FN Thomson Reuters Web of Science™ VR 1.0 PT J AU CHOW, WH DOSEMECI, M ZHENG, W VETTER, R MCLAUGHLIN, JK GAO, YT BLOT, WJ AF CHOW, WH DOSEMECI, M ZHENG, W VETTER, R MCLAUGHLIN, JK GAO, YT BLOT, WJ TI PHYSICAL-ACTIVITY AND OCCUPATIONAL RISK OF COLON CANCER IN SHANGHAI, CHINA SO INTERNATIONAL JOURNAL OF EPIDEMIOLOGY LA English DT Article ID LARGE-BOWEL CANCER; COLORECTAL-CANCER; DIETARY EPIDEMIOLOGY; NORTH-AMERICA; HYPOTHESIS; SUBSITE; SEX; FAT AB Using occupational data for over 2000 colon cancer cases diagnosed between 1980 and 1984 in Shanghai, and employment information from the 1982 census for the Shanghai population, standardized incidence ratios (SIR) were computed for occupational groups classified by job types and physical activity levels. Men employed in occupations with low physical activity levels had modest but significantly elevated risks of colon cancer. SIR for jobs with low activity based on sitting time was 121 (95% confidence interval, Cl : 108-135) and based on energy expenditure was 126 (95% Cl : 115-138). Corresponding SIR for women were 99 195% Cl : 83-118) and 113 (95% Cl : 100-127). The data were also used to screen for specific occupations with elevated SIR to generate leads to occupational colon cancer. Increased incidence was observed for professional and other white collar workers, and male chemical processors and female textile workers. The findings add to the emerging evidence that workplace activity may influence the risk of this common cancer. C1 SHANGHAI CANC INST,DEPT EPIDEMIOL,SHANGHAI,PEOPLES R CHINA. RP CHOW, WH (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,6130 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 55 TC 46 Z9 46 U1 1 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0300-5771 J9 INT J EPIDEMIOL JI Int. J. Epidemiol. PD FEB PY 1993 VL 22 IS 1 BP 23 EP 29 DI 10.1093/ije/22.1.23 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KP203 UT WOS:A1993KP20300004 PM 8449643 ER PT J AU JOHNSON, R AF JOHNSON, R TI EVENT-RELATED POTENTIAL EVIDENCE OF MULTIPLE MEMORY SYSTEM ACTIVITY DURING RECOGNITION MEMORY SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. J. Psychophysiol. PD FEB PY 1993 VL 14 IS 2 BP 129 EP 129 DI 10.1016/0167-8760(93)90178-R PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA KU039 UT WOS:A1993KU03900071 ER PT J AU ROHRBAUGH, JW VARNER, JL LAW, SK ZUBOVIC, EA ECKARDT, MJ AF ROHRBAUGH, JW VARNER, JL LAW, SK ZUBOVIC, EA ECKARDT, MJ TI SYNTHESIS OF THE AUDITORY 40 HZ RHYTHM FROM INDIVIDUAL MIDDLE LATENCY RESPONSE COMPONENTS SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. UNIV NEBRASKA,NIAAA,LINCOLN,NE 68588. NR 0 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. J. Psychophysiol. PD FEB PY 1993 VL 14 IS 2 BP 145 EP 145 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA KU039 UT WOS:A1993KU03900129 ER PT J AU FISHERMAN, JS OSBORN, BL CHUN, HG PLOWMAN, J SMITH, AC CHRISTIAN, MC ZAHARKO, DS SHOEMAKER, RH AF FISHERMAN, JS OSBORN, BL CHUN, HG PLOWMAN, J SMITH, AC CHRISTIAN, MC ZAHARKO, DS SHOEMAKER, RH TI CHLOROQUINOXALINE SULFONAMIDE - A SULFANILAMIDE ANTITUMOR AGENT ENTERING CLINICAL-TRIALS SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE CHLOROQUINOXALINE SULFONAMIDE; TOXICITY; PHARMACOKINETICS ID COLONY-FORMING ASSAY; TUMOR AB Chloroquinoxaline sulfonamide (CQS) has been developed to the clinical trial stage based on its activity in the Human Tumor Colony Forming Assay (HTCFA). In the HTCFA, CQS demonstrated inhibition of colony formation against breast, lung, melanoma and ovarian carcinomas. The mechanism of action of CQS is unknown. It does not appear to inhibit folate metabolism as does the structurally similar sulfaquinoxaline. Preclinical toxicology studies in dogs and rats have shown that CQS is toxic to lymphoid organs, bone marrow, gastrointestinal tract, pancreas, CNS, adrenal glands and testes. Toxicity was generally reversible with the exception of testicular atrophy in dogs and rats which occurred late and was not reversible within the study time frame. The pharmacokinetic data indicate that CQS binds to serum proteins in a dose and species specific manner. Terminal half-lives appear to vary between species from 60 hours in mice, 15 hours in rats, and 45-132 hours in dogs. Preliminary data indicate a longer terminal half-life in humans. Two phase I trials are ongoing using a 60 min infusion schedule once every 28 days. The starting dose for each trial was 18 mg/m2. C1 NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,INVEST DRUG BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,TOXICOL BRANCH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,PHARMACOL BRANCH,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 16 TC 14 Z9 14 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PD FEB PY 1993 VL 11 IS 1 BP 1 EP 9 DI 10.1007/BF00873904 PG 9 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA LF647 UT WOS:A1993LF64700001 PM 8349430 ER PT J AU JOHNSON, BE PARKER, R TSAI, CM BALTZ, J MILLER, MJ SHOEMAKER, R PHELPS, R BASTIAN, A STOCKER, J PHARES, J MULSHINE, JL GAZDAR, AF IHDE, DC AF JOHNSON, BE PARKER, R TSAI, CM BALTZ, J MILLER, MJ SHOEMAKER, R PHELPS, R BASTIAN, A STOCKER, J PHARES, J MULSHINE, JL GAZDAR, AF IHDE, DC TI PHASE-I TRIAL OF DIHYDROLENPERONE IN LUNG-CANCER PATIENTS - A NOVEL COMPOUND WITH INVITRO ACTIVITY AGAINST LUNG-CANCER SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE DIHYDROLENPERONE; DRUG EVALUATION; DRUG SCREENING ASSAYS; ANTITUMOR; CARCINOMA; NONSMALL CELL LUNG CARCINOMA; OAT CELL ID TUMOR-CELL-LINES; COLORIMETRIC ASSAY; GROWTH; FEASIBILITY; SENSITIVITY; SURVIVAL AB Antitumor activity of the butyrophenone dihydrolenperone in non-small cell lung cancer was initially suggested by in vitro screening against tumor cells derived from fresh surgical samples using the human tumor colony-forming assay. We have completed a directed phase I trial in patients with lung cancer. Thirty-two patients with lung cancer have completed 25 courses of therapy at doses of 10 to 60 mg/square meter orally on a twice daily schedule. Twenty-three men and 9 women with a median age of 55 (range 24-69) were entered. Twenty-four were performance status 0 or 1 and 8 were 2. The maximum tolerated dose was 50 mg/square meter orally twice daily and the dose limiting toxicity was somnolence. Of the 32 patients, 18 developed symptomatic hypotension (grade 1 or 2). There was no significant hematologic, renal, or hepatic toxicity. In vitro drug testing using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (thiazolyl blue)] assay confirmed 50% inhibition of non-small cell and small cell lung cancer cell line growth at 70-450 micromolar concentrations. Plasma dihydrolenperone levels were at least 75-fold less than levels at which in vitro activity was observed. We conclude: 1) the maximum tolerated dose in our study is 50 mg/square meter orally twice daily, 2) the dose-limiting side effect of dihydrolenperone is somnolence, and 3) the concentrations of dihydrolenperone observed in plasma are significantly lower than those associated with in vitro activity. C1 NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20889. NATL NAVAL CTR,BETHESDA,MD 20889. US FDA,ROCKVILLE,MD 20850. NCI,DEV THERAPEUT PROGRAM,FREDERICK,MD 21701. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20889. NR 16 TC 3 Z9 3 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PD FEB PY 1993 VL 11 IS 1 BP 29 EP 37 DI 10.1007/BF00873907 PG 9 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA LF647 UT WOS:A1993LF64700004 PM 8349433 ER PT J AU BENBARUCH, N DENICOFF, AM GOLDSPIEL, BR OSHAUGHNESSY, JA COWAN, KH AF BENBARUCH, N DENICOFF, AM GOLDSPIEL, BR OSHAUGHNESSY, JA COWAN, KH TI PHASE-II STUDY OF FAZARABINE (NSC-281272) IN PATIENTS WITH METASTATIC COLON-CANCER SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE FAZARABINE (ARABINOFURANOSYL-5-AZACYTOSINE; ARA-AC; NSC-281272); PHASE-II; COLON CANCER ID ARABINOSYL-5-AZACYTOSINE; TRIAL AB Fazarabine (Arabinofuranosyl-5-azacytosine) is a synthetic pyrimidine nucleoside which combines the arabinose sugar of cytosine arabinoside with the triazine base of 5-azacytidine. It has demonstrated activity against a variety of human solid tumor xenografts including colon, lung and breast cancers. Eighteen patients with refractory metastatic colon cancer were enrolled in a phase II trial of fazarabine. The drug was administered as a 72 hr continuous infusion every 3-4 weeks; the starting dose was 2 mg/m2/hr as established in a previous phase I study. The major toxicity was neutropenia, as predicted from the phase I study. The median time to nadir for cycle 1 was 20 days, with a median granulocyte count of 437/mul (range 36-1600/mul); recovery was within 2-4 days, with only one incidence of fever and neutropenia in 42 cycles. Especially noted for their absence were thrombocytopenia, nausea, vomiting and stomatitis. No objective clinical responses were seen; one patient had stabilization of rapidly growing liver metastases for a period of 7 months. In view of fazarabine's narrow range of toxicities, future dose intensification trials utilizing fazarabine in combination with hematopoietic growth factors are worthy of consideration. C1 NCI,MED BRANCH,BLDG 10,ROOM 12N226,BETHESDA,MD 20892. NR 10 TC 7 Z9 8 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PD FEB PY 1993 VL 11 IS 1 BP 71 EP 74 DI 10.1007/BF00873915 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA LF647 UT WOS:A1993LF64700012 PM 7688714 ER PT J AU LAYCOCK, KA LEE, SF STULTING, RD CROEN, KD OSTROVE, JM STRAUS, SE PEPOSE, JS AF LAYCOCK, KA LEE, SF STULTING, RD CROEN, KD OSTROVE, JM STRAUS, SE PEPOSE, JS TI HERPES-SIMPLEX VIRUS TYPE-1 TRANSCRIPTION IS NOT DETECTABLE IN QUIESCENT HUMAN STROMAL KERATITIS BY INSITU HYBRIDIZATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE CORNEA; HERPES SIMPLEX KERATITIS; HERPES SIMPLEX VIRUS; INSITU HYBRIDIZATION; LATENCY ASSOCIATED TRANSCRIPTS ID HUMAN TRIGEMINAL GANGLIA; INFECTED-RABBITS; MESSENGER-RNA; LATENCY; CORNEAS; RECOVERY; NEURONS; TISSUES; PROBES; MICE AB Purpose. The purpose of this study was to determine whether herpes simplex virus (HSV) transcripts are present in the corneas of patients with chronic herpetic stromal keratitis. Methods. Corneal buttons from patients with a history of stromal keratitis, but no ongoing active disease, together with positive and negative control tissues, were analyzed by in situ hybridization using single-stranded RNA probes for all three classes of viral lytic cycle transcripts as well as for the latency-associated transcripts (LATs). Tissues also were screened for presence of HSV genomic DNA using the polymerase chain reaction (PCR). Results. HSV DNA was detected in 7 of 13 quiescent corneas by PCR, but no viral transcripts were detected in any of these corneas by in situ hybridization. Conclusions. At the level of detection afforded by in situ hybridization, HSV persistent in scarred human corneas after stromal keratitis appears to be transcriptionally dormant. This contrasts with the situation in neurons of latently infected sensory ganglia, in which LATs are present at high levels. C1 WASHINGTON UNIV,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,660 S EUCLID AVE,BOX 8096,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. EMORY UNIV,DEPT OPHTHALMOL,ATLANTA,GA 30322. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. FU NEI NIH HHS [EY07057] NR 28 TC 26 Z9 26 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD FEB PY 1993 VL 34 IS 2 BP 285 EP 292 PG 8 WC Ophthalmology SC Ophthalmology GA KP018 UT WOS:A1993KP01800004 PM 8382667 ER PT J AU STANLEY, SK FAUCI, AS AF STANLEY, SK FAUCI, AS TI T-CELL HOMEOSTASIS IN HIV-INFECTION - PART OF THE SOLUTION, OR PART OF THE PROBLEM SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Editorial Material ID CD4 RP STANLEY, SK (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 6A-17,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 7 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD FEB PY 1993 VL 6 IS 2 BP 142 EP 143 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KK252 UT WOS:A1993KK25200006 PM 8433279 ER PT J AU VERMUND, SH AF VERMUND, SH TI DECISION-MAKING FOR CLINICAL-TRIALS AND PREVENTION RESEARCH - COMMENTARY ON THE MODEL OF PALTIEL AND KAPLAN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Editorial Material ID ZIDOVUDINE; AIDS; INFECTION; HIV-1 RP VERMUND, SH (reprint author), NIAID,DIV AIDS,CLIN RES PROGRAM,VACCINE TRIALS & EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. OI Vermund, Sten/0000-0001-7289-8698 NR 16 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD FEB PY 1993 VL 6 IS 2 BP 176 EP 178 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KK252 UT WOS:A1993KK25200011 PM 8433282 ER PT J AU SHAPSHAK, P MCCOY, CB RIVERS, JE CHITWOOD, DD MASH, DC WEATHERBY, NL INCIARDI, JA SHAH, SM BROWN, BS AF SHAPSHAK, P MCCOY, CB RIVERS, JE CHITWOOD, DD MASH, DC WEATHERBY, NL INCIARDI, JA SHAH, SM BROWN, BS TI INACTIVATION OF HUMAN IMMUNODEFICIENCY VIRUS-1 AT SHORT-TIME INTERVALS USING UNDILUTED BLEACH SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Letter C1 UNIV MIAMI,SCH MED,DEPT NEUROL,MIAMI,FL 33152. UNIV MIAMI,SCH MED,DEPT PATHOL,MIAMI,FL 33152. UNIV MIAMI,SCH MED,DEPT MICROBIOL IMMUNOL,MIAMI,FL 33152. UNIV MIAMI,SCH MED,DEPT PHARMACOL,MIAMI,FL 33152. UNIV MIAMI,SCH MED,DEPT EPIDEMIOL & PUBL HLTH,MIAMI,FL 33152. UNIV MIAMI,SCH MED,DEPT SOCIOL,MIAMI,FL 33152. UNIV DELAWARE,CTR DRUG & ALCOHOL STUDIES,NEWARK,DE 19718. NIDR,COMMUNITY RES BRANCH,BETHESDA,MD 20892. RP SHAPSHAK, P (reprint author), UNIV MIAMI,SCH MED,DEPT PSYCHIAT,COMPREHENS DRUG RES CTR,MIAMI,FL 33152, USA. FU NIDA NIH HHS [DA04787, DA04433, DA06227] NR 15 TC 38 Z9 38 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD FEB PY 1993 VL 6 IS 2 BP 218 EP 219 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA KK252 UT WOS:A1993KK25200018 PM 8433288 ER PT J AU KOWALSKI, ML SLIWINSKAKOWALSKA, M IGARASHI, Y WHITE, MV WOJCIECHOWSKA, B BRAYTON, P KAULBACH, H ROZNIECKI, J KALINER, MA AF KOWALSKI, ML SLIWINSKAKOWALSKA, M IGARASHI, Y WHITE, MV WOJCIECHOWSKA, B BRAYTON, P KAULBACH, H ROZNIECKI, J KALINER, MA TI NASAL SECRETIONS IN RESPONSE TO ACETYLSALICYLIC-ACID SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article DE ASPIRIN SENSITIVITY; RHINITIS; NASAL CHALLENGE; HISTAMINE; PGD2; LTC4; NASAL SECRETIONS ID ASPIRIN-SENSITIVE RHINOSINUSITIS; PATHO-PHYSIOLOGY; INDUCED ASTHMA; HISTAMINE-RELEASE; ARACHIDONIC-ACID; INDUCED RHINITIS; LEUKOTRIENES; CHALLENGE; PROTEIN; DESENSITIZATION AB Background: Acetylsalicylic acid (ASA) induces rhinorrhea in a subset of patients with asthma or chronic rhinosinusitis or both and nasal polyps. The underlying mechanism of the reaction is obscure. Methods: To assess the nasal response to ASA challenge, four groups of patients were challenged orally with ASA: group A (10 ASA-sensitive patients); group B (nine patients with nasal polyps and histories of tolerance to ASA); group C (nine ASA-tolerant patients with chronic allergic rhinitis); and group D (eight healthy nonatopic subjects). Results: Nasal lavages obtained before and after ASA challenge were assayed for proteins (total protein, lactoferrin, lysozyme, albumin) and inflammatory mediators (histamine, prostaglandin D2, and leukotriene C4). ASA challenges induced severe rhinorrhea and congestion and significant increases in mean concentrations of all measured nasal proteins in group A. Histamine and prostaglandin D2 rose, but not significantly. In the two control groups with chronic rhinitis, ASA induced increases in the concentration of proteins and histamine. Leukotriene C4 concentrations were significantly elevated in nasal lavages after ASA challenge in groups A and C only. In group D no symptoms or changes in nasal proteins were observed after aspirin challenge. Conclusions: These observations suggest that production of lipoxygenase products of arachidonate may induce glandular secretions that may participate in the clinical changes associated with ASA sensitivity. C1 NIAID,CLIN INVEST LAB,ALLERG DIS SECT,BETHESDA,MD 20892. RP KOWALSKI, ML (reprint author), MED ACAD LODZ,FAC MED,DEPT PULM & ALLERGOL,KOPCINSKIEGO 22,PL-90153 LODZ,POLAND. RI Sliwinska-Kowalska, Mariola/F-6119-2010 OI Sliwinska-Kowalska, Mariola/0000-0001-7569-3882 NR 61 TC 62 Z9 62 U1 1 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD FEB PY 1993 VL 91 IS 2 BP 580 EP 598 DI 10.1016/0091-6749(93)90264-G PG 19 WC Allergy; Immunology SC Allergy; Immunology GA KN548 UT WOS:A1993KN54800006 PM 8436774 ER PT J AU WAISMAN, Y EICHACKER, PQ BANKS, SM HOFFMAN, WD MACVITTIE, TJ NATANSON, C AF WAISMAN, Y EICHACKER, PQ BANKS, SM HOFFMAN, WD MACVITTIE, TJ NATANSON, C TI ACUTE HEMORRHAGE IN DOGS - CONSTRUCTION AND VALIDATION OF MODELS TO QUANTIFY BLOOD-LOSS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE ACUTE BLEEDS; PREDICTION MODELS; CONSTRAINED LINEAR REGRESSION ID SPLENECTOMIZED DOGS; OXYGEN DEBT; SHOCK; VOLUME; PREDICTORS; SEVERITY AB We examined the ability of commonly used clinical parameters to quantify acute hemorrhage in dogs. Eight animals were bled 40 ml/kg body wt over 100 min. Ten hemodynamic and 20 blood laboratory parameters were obtained every 10 min to construct, with use of linear regression analysis, models that quantify blood loss. During model construction, the best indicator of quantity of hemorrhage was arterial base deficit [ABD; coefficient of variation (CV) 35%]. This model was more accurate (P < 0.05) than 27 others (CV range 43 to 63%) and similar to systolic (CV 40%) and mean (CV 40%) arterial pressures. In validation studies in 10 additional animals, our best models based on ABD and systolic and mean arterial pressures each unexpectedly showed a significant (P < 0.05) decrease in accuracy (CV 86, 57, and 60%, respectively) attributable to large baseline (before hemorrhage) variability among animals. To eliminate this variability, models based on changes from baseline measurements were investigated. The best predictor of change in blood volume was change in ABD (CV 27%). This model was significantly (P < 0.05) more accurate than any of 27 others (CV range 36 to 65%) and similar to change in venous base deficit and venous pH (each CV 31%). When validated, acid-base models such as ABD, venous pH, and arterial bicarbonate were the best predictors of volume change (CV range 28 to 40%). With the use of multivariate analysis, pairwise combinations of single parameter models (n = 465) improved prediction errors only minimally. In summary, most commonly used hemodynamic and blood indexes could not be validated as accurate measurements in quantifying hemorrhage. In contrast, changes in acid-base parameters were validated as moderately accurate predictors of blood volume changes and therefore may have utility in the assessment of patients with ongoing hemorrhage. C1 DEF NUCL AGCY,ARMED FORCES RADIOBIOL RES INST,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,CTR EMERGENCY MED TRAUMA,WASHINGTON,DC 20010. RP WAISMAN, Y (reprint author), NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892, USA. NR 26 TC 29 Z9 29 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD FEB PY 1993 VL 74 IS 2 BP 510 EP 519 PG 10 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA KN704 UT WOS:A1993KN70400002 PM 8458764 ER PT J AU HEINEMANN, JA ANKENBAUER, RG AF HEINEMANN, JA ANKENBAUER, RG TI RETROTRANSFER IN ESCHERICHIA-COLI CONJUGATION - BIDIRECTIONAL EXCHANGE OR DENOVO MATING SO JOURNAL OF BACTERIOLOGY LA English DT Article ID CHROMOSOMAL MARKERS; REPLICATION; NUCLEOTIDE; PLASMIDS; BACTERIA; DNA AB DNA can be transferred among eubacteria and to plants and fungi by related, plasmid-mediated processes collectively referred to as bacterial conjugation. Conjugation occurs between cells in contact with one another and results in the unidirectional delivery of DNA from a bacterial donor to a recipient. Recent experiments that have reexamined the directionality of DNA flow during conjugation have come to different conclusions, some suggesting that genetic material also flows from recipient cells into the donor and that this process, termed retrotransfer, is likewise directed by donor-encoded functions. Given that bacteria are perhaps united with all living creatures by conjugation, the possibility of gene flow into donor bacteria during conjugation raises interesting evolutionary and biocontainment issues. Here we report that plasmid transmission from bacterial recipients to donors is not a donor-mediated event. Movement of genetic material from recipients to donors was inhibited by streptomycin, which does not inhibit the conjugative donor, indicating that retrotransfer requires gene expression in recipients. Furthermore, retrotransfer was reduced in matings mediated by plasmids that encode strong entry exclusion, to a similar degree as matings between two donors. Therefore we suggest that retrotransfer is in fact newly initiated conjugation between transconjugants and donors. RP HEINEMANN, JA (reprint author), NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840, USA. NR 21 TC 27 Z9 27 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD FEB PY 1993 VL 175 IS 3 BP 583 EP 588 PG 6 WC Microbiology SC Microbiology GA KJ722 UT WOS:A1993KJ72200002 PM 8423133 ER PT J AU DORGAI, L OBERTO, J WEISBERG, RA AF DORGAI, L OBERTO, J WEISBERG, RA TI XIS AND FIS PROTEINS PREVENT SITE-SPECIFIC DNA INVERSION IN LYSOGENS OF PHAGE HK022 SO JOURNAL OF BACTERIOLOGY LA English DT Article ID UNUSUAL CHROMOSOMAL LOCATIONS; BACTERIOPHAGE-LAMBDA; ATTACHMENT SITES; COLIPHAGE LAMBDA; GENETIC-ANALYSIS; PROPHAGE LAMBDA; RECOMBINATION; DETERMINANTS; INTEGRATION; MUTATIONS AB HK022, a temperate coliphage related to lambda, forms lysogens by inserting its DNA into the bacterial chromosome through site-specific recombination. The Escherichia coli Fis and phage Xis proteins promote excision of HK022 DNA from the bacterial chromosome. These two proteins also act during lysogenization to prevent a prophage rearrangement: lysogens formed in the absence of either Fis or Xis frequently carried a prophage that had suffered a site-specific internal DNA inversion. The inversion is a product of recombination between the phage attachment site and a secondary attachment site located within the HK022 left operon. In the absence of both Fis and Xis, the majority of lysogens carried a prophage with an inversion. Inversion occurs during lysogenization at about the same time as prophage insertion but is rare during lytic phage growth. Phages carrying the inverted segment are viable but have a defect in lysogenization, and we therefore suggest that prevention of this rearrangement is an important biological role of Xis and Fis for HK022. Although Fis and Xis are known to promote excision of lambda prophage, they had no detectable effect on lambda recombination at secondary attachment sites. HK022 cIts lysogens that were blocked in excisive recombination because of mutation in fis or xis typically produced high yields of phage after thermal induction, regardless of whether they carried an inverted prophage. The usual requirement for prophage excision was bypassed in these lysogens because they carried two or more prophages inserted in tandem at the bacterial attachment site; in such lysogens, viable phage particles can be formed by in situ packaging of unexcised chromosomes. C1 NICHHD,MOLEC GENET LAB,MICROBIAL GENET SECT,BETHESDA,MD 20892. NR 46 TC 19 Z9 19 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD FEB PY 1993 VL 175 IS 3 BP 693 EP 700 PG 8 WC Microbiology SC Microbiology GA KJ722 UT WOS:A1993KJ72200017 PM 8423145 ER PT J AU MARCONI, RT SAMUELS, DS GARON, CF AF MARCONI, RT SAMUELS, DS GARON, CF TI TRANSCRIPTIONAL ANALYSES AND MAPPING OF THE OSPC GENE IN LYME-DISEASE SPIROCHETES SO JOURNAL OF BACTERIOLOGY LA English DT Article ID BACTERIUM BORRELIA-BURGDORFERI; MAJOR SURFACE-PROTEINS; IMMUNOLOGICAL ANALYSIS; MOLECULAR ANALYSIS; PLASMID; DNA; HETEROGENEITY; CULTIVATION; AGENT AB In Lyme disease spirochetes, the ospC gene encodes a 22.7-kDa protein referred to as either the pC or the OspC protein. Using a variety of electrophoretic approaches followed by Southern blotting and probing with oligonudeotide probes, we mapped the ospC gene to a circular 26-kb plasmid. The ospC gene represents the first gene to be mapped to a circular plasmid in Lyme disease spirochetes. The occurrence of this gene in isolates belonging to each of the three Lyme disease-associated species, Borrelia burgdorferi, Borrelia garinii, and the VS461 group, was evaluated. The ospC gene was found to occur in all 21 isolates tested from each of the three species. Differential hybridization with a series of ospC probes in both Northern (RNA) and Southern blot analyses demonstrated that there is sequence variability in the ospC gene among isolates. While the gene was found to be present in all isolates, not all actively transcribed the gene. Transcriptional start site analyses suggest that the gene may be under the control of multiple promoters that are highly similar in nucleotide sequence. RP MARCONI, RT (reprint author), NIAID,ROCKY MT LABS,VECTORS & PATHOGENS LAB,HAMILTON,MT 59840, USA. RI Samuels, D Scott/B-7549-2012 OI Samuels, D Scott/0000-0001-8352-7593 NR 32 TC 143 Z9 144 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD FEB PY 1993 VL 175 IS 4 BP 926 EP 932 PG 7 WC Microbiology SC Microbiology GA KL849 UT WOS:A1993KL84900002 PM 7679385 ER PT J AU CORDELLAMIELE, E MIELE, L BENINATI, S MUKHERJEE, AB AF CORDELLAMIELE, E MIELE, L BENINATI, S MUKHERJEE, AB TI TRANSGLUTAMINASE-CATALYZED INCORPORATION OF POLYAMINES INTO PHOSPHOLIPASE-A2 SO JOURNAL OF BIOCHEMISTRY LA English DT Article ID PANCREATIC PHOSPHOLIPASE-A2; GAMMA-GLUTAMYL; CROSS-LINKING; PROTEIN; DIFFERENTIATION; EPSILON-(GAMMA-GLUTAMYL)LYSINE; DERIVATIVES; INHIBITION; DIAMINES; SEQUENCE AB We have previously demonstrated that when phospholipase A2 is treated with either tissue transglutaminase or human plasma Factor XIIIa, a striking increase of its catalytic activity is observed, due to the formation of an intramolecular epsilon-(gamma-glutamyl)-lysine crosslink [Cordella-Miele et al. (1990) J. Biol. Chem. 265,17180-17188]. Here, we report the effect of transglutaminase substrates such as mono-, di-, and polyamines on this transglutaminase-catalyzed post-translational modification of phospholipase A2. Incorporation of radioactively labeled polyamines into phospholipase A2 was demonstrated by using porcine pancreatic phospholipase A2 as a substrate in a conventional transglutaminase assay. These results were further confirmed by SDS-polyacrylamide gel electrophoresis followed by fluorography. Additionally, gamma-glutamyl-polyamine was detected and unequivocally identified in proteolytic digests of polyaminated phospholipase A2. When phospholipase A2 was incubated with transglutaminase in the presence of putrescine, spermine, spermidine, dansylcadaverine, or methylamine, a 2-3-fold increase in phospholipase A2 activity was observed. The increase of phospholipase A2 activity was found to be dependent upon the concentration of phospholipase A2, preincubation time, and the duration of the reaction. Increase in phospholipase A2 activity after transglutaminase treatment in the presence of polyamines was demonstrated using two different assay systems. Kinetic studies on phospholipase A2 pretreated with spermidine and transglutaminase demonstrated a significant increase of the apparent V(max) but no significant change in the apparent K(m). Unlike phospholipase A2 pretreated with transglutaminase alone, polyaminated phospholipase A2 does not undergo non-covalent dimerization in solution. Polyaminated phospholipase A2 was further purified by chromatofocusing and was found to contain N-mono(gamma-glutamyl)-spermidine in a molar ratio of about 1:1 to phospholipase A2. Freshly purified, polyaminated phospholipase A2 had a specific activity approximately 3-fold higher than that of control phospholipase A2 treated in an identical way except for the absence of transglutaminase. To our knowledge, this is the first demonstration that transglutaminase catalyzes the incorporation of amines into a phospholipase, and that this post-translational modification increases phospholipase A2 activity. C1 NICHHD,HUMAN GENET BRANCH,DEV GENET SECT,BLDG 10,ROOM 9S242,BETHESDA,MD 20892. OI Beninati, Simone/0000-0002-2704-0745 NR 59 TC 60 Z9 61 U1 0 U2 0 PU JAPANESE BIOCHEMICAL SOC PI TOKYO PA ISHIKAWA BLDG-3F 25-16 HONGO-5-CHOME, TOKYO TOKYO 113, JAPAN SN 0021-924X J9 J BIOCHEM-TOKYO JI J. Biochem. (Tokyo) PD FEB PY 1993 VL 113 IS 2 BP 164 EP 173 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KK778 UT WOS:A1993KK77800010 PM 8096844 ER PT J AU NAKATA, H AF NAKATA, H TI ANTIBODIES RAISED AGAINST THE ADENOSINE RECEPTOR AGONIST, 5'-N-ETHYLCARBOXAMIDOADENOSINE (NECA) SO JOURNAL OF BIOCHEMISTRY LA English DT Article ID BINDING-SITES; ADENYLATE-CYCLASE; MEMBRANES; PURIFICATION AB Antisera against the non-selective adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) have been raised by immunizing rabbits with NECA-coupled bovine serum albumin. The antisera which bind [H-3]NECA with high affinity were purified by affinity chromatography using NECA-coupled Sepharose as the affinity gel without significant changes in [H-3]NECA-binding properties. The order of the affinity for various adenosine receptor ligands of the purified or unpurified antisera was 5'-N-cyclopropylcarboxamidoadenosine greater-than-or-equal-to NECA > 2',5'-dideoxyadenosine > 2-chloroadenosine > theophylline > isobutylmethylxanthine > (R)-N6-phenylisopropyladenosine = N6-cyclohexyladenosine. This specificity was found to be similar to that of the non-receptor NECA-binding sites, which had been found in various tissues such as human placentas and mouse P815 mastocytoma cells, rather than to that of adenosine receptors. These anti-NECA antibodies will be useful as immunochemical agents in the search for endogenous ligand(s) to the non-receptor NECA-binding sites. 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,FUCHU,TOKYO 183,JAPAN. NR 20 TC 0 Z9 0 U1 0 U2 0 PU JAPANESE BIOCHEMICAL SOC PI TOKYO PA ISHIKAWA BLDG-3F 25-16 HONGO-5-CHOME, TOKYO TOKYO 113, JAPAN SN 0021-924X J9 J BIOCHEM-TOKYO JI J. Biochem. (Tokyo) PD FEB PY 1993 VL 113 IS 2 BP 241 EP 244 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KK778 UT WOS:A1993KK77800022 PM 8468331 ER PT J AU TOMAZIC, BB BROWN, WE EANES, ED AF TOMAZIC, BB BROWN, WE EANES, ED TI A CRITICAL-EVALUATION OF THE PURIFICATION OF BIOMINERALS BY HYPOCHLORITE TREATMENT SO JOURNAL OF BIOMEDICAL MATERIALS RESEARCH LA English DT Article ID BONE AB The quantitative deproteination of calcific deposits from surgically explanted heart valve bioprostheses was carried out by both hypochlorite and hydrazine extraction to establish which is the better procedure for preparing purified mineral suitable for detailed chemical and structural characterization. Hypochlorite treatment resulted in a material with a higher Ca/PO4 ratio than that of the untreated deposits. The hydrazine treatment did not produce such an effect. A systematic comparison of x-ray diffraction patterns of calcific deposits showed an increase in crystallinity of hypochlorite-treated versus native material, while the crystallinity of hydrazine-treated materials did not change. One other result of the hypochlorite treatment was a pronounced disaggregation of well-ground calcific deposits into a particle populations ranging from 50-300 nm in size, as shown by scanning electron microscopy. Results comparable to the above findings were also obtained when the two treatments were applied to other bioapatites. On the other hand, mineral solubilities were comparable, regardless of which deproteination treatment was used. The principal conclusion from this study is that hydrazine deproteination is preferable to hypochlorite extraction in isolating pathologic mineral deposits from bioprosthetic materials for further study. C1 NATL INST STAND & TECHNOL,NIDR,BONE RES ASSOCIATE PROGRAM,GAITHERSBURG,MD 20899. RP TOMAZIC, BB (reprint author), AMER DENT ASSOC,HLTH FDN,PAFFENBARGER RES CTR,GAITHERSBURG,MD 20899, USA. FU NHLBI NIH HHS [HL 30035] NR 13 TC 24 Z9 24 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9304 J9 J BIOMED MATER RES JI J. Biomed. Mater. Res. PD FEB PY 1993 VL 27 IS 2 BP 217 EP 225 DI 10.1002/jbm.820270211 PG 9 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA KG410 UT WOS:A1993KG41000010 PM 8436578 ER PT J AU KATZ, RW HOLLINGER, JO REDDI, AH AF KATZ, RW HOLLINGER, JO REDDI, AH TI THE FUNCTIONAL EQUIVALENCE OF DEMINERALIZED BONE AND TOOTH MATRICES IN ECTOPIC BONE INDUCTION SO JOURNAL OF BIOMEDICAL MATERIALS RESEARCH LA English DT Article ID INCISOR DENTIN CONTAINS; WATER-SOLUBLE PROTEINS; DISSOCIATIVE EXTRACTION; MORPHOGENETIC PROTEIN; EXTRACELLULAR-MATRIX; DELIVERY VEHICLE; CELLS-INVITRO; BOVINE; DIFFERENTIATION; PURIFICATION AB The objective of this study was to determine whether demineralized rat incisor matrices were a more potent inducer of ectopic endochondral bone formation than demineralized diaphyseal bone matrices derived from the same donors. Twenty-five-milligram disks of de-mineralized bone or tooth matrix obtained from adolescent Long-Evans rats were implanted in a standardized ectopic site. Biochemical and histometric measurements of bone formation revealed that the two matrices were functionally equivalent inducers of endochondral bone formation. The induced pellicle of bone reached a maturation point 18 days after implantation. Dentin matrix implants generated a significantly greater amount of mineralized tissue than did bone matrix implants. This difference could be explained on the basis of remineralization of the dentin particles to a greater degree than the bone matrix particles. Initial observations suggesting a more robust osteoinductive activity in demineralized incisor matrix can be attributed to the decreasing activity of bone matrix from older donors when compared to younger donors. The extent of osteoinduction by the two substrata was equivalent when the matrices were matched for age. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,INST DENT RES,BONE PHYSIOL BRANCH,WASHINGTON,DC 20307. JOHNS HOPKINS UNIV,MED CTR,DEPT ORTHOPED SURG,BALTIMORE,MD 21205. NR 34 TC 13 Z9 14 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9304 J9 J BIOMED MATER RES JI J. Biomed. Mater. Res. PD FEB PY 1993 VL 27 IS 2 BP 239 EP 245 DI 10.1002/jbm.820270214 PG 7 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA KG410 UT WOS:A1993KG41000013 PM 8436581 ER PT J AU HENRICH, DE CRAM, AE PARK, JB LIU, YK REDDI, H AF HENRICH, DE CRAM, AE PARK, JB LIU, YK REDDI, H TI INORGANIC BONE AND DEMINERALIZED BONE-MATRIX IMPREGNATED BONE-CEMENT - A PRELIMINARY INVIVO STUDY SO JOURNAL OF BIOMEDICAL MATERIALS RESEARCH LA English DT Note C1 NIH,BETHESDA,MD 20205. UNIV IOWA,COLL ENGN,DEPT SURG,IOWA CITY,IA 52242. UNIV IOWA,COLL ENGN,DEPT BIOMED ENGN,IOWA CITY,IA 52242. RP HENRICH, DE (reprint author), UNIV IOWA,COLL MED,IOWA CITY,IA 52242, USA. NR 13 TC 14 Z9 14 U1 1 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9304 J9 J BIOMED MATER RES JI J. Biomed. Mater. Res. PD FEB PY 1993 VL 27 IS 2 BP 277 EP 280 DI 10.1002/jbm.820270218 PG 4 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA KG410 UT WOS:A1993KG41000017 PM 8436585 ER PT J AU VETTER, U WEIS, MA MORIKE, M EANES, ED EYRE, DR AF VETTER, U WEIS, MA MORIKE, M EANES, ED EYRE, DR TI COLLAGEN CROSS-LINKS AND MINERAL CRYSTALLINITY IN BONE OF PATIENTS WITH OSTEOGENESIS IMPERFECTA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID I COLLAGEN; MOLECULES; LINKING; GENE AB In cortical bone samples from patients with osteogenesis imperfecta (OI), the concentrations of hydroxypyridinium cross-linking amino acids in collagen were measured by reversed-phase HPLC and the x-axis crystallinity of the apatite mineral phase was determined by x-ray diffraction. Bone samples from three patients with type I, nine patients with type III, and eight patients with type IV OI were analyzed and compared with human bone from nine controls. The concentration of the two chemical forms of the mature collagen crosslinking amino acids, hydroxylysylpyridinoline (HP) and lysylpyridinoline (LP), and the ratio HP/LP were found to be alike in bone collagen of OI patients and healthy controls. However, the c-axis crystallinity of the apatite was found to be reduced in the type III and IV OI patients compared with controls. Regression analysis of crosslink concentrations and c-axis crystallinity in OI bones did not show any correlation. Therefore, collagen molecules deposited in the extracellular matrix of OI bone appear to fulfill the structural requirements for the action of the enzyme lysyl oxidase, such that a normal concentration of intermolecular crosslinks is formed compared with healthy bone. Consequently, crosslink formation and apatite crystal growth seem to be regulated independently in OI bone. C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. UNIV WASHINGTON,DEPT ORTHOPAED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT BIOCHEM,SEATTLE,WA 98195. UNIV ULM,KINKERKLIN,BINDEGEWEBSLABOR,W-7900 ULM,GERMANY. RP VETTER, U (reprint author), UNIV FRANKFURT,KINDERKLIN,THEODOR STERN KAI 7,W-6000 FRANKFURT 1,GERMANY. FU NIAMS NIH HHS [R37 AR037318, AR 37318, R01 AR036794] NR 28 TC 35 Z9 35 U1 0 U2 4 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD FEB PY 1993 VL 8 IS 2 BP 133 EP 137 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KL829 UT WOS:A1993KL82900002 PM 8442432 ER PT J AU OERTER, KE KAMP, GA MUNSON, PJ NIENHUIS, AW CASSORLA, FG MANASCO, PK AF OERTER, KE KAMP, GA MUNSON, PJ NIENHUIS, AW CASSORLA, FG MANASCO, PK TI MULTIPLE HORMONE DEFICIENCIES IN CHILDREN WITH HEMOCHROMATOSIS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID BETA-THALASSEMIA MAJOR; GH-RELEASING HORMONE; SEXUAL-MATURATION; GONADAL-FUNCTION; GROWTH; PITUITARY; SECRETION; GIRLS; BOYS; THERAPY AB Patients with thalassemia major require multiple blood transfusions leading to hemochromatosis. These patients often have pubertal delay and growth failure, the etiology of which has not been fully elucidated. We performed an extensive endocrine evaluation which included measurements of spontaneous and stimulated levels of gonadotropins, GH, thyroid hormone, and adrenal hormones in 17 patients between the ages of 12 and 18 yr with hemochromatosis receiving desferoxamine therapy. All of the 17 patients had at least one endocrine abnormality, and 12 had more than one abnormality. Abnormalities of the hypothalamic-pituitary-gonadal axis were the most common. Six patients had clinical evidence of delayed puberty with spontaneous and stimulated gonadotropin and sex steroid levels appropriate for their delayed pubertal stage. All 14 children in puberty LH pulsatility index below the mean for pubertal stage compared to normal children. Six of the 14 had LH pulsatility index more than 2 SD below the mean for pubertal stage. This may be an indicator of abnormal pituitary function. Six patients failed either the provocative GH tests (peak GH < 7 mug/L) or had a mean spontaneous GH less than 1 mug/L. The 4 patients who failed provocative tests had growth velocities more than 2 SD below the mean for bone age. Three patients had evidence of primary hypothyroidism. We conclude that all patients with hemochromatosis need periodic careful endocrine evaluations because the incidence of endocrine dysfunction is substantial and they may benefit from hormonal therapy. C1 NHLBI, CLIN HEMATOL BRANCH, BETHESDA, MD 20892 USA. RP OERTER, KE (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA. NR 30 TC 48 Z9 49 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD FEB PY 1993 VL 76 IS 2 BP 357 EP 361 DI 10.1210/jc.76.2.357 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KM445 UT WOS:A1993KM44500018 PM 8432779 ER PT J AU MIXSON, AJ FRIEDMAN, TC KATZ, DA FEUERSTEIN, IM TAUBENBERGER, JK COLANDREA, JM DOPPMAN, JL OLDFIELD, EH WEINTRAUB, BD AF MIXSON, AJ FRIEDMAN, TC KATZ, DA FEUERSTEIN, IM TAUBENBERGER, JK COLANDREA, JM DOPPMAN, JL OLDFIELD, EH WEINTRAUB, BD TI THYROTROPIN-SECRETING PITUITARY CARCINOMA SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID MEDULLARY-THYROID CARCINOMA; INAPPROPRIATE SECRETION; SOMATOSTATIN ANALOG; HYPERTHYROIDISM; ADENOMAS; HETEROGENEITY; BROMOCRIPTINE; DISSEMINATION; METASTASES; SUBUNIT AB Pituitary tumors rarely metastasize outside the central nervous system. Of the more than 100 reported TSH-secreting adenomas, we now describe the first carcinoma. A 40-yr-old woman had transsphenoidal surgery for a large TSH-secreting pituitary adenoma in 1984. She had increased thyroid hormone levels with a TSH that varied from 16-31 muU/mL, and an unusually high alpha-subunit that ranged from 125-150 ng/mL. Because of residual tumor, she had a left craniotomy in 1985 followed by radiation. Despite these therapies, she had a residual tumor that remained stable until January 1989 when her tumor nearly doubled in size. She received radiation therapy and octreotide with marked diminution of the tumor and clinical improvement. In August 1989, she presented with leg weakness, and magnetic resonance imaging revealed a large sacral mass. A biopsy confirmed that the sacral mass was a metastasis from the pituitary tumor. Due to additional metastases in the lung, she received 5-florouracil, cytoxan, and adriamycin, with marked decrease in her lesions. Further substantiation of the metastatic pituitary tumor was made when the patient returned in December 1989 with a pleural effusion containing pituitary tumor cells. Of all the reported cases of TSH-secreting adenomas, this case had the highest a-subunit portending future metastases. Furthermore, the apparent response to octreotide and response to chemotherapy are encouraging and suggest that new therapies should be explored. Finally, since TSH-secreting adenomas tend to be more invasive than other pituitary tumors, this case underscores the need for early diagnosis and aggressive treatment of these tumors. C1 NIDDKD, BLDG 10, ROOM 8D14, BETHESDA, MD 20892 USA. NICHHD, BETHESDA, MD 20892 USA. NINCDS, BETHESDA, MD 20892 USA. NCI, BETHESDA, MD 20892 USA. WARREN GRANT MAGNUSON CLIN CTR, BETHESDA, MD 20892 USA. NR 30 TC 66 Z9 66 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD FEB PY 1993 VL 76 IS 2 BP 529 EP 533 DI 10.1210/jc.76.2.529 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA KM445 UT WOS:A1993KM44500050 PM 8432799 ER PT J AU DERSIMONIAN, R CLEMENS, J SPIRTAS, R PERLMAN, J AF DERSIMONIAN, R CLEMENS, J SPIRTAS, R PERLMAN, J TI VASECTOMY AND PROSTATE-CANCER RISK - METHODOLOGICAL REVIEW OF THE EVIDENCE SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE VASECTOMY; PROSTATE CANCER; EPIDEMIOLOGY; STATISTICS; DETECTION BIAS; HETEROGENEITY ID EPIDEMIOLOGY; ASSOCIATION; HEALTH; COHORT AB Two recent studies have reported a significantly elevated risk of prostate cancer among vasectomized men. To assess whether the new results conflict with earlier studies that found no significant overall association, and, if so, whether such a conflict could have a methodological basis, we reviewed the six major epidemiological studies of this topic. Statistical analysis revealed significant (p < 0.01) heterogeneity among the associations in the six studies, attributable to one of the recent studies. Scrutiny of the studies for fulfilment of eight methodological standards for scientific validity revealed that no study completely fulfilled more than four standards, and that all studies were deficient in avoiding detection bias and obtaining accurate vasectomy histories. Our review indicates that the evidence on this topic is indeed conflicting, that the quality of the evidence does not resolve the conflict, and that future studies of this topic. designed to ensure scientific credibility of results, are needed. RP DERSIMONIAN, R (reprint author), NICHHD,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 32 TC 27 Z9 28 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD FEB PY 1993 VL 46 IS 2 BP 163 EP 172 DI 10.1016/0895-4356(93)90054-5 PG 10 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA KP705 UT WOS:A1993KP70500005 PM 8437032 ER PT J AU HARRIS, T FELDMAN, JJ MAKUC, DM SCHATZKIN, AG ETTINGER, WH AF HARRIS, T FELDMAN, JJ MAKUC, DM SCHATZKIN, AG ETTINGER, WH TI CHOLESTEROL AND MORTALITY - RESPONSE SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Letter RP HARRIS, T (reprint author), NIA,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 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 FEB PY 1993 VL 46 IS 2 BP 210 EP 210 DI 10.1016/0895-4356(93)90067-B PG 1 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA KP705 UT WOS:A1993KP70500018 ER PT J AU RADER, DJ CAIN, W ZECH, LA USHER, D BREWER, HB AF RADER, DJ CAIN, W ZECH, LA USHER, D BREWER, HB TI VARIATION IN LIPOPROTEIN(A) CONCENTRATIONS AMONG INDIVIDUALS WITH THE SAME APOLIPOPROTEIN(A) ISOFORM IS DETERMINED BY THE RATE OF LIPOPROTEIN(A) PRODUCTION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ATHEROSCLEROSIS; CHOLESTEROL; METABOLISM; KINETICS; APOLIPOPROTEIN ID LP(A) GLYCOPROTEIN PHENOTYPES; CORONARY HEART-DISEASE; FAMILIAL HYPERCHOLESTEROLEMIA; GEL-ELECTROPHORESIS; RECEPTOR GENE; RISK FACTOR; PLASMA; HETEROGENEITY; ATHEROSCLEROSIS; ASSOCIATION AB Lipoprotein(a) [Lp(a)] is an atherogenic lipoprotein which is similar in structure to, but metabolically distinct from, LDL. Factors regulating plasma concentrations of Lp(a) are poorly understood. Apo(a), the protein that distinguishes Lp(a) from LDL, is highly polymorphic, and apo(a) size is inversely correlated with plasma Lp(a) level. Even within the same apo(a) isoform class, however, plasma Lp(a) concentrations vary widely. A series of in vivo kinetic studies were performed using purified radiolabeled Lp(a) in individuals with the same apo(a) isoform but different Lp(a) levels. In a group of seven subjects with a single S4-apo(a) isoform and Lp(a) levels ranging from 1 to 13.2 mg/dl, the fractional catabolic rate (FCR) of I-131-labeled S2-Lp(a) (mean 0.328 day-1) was not correlated with the plasma Lp(a) level (r = -0.346, P = 0.45). In two S4-apo(a) subjects with a 10-fold difference in Lp(a) level, the FCR's of I-125-labeled S4-Lp(a) were very similar in both subjects and not substantially different from the FCRs of I-131-S2-Lp(a) in the same subjects. In four subjects with a single S2-apo (a) isoform and Lp (a) levels ranging from 9.4 to 91 mg / dl, Lp (a) concentration was highly correlated with Lp (a) production rate (r = 0.993, P = 0.007), but poorly correlated with Lp(a) FCR (mean 0.304 day 1). Analysis of Lp(a) kinetic parameters in all 11 subjects revealed no significant correlation of Lp(a) level with Lp(a) FCR (r = -0.53, P = 0.09) and a strong correlation with Lp(a) production rate (r = 0.99, P < 0.0001). We conclude that the substantial variation in Lp(a) levels among individuals with the same apo(a) phenotype is caused primarily by differences in Lp(a) production rate. C1 UNIV DELAWARE,SCH LIFE & HLTH SCI,NEWARK,DE 19716. RP RADER, DJ (reprint author), NHLBI,MOLEC DIS BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM 7N117,BETHESDA,MD 20892, USA. NR 35 TC 146 Z9 146 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 FEB PY 1993 VL 91 IS 2 BP 443 EP 447 DI 10.1172/JCI116221 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KM222 UT WOS:A1993KM22200014 PM 8432853 ER PT J AU UDELSMAN, R BLAKE, MJ STAGG, CA LI, DG PUTNEY, DJ HOLBROOK, NJ AF UDELSMAN, R BLAKE, MJ STAGG, CA LI, DG PUTNEY, DJ HOLBROOK, NJ TI VASCULAR HEAT-SHOCK PROTEIN EXPRESSION IN RESPONSE TO STRESS - ENDOCRINE AND AUTONOMIC REGULATION OF THIS AGE-DEPENDENT RESPONSE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ADRENERGIC REGULATION; AGING; HEAT SHOCK PROTEIN; STRESS; VASCULAR STRESS RESPONSE ID CORTICOTROPIN-RELEASING HORMONE; MESSENGER-RNA; IMMUNOHISTOCHEMICAL LOCALIZATION; ATHEROSCLEROTIC SPECIMENS; CONSTITUTIVE EXPRESSION; DIPLOID FIBROBLASTS; SURGICAL STRESS; GENE-EXPRESSION; ADRENAL-CORTEX; HUMAN ARTERIES AB Adaptation to stress requires coordinated interactions between the vascular and endocrine systems. Previously we demonstrated that restraint stress induces the expression of the major heat shock protein, HSP70, in the adrenal cortex of the rat. Here we demonstrate that restraint also induces expression of HSP70 in the vasculature. We further demonstrate that the adrenal and vascular responses are differentially regulated: the adrenal response is adrenocorticotropin dependent, whereas the vascular response is under adrenergic control. In addition, the adrenal response is restricted to members of the HSP70 gene family, whereas in vascular tissue the low molecular weight HSP, HSP27, is also induced by restraint. Further characterization of the vascular response revealed that HSP70 induction occurred in both the thoracic and abdominal aortas as well as in the vena cava. However, no HSP70 induction was apparent in the heart or in a wide variety of other tissues examined. In situ hybridization showed that the vascular expression was localized to the aortic smooth muscle cells with minimal expression in the endothelium. Induction of HSP70 mRNA in both the adrenal cortex and aorta was followed by an elevation in HSP70 protein. Maximum HSP70 protein levels were seen within 3-12 h after restraint, but declined thereafter. Stress induced HSP70 expression was dramatically reduced with age, which may explain, in part, the diminished tolerance to stress seen in elderly individuals. C1 NIA,GERONTOL RES CTR,MOLEC GENET LAB,BALTIMORE,MD 21224. RP UDELSMAN, R (reprint author), JOHNS HOPKINS UNIV HOSP,DIV ENDOCRINE SURG,OSLER 624,600 N WOLFE ST,BALTIMORE,MD 21287, USA. FU NIDDK NIH HHS [K08 DK02064-01] NR 53 TC 196 Z9 199 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD FEB PY 1993 VL 91 IS 2 BP 465 EP 473 DI 10.1172/JCI116224 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KM222 UT WOS:A1993KM22200017 PM 8094399 ER PT J AU SOMMERCORN, J FIELDS, R RAZ, I MAEDA, R AF SOMMERCORN, J FIELDS, R RAZ, I MAEDA, R TI ABNORMAL REGULATION OF RIBOSOMAL-PROTEIN S6 KINASE BY INSULIN IN SKELETAL-MUSCLE OF INSULIN-RESISTANT HUMANS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE NON-INSULIN-DEPENDENT DIABETES-MELLITUS; INSULIN RESISTANCE; INSULIN SIGNAL TRANSDUCTION; PROTEIN PHOSPHORYLATION; PROTEIN KINASE ID PHOSPHATASE-ACTIVITY; PIMA-INDIANS; RECEPTOR; PURIFICATION; SEQUENCE; INVIVO; GROWTH; IDENTIFICATION; STIMULATION; ACTIVATION AB Insulin resistance in Pima Indians appears to result from a post-receptor impairment of insulin signal transduction that affects only some responses to insulin. To identify the primary lesion responsible for insulin resistance, we investigated the influence of insulin on ribosomal protein S6 kinase activities in skeletal muscle of insulin-sensitive and insulin-resistant nondiabetic Pima Indians during a 2-h hyperinsulinemic, euglycemic clamp. In sensitive subjects, S6 kinase activity was transiently activated fivefold over basal activity by 45 min of insulin infusion. Although basal activities in the two groups were similar, the response to insulin was delayed and restricted to about threefold over basal in subjects resistant to insulin. Two major S6 kinase activities in extracts of human muscle were resolved by chromatography on Mono Q. Peak 1, which accounted for basal activity owes to an enzyme antigenically related to the 90-kD S6 kinase II, a member of the rsk gene family. The major insulin-stimulated S6 kinase eluted as peak 2 and is antigenically related to a 70-kD S6 kinase. Our results show that insulin resistance impairs signaling to the 70-kD S6 kinase. RP SOMMERCORN, J (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,PHOENIX,AZ 85016, USA. NR 43 TC 9 Z9 9 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 FEB PY 1993 VL 91 IS 2 BP 509 EP 513 DI 10.1172/JCI116229 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KM222 UT WOS:A1993KM22200022 PM 8432859 ER PT J AU SANO, H ENGLEKA, K MATHERN, P HLA, T CROFFORD, LJ REMMERS, EF JELSEMA, CL GOLDMUNTZ, E MACIAG, T WILDER, RL AF SANO, H ENGLEKA, K MATHERN, P HLA, T CROFFORD, LJ REMMERS, EF JELSEMA, CL GOLDMUNTZ, E MACIAG, T WILDER, RL TI COEXPRESSION OF PHOSPHOTYROSINE-CONTAINING PROTEINS, PLATELET-DERIVED GROWTH FACTOR-B, AND FIBROBLAST GROWTH FACTOR-I INSITU IN SYNOVIAL TISSUES OF PATIENTS WITH RHEUMATOID-ARTHRITIS AND LEWIS RATS WITH ADJUVANT OR STREPTOCOCCAL CELL-WALL ARTHRITIS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE GLUCOCORTICOIDS; GROWTH FACTORS; FIBROBLAST GROWTH FACTOR-I; INFLAMMATION; PHOSPHORYLATION; PLATELET-DERIVED GROWTH FACTOR ID TRANSFORMATION-ASSOCIATED METALLOPROTEINASE; STIMULATES TYROSINE PHOSPHORYLATION; TRANSIN STROMELYSIN EXPRESSION; SIGNAL TRANSDUCTION; PDGF RECEPTOR; FACTOR-I; KINASE-ACTIVITY; FACTOR-BETA; BINDING; SYNOVIOCYTES AB Fibroblast growth factor (FGF)-1 and PDGF-B-like factors have been implicated in the pathobiology of RA and animal models of this disease. Since the receptors for FGF-1 and PDGF are tyrosine kinases, we examined the expression of tyrosine phosphorylated proteins (phosphotyrosine, P-Tyr) in synovial tissues from patients with RA and osteoarthritis (OA), and rats with streptococcal cell wall (SCW) and adjuvant arthritis (AA). Synovia from patients with RA and LEW/N rats with SCW and AA arthritis, in contrast to controls, stained intensely with anti-P-Tyr antibody. The staining colocalized with PDGF-B and FGF-1 staining. Comparative immunoblot analysis showed markedly enhanced expression of a 45-kD P-Tyr protein in the inflamed synovia. Treatment with physiological concentrations of dexamethasone suppressed both arthritis and P-Tyr expression in AA. P-Tyr was only transiently expressed in athymic nude Lewis rats and was not detected in relatively arthritis-resistant F344/N rats. These data suggest that (a) FGF-1 and PDGF-B-like factors are upregulated and may induce tyrosine phosphorylation of proteins in vivo in inflammatory joint diseases, (b) persistent high level P-Tyr expression is T lymphocyte dependent, correlates with disease severity, and is strain dependent in rats, (c) corticosteroids, in physiological concentrations, downregulate P-Tyr expression in these lesions. C1 NIAMSD,ARTHRITIS & RHEUMATISH BRANCH,BLDG 10,ROOM 9N240,BETHESDA,MD 20892. AMER RED CROSS,DEPT MOLEC BIOL,HOLLAND LAB,ROCKVILLE,MD 20855. RI Hla, Timothy/G-5873-2012; Crofford, Leslie/J-8010-2013 OI Hla, Timothy/0000-0001-8355-4065; FU NHLBI NIH HHS [HL-32348] NR 49 TC 60 Z9 65 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 FEB PY 1993 VL 91 IS 2 BP 553 EP 565 DI 10.1172/JCI116235 PG 13 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA KM222 UT WOS:A1993KM22200028 PM 7679410 ER PT J AU LONGO, DL AF LONGO, DL TI WHATS THE DEAL WITH FOLLICULAR LYMPHOMAS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID NON-HODGKINS-LYMPHOMA; NODULAR HISTIOCYTIC LYMPHOMA; BONE-MARROW TRANSPLANTATION; DISEASE-FREE SURVIVAL; HISTOLOGIC PROGRESSION; PROGNOSTIC FACTORS; MIXED LYMPHOMA; CELL LYMPHOMA; CHEMOTHERAPY; ABNORMALITIES RP LONGO, DL (reprint author), NCI,FREDERICK,MD 21701, USA. NR 32 TC 45 Z9 47 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD FEB PY 1993 VL 11 IS 2 BP 202 EP 208 PG 7 WC Oncology SC Oncology GA KK441 UT WOS:A1993KK44100002 PM 8426195 ER PT J AU BORNER, MM SARTOR, O AF BORNER, MM SARTOR, O TI MORE IS NOT ALWAYS BETTER - A CASE FOR LOW-DOSE LEUCOVORIN SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter ID COLON ADENOCARCINOMA XENOGRAFTS; BIOCHEMICAL MODULATION; COLORECTAL-CARCINOMA; FLUOROURACIL; CANCER; POOLS RP BORNER, MM (reprint author), NCI,BETHESDA,MD 20892, USA. RI Borner, Markus/B-7583-2011 NR 9 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD FEB PY 1993 VL 11 IS 2 BP 382 EP 383 PG 2 WC Oncology SC Oncology GA KK441 UT WOS:A1993KK44100028 PM 8426218 ER PT J AU GIFT, HC AF GIFT, HC TI NEEDED - A RESEARCH AGENDA FOR WOMEN S ORAL HEALTH SO JOURNAL OF DENTAL RESEARCH LA English DT Editorial Material ID ESTROGEN RP GIFT, HC (reprint author), NIDR,EPIDEMIOL & ORAL DIS PREVENT PROGRAM,BETHESDA,MD 20892, USA. NR 21 TC 4 Z9 4 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD FEB PY 1993 VL 72 IS 2 BP 552 EP 553 DI 10.1177/00220345930720021301 PG 2 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KK857 UT WOS:A1993KK85700013 PM 8423253 ER PT J AU RESTIFO, NP ESQUIVEL, F KAWAKAMI, Y YEWDELL, JW MULE, JJ ROSENBERG, SA BENNINK, JR AF RESTIFO, NP ESQUIVEL, F KAWAKAMI, Y YEWDELL, JW MULE, JJ ROSENBERG, SA BENNINK, JR TI IDENTIFICATION OF HUMAN CANCERS DEFICIENT IN ANTIGEN PROCESSING SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-II REGION; TUMOR-INFILTRATING LYMPHOCYTES; CELL LUNG-CANCER; ADOPTIVE IMMUNOTHERAPY; DEFECTIVE PRESENTATION; VIRAL PEPTIDES; VACCINIA VIRUS; MURINE TUMOR; MHC AB Intracellular antigens must be processed before presentation to CD8+ T cells by major histocompatibility complex (MHC) class I molecules. Using a recombinant vaccinia virus (Vac) to transiently express the K(d) molecule, we studied the antigen processing efficiency of 26 different human tumor lines. Three cell lines, all human small cell lung carcinoma, consistently failed to process endogenously synthesized proteins for presentation to K(d)-restricted, Vac-specific T cells. Pulse-chase experiments showed that MHC class I molecules were not transported by these cell lines from the endoplasmic reticulum to the cell surface. This finding suggested that peptides were not available for binding to nascent MHC molecules in the endoplasmic reticulum. Northern blot analysis of these cells revealed low to nondetectable levels of mRNAs for MHC-encoded proteasome components LMP-7 and LMP-2, as well as the putative peptide transporters TAP-1 and TAP-2. Treatment of cells with interferon gamma enhanced expression of these mRNAs and reversed the observed functional and biochemical deficits. Our findings suggest that downregulation of antigen processing may be one of the strategies used by tumors to escape immune surveillance. Potential therapeutic applications of these findings include enhancing antigen processing at the level of the transcription of MHC-encoded proteasome and transporter genes. C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RP RESTIFO, NP (reprint author), NCI,DIV CANC TREATMENT,SURG BRANCH,BLDG 10,ROOM 2B42,BETHESDA,MD 20892, USA. RI Restifo, Nicholas/A-5713-2008; yewdell, jyewdell@nih.gov/A-1702-2012; Kawakami, Yutaka /E-7429-2013; OI Kawakami, Yutaka /0000-0003-4836-2855; Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z01 BC010763-01, Z99 CA999999] NR 55 TC 532 Z9 536 U1 1 U2 8 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 FEB 1 PY 1993 VL 177 IS 2 BP 265 EP 272 DI 10.1084/jem.177.2.265 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KJ441 UT WOS:A1993KJ44100003 PM 8426105 ER PT J AU DUFFY, PE PIMENTA, P KASLOW, DC AF DUFFY, PE PIMENTA, P KASLOW, DC TI PGS28 BELONGS TO A FAMILY OF EPIDERMAL GROWTH-FACTOR LIKE ANTIGENS THAT ARE TARGETS OF MALARIA TRANSMISSION-BLOCKING ANTIBODIES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID PLASMODIUM-FALCIPARUM; SEXUAL STAGES; GALLINACEUM; IMMUNITY; DNA; TRANSFORMATION; EXPRESSION; PROTEINS; ZYGOTES; VACCINE AB Although Pgs28, a 28-kD surface protein of Plasmodium gallinaceum ookinetes, was previously thought not to be a target of transmission-blocking antibodies, we found that polyclonal antisera to Pgs28 completely blocked parasite infectivity to Aedes aegypti mosquitoes. Antisera raised against reduced Pgs28 were less effective in blocking transmission than were antisera to nonreduced Pgs28; thus, the target epitope(s) of transmission-blocking antibodies appears to be conformation dependent. In stage-specific assays, polyclonal antisera impaired the in vitro transformation of zygotes to mature ookinetes, as well as the in vivo development of mature ookinetes to oocysts. Using microsequence of immunoaffinity-purified Pgs28, we cloned the 666-bp open reading frame of the Pgs28 gene. The deduced amino acid sequence of Pgs28 is strikingly similar to that of a R gallinaceum zygote surface protein, Pgs25, and its P. falciparum analogue, Pfs25. Pgs28, like Pgs25 and Pfs25, has a presumptive secretory signal sequence, followed by four epidermal growth factor-like domains, and a terminal hydrophobic region. C1 NIAID,MALARIA RES LAB,MOLEC VACCINE SECT,BLDG 4 ROOM B1-37,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. WALTER REED ARMY INST RES,DEPT MED,WASHINGTON,DC 20307. NR 22 TC 80 Z9 84 U1 1 U2 1 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 FEB 1 PY 1993 VL 177 IS 2 BP 505 EP 510 DI 10.1084/jem.177.2.505 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA KJ441 UT WOS:A1993KJ44100027 PM 8426118 ER PT J AU PURCELL, L GRUIAGRAY, J SCANGA, S RINGUETTE, M AF PURCELL, L GRUIAGRAY, J SCANGA, S RINGUETTE, M TI DEVELOPMENTAL ANOMALIES OF XENOPUS EMBRYOS FOLLOWING MICROINJECTION OF SPARC ANTIBODIES SO JOURNAL OF EXPERIMENTAL ZOOLOGY LA English DT Article ID BINDING PROTEIN SPARC; CREST CELL-MIGRATION; EXTRACELLULAR-MATRIX; AMPHIBIAN EMBRYOS; ENDOTHELIAL-CELLS; OSTEONECTIN; EXPRESSION; THROMBOSPONDIN; FIBRONECTIN; TENASCIN AB The function of SPARC (Secreted Protein, Acidic, Rich in Cysteine) in early embryonic development was assayed by microinjecting affinity-purified antibodies directed against SPARC into the blastocoel cavity of Xenopus embryos. Microinjection of SPARC antibodies did not appear to interfere with development until late neurulation. By hatching, a broad spectrum of external developmental anomalies were observable, including bent embryonic axes, accentuated ventral masses, shortened embryonic axes, and lack of visible eye pigment. Histological sections of injected embryos demonstrated that lack of visible eye pigmentation was often associated with deformities in eye development. Bending and shortening of the embryonic axis was associated with highly disorganized myotome patterns and loss of segmental boundaries. The results indicate a requirement for SPARC in the early morphological development of several tissues in Xenopus. C1 UNIV TORONTO,DEPT ZOOL,25 HARBORD ST,TORONTO M5S 1A1,ONTARIO,CANADA. NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. NR 33 TC 36 Z9 36 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 0022-104X J9 J EXP ZOOL JI J. Exp. Zool. PD FEB 1 PY 1993 VL 265 IS 2 BP 153 EP 164 DI 10.1002/jez.1402650207 PG 12 WC Zoology SC Zoology GA KK281 UT WOS:A1993KK28100006 PM 8423439 ER PT J AU BIANCO, P RIMINUCCI, M BONUCCI, E TERMINE, JD ROBEY, PG AF BIANCO, P RIMINUCCI, M BONUCCI, E TERMINE, JD ROBEY, PG TI BONE SIALOPROTEIN (BSP) SECRETION AND OSTEOBLAST DIFFERENTIATION - RELATIONSHIP TO BROMODEOXYURIDINE INCORPORATION, ALKALINE-PHOSPHATASE, AND MATRIX DEPOSITION SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article DE BONE SIALOPROTEIN; ALKALINE PHOSPHATASE; BROMODEOXYURIDINE; OSTEOGENESIS; OSTEOBLAST DIFFERENTIATION ID TARGET-CELL; MARROW; 5-BROMODEOXYURIDINE; LOCALIZATION; EXPRESSION; TISSUES; EMBRYO AB We defined two distinct maturational compartments (proliferative and secretory) of osteogenic cells in vivo on the basis of ALP activity, BrdU incorporation, cell shape, and BSP production. BSP immunoreactivity was found to mark cells in the secretory but not in the proliferative compartment. We established the phenotypic similarity of primitive marrow stromal cells with proliferating perichondral cells (fibro-blast-like, ALP+, BrdU+, BSP-). This suggests the potential functional equivalence of the two cell types as committed non-secretory osteogenic cells and points to the duality of osteogenic cell compartments as a generalized feature of bone formation. We further showed that although BSP secretion is a hallmark of the onset of osteogenesis, BSP antigenicity is lost both in osteoid and in a large proportion of mature osteoblasts during subsequent phases of bone deposition. This suggests that bone formation may not be a uniform event, as bone cells actually deposit antigenically, and likely biochemically, distinct matrices at specific times. C1 UNIV ROME,DIPARTIMENTO BIOPATOL UMANA,I-00100 ROME,ITALY. ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. NIDR,BETHESDA,MD 20892. