplasmataceae) and two genera (Mycoplasma and Ureaplasma) for classification of sterol-requiring mollicutes primarily associated with vertebrates. Emended descriptions of the order and family for the above taxa are hereby included. Proposed order II (Entomoplasmatales ord. nov.) contains subtaxa for either nonhelical (Entomoplasmataceae fam. nov.) or helical (Spiroplasmataceae) mollicutes; the latter family is hereby transferred from the order Mycoplasmataks. The new order and family permit designation and classification of a monophyletic cluster of mollicute strains associated primarily with arthropods. It is proposed that nonhelical, sterol-requiring insect and plant mollicutes previously designated Mycoplasma ellychniae (Tully et al., 1989), Mycoplasma melaleucae (Tully et al., 1990), Mycoplasma somnilux (Williamson et al., 1990), Mycoplasma luminosum (Williamson et al., 19''), and Mycoplasma lucivorar (Williamson et al., 1990) be transferred to Entomoplasma gen. nov., family Entomoplasmataceae fam. nov., as Entomoplasma ellychniae comb. nov., Entomoplasma melaleucae comb. nov., Entomoplasma somnilux comb. nov, Entomoplasma luminosum comb. nov., and Entomoplasma lucivorar comb. nov. Furthermore, the genus Mesoplasma gen. nov. within the family Entomoplasmataceae fam. nov. is proposed for four non-sterol-requiring insect and plant mollicutes. This designation requires the transfer of Acholeplasma florum (McCoy et al., 1984), Achokplasma entomophilum (Tully et al., 1988), Acholeplasma seiffertii (Bonnet et al., 1991), and Mycoplasma lactucae (Rose et al., 1990) to Mesoplasma florum comb. nov., Mesoplasma entomophilum comb. nov., Mesoplasma seiffertii comb. nov., and Mesoplasma lactucae comb. nov., respectively. Previously established orders Achokplasmatales and Anaeroplasmatales within the class Mollicutes are designated orders III and IV, respectively, in the proposed revision. Classification and characteristics of lower taxa within these two orders remain as previously given. The proposal outlined here does not consider the large cluster of nonculturable, arthropod-associated, plant-pathogenic mollicutes (''mycoplasma-like organisms'') recently shown to be more closely related to members of the order Achokplasmataks. C1 INRA,BIOL CELLULAIRE & MOLEC LAB,F-33883 VILLENAVE DORNON,FRANCE. UNIV BORDEAUX 2,F-33883 VILLENAVE DORNON,FRANCE. USDA,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705. RP TULLY, JG (reprint author), NIAID,FREDERICK CANC RES & DEV CTR,MYCOPLASMA SECT,FREDERICK,MD 21702, USA. NR 54 TC 83 Z9 85 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1993 VL 43 IS 2 BP 378 EP 385 PG 8 WC Microbiology SC Microbiology GA KX917 UT WOS:A1993KX91700031 ER PT J AU HAMASAKI, DI SATO, H SANTHANAKRISHNAN, S SHINOHARA, T AF HAMASAKI, DI SATO, H SANTHANAKRISHNAN, S SHINOHARA, T TI CORRELATION BETWEEN THE PHYSIOLOGICAL AND MORPHOLOGIC CHANGES IN EXPERIMENTAL AUTOIMMUNE UVEITIS INDUCED BY PEPTIDE-G OF S-ANTIGEN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE EXPERIMENTAL AUTOIMMUNE UVEITIS; ELECTRORETINOGRAM; PEPTIDE-G; HISTOPATHOLOGIC CHANGES IN EAU; CORRELATION OF EAU AND ERG ID BIRDSHOT RETINOCHOROIDOPATHY; RATS; DROSOPHILA; ARRESTIN; UVEORETINITIS; IMMUNIZATION; RETINITIS; HOMOLOG AB Purpose. The authors followed and correlated the physiologic and morphologic changes occurring in experimental autoimmune uveitis (EAU) induced by the peptide G of S-antigen. Methods. EAU was induced in Lewis rats by footpad inoculation of a 13-amino acid synthetic peptide (peptide G) in complete Freund's adjuvant. Electroretinography (ERG) was used to follow the physiologic changes, and light and electron microscopy were used to examine the morphologic changes. Results. Serial ERG recordings showed a progressive decrease in the b-wave amplitude and a depression of retinal sensitivity beginning on day 18-21 postinoculation (PI). By day 35 PI, the b-wave was decreased by 91%, and the sensitivity was depressed by 4.68 log units. Negative ERG were recorded during the intermediate and late stage. Light and electron microscopy of the retina showed better correlation of the pathologic changes with b-wave depression than with PI day. Conclusions. ERG recordings were a good method to detect, follow, and quantify the severity of EAU. Their good correlation with the morphologic changes showed that this method can be used to assess the condition of the retina noninvasively. C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD. RP HAMASAKI, DI (reprint author), UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,MIAMI,FL 33136, USA. FU NEI NIH HHS [5 P30 EY 021180-15] NR 30 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD APR PY 1993 VL 34 IS 5 BP 1861 EP 1871 PG 11 WC Ophthalmology SC Ophthalmology GA KX212 UT WOS:A1993KX21200024 PM 8473123 ER PT J AU ZINK, S JAFFE, CC AF ZINK, S JAFFE, CC TI MEDICAL IMAGING DATABASES - A NATIONAL INSTITUTES OF HEALTH WORKSHOP SO INVESTIGATIVE RADIOLOGY LA English DT Article ID CHEST RADIOGRAPHS C1 YALE UNIV,SCH MED,DEPT DIAGNOST RADIOL & INTERNAL MED,CARDIAC RADIOL SECT,NEW HAVEN,CT 06510. RP ZINK, S (reprint author), NCI,DIV CANC TREATMENT,RADIAT RES PROGRAM,6130 EXECUT BLVD,EPM-800,BETHESDA,MD 20892, USA. NR 21 TC 21 Z9 21 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD APR PY 1993 VL 28 IS 4 BP 366 EP 372 DI 10.1097/00004424-199304000-00019 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KW595 UT WOS:A1993KW59500015 PM 8097506 ER PT J AU PUTMAN, CE FRANK, JA AF PUTMAN, CE FRANK, JA TI ACTIVITIES OF THE CONJOINT COMMITTEE - ENHANCEMENT OF DIAGNOSTIC RADIOLOGIC RESEARCH AND EDUCATION SO INVESTIGATIVE RADIOLOGY LA English DT Article; Proceedings Paper CT 5TH GRANTSMANSHIP WORKSHOP CY NOV 08-09, 1991 CL WASHINGTON, DC SP AMER COLL RADIOL, ASSOC UNIV RADIOLOGISTS, SOC CHAIRMAN ACAD RADIOL DEPT C1 NIH,CTR CLIN,DEPT DIAGNOST RADIOL,MRI,DIAGN RADIOL RES PROGRAM,BETHESDA,MD 20892. RP PUTMAN, CE (reprint author), DUKE UNIV,DEPT RADIOL,203 ALLEN BLDG,DURHAM,NC 27706, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD APR PY 1993 VL 28 SU 2 BP S52 EP S56 DI 10.1097/00004424-199304001-00014 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KX111 UT WOS:A1993KX11100014 PM 8478190 ER PT J AU WINGATE, CL AF WINGATE, CL TI NIH PEER-REVIEW OF GRANT APPLICATIONS - DEFINITIONS, PROCEDURES, AND SUGGESTIONS SO INVESTIGATIVE RADIOLOGY LA English DT Article; Proceedings Paper CT 5TH GRANTSMANSHIP WORKSHOP CY NOV 08-09, 1991 CL WASHINGTON, DC SP AMER COLL RADIOL, ASSOC UNIV RADIOLOGISTS, SOC CHAIRMAN ACAD RADIOL DEPT RP WINGATE, CL (reprint author), NIH,DIV RES GRANTS,DIAGN RADIOL STUDY SECT,WESTWOOD BLDG,ROOM 357,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD APR PY 1993 VL 28 SU 2 BP S38 EP S40 DI 10.1097/00004424-199304001-00010 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KX111 UT WOS:A1993KX11100010 PM 8478186 ER PT J AU HAMER, DH AF HAMER, DH TI HEAVY-METALS AND GENE-REGULATION - TOXICOLOGICAL ASPECTS SO JAPANESE JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH LA English DT Article; Proceedings Paper CT 18TH SYMP ON TOXICOLOGY AND ENVIRONMENTAL HEALTH CY OCT 27-28, 1992 CL TOKYO, JAPAN C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHARMACEUTICAL SOC JAPAN PI TOKYO PA 2-12-15-201 SHIBUYA, SHIBUYA-KU, TOKYO 150, JAPAN SN 0013-273X J9 JPN J TOX ENV HEALTH JI Jpn. J. Toxicol. Environ. Health PD APR PY 1993 VL 39 IS 2 BP P32 EP P33 PG 2 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA LG867 UT WOS:A1993LG86700012 ER PT J AU ATKINS, MS STOFF, DM AF ATKINS, MS STOFF, DM TI INSTRUMENTAL AND HOSTILE AGGRESSION IN CHILDHOOD DISRUPTIVE BEHAVIOR DISORDERS SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article; Proceedings Paper CT 1990 ANNUAL MEETING OF THE SOC FOR RESEARCH IN CHILD AND ADOLESCENT PSYCHOTHERAPY CY JAN, 1990 CL COSTA MESA, CA SP SOC RES CHILD & ADOLESCENT PSYCHOTHERAPY ID ATTENTION DEFICIT DISORDER; ANTISOCIAL-BEHAVIOR; CONDUCT DISORDER; HYPERACTIVITY; BOYS; CHILDREN; RATINGS; DELINQUENCY AB An analogue task of instrumental and hostile aggression during a competitive game was evaluated in a sample of clinically-referred 8- to 12-year-old aggressive boys. Similar to a prior task in a normative sample (Hoving, Wallace, & La Forme, 1979), both types of aggression increased during provocation as compared to baseline, indicating the success of the provocation manipulation, with moderate correlations between the two aggressive responses. The aggressive group with attention-deficit hyperactivity disorder (ADHD) and the aggressive group without ADHD each had higher rates of instrumental aggression than controls. Only the aggressive/ADHD group had higher rates of hostile aggression than controls. Parent Child Behavior Checklist ratings indicated a modest but significant unique relationship between instrumental aggression and delinquency. The high rate of both types of aggression in the aggressive/ADHD group suggests that comorbid ADHD and aggression may result in qualitative differences in aggressive behavior. The high rate of hostile aggression in the aggressive-ADHD group supports theoretical assumptions regarding the relationship of hostile aggression to poor impulse control. C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. NIMH,ROCKVILLE,MD 20857. FU BHP HRSA HHS [DH26979]; NIMH NIH HHS [MH40364, MH4682] NR 33 TC 55 Z9 55 U1 2 U2 6 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0091-0627 J9 J ABNORM CHILD PSYCH JI J. Abnorm. Child Psychol. PD APR PY 1993 VL 21 IS 2 BP 165 EP 178 DI 10.1007/BF00911314 PG 14 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA KZ070 UT WOS:A1993KZ07000003 PM 8491930 ER PT J AU CAUSSY, D TERRINHA, A EVANS, AC REIS, DD NUNES, JFM BLATTNER, WA AF CAUSSY, D TERRINHA, A EVANS, AC REIS, DD NUNES, JFM BLATTNER, WA TI CHANGES IN HIV-2 SEROPREVALENCE IN CAPE-VERDE, WEST AFRICA SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Letter C1 PORTUGUESE INST ONCOL,VIROL LAB,LISBON,PORTUGAL. HOSP DR AGOSTINHO NETO,PRAIA,CAPE VERDE. RP CAUSSY, D (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,ROCKVILLE,MD, USA. FU NCI NIH HHS [N01-CP-31041-03] NR 6 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD APR PY 1993 VL 6 IS 4 BP 432 EP 433 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KU221 UT WOS:A1993KU22100022 PM 8455152 ER PT J AU ENGEL, BT TALAN, MI CHEW, PH AF ENGEL, BT TALAN, MI CHEW, PH TI ROLE OF POSTURAL STATUS IN THE NOCTURNAL HEMODYNAMIC PATTERNS OF NONHUMAN-PRIMATES SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE DIURNAL; HEMODYNAMICS; POSTURE ID PRESSURE AB We compared the nocturnal hemodynamic patterns of seven tethered monkeys (Macaca mulatta) with those of seven chaired animals to determine whether the overnight changes are comparable in the two conditions. In both groups, we found a consistent hemodynamic pattern characterized by an overnight fall in cardiac output and central venous pressure and a rise in total peripheral resistance that maintained blood pressure homeostasis. The pattern of overnight change occurred despite major differences in response levels: cardiac output and central venous pressure were significantly elevated, and total peripheral resistance was significantly reduced at all times (from 1800 to 1200 h the following day) in the chaired animals relative to the tethered animals. This difference was probably due to an expanded plasma volume in the chaired animals, because stroke volume was also significantly elevated. Because the nocturnal hemodynamic pattern occurred under both conditions, it is likely that it is a stable biologic effect, which is probably related to an overnight loss in fluid volume that is not replaced in animals that sleep throughout the night. RP ENGEL, BT (reprint author), NIA,GERONTOL RES CTR,BEHAV SCI LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 10 TC 5 Z9 5 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD APR PY 1993 VL 74 IS 4 BP 1684 EP 1688 PG 5 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA KZ594 UT WOS:A1993KZ59400030 PM 8514683 ER PT J AU EICHACKER, PQ HOFFMAN, WD FARESE, A DANNER, RL SUFFREDINI, AF WAISMAN, Y BANKS, SM MOUGINIS, T WILSON, L ROTHLEIN, R ELIN, RJ HOSSEINI, JM MACVITTIE, TJ NATANSON, C AF EICHACKER, PQ HOFFMAN, WD FARESE, A DANNER, RL SUFFREDINI, AF WAISMAN, Y BANKS, SM MOUGINIS, T WILSON, L ROTHLEIN, R ELIN, RJ HOSSEINI, JM MACVITTIE, TJ NATANSON, C TI LEUKOCYTE CD18 MONOCLONAL-ANTIBODY WORSENS ENDOTOXEMIA AND CARDIOVASCULAR INJURY IN CANINES WITH SEPTIC SHOCK SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE NEUTROPHIL AND ENDOTHELIAL INTERACTIONS; SEPSIS-ASSOCIATED TISSUE INJURY; CARDIOVASCULAR INJURY ID TUMOR NECROSIS FACTOR; RESPIRATORY-DISTRESS SYNDROME; ACUTE LUNG INJURY; REDUCES ORGAN INJURY; NEUTROPHIL ADHERENCE; GRANULOCYTE DEPLETION; ALVEOLAR MACROPHAGES; ADHESION MOLECULES; HEMORRHAGIC-SHOCK; RABBITS AB We investigated the effects of a murine monoclonal antibody directed against the canine leukocyte CD11/18 adhesion complex (MAb R15.7) in a canine model of septic shock. Awake 2-yr-old purpose-bred beagles were studied 7 days before and 1, 2, 4, and 10 days after intraperitoneal placement of an Escherichia coli-infected fibrin clot. Starting 12 h before clot placement, animals received 0.5-1 mg/kg iv every 12 h (4 doses total) of either MAb R15.7 (MAb group, n = 8) or, as controls, murine serum protein (n = 8). After infected clot placement, all animals received antibiotic (ceftriaxone, 100 mg.kg-1.day-1 for 4 days). Two of eight control animals and four of eight MAb animals died (P = 0.4). During the first 8 h after clot placement, MAb animals, compared with control animals, had greater (P < 0.06) increases in serum endotoxin levels and higher (P < 0.05) neutrophil counts. Day 1 after clot placement, MAb animals, compared with control animals, had decreased (P < 0.05) central venous pressure and arterial pH and increased (P < 0.05) arterial lactate. Day 2 after clot placement, MAb animals, compared with control animals, had decreased (P < 0.05) cardiac index and mean arterial pressure. In summary, MAb R15.7, although associated with increased neutrophil counts, worsened serum endotoxemia, acidosis, and cardiovascular function in this canine model of septic shock. These data suggest that in septic shock, antibody directed against this leukocyte membrane protein complex may be harmful, possibly via impairment of normal leukocyte function. C1 ARMED FORCES RADIOBIOL RES INST,DEF NUCL AGCY,BETHESDA,MD 20814. CHILDRENS NATL MED CTR,CTR EMERGENCY MED TRAUMA,WASHINGTON,DC 20010. BOEHRINGER INGELHEIM CORP,RIDGEFIELD,CT 06877. RP EICHACKER, PQ (reprint author), NIH,CTR CLIN,DEPT CRIT CARE MED,BLDG 10,RM 7D43,BETHESDA,MD 20892, USA. NR 52 TC 48 Z9 48 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD APR PY 1993 VL 74 IS 4 BP 1885 EP 1892 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA KZ594 UT WOS:A1993KZ59400059 PM 8099906 ER PT J AU MORLEY, D MARAGOS, CM ZHANG, XY BOIGNON, M WINK, DA KEEFER, LK AF MORLEY, D MARAGOS, CM ZHANG, XY BOIGNON, M WINK, DA KEEFER, LK TI MECHANISM OF VASCULAR RELAXATION INDUCED BY THE NITRIC-OXIDE (NO) NUCLEOPHILE COMPLEXES, A NEW CLASS OF NO-BASED VASODILATORS SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article DE VASODILATION; MECHANISM; ENDOTHELIUM; NITRIC OXIDE; ENDOTHELIUM-DERIVED RELAXING FACTOR; SMOOTH MUSCLE ID RELAXING FACTOR; METHYLENE-BLUE; HEMOGLOBIN; AORTA AB Compounds formed by reacting nitric oxide (NO) with various nucleophiles have been shown to dilate aortic segments with a potency that correlates strongly with the amount of NO they release spontaneously in aqueous buffers. We performed experiments aimed at confirming their mechanism of action and using the data to design improvements in their pharmacologic properties. That the vasorelaxant action these agents induce is endothelium-independent was demonstrated by exposure of denuded versus intact aortic segments to the diethylamine/NO complex (DEA/NO); denudation had no significant effect on potency. Similarly, N(G)-monomethyl-L-arginine, an NO synthase inhibitor, did not affect the action of DEA/NO. However, both the vasorelaxant potency of DEA/NO and the amount of cyclic guanosine monophosphate it induced were significantly diminished by the guanylate cyclase inhibitor, methylene blue. The results support the view that the NO/nucleophile adducts induce vasodilation by spontaneously releasing NO, which then activates guanylate cyclase. This mechanistic conclusion suggests that not only potency but also duration of action, a clinically relevant parameter not studied in the previous investigation, might also be controllable by structural modification. We tested this hypothesis by comparing DEA/NO and the spermine/NO adduct (SPER/NO), whose half-lives (t 1/2) are 2.1 and 39 min, respectively, for persistence of their dilatory effects. The response to DEA/NO rapidly peaked (maximum at 5 min) and receded during the 60-min observation period; SPER/NO required 15 min to reach peak relaxation but maintained this level throughout the experiment. We conclude that the NO/nucleophile complexes provide an advantageous means of exposing biologic systems to NO in a defined and controlled fashion that should facilitate study of nitric oxide's effects on the vasculature in health and disease. C1 TEMPLE UNIV,HLTH SCI CTR,SCH MED,DEPT MED,CARDIOL SECT,PHILADELPHIA,PA 19140. NCI,FREDERICK CANC RES & DEV CTR,CHEM SECT,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21701. