FN Thomson Reuters Web of Science™ VR 1.0 PT J AU VELDHUIS, JD URBAN, RJ DUFAU, ML AF VELDHUIS, JD URBAN, RJ DUFAU, ML TI EVIDENCE THAT ANDROGEN NEGATIVE FEEDBACK REGULATES HYPOTHALAMIC GONADOTROPIN-RELEASING-HORMONE IMPULSE STRENGTH AND THE BURST-LIKE SECRETION OF BIOLOGICALLY-ACTIVE LUTEINIZING-HORMONE IN MEN SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; PULSATILE SECRETION; POSTMENOPAUSAL WOMEN; LH; PITUITARY; ESTROGEN; TESTOSTERONE; PUBERTY; BIOACTIVITY; DEFICIENT AB Testosterone injections or pharmacological amounts of dihydrotestosterone infused in men, and androgen-secreting tumors in women, can suppress plasma LH bioactivity assessed in an in vitro rat Leydig-cell bioassay. However, such observations do not define the physiological nature of endogenous androgen feedback actions on the hypothalamo-pituitary axis. To explore the feedback role of endogenous androgen on the male gonadotropic axis, we used a potent, selective, nonsteroidal competitive antagonist of the androgen receptor, flutamide HCl. Eight young men (ages 21-30) each received flutamide (750 mg orally daily x 3 days) and placebo and underwent blood sampling at 10-min intervals for 28 h, the last 2 h of which included two consecutive iv pulses of GhRH (10-mu-g). Plasma bioactive LH concentrations were measured in the rat Leydig cell bioassay. Deconvolution analysis was used to evaluate the number, amplitude, mass, and duration of bioactive LH secretory bursts and simultaneously estimate the half-life of endogenous LH. Flutamide treatment increased mean plasma bioactive LH concentrations from 27 +/- 2.3 to 54 +/- 9.1 IU/L (P = 0.018). Increased LH concentrations were achieved by a significantly amplified mass of LH secreted per burst, which rose from 14 +/- 1.8 (control) to 24 +/- 2.8 (flutamide) IU/L distribution volume. The amplitude (maximal secretion rate) of bioactive LH release episodes also increased from 1.3 +/- 0.21 (control) to 2.2 +/- 0.29 (flutamide) IU/L/min. These responses were specific, since flutamide did not influence bioactive LH half-life [49 +/- 6.5 (control) vs 52 +/- 4.1 (flutamide) min], LH secretory burst duration, frequency, or interburst interval. The total 24-h production rate of bioactive LH rose significantly from 310 +/- 35 (control) to 570 +/- 82 (flutamide) IU/L-day. In contrast, no features of LH secretory bursts evoked by exogenous GnRH pulses were altered significantly by antiandrogen. In summary, in vivo blockade of endogenous androgen negative feedback actions in normal men selectively amplifies the mass and amplitude of bioactive LH secretory bursts without altering their number or duration, or the half-life of LH, or the amount of LH released in response to exogenous GnRH. Therefore, we infer that in the steroid milieu of normal men endogenous androgen acting via the androgen receptor can negatively regulate hypothalamic GnRH stimulus strength, and hence the rate and mass of biologically active LH secretion in vivo. C1 NATL SCI FDN, CTR BIOL TIMING, CHARLOTTESVILLE, VA 22908 USA. NICHHD, REPROD ENDOCRINE RES BRANCH, BETHESDA, MD 20892 USA. RP VELDHUIS, JD (reprint author), UNIV VIRGINIA, HLTH SCI CTR, DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, BOX 202, CHARLOTTESVILLE, VA 22908 USA. FU NCRR NIH HHS [RR-00847-15, RR-00847]; NICHD NIH HHS [1-K04-HD00634] NR 40 TC 61 Z9 61 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JUN PY 1992 VL 74 IS 6 BP 1227 EP 1235 DI 10.1210/jc.74.6.1227 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HX258 UT WOS:A1992HX25800003 PM 1592863 ER PT J AU DEMITRACK, MA KALOGERAS, KT ALTEMUS, M PIGOTT, TA LISTWAK, SJ GOLD, PW AF DEMITRACK, MA KALOGERAS, KT ALTEMUS, M PIGOTT, TA LISTWAK, SJ GOLD, PW TI PLASMA AND CEREBROSPINAL-FLUID MEASURES OF ARGININE VASOPRESSIN SECRETION IN PATIENTS WITH BULIMIA-NERVOSA AND IN HEALTHY-SUBJECTS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID OSMOREGULATION; ABNORMALITIES; DISORDERS; THIRST; RHYTHM AB Bulimia nervosa is a psychiatric syndrome associated with intense hunger, deficient satiety mechanisms, an obsessional preoccupation with the adverse consequences of eating, ritualistic binge eating, and subsequent purging to forestall the effects of the binge. The morbidity of this illness reflects both the psychological suffering associated with a life organized around pathological eating behaviors, as well as medical complications such as fluid and electrolyte imbalances that occur largely as a result of purging and laxative abuse. We report here a study of the osmoregulation of plasma arginine vasopressin secretion and of vasopressin levels in the cerebrospinal fluid. This study was undertaken because vasopressin not only functions as the antidiuretic hormone, and thus as a principal modulator of fluid and electrolyte balance, but also because, in animals, centrally directed vasopressin delays the extinction of behaviors acquired during aversive conditioning. Thirteen normal-weight female patients with bulimia nervosa were studied after at least 1 month of nutritional stabilization and supervised abstinence from binge eating and purging. Plasma vasopressin, plasma sodium, and subjective thirst were measured serially before and during at 2-h infusion of 3% hypertonic saline (0.1 ml/kg min). In addition, cerebrospinal fluid was obtained by lumbar puncture upon admission and at 1 week before hypertonic saline infusion in 11 of these patients and in an additional 11 female patients who did not participate in the hypertonic infusion study. Fifteen healthy normal weight individuals (4 female, 11 male) served as controls for the hypertonic saline infusion and a separate group of 11 healthy normal weight female controls underwent lumbar puncture. Compared to controls, bulimic subjects showed a significant reduction in the plasma vasopressin response to hypertonic saline; in 12/13, plasma vasopressin correlated closely with plasma sodium, whereas in one patient vasopressin fluctuated erratically, with no relation to plasma sodium. Cerebrospinal fluid vasopressin levels were significantly higher in patients, and correlated positively with basal thirst level, which was enhanced in bulimics. Compared to controls, patients showed significant polyuria. We conclude that patients with bulimia nervosa have abnormal levels of vasopressin in their plasma and cerebrospinal fluid during abstinence from binge eating and purging. The disturbance in osmoregulation may aggravate the maintenance of adequate fluid volume in these patients, while the increase in centrally directed vasopressin may have relevance to their obsessional preoccupation with the aversive consequences of eating and weight gain. C1 NIMH, CLIN NEUROENDOCRINOL BRANCH, BETHESDA, MD 20814 USA. NIMH, CLIN SCI LAB, BETHESDA, MD 20892 USA. RP DEMITRACK, MA (reprint author), UNIV MICHIGAN, MED CTR, DEPT PSYCHIAT, MICHIGAN EATING DISORDERS PROGRAM, 1500 E MED CTR DR, ANN ARBOR, MI 48109 USA. RI Demitrack, Mark/I-7697-2013 NR 30 TC 18 Z9 18 U1 1 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JUN PY 1992 VL 74 IS 6 BP 1277 EP 1283 DI 10.1210/jc.74.6.1277 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HX258 UT WOS:A1992HX25800011 PM 1592871 ER PT J AU HARRIS, T FELDMAN, JJ KLEINMAN, JC ETTINGER, WH MAKUC, DM SCHATZKIN, AG AF HARRIS, T FELDMAN, JJ KLEINMAN, JC ETTINGER, WH MAKUC, DM SCHATZKIN, AG TI THE LOW CHOLESTEROL MORTALITY ASSOCIATION IN A NATIONAL COHORT SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE CHOLESTEROL; MORTALITY; AGED; EPIDEMIOLOGY; GERIATRICS ID CORONARY HEART-DISEASE; FACTOR INTERVENTION TRIAL; SERUM-CHOLESTEROL; RISK FACTOR; FOLLOW-UP; CANCER; FRAMINGHAM; WOMEN; MEN AB The relationship of low serum cholesterol and mortality was examined in data from the NHANES I Epidemiologic Followup Study (NHEFS) for 10,295 persons aged 35-74, 5833 women with 1281 deaths and 4462 men with 1748 deaths (mean followup = 14.1 years). Serum cholesterol below 4.1 mmol/l was associated with increased risk of death in comparison with serum cholesterol of 4.1-5.1 mmol/l (relative risk (RR) for women = 1.7, 95% confidence interval (CI) = (1.2, 2.3); for men RR = 1.4, CI = (1.1, 1.7)). However, the low serum cholesterol-mortality relationship was modified by time, age, and among older persons, activity level. The low serum cholesterol-mortality association was strongest in the first 10 years of followup. Moreover, this relationship occurred primarily among older persons (RR for low serum cholesterol for women 35-59 = 1.0 (0.6, 1.8), for women 70-74, RR = 2.1 (1.2, 3.7); RR for low serum cholesterol for men 35-59 = 1.2 (0.8, 2.0), for men 70-74, RR = 1.9 (1.3, 2.7)). Among older persons, however, the low serum cholesterol-mortality association was confined only to those with low activity at baseline. Factors related to underlying health status, rather than a mortality-enhancing effect of low cholesterol, likely accounts for the excess risk of death among persons with low cholesterol. The observed low cholesterol-mortality association therefore should not discourage public health programs directed at lowering serum cholesterol. C1 NATL CTR HLTH STAT,OFF ANAL & EPIDEMIOL,HYATTSVILLE,MD 20782. BOWMAN GRAY SCH MED,HYATTSVILLE,MD 20782. NCI,HYATTSVILLE,MD 20782. NR 34 TC 72 Z9 73 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD JUN PY 1992 VL 45 IS 6 BP 595 EP 601 DI 10.1016/0895-4356(92)90131-6 PG 7 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA JA226 UT WOS:A1992JA22600004 PM 1607898 ER PT J AU PSATY, BM LEE, M SAVAGE, PJ RUTAN, GH GERMAN, PS LYLES, M AF PSATY, BM LEE, M SAVAGE, PJ RUTAN, GH GERMAN, PS LYLES, M TI ASSESSING THE USE OF MEDICATIONS IN THE ELDERLY - METHODS AND INITIAL EXPERIENCE IN THE CARDIOVASCULAR HEALTH STUDY SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE DRUG UTILIZATION; PRESCRIPTION DRUGS; ELDERLY; PHARMACOEPIDEMIOLOGY; CARDIOVASCULAR DISEASE; METHODS; COMPUTER PROGRAM; DATABASE ID CORONARY HEART-DISEASE; ESTROGEN USE; BETA-BLOCKERS; DRUG-USE; MORTALITY; VALIDATION; RECORDS; CANCER; RECALL; TRIALS AB The Cardiovascular Health Study (CHS), a cohort study of risk factors for coronary heart disease and stroke, recruited 5201 community-dwelling adults aged 65 years or older. To assess the prevalence of medication use at baseline, we used the method of medication inventory and transcribed information about drug names and doses from prescription bottles. Using a specially-written computer program, persons without a knowledge of drug nomenclature coded 10,511 (89%) of the 11,846 medicines entered. We compared the results of the medication inventory and answers to questions on specific medications for reliability and validity. The use of beta-blockers and beta-agonists assessed by the method of medication inventory, but not by the method of directed recall, was associated with a significant effect on mean heart rate. Among 5197 participants with medication data, 76.1% were taking at least one medicine, and the mean number of drugs per person was 2.28. Among those with a reported history of high blood pressure, participants with cardiovascular disease (CVD) were more likely to be treated, and they were more likely to be taking beta-blockers and calcium-channel blockers than those without CVD. Daily aspirin use was also more common among those with CVD (30.5% of women and 43.2% of men) than among those without CVD (14.0% of women and 14.0% of men). The prevalence of post-menopausal estrogen use differed significantly among the four clinical centers (range = 5.5%-22.5% of women). We conclude that this method of assessing medications was easy to use and provided estimates of exposure to drugs that may affect risk of cardiovascular disease. C1 UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT HLTH SERV,SEATTLE,WA 98195. UNIV CALIF DAVIS,SCH MED,DEPT COMMUNITY HLTH,DAVIS,CA 95616. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,EPIDEMIOL & BIOMETRY PROGRAM,BETHESDA,MD 20892. UNIV PITTSBURGH,VET AFFAIRS MED CTR,SCH MED,DIV CLIN PHARMACOL,PITTSBURGH,PA 15260. GRAP SCH PUBL HLTH,DEPT EPIDEMIOL,PITTSBURGH,PA. CTR HLTH SERV RES,BALTIMORE,MD. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT INTERNAL MED,WINSTON SALEM,NC 27103. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,WINSTON SALEM,NC 27103. RP PSATY, BM (reprint author), UNIV WASHINGTON,DEPT MED,CARDIOVASC HLTH STUDY COORDINATING CTR,JD-30,1107 NE 45TH ST,SEATTLE,WA 98195, USA. FU NHLBI NIH HHS [N01-HC-85082, N01-HC-85081, N01-HC-85083] NR 38 TC 240 Z9 242 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD JUN PY 1992 VL 45 IS 6 BP 683 EP 692 DI 10.1016/0895-4356(92)90143-B PG 10 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA JA226 UT WOS:A1992JA22600016 PM 1607909 ER PT J AU COHEN, MS SPARLING, PF AF COHEN, MS SPARLING, PF TI MUCOSAL INFECTION WITH NEISSERIA-GONORRHOEAE - BACTERIAL ADAPTATION AND MUCOSAL DEFENSES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Review ID OUTER-MEMBRANE PROTEIN; FALLOPIAN-TUBE MUCOSA; GONOCOCCAL-INFECTION; HUMAN-NEUTROPHILS; EPITOPE EXPRESSION; PHAGOCYTIC-CELLS; STRUCTURAL GENE; DNA-SEQUENCE; SERUM; RESISTANCE C1 UNIV N CAROLINA,DEPT MICROBIOL,CHAPEL HILL,NC 27514. UNIV N CAROLINA,DEPT IMMUNOL,CHAPEL HILL,NC 27514. UNIV N CAROLINA,NIH,COOPERAT SEXUALLY TRANSMITTED INFECT RES CTR,CHAPEL HILL,NC 27514. RP COHEN, MS (reprint author), UNIV N CAROLINA,DEPT MED INFECT DIS,CB 7030,547 BURNETT WOMACK,CHAPEL HILL,NC 27599, USA. FU NIAID NIH HHS [UO1-AI31496] NR 85 TC 33 Z9 33 U1 0 U2 1 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 JUN PY 1992 VL 89 IS 6 BP 1699 EP 1705 DI 10.1172/JCI115770 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HX974 UT WOS:A1992HX97400001 PM 1601981 ER PT J AU KUHNS, DB DECARLO, E HAWK, DM GALLIN, JI AF KUHNS, DB DECARLO, E HAWK, DM GALLIN, JI TI DYNAMICS OF THE CELLULAR AND HUMORAL COMPONENTS OF THE INFLAMMATORY RESPONSE ELICITED IN SKIN BLISTERS IN HUMANS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CYTOKINES; NEUTROPHILS; EPIDERMIS; INTERFERON-GAMMA; C5A ID TUMOR-NECROSIS-FACTOR; HUMAN POLYMORPHONUCLEAR NEUTROPHILS; COLONY-STIMULATING FACTOR; INTERFERON-GAMMA; FACTOR-ALPHA; LEUKOCYTES; KERATINOCYTES; INTERLEUKIN-6; CHAMBER; LYMPHOCYTES AB Skin blisters induced by suction on the forearm of normal volunteers provide a convenient model to study the inflammatory response in vivo in man. In our study, after removal of the roof of the blister, i.e., the epidermis, the exposed floor of the blister (dermal-epidermal interface) was bathed with 70% autologous serum using a multiwell skin chamber. Migration of leukocytes (90-95% neutrophils) into the chamber fluid was detectable within 3 h, and appeared to plateau at 16-24 h. Sampling of the dermal-epidermal interface revealed primarily mononuclear cells during the first 8 h of the inflammatory response; however, their prevalence at 24 h was greatly diminished due to neutrophil infiltration. Accompanying the cellular immune response was the accumulation of inflammatory mediators in the bathing medium. The accumulation of IFN-gamma reached a plateau within 3 h; significant accumulations of the complement fragment, C5a, and of leukotriene B4 were also detected at 3 h. The accumulation of C5a did not peak until 5 h, whereas leukotriene B4 continued to accumulate through 24 h. IL-6 and IL-8 concentrations were minimal at 3-8 h but dramatic by 24 h while IL-1-beta, tumor necrosis factor-alpha, and granulocyte-macrophage colony-stimulating factor were undetectable within 3-8 h, but markedly elevated by 24 h. There was little accumulation of IL-4 and no accumulation of IL-1-alpha or IL-2 during the 24-h period. The sequential appearance of mediators at an inflammatory focus suggests that a carefully regulated dynamic system is responsible for controlling the evolution of the inflammatory response. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,CLIN IMMUNOL SERV,FREDERICK,MD 21702. RP GALLIN, JI (reprint author), NIAID,HOST DEFENSES LAB,BLDG 10,ROOM 11C103,BETHESDA,MD 20892, USA. FU NCI NIH HHS [N01-CO-74102]; PHS HHS [9175767502] NR 35 TC 71 Z9 72 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 JUN PY 1992 VL 89 IS 6 BP 1734 EP 1740 DI 10.1172/JCI115775 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HX974 UT WOS:A1992HX97400006 PM 1601984 ER PT J AU UGEN, KE GOEDERT, JJ BOYER, J REFAELI, Y FRANK, I WILLIAMS, WV WILLOUGHBY, A LANDESMAN, S MENDEZ, H RUBINSTEIN, A KIEBEREMMONS, T WEINER, DB AF UGEN, KE GOEDERT, JJ BOYER, J REFAELI, Y FRANK, I WILLIAMS, WV WILLOUGHBY, A LANDESMAN, S MENDEZ, H RUBINSTEIN, A KIEBEREMMONS, T WEINER, DB TI VERTICAL TRANSMISSION OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) INFECTION - REACTIVITY OF MATERNAL SERA WITH GLYCOPROTEIN-120 AND 41 PEPTIDES FROM HIV TYPE-1 SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE SYNTHETIC PEPTIDES; PROTECTIVE HUMORAL IMMUNITY; NEUTRALIZATION; SYNCYTIA; PEPTIDE-BASED IMMUNITY ID IMMUNE-DEFICIENCY SYNDROME; NEUTRALIZING ANTIBODIES; CHILDREN BORN; MONOCLONAL-ANTIBODIES; LAV/HTLV-III; AIDS; MOTHERS; CYTOTOXICITY; ASSOCIATION; RETROVIRUS AB The observation that approximately 70% of HIV-infected pregnant women do not transmit infection vertically suggests that antibody therapy may be effective in the prevention of transmission of HIV infection from mother to child. Currently, there is an incomplete understanding of the processes involved in vertical transmission of HIV infection. The elucidation of the serological basis of maternal immunity as it relates to protection from vertical transmission is the goal of this study. We have screened 20 maternal sera from HIV+ individuals of known vertical transmission status for reactivity with 31 peptides spanning the entire envelope glycoprotein of HIV-1. Of interest was reactivity to regions outside of the V3 loop of gp120. The findings have been examined in relationship to transmission status, as well as to in vitro anti-HIV-1 biological activity. Our results indicate that lack of vertical transmission is correlated with high viral neutralization activity, but not with antisyncytial activity nor with binding to the V3 peptides examined in this study. Also, the transmission group bound to fewer gp41 peptides when compared with the nontransmission group, suggesting that immune responses to gp41 may be important in preventing transmission. These findings may provide insights into the design of passive immunotherapies. C1 WISTAR INST,3601 SPRUCE ST,PHILADELPHIA,PA 19104. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. NCI,VIRAL EPIDEMIOL LAB,FREDERICK,MD 21701. NICHHD,ROCKVILLE,MD 20852. SUNY HLTH SCI CTR,BROOKLYN,NY 11203. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. RI Ugen, Kenneth/H-6544-2011; Weiner, David/H-8579-2014 NR 36 TC 80 Z9 80 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 JUN PY 1992 VL 89 IS 6 BP 1923 EP 1930 DI 10.1172/JCI115798 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HX974 UT WOS:A1992HX97400029 PM 1601999 ER PT J AU EASTMAN, RC CARSON, RE ORLOFF, DG COCHRAN, CS PERDUE, JF RECHLER, MM LANAU, F ROBERTS, CT SHAPIRO, J ROTH, J LEROITH, D AF EASTMAN, RC CARSON, RE ORLOFF, DG COCHRAN, CS PERDUE, JF RECHLER, MM LANAU, F ROBERTS, CT SHAPIRO, J ROTH, J LEROITH, D TI GLUCOSE-UTILIZATION IN A PATIENT WITH HEPATOMA AND HYPOGLYCEMIA - ASSESSMENT BY A POSITRON EMISSION TOMOGRAPHY SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE HYPOGLYCEMIA; HEPATOMA; INSULIN-LIKE GROWTH FACTOR-II; POSITRON EMISSION TOMOGRAPHY; NON-ISLET-CELL TUMOR ID GROWTH FACTOR-II; BRAIN TRANSFER CONSTANTS; NONISLET CELL TUMORS; TIME UPTAKE DATA; INSULIN-LIKE; IGF-I; EXTRAPANCREATIC TUMORS; GRAPHICAL EVALUATION; RADIORECEPTOR ASSAY; HORMONE SECRETION AB Tumor glucose use in patients with non-islet-cell tumors has been difficult to measure, particularly in hepatoma, because of hepatic involvement by neoplasm. We studied a patient with nonhepatic recurrence of hepatoma after successful liver transplantation. Tumor tissue contained messenger RNA for insulin-like growth factor-II (IGF-II), and circulating high molecular weight components and E-peptide of IGF-II were increased. Glucose use measured by isotope dilution with [3-H-3]glucose was 7.94 mg/kg fat-free mass per min, and splanchnic glucose production was 0.93 mg/kg fat-free mass per min. Glucose uptake and glucose model parameters were independently measured in tissues by positron emission tomography with F-18-fluoro-2-deoxy-D-glucose. Glucose uptake by heart muscle, liver, skeletal muscle, and neoplasm accounted for 0.8, 14, 44, and 15% of total glucose use, respectively. Model parameters in liver and neoplasm were not significantly different, and glucose transport and phosphorylation were twofold and fourfold greater than in muscle. This suggests that circulating IGF-II-like proteins are partial insulin agonists, and that hypoglycemia in hepatoma with IGF-II production is predominantly due to glucose uptake by skeletal muscle and suppression of glucose production. C1 NIH,CTR CLIN,DEPT POSITRON EMISS TOMOG,BETHESDA,MD 20892. NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NIH,CTR CLIN,DEPT NURSING,BETHESDA,MD 20892. AMER RED CROSS,JEROME H HOLLAND LAB BIOMED SCI,MOLEC BIOL LAB,ROCKVILLE,MD 20855. NIDDK,MOLEC CELLULAR & NUTR ENDOCRINOL BRANCH,GROWTH & DEV SECT,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,JOHNS HOPKINS ALLERGY & ASTHMA CTR,SCH MED,BALTIMORE,MD 21224. RP EASTMAN, RC (reprint author), NIDDKD,DIV DIABET ENDOCRINOL & METAB,DIABET BRANCH,BLDG 31,ROOM 9A-16,BETHESDA,MD 20892, USA. RI Carson, Richard/H-3250-2011; OI Carson, Richard/0000-0002-9338-7966; Roberts, Charles/0000-0003-1756-5772 NR 63 TC 49 Z9 49 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 JUN PY 1992 VL 89 IS 6 BP 1958 EP 1963 DI 10.1172/JCI115803 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HX974 UT WOS:A1992HX97400034 PM 1318326 ER PT J AU ROSENFELD, SJ YOSHIMOTO, K KAJIGAYA, S ANDERSON, S YOUNG, NS FIELD, A WARRENER, P BANSAL, G COLLETT, MS AF ROSENFELD, SJ YOSHIMOTO, K KAJIGAYA, S ANDERSON, S YOUNG, NS FIELD, A WARRENER, P BANSAL, G COLLETT, MS TI UNIQUE REGION OF THE MINOR CAPSID PROTEIN OF HUMAN PARVOVIRUS B19 IS EXPOSED ON THE VIRION SURFACE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE NEUTRALIZATION; ANTIBODIES; VACCINE; EPITOPE; IMMUNOPRECIPITATION ID AMINO-ACID SEQUENCES; ANTIGENIC DETERMINANTS; POLIOVIRUS; INFECTION; VIRUS; ORGANIZATION; HIV-1 AB Capsids of the B19 parvovirus are composed of major (VP2; 58 kD) and minor (VP1; 83 kD) structural proteins. These proteins are identical except for a unique 226 amino acid region at the amino terminus of VP1. Previous immunization studies with recombinant empty capsids have demonstrated that the presence of VP1 was required to elicit virus-neutralizing antibody activity. However, to date, neutralizing epitopes have been identified only on VP2. Crystallographic studies of a related parvovirus (canine parvovirus) suggested the unique amino-terminal portion of VP1 assumed an internal position within the viral capsid. To determine the position of VP1 in both empty capsids and virions, we expressed a fusion protein containing the unique region of VP1. Antisera raised to this protein recognized recombinant empty capsids containing VP1 and VP2, but not those containing VP2 alone, in an enzyme-linked immunosorbent assay. The antisera immunoprecipitated both recombinant empty capsids and human plasma-derived virions, and agglutinated the latter as shown by immune electron microscopy. The sera contained potent neutralizing activity for virus infectivity in vitro. These data indicate that a portion of the amino terminus of VPI is located on the virion surface, and that this region contains intrinsic neutralizing determinants. The external location of the VP1-specific tail may provide a site for engineered heterologous epitope presentation in novel recombinant vaccines. C1 PUBL HLTH LAB SERV,VIRUS REFERENCE LAB,LONDON NW9 5HT,ENGLAND. MEDIMMUNE INC,GAITHERSBURG,MD 20878. RP ROSENFELD, SJ (reprint author), NHLBI,CLIN HEMATOL BRANCH,CELL BIOL SECT,BLDG 10,ROOM 7C108,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 23 TC 89 Z9 96 U1 0 U2 1 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 JUN PY 1992 VL 89 IS 6 BP 2023 EP 2029 DI 10.1172/JCI115812 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HX974 UT WOS:A1992HX97400043 PM 1376332 ER PT J AU GENTSCH, JR GLASS, RI WOODS, P GOUVEA, V GORZIGLIA, M FLORES, J DAS, BK BHAN, MK AF GENTSCH, JR GLASS, RI WOODS, P GOUVEA, V GORZIGLIA, M FLORES, J DAS, BK BHAN, MK TI IDENTIFICATION OF GROUP-A ROTAVIRUS GENE-4 TYPES BY POLYMERASE CHAIN-REACTION SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID NUCLEOTIDE-SEQUENCE; SEROTYPE; RNA; NEUTRALIZATION; HYBRIDIZATION; SPECIFICITIES; SPECIMENS; PATTERNS; PROBES; VP7 AB Five genetically distinct human rotavirus (HRV) gene 4 groups have been described on the basis of comparative nucleotide sequencing and the predicted amino acid sequences, and at least four of them represent distinct VP4 antigenic types. To identify each gene 4 type and investigate its distribution in HRV isolates from patients with diarrhea, we developed a polymerase chain reaction (PCR) typing method using sequence information available for four genetically distinct gene 4 types. Rotavirus double-stranded RNAs (dsRNAs) isolated from stool samples were first reverse transcribed and amplified by PCR by using two oligonucleotide primers that correspond to regions that are highly conserved among all known HRV gene 4 types. The 876-bp dsDNA products were then reamplified by PCR in the presence of a cocktail containing one conserved plus-sense primer and four type-specific minus-sense primers (selected from the hypervariable region of gene 4), resulting in products of 345, 483, 267, and 391 bp corresponding to gene 4 types 1, 2, 3, and 4, respectively. This method reliably identified the gene 4 types of 16 well-characterized HRV isolates. Our results were independently confirmed for all 16 strains by reverse transcription and PCR amplification of HRV dsRNA in the presence of alternate type-specific primer pairs. For direct gene 4 typing of HRV in stool samples, we developed a method to extract rotavirus dsRNA from stool specimens by using glass powder. Our results suggest that gene 4 typing will be useful in providing more a complete characterization of HRV strains of epidemiologic or vaccine-related interest. C1 US FDA,DIV MICROBIOL,MOLEC BIOL BRANCH,WASHINGTON,DC 20204. ALL INDIA INST MED SCI,NEW DELHI 110016,INDIA. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. RP GENTSCH, JR (reprint author), CTR DIS CONTROL,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIAL DIS,ATLANTA,GA 30333, USA. NR 34 TC 939 Z9 971 U1 4 U2 9 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 JUN PY 1992 VL 30 IS 6 BP 1365 EP 1373 PG 9 WC Microbiology SC Microbiology GA HU603 UT WOS:A1992HU60300001 PM 1320625 ER PT J AU MYERS, C COOPER, M STEIN, C LAROCCA, R WALTHER, MM WEISS, G CHOYKE, P DAWSON, N STEINBERG, S UHRICH, MM CASSIDY, J KOHLER, DR TREPEL, J LINEHAN, WM AF MYERS, C COOPER, M STEIN, C LAROCCA, R WALTHER, MM WEISS, G CHOYKE, P DAWSON, N STEINBERG, S UHRICH, MM CASSIDY, J KOHLER, DR TREPEL, J LINEHAN, WM TI SURAMIN - A NOVEL GROWTH-FACTOR ANTAGONIST WITH ACTIVITY IN HORMONE-REFRACTORY METASTATIC PROSTATE-CANCER SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID FACTOR RECEPTOR; DOWN-REGULATION; ADRENAL-CORTEX; ANTIGEN; CELLS; TRANSFORMATION; ADENOCARCINOMA; HYPERPLASIA; INHIBITION; ACTIVATION C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT RADIOL,BETHESDA,MD 20892. NIH,WARREN G MAGNUSON CLIN CTR,DEPT NURSING,BETHESDA,MD 20892. NIH,WARREN G MAGNUSON CLIN CTR,DEPT PHARM,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,DIV HEMATOL ONCOL,WASHINGTON,DC 20307. NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,SURG BRANCH,BETHESDA,MD 20892. RP MYERS, C (reprint author), NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,CLIN PHARMACOL BRANCH,BLDG 10,ROOM 12C103,BETHESDA,MD 20892, USA. NR 43 TC 227 Z9 227 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 JUN PY 1992 VL 10 IS 6 BP 881 EP 889 PG 9 WC Oncology SC Oncology GA HW164 UT WOS:A1992HW16400003 PM 1375283 ER PT J AU LICHTER, AS LIPPMAN, ME DANFORTH, DN DANGELO, T STEINBERG, SM DEMOSS, E MACDONALD, HD REICHERT, CM MERINO, M SWAIN, SM COWAN, K GERBER, LH BADER, JL FINDLAY, PA SCHAIN, W GORRELL, CR STRAUS, K ROSENBERG, SA GLATSTEIN, E AF LICHTER, AS LIPPMAN, ME DANFORTH, DN DANGELO, T STEINBERG, SM DEMOSS, E MACDONALD, HD REICHERT, CM MERINO, M SWAIN, SM COWAN, K GERBER, LH BADER, JL FINDLAY, PA SCHAIN, W GORRELL, CR STRAUS, K ROSENBERG, SA GLATSTEIN, E TI MASTECTOMY VERSUS BREAST-CONSERVING THERAPY IN THE TREATMENT OF STAGE-I AND STAGE-II CARCINOMA OF THE BREAST - A RANDOMIZED TRIAL AT THE NATIONAL CANCER INSTITUTE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID PRIMARY RADIATION-THERAPY; EARLY LOCAL RECURRENCE; DNA FLOW-CYTOMETRY; CONSERVATIVE SURGERY; DEFINITIVE IRRADIATION; ADJUVANT CHEMOTHERAPY; PROGNOSTIC FACTORS; EXCISIONAL BIOPSY; SYSTEMIC THERAPY; TIME-COURSE C1 NCI,DEPT REHABIL MED,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD. NCI,SURG BRANCH,BETHESDA,MD. NCI,CANC NURSING SERV,BIOSTAT & DATA MANAGEMENT SECT,SURG PATHOL BRANCH,BETHESDA,MD. NR 60 TC 193 Z9 202 U1 1 U2 3 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 JUN PY 1992 VL 10 IS 6 BP 976 EP 983 PG 8 WC Oncology SC Oncology GA HW164 UT WOS:A1992HW16400016 PM 1588378 ER PT J AU WELLER, M AF WELLER, M TI DIAGNOSTIC-VALUE OF FIBRONECTIN DETERMINATION IN CEREBROSPINAL-FLUID SO JOURNAL OF CLINICAL PATHOLOGY LA English DT Letter RP WELLER, M (reprint author), NIH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0021-9746 J9 J CLIN PATHOL JI J. Clin. Pathol. PD JUN PY 1992 VL 45 IS 6 BP 548 EP 549 DI 10.1136/jcp.45.6.548-d PG 2 WC Pathology SC Pathology GA HY091 UT WOS:A1992HY09100031 PM 1624613 ER PT J AU PIGOTT, TA LHEUREUX, F RUBENSTEIN, CS BERNSTEIN, SE HILL, JL MURPHY, DL AF PIGOTT, TA LHEUREUX, F RUBENSTEIN, CS BERNSTEIN, SE HILL, JL MURPHY, DL TI A DOUBLE-BLIND, PLACEBO CONTROLLED-STUDY OF TRAZODONE IN PATIENTS WITH OBSESSIVE-COMPULSIVE DISORDER SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID SEROTONERGIC RESPONSIVITY; CONTROLLED TRIAL; EFFICACY; FLUVOXAMINE; CLOMIPRAMINE; FLUOXETINE; DEPRESSION; IMIPRAMINE; CHLOROPHENYLPIPERAZINE; TRYPTOPHAN AB Patients with obsessive-compulsive disorder (OCD) have been shown to be preferentially responsive to serotonin (5-HT) uptake-inhibiting antidepressants including clomipramine, fluoxetine, fluvoxamine, and sertraline. The nontricyclic antidepressant, trazodone, also possesses serotonin reuptake inhibiting properties and has been reported to be efficacious in OCD in several case reports and open trials. In order to investigate trazodone's potential antiobsessive efficacy in a controlled fashion, 21 patients with OCD were entered into a double-blind, parallel design comparison of trazodone and placebo. There were no significant differences in baseline rating scores of OCD or depressive symptoms between those who entered the trazodone phase (N = 13) versus those who entered the placebo phase (N = 8). As measured by standardized OCD and depression rating scales, there was no significant difference in OCD or depressive symptoms in the 17 patients who completed 10 weeks of trazodone (N = 11, mean daily dose, 235 +/- 10 mg) versus 10 weeks of placebo (N = 6) administration. In comparison to clomipramine and fluoxetine treatment which we have found to be associated with >95% reduction in platelet 5-HT concentration, there was only a 26% mean reduction in platelet 5-HT concentration after 10 weeks of trazodone administration. These results indicate that trazodone lacks substantial antiobsessive effects and is associated with only modest reductions in platelet 5-HT concentrations. RP PIGOTT, TA (reprint author), NIMH,CTR CLIN,CLIN SCI LAB,CLIN NEUROPHARMACOL SECT,10-3D41,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 45 TC 46 Z9 47 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 JUN PY 1992 VL 12 IS 3 BP 156 EP 162 PG 7 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA HX648 UT WOS:A1992HX64800002 PM 1629380 ER PT J AU HILAKIVICLARKE, LA LISTER, RG AF HILAKIVICLARKE, LA LISTER, RG TI ARE THERE PREEXISTING BEHAVIORAL-CHARACTERISTICS THAT PREDICT THE DOMINANT STATUS OF MALE NIH SWISS MICE (MUS-MUSCULUS) SO JOURNAL OF COMPARATIVE PSYCHOLOGY LA English DT Article ID PLUS-MAZE; EXPLORATION; DESPAIR; ANXIETY; STRESS; DEFEAT AB The behavior of isolated Cr:NIH(S) mice (Mus musculus) was studied in a holeboard test of exploration, in a plus-maze test of anxiety, in the resident-intruder paradigm of aggression, and in the swim test. Thereafter, mice that were matched for body weight were housed together in groups of 4-5. Within a week, 1 mouse per cage (the alpha) had attacked all its subordinate cagemates but lacked any signs of attack itself Subordinate mice had bite marks on their tails and backs. When mice were isolated, no differences were found between the behavior of those that later became alphas and those that became subordinates. In contrast, after the establishment of the social hierarchy, alpha mice spent less time immobile in the swim test and had higher locomotor activities than did the subordinate mice. The results suggest that the differences in behavior between the alpha and subordinate mice result from aggressive social interactions in the home cage. RP HILAKIVICLARKE, LA (reprint author), NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,BETHESDA,MD 20892, USA. NR 26 TC 19 Z9 19 U1 0 U2 2 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7036 J9 J COMP PSYCHOL JI J. Comp. Psychol. PD JUN PY 1992 VL 106 IS 2 BP 184 EP 189 DI 10.1037//0735-7036.106.2.184 PG 6 WC Behavioral Sciences; Psychology; Psychology, Multidisciplinary; Zoology SC Behavioral Sciences; Psychology; Zoology GA HW969 UT WOS:A1992HW96900010 PM 1600723 ER PT J AU BORSTEIN, MH AF BORSTEIN, MH TI SOCIAL INFLUENCES AND SOCIALIZATION IN INFANCY - LEWIS,M, FEINMAN,S SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review RP BORSTEIN, MH (reprint author), NICHHD,CHILD & FAMILY RES,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD JUN PY 1992 VL 13 IS 3 BP 234 EP 234 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA HY701 UT WOS:A1992HY70100018 ER PT J AU LAUNER, LJ FORMAN, MR HUNDT, GL SAROV, B CHANG, D BERENDES, HW NAGGAN, L AF LAUNER, LJ FORMAN, MR HUNDT, GL SAROV, B CHANG, D BERENDES, HW NAGGAN, L TI MATERNAL RECALL OF INFANT-FEEDING EVENTS IS ACCURATE SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH LA English DT Article AB Study objective-Retrospective infant feeding data are important to the study of child and adult health patterns. The accuracy of maternal recall of past infant feeding events was examined and specifically the infant's age when breast feeding was stopped and formula feeding and solid foods were introduced. Design and setting-The sample consisted of Bedouin Arab women (n=318) living in the Negev in Israel who were a part of a larger cohort participating in a prospective study of infant health and who were delivered of their infants between July 1 and December 15, 1981. Data from interviews conducted 12 and 18 months postpartum were compared to the standard data collected six months postpartum. Main results-As length of recall increased there was a small increase in the mean difference, and its standard deviation, between the standard and recalled age when breast feeding was stopped and formula feeding and solid foods were started. Recall on formula feeding was less accurate than recall on solid foods and breast feeding. In particular, among those 61% reporting formula use at the six month interview, 51% did not recall introducing formula when interviewed at 18 months. The odds ratio (95% CI) of stunting versus normal length for age for formula fed versus breast fed infants based on recall data (OR=2.07; 95%CI 0.82-5.22) differed only slightly from those based on the standard data (OR=2.21; 95%CI 0.77-6.37). The accuracy of a mother's recall varied with her child's nutritional status at the time of the interview, but not with other sociodemographic, infant, or interviewer characteristics. Conclusions-Retrospective infant feeding data based on maternal recall of events up to 18 months in the past can be used with confidence in epidemiological studies. However, data on formula feeding may not be as accurate as data on breast feeding and solid food feeding, and accuracy may decrease as length of recall increases. C1 NICHHD,DIV PREVENT RES,EPN RM 640,BETHESDA,MD 20892. COMP DATA SYST INC,ROCKVILLE,MD. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. BEN GURION UNIV NEGEV,FAC HLTH SCI,DIV HLTH COMMUNITY,SOCIOL HLTH UNIT,IL-84105 BEER SHEVA,ISRAEL. BEN GURION UNIV NEGEV,CTR HLTH SCI,EPIDEMIOL & HLTH SERV EVALUAT UNIT,IL-84105 BEER SHEVA,ISRAEL. NR 26 TC 71 Z9 72 U1 0 U2 1 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0143-005X J9 J EPIDEMIOL COMMUN H JI J. Epidemiol. Community Health PD JUN PY 1992 VL 46 IS 3 BP 203 EP 206 DI 10.1136/jech.46.3.203 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HY568 UT WOS:A1992HY56800008 PM 1645071 ER PT J AU KOZLOWSKI, S CORR, M TAKESHITA, T BOYD, LF PENDLETON, CD GERMAIN, RN BERZOFSKY, JA MARGULIES, DH AF KOZLOWSKI, S CORR, M TAKESHITA, T BOYD, LF PENDLETON, CD GERMAIN, RN BERZOFSKY, JA MARGULIES, DH TI SERUM ANGIOTENSIN-1 CONVERTING ENZYME-ACTIVITY PROCESSES A HUMAN IMMUNODEFICIENCY VIRUS-1 GP160 PEPTIDE FOR PRESENTATION BY MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I MOLECULES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TOXIC LYMPHOCYTES-T; ANTIGEN PRESENTATION; SOLUBLE-PROTEIN; BETA-2-MICROGLOBULIN; INHIBITORS; BINDING; PATHWAY; CELLS AB T cell stimulation by the human immunodeficiency virus 1 gp160-derived peptide p18 presented by H-2D(d) class I major histocompatibility complex molecules in a cell-free system was found to require proteolytic cleavage. This extracellular processing was mediated by peptidases present in fetal calf serum. In vitro processing of p18 resulted in a distinct reverse phase high performance liquid chromatography profile, from which a biologically active product was isolated and sequenced. This peptide processing can be specifically blocked by the angiotensin-1 converting enzyme (ACE) inhibitor captopril, and can occur by exposing p18 to purified ACE. The ability of naturally occurring extracellular proteases to convert inactive peptides to T cell antigens has important implications for understanding cytotoxic T lymphocyte responses in vivo, and for rational peptide vaccine design. C1 NIAID,IMMUNOL LAB,MOLEC BIOL SECT,BLDG 10,ROOM 11N311,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BETHESDA,MD 20892. NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD 20892. RI Margulies, David/H-7089-2013; OI Margulies, David/0000-0001-8530-7375 NR 32 TC 112 Z9 112 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 JUN 1 PY 1992 VL 175 IS 6 BP 1417 EP 1422 DI 10.1084/jem.175.6.1417 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HV676 UT WOS:A1992HV67600001 PM 1316930 ER PT J AU RESTIFO, NP SPIESS, PJ KARP, SE MULE, JJ ROSENBERG, SA AF RESTIFO, NP SPIESS, PJ KARP, SE MULE, JJ ROSENBERG, SA TI A NONIMMUNOGENIC SARCOMA TRANSDUCED WITH THE CDNA FOR INTERFERON-GAMMA ELICITS CD8+ T-CELLS AGAINST THE WILD-TYPE TUMOR - CORRELATION WITH ANTIGEN PRESENTATION CAPABILITY SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TOXIC LYMPHOCYTES-T; CLASS-I GENE; INFILTRATING LYMPHOCYTES; MURINE TUMOR; ADOPTIVE IMMUNOTHERAPY; MHC ANTIGENS; INTERLEUKIN-2; EXPRESSION; CANCER; TRANSCRIPTION AB To be recognized by CD8+ T lymphocytes, target cells must process and present peptide antigens in the context of major histocompatibility complex (MHC) class I molecules. The nonimmunogenic, low class I-expressing, methylcholanthrene (MCA)-induced murine sarcoma cell line, MCA 101, is a poor presenter of endogenously generated viral antigens to specific CD8+ T lymphocytes and cannot be used to generate tumor infiltrating lymphocytes (TIL). Since interferon-gamma (IFN-gamma) has been shown to upregulate three sets of molecules important for antigen processing and presentation, we retrovirally transduced wild-type MCA 101 (101.WT) tumor with the mIFN-gamma-cDNA to create the 101.NAT cell line. Unlike 101.WT, some clones of retrovirally transduced 101.NAT tumor expressed high levels of class I, and could be used to generate CD8+ TIL. More importantly, these TIL were therapeutic in vivo against established pulmonary metastases from the wild-type tumor. Although not uniformly cytotoxic amongst several separate cultures, these TIL did specifically release cytokines (IFN-gamma and tumor necrosis factor-alpha) in response to 101.WT targets. 101.WT's antigen presentation deficit was also reversed by gene modification with mIFN-gamma-cDNA. 101.NAT had a greatly improved capacity to present viral antigens to CD8+ cytotoxic T lymphocytes. These findings show that a nonimmunogenic tumor, incapable of generating a CD8+ T cell immune response, could be gene-modified to generate a therapeutically useful immune response against the wild-type tumor. This strategy may be useful in developing treatments for tumor histologies not thought to be susceptible to T cell-based immunotherapy. RP RESTIFO, NP (reprint author), NCI,DIV CANC TREATMENT,SURG BRANCH,BETHESDA,MD 20892, USA. RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z01 BC010763-01, Z99 CA999999] NR 48 TC 187 Z9 187 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 JUN 1 PY 1992 VL 175 IS 6 BP 1423 EP 1431 DI 10.1084/jem.175.6.1423 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HV676 UT WOS:A1992HV67600002 PM 1588273 ER PT J AU TOURAY, MG WARBURG, A LAUGHINGHOUSE, A KRETTLI, AU MILLER, LH AF TOURAY, MG WARBURG, A LAUGHINGHOUSE, A KRETTLI, AU MILLER, LH TI DEVELOPMENTALLY REGULATED INFECTIVITY OF MALARIA SPOROZOITES FOR MOSQUITO SALIVARY-GLANDS AND THE VERTEBRATE HOST SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID PLASMODIUM-KNOWLESI; CIRCUMSPOROZOITE PROTEINS; PARASITES; ANTIBODIES AB Sporozoites are an invasive stage of the malaria parasite in both the mosquito vector and the vertebrate host. We developed an in vivo assay for mosquito salivary gland invasion by preparing Plasmodium gallinaceum sporozoites from infected Aedes aegypti mosquitoes under physiological conditions and inoculating them into uninfected female Ae. aegypti. Sporozoites from mature oocysts were isolated from mosquito abdomens 10 or 11 d after an infective blood meal. Salivary gland sporozoites were isolated 13 or 14 d after an infective blood meal. Purified oocyst sporozoites that were inoculated into uninfected female mosquitoes invaded their salivary glands. Using the same assay system, sporozoites derived from salivary glands did not reinvade the salivary glands after inoculation. Conversely, as few as 10 to 50 salivary gland sporozoites induced infection in chickens, while only 2 of 10 chickens inoculated with 5,000 oocyst sporozoites were infected. Both sporozoite populations were found to express a circumsporozoite protein on the sporozoite surface as determined by immunofluorescence assay and circumsporozoite precipitation test using a circumsporozoite protein-specific monoclonal antibody. We conclude that molecules other than this circumsporozoite protein may be responsible for the differential invasion of mosquito salivary glands or infection of the vertebrate host. C1 NIAID,MALARIA RES LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892. FDN OSWALDO CRUZ,CTR PESQUISAS R RACHOU,BR-30190 BELO HORIZONTE,MG,BRAZIL. NR 22 TC 59 Z9 60 U1 0 U2 3 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 JUN 1 PY 1992 VL 175 IS 6 BP 1607 EP 1612 DI 10.1084/jem.175.6.1607 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HV676 UT WOS:A1992HV67600022 PM 1588284 ER PT J AU JACOBSEN, SEW RUSCETTI, FW DUBOIS, CM KELLER, JR AF JACOBSEN, SEW RUSCETTI, FW DUBOIS, CM KELLER, JR TI TUMOR-NECROSIS-FACTOR-ALPHA DIRECTLY AND INDIRECTLY REGULATES HEMATOPOIETIC PROGENITOR-CELL PROLIFERATION - ROLE OF COLONY-STIMULATING FACTOR RECEPTOR MODULATION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID GROWTH-FACTORS; INTERFERON-GAMMA; SURFACE RECEPTOR; STEM-CELLS; FACTOR-I; GM-CSF; INVITRO; MURINE; DIFFERENTIATION; LEUKEMIA AB Tumor necrosis factor-alpha (TNF-alpha) has been shown to both stimulate and inhibit the proliferation of hematopoietic progenitor cells (HPCs) in vitro, but its mechanisms of action are not known. We demonstrate that the direct effects of TNF-alpha on murine bone marrow progenitors are only inhibitory and mediated at least in part through downmodulation of colony-stimulating factor receptor (CSF-R) expression. The stimulatory effects of TNF-alpha are indirectly mediated through production of hematopoietic growth factors, which subsequently results in increased granulocyte-macrophage CSF and interleukin 3 receptor expression. In addition, the effects of TNF-alpha (stimulatory or inhibitory) are strictly dependent on the particular CSF stimulating growth as well as the concentration of TNF-alpha present in culture. A model is proposed to explain how TNF-alpha night directly and indirectly regulate HPC growth through modulation of CSF-R expression. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RP JACOBSEN, SEW (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 68 TC 103 Z9 104 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 JUN 1 PY 1992 VL 175 IS 6 BP 1759 EP 1772 DI 10.1084/jem.175.6.1759 PG 14 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HV676 UT WOS:A1992HV67600038 PM 1375270 ER PT J AU TULLI, HM CARLSON, CS JAYO, MJ FISHER, LW TRACY, RP MANN, KG AF TULLI, HM CARLSON, CS JAYO, MJ FISHER, LW TRACY, RP MANN, KG TI IMMUNOHISTOCHEMICAL METHOD FOR THE SIMULTANEOUS DEMONSTRATION OF 3 PROTEINS IN EDTA DECALCIFIED PARAFFIN EMBEDDED BONE SECTIONS SO JOURNAL OF HISTOTECHNOLOGY LA English DT Article DE ACTIN; ALKALINE PHOSPHATASE; BONE; EDTA; IMMUNOHISTOCHEMISTRY; OSTEOCALCIN ID GAMMA-CARBOXYGLUTAMIC ACID; ALKALINE-PHOSPHATASE; IMMUNOCYTOCHEMICAL LOCALIZATION; INSITU HYBRIDIZATION; RAT BONE; OSTEOCALCIN; ANTIBODY; TISSUE AB Immunohistochemistry was used to demonstrate the presence of three proteins (actin, osteocalcin and alkaline phosphatase) within the same ethylenediaminetetraacetic acid (EDTA) decalcified and paraffin embedded bone tissue section. EDTA chelated calcium ions, causing endogenous alkaline phosphatase (ALP) to be inactivated. By ablating endogenous ALP activity through chelation, we were able to use an ALP based detection system before reactivation of the endogenous enzyme with magnesium chloride. After reactivation, endogenous ALP itself was demonstrated immunohistochemically. C1 NIH,BETHESDA,MD 20892. UNIV VERMONT,COLL MED,BURLINGTON,VT 05405. RP TULLI, HM (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,COMPARAT MED CLIN RES CTR,MED CTR BLVD,WINSTON SALEM,NC 27157, USA. NR 20 TC 4 Z9 4 U1 0 U2 1 PU NATL SOC HISTOTECHNOLOGY PI BOWIE PA 4201 NORTHVIEW DR, STE 502, BOWIE, MD 20716-1073 SN 0147-8885 J9 J HISTOTECHNOL JI J. Histotechnol. PD JUN PY 1992 VL 15 IS 2 BP 93 EP 97 PG 5 WC Cell Biology SC Cell Biology GA HY327 UT WOS:A1992HY32700003 ER PT J AU MAHANTY, S ABRAMS, JS KING, CL LIMAYE, AP NUTMAN, TB AF MAHANTY, S ABRAMS, JS KING, CL LIMAYE, AP NUTMAN, TB TI PARALLEL REGULATION OF IL-4 AND IL-5 IN HUMAN HELMINTH INFECTIONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELLS AB To investigate the relationship between cytokine production and the increased levels of serum IgE and peripheral eosinophilia commonly accompanying human helminth infections, we studied the ability of PBMC of normal (N1) (n = 18) and eosinophilic individuals with helminth infections (H1) (n = 9) to produce IL-3, IL-4, IL-5, granulocyte-macrophage-CSF, and IFN-gamma in vitro after stimulation with PMA (50 ng/ml) and ionomycin (1-mu-g/ml). The two groups differed in both the levels of serum IgE and eosinophilia. For mitogen-induced production of granulocyte-macrophage-CSF and IFN-gamma, there was no difference in cytokine production between the two groups. In marked contrast, supernatants from PBMC of infected individuals had significantly higher levels of IL-4 (mean = 213 pg/ml for N1 and 944 pg/ml for H1, p < 0.02), IL-5 (mean = 180 pg/ml for N1 and 1118 pg/ml for HL, p < 0.001), and IL-3 (mean = 13900 pg/ml for N1, 28029 pg/ml for H1, p < 0.05). In addition, helminth-infected patients had approximately 5-fold greater numbers of T cells capable of producing IL-5 and 2.5-fold greater frequency of IL-4-secreting cells than did normal individuals; GM-CSF-and IFN-gamma-producing T cell numbers were not significantly different in the two groups. IL-3-producing cell frequencies could not be evaluated by this method. There was a direct correlation between IL-4 production and IL-5 production at the level of both protein production and frequency of T cells capable of producing these cytokines. These data indicate that individuals with reactive eosinophilia and elevated serum IgE have an expanded population of lymphocytes producing IL-4 and IL-5 and the association of the two suggests that the regulation of IL-4 and IL-5 may be linked. C1 DNAX RES INST MOLEC & CELLULAR BIOL INC,RES INST,PALO ALTO,CA 94304. RP MAHANTY, S (reprint author), NIAID,CLIN PARASITOL SECT,PARASIT DIS LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. OI Mahanty, Siddhartha/0000-0003-1068-0524 NR 25 TC 111 Z9 111 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 JUN 1 PY 1992 VL 148 IS 11 BP 3567 EP 3571 PG 5 WC Immunology SC Immunology GA HW136 UT WOS:A1992HW13600034 PM 1350292 ER PT J AU OSWALD, IP GAZZINELLI, RT SHER, A JAMES, SL AF OSWALD, IP GAZZINELLI, RT SHER, A JAMES, SL TI IL-10 SYNERGIZES WITH IL-4 AND TRANSFORMING GROWTH-FACTOR-BETA TO INHIBIT MACROPHAGE CYTOTOXIC ACTIVITY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SCHISTOSOMA-MANSONI; MURINE MACROPHAGES; CONCOMITANT IMMUNITY; INTERFERON-GAMMA; EFFECTOR-CELLS; CYTO-TOXICITY; MOUSE; RESISTANCE; MICE; FACTOR-BETA-1 AB After activation with IFN-gamma, thioglycollate-elicited murine peritoneal macrophages kill schistosomula of Schistosoma mansoni in vitro by an L-arginine-dependent mechanism which involves the production of reactive nitrogen oxides (NO). In the present study we demonstrate that the regulatory cytokines IL-10, IL-4, and transforming growth factor-beta (TGF-beta) are potent inhibitors of this extracellular killing function of activated macrophages. Each cytokine was found to suppress killing of schistosomula in a dose-dependent fashion. The activity of IL-10 was not permanent, because subsequent treatment with additional IFN-gamma 2 to 6 h later reversed the inhibition of macrophage larval killing. More importantly, the combination of suboptimal levels of any two of these three cytokines was found to give a potent synergistic suppression of schistosomulum killing by IFN-gamma-treated macrophages. Similarly, IL-10, IL-4, or TGF-beta alone blocked the production of NO, and when used in combination these cytokines exhibited an enhanced inhibitory effect on nitrite production. Macrophage-mediated killing of schistosomula through the generation of NO has been shown previously to be a major effector mechanism of schistosome immunity. The results presented here suggest that the suppression of this mechanism by induction of the regulatory cytokines IL-10, IL-4, and TGF-beta, which are known to be produced during schistosome infection, may be an important strategy used by the parasite to evade macrophage-mediated immune destruction. RP OSWALD, IP (reprint author), NIAID,IMMUNOL & CELL BIOL SECT,PARASIT DIS LAB,BLDG 4,RM 126,BETHESDA,MD 20892, USA. RI OSWALD, Isabelle/A-8497-2013; OI OSWALD, Isabelle/0000-0001-9918-277X NR 40 TC 413 Z9 415 U1 2 U2 6 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 1 PY 1992 VL 148 IS 11 BP 3578 EP 3582 PG 5 WC Immunology SC Immunology GA HW136 UT WOS:A1992HW13600036 PM 1588047 ER PT J AU KIM, JM BRANNAN, CI COPELAND, NG JENKINS, NA KHAN, TA MOORE, KW AF KIM, JM BRANNAN, CI COPELAND, NG JENKINS, NA KHAN, TA MOORE, KW TI STRUCTURE OF THE MOUSE IL-10 GENE AND CHROMOSOMAL LOCALIZATION OF THE MOUSE AND HUMAN GENES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NUCLEOTIDE-SEQUENCE; HEPATITIS-VIRUS; B-CELLS; INTERLEUKIN-10; EXPRESSION; ANTIGEN; GENOME AB The nucleotide sequence of a 7.2-kb segment containing the mouse IL-10 (mIL-10) gene was determined. Comparison to the mIL-10 cDNA sequence (Moore, K. W., et al. 1990. Science 248:1230; 250:494) revealed the presence of five exons that span approximately 5.1 kb of genomic DNA. The noncoding regions of the mIL-10 gene contain sequences that have been associated with transcriptional regulation of several cytokine genes. The mIL-10 gene was mapped to mouse chromosome 1 and the human IL-10 gene was also mapped to human chromosome 1. C1 DNAX RES INST MOLEC & CELLULAR BIOL INC,DEPT IMMUNOL,MOLEC & CELLULAR BIOL RES INST,PALO ALTO,CA 94304. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 35 TC 195 Z9 201 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 1 PY 1992 VL 148 IS 11 BP 3618 EP 3623 PG 6 WC Immunology SC Immunology GA HW136 UT WOS:A1992HW13600042 PM 1350294 ER PT J AU FARCI, P LONDON, WT WONG, DC DAWSON, GJ VALLARI, DS ENGLE, R PURCELL, RH AF FARCI, P LONDON, WT WONG, DC DAWSON, GJ VALLARI, DS ENGLE, R PURCELL, RH TI THE NATURAL-HISTORY OF INFECTION WITH HEPATITIS-C VIRUS (HCV) IN CHIMPANZEES - COMPARISON OF SEROLOGIC RESPONSES MEASURED WITH 1ST-GENERATION AND 2ND-GENERATION ASSAYS AND RELATIONSHIP TO HCV VIREMIA SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID NON-B-HEPATITIS; NON-A-HEPATITIS; DELTA-VIRUS; ANTIBODIES; BLOOD AB The sensitivity of first- and second-generation tests for antibody to hepatitis C virus (HCV) and the relationship among the patterns of antibody response and HCV viremia were examined in serial serum samples from 6 chimpanzees experimentally infected with HCV and followed less-than-or-equal-to 3 years. HCV infection was transient in 4 chimpanzees and became chronic in 2. All chimpanzees developed antibodies to HCV detectable by second-generation assays, while only 5 of the 6 became positive by first-generation assay. Second-generation were consistently more sensitive than first-generation assays for the early diagnosis of primary HCV infection. The pattern observed with second-generation assays was not influenced by the outcome of HCV infection, since antibodies remained persistently detectable throughout follow-up regardless of whether viremia was transient or persistent. In contrast, the first-generation antibody response was variable: It usually disappeared after loss of viremia, whereas its presence paralleled HCV viremia in chimpanzees with chronic infection. C1 GEORGETOWN UNIV,DEPT MICROBIOL,DIV MOLEC VIROL & IMMUNOL,ROCKVILLE,MD. ABBOTT LABS,ABBOTT PK,IL. UNIV CAGLIARI,DEPT INTERNAL MED,I-09100 CAGLIARI,ITALY. RP FARCI, P (reprint author), NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BLDG 7,ROOM 200,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 23 TC 77 Z9 77 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JUN PY 1992 VL 165 IS 6 BP 1006 EP 1011 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HV960 UT WOS:A1992HV96000004 PM 1374781 ER PT J AU CLERICI, M GIORGI, JV CHOU, CC GUDEMAN, VK ZACK, JA GUPTA, P HO, HN NISHANIAN, PG BERZOFSKY, JA SHEARER, GM AF CLERICI, M GIORGI, JV CHOU, CC GUDEMAN, VK ZACK, JA GUPTA, P HO, HN NISHANIAN, PG BERZOFSKY, JA SHEARER, GM TI CELL-MEDIATED IMMUNE-RESPONSE TO HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) TYPE-1 IN SERONEGATIVE HOMOSEXUAL MEN WITH RECENT SEXUAL EXPOSURE TO HIV-1 SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID MULTICENTER AIDS COHORT; ENVELOPE GLYCOPROTEIN; DEFICIENCY SYNDROME; LYMPHOCYTES-T; WESTERN BLOT; INFECTION; RECOGNITION; INDIVIDUALS; ACTIVATION; POPULATION AB Although human immunodeficiency virus (HIV) type 1 infection is efficiently transmitted by sexual intercourse, some individuals whose sexual behavior places them at extremely high risk for infection have nevertheless remained HIV-1-seronegative. An investigation was undertaken to determine whether such individuals have circulating T helper cells that are sensitized to HIV-1. Five very high risk men who had recent sexual exposure to HIV-1 were studied. Peripheral blood mononuclear cells from all 5 produced interleukin (IL)-2 in culture in response to synthetic amphipathic HIV-1 envelope peptides. One of the 5 high-risk men has subsequently seroconverted, while 4 have remained seronegative. All were initially culture-negative, and those who have remained seronegative were also virus-negative by polymerase chain reaction (PCR) testing 10 months after they were first studied. These results demonstrate that a cell-mediated immune response to HIV-1 can be detected in the absence of a humoral immune response in individuals recently exposed to HIV-1. Furthermore, IL-2 production by T cells in response to synthetic peptides may be a more sensitive test for exposure to HIV-1 than antibody, lymphoproliferation, or PCR tests. C1 NCI,METAB BRANCH,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. JONSSON COMPREHENS CAN CTR,LOS ANGELES,CA. MULTICENTER AIDS COHORT STUDY,LOS ANGELES,CA. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,PITTSBURGH,PA 15260. RP CLERICI, M (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B17,BETHESDA,MD 20892, USA. OI Ho, Hong-Nerng/0000-0002-7207-0089 FU NIAID NIH HHS [AI-72631, AI-72656] NR 39 TC 370 Z9 375 U1 0 U2 7 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 JUN PY 1992 VL 165 IS 6 BP 1012 EP 1019 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HV960 UT WOS:A1992HV96000005 PM 1533867 ER PT J AU CASADEVALL, A MUKHERJEE, J DEVI, SJN SCHNEERSON, R ROBBINS, JB SCHARFF, MD AF CASADEVALL, A MUKHERJEE, J DEVI, SJN SCHNEERSON, R ROBBINS, JB SCHARFF, MD TI ANTIBODIES ELICITED BY A CRYPTOCOCCUS-NEOFORMANS TETANUS TOXOID CONJUGATE VACCINE HAVE THE SAME SPECIFICITY AS THOSE ELICITED IN INFECTION SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID CAPSULAR POLYSACCHARIDE; MONOCLONAL-ANTIBODIES; IMMUNOLOGICAL-UNRESPONSIVENESS; SOLUBLE POLYSACCHARIDE; SEROTYPE-A; PASSIVE-IMMUNIZATION; MICE; GALACTOXYLOMANNAN; PHAGOCYTOSIS; MACROPHAGES AB The antibody responses of BALB/c mice to serotype A Cryptococcus neoformans capsular polysaccharide (CNPS) were compared after cryptococcal infection and immunization with a serotype A glucuronoxylomannan-tetanus toxoid conjugate (GXM-TT). Infection rarely resulted in a rise of serum antibody titer to CNPS. In contrast, mice immunized with GXM-TT produced serum IgM and IgG to CNPS. Six IgM and one IgG1 monoclonal antibodies (MAbs) were generated from the spleen of one infected mouse. Nine IgM, 1 IgG3, 16 IgG1, and 7 IgA MAbs were generated from the spleen of one GXM-TT-immunized mouse. All MAbs generated from both mice bound to the GXM fraction of the capsular polysaccharide. For some MAbs, de-O-acetylation of serotype A GXM abolished or greatly reduced MAb binding compared with the native GXM. All MAbs reacted with CNPS from C. neoformans serotypes A-D. MAbs generated from the infected mouse competitively inhibited the binding of MAbs generated from the GXM-TT-immunized mouse. These results indicate that some antibodies elicited by infection with C. neoformans or by immunization with GXM-TT bind to the same antigenic determinant in the GXM. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,DIV INFECT DIS,BRONX,NY 10461. NICHHD,DEV & MOLEC IMMUN LAB,BETHESDA,MD 20892. RP CASADEVALL, A (reprint author), YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT CELL BIOL,ULLMANN BLDG,ROOM 1219,1300 MORRIS PK AVE,BRONX,NY 10461, USA. FU NCI NIH HHS [CA-39838, CA-13330]; NIAID NIH HHS [AI-10702] NR 49 TC 114 Z9 116 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 JUN PY 1992 VL 165 IS 6 BP 1086 EP 1093 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HV960 UT WOS:A1992HV96000016 PM 1583327 ER PT J AU ROMPALO, AM CANNON, RO QUINN, TC HOOK, EW AF ROMPALO, AM CANNON, RO QUINN, TC HOOK, EW TI ASSOCIATION OF BIOLOGIC FALSE-POSITIVE REACTIONS FOR SYPHILIS WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID SECONDARY SYPHILIS; RISK AB The prevalence of biologic false-positive (BFP) reactions for syphilis (reactive rapid plasma reagin [RPR] test, nonreactive fluorescent treponemal antibody absorption [FTA-ABS] test) among patients attending two sexually transmitted disease (STD) clinics was evaluated to assess relationships between BFP reactions and human immunodeficiency virus (HIV) infection. Among 4863 patients, 357 (7.3%) had serologic evidence of syphilis and 4.9% had HIV infection. Only 40 patients (0.8% of total patients, 11% of those with reactive RPR tests) had BFP serologic tests for syphilis. There were no demographic differences between true syphilis and BFP patients as to sex, age, or intravenous drug use. BFP patients tended to have lower RPR titers (less-than-or-equal-to 1:4) than did true syphilis patients. After excluding 317 patients with reactive FTA-ABS tests, BFP RPR tests were seen in 6 (4%) of 159 HIV-seropositive patients and 34 (0.8%) of 4387 HIV-seronegative patients (odds ratio, 5.0; 95% confidence interval, 1.9-12.7). Although more common among HIV-infected than HIV-uninfected patients, BFP reactions are relatively rare among STD clinic patients, and 89% of patients with reactive RPR or VDRL serologic tests for syphilis had current or prior syphilis infection. The RPR test remains useful for guiding decisions regarding therapy for syphilis. C1 JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21205. BALTIMORE CITY DEPT HLTH,BALTIMORE,MD. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. CTR DIS CONTROL,DIV SEXUALLY TRANSMITTED DIS HIV PREVENT,ATLANTA,GA 30333. FU NIAID NIH HHS [AI-27727] NR 10 TC 65 Z9 66 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 JUN PY 1992 VL 165 IS 6 BP 1124 EP 1126 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HV960 UT WOS:A1992HV96000023 PM 1583332 ER PT J AU LUNDGREN, B LUNDGREN, JD NIELSEN, T MATHIESEN, L NIELSEN, JO KOVACS, JA AF LUNDGREN, B LUNDGREN, JD NIELSEN, T MATHIESEN, L NIELSEN, JO KOVACS, JA TI ANTIBODY-RESPONSES TO A MAJOR PNEUMOCYSTIS-CARINII ANTIGEN IN HUMAN-IMMUNODEFICIENCY-VIRUS INFECTED PATIENTS WITH AND WITHOUT PNEUMOCYSTIS-CARINII PNEUMONIA SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID PROTEINS AB Antibody responses to a major purified human Pneumocystis carinii surface antigen (gp95) were determined by ELISA in human immunodeficiency virus (HIV)-infected patients. Serum IgG directed against gp95 was measured in 129 consecutive HIV-infected patients who underwent bronchoscopy for evaluation of pulmonary symptoms. Significantly more patients with P. carinii pneumonia (PCP) had detectable antibodies compared with HIV-infected patients without PCP and with HIV-negative controls (50 [66%] of 76 vs. 18 [34%] of 53 and 7 [35%] of 20, respectively; P < .001), and the level of antibody response was higher (mean optical density ratio: 0.6 vs. 0.23 and 0.2, respectively; P < .01). Changes in antibody response were investigated in 78 patients for whom serial serum samples taken around the time of bronchoscopy were available. Of the 47 patients with verified PCP, 20 (43%) mounted an antibody response, compared with only 1 (3%) of 31 patients without PCP (P < .001). This patient had PCP on the basis of clinical criteria, including response to therapy. Thus, despite severe immunosuppression, a proportion of HIV-infected patients with PCP can mount a specific IgG-mediated antibody response to P. carinii. C1 UNIV COPENHAGEN,HVIDOVRE HOSP,DEPT MICROBIOL,DK-2650 HVIDOVRE,DENMARK. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RP LUNDGREN, B (reprint author), UNIV COPENHAGEN,HVIDOVRE HOSP,DEPT INTERNAL MED,144,DK-2650 HVIDOVRE,DENMARK. NR 15 TC 42 Z9 42 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 JUN PY 1992 VL 165 IS 6 BP 1151 EP 1155 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HV960 UT WOS:A1992HV96000030 PM 1583338 ER PT J AU STEEL, C NUTMAN, TB AF STEEL, C NUTMAN, TB TI CELLULAR AND HUMORAL IMMUNE-RESPONSE IN ONCHOCERCIASIS - REPLY SO JOURNAL OF INFECTIOUS DISEASES LA English DT Letter ID VOLVULUS INFECTION; VACCINATIONS; ANTIGEN; HUMANS; BCG RP STEEL, C (reprint author), NIH,PARASIT DIS LAB,BLDG 4,RM 126,BETHESDA,MD 20892, USA. NR 12 TC 0 Z9 0 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 JUN PY 1992 VL 165 IS 6 BP 1162 EP 1162 PG 1 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HV960 UT WOS:A1992HV96000035 ER PT J AU BAKER, PJ AF BAKER, PJ TI T-CELL REGULATION OF THE ANTIBODY-RESPONSE TO BACTERIAL POLYSACCHARIDE ANTIGENS - AN EXAMINATION OF SOME GENERAL-CHARACTERISTICS AND THEIR IMPLICATIONS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT CONF ON EPIDEMIOLOGY, PATHOGENESIS, AND PREVENTION OF HAEMOPHILUS INFLUENZAE DISEASE CY SEP 24-28, 1990 CL VELDHOVEN, NETHERLANDS SP MERCK SHARP & DOHME, PRAXIS BIOLOGICS, CONNAUGHT LABS, PASTEUR MERIEUX SERUMS & VACCINS, HOECHST ROUSSEL PHARM, MENINGITIS TRUST GREAT BRITAIN, UPJOHN, BAYER PHARM, GLAXO PHARM, ELI LILLY ID III PNEUMOCOCCAL POLYSACCHARIDE; LOW-DOSE PARALYSIS; B-CELLS; IMMUNOLOGICAL-UNRESPONSIVENESS; CAPSULAR POLYSACCHARIDE; SUPPRESSOR CELLS; CONCANAVALIN-A; LIPID-A; MICE; AMPLIFIER AB The characteristics of thymus-derived (T) lymphocytes that regulate the magnitude of the antibody response to the capsular polysaccharide antigen of type III Streptococcus pneumoniae are considered within the context of a general homeostatic model for controlling the antibody response to microbial antigens of medical importance. Some experimental approaches are described in which the activities of such regulatory T cells are modulated to provide an increase in the development of host immunity, to improve the immunogenicity of poorly immunogenic antigens, or to eliminate the inhibitory effects of suppressor T cells. RP BAKER, PJ (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK-II RES FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 41 TC 31 Z9 31 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 JUN PY 1992 VL 165 SU 1 BP S44 EP S48 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HW745 UT WOS:A1992HW74500014 PM 1588176 ER PT J AU FOJO, SS BREWER, HB AF FOJO, SS BREWER, HB TI HYPERTRIGLYCERIDEMIA DUE TO GENETIC-DEFECTS IN LIPOPROTEIN-LIPASE AND APOLIPOPROTEIN-C-II SO JOURNAL OF INTERNAL MEDICINE LA English DT Article DE APOC-II DEFICIENCY; CHYLOMICRONEMIA; LIPOPROTEIN; LIPOPROTEIN LIPASE DEFICIENCY; MOLECULAR DEFECTS; PANCREATITIS ID POLYMERASE CHAIN-REACTION; NUCLEIC-ACID SEQUENCE; CII DEFICIENCY; HUMAN CHROMOSOME-19; NONSENSE MUTATION; MISSENSE MUTATION; POINT MUTATIONS; SPLICE SITE; PATIENT; DNA AB Hypertriglyceridaemia, as defined by fasting triglyceride levels of > 2.8mmol 1-1, is a prevalent dyslipoproteinaemia in our population. The underlying pathophysiological mechanisms that result in elevations of plasma triglycerides are heterogeneous and, in most cases, incompletely understood. However, in a subset of patients presenting with this lipid disorder, the biochemical and genetic defects that lead to hypertriglyceridaemia have been well characterized. These individuals present with the familial chylomicronaemia syndrome, a rare genetic disorder that is inherited as an autosomal recessive trait, and is characterized by severe fasting hypertriglyceridaemia, massive accumulations of chylomicrons in plasma, and recurrent bouts of pancreatitis. The two major causes of the familial chylomicronaemia syndrome are a deficiency of the enzyme, lipoprotein lipase (LPL), or its cofactor, apolipoprotein (apo) C-II. Together, these two proteins initiate the hydrolysis of triglycerides present in chylomicrons and very-low density lipoproteins. In the past decade our understanding of the underlying molecular defects that lead to familial chylomicronaemia has been greatly enhanced by the identification of mutations in the genes for LPL and apoC-II. Characterization of these defects has provided new insights into the structure and function of apoC-II and LPL and established the important role that these two proteins play in normal triglyceride metabolism. RP FOJO, SS (reprint author), NHLBI,MOLEC DIS BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM 7N117,BETHESDA,MD 20892, USA. NR 67 TC 75 Z9 76 U1 0 U2 4 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0954-6820 J9 J INTERN MED JI J. Intern. Med. PD JUN PY 1992 VL 231 IS 6 BP 669 EP 677 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA JB709 UT WOS:A1992JB70900016 PM 1619390 ER PT J AU ACCILI, D BARBETTI, F CAMA, A KADOWAKI, H KADOWAKI, T IMANO, E LEVYTOLEDANO, R TAYLOR, SI AF ACCILI, D BARBETTI, F CAMA, A KADOWAKI, H KADOWAKI, T IMANO, E LEVYTOLEDANO, R TAYLOR, SI TI MUTATIONS IN THE INSULIN-RECEPTOR GENE IN PATIENTS WITH GENETIC SYNDROMES OF INSULIN RESISTANCE AND ACANTHOSIS NIGRICANS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article; Proceedings Paper CT 40TH ANNUAL SYMP ON THE BIOLOGY OF SKIN : CELL RECEPTORS, INTRACELLULAR SIGNALING, AND TRANSCRIPTIONAL RESPONSE ELEMENTS CY JUN 15-18, 1991 CL SNOWMASS VILLAGE, CO SP ORENTREICH FDN ADV SCI, COSMAIR, DERMIK LABS, HERBERT LABS, HOECHST ROUSSEL PHARM, JOHNSON & JOHNSON CONSUMER PROD, NATL PSORIASIS FDN, NEUTROGENA DERMATOLOG, ORTHO PHARM, OWEN GALDERMA ID TYROSINE KINASE-ACTIVITY; CULTURED LYMPHOCYTES; IMPAIRS TRANSPORT; BINDING REGION; MUTANT ALLELES; POINT MUTATION; HUMAN-DISEASE; CELL; SITE; PHOSPHORYLATION AB Mutations of the insulin receptor gene have been identified in patients with genetic syndromes of insulin resistance associated with acanthosis nigricans. These mutations impair insulin responses by reducing the number of insulin receptors on the surface of target cells, or by reducing the receptor's ability to bind insulin or to undergo insulin-stimulated autophosphorylation, an important step iii insulin action. Studies of mutant receptors expressed in transfection systems have contributed to our understanding of the structure-function relationships of the insulin receptor. RP ACCILI, D (reprint author), NIDDK,DIABET BRANCH,BETHESDA,MD 20892, USA. NR 47 TC 11 Z9 11 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JUN PY 1992 VL 98 IS 6 SU S BP S77 EP S81 DI 10.1111/1523-1747.ep12462281 PG 5 WC Dermatology SC Dermatology GA HX764 UT WOS:A1992HX76400015 PM 1588128 ER PT J AU CAUGHMAN, SW LI, LJ DEGITZ, K AF CAUGHMAN, SW LI, LJ DEGITZ, K TI HUMAN INTERCELLULAR-ADHESION MOLECULE-1 GENE AND ITS EXPRESSION IN THE SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article; Proceedings Paper CT 40TH ANNUAL SYMP ON THE BIOLOGY OF SKIN : CELL RECEPTORS, INTRACELLULAR SIGNALING, AND TRANSCRIPTIONAL RESPONSE ELEMENTS CY JUN 15-18, 1991 CL SNOWMASS VILLAGE, CO SP ORENTREICH FDN ADV SCI, COSMAIR, DERMIK LABS, HERBERT LABS, HOECHST ROUSSEL PHARM, JOHNSON & JOHNSON CONSUMER PROD, NATL PSORIASIS FDN, NEUTROGENA DERMATOLOG, ORTHO PHARM, OWEN GALDERMA ID TUMOR NECROSIS FACTOR; FUNCTION-ASSOCIATED ANTIGEN-1; INTERFERON-GAMMA; MONOCLONAL-ANTIBODIES; EPIDERMAL-KERATINOCYTES; ULTRAVIOLET-RADIATION; ENDOTHELIAL-CELLS; ICAM-1 EXPRESSION; IMMUNE-SYSTEM; LYMPHOCYTES-T AB Cell adhesion molecules are cell-surface proteins that allow specific cell-cell interactions among leukocytes, as well as between leukocytes and other cells. Recent studies have shown that the differential expression of selected cell-adhesion molecules plays a critical role in cutaneous inflammation, immunologic responses, and wound repair. Intercellular adhesion molecule-1 (ICAM-1) is a cell-adhesion molecule that is constitutively expressed on human dermal microvascular endothelial cells (HDMEC) and is inducible on human keratinocytes (HK). Its regulated expression is vital to the initiation and evolution of localized inflammatory processes in the skin. ICAM-1 serves as a specific ligand for lymphocyte function-associated antigen-1 (LFA-1), a cell-surface protein expressed on all leukocytes. The regulated expression of ICAM-1 allows leukocytes to bind to endothelial cells at sites of inflammation and, after exiting into the tissue, to interact with specific target cells, such as HK. Furthermore, specific cytokines are capable of differentially regulating ICAM-1 expression on HDMEC, HK, and other cells. The biologic relevance of ICAM-1 expression in cutaneous inflammation is further supported by functional studies demonstrating the critical role of ICAM-l/LFA-1 interactions in mediating the binding of peripheral blood leukocytes to HDMEC and to HK-cells known to be participants and targets in specific cutaneous immunologic responses. Thus, the delineation of precise molecular mechanisms that regulate the tissue-specific and cytokine-specific expression if ICAM-1 is important to both our understanding of the biology of localized inflammation and to the development of directed anti-inflammatory therapeutic strategies. Current evidence indicates that ICAM-1 expression is regulated at the level of gene transcription. Recently our laboratory has isolated and characterized a human genomic clone that contains the 5' regulatory region of the ICAM-1 gene. In the current studies, we further describe the genomic ICAM-1 clones isolated to date and demonstrate the presence of consensus regulatory elements located within the 5' flanking region of the ICAM-1 gene that are potentially involved in regulating ICAM-1 gene transcription. C1 VET AFFAIRS MED CTR,DEPT DERMATOL,ATLANTA,GA. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. DERMATOL KLIN & POLIKLIN,MUNICH,GERMANY. RP CAUGHMAN, SW (reprint author), EMORY UNIV,SCH MED,DEPT DERMATOL,5001 WOODRUFF MEM BLDG,ATLANTA,GA 30322, USA. NR 56 TC 13 Z9 13 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JUN PY 1992 VL 98 IS 6 SU S BP S61 EP S65 DI 10.1111/1523-1747.ep12462226 PG 5 WC Dermatology SC Dermatology GA HX764 UT WOS:A1992HX76400012 PM 1350296 ER PT J AU BRODY, AR BONNER, JC OVERBY, LH BADGETT, A KALTER, V KUMAR, RK BENNETT, RA AF BRODY, AR BONNER, JC OVERBY, LH BADGETT, A KALTER, V KUMAR, RK BENNETT, RA TI INTERSTITIAL PULMONARY MACROPHAGES PRODUCE PLATELET-DERIVED GROWTH-FACTOR THAT STIMULATES RAT LUNG FIBROBLAST PROLIFERATION INVITRO SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE PULMONARY MACROPHAGES; GROWTH FACTORS; FIBROBLAST PROLIFERATION LUNG FIBROSIS; MACROPHAGE-FIBROBLAST INTERACTIONS ID CHRYSOTILE ASBESTOS INHALATION; ALVEOLAR MACROPHAGES; INORGANIC PARTICLES; TRITIATED-THYMIDINE; DEPOSITION PATTERN; CELLS; MORPHOLOGY; RECEPTORS; HOMOLOG; SECRETION AB Alveolar macrophages from humans and several animal species produce factors in vitro that modulate fibroblast growth and have been proposed as mediators of interstitial pulmonary fibrosis. Pulmonary interstitial macrophages (IMs) have not been studied previously in this regard. Pulmonary IMs were isolated from prelavaged rat lungs by enzymatic digestion of tissue and subsequent differential adherence of cells to culture dishes. The ability of IMs to release modulators of fibroblast growth into the culture medium was assessed by measuring [H-3]thymidine incorporation into DNA and/or nuclear labeling of early-passage rat lung fibroblasts exposed to medium conditioned by IMs. The percentages of nuclei labeled in fibroblast cultures exposed to interstitial macrophage-conditioned medium (IMCM) alone did not significantly differ from that observed in controls, but fibroblasts exposed to IMCM supplemented with 2% platelet-poor plasma showed a 2.6-fold increase in labeling, indicating that IMCM contains predominantly "competence" growth factor activity. Similar results were obtained using purified human platelet-derived growth factor (PDGF). The level of growth factor activity released by IMs increased in cells that had phagocytized iron spheres during the culture period. In addition, fractionation of IMCM by high-performance liquid chromatography demonstrated most of the growth factor activity at a relative molecular mass of about 35 kd. Subsequent quantitative analysis of the fractions by an enzyme immunoassay for PDGF demonstrated that IMCM contains a homologue of human PDGF. These results show that IMs are capable of producing a PDGF-like growth factor for autologous fibroblasts and that release of this factor is enhanced by exposure to an insoluble inorganic particle. Because PDGF is a potent growth factor for fibroblasts and is released by IMs, it is essential to ask in future studies whether this or similar macrophage products play a significant role in mediating fibroblast proliferation in vivo. C1 NIEHS,NATL TOXICOL PROGRAM,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. RI Kumar, Rakesh/J-6124-2012 OI Kumar, Rakesh/0000-0002-9531-8411 NR 42 TC 45 Z9 45 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD JUN PY 1992 VL 51 IS 6 BP 640 EP 648 PG 9 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA JQ367 UT WOS:A1992JQ36700016 PM 1613399 ER PT J AU ZHU, GA BAX, A AF ZHU, GA BAX, A TI 2-DIMENSIONAL LINEAR PREDICTION FOR SIGNALS TRUNCATED IN BOTH DIMENSIONS SO JOURNAL OF MAGNETIC RESONANCE LA English DT Note ID NMR-SPECTROSCOPY; RESOLUTION; EXTRAPOLATION; RESONANCE; PHASE C1 UNIV MARYLAND,CHEM PHYS PROGRAM,COLLEGE PK,MD 20742. RP ZHU, GA (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 15 TC 64 Z9 64 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 0022-2364 J9 J MAGN RESON JI J. Magn. Reson. PD JUN 1 PY 1992 VL 98 IS 1 BP 192 EP 199 DI 10.1016/0022-2364(92)90124-P PG 8 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA HZ094 UT WOS:A1992HZ09400021 ER PT J AU ROTH, BJ AF ROTH, BJ TI HOW THE ANISOTROPY OF THE INTRACELLULAR AND EXTRACELLULAR CONDUCTIVITIES INFLUENCES STIMULATION OF CARDIAC-MUSCLE SO JOURNAL OF MATHEMATICAL BIOLOGY LA English DT Article DE BIDOMAIN; VIRTUAL CATHODE; CONDUCTIVITY; ANISOTROPY; CARDIAC MUSCLE ID 3-DIMENSIONAL PERIODIC MYOCARDIUM; WAVE-FRONT PROPAGATION; ASYMPTOTIC ANALYSIS; CYLINDRICAL BUNDLE; POTENTIAL DISTRIBUTION; SYNCYTIAL TISSUES; SKELETAL-MUSCLE; MODEL; FIBER; EXCITATION AB The bidomain model, which describes the behavior of many electrically active tissues, is equivalent to a multi-dimensional cable model and can be represented by a network of resistors and capacitors. For a two-dimensional sheet of tissue, the intracellular and extracellular conductivity tensors can be visualized as two ellipses. For any pair of conductivity tensors, a coordinate transformation can be found that reduces the extracellular ellipse to a circle and aligns the intracellular ellipse with the coordinate axes. The eccentricity of the intracellular ellipse in this new coordinate system is an important parameter. It can have two special values: zero (in which case the tissue has equal anisotropy ratios) or one (in which case the tissue is comprised of one-dimensional fibers coupled through the two-dimensional extracellular space). Thus the bidomain model provides a unifying framework within which the electrical behavior of a wide variety of nerve and muscle tissues can be studied. When the anisotropy ratios in the intracellular and extracellular domains are not equal, stimulation with an anode always causes depolarization of some region of tissue. An analogous effect occurs in models that describe one-dimensional fibers, in which an "activating function" determines the site of stimulation. Experiments indicate that cardiac muscle does not have equal anisotropy ratios. Therefore, models developed to describe stimulation of axons may also help in understanding stimulation of two- or three-dimensional cardiac tissue, and may explain the concept of anodal stimulation of cardiac tissue through a "virtual cathode". RP ROTH, BJ (reprint author), NIH, NATL CTR RES RESOURCES, BIOMED ENGN & INSTRUMENTAT PROGRAM, BLDG 13, BETHESDA, MD 20892 USA. RI Roth, Bradley/A-4920-2008 NR 60 TC 64 Z9 64 U1 1 U2 4 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0303-6812 J9 J MATH BIOL JI J. Math. Biol. PD JUN PY 1992 VL 30 IS 6 BP 633 EP 646 DI 10.1007/BF00948895 PG 14 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA JA815 UT WOS:A1992JA81500006 PM 1640183 ER PT J AU POTKAY, S AF POTKAY, S TI DISEASES OF THE CALLITRICHIDAE - A REVIEW SO JOURNAL OF MEDICAL PRIMATOLOGY LA English DT Review DE TAMARINS; MARMOSETS; CALLITRICHIDS; SAGUINUS; CALLITHRIX; CEBUELLA; LEONTOPITHECUS ID MARMOSETS CALLITHRIX-JACCHUS; COTTON-TOP TAMARINS; EPSTEIN-BARR VIRUS; NON-B-HEPATITIS; SAGUINUS-OEDIPUS-OEDIPUS; GOLDEN LION TAMARINS; RED-BELLIED TAMARINS; VARICELLA-ZOSTER VIRUS; HUMAN NON-A; COMMON MARMOSETS AB The Callitrichidae contains four genera that embrace up to 50 species and subspecies found in neotropical habitats. Certain members have either naturally occurring or induced conditions that serve as important models of human disease. They include viral, bacterial, and parasitic infections, nutritional deficiencies, neoplasia, and various other conditions. The spontaneous diseases of captive callitrichids and those to which these species are experimentally susceptible were reviewed. C1 NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,BETHESDA,MD 20892. NR 525 TC 63 Z9 66 U1 2 U2 10 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0047-2565 J9 J MED PRIMATOL JI J. Med. Primatol. PD JUN PY 1992 VL 21 IS 4 BP 189 EP 236 PG 48 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA JJ887 UT WOS:A1992JJ88700001 PM 1527793 ER PT J AU SPANDE, TF GARRAFFO, HM YEH, HJC PU, QL PANNELL, LK DALY, JW AF SPANDE, TF GARRAFFO, HM YEH, HJC PU, QL PANNELL, LK DALY, JW TI A NEW CLASS OF ALKALOIDS FROM A DENDROBATID POISON FROG - A STRUCTURE FOR ALKALOID-251F SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID SKIN ALKALOIDS; CLASSIFICATION; MYOBATRACHIDAE AB Alkaloids of a new class are present in skin extracts of the dendrobatid poison frog, Minyobates bombetes, of Colombia. The structure of the major alkaloid of this class, 251F, has been determined as a trimethylcyclopenta{b}quinolizidinemethanol 1 by nmr, gc-Ft-ir, and ms studies including ms-ms. At least nine congeners of 251F were detected in these extracts. C1 NIDDKD, BIOORGAN CHEM LAB, BLDG 8, ROOM 1A17, BETHESDA, MD 20892 USA. NIDDKD, ANALYT CHEM LAB, BETHESDA, MD 20892 USA. NR 15 TC 35 Z9 36 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD JUN PY 1992 VL 55 IS 6 BP 707 EP 722 DI 10.1021/np50084a002 PG 16 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA HX566 UT WOS:A1992HX56600002 PM 1522417 ER PT J AU WOO, EH WOO, WS CHMURNY, GN HILTON, BD AF WOO, EH WOO, WS CHMURNY, GN HILTON, BD TI MELANDRIOSIDE-A, A SAPONIN FROM MELANDRIUM-FIRMUM SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID NMR-SPECTROSCOPY; SPECTRA AB A new nortriterpene glycoside named melandrioside A {1} was isolated from Melandrium firmum, and its structure was elucidated as 3-O- {beta-D-galactopyranosyl-(1-->2)-{alpha-L-rhamnopyranosyl-(1-->4)}-beta-D-glucuronopyranosyl} -melandrigenin by use of modern nmr spectroscopic techniques. C1 SEOUL NATL UNIV,NAT PROD RES INST,SEOUL 151,SOUTH KOREA. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74102] NR 17 TC 9 Z9 9 U1 0 U2 1 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD JUN PY 1992 VL 55 IS 6 BP 786 EP 794 DI 10.1021/np50084a013 PG 9 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA HX566 UT WOS:A1992HX56600013 PM 1522420 ER PT J AU ROTHSTEIN, JD GARLAND, W PUIA, G GUIDOTTI, A WEBER, RJ COSTA, E AF ROTHSTEIN, JD GARLAND, W PUIA, G GUIDOTTI, A WEBER, RJ COSTA, E TI PURIFICATION AND CHARACTERIZATION OF NATURALLY-OCCURRING BENZODIAZEPINE RECEPTOR LIGANDS IN RAT AND HUMAN BRAIN SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE BENZODIAZEPINE; ENDOZEPINE; HPLC; GAMMA-AMINOBUTYRIC ACID MASS-SPECTROMETRY ID GABA-A RECEPTORS; STEROID-HORMONE METABOLITES; HEPATIC-ENCEPHALOPATHY; MONOCLONAL-ANTIBODY; ANTAGONIST FLUMAZENIL; MAMMALIAN BRAIN; BINDING-SITES; ANIMAL-MODEL; DIAZEPAM; MOLECULES AB Chemicals that are active at the benzodiazepine receptor (endozepines) are naturally present in the CNS. These substances are present in tissue from humans and animals and in plants and fungi. Using selective extraction protocols, HPLC purification, receptor binding displacement studies, and selective anti-benzodiazepine antibodies, we have identified six or seven peaks of endozepines in rat and human brain. All material could competitively displace [H-3]flunitrazepam binding to cerebellar benzodiazepine binding sites. Two peaks also competitively displaced Ro 5-4864 binding to the mitochondrial benzodiazepine binding site. Total amounts of brain endozepines were estimated to be present in potentially physiological concentrations, based on their ability to displace [H-3]flunitrazepam binding. Although endozepine peaks 1 and 2 had HPLC retention profiles similar to those of nordiazepam and diazepam, respectively, gas chromatography-mass spectrometry as well as high-performance TLC revealed biologically insignificant amounts of diazepam (< 0.02 pg/g) and nordiazepam (< 0.02 pg/g) in the purified material. Electrophysiologically, some purified endozepines positively modulated gamma-aminobutyric acid (GABA) action on Cl- conductance, monitored in patch-clamped cultured cortical neurons or in mammalian cells transfected with cDNA encoding various GABA(A) receptor subunits. These studies demonstrate that mammalian brains contain endozepines that could serve as potent endogenous positive allosteric modulators of GABA(A) receptors. C1 NIDDK,MED CHEM LAB,NEUROIMMUNOL UNIT,BETHESDA,MD. GEORGETOWN UNIV,SCH MED,FIDIA,GEORGETOWN INST NEUROSCI,WASHINGTON,DC. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. RP ROTHSTEIN, JD (reprint author), JOHNS HOPKINS UNIV,DEPT NEUROL,MEYER 5-119,600 N WOLFE ST,BALTIMORE,MD 21205, USA. RI rothstein, jeffrey/C-9470-2013; Puja, Giulia/C-3540-2015 OI Puja, Giulia/0000-0001-8385-6020 FU NINDS NIH HHS [1 KO8 NSO1355-01] NR 63 TC 58 Z9 58 U1 0 U2 5 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JUN PY 1992 VL 58 IS 6 BP 2102 EP 2115 DI 10.1111/j.1471-4159.1992.tb10952.x PG 14 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HT463 UT WOS:A1992HT46300015 PM 1315376 ER PT J AU WEINBERGER, DR JONES, D REBA, RC MANN, U COPPOLA, R GIBSON, R GOREY, J BRAUN, A CHASE, TN AF WEINBERGER, DR JONES, D REBA, RC MANN, U COPPOLA, R GIBSON, R GOREY, J BRAUN, A CHASE, TN TI A COMPARISON OF FDG PET AND IQNB SPECT IN NORMAL SUBJECTS AND IN PATIENTS WITH DEMENTIA SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; MUSCARINIC ACETYLCHOLINE-RECEPTORS; HUMAN CEREBRAL METABOLISM; ALZHEIMERS-DISEASE; SENILE DEMENTIA; COMPUTED-TOMOGRAPHY; PICKS DISEASE; PHYSOSTIGMINE; INVIVO AB Prior studies of patients with dementia have found similar qualitative patterns of cerebral glucose utilization with [F-18]2-fluoro-2-deoxyglucose (FDG) PET and of putative muscarinic receptor activity with [I-123]3-quinuclidinyl-4-iodobenzilate (IQNB). This raised doubts about whether receptor binding determines IQNB distribution and whether clinical information in IQNB scans is unique. To compare the methods directly, 4 normal volunteers and 7 patients with dementia underwent FDG PET and high-resolution IQNB SPECT scans. In normal subjects, relative regional activity from the paired scans was only weakly correlated (r = 0.29). Some regions (e.g., thalamus, frontal cortex) showed a clear disassociation of activity. In demented patients, IQNB scans tended to show larger defects than FDG scans, although one focal defect appeared only with PET. Results suggest that IQNB SPECT data are not primarily related to general physiological activity or regional cerebral blood flow and are not explained by attenuation or volume-averaging artifacts. Further studies should investigate whether IQNB scanning is a more sensitive in vivo measure of the extent of Alzheimer's disease than is FDG PET. C1 GEORGE WASHINGTON UNIV,DIV NUCL MED,WASHINGTON,DC 20052. NINCDS,EXPTL THERAPEUT BRANCH,WASHINGTON,DC. RP WEINBERGER, DR (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. FU PHS HHS [22215] NR 35 TC 42 Z9 43 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SUM PY 1992 VL 4 IS 3 BP 239 EP 248 PG 10 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JG128 UT WOS:A1992JG12800001 PM 1498576 ER PT J AU HENDERSON, R KURLAN, R KERSUN, JM COMO, P AF HENDERSON, R KURLAN, R KERSUN, JM COMO, P TI PRELIMINARY EXAMINATION OF THE COMORBIDITY OF ANXIETY AND DEPRESSION IN PARKINSONS-DISEASE SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID ATYPICAL DEPRESSION; DISORDERS AB Significant anxiety in combination with depression may represent a specific depressive subtype in Parkinson's disease (PD). To ascertain the prevalence of this symptom complex, we administered a self-report survey and standardized psychological tests that measure anxiety and depression to 164 PD patients and 150 age-matched healthy spouse control subjects. The reporting of depression in combination with panic/anxiety best differentiated the two populations (38% vs. 8%). Depression and anxiety were highly correlated in relationship to clinical features of PD. Our findings suggest that clinically significant levels of depression and anxiety may frequently coexist in PD. The specific neuropathology of PD may predispose to this pattern behavioral disturbance. C1 UNIV ROCHESTER,SCH MED,DEPT PSYCHIAT,ROCHESTER,NY 14627. UNIV ROCHESTER,SCH MED,DEPT NEUROL,ROCHESTER,NY 14627. UNIV ROCHESTER,NIMH,CLIN PSYCHOPATHOL ELDERLY RES CTR,ROCHESTER,NY 14627. FU NIMH NIH HHS [MH40381] NR 25 TC 90 Z9 92 U1 1 U2 4 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SUM PY 1992 VL 4 IS 3 BP 257 EP 264 PG 8 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JG128 UT WOS:A1992JG12800003 PM 1498578 ER PT J AU MARTIN, A HEYES, MP SALAZAR, AM KAMPEN, DL WILLIAMS, J LAW, WA COATS, ME MARKEY, SP AF MARTIN, A HEYES, MP SALAZAR, AM KAMPEN, DL WILLIAMS, J LAW, WA COATS, ME MARKEY, SP TI PROGRESSIVE SLOWING OF REACTION-TIME AND INCREASING CEREBROSPINAL-FLUID CONCENTRATIONS OF QUINOLINIC ACID IN HIV-INFECTED INDIVIDUALS SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID AIDS DEMENTIA COMPLEX; IMMUNODEFICIENCY-VIRUS-INFECTION; CHOICE REACTION-TIME; HUNTINGTONS-DISEASE; ALZHEIMERS-DISEASE; KYNURENIC ACID; L-TRYPTOPHAN; RAT-BRAIN; LESIONS; SYSTEM AB Neuropsychological functioning and cerebrospinal fluid concentrations of an endogenous neurotoxin, quinolinic acid (QUIN) were evaluated in 52 HIV-positive individuals (71 % without constitutional symptoms) and 33 HIV-seronegative controls (including 15 psychiatric patients with adjustment disorders). Although the HIV-positive subjects did not differ from controls on standard neuropsychological tests, simple and choice reactions times (RT) were slow at initial evaluation (P < 0.01) and became progressively slower at 6-month reevaluation (P < 0.05). Cerebrospinal fluid (CSF) QUIN was elevated at initial evaluation and increased during the 6-month interval (P < 0.05). Moreover, during this 6-month interval, progressive slowing of RT was highly correlated with increasing levels of CSF QUIN (r = 0.85, df = 15, P < 0.0001) but not with changes in mood, constitutional symptoms, or CD4 cell count. These findings suggest that RT may provide a sensitive behavioral measure of relatively early central nervous system involvement in HIV-infected individuals and that QUIN may play an important role in the pathogenesis of HIV-related neurological dysfunction. C1 HENRY M JACKSON FDN ADV MILIT MED,ROCKVILLE,MD. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. UNIFORMED SERV UNIV HLTH SCI,DEPT NEUROL,BETHESDA,MD 20814. RP MARTIN, A (reprint author), NIMH,CLIN SCI LAB,BLDG 10,ROOM 3D-41,BETHESDA,MD 20892, USA. RI martin, alex/B-6176-2009 NR 49 TC 97 Z9 100 U1 0 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SUM PY 1992 VL 4 IS 3 BP 270 EP 279 PG 10 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JG128 UT WOS:A1992JG12800005 PM 1386770 ER PT J AU BRADLEY, DJ TOWLE, HC YOUNG, WS AF BRADLEY, DJ TOWLE, HC YOUNG, WS TI SPATIAL AND TEMPORAL EXPRESSION OF ALPHA-THYROID AND BETA-THYROID HORMONE RECEPTOR MESSENGER-RNAS, INCLUDING THE BETA-2-SUBTYPE, IN THE DEVELOPING MAMMALIAN NERVOUS-SYSTEM SO JOURNAL OF NEUROSCIENCE LA English DT Article ID INSITU HYBRIDIZATION HISTOCHEMISTRY; RAT-BRAIN; PARAVENTRICULAR NUCLEUS; GENE-TRANSCRIPTION; ERBA-ALPHA; IDENTIFICATION; CEREBELLUM; PITUITARY; PROTEIN; TISSUES AB Thyroid hormone exerts profound effects on the developing mammalian brain, and its deficiency can lead to severe mental retardation and motor abnormalities. To identify specific anatomic targets of thyroid hormone action in the developing mammalian nervous system, we examined thyroid hormone receptor gene expression by hybridization histochemistry on serial adjacent sections f rom 1 2 stages of the developing rat nervous system. S-35-labeled cRNA probes were generated from divergent sequences of rat alpha-1-, alpha-2-,beta-1-, and beta-2-thyroid hormone receptor and related cDNAs. We found that alpha- and beta-thyroid hormone receptor genes have distinct patterns of spatiotemporal expression in the embryonic and postnatal rat nervous system. alpha-1- and alpha-2-mRNAs were widely expressed in similar patterns; highest levels were found in the fetal neocortical plate, site of cortical neuronal differentiation. In contrast, beta-1-transcripts were restricted in distribution, with prominent expression in zones of neuroblast proliferation such as the germinal trigone and the cortical ventricular layer. Surprisingly, the "pituitary-specific" beta-2-transcript was detected in the developing hippocampus and striatum. Our results suggest that alpha- and beta-thyroid hormone receptors may play distinct functional roles during development of the mammalian nervous system. C1 NIMH,CELL BIOL LAB,BLDG 36,ROOM 2D10,BETHESDA,MD 20892. UNIV MINNESOTA,DEPT BIOCHEM,MINNEAPOLIS,MN 55455. RI Young, W Scott/A-9333-2009 OI Young, W Scott/0000-0001-6614-5112 NR 65 TC 396 Z9 403 U1 2 U2 5 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 JUN PY 1992 VL 12 IS 6 BP 2288 EP 2302 PG 15 WC Neurosciences SC Neurosciences & Neurology GA HY156 UT WOS:A1992HY15600027 PM 1607941 ER PT J AU AKBASAK, A OLDFIELD, EH SARIS, SC AF AKBASAK, A OLDFIELD, EH SARIS, SC TI MAJOR HISTOCOMPATIBILITY ANTIGENS IN MURINE TUMORS - RESPONSE SO JOURNAL OF NEUROSURGERY LA English DT Letter ID CELLS C1 TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111. RP AKBASAK, A (reprint author), NIH,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD JUN PY 1992 VL 76 IS 6 BP 1049 EP 1050 PG 2 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA HV485 UT WOS:A1992HV48500040 ER PT J AU MCCORD, ME BACHARACH, SL BONOW, RO DILSIZIAN, V CUOCOLO, A FREEDMAN, N AF MCCORD, ME BACHARACH, SL BONOW, RO DILSIZIAN, V CUOCOLO, A FREEDMAN, N TI MISALIGNMENT BETWEEN PET TRANSMISSION AND EMISSION SCANS - ITS EFFECT ON MYOCARDIAL IMAGING SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID ATTENUATION CORRECTION AB Patient movement between PET scanning sequences can produce misalignment between attenuation and emission scans. Such misalignment introduces errors in the emission image. This study evaluates the severity of these errors and their effect upon quantitation of regional myocardial activity. Myocardial FDG scans from 14 patients were reconstructed with simulated translational, rotational and out-of-plane patient movement. Eight myocardial regions from each patient were examined to determine the effect such misalignment might have on regional myocardial activity. A 2-cm shift between attenuation and emission scans produced up to a 30% change in regional activity. Some regions of the myocardium increased while others decreased for a given magnitude and direction of shift, producing anomalous regional myocardial inhomogeneities in the image. Such changes could easily cause qualitative and quantitative misinterpretations. We present data permitting the reader to assess the magnitude of this effect in his/her own clinical setting. C1 NIH,DEPT NUCL MED,BLDG 10,RM 1C-401,BETHESDA,MD 20892. POSITRON CORP,HOUSTON,TX. OI Cuocolo, Alberto/0000-0003-3431-7658 NR 6 TC 59 Z9 59 U1 0 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JUN PY 1992 VL 33 IS 6 BP 1209 EP 1214 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HX245 UT WOS:A1992HX24500027 PM 1597741 ER PT J AU WALKER, WJ AF WALKER, WJ TI WHOS TO SHOULDER THE BURDEN OF LOW-LEVEL RADIOACTIVE-WASTE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material RP WALKER, WJ (reprint author), NIH,RADIAT SAFETY BRANCH,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JUN PY 1992 VL 33 IS 6 BP N20 EP & PG 0 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HX245 UT WOS:A1992HX24500005 PM 1597753 ER PT J AU MILLS, JL TUOMILEHTO, J YU, KF COLMAN, N BLANER, WS KOSKELA, P RUNDLE, WE FORMAN, M TAIVANEN, L RHOADS, GG AF MILLS, JL TUOMILEHTO, J YU, KF COLMAN, N BLANER, WS KOSKELA, P RUNDLE, WE FORMAN, M TAIVANEN, L RHOADS, GG TI MATERNAL VITAMIN LEVELS DURING PREGNANCIES PRODUCING INFANTS WITH NEURAL-TUBE DEFECTS SO JOURNAL OF PEDIATRICS LA English DT Article ID PERICONCEPTIONAL USE; SERUM FOLATE; SUPPLEMENTATION; PREVENTION; RECURRENCES; TRIAL AB Women at very high risk for having a child with a neural tube defect (NTD) because they had previously delivered affected children significantly reduced their recurrence rate by taking folate supplements before conception. To clarify how these results might apply to a lower-risk general obstetric population, we measured folate, vitamin B12, and retinol levels in maternal serum drawn early in 89 pregnancies resulting in NTD offspring and 178 control pregnancies identified from the Finnish Registry of Congenital Malformations. In 86.5% of the subjects, specimens were collected within 8 weeks after neural tube closure. In the NTD case mothers the mean (+/-SD) levels were not significantly lower than in control mothers: folate, 4.13 +/- 2.36 versus 4.28 +/- 2.52 ng/ml; vitamin B12, 482.8 +/- 161.1 versus 520.3 +/- 191.9 pg/ml; and retinol, 51.2 +/- 17.0 versus 50.5 +/- 16.9-mu-g/dl. After adjustment for age of the specimen, gestational age at which the specimen was drawn, maternal age, and maternal employment status, the odds ratios for being a case mother were 1.00 (95% confidence interval [Cl] 0.91 to 1.10) for folate, 1.05 (95% Cl 0.92 to 1.19) for vitamin B12, and 0.99 (95% Cl 0.88 to 1.10) for retinol. Excluding NTD cases with known or suspected causes unrelated to vitamins, restricting the analyses to interviewed subjects, and excluding subjects whose specimens were collected after 15 gestational weeks confirmed that NTD case and control vitamin levels did not differ significantly. This population-based investigation in a low rate area demonstrated no relationship between maternal serum folate, vitamin B12, or retinol levels during pregnancy and the risk of NTDs. C1 NATL PUBL HLTH INST, SF-00280 HELSINKI 28, FINLAND. MT SINAI MED CTR, NEW YORK, NY 10029 USA. COLUMBIA UNIV COLL PHYS & SURG, NEW YORK, NY 10032 USA. NCI, BETHESDA, MD 20892 USA. NATL PUBL HLTH INST, KUOPIO, FINLAND. UNIV MED & DENT NEW JERSEY, ROBERT WOOD JOHNSON MED SCH, PISCATAWAY, NJ 08854 USA. RP MILLS, JL (reprint author), NICHHD, DESPR,EPIDEMIOL BRANCH,PEDIAT EPIDEMIOL SECT, EPN BLDG, ROOM 640, BETHESDA, MD 20892 USA. NR 31 TC 77 Z9 77 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD JUN PY 1992 VL 120 IS 6 BP 863 EP 871 DI 10.1016/S0022-3476(05)81951-1 PG 9 WC Pediatrics SC Pediatrics GA HY116 UT WOS:A1992HY11600003 PM 1593344 ER PT J AU LEE, JW SEIBEL, NL AMANTEA, M WHITCOMB, P PIZZO, PA WALSH, TJ AF LEE, JW SEIBEL, NL AMANTEA, M WHITCOMB, P PIZZO, PA WALSH, TJ TI SAFETY AND PHARMACOKINETICS OF FLUCONAZOLE IN CHILDREN WITH NEOPLASTIC DISEASES SO JOURNAL OF PEDIATRICS LA English DT Article ID CEREBROSPINAL-FLUID; ANTIFUNGAL AGENTS; SYSTEMIC MYCOSES; PENETRATION; INFECTIONS; HUMANS AB To evaluate the safety, tolerance, and pharmacokinetics of fluconazole in children with neoplastic diseases, we studied fluconazole in 26 children, aged 5 to 15 years, with normal renal function who were receiving treatment for cancer. The patients received fluconazole, 2, 4, or 8 mg/kg per day for 7 days intravenously for a 2-hour period. Patients had no nausea or vomiting related to fluconazole; three patients had an asymptomatic rise in hepatic aminotransferase values after four to six doses (one patient at 2 mg/kg per day and two patients at 8 mg/kg per day), which returned to normal within 2 weeks after discontinuation of the drug. Fluconazole showed linear first-order kinetics over the dosage range tested and during multiple dosing. After the first dose, mean clearance was 22.8 +/- 2.3 ml/min, volume of distribution 0.87 +/- 0.06 L/kg, and terminal elimination half-life 16.8 +/- 1.1 hours. Similarly, after the last dose, clearance was 19.4 +/- 1.3 ml/min, volume of distribution 0.84 +/- 0.04 L/kg, and terminal elimination half-life 18.1 +/- 1.2 hours. Patients receiving their first fluconazole dose of 8 mg/kg achieved peak serum levels of 9.5 +/- 0.4-mu-g/ml and trough levels of 2.7 +/- 0.5-mu-g/ml 24 hours later, and an area under the serum concentration-time curve from time zero to infinity of 186 +/- 16-mu-g . hr per milliliter. Renal clearance of fluconazole was 65% +/- 5% of total clearance and demonstrated the predominantly renal excretion of this drug. We suggest that the shorter serum half-life and the higher frequency of aminotransferase elevations in comparison with those of adults warrant careful investigation of fluconazole in controlled clinical trials. C1 NCI, PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,RM 13N-240, BETHESDA, MD 20892 USA. CHILDRENS HOSP, NATL MED CTR, WASHINGTON, DC 20010 USA. NIH, WARREN GRANT MAGNUSEN CLIN CTR, DEPT PHARM, BETHESDA, MD 20892 USA. NR 21 TC 96 Z9 98 U1 0 U2 1 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD JUN PY 1992 VL 120 IS 6 BP 987 EP 993 DI 10.1016/S0022-3476(05)81975-4 PG 7 WC Pediatrics SC Pediatrics GA HY116 UT WOS:A1992HY11600026 PM 1593362 ER PT J AU LOE, H ANERUD, A BOYSEN, H AF LOE, H ANERUD, A BOYSEN, H TI THE NATURAL-HISTORY OF PERIODONTAL-DISEASE IN MAN - PREVALENCE, SEVERITY, AND EXTENT OF GINGIVAL RECESSION SO JOURNAL OF PERIODONTOLOGY LA English DT Article DE GINGIVAL RECESSION EPIDEMIOLOGY ID ORAL HYGIENE; AGE AB THIS PAPER DESCRIBES THE occurrence and levels of gingival recession in 2 cohorts of individuals participating in parallel longitudinal studies in Norway (1969-1988) and Sri Lanka (1970-1990), covering the age range from 15 to 50 years. In the Norwegian cohort gingival recession had begun early in life. It occurred in greater-than-or-equal-to 60% of the 20 year-olds and was confined to the buccal surfaces. At 30, greater-than-or-equal-to 70% had recession, which still was found mainly on buccal surfaces. As the group approached 50 years of age, more than 90% had gingival recession; greater-than-or-equal-to 25% of the buccal surfaces were involved, greater-than-or-equal-to 15% of lingual, and 3 to 4% of the interproximal surfaces. In the Sri Lankan cohort greater-than-or-equal-to 30% exhibited gingival recession before the age of 20 years. By 30 years, 90% had recession on buccal, lingual, and interproximal surfaces; and at 40 years, 100% of the Sri Lankans had recession. As they approached 50 years, gingival recession occurred in greater-than-or-equal-to 70% of the buccal, greater-than-or-equal-to 50% of the lingual, and 40% of the interproximal surfaces. Based on the special features of the two cohorts, the working hypothesis is advanced that there is more than one type of gingival recession and probably several factors determining the initiation and development of these lesions. RP LOE, H (reprint author), NIDR,BLDG 31,ROOM 2C39,BETHESDA,MD 20892, USA. FU NIDCR NIH HHS [Z01-DE00410-05EE] NR 21 TC 187 Z9 204 U1 3 U2 15 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD JUN PY 1992 VL 63 IS 6 BP 489 EP 495 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HZ496 UT WOS:A1992HZ49600001 PM 1625148 ER PT J AU MCCRAE, RR JOHN, OP AF MCCRAE, RR JOHN, OP TI AN INTRODUCTION TO THE 5-FACTOR MODEL AND ITS APPLICATIONS SO JOURNAL OF PERSONALITY LA English DT Review ID TRAIT-DESCRIPTIVE TERMS; PERSONALITY STRUCTURE; NATURAL-LANGUAGE; DIMENSIONS; SCALES; OPENNESS; EYSENCK; PSYCHOTICISM; UNIVERSALITY; INTROVERSION AB The five-factor model of personality is a hierarchical organization of personality traits in terms of five basic dimensions: Extraversion, Agreeableness, Conscientiousness, Neuroticism, and Openness to Experience. Research using both natural language adjectives and theoretically based personality questionnaires supports the comprehensiveness of the model and its applicability across observers and cultures. This article summarizes the history of the model and its supporting evidence; discusses conceptions of the nature of the factors; and outlines an agenda for theorizing about the origins and operation of the factors. We argue that the model should prove useful both for individual assessment and for the elucidation of a number of topics of interest to personality psychologists. C1 NIA,BALTIMORE,MD 21224. UNIV CALIF BERKELEY,BERKELEY,CA 94720. NR 142 TC 1559 Z9 1594 U1 73 U2 429 PU DUKE UNIV PRESS PI DURHAM PA BOX 90660, DURHAM, NC 27708-0660 SN 0022-3506 J9 J PERS JI J. Pers. PD JUN PY 1992 VL 60 IS 2 BP 175 EP 215 DI 10.1111/j.1467-6494.1992.tb00970.x PG 41 WC Psychology, Social SC Psychology GA JB395 UT WOS:A1992JB39500001 PM 1635039 ER PT J AU MCCRAE, RR AF MCCRAE, RR TI TUPES AND CHRISTAL - INTRODUCTION SO JOURNAL OF PERSONALITY LA English DT Editorial Material ID PERSONALITY C1 NIA,BALTIMORE,MD 21224. NR 13 TC 6 Z9 6 U1 0 U2 4 PU DUKE UNIV PRESS PI DURHAM PA BOX 90660, DURHAM, NC 27708-0660 SN 0022-3506 J9 J PERS JI J. Pers. PD JUN PY 1992 VL 60 IS 2 BP 217 EP 219 DI 10.1111/j.1467-6494.1992.tb00971.x PG 3 WC Psychology, Social SC Psychology GA JB395 UT WOS:A1992JB39500002 PM 1635041 ER PT J AU IRIE, T FUKUNAGA, K PITHA, J AF IRIE, T FUKUNAGA, K PITHA, J TI HYDROXYPROPYLCYCLODEXTRINS IN PARENTERAL USE .1. LIPID DISSOLUTION AND EFFECTS ON LIPID TRANSFERS INVITRO SO JOURNAL OF PHARMACEUTICAL SCIENCES LA English DT Article ID CYCLODEXTRINS; HYPERVITAMINOSIS; DERIVATIVES; TOXICITY AB Hydroxypropyl ethers of cyclodextrins form water-soluble inclusion complexes with lipids. Of the three hydroxypropylcycldextrins examined, hydroxypropyl-alpha-cyclodextrin had limited specificity for phospholipids, and hydroxypropyl-beta-cyclodextrin had limited specificity for cholesterol, and hydroxypropyl-gamma-cyclodextrin was nonspecific. The formation of inclusion complexes was found to be a fast and reversible process in which complexation of cholesterol did not inhibit its oxidation by cholesterol oxidase, and cholesterol of the erythrocyte membrane could be exchanged within a minute for cholesteryl methyl ether which was in the inclusion complex. Thus, hydroxypropylcyclodextrin in the circulation may catalyze the transport of lipids in the direction of equilibrium distribution. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. KUMAMOTO UNIV,FAC PHARMACEUT SCI,KUMAMOTO 862,JAPAN. NR 17 TC 103 Z9 105 U1 0 U2 5 PU AMER PHARMACEUTICAL ASSN PI WASHINGTON PA 2215 CONSTITUTION AVE NW, WASHINGTON, DC 20037 SN 0022-3549 J9 J PHARM SCI JI J. Pharm. Sci. PD JUN PY 1992 VL 81 IS 6 BP 521 EP 523 DI 10.1002/jps.2600810609 PG 3 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA HW638 UT WOS:A1992HW63800008 PM 1522487 ER PT J AU IRIE, T FUKUNAGA, K GARWOOD, MK CARPENTER, TO PITHA, J PITHA, J AF IRIE, T FUKUNAGA, K GARWOOD, MK CARPENTER, TO PITHA, J PITHA, J TI HYDROXYPROPYLCYCLODEXTRINS IN PARENTERAL USE .2. EFFECTS ON TRANSPORT AND DISPOSITION OF LIPIDS IN RABBIT AND HUMANS SO JOURNAL OF PHARMACEUTICAL SCIENCES LA English DT Article ID LOW-DENSITY LIPOPROTEIN; CHOLESTEROL; ATHEROSCLEROSIS; RETINOL; LIVER; RAT AB Hydroxypropyl ethers of cyclodextrins, after parenteral administration, come into contact with lipids in tissues and in circulation and form water-soluble inclusion complexes with these lipids. A single intravenous administration of hydroxypropyl-beta-cyclodextrin to a hereditary hyperlipidemic Watanabe rabbit slightly and temporarily decreased the level of total cholesterol in serum. Single injections of hydroxypropyl-alpha-cyclodextrin and of the corresponding gamma-homologue, both of which are less potent solubilizers of cholesterol, had lesser effects. Repeated administration of hydroxypropyl-beta-cyclodextrin to rabbits led to a gradual increase in total cholesterol in circulation and eventually to a slight relief of atherosclerotic lesions in the thoracic aorta. The only untoward effects of repeated treatments (total doses of up to 40 g/kg) were vacuoles in cells of proximal convoluted tubules in the kidneys. Repeated administration also strongly increased cholesterol in urine, probably because of excretion of the soluble cholesterol-hydroxypropyl-beta-cyclodextrin complex. Proteins in urine increased significantly, whereas triglycerides increased only moderately after repeated administrations. Intravenous infusion of hydroxypropyl-beta-cyclodextrin into a patient with hypervitaminosis A led to a release of liver-stored retinoids into serum in quantities much higher than those that could be directly solubilized by hydroxypropyl-beta-cyclodextrin. Levels of total cholesterol in the circulation of this patient decreased during the infusion. Thus, hydroxypropylcyclodextrins may serve as artificial lipid carriers in the circulation, and because the exchanges that involve inclusion complexation occur very quickly, the presence of hydroxypropylcyclodextrins in organisms may catalytically augment the establishment of equilibria in lipid distribution. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. US DEPT DEF,FT GEORGE G MEADE,MD 20755. KUMAMOTO UNIV,FAC PHARMACEUT SCI,KUMAMOTO 862,JAPAN. YALE UNIV,SCH MED,DEPT PEDIAT,NEW HAVEN,CT 06510. VET ADM MED CTR,OKLAHOMA CITY,OK 73104. NR 28 TC 36 Z9 37 U1 1 U2 4 PU AMER PHARMACEUTICAL ASSN PI WASHINGTON PA 2215 CONSTITUTION AVE NW, WASHINGTON, DC 20037 SN 0022-3549 J9 J PHARM SCI JI J. Pharm. Sci. PD JUN PY 1992 VL 81 IS 6 BP 524 EP 528 DI 10.1002/jps.2600810610 PG 5 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA HW638 UT WOS:A1992HW63800009 PM 1522488 ER PT J AU NAKAJIMA, T WANG, RS KATAKURA, Y KISHI, R ELOVAARA, E PARK, SS GELBOIN, HV VAINIO, H AF NAKAJIMA, T WANG, RS KATAKURA, Y KISHI, R ELOVAARA, E PARK, SS GELBOIN, HV VAINIO, H TI SEX-INDUCED, AGE-INDUCED AND PREGNANCY-INDUCED CHANGES IN THE METABOLISM OF TOLUENE AND TRICHLOROETHYLENE IN RAT-LIVER IN RELATION TO THE REGULATION OF CYTOCHROME-P450IIE1 AND CYTOCHROME-P450IIC11 CONTENT SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID MONOCLONAL-ANTIBODIES; HEPATIC CYTOCHROME-P-450; MICROSOMES; ETHANOL; ENZYMES; BENZENE; FORMS AB Sex-, age- and pregnancy-induced changes in the metabolism of toluene and trichloroethylene in rat liver were investigated in relation to the regulation of cytochrome P450IIE1 and P450IIC11 content using monoclonal antibodies. Immature male rats had a higher level of microsomal protein than females, and this increased with development; however, no difference by sex was found at puberty. No difference in cytochrome P450 content was seen between immature male and female rats; the content increased with development only in males, so that a sex difference in cytochrome P450 content occurred at puberty. Pregnancy decreased the cytochrome P450 content but not that of the microsomal protein. The rate of formation of benzyl alcohol from toluene was 4 times higher in mature than in immature male rats at a high concentration of toluene, but no difference was seen at a low toluene concentration. In contrast, the rate was lower in mature female rats than in immature ones at a low toluene level and no diff erence was seen at the high concentration. A sex difference was thus found in benzyl alcohol formation at puberty at both concentrations of toluene. The levels of oand p-cresol formation in liver were similar in males and females but the rate decreased during development of females. The rate of metabolism of trichloroethylene was higher in immature than in mature male and female rats, especially at a low substrate level, and no sex difference in metabolism was seen with either age or concentration of trichloroethylene. Pregnancy decreased the metabolism of both toluene and trichloroethylene. Monoclonal antibody-directed analysis showed that the level of P450IIE1 was lower in mature rats than in immature rats, and at puberty the level of the isoenzyme was higher in females than in males; P450IIC11/6 increased dramatically with development in male rats and only slightly in female rats, so that much higher levels were found in adult males than in adult females. The differences in the metabolism of toluene and trichloroethylene with age and sex may be due, in part, to different expression of these P450 isozymes and a different affinity of the hydrocarbons to the two isozymes. The decreased metabolism of toluene and trichloroethylene in pregnant rats may also be due to a decrease in the levels of P450IIE1 and/or P450IIC11/6. C1 SAPPORO MED COLL,DEPT PUBL HLTH,CHUO KU,SAPPORO,HOKKAIDO 060,JAPAN. INST OCCUPAT HLTH,DEPT IND HYG & TOXICOL,SF-00250 HELSINKI,FINLAND. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP NAKAJIMA, T (reprint author), SHINSHU UNIV,SCH MED,DEPT HYG,MATSUMOTO,NAGANO 390,JAPAN. RI Kishi, Reiko/D-6745-2012 NR 28 TC 45 Z9 46 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 JUN PY 1992 VL 261 IS 3 BP 869 EP 874 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JA184 UT WOS:A1992JA18400006 PM 1602390 ER PT J AU SCHWERI, MM THURKAUF, A MATTSON, MV RICE, KC AF SCHWERI, MM THURKAUF, A MATTSON, MV RICE, KC TI FOURPHIT - A SELECTIVE PROBE FOR THE METHYLPHENIDATE BINDING-SITE ON THE DOPAMINE TRANSPORTER SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID THREO-(+/-)-METHYLPHENIDATE BINDING; COCAINE RECEPTORS; RAT-BRAIN; METAPHIT; PHENCYCLIDINE; COMPLEX; STRIATUM AB Fourphit, a phencyclidine derivative containing an isothiocyanate substitution at the 4-position of the piperidine ring, inhibits the binding of the radiolabeled psychomotor stimulant, [H-3]methylphenidate, to sites on the dopamine transport complex in membranes prepared from the crude synaptosomal fraction of rat striatal tissue with an IC50 of 7.1-mu-M. The inhibition caused by Fourphit is irreversible and is associated with a decrease in the B(max), but not the K(D), of [H-3]methylphenidate binding. Pretreatment with saturating concentrations of unlabeled methylphenidate effected a modest (but statistically significant) protection of the stimulant binding site from inactivation by Fourphit, indicating that the acylating phencyclidine derivative may act directly at this site. Preincubation with Fourphit rather than vehicle did not alter the dissociation rate of [H-3]methylphenidate when measured in the presence of excess amfonelic acid, nor was any difference detected in the off-rate of [H-3]methylphenidate when excess Fourphit was substituted for excess unlabeled methylphenidate as the displacing agent. This lack of effect on the dissociation kinetics of [H-3]methylphenidate provides further evidence that Fourphit does not act allosterically at the methylphenidate binding site. Unlike Metaphit (an isomer of Fourphit containing the isothiocyanate moiety at the meta position of the aromatic ring), Fourphit can discriminate between the methylphenidate binding site and the phencyclidine binding site associated with the N-methyl-D-aspartate receptor: Metaphit irreversibly inactivates both binding sites, whereas Fourphit binds reversibly to the phencyclidine binding site. The data suggest that Fourphit may be useful as a relatively selective affinity label for the site on the dopamine transport complex recognized by methylphenidate and other psychomotor stimulants. C1 NIDDK,MED CHEM LAB,BETHESDA,MD. RP SCHWERI, MM (reprint author), MERCER UNIV,SCH MED,DIV BASIC MED SCI,1550 COLL ST,MACON,GA 31207, USA. FU NIDA NIH HHS [DA06305]; NINDS NIH HHS [NS28584] NR 25 TC 13 Z9 13 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 JUN PY 1992 VL 261 IS 3 BP 936 EP 942 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JA184 UT WOS:A1992JA18400016 PM 1602399 ER PT J AU ISADA, NB PAAR, DP GROSSMAN, JH STRAUS, SE AF ISADA, NB PAAR, DP GROSSMAN, JH STRAUS, SE TI TORCH INFECTIONS - DIAGNOSIS IN THE MOLECULAR AGE SO JOURNAL OF REPRODUCTIVE MEDICINE LA English DT Review ID POLYMERASE CHAIN-REACTION; HERPES-SIMPLEX VIRUS; CONGENITAL CYTOMEGALOVIRUS-INFECTION; HUMAN IMMUNODEFICIENCY VIRUS; VARICELLA-ZOSTER VIRUS; HUMAN PARVOVIRUS B19; PRENATAL-DIAGNOSIS; AMNIOTIC-FLUID; RESPIRATORY PAPILLOMATOSIS; TOXOPLASMA INFECTION AB TORCH agents cause a varied spectrum of disease. Advances in ultrasound, invasive perinatal procedures and molecular diagnostics have allowed in utero evaluation. Infected fetuses, especially those which are sonographically abnormal, may be treated in utero depending upon the pathogen and attendant pathophysiology. Subclinical perinatal infections may lead to later childhood deficits. Such infected fetuses may benefit from early diagnosis and prompt initiation of rehabilitative measures. C1 NIAID,CLIN INVEST LAB,MED VIROL SECT,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,MED CTR,DEPT OBSTET & GYNECOL,DIV MATERNAL FETAL MED,WASHINGTON,DC 20037. RP ISADA, NB (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,DEPT OBSTET & GYNECOL,DIV REPROD GENET,DETROIT,MI 48201, USA. NR 104 TC 4 Z9 4 U1 0 U2 2 PU SCI PRINTERS & PUBL INC PI ST LOUIS PA P.O. DRAWER 12425 8342 OLIVE BLVD, ST LOUIS, MO 63132 SN 0024-7758 J9 J REPROD MED JI J. Reprod. Med. PD JUN PY 1992 VL 37 IS 6 BP 499 EP 507 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HZ272 UT WOS:A1992HZ27200002 PM 1619602 ER PT J AU KARSON, EM POLVINO, W ANDERSON, WF AF KARSON, EM POLVINO, W ANDERSON, WF TI PROSPECTS FOR HUMAN GENE-THERAPY SO JOURNAL OF REPRODUCTIVE MEDICINE LA English DT Article ID BONE-MARROW TRANSPLANTATION; HUMAN ADENOSINE-DEAMINASE; UMBILICAL-CORD BLOOD; RETROVIRAL VECTORS; STEM-CELLS; EXPRESSION; MOUSE; RECONSTITUTION; ANEMIA; MICE AB Retroviral vectors containing marker genes and the sequence for human proteins have been used to transduce cultured lymphocytes, which have then been reinfused into patients. Circulating hematopoietic progenitor cells from human fetal cord blood obtained at the time of term and premature deliveries as early as 19 weeks of gestation have been shown to express such transduced genes in vitro. Cord blood cells from fetal sheep sampled and transduced ex vivo and transfused back in utero expressed marker genes up to two years after birth. Although the efficiency of gene transfer into cells and their long-term expression need to be improved, the potential exists for treating some genetic diseases after prenatal diagnosis either in utero or shortly after birth. C1 NHLBI,MOLEC HEMATOL BRANCH,BLDG 10,ROOM 70-18,BETHESDA,MD 20892. NR 27 TC 5 Z9 5 U1 0 U2 0 PU SCI PRINTERS & PUBL INC PI ST LOUIS PA P.O. DRAWER 12425 8342 OLIVE BLVD, ST LOUIS, MO 63132 SN 0024-7758 J9 J REPROD MED JI J. Reprod. Med. PD JUN PY 1992 VL 37 IS 6 BP 508 EP 514 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HZ272 UT WOS:A1992HZ27200003 PM 1619603 ER PT J AU EARLS, FT SLABY, RG SPIRITO, A SALTZMAN, LE THORNTON, T BERMAN, A DAVIDSON, L FAGAN, J GOODMAN, A HAWKINS, D KRAUS, JF LOFTIN, C MOSCICKI, E MUEHRER, P OCARROLL, P SUDAK, H VISHER, C WIDOM, CS WINTEMUTE, G BAER, K AF EARLS, FT SLABY, RG SPIRITO, A SALTZMAN, LE THORNTON, T BERMAN, A DAVIDSON, L FAGAN, J GOODMAN, A HAWKINS, D KRAUS, JF LOFTIN, C MOSCICKI, E MUEHRER, P OCARROLL, P SUDAK, H VISHER, C WIDOM, CS WINTEMUTE, G BAER, K TI PREVENTION OF VIOLENCE AND INJURIES DUE TO VIOLENCE SO JOURNAL OF SAFETY RESEARCH LA English DT Article C1 EDUC DEV CTR,NEWTON,MA. RHODE ISL HOSP,PROVIDENCE,RI 02902. CTR DIS CONTROL,NATL CTR ENVIRONM HLTH & INJURY CONTROL,DIV INJURY CONTROL,ATLANTA,GA 30333. WASHINGTON PSYCHOL CTR,WASHINGTON,DC. EMORY UNIV,SCH MED,ATLANTA,GA 30322. RUTGERS STATE UNIV,NEW BRUNSWICK,NJ 08903. NEW YORK CITY DEPT HLTH,NEW YORK,NY 10013. UNIV ILLINOIS,BLACK STUDIES PROGRAM,CHICAGO,IL 60680. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,LOS ANGELES,CA 90024. UNIV MARYLAND,COLLEGE PK,MD 20742. NIMH,ROCKVILLE,MD 20857. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. NATL INST JUSTICE,WASHINGTON,DC. INDIANA UNIV,BLOOMINGTON,IN 47401. UNIV CALIF DAVIS,SCH MED,DAVIS,CA 95616. MACRO INT INC,ATLANTA,GA. RP EARLS, FT (reprint author), HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115, USA. NR 1 TC 1 Z9 1 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0022-4375 J9 J SAFETY RES JI J. Saf. Res. PD SUM PY 1992 VL 23 IS 2 BP 117 EP 119 PG 3 WC Ergonomics; Public, Environmental & Occupational Health; Social Sciences, Interdisciplinary; Transportation SC Engineering; Public, Environmental & Occupational Health; Social Sciences - Other Topics; Transportation GA HV253 UT WOS:A1992HV25300008 ER PT J AU ROBERTSON, L STALLONES, L BRANCHEDORSEY, CM NOWAK, N BAKER, S BENDER, TR DUFOUR, M LUMPKIN, J MCLOUGHLIN, E MICIK, S ORY, M PLANEK, TW RIVARA, F RUTHERFORD, GW SCHEIDT, PC WIDOME, M LEZIN, N AF ROBERTSON, L STALLONES, L BRANCHEDORSEY, CM NOWAK, N BAKER, S BENDER, TR DUFOUR, M LUMPKIN, J MCLOUGHLIN, E MICIK, S ORY, M PLANEK, TW RIVARA, F RUTHERFORD, GW SCHEIDT, PC WIDOME, M LEZIN, N TI HOME AND LEISURE INJURY PREVENTION .1. SELECTED INJURIES SO JOURNAL OF SAFETY RESEARCH LA English DT Article C1 COLORADO STATE UNIV,FT COLLINS,CO 80523. CTR DIS CONTROL,NATL CTR ENVIRONM HLTH & INJURY CONTROL,DIV INJURY CONTROL,ATLANTA,GA 30333. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. CTR DIS CONTROL,NIOSH,MORGANTOWN,WV. NIAAA,ROCKVILLE,MD 20852. ILLINOIS DEPT PUBL HLTH,SPRINGFIELD,IL. SAN FRANCISCO GEN HOSP,SAN FRANCISCO,CA 94110. NORTH CTY HLTH SERV,SAN MARCOS,CA. NIA,BETHESDA,MD 20892. NATL SAFETY COUNCIL,CHICAGO,IL. HARBORVIEW INJURY PREVENT & RES CTR,SEATTLE,WA. CONSUMER PROD SAFETY COMMISS,BETHESDA,MD. NICHHD,ROCKVILLE,MD. PENN STATE UNIV,MILTON S HERSHEY MED CTR,COLL MED,HERSHEY,PA 17033. MACRO INT INC,ATLANTA,GA. RP ROBERTSON, L (reprint author), NANLEE RES,BRANFORD,CT 06405, USA. NR 2 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 0022-4375 J9 J SAFETY RES JI J. Saf. Res. PD SUM PY 1992 VL 23 IS 2 BP 121 EP 126 PG 6 WC Ergonomics; Public, Environmental & Occupational Health; Social Sciences, Interdisciplinary; Transportation SC Engineering; Public, Environmental & Occupational Health; Social Sciences - Other Topics; Transportation GA HV253 UT WOS:A1992HV25300009 ER PT J AU BURACCO, P GUGLIELMINO, R ABATE, O BOCCHINI, V CORNAGLIA, E DENICOLA, DB CILLI, M PONZIO, P AF BURACCO, P GUGLIELMINO, R ABATE, O BOCCHINI, V CORNAGLIA, E DENICOLA, DB CILLI, M PONZIO, P TI LARGE GRANULAR LYMPHOMA IN AN FIV-POSITIVE AND FELV-NEGATIVE CAT SO JOURNAL OF SMALL ANIMAL PRACTICE LA English DT Note ID IMMUNODEFICIENCY VIRUS-INFECTION; LYMPHOCYTIC-LEUKEMIA; DOMESTIC CATS; NEOPLASM; BLOOD; CELLS AB The clinical course of a feline leukaemia virus (FeLV)-negative and feline immunodeficiency virus (FIV)-positive cat affected with a large granular lymphocyte lymphoma is presented. Cytological examination showed neoplastic cells in the pleural effusion and in two abdominal masses. Bone marrow and peripheral blood were moderately involved and chemotherapy was used to control the tumour. Cytochemistry, immunohistochemistry and ultrastructural studies were applied to define the cellular lineage; cytochemistry suggested a T-cell lineage. C1 NATL CANC INST,GENOA,ITALY. PURDUE UNIV,SCH VET MED,W LAFAYETTE,IN 47907. RP BURACCO, P (reprint author), UNIV TURIN,DIPARTIMENTO PATOL ANIM,VIA NIZZA 52,I-10126 TURIN,ITALY. RI Buracco, Paolo/J-8251-2014 OI Buracco, Paolo/0000-0002-0181-0887 NR 36 TC 11 Z9 11 U1 0 U2 2 PU BRITISH VETERINARY ASSOC PI LONDON PA 7 MANSFIELD ST, LONDON, ENGLAND W1M 0AT SN 0022-4510 J9 J SMALL ANIM PRACT JI J. Small Anim. Pract. PD JUN PY 1992 VL 33 IS 6 BP 279 EP 284 DI 10.1111/j.1748-5827.1992.tb01143.x PG 6 WC Veterinary Sciences SC Veterinary Sciences GA HY321 UT WOS:A1992HY32100007 ER PT J AU BLITHE, DL KHAN, MS ROSNER, W AF BLITHE, DL KHAN, MS ROSNER, W TI COMPARISON OF THE CARBOHYDRATE-COMPOSITION OF RAT AND HUMAN CORTICOSTEROID-BINDING GLOBULIN - SPECIES-SPECIFIC GLYCOSYLATION SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article ID ASPARAGINE-LINKED OLIGOSACCHARIDES; PITUITARY GLYCOPROTEIN HORMONES; HUMAN CHORIONIC-GONADOTROPIN; HUMAN TRANSCORTIN; SIALYLATED OLIGOSACCHARIDES; ALPHA-SUBUNIT; HUMAN-PLASMA; THYROTROPIN; CHROMATOGRAPHY; GLYCOPEPTIDES AB We have examined the carbohydrate composition of corticosteroid-binding globulin (CBG) obtained from rat and human serum. Rat CBG contained a carbohydrate composition that was strikingly different from that of human CBG. Like other glycoproteins that circulate in human plasma, human CBG had a carbohydrate composition that was consistent with the presence of biantennary and triantennary oligosaccharide structures. In contrast, the carbohydrate composition of rat CBG indicated the presence of more than one sialic acid residue per antenna. It is not clear whether rat CBG contains a carbohydrate structure with sialic acids attached to both galactose and N-acetylglucosamine on the same antenna, or a terminal disialylated structure (sialic acid linked alpha-2-8 to sialic acid). These structural variations may play a role in the interaction of CBG with its receptor. C1 COLUMBIA UNIV,ST LUKES ROOSEVELT HOSP CTR,COLL PHYS & SURG,DEPT MED,NEW YORK,NY 10019. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. FU NIDDK NIH HHS [DK 36714] NR 29 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-0760 J9 J STEROID BIOCHEM JI J. Steroid Biochem. Mol. Biol. PD JUN PY 1992 VL 42 IS 5 BP 475 EP 478 DI 10.1016/0960-0760(92)90259-L PG 4 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA JC605 UT WOS:A1992JC60500005 PM 1616876 ER PT J AU LANGE, JR ALEXANDER, HR MERINO, MJ DOHERTY, GM NORTON, JA AF LANGE, JR ALEXANDER, HR MERINO, MJ DOHERTY, GM NORTON, JA TI INTERLEUKIN-1-ALPHA PREVENTION OF THE LETHALITY OF ESCHERICHIA-COLI PERITONITIS SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE ASSOC FOR ACADEMIC SURGERY CY NOV 20-23, 1991 CL COLORADO SPRINGS, CO SP ASSOC ACAD SURG ID TUMOR NECROSIS FACTOR; RECOMBINANT HUMAN INTERLEUKIN-1-ALPHA; BACTERIAL-INFECTION; MICE; RESISTANCE; PRETREATMENT C1 NCI,PATHOL LAB,BETHESDA,MD 20892. RP LANGE, JR (reprint author), NCI,SURG BRANCH,SURG METAB SECT,BETHESDA,MD 20892, USA. NR 17 TC 11 Z9 12 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD JUN PY 1992 VL 52 IS 6 BP 555 EP 559 DI 10.1016/0022-4804(92)90128-M PG 5 WC Surgery SC Surgery GA JN405 UT WOS:A1992JN40500004 PM 1528030 ER PT J AU HENDERSON, CT TRUMBORE, LS MOBARHAN, S BENYA, R MILES, TP AF HENDERSON, CT TRUMBORE, LS MOBARHAN, S BENYA, R MILES, TP TI PROLONGED TUBE-FEEDING IN LONG-TERM CARE - NUTRITIONAL-STATUS AND CLINICAL OUTCOMES SO JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION LA English DT Article DE ENTERAL TUBE FEEDING; LONG-TERM CARE; NUTRITIONAL ASSESSMENT; AGING; SERUM ZINC; PRESSURE ULCERS; HYPOCHOLESTEROLEMIA; HYPOPROTEINEMIA ID SUPPLYING ENERGY-REQUIREMENTS; NURSING-HOME PATIENTS; HOSPITALIZED-PATIENTS; ELDERLY PATIENTS; MORTALITY; MEN; COMPLICATIONS; CHOLESTEROL; BACTEREMIA; EFFICACY AB This study examines nutritional status and clinical outcomes, including pressure ulcers and death in 40 chronically tube-fed long-term care patients. Anthropometric, biochemical, clinical and dietary data were collected over a 3-month period, with follow-up of mortality at 1 year. Subjects' functional and cognitive status was generally poor. Adequate calories and protein were provided, with sample means exceeding standard means for energy, protein and micronutrients. Still, subjects showed weight loss and severe depletion of lean and fat body mass. Mean serum protein and micronutrient status measures were in the low normal range. Hemoglobin, hematocrit, and serum zinc and carotenoid levels were below normal in a sizable proportion of patients. Pressure ulcers were present in 65% of patients. Weight loss was associated with longer time on tube feeding and more pressure ulcers. Negative correlations with ulcer number were observed for cholesterol, albumin, zinc, retinol, alpha-tocopherol and iron. This study shows that despite administration of apparently adequate formula, micronutrient deficiencies and marasmic malnutrition exist in chronically ill patients. Causes may include the combined effects of chronic disease, sepsis, immobility, and severe neurologic deficits. Clinical outcomes may be expressions of an organism-wide diminution of protein synthesis, the cause of which is unknown. For clinical management, serial measures of weight, albumin, cholesterol, hemoglobin and hematocrit are recommended. Future research must address the many subsets of the population of chronically tube-fed patients. C1 LOYOLA UNIV,MED CTR,CLIN NUTR UNIT,MAYWOOD,IL 60153. NIDDKD,BETHESDA,MD. UNIV ILLINOIS,SCH PUBL HLTH,DEPT EPIDEMIOL & BIOSTAT,CHICAGO,IL 60680. RP HENDERSON, CT (reprint author), OAK FOREST HOSP COOK CTY,DEPT GERIATR MED & CHRON DIS,15900 S CICERO AVE,OAK FOREST,IL 60452, USA. NR 37 TC 68 Z9 70 U1 1 U2 5 PU AMER COLL NUTRITION PI NEW YORK PA C/O HOSP. JOINT DIS. 301 E. 17TH ST., NEW YORK, NY 10003 SN 0731-5724 J9 J AM COLL NUTR JI J. Am. Coll. Nutr. PD JUN PY 1992 VL 11 IS 3 BP 309 EP 325 PG 17 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HX575 UT WOS:A1992HX57500011 PM 1619183 ER PT J AU DIONNE, RA AF DIONNE, RA TI NEW APPROACHES TO PREVENTING AND TREATING POSTOPERATIVE PAIN SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article ID DENTAL PAIN; ORAL-SURGERY; C-FOS; IBUPROFEN; PLACEBO; CODEINE; ACETAMINOPHEN; HYDROCHLORIDE; FLURBIPROFEN; SUPPRESSION AB Dental pain is estimated to account for 15 million lost U.S. work days each year. A flexible analgesic scheme, described in this report, can effectively manage acute pain so patients won't avoid dental treatment they perceive as painful. RP DIONNE, RA (reprint author), NIDR,CLIN PHARMACOL UNIT,NEUROL & ANESTHESIOL BRANCH,BETHESDA,MD 20892, USA. NR 35 TC 3 Z9 3 U1 0 U2 0 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD JUN PY 1992 VL 123 IS 6 BP 26 EP 34 PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HX975 UT WOS:A1992HX97500009 PM 1619142 ER PT J AU BLOCK, G THOMPSON, FE HARTMAN, AM LARKIN, FA GUIRE, KE AF BLOCK, G THOMPSON, FE HARTMAN, AM LARKIN, FA GUIRE, KE TI COMPARISON OF 2 DIETARY QUESTIONNAIRES VALIDATED AGAINST MULTIPLE DIETARY RECORDS COLLECTED DURING A 1-YEAR PERIOD SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID FOOD FREQUENCY QUESTIONNAIRE; VALIDITY; REPRODUCIBILITY; VARIABILITY; DESIGN AB The validity of two dietary history questionnaires was examined, one the Health Habits and History Questionnaire (HHHQ) developed by Block et al and the other a questionnaire developed by investigators at the University of Michigan (UM). The reference data consisted of the mean of four 4-day dietary records and recalls collected for 1 year before administration of the questionnaires. The sample of 85 persons included black and white men and women aged 25 to 50 years. The HHHQ was entirely self-administered; the UM questionnaire had both self- and interviewer-administered components. The HHHQ group means were similar to food record estimates for energy and most nutrients, whereas the UM questionnaire produced overestimates for energy and all nutrients examined. Correlations ranged from .31 to .60 (median = .48) for the UM questionnaire and from .42 to .68 (median = .57) for the HHHQ. Use of respondent-reported portion sizes with the HHHQ produced higher correlations than use of investigator-determined "standard" portion sizes (median r = .43 vs .57). Food frequency questionnaires can provide useful nutrient data for individuals as well as groups. C1 NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. UNIV MICHIGAN,SCH PUBL HLTH,HUMAN NUTR PROGRAM,ANN ARBOR,MI 48109. RP BLOCK, G (reprint author), UNIV CALIF BERKELEY,SCH PUBL HLTH,PUBL HLTH NUTR PROGRAM,BERKELEY,CA 94720, USA. RI Block, Gladys/E-3304-2010 NR 27 TC 355 Z9 357 U1 2 U2 13 PU AMER DIETETIC ASSOC PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD JUN PY 1992 VL 92 IS 6 BP 686 EP 693 PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HY825 UT WOS:A1992HY82500014 PM 1607564 ER PT J AU FOX, TA HEIMENDINGER, J AF FOX, TA HEIMENDINGER, J TI TELEPHONE SURVEYS AS A METHOD FOR OBTAINING DIETARY INFORMATION - A REVIEW SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Article ID VALIDITY; QUESTIONNAIRE; STRATEGIES; RECALLS; DESIGN; MAIL AB The use of telephone surveys has increased significantly in the past decade. One advantage of telephone surveys is the ability to reach a large number of individuals: 97% of the US population owns telephones. Another advantage is cost savings: telephone surveys cost as little as one quarter to one half the amount of face-to-face surveys. Computer-assisted telephone interviewing has improved data collection, coding, and analysis. Random-digit dialing and a number of statistical advances such as weighting and stratification have significantly enhanced sample selection and research design of telephone surveys. The increasing need to collect dietary information from populations in an affordable fashion has expanded the use of telephone dietary surveys. To date, telephone dietary surveys have been used for follow-up after initial face-to-face contact has been made. The most common dietary instruments used are the 24-hour recall and the food frequency questionnaire. This review indicates that well-designed and well-administered telephone surveys are as good as, and may be better than, other methods for obtaining dietary information. C1 UNIV CALIF BERKELEY,PUBL HLTH NUTR,BERKELEY,CA 94720. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. RP FOX, TA (reprint author), USDA,FOOD & NUTR SERV,DIV CHILD NUTR,ALEXANDRIA,VA 22302, USA. RI Block, Gladys/E-3304-2010 NR 33 TC 51 Z9 51 U1 0 U2 1 PU AMER DIETETIC ASSOC PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD JUN PY 1992 VL 92 IS 6 BP 729 EP 732 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HY825 UT WOS:A1992HY82500022 PM 1607571 ER PT J AU WILBUR, WJ AF WILBUR, WJ TI RETRIEVAL TESTING BY THE COMPARISON OF STATISTICALLY INDEPENDENT RETRIEVAL METHODS SO JOURNAL OF THE AMERICAN SOCIETY FOR INFORMATION SCIENCE LA English DT Article ID INFORMATION-RETRIEVAL; RELEVANCE AB A procedure for retrieval testing is developed which is based on the comparison of statistically independent methods of retrieval applied to the same database. This is, in essence, a form of relative retrieval testing in which, due to the independence assumption, the conclusions drawn may be taken as absolute. The methodology is illustrated on a large database of MEDLINE records where documents are themselves used as queries. Test results in this setting indicate that, among the several methods tested, a form of cosine coefficient retrieval will give the best performance for the purpose of clustering documents or producing nearest neighbors of documents. RP WILBUR, WJ (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 19 TC 6 Z9 6 U1 2 U2 3 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0002-8231 J9 J AM SOC INFORM SCI JI J. Am. Soc. Inf. Sci. PD JUN PY 1992 VL 43 IS 5 BP 358 EP 370 DI 10.1002/(SICI)1097-4571(199206)43:5<358::AID-ASI4>3.0.CO;2-I PG 13 WC Computer Science, Information Systems; Information Science & Library Science SC Computer Science; Information Science & Library Science GA HV360 UT WOS:A1992HV36000003 ER PT J AU HAN, JS THOMPSON, KA CHOU, CL KNEPPER, MA AF HAN, JS THOMPSON, KA CHOU, CL KNEPPER, MA TI EXPERIMENTAL TESTS OF 3-DIMENSIONAL MODEL OF URINARY CONCENTRATING MECHANISM SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE RAT; COLLECTING DUCT; LOOP OF HENLE; OSMOTIC WATER PERMEABILITY ID MEDULLARY COLLECTING DUCT; THIN ASCENDING LIMB; ANTIDIURETIC-HORMONE; MATHEMATICAL-MODEL; TRANSPORT; WATER; SYSTEM; UREA; HENLE; PERMEABILITY AB Recently, a new model of the urinary concentrating process has been proposed that takes into account the three-dimensional architecture of the renal medulla. Under the assumptions of the model, computer simulations predicted significant axial osmolality gradients in the inner medulla without active transport by the inner medullary loop of Henle. Two of the model assumptions (which constitute hypotheses for this study) were: (1) the osmotic water permeability of the initial part of the inner medullary collecting duct (initial IMCD) is very low even in the presence of vasopressin; and (2) there is significant lateral separation of structures such that thin descending limbs are far from the collecting ducts at the same inner medullary level. The first hypothesis was addressed by perfusing rat initial IMCD segments in vitro and measuring osmotic water permeability. With the osmotic gradient oriented as predicted by the model (lumen > bath), vasopressin increased the osmotic water permeability from 286 to 852-mu-m/s. Three additional series of experiments confirmed the high water permeability in the presence of vasopressin. The second hypothesis was addressed by morphometric analysis of histologic cross-sections of the rat renal medulla. Mean distances of descending limbs to the nearest adjacent collecting duct were very small throughout the inner medulla (<6-mu-m) and substantially less than in the outer Medulla (28-mu-m). It was concluded that the data are inconsistent with both hypotheses and therefore do not support the feasibility of the 'three-dimensional' model of the renal inner medulla. The axial distributions of loops of Henle and collecting ducts in the rat renal medulla are also reported. C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BLDG 10,ROOM 6N307,BETHESDA,MD 20892. NR 30 TC 56 Z9 56 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD JUN PY 1992 VL 2 IS 12 BP 1677 EP 1688 PG 12 WC Urology & Nephrology SC Urology & Nephrology GA JC614 UT WOS:A1992JC61400006 PM 1498275 ER PT J AU ELLENBERG, SS FINKELSTEIN, DM SCHOENFELD, DA AF ELLENBERG, SS FINKELSTEIN, DM SCHOENFELD, DA TI STATISTICAL ISSUES ARISING IN AIDS CLINICAL-TRIALS SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION LA English DT Article DE ACQUIRED IMMUNE DEFICIENCY SYNDROME; CLINICAL TRIALS; HUMAN IMMUNODEFICIENCY VIRUS ID SURROGATE ENDPOINTS; DESIGN; INFECTION; CANCER AB In the 11 years since AIDS became a defined disease, programs for the development and evaluation of new drugs for this disease have grown rapidly. Although the fundamental principles that drive the design, conduct, and analysis of clinical trials are as applicable to AIDS as to other diseases, there is no question that we have been confronted with unusually difficult challenges in studying therapeutic approaches for this disease. These include the multiple treatment needs of individual patients, identification of appropriate endpoints, rapidly changing "natural history," and the need for interaction with an informed and vocal patient community that continues to express dissatisfaction with the pace of research. In this context, statisticians have taken a leadership role in identifying and addressing important methodological issues in the evaluation of AIDS drugs. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ELLENBERG, SS (reprint author), NIAID,BIOCHEM RES BRANCH,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 33 TC 27 Z9 27 U1 0 U2 1 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 SN 0162-1459 J9 J AM STAT ASSOC JI J. Am. Stat. Assoc. PD JUN PY 1992 VL 87 IS 418 BP 562 EP 569 DI 10.2307/2290291 PG 8 WC Statistics & Probability SC Mathematics GA HW622 UT WOS:A1992HW62200036 ER PT J AU ELLENBERG, SS FINKELSTEIN, DM SCHOENFELD, DA AF ELLENBERG, SS FINKELSTEIN, DM SCHOENFELD, DA TI STATISTICAL ISSUES ARISING IN AIDS CLINICAL-TRIALS - REJOINDER SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION LA English DT Note C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ELLENBERG, SS (reprint author), NIAID,BIOCHEM RES BRANCH,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 SN 0162-1459 J9 J AM STAT ASSOC JI J. Am. Stat. Assoc. PD JUN PY 1992 VL 87 IS 418 BP 581 EP 583 PG 3 WC Statistics & Probability SC Mathematics GA HW622 UT WOS:A1992HW62200042 ER PT J AU ROBERTSON, MN SPANGRUDE, GJ HASENKRUG, K PERRY, L NISHIO, J WEHRLY, K CHESEBRO, B AF ROBERTSON, MN SPANGRUDE, GJ HASENKRUG, K PERRY, L NISHIO, J WEHRLY, K CHESEBRO, B TI ROLE AND SPECIFICITY OF T-CELL SUBSETS IN SPONTANEOUS-RECOVERY FROM FRIEND VIRUS-INDUCED LEUKEMIA IN MICE SO JOURNAL OF VIROLOGY LA English DT Article ID HELPER LYMPHOCYTES-T; HERPES-SIMPLEX VIRUS; HOST GENETIC-CONTROL; MONOCLONAL-ANTIBODIES; INDUCED ERYTHROLEUKEMIA; MOLECULAR-BIOLOGY; SURFACE ANTIGENS; IMMUNE-RESPONSE; RETROVIRUS; IDENTIFICATION AB Spontaneous recovery from Friend virus complex-induced leukemic splenomegaly in H-2D(b/b) mice correlated with the appearance of Friend virus complex-specific cytotoxic T lymphocytes (CTL) detectable directly in spleen cell populations. By testing CTL on target cells containing expression vectors encoding individual retroviral structural proteins, the main viral protein recognized was shown to be the Friend murine leukemia helper virus envelope glycoprotein. In vivo depletion of CD8-positive T cells drastically reduced the incidence of recovery, providing direct evidence for the role of CD8-positive CTL in the spontaneous recovery process. In vivo depletion of CD4-positive cells had little effect on the early stages of recovery but did cause a marked reduction in the final incidence of recovery at 60 to 90 days. Thus, CD8-positive cells were required for the initiation of the recovery process, whereas CD4-positive cells appeared to be required for maintenance of the recovered status. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 57 TC 74 Z9 74 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3271 EP 3277 PG 7 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900001 PM 1374804 ER PT J AU CZUB, M MCATEE, FJ PORTIS, JL AF CZUB, M MCATEE, FJ PORTIS, JL TI MURINE RETROVIRUS-INDUCED SPONGIFORM ENCEPHALOMYELOPATHY - HOST AND VIRAL FACTORS WHICH DETERMINE THE LENGTH OF THE INCUBATION PERIOD SO JOURNAL OF VIROLOGY LA English DT Article ID WILD MOUSE RETROVIRUS; MOTOR NEURON DISEASE; LONG TERMINAL REPEAT; LEUKEMIA-VIRUS; NEUROTROPIC RETROVIRUS; SLOW DISEASE; PATHOGENESIS; INFECTION; PARALYSIS; MICE AB A molecular clone of wild mouse ecotropic retrovirus CasBrE (clone 15-1) causes a spongiform neurodegenerative disease with a long incubation period, greater-than-or-equal-to 6 months. This virus infects the central nervous system (CNS) at low levels. In contrast, a chimeric virus, FrCaS(E), containing env and 3' pol sequences of 15-1 in a Friend murine leukemia virus background, infects the CNS at high levels and causes a rapid neurodegenerative disease with an incubation period of only 16 days. With both viruses, the induction of neurologic disease is dependent on inoculation during the perinatal period. Since the length of the incubation period of this disease appears to be a function of the relative level of CNS infection, we have attempted to identify the viral and host factors which determine the relative level of virus infection of the CNS. It was previously shown that the CNS is susceptible to infection only during the perinatal period (M. Czub, S. Czub, F. J. McAtee, and J. L. Portis, J. Virol. 65:2539-2544, 1991). Here we have found that the susceptibility of the CNS wanes progressively or gradually as a function of the age of the host, this age-dependent resistance being complete by 12 to 14 days of age. Utilizing a group of chimeric viruses, we found that the relative level of CNS infection achieved after inoculation of mice at 1 day of age was a function of the kinetics of virus replication and spread in peripheral organs. Viruses which reached peak viremia titers early (5 to 7 days of age) infected the CNS at high levels, and viruses which reached peak titers later infected the CNS at lower levels. Among the group of viruses examined in the current study, the kinetics of peripheral virus replication and spread appeared to be influenced primarily by sequences within the R-U5-5' leader region of the viral genome. These results suggested that the relative level of CNS infection was determined very early in life and appeared to be a function of a dynamic balance between the kinetics of virus replication in the periphery and a progressively developing restriction of virus replication in the CNS. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 36 TC 46 Z9 46 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3298 EP 3305 PG 8 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900004 PM 1316449 ER PT J AU PETROPOULOS, CJ PAYNE, W SALTER, DW HUGHES, SH AF PETROPOULOS, CJ PAYNE, W SALTER, DW HUGHES, SH TI USING AVIAN RETROVIRAL VECTORS FOR GENE-TRANSFER SO JOURNAL OF VIROLOGY LA English DT Article ID CHICKEN ACTIN GENES; ROUS-SARCOMA VIRUS; SKELETAL-MUSCLE; TRANSGENIC MICE; CARDIAC ACTIN; GERM-LINE; PHOSPHOENOLPYRUVATE CARBOXYKINASE; REGULATED EXPRESSION; TISSUE TROPISM; PROMOTER AB The promoter regions of the chicken skeletal muscle alpha-actin (alpha(sk)-actin) and the cytoplasmic beta-actin genes were linked to the bacterial chloramphenicol acetyltransferase (CAT) gene. Replication-competent retroviral vectors were used to introduce these two actin/CAT cassettes into the chicken genome. Chickens infected with retroviruses containing the alpha(sk)-actin promoter expressed high levels of CAT activity in striated muscle (skeletal muscle and heart); much lower levels of CAT activity were produced in the other nonmuscle tissues. In contrast, chickens infected with retroviruses containing the beta-actin promoter linked to the CAT gene expressed low levels of CAT activity in many different tissue types and with no discernible tissue specificity. Data are presented to demonstrate that the high levels of CAT activity that were detected in the skeletal muscle of chickens infected with the retrovirus containing the alpha(sk)-actin promoter/CAT cassette were not due to preferential infectivity, integration, or replication of the retrovirus vector in the striated muscles of these animals. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,POB B,FREDERICK,MD 21702. USDA ARS,AVIAN DIS & ONCOL LAB,E LANSING,MI 48823. MICHIGAN STATE UNIV,DEPT MICROBIOL,E LANSING,MI 48824. MICHIGAN STATE UNIV,DEPT ANIM SCI,E LANSING,MI 48824. FU NCI NIH HHS [N01-CO-74101] NR 57 TC 64 Z9 68 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3391 EP 3397 PG 7 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900016 PM 1637416 ER PT J AU ROBERTGUROFF, M ALDRICH, K MULDOON, R STERN, TL BANSAL, GP MATTHEWS, TJ MARKHAM, PD GALLO, RC FRANCHINI, G AF ROBERTGUROFF, M ALDRICH, K MULDOON, R STERN, TL BANSAL, GP MATTHEWS, TJ MARKHAM, PD GALLO, RC FRANCHINI, G TI CROSS-NEUTRALIZATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 AND TYPE-2 AND SIMIAN IMMUNODEFICIENCY VIRUS ISOLATES SO JOURNAL OF VIROLOGY LA English DT Article ID HTLV-III; POINT MUTATION; ANTIBODIES; ENVELOPE; SEQUENCE; HIV-1; INFECTION; RETROVIRUS; MONKEYS; EPITOPE AB In contrast to infrequent and low-titer cross-neutralization of human immunodeficiency virus type 1 (HIV-1) isolates by HIV-2- and simian immunodeficiency virus (SIV)-positive sera, extensive cross-neutralization of HIV-2NIH-Z, SIV(MAC251), and SIV(AGM208K) occurs with high titer, suggesting conservation of epitopes and mechanism(s) of neutralization. The V3 regions of HIV-2 and SIV isolates, minimally related to the HIV-1 homolog, share significant sequence homology and are immunogenic in monkeys as well as in humans. Whereas the crown of the V3 loop is cross-reactive among HIV-1 isolates and elicits neutralizing antibodies of broad specificity, the SIV and especially HIV-2 crown peptides were not well recognized by cross-neutralizing antisera. V3 loop peptides of HIV-2 isolates did not elicit neutralizing antibodies in mice, guinea pigs, or a goat and together with SIV V3 peptides did not inhibit serum neutralization of HIV-2 and SIV. Thus, the V3 loops of HIV-2 and SIV do not appear to constitute simple linear neutralizing epitopes. In view of the immunogenicity of V3 peptides, the failure of conserved crown peptides to react with natural sera implies a significant role of loop conformation in antibody recognition. Our studies suggest that in addition to their grouping by envelope genetic relatedness, HIV-2 and SIV are neutralized similarly to each other but differently from HIV-1. The use of linear peptides of HIV-2 and SIV as immunogens may require greater attention to microconformation, and alternate subunit approaches may be needed in exploiting these viruses as vaccine models. Such approaches may also be applicable to the HIV-1 system in which conformational epitopes, in addition to the V3 loop, participate in virus neutralization. C1 ADV BIOSCI LABS INC,KENSINGTON,MD 20895. DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. RP ROBERTGUROFF, M (reprint author), NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 41 TC 61 Z9 61 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3602 EP 3608 PG 7 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900039 PM 1374810 ER PT J AU DINMAN, JD WICKNER, RB AF DINMAN, JD WICKNER, RB TI RIBOSOMAL FRAMESHIFTING EFFICIENCY AND GAG GAG-POL RATIO ARE CRITICAL FOR YEAST M(1) DOUBLE-STRANDED-RNA VIRUS PROPAGATION SO JOURNAL OF VIROLOGY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; SACCHAROMYCES-CEREVISIAE; EXPRESSION; POLYMERASE; PROTEIN; SIGNAL; GENE; ORGANIZATION; MUTATIONS; REGION AB About 1.9% of ribosomes translating the gag open reading frame of the yeast L-A double-stranded RNA virus positive strand undergo a - 1 frameshift and continue translating in the pol open reading frame to make a 170-kDa gag-pol fusion protein. The importance of frameshifting efficiency for viral propagation was tested in a system where the M1 (killer toxin-encoding) satellite RNA is supported by a full-length L-A cDNA clone. Either increasing or decreasing the frameshift efficiency more than twofold by alterations in the slippery site disrupted viral propagation. A threefold increase caused by a chromosomal mutation, hsh1 (high shifter), had the same effect. Substituting a +1 ribosomal frameshift site from Tyl with the correct efficiency also allowed support of M, propagation. The normal -1 frameshift efficiency is similar to the observed molar ratio in viral particles of the 170-kDa gag-pol protein to the 70-kDa gag gene product, the major coat protein. The results are interpreted in terms of a packaging model for L-A. RP DINMAN, JD (reprint author), NIDDKD, BIOCHEM PHARMACOL LAB, GENET SIMPLE EUKARYOTES SECT, BETHESDA, MD 20892 USA. OI Dinman, Jonathan/0000-0002-2402-9698 NR 39 TC 162 Z9 168 U1 3 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X EI 1098-5514 J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3669 EP 3676 PG 8 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900047 PM 1583726 ER PT J AU MONK, RJ MALIK, FG STOKESBERRY, D EVANS, LH AF MONK, RJ MALIK, FG STOKESBERRY, D EVANS, LH TI DIRECT DETERMINATION OF THE POINT MUTATION-RATE OF A MURINE RETROVIRUS SO JOURNAL OF VIROLOGY LA English DT Article ID INFECTIOUS-ANEMIA VIRUS; SINGLE REPLICATION CYCLE; SPLEEN NECROSIS VIRUS; FOCUS-FORMING VIRUSES; INFLUENZA-A VIRUS; HTLV-III LAV; LEUKEMIA VIRUSES; NUCLEOTIDE-SEQUENCE; PERSISTENT INFECTION; GENETIC-VARIATION AB The point mutation rate of a murine leukemia virus (MuLV) genome (AKV) was determined under conditions in which the number of replicative cycles was carefully controlled and the point mutation rate was determined by direct examination of the RNA genomes of progeny viruses. A clonal cell line infected at a low multiplicity of infection (2 x 10(-3)) was derived to provide a source of virus with high genetic homogeneity. Virus stocks from this cell line were used to infect cells at a low multiplicity of infection, and the cells were seeded soon after infection to obtain secondary clonal cell lines. RNase T1-oligonucleotide fingerprinting analyses of virion RNAs from 93 secondary lines revealed only 3 base changes in nearly 130,000 bases analyzed. To obtain an independent assessment of the mutation rate, we directly sequenced virion RNAs by using a series of DNA oligonucleotide primers distributed across the genome. RNA sequencing detected no mutations in over 21,000 bases analyzed. The combined fingerprinting and sequencing analyses yielded a mutation rate for infectious progeny viruses of one base change per 50,000 (2 x 10(-5)) bases per replication cycle. Our results suggest that over 80% of infectious progeny MuLVs may be replicated with complete fidelity and that only a low percentage undergo more than one point mutation during a replication cycle. Previous estimates of retroviral mutation rates suggest that the majority of infectious progeny viruses have undergone one or more point mutations. Recent studies of the mutation rates of marker genes in spleen necrosis virus-based vectors estimate a base substitution rate lower than estimates for infectious avian retroviruses and nearly identical to our determinations with AKV. The differences between mutation rates observed in studies of retroviruses may reflect the imposition of different selective conditions. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 51 TC 36 Z9 36 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3683 EP 3689 PG 7 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900049 PM 1316475 ER PT J AU HOLLAND, SM CHAVEZ, M GERSTBERGER, S VENKATESAN, S AF HOLLAND, SM CHAVEZ, M GERSTBERGER, S VENKATESAN, S TI A SPECIFIC SEQUENCE WITH A BULGED GUANOSINE RESIDUE(S) IN A STEM-BULGE-STEM STRUCTURE OF REV-RESPONSIVE ELEMENT RNA IS REQUIRED FOR TRANSACTIVATION BY HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REV SO JOURNAL OF VIROLOGY LA English DT Article ID VIRAL MESSENGER-RNA; TARGET SEQUENCE; SECONDARY STRUCTURE; PROTEIN; HIV-1; BINDING; RECOGNITION; TRANSACTIVATION; DETERMINANT; REGION AB We demonstrate that both the in vitro RNA binding and in vivo trans activation functions of human immunodeficiency virus type 1 Rev regulatory protein Rev require the presence of a 9-nucleotide 5'-CACUAUGGG-3' RNA motif on its cognate target, the Rev-responsive element RNA. For optimal Rev recognition, this sequence must be presented as a stem-bulge-stem structure and must contain at least two G's, one of which must be unpaired, and include some or all of the CACUAU sequence upstream of the three G's. Distal mutations which result in the base pairing of the G's eliminate the Rev response. The first G is crucial, but changes at the other G's are tolerated if at least one G is unpaired. The secondary structure or the three-dimensional orientation of the B1 and B2 stem-loops of the Rev-responsive element are not relevant as long as the 5'-CACUAUGGG-3' sequence is preserved, with at least one bulged G residue. C1 NIAID, MOLEC MICROBIOL LAB, HAMILTON, MT 59840 USA. NR 43 TC 33 Z9 33 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3699 EP 3706 PG 8 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900051 PM 1583728 ER PT J AU THIERRY, F SPYROU, G YANIV, M HOWLEY, P AF THIERRY, F SPYROU, G YANIV, M HOWLEY, P TI 2 AP1 SITES BINDING JUNB ARE ESSENTIAL FOR HUMAN PAPILLOMAVIRUS TYPE-18 TRANSCRIPTION IN KERATINOCYTES SO JOURNAL OF VIROLOGY LA English DT Article ID HPV18 REGULATORY REGION; C-JUN; GLUCOCORTICOID RECEPTOR; CERVICAL-CARCINOMA; GENE-PRODUCT; NONCODING REGION; DNA-BINDING; FOS; ENHANCER; PROTEINS AB The activity and epithelial tropism of the human papillomavirus type 18 P105 early promoter, which directs the synthesis of the E6 and E7 transforming genes, are controlled by cis elements included in the viral long control region. To identify potential cellular regulators of this promoter, we mutagenized one or both of the 5'-TGACTAA-3' cis elements capable of interacting with the AP1 transcription factor, which is composed either of homodimers or heterodimers of the Jun products or of heterodimers of Jun and Fos. Mutation of both elements completely abolished P105 promoter activity in human keratinocytes. We show that either AP1 site can interact efficiently in vitro with any of the three different Jun products as heterodimers with c-Fos. However, in nuclear extracts prepared from human keratinocytes, JunB was the predominant Jun component bound to the DNA probe containing this cis element. These results implicate JunB as an important factor in human papillomavirus type 18 transcription in keratinocytes and strongly suggest a potential role of this Jun gene product in the tissue-specific transcription of the genital papillomaviruses. C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. RP THIERRY, F (reprint author), INST PASTEUR,CNRS,UNITE VIRUS ONCOGENES 1149,28 RUE DR ROUX,F-75724 PARIS 15,FRANCE. NR 57 TC 137 Z9 139 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3740 EP 3748 PG 9 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900056 PM 1316480 ER PT J AU CHOYKE, PL AUSTIN, HA FRANK, JA GIRTON, ME DIGGS, RL DWYER, AJ MILLER, L NUSSENBLATT, R MCFARLAND, H SIMON, T AF CHOYKE, PL AUSTIN, HA FRANK, JA GIRTON, ME DIGGS, RL DWYER, AJ MILLER, L NUSSENBLATT, R MCFARLAND, H SIMON, T TI HYDRATED CLEARANCE OF GADOLINIUM-DTPA AS A MEASUREMENT OF GLOMERULAR-FILTRATION RATE SO KIDNEY INTERNATIONAL LA English DT Article ID CREATININE CLEARANCE; RENAL-INSUFFICIENCY; TC-99M-DTPA AB Hydrated clearance of gadolinium-DTPA as a measurement of glomerular filtration rate. Technetium (Tc-99m)-diethylene triamine pentaacetic acid (DTPA) hydrated clearance studies are accurate for determining GFR but require special facilities for handling and measuring samples. We investigated the potential of a non-radioactive paramagnetic analog, Gadolinium (Gd)-diethylene triamine pentaacetic acid (DTPA), an approved NMR contrast agent, as a glomerular filtration marker. Instead of relying on the radioactivity of technetium, this test is based on the fact that gadolinium induces alterations in the NMR T1 relaxation times in blood and urine samples. Ninety patients underwent simultaneous determinations of GFR using 1 mCi of Tc-DTPA and 0.05 mmol/kg Gd-DTPA (Berlex Labs) IV. The patients were hydrated with oral and intravenous fluid. Following a one hour equilibrium period, three or four consecutive urine collections were obtained; plasma samples were acquired at the beginning and end of each approximately 20-minute interval. Tc-99m-DTPA radioactivity was determined with a scintillation counter. T1 relaxation times were measured on a 10 MHz NMR spectrometer. These were converted to Gd-DTPA concentration by comparison with standard solutions. The Gd-DTPA derived GFR closely approximated the Tc-99m-DTPA derived GFR which ranged from 15 to 147 ml/min. The equation and correlation coefficient of the regression line is y = 1.04 x -2.2, r = 0.94. Thus, Gd-DTPA is a safe, non-radioactive indicator of GFR that may provide an alternative renal clearance method for clinical studies of progressive renal disease and nephrotoxicity. C1 NIDDKD,KIDNEY DIS SECT,BETHESDA,MD 20892. NIDDKD,DEPT NUCL MED,BETHESDA,MD 20892. NINCDS,BETHESDA,MD 20892. RP CHOYKE, PL (reprint author), NIDDKD,DEPT RADIOL,BLDG 10,ROOM 1C 660,BETHESDA,MD 20892, USA. NR 20 TC 55 Z9 59 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JUN PY 1992 VL 41 IS 6 BP 1595 EP 1598 DI 10.1038/ki.1992.230 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA HW904 UT WOS:A1992HW90400014 PM 1501414 ER PT J AU WALSH, TJ LEE, JW BACHER, J KELLY, P PIZZO, PA AF WALSH, TJ LEE, JW BACHER, J KELLY, P PIZZO, PA TI CONTINUOUS INTRAVENOUS-INFUSION AND SIMULTANEOUS PHARMACOKINETIC MONITORING IN AMBULATORY RABBITS WITH A PROGRAMMABLE MICROPUMP AND DUAL SUBCUTANEOUS SILASTIC(TM) CENTRAL VENOUS CATHETERS SO LABORATORY ANIMAL SCIENCE LA English DT Article ID TISSUE PENETRATION; CILOFUNGIN; RATS AB We describe a newly developed method of continuous intravenous infusion and simultaneous monitoring of plasma levels of investigational compounds in ambulatory untethered rabbits. Continuous infusion was administered by means of a portable programmable external micropump which permitted adjustable dosing. Simultaneous plasma pharmacokinetic monitoring during infusion was accomplished by dual silastic central venous catheters. The potential applications of the micropump infusion system as an alternative to current methods of continuous infusion in other species and in other studies are further discussed. This method provided a safe, reliable, and well-tolerated method of adjustable continuous intravenous infusion and simultaneous sampling of central venous blood in rabbits. C1 NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,BETHESDA,MD 20892. RP WALSH, TJ (reprint author), NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,RM 13N240,BETHESDA,MD 20892, USA. NR 16 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI CORDOVA PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018 SN 0023-6764 J9 LAB ANIM SCI JI Lab. Anim. Sci. PD JUN PY 1992 VL 42 IS 3 BP 286 EP 292 PG 7 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA JA579 UT WOS:A1992JA57900012 PM 1320161 ER PT J AU DUELAND, AN MARTIN, JR DEVLIN, ME WELLISH, M MAHALINGAM, R COHRS, R SOIKE, KF GILDEN, DH AF DUELAND, AN MARTIN, JR DEVLIN, ME WELLISH, M MAHALINGAM, R COHRS, R SOIKE, KF GILDEN, DH TI ACUTE SIMIAN VARICELLA INFECTION - CLINICAL, LABORATORY, PATHOLOGICAL, AND VIROLOGICAL FEATURES SO LABORATORY INVESTIGATION LA English DT Article DE PRIMARY INFECTION; GANGLIA ID DELTA-HERPESVIRUS INFECTION; ZOSTER VIRUS; GANGLION AB Five African green monkeys inoculated intratracheally with 7.5 x 10(3) to 1.4 x 10(5) plaque-forming units of simian varicella virus (SVV) were subjected to clinical, laboratory, pathologic, and virologic analyses to study the pathogenesis of acute varicella. All animals developed viremia and rash and were sacrificed 8 to 11 days post-infection. No serum was available for postmortem serologic studies. Examination of multiple organs for pathologic changes and for SVV-specific antigen and nucleic acid revealed inflammation, hemorrhagic necrosis, and intranuclear Cowdry A inclusions in liver, lung, lymph node, and spleen; mild inflammation without necrosis in adrenal gland, kidney, and bone marrow, and SVV-specific antigen and nucleic acids in all viscera examined. No pathologic changes, SVV antigen or nucleic acids were detected in the spinal cord or in the brain from any of the monkeys. Ganglia revealed mild inflammation but no necrosis, and intranuclear inclusion bodies in non-neuronal cells of one trigeminal ganglion; SVV antigen and nucleic acids were detected in both non-neuronal and neuronal cells in ganglia. The pathologic and virologic findings in viscera are consistent with those described in viscera of humans with disseminated zoster, but the mild inflammatory changes in ganglia during acute simian varicella infection contrast with the extensive hemorrhagic necrosis and intranuclear inclusion bodies seen in human ganglia after disseminated varicella or zoster. Nevertheless, these studies show that ganglia become infected with varicella virus during primary infection, although the route of primary ganglionic infection remains to be determined, and indicate the possible usefulness of the SVV model to study varicella pathogenesis in humans. C1 UNIV COLORADO,SCH MED,DEPT MICROBIOL & IMMUNOL,DENVER,CO 80262. NIH,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. TULANE UNIV,DELTA REG PRIMATE RES CTR,COVINGTON,LA 70433. RP DUELAND, AN (reprint author), UNIV COLORADO,SCH MED,DEPT NEUROL,4200 E 9TH AVE,CAMPUS BOX B-182,DENVER,CO 80262, USA. FU NIA NIH HHS [AG-07347, AG-06127]; NINDS NIH HHS [NS-07321] NR 25 TC 49 Z9 49 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JUN PY 1992 VL 66 IS 6 BP 762 EP 773 PG 12 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HZ657 UT WOS:A1992HZ65700013 PM 1602744 ER PT J AU BERNEMAN, ZN GARTENHAUS, RB REITZ, MS KLOTMAN, ME GALLO, RC AF BERNEMAN, ZN GARTENHAUS, RB REITZ, MS KLOTMAN, ME GALLO, RC TI CDNA SEQUENCING CONFIRMS HTLV-I EXPRESSION IN ADULT T-CELL LEUKEMIA LYMPHOMA AND DIFFERENT SEQUENCE VARIATIONS IN INVIVO AND INVITRO SO LEUKEMIA LA English DT Article; Proceedings Paper CT 15TH SYMP OF THE INTERNATIONAL ASSOC FOR COMPARATIVE RESEARCH ON LEUKEMIA AND RELATED DISEASES CY OCT 06-11, 1991 CL PADUA, ITALY SP INT ASSOC COMPARAT RES LEUKEMIA & RELATED DIS, ASSOC ITALIANA RIC CANC, LEUKEMIA SOC AMER, NCI, FIDIA RES LABS, BANCO SAN MARCO, AMMINISTRAZIONE PROV PADOVA, CITY PADOVA, UNIV PADOVA ID VIRUS TYPE-I; TROPICAL SPASTIC PARAPARESIS; COMPLETE NUCLEOTIDE-SEQUENCE; MOLECULAR-CLONING; MESSENGER-RNA; PROVIRUS; DNA; PX; MYELOPATHY; GENE AB Human T-lymphotropic virus type I (HTLV-I) is the etiological agent of adult T-cell leukemia/lymphoma (ATL) and of tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM). In both diseases, expression of viral message can generally only be demonstrated by the reverse transcriptase-polymerase chain reaction (RT-PCR) technique. We have previously reported on the the expression of at least four types of alternatively spliced pX mRNAs in vitro and in vivo (1). The sequence variation between HTLV-I pX cDNAs cloned from two different HTLV-I-infected cell lines and from uncultured primary peripheral blood mononuclear cells (PBMC) from two ATL patients was examined. None of the cDNA clones from one or the ATL samples was completely identical to any of the previously cloned cell line messages, establishing that the demonstration of HTLV-I mRNA in ATL is not the result of PCR contamination. Sequence analysis showed that differences between samples can be clustered according to their geographic origin. Cell line cDNAs showed a more marked sequence drift than ATL CDNAs, especially in the long terminal repeat (LTR), demonstrating association of intrastrain variability with culture in vitro. Intrastrain cDNA variability in vivo also suggests ongoing viral replication in infected individuals. A premature stop codon in the pX-II open reading frame (orr) was a common finding, suggesting that the complete putative pX-II protein is not essential for T-cell immortalization or HTLV-I replication. RP BERNEMAN, ZN (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,ROOM 6A09,BETHESDA,MD 20892, USA. RI klotman, mary/A-1921-2016 NR 38 TC 10 Z9 10 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD JUN PY 1992 VL 6 SU 3 BP S67 EP S71 PG 5 WC Oncology; Hematology SC Oncology; Hematology GA JD266 UT WOS:A1992JD26600020 PM 1602830 ER PT J AU BRODER, S AF BRODER, S TI FACTORS IN THE DEVELOPMENT OF AIDS-RELATED LYMPHOMAS SO LEUKEMIA LA English DT Article; Proceedings Paper CT 15TH SYMP OF THE INTERNATIONAL ASSOC FOR COMPARATIVE RESEARCH ON LEUKEMIA AND RELATED DISEASES CY OCT 06-11, 1991 CL PADUA, ITALY SP INT ASSOC COMPARAT RES LEUKEMIA & RELATED DIS, ASSOC ITALIANA RIC CANC, LEUKEMIA SOC AMER, NCI, FIDIA RES LABS, BANCO SAN MARCO, AMMINISTRAZIONE PROV PADOVA, CITY PADOVA, UNIV PADOVA ID IMMUNODEFICIENCY-VIRUS INFECTION; GENE; HIV; NEOPLASIA; PROTEIN; DISEASE RP BRODER, S (reprint author), NCI,BETHESDA,MD 20892, USA. NR 42 TC 3 Z9 3 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD JUN PY 1992 VL 6 SU 3 BP S6 EP S9 PG 4 WC Oncology; Hematology SC Oncology; Hematology GA JD266 UT WOS:A1992JD26600004 PM 1318478 ER PT J AU LEVINE, PH AF LEVINE, PH TI THE EPIDEMIOLOGY OF HUMAN VIRUS-ASSOCIATED HEMATOLOGIC MALIGNANCIES SO LEUKEMIA LA English DT Article; Proceedings Paper CT 15TH SYMP OF THE INTERNATIONAL ASSOC FOR COMPARATIVE RESEARCH ON LEUKEMIA AND RELATED DISEASES CY OCT 06-11, 1991 CL PADUA, ITALY SP INT ASSOC COMPARAT RES LEUKEMIA & RELATED DIS, ASSOC ITALIANA RIC CANC, LEUKEMIA SOC AMER, NCI, FIDIA RES LABS, BANCO SAN MARCO, AMMINISTRAZIONE PROV PADOVA, CITY PADOVA, UNIV PADOVA ID EPSTEIN-BARR VIRUS; NON-HODGKIN LYMPHOMA; T-CELL LYMPHOMA; BURKITT-LYMPHOMA; KAPOSIS-SARCOMA; DISEASE; LEUKEMIA; INFECTION; ANTIBODIES; PARTICLES AB The long history of studies etiologically linking viruses to a number of animal tumors (1) forecast the subsequent detection of human oncogenic viruses and their association with a variety of human malignancies (2). It is apparent that oncogenic viruses cause a wide spectrum of diseases. Epstein-Barr virus (EBV), for example, the cause of infectious mononucleosis (3), has also been etiologically linked to nasopharyngeal carcinoma (4), Burkitt's lymphoma (5) and other malignant lymphoproliferative diseases (6). Similarly, HTLV-I, the cause of most cases of adult T-cell leukemia/lymphoma (ATL) (7), has also been etiologically linked to HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) (8) and infective dermatitis (9). In this report, however, we will only review the epidemiology of human hematologic malignancies that have been linked to specific viruses. RP LEVINE, PH (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 65 TC 12 Z9 12 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD JUN PY 1992 VL 6 SU 3 BP S54 EP S59 PG 6 WC Oncology; Hematology SC Oncology; Hematology GA JD266 UT WOS:A1992JD26600017 PM 1318477 ER PT J AU PAVLAKIS, GN FELBER, BK CIMINALE, V UNGE, T SOLOMIN, L HARRISON, JE AF PAVLAKIS, GN FELBER, BK CIMINALE, V UNGE, T SOLOMIN, L HARRISON, JE TI STRUCTURE, REGULATION AND ONCOGENIC MECHANISMS OF HTLV-I AND HTLV-II SO LEUKEMIA LA English DT Article ID CELL LEUKEMIA-VIRUS; GENE-EXPRESSION; TRANSGENIC MICE; DNA-BINDING; TAT GENE; ACTIVATION; PROTEINS; TYPE-1; INTERLEUKIN-2; PROMOTER C1 NCI, FREDERICK CANC RES & DEV CTR, HUMAN RETROVIRUS SECT, FREDERICK, MD 21701 USA. NCI, FREDERICK CANC RES & DEV CTR, HUMAN RETROVIRUS PATHOGENESIS GRP, FREDERICK, MD 21701 USA. FU NCI NIH HHS [N01-CO-74101] NR 48 TC 2 Z9 2 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0887-6924 J9 LEUKEMIA JI Leukemia PD JUN PY 1992 VL 6 SU 3 BP S176 EP S180 PG 5 WC Oncology; Hematology SC Oncology; Hematology GA JD266 UT WOS:A1992JD26600051 PM 1602819 ER PT J AU KOIZUMI, S ALLEGRA, CJ AF KOIZUMI, S ALLEGRA, CJ TI ENZYME STUDIES OF METHOTREXATE-RESISTANT HUMAN LEUKEMIC-CELL (K562) SUBCLONES SO LEUKEMIA RESEARCH LA English DT Article DE METHOTREXATE; TRIMETREXATE; DRUG-RESISTANCE; DIHYDROFOLATE REDUCTASE; FOLATE; K562 CELLS ID THYMIDYLATE SYNTHETASE-ACTIVITY; BREAST CANCER-CELLS; DIHYDROFOLATE-REDUCTASE; MEMBRANE-TRANSPORT; KINETIC-PROPERTIES; LUNG-CANCER; LINES; POLYGLUTAMATES; LYMPHOBLASTS; SENSITIVITY AB Five methotrexate (MTX)-resistant K562 cell subclones (K562/MTX-1 is similar to -5) were established and were examined for mechanisms of drug resistance. Impairment of MTX-polyglutamate formation, with membrane transport alteration, in the resistant cells was demonstrated in the previous studies (Koizumi, S. (1988) Jpn. J. Cancer Res. 79, 1230). Further analysis of sensitivity of the cells to trimetrexate (TMQ), which is not polyglutamated and does not require the reduced folate transporter, but is a potent inhibitor of human DHFR, revealed a modest decrease in sensitivity to TMQ (2.4- to 15-fold). Enzyme studies showed that the dihydrofolate reductase (DHFR) activities of these resistant subclones were very similar to that of the parent cells. The number of binding sites of these subclones for MTX calculated from Scatchard analysis was increased up to 7-fold in the K562/MTX-1 and -4 subclones and up to 3-fold in the other 3 subclones as compared to the parent cells. K(D) values of MTX for the DHFR in the K562/MTX-1 and -4 subclones also appeared to be altered relative to the parent cell line. Further, thymidylate synthase (TS) activity of the resistant subclones was reduced to 50% in K562/MTX-1 and 4 cells, and to 11-25% in the other subclones as compared to the parent cell line. These findings suggest that antifolate resistance in the newly established K562/MTX subclones is multifactorial with polyglutamation and transport defects accounting for the majority of resistance to MTX, and that alteration in the binding affinity of DHFR for MTX and diminished levels of TS may contribute to the 'residual' drug resistance to TMQ and have importance with respect to MTX. C1 NCI,DIV CANC TREATMENT,MED BRANCH,BETHESDA,MD 20892. RP KOIZUMI, S (reprint author), KANAZAWA UNIV,SCH MED,DEPT PEDIAT,13-1 TAKARAMACHI,KANAZAWA,ISHIKAWA 920,JAPAN. NR 25 TC 5 Z9 5 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD JUN-JUL PY 1992 VL 16 IS 6-7 BP 565 EP 569 DI 10.1016/0145-2126(92)90003-P PG 5 WC Oncology; Hematology SC Oncology; Hematology GA JE989 UT WOS:A1992JE98900003 PM 1378915 ER PT J AU LINET, MS MCLAUGHLIN, JK HSING, AW WACHOLDER, S CHIEN, HTC SCHUMAN, LM BJELKE, E BLOT, WJ AF LINET, MS MCLAUGHLIN, JK HSING, AW WACHOLDER, S CHIEN, HTC SCHUMAN, LM BJELKE, E BLOT, WJ TI IS CIGARETTE-SMOKING A RISK FACTOR FOR NON-HODGKINS-LYMPHOMA OR MULTIPLE-MYELOMA - RESULTS FROM THE LUTHERAN BROTHERHOOD COHORT STUDY SO LEUKEMIA RESEARCH LA English DT Article DE CIGARETTE SMOKING; NON-HODGKINS LYMPHOMA; MULTIPLE MYELOMA; PROSPECTIVE STUDY; UNITED-STATES ID UNITED-STATES; LEUKEMIA; CANCER; ASSOCIATION; MORTALITY; TOBACCO; WHITES AB Among 17 633 U.S. white male insurance policy holders whose use of tobacco was characterized in a 1966 self-administered questionnaire, there were 49 deaths from non-Hodgkin's lymphoma (NHL) and 21 from multiple myeloma (MM) during a 20-year follow-up. Men who had ever smoked cigarettes had an elevated mortality from NHL (RR = 2.1; CI = 0.9-4.9), with risk almost four-fold greater among the heaviest smokers (RR = 3.8; CI = 1.4-10.1) compared with those who used no tobacco. In contrast, risk of MM was only slightly elevated among those who had ever smoked cigarettes (RR = 1.3; CI = 0.4-3.9) and without evidence of a dose-response trend. Since this is the first cohort study suggesting a link between cigarette smoking and NHL and findings from case-control studies have been inconsistent, additional clarification should be sought from larger incidence-based cohort investigations. C1 WESTAT CORP,ROCKVILLE,MD 20850. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV BERGEN,CTR EPIDEMIOL RES,N-5014 BERGEN,NORWAY. RP LINET, MS (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,AS BB EBP DCE,BETHESDA,MD 20892, USA. NR 29 TC 61 Z9 62 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD JUN-JUL PY 1992 VL 16 IS 6-7 BP 621 EP 624 DI 10.1016/0145-2126(92)90011-U PG 4 WC Oncology; Hematology SC Oncology; Hematology GA JE989 UT WOS:A1992JE98900011 PM 1635380 ER PT J AU UPPENKAMP, M DRESEN, IG BECHER, R RAFFELD, M MEUSERS, P AF UPPENKAMP, M DRESEN, IG BECHER, R RAFFELD, M MEUSERS, P TI MOLECULAR ANALYSIS OF AN ATAXIA TELANGIECTASIA T-CELL CLONE WITH A CHROMOSOMAL TRANSLOCATION T(14,18) - EVIDENCE FOR A BREAKPOINT IN THE T-CELL RECEPTOR DELTA-CHAIN GENE SO LEUKEMIA RESEARCH LA English DT Article DE ATAXIA TELANGIECTASIA; T-CELL LYMPHOCYTIC LYMPHOMA; RECIPROCAL CHROMOSOMAL TRANSLOCATION; T-CELL RECEPTOR GENE REARRANGEMENTS; T-CELL RECEPTOR DELTA-CHAIN GENE ID CONSTANT REGION GENES; MYELIN-BASIC-PROTEIN; ACUTE LYMPHOBLASTIC-LEUKEMIA; ALPHA-CHAIN; LYMPHOCYTIC-LEUKEMIA; LOCUS; DIVERSITY; ORGANIZATION; DIFFERENTIATION; REARRANGEMENTS AB We established a clonal T-cell line with a reciprocal chromosomal translocation t(14;18)(q11;q23) from a patient with ataxia telangiectasia (AT) and T-cell chronic lymphocytic leukemia (T-CLL). The tumor cells and the derived T-cell line were compared with respect to phenotype, karyotype, and rearrangement pattern. Restriction fragment analyses of the T-cell receptor (TCR)-delta gene, which is located within the TCR-alpha gene on chromosome 14q11, indicated that the breakpoint is located within the TCR-delta locus, splitting the TCR-delta gene between the variable and joining segments. This specific chromosomal translocation was only detected in the derived T-cell line and may be involved in the genesis of T-cell malignancies in AT. C1 UNIV ESSEN GESAMTHSCH,W GERMAN TUMOR CTR,W-4300 ESSEN 1,GERMANY. NCI,DEPT PATHOL,HEMATOPATHOL SECT,BETHESDA,MD 20892. RP UPPENKAMP, M (reprint author), UNIV ESSEN GESAMTHSCH,DEPT INTERNAL MED,DIV HEMATOL,HUFELANDSTR 55,W-4300 ESSEN 1,GERMANY. NR 46 TC 1 Z9 1 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD JUN-JUL PY 1992 VL 16 IS 6-7 BP 681 EP 691 DI 10.1016/0145-2126(92)90019-4 PG 11 WC Oncology; Hematology SC Oncology; Hematology GA JE989 UT WOS:A1992JE98900019 PM 1353132 ER PT J AU PURI, RK LELAND, P AF PURI, RK LELAND, P TI SYSTEMIC ADMINISTRATION OF RECOMBINANT INTERLEUKIN-6 IN MICE INDUCES PROLIFERATION OF LYMPHOID-CELLS INVIVO SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID PLASMACYTOMA GROWTH-FACTOR; ACTIVATED KILLER-CELLS; LYMPHOCYTES-T; INDUCTION; IL-6; DIFFERENTIATION; INTERFERON; BSF-2; IFN-BETA-2; PROTEIN AB Interleukin-6 (IL-6) is a pleiotropic cytokine and has been shown to support the growth of T and B lymphocytes in the presence of mitogens in vitro. IL-6 can induce human natural killer (NK) and interleukin-2 (IL-2)-induced lymphokine-activated killer cell (LAK) activity in vitro. It can also mediate antitumor effects in various murine models. In order to understand the mechanism of in vivo action, we have investigated the proliferation of lymphoid cells in vivo and the effects on NK, and LAK cell activities in response to IL-6 administration in mice. In vivo proliferation was measured by labeling the DNA of dividing cells with [I-125]iodo-2'-deoxyuridine. C57BL/6 mice were injected ip with either IL-6 or HBSS control two times a day for 3 days and in vivo proliferation was measured. For comparative purpose IL-2 was administered and in vivo effects were analyzed. IL-6 caused significant proliferation of cells mainly in the spleen, while, IL-2 caused proliferation in the lungs, liver, spleen, and kidneys. Pretreatment irradiation (500 rad) of mice abrogated the IL-6-induced proliferation indicating radiosensitive cells are involved. Furthermore, in vivo proliferation was not observed in young nude mice treated with IL-6. To investigate whether the proliferating cells were cytotoxic, we tested for LAK (vs. fresh MCA-102 tumor targets) and NK (vs. Yac-1 tumor targets) activities in the organs of mice treated with IL-6 or IL-2 by 4 h Cr-51-release assay. IL-2 administration induced the generation of LAK activity and increased NK cytotoxicity in various organs, but IL-6 had no effect. Cytofluorometric analysis of splenocytes from IL-6-treated naive mice revealed that absolute number of B cells and in alloantigen-immunized mice absolute number of CD8, CD4, and Thy 1.2+ T cells were increased. IL-2 also increased T cells and ASGM-1-positive cells, however, IL-6 did not increase ASGM-1 cells. These studies indicate that IL-6 can induce the proliferation of endogenous lymphocytes in the spleen and its antitumor effects may not be mediated by LAK and NK cells. RP PURI, RK (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,CELLULAR IMMUNOL LAB,NIH BLDG 29A,ROOM 2B20,BETHESDA,MD 20892, USA. NR 29 TC 13 Z9 13 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0277-6766 J9 LYMPHOKINE CYTOK RES JI Lymphokine Cytokine Res. PD JUN PY 1992 VL 11 IS 3 BP 133 EP 139 PG 7 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA JA055 UT WOS:A1992JA05500001 PM 1391232 ER PT J AU ZIPFEL, PF WHARTON, KA VILLALOBOS, J IRVING, SG KELLY, K SIEBENLIST, U AF ZIPFEL, PF WHARTON, KA VILLALOBOS, J IRVING, SG KELLY, K SIEBENLIST, U TI EMPLOYMENT OF ANTIPEPTIDE ANTISERA TO DISTINGUISH 2 CLOSELY RELATED CYTOKINES INDUCED IN HUMAN T-CELLS SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID MITOGENIC ACTIVATION; GENES; CLONING AB AT464 and AT744 are two cytokines encoded by mitogen-induced genes from human T lymphocytes. These proteins belong to a family of structurally related chemotactic proteins associated with inflammation. By expression of their full length cDNAs in COS cells and in baculovirus-infected Sf9 cells, we found that pAT464 and pAT744 cDNAs represent secreted polypeptides of a molecular mass of about 8,000 and 11,000 Da, respectively. Biochemical characterization of these proteins has been persued through polyclonal antisera, which were derived to synthetic peptides. Using these sera for Western blotting analyses the recombinant AT464 and AT744 proteins could be detected as secreted products from transfected COS cells and from baculovirus-infected Sf9 cells. Similarly the native proteins could be detected in the supernatants of activated human peripheral blood T cells. The recombinant and the T cell-secreted AT464 and AT744 proteins appear to be identical as judged by their mobility by SDS-PAGE and by their reactivity with the rabbit polyclonal antisera. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20007. NCI,PATHOL LAB,BETHESDA,MD 20892. RP ZIPFEL, PF (reprint author), BERNHARD NOCHT INST TROP MED,BERNHARD NOCHT STR 74,W-2000 HAMBURG 36,GERMANY. NR 17 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0277-6766 J9 LYMPHOKINE CYTOK RES JI Lymphokine Cytokine Res. PD JUN PY 1992 VL 11 IS 3 BP 141 EP 148 PG 8 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA JA055 UT WOS:A1992JA05500002 PM 1391233 ER PT J AU HUNTER, L AF HUNTER, L TI KNOWLEDGE ACQUISITION PLANNING - USING MULTIPLE SOURCES OF KNOWLEDGE TO ANSWER QUESTIONS IN BIOMEDICINE SO MATHEMATICAL AND COMPUTER MODELLING LA English DT Article AB By combining techniques from machine learning and robot planning, knowledge acquisition planning provides a framework for automatically deploying diverse and complex analytical tools to extremely large collections of data. KA planning is the process of automatically combining inferential tools such as induction, search, database lookup and statistical analysis into methods for addressing complex query statements. This process depends both on having a domain model that supports subgoal decomposition and a library of KA actions annotated with the type and form of required input data, expected outcomes of the action, estimates of computational resources needed, and so on. By annotating analytical tools in this way, it is possible to automatically select and deploy them and combine their results, even if they run on incompatible platforms. Knowledge acquisition planning was first implemented in a program that learned about diagnosing lung tumors. A larger project is currently underway in the domain of molecular biology. RP HUNTER, L (reprint author), NATL LIB MED,LISTER HILL CTR MS54,BETHESDA,MD 20894, USA. OI Hunter, Lawrence/0000-0003-1455-3370 NR 18 TC 0 Z9 0 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-7177 J9 MATH COMPUT MODEL JI Math. Comput. Model. PD JUN-JUL PY 1992 VL 16 IS 6-7 BP 79 EP 91 DI 10.1016/0895-7177(92)90153-C PG 13 WC Computer Science, Interdisciplinary Applications; Computer Science, Software Engineering; Mathematics, Applied SC Computer Science; Mathematics GA JA602 UT WOS:A1992JA60200007 ER PT J AU RIPAMONTI, U MA, S REDDI, AH AF RIPAMONTI, U MA, S REDDI, AH TI THE CRITICAL ROLE OF GEOMETRY OF POROUS HYDROXYAPATITE DELIVERY SYSTEM IN INDUCTION OF BONE BY OSTEOGENIN, A BONE MORPHOGENETIC PROTEIN SO MATRIX LA English DT Article DE BONE INDUCTION; BONE MATRIX; BONE MORPHOGENETIC PROTEINS; DELIVERY SYSTEM; HYDROXYAPATITE; OSTEOGENIN ID EXTRACELLULAR-MATRIX; BASEMENT-MEMBRANE; GROWTH-HORMONE; IV COLLAGEN; DIFFERENTIATION; TRANSFORMATION; FIBROBLASTS; COMPONENTS; CARTILAGE; LAMININ AB The collagenous extracellular matrix of bone obtained after dissociative extraction with 4 M guanidine-HCI is an optimal substratum for bone induction by osteogenin, a bone morphogenetic protein. As a proteinaceous substratum, this matrix and other collagen-based materials may be immunogenic. Thus, the search and discovery of a non-immunogenic substratum is a necessary prerequisite for the therapeutic application of the principle of bone induction to skeletal repair. Bovine osteogenin, purified greater than 50,000-fold and with an apparent molecular mass of 28-42 kilodaltons, was delivered into nonresorbable porous hydroxyapatite in granular and disc configuration. A total of 328 preparations were bioassayed for osteogenic activity by subcutaneous implantation into 164 Long-Evans rats. Specimens were harvested at day 7, 11 and 21 after implantation and subjected to alkaline phosphatase activity determination and histologic analysis. Osteogenin combined with discs of porous hydroxyapatite induced in vivo differentiation of the osteogenic phenotype in mesenchymal cells invading the three-dimensional porous space of the inorganic substratum. The geometry of the substratum had a profound influence on bone induction, since the expression of the osteogenic phenotype was solely confined in porous hydroxyapatite with disc configuration. Osteogenin did not induce bone differentiation when combined with granules of porous hydroxyapatite with identical pore dimensions. The finding that the biological activity of osteogenin can be restored and delivered by a substratum with defined geometry other than the insoluble collagenous matrix may form the basis of the potential therapeutic application of bone morphogenetic proteins. RP RIPAMONTI, U (reprint author), NIDR,BONE CELL BIOL SECT,BETHESDA,MD 20892, USA. NR 40 TC 145 Z9 148 U1 0 U2 8 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0934-8832 J9 MATRIX JI Matrix PD JUN PY 1992 VL 12 IS 3 BP 202 EP 212 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HY484 UT WOS:A1992HY48400005 PM 1328828 ER PT J AU GIORDANO, T JOHNSON, SA SAKAMOTO, K HOWARD, BH AF GIORDANO, T JOHNSON, SA SAKAMOTO, K HOWARD, BH TI EXPRESSION OF ALU AND 7SL-RNA IN ALZHEIMERS AND CONTROL BRAINS SO MECHANISMS OF AGEING AND DEVELOPMENT LA English DT Article DE 7SL RNA; ALU; ALZHEIMERS DISEASE ID DENSITY LIPOPROTEIN RECEPTOR; PRECURSOR MESSENGER-RNA; FAMILIAL HYPERCHOLESTEROLEMIA; DISEASE; GENE; PROTEIN; SEQUENCES; RECOMBINATION; PSEUDOGENES; EVOLUTION AB We investigated whether changes in expression of RNA polymerase III (pol III) or heterodisperse RNA polymerase II (pol II) transcripts hybridizing to Alu could be detected in Alzheimer's disease (AD). RNA samples obtained from AD and control brain tissues were examined by Northern analysis for Alu and 7SL RNA expression. All RNA samples contained a prominent band of approximately 300 nucleotides which corresponds to 7SL RNA, the Alu-homologous RNA component of the signal recognition particle. In addition, three small (i.e. <300 nucleotide) 7SL/Alu-hybridizing transcripts were detected. The two larger of the low molecular weight transcripts hybridized preferentially to the 7SL RNA probe, while the smallest transcript hybridized to the Alu probe. These transcripts and the heterodisperse RNA were variable in quantity and displayed a lack of correlation with AD. C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. UNIV SO CALIF,ETHEL PERCY ANDRUS GERONTOL CTR,LOS ANGELES,CA 90089. UNIV SO CALIF,DEPT BIOL SCI,LOS ANGELES,CA 90089. NR 27 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0047-6374 J9 MECH AGEING DEV JI Mech. Ageing. Dev. PD JUN PY 1992 VL 64 IS 1-2 BP 13 EP 20 DI 10.1016/0047-6374(92)90092-R PG 8 WC Cell Biology; Geriatrics & Gerontology SC Cell Biology; Geriatrics & Gerontology GA HZ161 UT WOS:A1992HZ16100002 PM 1378521 ER PT J AU BARANOWSKI, T BOUCHARD, C BAROR, O BRICKER, T HEATH, G KIMM, SYS MALINA, R OBARZANEK, E PATE, R STRONG, WB TRUMAN, B WASHINGTON, R AF BARANOWSKI, T BOUCHARD, C BAROR, O BRICKER, T HEATH, G KIMM, SYS MALINA, R OBARZANEK, E PATE, R STRONG, WB TRUMAN, B WASHINGTON, R TI ASSESSMENT, PREVALENCE, AND CARDIOVASCULAR BENEFITS OF PHYSICAL-ACTIVITY AND FITNESS IN YOUTH SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Review ID WHITE MALE-ADOLESCENTS; DOUBLY LABELED WATER; COLD PRESSOR TEST; SERUM-LIPIDS; BLOOD-PRESSURE; RISK-FACTORS; HYPERTENSIVE ADOLESCENTS; ENERGY-EXPENDITURE; BLACK-CHILDREN; COLLEGE ALUMNI C1 UNIV LAVAL, QUEBEC CITY G1K 7P4, QUEBEC, CANADA. MCMASTER UNIV, HAMILTON L8S 4L8, ONTARIO, CANADA. BAYLOR COLL MED, HOUSTON, TX 77030 USA. CTR DIS CONTROL, ATLANTA, GA 30333 USA. UNIV PITTSBURGH, SCH MED, PITTSBURGH, PA 15261 USA. UNIV TEXAS, AUSTIN, TX 78712 USA. NHLBI, BETHESDA, MD 20892 USA. UNIV S CAROLINA, COLUMBIA, SC 29208 USA. COLORADO CHILDRENS HOSP, DENVER, CO USA. RP BARANOWSKI, T (reprint author), MED COLL GEORGIA, GEORGIA PREVENT INST, DEPT PEDIAT, MAIL STOP HS 1640, AUGUSTA, GA 30912 USA. RI Bouchard, Claude/A-7637-2009 NR 108 TC 76 Z9 77 U1 3 U2 11 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD JUN PY 1992 VL 24 IS 6 SU S BP S237 EP S247 PG 11 WC Sport Sciences SC Sport Sciences GA HX754 UT WOS:A1992HX75400006 PM 1625549 ER PT J AU HASKELL, WL LEON, AS CASPERSEN, CJ FROELICHER, VF HAGBERG, JM HARLAN, W HOLLOSZY, JO REGENSTEINER, JG THOMPSON, PD WASHBURN, RA WILSON, PWF AF HASKELL, WL LEON, AS CASPERSEN, CJ FROELICHER, VF HAGBERG, JM HARLAN, W HOLLOSZY, JO REGENSTEINER, JG THOMPSON, PD WASHBURN, RA WILSON, PWF TI CARDIOVASCULAR BENEFITS AND ASSESSMENT OF PHYSICAL-ACTIVITY AND PHYSICAL-FITNESS IN ADULTS SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Review ID CORONARY HEART-DISEASE; HIGH-DENSITY-LIPOPROTEIN; MIDDLE-AGED MEN; PERIPHERAL ARTERIAL-DISEASE; ALL-CAUSE MORTALITY; MYOCARDIAL-INFARCTION; ENERGY-EXPENDITURE; LEISURE-TIME; SELF-REPORT; CARDIAC REHABILITATION C1 UNIV MINNESOTA,MINNEAPOLIS,MN 55455. CTR DIS CONTROL,ATLANTA,GA 30333. UNIV MARYLAND,COLLEGE PK,MD 20742. NIH,BETHESDA,MD 20892. WASHINGTON UNIV,ST LOUIS,MO 63130. UNIV COLORADO,BOULDER,CO 80309. MERIAM HOSP,CLEVELAND,OH. NEW ENGLAND RES INST,WATERTOWN,MA. NHLBI,FRAMINGHAM HEART STUDY,BETHESDA,MD 20892. RP HASKELL, WL (reprint author), STANFORD UNIV,SCH MED,730 WELCH RD,PALO ALTO,CA 94304, USA. RI Caspersen, Carl/B-2494-2009 NR 197 TC 93 Z9 93 U1 4 U2 12 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD JUN PY 1992 VL 24 IS 6 SU S BP S201 EP S220 DI 10.1249/00005768-199206001-00004 PG 20 WC Sport Sciences SC Sport Sciences GA HX754 UT WOS:A1992HX75400004 PM 1625547 ER PT J AU KING, AC BLAIR, SN BILD, DE DISHMAN, RK DUBBERT, PM MARCUS, BH OLDRIDGE, NB PAFFENBARGER, RS POWELL, KE YEAGER, KK AF KING, AC BLAIR, SN BILD, DE DISHMAN, RK DUBBERT, PM MARCUS, BH OLDRIDGE, NB PAFFENBARGER, RS POWELL, KE YEAGER, KK TI DETERMINANTS OF PHYSICAL-ACTIVITY AND INTERVENTIONS IN ADULTS SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Review ID CORONARY HEART-DISEASE; MIDDLE-AGED MEN; ACUTE MYOCARDIAL-INFARCTION; LEISURE-TIME EXERCISE; HEALTH PROMOTION; SELF-EFFICACY; RISK-FACTORS; PRIMARY-CARE; DESCRIPTIVE EPIDEMIOLOGY; INCREASING EXERCISE C1 NHLBI,COOPER INST AEROB RES,BETHESDA,MD 20892. UNIV GEORGIA,ATHENS,GA 30602. VET ADM MED CTR,WASHINGTON,DC 20422. STANFORD UNIV,MED CTR,SCH MED,CTR DIS CONTROL,STANFORD,CA 94305. SAN DIEGO STATE UNIV,SAN DIEGO,CA 92182. RP KING, AC (reprint author), STANFORD UNIV,SCH MED,STANFORD CTR RES DIS PREVENT,730 WELCH RD,SUITE B,PALO ALTO,CA 94304, USA. RI Freeman, Lance/B-8774-2009; Loureiro, Nuno/I-6400-2012 OI Loureiro, Nuno/0000-0002-1166-3219 NR 159 TC 248 Z9 251 U1 10 U2 39 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD JUN PY 1992 VL 24 IS 6 SU S BP S221 EP S236 PG 16 WC Sport Sciences SC Sport Sciences GA HX754 UT WOS:A1992HX75400005 PM 1625548 ER PT J AU LENFANT, C AF LENFANT, C TI PHYSICAL-ACTIVITY AND CARDIOVASCULAR HEALTH - SPECIAL EMPHASIS ON WOMEN AND YOUTH SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Editorial Material RP LENFANT, C (reprint author), NHLBI,BETHESDA,MD 20892, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD JUN PY 1992 VL 24 IS 6 SU S BP S191 EP S191 PG 1 WC Sport Sciences SC Sport Sciences GA HX754 UT WOS:A1992HX75400001 ER PT J AU LOUCKS, AB VAITUKAITIS, J CAMERON, JL ROGOL, AD SKRINAR, G WARREN, MP KENDRICK, J LIMACHER, MC AF LOUCKS, AB VAITUKAITIS, J CAMERON, JL ROGOL, AD SKRINAR, G WARREN, MP KENDRICK, J LIMACHER, MC TI THE REPRODUCTIVE-SYSTEM AND EXERCISE IN WOMEN SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Article ID DISTANCE RUNNERS; FEMALE RATS; ATHLETIC AMENORRHEA; LORDOSIS BEHAVIOR; EATING DISORDERS; ESTROUS CYCLES; BODY-FAT; VOLUNTARY; RESPONSES; SECRETION C1 NIH,NATL CTR RES RESOURCES,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT PSYCHIAT,PITTSBURGH,PA 15213. UNIV VIRGINIA,DEPT PEDIAT,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,DEPT PHARMACOL,CHARLOTTESVILLE,VA 22908. BOSTON UNIV,DEPT HLTH SCI,BOSTON,MA 02215. ST LUKES ROOSEVELT HOSP,DEPT MED & OBSTET GYNECOL,NEW YORK,NY 10019. CTR DIS CONTROL,DIV REPROD HLTH,ATLANTA,GA 30333. UNIV FLORIDA,J HILLIS MILLER HLTH CTR,DIV CARDIOL,GAINESVILLE,FL 32610. RP LOUCKS, AB (reprint author), OHIO UNIV,DEPT BIOL SCI,ATHENS,OH 45701, USA. NR 37 TC 39 Z9 43 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD JUN PY 1992 VL 24 IS 6 SU S BP S288 EP S293 PG 6 WC Sport Sciences SC Sport Sciences GA HX754 UT WOS:A1992HX75400011 PM 1625553 ER PT J AU SALLIS, JF SIMONSMORTON, BG STONE, EJ CORBIN, CB EPSTEIN, LH FAUCETTE, N IANNOTTI, RJ KILLEN, JD KLESGES, RC PETRAY, CK ROWLAND, TW TAYLOR, WC AF SALLIS, JF SIMONSMORTON, BG STONE, EJ CORBIN, CB EPSTEIN, LH FAUCETTE, N IANNOTTI, RJ KILLEN, JD KLESGES, RC PETRAY, CK ROWLAND, TW TAYLOR, WC TI DETERMINANTS OF PHYSICAL-ACTIVITY AND INTERVENTIONS IN YOUTH SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Article ID CHILDHOOD OBESITY; AEROBIC EXERCISE; RISK REDUCTION; HEART-DISEASE; CHILDREN; HEALTH; FITNESS; SCHOOL; PROGRAM; ADOLESCENTS C1 UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. NHLBI,BETHESDA,MD 20892. ARIZONA STATE UNIV,TEMPE,AZ 85287. UNIV PITTSBURGH,PITTSBURGH,PA 15260. UNIV S FLORIDA,TAMPA,FL 33620. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20007. STANFORD UNIV,CTR RES DIS PREVENT,STANFORD,CA 94305. MEMPHIS STATE UNIV,MEMPHIS,TN 38152. CALIF STATE UNIV LONG BEACH,LONG BEACH,CA 90840. TUFTS UNIV,SCH MED,BOSTON,MA 02111. UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. RP SALLIS, JF (reprint author), SAN DIEGO STATE UNIV,DEPT PSYCHOL,SAN DIEGO,CA 92182, USA. NR 78 TC 140 Z9 144 U1 6 U2 20 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD JUN PY 1992 VL 24 IS 6 SU S BP S248 EP S257 PG 10 WC Sport Sciences SC Sport Sciences GA HX754 UT WOS:A1992HX75400007 PM 1625550 ER PT J AU SOPKO, G OBARZANEK, E STONE, E AF SOPKO, G OBARZANEK, E STONE, E TI OVERVIEW OF THE NATIONAL-HEART, LUNG, AND BLOOD INSTITUTE WORKSHOP ON PHYSICAL-ACTIVITY AND CARDIOVASCULAR HEALTH SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE LA English DT Article C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. RP SOPKO, G (reprint author), NHLBI,DIV HEART & VASC DIS,FED BLDG,3C06,7500 WISCONSIN AVE,BETHESDA,MD 20892, USA. NR 2 TC 10 Z9 10 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0195-9131 J9 MED SCI SPORT EXER JI Med. Sci. Sports Exerc. PD JUN PY 1992 VL 24 IS 6 SU S BP S192 EP S195 PG 4 WC Sport Sciences SC Sport Sciences GA HX754 UT WOS:A1992HX75400002 PM 1625545 ER PT J AU KIM, SJ ONWUTA, US LEE, YI LI, R BOTCHAN, MR ROBBINS, PD AF KIM, SJ ONWUTA, US LEE, YI LI, R BOTCHAN, MR ROBBINS, PD TI THE RETINOBLASTOMA GENE-PRODUCT REGULATES SP1-MEDIATED TRANSCRIPTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SUSCEPTIBILITY GENE; ENCODED PROTEIN; OSTEO-SARCOMA; RB GENE; II GENE; EXPRESSION; CARCINOMA; IDENTIFICATION; INACTIVATION; ANTIONCOGENE AB We have demonstrated that the retinoblastoma gene product (Rb) can positively regulate transcription from the fourth promoter of the insulinlike growth factor II gene. Two copies of a motif (the retinoblastoma control element) similar to that found in the human c-fos, transforming growth factor beta-1, and c-myc promoters are responsible for conferring Rb regulation to the fourth promoter of the insulinlike growth factor II gene. We have shown that the transcription factor Sp1 can bind to and stimulate transcription from the retinoblastoma control element motif. Moreover, by using a GAL4-Sp1 fusion protein, we have directly demonstrated that Rb positively regulates Sp1 transcriptional activity in vivo. These results indicate that Rb can function as a positive regulator of transcription and that Sp1 is one potential target, either directly or indirectly, for transcriptional regulation by Rb. C1 UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. KOREA ADV INST SCI & TECHNOL,GENET ENGN RES INST,TAEJON,SOUTH KOREA. UNIV CALIF BERKELEY,DEPT MOLEC & CELLULAR BIOL,DIV BIOCHEM & MOLEC BIOL,BERKELEY,CA 94720. FU PHS HHS [30490, 55227] NR 41 TC 271 Z9 271 U1 1 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JUN PY 1992 VL 12 IS 6 BP 2455 EP 2463 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HV309 UT WOS:A1992HV30900001 PM 1588949 ER PT J AU CURCIO, MJ GARFINKEL, DJ AF CURCIO, MJ GARFINKEL, DJ TI POSTTRANSLATIONAL CONTROL OF TY1 RETROTRANSPOSITION OCCURS AT THE LEVEL OF PROTEIN PROCESSING SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID VIRUS-LIKE PARTICLES; SACCHAROMYCES-CEREVISIAE; ELEMENT TRANSPOSITION; RNA INTERMEDIATE; ESCHERICHIA-COLI; SPT3 GENE; YEAST; TRANSFORMATION; TRANSCRIPTION; SEQUENCE AB High-level expression of a transpositionally competent Ty1 element fused to the inducible GAL1 promoter on a 2-mu-m plasmid (pGTy1) overcomes transpositional dormancy in Saccharomyces cerevisiae. To investigate the mechanisms controlling the rate of Ty1 retrotransposition, we quantitated transposition and Ty1 gene products in cells induced and uninduced for expression of pGTy1. The increase in Ty1 transposition was 45- to 125-fold greater than the increase in Ty1 RNA effected by pGTy1 induction. Translational efficiency of Ty1 RNA was not altered in transposition-induced cells, since p190TYA1-TYB1 protein synthesis increased in proportion to steady-state Ty1 RNA levels. Therefore, expression of a pGTy1 element increases the efficiency of Ty1 transposition at a posttranslational level. Galactose induction of pGTy1 enhanced TYA1 protein processing and allowed detection of processed TYB1 proteins, which are normally present at very low levels in uninduced cells. When the ability of genomic Ty1 elements to complement defined mutations in HIS3-marked pGTy1 elements was examined, mutations in the protease domain or certain mutations in the integrase domain failed to be complemented, but mutations in the reverse transcriptase domain were partially complemented by genomic Ty1 elements. Therefore, the activity of Ty1 elements in yeast cells may be limited by the availability of Ty1 protease and possibly integrase. These results suggest that Ty1 transposition is regulated at the level of protein processing and that this regulation is overcome by expression of a pGTy1 element. C1 NCI,FREDERICK CANC RES FACIL,ABL BASIC RES PROGRAM,EUKARYOT GENE EXPRESS LAB,POB B,BLDG 539,FREDERICK,MD 21701. OI Curcio, M. Joan/0000-0001-5361-3909 FU NCI NIH HHS [N01-CO-74101] NR 38 TC 64 Z9 64 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JUN PY 1992 VL 12 IS 6 BP 2813 EP 2825 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HV309 UT WOS:A1992HV30900039 PM 1317008 ER PT J AU YANO, M FALVEY, E GONZALEZ, FJ AF YANO, M FALVEY, E GONZALEZ, FJ TI ROLE OF THE LIVER-ENRICHED TRANSCRIPTION FACTOR DBP IN EXPRESSION OF THE CYTOCHROME P450 CYP2C6 GENE SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ALBUMIN GENE; DIFFERENTIAL REGULATION; MAMMALIAN-CELLS; HEPATOMA-CELLS; RAT; PROTEIN; PROMOTER; DNA; CONVERSION; ACTIVATOR AB The CYP2C6 gene becomes maximally transcriptionally activated in livers of postpubertal rats. We examined the role of upstream DNA and liver-specific transcription factors in regulation of this promoter by use of transient transfection of heterologous chloramphenicol acetyltransferase gene constructs and vectors containing cDNAs encoding the liver-enriched transcription factors HNF-1-alpha, C/EBP, and DBP. Only DBP was able to activate the CYP2C6 promoter in HepG2 cells. Transactivation was not observed in one mouse and two human nonhepatic origin cell lines tested. Analysis of various constructs in which CYP2C6 upstream DNA was deleted revealed that DNA between -38 to -103 was involved in DBP-mediated activation. A partially purified preparation of DBP produced a footprint between -43 and -64 bp upstream of the transcription start site. A P-32-labeled double-stranded oligonucleotide, containing sequence information corresponding to -40 to -65, bound to both partially pure DBP and extracts from livers of rats as young as 1 week and as old as 25 weeks of age, as assessed by gel mobility shift analysis. This binding was eliminated by coincubation with excess unlabeled -40/-65 double-stranded oligonucleotide and by an oligonucleotide corresponding to the D site of the rat albumin gene. A gel mobility shift-Western immunoblot analysis revealed that the -40/-65 sequence bound to DBP only in liver nuclear extracts from rats older than 3 weeks; maximal binding was observed by 7 weeks of age, and no binding was detected from 1-week-old rat liver extracts. Interestingly, the DBP-binding regions of both CYP2C6 and albumin bind to C/EBP, but this factor is capable of transactivating only the latter gene. Although the DBP-binding regions in these two genes share no obvious sequence similarities, the CYP2C6 region contains consensus palindromic half sites for DBP-related binding proteins and affinity for recombinant DBP of 17-fold greater than that of the D site of albumin. This difference in affinity is probably responsible for the markedly lower amounts of DBP required for half-maximal activation of the CYP2C6 promoter, as compared with the albumin promoter, in transactivation transfection assays. These data indicate that the CYP2C6 gene may be regulated, at least in part, by DBP, a liver transcription factor produced when rats reach puberty that may also be involved in maintenance of albumin gene transcription. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. UNIV GENEVA,DEPT MOLEC BIOL,CH-1211 GENEVA 4,SWITZERLAND. NR 30 TC 46 Z9 46 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JUN PY 1992 VL 12 IS 6 BP 2847 EP 2854 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HV309 UT WOS:A1992HV30900042 PM 1588973 ER PT J AU KLEIN, DC ROSEBOOM, PH DONOHUE, SJ MARRS, BL AF KLEIN, DC ROSEBOOM, PH DONOHUE, SJ MARRS, BL TI EVOLUTION OF MELATONIN AS A NIGHT SIGNAL - CONTRIBUTION FROM A PRIMITIVE PHOTOSYNTHETIC ORGANISM SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID BIOSYNTHESIS; SEQUENCE C1 DUPONT CO,DEPT CENT RES & DEV EXPTL STN,WILMINGTON,DE 19880. RP KLEIN, DC (reprint author), NATL INST CHILD HLTH & HUMAN DEV,DEV NEUROBIOL LAB,NEUROENDOCRINOL SECT,BETHESDA,MD 20892, USA. NR 14 TC 11 Z9 11 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell Neurosci. PD JUN PY 1992 VL 3 IS 3 BP 181 EP 183 DI 10.1016/1044-7431(92)90036-2 PG 3 WC Neurosciences SC Neurosciences & Neurology GA HV947 UT WOS:A1992HV94700001 PM 19912858 ER PT J AU MORROW, AL HERBERT, JS MONTPIED, P AF MORROW, AL HERBERT, JS MONTPIED, P TI DIFFERENTIAL-EFFECTS OF CHRONIC ETHANOL ADMINISTRATION ON GABA-A RECEPTOR ALPHA-1 AND ALPHA-6 SUBUNIT MESSENGER-RNA LEVELS IN RAT CEREBELLUM SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID GAMMA-AMINOBUTYRIC ACID; OPERATED CHLORIDE CHANNELS; MEDIAL SEPTAL AREA; BRAIN SYNAPTONEUROSOMES; REGIONAL DISTRIBUTION; ALCOHOL ANTAGONIST; TRANSFECTED CELLS; INVERSE AGONIST; BINDING-SITES; NEURONS C1 UNIV N CAROLINA,SCH MED,CTR ALCOHOL STUDIES,CHAPEL HILL,NC 27599. NIMH,MOLEC PHARMACOL SECT,BETHESDA,MD 20892. RP MORROW, AL (reprint author), UNIV N CAROLINA,SCH MED,DEPT PSYCHIAT,CB 7175,MED RES BLDG A,CHAPEL HILL,NC 27599, USA. NR 46 TC 81 Z9 81 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 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell Neurosci. PD JUN PY 1992 VL 3 IS 3 BP 251 EP 258 DI 10.1016/1044-7431(92)90045-4 PG 8 WC Neurosciences SC Neurosciences & Neurology GA HV947 UT WOS:A1992HV94700010 PM 19912867 ER PT J AU ORDRONNEAU, P WOODLEY, JC GROSSMAN, G ABDULLAH, LH LAZARUS, LH PETRUSZ, P AF ORDRONNEAU, P WOODLEY, JC GROSSMAN, G ABDULLAH, LH LAZARUS, LH PETRUSZ, P TI CHARACTERIZATION OF AN ANTISERUM TO GLYCYL-D-ASPARTATE (GDA) AND ITS USE AS A PROBE FOR ENDOGENOUS N-METHYL-D-ASPARTATE (NMDA)-LIKE COMPOUNDS SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID RAT-BRAIN; IMMUNOCYTOCHEMICAL LOCALIZATION; GLUTAMATE; ANTIBODY; NEURONS; ACID C1 UNIV N CAROLINA,CURRICULUM NEUROBIOL,CHAPEL HILL,NC 27599. NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. RP ORDRONNEAU, P (reprint author), UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27599, USA. NR 16 TC 2 Z9 2 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 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell Neurosci. PD JUN PY 1992 VL 3 IS 3 BP 259 EP 266 DI 10.1016/1044-7431(92)90046-5 PG 8 WC Neurosciences SC Neurosciences & Neurology GA HV947 UT WOS:A1992HV94700011 PM 19912868 ER PT J AU MANECKJEE, R MINNA, JD AF MANECKJEE, R MINNA, JD TI BIOLOGICALLY-ACTIVE MK-801 AND SKF-10 047 BINDING-SITES DISTINCT FROM THOSE IN RAT-BRAIN ARE EXPRESSED ON HUMAN LUNG-CANCER CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article ID SIGMA-RECEPTORS; ASPARTATE NEUROTOXICITY; ANTICONVULSANT MK-801; PHENCYCLIDINE; GROWTH; LINES; DOG; IDENTIFICATION; ANTAGONISTS; ENANTIOMERS AB We have shown previously that cultured human lung cancer cells of different histologic types express multiple opioid receptors that can regulate their growth. In this report, we show that these cells also express specific, saturable, and high-affinity binding sites (Kd approximately 1 nM) for the non-opioid phencyclidine (PCP), {(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine hydrogen maleate} (MK-801) and sigma-N-allylnormetazocine (SKF-10 047) receptor ligands. Characterization of these binding sites showed them to be protein in nature and sensitive to the guanine nucleotide GTP, Pharmacological studies showed that (+) MK-801 and (+) SKF-10 047 competed with each other for their binding sites and also for the methadone binding site present in these cells. However, the mu and delta-opioid ligands did not compete for (+) MK-801 and (+) SKF-10 047 binding sites. In addition, these binding sites on lung cancer cells appear to be distinct from the N-methyl D-aspartate/PCP receptor ionophore complex reported to be present in rat brain. MK-801 and SKF-10 047, at nM concentrations, were found to inhibit the growth of these cells in culture within a few hours of exposure, and this effect was irreversible after 24 h. The growth effects of these ligands could not be reversed by the opioid antagonist naloxone, suggesting involvement of nonopioid type receptors in the actions of these ligands. The abundant expression of biologically active MK-801 and SKF-10 047 binding sites in these cell lines, distinct from those in rat brain, suggests that these cell lines may prove to be a valuable source for further characterization and purification of these binding sites. C1 UNIV TEXAS,SW MED CTR,SIMMON CANC CTR,DALLAS,TX 75235. RP MANECKJEE, R (reprint author), USN,NCI,MED ONCOL BRANCH,DIV CANC TREATMENT,BETHESDA,MD 20889, USA. NR 32 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD JUN PY 1992 VL 3 IS 6 BP 613 EP 619 PG 7 WC Cell Biology SC Cell Biology GA JD737 UT WOS:A1992JD73700004 PM 1323349 ER PT J AU PLOTZ, PH AF PLOTZ, PH TI THE ROLE OF AUTOANTIGENS IN THE INDUCTION AND MAINTENANCE OF AUTOIMMUNITY SO MOLECULAR BIOLOGY REPORTS LA English DT Article DE AUTOANTIBODY; AUTOANTIGEN; AUTOIMMUNITY; B-CELL EPITOPE; SYNTHETASE ID TRANSFER RNA-SYNTHETASE; LUPUS-ERYTHEMATOSUS; SOMATIC MUTATION; CUTANEOUS LUPUS; LEWIS RATS; AUTOANTIBODIES; ANTIBODIES; MYOSITIS; ANTIGEN; HETEROGENEITY RP PLOTZ, PH (reprint author), NIAMSD,ARTHRITIS & RHEUMATISM BRANCH,CONNECT TISSUE DIS SECT,BETHESDA,MD 20892, USA. NR 56 TC 8 Z9 8 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0301-4851 J9 MOL BIOL REP JI Mol. Biol. Rep. PD JUN PY 1992 VL 16 IS 3 BP 127 EP 132 DI 10.1007/BF00464699 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JE191 UT WOS:A1992JE19100001 PM 1508159 ER PT J AU EDWARDS, RA TRAINER, VL BADEN, DG AF EDWARDS, RA TRAINER, VL BADEN, DG TI BREVETOXINS BIND TO MULTIPLE CLASSES OF SITES IN RAT-BRAIN SYNAPTOSOMES SO MOLECULAR BRAIN RESEARCH LA English DT Article DE TOXIN; BREVETOXIN; SITE MULTIPLICITY; SODIUM CHANNEL ID SENSITIVE SODIUM-CHANNELS; PTYCHODISCUS-BREVIS; TOXIN; CELLS AB The brevetoxins (PbTx series), neurotoxins produced by the marine dinoflagellate Ptychodiscus brevis, cause dose-dependent activation of the voltage-sensitive sodium channel (VSSC). Saturation binding studies employing adult rat brain synaptosomes suggest the existence of a high affinity/low capacity (HA/LC) and a second, lower affinity/higher capacity (LA/HC) class of binding site. LIGAND analysis of saxitoxin and brevetoxin saturation binding data yields a statistically identical B(max) for the brevetoxin high affinity/low capacity (HA/LC) site (1.9 +/- 0.98 pmol/mg protein) and for saxitoxin (1.72 +/- 0.78 pmol/mg protein; P < 0.001). The stoichiometry of HA/LC brevetoxin binding and saxitoxin binding approaches 1:1. Covalent modification of synaptosomes with a brevetoxin photoaffinity probe preferentially blocks the HA/LC binding site. Hill plots of saturation binding data yield a coefficient of 1.0 +/- 0.02, demonstrating a lack of cooperativity between brevetoxin binding site classes. K(d) and B(max) for toxin binding are independent of membrane polarity, intimating that the observed low affinity/high capacity (LA/HC) binding characteristics are not due to modification of the HA/LC site, and strongly argue for the presence of multiple brevetoxin binding site classes. Half-maximal binding at the LA/HC site occurs at concentration ranges for which the brevetoxins allosterically modulate binding of other natural toxins to their specific sites. C1 UNIV MIAMI,ROSENSTIEL SCH MARINE & ATMOSPHER SCI,NIEHS,CTR MARINE & FRESHWATER BIOMED SCI,MIAMI,FL 33149. UNIV MIAMI,SCH MED,DEPT BIOCHEM & MOLEC BIOL,MIAMI,FL 33101. NR 19 TC 18 Z9 18 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD JUN PY 1992 VL 14 IS 1-2 BP 64 EP 70 DI 10.1016/0169-328X(92)90011-Y PG 7 WC Neurosciences SC Neurosciences & Neurology GA JA590 UT WOS:A1992JA59000010 PM 1323018 ER PT J AU BARTALENA, L FARSETTI, A FLINK, IL ROBBINS, J AF BARTALENA, L FARSETTI, A FLINK, IL ROBBINS, J TI EFFECTS OF INTERLEUKIN-6 ON THE EXPRESSION OF THYROID HORMONE-BINDING PROTEIN GENES IN CULTURED HUMAN HEPATOBLASTOMA-DERIVED (HEP-G2) CELLS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; ACUTE-PHASE RESPONSE; HEPATOCYTE-STIMULATING FACTORS; CENTRAL NERVOUS-SYSTEM; THYROTROPIN TSH SURGE; TRANSCRIPTIONAL REGULATION; RHEUMATOID-ARTHRITIS; INTERFERON-GAMMA; PLASMA-PROTEINS; FACTOR-II AB T4-binding globulin (TBG) shares a high degree of homology with two serpin antiproteases, alpha-1-antichymotrypsin (ACT) and alpha-1-antitrypsin (AT), whose synthesis is increased during the acute phase phenomenon, which accompanies trauma, infections, and neoplasms. Interleukin-6 (IL-6) is believed to be the main effector of the acute phase response. When evaluated in human hepatoblastoma-derived (Hep G2) cells exposed to different doses of the recombinant human cytokine for variable time intervals, IL-6 caused a dose- and time-dependent decrease in the secretion of [S-35]methionine-labeled TBG, transthyretin (TTR), and albumin. The secretion of ACT and AT was increased. These changes were not due to alterations in the secretory process, since the kinetics of secretion of newly synthesized proteins were not modified. IL-6 did, however, cause a decrease in the steady state levels of mRNA for TTR, TBG, and albumin and an increase in ACT and AT mRNAs. In addition, nuclear run-off assay demonstrated a decrease in the transcription of TTR, TBG, and albumin genes and an increased transcription of the ACT gene. Quantitation of the results showed that changes in the secretion of proteins, in steady state mRNA levels, and in gene transcription were superimposable for each protein, indicating that IL-6 exerts its effect on thyroid hormone-binding proteins mostly at the transcriptional level and that TTR is the thyroid hormone-binding protein showing the most pronounced negative regulation by IL-6. The opposite effect of IL-6 on TBG and the antiproteases, despite their structural homology, underscores gene divergence among these proteins. C1 NIDDKD, GENET & BIOCHEM BRANCH, BETHESDA, MD 20892 USA. UNIV ARIZONA, ARIZONA HLTH SCI CTR, TUCSON, AZ 85724 USA. NR 53 TC 57 Z9 58 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD JUN PY 1992 VL 6 IS 6 BP 935 EP 942 DI 10.1210/me.6.6.935 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HZ964 UT WOS:A1992HZ96400011 PM 1323058 ER PT J AU BURT, DW JAKOWLEW, SB AF BURT, DW JAKOWLEW, SB TI A NEW INTERPRETATION OF A CHICKEN TRANSFORMING GROWTH FACTOR-BETA-4 COMPLEMENTARY-DNA SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID FACTOR-BETA; SEQUENCE; CLONING C1 NCI, CHEMOPREVENT LAB, BETHESDA, MD 20892 USA. RP BURT, DW (reprint author), AFRC, INST ANIM PHYSIOL & GENET RES, DEPT CELLULAR & MOLEC BIOL, EDINBURGH RES STN, ROSLIN EH25 9PS, MIDLOTHIAN, SCOTLAND. NR 8 TC 32 Z9 35 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD JUN PY 1992 VL 6 IS 6 BP 989 EP 992 DI 10.1210/me.6.6.989 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HZ964 UT WOS:A1992HZ96400017 PM 1353860 ER PT J AU KOCH, WH ENNIS, DG LEVINE, AS WOODGATE, R AF KOCH, WH ENNIS, DG LEVINE, AS WOODGATE, R TI ESCHERICHIA-COLI UMUDC MUTANTS - DNA-SEQUENCE ALTERATIONS AND UMUD CLEAVAGE SO MOLECULAR & GENERAL GENETICS LA English DT Article DE ESCHERICHIA-COLI UMUDC MUTANTS; SOS MUTAGENESIS; PCR AMPLIFICATION; DNA SEQUENCE ANALYSIS; CHEMILUMINESCENT IMMUNODETECTION ID POLYMERASE CHAIN-REACTION; RECA-PROTEIN; ULTRAVIOLET-LIGHT; SOS MUTAGENESIS; UV MUTAGENESIS; INDUCIBLE MUTAGENESIS; CHEMICAL MUTAGENESIS; OPERON; GENE; MUTATIONS AB The products of the chromosomally encoded umuDC genes are directly required for mutagenesis in Escherichia coli. Strains with either umuD or umuC mutations are rendered phenotypically non-mutable. To ascertain the molecular basis of this non-mutability, we determined the DNA sequence alterations of seven chromosomal umuDC mutants. Six mutants (umuD1, umuD44, umuD77, umuC36, umuC25, and umuC104) were found to be single base-pair substitutions that resulted in missense mutations. The Tn5 transposon insertion mutation (umuC122) resulted in a missense mutation followed immediately by a termination codon, producing a truncated UmuC protein lacking 102 carboxyl-terminal amino acids. All of the mutations were found to reside in regions of the UmuD and UmuC proteins that share high homology with analogous proteins. Chemiluminescent immunoassays revealed that the umuD1, umuD44, and umuD77 mutations all resulted in a non-cleavable UmuD protein. Because UmuD cleavage is a prerequisite for mutagenesis, the lack of UmuD processing appears to be the molecular basis for the non-mutable phenotype in these strains. These studies re-emphasize the critical nature of the RecA-mediated cleavage of UmuD for inducible mutagenesis and provide insights into the functional domains of the UmuC protein. C1 NICHHD,VIRUSES & CELLULAR BIOL SECT,BETHESDA,MD 20892. US FDA,MOLEC BIOL BRANCH,WASHINGTON,DC 20204. NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. NR 45 TC 31 Z9 33 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD JUN PY 1992 VL 233 IS 3 BP 443 EP 448 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA JB372 UT WOS:A1992JB37200015 PM 1320188 ER PT J AU PINCUS, SH COLE, R PISETSKY, DS AF PINCUS, SH COLE, R PISETSKY, DS TI A DEFECT IN THE HUMORAL IMMUNE-RESPONSE TO PROTEIN ANTIGENS AND HAPTENS IN IMMUNOGLOBULIN-MU HEAVY-CHAIN TRANSGENIC MICE SO MOLECULAR IMMUNOLOGY LA English DT Article ID ENDOGENOUS IMMUNOGLOBULIN; SYNTHETIC POLYPEPTIDES; VARIABLE REGIONS; B-CELLS; ANTIBODIES; GENES; ACTIVATION; EXPRESSION; REPERTOIRE; LINE AB We have examined the antibody response in mice expressing a functionally rearranged mu Ig heavy chain derived from a hybridoma antibody with specificity for the hapten 4-hydroxy-3-nitrophenyl (NP). Transgenic mice and their normal litter-mates were immunized with the antigens NP-OVA, the synthetic polypeptide (Tyr,Glu)-Ala-Lys ((T,G)-A-L), or saline. The presence of serum antibodies to NP-BSA, OVA, (T,G)-A-L, and BSA was examined by ELISA. Sera were evaluated prior to immunization and at periods of up to 4 months following immunization. Prior to immunization, transgenic mice had high levels of IgM anti-NP antibody but no detectable antibody to the other antigens. Both the primary and secondary antibody responses of transgenic mice to NP, OVA, and (T,G)-A-L were depressed when compared with the response of nontransgenic mice. Because of reports that these transgenic mice have increased proportions of CD5+ B-cells. a subpopulation associated with the production of autoantibodies. we examined these mice for the production of both IgG and IgM rheumatoid factors and anti-DNA antibodies. Transgenic mice had a modest increase in the spontaneous production of IgM anti-DNA. These data demonstrate a functional defect in the humoral immune response of mu transgenic mice. C1 DUKE UNIV,DURHAM VET ADM MED CTR,DURHAM,NC 27705. RP PINCUS, SH (reprint author), NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840, USA. FU NIAID NIH HHS [AI-23308, AI-19368]; NIAMS NIH HHS [AR-39162] NR 19 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD JUN PY 1992 VL 29 IS 6 BP 801 EP 806 DI 10.1016/0161-5890(92)90190-9 PG 6 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA HY941 UT WOS:A1992HY94100011 PM 1603097 ER PT J AU HARRY, GJ AF HARRY, GJ TI ACRYLAMIDE-INDUCED ALTERATIONS IN AXONAL-TRANSPORT - BIOCHEMICAL AND AUTORADIOGRAPHIC STUDIES SO MOLECULAR NEUROBIOLOGY LA English DT Article; Proceedings Paper CT SATELLITE SYMP ON AXONAL TRANSPORT AND THE CYTOSKELETON, AT THE 13TH BIENNIAL MEETING OF THE INTERNATIONAL SOC FOR NEUROCHEMISTRY CY JUL 20-22, 1991 CL CAIRNS, AUSTRALIA SP INT SOC NEUROCHEM DE ACRYLAMIDE; AXONAL TRANSPORT; PERIPHERAL NEUROPATHY; GLYCOPROTEINS; NEUROTOXICOLOGY ID RAT SCIATIC-NERVE; FAST AXOPLASMIC-TRANSPORT; INDUCED NEUROPATHY; PERIPHERAL-NERVE; DYING-BACK; INTOXICATION; DEGENERATION; PROTEINS; IMPAIRMENT; DEPOSITION AB Alterations in the axonal transport of proteins, glycoproteins, and gangliosides in sensory neurons of the sciatic nerve were examined in adult male rats exposed to acrylamide (40 mg ip/kg body wt/d for nine consecutive days). Twenty-four hours after the last dose, the L5 dorsal root ganglion (DRG) was injected with either [S-35]methionine to label proteins or [H-3]glucosamine to label glycoproteins and gangliosides. The downflow patterns of radioactivity for [S-35]methionine-labeled proteins and [H-3]glucosamine-labeled gangliosides were unaltered by acrylamide treatment. In contrast, the outflow pattern of labeled glycoproteins displayed a severely attenuated crest with no alteration in velocity, suggesting a preferential transfer with the unlabeled stationary components in the axolemma. Retrograde accumulation of transported glycoproteins and gangliosides was unaltered for at least 6 h; however, by 24 h, there was a 75% decrease in the amount of accumulated material. The accumulation of [S-35]methionine-labeled proteins was not altered . Autoradiographic analysis revealed an acrylamide-induced paucity of transported radiolabeled glycoproteins selectively in myelinated axons with no effect on "nonmyelinated" axons. The pattern of transported proteins was similar in both control and acrylamide-exposed animals. These results suggest a preferential inhibition of glycosylation or axonal transport of glycoproteins in neurons bearing myelinated axons. More importantly, it suggests that interpretations of axonal transport data must be made with the consideration of alterations in selective nerve fibers and not with the tacit assumption that all fibers in the nerve population are equally affected. RP HARRY, GJ (reprint author), NIEHS,SYST TOXIC BRANCH,DEV & REPROD TOXICOL GRP,RES TRIANGLE PK,NC 27709, USA. FU NICHD NIH HHS [HD-03110]; NIEHS NIH HHS [ES01105]; NINDS NIH HHS [NS-11615] NR 53 TC 27 Z9 27 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD SUM-FAL PY 1992 VL 6 IS 2-3 BP 203 EP 216 PG 14 WC Neurosciences SC Neurosciences & Neurology GA KB783 UT WOS:A1992KB78300010 PM 1282332 ER PT J AU OVERBY, LH NISHIO, S WEIR, A CARVER, GT PLOPPER, CG PHILPOT, RM AF OVERBY, LH NISHIO, S WEIR, A CARVER, GT PLOPPER, CG PHILPOT, RM TI DISTRIBUTION OF CYTOCHROME P450-1A1 AND NADPH-CYTOCHROME P450 REDUCTASE IN LUNGS OF RABBITS TREATED WITH 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN - ULTRASTRUCTURAL IMMUNOLOCALIZATION AND INSITU HYBRIDIZATION SO MOLECULAR PHARMACOLOGY LA English DT Article ID MICROSOMAL PREPARATIONS; MONOOXYGENASE SYSTEM; ENZYME COMPONENTS; RIBONUCLEIC-ACID; LOCALIZATION; PULMONARY; LIVER; IDENTIFICATION; METABOLISM; ISOZYME-6 AB Induction of cytochrome P450 1 Al (P450 1 Al) in a variety of tissues is a well established consequence of exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds. Although localization of the induced protein within the lung has been described, the precise intracellular distribution of the enzyme is not clear. Analysis of tissue sections, microsomal proteins, and mRNA from lungs of treated and untreated rabbits established that P450 1 Al had been induced by treatment with TCDD. Rabbit lungs from animals treated with TCDD were examined with immunocytochemistry and in situ hybridization, to identify the cell types that contain P450 1A1 and those that contain mRNA encoding P450 lAl. Endothelial cells of the entire vascular bed of rabbit lung reacted markedly with anti-P450 1 Al. Likewise, cells lining both arteries and veins, as well as capillary endothelial cells, reacted strongly with the cDNA probe for mRNA encoding P450 lAl. Clara cells at all levels of airway labeled prominently for both P-450 lAl and P450 lAl mRNA. In addition, type 2 cells, alveolar macrophages, and, to a lesser degree, ciliated cells reacted with the cDNA probe. P450 reductase, which is required for P450 activity, has previously been identified in Clara cells, type 2 cells, and alveolar macrophages, but not in endothelium of rabbit lung. We have now obtained similar results for the localization of mRNA encoding P-450 reductase. This finding brings into question the function of P450 1 Al in endothelium. C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,POB 12233,MD 19-08,RES TRIANGLE PK,NC 27709. UNIV CALIF DAVIS,SCH VET MED,DEPT ANAT,DAVIS,CA 95616. NR 38 TC 48 Z9 48 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JUN PY 1992 VL 41 IS 6 BP 1039 EP 1046 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JA586 UT WOS:A1992JA58600008 PM 1614408 ER PT J AU IORIO, KR REINLIB, L TABAKOFF, B HOFFMAN, PL AF IORIO, KR REINLIB, L TABAKOFF, B HOFFMAN, PL TI CHRONIC EXPOSURE OF CEREBELLAR GRANULE CELLS TO ETHANOL RESULTS IN INCREASED N-METHYL-D-ASPARTATE RECEPTOR FUNCTION SO MOLECULAR PHARMACOLOGY LA English DT Article ID CALCIUM-CHANNEL ANTAGONISTS; WITHDRAWAL SEIZURES; NMDA RECEPTOR; INTRACELLULAR CA-2+; PHYSICAL-DEPENDENCE; NEURAL CELLS; PC12 CELLS; ADULT-RAT; BRAIN; INHIBITION AB In primary cultures of cerebellar granule cells, activation of the N-methyl-D-aspartate (NMDA) receptor leads to Ca2+ influx. Previous work showed that this response is selectively inhibited by acute exposure to low concentrations of ethanol. The present results demonstrate that the response to NMDA (measured as an increase in intracellular Ca2+ concentration, using fura-2 fluorescence) is significantly enhanced after chronic in vitro exposure of the cells to ethanol (100 mM for 2-4 days; 20 mM for 3 or more days). This enhancement is consistent with an increased number of NMDA receptors, with no change in receptor properties. Specifically, there was no change in the EC50 values for NMDA and glycine or in the magnitude of inhibition of the NMDA response by competitive or uncompetitive antagonists. There was also no change in the ability of acute ethanol to inhibit the NMDA response after chronic exposure of the cells to ethanol. Furthermore, chronic ethanol exposure did not alter depolarization-dependent increases in intracellular Ca2+ observed after exposure of the cells to 30 mM KCl. The data suggest that chronic ethanol exposure produces a selective up-regulation of NMDA receptor function. In the intact animal, such a change may be associated with particular symptoms of ethanol withdrawal, i.e., withdrawal seizures. C1 UNIV COLORADO, HLTH SCI CTR,DEPT PHARMACOL,C-236,4200 E 9TH AVE, DENVER, CO 80262 USA. NIAAA, DIV INTRAMURAL CLIN & BIOL RES, ROCKVILLE, MD 20852 USA. FU NIAAA NIH HHS [AA 9005] NR 46 TC 165 Z9 165 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JUN PY 1992 VL 41 IS 6 BP 1142 EP 1148 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JA586 UT WOS:A1992JA58600022 PM 1535416 ER PT J AU ROBERTS, AB SPORN, MB AF ROBERTS, AB SPORN, MB TI DIFFERENTIAL EXPRESSION OF THE TGF-BETA ISOFORMS IN EMBRYOGENESIS SUGGESTS SPECIFIC ROLES IN DEVELOPING AND ADULT TISSUES SO MOLECULAR REPRODUCTION AND DEVELOPMENT LA English DT Article; Proceedings Paper CT SYMP ON TGF-BETA AND RELATED PROTEINS IN DEVELOPMENT CY SEP 20-23, 1991 CL IOWA STATE UNIV, AMES, IA SP NIH, IOWA STATE UNIV, BIOTECHNOL COUNCIL, IOWA STATE UNIV, GRAD COLL, CELTRIX LABS, GENENTECH, IOWA BEEF IND COUNCIL, JOHNSON & JOHNSON, LILLY RES LABS, NATL ANIM DIS CTR AMES, MIDLAND UNITED DAIRY IND ASSOC HO IOWA STATE UNIV DE TRANSFORMING GROWTH FACTOR-BETA; EMBRYOGENESIS; ISOFORMS ID GROWTH-FACTOR-BETA; TRANSFORMED-CELLS; FACTOR-BETA-1; PROMOTER AB The TGF-beta's are multifunctional, pleiotropic molecules with major effects in control of cellular migration, cellular proliferation, and elaboration of extracellular matrix. Thus far, five distinct isoforms of TGF-beta have been described, each approximately 65-85% homologous and containing the characteristic 9 positionally conserved cysteine residues. Although the actions of the activated mature forms of the different isoforms on cells are qualitatively similar in most cases, there are a few examples of distinct activities. For example, TGF-beta's 1 and 3, but not TGF-beta-2, inhibit the growth of large vessel endothelial cells, and TGF-beta's 2 and 3, but not TGF-beta-1, inhibit the survival of cultured embryonic chick ciliary ganglionic neurons. In addition, selective targeting of the latent forms of the TGF-beta's is suggested by the observation that latent TGF-beta-2 is the prominent isoform found in body fluids such as amniotic fluid, breast milk, and the aqueous and vitreous humor of the eye; it is noteworthy in this regard that TGF-beta-2 is unique among various isoforms in that it lacks a RGD integrin-binding sequence in its precursor. The most dramatic differences in the TGF-beta isoforms are seen at the level of expression, where there is now a wealth of data demonstrating both spatially and temporally distinct expression of both the mRNAs and proteins in developing tissues, regenerating tissues, and in pathologic responses. Moreover, the post-transcriptional regulation of TGF-beta expression by members of the steroid/retinoid family of nuclear receptors is also isoform-specific; thus, treatment of keratinocytes with retinoids induces secretion of TGF-beta-2, whereas treatment of breast cancer cells with gestodene, a synthetic progestin, induces secretion of TGF-beta-1. Recent characterization of the 5' regulatory regions of the human TGF-beta-1, 2, and 3 genes suggests that distinct features of the promoters, including the presence of TATAA boxes and transcription factor binding sites, form the basis for the observed differential transcription. RP ROBERTS, AB (reprint author), NCI,CHEMOPREVENT LAB,BLDG 41,ROOM C629,BETHESDA,MD 20892, USA. NR 28 TC 136 Z9 143 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 1040-452X J9 MOL REPROD DEV JI Mol. Reprod. Dev. PD JUN PY 1992 VL 32 IS 2 BP 91 EP 98 DI 10.1002/mrd.1080320203 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology GA HY940 UT WOS:A1992HY94000002 PM 1637557 ER PT J AU DAWID, IB TAIRA, M GOOD, PJ REBAGLIATI, MR AF DAWID, IB TAIRA, M GOOD, PJ REBAGLIATI, MR TI THE ROLE OF GROWTH-FACTORS IN EMBRYONIC INDUCTION IN XENOPUS-LAEVIS SO MOLECULAR REPRODUCTION AND DEVELOPMENT LA English DT Article; Proceedings Paper CT SYMP ON TGF-BETA AND RELATED PROTEINS IN DEVELOPMENT CY SEP 20-23, 1991 CL IOWA STATE UNIV, AMES, IA SP NIH, IOWA STATE UNIV, BIOTECHNOL COUNCIL, IOWA STATE UNIV, GRAD COLL, CELTRIX LABS, GENENTECH, IOWA BEEF IND COUNCIL, JOHNSON & JOHNSON, LILLY RES LABS, NATL ANIM DIS CTR AMES, MIDLAND UNITED DAIRY IND ASSOC HO IOWA STATE UNIV DE GROWTH FACTORS; INDUCTION; EMBRYOGENESIS ID MESODERM-INDUCING FACTOR; MESSENGER-RNA; CAENORHABDITIS-ELEGANS; RETINOIC ACID; ACTIVIN-A; TGF-BETA; GENE; IDENTIFICATION; ACTIVATION; PROTEIN AB Establishment of the body pattern in all animals, and especially in vertebrate embryos, depends on cell interactions. During the cleavage and blastula stages in amphibians, signal(s) from the vegetal region induce the equatorial region to become mesoderm. Two types of peptide growth factors have been shown by explant culture experiments to be active in mesoderm induction. First, there are several isoforms of fibroblast growth factor (FGF), including aFGF, bFGF, and hst/kFGF. FGF induces ventral, but not the most dorsal, levels of mesodermal tissue; bFGF and its mRNA, and an FGF receptor and its mRNA, are present in the embryo. Thus, FGF probably has a role in mesoderm induction, but is unlikely to be the sole inducing agent in vivo. Second, members of the transforming growth factor-beta (TGF-beta) family. TGF-beta-2 and TGF-beta-3 are active in induction, but the most powerful inducing factors are the distant relatives of TGF-beta named activin A and activin B, which are capable of inducing all types of mesoderm. An important question relates to the establishment of polarity during the induction of mesoderm. While all regions of the animal hemisphere of frog embryos are competent to respond to activins by mesoderm differentiation, only explants that include cells close to the equator form structures with some organization along dorsoventral and anteroposterior axes. These observations suggest that cells in the blastula animal hemisphere are already polarized to some extent, although inducers are required to make this polarity explicit. How do inducing factors affect the differentiation of the responsive tissue? One approach to this question has been to look for gene expression in response to induction, especially the activation of regulatory loci like homeobox genes. Several homeobox-containing genes including Mix.1, Xhox3, X1Hbox1, and X1Hbox6, goosecoid and members of a new class of genes named Xlim, are activated by inducing factors with different patterns of expression in the embryo. Differential expression of regulatory genes probably controls the formation of distinct tissues in an orderly pattern during embryogenesis. RP DAWID, IB (reprint author), NICHHD,MOLEC GENET LAB,BLDG 6,RM 408,BETHESDA,MD 20892, USA. NR 48 TC 17 Z9 17 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1040-452X J9 MOL REPROD DEV JI Mol. Reprod. Dev. PD JUN PY 1992 VL 32 IS 2 BP 136 EP 144 DI 10.1002/mrd.1080320209 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology GA HY940 UT WOS:A1992HY94000008 PM 1353352 ER PT J AU BARNETT, LB LOVELL, DP FELTON, CF GIBSON, BJ COBB, RR SHARPE, DS SHELBY, MD LEWIS, SE AF BARNETT, LB LOVELL, DP FELTON, CF GIBSON, BJ COBB, RR SHARPE, DS SHELBY, MD LEWIS, SE TI ETHYLENE DIBROMIDE - NEGATIVE RESULTS WITH THE MOUSE DOMINANT LETHAL ASSAY AND THE ELECTROPHORETIC SPECIFIC-LOCUS TEST SO MUTATION RESEARCH LA English DT Article DE ETHYLENE DIBROMIDE; DOMINANT LETHAL ASSAY; GERM CELLS; SPECIFIC-LOCUS TEST, ELECTROPHORETIC ID SISTER-CHROMATID EXCHANGES; MICE; 1,2-DIBROMOETHANE; MUTAGENICITY; GLUTATHIONE; INDUCTION; MUTATIONS AB Ethylene dibromide (1,2-dibromoethane; EDB) was tested for the induction of dominant lethal and electrophoretically-detectable specific-locus mutations in the germ cells of DBA/2J male mice. Males were treated with a single intraperitoneal injection of 100 mg/kg EDB and mated to two C57BL/6J females. In the dominant lethal assay, matings were carried out to measure the effect of EDB on meiotic and postmeiotic stages; germ cells representing spermatogonial stem cells were analyzed in the electrophoretic specific-locus test. Neither of these germ cell tests produced any evidence that EDB is a germ cell mutagen. It appears from these data and those reported in the literature that EDB, a genotoxic carcinogen that affects male fertility in some mammalian species, is not mutagenic in the germ cells of the male mouse. C1 BRITISH IND BIOL RES ASSOC, CARSHALTON SM5 4DS, SURREY, ENGLAND. NIEHS, RES TRIANGLE PK, NC 27709 USA. RP BARNETT, LB (reprint author), RES TRIANGLE INST, POB 12194, RES TRIANGLE PK, NC 27709 USA. FU NIEHS NIH HHS [N01-ES-55078] NR 29 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES JI Mutat. Res. PD JUN PY 1992 VL 282 IS 2 BP 127 EP 133 DI 10.1016/0165-7992(92)90085-V PG 7 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HY734 UT WOS:A1992HY73400011 PM 1377351 ER PT J AU CARTY, MP LEVINE, AS DIXON, K AF CARTY, MP LEVINE, AS DIXON, K TI HELA-CELL SINGLE-STRANDED DNA-BINDING PROTEIN INCREASES THE ACCURACY OF DNA-SYNTHESIS BY DNA-POLYMERASE ALPHA INVITRO SO MUTATION RESEARCH LA English DT Article DE DNA POLYMERASE ALPHA; ACCURACY OF DNA REPLICATION; SINGLE-STRANDED DNA-BINDING PROTEIN ID SIMIAN VIRUS-40 DNA; SHUTTLE VECTOR PLASMID; REPLICATION PROTEINS; CALF THYMUS; DROSOPHILA-MELANOGASTER; ESCHERICHIA-COLI; HIGH FIDELITY; TEMPLATE; DELTA; SUBSTITUTION AB To determine whether cellular replication factors can influence the fidelity of DNA replication, the effect of HeLa cell single-stranded DNA-binding protein (SSB) on the accuracy of DNA replication by HeLa cell DNA polymerase-alpha has been examined. An in vitro gap-filling assay, in which the single-stranded gap contains the supF target gene, was used to measure mutagenesis. Addition of SSB to the in vitro DNA synthesis reaction increased the accuracy of DNA polymerase-alpha by 2- to 8-fold. Analysis of the products of DNA synthesis indicated that SSB reduces pausing by the polymerase at specific sites in the single-stranded supF template. Sequence analysis of the types of errors resulting from synthesis in the absence or presence of SSB reveals that, while the errors are primarily base substitutions under both conditions, SSB reduces the number of errors found at 3 hotspots in the supF gene. Thus, a cellular replication factor (SSB) can influence the fidelity of a mammalian DNA polymerase in vitro, suggesting that the high accuracy of cellular DNA replication may be determined in part by the interaction between replication factors, DNA polymerase and the DNA template in the replication complex. C1 NICHHD,VIRUSES & CELLULAR BIOL SECT,BETHESDA,MD 20892. NR 44 TC 20 Z9 20 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD JUN PY 1992 VL 274 IS 1 BP 29 EP 43 DI 10.1016/0921-8777(92)90041-Z PG 15 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HV725 UT WOS:A1992HV72500004 PM 1375330 ER PT J AU DABHOLKAR, M PARKER, R REED, E AF DABHOLKAR, M PARKER, R REED, E TI DETERMINANTS OF CISPLATIN SENSITIVITY IN NONMALIGNANT NON-DRUG-SELECTED HUMAN T-CELL LINES SO MUTATION RESEARCH LA English DT Article DE CISPLATIN SENSITIVITY; T-LYMPHOCYTE CELL LINES, HUMAN ID OVARIAN-CANCER PATIENTS; ACETYLTRANSFERASE GENE-EXPRESSION; DNA ADDUCT LEVELS; RAPID ASSAY; PLATINUM; CIS-DIAMMINEDICHLOROPLATINUM(II); REACTIVATION; QUANTITATION; CHEMOTHERAPY AB We have studied molecular mechanisms of cisplatin sensitivity and resistance in 3 non-malignant, non-drug-selected human T lymphocyte cell lines. HuT 78, H9, and MOLT-4 cells were assessed for sensitivity to cisplatin, DNA damage levels following defined drug exposures, drug accumulation, and DNA repair efficiency as measured by adduct removal from cellular DNA and by host-cell reactivation of cisplatin-modified plasmid DNA. Based on 3-day continuous drug exposures, the IC50 values for the cell lines were: HuT 78, 0.83-mu-M; H9, 0.45-mu-M; and MOLT-4, 0.33-mu-M. These cells retained this order with respect to DNA repair capability, whether measured by platinum-DNA adduct removal from cellular DNA or by host-cell reactivation assays. DNA repair values measured by these two assays were directly related to one another with a linear correlation coefficient of 0.993. At sublethal cisplatin doses the more resistant cells showed the highest levels of drug uptake. When drug uptake levels were 'corrected' for drug-induced cell kill, there were equal levels of DNA repair efficiency for a given level of drug uptake. Absolute levels of cisplatin-DNA adduct repair increased with increasing drug dose. However, at supralethal doses of drug, efficient DNA repair could be overcome in all 3 cell lines with percentage-adduct-removal dropping from a 60-80% range to a < 30% range. We conclude that in non-malignant non-drug-selected human T cells, DNA repair appears to be the primary determinant of cisplatin sensitivity/resistance and that enhanced DNA repair may be a biologic compensatory mechanism for cells that cannot prevent cellular uptake of DNA-damaging agents. C1 NCI,MED BRANCH,BLDG 10,RM 12N226,BETHESDA,MD 20892. NR 23 TC 22 Z9 22 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD JUN PY 1992 VL 274 IS 1 BP 45 EP 56 DI 10.1016/0921-8777(92)90042-2 PG 12 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HV725 UT WOS:A1992HV72500005 PM 1375331 ER PT J AU BOONE, CW STEELE, VE KELLOFF, GJ AF BOONE, CW STEELE, VE KELLOFF, GJ TI SCREENING FOR CHEMOPREVENTIVE (ANTICARCINOGENIC) COMPOUNDS IN RODENTS SO MUTATION RESEARCH LA English DT Article; Proceedings Paper CT WORKSHOP ON ASSESSMENT OF ANTIMUTAGENICITY AND ANTICARCINOGENICITY : END-POINTS AND SYSTEMS, AT THE 3RD INTERNATIONAL CONF ON ANTIMUTAGENESIS AND ANTICARCINOGENESIS CY MAY 05-10, 1991 CL IL CIOCCO, ITALY DE ANTICARCINOGENESIS; ANTIMUTAGENESIS; CHEMOPREVENTION; INHIBITION OF ANTICARCINOGENESIS AND ANTIMUTAGENESIS ID NONSTEROIDAL ANTIINFLAMMATORY DRUG; DIETARY GLUCARATE; CHEMICAL CARCINOGENESIS; MAMMARY TUMORIGENESIS; COLON CARCINOGENESIS; INHIBITION; MICE; RATS; DEHYDROEPIANDROSTERONE; RETINOIDS AB The Chemoprevention Branch is testing dozens of candidate chemopreventive compounds in the following rodent model carcinogenesis systems: mouse skin papillomas, DMBA/TPA induced, rat mammary adenocarcinoma, DMBA and MNU induced, hamster tracheal squamous cell carcinoma, MNU induced, and lung adenocarcinoma, DEN induced, rat and mouse colon adenocarcinoma, AOM and MAM acetate induced, respectively, and mouse bladder carcinoma, hydroxy BBN induced. Significant chemopreventive (i.e., anticancer) effects have been produced with 4-hydroxy-phenylretinamide, difluoromethylornithine, piroxicam, oltipraz (a dithiolthione), calcium glucarate, N-acetylcysteine, beta-carotene, ibuprofen, dehydroepiandrosterone (DHEA) and a 16-fluoro DHEA analog, 8354, tamoxifen, glycyrrhetinic acid, molybdate, selenite, curcumin, and fumaric acid. RP BOONE, CW (reprint author), NCI,CHEMOPREVENT BRANCH,BETHESDA,MD 20892, USA. NR 25 TC 77 Z9 78 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD JUN PY 1992 VL 267 IS 2 BP 251 EP 255 DI 10.1016/0027-5107(92)90069-E PG 5 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HZ647 UT WOS:A1992HZ64700011 PM 1376427 ER PT J AU KELLOFF, GJ BOONE, CW MALONE, WF STEELE, VE AF KELLOFF, GJ BOONE, CW MALONE, WF STEELE, VE TI CHEMOPREVENTION CLINICAL-TRIALS SO MUTATION RESEARCH LA English DT Article; Proceedings Paper CT WORKSHOP ON ASSESSMENT OF ANTIMUTAGENICITY AND ANTICARCINOGENICITY : END-POINTS AND SYSTEMS, AT THE 3RD INTERNATIONAL CONF ON ANTIMUTAGENESIS AND ANTICARCINOGENESIS CY MAY 05-10, 1991 CL IL CIOCCO, ITALY DE ANTICARCINOGENESIS; CHEMOPREVENTION; CANCER PREVENTION; RETINOIDS; BETA-CAROTENE; CALCIUM COMPOUNDS ID SQUAMOUS-CELL CARCINOMA; ORAL LEUKOPLAKIA; BETA-CAROTENE; PREVENTION; HEAD; NECK AB As part of a program to develop drugs which will delay or prevent cancer in humans, the Chemoprevention Branch, National Cancer Institute, National Institutes of Health, is sponsoring 12 Phase I and 22 Phase II and III clinical trials. Three agent classes are significantly advanced in the trials. These are the retinoids, including 13-cis-retinoic acid, retinol, and 4-hydroxyphenylretinamide (nine studies), beta-carotene (seven studies), and calcium compounds (three studies). In addition, six promising new compounds are in Phase I or Phase II trials. These are: piroxicam, ibuprofen, oltipraz (a dithiolthione), difluoromethylornithine, glycyrrhetinic acid, and N-acetylcysteine. Key concepts related to the development of cancer chemopreventive agents are (1) the need for long-term administration, (2) the need for oral route of administration, (3) the matching of toxic side effects to degree of cancer risk. RP KELLOFF, GJ (reprint author), NCI,CHEMOPREVENT BRANCH,BETHESDA,MD 20892, USA. NR 8 TC 45 Z9 45 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD JUN PY 1992 VL 267 IS 2 BP 291 EP 295 DI 10.1016/0027-5107(92)90073-B PG 5 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HZ647 UT WOS:A1992HZ64700015 PM 1376431 ER PT J AU BOJE, KM SKOLNICK, P RABER, J FLETCHER, RT CHADER, G AF BOJE, KM SKOLNICK, P RABER, J FLETCHER, RT CHADER, G TI STRYCHNINE-INSENSITIVE GLYCINE RECEPTORS IN EMBRYONIC CHICK RETINA - CHARACTERISTICS AND MODULATION OF NMDA NEUROTOXICITY SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article ID D-ASPARTATE RECEPTORS; N-METHYL ASPARTATE; AMINO-ACIDS; H-3 GLYCINE; RAT-BRAIN; GLUTAMATE NEUROTOXICITY; CHANNEL COMPLEX; MK-801 BINDING; ION CHANNEL; SITES AB In the mammalian brain, the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor is coupled to a cation channel and a strychnine-insensitive glycine receptor. The present paper demonstrates the presence of NMDA receptor-coupled strychnine-insensitive glycine receptors in embryonic chick retina. Both glycine and 1-aminocyclopropanecarboxylic acid (ACPC) exhibited similar potencies (271 +/- 39 vs 247 +/- 39 nM, respectively) as inhibitors of strychnine-insensitive [H-3]glycine binding to retinal membranes. Moreover, glycine and ACPC enhanced [H-3]MK-801 binding to sites within the NMDA-coupled cation channel in retinal membranes with potencies comparable to those reported in rat brain. While the potency of ACPC was significantly higher than glycine (EC50 54 +/- 12 vs 256 +/- 57 nM, P < 0.02) nn this measure, there were no significant differences in the maximum enhancement (efficacy) of [H-3]MK-801 binding by these compounds. Since glycine appears to be required for the operation of NMDA-coupled cation channels, we examined the effects of glycine and ACPC on NMDA-induced acute excitotoxicity in the 14-day embryonic chick retina. Histological evaluation of retina revealed that either ACPC (10 100-mu-M) or glycine (200-mu-M) attenuated NMDA-induced (200-mu-M) retinal damage, and a combination of these agents produced an enhanced protection against acute NMDA toxicity. ACPC (100-mu-M), but not MK-801 (1-mu-M) also afforded a modest protection against kainate-induced (25-mu-M) retinal damage. These findings demonstrate that while strychnine-insensitive glycine receptors are present in embryonic chick retina, occupation of these sites does not augment the cytotoxic actions of NMDA. Moreover, the ability of ACPC and glycine to attenuate NMDA-induced cytotoxicity does not appear to be mediated through occupation of these sites. C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. RP BOJE, KM (reprint author), NIADDKD,NEUROSCI LAB,BETHESDA,MD 20892, USA. NR 39 TC 11 Z9 11 U1 2 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD JUN PY 1992 VL 20 IS 4 BP 473 EP 486 DI 10.1016/0197-0186(92)90026-N PG 14 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HU629 UT WOS:A1992HU62900006 PM 1339019 ER PT J AU PARKS, RW LEVINE, DS LONG, DL CROCKETT, DJ DALTON, IE WEINGARTNER, H FEDIO, P COBURN, KL SILER, G MATTHEWS, JR BECKER, RE AF PARKS, RW LEVINE, DS LONG, DL CROCKETT, DJ DALTON, IE WEINGARTNER, H FEDIO, P COBURN, KL SILER, G MATTHEWS, JR BECKER, RE TI PARALLEL DISTRIBUTED-PROCESSING AND NEUROPSYCHOLOGY - A NEURAL NETWORK MODEL OF WISCONSIN CARD SORTING AND VERBAL FLUENCY SO NEUROPSYCHOLOGY REVIEW LA English DT Review DE PARALLEL DISTRIBUTED PROCESSING; NEURAL NETWORKS; ASSOCIATIONISM; ARTIFICIAL INTELLIGENCE; WISCONSIN CARD SORTING; VERBAL FLUENCY; NEUROPSYCHOLOGY ID FRONTAL-LOBE; COGNITIVE ARCHITECTURE; INTERACTIVE ACTIVATION; CONNECTIONIST MODELS; HUMAN-BRAIN; PERCEPTION; PSYCHOLOGY; KNOWLEDGE; DYNAMICS; LANGUAGE AB Neural networks can be used as a tool in the explanation of neuropsychological data. Using the Hebbian Learning Rule and other such principles as competition and modifiable interlevel feedback, researchers have successfully modeled a widely used neuropsychological test, the Wisconsin Card Sorting Test. One of these models is reviewed here and extended to a qualitative analysis of how verbal fluency might be modeled, which demonstrates the importance of accounting for the attentional components of both tests. Difficulties remain in programming sequential cognitive processes within a parallel distributed processing (PDP) framework and integrating exceedingly complex neuropsychological tests such as Proverbs. PDP neural network methodology offers neuropsychologists co-validation procedures within narrowly defined areas of reliability and validity. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. NIMH,PSYCHOTHERAPEUT MEDICAT DEV PROGRAM,BETHESDA,MD 20892. SO ILLINOIS UNIV,SCH MED,DEPT PSYCHIAT,DIV NEUROPSYCHOL,SPRINGFIELD,IL 62794. DIGITAL SYST RESOURCES,FAIRFAX,VA. UNIV TEXAS,DEPT MATH,ARLINGTON,TX 76019. UNIV BRITISH COLUMBIA,DEPT PSYCHIAT,VANCOUVER V6T 1W5,BC,CANADA. NINCDS,BETHESDA,MD 20892. UNIV CALIF DAVIS,DEPT PSYCHOL,DAVIS,CA 95616. MERCER UNIV,SCH MED,DEPT PSYCHIAT,MACON,GA 31207. FU NIA NIH HHS [P30 AG08014]; NIMH NIH HHS [R01 MH/AG41821-01, R01 MH/AG41821-02] NR 110 TC 11 Z9 11 U1 2 U2 6 PU PLENUM PUBL CORP PI NEW YORK PA CONSULTANTS BUREAU 233 SPRING ST, NEW YORK, NY 10013 SN 1040-7308 J9 NEUROPSYCHOL REV JI Neuropsychol. Rev. PD JUN PY 1992 VL 3 IS 2 BP 213 EP 233 DI 10.1007/BF01108843 PG 21 WC Psychology, Clinical; Neurosciences SC Psychology; Neurosciences & Neurology GA KE910 UT WOS:A1992KE91000003 PM 1338621 ER PT J AU DETERAWADLEIGH, SD BERRETTINI, WH GOLDIN, LR MARTINEZ, M HSIEH, WT HOEHE, MR ENCIO, IJ COFFMAN, D ROLLINS, DY MUNIEC, D CHOI, H GUROFF, JJ WIESCH, D THAI, N GERSHON, ES AF DETERAWADLEIGH, SD BERRETTINI, WH GOLDIN, LR MARTINEZ, M HSIEH, WT HOEHE, MR ENCIO, IJ COFFMAN, D ROLLINS, DY MUNIEC, D CHOI, H GUROFF, JJ WIESCH, D THAI, N GERSHON, ES TI A SYSTEMATIC SEARCH FOR A BIPOLAR PREDISPOSING LOCUS ON CHROMOSOME-5 SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE MAPPING; BIPOLAR ILLNESS; CHROMOSOME-5; MARKERS; RESTRICTION FRAGMENT LENGTH POLYMORPHISMS ID LIFETIME PSYCHIATRIC-DIAGNOSIS; POLYMERASE CHAIN-REACTION; MANIC-DEPRESSIVE ILLNESS; INSITU HYBRIDIZATION; GENETIC-LINKAGE; X-CHROMOSOME; DNA POLYMORPHISMS; RECEPTOR GENE; LONG ARM; MAPS AB Chromosome 5 markers spanning the pter to the qter were used to examine linkage to bipolar illness in 14 pedigrees. Twenty-four loci were examined in 237 individuals, of whom 69 were either bipolars or schizoaffectives. Marker genotypes were determined for each individual and lod scores were calculated under a dominant disease model with a maximum penetrance of 85%, a disease gene frequency of 0.015, a variable age of onset, and a phenocopy rate of 0.001. Under the assumption that bipolar illness is genetically homogeneous, the total lod scores from all pedigrees with each marker were uniformly lower than -2.0, suggesting the absence of linkage to disease at any of these loci. Multipoint analysis allowed exclusion of intervals between markers. When lod scores were calculated allowing for heterogeneity, no subset of linked families was found. These results indicate that in our pedigree series almost the entire mapped region of chromosome 5 can be excluded for linkage to bipolar illness. RP DETERAWADLEIGH, SD (reprint author), NIMH,CLIN NEUROSCI BRANCH,BLDG 10,ROOM 3N218,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Martinez, Maria/B-3111-2013; OI Martinez, Maria/0000-0003-2180-4537; Encio, Ignacio/0000-0003-1732-1989 NR 58 TC 28 Z9 28 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD JUN PY 1992 VL 6 IS 4 BP 219 EP 229 PG 11 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA HW998 UT WOS:A1992HW99800003 PM 1632891 ER PT J AU HILL, JM HARRIS, A HILTONCLARKE, DI AF HILL, JM HARRIS, A HILTONCLARKE, DI TI REGIONAL DISTRIBUTION OF GUANINE NUCLEOTIDE-SENSITIVE AND GUANINE NUCLEOTIDE-INSENSITIVE VASOACTIVE-INTESTINAL-PEPTIDE RECEPTORS IN RAT-BRAIN SO NEUROSCIENCE LA English DT Article ID SUPERIOR CERVICAL-GANGLION; ADENYLATE-CYCLASE; PLASMA-MEMBRANES; CEREBRAL-CORTEX; POLYPEPTIDE VIP; BINDING; LIVER; HETEROGENEITY; PITUITARY; GLUCAGON AB Based on the ability of guanine nucleotides to inhibit the binding of vasoactive intestinal peptide to its receptors, a guanosine 5'-triphosphate analog, guanylyl-imidodiphosphate, was used to differentiate two subtypes (or different functional states of a single subtype) of vasoactive intestinal peptide receptor in brain with in vitro autoradiography. In most brain regions, guanylyl-imidodiphosphate reduced vasoactive intestinal peptide binding between 40 and 60%. However, in the supraoptic nucleus, locus coeruleus, interpeduncular nucleus, facial nucleus, olfactory tubercle and periventricular hypothalamic nucleus, 80% or more of vasoactive intestinal peptide binding was inhibited. In other brain regions, including the medial geniculate, olfactory bulbs, and ventral thalamic nuclei, guanylyl-imidodiphosphate had little effect on vasoactive intestinal peptide binding. In liver, lung and intestine it also partly inhibited vasoactive intestinal peptide binding. Electrophoretic analysis of vasoactive intestinal peptide, covalently cross-linked to its receptors in brain membranes, revealed a pair of bands between 44,000 and 52,000 mol. wt, a component at 64,000 mol. wt and another at 92,000 mol. wt. All were displaceable with vasoactive intestinal peptide but guanylyl-imidodiphosphate displaced only the 64,000 mol. wt band suggesting that the GTP-sensitive vasoactive intestinal peptide receptor seen in brain sections has a molecular weight of about 61,000. The differential sensitivity to guanylyl-imidodiphosphate suggests the existence of at least two vasoactive intestinal peptide receptor subtypes in brain, with distinct regional distribution, and may reflect differential coupling to second messenger systems. C1 PEPTIDE DESIGN LP, GERMANTOWN, MD 20874 USA. RP NICHHD, DEV NEUROBIOL LAB, NEUROCHEM UNIT, 36-2A21, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 29 TC 47 Z9 47 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0306-4522 EI 1873-7544 J9 NEUROSCIENCE JI Neuroscience PD JUN PY 1992 VL 48 IS 4 BP 925 EP 932 DI 10.1016/0306-4522(92)90280-F PG 8 WC Neurosciences SC Neurosciences & Neurology GA HZ792 UT WOS:A1992HZ79200017 PM 1321366 ER PT J AU JOHNSON, EO KAMILARIS, TC CHROUSOS, GP GOLD, PW AF JOHNSON, EO KAMILARIS, TC CHROUSOS, GP GOLD, PW TI MECHANISMS OF STRESS - A DYNAMIC OVERVIEW OF HORMONAL AND BEHAVIORAL HOMEOSTASIS SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE STRESS; HPA AXIS; AUTONOMIC SYSTEM; AGING; REPRODUCTIVE SUPPRESSION; GROWTH RETARDATION; IMMUNOSUPPRESSION; DEPRESSION ID CORTICOTROPIN-RELEASING-FACTOR; CENTRAL NERVOUS-SYSTEM; PITUITARY-ADRENAL SYSTEM; INHIBIT GROWTH-HORMONE; LUTEINIZING-HORMONE; ANOREXIA-NERVOSA; LOCUS COERULEUS; BETA-ENDORPHIN; FACTOR CRF; IMMUNOREACTIVE NEURONS AB Environmental events, both physical and emotional, can produce stress reactions to widely varying degrees. Stress can affect many aspects of physiology, and levels of stress, emotional status, and means of coping with stress can influence health and disease. The stress system consists of brain elements, of which the main components are the corticotropin-releasing hormone (CRH) and locus ceruleus (LC)-norepinephrine (NE)/autonomic systems, as well as their peripheral effectors, the pituitary-adrenal axis and the autonomic system, which function to coordinate the stress response. Activation of the stress system results in behavioral and physical changes which allow the organism to adapt. This system is closely integrated with other central nervous system elements involved in the regulation of behavior and emotion, in addition to the axes responsible for reproduction, growth and immunity. With current trends in stress research which focus on understanding the mechanisms through which the stress-response is adaptive or becomes maladaptive, there is a growing association of stress system dysfunction, characterized by hyperactivity and/or hypoactivity to various pathophysiological states. The purpose of this review is to 1) define the concepts of stress and the stress response from a historical perspective, 2) present a dynamic overview of the biobehavioral mechanisms that participate in the stress response, and 3) examine the consequences of stress on the physiologic and behavioral well-being of the organism by integrating knowledge from apparently disparate fields of science. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RP JOHNSON, EO (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N262,BETHESDA,MD 20892, USA. NR 217 TC 447 Z9 458 U1 8 U2 83 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0149-7634 J9 NEUROSCI BIOBEHAV R JI Neurosci. Biobehav. Rev. PD SUM PY 1992 VL 16 IS 2 BP 115 EP 130 DI 10.1016/S0149-7634(05)80175-7 PG 16 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA HX369 UT WOS:A1992HX36900001 PM 1630726 ER PT J AU ELDRIDGE, R PARRY, D AF ELDRIDGE, R PARRY, D TI VESTIBULAR SCHWANNOMA (ACOUSTIC NEUROMA) CONSENSUS DEVELOPMENT CONFERENCE - SUMMARY SO NEUROSURGERY LA English DT Editorial Material RP ELDRIDGE, R (reprint author), NCI,CLIN EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 35 Z9 37 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD JUN PY 1992 VL 30 IS 6 BP 962 EP 964 PG 3 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA HV274 UT WOS:A1992HV27400030 PM 1614607 ER PT J AU FALETTO, DL TSARFATY, I KMIECIK, TE GONZATTI, M SUZUKI, T WOUDE, GFV AF FALETTO, DL TSARFATY, I KMIECIK, TE GONZATTI, M SUZUKI, T WOUDE, GFV TI EVIDENCE FOR NONCOVALENT CLUSTERS OF THE C-MET PROTOONCOGENE PRODUCT SO ONCOGENE LA English DT Article ID GROWTH-FACTOR RECEPTOR; SCATTER FACTOR; SIGNAL TRANSDUCTION; TYROSINE KINASES; PURIFICATION; HEPATOCYTES; CELLS; DIMERIZATION; MECHANISM; MOBILITY AB The met proto-oncogene is a member of the tyrosine kinase growth factor receptor family and is the receptor for hepatocyte growth factor (HGF) or scatter factor. The primary met product is a 150 kDa precursor that is glycosylated to generate a 170 kDa (p170met) proreceptor protein. The mature form of the receptor is generated by cleavage of p170met to yield a disulfide-linked 140 kDa beta-subunit (p140met) and a 45 kDa alpha-subunit (p45met). Both products are glycosylated. Under non-reducing conditions both p170met and the alpha, beta-disulfide-linked protein are detected as a 185 kDa product (p185met), but only alpha-beta heterodimeric p185met is cross-linked and rendered resistant to disulfide reduction with membrane-impermeable 6.4 angstrom. linker length cross-linking reagents. These data indicate that the p170 precursor is not on the cell surface. Cross-linking experiments using 12-angstrom linker reagents yield multimeric forms of alpha-beta heterodimeric p185met greater than 500 kDa in size. These multimeric forms are produced in all cell lines tested regardless of the levels of protein expressed. These data suggest that alpha-beta heterodimeric p185met occurs in clusters or patches on the cell surface. Immunohistochemical analysis of met protein in the absence of ligand reveals a clustered staining pattern on the cell surface. C1 FUKUSHIMA MED SCH,DEPT PATHOL 2,FUKUSHIMA 96012,JAPAN. RP WOUDE, GFV (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 40 TC 41 Z9 41 U1 2 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JUN PY 1992 VL 7 IS 6 BP 1149 EP 1157 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HU642 UT WOS:A1992HU64200012 PM 1317541 ER PT J AU WANG, YS SUGIYAMA, H AXELSON, H PANDA, CK BABONITS, M MA, A STEINBERG, JM ALT, FW KLEIN, G WIENER, F AF WANG, YS SUGIYAMA, H AXELSON, H PANDA, CK BABONITS, M MA, A STEINBERG, JM ALT, FW KLEIN, G WIENER, F TI FUNCTIONAL HOMOLOGY BETWEEN N-MYC AND C-MYC IN MURINE PLASMACYTOMAGENESIS - PLASMACYTOMA DEVELOPMENT IN N-MYC TRANSGENIC MICE SO ONCOGENE LA English DT Article ID LEUKEMIA-VIRUS; V-ABL; CHROMOSOMAL TRANSLOCATIONS; CELLULAR ONCOGENES; KINASE-ACTIVITY; BALB/C MICE; B-CELLS; GENE; EXPRESSION; AMPLIFICATION AB Mouse plasmacytomas induced by pristane oil alone, or in combination with Abelson murine leukemia virus (A-MuLV), regularly carry one of three alternative chromosomal translocations that juxtapose c-myc to immunoglobulin heavy- or light-chain loci. E-mu-c-myc transgenic mice develop translocation-free plasmacytomas after induction by pristane oil and/or A-MuLV [Sugiyama, H., Silva, S., Wang, Y., Weber, G., Babonits, M., Rosen, A., Wiener, F. & Klein, G. (1990). Int. J. Cancer, 46, 845-8521. In order to test whether another member of the myc family, N-myc, could play a similar role as c-myc, we treated E-mu- N -myc transgenic mice with pristane and helper-free A-MuLV. Of 20 mice that received a single pristane injection followed by A-MuLV, 17 developed plasmacytomas with a mean latency period of 54 +/- 20 days. In a corresponding group that only received a single pristane injection, five out of six transgenic mice developed plasmacytomas with a mean latency period of 142 +/- 32 days. However, after three monthly injections of pristane, all 15 transgenic mice developed plasmacytomas with a mean latency period of 128 +/- 20 days. All plasmacytomas expressed the N-myc transgene, while none of them expressed either c-myc or endogenous N-myc. None of the tumors carried the usual plasmacytoma-associated translocations. C1 COLUMBIA UNIV COLL PHYS & SURG,HOWARD HUGHES MED INST,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT BIOCHEM,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT MICROBIOL,NEW YORK,NY 10032. NCI,GENET LAB,BETHESDA,MD 20892. RP WANG, YS (reprint author), KAROLINSKA INST,DEPT TUMOR BIOL,BOX 60400,S-10401 STOCKHOLM 60,SWEDEN. FU NCI NIH HHS [5 RO1 CA 14054-15] NR 38 TC 18 Z9 18 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JUN PY 1992 VL 7 IS 6 BP 1241 EP 1247 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HU642 UT WOS:A1992HU64200023 PM 1375720 ER PT J AU PEPOSE, JS BUERGER, DG PAUL, DA QUINN, TC DARRAGH, TM DONEGAN, E AF PEPOSE, JS BUERGER, DG PAUL, DA QUINN, TC DARRAGH, TM DONEGAN, E TI NEW DEVELOPMENTS IN SEROLOGIC SCREENING OF CORNEAL DONORS FOR HIV-1 AND HEPATITIS-B VIRUS-INFECTIONS SO OPHTHALMOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; SURFACE-ANTIGEN; ENZYME-IMMUNOASSAY; HOMOSEXUAL MEN; HTLV-III; AQUEOUS-HUMOR; ANTIBODY; TRANSMISSION; MARKERS; SERUM AB Purpose: The authors evaluated different methods to serologically screen potential cadaveric corneal donors for human immunodeficiency virus type 1 (HIV-1) and hepatitis B virus (HBV) infections. Methods: Three commercially available enzyme-linked immunosorbent assays (ELISAs) for antibodies against HIV-1, a supplemental ELISA test for HIV antigen, and a radioimmunoassay and two ELISAs for hepatitis B surface antigen were compared using serum from cadavers with acquired immune deficiency syndrome (AIDS), cadavers with high risk factors for HIV infection, and cadavers with no known risk of HIV infection, along with respective confirmatory testing. Results: The ELISA tests for HIV antibodies from Abbott Laboratories, Electronucleonics, and Organon-Teknika showed sensitivities of 94.3%, 94.3%, and 97.1%, respectively, compared with the autopsy diagnosis of AIDS in 35 cadavers. The sensitivities of the HIV-1 antibody ELISAs ranged between 73% and 87% compared with positive Western blots in testing 118 sera from cadavers at high risk of HIV-infection, but not manifesting AIDS at the time of death. Supplemental ELISA testing for HIV-1 antigen, in an effort to close the seronegative window, failed to identify any HIV antigen-positive sera confirmed by neutralization that were not also positive for antibodies to HIV-1 by ELISA and Western blot. The ELISA for HBV surface antigen had an overall sensitivity of 92.9% and specificity of only 81.3% compared with radioimmunoassay in testing 409 sera. Monoclonal ELISAs for HIV-1 antigen and HBV surface antigen paradoxically had lower specificity than polyclonal ELISAs, with false positivity correlating with hemolysis and with increasing death to puncture time. Conclusion. ELISA testing for antibodies against HIV-1 is relatively but not absolutely effective, should be accompanied by historical screening for risk factors, and does not appear to benefit from supplemental ELISA testing for HIV-1 antigen. ELISA testing for HBV surface antigen has lower specificity in screening cadaveric sera when compared with radioimmunoassay. C1 WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. NIAID,BETHESDA,MD 20892. ABBOTT LABS,N CHICAGO,IL 60064. UNIV CALIF SAN FRANCISCO,SCH MED,DEPT PATHOL,SAN FRANCISCO,CA 94143. RP PEPOSE, JS (reprint author), WASHINGTON UNIV,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,BOX 8096,660 S EUCLID AVE,ST LOUIS,MO 63110, USA. FU NEI NIH HHS [EY 08143] NR 64 TC 21 Z9 21 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD JUN PY 1992 VL 99 IS 6 BP 879 EP 888 PG 10 WC Ophthalmology SC Ophthalmology GA HX373 UT WOS:A1992HX37300014 PM 1630777 ER PT J AU ELDRIDGE, R PARRY, DM AF ELDRIDGE, R PARRY, DM TI SUMMARY OF THE VESTIBULAR SCHWANNOMA CONSENSUS DEVELOPMENT CONFERENCE - NATIONAL-INSTITUTES-OF-HEALTH, BETHESDA, MARYLAND, DECEMBER 11-13, 1991 SO OTOLARYNGOLOGIC CLINICS OF NORTH AMERICA LA English DT Article C1 US PHS,BETHESDA,MD. NCI,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 0030-6665 J9 OTOLARYNG CLIN N AM JI Otolaryngol. Clin. N. Am. PD JUN PY 1992 VL 25 IS 3 BP 729 EP 732 PG 4 WC Otorhinolaryngology SC Otorhinolaryngology GA HW298 UT WOS:A1992HW29800011 ER PT J AU BAUM, BJ AF BAUM, BJ TI AGE-RELATED VULNERABILITY SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID SJOGRENS-SYNDROME; PAROTID-SALIVA; FLOW-RATE; SECRETION; FEATURES; GLANDS AB This presentation considers the vulnerability of the upper alimentary and respiratory tracts to environmental insults during aging. A specific example, salivary gland secretion, is discussed. Available data suggest that while aging per se does not affect salivary performance adversely, it does appear to compromise the glands in such a way that older persons are more vulnerable to exogenous factors that can reduce secretory capacity and, consequently, diminish oropharyngeal health. RP BAUM, BJ (reprint author), NIDR,CLIN INVEST & PATIENT CARE BRANCH,BLDG 10,ROOM 1N-113,BETHESDA,MD 20892, USA. NR 22 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD JUN PY 1992 VL 106 IS 6 BP 730 EP 732 PG 3 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA JA316 UT WOS:A1992JA31600019 PM 1608640 ER PT J AU TRAUB, RJ PECHMAN, P IADAROLA, MJ GEBHART, GF AF TRAUB, RJ PECHMAN, P IADAROLA, MJ GEBHART, GF TI FOS-LIKE PROTEINS IN THE LUMBOSACRAL SPINAL-CORD FOLLOWING NOXIOUS AND NONNOXIOUS COLORECTAL DISTENSION IN THE RAT SO PAIN LA English DT Article DE PAIN; C-FOS; COLORECTAL DISTENSION; INFLAMMATION; DORSAL HORN ID PEPTIDE-LIKE IMMUNOREACTIVITY; VISCERAL AFFERENT-FIBERS; C-FOS; URINARY-BLADDER; PELVIC NERVE; MECHANICAL STIMULATION; FUNCTIONAL-PROPERTIES; CONDUCTION-VELOCITY; PROJECTION NEURONS; GENE-EXPRESSION AB The rat lumbosacral spinal cord was immunocytochemically stained for Fos-like immunoreactivity following repetitive colorectal distention (CRD) to 20, 40 or 80 mm Hg. Following all 3 distention pressures, Fos-like immunoreactive (Fos-ir) nuclei were observed primarily in laminae I-II, V-VII and X, although some labeled nuclei were observed in laminae III-IV. Eighty mm Hg CRD resulted in significantly more Fos-ir nuclei than 20 or 40 mm Hg CRD. Morphological examination of the colon revealed clear signs of inflammation following 80 but not 20 mm Hg CRD. Acute 20 mm Hg CRD is a non-noxious stimulus, suggesting that both noxious and non-noxious visceral stimuli can induce Fos-like immunoreactivity in the spinal cord. It is suggested that activation of neuropeptide-containing small-diameter primary afferents is necessary, although not necessarily sufficient, to induce c-fos in the rat spinal cord. C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. RP TRAUB, RJ (reprint author), UNIV IOWA,COLL MED,DEPT PHARMACOL,IOWA CITY,IA 52242, USA. OI Traub, Richard/0000-0001-8633-6311 FU NHLBI NIH HHS [HL 32295]; NINDS NIH HHS [NS 19912] NR 62 TC 109 Z9 115 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD JUN PY 1992 VL 49 IS 3 BP 393 EP 403 DI 10.1016/0304-3959(92)90247-9 PG 11 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA JA872 UT WOS:A1992JA87200015 PM 1408305 ER PT J AU CHRISTOFFEL, KK SCHEIDT, PC AGRAN, PF KRAUS, JF MCLOUGHLIN, E PAULSON, JA AF CHRISTOFFEL, KK SCHEIDT, PC AGRAN, PF KRAUS, JF MCLOUGHLIN, E PAULSON, JA TI STANDARD DEFINITIONS FOR CHILDHOOD INJURY RESEARCH - EXCERPTS OF A CONFERENCE REPORT SO PEDIATRICS LA English DT Article DE INJURIES; MOTOR VEHICLE INJURY; DROWNING; BURNS; VIOLENCE; FALLS AB As awareness of the huge human and other costs of injury has grown, research has expanded. There has not been any standard set of terminology for use in this research. As a result, research and surveillance data are too often difficult to interpret and compare. To overcome this impediment to gains in needed knowledge about childhood injuries, a conference was held in 1989 by the National Institute of Child Health and Human Development to develop a set of standard definitions. The full conference report is available from the US Government Printing Office. This report presents excerpts, emphasizing those-core-variables likely to be of use to the largest number of investigators. The conference recommendations presented address cross-cutting factors (age, race/ethnicity, location, socioeconomic status, and biopsychosocial development), effect modifiers (exposure, medical risk factors, substance abuse, time, injury severity, and social risk factors), and specific injuries (motor vehicle injuries, central nervous system injuries, falls, fire/burns, drowning and violence). It is expected that childhood injury investigators will strive to meet the recommendations of this conference and that use of these definitions will lead to improvements in research and, ultimately, to revision of the definitions. RP CHRISTOFFEL, KK (reprint author), NICHHD,OFF RES REPORTING,BLDG 31,RM 2A32,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 18 TC 44 Z9 44 U1 0 U2 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUN PY 1992 VL 89 IS 6 BP 1027 EP 1034 PN 1 PG 8 WC Pediatrics SC Pediatrics GA HX376 UT WOS:A1992HX37600006 PM 1594342 ER PT J AU KLEINMAN, RE BAKER, SS BELL, EF HATCH, TF KLISH, WJ LEIBEL, RL UDALL, JN CHENEY, M CHOPRA, J FORD, C HUBBARD, VS LEVIN, E PRENDERGAST, A STEMARIE, M SMITH, A YIP, R LAUER, RM AF KLEINMAN, RE BAKER, SS BELL, EF HATCH, TF KLISH, WJ LEIBEL, RL UDALL, JN CHENEY, M CHOPRA, J FORD, C HUBBARD, VS LEVIN, E PRENDERGAST, A STEMARIE, M SMITH, A YIP, R LAUER, RM TI THE USE OF WHOLE COWS MILK IN INFANCY SO PEDIATRICS LA English DT Article ID IRON NUTRITIONAL-STATUS; DECLINING PREVALENCE; OLDER INFANTS; UNITED-STATES; BLOOD-LOSS; FORMULA; DEFICIENCY; ANEMIA; RATS; ABSORPTION C1 BUR NUTR SCI,OTTAWA,ONTARIO,CANADA. US FDA,BETHESDA,MD 20014. USDA,ATHENS,GA 30601. NIDDKD,PHOENIX,AZ. NICHHD,BETHESDA,MD 20892. CTR DIS CONTROL,ATLANTA,GA 30333. AMER ACAD PEDIAT,CARDIOL SECT,EVANSTON,IL 60204. RP KLEINMAN, RE (reprint author), AMER ACAD PEDIAT,COMM NUTR,EVANSTON,IL 60204, USA. NR 45 TC 66 Z9 66 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUN PY 1992 VL 89 IS 6 BP 1105 EP 1109 PN 1 PG 5 WC Pediatrics SC Pediatrics GA HX376 UT WOS:A1992HX37600024 ER PT J AU SCHEIDT, PC WILSON, MH STERN, MS AF SCHEIDT, PC WILSON, MH STERN, MS TI BICYCLE HELMET LAW FOR CHILDREN - A CASE-STUDY OF ACTIVISM IN INJURY CONTROL SO PEDIATRICS LA English DT Article DE BICYCLE HELMET; INJURY PREVENTION; LEGISLATION ID SAFETY; CAMPAIGN AB In 1990, the first regulation requiring the use of helmets for bicyclists younger than 16 years of age was passed in Howard County, Maryland. This unexpected injury control measure resulted from the convergence of multiple factors and efforts: the bicycle-related deaths of two children from the same middle school, creative students and teachers motivated by these deaths, a responsive legislator to introduce the legislation, available surveillance and research statistics supporting the need and efficacy for helmet use, increased national awareness of the importance of helmet use to prevent bicycle-related head injuries, and organized national and local public health groups to support the legislation. This case study of activism in injury control illustrates the importance of supporting research, of well-organized public health coalitions and groups, and of creative community activists motivated by local circumstances. C1 JOHNS HOPKINS UNIV HOSP,DEPT PEDIAT,BALTIMORE,MD 21205. AMER ACAD PEDIAT,MARYLAND CHAPTER,LEGISLAT COMM,HIGHLAND,MD. RP SCHEIDT, PC (reprint author), NICHHD,CTR RES MOTHERS & CHILDREN,HUMAN LEARNING & BEHAV BRANCH,BETHESDA,MD 20892, USA. NR 14 TC 15 Z9 15 U1 0 U2 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUN PY 1992 VL 89 IS 6 BP 1248 EP 1250 PN 2 PG 3 WC Pediatrics SC Pediatrics GA HX377 UT WOS:A1992HX37700022 PM 1594383 ER PT J AU COSTA, PT MCCRAE, RR AF COSTA, PT MCCRAE, RR TI 4 WAYS 5 FACTORS ARE BASIC SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article; Proceedings Paper CT MEETING OF THE INTERNATIONAL SOC FOR THE STUDY OF INDIVIDUAL DIFFERENCES CY JUL, 1991 CL OXFORD, ENGLAND SP INT SOC STUDY INDIVIDUAL DIFFERENCES ID 5-FACTOR MODEL; INDIVIDUAL-DIFFERENCES; NATURAL-LANGUAGE; PERSONALITY; DIMENSIONS; INVENTORY; SCALES; QUESTIONNAIRES; UNIVERSALITY; JAPANESE AB The five-factor model has recently received wide attention as a comprehensive model of personality traits. The claim that these five factors represent basic dimensions of personality is basad on four lines of reasoning and evidence: (a) longitudinal and cross-observer studies demonstrate that all five factors are enduring dispositions that are manifest in patterns of behavior; (b) traits related to each of the factors are found in a variety of personality systems and in the natural language of trait description; (c) the factors are found in different age, sex, race, and language groups, although they may be somewhat differently expressed in different cultures; and (d) evidence of heritability suggests that all have some biological basis. To clarify some remaining confusions about the five-factor model, the relation between Openness and psychometric intelligence is described, and problems in factor rotation are discussed. RP COSTA, PT (reprint author), NIA,GERONTOL RES CTR,BALTIMORE,MD 21224, USA. NR 107 TC 619 Z9 628 U1 31 U2 183 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0191-8869 J9 PERS INDIV DIFFER JI Pers. Individ. Differ. PD JUN PY 1992 VL 13 IS 6 BP 653 EP 665 DI 10.1016/0191-8869(92)90236-I PG 13 WC Psychology, Social SC Psychology GA HT554 UT WOS:A1992HT55400003 ER PT J AU OWENS, IS RITTER, JK AF OWENS, IS RITTER, JK TI THE NOVEL BILIRUBIN PHENOL UDP-GLUCURONOSYLTRANSFERASE UGT1 GENE LOCUS - IMPLICATIONS FOR MULTIPLE NONHEMOLYTIC FAMILIAL HYPERBILIRUBINEMIA PHENOTYPES SO PHARMACOGENETICS LA English DT Review AB At least three types of congenital nonhemolytic unconjugated hyperbilirubinemias, including the rare Crigler-Najjar (CN) diseases (Types I or II) and Gilbert's syndrome (affecting 6% of the population) are associated with either absent or reduced hepatic UDP-glucuronosyltransferase (transferase) activity towards the potentially toxic endogenous acceptor, bilirubin. Here, we review the biochemical studies associated with these deficiencies. Accumulated evidence from studies with an animal model of CN Type I syndrome, the Gunn strain of hyperbilirubinemic rats, suggested that multiple isozymes are absent. These confounding observations have been clarified by a flurry of reports which have revealed the molecular basis for the complex disease phenotype in the Gunn rat and by the isolation and description of a novel human gene complex, UGT1, which encodes multiple and independently-regulated transferase isozymes that contain identical carboxyl terminal regions (246 amino acids). Finally, we discuss the implications of the gene organization and genetic defects determined for four different CN Type I individuals as a basis for a model which explains the inheritance pattern and genotypes of other familial unconjugated hyperbilirubinemias. RP OWENS, IS (reprint author), NICHHD,GENET DISORDERS DRUG METAB SECT,HUMAN GENET BRANCH,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 72 Z9 75 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD JUN PY 1992 VL 2 IS 3 BP 93 EP 108 DI 10.1097/00008571-199206000-00001 PG 16 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA LG853 UT WOS:A1992LG85300001 PM 1306114 ER PT J AU WOODS, JH KATZ, JL WINGER, G AF WOODS, JH KATZ, JL WINGER, G TI BENZODIAZEPINES - USE, ABUSE, AND CONSEQUENCES SO PHARMACOLOGICAL REVIEWS LA English DT Review ID PSYCHOTROPIC-DRUG USE; NEW-YORK-STATE; TERM THERAPEUTIC USE; DEPENDENT PSYCHIATRIC-INPATIENTS; CUMULATIVE DOSING PROCEDURE; INTERMEDIATE-CARE FACILITY; PSYCHOACTIVE SUBSTANCE USE; NERVOUS-SYSTEM REACTIVITY; GENERAL MEDICAL PATIENTS; SYMBOL SUBSTITUTION TEST C1 NIDA,ADDICT RES CTR,PSYCHOBIOL LAB,BALTIMORE,MD. RP WOODS, JH (reprint author), UNIV MICHIGAN,SCH MED,DEPT PHARMACOL,M6322 MED SCI I,ANN ARBOR,MI 48109, USA. OI Katz, Jonathan/0000-0002-1068-1159 NR 867 TC 438 Z9 442 U1 10 U2 28 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-6997 J9 PHARMACOL REV JI Pharmacol. Rev. PD JUN PY 1992 VL 44 IS 2 BP 151 EP 347 PG 197 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KG619 UT WOS:A1992KG61900001 PM 1356276 ER PT J AU FALLOON, J AF FALLOON, J TI CURRENT THERAPY FOR HIV-INFECTION AND ITS INFECTIOUS COMPLICATIONS - A PRACTICAL SUMMARY FOR PRIMARY CARE PHYSICIANS SO POSTGRADUATE MEDICINE LA English DT Article ID DIAGNOSIS AB Primary care physicians can play a crucial role in the care of patients with HIV infection. Treatment often requires orchestration of many complex drug regimens. In addition, the patient must make informed decisions about a broad range of care-related issues. Steps in the care of such patients include (1) staging of HIV infection, (2) instituting antiretroviral therapy, and (3) preventing opportunistic infections plus treating opportunistic infections when present. A wide range of established and investigational agents are available for these purposes, and new ones are continually being discovered. RP FALLOON, J (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BLDG 10,RM 7D43,BETHESDA,MD 20892, USA. NR 15 TC 0 Z9 0 U1 0 U2 0 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 0032-5481 J9 POSTGRAD MED JI Postgrad. Med. PD JUN PY 1992 VL 91 IS 8 BP 115 EP & PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA HZ530 UT WOS:A1992HZ53000014 PM 1603746 ER PT J AU BUKH, J PURCELL, RH MILLER, RH AF BUKH, J PURCELL, RH MILLER, RH TI SEQUENCE-ANALYSIS OF THE 5' NONCODING REGION OF HEPATITIS-C VIRUS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE NON-A, NON-B HEPATITIS; GENETIC HETEROGENEITY; VIRUS EVOLUTION ID HOG-CHOLERA VIRUS; NON-B-HEPATITIS; MOLECULAR-CLONING; NUCLEOTIDE-SEQUENCE; NON-A; GENOME AB We have determined the nucleotide sequence of the 5' noncoding (NC) region of the hepatitis C virus (HCV) genome in 44 isolates from around the world. We have identified several HCV isolates with significantly greater sequence heterogeneity than reported previously within the 5' NC region. The most distantly related isolates were only 90.1 % identical. Nucleotide insertions were seen in three isolates. Analysis of the nucleotide sequence from 44 HCV isolates in this study combined with that of 37 isolates reported in the literature reveals that the 5' NC region of HCV consists of highly conserved domains interspersed with variable domains. The consensus sequence was identical to the prototype HCV sequence. Nucleotide variations were found in 45 (16 %) of the 282 nucleotide positions analyzed and were primarily located in three domains of significant heterogeneity (positions -239 to -222, -167 to -118, and -100 to -72). Conversely, there were three highly conserved domains consisting of 18, 22, and 63 completely invariant nucleotides (positions -263 to -246, -199 to -178, and -65 to -3, respectively). Two nucleotide domains within the 5' NC region, conserved among all HCV isolates studied to date, shared statistically significant similarity with pestivirus 5' NC sequences, providing further evidence for a close evolutionary relationship between these two groups of viruses. Additional analysis revealed the presence of short open reading frames in all HCV isolates. Our sequence analysis of the 5' NC region of the HCV genome provides additional information about conserved elements within this region and suggests a possible functional role for the region in viral replication or gene expression. These data also have implications for selection of optimal primer sequences for the detection of HCV RNA by the PCR assay. C1 NIAID, INFECT DIS LAB, HEPATITIS VIRUSES SECT, BETHESDA, MD 20892 USA. NR 24 TC 367 Z9 375 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 1 PY 1992 VL 89 IS 11 BP 4942 EP 4946 DI 10.1073/pnas.89.11.4942 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HX168 UT WOS:A1992HX16800034 PM 1317578 ER PT J AU RAUSCHECKER, JP TIAN, B KORTE, M EGERT, U AF RAUSCHECKER, JP TIAN, B KORTE, M EGERT, U TI CROSSMODAL CHANGES IN THE SOMATOSENSORY VIBRISSA BARREL SYSTEM OF VISUALLY DEPRIVED ANIMALS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CAT; MOUSE; PLASTICITY ID SUPERIOR COLLICULUS; CORTEX; MOUSE; RAT; REPRESENTATION; ORGANIZATION; INNERVATION; DEPRIVATION AB Cats deprived of vision from birth adapt remarkably well to their situation and show little behavioral impairment. They seem to compensate for their lack of vision by relying more on their auditory and tactile senses. We report here that the facial vibrissae, which are most important for tactile orientation in many animals, show supernormal growth in both cats and mice that have been deprived of vision from birth. Furthermore, the whisker representation in the somatosensory cortical barrel field shows a concomitant enlargement in binocularly enucleated mice: individual barrels are expanded in size by up to one-third. The increased use of the vibrissae in visually deprived animals may stimulate both their own growth and, via activation of the respective neural pathways, the expansion of their central representation. C1 MAX PLANCK INST BIOL CYBERNET,W-7400 TUBINGEN,GERMANY. RP RAUSCHECKER, JP (reprint author), NIMH,NATL INST HLTH ANIM CTR,POB 289,POOLESVILLE,MD 20837, USA. RI Rauschecker, Josef/A-4120-2013; Egert, Ulrich/D-3954-2009 OI Egert, Ulrich/0000-0002-4583-0425 NR 35 TC 73 Z9 73 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 1 PY 1992 VL 89 IS 11 BP 5063 EP 5067 DI 10.1073/pnas.89.11.5063 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HX168 UT WOS:A1992HX16800059 PM 1594614 ER PT J AU KINOSHITA, CM GEWURZ, AT SIEGEL, JN YING, SC HUGLI, TE COE, JE GUPTA, RK HUCKMAN, R GEWURZ, H AF KINOSHITA, CM GEWURZ, AT SIEGEL, JN YING, SC HUGLI, TE COE, JE GUPTA, RK HUCKMAN, R GEWURZ, H TI A PROTEASE-SENSITIVE SITE IN THE PROPOSED CA2+-BINDING REGION OF HUMAN SERUM AMYLOID-P COMPONENT AND OTHER PENTRAXINS SO PROTEIN SCIENCE LA English DT Article DE CALCIUM-BINDING PROTEIN; C-REACTIVE PROTEIN; HAMSTER FEMALE PROTEIN; PENTRAXIN; SERUM AMYLOID-P COMPONENT ID C-REACTIVE PROTEIN; AMINO-ACID-SEQUENCE; GALACTOSE-BINDING PROTEIN; HUMAN-TISSUE; CALCIUM; LOCALIZATION; FIBRINOGEN; SUBCOMPONENT; CALMODULIN; COMPLEMENT AB Serum amyloid P component (SAP) is a decamer of 10 identical 25.5-kDa subunits. Limited proteolysis of SAP with alpha-chymotrypsin cleaves the subunit into two fragments of 18 and 7.5 kDa, although the fragments stay together in the decamer under nondenaturing conditions. Proteolysis does not occur in the presence of Ca2+ (10 mM). Cleavage with alpha-chymotrypsin prevents the Ca2+-dependent binding of SAP to zymosan extract, nucleosomes, and DNA. The alpha-chymotrypsin cleavage site identified is in a region of SAP that is highly conserved in members of the human C-reactive protein (CRP) family of proteins (pentraxins) to which SAP belongs and is similar to the Ca2+-binding site in calmodulin and related Ca2+-binding proteins (Nguyen, N.Y., Suzuki, A., Boykins, R.A., & Liu, T.-Y., 1986, J. Biol. Chem. 261, 10456-10465). Treatment of SAP with other proteases (trypsin, Pronase, and Nagarse protease) yields fragmentation patterns upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) that are similar to those obtained with alpha-chymotrypsin. Two other members of the pentraxin family of proteins, hamster female protein and rabbit CRP, also exhibit similar fragmentation patterns on SDS-PAGE when treated with the various proteases. Recently, it has been shown that the homologous protein, human CRP, is cleaved in the same homologous position as cleavage of SAP by alpha-chymotrypsin, resulting in the loss of Ca2+ binding (as shown by equilibrium dialysis) and Ca2+-dependent binding reactivities (Kinoshita, C.M., Ying, S.-C., Hugli, T.E., Siegel, J.N., Potempa, L.A., Jiang, H.J., Houghten, R.A., & Gewurz, H., 1989, Biochemistry 28, 9840-9848). These results indicate that the protease sensitivity of this proposed Ca2+-binding region has been conserved and may play an important regulatory role, perhaps via the control of Ca2+-dependent properties of these proteins. C1 RUSH MED COLL,DEPT IMMUNOL MICROBIOL,CHICAGO,IL 60612. SCRIPPS CLIN & RES FDN,DEPT IMMUNOL,LA JOLLA,CA 92037. NIH,ROCKY MT LABS,HAMILTON,MT 59840. NR 54 TC 37 Z9 38 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0961-8368 J9 PROTEIN SCI JI Protein Sci. PD JUN PY 1992 VL 1 IS 6 BP 700 EP 709 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JA625 UT WOS:A1992JA62500001 PM 1304912 ER PT J AU BIHARI, K HILL, JL MURPHY, DL AF BIHARI, K HILL, JL MURPHY, DL TI OBSESSIVE-COMPULSIVE CHARACTERISTICS IN PATIENTS WITH IDIOPATHIC SPASMODIC TORTICOLLIS SO PSYCHIATRY RESEARCH LA English DT Article DE BASAL GANGLIA; MOTOR DISORDERS; DYSTONIA; YALE-BROWN OBSESSIVE-COMPULSIVE SCALE; SYMPTOM CHECKLIST-90-REVISED ID DOUBLE-BLIND; DISORDER; DEPRESSION AB To explore suggested relationships between involuntary motor disorders and obsessive-compulsive disorder (OCD), we evaluated obsessive-compulsive characteristics in patients with idiopathic spasmodic torticollis (IST). Twenty-two patients with IST had significantly higher scores than 29 age- and sex-matched healthy controls on the Yale-Brown Obsessive-Compulsive Scale and the obsessionality subscale of the Symptom Checklist-90-Revised. The IST patients also had higher (though not significantly so) scores on the Maudsley Obsessive-Compulsive Inventory. Their Beck Depression Inventory scores were likewise higher than those of controls. These results provide additional support for the theory of a link between basal ganglia disorders and psychiatric disorders. C1 NIMH,INTRAMURAL RES PROGRAM,CLIN SCI LAB,BETHESDA,MD 20892. NR 26 TC 36 Z9 37 U1 1 U2 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD JUN PY 1992 VL 42 IS 3 BP 267 EP 272 DI 10.1016/0165-1781(92)90118-M PG 6 WC Psychiatry SC Psychiatry GA JD717 UT WOS:A1992JD71700007 PM 1496058 ER PT J AU ROBINSON, JK AF ROBINSON, JK TI QUANTITATIVE-ANALYSES OF CHOICE IN RAT AND PIGEON SO PSYCHOLOGICAL RECORD LA English DT Article ID INTERVAL SCHEDULES; CONCURRENT; PERFORMANCE; REINFORCEMENT; CHANGEOVER; MULTIPLE AB Studies of choice in nonhuman animals that presented concurrent variable-interval variable-interval schedules of reinforcement were quantitatively reviewed. Empirical parameters representing bias and sensitivity in the generalized matching equation were calculated across studies and compared. Undermatching was the most common relationship observed. No consistent bias was shown. An analysis of moderating variables also revealed that the laboratory in which an experiment was conducted, and the year of publication were related to the sensitivity parameter. This reanalysis confirms that a proportional relationship between the ratios of response rates and ratios of reinforcement rates is not an accurate description of concurrent VI VI performance. C1 UNIV NEW HAMPSHIRE,DURHAM,NH 03824. RP ROBINSON, JK (reprint author), NIMH,EXPTL THERAPEUT BRANCH,BEHAV NEUROPHARMACOL UNIT,BLDG 10,ROOM 4N214,BETHESDA,MD 20892, USA. NR 43 TC 4 Z9 4 U1 1 U2 2 PU PSYCHOLOGICAL RECORD PI GAMBIER PA KENYON COLLEGE, GAMBIER, OH 43022 SN 0033-2933 J9 PSYCHOL REC JI Psychol. Rec. PD SUM PY 1992 VL 42 IS 3 BP 437 EP 445 PG 9 WC Psychology, Multidisciplinary SC Psychology GA JB409 UT WOS:A1992JB40900009 ER PT J AU KATZ, JL WITKIN, JM AF KATZ, JL WITKIN, JM TI EFFECTS OF QUINPIROLE AND SKF-38393 ALONE AND IN COMBINATION IN SQUIRREL-MONKEYS TRAINED TO DISCRIMINATE COCAINE SO PSYCHOPHARMACOLOGY LA English DT Article DE COCAINE; QUINPIROLE; SKF-38393; D1 AGONIST; D2 AGONIST; DRUG INTERACTIONS; ROUTE OF ADMINISTRATION; DISCRIMINATIVE-STIMULUS EFFECTS; BEHAVIOR; SQUIRREL MONKEYS ID DOPAMINE RECEPTOR; RHESUS-MONKEYS; D1; AGONISTS; BLOCKADE AB The present study was designed to assess the behavioral similarity of the effects of prototype dopamine receptor-subtype selective agonists and cocaine. Squirrel monkeys (N = 4) were trained with food reinforcement to press one of two levers after administration of IV cocaine (0.3 mg/kg) or the other lever after saline. After training, IV cocaine-produced reliable responding on the cocaine lever (> 98%), whereas saline produced reliable responding on the alternate lever (> 98%). The D2 agonist, quinpirole (0.003-1.0 mg/kg, IM), produced dose-related increases in cocaine-appropriate responding, with maximal effects of 62%. When delivered IV, quinpirole (0.01-0.17 mg/kg) was approximately twice as potent, but no more effective. The D1 agonist, SKF 38393 (0.3-30.0 mg/kg, IM or 3.0-17.0 mg/kg, IV) failed to produce any significant cocaine-appropriate responding. Further, pretreatment with SKF 38393 (either 0.3 or 10.0 mg/kg, IM) did not significantly alter the the quinpirole (0.01-1.0 mg/kg, IM) dose-effect curve. The effects of these drugs differ from those previously reported in rats, suggesting a species difference that may be of importance in evaluating the behavioral pharmacology of cocaine. RP KATZ, JL (reprint author), NIDA,ADDICT RES CTR,PRECLIN PHARMACOL BRANCH,PSYCHOBIOL LAB,POB 5180,BALTIMORE,MD 21224, USA. OI Katz, Jonathan/0000-0002-1068-1159 NR 16 TC 18 Z9 18 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD JUN PY 1992 VL 107 IS 2-3 BP 217 EP 220 DI 10.1007/BF02245140 PG 4 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA HQ547 UT WOS:A1992HQ54700009 PM 1352052 ER PT J AU ULRICHSEN, J PARTILLA, JS DAX, EM AF ULRICHSEN, J PARTILLA, JS DAX, EM TI LONG-TERM ADMINISTRATION OF META-CHLOROPHENYLPIPERAZINE (META-CPP) TO RATS INDUCES CHANGES IN SEROTONIN RECEPTOR-BINDING, DOPAMINE LEVELS AND LOCOMOTOR-ACTIVITY WITHOUT ALTERING PROLACTIN AND CORTICOSTERONE SECRETION SO PSYCHOPHARMACOLOGY LA English DT Article DE SEROTONIN; META-CHLOROPHENYLPIPERAZINE; RECEPTORS, 5-HT1A, 5-HT1B, 5-HT2; LOCOMOTOR ACTIVITY; NEUROTRANSMITTERS; PROLACTIN; CORTICOSTERONE ID ANTI-DEPRESSANT TREATMENT; FRONTAL-CORTEX; LIGAND-BINDING; AGONIST; BRAIN; 5-HYDROXYTRYPTAMINE; IMIPRAMINE; SITES; HIPPOCAMPUS; RESPONSES AB Meta-chlorophenylpiperazine (mCPP) is a serotonin (5-HT) agonist with antidepressant actions. In order to investigate the effects of chronic mCPP treatment the drug was administered to rats for 15 days (5 mg/kg twice daily). Controls were administered saline. Long-term mCPP treatment led to a 36% increase in [H-3]8-hydroxy-2-(di-n-propylamino)tetralin ([H-3]8-OH-DPAT) binding to 5-HT1a receptors in hippocampus and a 74% decrease in [H-3]ketanserin binding to 5-HT2 receptors in cortex, while (-)[I-125]iodocyanopindolol ([I-125]CYP) binding to 5-HT1b receptors in hypothalamus and striatum was unchanged. In hypothalamus, chronic mCPP treatment decreased the levels of dopamine (DA) but not 5-HT. The usual suppression of locomotor activity induced by acute mCPP administration was less after long-term mCPP treatment. Brain and plasma levels of mCPP following an acute dose were not different between controls and rats previously administered mCPP, suggesting that altered rate of metabolism of the drug did not explain the tolerance to the mCPP-induced decrease in locomotor activity. mCPP-induced prolactin (PRL) and corticosterone release were not changed by previous long-term mCPP administration. Thus, chronic mCPP administration to rats induced alterations in density of 5-HT receptor subtypes, hypothalamic levels of DA and locomotor behavior. RP ULRICHSEN, J (reprint author), NIDA,ADDICT RES CTR,NEUROENDOCRINOL IMMUNOL LAB,POB 5180,BALTIMORE,MD 21224, USA. NR 40 TC 35 Z9 35 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD JUN PY 1992 VL 107 IS 2-3 BP 229 EP 235 DI 10.1007/BF02245142 PG 7 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA HQ547 UT WOS:A1992HQ54700011 PM 1352053 ER PT J AU KATZ, JL RICAURTE, GA WITKIN, JM AF KATZ, JL RICAURTE, GA WITKIN, JM TI REINFORCING EFFECTS OF ENANTIOMERS OF N,N-DIMETHYLAMPHETAMINE IN SQUIRREL-MONKEYS SO PSYCHOPHARMACOLOGY LA English DT Article DE REINFORCING EFFECTS OF DRUGS; DRUG SELF ADMINISTRATION; N,N-DIMETHYLAMPHETAMINE; STEREOISOMERS; ABUSE LIABILITY ASSESSMENT; FIXED-RATIO SCHEDULE; SQUIRREL MONKEYS ID AMPHETAMINE; METHYLAMPHETAMINE; ISOMERS; RATS AB Reinforcing effects of the (+)- and (-)-enantiomers of N,N-dimethylamphetamine, a drug that is abused in humans, were studied in squirrel monkeys (Siamiri sciureus) trained under schedules of intermittent cocaine reinforcement. During training, each 30th response produced an injection of cocaine (fixed-ratio schedule), which was followed by a 1-min period during which lights were out and responses had no scheduled consequences (timeout). Sessions in which cocaine injections were scheduled alternated in an irregular sequence with sessions in which saline injections were scheduled. After training, response rates were well maintained by cocaine (response rates approximated 1.4 responses per second) but occurred relatively infrequently during sessions in which saline was injected (response rates approximated 0.3 responses per second). Doses of 10 to 56-mu-g/kg/injection of (+)-N,N-dimethylamphetamine maintained rates of responding significantly higher than those maintained by saline. The (-)-enantiomer did not maintain rates of responding that were higher than those maintained by saline when tested at doses up to 100-mu-g/kg/injection. These findings support previous results indicating that N,N-dimethylamphetamine will function as a reinforcer in laboratory animals. Further, they suggest that the significant reinforcing activity of this drug is restricted to the (+)-enantiomer. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21224. RP KATZ, JL (reprint author), NIDA,ADDICT RES CTR,PSYCHOBIOL LAB,POB 5180,BALTIMORE,MD 21224, USA. OI Katz, Jonathan/0000-0002-1068-1159 NR 22 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD JUN PY 1992 VL 107 IS 2-3 BP 315 EP 318 DI 10.1007/BF02245154 PG 4 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA HQ547 UT WOS:A1992HQ54700023 PM 1615131 ER PT J AU SKOLNICK, P MILLER, R YOUNG, A BOJE, K TRULLAS, R AF SKOLNICK, P MILLER, R YOUNG, A BOJE, K TRULLAS, R TI CHRONIC TREATMENT WITH 1-AMINOCYCLOPROPANECARBOXYLIC ACID DESENSITIZES BEHAVIORAL-RESPONSES TO COMPOUNDS ACTING AT THE N-METHYL-D-ASPARTATE RECEPTOR COMPLEX SO PSYCHOPHARMACOLOGY LA English DT Article DE GLYCINE; 1-AMINOCYCLOPROPANECARBOXYLIC ACID; MK-801; N-METHYL-D-ASPARTATE; FORCED SWIM TEST ID LONG-TERM POTENTIATION; FUNCTIONAL ANTAGONISTS; ANTICONVULSANT MK-801; RAT HIPPOCAMPUS; BINDING-SITES; AMINO-ACIDS; GLYCINE; ANTIDEPRESSANTS; PHENCYCLIDINE; GLUTAMATE AB Functional antagonists at the N-methyl-D-aspartate (NMDA) receptor complex produce anti-depressant-like actions in preclinical models. Thus, an injection of a glycine partial agonist (1-aminocyclopropanecarboxylic acid; ACPC), a competitive NMDA antagonist (2-amino-7-phosphonoheptanoic acid; AP-7) or a use-dependent cation channel blocker (MK-801) reduced immobility in the forced swim test (FST) with efficacies comparable to imipramine (Trullas and Skolnick 1990). Seven daily injections of ACPC (200-400 mg/kg) abolished the effects of both this compound (200-1200 mg/kg) and AP-7 (200-300 mg/kg) in the FST. The loss in effectiveness of ACPC required 7 days of treatment to become fully manifest, and was reversed by discontinuing treatment. Other agents active in the FST (e.g. MK-801, imipramine, and nifedipine) were unaffected by this regimen. Moreover, ACPC and AP-7 remained active in the FST following repeated injections of MK-801, AP-7, or imipramine. Chronic treatment with ACPC did not affect its actions in the elevated plus-maze, but significantly attenuated the convulsant and lethal effects of NMDA (125 mg/kg). Tissue levels of ACPC indicate the modified behavioral responses produced by chronic treatment are not attributable to pharmacokinetic factors. These findings suggest repeated administration of ACPC may effect an "uncoupling" of NMDA and glycine receptors, resulting in an apparent desensitization of the behavioral actions of substances acting at these sites. RP SKOLNICK, P (reprint author), NIDDK,NEUROSCI LAB,BETHESDA,MD 20892, USA. RI Trullas, Ramon/D-2197-2016 OI Trullas, Ramon/0000-0001-7951-9881 NR 39 TC 77 Z9 77 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD JUN PY 1992 VL 107 IS 4 BP 489 EP 496 DI 10.1007/BF02245261 PG 8 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA HU011 UT WOS:A1992HU01100005 PM 1534910 ER PT J AU SHTERN, F AF SHTERN, F TI DIGITAL MAMMOGRAPHY AND RELATED TECHNOLOGIES - A PERSPECTIVE FROM THE NATIONAL-CANCER-INSTITUTE SO RADIOLOGY LA English DT Editorial Material DE BREAST RADIOGRAPHY, TECHNOLOGY; COMPUTERS, DIAGNOSTIC AID; IMAGES, TRANSMISSION ID DIAGNOSIS AB The National Cancer Institute held a workshop entitled "Breast Imaging: State-of-the-Art and Technologies of the Future" in September 1991. This article describes some of the presentations given at the workshop as well as relevant data in the literature and discusses their implications. The workshop faculty identified digital mammography as the evolving technology with the greatest potential impact on management of breast cancer. On the basis of the workshop findings and literature review, the author proposed to from the National Digital Mammography Development Group, which will stimulate research in digital mammography and its integration with related technologies: image processing for improved lesion contrast, automated computer-aided diagnosis for enhanced breast cancer detection and characterization, and teleradiology for facilitated radiologic consultation with recognized experts in the field. It is expected that the National Digital Mammography Development Group will facilitate transfer of advanced digital imaging technology to breast cancer clinics. RP SHTERN, F (reprint author), NCI,DIV CANC TREATMENT,RADIAT RES PROGRAM,DIAGNOST IMAGING RES BRANCH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 11 TC 82 Z9 84 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JUN PY 1992 VL 183 IS 3 BP 629 EP 630 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HV578 UT WOS:A1992HV57800008 PM 1584908 ER PT J AU MILLER, DL AF MILLER, DL TI NEUROLOGIC COMPLICATIONS OF PETROSAL SINUS SAMPLING SO RADIOLOGY LA English DT Letter C1 GEORGETOWN UNIV,SCH MED,DEPT RADIOL,WASHINGTON,DC 20057. RP MILLER, DL (reprint author), NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892, USA. NR 2 TC 2 Z9 2 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JUN PY 1992 VL 183 IS 3 BP 878 EP 878 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HV578 UT WOS:A1992HV57800061 PM 1584954 ER PT J AU BROWN, DP AF BROWN, DP TI MORTALITY OF WORKERS EMPLOYED AT ORGANOCHLORINE PESTICIDE MANUFACTURING PLANTS - AN UPDATE SO SCANDINAVIAN JOURNAL OF WORK ENVIRONMENT & HEALTH LA English DT Article DE ALDRIN, CANCER; CHLORDANE; DICHLORODIPHENYLTRICHLOROETHANE; DIELDRIN; EPIDEMIOLOGY; HEPTACHLOR; LIVER CANCER; ORGANOCHLORINE PESTICIDES ID COHORT AB A previous mortality study among four organochlorine pesticide manufacturers was updated through 1987. The organochlorine pesticides included chlordane; heptachlor and endrin; aldrin, dieldrin and endrin; and dichlorodiphenyltrichloroethane. The mortality for all causes and all malignant neoplasms at each of the plants was lower than expected. There was a statistically significant increase in liver and biliary tract cancer among workers at plant 3 (5 observed, standardized mortality ratio 393, 95% confidence interval 1.27-9.20). These results are somewhat consistent with experimental animal findings showing benign and malignant tumors of the liver after exposure to aldrin and dieldrin. However, the deaths were due to a mixture of intra- and extra-hepatic tumors, and the dose-response analysis was limited because of the small number of deaths and lack of exposure data. Additional study of this group should include continued follow-up of the total cohort and a case-referent analysis of the deaths from liver and biliary tract cancer. C1 NIOSH,DIV SURVEILLANCE,INDUSTRYWIDE STUDIES BRANCH,CINCINNATI,OH 45226. RP BROWN, DP (reprint author), NIEHS,OFF OCCUPAT HLTH & TECH SERV,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 14 TC 28 Z9 29 U1 3 U2 4 PU SCAND J WORK ENV HEALTH PI HELSINKI PA TOPELIUKSENKATU 41A, SF-00250 HELSINKI, FINLAND SN 0355-3140 J9 SCAND J WORK ENV HEA JI Scand. J. Work Environ. Health PD JUN PY 1992 VL 18 IS 3 BP 155 EP 161 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HZ558 UT WOS:A1992HZ55800002 PM 1615289 ER PT J AU GARRISON, HH HERMAN, SS LIPTON, JA AF GARRISON, HH HERMAN, SS LIPTON, JA TI MEASURING CHARACTERISTICS OF SCIENTIFIC-RESEARCH - A COMPARISON OF BIBLIOGRAPHIC AND SURVEY DATA SO SCIENTOMETRICS LA English DT Article ID PRODUCTIVITY AB Three characteristics of scientific research (subject matter, researchers' institutional sectors, and funding sources) were compared using bibliographic and survey data from a study of restorative dental materials research. Both types of data yielded similar findings on the distribution of research across subject areas and the distribution of researchers in government, university and industry sectors. Findings on the sources of research funding, however, were dissimilar and university research support appeared underreported in the bibliographic data. In general, data on publications (from bibliographic files or surveys) yielded lower estimates of industrial participation in research than data pertaining to projects. C1 NIDR,BETHESDA,MD 20892. RP GARRISON, HH (reprint author), ASPEN SYST CORP,962 WAYNE AVE,SILVER SPRING,MD 20910, USA. OI Garrison, Howard/0000-0001-9455-3527 NR 13 TC 3 Z9 3 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0138-9130 J9 SCIENTOMETRICS JI Scientometrics PD JUN PY 1992 VL 24 IS 2 BP 359 EP 370 DI 10.1007/BF02017915 PG 12 WC Computer Science, Interdisciplinary Applications; Information Science & Library Science SC Computer Science; Information Science & Library Science GA JH395 UT WOS:A1992JH39500008 ER PT J AU RODGERS, GP AF RODGERS, GP TI SPECTRUM OF FETAL HEMOGLOBIN RESPONSES IN SICKLE-CELL PATIENTS TREATED WITH HYDROXYUREA - THE NATIONAL INSTITUTES OF HEALTH EXPERIENCE SO SEMINARS IN ONCOLOGY LA English DT Article ID GAMMA-GLOBIN SYNTHESIS; 5-AZACYTIDINE; ANEMIA; DISEASE; STIMULATION; BABOONS; ERYTHROPOIETIN; AUGMENTATION; THALASSEMIA; MECHANISM RP RODGERS, GP (reprint author), NIDDK,CHEM BIOL LAB,BLDG 10,ROOM 9N-318,BETHESDA,MD 20892, USA. NR 26 TC 11 Z9 12 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD JUN PY 1992 VL 19 IS 3 SU 9 BP 67 EP 73 PG 7 WC Oncology SC Oncology GA JG078 UT WOS:A1992JG07800010 PM 1379375 ER PT J AU VAMVAKOPOULOS, NC MAYOL, V MARGIORIS, AN CHROUSOS, GP AF VAMVAKOPOULOS, NC MAYOL, V MARGIORIS, AN CHROUSOS, GP TI LACK OF DEXAMETHASONE MODULATION OF MESSENGER-RNAS INVOLVED IN THE GLUCOCORTICOID SIGNAL TRANSDUCTION PATHWAY IN 2 CELL SYSTEMS SO STEROIDS LA English DT Article DE GLUCOCORTICOIDS-DEXAMETHASONE TREATMENT; GLUCOCORTICOID RECEPTOR MESSENGER RNA; CHICKEN OVALBUMIN UPSTREAM PROMOTER TRANSCRIPTION FACTOR (COUP-TF); HEAT SHOCK PROTEINS; HYPOTHALAMIC-PITUITARY-ADRENAL AXIS; MAMMALIAN STRESS RESPONSE; GLUCOCORTICOID SIGNAL TRANSDUCTION PATHWAY; STEROIDS; HUMAN LYMPHOCYTES; EPSTEIN-BARR-VIRUS (EBV) TRANSFORMATION ID HEAT-SHOCK PROTEIN; STEROID-RECEPTOR SUPERFAMILY; TRANSCRIPTION FACTOR; HUMAN-LYMPHOCYTES; GENE; INHIBITION; EXPRESSION; SECRETION; INDUCTION; PROMOTER AB Glucocorticoids are final effectors of the stress response. These hormones exert negative feedback action at multiple levels of the hypothalamic-pituitary-adrenal axis and regulate a large number of central nervous system and peripheral target genes. The inactive form of the glucocorticoid receptor in the cytoplasm appears to be bound to heat shock proteins of the 90K family (hsp90-alpha and hsp90-beta). This interaction facilitates binding of glucocorticoid to its receptor and, therefore, its activation. The chicken ovalbumin upstream promoter transcription factor (COUP-TF) binds on a negative glucocorticoid response element in the 5' regulatory region of the proopiomelanocortin gene and prevents the repressive effect of glucocorticoids on this gene. The aim of this study was to examine the effect of glucocorticoids on the steady-state mRNAs of their own receptor, the two hsp90s, and COUP-TF. Quantitative Northern blot analysis in primary leukocytes and Epstein-Barr virus-transformed human lymphocytes (EBV-THL) basally and after a 24-hour exposure to 50 nM dexamethasone was performed. Treatment of primary leukocytes or normally growing EBV-THL with dexamethasone had no effect on the mRNA level of glucocorticoid receptor, hsp90-alpha, hsp90-beta, or COUP-TF. Similar treatment of EBV-THL grown in charcoal-stripped media, resulted in minimal changes in the mRNAs of these factors. Our findings suggest that glucocorticoids do not regulate the steady-state mRNA levels of these core components of the mammalian stress response in human primary and Epstein-Barr virus-transformed lymphocytes. C1 UNIV CRETE,SCH MED,DEPT CLIN CHEM,IRAKLION,GREECE. RP VAMVAKOPOULOS, NC (reprint author), NICHHD,PEDIAT ENDOCRINOL SECT,BLDG 10,ROOM 10N-240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 41 TC 15 Z9 15 U1 0 U2 1 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0039-128X J9 STEROIDS JI Steroids PD JUN PY 1992 VL 57 IS 6 BP 282 EP 287 DI 10.1016/0039-128X(92)90061-D PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA HX938 UT WOS:A1992HX93800005 PM 1279841 ER PT J AU SCHEFFEL, U DANNALS, RF CLINE, EJ RICAURTE, GA CARROLL, FI ABRAHAM, P LEWIN, AH KUHAR, MJ AF SCHEFFEL, U DANNALS, RF CLINE, EJ RICAURTE, GA CARROLL, FI ABRAHAM, P LEWIN, AH KUHAR, MJ TI [I-123-125I]RTI-55, AN INVIVO LABEL FOR THE SEROTONIN TRANSPORTER SO SYNAPSE LA English DT Article DE [123/125I]RTI-55; COCAINE BINDING SITES; DA TRANSPORTER; 5-HT TRANSPORTER; INVIVO LABELING; 5-HT NEUROTOXICITY ID UPTAKE SITES; H-3 6-NITROQUIPAZINE; RAT-BRAIN; PAROXETINE AB [I-123]RTI-55, an iodinated derivative of the cocaine analog 3-beta-phenyltropane-2-beta-carboxylic acid methyl ester, was evaluated as an agent for in vivo labeling of the serotonin transporter. Labeling of the precursor of RTI-55 with I-123 was efficient and yielded a high specific activity product. After intravenous injection of [I-123]RTI-55 into rats, the tracer accumulated in regions with high densities of serotonin and dopamine uptake sites. The distribution of [I-123]RTI-55 binding in areas rich in serotonin uptake sites correlated with [H-3]serotonin uptake measured in vitro in the same regions. Specific [I-123]RTI-55 binding to serotonin uptake sites was inhibited by paroxetine but not by GBR 12,909. Treatment of rats with neurotoxic doses of fenfluramine caused decreases of 66% (in the hypothalamus) to 83% (in the superior colliculi) of specific [I-125]RTI-55 binding in all areas except in the striatum and the olfactory tubercles (regions rich in dopamine transporters). These results indicate that [I-123/125]RTI-55 binds, although not selectively, to the serotonin transporter in vivo. Furthermore, they suggest that [I-123]RTI-55 holds promise as a SPECT imaging agent for the study of the serotonin transporter in humans in health and disease. C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. JOHNS HOPKINS MED INST,DEPT NEUROL,BALTIMORE,MD 21205. NIDA,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21205. RP SCHEFFEL, U (reprint author), JOHNS HOPKINS MED INST,DEPT RADIOL,DIV NUCL MED,BALTIMORE,MD 21205, USA. FU NCI NIH HHS [CA 32845]; NIDA NIH HHS [DA 06309]; NINDS NIH HHS [NS 15080] NR 24 TC 85 Z9 85 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 0887-4476 J9 SYNAPSE JI Synapse PD JUN PY 1992 VL 11 IS 2 BP 134 EP 139 DI 10.1002/syn.890110206 PG 6 WC Neurosciences SC Neurosciences & Neurology GA HV171 UT WOS:A1992HV17100005 PM 1385663 ER PT J AU SABOURIN, PJ MEDINSKY, MA BIRNBAUM, LS GRIFFITH, WC HENDERSON, RF AF SABOURIN, PJ MEDINSKY, MA BIRNBAUM, LS GRIFFITH, WC HENDERSON, RF TI EFFECT OF EXPOSURE CONCENTRATION ON THE DISPOSITION OF INHALED BUTOXYETHANOL BY F344 RATS SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID GLYCOL MONOBUTYL ETHER; INHALATION; 2-BUTOXYETHANOL; TOXICITY; METABOLISM; EXCRETION C1 LOVELACE BIOMED & ENVIRONM RES INST,INHALAT TOXICOL RES INST,POB 5890,ALBUQUERQUE,NM 87185. NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [222-ES-20092] NR 16 TC 11 Z9 12 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD JUN PY 1992 VL 114 IS 2 BP 232 EP 238 DI 10.1016/0041-008X(92)90073-2 PG 7 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA HY258 UT WOS:A1992HY25800008 PM 1609415 ER PT J AU SABOURIN, PJ MUGGENBURG, BA COUCH, RC LEFLER, D LUCIER, G BIRNBAUM, LS HENDERSON, RF AF SABOURIN, PJ MUGGENBURG, BA COUCH, RC LEFLER, D LUCIER, G BIRNBAUM, LS HENDERSON, RF TI METABOLISM OF [C-14] BENZENE BY CYNOMOLGUS MONKEYS AND CHIMPANZEES SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID BENZENE METABOLITES; B6C3F1 MICE; EXPOSURE; RATS; TOXICITY; PHENOL; ACID; TRANS,TRANS-MUCONALDEHYDE; MYELOTOXICITY; EXCRETION C1 LOVELACE BIOMED & ENVIRONM RES INST,INHALAT TOXICOL RES INST,POB 5890,ALBUQUERQUE,NM 87185. WHITE SANDS RES CTR,ALAMOGORDO,NM 88330. NIEHS,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [222-402-ES-20092] NR 27 TC 35 Z9 35 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD JUN PY 1992 VL 114 IS 2 BP 277 EP 284 DI 10.1016/0041-008X(92)90078-7 PG 8 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA HY258 UT WOS:A1992HY25800013 PM 1609420 ER PT J AU STEIN, PH REES, MA SINGER, A AF STEIN, PH REES, MA SINGER, A TI RECONSTITUTION OF (BALB/C X B6)F1 NORMAL MICE WITH STEM-CELLS AND THYMUS FROM NONOBESE DIABETIC MICE RESULTS IN AUTOIMMUNE INSULITIS OF THE NORMAL HOSTS PANCREASES SO TRANSPLANTATION LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; ALLOGENEIC BONE-MARROW; NOD MICE; CLASS-II; TRANSGENIC MICE; MONOCLONAL-ANTIBODIES; BETA-CELLS; MOUSE; TRANSPLANTATION; EXPRESSION AB The NOD mouse develops immune-mediated diabetes mellitus characterized by T cell infiltration and destruction of pancreatic islet tissue. We wished to determine whether one contributing factor was an abnormality of the NOD pancreas that caused it to elicit an attack by NOD T cells. Therefore we constructed mice that had an NOD immune system and a non-NOD host pancreas. We found that these animals with only an NOD immune system developed both insulitis and diabetes in their non-NOD pancreas. We conclude that the NOD pancreas is not unique in its ability to elicit an autoimmune attack from NOD T cells. C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B-17,BETHESDA,MD 20892. NR 40 TC 5 Z9 5 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD JUN PY 1992 VL 53 IS 6 BP 1347 EP 1352 DI 10.1097/00007890-199206000-00032 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HZ486 UT WOS:A1992HZ48600032 PM 1604490 ER PT J AU KOONIN, EV SENKEVICH, TG CHERNOS, VI AF KOONIN, EV SENKEVICH, TG CHERNOS, VI TI A FAMILY OF DNA VIRUS GENES THAT CONSISTS OF FUSED PORTIONS OF UNRELATED CELLULAR GENES SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Article ID PROTEIN; SEQUENCE C1 ACAD MED SCI USSR,INST VIRUS PREPARAT,MOSCOW 109088,USSR. RP KOONIN, EV (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BLDG 38A,BETHESDA,MD 20894, USA. NR 13 TC 41 Z9 41 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0968-0004 J9 TRENDS BIOCHEM SCI JI Trends Biochem.Sci. PD JUN PY 1992 VL 17 IS 6 BP 213 EP 214 DI 10.1016/0968-0004(92)90379-N PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HZ509 UT WOS:A1992HZ50900006 PM 1502722 ER PT J AU CRAIGIE, R AF CRAIGIE, R TI HOTSPOTS AND WARM SPOTS - INTEGRATION SPECIFICITY OF RETROELEMENTS SO TRENDS IN GENETICS LA English DT Article ID RETROVIRAL DNA INTEGRATION; VIRAL-DNA; PROTEIN; INVITRO; TARGETS RP CRAIGIE, R (reprint author), NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 27 TC 94 Z9 95 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0168-9525 J9 TRENDS GENET JI Trends Genet. PD JUN PY 1992 VL 8 IS 6 BP 187 EP 190 DI 10.1016/0168-9525(92)90223-Q PG 4 WC Genetics & Heredity SC Genetics & Heredity GA HW747 UT WOS:A1992HW74700001 PM 1323152 ER PT J AU KLAR, AJS AF KLAR, AJS TI DEVELOPMENTAL CHOICES IN MATING-TYPE INTERCONVERSION IN FISSION YEAST SO TRENDS IN GENETICS LA English DT Review ID SCHIZOSACCHAROMYCES-POMBE; CELL LINEAGE; DNA STRANDS; HO GENE; CASSETTES; ASYMMETRY; PATTERN; DIRECTIONALITY; TRANSPOSITION; RECOMBINATION AB Fission yeast cells follow a specific pattern of mating (cell) type switching in single cell pedigrees. Asymmetric cell divisions producing sisters of different developmental fates result from inheritance of specific parental DNA strands according to the classical model of semiconservative replication and segregation. RP KLAR, AJS (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,POB B,BLDG 539,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 33 TC 30 Z9 30 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0168-9525 J9 TRENDS GENET JI Trends Genet. PD JUN PY 1992 VL 8 IS 6 BP 208 EP 213 DI 10.1016/0168-9525(92)90100-I PG 6 WC Genetics & Heredity SC Genetics & Heredity GA HW747 UT WOS:A1992HW74700006 PM 1496556 ER PT J AU COCKERELL, GL JENSEN, WA ROVNAK, J ENNIS, WH GONDA, MA AF COCKERELL, GL JENSEN, WA ROVNAK, J ENNIS, WH GONDA, MA TI SEROPREVALENCE OF BOVINE IMMUNODEFICIENCY-LIKE VIRUS AND BOVINE LEUKEMIA-VIRUS IN A DAIRY-CATTLE HERD SO VETERINARY MICROBIOLOGY LA English DT Article ID LYMPHOCYTOSIS; PATHOGENESIS; ANTIBODIES; INFECTION AB To determine the prevalence of single vs. dual infection with bovine immunodeficiency virus (BIV) and bovine leukemia virus (BLV), sera (n = 95) from a dairy cattle herd were analyzed for anti-BIV and anti-BLV antibodies by an enzyme linked immunosorbent assay. Twenty-one percent (20/95) of samples were BIV-seropositive, while 52% (49/95) of the same samples were BLV-seropositive. A significantly greater percentage of BIV-seronegative samples were BLV-seropositive, 57% (43/75), than were BIV-seropositive samples, 30% (6/20). There was no significant correlation between data ranked from least to greatest amount of anti-viral antibody. Five cattle had persistent lymphocytosis (PL); all five were BLV-seropositive and two were BIV-positive. The mean anti-BLV titer was significantly greater in PL cattle, as compared at non-PL cattle, whereas there was no significant difference between the mean anti-BIV titer in PL cattle, as compared with non-PL cattle. These results provide additional information on the seroprevalence of naturally occurring BIV infection, and indicate that BIV can exist independent of other common infectious agents, such as BLV. Further, the results suggest that infection with BIV is not associated with an increased rate of infection with other infectious agents such as BLV. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701. RP COCKERELL, GL (reprint author), COLORADO STATE UNIV,DEPT PATHOL,FT COLLINS,CO 80523, USA. FU NCI NIH HHS [CA43728, N01-CO-74102] NR 15 TC 53 Z9 53 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1135 J9 VET MICROBIOL JI Vet. Microbiol. PD JUN 1 PY 1992 VL 31 IS 2-3 BP 109 EP 116 DI 10.1016/0378-1135(92)90069-6 PG 8 WC Microbiology; Veterinary Sciences SC Microbiology; Veterinary Sciences GA HY714 UT WOS:A1992HY71400002 PM 1320785 ER PT J AU SEMMES, OJ JEANG, KT AF SEMMES, OJ JEANG, KT TI HTLV-I TAX IS A ZINC-BINDING PROTEIN - ROLE OF ZINC IN TAX STRUCTURE AND FUNCTION SO VIROLOGY LA English DT Article ID VIRUS TYPE-I; TRANSCRIPTION FACTOR-IIIA; LONG TERMINAL REPEAT; TRANS-ACTIVATOR PROTEIN; DNA-BINDING; LEUCINE ZIPPER; DIRECTED MUTAGENESIS; MUTATIONAL ANALYSIS; MAMMALIAN-CELLS; GENE-EXPRESSION C1 NIAID, MOLEC MICROBIOL LAB, BETHESDA, MD 20892 USA. RI Jeang, Kuan-Teh/A-2424-2008 NR 61 TC 30 Z9 31 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD JUN PY 1992 VL 188 IS 2 BP 754 EP 764 DI 10.1016/0042-6822(92)90530-3 PG 11 WC Virology SC Virology GA HU511 UT WOS:A1992HU51100036 PM 1585646 ER PT J AU POTTS, BJ HOGGAN, MD LAMPERTH, L SPIVAK, J AF POTTS, BJ HOGGAN, MD LAMPERTH, L SPIVAK, J TI REPLICATION OF HIV-1 AND HIV-2 IN HUMAN BONE-MARROW CULTURES SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-DEFICIENCY SYNDROME; HEMATOPOIETIC PROGENITOR CELLS; INSITU HYBRIDIZATION; HUMAN RETROVIRUS; HOMOSEXUAL MEN; SCHWANN-CELLS; MESSENGER-RNA; INFECTION; AIDS C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NINCDS,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV HEMATOL,BALTIMORE,MD 21205. FU NIDDK NIH HHS [DK 16702] NR 37 TC 12 Z9 12 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JUN PY 1992 VL 188 IS 2 BP 840 EP 849 DI 10.1016/0042-6822(92)90539-2 PG 10 WC Virology SC Virology GA HU511 UT WOS:A1992HU51100045 PM 1585651 ER PT J AU SCHNIERLE, BS MOSS, B AF SCHNIERLE, BS MOSS, B TI VACCINIA VIRUS-MEDIATED INHIBITION OF HOST PROTEIN-SYNTHESIS INVOLVES NEITHER DEGRADATION NOR UNDERPHOSPHORYLATION OF COMPONENTS OF THE CAP-BINDING EUKARYOTIC TRANSLATION INITIATION-FACTOR COMPLEX ELF-4F SO VIROLOGY LA English DT Note ID LATE MESSENGER-RNAS; POLIOVIRUS RNA; POLY(A) SEQUENCES; PHOSPHORYLATION; LEADER; IDENTIFICATION; RIBOSOMES; INVITRO; EIF-4F; REGION C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 35 TC 13 Z9 13 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JUN PY 1992 VL 188 IS 2 BP 931 EP 933 DI 10.1016/0042-6822(92)90556-5 PG 3 WC Virology SC Virology GA HU511 UT WOS:A1992HU51100062 PM 1585660 ER PT J AU GARCIABEATO, R FREIJE, JMP LOPEZOTIN, C BLASCO, R VINUELA, E SALAS, ML AF GARCIABEATO, R FREIJE, JMP LOPEZOTIN, C BLASCO, R VINUELA, E SALAS, ML TI A GENE HOMOLOGOUS TO TOPOISOMERASE-II IN AFRICAN SWINE FEVER VIRUS SO VIROLOGY LA English DT Note ID COLI DNA GYRASE; ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; VACCINIA VIRUS; GYRB GENE; CLONING; SITE; SUBUNIT; PURIFICATION; TRANSLATION C1 UNIV AUTONOMA MADRID, FAC CIENCIAS, CSIC, CTR BIOL MOLEC, CANTOBLANCO, E-28049 MADRID, SPAIN. UNIV OVIEDO, FAC MED, DEPT BIOL FUNC, E-33006 OVIEDO, SPAIN. NIAID, VIRAL DIS LAB, BETHESDA, MD 20892 USA. RI Freije, Jose M.P./A-6535-2008; Blasco, Rafael/B-5829-2016; Lopez-Otin, Carlos/C-6657-2013 OI Freije, Jose M.P./0000-0002-4688-8266; Lopez-Otin, Carlos/0000-0001-6964-1904 NR 55 TC 35 Z9 37 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD JUN PY 1992 VL 188 IS 2 BP 938 EP 947 DI 10.1016/0042-6822(92)90558-7 PG 10 WC Virology SC Virology GA HU511 UT WOS:A1992HU51100064 PM 1316688 ER PT J AU TAN, GT MILLER, JF KINGHORN, AD HUGHES, SH PEZZUTO, JM AF TAN, GT MILLER, JF KINGHORN, AD HUGHES, SH PEZZUTO, JM TI HIV-1 AND HIV-2 REVERSE TRANSCRIPTASES - A COMPARATIVE-STUDY OF SENSITIVITY TO INHIBITION BY SELECTED NATURAL-PRODUCTS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID IMMUNODEFICIENCY VIRUS TYPE-2; ESCHERICHIA-COLI; AIDS; RETROVIRUS; FAGARONINE C1 UNIV ILLINOIS,COLL PHARM,DEPT MED CHEM & PHARMACOGNOSY,PROGRAM COLLABORAT RES PHARMACEUT SCI,CHICAGO,IL 60612. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. UNIV ILLINOIS,COLL MED,CTR SPECIALIZED CANC,CHICAGO,IL 60612. OI Kinghorn, A. Douglas/0000-0002-6647-8707 FU NCI NIH HHS [N01-CO-740101] NR 22 TC 45 Z9 47 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAY 29 PY 1992 VL 185 IS 1 BP 370 EP 378 DI 10.1016/S0006-291X(05)80995-7 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HW513 UT WOS:A1992HW51300056 PM 1376118 ER PT J AU RAMSAY, DA DRACHMAN, DB DRACHMAN, RJ STANLEY, EF AF RAMSAY, DA DRACHMAN, DB DRACHMAN, RJ STANLEY, EF TI STABILIZATION OF ACETYLCHOLINE-RECEPTORS AT THE NEUROMUSCULAR SYNAPSE - THE ROLE OF THE NERVE SO BRAIN RESEARCH LA English DT Article DE ACETYLCHOLINE RECEPTOR; NEUROMUSCULAR JUNCTION; RECEPTOR STABILIZATION; RECEPTOR TURNOVER; PLASTICITY; RECEPTOR KINETICS ID SKELETAL-MUSCLE; ALPHA-BUNGAROTOXIN; RAT DIAPHRAGM; MYASTHENIC IMMUNOGLOBULIN; BETA-SUBUNIT; DEGRADATION; JUNCTIONS; MEMBRANE; TURNOVER; STABILITY AB The majority of acetylcholine receptors (AChRs) at innervated neuromuscular junctions (NMJs) are stable, with half-lives averaging about 11 days in rodent muscles. In addition to the stable AChRs, approximately 18% of AChRs at these innervated junctions are rapidly turned over (RTOs), with half lives of less than 24 h. We have postulated that RTOs may be precursors of stable AChRs, and that the motor nerve may influence their stabilization. This hypothesis was tested by: (i) labeling AChRs in mouse sternomastoid (SM) muscles with I-125-alpha-BuTx; (ii) denervating one SM muscle in each mouse, and (iii) following the fate of the labeled AChRs through a 5-day period when RTOs were either stabilized or degraded. The hypothesis predicts that denervation should preclude stabilization of RTOs, resulting in a deficit of stable AChRs in denervated muscles. The results showed a highly significant (P < 0.002) deficit of stable AChRs in denervated as compared with innervated muscles. Control experiments excluded the possibility that this deficit could be attributed to independent accelerated degradation of either RTOs or pre-existing stable AChRs. The observed deficit was quantitatively consistent with the deficit predicted by a mathematical model based on interruption of stabilization following denervation. We conclude that: (i) the observed deficit after denervation of NMJs is due to failure of stabilization of pre-existing RTOs; (ii) RTOs at normally innervated NMJs are precursors of stable AChRs; (iii) stabilization occurs after the insertion of AChRs at NMJs, and (iv) motor nerves play a key role in stabilization of RTOs. The concept of receptor stabilization has important implications for understanding the biology of the neuromuscular junction and post-synaptic plasticity. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,600 N WOLFE ST,BALTIMORE,MD 21205. VICTORIA HOSP,DEPT NEUROPATHOL,LONDON N6A 4G5,ONTARIO,CANADA. NASA,GODDARD SPACE FLIGHT CTR,ASTRON & SOLAR PHYS LAB,GREENBELT,MD 20771. NIH,BETHESDA,MD 20892. FU NINDS NIH HHS [1R01 NS23719] NR 53 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAY 29 PY 1992 VL 581 IS 2 BP 198 EP 207 DI 10.1016/0006-8993(92)90709-I PG 10 WC Neurosciences SC Neurosciences & Neurology GA JB033 UT WOS:A1992JB03300003 PM 1393528 ER PT J AU ENGBER, TM BOLDRY, RC KUO, S CHASE, TN AF ENGBER, TM BOLDRY, RC KUO, S CHASE, TN TI DOPAMINERGIC MODULATION OF STRIATAL NEUROPEPTIDES - DIFFERENTIAL-EFFECTS OF D(1) AND D(2) RECEPTOR STIMULATION ON SOMATOSTATIN, NEUROPEPTIDE-Y, NEUROTENSIN, DYNORPHIN AND ENKEPHALIN SO BRAIN RESEARCH LA English DT Article DE SKF-38393; QUINPIROLE; 6-HYDROXYDOPAMINE; RADIOIMMUNOASSAY; NEUROPEPTIDE ID INSITU HYBRIDIZATION HISTOCHEMISTRY; PREPROSOMATOSTATIN MESSENGER-RNA; RAT CAUDATE-NUCLEUS; SUBSTANTIA-NIGRA; GENE-EXPRESSION; BASAL GANGLIA; IMMUNOREACTIVE NEURONS; CAT; INTERMITTENT; NEOSTRIATUM AB Dopaminergic modulation of neuropeptides in rat striatum was investigated by examining the effects of prolonged D1 or D2 receptor stimulation on levels of somatostatin, neuropeptide Y, neurotensin, dynorphin and enkephalin. Rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of the nigrostriatal pathway were treated for 7 days with either the D1 agonist SKF 38393 (12.5 mg/kg/day) or the D2 agonist quinpirole (1 mg/kg/day). Two regimens of agonist treatment were compared: continuous infusion via osmotic pump implanted i.p. and intermittent (once daily) i.p. injection. Rats were sacrificed 3 h after the last injection and peptide levels measured in the striatum bilaterally by radioimmunoassay; alterations in peptide content were observed primarily in the denervated striatum. In comparison to values from lesioned, vehicle-treated controls, intermittent administration of SKF 38393 reduced somatostatin and neuropeptide Y (down 61% and 57%, respectively), increased neurotensin (up 105%) and dynorphin (up 184%) and had no effect on enkephalin; continuous SKF 38393 decreased neuropeptide Y by 39% but did not alter levels of the other peptides. Continuous quinpirole elevated somatostatin and neuropeptide Y levels (up 43% and 33%, respectively), but reduced the lesion-induced increases in both neurotensin (down 51%) and enkephalin (down 24%) content. Conversely, intermittent quinpirole decreased somatostatin (down 35%) and neuropeptide Y (down 27%), increased neurotensin content by 79% and had no effect on enkephalin. Dynorphin levels were not altered by either continuous or intermittent quinpirole. These findings reveal the complexity of dopaminergic influences on striatal neuropeptides. Somatostatin, neuropeptide Y and neurotensin levels are modulated by both D1 and D2 dopamine receptors: somatostatin and neuropeptide Y show parallel changes, but the alterations in neurotensin are opposite in direction to those of somatostatin and neuropeptide Y. Striatal dynorphin content is influenced only by D1 receptor stimulation, while enkephalin is modulated only by D2 receptors. The data also demonstrate that striatal neuropeptides are profoundly influenced by the temporal characteristics of dopamine receptor stimulation. RP NINCDS, EXPTL THERAPEUT BRANCH, NIH BLDG 10, ROOM 5C215, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 46 TC 111 Z9 111 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 EI 1872-6240 J9 BRAIN RES JI Brain Res. PD MAY 29 PY 1992 VL 581 IS 2 BP 261 EP 268 DI 10.1016/0006-8993(92)90716-M PG 8 WC Neurosciences SC Neurosciences & Neurology GA JB033 UT WOS:A1992JB03300010 PM 1356580 ER PT J AU ROSNER, M DESANTO, RJ ARNHEITER, H STAUDT, LM AF ROSNER, M DESANTO, RJ ARNHEITER, H STAUDT, LM TI RETRACTION - OCT-3 IS A MATERNAL FACTOR REQUIRED FOR THE 1ST MOUSE EMBRYONIC DIVISION SO CELL LA English DT Letter RP ROSNER, M (reprint author), NCI,BETHESDA,MD 20892, USA. NR 1 TC 5 Z9 5 U1 1 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAY 29 PY 1992 VL 69 IS 5 BP 724 EP 724 DI 10.1016/0092-8674(92)90284-J PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HW838 UT WOS:A1992HW83800003 PM 1591774 ER PT J AU GUSTAFSON, KR CARDELLINA, JH MCMAHON, JB GULAKOWSKI, RJ ISHITOYA, J SZALLASI, Z LEWIN, NE BLUMBERG, PM WEISLOW, OS BEUTLER, JA BUCKHEIT, RW CRAGG, GM COX, PA BADER, JP BOYD, MR AF GUSTAFSON, KR CARDELLINA, JH MCMAHON, JB GULAKOWSKI, RJ ISHITOYA, J SZALLASI, Z LEWIN, NE BLUMBERG, PM WEISLOW, OS BEUTLER, JA BUCKHEIT, RW CRAGG, GM COX, PA BADER, JP BOYD, MR TI A NONPROMOTING PHORBOL FROM THE SAMOAN MEDICINAL PLANT HOMALANTHUS-NUTANS INHIBITS CELL KILLING BY HIV-1 SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; HUMAN-IMMUNODEFICIENCY-VIRUS; POTENT TUMOR PROMOTERS; ENVELOPE GLYCOPROTEIN; MYRISTATE ACETATE; ARACHIDONIC-ACID; T-CELLS; EXPRESSION; ESTERS; ACTIVATION AB Extracts of Homalanthus nutans, a plant used in Samoan herbal medicine, exhibited potent activity in an in vitro, tetrazolium-based assay which detects the inhibition of the cytopathic effects of human immunodeficiency virus (HIV-1). The active constituent was identified as prostratin, a relatively polar 12-deoxyphorbol ester. Noncytotoxic concentrations of prostratin from greater-than-or-equal-to 0.1 to >25-mu-M protected T-lymphoblastoid CEM-SS and C-8166 cells from the killing effects of HIV-1. Cytoprotective concentrations of prostratin greater-than-or-equal-to 1-mu-M essentially stopped virus reproduction in these cell lines, as well as in the human monocytic cell line U937 and in freshly isolated human monocyte/macrophage cultures. Prostratin bound to and activated protein kinase C in vitro in CEM-SS cells and elicited other biochemical effects typical of phorbol esters in C3H10T1/2 cells; however, the compound does not appear to be a tumor promoter. In skin of CD-1 mice, high doses of prostratin induced ornithine decarboxylase only to 25-30% of the levels induced by typical phorbol esters at doses 1/30 or less than that used for prostratin, produced kinetics of edema formation characteristic of the nonpromoting 12-deoxyphorbol 13-phenylacetate, and failed to induce the acute or chronic hyperplasias typically caused by tumor-promoting phorbols at doses of 1/100 or less than that used for prostratin. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702. BRIGHAM YOUNG UNIV,DEPT BOT & RANGE SCI,PROVO,UT 84602. NCI,DCT,DTP,ANTIVIRAL EVALUAT BRANCH,ROCKVILLE,MD 20892. NCI,DIV CANC ETIOL,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. DYNCORP PROGRAM RESOURCES INC,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. SO RES INST,BIRMINGHAM,AL 35255. NCT,FREDERICK CANC RES & DEV CTR,DCT,DTP,NAT PROD BRANCH,FREDERICK,MD 21702. RI Beutler, John/B-1141-2009 OI Beutler, John/0000-0002-4646-1924 NR 59 TC 132 Z9 140 U1 1 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD MAY 29 PY 1992 VL 35 IS 11 BP 1978 EP 1986 DI 10.1021/jm00089a006 PG 9 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA HX265 UT WOS:A1992HX26500006 PM 1597853 ER PT J AU ENGEL, I OTTENHOFF, THM KLAUSNER, RD AF ENGEL, I OTTENHOFF, THM KLAUSNER, RD TI HIGH-EFFICIENCY EXPRESSION AND SOLUBILIZATION OF FUNCTIONAL T-CELL ANTIGEN RECEPTOR HETERODIMERS SO SCIENCE LA English DT Article ID ENDOPLASMIC-RETICULUM; CYTOCHROME-C; DEGRADATION; RECOGNITION; IA; COMPLEX; CHAINS; GENE; ZETA; BETA AB The T cell receptor (TCR) zeta-chain was attached to the TCR-alpha and beta-extracellular domains to induce efficient expression of alpha-beta-heterodimers that can recognize complexes of antigen with major histocompatibility complex (MHC) molecules. Chimeric constructs expressed in RBL-2H3 cells were efficiently transported to the cell surface uniquely as disulfide-linked heterodimers. Transfectants were activated by specific antigen-MHC complexes, which demonstrated that the expressed-alpha-beta was functional and that CD3 was not required for antigen-MHC binding. Constructs with thrombin cleavage sites were efficiently cleaved to soluble disulfide-linked heterodimers. Thus, attachment of TCR-zeta-domains and protease cleavage sites to TCR-alpha and beta induces expression of demonstrably functional heterodimers that can be solubilized. RP ENGEL, I (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 30 TC 76 Z9 76 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAY 29 PY 1992 VL 256 IS 5061 BP 1318 EP 1321 DI 10.1126/science.1598575 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HW135 UT WOS:A1992HW13500033 PM 1598575 ER PT J AU PARK, SS WALKER, W AOYAMA, T LAPENSON, DP WAXMAN, DJ GONZALEZ, FJ GELBOIN, HV AF PARK, SS WALKER, W AOYAMA, T LAPENSON, DP WAXMAN, DJ GONZALEZ, FJ GELBOIN, HV TI MONOCLONAL-ANTIBODIES TO RAT-LIVER MICROSOMAL CYTOCHROME-B5 SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID FISH STENOTOMUS-CHRYSOPS; CATALYTIC ACTIVITY; PURIFICATION; METABOLISM; FORMS; CARCINOGENESIS; SEQUENCE; ENZYMES; TISSUES; CDNA AB Hybridomas obtained by the fusion of spleen cells from rat cytochrome b5-immunized mice with mouse myeloma cells produced five groups of monoclonal antibodies (MAbs) with three mouse immunoglobulin subtypes: IgG1, IgG2b and IgM. All of the MAbs bound strongly to rat cytochrome b5 as measured by radioimmunoassay (RIA). Four clones of MAbs were also strongly immunoreactive with cytochrome b5 when tested by Western blotting, but only one of the MAbs (1-39-2) weakly immunoprecipitated cytochrome b5 in an Ouchterlony double-immunodiffusion test. Two of the MAbs partially inhibited cytochrome b5-mediated NADH cytochrome c reduction catalyzed by liver microsomes (24-36%). Expression of immunodetectable cytochrome b5 was highest in the liver, next highest in the kidney, and quite low in the other tissues examined with MAb 1-17-1 by Western blotting. This MAb recognized homologous cytochrome b5 of human liver microsomes and in homogenates of TK- cells infected with recombinant vaccinia virus encoding human cytochrome b5. These MAbs to cytochrome b5 will be useful for the identification, quantification, and purification of cytochrome b5 from animal and human tissues, and for understanding its role in cytochrome P450 catalyzed drug metabolism and carcinogen activation with respect to tissue, organ and individual differences. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NR 32 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAY 28 PY 1992 VL 43 IS 10 BP 2201 EP 2208 DI 10.1016/0006-2952(92)90179-M PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HZ254 UT WOS:A1992HZ25400020 PM 1599506 ER PT J AU LUBIN, JH LI, JY XUAN, XZ CAI, SK LUO, QS YANG, LF WANG, JZ YANG, L BLOT, WJ AF LUBIN, JH LI, JY XUAN, XZ CAI, SK LUO, QS YANG, LF WANG, JZ YANG, L BLOT, WJ TI RISK OF LUNG-CANCER AMONG CIGARETTE AND PIPE SMOKERS IN SOUTHERN CHINA SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT 3RD BIENNIAL JAPANESE / GERMAN WORKSHOP ON MOLECULAR AND CELLULAR ASPECTS OF CARCINOGENESIS CY OCT 24-26, 1991 CL ESSEN, GERMANY SP DEUT FORSCHUNGSGEMEINSCH, FED REP GER MINIST RES & TECHNOL, FDN PROMOT CANC RES JAPAN, MINIST EDUC SCI & CULTURE JAPAN, INT SCI RES PROGRAM ID TIN MINERS; YUNNAN PROVINCE; SMOKING; TAR; HISTOPATHOLOGY; EXPOSURE; TOBACCO; RATES; RADON; YIELD AB Studies in Shanghai and in north-east China indicate that cigarette smoking is a major contributor to the high rates of lung cancer in those areas, but doubts persist regarding the influence of cigarette use on lung cancer rates in other areas of China. In addition, the risk of lung cancer associated with other methods of tobacco consumption-in particular, the use of bamboo water-pipes and long-stem pipes-is uncertain. A population-based case-control study of 427 male lung cancer patients residing in a mining area of Southern China and 1,011 controls was carried out to address this and other issues. Of these patients, 63% smoked cigarettes and (water and long-stem) pipes; 17% and 14% smoked only cigarettes or pipes, respectively; and 6% did not smoke. Compared to nonsmokers, smokers of cigarettes only, smokers of pipes only and mixed smokers were at increased risk; OR = 2.6 (95% Cl 1.1-6.2), 1.8 (95% Cl 0.8-4.2) and 4.1 (95% Cl 2.3-9.2), respectively. Risk increased with duration of tobacco use; however, the rate of increase with years of cigarette use was significantly greater than for years of pipe use (p = 0.03). In addition, risks increased 8-fold in the highest quartile of number of cigarettes per day compared to non-cigarette smokers vs. 2.3-fold for the highest quartile of number of liang (50 g) smoked per month compared to non-pipe-smokers; the trends in the ORs differed significantly (p < 0.001). Results suggest that, in this area of China, tobacco use is an important cause of lung cancer, and that smoking cigarettes may be more deleterious than smoking pipes (primarily water pipes). C1 CHINESE ACAD MED SCI,DEPT EPIDEMIOL,BEIJING,PEOPLES R CHINA. YUNNAN TIN CORP,INST LAB PROTECT,GEJIU,PEOPLES R CHINA. OFF CANC PREVENT & CONTROL,GEJIU,PEOPLES R CHINA. RP LUBIN, JH (reprint author), NCI,BIOSTAT BRANCH,6130 EXECUT BLVD,EPN-403,ROCKVILLE,MD 20892, USA. NR 36 TC 34 Z9 34 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD MAY 28 PY 1992 VL 51 IS 3 BP 390 EP 395 DI 10.1002/ijc.2910510310 PG 6 WC Oncology SC Oncology GA HW455 UT WOS:A1992HW45500009 PM 1592530 ER PT J AU LOLAIT, SJ OCARROLL, AM MCBRIDE, OW KONIG, M MOREL, A BROWNSTEIN, MJ AF LOLAIT, SJ OCARROLL, AM MCBRIDE, OW KONIG, M MOREL, A BROWNSTEIN, MJ TI CLONING AND CHARACTERIZATION OF A VASOPRESSIN V2 RECEPTOR AND POSSIBLE LINK TO NEPHROGENIC DIABETES-INSIPIDUS SO NATURE LA English DT Article ID ARGININE-VASOPRESSIN; MESSENGER-RNAS; BINDING-SITES; LOCALIZATION; DNA; AMPLIFICATION; ANTAGONISTS; EXPRESSION; PRIMER; POTENT AB THE antidiuretic effect of arginine vasopressin (AVP) is mediated by renal-type (V2) receptors linked to adenylyl cyclase 1. We report here the cloning of the rat kidney V2 AVP receptor complementary DNA that encodes a 370-amino-acid protein with a transmembrane topography characteristic of G protein-coupled receptors, and with similarity to the V1a (hepatic) AVP receptor 2 in its seven membrane-spanning domains. Expression of the cloned cDNA in mammalian cells showed specific ligand binding and activity characteristic of the native V2 AVP receptor. The receptor messenger RNA is detected only in the kidney. The human V2 receptor gene has been localized to the long arm of the X chromosome close to the locus for nephrogenic diabetes insipidus, an X-linked recessive disorder characterized by renal resistance to the antidiuretic action of AVP 3-6. C1 NIMH,CELL BIOL LAB,BLDG 36,ROOM 3A-17,BETHESDA,MD 20892. GRP NEUROBIOCHIM CELLULAIRE & MOLEC,F-75006 PARIS,FRANCE. NCI,CHEM LAB,BETHESDA,MD 20892. RI Brownstein, Michael/B-8609-2009 NR 28 TC 446 Z9 449 U1 1 U2 12 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAY 28 PY 1992 VL 357 IS 6376 BP 336 EP 339 DI 10.1038/357336a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HW132 UT WOS:A1992HW13200050 PM 1534150 ER PT J AU JOHNSON, RE JAFFE, JH FUDALA, PJ AF JOHNSON, RE JAFFE, JH FUDALA, PJ TI A CONTROLLED TRIAL OF BUPRENORPHINE TREATMENT FOR OPIOID DEPENDENCE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID HEROIN-ADDICTS; METHADONE; MAINTENANCE; OPIATE; ABUSE; DETOXIFICATION AB Objective.-To assess the efficacy of buprenorphine for short-term maintenance/detoxification. Design.-A randomized, double-blind, parallel group study comparing buprenorphine, 8 mg/d, methadone, 60 mg/d, and methadone, 20 mg/d, in a 17-week maintenance phase followed by an 8-week detoxification phase. Setting.-Outpatient facilities at the Addiction Research Center, Baltimore, Md. Patients.-One hundred sixty-two volunteers seeking treatment for opioid dependence. Intervention.-In addition to the medication, counseling using a relapse prevention model was offered but not required. Primary Outcome Measures.-Retention time in treatment, urine samples negative for opioids, and failure to maintain abstinence. Results.-Throughout the maintenance phase, retention rates were significantly greater for buprenorphine (42%) than for methadone, 20 mg/d (20%, P < .04); the percentage of urine samples negative for opioids was significantly greater for buprenorphine (53%, P < .001) and methadone, 60 mg/d (44%, P < .04), than for methadone, 20 mg/d (29%). Failure to maintain abstinence during the maintenance phase was significantly greater for methadone, 20 mg/d, than for buprenorphine (P < .03). During the detoxification phase, no differences were observed between groups with respect to urine samples negative for opioids. For the entire 25 weeks, retention rates for buprenorphine (30%, P < .01) and methadone, 60 mg/d (20%, P < .05), were significantly greater than for methadone, 20 mg/d (6%). All treatments were well tolerated, with similar profiles of self-reported adverse effects. The percentages of patients who received counseling did not differ between groups. Conclusions.-Buprenorphine was as effective as methadone, 60 mg/d, and both were superior to methadone, 20 mg/d, in reducing illicit opioid use and maintaining patients in treatment for 25 weeks. C1 NIDA,ADDICT RES CTR,BALTIMORE,MD. NR 45 TC 389 Z9 393 U1 3 U2 19 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAY 27 PY 1992 VL 267 IS 20 BP 2750 EP 2755 DI 10.1001/jama.267.20.2750 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HV265 UT WOS:A1992HV26500021 PM 1578593 ER PT J AU SODERSTROM, CA DISCHINGER, PC SMITH, GS MCDUFF, DR HEBEL, JR GORELICK, DA AF SODERSTROM, CA DISCHINGER, PC SMITH, GS MCDUFF, DR HEBEL, JR GORELICK, DA TI PSYCHOACTIVE SUBSTANCE DEPENDENCE AMONG TRAUMA CENTER PATIENTS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID ALCOHOL; RECOGNITION; PREVALENCE; ABUSE; SEVERITY AB Introduction.-The practice of assessing only trauma patients with elevated blood alcohol concentrations (BACs) or positive drug screens for psychoactive substance use disorders (PSUDs) was evaluated. Methods.-Twenty-four BAC-negative (BAC-) (BAC, 0) and 21 BAC-positive (BAC+) (BAC, greater-than-or-equal-to 22 mmol/L or 100 mg/dL; mean, 41 mmol/L; range, 24.3 to 79 mmol/L) adult trauma patients were evaluated for alcoholism and other PSUDs using the Structured Clinical Interview (SCI) from the Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (DSM-III-R). Approximately half were vehicular crash victims and 78% were men. Results.-A total of 64 PSUDs were diagnosed in 31 (68.9%) of the 45 patients; all but one was for dependence (vs abuse). Of the BAC+ patients, 14 (66.7%) met DSM-III-R criteria for alcohol dependence, 11 (78.6%) of whom also had other PSUDs not related to alcohol. Two other BAC+ patients had nonalcohol PSUDs. Of the BAC- patients, 11 (45.8%) had alcohol dependence, six (54.5%) of whom also had nonalcohol PSUDs. Another four BAC- patients had nonalcohol PSUDs. Overall, 76.2% of the BAC+ patients and 62.5% of the BAC- patients had a diagnosis of psychoactive substance dependence. Conclusion.-All patients admitted to trauma centers should be assessed for alcoholism and other PSUDs. C1 CHARLES MATHIAS NATL STUDY CTR TRAUMA & EMERGENCY MED SYST,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,CTR INJURY PREVENT,BALTIMORE,MD 21218. UNIV MARYLAND,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT EPIDEMIOL & PREVENT MED,BALTIMORE,MD 21201. NIDA,BETHESDA,MD. RP SODERSTROM, CA (reprint author), MARYLAND INST EMERGENCY MED SERV SYST,R ADAMS COWLEY SHOCK TRAUMA CTR,DEPT SURG,22 S GREENE ST,BALTIMORE,MD 21201, USA. OI Smith, Gordon/0000-0002-2911-3071 FU NIAAA NIH HHS [R29AA07700] NR 38 TC 94 Z9 96 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAY 27 PY 1992 VL 267 IS 20 BP 2756 EP 2759 DI 10.1001/jama.267.20.2756 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HV265 UT WOS:A1992HV26500022 PM 1578594 ER PT J AU TOZSER, J WEBER, IT GUSTCHINA, A BLAHA, I COPELAND, TD LOUIS, JM OROSZLAN, S AF TOZSER, J WEBER, IT GUSTCHINA, A BLAHA, I COPELAND, TD LOUIS, JM OROSZLAN, S TI KINETIC AND MODELING STUDIES OF S3-S3' SUBSITES OF HIV PROTEINASES SO BIOCHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; MURINE LEUKEMIA-VIRUS; TYPE-1 PROTEASE; SUBSTRATE; INFECTIVITY; RESOLUTION; INHIBITOR; COMPLEX; GAG; POLYPROTEINS AB Kinetic analysis and modeling studies of HIV-1 and HIV-2 proteinases were carr [GRAPHICS] and its analogs containing single amino acid substitutions in P3-P3' positions. The two proteinases acted similarly on the substrates except those having certain hydrophobic amino acids at P2, P1, P2', and P3' positions (Ala, Leu, Met, Phe). Various amino acids seemed to be acceptable at P3 and P3' positions, while the P2 and P2' positions seemed to be more restrictive. Polar uncharged residues resulted in relatively good binding at P3 and P2 positions, while at P2' and P3' positions they gave very high K(m) values, indicating substantial differences in the respective S and S' subsites of the enzyme. Lys prevented substrate hydrolysis at any of the P2-P2' positions. The large differences for subsite preference at P2 and P2' positions seem to be at least partially due to the different internal interactions of P2 residue with P1', and P2' residue with P1. As expected on the basis of amino acid frequency in the naturally occurring cleavage sites, hydrophobic residues at P1 position resulted in cleavable peptides, while polar and beta-branched amino acids prevented hydrolysis. On the other hand, changing the P1' Pro to other amino acids prevented substrate hydrolysis, even if the substituted amino acid had produced a good substrate in other oligopeptides representing naturally occurring cleavage sites. The results suggest that the subsite specificity of the HIV proteinases may strongly depend on the sequence context of the substrate. C1 NCI, FREDERICK CANC RES & DEV CTR, MOLEC VIROL & CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MACROMOLEC STRUCT LAB, FREDERICK, MD 21702 USA. NIDDKD, CELLULAR & DEV BIOL LAB, BETHESDA, MD 20892 USA. RI Tozser, Jozsef/A-7840-2008; OI Tozser, Jozsef/0000-0003-0274-0056; Tozser, Jozsef/0000-0001-5076-8729 FU NCI NIH HHS [N01-CO-74101] NR 52 TC 88 Z9 88 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAY 26 PY 1992 VL 31 IS 20 BP 4793 EP 4800 DI 10.1021/bi00135a008 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HW138 UT WOS:A1992HW13800008 PM 1591240 ER PT J AU CLIMENT, I SJOBERG, BM HUANG, CY AF CLIMENT, I SJOBERG, BM HUANG, CY TI SITE-DIRECTED MUTAGENESIS AND DELETION OF THE CARBOXYL TERMINUS OF ESCHERICHIA-COLI RIBONUCLEOTIDE REDUCTASE PROTEIN R2 - EFFECTS ON CATALYTIC ACTIVITY AND SUBUNIT INTERACTION SO BIOCHEMISTRY LA English DT Article ID PROMOTER SYSTEM; IRON CENTER; DIPHOSPHATES; INHIBITION; CLONING; ENZYME AB Ribonucleotide reductase from Escherichia coli consists of two dissociable, nonidentical homodimeric proteins called R1 and R2. The role of the C-terminal region of R2 in forming the R1R2 active complex has been studied. A heterodimeric R2 form with a full-length polypeptide chain and a truncated one missing the last 30 carboxyl-terminal residues was engineered by site-directed mutagenesis. Kinetic analysis of the binding of this protein to R1, compared with full-length or truncated homodimer, revealed that the C-terminal end of R2 accounts for all of its interactions with R1. The intrinsic dissociation constant of the heterodimeric R2 form, with only one contact to R1, 13-mu-M, is of the same magnitude as that obtained previously [Climent, I., Sjoberg, B.-M., & Huang, C. Y. (1991) Biochemistry 30, 5164-5171] for synthetic C-terminal peptides, 15-18-mu-M. We have also mutagenized the only two invariant residues localized at the C-terminal region of R2, glutamic acid-350 and tyrosine-356, to alanine. The binding of these mutant proteins to R1 remains tight, but their catalytic activity is severely affected. While E350A protein exhibits a low (240 times less active than the wild-type) but definitive activity, Y356A is completely inactive. A catalytic rather than structural role for these residues is discussed. C1 UNIV STOCKHOLM, DEPT MOLEC BIOL, S-10691 STOCKHOLM, SWEDEN. NHLBI, BIOCHEM LAB, BETHESDA, MD 20892 USA. NR 34 TC 125 Z9 127 U1 0 U2 7 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAY 26 PY 1992 VL 31 IS 20 BP 4801 EP 4807 DI 10.1021/bi00135a009 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HW138 UT WOS:A1992HW13800009 PM 1591241 ER PT J AU SCHWALBE, RA DAHLBACK, B COE, JE NELSESTUEN, GL AF SCHWALBE, RA DAHLBACK, B COE, JE NELSESTUEN, GL TI PENTRAXIN FAMILY OF PROTEINS INTERACT SPECIFICALLY WITH PHOSPHORYLCHOLINE AND OR PHOSPHORYLETHANOLAMINE SO BIOCHEMISTRY LA English DT Article ID C-REACTIVE PROTEIN; AMYLOID-P-COMPONENT; HAMSTER FEMALE PROTEIN; C4B-BINDING PROTEIN; HUMAN-PLASMA; SYRIAN-HAMSTERS; BINDING PROTEIN; SERUM; COMPLEX; CHROMATIN AB Pentraxins are a family of serum proteins characterized by five identical subunits that are noncovalently linked. The two major types of pentraxins are C-reactive protein (CRP) and serum amyloid P component (SAP). CRP proteins are identified by their calcium-dependent interaction with phosphorylcholine. This study showed that SAP also bound to phosphorylated compounds but had a high specificity for phosphorylethanolamine. Thus, human CRP and SAP show high specificity that is complementary for the related compounds, phosphorylcholine and phosphorylethanolamine, respectively. This relationship suggests a complementary and/or related function for the pentraxins. Pentraxins from other species were also examined. Mouse SAP showed binding interactions and specificity similar to human SAP. Female protein (FP) from hamster and rat CRP showed a hybrid specificity and bound to both phosphorylethanolamine and phosphorylcholine. All of the proteins that bound phosphorylethanolamine also associated with human C4b-binding protein (C4BP). With the exception of human and rat CRP, all the proteins also bound to vesicles containing acidic phospholipids. All of these binding interactions were calcium-dependent and mutually exclusive, suggesting that they involved the same site on the protein. These findings suggest possible ways to examine the function of the pentraxins. C1 UNIV MINNESOTA,DEPT BIOCHEM,ST PAUL,MN 55108. UNIV LUND,MALMO GEN HOSP,DEPT CLIN CHEM,S-21401 MALMO,SWEDEN. NIAID,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. FU NHLBI NIH HHS [HL15728] NR 51 TC 84 Z9 87 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAY 26 PY 1992 VL 31 IS 20 BP 4907 EP 4915 DI 10.1021/bi00135a023 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HW138 UT WOS:A1992HW13800023 PM 1375509 ER PT J AU EVANS, GA LINNEKIN, D GROVE, S FARRAR, WL AF EVANS, GA LINNEKIN, D GROVE, S FARRAR, WL TI SPECIFIC PROTEIN-KINASES MODULATED DURING T-CELL MITOGENESIS - ACTIVITY OF A 55-KDA SERINE KINASE IS ASSOCIATED WITH GROWTH ARREST IN HUMAN T-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CYCLIN MESSENGER-RNA; HUMAN LYMPHOCYTES-T; DEPENDENT PHOSPHORYLATION; CDC2 PROTEIN; INTERLEUKIN-2; ACTIVATION; RETINOBLASTOMA; MITOSIS; SUBUNIT; GENE AB The intracellular events which are involved in controlling the G1 to S phase transition during the eucaryotic cell cycle are important to define in order to understand the mechanisms by which mitogenic and growth arrest-inducing agents control cell growth. Because a change in protein kinase activity is associated with the initial response of cells to mitogenic stimulants and growth factors, we used a kinase renaturation assay to identify specific protein kinases which are modulated as human T cells make the G1 to S phase transition after mitogenic stimulation with lectin. We identified four protein serine/threonine kinases of 180, 97, 85, and 38 kilodaltons which are increased in activity as these cells enter S phase. A-55 kDa serine/threonine kinase (PK55) was shown to have maximal activity during G0 and its activity was reduced by 95% upon movement into S phase. PK55 is inducible in human T cells by removal of interleukin 2 and low serum incubation which arrests cells in G1 phase, indicating that it is closely associated with G1 phase growth arrest. Furthermore, a similar PK55 activity was induced upon growth arrest in HL-60 cells treated with dimethyl sulfoxide and in Daudi cells treated with interferon-alpha. Because the cAMP-dependent protein kinase (PK-A) family has been shown to be antiproliferative to lectin stimulated T cells, we were interested in determining whether PK55 was in fact an isozyme of PK-A. Comparative analysis using a specific peptide inhibitor of PK-A activity revealed that PK55 is catalytically distinct from PK-A. This data suggest that increases in PK55 may be associated with the growth-arrested state and further that PK55 is distinct from PK-A. C1 DYNCORP,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RP EVANS, GA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BCDP,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 26 TC 4 Z9 4 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10313 EP 10317 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000019 PM 1534085 ER PT J AU YANG, J CLARK, AE KOZKA, IJ CUSHMAN, SW HOLMAN, GD AF YANG, J CLARK, AE KOZKA, IJ CUSHMAN, SW HOLMAN, GD TI DEVELOPMENT OF AN INTRACELLULAR POOL OF GLUCOSE TRANSPORTERS IN 3T3-L1 CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INSULIN-STIMULATED TRANSLOCATION; RAT SKELETAL-MUSCLE; HEXOSE-TRANSPORT; PLASMA-MEMBRANE; MURINE FIBROBLASTS; ADIPOSE-CELLS; MESSENGER-RNA; ADIPOCYTES; HEPG2; EXPRESSION AB The membrane-impermeant bis-mannose photolabel 2-N-4-(1-azi-2,2,2-trifluoroethyl)benzoyl-1,3-bis-(D-mannos-4-yloxy)-2-propylamine (ATB-BMPA) has been used to study the development of an intracellular pool of glucose transporters in 3T3-L1 cells. The subcellular distributions of the transporter isoforms GLUT1 and GLUT4 were determined by comparing the labeling obtained in cells in which the impermeant reagent only had access to the cell surface and the labeling obtained in digitonin-permeabilized cells. ATB-BMPA labeling showed that only GLUT1 was present in preconfluent fibroblasts and that most of the transporters were distributed to the cell surface. In preconfluent fibroblasts, the 2-deoxy-D-glucose transport activity was almost-equal-to 5 times higher than in confluent fibroblasts. ATB-BMPA labeling showed that the decrease in transport as cells reached confluence was associated with a decrease in the proportion of GLUT1 distributed to the cell surface. The sequestration of these transporters was associated with the development of an insulin-responsive transport activity which increased by almost-equal-to 2.5-fold compared with unstimulated confluent cells. ATB-BMPA labeling showed that insulin stimulation resulted in an almost-equal-to 2-fold increase in surface GLUT1 so that about one-half of the available transporters became recruited to the cell surface. Measurements of the changes in the distribution of both GLUT1 and GLUT4 throughout the differentiation of confluent fibroblasts into adipocytes showed that both transporters were sequestered in parallel. Basal levels of transport and photolabeling remained low throughout the differentiation period when the total pool of transporters (GLUTI plus GLUT4) was increased by almost-equal-to 5-fold. These results suggest that the sequestration process was present before new transporters were synthesized. Thus, the sequestration mechanism develops in confluent growth-arrested fibroblasts although the capacity to sequester additional transporters may increase as differentiation proceeds. C1 NIDDKD,DIABET BRANCH,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD 20892. RP YANG, J (reprint author), UNIV BATH,DEPT BIOCHEM,BATH BA2 7AY,AVON,ENGLAND. NR 37 TC 82 Z9 82 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10393 EP 10399 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000032 PM 1587825 ER PT J AU WAHL, MI JONES, GA NISHIBE, S RHEE, SG CARPENTER, G AF WAHL, MI JONES, GA NISHIBE, S RHEE, SG CARPENTER, G TI GROWTH-FACTOR STIMULATION OF PHOSPHOLIPASE-C-GAMMA-1 ACTIVITY - COMPARATIVE PROPERTIES OF CONTROL AND ACTIVATED ENZYMES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; TYROSINE PHOSPHORYLATION; FACTOR RECEPTOR; INTRACELLULAR STORES; INOSITOL PHOSPHATES; KINETIC-ANALYSIS; CYTOSOLIC CA-2+; MIXED MICELLES; BOVINE BRAIN; A-431 CELLS AB We demonstrated previously tyrosine phosphorylation-dependent modulation of phospholipase C-gamma-1 (PLC-gamma-1) catalytic activity (Nishibe, S., Wahl, M. I., Hernandez-Sotomayor, S. M. T., Tonks, N. K., Rhee, S. G., and Carpenter, G. (1990) Science 250, 1253-1256). The increase in PLC-gamma-1 catalytic activity in A-431 cells occurs rapidly, with maximal activation 5 min after epidermal growth factor (EGF) stimulation. Certain other growth factors (fibroblast growth factor, platelet-derived growth factor) also stimulate PLC-gamma-1 catalytic activity, whereas insulin does not. A similar increase in PLC-gamma-1 specific activity (2-3-fold) was observed in both soluble (cytosol) and particulate (membrane) preparations from EGF-treated cells. Tyrosine-phosphorylated PLC-gamma-1 was detected in both cytosol and membrane fractions in lysates from EGF-treated A-431 cells, but the proportion of tyrosine-phosphorylated PLC-gamma-1 was higher in the cytosol (approximately 50%) than in the membrane (approximately 20%). Because a micellar concentration of the non-ionic detergent Triton X-100 allows detection of the tyrosine phosphorylation-dependent increase in PLC-gamma-1 catalytic activity in this assay, we evaluated the kinetic properties of PLC-gamma-1, immunoprecipitated from cytosol of control or EGF-treated cells, using substrate, phosphatidylinositol 4,5-bisphosphate (PtdIns 4,5-P2), solubilized in Triton X-100 at various molar ratios. The behavior of the control enzyme differed from the EGF-activated enzyme with respect to both K8 and K(m). The control enzyme has a 7.5-fold higher K8 value than the activated enzyme (1.5 mm as compared with 0.22 mm). Activation by EGF is also a positive allosteric modifier of PLC-gamma-1-catalyzed PtdIns 4,5-P2 hydrolysis, i.e. the activated enzyme displayed apparent Michalis-Menton kinetics, with a K(m) of 0.6 mol fraction PtdIns 4,5-P2, whereas the control enzyme displayed sigmoidal kinetics with respect to PtdIns 4,5-P2 hydrolysis. At low substrate mol fractions (e.g. 0.07), the reaction velocity of the control enzyme was 4-fold lower than the activated enzyme. However, at a high substrate mol fraction (e.g. 0.33), the estimated maximal reaction velocities (V(max)) for both forms of PLC-gamma-1 were equivalent. PLC-gamma-1 activity from both control and EGF-treated cells was stimulated by increasing nanomolar Ca2+ concentrations. Although the catalytic activity of PLC-gamma-1 from EGF-treated cells was greater than control PLC-gamma-1 at every Ca2+ concentration tested, the relative stimulation of activity was markedly greater at Ca2+ concentrations above approximately 300 nM. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT BIOCHEM,NASHVILLE,TN 37232. VANDERBILT UNIV,MED CTR,SCH MED,DEPT MED,NASHVILLE,TN 37232. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA43720, CA09582]; NIGMS NIH HHS [GM07347] NR 48 TC 150 Z9 150 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10447 EP 10456 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000039 PM 1316902 ER PT J AU MOSS, J STANLEY, SJ NIGHTINGALE, MS MURTAGH, JJ MONACO, L MISHIMA, K CHEN, HC WILLIAMSON, KC TSAI, SC AF MOSS, J STANLEY, SJ NIGHTINGALE, MS MURTAGH, JJ MONACO, L MISHIMA, K CHEN, HC WILLIAMSON, KC TSAI, SC TI MOLECULAR AND IMMUNOLOGICAL CHARACTERIZATION OF ADP-RIBOSYLARGININE HYDROLASES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID POLYMERASE CHAIN-REACTION; AMINO-ACID SEQUENCE; TURKEY ERYTHROCYTES; RIBOSYLTRANSFERASE ACTIVITY; SUBSTRATE-SPECIFICITY; RIBOSYLATION FACTOR; CHOLERA-TOXIN; PROTEIN; NUCLEOTIDE; IDENTIFICATION AB Mono-ADP-ribosylation is a reversible modification of proteins with NAD:arginine ADP-ribosyltransferases and ADP-ribosylarginine hydrolases catalyzing the forward and reverse reactions, respectively. Hydrolase activities were present in a variety of animal species, with the highest specific activities found in rat and mouse brain, spleen, and testis. Rat and mouse hydrolases were dithiothreitol- and Mg2+-dependent, whereas the bovine and guinea pig enzymes were dithiothreitol-independent. A rat brain hydrolase was purified approximately 20,000-fold and represented the major approximately 39-kDa protein on denaturing gels. Immunoaffinity-purified rabbit polyclonal antibodies reacted with 39-kDa proteins from turkey erythrocytes and rat, mouse, and calf brains. A rat brain cDNA library was screened using oligonucleotide and polymerase chain reaction-generated cDNA probes. Inserts from two overlapping clones yielded a composite sequence that included a 1086-base pair open reading frame, which contained amino acid sequences found in the purified hydrolase. A hydrolase fusion protein, synthesized in Escherichia coli, reacted with anti-39-kDa polyclonal antibodies and exhibited Mg2+- and dithiothreitol-dependent hydrolase activity. A coding region cDNA hybridized readily to a 1.7-kilobase band in rat and mouse poly(A)+ RNA, but poorly to bovine, chicken, rabbit, and human poly(A)+ RNA. The immunological and molecular biological data are consistent with partial conservation of hydrolase structure across animal species. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. RP MOSS, J (reprint author), NHLBI,CELLULAR METAB LAB,ROOM 5N-307,BLDG 10,BETHESDA,MD 20892, USA. RI Monaco, Lucia/A-4031-2010 NR 39 TC 85 Z9 86 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10481 EP 10488 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000043 PM 1375222 ER PT J AU MORROW, CS CHIU, J COWAN, KH AF MORROW, CS CHIU, J COWAN, KH TI POSTTRANSCRIPTIONAL CONTROL OF GLUTATHIONE-S-TRANSFERASE-PI GENE-EXPRESSION IN HUMAN BREAST-CANCER CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ESTROGEN-RECEPTOR CONTENT; MESSENGER-RNA STABILITY; C-MYC ONCOGENE; DRUG-RESISTANCE; PLACENTAL FORM; STEM-LOOP; RAT; REGION; CDNA; HEPATOCARCINOGENESIS AB The glutathione S-transferase pi-gene (GST-pi) is highly expressed in estrogen receptor negative (ER-) but not expressed in ER+ human breast cancer cell lines. To define regulatory mechanisms of GST-pi gene expression, we analyzed both the activity of the GST-pi promoter and the posttranscriptional fate of GST-pi RNA sequences in three ER+ and three ER- breast cancer cell lines. Expression of a transiently transfected CAT reporter gene driven by the GST-pi promoter and 2203 nucleotides of 5'-flanking sequences were similar in all six cell lines regardless of ER status. Endogenous GST-pi transcription rates in nuclei isolated from ER- cells were quite low despite high steady state levels of cytoplasmic mRNA. Furthermore, the endogenous GST-pi gene was transcribed in ER+ nuclei at rates similar to those obtained in ER- nuclei. We determined the stabilities of mRNAs transcribed from the endogenous GST-pi gene (ER- cells) and from a stably transfected GST-pi cDNA expression vector (ER+ and ER- cells). The endogenous GST-pi mRNA was extraordinarily stable in ER- cells. Comparisons between transfected ER+ and ER- cells revealed no significant differences in the stabilities of transfection-derived GST-pi mRNA sequences. We conclude that GST-pi mRNA stability contributes significantly to the high levels of cytoplasmic mRNA observed in ER-cells, but that the differential expression of GST-pi in ER+ versus ER- cells is governed by other posttranscriptional processes. RP MORROW, CS (reprint author), NCI,MED BRANCH,BLDG 10,RM 12N226,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 54 TC 48 Z9 49 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10544 EP 10550 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000051 PM 1587835 ER PT J AU OLAH, ME REN, HZ OSTROWSKI, J JACOBSON, KA STILES, GL AF OLAH, ME REN, HZ OSTROWSKI, J JACOBSON, KA STILES, GL TI CLONING, EXPRESSION, AND CHARACTERIZATION OF THE UNIQUE BOVINE-A1 ADENOSINE RECEPTOR - STUDIES ON THE LIGAND-BINDING SITE BY SITE-DIRECTED MUTAGENESIS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MUSCARINIC ACETYLCHOLINE-RECEPTOR; ADENYLATE CYCLASE SYSTEM; MOLECULAR-CLONING; ALPHA-1-ADRENERGIC RECEPTOR; CEREBRAL-CORTEX; BRAIN MEMBRANES; CDNA; A1-ADENOSINE; ANTAGONIST; SUBTYPES AB The bovine brain A1 adenosine receptor (A1AR) is distinct from other A1ARs in that it displays the unique agonist potency series of N6-R-phenylisopropyladenosine (R-PIA) > N6-S-phenylisopropyladenosine (S-PIA) > 5'-N-ethylcarboxamidoadenosine and has a 5-10-fold higher affinity for both agonists and antagonists. The cDNA for this receptor has been cloned from a size-selected (2-4-kb) bovine brain library and sequenced. The 2.0-kb cDNA encodes a protein of 326 amino acid residues with a molecular mass of 36,570 daltons. The amino acid sequence fits well into the seven-transmembrane domain motif typical of G protein-coupled receptors. Northern analysis in bovine tissue using the full length cDNA demonstrates mRNAs of 3.4 and 5.7 kb with a tissue distribution consistent with A1AR binding. Subcloning of the cDNA in a pCMV5 expression vector with subsequent transfection into both COS7 and Chinese hamster ovary cells revealed a fully functional A1AR which could inhibit adenylylcyclase and retained the unique pharmacologic properties of the bovine brain A1AR. The A1AR was found to have a single histidine residue in each of transmembrane domains 6 and 7. Histidine residues have been postulated by biochemical studies to be important for ligand binding. Mutation of His-278 to Leu-278 (seventh transmembrane domain) dramatically decreased both agonist and antagonist binding by > 90%. In contrast, mutation of His-251 to Leu-251 decreased antagonist affinity and the number of receptors recognized by an antagonist radioligand. In contrast, agonist affinity was not perturbed but the number of receptors detected by an agonist radioligand was also reduced. These data suggest that both histidines are important for both agonist and antagonist binding, but His-278 appears critical for ligand binding to occur. C1 DUKE UNIV,MED CTR,DEPT MED,BOX 3444,DURHAM,NC 27710. NIDDKD,CHEM LAB,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT BIOCHEM,DURHAM,NC 27710. DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DURHAM,NC 27710. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999]; NHLBI NIH HHS [R01-HL35134]; NIGMS NIH HHS [1F32-GM-13713-01] NR 46 TC 153 Z9 154 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10764 EP 10770 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000084 PM 1587851 ER PT J AU GLASGOW, WC AFSHARI, CA BARRETT, JC ELING, TE AF GLASGOW, WC AFSHARI, CA BARRETT, JC ELING, TE TI MODULATION OF THE EPIDERMAL GROWTH-FACTOR MITOGENIC RESPONSE BY METABOLITES OF LINOLEIC AND ARACHIDONIC-ACID IN SYRIAN-HAMSTER EMBRYO FIBROBLASTS - DIFFERENTIAL-EFFECTS IN TUMOR SUPPRESSOR GENE (+) AND (-) PHENOTYPES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHOSPHOLIPASE-C-GAMMA; PROTEIN-TYROSINE KINASE; PERFORMANCE LIQUID-CHROMATOGRAPHY; MAMMARY EPITHELIAL-CELLS; PROSTAGLANDIN-H SYNTHASE; EGF RECEPTOR; 5-LIPOXYGENASE-ACTIVATING PROTEIN; PROLIFERATIVE RESPONSE; LEUKOTRIENE SYNTHESIS; ENDOTHELIAL-CELLS AB Specific metabolites of arachidonic and linoleic acid have been proposed as serving a regulatory function in growth factor signal transduction in fibroblasts. In studies with Syrian hamster embryo (SHE) fibroblasts, we found lipoxygenase inhibitors to be potent blockers of epidermal growth factor (EGF)-dependent mitogenesis. Analytical chemical characterization of arachidonic and linoleic acid metabolism in SHE cells demonstrated that the major lipoxygenase product was 13-hydroxyoctadecadienoic acid (HODE). EGF stimulation of quiescent SHE cells resulted in an enhancement of HODE biosynthesis. The primary arachidonate products were prostaglandin E2 and F2-alpha formed via the cyclooxygenase pathway. Inhibition of cyclooxygenase activity did not alter the EGF-mitogenic response in SHE cells. Addition of lipoxygenase-derived linoleate metabolites (10(10)-10(-6) M) produced a 2-4-fold potentiation of EGF-stimulated [H-3]thymidine incorporation in SHE cells. Interestingly, the linoleate products did not enhance the EGF mitogenic effect in variant SHE cells that had lost tumor suppressor gene function. These results were confirmed by autoradiographic studies of DNA synthesis and suggest that loss of tumor suppressor phenotype correlates with a lack of responsiveness to linoleate products in signal transduction. In studies on the mechanism of EGF regulation of linoleic acid metabolism, inhibitors of EGF receptor tyrosine kinase activity were observed to block EGF-stimulated HODE biosynthesis. In addition, both cyclohexamide and actinomycin D attenuated the ability of EGF to increase linoleic acid metabolism in SHE cells. EGF induction of the linoleate pathway appears to be linked to activation of the EGF receptor and may be modulated at transcriptional or translational levels. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 53 TC 146 Z9 146 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10771 EP 10779 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000085 PM 1587852 ER PT J AU PARK, K CHUNG, M KIM, SJ AF PARK, K CHUNG, M KIM, SJ TI INHIBITION OF MYOGENESIS BY OKADAIC ACID, AN INHIBITOR OF PROTEIN PHOSPHATASES-1 AND PHOSPHATASES-2A, CORRELATES WITH THE INDUCTION OF AP1 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SERUM RESPONSE ELEMENT; GENE FAMILY; TRANSCRIPTION FACTOR; COLLAGENASE GENE; TUMOR PROMOTER; GROWTH-FACTOR; ONCOGENE FOS; MYOD FAMILY; BINDING; MEMBER AB Recently, we demonstrated that okadaic acid, an inhibitor of protein phosphatases 1 and 2A, inhibits myogenesis by extinguishing the expression of MyoD1 and inducing the expression of Id. Since it has been reported that transformation by c-fos also inhibits myogenesis through inhibition of MyoD1 expression, we examined the effects of okadaic acid on the activation of the c-fos and jun family of proto-oncogenes in an attempt to understand the mechanism by which okadaic acid inhibits the myogenic differentiation. Treatment of C2C12 cells in growth medium with okadaic acid increased expression of the mRNAs for the c-fos family continuously and for the jun family to a lesser extent. In contrast, in differentiation medium, the induction of c-fos, c-jun, and fos B mRNAs by okadaic acid was transient, whereas fra-1, jun D, and jun B mRNAs were induced continuously, suggesting that okadaic acid regulates the expression of the c-fos and jun family through complex regulatory mechanisms depending on the state of differentiation of the cells. Transfection of c-jun and c-fos promoter-chloramphenicol acetyltransferase constructs demonstrated that the effects of okadaic acid on the induction of c-fos and c-jun are mediated through the activation of promoter elements. These results suggest that some of the targets of protein phosphatases 1 and 2A may include transcription factors capable of forming AP1 complexes and that these factors may play an important role during myogenic differentiation. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 46 TC 43 Z9 43 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10810 EP 10815 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000091 PM 1316910 ER PT J AU WALKER, B KRISHNASASTRY, M ZORN, L KASIANOWICZ, J BAYLEY, H AF WALKER, B KRISHNASASTRY, M ZORN, L KASIANOWICZ, J BAYLEY, H TI FUNCTIONAL EXPRESSION OF THE ALPHA-HEMOLYSIN OF STAPHYLOCOCCUS-AUREUS IN INTACT ESCHERICHIA-COLI AND IN CELL LYSATES - DELETION OF 5 C-TERMINAL AMINO-ACIDS SELECTIVELY IMPAIRS HEMOLYTIC-ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DEPENDENT PROTEIN-KINASE; MEMBRANE DAMAGE; REGULATORY SUBUNIT; TOXIN; BINDING; SITE; MECHANISM; CHANNEL; GENE; MUTAGENESIS AB The alpha-hemolysin gene from Staphylococcus aureus, excluding the 5' region encoding the hydrophobic leader sequence, was amplified from genomic DNA. The identity of the disputed C terminus has been confirmed and revisions made to the internal sequence. The hemolysin is expressed at high levels in Escherichia coli and has been purified to homogeneity from this source. In addition, active [S-35-Met]alpha-hemolysin of high specific radioactivity can be generated in an E. coli transcription-translation system. By criteria based on protein chemistry, and biological and electrophysiological assays, the recombinant polypeptide is closely similar to the staphylococcal polypeptide ruling out the possibility of functionally important posttranslational modifications in S. aureus. Convenient new assays utilizing the S-35-labeled polypeptide to measure erythrocyte binding, oligomer formation in detergent and on target cells, and hemolysis have been developed. They have been used to demonstrate that a deletion mutant of alpha-hemolysin, in which five C-terminal amino acids are absent, is severely compromised in its ability both to oligomerize and to lyse rabbit erythrocytes. The mutant polypeptide nevertheless binds tightly to erythrocytes as a monomer, strengthening the idea that oligomerization is required for cell lysis. C1 UNIV MASSACHUSETTS,CTR MED,GRAD SCH BIOMED SCI,WORCESTER,MA 01655. NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. RP WALKER, B (reprint author), WORCESTER FDN EXPTL BIOL INC,SHREWSBURY,MA 01545, USA. NR 45 TC 76 Z9 81 U1 3 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10902 EP 10909 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000103 PM 1587866 ER PT J AU AGOSTON, DV COLBURN, S KRAJNIAK, KG WASCHEK, JA AF AGOSTON, DV COLBURN, S KRAJNIAK, KG WASCHEK, JA TI DISTINCT REGULATION OF VASOACTIVE-INTESTINAL-PEPTIDE (VIP) EXPRESSION AT MESSENGER-RNA AND PEPTIDE LEVELS IN HUMAN NEUROBLASTOMA-CELLS SO NEUROSCIENCE LETTERS LA English DT Article DE VASOACTIVE INTESTINAL PEPTIDE; NEUROBLASTOMA; MESSENGER RNA; SH-SY5Y; DIFFERENTIATION ID NEURO-BLASTOMA CELLS; POLYPEPTIDE VIP; CHROMAFFIN CELLS; BRAIN; FORM; RAT AB Neuronal differentiation was induced in cultures of the human neuroblastoma cell line subclone SH-SY5Y by 14-day treatment with dibutyryl cAMP (dBcAMP), retinoic acid, and phorbol 12-myristate 13-acetate (PMA). An approximate 4-fold increase in vasoactive intestinal peptide (VIP) mRNA concentration was observed after differentiation with retinoic acid, whereas no change in VIP mRNA concentration was observed after differentiation with dBcAMP or PMA. A short-term treatment of cells with PMA did however result in a 5-fold transient increase in VIP mRNA; prior differentiation with retinoic acid or dBcAMP diminished this effect. Observed increases in VIP mRNA were in all cases accompanied by increases in VIP immunoreactivity. Remarkably, however, long-term treatment of cells with dBcAMP, which caused no change in mRNA levels, resulted in a six-fold increase in VIP immunoreactivity. Acute (36-h) treatment with carbachol also caused an increase in VIP immunoreactivity (about 2-fold, and blocked by atropine) without an increase in VIP mRNA level. Thus, a quantitative change in gene transcription or mRNA stability appears not to be a prerequisite for increased VIP expression, indicating that regulation can occur at translational or post-translational steps. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,MENTAL RETARDAT RES CTR,LOS ANGELES,CA 90024. FU NICHD NIH HHS [HD04612, HD06576] NR 24 TC 19 Z9 19 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD MAY 25 PY 1992 VL 139 IS 2 BP 213 EP 216 DI 10.1016/0304-3940(92)90555-L PG 4 WC Neurosciences SC Neurosciences & Neurology GA HW694 UT WOS:A1992HW69400018 PM 1319016 ER PT J AU DRIGGERS, PH ELENBAAS, BA AN, JB LEE, IJ OZATO, K AF DRIGGERS, PH ELENBAAS, BA AN, JB LEE, IJ OZATO, K TI 2 UPSTREAM ELEMENTS ACTIVATE TRANSCRIPTION OF A MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I GENE INVITRO SO NUCLEIC ACIDS RESEARCH LA English DT Article ID ENHANCER BINDING-PROTEIN; MULTIPLE NUCLEAR FACTORS; RNA POLYMERASE-II; CELL-FREE SYSTEM; NF-KAPPA-B; REGULATORY ELEMENT; GLUCOCORTICOID RECEPTOR; NUCLEOTIDE-SEQUENCE; FACTORS INTERACT; MAMMALIAN-CELLS AB Expression of major histocompatibility complex (MHC) class I genes exhibits unique tissue and developmental specificity. In an effort to study molecular mechanisms of MHC class I gene regulation, an in vitro transcription system has been established. In B cell nuclear extracts a template DNA containing the mouse H-2L(d) promoter sequence accurately directed RNA polymerase II-dependent transcription of a G-free cassette. A conserved class I regulatory complex previously shown to moderately enhance promoter activity in vivo enhanced transcription in vitro by 2 - 3 fold. Much of this enhancement was accounted for by a 40 bp fragment within the complex, which was capable of activating a basal H-2L(d) promoter in either orientation. Farther downstream, another element called site B was identified, which independently activated MHC class I transcription in vitro by 2-4 fold. Site B bound a specific nuclear factor(s) through an NF-1 binding site but not through a neighboring CCAAT site. The functional significance of site B in vivo was demonstrated in transfection experiments in which site B enhanced MHC class I promoter activity to a degree comparable to that seen in vitro. With the identification of the two upstream activators, MHC class I genes may serve as a model to study roles of sequence-specific DNA-binding proteins in transcription in vitro. C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NR 70 TC 27 Z9 27 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAY 25 PY 1992 VL 20 IS 10 BP 2533 EP 2540 DI 10.1093/nar/20.10.2533 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HX134 UT WOS:A1992HX13400019 PM 1598211 ER PT J AU TOYAMA, R BENDE, SM DHAR, R AF TOYAMA, R BENDE, SM DHAR, R TI TRANSCRIPTIONAL ACTIVITY OF THE HUMAN IMMUNODEFICIENCY VIRUS-1 LTR PROMOTER IN FISSION YEAST SCHIZOSACCHAROMYCES-POMBE SO NUCLEIC ACIDS RESEARCH LA English DT Article ID LONG TERMINAL REPEAT; SACCHAROMYCES-CEREVISIAE; TRANS-ACTIVATOR; MUTATIONAL ANALYSIS; TAR RNA; HIV-1; PROTEIN; GENE; IDENTIFICATION; ELEMENT AB We have analyzed the transcriptional activity of the human immunodeficiency virus type I (HIV-1) LTR Promoter in the fission yeast Schizosaccharomyces pombe (S. pombe). The ability of a series Of 5'-deleted forms of the HIV-1 LTR Promoter to direct transcription of the chloramphenicol acetyltransferase reporter gene was studied. We found that the HIV-1 promoter is functional in S. pombe and that deletion of sequences upstream of the NF-kB binding site previously identified to contain the negative regulatory element (NRE) in mammalian cells, resulted in an about thirty-fold increase in transcriptional activity. Sequences in the HIV-1 promoter that bind NF-kB were found to be essential for transcriptional activation in S. pombe. In mammalian cells, transactivation of the HIV-1 LTR requires TAR sequences and the viral Tat protein. In fission yeast, Tat failed to transactivate the HIV-1 LTR, suggesting that S. pombe may lack a cellular factor(s) required for the Tat transactivation process. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 29 TC 13 Z9 13 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAY 25 PY 1992 VL 20 IS 10 BP 2591 EP 2596 DI 10.1093/nar/20.10.2591 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HX134 UT WOS:A1992HX13400027 PM 1598218 ER PT J AU HAYNES, SR DOLLARD, C WINSTON, F BECK, S TROWSDALE, J DAWID, IB AF HAYNES, SR DOLLARD, C WINSTON, F BECK, S TROWSDALE, J DAWID, IB TI THE BROMODOMAIN - A CONSERVED SEQUENCE FOUND IN HUMAN, DROSOPHILA AND YEAST PROTEINS SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. RP HAYNES, SR (reprint author), NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892, USA. NR 9 TC 253 Z9 259 U1 1 U2 12 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAY 25 PY 1992 VL 20 IS 10 BP 2603 EP 2603 DI 10.1093/nar/20.10.2603 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HX134 UT WOS:A1992HX13400034 PM 1350857 ER PT J AU WURTZ, RH DUFFY, CJ AF WURTZ, RH DUFFY, CJ TI NEURONAL CORRELATES OF OPTIC FLOW STIMULATION SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID SUPERIOR TEMPORAL SULCUS; MACAQUE MONKEY; VISUAL AREA; EXPANSION CONTRACTION; RESPONSE SELECTIVITY; ROTATION CELLS; EYE-MOVEMENTS; FIELD STIMULI; DORSAL PART; MST NEURONS RP WURTZ, RH (reprint author), NEI, SENSORIMOTOR RES LAB, BLDG 10, ROOM 10C101, BETHESDA, MD 20892 USA. NR 20 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAY 22 PY 1992 VL 656 BP 205 EP 219 PG 15 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM221 UT WOS:A1992JM22100015 ER PT J AU MILES, FA BUSETTINI, C AF MILES, FA BUSETTINI, C TI OCULAR COMPENSATION FOR SELF-MOTION - VISUAL MECHANISMS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID PURSUIT EYE-MOVEMENTS; RABBITS CEREBELLAR FLOCCULUS; ACCESSORY OPTIC-SYSTEM; TERM ADAPTIVE-CHANGES; OPTOKINETIC NYSTAGMUS; SMOOTH-PURSUIT; VESTIBULOOCULAR REFLEX; SPATIAL-ORGANIZATION; VESTIBULAR INTERACTIONS; RESPONSE PROPERTIES C1 UNIV TRIESTE,DIPARTIMENTO ELETTROTECN ELETTRON & INFORMAT,I-34100 TRIESTE,ITALY. RP MILES, FA (reprint author), NEI,SENSORIMOTOR RES LAB,BLDG 10,ROOM 10C101,BETHESDA,MD 20892, USA. NR 78 TC 34 Z9 34 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD MAY 22 PY 1992 VL 656 BP 220 EP 232 DI 10.1111/j.1749-6632.1992.tb25211.x PG 13 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM221 UT WOS:A1992JM22100016 PM 1599145 ER PT J AU WALKER, JM BOWEN, WD GOLDSTEIN, SR ROBERTS, AH PATRICK, SL HOHMANN, AG DECOSTA, B AF WALKER, JM BOWEN, WD GOLDSTEIN, SR ROBERTS, AH PATRICK, SL HOHMANN, AG DECOSTA, B TI AUTORADIOGRAPHIC DISTRIBUTION OF [H-3] (+)-PENTAZOCINE AND [H-3] 1,3-DI-ORTHO-TOLYLGUANIDINE (DTG) BINDING-SITES IN GUINEA-PIG BRAIN - A COMPARATIVE-STUDY SO BRAIN RESEARCH LA English DT Article DE SIGMA RECEPTOR; RED NUCLEUS; 1,3-DI-ORTHO-TOLYLGUANIDINE; N-ALLYL-NORMETAZOCINE; PENTAZOCINE; (+)-3-PPP; AUTORADIOGRAPHY; BRAIN ID ANTIPSYCHOTIC-DRUGS; SIGMA-RECEPTOR; OPIATE RECEPTORS; RAT-BRAIN; LOCALIZATION; LIGAND AB Binding studies suggested the selectivity of (+)-pentazocine for sigma receptors, and subsequent synthesis and testing of [H-3](+)-pentazocine confirmed its high potency and selectivity for sigma sites. Newer data have demonstrated the selectivity of (+)-pentazocine for a subtype of the sigma receptor called sigma-1. Based on these findings, the distribution of [H-3](+)-pentazocine binding sites in the guinea pig brain was examined using in vitro autoradiography. [H-3](+)-Pentazocine binding was high in the cingulate cortex, dorsal diagonal band, periaqueductal gray, cerebellum and cranial nerve nuclei. It was relatively low in the nucleus accumbens, neocortical areas and caudate nucleus. A significant correlation was found between the binding of [H-3](+)-pentazocine and [H-3]1,3-di-o-tolylguanidine, a selective sigma ligand across brain regions. However, certain nuclei exhibited markedly different ratios of binding of the two ligands. Since DTG is not selective for the sigma subtypes, while (+)-pentazocine is selective for the sigma-1 type, the data are suggestive of relative differences in the distributions of sigma-1 and sigma-2 sites. C1 BROWN UNIV,DIV BIOL & MED,BIOCHEM SECT,PROVIDENCE,RI 02912. NIDDK,MED CHEM LAB,BETHESDA,MD 20892. RP WALKER, JM (reprint author), BROWN UNIV,DEPT PSYCHOL,SCHRIER RES LAB,89 WATERMAN ST,POB 1853,PROVIDENCE,RI 02912, USA. NR 23 TC 62 Z9 65 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAY 22 PY 1992 VL 581 IS 1 BP 33 EP 38 DI 10.1016/0006-8993(92)90340-F PG 6 WC Neurosciences SC Neurosciences & Neurology GA HZ943 UT WOS:A1992HZ94300004 PM 1323368 ER PT J AU LEPPIN, C FINIELSMARLIER, F CRAWLEY, JN MONTPIED, P PAUL, SM AF LEPPIN, C FINIELSMARLIER, F CRAWLEY, JN MONTPIED, P PAUL, SM TI FAILURE OF A PROTEIN-SYNTHESIS INHIBITOR TO MODIFY GLUTAMATE RECEPTOR-MEDIATED NEUROTOXICITY INVIVO SO BRAIN RESEARCH LA English DT Note DE EXCITOTOXICITY; GLUTAMATE RECEPTOR; PROTEIN SYNTHESIS INHIBITOR ID NEURONAL DEATH; MK-801 AB The delayed neuronal death (DND) resulting from brief forebrain ischemia has recently been reported to be markedly attenuated by parenteral administration of the reversible protein synthesis inhibitor, anisomycin. Previous work suggests that ischemia-induced DND is mediated by glutamate acting at one or more glutamate receptors, since glutamate receptor antagonists have been reported to reduce ischemia-induced DND. Consequently, we tested whether anisomycin could modify DND induced by direct intracerebral administration of the excitotoxins, N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methylisoxasole (AMPA) or kainic acid. Anisomycin, administered parenterally, in multiple doses did not alter DND induced by any of these excitotoxins, nor did combined parenteral and direct intracerebral injection of anisomycin protect against DND induced by AMPA. Thus, neurotoxicity induced by direct intracerebral administration of NMDA, AMPA or kainic acid does not appear to require de novo protein synthesis, and, therefore, is not likely to be mediated by the expression of a programmed cell death cascade. C1 NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BLDG 10,ROOM 4N224,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 8 TC 30 Z9 30 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAY 22 PY 1992 VL 581 IS 1 BP 168 EP 170 DI 10.1016/0006-8993(92)90359-H PG 3 WC Neurosciences SC Neurosciences & Neurology GA HZ943 UT WOS:A1992HZ94300023 PM 1379868 ER PT J AU ZIEGLER, T SUTORIS, H GLAUDEMANS, CPJ AF ZIEGLER, T SUTORIS, H GLAUDEMANS, CPJ TI BINDING-STUDIES ON INTERNAL IMMUNODETERMINANTS - SYNTHESIS OF BETA-(1-]6)-LINKED OLIGOSACCHARIDE METHYL GLYCOSIDES HAVING ONE TO 4 INTERNAL D-GALACTOPYRANOSYL RESIDUES FLANKED BY GENTIOBIOSE RESIDUES SO CARBOHYDRATE RESEARCH LA English DT Article ID POLYSACCHARIDE ANTIGEN; MONOCLONAL-ANTIBODY; COMBINING SITES; BETA-GLYCOSIDES; (1->6)-BETA-D-GALACTO-OLIGOSACCHARIDES AB The oligosaccharide glycosides beta-D-Glc p-(1 --> 6)-beta-D-Glc p-(1 --> 6)-[beta-D-Gal p-(1 --> 6)]n-beta-D-Glc p-(1 --> 6)-beta-D-Glc p-1 --> OMe (n = 1-4) were prepared by a convergent block synthesis. Haloacetyl, tert-butyldiphenylsilyl, and dimethylthexylsilyl groups were used as temporary protective groups for the preparation of the intermediate glycosyl donors and acceptors. The deoxygenated trisaccharide glyco-sides beta-D-Glc p-(1 --> 6)-beta-D-Gal p-(1 --> 6)-4-deoxy-beta-D-xylo-Hex p-1 --> OMe and beta-D-Glc p-(1 --> 6)-4-deoxy-beta-D-xylo-Hex p-(1 --> 6)-beta-D-Gal p-1 --> OMe were also synthesized. The binding of each glycoside to the monoclonal antigalactan antibody IgA 1539 was studied and the results support the previous finding that J539 can bind to internal antigenic epitopes. The data are consistent with the interpretation that subsite C of that antibody binds glucose with a K(a) of approximately 6 (cf. 10.9 for galactose). C1 NIDDK,BETHESDA,MD 20892. RP ZIEGLER, T (reprint author), UNIV STUTTGART,INST ORGAN CHEM,PFAFFENWALDRING 55,W-7000 STUTTGART 80,GERMANY. NR 24 TC 10 Z9 10 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD MAY 22 PY 1992 VL 229 IS 2 BP 271 EP 291 DI 10.1016/S0008-6215(00)90575-5 PG 21 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA HZ275 UT WOS:A1992HZ27500006 PM 1382854 ER PT J AU TOKUYAMA, T DALY, JW GARRAFFO, HM SPANDE, TF AF TOKUYAMA, T DALY, JW GARRAFFO, HM SPANDE, TF TI PYRROLIZIDINE OXIMES - A NOVEL NEW CLASS OF DENDROBATID ALKALOIDS SO TETRAHEDRON LA English DT Article ID SPECTRA AB Analysis of GC-FTIR spectra and reexamination of H-1- and C-13-NMR data led to revised structures for three closely related tricyclic alkaloids from a dendrobatid poison-frog Dendrobates pumilio. The simplest member, 222, is a spiropentano-pyrrolizidine oxime, while 236 is the corresponding O-methyl oxime and 252, a hydroxy-O-methyl oxime. C1 NIDDKD,BETHESDA,MD 20892. RP TOKUYAMA, T (reprint author), OSAKA CITY UNIV,FAC SCI,OSAKA 558,JAPAN. NR 16 TC 11 Z9 11 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4020 J9 TETRAHEDRON JI Tetrahedron PD MAY 22 PY 1992 VL 48 IS 21 BP 4247 EP 4258 DI 10.1016/S0040-4020(01)80437-3 PG 12 WC Chemistry, Organic SC Chemistry GA HV886 UT WOS:A1992HV88600001 ER PT J AU SLATER, JL HUANG, CH LEVIN, IW AF SLATER, JL HUANG, CH LEVIN, IW TI INTERDIGITATED BILAYER PACKING MOTIFS - RAMAN-SPECTROSCOPIC STUDIES OF THE EUTECTIC PHASE-BEHAVIOR OF THE 1-STEAROYL-2-CAPRYLPHOSPHATIDYLCHOLINE DIMYRISTOYLPHOSPHATIDYLCHOLINE BINARY MIXTURE SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE RAMAN SPECTROSCOPY; PHOSPHOLIPID BINARY MIXTURE; EUTECTIC PHASE BEHAVIOR; 1-STEAROYL-2-CAPRYLPHOSPHATIDYLCHOLINE; DIMYRISTOYLPHOSPHATIDYLCHOLINE; MIXED INTERDIGITATED BILAYER ID HYDROCARBON CHAIN INTERDIGITATION; PHOSPHOLIPID-BILAYERS; SPECTRAL PARAMETERS; DISPERSIONS; PHOSPHATIDYLCHOLINES; MODEL; DIPALMITOYLPHOSPHATIDYLCHOLINE; DIHEXADECYLPHOSPHATIDYLCHOLINE; LONG AB The thermotropic properties and acyl chain packing characteristics of multilamellar dispersions of binary mixtures of 1-stearoyl-2-caprylphosphatidylcholine (C(18): C(10)PC), an asymmetric chain species, and dimyristoylphosphatidylcholine (C(14): C(14)PC), a symmetric chain lipid, were monitored by vibrational Raman spectroscopy. In order to examine each component of the binary mixture separately, the acyl chains of the symmetric chain species were perdeuterated. As shown by differential scanning calorimetry, the mismatch in the gel phase bilayer thickness between the two lipid components generates a lateral phase separation resulting in two distinct gel phases, G(I) and G(II). which coexist over much of the composition range. The Raman data demonstrate that the mixed interdigitated phase (three chains per headgroup), analogous to single component phase behavior, is retained when the C(18): C(10)PC component act as a host for the G(I) gel phase. In contrast, the C(18): C(10)PC molecules exhibit partial interdigitation (two chains per headgroup) when they are included as guests within the C(14): C(14)PC host matrix to form the G(II) gel phase. Compared to pure C(14): C(t4)PC bilayers at equivalent reduced temperatures, the host G(II) gel phase C(14):C(14)PC molecules exhibit an increased acyl chain order, while for the host G(I) gel phase thc C(14): C(14)PC lipid species show increased intrachain disorder. C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. UNIV VIRGINIA,HLTH SCI CTR,DEPT BIOCHEM,CHARLOTTESVILLE,VA 22903. NR 24 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD MAY 21 PY 1992 VL 1106 IS 2 BP 242 EP 250 DI 10.1016/0005-2736(92)90002-4 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HZ063 UT WOS:A1992HZ06300002 PM 1596504 ER PT J AU MILLER, FW LEITMAN, SF CRONIN, ME HICKS, JE LEFF, RL WESLEY, R FRASER, DD DALAKAS, M PLOTZ, PH AF MILLER, FW LEITMAN, SF CRONIN, ME HICKS, JE LEFF, RL WESLEY, R FRASER, DD DALAKAS, M PLOTZ, PH TI CONTROLLED TRIAL OF PLASMA-EXCHANGE AND LEUKAPHERESIS IN POLYMYOSITIS AND DERMATOMYOSITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID RHEUMATOID-ARTHRITIS; DOUBLE-BLIND; INFLAMMATORY MYOPATHIES; RANDOMIZED TRIAL; PLASMAPHERESIS; LYMPHOPLASMAPHERESIS; RECOGNITION; MYOSITIS; THERAPY; SUBSETS AB Background. The therapeutic options for patients with polymyositis or dermatomyositis that is resistant to corticosteroids are limited, unproved, and often toxic. Uncontrolled trials concluded that both plasma exchange and leukapheresis are beneficial, but despite the considerable use of these approaches, proof of their efficacy is lacking. Methods. Thirty-nine patients with definite polymyositis or dermatomyositis were randomly assigned to receive plasma exchange (replacement of one volume of plasma with 5 percent albumin in saline), leukapheresis (removal of 5 x 10(9) to 10 x 10(9) lymphocytes), or sham apheresis in a double-blind manner, with 12 treatments given over a one-month period. Muscle strength, functional capacity, and serum levels of muscle-associated enzymes were measured before and after the 12 procedures. Results. In each group 3 of 13 patients had improvements in strength and functional capacity. The condition of 3 patients treated with leukapheresis and 1 treated with plasma exchange deteriorated, and it was unchanged in the other 26 patients. Adverse effects of apheresis included the need for a central venous catheter (9 patients), major vasovagal episodes (3 patients), and severe citrate reactions (2 patients). Despite the occurrence of significant reductions in the serum levels of muscle enzymes with plasma exchange (P < 0.001) and significant decreases in lymphocyte counts with leukapheresis (P = 0.002), there were no significant differences among the three treatment groups in the final muscle strength or functional capacity of the patients. Conclusions. As treatments for corticosteroid-resistant polymyositis or dermatomyositis, leukapheresis and plasma exchange are no more effective than sham apheresis. C1 NIH,DEPT TRANSFUS MED,BETHESDA,MD 20892. NIH,DEPT REHABIL MED,BETHESDA,MD 20892. NIH,CTR CLIN,BETHESDA,MD 20892. NINCDS,BETHESDA,MD 20892. OI Miller, Frederick/0000-0003-2831-9593 NR 27 TC 186 Z9 190 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 21 PY 1992 VL 326 IS 21 BP 1380 EP 1384 DI 10.1056/NEJM199205213262102 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HU890 UT WOS:A1992HU89000002 PM 1472183 ER PT J AU KELEN, GD GREEN, GB PURCELL, RH CHAN, DW QAQISH, BF SIVERTSON, KT QUINN, TC AF KELEN, GD GREEN, GB PURCELL, RH CHAN, DW QAQISH, BF SIVERTSON, KT QUINN, TC TI HEPATITIS-B AND HEPATITIS-C IN EMERGENCY DEPARTMENT PATIENTS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; NON-A; HEPATOCELLULAR-CARCINOMA; SEXUAL TRANSMISSION; UNITED-STATES; CIRCULATING ANTIBODIES; RISK; INFECTION; EPIDEMIOLOGY; PREVALENCE AB Background. Infections with hepatitis B virus (HBV), hepatitis C virus (HCV), and the human immunodeficiency virus type 1 (HIV-1) are common in inner-city populations, but their frequency and interrelations are not well established. Methods. During a six-week period, excess serum samples were collected, along with information on risk factors, from all adult patients presenting to an inner-city emergency department. The samples were assayed for hepatitis B surface antigen (HBsAg) and antibodies to HCV and HIV-1. Results. Of the 2523 patients tested, 612 (24 percent) were infected with at least one of the three viruses. Five percent were seropositive for HBV, 18 percent for HCV, and 6 percent for HIV-1. HCV was found in 145 of the 175 intravenous drug users (83 percent), 36 of the 171 transfusion recipients (21 percent), and 5 of the 24 homosexual men (21 percent). Among black men 35 to 44 years of age, the seroprevalence of HCV was 51 percent. HBsAg was present in 9 percent of those whose only identifiable risk was possible heterosexual exposure. At least one viral marker was found in about 30 percent of the patients who were actively bleeding or in whom procedures were performed. Testing for HIV-1 alone would have failed to identify 87 percent of the patients infected with HBV and 80 percent of those infected with HCV. Conclusions. In a population of patients in an inner-city emergency room, HBV, HCV, and HIV-1 are all highly prevalent. However, routine screening for HIV-1 alone would identify only a small fraction of the patients who pose risks of severe viral infections, including HBV and HCV, to providers. C1 JOHNS HOPKINS UNIV,SCH MED,DIV EMERGENCY MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV HOSP,DEPT LAB MED,BALTIMORE,MD 21205. UNIV N CAROLINA,DEPT BIOSTAT,CHAPEL HILL,NC 27514. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RI Quinn, Thomas/A-2494-2010; OI Kelen, Gabor/0000-0002-3236-8286 NR 54 TC 226 Z9 228 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 21 PY 1992 VL 326 IS 21 BP 1399 EP 1404 DI 10.1056/NEJM199205213262105 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HU890 UT WOS:A1992HU89000005 PM 1373867 ER PT J AU WEHR, TA AF WEHR, TA TI THE MOOD-ELEVATING EFFECTS OF SLEEP-DEPRIVATION IN DEPRESSION - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP WEHR, TA (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAY 20 PY 1992 VL 267 IS 19 BP 2605 EP 2605 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HT823 UT WOS:A1992HT82300020 ER PT J AU JOSHUATOR, L FROLOW, F APPELLA, E HOPE, H RABINOVICH, D SUSSMAN, JL AF JOSHUATOR, L FROLOW, F APPELLA, E HOPE, H RABINOVICH, D SUSSMAN, JL TI 3-DIMENSIONAL STRUCTURES OF BULGE-CONTAINING DNA FRAGMENTS SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE DNA STRUCTURE; X-RAY DIFFRACTION; BULGED BASES; FRAMESHIFT MUTATION ID CONTAINING DEOXYTRIDECANUCLEOTIDE DUPLEXES; EXTRA ADENOSINE STACKS; LOOPED-OUT BASES; CRYSTAL-STRUCTURE; B-DNA; DOUBLE-HELIX; CONFORMATIONAL TRANSITIONS; MACROMOLECULAR STRUCTURES; ENERGY MINIMIZATION; MOLECULAR-STRUCTURE C1 WEIZMANN INST SCI,DEPT STRUCT BIOL,IL-76100 REHOVOT,ISRAEL. UNIV CALIF DAVIS,DEPT CHEM,DAVIS,CA 95616. NCI,CELL BIOL LAB,BETHESDA,MD 20205. RI Frolow, Felix/A-1760-2013 NR 96 TC 88 Z9 88 U1 1 U2 4 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD MAY 20 PY 1992 VL 225 IS 2 BP 397 EP 431 DI 10.1016/0022-2836(92)90929-E PG 35 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HX080 UT WOS:A1992HX08000013 PM 1593627 ER PT J AU FRIEDMAN, MA MCCABE, MS AF FRIEDMAN, MA MCCABE, MS TI ASSIGNING CARE COSTS ASSOCIATED WITH THERAPEUTIC ONCOLOGY RESEARCH - A MODEST PROPOSAL SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID PATIENT-CARE; REIMBURSEMENT RP FRIEDMAN, MA (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,EXECUT PLAZA N,RM 742F,BETHESDA,MD 20892, USA. NR 8 TC 18 Z9 18 U1 1 U2 3 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAY 20 PY 1992 VL 84 IS 10 BP 760 EP 763 DI 10.1093/jnci/84.10.760 PG 4 WC Oncology SC Oncology GA HU582 UT WOS:A1992HU58200012 PM 1573661 ER PT J AU CARTER, CL HU, N WU, M LIN, PZ MURIGANDE, C BONNEY, GE AF CARTER, CL HU, N WU, M LIN, PZ MURIGANDE, C BONNEY, GE TI SEGREGATION ANALYSIS OF ESOPHAGEAL CANCER IN 221 HIGH-RISK CHINESE FAMILIES SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID REGRESSIVE MODELS; GENETIC-ANALYSIS; UNIFIED MODEL; TRAITS AB Background: Until recently, environmental factors were considered of greatest importance in the etiology of esophageal cancer. Recent studies, however, have suggested that genetic factors also have a role. Purpose: Since no formal genetic study of this cancer has been previously reported, we carried out a statistical analysis to determine how important genetic factors are in the etiology of esophageal cancer in high-incidence areas of North China. Methods: Using a logistic regressive model, we performed a segregation analysis on 221 high-risk nuclear families from the Yaocun Commune, Linxian, Henan Province of China, with at least one affected family member and with all off-spring aged 40 years or older. Three models, the mendelian, the environmental, and the no-transmission models, were each compared with the general-transmission model that incorporated both genetic and environmental factors. Results: According to Akaike's Information Criterion, the mendelian model provided the best fit for the data. By the chi-square test, the mendelian inheritance model was not rejected, but the environmental and the no-transmission models were both rejected. Conclusion: The segregation analysis indicated an autosomal recessive mendelian inheritance, with the alleged mendelian gene present at a frequency of 19%, causing 4% of this population to be predisposed to develop esophageal cancer. Large, unmeasured, residual familial factors, however, were also significant. Implications: Both an autosomal recessive gene and unexplained environmental factors appear to be important in the etiology of esophageal cancer in the subpopulation studied. C1 CHINESE ACAD MED SCI,INST CANC,DEPT CELL BIOL,BEIJING,PEOPLES R CHINA. NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,ROCKVILLE,MD. HOWARD UNIV,CTR CANC,DIV BIOSTAT & EPIDEMIOL,WASHINGTON,DC 20059. CHINESE ACAD MED SCI,INST CANC,DEPT ETIOL,BEIJING,PEOPLES R CHINA. FOX CHASE CANC INST,DEPT BIOSTAT,PHILADELPHIA,PA 19111. NR 23 TC 41 Z9 44 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAY 20 PY 1992 VL 84 IS 10 BP 771 EP 776 DI 10.1093/jnci/84.10.771 PG 6 WC Oncology SC Oncology GA HU582 UT WOS:A1992HU58200014 PM 1573663 ER PT J AU MICKISCH, GH RAHMAN, A PASTAN, I GOTTESMAN, MM AF MICKISCH, GH RAHMAN, A PASTAN, I GOTTESMAN, MM TI INCREASED EFFECTIVENESS OF LIPOSOME-ENCAPSULATED DOXORUBICIN IN MULTIDRUG-RESISTANT-TRANSGENIC MICE COMPARED WITH FREE DOXORUBICIN SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Note ID BREAST-CANCER; CARDIOTOXICITY; ANTITUMOR C1 NCI,DIV CANC BIOL DIAG & CTRS,MOLEC BIOL LAB,BLDG 37,RM 1B22,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,DEPT MED,DIV CLIN PHARMACOL,WASHINGTON,DC 20007. NCI,DIV CANC BIOL DIAG & CTRS,CELL BIOL LAB,BETHESDA,MD 20892. NR 19 TC 45 Z9 45 U1 0 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAY 20 PY 1992 VL 84 IS 10 BP 804 EP 805 DI 10.1093/jnci/84.10.804 PG 2 WC Oncology SC Oncology GA HU582 UT WOS:A1992HU58200021 PM 1573669 ER PT J AU LEFF, RL LOVE, LA MILLER, FW GREENBERG, SJ KLEIN, EA DALAKAS, MC PLOTZ, PH AF LEFF, RL LOVE, LA MILLER, FW GREENBERG, SJ KLEIN, EA DALAKAS, MC PLOTZ, PH TI VIRUSES IN IDIOPATHIC INFLAMMATORY MYOPATHIES - ABSENCE OF CANDIDATE VIRAL GENOMES IN MUSCLE SO LANCET LA English DT Article ID INCLUSION-BODY MYOSITIS; POLYMYOSITIS; DERMATOMYOSITIS; RNA; AMPLIFICATION; PICORNAVIRUS; MYOCARDITIS; POLYMERASE; RETROVIRUS; MODEL AB There is indirect evidence that various viruses have aetiological roles in the idiopathic inflammatory myopathies. By means of a sensitive and specific method based on the polymerase chain reaction (PCR), we sought direct evidence for the presence in affected muscle of nucleic acid sequences from Coxsackie virus, mumps virus, encephalomyocarditis virus, adenovirus, human T-lymphotropic virus types I and II, and human immunodeficiency virus. RNA was extracted from muscle biopsy samples obtained from 44 patients with idiopathic inflammatory myopathies a mean of 45 (range 0-216) months after disease onset. All the subjects were older than 16 years at disease onset. The integrity of the mRNA extracted was confirmed by the successful PCR amplification of insulin receptor mRNA in all samples. The PCR method was able to detect between 1 and 20 molecules of added viral nucleic acid for the picornaviruses sought. No detectable virus sequences were found, however, in any of the patients' muscle samples or in samples from 13 controls. We tested for retroviral DNA in 22 samples (17 patients, 5 controls) that met our criterion for adequate DNA extraction (detectable beta-actin DNA by PCR); again no virus sequences were found. Persistence in muscle of these or closely related viruses is unlikely to be a continuing stimulus for disease in the idiopathic inflammatory myopathies. C1 ROSWELL PK CANC INST,DEPT NEUROL,BUFFALO,NY. SUNY BUFFALO,BUFFALO,NY 14260. NINCDS,BETHESDA,MD 20892. RP LEFF, RL (reprint author), NIAMS,ARTHRIT & RHEUMATISM BRANCH,BLDG 10,ROOM 9N228,BETHESDA,MD 20892, USA. OI Miller, Frederick/0000-0003-2831-9593 NR 28 TC 101 Z9 101 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAY 16 PY 1992 VL 339 IS 8803 BP 1192 EP 1195 DI 10.1016/0140-6736(92)91134-T PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HU684 UT WOS:A1992HU68400004 PM 1349938 ER PT J AU THOMPSON, DC JOSEPHY, PD CHU, JWK ELING, TE AF THOMPSON, DC JOSEPHY, PD CHU, JWK ELING, TE TI ENHANCED MUTAGENICITY OF ANISIDINE ISOMERS IN BACTERIAL STRAINS CONTAINING ELEVATED N-ACETYLTRANSFERASE ACTIVITY SO MUTATION RESEARCH LA English DT Article DE PARA-ANISIDINE; ORTHO-ANISIDINE; N-ACETYLTRANSFERASE ID PROSTAGLANDIN-H SYNTHASE; SALMONELLA-TYPHIMURIUM; ACTIVATION; BENZIDINE; MUTAGENESIS; PEROXIDASE; ASSAY; ARYLAMINES; CHEMICALS; REDUCTION AB In previous studies on the mutagenicity of anisidine isomers, the ortho isomer was considered to be mutagenic towards standard Ames tester strains, while the para isomer gave equivocal results. In the present study we show that both para- and ortho-anisidine isomers are mutagenic in a Salmonella typhimurium tester strain containing elevated levels of N-acetyltransferase (YG1029). p-Anisidine gave a positive mutagenic response using either hamster S9 or ram seminal vesicle microsomes (RSVM) as an activating system, while o-anisidine gave a positive response only with the hamster S9 fraction. The mutagenic response from p-anisidine was greater than with o-anisidine in each case. In tests with p-anisidine and RSVM, the addition of arachidonic acid was not necessary to observe a mutagenic response. Catalase produced a dose-dependent decrease in the mutagenic response with p-anisidine and RSVM; this indicates that endogenous hydrogen peroxide from the bacteria acts as a substrate for the peroxidase activity of RSVM prostaglandin H synthase. These results demonstrate that both anisidine isomers are mutagenic and that N-acetyltransferase enzymes play an important role in their metabolism to mutagenic species. C1 NIEHS,MOLEC BIOPHYS LAB,EICOSANOID BIOCHEM SECT,POB 12233,RES TRIANGLE PK,NC 27709. UNIV GUELPH,DEPT CHEM & BIOCHEM,GUELPH N1G 2W1,ONTARIO,CANADA. NR 24 TC 21 Z9 22 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD MAY 16 PY 1992 VL 279 IS 2 BP 83 EP 89 DI 10.1016/0165-1218(92)90249-Y PG 7 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HW435 UT WOS:A1992HW43500002 PM 1375342 ER PT J AU MALLING, HV BURKHART, JG AF MALLING, HV BURKHART, JG TI COMPARISON OF MUTATION FREQUENCIES OBTAINED USING TRANSGENES AND SPECIFIC-LOCUS MUTATION SYSTEMS IN MALE-MOUSE GERM-CELLS SO MUTATION RESEARCH LA English DT Article DE MALE GERMINAL CELLS; MUTATION FREQUENCIES; TRANSGENES; SPECIFIC-LOCUS SYSTEMS ID DNA; ETHYLNITROSOUREA RP MALLING, HV (reprint author), NIEHS,GENET LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 10 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD MAY 16 PY 1992 VL 279 IS 2 BP 149 EP 151 PG 3 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HW435 UT WOS:A1992HW43500011 PM 1375340 ER PT J AU FURBERG, CD MANOLIO, TA PSATY, BM BILD, DE BORHANI, NO NEWMAN, A TABATZNIK, B RAUTAHARJU, PM AF FURBERG, CD MANOLIO, TA PSATY, BM BILD, DE BORHANI, NO NEWMAN, A TABATZNIK, B RAUTAHARJU, PM TI MAJOR ELECTROCARDIOGRAPHIC ABNORMALITIES IN PERSONS AGED 65 YEARS AND OLDER (THE CARDIOVASCULAR HEALTH STUDY) SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID UNRECOGNIZED MYOCARDIAL-INFARCTION; PROGNOSIS AB Electrocardiographic abnormalities are often found in older patients, but their prevalence in free-living elderly populations is not well-defined. In addition, the clinical significance of many of these abnormalities is uncertain. The prevalence of major electrocardiographic abnormalities was determined in 5,150 adults aged greater-than-or-equal-to 65 years from the Cardiovascular Health Study - a study of risk factors for stroke and coronary heart disease in the elderly. Ventricular conduction defects, major Q/QS waves, left ventricular hypertrophy, isolated major ST-T-wave abnormalities, atrial fibrillation and first-degree atrioventricular block were collectively categorized as major electrocardiographic abnormalities. Prevalence of any major electrocardiographic abnormality was 29% in the entire cohort, 19% among 2,413 participants who reported no history of coronary artery disease or systemic hypertension, and 37% among 2,737 participants with a history of coronary artery disease or hypertension. Prevalence of major electrocardiographic abnormalities was higher in men than in women regardless of history, and tended to increase with age. Major Q/QS waves were found in 5.2%, and more than half were in those who did not report a previous myocardial infarction. Major electrocardiographic abnormalities are common in elderly men and women irrespective of the history of heart disease. C1 WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SERV,WINSTON SALEM,NC 27103. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT HLTH SERV,SEATTLE,WA 98195. UNIV CALIF DAVIS,SCH MED,DEPT INTERNAL MED,DAVIS,CA 95616. UNIV CALIF DAVIS,SCH MED,DEPT COMMUNITY HLTH,DAVIS,CA 95616. UNIV PITTSBURGH,GRAD SCH PUBL HLTH,PITTSBURGH,PA 15260. JOHNS HOPKINS UNIV,DEPT MED,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,DEPT EPIDEMIOL,BALTIMORE,MD 21218. UNIV ALBERTA,DEPT MED,CTR EPICORE,EDMONTON T6G 2E1,ALBERTA,CANADA. RI Newman, Anne/C-6408-2013 OI Newman, Anne/0000-0002-0106-1150 FU NHLBI NIH HHS [N01-HC-85079, N01-HC-85080, N01-HC-85081] NR 15 TC 151 Z9 151 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAY 15 PY 1992 VL 69 IS 16 BP 1329 EP 1335 DI 10.1016/0002-9149(92)91231-R PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HU939 UT WOS:A1992HU93900017 PM 1585868 ER PT J AU GRIDLEY, G MCLAUGHLIN, JK BLOCK, G BLOT, WJ GLUCH, M FRAUMENI, JF AF GRIDLEY, G MCLAUGHLIN, JK BLOCK, G BLOT, WJ GLUCH, M FRAUMENI, JF TI VITAMIN SUPPLEMENT USE AND REDUCED RISK OF ORAL AND PHARYNGEAL CANCER SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE MOUTH NEOPLASMS; NEOPLASMS; PHARYNGEAL NEOPLASMS; RETROSPECTIVE STUDIES; RISK FACTORS; VITAMIN-E; VITAMINS ID UNITED-STATES; ALPHA-TOCOPHEROL; DIET; PREVENTION; NUTRIENTS; CARCINOGENESIS; ETIOLOGY; SELENIUM AB Use of vitamin and mineral supplements was assessed in a population-based case-control study of oral and pharyngeal cancer, conducted during 1984-1985 in four areas of the United States. There was no association with intake of multivitamin products, but users of supplements of individual vitamins, including vitamins A, B, C, and E, were at lower risk after controlling for the effects of tobacco, alcohol, and other risk factors for these cancers. After further adjustment for use of other supplements, vitamin E was the only supplement that remained associated with a significantly reduced cancer risk. The adjusted odds ratio of oral and pharyngeal cancer for "ever regularly used" vitamin E was 0.5 (95% confidence interval 0.4-0.6). To the authors' knowledge, this is the first epidemiologic study to show a reduced oral cancer risk with vitamin E use. Although it is not clear that the lower risk among consumers of vitamin E supplements is due to the vitamin per se, the findings are consistent with experimental evidence and should prompt further research on the role of vitamin E and other micronutrients as inhibitors of oral and pharyngeal cancer. C1 NCI,DIV CANC PREVENT,BETHESDA,MD 20892. NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. RP GRIDLEY, G (reprint author), NCI,DIV CANC ETIOL,EXECUT PLAZA N,ROOM 443,BETHESDA,MD 20892, USA. RI Block, Gladys/E-3304-2010 NR 35 TC 97 Z9 98 U1 0 U2 0 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 MAY 15 PY 1992 VL 135 IS 10 BP 1083 EP 1092 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JF484 UT WOS:A1992JF48400002 PM 1632421 ER PT J AU SAAH, AJ MUNOZ, A KUO, V FOX, R KASLOW, RA PHAIR, JP RINALDO, CR DETELS, R POLK, BF AF SAAH, AJ MUNOZ, A KUO, V FOX, R KASLOW, RA PHAIR, JP RINALDO, CR DETELS, R POLK, BF TI PREDICTORS OF THE RISK OF DEVELOPMENT OF ACQUIRED-IMMUNODEFICIENCY-SYNDROME WITHIN 24 MONTHS AMONG GAY MEN SEROPOSITIVE FOR HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 - A REPORT FROM THE MULTICENTER AIDS COHORT STUDY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; HELPER CELLS; HIV; HOMOSEXUALITY; LYMPHOCYTES-T ID HOMOSEXUAL MEN; HIV-INFECTION; PROGRESSION AB The natural history of infection with human immunodeficiency virus type 1 (HIV-1) is characterized by a relentless decline in CD4-positive lymphocytes and the ultimate development of acquired immunodeficiency syndrome (AIDS). However, variables other than the CD4-positive lymphocyte level contribute to the measurement of risk for AIDS and can be used as predictors of AIDS onset. This study was undertaken to identify factors that, independently of the CD4-positive lymphocyte level, would predict the risk of AIDS over 24 months in a cohort of HIV-1 seropositive homosexual men receiving no antiretroviral therapy. Demographic, clinical, and laboratory data from 1,325 white, HIV-1 seropositive participants in the Multicenter AIDS Cohort Study who have been studied for 4 years were analyzed with univariate and multivariate methods. To control for stage of infection, the baseline percentage of CD4-positive lymphocytes (a known marker of disease progression), and the decline of CD4-positive cells during the first 6 months of observation were used as continuous variables. The variables that were independently associated with an increased risk of developing AIDS were: low baseline CD4 percentage, decline in the CD4 percentage during the first 6 months of follow-up, the presence of serum immunoglobulin A at baseline, decrease in hemoglobin during the first 6 months of follow-up, incident fatigue, and the interaction of decline in the CD4 percentage and incident thrush. While low CD4 percentage and other variables have been previously described as prognostic markers, decline in the CD4 percentage and the interaction of that decline and incident thrush have not previously been described as being of prognostic importance. These variables and the analytic method for estimating prognosis may prove useful for selecting and evaluating antiretroviral therapy, instituting prophylactic measures against certain opportunistic infections, and recruitment into clinical trials. Because study participants received no antiretroviral prophylaxis during the period under analysis, the method could be used to estimate the prognosis for those receiving investigational treatment were they to remain untreated, effectively making any participant in a clinical trial his own untreated control. C1 UNIV PITTSBURGH,GRAD SCH PUBL HLTH,PITTSBURGH,PA 15260. HOWARD BROWN MEM CLIN,EVANSTON,IL. NIAID,BETHESDA,MD 20892. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,LOS ANGELES,CA 90024. NORTHWESTERN UNIV,SCH MED,EVANSTON,IL 60201. RP SAAH, AJ (reprint author), JOHNS HOSP UNIV,SCH HYG & PUBL HLTH,624 N BROADWAY,SUITE 763,BALTIMORE,MD 21205, USA. FU NIAID NIH HHS [N01-AI-72634, N01-AI-72631, N01-AI-72632] NR 16 TC 59 Z9 59 U1 0 U2 0 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 MAY 15 PY 1992 VL 135 IS 10 BP 1147 EP 1155 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JF484 UT WOS:A1992JF48400009 PM 1352940 ER PT J AU GABRIEL, O GERSTEN, DM AF GABRIEL, O GERSTEN, DM TI STAINING FOR ENZYMATIC-ACTIVITY AFTER GEL-ELECTROPHORESIS .1. SO ANALYTICAL BIOCHEMISTRY LA English DT Review ID SODIUM DODECYL-SULFATE; RED BLOOD-CELLS; PHOSPHOENOLPYRUVATE CARBOXYLASE ACTIVITY; NUCLEOTIDE-LINKED DEHYDROGENASES; ALKALINE-PHOSPHATASE ISOENZYMES; PATHOGENESIS-RELATED PROTEINS; ALPHA-L-FUCOSIDASE; POLYACRYLAMIDE-GEL; PRODUCE PHOSPHATE; GENERAL-METHOD C1 NIH,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,ROCKVILLE,MD 20850. GEORGETOWN UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20007. RP GABRIEL, O (reprint author), NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892, USA. NR 323 TC 77 Z9 79 U1 0 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD MAY 15 PY 1992 VL 203 IS 1 BP 1 EP 21 DI 10.1016/0003-2697(92)90036-7 PG 21 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA HU613 UT WOS:A1992HU61300001 PM 1381872 ER PT J AU LEROITH, D CLEMMONS, D NISSLEY, P RECHLER, MM AF LEROITH, D CLEMMONS, D NISSLEY, P RECHLER, MM TI INSULIN-LIKE GROWTH-FACTORS IN HEALTH AND DISEASE SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE ACROMEGALY; INSULIN-LIKE GROWTH FACTORS; GROWTH DISORDERS; DIABETES-MELLITUS; SOMATOMEDINS; HYPOGLYCEMIA ID FACTOR-BINDING-PROTEIN; SOMATOMEDIN-C LEVELS; FACTOR IGF BINDING; EXTRAPANCREATIC TUMOR HYPOGLYCEMIA; NONISLET CELL TUMORS; FACTOR-II; SHORT STATURE; RAT-HEART; HORMONE; SERUM AB The insulin-like growth factor (IGF) family of peptides, binding proteins, and receptors are ubiquitous and important for normal human growth and development. Modern techniques including specific radioimmunoassays, radioreceptor assays and recombinant DNA technology have improved our understanding of the role of IGFs in growth and development. In addition to enhancing our understanding of normal physiology, these techniques assess changes in these hormones, binding proteins, and receptors in pathologic conditions including growth retardation, acromegaly, malnutrition, diabetes, and malignancy. Further, these studies have led to improvement in the assessment of responses to certain therapies used in the treatment of these diseases and may lead to improvements in these therapies. C1 NCI,BETHESDA,MD 20892. UNIV N CAROLINA,DIV ENDOCRINOL,CHAPEL HILL,NC 27599. RP LEROITH, D (reprint author), NIDDKD,DIABET BRANCH,ROOM 8S423,BLDG 10,BETHESDA,MD 20892, USA. NR 70 TC 145 Z9 148 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 MAY 15 PY 1992 VL 116 IS 10 BP 854 EP 862 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA HT802 UT WOS:A1992HT80200012 PM 1373590 ER PT J AU POSTON, JM PARENTEAU, GL FLYNN, DM KELLY, GD AF POSTON, JM PARENTEAU, GL FLYNN, DM KELLY, GD TI BIOCHEMICAL EFFECTS OF ISCHEMIA ON ISOLATED, PERFUSED RAT-HEART TISSUES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID GLUTAMINE-SYNTHETASE; FREE-RADICALS; PURIFICATION; MYOCARDIUM; CATABOLISM; PROTEASE; INJURY; DAMAGE; BRAIN C1 NHLBI,SURG BRANCH,BETHESDA,MD 20892. RP POSTON, JM (reprint author), NHLBI,BIOCHEM LAB,BETHESDA,MD 20892, USA. NR 29 TC 29 Z9 29 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD MAY 15 PY 1992 VL 295 IS 1 BP 35 EP 41 DI 10.1016/0003-9861(92)90484-E PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HQ209 UT WOS:A1992HQ20900006 PM 1575515 ER PT J AU HANNA, PM MASON, RP AF HANNA, PM MASON, RP TI DIRECT EVIDENCE FOR INHIBITION OF FREE-RADICAL FORMATION FROM CU(I) AND HYDROGEN-PEROXIDE BY GLUTATHIONE AND OTHER POTENTIAL LIGANDS USING THE EPR SPIN-TRAPPING TECHNIQUE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID SINGLE-STRAND BREAKAGE; HISTIDINE-RESIDUES; HYDROXYL RADICALS; FENTON REACTIONS; IMIDAZOLE RING; ASCORBIC-ACID; CUPRIC IONS; DNA DAMAGE; COPPER; OXIDATION RP HANNA, PM (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 51 TC 119 Z9 121 U1 1 U2 17 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 MAY 15 PY 1992 VL 295 IS 1 BP 205 EP 213 DI 10.1016/0003-9861(92)90507-S PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HQ209 UT WOS:A1992HQ20900029 PM 1315504 ER PT J AU SHARIEF, FS LI, SSL AF SHARIEF, FS LI, SSL TI STRUCTURE OF HUMAN PROSTATIC ACID-PHOSPHATASE GENE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID SEQUENCE; CLONING C1 NIEHS,GENET LAB,RES TRIANGLE PK,NC 27709. NR 14 TC 14 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAY 15 PY 1992 VL 184 IS 3 BP 1468 EP 1476 DI 10.1016/S0006-291X(05)80048-8 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HV388 UT WOS:A1992HV38800048 PM 1375464 ER PT J AU ALAVA, MA DEBELL, KE CONTI, A HOFFMAN, T BONVINI, E AF ALAVA, MA DEBELL, KE CONTI, A HOFFMAN, T BONVINI, E TI INCREASED INTRACELLULAR CYCLIC-AMP INHIBITS INOSITOL PHOSPHOLIPID HYDROLYSIS INDUCED BY PERTURBATION OF THE T-CELL RECEPTOR CD3 COMPLEX BUT NOT BY G-PROTEIN STIMULATION - ASSOCIATION WITH PROTEIN KINASE-A-MEDIATED PHOSPHORYLATION OF PHOSPHOLIPASE C-GAMMA-1 SO BIOCHEMICAL JOURNAL LA English DT Article ID CYTOPLASMIC FREE CALCIUM; ANTIGEN RECEPTOR; LYMPHOCYTES-T; ADENYLATE-CYCLASE; CHOLERA-TOXIN; TYROSINE PHOSPHORYLATION; SURFACE MOLECULES; ACTIVATION; CAMP; BINDING AB Modulation of inositol phospholipid (InsPL) hydrolysis in response to increasing intracellular concentrations of cyclic AMP (cAMP) was studied in a murine T helper type II (Th2) lymphocyte clone, 8-5-5. Intact 8-5-5 cells produced maximal amounts of cAMP in response to prostaglandin E2 (PGE2), cholera toxin (CTx) or 7-beta-deacetyl-7-beta-(gamma-N-methylpiperazino)butyryl forskolin (dmpb-forskolin). cAMP generation reached a plateau after 5 min of treatment with dmpb-forskolin (300-mu-M) or PGE2 (1-mu-M), but required 60 min of treatment with CTx (1-mu-g/ml). Preincubation of 8-5-5 cells with 1-mu-M-PGE2 or 300-mu-M-dmpb-forskolin (10 min at 37-degrees-C) or with 1-mu-g of CTx/ml (60 min at 37-degrees-C) completely inhibited InsPL hydrolysis induced by perturbation of the T cell receptor (TCR)/CD3 complex with the monoclonal antibody 145.2C11. Preincubation with the cAMP analogue 8-bromo-cyclic AMP (8-Br-cAMP) also inhibited InsPL hydrolysis. Tetanolysin-permeabilized 8-5-5 cells produced cAMP in response to PGE2, dmpb-forskolin and guanosine 5'-[gamma-thio]triphosphate (GTP[S]), a non-cell-permeating, non-hydrolysable analogue of GTP that directly activates G-proteins. No inhibition of TCR/CD3-induced InsPL hydrolysis was observed under these conditions. InsPL hydrolysis was also unaffected when permeabilized cells were incubated with up to 10 mM-8-Br-cAMP, suggesting that permeabilized cells lost (a) soluble effector molecule(s) involved in mediating the inhibitory effect observed in intact cells. Treatment of 8-5-5 cells with dmpb-forskolin or CTx prior to permeabilization resulted in inhibition of TCR/CD3-induced InsPL hydrolysis, but did not affect InsPL hydrolysis induced via G-protein stimulation with GTP[S]. Treatment of permeabilized 8-5-5 cells with purified cAMP-dependent protein kinase (PKA) resulted in inhibition of TCR/CD3- but not GTP[S]-induced InsPL hydrolysis. This effect was associated with phosphorylation of phospholipase (PLC)-gamma-l in the absence of phosphorylation of components of the TCR/CD3 complex. These results suggest that PKA-mediated phosphorylation of PLC may regulate TCR/CD3-induced InsPL hydrolysis. RP ALAVA, MA (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL,CELL BIOL LAB,NIH CAMPUS,BLDG 29,ROOM 231,BETHESDA,MD 20892, USA. NR 48 TC 49 Z9 49 U1 1 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAY 15 PY 1992 VL 284 BP 189 EP 199 PN 1 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV223 UT WOS:A1992HV22300027 PM 1318020 ER PT J AU LEMAISTRE, CF MENEGHETTI, C ROSENBLUM, M REUBEN, J PARKER, K SHAW, J DEISSEROTH, A WOODWORTH, T PARKINSON, DR AF LEMAISTRE, CF MENEGHETTI, C ROSENBLUM, M REUBEN, J PARKER, K SHAW, J DEISSEROTH, A WOODWORTH, T PARKINSON, DR TI PHASE-I TRIAL OF AN INTERLEUKIN-2 (IL-2) FUSION TOXIN (DAB486IL-2) IN HEMATOLOGIC MALIGNANCIES EXPRESSING THE IL-2 RECEPTOR SO BLOOD LA English DT Article ID CHRONIC LYMPHOCYTIC-LEUKEMIA; HAIRY-CELL LEUKEMIA; HIGH-AFFINITY RECEPTORS; ELEVATED SERUM LEVELS; TAC-ANTIGEN; DIPHTHERIA-TOXIN; CYTO-TOXICITY; PROTEIN; LYMPHOMAS; DISTINCT C1 UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX 77025. SERAGEN INC,HOPKINTON,MA. NCI,BETHESDA,MD 20892. RP LEMAISTRE, CF (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 43 TC 146 Z9 148 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 MAY 15 PY 1992 VL 79 IS 10 BP 2547 EP 2554 PG 8 WC Hematology SC Hematology GA HW618 UT WOS:A1992HW61800008 PM 1586707 ER PT J AU YOSHIMURA, K CRYSTAL, RG AF YOSHIMURA, K CRYSTAL, RG TI TRANSCRIPTIONAL AND POSTTRANSCRIPTIONAL MODULATION OF HUMAN NEUTROPHIL ELASTASE GENE-EXPRESSION SO BLOOD LA English DT Article ID PROMYELOCYTIC LEUKEMIA-CELLS; HUMAN CATHEPSIN-G; AMINO-ACID SEQUENCE; MESSENGER-RNA; HUMAN MYELOPEROXIDASE; NUCLEOTIDE-SEQUENCE; HL-60 CELLS; MOLECULAR-CLONING; SERINE PROTEASE; CDNA CLONES C1 NHLBI,PULM BRANCH,BLDG 10,ROOM 6D03,BETHESDA,MD 20892. NR 52 TC 26 Z9 26 U1 0 U2 1 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 MAY 15 PY 1992 VL 79 IS 10 BP 2733 EP 2740 PG 8 WC Hematology SC Hematology GA HW618 UT WOS:A1992HW61800033 PM 1586720 ER PT J AU INGRAM, DK GAROFALO, P SPANGLER, EL MANTIONE, CR ODANO, I LONDON, ED AF INGRAM, DK GAROFALO, P SPANGLER, EL MANTIONE, CR ODANO, I LONDON, ED TI REDUCED DENSITY OF NMDA RECEPTORS AND INCREASED SENSITIVITY TO DIZOCILPINE-INDUCED LEARNING IMPAIRMENT IN AGED RATS SO BRAIN RESEARCH LA English DT Article DE GLUTAMATE RECEPTOR; MEMORY; AGING; EXCITATORY AMINO ACID; MK-801; N-METHYL-D-ASPARTATE ID METHYL-D-ASPARTATE; EXCITATORY AMINO-ACIDS; LONG-TERM POTENTIATION; L-GLUTAMATE BINDING; 14-UNIT T-MAZE; ALZHEIMERS-DISEASE; CHOLINERGIC HYPOTHESIS; MEMORY DYSFUNCTION; HIPPOCAMPAL DAMAGE; PERFORMANCE AB About 20 min prior to training in a shock-motivated 14-unit T-maze, young (3-4 months) and aged (24-25 months) male Fischer-344 rats were given s.c. injections of either saline or dizocilpine (MK-801, 0.02 or 0.04 mg/kg), a non-competitive antagonist of the N-methyl-D-asparate (NMDA) receptor. The aged rats showed a dose-dependent impairment in maze performance. Deficiencies were manifested as increases in errors, in runtime from start to goal, and in the number and duration of shocks received. In contrast, young rats exhibited no detrimental effects of dizocilpine on maze performance. Analysis of [H-3]glutamate binding in these rats revealed a marked age-related decline in NMDA receptor binding in hippocampus. A significant correlation was observed between errors in the maze and hippocampal [H-3]glutamate binding, but the correlation was positive, i.e., rats that made the most errors had the highest level of NMDA receptor binding. Thus, compared to young rats, aged rats were more sensitive to the behavioral effects of NMDA receptor antagonism and they showed a hippocampal loss of [H-3]glutamate in binding, which may be related to the increased sensitivity to dizocilpine. The positive correlation between poor maze performance and NMDA receptor binding suggests that the behaviors assessed involve complex interactions between NMDA receptors and other neuronal systems in the hippocampus. RP NIA, GERONTOL RES CTR, NATHAN W SHOCK LABS, MOLEC PHYSIOL & GENET SECT, BALTIMORE, MD 21224 USA. NR 80 TC 62 Z9 63 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 EI 1872-6240 J9 BRAIN RES JI Brain Res. PD MAY 15 PY 1992 VL 580 IS 1-2 BP 273 EP 280 DI 10.1016/0006-8993(92)90954-8 PG 8 WC Neurosciences SC Neurosciences & Neurology GA HZ747 UT WOS:A1992HZ74700036 PM 1387035 ER PT J AU KASPRZYK, PG SONG, SU DIFIORE, PP KING, CR AF KASPRZYK, PG SONG, SU DIFIORE, PP KING, CR TI THERAPY OF AN ANIMAL-MODEL OF HUMAN GASTRIC-CANCER USING A COMBINATION OF ANTI-ERBB-2 MONOCLONAL-ANTIBODIES SO CANCER RESEARCH LA English DT Article ID HUMAN-BREAST CANCER; GROWTH-FACTOR RECEPTOR; ERBB-2 MESSENGER-RNA; HER-2 NEU ONCOGENE; HETEROGENEOUS EXPRESSION; PROTO-ONCOGENE; OVARIAN-CANCER; POOR SURVIVAL; CELL-LINES; AMPLIFICATION AB Amplification and/or overexpression of the erbB-2 gene have been demonstrated in 20-30% of adenocarcinomas of the breast, ovary, lung, and stomach and are associated with aggressive clinical course and poor prognosis. Interference with erbB-2 function by the use of monoclonal antibodies is a promising approach to the treatment of these diseases. In this study we demonstrate that a combination of two anti-erbB-2-specific antibodies inhibited the growth of human gastric tumor cells in vitro. This combination antibody therapy also inhibited the growth of human tumor cell lines growing as xenografts in nude mice and was able to dramatically reduce established tumors. This is the first reported observation of tumor regression induced by anti-erbB-2 monoclonal antibodies. Treatment was not curative in that tumors regrew after 6 weeks. Treatment with either single antibody alone did not inhibit cell growth or tumor formation. Pulse chase and tyrosine kinase activity experiments were used to investigate the activity of the erbB-2 gene product (gp185erbB-2). The formation of complexes by two antibodies was found to interfere with receptor function and mimic some properties of a typical receptor ligand. Selective interference of the erbB-2 receptor by combination antibody therapy may be advantageous for the treatment of human cancers. C1 MOLEC ONCOL INC,19 FIRSTFIELD RD,GAITHERSBURG,MD 20878. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. RI Di Fiore, Pier Paolo/K-2130-2012 OI Di Fiore, Pier Paolo/0000-0002-2252-0950 FU NCI NIH HHS [2 R44 CA50077-02] NR 29 TC 125 Z9 126 U1 0 U2 2 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 MAY 15 PY 1992 VL 52 IS 10 BP 2771 EP 2776 PG 6 WC Oncology SC Oncology GA HU222 UT WOS:A1992HU22200001 PM 1349849 ER PT J AU SHOEMAKER, RH SMYTHE, AM WU, L BALASCHAK, MS BOYD, MR AF SHOEMAKER, RH SMYTHE, AM WU, L BALASCHAK, MS BOYD, MR TI EVALUATION OF METASTATIC HUMAN TUMOR BURDEN AND RESPONSE TO THERAPY IN A NUDE-MOUSE XENOGRAFT MODEL USING A MOLECULAR PROBE FOR REPETITIVE HUMAN DNA-SEQUENCES SO CANCER RESEARCH LA English DT Article ID HUMAN CANCER METASTASIS; CARCINOMA CELL-LINE; HUMAN-MELANOMA; MICE; GROWTH; LUNG; ESTABLISHMENT; VARIANT AB A sensitive DNA dot-blot assay for repetitive human DNA sequences was developed and applied to the quantitative determination of spontaneous metastases of a human melanoma in various tissues of nude mice. The assay was useful for defining the time course and pattern of tissue distribution of metastatic cells as well as for assessing response to therapy. The methodology is relatively simple, can be performed using nonradioactive DNA probes, and should be broadly applicable to studies of metastasis of human tumors in nude mice. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21702. RP SHOEMAKER, RH (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702, USA. NR 35 TC 7 Z9 8 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 MAY 15 PY 1992 VL 52 IS 10 BP 2791 EP 2796 PG 6 WC Oncology SC Oncology GA HU222 UT WOS:A1992HU22200004 PM 1581891 ER PT J AU TENNENBAUM, T YUSPA, SH GROVER, A CASTRONOVO, V SOBEL, ME YAMADA, Y DE LUCA, LM AF TENNENBAUM, T YUSPA, SH GROVER, A CASTRONOVO, V SOBEL, ME YAMADA, Y DE LUCA, LM TI EXTRACELLULAR-MATRIX RECEPTORS AND MOUSE SKIN CARCINOGENESIS - ALTERED EXPRESSION LINKED TO APPEARANCE OF EARLY MARKERS OF TUMOR PROGRESSION SO CANCER RESEARCH LA English DT Article ID CELL-SURFACE RECEPTORS; BASEMENT-MEMBRANE; EPIDERMAL CARCINOGENESIS; INTEGRIN HETERODIMER; MULTIPLE RECEPTORS; LAMININ; DIFFERENTIATION; CARCINOMA; BASAL; ALPHA-6-BETA-4 AB Interaction of cells with the basement membrane is important for cell proliferation and differentiation. Disruption of the basement membrane is an early event during progression of benign tumors to cancer. Using the techniques of immunohistochemistry and immunofluorescence, we show that cell-matrix interactions via the cell surface integrin receptors alpha-3-beta-1, alpha-5-beta-1, alpha-6-beta-4, the M(r) 67,000 laminin receptor (67LR) laminin-binding protein, and the secreted matrix protein laminin are strictly regulated during differentiation of mouse epidermis. While alpha-6-beta-4 and alpha-5-beta-1 are polarized to the basal surface of basal cells in contact with the basement membrane, alpha-3-beta-1 and the non-integrin 67LR are primarily detected in the cell periphery of suprabasal cells, where cell to cell contacts are found. Sequential changes in expression of matrix receptors occur following multistage carcinogenesis of mouse skin. In an analysis of benign and malignant skin tumors induced by chemical carcinogens or oncogene transduction, we found that alpha-3-beta-1 and alpha-5-beta-1 as well as the non-integrin 67LR are sequentially down-regulated in the progression from benign to malignant, while alpha-6-beta-4 is the predominant receptor expressed in the carcinomas. Tumor expression of alpha-6-beta-4 is not polarized and is dissociated from its colocalized normal partner bullous pemphigoid antigen, which remains restricted to the basement membrane. The changes in matrix receptors are linked to appearance of keratin 13 in suprabasal regions, but always in alpha-6-beta-4 negative cells. The predominance of alpha-6-beta-4 in the proliferating cells during progression is associated with decreased expression of keratin 13 in carcinomas. These results suggest that matrix interactions with its receptors are important determinants of ordered differentiation in normal skin and show characteristic alterations during carcinogenesis that parallel changes in differentiation of the tumors. C1 NCI, TUMOR PATHOL LAB, BETHESDA, MD 20892 USA. NIDR, DEV BIOL LAB, BETHESDA, MD 20892 USA. RP TENNENBAUM, T (reprint author), NCI, DIV CANC ETIOL, CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB, BLDG 37, BETHESDA, MD 20892 USA. NR 68 TC 69 Z9 71 U1 0 U2 1 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 MAY 15 PY 1992 VL 52 IS 10 BP 2966 EP 2976 PG 11 WC Oncology SC Oncology GA HU222 UT WOS:A1992HU22200032 PM 1533815 ER PT J AU HSU, VW SHAH, N KLAUSNER, RD AF HSU, VW SHAH, N KLAUSNER, RD TI A BREFELDIN-A-LIKE PHENOTYPE IS INDUCED BY THE OVEREXPRESSION OF A HUMAN ERD-2-LIKE PROTEIN, ELP-1 SO CELL LA English DT Article ID LUMINAL ER PROTEINS; ENDOPLASMIC-RETICULUM; GOLGI PROTEINS; TRANSPORT; SYSTEM; PATHWAY; GENE; IDENTIFICATION; EXPRESSION; RETENTION AB Brefeldin A (BFA) is a unique drug affecting the molecular mechanisms that regulate membrane traffic and organelle structure. BFA's ability to alter retrograde traffic from the Golgi to the endoplasmic reticulum (ER) led us to ask whether the ERD-2 retrieval receptor, proposed to return escaped ER resident proteins from the Golgi, might either interfere with or mimic the effects of the drug. When either human ERD-2 or a novel human homolog (referred to as ELP-1) is overexpressed in a variety of cell types, the effects are phenotypically indistinguishable from the addition of BFA. These include the redistribution of the Golgi coat protein, beta-COP, to the cytosol, the loss of the Golgi apparatus as a distinct organelle, the mixing of this organelle with the ER, the addition of complex oligosaccharides to resident ER glycoproteins, and the block of anterograde traffic. Thus, these receptors may provide signals that regulate retrograde traffic between the Golgi and the ER. RP HSU, VW (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 46 TC 108 Z9 109 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAY 15 PY 1992 VL 69 IS 4 BP 625 EP 635 DI 10.1016/0092-8674(92)90226-3 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HV089 UT WOS:A1992HV08900007 PM 1316805 ER PT J AU STEELE, FR WASHBURN, T RIEGER, R OTOUSA, JE AF STEELE, FR WASHBURN, T RIEGER, R OTOUSA, JE TI DROSOPHILA RETINAL-DEGENERATION-C (RDGC) ENCODES A NOVEL SERINE THREONINE PROTEIN PHOSPHATASE SO CELL LA English DT Article ID LIGHT-INDUCED PHOSPHORYLATION; CALCIUM-BINDING PROTEINS; CHROMOSOMAL LOCALIZATION; NERVOUS-SYSTEM; GENE; MELANOGASTER; RHODOPSIN; POLYPEPTIDES; SEQUENCE; KINASES AB The Drosophila retinal degeneration C (rdgC) gene is required to prevent light-induced retinal degeneration. Molecular analysis shows that the rdgC transcription unit encodes a novel serine/threonine protein phosphatase. Amino acids 153-393 define a domain that has 30% identity with the catalytic domains of types 1, 2A, and 2B serine/threonine protein phosphatases. A putative regulatory domain is appended that contains multiple potential Ca2+-binding sites or "EF hand motifs." Thus, the analysis suggests that the rdgC protein is a novel type of serine/threonine protein phosphatase that is directly regulated by Ca2+. rdgC is expressed in the visual systems of the fly, as well as in the mushroom bodies of the central brain. C1 UNIV NOTRE DAME, DEPT BIOL SCI, NOTRE DAME, IN 46556 USA. RP NEI, IMMUNOL LAB, BETHESDA, MD 20892 USA. OI O'Tousa, Joseph/0000-0001-9754-6816 FU NEI NIH HHS [EY06808] NR 55 TC 124 Z9 125 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0092-8674 EI 1097-4172 J9 CELL JI Cell PD MAY 15 PY 1992 VL 69 IS 4 BP 669 EP 676 DI 10.1016/0092-8674(92)90230-A PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HV089 UT WOS:A1992HV08900011 PM 1316807 ER PT J AU NAKATA, H AF NAKATA, H TI BIOCHEMICAL AND IMMUNOLOGICAL CHARACTERIZATION OF ADENOSINE-A1-RECEPTORS PURIFIED FROM HUMAN BRAIN MEMBRANES SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article ID A1 ADENOSINE RECEPTOR; RAT-BRAIN; POLYACRYLAMIDE GELS; BINDING; PROTEIN; PURIFICATION AB The A1 adenosine receptor was purified approximately 13000-fold to apparent homogeneity from human cerebral cortex membranes using a novel affinity-chromatography system developed for the purification of rat brain and rat testis A1 adenosine receptors [Nakata, H. (1989) J. Biol. Chem. 264, 16 545 - 16 551; Nakata, H. (1990) J. Biol. Chem. 265, 671 - 6771. The purified human brain receptor showed the ligand-binding specificity expected of the A1 adenosine receptor. The B(max) and K(d) for the purified receptor with a specific A1 adenosine receptor antagonist, 8-cyclopentyl-1,3-[H-3]dipropylxanthine, were approximately 16 nmol/mg protein and 2 nM, respectively. SDS/PAGE of the purified receptor preparation showed one broad protein band of molecular mass of approximately 35 kDa, which is very similar to that of purified A1 adenosine receptor from rat brain membranes. Endoglycosidase F treatment of the purified receptor reduced the molecular mass to approximately 30 kDa, suggesting that the human brain A1 adenosine receptor is a glycoprotein. Comparison of the purified human and rat brain A1 adenosine receptors by peptide mapping after the proteolytic digestion showed minor differences between these receptors. Immunological comparisons of the human brain A1 adenosine receptor with rat brain A1 adenosine receptor using polyclonal antibodies against the purified rat brain A1 adenosine receptor showed that the antibodies react preferentially with the rat brain receptor and weakly with human brain receptor. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP NAKATA, H (reprint author), TOKYO METROPOLITAN INST NEUROSCI,DEPT MOLEC & CELLULAR NEUROBIOL,2-6 MUSASHIDAI,FUCHU,TOKYO 183,JAPAN. NR 24 TC 19 Z9 19 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD MAY 15 PY 1992 VL 206 IS 1 BP 171 EP 177 DI 10.1111/j.1432-1033.1992.tb16914.x PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HW764 UT WOS:A1992HW76400021 PM 1316839 ER PT J AU KOHIDAI, L BARSONY, J ROTH, J MARX, SJ AF KOHIDAI, L BARSONY, J ROTH, J MARX, SJ TI RAPID EFFECTS OF INSULIN ON CYCLIC-GMP LOCATION IN AN INTACT PROTOZOAN SO EXPERIENTIA LA English DT Article DE INSULIN; CYCLIC GMP; IMMUNOCYTOLOGY; TETRAHYMENA-PYRIFORMIS ID DEPENDENT GUANYLATE-CYCLASE; ADENYLATE-CYCLASE; SODIUM-NITROPRUSSIDE; DOWN-REGULATION; PROTEIN-KINASE; RAT ADIPOCYTES; TETRAHYMENA; RECEPTOR; CELL; CALMODULIN AB We studied rapid changes in location of cyclic GMP in Tetrahymena pyriformis. Insulin caused cGMP localization in cilia and near the plasma membrane (0.5 - 1 min). Later (1 - 5 min) cGMP localization was diffuse in cytoplasm with perinuclear accentuation. Inactive insulin analogs did not elicit these changes. C1 NIDDK,METAB DIS BRANCH,BLD 10,RM 9C-101,BETHESDA,MD 20892. NIDDK,DIABET BRANCH,BETHESDA,MD 20892. OI Kohidai, Laszlo/0000-0002-9002-0296 NR 37 TC 43 Z9 45 U1 0 U2 0 PU BIRKHAUSER VERLAG AG PI BASEL PA PO BOX 133 KLOSTERBERG 23, CH-4010 BASEL, SWITZERLAND SN 0014-4754 J9 EXPERIENTIA JI Experientia PD MAY 15 PY 1992 VL 48 IS 5 BP 476 EP 481 DI 10.1007/BF01928167 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HX600 UT WOS:A1992HX60000010 PM 1376280 ER PT J AU YANAGISHITA, M HASCALL, VC AF YANAGISHITA, M HASCALL, VC TI CELL-SURFACE HEPARAN-SULFATE PROTEOGLYCANS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID OVARIAN GRANULOSA-CELLS; GROWTH-FACTOR-BETA; INTRACELLULAR DEGRADATION; TRANSPORT; CULTURE; NUCLEI; GLYCOSAMINOGLYCANS; ANTITHROMBIN; HEPATOCYTES; METABOLISM RP YANAGISHITA, M (reprint author), NIDR,BONE RES BRANCH,BETHESDA,MD 20892, USA. NR 49 TC 384 Z9 389 U1 0 U2 7 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9451 EP 9454 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500001 PM 1577788 ER PT J AU SANDBERG, K JI, H CLARK, AJL SHAPIRA, H CATT, KJ AF SANDBERG, K JI, H CLARK, AJL SHAPIRA, H CATT, KJ TI CLONING AND EXPRESSION OF A NOVEL ANGIOTENSIN-II RECEPTOR SUBTYPE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID ADRENAL GLOMERULOSA CELLS; ADRENERGIC-RECEPTORS; CALCIUM; ACTIVATION; OOCYTES; RAT AB Angiotensin II (AII) is a major regulator of cardiovascular function and fluid homeostasis. Recently. the cDNA for an AII receptor (AT1) was cloned from rat smooth muscle and bovine adrenal. To search for AII receptor subtypes, we amplified rat adrenal cortex cDNA by PCR using primers based on the AT1 receptor. The product was distinct from the AT1 receptor as indicated by restriction enzyme analysis and DNA sequencing. A full-length cDNA clone (2.2 kilobase pairs) encoding a novel All receptor (AT3) Was obtained by screening an adrenal cortex library. The AT3 cDNA encodes a M(r) 40,959 protein with 95% amino acid identity to the rat smooth muscle receptor, but the overall nucleotide similarity is 71% due to low homology in the 5'- (58%) and 3'- (62%) untranslated regions. Expressed AT3 receptors in Xenopus oocytes and COS-7 cells mediate agonist-induced Ca2+ mobilization but are pharmacologically distinct from the AT1 receptors. AT3 mRNA is most abundant in the adrenal cortex and pituitary and differs from AT1 mRNA in its tissue distribution. The structural features of the AT3 receptor, including two additional potential phosphorylation sites for protein kinase C, could be related to the distinctive binding properties of the adrenal and vascular receptors and to their differential regulation during altered sodium intake. C1 NINCDS,NEUROCHEM LAB,BETHESDA,MD 20892. RP SANDBERG, K (reprint author), NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 10,RM B1-L400,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 28 TC 262 Z9 264 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9455 EP 9458 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500002 PM 1374402 ER PT J AU GRINDE, B CAMERON, CE LEIS, J WEBER, IT WLODAWER, A BURSTEIN, H BIZUB, D SKALKA, AM AF GRINDE, B CAMERON, CE LEIS, J WEBER, IT WLODAWER, A BURSTEIN, H BIZUB, D SKALKA, AM TI MUTATIONS THAT ALTER THE ACTIVITY OF THE ROUS-SARCOMA VIRUS PROTEASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AVIAN RETROVIRAL PROTEASE; SYNTHETIC HIV-1 PROTEASE; CRYSTAL-STRUCTURE; ASPARTIC PROTEASES; POL POLYPROTEINS; ESCHERICHIA-COLI; 2-A RESOLUTION; INHIBITOR; COMPLEX AB Mutations designed by analysis of the Rous sarcoma virus (RSV) and human immunodeficiency virus (HIV)-1 protease (PR) crystal structures were introduced into 1) the substrate binding pocket, 2) the substrate enclosing "flaps," and 3) surface loops of RSV PR. Each mutant PR was expressed in Escherichia coli. Changes in activity were detected by following cleavage of a truncated (NC-PR) precursor polypeptide in E. coli and cleavage of synthetic peptide substrates representing RSV and HIV-1 PR cleavage sites in vitro. Mutations in the substrate binding pocket exchanged amino acid residues located close to the substrate in the HIV-1 PR for structurally equivalent residues in the RSV PR. Changing histidine 65 to glycine (H65G) gave an inactive enzyme, while a double mutant R105P,G106V, as well as the triple mutant, H65G,R105P,G106V, produced enzymes which showed significant activity toward a substrate that represented a HIV-1 cleavage site. Mutating the catalytic aspartate (D37S) or an adjacent conserved alanine to threonine (A40T), produced inactive enzymes. In contrast, the substitution A40S was active, but showed a reduced rate of catalysis. Mutations in the flaps of conserved glycines (G69L, G70L) produced inactive PRs. Two extended RSV PR surface loops were shortened to the size found in HIV-1 PR and resulted in drastically reduced activity. These results have confirmed some of the basic predictions made from structural models but have also revealed unexpected roles and interactions in the protein. C1 CASE WESTERN RESERVE UNIV, SCH MED, CLEVELAND, OH 44106 USA. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA. FOX CHASE CANC INST, INST CANC RES, PHILADELPHIA, PA 19111 USA. FU NCI NIH HHS [CA06927, CA38046, CA47486] NR 42 TC 41 Z9 41 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9481 EP 9490 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500009 PM 1315755 ER PT J AU GRINDE, B CAMERON, CE LEIS, J WEBER, IT WLODAWER, A BURSTEIN, H SKALKA, AM AF GRINDE, B CAMERON, CE LEIS, J WEBER, IT WLODAWER, A BURSTEIN, H SKALKA, AM TI ANALYSIS OF SUBSTRATE INTERACTIONS OF THE ROUS-SARCOMA VIRUS WILD-TYPE AND MUTANT PROTEASES AND HUMAN IMMUNODEFICIENCY VIRUS-1 PROTEASE USING A SET OF SYSTEMATICALLY ALTERED PEPTIDE-SUBSTRATES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SYNTHETIC HIV-1 PROTEASE; CRYSTAL-STRUCTURE; RETROVIRAL PROTEASE; ASPARTIC PROTEASE; RESOLUTION; INHIBITOR; COMPLEX AB In the preceding study, mutant Rous sarcoma virus (RSV) proteases are described in which three amino acids found in the human immunodeficiency virus-1 (HIV-1) protease (PR) were substituted into structurally comparable positions (Grinde, B., Cameron, C. E., Leis, J., Weber, I., Wlodawer, A., Burstein, H., Bizub, D., and Skalka, A. M. (1992) J. Biol. Chem. 267, 9481-9490). In this report, the activity of the wild type and these mutant PRs are compared using a set of RSV NC-PR peptide substrates with single amino acid substitutions in each of the P4 to P3' positions. With most substrates, the relative activities of the two active mutants followed that of the RSV PR. Substitutions in the P1 and P1' positions were an exception; in this case, the mutants behaved more like the HIV-1 PR. These results confirm predictions from structural analyses which indicate that residues 105 and 106 of the RSV PR are important in forming the S1 and S1' binding subsites. These results, further analyzed with the aid of computer modeling of the RSV PR with different substrates, provide an explanation for why only partial HIV-1 PR-like behavior was introduced into the above RSV PR mutants. C1 CASE WESTERN RESERVE UNIV, SCH MED, CLEVELAND, OH 44106 USA. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA. FOX CHASE CANC INST, INST CANC RES, PHILADELPHIA, PA 19111 USA. FU NCI NIH HHS [CA06927, CA38046, CA47486] NR 22 TC 49 Z9 49 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9491 EP 9498 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500010 PM 1315756 ER PT J AU YANAGISHITA, M AF YANAGISHITA, M TI METABOLIC LABELING OF GLYCOSYLPHOSPHATIDYLINOSITOL-ANCHOR OF HEPARAN-SULFATE PROTEOGLYCANS IN RAT OVARIAN GRANULOSA-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GLYCOSYL-PHOSPHATIDYLINOSITOL; FUNCTIONAL ROLES; MEMBRANE ANCHOR; PROTEINS; BIOSYNTHESIS; GLYCOPROTEIN; INSULIN; CULTURE AB The glycosylphosphatidylinositol (GPI)-anchor of the plasma membrane-associated heparan sulfate (HS) proteoglycan was metabolically radiolabeled with [H-3] myristic acid, [H-3]palmitic acid, [H-3]inositol, [H-3]ethanolamine, or [P-32]phosphate in rat ovarian granulosa cell culture. Cell cultures labeled with [H-3]myristic acid or [H-3]palmitic acid were extracted with 4 M guanidine HCl buffer containing 2% Triton X-100 and the proteoglycans were purified by ion exchange chromatography after extensive delipidation. Specific incorporation of H-3 into GPI-anchor was demonstrated by removing the label with a phosphatidylinositol-specific phospholipase C (PI-PLC). Incorporation of H-3 activity into glycosaminoglycans and core glycoproteins was also demonstrated. However, the specific activity of H-3 in these structures was approximately 2 orders of magnitude lower than that in the GPI-anchor, suggesting that H-3 label was the result of the metabolic utilization of catabolic products of the H-3-labeled fatty acids. PI-PLC treatment of cell cultures metabolically labeled with [H-3]inositol, [H-3]ethanolamine, or [P-32]phosphate specifically released radiolabeled cell surface-associated HS proteoglycans indicating the presence of GPI-anchor in these proteoglycans. GPI-anchored HS proteoglycans accounted for 20-30% of the total cell surface-associated HS proteoglycans and virtually all of them were removed by PI-PLC. These results further substantiate the presence of GPI-anchored heparan sulfate proteoglycan in ovarian granulosa cells and its cell surface localization. RP YANAGISHITA, M (reprint author), NIDR, BONE RES BRANCH, BETHESDA, MD 20892 USA. NR 25 TC 6 Z9 8 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9499 EP 9504 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500011 PM 1533635 ER PT J AU YANAGISHITA, M AF YANAGISHITA, M TI GLYCOSYLPHOSPHATIDYLINOSITOL-ANCHORED AND CORE PROTEIN-INTERCALATED HEPARAN-SULFATE PROTEOGLYCANS IN RAT OVARIAN GRANULOSA-CELLS HAVE DISTINCT SECRETORY, ENDOCYTOTIC, AND INTRACELLULAR DEGRADATIVE PATHWAYS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GLYCOSYL-PHOSPHATIDYLINOSITOL; SURFACE; CULTURE; ASSOCIATION; METABOLISM; TRANSPORT; INSULIN AB Rat ovarian granulosa cells synthesize two distinct species of plasma membrane-intercalated heparan sulfate (HS) proteoglycans; glycosylphosphatidylinositol (GPI)-anchored and core protein-intercalated HS proteoglycans. Both species of HS proteoglycans are primarily localized on the plasma membrane. Cell surface localization of GPI-anchored and protein-intercalated HS proteoglycans can be determined by their accessibility to exogenously added phosphatidylinositol-specific phospholipase C (PI-PLC) and trypsin, respectively. Kinetic parameters for the processes involving their transfer from the Golgi to the cell surface, endocytosis and secretion, and the modes of intracellular degradation were determined by metabolic labeling experiments using [S-35]sulfate and various chase protocols in combination with the use of PI-PLC and trypsin in rat ovarian granulosa cells. The experiments demonstrated that (i) both HS proteoglycan species are transferred from the Golgi to the cell surface with an average transit time of approximately 12 min. (ii) GPI-anchored HS proteoglycans are endocytosed with a t1-2 approximately 3 h, without being shed into the medium, and they are rapidly degraded, t1/2 approximately 25 min, without generating recognizable degradation intermediates. (iii) Protein-intercalated HS proteoglycans are partly (approximately 30%) shed from the cell surface into the medium and the remaining approximately 70% are endocytosed with a t1/2 approximately 4 h. After endocytosis, they undergo a slow (t1/2 approximately 4 h) stepwise degradation generating distinct HS oligosaccharides as degradation intermediates. These results indicate that the GPI-anchored and the protein-intercalated HS proteoglycans have distinct secretory, endocytotic, and intracellular degradation pathways probably due to the differences in their anchor structures. RP YANAGISHITA, M (reprint author), NIDR,BONE RES BRANCH,BETHESDA,MD 20892, USA. NR 23 TC 55 Z9 55 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9505 EP 9511 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500012 PM 1533636 ER PT J AU CHAMULITRAT, W MASON, RP RIENDEAU, D AF CHAMULITRAT, W MASON, RP RIENDEAU, D TI NITROXIDE METABOLITES FROM ALKYLHYDROXYLAMINES AND N-HYDROXYUREA DERIVATIVES RESULTING FROM REDUCTIVE INHIBITION OF SOYBEAN LIPOXYGENASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ELECTRON-SPIN RESONANCE; 5-LIPOXYGENASE; ACID; DESFERRIOXAMINE; BIOSYNTHESIS; INACTIVATION; OXIDATION; POTENT; DRUGS; ESR AB One proposed mechanism of the inactivation of lipoxygenase by inhibitors is the reduction of the catalytically active ferric form of the enzyme to its ferrous form. Recent studies have shown that compounds containing the hydroxamate moiety are potent inhibitors of lipoxygenase. The hydroxamate portion of the inhibitor is thought to bind to iron at the catalytic site of the enzyme. We now report evidence that the NOH of the hydroxamate group of N-(4-chlorophenyl)-N-hydroxy-N'-(3-chlorophenyl)urea, N-[(E)-3-(3-phenoxyphenyl)prop-2-enyl]acetohydroxamic (BW A4C), and N-(1-benzo(b)thien-2-ylethyl)-N-hydroxyurea (Zileuton) is oxidized by lipoxygenase to form their corresponding nitroxides, which are directly detected by electron paramagnetic resonance spectroscopy. It is consistently found that the selected NOH-containing compounds, e.g. alkylhydroxylamines or N-hydroxyureas, are also oxidized by lipoxygenase to form their corresponding nitroxides. C1 MERCK FROSST CTR THERAPEUT RES,DEPT BIOCHEM,POINTE CLAIRE H9R 4P8,QUEBEC,CANADA. RP CHAMULITRAT, W (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 29 TC 30 Z9 30 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9574 EP 9579 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500022 PM 1315759 ER PT J AU MURTAGH, JJ MOWATT, MR LEE, CM LEE, FJS MISHIMA, K NASH, TE MOSS, J VAUGHAN, M AF MURTAGH, JJ MOWATT, MR LEE, CM LEE, FJS MISHIMA, K NASH, TE MOSS, J VAUGHAN, M TI GUANINE NUCLEOTIDE-BINDING PROTEINS IN THE INTESTINAL PARASITE GIARDIA-LAMBLIA - ISOLATION OF A GENE ENCODING AN SIMILAR-TO-20-KDA ADP-RIBOSYLATION FACTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID POLYMERASE CHAIN-REACTION; CHOLERA-TOXIN; MESSENGER-RNA; ALPHA-SUBUNIT; SACCHAROMYCES-CEREVISIAE; MOLECULAR-CLONING; GTP; DNA; YEAST; SEQUENCES AB Giardia lamblia is a protozoan intestinal parasite that has characteristics of both eukaryotes and prokaryotes. To determine whether genes for guanine nucleotide-binding proteins are present in Giardia, genomic DNA and cDNA libraries were screened by polymerase chain reaction and by hybridization with mixed oligonucleotide probes complementary to sequences encoding conserved GTP-binding domains. A gene with a high degree of sequence identity with mammalian ADP-ribosylation factors (ARFs), believed to be important in vesicular transport, was identified. The Giardia ARF gene had a 573-base open reading frame encoding 191 amino acids which are 63-70% identical with known mammalian and yeast ARFs. Sequence conservation among ARFs was greatest in putative GTP-binding domains. A single ARF mRNA species of approximately 750 bases was found in two different Giardia isolates. Primer extension and RNA sequencing of the Giardia ARF transcript revealed a short (6-base) 5'-untranslated region similar in size to those found in other Giardia transcripts. Giardia extracts contained ARF activity, as shown by stimulation of cholera toxin-catalyzed ADP-ribosylation and a Giardia ARF expressed in Escherichia coli as a fusion protein likewise exhibited biochemical activity. Its presence in Giardia is consistent with the view that ARF emerged before the divergence of this protozoan from other eukaryotes (approximately 1.5 billion years ago), and that an ARF-like protein may have been the ancestor of several other classes of signal-transducing guanine nucleotide-binding proteins, including the a subunits of the heterotrimeric G proteins. C1 NHLBI,CELLULAR METAB LAB,BLDG 10-5N307,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. OI LEE, CHII-MING/0000-0002-1075-5787 NR 62 TC 74 Z9 75 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9654 EP 9662 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500033 PM 1577802 ER PT J AU SILVERMAN, TA NOGUCHI, M SAFER, B AF SILVERMAN, TA NOGUCHI, M SAFER, B TI ROLE OF SEQUENCES WITHIN THE 1ST INTRON IN THE REGULATION OF EXPRESSION OF EUKARYOTIC INITIATION FACTOR-2-ALPHA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FIREFLY LUCIFERASE; PROTEIN-SYNTHESIS; GENE-EXPRESSION; MAMMALIAN-CELLS; TRANSCRIPTION; DNA; IDENTIFICATION; LYMPHOCYTES; ACTIVATION; PROMOTER AB Resting human peripheral blood T cells synthesize proteins at very low rates and contain very low levels of eukaryotic initiation factor (eIF) 2-alpha mRNA. Daring mitogenic activation, the level of eIF-2-alpha mRNA increases at least 50-fold, an effect thought to be due primarily to intranuclear stabilization of the primary transcript (Cohen, R. B., Boal, T. R., and Safer, B. (1990) EMBO J. 9, 3831-3837). Analysis of sequences within the first intron revealed a region with homology to the "initiator" (Inr) sequence first described by Smale and Baltimore (Smale, S. T., and Baltimore, D. (1989) Cell 57, 103-113). This Inr element is positioned 450 bases downstream of the eIF-2-alpha promoter and is oriented to generate an overlapping antisense transcript. Deletion or mutation of the Inr element results in a reproducible 5-8-fold increase in the activity of an eIF-2-alpha promoter-driven CAT reporter gene and a corresponding 2.5-fold decrease in activity of an antisense driven luciferase reporter gene in vivo in 293 cells. In vitro transcription analysis also reveals antisense transcripts which depend on an intact Inr element and whose 5' ends map to sequences surrounding the Inr consensus sequence. A potential role for double-stranded RNA generated by these overlapping divergent transcription units in the regulation of eIF-2-alpha gene expression in T cells is suggested. C1 NHLBI,PROT & RNA BIOSYNTH SECT,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NR 27 TC 36 Z9 37 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9738 EP 9742 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500047 PM 1374407 ER PT J AU WEITZ, G PROIA, RL AF WEITZ, G PROIA, RL TI ANALYSIS OF THE GLYCOSYLATION AND PHOSPHORYLATION OF THE ALPHA-SUBUNIT OF THE LYSOSOMAL-ENZYME, BETA-HEXOSAMINIDASE-A, BY SITE-DIRECTED MUTAGENESIS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHAIN BINDING-PROTEIN; TAY-SACHS DISEASE; IMMUNOGLOBULIN HEAVY-CHAIN; VIRUS-G PROTEIN; INTRACELLULAR-TRANSPORT; EXTENSIVE HOMOLOGY; FIBROBLASTS; SEQUENCE; OLIGOSACCHARIDES; HEMAGGLUTININ AB The glycosylation and subsequent phosphorylation of mannose residues is a pivotal modification during the biosynthesis of lysosomal enzymes. We have identified the sites of N-linked glycosylation and oligosaccharide phosphorylation on the alpha-subunit of beta-hexosaminidase and have determined the influence of the oligosaccharides on the folding and transport of the enzyme. The potential glycosylation sequences, either singly or in combination, were eliminated through site-directed mutagenesis of the cDNA. By expression of the mutant cDNAs in COS-1 cells, each of the three glycosylation sites on the alpha-subunit was found to be modified by an oligosaccharide. One of the three oligosaccharides was the preferred site of phosphorylation. The absence of any individual oligosaccharide did not diminish the expression of the catalytic activity associated with the alpha-chain, implying proper folding and assembly of subunits. A profound effect was observed, however, when all three oligosaccharides were absent. The unglycosylated alpha-subunit, resulting from genetic alteration of all three glycosylation sites or synthesis of the wild-type protein in the presence of tunicamycin, was catalytically inactive. It was found to be improperly folded into an insoluble aggregate, linked through inappropriate disulfide bonds. The unglycosylated protein was trapped in the lumen of the endoplasmic reticulum and was found in a complex with the Ig heavy chain-binding protein, BiP. The properties of the nonglycosylated, misfolded alpha-subunit were similar to some mutant alpha-subunits in Tay-Sachs disease patients. The results indicate that the oligosaccharides are essential, although not in a site-specific manner, for proper folding and cellular transport of the alpha-subunit. C1 NIDDKD,GENET & BIOCHEM BRANCH,BLDG 10,RM 9D-15,BETHESDA,MD 20892. RI Proia, Richard/A-7908-2012 NR 40 TC 55 Z9 56 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 10039 EP 10044 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500089 PM 1533633 ER PT J AU DING, L SHEVACH, EM AF DING, L SHEVACH, EM TI IL-10 INHIBITS MITOGEN-INDUCED T-CELL PROLIFERATION BY SELECTIVELY INHIBITING MACROPHAGE COSTIMULATORY FUNCTION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MONOCLONAL-ANTIBODIES; B-CELLS; MOUSE MACROPHAGE; ACCESSORY CELLS; ANTIGENS; UNRESPONSIVENESS; INTERLEUKIN-10; EXPRESSION; ACTIVATION; RECEPTORS AB IL-10, a newly designated cytokine primarily produced by the Th2 subset of CD4+ T lymphocytes and Ly-1+ B lymphocytes, has recently been hypothesized to inhibit cytokine production by Thl T cell clones by blocking accessory cell- (AC) dependent costimulatory function. To evaluate the effect of IL-10 on Con A-induced proliferative responses of resting murine T cells, purified T cells were cultured with different types of AC. The addition of IL-10 produced a 70 to 90% inhibition of resting T lymphocyte proliferation when purified populations of macrophages were used as AC, but had no effect on the AC function of T-depleted spleen cells, activated B cells, dendritic cells, or L cells. The inhibitory effects of IL-10 were inversely related to the concentration of mitogen and could be reversed by the addition of the neutralizing anti-IL-10 mAb, SXC1. The inhibition of macrophage AC function was not related to the induction of a suppressor cytokine as stimulation by mixtures of macrophages and limiting numbers of dendritic cells was not inhibited. The decrease in proliferative responses was primarily secondary to inhibition of IL-2 production although the failure of exogenous IL-2 to completely reconstitute the response suggested that IL-10 may also exert inhibitory effects on the induction of expression of a functional IL-2R. These results are most consistent with a model in which IL-10 inhibits the induction of expression on macrophages of a critical costimulatory molecule that may be constitutively expressed on other types of AC. C1 NIAID,IMMUNOL LAB,BLDG 10,ROOM 11N 315,BETHESDA,MD 20892. NR 35 TC 367 Z9 368 U1 1 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 15 PY 1992 VL 148 IS 10 BP 3133 EP 3139 PG 7 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600023 PM 1578140 ER PT J AU SUNDT, TM LEGUERN, C GERMANA, S SMITH, CV NAKAJIMA, K LUNNEY, JK SACHS, DH AF SUNDT, TM LEGUERN, C GERMANA, S SMITH, CV NAKAJIMA, K LUNNEY, JK SACHS, DH TI CHARACTERIZATION OF A POLYMORPHISM OF CD4 IN MINIATURE SWINE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CLASS-II MHC; MONOCLONAL-ANTIBODIES; T-CELLS; SIGNAL TRANSDUCTION; EPITOPE; HETEROGENEITY; LYMPHOCYTES; ANTIGENS; BINDING; OKT4 AB A polymorphism of CD4 in miniature swine has been identified by failure of cells from some animals to react with mAb 74-12-4. The phenotypic, molecular genetic, and functional characteristics of these animals have been defined. Cells from heterozygous animals bear approximately 50% the number of 74-12-4-reactive molecules on their surface as do cells from animals homozygous for the wild type. Animals of both phenotypes demonstrate similar flow cytometric profiles for CD8+ T cells. Northern blot analysis confirms the presence of mRNA for CD4 among PBL of animals failing to stain with 74-12-4. CD4 allelism is confirmed by Southern blot analysis, revealing RFLP. Function of the CD4 subset in vivo, as demonstrated by antibody production against a T cell-dependent Ag, is similar between animals of both phenotypes. Proliferative responses to PHA and alloantigen stimulation by a full haplotype mismatch or a class II mismatch alone are equivalent for animals of both phenotypes. These data suggest that the allelic form of CD4, designated CD4.2 in contrast to the wild-type CD4.1, is capable of performing normally as an accessory molecule in the generation of immune responses. Furthermore, antixenogeneic responses to C57B10.BR were equivalent, suggesting that both CD4 molecular types may be capable of interacting with xenogeneic class II molecules. Although the polymorphism includes differences in exons 3 and 4, regions thought to encode portions of the molecule interacting with MHC class II, these results imply that this naturally occurring CD4 polymorphism does not affect the interaction with class II molecules. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. NR 29 TC 15 Z9 17 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 MAY 15 PY 1992 VL 148 IS 10 BP 3195 EP 3201 PG 7 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600032 PM 1578144 ER PT J AU CHEEVER, AW FINKELMAN, FD CASPAR, P HEINY, S MACEDONIA, JG SHER, A AF CHEEVER, AW FINKELMAN, FD CASPAR, P HEINY, S MACEDONIA, JG SHER, A TI TREATMENT WITH ANTI-IL-2 ANTIBODIES REDUCES HEPATIC PATHOLOGY AND EOSINOPHILIA IN SCHISTOSOMA-MANSONI-INFECTED MICE WHILE SELECTIVELY INHIBITING T-CELL IL-5 PRODUCTION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SUPPRESSOR EFFECTOR FACTOR; GRANULOMA-FORMATION; MOLECULAR-BASIS; INVIVO; EXPRESSION; INDUCTION; PATTERNS; FIBROSIS; INVITRO AB Granulomas around Schistosoma mansoni eggs are a principal cause of morbidity in mice infected with this helminth. In vivo treatment of infected mice with anti-IL-2 antibodies, with or without anti-IL-2 receptor antibodies, significantly diminished the size of circumoval granulomas in the liver and decreased hepatic fibrosis to half that in untreated mice. Antibody-treated animals also displayed a marked reduction in both peripheral blood and tissue eosinophilia while IgE levels were unchanged or increased. Spleen cell cytokine production in response to Ag or mitogen stimulation was selectively altered by in vivo anti-IL-2 administration. IL-5 responses were dramatically reduced, whereas IL-4, IL-2, and IFN-gamma responses were not consistently changed. These findings confirm previous observations, suggesting a role for IL-2 in egg-induced pathology but indicate that the primary function of this cytokine in schistosome-infected mice may be in the generation of Th2- rather than Thl-associated responses. 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,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [R01 AI21328] NR 28 TC 68 Z9 69 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 15 PY 1992 VL 148 IS 10 BP 3244 EP 3248 PG 5 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600039 PM 1533655 ER PT J AU KULLBERG, MC PEARCE, EJ HIENY, SE SHER, A BERZOFSKY, JA AF KULLBERG, MC PEARCE, EJ HIENY, SE SHER, A BERZOFSKY, JA TI INFECTION WITH SCHISTOSOMA-MANSONI ALTERS TH1/TH2 CYTOKINE RESPONSES TO A NON-PARASITE ANTIGEN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID DELAYED-HYPERSENSITIVITY; GRANULOMA-FORMATION; IGE RESPONSES; TH2 CLONES; T-CELLS; GAMMA; ANTIBODY; MOUSE; MICE; IL-4 AB Schistosoma mansoni infection in the mouse has been shown to be accompanied by a down-regulation in parasite-Ag- and mitogen-induced Th1 cytokine secretion (IL-2 and IFN-gamma) with a simultaneous increase in the production of Th2 cytokines (IL-4, IL-5, and IL-10), suggesting a generalized imbalance in lymphocyte function. In the present study, we examined whether infection with S. mansoni would also influence the character of immune responses to a non-parasite Ag, sperm whale myoglobin (SwMb). When spleen cells (SC) from schistosome-infected SwMb-immunized animals were stimulated with SwMb, their production of IL-2 and IFN-gamma per CD4+ cell was found to be significantly reduced (by 45% and 59%, respectively) compared with the responses observed in immunized uninfected animals. Moreover, SwMb-induced secretion of IL-4 per CD4+ cell was increased threefold in SC cultures from infected mice. No myoglobin-induced IL-5 was detected in the same cultures. Addition to SC cultures of a neutralizing mAb specific for IL-10 partly restored the suppressed IFN-gamma response to SwMb seen in infected mice, suggesting a role for IL-10 in the observed down-regulation. S. mansoni-infected mice also showed an impaired antibody response to SwMb, with levels ranging from 10% to 27% of those observed in uninfected mice, although no differences in IgG isotype were evident. Taken together, these results suggest that infection with S. mansoni induces a down-regulation of Thl responses and elevation of Th2 responses to unrelated foreign immunogens as well as to parasite Ag themselves. One implication of these findings is that helminth-infected individuals may have altered cell-mediated immune function to other microbial agents. C1 NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BETHESDA,MD 20892. NR 46 TC 223 Z9 227 U1 2 U2 6 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 15 PY 1992 VL 148 IS 10 BP 3264 EP 3270 PG 7 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600042 PM 1533656 ER PT J AU CARROLL, FI GAO, YG ABRAHAM, P LEWIN, AH LEW, R PATEL, A BOJA, JW KUHAR, MJ AF CARROLL, FI GAO, YG ABRAHAM, P LEWIN, AH LEW, R PATEL, A BOJA, JW KUHAR, MJ TI PROBES FOR THE COCAINE RECEPTOR - POTENTIALLY IRREVERSIBLE LIGANDS FOR THE DOPAMINE TRANSPORTER SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article AB Several potentially irreversible ligands (i.e., wash-resistant binding inhibitors) for the cocaine receptor site on the dopamine transporter, derived from (-)-cocaine or 3-beta-phenyltropan-2-beta-carboxylic acid methyl ester (WIN 35,065-2), were prepared and shown to produce wash-resistant inhibition of [H-3]-3-beta-(p-fluorophenyl)tropan-2-beta-carboxylic acid methyl ester ([H-3]WIN 35,428) binding. All the compounds prepared had the same absolute configuration as cocaine; they include analogues possessing chemically reactive groups such as the isothiocyanato and bromoacetamido as well as photoactive azido groups. The potentially irreversible ligands, as well as all the intermediates prepared in this study, were evaluated for their ability to inhibit the binding of [H-3]WIN 35,428 in coincubation experiments. Of the potentially irreversible ligands, 3-beta-(p-chlorophenyl)tropan-2-beta-carboxylic acid 2-[p-(bromoacetamido)phenyl]ethyl ester (6c) had the highest apparent potency. The potentially irreversible ligands were also preincubated, and inhibition of [H-3]WIN 35,428 binding was determined both before and after washing the ligand-exposed tissues. The most effective ligands in this regard were 3-beta-(3-iodo-4-azidophenyl)tropan-2-beta-carboxylic acid methyl ester (5) and 3-beta-(p-chlorophenyl)tropan-2-beta-carboxylic acid 2-(3-iodo-4-azidophenyl)ethyl ester (6d). The structure-activity relationships of these data are discussed. C1 NIDA, ADDICT RES CTR, NEUROSCI BRANCH, BALTIMORE, MD 21224 USA. RP RES TRIANGLE INST, POB 12194, RES TRIANGLE PK, NC 27709 USA. FU NIDA NIH HHS [DA05477] NR 16 TC 59 Z9 59 U1 0 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 EI 1520-4804 J9 J MED CHEM JI J. Med. Chem. PD MAY 15 PY 1992 VL 35 IS 10 BP 1813 EP 1817 DI 10.1021/jm00088a017 PG 5 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA HU927 UT WOS:A1992HU92700017 PM 1588560 ER PT J AU DAYAN, I GITTERMAN, M WEISS, GH AF DAYAN, I GITTERMAN, M WEISS, GH TI ON THE ENTROPY OF A CLASS OF CONSTRAINED RANDOM-WALKS SO PHYSICA A LA English DT Article AB We define and calculate the entropy of some random walks which have two endpoints fixed, and for which displacements are allowed to take all possible values. An example is given in which the entropy can either be increased or decreased by imposing a constraint. It is also shown, by example, that when the constrained entropy approaches its unconstrained value, the rate of approach is asymtotically O(In n)/n). C1 NIH,BETHESDA,MD 20892. RP DAYAN, I (reprint author), BAR ILAN UNIV,DEPT PHYS,IL-52100 RAMAT GAN,ISRAEL. NR 4 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4371 J9 PHYSICA A JI Physica A PD MAY 15 PY 1992 VL 183 IS 4 BP 508 EP 518 DI 10.1016/0378-4371(92)90297-4 PG 11 WC Physics, Multidisciplinary SC Physics GA HX665 UT WOS:A1992HX66500008 ER PT J AU MASOLIVER, J WEISS, GH AF MASOLIVER, J WEISS, GH TI 1ST PASSAGE TIMES FOR A GENERALIZED TELEGRAPHERS EQUATION SO PHYSICA A LA English DT Article ID DIFFUSION AB All definitions and analyses of the one-dimensional telegrapher's equation assume an underlying translational invariant space. We here generalize this model to allow for nonuniform spatial properties, and derive the form of the backward equation and the associated boundary conditions in the presence of trapping points. We show that moments of the first-passage time till trapping can be calculated in closed form from a formalism based on the backward equation. C1 NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. RP MASOLIVER, J (reprint author), UNIV BARCELONA,DEPT FIS FONAMENTAL,DIAGONAL 647,E-08028 BARCELONA,SPAIN. RI Masoliver, Jaume/F-7198-2016 OI Masoliver, Jaume/0000-0002-5810-879X NR 10 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4371 J9 PHYSICA A JI Physica A PD MAY 15 PY 1992 VL 183 IS 4 BP 537 EP 548 DI 10.1016/0378-4371(92)90299-6 PG 12 WC Physics, Multidisciplinary SC Physics GA HX665 UT WOS:A1992HX66500010 ER PT J AU LARRALDE, H TRUNFIO, P HAVLIN, S STANLEY, HE WEISS, GH AF LARRALDE, H TRUNFIO, P HAVLIN, S STANLEY, HE WEISS, GH TI NUMBER OF DISTINCT SITES VISITED BY N-RANDOM WALKERS SO PHYSICAL REVIEW A LA English DT Article ID DIFFUSION; RELAXATION AB We study the number of distinct sites visited by N random walkers after t steps S(N)(t) under the condition that all the walkers are initially at the origin. We derive asymptotic expressions for the mean number of distinct sites [S(N)(t)] in one, two, and three dimensions. We find that [S(N)(t)] passes through several growth regimes, at short times [S(N)(t)] approximately t(d) (regime I), for t(x) << t << t'x we find that [S(N)(t)] approximately (t ln[N S1(t)/t(d/2)])d/2 (regime II), and for t >> t'x, [S(N)(t)) approximately NS1(t) (regime III). The crossover times are t(x) approximately ln N for all dimensions, and t'x approximately infinity, exp N, and N2 for one, two, and three dimensions, respectively. We show that in regimes II and III [S(N)(t)] satisfies a scaling relation of the form [S(N)(t)] approximately t(d/2) f(x), with x = N[S1(t)]/t(d/2). We also obtain asymptotic results for the complete probability distribution of S(N)(t) for the one-dimensional case in the limit of large N and t. C1 BOSTON UNIV, DEPT PHYS, BOSTON, MA 02215 USA. NIH, DIV COMP RES & TECHNOL, PHYS SCI LAB, BETHESDA, MD 20892 USA. RP BOSTON UNIV, CTR POLYMER STUDIES, BOSTON, MA 02215 USA. NR 34 TC 73 Z9 73 U1 1 U2 3 PU AMER PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 2469-9926 EI 2469-9934 J9 PHYS REV A JI Phys. Rev. A PD MAY 15 PY 1992 VL 45 IS 10 BP 7128 EP 7138 DI 10.1103/PhysRevA.45.7128 PG 11 WC Optics; Physics, Atomic, Molecular & Chemical SC Optics; Physics GA HV267 UT WOS:A1992HV26700027 ER PT J AU HAVLIN, S NOSSAL, R TRUS, B WEISS, GH AF HAVLIN, S NOSSAL, R TRUS, B WEISS, GH TI PHOTON MIGRATION IN DISORDERED MEDIA SO PHYSICAL REVIEW A LA English DT Article ID OPTICAL-PROPERTIES; TISSUE; TIME; FRACTALS; INVERSION; DENSITY; MODEL; WALKS AB Numerical and analytical methods are used to study a model for the multiple scattering of photons in the presence of randomly reflecting inclusions. The photons are injected into a semi-infinite medium near its surface, and are absorbed by the surface or within the medium. In the medium the photons can diffuse only through voids between the reflecting inclusions, where the void structure has been modeled as a fractal object. Our analytical approach is based on an analogy between the kinetics of a continuous-time random-walk model and the movement of random walkers on fractals. For the case of nonabsorbing media, we find the survival of photons within the medium after n steps to be S(n) is-proportional-to n-1+1/d(w) and the intensity profile at a distance-rho from the injection point to be GAMMA(rho) is-proportional-to rho(-d)w, where d(w) is the diffusion exponent for fractals. For the case of absorbing media, GAMMA(rho) scales as mu(theta)rho(-lambda)exp(-gamma-mu-1/d(w) rho), where mu is the absorption coefficient of the fractal medium, theta and lambda are exponents related to the fractal dimensions, and gamma is a constant. We also calculate the mean time and the average maximal depth of photons that emerge at a distance-rho. RP NIH, BETHESDA, MD 20892 USA. NR 40 TC 4 Z9 4 U1 0 U2 1 PU AMER PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 2469-9926 EI 2469-9934 J9 PHYS REV A JI Phys. Rev. A PD MAY 15 PY 1992 VL 45 IS 10 BP 7511 EP 7519 DI 10.1103/PhysRevA.45.7511 PG 9 WC Optics; Physics, Atomic, Molecular & Chemical SC Optics; Physics GA HV267 UT WOS:A1992HV26700068 ER PT J AU HECK, DV YEE, CL HOWLEY, PM MUNGER, K AF HECK, DV YEE, CL HOWLEY, PM MUNGER, K TI EFFICIENCY OF BINDING THE RETINOBLASTOMA PROTEIN CORRELATES WITH THE TRANSFORMING CAPACITY OF THE E7 ONCOPROTEINS OF THE HUMAN PAPILLOMAVIRUSES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ADENOVIRUS E1A PROTEINS; ESCHERICHIA-COLI; GENE-PRODUCT; TYPE-16; TRANSCRIPTION; SV40; KERATINOCYTES; E7-PROTEIN; CELLS; TRANSACTIVATION AB The human papillomaviruses (HPVs) associated with genital tract lesions can be classified as either "high risk" or "low risk" based on their association with human anogenital cancer. The E7 proteins of the. high-risk and the low-risk viruses are quite similar in their amino acid composition and structural organization yet differ in their transforming potential and in a number of biochemical properties. A series of chimeric proteins consisting of segments of the high-risk HPV-16 and the low-risk HPV-6 E7 proteins were constructed in order to define which domains within the amino-terminal half of E7 were responsible for the different biological and biochemical properties. The E7 oncogenic capacity, which was determined by assaying transformation of baby rat kidney cells in cooperation with an activated ras oncogene, segregated with the retinoblastoma tumor suppressor protein (pRB) binding domain of the HPV-16 E7 protein. A comparison of the pRB binding sites of the sequenced genital tract HPVs revealed a consistent amino acid difference (aspartic acid/glycine) between the high-risk and low-risk viruses. Single amino acid substitution mutations were generated at this position in the HPV-6 and HPV-16 E7 proteins, and this single amino acid residue was shown to be the principal determinant responsible for the differences in the apparent pRB binding affinity and transformation capacity distinguishing the HPV E7 proteins of the high-risk and low-risk HPVs. C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. OI Munger, Karl/0000-0003-3288-9935 NR 44 TC 261 Z9 266 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 15 PY 1992 VL 89 IS 10 BP 4442 EP 4446 DI 10.1073/pnas.89.10.4442 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU977 UT WOS:A1992HU97700046 PM 1316608 ER PT J AU MURPHY, WJ DURUM, SK LONGO, DL AF MURPHY, WJ DURUM, SK LONGO, DL TI HUMAN GROWTH-HORMONE PROMOTES ENGRAFTMENT OF MURINE OR HUMAN T-CELLS IN SEVERE COMBINED IMMUNODEFICIENT MICE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE NEUROENDOCRINE IMMUNE EFFECTS; IMMUNE RECONSTITUTION; AIDS ANIMAL MODEL ID LYMPHOCYTES; RECEPTOR; BINDING; MOUSE AB Growth hormone (GH) has previously been implicated in T-cell development, and here we test its efficacy in promoting T-lymphocyte engraftment in mice with severe combined immune deficiency (SCID). SCID mice receiving syngeneic thymocytes and treated with recombinant human GH (rhGH) had significantly better T-cell engraftment in their lymph nodes. Human T-cell engraftment was also strongly promoted by rhGH in SCID recipients receiving human peripheral blood lymphocytes. Additionally, although mature human cells have not been thought to enter the murine thymus, human T cells were detected in the SCID thymus after rhGH treatment. Thus, rhGH can be used to optimize long-term peripheral T-cell engraftment in these human-mouse chimeras and may also be useful clinically in treating T-cell deficiencies. RP MURPHY, WJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702, USA. NR 19 TC 93 Z9 95 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 15 PY 1992 VL 89 IS 10 BP 4481 EP 4485 DI 10.1073/pnas.89.10.4481 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU977 UT WOS:A1992HU97700054 PM 1584780 ER PT J AU UCHIDA, K STADTMAN, ER AF UCHIDA, K STADTMAN, ER TI MODIFICATION OF HISTIDINE-RESIDUES IN PROTEINS BY REACTION WITH 4-HYDROXYNONENAL SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID LOW-DENSITY-LIPOPROTEIN; ASCITES TUMOR-CELLS; LIPID-PEROXIDATION; OXIDATIVE MODIFICATION; GLUTAMINE-SYNTHETASE; CATALYZED OXIDATION; PRODUCT; ALDEHYDES; MECHANISM AB We find that histidine residues in proteins are major targets for reaction with the lipid peroxidation product 4-hydroxynon-2-enal (HNE). Reaction of insulin (which contains no sulfhydryl groups) with HNE leads to the generation of HNE-protein adducts, which are converted to radioactive derivatives upon subsequent treatment with NaB[H-3]H-4. Amino acid analysis of the modified protein showed that the HNE treatment leads to the selective loss of histidine residues and the stoichiometric formation of H-3-labeled amino acid derivatives. The same labeled products were detected in acid hydrolysates of polyhistidine and N-acetylhistidine after their reactions with HNE and NaB[H-3]H-4. The reaction of N-acetylhistidine with HNE led to the production of two compounds. Upon acid hydrolysis, both derivatives yielded stoichiometric amounts of histidine. However, after reduction with NaBH4, acid hydrolysis led to a mixture of amino acid derivatives [presumably, isomeric forms of N(pi)(N(tau))-1,4-dihydroxynonanylhistidine] that were indistinguishable from those obtained from insulin and polyhistidine after similar treatment. Although other possibilities are not excluded, it is suggested that the modification of histidine residues in proteins by HNE involves a Michael-type addition of the imidazole nitrogen atom of histidine to the alpha,beta-unsaturated bond of HNE, followed by secondary reaction involving the aldehyde group with the C-4 hydroxyl group of HNE. The reaction of histidine residues with HNE provides the basis for methods by which the contributions of HNE in the modification of proteins can be determined. C1 NHLBI,BIOCHEM LAB,9000 ROCKVILLE PIKE,BLDG 3,ROOM 222,BETHESDA,MD 20892. NR 32 TC 402 Z9 410 U1 3 U2 12 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 15 PY 1992 VL 89 IS 10 BP 4544 EP 4548 DI 10.1073/pnas.89.10.4544 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU977 UT WOS:A1992HU97700067 PM 1584790 ER PT J AU CHELLAPPAN, S KRAUS, VB KROGER, B MUNGER, K HOWLEY, PM PHELPS, WC NEVINS, JR AF CHELLAPPAN, S KRAUS, VB KROGER, B MUNGER, K HOWLEY, PM PHELPS, WC NEVINS, JR TI ADENOVIRUS-E1A, SIMIAN VIRUS-40 TUMOR-ANTIGEN, AND HUMAN PAPILLOMAVIRUS-E7 PROTEIN SHARE THE CAPACITY TO DISRUPT THE INTERACTION BETWEEN TRANSCRIPTION FACTOR-E2F AND THE RETINOBLASTOMA GENE-PRODUCT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CELL-CYCLE; RB GENE; SUSCEPTIBILITY GENE; BINDING-ACTIVITY; EXPRESSION; E2F; TRANSFORMATION; CARCINOMA; COMPLEX; PHOSPHORYLATION AB The adenovirus E1A gene product, the simian virus 40 large tumor antigen, and the human papillomavirus E7 protein share a short amino acid sequence that constitutes a domain required for the transforming activity of these proteins. These sequences are also required for these proteins to bind to the retinoblastoma gene product (pRb). Recent experiments have shown that E1A can dissociate complexes containing the transcription factor E2F bound to pRb, dependent on this conserved sequence element. We now show that the E7 protein and the simian virus 40 large tumor antigen can dissociate the E2F-pRb complex, dependent on this conserved sequence element. We also find that the E2F-pRb complex is absent in various human cervical carcinoma cell lines that either express the E7 protein or harbor an RB1 mutation, suggesting that the loss of the E2F-pRb interaction may be an important aspect in human cervical carcinogenesis. We suggest that the ability of E1A, the simian virus 40 large tumor antigen, and E7 to dissociate the E2F-pRb complex may be a common activity of these viral proteins that has evolved to stimulate quiescent cells into a proliferating state so that viral replication can proceed efficiently. In circumstances in which a lytic infection does not proceed, the consequence of this action may be to initiate the oncogenic process in a manner analogous to the mutation of the RB1 gene. C1 BURROUGHS WELLCOME CO,DIV VIROL,RES TRIANGLE PK,NC 27709. NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. RP CHELLAPPAN, S (reprint author), DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT MICROBIOL & IMMUNOL,GENET SECT,DURHAM,NC 27710, USA. OI Munger, Karl/0000-0003-3288-9935 NR 50 TC 467 Z9 479 U1 1 U2 10 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 15 PY 1992 VL 89 IS 10 BP 4549 EP 4553 DI 10.1073/pnas.89.10.4549 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU977 UT WOS:A1992HU97700068 PM 1316611 ER PT J AU IGNARTROWBRIDGE, DM NELSON, KG BIDWELL, MC CURTIS, SW WASHBURN, TF MCLACHLAN, JA KORACH, KS AF IGNARTROWBRIDGE, DM NELSON, KG BIDWELL, MC CURTIS, SW WASHBURN, TF MCLACHLAN, JA KORACH, KS TI COUPLING OF DUAL SIGNALING PATHWAYS - EPIDERMAL GROWTH-FACTOR ACTION INVOLVES THE ESTROGEN-RECEPTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MESSENGER RIBONUCLEIC-ACID; BREAST-CANCER CELLS; PROGESTERONE-RECEPTOR; MOUSE UTERUS; TYROSINE PHOSPHORYLATION; ANTIESTROGENS; PROTEIN AB Epidermal growth factor (EGF) reproduces many of the effects of estrogen on the murine female reproductive tract and may partially mediate estrogen-induced growth and differentiation. This study was performed to investigate the mechanism by which EGF elicits estrogen-like actions in the whole animal. EGF was administered to adult ovariectomized mice by slow release pellets implanted under the kidney capsule. The induction of uterine DNA synthesis and phosphatidylinositol lipid turnover by EGF or administration of diethylstilbestrol (5-mu-g/kg), a potent estrogen, was attenuated by the estrogen receptor antagonist ICI 164,384. Furthermore, EGF mimicked the effects of estrogen on enhanced nuclear localization of the estrogen receptor and the formation of a unique form of the estrogen receptor found exclusively in the nucleus. These results suggest that EGF may induce effects similar to those of estrogen in the mouse uterus by an interaction between the EGF signaling pathway and the classical estrogen receptor. The demonstration of cross-talk between polypeptide growth factors and steroid hormone receptors may be of importance to our understanding of the regulation of normal growth and differentiation as well as the mechanisms of transmission of extracellular mitogen signals to the nucleus. C1 NIEHS, REPROD & DEV TOXICOL LAB, RES TRIANGLE PK, NC 27709 USA. OI Korach, Kenneth/0000-0002-7765-418X NR 30 TC 440 Z9 444 U1 0 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 15 PY 1992 VL 89 IS 10 BP 4658 EP 4662 DI 10.1073/pnas.89.10.4658 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU977 UT WOS:A1992HU97700090 PM 1584801 ER PT J AU VOGEL, SS ZIMMERBERG, J AF VOGEL, SS ZIMMERBERG, J TI PROTEINS ON EXOCYTIC VESICLES MEDIATE CALCIUM-TRIGGERED FUSION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SECRETION; SEA URCHIN EGG; FERTILIZATION; EXOCYTOSIS ID SEA-URCHIN EGGS; PLASMA-MEMBRANE; SECRETORY VESICLES; MAST-CELLS; INVITRO; GRANULES; DISCHARGE; CORTICES; RELEASE; ASSAY AB In many exocytic systems, micromolar concentrations of intracellular Ca2+ trigger fusion. We find that aggregates of secretory granules isolated from sea urchin eggs fuse together when perfused with greater-than-or-equal-to 10-mu-M free Ca2+. Mixing of membrane components was demonstrated by transfer of fluorescent lipophilic dye, and melding of granule contents was seen with differential interference microscopy. A technique based upon light scattering was developed to conveniently detect fusion. Two protein modifiers, trypsin and N-ethylmaleimide, inhibit granule-granule fusion at concentrations similar to those that inhibit granule-plasma membrane fusion. We suggest that molecular machinery sufficient for Ca2+-triggered fusion resides on secretory granules as purified and that at least some of these essential components are proteinaceous. C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. RP VOGEL, SS (reprint author), NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892, USA. RI Vogel, Steven/A-3585-2012; OI Vogel, Steven/0000-0002-3005-2667 NR 30 TC 39 Z9 40 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 15 PY 1992 VL 89 IS 10 BP 4749 EP 4753 DI 10.1073/pnas.89.10.4749 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU977 UT WOS:A1992HU97700109 PM 1584814 ER PT J AU PAVLIAK, V KOVAC, P GLAUDEMANS, CPJ AF PAVLIAK, V KOVAC, P GLAUDEMANS, CPJ TI SYNTHESIS OF LIGANDS RELATED TO THE O-SPECIFIC ANTIGEN OF SHIGELLA-DYSENTERIAE TYPE-1 .2. STEREOSELECTIVE SYNTHESES OF A DISACCHARIDE, TRISACCHARIDE, AND TETRASACCHARIDE FRAGMENT OF SHIGELLA-DYSENTERIAE TYPE-1 O-ANTIGEN USING 3,4,6-TRI-O-ACETYL-2-AZIDO-2-DEOXY-ALPHA-D-GLUCOPYRANOSYL CHLORIDE AS A GLYCOSYL DONOR SO CARBOHYDRATE RESEARCH LA English DT Article ID LINKED DISACCHARIDES; FACILE PREPARATION; BUILDING UNITS; OLIGOSACCHARIDES; DERIVATIVES; 2-AMINO-2-DEOXY-D-GLUCOPYRANOSE; SHIGELLA-DYSENTERIAE-1; GLUCOSAMINE; PRECURSORS; VIRULENCE AB Methyl 2,4-di-O-benzoyl-alpha-L-rhamnopyranoside (1) furnished a crystalline 3-0-bromoacetyl derivative that was treated with the dichloromethyl methyl ether-ZnCl2 reagent to give 2,4-di-O-benzoyl-3-O-bromoacetyl-alpha-L-rhamnopyranosyl chloride (3). Compounds 1 and 3 were condensed under the conditions of base-deficient, silver trifluoromethanesulfonate-mediated glycosylation to give a fully protected rhamnobioside, which on O-debromoacetylation afforded the disaccharide nucleophile 10. Similar condensation of 3 with methyl 3-O-benzoyl-4,6-O-benzylidene-alpha-D-galactopyranoside, followed by O-debromoacetylation and condensation of the thus formed methyl O-(2,4-di-O-benzoyl-alpha-L-rhamopyranosyl)-(1 --> 2)-4,6-O-benzylidene-3-O-benzoyl-alpha-D-galactopyranoside again with 3, gave the trisaccharide glycoside. Subsequent O-debromoacetylation gave 17, having only HO-3(3) unsubstituted. Silver perchlorate-mediated glycosylations of 1, 10, and 17 with 3.4.6-tri-O-acetyl-2-azido-2-deoxy-alpha-D-glucopyranosyl chloride afforded, with high alpha stereoselectivity, protected di-, tri-, and tetra-saccharide glycosides. Subsequent hydrogenation, followed by N-acetylation and O-deacylation, afforded three oligosaccharide glycosides having nonreducing terminal 2-acetamido-2-deoxy-alpha-D-glucopyranosyl residues and comprising successively larger portions of the repeating unit of Shigella dysenteriae type 1 O-antigen. C1 NIH,BETHESDA,MD 20892. NR 26 TC 11 Z9 11 U1 2 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD MAY 14 PY 1992 VL 229 IS 1 BP 103 EP 116 DI 10.1016/S0008-6215(00)90483-X PG 14 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA HW844 UT WOS:A1992HW84400008 PM 1381283 ER PT J AU ZWANZIG, R AF ZWANZIG, R TI DIFFUSION PAST AN ENTROPY BARRIER SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID BROWNIAN PARTICLE; COEFFICIENT AB Diffusion in a tube or channel of varying cross section has been treated, by Fick and Jacobs, as one-dimensional diffusion past an entropy barrier determined by the tube cross-sectional area or channel width. The Fick-Jacobs diffusion equation is rederived, along with corrections involving the curvature of the tube or channel. On comparison with two exactly solvable examples, the Fick-Jacobs equation appears to be quite reliable as long as the curvature is not too great. RP ZWANZIG, R (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 2,BETHESDA,MD 20892, USA. NR 9 TC 273 Z9 274 U1 3 U2 26 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3654 J9 J PHYS CHEM-US JI J. Phys. Chem. PD MAY 14 PY 1992 VL 96 IS 10 BP 3926 EP 3930 DI 10.1021/j100189a004 PG 5 WC Chemistry, Physical SC Chemistry GA HV240 UT WOS:A1992HV24000004 ER PT J AU RUBINSTEIN, LV KOUTSOUKOS, AD AF RUBINSTEIN, LV KOUTSOUKOS, AD TI ARTISTS OFFSPRING SO NATURE LA English DT Letter RP RUBINSTEIN, LV (reprint author), NCI,BIOMETR RES BRANCH,ROCKVILLE,MD 20892, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAY 14 PY 1992 VL 357 IS 6374 BP 106 EP 106 DI 10.1038/357106c0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU122 UT WOS:A1992HU12200021 PM 1579157 ER PT J AU BOICE, JD MILLER, RW AF BOICE, JD MILLER, RW TI RISK OF BREAST-CANCER IN ATAXIA TELANGIECTASIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP BOICE, JD (reprint author), NCI,BETHESDA,MD 20892, USA. NR 6 TC 22 Z9 22 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 14 PY 1992 VL 326 IS 20 BP 1357 EP 1358 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HT803 UT WOS:A1992HT80300013 PM 1565151 ER PT J AU LAND, CE AF LAND, CE TI RISK OF BREAST-CANCER IN ATAXIA TELANGIECTASIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP LAND, CE (reprint author), NCI,BETHESDA,MD 20892, USA. NR 4 TC 7 Z9 7 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 14 PY 1992 VL 326 IS 20 BP 1359 EP 1360 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HT803 UT WOS:A1992HT80300016 PM 1304719 ER PT J AU LAGAKOS, SW FISCHL, MA STEIN, DS VOLBERDING, PA AF LAGAKOS, SW FISCHL, MA STEIN, DS VOLBERDING, PA TI THE EFFECT OF ZIDOVUDINE ON PATIENT SUBGROUPS - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter C1 UNIV MIAMI,CORAL GABLES,FL 33124. NIAID,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. RP LAGAKOS, SW (reprint author), HARVARD UNIV,CAMBRIDGE,MA 02138, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAY 13 PY 1992 VL 267 IS 18 BP 2473 EP 2473 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HT068 UT WOS:A1992HT06800022 ER PT J AU MAYER, ML BENVENISTE, M PATNEAU, DK VYKLICKY, L AF MAYER, ML BENVENISTE, M PATNEAU, DK VYKLICKY, L TI PHARMACOLOGICAL PROPERTIES OF NMDA RECEPTORS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID METHYL-D-ASPARTATE; AMINO-ACID RECEPTORS; CULTURED HIPPOCAMPAL-NEURONS; MOUSE CENTRAL NEURONS; SYNAPTIC TRANSMISSION; ACTIVATED CHANNELS; MOLECULAR-CLONING; DIVALENT-CATIONS; KINETIC-ANALYSIS; RAT HIPPOCAMPUS RP MAYER, ML (reprint author), NICHHD, DEV NEUROBIOL LAB, NEUROPHYSIOL & BIOPHYS SECT, BLDG 36, ROOM 2A21, BETHESDA, MD 20892 USA. RI Vyklicky, Ladislav/C-1851-2012; Mayer, Mark/H-5500-2013 OI Vyklicky, Ladislav/0000-0002-0015-0098; NR 44 TC 28 Z9 29 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD MAY 11 PY 1992 VL 648 BP 194 EP 204 DI 10.1111/j.1749-6632.1992.tb24538.x PG 11 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM216 UT WOS:A1992JM21600023 PM 1386202 ER PT J AU LEHMANN, J DESOUZA, EB CULP, S ZACZEK, R AF LEHMANN, J DESOUZA, EB CULP, S ZACZEK, R TI REGIONAL DISTRIBUTION TO RECOVERY OF 5-HT LEVELS AFTER ADMINISTRATION OF ATROPHINS MDMA AND D,L-FENFLURAMINE - STEREOSPECIFICITY AND COMPARISON WITH 5,7-DIHYDROXYTRYPTAMINE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID MEDIAN RAPHE NUCLEI; ALZHEIMERS-DISEASE; RAT-BRAIN; REPEATED FENFLURAMINE; AXON TERMINALS; SEROTONIN; DORSAL C1 NIDA,DEPT NEUROSCI,BETHESDA,MD 20892. RP LEHMANN, J (reprint author), HAHNEMANN UNIV,DIV BEHAV NEUROBIOL,DEPT MENTAL HLTH SERV,PHILADELPHIA,PA 19102, USA. NR 13 TC 6 Z9 6 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD MAY 11 PY 1992 VL 648 BP 291 EP 295 DI 10.1111/j.1749-6632.1992.tb24560.x PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM216 UT WOS:A1992JM21600045 PM 1379013 ER PT J AU RABINOVITZ, M AF RABINOVITZ, M TI THE PLEIOTYPIC RESPONSE TO AMINO-ACID DEPRIVATION IS THE RESULT OF INTERACTIONS BETWEEN COMPONENTS OF THE GLYCOLYSIS AND PROTEIN-SYNTHESIS PATHWAYS SO FEBS LETTERS LA English DT Article DE AMINO ACID DEFICIENCY; TRANSFER RNA; AMINOACYL-TRANSFER RNA; PHOSPHOFRUCTOKINASE; FRUCTOSE-1,6-DIPHOSPHATE; INSULIN; CYCLIC AMP ID ELONGATION-FACTOR-TU; POLYPEPTIDE-CHAIN INITIATION; RAT SKELETAL-MUSCLE; MAMMALIAN-CELLS; HUMAN-LYMPHOBLASTS; PURINE SYNTHESIS; 3T3 CELLS; INSULIN; PHOSPHOFRUCTOKINASE; STARVATION AB Several diverse metabolic events become compromised when mammalian cells are made deficient in essential amino acids or when charging of their tRNA is blocked by amino acid analogs. This rapid general demise of cell function can be due to inhibition of phosphofructokinase (PFK) by uncharged tRNA. It has now been demonstrated that when tRNA is added to PFK in an assay dependent upon the reassociation of inactive, dissociated enzyme subunits, nanomolar concentrations cause complete inhibition. The model for control suggests that charged tRNA becomes associated with EF-1, which is specific for aminoacyl-tRNAs and is present in sufficiently high concentrations in cells to sequester the charged forms from an inhibitory role. Support for this model include: (1) the rapid onset of inhibition of glycolysis and glucose uptake upon amino acid deficiency; (2) the unique role of the product of PFK activity, fructose-1,6-diphosphate, in reactions of peptide chain initiation, particularly its role as a co-factor for purified eIF-2B, the GDP/GTP exchange factor; (3) the correlations of this interaction with the cellular and molecular lesions of insulin insufficiency; (4) the recognition that the anomalous role of high concentrations of cAMP as a stimulant of peptide chain initiation in energy depleted or gel-filtered cell lysates correlates with its stimulatory action on PFK as an analog for the positive effector, adenosine-5'-monophosphate; and (5) the role of fructose-1,6-diphosphate in the formation of glyceraldehyde-3-phosphate, a substrate for synthesis of ribose-5-phosphate via the non-oxidative portion of the pentose phosphate pathway, which, as a precursor of phosphoribosylpyrophosphate, is essential for nucleic acid synthesis. RP RABINOVITZ, M (reprint author), NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,PROGRAM DEV THERAPEUT,BETHESDA,MD 20892, USA. NR 33 TC 19 Z9 19 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAY 11 PY 1992 VL 302 IS 2 BP 113 EP 116 DI 10.1016/0014-5793(92)80418-G PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA HU897 UT WOS:A1992HU89700003 PM 1321723 ER PT J AU GHOSH, D AF GHOSH, D TI TFD - THE TRANSCRIPTION FACTORS DATABASE SO NUCLEIC ACIDS RESEARCH LA English DT Article RP GHOSH, D (reprint author), NATL CTR BIOTECHNOL INFORMAT,NLM,BETHESDA,MD 20894, USA. NR 6 TC 79 Z9 80 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAY 11 PY 1992 VL 20 SU S BP 2091 EP 2093 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HY931 UT WOS:A1992HY93100009 PM 1598237 ER PT J AU LEWIN, NE DELLAQUILA, ML PETTIT, GR BLUMBERG, PM WARREN, BS AF LEWIN, NE DELLAQUILA, ML PETTIT, GR BLUMBERG, PM WARREN, BS TI BINDING OF [H-3] BRYOSTATIN-4 TO PROTEIN-KINASE-C SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID PHORBOL ESTER BINDING; MOUSE EPIDERMAL-CELLS; TUMOR PROMOTERS; RAT-BRAIN; ACRIDINE; TUMORIGENICITY; DERIVATIVES AB The present study describes the synthesis and configurational assignment of four enantiomerically pure, bay-region 10,11-diol 8,9-epoxide diastereomers 14-17 of dibenz[a,h]acridine (1) from the corresponding optically pure trans-10,11-dihydroxy-10,11-dihydrodibenz[a,h]acridine enantiomers 6 and 7. Racemic trans-10,11-di-hydroxy-10, 11-dihydrodibenz[a,h]acridine (3) was resolved via its conversion to the diastereomeric bis((-)-methyloxy) esters, separation of the diastereomers by short bed/continuous developing preparative TLC, and finally saponification of the individual diastereomers. Assignment of (10R,11R)-absolute configuration to (-)-trans-10,11-dihydroxy-10,11-dihydrodibenz[a,h]acridine (6) was achieved through the application of exciton circular dichroism technique to the bis[p-(dimethylamino)cinnamic] ester 13 of its tetrahydro analogue 11. C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RP KUMAR, S (reprint author), SUNY COLL BUFFALO,CTR ENVIRONM RES & EDUC,DIV ENVIRONM TOXICOL & CHEM,BUFFALO,NY 14222, USA. NR 30 TC 8 Z9 8 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD MAY 8 PY 1992 VL 57 IS 10 BP 2784 EP 2787 DI 10.1021/jo00036a006 PG 4 WC Chemistry, Organic SC Chemistry GA HT853 UT WOS:A1992HT85300006 ER PT J AU GUSTAFSON, KR CARDELLINA, JH MCMAHON, JB PANNELL, LK CRAGG, GM BOYD, MR AF GUSTAFSON, KR CARDELLINA, JH MCMAHON, JB PANNELL, LK CRAGG, GM BOYD, MR TI HIV INHIBITORY NATURAL-PRODUCTS .6. THE PELTATOLS, NOVEL HIV-INHIBITORY CATECHOL DERIVATIVES FROM POTHOMORPHE-PELTATA SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Article ID RECEPTOR AB Three new prenylated catechol dimers have been isolated from the tropical shrub Pothomorphe peltata (Piperaceae). The structures of peltatol A (1), peltatol B (2), and peltatol C (3) were determined by extensive spectroscopic analyses. Peltatols A-C inhibited HIV-1 induced cell killing at subcytotoxic concentrations of 1-10-mu-g/mL. The monomeric catechol derivative 4-nerolidyleatechol (4) was active in a phorbol receptor binding assay (IC50 = 35-mu-g/mL) but inactive against HIV. The diphenyl ethers, peltatols B (2) and C (3), were interconvertible in solution (MeOH, DMSO) at room temperature. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES & DEV LAB,BLDG 1052,ROOM 121,FREDERICK,MD 21702. NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 7 TC 39 Z9 44 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD MAY 8 PY 1992 VL 57 IS 10 BP 2809 EP 2811 DI 10.1021/jo00036a010 PG 3 WC Chemistry, Organic SC Chemistry GA HT853 UT WOS:A1992HT85300010 ER PT J AU ANDERSON, WF AF ANDERSON, WF TI HUMAN GENE-THERAPY SO SCIENCE LA English DT Article ID TUMOR-INFILTRATING LYMPHOCYTES; METASTATIC MELANOMA; ETHICAL ISSUES; STEM-CELLS; RETROVIRUS; EXPRESSION; INTERLEUKIN-2; IMMUNOTHERAPY; TRANSDUCTION; PRECURSORS AB Human gene therapy is a procedure that is being used in an attempt to treat genetic and other diseases. Eleven clinical protocols are under way at the present time, each with scientific and clinical objectives. Human genetic engineering raises unique safety, social, and ethical concerns. RP ANDERSON, WF (reprint author), NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892, USA. NR 91 TC 712 Z9 736 U1 3 U2 59 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAY 8 PY 1992 VL 256 IS 5058 BP 808 EP 813 DI 10.1126/science.1589762 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HT235 UT WOS:A1992HT23500035 PM 1589762 ER PT J AU BRECHBIEL, MW GANSOW, OA AF BRECHBIEL, MW GANSOW, OA TI SYNTHESIS OF C-FUNCTIONALIZED TRANS-CYCLOHEXYLDIETHYLENETRIAMINEPENTA-ACETIC ACIDS FOR LABELING OF MONOCLONAL-ANTIBODIES WITH THE BISMUTH-212 ALPHA-PARTICLE EMITTER SO JOURNAL OF THE CHEMICAL SOCIETY-PERKIN TRANSACTIONS 1 LA English DT Article ID RADIOIMMUNOTHERAPY; COMPLEXES AB Several C-functionalized cyclohexyldiethylenetriaminepenta-acetic acid derivatives have been prepared from (+/-)-4-nitrophenylalanine and (+/-)-trans-cyclohexane-1,2-diamine to produce two sets of diastereoisomeric enantiomers. A modification of this synthesis has been employed to prepare a single enantiomer in order to define the absolute configurations of the products. RP BRECHBIEL, MW (reprint author), NCI,RADIAT ONCOL BRANCH,INORGAN & RADIOIMMUNE CHEM SECT,BLDG 10,ROOM B3B69,BETHESDA,MD 20892, USA. NR 29 TC 52 Z9 53 U1 0 U2 0 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON ROAD, CAMBRIDGE, CAMBS, ENGLAND CB4 4WF SN 0300-922X J9 J CHEM SOC PERK T 1 JI J. Chem. Soc.-Perkin Trans. 1 PD MAY 7 PY 1992 IS 9 BP 1173 EP 1178 DI 10.1039/p19920001173 PG 6 WC Chemistry, Organic SC Chemistry GA HT706 UT WOS:A1992HT70600016 ER PT J AU FLATEN, TP GARRUTO, RM AF FLATEN, TP GARRUTO, RM TI POLYNUCLEAR IONS IN ALUMINUM TOXICITY SO JOURNAL OF THEORETICAL BIOLOGY LA English DT Letter ID INVITRO C1 NIH,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. RI Flaten, Trond Peder/I-3756-2013 NR 13 TC 22 Z9 23 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-5193 J9 J THEOR BIOL JI J. Theor. Biol. PD MAY 7 PY 1992 VL 156 IS 1 BP 129 EP 132 DI 10.1016/S0022-5193(05)80660-5 PG 4 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA HU549 UT WOS:A1992HU54900007 PM 1640718 ER PT J AU PAUL, WE AF PAUL, WE TI CYTOKINES - POKING HOLES IN THE NETWORK SO NATURE LA English DT Editorial Material ID STIMULATORY FACTOR-I RP PAUL, WE (reprint author), NIAID,IMMUNOL LAB,BETHESDA,MD 20892, USA. NR 10 TC 5 Z9 5 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAY 7 PY 1992 VL 357 IS 6373 BP 16 EP 17 DI 10.1038/357016a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HT229 UT WOS:A1992HT22900027 PM 1349426 ER PT J AU ARNOLD, E JACOBOMOLINA, A NANNI, RG WILLIAMS, RL LU, XD DING, JP CLARK, AD ZHANG, AQ FERRIS, AL CLARK, P HIZI, A HUGHES, SH AF ARNOLD, E JACOBOMOLINA, A NANNI, RG WILLIAMS, RL LU, XD DING, JP CLARK, AD ZHANG, AQ FERRIS, AL CLARK, P HIZI, A HUGHES, SH TI STRUCTURE OF HIV-1 REVERSE-TRANSCRIPTASE DNA COMPLEX AT 7-A RESOLUTION SHOWING ACTIVE-SITE LOCATIONS SO NATURE LA English DT Article ID NUCLEOTIDE-SEQUENCE; AIDS VIRUS; REPLICATION; INHIBITION AB AIDS, caused by human immunodeficiency virus (HIV), is one of the world's most serious health problems, with current protocols being inadequate for either prevention or successful long-term treatment. In retroviruses such as HIV, the enzyme reverse transcriptase copies the single-stranded RNA genome into double-stranded DNA that is then integrated into the chromosomes of infected cells. Reverse transcriptase is the target of the most widely used treatments for AIDS, 3'-azido-3'-deoxythymidine (AZT) and 2',3'-dideoxyinosine (ddI), but resistant strains of HIV-1 arise in patients after a relatively short time 1,2. There are several non-nucleoside inhibitors of HIV-1 reverse transcriptase 3-6, but resistance to such agents also develops rapidly 7. We report here the structure at 7 angstrom resolution of a ternary complex of the HIV-1 reverse transcriptase heterodimer, a monoclonal antibody Fab fragment 8, and a duplex DNA template-primer. The double-stranded DNA binds in a groove on the surface of the enzyme. The electron density near one end of the DNA matches well with the known structure of the HIV-1 reverse transcriptase RNase H domain 12. At the opposite end of the DNA, a mercurated derivative of UTP has been localized by difference Fourier methods, allowing tentative identification of the polymerase nucleoside triphosphate binding site. We also determined the structure of the reverse transcriptase/Fab complex in the absence of template-primer to compare the bound and free forms of the enzyme. The presence of DNA correlates with movement of protein electron density in the vicinity of the putative template-primer binding groove. These results have important implications for developing improved inhibitors of reverse transcriptase for the treatment of AIDS. C1 RUTGERS STATE UNIV,DEPT CHEM,PISCATAWAY,NJ 08854. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. PROGRAM RESOURCES INC,FREDERICK,MD 21702. TEL AVIV UNIV,SACKLER SCH MED,DEPT CELL BIOL & HISTOL,IL-69978 TEL AVIV,ISRAEL. RP ARNOLD, E (reprint author), CTR ADV BIOTECHNOL & MED,679 HOES LANE,PISCATAWAY,NJ 08854, USA. NR 22 TC 170 Z9 174 U1 0 U2 2 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAY 7 PY 1992 VL 357 IS 6373 BP 85 EP 89 DI 10.1038/357085a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HT229 UT WOS:A1992HT22900065 PM 1374166 ER PT J AU MAX, MB LYNCH, SA MUIR, J SHOAF, SE SMOLLER, B DUBNER, R AF MAX, MB LYNCH, SA MUIR, J SHOAF, SE SMOLLER, B DUBNER, R TI EFFECTS OF DESIPRAMINE, AMITRIPTYLINE, AND FLUOXETINE ON PAIN IN DIABETIC NEUROPATHY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID RELIEVES POSTHERPETIC NEURALGIA; DOUBLE-BLIND CROSSOVER; TOOTH-PULP SENSATIONS; RATIO SCALES; ANTIDEPRESSANTS; PHARMACOKINETICS; DESCRIPTORS; MECHANISMS; RECEPTORS; ANALGESIA AB Background. Amitriptyline reduces the pain caused by peripheral-nerve disease, but treatment is often limited by side effects related to the drug's many pharmacologic actions. Selective agents might be safer and more effective. Methods. We carried out two randomized, double-blind, crossover studies in patients with painful diabetic neuropathy, comparing amitriptyline with the relatively selective blocker of norepinephrine reuptake desipramine in 38 patients, and comparing the selective blocker of serotonin reuptake fluoxetine with placebo in 46 patients. Fifty-seven patients were randomly assigned to a study as well as to the order of treatment, permitting comparison among all three drugs and placebo as the first treatment. The patients rated the degree of pain present each day using verbal descriptors, and they also assessed the extent of pain relief globally at the end of each treatment period. Results. After individual dose titration, the mean daily doses of the drugs were as follows: amitriptyline, 105 mg; desipramine, 111 mg; and fluoxetine, 40 mg. There was moderate or greater relief of pain in 28 of the 38 patients (74 percent) who received amitriptyline, 23 of the 38 patients (61 percent) who received desipramine, 22 of the 46 patients (48 percent) who received fluoxetine, and 19 of the 46 patients (41 percent) who received placebo. The differences in responses between amitriptyline and desipramine and between fluoxetine and placebo were not statistically significant, but both amitriptyline and desipramine were superior to placebo. Amitriptyline and desipramine were as effective in patients who were not depressed as in depressed patients, but fluoxetine was effective only in depressed patients. Conclusions. Desipramine relieves pain caused by diabetic neuropathy with efficacy similar to that of amitriptyline, offering an alternative for patients unable to tolerate the latter. Blockade of norepinephrine reuptake is likely to mediate the analgesic effect of these antidepressant drugs in diabetic neuropathy. Fluoxetine, which blocks serotonin uptake, is no more effective than placebo for the relief of pain. C1 NIAAA,CTR CLIN,DEPT NURSING,BETHESDA,MD. NIAAA,CLIN STUDIES LAB,BETHESDA,MD. RP MAX, MB (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,PAIN RES CLIN,BLDG 10,RM 3C-405,BETHESDA,MD 20892, USA. NR 42 TC 712 Z9 726 U1 7 U2 26 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 7 PY 1992 VL 326 IS 19 BP 1250 EP 1256 DI 10.1056/NEJM199205073261904 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA HR447 UT WOS:A1992HR44700004 PM 1560801 ER PT J AU PIERCE, JP ANDERSON, DM ROMANO, RM MEISSNER, HI ODENKIRCHEN, JC AF PIERCE, JP ANDERSON, DM ROMANO, RM MEISSNER, HI ODENKIRCHEN, JC TI PROMOTING SMOKING CESSATION IN THE UNITED-STATES - EFFECT OF PUBLIC-SERVICE ANNOUNCEMENTS ON THE CANCER-INFORMATION-SERVICE TELEPHONE LINE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID CIGARETTE-SMOKING; QUIT SMOKING; TRENDS; CAMPAIGN AB Background: Although many smokers report making attempts to quit, few seek help or are successful in their attempts. Some of the barriers to seeking help can be overcome by a telephone counseling and information service like that offered by the Cancer Information Service of the National Cancer Institute. This service has been promoted by antismoking public service announcements produced by the Office on Smoking and Health, Centers for Disease Control, Public Health Service, U.S. Department of Health and Human Services. Purpose: We determined whether such nationally televised public service announcements were associated with increased use of the Cancer Information Service. We assessed the importance of specifically promoting the telephone line and identified the characteristics of the individuals who responded to such promotion. Methods: We combined the frequency-of-call data from the Cancer Information Service with the data on the frequency and reach of the television spots. Results: During this 5-year study (1983-1987), the Cancer Information Service received a notably disproportionate number of calls in 3 specific months (August 1983, January 1985, and January 1987). In each case, more than 20% of all calls in that year were received in that month (expected percentage = 8% if the calls had been evenly distributed). These peak periods were associated with the showing of the three public service announcements that mentioned the telephone number of the Cancer Information Service. These promotions were particularly effective in increasing the percentage of callers who were male, who were under the age of 40 years, or who had received a high school education or less. Conclusions: Television is an effective medium for supporting antismoking goals by motivating more smokers to seek help to quit. Implications: It is important to identify whether the aid offered by the Cancer Information Service hotline is effective in helping the caller to quit. Future work must concentrate on the most effective strategies for using this initial contact to provide aid to prevent relapse, thus maximizing the potential impact of the public service announcement campaigns. C1 NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. CTR DIS CONTROL,CTR CHRON DIS PREVENT & HLTH PROMOT,OFF SMOKING & HLTH,ATLANTA,GA 30333. UNIV CALIF SAN DIEGO,CTR CANC,LA JOLLA,CA 92093. NR 23 TC 43 Z9 43 U1 0 U2 1 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAY 6 PY 1992 VL 84 IS 9 BP 677 EP 683 DI 10.1093/jnci/84.9.677 PG 7 WC Oncology SC Oncology GA HR763 UT WOS:A1992HR76300013 PM 1569601 ER PT J AU HERZOG, CE TREPEL, JB MICKLEY, LA BATES, SE FOJO, AT AF HERZOG, CE TREPEL, JB MICKLEY, LA BATES, SE FOJO, AT TI VARIOUS METHODS OF ANALYSIS OF MDR-1/P-GLYCOPROTEIN IN HUMAN COLON CANCER CELL-LINES SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID MULTIDRUG-RESISTANCE GENE; P-GLYCOPROTEIN EXPRESSION; MULTIPLE-DRUG RESISTANCE; BREAST-CANCER; TUMOR-CELLS; VINCRISTINE; LEUKEMIA; INVITRO; TISSUES AB Background: Multidrug resistance (MDR) mediated by high levels of mdr-l (also known as PGY1)/P-glycoprotein (Pgp) has been studied in tissue culture systems; however, most tumor samples which express mdr-l/Pgp have much lower levels. Purpose: We wanted to determine if levels seen clinically could be detected by commonly used methods and to determine if these levels conferred MDR reversible by Pgp antagonists. Methods: We studied multidrug-resistant cell lines and sublines with levels of mdr-l/Pgp expression comparable to those seen clinically. We evaluated the expression of mdr-l RNA by Northern blot analysis, slot blot analysis, polymerase chain reaction (PCR) analysis, and in situ hybridization. We evaluated protein expression by immunofluorescence, immunohistochemistry, fluorescence-activated cell sorting, and immunoblotting analyses. Drug resistance and reversibility were determined by cell growth during continuous drug exposure. Results: In most cases, the low level of mdr-l/Pgp present in these cell lines could be detected by each method, but the assays were at the limit of sensitivity for all methods except the PCR method. These low levels of mdr-l/Pgp are capable of conferring MDR, which can be antagonized by verapamil. Conclusions: Levels of mdr-l/Pgp similar to those found in clinical samples can be detected by each of these methods, but the PCR method was the most sensitive and most reliably quantitative. Implications: In vitro sensitization by the addition of verapamil in cell lines with these low levels of mdr-l/Pgp suggests that clinically detected levels may confer drug resistance in vivo. C1 NCI,DIV CANC TREATMENT,MED BRANCH,BETHESDA,MD 20892. RP HERZOG, CE (reprint author), NCI,DIV CANC TREATMENT,PEDIAT BRANCH,BLDG 10,RM 13N240,BETHESDA,MD 20892, USA. NR 21 TC 98 Z9 98 U1 1 U2 3 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAY 6 PY 1992 VL 84 IS 9 BP 711 EP 716 DI 10.1093/jnci/84.9.711 PG 6 WC Oncology SC Oncology GA HR763 UT WOS:A1992HR76300020 PM 1349044 ER PT J AU POWERS, R GARRETT, DS MARCH, CJ FRIEDEN, EA GRONENBORN, AM CLORE, GM AF POWERS, R GARRETT, DS MARCH, CJ FRIEDEN, EA GRONENBORN, AM CLORE, GM TI H-1, N-15, C-13 AND (CO)-C-13 ASSIGNMENTS OF HUMAN INTERLEUKIN-4 USING 3-DIMENSIONAL DOUBLE-RESONANCE AND TRIPLE-RESONANCE HETERONUCLEAR MAGNETIC-RESONANCE SPECTROSCOPY SO BIOCHEMISTRY LA English DT Article ID NMR-SPECTROSCOPY; PRACTICAL ASPECTS; LARGER PROTEINS; SPECTRA; PURIFICATION; EXPRESSION; PHASE; YEAST; 2D AB The assignment of the H-1, N-15, (CO)-C-13, and C-13 resonances of recombinant human interleukin-4 (IL-4), a protein of 133 residues and molecular mass of 15.4 kDa, is presented based on a series of 11 three-dimensional (3D) double- and triple-resonance heteronuclear NMR experiments. These studies employ uniformly labeled N-15- and N-15/C-13-labeled IL-4 with an isotope incorporation of > 95% for the protein expressed in yeast. Five independent sequential connectivity pathways via one-, two-, and three-bond heteronuclear J couplings are exploited to obtain unambiguous sequential assignments. Specifically, CO(i)-N(i + 1),NH(i + 1) correlations are observed in the HNCO experiment, the C(alpha)H(i),C(alpha)(i)-N(i + 1) correlations in the HCA(CO)N experiment, the C(alpha)(i)-N(i + 1),NH(i + 1) correlations in the HNCA and HN(CO)CA experiments, the C(alpha)H(i)-N(i + 1),NH(i + 1) correlations in the H(CA)NH and HN(CO)HB experiments, and the C(beta)H(i)-N(i + 1),NH(i + 1) correlations in the HN(CO)HB experiments. The backbone intraresidue C(alpha)H(i)-N-15(i)-NH(i) correlations are provided by the N-15-edited Hartmann-Hahn (HOHAHA) and H(CA)NH experiments, the C(beta)H(i)-N-15(i)-NH(i) correlations by the N-15-edited HOHAHA and HNHB experiments, the C-13-(alpha)(i)-N-15(i)-NH(i) correlations by the HNCA experiment, and the C(alpha)H(i)-C-13(alpha)(i)-(CO)-C-13(i) correlations by the HCACO experiment. Aliphatic side-chain spin systems are assigned by 3D H-1-C-13-C-13-H-1 correlated (HCCH-COSY) and total correlated (HCCH-TOCSY) spectroscopy. Because of the high resolution afforded by these experiments, as well as the availability of multiple sequential connectivity pathways, ambiguities associated with the limited chemical shift dispersion associated with helical proteins are readily resolved. Further, in the majority of cases (88%), four or more sequential correlations are observed between successive residues. Consequently, the interpretation of these experiments readily lends itself to semiautomated analysis which significantly simplifies and speeds up the assignment process. The assignments presented in this paper provide the essential basis for studies aimed at determining the high-resolution three-dimensional structure of IL-4 in solution. C1 NIDDKD,CHEM PHYS LAB,BLDG 2,BETHESDA,MD 20892. IMMUNEX CORP,SEATTLE,WA 98101. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 59 TC 51 Z9 52 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAY 5 PY 1992 VL 31 IS 17 BP 4334 EP 4346 DI 10.1021/bi00132a026 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR856 UT WOS:A1992HR85600026 PM 1567880 ER PT J AU GARRETT, DS POWERS, R MARCH, CJ FRIEDEN, EA CLORE, GM GRONENBORN, AM AF GARRETT, DS POWERS, R MARCH, CJ FRIEDEN, EA CLORE, GM GRONENBORN, AM TI DETERMINATION OF THE SECONDARY STRUCTURE AND FOLDING TOPOLOGY OF HUMAN INTERLEUKIN-4 USING 3-DIMENSIONAL HETERONUCLEAR MAGNETIC-RESONANCE SPECTROSCOPY SO BIOCHEMISTRY LA English DT Article ID NOESY-HMQC SPECTROSCOPY; COUPLING-CONSTANTS; NMR-SPECTROSCOPY; C-13-LABELED PROTEIN; CONFORMATION; ASSIGNMENT; SPECTRA AB The secondary structure of human recombinant interleukin-4 (IL-4) has been investigated by three-dimensional (3D) N-15- and C-13-edited nuclear Overhauser (NOE) spectroscopy on the basis of the H-1, N-15, and C-13 assignments presented in the preceding paper [Powers, R., Garrett, D. S., March, C. J., Frieden, E. A., Gronenborn, A. M., & Clore, G. M. (1992) Biochemistry (preceding paper in this issue)]. Based on the NOE data involving the NH, C(alpha)H, and C(beta)H protons, as well as 3J(HN-alpha) coupling constant, amide exchange, and C-13(alpha) and C-13(beta) secondary chemical shift data, it is shown that IL-4 consists of four long helices (residues 9-21, 45-64, 74-96, and 113-129), two small helical turns (residues 27-29 and 67-70), and a mini antiparallel beta-sheet (residues 32-34 and 110-112). In addition, the topological arrangement of the helices and the global fold could be readily deduced from a number of long-range interhelical NOEs identified in the 3D C-13-edited NOE spectrum in combination with the spatial restrictions imposed by three disulfide bridges. These data indicate that the helices of interleukin-4 are arranged in a left-handed four-helix bundle with two overhand connections. C1 NIDDKD,CHEM PHYS LAB,BLDG 2,BETHESDA,MD 20892. IMMUNEX CORP,SEATTLE,WA 98101. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 38 TC 24 Z9 25 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAY 5 PY 1992 VL 31 IS 17 BP 4347 EP 4353 DI 10.1021/bi00132a027 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR856 UT WOS:A1992HR85600027 PM 1567881 ER PT J AU KINDT, JT WOODS, A MARTIN, BM COTTER, RJ OSAWA, Y AF KINDT, JT WOODS, A MARTIN, BM COTTER, RJ OSAWA, Y TI COVALENT ALTERATION OF THE PROSTHETIC HEME OF HUMAN HEMOGLOBIN BY BRCCL3 - CROSS-LINKING OF HEME TO CYSTEINE RESIDUE-93 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ADDUCT FORMATION; BINDING; BENZOPYRENE; DENATURATION; RESOLUTION; MECHANISM; MYOGLOBIN; PROTEIN; MOUSE; RATS AB Recent studies have shown that a protein-bound heme adduct formed from the reaction of BrCCl3 with myoglobin was due to bonding of the proximal histidine residue through the ring I vinyl of a heme-CCl2 moiety. The present study reveals that BrCCl3 also reacts with the heme of reduced human hemoglobin to form two protein-bound heme adducts. Edman degradation and mass spectrometry provided evidence that these protein-bound heme adducts were addition products in which heme-CCl2 or heme-CCl3 were bound to cysteine residue 93 of the beta-chain of hemoglobin. It appeared that the cysteine residue was bonded regiospecifically to the ring I vinyl group of the altered heme moiety, because the nonprotein-bound products of the reaction included the beta-carboxyvinyl and alpha-hydroxy-beta-trichloromethylethyl derivatives of the ring I vinyl moiety of heme. The absorption spectra of the protein-bound adducts in both the oxidized and reduced states were highly similar to those described for hemichromes, which are thought to be involved in the formation of Heinz bodies and subsequent red cell lysis. C1 NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,MIDDLE ATLANTIC MASS SPECTROMETRY LAB,BALTIMORE,MD 21205. NR 36 TC 29 Z9 29 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 5 PY 1992 VL 267 IS 13 BP 8739 EP 8743 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR854 UT WOS:A1992HR85400008 PM 1577716 ER PT J AU MINNITI, CP KOHN, EC GRUBB, JH SLY, WS OH, Y MULLER, HL ROSENFELD, RG HELMAN, LJ AF MINNITI, CP KOHN, EC GRUBB, JH SLY, WS OH, Y MULLER, HL ROSENFELD, RG HELMAN, LJ TI THE INSULIN-LIKE GROWTH FACTOR-II (IGF-II) MANNOSE 6-PHOSPHATE RECEPTOR MEDIATES IGF-II-INDUCED MOTILITY IN HUMAN RHABDOMYOSARCOMA CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN-MELANOMA CELLS; AUTOCRINE GROWTH; TUMOR CELLS; CLONING; BINDING; PROTEIN; HETEROGENEITY; EXPRESSION; AFFINITY; SEQUENCE AB Insulin-like growth factor-II (IGF-II) is an autocrine growth and motility factor for human rhabdomyosarcoma. It interacts with three different receptors: the IGF-I, the IGF-II, and the insulin receptor. A specific function of the IGF-II receptor in mediating IGF-II responses has not been defined. In this report we investigate the mechanism of IGF-II-mediated motility in rhabdomyosarcoma cells. We demonstrate that IGF-II and [Leu27]IGF-II, an analog selective for the IGF-II receptor, stimulate motility at concentrations in which they interact only with their own receptor. An antibody that blocks the IGF-I receptor does not inhibit either peptide activity, while an antibody specific for the IGF-II receptor suppresses the IGF-II-induced motility. This antibody does not interfere with rhabdomyosarcoma cell proliferation. We conclude that in rhabdomyosarcoma cells IGF-II stimulates two different responses mediated by distinct receptors: 1) a mitogenic response through the type I receptor and 2) a motility response through the type II receptor. C1 ST LOUIS UNIV,SCH MED,DEPT BIOCHEM,ST LOUIS,MO 63104. STANFORD UNIV,MED CTR,STANFORD,CA 94305. RP MINNITI, CP (reprint author), NCI,PEDIAT BRANCH,MOLEC GENET SECT,BLDG 10,RM 13N240,BETHESDA,MD 20892, USA. NR 41 TC 112 Z9 115 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 5 PY 1992 VL 267 IS 13 BP 9000 EP 9004 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR854 UT WOS:A1992HR85400047 PM 1315746 ER PT J AU LEE, CM HAUN, RS TSAI, SC MOSS, J VAUGHAN, M AF LEE, CM HAUN, RS TSAI, SC MOSS, J VAUGHAN, M TI CHARACTERIZATION OF THE HUMAN GENE ENCODING ADP-RIBOSYLATION FACTOR-I, A GUANINE NUCLEOTIDE-BINDING ACTIVATOR OF CHOLERA-TOXIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MESSENGER-RNA; TRANSCRIPTION FACTOR; PROTEIN; PROMOTER; SEQUENCE; ACID; MATURATION; POLY(A); SUBUNIT; SITE AB Mammalian ADP-ribosylation factors (ARFs), approximately 20-kDa guanine nucleotide-binding proteins that stimulate cholera toxin ADP-ribosyltransferase activity, were grouped into three classes based on deduced amino acid sequence. Human ARF 1, a class I ARF, is identical with its bovine counterpart, has a distinctive pattern of tissue and developmental expression, and is encoded by a approximately 1.9-kilobase mRNA. ARF 1 cDNAs were isolated from a human fibroblast cDNA library; one arose via an alternative polyadenylation signal (AA-TACA) 84 nucleotides 5' to the polyadenylation signal (AATAAA) used in the 1815-base pair cDNA. The polyadenylation signals, their respective locations, and the surrounding nucleotide sequences are conserved in human and rat. The human ARF 1 gene, with four introns, spans approximately 16.5 kilobases. Exon 1 (46 base pairs) contains only untranslated sequence. Translation initiates in exon 2, which encodes the sequence GXXXXGK involved in phosphate binding (GTP hydrolysis). The sequence DVGG is encoded in exon 3, and NKQD, which is involved in the interaction with the guanine ring, is interrupted following the codon for Q by intron 4. The carboxyl-terminal 53 amino acids and > 1110 base pairs of 3'-untranslated region are encoded in exon 5. Primer extension and mung bean and S1 nuclease mapping indicated multiple transcription initiation sites and were consistent with Northern analyses. The 5'-flanking region has a high GC content but no TATA or CAAT box, as found in housekeeping genes. In addition, the two human class I ARF genes, ARF 1 and ARF 3, have similar exon/intron organizations and use GC-rich promoters. RP LEE, CM (reprint author), NHLBI,CELLULAR METAB LAB,RM 5N307,BLDG 10,BETHESDA,MD 20892, USA. OI LEE, CHII-MING/0000-0002-1075-5787 NR 36 TC 41 Z9 42 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 5 PY 1992 VL 267 IS 13 BP 9028 EP 9034 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR854 UT WOS:A1992HR85400051 PM 1577740 ER PT J AU OLSON, D POLLANEN, J HOYERHANSEN, G RONNE, E SAKAGUCHI, K WUN, TC APPELLA, E DANO, K BLASI, F AF OLSON, D POLLANEN, J HOYERHANSEN, G RONNE, E SAKAGUCHI, K WUN, TC APPELLA, E DANO, K BLASI, F TI INTERNALIZATION OF THE UROKINASE-PLASMINOGEN ACTIVATOR INHIBITOR TYPE-1 COMPLEX IS MEDIATED BY THE UROKINASE RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID EXTRACELLULAR-MATRIX DEGRADATION; BOUND UROKINASE; CELL-SURFACE; U937 MONOCYTES; PRO-UROKINASE; SARCOMA-CELLS; BINDING; PROUROKINASE; SYSTEM; PURIFICATION AB The role of the urokinase receptor (uPAR) in the internalization of the urokinase-plasminogen activator inhibitor type-1 (uPA.PAI-1) complex has been investigated. First, exploiting the species specificity of uPA binding, we show that mouse LB6 cells (that express a mouse uPAR) were unable to bind or degrade the human uPA.PAI-1 complex. On the other hand, LB6 clone 19 cells, which express a transfected human uPAR, degraded uPA.PAI-1 complexes with kinetics identical to the human monocytic U937 cells. We also show by immunofluorescence experiments with anti-uPA antibodies that in LB6 clone 19 cells, the uPA.PAI-1 complex is indeed internalized. While at 4-degrees-C uPA fluorescence was visible at the cell surface, shift of the temperature to 37-degrees-C caused a displacement of the immunoreactivity to the cytoplasmic compartment, with a pattern indicating lysosomal localization. If uPA.PAI-1 internalization/degradation is mediated by uPAR, inhibition of uPA.PAI-1 binding to uPAR should block degradation. Three different treatments, competition with the agonist amino-terminal fragment of uPA, treatment with a monoclonal antibody directed toward the binding domain of uPAR or release of uPAR from the cell surface with phosphatidylinositol-specific phospholipase C completely prevented uPA.PAI-1 degradation. The possibility that a serpin-enzyme complex receptor might be primarily or secondarily involved in the internalization process was excluded since a serpin-enzyme complex peptide failed to inhibit uPA.PAI-1 binding and degradation. Similarly, complexes of PAI-1 with low molecular mass uPA (33 kDa uPA), which lacks the uPAR binding domain, were neither bound nor degraded. Finally we also show that treatment of cells with uPA.PAI-1 complex caused a specific but partial down-regulation of uPAR. A similar result was obtained when PAI-1 was allowed to complex to uPA that had been previously bound to the receptor. The possibility therefore exists that the entire complex uPA.PAI-1-uPAR is internalized. All these data allow us to conclude that internalization of the uPA.PAI-1 complex is mediated by uPAR. C1 UNIV COPENHAGEN,INST MICROBIOL,OSTER FARIMAGSGADE 2A,DK-1353 COPENHAGEN,DENMARK. MONSANTO CO,CHESTERFIELD,MO 63198. FINSEN INST,DK-2100 COPENHAGEN,DENMARK. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 38 TC 162 Z9 165 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 5 PY 1992 VL 267 IS 13 BP 9129 EP 9133 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR854 UT WOS:A1992HR85400066 PM 1315748 ER PT J AU TAMURA, JK BATES, AD GELLERT, M AF TAMURA, JK BATES, AD GELLERT, M TI SLOW INTERACTION OF 5'-ADENYLYL-BETA,GAMMA-IMIDODIPHOSPHATE WITH ESCHERICHIA-COLI DNA GYRASE - EVIDENCE FOR COOPERATIVITY IN NUCLEOTIDE BINDING SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID P-N-P; ADENOSINE-TRIPHOSPHATE; ATPASE ACTIVITY; NALIDIXIC-ACID; FREE-ENERGY; BASE-PAIRS; A-PROTEIN; TOPOISOMERASES; SUBUNIT; SITE AB We have examined the kinetics of interaction between Escherichia coli DNA gyrase and the nonhydrolyzable ATP analog 5'-adenylyl-beta, gamma-imidodiphosphate (ADPNP) in the presence and absence of ATP. In the absence of ATP, [alpha-P-32]ADPNP binds extremely slowly to gyrase, with an apparent second-order rate constant (k1) of 120 M-1 min-1. Similarly, the limited negative supercoiling of closed-circular DNA caused by ADPNP binding is slow, requiring at least 2 h to reach completion in the presence of 100-mu-M ADPNP. A very slow but detectable rate of dissociation of ADPNP from gyrase was measured, with a rate constant of 3.5 x 10(-4) min-1. The calculated dissociation constant for ADPNP is thus 2.9-mu-M. ADPNP is a potent competitive inhibitor of ATP-dependent DNA supercoiling. Inhibition is established much more rapidly than can be accounted for by the slow rate of ADPNP binding in the absence of ATP. We have found that ATP can accelerate the rate of [P-32]ADPNP binding by more than 15-fold (k1 = 1,850 M-1 min-1). The ATP-promoted rate enhancement requires the presence of DNA; in the absence of DNA, ATP has no effect on the rate of binding. Relaxed closed-circular, nicked-circular, and linear pBR322 DNA are all equally effective cofactors for ATP-stimulated binding of ADPNP. After a short lag, the presence of ATP also greatly speeds up ADPNP dissociation from gyrase bound initially to closed-circular DNA, with the restoration of DNA supercoiling activity. This effect is not observed in the presence of nicked-circular or linear DNA, suggesting that ADPNP dissociates more rapidly from gyrase bound to supercoiled DNA. The results of ADPNP binding provide evidence for cooperative interactions between the nucleotide binding sites. To account for these data, a model is proposed for the interaction of nucleotides at the two ATP binding sites on DNA gyrase. RP TAMURA, JK (reprint author), NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 47 TC 44 Z9 44 U1 2 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 5 PY 1992 VL 267 IS 13 BP 9214 EP 9222 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR854 UT WOS:A1992HR85400078 PM 1315750 ER PT J AU ZORETIC, PA WENG, XY BIGGERS, CK BIGGERS, MS CASPAR, ML DAVIS, DG AF ZORETIC, PA WENG, XY BIGGERS, CK BIGGERS, MS CASPAR, ML DAVIS, DG TI MANGANESE(III)-PROMOTED OXIDATIVE FREE-RADICAL CYCLIZATIONS OF BETA-KETO IMIDES - ASYMMETRIC INDUCTION WITH OPPOLZERS CHIRAL SULTAM SO TETRAHEDRON LETTERS LA English DT Article ID ORGANIC-SYNTHESIS; CHAIN REACTIONS; DESIGN AB Oxidative free-radical cyclization of the unsaturated beta-keto imide 3 containing Oppolzer's D-camphor sultam as a chiral auxiliary was studied. Intramolecularly promoted oxidative free-radical cyclization of 3 with Mn (III) in the presence of Cu (II) produced the stereoisomeric cis-hydrindanones 4 and 5 in a 3:1 ratio at 25-degrees-C. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RP ZORETIC, PA (reprint author), E CAROLINA UNIV,DEPT CHEM,GREENVILLE,NC 27858, USA. NR 16 TC 32 Z9 33 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD MAY 5 PY 1992 VL 33 IS 19 BP 2637 EP 2640 DI 10.1016/S0040-4039(00)79045-9 PG 4 WC Chemistry, Organic SC Chemistry GA HT782 UT WOS:A1992HT78200006 ER PT J AU DAVIDSON, WF PIERCE, JH HOLMES, KL AF DAVIDSON, WF PIERCE, JH HOLMES, KL TI EVIDENCE FOR A DEVELOPMENTAL RELATIONSHIP BETWEEN CD5+ B-LINEAGE CELLS AND MACROPHAGES SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID COLONY-STIMULATING FACTOR; LYMPHOID PROGENITOR-CELL; MYELOID LEUKEMIC-CELLS; PRE-B; STEM-CELLS; INVITRO TRANSFORMATION; AUTOCRINE STIMULATION; HEMATOPOIETIC-CELLS; AUTONOMOUS GROWTH; RECEPTOR GENES C1 NCI, CELLULAR & MOLEC BIOL LAB, BETHESDA, MD 20892 USA. NIAID, BIOL RESOURCES BRANCH, FLOW CYTOMETRY SECT, BETHESDA, MD 20892 USA. RP DAVIDSON, WF (reprint author), NCI, GENET LAB, BETHESDA, MD 20892 USA. NR 46 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAY 4 PY 1992 VL 651 BP 112 EP 129 PG 18 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM219 UT WOS:A1992JM21900014 ER PT J AU KEHRL, JH RIECKMANN, P KOZLOW, E FAUCI, AS AF KEHRL, JH RIECKMANN, P KOZLOW, E FAUCI, AS TI LYMPHOKINE PRODUCTION BY B-CELLS FROM NORMAL AND HIV-INFECTED INDIVIDUALS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; GROWTH-FACTOR-BETA; FACTOR-ALPHA; LYMPHOCYTES-B; TRANSCRIPTION FACTOR; INTERLEUKIN-6 GENE; IL-6 PRODUCTION; MESSENGER-RNA; T-CELLS RP KEHRL, JH (reprint author), NIAID, IMMUNOREGULAT LAB, BETHESDA, MD 20892 USA. NR 30 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAY 4 PY 1992 VL 651 BP 220 EP 227 PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM219 UT WOS:A1992JM21900030 ER PT J AU IKEMATSU, H HARINDRANATH, N CASALI, P AF IKEMATSU, H HARINDRANATH, N CASALI, P TI SOMATIC MUTATIONS IN THE V(H) GENES OF HIGH-AFFINITY ANTIBODIES TO SELF AND FOREIGN ANTIGENS PRODUCED BY HUMAN CD5+ AND CD5- LYMPHOCYTES-B SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID VARIABLE REGION GENES; GERM-LINE GENES; RHEUMATOID FACTORS; MONOCLONAL IGM; VH-GENE; AUTOANTIBODIES; CELLS; POLYMORPHISM; FAMILIES; SEQUENCE C1 NYU, SCH MED, DEPT PATHOL, MSB-599, 550 1ST AVE, NEW YORK, NY 10016 USA. NYU, SCH MED, KAPLAN CANC CTR, NEW YORK, NY 10016 USA. NIH, ORAL MED LAB, BETHESDA, MD 20892 USA. RI Casali, Paolo/F-6579-2010 NR 22 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAY 4 PY 1992 VL 651 BP 319 EP 327 PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM219 UT WOS:A1992JM21900044 ER PT J AU BERTIN, PA MARTI, GE AF BERTIN, PA MARTI, GE TI EXPRESSION OF IMMUNOGLOBULIN HEAVY-CHAIN VARIABLE GENE (V(H)) IN B-CHRONIC LYMPHOCYTIC-LEUKEMIA (B-CLL) AND B-PROLYMPHOCYTIC LEUKEMIA (B-PLL) CELL-LINES - RESTRICTED USAGE OF V(H)3 FAMILY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article RP BERTIN, PA (reprint author), NIH, US FDA, CTR BIOL EVALUAT & RES, DIV BIOCHEM & BIOPHYS, BETHESDA, MD 20892 USA. NR 4 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAY 4 PY 1992 VL 651 BP 464 EP 464 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM219 UT WOS:A1992JM21900059 ER PT J AU MARTI, GE FAGUET, G BERTIN, P AGEE, J WASHINGTON, G RUIZ, S CARTER, P ZENGER, V VOGT, R NOGUCHI, P AF MARTI, GE FAGUET, G BERTIN, P AGEE, J WASHINGTON, G RUIZ, S CARTER, P ZENGER, V VOGT, R NOGUCHI, P TI CD20 AND CD5 EXPRESSION IN B-CHRONIC LYMPHOCYTIC-LEUKEMIA SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID CELLS C1 MED COLL GEORGIA, VET ADM MED CTR, DEPT MED, AUGUSTA, GA 30912 USA. MED COLL GEORGIA, VET ADM MED CTR, DEPT BIOCHEM & MOLEC BIOL, AUGUSTA, GA 30912 USA. CTR DIS CONTROL, DIV ENVIRONM HLTH LAB SCI, ATLANTA, GA 30333 USA. RP MARTI, GE (reprint author), NIH, US FDA, CTR BIOL EVALUAT & RES, DIV BIOCHEM & BIOPHYS, BETHESDA, MD 20892 USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAY 4 PY 1992 VL 651 BP 480 EP 483 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM219 UT WOS:A1992JM21900064 ER PT J AU DAVIS, MD KAUFMAN, S MILSTIEN, S AF DAVIS, MD KAUFMAN, S MILSTIEN, S TI DISTRIBUTION OF 4A-HYDROXYTETRAHYDROPTERIN DEHYDRATASE IN RAT-TISSUES - COMPARISON WITH THE AROMATIC AMINO-ACID HYDROXYLASES SO FEBS LETTERS LA English DT Article DE PHENYLALANINE; HYPERPHENYLALANINEMIA; TETRAHYDROBIOPTERIN; 7-BIOPTERIN; PHENYLALANINE HYDROXYLASE; 4A-CARBINOLAMINE DEHYDRATASE; 4A-HYDROXY TETRAHYDROBIOPTERIN ID PHENYLALANINE-HYDROXYLASE; 7-SUBSTITUTED PTERINS; LIVER; PROTEIN; STIMULATOR; ENZYME AB A 4a-carbinolamine intermediate is generated stoichiometrically during the tetrahydrobiopterin-dependent phenylalanine hydroxylation reaction catalyzed by phenylalanine hydroxylase. The dehydration of the carbinolamine is catalyzed by the enzyme, 4a-hydroxytetrahydropterin dehydratase. We have now examined the distribution of the dehydratase activity in various rat tissues by activity measurements and by immunoblot analysis to explore the possibility that the dehydratase may also play a role in tyrosine and tryptophan hydroxylation. The only two tissues that express relatively high dehydratase activity are liver and kidney, which are also the only two tissues that express phenylalanine hydroxylase activity. The dehydratase activity was generally very low in those tissues which contain high levels of tyrosine and tryptophan hydroxylase activity, except for the pineal gland. These results suggest that the dehydratase may not play an important role in the regulation of the synthesis of those neurotransmitters which are derived from the hydroxylated aromatic amino acids. C1 NIMH,NEUROCHEM LAB,BLDG 36 RM,3D-30,BETHESDA,MD 20892. NR 14 TC 35 Z9 35 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAY 4 PY 1992 VL 302 IS 1 BP 73 EP 76 DI 10.1016/0014-5793(92)80288-R PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA HT129 UT WOS:A1992HT12900020 PM 1350256 ER PT J AU WINDLE, C LALLEY, TL AF WINDLE, C LALLEY, TL TI RECENT FINDINGS FROM NIMHS SERVICES RESEARCH-PROGRAM SO ADMINISTRATION AND POLICY IN MENTAL HEALTH LA English DT Article ID MENTAL-HEALTH-CARE; COVERAGE; OUTCOMES; COSTS RP WINDLE, C (reprint author), NIMH,SERV RES PROGRAM,ROCKVILLE,MD 20857, USA. NR 21 TC 0 Z9 0 U1 0 U2 0 PU HUMAN SCI PRESS INC PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 SN 0894-587X J9 ADM POLICY MENT HLTH JI Adm. Policy. Ment. Health PD MAY PY 1992 VL 19 IS 5 BP 367 EP 372 DI 10.1007/BF00707142 PG 6 WC Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA HZ185 UT WOS:A1992HZ18500006 ER PT J AU DUBLIN, S ROSENBERG, PS GOEDERT, JJ AF DUBLIN, S ROSENBERG, PS GOEDERT, JJ TI PATTERNS AND PREDICTORS OF HIGH-RISK SEXUAL-BEHAVIOR IN FEMALE PARTNERS OF HIV-INFECTED MEN WITH HEMOPHILIA SO AIDS LA English DT Article DE SAFE SEX; CONDOMS; CONTRACEPTIVES; EDUCATION; COUNSELING; LOGISTIC REGRESSION; SURVIVAL ANALYSIS; HEMOPHILIA; AIDS; HIV ID HUMAN IMMUNODEFICIENCY VIRUS; SAN-FRANCISCO; BISEXUAL MEN; CONDOM USE; TRANSMISSION; HETEROSEXUALS; HEALTH; GAY AB Objective: To characterize and quantify high-risk heterosexual activity in HIV-discordant couples. Design: Analysis of cross-sectional and longitudinal questionnaire data from 217 HIV-negative female sexual partners of HIV-infected hemophilic men. Methods: Comparison of prevalence rates of anal sex, oral sex, vaginal intercourse with or without condoms, and use of other contraceptives between 1985 and 1991. Logistic regression analysis of demographic, sexual and clinical variables to predict unprotected vaginal sex. Actuarial estimates of semi-annual relapse rates to unsafe sex. Results: The proportion of women at low risk increased from 7 to 69% between 1985 and 1991, mainly because more women were using condoms during all acts of vaginal intercourse. Other contraceptive practices did not change during this time. The proportion engaging in oral or anal sex decreased (from 26 to 13% and 13 to 4%, respectively). Unprotected vaginal sex was more common among women who enrolled earlier, had less education, engaged in oral or anal sex, and among those whose partners had not had AIDS. Unprotected vaginal sex before enrollment was the strongest predictor of this high-risk activity during follow-up. Two-year rates of relapse to high-risk behavior were significantly higher among women who enrolled at high risk compared with those who enrolled at low risk (39 versus 8%, P = 0.005). Conclusions: Although high-risk sexual behavior became much less prevalent in this population between 1985 and 1991, many continued to have unprotected vaginal sex occasionally. Counseling efforts should target couples who have been the most sexually active or have less education, and should emphasize not only initial risk reduction but also maintenance of low-risk behavior. C1 UNIV GENEVA,HOP CANTONAL,CH-1211 GENEVA 4,SWITZERLAND. PENN STATE UNIV,MILTON S HERSHEY MED CTR,SCH MED,HERSHEY,PA 17033. RES TRIANGLE INST,WASHINGTON,DC. TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. UNIV MUNICH,W-8000 MUNICH 2,GERMANY. UNIV COLORADO,DENVER,CO 80202. UNIV N CAROLINA,CHAPEL HILL,NC 27514. UNIV VIENNA,A-1010 VIENNA,AUSTRIA. NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. UNIV ATHENS,SCH MED,ATHENS,GREECE. UNIV ATHENS,LAIKON GEN HOSP,ATHENS,GREECE. CARDEZA FDN HEMOPHILIA CTR,PHILADELPHIA,PA. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010. CORNELL UNIV,MED CTR,NEW YORK,NY 10021. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. MT SINAI MED CTR,NEW YORK,NY 10029. FU NCI NIH HHS [N01-CP-85648] NR 29 TC 24 Z9 24 U1 2 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD MAY PY 1992 VL 6 IS 5 BP 475 EP 482 DI 10.1097/00002030-199205000-00006 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA HT197 UT WOS:A1992HT19700006 PM 1616653 ER PT J AU VARNIER, OE KINDT, TJ AF VARNIER, OE KINDT, TJ TI CURRENT STATUS OF HIV-1 INFECTION IN THE RABBIT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Letter ID HUMAN IMMUNODEFICIENCY VIRUS; T-CELL; LEUKEMIA-VIRUS; DEFINITION; INDUCTION; LINES C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. RP VARNIER, OE (reprint author), SCH MED,INST MICROBIOL,HUMAN RETROVIROL LAB,GENOA,ITALY. NR 26 TC 8 Z9 8 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 MAY PY 1992 VL 8 IS 5 BP 533 EP 535 DI 10.1089/aid.1992.8.533 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300001 PM 1515208 ER PT J AU TRUJILLO, JM CONCHA, M MUNOZ, A BERGONZOLI, G MORA, C BORRERO, I GIBBS, CJ ARANGO, C AF TRUJILLO, JM CONCHA, M MUNOZ, A BERGONZOLI, G MORA, C BORRERO, I GIBBS, CJ ARANGO, C TI SEROPREVALENCE AND COFACTORS OF HTLV-I INFECTION IN TUMACO, COLOMBIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID TROPICAL SPASTIC PARAPARESIS; T-CELL LEUKEMIA; VIRUS TYPE-I; TRANSMISSION; ANTIBODIES; JAPAN; RISK; PREFECTURE; TRINIDAD; ANTIGEN AB This study presents an analysis of the factors associated with HTLV-I seroprevalence in the endemic area of Tumaco, Colombia. During June to August 1988, 1,077 individuals were selected at random from a population of 45,594. The overall prevalence rate of HTLV-I antibodies was 2.8%. Among females prevalence was significantly higher (p < 0.02) than among males. Rates increased substantially with age. HTLV-I prevalence among individuals with history of use of intravenous medications was significantly higher (p < 0.001) than in those without such history. Logistic regression analysis included age in years, indicators for male gender, and for i.v. injections, and their interactions. Age was very strongly associated to HTLV-I infection among females. At early ages prevalence was not different between sexes, but females presented a significantly higher rate than males after age 42. History of i.v. administered medications was verv strongly associated in the univariate analysis and, although significance was borderline in the multivariate analysis, it had the effect of doubling the odds of HTLV-I infection. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21205. UNIV VALLE,FAC HLTH,DEPT SOCIAL MED,CALI,COLOMBIA. UNIV VALLE,FAC HLTH,DEPT MICROBIOL,CALI,COLOMBIA. UNIV VALLE,FAC HLTH,DEPT INTERNAL MED,CALI,COLOMBIA. NIH,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. RP TRUJILLO, JM (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT IMMUNOL & INFECT DIS,615 N WOLFE ST,BALTIMORE,MD 21205, USA. NR 38 TC 27 Z9 27 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 MAY PY 1992 VL 8 IS 5 BP 651 EP 657 DI 10.1089/aid.1992.8.651 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300016 PM 1515216 ER PT J AU SARVER, N BLACK, RJ BRIDGES, S CHRISEY, L AF SARVER, N BLACK, RJ BRIDGES, S CHRISEY, L TI FRONTIERS IN HIV-1 THERAPY - 4TH CONFERENCE OF THE NIAID NATIONAL COOPERATIVE DRUG DISCOVERY GROUPS-HIV SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material AB This summary describes current studies in antiviral targeting as reported at the Frontiers in HIV Therapy conference, November 3-7, 1991, in San Diego, California. In parallel with the progressive steps in HIV-1 replication, the meeting covered potential antiviral targets starting from the time HIV-1 docks with the CD4 receptor to virus release. The summary concludes with current research trends to block HIV-1 growth. C1 USN,RES LAB,WASHINGTON,DC 20375. RP SARVER, N (reprint author), NIAID,DIV AIDS,BASIC RES & DEV PROGRAM,DEV THERAPEUT BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 12 Z9 12 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 659 EP 667 DI 10.1089/aid.1992.8.659 PG 9 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300017 PM 1515217 ER PT J AU FAUCI, AS AF FAUCI, AS TI PHARMACOLOGICAL REGULATION OF HIV EXPRESSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL ID HUMAN IMMUNODEFICIENCY VIRUS; LYMPHADENOPATHY-ASSOCIATED VIRUS; IMMUNE-DEFICIENCY SYNDROME; T-LYMPHOTROPIC RETROVIRUS; COLORECTAL CELL-LINES; REGRESSIVE ENCEPHALOPATHY; PERSISTENT INFECTION; SEROPOSITIVE MAN; SYNDROME AIDS; LAV RP FAUCI, AS (reprint author), NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892, USA. NR 35 TC 2 Z9 2 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 MAY PY 1992 VL 8 IS 5 BP 707 EP 718 PG 12 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300020 PM 1515220 ER PT J AU BRADY, JN AF BRADY, JN TI EXTRACELLULAR TAX(1) PROTEIN STIMULATES NF-KB AND EXPRESSION OF NF-KB-RESPONSIVE IG KAPPA AND TNF(BETA) GENES IN LYMPHOID-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL RP BRADY, JN (reprint author), NCI,MOLEC VIROL LAB,BETHESDA,MD 20892, USA. NR 4 TC 16 Z9 16 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 MAY PY 1992 VL 8 IS 5 BP 724 EP 727 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300022 PM 1515222 ER PT J AU MASUR, H AF MASUR, H TI NEW ADVANCES IN THE MANAGEMENT OF AIDS ASSOCIATED OPPORTUNISTIC INFECTIONS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL RP MASUR, H (reprint author), NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 728 EP 731 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300023 PM 1515223 ER PT J AU SHACTER, E ARZADON, G AF SHACTER, E ARZADON, G TI ELEVATION OF IL-6 IN PLASMA-CELL TUMORIGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL RP SHACTER, E (reprint author), NCI,GENET LAB,BETHESDA,MD 20892, USA. NR 4 TC 2 Z9 2 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 MAY PY 1992 VL 8 IS 5 BP 754 EP 756 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300029 PM 1515225 ER PT J AU GERMAIN, RN AF GERMAIN, RN TI ANTIGEN PROCESSING AND PRESENTATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL RP GERMAIN, RN (reprint author), NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 769 EP 776 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300033 PM 1515228 ER PT J AU YAMADA, KM AF YAMADA, KM TI FUNCTIONS OF INTEGRINS IN CELL-ADHESION AND MIGRATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL RP YAMADA, KM (reprint author), NIDR,DEV BIOL LAB,BETHESDA,MD 20892, USA. OI Yamada, Kenneth/0000-0003-1512-6805 NR 0 TC 5 Z9 5 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 786 EP 793 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300035 PM 1515229 ER PT J AU TABOR, E AF TABOR, E TI HEPATITIS-C VIRUS AND HEPATOCELLULAR-CARCINOMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL RP TABOR, E (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 793 EP 796 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300036 PM 1325172 ER PT J AU SCHULZ, N VANDEWOUDE, GF AF SCHULZ, N VANDEWOUDE, GF TI A TRANSGENIC MOUSE MODEL FOR MEN .2. SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL RP SCHULZ, N (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 820 EP 823 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300040 PM 1355348 ER PT J AU PAPAS, TS AF PAPAS, TS TI ONCOGENES AS PROBES FOR CELLULAR SIGNAL PROCESSES - THE FAMILY OF ETS GENES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE LABORATORY OF TUMOR CELL BIOLOGY CY SEP 01-08, 1991 CL BETHESDA, MD SP LAB TUMOR CELL BIOL RP PAPAS, TS (reprint author), NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702, USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 824 EP 833 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300041 PM 1515233 ER PT J AU ANDERSON, WF AF ANDERSON, WF TI HUMAN GENE-THERAPY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 859 EP 859 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300044 ER PT J AU ROSENBERG, SA AF ROSENBERG, SA TI GENE-THERAPY OF CANCER SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 859 EP 859 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300046 ER PT J AU OROSZLAN, S AF OROSZLAN, S TI THE BIOCHEMISTRY OF HIV PROTEASE AND ITS INHIBITORS AS ANTIVIRAL AGENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 860 EP 860 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300050 ER PT J AU CHANG, HK LISZIEWICZ, J GALLO, RC ENSOLI, B AF CHANG, HK LISZIEWICZ, J GALLO, RC ENSOLI, B TI INHIBITION OF HIV-1 REGULATORY GENE-EXPRESSION (TAT AND REV) BY ANTISENSE EXPRESSING PLASMIDS IN HUMAN T-CELL LINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 861 EP 861 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300053 ER PT J AU LISZIEWICZ, J SMYTHE, J SUN, D READCONNOLE, B LUSSO, P GALLO, R REITZ, M AF LISZIEWICZ, J SMYTHE, J SUN, D READCONNOLE, B LUSSO, P GALLO, R REITZ, M TI GENETIC APPROACHES TO HIV THERAPY - DEVELOPMENT OF PROTECTIVE GENES CONTAINING POLY-TAR ELEMENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 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 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 MAY PY 1992 VL 8 IS 5 BP 861 EP 861 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300055 ER PT J AU LISZIEWICZ, J DAEFLER, S LI, G SUN, D ZON, G WONGSTAAL, F KLOTMAN, ME AF LISZIEWICZ, J DAEFLER, S LI, G SUN, D ZON, G WONGSTAAL, F KLOTMAN, ME TI ANTISENSE OLIGONUCLEOTIDES DIRECTED AGAINST THE REV PROTEIN-BINDING SITE OF THE REV RESPONSIVE ELEMENT BLOCK REV ACTIVITY AND HIV-INFECTION INVITRO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 861 EP 861 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300054 ER PT J AU MITSUYA, H AOKISEI, S AF MITSUYA, H AOKISEI, S TI QUANTITATIVE-ANALYSIS OF HIV-1 IN CLINICAL SPECIMENS FROM PATIENTS (PT) WITH HIV-1 INFECTION BY POLYMERASE CHAIN-REACTION (PCR) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 862 EP 862 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300059 ER PT J AU MORGAN, RA COUTURE, L MASON, J RAGHEB, J GALLO, RC ANDERSON, WF AF MORGAN, RA COUTURE, L MASON, J RAGHEB, J GALLO, RC ANDERSON, WF TI GENE-TRANSFER AS AN ANTI-HIV THERAPY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 862 EP 862 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300056 ER PT J AU YARCHOAN, R VENZON, D LIETZAU, J PLUDA, JM WYVILL, KM STEINBERG, S BRODER, S AF YARCHOAN, R VENZON, D LIETZAU, J PLUDA, JM WYVILL, KM STEINBERG, S BRODER, S TI RELATIONSHIP BETWEEN THE CD4 COUNT AND MORTALITY IN HIV-INFECTED PATIENTS ON ANTIRETROVIRAL THERAPY FOLLOWED AT A RESEARCH HOSPITAL SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 862 EP 862 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300057 ER PT J AU BABOONIAN, C DALGLEISH, A BOUNTIFF, L GROSS, J OROSZLAN, S RICKETT, G SMITHBURCHNELL, C TROKE, P MERSON, J AF BABOONIAN, C DALGLEISH, A BOUNTIFF, L GROSS, J OROSZLAN, S RICKETT, G SMITHBURCHNELL, C TROKE, P MERSON, J TI HIV-1 PROTEINASE IS REQUIRED FOR SYNTHESIS OF PRO-VIRAL DNA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CLIN RES CTR,HARROW HA1 3UJ,MIDDX,ENGLAND. PFIZER LTD,CENT RES,SANDWICH CT13 9NJ,KENT,ENGLAND. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 863 EP 863 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300061 ER PT J AU SARVER, N AF SARVER, N TI RIBOZYMES - PRESENT AND POTENTIAL FUTURE-DIRECTION IN BIOMEDICAL APPLICATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,DIV AIDS,DEV THERAPEUT BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 863 EP 863 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300063 ER PT J AU CLERICI, M LANDAY, AL KESSLER, HA LUCEY, DR HENDRIX, CW PIZZO, PA ROILIDES, E SHEARER, GM AF CLERICI, M LANDAY, AL KESSLER, HA LUCEY, DR HENDRIX, CW PIZZO, PA ROILIDES, E SHEARER, GM TI A NOVEL SURROGATE MARKER - T-HELPER (TH) FUNCTION IN HIV+ PATIENTS ON ANTIRETROVIRAL THERAPY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. WILFORD HALL USAF MED CTR,LACKLAND AFB,TX 78236. RI Hendrix, Craig/G-4182-2014 OI Hendrix, Craig/0000-0002-5696-8665 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 864 EP 864 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300065 ER PT J AU SHIRASAKA, T YARCHOAN, R HUSSON, R OBRIEN, MC SHIMADA, T WYVILL, KM BRODER, S MITSUYA, H AF SHIRASAKA, T YARCHOAN, R HUSSON, R OBRIEN, MC SHIMADA, T WYVILL, KM BRODER, S MITSUYA, H TI HIV MAY DEVELOP RESISTANCE PREFERENTIALLY TO AZIDOTHYMIDINE (AZT) AS COMPARED TO DIDEOXYCYTIDINE (DDC) AND DIDEOXYINOSINE (DDI) IN PATIENTS RECEIVING ANTIVIRAL THERAPY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 864 EP 864 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300067 ER PT J AU WEINSTEIN, JN BUNOW, B AF WEINSTEIN, JN BUNOW, B TI NEW CONCEPTS FOR THE DESIGN AND ANALYSIS OF EXPERIMENTS ON COMBINATION THERAPY OF AIDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CIVILIZED SOFTWARE INC,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 864 EP 864 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300064 ER PT J AU PAVLAKIS, GN SCHWARTZ, S BENKO, DM FELBER, BK SOLOMIN, L HARRISON, JE AF PAVLAKIS, GN SCHWARTZ, S BENKO, DM FELBER, BK SOLOMIN, L HARRISON, JE TI REGULATION OF THE STABILITY TRANSPORT, AND TRANSLATION OF RRE-CONTAINING HIV-1 MESSENGER-RNAS BY REV SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS SECT,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS PATHOGENESIS GRP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 867 EP 867 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300073 ER PT J AU FRANCO, L VERONESE, F DEVICO, A LUSSO, P BOYER, C REITZ, MS GALLO, RC AF FRANCO, L VERONESE, F DEVICO, A LUSSO, P BOYER, C REITZ, MS GALLO, RC TI VIRAL-DNA IS CARRIED BY HIV-1 VIRIONS ASSOCIATED WITH REVERSE-TRANSCRIPTASE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 869 EP 869 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300081 ER PT J AU BOHAN, CA KASHANCHI, F ENSOLI, B BUONAGURO, L BRADY, JN AF BOHAN, CA KASHANCHI, F ENSOLI, B BUONAGURO, L BRADY, JN TI HIV-1 TAT PROTEIN STIMULATES TRANSCRIPTION PREINITIATION COMPLEX-FORMATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 871 EP 871 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300089 ER PT J AU BRESSLER, P BROWN, K TIMMER, W BOURS, V SIEBENLIST, U FAUCI, A AF BRESSLER, P BROWN, K TIMMER, W BOURS, V SIEBENLIST, U FAUCI, A TI MUTATIONAL ANALYSIS OF THE NF-KAPPA-B P50 PROTEIN AND INHIBITION OF NF-KAPPA-B ACTIVITY BY TRANSDOMINANT MUTANTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 871 EP 871 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300088 ER PT J AU DAYTON, ET KONINGS, DAM POWELL, DM SHAPIRO, BA BUTINI, L PANTALEO, G POLI, G MAIZEL, JV FAUCI, AS DAYTON, AI AF DAYTON, ET KONINGS, DAM POWELL, DM SHAPIRO, BA BUTINI, L PANTALEO, G POLI, G MAIZEL, JV FAUCI, AS DAYTON, AI TI THE REV AXIS OF HIV-1 AUTOREGULATION CAN CONTRIBUTE TO CELL-TYPE SPECIFIC VIRAL TROPISM SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NCI,DIV CANC BIOL & DIAG,MATH BIOL LAB,FREDERICK,MD 21701. GEORGE WASHINGTON UNIV,DEPT GENET,WASHINGTON,DC 20052. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 871 EP 871 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300086 ER PT J AU RAPPAPORT, J SUHASINI, M REDDY, T BITTERLICH, G RICHARDSON, MW KRAUS, G ARYA, S WONGSTAAL, F AF RAPPAPORT, J SUHASINI, M REDDY, T BITTERLICH, G RICHARDSON, MW KRAUS, G ARYA, S WONGSTAAL, F TI HIV-1 TAT AND TAR RNA-BINDING CELLULAR FACTORS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DEPT HYDROCARBON RES,LA JOLLA,CA 92093. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 871 EP 871 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300087 ER PT J AU BUONAGURO, L CHANG, HK BOHAN, C BARILLARI, G KAO, V BRADY, J GALLO, RC ENSOLI, B AF BUONAGURO, L CHANG, HK BOHAN, C BARILLARI, G KAO, V BRADY, J GALLO, RC ENSOLI, B TI TAT, THE TRANSACTIVATOR GENE OF HIV-1, ACTIVATES THE EXPRESSION OF TUMOR NECROSIS FACTOR-BETA (TNF-BETA) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 872 EP 872 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300092 ER PT J AU ENSOLI, B BUONAGURO, L BARILLARI, G FIORELLI, V GENDELMAN, R MORGAN, R WINGFIELD, P GALLO, RC AF ENSOLI, B BUONAGURO, L BARILLARI, G FIORELLI, V GENDELMAN, R MORGAN, R WINGFIELD, P GALLO, RC TI RELEASE-UPTAKE OF HIV-1 TAT AND MECHANISMS OF TAT-INDUCED PARACRINE BIOLOGICAL EFFECTS (TAT DOMAINS AND PATHWAYS FOR CELL-GROWTH AND TRANSACTIVATION ACTIVITY) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NIH,PROT EXPRESS LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 872 EP 872 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300090 ER PT J AU GURGO, C GALLO, RC LUSSO, P AF GURGO, C GALLO, RC LUSSO, P TI MOLECULAR PATHOGENICITY OF HIV-1 IN THE ABSENCE OF ENVELOPE PROTEIN EXPRESSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,LTCB,BETHESDA,MD 20892. CNR,CEOS,NAPLES,ITALY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 873 EP 873 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300097 ER PT J AU CHATTERJEE, P ARYA, SK AF CHATTERJEE, P ARYA, SK TI DIVERSITY OF HIV-2 REGULATORY GENE TRANSCRIPTS - ROLE IN LATENCY AND PATHOGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 874 EP 874 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300098 ER PT J AU WEEKS, BS DESAI, K LOEWENSTEIN, PM KLOTMAN, ME KLOTMAN, PE GREEN, M KLEINMAN, HK AF WEEKS, BS DESAI, K LOEWENSTEIN, PM KLOTMAN, ME KLOTMAN, PE GREEN, M KLEINMAN, HK TI IDENTIFICATION OF RECOGNITION SEQUENCES FOR CELL ATTACHMENT IN THE HIV-1 TAT PROTEIN AND A 90 KDA CELL-SURFACE TAT-BINDING PROTEIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. ST LOUIS UNIV,MED CTR,INST MOLEC VIROL,ST LOUIS,MO 63110. 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 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 MAY PY 1992 VL 8 IS 5 BP 874 EP 874 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300099 ER PT J AU BARILLARI, G CROWLEY, R GENDELMAN, R BIBERFELD, P GALLO, RC ENSOLI, B AF BARILLARI, G CROWLEY, R GENDELMAN, R BIBERFELD, P GALLO, RC ENSOLI, B TI INFLAMMATORY CYTOKINES INCREASE MESENCHYMAL CELL-GROWTH AND ATTACHMENT INDUCED BY HIV-1 TAT PROTEIN AND ADHESION MOLECULES - IMPLICATIONS FOR AIDS-KAPOSIS SARCOMA PATHOGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. KAROLINSKA INST,DEPT PATHOL,S-10401 STOCKHOLM 60,SWEDEN. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 876 EP 876 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300106 ER PT J AU ENSOLI, B BARILLARI, G BUONAGURO, L FIORELLI, V GALLO, RC AF ENSOLI, B BARILLARI, G BUONAGURO, L FIORELLI, V GALLO, RC TI ROLE OF CYTOKINES FROM ACTIVATED T-CELLS AND HIV-1 TAT PROTEIN IN THE PATHOGENESIS OF AIDS-ASSOCIATED KAPOSIS-SARCOMA (AIDS-KS) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 876 EP 876 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300104 ER PT J AU WILLIAMS, AO FOGARTY, MD AF WILLIAMS, AO FOGARTY, MD TI KAPOSIGENESIS AND A NEW CLASSIFICATION OF KAPOSIS-SARCOMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,CTR INT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 876 EP 876 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300105 ER PT J AU LUNARDIISKANDAR, Y LAM, HH JUDDE, JG GALLO, RC AF LUNARDIISKANDAR, Y LAM, HH JUDDE, JG GALLO, RC TI CYTOKINE AND HORMONE RECEPTORS ON AIDS-KAPOSIS SARCOMA (KS)-DERIVED CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 877 EP 877 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300108 ER PT J AU SARNGADHARAN, MG DEVICO, AL NAIR, BC NAKAMURA, S COPELAND, TD OROSZLAN, S PATEL, A GALLO, RC AF SARNGADHARAN, MG DEVICO, AL NAIR, BC NAKAMURA, S COPELAND, TD OROSZLAN, S PATEL, A GALLO, RC TI PURIFICATION AND PARTIAL CHARACTERIZATION OF THE 30 KD FACTOR THAT SUPPORTS THE GROWTH OF KAPOSIS SARCOMA-DERIVED CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ADV BIOSCI LABS INC,KENSINGTON,MD. LAB TUMOR CELL BIOL,ROCKVILLE,MD. FREDERICK CANC RES & DEV CTR,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 877 EP 877 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300107 ER PT J AU HAVERKOS, HW AF HAVERKOS, HW TI NITRITE INHALANT ABUSE IN AIDS-RELATED KAPOSIS-SARCOMA (KS) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDA,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 878 EP 878 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300112 ER PT J AU ALBINI, A ADATIA, R DECUPIS, A COLACCI, A POGGI, L THOMPSON, EW ENSOLI, B GALLO, RC AF ALBINI, A ADATIA, R DECUPIS, A COLACCI, A POGGI, L THOMPSON, EW ENSOLI, B GALLO, RC TI AIDS-CELL INDUCED ENDOTHELIAL-CELL INVASION - STUDIES ON MECHANISMS AND INHIBITION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 IST NAZL RIC CANC,I-16132 GENOA,ITALY. VT LOMBARDI CANC CTR,WASHINGTON,DC. NCI,BETHESDA,MD 20892. RI Thompson, Erik/A-1425-2009; Ensoli, Barbara/J-9169-2016 OI Thompson, Erik/0000-0002-9723-4924; Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 2 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 MAY PY 1992 VL 8 IS 5 BP 879 EP 879 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300116 ER PT J AU WILLIAMS, AO REITZ, M WARD, JM JACKSON, MA LI, F FRIEDLAND, G BECKER, N WAMUKOTA, W MUGERWA, J GERSHYDAMET, GM EHOUBAIN, A AF WILLIAMS, AO REITZ, M WARD, JM JACKSON, MA LI, F FRIEDLAND, G BECKER, N WAMUKOTA, W MUGERWA, J GERSHYDAMET, GM EHOUBAIN, A TI DETECTION OF HIV-1 DNA-SEQUENCES AND IMMUNOHISTOCHEMICAL LOCALIZATION OF HIV-1 ANTIGEN IN AFRICAN AND AFRICAN-AMERICANS WITH KAPOSIS-SARCOMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,FOGARTY INT CTR,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. HOWARD UNIV,DEPT PATHOL,WASHINGTON,DC 20059. N CENT BRONX HOSP,BRONX,NY. MONTEFIORE MED CTR,BRONX,NY 10467. MAKERERE UNIV,KAMPALA,UGANDA. INST PASTEUR,ABIDJAN,COTE IVOIRE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 879 EP 879 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300115 ER PT J AU KLEINMAN, HK GRANT, DS AF KLEINMAN, HK GRANT, DS TI ROLE OF BASEMENT-MEMBRANE IN ANGIOGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 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 MAY PY 1992 VL 8 IS 5 BP 880 EP 880 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300121 ER PT J AU YAMADA, KM AF YAMADA, KM TI FUNCTIONS OF INTEGRINS IN CELL-ADHESION AND MIGRATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 880 EP 880 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300118 ER PT J AU PAPAS, TS AF PAPAS, TS TI ONCOGENES AS PROBES FOR CELLULAR SIGNAL PROCESSES - THE FAMILY OF ETS GENES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 882 EP 882 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300125 ER PT J AU VANDEWOUDE, GF AF VANDEWOUDE, GF TI ONCOGENES, CELL-CYCLE AND ANTINEOPLASTIC DRUGS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 882 EP 882 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300126 ER PT J AU TABOR, E AF TABOR, E TI HEPATITIS-C VIRUS (HCV) AND HEPATOCELLULAR-CARCINOMA (HCC) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 883 EP 883 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300128 ER PT J AU ABLASHI, DV HUNG, CL BALACHANDRAN, N KRUEGER, GRF GALLO, RC AF ABLASHI, DV HUNG, CL BALACHANDRAN, N KRUEGER, GRF GALLO, RC TI CHARACTERIZATION OF HHV-6 ISOLATES AND REACTIVATION OF HHV-6 IN SOME DISEASES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. PHARMACIA DIAGNOST INC,SILVER SPRING,MD. UNIV KANSAS,MED CTR,KANSAS CITY,KS 66103. UNIV COLOGNE,W-5000 COLOGNE 41,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 885 EP 885 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300133 ER PT J AU IYENGAR, S LEVINE, PH ABLASHI, D NEEQUAYE, J PEARSON, GR AF IYENGAR, S LEVINE, PH ABLASHI, D NEEQUAYE, J PEARSON, GR TI SEROEPIDEMIOLOGIC INVESTIGATIONS ON HUMAN HERPESVIRUS-6 (HHV-6) INFECTIONS USING A NEWLY DEVELOPED EARLY ANTIGEN-ASSAY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NCI,BETHESDA,MD 20892. BURKITT TUMOR PROJECT,ACCRA,GHANA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 885 EP 885 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300134 ER PT J AU BERNEMAN, ZN SAXINGER, C JOSEPHS, SF LI, G ABLASHI, DV GALLO, RC AF BERNEMAN, ZN SAXINGER, C JOSEPHS, SF LI, G ABLASHI, DV GALLO, RC TI MOLECULAR STUDIES OF HUMAN HERPESVIRUS-6 (HHV-6) AND HUMAN HERPESVIRUS-7 (HHV-7) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 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 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 MAY PY 1992 VL 8 IS 5 BP 886 EP 886 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300139 ER PT J AU BERNEMAN, ZN ABLASHI, DV EGERFLETCHER, M KLOTMAN, ME LEVINE, P WEEKS, B THOMAS, L HUNG, CL KRAMARSKY, B KOMAROFF, A BRUS, I GALLO, RC AF BERNEMAN, ZN ABLASHI, DV EGERFLETCHER, M KLOTMAN, ME LEVINE, P WEEKS, B THOMAS, L HUNG, CL KRAMARSKY, B KOMAROFF, A BRUS, I GALLO, RC TI AN INDEPENDENT ISOLATE OF HUMAN HERPESVIRUS-7 (HHV-7) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. PHARMACIA DIAGNOST,SILVER SPRING,MD. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RI klotman, mary/A-1921-2016 NR 1 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 886 EP 886 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300137 ER PT J AU PELLETT, PE LINDQUESTER, GJ STAMEY, FR DANOVITCH, RM SCHIRMER, EG FRENKEL, N ANTON, ED GREENAMOYER, CA OBRIAN, JJ STACK, S DAMBAUGH, TR AF PELLETT, PE LINDQUESTER, GJ STAMEY, FR DANOVITCH, RM SCHIRMER, EG FRENKEL, N ANTON, ED GREENAMOYER, CA OBRIAN, JJ STACK, S DAMBAUGH, TR TI GENOMIC AND GENETIC ARCHITECTURE OF HUMAN HERPESVIRUS-6 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CTR DIS CONTROL,ATLANTA,GA 30333. RHODES COLL,MEMPHIS,TN 38112. NIH,BETHESDA,MD 20892. DUPONT MERCK PHARMACEUT,WILMINGTON,DE 19880. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 886 EP 886 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300138 ER PT J AU RICCIARDI, RP AGULNICK, A THOMPSON, J IYENGAR, S PEARSON, GR GALLO, RC ABLASHI, V AF RICCIARDI, RP AGULNICK, A THOMPSON, J IYENGAR, S PEARSON, GR GALLO, RC ABLASHI, V TI CLONING AND EXPRESSION OF HUMAN HERPES VIRUS-6 EARLY GENES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 WISTAR INST,PHILADELPHIA,PA 19104. GEORGETOWN UNIV,WASHINGTON,DC 20007. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 886 EP 886 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300140 ER PT J AU INAMDAR, A THOMPSON, J BRADY, J ROSENTHAL, L AF INAMDAR, A THOMPSON, J BRADY, J ROSENTHAL, L TI MTRII OF HCMV IS A 79AA ORF SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 887 EP 887 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300142 ER PT J AU LEVINE, P AF LEVINE, P TI THE EPIDEMIOLOGY OF HUMAN HERPESVIRUS-6 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 888 EP 888 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300147 ER PT J AU LUSSO, P MALNATI, M DEMO, AG DEROCCO, SE ARYA, SK GALLO, RC AF LUSSO, P MALNATI, M DEMO, AG DEROCCO, SE ARYA, SK GALLO, RC TI HHV-6 AS A POTENTIAL COFACTOR IN AIDS - TRANSCRIPTIONAL REGULATION OF CD3, CD4, CD25 AND THE HIV-1 LTR BY DIFFERENT VIRAL ISOLATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIAID,LIG,BETHESDA,MD 20892. CADV BIOSCI LABS INC,KENSINGTON,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 888 EP 888 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300145 ER PT J AU DEMO, AG ARYA, SK BUONAGURO, L ENSOLI, B GALLO, RC LUSSO, P AF DEMO, AG ARYA, SK BUONAGURO, L ENSOLI, B GALLO, RC LUSSO, P TI TRANSCRIPTIONAL ACTIVATION OF CD25 AND TNF-BETA PROMOTERS BY HHV-6 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 889 EP 889 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300151 ER PT J AU MALNATI, MS LUSSO, P MARTIN, R LONG, EO AF MALNATI, MS LUSSO, P MARTIN, R LONG, EO TI SPECIFIC KILLING OF HHV6-INFECTED CELLS BY CD3-CD56+ NATURAL-KILLER LYMPHOCYTES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 889 EP 889 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300152 ER PT J AU DEROCCO, SE MARKHAM, PD NORBECK, D GALLO, RC AF DEROCCO, SE MARKHAM, PD NORBECK, D GALLO, RC TI INVITRO INHIBITION OF HHV-6 BY ANTIVIRAL AGENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ABL,DCB,KENSINGTON,MD. ABBOTT LABS,ABBOTT PK,IL. NCI,LTCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 890 EP 890 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300153 ER PT J AU PLUDA, JM BRODER, S VENZON, D TOSATO, G LIETZAU, J YARCHOAN, R AF PLUDA, JM BRODER, S VENZON, D TOSATO, G LIETZAU, J YARCHOAN, R TI FACTORS PREDICTIVE OF OPPORTUNISTIC NON-HODGKINS-LYMPHOMA (NHL) IN SEVERELY IMMUNOCOMPROMISED HIV-INFECTED PATIENTS ON LONG-TERM ANTIRETROVIRAL THERAPY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CTR BIOL EVALUAT & RES,BETHESDA,MD. RI Venzon, David/B-3078-2008 NR 1 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 892 EP 892 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300159 ER PT J AU BIBERFELD, P FEICHTINGER, H LI, SL KAAYA, EE GENDELMAN, R GRUNEWALD, K PUTKONEN, P ABLASHI, D BIBERFELD, G AF BIBERFELD, P FEICHTINGER, H LI, SL KAAYA, EE GENDELMAN, R GRUNEWALD, K PUTKONEN, P ABLASHI, D BIBERFELD, G TI EBV-ASSOCIATED LYMPHOMAGENESIS IN SIV-IMMUNOSUPPRESSED MONKEYS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 KAROLINSKA INST,IMMUNOPATHOL LAB,S-10401 STOCKHOLM 60,SWEDEN. NATL BACTERIOL LAB,DEPT IMMUNOL,S-10521 STOCKHOLM,SWEDEN. UNIV INNSBRUCK,DEPT PATHOL,A-6020 INNSBRUCK,AUSTRIA. UNIV INNSBRUCK,DEPT INTERNAL MED,MOLEC GENET LAB,A-6020 INNSBRUCK,AUSTRIA. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. MUHIMBILI MED CTR,DEPT PATHOL,DAR ES SALAAM,TANZANIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 894 EP 894 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300167 ER PT J AU COLOMBINI, S ABLASHI, D BIBERFELD, P GALLO, RC AF COLOMBINI, S ABLASHI, D BIBERFELD, P GALLO, RC TI EPSTEIN-BARR-VIRUS (EBV) INFECTION PRECEDES THE ONSET OF LYMPHOMAS IN IMMUNODEFICIENT, SIV-POSITIVE CYNOMOLGUS MONKEYS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. KAROLINSKA INST,S-10401 STOCKHOLM 60,SWEDEN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 894 EP 894 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300166 ER PT J AU MORSE, HC GAZZINELLI, R MAKINO, M SNAPPER, CM CHATTOPADHYAY, SK HARTLEY, JW FREDRICKSON, TN AF MORSE, HC GAZZINELLI, R MAKINO, M SNAPPER, CM CHATTOPADHYAY, SK HARTLEY, JW FREDRICKSON, TN TI CHRONIC ACTIVATION OF T HELPER-CELLS IN MAIDS - RELATION TO THE DEVELOPMENT OF B-CELL LINEAGE LYMPHOMAS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,LIP,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 894 EP 894 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300165 ER PT J AU BEECHAM, EJ MUSHINSKI, JF SHACTER, KHE POTTER, M BOHR, VA AF BEECHAM, EJ MUSHINSKI, JF SHACTER, KHE POTTER, M BOHR, VA TI DNA-REPAIR IN THE C-MYC LOCUS IN LYMPHOCYTES-B SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NCI,GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 895 EP 895 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300171 ER PT J AU BOHR, V AF BOHR, V TI GENE SPECIFIC DAMAGE AND REPAIR SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 895 EP 895 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300169 ER PT J AU SHACTER, E ARZADON, G AF SHACTER, E ARZADON, G TI ELEVATION OF IL-6 IN PLASMA-CELL TUMORIGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 895 EP 895 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300170 ER PT J AU BENVENISTE, R HEIDECKER, G EDDY, G LEWIS, M BURKE, D SHAFFERMAN, A MORTON, W HU, SL AF BENVENISTE, R HEIDECKER, G EDDY, G LEWIS, M BURKE, D SHAFFERMAN, A MORTON, W HU, SL TI RECOMBINANT VACCINES PROTECT MACAQUES AGAINST HOMOLOGOUS SIV OR TYPE-D RETROVIRUS INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21701. WASHINGTON PRIMATE CTR,SEATTLE,WA. JACKSON FDN,ROCKVILLE,MD. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. ISRAEL INST BIOL RES,IL-70450 NESS ZIONA,ISRAEL. ONCOGEN,SEATTLE,WA. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 896 EP 896 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300176 ER PT J AU SHAFFERMAN, A EDDY, GA JAHRLING, PB LEWIS, MG BENVENISTE, RE EDENMCCUTCHAN, F BURKE, DS AF SHAFFERMAN, A EDDY, GA JAHRLING, PB LEWIS, MG BENVENISTE, RE EDENMCCUTCHAN, F BURKE, DS TI PROTECTION OF MACAQUES WITH A VACCINE OF SIV ENVELOPE PEPTIDES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ISRAEL INST BIOL RES,IL-70450 NESS ZIONA,ISRAEL. HENRY M JACKSON FDN,ROCKVILLE,MD. USA,MED RES INST INFECT DIS,FREDERICK,MD 21701. NCI,VIRAL CARCINOGENESIS LAB,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 897 EP 897 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300179 ER PT J AU GONDA, MA PIFAT, DY PALLANSCH, LA RASMUSSEN, L AF GONDA, MA PIFAT, DY PALLANSCH, LA RASMUSSEN, L TI BOVINE IMMUNODEFICIENCY-LIKE VIRUS (BIV) - CHARACTERIZATION OF VIRUS GENE-EXPRESSION INVITRO AND INFECTIONS IN RABBITS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,CELL & MOLEC STRUCT LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 898 EP 898 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300184 ER PT J AU ABIMIKU, AG FRANCHINI, G MARKHAM, PD GARD, E GALLO, RC ROBERTGUROFF, M AF ABIMIKU, AG FRANCHINI, G MARKHAM, PD GARD, E GALLO, RC ROBERTGUROFF, M TI HUMORAL AND CELL-MEDIATED-IMMUNITY IN RHESUS MACAQUES INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-2 (HIV-2) MUTANTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 900 EP 900 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300188 ER PT J AU FRANCHINI, G MARKHAM, P HATTORI, N MARCON, L GARD, E GALLO, RC AF FRANCHINI, G MARKHAM, P HATTORI, N MARCON, L GARD, E GALLO, RC TI INFECTIVITY OF HIV-2 MUTANTS IN RHESUS MACAQUES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. ADV BIOSCI LAB INC,KENSINGTON,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 900 EP 900 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300189 ER PT J AU KINDT, TJ SAWASDIKOSOL, S HAGUE, B GORDON, M TRUCKENMILLER, ME KUTA, E BOWERS, F BROWN, TJ AF KINDT, TJ SAWASDIKOSOL, S HAGUE, B GORDON, M TRUCKENMILLER, ME KUTA, E BOWERS, F BROWN, TJ TI INFECTION OF LABORATORY RABBITS WITH HIV-1 AND HTLV-I SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,TWINBROOK FACIL 2,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 901 EP 901 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300193 ER PT J AU SANTORO, TJ BRYANT, JL PELLICORO, JA KLOTMAN, ME WAHL, SM KOPP, JB NOTKINS, AL KLOTMAN, PE AF SANTORO, TJ BRYANT, JL PELLICORO, JA KLOTMAN, ME WAHL, SM KOPP, JB NOTKINS, AL KLOTMAN, PE TI AIDS-LIKE CACHEXIA SYNDROME IN TRANSGENIC MICE BEARING NONREPLICATING HIV-1 PROVIRAL DNA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDR,LDB,BETHESDA,MD 20892. NIDR,LOM ACU,BETHESDA,MD 20892. NIDR,LMI,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 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 MAY PY 1992 VL 8 IS 5 BP 901 EP 901 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300194 ER PT J AU KOPP, JB KLOTMAN, ME MARINOS, NJ BRYANT, JL NOTKINS, AL KLOTMAN, PE AF KOPP, JB KLOTMAN, ME MARINOS, NJ BRYANT, JL NOTKINS, AL KLOTMAN, PE TI NEPHROPATHY IN HIV-TRANSGENIC MICE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDR,LDB,BETHESDA,MD 20892. NIDR,LOM,ACU,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 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 MAY PY 1992 VL 8 IS 5 BP 903 EP 903 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300202 ER PT J AU EIDEN, LE RAUSCH, DM KALYANARAMAN, YS BUCK, D HWANG, KM LIFSON, JD BERGER, EA AF EIDEN, LE RAUSCH, DM KALYANARAMAN, YS BUCK, D HWANG, KM LIFSON, JD BERGER, EA TI ROLE OF THE CDR3-LIKE DOMAIN OF CD4 IN HIV-1 INFECTION AND CYTOPATHOGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. BIONET RES INST,ROCKVILLE,MD. BECTON DICKINSON MONOCLONAL CTR INC,MT VIEW,CA. GENELABS INC,REDWOOD CITY,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 906 EP 906 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300211 ER PT J AU SMYTHE, JA NARDELLI, B CHATTERJEE, P GALLO, RC GERSHONI, JM AF SMYTHE, JA NARDELLI, B CHATTERJEE, P GALLO, RC GERSHONI, JM TI LINEAR-POLYMERS OF CD4 AS POLYVALENT MOLECULAR DECOYS FOR HIV GP120 BINDING SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ROCKEFELLER UNIV,NEW YORK,NY 10021. TEL AVIV UNIV,DEPT CELL BIOL,IL-69978 TEL AVIV,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 907 EP 907 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300215 ER PT J AU GERMAIN, RN AF GERMAIN, RN TI ANTIGEN PROCESSING AND PRESENTATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 908 EP 908 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300218 ER PT J AU SAMELSON, LE EGERTON, ML THOMAS, PM SAROSI, GL LANE, HC COHEN, DI AF SAMELSON, LE EGERTON, ML THOMAS, PM SAROSI, GL LANE, HC COHEN, DI TI BIOCHEMICAL ASPECTS OF T-CELL ACTIVATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 908 EP 908 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300219 ER PT J AU NOTKINS, AL AF NOTKINS, AL TI HUMAN MONOCLONAL-ANTIBODIES AND CLONAL ANALYSIS OF THE B-CELL REPERTOIRE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 909 EP 909 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300220 ER PT J AU PASTAN, I AF PASTAN, I TI ONCOTOXINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,DIV CANC BIOL DIAGNOSIS & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 909 EP 909 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300221 ER PT J AU COHEN, DI TIAN, H LANE, HC SAMELSON, LE AF COHEN, DI TIAN, H LANE, HC SAMELSON, LE TI EFFECTS OF HIV-ENVELOPE PROTEIN EXPRESSION ON T-CELL ACTIVATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 910 EP 910 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300225 ER PT J AU WATKINS, BA GALLO, RC REITZ, MS AF WATKINS, BA GALLO, RC REITZ, MS TI THE GENERATION OF COMBINATORIAL HUMAN ANTI-HIV-1 ANTIBODY LIBRARIES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 910 EP 910 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300224 ER PT J AU AGGARWAL, A NASH, TE DIAMOND, LS GALLO, RC FRANCHINI, G AF AGGARWAL, A NASH, TE DIAMOND, LS GALLO, RC FRANCHINI, G TI ENTAMOEBA-HISTOLYTICA AND GIARDIA-LAMBLIA - HUMAN PARASITES AS POTENTIAL CARRIERS OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIAID,LPD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 911 EP 911 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300229 ER PT J AU FAUCI, AS AF FAUCI, AS TI PHARMACOLOGICAL REGULATION OF HIV EXPRESSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 913 EP 913 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300233 ER PT J AU MANN, D GOEDERT, JJ ODONNELL, M MILLER, T CARRINGTON, M AF MANN, D GOEDERT, JJ ODONNELL, M MILLER, T CARRINGTON, M TI HLA GENES GENE-PRODUCTS INFLUENCE RATE OF DISEASE PROGRESSION AND OUT COME IN HIV-1 INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,PRI DYNCORP,IMMUNOGENET SECT,BETHESDA,MD 20892. NCI,PRI DYNCORP,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 914 EP 914 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300239 ER PT J AU SHEARER, GM CLERICI, M TACKET, CO GIORGI, JV BERZOFSKY, JA AF SHEARER, GM CLERICI, M TACKET, CO GIORGI, JV BERZOFSKY, JA TI DOES TH1 - TH2 CROSS-REGULATION PLAY A ROLE IN IMMUNE PROTECTION AND SUSCEPTIBILITY TO AIDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV MARYLAND,BALTIMORE,MD 21201. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 914 EP 914 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300238 ER PT J AU AOKISEI, S KLEINER, DE CHANDRA, R YARCHOAN, R HUSSON, R PIZZO, PA BRODER, S MITSUYA, H AF AOKISEI, S KLEINER, DE CHANDRA, R YARCHOAN, R HUSSON, R PIZZO, PA BRODER, S MITSUYA, H TI QUANTITATIVE-ANALYSIS OF HIV-1 DNA AND RNA IN VARIOUS TISSUES FROM PATIENTS WITH AIDS OR ARC BY POLYMERASE CHAIN-REACTION (PCR) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CLIN CTR,BETHESDA,MD. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 915 EP 915 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300243 ER PT J AU GRAZIOSI, C PANTALEO, G BUTINI, L SCHNITTMAN, S PIZZO, P KOTLER, DP FAUCI, AS AF GRAZIOSI, C PANTALEO, G BUTINI, L SCHNITTMAN, S PIZZO, P KOTLER, DP FAUCI, AS TI HEAVY VIRAL BURDEN IN THE LYMPHOID ORGANS OF HIV INFECTED PATIENTS IN THE EARLY STAGES OF DISEASE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. ST LUKES ROOSEVELT HOSP,NEW YORK,NY 10025. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 915 EP 915 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300241 ER PT J AU LUSSO, P BALOTTA, C VERONESE, FD LORI, F PAL, R GALLO, RC REITZ, MS AF LUSSO, P BALOTTA, C VERONESE, FD LORI, F PAL, R GALLO, RC REITZ, MS TI A HUMAN CD4+ B-CELL LINE SUSCEPTIBLE TO A PURELY MACROPHAGE-TROPIC HIV-1 ISOLATE (HIV-1BAL-PHI) - LACK OF CYTOPATHIC EFFECT, CD4 DOWN-REGULATION AND RECEPTOR INTERFERENCE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,DCB,KENSINGTON,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 916 EP 916 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300245 ER PT J AU KLOTMAN, ME WEEKS, BS KLEINMAN, HK YAMADA, KM KLOTMAN, PE AF KLOTMAN, ME WEEKS, BS KLEINMAN, HK YAMADA, KM KLOTMAN, PE TI ACUTE HIV-1 INFECTION OF PRIMARY LYMPHOCYTES AND CELL-LINES IS ASSOCIATED WITH INCREASED EXPRESSION OF INTEGRINS INVOLVED IN BINDING TO FIBRONECTIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 917 EP 917 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300248 ER PT J AU PANTALEO, G BUTINI, L GRAZIOSI, C POLI, G FAUCI, AS AF PANTALEO, G BUTINI, L GRAZIOSI, C POLI, G FAUCI, AS TI HIV MEDIATED SYNCYTIA FORMATION IS AN LFA-1-DEPENDENT BUT ICAM-1/ICAM-2-INDEPENDENT PHENOMENON SO AIDS RESEARCH AND HUMAN RETROVIRUSES 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 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 MAY PY 1992 VL 8 IS 5 BP 917 EP 917 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300250 ER PT J AU STANLEY, SK KESSLER, SW JUSTEMENT, JS SCHNITTMAN, SM GREENHOUSE, JJ BROWN, CC MUSONGELA, L FAUCI, AS AF STANLEY, SK KESSLER, SW JUSTEMENT, JS SCHNITTMAN, SM GREENHOUSE, JJ BROWN, CC MUSONGELA, L FAUCI, AS TI CD34+ BONE-MARROW CELLS ARE INFECTED WITH HIV IN A SUBSET OF SEROPOSITIVE INDIVIDUALS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. USN,MED RES INST,BETHESDA,MD 20814. MAMA YEMO HOSP,KINSHASA,ZAIRE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 917 EP 917 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300249 ER PT J AU GOLDING, H DIMITROV, D BLUMENTHAL, R AF GOLDING, H DIMITROV, D BLUMENTHAL, R TI LFA-1 ADHESION MOLECULE IS INVOLVED IN HIV-1 ENV-MEDIATED SYNCYTIA FORMATION BUT NOT IN EARLY STAGES OF CELL-FUSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 US FDA,DIV VIROL,BETHESDA,MD 20014. NCI,LMMB,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 918 EP 918 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300251 ER PT J AU POLI, G BISWAS, P KINTER, AL JUSTEMENT, JS ORENSTEIN, JM FAUCI, AS AF POLI, G BISWAS, P KINTER, AL JUSTEMENT, JS ORENSTEIN, JM FAUCI, AS TI DIFFERENTIAL ROLES OF INTERFERONS AS MODULATORS OF HIV EXPRESSION IN CHRONICALLY INFECTED-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20052. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 919 EP 919 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300257 ER PT J AU GESSAIN, A YANAGIHARA, R GAJDUSEK, C GALLO, RC FRANCHINI, G AF GESSAIN, A YANAGIHARA, R GAJDUSEK, C GALLO, RC FRANCHINI, G TI MOLECULAR EPIDEMIOLOGY OF HTLV-I IN THE WORLD - IDENTIFICATION OF NOVEL HTLV-I VARIANTS IN AFRICA AND MELANESIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NINCDS,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 923 EP 923 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300271 ER PT J AU RAUSCH, DM LENDVAY, J SHARER, LR REHM, S WARD, J HEYES, M EIDEN, LE MURRAY, EA AF RAUSCH, DM LENDVAY, J SHARER, LR REHM, S WARD, J HEYES, M EIDEN, LE MURRAY, EA TI SIVSMMB670 INFECTION OF RHESUS MACAQUES CAUSES COGNITIVE AND MOTOR DEFICITS REMINISCENT OF CNS DYSFUNCTION IN HUMAN AIDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. FREDERICK CANC RES & DEV CTR,FREDERICK,MD. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,NEWARK,NJ 07103. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 923 EP 923 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300272 ER PT J AU BERNEMAN, ZN GARTENHAUS, RB REITZ, MS GALLO, RC KLOTMAN, ME AF BERNEMAN, ZN GARTENHAUS, RB REITZ, MS GALLO, RC KLOTMAN, ME TI HTLV-I MESSENGER-RNA IS EXPRESSED AND ALTERNATIVELY SPLICED IN ADULT T-CELL LEUKEMIA/LYMPHOMA (ATL) AND IN HEALTHY CARRIERS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 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 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 MAY PY 1992 VL 8 IS 5 BP 925 EP 925 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300278 ER PT J AU LINDHOLM, PF BRADY, JN AF LINDHOLM, PF BRADY, JN TI EXTRACELLULAR TAX, PROTEIN STIMULATION OF IMMUNOGLOBULIN KAPPA LIGHT CHAIN (IGK) AND TUMOR NECROSIS FACTOR-BETA (TNF-BETA) GENES IN LYMPHOID-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 925 EP 925 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300275 ER PT J AU WALDMANN, TA AF WALDMANN, TA TI THE MULTISUBUNIT IL-2 RECEPTOR - A TARGET FOR IMMUNOTHERAPY IN PATIENTS WITH HTLV-I-ASSOCIATED LEUKEMIA LYMPHOMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 925 EP 925 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300277 ER PT J AU FELBER, BK CIMINALE, V UNGE, T SOLOMIN, L CUNNINGHAM, CP MELLINI, M DERSE, D PAVLAKIS, GN AF FELBER, BK CIMINALE, V UNGE, T SOLOMIN, L CUNNINGHAM, CP MELLINI, M DERSE, D PAVLAKIS, GN TI GENOME ORGANIZATION AND REGULATION OF EXPRESSION OF HTLV-1 BY REX SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,HUMAN RETROVIRUS PATHOGENESIS GRP,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 926 EP 926 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300279 ER PT J AU KORALNIK, IJ GESSAIN, A KLOTMAN, M BERNEMAN, ZN FRANCHINI, G AF KORALNIK, IJ GESSAIN, A KLOTMAN, M BERNEMAN, ZN FRANCHINI, G TI ALTERNATIVE SPLICING ENABLES THE PROCESSING OF MESSENGER-RNAS FOR THE HTLV-I OPEN READING FRAMES-I AND FRAMES-II SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 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 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 MAY PY 1992 VL 8 IS 5 BP 926 EP 926 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300281 ER PT J AU KORALNIK, IJ GESSAIN, A HIRSH, V LOMONICO, A GUO, HG KALYANARAMAN, VS SAXINGER, C GALLO, RC FRANCHINI, G AF KORALNIK, IJ GESSAIN, A HIRSH, V LOMONICO, A GUO, HG KALYANARAMAN, VS SAXINGER, C GALLO, RC FRANCHINI, G TI STLVS AND HTLVS GENETIC-RELATIONSHIPS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20007. ABL,KENSINGTON,MD. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 926 EP 926 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300280 ER PT J AU MARRIOTT, SJ BRADY, JN AF MARRIOTT, SJ BRADY, JN TI EXTRACELLULAR HTLV-I TAX, ACTIVATES EXPRESSION OF THE INTERLEUKIN-2 RECEPTOR IN PRIMARY HUMAN-LYMPHOCYTES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 926 EP 926 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300282 ER PT J AU GARTENHAUS, RB LUNARDIISKANDER, Y BERNEMAN, Z REITZ, M GALLO, RC KLOTMAN, ME AF GARTENHAUS, RB LUNARDIISKANDER, Y BERNEMAN, Z REITZ, M GALLO, RC KLOTMAN, ME TI INVITRO EFFECTS OF SOLUBLE RECOMBINANT TAX PROTEIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 927 EP 927 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300283 ER PT J AU LUNARDIISKANDAR, Y GESSAIN, A LAM, HH GALLO, RC AF LUNARDIISKANDAR, Y GESSAIN, A LAM, HH GALLO, RC TI ABNORMAL INVITRO PROLIFERATION AND DIFFERENTIATION OF T-CELL COLONY-FORMING CELLS (T-CFC) IN PATIENTS WITH TROPICAL SPASTIC PARAPARESIS/HTLV-I-ASSOCIATED MYELOPATHY (TSP/HAM) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 927 EP 927 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300285 ER PT J AU MUKHOPADHYAYA, R GESSAIN, A RODGERSJOHNSON, P GIBBS, CJ GALLO, RC SADAIE, MR AF MUKHOPADHYAYA, R GESSAIN, A RODGERSJOHNSON, P GIBBS, CJ GALLO, RC SADAIE, MR TI PRODUCTION OF IL-6 AND TNF-ALPHA BY HTLV-I TRANSFORMED-CELL LINES DO NOT DISCRIMINATE BETWEEN TSP/HAM AND ATL ISOLATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NINCDS,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. TATA CANC RES INST,BOMBAY,INDIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 927 EP 927 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300286 ER PT J AU KULAGA, H COGGIANO, M TRUCKENMILLER, ME RONNETT, G SYNDER, SH WYATT, R SWEETNAM, P AF KULAGA, H COGGIANO, M TRUCKENMILLER, ME RONNETT, G SYNDER, SH WYATT, R SWEETNAM, P TI HIV-1 INFECTION OF THE CENTRAL-NERVOUS-SYSTEM - CHARACTERIZATION USING A HUMAN CORTICAL NEURONAL CELL-LINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIMH,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. NOVA PHARMACEUT CORP,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 929 EP 929 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300292 ER PT J AU BLATTNER, WA AF BLATTNER, WA TI HUMAN RETROVIRUSES IN CANCER AND EPIDEMIOLOGIC PROSPECTIVE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 930 EP 930 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300293 ER PT J AU GOEDERT, JJ DULIEGE, AM AMOS, CI AF GOEDERT, JJ DULIEGE, AM AMOS, CI TI THE INTERNATIONAL REGISTRY OF HIV-EXPOSED TWINS - A 1ST REPORT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TWINS REGISTRY GRP,BETHESDA,MD 20892. GENENTECH INC,S SAN FRANCISCO,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 930 EP 930 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300294 ER PT J AU MASUR, H AF MASUR, H TI NEW ADVANCES IN THE MANAGEMENT OF AIDS ASSOCIATED OPPORTUNISTIC INFECTIONS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,CTR CLIN,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 930 EP 930 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300295 ER PT J AU BIGGAR, RJ MALONEY, E NEEL, JV BLATTNER, WA AF BIGGAR, RJ MALONEY, E NEEL, JV BLATTNER, WA TI HTLV-II IS A NEW-WORLD VIRUS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 MAY PY 1992 VL 8 IS 5 BP 931 EP 931 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300300 ER PT J AU TAKAHASHI, H HALL, WW KAPLAN, MH LIU, CR SCHNEEWIND, O CORONESI, M NAGASHIMA, K GALLO, RC AF TAKAHASHI, H HALL, WW KAPLAN, MH LIU, CR SCHNEEWIND, O CORONESI, M NAGASHIMA, K GALLO, RC TI MULTIPLE ISOLATES AND CHARACTERISTICS OF HUMAN T-CELL LEUKEMIA-VIRUS, TYPE-II (HTLV-II) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CORNELL UNIV,N SHORE UNIV HOSP,COLL MED,MANHASSET,NY 11030. ROCKEFELLER UNIV,NEW YORK,NY 10021. HOKKAIDO UNIV,SAPPORO,HOKKAIDO 060,JAPAN. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 932 EP 932 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300303 ER PT J AU RABKIN, CS HIRA, S PALEFSKY, J BIGGAR, R AF RABKIN, CS HIRA, S PALEFSKY, J BIGGAR, R TI HUMAN PAPILLOMAVIRUS, HIV, AND CERVICAL DYSPLASIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV TEACHING HOSP,LUSAKA,SENEGAMBIA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 934 EP 934 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300312 ER PT J AU MADELEINE, MM WIKTOR, SZ GOEDERT, JJ BLATTNER, WA AF MADELEINE, MM WIKTOR, SZ GOEDERT, JJ BLATTNER, WA TI WORLDWIDE DISTRIBUTION OF HTLV-I IMMUNOBLOT REACTIVITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL SECT,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 935 EP 935 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300314 ER PT J AU WEINHOLD, KJ FERRARI, G ARTHUR, LO AF WEINHOLD, KJ FERRARI, G ARTHUR, LO TI COMPARISON OF CELLULAR ANTIVIRAL CYTOTOXICITIES PRESENT IN HIV-1 INFECTED HUMANS AND CHIMPANZEES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. UNIV GENOA,IST MICROBIOL,I-16126 GENOA,ITALY. NCI,FREDERICK CANC & RES DEV CTR,PRI DYNCORP,FREDERICK,MD 21701. RI Ferrari, Guido/A-6088-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 938 EP 938 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300326 ER PT J AU GOLDSTEIN, AL NAYLOR, PH SARIN, PS OTOOLE, C KIRKLEY, JE RIOS, A ZAGURY, D ACHOUR, A GAZZARD, B GIBBS, CJ YOULE, M AF GOLDSTEIN, AL NAYLOR, PH SARIN, PS OTOOLE, C KIRKLEY, JE RIOS, A ZAGURY, D ACHOUR, A GAZZARD, B GIBBS, CJ YOULE, M TI PROGRESS IN THE DEVELOPMENT OF A P17 BASED HIV VACCINE - SAFETY AND POTENTIAL EFFICACY OF THE HGP-30 SYNTHETIC PEPTIDE VACCINE IN HUMANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NIH,BETHESDA,MD 20892. SW MEM HOSP,HOUSTON,TX. UNIV LONDON,LONDON,ENGLAND. ST STEPHENS HOSP,LONDON SW10 9TH,ENGLAND. MARIE & PIERRE CURIE INST PASTEUR,PARIS,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 939 EP 939 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300328 ER PT J AU MONTEFIORI, DC JOHNSON, PR AF MONTEFIORI, DC JOHNSON, PR TI COMPLEMENT-MEDIATED, INFECTION-ENHANCING ANTIBODIES IN HIV AND SIV INFECTION AND VACCINE TRIALS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 VANDERBILT UNIV,MED CTR,SCH MED,NASHVILLE,TN 37232. GEORGETOWN UNIV,WASHINGTON,DC 20007. NIAID,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 940 EP 940 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300331 ER PT J AU LAYNE, SP MERGES, MJ DEMBO, M SPOUGE, JL NARA, PL AF LAYNE, SP MERGES, MJ DEMBO, M SPOUGE, JL NARA, PL TI RELATIONSHIPS BETWEEN ENVELOPE SHEDDING, CELL-DENSITY AND HUMORAL BLOCKING ACTIVITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 LOS ALAMOS NATL LAB,LOS ALAMOS,NM 87544. NCI,FREDERICK,MD 21701. NATL LIB MED,BETHESDA,MD 20209. RI Dembo, Micah/C-2755-2013 NR 0 TC 0 Z9 0 U1 0 U2 2 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 MAY PY 1992 VL 8 IS 5 BP 941 EP 941 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300335 ER PT J AU SPOUGE, JL NARA, PL LAYNE, SP AF SPOUGE, JL NARA, PL LAYNE, SP TI VACMAN - A PRACTICAL COMPUTER-PROGRAM FOR ANALYZING VIRAL INFECTIVITY ASSAYS AND VACCINE TRIALS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NATL LIB MED,BETHESDA,MD 20209. NCI,LTCB,FREDERICK,MD 21702. LOS ALAMOS NATL LAB,BIOPHYS GRP,LOS ALAMOS,NM 87544. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 941 EP 941 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300334 ER PT J AU AGGARWAL, A SADOFF, J MARKHAM, P GARD, E FUERST, T GALLO, RC FRANCHINI, G AF AGGARWAL, A SADOFF, J MARKHAM, P GARD, E FUERST, T GALLO, RC FRANCHINI, G TI HIV-2 RECOMBINANT VACCINES INDUCE CD8+ SPECIFIC CYTOTOXIC LYMPHOCYTES-T IN RODENTS AND PRIMATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. ADV BIOTECHNOL LABS,KENSINGTON,MD. MEDIMMUNE,GAITHERSBURG,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 942 EP 942 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300338 ER PT J AU SADOFF, J AGGARWAL, A BARON, L HONG, H ELSINGHORST, E LANAR, D WARREN, R AF SADOFF, J AGGARWAL, A BARON, L HONG, H ELSINGHORST, E LANAR, D WARREN, R TI LIVE ORAL RECOMBINANT SALMONELLA CARRIER VACCINES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. NIH,BETHESDA,MD 20892. RI Lanar, David/B-3560-2011 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 942 EP 942 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300336 ER PT J AU BLAY, R BETTS, M CLERICI, M HOFFMAN, T GOLDING, B AF BLAY, R BETTS, M CLERICI, M HOFFMAN, T GOLDING, B TI BRUCELLA-ABORTUS IS CAPABLE OF STIMULATING HUMAN T-CELLS FROM NONINFECTED AND HIV-1 INFECTED INDIVIDUALS TO SECRETE INTERFERON-GAMMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 US FDA,CBER,DIV HEMATOL CELL BIOL LAB,BETHESDA,MD 20014. NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 944 EP 944 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300346 ER PT J AU BERZOFSKY, JA PENDLETON, CD CLERICI, M AHLERS, J LUCEY, DR PUTNEY, SD SHEARER, GM AF BERZOFSKY, JA PENDLETON, CD CLERICI, M AHLERS, J LUCEY, DR PUTNEY, SD SHEARER, GM TI PROMISCUOUS HIV-1 HELPER T-CELL PEPTIDES FOR MURINE AND HUMAN MHC MOLECULES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 945 EP 945 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300347 ER PT J AU NARA, P GARRITY, R MINASSIAN, A GOUDSMIT, J AF NARA, P GARRITY, R MINASSIAN, A GOUDSMIT, J TI BINDING OF V3-SPECIFIC MOABS DOES NOT ALWAYS CORRELATE WITH NEUTRALIZATION - IMPLICATIONS TO HUMORAL VACCINE DESIGN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. HUMAN RETROVIRUS LAB,AMSTERDAM,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 945 EP 945 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300350 ER PT J AU PAUL, JR TROCHA, A EARL, P MOSS, B BUCHANAN, TM WALKER, BD AF PAUL, JR TROCHA, A EARL, P MOSS, B BUCHANAN, TM WALKER, BD TI EFFECTS OF GAG AND ENVELOPE SEQUENCE VARIATION ON EPITOPE RECOGNITION BY HIV-1-SPECIFIC CYTOTOXIC LYMPHOCYTE-T CLONES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NIAID,BETHESDA,MD 20892. UNIV WASHINGTON,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 945 EP 945 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300349 ER PT J AU ROBERTGUROFF, M ALDRICH, K MULDOON, R STERN, T VERONESE, FD MARKHAM, P BONSAL, G FUERST, T PAOLETTI, E MATTHEWS, T GALLO, RC FRANCHINI, G AF ROBERTGUROFF, M ALDRICH, K MULDOON, R STERN, T VERONESE, FD MARKHAM, P BONSAL, G FUERST, T PAOLETTI, E MATTHEWS, T GALLO, RC FRANCHINI, G TI CROSS-NEUTRALIZATION OF HIV-1, HIV-2, AND SIV ISOLATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. ADV BIOSCI LABS,KENSINGTON,MD. MEDIMMUNE INC,GAITHERSBURG,MD. VIROGENET CORP,TROY,NY. DUKE UNIV,DURHAM,NC 27706. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 945 EP 945 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300348 ER PT J AU GOUDSMIT, J BAKKER, M MELOEN, R DEWOLF, F THIRIART, C BRUCK, C NARA, P MCENTEE, M NARAYAN, O HEENEY, J AF GOUDSMIT, J BAKKER, M MELOEN, R DEWOLF, F THIRIART, C BRUCK, C NARA, P MCENTEE, M NARAYAN, O HEENEY, J TI CHARACTERIZATION OF TYPE-SPECIFIC ANTIBODY-RESPONSES TO THE V2 NEUTRALIZATION DOMAIN OF SIVMAC251 DURING SERIAL SIVMAC251 AND SIVDELTAB670 INVIVO PASSAGE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV AMSTERDAM,HUMAN RETROVIRUS LAB,AMSTERDAM,NETHERLANDS. NETHERLANDS RED CROSS,BLOOD TRANSFUS SERV,CENT LAB,AMSTERDAM,NETHERLANDS. SMITHKLINE BEECHAM,RIXENSART,BELGIUM. NCI,FREDERICK CANC RES FACIL,FREDERICK,MD 21701. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. TNO,ITRI,VIRAL PATHOGENESIS LAB,2280 HV RIJSWIJK,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 946 EP 946 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300352 ER PT J AU PINCUS, SH MESSER, K AF PINCUS, SH MESSER, K TI HUMORAL IMMUNE-RESPONSE TO HOMOLOGOUS ENVELOPE PEPTIDES IN LAB WORKERS INFECTED WITH HIV SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 946 EP 946 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300353 ER PT J AU VERONESE, FD LUSSO, P ROBERTGUROFF, M LORI, F BOYER, C REITZ, M GALLO, RC AF VERONESE, FD LUSSO, P ROBERTGUROFF, M LORI, F BOYER, C REITZ, M GALLO, RC TI A SINGLE MUTATION IN THE V3 LOOP OF HIV-1(IIIB) ABOLISHES RECOGNITION OF GP120 AND INHIBITION OF SYNCYTIUM FORMATION BY A MONOCLONAL-ANTIBODY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ADV BIOSCI LABS INC,KENSINGTON,MD. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 947 EP 947 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300358 ER PT J AU WATSON, PM NIGIDA, SM ARTHUR, LO AF WATSON, PM NIGIDA, SM ARTHUR, LO TI MURINE MONOCLONAL-ANTIBODIES RECOGNIZING HIV-1 GAG PRODUCTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 948 EP 948 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300362 ER PT J AU ARYA, SK SADAIE, MR AF ARYA, SK SADAIE, MR TI HIV-2 FUSOGENICITY AND CYTOPATHICITY - ANALYSIS WITH CHIMERIC PROVIRUSES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 949 EP 949 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300365 ER PT J AU REITZ, MS LORI, F HALL, L MICHAELS, F LUSSO, P MARKHAM, P POPOVIC, M GALLO, RC AF REITZ, MS LORI, F HALL, L MICHAELS, F LUSSO, P MARKHAM, P POPOVIC, M GALLO, RC TI CHARACTERIZATION OF MACROPHAGE-COMPETENT BIOLOGICALLY-ACTIVE MOLECULAR CLONES OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,LTCB,BETHESDA,MD 20892. ADV BIOSCI LAB,KENSINGTON,MD 20895. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 949 EP 949 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300363 ER PT J AU LAUTENBERGER, JA STEPHENS, JC OBRIEN, SJ AF LAUTENBERGER, JA STEPHENS, JC OBRIEN, SJ TI PHYLOGENETIC ANALYSIS OF HIV-1 SEQUENCES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 950 EP 950 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300368 ER PT J AU NIGIDA, SM SMITH, CH ARTHUR, LO AF NIGIDA, SM SMITH, CH ARTHUR, LO TI PROPERTIES OF CLONED H9/HIV-1(MN) CELL-LINES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 950 EP 950 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300370 ER PT J AU BALOTTA, C LUSSO, P COCCHI, F GALLO, RC REITZ, MS AF BALOTTA, C LUSSO, P COCCHI, F GALLO, RC REITZ, MS TI BIOLOGICAL PROPERTIES OF ENVELOPE CHIMERIC CONSTRUCTS OF HIV-1(BAL) AND HIV-1(HXB2) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,LTCB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 951 EP 951 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300372 ER PT J AU BOERI, E FERRO, A SABBATANI, S VARNIER, O GUROFF, MR VERANI, P DIMARZO, F GALLO, RC FRANCHINI, G AF BOERI, E FERRO, A SABBATANI, S VARNIER, O GUROFF, MR VERANI, P DIMARZO, F GALLO, RC FRANCHINI, G TI GENETIC-VARIABILITY OF THE IMMUNODOMINANT V3-LOOP EPITOPE OF HIV-2 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,LTCB,BETHESDA,MD 20892. UNIV BOLOGNA,I-40126 BOLOGNA,ITALY. INST MICROBIOL,GENEVA,SWITZERLAND. IST SUPER SANITA,I-00161 ROME,ITALY. ADV BIOSCI LAB,KENSINGTON,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 951 EP 951 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300373 ER PT J AU WATERS, DJ WILSON, C MILEY, W ARTHUR, L BLATTNER, W REITZ, M AF WATERS, DJ WILSON, C MILEY, W ARTHUR, L BLATTNER, W REITZ, M TI AN ADHERENT CELL, NONISOTOPIC, TRANSACTIVATION-BASED ASSAY FOR THE DETECTION AND TITRATION OF INFECTIOUS HIV-1 AND HIV-2 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD 21701. NCI,BETHESDA,MD 20892. NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 951 EP 951 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300371 ER PT J AU COHEN, SG AF COHEN, SG TI ASTHMA IN ANTIQUITY - THE EBERS PAPYRUS SO ALLERGY PROCEEDINGS LA English DT Article RP COHEN, SG (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 0 TC 8 Z9 8 U1 0 U2 5 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 SN 1046-9354 J9 ALLERGY PROC JI Allergy Proc. PD MAY-JUN PY 1992 VL 13 IS 3 BP 147 EP 154 DI 10.2500/108854192778878746 PG 8 WC Allergy SC Allergy GA JB229 UT WOS:A1992JB22900008 PM 1505756 ER PT J AU LENFANT, C FULWOOD, R AF LENFANT, C FULWOOD, R TI NEW DIRECTIONS FOR ASTHMA MANAGEMENT IN THE 1990S SO AMERICAN FAMILY PHYSICIAN LA English DT Editorial Material RP LENFANT, C (reprint author), NHLBI,NATL ASTHMA EDUC PROGRAM,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD MAY PY 1992 VL 45 IS 5 BP 2027 EP 2028 PG 2 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA HU008 UT WOS:A1992HU00800008 PM 1575104 ER PT J AU LAUER, RM BARNESS, LA CLARK, R DECKELBAUM, RJ FINBERG, L KWITEROVICH, PO MCBRIDE, PE SCHIEKEN, RM SCOTT, LW STRONG, JP WEIDMAN, WH ZIEGLER, EE CLEEMAN, JI ERNST, N HARLAN, WR RIFKIND, B ROSSOUW, JE QUINTADLER, L MCNEIL, CT AF LAUER, RM BARNESS, LA CLARK, R DECKELBAUM, RJ FINBERG, L KWITEROVICH, PO MCBRIDE, PE SCHIEKEN, RM SCOTT, LW STRONG, JP WEIDMAN, WH ZIEGLER, EE CLEEMAN, JI ERNST, N HARLAN, WR RIFKIND, B ROSSOUW, JE QUINTADLER, L MCNEIL, CT TI HIGHLIGHTS OF THE REPORT OF THE EXPERT PANEL ON BLOOD CHOLESTEROL LEVELS IN CHILDREN AND ADOLESCENTS SO AMERICAN FAMILY PHYSICIAN LA English DT Article RP LAUER, RM (reprint author), NHLBI,NATL CHOLESTEROL EDUC PROGRAM,9000 ROCKVILLE PIKE,BLDG 3,ROOM 4A05,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD MAY PY 1992 VL 45 IS 5 BP 2127 EP 2136 PG 10 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA HU008 UT WOS:A1992HU00800013 ER PT J AU GONZALES, JJ STERN, TA EMMERICH, AD RAUCH, SL AF GONZALES, JJ STERN, TA EMMERICH, AD RAUCH, SL TI RECOGNITION AND MANAGEMENT OF BENZODIAZEPINE DEPENDENCE SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Primary care physicians prescribe the majority of benzodiazepines and thus may see most patients who are dependent on these drugs. The diagnosis of benzodiazepine misuse is based on the history, the physical examination and drug use patterns. The treatment of benzodiazepine misuse can be a challenging process that requires the physician's patience, caution and sound clinical judgement. Patients who misuse benzodiazepines may have coexisting psychiatric problems that require treatment, such as depression or panic disorder. Family physicians can manage these patients but should be prepared to refer them for hospitalization when habituation and withdrawal reactions are complicated by medical instability, noncompliance or clinical deterioration. RP GONZALES, JJ (reprint author), NIMH,ROCKVILLE,MD 20857, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD MAY PY 1992 VL 45 IS 5 BP 2269 EP 2276 PG 8 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA HU008 UT WOS:A1992HU00800026 PM 1575121 ER PT J AU LIANG, CS STEWART, DK LEJEMTEL, TH KIRLIN, PC MCINTYRE, KM ROBERTSON, HT BROWN, R MOORE, AW WELLINGTON, KL CAHILL, L GALVAO, M WOODS, PA GARCES, C HELD, P AF LIANG, CS STEWART, DK LEJEMTEL, TH KIRLIN, PC MCINTYRE, KM ROBERTSON, HT BROWN, R MOORE, AW WELLINGTON, KL CAHILL, L GALVAO, M WOODS, PA GARCES, C HELD, P TI CHARACTERISTICS OF PEAK AEROBIC CAPACITY IN SYMPTOMATIC AND ASYMPTOMATIC SUBJECTS WITH LEFT-VENTRICULAR DYSFUNCTION SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID CONGESTIVE-HEART-FAILURE; EXERCISE CAPACITY; ANAEROBIC THRESHOLD; EJECTION FRACTION; WOMEN; AGE AB Expired gas analysis was used to determine the aerobic exercise performance of subjects with depressed left ventricular (LV) systolic function and congestive heart failure (CHF). To determine whether subjects with no or minimal CHF have better aerobic exercise performance than do those with overt CHF, oxygen consumption (VO2) at anaerobic threshold (AT) and peak exercise was measured in 184 subjects with LV ejection fraction less-than-or-equal-to 0.35 who participated in the Studies of Left Ventricular Dysfunction. Subjects were divided into those with overt CHF needing treatment (treatment trial; n = 20) and those who had neither overt CHF nor treatment for CHF (prevention trial; n = 164). Treatment trial subjects had a lower LV ejection fraction (0.25 +/- 0.07) than did prevention trial ones (0.29 +/- 0.05; p = 0.001), but there were no differences in age, gender, body weight, resting heart rate and blood pressure. Treadmill exercise testing was performed after 2 to 3 weeks of placebo (no angiotensin-converting enzyme inhibitor) treatment. Treatment trial subjects exercised for a shorter time (493 +/- 160 seconds) and attained a lower peak VO2 (13 +/- 4 ml/kg/min) and VO2 at AT (11 +/- 4 ml/kg/min) than did prevention trial ones (842 +/- 277 seconds, and 20 +/- 6 and 16 +/- 5 ml/kg/min, respectively). Analysis of covariance showed that the differences in peak VO2 and VO2 at AT were statistically significant between the 2 trials after adjusting for age, gender, LV ejection fraction and New York Heart Association functional class. In contrast, there was no correlation between the expired gas measurements and LV ejection fraction or New York Heart Association classification after adjusting for other factors. Thus, it is concluded that of subjects with reduced LV ejection fraction, those with no or minimal CHF have higher aerobic exercise performance than do those with overt CHF, and this difference cannot be explained by gender, age, LV ejection fraction or New York Heart Association functional class. C1 UNIV WASHINGTON,MED CTR,SEATTLE,WA 98195. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. MICHIGAN STATE UNIV,E LANSING,MI 48824. VET AFFAIRS MED CTR,BOSTON,MA. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV N CAROLINA,CHAPEL HILL,NC 27514. NHLBI,CLIN TRIALS BRANCH,BETHESDA,MD 20892. RP LIANG, CS (reprint author), UNIV ROCHESTER,MED CTR,CARDIOL UNIT,BOX 679,601 ELMWOOD AVE,ROCHESTER,NY 14642, USA. NR 24 TC 23 Z9 24 U1 1 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAY 1 PY 1992 VL 69 IS 14 BP 1207 EP 1211 DI 10.1016/0002-9149(92)90937-T PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HQ723 UT WOS:A1992HQ72300016 PM 1575192 ER PT J AU SPIRITO, P LAKATOS, E MARON, BJ AF SPIRITO, P LAKATOS, E MARON, BJ TI DEGREE OF LEFT-VENTRICULAR HYPERTROPHY IN PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY AND CHRONIC ATRIAL-FIBRILLATION SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID SUBAORTIC STENOSIS; EXTENT; ABNORMALITIES; PROGRESSION; PROGNOSIS; GRADIENT AB It has been generally assumed that most patients with hypertrophic cardiomyopathy (HC) who develop atrial fibrillation (AF) have marked left ventricular (LV) hypertrophy and subaortic obstruction. The morphologic and functional features of this subset of patients with HC have not been systematically investigated. The LV morphology and functional profile of 46 patients with HC and chronic AF were compared with those of 81 control patients with HC and normal sinus rhythm. Contrary to expectations, LV hypertrophy (assessed with 2-dimensional echocardiography) was substantially less marked in the patients with AF than in the control patients, and prevalence of subaortic obstruction was similar in the 2 groups. Maximal LV wall thickness and wall thickness index were lower in patients with AF (18 +/- 2 and 56 +/- 7 mm, respectively) than in control patients (22 +/- 6 and 67 +/- 16 mm, respectively; p < 0.001). Furthermore, mild LV hypertrophy (maximal LV wall thickness less-than-or-equal-to 17 mm confined to 1 ventricular segment) was almost twice as frequent in patients with AF (63%) than in control patients (36%; p < 0.005). Subaortic obstruction was present in 9 patients with AF (20%) and in 28 control patients (35%; p > 0.05). In a subgroup of 22 patients with AF who were followed for 4 to 10 years, 5 patients had marked LV wall thinning (greater-than-or-equal-to 5 mm, range 5 to 14). In conclusion, these results demonstrate that most patients with HC and chronic AF have the nonobstructive form of HC, and relatively mild LV hypertrophy. In many of these patients, progressive LV wall thinning is probably responsible for the mild LV hypertrophy. C1 NHLBI,BIOSTAT RES BRANCH,BETHESDA,MD 20892. NHLBI,CARDIOL BRANCH,ECHOCARDIOG LAB,BETHESDA,MD 20892. RP SPIRITO, P (reprint author), ENTE OSPED OSPEDALI GALLIERA,DIV CARDIOL,VIA VOLTA 8,I-16128 GENOA,ITALY. NR 26 TC 29 Z9 29 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAY 1 PY 1992 VL 69 IS 14 BP 1217 EP 1222 DI 10.1016/0002-9149(92)90939-V PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HQ723 UT WOS:A1992HQ72300018 PM 1533490 ER PT J AU SLATTERY, ML MCDONALD, A BILD, DE CAAN, BJ HILNER, JE JACOBS, DR LIU, K AF SLATTERY, ML MCDONALD, A BILD, DE CAAN, BJ HILNER, JE JACOBS, DR LIU, K TI ASSOCIATIONS OF BODY-FAT AND ITS DISTRIBUTION WITH DIETARY-INTAKE, PHYSICAL-ACTIVITY, ALCOHOL, AND SMOKING IN BLACKS AND WHITES SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE ALCOHOL; BODY FAT; CIGARETTE SMOKING; DIETARY INTAKE; PHYSICAL ACTIVITY ID CIGARETTE-SMOKING; CARBOHYDRATE; ADIPOSITY; EXERCISE; OBESITY; BALANCE; WEIGHT; RISK; SEX AB Cross-sectional associations between body fat and its distribution and environmental factors influencing energy balance were examined in 5115 young adults. Protein was directly associated with body mass index (BMI) in all race and sex groups (P < 0.01) after age, education, cigarette-smoking status, alcohol intake, and physical activity were adjusted for. Carbohydrate intake was inversely associated with BMI in males (P = 0.02). Total physical activity was inversely associated with BMI in white women and with skinfold-thickness measures (P < 0.01) in all groups. Waist-to-hip-circumference ratio (WHCR) was positively associated with total kilojoules (kilocalories) in women, inversely associated with percent of kilojoules (kilocalories) from carbohydrates in whites, grams of crude fiber/4184 kJ (1000 kcal) (except in black men), and physical activity (except in white women). WHCR was directly associated with cigarette smoking except in black men, and with total alcohol intake in men. Beer was consistently associated with WHCR in all race and sex groups. C1 UNIV ILLINOIS,DEPT NUTR & MED DIETET,CHICAGO,IL 60680. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. KAISER PERMANENTE MED CARE PROGRAM,DIV RES,NO CALIF REG,OAKLAND,CA. UNIV ALABAMA,CARDIA COORDINATING CTR,BIRMINGHAM,AL 35294. UNIV MINNESOTA,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. NORTHWESTERN UNIV,SCH MED,DEPT COMMUNITY HLTH & PREVENT MED,CHICAGO,IL 60611. RP SLATTERY, ML (reprint author), UNIV UTAH,SCH MED,DEPT FAMILY & PREVENT MED,SALT LAKE CITY,UT 84132, USA. FU NHLBI NIH HHS [N01-HC-48047, N01-HC-48049, N01-HC-48048] NR 36 TC 149 Z9 148 U1 2 U2 7 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 MAY PY 1992 VL 55 IS 5 BP 943 EP 949 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HR468 UT WOS:A1992HR46800005 PM 1570801 ER PT J AU WACHOLDER, S MCLAUGHLIN, JK SILVERMAN, DT MANDEL, JS AF WACHOLDER, S MCLAUGHLIN, JK SILVERMAN, DT MANDEL, JS TI SELECTION OF CONTROLS IN CASE-CONTROL STUDIES .1. PRINCIPLES SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE BIAS (EPIDEMIOLOGY); EPIDEMIOLOGIC METHODS; PROSPECTIVE STUDIES; RETROSPECTIVE STUDIES ID CONTROL DEFINITION; COHORT ANALYSIS; MISCLASSIFICATION; EXPOSURE; CANCER; DESIGN; BIAS; MORTALITY; EFFICACY; ERRORS AB A synthesis of classical and recent thinking on the issues involved in selecting controls for case-control studies is presented in this and two companion papers (S. Wacholder et al. Am J Epidemiol 1992;135:1029-50). In this paper, a theoretical framework for selecting controls in case-control studies is developed. Three principles of comparability are described: 1) study base, that all comparisons be made within the study base; 2) deconfounding, that comparisons of the effects of the levels of exposure on disease risk not be distorted by the effects of other factors; and 3) comparable accuracy, that any errors in measurement of exposure be nondifferential between cases and controls. These principles, if adhered to in a study, can reduce selection, confounding, and information bias, respectively. The principles, however, are constrained by an additional efficiency principle regarding resources and time. Most problems and controversies in control selection reflect trade-offs among these four principles. C1 NCI,BIOSTAT BRANCH,BETHESDA,MD 20892. UNIV MINNESOTA,SCH PUBL HLTH,DEPT ENVIRONM & OCCUPAT HLTH,MINNEAPOLIS,MN 55455. NR 52 TC 475 Z9 485 U1 1 U2 24 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 MAY 1 PY 1992 VL 135 IS 9 BP 1019 EP 1028 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HY092 UT WOS:A1992HY09200008 PM 1595688 ER PT J AU WACHOLDER, S SILVERMAN, DT MCLAUGHLIN, JK MANDEL, JS AF WACHOLDER, S SILVERMAN, DT MCLAUGHLIN, JK MANDEL, JS TI SELECTION OF CONTROLS IN CASE-CONTROL STUDIES .2. TYPES OF CONTROLS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE BIAS (EPIDEMIOLOGY); EPIDEMIOLOGIC METHODS; RETROSPECTIVE STUDIES ID DEAD CONTROLS; RISK-FACTORS; ENDOMETRIAL CANCER; PROXY RESPONDENTS; CHILDHOOD-CANCER; BIAS; POPULATION; RELIABILITY; SMOKING; DISEASE AB Types of control groups are evaluated using the principles described in paper 1 of the series, "Selection of Controls in Case-Control Studies" (S. Wacholder et al. Am J Epidemiol 1992;135:1019-28). Advantages and disadvantages of population controls, neighborhood controls, hospital or registry controls, medical practice controls, friend controls, and relative controls are considered. Problems with the use of deceased controls and proxy respondents are discussed. C1 NCI, BIOSTAT BRANCH, BETHESDA, MD 20892 USA. UNIV MINNESOTA, SCH PUBL HLTH, DEPT ENVIRONM & OCCUPAT HLTH, MINNEAPOLIS, MN 55455 USA. RI Osborne, Nicholas/N-4915-2015 OI Osborne, Nicholas/0000-0002-6700-2284 NR 73 TC 386 Z9 391 U1 1 U2 15 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAY 1 PY 1992 VL 135 IS 9 BP 1029 EP 1041 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HY092 UT WOS:A1992HY09200009 PM 1595689 ER PT J AU WACHOLDER, S SILVERMAN, DT MCLAUGHLIN, JK MANDEL, JS AF WACHOLDER, S SILVERMAN, DT MCLAUGHLIN, JK MANDEL, JS TI SELECTION OF CONTROLS IN CASE-CONTROL STUDIES .3. DESIGN OPTIONS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE BIAS (EPIDEMIOLOGY); EPIDEMIOLOGIC METHODS; RETROSPECTIVE STUDIES ID CASE-COHORT DESIGN; BIASED SELECTION; NONMALFORMED INFANTS; LOGISTIC-REGRESSION; REPORTING ACCURACY; RARE DISEASE; RISK; EFFICIENCY; APPRAISAL; EXPOSURE AB Several design options available in the planning stage of case-control studies are examined. Topics covered include matching, control/case ratio, choice of nested case-control or case-cohort design, two-stage sampling, and other methods that can be used for control selection. The effect of potential problems in obtaining comparable accuracy of exposure is also examined. A discussion of the difficulty in meeting the principles of study base, deconfounding, and comparable accuracy (S. Wacholder et al. Am J Epidemiol 1992; 1 35:1019-28) in a single study completes this series of papers. C1 NCI,BIOSTAT BRANCH,BETHESDA,MD 20892. UNIV MINNESOTA,SCH PUBL HLTH,DEPT ENVIRONM & OCCUPAT HLTH,MINNEAPOLIS,MN 55455. NR 54 TC 240 Z9 244 U1 3 U2 20 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 MAY 1 PY 1992 VL 135 IS 9 BP 1042 EP 1050 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HY092 UT WOS:A1992HY09200010 PM 1595690 ER PT J AU FARRER, LA GRUNDFAST, KM AMOS, J ARNOS, KS ASHER, JH BEIGHTON, P DIEHL, SR FEX, J FOY, C FRIEDMAN, TB GREENBERG, J HOTH, C MARAZITA, M MILUNSKY, A MORELL, R NANCE, W NEWTON, V RAMESAR, R SANAGUSTIN, TB SKARE, J STEVENS, CA WAGNER, RG WILCOX, ER WINSHIP, I READ, AP AF FARRER, LA GRUNDFAST, KM AMOS, J ARNOS, KS ASHER, JH BEIGHTON, P DIEHL, SR FEX, J FOY, C FRIEDMAN, TB GREENBERG, J HOTH, C MARAZITA, M MILUNSKY, A MORELL, R NANCE, W NEWTON, V RAMESAR, R SANAGUSTIN, TB SKARE, J STEVENS, CA WAGNER, RG WILCOX, ER WINSHIP, I READ, AP TI WAARDENBURG SYNDROME (WS) TYPE-I IS CAUSED BY DEFECTS AT MULTIPLE LOCI, ONE OF WHICH IS NEAR ALPP ON CHROMOSOME-2 - 1ST REPORT OF THE WS CONSORTIUM SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID FRAGMENT LENGTH POLYMORPHISMS; ALKALINE-PHOSPHATASE GENE; LINKAGE ANALYSIS; HIRSCHSPRUNG MEGACOLON; DISEASE; HETEROGENEITY; HUMANS; RFLP; MAP; STRATEGIES AB Previous studies have localized the gene for Waardenburg syndrome (WS) type I to the distal portion of chromosome 2q, near the ALPP locus. We pooled linkage data obtained from 41 WS type I and 3 WS type II families which were typed for six polymorphic loci on chromosome 2q in order to refine the location of the WS locus (WS1) and evaluate the extent of genetic heterogeneity. In the course of this work, we developed diagnostic criteria for genetic and phenotypic studies. Our findings, based on two-locus and multilocus analysis using a linkage map established from reference pedigrees, suggest that there are two or more mutations causing WS, one of which (i.e., WS1) is located on chromosome 2q, between the ALPP and FN1 loci, at distances of 7.8 cM and 11.2 cM for each marker, respectively. The results also indicate that WS1 is responsible for the illness in approximately 45% of all families in this sample. However, the odds favoring this position over a location between ALPP and SAG are only 2:1 when alternate assumptions about the proportion of linked families are considered. We conclude that a more saturated map of this region of chromosome 2q, including highly polymorphic markers, will be needed to accurately distinguish linked families and, ultimately, isolate the mutant gene. C1 BOSTON UNIV,SCH PUBL HLTH,BOSTON,MA 02215. NATL INST DEAFNESS & OTHER COMMUNICAT DISORDERS,MOLEC CYTOL LAB,BETHESDA,MD. GALLAUDET UNIV,WASHINGTON,DC. MICHIGAN STATE UNIV,DEPT ZOOL,E LANSING,MI 48824. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT HUMAN GENET,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PSYCHIAT,RICHMOND,VA 23298. BOSTON UNIV,CTR HUMAN GENET,BOSTON,MA 02215. MICHIGAN STATE UNIV,GENET GRAD PROGRAM,E LANSING,MI 48824. UNIV CAPE TOWN,DEPT HUMAN GENET,CAPE TOWN,SOUTH AFRICA. UNIV MANCHESTER,DEPT MED GENET,MANCHESTER M13 9PL,LANCS,ENGLAND. UNIV MANCHESTER,CTR AUDIOL,MANCHESTER M13 9PL,LANCS,ENGLAND. RP FARRER, LA (reprint author), BOSTON UNIV,SCH MED,DEPT NEUROL,80 E CONCORD ST,BOSTON,MA 02118, USA. RI Ramesar, Raj/I-6941-2015; OI Ramesar, Raj/0000-0001-5688-1634; Morell, Robert/0000-0003-1537-7356; Farrer, Lindsay/0000-0001-5533-4225; Winship, Ingrid/0000-0001-8535-6003 FU NIDCD NIH HHS [DC00038]; NIMHD NIH HHS [263-MD-117512] NR 55 TC 96 Z9 116 U1 0 U2 4 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 MAY PY 1992 VL 50 IS 5 BP 902 EP 913 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA HR473 UT WOS:A1992HR47300004 PM 1349198 ER PT J AU JOHNSON, ES LUCIER, G AF JOHNSON, ES LUCIER, G TI PERSPECTIVES ON RISK ASSESSMENT IMPACT OF RECENT REPORTS ON BENZENE SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Editorial Material DE BENZENE RISK; MUCONIC ACID BIO-MARKER; GENERAL POPULATION EXPOSURES; OCCUPATIONAL EXPOSURES ID TRANS-MUCONALDEHYDE; B6C3F1 MICE; EXPOSURE; LEUKEMIA; SMOKING; METABOLISM; RATS; CARCINOGENICITY; TOXICITY; ACID AB Very sensitive methods that can detect the benzene metabolite muconic acid (MA) in the urine of virtually all members of the general population have recently become available and have been used in a few occupational studies as a marker of benzene exposure. Preliminary findings from these studies suggest that urinary MA may be a reliable marker of occupational exposure to > 5 ppm benzene. It was also consistently observed that a certain proportion of the general population have urinary MA levels compatible with those seen in persons occupationally exposed to > 1 ppm benzene. It is unlikely that these elevated levels can be explained solely as being artifactual. The frequency with which they occur for a given individual, and the duration with which they are maintained, are not known. Information on these two factors is needed in order to adequately assess whether or not these levels present a significant risk for a segment of the general population. RP JOHNSON, ES (reprint author), NIEHS,DIV BIOMETRY & RISK ASSESSMENT,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 30 TC 34 Z9 35 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD MAY PY 1992 VL 21 IS 5 BP 749 EP 757 DI 10.1002/ajim.4700210513 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HQ043 UT WOS:A1992HQ04300012 PM 1609819 ER PT J AU RIEVES, RD AF RIEVES, RD TI CHRISTMAS, 1985 - MEDICAL INTENSIVE-CARE UNIT SO AMERICAN JOURNAL OF MEDICINE LA English DT Article C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 MAY PY 1992 VL 92 IS 5 BP 549 EP 550 DI 10.1016/0002-9343(92)90752-W PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HU612 UT WOS:A1992HU61200014 ER PT J AU STURGEON, SR BRINTON, LA DEVESA, SS KURMAN, RJ AF STURGEON, SR BRINTON, LA DEVESA, SS KURMAN, RJ TI INSITU AND INVASIVE VULVAR CANCER INCIDENCE TRENDS (1973 TO 1987) SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE VULVAR CANCER; INCIDENCE RATES; TIME TRENDS ID CARCINOMA INSITU; HUMAN PAPILLOMAVIRUS; NEOPLASIA; CHALLENGE; WOMEN AB OBJECTIVE: The objective of this study was to examine recent trends in the incidence of vulvar cancer. STUDY DESIGN: Cases of in situ and invasive squamous cell vulvar cancer were identified from nine Surveillance, Epidemiology, and End Results cancer registries. RESULTS: The incidence rate of in situ vulvar cancer nearly doubled between 1973 to 1976 and 1985 to 1987, whereas the rate of invasive squamous cell carcinoma remained relatively stable. CONCLUSIONS: Possible reasons for this discordance include the following: (1) Women affected by the "sexual revolution" are not yet old enough to have invasive vulvar carcinoma; (2) early diagnosis and treatment of in situ carcinoma have mitigated anticipated increases in invasive vulvar carcinoma incidence; (3) in situ and invasive carcinomas of the vulva have different etiologies, with the sexually transmitted human papillomavirus involved in the etiology of in situ carcinoma and other factors involved with most invasive squamous cell carcinoma. C1 NCI,BIOSTAT BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,DEPT GYNECOL & OBSTET & PATHOL,BALTIMORE,MD 21218. RP STURGEON, SR (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 443,BETHESDA,MD 20892, USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 25 TC 129 Z9 134 U1 0 U2 2 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 MAY PY 1992 VL 166 IS 5 BP 1482 EP 1485 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HU954 UT WOS:A1992HU95400029 PM 1595803 ER PT J AU HILBERT, SL FERRANS, VJ MCALLISTER, HA COOLEY, DA AF HILBERT, SL FERRANS, VJ MCALLISTER, HA COOLEY, DA TI IONESCU-SHILEY BOVINE PERICARDIAL BIOPROSTHESES - HISTOLOGIC AND ULTRASTRUCTURAL STUDIES SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID HEART-VALVE BIOPROSTHESES; PRIMARY TISSUE FAILURE; AORTIC POSITION; CARDIAC VALVES; FOLLOW-UP; PATHOLOGIC FINDINGS; XENOGRAFT; HANCOCK; CLASSIFICATION; HETEROGRAFTS AB Studies were done on the structural changes that develop in Ionescu-Shiley valves that are used as replacement heart valves for 4 to 8 years. These changes were compared with those found in similarly used porcine aortic valve (PAV) bioprostheses. A variety of morphologic differences were observed between bovine pericardial valve (BPV) and PAV bioprostheses after orthotopic implantation including: primary tissue failure associated with the use of an alignment suture, thickening of valve leaflet, leaflet tissue delamination, leaflet calcification, and dystrophic alterations of collagen. These findings indicate that valve design criteria directly influence the durability of pericardial valves. However, other factors unique to pericardial tissue also affect the durability and performance of BPVs. These factors include the inability of pericardial tissue to accommodate dynamic stresses; the extensive insudation of plasma proteins and lipids; and the inability to reduce leaflet calcification using agents that effectively mitigate calcification in PAV bioprostheses. C1 NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. TEXAS HEART INST,DEPT PATHOL,HOUSTON,TX 77025. TEXAS HEART INST,DIV SURG,HOUSTON,TX 77025. RP HILBERT, SL (reprint author), US FDA,CTR DEVICES & RADIOL HLTH,DIV MECH & MAT SCI,OFF SCI & TECHNOL,12200 WILKINS AVE,ROCKVILLE,MD 20852, USA. NR 28 TC 28 Z9 28 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 MAY PY 1992 VL 140 IS 5 BP 1195 EP 1204 PG 10 WC Pathology SC Pathology GA HU007 UT WOS:A1992HU00700022 PM 1580331 ER PT J AU MANTHEY, CL KOSSMANN, T ALLEN, JB CORCORAN, ML BRANDES, ME WAHL, SM AF MANTHEY, CL KOSSMANN, T ALLEN, JB CORCORAN, ML BRANDES, ME WAHL, SM TI ROLE OF KUPFFER CELLS IN DEVELOPING STREPTOCOCCAL CELL-WALL GRANULOMAS - STREPTOCOCCAL CELL-WALL INDUCTION OF INFLAMMATORY CYTOKINES AND MEDIATORS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID GROWTH FACTOR-BETA; TUMOR NECROSIS FACTOR; INDUCED HEPATIC GRANULOMAS; HUMAN-MONOCYTES; EXPRESSION; STIMULATION; INVIVO; RAT; MACROPHAGES; MODULATION AB Hepatic granulomas are induced by intraperitoneal injection of streptococcal cell walls (SCW) into Lewis rats. Kupffer cells rapidly clear SCW from the blood, and the authors examined Kupffer cells further for a role in SCW-hepatic inflammation. Isolated Kupffer cells cultured with SCW secreted high levels of tumor necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1), transforming growth factor beta (TGF-beta), and prostaglandin E2 (PGE2). SCW transiently induced increased steady-state levels of IL-1-beta and TNF-alpha mRNA; in contrast, constitutive expression of TGF-beta-1 mRNA in Kupffer cells was not affected by SCW. Low concentrations of SCW induced the accumulation of intracellular IL-1 and TGF-beta bioactivity, with intracellular IL-1 bioactivity remaining high through at least 72 hours of culture. Kupffer cells isolated 1, 7, and 21 days after SCW injection did not express IL-1-beta or TNF-alpha mRNA greater than control levels and exhibited marked hyporesponsiveness to secondary in vitro stimulation with SCW or LPS. SCW transiently induces Kupffer cells to secrete a variety of soluble mediators that contribute to hepatic inflammation by inducing leukocyte recruitment and activation and fibroproliferation. The transient nature of the Kupffer cell response and the hyporesponsiveness to secondary stimulation may be a mechanism by which the hepatic inflammation is negatively regulated. C1 NIDR,CELLULAR IMMUNOL SECT,IMMUNOL LAB,BLDG 30,ROOM 326,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT MICROBIOL,BETHESDA,MD 20814. NR 43 TC 19 Z9 20 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 MAY PY 1992 VL 140 IS 5 BP 1205 EP 1214 PG 10 WC Pathology SC Pathology GA HU007 UT WOS:A1992HU00700023 PM 1580332 ER PT J AU PROROK, PC AF PROROK, PC TI EPIDEMIOLOGIC APPROACH FOR CANCER SCREENING - PROBLEMS IN DESIGN AND ANALYSIS OF TRIALS SO AMERICAN JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY LA English DT Article DE CANCER SCREENING; STUDY DESIGN; ANALYSIS ID BREAST-CANCER; MORTALITY; EFFICACY; MAMMOGRAPHY; DEFINITION; PROGRAMS; DISEASE AB The goal of cancer screening is early detection and treatment of disease with a consequent reduction in mortality. The difficult task of evaluating whether a particular screening program can achieve this goal is the theme of this article. Our focus is on the two principal components of the screening process. The first component is the ability of the screening test to detect cancer early, while minimizing the number of false positive results. In this regard, the specificity of the test ordinarily must be very high, approaching 99%. The second component in the screening process is evaluating the overall impact of a screening program. For this, various study designs have been proposed. The best procedure, the randomized controlled trial, is discussed in detail, but alternative designs are also considered. The endpoint in any such study should be cancer-specific mortality. The problems inherent in other outcome variables, such as stage shift and increased length of survival due to lead time and length biases are addressed. Also considered are major difficulties in study design and evaluation, such as inadequate knowledge of the natural history of the disease, particularly of preclinical lesions. Key data items that should be collected for evaluation are listed. RP PROROK, PC (reprint author), NCI,DCPC,BIOMETRY BRANCH,SCREENING SECT,EXECUT PLAZA N,SUITE 344,BETHESDA,MD 20892, USA. NR 40 TC 50 Z9 50 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-8562 J9 AM J PEDIAT HEMATOL PD MAY PY 1992 VL 14 IS 2 BP 117 EP 128 PG 12 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA HN758 UT WOS:A1992HN75800005 PM 1530116 ER PT J AU MIYAMOTO, A VILLALOBOSMOLINA, R KOWATCH, MA ROTH, GS AF MIYAMOTO, A VILLALOBOSMOLINA, R KOWATCH, MA ROTH, GS TI ALTERED COUPLING OF ALPHA-1-ADRENERGIC RECEPTOR-G PROTEIN IN RAT PAROTID DURING AGING SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ALPHA-ADRENERGIC ACTION; INOSITOL 1,4,5-TRISPHOSPHATE ID NUCLEOTIDE BINDING-PROTEINS; PHOSPHOLIPASE-C ACTIVITY; GUANINE-NUCLEOTIDE; SIGNAL TRANSDUCTION; ACTIVATION; MEMBRANES; CELLS; RESPONSIVENESS; IDENTIFICATION; MECHANISMS AB A possible role for altered signal transduction mechanisms in impaired alpha(1)-adrenergic-stimulated secretory function during aging was investigated in parotid cells prepared from adult (6 mo) and old (24 mo) rats. Compared with adults, epinephrine-stimulated Ca-45(2+) efflux and inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] production were reduced 31 and 36% in cells of old rats, respectively. There was a highly significant correlation between Ca-45(2+) efflux and Ins(1,4,5)P3 production. In saponinpermeabilized cells, no significant differences in Ins(1,4,5)P3-stimulated Ca-45(2+) efflux in adult and old preparations were observed. When G proteins were stimulated by guanosine 5'-O-(3-thiotriphosphate) or NaF, no age differences in Ins(1,4,5)P3 production were detected. Stimulation of phosphoinositide-specific phospholipase C (PLC) by CaCl2 in adult and old cells was also comparable. Moreover, no differences in immunolabeled common alpha (GTP binding site), G(i)alpha, PLC-gamma, or PLC-DELTA could be detected in either cytosol or membranes of adult and old preparations. In the absence of 5'-guanylylimidodiphosphate [Gpp(NH)p], no age-related changes in epinephrine competition for [H-3]prazosin binding sites were observed. Approximately 30% of the agonist binding sites existed in a high-affinity form at both ages. Gpp(NH)p caused large rightward shifts of epinephrine displacement curves in adult membranes (converting all binding sites to the low-affinity form), but not old. Moreover, epinephrine was much more effective in stimulating G protein low-K(m) GTPase in parotid membranes from adult than old rats. These data suggest that age-related impairments in alpha(1)-adrenergic responsiveness are mediated, at least in part, by the functional alterations in the coupling of G proteins with alpha(1)-adrenergic receptors. C1 NIA,FRANCIS SCOTT KEY MED CTR,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 33 TC 34 Z9 34 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 MAY PY 1992 VL 262 IS 5 BP C1181 EP C1188 PN 1 PG 8 WC Physiology SC Physiology GA HV370 UT WOS:A1992HV37000013 ER PT J AU SAMAHA, FF HEINEMAN, FW INCE, C FLEMING, J BALABAN, RS AF SAMAHA, FF HEINEMAN, FW INCE, C FLEMING, J BALABAN, RS TI ATP-SENSITIVE POTASSIUM CHANNEL IS ESSENTIAL TO MAINTAIN BASAL CORONARY VASCULAR TONE INVIVO SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CARDIAC ISCHEMIA; TRANSMEMBRANE POTENTIAL; CORONARY BLOOD FLOW; GLIBENCLAMIDE; SULFONYLUREAS ID SMOOTH-MUSCLE; ADENOSINE; HEART; P-31-NMR AB Glibenclamide, a known selective inhibitor of ATP-sensitive potassium channels, was infused into the coronary vasculature of anesthetized dogs and of isolated perfused rabbit hearts to assess the role of this channel in the maintenance of basal coronary resistance. Infusion of glibenclamide at a concentration of 55-80-mu-M in the dogs resulted in a twofold steady-state increase in coronary resistance with resultant tissue ischemia. Infusion of 1-mu-M glibenclamide in the isolated hearts resulted in a 67% increase in coronary resistance with resultant tissue ischemia. The ischemic changes were reversible upon removal of the drug. These findings indicate that the ATP-sensitive K+ channel plays a significant role in the maintenance of basal coronary resistance in vivo. Higher concentrations of glibenclamide (80-100-mu-M) in the in vivo dog heart consistently gave rise to an oscillating pattern of coronary flow. These oscillations were either eliminated or decreased in amplitude and frequency by the infusion of 8-phenyltheophylline, a specific competitive inhibitor of adenosine receptors. P-31-nuclear magnetic resonance spectroscopy performed at the peaks and troughs of these oscillations revealed oscillation of the phosphorylation potential at the same frequency. Thus adenosine release caused by tissue ischemia appears to play a major role in creating the oscillating pattern of coronary blood flow, that occurs during the inhibition of ATP-sensitive K+ channels by glibenclamide. RP SAMAHA, FF (reprint author), NHLBI,CARDIAC ENERGET LAB,BLDG 1-B3-07,BETHESDA,MD 20892, USA. RI Balaban, Robert/A-7459-2009 OI Balaban, Robert/0000-0003-4086-0948 NR 29 TC 162 Z9 162 U1 1 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAY PY 1992 VL 262 IS 5 BP C1220 EP C1227 PN 1 PG 8 WC Physiology SC Physiology GA HV370 UT WOS:A1992HV37000018 ER PT J AU GAWIN, AZ BARANIUK, JN KALINER, M AF GAWIN, AZ BARANIUK, JN KALINER, M TI EFFECTS OF HISTAMINE ON GUINEA-PIG NASAL MUCOSAL SECRETION SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE NASAL MUCOSA; NASAL SECRETION; ATROPINE; CHLORPHENIRAMINE; CIMETIDINE; ALBUMIN ID INFLAMMATORY MEDIATORS; ANTIGEN CHALLENGE; PATHO-PHYSIOLOGY; HUMAN AIRWAYS; RELEASE; RECEPTORS; RHINITIS; INVITRO; H-1; STIMULATION AB A guinea pig model of nasal secretory responses was developed to assess the contributions of vascular permeability and glandular secretion in the production of nasal secretions. The secretory responses to saline, histamine, chlorpheniramine (H-1-antagonist), cimetidine (H-2 antagonist), and atropine (muscarinic antagonist) on ipsilateral and contralateral (reflex) secretory responses were analyzed by measurement of total protein (Lowry method), I-125-labeled bovine serum albumin (I-125-BSA; administered intravenously) and guinea pig albumin (measured by enzyme-linked immunoabsorbant assay) in nasal secretions. Significant, dose-dependent secretion of total protein, I-125-BSA, and albumin occurred after histamine provocation on the ipsilateral challenged nostril and at several doses on the contralateral (unchallenged) nostril. Histamine-induced total protein and albumin secretion were blocked by chlorpheniramine but not cimetidine. Atropine pretreatment partially reduced total protein secretion. Guinea pig albumin immunoreactive material was detected by immunohistochemistry in superficial vessels, interstitial areas, the epithelium, between glandular cells of submucosal glands, and in gland lumens. Approximately 10% of submucosal gland cells contained albumin immunoreactive material in their cytoplasm. Autoradiography demonstrated that intravenously injected I-125-BSA moved quickly into extracellular areas and then to the epithelium and glands. These observations suggest that histamine stimulates vascular permeability, glandular secretion, and sensory nerve stimulation and that the ipsilateral and contralateral glandular secretion was at least partly due to an atropine-inhibitable cholinergic reflex. RP GAWIN, AZ (reprint author), NIAID,ALLERG DIS SECT,CLIN INVEST LAB,BETHESDA,MD 20892, USA. NR 32 TC 10 Z9 10 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAY PY 1992 VL 262 IS 5 BP L590 EP L599 PN 1 PG 10 WC Physiology SC Physiology GA HV370 UT WOS:A1992HV37000093 PM 1350423 ER PT J AU YONKERS, KA KANDO, JC COLE, JO BLUMENTHAL, S AF YONKERS, KA KANDO, JC COLE, JO BLUMENTHAL, S TI GENDER DIFFERENCES IN PHARMACOKINETICS AND PHARMACODYNAMICS OF PSYCHOTROPIC MEDICATION SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID ORAL-CONTRACEPTIVE STEROIDS; MENSTRUAL-CYCLE; SEX-DIFFERENCES; SCHIZOPHRENIC-PATIENTS; ANTIDEPRESSANT DRUGS; AFFECTIVE-DISORDER; PLASMA-LEVELS; AGE; DISPOSITION; WOMEN AB Objective: This review explores the theoretical background for and empirical evidence supporting gender-related differences in pharmacokinetics and pharmacodynamic properties of psychotropic medications. Method: The authors reviewed all English-language articles on this topic that involved original research using human subjects. Results: Limited evidence suggests that young women seem to respond better to and require lower doses of antipsychotic agents and benzodiazepines than young men. The administration of exogenous hormones interacts with medications, changing plasma levels and possibly conferring greater risks for toxicity. Young women may have an enhanced response to nontricyclic antidepressants. Conclusions: Too little basic and clinical research has been conducted on sex differences in therapeutic effects and side effects of psychopharmacological treatments. Addressing these differences as well as similarities will lead to safer and more effective treatment for all patients. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MCLEAN HOSP,NIMH,BEHAV MED PROGRAM,BELMONT,MA 02178. FU NIMH NIH HHS [MH-32675] NR 58 TC 201 Z9 204 U1 1 U2 6 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 MAY PY 1992 VL 149 IS 5 BP 587 EP 595 PG 9 WC Psychiatry SC Psychiatry GA HR721 UT WOS:A1992HR72100001 PM 1575248 ER PT J AU ADLER, KB AKLEY, NJ GLASGOW, WC AF ADLER, KB AKLEY, NJ GLASGOW, WC TI PLATELET-ACTIVATING-FACTOR PROVOKES RELEASE OF MUCIN-LIKE GLYCOPROTEINS FROM GUINEA-PIG RESPIRATORY EPITHELIAL-CELLS VIA A LIPOXYGENASE-DEPENDENT MECHANISM SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID FACTOR STIMULATES SECRETION; ARACHIDONIC-ACID; FACTOR PAF; CULTURE; ASTHMA; GLYCOCONJUGATE; PROSTAGLANDINS; LEUKOTRIENES; EOSINOPHILS; METABOLITES AB Primary cultures of guinea pig tracheal epithelial cells maintained in an air/liquid interface system that maintains differentiated characteristics were grown to near confluence and exposed for 1 h to platelet-activating factor (PAF) on both apical and basal sides. PAF provoked release of high-molecular-weight mucin-like glycoproteins (MLG) from the cells, with maximal stimulation occurring at 10(-8) and 10(-9) M. The inactive form of PAF, lyso-PAF, was without effect. Indomethacin, the cyclooxygenase inhibitor, did not affect secretion stimulated by PAF, but nordihydroguiaretic acid (NDGA), a mixed cyclooxygenase and lipoxygenase inhibitor, attenuated secretion stimulated by PAF in a concentration-dependent manner. High performance liquid chromatography assay of the culture medium after addition of PAF revealed increased production of 15-, 12-, and 5-hydroxyeicosatetraenoic acids (15-, 12-, and 5-HETEs). The stimulatory effect of PAF on both mucin secretion and formation of HETEs was inhibited by the PAF receptor antagonists, CV-3988 and Ro 19 3704, with Ro 19 3704 acting at a concentration 10-fold lower than CV-3988 in inhibiting both effects. When added exogenously to the cell cultures, the combination of 5-, 12-, and 15-HETEs stimulated MLG release in a concentration-dependent manner. The results suggest that PAF stimulates release of MLG by guinea pig airway epithelium in vitro by a mechanism involving binding of PAF to receptors on epithelial cell surfaces, stimulation of lipoxygenase metabolism of arachidonic acid to HETEs within the epithelium, and stimulation of secretion by these epithelial-derived HETEs via an autocrine or paracrine mechanism. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RP ADLER, KB (reprint author), N CAROLINA STATE UNIV,COLL VET MED,DEPT ANAT PHYSIOL SCI & RADIOL,4700 HILLSBOROUGH ST,RALEIGH,NC 27606, USA. FU NHLBI NIH HHS [HL-36736, HL-36982] NR 35 TC 41 Z9 41 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 MAY PY 1992 VL 6 IS 5 BP 550 EP 556 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA HU715 UT WOS:A1992HU71500013 PM 1316134 ER PT J AU MEDEIROS, LJ JAFFE, ES CHEN, YY WEISS, LM AF MEDEIROS, LJ JAFFE, ES CHEN, YY WEISS, LM TI LOCALIZATION OF EPSTEIN-BARR VIRAL GENOMES IN ANGIOCENTRIC IMMUNOPROLIFERATIVE LESIONS SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE ANGIOCENTRIC IMMUNOPROLIFERATIVE LESIONS; EPSTEIN-BARR VIRUS; INSITU HYBRIDIZATION; T-CELL LINEAGE ID T-CELL LYMPHOMAS; GRANULOMATOSIS; VIRUS; DISEASE; DNA AB Epstein-Barr virus has been demonstrated in angiocentric immunoproliferative lesions. However, these studies, which have used the polymerase chain reaction technique or Southern blot analysis, have not revealed the identity of the cell population harboring the virus. To address this issue, we analyzed 12 angiocentric immunoproliferative lesions (14 biopsy specimens) for Epstein-Barr virus RNA using a sensitive and specific in situ hybridization method. Epstein-Barr virus RNA was detected in five of 12 cases. Each positive lesion was a high-grade angiocentric immunoproliferative lesion (i.e., angiocentric lymphoma) in which Epstein-Barr virus was identified in numerous cells. Furthermore, the Epstein-Barr virus-positive cells were often larger than normal lymphocytes and thus were most likely the malignant cells. Double-labeling immunohistochemistry/in situ hybridization studies revealed that the majority of Epstein-Barr virus-positive cells were CD43-positive and CD20-negative, consistent with T-cell lineage. The remaining seven cases, all grade I or II angiocentric immunoproliferative lesions, were either completely negative (four cases) or had only rare to occasional Epstein-Barr virus-positive cells (three cases). The results obtained with the polymerase chain reaction and Southern blot hybridization studies generally confirmed those obtained with in situ hybridization. We conclude that Epstein-Barr virus is frequently associated with angiocentric immunoproliferative lesions, particularly within high-grade lesions, in which the virus is probably present within the neoplastic cells. These findings also suggest that Epstein-Barr virus may be involved in the transformation of low-grade angiocentric immunoproliferative lesions to histologically unequivocal angiocentric lymphomas. C1 CITY HOPE NATL MED CTR,DEPT PATHOL,DUARTE,CA 91010. RP MEDEIROS, LJ (reprint author), NCI,HEMATOPATHOL SECT,PATHOL LAB,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA 50341] NR 24 TC 138 Z9 138 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAY PY 1992 VL 16 IS 5 BP 439 EP 447 DI 10.1097/00000478-199205000-00002 PG 9 WC Pathology; Surgery SC Pathology; Surgery GA HQ199 UT WOS:A1992HQ19900002 PM 1318000 ER PT J AU CAMPO, E MERINO, MJ TAVASSOLI, FA CHARONIS, AS STETLERSTEVENSON, WG LIOTTA, LA AF CAMPO, E MERINO, MJ TAVASSOLI, FA CHARONIS, AS STETLERSTEVENSON, WG LIOTTA, LA TI EVALUATION OF BASEMENT-MEMBRANE COMPONENTS AND THE 72-KDA TYPE-IV COLLAGENASE IN SEROUS TUMORS OF THE OVARY SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE OVARY; SEROUS TUMOR OF LOW MALIGNANT POTENTIAL; CYSTADENOMA; MICROINVASION; BASEMENT MEMBRANE; LAMININ; TYPE-IV COLLAGEN; TYPE-IV COLLAGENASE; METALLOPROTEINASE ID BRONCHIAL EPITHELIAL-CELLS; TISSUE INHIBITOR; HA-RAS; EXPRESSION; LAMININ; INVASION; BENIGN; TIMP-2; MICROINVASION; BORDERLINE AB We studied the distribution of the basement membrane components laminin and type IV collagen in 46 serous tumors of the ovary, including a group of low malignant potential tumors with microinvasion. The findings were correlated with the expression of the 72 kDa type IV collagenase, an enzyme that initiates the degradation of type IV collagen and consequently may play a role in the process of invasion. Benign cystadenomas and tumors of low malignant potential without microinvasion showed a continuous basement membrane; whereas invasive carcinomas, peritoneal implants, and lymph node metastasis had frequent disruptions and extensive areas without basement membrane components. Early invasion in tumors of low malignant potential was characterized by focal disruptions in basement membranes and complete absence of laminin and type IV collagen around single or clusters of microinvasive cells. Type IV collagenase was negative or minimally expressed in cystadenomas, whereas in invasive carcinomas and metastasis the reactivity was moderate to intense. Microinvasive cells in tumors of low malignant potential were strongly positive. The collagenase IV was also localized in cell clusters elsewhere in the tumors where the basement membrane was still preserved. These cells had a similar morphology to that of the microinvasive cells. We conclude that detection of basement membrane components may be useful in recognizing early invasion in this group of ovarian neoplasms. The correlation between progressive anomalies of the basement membrane and expression of type IV collagenase suggests that this enzyme functions directly in the degradation of basement membrane components and faciliates the invasive process. C1 ARMED FORCES INST PATHOL,DEPT GYNECOL & BREAST PATHOL,WASHINGTON,DC 20306. UNIV MINNESOTA,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. RP CAMPO, E (reprint author), NCI,PATHOL LAB,BLDG 10,ROOM 2N212,BETHESDA,MD 20892, USA. RI Stetler-Stevenson, William/H-6956-2012; OI Stetler-Stevenson, William/0000-0002-5500-5808; Charonis, Aristidis/0000-0001-9956-732X; Campo, elias/0000-0001-9850-9793 NR 41 TC 116 Z9 117 U1 0 U2 3 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 MAY PY 1992 VL 16 IS 5 BP 500 EP 507 DI 10.1097/00000478-199205000-00009 PG 8 WC Pathology; Surgery SC Pathology; Surgery GA HQ199 UT WOS:A1992HQ19900009 PM 1318001 ER PT J AU FERNANDEZ, PL GOMEZ, M CABALLERO, T MEDINA, T AGUILAR, D AF FERNANDEZ, PL GOMEZ, M CABALLERO, T MEDINA, T AGUILAR, D TI PROSTATIC ACID-PHOSPHATASE IN CLOACAL DERIVATIVES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Letter C1 FAC MED GRANADA,DEPT ANAT PATOL,GRANADA,SPAIN. RP FERNANDEZ, PL (reprint author), NCI,DEPT PATHOL,BETHESDA,MD 20892, USA. NR 2 TC 2 Z9 2 U1 0 U2 2 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 MAY PY 1992 VL 16 IS 5 BP 526 EP 526 DI 10.1097/00000478-199205000-00013 PG 1 WC Pathology; Surgery SC Pathology; Surgery GA HQ199 UT WOS:A1992HQ19900013 PM 1599030 ER PT J AU LANGE, JV ELDESSOUKY, AG MANOR, E MERDAN, AI AZAD, AF AF LANGE, JV ELDESSOUKY, AG MANOR, E MERDAN, AI AZAD, AF TI SPOTTED-FEVER RICKETTSIAE IN TICKS FROM THE NORTHERN SINAI GOVERNATE, EGYPT SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID POLYMERASE CHAIN-REACTION; TYPHUS INFECTION; DIAGNOSIS AB A field study was initiated in 1988 to investigate whether spotted fever group rickettsiae occur in geographic areas in Egypt that are adjacent to an area in the southern Israeli Negev that has a defined focus of spotted fever disease. Ticks were collected from dogs, sheep, and camels at four study sites in the northern Sinai. Tick hemolymph was processed for rickettsial detection by staining with fluorescein isothiocyanate-conjugated antibody to Rickettsia rickettsii. Of the 442 hemolymphs examined, 15 contained immunofluorescent rickettsiae. Eight hemolymph test-positive (HT+) ticks were Rhipicephalus phalus sanguineus removed from dogs; the other HT+ ticks comprised three Hyalomma species, H. anatolicum, H. impeltatum, and H. dromedarii. Both HT+ and HT- ticks were tested for rickettsial DNA using the polymerase chain reaction (PCR). Eight of 10 HT+ field-collected ticks were PCR positive (PCR+). All laboratory colony R. rickettsii-infected ticks were PCR+. No HT- ticks from field or laboratory isolates were PCR+. C1 AIN SHAMS UNIV,RES & TRAINING CTR VECTORS DIS,CAIRO,EGYPT. BEN GURION UNIV NEGEV,VIROL UNIT,IL-84105 BEER SHEVA,ISRAEL. UNIV MARYLAND,SCH MED,DEPT MICROBIOL & IMMUNOL,BALTIMORE,MD 21201. RP LANGE, JV (reprint author), NIAID,OFF TROP MED & INT RES,BLDG CDB-3C25,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI-17828]; PHS HHS [ANE-0158-P-HZ-7020-00] NR 17 TC 17 Z9 17 U1 1 U2 1 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 MAY PY 1992 VL 46 IS 5 BP 546 EP 551 PG 6 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA HX463 UT WOS:A1992HX46300007 PM 1599048 ER PT J AU HIBBS, JR ISSARAGRISIL, S YOUNG, NS AF HIBBS, JR ISSARAGRISIL, S YOUNG, NS TI HIGH PREVALENCE OF HEPATITIS-C VIREMIA AMONG APLASTIC-ANEMIA PATIENTS AND CONTROLS FROM THAILAND SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID NON-B-HEPATITIS; POLYMERASE CHAIN-REACTION; NON-A; BLOOD-DONORS; LIVER-TRANSPLANTATION; VIRAL-HEPATITIS; VIRUS; ANTIBODIES; HEMOPHILIACS; SEQUENCES AB Aplastic anemia is a rare, life-threatening disease of unknown etiology, with unusually high prevalence in Thailand. It is sometimes associated with non-A, non-B hepatitis (NANBH). The hepatitis C virus (HCV), one of the causes of NANBH, is similar to flaviviridiae, a family of viruses many of whose members cause acute bone marrow suppression. To test the hypothesis that HCV viremia is associated with aplastic anemia among patients in Thailand, we compared 53 untransfused hospitalized aplastic anemia patients and 39 untransfused controls hospitalized for other conditions. We used the polymerase chain reaction to identify HCV viremia in three (5.7%) untransfused patients and two (5.1%) untransfused controls (P = 1.0, by Fisher's two-tailed exact test). Although our data do not exclude the possibility that a small subset of aplastic anemia cases are precipitated by HCV, we conclude that HCV viremia is not generally associated with aplastic anemia in Thailand. Our results also imply that the prevalence of HCV viremia may be unexpectedly high among untransfused persons in Thailand, a hypothesis that should be tested in other populations. C1 MAHIDOL UNIV,SIRIRAJ HOSP,DEPT MED,DIV HEMATOL,BANGKOK 10700,THAILAND. RP HIBBS, JR (reprint author), NHLBI,CLIN HEMATOL BRANCH,BLDG 10,ROOM 7C103,9000 ROCKVILLE PIKE,BETHESDA,MD 20814, USA. OI Issaragrisil, Surapol/0000-0002-8924-0646 FU NHLBI NIH HHS [HL-35068] NR 40 TC 17 Z9 17 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD MAY PY 1992 VL 46 IS 5 BP 564 EP 570 PG 7 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA HX463 UT WOS:A1992HX46300010 PM 1318006 ER PT J AU EICHACKER, PQ FARESE, A HOFFMAN, WD BANKS, SM MOUGINIS, T RICHMOND, S KUO, GC MACVITTIE, TJ NATANSON, C AF EICHACKER, PQ FARESE, A HOFFMAN, WD BANKS, SM MOUGINIS, T RICHMOND, S KUO, GC MACVITTIE, TJ NATANSON, C TI LEUKOCYTE CD11B/18 ANTIGEN-DIRECTED MONOCLONAL-ANTIBODY IMPROVES EARLY SURVIVAL AND DECREASES HYPOXEMIA IN DOGS CHALLENGED WITH TUMOR-NECROSIS-FACTOR SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID ACUTE LUNG INJURY; SEPTIC SHOCK; NEUTROPHIL ADHERENCE; VASCULAR ENDOTHELIUM; REPERFUSION INJURY; CACHECTIN; ADHESION; ALPHA; INTERLEUKIN-1; BACTEREMIA AB This study examined the effect of monoclonal antibody (MAb) directed against leukocyte CD11b/18 glycoprotein complex (904MAb) on cardiopulmonary injury induced by tumor necrosis factor (TNF), and death. Eighteen 2-yr-old, purpose-bred beagles with chronic tracheostomies were challenged with TNF (60-mu-g/kg of body weight) intravenously. Nine of 18 animals were treated with 0.5 to 1.0 mg/kg of body weight 904MAb intravenously 45 min before and 12, 36, and 48 h after TNF infusion. Serial femoral and pulmonary arterial catheter hemodynamics, blood gas analysis, and radionuclide cineangiographic left ventricular election fractions (EF) were done before and after a fluid challenge. Serial bronchoalveolar lavages (BAL) with cell and protein analysis also were performed using the chronic tracheostomies. Compared with animals given TNF alone, animals treated with 904MAb did not differ in overall survival (TNF alone, 219; 904MAb, 319); however, the group of animals treated with 904MAb had significantly (p < 0.01) fewer deaths within the first 30 h of TNF challenge. At 4 h after TNF challenge, all animals had significantly (p < 0.05) reduced PaO2 after fluid challenge; however, animals given 904MAb (compared with animals given TNF alone) had significantly (p < 0.05) smaller reductions in PaO2. Throughout the study, animals given 904MAb before TNF or TNF alone had similar changes in cardiac Index, mean arterial pressure, EF, and BAL protein and neutrophil concentration. Thus, MAb directed against the leukocyte CD11b/18 glycoprotein complex prolonged survival and reduced the hypoxemia occurring after TNF challenge, but this antibody did not improve overall survival or cardiopulmonary function. These results suggest that the leukocyte CD11b/18 glycoprotein complex contributes to the acute pulmonary injury and early lethality induced by TNF. C1 DEF NUCL AGCY,ARMED FORCES RADIOBIOL RES INST,BETHESDA,MD 20014. COULTER IMMUNOL,HIALEAH,FL. CHIRON CORP,EMERYVILLE,CA. RP EICHACKER, PQ (reprint author), NIH,CTR CLIN,DEPT CRIT CARE MED,BLDG 10,ROOM 10D48,BETHESDA,MD 20892, USA. NR 24 TC 41 Z9 41 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 MAY PY 1992 VL 145 IS 5 BP 1023 EP 1029 PG 7 WC Respiratory System SC Respiratory System GA HU614 UT WOS:A1992HU61400008 PM 1586042 ER PT J AU DUBOIS, RM KIRBY, M BALBI, B SALTINI, C CRYSTAL, RG AF DUBOIS, RM KIRBY, M BALBI, B SALTINI, C CRYSTAL, RG TI LYMPHOCYTES-T THAT ACCUMULATE IN THE LUNG IN SARCOIDOSIS HAVE EVIDENCE OF RECENT STIMULATION OF THE T-CELL ANTIGEN RECEPTOR SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID ACTIVE PULMONARY SARCOIDOSIS; PROTEIN KINASE-C; MAJOR HISTOCOMPATIBILITY COMPLEX; LOWER RESPIRATORY-TRACT; INSITU HYBRIDIZATION; SPONTANEOUS RELEASE; BRONCHOALVEOLAR LAVAGE; T3-MOLECULAR COMPLEX; ALVEOLAR MACROPHAGES; CHRONIC INFLAMMATION AB Sarcoidosis, a granulomatous disease of unknown etiology, is characterized at sites of disease such as the lung by the accumulation of large numbers of T-lymphocytes. To differentiate whether the T-cells accumulate in organs nonspecifically (e.g., through chemotaxis or tumorlike proliferation) or more specifically through an antigen-driven ordered immune response, the present study capitalized on the knowledge that specific antigen stimulation of T-cells requires antigen interactions with the T-cell antigen receptor (TCR), resulting in a decrease in the number of surface TCR and a concomitant increase in TCR mRNA levels, i.e., if lung T-cell accumulation in pulmonary sarcoid results from an ordered immune response, lung, but not blood, T-cells should demonstrate evidence of recent triggering of the alpha-beta-receptor, the most abundant type of TCR. The surface density of T-cell surface-alpha-beta-TCR expression was evaluated by flow cytometry with an anti-alpha-beta-antibody and TCR-beta-chain mRNA transcript number quantified by in situ hybridization with S-35-labeled antisense and sense cRNA probes. Control studies utilizing normal blood T-lymphocytes stimulated with the anti-CD3 monoclonal antibody, OKT3, in the presence of autologous monocytes, demonstrated the expected down-regulation of surface-alpha-beta-TCR expression and increased beta-chain mRNA transcript number. When lung and blood T-cells of patients with pulmonary sarcoidosis were compared immediately upon recovery (i.e., without in vitro stimulation), the lung T-cells of 10 of 10 subjects demonstrated a decreased surface density of alpha-beta-TCR compared with their autologous blood T-cells. Furthermore, lung T-cells of eight of nine of these subjects exhibited an increase in beta-chain mRNA transcripts compared with their autologous blood T-lymphocytes. Together, these observations are consistent with the concept that lung, but not blood, T-cells in active pulmonary sarcoidosis have recently been activated through a mechanism that modulates T-cell surface antigen receptor. This process is likely antigen-driven although activation via other ligand-receptor bindings may occur and have not been directly excluded in this study. Overall, these data give support to the hypothesis that the T-cells accumulate in the lung in pulmonary sarcoid in response to persistent antigenic stimulation. C1 NHLBI,PULM BRANCH,BLDG 10,ROOM 6D03,BETHESDA,MD 20892. NR 65 TC 82 Z9 82 U1 0 U2 2 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 MAY PY 1992 VL 145 IS 5 BP 1205 EP 1211 PG 7 WC Respiratory System SC Respiratory System GA HU614 UT WOS:A1992HU61400039 PM 1533998 ER PT J AU DANIELE, RP BARNES, PJ GOETZL, EJ NADEL, J ODORISIO, S KILEY, J JACOBS, T AF DANIELE, RP BARNES, PJ GOETZL, EJ NADEL, J ODORISIO, S KILEY, J JACOBS, T TI NEUROIMMUNE INTERACTIONS IN THE LUNG SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Editorial Material C1 NHLBI,DIV LUNG DIS,WESTWOOD BLDG,5333 WESTBARD AVE,ROOM 6A09,BETHESDA,MD 20892. NR 0 TC 16 Z9 16 U1 0 U2 2 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 MAY PY 1992 VL 145 IS 5 BP 1230 EP 1235 PG 6 WC Respiratory System SC Respiratory System GA HU614 UT WOS:A1992HU61400046 PM 1586073 ER PT J AU ANTONY, VB SAHN, SA MOSSMAN, B GAIL, DB KALICA, A AF ANTONY, VB SAHN, SA MOSSMAN, B GAIL, DB KALICA, A TI PLEURAL CELL BIOLOGY IN HEALTH AND DISEASE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Editorial Material C1 NHLBI,DIV LUNG DIS,WESTWOOD BLDG,ROOM 6A07,5333 WESTBARD AVE,BETHESDA,MD 20892. NR 0 TC 35 Z9 36 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 MAY PY 1992 VL 145 IS 5 BP 1236 EP 1239 PG 4 WC Respiratory System SC Respiratory System GA HU614 UT WOS:A1992HU61400047 PM 1586074 ER PT J AU PIEGORSCH, WW AF PIEGORSCH, WW TI COMPLEMENTARY LOG REGRESSION FOR GENERALIZED LINEAR-MODELS SO AMERICAN STATISTICIAN LA English DT Article DE BINOMIAL MODEL; DATA TRUNCATION; EXTENDED LINK FAMILY; GOODNESS-OF-LINK TESTING; LOGISTIC REGRESSION; NONLINEAR REGRESSION ID MAXIMUM-LIKELIHOOD ESTIMATION; RESPONSE MODELS; RISK RATIOS; TRANSFORMATIONS; GLIM AB Use and implementation of the complementary log regression model are discussed, integrating various separate applications of the model under the form of a generalized linear model. Some motivation is drawn from cases where an underlying random variable is reduced to a dichotomous form. Estimation and testing are facilitated by recognizing the complementary log as a specific link function within a generalized linear framework. Testing for goodness of link via efficient scores is also discussed. RP PIEGORSCH, WW (reprint author), NIEHS,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709, USA. NR 39 TC 13 Z9 13 U1 1 U2 4 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 SN 0003-1305 J9 AM STAT JI Am. Stat. PD MAY PY 1992 VL 46 IS 2 BP 94 EP 99 DI 10.2307/2684172 PG 6 WC Statistics & Probability SC Mathematics GA HR034 UT WOS:A1992HR03400004 ER PT J AU KOZIOL, DE HENDERSON, DK AF KOZIOL, DE HENDERSON, DK TI EVOLVING EPIDEMIOLOGY OF HIV-INFECTION AMONG ADULTS SO ANNALS OF ALLERGY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; HTLV-III ANTIBODY; SEXUALLY-TRANSMITTED DISEASES; PLACEBO-CONTROLLED TRIAL; INTRAVENOUS DRUG-USERS; HOMOSEXUAL MEN; RISK-FACTORS; UNITED-STATES; CEREBROSPINAL-FLUID C1 NIH,WARREN G MAGNUSON CLIN CTR,HOSP EPIDEMIOL SERV,BLDG 10,RM 2C 146,BETHESDA,MD 20892. NR 175 TC 1 Z9 1 U1 0 U2 0 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 MAY PY 1992 VL 68 IS 5 BP 375 EP 385 PG 11 WC Allergy SC Allergy GA HU230 UT WOS:A1992HU23000002 PM 1586001 ER PT J AU FOY, JL EASTMAN, RC NEALON, RC BOWEN, PM PENGELLY, ML DRASS, JA DORWORTH, TE PUCINO, F AF FOY, JL EASTMAN, RC NEALON, RC BOWEN, PM PENGELLY, ML DRASS, JA DORWORTH, TE PUCINO, F TI AUTOMATED THERAPEUTIC DRUG-MONITORING IN AN AMBULATORY CARE ENDOCRINE CLINIC SO ANNALS OF PHARMACOTHERAPY LA English DT Article ID BONE-DENSITY; L-THYROXINE; HYPERTHYROIDISM; THYROTOXICOSIS AB OBJECTIVE: To develop and implement an automated therapeutic drug monitoring system for accessing data from endocrine clinic patients who had been prescribed insulin, oral hypoglycemic agents (OHA), or levothyroxine. DATA SOURCES: We designed a computer system to retrieve clinical data from the Medical Information System (MIS), a centralized hospital computer system, and import this information directly into a Macintosh personal computer. Physician entry of prescriptions for insulin, OHA, or levothyroxine into MIS formed the basis for a computer program to retrieve daily diagnostic and prescription information, demographics, and laboratory analyses, including blood glucose and glycosylated hemoglobin for insulin and OHA orders and free and total thyroxine, total triiodothyronine, and thyroid stimulating hormone for levothyroxine orders. The information was imported into a database program (4th Dimension). RESULTS: The system identifies laboratory values outside of predetermined therapeutic ranges, maintains an up-to-date patient profile, and edits and generates reports. Preliminary experience suggests that automation eliminates 75-90 percent of the time required to manually collect the same information, and improves the accuracy, comprehensiveness, and utility of reports. CONCLUSIONS: Automated therapeutic drug monitoring minimizes the time required to collect clinical data, alerts clinicians to potential problems, and provides a means to assess overall therapeutic management. Our methodology can be used to evaluate other medications in a variety of general or specialty clinics. C1 NIH,DEPT PHARM,WARREN GRANT MAGNUSON CLIN CTR,BLDG 10,RM 1N-257,BETHESDA,MD 20892. NIDDKD,DEPT INFORMAT SYST,BETHESDA,MD. NIDDKD,DIABET BRANCH,BETHESDA,MD. NIH,DEPT INFORMAT SYST,BETHESDA,MD 20892. NIH,DEPT PHARM,OUTPATIENT PHARM SECT,BETHESDA,MD 20892. NR 22 TC 7 Z9 7 U1 0 U2 0 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 1060-0280 J9 ANN PHARMACOTHER JI Ann. Pharmacother. PD MAY PY 1992 VL 26 IS 5 BP 675 EP 678 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HT842 UT WOS:A1992HT84200015 PM 1591429 ER PT J AU GOMES, MN CHOYKE, PL WALLACE, RB AF GOMES, MN CHOYKE, PL WALLACE, RB TI INFECTED AORTIC-ANEURYSMS - A CHANGING ENTITY SO ANNALS OF SURGERY LA English DT Article; Proceedings Paper CT 103RD ANNUAL SCIENTIFIC SESSION OF THE SOUTHERN SURGICAL ASSOC CY DEC 01-04, 1991 CL HOT SPRINGS, VA SP SO SURG ASSOC ID ABDOMINAL-AORTA; MYCOTIC-ANEURYSM; MANAGEMENT; DIAGNOSIS; EVOLUTION; SURVIVAL AB Infected (mycotic) aortic aneurysms are infrequent and, without surgical intervention, usually lead to uncontrolled sepsis or catastrophic hemorrhage. Symptoms are frequently absent or non-specific during the early stages, and a high index of suspicion is essential to make the diagnosis. Surgery performed after rupture carries high morbidity and mortality rates. Bacterial endocarditis with streptococcus pyogenes was the most common cause of infected aortic aneurysm in the pre-antibiotic era. Today, arterial trauma due to iatrogenic manipulation and depressed immuno-competence have become more common risk factors. Staphylococcus aureus and Salmonella are the most frequent bacteria identified. The authors' recent experience in six patients with infected aortic aneurysms who underwent arteriography and computed tomography was reviewed and these diagnostic methods compared. Computed tomography was found to be more sensitive in the diagnosis of the early stages of the disease, allowing for follow-up by serial scans in a noninvasive and less costly manner. Successful treatment, in four of these patients, was accomplished by aneurysmal resection and extra-anatomic bypass or in situ prosthetic reconstruction. A higher clinical awareness of this disease, leading to early computed tomography evaluation and prompt surgical intervention under appropriate and intensive antibiotic therapy, appears to offer the best chance of survival in patients with this difficult condition. C1 NIH,WARREN GRANT MAGNUSSON CLIN CTR,DEPT RADIOL,BETHESDA,MD 20892. RP GOMES, MN (reprint author), GEORGETOWN UNIV,MED CTR,DEPT SURG,3800 RESERVOIR RD NW,WASHINGTON,DC 20007, USA. NR 43 TC 103 Z9 105 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD MAY PY 1992 VL 215 IS 5 BP 435 EP 442 DI 10.1097/00000658-199205000-00005 PG 8 WC Surgery SC Surgery GA JB515 UT WOS:A1992JB51500005 PM 1616380 ER PT J AU KAGEYAMA, S WEINSTEIN, JN SHIRASAKA, T KEMPF, DJ NORBECK, DW PLATTNER, JJ ERICKSON, J MITSUYA, H AF KAGEYAMA, S WEINSTEIN, JN SHIRASAKA, T KEMPF, DJ NORBECK, DW PLATTNER, JJ ERICKSON, J MITSUYA, H TI INVITRO INHIBITION OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) TYPE-1 REPLICATION BY C2 SYMMETRY-BASED HIV PROTEASE INHIBITORS AS SINGLE AGENTS OR IN COMBINATIONS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID AIDS-RELATED COMPLEX; PHASE-I TRIAL; HTLV-III; 2',3'-DIDEOXYINOSINE DDI; ZIDOVUDINE AZT; INFECTION; THERAPY; 3'-AZIDO-3'-DEOXYTHYMIDINE; MATURATION; III/LAV AB C2 symmetry-based human immunodeficiency virus (HIV) protease inhibitors were examined in vitro as single agents or in combination with 3'-azido-2',3'-dideoxythymidine (AZT) or 2',3'-dideoxyinosine for activity against HIV type 1 (HIV-1). Ten C2 symmetry-based or pseudo-C2 symmetry-based HIV protease inhibitors were active against a laboratory strain (HIV-1IIIB) in the HIV-1 cytopathic effect inhibition assay. Three inhibitors, A75925, A76928, and A77003, selected to represent a range of aqueous solubility and antiviral activity, were active against four different HIV-1 strains tested. These three inhibitors exhibited a significant inhibition of the cytopathic effect of HIV-1 against the CD4+ ATH8 cell line, with 90% inhibitory concentrations ranging from 0.1 to 4-mu-M. Cellular toxicity was negligible at up to 20-mu-M. Furthermore, they completely inhibited the replication of monocytotropic strain HIV-1Ba-L in purified monocytes and macrophages at 0.75 to 2-mu-M. Potent inhibitory activity against a primary HIV-1 isolate and an AZT-resistant HIV-1 variant was also observed for all three inhibitors in phytohemagglutinin-activated peripheral blood mononuclear cells. When these three HIV protease inhibitors and AZT or 2',3'-dideoxyinosine were used in combinations against a primary HIV isolate in phytohemagglutinin-activated peripheral blood mononuclear cells and the results were analyzed with the COMBO program package, their antiviral activities were identified to be synergistic in some cases and additive in others. The present data warrant further investigations of these compounds as potential antiviral agents for the therapy of HIV infections. C1 NCI,MED BRANCH,EXPTL RETROVIROL SECT,BETHESDA,MD 20892. ABBOTT LABS,DIV PHARMACEUT PROD,ABBOTT PK,IL 60064. NCI,MATH BIOL LAB,THEORET IMMUNOL SECT,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,DYN CORP,PROGRAM RESOURCES INC,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702. FU NIAID NIH HHS [AI 27220] NR 33 TC 56 Z9 56 U1 0 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 MAY PY 1992 VL 36 IS 5 BP 926 EP 933 PG 8 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA HT589 UT WOS:A1992HT58900004 PM 1510415 ER PT J AU RAMPHAL, R BOLGER, M OBLON, DJ SHERERTZ, RJ MALONE, JD RAND, KH GILLIOM, M SHANDS, JW KRAMER, BS AF RAMPHAL, R BOLGER, M OBLON, DJ SHERERTZ, RJ MALONE, JD RAND, KH GILLIOM, M SHANDS, JW KRAMER, BS TI VANCOMYCIN IS NOT AN ESSENTIAL COMPONENT OF THE INITIAL EMPIRIC TREATMENT REGIMEN FOR FEBRILE NEUTROPENIC PATIENTS RECEIVING CEFTAZIDIME - A RANDOMIZED PROSPECTIVE-STUDY SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID CANCER-PATIENTS; ANTIBIOTIC-THERAPY; CLINICAL-TRIAL; ACUTE-LEUKEMIA; CARBENICILLIN; CEPHALOTHIN; GENTAMICIN; GRANULOCYTOPENIA; BACTEREMIA AB The use of vancomycin as part of the initial antibiotic therapy of febrile neutropenic patients has become a controversial issue. Some studies support its incorporation in the initial regimen, and others suggest that vancomycin can be added later. We examined this issue in a prospective, randomized trial. We randomized 127 febrile neutropenic patients to receive either ceftazidime alone or ceftazidime plus vancomycin as the initial empiric antibiotic treatment. We added vancomycin to the ceftazidime arm of the study when fever persisted after 96 h of monotherapy, when new fever occurred after this time, or when a moderately ceftazidime-resistant gram-positive bacterium was isolated. Each of these regimens had similar initial response rates, similar durations of initial fever, similar frequencies of new fever during therapy, similar microbiological cure rates, similar superinfection rates, and similar survival rates. We observed more renal and cutaneous toxicities in patients receiving vancomycin and ceftazidime as initial therapy. We conclude that ceftazidime is appropriate as initial therapy for febrile neutropenic patients and that the addition of vancomycin is appropriate when fever persists after 4 days of monotherapy or when fever recurs following an initial response. C1 NATL NAVAL MED CTR, NCI, NAVY MED ONCOL BRANCH, BETHESDA, MD 20814 USA. RP RAMPHAL, R (reprint author), UNIV FLORIDA, DEPT MED, GAINESVILLE, FL 32610 USA. NR 20 TC 86 Z9 86 U1 0 U2 0 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 MAY PY 1992 VL 36 IS 5 BP 1062 EP 1067 PG 6 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA HT589 UT WOS:A1992HT58900029 PM 1510394 ER PT J AU VIZA, D ARANDAANZALDO, A ABLASHI, D KRAMARSKY, B AF VIZA, D ARANDAANZALDO, A ABLASHI, D KRAMARSKY, B TI HHV-6 INHIBITION BY 2 POLAR COMPOUNDS SO ANTIVIRAL RESEARCH LA English DT Article DE HHV-6; POLAR COMPOUND; VIRAL INHIBITION; DIMETHYL SULFOXIDE; DIMETHYL FORMAMIDE ID VIRUS HUMAN HERPESVIRUS-6; CELLS IN-VITRO; DIMETHYL-SULFOXIDE; ERYTHROID DIFFERENTIATION; ERYTHROLEUKEMIA CELLS; HEMOGLOBIN SYNTHESIS; TYPE-1 REPLICATION; INDUCTION; LEUKEMIA; INDUCERS AB Dimethyl sulphoxide and dimethyl formamide, two polar compounds and powerful cell differentiation inducers, inhibit HHV-6 infection when added to HHV-6-infected HSB2 cultures. This was established by a delay in the time-course of infection and in the development of virus-induced cytopathic effects. Furthermore, viral titration of supernatants showed a significant reduction (3 log10) of the number of infectious particles. Electron microscopy confirmed that viable cells and extracellular virions were present in the cultures containing the polar compounds, while in the non-treated cultures all cells were lysed and no extracellular virus was evident. The mode of action of these compounds is still unclear and warrants further investigation. C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. PHARMACIA DIAGNOST INC,SILVER SPRING,MD. RP VIZA, D (reprint author), FAC MED PARIS,IMMUNOBIOL LAB,CNRS,45 RUE SAINTS PERES,F-75006 PARIS,FRANCE. RI Aranda-Anzaldo, Armando/A-6513-2014 OI Aranda-Anzaldo, Armando/0000-0002-5583-5465 NR 28 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD MAY PY 1992 VL 18 IS 1 BP 27 EP 38 DI 10.1016/0166-3542(92)90003-N PG 12 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA HT092 UT WOS:A1992HT09200002 PM 1329644 ER PT J AU SAFAVI, K AF SAFAVI, K TI PREVALENCE OF ALOPECIA-AREATA IN THE 1ST-NATIONAL-HEALTH-AND-NUTRITION-EXAMINATION-SURVEY SO ARCHIVES OF DERMATOLOGY LA English DT Letter RP SAFAVI, K (reprint author), NIAMSD,OFF PREVENT EPIDEMIOL & CLIN APPLICAT,BLDG 31,ROOM 4C13,BETHESDA,MD 20892, USA. NR 3 TC 66 Z9 71 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD MAY PY 1992 VL 128 IS 5 BP 702 EP 702 PG 1 WC Dermatology SC Dermatology GA HU003 UT WOS:A1992HU00300027 PM 1575541 ER PT J AU PICKAR, D OWEN, RR LITMAN, RE KONICKI, PE GUTIERREZ, R RAPAPORT, MH AF PICKAR, D OWEN, RR LITMAN, RE KONICKI, PE GUTIERREZ, R RAPAPORT, MH TI CLINICAL AND BIOLOGIC RESPONSE TO CLOZAPINE IN PATIENTS WITH SCHIZOPHRENIA - CROSSOVER COMPARISON WITH FLUPHENAZINE SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PLASMA HOMOVANILLIC-ACID; CEREBROSPINAL-FLUID; PHARMACOLOGICAL TREATMENT; ELECTROCHEMICAL DETECTION; NEUROLEPTIC TREATMENT; DOPAMINE; NOREPINEPHRINE; CHLORPROMAZINE; RECEPTORS; PSYCHOSIS AB Twenty-one patients with schizophrenia who met criteria for neuroleptic treatment resistance or intolerance participated in a crossover, placebo-controlled, double-blind comparison of long-term typical neuroleptic and clozapine treatment. Clozapine significantly reduced total as well as positive and negative symptoms in comparison with both fluphenazine and placebo. Of the 21 patients, eight (38%) showed clozapine superiority on the basis of prospective response criteria. High levels of extrapyramidal side effects during fluphenazine treatment and later onset of illness were clinical predictors of clozapine superiority. Clozapine and fluphenazine equally reduced plasma homovanillic acid levels in comparison with placebo, although fluphenazine but not clozapine increased plasma prolactin level. A striking biologic difference between clozapine and fluphenazine was clozapine's enhancement of indexes of noradrenergic activity. Superior clozapine response was predicted by low ratios of cerebrospinal fluid homovanillic acid to 5-hydroxyindoleacetic acid, consistent with the notion that balance between dopaminergic and serotoninergic systems is important for clozapine's mechanism of action. RP PICKAR, D (reprint author), NIMH,EXPTL THERAPEUT BRANCH,CLIN STUDIES SECT,BLDG 10,ROOM 4N214,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 66 TC 311 Z9 313 U1 4 U2 8 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD MAY PY 1992 VL 49 IS 5 BP 345 EP 353 PG 9 WC Psychiatry SC Psychiatry GA HV122 UT WOS:A1992HV12200001 PM 1375019 ER PT J AU SOGN, DD EVANS, R SHEPHERD, GM CASALE, TB CONDEMI, J GREENBERGER, PA KOHLER, PF SAXON, A SUMMERS, RJ VANARSDEL, PP MASSICOT, JG BLACKWELDER, WC LEVINE, BB AF SOGN, DD EVANS, R SHEPHERD, GM CASALE, TB CONDEMI, J GREENBERGER, PA KOHLER, PF SAXON, A SUMMERS, RJ VANARSDEL, PP MASSICOT, JG BLACKWELDER, WC LEVINE, BB TI RESULTS OF THE NATIONAL-INSTITUTE-OF-ALLERGY-AND-INFECTIOUS-DISEASES COLLABORATIVE CLINICAL-TRIAL TO TEST THE PREDICTIVE VALUE OF SKIN TESTING WITH MAJOR AND MINOR PENICILLIN DERIVATIVES IN HOSPITALIZED ADULTS SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID HYPERSENSITIVITY; EXPERIENCE; DIAGNOSIS AB Background. - A history (or lack thereof) of penicillin allergy is known to be unreliable in predicting reactions on subsequent administration of the drug. This study tests the usefulness of four penicillin allergen skin tests in the prediction of IgE-mediated reactions subsequent to administration of penicillin. Methods. - Eight centers cooperated in the National Institute of Allergy and Infectious Diseases trial of the predictive value of skin testing with major and minor penicillin derivatives. Hospitalized adults were tested with a major determinant (octa-benzylpenicilloyl-octalysine) and a minor determinant mixture and its components (potassium benzylpenicillin, benzylpenicilloate, and benzylpenicilloyl-N-propylamine). Patients then received a therapeutic course of penicillin and were observed, for 48 hours, for adverse reactions compatible with an IgE-mediated immediate or accelerated allergy. Results. - Among 726 history-positive patients, 566 with negative skin tests received penicillin and only seven (1.2%) had possibly IgE-mediated reactions. Among 600 history-negative patients, 568 with negative skin tests received penicillin and none had a reaction. Only nine of the 167 positive skin test reactors received a penicillin agent and then usually by cautious incremental dosing. Two (22%) of these nine patients had reactions compatible with IgE-mediated immediate or accelerated penicillin allergy; both were positive to the two determinants. Conclusions. - These data corroborate previous data about the negative predictive value of negative skin tests to these materials. The reaction rate in skin test-positive patients was significantly higher than in those with negative skin tests, demonstrating the positive predictive value of positive tests to both major and minor determinants. The number of patients positive only to the major determinant or only to the minor determinant mix was too small to draw conclusions about the positive predictive value of either reagent alone. C1 NIAID,BETHESDA,MD 20892. NIH,NATL CTR RES RESOURCES,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. NORTHWESTERN UNIV,CHICAGO,IL 60611. CORNELL UNIV,ITHACA,NY 14853. UNIV IOWA,IOWA CITY,IA 52242. UNIV ROCHESTER,ROCHESTER,NY 14627. UNIV COLORADO,DENVER,CO 80202. TULANE UNIV,NEW ORLEANS,LA 70118. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. UNIV WASHINGTON,SEATTLE,WA 98195. NHLBI,BETHESDA,MD 20892. NYU,NEW YORK,NY 10003. RI Casale, Thomas/K-4334-2013 OI Casale, Thomas/0000-0002-3149-7377 FU NIAID NIH HHS [N01 AI-92629, N01 AI-92630, N01 AI-92631] NR 21 TC 187 Z9 191 U1 1 U2 5 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD MAY PY 1992 VL 152 IS 5 BP 1025 EP 1032 DI 10.1001/archinte.152.5.1025 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA HU616 UT WOS:A1992HU61600020 PM 1580706 ER PT J AU SWAN, GE LARUE, A CARMELLI, D REED, TE FABSITZ, RR AF SWAN, GE LARUE, A CARMELLI, D REED, TE FABSITZ, RR TI DECLINE IN COGNITIVE PERFORMANCE IN AGING TWINS - HERITABILITY AND BIOBEHAVIORAL PREDICTORS FROM THE NATIONAL-HEART-LUNG-AND-BLOOD-INSTITUTE TWIN STUDY SO ARCHIVES OF NEUROLOGY LA English DT Article ID PSYCHOMETRIC DIFFERENTIATION; NHLBI TWIN; INTELLIGENCE; ABILITIES; DEMENTIA; PRESSURE; AGE AB The present study examined the contribution of genetic factors to Digit Symbol performance and its decline in 23 monozygotic twin pairs (mean age at examination 1, 57.1 years) and 21 dizygotic twin pairs (mean age at examination 1, 56.3 years). These men were assessed twice during a 5-year interval as part of the National Heart, Lung, and Blood institute Twin Study. The prevalence of decline (a change, > 1 SD) during the 5-year interval was 35% and 39% for monozygotic and dizygotic twins, respectively. The pairwise concordance for decline was 45% in monozygotic and 8% in dizygotic twin pairs, suggesting a possible role for genetic factors in the decline in Digit Symbol performance in this sample. A comparison of baseline biologic and behavioral characteristics within monozygotic twin pairs discordant for decline in Digit Symbol performance revealed that decliners had higher initial systolic blood pressures, lower serum cholesterol levels, and lower heart rates than nondecliners. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. INDIANA UNIV,SCH MED,DEPT MED GENET,INDIANAPOLIS,IN 46202. NHLBI,DIV EPIDEMIOL,BETHESDA,MD 20892. RP SWAN, GE (reprint author), STANFORD RES INST,HLTH SCI PROGRAM,333 RAVENSWOOD AVE,MENLO PK,CA 94025, USA. FU NHLBI NIH HHS [N01-HC-55029] NR 43 TC 69 Z9 70 U1 1 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD MAY PY 1992 VL 49 IS 5 BP 476 EP 481 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA HT678 UT WOS:A1992HT67800010 PM 1580808 ER PT J AU LINET, MS ZIEGLER, DK STEWART, WF AF LINET, MS ZIEGLER, DK STEWART, WF TI HEADACHES PRECEDED BY VISUAL AURA AMONG ADOLESCENTS AND YOUNG-ADULTS - A POPULATION-BASED SURVEY SO ARCHIVES OF NEUROLOGY LA English DT Article ID CLINIC POPULATION; MIGRAINE; SYMPTOMS; WOMEN AB Clinical descriptions of migraine preceded by visual aura often include a composite of striking and severe symptoms of several attacks in individual patients, but few studies have characterized the spectrum of such attacks. In a population-based telephone survey of 8920 Washington County, Maryland, residents 12 through 29 years old, the attack rate for visual aura headaches during the week prior to the standardized interview was 3.7% in male and 6.1% in female subjects. Among female subjects, the risk for visual aura headache with tension-type symptoms increased with age, whereas the risk for visual aura headache without tension symptoms decreased with increasing age. No clear age-related patterns were observed among male subjects for either type of aura headache. The severity of visual aura headache with and without tension symptoms increased with age among female subjects, but showed an inconsistent pattern among male subjects except for decreasing disability with increasing age. The median interval between the onset of aura symptoms and the onset of headache (aura interval) was 15 minutes in male subjects and 25 minutes in female subjects, with aura intervals longer than 60 minutes reported by 12% of male subjects 'and 20% of female subjects. In one of the first large population-based studies to characterize the spectrum of visual aura headache, differing age, gender, and subtype patterns were found. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21218. UNIV KANSAS,MED CTR,DEPT NEUROL,KANSAS CITY,KS 66103. RP LINET, MS (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BIOSTAT BRANCH,ANALYT STUDIES SECT,EPN 415B,ROCKVILLE,MD 20892, USA. FU NINDS NIH HHS [NS-19381] NR 23 TC 10 Z9 10 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD MAY PY 1992 VL 49 IS 5 BP 512 EP 516 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA HT678 UT WOS:A1992HT67800016 PM 1580814 ER PT J AU RUMSEY, JM ANDREASON, P ZAMETKIN, AJ AQUINO, T KING, AC HAMBURGER, SD PIKUS, A RAPOPORT, JL COHEN, RM AF RUMSEY, JM ANDREASON, P ZAMETKIN, AJ AQUINO, T KING, AC HAMBURGER, SD PIKUS, A RAPOPORT, JL COHEN, RM TI FAILURE TO ACTIVATE THE LEFT TEMPOROPARIETAL CORTEX IN DYSLEXIA - AN O-15 POSITRON EMISSION TOMOGRAPHIC STUDY SO ARCHIVES OF NEUROLOGY LA English DT Article ID DEVELOPMENTAL DYSLEXIA; READING-DISABILITY; ANATOMY AB To test the hypothesis of left temporoparietal dysfunction in dyslexia, suggested by neuropsychological and neuropathologic data, cerebral blood flow was measured with positron emission tomography in 14 right-handed men with severe developmental dyslexia (mean [SD] age, 27 [5] years; median reading level, fifth grade) and 14 matched controls at rest and during an auditory phonologic task (rhyme detection) and an auditory attention task involving the detection of target tones. As expected, normal readers activated left temporoparietal cortex during rhyme detection but not during the nonphonologic attentional task. Dyslexic men failed to activate those left temporoparietal regions activated in controls during rhyme detection but did not differ from controls in these regions during rest or attentional testing. Thus, the expected left temporoparietal dysfunction was demonstrated only when specific probes for these regions were employed. C1 NIMH,CEREBRAL METAB LAB,CLIN BRAIN IMAGING SECT,BETHESDA,MD 20892. NIDCD,CLIN AUDIOL HEARING SECT,BETHESDA,MD. RP RUMSEY, JM (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,BETHESDA,MD 20892, USA. NR 28 TC 225 Z9 226 U1 3 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD MAY PY 1992 VL 49 IS 5 BP 527 EP 534 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA HT678 UT WOS:A1992HT67800018 PM 1580816 ER PT J AU WHITCUP, SM CHAN, CC LI, Q NUSSENBLATT, RB AF WHITCUP, SM CHAN, CC LI, Q NUSSENBLATT, RB TI EXPRESSION OF CELL-ADHESION MOLECULES IN POSTERIOR UVEITIS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID HUMAN-ENDOTHELIAL CELLS; NECROSIS FACTOR-ALPHA; INTERFERON-GAMMA; IMMUNE-SYSTEM; RECEPTORS; ICAM-1; LFA-1; MECHANISMS; INTEGRINS AB Cells in the eye express surface molecules that direct leukocyte migration during ocular inflammation. We studied the expression of intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and endothelial leukocyte adhesion molecule-1 in six enucleated eyes from patients with uveitis and in seven normal control eyes. Lymphocyte function-associated antigen-1 was expressed on infiltrating lymphocytes and intercellular adhesion molecule-1 was expressed on endothelial cells of retinal and choroidal blood vessels and the retinal pigment epithelium in all uveitic eyes, but in none of the normal control eyes. Ocular inflammatory cells stained strongly positive for tumor necrosis factor-alpha in all eyes with uveitis, but four of six uveitic eyes showed mild staining for tumor necrosis factor-beta and interferon gamma. Cell adhesion molecules are expressed in eyes with posterior uveitis and may be regulated by cytokines such as tumor necrosis factor-alpha. RP WHITCUP, SM (reprint author), NEI,IMMUNOL LAB,BLDG 10,RM 10N202,BETHESDA,MD 20892, USA. NR 27 TC 68 Z9 70 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAY PY 1992 VL 110 IS 5 BP 662 EP 666 PG 5 WC Ophthalmology SC Ophthalmology GA HT822 UT WOS:A1992HT82200025 PM 1374609 ER PT J AU BECHTOLD, WE SUN, JD BIRNBAUM, LS YIN, SN LI, GL KASICKI, S LUCIER, G HENDERSON, RF AF BECHTOLD, WE SUN, JD BIRNBAUM, LS YIN, SN LI, GL KASICKI, S LUCIER, G HENDERSON, RF TI S-PHENYLCYSTEINE FORMATION IN HEMOGLOBIN AS A BIOLOGICAL EXPOSURE INDEX TO BENZENE SO ARCHIVES OF TOXICOLOGY LA English DT Article DE BENZENE; HEMOGLOBIN; ADDUCTS; S-PHENYLCYSTEINE; BIOLOGICAL EXPOSURE INDEX ID METABOLISM; ADDUCTS; BINDING; IDENTIFICATION; BENZOQUINONE; RAT AB Benzene is metabolized to intermediates that bind to hemoglobin, forming adducts. These hemoglobin adducts may be usable as biomarkers of exposure. In this paper, we describe the development of a gas chromatography/mass spectroscopy assay for quantitating the binding of the benzene metabolite, benzene oxide, to cysteine groups in hemoglobin. We used this assay to study the hemoglobin adduct, S-phenylcysteine (SPC), in the blood of rats and mice exposed to benzene either by inhalation or by gavage. We were able to detect SPC in the hemoglobin of exposed rats and mice, to show the linearity of the exposure dose-response relationship, and to establish the sensitivity limits of this assay. For the same exposure regime, rats showed considerably higher levels of SPC than did mice. As yet, we have not been able to detect SPC in the globin of humans occupationally exposed to benzene. We attempted to determine whether the SPC found in hemoglobin originated from the metabolism of benzene within or outside of the red blood cell. We hypothesized that the greatest red blood cell metabolism would be associated with peripheral reticulocytes, which retain high metabolic capacity. After exposing rats to benzene, we isolated the red blood cells and used discontinuous Percoll gradients to fractionate them into age groups. No differences in SPC levels were found among any of the fractions, suggesting that the SPC found in globin originates from the metabolism of benzene to benzene oxide in a location external to the red blood cell. To our knowledge, this is the first demonstration of the nonenzymatic binding of the benzene metabolite, benzene oxide, to protein. The products of the interaction of benzene oxide with protein are particularly appealing as potential biomarkers. These adducts are stable both in vivo and during isolation, and because high background levels in unexposed individuals are unlikely, the presence of such adducts should be a specific indicator of exposure to benzene. If SPC can be detected in humans, the present assay, with some modification, may be amenable to routine monitoring of worker exposures to benzene. C1 US EPA,HLTH EFFECTS RES LAB,DIV ENVIRONM TOXICOL,RES TRIANGLE PK,NC 27711. CHINESE ACAD PREVENT MED,INST OCCUPAT MED,BEIJING,PEOPLES R CHINA. NIEHS,RES TRIANGLE PK,NC 27709. RP BECHTOLD, WE (reprint author), LOVELACE BIOMED & ENVIRONM RES INST,INHALAT TOXICOL RES INST,POB 5890,ALBUQUERQUE,NM 87185, USA. FU NIEHS NIH HHS [222-Y02-ES-20092] NR 25 TC 34 Z9 35 U1 1 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-5761 J9 ARCH TOXICOL JI Arch. Toxicol. PD MAY PY 1992 VL 66 IS 5 BP 303 EP 309 DI 10.1007/BF01973623 PG 7 WC Toxicology SC Toxicology GA HV511 UT WOS:A1992HV51100001 PM 1610291 ER PT J AU STEINBERG, AD AF STEINBERG, AD TI A CRITIQUE OF THE NIH LUPUS NEPHRITIS SURVEY - REPLY SO ARTHRITIS AND RHEUMATISM LA English DT Letter RP STEINBERG, AD (reprint author), NIH,BETHESDA,MD 20892, USA. NR 14 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD MAY PY 1992 VL 35 IS 5 BP 605 EP 607 DI 10.1002/art.1780350521 PG 3 WC Rheumatology SC Rheumatology GA HV713 UT WOS:A1992HV71300021 ER PT J AU HEYES, MP SAITO, K MARKEY, SP AF HEYES, MP SAITO, K MARKEY, SP TI HUMAN MACROPHAGES CONVERT L-TRYPTOPHAN INTO THE NEUROTOXIN QUINOLINIC ACID SO BIOCHEMICAL JOURNAL LA English DT Note ID CEREBROSPINAL-FLUID; RHESUS MACAQUES; KYNURENIC ACID; RAT-BRAIN; QUANTIFICATION AB Substantial increases in the concentrations of the excitotoxin and N-methyl-D-aspartate-receptor agonist quinolinic acid (QUIN) occur in human patients and non-human primates with inflammatory diseases. Such increases were postulated to be secondary to induction of indoleamine 2.3-dioxygenase in inflammatory cells, particularly macrophages, by interferon-gamma. To test this hypothesis, human peripheral-blood macrophages were incubated with L-[C-13(6)]tryptophan in the absence or presence of interferon-gamma. [C-13(6)]QUIN was quantified by gas chromatography and electron-capture negative-chemical-ionization mass spectrometry. [C-13(6)]QUIN was detected in the incubation medium of both unstimulated and stimulated cultures. Exposure to interferon-gamma substantially increased the accumulation of [C-13(6)]QUIN in a dose- and time-dependent manner. The QUIN concentrations achieved exceeded those reported in both cerebrospinal fluid and blood of patients and of non-human primates with inflammatory diseases. Macrophages stimulated with interferon-gamma may be an important source of accelerated L-tryptophan conversion into QUIN in inflammatory diseases. RP HEYES, MP (reprint author), NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BETHESDA,MD 20892, USA. NR 17 TC 190 Z9 191 U1 0 U2 3 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAY 1 PY 1992 VL 283 BP 633 EP 635 PN 3 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR720 UT WOS:A1992HR72000002 PM 1534219 ER PT J AU KLEIN, DC SCHAAD, NL NAMBOORDIRI, MAA YU, L WELLER, JL AF KLEIN, DC SCHAAD, NL NAMBOORDIRI, MAA YU, L WELLER, JL TI REGULATION OF PINEAL SEROTONIN N-ACETYLTRANSFERASE ACTIVITY SO BIOCHEMICAL SOCIETY TRANSACTIONS LA English DT Article; Proceedings Paper CT 641ST MEETING OF THE BIOCHEMICAL SOC CY DEC 17-20, 1991 CL ROYAL HOLLOWAY & BEDFORD NEW COLL, LONDON, ENGLAND SP BIOCHEM SOC HO ROYAL HOLLOWAY & BEDFORD NEW COLL ID PROTEIN KINASE-C; BETA-ADRENERGIC STIMULATION; RAT PINEALOCYTES; CIRCADIAN-RHYTHM; ADENOSINE 3',5'-MONOPHOSPHATE; DISULFIDE EXCHANGE; MELATONIN; GLAND; DECREASE; CALCIUM C1 GEORGETOWN UNIV,DEPT BIOL,WASHINGTON,DC 20057. UNIV ST LOUIS,INST MOLEC VIROL,ST LOUIS,MO 63100. RP KLEIN, DC (reprint author), NICHHD,DEV NEUROBIOL LAB,NEUROENDOCRINOL RES LAB,BETHESDA,MD 20892, USA. NR 42 TC 57 Z9 57 U1 1 U2 2 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0300-5127 J9 BIOCHEM SOC T JI Biochem. Soc. Trans. PD MAY PY 1992 VL 20 IS 2 BP 299 EP 304 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV728 UT WOS:A1992HV72800012 PM 1397615 ER PT J AU CHOCHUNG, YS AF CHOCHUNG, YS TI SUPPRESSION OF MALIGNANCY TARGETING CYCLIC-AMP SIGNAL TRANSDUCING PROTEINS SO BIOCHEMICAL SOCIETY TRANSACTIONS LA English DT Article; Proceedings Paper CT 641ST MEETING OF THE BIOCHEMICAL SOC CY DEC 17-20, 1991 CL ROYAL HOLLOWAY & BEDFORD NEW COLL, LONDON, ENGLAND SP BIOCHEM SOC HO ROYAL HOLLOWAY & BEDFORD NEW COLL ID MAMMARY EPITHELIAL-CELLS; SELECTIVE CAMP ANALOGS; II REGULATORY SUBUNIT; CATALYTIC SUBUNIT; MOLECULAR-CLONING; ADENOSINE-MONOPHOSPHATE; GENE-EXPRESSION; MESSENGER-RNA; HUMAN TESTIS; KINASE RP CHOCHUNG, YS (reprint author), NCI,BETHESDA,MD 20892, USA. NR 50 TC 25 Z9 25 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0300-5127 J9 BIOCHEM SOC T JI Biochem. Soc. Trans. PD MAY PY 1992 VL 20 IS 2 BP 425 EP 430 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV728 UT WOS:A1992HV72800045 PM 1327918 ER PT J AU KARTON, Y BAUMGOLD, J HANDEN, JS JACOBSON, KA AF KARTON, Y BAUMGOLD, J HANDEN, JS JACOBSON, KA TI MOLECULAR PROBES FOR MUSCARINIC RECEPTORS - DERIVATIVES OF THE M1-ANTAGONIST TELENZEPINE SO BIOCONJUGATE CHEMISTRY LA English DT Article ID ACETYLCHOLINE-RECEPTOR; AFFINITY; DRUG; TRANSPORTER; INHIBITION; AGONIST; LIGANDS; GENES AB Functionalized congeners of the M1-selective muscarinic antagonist telenzepine (4,9-dihydro-3-methyl-4-[(4-methyl-1-piperazinyl)acetyl]-10H-thieno[3,4-b][1,5]benzodiazepin-10-one) were developed and found to bind to the receptor with affinities (K(i) values) in approximately the nanomolar range. The derivatives contain a 10-aminodecyl group, which provides a nucleophilic functionality for further derivatization. The attachment of a spacer chain to the distal piperazinyl nitrogen was based on previous findings of enhanced affinity at muscarinic receptors in an analogous series of alkylamino derivatives of pirenzepine [J. Med. Chem. (1991) 34, 2133-2145]. The telenzepine derivatives contain prosthetic groups for radioiodination, protein cross-linking, photoaffinity labeling, and fluorescent labeling and biotin for avidin complexation. The affinity for muscarinic receptors in rat forebrain (mainly m1 subtype) was determined in competitive binding assays vs [H-3]-N-methylscopolamine. A (P-aminophenyl)acetyl derivative for photoaffinity labeling had a K(i) value of 0.29 nM at forebrain muscarinic receptors (16-fold higher affinity than telenzepine). A biotin conjugate displayed a K(i) value of 0.60 nM at m2-receptors and a 5-fold selectivity versus forebrain. The high affinity of these derivatives makes them suitable for the characterization of muscarinic receptors in pharmacological and spectroscopic studies, for peptide mapping, and for histochemical studies. C1 NIDDK,BIOORGAN CHEM LAB,BLDG 8A,RM B1A 17,BETHESDA,MD 20892. ISRAEL INST BIOL RES,IL-70450 NESS ZIONA,ISRAEL. GEORGE WASHINGTON UNIV,MED CTR,DEPT RADIOL,WASHINGTON,DC 20037. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031115-24, Z99 DK999999] NR 25 TC 12 Z9 12 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD MAY-JUN PY 1992 VL 3 IS 3 BP 234 EP 240 DI 10.1021/bc00015a006 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA HX055 UT WOS:A1992HX05500006 PM 1520727 ER PT J AU KUNKEL, TA AF KUNKEL, TA TI BIOLOGICAL ASYMMETRIES AND THE FIDELITY OF EUKARYOTIC DNA-REPLICATION SO BIOESSAYS LA English DT Review ID INVITRO REPLICATION; MAMMALIAN GENOME; MUTATION-RATES; CELLS; MISALIGNMENT; MISMATCH; REGIONS; REPAIR AB A diploid human genome contains approximately six billion nucleotides. This enormous amount of genetic information can be replicated with great accuracy in only a few hours. However, because DNA strands are oriented antiparallel while DNA polymerization only occurs in the 5' --> 3' direction, semi-conservative replication of double-stranded DNA is an asymmetric process, i.e., there is a leading and a lagging strand. This provides a considerable opportunity for non-random error rates, because the architecture of the two strands as well as the DNA polymerases that replicate them may be different. In addition, the proteins that start or finish chains may well be different from those that perform the bulk of chain elongation. Furthermore, while replication fidelity depends on the absolute and relative concentrations of the four deoxyribonucleotide precursors, these are not equal in vivo, not constant throughout the cell cycle, and not necessarily equivalent in all cell types. Finally, the fidelity of DNA synthesis is sequence-dependent and the eukaryotic nuclear genome is a heterogeneous substrate. It contains repetitive and nonrepetitive sequences and can actually be considered as two subgenomes that differ in nucleotide composition and gene content and that replicate at different times. The effects that each of these asymmetries may have on error rates during replication of the eukaryotic genome are discussed. RP KUNKEL, TA (reprint author), NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709, USA. NR 44 TC 90 Z9 91 U1 2 U2 4 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD MAY PY 1992 VL 14 IS 5 BP 303 EP 308 DI 10.1002/bies.950140503 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA HX062 UT WOS:A1992HX06200002 PM 1637361 ER PT J AU RUBINOW, DR POST, RM AF RUBINOW, DR POST, RM TI IMPAIRED RECOGNITION OF AFFECT IN FACIAL EXPRESSION IN DEPRESSED-PATIENTS SO BIOLOGICAL PSYCHIATRY LA English DT Article ID EMOTION; ASYMMETRY; DISORDERS; AMYGDALA; BEHAVIOR; NEURONS; LESION; MONKEY; FACES AB Measures of recognition of seven affects in facial and verbal expressions to 17 depressed patients and 31 controls were administered. Depressed patients were significantly impaired in the recognition of affect in the facial, but not verbal, expressions. Among the seven affects examined, depressed patients made significantly or near significantly fewer correct matches for sad, happy, and interested face items. The performance of the depressed patients was similar to that observed by Kolb and Taylor in patients with right, but not left, hemisphere cortical excisions. The neurobiology of facial recognition is reviewed, and the relevance of the observed perceptual deficit in depressed patients to the pathophysiology and symptomatology of depression is discussed. RP RUBINOW, DR (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BEHAV ENDOCRINOL SECT,BLDG 10,ROOM 3N238,BETHESDA,MD 20892, USA. NR 27 TC 160 Z9 163 U1 1 U2 17 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 MAY 1 PY 1992 VL 31 IS 9 BP 947 EP 953 DI 10.1016/0006-3223(92)90120-O PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JD610 UT WOS:A1992JD61000009 PM 1637932 ER PT J AU JOLKKONEN, J PITKANEN, A RIEKKINEN, PJ KORPI, ER KAUFMANN, CA WEINBERGER, DR AF JOLKKONEN, J PITKANEN, A RIEKKINEN, PJ KORPI, ER KAUFMANN, CA WEINBERGER, DR TI SOMATOSTATIN-LIKE IMMUNOREACTIVITY IN CSF OF SCHIZOPHRENIC-PATIENTS DURING HALOPERIDOL TREATMENT SO BIOLOGICAL PSYCHIATRY LA English DT Note ID CEREBROSPINAL-FLUID CONCENTRATIONS; BRAIN; NEUROPEPTIDES; RAT C1 UNIV KUOPIO,DEPT NEUROL,KUOPIO,FINLAND. ALKO LTD,RES LABS,HELSINKI,FINLAND. NIMH,IRP,CLIN BRAIN DISORDERS BRANCH,NEUROSCI CTR ST ELIZABETHS,WASHINGTON,DC 20032. COLUMBIA UNIV,DEPT PSYCHIAT,NEW YORK,NY 10027. RP JOLKKONEN, J (reprint author), VAAJASALO HOSP,SF-71130 KORTEJOKI,FINLAND. NR 16 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 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1992 VL 31 IS 9 BP 962 EP 964 DI 10.1016/0006-3223(92)90122-G PG 3 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JD610 UT WOS:A1992JD61000011 PM 1637934 ER PT J AU GLOVINSKY, D KIRCH, DG WYATT, RJ AF GLOVINSKY, D KIRCH, DG WYATT, RJ TI EARLY ANTIPSYCHOTIC RESPONSE TO RESUMPTION OF NEUROLEPTICS IN DRUG-FREE CHRONIC-SCHIZOPHRENIC PATIENTS SO BIOLOGICAL PSYCHIATRY LA English DT Note ID RAPID TREATMENT; HALOPERIDOL; PSYCHOSIS; DOPAMINE C1 NIMH,DIV CLIN RES,ROCKVILLE,MD 20857. RP GLOVINSKY, D (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032, USA. NR 13 TC 31 Z9 31 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 1 PY 1992 VL 31 IS 9 BP 968 EP 970 DI 10.1016/0006-3223(92)90124-I PG 3 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JD610 UT WOS:A1992JD61000013 PM 1637936 ER PT J AU MORI, C WELCH, JE SAKAI, Y EDDY, EM AF MORI, C WELCH, JE SAKAI, Y EDDY, EM TI INSITU LOCALIZATION OF SPERMATOGENIC CELL-SPECIFIC GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE (GAPD-S) MESSENGER-RIBONUCLEIC-ACID IN MICE SO BIOLOGY OF REPRODUCTION LA English DT Article ID ROUND SPERMATIDS; DNA FRAGMENTS; TESTIS; MOUSE; HYBRIDIZATION; RNAS; LACTATE; GENE; METABOLISM; EXPRESSION AB Northern blot analysis with a cDNA clone for mouse spermatogenic cell-specific glyceraldehyde 3-phosphate dehydrogenase (Gapd-s) previously identified transcripts in isolated round spermatids, but not in isolated pachytene spermatocyte's, strongly suggesting that Gapd-s transcription first occurs in haploid germ cells- In the present study, in situ hybridization was carried out with a [S-35]-labeled anti-sense RNA probe of Gapd-s to define more precisely the temporal expression and spatial distribution of Gapd-s mRNA in adult mouse testes. Gapd-s transcripts were not detected in spermatogonia, primary spermatocytes, secondary spermatocytes, or spermatozoa. However, they were abundant in round spermatids and condensing spermatids. Transcripts were not detected in somatic cells of the testis, in oocytes in pre-antral or antral follicles, or in skeletal muscle. Grain counts were used to define when the Gapd-s gene was expressed during round spermatid development in adult mice. The number of silver grains first exceeded background levels in step 4-6 spermatids (early cap phase of spermiogenesis) and were high in step 7-15 spermatids (acrosome and elongation phases of spermiogenesis). However, they returned to background levels in step 16 spermatids, the final step of spermiogenesis in the mouse. In 20-day-old juvenile mice, Gapd-s transcripts were first detected in round spermatids during the early cap phase of development. These observations confirmed that Gapd-s mRNA is expressed during the post-meiotic phase of male germ cell development, demonstrated that Gapd-s transcripts are present in step 4-15 spermatids, and established that transcription begins in round spermatids during the early cap phase of spermiogenesis in both juvenile and adult mice. C1 NIEHS,REPROD & DEV TOXICOL LAB,DEV ENDOCRINOL & PHARMACOL SECT,C4-01,RES TRIANGLE PK,NC 27709. NIEHS,REPROD & DEV TOXICOL LAB,GAMETE BIOL SECT,RES TRIANGLE PK,NC 27709. NR 30 TC 39 Z9 40 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD MAY PY 1992 VL 46 IS 5 BP 859 EP 868 DI 10.1095/biolreprod46.5.859 PG 10 WC Reproductive Biology SC Reproductive Biology GA HP390 UT WOS:A1992HP39000013 PM 1591341 ER PT J AU WELCH, JE SCHATTE, EC OBRIEN, DA EDDY, EM AF WELCH, JE SCHATTE, EC OBRIEN, DA EDDY, EM TI EXPRESSION OF A GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GENE SPECIFIC TO MOUSE SPERMATOGENIC CELLS SO BIOLOGY OF REPRODUCTION LA English DT Article ID ROUND SPERMATIDS; MESSENGER-RNA; SERTOLI CELLS; MORPHOLOGICAL CHARACTERIZATION; NUCLEOTIDE-SEQUENCES; PREFERRED SUBSTRATE; GLUCOSE-METABOLISM; RIBONUCLEIC-ACID; ANTIBODY PROBES; CDNA LIBRARIES AB A cDNA clone encoding a putative glyceraldehyde 3-phosphate dehydrogenase (GAPD-S) protein specific to spermatogenic cells was isolated from a mouse spermatogenic cell expression library. The Gapd-s cDNA contained 1451 bp of transcribed sequence, including an ATG initiation codon and a poly(A) addition signal. The location of the Gapd-s initiation codon differed from that of other Gapd sequences, resulting in a germ cell GAPD-S protein predicted to contain 105 additional residues at the amino terminus. While GAPD is constitutively expressed in somatic tissues, Northern blot analysis demonstrated that a Gapd-s probe hybridized to a 1.5-kb transcript present only in the testis. The Gapd-s mRNA was first detected during postnatal development in the testes of 20-day-old mice, suggesting that gene expression begins shortly after the appearance of haploid round spermatids. Northern analysis of RNA from isolated mouse pachytene spermatocytes and spermatids confirmed that Gapd-s expression is confined to post-meiotic germ cells. GAPD has been previously proposed to be the key enzyme regulating glycolysis in isolated round spermatids. We hypothesize that the GAPD-S enzyme plays an important role in regulating the switch between different pathways for energy production during spermiogenesis and in the spermatozoon. C1 UNIV N CAROLINA,REPROD BIOL LABS,CHAPEL HILL,NC 27595. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC 27595. UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27595. RP WELCH, JE (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,GAMETE BIOL SECT,BLDG 101,C4-03,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU NICHD NIH HHS [P30-HD-18968, R01 HD026485, HD-26485] NR 90 TC 119 Z9 121 U1 0 U2 2 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD MAY PY 1992 VL 46 IS 5 BP 869 EP 878 DI 10.1095/biolreprod46.5.869 PG 10 WC Reproductive Biology SC Reproductive Biology GA HP390 UT WOS:A1992HP39000014 PM 1375514 ER PT J AU DONOGHUE, AM JOHNSTON, LA MUNSON, L BROWN, JL WILDT, DE AF DONOGHUE, AM JOHNSTON, LA MUNSON, L BROWN, JL WILDT, DE TI INFLUENCE OF GONADOTROPIN TREATMENT INTERVAL ON FOLLICULAR MATURATION, INVITRO FERTILIZATION, CIRCULATING STEROID CONCENTRATIONS, AND SUBSEQUENT LUTEAL FUNCTION IN THE DOMESTIC CAT SO BIOLOGY OF REPRODUCTION LA English DT Article ID OVARIAN ACTIVITY; SEXUAL-BEHAVIOR; OOCYTES; PHASE; PROGESTERONE; ASPIRATION; CYCLICITY; PREGNANCY; ESTRADIOL; HORMONES AB The impact of the eCG-hCG interval on in vitro fertilization (IVF), endogenous hormonal patterns, and luteal integrity was studied in the domestic cat. Adult cats with inactive ovaries were given eCG (i.m.) and then hCG (i.m.) 80, 84, 88, 92, or 96 h later. Oocytes were aspirated 25-27 h after hCG and co-cultured with swim-up-processed cat spermatozoa. Blood samples were collected daily from 2 days before eCG treatment (Day -2) through Day 14, and sera were analyzed for estradiol-17-beta and progesterone. The mean number of oocytes recovered from the 80-92-h groups (range, 17.2 +/- 2.1 to 21.1 +/- 3.0) did not differ (p > 0.05); however, oocyte number was reduced (p < 0.05) in the 96-h group (10.3 +/- 2.1). The proportion of all oocytes classified as mature was greater (p < 0.05) when hCG was given 80, 84, or 88 h compared to 92 or 96 h after eCG. Delaying hCG treatment until 96 h caused more than 25% of all oocytes to degenerate, which was a greater rate (p < 0.05) than in all other groups. The IVF rate at 80 (57%), 84 (56.5%), 88 (65.0%), and 92 (52.5%) h was greater (p < 0.05) than that observed at 96 h (33.6%). Circulating estradiol-17-beta concentrations began to rise above nadir within 24 h of eCG injection in all interval groups. On the basis of areas under the curve, cats in the 80- and 84-h treatments produced more (p < 0.05) estradiol-17-beta than other groups. Circulating progesterone rose above nadir within the first 24 h of follicular aspiration, and there were no marked temporal differences among groups. Mean CL number on Day 14 ranged from 11.8 in the 96-h group to 20.3 in the 84-h group, but was not different (p > 0.05) because of wide variation among individual animals. Mean luteal weight per ovary was higher (p < 0.05) in the 80-92-h intervals (range, 0.13 +/- 0.01 to 0.21 +/- 0.14 g/ovary) than in the 96-h group (0.07 +/- 0.01 g/ovary), resulting in greater overall progesterone content per ovary (p < 0.05). However, neither progesterone concentration per unit mass of luteal tissue nor luteal histology differed (p > 0.05) among interval groups. Although cat oocytes normally reside within Graafian follicles for unpredictable intervals awaiting copulation, these oocytes are sensitive to the timing of the hormonal stimulus that triggers final maturation, but only if the interval between the FSH-like and LH-like stimulus exceeds 88 h. The effect is expressed by variation in the number and maturity of oocytes recovered and by as yet undefined alterations that influence fertilizability in vitro but not CL composition or function. C1 UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. UNIV TENNESSEE,COLL VET MED,KNOXVILLE,TN 37901. RP DONOGHUE, AM (reprint author), SMITHSONIAN INST,NATL ZOOL PK,DEPT ANIM HLTH,WASHINGTON,DC 20008, USA. FU NICHD NIH HHS [HD 23853] NR 42 TC 45 Z9 47 U1 1 U2 6 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD MAY PY 1992 VL 46 IS 5 BP 972 EP 980 DI 10.1095/biolreprod46.5.972 PG 9 WC Reproductive Biology SC Reproductive Biology GA HP390 UT WOS:A1992HP39000028 PM 1591354 ER EF