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 33 TC 84 Z9 85 U1 0 U2 3 PU HISTOCHEMICAL SOC INC PI NEW YORK PA MT SINAI MEDICAL CENTER 19 EAST 98TH ST SUTIE 9G, NEW YORK, NY 10029 SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD FEB PY 1993 VL 41 IS 2 BP 183 EP 191 PG 9 WC Cell Biology SC Cell Biology GA KH749 UT WOS:A1993KH74900005 PM 8419458 ER PT J AU BIANCO, P RIMINUCCI, M SILVESTRINI, G BONUCCI, E TERMINE, JD FISHER, LW ROBEY, PG AF BIANCO, P RIMINUCCI, M SILVESTRINI, G BONUCCI, E TERMINE, JD FISHER, LW ROBEY, PG TI LOCALIZATION OF BONE SIALOPROTEIN (BSP) TO GOLGI AND POST-GOLGI SECRETORY STRUCTURES IN OSTEOBLASTS AND TO DISCRETE SITES IN EARLY BONE-MATRIX SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article DE BONE SIALOPROTEIN; OSTEOBLAST; IMMUNOCYTOCHEMISTRY; ULTRASTRUCTURE; GOLGI; CELL ADHESION; MINERALIZATION ID GAMMA-CARBOXYGLUTAMIC ACID; DEVELOPING RAT BONES; PHOSPHOPROTEIN; PROTEIN; IMMUNOLOCALIZATION; COMPARTMENT; EXPRESSION; ADHESION; TISSUES AB Bone sialoprotein (BSP), a bone matrix-enriched glycoprotein containing the Arg-Gly-Asp (RGD) motif and endowed with cell binding properties, was localized in osteoblasts and early bone matrix of developing rat bone at the ultrastructural level. Preliminary light microscopic observations indicated that intracellular labelling was restricted to a paranuclear dot corresponding to the ''negative Golgi image'' of classical histology. The same pattern was observed whether antisera against the fully glycosylated protein or a peptide antiserum to a stretch of amino acids in human BSP sequence were employed. At the EM level, we obtained labeling over the Golgi area of osteoblasts but not over the rER. The labeling was concentrated over distensions of the trans Golgi and over pro-secretory granules. In the matrix, BSP was distributed in a non-random manner. The label was concentrated over spherical aggregates of finely fibrillar material corresponding to the sites of early mineral deposition (so-called ''mineralization nodules''). Such BSP-positive foci were seen both close to and away from the cell surface. The predominant association of BSP with Golgi and post-Golgi secretory structures and its absence from rER, as well as the reproducibility of the same pattern of localization with different antisera, might indicate a slow transit of the protein through the Golgi, not necessarily associated with protein glycosylation. C1 UNIV ROME,DIPARTIMENTO BIOPATOL UMANA,I-00100 ROME,ITALY. ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. NIDR,BETHESDA,MD 20892. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 33 TC 119 Z9 119 U1 0 U2 1 PU HISTOCHEMICAL SOC INC PI NEW YORK PA MT SINAI MEDICAL CENTER 19 EAST 98TH ST SUTIE 9G, NEW YORK, NY 10029 SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD FEB PY 1993 VL 41 IS 2 BP 193 EP 203 PG 11 WC Cell Biology SC Cell Biology GA KH749 UT WOS:A1993KH74900006 PM 8419459 ER PT J AU OLSON, MJ MARTIN, JL LAROSA, AC BRADY, AN POHL, LR AF OLSON, MJ MARTIN, JL LAROSA, AC BRADY, AN POHL, LR TI IMMUNOHISTOCHEMICAL LOCALIZATION OF CARBOXYLESTERASE IN THE NASAL-MUCOSA OF RATS SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Note DE CARBOXYLESTERASE; IMMUNOHISTOCHEMISTRY; RAT; NASAL MUCOSA ID RESPIRATORY TRACTS; PURIFICATION; METABOLISM; TOXICITY; ACRYLATE; ACETATE; ESTERS; LIVER AB The enzymatic esterase activity of carboxylesterases is integral to the nasal toxicity of many esters used as industrial solvents or in polymer manufacture, including propylene glycol monomethyl ether acetate, dimethyl glutarate, dimethyl succinate, dimethyl adipate, and ethyl acrylate. Inhalation of these chemicals specifically damages the olfactory mucosa of rodents. We report the localization and differential distribution of a 59 KD carboxylesterase in nasal tissues of the rat by immunohistochemistry. Rabbit antiserum against the 59 KD rat liver microsomal carboxylesterase bound most prominently to the olfactory mucosa when applied to decalcified, paraffin-embedded sections of rat nasal turbinates. Within the olfactory mucosa, anti-carboxylesterase did not bind to sensory neurons, the target cell for ester-initiated toxicity; these cells apparently lack carboxylesterase. Instead, the antibody was preferentially bound by cells of Bowman's glands and sustentacular epithelial cells which are immediately adjacent to the olfactory nerve cells. In contrast, non-olfactory tissues (respiratory mucosa and squamous epithelium), which are more resistant to the toxicity of esters, had less carboxylesterase content. The distribution of immunoreactivity correlated well with the distribution of carboxylesterase catalytic activity described elsewhere. These findings help to link the metabolic fate of inhaled esters to the site-specific pathological findings that follow exposure to such chemicals. C1 JOHNS HOPKINS MED INST,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205. NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. RP OLSON, MJ (reprint author), GM CORP,RES & ENVIRONM STAFF,DEPT BIOMED SCI,30500 MOUND RD,BOX 9055,WARREN,MI 48090, USA. NR 18 TC 18 Z9 19 U1 0 U2 1 PU HISTOCHEMICAL SOC INC PI NEW YORK PA MT SINAI MEDICAL CENTER 19 EAST 98TH ST SUTIE 9G, NEW YORK, NY 10029 SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD FEB PY 1993 VL 41 IS 2 BP 307 EP 311 PG 5 WC Cell Biology SC Cell Biology GA KH749 UT WOS:A1993KH74900018 PM 8419465 ER PT J AU SHIRAI, A HOLMES, K KLINMAN, D AF SHIRAI, A HOLMES, K KLINMAN, D TI DETECTION AND QUANTITATION OF CELLS SECRETING IL-6 UNDER PHYSIOLOGICAL CONDITIONS IN BALB/C MICE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; TUMOR NECROSIS FACTOR; MARROW STROMAL CELLS; MOUSE BONE-MARROW; GROWTH-FACTOR; T-CELL; B-CELLS; ANTIBODY-FORMATION; MONOCLONAL-ANTIBODY; STIMULATING FACTORS AB IL-6 is a pleiotropic cytokine involved in the regulation of hematopoiesis and lymphocyte activation. An extremely sensitive ELIspot assay was developed to detect and enumerate individual cells secreting IL-6 in normal BALB/c mice. Under physiologic conditions, the frequency of cells producing IL-6 in the bone marrow, spleen, and mesenteric lymph nodes of normal adult animals was approximately 0.5, 0.1, and 0.01%, respectively. FACS analysis revealed that macrophages and Macl- B220- cells accounted for the vast majority of IL-6 production in the bone marrow, whereas T and B lymphocytes accounted for 4% and 38% of IL-6 production in the spleen. Simultaneous studies comparing cell number with IL-6 levels indicated that the average activated cell produced approximately 85 molecules of IL-6/s. C1 US FDA,CTR BIOL EVALUAT & RES,DIV VIROL,RETROVIRUS RES LAB,BLDG 29A,RM 3D10,BETHESDA,MD 20892. NIAID,BIOL RESOURCES BRANCH,FLOW CYTOMETRY SECT,BETHESDA,MD 20892. NR 60 TC 60 Z9 61 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 FEB 1 PY 1993 VL 150 IS 3 BP 793 EP 799 PG 7 WC Immunology SC Immunology GA KJ095 UT WOS:A1993KJ09500010 PM 8423340 ER PT J AU WADSWORTH, S HALVORSON, MJ CHANG, AC COLIGAN, JE AF WADSWORTH, S HALVORSON, MJ CHANG, AC COLIGAN, JE TI MULTIPLE CHANGES IN VLA PROTEIN GLYCOSYLATION, EXPRESSION, AND FUNCTION OCCUR DURING MOUSE T-CELL ONTOGENY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID FIBRONECTIN RECEPTOR; EXTRACELLULAR-MATRIX; LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; IMMATURE THYMOCYTES; ADHESION MOLECULES; INTEGRIN RECEPTORS; BINDING; DIFFERENTIATION; SURFACE AB VLA molecules (beta1 integrins) are cell-surface alphabeta heterodimers that bind to extracellular matrix (ECM) proteins such as fibronectin, laminin, and collagen. We analyzed the expression, structure, and function of VLAs on mouse thymocytes, as a first step toward understanding their role in T cell development. Two major forms of beta1 were detected, which differed in their extent of N-glycosylation and sialylation. No evidence for alternative splicing of beta1 mRNA was obtained by PCR analyses. The larger (135 kDa, nonreduced) more basic beta1 was the only form on nonmature (J11d+) adult thymocytes, with 135 kDa and larger beta1-chains expressed on fetal thymocytes from day 14 of gestation through birth. The smaller (120 kDa, nonreduced), more acidic beta-chain was found exclusively on mature (J11d-) thymocytes and peripheral lymphocytes. VLAalpha-chain expression was also analyzed. Virtually all thymocytes were VLA-alpha4+, -alpha6+. VLA-alpha5 was detected in both J11d+ and J11d- thymocytes by immunoprecipitation, but could not be analyzed in detail because of the lack of an appropriate mAb for flow cytometry. VLA-alpha1 and -alpha2 Were immunoprecipitated only from cells within the J11d- population. Only J11d+ thymocytes (12 to 15%) bound to fibronectin (via VLA-4 and VLA-5) and binding to laminin (via VLA-6) was two to fourfold higher in J11d+ compared with J11d- thymocytes (60 to 80% vs 20 to 30%). The high percentage of J11d+ thymocytes adhering to laminin suggests that VLA-6 exists in an activated state on most thymocytes, in contrast to resting peripheral T cells. These data show that major changes in VLA glycosylation, expression, and ECM-binding capacity occur as thymocytes mature, supporting the hypothesis that VLA-ECM interactions play a role in T cell ontogeny. C1 NIAID,BIOL RESOURCES BRANCH,BLDG 4,ROOM 413,BETHESDA,MD 20892. NR 48 TC 38 Z9 39 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 FEB 1 PY 1993 VL 150 IS 3 BP 847 EP 857 PG 11 WC Immunology SC Immunology GA KJ095 UT WOS:A1993KJ09500015 PM 7678625 ER PT J AU KARP, SE FARBER, A SALO, JC HWU, P JAFFE, G ASHER, AL SHILONI, E RESTIFO, NP MULE, JJ ROSENBERG, SA AF KARP, SE FARBER, A SALO, JC HWU, P JAFFE, G ASHER, AL SHILONI, E RESTIFO, NP MULE, JJ ROSENBERG, SA TI CYTOKINE SECRETION BY GENETICALLY MODIFIED NONIMMUNOGENIC MURINE FIBROSARCOMA - TUMOR-INHIBITION BY IL-2 BUT NOT TUMOR-NECROSIS-FACTOR SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ACTIVATED KILLER CELLS; GENE-TRANSFER; FACTOR-ALPHA; REDUCED TUMORIGENICITY; ANTITUMOR-ACTIVITY; ADVANCED CANCER; INVIVO; INTERLEUKIN-2; TNF; LYMPHOCYTES AB Recent investigations have demonstrated that the in vivo growth of weakly immunogenic murine tumors can be inhibited by genetic manipulations that enable them to secrete a variety of cytokines. Inasmuch as most human tumors fail to elicit a detectable host immune response we questioned whether the growth of a nonimmunogenic murine tumor could be inhibited by the secretion of cytokines. We have thus inserted the cDNA encoding for human IL-2 or TNF into the nonimmunogenic murine fibrosarcoma MCA 102. Tumor cells secreting IL-2 failed to grow in vivo despite normal in vitro growth. This growth inhibition required an intact immune system as tumors grew progressively in mice sublethally irradiated before tumor injection. Tumor inhibition was abrogated by the in vivo depletion, by specific mAb before tumor injection, of either CD8+ T cells or NK cells, but not CD4+ T cells. IL-2 secretion by tumor afforded a significant survival benefit to the animal, and IL-2-secreting tumor limited the growth of admixed nonsecreting parental tumor. Histologic evidence and FACS analyses revealed a dense lymphocytic infiltration of IL-2-secreting tumors composed of both CD4+ and CD8+ T cells. In contrast, secretion of TNF failed to inhibit the growth of MCA 102, and similar lymphocyte subset depletions, or administration of specific anti-TNF mAb had no effect on the growth of TNF secreting MCA 102. In summary, these investigations demonstrated that the host response to this nonimmunogenic tumor can be markedly enhanced by the genetic manipulation of the tumor cells to secrete IL-2, but not TNF. This strategy has potential application for the development of immunotherapies for nonimmunogenic tumors. C1 NCI,SURG BRANCH,BLDG 10,ROOM 2B46,BETHESDA,MD 20892. NCI,PATHOL BRANCH,BETHESDA,MD 20892. RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z99 CA999999, Z01 BC010763-01] NR 37 TC 101 Z9 102 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 FEB 1 PY 1993 VL 150 IS 3 BP 896 EP 908 PG 13 WC Immunology SC Immunology GA KJ095 UT WOS:A1993KJ09500020 PM 8423345 ER PT J AU DJEU, JY LIU, JH WEI, S RUI, H PEARSON, CA LEONARD, WJ BLANCHARD, DK AF DJEU, JY LIU, JH WEI, S RUI, H PEARSON, CA LEONARD, WJ BLANCHARD, DK TI FUNCTION ASSOCIATED WITH IL-2 RECEPTOR-BETA ON HUMAN NEUTROPHILS - MECHANISM OF ACTIVATION OF ANTIFUNGAL ACTIVITY AGAINST CANDIDA-ALBICANS BY IL-2 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; TUMOR NECROSIS FACTOR; INTERLEUKIN-2 RECEPTOR; INTERFERON-GAMMA; CELLS; EXPRESSION; DISTINCT; IDENTIFICATION AB Polymorphonuclear neutrophils (PMN) are essential components of the host defense system against a wide variety of pathogens. We report here the novel finding that freshly isolated human PMN constitutively express detectable surface levels of IL-2Rbeta, but not IL-2Ralpha, as analyzed by flow cytometry. Northern blot analysis confirmed the constitutive expression of mRNA for IL-2Rbeta in PMN. Scatchard analysis using I-125-labeled IL-2 demonstrated the presence of approximately 600 intermediate binding IL-2R per PMN, with a dissociation constant of 1.1 X 10(-9) M, similar to that of IL-2 binding to YT-1 tumor cells that specifically express IL-2Rbeta. More importantly, PMN were able to respond functionally to IL-2 by enhanced growth-inhibitory activity against an opportunistic fungal pathogen, Candida albicans. IL-2 activation of antifungal activity was dose-dependent, with some functional activation detected at 1 U/ml of rIL-2 and maximal activation at 1000 U/ml. The action of IL-2 was rapid, with maximal PMN activation after 30-min incubation with IL-2. The IL-2 enhancement of antifungal activity could be blocked by a specific antibody against IL-2Rbeta, but not by anti-IL-2Ralpha. Analysis of the mechanism of IL-2 activation of PMN indicated that oxidative metabolism, as measured by superoxide anion production, was not involved. Instead, PMN release of lactoferrin appeared to be responsible for the heightened activity against C albicans in IL-2-treated PMN. Not only was lactoferrin detected in the supernatants of IL-2-treated PMN, but also the antifungal activity of PMN activated by IL-2 could be blocked in the presence of antilactoferrin. These results, taken together, indicate that normal PMN are capable of functionally responding to IL-2 via expression of the IL-2Rbeta chain. C1 NHLBI,PULM & MOLEC IMMUNOL SECT,BETHESDA,MD 20892. RP DJEU, JY (reprint author), UNIV S FLORIDA,COLL MED,DEPT MED MICROBIOL & IMMUNOL,IMMUNOL PROGRAM,H LEE MOFFITT CANC CTR,TAMPA,FL 33612, USA. FU NCI NIH HHS [CA-46820]; NIAID NIH HHS [AI-24699] NR 36 TC 86 Z9 87 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 FEB 1 PY 1993 VL 150 IS 3 BP 960 EP 970 PG 11 WC Immunology SC Immunology GA KJ095 UT WOS:A1993KJ09500027 PM 8380826 ER PT J AU BUHL, R JAFFE, HA HOLROYD, KJ BOROK, Z ROUM, JH MASTRANGELI, A WELLS, FB KIRBY, M SALTINI, C CRYSTAL, RG AF BUHL, R JAFFE, HA HOLROYD, KJ BOROK, Z ROUM, JH MASTRANGELI, A WELLS, FB KIRBY, M SALTINI, C CRYSTAL, RG TI ACTIVATION OF ALVEOLAR MACROPHAGES IN ASYMPTOMATIC HIV-INFECTED INDIVIDUALS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID IMMUNODEFICIENCY-VIRUS INFECTION; TUMOR NECROSIS FACTOR; INTERFERON-GAMMA; PERIPHERAL-BLOOD; LYMPHOCYTES-T; SEROPOSITIVE INDIVIDUALS; MONONUCLEAR PHAGOCYTES; BRONCHOALVEOLAR LAVAGE; OXIDATIVE-METABOLISM; CIGARETTE SMOKERS AB After the initial infection with HIV, there is evidence of immune dysfunction despite an apparent normal clinical state. In the context that the lung is a major site affected by opportunistic infection during the progression of this immune dysfunction, and that some components of the immune system are activated during early HIV infection, we hypothesized that there may be activation of alveolar macrophages (AM), a key component of the pulmonary host defense system, during the asymptomatic phase of HIV infection. Compared to normals, in HIV-infected individuals the class II MHC molecules DR, DQ, and DP were all expressed more frequently and in greater cell surface density on AM (p < 0.03, all comparisons), and there was increased spontaneous release of superoxide anion (O2 radical-anion) by AM (p < 0.002). To gain insight into whether the activation of the AM was an inherent property of the cells or dependent on the in vivo milieu, AM were evaluated after 24 h in culture for O2 radical-anion release. In contrast to the findings in fresh AM, after 24 h in culture, O2 radical-anion release by HIV AM was not different from normals (p > 0.7), suggesting that these AM had been activated in vivo. To assess whether IFN-gamma could be mediating these effects, mRNA levels of the IP-10 gene (a gene specifically induced by increased concentrations of IFN-gamma) were quantified in AM. Strikingly, the IP-10 gene was expressed only in AM of HIV-seropositive individuals, suggesting the AM had been exposed to IFN-gamma in vivo. Overall, these observations are consistent with the concept that the HIV-seropositive state is associated with activation of AM, in part due to local exposure to IFN-gamma. C1 NHLBI,PULM BRANCH,BLDG 10,ROOM 6D03,BETHESDA,MD 20892. NR 60 TC 79 Z9 79 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 FEB 1 PY 1993 VL 150 IS 3 BP 1019 EP 1028 PG 10 WC Immunology SC Immunology GA KJ095 UT WOS:A1993KJ09500033 PM 8380824 ER PT J AU TWU, SJ DETELS, R NELSON, K VISSCHER, BR KASLOW, R PALENICEK, J PHAIR, J AF TWU, SJ DETELS, R NELSON, K VISSCHER, BR KASLOW, R PALENICEK, J PHAIR, J TI RELATIONSHIP OF HEPATITIS-B VIRUS-INFECTION TO HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID LONG TERMINAL REPEAT; MULTICENTER AIDS COHORT; X-PROTEIN; SEROCONVERSION; ACTIVATION; RISK; MEN AB The Multicenter AIDS Cohort Study (MACS) was designed to study the natural history of human immunodeficiency virus type 1 (HIV-1) infection, including the relationship between hepatitis B virus (HBV) and HIV-1 infection. In total, 4954 homosexual men were recruited from April 1984 through March 1985 and have been followed up thereafter every 6 months. Hepatitis B surface antigen and hepatitis B core antibody were tested for at the first visit by RIA or EIA; HIV-1 antibody testing was done at each visit by ELISA and confirmed by Western blot assay. The role of HBV infection in HIV-1 seroconversion was studied by stratification for sexual behavior and disease visit by visit. The adjusted risk ratio was 2.02 for hepatitis B surface antigen carriers and 2.14 for hepatitis-immune cases compared with hepatitis B-susceptible subjects. Similar results were obtained using a logistic regression model. After taking into account changes in sexual behavior and disease over time, the authors conclude that past HBV infection remains suspect as a cofactor or as a surrogate for other factors associated with HIV-1 seroconversion. C1 UNIV CALIF LOS ANGELES, SCH PUBL HLTH, DEPT EPIDEMIOL, 10833 LE CONTE AVE, LOS ANGELES, CA 90024 USA. JOHNS HOPKINS UNIV, SCH HYG & PUBL HLTH, BALTIMORE, MD 21218 USA. NIAID, BETHESDA, MD 20892 USA. NORTHWESTERN UNIV, SCH MED, CHICAGO, IL 60611 USA. FU NIAID NIH HHS [AI-72676, AI-72631, AI-72634] NR 21 TC 19 Z9 20 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0022-1899 EI 1537-6613 J9 J INFECT DIS JI J. Infect. Dis. PD FEB PY 1993 VL 167 IS 2 BP 299 EP 304 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KJ487 UT WOS:A1993KJ48700007 PM 8421164 ER PT J AU DANNER, RL EICHACKER, PQ DOERFLER, ME HOFFMAN, WD REILLY, JM WILSON, J MACVITTIE, TJ STUETZ, P PARRILLO, JE NATANSON, C AF DANNER, RL EICHACKER, PQ DOERFLER, ME HOFFMAN, WD REILLY, JM WILSON, J MACVITTIE, TJ STUETZ, P PARRILLO, JE NATANSON, C TI THERAPEUTIC TRIAL OF LIPID X IN A CANINE MODEL OF SEPTIC SHOCK SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID GRAM-NEGATIVE BACTEREMIA; STAPHYLOCOCCUS-AUREUS CHALLENGES; ESCHERICHIA-COLI CHALLENGES; PROTEIN KINASE-C; CARDIOVASCULAR DYSFUNCTION; RHODOPSEUDOMONAS-SPHAEROIDES; ANTIENDOTOXIN ACTIVITY; LETHAL ENDOTOXEMIA; HUMAN SEPSIS; MORTALITY AB Three groups of dogs were given lipid X (0, 1, or 10 mg/kg) every 8 h for seven doses, starting simultaneously with the intraperitoneal placement of Escherichia coli-containing fibrin clots. All animals developed bacteremia, hypotension, and a pattern of decreased left ventricular ejection fraction characteristic of septic shock (P = .01). Survival rates and survival times were not significantly different between treatment groups (P > .2). In a similar experiment, higher doses of lipid X resulted in a significantly decreased survival time compared with concurrent controls (P .04). Animals receiving lipid X did not differ from controls in serial determinations of temperature, hemodynamic measurements, or laboratory parameters (except serum total protein). Although lipid X has antiendotoxin effects. no benefit could be demonstrated in this antibiotic-treated, gram-negative bacillary-infected model of septic shock. These data do not support a therapeutic role for lipid X in the treatment of gram negative sepsis. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD 20892. DEF NUCL AGCY,ARMED FORCES RADIOBIOL RES INST,BETHESDA,MD 20014. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. RP DANNER, RL (reprint author), NIH,DEPT CRIT CARE MED,BLDG 10,ROOM 7D43,BETHESDA,MD 20892, USA. NR 47 TC 19 Z9 19 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 FEB PY 1993 VL 167 IS 2 BP 378 EP 384 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA KJ487 UT WOS:A1993KJ48700017 PM 8421172 ER PT J AU KAMEYAMA, K TAKEMURA, T HAMADA, Y SAKAI, C KONDOH, S NISHIYAMA, S URABE, K HEARING, VJ AF KAMEYAMA, K TAKEMURA, T HAMADA, Y SAKAI, C KONDOH, S NISHIYAMA, S URABE, K HEARING, VJ TI PIGMENT PRODUCTION IN MURINE MELANOMA-CELLS IS REGULATED BY TYROSINASE, TYROSINASE-RELATED PROTEIN-1 (TRP1), DOPACHROME TAUTOMERASE (TRP2), AND A MELANOGENIC INHIBITOR SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID MAMMALIAN MELANOGENESIS; PURIFICATION; BIOSYNTHESIS; MELANOCYTES; TRANSCRIPTS; HORMONE; MOUSE; CHAIN AB Using antibodies that recognize either tyrosinase, tyrosinase-related protein-1 (TRP1), or tyrosinase-related protein-2 (TRP2, DOPAchrome tautomerase), the quantities of those melanogenic enzymes were analyzed in five melanoma cell lines that possess various degrees of melanin production. All cells except JB/MS-W increased melanin production four to 30 times after 4 d of melanocyte-stimulating hormone (MSH) treatment. Melanin production by JB/MS-W cells was always under background, with or without MSH treatment. There was a positive correlation between quantities and synthetic rates of those melanogenic enzymes and their melanin formation or DOPAchrome tautomerase activities. The activity of a heat-resistant melanogenic inhibitory factor was also analyzed. The results showed, surprisingly, that pigmented cells showed higher levels of melanogenic inhibitors activity. Tyrosinase activity was increased dramatically whereas the level of melanogenic inhibitor was remarkably decreased following MSH treatment. Interestingly, melanogenic inhibitor derived from JB/MS-W cells suppressed not only tyrosinase but also DOPAchrome tautomerase, another enzyme functional in melanin production. These results clearly suggest that melanin production is regulated by a subtle balance between the activities of these enzymes and other factors such as the melanogenic inhibitor. C1 KITASATO UNIV,SCH MED,DEPT DERMATOL,SAGAMIHARA,KANAGAWA 228,JAPAN. NIH,CELL BIOL LAB,BETHESDA,MD 20892. NR 25 TC 74 Z9 75 U1 0 U2 3 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD FEB PY 1993 VL 100 IS 2 BP 126 EP 131 DI 10.1111/1523-1747.ep12462778 PG 6 WC Dermatology SC Dermatology GA KM220 UT WOS:A1993KM22000006 PM 8429235 ER PT J AU GRZESIEK, S ANGLISTER, J BAX, A AF GRZESIEK, S ANGLISTER, J BAX, A TI CORRELATION OF BACKBONE AMIDE AND ALIPHATIC SIDE-CHAIN RESONANCES IN C-13/N-15-ENRICHED PROTEINS BY ISOTROPIC MIXING OF C-13 MAGNETIZATION SO JOURNAL OF MAGNETIC RESONANCE SERIES B LA English DT Note ID 3D NMR-SPECTROSCOPY; 2D; ASSIGNMENT; SPECTRA; PHASE; H-1 RP GRZESIEK, S (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 17 TC 512 Z9 515 U1 2 U2 17 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1064-1866 J9 J MAGN RESON SER B JI J. Magn. Reson. Ser. B PD FEB PY 1993 VL 101 IS 1 BP 114 EP 119 DI 10.1006/jmrb.1993.1019 PG 6 WC Physics, Atomic, Molecular & Chemical SC Physics GA KW231 UT WOS:A1993KW23100019 ER PT J AU RICHARDS, FM MAHER, ER LATIF, F PHIPPS, ME TORY, K LUSH, M CROSSEY, PA OOSTRA, B GUSTAVSON, KH GREEN, J TURNER, G YATES, JRW LINEHAN, WM AFFARA, NA LERMAN, M ZBAR, B FERGUSONSMITH, MA AF RICHARDS, FM MAHER, ER LATIF, F PHIPPS, ME TORY, K LUSH, M CROSSEY, PA OOSTRA, B GUSTAVSON, KH GREEN, J TURNER, G YATES, JRW LINEHAN, WM AFFARA, NA LERMAN, M ZBAR, B FERGUSONSMITH, MA TI DETAILED GENETIC-MAPPING OF THE VONHIPPEL-LINDAU DISEASE TUMOR SUPPRESSOR GENE SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID RENAL-CELL CARCINOMA; LINKAGE ANALYSIS; SMALL REGION; SHORT ARM; CHROMOSOME-3; MEMBERS; LOCUS; MAPS AB Von Hippel-Lindau (VHL) disease is an autosomal dominant inherited familial cancer syndrome characterised by a predisposition to the development of retinal, cerebellar, and spinal haemangioblastomas, renal cell carcinoma, and phaeochromocytoma. The gene for VHL disease has been mapped to chromosome 3p25-p26 and flanking markers identified. We report the detailed genetic mapping of the VHL disease locus in 38 families. Significant linkage was detected between VHL disease and D3S601 (Zmax = 18.86 at theta = 0.0, CI 0.0-0.025), D3S18 (Zmax = 11.42 at theta = 0.03, CI 0.005-0.08), RAF1 (Zmax = 11.02 at theta = 0.04, CI 0.007-0.01), and D3S1250 (Zmax = 4.73 at theta = 0.05, CI 0.005-0.15). Multipoint linkage analysis mapped the VHL disease locus between D3S1250 and D3S18 close to D3S601. There was no evidence of locus heterogeneity. This study has (1) confirmed the tight linkage between VHL disease and D3S601, (2) identified D3S1250 as the first marker telomeric to RAF1 which maps centromeric to the VHL disease gene, and (3) narrowed the target region for isolation of the VHL disease gene by positional cloning techniques to a 4 cM interval between D3S1250 and D3S18. These findings will improve the clinical management of families with VHL disease by improving the accuracy of presymptomatic diagnosis using linked DNA markers, and will enhance progress towards isolating the VHL disease gene. C1 UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE,ENGLAND. NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,FREDERICK,MD 21701. YORKSHIRE REG GENET SERV,LEEDS,ENGLAND. ERASMUS UNIV,3000 DR ROTTERDAM,NETHERLANDS. UNIV UPPSALA,S-75105 UPPSALA,SWEDEN. MEM UNIV NEWFOUNDLAND,DIV COMMUNITY MED,ST JOHNS A1C 5S7,NEWFOUNDLAND,CANADA. ICRF,GENET EPIDEMIOL LAB,LEEDS,ENGLAND. RI MAHER, EAMONN/A-9507-2008 OI MAHER, EAMONN/0000-0002-6226-6918 NR 27 TC 36 Z9 36 U1 0 U2 3 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD FEB PY 1993 VL 30 IS 2 BP 104 EP 107 DI 10.1136/jmg.30.2.104 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA KL081 UT WOS:A1993KL08100005 PM 8445612 ER PT J AU BENVENISTE, RE KULLER, L ROODMAN, ST HU, SL MORTON, WR AF BENVENISTE, RE KULLER, L ROODMAN, ST HU, SL MORTON, WR TI LONG-TERM PROTECTION OF MACAQUES AGAINST HIGH-DOSE TYPE-D RETROVIRUS CHALLENGE AFTER IMMUNIZATION WITH RECOMBINANT VACCINIA VIRUS EXPRESSING ENVELOPE GLYCOPROTEINS SO JOURNAL OF MEDICAL PRIMATOLOGY LA English DT Article; Proceedings Paper CT 10TH ANNUAL MEETING ON NONHUMAN PRIMATE MODELS FOR AIDS 5 CY NOV 17-20, 1991 CL UNIV PUERTO RICO, CARIBBEAN PRIMATES CTR, SAN JUAN, PR HO UNIV PUERTO RICO, CARIBBEAN PRIMATES CTR DE SIMIAN AIDS; SRV-2; VACCINE; RETROPERITONEAL FIBROMATOSIS; PIG-TAILED MACAQUES ID ACQUIRED IMMUNODEFICIENCY SYNDROME; PFIZER MONKEY VIRUS; SIMIAN AIDS; RETROPERITONEAL FIBROMATOSIS; LENTIVIRUS AB Recombinant vaccinia virus expressing the envelope proteins of type D retrovirus-Washington (SRV-2/W) was used to immunize macaques against SRV-2 infection. Four immunized macaques which had resisted a prior low-dose challenge were rechallenged with a high dose (10(6) infectious particles) of SRV-2 two years after being immunized. All four nonimmunized control macaques became infected, but the four vaccinated animals resisted this intravenous challenge, as determined by the inability to detect SRV-2 in peripheral blood mononuclear cells and by the lack of seroconversion to new viral antigens. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. WASHINGTON REG PRIMATE RES CTR,SEATTLE,WA. ST LOUIS UNIV,SCH MED,ST LOUIS,MO. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 FU NCRR NIH HHS [RR00166]; PHS HHS [N01-74102] NR 16 TC 20 Z9 20 U1 0 U2 0 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 FEB-MAY PY 1993 VL 22 IS 2-3 BP 74 EP 79 PG 6 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA MC758 UT WOS:A1993MC75800002 PM 8411111 ER PT J AU HU, SL STALLARD, V ABRAMS, K BARBER, GN KULLER, L LANGLOIS, AJ MORTON, WR BENVENISTE, RE AF HU, SL STALLARD, V ABRAMS, K BARBER, GN KULLER, L LANGLOIS, AJ MORTON, WR BENVENISTE, RE TI PROTECTION OF VACCINIA-PRIMED MACAQUES AGAINST SIV(MNE) INFECTION BY COMBINATION IMMUNIZATION WITH RECOMBINANT VACCINIA VIRUS AND SIV(MNE) GP160 SO JOURNAL OF MEDICAL PRIMATOLOGY LA English DT Article; Proceedings Paper CT 10TH ANNUAL MEETING ON NONHUMAN PRIMATE MODELS FOR AIDS 5 CY NOV 17-20, 1991 CL UNIV PUERTO RICO, CARIBBEAN PRIMATES CTR, SAN JUAN, PR HO UNIV PUERTO RICO, CARIBBEAN PRIMATES CTR DE ENVELOPE GLYCOPROTEINS; BACULOVIRUS; HIV-1; AIDS; PATHOGENESIS; SUBUNIT VACCINE; NEUTRALIZING ANTIBODIES ID ENVELOPE GLYCOPROTEINS; SUBUNIT VACCINES; D RETROVIRUS; AIDS VIRUS; RESPONSES; CELLS; LENTIVIRUS; ANTIBODIES; GENE AB Two Macaca fascicularis with preexisting immunity to vaccinia virus were immunized twice with recombinant vaccinia virus expressing SIVmne gp160. Their SIV-specific antibody responses were lower than that of vaccinia-naive animals immunized similarly. Upon repeated boosting with gp160, the SIV-specific antibody titers in vaccinia-primed animals reached similar levels as vaccinia-naive animals and with comparable neutralizing titers. Both animals were protected against repeated intravenous challenge with low-dose SIV(mne)E11S. These results are significant because SIV(mne)E11S infection in M. fascicularis is pathogenic and leads to AIDS-like diseases. C1 UNIV WASHINGTON,WASHINGTON REG PRIMATE RES CTR,SEATTLE,WA. DUKE UNIV,MED CTR,DURHAM,NC. NCI,FREDERICK,MD 21701. RP HU, SL (reprint author), BRISTOL MYERS SQUIBB PHARMACEUT RES INST,3005 1ST AVE,SEATTLE,WA 98121, USA. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 FU NCRR NIH HHS [RR00166]; NIAID NIH HHS [AI26503] NR 27 TC 23 Z9 23 U1 0 U2 0 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 FEB-MAY PY 1993 VL 22 IS 2-3 BP 92 EP 99 PG 8 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA MC758 UT WOS:A1993MC75800005 PM 8411113 ER PT J AU BENVENISTE, RE HILL, RW KNOTT, WB TSAI, CC KULLER, L MORTON, WR AF BENVENISTE, RE HILL, RW KNOTT, WB TSAI, CC KULLER, L MORTON, WR TI DETECTION OF SERUM ANTIBODIES IN ETHIOPIAN BABOONS THAT CROSS-REACT WITH SIV, HTLV-I, AND TYPE-D RETROVIRAL ANTIGENS SO JOURNAL OF MEDICAL PRIMATOLOGY LA English DT Article; Proceedings Paper CT 10TH ANNUAL MEETING ON NONHUMAN PRIMATE MODELS FOR AIDS 5 CY NOV 17-20, 1991 CL UNIV PUERTO RICO, CARIBBEAN PRIMATES CTR, SAN JUAN, PR HO UNIV PUERTO RICO, CARIBBEAN PRIMATES CTR DE PRIMATE SEROEPIDEMIOLOGY; PAPIO CYNOCEPHALUS; AIDS; GAG PROTEINS ID CELL LEUKEMIA-VIRUS; SIMIAN IMMUNODEFICIENCY VIRUS; AFRICAN-GREEN MONKEYS; NON-HUMAN PRIMATES; T-LYMPHOTROPIC RETROVIRUS; SEROEPIDEMIOLOGIC SURVEY; CERCOCEBUS-ATYS; MACAQUES; LENTIVIRUS; MANGABEYS AB Baboons (Papio cynocephalus) imported from Ethiopia were screened for antibodies to various primate retroviruses by immunoblotting. Antibodies that cross-reacted with SIV/Mne or with type D viral antigens were detected in approximately one-third of these animals. In addition, 20% of these baboons had antibodies that cross-reacted with HTLV-I viral antigens. These data suggest that wild-caught baboons are infected with retroviruses only partially related to known primate viral isolates. C1 WASHINGTON REG PRIMATE RES CTR,SEATTLE,WA. NCI,FCRDC,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. RP BENVENISTE, RE (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,BLDG 560,FREDERICK,MD 21702, USA. FU NCRR NIH HHS [RR00166] NR 30 TC 8 Z9 8 U1 0 U2 0 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 FEB-MAY PY 1993 VL 22 IS 2-3 BP 124 EP 128 PG 5 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA MC758 UT WOS:A1993MC75800010 PM 8411104 ER PT J AU OCHS, HD MORTON, WR KULLER, LD ZHU, Q TSAI, CC AGY, MB BENVENISTE, RE AF OCHS, HD MORTON, WR KULLER, LD ZHU, Q TSAI, CC AGY, MB BENVENISTE, RE TI INTRAAMNIOTIC INOCULATION OF PIGTAILED MACAQUE (MACACA-NEMESTRINA) FETUSES WITH SIV AND HIV-1 SO JOURNAL OF MEDICAL PRIMATOLOGY LA English DT Article; Proceedings Paper CT 10TH ANNUAL MEETING ON NONHUMAN PRIMATE MODELS FOR AIDS 5 CY NOV 17-20, 1991 CL UNIV PUERTO RICO, CARIBBEAN PRIMATES CTR, SAN JUAN, PR HO UNIV PUERTO RICO, CARIBBEAN PRIMATES CTR DE PEDIATRIC AIDS; MATERNAL; FETAL TRANSMISSION; INTRAUTERINE INFECTION WITH SIV/HIV-1 ID IMMUNODEFICIENCY-VIRUS TYPE-1; TRANSMISSION; INFECTION; LENTIVIRUS AB Six pregnant pigtailed macaques (Macaca nemestrina) were inoculated intra-amniotically (i.a.) with SIVMne. All became viremic and seroconverted; three viable offspring were SIV-positive and at autopsy showed disseminated viral infection; one of three abortuses had SIV-infected thymic macrophages. Three of five pregnant macaques inoculated i.v. and/or i.a. with HIV-1(LAI) became virus-positive, and four seroconverted, suggesting fetal-maternal transmission. One abortus had HIV-1-antigen in lymph nodes and brain; one infant, culture-positive at birth, died at age 11 days of disseminated HIV-1 infection. C1 UNIV WASHINGTON,REG PRIMATE RES CTR,SEATTLE,WA 98195. NCI,FREDERICK,MD 21701. RP OCHS, HD (reprint author), UNIV WASHINGTON,SCH MED,DEPT PEDIAT,RD-20,SEATTLE,WA 98195, USA. FU NCRR NIH HHS [RR00166]; NIAID NIH HHS [AI27757, AI26503] NR 15 TC 7 Z9 7 U1 0 U2 0 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 FEB-MAY PY 1993 VL 22 IS 2-3 BP 162 EP 168 PG 7 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA MC758 UT WOS:A1993MC75800015 PM 8411108 ER PT J AU ENGELMANN, GL BIRCHENALLROBERTS, MC RUSCETTI, FW SAMAREL, AM AF ENGELMANN, GL BIRCHENALLROBERTS, MC RUSCETTI, FW SAMAREL, AM TI FORMATION OF FETAL-RAT CARDIAC CELL CLONES BY RETROVIRAL TRANSFORMATION - RETENTION OF SELECT MYOCYTE CHARACTERISTICS SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE MYOCYTE; CELL LINE; RETROVIRUS; PROLIFERATION; GENE EXPRESSION ID FIBROBLAST GROWTH-FACTOR; V-MYC ONCOGENE; C-MYC; REGIONAL DIFFERENCES; HYPERTENSIVE RATS; CREATINE-KINASE; TRANSGENIC MICE; RETINOIC ACID; TGF-BETA; EXPRESSION C1 NCI, FREDERICK CANC RES & DEV CTR, PROGRAM RESOURCES INC, FREDERICK, MD 21701 USA. LOYOLA UNIV, STRITCH SCH MED, DEPT CELL BIOL, MAYWOOD, IL 60153 USA. NCI, DIV CANC TREATMENT, BIOL RESPONSE MODIFIERS PROGRAM, MOLEC REGULAT LAB, FREDERICK, MD 21701 USA. LOYOLA UNIV, STRITCH SCH MED, DEPT MED & PHYSIOL, MAYWOOD, IL 60153 USA. RP ENGELMANN, GL (reprint author), LOYOLA UNIV, STRITCH SCH MED, DEPT MED, RM 0730, 2160 S 1ST AVE, MAYWOOD, IL 60153 USA. FU NHLBI NIH HHS [HL-42218, HL-34328] NR 64 TC 24 Z9 24 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD FEB PY 1993 VL 25 IS 2 BP 197 EP 213 DI 10.1006/jmcc.1993.1022 PG 17 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA KR244 UT WOS:A1993KR24400007 PM 8386255 ER PT J AU DUBERSTEIN, PR CONWELL, Y CAINE, ED AF DUBERSTEIN, PR CONWELL, Y CAINE, ED TI INTERPERSONAL STRESSORS, SUBSTANCE-ABUSE, AND SUICIDE SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID SAN-DIEGO SUICIDE; LIFE EVENTS AB In contrast to suicide in depression, suicide associated with alcoholism and substance dependence may be preceded more often by interpersonal loss and conflict 6 weeks prior to death. We used psychological autopsy methodology in an effort to clarify and extend these findings using a more comprehensive typology of interpersonal stressors. Subjects included 57 suicide victims with diagnoses of alcohol/substance dependence (A/SD; N = 30) and mood/anxiety disorders (M/AD; N = 27). Consistent with previous studies, a substantial majority of the A/SD suicide victims were confronted with interpersonal stressors in the 6 weeks prior to death. Our investigation extends previous findings by indicating that a) A/SD suicide victims are confronted with a broader range of interpersonal stressors than M/AD suicide completers and b) the types of interpersonal stressors experienced by A/SD subjects in the weeks prior to suicide involve conflicts/arguments and attachment disruptions. RP DUBERSTEIN, PR (reprint author), UNIV ROCHESTER,MED CTR,DEPT PSYCHIAT,NIMH,CLIN RES CTR STUDY PSYCHOPATHOL ELDERLY,ROCHESTER,NY 14642, USA. FU NIMH NIH HHS [MH00748, MH18911, MH40381] NR 33 TC 77 Z9 77 U1 2 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD FEB PY 1993 VL 181 IS 2 BP 80 EP 85 DI 10.1097/00005053-199302000-00002 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA KL710 UT WOS:A1993KL71000002 PM 8426175 ER PT J AU VALCHAR, M HANBAUER, I AF VALCHAR, M HANBAUER, I TI COMPARISON OF [H-3] WIN 35,428 BINDING, A MARKER FOR DOPAMINE TRANSPORTER, IN EMBRYONIC MESENCEPHALIC NEURONAL CULTURES WITH STRIATAL MEMBRANES OF ADULT-RATS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE DOPAMINE TRANSPORTER; VENTRAL MESENCEPHALON; PRIMARY CULTURES; [H-3]DOPAMINE UPTAKE; [H-3]WIN 35,428 BINDING ID UPTAKE SITES; H-3 COCAINE; GBR-12935 BINDING; LIGAND-BINDING; UPTAKE COMPLEX; NOREPINEPHRINE; RECEPTORS; INVITRO; BRAIN AB In contrast to striatal membranes of adult rats, where high- (K(D1) = 34 nM) and low- (K(D2) = 48,400 nM) affinity binding sites for [H-3]WIN 35,428 are present, in primary cultures of ventral mesencephalon neurons (CVMNs) only low-affinity binding sites were found (K(D) = 336,000 nM). The binding of [H-3]WIN 35,428 in CVMNs prepared from rat embryos was reversible, saturable, and located in cytosol. Although dopamine (DA) uptake blockers inhibited [H-3]DA uptake at nanomolar concentrations in CVMNs, the displacement of [H-3]WIN 35,428 binding in CVMNs by DA uptake inhibitors required 100-8,000 times higher concentrations than were needed to displace [H-3]WIN 35,428 binding in striatal membranes. Piperazine derivatives, e.g., GBR-12909, GBR-12935, and rimcazole, inhibited [H-3]WIN 35,428 binding in CVMNs more effectively than did cocaine, WIN 35,428, mazindol, nomifensine, or benztropin. A positive correlation (r = 0.779; p < 0.001) was found between drug affinities for the striatal membrane sites labeled by [H-3]WIN 35,428 and their abilities to inhibit DA uptake in CVMNs, whereas no correlation existed between the IC50 values of drugs that inhibited [H-3]WIN 35,428 binding and [H-3]DA uptake in CVMNs. The cytosolic [H-3]WIN 35,428 binding sites may be a piperazine acceptor and may not be involved in the regulation of the DA transporter. C1 NHLBI,CHEM PHARMACOL LAB,BLDG 10,ROOM 8N-102,BETHESDA,MD 20892. NR 18 TC 26 Z9 26 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD FEB PY 1993 VL 60 IS 2 BP 469 EP 476 DI 10.1111/j.1471-4159.1993.tb03174.x PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KG671 UT WOS:A1993KG67100010 PM 8419533 ER PT J AU DOYU, M SOBUE, G KEN, E KIMATA, K SHINOMURA, T YAMADA, Y MITSUMA, T TAKAHASHI, A AF DOYU, M SOBUE, G KEN, E KIMATA, K SHINOMURA, T YAMADA, Y MITSUMA, T TAKAHASHI, A TI LAMININ-A, LAMININ-B1, AND LAMININ-B2 CHAIN GENE-EXPRESSION IN TRANSECTED AND REGENERATING NERVES - REGULATION BY AXONAL SIGNALS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE LAMININ; NORTHERN BLOT ANALYSIS; PERIPHERAL NERVE; REGENERATION; DEGENERATION; AXON-SCHWANN CELL CONTACT ID CULTURED SCHWANN-CELLS; RAT SCIATIC-NERVE; BASEMENT-MEMBRANE PROTEIN; GROWTH-FACTOR RECEPTOR; PERIPHERAL-NERVE; WALLERIAN DEGENERATION; NEURITE OUTGROWTH; BASAL LAMINA; MULTIDOMAIN PROTEIN; ENRICHED FRACTIONS AB Laminin A, B1, and B2 chain mRNA levels in degenerating and regenerating mouse sciatic nerves were examined using northern blot analysis. In normal intact nerves, B1 and B2 mRNA steady-state levels were high, but when the nerves were crushed, the steady-state levels of B1 and B2 mRNA per milligram wet tissue weight of the distal segments of the nerves increased five- to eightfold over that of control levels as the total RNA and beta-actin mRNA levels increased, suggesting that these increases were the consequence of Schwann cell proliferation after axotomy. When the steady-state levels of B1 and B2 mRNA were normalized as the ratio to total RNA or beta-actin mRNA levels, however, they drastically decreased to about 20% of the normal nerve levels in the nerve segments distal to both the crush and transection sites 1 day after injury. In the crushed nerves, B1 and B2 mRNA levels gradually increased as the regenerating nerves arrived at the distal segments and reestablished normal axon-Schwann cell contact, and then returned to normal levels on the 21 st day. In the transected nerves, where Schwann cells continued to be disconnected from axons, both B1 and B2 mRNA levels remained low. Cultured Schwann cells expressed detectable levels of B1 and B2 chain mRNA which significantly increased when the cells were cocultured with sensory neurons. However, mRNA for A chain was not detectable in the normal, axotomized nerves or in cultured Schwann cells. These data indicate that Schwann cells express laminin B1 and B2 chain mRNA that are up-regulated by axonal or neuronal contact, but they do not express A chain mRNA. C1 AICHI MED UNIV,DEPT INTERNAL MED 4,DIV NEUROL,NAGAKUTE,AICHI 48011,JAPAN. NAGOYA UNIV,SCH MED,DEPT NEUROL,NAGOYA,AICHI 464,JAPAN. AICHI MED UNIV,INST MOLEC SCI & MED,NAGAKUTE,AICHI 48011,JAPAN. NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. NR 56 TC 49 Z9 50 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD FEB PY 1993 VL 60 IS 2 BP 543 EP 551 DI 10.1111/j.1471-4159.1993.tb03183.x PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KG671 UT WOS:A1993KG67100019 PM 8419535 ER PT J AU ABI-DARGHAM, A LARUELLE, M WONG, DT ROBERTSON, DW WEINBERGER, DR KLEINMAN, JE AF ABI-DARGHAM, A LARUELLE, M WONG, DT ROBERTSON, DW WEINBERGER, DR KLEINMAN, JE TI PHARMACOLOGICAL AND REGIONAL CHARACTERIZATION OF [H-3] LY278584 BINDING-SITES IN HUMAN BRAIN SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE 5-HYDROXYTRYPTAMINE3 RECEPTORS; [H-3]LY278584; LIMBIC SYSTEM; STRIATUM ID 5-HT3 RECEPTOR ANTAGONIST; CENTRAL NERVOUS-SYSTEM; RAT-BRAIN; RECOGNITION SITES; H-3 QUIPAZINE; 5-HYDROXYTRYPTAMINE3 RECEPTORS; RADIOLIGAND BINDING; CORTICAL MEMBRANES; IDENTIFICATION; DOPAMINE AB Binding of [H-3]LY278584, which has been previously shown to label 5-hydroxytryptamine3 (5-HT3) receptors in rat cortex, was studied in human brain. Saturation experiments revealed a homogeneous population of saturable binding sites in amygdala (K(D) = 3.08 +/- 0.67 nM, B(max) = 11.86 +/- 1.87 fmol/mg of protein) as well as in hippocampus, caudate, and putamen. Specific binding was also high in nucleus accumbens and entorhinal conex. Specific binding was negligible in neocortical areas. Kinetic studies conducted in human hippocampus revealed a K(on) of 0.025 +/- 0.009 nM-1 min-1 and a K(off) of 0.010 +/- 0.002 min-1. The kinetics of [H-3]LY278584 binding were similar in the caudate. Pharmacological characterization of [H-3]LY278584 specific binding in caudate and amygdala indicated the compound was binding to 5-HT, receptors. We conclude that 5-HT3 receptors labeled by [H-3]LY278584 are present in both limbic and striatal areas in human brain, suggesting that 5-HT, receptor antagonists may be able to influence the dopamine system in humans, similarly to their effects in rodent studies. C1 NIMH, NEUROSCI CTR ST ELIZABETHS, IRP, CLIN BRAIN DISORDERS BRANCH, WASHINGTON, DC 20032 USA. LIGAND PHARMACEUT, SAN DIEGO, CA USA. ELI LILLY & CO, LILLY RES LAB, LILLY CORP CTR, INDIANAPOLIS, IN 46285 USA. NR 30 TC 45 Z9 46 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0022-3042 EI 1471-4159 J9 J NEUROCHEM JI J. Neurochem. PD FEB PY 1993 VL 60 IS 2 BP 730 EP 737 DI 10.1111/j.1471-4159.1993.tb03208.x PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA KG671 UT WOS:A1993KG67100044 PM 8419547 ER PT J AU SHAMMA, SA FLESHMAN, JW WISER, PR VERSNEL, H AF SHAMMA, SA FLESHMAN, JW WISER, PR VERSNEL, H TI ORGANIZATION OF RESPONSE AREAS IN FERRET PRIMARY AUDITORY-CORTEX SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID AMPLITUDE-SPECTRUM REPRESENTATION; INFERIOR COLLICULUS; SOUND-LOCALIZATION; TOPOGRAPHICAL ORGANIZATION; TONOTOPIC ORGANIZATION; MUSTELA-PUTORIUS; COCHLEAR NUCLEUS; COMPLEX TONES; MUSTACHE BAT; CAT AB 1. We studied the topographic organization of the response areas obtained from single- and multiunit recordings along the isofrequency planes of the primary auditory cortex in the barbiturate-anesthetized ferret. 2. Using a two-tone stimulus, we determined the excitatory and inhibitory portions of the response areas and then parameterized them in terms of an asymmetry index. The index measures the balance of excitatory and inhibitory influences around the best frequency (BF). 3. The sensitivity of responses to the direction of a frequency-modulated (FM) tone was tested and found to correlate strongly with the asymmetry index of the response areas. Specifically, cells with strong inhibition from frequencies above the BF preferred upward sweeps, and those from frequencies below the BF preferred downward sweeps. 4. Responses to spectrally shaped noise were also consistent with the asymmetry of the response areas. For instance, cells that were strongly inhibited by frequencies higher than the BF responded best to stimuli that contained least spectral energy above the BF, i.e., stimuli with the opposite asymmetry. 5. Columnar organization of the response area types was demonstrated in 66 single units from 16 penetrations. Consistent with this finding, it was also shown that response area asymmetry measured from recordings of a cluster of cells corresponded closely with those measured from its single-unit constituents. Thus, in a local region, most cells exhibited similar response area types and other response features, e.g., FM directional sensitivity. 6. The distribution of the asymmetry index values along the isofrequency planes revealed systematic changes in the symmetry of the response areas. At the center, response areas with narrow and symmetric inhibitory sidebands predominated. These gave way to asymmetric inhibition, with high-frequency inhibition (relative to the BF) becoming more effective caudally and low-frequency inhibition more effective rostrally. These response types tended to cluster along repeated bands that paralleled the tonotopic axis. 7. Response features that correlated with the response area types were also mapped along the isofrequency planes. Thus, in four animals, a map of FM directional sensitivity was shown to be superimposed on the response area map. Similarly, it was demonstrated in six animals that the spectral gradient of the most effective noise stimulus varied systematically along the isofrequency planes. 8. One functional implication of the response area organization is that cortical responses encode the locally averaged gradient of the acoustic spectrum by their differential distribution along the isofrequency planes. This enhances the representation of such features as the symmetry of spectral peaks and edges and the spectral envelope. This scheme can be viewed as the one-dimensional analogue of spatial phase sensitivity in simple cells of the primary visual cortex, which there gives rise to spatial frequency channels and orientation columns. C1 UNIV MARYLAND,INST ADV COMP STUDIES,DEPT ELECT ENGN,COLL PK,MD 20742. NIDDKD,MATH RES BRANCH,BETHESDA,MD 20892. RP SHAMMA, SA (reprint author), UNIV MARYLAND,SYST RES CTR,AV WILLIAMS BLDG,COLL PK,MD 20742, USA. RI Shamma, Shihab/F-9852-2012 NR 58 TC 185 Z9 189 U1 0 U2 6 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD FEB PY 1993 VL 69 IS 2 BP 367 EP 383 PG 17 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA KN819 UT WOS:A1993KN81900007 PM 8459273 ER PT J AU MAUREA, S CUOCOLO, A REYNOLDS, JC TUMEH, SS BEGLEY, MG LINEHAN, WM NORTON, JA WALTHER, MM KEISER, HR NEUMANN, RD AF MAUREA, S CUOCOLO, A REYNOLDS, JC TUMEH, SS BEGLEY, MG LINEHAN, WM NORTON, JA WALTHER, MM KEISER, HR NEUMANN, RD TI IODINE-131-METAIODOBENZYLGUANIDINE SCINTIGRAPHY IN PREOPERATIVE AND POSTOPERATIVE EVALUATION OF PARAGANGLIOMAS - COMPARISON WITH CT AND MRI SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID COMPUTED-TOMOGRAPHY; ADRENAL MASSES; I-131 MIBG; PHEOCHROMOCYTOMA; LOCALIZATION; DISEASE; METAIODOBENZYLGUANIDINE; IODOBENZYLGUANIDINE; DIAGNOSIS AB Iodine-131-metaiodobenzylguanidine (MIBG) scintigraphy, transmission computed tomography and magnetic resonance imaging were used to evaluate 36 patients with clinically suspected functioning paragangliomas. The patients were divided into two groups. In Group 1 (n = 21), studied before surgery, patients mainly had benign adrenal disease. In Group 2 (n = 15), studied after surgery, patients frequently had malignant or extra-adrenal tumors. In Group 1, transmission computed tomography and magnetic resonance imaging were more sensitive (100% for both) than MIBG scintigraphy (82%), which, however, was the most specific (100%). In Group 2, MIBG scintigraphy and magnetic resonance imaging were more sensitive (83% for both) than transmission computed tomography (75%), but MIBG was again the most specific (100%). Thus, all three were complementary modalities for localizing paragangliomas both preoperatively and postoperatively. MIBG imaging is indicated for both groups but it is especially recommended for postsurgical patients with recurrence because the disease is often malignant or extra-adrenal. C1 NCI,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,BLDG 10,ROOM 1C-401,BETHESDA,MD 20892. NCI,WARREN G MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NHLBI,HYPERTENS ENDOCRINE BRANCH,BETHESDA,MD 20892. OI Cuocolo, Alberto/0000-0003-3431-7658 NR 38 TC 96 Z9 99 U1 0 U2 2 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 FEB PY 1993 VL 34 IS 2 BP 173 EP 179 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK926 UT WOS:A1993KK92600005 PM 8381474 ER PT J AU BACHARACH, SL DOUGLAS, MA CARSON, RE KALKOWSKI, PJ FREEDMAN, NMT PERRONEFILARDI, P BONOW, RO AF BACHARACH, SL DOUGLAS, MA CARSON, RE KALKOWSKI, PJ FREEDMAN, NMT PERRONEFILARDI, P BONOW, RO TI 3-DIMENSIONAL REGISTRATION OF CARDIAC POSITRON EMISSION TOMOGRAPHY ATTENUATION SCANS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article AB A method is described and tested which allows three-dimensional registration of two cardiac PET attenuation scans of the same subject acquired at different times. The alignment method is based on maximizing the correlation coefficient between the stacks of slices obtained during each of the two imaging sessions. The method appears accurate to better than 1 mm in x, y and z, and better than 1.5-degrees in the three angles of rotation. The method has been tested by using it to realign deliberately misaligned attenuation scans, and also by using realigned attenuation scans to correct fluorodeoxyglucose (FDG) emission scan data. The FDG emission data reconstructed with the realigned attenuation scans do not differ appreciably from the FDG data obtained using the original attenuation data. The method should be useful in realigning emission data (using the alignment coordinates predicted by realigning the attenuation scans), correcting for subject motion between scans (especially multiple intervention scans) and may allow a subject to leave the scanning table between scans during long imaging sessions. C1 POSITRON CORP,HOUSTON,TX. RP BACHARACH, SL (reprint author), NIH,DEPT NUCL MED,BLDG 10,RM 1C401,BETHESDA,MD 20892, USA. RI Carson, Richard/H-3250-2011 OI Carson, Richard/0000-0002-9338-7966 NR 8 TC 41 Z9 41 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 FEB PY 1993 VL 34 IS 2 BP 311 EP 321 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK926 UT WOS:A1993KK92600030 PM 8429355 ER PT J AU WEINER, R NEUMANN, RD AF WEINER, R NEUMANN, RD TI CELLULAR BASIS FOR ELEVATED GA-67 UPTAKE IN RHEUMATOID LUNG PATIENT SO JOURNAL OF NUCLEAR MEDICINE LA English DT Letter ID POLYMORPHONUCLEAR LEUKOCYTES; BINDING-SITES; LACTOFERRIN; TRANSFERRIN; SURFACE; IRON C1 NIH,BETHESDA,MD 20892. RP WEINER, R (reprint author), UNIV CONNECTICUT,CTR HLTH,FARMINGTON,CT 06032, USA. NR 11 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 FEB PY 1993 VL 34 IS 2 BP 351 EP 352 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KK926 UT WOS:A1993KK92600036 PM 8429361 ER PT J AU POTISCHMAN, N AF POTISCHMAN, N TI NUTRITIONAL EPIDEMIOLOGY OF CERVICAL NEOPLASIA SO JOURNAL OF NUTRITION LA English DT Article; Proceedings Paper CT SYMP ON HISTORICAL VIEW OF THE SAFETY OF THE FOOD SUPPLY, AT THE 76TH ANNUAL MEETING OF THE FEDERATION OF AMERICAN SOC FOR EXPERIMENTAL BIOLOGY CY APR 28, 1992 CL ANAHEIM, CA SP AMER SOC EXPTL BIOL DE CERVIX NEOPLASIA; DIET; SERUM; VITAMIN-A; VITAMIN-C; VITAMIN-E; CAROTENE; FOLATE ID SERUM VITAMIN-A; BETA-CAROTENE; UNITED-STATES; INTRAEPITHELIAL NEOPLASIA; WHITE WOMEN; FOLIC-ACID; CANCER; RISK; DYSPLASIA; PLASMA AB There appears to be a natural progression of some preinvasive cervical lesions to more advanced lesions. Although research has evaluated the associations between nutrients and particular preinvasive lesions or invasive disease, little work has been done to compare results across the spectrum of lesions in the progression to invasive disease. This review complies studies that have evaluated the relation between nutrients and cervical neoplasia and evaluates the general consistency of the literature across stage of disease. Preformed vitamin A does not appear to be related to risk of any preinvasive or invasive lesions, whereas vitamin C has been associated with a reduced risk for dysplasia, in situ cancer, and invasive disease, particularly among smokers. There was evidence of reduced risks associated with various carotenoids and vitamin E at all stages of the disease process, although these studies were inconsistent and further work is needed. Folate was the only nutrient that appeared to be protective for dysplastic lesions and not related to risk of in situ or invasive disease. Red blood cell folate was a better predictor of dysplasia than were serum or dietary folate, and further investigation using this marker of folate status is warranted. Research is needed across a spectrum of lesions within one study, with particular attention to interactions between nutrients and other risk factors for disease. RP POTISCHMAN, N (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,ENVIRONM STUDIES SECT,BETHESDA,MD 20892, USA. NR 37 TC 30 Z9 30 U1 0 U2 0 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD FEB PY 1993 VL 123 IS 2 SU S BP 424 EP 429 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA KM528 UT WOS:A1993KM52800033 PM 8429398 ER PT J AU ANDERSSON, HC MARKELLO, TC SCHNEIDER, JA GAHL, WA AF ANDERSSON, HC MARKELLO, TC SCHNEIDER, JA GAHL, WA TI GROWTH-HORMONE THERAPY IN NEPHROPATHIC CYSTINOSIS - REPLY SO JOURNAL OF PEDIATRICS LA English DT Letter RP ANDERSSON, HC (reprint author), NICHHD, BETHESDA, MD 20892 USA. NR 4 TC 0 Z9 0 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 FEB PY 1993 VL 122 IS 2 BP 329 EP 330 DI 10.1016/S0022-3476(06)80156-3 PG 2 WC Pediatrics SC Pediatrics GA KL328 UT WOS:A1993KL32800043 ER PT J AU LILJEQUIST, S TABAKOFF, B AF LILJEQUIST, S TABAKOFF, B TI BICUCULLINE-PRODUCED REGIONAL DIFFERENCES IN THE MODULATION OF S-35 TBPS BINDING BY GABA, PENTOBARBITAL AND DIAZEPAM IN MOUSE CEREBELLUM AND CORTEX SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID AMINOBUTYRIC ACIDA RECEPTOR; CENTRAL-NERVOUS-SYSTEM; A RECEPTOR; RAT-BRAIN; BENZODIAZEPINE RECEPTORS; ALPHA-SUBUNIT; FUNCTIONAL EXPRESSION; GAMMA-2 SUBUNIT; SITES; HETEROGENEITY AB The modulation of S-35-t-butylbicyclophosphorothionate (S-35-TBPS) binding by in vitro addition of gamma-aminobutyric acid (GABA), diazepam, pentobarbital, etomidate and etazolate was studied in the presence of KCl (100 mM) in the cerebellum and in the cortex of C57Bl mice. In the cortex, all of the depressant drugs caused a biphasic effect (stimulation followed by inhibition) on S-35-TBPS binding, whereas in the cerebellum only inhibition was observed. Saturation analysis revealed that the enhancement of S-35-TBPS binding was due to an increase in the affinity of S-35-TBPS for its binding sites. The introduction of a GABA(A) receptor antagonist, bicuculline methiodide (10 muM), into assay media altered the effects of the depressants. except for those of diazepam, on S-35-TBPS binding in a complex manner. Our results indicate that bicuculline, in addition to its GABA(A) receptor blocking properties, also influenced the binding of S-35-TBPS through some other, as yet unknown, mechanism(s). Thus, bicuculline not only produced a rightward shift of the dose-response curves of the central depressant drugs in the cortex, but also increased the maximal stimulation of S-35-TBPS binding. Furthermore, in the cerebellum, the previously observed drug-induced inhibition of S-35-TBPS binding was replaced by stimulation followed by inhibition in the presence of bicuculline. Finally, it was found that the in vitro addition of bicuculline had no effect on the diazepam-induced stimulation of S-35-TBPS binding. It is suggested that the regional differences in the modulation of S-35-TBPS binding in various brain structures may be due to endogenous differences in the molecular composition of GABA(A) receptors in various brain areas. C1 NIAAA,DIV INTRAMURAL CLIN & BIOL RES,SPECIAL PROJECTS UNIT,ROCKVILLE,MD 20852. NR 46 TC 23 Z9 23 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 FEB PY 1993 VL 264 IS 2 BP 638 EP 647 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KM432 UT WOS:A1993KM43200017 PM 8382279 ER PT J AU WILD, KD CARLISI, VJ MOSBERG, HI BOWEN, WD PORTOGHESE, PS SULTANA, M TAKEMORI, AE HRUBY, VJ PORRECA, F AF WILD, KD CARLISI, VJ MOSBERG, HI BOWEN, WD PORTOGHESE, PS SULTANA, M TAKEMORI, AE HRUBY, VJ PORRECA, F TI EVIDENCE FOR A SINGLE FUNCTIONAL OPIOID DELTA RECEPTOR SUBTYPE IN THE MOUSE ISOLATED VAS-DEFERENS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID OPIATE RECEPTORS; RAT-BRAIN; NALTRINDOLE 5'-ISOTHIOCYANATE; DIFFERENTIAL ANTAGONISM; ENKEPHALIN; AFFINITY; AGONISTS; MICE; ANTINOCICEPTION; PEPTIDES AB The identification of opioid delta receptor subtypes in mouse brain led to the investigation of the nature of the opioid delta receptors in the mouse isolated vas deferens in vitro. Noncumulative concentration-effect curves were constructed for DPDPE (delta1 agonist) and [D-Ala2, Glu4]deltorphin (delta2 agonist) in control tissues, or in tissues which had been incubated with either [D-Ala2, Leu5, Cys6] enkephalin (DALCE) (noncompetitive delta1 antagonist) or 5'-naltrindole isothiocyanate (5'-NTII) (noncompetitive delta2 antagonist). Incubation of the tissues with DALCE, under either oxygenated or nonoxygenated conditions, did not alter the concentration-effect curves for either agonist. In contrast, incubation of the tissues with 5'-NTII resulted in a significant rightward displacement of the concentration-effect curves of both DPDPE and [D-Ala2, Glu4] deltorphin. Additionally, naltriben, a selective and competitive delta2 antagonist, showed no significant difference in its ability to antagonize a fixed, submaximal concentration of either DPDPE or [D-Ala2, Glu4]deltorphin. Furthermore, there was no significant difference in the affinity of naloxone (i.e., pA2) at the receptor(s) acted upon by either DPDPE or [D-Ala2, Glu4]deltorphin. Tolerance to DPDPE or [D-Ala2, Glu4]deltorphin was produced by incubation of the tissues with these agonists; construction of the [D-Ala2, Glu4]deltorphin concentration-effect curve in DPDPE-tolerant tissues demonstrated cross-tolerance between these agonists and, conversely, construction of DPDPE concentration-effect curves in [D-Ala2, Glu4]deltorphin-tolerant tissues revealed cross-tolerance between these agonists. Thus, the present data provide support for one subtype of opioid delta receptor in the mouse isolated vas deferens based on 1) the lack of antagonism of the effects of both agonists selective for delta1 and delta2 receptor subtypes by DALCE, a delta1 antagonist. 2) the antagonism of delta1 and delta2 agonists by 5'-NTII or naltriben (delta2 antagonists), 3) the similar antagonist potency of NTB against either DPDPE or [D-Ala2, Glu4]deltorphin, 4) the lack of significant difference in the naloxone pA2 against either delta agonist and 5) the demonstration of two-way cross-tolerance between the effects of DPDPE and [D-Ala2, Glu4]deltorphin in this tissue. C1 UNIV ARIZONA,ARIZONA HLTH SCI CTR,DEPT PHARMACOL,TUCSON,AZ 85724. NIDDKD,MED CHEM LAB,RECEPTOR BIOCHEM & PHARMACOL UNIT,BETHESDA,MD. UNIV ARIZONA,ARIZONA HLTH SCI CTR,DEPT CHEM,TUCSON,AZ 85724. UNIV MICHIGAN,COLL PHARM,ANN ARBOR,MI 48109. UNIV MINNESOTA,DEPT MED CHEM,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT PHARMACOL,MINNEAPOLIS,MN 55455. NR 34 TC 31 Z9 31 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD FEB PY 1993 VL 264 IS 2 BP 831 EP 838 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KM432 UT WOS:A1993KM43200043 PM 8382281 ER PT J AU PATTERSON, GML BAKER, KK BALDWIN, CL BOLIS, CM CAPLAN, FR LARSEN, LK LEVINE, IA MOORE, RE NELSON, CS TSCHAPPAT, KD TUANG, GD BOYD, MR CARDELLINA, JH COLLINS, RP GUSTAFSON, KR SNADER, KM WEISLOW, OS LEWIN, RA AF PATTERSON, GML BAKER, KK BALDWIN, CL BOLIS, CM CAPLAN, FR LARSEN, LK LEVINE, IA MOORE, RE NELSON, CS TSCHAPPAT, KD TUANG, GD BOYD, MR CARDELLINA, JH COLLINS, RP GUSTAFSON, KR SNADER, KM WEISLOW, OS LEWIN, RA TI ANTIVIRAL ACTIVITY OF CULTURED BLUE-GREEN-ALGAE (CYANOPHYTA) SO JOURNAL OF PHYCOLOGY LA English DT Article DE ANTIVIRAL; CYANOBACTERIA; CYANOPHYTE; HERPES VIRUS; HIV-1; HSV-2; HUMAN IMMUNODEFICIENCY VIRUS; NATURAL PRODUCTS; PHARMACEUTICAL; RESPIRATORY SYNCYTIAL VIRUS ID NATURAL-PRODUCTS; MARINE AB Lipophilic and hydrophilic extracts from approximately 600 strains of cultured cyanophytes, representing some 300 species, were examined for antiviral activity against three pathogenic viruses. Approximately 10% of the cultures produced substances that caused significant reduction in cytopathic effect normally associated with. viral infection. The screening program identified the order Chroococcales as commonly producing antiviral agents. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NCI FCRF,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21702. UNIV CALIF SAN DIEGO,SCRIPPS INST OCEANOG,LA JOLLA,CA 92093. RP PATTERSON, GML (reprint author), UNIV HAWAII,DEPT CHEM,HONOLULU,HI 96822, USA. NR 16 TC 50 Z9 58 U1 0 U2 4 PU PHYCOLOGICAL SOC AMER INC PI LAWRENCE PA 810 EAST 10TH ST, LAWRENCE, KS 66044 SN 0022-3646 J9 J PHYCOL JI J. Phycol. PD FEB PY 1993 VL 29 IS 1 BP 125 EP 130 DI 10.1111/j.1529-8817.1993.tb00290.x PG 6 WC Plant Sciences; Marine & Freshwater Biology SC Plant Sciences; Marine & Freshwater Biology GA KP046 UT WOS:A1993KP04600018 ER PT J AU XU, SE BRENNER, B YU, LC AF XU, SE BRENNER, B YU, LC TI STATE-DEPENDENT RADIAL ELASTICITY OF ATTACHED CROSS-BRIDGES IN SINGLE SKINNED FIBERS OF RABBIT PSOAS MUSCLE SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Article ID X-RAY-DIFFRACTION; SKELETAL-MUSCLE; FIBERS; RIGOR; CROSSBRIDGES; STIFFNESS; FORCE; ACTIN; BINDING AB 1. In a single skinned fibre of rabbit psoas muscle, upon attachment of cross-bridges to actin in the presence of ADP or pyrophosphate (PP(i)), the separation between the contractile filaments, as determined by equatorial X-ray diffraction, is found to decrease, suggesting that force is generated in the radial direction. 2. The single muscle fibres were subjected to compression by 0-8% of dextran T500. The changes in lattice spacings by dextran compression were compared with changes induced by cross-bridge attachment to actin. Based on this comparison, the magnitude and the direction of the radial force generated by the attached cross-bridges were estimated. The radial cross-bridge force varied with filament separation, and the magnitude of the radial cross-bridge force reached as high as the maximal axial force produced during isometric contraction. 3. One key parameter of the radial elasticity, i.e. the equilibrium spacing where the radial force is zero, was found to depend on the ligand bound to the myosin head. In the presence of ADP, the equilibrium spacing was 36 nm. In the presence of MgPP(i) the equilibrium spacing shifted to 35 nm and Ca2+ had little effect on the equilibrium spacing. 4. The equilibrium spacing was independent of the fraction of cross-bridges attached to actin. The fraction of cross-bridges attached in rigor was modulated from 100 % to close to 0 % by adding up to 10 mm of ATPgammaS in the rigor solution. The lattice spacing remained at 38 nm, the equilibrium spacing for nucleotide-free cross-bridges at mu = 170 mm. 5. Radial force generated by cross-bridges in rigor at large lattice spacings (38 nm less-than-or-equal-to d10 less-than-or-equal-to 46 nm) appeared to vary linearly with lattice spacing. 6. The titration of ATPgammaS to fibres in rigor provided a correlation between the radial stiffness of the nucleotide-free cross-bridges and the equatorial intensities. The relation between the equatorial intensity ratio I11/I10 and radial stiffness appeared to be approximately linear. 7. The fibres under different conditions showed a wide range of radial stiffness, which was not proportional to the apparent axial stiffness of the fibre. If the apparent axial stiffness is a measure of the fraction of cross-bridges bound to actin, it follows that the radial elastic constant is state dependent; or vice versa. 8. Differences in equilibrium lattice spacing and in radial elastic constant. most probably reflect differences in the molecular structure of the acto-myosin complex and there is more than one single conformation of the variouS Strongly bound cross-bridge states. 