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 NR 24 TC 73 Z9 73 U1 0 U2 4 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. PD APR PY 1993 VL 21 IS 4 BP 670 EP 676 PG 7 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA KV370 UT WOS:A1993KV37000023 PM 7681915 ER PT J AU LAMORTE, VJ HAROOTUNIAN, AT SPIEGEL, AM TSIEN, RY FERAMISCO, JR AF LAMORTE, VJ HAROOTUNIAN, AT SPIEGEL, AM TSIEN, RY FERAMISCO, JR TI MEDIATION OF GROWTH-FACTOR INDUCED DNA-SYNTHESIS AND CALCIUM MOBILIZATION BY G(Q) AND G(I2) SO JOURNAL OF CELL BIOLOGY LA English DT Article ID G-PROTEIN; ALPHA-SUBUNITS; INOSITOL PHOSPHATES; SIGNAL TRANSDUCTION; PHOSPHOLIPASE-C; RECEPTOR; INHIBITION; ANTIBODIES; ACTIVATION; PROLIFERATION AB A newly identified subclass of the heterotrimeric GTP binding regulatory protein family, G(q), has been found to be expressed in a diverse range of cell types. We investigated the potential role of this protein in growth factor signal transduction pathways and its potential relationship to the function of other Galpha subclasses. Recent biochemical studies have suggested that G(q) regulates the beta 1 isozyme of phospholipase C (PLCbeta1), an effector for some growth factors. By microinjection of inhibitory antibodies specific to distinct G alpha subunits into living cells, we have determined that Galpha(q) transduces bradykinin- and thrombin-stimulated intracellular calcium transients which are likely to be mediated by PLCbeta1. Moreover, we found that Galpha(q) function is required for the mitogenic action of both of these growth factors. These results indicate that both thrombin and bradykinin utilize G(q) to couple to increases in intracellular calcium, and that G(q) is a necessary component of the mitogenic action of these factors. While microinjection of antibodies against Galpha(i2) did not abolish calcium transients stimulated by either of these factors, such microinjection prevented DNA synthesis in response to thrombin but not to bradykinin. These data suggest that thrombin-induced mitogenesis requires both G(q) and G(i2), whereas bradykinin needs only the former. Thus, different growth factors operating upon the same cell type use overlapping yet distinct sets of Galpha subtypes in mitogenic signal transduction pathways. The direct identification of the coupling of both a pertussis toxin sensitive and insensitive G protein subtype in the mitogenic pathways utilized by thrombin offers an in vivo biochemical clarification of previous results obtained by pharmacologic studies. C1 UNIV CALIF SAN DIEGO,DEPT PHARMACOL,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,CTR CANC,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,HOWARD HUGHES INST,LA JOLLA,CA 92093. NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892. RP LAMORTE, VJ (reprint author), UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093, USA. FU NIGMS NIH HHS [GM07752]; PHS HHS [39811] NR 34 TC 108 Z9 108 U1 1 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1993 VL 121 IS 1 BP 91 EP 99 DI 10.1083/jcb.121.1.91 PG 9 WC Cell Biology SC Cell Biology GA KU174 UT WOS:A1993KU17400009 PM 8458876 ER PT J AU SIPES, JM GUO, NH NEGRE, E VOGEL, T KRUTZSCH, HC ROBERTS, DD AF SIPES, JM GUO, NH NEGRE, E VOGEL, T KRUTZSCH, HC ROBERTS, DD TI INHIBITION OF FIBRONECTIN BINDING AND FIBRONECTIN-MEDIATED CELL-ADHESION TO COLLAGEN BY A PEPTIDE FROM THE 2ND TYPE-I REPEAT OF THROMBOSPONDIN SO JOURNAL OF CELL BIOLOGY LA English DT Article ID PLATELET THROMBOSPONDIN; PLASMA FIBRONECTIN; ENDOTHELIAL-CELLS; MELANOMA-CELLS; PROTEINS; GROWTH; GLYCOPROTEIN; DROSOPHILA; ATTACHMENT; RECEPTORS AB The platelet and extracellular matrix glycoprotein thrombospondin interacts with various types of cells as both a positive and negative modulator of cell adhesion, motility, and proliferation. These effects may be mediated by binding of thrombospondin to cell surface receptors or indirectly by binding to other extracellular matrix components. The role of peptide sequences from the type I repeats of thrombospondin in its interaction with fibronectin were investigated. Fibronectin bound specifically to the peptide Gly-Gly-Trp-Ser-His-Trp from the second type I repeat of thrombospondin but not to the corresponding peptides from the first or third repeats or flanking sequences from the second repeat. The two Trp residues and the His residue were essential for binding, and the two Gly residues enhanced the affinity of binding. Binding of the peptide and intact thrombospondin to fibronectin were inhibited by the gelatin-binding domain of fibronectin. The peptide specifically inhibited binding of fibronectin to gelatin or type I collagen and inhibited fibronectin-mediated adhesion of breast carcinoma and melanoma cells to gelatin or type I collagen substrates but not direct adhesion of the cells to fibronectin, which was inhibited by the peptide Gly-Arg-Gly-Asp-Ser. Thus, the fibronectin-binding thrombospondin peptide Gly-Gly-Trp-Ser-His-Trp is a selective inhibitor of fibronectin-mediated interactions of cells with collagen in the extracellular matrix. C1 NCI,PATHOL LAB,BLDG 10,ROOM 2A33,BETHESDA,MD 20892. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 40 TC 46 Z9 46 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1993 VL 121 IS 2 BP 469 EP 477 DI 10.1083/jcb.121.2.469 PG 9 WC Cell Biology SC Cell Biology GA KY008 UT WOS:A1993KY00800022 PM 8468356 ER PT J AU SHAKOORI, AR OWEN, TA SHALHOUB, V STEIN, JL BUSTIN, M STEIN, GS LIAN, JB AF SHAKOORI, AR OWEN, TA SHALHOUB, V STEIN, JL BUSTIN, M STEIN, GS LIAN, JB TI DIFFERENTIAL EXPRESSION OF THE CHROMOSOMAL HIGH MOBILITY GROUP PROTEIN-14 AND PROTEIN-17 DURING THE ONSET OF DIFFERENTIATION IN MAMMALIAN OSTEOBLASTS AND PROMYELOCYTIC LEUKEMIA-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE HL-60; GENE REGULATION; HMG14; HMG17; PROLIFERATION; OSTEOBLASTS; CHROMOSOMAL PROTEINS ID H-4 HISTONE GENE; CHROMATIN STRUCTURE; MESSENGER-RNA; CYCLE; GROWTH; ORGANIZATION; INDUCTION; CLONING; HMG-17 AB The expression of chromosomal proteins HMG 14 and HMG 17 during proliferation and differentiation into the osteoblast and monocyte phenotypes was studied. Cellular levels of HMG 14 and HMG 17 mRNA were assayed in primary cultures of calvarial-derived rat osteoblasts under conditions that (1) support complete expression of the mature osteocytic phenotype and development of a bone tissue-like organization; and (2) where development of osteocytic phenotypic properties are both delayed and reduced in extent of expression. HMG 14 and HMG 17 are preferentially expressed in proliferating osteoblasts and decline to basal levels post-proliferatively at the onset of extracellular matrix mineralization. In contrast, under conditions that are not conducive to extracellular matrix mineralization, HMG 14 is maximally expressed following the downregulation of proliferation. Consistent with previous reports by Bustin and co-workers [Crippa et al., 1990], HMG 14 and HMG 17 are expressed in proliferating HL-60 promyelocytic leukemia cells and downregulated post-proliferatively following phorbol ester-induced monocytic differentiation. However, differentiation into the monocyte phenotype is accompanied by reinitiation of HMG 17 gene expression. The results indicate that the levels of HMG 1.4 and HMG 17 mRNA are selectively down-regulated during differentiation. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP SHAKOORI, AR (reprint author), UNIV MASSACHUSETTS,MED CTR,DEPT CELL BIOL,55 LAKE AVE N,WORCESTER,MA 01655, USA. RI Shakoori, Abdul Rauf/F-3026-2015; Bustin, Michael/G-6155-2015 FU NIAMS NIH HHS [AR35166, AR39588, AR33920] NR 35 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR PY 1993 VL 51 IS 4 BP 479 EP 487 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KW487 UT WOS:A1993KW48700013 PM 8496248 ER PT J AU TIMMER, WC VILLALOBOS, JM AF TIMMER, WC VILLALOBOS, JM TI THE POLYMERASE CHAIN-REACTION SO JOURNAL OF CHEMICAL EDUCATION LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; DNA AMPLIFICATION; MESSENGER-RNA; NUCLEIC-ACIDS; STRANDED-DNA; INDIVIDUALS; SEQUENCES; PCR; QUANTITATION; INFANTS C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 48 TC 9 Z9 9 U1 3 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0021-9584 J9 J CHEM EDUC JI J. Chem. Educ. PD APR PY 1993 VL 70 IS 4 BP 273 EP 280 PG 8 WC Chemistry, Multidisciplinary; Education, Scientific Disciplines SC Chemistry; Education & Educational Research GA KZ720 UT WOS:A1993KZ72000007 ER PT J AU FLACK, MR PYLE, RG MULLEN, NM LORENZO, B WU, YW KNAZEK, RA NISULA, BC REIDENBERG, MM AF FLACK, MR PYLE, RG MULLEN, NM LORENZO, B WU, YW KNAZEK, RA NISULA, BC REIDENBERG, MM TI ORAL GOSSYPOL IN THE TREATMENT OF METASTATIC ADRENAL CANCER SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID MALE CONTRACEPTIVE DRUG; ADRENOCORTICAL CARCINOMA; CORTICAL CARCINOMA; CLINICAL-TRIAL; ANTITUMOR; CISPLATIN; ENANTIOMERS; RESISTANCE; INVIVO; AGENT AB Medical treatment of metastatic adrenal cancer is largely unsuccessful and has considerable toxicity. We previously demonstrated the activity of the plant toxin gossypol against human adrenal cancers in nude mice. We therefore examined the efficacy and toxicity of oral gossypol as a treatment for adrenal cancer in humans. Twenty-one patients with metastatic adrenal cancer received oral gossypol at doses of 30-70 mg/day. Patients were monitored for side effects of gossypol, changes in hormone secretion, and tumor response. Eighteen patients completed at least 6 weeks of gossypol treatment. Three of these patients, whose tumors were refractory to other chemotherapeutic agents, had partial tumor responses (greater=than-or-equal-to 50% decrease in tumor volume) that lasted from several months to over 1 yr. One patient had a minor response followed by resection of her remaining disease, 1 patient had stable disease, and 13 patients bad disease progression. Three patients died of their disease without receiving sufficient gossypol to achieve detectable drug levels, and were eliminated from the final analysis. The side effects of gossypol were generally well tolerated; the only serious side effect was abdominal ileus that resolved when the drug was temporarily withheld and restarted at a lower dose. We conclude that oral gossypol can be used relatively safely on an outpatient basis for the treatment of metastatic adrenal cancer. The response rate is similar to the other agents currently available for adrenal cancer, and responses were seen in patients who had failed other chemotherapeutic regimens. This study provides the first indication that gossypol may have activity against cancer in humans, suggesting the need for further investigation of gossypol as an antitumor agent. C1 CELLCO BIOREACTORS INC, GAITHERSBURG, MD USA. CORNELL UNIV, MED CTR, COLL MED, DEPT PHARMACOL, NEW YORK, NY 10021 USA. CORNELL UNIV, MED CTR, COLL MED, DEPT MED, NEW YORK, NY 10021 USA. RP FLACK, MR (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N262, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. FU NCRR NIH HHS [RR-47]; NIGMS NIH HHS [GM-07488] NR 21 TC 123 Z9 126 U1 2 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 APR PY 1993 VL 76 IS 4 BP 1019 EP 1024 DI 10.1210/jc.76.4.1019 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KW773 UT WOS:A1993KW77300039 PM 8473376 ER PT J AU LOCKSHIN, MD AF LOCKSHIN, MD TI PREVENTING ANTIPHOSPHOLIPID ANTIBODY-INDUCED FETAL LOSS - A NEW IDEA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Editorial Material RP LOCKSHIN, MD (reprint author), NIAMSD,BETHESDA,MD, USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1993 VL 91 IS 4 BP 1267 EP 1267 DI 10.1172/JCI116323 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KY052 UT WOS:A1993KY05200002 PM 8473480 ER PT J AU CHUNG, KN SAIKAWA, Y PAIK, TH DIXON, KH MULLIGAN, T COWAN, KH ELWOOD, PC AF CHUNG, KN SAIKAWA, Y PAIK, TH DIXON, KH MULLIGAN, T COWAN, KH ELWOOD, PC TI STABLE TRANSFECTANTS OF HUMAN MCF-7 BREAST-CANCER CELLS WITH INCREASED LEVELS OF THE HUMAN FOLATE RECEPTOR EXHIBIT AN INCREASED SENSITIVITY TO ANTIFOLATES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CELL GROWTH; DRUG RESISTANCE; FOLATE BINDING PROTEINS; FOLIC ACID; METHOTREXATE ID HUMAN KB CELLS; HAMSTER OVARY CELLS; BINDING-PROTEIN; METHOTREXATE TRANSPORT; LEUKEMIA-CELLS; L1210 CELLS; FLUORESCEINATED METHOTREXATE; MEMBRANE; EXPRESSION; CULTURE AB A major problem in cancer therapy is tumor drug resistance such as is found with antifolates (e.g., methotrexate [MTX]). We are specifically interested in the role of the human folate receptor (hFR) in MTX resistance. To investigate whether transfection of hFR results in increased MTX uptake and increased drug sensitivity, human mammary carcinoma (MCF-7) cells and Chinese hamster ovary cells (CHO) (cells which do not express detectable levels of hFR) were transfected with hFR cDNA. Stable human mammary carcinoma and Chinese hamster ovary transfectants expressing high levels of hFR were selected for further analysis. Transfected cells which express increased levels of hFR grow more rapidly than mock, transfected or wild type cells in media containing physiologic concentrations of folates. The hFR expressed by these cells is sorted to the plasma membrane and is functional as determined by cell surface binding of a radiolabeled folic acid derivative and by internalization of [H-3]methotrexate. The stable transfectants that express increased levels of hFR are also more sensitive to MTX in physiologic concentrations of folates. We conclude that increased expression of hFR by human mammary carcinoma and Chinese hamster ovary cells cultured under these conditions results in an enhanced growth rate, increased folic acid binding, and increased MTX uptake and cytotoxicity. RP CHUNG, KN (reprint author), NCI,MED BRANCH,BLDG 10,ROOM 12N226,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 36 TC 59 Z9 59 U1 0 U2 5 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1993 VL 91 IS 4 BP 1289 EP 1294 DI 10.1172/JCI116327 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KY052 UT WOS:A1993KY05200006 PM 7682567 ER PT J AU ROMA, P GREGG, RE MENG, MS RONAN, R ZECH, LA FRANCESCHINI, G SIRTORI, CR BREWER, HB AF ROMA, P GREGG, RE MENG, MS RONAN, R ZECH, LA FRANCESCHINI, G SIRTORI, CR BREWER, HB TI INVIVO METABOLISM OF A MUTANT FORM OF APOLIPOPROTEIN A-I, APO A-I(MILANO), ASSOCIATED WITH FAMILIAL HYPOALPHALIPOPROTEINEMIA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE KINETICS; LIPOPROTEINS; GENETIC DEFECTS; HYPOALPHALIPOPROTEINEMIA; APOLIPOPROTEIN A-I; LIPOPROTEINS; HDL ID HIGH-DENSITY-LIPOPROTEIN; CORONARY HEART-DISEASE; IMILANO APOPROTEIN; CHOLESTEROL ACYLTRANSFERASE; IDENTIFICATION; AIMILANO; VARIANT; PLASMA; CONVERSION; LECITHIN AB Apo A-I(Milano) is a mutant form of apo A-I in which cysteine is substituted for arginine at amino acid 173. Subjects with apo A-I(Milano) are characterized by having low levels of plasma HDL cholesterol and apo A-I. To determine the kinetic etiology of the decreased plasma levels of the apo A-I in these individuals, normal and mutant apo A-I were isolated, radiolabeled with either I-125 or I-131, and both types of apo A-I were simultaneously injected into two normal control subjects and two subjects heterozygous for apo A-I(Milano). In the normal subjects, apo A-I(Milano) was catabolized more rapidly than the normal apo A-I (mean residence times of 5.11 d for normal apo A-I vs. 3.91 d for apo A-I(Milano)), clearly establishing that apo A-I(Milano) is kinetically abnormal and that it has a shortened residence time in plasma. In the two apo A-I(Milano) subjects, both types of apo A-I were catabolized more rapidly than normal (residence times ranging from 2.63 to 3.70 d) with normal total apo A-I production rates (mean of 10.3 vs. 10.4 mg/kg per d in the normal subjects). Therefore, in the subjects with apo A-I(Milano), the decreased apo A-I levels are caused by rapid catabolism of apo A-I and not to a decreased production rate, and the abnormal apo A-I(Milano) leads to the rapid catabolism of both the normal and mutant forms of apo A-I in the affected subjects. C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. IST SCI FARMACOL,CTR E GROSSI PAOLETTI,MILAN,ITALY. RI Sirtori, Cesare/F-4658-2012; OI FRANCESCHINI, GUIDO/0000-0003-2687-1771 NR 32 TC 93 Z9 98 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1993 VL 91 IS 4 BP 1445 EP 1452 DI 10.1172/JCI116349 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KY052 UT WOS:A1993KY05200028 PM 8473493 ER PT J AU PALIOGIANNI, F RAPTIS, A AHUJA, SS NAJJAR, SM BOUMPAS, DT AF PALIOGIANNI, F RAPTIS, A AHUJA, SS NAJJAR, SM BOUMPAS, DT TI NEGATIVE TRANSCRIPTIONAL REGULATION OF HUMAN INTERLEUKIN-2 (IL-2) GENE BY GLUCOCORTICOIDS THROUGH INTERFERENCE WITH NUCLEAR TRANSCRIPTION FACTORS AP-1 AND NF-AT SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE GLUCOCORTICOIDS; INTERLEUKIN-2; GENE TRANSCRIPTION; NUCLEAR FACTOR AP-1; NUCLEAR FACTOR AT ID ONCOGENE JUN ENCODES; CYCLOSPORINE-A; ANTIGEN RECEPTOR; LYMPHOCYTES-T; KAPPA-B; DNA-BINDING; C-JUN; EXPRESSION; PROTEIN; ACTIVATION AB IL-2 gene transcription is affected by several nuclear proteins. We asked whether dexamethasone (Dex) and cyclosporin A (CsA) inhibit IL-2 gene transcription by interfering with the activity of nuclear proteins that bind to the IL-2 promoter. Nuclear extracts from primary human T lymphocytes were analyzed by electrophoretic DNA mobility shift assays. Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter. To correlate changes in nuclear factor binding in vitro with transcriptional activity in vivo and define the structural requirements for IL-2 promoter repression, we used transient DNA transfections. Jurkat cells were transfected with plasmids containing either the intact IL-2 promoter or its AP-1, NF-AT, and NF-kB motifs. Dex inhibited the IL-2 promoter and the AP-1, but not the NF-AT and NF-kB plasmids. In contrast, CsA inhibited the IL-2 promoter and the NF-AT, but not the AP-1 and NF-kB plasmids. These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT. We propose that, while maximum inhibition may involve interaction with both transcription factors, AP-1 is the primary target of Dex. C1 NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. RP PALIOGIANNI, F (reprint author), NIDDKD,KIDNEY DIS SECT,BLDG 10,ROOM 3N-114,BETHESDA,MD 20892, USA. NR 40 TC 173 Z9 175 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1993 VL 91 IS 4 BP 1481 EP 1489 DI 10.1172/JCI116353 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KY052 UT WOS:A1993KY05200032 PM 8473495 ER PT J AU KARP, CL ELSAFI, SH WYNN, TA SATTI, MMH KORDOFANI, AM HASHIM, FA HAGALI, M NEVA, FA NUTMAN, TB SACKS, DL AF KARP, CL ELSAFI, SH WYNN, TA SATTI, MMH KORDOFANI, AM HASHIM, FA HAGALI, M NEVA, FA NUTMAN, TB SACKS, DL TI INVIVO CYTOKINE PROFILES IN PATIENTS WITH KALA-AZAR - MARKED ELEVATION OF BOTH INTERLEUKIN-10 AND INTERFERON-GAMMA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CYTOKINES; LEISHMANIASIS; POLYMERASE CHAIN REACTION; HUMAN; MACROPHAGE ID TRANSFORMING GROWTH-FACTOR; VISCERAL LEISHMANIASIS; MURINE LEISHMANIASIS; FACTOR-BETA; CELL; INFECTION; IL-10; MACROPHAGES; EXPRESSION; TH1 AB The immunological mechanisms underlying the susceptibility to disseminated visceral parasitism of mononuclear phagocytes in patients with kala-azar remain undefined. Resistance and susceptibility are correlated with distinct patterns of cytokine production in murine models of disseminated leishmanial disease. To assess lesional cytokine profiles in patients with kala-azar, bone marrow aspirates were analyzed using a quantitative reverse transcriptase PCR technique to amplify specific mRNA sequences of multiple Th1-, Th2-, and/or macrophage-associated cytokines. Transcript levels of IL-10 as well as IFN-gamma were significantly elevated in patients with active visceral leishmaniasis; IL-10 levels decreased markedly with resolution of disease. These findings suggest that IL-10, a potent, pleiotropic suppressor of all known microbicidal effector functions of macrophages, may contribute to the pathogenesis of kala-azar by inhibiting the cytokine-mediated activation of host macrophages that is necessary for the control of leishmanial infection. C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. UNIV KHARTOUM,FAC MED,KHARTOUM,SUDAN. NATL RES COUNCIL,KHARTOUM,SUDAN. RI Wynn, Thomas/C-2797-2011 FU NIAID NIH HHS [2PO1 AI 16312] NR 38 TC 294 Z9 295 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1993 VL 91 IS 4 BP 1644 EP 1648 DI 10.1172/JCI116372 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KY052 UT WOS:A1993KY05200051 PM 8097208 ER PT J AU CHIN, E ZHOU, J BONDY, C AF CHIN, E ZHOU, J BONDY, C TI ANATOMICAL AND DEVELOPMENTAL PATTERNS OF FACILITATIVE GLUCOSE TRANSPORTER GENE-EXPRESSION IN THE RAT-KIDNEY SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE GLUCOSE METABOLISM; NEPHRON; VASOPRESSIN; INSULIN-LIKE GROWTH FACTOR; MESSENGER RNA ID INSULIN-RESPONSIVE TISSUES; MESSENGER-RNA; CLONING; LOCALIZATION; METABOLISM; INTESTINE; PROTEIN; FAMILY; MUSCLE AB In situ hybridization was used to map cellular patterns of gene expression for facilitative glucose transporters (GTs) 1-5 in the developing and adult rat kidney. GT3 was not detected. GT1 mRNA was present in the proximal straight tubule (PST), distal nephron and collecting duct. GT2 mRNA was localized in both proximal convoluted and PST, while GT5 mRNA was detected only in the PST. GT4 mRNA and immunoreactivity were focally localized in the thick ascending limb of Henle's loop and were coexpressed with IGF-I. Thus, each of the four different isoforms demonstrated a distinct renal distribution, with GTs 1, 2, and 5 coexpressed in the PST. Renal GT1 and GT5 gene expression were unchanged throughout development, while GT2 was most abundant before weaning and GT4 was first detected after weaning. Only GT4 appeared to be hormonally regulated: It was decreased after hypophysectomy and increased after vasopressin treatment, but was not affected by 1 or 4 d of insulinopenic diabetes mellitus. The coexpression of GT4 and IGF-I in the thick ascending limb segment of the nephron suggests a novel autocrine/paracrine mechanism by which cells may control local fuel economy independently from that of the larger structure to which they belong and from the systemic hormonal milieu. RP CHIN, E (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10-10W262,BETHESDA,MD 20892, USA. NR 35 TC 54 Z9 54 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1993 VL 91 IS 4 BP 1810 EP 1815 DI 10.1172/JCI116392 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KY052 UT WOS:A1993KY05200071 PM 8473519 ER PT J AU STEINHOFF, MC FRIES, LF KARRON, RA CLEMENTS, ML MURPHY, BR AF STEINHOFF, MC FRIES, LF KARRON, RA CLEMENTS, ML MURPHY, BR TI EFFECT OF HETEROSUBTYPIC IMMUNITY ON INFECTION WITH ATTENUATED INFLUENZA-A VIRUS-VACCINES IN YOUNG-CHILDREN SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID AVIAN-HUMAN; H3N2; H1N1; VIRULENCE; INFANTS AB Resistance to infection with an influenza A virus conferred by previous infection with an influenza A virus belonging to another subtype is called heterosubtypic immunity. Heterosubtypic immunity is demonstrable in laboratory animals but is believed to be weak in humans. The present study examined whether heterosubtypic immunity from previous influenza virus infection induced resistance to infection with an attenuated influenza A vaccine virus. Two groups of vaccinees consisting of young infants and children who received either influenza A H1N1 or H3N2 attenuated virus were studied. Influenza A H3N2 virus vaccine recipients were classified by their preexisting H1N1 heterosubtypic antibody level induced by prior infection with wild-type virus, and the H1N1 vaccinees were classified by their history of infection with H3N2 vaccine virus. For both groups of vaccinees, the rates of seroconversion and virus shedding and the level of vaccine virus replication were compared in subjects with and without heterosubtypic immunity. In 48 influenza A H3N2 virus and 39 H1N1 virus vaccinees, heterosubtypic immunity had no demonstrable effect on infectivity, immunogenicity, or replication of attenuated vaccine virus. These observations confirm the weak nature of heterosubtypic immunity in humans and suggest that it will not limit the utility of live attenuated influenza A viruses in young infants and children. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. NIH,INFECT DIS LAB,BETHESDA,MD 20814. RP STEINHOFF, MC (reprint author), JOHNS HOPKINS UNIV,CTR IMMUNIZAT RES,SCH HYG & PUBL HLTH,DEPT INT HLTH,BALTIMORE,MD 21205, USA. FU NIAID NIH HHS [N01-AI-62515] NR 9 TC 30 Z9 31 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1993 VL 31 IS 4 BP 836 EP 838 PG 3 WC Microbiology SC Microbiology GA KT445 UT WOS:A1993KT44500014 PM 8463393 ER PT J AU GOUVEA, V RAMIREZ, C LI, BG SANTOS, N SAIF, L CLARK, HF HOSHINO, Y AF GOUVEA, V RAMIREZ, C LI, BG SANTOS, N SAIF, L CLARK, HF HOSHINO, Y TI RESTRICTION ENDONUCLEASE ANALYSIS OF THE VP7 GENES OF HUMAN AND ANIMAL ROTAVIRUSES SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; SEQUENCE-ANALYSIS; G-SEROTYPE; NEUTRALIZATION; IDENTIFICATION; HYBRIDIZATION; STRAINS; FELINE; ACID AB The vp7 genes of 194 strains of group A rotaviruses representing all known G types were analyzed with three restriction enzymes by direct digestion of amplified cDNA copies or by deduction of the restriction patterns from known sequences. Mammalian rotavirus strains were classified into 28 restriction patterns consisting of combinations of the 6 profiles (s1 to s6) obtained by digestion with Sau96I endonuclease, 9 profiles (h1 to h9) obtained with HaeIII, and 15 profiles (b1 to b15) obtained with BstYI. Digestion with Sau96I and HaeIII identified restriction sites common to all, or almost all, rotavirus strains studied, whereas BstYI was the most discriminating among rotavirus strains. A clear correlation between some restriction patterns or individual profiles and G type and/or host species of origin was found. Several discriminatory restriction sites consisted of type-specific nucleic acid sequences that encoded conserved amino acid residues. Although not directly involved in antigenic diversity, these sites appear to indicate the G type of the isolate. The technique permits rapid comparison of a large number of virus isolates directly from fecal specimens and provides useful markers for investigating the evolution of rotavirus vp7 genes and tracing vaccine virus and interspecies transmission. C1 OHIO STATE UNIV,OHIO AGR RES & DEV CTR,WOOSTER,OH 44691. CHILDRENS HOSP PHILADELPHIA,DIV INFECT DIS,PHILADELPHIA,PA 19104. NIH,INFECT DIS LAB,BETHESDA,MD 20892. RP GOUVEA, V (reprint author), US FDA,DIV MICROBIOL,WASHINGTON,DC 20204, USA. RI Santos, Norma/H-6986-2015 OI Santos, Norma/0000-0002-5123-9172 NR 26 TC 44 Z9 44 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1993 VL 31 IS 4 BP 917 EP 923 PG 7 WC Microbiology SC Microbiology GA KT445 UT WOS:A1993KT44500028 PM 8385152 ER PT J AU MIDTHUN, K GREENBERG, HB KURTZ, JB GARY, GW LIN, FY KAPIKIAN, AZ AF MIDTHUN, K GREENBERG, HB KURTZ, JB GARY, GW LIN, FY KAPIKIAN, AZ TI CHARACTERIZATION AND SEROEPIDEMIOLOGY OF A TYPE-5 ASTROVIRUS ASSOCIATED WITH AN OUTBREAK OF GASTROENTERITIS IN MARIN-COUNTY, CALIFORNIA SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID INFECTIOUS NONBACTERIAL GASTROENTERITIS; MOUNTAIN AGENT GASTROENTERITIS; NON-BACTERIAL GASTROENTERITIS; IMMUNE ELECTRON-MICROSCOPY; TO-PERSON SPREAD; SNOW MOUNTAIN; NORWALK VIRUS; EPIDEMIC GASTROENTERITIS; VIRAL GASTROENTERITIS; CHILDREN AB The Marin County strain of type 5 astrovirus was associated with two separate outbreaks of nonbacterial gastroenteritis in California in 1978. A safety-tested, bacterium-free filtrate prepared from a stool specimen of an individual who was ill during the original outbreak was given orally to 19 adult volunteers. One volunteer developed a gastrointestinal illness, and nine had serologic responses. Several diarrheal stool specimens from the ill volunteer contained a large number of 27-nm particles. By using immune electron microscopy with acute- and convalescent-phase sera from the original outbreak, these 27-nm particles were shown to be identical to the viral inoculum. The Marin County virus, purified from the stool of the ill volunteer, was shown by immunoprecipitation and polyacrylamide gel electrophoresis to contain a single structural protein with a molecular weight of 30,000. The buoyant density of the virion was 1.39 g/cm3 in cesium chloride. By electron microscopy, approximately 5% of the particles had the characteristic stellate configuration of astrovirus, and serologic studies by immunofluorescence technique confirmed previous classification of the Marin County virus as a type 5 astrovirus. Radioimmunoassay and biotin-avidin immunoassay were used to detect antibody to the Marin County virus in paired acute- and convalescent-phase sera from 32 outbreaks of nonbacterial gastroenteritis, but none of these outbreaks could be attributed to this virus. Prevalence of antibody to this strain of astrovirus was approximately 13% in children 6 months to 3 years of age and increased to 41% in older children and young adults. C1 NIAID,INFECT DIS LAB,BETHESDA,MD 20892. JOHN RADCLIFFE HOSP,DEPT VIROL,OXFORD OX3 9DU,ENGLAND. CTR DIS CONTROL,RESP & ENTEROVIRUS BRANCH,ATLANTA,GA 30333. CTR CLIN EPIDEMIOL,DEPT HLTH & MENTAL HYG,BALTIMORE,MD. NR 50 TC 31 Z9 34 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1993 VL 31 IS 4 BP 955 EP 962 PG 8 WC Microbiology SC Microbiology GA KT445 UT WOS:A1993KT44500034 PM 8385155 ER PT J AU MARCONI, RT GARON, CF AF MARCONI, RT GARON, CF TI DEVELOPMENT OF POLYMERASE CHAIN-REACTION PRIMER SETS FOR DIAGNOSIS OF LYME-DISEASE AND FOR SPECIES-SPECIFIC IDENTIFICATION OF LYME-DISEASE ISOLATES BY 16S RIBOSOMAL-RNA SIGNATURE NUCLEOTIDE ANALYSIS (VOL 30, PG 2831, 1992) SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Correction, Addition RP MARCONI, RT (reprint author), US PHS,NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA. NR 1 TC 6 Z9 6 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1993 VL 31 IS 4 BP 1026 EP 1026 PG 1 WC Microbiology SC Microbiology GA KT445 UT WOS:A1993KT44500053 ER PT J AU CURTI, BD LONGO, DL OCHOA, AC CONLON, KC SMITH, JW ALVORD, WG CREEKMORE, SP FENTON, RG GAUSE, BL HOLMLUND, J JANIK, JE OCHOA, J RICE, PA SHARFMAN, WH SZNOL, M URBA, WJ AF CURTI, BD LONGO, DL OCHOA, AC CONLON, KC SMITH, JW ALVORD, WG CREEKMORE, SP FENTON, RG GAUSE, BL HOLMLUND, J JANIK, JE OCHOA, J RICE, PA SHARFMAN, WH SZNOL, M URBA, WJ TI TREATMENT OF CANCER-PATIENTS WITH EXVIVO ANTI-CD3-ACTIVATED KILLER-CELLS AND INTERLEUKIN-2 SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID TUMOR-INFILTRATING LYMPHOCYTES; METASTATIC MALIGNANT-MELANOMA; HIGH-DOSE INTERLEUKIN-2; PHASE-II; CYTO-TOXICITY; NITRIC-OXIDE; L-ARGININE; IMMUNOTHERAPY; OXIDATION; ANTI-CD3 C1 FREDERICK MEM HOSP,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,DATA MANAGEMENT SERV,FREDERICK,MD 21701. UNIV PITTSBURGH,DEPT SURG,PITTSBURGH,PA 15260. NCI,DIV CANC TREATMENT,INVEST DRUG BRANCH,CANC THERAPY EVALUAT PROGRAM,FREDERICK,MD 21701. RP CURTI, BD (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74102] NR 29 TC 38 Z9 42 U1 0 U2 1 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 APR PY 1993 VL 11 IS 4 BP 652 EP 660 PG 9 WC Oncology SC Oncology GA KV515 UT WOS:A1993KV51500010 PM 8257476 ER PT J AU ATKINS, MB SPARANO, J FISHER, RI WEISS, GR MARGOLIN, KA FINK, KI RUBINSTEIN, L LOUIE, A MIER, JW GUCALP, R SOSMAN, JA BOLDT, DH DOROSHOW, JH ARONSON, FR SZNOL, M AF ATKINS, MB SPARANO, J FISHER, RI WEISS, GR MARGOLIN, KA FINK, KI RUBINSTEIN, L LOUIE, A MIER, JW GUCALP, R SOSMAN, JA BOLDT, DH DOROSHOW, JH ARONSON, FR SZNOL, M TI RANDOMIZED PHASE-II TRIAL OF HIGH-DOSE INTERLEUKIN-2 EITHER ALONE OR IN COMBINATION WITH INTERFERON-ALFA-2B IN ADVANCED RENAL-CELL CARCINOMA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACTIVATED KILLER-CELLS; RECOMBINANT HUMAN INTERLEUKIN-2; METASTATIC MALIGNANT-MELANOMA; ESTABLISHED PULMONARY METASTASES; ALPHA-INTERFERON; PROPHYLACTIC ANTIBIOTICS; ADOPTIVE IMMUNOTHERAPY; HEPATIC METASTASES; CANCER-PATIENTS; CLINICAL-TRIAL C1 UNIV TEXAS,AUDI L MURPHY VET ADM MED CTR,HLTH SCI CTR,SAN ANTONIO,TX 78285. MONTEFIORE MED CTR,ALBERT EINSTEIN MED CTR,EXTRAMURAL IL-2 WORKING GRP,BRONX,NY 10467. LOYOLA UNIV,MED CTR,EXTRAMURAL IL-2 WORKING GRP,MAYWOOD,IL 60153. CITY HOPE NATL MED CTR,EXTRAMURAL IL-2 WORKING GRP,DUARTE,CA 91010. UNIV CALIF SAN FRANCISCO,MED CTR,EXTRAMURAL IL-2 WORKING GRP,SAN FRANCISCO,CA 94143. NCI,DIV CANC TREATMENT,INVEST DRUG BRANCH,CANC THERAPY EVALUAT PROGRAM,FREDERICK,MD 21701. CETUS CORP,DIV ONCOL,EMERYVILLE,CA 94608. RP ATKINS, MB (reprint author), TUFTS UNIV,NEW ENGLAND MED CTR,DIV HEMATOL ONCOL,EXTRAMURAL IL-2 WORKING GRP,BOX 245,BOSTON,MA 02111, USA. FU NCI NIH HHS [N01-CM73702-7]; NCRR NIH HHS [M01-RR00054, M01-RR00079] NR 64 TC 159 Z9 159 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 APR PY 1993 VL 11 IS 4 BP 661 EP 670 PG 10 WC Oncology SC Oncology GA KV515 UT WOS:A1993KV51500011 PM 8478661 ER PT J AU KORN, EL SIMON, R AF KORN, EL SIMON, R TI USING THE TOLERABLE-DOSE DIAGRAM IN THE DESIGN OF PHASE-I COMBINATION CHEMOTHERAPY TRIALS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID METASTATIC COLORECTAL-CARCINOMA; REFRACTORY OVARIAN-CANCER; CALIFORNIA-ONCOLOGY-GROUP; CYCLOPHOSPHAMIDE THERAPY; HYPERTONIC SALINE; AUTOLOGOUS MARROW; ADVANCED BREAST; SOLID TUMORS; CISPLATIN; FLUOROURACIL RP KORN, EL (reprint author), NCI,BIOMETR RES BRANCH,EPN 739,BETHESDA,MD 20892, USA. NR 28 TC 32 Z9 32 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 APR PY 1993 VL 11 IS 4 BP 794 EP 801 PG 8 WC Oncology SC Oncology GA KV515 UT WOS:A1993KV51500027 PM 8478673 ER PT J AU KHOT, V DEVANE, CL KORPI, ER VENABLE, D BIGELOW, LB WYATT, RJ KIRCH, DG AF KHOT, V DEVANE, CL KORPI, ER VENABLE, D BIGELOW, LB WYATT, RJ KIRCH, DG TI THE ASSESSMENT AND CLINICAL IMPLICATIONS OF HALOPERIDOL ACUTE-DOSE, STEADY-STATE, AND WITHDRAWAL PHARMACOKINETICS SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID SCHIZOPHRENIC-PATIENTS; PLASMA-CONCENTRATIONS; REDUCED HALOPERIDOL; PREDICTION; LEVEL; BIOAVAILABILITY; SMOKING; DOSAGE; SERUM; DRUGS AB In order to evaluate comprehensively haloperidol pharmacokinetics under fixed-dose treatment conditions, psychiatric patients were studied after treatment with an acute dose, during maintenance therapy, and after withdrawal from haloperidol following steady-state conditions. After single doses, haloperidol appeared rapidly in serum, achieving peak concentration at a mean of 4.5 hours. The range of observed elimination half-life was broad, between 8.5 and 66.6 hours, with a mean of 19.5 hours. Under conditions of chronic dosing, serial measurements of steady-state serum concentration revealed intrapatient coefficients of variation between 2 and 72%. The mean for all patients was 26.4%. Body clearance decreased nonsignificantly and elimination half-life increased significantly after chronic dosing compared with kinetic parameters determined after a single dose. The concentration of haloperidol in serum obtained at 8 hours after a single dose correlated most strongly (r = 0.73; p < 0.0001) with steady-state concentration resulting from chronic dosing. A value of 4 ng/ml or lower determined 8 hours after a single oral dose of 0.2 mg/kg identified patients who did not accumulate haloperidol during chronic dosing of 0.4 mg/kg per day above a presumed therapeutic range for haloperidol of 5 to 15 ng/ml. The implications or these data for the clinical use of haloperidol are discussed. C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. UNIV FLORIDA,DEPT PHARM PRACTICE,GAINESVILLE,FL 32611. UNIV FLORIDA,DEPT PSYCHIAT,GAINESVILLE,FL 32611. NR 33 TC 10 Z9 10 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1993 VL 13 IS 2 BP 120 EP 127 PG 8 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA KR982 UT WOS:A1993KR98200006 PM 8463444 ER PT J AU SAROKIN, D SCHULKIN, J AF SAROKIN, D SCHULKIN, J TI THE NECESSITY OF ENVIRONMENTAL ECONOMICS SO JOURNAL OF ENVIRONMENTAL MANAGEMENT LA English DT Article DE ENVIRONMENTAL ECONOMICS; SUSTAINABLE DEVELOPMENT; ENVIRONMENTAL RESPONSIBILITY C1 UNIV PENN, DEPT DECIS SCI, PHILADELPHIA, PA 19104 USA. NIMH, NEUROENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. RP SAROKIN, D (reprint author), US EPA, TS-792A, 401 M ST SW, WASHINGTON, DC 20460 USA. NR 53 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0301-4797 EI 1095-8630 J9 J ENVIRON MANAGE JI J. Environ. Manage. PD APR PY 1993 VL 37 IS 4 BP 259 EP 280 DI 10.1006/jema.1993.1021 PG 22 WC Environmental Sciences SC Environmental Sciences & Ecology GA LB214 UT WOS:A1993LB21400002 ER PT J AU RACIOPPI, L RONCHESE, F MATIS, LA GERMAIN, RN AF RACIOPPI, L RONCHESE, F MATIS, LA GERMAIN, RN TI PEPTIDE MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II COMPLEXES WITH MIXED AGONIST ANTAGONIST PROPERTIES PROVIDE EVIDENCE FOR LIGAND-RELATED DIFFERENCES IN T-CELL RECEPTOR DEPENDENT INTRACELLULAR SIGNALING SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MEDIATED GENE-TRANSFER; KINASE-C ACTIVATION; COSTIMULATORY SIGNAL; ANTIGEN PRESENTATION; LYMPHOCYTE-T; CYTOCHROME-C; TYROSINE PHOSPHORYLATION; PROLIFERATIVE RESPONSE; IMMUNOGENIC PEPTIDES; ENDOGENOUS ANTIGENS AB Clonal activation of CD4+ and CD8+ T lymphocytes depends on binding of peptide-major histocompatibility complex (MHC) molecule complexes by their alpha/beta receptors, eventually resulting in sufficient aggregation to initiate second messenger generation. The nature of intracellular signals resulting from such T cell receptor (TCR) occupancy is believed to be independent of the specific structure of the ligand being bound, and to vary quantitatively, not qualitatively, with the concentration of ligand offered and the affinity of the receptor for the peptide-MHC molecule complex. In contrast to the expectations of this model, the analysis of the response of a T helper type 1 clone to mutant EalphaEbeta(k) molecules in the absence or presence of a peptide antigen revealed that peptide inhibited the interleukin 2 (IL-2) response to an otherwise allostimulatory mutant form of this MHC class II molecule. The inhibition was not due to competition for formation of alloantigen, it required TCR recognition of peptide-mutant MHC molecule complexes, and it decreased IL-2 production without affecting receptor-dependent IL-3, IL-2 receptor alpha, or size enlargement responses. This preferential reduction in IL-2 secretion could be correlated with the costimulatory signal dependence of this cytokine response, but could not be overcome by crosslinking the CD28 molecule on the T cell. These results define a new class of TCR ligands with mixed agonist/antagonist properties, and point to a ligand-related variation in the quality of clonotypic receptor signaling events or their integration with other signaling processes. It was also found that a single TCR ligand showed greatly different dose thresholds for the elicitation of distinct effector responses from a cloned T cell population. The observations that changes in ligand structure can result in qualitative alterations in the effects of receptor occupancy and that quantitative variations in ligand density can be translated into qualitative differences in T cell responses have important implications for models of intrathymic selection and control of the results of active immunization. C1 NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BLDG 10,ROOM 11N311,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NCI,BIOL RESPONSE MODIFIER BRANCH,BETHESDA,MD 20892. OI racioppi, luigi/0000-0002-9207-6752 NR 78 TC 249 Z9 251 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1993 VL 177 IS 4 BP 1047 EP 1060 DI 10.1084/jem.177.4.1047 PG 14 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KU080 UT WOS:A1993KU08000018 PM 8384651 ER PT J AU WELLS, FB TATSUMI, Y BLUESTONE, JA HEDRICK, SM ALLISON, JP MATIS, LA AF WELLS, FB TATSUMI, Y BLUESTONE, JA HEDRICK, SM ALLISON, JP MATIS, LA TI PHENOTYPIC AND FUNCTIONAL-ANALYSIS OF POSITIVE SELECTION IN THE GAMMA/DELTA T-CELL LINEAGE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID ANTIGEN RECEPTOR; CYCLOSPORINE-A; LYMPHOCYTES-T; SIGNAL TRANSDUCTION; IMMATURE THYMOCYTES; DEFICIENT MICE; INTERLEUKIN-2; ACTIVATION; EXPRESSION; MATURE AB Recent evidence suggests that T cells expressing gamma/delta antigen receptors (T cell receptor [TCR]) are subject to positive selection during development. We have shown that T cells expressing a class I major histocompatibility complex (MHC)-specific gamma/delta TCR transgene (tg) are not positively selected in class I MHC-deficient, beta2-microglobulin (beta2m) gene knockout mice (tg+ beta2m-). In this report, we examine phenotypic and functional parameters of gamma/delta positive selection in this transgenic model system. TCR-gamma/delta tg+ thymocytes of mature surface phenotype (heat stable antigen-, CD5hi) were found in beta2m+ but not in beta2m- mice. Moreover, subsets of tg+ thymocytes with the phenotype of activated T cells (interleukin [IL]2R+, CD44hi, or Mel-14lo) were also present only in the beta2m+ mice. Cyclosporine A, which blocks positive selection of TCR-alpha/beta T cells, also inhibited gamma/delta tg+ T cell development. These results support the idea that positive selection of TCR-gamma/delta requires active TCR-mediated signal transduction. Whereas tg+ beta2m+ thymocytes produced IL-2 and proliferated when stimulated by alloantigen, TCR engagement of tg+ beta2m- thymocytes by antigen induced IL-2R expression but was uncoupled from the signal transduction pathway leading to IL-2 production and autocrine proliferation. Overall, these results demonstrate significant parallels between gamma/delta and alpha/beta lineage development, and suggest a general role for TCR signaling in thymic maturation. C1 PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. UNIV CHICAGO,DEPT PATHOL,CHICAGO,IL 60637. UNIV CHICAGO,COMM IMMUNOL,CHICAGO,IL 60637. UNIV CALIF SAN DIEGO,DEPT BIOL,LA JOLLA,CA 92093. UNIV CALIF BERKELEY,DEPT BIOL,BERKELEY,CA 94720. UNIV CALIF BERKELEY,CTR CANC,BERKELEY,CA 94720. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74102, CA-40041]; NIAID NIH HHS [AI00602] NR 65 TC 33 Z9 35 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1993 VL 177 IS 4 BP 1061 EP 1070 DI 10.1084/jem.177.4.1061 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KU080 UT WOS:A1993KU08000019 PM 8459203 ER PT J AU BONOMO, A MATZINGER, P AF BONOMO, A MATZINGER, P TI THYMUS EPITHELIUM INDUCES TISSUE-SPECIFIC TOLERANCE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID HISTOCOMPATIBILITY COMPLEX ANTIGENS; T-CELL TOLERANCE; NEONATAL TOLERANCE; CD4+8+ THYMOCYTES; IMMUNE-RESPONSES; CLONAL DELETION; TRANSGENIC MICE; MHC MOLECULES; ALLOGRAFTS; DEOXYGUANOSINE AB Most current models of T cell development include a positive selection step in the thymus that occurs when T cells interact with thymic epithelium and a negative selection step after encounters with bone marrow-derived cells. We show here that developing T cells are tolerized when they recognize antigens expressed by thymic epithelium, that the tolerance is tissue specific, and that it can occur by deletion of the reactive T cells. RP BONOMO, A (reprint author), NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892, USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 69 TC 109 Z9 109 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1993 VL 177 IS 4 BP 1153 EP 1164 DI 10.1084/jem.177.4.1153 PG 12 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KU080 UT WOS:A1993KU08000028 PM 8459209 ER PT J AU KOONIN, EV AF KOONIN, EV TI COMPUTER-ASSISTED IDENTIFICATION OF A PUTATIVE METHYLTRANSFERASE DOMAIN IN NS5 PROTEIN OF FLAVIVIRUSES AND LAMBDA-2 PROTEIN OF REOVIRUS SO JOURNAL OF GENERAL VIROLOGY LA English DT Note ID DEPENDENT RNA-POLYMERASES; POSITIVE-STRAND; SACCHAROMYCES-CEREVISIAE; NUCLEOTIDE-SEQUENCE; GENE; REPLICATION; EXPRESSION; HELICASES; VIRUSES; CLONING AB A sequence motif that is conserved in a number of S-adenosylmethionine (SAM)-utilizing methyltransferases and is implicated in SAM binding was identified in the N-terminal portion of NS5 proteins of flaviviruses and in lambda2 protein of reovirus. An additional conserved motif was shared by these viral proteins and two distinct groups of methyltransferases including as the prototypes Rhodobacter capsulatus hydroxyneurosporene methylase (crtF gene product) and yeast 3,4-dihydroxy-5-hexaprenylbenzoate methylase (COQ3 gene product), respectively. Statistically significant similarity was revealed between the region of flavivirus NS5 containing the SAM-binding motif and a newly characterized family of putative methyltransferases from bacteria, yeast and plants, which is related to the Coq3 group. Amino acid sequence signatures were derived that are unique for NS5 proteins and different subsets of (putative) cellular methyltransferases. It is hypothesized that the N-terminal domain of NS5 is a methyltransferase involved in viral RNA capping. Thus NS5 may be a two-domain protein. with its C-terminal domain comprising the RNA-dependent RNA polymerase. The putative methyltransferase domain of flaviviruses is unrelated to the methyltransferase domain previously characterized in positive-strand RNA viruses of the alphavirus-like supergroup. The lack of sequence similarity and different location of the putative methyltransferase domain underscores the drastic difference in the genome layout of flaviviruses and alphaviruses. The identification of the putative methyltransferase domain in reovirus lambda2 protein is compatible with the available evidence that this protein is the viral capping enzyme. C1 RUSSIAN ACAD SCI,INST MICROBIOL,MOSCOW,RUSSIA. RP KOONIN, EV (reprint author), NIH,NATL LIB MED NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,BETHESDA,MD 20892, USA. NR 42 TC 169 Z9 180 U1 1 U2 4 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1317 J9 J GEN VIROL JI J. Gen. Virol. PD APR PY 1993 VL 74 BP 733 EP 740 DI 10.1099/0022-1317-74-4-733 PN 4 PG 8 WC Biotechnology & Applied Microbiology; Virology SC Biotechnology & Applied Microbiology; Virology GA KW696 UT WOS:A1993KW69600022 PM 8385698 ER PT J AU RISCO, C DASILVA, PP AF RISCO, C DASILVA, PP TI BINDING OF BACTERIAL-ENDOTOXINS TO THE MACROPHAGE SURFACE - VISUALIZATION BY FRACTURE-FLIP AND IMMUNOCYTOCHEMISTRY SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article DE BACTERIAL ENDOTOXINS; LIPOPOLYSACCHARIDE; LPS; RAT ALVEOLAR MACROPHAGES; FRACTURE-FLIP; IMMUNOCYTOCHEMISTRY ID LIPOPOLYSACCHARIDE LPS; HUMAN-MONOCYTES; TUMOR-NECROSIS; CELL-SURFACE; RECEPTOR; SHOCK AB Endotoxins (lipopolysaccharides, LPS) are surface components of gram-negative bacteria that stimulate macrophage activation and cause endotoxic shock. How LPS is recognized by host cells is still an open question, but it is generally accepted that many effects of endotoxins follow the overproduction of cytokines by macrophages. In the present study, we used fracture-flip and immunolabeling to study the morphology of isolated commercial LPS (C-LPS), the endotoxin release from the bacterial wall in presence of serum (S-LPS), and the distribution of these two endotoxins on the macrophage surface. Cells treated with C-LPS exhibited large LPS aggregates bound to smooth and particulate areas of the membrane and to microvilli. In contrast, macrophages incubated with S-LPS showed a uniform monodispersed labeling over the free surface of the membrane. Our results show that fracture-flip provides high-resolution images of the binding of ligands to the cell surface. They also suggest the importance of using highly dispersed LPS suspensions when the mechanisms of cell activation and damage by endotoxins are studied. RP RISCO, C (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DEPT MATH BIOL,STRUCT BIOL SECT,FREDERICK,MD 21702, USA. NR 31 TC 12 Z9 12 U1 0 U2 3 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 APR PY 1993 VL 41 IS 4 BP 601 EP 608 PG 8 WC Cell Biology SC Cell Biology GA KT973 UT WOS:A1993KT97300014 PM 8450199 ER PT J AU LIAO, F SHIN, HS RHEE, SG AF LIAO, F SHIN, HS RHEE, SG TI CROSS-LINKING OF FC-GAMMA-RIIIA ON NATURAL-KILLER-CELLS RESULTS IN TYROSINE PHOSPHORYLATION OF PLC-GAMMA-1 AND PLC-GAMMA-2 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID RECEPTOR ZETA-CHAIN; T-CELL; PHOSPHOLIPASE C-GAMMA-1; SIGNAL TRANSDUCTION; IGG FC; ACTIVATION; IMMUNOGLOBULIN; STIMULATION; ENGAGEMENT; INHIBITION AB The FcgammaRIIIA, which is composed of a transmembrane IgG-binding glycoprotein and either a disulfide-linked homodimer (zetazeta, gammagamma) or heterodimer (zetagamma), mediates the antibody-dependent cellular cytotoxicity in NK cells. The role of phospholipase C (PLC) isozymes in FcgammaRIIIA-mediated signal transduction was investigated. The NK cell line NK3.3 was found to contain PLC-gamma1 and an especially high concentration of PLC-gamma2, but PLC-beta1 and PLC-delta1 were not detected. Cross-linking of FcgammaRIIIA on NK3.3 cells induced a rapid phosphorylation of PLC-gamma1 and PLC-gamma2 on tyrosine residues. Pretreatment of NK3.3 cells with a tyrosine kinase inhibitor, herbimycin A, prevented the tyrosine phosphorylation of both PLC-gamma1 and PLC-gamma2. These results indicate that activation of FcgammaRIIIA on NK3.3 cells is coupled either directly or indirectly to a nonreceptor tyrosine kinase, which phosphorylates, and thereby activates PLC-gamma1 and PLC-gamma2. C1 NHLBI,BIOCHEM LAB,BLDG 3,ROOM 122,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. NR 40 TC 46 Z9 46 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1993 VL 150 IS 7 BP 2668 EP 2674 PG 7 WC Immunology SC Immunology GA KT805 UT WOS:A1993KT80500012 PM 8454849 ER PT J AU BRINKMANN, U LEE, BK PASTAN, I AF BRINKMANN, U LEE, BK PASTAN, I TI RECOMBINANT IMMUNOTOXINS CONTAINING THE VH OR VL DOMAIN OF MONOCLONAL-ANTIBODY B3 FUSED TO PSEUDOMONAS EXOTOXIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LIGHT CHAIN DIMER; ESCHERICHIA-COLI; 3-DIMENSIONAL STRUCTURE; CHIMERIC TOXINS; CRYSTAL; COMPLEX; CLONING; PROTEIN; RESOLUTION; REPERTOIRE AB We prepared recombinant immunotoxins in Escherichia coli in which the V(H) or V(L) domains of mAb B3 were fused to a truncated form of Pseudomonas exotoxin (PE) (PE38KDEL). mAb B3 binds to a carbohydrate Ag found on the surfaces of many types of cancers and only a few normal tissues. PE38KDEL is a 38-kDa form of PE (66 kDa) that is missing the cell-binding domain of PE and has the carboxyl end changed from REDLK to KDEL. We show that immunotoxins in which the H chain or the L chain V region is fused to PE38KDEL bind to and kill carcinoma cells containing the B3 Ag. B3 Ag-negative cells were not affected. The cytotoxicity of these molecules is between 20- and 100-fold less than B3(Fv)-immunotoxins, containing both the H and L chain V regions. The V(L)-containing toxin was more active than the V(H)-containing toxin, indicating that the L chain of mAb B3 probably contributes more to Ag-binding than the H chain. Refolding experiments show that B3(V(L))-PE38KDEL aggregates less than the V(H)-derivative or than a single chain immunotoxin B3(Fv)-PE38KDEL, which contains both domains in a single chain form. Furthermore, in addition to monomers, active homodimers of B3(V(H))- and B3(V(L))-PE38KDEL were obtained from renaturation experiments. The V(L)-toxin dimers, which might have their binding regions arranged in a manner similar to Bence Jones proteins (L chain homodimers), were found to have almost the same cytotoxicity as the monomers, whereas the V(H)-toxin dimers had decreased cytotoxic activity. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BLDG 37,ROOM 4E16,BETHESDA,MD 20892. NR 34 TC 27 Z9 28 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1993 VL 150 IS 7 BP 2774 EP 2782 PG 9 WC Immunology SC Immunology GA KT805 UT WOS:A1993KT80500023 PM 8454854 ER PT J AU CHEN, HT ALEXANDER, CB YOUNGCOOPER, GO MAGE, RG AF CHEN, HT ALEXANDER, CB YOUNGCOOPER, GO MAGE, RG TI VH GENE-EXPRESSION AND REGULATION IN THE MUTANT ALICIA RABBIT - RESCUE OF VHA2 ALLOTYPE EXPRESSION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CHAIN VARIABLE-REGION; IMMUNOGLOBULIN HEAVY-CHAINS; SOMATIC DIVERSIFICATION; B-CELLS; SUPPRESSED RABBITS; ANTIBODY DIVERSITY; JOINING REGION; VDJ GENES; IG-VH; SEQUENCES AB Rabbits of the Alicia strain, derived from rabbits expressing the V(H)a2 allotype, have a mutation in the H chain locus that has a cis effect upon the expression of V(H)a2 and V(H)a- genes. A small deletion at the most J-proximal (3') end of the V(H) locus leads to low expression of all the genes on the entire chromosome in heterozygous ali mutants and altered relative expression of V(H) genes in homozygotes. To study V(H) gene expression and regulation, we used the polymerase chain reaction to amplify the V(H) genes expressed in spleens of young and adult wild-type and mutant Alicia rabbits. The cDNA from reverse transcription of splenic mRNA was amplified and polymerase chain reaction libraries were constructed and screened with oligonucleotides from framework regions 1 and 3, as well as J(H). Thirty-three V(H)-positive clones were sequenced and analyzed. We found that in mutant Alicia rabbits, products of the first functional V(H) gene (V(H)4a2), (or V(H)4a2-like genes) were expressed in 2- to 8-wk-olds. Expression of both the V(H)x and V(H)y types of V(H)a- genes was also elevated but the relative proportions of V(H)x and V(H)y, especially V(H)x, decreased whereas the relative levels of expression of V(H)4a2 or V(H)4a2-like genes increased with age. Our results suggest that the appearance of sequences resembling that of the V(H)1a2, which is deleted in the mutant ali rabbits, could be caused by alterations of the sequences of the rearranged V(H)4a2 genes by gene conversions and/or rearrangement of upstream V(H)1a2-like genes later in development. C1 NIAID,IMMUNOL LAB,MOLEC IMMUNOGENET SECT,BETHESDA,MD 20892. NR 53 TC 24 Z9 24 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1993 VL 150 IS 7 BP 2783 EP 2793 PG 11 WC Immunology SC Immunology GA KT805 UT WOS:A1993KT80500024 PM 8454855 ER PT J AU SINGER, II KAWKA, DW DEMARTINO, JA DAUGHERTY, BL ELLISTON, KO ALVES, K BUSH, BL CAMERON, PM CUCA, GC DAVIES, P FORREST, MJ KAZAZIS, DM LAW, MF LENNY, AB MACINTYRE, DE MEURER, R PADLAN, EA PANDYA, S SCHMIDT, JA SEAMANS, TC SCOTT, S SILBERKLANG, M WILLIAMSON, AR MARK, GE AF SINGER, II KAWKA, DW DEMARTINO, JA DAUGHERTY, BL ELLISTON, KO ALVES, K BUSH, BL CAMERON, PM CUCA, GC DAVIES, P FORREST, MJ KAZAZIS, DM LAW, MF LENNY, AB MACINTYRE, DE MEURER, R PADLAN, EA PANDYA, S SCHMIDT, JA SEAMANS, TC SCOTT, S SILBERKLANG, M WILLIAMSON, AR MARK, GE TI OPTIMAL HUMANIZATION OF 1B4, AN ANTI-CD18 MURINE MONOCLONAL-ANTIBODY, IS ACHIEVED BY CORRECT CHOICE OF HUMAN V-REGION FRAMEWORK SEQUENCES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID REDUCES ORGAN INJURY; LEUKOCYTE ADHESION; NEUTROPHIL ADHERENCE; TRANSENDOTHELIAL MIGRATION; INTERLEUKIN-2 RECEPTOR; REPERFUSION INJURY; TRANSIENT ADHESION; HEMORRHAGIC-SHOCK; ENDOTHELIAL-CELLS; INTERFERON-GAMMA AB The murine anti-CD18 mAb 1B4 has been humanized using CDR grafting. Three V(H) (Gal, Jon, and New) and two V(L) (Rei and, Len) human frameworks, whose selection was based exclusively on their sequence identity with m1B4, were used to construct five human gamma4/kappa recombinant antibodies: Gal/Rei, Gal/Len, Jon/Rei, and New/Rei, and a ''hemichimeric'' antibody pairing the V(H) of m1B4 with grafted Rei. Each of these h1B4 constructs completely inhibited the binding of m1B4 to activated human leukocytes with avidities (IC50) ranging from 1.5 to 8.0 nM, compared to 0.5 nM for m1B4. Replacement of three V(H) residues in the best V(H) framework, Gal, with the corresponding m1B4 ''packing'' (nonsolvent exposed) residues gave an h1B4 (mutant Gal/Rei) with the same avidity as m1B4. Avidity correlated with overall percent identity between the human and murine V(H) frameworks and, in particular, with conservation of ''packing'' residues. Rei and Len V(L) frameworks proved to be interchangeable. Further characterization showed that the Gal/Rei prototype was equipotent to m1B4 in blocking adhesion of polymorphonuclear leukocytes and monocytes to human vascular endothelium in vitro, and polymorphonuclear leukocyte extravasation into C5a-injected rabbit or monkey skin sites. Dual-label immunofluorescence microscopy of bone marrow cells with Gal/Rei h1B4 and m1B4 demonstrated that the fine specificity of the combining sites had not been altered by humanization. Reduced immunogenicity was demonstrated in rhesus monkeys that tolerated weekly treatment with h1B4 for 6 wk, whereas m1B4 induced profound anaphylaxis at 3 wk. Anti-1B4 titers in h1B4-treated rhesus were 50 to 66% lower and developed 1 wk later than in ml B4-treated monkeys. Crucially, the anti-h1B4 antibodies were anti-idiotypic while the anti-m1B4 antibodies were directed against constant and framework regions. We conclude that sequence identity searches are sufficient to identify suitable human frameworks for CDR-grafting of m1B4, yielding functionally equivalent humanized antibodies that are tolerated better in primates. C1 MERCK SHARP & DOHME LTD,DEPT CELLULAR & MOLEC BIOL,RAHWAY,NJ 07065. MERCK SHARP & DOHME LTD,DEPT BIOPHYS CHEM,RAHWAY,NJ 07065. MERCK SHARP & DOHME LTD,DEPT BIOCHEM & MOLEC PATHOL,RAHWAY,NJ 07065. MERCK SHARP & DOHME LTD,DEPT CELLULAR & MOLEC PHARMACOL,RAHWAY,NJ 07065. MERCK SHARP & DOHME LTD,DEPT BIOL DATA,RAHWAY,NJ 07065. MERCK SHARP & DOHME LTD,DEPT IMMUNOL & INFLAMMAT,RAHWAY,NJ 07065. MERCK SHARP & DOHME LTD,DEPT MOLEC SYST,RAHWAY,NJ 07065. NIDDKD,MOLEC BIOL LAB,MOLEC STRUCT SECT,BETHESDA,MD 20892. NR 68 TC 45 Z9 46 U1 2 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1993 VL 150 IS 7 BP 2844 EP 2857 PG 14 WC Immunology SC Immunology GA KT805 UT WOS:A1993KT80500030 PM 8095956 ER PT J AU WANG, JM SHERRY, B FIVASH, MJ KELVIN, DJ OPPENHEIM, JJ AF WANG, JM SHERRY, B FIVASH, MJ KELVIN, DJ OPPENHEIM, JJ TI HUMAN RECOMBINANT MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA AND PROTEIN-1-BETA AND MONOCYTE CHEMOTACTIC AND ACTIVATING FACTOR UTILIZE COMMON AND UNIQUE RECEPTORS ON HUMAN MONOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN INTERLEUKIN-8 RECEPTOR; COLONY FORMATION INVITRO; HUMAN-NEUTROPHILS; PROGENITOR CELLS; CYTOKINE FAMILY; MURINE; IDENTIFICATION; CLONING; MIGRATION; PROTEINS AB The human macrophage inflammatory proteins-1alpha and -beta (MIP-1alpha and -beta), which a real so known as LD78 and ACT2, respectively, are distinct but highly related members of the chemoattractant cytokine (chemokine) family. rMIP-1alpha and -beta labeled with I-125 specifically bind to human peripheral blood monocytes, the monocytic cell line THP-1, peripheral blood T cells, and the YT cell line. Steady state binding experiments revealed approximately 3000 high affinity binding sites/cell for MIP-1alpha on human monocytes and on THP-1 cells, with K(d) values of 383 pM and 450 pM, respectively. Human MIP-1alpha and -beta had nearly identical affinities for the binding sites and each competed equally well for binding. Human monocyte chemotactic and activating factor (MCAF), a member of the same chemokine family, consistently displaced about 25% of human MIP-1alpha and -beta binding on monocytes but not on YT cells, which did not bind MCAF. On the other hand, human rMIP-1alpha and -beta partially inhibited binding of radiolabeled MCAF to monocytes. Both MIP-1alpha and -beta were chemotactic for human monocytes. Preincubation of monocytes with human rMIP-1alpha or -beta markedly reduced cell migration towards the other cytokine, whereas preincubation with human rMCAF only partially desensitized the monocyte chemotaxis response to human rMIP-1alpha or -beta. These data suggest the existence of three subtypes of receptors, i.e., one unique receptor shared by MIP-1alpha and -beta, a second unique receptor for MCAF, and a third species that recognizes both MCAF and MIP-1 peptides. C1 PICOWER INST MED RES,MANHASSET,NY 11030. NCI,FREDERICK CANC RES & DEV CTR,COMP SERV,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,STAT SERV,FREDERICK,MD 21702. RP WANG, JM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702, USA. NR 26 TC 114 Z9 115 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1993 VL 150 IS 7 BP 3022 EP 3029 PG 8 WC Immunology SC Immunology GA KT805 UT WOS:A1993KT80500047 PM 8454871 ER PT J AU TSANG, KY KASHMIRI, SVS DEFILIPPI, R QI, CF CALVO, B SHU, LM NIERODA, CA GREINER, JW SCHLOM, J AF TSANG, KY KASHMIRI, SVS DEFILIPPI, R QI, CF CALVO, B SHU, LM NIERODA, CA GREINER, JW SCHLOM, J TI A HUMAN T-CELL LINE ENGINEERED TO SECRETE CHIMERIC MONOCLONAL-ANTIBODY SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE TUMOR IMMUNOTHERAPY; CHIMERIC MONOCLONAL ANTIBODIES; TUMOR-INFILTRATING LYMPHOCYTES; ANTIBODY-DEPENDENT CELL-MEDIATED CYTOTOXICITY ID TUMOR-INFILTRATING LYMPHOCYTES; COLON-CARCINOMA XENOGRAFTS; METASTATIC MELANOMA; GENE-TRANSFER; IMMUNOGLOBULIN GENE; RETROVIRAL VECTORS; EFFECTOR-CELLS; LYMPHOID-CELLS; EXPRESSION; CANCER AB Both monoclonal antibodies (MAbs) and human T cells have been used in human tumor immunotherapy protocols. Tumor-infiltrating lymphocytes (TILs) and MAbs that can mediate antibody-dependent cell-mediated cytotoxicity (ADCC) via human effector cells have shown antitumor effects in both animal models and clinical trials. One potential novel approach would be to combine these two modalities in the creation of a T cell capable of secreting antitumor immunoglobulins (1g), in essence, creating an antitumor Ig ''factory'' at the tumor site. In the studies reported here, we have cloned the D612 MAb Ig genes and generated a chimeric D612 IgG1 containing the murine variable region and human constant region. D612 MAb has been shown to mediate lysis of human colon carcinomas via effector cell-mediated ADCC. We have demonstrated that following transfection, chimeric D612 can be expressed and secreted by the human T-cell line MOLT-4 at a rate of 0.25 mug/ml per 10(6) cells in 72 hours. The secreted Ig retained its antigen-binding properties as assayed by competition radioimmunoassay and also its ability to mediate ADCC against human tumor cells. To our knowledge, this is the first demonstration of the production of a chimeric IgG by human T cells and opens the possibility of a therapeutic approach in which TILs secrete humanized antitumor MAb capable of mediating ADCC at the tumor site. RP TSANG, KY (reprint author), NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892, USA. NR 51 TC 7 Z9 7 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD APR PY 1993 VL 13 IS 3 BP 143 EP 152 DI 10.1097/00002371-199304000-00001 PG 10 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA KU065 UT WOS:A1993KU06500001 PM 8471589 ER PT J AU KOPP, WC SMITH, JW EWEL, CH ALVORD, WG MAIN, C GUYRE, PM STEIS, RG LONGO, DL URBA, WJ AF KOPP, WC SMITH, JW EWEL, CH ALVORD, WG MAIN, C GUYRE, PM STEIS, RG LONGO, DL URBA, WJ TI IMMUNOMODULATORY EFFECTS OF INTERFERON-GAMMA IN PATIENTS WITH METASTATIC MALIGNANT-MELANOMA SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE INTERFERON-GAMMA; NEOPTERIN; MELANOMA; IMMUNOLOGICAL MONITORING; CD14; CD64 ID HUMAN MONONUCLEAR PHAGOCYTES; HUMAN-MONOCYTES; CANCER-PATIENTS; LIPOPOLYSACCHARIDE LPS; MONOCLONAL-ANTIBODIES; ANTIGEN EXPRESSION; FC-RECEPTORS; PHASE-II; INDUCTION; CD14 AB Interferon-gamma (IFN-gamma) is a potent monocyte/macrophage activating agent that in animal models exhibits a bell-shaped dose-response curve of immunomodulatory activity and antitumor efficacy. Previous clinical trials of IFN-gamma conducted at the maximal tolerated dose (MTD) have been associated with low response rates that may have been due to failure to treat at an optimal immunomodulatory dose (OID). The objective of this study was to test the hypothesis that optimal immunomodulatory activity of IFN-gamma in patients with metastatic melanoma would be obtained at a dose below the MTD. Groups of five patients each were given daily subcutaneous injections of IFN-gamma at doses of 0.0 1, 0.1, or 0.25 mg/m2. In vivo immunomodulation was assessed by serial measurement of serum neopterin and by flow cytometry. IFN-gamma doses of 0. 1 or 0.25 mg/m2 induced significantly greater immunomodulation of monocyte-associated immune parameters than 0.01 mg/m2. Changes in immunologic parameters included marked elevation of serum neopterin levels, significant increases in monocyte expression of CD64, beta2-microglobulin, and HLA-ABC, and decreased monocyte expression of CD14. The most dramatic decreases in CD14 expression were observed on monocytes obtained from patients treated at 0.25 mg/M2 . The 0.25-mg/m2 dose group had significantly lower white blood cell counts on day 14. No bell-shaped curve of immunologic response was observed over the dosage range tested. Based on the similarity of the immunologic effects at 0. 1 and 0.25 mg/M2, treatment at the MTD of IFN-gamma (0.25 mg/m2) represents treatment at the OID for patients with metastatic malignant melanoma. C1 NCI,FREDERICK CANC RES & DEV CTR,DATA MANAGEMENT SERV INC,FREDERICK,MD 21701. NCI,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. FREDERICK MEM HOSP,FREDERICK,MD. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT PHYSIOL,HANOVER,NH 03756. RP KOPP, WC (reprint author), NCI,FCRDC,INC DYNCORP,PROGRAM RESOURCES,CLIN SERV PROGRAM,CLIN IMMUNOL SERV,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 33 TC 17 Z9 19 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD APR PY 1993 VL 13 IS 3 BP 181 EP 190 DI 10.1097/00002371-199304000-00005 PG 10 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA KU065 UT WOS:A1993KU06500005 PM 8471592 ER PT J AU ROILIDES, E HOLMES, A BLAKE, C PIZZO, PA WALSH, TJ AF ROILIDES, E HOLMES, A BLAKE, C PIZZO, PA WALSH, TJ TI IMPAIRMENT OF NEUTROPHIL ANTIFUNGAL ACTIVITY AGAINST HYPHAE OF ASPERGILLUS-FUMIGATUS IN CHILDREN INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID CHRONIC GRANULOMATOUS-DISEASE; PULMONARY ASPERGILLOSIS; ENVELOPE GLYCOPROTEIN; HOST DEFENSE; INVITRO; DAMAGE; AIDS; MONONUCLEAR; PHAGOCYTES; INHIBITION AB Human immunodeficiency virus (HIV)-infected patients may acquire invasive aspergillosis without previously recognized risk factors, such as neutropenia or corticosteroid therapy. Because neutrophils (PMNL) are an important component of host defense in aspergillosis, the antifungal activity of PMNL against hyphae of Aspergillus fumigatus in 31 HIV-infected children was assessed. Hyphal damage was unaffected in 15 HIV-infected children with age-adjusted CD4 cell counts greater-than-or-equal-to 25% of the normal median value; it was decreased in 16 with CD4 cell counts <25% (both vs. 20 healthy controls, P = .001. Incubation with sera from 12 of 14 HIV-infected children but not with the recombinant HIV proteins gp 1 20, gp41, and p24 suppressed antifungal activity of normal PMNL compared with normal serum (P = .002). Pretreatment of defective PMNL from 5 patients with granulocyte colony-stimulating factor (G-CSF) partially corrected the defect (P = .002). These findings suggest that impaired serum-mediated antifungal activity against Aspergillus hyphae exists in PMNL of HIV-infected patients with low CD4 cell counts; G-CSF may improve this activity. C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,ROOM 13N240,BETHESDA,MD 20892. NR 41 TC 82 Z9 85 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1993 VL 167 IS 4 BP 905 EP 911 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KU086 UT WOS:A1993KU08600016 PM 8450255 ER PT J AU HALL, SL SARRIS, CM TIERNEY, EL LONDON, WT MURPHY, BR AF HALL, SL SARRIS, CM TIERNEY, EL LONDON, WT MURPHY, BR TI A COLD-ADAPTED MUTANT OF PARAINFLUENZA VIRUS TYPE-3 IS ATTENUATED AND PROTECTIVE IN CHIMPANZEES SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID INFLUENZA AB A live attenuated cold-adapted parainfluenza virus type 3 (PIV-3) vaccine is being developed to prevent the serious lower respiratory tract disease caused by this virus in infants and young children. This cold-passaged mutant (cp45) was evaluated in seronegative chimpanzees and found to be highly attenuated in both the upper and lower respiratory tracts compared to its wild-type parent. Animals immunized with cp45 were also highly resistant to wild-type PIV-3 challenge. Stability of the attenuation phenotype was demonstrated by the administration to 2 additional chimpanzees of an isolate of cp45 obtained after 10 days of replication in a chimpanzee. It was attenuated in both the upper and lower respiratory tracts. The cp45 virus present in the respiratory tract secretions of chimpanzees retained the temperature-sensitive (ts) phenotype, but some loss of ts property was observed in the isolates. These results provide a basis on which to proceed to clinical trials in seronegative human infants and children. RP HALL, SL (reprint author), NIAID,INFECT DIS LAB,RESP VIRUSES SECT,BETHESDA,MD 20892, USA. NR 13 TC 25 Z9 25 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1993 VL 167 IS 4 BP 958 EP 962 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KU086 UT WOS:A1993KU08600026 PM 8383726 ER PT J AU HYAMS, KC MALONE, JD KAPIKIAN, AZ ESTES, MK JIANG, X BOURGEOIS, AL PAPARELLO, S HAWKINS, RE GREEN, KY AF HYAMS, KC MALONE, JD KAPIKIAN, AZ ESTES, MK JIANG, X BOURGEOIS, AL PAPARELLO, S HAWKINS, RE GREEN, KY TI NORWALK VIRUS-INFECTION AMONG DESERT STORM TROOPS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Letter ID GASTROENTERITIS; OUTBREAK C1 NATL NAVAL MED CTR, BETHESDA, MD 20814 USA. NIH, INFECT DIS LAB, BETHESDA, MD 20892 USA. BAYLOR COLL MED, DIV MOLEC VIROL, HOUSTON, TX 77030 USA. RP HYAMS, KC (reprint author), USN, MED RES INST, DEPT INFECT DIS, 12300 WASHINGTON AVE, ROCKVILLE, MD 20852 USA. FU NIAID NIH HHS [AI-30488] NR 10 TC 42 Z9 43 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 APR PY 1993 VL 167 IS 4 BP 986 EP 987 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KU086 UT WOS:A1993KU08600033 PM 8383727 ER PT J AU HASHIMOTO, T EBIHARA, T ISHIKO, A SHIMIZU, H BHOGAL, BS BLACK, MM STANLEY, JR NISHIKAWA, T AF HASHIMOTO, T EBIHARA, T ISHIKO, A SHIMIZU, H BHOGAL, BS BLACK, MM STANLEY, JR NISHIKAWA, T TI COMPARATIVE-STUDY OF BULLOUS PEMPHIGOID ANTIGENS AMONG JAPANESE, BRITISH, AND UNITED-STATES PATIENTS INDICATES SIMILAR ANTIGEN PROFILES WITH THE 170-KD ANTIGEN PRESENT BOTH IN THE BASEMENT-MEMBRANE AND ON THE KERATINOCYTE CELL-MEMBRANE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID CDNA CLONING; ANTIBODIES; 230-KD; EXPRESSION; PROTEIN; SERA; IMMUNOFLUORESCENCE; IDENTIFICATION; HETEROGENEITY; HEMIDESMOSOME AB There are a number of controversies relating to studies of bullous pemphigoid (BP) antigens from different institutions, mainly regarding the detection of the 230-kD and 170-kD BP antigens. In this study, in an attempt to resolve the discrepancies, we have examined and compared the reactivity by immunofluorescence, immunoblotting, and immunoprecipitation among the sera from Japanese, British and U.S. BP patients. Both the 230-kD and 170-kD BP antigens were detected by various sera from all populations with immunoblotting, whereas immunoprecipitation detected only the 230-kD BP antigen but not the 170-kD BP antigen. Immunoprecipitation was more sensitive than immunoblotting to detect the 230-kD antigen. These results indicate that both the 230-kD and 170-kD proteins are BP antigens found in all three populations. By immunofluorescence cell surface staining in the lower epidermis in addition to basement membrane zone staining was shown by a considerable number of patients' sera in all populations. Comparison between the results of immunofluorescence and immunoblotting revealed a clear correlation of this cell surface staining with the presence of antibodies against the 170-kD BP antigen. That the affinity-purified antibodies specific to the 170-kD BP antigen showed this cell surface staining further confirmed this correlation. These results may indicate a different nature of the 170-kD BP antigen from that of the 230-kD BP antigen. C1 ST THOMAS HOSP,SKIN UNIT,LONDON SE1 7EH,ENGLAND. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. RP HASHIMOTO, T (reprint author), KEIO UNIV,SCH MED,DEPT DERMATOL,35 SHINANOMACHI,SHINJUKU KU,TOKYO 160,JAPAN. RI Shimizu, Hiroshi/A-5193-2012 NR 27 TC 17 Z9 17 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 385 EP 389 DI 10.1111/1523-1747.ep12471985 PG 5 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500007 PM 7681090 ER PT J AU KORGE, BP STEINERT, PM MISCHKE, D AF KORGE, BP STEINERT, PM MISCHKE, D TI C-TERMINAL DELETION IN KERATIN-1 GENE IS THE MOLECULAR-BASIS FOR THE 2 ALLELES DESCRIBED FOR THE HUMAN KERATIN-1 PROTEIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD 20892. FREE UNIV BERLIN,MED CTR RUDOLF VIRCHOW,INST EXP ONCOL & TRANSPLANTAT MED,W-1000 BERLIN 33,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 441 EP 441 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500050 ER PT J AU ENK, AH ANGELONI, VL UDEY, MC KATZ, SI AF ENK, AH ANGELONI, VL UDEY, MC KATZ, SI TI AN ESSENTIAL ROLE FOR INTERLEUKIN-1-BETA IN THE INDUCTION OF PRIMARY IMMUNE-RESPONSES IN SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 447 EP 447 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500085 ER PT J AU ROCKEN, M BOULAY, JL PAUL, WE SHEVACH, EM AF ROCKEN, M BOULAY, JL PAUL, WE SHEVACH, EM TI INDUCTION OF IL-4 PRODUCTION INVIVO - A MODEL FOR THE STUDY OF ATOPY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 489 EP 489 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500306 ER PT J AU MOLES, JP SCHILLERT, J LEIGH, I TESNIERE, A GUILHOU, JJ BASSETSEQUIN, N AF MOLES, JP SCHILLERT, J LEIGH, I TESNIERE, A GUILHOU, JJ BASSETSEQUIN, N TI CORRELATION BETWEEN CK 19 EXPRESSION AND P53 ACTIVITY IN HUMAN KERATINOCYTES INVITRO AND INVIVO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. ICRF,LONDON,ENGLAND. RP MOLES, JP (reprint author), LAB DERMATOL MOLEC,MONTPELLIER,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 493 EP 493 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500330 ER PT J AU WEINBERG, WC CHAPMAN, K PELLING, J LEVINE, A YUSPA, SH AF WEINBERG, WC CHAPMAN, K PELLING, J LEVINE, A YUSPA, SH TI P53 SYNTHESIS AND P53-DEPENDENT TRANSCRIPTIONAL ACTIVITY ARE MODULATED FOLLOWING INDUCTION OF KERATINOCYTE DIFFERENTIATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. EPPLEY INST CANC RES,OMAHA,NE. PRINCETON UNIV,PRINCETON,NJ 08544. RI Weinberg, Wendy/A-8920-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 493 EP 493 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500328 ER PT J AU DENNING, MF DLUGOSZ, AA YUSPA, SH AF DENNING, MF DLUGOSZ, AA YUSPA, SH TI REDISTRIBUTION OF SPECIFIC PROTEIN-KINASE-C ISOZYMES ACCOMPANY CA-2+-INDUCED KERATINOCYTE DIFFERENTIATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 495 EP 495 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500342 ER PT J AU SZALLASI, Z SMITH, CB DENNING, MF DLUGOSZ, AA YUSPA, SH PETTIT, GR BLUMBERG, PM AF SZALLASI, Z SMITH, CB DENNING, MF DLUGOSZ, AA YUSPA, SH PETTIT, GR BLUMBERG, PM TI DIFFERENTIAL REGULATION OF PROTEIN-KINASE-C ISOZYMES BY INHIBITORY 12-DEOXYPHORBOL 13-MONOESTERS, BRYOSTATIN-1 AND PHORBOL 12-MYRISTATE 13-ACETATE (PMA) IN MOUSE KERATINOCYTES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. ARIZONA STATE UNIV,CANC RES INST,TEMPE,AZ 85287. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 495 EP 495 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500340 ER PT J AU LI, LW HENNINGS, H YUSPA, SH AF LI, LW HENNINGS, H YUSPA, SH TI THAPSIGARGIN AND CYCLOPIAZONIC ACID INHIBIT CA-2+-INDUCED KERATINOCYTE TERMINAL DIFFERENTIATION INVITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 496 EP 496 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500346 ER PT J AU KIRNBAUER, R RODEN, R LOWY, DR SCHILLER, JT AF KIRNBAUER, R RODEN, R LOWY, DR SCHILLER, JT TI PAPILLOMAVIRUS-LIKE PARTICLES PRODUCED IN INSECT CELLS - POTENTIAL APPLICATION TO VACCINE DEVELOPMENT, BASIC BIOLOGY AND SERODIAGNOSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 497 EP 497 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500354 ER PT J AU AMAGAI, M KLAUSKOVTUN, V UDEY, MC STANLEY, JR AF AMAGAI, M KLAUSKOVTUN, V UDEY, MC STANLEY, JR TI EXPRESSION OF THE EXTRACELLULAR (EC) REGION OF PEMPHIGUS-VULGARIS ANTIGEN (PVA) ON MOUSE FIBROBLASTS (L CELLS) CAUSES CELL-TO-CELL ADHESION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 498 EP 498 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500358 ER PT J AU HOLLERAN, WM MENON, GK ELIAS, PM GINNS, EI SIDRANSKY, E AF HOLLERAN, WM MENON, GK ELIAS, PM GINNS, EI SIDRANSKY, E TI BETA-GLUCOCEREBROSIDASE-DEFICIENT TRANSGENIC MICE HAVE ABNORMAL STRATUM-CORNEUM LAMELLAR BILAYERS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,DEPT DERMATOL,SAN FRANCISCO,CA 94143. VET ADM MED CTR,DERMATOL SERV,SAN FRANCISCO,CA 94121. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 498 EP 498 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500357 ER PT J AU COMPTON, JG IDLER, WW AF COMPTON, JG IDLER, WW TI ORGANIZATION OF THE KERATIN GENE-CLUSTER ON HUMAN CHROMOSOME-12 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 500 EP 500 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500369 ER PT J AU MAREKOV, L STEINERT, PM PARRY, DAD AF MAREKOV, L STEINERT, PM PARRY, DAD TI THE DETERMINATION OF THE MOLECULAR DIMENSIONS AND MODE OF ASSEMBLY OF KERATIN INTERMEDIATE FILAMENTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. MASSEY UNIV,PALMERSTON NORTH,NEW ZEALAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 500 EP 500 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500372 ER PT J AU STEINERT, PM KHOUN, S GOLDMAN, RD AF STEINERT, PM KHOUN, S GOLDMAN, RD TI USE OF SYNTHETIC PEPTIDES TO PROBE THE HIGHLY DYNAMIC STRUCTURES OF KERATIN INTERMEDIATE FILAMENTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 500 EP 500 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500371 ER PT J AU JANG, S MARKOVA, NG STEINERT, PM AF JANG, S MARKOVA, NG STEINERT, PM TI POSITIVE AND NEGATIVE ELEMENTS INVOLVED IN THE TRANSCRIPTION OF THE HUMAN PROFILAGGRIN GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 501 EP 501 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500376 ER PT J AU WILMER, JL BURLESON, FG KAYAMA, F KANNO, J LUSTER, MI AF WILMER, JL BURLESON, FG KAYAMA, F KANNO, J LUSTER, MI TI RELATION OF CHEMICALLY-INDUCED INFLAMMATION IN MOUSE SKIN TO PATTERNS OF CYTOKINE PRODUCTION IN HUMAN KERATINOCYTES EXPOSED TO SKIN TOXICANTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 501 EP 501 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500377 ER PT J AU DUGAN, EM WASSERMANN, EM COHEN, PJ ALLEN, RH KATZ, SI HORNE, MK AF DUGAN, EM WASSERMANN, EM COHEN, PJ ALLEN, RH KATZ, SI HORNE, MK TI COBALAMIN DEFICIENCY IN DERMATITIS-HERPETIFORMIS PATIENTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV COLORADO,DENVER,CO 80202. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 509 EP 509 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500427 ER PT J AU GLICK, AB KULKARNI, AB TENNENBAUM, T KARLSSON, S YUSPA, SH AF GLICK, AB KULKARNI, AB TENNENBAUM, T KARLSSON, S YUSPA, SH TI ANALYSIS OF TGF-ALPHA FUNCTION IN THE EPIDERMIS USING TGF-BETA-1 KNOCKOUT MICE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NINOS,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 510 EP 510 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500430 ER PT J AU SELLHEVER, K ROTHNAGEL, J BUNDMAN, D LONGLEY, M GEISER, A ROBERTS, A ROOP, D AF SELLHEVER, K ROTHNAGEL, J BUNDMAN, D LONGLEY, M GEISER, A ROBERTS, A ROOP, D TI TARGETED EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA-1 (TGF-BETA-1) TO THE EPIDERMIS LEADS TO LIVEBORN BUT NONVIABLE TRANSGENIC MICE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. BAYLOR COLL MED,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 510 EP 510 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500432 ER PT J AU LEE, SC KIM, IG MAREKOV, L OKEEFE, EJ PARRY, DAD STEINERT, PM AF LEE, SC KIM, IG MAREKOV, L OKEEFE, EJ PARRY, DAD STEINERT, PM TI THE STRUCTURE OF HUMAN TRICHOHYALIN - A MULTIFUNCTIONAL EF-HAND-TYPE CALCIUM-BINDING PROTEIN, CORNIFIED CELL-ENVELOPE PRECURSOR AND KERATIN INTERMEDIATE FILAMENT ASSOCIATED PROTEIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. UNIV N CAROLINA,DEPT DERMATOL,CHAPEL HILL,NC 27514. MASSEY UNIV,PALMERSTON NORTH,NEW ZEALAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 511 EP 511 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500438 ER PT J AU MARKOVA, NG GAN, SQ STEINERT, PM AF MARKOVA, NG GAN, SQ STEINERT, PM TI COMPLEXITY OF PROFILAGGRIN GENE-EXPRESSION IN MAMMALIAN EPIDERMIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 511 EP 511 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500435 ER PT J AU SCANDURRO, AB WANG, QZ GOODMAN, L LEDBETTER, S YUSPA, SH LICHTI, U AF SCANDURRO, AB WANG, QZ GOODMAN, L LEDBETTER, S YUSPA, SH LICHTI, U TI INTERACTION OF IMMATURE HAIR FOLLICLE BUDS WITH IMMORTALIZED DERMAL PAPILLA CELLS IN COLLAGEN MATRIX COCULTURE LEADS TO ACTIVATION OF TYPE-IV COLLAGENASES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROTECT LAB,BETHESDA,MD 20892. NCI,BIOL CHEM LAB,BETHESDA,MD 20892. UPJOHN CO,KALAMAZOO,MI 49001. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 512 EP 512 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500441 ER PT J AU LEVY, DD TANAKA, K KRAEMER, KH AF LEVY, DD TANAKA, K KRAEMER, KH TI EXPRESSION OF A TRANSFECTED DNA-REPAIR GENE (XPAC) IN XERODERMA-PIGMENTOSUM GROUP A CELLS IMPROVES DNA-REPAIR AND MUTAGENESIS OF UV-TREATED PLASMIDS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. OSAKA UNIV,OSAKA,JAPAN. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 514 EP 514 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500457 ER PT J AU CHIPEY, CC YANG, JM STEINERT, PM COMPTON, JG AF CHIPEY, CC YANG, JM STEINERT, PM COMPTON, JG TI MUTATIONS IN THE KERATIN 10 GENE IN PATIENTS WITH EPIDERMOLYTIC HYPERKERATOSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 516 EP 516 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500468 ER PT J AU BORKOWSKI, T LEE, MG UDEY, MC AF BORKOWSKI, T LEE, MG UDEY, MC TI EXPRESSION OF THE COSTIMULATORY MOLECULE B7 BY CULTURED MURINE LANGERHANS CELLS IS REGULATED AT THE MESSENGER-RNA LEVEL SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 521 EP 521 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500494 ER PT J AU LEE, MG TANG, A UDEY, MC AF LEE, MG TANG, A UDEY, MC TI A ROLE FOR E-CADHERIN (E-CAD) IN ADHESION OF MURINE EPIDERMAL GAMMA-DELTA T-CELLS (GAMMA-DELTA-TC) TO KERATINOCYTES (KC) INVITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 521 EP 521 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500497 ER PT J AU YONEDA, K STEINERT, PM AF YONEDA, K STEINERT, PM TI THE CORRECT EXPRESSION OF THE HUMAN LORICRIN GENE IN TRANSGENIC MICE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 522 EP 522 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500505 ER PT J AU DLUGOSZ, AA DHARIA, AG CHENG, C YUSPA, SH AF DLUGOSZ, AA DHARIA, AG CHENG, C YUSPA, SH TI EXPRESSION OF GRANULAR-CELL DIFFERENTIATION MARKERS IS COORDINATELY REGULATED BY PROTEIN-KINASE-C SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 523 EP 523 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500506 ER PT J AU KIM, SY KIM, JG STEINERT, PM AF KIM, SY KIM, JG STEINERT, PM TI PROCESSING OF THE MEMBRANE-ASSOCIATED TRANSGLUTAMINASE-1 DURING EPIDERMAL DIFFERENTIATION - STRUCTURE AND FUNCTIONAL-RELATIONSHIPS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 523 EP 523 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500509 ER PT J AU GAUDET, SJ SLOMINSKI, A ETMINAN, M PRUSKI, D PAUS, R NAMBOODIRI, MAA AF GAUDET, SJ SLOMINSKI, A ETMINAN, M PRUSKI, D PAUS, R NAMBOODIRI, MAA TI IDENTIFICATION AND CHARACTERIZATION OF 2 ISOZYMIC FORMS OF ARYLAMINE N-ACETYLTRANSFERASE IN SYRIAN-HAMSTER SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. ALBANY MED COLL,DEPT MICROBIOL IMMUNOL & MOLEC GENET,ALBANY,NY 12208. GEORGETOWN UNIV,DEPT BIOL,WASHINGTON,DC 20057. UKRV FU BERLIN,DEPT DERMATOL,BERLIN,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 537 EP 537 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500590 ER PT J AU DIGIOVANNA, JJ COMPTON, JG BALE, SJ AF DIGIOVANNA, JJ COMPTON, JG BALE, SJ TI CLINICAL HETEROGENEITY IN EPIDERMOLYTIC HYPERKERATOSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAMS,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 538 EP 538 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500600 ER PT J AU TURNER, ML MOSHELL, A CORBETT, DW STERN, JB ROTH, MJ DIGIOVANNA, JD HORN, TD KRAEMER, KH AF TURNER, ML MOSHELL, A CORBETT, DW STERN, JB ROTH, MJ DIGIOVANNA, JD HORN, TD KRAEMER, KH TI CLEARING OF MELANOMA-INSITU WITH INTRALESIONAL ALPHA-INTERFERON IN A PATIENT WITH XERODERMA-PIGMENTOSUM SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NNMC,BETHESDA,MD. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 538 EP 538 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500598 ER PT J AU MILSTONE, LM BALE, SJ INSOGNA, KL AF MILSTONE, LM BALE, SJ INSOGNA, KL TI SECONDARY HYPERPARATHYROIDISM IN PATIENTS WHO HAVE ICHTHYOSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT DERMATOL,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT INTERNAL MED,NEW HAVEN,CT 06510. NIAMS,CT & SKIN BIOL BRANCH,BETHESDA,MD. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 541 EP 541 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500614 ER PT J AU KARPATI, S AMAGAI, M PRUSSICK, R CEHRS, K STANLEY, JR AF KARPATI, S AMAGAI, M PRUSSICK, R CEHRS, K STANLEY, JR TI PEMPHIGUS-VULGARIS ANTIGEN (PVA) IS LOCATED WITHIN HUMAN KERATINOCYTE DESMOSOMES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 545 EP 545 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500638 ER PT J AU HALABAN, R TYRRELL, L LONGLEY, J RUBIN, J AF HALABAN, R TYRRELL, L LONGLEY, J RUBIN, J TI UVB IRRADIATION INDUCES THE SECRETION OF GROWTH-FACTORS FROM KERATINOCYTES AND FIBROBLASTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT DERMATOL,NEW HAVEN,CT 06510. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 557 EP 557 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500711 ER PT J AU ENK, AH KATZ, SI AF ENK, AH KATZ, SI TI HEAT-STABLE ANTIGEN - A CRITICAL COSTIMULATORY MOLECULE ON EPIDERMAL LANGERHANS CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV MAINZ,DEPT DERMATOL,W-6500 MAINZ,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 560 EP 560 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500728 ER PT J AU TENNENBAUM, T WILDNAUER, T BELANGER, A MROZ, A BROWN, LJ POTE, J GORDON, JS AF TENNENBAUM, T WILDNAUER, T BELANGER, A MROZ, A BROWN, LJ POTE, J GORDON, JS TI COMPARISON OF THE EFFECTS OF RETINOIC ACID AND AN IRRITANT, HEXADECANE, ON HAIRLESS MOUSE SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,LCCTP,BETHESDA,MD 20892. JOHNSON & JOHNSON CONSUMER PROD INC,SKILLMAN,NJ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 580 EP 580 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500851 ER PT J AU YANG, JM CHIPEV, CC STEINERT, PM COMPTON, JG AF YANG, JM CHIPEV, CC STEINERT, PM COMPTON, JG TI IS PALMOPLANTAR INVOLVEMENT IN EPIDERMOLYTIC HYPERKERATOSIS ASSOCIATED WITH SPECIFIC KERATIN MUTATIONS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1993 VL 100 IS 4 BP 581 EP 581 PG 1 WC Dermatology SC Dermatology GA KW395 UT WOS:A1993KW39500858 ER PT J AU BOYE, O GETAHUN, Z GROVER, S HAMEL, E BROSSI, A AF BOYE, O GETAHUN, Z GROVER, S HAMEL, E BROSSI, A TI SYNTHESIS OF C-14-LABELED ELECTROPHILIC LIGANDS OF THE COLCHICINE BINDING-SITE OF TUBULIN - CHLOROACETATES OF DEMETHYLTHIOCOLCHICINES AND OF N-ACETYLCOLCHINOL - ISOTHIOCYANATE OF 9-DEOXY-N-ACETYLCOLCHINOL SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE COLCHICINE; AFFINITY LIGAND; TUBULIN; MICROTUBULE; C-14-RADIOLABELED LIGAND ID ANALOGS; THIOCOLCHICINE AB C-14-Chloroacetates of 2-demethylthiocolchicine 7 (specific activity 55.0 MCi/mmol, radiochemical yield 26.1%), and of 3-demethylthiocolchicine 8 (specific activity 55.0 mCi/mmol, radiochemical yield 5.7%) were synthesized and found to covalently bind with high specificity to the beta-subunit of tubulin. The C-14-chloroacetate of N-acetylcolchinol 5 (specific activity 56.0 mCi/mmol, radiochemical yield 7.8%) and the C-14-isothiocyanate 6 (specific activity 50.0 mCi/mmol, radiochemical yield 32%) were also prepared and found to react covalently with tubulin but in a nonspecific manner. With the radiolabelled chloroacetates 7 and 8 two compounds are now available to further characterize the colchicine binding site on the beta subunit of tubulin. C1 NCI,DCT,DTP,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RP BOYE, O (reprint author), NIDDK,NAT PROD SECT,STRUCT BIOL LAB,BETHESDA,MD 20892, USA. NR 16 TC 1 Z9 1 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 APR PY 1993 VL 33 IS 4 BP 293 EP 299 DI 10.1002/jlcr.2580330407 PG 7 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA KW685 UT WOS:A1993KW68500006 ER PT J AU SAYERS, TJ MASON, LH PILARO, A WILTROUT, TA KOMSCHLIES, K MUNGER, WL WILTROUT, RH AF SAYERS, TJ MASON, LH PILARO, A WILTROUT, TA KOMSCHLIES, K MUNGER, WL WILTROUT, RH TI SUBSTRATE-SPECIFIC PROTEASES (BLT-ESTERASE) ARE LOCALIZED PREDOMINANTLY IN THE NATURAL-KILLER-CELLS OF UNPRIMED MICE SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE NATURAL KILLER CELLS; BLT-ESTERASE; SERINE PROTEASES; BIOLOGICAL RESPONSE MODIFIERS ID TOXIC LYMPHOCYTE-T; METRIAL GLAND-CELLS; SERINE ESTERASE; CYTOPLASMIC GRANULES; EFFECTOR-CELLS; EXPRESSION; INVIVO; MOUSE; GENES; RECEPTOR AB In leukocytes isolated from unprimed mice, the levels of extractable Nalpha-Cbz-Lys-thiobenzylesteresterase (BLT-esterase) closely correlated with the number of natural killer (NK) cells. The spleens of mice that exhibit severe combined immunodeficiency (SCID) contained much higher levels of this enzyme than other mouse strains. Treatments that resulted in a local accumulation of NK cells (as assessed by lytic activity) produced a concomitant increase in BLT-esterase activity. However, short-term in vitro treatment of spleen cells with interferon (IFN)-alpha/beta indicated that BLT-esterase levels correlated more closely with absolute numbers of NK cells than with their lytic capacity. There was a very good correlation between the numbers of cells bearing the NK phenotype (NK-1.1+) and BLT-esterase levels. Cells positively sorted using the NK-specific antibodies NK-1.1 and LGL-1 had high enzymatic activity. The BLT-esterase levels were high in both the NK-1.1+/LGL-1- and NK-1.1+/LGL-1+ subsets. Highly purified CD4+ and CD8+ T cells and sIg+ B cells demonstrated negligible enzyme, as did populations of cells highly enriched for macrophages or neutrophils. However, it should be stressed that the inbred mice used on this study have been maintained in a pathogen-free facility. It would be anticipated that mice maintained under less stringent conditions could exhibit appreciable levels of BLT-esterase activity in their T cells. Nonetheless, BLT-esterase is present at high levels in NK cells and cannot be regarded as a T cell-specific enzyme. C1 NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. IMMUNEX CORP,SEATTLE,WA. RP SAYERS, TJ (reprint author), NCI,FCRDC,PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,BLDG 560,ROOM 31-28,FREDERICK,MD 21702, USA. RI Sayers, Thomas/G-4859-2015 NR 42 TC 15 Z9 15 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD APR PY 1993 VL 53 IS 4 BP 454 EP 461 PG 8 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA LB373 UT WOS:A1993LB37300014 PM 8482926 ER PT J AU THOMPSON, MB DAVIS, DG MORRIS, RW AF THOMPSON, MB DAVIS, DG MORRIS, RW TI TAURINE CONJUGATE OF 3-ALPHA,6-BETA,7-BETA-TRIHYDROXY-5-BETA,22-CHOLEN-24-OIC ACID (TAURO-DELTA-22-BETA-MURICHOLATE) - THE MAJOR BILE-ACID IN THE SERUM OF FEMALE RATS TREATED WITH ALPHA-NAPHTHYLISOTHIOCYANATE AND ITS SECRETION BY LIVER SLICES SO JOURNAL OF LIPID RESEARCH LA English DT Article DE BILE ACIDS AND SALTS; HPLC; CHOLESTASIS; BETA-MURICHOLATE; DELTA-22-BETA-MURICHOLATE ID DUCT LIGATION; GNOTOBIOTIC-RATS; CHOLESTASIS; HEPATOCYTES; CHOLESTEROL; METABOLISM; EXCRETION AB The taurine conjugate of 3alpha,6beta,7beta-trihydroxy-5beta, 22-cholen-24-oic acid (tauro-DELTA22-beta-muricholate) has been identified in the serum of female rats treated with alpha-naphthylisothiocyanate. Using a high performance liquid chromatographic/enzymatic method for measurement of bile acids, tauro-DELTA22-beta-muricholate was the predominant bile acid in the serum of female Fischer 344 rats treated for 3 days with alpha-naphthylisothiocyanate. Other significant changes in concentrations of serum bile acids included increases in tauro-alpha-muricholate, tauro-beta-muricholate, taurocholate, taurochenodeoxycholate, and several unknown bile acids. The formation of tauro-DELTA22-beta-muricholate was examined in vitro using liver slices from control rats and rats treated with alpha-naphthylisothiocyanate. Slices were incubated for 7 h in William's E medium containing no bile acids or 25 mumol/l of one of the following: beta-muricholate, tauro-beta-muricholate, or cholate. Tauro-DELTA22-beta-muricholate was secreted by slices from control and treated rats and the rate was increased significantly by the addition of beta-muricholate (2.9-5.6-fold) but not tauro-beta-muricholate or cholate to the medium. Tauro-DELTA-beta-muricholate was formed by liver slices from endogenous precursors and from exogenous beta-muricholate. Pretreatment of rats with alpha-naphthylisothiocyanate did not alter total secretion rates but those of some important individual bile acids were affected. Because of the increased secretion of tauro-DELTA-beta-muricholate by liver slices with the addition of beta-muricholate to the medium, the liver may be the primary site of formation for this unsaturated bile acid. C1 ANALYT SCI INC,RES TRIANGLE PK,NC 27709. RP THOMPSON, MB (reprint author), NIEHS,MD C2-08,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 37 TC 27 Z9 27 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 APR PY 1993 VL 34 IS 4 BP 553 EP 561 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX501 UT WOS:A1993KX50100003 PM 8496661 ER PT J AU DAVIS, DG THOMPSON, MB AF DAVIS, DG THOMPSON, MB TI NUCLEAR-MAGNETIC-RESONANCE IDENTIFICATION OF THE TAURINE CONJUGATE OF 3-ALPHA,6-BETA,7-BETA-TRIHYDROXY-5-BETA,22-CHOLEN-24-OIC ACID (TAURO-DELTA-22-BETA-MURICHOLATE) IN THE SERUM OF FEMALE RATS TREATED WITH ALPHA-NAPHTHYLISOTHIOCYANATE SO JOURNAL OF LIPID RESEARCH LA English DT Article DE PROTON CARBON CHEMICAL SHIFTS; 1D-HOHAHA; 2D-HSQC; INDIRECT DETECTION; BETA-MURICHOLATE; ISOTROPIC MIXING; STEREOSPECIFIC PROTON ASSIGNMENTS; SCALAR CONNECTIVITY ID BILE-ACIDS; SPECTROSCOPY; NMR; CHOLESTASIS; ASSIGNMENTS; SPECTRA; PHASE AB Recently developed H-1 nuclear magnetic resonance methods, including 2-dimensional, H-1-detected-{C-13} shift correlation spectroscopy and 1-dimensional HOHAHA spectroscopy at 500 MHz have been used to identify the major bile acid in the serum of rats treated with alpha-naphthylisothiocyanate as the taurine conjugate of 3alpha,6beta,7beta-trihydroxy-5beta,22-cholen-24-oic acid (tauro-DELTA22-beta-muricholate), a derivative of beta-muricholate having an unsaturated bond in the acyclic side chain. Complete stereospecific assignments of the H-1 and protonated C-13 spectra of the title compound and beta-muricholate are reported. The assignments were based entirely on H-1-H-1 and H-1-C-13 scalar connectivities and were made using approximately 0.5-2.0 mg of material. It is suggested that these new methods will be of general value for identifying the structure and assigning the spectra of other scarce steroid-like molecules. RP DAVIS, DG (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 26 TC 9 Z9 9 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 APR PY 1993 VL 34 IS 4 BP 651 EP 661 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KX501 UT WOS:A1993KX50100014 PM 8388431 ER PT J AU VUISTER, GW CLORE, GM GRONENBORN, AM POWERS, R GARRETT, DS TSCHUDIN, R BAX, A AF VUISTER, GW CLORE, GM GRONENBORN, AM POWERS, R GARRETT, DS TSCHUDIN, R BAX, A TI INCREASED RESOLUTION AND IMPROVED SPECTRAL QUALITY IN 4-DIMENSIONAL C-13/C-13-SEPARATED HMQC-NOESY-HMQC SPECTRA USING PULSED-FIELD GRADIENTS SO JOURNAL OF MAGNETIC RESONANCE SERIES B LA English DT Note ID NMR-SPECTROSCOPY; LARGER PROTEINS RP VUISTER, GW (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 23 TC 171 Z9 172 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 1064-1866 J9 J MAGN RESON SER B JI J. Magn. Reson. Ser. B PD APR PY 1993 VL 101 IS 2 BP 210 EP 213 DI 10.1006/jmrb.1993.1035 PG 4 WC Physics, Atomic, Molecular & Chemical SC Physics GA KZ352 UT WOS:A1993KZ35200016 ER PT J AU CURRAN, MJ COHEN, FS CHANDLER, DE MUNSON, PJ ZIMMERBERG, J AF CURRAN, MJ COHEN, FS CHANDLER, DE MUNSON, PJ ZIMMERBERG, J TI EXOCYTOTIC FUSION PORES EXHIBIT SEMI-STABLE STATES SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE MEMBRANES; MAST CELLS; SECRETION; ELECTROPHYSIOLOGY; FREEZE-FRACTURE; EXOCYTOSIS ID SEA-URCHIN EGGS; CORTICAL GRANULE EXOCYTOSIS; ADRENAL CHROMAFFIN CELLS; MOUSE MAST-CELLS; MEMBRANE-FUSION; CAPACITANCE MEASUREMENTS; SECRETORY VESICLE; PARAMECIUM CELLS; MATRIX; EVENTS AB Rapid-freezing/freeze-fracture electron microscopy and whole-cell capacitance techniques were used to study degranulation in peritoneal mast cells of the rat and the mutant beige mouse. These studies allowed us to create a time-resolved picture for fusion pore formation. After stimulation, a dimple in the plasma membrane formed a small contact area with the secretory granule membrane. Within this zone of apposition no ordered proteinaceous specializations were seen. Electrophysiological technique measured a small fusion pore which widened rapidly to 1 nS. Thereafter, the fusion pore remained at semi-stable conductances between 1 and 20 nS for a wide range of times, between 10 and 15,000 msec. These conductances correspond to pore diameters 25-36 nm. Ultrastructural data confirmed small pores of hourglass morphology, composed of biological membrane co-planar with both the plasma and granular membranes. Later, the fusion pore rapidly increased in conductance, consistent with the observed morphology of omega-figures. The hallmarks of channel-like behavior, instantaneous jumps in pore conductance between defined levels, and sharp peaks in histograms of conductance dwell-time, were not seen. Since the morphology of small pores shows contiguous fracture planes, the electrical data represent pores that contain lipid. These combined morphological and electrophysiological data are consistent with a lipid/protein complex mediating both the initial and later stages of membrane fusion. C1 ARIZONA STATE UNIV,DEPT ZOOL,TEMPE,AZ 85287. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NIH,DIV COMP RES & TECHNOL,BIOSTAT SECT,BETHESDA,MD 20892. RUSH MED COLL,DEPT PHYSIOL,CHICAGO,IL 60612. FU NIGMS NIH HHS [GM-27367] NR 29 TC 61 Z9 62 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 APR PY 1993 VL 133 IS 1 BP 61 EP 75 PG 15 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA KY115 UT WOS:A1993KY11500006 PM 8320720 ER PT J AU ESHET, R WERNER, H KLINGER, B SILBERGELD, A LARON, Z LEROITH, D ROBERTS, CT AF ESHET, R WERNER, H KLINGER, B SILBERGELD, A LARON, Z LEROITH, D ROBERTS, CT TI UP-REGULATION OF INSULIN-LIKE GROWTH FACTOR-I (IGF-I) RECEPTOR GENE-EXPRESSION IN PATIENTS WITH REDUCED SERUM IGF-I LEVELS SO JOURNAL OF MOLECULAR ENDOCRINOLOGY LA English DT Article ID HUMAN-ERYTHROCYTES; MONONUCLEAR-CELLS AB We have analysed the expression of the IGF-I receptor gene in lymphocytes of patients with low levels of circulating IGF-I (four patients with isolated GH deficiency (IGHD) and one Laron-type dwarf (LTD)) in comparison with a control group exhibiting normal serum IGF-I levels and endocrine profiles. I-125-Labelled IGF-I binding assays were performed on erythrocytes to determine the number of IGF-I binding sites per cell and their dissociation constants. Erythrocytes from patients with IGHD or LTD contained significantly (P=0.002) more receptors per cell (10-9+/-3.1 binding sites/cell), with a reduced affinity (K(d)=0.49+/-0.05 nm), than erythrocytes from controls (2.0+/-0.4 sites/cell; K(d)= 0.14 nM). The levels of IGF-I receptor mRNA in circulating lymphocytes were determined by an RNA template-specific reverse transcription/polymerase chain reaction method. There was a statistically significant increase in IGF-I receptor mRNA levels in lymphocytes from patients with LTD or IGHD when compared with controls (3108-1+/-775.9 vs 576.0+/-465.7 arbitrary units, P=0.006). The increased level of IGF-I binding due to increased IGF-I receptor gene expression may represent a compensatory up-regulation process activated in response to the low levels of IGF-I in the circulation of patients with LTD or IGHD. C1 NIDDKD,DIABET BRANCH,BLDG 10,ROOM 8S-239,BETHESDA,MD 20892. BEILINSON MED CTR,INST PEDIAT & ADOLESCENT ENDOCRINOL,IL-49100 PETAH TIQWA,ISRAEL. TEL AVIV UNIV,SACKLER FAC MED,IL-69978 TEL AVIV,ISRAEL. OI Roberts, Charles/0000-0003-1756-5772 NR 23 TC 37 Z9 37 U1 0 U2 1 PU J ENDOCRINOLOGY LTD PI BRISTOL PA 17/18 THE COURTYARD, WOODLANDS, ALMONDSBURY, BRISTOL, ENGLAND BS12 4NQ SN 0952-5041 J9 J MOL ENDOCRINOL JI J. Mol. Endocrinol. PD APR PY 1993 VL 10 IS 2 BP 115 EP 120 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KW677 UT WOS:A1993KW67700002 PM 8484860 ER PT J AU PATERSON, BM SHIRAKATA, M MITSUI, K QIN, W AF PATERSON, BM SHIRAKATA, M MITSUI, K QIN, W TI STUDIES ON THE ROLE OF HYDROPHILIC AMINO-ACIDS AND PHOSPHORYLATION IN THE DIMERIZATION OF THE MYOD FAMILY OF MYOGENIC REGULATORY FACTORS SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0142-4319 J9 J MUSCLE RES CELL M JI J. Muscle Res. Cell Motil. PD APR PY 1993 VL 14 IS 2 BP 220 EP 221 PG 2 WC Cell Biology SC Cell Biology GA KZ904 UT WOS:A1993KZ90400014 ER PT J AU KRAFT, T SCHNEKENBUHL, S YU, LC CHALOVICH, JM BRENNER, B AF KRAFT, T SCHNEKENBUHL, S YU, LC CHALOVICH, JM BRENNER, B TI P(I) EFFECTS ON CROSSBRIDGE TURNOVER KINETICS IN SKINNED SKELETAL-MUSCLE FIBERS ACTIVATED BY NEM-S1 OR CALCIUM SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Meeting Abstract C1 UNIV ULM,W-7900 ULM,GERMANY. NIH,BETHESDA,MD 20892. E CAROLINA UNIV,GREENVILLE,NC 27834. NR 1 TC 0 Z9 0 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0142-4319 J9 J MUSCLE RES CELL M JI J. Muscle Res. Cell Motil. PD APR PY 1993 VL 14 IS 2 BP 267 EP 267 PG 1 WC Cell Biology SC Cell Biology GA KZ904 UT WOS:A1993KZ90400173 ER PT J AU SCHNEKENBUHL, S KRAFT, T YU, LC BRENNER, B CHALOVICH, JM AF SCHNEKENBUHL, S KRAFT, T YU, LC BRENNER, B CHALOVICH, JM TI CHARACTERIZATION OF NEM-S-1-BINDING TO REGULATED ACTIN IN SOLUTION AND ITS EFFECTS ON ACTOMYOSIN ATPASES SO JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY LA English DT Meeting Abstract C1 UNIV ULM,W-7900 ULM,GERMANY. NIH,BETHESDA,MD 20892. E CAROLINA UNIV,GREENVILLE,NC 27834. NR 2 TC 0 Z9 0 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0142-4319 J9 J MUSCLE RES CELL M JI J. Muscle Res. Cell Motil. PD APR PY 1993 VL 14 IS 2 BP 271 EP 271 PG 1 WC Cell Biology SC Cell Biology GA KZ904 UT WOS:A1993KZ90400188 ER PT J AU FREED, WJ ROSENSTEIN, JM AF FREED, WJ ROSENSTEIN, JM TI NEURAL TRANSPLANTATION - A REPORT ON THE IVTH INTERNATIONAL-SYMPOSIUM SO JOURNAL OF NEURAL TRANSPLANTATION & PLASTICITY LA English DT Editorial Material ID ADRENAL-MEDULLA GRAFTS; CENTRAL-NERVOUS-SYSTEM; RIGHT CAUDATE-NUCLEUS; PARKINSONS-DISEASE; DOPAMINE NEURONS; GROWTH-FACTOR; RAT MODEL; FOLLOW-UP; BRAIN; CELLS C1 GEORGE WASHINGTON UNIV,DEPT ANAT,WASHINGTON,DC 20052. RP FREED, WJ (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,2700 MARTIN LUTHER KING AVE,WASHINGTON,DC 20032, USA. NR 162 TC 2 Z9 2 U1 0 U2 0 PU FREUND PUBLISHING HOUSE PI LONDON PA STE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA SN 0792-8483 J9 J NEURAL TRANSP PLAS JI J. Neural Transplant. Plast. PD APR-JUN PY 1993 VL 4 IS 2 BP 61 EP 96 PG 36 WC Neurosciences; Transplantation SC Neurosciences & Neurology; Transplantation GA MG888 UT WOS:A1993MG88800001 PM 7906551 ER PT J AU CANNONSPOOR, HE AF CANNONSPOOR, HE TI THE VISUAL-SYSTEM - (REPORT ON SESSION 25.0) WASHINGTON, DC, JULY 15, 1992 SO JOURNAL OF NEURAL TRANSPLANTATION & PLASTICITY LA English DT Editorial Material ID SUPERIOR COLLICULUS; BRAIN; RAT; PROJECTIONS; RETINA; CELLS RP CANNONSPOOR, HE (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT LAB,WASHINGTON,DC 20032, USA. NR 18 TC 0 Z9 0 U1 0 U2 0 PU FREUND PUBLISHING HOUSE PI LONDON PA STE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA SN 0792-8483 J9 J NEURAL TRANSP PLAS JI J. Neural Transplant. Plast. PD APR-JUN PY 1993 VL 4 IS 2 BP 101 EP 104 PG 4 WC Neurosciences; Transplantation SC Neurosciences & Neurology; Transplantation GA MG888 UT WOS:A1993MG88800003 PM 7906547 ER PT J AU REDMOND, DE HOFFER, BJ AEBISCHER, P BAETGE, E BAKAY, R BUNGE, R CARVEY, P FREED, C FREED, WJ FREEMAN, T GAGE, F GASH, D HITCHCOCK, E HODGES, H HORELLOU, P KROMER, L LINDVALL, O LOPEZLOZANO, J MADRAZO, I ROBBINS, R SANBERG, P SLADEK, J SOTELO, C ZIMMER, J AF REDMOND, DE HOFFER, BJ AEBISCHER, P BAETGE, E BAKAY, R BUNGE, R CARVEY, P FREED, C FREED, WJ FREEMAN, T GAGE, F GASH, D HITCHCOCK, E HODGES, H HORELLOU, P KROMER, L LINDVALL, O LOPEZLOZANO, J MADRAZO, I ROBBINS, R SANBERG, P SLADEK, J SOTELO, C ZIMMER, J TI IVTH INTERNATIONAL-SYMPOSIUM ON NEURAL TRANSPLANTATION TRANSCRIPT OF THE CLOSING DISCUSSION (EDITED) - (SESSION 44.0) WASHINGTON, DC - JULY 16, 1992 SO JOURNAL OF NEURAL TRANSPLANTATION & PLASTICITY LA English DT Editorial Material C1 UNIV COLORADO,HLTH SCI CTR,DEPT PHARMACOL,DENVER,CO 80262. BROWN UNIV,DEPT NEUROBIOL,PROVIDENCE,RI 02912. CYTOTHERAPEUT INC,PROVIDENCE,RI 02906. EMORY CLIN NEUROL SURG,ATLANTA,GA 30322. UNIV MIAMI,SCH MED,MIAMI PROJECT,MIAMI,FL 33136. RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT NEUROL SCI & PHARMACOL,NEUROPHARMACOL RES LABS,CHICAGO,IL 60612. NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. UNIV S FLORIDA,DIV NEUROSURG,TAMPA,FL 33606. UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. UNIV ROCHESTER,MED CTR,DEPT NEUROBIOL & ANAT,ROCHESTER,NY 14642. MIDLAND CTR NEUROSURG & NEUROL,SMETHWICK B67 7JX,W MIDLANDS,ENGLAND. INST PSYCHIAT,DEPT PSYCHOL,LONDON SE5 8AF,ENGLAND. CNRS,NEUROBIOL LAB,F-9119 GIF SUR YVETTE,FRANCE. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262. LUND UNIV,DEPT HISTOL,S-22362 LUND,SWEDEN. HOSP PUERTA HIERRO,INSALUD,NEUROBIOL LAB,E-28035 MADRID,SPAIN. CTR MED SIGLO XXIIMSS,CAMINO A SANTA TERESA 1055,MEXICO CITY 10700,DF,MEXICO. YALE UNIV,NEURAL TRANSPLANT PROGRAM,NEW HAVEN,CT 06510. CHICAGO MED SCH,INST NEUROSCI,N CHICAGO,IL 60064. HOP LA PITIE SALPETRIERE,INSERM,U106,F-75651 PARIS 13,FRANCE. AARHUS UNIV,INST NEUROBIOL,DK-8000 AARHUS,DENMARK. GEORGETOWN UNIV,SCH MED,DEPT ANAT,WASHINGTON,DC 20007. RP REDMOND, DE (reprint author), YALE UNIV,SCH MED,NEUROBEHAV LAB,333 CEDAR ST,POB 3333,NEW HAVEN,CT 06510, USA. RI Sanberg, Paul/A-6753-2009; Aebischer, Patrick/E-1387-2013 NR 21 TC 0 Z9 0 U1 0 U2 0 PU FREUND PUBLISHING HOUSE PI LONDON PA STE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA SN 0792-8483 J9 J NEURAL TRANSP PLAS JI J. Neural Transplant. Plast. PD APR-JUN PY 1993 VL 4 IS 2 BP 113 EP 125 PG 13 WC Neurosciences; Transplantation SC Neurosciences & Neurology; Transplantation GA MG888 UT WOS:A1993MG88800006 PM 7906550 ER PT J AU YU, L SCHAAD, NC KLEIN, DC AF YU, L SCHAAD, NC KLEIN, DC TI CALCIUM POTENTIATES CYCLIC-AMP STIMULATION OF PINEAL ARYLALKYLAMINE N-ACETYLTRANSFERASE SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE N-ACETYLTRANSFERASE; PINEAL GLAND; CYCLIC AMP; CALCIUM STIMULATION ID PROTEIN KINASE-C; ELEMENT-BINDING PROTEIN; RAT PINEALOCYTES; GUANOSINE 3',5'-MONOPHOSPHATE; ADRENERGIC-STIMULATION; CAMP; ADENOSINE-3',5'-MONOPHOSPHATE; CGMP; PHOSPHORYLATION; TRANSCRIPTION AB Pineal arylalkylamine N-acetyltransferase (N-acetyltransferase) controls large daily changes in melatonin production. It is generally thought that the activity of this enzyme is controlled by norepinephrine acting exclusively via elevation of cyclic AMP. However, norepinephrine also elevates pineal intracellular Ca2+ concentration ([Ca2+]i), and it is not known whether Ca2+ is involved in regulating N-acetyltransferase activity other than through its established role in cyclic AMP production. In this study, the issue of whether Ca2+ enhances the effects of cyclic AMP on N-acetyltransferase activity was investigated. The effects of cyclic AMP protagonists (isobutylmethylxanthine, N6, 2'-O-dibutyryladenosine 3',5'-cyclic monophosphate, 8-bromoadenosine 3',5'-cyclic monophosphate, and adenosine 3',5'-cyclic monophosphothioate, Sp-diastereomer) were examined in combination with [Ca2+]i protagonists (A23187, ionomycin, and phenylephrine). All [Ca2+]i protagonists potentiated the effects of cyclic AMP protagonists. For example, ionomycin potentiated the effects of low concentrations of 8-bromoadenosine 3',5'-cyclic monophosphate, and A23187 potentiated the effects of isobutylmethylxanthine without altering cyclic AMP accumulation. These findings indicate that Ca2+ and cyclic AMP probably act physiologically in a coordinated manner to stimulate N-acetyltransferase activity; these second messengers could act directly at one or more sites or through indirect actions mediated by kinases. C1 NICHHD,DEV NEUROBIOL LAB,NEUROENDOCRINOL SECT,BLDG 36,ROOM 4A07,BETHESDA,MD 20892. NR 31 TC 31 Z9 31 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 APR PY 1993 VL 60 IS 4 BP 1436 EP 1443 DI 10.1111/j.1471-4159.1993.tb03306.x PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KT837 UT WOS:A1993KT83700030 PM 7681102 ER PT J AU MUTOH, T TOKUDA, A GUROFF, G FUJIKI, N AF MUTOH, T TOKUDA, A GUROFF, G FUJIKI, N TI THE EFFECT OF THE B-SUBUNIT OF CHOLERA-TOXIN ON THE ACTION OF NERVE GROWTH-FACTOR ON PC12 CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE PC12 CELLS; GANGLIOSIDE GM1; B-SUBUNIT OF CHOLERA TOXIN; NERVE GROWTH FACTOR; S6 KINASE; TRK; PHOSPHORYLATION ID GANGLIOSIDE GM1; NEURITE OUTGROWTH; PHEOCHROMOCYTOMA CELLS; EXOGENOUS GANGLIOSIDES; RECEPTOR; FIBROBLASTS; PC12-CELLS; BINDING; INVITRO; NEURONS AB Exogenous gangliosides, especially ganglioside GM 1 (GM 1), seem to potentiate the action of nerve growth factor (NGF). We have examined the possible regulation of the NGF signaling pathway in PC12 cells by the B subunit of cholera toxin (CTB), which binds to endogenous GM1 specifically and with a high affinity. CTB treatment (1 mug/ml) enhanced NGF-induced neurite outgrowth from PC12 cells, NGF-induced activation of ribosomal protein S6 kinase, and NGF-induced stimulation of trk phosphorylation. CTB plus NGF also caused a greater inhibition of [H-3]thymidine incorporation into DNA than did NGF alone. These enhancing effects of CTB were blocked by the presence of cytochalasin B in the culture medium but were not affected by the presence of colchicine or by the depletion of Ca2+ in the medium. I-125-NGF binding experiments revealed that CTB treatment did not affect the specific binding of NGF to the cells. These results strongly suggest that the binding of cell surface GM1 by CTB modulates the pathway of intracellular signaling initiated by NGF and that the association of CTB with a cytoskeletal component is essential for these effects. C1 NICHHD,GROWTH FACTORS SECT,BLDG 6,ROOM 130,BETHESDA,MD 20892. FUKUI MED SCH,DEPT INTERNAL MED 2,DIV NEUROL,FUKUI 91011,JAPAN. NR 44 TC 37 Z9 38 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 APR PY 1993 VL 60 IS 4 BP 1540 EP 1547 DI 10.1111/j.1471-4159.1993.tb03319.x PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KT837 UT WOS:A1993KT83700043 PM 8455041 ER PT J AU LENNARD, DE ECKERT, WA MERCHENTHALER, I AF LENNARD, DE ECKERT, WA MERCHENTHALER, I TI CORTICOTROPIN-RELEASING HORMONE NEURONS IN THE PARAVENTRICULAR NUCLEUS PROJECT TO THE EXTERNAL ZONE OF THE MEDIAN-EMINENCE - A STUDY COMBINING RETROGRADE LABELING WITH IMMUNOCYTOCHEMISTRY SO JOURNAL OF NEUROENDOCRINOLOGY LA English DT Article DE CORTICOTROPIN-RELEASING HORMONE; IMMUNOCYTOCHEMISTRY; RETROGRADE LABELING ID FACTOR CRF; RAT HYPOTHALAMUS; IMMUNOREACTIVE NEURONS; BRAIN; FIBERS; SYSTEM; IDENTIFICATION; LOCALIZATION; PITUITARY; LESIONS AB Corticotropin-releasing hormone (CRH) is the major regulator of the pituitary-adrenal axis. CRH-immunoreactive perikarya are widely distributed in the central nervous system; however, only those which participate directly in the regulation of adrenocorticotropin are connected to the portal circulation in the external zone of the median eminence. The present study describes the identification of these hypophysiotropic neurons using retrograde labeling and CRH immunocytochemistry. Fluoro-Gold was injected peripherally then, 5 days later, the animals were treated with colchicine. Twenty-four hours later the animals were sacrificed, and their brains were immunostained for CRH with the indirect immunofluorescence technique. The results indicate that the vast majority of the Fluoro-Gold-accumulating and CRH-immunopositive perikarya (hypophysiotropic neurons) are located in the medial parvicellular subdivision of the paraventricular nucleus (PVN). However, not each CRH-immunoreactive neuron contains Fluoro-Gold, i.e. a small portion of these neurons project to areas of the brain other than the median eminence. The anterior, lateral and periventricular subdivisions of the PVN also contain hypophysiotropic CRH-immunoreactive perikarya, however, their number is much less than in the medial parvicellular subdivision. Scattered double-labeled cells are also present in the medial preoptic area and the dorsal hypothalamus, just behind the PVN. These results support previous observations that the PVN, particularly the medial parvicellular subdivision, is the predominant source of the hypophysiotropic CRH neurons. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,FUNCT MORPHOL SECT,MD C4-07,RES TRIANGLE PK,NC 27709. NR 28 TC 27 Z9 27 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. PD APR PY 1993 VL 5 IS 2 BP 175 EP 181 DI 10.1111/j.1365-2826.1993.tb00378.x PG 7 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA KX724 UT WOS:A1993KX72400007 PM 8485552 ER PT J AU WELLER, M AF WELLER, M TI ANTERIOR OPERCULAR CORTEX LESIONS CAUSE DISSOCIATED LOWER CRANIAL NERVE PALSIES AND ANARTHRIA BUT NO APHASIA - FOIX-CHAVANY-MARIE SYNDROME AND AUTOMATIC VOLUNTARY DISSOCIATION REVISITED SO JOURNAL OF NEUROLOGY LA English DT Editorial Material DE FOIX-CHAVANY-MARIE SYNDROME; OPERCULUM; DISSOCIATION; SUPRABULBAR PALSY; ANARTHRIA ID BILATERAL PERISYLVIAN SOFTENINGS; ACUTE PSEUDOBULBAR PALSY; BRAIN-LESIONS; FACIAL EXPRESSIONS; ROLANDIC OPERCULUM; STATUS EPILEPTICUS; CLINICAL REPORT; STROKE PATIENTS; CT; SPEECH AB Anarthria and bilateral central facio-linguo-velo-pharyngeo-masticatory paralysis with ''automatic voluntary dissociation'' are the clinical hallmarks of Foix-Chavany-Marie syndrome (FCMS), the corticosubcortial type of suprabulbar palsy. A literature review of 62 FCMS reports allowed the differentiation of five clinical types of FCMS: (a) the classical and most common form associated with cerebrovascular disease, (b) a subacute form caused by central nervous system infections, (c) a developmental form probably most often related to neuronal migration disorders, (d) a reversible form in children with epilepsy, and (e) a rare type associated with neurodegenerative disorders. Bilateral opercular lesions were confirmed in 31 of 41 patients who had CT or MRI performed, and by necropsy in 7 of 10 patients. FCMS could be attributed to unilateral lesions in 2 patients. The typical presentation and differential diagnosis of FCMS provide important clues to lesion localization in clinical neurology. FCMS is a paretic and not an apraxic disorder and is not characterized by language disturbances. Its clinical features prove divergent corticobulbar pathways for voluntary and automatic motor control of craniofacial muscles. Precise clinico-neuroradiological correlations should facilitate the identification of the structural substrate of ''automatic voluntary dissociation'' in FCMS. C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 113 TC 91 Z9 95 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-5354 J9 J NEUROL JI J. Neurol. PD APR PY 1993 VL 240 IS 4 BP 199 EP 208 DI 10.1007/BF00818705 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA KV744 UT WOS:A1993KV74400001 PM 7684439 ER PT J AU STEVENS, A WELLER, M WIETHOLTER, H AF STEVENS, A WELLER, M WIETHOLTER, H TI A CHARACTERISTIC GANGLIOSIDE ANTIBODY PATTERN IN THE CSF OF PATIENTS WITH AMYOTROPHIC-LATERAL-SCLEROSIS SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID MOTOR-NEURON DISEASE; PLASMA-CELL DYSCRASIA; SPINAL-CORD; GM1 GANGLIOSIDE; CEREBROSPINAL-FLUID; IMMUNOGLOBULIN-M; SERUM; ALS; INFILTRATION; REACTIVITY AB Paired cerebrospinal fluid and serum samples of patients with amyotrophic lateral sclerosis (n = 35) revealed no consistent abnormalities of CSF cell count, CSF albumin, CSF IgG, CSF IgM, IgG or IgM index, or oligoclonal immunoglobulin band formation in the CSF. Determination of IgG and IgM CSF and serum antibodies to gangliosides GM1, GM2, GM3, AGM1, GD1a, GD1b, and GT1b showed a characteristic pattern which allowed the differentiation of amyotrophic lateral sclerosis from controls and from patients with other neurological disorders including multiple sclerosis. Specifically, patients with the disease had elevated CSF IgM antibodies to all gangliosides except AGM1. The lack of correlation between the CSF findings and corresponding serum antibodies suggests a chronic, compartmental, intrathecal immune response of low activity in amyotrophic lateral sclerosis. Whether this immune response is primary and of pathogenetic significance, or an epiphenomenon of neuronal degeneration, remains to be investigated. C1 UNIV TUBINGEN,DEPT NEUROL,W-7400 TUBINGEN 1,GERMANY. NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BETHESDA,MD 20892. NR 29 TC 26 Z9 26 U1 0 U2 1 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 APR PY 1993 VL 56 IS 4 BP 361 EP 364 DI 10.1136/jnnp.56.4.361 PG 4 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA KW665 UT WOS:A1993KW66500006 PM 7683329 ER PT J AU KAPOULA, Z ROBINSON, DA OPTICAN, LM AF KAPOULA, Z ROBINSON, DA OPTICAN, LM TI VISUALLY INDUCED CROSS-AXIS POSTSACCADIC EYE DRIFT SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID PATCHING ONE EYE; VESTIBULOOCULAR REFLEX; SACCADIC SYSTEM; BINOCULAR COORDINATION; ADAPTIVE-CHANGES; MOVEMENTS; PLASTICITY; MONKEY; GENERATION; NEURONS AB 1. It has been previously shown that, if a visual pattern is transiently moved just after every saccade, it is possible to induce horizontal, postsaccadic, ocular drift after horizontal saccades that persists in the dark. In this study we show that horizontal ocular drift can also be created after vertical saccades. Five human subjects viewed binocularly the interior of a full-field hemisphere filled with a random-dot pattern. They were encouraged to make frequent vertical saccades. During training, eye movements were recorded by the electrooculogram. A computer detected the end of every saccade and immediately moved the pattern to the left after up saccades and right after down saccades. The motion was exponential, its amplitude was 25% of the vertical component of the antecedent saccade, its time constant was 50 ms. Before and after 2-3 h of training, movements of both eyes were measured by the eye-coil/magnetic-field method while subjects were instructed to make vertical saccades in the dark, in the presence of the movable adapting pattern, and between stationary targets for calibration. 2. After training (approximately 20,000 saccades) all subjects developed a zero-latency, exponential ocular drift to the left after up saccades and to the right after down saccades. The amplitude of the horizontal drift, expressed as a percentage of the vertical component of the preceding saccade, was 2.7% in the dark. This rose to 10.2% in the presence of the movable adapting stimulus. The latter rise is not due to visual following systems but to a zero-latency increase in initial drift velocity. 