9. Determining equilibrium spacings of the radial elasticity appears to be an effective new approach in detecting structural differences among the attached cross-bridges. since this approach is independent of the fraction of cross-bridges attached, a factor that frequently encumbers the interpretation of structural studies of attached cross-bridge states. C1 NIH,BETHESDA,MD 20892. UNIV ULM,W-7900 ULM,GERMANY. NR 32 TC 13 Z9 13 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD FEB PY 1993 VL 461 BP 283 EP 299 PG 17 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA KN980 UT WOS:A1993KN98000017 PM 16993186 ER PT J AU MOORE, J CAMPANA, J LAM, M SANDAUCHRISTOPHER, D SADLER, J SCALISE, D GAY, N STALVEY, R SCHROEDER, J PELTON, J BIEHR, BJ HARRIS, J STRUNK, N CHIOTTI, R OWENSNAUSLER, J GRENERT, B CHIODA, D COLE, D MEURER, K ABELSON, G SHEFFIELD, A RUZICKA, P BALSLEY, C SUTTER, M CHERNECO, MD FRASER, J CARR, M WORD, E SIMPSON, P LACY, L TYE, S NEHLSLOWE, B ANDERSON, B AF MOORE, J CAMPANA, J LAM, M SANDAUCHRISTOPHER, D SADLER, J SCALISE, D GAY, N STALVEY, R SCHROEDER, J PELTON, J BIEHR, BJ HARRIS, J STRUNK, N CHIOTTI, R OWENSNAUSLER, J GRENERT, B CHIODA, D COLE, D MEURER, K ABELSON, G SHEFFIELD, A RUZICKA, P BALSLEY, C SUTTER, M CHERNECO, MD FRASER, J CARR, M WORD, E SIMPSON, P LACY, L TYE, S NEHLSLOWE, B ANDERSON, B TI SELECTED BEHAVIORS THAT INCREASE RISK FOR HIV-INFECTION, OTHER SEXUALLY-TRANSMITTED DISEASES, AND UNINTENDED PREGNANCY AMONG HIGH-SCHOOL-STUDENTS - UNITED-STATES, 1991 SO JOURNAL OF SCHOOL HEALTH LA English DT Article C1 PENNSYLVANIA DEPT EDUC,HARRISBURG,PA. S CAROLINA DEPT EDUC,COLUMBIA,SC. S DAKOTA DEPT EDUC & CULTURAL AFFAIRS,PIERRE,SD. TENNESSEE DEPT EDUC,NASHVILLE,TN. DALLAS INDEPENDENT SCH DIST,DALLAS,TX. UTAH OFF EDUC,SALT LAKE CITY,UT. WISCONSIN DEPT PUBL INSTRUCT,MADISON,WI. WYOMING DEPT EDUC,CHEYENNE,WY. NIDA,SUBST ABUSE & MENTAL HLTH SERV ADM,DIV EPIDEMIOL & PREVENT RES,ATLANTA,GA 30341. CTR DIS CONTROL,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,DIV ADOLESCENT & SCH HLTH,ATLANTA,GA. CTR DIS CONTROL,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,DIV REPROD HLTH,ATLANTA,GA. SAN DIEGO UNIFIED SCH DIST,SAN DIEGO,CA. SAN FRANCISCO UNIFIED SCH DIST,SAN FRANCISCO,CA. COLORADO DEPT EDUC,DENVER,CO 80203. DIST COLUMBIA PUBL SCH,WASHINGTON,DC. GEORGIA DEPT EDUC,ATLANTA,GA 30334. HAWAII DEPT EDUC,HONOLULU,HI 96813. IDAHO DEPT EDUC,BOISE,ID 83720. CHICAGO PUBL SCH,CHICAGO,IL. IOWA DEPT EDUC,DES MOINES,IA. BOSTON PUBL SCH SYST,BOSTON,MA. MONTANA OFF PUBL INSTRUCT,HELENA,MT. NEBRASKA DEPT EDUC,LINCOLN,NE. NEW HAMPSHIRE DEPT EDUC,CONCORD,NH. JERSEY CITY BOARD EDUC,JERSEY CITY,NJ. NEW JERSEY DEPT HIGHER EDUC,TRENTON,NJ. NEW MEXICO DEPT EDUC,SANTA FE,NM. NEW YORK CITY BOARD EDUC,NEW YORK,NY. NEW YORK STATE DEPT EDUC,ALBANY,NY 12224. OREGON DEPT EDUC,SALEM,OR. SCH DIST PHILADELPHIA,PHILADELPHIA,PA. RP MOORE, J (reprint author), ALABAMA DEPT EDUC,MONTGOMERY,AL 36130, USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU AMER SCHOOL HEALTH ASSOC PI KENT PA PO BOX 708, KENT, OH 44240 SN 0022-4391 J9 J SCHOOL HEALTH JI J. Sch. Health PD FEB PY 1993 VL 63 IS 2 BP 116 EP 118 PG 3 WC Education & Educational Research; Education, Scientific Disciplines; Health Care Sciences & Services; Public, Environmental & Occupational Health SC Education & Educational Research; Health Care Sciences & Services; Public, Environmental & Occupational Health GA KV374 UT WOS:A1993KV37400009 ER PT J AU WAHBA, ZZ COOGAN, TP RHODES, SW WAALKES, MP AF WAHBA, ZZ COOGAN, TP RHODES, SW WAALKES, MP TI PROTECTIVE EFFECTS OF SELENIUM ON CADMIUM TOXICITY IN RATS - ROLE OF ALTERED TOXICOKINETICS AND METALLOTHIONEIN SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH LA English DT Article ID HEMOGLOBIN AFFINITY ASSAY; WISTAR CRL-(WI)BR RATS; ZINC-INDUCED TOLERANCE; DOSE-RESPONSE ANALYSIS; GLUTATHIONE-PEROXIDASE; RAPID-DETERMINATION; BIOLOGICAL TISSUES; LIPID-PEROXIDATION; POSSIBLE MECHANISM; BINDING-PROTEINS AB Selenium prevents the toxicity of the carcinogenic metal cadmium through undefined mechanisms. In this study, we determined the effects of selenium on cadmium toxicokinetics and on the ability of cadmium to induce metallothionein, a metal-binding protein that is thought to confer tolerance to cadmium toxicity. To assess the acute protective effects of selenium, male Wistar (WF/NCr) rats were given selenium (as SeO2; 10 mumol/kg, sc) at -24, 0, and +24 h relative to cadmium (as CdCl2; 45 mumol/kg, sc). Over a 14-d period this dose of cadmium killed 6 out of 10 rats, while 100% of the cadmium-treated rats given concurrent selenium treatments survived. The acute increases in testicular weight that were seen with cadmium, indicative of edematous damage, were also prevented by concurrent selenium treatments. Further studies assessed the distribution and excretion of cadmium and its ability to induce metallothionein in rats given 40 mumol Cd/kg, sc, at time 0 and selenium (10 mumol/kg, sc) at -24 and 0 h. Selenium treatments enhanced cadmium accumulation at 24 h in the liver (23%), testes (145%), and epididymis (35%) but reduced renal accumulation by more than half. Urine samples, collected at 0-3, 3-6, and 6-24 h following cadmium administration, indicated a markedly reduced excretion of cadmium in selenium treated rats during all time periods. The synthesis of metallothionein was stimulated to a much lesser extent by cadmium in selenium-treated rat kidney (41% decrease) but was unaffected in liver. The levels of cadmium-binding proteins within the testes were markedly reduced by cadmium treatment, an effect unmodified by selenium treatments. These results suggest selenium prevents acute cadmium toxicity through a mechanism that does not involve induction of metallothionein and in spite of a markedly enhanced retention of cadmium. C1 NCI,FCRDC,COMPARAT CARCINOGENESIS LAB,INORGAN CARCINOGENESIS SECT,BLDG 538,ROOM 205E,FREDERICK,MD 21702. NR 51 TC 40 Z9 43 U1 1 U2 4 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0098-4108 J9 J TOXICOL ENV HEALTH JI J. Toxicol. Environ. Health PD FEB PY 1993 VL 38 IS 2 BP 171 EP 182 PG 12 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA KM835 UT WOS:A1993KM83500006 PM 8433401 ER PT J AU ERNST, DR RACE, RE AF ERNST, DR RACE, RE TI COMPARATIVE-ANALYSIS OF SCRAPIE AGENT INACTIVATION METHODS SO JOURNAL OF VIROLOGICAL METHODS LA English DT Article DE SCRAPIE; LPH; SPONGIFORM ENCEPHALOPATHY; NEURO-DEGENERATIVE; KURU; GERSTMANN-STRAUSSLER-SCHEINKER DISEASE; CREUTZFELDT-JAKOB DISEASE ID CREUTZFELDT-JAKOB-DISEASE; BOVINE SPONGIFORM ENCEPHALOPATHY; PERSON TRANSMISSION; SUFFOLK SHEEP; VIRUS; INFECTIVITY; DISINFECTION; IRRADIATION; PRIMATES; BRAIN AB A scrapie-infected hamster brain homogenate was subjected to several different potential inactivation methods. Methods included autoclaving for various lengths of time, either alone or in combination with different concentrations of sodium hydroxide or LpH, an aqueous acid phenolic derivative (Calgon Vestal Laboratories in St. Louis, MO). Inactivation treatments utilizing either NaOH or LpH alone were also evaluated. It was determined that several of the treatments inactivated all of the detectable infectivity. RP ERNST, DR (reprint author), NIAID,PERSISTENT VIRAL DIS LAB,ROCKY MT LABS,HAMILTON,MT 59840, USA. NR 52 TC 82 Z9 82 U1 2 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-0934 J9 J VIROL METHODS JI J. Virol. Methods PD FEB PY 1993 VL 41 IS 2 BP 193 EP 201 DI 10.1016/0166-0934(93)90126-C PG 9 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Virology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Virology GA KL943 UT WOS:A1993KL94300006 PM 8496294 ER PT J AU CAUGHEY, B RAYMOND, GJ AF CAUGHEY, B RAYMOND, GJ TI SULFATED POLYANION INHIBITION OF SCRAPIE-ASSOCIATED PRP ACCUMULATION IN CULTURED-CELLS SO JOURNAL OF VIROLOGY LA English DT Article ID GERSTMANN-STRAUSSLER SYNDROME; CREUTZFELDT-JAKOB DISEASE; PRION PROTEIN; DEXTRAN SULFATE; HEPARAN-SULFATE; INCUBATION PERIOD; PHOSPHOLIPASE-C; AMYLOID PLAQUES; MOUSE SCRAPIE; INFECTION AB The accumulation of an abnormal, protease-resistant form of the protein PrP (PrP-res) in hosts with scrapie and related transmissible spongiform encephalopathies appears to be important in disease pathogenesis. To pin insight into the mechanism of PrP-res accumulation and the in vivo antiscrapie activity of certain polyanions, we have studied effects of sulfated glycans on PrP metabolism in scrapie-infected neuroblastoma cells. Pentosan polysulfate, like the amyloid-binding dye Congo red, potently inhibited the accumulation of PrP-res in these cells without apparent effects on the metabolism of the normal isoform. The inhibition was due primarily to prevention of new PrP-res accumulation rather than destabilization of preexisting PrP-res. PrP-res accumulation remained depressed in the cultures after removal of the inhibitors. The activities of other sulfated glycans, nonsulfated polyanions, dextran, and DEAE-dextran were compared with those of pentosan polysulfate and Congo red. This comparison provided evidence that the density of sulfation and molecular size are factors influencing anti-PrP-res activity of sulfated glycans. The relative potencies of these compounds corresponded well with their previously determined antiscrapie activities in vivo, suggesting that the prophylactic effects of sulfated polyanions may be due to inhibition of PrP-res accumulation. Since PrP-res amyloid is known to contain sulfated glycosaminoglycans, we reason that these inhibitors may competitively block an interaction between PrP and endogenous glycosaminoglycans that is essential for its accumulation in a protease-resistant, potentially amyloidogenic state. RP CAUGHEY, B (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 63 TC 307 Z9 319 U1 1 U2 11 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 FEB PY 1993 VL 67 IS 2 BP 643 EP 650 PG 8 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000003 PM 7678300 ER PT J AU CHANG, LJ MCNULTY, E MARTIN, M AF CHANG, LJ MCNULTY, E MARTIN, M TI HUMAN IMMUNODEFICIENCY VIRUSES CONTAINING HETEROLOGOUS ENHANCER PROMOTERS ARE REPLICATION COMPETENT AND EXHIBIT DIFFERENT LYMPHOCYTE TROPISMS SO JOURNAL OF VIROLOGY LA English DT Article ID LONG TERMINAL REPEAT; NF-KAPPA-B; TRANS-ACTIVATOR GENE; HUMAN CYTOMEGALO-VIRUS; IMMEDIATE-EARLY GENE; T-CELL; HIV-1 TAT; HTLV-III; TRANSCRIPTIONAL ELONGATION; BINDING PROTEIN AB The human immunodeficiency virus (HIV) type 1 long terminal repeat (LTR) contains binding sites for nuclear factor kappaB (NF-kappaB) and the constitutively expressed transcription factor Sp1, both of which are highly conserved in HIV and simian immunodeficiency virus isolates. To delineate the effects of these motifs on the replicative capacity of HIV and to explore the possibility of extending the virus host range, known heterologous enhancer/promoters were inserted into the HIV-1 LTR in place of the NF-kappaB and Sp1 binding sites. The effects of these substitutions on viral replication in transfected HeLa cells and on HIV infection of human peripheral blood lymphocytes or continuous T-leukemia cell lines were evaluated. HIVs in which the NF-kappaB/Sp1 enhancer plus the downstream TATA element were replaced with heterologous enhancer/promoters were also constructed. Viruses containing the human cytomegalovirus immediate-early enhancer exhibited infectious kinetics similar to that of wild-type HIV in activated human peripheral blood lymphocytes and AA2 cells but replicated less efficiently in H9 and CEM cells. These studies indicate that heterologous enhancer elements are capable of restoring Tat responsiveness to the HIV LTR in the context of directing reporter gene expression as well as in the production of infectious progeny virions. RP CHANG, LJ (reprint author), NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892, USA. NR 58 TC 38 Z9 38 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 FEB PY 1993 VL 67 IS 2 BP 743 EP 752 PG 10 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000014 PM 8419644 ER PT J AU ROTHMAN, AL KURANE, I LAI, CJ BRAY, M FALGOUT, B MEN, R ENNIS, FA AF ROTHMAN, AL KURANE, I LAI, CJ BRAY, M FALGOUT, B MEN, R ENNIS, FA TI DENGUE VIRUS PROTEIN RECOGNITION BY VIRUS-SPECIFIC MURINE CD8+ CYTOTOXIC LYMPHOCYTES-T SO JOURNAL OF VIROLOGY LA English DT Article ID RECOMBINANT VACCINIA VIRUS; NONSTRUCTURAL PROTEINS; STRUCTURAL PROTEINS; ENCEPHALITIS; INFECTIONS; EXPRESSION; GENES; MICE; IMMUNIZATION; VACCINATION AB The identification of the protein targets for dengue virus-specific T lymphocytes may be useful for planning the development of subunit vaccines against dengue. We studied the recognition by murine dengue virus-specific major histocompatibility complex class I-restricted, CD8+ cytotoxic T lymphocytes (CTL) of dengue virus proteins using recombinant vaccinia viruses containing segments of the dengue virus genome. CTL from H-2k mice recognized a single serotype-cross-reactive epitope on the nonstructural (NS) protein NS3. CTL from H-2b mice recognized a serotype-cross-reactive epitope that was localized to NS4a or NS4b. CTL from H-2d mice recognized at least three epitopes: a serotype-specific epitope on one of the structural proteins, a serotype-cross-reactive epitope on NS3, and a serotype-cross-reactive epitope on NS1 or NS2a. Our findings demonstrate the limited recognition of dengue virus proteins by CTL from three inbred mouse strains and the predominance of CTL epitopes on dengue virus nonstructural proteins, particularly NS3. Since human dengue virus-specific CTL show similar patterns of recognition, these findings suggest that nonstructural proteins should be considered in designing vaccines against dengue. C1 UNIV MASSACHUSETTS,MED CTR,DEPT MED,WORCESTER,MA 01655. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. FU NIAID NIH HHS [T32-AI07272, K11-AI00971] NR 30 TC 54 Z9 56 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 FEB PY 1993 VL 67 IS 2 BP 801 EP 806 PG 6 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000021 PM 7678307 ER PT J AU BEISEL, CE EDWARDS, JF DUNN, LL RICE, NR AF BEISEL, CE EDWARDS, JF DUNN, LL RICE, NR TI ANALYSIS OF MULTIPLE MESSENGER-RNAS FROM PATHOGENIC EQUINE INFECTIOUS-ANEMIA VIRUS (EIAV) IN AN ACUTELY INFECTED HORSE REVEALS A NOVEL PROTEIN, TTM, DERIVED FROM THE CARBOXY TERMINUS OF THE EIAV TRANSMEMBRANE PROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID SIMIAN IMMUNODEFICIENCY VIRUS; ENDOPLASMIC-RETICULUM; PERSISTENT INFECTION; MOLECULAR CLONES; ENVELOPE PROTEIN; FUSION PROTEIN; REV PROTEINS; PUTATIVE REV; VISNA VIRUS; HUMAN-CELLS AB Transcription of pathogenic equine infectious anemia virus (EIAV) in an acutely infected horse was examined by using the polymerase chain reaction and nucleotide sequencing. Four spliced transcripts were identified in liver tissue, in contrast to the multiplicity of alternatively spliced messages reported for in vitro-propagated human immunodeficiency virus, simian immunodeficiency virus, and, to a lesser extent, EIAV. Nucleotide sequence analysis demonstrated that three of these mRNAs encode known viral proteins: the envelope precursor, the product of the S2 open reading frame, and the regulatory proteins Tat and Rev. The fourth transcript encodes a novel Tat-TM fusion protein, Ttm. Ttm is a 27-kDa protein translated from the putative tat CTG initiation codon and containing the carboxy-terminal portion of TM immediately downstream from the membrane-spanning domain. p27ttm is expressed in EIAV-infected canine cells and was recognized by peptide antisera against both Tat and TM. Cells transfected with ttm cDNA also expressed p27ttm, which appeared to be localized to the endoplasmic reticulum or Golgi apparatus by indirect immunofluorescence. The carboxy terminus of lentiviral TM proteins has previously been shown to influence viral infectivity, growth kinetics, and cytopathology, suggesting that Ttm plays an important role in the EIAV life cycle. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOLEC VIROL & CARCINOGENESIS LAB,POB B,FREDERICK,MD 21702. TEXAS A&M UNIV SYST,COLL VET MED,DEPT VET PATHOL,COLL STN,TX 77843. FU NCI NIH HHS [N01-CO-74101] NR 69 TC 25 Z9 26 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 FEB PY 1993 VL 67 IS 2 BP 832 EP 842 PG 11 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000025 PM 8419648 ER PT J AU BRODER, CC BERGER, EA AF BRODER, CC BERGER, EA TI CD4 MOLECULES WITH A DIVERSITY OF MUTATIONS ENCOMPASSING THE CDR3 REGION EFFICIENTLY SUPPORT HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEIN-MEDIATED CELL-FUSION SO JOURNAL OF VIROLOGY LA English DT Article ID RECOMBINANT VACCINIA VIRUS; SOLUBLE CD4; SYNCYTIUM FORMATION; HIV-INFECTION; BINDING-SITE; DEXTRAN SULFATE; PEPTIDE DERIVATIVES; CD4-BEARING CELLS; T-CELLS; GP120 AB The third complementarity-determining region (CDR3) within domain 1 of the human CD4 molecule has been suggested to play a critical role in membrane fusion mediated by the interaction of CD4 with the human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein. To analyze in detail the role of CDR3 and adjacent regions in the fusion process, we used cassette mutagenesis to construct a panel of 30 site-directed mutations between residues 79 and 96 of the full-length CD4 molecule. The mutant proteins were transiently expressed by using recombinant vaccinia virus vectors and were analyzed for cell surface expression, recombinant gp120-binding activity, and overall structural integrity as assessed by reactivity with a battery of anti-CD4 monoclonal antibodies. Cells expressing the CD4 mutants were assayed for their ability to form syncytia when mixed with cells expressing the HIV-1 envelope glycoprotein. Surprisingly in view of published data from others, most of the mutations had little effect on syncytium-forming activity. Normal fusion was observed in 21 mutants, including substitution of human residues 85 to 95 with the corresponding sequences from either chimpanzee, rhesus, or mouse CD4; a panel of Ser-Arg double insertions after each residue from 86 to 91; and a number of other charge, hydrophobic, and proline substitutions and insertions within this region. The nine mutants that showed impaired fusion all displayed defective gp120 binding and disruption of overall structural integrity. In further contrast with results of other workers, we observed that transformant human cell lines expressing native chimpanzee or rhesus CD4 efficiently formed syncytia when mixed with cells expressing the HIV-1 envelope glycoprotein. These data refute the conclusion that certain mutations in the CDR3 region of CD4 abolish cell fusion activity, and they suggest that a wide variety of sequences can be functionally tolerated in this region, including those from highly divergent mammalian species. Syncytium formation mediated by several of the CDR3 mutants was partially or completely resistant to inhibition by the CDR3-directed monoclonal antibody L71, suggesting that the corresponding epitope is not directly involved in the fusion process. We observed that CDR3 synthetic peptide derivatives inhibited syncytium formation mediated by the mutant CD4 molecules with the same potency as for wild-type CD4. In contrast with our earlier findings with such peptides, we observed that mutation of the CDR3 region (E87G) in the soluble CD4 protein had no effect on its ability to inhibit syncytium formation or to stimulate gp120 release from the HIV-1 envelope glycoprotein. These results suggest that the previously described fusion-related activities of the CDR3 peptide derivatives are not due to their ability to compete for or to mimic the function of the corresponding region in the native CD4 protein. Taken together, the present findings challenge the prevailing notion that the CDR3 region of CD4 plays a critical role in HIV-1 envelope glycoprotein-mediated membrane fusion. C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 56 TC 49 Z9 50 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 FEB PY 1993 VL 67 IS 2 BP 913 EP 926 PG 14 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000033 PM 8419649 ER PT J AU YEWDELL, JW TAYLOR, A YELLEN, A CATON, A GERHARD, W BACHI, T AF YEWDELL, JW TAYLOR, A YELLEN, A CATON, A GERHARD, W BACHI, T TI MUTATIONS IN OR NEAR THE FUSION PEPTIDE OF THE INFLUENZA-VIRUS HEMAGGLUTININ AFFECT AN ANTIGENIC SITE IN THE GLOBULAR REGION SO JOURNAL OF VIROLOGY LA English DT Article ID MEDIATED MEMBRANE-FUSION; INTRACELLULAR-TRANSPORT; MONOCLONAL-ANTIBODIES; CONFORMATIONAL-CHANGES; PH OPTIMUM; GLYCOPROTEIN; ACTIVATION; MUTANT; DETERMINANTS; SELECTION AB We previously described a monoclonal antibody (Y8-10C2) that binds influenza virus hemagglutinin (HA) monomers but not native trimers. In this study, we demonstrated that Y8-10C2 binds to the globular domain of HA and found evidence that its epitope is located at the interface of adjacent subunits. We further showed that at elevated temperatures, the Y8-10C2 epitope is transiently exposed in trimers for antibody binding. Introduction of intrasubunit chemical cross-links into RA reversibly inhibited both Y8-10C2 binding to trimers at elevated temperatures and viral fusion activity, indicating that exposure of the epitope requires the normal conformational flexibility of the molecule. Prolonged incubation of Y8-10C2 with virus at an elevated temperature resulted in neutralization of viral infectivity, allowing selection of neutralization-resistant virus mutants. Mutants were divided into two classes based on a radioimmunoassay in which the virus is attached to polyvinyl: those with reduced affinity for Y8-10C2 or other monoclonal antibodies specific for the globular domain and those with no alteration in their interaction with Y8-10C2 or other antibodies. DNA sequencing of HA genes revealed that the first type of mutants possessed single amino acid substitutions in the Y8-10C2 epitope itself, while remarkably, the second type of mutants possessed single amino acid substitutions in or near the fusion peptide of the RA, which is located in the stem of the HA at a considerable distance from the Y8-10C2 epitope. These findings indicate that the conformational flexibility of the RA affects its antigenicity and that single amino acid substitutions in or near the fusion peptide influence the flexibility of the globular domains. C1 WISTAR INST,PHILADELPHIA,PA 19104. UNIV ZURICH,ELECTRON MICROSCOPY LAB,CH-8028 ZURICH,SWITZERLAND. RP YEWDELL, JW (reprint author), NIAID,VIRAL DIS LAB,BETHESDA,MD 20892, USA. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 34 TC 37 Z9 37 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 FEB PY 1993 VL 67 IS 2 BP 933 EP 942 PG 10 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000035 PM 7678310 ER PT J AU HARIHARAN, K NARA, PL CARALLI, VM NORTON, FL HAIGWOOD, N KANG, CY AF HARIHARAN, K NARA, PL CARALLI, VM NORTON, FL HAIGWOOD, N KANG, CY TI ANALYSIS OF THE CROSS-REACTIVE ANTI-GP120 ANTIBODY POPULATION IN HUMAN IMMUNODEFICIENCY VIRUS-INFECTED ASYMPTOMATIC INDIVIDUALS SO JOURNAL OF VIROLOGY LA English DT Article ID HUMAN MONOCLONAL-ANTIBODY; TYPE-1 NEUTRALIZATION; ENVELOPE GLYCOPROTEIN; CD4 BINDING; HIV-1 GP120; EPITOPE; CHIMPANZEES; INVIVO; SERA; AIDS AB This study was undertaken to analyze the specificity and neutralizing properties of cross-reactive anti-gp120 antibodies (Abs) in the sera of two human immunodeficiency virus (HIV)-infected asymptomatic individuals. Two panels of murine monoclonal anti-idiotype Abs (anti-id MAbs) were established against cross-reactive polyclonal anti-gp120 Abs purified from HIV+ sera by sequential affinity chromatography using gp120SF2- and gp120IIIB-Sepharose columns. These panels of anti-id MAbs were then used to affinity purify idiotype-positive (Id+) anti-gp120 Abs from HIV' sera. The recovery of each of these Id+ Abs by purification indicated that several idiotypically distinct cross-reactive anti-gp120 Abs are present in sera over a wide range of concentrations. Immunological and biological studies showed that although all of the Id+ Abs were reactive against gp120SF2 and gp120IIIB, they exhibited unique epitope specificities and distinct neutralizing activities. Most of the Id+ Abs were directed against epitopes in the CD4 attachment site (CD4 site epitopes) of gp120 and exhibited a spectrum of broadly neutralizing activities. On the other hand, a minor population of Id+ Abs showed specificity for the V3 region of gp120 and exhibited limited cross-neutralizing activities. Together, these studies indicate that the CD4 site epitope-specific Abs are heterogeneous with respect to their clonality, neutralizing activity, and concentration in sera. This heterogeneity suggests that anti-gp120 Abs to the CD4 attachment site are developed in response to multiple overlapping epitopes present on the original virus isolate and/or epitopes on mutated variants which emerged over time. C1 IDEC PHARMACEUT CORP,11099 N TORREY PINES RD,LA JOLLA,CA 92037. NCI,FREDERICK CANC RES CTR,VIRUS BIOL UNIT,FREDERICK,MD 21701. CHIRON CORP,EMERYVILLE,CA 94608. FU NIAID NIH HHS [AI31310] NR 35 TC 16 Z9 16 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 FEB PY 1993 VL 67 IS 2 BP 953 EP 960 PG 8 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000037 PM 7678311 ER PT J AU OWENS, RA WEITZMAN, MD KYOSTIO, SRM CARTER, BJ AF OWENS, RA WEITZMAN, MD KYOSTIO, SRM CARTER, BJ TI IDENTIFICATION OF A DNA-BINDING DOMAIN IN THE AMINO TERMINUS OF ADENOASSOCIATED VIRUS REP PROTEINS SO JOURNAL OF VIROLOGY LA English DT Article ID HUMAN-CELLS; WILD-TYPE; REPLICATION; GENE; MUTANTS; ORIGIN; GENOME; SITE; MUTAGENESIS; ANTIBODIES AB The Rep78 and Rep68 proteins of adeno-associated virus (AAV) bind to the AAV terminal repeat hairpin DNA and are required for viral replication. We have expressed a series of mutant rep genes from the human immunodeficiency virus type 1 long terminal repeat promoter in human 293 cells and in an in vitro transcription-translation system. Mutant proteins were analyzed for AAV hairpin DNA binding and AAV terminal resolution functions. Deletion of amino acid residues 523 through 621 of Rep78 had no effect on these functions. Amber mutant Rep proteins truncated at either amino acid 237 or amino acid 243 showed no detectable hairpin DNA binding or terminal resolution activity. A frameshift mutant Rep protein which contained Rep78 amino acids 1 through 241 lacked terminal resolution functions but bound specifically to the AAV hairpin DNA. The carboxyl-terminal missense sequence in this mutant appeared to have complemented an AAV-specific DNA-binding domain within the amino terminus of the Rep protein. A mutant Rep protein in which methionine 225 of Rep78 was deleted (M225dl) was reduced threefold in AAV hairpin binding and had no terminal resolution functions. A mutant Rep protein in which a glycine was substituted at position 225 (M225G) was fully functional in these assays. When M225dl extract was mixed with wild-type Rep78 extract, AAV terminal resolution by Rep78 was inhibited. These results suggest that the amino-terminal portion of Rep78 and Rep68 contains a domain which can direct binding to AAV terminal hairpin DNA and that elements within the central region of the protein stabilize binding. RP OWENS, RA (reprint author), NIDDKD,MOLEC & CELLULAR BIOL LAB,BLDG 8,ROOM 304,BETHESDA,MD 20892, USA. NR 34 TC 93 Z9 93 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 FEB PY 1993 VL 67 IS 2 BP 997 EP 1005 PG 9 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000042 PM 8380475 ER PT J AU GESSAIN, A BOERI, E YANAGIHARA, R GALLO, RC FRANCHINI, G AF GESSAIN, A BOERI, E YANAGIHARA, R GALLO, RC FRANCHINI, G TI COMPLETE NUCLEOTIDE-SEQUENCE OF A HIGHLY DIVERGENT HUMAN T-CELL LEUKEMIA (LYMPHOTROPIC) VIRUS TYPE-I (HTLV-I) VARIANT FROM MELANESIA - GENETIC AND PHYLOGENETIC RELATIONSHIP TO HTLV-I STRAINS FROM OTHER GEOGRAPHICAL REGIONS SO JOURNAL OF VIROLOGY LA English DT Article ID PAPUA-NEW-GUINEA; TROPICAL SPASTIC PARAPARESIS; SYNTHETIC PEPTIDES; TRANSCRIPTIONAL ACTIVATOR; SOLOMON-ISLANDS; MESSENGER-RNA; PX PROTEIN; IDENTIFICATION; ANTIBODY; P27X-III AB The high prevalences of antibodies against human T-cell leukemia (lymphotropic) virus type I (HTLV-1) reported for remote populations in Papua New Guinea and the Solomon Islands and for some aboriginal populations in Australia have been verified by virus isolation. Limited genetic analysis of the transmembrane portion (gp21) of the envelope gene of these viruses indicates the existence of highly divergent HTLV-I strains in Melanesia. Here, we report the complete nucleotide sequence of an HTLV-1 isolate (designated HTLV-I(MELS)) from the Solomon Islands. The overall nucleotide divergence of HTLV-I(MELS) from the prototype HTLV-I(ATK) was approximately 8.5%. The degree of variability in the amino acid sequences of structural genes ranged between 3 and 11% and was higher (8.5 to 25%) for the regulatory (tax and rex) genes and the other genes encoded by the pX region. Since HTLV-I(MELS) was as distantly related to HTLV-II as to the other known HTLV-I strains, it could not have arisen from a recombinational event involving HTLV-II but rather might be an example of independent viral evolution in this remote population. These data provide important insights and raise new questions about the origin and global dissemination of HTLV-I. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NATL INST NEUROL DISORDERS & STROKE,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. NR 53 TC 160 Z9 169 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 FEB PY 1993 VL 67 IS 2 BP 1015 EP 1023 PG 9 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000044 PM 8419636 ER PT J AU KULKARNI, AB CONNORS, M FIRESTONE, CY MORSE, HC MURPHY, BR AF KULKARNI, AB CONNORS, M FIRESTONE, CY MORSE, HC MURPHY, BR TI THE CYTOLYTIC ACTIVITY OF PULMONARY CD8+ LYMPHOCYTES, INDUCED BY INFECTION WITH A VACCINIA VIRUS RECOMBINANT EXPRESSING THE M2 PROTEIN OF RESPIRATORY SYNCYTIAL VIRUS (RSV), CORRELATES WITH RESISTANCE TO RSV INFECTION IN MICE SO JOURNAL OF VIROLOGY LA English DT Article ID T-CELL MEMORY; INFLUENZA-VIRUS; F-GLYCOPROTEIN; HOST IMMUNITY; COTTON RATS; NUCLEOPROTEIN; HEMAGGLUTININ; SPECIFICITY; PROTECTION; ANTIGENS AB Previous studies demonstrated that the pulmonary resistance to respiratory syncytial virus (RSV) challenge induced by immunization with a recombinant vaccinia virus expressing the M2 protein of RSV (vac-M2) was significantly greater 9 days after immunization than at 28 days and was mediated predominantly by CD8+ T cells. In this study, we have extended these findings and sought to determine whether the level of CD8+ cytotoxic T-lymphocyte (CTL) activity measured in vitro correlates with the resistance to RSV challenge in vivo. Three lines of evidence documented an association between the presence of pulmonary CTL activity and resistance to RSV challenge. First, vac-M2 immunization induced pulmonary CD8+ CTL activity and pulmonary resistance to RSV infection in BALB/c (H-2d) mice, whereas significant levels of pulmonary CTL activity and resistance to RSV infection were not seen in BALB.K (H-2k) or BALB.B (H-2b) mice. Second, pulmonary CD8+ CTL activity was not induced by infection with other vaccinia virus-RSV recombinants that did not induce resistance to RSV challenge. Third, the peak of pulmonary CTL activity correlated with the peak of resistance to RSV replication (day 6), with little resistance being observed 45 days after immunization. An accelerated clearance of virus was not observed when mice were challenged with RSV 45 days after immunization with vac-M2. The results indicate that resistance to RSV induced by immunization with vac-M2 is mainly mediated by primary pulmonary CTLs and that this resistance decreases to very low levels within 2 months following immunization. The implications for inclusion of CTL epitopes into RSV vaccines are discussed in the context of these observations. C1 NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. RP KULKARNI, AB (reprint author), NIAID,INFECT DIS LAB,RESP VIRUSES SECT,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI Morse, Herbert/0000-0002-9331-3705 NR 40 TC 58 Z9 58 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 FEB PY 1993 VL 67 IS 2 BP 1044 EP 1049 PG 6 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000047 PM 8419638 ER PT J AU EGLITIS, MA KADAN, MJ WONILOWICZ, E GOULD, L AF EGLITIS, MA KADAN, MJ WONILOWICZ, E GOULD, L TI INTRODUCTION OF HUMAN GENOMIC SEQUENCES RENDERS CHO-K1 CELLS SUSCEPTIBLE TO INFECTION BY AMPHOTROPIC RETROVIRUSES SO JOURNAL OF VIROLOGY LA English DT Note ID ECOTROPIC MURINE RETROVIRUSES; LEUKEMIA VIRUSES; GENE ENCODES; RECEPTOR; PROTEIN; VECTORS AB To learn more about the nature of the block to infection by amphotropic retroviruses exhibited by Chinese hamster cells (CHO-K1), CHO-K1 cells were made susceptible to amphotropic retrovirus infection by introducing genomic DNA from infectable human cells. A clone, designated CHO18, was obtained and shown to be infected as efficiently as NIH 3T3 fibroblasts. Susceptibility of CHO18 cells to infection was specific to retroviruses and vectors bearing an amphotropic envelope. By comparison to CHO-K1 cells, CHO18 cells may provide a useful model for analysis of the molecular events involved in the retrovirus-receptor interaction. C1 GENET THERAPY INC,GAITHERSBURG,MD 20878. RP EGLITIS, MA (reprint author), NIMH,CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 21 TC 6 Z9 6 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 FEB PY 1993 VL 67 IS 2 BP 1100 EP 1104 PG 5 WC Virology SC Virology GA KG400 UT WOS:A1993KG40000056 PM 8380456 ER PT J AU BAYNE, KAL DEXTER, SL HURST, JK STRANGE, GM HILL, EE AF BAYNE, KAL DEXTER, SL HURST, JK STRANGE, GM HILL, EE TI KONG(R) TOYS FOR LABORATORY PRIMATES - ARE THEY REALLY AN ENRICHMENT OR JUST FOMITES SO LABORATORY ANIMAL SCIENCE LA English DT Article ID RHESUS-MONKEYS; BEHAVIOR AB Simple toys as enrichment devices have been associated with a rapid decline in their use by nonhuman primates. Other facets of toy presentation have not been described previously. For example, a comparison of the effect(s) of an enrichment device between two facilities should be validated if enrichment recommendations are to be made that affect diverse research facilities across the country. Additionally, a comparison of two methods of presentation (one highly accessible to the animal and the other less accessible) of the same enrichment device for potential differences in efficacy could provide direction in implementing an enrichment program based on simple toys. The handling of enrichment devices by nonhuman primates can lead to the spread of microbial contamination. The typical enrichment program rotates enrichment devices among animals to maximize the variety of stimuli available to each primate in the most economic manner. An adequate sanitation program is therefore pivotal to minimizing the potential for enrichment devices to be fomites. We conducted three experiments that addressed these issues. The results confirmed that, although the presence of a simple toy reduced behavioral pathology, there was variability in behavioral effect for an enrichment technique between facilities. Two methods of presentation (on floor and suspended) of a simple toy did not produce any significant differences in use. Finally, we demonstrated that microbial growth can persist on enrichment devices after they have been sanitized in a commercial cagewasher. RP BAYNE, KAL (reprint author), NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,SCI SERV BRANCH,BETHESDA,MD 20892, USA. NR 17 TC 20 Z9 20 U1 1 U2 4 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 FEB PY 1993 VL 43 IS 1 BP 78 EP 85 PG 8 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA KP472 UT WOS:A1993KP47200012 PM 8459682 ER PT J AU LOCKSHIN, MD AF LOCKSHIN, MD TI DOES LUPUS FLARE DURING PREGNANCY SO LUPUS LA English DT Editorial Material ID ERYTHEMATOSUS RP LOCKSHIN, MD (reprint author), NIAMSD,BETHESDA,MD 20892, USA. NR 9 TC 27 Z9 27 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0961-2033 J9 LUPUS JI Lupus PD FEB PY 1993 VL 2 IS 1 BP 1 EP 2 DI 10.1177/096120339300200101 PG 2 WC Rheumatology SC Rheumatology GA KT677 UT WOS:A1993KT67700001 PM 8485554 ER PT J AU AVERBOOK, BJ WEI, JP PERRYLALLEY, DM ROSENBERG, SA YANG, JC AF AVERBOOK, BJ WEI, JP PERRYLALLEY, DM ROSENBERG, SA YANG, JC TI A TUMOR-ELABORATED SUPERNATANT FACTOR CHEMOTACTIC FOR IL-2 EXPANDED TUMOR INFILTRATING T-LYMPHOCYTES SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID RECOMBINANT INTERLEUKIN-2 INVIVO; ESTABLISHED PULMONARY METASTASES; ACTIVATED KILLER CELLS; ADOPTIVE IMMUNOTHERAPY; GENE-EXPRESSION; NECROSIS-FACTOR; MELANOMA; LOCOMOTION; EFFICACY; MOLECULE AB Very little is known about factors influencing the migration of highly activated T-lymphocytes. One such lymphocyte population is the IL-2 expanded population of T cells infiltrating tumors. These tumor-infiltrating lymphocytes (TIL) can cause tumor regression in patients with metastatic cancer and in murine tumor models when given in adoptive transfer. In patients with melanoma, these TIL have been shown to migrate to sites of tumor and this may be a critical factor in their antitumor activity. In this study, a 48-well microchemotaxis chamber and a 5 mum pore nitrocellulose filter membrane system was utilized to study the motility of murine TIL. A chemotactic response was observed to supernatants from freshly explanted, autologous, and nonautologous tumor cultured for 24 h. Serially passaged autologous and nonautologous tumors also produced supernatants with chemotactic activity. Supernatants from single cell suspensions of normal tissues prepared and cultured identically did not elicit chemotaxis. Chemotactic activity for TIL was not removed by dialysis (2000 MW exclusion limit), its activity was undiminished by heat treatment at 60-degrees-C for up to 60 min, and it was trypsin sensitive. Tumor supernatants were also chemotactic for two IL-2-dependent specifically alloreactive CTL lines (CTL-TIM and OE-4), but not two helper T cell lines (D-10 and D-1.5) or normal resting lymphocytes. This is the first demonstration of a chemotactic effect on IL-2-dependent, activated T cells. Characterization and purification of factors from tumor responsible for this directed migration are in progress. C1 MED COLL GEORGIA,DEPT SURG,BIW 442,AUGUSTA,GA 30912. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 36 TC 5 Z9 5 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 FEB PY 1993 VL 12 IS 1 BP 1 EP 8 PG 8 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA KQ623 UT WOS:A1993KQ62300001 PM 8457627 ER PT J AU JESSOP, JJ HOFFMAN, T AF JESSOP, JJ HOFFMAN, T TI PRODUCTION AND RELEASE OF IL-1-BETA BY HUMAN PERIPHERAL-BLOOD MONOCYTES IN RESPONSE TO DIVERSE STIMULI - POSSIBLE ROLE OF MICRODAMAGE TO ACCOUNT FOR UNREGULATED RELEASE SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID HUMAN PROINTERLEUKIN-1-BETA; HUMAN INTERLEUKIN-1; ACTIVATING FACTOR; SIGNAL SEQUENCE; PROTEIN-KINASE; SECRETION; CALCIUM; IL-1; LOCALIZATION; EXOCYTOSIS AB Three different stimuli [lipopolysaccharide (LPS), concanavalin A (Con A), and phorbol myristate acetate (PMA)] all induced production and release of interleukin-1beta (IL-1beta) from human monocytes in vitro. Of the three, LPS demonstrated the greatest potency for IL-1beta production. LPS and Con A demonstrated similar efficacy with respect to IL-1beta release. LPS was approximately 1000 times more potent than Con A in this regard. LPS- and Con A-induced IL-1beta release occurred within 3 h and 12-24 h, respectively. Challenge with PMA induced low levels of IL-1beta production with a relatively large percentage released. IL-1beta release by all three stimuli occurred at concentrations greater than or equal to those required for optimal IL-1beta production. The amount of IL-1beta released correlated with total IL-1beta produced and was associated with release of lactate dehydrogenase (LDH), a cytosolic enzyme marker used to evaluate cell membrane integrity. IL-1beta release preceded LDH release temporally. LPS and Con A had no effect on total cell protein synthesis, a measure of overt toxicity, while PMA inhibited protein synthesis in a dose-dependent fashion. LPS and Con A both induced expression of a 33- and 29-kDa precursor IL-1beta, but only the 17-kDa form was released. These data suggest that IL-1beta is released by a process different from regulated secretion. While PMA induces a more profound damage, LPS and Con A may stimulate release of IL-1beta from human monocytes in vitro through induction of microdamage to the cell membrane. RP JESSOP, JJ (reprint author), US FDA,PHS,CTR BIOL EVALUAT & RES,OBR,DIV HEMATOL,CELL BIOL LAB,NIH CAMPUS,BLDG 29,RM 223,BETHESDA,MD 20892, USA. NR 32 TC 12 Z9 12 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 FEB PY 1993 VL 12 IS 1 BP 51 EP 58 PG 8 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA KQ623 UT WOS:A1993KQ62300008 PM 8457632 ER PT J AU KIM, DK CECKLER, TL HASCALL, VC CALABRO, A BALABAN, RS AF KIM, DK CECKLER, TL HASCALL, VC CALABRO, A BALABAN, RS TI ANALYSIS OF WATER-MACROMOLECULE PROTON MAGNETIZATION TRANSFER IN ARTICULAR-CARTILAGE SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE COLLAGEN; PROTEOGLYCAN; SPIN-LATTICE RELAXATION; SATURATION TRANSFER ID TRANSFER CONTRAST; CROSS-RELAXATION; PROTEOGLYCANS; ARTHRITIS; INVIVO; KNEE AB These studies were designed to establish which structural elements of cartilage are responsible for proton magnetization transfer between water (Hf) and macromolecules (Hr) observed in MRI studies on articular cartilage. Saturation transfer techniques were used to monitor magnetization transfer in vitro on samples of the two major constituents of cartilage: collagen and proteoglycan. Articular cartilage samples were also evaluated in vitro before and after the removal of the proteoglycan fraction. Isolated hydrated collagen exhibited a significant proton magnetization transfer rate with water. In contrast, proteoglycans exhibited no proton magnetization transfer. Articular cartilage, in vitro, exhibited a high degree of magnetization transfer with water protons consistent with previous MRI studies in vivo. Enzymatic removal of proteoglycan from the cartilage did not alter the magnetization transfer rate between Hr and Hf. These data demonstrate that the structure and concentration of the collagen matrix are the predominant determinants of the magnetization transfer process in articular cartilage with little or no contribution from proteoglycans. This specificity of the magnetization transfer effect may prove useful in the noninvasive evaluation of cartilage composition and structure in vivo. C1 NHLBI,CARDIAC ENERGET LAB,BLDG 10,ROOM BID-161,BETHESDA,MD 20892. NIDR,BONE RES BRANCH,BETHESDA,MD 20892. RI Balaban, Robert/A-7459-2009 OI Balaban, Robert/0000-0003-4086-0948 NR 24 TC 138 Z9 142 U1 0 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD FEB PY 1993 VL 29 IS 2 BP 211 EP 215 DI 10.1002/mrm.1910290209 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KM064 UT WOS:A1993KM06400008 PM 8429785 ER PT J AU TURNER, R JEZZARD, P WEN, H KWONG, KK LEBIHAN, D ZEFFIRO, T BALABAN, RS AF TURNER, R JEZZARD, P WEN, H KWONG, KK LEBIHAN, D ZEFFIRO, T BALABAN, RS TI FUNCTIONAL MAPPING OF THE HUMAN VISUAL-CORTEX AT 4 AND 1.5 TESLA USING DEOXYGENATION CONTRAST EPI SO MAGNETIC RESONANCE IN MEDICINE LA English DT Note ID BLOOD; FIELDS; IMAGE; BRAIN; TIME AB The effects of photic stimulation on the visual cortex of human brain were studied by means of gradient-echo echo-planar imaging (EPI). Whole-body 4 and 1.5 T MRI systems, equipped with a small z axis head gradient coil, were used. Variations of image intensity of up to 28% at 4 T, and up to 7% at 1.5 T, were observed in primary visual cortex, corresponding to an increase of blood oxygenation in regions of increased neural activity. The larger effects at 4 T are due to the increased importance of the susceptibility difference between deoxygenated and oxygenated blood at high fields, C1 MASSACHUSETTS GEN HOSP,CTR NMR,BOSTON,MA 02114. NIH,DEPT DIAGNOST RADIOL,CTR CLIN,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892. RP TURNER, R (reprint author), NHLBI,CARDIAC ENERGET LAB,BLDG 10,ROOM B10161,BETHESDA,MD 20892, USA. RI Turner, Robert/C-1820-2008; Balaban, Robert/A-7459-2009; Wen, Han/G-3081-2010; OI Balaban, Robert/0000-0003-4086-0948; Wen, Han/0000-0001-6844-2997; Jezzard, Peter/0000-0001-7912-2251 NR 14 TC 360 Z9 363 U1 0 U2 6 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD FEB PY 1993 VL 29 IS 2 BP 277 EP 279 DI 10.1002/mrm.1910290221 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KM064 UT WOS:A1993KM06400020 PM 8429797 ER PT J AU GOLDSTEIN, AM TUCKER, MA CRUTCHER, WA HARTGE, P SAGEBIEL, RW AF GOLDSTEIN, AM TUCKER, MA CRUTCHER, WA HARTGE, P SAGEBIEL, RW TI THE INHERITANCE PATTERN OF DYSPLASTIC NEVI IN FAMILIES OF DYSPLASTIC NEVUS PATIENTS SO MELANOMA RESEARCH LA English DT Article DE DYSPLASTIC NEVI; GENETICS; INHERITANCE; MELANOMA AB Dysplastic naevi (DN) are the major precursor lesions of malignant melanoma, yet the presumed mode of inheritance or genetic aetiology of DN remains controversial. The inheritance pattern of DN in families from a randomly selected population of 26 dysplastic naevus patients was investigated by estimating the segregation ratio in families ascertained through an offspring with DN (incomplete ascertainment). For families ascertained through a parent with DN (complete ascertainment) the transmission pattern was examined by comparing the observed number of affected offspring to the expected number using a chi2 goodness-of-fit test. Results from the chi2 tests and the estimated segregation ratio of 0.52 (95% confidence interval: 0.31, 0.73) suggest that the inheritance pattern for dysplastic naevi in these families is consistent with autosomal dominant transmission, although the present study was limited because of a small sample size. The findings, therefore, need to be confirmed by a much larger study that is able to test more rigorously specific genetic hypotheses. RP GOLDSTEIN, AM (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,6130 EXECUT BLVD,ROOM 439,BETHESDA,MD 20892, USA. RI Tucker, Margaret/B-4297-2015 NR 0 TC 21 Z9 21 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0960-8931 J9 MELANOMA RES JI Melanoma Res. PD FEB PY 1993 VL 3 IS 1 BP 15 EP 22 DI 10.1097/00008390-199304000-00003 PG 8 WC Oncology; Dermatology; Medicine, Research & Experimental SC Oncology; Dermatology; Research & Experimental Medicine GA KW653 UT WOS:A1993KW65300002 PM 8471833 ER PT J AU MCDANIEL, JP DVORAK, JA AF MCDANIEL, JP DVORAK, JA TI IDENTIFICATION, ISOLATION, AND CHARACTERIZATION OF NATURALLY-OCCURRING TRYPANOSOMA-CRUZI VARIANTS SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE TRYPANOSOMA-CRUZI; DNA; KARYOTYPE POLYMORPHISM; CLONAL STABILITY; ISOENZYME; SCHIZODEME; FLOW CYTOMETRY ID SURFACE-ANTIGEN GENE; FLOW CYTOMETRIC ANALYSIS; MOLECULAR KARYOTYPE; CHROMOSOME-SIZE; DNA-MOLECULES; LEISHMANIA; STRAIN; EXPRESSION; CLONING; POLYMORPHISMS AB Naturally occurring DNA variants of the single-cell-derived Y-02 stock of Trypanosoma cruzi were discovered during a routine assay of the stock. Three DNA variant types were isolated. One type was indistinguishable from the parental Y-02 stock on the basis of total DNA cell- 1. The other two types contained approximately 30% and 70% more DNA cell-1 than the parental Y-02 stock. Both the nucleus and kinetoplast were involved in the DNA content differences. The increase in DNA cell-1 was not G-C- or A-T-specific and was unrelated to the developmental stage of the parasite. Epimastigote population doubling times, isoenzymes, and schizodeme analyses could not differentiate the variant stocks. However, marked karyotype polymorphisms were observed by pulse-field gel electrophoresis, and restriction-fragment-length-polymorphisms were detected in hybridizations of some endonuclease-restricted samples to the spliced leader probe. We postulate that the Y-02 variants are genetic homologs. The ability to form viable hybrids or aneuploids provides T. cruzi with a mechanism to survive environmental stress, promote intra-specific heterogeneity and generate the diversity observed in the presentation and course of Chagas' disease. C1 NIAID,PARASIT DIS LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 42 TC 42 Z9 42 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-6851 J9 MOL BIOCHEM PARASIT JI Mol. Biochem. Parasitol. PD FEB PY 1993 VL 57 IS 2 BP 213 EP 222 DI 10.1016/0166-6851(93)90197-6 PG 10 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA KG986 UT WOS:A1993KG98600004 PM 8433713 ER PT J AU CHAN, AML FLEMING, TP MCGOVERN, ES CHEDID, M MIKI, T AARONSON, SA AF CHAN, AML FLEMING, TP MCGOVERN, ES CHEDID, M MIKI, T AARONSON, SA TI EXPRESSION CDNA CLONING OF A TRANSFORMING GENE ENCODING THE WILD-TYPE G-ALPHA-12 GENE-PRODUCT SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SOFT-TISSUE SARCOMAS; NIH 3T3 CELLS; ALPHA-SUBUNIT; G-PROTEINS; MITOGENESIS; MUTATIONS; CYCLASE; CANCER; TUMORS; SYSTEM AB Using an expression cDNA cloning approach, we examined human tumor cell lines for novel oncogenes that might evade detection by conventional techniques. We isolated a transforming sequence that was highly efficient in transforming NIH 3T3 mouse fibroblasts. DNA sequence analysis identified the gene as the human homolog of a recently cloned alpha subunit of mouse GTP-binding protein Galpha12. NIH 3T3 cells transfected with Galpha12 cDNA grew in soft apr and were tumorigenic in nude mice. There were no apparent mutations in the cloned cDNA in comparison with a Galpha12 cDNA clone isolated from a normal human epithelial cell library, implying that overexpression alone was sufficient to cause NIH 3T3 cell transformation. The observed altered growth properties mediated by Galpha12 showed a certain degree of dependency on serum factors, and its mitogenic potential was also potently inhibited by suramin treatment. C1 NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,ROOM 1E24,BETHESDA,MD 20892. NR 33 TC 127 Z9 128 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 FEB PY 1993 VL 13 IS 2 BP 762 EP 768 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300004 PM 8423800 ER PT J AU HUIBREGTSE, JM SCHEFFNER, M HOWLEY, PM AF HUIBREGTSE, JM SCHEFFNER, M HOWLEY, PM TI CLONING AND EXPRESSION OF THE CDNA FOR E6-AP, A PROTEIN THAT MEDIATES THE INTERACTION OF THE HUMAN PAPILLOMAVIRUS E6 ONCOPROTEIN WITH P53 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CARCINOMA CELL-LINES; RETINOBLASTOMA GENE-PRODUCT; TUMOR SUPPRESSOR GENE; WILD-TYPE P53; CERVICAL-CARCINOMA; TRANSFORMED-CELLS; ANTI-ONCOGENE; DNA; KERATINOCYTES; ASSOCIATION AB The E6 oncoproteins of the cancer-associated or high-risk human papillomaviruses (HPVs) target the cellular p53 protein. The association of E6 with p53 leads to the specific ubiquitination and degradation of p53 in vitro, suggesting a model by which E6 deregulates cell growth control by the elimination of the p53 tumor suppressor protein. Complex formation between E6 and p53 requires an additional cellular factor, designated E6-AP (E6-associated protein), which has a native and subunit molecular mass of approximately 100 kDa. Here we report the purification of E6-AP and the cloning of its corresponding cDNA, which contains a novel open reading frame encoding 865 amino acids. E6-AP, translated in vitro, has the following properties: (i) it associates with wild-type p53 in the presence of the HPV16 E6 protein and simultaneously stimulates the association of E6 with p53, (ii) it associates with the high-risk HPV16 and HPV18 E6 proteins in the absence of p53, and (iii) it induces the E6- and ubiquitin-dependent degradation of p53 in vitro. RP HUIBREGTSE, JM (reprint author), NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892, USA. RI Scheffner, Martin/K-2940-2012 OI Scheffner, Martin/0000-0003-2229-0128 NR 49 TC 403 Z9 409 U1 1 U2 5 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 FEB PY 1993 VL 13 IS 2 BP 775 EP 784 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300006 PM 8380895 ER PT J AU TOLEDANO, MB GHOSH, D TRINH, F LEONARD, WJ AF TOLEDANO, MB GHOSH, D TRINH, F LEONARD, WJ TI N-TERMINAL DNA-BINDING DOMAINS CONTRIBUTE TO DIFFERENTIAL DNA-BINDING SPECIFICITIES OF NF-KAPPA-B P50 AND P65 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID TRANSCRIPTION FACTOR; CRYSTAL-STRUCTURE; 65-KD SUBUNIT; OPERATOR COMPLEX; PROTEIN; REL; RECEPTOR; SEQUENCE; RECOGNITION; ACTIVATION AB We previously reported that either oxidation or alkylation of NF-kappaB in vitro abrogates DNA binding. We used this phenomenon to help elucidate structural determinants of NF-kappaB binding. We now demonstrate that Cys-62 of NF-kappaB p50 mediates the redox effect and lies within an N-terminal region required for DNA binding but not for dimerization. Several point mutations in this region confer a transdominant negative binding phenotype to p50. The region is highly conserved in all Rel family proteins, and we have determined that it is also critical for DNA binding of NF-kappaB p65. Replacement of the N-terminal region of p65 with the corresponding region from p50 changes its DNA-binding specificity towards that of p50. These data suggest that the N-terminal regions of p50 and p65 are critical for DNA binding and help determine the DNA-binding specificities of p50 and p65. We have defined within the N-terminal region a sequence motif, R(F/G)(R/K)YXCE, which is present in Rel family proteins and also in zinc finger proteins capable of binding to kappaB sites. The potential significance of this finding is discussed. C1 NHLBI,PULM & MOLEC,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892. NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BASIC RES BRANCH,BETHESDA,MD 20892. NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NR 52 TC 109 Z9 111 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 FEB PY 1993 VL 13 IS 2 BP 852 EP 860 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300014 PM 8423807 ER PT J AU GONG, QH DEAN, A AF GONG, QH DEAN, A TI ENHANCER-DEPENDENT TRANSCRIPTION OF THE EPSILON-GLOBIN PROMOTER REQUIRES PROMOTER-BOUND GATA-1 AND ENHANCER-BOUND AP-1/NF-E2 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PORPHOBILINOGEN DEAMINASE GENE; PROTEIN DNA INTERACTIONS; DOMINANT CONTROL REGION; TRANSGENIC MICE; ERYTHROID PROMOTER; BINDING FACTOR; EXPRESSION; INVIVO; CELLS; SITE AB We analyzed epsilon-globin transcription in erythroid cells and in erythroid extracts to determine the requirements for enhancer-dependent expression of this gene. Mutations that abolished GATA-1 binding at a single position in the promoter prevented interaction with enhancers, whereas elimination of a second more distal promoter GATA-1 site had no effect. Deletion or mutation of the GATA-1 sites in either the human beta-globin locus control region DNase-hypersensitive site II enhancer or the chicken beta(A)/epsilon-globin enhancer did not diminish the ability of the enhancers to interact with the promoter. In contrast, mutation of the AP-1/NF-E2 sites in these enhancers resulted in elimination of enhancement. In vitro transcription of these constructs was promoter dependent and was not sensitive to abolition of GATA-1 binding in the promoter, consistent with the role of GATA-1 solely as a mediator of the enhancer effect. Thus, GATA-1 regulates the response of the epsilon-globin gene to enhancers through a specific site in the promoter and requires enhancer AP-1/NF-E2 binding to transduce the enhancer effect on transcription. C1 NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. NR 49 TC 59 Z9 61 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 FEB PY 1993 VL 13 IS 2 BP 911 EP 917 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300020 PM 8423810 ER PT J AU BONNER, WM MANNIRONI, C ORR, A PILCH, DR HATCH, CL AF BONNER, WM MANNIRONI, C ORR, A PILCH, DR HATCH, CL TI HISTONE H2AX GENE-TRANSCRIPTION IS REGULATED DIFFERENTLY THAN TRANSCRIPTION OF OTHER REPLICATION-LINKED HISTONE GENES SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MESSENGER-RNA DEGRADATION; PROTEIN-SYNTHESIS; DNA-REPLICATION; CELL-CYCLE; S-PHASE; 3' END; SEQUENCE; PHOSPHORYLATION; INHIBITION; EXPRESSION AB Histone H2A.X is a replication-independent histone H2A isoprotein species that is encoded by a transcript alternatively processed at the 3' end to yield two mRNAs: a 0.6-kb mRNA ending with the stem-loop structure characteristic of the mRNAs for replication-linked histone species, and a second, polyadenylated 1.6-kb mRNA ending about 1 kb further downstream (C. Mannironi, W. M. Bonner, and C. L. Hatch, Nucleic Acids Res. 17:9113-9126, 1989). Of the two, the 0.6-kb H2A.X stem-loop mRNA predominates in many cell lines, indicating that the presence of two types of mRNA may not completely account for the replication independence of H2A.X protein synthesis. The ambiguity is resolved by the finding that the level of the 0.6-kb H2A.X mRNA is only weakly downregulated during the inhibition of DNA replication and only weakly upregulated during the inhibition of protein synthesis, while the levels of other replication-linked mRNAs are strongly down- or upregulated under these two conditions. Analysis of the nuclear transcription rates of specific H2A genes showed that while the rates of transcription of replication-linked H2A genes decreased substantially during the inhibition of DNA synthesis and increased substantially during the inhibition of protein synthesis, the rate of H2A.X gene transcription decreased slightly under both conditions. These differences in transcriptional regulation between the H2A.X gene and other replication-linked histone genes are sufficient to account for the differences in regulation of their respective stem-loop mRNAs. RP BONNER, WM (reprint author), NCI,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892, USA. RI mannironi, cecilia/I-3542-2013 NR 46 TC 28 Z9 28 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 FEB PY 1993 VL 13 IS 2 BP 984 EP 992 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300029 PM 8423818 ER PT J AU SPRENGER, F TROSCLAIR, MM MORRISON, DK AF SPRENGER, F TROSCLAIR, MM MORRISON, DK TI BIOCHEMICAL-ANALYSIS OF TORSO AND D-RAF DURING DROSOPHILA EMBRYOGENESIS - IMPLICATIONS FOR TERMINAL SIGNAL TRANSDUCTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MATERNAL-EFFECT MUTATIONS; RECEPTOR TYROSINE KINASE; PROTEIN-KINASE; FEMALE-STERILE; EMBRYONIC TERMINI; GENE TAILLESS; C-FOS; PATTERN; MELANOGASTER; REQUIREMENT AB Determination of anterior and posterior terminal structures of Drosophila embryos requires activation of two genes encoding putative protein kinases, torso and D-raf. In this study, we demonstrate that Torso has intrinsic tyrosine kinase activity and show that it is transiently tyrosine phosphorylated (activated) at syncytial blastoderm stages. Torso proteins causing a gain-of-function phenotype are constitutively tyrosine phosphorylated, while Torso proteins causing a loss-of-function phenotype lack tyrosine kinase activity. The D-raf gene product, which is required for Torso function, is identified as a 90-kDa protein with intrinsic serine/threonine kinase activity. D-Raf is expressed throughout embryogenesis; however, the phosphorylation state of the protein changes during development. In wild-type embryos, D-Raf is hyperphosphorylated at 1 to 2 h after egg laying, and thereafter only the most highly phosphorylated form is detected. Embryos lacking Torso activity, however, show significant reductions in D-Raf protein expression rather than major alterations in the protein's phosphorylation state. This report provides the first biochemical analysis of the terminal signal transduction pathway in Drosophila embryos. C1 NCI,FREDERICK CANC RES & DEV CTR,MOLEC MECHAN CARCINOGENESIS LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM & BIOPHYS,SAN FRANCISCO,CA 94143. MAX PLANCK INST ENTWICKLUNGSBIOL,GENET ABT,W-7400 TUBINGEN,GERMANY. FU NCI NIH HHS [N01-CO-74101] NR 49 TC 46 Z9 52 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD FEB PY 1993 VL 13 IS 2 BP 1163 EP 1172 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KH793 UT WOS:A1993KH79300047 PM 8423783 ER PT J AU WADA, E BATTEY, J WRAY, S AF WADA, E BATTEY, J WRAY, S TI BOMBESIN RECEPTOR GENE-EXPRESSION IN RAT EMBRYOS - TRANSIENT GRP-R GENE-EXPRESSION IN THE POSTERIOR PITUITARY SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID GASTRIN-RELEASING PEPTIDE; HYPOTHALAMO-NEUROHYPOPHYSEAL SYSTEM; DEVELOPING NEURAL LOBE; CELL LUNG-CANCER; SWISS 3T3 CELLS; NERVOUS-SYSTEM; GROWTH-FACTORS; NEUROMEDIN-B; FETAL LUNG; SUBTYPES C1 NCI,DCT,DTP,BIOL CHEM LAB,BETHESDA,MD 20892. RP WADA, E (reprint author), NINCDS,NEUROCHEM LAB,BETHESDA,MD 20892, USA. OI wray, susan/0000-0001-7670-3915 NR 36 TC 19 Z9 19 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 FEB PY 1993 VL 4 IS 1 BP 13 EP 24 DI 10.1006/mcne.1993.1002 PG 12 WC Neurosciences SC Neurosciences & Neurology GA KH312 UT WOS:A1993KH31200002 PM 19912903 ER PT J AU SUH, HH MCMILLIAN, MK HUDSON, PM PENNYPACKER, KR HONG, JS AF SUH, HH MCMILLIAN, MK HUDSON, PM PENNYPACKER, KR HONG, JS TI EXPRESSION OF THE PROENKEPHALIN-A GENE AND [MET(5)]ENKEPHALIN SECRETION INDUCED BY PROSTAGLANDIN-E(2) IN BOVINE ADRENAL-MEDULLARY CHROMAFFIN CELLS - INVOLVEMENT OF 2ND MESSENGERS SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID CATECHOLAMINE RELEASE; PHOSPHOINOSITIDE METABOLISM; ENKEPHALIN BIOSYNTHESIS; GEL-ELECTROPHORESIS; CA-2+ MOBILIZATION; CYCLIC-AMP; CALMODULIN; CHANNELS; INHIBITORS; RESPONSES RP SUH, HH (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,NEUROPHARMACOL SECT,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Pennypacker, Keith/I-5092-2012 NR 34 TC 10 Z9 10 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 FEB PY 1993 VL 4 IS 1 BP 113 EP 120 DI 10.1006/mcne.1993.1013 PG 8 WC Neurosciences SC Neurosciences & Neurology GA KH312 UT WOS:A1993KH31200013 PM 19912914 ER PT J AU TILLY, K HAUSER, R CAMPBELL, J OSTHEIMER, GJ AF TILLY, K HAUSER, R CAMPBELL, J OSTHEIMER, GJ TI ISOLATION OF DNAJ, DNAK, AND GRPE HOMOLOGS FROM BORRELIA-BURGDORFERI AND COMPLEMENTATION OF ESCHERICHIA-COLI MUTANTS SO MOLECULAR MICROBIOLOGY LA English DT Article ID HEAT-SHOCK PROTEINS; POLYMERASE CHAIN-REACTION; LYME-DISEASE SPIROCHETE; F PLASMID REPLICATION; NUCLEOTIDE-SEQUENCE; GENE-PRODUCT; ARTHRITIS; IDENTIFICATION; CHROMOSOME; GROWTH AB The heat-shock proteins DnaJ, DnaK, and GrpE are involved in the replication of various species of DNA in Escherichia coli, in addition to their roles in other processes, including protein disaggregation and export. We have cloned the Borrelia burgdorferi homologues of these genes. DNA sequence analysis revealed an open reading frame encoding a protein that is 62% identical to the E. coli DnaK protein. Genes homologous to the E. coli grpE and dnaJ genes, encoding products 28% and 39% identical to their homologues, are located up- and downstream, respectively, of the B. burgdorferi dnaK gene. No obvious promoters were detected in the sequenced DNA, although a potential transcription terminator was found downstream of the dnaJ gene, so these three genes may form an operon, perhaps with a fourth gene located upstream of the grpE gene. The grpE homologue complemented an E. coli grpE mutant and the dnaJ homologue complemented an E. coli dnaJ mutant, whereas the B. burgdorferi dnaK gene did not complement dnaK mutants. RP TILLY, K (reprint author), NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840, USA. NR 64 TC 47 Z9 50 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0950-382X J9 MOL MICROBIOL JI Mol. Microbiol. PD FEB PY 1993 VL 7 IS 3 BP 359 EP 369 DI 10.1111/j.1365-2958.1993.tb01128.x PG 11 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA KK976 UT WOS:A1993KK97600004 PM 8459764 ER PT J AU KAMINSKY, LS DEMORAIS, SMF FALETTO, MB DUNBAR, DA GOLDSTEIN, JA AF KAMINSKY, LS DEMORAIS, SMF FALETTO, MB DUNBAR, DA GOLDSTEIN, JA TI CORRELATION OF HUMAN CYTOCHROME P4502C SUBSTRATE SPECIFICITIES WITH PRIMARY STRUCTURE - WARFARIN AS A PROBE SO MOLECULAR PHARMACOLOGY LA English DT Article ID HUMAN-LIVER-MICROSOMES; MEPHENYTOIN HYDROXYLATION; CHROMOSOMAL LOCALIZATION; COMPLEMENTARY DNAS; MULTIPLE MEMBERS; SUBFAMILY; CLONING; PURIFICATION; METABOLITES; EXPRESSION AB The regio- and stereoselectivity of warfarin metabolism have been used to assess structure-function relationships of human P4502C subfamily members. Metabolism was investigated using a yeast cDNA expression system in which full length cDNAs for P4502C8,-2C9 (alleles Arg144 Tyr358 Ile359 Gly417 and Arg114 Tyr358 Leu359 Gly417), -2C18 (alleles Thr385 and Met385), and -2C19 were expressed. Additionally, two mutations reported in other P4502C9/2C10 alleles were individually introduced into P4502C9 by site-directed mutagenesis, to yield Cys144 Tyr358 Ile359 Gly417, Arg144 Tyr358 Ile359 Asp417, and Arg144 Cys358 Ile359 Gly417, which were expressed in yeast; their ability to metabolize warfarin was then studied. Warfarin metabolism by purified preparations of P4502C9 allele Arg144 Tyr358 Ile359 Gly417 and its Leu359 mutant was also investigated in reconstituted systems. Both alleles of P4502C18 were regioselective for 4'-hydroxywarfarin, without any significant stereoselectivity. Both also metabolized warfarin at the 6-position, but to a lesser extent, and metabolism at this site was stereoselective for (R)-warfarin. P4502C8 metabolized warfarin at the 7-position and was stereospecific for (R)-warfarin. It also metabolized warfarin to a lesser extent at the 4'-position, and metabolism at this site was stereoselective for (R)-warfarin. P4502C19 was regioselective for 6- and 8-hydroxywarfarin and was stereoselective for (R)-warfarin. The highly conservative mutation of Ile359 to Leu359 in P4502C9 profoundly altered the regio- and stereoselectivity of warfarin metabolism, from regioselective for 7-hydroxywarfarin, with stereospecificity for (S)-warfarin, to regioselective for 4'-hydroxywarfarin, with stereoselectivity for (R)-warfarin, which was confirmed in a reconstituted system using purified recombinant enzymes. In contrast, individual mutations of P4502C9 of Arg144 to Cys, Tyr358 to Cys, and Gly417 to Asp did not markedly affect the regio- or stereoselectivity of warfarin metabolism, although the overall rates of warfarin metabolism were apparently increased by these changes. We conclude that residue 359 is at the substrate binding site of P4502C9, whereas residues 144, 358, and 417, and residue 385 of P4502C18, are not. C1 NIEHS,RES TRIANGLE PK,NC 27709. RP KAMINSKY, LS (reprint author), NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,POB 509,ALBANY,NY 12201, USA. FU NIEHS NIH HHS [2PO1ES04238] NR 35 TC 157 Z9 160 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 FEB PY 1993 VL 43 IS 2 BP 234 EP 239 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KN002 UT WOS:A1993KN00200014 PM 8429826 ER PT J AU ONARAN, HO COSTA, T RODBARD, D AF ONARAN, HO COSTA, T RODBARD, D TI BETA-GAMMA SUBUNITS OF GUANINE NUCLEOTIDE-BINDING PROTEINS AND REGULATION OF SPONTANEOUS RECEPTOR ACTIVITY - THERMODYNAMIC MODEL FOR THE INTERACTION BETWEEN RECEPTORS AND GUANINE NUCLEOTIDE-BINDING PROTEIN SUBUNITS SO MOLECULAR PHARMACOLOGY LA English DT Article ID ADENYLATE-CYCLASE SYSTEM; TERNARY COMPLEX MODEL; ADRENERGIC-RECEPTOR; K+ CHANNEL; D2-DOPAMINE RECEPTOR; ANTERIOR-PITUITARY; LIGAND-BINDING; BOUND GDP; GI-ALPHA; GTP AB We used a thermodynamic model to examine the interactions between receptor, guanine nucleotide-binding protein (G protein), and their ligands. The model describes the interactions as multiple equilibria occurring between three distinct protein species (receptor, G(alpha) subunit, and G(betagamma) complex) and two small ligands, i.e., agonist (which interacts with receptor) and guanine nucleotide (which binds to G(alpha)). The equilibrium distribution of free and complexed species is determined by the total concentration of the components, the affinities that govern the bimolecular reactions, and the allosteric interactions that ligands exert on each other when they are simultaneously bound to the same species. These allosteric factors are given in terms of free energy coupling. The model explains a number of experimental observations, as follows. (i) Both GTP and GDP can reduce agonist affinity, whereas the agonist enhances the net binding of GTP and diminishes that of GDP. (ii) G(betagamma), is more effective in reducing agonist-independent than agonist-dependent receptor activity. (iii) Removal of guanine nucleotides increases the ratio between agonist-independent and -dependent activation of G protein. The model leads to a number of interesting predictions. (i) Not only G(alpha) but also G(betagamma) has effects on hormone binding. (ii) As long as the distribution of protein species is [G(betagamma)] > [G(alpha)] > [receptor] (as often observed in the cell membrane), small changes in the concentration of G(betagamma), do not alter the overall response induced by agonist. (iii) Agonist activity examined at low concentrations of guanine nucleotide is inevitably different from that observed at high concentrations, typical of intact systems. (iv) Differences in potencies and maximal effects for various guanine nucleotide analogues may reflect differences in their coupling constants that are experimentally measurable. The present model suggests several experimentally testable hypotheses that could be important in elucidating the activation mechanism and regulatory flexibility of G protein-dependent transduction systems. C1 NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20014. NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20014. OI costa, tommaso/0000-0002-8729-3357 NR 52 TC 49 Z9 49 U1 0 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD FEB PY 1993 VL 43 IS 2 BP 245 EP 256 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KN002 UT WOS:A1993KN00200016 PM 8381511 ER PT J AU BURKITT, MJ KADIISKA, MB HANNA, PM JORDAN, SJ MASON, RP AF BURKITT, MJ KADIISKA, MB HANNA, PM JORDAN, SJ MASON, RP TI ELECTRON-SPIN-RESONANCE SPIN-TRAPPING INVESTIGATION INTO THE EFFECTS OF PARAQUAT AND DESFERRIOXAMINE ON HYDROXYL RADICAL GENERATION DURING ACUTE IRON POISONING SO MOLECULAR PHARMACOLOGY LA English DT Article ID BIPYRIDYLIUM QUATERNARY-SALTS; ESCHERICHIA-COLI; SUPEROXIDE FORMATION; PULSE-RADIOLYSIS; METHYL VIOLOGEN; OXYGEN; MECHANISM; TOXICITY; INVIVO; CHLOROPLASTS AB We have previously described a secondary radical-trapping technique for the detection of in vivo hydroxyl radical generation during acute iron overload. With this technique, the hydroxyl radical (.OH) reacts with dimethylsulfoxide to form the methyl radical (.CH3), which is then detected by ESR spectroscopy as its adduct with the spin trap phenyl-N-tert-butylnitrone in the bile of treated animals. In this study, we report both the individual and combined effects of the futile-cycling agent paraquat (PQ2+) and the iron-chelating agent desferrioxamine (DFO) on iron-dependent .OH generation. Interactions between iron and the partially reduced oxygen species superoxide and hydrogen peroxide, which are generated during the metabolism of pQ2+, might be expected to stimulate .OH generation to a level above that seen in the presence of the metal ion alone. Although pQ2+ was often found to promote further .OH generation when administered to animals also given iron, the large variation observed between individual animals in response to the reagent meant that the effect was not statistically significant (p < 0.05). DFO was found to abolish iron-dependent .OH generation, both in the presence and in the absence of PQ2+. This is believed to result from the chelation of iron by DFO, to form an essentially redox-inert iron(III) complex that is unable to catalyze .OH radical formation. In addition, it was found that the iron(II) complex of DFO can reduce PQ2+ to its radical cation in vitro, indicating, therefore, that the chelation of iron by DFO may not necessarily prevent its participation in free radical reactions. C1 BULGARIAN ACAD SCI,INST PHYSIOL,BU-1113 SOFIA,BULGARIA. NIEHS,RES TRIANGLE PK,NC 27709. RP BURKITT, MJ (reprint author), ROWETT RES INST,GREENBURN RD,BUCKSBURN AB2 9SB,ABERDEEN,SCOTLAND. NR 35 TC 43 Z9 44 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD FEB PY 1993 VL 43 IS 2 BP 257 EP 263 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KN002 UT WOS:A1993KN00200017 PM 8381512 ER PT J AU OBRIEN, SJ WOMACK, JE LYONS, LA MOORE, KJ JENKINS, NA COPELAND, NG AF OBRIEN, SJ WOMACK, JE LYONS, LA MOORE, KJ JENKINS, NA COPELAND, NG TI ANCHORED REFERENCE LOCI FOR COMPARATIVE GENOME MAPPING IN MAMMALS SO NATURE GENETICS LA English DT Review ID GENETIC-LINKAGE MAP; MOUSE X-CHROMOSOME; INTERSPECIFIC BACKCROSS MICE; SOMATIC-CELL HYBRIDIZATION; DOMESTIC CAT; BINDING-PROTEIN; GROWTH-FACTOR; SYNTENIC CONSERVATION; THYROGLOBULIN GENE; BETA-SUBUNIT AB Recent advances in gene mapping technologies have led to increased emphasis in developing representative genetic maps for several species, particularly domestic plants and animals. These maps are being compiled with two distinct goals: to provide a resource for genetic analysis, and to help dissect the evolution of genome organization by comparing linkage relationships of homologous genes. We propose here a list of 321 reference anchor loci suitable for comparative gene mapping in mammals and other vertebrate classes. We selected cloned mouse and human functional genes spaced an average of 5-10 centiMorgans throughout their respective genomes. We also attempted to include loci that are evolutionarily conserved and represented in comparative gene maps in other mammalian orders, particularly cattle and the domestic cat. We believe that the map may provide the basis for a unified approach to comparative analysis of mammalian species genomes. C1 TEXAS A&M UNIV SYST,DEPT VET PATHOBIOL,COLL STN,TX 77843. TEXAS A&M UNIV SYST,CTR ANIM GENET,INST BIOSCI & TECHNOL,COLL STN,TX 77843. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP OBRIEN, SJ (reprint author), NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 154 TC 451 Z9 459 U1 2 U2 9 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD FEB PY 1993 VL 3 IS 2 BP 103 EP & DI 10.1038/ng0293-103 PG 0 WC Genetics & Heredity SC Genetics & Heredity GA KL010 UT WOS:A1993KL01000005 PM 8499943 ER PT J AU IRIS, FJM BOUGUELERET, L PRIEUR, S CATERINA, D PRIMAS, G PERROT, V JURKA, J RODRIGUEZTOME, P CLAVERIE, JM DAUSSET, J COHEN, D AF IRIS, FJM BOUGUELERET, L PRIEUR, S CATERINA, D PRIMAS, G PERROT, V JURKA, J RODRIGUEZTOME, P CLAVERIE, JM DAUSSET, J COHEN, D TI DENSE ALU CLUSTERING AND A POTENTIAL NEW MEMBER OF THE NF KAPPA-B FAMILY WITHIN A 90 KILOBASE HLA CLASS-III SEGMENT SO NATURE GENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; NUCLEOTIDE-SEQUENCE; HUMAN GENOME; GENE; EVOLUTION; DISEASE; PROTEIN; REGION; ALPHA; ASSOCIATIONS AB We have conducted a detailed structural analysis of 90 kilobases (kb) of the HLA Class III region from the Bat2 gene at the centromeric end to 23 kb beyond TNF. A single contig of 80 kb was sequenced entirely with a group of four smaller contigs covering 10 kb being only partly sequenced. This region contains four known genes and a novel telomeric potential coding region. The genes are bracketed by long, dense clusters of Alu repeats belonging to all the major families. At least six new families of MER repeats and one pseudogene are intercalated within and between the Alu clusters. The most telomeric 3.8 kb contains three potential exons, one of which bears strong homology to the ankyrin domain of the DNA binding factors NF kappaB and I kappaB. C1 LINUS PAULING INST SCI & MED,PALO ALTO,CA 94306. NIH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BETHESDA,MD 20892. RP IRIS, FJM (reprint author), CTR ETUD POLYMORPHISME HUMAIN,27 RUE JULIETTE DODU,F-75010 PARIS,FRANCE. NR 48 TC 102 Z9 107 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD FEB PY 1993 VL 3 IS 2 BP 137 EP 145 DI 10.1038/ng0293-137 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA KL010 UT WOS:A1993KL01000011 PM 8499947 ER PT J AU CHU, CS TRAPNELL, BC CURRISTIN, S CUTTING, GR CRYSTAL, RG AF CHU, CS TRAPNELL, BC CURRISTIN, S CUTTING, GR CRYSTAL, RG TI GENETIC-BASIS OF VARIABLE EXON-9 SKIPPING IN CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR MESSENGER-RNA SO NATURE GENETICS LA English DT Article ID 3' SPLICE-SITE; MAMMALIAN INTRONS; XENOPUS OOCYTES; CL CHANNEL; CFTR GENE; IDENTIFICATION; SEQUENCES; CELLS; DNA; MUTATIONS AB Variable in-frame skipping of exon 9 in cystic fibrosis transmembrane conductance regulator (CFTR) mRNA transcripts (exon 9-) occurs in the respiratory epithelium. To explore the genetic basis of this event, we evaluated respiratory epithelial cells and blood leukocytes from 124 individuals (38 with cystic fibrosis (CF), 86 without CF). We found an inverse relationship between the length of the polythymidine tract at the exon 9 splice branch/acceptor site and the proportion of exon 9- CFTR mRNA transcripts. These results strongly indicate a genetic basis in vivo modulating post-transcriptional processing of CFTR mRNA transcripts. C1 JOHNS HOPKINS UNIV HOSP,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV HOSP,CTR MED GENET,BALTIMORE,MD 21205. RP CHU, CS (reprint author), NHLBI,PULM BRANCH,BETHESDA,MD 20892, USA. NR 51 TC 366 Z9 370 U1 1 U2 8 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD FEB PY 1993 VL 3 IS 2 BP 151 EP 156 DI 10.1038/ng0293-151 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA KL010 UT WOS:A1993KL01000013 PM 7684646 ER PT J AU BODDEKE, HWGM HOFFMAN, BJ PALACIOS, JM KNOT, H HOYER, D AF BODDEKE, HWGM HOFFMAN, BJ PALACIOS, JM KNOT, H HOYER, D TI CHARACTERIZATION OF FUNCTIONAL-RESPONSES IN A9-CELLS TRANSFECTED WITH CLONED RAT 5-HT1C RECEPTORS SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY LA English DT Article DE 5-HT1C RECEPTORS; A9 CELLS POTASSIUM CONDUCTANCE; CALCIUM RESPONSE; FURA-2 FLUO-3 ID 5-HYDROXYTRYPTAMINE BINDING-SITES; PIG CHOROID-PLEXUS; INOSITOL 1,4,5-TRISPHOSPHATE; XENOPUS OOCYTES; CELLS; CDNA; TRISPHOSPHATE; INDICATORS; LIGANDS; BRAIN AB Functional responses to stimulation of rat 5-HT1C receptors expressed in A9 cells were studied using whole cell voltage clamp and calcium recording techniques. Stimulation of 5-HT1C receptors evoked outward currents clamped at - 50 mV. The outward currents were reduced when GTP was excluded from the intracellular recording solution or when GDP-beta-S was added. 8-Bromo cyclic AMP (5 mmol/1) neither produced an effect per se nor affected the 5-HT-induced outward current in A9 cells, thus excluding cAMP as a second messenger involved in 5-HT1C receptor activation. Phorbol myristic acetate (PMA; 10 mumol/1) did not affect the electrical activity of the transfected A9 cells but reduced the 5-HT-induced current amplitude to 71+/-9% of the control value (n = 12). This indicates that activation of protein kinase C does not play a direct role in the 5-HT-induced response in these cells. The 5-HT induced currents mainly involved potassium ions, although a small contribution of chloride ions was also observed. The 5-HT-induced current was inhibited by the K+ channel blocking agents tetraethylammonium (1 mmol/1), apamin (0,5 mumol/1) and 4-aminopyridine (5 mmol/1). The 5-HT-induced currents recorded at - 50 mV were unaffected by removal of extracellular calcium, but inclusion of the calcium chelator BAPTA (5 mmol/1) in the intracellular solutions abolished the current. Measurement with the calcium indicator Fluo-3 revealed a 5-HT-induced increase in intracellular calcium which was not affected by removal of extracellular calcium but declined after repeated stimulation. Determinated of pD2 and K(B) values of several 5-HT ligands using Fura-2 calcium measurements confirmed the pharmacology of the 5-HTc receptor. The results show that cloned rat 5-HT1C receptors expressed in A9 cells activate a calcium-dependent potassium conductance. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. LABS ALMIRALL SA,E-08024 BARCELONA,SPAIN. UNIV VERMONT,COLCHESTER,VT 05446. RP BODDEKE, HWGM (reprint author), SANDOZ PHARMA LTD,PRECLIN RES,CH-4002 BASEL,SWITZERLAND. OI Hoyer, Daniel/0000-0002-1405-7089 NR 26 TC 14 Z9 15 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0028-1298 J9 N-S ARCH PHARMACOL JI Naunyn-Schmiedebergs Arch. Pharmacol. PD FEB PY 1993 VL 347 IS 2 BP 119 EP 124 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KP023 UT WOS:A1993KP02300001 PM 8474532 ER PT J AU BREITNER, JCS GATZ, M BERGEM, ALM CHRISTIAN, JG MORTIMER, JA MCCLEARN, GE HESTON, LL WELSH, KA ANTHONY, JC FOLSTEIN, MF RADEBAUGH, TS AF BREITNER, JCS GATZ, M BERGEM, ALM CHRISTIAN, JG MORTIMER, JA MCCLEARN, GE HESTON, LL WELSH, KA ANTHONY, JC FOLSTEIN, MF RADEBAUGH, TS TI USE OF TWIN COHORTS FOR RESEARCH IN ALZHEIMERS-DISEASE SO NEUROLOGY LA English DT Article ID PRECURSOR PROTEIN GENE; FAMILIAL AGGREGATION; 1ST-DEGREE RELATIVES; DEMENTING ILLNESSES; CLINICAL GENETICS; MONOZYGOTIC TWIN; SENILE DEMENTIA; DOWNS-SYNDROME; RISK-FACTORS; EARLY-ONSET AB The causes of Alzheimer's disease (AD) remain a mystery despite the recent identification of several putative environmental risk factors and the discovery of several linked genetic loci and point mutations associated with the disease. Particularly uncertain is the generalizability of the genetic findings to the common forms of disease encountered in clinical practice or population research. Twin studies of AD can illuminate causal mechanisms, both genetic and environmental. This consensus document explores the rationale for such twin studies, as well as a number of methodologic problems that render them difficult to implement or interpret. We review existing twin studies of AD and note several ambitious new studies. Finally, we delineate several practical strategies for the near future of twin research in AD. C1 DUKE UNIV, MED CTR, KATHLEEN BRYAN ALZHEIMERS DIS RES CTR, DURHAM, NC 27710 USA. VET ADM MED CTR, CTR GERIATR RES EDUC & CLIN, MINNEAPOLIS, MN USA. WASHINGTON INST MENTAL ILLNESS RES & TRAINING, FT STEILACOOM, WA USA. UNIV MINNESOTA, DEPT NEUROL, MINNEAPOLIS, MN 55455 USA. JOHNS HOPKINS UNIV, DEPT PSYCHIAT & BEHAV SCI, BALTIMORE, MD 21218 USA. JOHNS HOPKINS UNIV, DEPT MENTAL HYG, BALTIMORE, MD 21218 USA. UNIV SO CALIF, DEPT PSYCHOL, LOS ANGELES, CA 90089 USA. NIA, BETHESDA, MD 20892 USA. UNIV OSLO, DEPT PSYCHIAT, OSLO 3, NORWAY. PENN STATE UNIV, COLL HLTH & HUMAN DEV, UNIV PK, PA 16802 USA. INDIANA UNIV, SCH MED, DEPT MED & MOLEC GENET, INDIANAPOLIS, IN 46202 USA. RP BREITNER, JCS (reprint author), DUKE UNIV, MED CTR, DEPT PSYCHIAT, BOX 3925, DURHAM, NC 27710 USA. NR 91 TC 30 Z9 31 U1 1 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 EI 1526-632X J9 NEUROLOGY JI Neurology PD FEB PY 1993 VL 43 IS 2 BP 261 EP 267 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA KM768 UT WOS:A1993KM76800004 PM 8437688 ER PT J AU JAKAB, G WEBSTER, HD SALAMON, I MEZEY, E AF JAKAB, G WEBSTER, HD SALAMON, I MEZEY, E TI NEURAL AND NONNEURAL ORIGIN OF CALCITONIN GENE-RELATED PEPTIDE (CGRP) IN THE GASTRIC-MUCOSA SO NEUROPEPTIDES LA English DT Article ID RAT GASTROINTESTINAL-TRACT; ACID-SECRETION; SUBSTANCE-P; MESSENGER-RNAS; BLOOD-FLOW; STOMACH; RELEASE; IMMUNOREACTIVITY; POLYPEPTIDE; CAPSAICIN AB We have used immunohistochemistry and in situ hybridization histochemistry to visualize CGRP and the mRNA encoding the CGRP precursor in the stomach. CGRP is present in nerve fibers in the mucosa. CGRP mRNA and CGRP itself are also found in non-neural cells in the lamina propria. These cells are likely to be macrophages or B-lymphocytes. C1 NIMH,LCB,BETHESDA,MD 20892. SEMMELWEIS UNIV MED,SCH MED,DEPT ANAT 2,H-1085 BUDAPEST 8,HUNGARY. RP JAKAB, G (reprint author), NINCDS,EXPTL NEUROPATHOL LAB,9000 ROCKVILLE PIKE,BLDG 36,ROOM 4A29,BETHESDA,MD 20892, USA. NR 31 TC 16 Z9 17 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0143-4179 J9 NEUROPEPTIDES JI Neuropeptides PD FEB PY 1993 VL 24 IS 2 BP 117 EP 122 DI 10.1016/0143-4179(93)90030-E PG 6 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA KN343 UT WOS:A1993KN34300008 PM 8459910 ER PT J AU GHANSAH, E KOPSOMBUT, P MALEQUE, MA BROSSI, A AF GHANSAH, E KOPSOMBUT, P MALEQUE, MA BROSSI, A TI EFFECTS OF MESCALINE AND SOME OF ITS ANALOGS ON CHOLINERGIC NEUROMUSCULAR-TRANSMISSION SO NEUROPHARMACOLOGY LA English DT Article DE MESCALINE; HALLUCINOGEN; TETRAHYDROISOQUINOLINE; CHOLINERGIC NEUROTRANSMISSION; RECEPTOR BINDING; NEUROMUSCULAR TRANSMISSION ID HALLUCINOGENIC DRUGS; SKELETAL-MUSCLE; RECEPTORS; BRAIN; BINDING AB Mescaline (3,4,5-trimethoxyphenylethylamine; MES) and its analogs, anhalinine (ANH) and methylenemescaline trimer (MMT) were investigated, using sciatic-sartorius preparations of the frog and cortical tissue from the rat. The effects of MES and its analogs were examined with respect to muscle twitch, resting membrane potential and nicotinic receptor binding. Mescaline and its analogs (10-100 muM) blocked both directly and neurally evoked twitches but their effects on neurally evoked twitches were greater than those on directly evoked twitches. Mescaline, ANH and MMT decreased amplitude of the miniature endplate and endplate potentials, decreased acetylcholine (ACh) quantal content, hyperpolarized the resting membrane potential and prolonged duration of the action potential. They did not significantly displace the binding of [I-125]-alpha-bungarotoxin (alpha-BTX) to nicotinic receptors, at concentrations which blocked neuromuscular transmission. These results suggest that MES and its analogs inhibit cholinergic neuromuscular transmission by blocking release of ACh; they also affect K+ conductance. C1 MEHARRY MED COLL, DEPT PHARMACOL, 1005 DB TODD BLVD, NASHVILLE, TN 37208 USA. NIH, MED CHEM LAB, BETHESDA, MD 20205 USA. FU NCRR NIH HHS [G12RR03032, SO6-RR08037-A1] NR 23 TC 7 Z9 7 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0028-3908 EI 1873-7064 J9 NEUROPHARMACOLOGY JI Neuropharmacology PD FEB PY 1993 VL 32 IS 2 BP 169 EP 174 DI 10.1016/0028-3908(93)90097-M PG 6 WC Neurosciences; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA KJ844 UT WOS:A1993KJ84400009 PM 8383816 ER PT J AU ROSENTHAL, NE MOUL, DE HELLEKSON, CJ OREN, DA FRANK, A BRAINARD, GC MURRAY, MG WEHR, TA AF ROSENTHAL, NE MOUL, DE HELLEKSON, CJ OREN, DA FRANK, A BRAINARD, GC MURRAY, MG WEHR, TA TI A MULTICENTER STUDY OF THE LIGHT VISOR FOR SEASONAL AFFECTIVE-DISORDER - NO DIFFERENCE IN EFFICACY FOUND BETWEEN 2 DIFFERENT INTENSITIES SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE SEASONAL AFFECTIVE DISORDER; PHOTOTHERAPY; LIGHT; CIRCADIAN RHYTHMS; SEASONS; DEPRESSION ID THERAPY; PHOTOTHERAPY AB Fifty-five patients with winter seasonal affective disorder (SAD) were treated with a light visor, a newly developed portable light-delivery system, in a controlled parallel design. A dim (400 lux) visor was compared with a bright (6000 lux) visor for either 30 or 60 minutes in the morning for 1 week. Response rates for these two treatments were 36% and 56%, respectively; the duration of treatment sessions did not affect outcome. There was no evidence that the brighter visor was superior in efficacy to the dimmer one. Significantly greater relapse occurred following withdrawal of the dimmer visor. Alternative explanations for these findings are that the light visor is acting as a placebo or that it is equally effective over a wide range of intensities. C1 PROVIDENCE HOSP,PROVIDENCE SLEEP DISORDERS CTR,SEATTLE,WA. BROOKSIDE HOSP,NASHUA,NH. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT NEUROL,PHILADELPHIA,PA 19107. RP ROSENTHAL, NE (reprint author), NIMH,DIRP,CLIN PSYCHOBIOL BRANCH,ENVIRONM PSYCHIAT SECT,BLDG 10-4S-239,BETHESDA,MD 20892, USA. NR 34 TC 38 Z9 38 U1 0 U2 0 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 FEB PY 1993 VL 8 IS 2 BP 151 EP 160 PG 10 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KK807 UT WOS:A1993KK80700008 PM 8471127 ER PT J AU HILAKIVICLARKE, L DURCAN, M GOLDBERG, R AF HILAKIVICLARKE, L DURCAN, M GOLDBERG, R TI EFFECT OF ALCOHOL ON ELEVATED AGGRESSIVE-BEHAVIOR IN MALE TRANSGENIC TGF-ALPHA MICE SO NEUROREPORT LA English DT Article DE TRANSFORMING GROWTH FACTOR-ALPHA; TRANSGENIC MICE; ALCOHOL; AGGRESSION; ALCOHOL SENSITIVITY ID ETHANOL; ONSET; BRAIN; AGE AB THE effect of alcohol on aggressive behavior was studied in the highly aggressive transgenic TGFalpha male mouse. In contrast to findings obtained in other aggressive animals, low and moderate doses of alcohol failed to reduce this behavior in the TGFalpah mice; only a high dose reduced aggression. The plasma levels of alcohol were similar in the TGFalpha mice and non-transgenic control mice. However, the loss of righting reflex following an alcohol administration was significantly lengthened in the TGFalpha mice. These results suggest that the male TGFalpha mice can be used to investigate the mechanisms determining the physiological sensitivity to alcohol. Furthermore, these mice represent the first animal model supporting the findings obtained in humans that alcohol maintains pathological aggression. C1 GEORGETOWN UNIV,SCH MED,VINCENT T LOMBARDI RES CTR,WASHINGTON,DC 20007. NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20852. RP HILAKIVICLARKE, L (reprint author), GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,3800 RESERVOIR RD NW,WASHINGTON,DC 20007, USA. NR 20 TC 13 Z9 13 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD FEB PY 1993 VL 4 IS 2 BP 155 EP 158 DI 10.1097/00001756-199302000-00010 PG 4 WC Neurosciences SC Neurosciences & Neurology GA KQ676 UT WOS:A1993KQ67600010 PM 8453053 ER PT J AU BELL, JA AF BELL, JA TI SELECTIVE BLOCKADE OF SPINAL REFLEXES BY OMEGA-CONOTOXIN IN THE ISOLATED SPINAL-CORD OF THE NEONATAL RAT SO NEUROSCIENCE LA English DT Article ID MULTIPLE CALCIUM CHANNELS; CHICK SENSORY NEURONS; ROOT GANGLION NEURONS; PERIPHERAL NEURONS; SUBSTANCE-P; N-TYPE; RELEASE; SENSITIVITY; CURRENTS; INHIBITION AB High-voltage-activated calcium currents can be pharmacologically separated into two components: omega-conotoxin-sensitive, dihydropyridine resistant (N-type) and dihydropyridine sensitive, omega-conotoxin-resistant (L-type). In the present study, omega-conotoxin completely blocked spinal monosynaptic responses and long-latency electrically evoked polysynaptic reflexes were 93% blocked. Short-latency electrically evoked and capsaicin-evoked polysynaptic reflexes were partially blocked (39 and 37% block, respectively). Nifedipine, a dihydropyridine type antagonist, had no effect on any evoked responses and Bay K 8644, a dihydropyridine agonist, only increased spontaneous firing. Dynorphin A blocks N currents, but its depressant effects were not altered by irreversible blockade of omega-conotoxin-sensitive N channels. These results demonstrate that omega-conotoxin-sensitive N channels play a major role in the synaptic transmission that mediates monosynaptic and electrically evoked slow polysynaptic reflexes, and a lesser but significant role in fast and capsaicin-evoked polysynaptic spinal reflexes. L-type channels play a minor role. Furthermore, dynorphin A depresses synaptic transmission by blockade of high threshold calcium channels that are distinct from the omega-conotoxin-sensitive N channel, or by a mechanism that does not directly involve calcium channels. RP NIDA, ADDICT RES CTR, NEUROIMAGING & DRUG ACT SECT, POB 5180, BALTIMORE, MD 21224 USA. NR 26 TC 12 Z9 12 U1 0 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 FEB PY 1993 VL 52 IS 3 BP 711 EP 716 DI 10.1016/0306-4522(93)90419-G PG 6 WC Neurosciences SC Neurosciences & Neurology GA KL974 UT WOS:A1993KL97400020 PM 7680794 ER PT J AU JOHN, CS KINUYA, S MINEAR, G KEAST, RK PAIK, CH AF JOHN, CS KINUYA, S MINEAR, G KEAST, RK PAIK, CH TI SYNTHESIS AND BIOLOGICAL EVALUATION OF GALLIUM POLYAMINOTHIOLS (PAT) SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Article ID BIODISTRIBUTION; GA-67; RADIOPHARMACEUTICALS; COMPLEXES; LIGANDS AB Two polyaminothiol ligands, one hexadentate, N,N',N''-tris[2-methyl(2-propanethiol)]-1,4,7-triazacyclononane (TACN), and another potentially heptadentate, tris[2-methyl(2-propanethiol)]aminoethylamine (TMAE), were synthesized and characterized using spectroscopic and analytical methods. Both ligands were labeled with gallium-67 at pH 3.0-3.5 in high yields. The resulting gallium chelates were lipophilic. The biodistribution studies for both the chelates showed hepatic uptake and biliary clearance. The total % ID activity for [Ga-67]TACN in liver and intestine at 5 min was 33.86 increasing gradually to 61.4% at 30 min. The chelates were in vivo stable to plasma-transferrin transchelation as confirmed by scintigraphic images obtained by [Ga-67]TACN in rats and by plasma incubation of the chelates. These results indicate that Ga-TACN is a potentially useful tracer for hepatobiliary imaging using PET. No brain uptake was found. C1 NIH,BETHESDA,MD 20892. RP JOHN, CS (reprint author), GEORGE WASHINGTON UNIV,MED CTR,RADIOPHARMACEUT CHEM SECT,662 ROSS HALL,2300 I ST NW,WASHINGTON,DC 20037, USA. NR 17 TC 10 Z9 10 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD FEB PY 1993 VL 20 IS 2 BP 217 EP 223 DI 10.1016/0969-8051(93)90118-E PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KL023 UT WOS:A1993KL02300015 PM 8448576 ER PT J AU COPPER, RL GOLDENBERG, RL CLIVER, SP DUBARD, MB HOFFMAN, HJ DAVIS, RO AF COPPER, RL GOLDENBERG, RL CLIVER, SP DUBARD, MB HOFFMAN, HJ DAVIS, RO TI ANTHROPOMETRIC ASSESSMENT OF BODY SIZE DIFFERENCES OF FULL-TERM MALE AND FEMALE INFANTS SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID BIRTH-WEIGHT; MORTALITY; SEX AB Objective: To determine gender-specific differences in anthropometric characteristics of full-term male and female infants. Methods: Twelve hundred five term newborn infants were examined. All measures of length and skinfold thickness were performed in a standardized manner. Results: After adjusting for confounding variables by regression analysis, we found that nearly all length and circumference measurements were significantly smaller in female infants than in male infants but that subcutaneous fat deposition in female infants was significantly increased. However, there was no difference in the ponderal index between male and female newborns, indicating that this measure does not correlate with newborn fat deposition Conclusions: Despite being shorter and having smaller circumferences, female infants have more subcutaneous fat than male infants. The ponderal index is not useful as a measure of fatness when the sexes are compared. We speculate that the greater subcutaneous fat deposition in female infants may be related to their better neonatal outcomes. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. RP COPPER, RL (reprint author), UNIV ALABAMA,DEPT OBSTET & GYNECOL,OBSTET SERV,PERINATAL EPIDEMIOL UNIT,1500 6TH AVE S,BIRMINGHAM,AL 35294, USA. FU NICHD NIH HHS [N01-HD-4-2811] NR 20 TC 24 Z9 25 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD FEB PY 1993 VL 81 IS 2 BP 161 EP 164 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KJ537 UT WOS:A1993KJ53700001 PM 8423940 ER PT J AU MAHER, JE GOLDENBERG, RL TAMURA, T CLIVER, SP JOHNSTON, KE HOFFMAN, HJ AF MAHER, JE GOLDENBERG, RL TAMURA, T CLIVER, SP JOHNSTON, KE HOFFMAN, HJ TI INDICATORS OF MATERNAL NUTRITIONAL-STATUS AND BIRTH-WEIGHT IN TERM DELIVERIES SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID GROWTH-RETARDATION; REPRODUCTIVE PROCESS; DUTCH FAMINE; FETAL GROWTH; 6 INDEXES; SERUM AB Objective: To determine the relationship between measures of maternal protein nutriture and fetal size at birth. Methods: We obtained serum samples at 18 and 30 weeks' gestation from 289 indigent multiparous women. The concentrations of albumin, prealbumin, and retinol-binding protein were correlated with birth weight, fetal growth retardation, and other measures of nutritional status. Results: Serum albumin levels at 18 weeks correlated inversely with birth weight (P = .05). This negative correlation was explained by an inverse relationship between albumin concentration and maternal body mass index (BMI), and disappeared in a regression analysis adjusting for BMI. There was no significant correlation between albumin levels at 30 weeks and birth weight or between birth weight and the concentrations of the other two proteins at either gestational age. In individual subjects, the concentration of each protein correlated significantly with the concentration of the other proteins, and the levels at 18 weeks correlated with those at 30 weeks. Conclusion: Serum protein levels are not predictive of birth weight or growth retardation at birth, but do correlate significantly with a number of other measures of nutritional status. C1 UNIV ALABAMA,DEPT NUTR SCI,BIRMINGHAM,AL 35233. NICHHD,PREVENT RES PROGRAM,BETHESDA,MD 20892. RP MAHER, JE (reprint author), UNIV ALABAMA,DEPT OBSTET & GYNECOL,DIV MATERNAL FETAL MED,PERINATAL EPIDEMIOL UNIT,BIRMINGHAM,AL 35233, USA. FU NCI NIH HHS [5PO1-CA28103]; NICHD NIH HHS [N01-HD-4-2811] NR 21 TC 11 Z9 11 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD FEB PY 1993 VL 81 IS 2 BP 165 EP 169 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KJ537 UT WOS:A1993KJ53700002 PM 8423941 ER PT J AU BRINTON, LA HOOVER, RN AF BRINTON, LA HOOVER, RN TI ESTROGEN REPLACEMENT THERAPY AND ENDOMETRIAL CANCER RISK - UNRESOLVED ISSUES SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID EXOGENOUS ESTROGEN; CONJUGATED ESTROGENS; ORAL-CONTRACEPTIVES; CARCINOMA; WOMEN; PROGESTOGENS; ASSOCIATION; PATTERNS; DISEASE AB Objective: To clarify several unresolved issues regarding the relationship of estrogens to endometrial cancer risk. Methods: We conducted a hospital-based case-control study involving 300 menopausal women newly diagnosed with epithelial endometrial cancer and 207 population controls matched to the cases for age, race, and residence. Results: Estrogen use significantly increased endometrial cancer risk (adjusted relative risk [RR] 3.0, 95% confidence interval [CI] 1.7-5.1). Although both short- and long-term use appeared to elevate the risk of early-stage tumors, an effect of estrogens on late-stage tumors was observed only for long-term use (RR 2.1, 95% CI 0.7-6.4). A small proportion of women reported having used progestogens simultaneously with estrogens, which was associated with a lower risk (RR 1.8) than use of estrogens alone (RR 3.4). Although the highest risks were for recent users of estrogens, persistent excess risks were seen even for those who had discontinued use of 5 or more years. There were no striking relationships according to the type of estrogen or regimen used, and associations with dose were inconsistent, although women who used low-dose preparations exclusively had the lowest risk. Estrogen injections or creams, used by only 5.9 and 5.1% of the subjects, respectively, were not significant risk factors after adjustment for estrogen pill use. Women who were thin or who smoked cigarettes appeared to be most adversely affected by estrogen use. Estrogen users failed to experience the protective effect normally associated with oral contraceptive use. Conclusion: The effect of estrogens on endometrial cancer risk appears to vary both by usage patterns and by patient characteristics. RP BRINTON, LA (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 34 TC 135 Z9 135 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD FEB PY 1993 VL 81 IS 2 BP 265 EP 271 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KJ537 UT WOS:A1993KJ53700024 PM 8380913 ER PT J AU KOLCH, W HEIDECKER, G TROPPMAIR, J YANAGIHARA, K BASSIN, RH RAPP, UR AF KOLCH, W HEIDECKER, G TROPPMAIR, J YANAGIHARA, K BASSIN, RH RAPP, UR TI RAF REVERTANT CELLS RESIST TRANSFORMATION BY NONNUCLEAR ONCOGENES AND ARE DEFICIENT IN THE INDUCTION OF EARLY RESPONSE GENES BY TPA AND SERUM SO ONCOGENE LA English DT Article ID PROTEIN KINASE-C; NIH 3T3 CELLS; SIGNAL TRANSDUCTION; V-RAF; TYROSINE PHOSPHORYLATION; NEGATIVE AUTOREGULATION; EXTRACELLULAR SIGNALS; NUCLEOTIDE-SEQUENCE; FLAT REVERTANTS; AUTO-REGULATION AB A revertant cell line was generated from v-raf transformed NIH/3T3 fibroblasts. These cells, termed CHP25, express a functional v-raf oncogene. However, they are non-tumorigenic, do not form colonies in soft agar and possess a flat morphology. CHP25 cell are resistant to re-transformation by sis, ras, tyrosine kinase as well as serine/threonine kinase-encoding oncogenes suggesting that Raf functions downstream of most membrane associated signal transducers. In contrast to v-raf transformed cells, in which the endogenous Raf-1 protein kinase is constitutively activated, v-Raf in CHP25 cells does not activate endogenous Raf-1 kinase. Since mitogen regulation of Raf-1 kinase in CHP25 cells is intact, we conclude that CHP25 cells are blocked at the level of Raf-1 substrate phosphorylation. Consistent with this interpretation CHP25 cells show specific alterations of early gene induction. The serum induction of c-fos and junD as well as the serum and TPA (12-O-tetradecanoylphorbol-13-acetate) induction of junB and egr-1 are almost completely abolished. Only v-fos can transform CHP25, whereas c-fos, v-myc, c-jun and junB are ineffective. These data suggest that the lesion responsible for the revertant phenotype of CHP25 cells is the inability to activate the AP-1 complex. We conclude that Raf-1 signaling is essential for transformation of NIH/3T3 cells by peripheral oncogenes and for regulation of a subset of early response genes by TPA and serum growth factors. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20855. OI Kolch, Walter/0000-0001-5777-5016 NR 71 TC 28 Z9 28 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB PY 1993 VL 8 IS 2 BP 361 EP 370 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN006 UT WOS:A1993KN00600015 PM 8426742 ER PT J AU LEE, MS YANG, JH SALEHI, Z ARNSTEIN, P CHEN, LS JAY, G RHIM, JS AF LEE, MS YANG, JH SALEHI, Z ARNSTEIN, P CHEN, LS JAY, G RHIM, JS TI NEOPLASTIC TRANSFORMATION OF A HUMAN KERATINOCYTE CELL-LINE BY THE V-FOS ONCOGENE SO ONCOGENE LA English DT Article ID OSTEO-SARCOMA VIRUS; HUMAN EPIDERMAL-KERATINOCYTES; PROTO-ONCOGENE; TRANSCRIPTION; EXPRESSION; PRODUCT; ACID; DNA; CARCINOMA; LEUKEMIAS AB To analyze the role of the fos oncogene in the growth of human epithelial cells, we have transfected a nontumorigenic human epidermal keratinocyte line (RHEK1) immortalized by the Ad12-SV40 hybrid virus with a plasmid carrying the v-fos gene together with plasmid pSV2-neo which confers resistance to neomycin. Individual neomycin-resistant clones were isolated and characterized with respect to morphological alteration. Of 16 independent clones analyzed, two appeared morphologically transformed and formed foci in culture. Only the two clones with a transformed phenotype were found by Southern blot hybridization analysis to contain the transfected v-fos gene. These clones formed colonies in soft agar and induced tumors when transplanted into nude mice. Analysis of fos specific mRNA and protein demonstrated that the transfected v-fos gene was expressed in these two clonal lines. These findings suggest that expression of the v-fos gene might facilitate the process of neoplastic transformation of human epithelial cells in culture. This appears to represent the first demonstration of the transforming potential of the v-fos gene in human cells. C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. JEROME H HOLLAND LAB,VIROL LAB,ROCKVILLE,MD 20855. RI Jay, Gregory/C-6346-2013 NR 40 TC 14 Z9 14 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB PY 1993 VL 8 IS 2 BP 387 EP 393 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN006 UT WOS:A1993KN00600018 PM 8426745 ER PT J AU MANO, H MANO, K TANG, B KOEHLER, M YI, T GILBERT, DJ JENKINS, NA COPELAND, NG IHLE, JN AF MANO, H MANO, K TANG, B KOEHLER, M YI, T GILBERT, DJ JENKINS, NA COPELAND, NG IHLE, JN TI EXPRESSION OF A NOVEL FORM OF TEC KINASE IN HEMATOPOIETIC-CELLS AND MAPPING OF THE GENE TO CHROMOSOME-5 NEAR KIT SO ONCOGENE LA English DT Article ID PROTEIN-TYROSINE KINASE; AMINO-TERMINAL DOMAIN; SENSITIVE V-ABL; SIGNAL TRANSDUCTION; C-ABL; DEVELOPMENTAL EXPRESSION; CYTOPLASMIC DOMAINS; ANTIGEN RECEPTOR; MESSENGER-RNA; MYELOID CELLS AB The Tec kinase was initially identified as a novel cytoplasmic protein tyrosine kinase that is preferentially expressed in the liver and is highly homologous to the Drosophila Dsrc28C src-related tyrosine kinase. In screening of interleukin 3 (IL-3)-dependent myeloid leukemia cells for protein tyrosine kinases, we observed that all cell lines examined expressed high levels of Tec transcripts. However, characterization of Tec cDNAs indicated that they differed significantly from the published sequence. Most strikingly, an insertion of 41 bp in the 5' region affects the initiation codon and results in replacing the published 13 amino acid amino-terminal sequences with 94 amino acids. Using polymerase chain reaction (PCR) analysis, only the form containing the insertion was detected in hematopoietic cells. In addition, we found an in-frame insertion of 66 bp that introduces an additional 22 amino acids into the SH3 domain. This insertion restores conserved SH3 sequences that are found in the src gene family and in the Dsrc28C gene. By PCR analysis, approximately equal levels of Tec transcripts containing the intact SH3 domain and containing the 22 amino acid deletion were found in hematopoietic cells. Lastly, by interspecies backcross analysis, we show that the Tec gene is tightly linked to the c-Kit gene on mouse chromosome 5. C1 ST JUDE CHILDRENS RES HOSP, DEPT BIOCHEM, 332 N LAUDERDALE, MEMPHIS, TN 38105 USA. NCI, FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM, MAMMALIAN GENET LAB, FREDERICK, MD 21702 USA. FU NCI NIH HHS [P30 CA21765, N01-CO-74101]; NIDDK NIH HHS [DK42932] NR 63 TC 161 Z9 164 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB PY 1993 VL 8 IS 2 BP 417 EP 424 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN006 UT WOS:A1993KN00600021 PM 7678927 ER PT J AU BOYER, PL COLMENARES, C STAVNEZER, E HUGHES, SH AF BOYER, PL COLMENARES, C STAVNEZER, E HUGHES, SH TI SEQUENCE AND BIOLOGICAL-ACTIVITY OF CHICKEN SNON CDNA CLONES SO ONCOGENE LA English DT Article ID V-SKI ONCOGENE; RETROVIRUS VECTORS; CELLS; GENE; VIRUSES; MUSCLE AB cDNA clones of the ski-related gene, sno, were isolated from a chicken cDNA library and sequenced. In contrast to the human system, from which two forms of sno cDNAs have been isolated, we obtained only one type of chicken sno cDNA, that encoding snoN. The coding region for chicken snoN was inserted into the retroviral vectors RCAS(A) and RCASBP(A) and introduced into chicken embryo fibroblasts (CEFs) or quail embryo cells (QECs). Like the various forms of ski, snoN appears to be localized in the nucleus, and high levels of snoN expression cause transformation of CEFs and muscle differentiation of QECs. In contrast to ski however, low-level expression of snoN cannot induce transformation, and is only weakly myogenic. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,POB B,FREDERICK,MD 21702. UNIV CINCINNATI,MED CTR,DEPT MOLEC GENET BIOCHEM & MICROBIOL,CINCINNATI,OH 45267. FU NCI NIH HHS [N01-CO-74101] NR 13 TC 85 Z9 87 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB PY 1993 VL 8 IS 2 BP 457 EP 466 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN006 UT WOS:A1993KN00600025 PM 8426750 ER PT J AU NEBREDA, AR PORRAS, A SANTOS, E AF NEBREDA, AR PORRAS, A SANTOS, E TI P21RAS-INDUCED MEIOTIC MATURATION OF XENOPUS OOCYTES IN THE ABSENCE OF PROTEIN-SYNTHESIS - MPF ACTIVATION IS PRECEDED BY ACTIVATION OF MAP AND S6 KINASES SO ONCOGENE LA English DT Article ID ONCOGENIC RAS PROTEIN; LAEVIS OOCYTES; M-PHASE; CELL-CYCLE; TYROSINE PHOSPHORYLATION; OKADAIC ACID; P21; P34CDC2; INVIVO; SUBSTRATE AB Microinjection of transforming p21ras into Xenopus oocytes caused a time-dependent increase in the level of total cell protein phosphorylation that culminated with germinal vesicle breakdown (GVBD). The same pattern of phosphorylation was observed in oocytes matured by either progesterone or insulin. Treatment with cycloheximide (CHX) completely blocked both GVBD and the associated de novo phosphorylations induced by the hormones, but did not abolish p21ras-induced maturation nor the occurrence of associated maturation promoting factor (MPF)-dependent and -independent phosphorylations. Thus, induction of GVBD by p21ras in the absence of protein synthesis correlated with the activation of cytosolic MPF-associated kinase activity similar in specificity on exogenous (histone H1) and endogenous (47 kDa and a 42 kDa proteins) substrates to the MPF activity of hormonally-matured oocytes. The injection of p21ras in the presence of CHX caused also activation of other kinase(s) preceding MPF activation which were responsible for the phosphorylation of endogenous substrates including a 41 kDa protein and a 92 kDa protein kinase that comigrated, respectively, with bands recognized specifically by antibodies to MAP2 kinase and S6 kinase. The phosphorylation of those bands correlated also with the activation of cytosolic kinases acting specifically on myelin basic protein (MBP) and a S6-derived peptide as substrates. These results indicate that, in the absence of protein synthesis, p21ras is able to activate phosphorylation events leading to GVBD and suggest that this oncoprotein can participate in at least two separate pathways of MPF activation. We propose that the activation of MAP/MBP kinases and S6 kinases is an early effect of p21ras oncoproteins. C1 NCI,CELLULAR & MOLEC BIOL LAB,BG 37,RM 1D28,BETHESDA,MD 20892. RI Porras, Almudena/N-2121-2015 OI Porras, Almudena/0000-0002-6495-3308 NR 50 TC 41 Z9 41 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB PY 1993 VL 8 IS 2 BP 467 EP 477 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA KN006 UT WOS:A1993KN00600026 PM 8381222 ER PT J AU KAUFMAN, E HARGREAVES, KM DIONNE, RA AF KAUFMAN, E HARGREAVES, KM DIONNE, RA TI COMPARISON OF ORAL TRIAZOLAM AND NITROUS-OXIDE WITH PLACEBO AND INTRAVENOUS DIAZEPAM FOR OUTPATIENT PREMEDICATION SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS LA English DT Article ID SCALE AB Triazolam was evaluated as an oral sedative agent for dental outpatients in two studies in the oral surgery model. The first study demonstrated that 0.25 mg of triazolam in combination with nitrous oxide provides therapeutic effects but with a more rapid recovery than a 0.50 mg dose in combination with nitrous oxide. In the second study, triazolam produced a significant anxiolytic effect that was comparable to the effects of diazepam titrated to the usual clinical endpoint (mean dose = 19.3 mg). Less impairment in cognitive-psychomotor impairment and ambulatory function was seen after triazolam in comparison with diazepam. Triazolam appears to be a safe, effective alternative to parenteral sedation with a benzodiazepine for dental outpatients. C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,CLIN PHARMACOL UNIT,BLDG 10,BETHESDA,MD 20892. RI Hargreaves, Kenneth/F-5308-2010 NR 20 TC 11 Z9 12 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1079-2104 J9 ORAL SURG ORAL MED O JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. PD FEB PY 1993 VL 75 IS 2 BP 156 EP 164 DI 10.1016/0030-4220(93)90086-J PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA KM018 UT WOS:A1993KM01800005 PM 8426714 ER PT J AU GRACELY, RH LYNCH, SA BENNETT, GJ AF GRACELY, RH LYNCH, SA BENNETT, GJ TI PAINFUL NEUROPATHY - ALTERED CENTRAL PROCESSING MAINTAINED DYNAMICALLY BY PERIPHERAL INPUT (PAIN, VOL 51, PG 175-194, 1992) SO PAIN LA English DT Correction, Addition RP GRACELY, RH (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 10,ROOM 1N 103,BETHESDA,MD 20892, USA. NR 1 TC 20 Z9 20 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 FEB PY 1993 VL 52 IS 2 BP 251 EP 251 DI 10.1016/0304-3959(93)90141-B PG 1 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA KN750 UT WOS:A1993KN75000018 ER PT J AU ROBINSON, TN HAMMER, LD KILLEN, JD KRAEMER, HC WILSON, DM HAYWARD, C TAYLOR, CB AF ROBINSON, TN HAMMER, LD KILLEN, JD KRAEMER, HC WILSON, DM HAYWARD, C TAYLOR, CB TI DOES TELEVISION VIEWING INCREASE OBESITY AND REDUCE PHYSICAL-ACTIVITY - CROSS-SECTIONAL AND LONGITUDINAL ANALYSES AMONG ADOLESCENT GIRLS SO PEDIATRICS LA English DT Article DE TELEVISION; OBESITY; ADIPOSITY; PHYSICAL ACTIVITY; ADOLESCENTS; FEMALES ID BODY-FAT DISTRIBUTION; EPIDEMIOLOGIC RESEARCH; SEXUAL-MATURATION; SELF-ASSESSMENT; BLOOD-PRESSURE; FOOD MESSAGES; MASS INDEX; CHILDREN; WEIGHT; DIET AB To examine the relationships between hours of television viewing and adiposity and physical activity among female adolescents, a cohort study with follow-up assessments 7,14, and 24 months after baseline was conducted. All sixth- and seventh-grade girls (N = 971) attending four northern California middle schools were eligible to participate. Six hundred seventy-one students had sufficient data for baseline cross-sectional analyses, and 279 students in a no-intervention cohort had sufficient data for longitudinal analyses. The baseline sample had a mean age of 12.4 years and was 43% white, 22% Asian, 21% Latino, 6% Pacific Islander, 4% black, 2% American Indian, and 2% other. Hours of after-school television viewing, level of physical activity, and stage of sexual maturation were assessed with self-report instruments. Height, weight, and triceps skinfold thickness were measured and body mass index (ratio of weight [in kilograms] to height [in meters] squared) and triceps skinfold thickness were adjusted by level of sexual maturity for the analyses. Baseline hours of after-school television viewing was not significantly associated with either baseline or longitudinal change in body mass index or triceps skinfold thickness. Baseline hours of after-school television viewing was weakly negatively associated with level of physical activity in cross-sectional analyses but not significantly associated with change in level of physical activity over time. All results were essentially unchanged when adjusted for age, race, parent education, and parent fatness. Among adolescent girls, television viewing time appears to have only weak, if any, meaningful associations with adiposity, physical activity, or change in either over time. C1 STANFORD UNIV,SCH MED,DEPT PEDIAT,PALO ALTO,CA 94304. STANFORD UNIV,SCH MED,DEPT PSYCHIAT,PALO ALTO,CA 94304. STANFORD UNIV,SCH MED,STANFORD CTR RES DIS PREVENT,PALO ALTO,CA 94304. NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. RP ROBINSON, TN (reprint author), STANFORD UNIV,SCH MED,ROBERT WOOD JOHNSON CLIN SCHOLARS PROGRAM,1000 WELCH RD,SUITE 203,PALO ALTO,CA 94304, USA. RI Loureiro, Nuno/I-6400-2012 OI Loureiro, Nuno/0000-0002-1166-3219 FU NICHD NIH HHS [R01 HD24240-01] NR 41 TC 224 Z9 226 U1 1 U2 11 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 FEB PY 1993 VL 91 IS 2 BP 273 EP 280 PG 8 WC Pediatrics SC Pediatrics GA KK578 UT WOS:A1993KK57800001 PM 8424000 ER PT J AU KORZEKWA, KR JONES, JP AF KORZEKWA, KR JONES, JP TI PREDICTING THE CYTOCHROME-P450 MEDIATED METABOLISM OF XENOBIOTICS SO PHARMACOGENETICS LA English DT Review ID LIVER MICROSOMAL CYTOCHROME-P-450; SEQUENCE REQUIREMENTS; CATALYTIC ACTIVITY; SUBSTRATE-SPECIFICITY; SECONDARY STRUCTURE; OXYGEN ACTIVATION; INSERTION SIGNAL; RABBIT LIVER; HYDROXYLATION; CYTOCHROMES-P-450 AB The cytochrome P450s play a unique role in the metabolism of xenobiotics. Characteristics which allow a vast number of foreign compounds to be metabolized by a limited number of enzymes include broad substrate specificity and broad regioselectivity. Because of their importance in both the metabolism and toxicity of drugs and environmental contaminants, efforts are being made to use computational methods to predict these biotransformation pathways. This review describes the recent progress towards the prediction of the tertiary structures of the various P450s and the determination of the electronic characteristics ot' substrates which determine their tendency to be oxidized by the P450s. C1 UNIV ROCHESTER,SCH MED,DEPT PHARMACOL,ROCHESTER,NY 14642. RP KORZEKWA, KR (reprint author), NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 75 TC 118 Z9 119 U1 2 U2 11 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD FEB PY 1993 VL 3 IS 1 BP 1 EP 18 DI 10.1097/00008571-199302000-00001 PG 18 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA KQ686 UT WOS:A1993KQ68600001 PM 8485584 ER PT J AU PENMAN, BW REECE, J SMITH, T YANG, CS GELBOIN, HV GONZALEZ, FJ CRESPI, CL AF PENMAN, BW REECE, J SMITH, T YANG, CS GELBOIN, HV GONZALEZ, FJ CRESPI, CL TI CHARACTERIZATION OF A HUMAN CELL-LINE EXPRESSING HIGH-LEVELS OF CDNA-DERIVED CYP2D6 SO PHARMACOGENETICS LA English DT Article ID DEBRISOQUINE METABOLIC PHENOTYPE; GENETIC-POLYMORPHISM; LUNG-CANCER; HUMAN-LIVER; CYTOCHROME-P-450 ISOZYMES; DRUG OXIDATION; TOBACCO-SMOKE; SPARTEINE; BUFURALOL; ACTIVATION AB We have developed a human B-lymphoblastoid cell, designated h2D6v2, which expresses high levels of CYP2D6 cDNA. Microsomal P450 contents of 160 pmol mg-1 protein were observed. NADPH-fortified microsomes exhibited a substantial capacity to hydroxylate the prototype CYP2D6 substrates bufuralol and debrisoquine. Kinetic parameters, apparent K(m), turnover number, K(i) for quinidine inhibition and stereospecificity of bufuralol hydroxylation, observed with the human lymphoblast expressed enzyme were similar to those observed in human liver microsomes or purified liver CYP2D6 proteins. Therefore, the human lymphoblast expressed material appears to faithfully reflect the authentic protein. Relative to control cells, h2D6v2 cells were more sensitive to the cytotoxicity and mutagenicity of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), supporting our previous observation with a cell line expressing lower levels of CYP2D6. h2D6v2 microsomes were capable of metabolizing NNK and NNK metabolism and mutagenicity were markedly inhibited by the addition of quinidine, a CYP2D6 inhibitor. h2D6v2 cells coupled with control cells, represent a useful in vitro system for studying xenobiotic metabolism by the clinically important, polymorphic CYP2D6. The human lymphoblast system offers the desirable ability to couple metabolic transformation studies with toxicological endpoints such as cytotoxicity and mutagenicity. C1 GENTEST CORP,6 HENSHAW ST,WOBURN,MA 01801. RUTGERS STATE UNIV,COLL PHARM,PISCATAWAY,NJ 08855. NCI,BETHESDA,MD 20892. NR 33 TC 68 Z9 69 U1 1 U2 2 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD FEB PY 1993 VL 3 IS 1 BP 28 EP 39 DI 10.1097/00008571-199302000-00003 PG 12 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA KQ686 UT WOS:A1993KQ68600003 PM 8485585 ER PT J AU LAWTON, MP PHILPOT, RM AF LAWTON, MP PHILPOT, RM TI MOLECULAR-GENETICS OF THE FLAVIN-DEPENDENT MONOOXYGENASES SO PHARMACOGENETICS LA English DT Article ID MULTIPLE FORMS; PRIMARY ALKYLAMINES; COVALENT STRUCTURE; LIVER-MICROSOMES; PRIMARY SEQUENCE; RABBIT LIVER; PIG-LIVER; LUNG; DISTINCT; RAT C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,POB 12233,RES TRIANGLE PK,NC 27709. NR 26 TC 21 Z9 21 U1 2 U2 2 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD FEB PY 1993 VL 3 IS 1 BP 40 EP 44 DI 10.1097/00008571-199302000-00004 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA KQ686 UT WOS:A1993KQ68600004 PM 8485586 ER PT J AU GONZALEZ, FJ LIU, SY YANO, M AF GONZALEZ, FJ LIU, SY YANO, M TI REGULATION OF CYTOCHROME-P450 GENES - MOLECULAR MECHANISMS SO PHARMACOGENETICS LA English DT Article ID ENRICHED TRANSCRIPTIONAL ACTIVATOR; DIOXIN RECEPTOR; EXPRESSION; HEPATOCYTES; SEQUENCE; MEMBER; HNF-1; DBP RP GONZALEZ, FJ (reprint author), NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 36 TC 90 Z9 97 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 FEB PY 1993 VL 3 IS 1 BP 51 EP 57 DI 10.1097/00008571-199302000-00006 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA KQ686 UT WOS:A1993KQ68600006 PM 8387380 ER PT J AU DALY, JW PADGETT, WL SECUNDA, SI THOMPSON, RD OLSSON, RA AF DALY, JW PADGETT, WL SECUNDA, SI THOMPSON, RD OLSSON, RA TI STRUCTURE-ACTIVITY-RELATIONSHIPS FOR 2-SUBSTITUTED ADENOSINES AT A1 AND A2 ADENOSINE RECEPTORS SO PHARMACOLOGY LA English DT Article DE ADENOSINE RECEPTORS; STRUCTURE ACTIVITY; ADENYLATE CYCLASE ID RAT FAT-CELLS; GUINEA-PIG ILEUM; 5'-CARBOXAMIDE DERIVATIVES; ADENYLATE-CYCLASE; HUMAN-PLATELETS; SELECTIVE AGONISTS; VAS-DEFERENS; PC12 CELLS; ANALOGS; POTENT AB A series of 55 2-alkyloxy-, 2-aryloxy- and 2-aralkyloxy-adenosines was screened as inhibitors of the binding of [H-3]R-phenyl-isopropyladenosine to A1 adenosine receptors in rat cerebral cortical membranes, and of the binding of [3]N-ethylcarboxamidoadenosine to A2 adenosine receptors in rat striatal membranes and as agonists at A2 adenosine receptors coupled to adenylate cyclase in rat pheochromocytoma PC12 cell membranes. The activities are consonant with a hydrophobic binding site in the A2 recpetors at a distance from the 2-position of the adenine ring corresponding to a spacer chain of -O-CH2-CH2-. There is little lateral steric tolerance in the region occupied by the spacer chain. Interaction with the hydrophobic binding site is greatest in the 2-alkyloxy series for 2-cyclohexylethoxy-, 2-cyclohexylpropoxy- and 2-cyclohexylbutoxyadenosines and in the 2-aralkoxy series for 2-phenylethoxy-, 2-(4-methylphenyl)ethoxy-, 2-(4-chlorophenyl)ethoxy-, and 2-naphthylethoxy-adenosine. The affinities of the 2-substituted adenosines for the rat cerebral cortical A1 receptors are not as markedly altered by structural changes and are in almost all cases two- to hundredfold less than the affinity of the 2-substituted adenosine for the rat striatal A2 recpetor. There is excellent correspondence of the present data on rat A2 receptors with reported potencies of these 2-substituted adenosines as coronary vasodilators in guinea pig heart preparations. C1 UNIV S FLORIDA,COLL MED,DEPT INTERNAL MED,TAMPA,FL 33612. RP DALY, JW (reprint author), NIDDKD,BIOORGAN CHEM LAB,BLDG 8,RM 1A15,BETHESDA,MD 20892, USA. NR 44 TC 37 Z9 38 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0031-7012 J9 PHARMACOLOGY JI Pharmacology PD FEB PY 1993 VL 46 IS 2 BP 91 EP 100 DI 10.1159/000139033 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KM271 UT WOS:A1993KM27100005 PM 8441759 ER PT J AU WEISS, GH AF WEISS, GH TI NEAREST-NEIGHBOR DISTANCE TO A TRAP IN A ONE-DIMENSIONAL SMOLUCHOWSKI MODEL SO PHYSICA A LA English DT Article ID DIFFUSION-CONTROLLED REACTIONS; STATISTICAL PROPERTIES; REACTION-KINETICS; MOBILE TRAP; DENSITY; MOTION AB We consider a one-dimensional Smoluchowski model for the reaction A + T --> T, with a single immobile trapping particle and noninteracting A particles which move by diffusion. It is known that when there is an initial density of A particles, the average value of the closest distance between the trap and an untrapped A is asymptotically proportional to t1/4. We show that this dependence also holds when the initial distances between adjacent A particles are independent identically distributed random variables with a finite mean. We also consider the case in which the trap is mobile and the A's are immobile. Here it is known that the asymptotic nearest-neighbor distance is proportional to t1/2. We show that for this to hold with a general initial distribution of A's one requires both the first and second moments of the initial distances to be finite. RP WEISS, GH (reprint author), NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892, USA. NR 13 TC 4 Z9 4 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 FEB 1 PY 1993 VL 192 IS 4 BP 617 EP 627 DI 10.1016/0378-4371(93)90112-H PG 11 WC Physics, Multidisciplinary SC Physics GA KL029 UT WOS:A1993KL02900007 ER PT J AU GITTERMAN, M WEISS, GH AF GITTERMAN, M WEISS, GH TI SMALL-NOISE APPROXIMATIONS TO THE SOLUTION OF THE SMOLUCHOWSKI EQUATION SO PHYSICAL REVIEW E LA English DT Article AB We explore the connection between the two perturbation methods that have been suggested for solving Smoluchowski-like equations with weak noise. A slight modification of the first of these methods (the size expansion of van Kampen) makes it identical to the second (the method of running coordinates). We point out that a number of modifications to both methods are possible and should be explored. We illustrate the advantages of both of these methods as applied to three solvable examples. C1 BAR ILAN UNIV,DEPT PHYS,IL-52100 RAMAT GAN,ISRAEL. RP GITTERMAN, M (reprint author), NIH,BETHESDA,MD 20892, USA. NR 12 TC 8 Z9 8 U1 1 U2 1 PU AMERICAN PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 1063-651X J9 PHYS REV E JI Phys. Rev. E PD FEB PY 1993 VL 47 IS 2 BP 976 EP 980 DI 10.1103/PhysRevE.47.976 PG 5 WC Physics, Fluids & Plasmas; Physics, Mathematical SC Physics GA KY136 UT WOS:A1993KY13600028 ER PT J AU KAMETANI, H SPANGLER, EL BRESNAHAN, EL KOBAYASHI, S LONG, JM INGRAM, DK AF KAMETANI, H SPANGLER, EL BRESNAHAN, EL KOBAYASHI, S LONG, JM INGRAM, DK TI IMPAIRED ACQUISITION IN A 14-UNIT T-MAZE FOLLOWING MEDIAL SEPTAL-LESIONS IN RATS IS CORRELATED WITH LESION SIZE AND HIPPOCAMPAL ACETYLCHOLINESTERASE STAINING SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE AGING; LEARNING; MEMORY; CHOLINERGIC SYSTEM; NEUROANATOMY; DENSITOMETRY ID FIMBRIA-FORNIX LESIONS; AGED RATS; CHOLINE-ACETYLTRANSFERASE; RETENTION PERFORMANCE; MUSCARINIC RECEPTORS; MEMORY IMPAIRMENT; BASAL FOREBRAIN; DIAGONAL BAND; YOUNG-RATS; DEFICITS AB Septohippocampal cholinergic system involvement in acquisition of an aversively motivated 14-unit T-maze was evaluated in 4-month-old male Fischer-344 rats. Each rat was assigned to one of two groups that received either a bilateral electrolytic lesion to the medial septal area (MSA) or a sham operation. One week after surgery, each rat began pretraining in one-way active avoidance (footshock = 0.8 mA) consisting of 10 trials per day on each of 3 consecutive days. Criterion for successful completion of pretraining was 8/10 avoidances on the third day. On the day following completion of pretraining, each rat received 10 trials in a shock-motivated 14-unit T-maze. The performance requirement was to move through each of five maze segments within 10 s to avoid footshock (0.8 mA). A second 10-trial session was provided 24 h later. Performance measures included errors, alternation errors, runtime, shock frequency, and duration. Following maze training, each rat was sacrificed, and formalin-fixed brains were frozen for histology, which included procedures for thionin Nissl and acetylcholinesterase (AChE) staining. MSA-lesioned rats were observed to be significantly impaired on all measures of maze performance compared to sham-operated controls. Densitometric analysis of hippocampal AChE staining revealed a 30% reduction in relative AChE staining of MSA-lesioned rats compared to sham-operated controls. Lesion size was observed to be highly positively correlated with maze errors. A negative correlation of mean error score with density of AChE staining was observed for MSA-lesioned rats, but not for sham-operated rats. These results are consistent with previous studies implicating the cholinergic system in the acquisition of this task and further support the use of this maze for the evaluation of age-related cholinergic dysfunction and cognitive deficits in rodent models. C1 NIA,FRANCIS SCOTT KEY MED CTR,GERONTOL RES CTR,NATHAN W SHOCK LABS,BALTIMORE,MD 21224. NR 39 TC 7 Z9 7 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD FEB PY 1993 VL 53 IS 2 BP 221 EP 228 DI 10.1016/0031-9384(93)90197-N PG 8 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA KK818 UT WOS:A1993KK81800002 PM 8446684 ER PT J AU WILDMAN, DE TAMIR, H LEBERER, E NORTHUP, JK DENNIS, M AF WILDMAN, DE TAMIR, H LEBERER, E NORTHUP, JK DENNIS, M TI PRENYL MODIFICATION OF GUANINE-NUCLEOTIDE REGULATORY PROTEIN-GAMMA-2 SUBUNITS IS NOT REQUIRED FOR INTERACTION WITH THE TRANSDUCIN ALPHA-SUBUNIT OR RHODOPSIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ADP-RIBOSYLATED ALPHA-39; BOVINE CEREBRAL-CORTEX; BETA-GAMMA-SUBUNITS; ROD OUTER SEGMENTS; G-PROTEINS; ADENYLATE-CYCLASE; GTP-BINDING; PHOSPHOLIPID-VESICLES; MOLECULAR-CLONING; BRAIN AB Guanine nucleotide-binding regulatory protein (G protein) betagamma dimers that were active in reconstitution assays were produced in insect cells using the baculovirus/Sf9 insect cell expression system. Sf9 cells were infected either singly or in combination with recombinant baculoviruses containing a human G-protein beta1 gene or a bovine G-protein gamma2 gene. It was possible to express the beta1 and gamma2 gene products independently of each other in this system, as determined by using immunological and metabolic labeling techniques. Further, the ability of recombinant beta and/or gamma chains to function in defined biochemical assays of betagamma activity was assessed for membrane extracts and supernatant fractions from infected Sf9 cells. Extracts of cells expressing beta or gamma chain alone were inactive in these assays, whereas those from cells coinfected with beta1 and gamma2 did display activity. These assays were used to identify recombinant betagamma dimer migration during chromatographic purification, and the recombinant dimers were purified to near homogeneity. Both the membrane-associated and soluble betagamma dimers facilitated rhodopsin-catalyzed guanosine 5'-[gamma-thio]triphosphate binding to G(t)alpha, the GTP-binding subunit of the retinal G protein transducin (K0.5 of 13 +/- 2 and 36 +/- 5 nM, respectively). Both recombinant betagamma dimers also facilitated the pertussis toxin-catalyzed ADP-ribosylation of G(t)alpha with equal potency (K0.5 of 9 +/- 1 and 10 +/- 3 nM for membrane and soluble dimers, respectively). [H-3]Mevalonolactone labeling showed that the gamma2 subunits of membrane-associated betagamma dimers incorporated radiolabel, whereas in the soluble form they did not. Thus, prenyl modification of gamma2 directs the membrane association of the beta1gamma2 dimer and increases its apparent affinity for receptor, but it is not required for the functional interaction(s) of the dimer. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06510. NATL RES COUNCIL CANADA,BIOTECHNOL RES INST,RECEPTOR GRP,MONTREAL H4P 2R2,PQ,CANADA. NR 47 TC 36 Z9 36 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 1 PY 1993 VL 90 IS 3 BP 794 EP 798 DI 10.1073/pnas.90.3.794 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KK813 UT WOS:A1993KK81300005 PM 8430087 ER PT J AU ACTOR, JK SHIRAI, M KULLBERG, MC BULLER, RML SHER, A BERZOFSKY, JA AF ACTOR, JK SHIRAI, M KULLBERG, MC BULLER, RML SHER, A BERZOFSKY, JA TI HELMINTH INFECTION RESULTS IN DECREASED VIRUS-SPECIFIC CD8+ CYTOTOXIC T-CELL AND TH1-CYTOKINE RESPONSES AS WELL AS DELAYED VIRUS CLEARANCE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SCHISTOSOMA-MANSONI; VACCINIA; CYTOTOXIC LYMPHOCYTE-T; IMMUNOREGULATION; PARASITE ID HEPATITIS-B INFECTION; LYMPHOCYTES-T; SCHISTOSOMIASIS-MANSONI; ENVELOPE GLYCOPROTEIN; DOWN-REGULATION; REPLICATION; INVITRO; GAMMA AB During the time of egg deposition, schistosome-infected mice exhibit a downregulation in interleukin 2 and interferon gamma production toward parasite antigens, mitogens, and foreign nonparasite protein antigens. To determine whether this imbalance in cytokine response would impact on CD8+ cytotoxic T-lymphocyte (CTL) responses, as well as on immune clearance of viral infections, we challenged Schistosoma mansoni-infected BALB/c mice, when cytokine imbalance was prominent, with a recombinant vaccinia virus expressing human immunodeficiency virus type 1 gp160. In contrast to control vaccinia-infected animals, S. mansoni plus vaccinia-infected mice did not produce significant Th1 cytokine responses upon in vitro stimulation with recombinant gp120, consistent with previous results for nonparasite antigens. However, more striking was the downregulation of the virus-specific CTL response not previously studied. Spleen cells from vaccinia-infected control mice displayed strong CD8+ cytolytic activity against gp160-transfected fibroblasts and fibroblasts pulsed with a peptide (P18) representing a CTL epitope of gp160. In contrast, mice coinfected with S. mansoni and vaccinia manifested absent or markedly reduced in vitro CTL activity even in the presence of exogenous interleukin 2. To determine whether this immune dysregulation might impact on viral clearance, we measured virus titers in tissues as a function of time. Mice infected with vaccinia virus alone rapidly cleared the virus, whereas in animals coinfected with S. mansoni, viral clearance was delayed by as much as 3 weeks in the liver and by several days in the spleen and lungs. These observations suggest that helminth infection may influence immune responses to concurrent viral infections. C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NCI,METAB BRANCH,BETHESDA,MD 20892. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. OI Actor, Jeffrey/0000-0002-9265-7012 NR 28 TC 288 Z9 292 U1 0 U2 7 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD FEB 1 PY 1993 VL 90 IS 3 BP 948 EP 952 DI 10.1073/pnas.90.3.948 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KK813 UT WOS:A1993KK81300036 PM 8094248 ER PT J AU JONES, TLZ WOODARD, C SPIEGEL, AM AF JONES, TLZ WOODARD, C SPIEGEL, AM TI BACULOVIRUS EXPRESSION AND PURIFICATION OF A SOLUBLE, MUTANT G-PROTEIN ALPHA-SUBUNIT SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article ID GUANINE-NUCLEOTIDE-BINDING; BETA-GAMMA-SUBUNITS; ACTIVATING PROTEIN; ESCHERICHIA-COLI; ADP-RIBOSYLATION; PERTUSSIS TOXIN; BOVINE BRAIN; MEMBRANE; MYRISTOYLATION; DISTINGUISH RP JONES, TLZ (reprint author), NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892, USA. NR 34 TC 9 Z9 9 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1046-5928 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD FEB PY 1993 VL 4 IS 1 BP 64 EP 71 DI 10.1006/prep.1993.1010 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA KJ886 UT WOS:A1993KJ88600010 PM 8425110 ER PT J AU POST, RM AF POST, RM TI ISSUES IN THE LONG-TERM MANAGEMENT OF BIPOLAR AFFECTIVE-ILLNESS SO PSYCHIATRIC ANNALS LA English DT Article ID AFFECTIVE-DISORDERS; FOLLOW-UP; CARBAMAZEPINE; LITHIUM; PROPHYLAXIS; MECHANISM; TOLERANCE RP POST, RM (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,ROOM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 32 TC 12 Z9 13 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD FEB PY 1993 VL 23 IS 2 BP 86 EP 93 PG 8 WC Psychiatry SC Psychiatry GA KM099 UT WOS:A1993KM09900010 ER PT J AU RICHTERS, JE AF RICHTERS, JE TI COMMUNITY VIOLENCE AND CHILDRENS DEVELOPMENT - TOWARD A RESEARCH AGENDA FOR THE 1990S SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article; Proceedings Paper CT NATIONAL CONF ON COMMUNITY VIOLENCE AND CHILDRENS DEVELOPMENT : RESEARCH AND CLINICAL IMPLICATIONS CY NOV 15-17, 1990 CL BETHESDA, MD SP NIMH, JOHN D & CATHERINE T MACARTHUR FDN, RES NETWORK AWARD, PSYCHIATRY, WASHINGTON SCH PSYCHIAT AB THE UNITED STATES is the most violent country in the industrialized world - particularly for young people. Homicide in the United States ranks as the second leading cause of death among those between 15 and 24 years of age (Earls et al. 1991). Males, especially, are at high risk. As indicated in Figure 1, those between 15 and 24 years of age were more likely to be murdered than their counterparts in all 22 other developed countries for which comparable homicide statistics were available during 1986-1987 (Fingerhut and Kleinman 1990). Young males were 4 times more likely to be murdered than their counterparts in the next highest country, Scotland; 7 times more likely than young males in Canada; 21 times more likely than those in West Germany; and 40 times more likely than same-age males in Japan. Moreover, the U.S. homicide rate for Black males (15 and 24 years) was more than 7 times the homicide rate for White males in this age range. These figures are all the more alarming in light of the fact that homicide rates in major U.S. cities have increased steadily since these data were recorded. RP RICHTERS, JE (reprint author), NIMH,DIV CLIN RES,CHILD & ADOLESCENT DISORDERS RES BRANCH,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. OI Richters, John/0000-0002-6780-1828 NR 12 TC 36 Z9 38 U1 0 U2 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD FEB PY 1993 VL 56 IS 1 BP 3 EP 6 PG 4 WC Psychiatry SC Psychiatry GA LC516 UT WOS:A1993LC51600002 PM 8488210 ER PT J AU RICHTERS, JE MARTINEZ, P AF RICHTERS, JE MARTINEZ, P TI THE NIMH COMMUNITY VIOLENCE PROJECT .1. CHILDREN AS VICTIMS OF AND WITNESSES TO VIOLENCE SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article; Proceedings Paper CT NATIONAL CONF ON COMMUNITY VIOLENCE AND CHILDRENS DEVELOPMENT : RESEARCH AND CLINICAL IMPLICATIONS CY NOV 15-17, 1990 CL BETHESDA, MD SP NIMH, JOHN D & CATHERINE T MACARTHUR FDN, RES NETWORK AWARD, PSYCHIATRY, WASHINGTON SCH PSYCHIAT AB THE 1980s WITNESSED an extraordinary increase in community violence in most major cities across the United States. In 1990 the homicide rate in Boston increased by 45% over the previous year; in Denver, by 29%; in Chicago, Dallas, and New Orleans, by more than 20%; in Los Angeles, by 16%; in New York, by 11%. In Washington, DC, which has the highest per capita homicide rate in the country, the 1990 murder rate set an all time record in the District's history (Escobar 1991). Across the country, 1 out of 5 teenage and young adult deaths was gun related in 1988 - the first year in which firearm death rates for both Black and White teenagers exceeded the total for all natural causes of death combined. Also in 1988, the firearm homicide rate for young Black males increased by 35%, and Black male teens were 11 times more likely than their White counterparts to be killed by guns (Christofel 1990). C1 NIMH,DEV PSYCHOL LAB,ROCKVILLE,MD 20857. RP RICHTERS, JE (reprint author), NIMH,DIV CLIN RES,CHILD & ADOLESCENT DISORDERS RES BRANCH,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. OI Richters, John/0000-0002-6780-1828 NR 11 TC 491 Z9 497 U1 2 U2 24 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD FEB PY 1993 VL 56 IS 1 BP 7 EP 21 PG 15 WC Psychiatry SC Psychiatry GA LC516 UT WOS:A1993LC51600003 PM 8488215 ER PT J AU MARTINEZ, P RICHTERS, JE AF MARTINEZ, P RICHTERS, JE TI THE NIMH COMMUNITY VIOLENCE PROJECT .2. CHILDRENS DISTRESS SYMPTOMS ASSOCIATED WITH VIOLENCE EXPOSURE SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article; Proceedings Paper CT NATIONAL CONF ON COMMUNITY VIOLENCE AND CHILDRENS DEVELOPMENT : RESEARCH AND CLINICAL IMPLICATIONS CY NOV 15-17, 1990 CL BETHESDA, MD SP NIMH, JOHN D & CATHERINE T MACARTHUR FDN, RES NETWORK AWARD, PSYCHIATRY, WASHINGTON SCH PSYCHIAT ID CAMBODIAN CHILDREN; NATURAL DISASTER; PSYCHIC TRAUMA; MASSIVE TRAUMA; ANXIETY LEVEL; STRESS; SCHOOL; PARENT AB THE rising tide of violence in American cities has placed the causes and consequences of violence squarely on the public health agenda. The U.S. Government's Year 2000 National Health Promotion and Disease Prevention Objectives includes a full chapter devoted to violence issues and delineates a number of goals and programs aimed at reducing the number of deaths and injuries associated with violence (Public Health Service 1990). Notably absent from these objectives, however, is attention to the possible adverse psychological consequences of exposure to acute or chronic violence. Nonetheless, in light of numerous media reports of children's exposure to community violence and recent reports documenting high levels of exposure even among very young children (Richters and Martinez 1993), it is reasonable to question whether the risks of exposure extend beyond death and physical injury to psychological well-being. C1 NIMH,DIV CLIN RES,CHILD & ADOLESCENT DISORDERS RES BRANCH,5600 FISHERS LANE,ROCKVILLE,MD 20857. NIMH,DEV PSYCHOL LAB,ROCKVILLE,MD 20857. OI Richters, John/0000-0002-6780-1828 NR 48 TC 308 Z9 312 U1 4 U2 16 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD FEB PY 1993 VL 56 IS 1 BP 22 EP 35 PG 14 WC Psychiatry SC Psychiatry GA LC516 UT WOS:A1993LC51600004 PM 8488209 ER PT J AU PUTNAM, FW TRICKETT, PK AF PUTNAM, FW TRICKETT, PK TI CHILD SEXUAL ABUSE - A MODEL OF CHRONIC TRAUMA SO PSYCHIATRY-INTERPERSONAL AND BIOLOGICAL PROCESSES LA English DT Article; Proceedings Paper CT NATIONAL CONF ON COMMUNITY VIOLENCE AND CHILDRENS DEVELOPMENT : RESEARCH AND CLINICAL IMPLICATIONS CY NOV 15-17, 1990 CL BETHESDA, MD SP NIMH, JOHN D & CATHERINE T MACARTHUR FDN, RES NETWORK AWARD, PSYCHIATRY, WASHINGTON SCH PSYCHIAT ID MULTIPLE PERSONALITY-DISORDER; POSTTRAUMATIC-STRESS-DISORDER; CHRONIC PELVIC PAIN; CHEMICAL DEPENDENCY; ADOLESCENT GIRLS; SUBSTANCE ABUSE; BODY-IMAGE; INCEST; WOMEN; MEN AB ALTHOUGH there is a general consensus among concerned professionals that exposure to community violence is likely to be stressful and may contribute significantly to immediate and long-term mental health problems, there is virtually no empirical research on either its acute or enduring effects. In the absence of data, investigators planning research in this area must look to other studies of the impact of chronic environmental trauma on children, including the effects of war and child maltreatment. Research on child abuse provides an important source of information on the effects of trauma on children because it draws on both prospective and retrospective studies crossing a variety of theoretical perspectives and disciplines. The existence of data on both the acute impact of abuse on children and its chronic effects and outcomes in adults informs the generation of developmentally based psychological and biological hypotheses. This paper utilizes data from research on the acute and chronic effects of sexual abuse to discuss three broad hypotheses that may be relevant to the study of the effects of community violence on children. C1 UNIV SO CALIF,DEPT PSYCHOL,LOS ANGELES,CA 90089. RP PUTNAM, FW (reprint author), NIMH,DEV PSYCHOL LAB,BLDG 15K,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 110 TC 48 Z9 48 U1 1 U2 6 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0033-2747 J9 PSYCHIATRY JI Psychiatry-Interpers. Biol. Process. PD FEB PY 1993 VL 56 IS 1 BP 82 EP 95 PG 14 WC Psychiatry SC Psychiatry GA LC516 UT WOS:A1993LC51600009 PM 8488216 ER PT J AU BREWERTON, TD GEORGE, MS HARDEN, RN AF BREWERTON, TD GEORGE, MS HARDEN, RN TI MIGRAINE AND THE EATING DISORDERS SO PSYCHIATRY RESEARCH LA English DT Letter ID NERVOSA C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. MED UNIV S CAROLINA,DEPT NEUROL,CHARLESTON,SC 29425. RP BREWERTON, TD (reprint author), MED UNIV S CAROLINA,INST PSYCHIAT,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 14 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD FEB PY 1993 VL 46 IS 2 BP 201 EP 202 DI 10.1016/0165-1781(93)90020-H PG 2 WC Psychiatry SC Psychiatry GA KU969 UT WOS:A1993KU96900008 PM 8483977 ER PT J AU GOLDBERG, TE TORREY, EF GOLD, JM RAGLAND, JD BIGELOW, LB WEINBERGER, DR AF GOLDBERG, TE TORREY, EF GOLD, JM RAGLAND, JD BIGELOW, LB WEINBERGER, DR TI LEARNING AND MEMORY IN MONOZYGOTIC TWINS DISCORDANT FOR SCHIZOPHRENIA SO PSYCHOLOGICAL MEDICINE LA English DT Article ID DORSOLATERAL PREFRONTAL CORTEX; ANTICHOLINERGIC DRUGS; WORKING MEMORY; TERM MEMORY; RECALL; DYSFUNCTION; DEFICIT; RECOGNITION; DISORDERS; PSYCHOSIS AB Learning and memory were assessed in 24 monozygotic (MZ) pairs of individuals discordant for schizophrenia or delusional disorder and seven normal pairs of MZ twins. On declarative memory tasks, the affected group displayed a pattern that might best be characterized as dysmnesic in that they performed significantly worse than the discordant unaffected group on story recall, paired associated learning, and visual recall of designs, but they learned over time, had relatively preserved recognition memory, and did not show profoundly accelerated rates of forgetting. Effortful, volitional retrieval from the lexicon, measured by verbal fluency, was also compromised in the affected group. On the other hand, procedural learning of the motor skill in a pursuit rotor task was relatively intact in the affected group. Comparisons of the normal group and unaffected group indicated that the latter group had very mild impairments in some aspects of episodic memory, namely, immediate and delayed recall of stories and delayed recall of designs. It is highly unlikely that the impairments observed in the affected group can be attributed to differences in genome, family environment, socioeconomic circumstance, or educational opportunity, as all of these were controlled by the twin paradigm. Rather, the impairments appear to be related to the intercession of disease. The neuropsychological profile is consistent with frontal lobe and medial temporal lobe dysfunction, as noted in this sample as well as other samples of schizophrenic singletons. Significant correlations between many measures of memory and global level of social and vocational functioning within the discordant group were also found. Thus difficulties in rapidly acquiring new information and propitiously retrieving old information may burden patients with schizophrenia in man of the transactions of everyday life. RP GOLDBERG, TE (reprint author), NIMH, NEUROSCI CTR ST ELIZABETHS, CLIN BRAIN DISORDERS BRANCH, WASHINGTON, DC 20032 USA. NR 82 TC 161 Z9 162 U1 2 U2 7 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD FEB PY 1993 VL 23 IS 1 BP 71 EP 85 PG 15 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA KT521 UT WOS:A1993KT52100009 PM 8475218 ER PT J AU HAERTZEN, C COVI, L BUXTON, K RICHARDS, H AF HAERTZEN, C COVI, L BUXTON, K RICHARDS, H TI SEASONAL-CHANGES IN RULE INFRACTIONS AMONG PRISONERS - A PRELIMINARY TEST OF THE TEMPERATURE-AGGRESSION HYPOTHESIS SO PSYCHOLOGICAL REPORTS LA English DT Article ID AMBIENT-TEMPERATURE; COLLECTIVE VIOLENCE; MANIA; HEAT AB To test the temperature-aggression hypothesis, seasonal changes in aggression as indexed by reported rule infractions were studied for prisoners located at the Patuxent Institution, Jessup, Maryland. 5383 reports of rule infractions occurred between July 1987 and March 1991. Rule infractions occurred more frequently during the hot summer months than the three other seasons of the year. This summer effect, though significant, is only a few percent above a theoretical chance level based on the number of days comprising the seasons. A much stronger monthly effect over 45 months was found, but the bases of erratic fluctuations are not known. C1 STATE MARYLAND DEPT PUBL SAFETY & CORRECT SERV,PATUXENT INST,JESSUP,MD. RP HAERTZEN, C (reprint author), NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 15 TC 8 Z9 8 U1 1 U2 4 PU PSYCHOLOGICAL REPORTS PI MISSOULA PA P O BOX 9229, MISSOULA, MT 59807 SN 0033-2941 J9 PSYCHOL REP JI Psychol. Rep. PD FEB PY 1993 VL 72 IS 1 BP 195 EP 200 PG 6 WC Psychology, Multidisciplinary SC Psychology GA KV528 UT WOS:A1993KV52800038 PM 8451356 ER PT J AU GARCHA, HS THOMAS, P SPIVAK, CE WONNACOTT, S STOLERMAN, IP AF GARCHA, HS THOMAS, P SPIVAK, CE WONNACOTT, S STOLERMAN, IP TI BEHAVIORAL AND LIGAND-BINDING STUDIES IN RATS WITH 1-ACETYL-4-METHYLPIPERAZINE, A NOVEL NICOTINIC AGONIST SO PSYCHOPHARMACOLOGY LA English DT Article DE NICOTINE; 1-ACETYL-4-METHYLPIPERAZINE; MECAMYLAMINE; DMPP; LIGAND BINDING; LOCOMOTOR ACTIVITY; DRUG DISCRIMINATION ID LOCOMOTOR-ACTIVITY; TOLERANT RATS; ISOARECOLONE; RECEPTORS; EXPOSURE; ANALOGS; SITES AB The novel nicotinic agonist 1-acetyl-4-methyl-piperazine (AMP) has been studied in ligand-binding and behavioural studies. AMP methiodide potently inhibited [H-3]-(-)-nicotine and [I-125]-alpha-bungarotoxin binding to P2 membranes from rat brain and [I-125]-alpha-bungarotoxin binding to rat skeletal muscles. AMP HCl also inhibited nicotinic binding, but it was 100 times less potent than AMP methiodide. In behavioural studies, AMP HCl reduced locomotor activity of experimentally naive rats and mecamylamine blocked this effect. In rats receiving (-)-nicotine chronically, AMP HCl did not increase locomotor activity consistently or to the same extent as (-)-nicotine. In rats trained to discriminate (-)-nicotine from saline in a two-bar operant conditioning procedure with food reinforcement, there was generalization to AMP HCl, but only at doses that reduced the overall rate of responding. The potency and effectiveness of AMP relative to (-)-nicotine varied across the different behavioural procedures. The results suggest that the pharmacodynamic action of AMP differs from that of (-)-nicotine and that it usefully extends the range of agonists that can be used as probes for central nicotinic mechanisms. C1 INST PSYCHIAT,DEPT PSYCHIAT,DE CRESPIGNY PK,LONDON SE5 8AF,ENGLAND. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. UNIV BATH,DEPT BIOCHEM,BATH BA2 7AY,AVON,ENGLAND. NR 19 TC 11 Z9 11 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 FEB PY 1993 VL 110 IS 3 BP 347 EP 354 DI 10.1007/BF02251292 PG 8 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA KL525 UT WOS:A1993KL52500014 PM 7831430 ER PT J AU KEMPNER, ES AF KEMPNER, ES TI DAMAGE TO PROTEINS DUE TO THE DIRECT ACTION OF IONIZING-RADIATION SO QUARTERLY REVIEWS OF BIOPHYSICS LA English DT Article ID MUSCLE SARCOPLASMIC-RETICULUM; TARGET SIZE ANALYSIS; INACTIVATION ANALYSIS; SKELETAL-MUSCLE; OLIGOMERIC STRUCTURE; MOLECULAR-WEIGHT; FUNCTIONAL UNIT; ENERGY-TRANSFER; 3-HYDROXY-3-METHYLGLUTARYL COENZYME; ASSIMILATORY NADH RP NIAMSD, BETHESDA, MD 20892 USA. NR 72 TC 40 Z9 40 U1 2 U2 5 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0033-5835 EI 1469-8994 J9 Q REV BIOPHYS JI Q. Rev. Biophys. PD FEB PY 1993 VL 26 IS 1 BP 27 EP 48 PG 22 WC Biophysics SC Biophysics GA LT397 UT WOS:A1993LT39700002 PM 8210312 ER PT J AU ZIGUN, JR FRANK, JA BARRIOS, FA JONES, DW FOO, TKF MOONEN, CTW PRESS, DZ WEINBERGER, DR AF ZIGUN, JR FRANK, JA BARRIOS, FA JONES, DW FOO, TKF MOONEN, CTW PRESS, DZ WEINBERGER, DR TI MEASUREMENT OF BRAIN ACTIVITY WITH BOLUS ADMINISTRATION OF CONTRAST AGENT AND GRADIENT-ECHO MR IMAGING SO RADIOLOGY LA English DT Article DE BLOOD, VOLUME; BRAIN, FUNCTION; BRAIN, MR; BRAIN, WHITE MATTER; MAGNETIC RESONANCE (MR), RAPID IMAGING ID CEREBRAL BLOOD-FLOW; TOMOGRAPHY; CORTEX AB This study was performed to measure changes in cerebral blood volume (CBV) associated with visual activation by use of bolus administration of contrast agent and conventional, clinically configured magnetic resonance (MR) hardware and software. Fast gradient-recalled acquisition in the steady state technique was used to study five healthy subjects during visual activation and a control dark state. MR images were obtained every 2.048 seconds for 2 minutes. A bolus of gadopentetate dimeglumine was injected during visual stimulation and darkness. Cine images produced from the series of rapid images clearly depicted arterial, capillary, and venous phases. Analysis of serial concentration maps derived from the rapid images revealed expected differences between the relative CBV of gray matter and that of white matter, as well as significantly increased relative CBV in calcarine cortex during visual activation versus the control state (mean increase, 15.24%; range, 6.41%-27.78%; P < .05). These results confirm those reported in echo-planar imaging studies and demonstrate that brain function can be assessed with the bolus method by means of MR imaging hardware and software with conventional clinical configurations. C1 NIMH,NEUROSCI CTR ST ELIZABETHS,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032. GE MED SYST,MILWAUKEE,WI. NIH,DIAGNOST RADIOL RES PROGRAM,BETHESDA,MD 20892. NIH,IN VIVO NMR RES CTR,BIOMED ENGN INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NIH,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. RI Barrios, Fernando/B-4295-2012; Barrios, Fernando/D-1591-2016; Moonen, Chrit/K-4434-2016 OI Barrios, Fernando/0000-0002-5699-4222; Moonen, Chrit/0000-0001-5593-3121 NR 14 TC 31 Z9 32 U1 0 U2 2 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD FEB PY 1993 VL 186 IS 2 BP 353 EP 356 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA KH843 UT WOS:A1993KH84300015 PM 8421733 ER PT J AU LOCKSHIN, MD AF LOCKSHIN, MD TI WHICH PATIENTS WITH ANTIPHOSPHOLIPID ANTIBODY SHOULD BE TREATED AND HOW SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; RECURRENT PREGNANCY LOSS; ANTICARDIOLIPIN ANTIBODIES; FETAL DEATH; CLINICAL-SIGNIFICANCE; ANTICOAGULANT; DISEASE; THROMBOCYTOPENIA; ASSOCIATION; CARDIOLIPIN RP LOCKSHIN, MD (reprint author), NIAMSD,EXTRAMURAL PROGRAM,BLDG 31,ROOM 4C-32,BETHESDA,MD 20892, USA. NR 46 TC 44 Z9 46 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-857X J9 RHEUM DIS CLIN N AM JI Rheum. Dis. Clin. North Am. PD FEB PY 1993 VL 19 IS 1 BP 235 EP 247 PG 13 WC Rheumatology SC Rheumatology GA LA281 UT WOS:A1993LA28100018 PM 8356257 ER PT J AU KLIPPEL, JH AF KLIPPEL, JH TI IS AGGRESSIVE THERAPY EFFECTIVE FOR LUPUS SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID INTRAVENOUS GAMMA-GLOBULIN; TOTAL LYMPHOID IRRADIATION; NON-HODGKINS LYMPHOMA; RHEUMATOID-ARTHRITIS; CYCLOPHOSPHAMIDE THERAPY; PULSE CYCLOPHOSPHAMIDE; ERYTHEMATOSUS; NEPHRITIS; BLADDER; PATIENT RP KLIPPEL, JH (reprint author), NIAMSD,BLDG 10,ROOM 9N 228,BETHESDA,MD 20892, USA. NR 64 TC 20 Z9 20 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-857X J9 RHEUM DIS CLIN N AM JI Rheum. Dis. Clin. North Am. PD FEB PY 1993 VL 19 IS 1 BP 249 EP 261 PG 13 WC Rheumatology SC Rheumatology GA LA281 UT WOS:A1993LA28100019 PM 8356258 ER PT J AU BACON, BR FRIED, MW DIBISCEGLIE, AM AF BACON, BR FRIED, MW DIBISCEGLIE, AM TI A 39-YEAR-OLD MAN WITH CHRONIC HEPATITIS, ELEVATED SERUM FERRITIN VALUES, AND A FAMILY HISTORY OF HEMOCHROMATOSIS SO SEMINARS IN LIVER DISEASE LA English DT Review ID TRANSFERRIN-BOUND IRON; IDIOPATHIC HEMOCHROMATOSIS; RAT-LIVER; B VIRUS; EXPRESSION; RECEPTOR; DISEASE; PLASMA; CLEARANCE; OVERLOAD C1 NIDDKD,HEPATITIS STUDIES SECT,BETHESDA,MD. RP BACON, BR (reprint author), ST LOUIS UNIV,SCH MED,DEPT INTERNAL MED,DIV GASTROENTEROL & HEPATOL,POB 15250,ST LOUIS,MO 63110, USA. NR 31 TC 12 Z9 12 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0272-8087 J9 SEMIN LIVER DIS JI Semin. Liver Dis. PD FEB PY 1993 VL 13 IS 1 BP 101 EP 105 DI 10.1055/s-2007-1007342 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA KQ458 UT WOS:A1993KQ45800011 PM 8446904 ER PT J AU SZNOL, M LONGO, DL AF SZNOL, M LONGO, DL TI CHEMOTHERAPY DRUG-INTERACTIONS WITH BIOLOGICAL AGENTS SO SEMINARS IN ONCOLOGY LA English DT Review ID TUMOR-NECROSIS-FACTOR; ADVANCED COLORECTAL-CARCINOMA; PHASE-I TRIAL; METASTATIC MALIGNANT-MELANOMA; LEUKOCYTE-A INTERFERON; SMALL-CELL LUNG; SYNERGISTIC ANTITUMOR-ACTIVITY; LOW-DOSE CYCLOPHOSPHAMIDE; HUMAN INTERLEUKIN 1-ALPHA; COLON-CARCINOMA C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BETHESDA,MD 20892. RP SZNOL, M (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,INVEST DRUG BRANCH,BETHESDA,MD 20892, USA. NR 134 TC 19 Z9 19 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 FEB PY 1993 VL 20 IS 1 BP 80 EP 93 PG 14 WC Oncology SC Oncology GA KM971 UT WOS:A1993KM97100010 PM 8475413 ER PT J AU LINDHOLM, PF KASHANCHI, F BRADY, JN AF LINDHOLM, PF KASHANCHI, F BRADY, JN TI TRANSCRIPTIONAL REGULATION IN THE HUMAN RETROVIRUS HTLV-1 SO SEMINARS IN VIROLOGY LA English DT Article DE HTLV-1; TAX1; TRANSCRIPTION; TRANSACTIVATION; CYTOKINE ID CELL LEUKEMIA-VIRUS; LONG-TERMINAL-REPEAT; NF-KAPPA-B; COLONY-STIMULATING FACTOR; DNA-BINDING PROTEINS; I TAX GENE; INTERLEUKIN-2 RECEPTOR; RESPONSIVE ELEMENT; TRANS-ACTIVATION; NUCLEAR PROTEINS RP LINDHOLM, PF (reprint author), NCI,MOLEC VIROL LAB,BETHESDA,MD 20892, USA. NR 86 TC 22 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 1044-5773 J9 SEMIN VIROL JI Semin. Virol. PD FEB PY 1993 VL 4 IS 1 BP 53 EP 60 DI 10.1016/1044-5773(93)80008-C PG 8 WC Virology SC Virology GA KW238 UT WOS:A1993KW23800007 ER PT J AU DERSE, D CARROLL, R CARVALHO, M AF DERSE, D CARROLL, R CARVALHO, M TI TRANSCRIPTIONAL REGULATION OF EQUINE INFECTIOUS-ANEMIA VIRUS SO SEMINARS IN VIROLOGY LA English DT Article DE EIAV; TAT; TRANSCRIPTIONAL REGULATION; DNA-BINDING PROTEINS; LONG TERMINAL REPEAT ID LONG TERMINAL REPEAT; HIV-1 TAT; TRANS-ACTIVATION; PERSISTENT INFECTION; MUTATIONAL ANALYSIS; FUNCTIONAL DOMAINS; GENE-EXPRESSION; LENTIVIRUS TAT; RNA; PROTEIN RP DERSE, D (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. NR 40 TC 9 Z9 12 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 1044-5773 J9 SEMIN VIROL JI Semin. Virol. PD FEB PY 1993 VL 4 IS 1 BP 61 EP 68 DI 10.1016/1044-5773(93)80009-D PG 8 WC Virology SC Virology GA KW238 UT WOS:A1993KW23800008 ER PT J AU KAFADAR, K KARON, JM AF KAFADAR, K KARON, JM TI AN ANALYSIS OF AIDS INCIDENCE DATA BY CLUSTERING TRENDS SO STATISTICS IN MEDICINE LA English DT Article ID FUTURE-TRENDS; UNITED-STATES; EPIDEMIC AB AIDS incidence trends vary greatly among geographic areas in the United States. We define clusters of areas within which AIDS incidence trends are similar, as areas within a cluster may have similar human immunodeficiency virus epidemic patterns and thus may lead to similar prevention/intervention strategies. Methods of exploratory data analysis are used to define such clusters from reported quarterly AIDS incidence to December 1990 (adjusted for estimated reporting delays) in homosexual and bisexual men not using intravenous drugs in 39 metropolitan statistical areas (MSAs) in the United States. After smoothing AIDS incidence in each MSA, we define groups from cluster analysis based on a measure of similarity between pairs of MSAs. A log-linear model gives estimates of the scale factors and the common trend for the MSAs in each group. Alternative metrics and simulated data suggest that the clustering is fairly robust to variations in AIDS incidence data. The resulting clusters separate MSAs with different trends, for example, MSAs in which AIDS incidence shows signs of reaching a plateau are separated from MSAs in which incidence continues to increase rapidly. C1 NATL CTR INFECT DIS,CTR DIS CONTROL,DIV HIV AIDS E-48,ATLANTA,GA 30333. RP KAFADAR, K (reprint author), NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892, USA. NR 24 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD FEB PY 1993 VL 12 IS 3-4 BP 311 EP 326 DI 10.1002/sim.4780120314 PG 16 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA KN880 UT WOS:A1993KN88000012 PM 8456214 ER PT J AU FERRUCCI, L BANDINELLI, S GURALNIK, JM LAMPONI, M BERTINI, C FALCHINI, M BARONI, A AF FERRUCCI, L BANDINELLI, S GURALNIK, JM LAMPONI, M BERTINI, C FALCHINI, M BARONI, A TI RECOVERY OF FUNCTIONAL STATUS AFTER STROKE - A POSTREHABILITATION FOLLOW-UP-STUDY SO STROKE LA English DT Article DE NEURONAL DAMAGE; REHABILITATION; STROKE ID REHABILITATION; DISABILITY; OUTCOMES; PERFORMANCE; SURVIVAL; PATIENT; NEED AB Background and Purpose: Information on predictors of long-term change in functional capacity after a rehabilitation program in stroke patients is scant. This study describes the long-term evolution of self-reported functional ability after discharge from rehabilitation and its relation with age, level of neural impairment at discharge, and changes in neural impairment during follow-up. Methods. Fifty patients (31 men and 19 women; mean +/- SD age, 66.0 +/- 9.9 years; range, 47-86 years) with a first unilateral stroke and no severe cognitive impairment were consecutively enrolled. Self-reported disability in activities of daily living and neural impairment measured by the Fugl-Meyer Scale were evaluated after discharge from a rehabilitation program and 3 and 6 months later. Results: Functional disability was significantly reduced after 3 and 6 months. Attenuation of disability occurred mainly among those patients with more severe baseline neural impairment. In this group, patients aged greater-than-or-equal-to 65 years were more disabled at baseline than younger individuals, but they had the same rate of improvement. In patients aged < 65 years, changes in disability over time could be attributed to changes in neural function, whereas older patients' functional recovery was greater than that expected from their improvement in neural impairment alone. Conclusions: These results suggest that in stroke patients with severe neural damage further functional improvement occurs even after completion of a rehabilitation program. There is evidence that older patients may be more likely to employ compensatory strategies to overcome some of the neural impairment that remains after stroke. C1 NATL INST AGING,7201 WISCONSIN AVE,GATEWAY BLDG,SUITE 3C309,BETHESDA,MD 20892. NATL INST RES & CARE ELDERLY,DEPT GERIATR,FLORENCE,ITALY. NR 35 TC 83 Z9 85 U1 0 U2 4 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD FEB PY 1993 VL 24 IS 2 BP 200 EP 205 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA KJ944 UT WOS:A1993KJ94400003 PM 8421819 ER PT J AU YONEMOTO, J SHIRAISHI, H SOMA, Y AF YONEMOTO, J SHIRAISHI, H SOMA, Y TI INVITRO ASSESSMENT OF TERATOGENIC POTENTIAL OF ORGANOTIN COMPOUNDS USING RAT EMBRYO LIMB BUD CELL-CULTURES SO TOXICOLOGY LETTERS LA English DT Article DE ORGANOTIN COMPOUNDS; TRI-N-BUTYLTIN; DI-N-BUTYLTIN; LIMB BUD CELL CULTURE; TERATOGENICITY SCREEN ID TRIBUTYLTIN; BIS(TRI-NORMAL-BUTYLTIN)OXIDE; ACCUMULATION; METABOLISM; CHEMISTRY; TBTO; TIN AB Assessment of the relative teratogenic potential of bis(tri-n-butyltin)oxide (TBTO), tri-n-butyltin chloride (TBT), and its metabolites, i.e., (3-OH)hydroxybutyl dibutyltin chloride ((3-OH-Bu)DBT), di-n-butyltin dichloride (DBT), and butyltin trichloride (MBT) have been conducted using rat embryo limb bud cell cultures (LBC) to gain some knowledge of TBT embryotoxicity and DBT teratogenicity. Triphenyltin chloride (TPT), trimethyltin chloride (TMT), and triethyltin bromide (TET) have also been tested to obtain data for validation of LBC as a teratogen prescreening for organotin compounds. Fifty percent inhibition concentration for cell proliferation (IP50), and for cell differentiation (ID50), and the ratio of the former to the latter (P/D ratio) were obtained. The ID50 values in increasing order were as follows; TPT, DBT < TBT, TBTO < (3-OH-Bu)DBT < TET < TMT much less than MBT. With the exception of MBT, organotin compounds tested were very strong inhibitors of cell differentiation (ID50; 0.13-1.71 muM) and cell proliferation (IP50; 0.12-2.81 muM). P/D ratios for TBT, (3-OH-Bu)DBT, DBT and MBT were 1.0, 1.43, 1.32 and 1.08, respectively. These results suggest that the proximal toxin of DBT teratogenicity is DBT itself, and TBT is rather embryocidal than teratogenic so that TBT might mask the teratogenic and/or fetotoxic effects of its metabolites. RP YONEMOTO, J (reprint author), NIEHS,DIV REG & COMMUNITY ENVIRONM,CHEM EXPOSURE & HLTH EFFECTS RES TEAM,16-2 ONOGAWA,TSUKUBA,IBARAKI 305,JAPAN. NR 28 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0378-4274 J9 TOXICOL LETT JI Toxicol. Lett. PD FEB PY 1993 VL 66 IS 2 BP 183 EP 191 PG 9 WC Toxicology SC Toxicology GA KM774 UT WOS:A1993KM77400008 PM 8430438 ER PT J AU HIRSCH, F PONCET, P FREEMAN, S GRESS, RE SACHS, DH DRUET, P HIRSCH, R AF HIRSCH, F PONCET, P FREEMAN, S GRESS, RE SACHS, DH DRUET, P HIRSCH, R TI ANTIFECTION - A NEW METHOD FOR TARGETED GENE TRANSFECTION SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID CELLS; MOUSE C1 CHILDRENS HOSP MED CTR,DIV RHEUMATOL,ELLAND & BETHESDA AVES,CINCINNATI,OH 45229. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,BOSTON,MA. TULANE UNIV,NEW ORLEANS,LA 70118. HOP BROUSSAIS,INSERM,U28,F-75674 PARIS 14,FRANCE. NR 5 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 138 EP 139 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100047 PM 8438253 ER PT J AU EMERY, DW SMITH, CV SHAFER, GE KARSON, EM SACHS, DH LEGUERN, C AF EMERY, DW SMITH, CV SHAFER, GE KARSON, EM SACHS, DH LEGUERN, C TI EXPRESSION OF ALLOGENEIC CLASS-II CDNA IN SWINE PERIPHERAL-BLOOD MONONUCLEAR-CELLS FOLLOWING RETROVIRAL-MEDIATED GENE-TRANSFER INTO BONE-MARROW SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID TRANSPLANTATION C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. NHLBI,BETHESDA,MD 20892. NR 7 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 140 EP 141 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100048 PM 7679808 ER PT J AU SACHS, DH BODINE, DM MOULTON, AD PEARSON, DA NIENHUIS, AW SYKES, M AF SACHS, DH BODINE, DM MOULTON, AD PEARSON, DA NIENHUIS, AW SYKES, M TI TOLERANCE INDUCTION USING AUTOLOGOUS BONE-MARROW MODIFIED WITH AN ALLOGENEIC CLASS-I MHC GENE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID TRANSPLANTS C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. RP SACHS, DH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,MGH E,BLDG 149,BOSTON,MA 02129, USA. FU PHS HHS [N01-H1-19054] NR 5 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 348 EP 349 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100128 PM 8438329 ER PT J AU SMITH, CV FISHBEIN, J NAKAJIMA, K ROSENGARD, BR GUZZETTA, PC SACHS, DH AF SMITH, CV FISHBEIN, J NAKAJIMA, K ROSENGARD, BR GUZZETTA, PC SACHS, DH TI EFFECT OF TOLERANCE TO ALLOGENEIC MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS ON REJECTION ACROSS MINOR ANTIGEN DIFFERENCES SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC, SANDOZ PHARMA, ORTHO CILAG PHARM, FUJISAW PHARM, UPJOHN, FRESENIUS, PASTEUR MERIEUX, SYNTEX INT, HOSPAL, DUPONT MERCK PHARM ID MINIATURE SWINE; TRANSPLANTATION C1 NCI,TRANSPLANTAT BIOL SECT,IMMUNOL BRANCH,BETHESDA,MD 20892. RP SMITH, CV (reprint author), MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH,BOSTON,MA 02129, USA. FU NIAID NIH HHS [IF32 AI08577-01, 5 R01 AI31046-02] NR 7 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 364 EP 365 PN 1 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN621 UT WOS:A1993KN62100136 PM 8438337 ER PT J AU SYKES, M ABRAHAM, VS HARTY, MW PEARSON, DA AF SYKES, M ABRAHAM, VS HARTY, MW PEARSON, DA TI SELECTIVE-INHIBITION OF CD4 GRAFT-VERSUS-HOST ACTIVITY IN IL-2-TREATED MICE SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT JEAN HAMBURGER MEMORIAL CONGRESS / 14TH INTERNATIONAL CONGRESS OF THE TRANSPLANTATION SOC CY AUG 16-21, 1992 CL PARIS, FRANCE SP TRANSPLANTAT SOC ID DISEASE C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. RP SYKES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,TRANSPLANTAT BIOL RES CTR,MGH-E,BLDG 149,BOSTON,MA 02129, USA. FU NCI NIH HHS [R01CA55290]; NIAID NIH HHS [R01AI31158] NR 6 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD FEB PY 1993 VL 25 IS 1 BP 1225 EP 1226 PN 2 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA KN622 UT WOS:A1993KN62200159 PM 8442096 ER PT J AU MENNITI, FS OLIVER, KG PUTNEY, JW SHEARS, SB AF MENNITI, FS OLIVER, KG PUTNEY, JW SHEARS, SB TI INOSITOL PHOSPHATES AND CELL SIGNALING - NEW VIEWS OF INSP5 AND INSP6 SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Review ID MYOINOSITOL 1,3,4,5,6-PENTAKISPHOSPHATE; AVIAN ERYTHROCYTES; ACINAR-CELLS; PENTAKISPHOSPHATE; METABOLISM; 3,4,5,6-TETRAKISPHOSPHATE; 1,3,4,6-TETRAKISPHOSPHATE; 1,4,5,6-TETRAKISPHOSPHATE; 1,3,4-TRISPHOSPHATE; TETRAKISPHOSPHATES AB Ins(1,3,4,5,6)P5 and InsP6 comprise the bulk of the inositol phosphate content of mammalian cells, but their intracellular functions are unknown. Until recently it seemed that these compounds were metabolically lethargic; this has diverted attention away from their possible role in short-term regulation of physiological processes. Interest in the idea that these polyphosphates play more dynamic roles is now increasing, following recent demonstrations that they are precursors of several inositol phosphates that turnover rapidly. C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,INOSITOL LIPID SECT,RES TRIANGLE PK,NC 27709. NIEHS,CALCIUM REGULAT SECT,RES TRIANGLE PK,NC 27709. RP MENNITI, FS (reprint author), PFIZER INC,CENT RES,EASTERN POINT RD,GROTON,CT 06340, USA. NR 33 TC 124 Z9 124 U1 1 U2 4 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 FEB PY 1993 VL 18 IS 2 BP 53 EP 56 DI 10.1016/0968-0004(93)90053-P PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KN139 UT WOS:A1993KN13900007 PM 8387704 ER PT J AU WISE, SP AF WISE, SP TI MONKEY MOTOR CORTEX - MOVEMENTS, MUSCLES, MOTONEURONS AND METRICS SO TRENDS IN NEUROSCIENCES LA English DT Editorial Material ID PRIMATE CORTICOMOTONEURONAL CELLS; ARM MOVEMENTS; CORTICOSPINAL NEURONS; RHESUS-MONKEYS; PRECISION GRIP; TASK; FACILITATION; DIRECTION; SPACE; FORCE RP WISE, SP (reprint author), NIMH,NEUROPHYSIOL LAB,POOLESVILLE,MD 20837, USA. NR 28 TC 23 Z9 23 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD FEB PY 1993 VL 16 IS 2 BP 46 EP 49 DI 10.1016/0166-2236(93)90014-D PG 4 WC Neurosciences SC Neurosciences & Neurology GA KK011 UT WOS:A1993KK01100003 PM 7680498 ER PT J AU LEAPMAN, RD HUNT, JA BUCHANAN, RA ANDREWS, SB AF LEAPMAN, RD HUNT, JA BUCHANAN, RA ANDREWS, SB TI MEASUREMENT OF LOW CALCIUM CONCENTRATIONS IN CRYOSECTIONED CELLS BY PARALLEL-EELS MAPPING SO ULTRAMICROSCOPY LA English DT Article ID CRYO-ELECTRON-MICROSCOPY; ENERGY-LOSS SPECTROMETRY; LOSS SPECTRA; MICROANALYSIS; SPECTROSCOPY; SECTIONS; STEM AB Electron energy loss spectroscopy (EELS) in the scanning transmission electron microscope provides a high sensitivity for microanalysis of certain important biological elements such as calcium whose physiological concentrations in cells are rather low. Application of parallel-EELS mapping to the analysis of freeze-dried cryosections of rapidly frozen tissue provides a means of detecting small amounts of calcium in structures with diameter approximately 50 nm. Detector pattern noise due to channel gain variations can be reduced by acquiring difference spectra at each pixel. By segmenting nitrogen maps that reflect the structure through the protein distribution it is possible to sum spectra from specific compartments. These are then processed by fitting reference spectra for the Ca L23-edge and the carbon background. It has been found that useful data can be collected at 100 keV beam energy from freeze-dried cryosections of cerebellar cortex cut to nominal thickness of 100 nm. The analysis results in a sensitivity of +/- 0.4 mmol Ca/kg dry weight with a total acquisition time of 400 s, a significant improvement over that achievable with energy-dispersive X-ray spectroscopy. C1 NINCDS, LAB, BETHESDA, MD 20892 USA. NINCDS, NEUROBIOL LAB, BETHESDA, MD 20892 USA. LEHIGH UNIV, DEPT MAT SCI & ENGN, BETHLEHEM, PA 18015 USA. RP LEAPMAN, RD (reprint author), NIH, NCRR, BIOMED ENGN & INSTRUMENTAT PROGRAM, BETHESDA, MD 20892 USA. NR 41 TC 42 Z9 42 U1 1 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3991 EI 1879-2723 J9 ULTRAMICROSCOPY JI Ultramicroscopy PD FEB PY 1993 VL 49 IS 1-4 BP 225 EP 234 DI 10.1016/0304-3991(93)90229-Q PG 10 WC Microscopy SC Microscopy GA KV567 UT WOS:A1993KV56700024 PM 8475601 ER PT J AU TERLAAK, EA TULLY, JG NOORDERGRAAF, HH ROSE, DL CARLE, P BOVE, JM SMITS, MA AF TERLAAK, EA TULLY, JG NOORDERGRAAF, HH ROSE, DL CARLE, P BOVE, JM SMITS, MA TI RECOGNITION OF MYCOPLASMA-CANIS AS PART OF THE MYCOPLASMAL FLORA OF THE BOVINE RESPIRATORY-TRACT SO VETERINARY MICROBIOLOGY LA English DT Article AB Mycoplasma strain C3b was isolated in the Netherlands from the lung of a pneumonic calf. Forty similar strains were isolated afterwards from calves in 19 other herds in different parts of the Netherlands. Eight strains from eight different herds were investigated in this study. Results of tests to determine whether the organism catabolized glucose were inconclusive. Four strains, including strain C3b, apparently catabolized glucose under some test conditions; the remaining four strains did not. Although strain C3b and similar strains were slightly different from canine M. canis strains in growth inhibition tests and glucose metabolism tests, we concluded that strain C3b and similar strains have to be classified as M. canis. A close contact between calves and dogs was observed in several herds where strain C3b or similar strains were isolated. This is the first report of M. canis isolated from cattle. C1 NIAID,FREDERICK CANC RES FACIL,MYCOPLASMA SECT,MOLEC MICROBIOL LAB,FREDERICK,MD 21701. INRA,BIOL CELLULAIRE & MOLEC LAB,F-33140 PONT DE LA MAYE,FRANCE. CENT VET INST,DEPT MOLEC BIOL,LELYSTAD,NETHERLANDS. RP TERLAAK, EA (reprint author), CENT VET INST,DEPT BACTERIOL,POB 65,8200 AB LELYSTAD,NETHERLANDS. RI smits, mari/J-4892-2013 OI smits, mari/0000-0002-3493-291X NR 26 TC 12 Z9 12 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 FEB PY 1993 VL 34 IS 2 BP 175 EP 189 DI 10.1016/0378-1135(93)90171-3 PG 15 WC Microbiology; Veterinary Sciences SC Microbiology; Veterinary Sciences GA KP136 UT WOS:A1993KP13600007 PM 8451833 ER PT J AU LEONMONZON, M SORIANO, V ESCUDERO, D GONZALEZLAHOZ, J AF LEONMONZON, M SORIANO, V ESCUDERO, D GONZALEZLAHOZ, J TI SEROLOGIC REACTIVITY VERSUS RETROVIRUS IN PATIENTS WITH SJOGRENS-SYNDROME SO MEDICINA CLINICA LA Spanish DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; HUMAN-IMMUNODEFICIENCY-VIRUS; EPSTEIN-BARR-VIRUS; MULTIPLE-SCLEROSIS; ANTIBODIES; EXOCRINOPATHY; POLYMYOSITIS; INFECTION; PROTEINS; COMPLEX AB BACKGROUND: The primary Sjogren's syndrome (SS) is a systemic disease which destroys the exocrine glands by autoimmune mechanisms. The etiology of this syndrome is unknown although different virus are involved in its genesis. METHODs: The presence of serologic reactivity IgG and IgM versus the human immunodeficiency virus (HIV-1), HIV-2, HTLV-I and HTLV-II were studied in 14 patients with SS and in 15 controls. Likewise, the presence of retroviral genomic sequences was analyzed in 7 of these patients by polymerase chain reaction (PCR). RESULTS: All the patients with SS were negative by enzymoimmunoassay (EIA) versus known retrovirus. However, more than 70 % presented reactivity versus different nuclear proteins, particularly versus p24 of HTLV-I in Western blot (WB). These results were negative in the control group. Genomic analysis by PCR did not confirm the presence of specific sequences in any of the known human retroviruses in the patients with SS, nonetheless, in 3 of the 7 samples analyzed by PCR, related retroviral sequences were detected. CONCLUSIONs: The presence of serologic reactivity in Western blot versus some viral proteins and the similarity of genomic sequences in some cases suggests that a retrovirus related with those which are currently known, particularly with the HTLV-I, may be involved in the genesis of Sjogren's syndrome. C1 INST SALUD CARLOS 3,CTR INVEST CLIN,SERV ENFERMEDADES INFECCIOSAS,RAFAEL CALVO 7,2-A,E-28010 MADRID,SPAIN. NINCDS,MED NEUROL BRANCH,EE,UU,BETHESDA,MD 20892. HOSP GERMANS TRIAS & PUJOL,SERV NEUROL,BARCELONA,SPAIN. NR 35 TC 2 Z9 2 U1 0 U2 0 PU EDICIONES DOYMA S/A PI BARCELONA PA TRAV DE GRACIA 17-21, 08021 BARCELONA, SPAIN SN 0025-7753 J9 MED CLIN-BARCELONA JI Med. Clin. PD JAN 30 PY 1993 VL 100 IS 4 BP 121 EP 124 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA KL153 UT WOS:A1993KL15300001 PM 8095086 ER PT J AU WANG, XJ AF WANG, XJ TI GENESIS OF BURSTING OSCILLATIONS IN THE HINDMARSH-ROSE MODEL AND HOMOCLINICITY TO A CHAOTIC SADDLE SO PHYSICA D-NONLINEAR PHENOMENA LA English DT Article ID SYSTEMS; SINKS AB We present two hypotheses on the mathematical mechanism underlying bursting dynamics in a class of differential systems: (1) that the transition from continuous firing of spikes to bursting is caused by a crisis which destabilizes a chaotic state of continuous spiking; and (2) that the bursting corresponds to a homoclinicity to this unstable chaotic state. These propositions are supported by a numerical test on the Hindmarsh-Rose model, a prototype of its kind. We conclude by a unified view for three types of complex multi-modal oscillations: homoclinic systems, bursting, and the Pomeau-Manneville intermittency. C1 UNIV CHICAGO, JAMES FRANCK INST, CHICAGO, IL 60637 USA. UNIV CHICAGO, DEPT MATH, CHICAGO, IL 60637 USA. RP WANG, XJ (reprint author), NIDDK, MATH RES BRANCH, BETHESDA, MD 20892 USA. RI Wang, Xiao-Jing/D-2722-2009 NR 34 TC 102 Z9 106 U1 2 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-2789 EI 1872-8022 J9 PHYSICA D JI Physica D PD JAN 30 PY 1993 VL 62 IS 1-4 BP 263 EP 274 DI 10.1016/0167-2789(93)90286-A PG 12 WC Mathematics, Applied; Physics, Multidisciplinary; Physics, Mathematical SC Mathematics; Physics GA KR114 UT WOS:A1993KR11400020 ER PT J AU ZHOU, SYJ KINGSLEY, LA TAYLOR, JMG CHMIEL, JS HE, DY HOOVER, DR SAAH, A FARZADEGAN, H MARGOLICK, J MCARTHUR, J PHAIR, JP CHMIEL, JS COHEN, B WESCH, J WOLINSKY, S RINALDO, CR GUPTA, P HO, M KINGSLEY, LA ANDERSON, R ZHOU, SYJ DETELS, R VISSCHER, BR DUDLEY, J FAHEY, JL GIORGI, JV IMAGAWA, D TAYLOR, J MUNOZ, A BACELLAR, H CAREY, V HOOVER, D JACOBSON, LP SU, S HE, DY VERMUND, S SCHRAGER, L KASLOW, RA VANRADEN, MJ AF ZHOU, SYJ KINGSLEY, LA TAYLOR, JMG CHMIEL, JS HE, DY HOOVER, DR SAAH, A FARZADEGAN, H MARGOLICK, J MCARTHUR, J PHAIR, JP CHMIEL, JS COHEN, B WESCH, J WOLINSKY, S RINALDO, CR GUPTA, P HO, M KINGSLEY, LA ANDERSON, R ZHOU, SYJ DETELS, R VISSCHER, BR DUDLEY, J FAHEY, JL GIORGI, JV IMAGAWA, D TAYLOR, J MUNOZ, A BACELLAR, H CAREY, V HOOVER, D JACOBSON, LP SU, S HE, DY VERMUND, S SCHRAGER, L KASLOW, RA VANRADEN, MJ TI A METHOD TO TEST FOR A RECENT INCREASE IN HIV-1 SEROCONVERSION INCIDENCE - RESULTS FROM THE MULTICENTER AIDS COHORT STUDY (MACS) SO STATISTICS IN MEDICINE LA English DT Article ID BOOTSTRAP CONFIDENCE-INTERVALS; FIELLER THEOREM; LIKELIHOOD; MEN AB We have formulated the problem of determining whether there has been an upturn in HIV-1 seroconversion incidence over the first five years of follow-up in the Multicenter AIDS Cohort Study (MACS) as that of locating the minimum of a quadratic regression or examination of two-knot piecewise spline models. Under a quadratic model, we propose a method to obtain a direct estimate and a bootstrap estimate for the location of the temporal turning point (local minimum) for HIV-1 seroconversion incidence and three methods to estimate confidence intervals for the location of the turning point for HIV seroconversion incidence: (1) Wald confidence interval estimate with or without log transformation assuming the asymptotic normality and applying the Delta method; (2) asymmetric confidence intervals using Fieller's Theorem and its modification; and (3) bootstrapping confidence intervals. Inferences for the temporal turning point based on Wald tests for a single regression term in a non-linear regression model were not reliable compared to inferences based on confidence intervals placed on calendar time. We present results using these different C1 UNIV PITTSBURGH, SCH PUBL HLTH, DEPT EPIDEMIOL, PITTSBURGH, PA 15213 USA. UNIV PITTSBURGH, GRAD SCH PUBL HLTH, PITTSBURGH, PA 15260 USA. UNIV CALIF LOS ANGELES, SCH PUBL HLTH, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH PUBL HLTH, DEPT BIOSTAT, LOS ANGELES, CA 90024 USA. NIAID, BETHESDA, MD 20892 USA. NORTHWESTERN UNIV, SCH MED, CTR CANC, BIOMETRY SECT, CHICAGO, IL 60611 USA. JOHNS HOPKINS UNIV, SCH HYG & PUBL HLTH, BALTIMORE, MD 21205 USA. NORTHWESTERN UNIV, HOWARD BROWN MEM CLIN, EVANSTON, IL 60201 USA. JOHNS HOPKINS UNIV, SCH PUBL HLTH, DEPT EPIDEMIOL, BALTIMORE, MD 21205 USA. RP ZHOU, SYJ (reprint author), UNIV PITTSBURGH, SCH AFRC, DEPT INFECT DIS & MICROBIOL, 200 MEYRAN AVE, SUITE 401, PITTSBURGH, PA 15213 USA. RI Wolinsky, Steven/B-2893-2012 FU NIAID NIH HHS [AI-72631, AI-72632, AI-72634] NR 22 TC 2 Z9 2 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0277-6715 J9 STAT MED JI Stat. Med. PD JAN 30 PY 1993 VL 12 IS 2 BP 153 EP 164 DI 10.1002/sim.4780120207 PG 12 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA KL743 UT WOS:A1993KL74300005 PM 8446810 ER PT J AU FREEDMAN, LS PARMAR, MKB BAKER, SG AF FREEDMAN, LS PARMAR, MKB BAKER, SG TI THE DESIGN OF OBSERVER AGREEMENT STUDIES WITH BINARY ASSESSMENTS SO STATISTICS IN MEDICINE LA English DT Article ID SUPERFICIAL BLADDER-CANCER; INTRAOBSERVER AB We discuss the design of observer agreement studies with binary assessments, with particular emphasis on the need for adequate sample size and the use of replicate observations. First, we present a method and tables for determining the sample size required for ensuring a desired precision for the estimate of the probability of disagreement between two observers. Second, for studies including replicate observations, we present a statistical model that allows estimation of the magnitude of within- and between-observer variation. We then derive sample sizes guaranteeing a specified precision for these estimates, present tables of these sample sizes and give examples of their use. C1 MRC,CANC TRIALS OFF,CAMBRIDGE CB2 2BB,ENGLAND. RP FREEDMAN, LS (reprint author), NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892, USA. NR 10 TC 19 Z9 19 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD JAN 30 PY 1993 VL 12 IS 2 BP 165 EP 179 DI 10.1002/sim.4780120208 PG 15 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA KL743 UT WOS:A1993KL74300006 PM 8446811 ER PT J AU HODIN, J WISTOW, G AF HODIN, J WISTOW, G TI 5'-RACE PCR OF MESSENGER-RNA FOR 3 TAXON-SPECIFIC CRYSTALLINS - FOR EACH GENE ONE PROMOTER CONTROLS BOTH LENS AND NONLENS EXPRESSION SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID ARGININOSUCCINATE LYASE GENE; DUCK LENS; STRUCTURAL PROTEIN; ALPHA-ENOLASE; EVOLUTION; ENZYME; DELTA-2-CRYSTALLIN; SEQUENCE C1 NEI,LMDB,MOLEC STRUCT & FUNCT SECT,6222,BETHESDA,MD 20892. NR 26 TC 10 Z9 10 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JAN 29 PY 1993 VL 190 IS 2 BP 391 EP 396 DI 10.1006/bbrc.1993.1060 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KK585 UT WOS:A1993KK58500012 PM 8427583 ER PT J AU SMITH, CJ KRALL, J MANGANIELLO, VC MOVSESIAN, MA AF SMITH, CJ KRALL, J MANGANIELLO, VC MOVSESIAN, MA TI CYTOSOLIC AND SARCOPLASMIC RETICULUM-ASSOCIATED LOW KM, CGMP-INHIBITED CAMP PHOSPHODIESTERASE IN MAMMALIAN MYOCARDIUM SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID CYCLIC-AMP PHOSPHODIESTERASE; NUCLEOTIDE PHOSPHODIESTERASE; CARDIAC-MUSCLE; VENTRICULAR MYOCARDIUM; CARDIOTONIC DRUGS; PHOSPHORYLATION; SUBCLASSES; PURIFICATION; ACTIVATION; BINDING C1 UNIV UTAH,MED CTR,DIV CARDIOL,50 N MED OR,SALT LAKE CITY,UT 84132. NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. SALT LAKE VET AFFAIRS MED CTR,DEPT INTERNAL MED,DIV CARDIOL,SALT LAKE CITY,UT. UNIV UTAH,SCH MED,SALT LAKE CITY,UT 84112. NR 19 TC 36 Z9 37 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 JAN 29 PY 1993 VL 190 IS 2 BP 516 EP 521 DI 10.1006/bbrc.1993.1078 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KK585 UT WOS:A1993KK58500030 PM 8381278 ER PT J AU ROWLAND, AS BAIRD, DD WEINBERG, CR AF ROWLAND, AS BAIRD, DD WEINBERG, CR TI NITROUS-OXIDE AND FERTILITY - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP ROWLAND, AS (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 2 TC 1 Z9 1 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 JAN 28 PY 1993 VL 328 IS 4 BP 284 EP 284 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KJ442 UT WOS:A1993KJ44200015 ER PT J AU ROSENBERG, PS GAIL, MH BIGGAR, RJ LEVY, ME MIXON, D AF ROSENBERG, PS GAIL, MH BIGGAR, RJ LEVY, ME MIXON, D TI HIV PREVALENCE AMONG WASHINGTON, DC, RESIDENTS HAVING ABORTIONS - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter C1 DIST COLUMBIA COMMISS PUBL HLTH,WASHINGTON,DC. RP ROSENBERG, PS (reprint author), NCI,ROCKVILLE,MD, USA. NR 3 TC 0 Z9 0 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 JAN 27 PY 1993 VL 269 IS 4 BP 472 EP 473 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KH385 UT WOS:A1993KH38500015 ER PT J AU HALL, WH AF HALL, WH TI TRIGLYCERIDE, HIGH-DENSITY-LIPOPROTEIN, AND CORONARY HEART-DISEASE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP HALL, WH (reprint author), NIH,OFF MED APPLICAT RES,FED BLDG,ROOM 618,BETHESDA,MD 20892, USA. NR 0 TC 197 Z9 198 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 JAN 27 PY 1993 VL 269 IS 4 BP 505 EP 510 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA KH385 UT WOS:A1993KH38500036 ER PT J AU NIMS, RW LUBET, RA JONES, CR MELLINI, DW THOMAS, PE AF NIMS, RW LUBET, RA JONES, CR MELLINI, DW THOMAS, PE TI COMPARATIVE PHARMACODYNAMICS OF CYP2B INDUCTION BY PHENOBARBITAL IN THE MALE AND FEMALE F344/NCR RAT SO BIOCHEMICAL PHARMACOLOGY LA English DT Note ID LIVER-MICROSOMES; HEPATIC CYTOCHROME-P-450; SEX; DEALKYLATION; DISTINGUISH; METABOLISM; ISOZYMES; FORMS; ASSAY; AGE AB The phenobarbital dose-CYP2B induction response relationships and pharmacodynamics of CYP2B induction have been characterized in female and male F344/NCr rats. The ED50 and EC50 values for the induction, by phenobarbital, of hepatic CYP2B1 or 2B1/2B2 protein or associated catalytic activities (benzyloxy- or pentoxyresorufin O-dealkylation or testosterone 16beta-hydroxylation) were 2- to 7-fold higher in the female than in the male rat, indicating a somewhat decreased potency for this effect in the female rat. In contrast, the maximal induction, expressed as the ratio of induced activity to control activity, was as great or greater in the female rat than in the male. Thus, any difference in the responsiveness of female rats to hepatic CYP2B induction by phenobarbital, compared to male rats, is reflected in potency but not degree of induction of catalytic activity or immunoreactive protein. C1 BCDP & CSAL PROGRAM RESOURCES INC DYNCORP,NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. RUTGERS STATE UNIV,COLL PHARM,PISCATAWAY,NJ 08855. RP NIMS, RW (reprint author), NCI,COMPARAT CARCINOGENESIS LAB,CHEM SECT,FREDERICK,MD 21702, USA. NR 28 TC 17 Z9 17 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 JAN 26 PY 1993 VL 45 IS 2 BP 521 EP 526 DI 10.1016/0006-2952(93)90092-B PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KL505 UT WOS:A1993KL50500032 PM 8435102 ER PT J AU WALKER, JM BOWEN, WD PATRICK, SL WILLIAMS, WE MASCARELLA, SW BAI, X CARROLL, FI AF WALKER, JM BOWEN, WD PATRICK, SL WILLIAMS, WE MASCARELLA, SW BAI, X CARROLL, FI TI A COMPARISON OF (-)-DEOXYBENZOMORPHANS DEVOID OF OPIATE ACTIVITY WITH THEIR DEXTROROTATORY PHENOLIC COUNTERPARTS SUGGESTS ROLE OF SIGMA-2 RECEPTORS IN MOTOR FUNCTION SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE NORMETAZOCINE; SIGMA-RECEPTORS; SUBSTANTIA-NIGRA; MOVEMENT; NALOXONE; OPIATES ID GUINEA-PIG BRAIN; BINDING-SITES; LIGANDS; RAT; AFFINITY; CELLS AB Three novel benzomorphans, (+)-N-benzylnormetazocine, (-)-deoxy-N-benzylnormetazocine, and (-)-deoxypentazocine were tested for their ability to produce circling behavior in rats following intranigral microinjections. Dose studies revealed the following rank order of potency: (-)-deoxypentazocine > (-)-deoxy-N-benzylnormetazocine > (+)-N-benzylnormetazocine. This rank order approximates that for affinities for sigma2 receptors but not sigma1 receptors. It is very unlikely that the effects of the (-)-deoxybenzomorphans were mediated by opiate receptors for the following reasons: (1) consistent with the known requirement for the phenolic hydroxyl group for opiate activity, both (-)-deoxy compounds showed very low affinity for opiate receptors; (2) naloxone (4 mug) co-administered with (-)-deoxy-N-benzylnormetazocine failed to reduce its efficacy; (3) both (-)-deoxy compounds failed to produce marked analgesic effects in the tail flick test following systemic injections of 20 mg/kg s.c. These findings suggest that sigma2 receptors mediate the motor effects of sigma ligands in rats. C1 NIDDKD,MED CHEM LAB,RECEPTOR BIOCHEM & PHARMACOL UNIT,BETHESDA,MD 20892. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. RP WALKER, JM (reprint author), BROWN UNIV,DEPT PSYCHOL,SCHRIER RES LAB,POB 1853,89 WATERMAN ST,PROVIDENCE,RI 02912, USA. OI Mascarella, Wayne/0000-0003-0092-8178 FU NIDA NIH HHS [DA05721, DA04988]; NIMH NIH HHS [MH48869] NR 28 TC 79 Z9 80 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD JAN 26 PY 1993 VL 231 IS 1 BP 61 EP 68 DI 10.1016/0014-2999(93)90684-A PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KM167 UT WOS:A1993KM16700009 PM 8383063 ER PT J AU SPANGRUDE, GJ AF SPANGRUDE, GJ TI DO MOUSE HEMATOPOIETIC STEM-CELLS SELF-RENEW SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 50 EP 50 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500173 ER PT J AU GRONENBORN, AM WINGFIELD, PT APPELLA, E MATSUSHIMA, K POWERS, R GARRETT, DS MARCH, CJ FRIEDEN, A CLORE, GM AF GRONENBORN, AM WINGFIELD, PT APPELLA, E MATSUSHIMA, K POWERS, R GARRETT, DS MARCH, CJ FRIEDEN, A CLORE, GM TI NMR STRUCTURE OF CYTOKINES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDKD,BETHESDA,MD. NIH,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. IMMUNEX CO,SEATTLE,WA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 51 EP 51 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500178 ER PT J AU WANG, LM KEEGAN, A LI, WG GUTKIND, S WHITE, M AARONSON, SA PAUL, W PIERCE, JH AF WANG, LM KEEGAN, A LI, WG GUTKIND, S WHITE, M AARONSON, SA PAUL, W PIERCE, JH TI IL-4 AND INSULIN INDUCE OVERLAPPING SIGNALING PATHWAYS IN FACTOR-DEPENDENT MYELOID CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Gutkind, J. Silvio/A-1053-2009 NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 52 EP 52 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500181 ER PT J AU FAUCI, AS AF FAUCI, AS TI THE ROLE OF CYTOKINES IN THE REGULATION OF HIV EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 58 EP 58 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500198 ER PT J AU FARESE, AM MCLAUGHLIN, E EICHACKER, P NATANSON, C MACVITTIE, TJ AF FARESE, AM MCLAUGHLIN, E EICHACKER, P NATANSON, C MACVITTIE, TJ TI THE STIMULATION OF CANINE NEUTROPHILS (PMN) BY RHIL-8 OR PHORBOL-12-MYRISTATE,13-ACETATE (PMA) FOLLOWING THE PROPHYLACTIC ADMINISTRATION OF RCG-CSF BEFORE AND AFTER THE INDUCTION OF GRAM-NEGATIVE SEPSIS (GNS) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,AFRRI,EXH,BETHESDA,MD 20892. NIH,CCMD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 62 EP 62 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500209 ER PT J AU GRZEGORZEWSKI, K KOMSCHLIES, K KANEDA, K FALTYNEK, C RUSCETTI, FW WILTROUT, RH AF GRZEGORZEWSKI, K KOMSCHLIES, K KANEDA, K FALTYNEK, C RUSCETTI, FW WILTROUT, RH TI RHIL7 INDUCES EXTRAMEDULLARY HEMATOPOIESIS IN MICE THROUGH THE EXPORTATION OF MYELOID PROGENITOR CELLS FROM THE BONE-MARROW TO PERIPHERAL SITES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP,BCDP,RH,FREDERICK,MD 21702. NCI,FCRDC,DCT,BRMP,LMI,LEI,FREDERICK,MD 21702. STERLING WINTHROP RES INST,DIV PHARMACEUT RES,MALVERN,PA 19355. NR 1 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 63 EP 63 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500213 ER PT J AU JACOBSEN, SEW SMELAND, EB LIEN, E RUSCETTI, FW ORTIZ, M KELLER, JR AF JACOBSEN, SEW SMELAND, EB LIEN, E RUSCETTI, FW ORTIZ, M KELLER, JR TI DIRECT EFFECTS OF SYNERGISTIC HEMATOPOIETIC GROWTH-FACTORS ON MURINE BONE-MARROW PROGENITOR CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NORWEGIAN RADIUM HOSP,DEPT IMMUNOL,OSLO 3,NORWAY. NCI,FCRDC,PRI DYNCORP,BCDP,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 65 EP 65 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500221 ER PT J AU KELLER, JR JACOBSEN, SEW ORTIZ, M GOOYA, J RUSCETTI, FW AF KELLER, JR JACOBSEN, SEW ORTIZ, M GOOYA, J RUSCETTI, FW TI MAST-CELL GROWTH-FACTOR PROMOTES THE SURVIVAL OF PROGENITOR CELLS IN THE ABSENCE OF CELL-DIVISION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,BRMP,LMI,PRI DYNCORP,BCDP,FREDERICK,MD 21702. NORWEGIAN RADIUM HOSP,OSLO 3,NORWAY. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 65 EP 65 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500223 ER PT J AU MUSZYNSKI, KW RAPP, UR RUSCETTI, FW KELLER, JR AF MUSZYNSKI, KW RAPP, UR RUSCETTI, FW KELLER, JR TI INHIBITION OF NORMAL HEMATOPOIESIS AND GROWTH FACTOR-DEPENDENT CELL-LINES BY C-RAF ANTISENSE OLIGONUCLEOTIDES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,LVC,BRMP,LMI,PRI DYNCORP,BCDP,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 67 EP 67 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500230 ER PT J AU NETA, R LIEDMAN, JE MITCHELL, J WILLIAMS, D AF NETA, R LIEDMAN, JE MITCHELL, J WILLIAMS, D TI COMPARISON OF C-KIT LIGAND AND PROINFLAMMATORY CYTOKINES IN RADIOPROTECTION OF MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,AFRRI,BETHESDA,MD 20892. IMMUNEX CORP,SEATTLE,WA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 67 EP 67 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500232 ER PT J AU DALESSANDRO, F COLAMONICI, O LOELOFF, M NORDAN, RP AF DALESSANDRO, F COLAMONICI, O LOELOFF, M NORDAN, RP TI IDENTIFICATION OF A VARIANT FORM OF THE INTERLEUKIN-6 RECEPTOR IN CELL-LINES OF DIFFERENT ORIGIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 74 EP 74 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500257 ER PT J AU HESTDAL, K RUSCETTI, FW CHIZZONITE, R ORTIZ, M GOOYA, J LONGO, DL KELLER, JR AF HESTDAL, K RUSCETTI, FW CHIZZONITE, R ORTIZ, M GOOYA, J LONGO, DL KELLER, JR TI ROLE OF THE TYPE-I AND TYPE-II INTERLEUKIN-1 RECEPTORS (IL-1R) ON HEMATOPOIETIC PROGENITOR GROWTH-INVITRO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,LMI BRMP,PRI DYNCORP INC,BCDP,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 77 EP 77 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500269 ER PT J AU WANG, JM MCVICAR, DW OPPENHEIM, JJ KELVIN, DJ AF WANG, JM MCVICAR, DW OPPENHEIM, JJ KELVIN, DJ TI PROMISCUITY OF RANTES RECEPTORS ON HUMAN MONOCYTIC CELLS - COMPETITION FOR BINDING AND DESENSITIZATION OF RANTES RECEPTORS BY RELATED CHEMOTACTIC CYTOKINES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,MOLEC IMMUNOREGULAT LABS,FREDERICK,MD 21702. NCI,FCRDC,BRMP,EXPTL IMMUNOL LABS,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 83 EP 83 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500294 ER PT J AU ZIMMERS, TA HANKINS, WD WILLIAMS, DM WANG, LM SCHECHTER, AN PIERCE, JH AF ZIMMERS, TA HANKINS, WD WILLIAMS, DM WANG, LM SCHECHTER, AN PIERCE, JH TI ANALYSIS OF HUMAN ERYTHROPOIETIN RECEPTOR FUNCTION BY MUTAGENESIS AND GENE-TRANSFER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,LCB,BETHESDA,MD 20892. NCI,LCMB,BETHESDA,MD 20892. RI Zimmers, Teresa/H-5892-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 84 EP 84 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500300 ER PT J AU ADAMS, DH TANAKA, Y STIFF, L YANNELLI, J SHAW, S AF ADAMS, DH TANAKA, Y STIFF, L YANNELLI, J SHAW, S TI DIVERSE GROWTH-FACTORS CYTOKINES INDUCE T-CELL MIGRATION INVITRO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 85 EP 85 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500301 ER PT J AU BERGER, M KOZAK, C PRYSTOWSKY, M AF BERGER, M KOZAK, C PRYSTOWSKY, M TI C10, A MEMBER OF THE SIG CYTOKINE FAMILY LOCATED ON MOUSE CHROMOSOME-11, CONTAINS A NOVEL 2ND-EXON NOT FOUND IN OTHER FAMILY MEMBERS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV PENN,SCH MED,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PATHOL,PHILADELPHIA,PA 19104. NIH,VIRAL BIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 86 EP 86 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500307 ER PT J AU CLERICI, M SHEARER, GM AF CLERICI, M SHEARER, GM TI TH1 AND TH2 LIKE CYTOKINE PRODUCTION IN ASYMPTOMATIC, HIV-SEROPOSITIVE INDIVIDUALS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 88 EP 88 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500316 ER PT J AU GAZZINELLI, RT ELTOUM, I WYNN, TA SHER, A AF GAZZINELLI, RT ELTOUM, I WYNN, TA SHER, A TI DUAL REQUIREMENT FOR TNF-ALPHA AND IFN-GAMMA IN CELL-MEDIATED IMMUNE CONTROL OF TOXOPLASMIC ENCEPHALITIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RI Wynn, Thomas/C-2797-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 91 EP 91 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500325 ER PT J AU LLOYD, A TAUB, D CONLON, K MATSUSHIMA, K OPPENHEIM, J KELVIN, D AF LLOYD, A TAUB, D CONLON, K MATSUSHIMA, K OPPENHEIM, J KELVIN, D TI REGULATION OF T-CELL SUBSET ADHESION BY CHEMOKINE FAMILY MEMBERS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BRMP,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. RI Lloyd, Andrew/E-7334-2017 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 92 EP 92 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500332 ER PT J AU MUSSO, T GUSELLA, GL BOSCO, MC LONGO, D VARESIO, L AF MUSSO, T GUSELLA, GL BOSCO, MC LONGO, D VARESIO, L TI LEUKEMIA INHIBITORY FACTOR (LIF) INDUCES IL8 EXPRESSION IN HUMAN MONOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP,BCDP,FREDERICK,MD 21702. NCI,FCRDC,BRMP,FREDERICK,MD 21702. RI Bosco, Maria Carla/J-7928-2016; varesio, luigi/J-8261-2016 OI Bosco, Maria Carla/0000-0003-1857-7193; varesio, luigi/0000-0001-5659-2218 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 95 EP 95 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500343 ER PT J AU TAKEYA, M SAKANASHI, Y YAMASHIRO, S TAKESHIMA, H YOSHIMURA, T TAKAHASHI, K AF TAKEYA, M SAKANASHI, Y YAMASHIRO, S TAKESHIMA, H YOSHIMURA, T TAKAHASHI, K TI EXPRESSION OF MONOCYTE CHEMOATTRACTANT PROTEIN-1 IN A RAT MODEL OF BLEOMYCIN-INDUCED LUNG INJURY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 KUMAMOTO UNIV,SCH MED,DEPT PATHOL 2,KUMAMOTO 860,JAPAN. NCI,FCRDC,IMMUNOBIOL LAB,IMMUNOPATHOL SECT,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 99 EP 99 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500357 ER PT J AU TAUB, D LLOYD, A CONLON, K MATSUSHIMA, K OPPENHEIM, J KELVIN, D AF TAUB, D LLOYD, A CONLON, K MATSUSHIMA, K OPPENHEIM, J KELVIN, D TI CHEMOATTRACTION OF T-CELL SUBSETS BY CHEMOKINE FAMILY MEMBERS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BRMP,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 99 EP 99 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500359 ER PT J AU YOSHIMURA, T AF YOSHIMURA, T TI CDNA CLONING OF GUINEA-PIG MONOCYTE CHEMOATTRACTANT PROTEIN-1 (MCP-1) AND THE EFFECT OF INTRADERMAL INJECTION OF THE RECOMBINANT PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,IMMUNOBIOL LAB,IMMUNOPATHOL SECT,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 102 EP 102 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500368 ER PT J AU CLOUSE, KA HOWARD, OMZ WEIH, KA SMITH, C GOODWIN, RG FARRAR, WL AF CLOUSE, KA HOWARD, OMZ WEIH, KA SMITH, C GOODWIN, RG FARRAR, WL TI INHIBITION OF HIV ACTIVATION USING SOLUBLE TUMOR-NECROSIS-FACTOR RECEPTOR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 US FDA,CBER,BETHESDA,MD 20895. NCI,FCRDC,BCDP,PRI DYNCORP,FREDERICK,MD 21702. IMMUNEX CORP,SEATTLE,WA 98101. NCI,FCRDC,BRMP,FREDERICK,MD 21702. RI Howard, O M Zack/B-6117-2012 OI Howard, O M Zack/0000-0002-0505-7052 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 103 EP 103 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500374 ER PT J AU JESSOP, JJ HENRY, S HOFFMAN, T AF JESSOP, JJ HENRY, S HOFFMAN, T TI EFFECTS OF THE SERINE PROTEASE INHIBITOR, TAME, ON INTERLEUKIN-1-BETA IN LIPOPOLYSACCHARIDE (LPS)-STIMULATED HUMAN MONOCYTES - THE RELATIONSHIP BETWEEN SYNTHESIS AND RELEASE OF A 33 KDA PRECURSOR AND THE 17 KDA BIOLOGICALLY-ACTIVE SPECIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,CELL BIOL LAB,DIV HEMATOL,CBER,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 105 EP 105 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500380 ER PT J AU NAGEL, JE SCHOONMAKER, MM CHREST, FJ ADLER, WH AF NAGEL, JE SCHOONMAKER, MM CHREST, FJ ADLER, WH TI EFFECT OF AGE ON IL-1-ALPHA, IL-1-BETA, IL-2, IL-3, IL-5, IL-6, IL-8, IFN-GAMMA, IFN-GAMMA-R, TNF-ALPHA, AND TNF-BETA MESSENGER-RNA EXPRESSION BY CON-A AND PHA ACTIVATED HUMAN IMMUNOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 106 EP 106 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500385 ER PT J AU SCHULICK, RD MILLER, MW SHEARER, GM AF SCHULICK, RD MILLER, MW SHEARER, GM TI EFFECTS OF CYCLOSPORINE ON THE PATHWAYS OF IL-2 GENERATION AND CELL-MEDIATED LYMPHOLYSIS IN A MURINE CARDIAC ALLOGRAFT MODEL SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 108 EP 108 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500393 ER PT J AU FARRAR, WL GARCIA, GG EVANS, G KIRKEN, R HOWARD, Z AF FARRAR, WL GARCIA, GG EVANS, G KIRKEN, R HOWARD, Z TI CHARACTERIZATION OF A 97 KDA TYROSINE KINASE ASSOCIATED WITH THE IL-2 RECEPTOR COMPLEX - LACK OF A REQUIREMENT FOR SRC-RELATED ENZYMES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PRI,DYN CORP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 111 EP 111 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500404 ER PT J AU GUSELLA, GL MUSSO, T BOSCO, MC RICE, NR LONGO, D VARESIO, L AF GUSELLA, GL MUSSO, T BOSCO, MC RICE, NR LONGO, D VARESIO, L TI P50 AND P65 SUBUNITS OF THE NF-KAPPA-B COMPLEX, BUT NOT C-REL, ARE INVOLVED IN IL-6 INDUCTION BY IL-2 IN HUMAN MONOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP,BCDP,FREDERICK,MD 21702. NCI,FCRDC,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21702. RI Bosco, Maria Carla/J-7928-2016; varesio, luigi/J-8261-2016 OI Bosco, Maria Carla/0000-0003-1857-7193; varesio, luigi/0000-0001-5659-2218 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 112 EP 112 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500408 ER PT J AU KMIECIK, T VANDEWOUDE, G RUSCETTI, F KELLER, J AF KMIECIK, T VANDEWOUDE, G RUSCETTI, F KELLER, J TI CHARACTERIZATION OF C-MET AND RELATED MESSENGER-RNAS IN NORMAL BONE-MARROW CELLS AND FACTOR-DEPENDENT PROGENITOR-CELL LINES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,MOLEC IMMUNOREGULAT LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,PRI DYNCORP INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NR 1 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 114 EP 114 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500415 ER PT J AU LINNEKIN, D HOWARD, OMZ PARK, L FARRAR, W FERRIS, D LONGO, DL AF LINNEKIN, D HOWARD, OMZ PARK, L FARRAR, W FERRIS, D LONGO, DL TI COUPLING OF THE HUMAN GM-CSF RECEPTOR TO BIOLOGICAL RESPONSES BY THE PROTOONCOGENE HCK SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. IMMUNEX RES & DEV CORP,SEATTLE,WA. RI Howard, O M Zack/B-6117-2012 OI Howard, O M Zack/0000-0002-0505-7052 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 115 EP 115 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500421 ER PT J AU RUI, H EVANS, GA DJEU, JY KELLY, PA FARRAR, WL AF RUI, H EVANS, GA DJEU, JY KELLY, PA FARRAR, WL TI RAPID LIGAND-INDUCED TYROSINE PHOSPHORYLATION OF A 120 KDA PROTEIN ASSOCIATED WITH PROLACTIN AND GROWTH-HORMONE RECEPTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,CYTOKINE MOLEC MECH SECT,LMI,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. UNIV S FLORIDA,H LEE MOFFITT CANC INST & RES CTR,TAMPA,FL 33612. UNIV PARIS 05,INSERM,U344,F-75730 PARIS 15,FRANCE. RI Kelly, Paul/A-7951-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 118 EP 118 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500430 ER PT J AU WANG, LM KEEGAN, AD PAUL, WE HEIDARAN, MA GUTKIND, JS PIERCE, JH AF WANG, LM KEEGAN, AD PAUL, WE HEIDARAN, MA GUTKIND, JS PIERCE, JH TI IL-4 ACTIVATES A DISTINCT SIGNAL TRANSDUCTION CASCADE FROM IL-3 IN FACTOR-DEPENDENT MYELOID CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NAIAD,IMMUNOL LAB,BETHESDA,MD. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. RI Gutkind, J. Silvio/A-1053-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 119 EP 119 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500437 ER PT J AU TING, CC LIANG, SM CHEN, YY HARGROVE, ME AF TING, CC LIANG, SM CHEN, YY HARGROVE, ME TI IL-4 AND PKC REGULATION OF GENE (PERFORIN) EXPRESSION AND PROTEIN (BLT-ESTERASE) SYNTHESIS IN T-CELL ACTIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CTR BIOL EVALUAT & RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 121 EP 121 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500443 ER PT J AU MORSE, HC HUGIN, A FLAVELL, R HARTLEY, J CHATTOPADHYAY, SK AF MORSE, HC HUGIN, A FLAVELL, R HARTLEY, J CHATTOPADHYAY, SK TI RETROVIRUS-INDUCED IMMUNODEFICIENCY IN THE MOUSE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 124 EP 124 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500447 ER PT J AU EISENBERG, R BLOOM, D BRADLEY, D CLARKE, S CREECH, E DAVIGNON, JL FISHER, C HALPERN, M KATAGIRI, T MCDANIEL, R NAKULAQUARONNE, D REAP, E RETTER, M SOBEL, E TREADWELL, E COHEN, P AF EISENBERG, R BLOOM, D BRADLEY, D CLARKE, S CREECH, E DAVIGNON, JL FISHER, C HALPERN, M KATAGIRI, T MCDANIEL, R NAKULAQUARONNE, D REAP, E RETTER, M SOBEL, E TREADWELL, E COHEN, P TI CELLULAR AND GENETIC MECHANISMS OF AUTOANTIBODY PRODUCTION IN SLE MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV N CAROLINA,CHAPEL HILL,NC 27599. STANFORD UNIV,STANFORD,CA 94305. INSERM,TOULOUSE,FRANCE. NCI,FREDERICK,MD 21701. UNIV TOKYO,TOKYO 113,JAPAN. E CAROLINA UNIV,GREENVILLE,NC 27834. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 130 EP 130 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500465 ER PT J AU DAVIDSON, WF ALLISON, JP GIESE, T AF DAVIDSON, WF ALLISON, JP GIESE, T TI ANTIBODIES TO TCR ALPHA/BETA AND CD28 REVERSE FUNCTIONAL ANERGY OF LPR AND GLD B220+ DN T-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD 20892. UNIV CALIF BERKELEY,DEPT MOLEC & CELLULAR BIOL,CANC RES LAB,BERKELEY,CA 94720. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 137 EP 137 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500486 ER PT J AU GIESE, T DAVIDSON, WF AF GIESE, T DAVIDSON, WF TI DIFFERENTIAL RESPONSE OF C3H-LPR T-CELL SUBSETS TO STIMULATION WITH S-ENTEROTOXIN-B INVITRO AND INVIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 138 EP 138 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500491 ER PT J AU MCDERMOTT, M KASTNER, DL HOLLOMAN, J SCHMIDTWOLF, G LUNDBERG, A SINHA, A AMOS, C KHAN, MA WOLFE, FO RUBIN, L MULCAHY, B CASHIN, P MOLLOY, MGM CLEGG, R WARD, R MCDEVITT, HO AF MCDERMOTT, M KASTNER, DL HOLLOMAN, J SCHMIDTWOLF, G LUNDBERG, A SINHA, A AMOS, C KHAN, MA WOLFE, FO RUBIN, L MULCAHY, B CASHIN, P MOLLOY, MGM CLEGG, R WARD, R MCDEVITT, HO TI SEGREGATION OF TCR-BETA CHAIN HAPLOTYPES IN MULTIPLEX RHEUMATOID-ARTHRITIS FAMILIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAMS,ARB,BETHESDA,MD. STANFORD UNIV,DEPT MICROBIOL & IMMUNOL,STANFORD,CA 94305. CASE WESTERN RESERVE UNIV,DEPT RHEUMATOL,CLEVELAND,OH 44106. UNIV KANSAS,DEPT RHEUMATOL,LAWRENCE,KS 66045. UNIV TORONTO,DEPT RHEUMATOL,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV UTAH,SALT LAKE CITY,UT 84112. UNIV CORK,DEPT RHEUMATOL,CORK,IRELAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 140 EP 140 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500497 ER PT J AU TANAKA, Y ADAMS, DH HUBSCHER, S HIRANO, H SIEBENLIST, U SHAW, S AF TANAKA, Y ADAMS, DH HUBSCHER, S HIRANO, H SIEBENLIST, U SHAW, S TI INDUCTION OF T-CELL ADHESION BY PROTEOGLYCAN-IMMOBILIZED MACROPHAGE INFLAMMATORY PROTEIN-1-BETA (MIP-1-BETA) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 143 EP 143 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500511 ER PT J AU DONNELLY, RP CROFFORD, LJ REMMERS, E OBIRI, N FENTON, MJ WILDER, RL AF DONNELLY, RP CROFFORD, LJ REMMERS, E OBIRI, N FENTON, MJ WILDER, RL TI TISSUE-SPECIFIC REGULATION OF IL-6 PRODUCTION BY IL-4 - DIFFERENTIAL-EFFECTS OF IL-4 ON MONOCYTES AND FIBROBLASTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 US FDA,CBER,DIV CYTOKINE BIOL,BETHESDA,MD 20892. NIAMS,ARTHRITIS & RHEUMAT BRANCH,BETHESDA,MD 20892. BOSTON UNIV,SCH MED,DEPT MED,BOSTON,MA 02118. RI Crofford, Leslie/J-8010-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 144 EP 144 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500515 ER PT J AU KANNO, H WOLFINBARGER, JB BLOOM, ME AF KANNO, H WOLFINBARGER, JB BLOOM, ME TI INTERLEUKIN-6 INDUCTION IN HUMAN MACROPHAGE CELL-LINE U937 BY ALEUTIAN MINK DISEASE PARVOVIRUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 146 EP 146 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500522 ER PT J AU PAUL, WE AF PAUL, WE TI HOW IS THE LYMPHOKINE-PRODUCING PHENOTYPE OF AN IMMUNE-RESPONSE ESTABLISHED SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 162 EP 162 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500572 ER PT J AU LAW, CL TORRES, RM SUNDBERG, HA PARKHOUSE, RME BRANNAN, CI COPELAND, NG JENKINS, NA CLARK, EA AF LAW, CL TORRES, RM SUNDBERG, HA PARKHOUSE, RME BRANNAN, CI COPELAND, NG JENKINS, NA CLARK, EA TI ORGANIZATION OF THE GENE LOCUS ENCODING MURINE CD22, CD22 - MAPPING TO CHROMOSOME-7 AND CHARACTERIZATION OF 2 ALLELES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV WASHINGTON,DEPT MICROBIOL,SEATTLE,WA 98195. INST ANIM HLTH,PIRBRIGHT,ENGLAND. FREDERICK CANC RES DEV CTR,MAMMALIAN GENET LAB,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 168 EP 168 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500593 ER PT J AU SADOFSKY, M GELLERT, M AF SADOFSKY, M GELLERT, M TI STUDIES OF RAG PROTEINS GENERATED IN A TISSUE-CULTURE SYSTEM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,MOLEC BIOL LAB,BETHESDA,MD 20897. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500657 ER PT J AU VICTORKOBRIN, C KUEHL, M AF VICTORKOBRIN, C KUEHL, M TI A CLONED MURINE B-LYMPHOMA HAS GENERATED VARIANTS WITH SOMATIC MUTATIONS IN H-CHAIN AND L-CHAIN V-REGIONS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,USN,MED ONCOL BRANCH,BETHESDA,MD 20889. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 186 EP 186 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500663 ER PT J AU PAUL, WE AF PAUL, WE TI HOW IS THE LYMPHOKINE-PRODUCING PHENOTYPE OF AN IMMUNE-RESPONSE ESTABLISHED SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 200 EP 200 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500709 ER PT J AU TAUBENBERGER, JK LANTZ, LM HOLMES, KL AF TAUBENBERGER, JK LANTZ, LM HOLMES, KL TI CHARACTERIZATION OF THE LIP-6 ANTIGEN, WHICH IS EXPRESSED BY MURINE BONE-MARROW B220-B-CELL PROGENITORS AND BY SUBPOPULATIONS OF MATURE PERIPHERAL B-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 211 EP 211 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500750 ER PT J AU HIRANO, H HATHCOCK, KS HODES, RJ AF HIRANO, H HATHCOCK, KS HODES, RJ TI CD44 EXPRESSION BY B-CELLS - EVIDENCE FOR ALTERATIONS OF CD44 ISOFORM INDUCED BY B-CELL ACTIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 214 EP 214 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500762 ER PT J AU KENNY, JJ MORATZ, CM CLAFLIN, JL LONGO, DL AF KENNY, JJ MORATZ, CM CLAFLIN, JL LONGO, DL TI A STRUCTURAL AND MOLECULAR-MODEL FOR T15-IDIOTYPE DOMINANCE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PROGRAM RESOURCES INC,DYNCORP,FREDERICK,MD 21702. UNIV ALABAMA,DEPT MICROBIOL & IMMUNOL,BIRMINGHAM,AL 35294. UNIV MICHIGAN,DEPT MICROBIOL & IMMUNOL,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 218 EP 218 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500778 ER PT J AU WEINSTEIN, PD ANDERSON, AO MAGE, RG AF WEINSTEIN, PD ANDERSON, AO MAGE, RG TI MOLECULAR GENETIC DIVERSIFICATION OF VARIABLE REGION GENES FROM GALT B-CELLS RESPONDING TO ENVIRONMENT ANTIGENS IN THE 2 PRIMARY GERMINAL CENTER COMPARTMENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. USA,MRIID,DAD,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 223 EP 223 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500796 ER PT J AU FUSCHIOTTI, P SADOFSKY, M HESSE, JE MAGE, RG AF FUSCHIOTTI, P SADOFSKY, M HESSE, JE MAGE, RG TI THE RECOMBINATION ACTIVATING GENES OF THE RABBIT - EXPRESSION AND FUNCTIONAL-STUDIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. NIDDK,LMB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 230 EP 230 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500823 ER PT J AU OCONNELL, C LONGO, D HILL, S HURST, J KENNY, J AF OCONNELL, C LONGO, D HILL, S HURST, J KENNY, J TI ENDOGENOUS IMMUNOGLOBULIN GENE-EXPRESSION DURING FETAL DEVELOPMENT OF IGA TRANSGENIC MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 233 EP 233 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500836 ER PT J AU ROTH, DB MENETSKI, JP NAKAJIMA, PB BOSMA, MJ GELLERT, M AF ROTH, DB MENETSKI, JP NAKAJIMA, PB BOSMA, MJ GELLERT, M TI V(D)J RECOMBINATION - BROKEN DNA WITH HAIRPIN CODING ENDS IN SCID MOUSE THYMUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,MOLEC BIOL LAB,BETHESDA,MD 20892. FOX CHASE CANC CTR,INST CANC RES,PHILADELPHIA,PA 19111. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 234 EP 234 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500838 ER PT J AU DUNNICK, W ELENICH, L BERRY, J CLAFLIN, JL CHU, CC AF DUNNICK, W ELENICH, L BERRY, J CLAFLIN, JL CHU, CC TI EFFECT OF A SV40 T-ANTIGEN TRANSGENE DRIVEN BY THE GAMMA-1-GERMLINE PROMOTER ON EXPRESSION OF THE ENDOGENOUS GAMMA-1-GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV MICHIGAN,DEPT MICROBIOL & IMMUNOL,ANN ARBOR,MI 48103. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 237 EP 237 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500853 ER PT J AU BEHRENS, TW JAGADEESH, J YEWDELL, JW STAUDT, LM AF BEHRENS, TW JAGADEESH, J YEWDELL, JW STAUDT, LM TI JAW-1, A LYMPHOID-RESTRICTED INTEGRAL MEMBRANE-PROTEIN LOCALIZED TO THE ENDOPLASMIC-RETICULUM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 240 EP 240 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500864 ER PT J AU BERGSAGEL, PL VICTORKOBRIN, C BRENTS, LA KUEHL, WM AF BERGSAGEL, PL VICTORKOBRIN, C BRENTS, LA KUEHL, WM TI THE IDENTIFICATION OF GENES SELECTIVELY EXPRESSED IN MURINE PLASMACYTOMAS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,USN,MED ONCOL BRANCH,BETHESDA,MD 20889. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 240 EP 240 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500863 ER PT J AU FISCHER, RT GUELDE, G LONGO, D KENNY, JJ AF FISCHER, RT GUELDE, G LONGO, D KENNY, JJ TI A NOVEL FORM OF PHOSPHOCHOLINE INDUCES PROTECTION AGAINST STREPTOCOCCUS-PNEUMONIAE INFECTION IN X-LINKED IMMUNODEFICIENT (XID) MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702. NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 241 EP 241 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500866 ER PT J AU HATHCOCK, KS HIRANO, H MURAKAMI, S HODES, RJ AF HATHCOCK, KS HIRANO, H MURAKAMI, S HODES, RJ TI ANALYSIS OF CD45 EXPRESSION ON UNSTIMULATED B-CELLS OR B-CELLS STIMULATED WITH EITHER LPS OR IL5 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 241 EP 241 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500868 ER PT J AU RIVA, A WILSON, GL KEHRL, JH AF RIVA, A WILSON, GL KEHRL, JH TI ANALYSIS OF THE HUMAN CD19 PROMOTER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 246 EP 246 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500885 ER PT J AU THEVENIN, C LUCAS, BP KEHRL, JH AF THEVENIN, C LUCAS, BP KEHRL, JH TI INVIVO FOOTPRINTING AND GEL SHIFT ANALYSIS OF THE HUMAN CD20 PROMOTER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 246 EP 246 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500888 ER PT J AU BECKWITH, M FENTON, RG KATONA, IM LONGO, DL AF BECKWITH, M FENTON, RG KATONA, IM LONGO, DL TI ANTI-IGM-MEDIATED TYROSINE PHOSPHORYLATION OF PI3 KINASE IS NOT ESSENTIAL FOR GROWTH-INHIBITION OF A HUMAN B-LYMPHOMA CELL-LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PEDIAT,BETHESDA,MD 20814. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. NCI,FCRDC,PRI DYNCORP INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 26 PY 1993 SU 17B BP 252 EP 252 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN465 UT WOS:A1993KN46500909 ER PT J AU GIFFORD, RW ALDERMAN, MH CHOBANIAN, AV CUNNINGHAM, SL DUSTAN, HP FRANCIS, CK FROHLICH, ED KAPLAN, NM MANN, RJ MOSER, M NICKEY, WA PERRY, HM REED, JW SHEPS, SG SHAMLER, J BROWN, C CUNNINGHAM, SL CUTLER, J HARLAN, WR IBRAHIM, M JULIUS, S KULLER, LH LEVINE, DM MURPHY, RS NEATON, JD REMINGTON, R SHEPS, SG WHEELER, FC WHELTON, PK CAMPESE, VM GRIMM, R BRITO, GT OPARIL, S SULLIVAN, JM VIDT, DG BLACK, HR BLAIR, SN BLAUFOX, MD ERNST, ND KOTCHEN, TA MOORE, MA SPITTELL, JA WINSTON, M AUGUST, P BERGE, K DEVEREUX, R DONATO, K FALKNER, B GOINS, MK GRIM, CE HALL, WD HORAN, MJ KUMANYIKA, SK PERRY, HM PORUSH, JG RANDALL, OS TAUBERT, KA ROCCELLA, EJ AF GIFFORD, RW ALDERMAN, MH CHOBANIAN, AV CUNNINGHAM, SL DUSTAN, HP FRANCIS, CK FROHLICH, ED KAPLAN, NM MANN, RJ MOSER, M NICKEY, WA PERRY, HM REED, JW SHEPS, SG SHAMLER, J BROWN, C CUNNINGHAM, SL CUTLER, J HARLAN, WR IBRAHIM, M JULIUS, S KULLER, LH LEVINE, DM MURPHY, RS NEATON, JD REMINGTON, R SHEPS, SG WHEELER, FC WHELTON, PK CAMPESE, VM GRIMM, R BRITO, GT OPARIL, S SULLIVAN, JM VIDT, DG BLACK, HR BLAIR, SN BLAUFOX, MD ERNST, ND KOTCHEN, TA MOORE, MA SPITTELL, JA WINSTON, M AUGUST, P BERGE, K DEVEREUX, R DONATO, K FALKNER, B GOINS, MK GRIM, CE HALL, WD HORAN, MJ KUMANYIKA, SK PERRY, HM PORUSH, JG RANDALL, OS TAUBERT, KA ROCCELLA, EJ TI THE 5TH REPORT OF THE JOINT NATIONAL COMMITTEE ON DETECTION, EVALUATION, AND TREATMENT OF HIGH BLOOD-PRESSURE (JNC V) SO ARCHIVES OF INTERNAL MEDICINE LA English DT Review ID LEFT-VENTRICULAR MASS; RANDOMIZED CONTROLLED TRIAL; CORONARY HEART-DISEASE; ALL-CAUSE MORTALITY; CARDIOVASCULAR-DISEASE; HYPERTENSIVE PATIENTS; MYOCARDIAL-INFARCTION; HEALTH-PROFESSIONALS; MILD HYPERTENSION; WEIGHT-REDUCTION C1 NHLBI, NATL HIGH BLOOD PRESSURE EDUC PROGRAM, OFF PREVENT, BETHESDA, MD 20892 USA. CLEVELAND CLIN EDUC FDN, CLEVELAND, OH 44106 USA. YESHIVA UNIV ALBERT EINSTEIN COLL MED, BRONX, NY 10461 USA. BOSTON UNIV, SCH MED, BOSTON, MA 02118 USA. UNIV WASHINGTON, SEATTLE, WA 98195 USA. UNIV ALABAMA, SCH MED, ESSEX, VT USA. COLUMBIA UNIV COLL PHYS & SURG, NEW YORK, NY 10032 USA. ALTON OCHSNER MED FDN & OCHSNER CLIN, NEW ORLEANS, LA 70121 USA. UNIV TEXAS, HLTH SCI CTR, SW MED SCH, DALLAS, TX 75235 USA. UNIV ARKANSAS MED SCI HOSP, LITTLE ROCK, AR 72205 USA. YALE UNIV, SCH MED, NEW HAVEN, CT 06510 USA. OSTEOPATH MED CTR, PHILADELPHIA, PA USA. WASHINGTON UNIV, SCH MED, ST LOUIS, MO 63110 USA. MOREHOUSE SCH MED, ATLANTA, GA USA. MAYO MED SCH & CLIN, ROCHESTER, MN USA. NORTHWESTERN UNIV, SCH MED, CHICAGO, IL 60611 USA. NIH, BETHESDA, MD 20892 USA. UNIV MICHIGAN, ANN ARBOR, MI 48109 USA. UNIV PITTSBURGH, PITTSBURGH, PA 15260 USA. JOHNS HOPKINS UNIV, SCH MED, BALTIMORE, MD 21205 USA. BROOKDALE HOSP MED CTR, BROOKLYN, NY 11212 USA. HOWARD UNIV HOSP, WASHINGTON, DC 20060 USA. UNIV RES CORP, BETHESDA, MD USA. NATL CTR HLTH STAT, CTR DIS CONTROL, HYATTSVILLE, MD 20782 USA. UNIV MINNESOTA, MINNEAPOLIS, MN 55455 USA. UNIV IOWA, IOWA CITY, IA 52242 USA. S CAROLINA DEPT HLTH & ENVIRONM CONTROL, COLUMBIA, SC 29201 USA. JOHNS HOPKINS MED INST, BALTIMORE, MD 21205 USA. UNIV SO CALIF, MED CTR, LOS ANGELES, CA 90089 USA. UNIV ILLINOIS, CHICAGO, IL 60680 USA. UNIV COLORADO, DENVER, CO 80202 USA. UNIV ALABAMA, BIRMINGHAM, AL 35294 USA. UNIV TENNESSEE CTR HLTH SCI, MEMPHIS, TN 38163 USA. RUSH PRESBYTERIAN ST LUKES MED CTR, CHICAGO, IL 60612 USA. PED, INST AEROB RES, DALLAS, TX USA. W VIRGINIA UNIV, MORGANTOWN, WV 26506 USA. BOWMAN GRAY SCH MED, DANVILLE, VA USA. UNIV N CAROLINA, UROL CLIN, CHAPEL HILL, NC 27514 USA. AMER HEART ASSOCIAT, DALLAS, TX USA. CORNELL UNIV, MED CTR, COLL MED, NEW YORK, NY 10021 USA. MED COLL PENN, PHILADELPHIA, PA 19129 USA. FAMILY HLTH CTR, HIALEAH, FL USA. CHARLES R DREW UNIV MED & SCI, LOS ANGELES, CA USA. EMORY UNIV, ATLANTA, GA 30322 USA. PENN STATE UNIV, MILTON S HERSHEY MED CTR, HERSHEY, PA 17033 USA. NR 117 TC 1257 Z9 1295 U1 3 U2 12 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-9926 EI 1538-3679 J9 ARCH INTERN MED JI Arch. Intern. Med. PD JAN 25 PY 1993 VL 153 IS 2 BP 154 EP 183 PG 30 WC Medicine, General & Internal SC General & Internal Medicine GA KK027 UT WOS:A1993KK02700002 ER PT J AU WHELTON, PK ADAMSCAMPBELL, LL APPEL, LJ CUTLER, J DONATO, K ELMER, PJ GRIMM, R HASKELL, WL HAVAS, S HORAN, MJ LASATER, TM LEVINE, DM MOSER, M SACKS, FM STAMLER, R ROCCELLA, EJ BRITO, GT AF WHELTON, PK ADAMSCAMPBELL, LL APPEL, LJ CUTLER, J DONATO, K ELMER, PJ GRIMM, R HASKELL, WL HAVAS, S HORAN, MJ LASATER, TM LEVINE, DM MOSER, M SACKS, FM STAMLER, R ROCCELLA, EJ BRITO, GT TI NATIONAL HIGH BLOOD-PRESSURE EDUCATION-PROGRAM WORKING GROUP-REPORT ON PRIMARY PREVENTION OF HYPERTENSION SO ARCHIVES OF INTERNAL MEDICINE LA English DT Review ID CORONARY HEART-DISEASE; RANDOMIZED CONTROLLED TRIAL; NUTRITION EXAMINATION SURVEY; ORAL CALCIUM SUPPLEMENTATION; MODERATE SODIUM RESTRICTION; MILD ESSENTIAL-HYPERTENSION; UNSATURATED FATTY-ACIDS; TIME PHYSICAL-ACTIVITY; BELGIAN-INTERUNIVERSITY-RESEARCH; RESEARCH CLINICS PREVALENCE C1 NHLBI, NATL HIGH BLOOD PRESSURE EDUC PROGRAM, OFF PREVENT EDUC & CONTROL, BETHESDA, MD 20892 USA. JOHNS HOPKINS MED INST, BALTIMORE, MD 21205 USA. HOWARD UNIV, CTR CANC, WASHINGTON, DC 20059 USA. UNIV MINNESOTA, MINNEAPOLIS, MN 55455 USA. STANFORD UNIV, MED CTR, SCH MED, STANFORD, CA 94305 USA. UNIV MARYLAND, BALTIMORE, MD 21201 USA. MEM HOSP, PAWTUCKET, RI 02860 USA. JOHNS HOPKINS UNIV, SCH MED, BALTIMORE, MD 21205 USA. YALE UNIV, SCH MED, NEW HAVEN, CT 06510 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. NORTHWESTERN UNIV, SCH MED, CHICAGO, IL 60611 USA. NR 325 TC 202 Z9 208 U1 4 U2 8 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-9926 EI 1538-3679 J9 ARCH INTERN MED JI Arch. Intern. Med. PD JAN 25 PY 1993 VL 153 IS 2 BP 186 EP 208 PG 23 WC Medicine, General & Internal SC General & Internal Medicine GA KK027 UT WOS:A1993KK02700003 ER PT J AU MAY, A NAIRN, RS OKUMOTO, DS WASSERMANN, K STEVNSNER, T JONES, JC BOHR, VA AF MAY, A NAIRN, RS OKUMOTO, DS WASSERMANN, K STEVNSNER, T JONES, JC BOHR, VA TI REPAIR OF INDIVIDUAL DNA STRANDS IN THE HAMSTER DIHYDROFOLATE-REDUCTASE GENE AFTER TREATMENT WITH ULTRAVIOLET-LIGHT, ALKYLATING-AGENTS, AND CISPLATIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INTERSTRAND CROSS-LINKS; UV-INDUCED MUTATIONS; ESCHERICHIA-COLI; OVARY CELLS; TRANSCRIBED STRAND; PREFERENTIAL REPAIR; PYRIMIDINE DIMERS; 6-4 PHOTOPRODUCTS; HUMAN FIBROBLASTS; MAMMALIAN-CELLS AB We have analyzed gene-specific and strand-specific DNA damage and repair in the dihydrofolate reductase gene in hamster cells. Cells were UV-irradiated or treated with two types of chemotherapeutics, alkylating agents or cisplatin. UV-induced pyrimidine dimers were detected using a previoulsy published technique in which the T4 endonuclease V enzyme is used to create nicks at the lesion sites. 6-4 photoproducts were detected in a similar assay using ABC excinuclease after prior reversal of the pyrimidine dimers with photolyase. Adducts formed by the alkylating agents nitrogen mustard and dimethyl sulfate were quantitated by generating strand breaks at abasic sites after neutral depurination. Cisplatin-induced intrastrand adducts were detected with ABC excinuclease, and cisplatin interstrand cross-links were detected using a denaturation-reannealing reaction before electrophoresis. In accord with previous reports by other investigators, we find distinct strand specificity of the repair of pyrimidine dimers after UV; the transcribed strand was much more efficiently repaired than the nontranscribed strand. In contrast, there was little or no strand bias in the repair of the 6-4 photoproducts. For alkylating agents, a slight bias toward repair in the transcribed strand was found after treatment with nitrogen mustard, but there appeared to be no bias in the repair after treatment with dimethyl sulfate. Cisplatin interstrand cross-links are repaired with equal efficiency from the two strands, but the more common cisplatin-induced lesion, the intrastrand adduct, is preferentially repaired from the transcribed strand. In conclusion, there is strand bias in the repair of pyrimidine dimers and cisplatin intrastrand adducts, but the strand specificity of repair may not be a general feature for all DNA lesions, as we found little or no strand bias in the repair of other lesions studied. C1 NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. UNIV TEXAS,MD ANDERSON CANC CTR,DIV SCI PK RES,SMITHVILLE,TX 78957. NR 46 TC 67 Z9 67 U1 1 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 JAN 25 PY 1993 VL 268 IS 3 BP 1650 EP 1657 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH620 UT WOS:A1993KH62000025 PM 8420940 ER PT J AU OZAWA, K SZALLASI, Z KAZANIETZ, MG BLUMBERG, PM MISCHAK, H MUSHINSKI, JF BEAVEN, MA AF OZAWA, K SZALLASI, Z KAZANIETZ, MG BLUMBERG, PM MISCHAK, H MUSHINSKI, JF BEAVEN, MA TI CA2+-DEPENDENT AND CA2+-INDEPENDENT ISOZYMES OF PROTEIN-KINASE-C MEDIATE EXOCYTOSIS IN ANTIGEN-STIMULATED RAT BASOPHILIC RBL-2H3 CELLS - RECONSTITUTION OF SECRETORY RESPONSES WITH CA2+ AND PURIFIED ISOZYMES IN WASHED PERMEABILIZED CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHORBOL ESTER BINDING; DIFFERENTIAL DOWN-REGULATION; 2H3 CELLS; HISTAMINE-RELEASE; LEUKEMIA-CELLS; CALCIUM SIGNAL; IGE RECEPTORS; CALPHOSTIN-C; MAST-CELLS; FAMILY AB Rat basophilic RBL-2H3 cells, which exhibit Ca2+-dependent secretion of granules when stimulated with antigen, contained the Ca2+-dependent alpha and beta and the Ca2+-independent delta, epsilon, and zeta isoforms of protein kinase C. These isoforms associated, to variable extents (i.e. delta the most and zeta the least), with the membrane fraction upon antigen stimulation but without external Ca2+; only the Ca2+-independent isoforms did so. Both types of isozymes were probably necessary for optimal responses to antigen as indicated by the following observations. All Ca2+-dependent isozymes were degraded in cells treated with 20 nM phorbol 12-myristate 13-acetate for 6 h, whereas the Ca2+-independent isozymes were not degraded and were retained when the cells were subsequently permeabilized and washed. Cells so treated still exhibited antigen-induced secretion (25-33% of normal) which was suppressed by selective inhibitors of protein kinase C (Ro31-7549 and calphostin C) thereby indicating a possible contribution of the Ca2+-independent isozymes in secretion. Normally, washed permeabilized cells lost all isozymes of protein kinase C and failed to secrete in response to antigen. A full secretory response to antigen could be reconstituted by the subsequent addition of nanomolar concentrations of either beta or delta isozymes of protein kinase C (other isozymes were much less effective) but only in the presence of 1 muM free Ca2+ to indicate distinct roles for Ca2+ and protein kinase C in exocytosis. C1 NHLBI, CHEM PHARMACOL LAB, BETHESDA, MD 20892 USA. NCI, CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB, BETHESDA, MD 20892 USA. NCI, GENET LAB, BETHESDA, MD 20892 USA. RI Mischak, Harald/E-8685-2011 NR 36 TC 380 Z9 381 U1 0 U2 5 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 JAN 25 PY 1993 VL 268 IS 3 BP 1749 EP 1756 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH620 UT WOS:A1993KH62000039 PM 8420951 ER PT J AU STAGSTED, J ZIEBE, S SATOH, S HOLMAN, GD CUSHMAN, SW OLSSON, L AF STAGSTED, J ZIEBE, S SATOH, S HOLMAN, GD CUSHMAN, SW OLSSON, L TI INSULINOMIMETIC EFFECT ON GLUCOSE-TRANSPORT BY EPIDERMAL GROWTH-FACTOR WHEN COMBINED WITH A MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I-DERIVED PEPTIDE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INSULIN-RECEPTOR; PLASMA-MEMBRANE; TYROSINE KINASE; RAT ADIPOCYTES; FAT-CELLS; STIMULATION; DEGRADATION; ANTIGENS; BINDING; TRANSLOCATION AB Peptides derived from the alpha1-region of the murine H-2D(k) molecule enhance glucose uptake in rat adipose cells above the maximum obtained with insulin stimulation alone (Stagsted, J., Reaven, G. M., Hansen, T., Goldstein, A., and Olsson, L. (1990) Cell 62, 297-307). We now describe that epidermal growth factor (EGF) in combination with the same peptides, D(k)-61-85) and D(k)-(62-85), stimulates cellular glucose uptake 5-7 times over the basal level, i.e. to 30-50% of the maximal insulin effect. EGF alone increased glucose uptake by only approximately 50% above basal and the peptide alone by 100% above basal. Maximal effect of EGF and peptide was reached in 10-20 min with 30 muM peptide (EC50 10-15 muM) and 50 nM EGF (EC50 1-2 nM). The effect of EGF and peptide on glucose uptake was additive to that of insulin and peptide until the maximal level attained with insulin and peptide was reached. The combined effect of EGF plus peptide on glucose transport was associated with a recruitment of GLUT4 molecules to the plasma membrane. However, the phosphatidylinositol (PI) kinase which is activated by insulin was not activated by EGF plus peptide. Thus, the effect of EGF plus peptide on glucose uptake seems independent of the activity status of the insulin receptor. I-125-Labeled EGF bound specifically to rat adipose cells with an apparent affinity of approximately 2 nM and B(max) approximately 5 x 10(3). However, the major histocompatibility complex (MHC) peptides did not affect EGF-stimulated internalization of EGF receptor, in contrast to their effect on the insulin receptors. Transforming growth factor(alpha) had an effect similar to EGF on glucose uptake. Three other peptides derived from other parts of murine MHC class I had no effect on glucose uptake in combination with EGF. Thus, EGF in combination with certain MHC class I-derived peptides is insulinomimetic concerning glucose transport and this effect is independent of the insulin receptor activity. C1 NIDDKD,DIABET BRANCH,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD 20892. UNIV BATH,DEPT BIOCHEM,BATH BA2 7AY,AVON,ENGLAND. RP STAGSTED, J (reprint author), RECEPTRON INC,CONCORD,CA 94520, USA. NR 28 TC 28 Z9 28 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 JAN 25 PY 1993 VL 268 IS 3 BP 1770 EP 1774 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH620 UT WOS:A1993KH62000042 PM 8420953 ER PT J AU SANDER, M CARTER, M HUANG, SM AF SANDER, M CARTER, M HUANG, SM TI EXPRESSION OF DROSOPHILA RRP1 PROTEIN IN ESCHERICHIA-COLI - ENZYMATIC AND PHYSICAL CHARACTERIZATION OF THE INTACT PROTEIN AND A CARBOXYL-TERMINALLY DELETED EXONUCLEASE-DEFICIENT MUTANT SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DNA STRAND EXCHANGE; SACCHAROMYCES-CEREVISIAE; HOMOLOGOUS RECOMBINATION; REPAIR ENZYMES; RECA PROTEIN; APURINIC ENDONUCLEASE; BRANCH MIGRATION; SEQUENCE; GENE; PURIFICATION AB Drosophila Rrp1 protein purified from embryos has four tightly associated enzymatic activities: DNA strand transfer, single-strand DNA renaturation, 3'-exonuclease, and apurinic endonuclease. Copurifying with these activities is a single polypeptide that has an apparent M(r) of 105,000 when estimated by SDS-polyacrylamide gel electrophoresis. To determine if this polypeptide is sufficient for these activities, it has been overexpressed in Escherichia coli. In crude extracts of E. coli cells, an ATP-independent Mg2+-dependent strand transfer activity is observed upon activation of the promoter that drives expression of Rrp1. Rrp1 protein purified from induced E. coli cells has electrophoretic, chromatographic, and enzymatic properties similar to those of Drosophila Rrp1 protein. The carboxyl-terminal region of Rrp1 (amino acids 428-679) is homologous to E. coli exonuclease III. Rrp1 deleted for this region cannot carry out DNA strand transfer, but can renature complementary single-strand DNA. The strand transfer activity of this truncated protein can be restored if DNA 3'-exonuclease is provided in trans by pretreating the double-strand DNA substrate with E. coli exonuclease III. This demonstrates a likely role of the exonuclease in the in vitro DNA strand transfer reaction carried out by Rrp1 protein. Such a role is also suggested by an analysis of the polarity of the strand transfer reaction. RP SANDER, M (reprint author), NIEHS,GENET LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 36 TC 22 Z9 22 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 JAN 25 PY 1993 VL 268 IS 3 BP 2075 EP 2082 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH620 UT WOS:A1993KH62000087 PM 7678415 ER PT J AU DALESSANDRO, F COLAMONICI, OR NORDAN, RP AF DALESSANDRO, F COLAMONICI, OR NORDAN, RP TI DIRECT ASSOCIATION OF INTERLEUKIN-6 WITH A 130-KDA COMPONENT OF THE INTERLEUKIN-6 RECEPTOR SYSTEM SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID STIMULATORY FACTOR-II; PLASMACYTOMA GROWTH-FACTOR; CROSS-LINKING; SIGNAL TRANSDUCER; CELLS; PROTEIN; DIFFERENTIATION; EXPRESSION; IL-6; INTERFERON-BETA-2 AB Affinity cross-linking of membrane bound I-125-interleukin-6 (IL-6) on several cell lines revealed a three-band pattern of IL-6-containing cross-linked complexes with molecular masses of 100, 120, and 150 kDa. To identify the membrane components that were associated with IL-6 in the three complexes, we employed the Denny-Jaffe reagent, a heterobifunctional, cleavable cross-linker that allows the transfer of I-125 from the ligand to its receptor. Samples cross-linked with Denny-Jaffe reagent were analyzed by two-dimensional SDS-polyacrylamide gel electrophoresis in which the cross-linker was cleaved prior to the second dimension. This analysis revealed that IL-6 directly associates with a 130-kDa membrane protein thus allowing the formation of the 150-kDa complex. In addition, both the 100- and 120-kDa cross-linked complexes were shown to include an 80-kDa membrane glycoprotein associated with one and two IL-6 molecules, respectively. C1 NCI,CLIN PHARMACOL BRANCH,BLDG 10,RM 13N268,BETHESDA,MD 20892. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. NR 32 TC 16 Z9 16 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 JAN 25 PY 1993 VL 268 IS 3 BP 2149 EP 2153 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH620 UT WOS:A1993KH62000097 PM 8420983 ER PT J AU GERSHON, PD MOSS, B AF GERSHON, PD MOSS, B TI STIMULATION OF POLY(A) TAIL ELONGATION BY THE VP39 SUBUNIT OF THE VACCINIA VIRUS-ENCODED POLY(A) POLYMERASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RNA-POLYMERASE; EARLY GENES; TRANSCRIPTION; POLYADENYLATION; SPECIFICITY; TERMINATION; DOWNSTREAM; SEQUENCE; VIRIONS; PROTEIN AB The VP55 subunit of the vaccinia virus-encoded poly(A) polymerase can add a maximum of 35 adenylates to the 3'-end of an RNA primer in a rapid and highly processive manner, whereas the VP55-VP39 heterodimer catalyzes the formation of poly(A) tails several hundred nucleotides in length. Here, we describe the overexpression of the VP39 subunit, its purification to near homogeneity, and its ability to associate physically with VP55 and to stimulate polyadenylation. Although VP39 possessed no independent poly(A) polymerase activity, RNA primers with oligo(A) tails greater than 30 adenylates in length could be extended nearly 40-fold more rapidly in the presence of VP39. VP39 enhanced the polyadenylation rate by converting the slow, nonprocessive polyadenylation occurring after the rapid burst in the presence of monomeric VP55, to a rapid, semiprocessive reaction. The effect of VP39 was dramatic when poly(A) primers were used as, 60 mm NaCl, VP39 enhanced the polyadenylation rate 500-fold, and at 90 mm NaCl VP39 was absolutely required. Nevertheless, the VP39-containing polymerase remained selective for polyadenylation of an mRNA 3'-end in the presence of excess poly(A). These data suggest that the role of VP39 in polyadenylation is to increase the affinity of the polymerase for the growing poly(A) tail. C1 NIAID,VIRAL DIS LAB,BLDG 4,RM 229,BETHESDA,MD 20892. NR 22 TC 51 Z9 52 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 JAN 25 PY 1993 VL 268 IS 3 BP 2203 EP 2210 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH620 UT WOS:A1993KH62000105 PM 8420988 ER PT J AU MILNE, GWA NICKLAUS, MC HODOSCEK, M AF MILNE, GWA NICKLAUS, MC HODOSCEK, M TI MOLECULAR MODELING IN SOLVENT SO JOURNAL OF MOLECULAR STRUCTURE LA English DT Article ID MONTE-CARLO SIMULATION; ABINITIO; DYNAMICS; CONTINUUM; TRIMERS; ENERGY; DIMERS; CH3OH AB The structures of a number of organic molecules have been modeled, both in vacuo and in a solvent environment. The differences between the minimum energy structures in the two environments are conformational in nature and stem primarily from hydrogen bonding. In polar solvents such as water, external hydrogen bonding tends to supplant all but the strongest intramolecular hydrogen bonds. Wherever intramolecular hydrogen bonds controlled the conformation in vacuo, but were destroyed in water, conformational changes were observed. The changes, however, are not usually major. These results have been generally supported by ab initio calculations. C1 NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. RP MILNE, GWA (reprint author), NCI,MED CHEM LAB,BETHESDA,MD 20892, USA. RI Nicklaus, Marc/N-4183-2014 NR 33 TC 12 Z9 12 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-2860 J9 J MOL STRUCT JI J. Mol. Struct. PD JAN 25 PY 1993 VL 291 IS 1 BP 89 EP 103 DI 10.1016/0022-2860(93)80255-T PG 15 WC Chemistry, Physical SC Chemistry GA KL115 UT WOS:A1993KL11500005 ER PT J AU MONTI, E MIMNAUGH, EG SINHA, BK AF MONTI, E MIMNAUGH, EG SINHA, BK TI SYNERGISTIC INTERACTIONS OF ETOPOSIDE AND INTERLEUKIN-1-ALPHA ARE NOT DUE TO DNA DAMAGE IN HUMAN-MELANOMA CELLS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE ETOPOSIDE; INTERLEUKIN-1-ALPHA; MELANOMA CELL; DNA DAMAGE; DNA REPAIR ID TUMOR-NECROSIS-FACTOR; TOPOISOMERASE-II; CYTO-TOXICITY; MECHANISM; CLEAVAGE; VP-16-213; CYTOTOXICITY; METABOLISM; BREAKAGE; BINDING AB Several possible mechanisms of the synergistic interactions of IL-1alpha and VP-16 against A375-C6 human melanoma cells were investigated. Studies indicate that IL-1alpha did not increase topoisomerase II-dependent VP-16-mediated DNA damage, nor did IL-1alpha inhibit the repair of VP-16-induced DNA damage in these cells. Furthermore, IL-1alpha by itself or in combination with VP-16 did not cause significant fragmentation of cellular DNA into oligomers, indicating programmed cell death (apoptosis) was not involved in the mechanism of synergy. In contrast, an IL-1-specific receptor antagonist significantly decreased IL-1alpha toxicity toward the melanoma cells and nearly eliminated the synergistic interactions of IL-1alpha with VP-16. These results strongly indicate that synergism of IL-1alpha with VP-16 was dependent upon an IL-1-receptor-mediated processes. DNA-strand breakage was unlikely to be a primary intracellular target for IL-1alpha cytotoxicity and synergism with VP-16. C1 NCI,CLIN PHARMACOL BRANCH,BIOCHEM & MOLEC PHARMACOL SECT,BLDG 10,ROOM 6N119,BETHESDA,MD 20892. NR 20 TC 8 Z9 8 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 JAN 22 PY 1993 VL 1180 IS 3 BP 231 EP 235 DI 10.1016/0925-4439(93)90043-Z PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KJ445 UT WOS:A1993KJ44500002 PM 8422427 ER PT J AU ANANDATHEERTHAVARADA, HK SHANKAR, SK BHAMRE, S BOYD, MR SONG, BJ RAVINDRANATH, V AF ANANDATHEERTHAVARADA, HK SHANKAR, SK BHAMRE, S BOYD, MR SONG, BJ RAVINDRANATH, V TI INDUCTION OF BRAIN CYTOCHROME-P-450IIE1 BY CHRONIC ETHANOL TREATMENT SO BRAIN RESEARCH LA English DT Article DE BRAIN; CYTOCHROME-P-450; ETHANOL; CYTOCHROME-P-450IIE1; MONOOXYGENASE ID RAT-BRAIN; REGIONAL DISTRIBUTION; MICROSOMES; OXIDATION; QUANTITATION; CONSUMPTION; DEMETHYLASE; REDUCTASE; BINDING; SYSTEM AB Cytochrome P-450 mediated metabolism is potentially involved in the expression of the pharmacological and/or toxicological effects of a wide variety of drugs and environmental chemicals upon tissues which contain this metabolic system. In the present investigation, the presence of cytochrome P-450IIEI and associated mono-oxygenase activities in brain and the effect of chronic ethanol treatment on brain cytochrome P-450 (P-450) were studied. Aniline hydroxylase, N-nitroso-dimethylamine N-demethylase and p-nitrophenol hydroxylase activities (known to be mediated by P-450IIE1) were detectable in brain microsomes from untreated rats and were about 5%, 125% and 8.3%, respectively, of the corresponding hepatic levels. Chronic ethanol treatment resulted in induction of the above enzyme activities in brain microsomes by 243%, 496% and 155%, respectively. Intake of ethanol for a prolonged period also resulted in the induction of total P-450 in the brain (150% of the control). Addition of the antisera raised against rat liver cytochrome P-450IIE1 markedly inhibited brain microsomal p-nitrophenol hydroxylase activity. Immunoblot analysis of rat brain microsomes using the above antisera also revealed the induction of brain cytochrome P-450IIE1 following chronic ethanol administration. Immunocytochemical localization of cytochrome P-450IIEI using the above antisera, revealed the preferential localization of the enzyme in the neuronal cell bodies in the cortex, hippocampus, basal ganglia, hypothalamic nuclei and reticular nuclei in the brainstem of rats treated chronically with ethanol. Based upon these studies, it is conceivable that chronic alcohol ingestion could enhance the sensitivity of certain regions of the brain to environmental chemicals that are metabolized to more toxic derivatives by the P-450 system. C1 NIMHANS,DEPT NEUROCHEM,HOSUR RD,BANGALORE 560029,INDIA. NIMHANS,DEPT NEUROPATHOL,BANGALORE,INDIA. NCI,FREDERICK CANC RES & DEV CTR,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. NIAAA,METAB & MOLEC BIOL LAB,ROCKVILLE,MD 20852. NR 35 TC 71 Z9 71 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 JAN 22 PY 1993 VL 601 IS 1-2 BP 279 EP 285 DI 10.1016/0006-8993(93)91721-4 PG 7 WC Neurosciences SC Neurosciences & Neurology GA KH884 UT WOS:A1993KH88400033 PM 8431773 ER PT J AU MATSUDA, LA BONNER, TI LOLAIT, SJ AF MATSUDA, LA BONNER, TI LOLAIT, SJ TI LOCALIZATION OF CANNABINOID RECEPTOR MESSENGER-RNA IN RAT-BRAIN SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE INSITU HYBRIDIZATION HISTOCHEMISTRY; CANNABIS; HIPPOCAMPUS; BASAL GANGLIA; TETRAHYDROCANNABINOL ID NEURONAL LOCALIZATION; DENTATE GYRUS; HORSERADISH-PEROXIDASE; OLFACTORY TUBERCLE; ADENYLATE-CYCLASE; AXONAL-TRANSPORT; GLOBUS PALLIDUS; PROJECTION; NUCLEI; CONNECTIONS AB Cannabinoid receptor mRNA was localized in adult rat brain by S-35-tailed oligonucleotide probes and in situ hybridization histochemistry. Labelling is described as uniform or non-uniform depending on the relative intensities of individual cells expressing cannabinoid receptor mRNA within a given region or nucleus. Uniform labelling was found in the hypothalamus, thalamus, basal ganglia, cerebellum and brainstem. Non-uniform labelling that resulted from the presence of cells displaying two easily distinguishable intensities of hybridization signals was observed in several regions and nuclei in the forebrain (cerebral cortex, hippocampus, amygdala, certain olfactory structures). Olfactory-associated structures, basal ganglia, hippocampus, and cerebellar cortex displayed the heaviest amounts of labelling. Many regions that displayed cannabinoid receptor mRNA could reasonably be identified as sources for cannabinoid receptors on the basis of well documented hodologic data. Other sites that were also clearly labelled could not be assigned as logical sources of cannabinoid receptors. The localization of cannabinoid receptor mRNA indicates that sensory, motor, cognitive, limbic, and autonomic systems should all be influenced by the activation of this receptor by either exogenous cannabimimetics, including marijuana, or the yet unknown endogenous ''cannabinoid'' ligand. C1 NIH,CELL BIOL LAB,BETHESDA,MD 20892. NR 56 TC 418 Z9 429 U1 1 U2 8 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JAN 22 PY 1993 VL 327 IS 4 BP 535 EP 550 DI 10.1002/cne.903270406 PG 16 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA KH555 UT WOS:A1993KH55500005 PM 8440779 ER PT J AU LAZAR, G MADERDRUT, JL TRASTI, SL LIPOSITS, Z TOTH, P KOZICZ, T MERCHENTHALER, I AF LAZAR, G MADERDRUT, JL TRASTI, SL LIPOSITS, Z TOTH, P KOZICZ, T MERCHENTHALER, I TI DISTRIBUTION OF PRONEUROPEPTIDE Y-DERIVED PEPTIDES IN THE BRAIN OF RANA-ESCULENTA AND XENOPUS-LAEVIS SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE AMPHIBIA; ELECTRON MICROSCOPY; EVOLUTION; HYPOTHALAMUS; IMMUNOCYTOCHEMISTRY; NEUROANATOMY; NEUROPEPTIDE-Y; OPTIC TECTUM; PANCREATIC POLYPEPTIDE ID IMMUNOREACTIVE AMACRINE CELLS; POLYPEPTIDE-LIKE IMMUNOREACTIVITY; TERMINAL FLANKING PEPTIDE; CENTRAL NERVOUS-SYSTEM; NEUROPEPTIDE-Y; PANCREATIC-POLYPEPTIDE; SPINAL-CORD; SUBSTANCE-P; (NPY)-LIKE IMMUNOREACTIVITY; IMMUNOHISTOCHEMICAL LOCALIZATION AB The distribution of proneuropeptide Y-containing perikarya and nerve fibers in the brain of Rana esculenta and Xenopus laevis was determined with antisera directed toward neuropeptide Y and the carboxyl terminal flanking peptide. The distribution of proneuropeptide Y-like immunoreactivity was similar in both anurans. In the telencephalon, immunoreactive perikarya were found in the olfactory bulb, all subdivisions of the pallium, the septum, pars lateralis of the amygdala, the nucleus accumbens, and the anterior preoptic area. In the diencephalon, labelled perikarya were detected in the ventromedial, ventrolateral and central thalamic nuclei, the magnocellular preoptic nucleus, the suprachiasmatic nucleus, the posterior tuberculum, and the infundibulum. Amacrine-like cells were stained in the retina. In the pretectal area, posterior thalamic neurons showed intense, Golgi-like immunostaining. In the mesencephalon, immunoreactive cells were found in the reticular nucleus, the anteroventral tegmental nucleus, the optic tectum, the interpeduncular nucleus, and the torus semicircularis. In the rhombencephalon, labelled perikarya were detected in the secondary visceral nucleus, the central gray, the nucleus of the solitary tract, the dorsal column nuclei, and the spinal nucleus of the trigeminal nerve. Immunoreactive nerve fibers were observed in all areas of the brain that contained labelled perikarya. The densest accumulations were found in the accessory olfactory bulb, pars lateralis of the amygdala, the ventral habenula, the posterior pituitary, the optic tectum, the interpeduncular nucleus, and the saccular nucleus. The distribution of proneuropeptide Y-like immunoreactivity in the anuran brain showed many similarities to the distribution described for the amniote brain. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,MDC4-07,POB 12233,RES TRIANGLE PK,NC 27709. UNIV PECS,DEPT ANAT,H-7643 PECS,HUNGARY. KENSINGTON TRACE,CHAPEL HILL,NC 27514. RI Kozicz MD, PhD, Tamas/G-3161-2012; Kozicz, Tamas/N-5154-2014 OI Kozicz MD, PhD, Tamas/0000-0001-6915-4364; NR 75 TC 63 Z9 65 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD JAN 22 PY 1993 VL 327 IS 4 BP 551 EP 571 DI 10.1002/cne.903270407 PG 21 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA KH555 UT WOS:A1993KH55500006 PM 8440780 ER PT J AU POTHEN, S CAO, T SMITH, R LEVINE, PH LEVINE, A PEARSON, GR AF POTHEN, S CAO, T SMITH, R LEVINE, PH LEVINE, A PEARSON, GR TI IDENTIFICATION OF T-CELL AND B-CELL EPITOPES ASSOCIATED WITH A RESTRICTED COMPONENT OF THE EPSTEIN-BARR VIRUS-INDUCED EARLY ANTIGEN COMPLEX SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID MONOCLONAL-ANTIBODIES; IMMUNODEFICIENCY; SEQUENCE AB Experiments were designed in an attempt to identify T- and B-cell epitopes expressed on the 17-kDa early-antigen-restricted (EA-R) polypeptide of the EBV-induced early antigen complex. Using Berzofsky's algorithm, 3 hypothetical T-cell epitopes on p17 were synthesized and employed in EBV-specific lymphoproliferative assays. Lymphocytes from all EBV-infected donors responded against one of these epitopes (p 17.1) irrespective of their serological status relative to antibodies to EA-R. Both CD4+ and CD8+ T-cell subpopulations from seropositive donors proliferated in the presence of p17.1 in short-term cultures. These experiments therefore identified one T-cell epitope on the 17-kDa polypeptide. In contrast, sera from anti-EA antibody-positive individuals reacted with all 3 synthetic peptides to varying degrees, with p17.1 being the most frequently reactive epitope. When the sera were grouped according to diagnosis, it was noted that 82% of the sera from patients with aggressive lymphomas, whether Africans with Burkitt's lymphoma or North Americans with intermediate-grade large-cell or high-grade B-cell lymphoma, contained antibody reactive with p17.1, while 64% were reactive with p17.2 and 29% with p17.3. In contrast, high anti-EA antibody-positive sera from nasopharyngeal carcinoma patients were relatively less reactive with these synthetic peptides (23% positive with p17.1; 19% with p17.2; and 13% with p 17.3). These results therefore identified 3 B-cell EA-R epitopes which might be potentially useful for clinical or epidemiological studies of EBV-associated lymphoproliferative diseases. C1 GEORGETOWN UNIV,SCH MED,DEPT MICROBIOL,MED DENT BLDG,53RD FLOOR,3900 RESERVOIR RD,WASHINGTON,DC 20007. JOHNSON & JOHNSON BIOTECHNOL CTR,SAN DIEGO,CA. NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. UNIV SO CALIF,DEPT HEMATOL,LOS ANGELES,CA 90089. NR 22 TC 9 Z9 9 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JAN 21 PY 1993 VL 53 IS 2 BP 199 EP 204 DI 10.1002/ijc.2910530204 PG 6 WC Oncology SC Oncology GA KH524 UT WOS:A1993KH52400003 PM 7678829 ER PT J AU MILLER, AC KARIKO, K MYERS, CE CLARK, EP SAMID, D AF MILLER, AC KARIKO, K MYERS, CE CLARK, EP SAMID, D TI INCREASED RADIORESISTANCE OF EJRAS-TRANSFORMED HUMAN OSTEOSARCOMA CELLS AND ITS MODULATION BY LOVASTATIN, AN INHIBITOR OF P21RAS ISOPRENYLATION SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID H-RAS; RESISTANCE; BIOSYNTHESIS; ONCOGENES; RADIATION; PROTEINS; GROWTH AB Alterations in ras oncogene expression have been associated with increased cellular resistance to ionizing radiation. As an extension of studies with murine cell models, we have now explored the radioresponses of human osteosarcoma (HOS) sub-clones that differ in their EJras expression. Quantitative analysis revealed a tight correlation between the amounts of ras-encoded mRNA and p21 produced, and the degree of cell radioresistance. Interestingly, treatment of the ras-transformed cells with lovastatin, an inhibitor of p21ras post-translational processing via the mevalonate pathway, markedly decreased their radioresistance. Under the experimental conditions used, lovastatin prevented the membrane association, but not the biosynthesis, of p21. The decline in radiation resistance following lovastatin treatment could not be attributed to perturbation of cholesterol metabolism or to non-specific cell-cycle effects. In agreement, lovastatin did not alter the radiation responses of control HOS cells that do not express EJras, or those with an activated met oncogene. The results indicate that elevation in ras gene expression can lead to increased radioresistance of human tumor cells. It appears, however, that p21ras membrane localization is critical for maintenance of the radioresistant phenotype, thus providing a target for pharmacological intervention. C1 NCI,DIV CANC TREATMENT,CLIN PHARMACOL SECT,BLDG 10,ROOM 12C103,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. UNIV PENN,SCH MED,DEPT MED,CARDIOVASC SECT,PHILADELPHIA,PA 19104. ARMED FORCES RADIOBIOL RES INST,DEPT RADIAT BIOCHEM,BETHESDA,MD 20889. NR 24 TC 110 Z9 112 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 JAN 21 PY 1993 VL 53 IS 2 BP 302 EP 307 DI 10.1002/ijc.2910530222 PG 6 WC Oncology SC Oncology GA KH524 UT WOS:A1993KH52400021 PM 8425769 ER PT J AU WHITE, RE LEE, AB SHCHERBATKO, AD LINCOLN, TM SCHONBRUNN, A ARMSTRONG, DL AF WHITE, RE LEE, AB SHCHERBATKO, AD LINCOLN, TM SCHONBRUNN, A ARMSTRONG, DL TI POTASSIUM CHANNEL STIMULATION BY NATRIURETIC PEPTIDES THROUGH CGMP-DEPENDENT DEPHOSPHORYLATION SO NATURE LA English DT Article ID CA-2+-ACTIVATED K+ CHANNELS; ANTERIOR-PITUITARY-CELLS; SMOOTH-MUSCLE CELLS; PROTEIN-KINASE; CALCIUM CHANNELS; CYCLIC-GMP; MODULATION; PHOSPHATASES; RECEPTOR; CYCLASE AB NATRIURETIC peptides inhibit the release and action of many hormones through cyclic guanosine monophosphate (cGMp)1,2, but the mechanism of cGMP action is unclear3. In frog ventricular muscle and guinea-pig hippocampal neurons, cGMP inhibits voltage-activated Ca2+ currents by stimulating phosphodiesterase activity and reducing intracellular cyclic AMP4,5; however, this mechanism is not involved in the action of cGMP on other channels6 or on Ca2+ channels in other cells7,8. Natriuretic peptide receptors in the rat pituitary also stimulate guanylyl cyclase activity but inhibit secretion by increasing membrane conductance to potassium9,10. In an electrophysiological study on rat pituitary tumour cells11, we identified the large-conductance, calcium- and voltage-activated potassium channels (BK) as the primary target of another inhibitory neuropeptide, somatostatin. Here we report that atrial natriuretic peptide also stimulates BK channel activity in GH4C1 cells through protein dephosphorylation. Unlike somatostatin, however, the effect of atrial natriuretic peptide on BK channel activity is preceded by a rapid and potent stimulation of cGMP production and requires cGMP-dependent protein kinase activity. Protein phosphatase activation by cGMP-dependent kinase could explain the inhibitory effects of natriuretic peptides on electrical excitability and the antagonism of cGMP and cAMP in many systems12. C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. UNIV ALABAMA,DEPT PATHOL,BIRMINGHAM,AL 35294. UNIV TEXAS,SCH MED,DEPT PHARMACOL,HOUSTON,TX 77225. NR 31 TC 232 Z9 238 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 JAN 21 PY 1993 VL 361 IS 6409 BP 263 EP 266 DI 10.1038/361263a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH614 UT WOS:A1993KH61400061 PM 7678699 ER PT J AU SINGH, J KLAR, AJS AF SINGH, J KLAR, AJS TI DNA POLYMERASE-ALPHA IS ESSENTIAL FOR MATING-TYPE SWITCHING IN FISSION YEAST SO NATURE LA English DT Article ID SCHIZOSACCHAROMYCES-POMBE; REPLICATION; GENES; CELLS; INITIATION; ASYMMETRY; STRANDS; PATTERN; SITE; MAT1 AB IN the fission yeast Schizosaccharomyces pombe, the double-stranded chromosomal break (DSB) at the mating-type locus (mat1) initiates recombination during mating-type switching1-3 . A constant DSB level is maintained throughout the cell-cycle'. In the strand-segregation model for mating-type switching, it was postulated that if the DSB is generated during or soon after mat1 replication4, one of the chromatids could be repaired and switched during replication in the next cell cycle, while the other chromatid inherits the break3-6. Here we report a molecular characterization of swi7, one of the genes required for DSB formation. Surprisingly, a gene complementing the swi7 mutation maps to chromosome I and encodes S. pombe DNA polymerase-alpha. Disruption of this gene is lethal in both switching and non-switching strains, as expected. S. pombe DNA polymerase-alpha must therefore play a role in generating the DSB at mat1, suggesting that DSB formation is coupled with DNA replication. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM,EUKARYOT GENE EXPRESS LAB, POB B,BLDG 539, FREDERICK, MD 21702 USA. NR 28 TC 58 Z9 59 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 EI 1476-4687 J9 NATURE JI Nature PD JAN 21 PY 1993 VL 361 IS 6409 BP 271 EP 273 DI 10.1038/361271a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH614 UT WOS:A1993KH61400064 PM 8423854 ER PT J AU MOORE, J CAMPANA, J LAM, M SANDAUCHRISTOPHER, D SADLER, J SCALISE, D GAY, N STALVEY, R SCHROEDER, J PELTON, J BIEHR, BJ HARRIS, J STRUNK, N CHIOTTI, R OWENSNAUSLER, J GRENERT, B CHIODA, D COLE, D MEURER, K ABELSON, G SHEFFIELD, A RUZICKA, P BALSLEY, C SUTTER, M CHERNECO, MD FRASER, J CARR, M WORD, E SIMPSON, P LACY, L TYE, S NEHLSLOWE, B ANDERSON, B AF MOORE, J CAMPANA, J LAM, M SANDAUCHRISTOPHER, D SADLER, J SCALISE, D GAY, N STALVEY, R SCHROEDER, J PELTON, J BIEHR, BJ HARRIS, J STRUNK, N CHIOTTI, R OWENSNAUSLER, J GRENERT, B CHIODA, D COLE, D MEURER, K ABELSON, G SHEFFIELD, A RUZICKA, P BALSLEY, C SUTTER, M CHERNECO, MD FRASER, J CARR, M WORD, E SIMPSON, P LACY, L TYE, S NEHLSLOWE, B ANDERSON, B TI SELECTED BEHAVIORS THAT INCREASE RISK FOR HIV-INFECTION, OTHER SEXUALLY-TRANSMITTED DISEASES, AND UNINTENDED PREGNANCY AMONG HIGH-SCHOOL-STUDENTS - UNITED-STATES, 1991 (REPRINTED FROM MMWR, VOL 41, PG 945-950, 1992) SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Reprint C1 SAN DIEGO UNIFIED SCH DIST,SAN DIEGO,CA. SAN FRANCISCO UNIFIED SCH DIST,SAN FRANCISCO,CA. DIST COLUMBIA PUBL SCH,WASHINGTON,DC. CHICAGO PUBL SCH,CHICAGO,IL. BOSTON PUBL SCH SYST,BOSTON,MA. NEW HAMPSHIRE STATE DEPT EDUC,CONCORD,NH 03301. JERSEY CITY BOARD EDUC,JERSEY CITY,NJ. NEW MEXICO STATE DEPT EDUC,SANTA FE,NM 87501. NEW YORK CITY BOARD EDUC,NEW YORK,NY. NEW YORK STATE DEPT EDUC,ALBANY,NY 12224. SCH DIST PHILADELPHIA,PHILADELPHIA,PA. DALLAS INDEPENDENT SCH DIST,DALLAS,TX. UTAH STATE OFF EDUC,SALT LAKE CITY,UT 84111. WISCONSIN DEPT PUBL INSTRUCT,MADISON,WI 53707. NIDA,LEXINGTON,KY 40583. CTR DIS CONTROL,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,DIV REPROD HLTH,ATLANTA,GA 30333. RP MOORE, J (reprint author), ALABAMA STATE DEPT EDUC,MONTGOMERY,AL 36130, USA. NR 11 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 JAN 20 PY 1993 VL 269 IS 3 BP 329 EP 330 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KG381 UT WOS:A1993KG38100007 ER PT J AU OBERTO, J CLERGET, M DITTO, M CAM, K WEISBERG, RA AF OBERTO, J CLERGET, M DITTO, M CAM, K WEISBERG, RA TI ANTITERMINATION OF EARLY TRANSCRIPTION IN PHAGE-HK022 - ABSENCE OF A PHAGE-ENCODED ANTITERMINATION FACTOR SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE ANTITERMINATION; TRANSCRIPTION TERMINATION; PHAGE-HK022 ID SITE-SPECIFIC RECOMBINATION; LAMBDA-N ANTITERMINATION; BACTERIOPHAGE-LAMBDA; ESCHERICHIA-COLI; CLONING VECTORS; TERMINATION SITES; DELETION MUTANTS; RNA-POLYMERASE; OPERON FUSIONS; REGION C1 NICHHD,MICROBIAL GENET SECT,MOLEC GENET LAB,BLDG 6B,ROOM 4B-413,BETHESDA,MD 20892. NR 53 TC 25 Z9 25 U1 0 U2 0 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 JAN 20 PY 1993 VL 229 IS 2 BP 368 EP 381 DI 10.1006/jmbi.1993.1040 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KL456 UT WOS:A1993KL45600009 PM 8429552 ER PT J AU KANG, HS KUROCHKINA, NA LEE, B AF KANG, HS KUROCHKINA, NA LEE, B TI ESTIMATION AND USE OF PROTEIN BACKBONE ANGLE PROBABILITIES SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE PHI-PSI PROBABILITIES; POLYPEPTIDE STRUCTURE PREDICTION; CHAIN CONFORMATIONAL ENTROPY; FOLDING INITIATION SITES ID IMMUNOGENIC PEPTIDE-FRAGMENTS; DYNAMIC MONTE-CARLO; SECONDARY STRUCTURE; GLOBULAR PROTEINS; HYDROGEN-EXCHANGE; WATER SOLUTION; NMR; CONFORMATION; PREDICTION; SEQUENCE C1 NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BLDG 37,ROOM 4B15,BETHESDA,MD 20892. NR 40 TC 44 Z9 45 U1 0 U2 1 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 JAN 20 PY 1993 VL 229 IS 2 BP 448 EP 460 DI 10.1006/jmbi.1993.1045 PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KL456 UT WOS:A1993KL45600014 PM 8429556 ER PT J AU RAGHUNATHAN, G MILES, HT SASISEKHARAN, V AF RAGHUNATHAN, G MILES, HT SASISEKHARAN, V TI SYMMETRY AND MOLECULAR-STRUCTURE OF A DNA TRIPLE HELIX - D(T)N.D(A)N.D(T)N SO BIOCHEMISTRY LA English DT Article ID STRAND FORMATION; INHIBITION; SEQUENCES; PLASMIDS; PROTEINS; PROMOTER; CELLS; FORM AB A structure for the triple helix d(T)n.d(A)n.d(T)n consistent with recent infrared spectral data is proposed, and its salient features are discussed. The present structure preserves the pseudodyad between the Watson-Crick base-paired adenine and thymine strands and in addition has a pseudorotational symmetry relating the Hoogsteen-paired adenine and thymine strands. The simultaneous presence of these two symmetries gives rise to a dyad between the two thymine polynucleotides. These symmetries result in identical backbone conformations for all three strands, unlike any previously proposed model for a triple helix. The proposed structure has an axial rise per residue of 3.26 angstrom and 12 residues per turn obtained from X-ray fiber diffraction [Arnott S., & Selsing, E. (1974) J. Mol. Biol. 88, 509-521]. The present structure is structurally and conformationally similar to double helical B-form DNA and has sugar pucker in the C2'-endo region. This structure is fundamentally different from the one proposed by Arnott and co-workers, which was based on structural and conformational features similar to double helical A-form DNA with C3'-endo sugar pucker. It is stereochemically satisfactory, and it does not have the disallowed nonbonded distances present in the earlier model of Arnott and co-workers. It is energetically much more favorable than their structure. Coordinates of the present structure are given. C1 NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. RP RAGHUNATHAN, G (reprint author), NCI,MATH BIOL LAB,ROOM 217,6010 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 43 TC 92 Z9 92 U1 1 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 JAN 19 PY 1993 VL 32 IS 2 BP 455 EP 462 DI 10.1021/bi00053a009 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH386 UT WOS:A1993KH38600009 PM 8422354 ER PT J AU MURAYAMA, T TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M AF MURAYAMA, T TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M TI EFFECTS OF TEMPERATURE ON ADP-RIBOSYLATION FACTOR STIMULATION OF CHOLERA-TOXIN ACTIVITY SO BIOCHEMISTRY LA English DT Article ID BINDING REGULATORY PROTEINS; NUCLEOTIDE-BINDING; ADENYLATE-CYCLASE; RIBOSYLTRANSFERASE ACTIVITY; ESCHERICHIA-COLI; BOVINE BRAIN; SOLUBLE-PROTEINS; ACTIVATION; GTP; MECHANISM AB The effects of cholera toxin, a secretory product of Vibrio cholerae, result from ADP-ribosylation of the stimulatory guanine nucleotide-binding (G(s)) protein of the adenylyl cyclase system. Cholera toxin A subunit (CTA) also uses agmatine, a simple guanidino compound, several proteins unrelated to G(s), and CTA itself as alternative ADP-ribose acceptors. The effects of toxin occur in the jejunum presumably at body core temperature. With agmatine as a model substrate, the optimal temperature for CTA-catalyzed ADP-ribosylation was 25-30-degrees-C, and that for CTA-catalyzed auto-ADP-ribosylation was 20-25-degrees-C. Both activities were significantly less at 37-degrees-C, reflecting lower initial velocities, not heat-inactivation of the toxin. All the transferase activities of CTA are enhanced by ADP-ribosylation factors (ARFs), approximately 20-kDa guanine nucleotide-binding proteins that are ubiquitous in mammalian cells. Phospholipids and a soluble brain ARF, in a GTP-dependent manner, activated toxin NAD:agmatine ADP-ribosyltransferase activity; their simultaneous effect was maximal at physiological temperatures (approximately 37-degrees-C). At lower temperatures, the stimulation by ARF was much less. There were similar effects on other toxin-catalyzed reactions, notably, the ADP-ribosylation of G(salpha) and the hydrolysis of NAD. Thus, host factors, such as ARF and phospholipid, synergistically increase cholera toxin activity at 37-degrees-C and may be important in toxin action in the mammalian gut. RP MURAYAMA, T (reprint author), NHLBI,CELLULAR METAB LAB,BLDG 10,ROOM 5N-307,BETHESDA,MD 20892, USA. NR 29 TC 38 Z9 38 U1 0 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 JAN 19 PY 1993 VL 32 IS 2 BP 561 EP 566 DI 10.1021/bi00053a022 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KH386 UT WOS:A1993KH38600022 PM 8422366 ER PT J AU SALVADORI, S BRYANT, SD TEMUSSI, PA BUNDY, DM ATTILA, M TOMATIS, R LAZARUS, LH AF SALVADORI, S BRYANT, SD TEMUSSI, PA BUNDY, DM ATTILA, M TOMATIS, R LAZARUS, LH TI RELATIONSHIP BETWEEN RECEPTOR AFFINITY AND TOPOGRAPHY OF N-TERMINALLY EXTENDED AND BRIDGED [TYR1-]ASP4]DELTORPHIN-C ANALOGS - NOVEL PROBES FOR THE DELTA-OPIOID RECEPTOR SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Note DE DELTORPHIN; OPIOID RECEPTORS; PEPTIDE SYNTHESIS; COMPUTER MODELING ID DERMORPHIN; PEPTIDES; SELECTIVITY; SITES; SEQUENCE AB Receptor binding of N-terminally extended Tyr1 deltorphin C analogues diminished delta and mu affinities, but with only a moderate loss in delta selectivity. Pseudopeptide bridged [Tyr1 --> Aps4]deltorphin C analogues drastically decreased delta affinity to yield peptides with poor delta selectivity. Low energy conformers of the peptides revealed that the bridge modifies the spatial orientation of the backbone of the N- and C-terminal sequences with respect to deltorphin C. The data indicate that the delta receptor site can accommodate an opioid peptide containing an N-terminal aliphatic extension on amino-Tyr1, but not a heptapeptide conformationally constrained between residues 1 and 4. C1 NIEHS,INTEGRAT BIOL LAB,PEPTIDE NEUROCHEM SECT,POB 12233,RES TRIANGLE PK,NC 27709. UNIV NAPLES,DEPT CHEM,I-80134 NAPLES,ITALY. UNIV FERRARA,DEPT PHARMACEUT SCI,I-44100 FERRARA,ITALY. OI SALVADORI, Severo/0000-0002-8224-2358 NR 16 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD JAN 19 PY 1993 VL 230 IS 3 BP 357 EP 361 DI 10.1016/0014-2999(93)90573-Z PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KM165 UT WOS:A1993KM16500017 PM 8382619 ER PT J AU WANG, LH MANTEY, SA LIN, JT FRUCHT, H JENSEN, RT AF WANG, LH MANTEY, SA LIN, JT FRUCHT, H JENSEN, RT TI LIGAND-BINDING, INTERNALIZATION, DEGRADATION AND REGULATION BY GUANINE-NUCLEOTIDES OF BOMBESIN RECEPTOR SUBTYPES - A COMPARATIVE-STUDY SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE BOMBESIN; RECEPTOR; LIGAND BINDING; GUANINE NUCLEOTIDE ID SWISS 3T3 CELLS; GASTRIN-RELEASING PEPTIDE; CENTRAL-NERVOUS-SYSTEM; RAT PANCREATIC ACINI; MUSCLE-CELLS; CANCER CELLS; LUNG-CANCER; GROWTH; BRAIN; LINE AB Recent cloning studies confirm two subtypes of Bn receptors exist, a neuromedin B-preferring receptor (NMB-R) and a gastrin-releasing peptide-preferring receptor (GRP-R). Both subtypes occur widely in GI tract and the CNS; however, to the GRP-R subtype little is known about the ligand-receptor interactions for the NMB-R. Therefore, in the present study we explored the ligand-receptor interactions including kinetics. stoichiometry, internalization. degradation and regulation by guanine nucleotide binding proteins with the NMB-R and compared it to the GRP-R. The rat glioblastoma C-6 cell line which possess functional NMB-R and 3T3 cells which possess functional GRP-R were used. I-125-[D-Tyr-degrees]NMB and I-125-[Tyr4]Bn were prepared using lodogen and purified on HPLC. At 37-degrees-C binding of I-125-[D-Tyr-degrees]NMB to NMB-R or I-125-[Tyr4]Bn to GRP-R was maximal by 5-15 min and decreased to 60-70% after 60 min. HPLC analysis of the 60 min supernatant showed that > 80% of each tracer was degraded. Addition of proteinase inhibitors had a varied inhibitory effect on degradation with the relative order of potency in C-6 cells being leupeptin > bacitracin > chymostatin > phosphoramidon much greater than bestatin and amastatin and 3T3 cells being bacitracin = phosphoramidon > leupeptin = bestatin > chymostatin > amastatin in 3T3 cells. By HPLC analysis addition of bacitracin prevented the degradation in both cell types. With both receptor subtypes dissociation of bound radioligands was slow. with 70-80% of either I-125-[D-Tyr-degrees]NMB or I-125-[Tyr4]Bn remained cell-associated after 60 min suggesting possible peptide internalization. With an acid wash procedure to remove surface bound radioligands, 60% of the C-6 cell-associated I-125-[D-Tyr-degrees]NMB and 52% of the 3T3 cell-associated I-125-[Tyr4]Bn were internalized after 30 min at 37-degrees-C. With membranes from cells possessing either receptor subtype, the stable guanine nucleotide GPP(NH)P inhibited in a dose-dependent fashion binding of ligands. Computer analysis demonstrated that GPP(NH)P decreased receptor affinity for ligands to both receptor subtypes. These results demonstrated that NMB receptors, similar to GRP receptors and rapidly internalize bound agonists and rapidly degrade agonists. The ligand-receptor interaction is regulated by a guanine nucleotide binding protein for both Bn receptor subtypes. C1 NIDDKD,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892. NR 55 TC 34 Z9 34 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD JAN 17 PY 1993 VL 1175 IS 2 BP 232 EP 242 DI 10.1016/0167-4889(93)90028-N PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KH713 UT WOS:A1993KH71300014 PM 8380344 ER PT J AU XIAO, OS WEI, Z POTISCHMAN, N BRINTON, LA HATCH, MC GAO, YT FRAUMENI, JF AF XIAO, OS WEI, Z POTISCHMAN, N BRINTON, LA HATCH, MC GAO, YT FRAUMENI, JF TI A POPULATION-BASED CASE-CONTROL STUDY OF DIETARY FACTORS AND ENDOMETRIAL CANCER IN SHANGHAI, PEOPLES-REPUBLIC-OF-CHINA SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE CASE-CONTROL STUDIES; DIETARY FATS; ENDOMETRIUM; NUTRITION; RISK FACTORS; UTERINE NEOPLASMS ID HORMONE CONCENTRATIONS; WOMEN; CONSUMPTION; RISK; FAT; VEGETARIAN; DISEASE; ALCOHOL AB The relation between diet and endometrial cancer was examined in a population-based case-control study conducted in Shanghai, People's Republic of China, between 1988 and 1990, involving interviews with 268 cases and 268 controls aged 18-74 years. The subjects' usual dietary intake of 63 major foods during the previous 10 years (disregarding any recent changes) was measured by means of a structured quantitative food questionnaire. Although women in the highest quartile of total caloric intake had a 2.1-fold increased risk of endometrial cancer, risk varied according to the source of calories. The highest quartiles of caloric intake from fat and protein were associated with odds ratios of 3.9 and 3.1, respectively, while calories from carbohydrates, the major contributor of total calories in this population, were not related to risk. The association of fat and protein with endometrial cancer risk was confined to foods of animal origin in the diet. After adjustment for age, body mass index (weight (kg)/height (m)2), and number of pregnancies, odds ratios were 3.5 (95% confidence interval (Cl) 2.0-6.0) and 3.0 (95% Cl 1.7-5.1) for women in the highest quartiles of intake of animal fat and animal protein, respectively. Food group analyses showed a similar pattern, with high consumption of meat, eggs, and fresh fish being associated with elevated risks. After adjustment for total calories, no significant association of risk was found with intake of vegetables or dark green/yellow vegetables, or with estimated carotene intake, although fruit and allium vegetables were associated with some reduction in risk. These results suggest that diets rich in animal fat and animal protein may play an important role in the etiology of endometrial cancer. C1 SHANGHAI CANC INST,DEPT EPIDEMIOL,SHANGHAI,PEOPLES R CHINA. COLUMBIA UNIV,DIV EPIDEMIOL,NEW YORK,NY 10027. NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 32 TC 3 Z9 3 U1 0 U2 2 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JAN 15 PY 1993 VL 137 IS 2 BP 155 EP 165 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KR948 UT WOS:A1993KR94800004 ER PT J AU MARINI, JC LEWIS, MB CHEN, K AF MARINI, JC LEWIS, MB CHEN, K TI MODERATELY SEVERE OSTEOGENESIS IMPERFECTA ASSOCIATED WITH SUBSTITUTIONS OF SERINE FOR GLYCINE IN THE ALPHA-1(I) CHAIN OF TYPE-I COLLAGEN SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL CONF ON OSTEOGENESIS IMPERFECTA CY SEP 09-12, 1990 CL UNIV PAVIA, COLL NUOVO, PAVIA, ITALY HO UNIV PAVIA, COLL NUOVO DE MOLECULAR PATHOGENESIS; COL1A1; OSTEOGENESIS IMPERFECTA ID TRIPLE-HELICAL DOMAIN; POINT MUTATIONS; PHENOTYPE; CYSTEINE AB We have examined the type I collagen protein, RNA, and cDNA of 2 children with moderately severe (type IV) osteogenesis imperfecta (OI). They have in common a non-lethal form of OI with ambulatory potential, over-modification of type I collagen protein, and a substitution of serine for glycine in the collagen chain produced by one alpha1(I) allele. The first child (Marini et al.: J Biol Chem 264:11893-11900,1989) is now 7 years old, with the height of a 3-year-old. Her course includes significant remodeling of lower long bones and 4 femur fractures. She walks independently. A mishmatch was detected in her alpha1(I) mRNA using RNA/RNA hybrids; it was demonstrated to be due to a G-->A point mutation in one allele of alpha1(I), resulting in the substitution of serine for glycine 832. The second child is now 6 1/2 years old, with the height of 1 1/2-year-old. Her history includes significant bowing of femurs and tibias, 6 femur fractures, S-curve scoliosis, compression of all lumbar vertebrae, and limited short-distance walking with braces. Her alpha1(I) mRNA has also been studied by RNA hybrid analysis; there is a single G-->A change in one alpha1(I) allele causing the substitution of serine for gly 352. Both children have moderately severe OI. However, the serine substitution at gly 352 is associated with a more severe phenotype then is the serine substitution at gly 832. Compared to substitutions described in other cases of OI, the serine 352 is located in the middle of a cluster of cysteine substitutions associated with non-lethal OI. The ser 832 is located near another non-lethal substitution of serine for glycine but is otherwise flanked by lethal substitutions. These data support a model of OI cause in which crucial and non-crucial regions are interspersed along the type I collagen chain. Whether a mutation located in a particular region causes OI type II or OI type IV would then depend on the importance of that region for the interaction of type I collagen with other matrix components or for intracellular processing. RP MARINI, JC (reprint author), NICHHD,HUMAN GENET BRANCH,CONNECT TISSUE DISORDERS,BLDG 10,ROOM 9S242,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 10 TC 5 Z9 6 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 15 PY 1993 VL 45 IS 2 BP 241 EP 245 DI 10.1002/ajmg.1320450217 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA KG480 UT WOS:A1993KG48000016 PM 8456809 ER PT J AU MARINI, JC BORDENICK, S HEAVNER, G ROSE, S CHROUSOS, GP AF MARINI, JC BORDENICK, S HEAVNER, G ROSE, S CHROUSOS, GP TI EVALUATION OF GROWTH-HORMONE AXIS AND RESPONSIVENESS TO GROWTH-STIMULATION OF SHORT CHILDREN WITH OSTEOGENESIS IMPERFECTA SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL CONF ON OSTEOGENESIS IMPERFECTA CY SEP 09-12, 1990 CL UNIV PAVIA, COLL NUOVO, PAVIA, ITALY HO UNIV PAVIA, COLL NUOVO DE OI TYPE-I; OI TYPE-III; OI TYPE-IV; GROWTH HORMONE; GROWTH HORMONE RELEASING FACTOR ID SHORT STATURE; GIRLS; BOYS AB Growth deficiency is a cardinal manifestation of severe Osteogenesis Imperfecta (OI) and occurs frequently in moderate to mild OI. We have investigated the status of the hormones related to growth in 28 children with OI. Our goals were to determine whether there were any abnormalities of these hormones, whether the abnormalities correlated with types of OI, and whether OI bone could be safely stimulated to grow. The study group included 14 females and 14 males. Using the criteria developed by Sillence et al. [1979], 13 children had OI type III, 12 had OI type IV, and 3 had OI type I. Evaluation included 3 standard hGH provocative tests (AITT, L-Dopa), GRF stimulation, 24 hr q20 minute sampling of unstimulated growth hormone, and a somatomedin generation test. All patients except one had normal responses to standard provocative stimuli. Responses to GRF fell into 2 groups: one with a mean response similar to that of normal children, and one with a mean response resembling that of GH deficient children. The group with low response to GRF had a significantly lower area under the curve in the 24-hr test of unstimulated GH than did the normal response group. The OI children as a group showed a blunted IGF-1 response during the Somatomedin Generation Test, with 18/28 children having less than a two-fold stimulation. No test results correlated with OI type. Ten OI children were enrolled in a pilot growth stimulation study. Two children received protropin and 8 received clonidine for at least 6 months. Both children treated with protropin and 4/8 treated with clonidine experienced at least a doubling of their pre-treatment growth rates. Lack of growth hormone response did not correlate with type of OI or parameters from the hormonal evaluation. We speculate that there is a group of OI children who have a hypoactive growth hormone axis. Some OI bone appears to respond to GH and a treatment trial with protropin is planned for a larger number of children. C1 NICHHD,DEPT NURSING,BETHESDA,MD 20892. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP MARINI, JC (reprint author), NICHHD,HUMAN GENET BRANCH,BLDG 10,ROOM 95242,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 10 TC 30 Z9 31 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 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 15 PY 1993 VL 45 IS 2 BP 261 EP 264 DI 10.1002/ajmg.1320450223 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA KG480 UT WOS:A1993KG48000022 PM 8456815 ER PT J AU BINDER, H CONWAY, A HASON, S GERBER, LH MARINI, J BERRY, R WEINTROB, J AF BINDER, H CONWAY, A HASON, S GERBER, LH MARINI, J BERRY, R WEINTROB, J TI COMPREHENSIVE REHABILITATION OF THE CHILD WITH OSTEOGENESIS IMPERFECTA SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL CONF ON OSTEOGENESIS IMPERFECTA CY SEP 09-12, 1990 CL UNIV PAVIA, COLL NUOVO, PAVIA, ITALY HO UNIV PAVIA, COLL NUOVO DE OSTEOGENESIS IMPERFECTA; REHABILITATION; PHYSICAL THERAPY AB Children with osteogenesis imperfecta (OI) that results in considerable deformity are often viewed as poor candidates for aggressive physical therapy and rehabilitation. To determine if this view is realistic, we have entered almost 50 children with OI type III and OI type IV into a comprehensive graduated rehabilitation program, based at the National Institutes of Health, but designed to be implemented by continuing involvement of community resources. Children are begun in the program early with emphasis on gain of head and trunk control and progression to sitting and walking, if possible, with the aid of a variety of physical supports, including internal and external bracing. Although not conducted in a randomized fashion, the program's success in bringing children into graded exercise regimes and fostering their increased involvement in school and social situations suggest that aggressive physical therapy and rehabilitation have a major place in the overall care of the infants and children with OI. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD 20892. ORTHOT PROSTHET CTR,FAIFAX,VA. RP BINDER, H (reprint author), CHILDRENS HOSP,NATL MED CTR,DEPT PHYS MED & REHABIL,111 MICHIGAN AVE NW,WASHINGTON,DC 20010, USA. NR 7 TC 19 Z9 19 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 15 PY 1993 VL 45 IS 2 BP 265 EP 269 DI 10.1002/ajmg.1320450224 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA KG480 UT WOS:A1993KG48000023 PM 8456816 ER PT J AU SILLENCE, DO RITCHIE, HE DIBBAYAWAN, T ETESON, D BROWN, K AF SILLENCE, DO RITCHIE, HE DIBBAYAWAN, T ETESON, D BROWN, K TI FRAGILITAS-OSSIUM (FRO/FRO) IN THE MOUSE - A MODEL FOR A RECESSIVELY INHERITED TYPE OF OSTEOGENESIS IMPERFECTA SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL CONF ON OSTEOGENESIS IMPERFECTA CY SEP 09-12, 1990 CL UNIV PAVIA, COLL NUOVO, PAVIA, ITALY HO UNIV PAVIA, COLL NUOVO DE OI TYPE-II; OI TYPE-III; VARIABLE EXPRESSION ID GENETIC-HETEROGENEITY; DELINEATION; PHENOTYPE AB The fragilitas ossium (fro/fro) mutation in the mouse has been demonstrated to have clinical, radiographic and morphologic manifestations similar to those which arise in autosomal recessive forms of osteogenesis imperfecta (OI) occurring in humans. Approximately 90% of mutant offspring in the mouse were perinatally lethal with clinical and roentgenographic findings similar to those of OI type II subgroup A in humans. The 10% of mutant mice surviving follow a course very similar to severe progressively deforming OI type III. In surviving mice, there is progressive fore-limb and hind-limb bowing in the absence of a high fracture frequency. C1 UNIV SYDNEY,DEPT PAEDIAT & CHILD HLTH,SYDNEY,NSW 2006,AUSTRALIA. UNIV SYDNEY,DEPT ANAT,SYDNEY,NSW 2006,AUSTRALIA. UNIV SYDNEY,ELECTRON MICROSCOPY UNIT,SYDNEY,NSW 2006,AUSTRALIA. NIDR,DEV BIOL & ANOMOLIES,BETHESDA,MD 20892. HARBOR UCLA MED CTR TORRANCE,TORRANCE,CA. RI Ritchie, Helen/B-9910-2016 OI Ritchie, Helen/0000-0001-9794-5702 NR 19 TC 17 Z9 18 U1 2 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 15 PY 1993 VL 45 IS 2 BP 276 EP 283 DI 10.1002/ajmg.1320450227 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA KG480 UT WOS:A1993KG48000026 PM 8456819 ER PT J AU ALWARD, WLM FARRELL, T HAYREH, S KOLDER, H CARNEY, B PHELPS, C GRESSEL, M COSTIN, J CRAVEN, P ZGRABIK, M SCHREMP, P SIMASHKEVICH, B HEUER, DK BAERVELDT, G MINCKLER, D IRVINE, J SADUN, A GREEN, R MCDONNELL, P LLOYD, M OBER, RR WALONKER, F PADILLA, M MARTONE, J LIGGETT, P LEAN, J GRIFFAY, E MILLERSCHOLTE, A KASS, M KOLKER, A FARBER, M GANS, L SMITH, M JONES, A KLENKE, S OWENSBY, A PARRISH, RK HODAPP, E PALMBERG, PF ANDERSON, DR DELCALVO, M MULE, M CARTER, A FAJARDO, A ROSARIO, Y SHERWOOD, M STERN, G DRIEBE, W GUY, J ADI, M FANOUS, M MANES, R CRAWFORD, P SMITH, MF DOYLE, W BENEKE, J SHAMIS, D ENGEL, H WILENSKY, J TESSLER, H FROHLICHSTEIN, D BARNES, R HIGGINBOTHAM, E LIU, S SHAHBOZ, M SCHOLES, G MOWERY, RL SURAN, A GOLDBERG, I DUDLEY, P SCHIFFMAN, J SCHWELM, R FEUER, W GILLINGS, D GUAL, L FURBERG, C DUEKER, D GREEN, SB LATIES, AM PERES, KE TAYLOR, RF LESKE, C AF ALWARD, WLM FARRELL, T HAYREH, S KOLDER, H CARNEY, B PHELPS, C GRESSEL, M COSTIN, J CRAVEN, P ZGRABIK, M SCHREMP, P SIMASHKEVICH, B HEUER, DK BAERVELDT, G MINCKLER, D IRVINE, J SADUN, A GREEN, R MCDONNELL, P LLOYD, M OBER, RR WALONKER, F PADILLA, M MARTONE, J LIGGETT, P LEAN, J GRIFFAY, E MILLERSCHOLTE, A KASS, M KOLKER, A FARBER, M GANS, L SMITH, M JONES, A KLENKE, S OWENSBY, A PARRISH, RK HODAPP, E PALMBERG, PF ANDERSON, DR DELCALVO, M MULE, M CARTER, A FAJARDO, A ROSARIO, Y SHERWOOD, M STERN, G DRIEBE, W GUY, J ADI, M FANOUS, M MANES, R CRAWFORD, P SMITH, MF DOYLE, W BENEKE, J SHAMIS, D ENGEL, H WILENSKY, J TESSLER, H FROHLICHSTEIN, D BARNES, R HIGGINBOTHAM, E LIU, S SHAHBOZ, M SCHOLES, G MOWERY, RL SURAN, A GOLDBERG, I DUDLEY, P SCHIFFMAN, J SCHWELM, R FEUER, W GILLINGS, D GUAL, L FURBERG, C DUEKER, D GREEN, SB LATIES, AM PERES, KE TAYLOR, RF LESKE, C TI 3-YEAR FOLLOW-UP OF THE FLUOROURACIL FILTERING SURGERY STUDY SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID FILTRATION SURGERY; 5-FLUOROURACIL; TRABECULECTOMY; GLAUCOMA AB Patients who participated in the Fluorouracil Filtering Surgery Study, a clinical trial in which patients were randomly assigned to treatment to determine the efficacy and safety of subconjunctivally injected 5-fluorouracil after filtering surgery in eyes with poor prognoses, were followed up for three years. Treatments in 49 of the 100 eyes in the 5-fluorouracil group and 73 of the 99 eyes (74%) in the standard treatment group were classified as failures, defined by reoperation for control of intraocular pressure or intraocular pressure greater than 21 mm Hg during the first three years postoperatively (P < .001, chi-square). Late-onset leakage of aqueous through the filtering bleb occurred more frequently in the 5-fluorouracil group (seven of 105 eyes, 7%) than in the standard treatment group (none of 108 eyes, 0%) (P = .006, Fisher's exact test). We recommend the use of 5-fluorouracil after trabeculectomy in eyes after previous cataract extraction or unsuccessful filtering surgery. The increased risk of late-onset conjunctival filtering bleb leaks associated with 5-fluorouracil cautions against its routine use in patients with good prognoses. C1 UNIV IOWA,CTR,IOWA CITY,IA 52242. LORAIN COMMUNITY HOSP,LORAIN,OH. UNIV SO CALIF,CTR,LOS ANGELES,CA 90089. WASHINGTON UNIV,CTR,ST LOUIS,MO 63130. UNIV MIAMI,CTR,MIAMI,FL 33152. UNIV FLORIDA,CTR,GAINESVILLE,FL 32611. UNIV ILLINOIS,CTR,CHICAGO,IL 60680. NEI,BETHESDA,MD 20892. UNIV MISSOURI,COLUMBIA,MO 65201. NR 9 TC 91 Z9 93 U1 0 U2 1 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD JAN 15 PY 1993 VL 115 IS 1 BP 82 EP 92 PG 11 WC Ophthalmology SC Ophthalmology GA KF915 UT WOS:A1993KF91500012 ER PT J AU RODRIGUES, MM KRUTH, HS RAJAGOPALAN, S JONES, K AF RODRIGUES, MM KRUTH, HS RAJAGOPALAN, S JONES, K TI UNESTERIFIED CHOLESTEROL IN GRANULAR, LATTICE, AND MACULAR DYSTROPHIES SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Letter ID CORNEAL-DYSTROPHY; PROTEOGLYCAN C1 RES PREVENT BLINDNESS INC,NEW YORK,NY. NHLBI,MOLEC DIS BRANCH,EXPTL ATHEROSCLEROSIS SECT,BETHESDA,MD 20892. RP RODRIGUES, MM (reprint author), UNIV MARYLAND,DEPT OPHTHALMOL,OPHTHALM PATHOL LAB,10 S PINE ST,MSTF,ROOM 5-00B,BALTIMORE,MD 21201, USA. NR 5 TC 1 Z9 1 U1 0 U2 1 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD JAN 15 PY 1993 VL 115 IS 1 BP 112 EP 114 PG 3 WC Ophthalmology SC Ophthalmology GA KF915 UT WOS:A1993KF91500019 PM 8420363 ER PT J AU LI, FP DECKER, HJH ZBAR, B STANTON, VP KOVACS, G SEIZINGER, BR ABURATANI, H SANDBERG, AA BERG, S HOSOE, S BROWN, RS AF LI, FP DECKER, HJH ZBAR, B STANTON, VP KOVACS, G SEIZINGER, BR ABURATANI, H SANDBERG, AA BERG, S HOSOE, S BROWN, RS TI CLINICAL AND GENETIC-STUDIES OF RENAL-CELL CARCINOMAS IN A FAMILY WITH A CONSTITUTIONAL CHROMOSOME-3,8 TRANSLOCATION - GENETICS OF FAMILIAL RENAL-CARCINOMA SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE CARCINOMA, RENAL CELL; NEOPLASTIC SYNDROMES, HEREDITARY; KIDNEY NEOPLASMS; CHROMOSOMES, HUMAN, PAIR-3; CHROMOSOMES, HUMAN, PAIR-8 ID VONHIPPEL-LINDAU DISEASE; GRADIENT GEL-ELECTROPHORESIS; TUMOR SUPPRESSOR GENES; SHORT ARM; HEREDITARY; DELETION; 3P; HETEROZYGOSITY; LOCALIZATION; INVOLVEMENT AB Objective: To describe the clinical course and genetic studies of renal carcinoma in members of a family with the constitutional chromosome translocation, t(3;8) (p14;q24). Design: A follow-up study that updates our 1979 report of renal carcinoma in 1 0 of these relatives. Setting: A cancer center and university hospital. Patients: Members of the family, including five carriers of the 3;8 translocation who were in remission of renal cancer. Measurements: Clinical follow-up of the family and genetic analyses of the renal cancer specimens of three patients. Results: Renal carcinoma recurred in all five patients in the family at 1 to 16 years of follow-up. Three patients have died of renal cancer, and two are in a second remission. The renal cancers from three family members consistently reveal loss of the entire derivative chromosome 8, which bears the chromosome 3p segment spanning band p14 to the telomere. In contrast, no genetic change was detected in the derivative chromosome 3 or in normal chromosomes 3 and 8. Conclusions: This family illustrates the importance of clinical follow-up of patients with a hereditary cancer that can develop at multiple foci and recur over time. The inherited 3;8 translocation and loss of the translocated distal chromosome 3p in tumor specimens of family members may help localize the gene or genes involved in the pathogenesis of both familial and sporadic renal carcinoma. C1 NCI,BETHESDA,MD 20892. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. SW BIOMED RES INST,SCOTTSDALE,AZ. RP LI, FP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,MAYER 3A27,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01 CA49455]; NHGRI NIH HHS [HG00299]; NHLBI NIH HHS [HL41484] NR 34 TC 74 Z9 74 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JAN 15 PY 1993 VL 118 IS 2 BP 106 EP 111 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA KF918 UT WOS:A1993KF91800005 PM 8416305 ER PT J AU COHEN, RB ABDALLAH, JM GRAY, JR FOSS, F AF COHEN, RB ABDALLAH, JM GRAY, JR FOSS, F TI REVERSIBLE NEUROLOGIC TOXICITY IN PATIENTS TREATED WITH STANDARD-DOSE FLUDARABINE PHOSPHATE FOR MYCOSIS-FUNGOIDES AND CHRONIC LYMPHOCYTIC-LEUKEMIA SO ANNALS OF INTERNAL MEDICINE LA English DT Note DE LEUKEMIA, LYMPHATIC, CHRONIC; MYCOSIS FUNGOIDES; FLUDARABINE PHOSPHATE; CENTRAL NERVOUS SYSTEM DISEASES; NEUROLOGIC MANIFESTATIONS ID NERVOUS-SYSTEM TOXICITY; PHASE-I AB Fludarabine phosphate is approved for the treatment of advanced B-cell chronic lymphocytic leukemia refractory to alkylating agents. We report two cases of disabling but reversible neurotoxicity in a patient with mycosis fungoides and a patient with chronic lymphocytic leukemia who received standard doses of fludarabine (20 to 25 mg m2 per day for 5 days) every 28 days for 6 to 8 cycles). Serial brain magnetic resonance imaging scans in the patient with mycosis fungoides showed rapid evolution of white-matter changes with subsequent complete resolution. C1 NCI,BETHESDA,MD 20892. RP COHEN, RB (reprint author), USN,NATL NAVAL MED CTR,NCI,MED ONCOL BRANCH,BETHESDA,MD 20889, USA. NR 9 TC 40 Z9 41 U1 0 U2 2 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JAN 15 PY 1993 VL 118 IS 2 BP 114 EP 116 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA KF918 UT WOS:A1993KF91800007 PM 8416307 ER PT J AU TUOMINEN, RK WERNER, MH YE, H MCMILLIAN, MK HUDSON, PM HANNUN, YA HONG, JS AF TUOMINEN, RK WERNER, MH YE, H MCMILLIAN, MK HUDSON, PM HANNUN, YA HONG, JS TI BIPHASIC GENERATION OF DIACYLGLYCEROL BY ANGIOTENSIN AND PHORBOL ESTER IN BOVINE ADRENAL CHROMAFFIN CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PROTEIN-KINASE-C; INOSITOL TRISPHOSPHATE; SIGNAL TRANSDUCTION; CELLULAR-REGULATION; MEDULLARY CELLS; HYDROLYSIS; PHOSPHOLIPIDS; ACCUMULATION; STIMULATION; ACTIVATION C1 DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. RP TUOMINEN, RK (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU PHS HHS [4066] NR 27 TC 9 Z9 9 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JAN 15 PY 1993 VL 190 IS 1 BP 181 EP 185 DI 10.1006/bbrc.1993.1028 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KH402 UT WOS:A1993KH40200028 PM 8380691 ER PT J AU HEEMSKERK, FMJ CHEN, HC HUANG, FL AF HEEMSKERK, FMJ CHEN, HC HUANG, FL TI PROTEIN-KINASE-C PHOSPHORYLATES SER152, SER156 AND SER163 BUT NOT SER160 OF MARCKS IN RAT-BRAIN SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PROMINENT CELLULAR SUBSTRATE; MOLECULAR-CLONING; PHORBOL ESTERS; PURIFICATION; CALMODULIN; 80-KDA; FIBROBLASTS; BINDING C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 10,ROOM B1-L400,BETHESDA,MD 20892. NR 18 TC 53 Z9 54 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 JAN 15 PY 1993 VL 190 IS 1 BP 236 EP 241 DI 10.1006/bbrc.1993.1036 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA KH402 UT WOS:A1993KH40200036 PM 8422248 ER PT J AU FRIDMAN, R BIRD, RE HOYHTYA, M OELKUCT, M KOMAREK, D LIANG, CM BERMAN, ML LIOTTA, LA STETLERSTEVENSON, WG FUERST, TR AF FRIDMAN, R BIRD, RE HOYHTYA, M OELKUCT, M KOMAREK, D LIANG, CM BERMAN, ML LIOTTA, LA STETLERSTEVENSON, WG FUERST, TR TI EXPRESSION OF HUMAN RECOMBINANT 72-KDA GELATINASE AND TISSUE INHIBITOR OF METALLOPROTEINASE-2 (TIMP-2) - CHARACTERIZATION OF COMPLEX AND FREE ENZYME SO BIOCHEMICAL JOURNAL LA English DT Article ID BRONCHIAL EPITHELIAL-CELLS; IV COLLAGENASE; VACCINIA VIRUS; RNA-POLYMERASE; ACTIVATION; SYSTEM; IDENTIFICATION; PROGELATINASE; FIBROBLASTS; PRECURSOR AB The human 72 kDa gelatinase/type IV collagenase is a metalloproteinase that is thought to play a role in metastasis and angiogenesis. The 72 kDa progelatinase can be isolated from conditioned media as a complex with the tissue inhibitor of metalloproteinase-2 (TIMP-2). To investigate 72 kDa gelatinase-TIMP-2 interactions and to compare the activity of the complex versus that of the free enzyme, we have expressed and purified human 72 kDa progelatinase and TIMP-2 as single proteins in a recombinant vaccinia virus mammalian cell expression system. The recombinant 72 kDa progelatinase was able to bind TIMP-2, and it digested gelatin and collagen type IV after activation by p-aminophenylmercuric acid (APMA). The specific activity of the recombinant free enzyme was 20-fold higher than the activity of an APMA-treated stoichiometric complex of recombinant 72 kDa progelatinase and TIMP-2. Also, TIMP-2 caused an 86% inhibition of activity when added to the activated enzyme at a 1:1 molar ratio. Activation of the free recombinant 72 kDa progelatinase yielded the 62 kDa species and two fragments of 46 and 35 kDa that cross-reacted with monoclonal antibodies to the 72 kDa proenzyme. TIMP-2 inhibited the conversion of the recombinant proenzyme to the 62 kDa species and the appearance of the 45 and 35 kDa bands. These results suggest that TIMP-2 is not only a potent inhibitor of the activated enzyme but also prevents the generation of low-molecular-mass species and full enzymic activity from the zymogen. C1 MOLEC ONCOL INC,GAITHERSBURG,MD 20878. MEDLUMMUNE INC,GAITHERSBURG,MD 20878. NCI,PATHOL LAB,BETHESDA,MD 20892. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NCI NIH HHS [1R43CA56257-01] NR 31 TC 77 Z9 77 U1 0 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 JAN 15 PY 1993 VL 289 BP 411 EP 416 PN 2 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KJ143 UT WOS:A1993KJ14300013 PM 8380993 ER PT J AU KOZLOW, EJ WILSON, GL FOX, CH KEHRL, JH AF KOZLOW, EJ WILSON, GL FOX, CH KEHRL, JH TI SUBTRACTIVE CDNA CLONING OF A NOVEL MEMBER OF THE IG GENE SUPERFAMILY EXPRESSED AT HIGH-LEVELS IN ACTIVATED LYMPHOCYTES-B SO BLOOD LA English DT Article ID IMMUNOGLOBULIN SUPERFAMILY; CELL ACTIVATION; SEQUENCE; ANTIGEN; PROTEIN; DIFFERENTIATION; TRANSCRIPTION; MEDIATOR; DOMAINS; MODEL C1 NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B-13,BETHESDA,MD 20892. NR 33 TC 68 Z9 73 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 JAN 15 PY 1993 VL 81 IS 2 BP 454 EP 461 PG 8 WC Hematology SC Hematology GA KH512 UT WOS:A1993KH51200025 PM 8422464 ER PT J AU AMBINDER, RF BROWNING, PJ LORENZANA, I LEVENTHAL, BG COSENZA, H MANN, RB MACMAHON, EME MEDINA, R CARDONA, V GRUFFERMAN, S OLSHAN, A LEVIN, A PETERSEN, EA BLATTNER, W LEVINE, PH AF AMBINDER, RF BROWNING, PJ LORENZANA, I LEVENTHAL, BG COSENZA, H MANN, RB MACMAHON, EME MEDINA, R CARDONA, V GRUFFERMAN, S OLSHAN, A LEVIN, A PETERSEN, EA BLATTNER, W LEVINE, PH TI EPSTEIN-BARR-VIRUS AND CHILDHOOD HODGKINS-DISEASE IN HONDURAS AND THE UNITED-STATES SO BLOOD LA English DT Article ID REED-STERNBERG CELLS; POLYMERASE CHAIN-REACTION; PREVIOUS INFECTIOUS-MONONUCLEOSIS; INSITU HYBRIDIZATION; SMALL RNAS; NASOPHARYNGEAL CARCINOMA; GENE-EXPRESSION; VIRAL GENOMES; LYMPHOMA; PROTEIN C1 UNIV NACL AUTONOMA HONDURAS, DEPT MICROBIOL, TEGUCIGALPA, HONDURAS. HOSP ESCUELA TEGUCIGALPA, DEPT PATHOL, TEGUCIGALPA, HONDURAS. RES TRIANGLE INST UNIT, HARROW, MIDDX, ENGLAND. JOHNS HOPKINS UNIV, SCH MED, DEPT PATHOL, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, DEPT MED, BALTIMORE, MD 21205 USA. NCI, BETHESDA, MD 20892 USA. UNIV PITTSBURGH, SCH MED, DEPT CLIN EPIDEMIOL & PREVENT MED, PITTSBURGH, PA 15261 USA. UNIV ARIZONA, TUCSON, AZ 85721 USA. PEDIAT ONCOL GRP, ST LOUIS, MO USA. RP AMBINDER, RF (reprint author), JOHNS HOPKINS UNIV, SCH MED, DEPT ONCOL, BALTIMORE, MD 21205 USA. FU NCI NIH HHS [R01 CA47473, U10 CA-28476] NR 55 TC 156 Z9 160 U1 1 U2 1 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD JAN 15 PY 1993 VL 81 IS 2 BP 462 EP 467 PG 6 WC Hematology SC Hematology GA KH512 UT WOS:A1993KH51200026 PM 8380725 ER PT J AU SCHLAIFER, D COOPER, MR ATTAL, M SARTOR, AO TREPEL, JB LAURENT, G MYERS, CE AF SCHLAIFER, D COOPER, MR ATTAL, M SARTOR, AO TREPEL, JB LAURENT, G MYERS, CE TI MYELOPEROXIDASE - AN ENZYME INVOLVED IN INTRINSIC VINCRISTINE RESISTANCE IN HUMAN MYELOBLASTIC-LEUKEMIA SO BLOOD LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; MULTIDRUG RESISTANCE; MYELOID-LEUKEMIA; CELL-LINE; PEROXIDASE; INVITRO; VINBLASTINE; EXPRESSION; PROTEINS; PATIENT C1 NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. RP SCHLAIFER, D (reprint author), CHR TOULOUSE,HOP PURPAN,CLIN DIEULAFOY,SERV HEMATOL,PL DOCTEUR BAYLAC,F-31059 TOULOUSE,FRANCE. NR 33 TC 22 Z9 22 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 JAN 15 PY 1993 VL 81 IS 2 BP 482 EP 489 PG 8 WC Hematology SC Hematology GA KH512 UT WOS:A1993KH51200029 PM 8380727 ER PT J AU MARLEY, RJ SHIMOSATO, K FRIEMAN, M GOLDBERG, SR AF MARLEY, RJ SHIMOSATO, K FRIEMAN, M GOLDBERG, SR TI GENETIC-DIFFERENCES IN THE TIME COURSE FOR THE DEVELOPMENT AND PERSISTENCE OF THE ANTICONVULSANT EFFECTS OF CARBAMAZEPINE AGAINST COCAINE SEIZURES SO BRAIN RESEARCH LA English DT Article DE CARBAMAZEPINE; COCAINE; PHARMACOGENETICS; PHARMACOKINETIC; INBRED MOUSE STRAIN; SEIZURE; ANTICONVULSANT; CYTOCHROME-P-450 ID EPOXIDE METABOLITE; KINDLED SEIZURES; RAT-LIVER; LIDOCAINE; MICE AB Initial studies of the effect of chronic carbamazepine (CBZ) against cocaine-induced seizures indicated that there were genetic differences in both the time course for the development of the anticonvulsant effects of CBZ against cocaine-induced seizures and the persistence of these effects. The present studies were initiated to investigate the time course for the development and persistence of the anticonvulsant effects of chronic CBZ against cocaine seizures in BALB/cByJ, C57Bl/6J and SJL/J mice. The anticonvulsant actions of CBZ were dependent on the duration of CBZ administration, requiring 4-7 days to achieve maximal efficacy. However, once the anticonvulsant effects of CBZ were manifest, the effect persisted for up to 5 days after stopping CBZ treatment depending on the genotype. The levels of CBZ and its active epoxide metabolite were determined in plasma and brain at various time points during and after chronic CBZ treatment. The levels of CBZ and CBZ-10,11-epoxide were substantially reduced over the course of treatment in all three strains, such that the levels of the two compounds in plasma and brain could not account for the decreased susceptibility to cocaine seizures observed following chronic CBZ. These results suggest that the effects of CBZ on cocaine seizures are mediated by relatively long-term changes in one or more biological systems associated with cocaine's convulsant effects. RP MARLEY, RJ (reprint author), NIDA,ADDICT RES CTR,BOX 5180,BALTIMORE,MD 21224, USA. NR 31 TC 4 Z9 4 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 JAN 15 PY 1993 VL 600 IS 2 BP 193 EP 200 DI 10.1016/0006-8993(93)91373-Z PG 8 WC Neurosciences SC Neurosciences & Neurology GA KG868 UT WOS:A1993KG86800003 PM 8435746 ER PT J AU EHRENREICH, H COSTA, T CLOUSE, KA PLUTA, RM OGINO, Y COLIGAN, JE BURD, PR AF EHRENREICH, H COSTA, T CLOUSE, KA PLUTA, RM OGINO, Y COLIGAN, JE BURD, PR TI THROMBIN IS A REGULATOR OF ASTROCYTIC ENDOTHELIN-1 SO BRAIN RESEARCH LA English DT Article DE THROMBIN; PRIMARY ASTROCYTE; ENDOTHELIN; ENDOTHELIN RECEPTOR; INOSITOLPHOSPHOLIPID TURNOVER; AP1; REVERSE TRANSCRIPTASE PCR ID MESSENGER-RNA; VASOCONSTRICTOR PEPTIDE; NEURITE OUTGROWTH; PROTEASE NEXIN-1; MESANGIAL CELLS; RAT ASTROBLASTS; UMBILICAL VEIN; GROWTH-FACTOR; GLIAL-CELLS; EXPRESSION AB Endothelin-1, a potent vasoconstrictor of cerebral vessels, is produced by rat primary astrocytes and is subject to autostimulatory regulation in these cells. In this study we examined the effect of thrombin on astrocytic endothelins and report that endothelin-1 is released into the culture fluid in response to thrombin treatment. However, increased production of endothelin-1 is not accompanied by a concomitant increase in steady-state levels of endothelin-1 mRNA as assessed by reverse transcriptase-polymerase chain reaction, even though thrombin stimulation leads to increased inositolphospholipid turnover and activation of the nuclear factor AP1. Thus, astrocytic production of endothelin-1 may be mainly post-transcriptionally regulated in response to thrombin stimulation. In addition, two endothelin receptor genes (ET(A) and ET(B)) were found to be transcribed simultaneously in primary astrocyte cultures, and both thrombin and endothelin-1 stimulation result in a distinct temporary decrease in ET(A) mRNA. These studies suggest a role for thrombin in the regulation of brain perfusion through astrocytic endothelin-1 expression. C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD 20892. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. OI costa, tommaso/0000-0002-8729-3357 NR 44 TC 93 Z9 94 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JAN 15 PY 1993 VL 600 IS 2 BP 201 EP 207 DI 10.1016/0006-8993(93)91374-2 PG 7 WC Neurosciences SC Neurosciences & Neurology GA KG868 UT WOS:A1993KG86800004 PM 7679602 ER PT J AU FREO, U RICCHIERI, GL HOLLOWAY, HW SONCRANT, TT AF FREO, U RICCHIERI, GL HOLLOWAY, HW SONCRANT, TT TI TIME-DEPENDENT AND DOSE-DEPENDENT EFFECTS OF THE SEROTONERGIC AGENT QUIPAZINE ON REGIONAL CEREBRAL METABOLISM IN RATS SO BRAIN RESEARCH LA English DT Article DE SEROTONIN; QUIPAZINE; RCMRGLC ID 5-HT3 RECEPTORS; GLUCOSE-UTILIZATION; RECOGNITION SITES; H-3 QUIPAZINE; AGONISTS; BRAIN; MEDIATION; BINDING; 5-HYDROXYTRYPTAMINE; ANTAGONISTS AB The time course and the relation to dose of regional cerebral metabolic rates for glucose (rCMRglc) were measured in awake male adult Fischer-344 rats after administration of quipazine, a serotonin 5-HT2-3 receptor agonist. rCMRglc was determined, using the quantitative autoradiographiC [C-14]deoxyglucose technique, in 92 brain regions at 30, 60, 90 and 120 min after quipazine 20 mg/kg i.p. and at 60 min after quipazine 5 mg/kg i.p. Peak metabolic effects were observed 60 min after quipazine 20 mg/kg i.p. when rCMRglc was significantly elevated in 27 (29%) brain regions (mean rise 17%). Quipazine increased rCMRglc in brain regions with high densities of 5-HT3 receptors (area postrema, olfactory tubercle, amygdala), in dopaminergic nuclei (substantia nigra pars compacta and pars reticulata) and terminal fields of their projections (zona incerta, subthalamic nucleus, preoptic magnocellular area, nucleus of facial nerve). The topographic distribution and direction of rCMRglc changes induced by quipazine are different from those produced by the 5-HT2 agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane and, consistent with the pharmacological and binding properties of quipazine, suggest a preferential activation of 5-HT3 receptors. C1 NIA,NEUROSCI LAB,PHARMACOL & PHARMACOKINET UNIT,BLDG 10,ROOM 6C103,BETHESDA,MD 20892. NR 60 TC 8 Z9 8 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 JAN 15 PY 1993 VL 600 IS 2 BP 249 EP 256 DI 10.1016/0006-8993(93)91380-B PG 8 WC Neurosciences SC Neurosciences & Neurology GA KG868 UT WOS:A1993KG86800010 PM 8435750 ER PT J AU CRAWLEY, JN ROBINSON, JK LANGEL, U BARTFAI, T AF CRAWLEY, JN ROBINSON, JK LANGEL, U BARTFAI, T TI GALANIN RECEPTOR ANTAGONIST-M40 AND ANTAGONIST-C7 BLOCK GALANIN-INDUCED FEEDING SO BRAIN RESEARCH LA English DT Article DE GALANIN; NEUROPEPTIDE; RECEPTOR ANTAGONIST; RECEPTOR BINDING; FEEDING; BEHAVIOR; HYPOTHALAMUS ID CENTRAL NERVOUS-SYSTEM; SUBSTANCE-P ANALOGS; BOMBESIN; PEPTIDE; STIMULATION; FRAGMENTS; BEHAVIOR; BINDING AB Two peptide antagonists of the galanin receptor, M40 (galanin[1-13]-Pro-Pro-[Ala-Leu]2-Ala amide) and C7 (galanin[1-13]-spantide amide), significantly inhibited galanin-induced consumption of a palatable wet cookie mash, when microinjected intraventricularly to satiated rats. Antagonists were effective at doses equimolar to or less than the active doses of galanin. Feeding induced by an overnight fast was not significantly different in rats microinjected with saline as compared to M40 or C7, at doses which inhibited galanin-induced feeding. The activity of the chimeric compound, C7, did not appear to be linked to the properties of its C-terminal spantide-like sequence, as C7 did not induce barrel rolling at doses which inhibited galanin-induced feeding. The IC50 for displacement of, I-125-[Tyr26]-porcine galanin 1-29 binding in rat hypothalamic membranes was 15 nM for M40, and 0.2 nM for C7, as compared to 0.8 nM for unlabelled porcine galanin(1-29). These two structurally different galanin antagonists, both demonstrating antagonist activity in vivo in awake, behaving rats, provide promising tools for further analyses of the functional activity of galanin in the mammalian brain. C1 UNIV STOCKHOLM,DEPT NEUROCHEM & NEUROTOXICOL,S-10691 STOCKHOLM,SWEDEN. RP CRAWLEY, JN (reprint author), NIMH,EXPTL THERAPEUT BRANCH,BEHAV NEUROPHARMACOL UNIT,BLDG 10,ROOM 4N214,BETHESDA,MD 20892, USA. NR 20 TC 97 Z9 100 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JAN 15 PY 1993 VL 600 IS 2 BP 268 EP 272 DI 10.1016/0006-8993(93)91382-3 PG 5 WC Neurosciences SC Neurosciences & Neurology GA KG868 UT WOS:A1993KG86800012 PM 7679604 ER PT J AU YANCIK, R MOORE, TD MARTIN, G OBRAMS, GI REED, E AF YANCIK, R MOORE, TD MARTIN, G OBRAMS, GI REED, E TI OLDER WOMEN AS THE FOCUS FOR RESEARCH AND TREATMENT OF OVARIAN-CANCER - AN OVERVIEW FOR THE NATIONAL-INSTITUTE-ON-AGING, NATIONAL-CANCER-INSTITUTE, AND AMERICAN-CANCER-SOCIETY MULTIDISCIPLINARY WORKING CONFERENCE SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE CONFERENCE AIMS; RATIONALE; SCOPE AB Ovarian cancer disproportionately affects women 65 years of age and older who are likely to have concomitant changes in physical ability, physiological functioning, and other chronic conditions associated with advancing age. The National Institute on Aging, National Cancer Institute, and the American Cancer Society cosponsored a multidisciplinary working conference, ''Perspectives on Ovarian Cancer in Older-Aged Women: Current Knowledge and Recommendations for Research,'' at the National Institutes of Health on November 20-21, 1991 to confront the age-related aspects of ovarian cancer in epidemiology, etiology, clinical investigations, and patient management. Conference participants devoted attention to such special topics as drug resistance, dose intensity, patterns of care, and screening potential for ovarian cancer. After exploring these areas with existing data, the task was then to generate recommendations for research and practice. The scope of the conference and an introduction to the proceedings are presented in this paper. C1 NIA,GERONTOL RES CTR,BETHESDA,MD 20892. NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. NCI,DIV CHEMOTHERAPY,CLIN ONCOL PROGRAM,MED BRANCH,BETHESDA,MD 20892. RP YANCIK, R (reprint author), NIA,OFF DIRECTOR,9000 ROCKVILLE PIKE,BLDG 31,ROOM 5C05,BETHESDA,MD 20892, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 514 EP 516 PG 3 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600002 PM 8420670 ER PT J AU YANCIK, R AF YANCIK, R TI OVARIAN-CANCER - AGE CONTRASTS IN INCIDENCE, HISTOLOGY, DISEASE STAGE AT DIAGNOSIS, AND MORTALITY SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE OVARIAN CANCER IN THE ELDERLY; AGE STAGE CONTRASTS; STAGE AGE RELATIONSHIPS; HISTOLOGY AB Background. Age comparisons for incidence, histology, disease stage at initial diagnosis, and mortality of more than 20,000 ovarian cancer patients diagnosed between 1973-1987 are the focus of this descriptive epidemiologic study. This paper highlights key issues and concerns regarding ovarian cancer in women 65 years and older as a frame of reference for the proceedings of the working conference, ''Perspectives on Ovarian Cancer in Older-Aged Women,'' co-sponsored by the National Institute on Aging, National Cancer Institute, and American Cancer Society held at the National Institutes of Health, November, 1991. Methods. Data are from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program and the National Center for Health Statistics. The SEER Program database represents approximately 9.6% of the U.S. population. Results. Ovarian cancer affects women in the age group 65 years and older more frequently than younger women. More than 48% of all ovarian cancers occur in women in this age group. Age-adjusted rates increase as age advances, peaking at 54.0 per 100,000 in the age group 75-79 years. Time trends also indicate increases in age-specific incidence rates. This malignancy takes its toll in mortality in women 65 years and older with 64% of all deaths due to this neoplasm (in 1989). Moreover, older women are more likely to be initially diagnosed with advanced disease. Conclusions. Important questions about ovarian cancer in older-aged women need urgent attention from the research community. New strategies for diagnostic leads have to be developed for older women. RP YANCIK, R (reprint author), NIA,9000 ROCKVILLE PIKE,BLDG 31,ROOM 5C05,BETHESDA,MD 20892, USA. NR 12 TC 180 Z9 184 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 517 EP 523 PG 7 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600003 PM 8420671 ER PT J AU RIES, LAG AF RIES, LAG TI OVARIAN-CANCER - SURVIVAL AND TREATMENT DIFFERENCES BY AGE SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE OVARIAN CANCER; ELDERLY; OLDER WOMEN; SURVIVAL; STAGE; TREATMENT AB Background. Cancer of the ovary is a disease of older American women with an incidence rate of 9.4 per 100,000 for those under 65 compared to 54.8 per 100,000 for those 65 years of age and over. Methods. Over 22,000 women were diagnosed with ovarian cancer between 1973 and 1987 within the Surveillance, Epidemiology and End Results (SEER) Program of the National Cancer Institute. SEER is a population-based program that covers nearly 10% of the U.S. population for cancer incidence and survival. Results. Ovarian cancer survival rates vary dramatically by stage. Within stage, however, differences are noted in survival by age, with younger women surviving better than older women even after adjustment for the general life expectancy of each age group (relative survival). For Stages III-IV disease, women under 45 years of age have a 5-year relative survival rate of over 45% compared to only 8% for those 85 years of age and over. Between 1973-1977 and 1983-1987, the treatment for Stages III-IV disease has changed. For all age groups, there were sharp increases in the percentage having surgery and chemotherapy/hormonal therapy and decreases in those having surgery and radiation as part of the first course of therapy. Over 40% of women 85 years of age and over did not receive any definitive treatment according to the hospital medical record. In 1983-1987, younger women received more combination therapy (surgery with chemotherapy/hormonal therapy) versus older women who received more single modalities such as surgery only or chemotherapy/hormonal therapy only. Conclusions. Older women with ovarian cancer are treated less aggressively than their younger counterparts and have poorer survival rates. RP RIES, LAG (reprint author), NCI,SEER PROGRAM,CANC STAT BRANCH,9000 ROCKVILLE PIKE,EPN 343J,BETHESDA,MD 20892, USA. NR 4 TC 99 Z9 101 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 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 524 EP 529 PG 6 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600004 PM 8420672 ER PT J AU MERINO, MJ JAFFE, G AF MERINO, MJ JAFFE, G TI AGE CONTRAST IN OVARIAN PATHOLOGY SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE OVARIAN CANCER; GERM CELL AND EPITHELIAL TUMORS ID SURFACE PAPILLARY CARCINOMA; EPITHELIAL TUMORS; SEROUS CARCINOMA; BRENNER TUMORS; BORDERLINE; CANCER; BEHAVIOR AB Background. Ovarian cancer accounts for approximately 23% of all gynecologic tumors and is the most common fatal gynecologic malignancy. These tumors can occur in women of all ages, but there are differences in the histologic types during various decades of life. Conclusions. During infancy and childhood, the predominant type of neoplasms are those of germ cell origin, such as teratomas, dysgerminomas, and endodermal sinus tumors. In adults, epithelial neoplasms, or tumors that originate from the epithelium that covers the ovarian surface, are the most common, accounting for almost 85% of all neoplasms after the age of 50 years. The peak incidence of benign epithelial tumors occurs between the ages of 20 and 40 years, Young women (30 to 40 years of age) are frequently affected by the so-called ''tumors of low malignant potential,'' which have excellent prognosis. Older women, on the other hand, usually have the most aggressive forms of ovarian cancer, present with advanced disease, and have a dismal prognosis. RP MERINO, MJ (reprint author), NCI,PATHOL LAB,BLDG 10,ROOM 2N212,BETHESDA,MD 20892, USA. NR 37 TC 23 Z9 23 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 537 EP 544 PG 8 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600006 PM 8420674 ER PT J AU KOHN, E AF KOHN, E TI AGING ISSUES IN INVASION AND METASTASIS - FERTILE GROUND FOR INVESTIGATION SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE AGING; INVASION; METASTASIS; OVARIAN CANCER ID AUTOCRINE MOTILITY FACTOR; HUMAN-BREAST-CANCER; GROWTH FACTOR-I; LAMININ RECEPTOR; MELANOMA-CELLS; TUMOR-CELLS; EXPRESSION; CHEMOTAXIS; L651582; MATRIX AB Background. Ovarian cancer is a disease of predominantly older women and one in which metastases occur early and extensively. The unusual pattern of local metastasis is fertile ground for laboratory and clinical investigation. Methods. Tools are now available with which to study the complex cascade of invasion and metastasis as it underlies invasive ovarian cancer. The metastatic cascade involves five repetitive steps: angiogenesis, adhesion to the vascular basement membrane, local proteolysis, migration into and out of the vasculature, and proliferation at the secondary sites. Both in vivo and in vitro models of ovarian cancer are available; however, there are no systems targeted to understanding age-related differences in ovarian cancer biology. Results. Progress in investigation of the biology of ovarian cancer has led to new diagnostic and therapeutic leads, including the use of adhesion receptors, protease secretion, and stimulation of tumor cell migration as potential markers and the identification of a new anticancer agent, CAI (NSC609974). Conclusions. CAI inhibits signal transduction pathways important in the regulation and activation of metastasis and proliferation. A phase I study has begun accrual at the National Cancer Institute; the protocol will contain no upper age limit. C1 NCI,MED BRANCH,BETHESDA,MD 20892. RP KOHN, E (reprint author), NCI,PATHOL LAB,BLDG 10,ROOM 2A33,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 34 TC 14 Z9 14 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 552 EP 557 PG 6 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600008 PM 8420676 ER PT J AU AMOS, CI STRUEWING, JP AF AMOS, CI STRUEWING, JP TI GENETIC EPIDEMIOLOGY OF EPITHELIAL OVARIAN-CANCER SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE OVARIAN CANCER; GENETICS; EPIDEMIOLOGY; FAMILY STUDIES; CYTOGENETICS ID ALLELE LOSS; GALACTOSE CONSUMPTION; FAMILY HISTORY; BREAST-CANCER; MILK-DRINKING; CELL-LINES; RISK; CARCINOMA; LOCUS; ABNORMALITIES AB Background. Aside from age, family history is the strongest predictor of ovarian cancer risk. Genetic components of risk for ovarian cancer have been evaluated by a number of designs, including case-control studies of family history and other risk factors, segregation and genetic linkage studies, and studies of biomarkers and tumor-specific cytogenetic abnormalities. Methods. Data were extracted from all available case-control studies that included family history. Cytogenetic, biomarker, segregation, analytic, and genetic linkage studies were reviewed. Results. Family history of ovarian cancer confers a 3.6-fold increased risk for this disease. Segregation studies of breast and ovarian cancer in five large families were consistent with dominant inheritance. Low levels of alpha-L-fucosidase confer mildly increased risk for ovarian cancer. Low galactose-1-phosphate uridyl transferase and type A blood group may increase risk for ovarian cancer. Cytogenetic and oncogene studies have identified regions that may be important in tumorigenesis and metastasis, but discriminating between early and late changes is difficult from these studies. Presence of a genetic susceptibility locus for breast and ovarian cancer has been confirmed on chromosome 17q21. Conclusions. Family history is an important predictor of ovarian cancer risk. In rare families, a specific dominantly acting gene can be identified, but in the vast majority of familial ovarian cancers the underlying mechanism remains unclear. Specific studies are needed for women with a family history of ovarian cancer because evidence suggests modification of the effects of oral contraceptive use and reproductive patterns in this population of women. C1 NCI,DIV CANC ETIOL,FAMILY STUDIES SECT,BETHESDA,MD 20892. RP AMOS, CI (reprint author), NIAMS,GENET STUDIES SECT,BLDG 6,ROOM 429,BETHESDA,MD 20892, USA. RI Struewing, Jeffery/C-3221-2008; Struewing, Jeffery/I-7502-2013 OI Struewing, Jeffery/0000-0002-4848-3334 NR 77 TC 53 Z9 54 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 566 EP 572 PG 7 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600010 PM 8420678 ER PT J AU KRAMER, BS GOHAGAN, J PROROK, PC SMART, C AF KRAMER, BS GOHAGAN, J PROROK, PC SMART, C TI A NATIONAL-CANCER-INSTITUTE SPONSORED SCREENING TRIAL FOR PROSTATIC, LUNG, COLORECTAL, AND OVARIAN CANCERS SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE OVARIAN CANCER; SCREENING; RANDOMIZED TRIAL; CA-125; TRANSVAGINAL ULTRASOUND ID STAGE-I; DIAGNOSIS AB Background. Ovarian cancer is the fifth most common cause of cancer-related death in American women. The median age at diagnosis is about 62 years; incidence rises rapidly after age 60. Pelvic examination has been the primary method for detection of ovarian carcinoma. It is insensitive for the detection of early disease, however: most women present with disease beyond the pelvis (Stages III and IV) and are not curable with existing techniques. Two new technologies may be useful as screening tools for earlier detection of ovarian cancer. CA 125 is an antigenic determinant expressed on an ovarian cancer cell line. Transvaginal ultrasound (TVUS) images the ovaries from within the vagina and can be performed by a technician in about 10 minutes. In small preoperative studies of women with ovarian masses, serum CA 125 levels have been elevated (typically above 35 U/ml) in over two-thirds of cases and in up to 50% of Stage I cases. The test is not absolutely specific: elevations have been reported with pregnancy, endometriosis, menstruation, benign ovarian tumors, and with cancers of the breast, colon, pancreas, lung, stomach, and liver. Nevertheless, the specificity of CA 125 in postmenopausal women has been reported at about 95% or more. TVUS provides higher resolving power for ovarian abnormalities than transabdominal ultrasound or physical examination; however, experience with it is limited. CA 125 and TVUS may be complementary. Conclusions. For these reasons, the National Cancer Institute is planning a randomized trial of all three tests versus routine medical care in women of ages 60-74 years. This is part of a larger trial to determine the efficacy of screening for lung, colorectal, and ovarian cancers in women, and for lung, colorectal, and prostatic cancers in men. Seventy-four thousand women will be randomized in the study. C1 NIH,BIOMETRY BRANCH,BETHESDA,MD 20892. RP KRAMER, BS (reprint author), NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT & COMMUNITY ONCOL PROGRAM,BETHESDA,MD 20892, USA. NR 16 TC 106 Z9 106 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 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 589 EP 593 PG 5 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600013 PM 8420681 ER PT J AU BICHER, A SAROSY, G KOHN, E ADAMO, DO DAVIS, P JACOB, J CHABNER, BA REED, E AF BICHER, A SAROSY, G KOHN, E ADAMO, DO DAVIS, P JACOB, J CHABNER, BA REED, E TI AGE DOES NOT INFLUENCE TAXOL DOSE INTENSITY IN RECURRENT CARCINOMA OF THE OVARY SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE TAXOL; DOSE INTENSITY; AGE; OVARIAN CANCER ID CANCER; CHEMOTHERAPY; EPIDEMIOLOGY; TRIALS AB Background. In the treatment of advanced-stage ovarian cancer, it is common practice to treat elderly patients in a less aggressive fashion than young patients. This approach is based on the notion that age is associated with poor patient tolerance to aggressive chemotherapy. Relatively little data exist to support this contention. The most exciting new chemotherapy agent to be developed in the last 10 years is taxol, a diterpeniod derivative of the Northwestern yew Taxus brevifolia. Methods. The ability to administer dose-intensive taxol to adult patients with recurrent ovarian cancer was assessed retrospectively, and the question was asked whether the administered dose intensity of taxol was unfavorably influenced by age. Forty-eight patients with recurrent ovarian carcinoma received taxol at an initial dose of 250 mg/m2 every 3 weeks. Age in this cohort ranged from 26 to 74 years, with a median of 55. Twenty-nine percent (14 of 48) of the patients treated were 61 years of age or greater. Criteria for administration of taxol included a creatinine clearance of > 45 ml/minute, minimal abnormalities in liver function tests, good performance status, and the absence of substantial comorbid disease. Results. Elderly patients in this cohort (age > 60 years) did not differ from younger patients with respect to administered dose intensity, number of cycles of therapy administered, or the occurrence of serious or mild toxicities. Conclusions. Age, in and of itself, should not be a factor in the consideration of dose modifications of taxol. C1 NCI,MED BRANCH,BLDG 10,ROOM 12N226,BETHESDA,MD 20892. NR 14 TC 36 Z9 36 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 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 594 EP 600 PG 7 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600014 PM 7678382 ER PT J AU CORNELISON, TL REED, E AF CORNELISON, TL REED, E TI DOSE INTENSITY ANALYSIS OF HIGH-DOSE CARBOPLATIN IN REFRACTORY OVARIAN-CARCINOMA RELATIVE TO AGE SO CANCER LA English DT Article; Proceedings Paper CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH DE DOSE INTENSITY; HIGH-DOSE CARBOPLATIN; OVARIAN CARCINOMA; AGE ID CANCER PATIENTS; CISPLATIN; CHEMOTHERAPY; TRIALS AB Background. Cisplatin and carboplatin are essential to management of advanced-stage epithelial ovarian carcinoma. No published data exist regarding carboplatin dose intensity importance in ovarian cancer, nor are there data for the effect of age on the ability to deliver dose-intensive carboplatin. Methods. Retrospective dose intensity analyses were performed for 93 patients with advanced-stage refractory ovarian carcinoma, who received single-agent, high-dose carboplatin chemotherapy (800 mg/m2/35 days or 160 mg/m2/week). These patients had been treated on one of three high-dose carboplatin studies conducted in the Medicine Branch of the National Cancer Institute during the 1980s. Eligibility criteria required age greater than or equal to 18 years, good end organ function, and good performance status. Results. Patients 60 years of age or older comprised 33% of the cohort and patients 70 years of age or older comprised 8% of the cohort. Administered dose intensity of carboplatin did not differ among age groups. Patients of age less-than-or-equal-to 39 years received a dose intensity of 136 +/- 28 mg/m2/week, those of age 40-59 years received 129 +/- 33, those of age greater-than-or-equal-to 60 years received 134 +/- 24, and those of age greater-than-or-equal-to 70 years received 129 +/- 19. Further, the administered carboplatin dose intensity did not differ among clinical response groups. Dose intensity in complete responders was 138 +/- 18 mg/m2/week; in partial responders, 121 +/- 29; and in nonresponders, 134 +/- 30. The age distribution of responders matched the age distribution of the cohort. Conclusions. These data demonstrate that elderly patients with good end organ function and good performance status tolerate the same level of dose-intensive platinum therapy as younger patients. Age alone should not be a determinant for carboplatin dose modification in the treatment of ovarian carcinoma. C1 NCI,MED BRANCH,BLDG 10,ROOM 12N226,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 21 TC 18 Z9 18 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 650 EP 655 PG 6 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600023 PM 8420690 ER PT J AU HOSKINS, WJ YANCIK, R TRIMBLE, E AF HOSKINS, WJ YANCIK, R TRIMBLE, E TI PERSPECTIVES ON OVARIAN-CANCER IN OLDER-AGED WOMEN - CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH - CONFERENCE SUMMARY - RECOMMENDATIONS FOR RESEARCH SO CANCER LA English DT Editorial Material CT WORKING CONF ON PERSPECTIVES ON OVARIAN CANCER IN OLDER-AGED WOMEN : CURRENT KNOWLEDGE AND RECOMMENDATIONS FOR RESEARCH CY NOV 20-21, 1991 CL NIH, BETHESDA, MD SP AMER CANC SOC, NIA, NCI HO NIH C1 NIA,OFF DIRECTOR,9000 ROCKVILLE PIKE,BLDG 31,ROOM 5C05,BETHESDA,MD 20892. MEM SLOAN KETTERING CANC CTR,DEPT SURG,GYNECOL SERV,NEW YORK,NY 10021. NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,CLIN INVEST BRANCH,SURG SECT,BETHESDA,MD 20892. NR 1 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 15 PY 1993 VL 71 IS 2 SU S BP 656 EP 658 PG 3 WC Oncology SC Oncology GA KH506 UT WOS:A1993KH50600024 ER PT J AU ANDERSON, LM CARTER, JP DRIVER, CL LOGSDON, DL KOVATCH, RM GINERSOROLLA, A AF ANDERSON, LM CARTER, JP DRIVER, CL LOGSDON, DL KOVATCH, RM GINERSOROLLA, A TI ENHANCEMENT OF TUMORIGENESIS BY N-NITROSODIETHYLAMINE, N-NITROSOPYRROLIDINE AND N6(METHYLNITROSO)-ADENOSINE BY ETHANOL SO CANCER LETTERS LA English DT Article DE NITROSAMINES; N-NITROSODIETHYLAMINE; N-NITROSOPYRROLIDINE; N6-(METHYLNITROSO)-ADENOSINE; ETHANOL; LUNG TUMORS; STOMACH TUMORS; THYMIC LYMPHOMAS ID SYRIAN GOLDEN-HAMSTERS; LIVER-MICROSOMES; HUMAN CANCER; NITROSODIMETHYLAMINE; METABOLISM; RAT; DIETHYLNITROSAMINE; ALCOHOL; CYTOCHROME-P450IIE1; DIMETHYLNITROSAMINE AB Inclusion of 10% ethanol with 6.8 ppm N-nitrosodiethylamine in the drinking water of strain A male mice resulted in a 4-fold enhancement of multiplicity of lung tumors and a 16-fold increase in incidence of fore-stomach tumors, compared with carcinogen alone. Given with 40 ppm N-nitrosopyrrolidine, ethanol caused a 5.5-fold increase in lung tumor multiplicity. The inclusion of 15 % ethanol with N6 (methylnitroso)adenosine, given orally to Swiss female mice, led to reduced body weights and shortened survival time related to hemangiosarcoma occurrence or increased incidence of thymic lymphoma, depending on dose of carcinogen. The data provide additional support for the proposal that co-administered ethanol increases the tumorigenicity of nitrosamines by blocking hepatic first-pass clearance. C1 NCI,COMPARAT CARCINOGENSIS LAB,FREDERICK,MD 21701. PATHOL ASSOCIATES INC,FREDERICK,MD 21701. UNIV FIORDIA,COLL MED,TAMPA,FL 33612. RP ANDERSON, LM (reprint author), PRI DYN CORP,NCL FREDERICK CANC RES & DEV CTR,BLDG 538,FREDERICK,MD 21702, USA. NR 32 TC 24 Z9 24 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD JAN 15 PY 1993 VL 68 IS 1 BP 61 EP 66 DI 10.1016/0304-3835(93)90220-4 PG 6 WC Oncology SC Oncology GA KH444 UT WOS:A1993KH44400009 PM 8422650 ER PT J AU PARKER, RJ VIONNET, JA BOSTICKBRUTON, F REED, E AF PARKER, RJ VIONNET, JA BOSTICKBRUTON, F REED, E TI ORMAPLATIN SENSITIVITY RESISTANCE IN HUMAN OVARIAN-CANCER CELLS MADE RESISTANT TO CISPLATIN SO CANCER RESEARCH LA English DT Article ID ACQUIRED-RESISTANCE; DNA-REPAIR; PLATINUM; CIS-DIAMMINEDICHLOROPLATINUM(II); TETRAPLATIN; LINES; GLUTATHIONE; 1,2-DIAMINOCYCLOHEXANE; MECHANISMS; COMPLEXES AB The human ovarian cancer cell lines A2780 and A2780/CP70 were studied to investigate the cellular basis for their relative sensitivities to tetrachloro(DL-trans)-1,2-diamminecyclohexaneplatinum(IV) (ormaplatin). Cells were exposed to ormaplatin for 1 h in all experiments. As assessed by colony formation assays, the A2780/CP70 cell line [50% inhibitory dose (IC50) = 3.6 muM] was 9.5-fold more resistant to ormaplatin than the A2780 cell line [IC50 = 0.38 muM]. For cisplatin, the IC50 doses were 40 and 3 muM, respectively. Both cell lines were treated with ormaplatin at doses ranging from 0.10 to 40 muM, for the purpose of studying drug accumulation and efflux, and DNA adduct formation and repair. When these cell lines were treated at their respective IC50 doses, drug accumulation was greater in the resistant cells. When treated at equal muM doses, the sensitive cells formed 8-fold more DNA adduct than the resistant cells. When cells were treated with ormaplatin so as to achieve equivalent levels of platinum-DNA modification, sensitive cells removed 53% of the platinum-DNA damage in the first 6 h after drug exposure, compared to 68% in the resistant cells. We conclude