3. The horizontal drifts were usually unequal between the two eyes, indicating the presence of disconjugate movements. We measured intrasaccadic disconjugate horizontal movements of all subjects. In agreement with studies by others of saccades in the light, we measured a divergence during up saccades (1.3-degrees) and a convergence for down (0.4-degrees), but in this case for spontaneous saccades in the dark. After training, these values increased for saccades in the dark but decreased in the light in the presence of the adapting stimulus. These changes were largely idiosyncratic and statistically significant in only a few subjects. 4. The cross-axis postsaccadic drifts were separated into their conjugate and disconjugate components. The disconjugate components were small and idiosyncratic, and the means were small for saccades in the dark. The only consistent trend was in the presence of the adapting stimulus where up saccades were often followed by convergence. The presence of these vergence components do not interfere with our conclusion that this paradigm demonstrated cross-axis plasticity in postsaccadic drift. 5. The induced drift was specific to the stimulus pattern. The horizontal induced drift became smaller for oblique saccades, decreased as their vertical components became smaller, and disappeared for horizontal saccades. There was no induced vertical drift after horizontal saccades. 6. We suggest a hypothesis of crossed innervation. During a vertical saccade, horizontal burst neurons are known to be bilaterally coactivated by a signal presumably from vertical burst neurons. Normally, these activities cancel each other to produce no net horizontal movement. Thus the lack of a horizontal component would seem to be not passive (no signal at all) but active and determined by a balance between opposing forces. The same argument can be made for the step of innervation. Plastic modification of synapses between the horizontal burst neurons and the horizontal neural integrator could therefore create, during a vertical saccade, a step of innervation to horizontal motoneurons in the absence of a pulse. This hypothesis, with the use of only demonstrable neural pathways, shows how one might create a step of innervation without a pulse and thus a horizontal postsaccadic drift without a horizontal saccade. C1 LAB PHYSIOL NEUROSENSORIELLE, CNRS, F-75006 PARIS, FRANCE. NEI, SENSORIMOTOR RES LAB, BETHESDA, MD 20892 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT OPHTHALMOL, BALTIMORE, MD 21287 USA. FU NEI NIH HHS [EY-00598, EY-01765] NR 26 TC 7 Z9 7 U1 3 U2 4 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3077 EI 1522-1598 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD APR PY 1993 VL 69 IS 4 BP 1031 EP 1043 PG 13 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA KX597 UT WOS:A1993KX59700004 PM 8492146 ER PT J AU MILLER, EK LI, L DESIMONE, R AF MILLER, EK LI, L DESIMONE, R TI ACTIVITY OF NEURONS IN ANTERIOR INFERIOR TEMPORAL CORTEX DURING A SHORT-TERM-MEMORY TASK SO JOURNAL OF NEUROSCIENCE LA English DT Article DE MACAQUE MONKEY; MEMORY; INFERIOR TEMPORAL CORTEX ID TWO-DIMENSIONAL PATTERNS; ENTORHINAL CORTEX; SINGLE UNITS; INFEROTEMPORAL CORTEX; HIPPOCAMPAL-FORMATION; PREFRONTAL LESIONS; RECOGNITION MEMORY; VISUAL-STIMULI; MONKEYS; PRIMATE AB Inferior temporal (IT) cortex of primates is known to play an important role in visual memory. Previous studies of IT neurons during performance of working memory tasks have found modulation of responses when a current stimulus matched an item in memory; however, this effect was lost if other stimuli intervened in the retention interval. To examine how IT cortex retains memories while new stimuli are activating the cells, we recorded from IT neurons while monkeys performed a delayed matching-to-sample task, with multiple intervening items between the sample and matching test stimulus. About half of the cells responded differently to a test stimulus if it matched the sample, and this difference was maintained following intervening stimuli. For most of the affected cells, the responses to matching stimuli were suppressed; however, for a few cells the opposite effect was seen. Temporal contiguity alone could not explain the results, as there was no modulation of responses when a stimulus on one trial was repeated on the next trial. Thus, an active reset mechanism appears to restrict the memory comparison to just the stimuli presented within a trial. The suppressive effects appear to be generated within or before IT cortex since the suppression of response to matching stimuli began almost immediately with the onset of the visual response. The memory of the sample stimulus affected not only the responses to matching stimuli but also those to nonmatching stimuli. There was suggestive evidence that the more similar a nonmatching stimulus to the sample, the more the response was suppressed. About a quarter of the cells showed stimulus-selective activity in the delay interval following the sample. However, this activity appeared to be eliminated by intervening stimuli. Thus, it is unlikely that delay-interval activity in IT contributed to the performance of this particular version of delayed matching to sample. To determine how much information about the match-nonmatch status of the stimulus was conveyed by individual neurons, we analyzed the responses with discriminant analysis. The responses of an individual IT neuron could be used to classify a stimulus as matching or nonmatching on about 60% of the trials. To achieve the same performance as the animal would require averaging the responses of a minimum of 25 IT neurons. There was rio evidence that mnemonic information was carried by temporal variations in the spike trains. By contrast, there was a modest amount of temporal variation in sensory responses to different visual stimuli. This variation appeared to be due to different stimuli having different effects on the early and late (transient and sustained) portions of the response. We propose that two populations of IT cells contribute to memory. One functions as adaptive mnemonic filters and the other provides a sensory referent. The difference in response between the two populations is a measure of the difference between the current stimulus and stored memory traces. A temporal ''figure-ground'' mechanism such as this could contribute to performance of a variety of mnemonic tasks, including working memory tasks. RP MILLER, EK (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 9,ROOM 1E104,BETHESDA,MD 20892, USA. NR 66 TC 484 Z9 485 U1 0 U2 7 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1993 VL 13 IS 4 BP 1460 EP 1478 PG 19 WC Neurosciences SC Neurosciences & Neurology GA KV711 UT WOS:A1993KV71100013 PM 8463829 ER PT J AU TROWBRIDGE, FL HARRIS, SS COOK, J DUNN, JT FLORENTINO, RF KODYAT, BA MANNAR, MGV REDDY, V TONTISIRIN, K UNDERWOOD, BA YIP, R AF TROWBRIDGE, FL HARRIS, SS COOK, J DUNN, JT FLORENTINO, RF KODYAT, BA MANNAR, MGV REDDY, V TONTISIRIN, K UNDERWOOD, BA YIP, R TI COORDINATED STRATEGIES FOR CONTROLLING MICRONUTRIENT MALNUTRITION - A TECHNICAL WORKSHOP SO JOURNAL OF NUTRITION LA English DT Article DE MICRONUTRIENT MALNUTRITION; IODINE; IRON; VITAMIN-A; HUMANS ID INTERVENTIONS; DEFICIENCY AB Participants in a November 1991 workshop concluded that coordinated strategies for controlling malnutrition due to iodine, iron, vitamin A and other micronutrients deficiencies are technically feasible and should be given consideration in planning control efforts. Coordinated surveys involving clinical, biochemical and dietary assessment of multiple micronutrients are feasible. Multiple fortification is also possible using such vehicles as salt, processed rice or sugar. Supplementation efforts can be integrated with existing health care programs. Food-based strategies are also effective. The best examples have been community-based and have included a strong nutrition and health education component designed to change food consumption patterns, improve food preservation and preparation practices, and link income-generating activities with food production activities. Successful coordinated efforts will require a strong political commitment and a supportive infrastructure. Specific recommendations include the formation of national coordinating bodies for micronutrient deficiency control, establishment of a micronutrient information network and expansion of technical exchange and training. C1 INT LIFE SCI INST RES FDN,INST HUMAN NUTR,WASHINGTON,DC 20036. CTR DIS CONTROL,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,DIV NUTR,ATLANTA,GA 30333. UNIV KANSAS,MED CTR,DIV HEMATOL,KANSAS CITY,KS 66103. UNIV VIRGINIA,SCH MED,INT COUNCIL CONTROL IODINE DEFICIENCY DISORDERS,CHARLOTTESVILLE,VA 22908. FOOD & NUTR INST,MANILA 1000,PHILIPPINES. MINIST HLTH,DIRECTORATE NUTR,JAKARTA 12950,INDONESIA. NATL INST NUTR,HYDERABAD 500007,ANDHRA PRADESH,INDIA. MAHIDOL UNIV SALAYA,INST NUTR,NAKHON PATHOM 73170,THAILAND. NEI,BETHESDA,MD 20892. NR 37 TC 20 Z9 21 U1 0 U2 1 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD APR PY 1993 VL 123 IS 4 BP 775 EP 787 PG 13 WC Nutrition & Dietetics SC Nutrition & Dietetics GA KU909 UT WOS:A1993KU90900021 PM 8463879 ER PT J AU YASAR, S SCHINDLER, CW THORNDIKE, EB SZELENYI, I GOLDBERG, SR AF YASAR, S SCHINDLER, CW THORNDIKE, EB SZELENYI, I GOLDBERG, SR TI EVALUATION OF THE STEREOISOMERS OF DEPRENYL FOR AMPHETAMINE-LIKE DISCRIMINATIVE STIMULUS EFFECTS IN RATS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID MONOAMINE-OXIDASE; METHAMPHETAMINE; (-)-DEPRENYL; METABOLITES; INHIBITORS; SELEGILINE AB The antiparkinsonian agent l-deprenyl, a selective monoamine oxidase (MAO)-B inhibitor, is a phenylalkylamine derivative which is metabolized in part to /-methamphetamine and l-amphetamine. As the clinical use of amphetamine-like psychostimulants is limited by their potential for abuse, we evaluated 1-deprenyl for amphetamine-like discriminative stimulus effects over a range of experimental conditions. Male Fisher rats were trained under a 5-response, fixed-ratio schedule of stimulus-shock termination or a 1 0-response, fixed-ratio schedule of food-presentation to discriminate between d-amphetamine (1.0 mg/kg i.p.) and saline in a two-lever, operant conditioning procedure. Full generalization was obtained to l-amphetamine (1.0-2.0 mg/kg), d-deprenyl (10.0-17.0 mg/kg) and /-deprenyl (17.0 and 30.0 mg/kg) under both the food-presentation and stimulus-shock termination schedules, and increases in responding on the lever appropriate to d-amphetamine were dose-dependent. The dose-effect functions for l-amphetamine, l-deprenyl and d-deprenyl were shifted slightly to the left under the stimulus-shock termination schedule compared to the food-presentation schedule. When l-deprenyl (3.0 or 5.6 mg/kg i.p.) was given 30 min before d-amphetamine it produced a small shift to the left in the dose-effect function for d-amphetamine under the food-presentation schedule. l-Deprenyl produced clear generalization to the d-amphetamine stimulus only at very high doses of 17.0 to 30.0 mg/kg, doses about 1 0-fold higher than those that have a selective action on MAO-B vs. MAO-A and which start to have marked rate decreasing actions on food-reinforced responding. Thus, the present findings are in accord with clinical findings that over almost 20 years of long-term clinical use l-deprenyl has shown no signs of abuse liability. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205. ASTA MEDICA AG,FRANKFURT,GERMANY. RP YASAR, S (reprint author), NIDA,ADDICT RES CTR,BEHAV PHARMACOL & GENET SECT,PRECLIN PHARMACOL LAB,POB 5180,BALTIMORE,MD 21224, USA. NR 26 TC 28 Z9 28 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1993 VL 265 IS 1 BP 1 EP 6 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KY066 UT WOS:A1993KY06600001 PM 8473997 ER PT J AU SHIPPENBERG, TS BALSKUBIK, R HERZ, A AF SHIPPENBERG, TS BALSKUBIK, R HERZ, A TI EXAMINATION OF THE NEUROCHEMICAL SUBSTRATES MEDIATING THE MOTIVATIONAL EFFECTS OF OPIOIDS - ROLE OF THE MESOLIMBIC DOPAMINE SYSTEM AND D-1 VS D-2 DOPAMINE-RECEPTORS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID VENTRAL TEGMENTAL AREA; FREELY MOVING RATS; NUCLEUS-ACCUMBENS; 6-HYDROXYDOPAMINE LESIONS; HEROIN REWARD; ANTAGONIST; MORPHINE; KAPPA; SCH-23390; AGONISTS AB Both the reinforcing and aversive effects of exogenous opioids have been attributed to the activation of opioid receptors within the mesolimbic dopamine (DA) system. At present, however, it is unclear whether the activity of DA neurons projecting to the nucleus accumbens (NAC) is necessary for the expression of these effects. The present study sought to address this issue in rats by examining the influence of 6-hydroxydopamine (6-OHDA) lesions of the NAC and microinjections of selective DA receptor antagonists into this brain area upon the place conditioning produced by systemically administered opioids. The mu-opioid receptor agonist morphine produced dose-related preferences for the drug-paired place in control animals, whereas the kappa-opioid agonist U-69593 produced place aversions. Bilateral 6-OHDA lesions of the NAC abolished the place conditioning produced by both opioids. Lesions of the caudate/putamen or medial prefrontal cortex were, however, without effect. Microinjection of the D-1 DA antagonist SCH-23390 into the NAC, at a dose which was as ineffective as a conditioning stimulus, attenuated the place conditioning produced by low doses of morphine and U-69593. Over the dose range tested, the D-2 DA antagonist (-)-sulpiride was without effect. Neither SCH-23390 nor 6-OHDA lesions of the NAC modified the place conditioning produced by lithium chloride, a drug of a different pharmacological class. These data demonstrate that the rewarding and aversive effects of opioids are dependent on DA neural transmission within the mesolimbic system and suggest a role for NAC D-1 DA receptors in the mediation of both motivational effects. C1 MAX PLANCK INST PSYCHIAT, DEPT NEUROPHARMACOL, W-8033 MARTINSRIED, GERMANY. RP SHIPPENBERG, TS (reprint author), NIDA, ADDICT RES CTR, BEHAV PHARMACOL & GENET SECT, PRECLIN PHARMACOL LAB, POB 5180, BALTIMORE, MD 21224 USA. NR 49 TC 218 Z9 220 U1 1 U2 5 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA SN 0022-3565 EI 1521-0103 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1993 VL 265 IS 1 BP 53 EP 59 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KY066 UT WOS:A1993KY06600009 PM 8386244 ER PT J AU COMPTON, DR RICE, KC DECOSTA, BR RAZDAN, RK MELVIN, LS JOHNSON, MR MARTIN, BR AF COMPTON, DR RICE, KC DECOSTA, BR RAZDAN, RK MELVIN, LS JOHNSON, MR MARTIN, BR TI CANNABINOID STRUCTURE-ACTIVITY-RELATIONSHIPS - CORRELATION OF RECEPTOR-BINDING AND INVIVO ACTIVITIES SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID PHARMACOLOGICAL EVALUATION; HIGH-AFFINITY; RADIOLIGAND-BINDING; DOPAMINE-RECEPTORS; ANALOGS; BRAIN; DELTA-8-TETRAHYDROCANNABINOL; MICE; CANNABIDIOL; SITES AB Although a receptor exists for cannabinoid drugs, it is uncertain which pharmacological actions this receptor mediates. This structure-activity relationship investigation was initiated to determine which effects might correspond to binding affinity for the cannabinoid receptor, as well as to explore the binding requirements of this site. The ability of nearly 60 cannabinoids to displace [H-3]CP-55,940 {(-)-3-[2-hydroxy-4-(1,1-dimethylhep-tyl)phenyl]-4-[3-hydroxy propyl] cyclohexan-1-ol} was determined before establishing correlations between receptor affinity and in vivo pharmacological potency. Analysis of [H-3]CP-55,940 binding indicated a Hill coefficient of 0.97, a B(max) of 499 pM (3.3 pmol/mg of protein) and an apparent K(d) of 924 pM. Closer inspection indicated the binding assay exhibited ''zone B'' characteristics, and use of correction equations indicated a true K(d) for CP-55,940 of 675 pM. The structure-activity relationship indicated the importance of side chain structure to high-affinity binding, with the most potent analogs (K(I) < 10 nM) possessing either a dimethylheptyl side-chain, a similarly complex branched side chain or a halogen substituent at the 5' position. Comparative analysis of K(I) values to in vivo potency in a mouse model indicated a high degree of correlation between parameters for the depression of spontaneous locomotor activity (r = 0.91) and for the production of antinociception (r = 0.90), hypothermia (r = 0.89) and catalepsy (r = 0.85). Similarly high correlations were demonstrated between binding affinity and in vivo potency in both the rat drug discrimination model (r = 0.81) and for psychotomimetic activity in humans (r = 0.88). Thus, these studies appear to indicate that the requirements for activation of the cannabinoid receptor are similar across different species, and that receptor binding is sufficient to mediate many of the known pharmacological effects of cannabinoids. C1 NIDDKD,MEDICINAL CHEM LAB,BETHESDA,MD. ORGAN INC,WOBURN,MA. PFIZER INC,GROTON,CT 06340. GLAXO INC,RES TRIANGLE PK,NC. RP COMPTON, DR (reprint author), VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298, USA. FU NIDA NIH HHS [DA 03672] NR 42 TC 339 Z9 348 U1 1 U2 17 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1993 VL 265 IS 1 BP 218 EP 226 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KY066 UT WOS:A1993KY06600031 PM 8474008 ER PT J AU MATHEWS, JM BEND, JR AF MATHEWS, JM BEND, JR TI N-ARALKYL DERIVATIVES OF 1-AMINOBENZOTRIAZOLE AS POTENT ISOZYME-SELECTIVE MECHANISM-BASED INHIBITORS OF RABBIT PULMONARY CYTOCHROME-P450 INVIVO SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID MONOOXYGENASE SYSTEM; STYRENE OXIDATION; RAT-LIVER; INACTIVATION; METABOLISM; MICROSOMES; SUBSTRATE; LUNG; STEREOSELECTIVITY; ADDUCT AB Two N-aralkylated (N-benzyl- and N-alpha-methylbenzyl-) derivatives of 1 -aminobenzotriazole, a mechanism-based inhibitor of cytochrome P450 with low isozyme selectivity, were previously shown to be potent and isozyme-selective suicide substrates for rabbit and guinea pig pulmonary P450 in vitro (Mathews and Bend, 1986; Woodcroft et al., 1990). These three compounds were compared as inhibitors in vivo after i.v. administration to rabbits treated with the cytochrome P450 inducers beta-naphthoflavone or phenobarbital. By 1 hr after administration of N-alpha-methylbenzyl-1-aminobenzotriazole (1 mumol/kg), 80% of P450 2Bs-catalyzed benzphetamine N-demethylation in lung of beta-naphthoflavone-treated rabbits was inactivated and about 35% of P450 was lost without inhibition of P450 1 Al -catalyzed activity; at a dose of 10 or 100 mumol/kg, this compound totally inactivated pulmonary P450 2Bs activity while exerting minimal effects on benzphetamine N-demethylation activity (<20% inhibition) in liver of beta-naphthoflavone-treated rabbits. N-benzyl-1-aminobenzotriazole was also an isozyme- and tissue-selective inhibitor of pulmonary P450 2Bs in vivo. Relatively high doses (100 mumol/kg) of these compounds were compared in phenobarbital-induced rabbits. Virtually all (-95%) of pulmonary P450 2Bs-dependent activity was inhibited by the two N-aralkylated compounds (vs. 50% for 1-aminobenzotriazole). At this dose, about 25% of hepatic P450 was destroyed by all three compounds, whereas 1-aminobenzotriazole and its N-benzyl and N-alpha-methylbenzyl derivatives inactivated 20, 50 and 85% of hepatic P450 2Bs-selective benzphetamine N-demethylation activity, respectively. Our data demonstrate that N-a-methylbenzyl-1-aminobenzotriazole and N-benzyl-1-aminobenzotriazole, but not 1-aminobenzotriazole, are highly selective for the inactivation of pulmonary P450 2Bs in rabbits in vivo. C1 UNIV WESTERN ONTARIO,DEPT PHARMACOL & TOXICOL,LONDON N6A 5C12,ON,CANADA. RES TRIANGLE INST,CTR CHEM LIFE SCI,RES TRIANGLE PK,NC 27709. NIEHS,PHARMACOL LAB,RES TRIANGLE PK,NC 27709. NR 35 TC 12 Z9 12 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1993 VL 265 IS 1 BP 281 EP 285 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KY066 UT WOS:A1993KY06600038 PM 8474011 ER EF