that in human ovarian cancer cells made resistant to cisplatin, there is moderate cross-resistance to ormaplatin. This cross-resistance is not explained by differences in drug accumulation but is associated with reduced platinum-DNA adduct formation, which may be attributable in part to cytosolic inactivation of drug. C1 NCI,MED BRANCH,BLDG 10,ROOM 12N 226,900 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 33 TC 17 Z9 17 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1993 VL 53 IS 2 BP 242 EP 247 PG 6 WC Oncology SC Oncology GA KF731 UT WOS:A1993KF73100010 PM 8417816 ER PT J AU BRUNNER, N BOULAY, V FOJO, A FRETER, CE LIPPMAN, ME CLARKE, R AF BRUNNER, N BOULAY, V FOJO, A FRETER, CE LIPPMAN, ME CLARKE, R TI ACQUISITION OF HORMONE-INDEPENDENT GROWTH IN MCF-7 CELLS IS ACCOMPANIED BY INCREASED EXPRESSION OF ESTROGEN-REGULATED GENES BUT WITHOUT DETECTABLE DNA AMPLIFICATIONS SO CANCER RESEARCH LA English DT Article ID HUMAN-BREAST-CANCER; MALIGNANT PROGRESSION; RECEPTOR EXPRESSION; PROGNOSTIC FACTORS; FACTOR-ALPHA; NUDE-MICE; LINES; RESISTANCE; INVITRO; INVIVO AB A hormone-independent but hormone-responsive subpopulation (MCF7/MIII) of the hormone-dependent MCF-7 human breast cancer cell line (R. Clarke et al. Proc. Natl. Acad. Sci. USA 86: 3649-3653, 1989) was further passaged in ovariectomized nude mice and re-established in vitro as the continuous cell line MCF7/LCC1. The lag time to the appearance of proliferating tumors in ovariectomized animals is significantly reduced in MCF7/LCC1 when compared with MCF7/MIII cells. In gel denaturation/renaturation analysis of tumor, genomic DNA does not reveal significant differences in the pattern of detectable DNA amplifications between parent MCF-7 cells and MCF7/LCC1 cells. In the absence of estrogen, steady-state levels of phosphoinositol turnover are similar in both MCF-7 and MCF7/LCC1 cells, but turnover is increased by estrogen only in MCF-7 cells. MCF7/MIII and MCF7/LCC1, but not MCF-7 cells, express a high baseline level of the estrogen-regulated pS2 mRNA. The baseline level of expression of progesterone receptor protein, but not mRNA, is higher in MCF7/LCC1 when compared with either MCF-7 or early passage MCF7/MIII cells. However, while the estrogen receptor is also an estrogen-regulated gene, MCF7/MIII and MCF7/LCC1 cells retain estrogen receptor levels equivalent to the parental MCF-7 cells. These data indicate that progression to hormone independence can occur without major gene amplifications or a high constitutive induction of phosphoinositide metabolism. Thus, DNA amplifications may be acquired during the early initiation and/or promotional events of carcinogenesis. Significantly, acquisition of a hormone-independent but responsive phenotype in human breast cancer is associated with perturbations in the expression of specific estrogen-regulated genes. C1 NCI,MED BRANCH,BETHESDA,MD 20892. RP CLARKE, R (reprint author), GEORGETOWN UNIV,VINCENT T LOMBARDI CANC RES CTR,SCH MED,3800 RESERVOIR RD NW,WASHINGTON,DC 20007, USA. RI Clarke, Robert/A-6485-2008 OI Clarke, Robert/0000-0002-9278-0854 FU NCI NIH HHS [1-R55-CA51782, 5-R01-CA58022, 5-U01-CA51908] NR 54 TC 97 Z9 98 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1993 VL 53 IS 2 BP 283 EP 290 PG 8 WC Oncology SC Oncology GA KF731 UT WOS:A1993KF73100017 PM 8380254 ER PT J AU THEUER, CP KREITMAN, RJ FITZGERALD, DJ PASTAN, I AF THEUER, CP KREITMAN, RJ FITZGERALD, DJ PASTAN, I TI IMMUNOTOXINS MADE WITH A RECOMBINANT FORM OF PSEUDOMONAS EXOTOXIN-A THAT DO NOT REQUIRE PROTEOLYSIS FOR ACTIVITY SO CANCER RESEARCH LA English DT Article ID RICINUS-COMMUNIS AGGLUTININ; ANTI-TRANSFERRIN RECEPTOR; ANTITUMOR-ACTIVITY; FUSION PROTEIN; MONOCLONAL-ANTIBODIES; ESCHERICHIA-COLI; HUMAN LYMPHOMA; CELL-LINES; DOMAIN-II; TOXIN AB We used recombinant DNA technology to construct a mutant form of Pseudomonas exotoxin A (PE) called cysPE35 that contains amino acids 280-364 and 381-613 of PE. cysPE35 begins at the native PE proteolytic cleavage site and contains a single cysteine residue at position 287 that can be used to conjugate the toxin to monoclonal antibodies (MAbs). Unlike immunotoxins containing larger mutant forms of PE, such as PE40 or PE38, immunotoxins containing cysPE35 linked through a disulfide bond do not require proteolysis to generate a toxin fragment able to translocate to the cytosol. cysPE35 was conjugated to several MAbs and their activities were studied in vitro and in vivo. The concentration of toxin that inhibited protein synthesis as measured by a decrease in [H-3]leucine incorporation of 50% of cysPE35 conjugated through a disulfide bond to the MAb HB21, which targets the human transferrin receptor, was 1 ng/ml on A431 cells. The MAb HB21 conjugated through a thioether bond to cysPE35 was much less active (concentration of toxin that inhibited protein synthesis as measured by a decrease in [H-3]leucine incorporation of 50%, 200 ng/ml). An immunotoxin containing PE38 conjugated through either a disulfide or thioether bond to the MAb HB21 had a concentration of toxin that inhibited protein synthesis as measured by a decrease in [H-3]leucine incorporation of 50 % of 5 ng/ml, indicating that proteolysis of PE38 may be rate limiting in the action of these immunotoxins. Two other MAbs, LL2 and B3, were also conjugated through a disulfide bond to cysPE35. Both immunotoxins were also more active against cultured cells than conjugates using PE38 or PE40, and caused complete regression of human tumor xenografts growing in nude mice. In conclusion, we have constructed a mutant form of PE which must be coupled to MAbs through a disulfide bond to produce fully active immunotoxins that do not require proteolysis to generate a toxin fragment able to reach the cell cytosol. RP THEUER, CP (reprint author), NCI,DIV CANC BIOL,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 40 TC 50 Z9 50 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1993 VL 53 IS 2 BP 340 EP 347 PG 8 WC Oncology SC Oncology GA KF731 UT WOS:A1993KF73100026 PM 8417828 ER PT J AU DEGUCHI, Y KEHRL, JH AF DEGUCHI, Y KEHRL, JH TI HIGH-LEVEL EXPRESSION OF THE HOMEOBOX GENE HB24 IN A HUMAN T-CELL LINE CONFERS THE ABILITY TO FORM TUMORS IN NUDE-MICE SO CANCER RESEARCH LA English DT Article ID MYELOID-LEUKEMIA; PRE-B; TRANSLOCATION AB The human homeobox gene HB24 is constitutively expressed in bone marrow progenitor cells and is inducible in lymphocytes. Transfection of HB24 into the T-cell line Jurkat under the control of the beta-actin promoter resulted in enhanced cell growth and induction of several growth-related genes. In this study we have examined whether the presence of high levels of HB24 alters the tumorigenicity of Jurkat cells in nude mice. Subcutaneous injection of 1-2 x 10(6) Jurkat cells or Jurkat cells transfected with a control expression vector into nude mice failed to produce tumors. However, injection of a similar number of HB24-transfected Jurkat cells resulted in local tumor formation within 4 weeks and grossly apparent metastatic lesions within 8 weeks. Histopathological analysis of tissues from the local and metastatic lesions demonstrated predominantly lymphoid cells, consistent with the morphological appearance of the injected cell line. Freshly isolated tumor cells from the nude mice incorporated similar levels of [H-3]thymidine as the HB24-transfected Jurkat cells and 2-fold more than the parent Jurkat cells. Northern blot analysis of RNA prepared from the tumors revealed expression of human interleukin 2, interleukin 2 receptor alpha-chain, HB24, and CD4. Flow cytometric analysis of the tumor cells revealed human CD4 expression but not murine CD4, confirming the human origin of the tumor cells. Media conditioned by the tumor cells contained large amounts of interleukin 2. Since natural killer cell activity is the primary immunological response against tumors in nude mice, the effects of HB24 on the responsiveness to natural killer cell-mediated cell lysis was examined. No differences in natural killer cell killing of the parent Jurkat cells and the HB24-transfected cells were observed. These data, in conjunction with recent data implicating other homeobox-containing genes in the pathogenesis of human leukemias, suggest that overexpression of HB24 in hematopoietic progenitors or T-cells may contribute to oncogenic transformation. C1 NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B-13,BETHESDA,MD 20892. OI Kehrl, John/0000-0002-6526-159X NR 18 TC 21 Z9 22 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1993 VL 53 IS 2 BP 373 EP 377 PG 5 WC Oncology SC Oncology GA KF731 UT WOS:A1993KF73100031 PM 8093351 ER PT J AU BELINSKY, SA STEFANSKI, SA ANDERSON, MW AF BELINSKY, SA STEFANSKI, SA ANDERSON, MW TI THE A/J MOUSE LUNG AS A MODEL FOR DEVELOPING NEW CHEMOINTERVENTION STRATEGIES SO CANCER RESEARCH LA English DT Article ID SQUAMOUS-CELL CARCINOMA; STRAIN-A MOUSE; RANDOMIZED TRIAL; RAS PROTOONCOGENE; MURINE TUMORS; GROWTH-RATE; DNA DAMAGE; CHEMOTHERAPY; CANCER; MICE AB The use of the A/J mouse lung as a model for developing new chemointervention strategies was investigated by first inducing lung tumors with a single dose of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Lungs were then staged for tumor development and intervention therapy was initiated 42 weeks after carcinogen treatment. At this time point, an average of 7 pulmonary lesions were present on a standard histological section and the relative frequency of lesions was distributed as alveolar hyperplasias (38%), adenomas (40%), and adenocarcinomas (22%). Mice were treated for 4 or 8 weeks with cis-platinum alone or in combination with either indomethacin, an inhibitor of prostaglandin synthesis, metoclopramide, an inducer of poly(ADP) ribosylation, or nifedipine, a calcium channel blocker. The effect of indomethacin, metoclopramide, and nifedipine on tumor growth was also determined. The most dramatic effects were observed in lungs from mice treated for 8 weeks. cis-Platinum treatment caused a 37% reduction in the size of carcinomas, while tumor mass was reduced by 50 to 60% with cis-platinum in combination with metoclopramide and/or indomethacin. The inclusion of indomethacin therapy in conjunction with cis-platinum significantly enhanced the effectiveness of cis-platinum for inhibiting the growth of adenocarcinomas. In contrast, nifedipine appeared to ameliorate any of the inhibitory growth effects seen with cis-platinum treatment. Although none of the therapeutic combinations affected the size of adenomas, morphological differences were observed among treatment groups. A moderate to marked decrease in cytoplasm was observed in adenomas from mice treated with cis-platinum in combination with indomethacin or metoclopramide, cis-platinum plus metoclopramide and indomethacin, or metoclopramide plus indomethacin. Taken together, the results from these studies demonstrate that the A/J mouse lung can be used as a model to study the effectiveness of new intervention therapies for controlling malignant tumor growth. This model should also be applicable for studying the effectiveness of cancer prevention therapies on the progression of pulmonary hyperplasia. C1 NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709. NR 38 TC 30 Z9 31 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1993 VL 53 IS 2 BP 410 EP 416 PG 7 WC Oncology SC Oncology GA KF731 UT WOS:A1993KF73100036 PM 8417832 ER PT J AU YAMAMURA, K KIBBEY, MC KLEINMAN, HK AF YAMAMURA, K KIBBEY, MC KLEINMAN, HK TI MELANOMA-CELLS SELECTED FOR ADHESION TO LAMININ PEPTIDES HAVE DIFFERENT MALIGNANT PROPERTIES SO CANCER RESEARCH LA English DT Article ID EXPERIMENTAL METASTASIS FORMATION; AMINO-ACID-SEQUENCE; BASEMENT-MEMBRANE; TUMOR-CELLS; A-CHAIN; SYNTHETIC PEPTIDE; NEURITE OUTGROWTH; IV COLLAGENASE; B1 CHAIN; IDENTIFICATION AB Laminin is an important promoter of cell-matrix interactions. A number of active laminin domains have been defined by use of synthetic peptides. The Tyr-Ile-Gly-Ser-Arg (YIGSR) sequence on the B1 chain in laminin can decrease tumor growth and metastasis, whereas another sequence containing Ser-Ile-Lys-Val-Ala-Val (SIKVAV) on the A chain can increase tumor growth and metastasis. Here, we selected B16-F10 melanoma cells by adherence or nonadherence to either YIGSR- or SIKVAV-coated dishes and established 3 B16-F10 variants: YIGSR-adherent cells (Y+), YIGSR-nonadherent cells (Y-), and SIKVAV-nonadherent cells (S-). SIKVAV-adherent cells were not selected because most of F10 cells attached to the SIKVAV-coated dish. These cell lines proliferated at the same rate as the parent F10 cells and attached equally to laminin, collagen IV, and fibronectin. Y+ cells produced rapidly growing tumors after s.c. injection and twice as many lung colonies as the parental F10 cells after i.v. injection. In contrast, Y- cells produced more slowly growing tumors after s.c. injection and produced one-third of the lung colonies relative to the parent cells after i.v. injection. S- cells produced slowly growing tumors after s.c. injection and yielded similar numbers but smaller colonies in the lung than the parental B16-F10 cells after i.v. injection. These data suggest that interactions of melanoma cells with the YIGSR site on laminin are probably important for both colony formation in a target organ (lung) and subsequent tumor growth, while the SIKVAV-containing site on laminin may be more important for tumor growth. C1 NIDR,DEV BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 42 TC 39 Z9 40 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1993 VL 53 IS 2 BP 423 EP 428 PG 6 WC Oncology SC Oncology GA KF731 UT WOS:A1993KF73100038 PM 8417834 ER PT J AU KLAUSNER, RD ROUAULT, TA HARFORD, JB AF KLAUSNER, RD ROUAULT, TA HARFORD, JB TI REGULATING THE FATE OF MESSENGER-RNA - THE CONTROL OF CELLULAR IRON-METABOLISM SO CELL LA English DT Review ID PAIRED FLANKING REGIONS; ELEMENT-BINDING-PROTEIN; RESPONSIVE ELEMENT; TRANSFERRIN RECEPTOR; UNTRANSLATED REGION; 5-AMINOLEVULINATE SYNTHASE; TRANSLATIONAL REGULATION; SECONDARY STRUCTURE; CHELATABLE IRON; HEAVY-SUBUNIT RP KLAUSNER, RD (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 75 TC 1109 Z9 1115 U1 2 U2 20 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JAN 15 PY 1993 VL 72 IS 1 BP 19 EP 28 DI 10.1016/0092-8674(93)90046-S PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KG955 UT WOS:A1993KG95500006 PM 8380757 ER PT J AU LEE, DY HAYES, JJ PRUSS, D WOLFFE, AP AF LEE, DY HAYES, JJ PRUSS, D WOLFFE, AP TI A POSITIVE ROLE FOR HISTONE ACETYLATION IN TRANSCRIPTION FACTOR ACCESS TO NUCLEOSOMAL DNA SO CELL LA English DT Article ID 5S RNA GENE; CHROMATIN CORE PARTICLES; LINKING NUMBER CHANGE; TUMOR VIRUS PROMOTER; SILENT MATING LOCI; FACTOR-IIIA; 5S-RNA GENE; C-FOS; BINDING; REPRESSION AB Acetylation of the N-terminal tails of the core histones directly facilitates the recognition by TFIIIA of the 5S RNA gene within model chromatin templates. This effect is independent of a reduction in the extent of histone-DNA interactions or a change in DNA helical repeat; it is also independent of whether a histone tetramer or octamer inhibits TFIIIA binding. Removal of the N-terminal tails from the core histones also facilitates the association of TFIIIA with nucleosomal templates. We suggest that the histone tails have a major role in restricting transcription factor access to DNA and that their acetylation releases this restriction by directing dissociation of the tails from DNA and/or inducing a change in DNA configuration on the histone core to allow transcription factor binding. Acetylation of core histones might be expected to exert a major influence on the accessibility of chromatin to regulatory molecules. RP LEE, DY (reprint author), NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892, USA. NR 75 TC 837 Z9 849 U1 3 U2 18 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JAN 15 PY 1993 VL 72 IS 1 BP 73 EP 84 DI 10.1016/0092-8674(93)90051-Q PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KG955 UT WOS:A1993KG95500011 PM 8422685 ER PT J AU ZAWIA, NH HARRY, GJ AF ZAWIA, NH HARRY, GJ TI CORRELATIONS BETWEEN DEVELOPMENTAL ORNITHINE DECARBOXYLASE GENE-EXPRESSION AND ENZYME-ACTIVITY IN THE RAT-BRAIN SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE ORNITHINE DECARBOXYLASE; CEREBELLUM MESSENGER RNA; NEOCORTEX; RAT ID MOUSE-BRAIN; METHYLMERCURY; POLYAMINES; INDUCTION; ANTIZYME; PROTEIN; RNA AB The rise and decline in cerebral ODC activity during specific stages of development has been attributed to cytoplasmic intermediates which regulate ornithine decarboxylase activity. Here we examine whether transcriptional regulation contributes to the production of the developmental profiles of ODC activity. Postnatal cerebellar and neocortical tissue were obtained from Long-Evans hooded rats at postnatal days (PND) 5, 10, 15, 20, 25, 30, 90 and probed for ODC and actin gene expression, by Northern analysis. Our results indicate that ODC gene expression in the cerebellum was elevated at PND 5 and 10 followed by a gradual drop to the adult low levels by PND 20. By contrast, high levels of ODC gene expression in the neocortex were seen at PND 5 with an abrupt decrease at day 10 to low adult levels. The expression of the ODC gene in the neocortex follows closely the pattern for the ODC enzyme activity; however, it tends to remain elevated longer in the cerebellum. The levels of actin gene expression exhibited a distinct developmental profile in the postnatally developing cerebellum. However, actin mRNA levels remained unchanged in the neocortex, consistent with the prenatal development of this region. Our findings suggest that ODC gene expression may play an important role in the production of the ontogenetic patterns of ODC activity. C1 NIEHS,SYST TOXIC BRANCH,DEV & REPROD TOXICOL GRP,POB 12233,MD-E102,RES TRIANGLE PK,NC 27709. NR 23 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD JAN 15 PY 1993 VL 71 IS 1 BP 53 EP 57 DI 10.1016/0165-3806(93)90104-I PG 5 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA KH259 UT WOS:A1993KH25900007 ER PT J AU MCMILLIAN, MK HUDSON, PM LEE, DY THAI, L HUNG, GH HONG, JS AF MCMILLIAN, MK HUDSON, PM LEE, DY THAI, L HUNG, GH HONG, JS TI DEVELOPMENTAL-CHANGES IN RAT ADRENAL ENKEPHALIN PRECURSOR - PEPTIDE RATIO SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE ADRENAL MEDULLA; ENKEPHALIN; PROENKEPHALIN; CARBOXYPEPTIDASE-E; NICOTINE ID PREPROENKEPHALIN MESSENGER-RNA; CRYPTIC MET-ENKEPHALIN; CHROMAFFIN CELLS; CARBOXYPEPTIDASE-E; INCREASES; MEDULLA; DENERVATION; PROENKEPHALIN; MODULATION; MECHANISMS AB Developmental changes in rat adrenal [Met5]enkephalin (ME) immunoreactivity and [Met5]enkephalinargininephenylalanine (MERF) immunoreactivity (which presumably reflects proenkephalin) were examined. The concentration of MERF appeared highest at the end of the first week postnatally and decreased fourfold to near adult values by day 21, while ME levels decreased only about twofold. This indicates a fall in the adrenal proenkephalin:ME ratio during the transition from the suckling to the weanling period in the rat. The elevated MERF levels during the suckling period may result from deficient processing of proenkephalin to free ME. An increase in the activity of the processing enzyme carboxypeptidase E was observed at day 15, which may contribute to the developmental fall in the adrenal proenkephalin to free ME ratio. Mimicking sympathetic activity by nicotine treatment (3 mg/kg i.p. twice daily from birth) produced a precocious decrease in the MERF: ME ratio at day 8, and also increased the activity of the processing enzyme. Denervation at day 10 markedly decreased adrenal ME and produced a three-fold increase in MERF: ME ratio when measured at day 30. Adrenal carboxypeptidase E activity was also decreased after denervation. In summary, these results suggest that increasing preganglionic sympathetic nerve activity during the third week postnatally stimulates proenkephalin processing and leads to the developmental decrease in MERF: ME ratio in the rat adrenal. RP MCMILLIAN, MK (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,BOX 12233,MAILDROP 14-06,RES TRIANGLE PK,NC 27709, USA. NR 29 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD JAN 15 PY 1993 VL 71 IS 1 BP 75 EP 80 DI 10.1016/0165-3806(93)90107-L PG 6 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA KH259 UT WOS:A1993KH25900010 ER PT J AU YAMADA, M KAKITA, A MIZUGUCHI, M RHEE, SG KIM, SU IKUTA, F AF YAMADA, M KAKITA, A MIZUGUCHI, M RHEE, SG KIM, SU IKUTA, F TI DEVELOPMENTAL PROFILE OF INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE IN RAT CEREBELLAR CORTEX - LIGHT AND ELECTRON-MICROSCOPIC IMMUNOHISTOCHEMICAL STUDIES SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE INOSITOL 1,4,5-TRISPHOSPHATE; INOSITOL 1,3,4,5-TETRAKISPHOSPHATE; INOSITOL 1,4,5-TRISPHOSPHATE 3-KINASE; IMMUNOHISTOCHEMISTRY; RAT; CEREBELLUM; DEVELOPMENT; ULTRASTRUCTURE ID PURKINJE-CELLS; DENDRITIC SPINES; MOLECULAR LAYER; PHOSPHOLIPASE-C; RECEPTOR; 1,3,4,5-TETRAKISPHOSPHATE; PHOSPHATES; CA-2+; BRAIN; CALCIUM AB Developmental expression and intracellular distribution of inositol 1,4,5-trisphosphate 3-kinase in the rat cerebellar cortex were studied immunohistochemically. Immunoreactivity appeared first at postnatal day 1 in the rostral region of the cerebellum and by day 15 had extended throughout the whole cerebellum, being localized in the Purkinje cell layer. Shortly after the expression of the enzyme in each Purkinje cell, the labelling showed a tendency to accumulate in the dendrites in a fine granular pattern. Electron microscopy revealed that immunoreactivity was present in the Purkinje dendritic trunks with accentuation in the distal segments during the early postnatal period, thereafter becoming concentrated in the dendritic spines at later developmental stages. Labelling was associated mainly with the plasmalemma, including the postsynaptic densities and open coated vesicles, and the subplasmalemmal vesicles of the smooth endoplasmic reticulum. Immunoreactivity was also evident in the perisomatic processes of immature Purkinje cells, which are transient projections synapsing with climbing fibers. In developing Purkinje axons, immunoreactivity was accentuated in the distal segments, associated with the plasmalemma and synaptic vesicles. These results suggest that inositol 1,4,5-trisphosphate 3-kinase is involved in the dendritic arborization and subsequent spine synaptogenesis of Purkinje cells, and that the developing presynaptic nerve endings of these cells are another functional site for the enzyme. C1 UNIV TOKYO,FAC MED,DEPT PEDIAT,TOKYO 113,JAPAN. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV BRITISH COLUMBIA,DEPT MED,DIV NEUROL,VANCOUVER V6T 1W5,BC,CANADA. RP YAMADA, M (reprint author), NIIGATA UNIV,BRAIN RES INST,DEPT PATHOL,ASAHIMACHI 1,NIIGATA 951,JAPAN. NR 33 TC 7 Z9 7 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD JAN 15 PY 1993 VL 71 IS 1 BP 137 EP 145 DI 10.1016/0165-3806(93)90114-P PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA KH259 UT WOS:A1993KH25900017 ER PT J AU VILNER, BJ BOWEN, WD AF VILNER, BJ BOWEN, WD TI SIGMA-RECEPTOR-ACTIVE NEUROLEPTICS ARE CYTOTOXIC TO C6 GLIOMA-CELLS IN CULTURE SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION LA English DT Note DE SIGMA-RECEPTORS; ANTIPSYCHOTIC DRUGS; CYTOTOXICITY ID GUINEA-PIG BRAIN; BINDING AB When exposed to neuroleptics (100 mum), C6 glioma cells exhibited marked changes in cell morphology, accompanied by cessation of cell division and ultimately cell death. The degree of activity generally correlated with binding affinity at sigma sites: fluphenazine = perphenazine = haloperidol = reduced haloperidol > pimozide = spiperone much greater than much greater than (-)-sulpiride. Sigma-inactive compounds (100 muM) which block dopamine, serotonin, phencyclidine, muscarinic receptors and adrenoceptors showed no effect. These results may suggest a role of sigma binding sites in maintenance of cell viability. C1 NIDDK,MED CHEM LAB,RECEPTOR BIOCHEM & PHARMACOL UNIT,BLDG 8,RM B1-23,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 8 TC 63 Z9 63 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0922-4106 J9 EUR J PHARM-MOLEC PH JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect. PD JAN 15 PY 1993 VL 244 IS 2 BP 199 EP 201 DI 10.1016/0922-4106(93)90029-9 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KH540 UT WOS:A1993KH54000015 PM 8094338 ER PT J AU IWASAKI, M DARDEN, TA PEDERSEN, LG DAVIS, DG JUVONEN, RO SUEYOSHI, T NEGISHI, M AF IWASAKI, M DARDEN, TA PEDERSEN, LG DAVIS, DG JUVONEN, RO SUEYOSHI, T NEGISHI, M TI ENGINEERING MOUSE P450COH TO A NOVEL CORTICOSTERONE 15-ALPHA-HYDROXYLASE AND MODELING STEROID-BINDING ORIENTATION IN THE SUBSTRATE POCKET SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID SITE-DIRECTED MUTAGENESIS; AMINO; CYTOCHROMES-P450; SPECIFICITY; MUTATION; SEQUENCE; PROTEINS; FIELD AB The F209L mutation alters specificity of P450coh from coumarin 7-hydroxylation to 15alpha-hydroxylation of 11-deoxysteroids such as testosterone and 11-deoxycorticosterone. Neither the wild-type nor F209L exhibits activity toward 11beta-hydroxysteroids including corticosterone. Mutation of Phe-209 to Asn, however, confers on mutant F209N a high corticosterone 15alpha-hydroxylase activity. F209V also exhibits low corticosterone 15alpha-hydroxylase activity; K(m) and V(max) are 10-fold higher and lower, respectively, than for F209N. The results are consistent with the hypothesis that direct interaction of Asn-209 with 11OH is responsible for high corticosterone 15alpha-hydroxylase activity. To support this hypothesis, a possible steroid-binding orientation is modeled in the substrate pocket of P450cam. Our weighted homology and constrained alignments map residue 209 of P450coh to Met-184 and Met- 191 of P450cam. Energy minimization of corticosterone in the substrate pocket results in the 11 OH of the steroid directed toward Met-184 (7 angstrom) and Met-191 (16 angstrom), and in C15 located near the sixth axial position of the heme. The steroid-binding model suggests that the P450cam's substrate pocket may be conserved in the mammalian P450 and can accommodate a steroid molecule, and that residue 209 appears to be located at the critical site that determines the steroid-substrate specificity of a P450 depending on the type of group at the 11-position of steroid molecule. C1 NIEHS,REPRODUCT & DEV TOXICOL LAB,PHARMACOGENET SECT,RES TRIANGLE PK,NC 27709. NIEHS,MOLEC TOXICOL LAB,RES TRIANGLE PK,NC 27709. NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 24 TC 57 Z9 57 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 JAN 15 PY 1993 VL 268 IS 2 BP 759 EP 762 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG077 UT WOS:A1993KG07700002 PM 8419350 ER PT J AU CHAUHAN, SS POPESCU, NC RAY, D FLEISCHMANN, R GOTTESMAN, MM TROEN, BR AF CHAUHAN, SS POPESCU, NC RAY, D FLEISCHMANN, R GOTTESMAN, MM TROEN, BR TI CLONING, GENOMIC ORGANIZATION, AND CHROMOSOMAL LOCALIZATION OF HUMAN CATHEPSIN-L SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MAJOR EXCRETED PROTEIN; BONE-RESORPTION; MESSENGER-RNAS; ACID-PROTEASE; GROWTH-FACTOR; CELL LINES; GENE; EXPRESSION; SEQUENCES; MURINE AB Cathepsin L is a lysosomal cysteine protease whose expression and secretion is induced by malignant transformation, growth factors, and tumor promoters. Many human tumors express high levels of cathepsin L, which is a broad spectrum protease with potent elastase and collagenase activities. Two published human cathepsin L cDNA sequences differ only in their 5'-untranslated regions. In this study, we demonstrate the concurrent expression of two distinct human cathepsin L mRNAs (hCATL-A and hCATL-B) in adenocarcinoma, hepatoma, and renal cancer cell lines. Cloning of the human cathepsin L gene by polymerase chain reaction amplification of genomic DNA and subsequent sequencing reveals that hCATL-A and hCATL-B mRNAs are encoded by a single gene. The 3' end of the first intron contains the 5' portion of hCATL-B and is contiguous to the second exon of the gene. These data suggest either the possibility of alternative splicing or the presence of a second promoter within the first intron of the hCATL gene. We mapped the hCATL gene to chromosome 9q21-22. Sequencing of both the mouse and human cathepsin L genes demonstrates almost complete conservation of exon and intron position, but significant divergence in intron structure, possibly reflecting differences in regulation of expression of the mouse and human cathepsin L genes. C1 UNIV NANCY 1,VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,INST GERONTOL,F-54506 VANDOEUVRE NANCY,FRANCE. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NCI,BIOL LAB,BETHESDA,MD 20892. NR 51 TC 80 Z9 81 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 JAN 15 PY 1993 VL 268 IS 2 BP 1039 EP 1045 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG077 UT WOS:A1993KG07700044 PM 8419312 ER PT J AU NAJJAR, SM ACCILI, D PHILIPPE, N JERNBERG, J MARGOLIS, R TAYLOR, SI AF NAJJAR, SM ACCILI, D PHILIPPE, N JERNBERG, J MARGOLIS, R TAYLOR, SI TI PP120 ECTO-ATPASE, AN ENDOGENOUS SUBSTRATE OF THE INSULIN-RECEPTOR TYROSINE KINASE, IS EXPRESSED AS 2 VARIABLY SPICED ISOFORMS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; PRE-MESSENGER RNA; GLYCOPROTEIN; PROTEIN; CLONING; COMMON; PHOSPHORYLATION; LOCALIZATION; ACTIVATION; ANTIGENS AB The insulin receptor possesses tyrosine kinase activity which is thought to mediate the biological effects of insulin upon target cells. pp120 is a liver-specific glycoprotein of apparent molecular size of 120 kDa that is phosphorylated on tyrosine residues by the receptors for insulin, insulin-like growth factor-I, and epidermal growth factor. Previously, we demonstrated that pp120 is identical to a liver-specific ecto-ATPase. In the present study, we have cloned the rat gene encoding pp120/ecto-ATPase. The gene is contained within approximately 15 kilobases of genomic DNA, and consists of nine exons interrupted by eight introns. Using the reverse transcriptase/polymerase chain reaction, we isolated cDNA clones complementary to rat liver mRNA encoding pp120/ecto-ATPase. Sequence analysis indicated the presence of two populations of cDNA's that differ by the presence or absence of a 53-base pair (bp) fragment encoding the juxtamembrane region of the cytoplasmic domain. By cloning the corresponding region of the ecto-ATPase gene, we demonstrated that the 53-bp represents exon 7 of the gene. This 53-bp exon undergoes alternative splicing, thereby giving rise to two mRNA variants. Deletion of this 53-bp cassette exon introduces a frameshift, and results in a premature chain termination codon that truncates the cytoplasmic domain. The truncated cytoplasmic domain contains 10 rather than 71 amino acid residues. Because the short isoform of ecto-ATPase lacks the putative sites for tyrosine- and serine-specific phosphorylation, this alternative splicing may have a major effect upon the physiological function of the enzyme. C1 NIDDKD,DIABET BRANCH,BLDG 10,RM 85-239,BETHESDA,MD 20892. NR 27 TC 84 Z9 85 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 JAN 15 PY 1993 VL 268 IS 2 BP 1201 EP 1206 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG077 UT WOS:A1993KG07700066 PM 8380406 ER PT J AU BRINI, AT LEE, GM KINET, JP AF BRINI, AT LEE, GM KINET, JP TI INVOLVEMENT OF ALU SEQUENCES IN THE CELL-SPECIFIC REGULATION OF TRANSCRIPTION OF THE GAMMA-CHAIN OF FC AND T-CELL RECEPTORS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NATURAL-KILLER-CELLS; ZETA-CHAIN; MOLECULAR-CLONING; ANTIGEN RECEPTOR; BINDING PROTEIN; MAMMALIAN-CELLS; NUCLEAR-PROTEIN; IGE; GENE; EXPRESSION AB The FcepsilonRI-gamma chains are expressed in a variety of hematopoietic cells where they play a critical role in signal transduction. They are part of the high affinity IgE receptor in mast cells, basophils, Langerhans cells, and possibly other cells; a component of the low affinity receptor for IgG (FcgammaRIIIA or CD16) in natural killer cells and macrophages; and part of the T cell antigen receptor in subsets of T cells. Here we have investigated the transcriptional regulation of the gamma chain gene by analyzing the 2.5-kilobase sequence upstream of the transcription start site. This sequence contains a promoter specific to cells of hematopoietic lineage. However, the tissue specificity of this promoter is only partial because it is active in all of the hematopoietic cells tested here, regardless of whether they constitutively express FcepsilonI- gamma chain transcripts. We have identified two adjacent cis-acting regulatory elements, both of which are part of an Alu repeat. The first (-445/-366) is a positive element active in both basophils and T cells. The second (-365/-264) binds to nuclear factors, which appear to be different in basophils and T cells, and acts as a negative element in basophils and as a positive one in T cells. Thus, this Alu repeat (90% identical to Alu consensus sequences) has evolved to become both a positive and negative regulator. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. OI Brini, Anna Teresa/0000-0002-7848-8099 NR 43 TC 74 Z9 74 U1 0 U2 4 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 JAN 15 PY 1993 VL 268 IS 2 BP 1355 EP 1361 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG077 UT WOS:A1993KG07700089 PM 8419337 ER PT J AU BOEHNCKE, WH TAKESHITA, T PENDLETON, CD HOUGHTEN, RA SADEGHNASSERI, S RACIOPPI, L BERZOFSKY, JA GERMAIN, RN AF BOEHNCKE, WH TAKESHITA, T PENDLETON, CD HOUGHTEN, RA SADEGHNASSERI, S RACIOPPI, L BERZOFSKY, JA GERMAIN, RN TI THE IMPORTANCE OF DOMINANT NEGATIVE EFFECTS OF AMINO-ACID SIDE-CHAIN SUBSTITUTION IN PEPTIDE-MHC MOLECULE INTERACTIONS AND T-CELL RECOGNITION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; ANTIGEN-BINDING SITE; CLASS-II MOLECULE; SURFACE EXPRESSION; SYNTHETIC PEPTIDE; CONTACT RESIDUES; LYMPHOCYTES-T; A-BETA; IDENTIFICATION; HYBRIDOMAS AB Previous studies on the role of specific residues of the peptide or MHC molecule in Ag presentation have revealed the sensitivity of this complex system to even small changes in structure. In our study, we have analyzed the effect of amino acid substitution in a major CD4+ T cell determinant (T1) of HIV-1 gp160 on binding and recognition in the context of various EalphaEbeta MHC class II molecules. Individual alanine substitutions at all but three positions had little or no negative effect on either MHC binding or recognition by a specific T hybridoma, whereas substitutions with larger side chains often diminished reactivity. A poly-alanine peptide containing only four of the original residues was an effective MHC class II binder and in vivo immunogen, although lacking the ability to stimulate the hybridoma. Replacement of a glutamic acid in T1 with alanine or a size-conservative, uncharged glutamine, but not a negatively charged aspartic acid produced a peptide at least 100-fold more potent than the parent peptide, indicating an inhibitory effect of the negative charge. Conversely, substitution of a glutamic acid for valine at position 29 in the floor of the peptide binding site of the EalphaEbeta molecule decreased functional presentation of this peptide by more than 2 logs. However, these two effects of glutamic acid were not complementary and were mediated by distinct mechanisms, as the change in the peptide altered the extent of binding to class II, but the change in the MHC molecule decreased recognition without inhibiting peptide binding. Taken together, the data all suggest the conclusion that changes in side-chains of peptides and MHC molecules affect Ag presentation and T cell stimulation most often by introducing dominant negative or interfering groups that prevent or alter the pattern of binding events primarily mediated by a very limited number of other residues in the Ag or presenting molecule. These results have important implications for understanding the biochemistry of peptide-MHC-TCR interactions and for the possible design of vaccines both more potent and less subject to allele-specific limitations on immunogenicity. C1 NIAID,IMMUNOL LAB,LYMPHOCYTE BIOL SECT,BLDG 10,ROOM 11N311,BETHESDA,MD 20892. NCI,METAB SECT,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD 20892. TORREY PINES INST MOLEC STUDIES,SAN DIEGO,CA 92121. OI racioppi, luigi/0000-0002-9207-6752 NR 49 TC 122 Z9 122 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1993 VL 150 IS 2 BP 331 EP 341 PG 11 WC Immunology SC Immunology GA KG469 UT WOS:A1993KG46900001 PM 8093457 ER PT J AU DENKERS, EY GAZZINELLI, RT HIENY, S CASPAR, P SHER, A AF DENKERS, EY GAZZINELLI, RT HIENY, S CASPAR, P SHER, A TI BONE-MARROW MACROPHAGES PROCESS EXOGENOUS TOXOPLASMA-GONDII POLYPEPTIDES FOR RECOGNITION BY PARASITE-SPECIFIC CYTOLYTIC LYMPHOCYTES-T SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HISTOCOMPATIBILITY COMPLEX BINDING; INFECTED CELLS; ANTIGEN; MICE; PEPTIDE; BETA-2-MICROGLOBULIN; INDUCTION; MOLECULES; ANTIBODY; PROTEIN AB CD8+ T cells from mice vaccinated with an attenuated strain of Toxoplasma gondii have previously been shown to have cytolytic activity against bone marrow macrophages (BMMO) preincubated with a soluble tachyzoite extract. In the present study, we show that class I-transfected L cells differ from BMMO in that although both cell types are recognized CTL after infection, only BMMO are killed after sensitization with soluble tachyzoite extract. Gel filtration studies indicated that the T. gondii Ag responsible for sensitization of BMMO are macro-molecules of M(r) greater-than-or-equal-to 12,000. In contrast, peptides.derived by tryptic digestion of this material were found to sensitize both transfected L cells and BMMO. Although exogenous beta2-microglobulin markedly enhanced peptide sensitization of BMMO, no such effect was observed using the macromolecular preparation. This result suggests a requirement for cellular internalization in the processing by BMMO of soluble Ag for class I-restricted recognition. In related experiments, infected and Ag-sensitized BMMO were found to express cross-reactive T. gondii epitopes, as determined by cold target inhibition studies. Supernatant derived by 100,000 x g centrifugation of tachyzoite extract had potent sensitizing activity, and after anion exchange chromatography most of the activity was associated with a single fraction. The p30 Ag was not detected by immunoblot analysis in the biologically active supernatant and chromatographic fractions. These findings establish the feasibility of identifying the parasite Ag recognized by CD8+ effectors by direct fractionation of T. gondii proteins coupled with sensitization of BMMO targets. RP DENKERS, EY (reprint author), NIAID,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. NR 34 TC 59 Z9 60 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1993 VL 150 IS 2 BP 517 EP 526 PG 10 WC Immunology SC Immunology GA KG469 UT WOS:A1993KG46900021 PM 8419484 ER PT J AU SWIETER, M MIDURA, RJ NISHIKATA, H OLIVER, C BERENSTEIN, EH MERGENHAGEN, SE HASCALL, VC SIRAGANIAN, RP AF SWIETER, M MIDURA, RJ NISHIKATA, H OLIVER, C BERENSTEIN, EH MERGENHAGEN, SE HASCALL, VC SIRAGANIAN, RP TI MOUSE 3T3 FIBROBLASTS INDUCE RAT BASOPHILIC LEUKEMIA (RBL-2H3) CELLS TO ACQUIRE RESPONSIVENESS TO COMPOUND-48/80 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INDUCED HISTAMINE-RELEASE; SKIN MAST-CELLS; C-KIT LIGAND; GROWTH-FACTOR; IMMUNOGLOBULIN-E; HIGH-AFFINITY; RECEPTOR; EXPRESSION; PEPTIDES; INVITRO AB 2H3 subline of rat basophilic leukemia (RBL-2H3) cells are mast cell analogs that lack responsiveness to nonimmunologic stimuli such as compound 48/80 and substance P. To determine if fibroblasts can influence this responsiveness, RBL-2H3 cells were cocultured with confluent monolayers of mouse 3T3 fibroblasts and assayed for secretagogue-induced histamine release. After 1 wk in coculture, RBL-2H3 cells began to respond to compound 48/80. Responsiveness reached a maximum at 2 wk in coculture and remained at this level for an additional 2 wk. Histamine release was specific, noncytotoxic, dose-dependent, and occurred even in the absence of extracellular Ca2+. No soluble factor from 3T3 cells was found that induced these alterations. Moreover, neither recombinant rat or mouse steel factor, at concentrations up to 250 ng/ml, was able to alter RBL-2H3 cell reactivity to compound 48/80. By 2 wk in coculture, RBL-2H3 cells also became responsive to substance P, although no changes in histamine content, Alcian blue+/safranin- staining or type of serine protease were detected. These results show that 3T3 fibroblasts cause an alteration in the functional repertoire of RBL-2H3 cells and that soluble steel factor cannot duplicate the effect. C1 NIDR,BONE RES BRANCH,PROTEOGLYCAN CHEM SECT,BETHESDA,MD 20892. RP SWIETER, M (reprint author), NIDR,IMMUNOL LAB,BLDG 10,RM 1A23,BETHESDA,MD 20892, USA. NR 34 TC 40 Z9 40 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 JAN 15 PY 1993 VL 150 IS 2 BP 617 EP 624 PG 8 WC Immunology SC Immunology GA KG469 UT WOS:A1993KG46900033 PM 7678278 ER PT J AU SCOTT, DE KISCH, WJ STEINBERG, AD AF SCOTT, DE KISCH, WJ STEINBERG, AD TI STUDIES OF T-CELL DELETION AND T-CELL ANERGY FOLLOWING INVIVO ADMINISTRATION OF SEB TO NORMAL AND LUPUS-PRONE MICE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID STAPHYLOCOCCAL ENTEROTOXIN-B; MRL-LPR/LPR MICE; MONOCLONAL-ANTIBODY; DEFECTIVE TOLERANCE; ANTIGEN RECEPTOR; CLONAL DELETION; MURINE MODELS; INDUCTION; NEPHRITIS; THYMUS AB This study examines the responses of lupus-prone NZB, (NZB X NZW) F1, BXSB, MRL-lpr/lpr and control mice (H-2 and Mls matched) to in vivo administration of the superantigen staphylococcal enterotoxin B (SEB). Two weeks after i.v. administration of 500 mug SEB, CD4+Vbeta8+ lymph node T cells were deleted equivalently by lupus-prone and control mice. However, IE+ strains deleted a greater proportion (47% to 77%) of their CD4+Vbeta8+ cells than did IE- strains (24% to 27%). CD8+Vbeta8+ cells were deleted less than CD4+Vbeta8+ cells by injection of 500 mug SEB. IE- strains failed to delete CD8+Vbeta8+ cells, whereas six of seven IE+ strains deleted >25% of their CD8+Vbeta8+ cells. IE+ MRL-lpr/lpr mice showed some impairment in deletion: they failed to delete CD8+Vbeta8+ cells at all doses of SEB and had reduced deletion of CD4+Vbeta8+ cells at low doses of in vivo SEB (10 and 50 mug). Peripheral expansion of the intrathymically deleted Vbeta7 TCR family was not observed in lupus-prone mice 2 wk after 500 mug in vivo SEB. In vitro restimulation with SEB of mice previously injected with 500 mug SEB demonstrated anergy in T cells from all strains, including the IE- and MRL-lpr/lpr. This result contrasts with previous reports of tolerance defects in lupus-prone strains using B cell read-out assays as measures of tolerance. The present study demonstrates that there is no global defect in peripheral T cell deletion or anergy in lupus-prone mice to the superantigen SEB. Although additional Ag would need to be studied, these experiments raise the possibility that some reported tolerance defects in lupus-prone strains may reflect excessive B cell responses to relatively normal T cell signals. C1 MITRE CORP,MCLEAN,VA 22102. RP SCOTT, DE (reprint author), NIAMSD,ARTHRIT & RHEUMATISM BRANCH,CELLULAR IMMUNOL SECT,BLDG 10,ROOM 9N-218,BETHESDA,MD 20892, USA. NR 45 TC 139 Z9 141 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1993 VL 150 IS 2 BP 664 EP 672 PG 9 WC Immunology SC Immunology GA KG469 UT WOS:A1993KG46900038 PM 8419493 ER PT J AU SOBEL, ES YOKOYAMA, WM SHEVACH, EM EISENBERG, RA COHEN, PL AF SOBEL, ES YOKOYAMA, WM SHEVACH, EM EISENBERG, RA COHEN, PL TI ABERRANT EXPRESSION OF THE VERY EARLY ACTIVATION ANTIGEN ON MRL/MP-LPR/LPR LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL-RECEPTOR; LPR LPR MICE; LYMPH-NODE CELLS; MONOCLONAL-ANTIBODY; RHEUMATOID-ARTHRITIS; TYROSINE PHOSPHORYLATION; DIFFERENTIATION ANTIGENS; INTERLEUKIN-2 RESPONSES; GENE; L3T4 AB MRL/Mp-lpr/lpr (MRL/lpr) mice develop marked lymphadenopathy, characterized predominantly by Thy1+CD3+CD4-CD8- cells (''double negative T cells''; DNT). It is paradoxical that DNT proliferate poorly in vitro when stimulated through CD3 or by mitogens. The hamster mAb H1.2F3, raised against dendritic epidermal DNT, recognizes a very early activation (VEA) Ag, which is generally absent on resting cells but expressed soon after T cell activation with Con A or phorbol ester. Cross-linking of this disulfide-linked dimer in the presence of APC and phorbol ester induces proliferation of normal T cells. Therefore, we tested to see whether MRL/lpr DNT expressed this Ag and whether it might play a role in DNT expansion. Unmanipulated cells from enlarged MRL/lpr lymph nodes expressed VEA in an age-dependent manner, peaking at 3 to 4 mo of age. Only limited expression in a small subset of lymphocytes from the congenic MRL/Mp-+/+ strain was seen. VEA expression on freshly harvested MRL/lpr lymphocytes was seen mainly on DNT, yet double staining of the DNT for VEA Ag and three other markers known to be present on lpr DNT showed that the DNT were a heterogeneous population. In addition, some CD4+ T cells expressed VEA Ag. Despite their constitutive VEA Ag expression, MRL/lpr DNT showed no proliferative response to cross-linking with the Hl.2F3 antibody. Furthermore, unlike normal T cells, they failed to respond to the antibody even when phorbol ester was added. The addition of supplementary cytokines did not correct this defect. These studies indicate that MRL/lpr DNT constitutively and aberrantly express VEA but do not respond when it is cross-linked. These abnormalities may result from the failure to express Fas, the recently reported apoptosis-inducing receptor defective in lpr mice. C1 UNIV N CAROLINA,DEPT MED,CHAPEL HILL,NC 27599. MT SINAI MED CTR,BROOKDALE CTR MOLEC BIOL,NEW YORK,NY 10029. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. FU NIAMS NIH HHS [AR34156, AR40620, AR26574] NR 62 TC 14 Z9 14 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1993 VL 150 IS 2 BP 673 EP 682 PG 10 WC Immunology SC Immunology GA KG469 UT WOS:A1993KG46900039 PM 8380429 ER PT J AU SUGIHARA, S FUJIWARA, H SHEARER, GM AF SUGIHARA, S FUJIWARA, H SHEARER, GM TI AUTOIMMUNE-THYROIDITIS INDUCED IN MICE DEPLETED OF PARTICULAR T-CELL SUBSETS - CHARACTERIZATION OF THYROIDITIS-INDUCING T-CELL LINES AND CLONES DERIVED FROM THYROID LESIONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NONOBESE DIABETIC MICE; MONOCLONAL-ANTIBODY; GRAVES-DISEASE; ALLERGIC ENCEPHALOMYELITIS; GENE USAGE; RECEPTOR; ANTIGEN; TOLERANCE; THYMOCYTES; REACTIVITY AB We have previously shown that autoimmune thyroiditis spontaneously develops in T cell-depleted (C57BL/6xC3H/He)F1 mice after adoptive transfer of syngeneic lymphoid cells that have been depleted of CD5bright T lymphocytes. This mouse model was considered to be an instructive model for Hashimoto's thyroiditis in humans, and suggested that CD5dull CD4+ autoreactive T cells are not deleted in normal lymphoid cell populations and induce thyroiditis after elimination of regulatory T cell subsets. in our study, we have established thyroid-derived T cell lines and clones by culturing thyroid-infiltrating lymphocytes with thyroid epithelial cells and syngeneic feeder cells in the presence of exogenous IL-2. Both CD4+ T cells and CD8+ T cells were identified and their CD5 expression was dull or negative. In our report, we focused on CD4+ T cells. Four CD4+ T cell lines and 19 clones were generated and characterized. CD4+ T cell clones derived from F1 hybrid (H-2b/k) mice responded to thyroid Ag in the context of not only class II MHC molecules from both parental strains (I-A(k) or I-A(b)), but also F1 unique MHC molecules. Thyroglobulin (Tg) was demonstrated to be a major autoantigen of the thyroid for T cell responses, and at least two epitopes of Tg were suggested to be recognized by T cell clones. An additional undefined thyroid component other than Tg was recognized by some T cell clones. Thyroid-derived T cells were all TCR-alphabeta+. Five types of Vbeta usage (Vbeta 2, 4, 8.3, 14, and an undefined Vbeta) were found in CD4+ T cells. Finally, the thyroid lesions could be transferred to syngeneic mice by five distinct groups of CD4+ T cell clones, which were distinguished on the basis of their Ag specificity, MHC restriction, and TCRVbeta usage. The considerable heterogeneity of TCRVbeta usage of thyroiditis-inducing T cell clones in this study may be attributed to the multiple patterns of their recognition of the thyroid autoantigens. These findings provide important implications for further understanding of organ-specific autoimmune processes induced by depletion of regulatory T cell subsets. C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B-17,BETHESDA,MD 20892. OSAKA UNIV,SCH MED,BIOMED RES CTR,OSAKA 565,JAPAN. NR 52 TC 34 Z9 34 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1993 VL 150 IS 2 BP 683 EP 694 PG 12 WC Immunology SC Immunology GA KG469 UT WOS:A1993KG46900040 PM 7678281 ER PT J AU CHOY, HE ADHYA, S AF CHOY, HE ADHYA, S TI RNA-POLYMERASE IDLING AND CLEARANCE IN GAL PROMOTERS - USE OF SUPERCOILED MINICIRCLE DNA-TEMPLATE MADE INVIVO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE TRANSCRIPTION; CYCLIC AMP; CYCLIC AMP RECEPTOR PROTEIN ID SITE-SPECIFIC RECOMBINATION; STEADY-STATE ASSAY; ESCHERICHIA-COLI; BACTERIOPHAGE-LAMBDA; INITIATION REACTION; RECEPTOR PROTEIN; GALACTOSE OPERON; CYCLIC-AMP; ATT SITE; TRANSCRIPTION AB We have developed an in vivo system to engender supercoiled ''minicircle'' DNA containing a single promoter by using the integrative recombination system of bacteriophage lambda. The resulting minicircle templates allow quantitative analysis of the stages of transcription initiation from a promoter, including synthesis of both full-length and aborted transcripts in the same reactions under physiological conditions. We have used such minicircle DNA templates to study in vitro transcription of the Escherichia coli gal promoter. The full-length transcripts from gal P1 and P2 promoters responded to cAMP-cAMP receptor protein in a manner identical to that observed in vivo. There is a 3.5 -fold stimulation of P1 and almost total inhibition of P2 in the presence of cAMP. Thus, the unitary promoter system described here duplicates the in vivo physiology. In spite of the synthesis in equimolar amounts of full-length transcripts from P1 and P2 in the absence of cAMP in vitro, as in vivo, RNA polymerase encountered different rate-limiting steps of transcription initiation at the two promoters. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 34 TC 57 Z9 57 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 15 PY 1993 VL 90 IS 2 BP 472 EP 476 DI 10.1073/pnas.90.2.472 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600024 PM 8380640 ER PT J AU CHU, E VOELLER, D KOELLER, DM DRAKE, JC TAKIMOTO, CH MALEY, GF MALEY, F ALLEGRA, CJ AF CHU, E VOELLER, D KOELLER, DM DRAKE, JC TAKIMOTO, CH MALEY, GF MALEY, F ALLEGRA, CJ TI IDENTIFICATION OF AN RNA-BINDING SITE FOR HUMAN THYMIDYLATE SYNTHASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID IRON-RESPONSIVE ELEMENT; MESSENGER-RNA; COAT PROTEIN; CELL-CYCLE; NUCLEOTIDE-SEQUENCE; ESCHERICHIA-COLI; RIBONUCLEIC-ACID; GENE; EXPRESSION; DNA AB Previous studies from this laboratory have shown that human TS mRNA translation is regulated by its protein product in a negative autoregulatory manner. In this paper, we identify an RNA binding site for TS protein located within the first 188 nt of TS RNA. A 36-nt RNA sequence contained within this 188-nt fragment, corresponding to nt 75-110 and including the translational initiation site, binds TS protein with an affinity similar to that of both the full-length and the 188-nt TS RNA sequences. Variant RNAs with either a deletion or a mutation at the translational initiation region are unable to compete for TS protein binding. UV crosslinking studies reveal that an RNA fragment of almost-equal-to 36 nt is protected from RNase T1 digestion by TS protein binding. A second TS protein-binding site is localized within the protein-coding region corresponding to nt 434-634. These findings demonstrate a specific interaction between human TS protein and its TS RNA and identify an RNA binding site that includes the translational initiation site. C1 UNIV WASHINGTON,DEPT MED,DIV MED GENET,SEATTLE,WA 98105. NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,ALBANY,NY 12201. RP CHU, E (reprint author), NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA44355] NR 33 TC 154 Z9 155 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 15 PY 1993 VL 90 IS 2 BP 517 EP 521 DI 10.1073/pnas.90.2.517 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600033 PM 8421684 ER PT J AU ANDERSON, SK GALLINGER, S RODER, J FREY, J YOUNG, HA ORTALDO, JR AF ANDERSON, SK GALLINGER, S RODER, J FREY, J YOUNG, HA ORTALDO, JR TI A CYCLOPHILIN-RELATED PROTEIN INVOLVED IN THE FUNCTION OF NATURAL-KILLER-CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE NATURAL KILLER TUMOR-RECOGNITION MOLECULE; HISTONE-RELATED; ARGININE-RICH AND SERINE-RICH DOMAINS ID A-BINDING-PROTEIN; CIS-TRANS ISOMERASE; LARGE GRANULAR LYMPHOCYTES; NK CELLS; GENE; EXPRESSION; RECOGNITION; MECHANISM; ENCODES; CLONES AB Natural killer cells are non-major histocompatibility complex-restricted large granular lymphocytes that can recognize and destroy tumor cells without prior stimulation. A 150-kDa molecule on the surface of human natural killer cells was identified as a component of a putative tumor-recognition complex. We report here the isolation of cDNAs coding for the 150-kDa tumor-recognition molecule from human and mouse cDNA libraries. The amino terminus of the predicted protein contains a large hydrophobic region followed by a domain that is highly homologous to cyclophilin/peptidylprolyl cis-trans isomerase. The remainder of the protein is extremely hydrophilic and contains three homologous positively charged clusters. There are also three regions that contain extensive arginine- and serine-rich repeats. Comparison of the human and mouse predicted amino acid sequences revealed >80% homology. C1 MT SINAI HOSP, RES INST, DIV MOLEC IMMUNOL & NEUROBIOL, TORONTO M5G 1X5, ONTARIO, CANADA. RP ANDERSON, SK (reprint author), NCI, FREDERICK CANC RES & DEV CTR, DIV CANC TREATMENT, BIOL RESPONSE MODIFIERS PROGRAM, FREDERICK, MD 21702 USA. RI Anderson, Stephen/B-1727-2012; Gallinger, Steven/E-4575-2013; Roder, John/G-6468-2013 OI Anderson, Stephen/0000-0002-7856-4266; NR 36 TC 117 Z9 120 U1 0 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 JAN 15 PY 1993 VL 90 IS 2 BP 542 EP 546 DI 10.1073/pnas.90.2.542 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600038 PM 8421688 ER PT J AU BRINKMANN, U GALLO, M BRINKMANN, E KUNWAR, S PASTAN, I AF BRINKMANN, U GALLO, M BRINKMANN, E KUNWAR, S PASTAN, I TI A RECOMBINANT IMMUNOTOXIN THAT IS ACTIVE ON PROSTATE-CANCER CELLS AND THAT IS COMPOSED OF THE FV REGION OF MONOCLONAL-ANTIBODY PR1 AND A TRUNCATED FORM OF PSEUDOMONAS EXOTOXIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SINGLE-CHAIN IMMUNOTOXIN; CHEMOTHERAPY; IMMUNOTHERAPY ID GENES; AFFINITY; B3 AB Monoclonal antibody PR1 binds to the surface of normal prostate cells and to adenocarcinomas of the prostate. The cDNAs coding for the heavy and light chain variable regions of monoclonal antibody PR1 were cloned by PCR techniques. A recombinant toxin was then constructed that has the heavy chain variable region of monoclonal antibody PR1 connected to the light chain variable region by a flexible peptide linker to create a single-chain Fv; the Fv in turn is fused to a truncated form of Pseudomonas exotoxin. The resulting recombinant immunotoxin PR1(Fv)-PE38KDEL was produced in Escherichia coli and accumulated in inclusion bodies. After denaturation and renaturation, active monomeric molecules with a molecular mass of almost-equal-to 65 kDa were purified to homogeneity. PR1(Fv)-PE38KDEL binds specifically to cells containing the PR1 antigen and is very cytotoxic toward a subset of LNCaP cells that express the PR1 antigen on their surface. C1 NCI,DIV CANC BIOL DIAGNOSIS,MOLEC BIOL LAB,BLDG 37,ROOM 4E16,BETHESDA,MD 20892. FU NCI NIH HHS [CA-12197]; NCRR NIH HHS [RR-04869] NR 21 TC 32 Z9 32 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 15 PY 1993 VL 90 IS 2 BP 547 EP 551 DI 10.1073/pnas.90.2.547 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600039 PM 8421689 ER PT J AU SHIRASAKA, T YARCHOAN, R OBRIEN, MC HUSSON, RN ANDERSON, BD KOJIMA, E SHIMADA, T BRODER, S MITSUYA, H AF SHIRASAKA, T YARCHOAN, R OBRIEN, MC HUSSON, RN ANDERSON, BD KOJIMA, E SHIMADA, T BRODER, S MITSUYA, H TI CHANGES IN DRUG SENSITIVITY OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 DURING THERAPY WITH AZIDOTHYMIDINE, DIDEOXYCYTIDINE, AND DIDEOXYINOSINE - AN INVITRO COMPARATIVE-STUDY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HIV-1 REVERSE-TRANSCRIPTASE; ZIDOVUDINE AZT; PHASE-I; 2',3'-DIDEOXYINOSINE; RESISTANCE; SEQUENCES; DDI AB Human immunodeficiency virus type 1 (HIV-1) strains were isolated from nine patients before and after prolonged therapy with either an alternating regimen of 3'-azido-3'-deoxythymidine (AZT) and 2',3'-dideoxycytidine (ddC) (AZT/ddC) or 2',3'-dideoxyinosine (ddI) alone. All strains obtained from four patients who received AZT/ddC for up to 41 mo were highly insensitive to AZT in vitro. Only one strain obtained after AZT/ddC therapy showed reduced susceptibility to ddC in addition to AZT and had previously unreported amino acid substitutions in the viral polymerase-encoding pol region, whereas three other strains had one or more of the five previously reported AZT-related mutations. In five HIV-1 strains from patients who received ddI for up to 29 mo, no appreciable decrease in sensitivity to ddI was detected. Two strains isolated after ddI therapy had no significant amino acid mutations, although three strains had a mutation reportedly associated with ddI administration. These data suggest that HIV-1 develops reduced susceptibility to AZT more readily than to ddC and ddI and/or that the reduced susceptibility to ddC and ddI is modest in degree. Moreover, the present data suggest that an alternating regimen of AZT and ddC does not block the emergence of AZT-insensitive variants. It should be noted, however, that the current results do not provide a basis for concluding that AZT/ddC or ddI is inferior, equivalent, or superior to AZT as therapy of AIDS. C1 NCI,MED BRANCH,EXPTL RETROVIROL SECT,BLDG 10,ROOM 5A11,BETHESDA,MD 20892. NHLBI,MED BRANCH,EXPTL RETROVIROL SECT,BETHESDA,MD 20892. NHLBI,MED BRANCH,RETROVIROL DIS SECT,BETHESDA,MD 20892. NHLBI,CLIN HAEMATOL BRANCH,BETHESDA,MD 20892. NR 19 TC 133 Z9 134 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 15 PY 1993 VL 90 IS 2 BP 562 EP 566 DI 10.1073/pnas.90.2.562 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600042 PM 8380641 ER PT J AU ARISPE, N ROJAS, E POLLARD, HB AF ARISPE, N ROJAS, E POLLARD, HB TI ALZHEIMER-DISEASE AMYLOID BETA-PROTEIN FORMS CALCIUM CHANNELS IN BILAYER-MEMBRANES - BLOCKADE BY TROMETHAMINE AND ALUMINUM SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CATION CHANNEL; PHOSPHOLIPID BILAYER ID AGGREGATION; PRECURSOR; DEMENTIA; BRAIN; CDNA; GENE AB Amyloid beta protein (AbetaP) is the 40- to 42-residue polypeptide implicated in the pathogenesis of Alzheimer disease. We have incorporated this peptide into phosphatidylserine liposomes and then fused the liposomes with a planar bilayer. When incorporated into bilayers the AbetaP forms channels, which generate linear current-voltage relationships in symmetrical solutions. A permeability ratio, P(K)/P(Cl), Of 11 for the open AbetaP channel was estimated from the reversal potential of the channel current in asymmetrical KCl solutions. The permeability sequence for different cations, estimated from the reversal potential of the AbetaP-channel current for each system of asymmetrical solutions, is P(Cs) > P(Li) > P(Ca) greater-than-or-equal-to P(K) > P(Na). AbetaP-channel current (either Cs+ or Ca2+ as charge carriers) is blocked reversibly by tromethamine (millimolar range) and irreversibly by Al3+ (micromolar range). The inhibition of the AbetaP-channel current by these two substances depends on transmembrane potential, suggesting that the mechanism of blockade involves direct interaction between tromethamine (or Al3+) and sites within the AbetaP channel. Hitherto, AbetaP has been presumed to be neurotoxic. On the basis of the present data we suggest that the channel activity of the polypeptide may be responsible for some or all of its neurotoxic effects. We further propose that a useful strategy for drug discovery for treatment of Alzheimer disease may include screening compounds for their ability to block or otherwise modify AbetaP channels. RP ARISPE, N (reprint author), NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. NR 28 TC 618 Z9 638 U1 3 U2 46 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 15 PY 1993 VL 90 IS 2 BP 567 EP 571 DI 10.1073/pnas.90.2.567 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600043 PM 8380642 ER PT J AU BIRO, S FU, YM YU, ZX EPSTEIN, SE AF BIRO, S FU, YM YU, ZX EPSTEIN, SE TI INHIBITORY EFFECTS OF ANTISENSE OLIGODEOXYNUCLEOTIDES TARGETING C-MYC MESSENGER-RNA ON SMOOTH-MUSCLE CELL-PROLIFERATION AND MIGRATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANGIOPLASTY; RESTENOSIS ID FIBROBLAST GROWTH-FACTOR; HUMAN LYMPHOCYTES-T; DNA-BINDING; CORONARY ANGIOPLASTY; PROTEIN EXPRESSION; EXTRACELLULAR ATP; GENE; ONCOGENE; CYCLE; RESTENOSIS AB Smooth muscle cell (SMC) proliferation and migration play pivotal roles in restenosis following angioplasty. c-myc is an immediate early response gene induced by various mitogens, and several lines of evidence derived from experiments using transformed or hematopoietic cell lines, or transgenic mice, suggest its protein product plays a role in numerous signaling transduction pathways, including those modulating cell division. We therefore reasoned that a strategy employing oligodeoxynucleotides (ODNs) complementary to c-myc mRNA (antisense ODNs) might be potent inhibitors of SMC proliferation and, perhaps, of SMC migration. To evaluate this concept, we tested several antisense ODNs targeted to c-myc mRNA (15- or 18-mer ODNs complementary to different c-myc mRNA sequences) by introducing them individually into the medium of cultured rat aortic SMCs. Phosphoroamidate-modified ODNs were employed to retard degradation. Antisense ODNs inhibited, in a concentration-dependent manner, SMC proliferation and SMC migration. Maximal inhibitory effect was 50% for proliferation and >90% for migration. These effects were associated with decreased SMC expression of c-myc-encoded protein by Western immunoblotting and immunocytochemical staining. ODNs with the same nucleotides but a scrambled sequence caused no effect. These results indicate that the c-myc gene product is involved in the signal transduction pathways mediating SMC proliferation and migration in the in vitro model we employed. The results also suggest a potential role of antisense strategies designed to inhibit c-myc expression for the prevention of coronary restenosis. C1 NHLBI,CARDIOL BRANCH,10-7B15,BETHESDA,MD 20892. NR 44 TC 168 Z9 176 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 15 PY 1993 VL 90 IS 2 BP 654 EP 658 DI 10.1073/pnas.90.2.654 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600061 PM 8421701 ER PT J AU KULKARNI, AB HUH, CG BECKER, D GEISER, A LYGHT, M FLANDERS, KC ROBERTS, AB SPORN, MB WARD, JM KARLSSON, S AF KULKARNI, AB HUH, CG BECKER, D GEISER, A LYGHT, M FLANDERS, KC ROBERTS, AB SPORN, MB WARD, JM KARLSSON, S TI TRANSFORMING GROWTH FACTOR-BETA-1 NULL MUTATION IN MICE CAUSES EXCESSIVE INFLAMMATORY RESPONSE AND EARLY DEATH SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HOMOLOGOUS RECOMBINATION; EMBRYONIC STEM CELLS; INFLAMMATION; AUTOIMMUNITY ID FACTOR-BETA; STEM-CELLS; ADHESIVENESS; LYMPHOCYTES; ACTIVATION; VASCULITIS; SEQUENCES; PROMOTER; ONCOGENE AB To delineate specific developmental roles of transforming growth factor beta1 (TGF-beta1) we have disrupted its cognate gene in mouse embryonic stem cells by homologous recombination to generate TGF-beta1 null mice. These mice do not produce detectable amounts of either TGF-beta1 RNA or protein. After normal growth for the first 2 weeks they develop a rapid wasting syndrome and die by 3-4 weeks of age. Pathological examination revealed an excessive inflammatory response with massive infiltration of lymphocytes and macrophages in many organs, but primarily in heart and lungs. Many lesions resembled those found in autoimmune disorders, graft-vs.-host disease, or certain viral diseases. This phenotype suggests a prominent role for TGF-beta1 in homeostatic regulation of immune cell proliferation and extravasation into tissues. C1 NINCDS,DEV & METAB NEUROL BRANCH,MOLEC MED GENET SECT,BLDG 10,ROOM 3D04,BETHESDA,MD 20892. NCI,DIV CANC ETIOL,COMPARAT CARCINOGENESIS LAB,CHEMOPREVENT LAB,BETHESDA,MD 20892. NCI,OFF LAB ANIM SCI,VET & TUMOR PATHOL SECT,FREDERICK,MD 21702. NR 37 TC 1375 Z9 1426 U1 3 U2 21 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 15 PY 1993 VL 90 IS 2 BP 770 EP 774 DI 10.1073/pnas.90.2.770 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KH516 UT WOS:A1993KH51600086 PM 8421714 ER PT J AU BENICHOU, J AF BENICHOU, J TI METHODS OF ADJUSTMENT FOR ESTIMATING THE ATTRIBUTABLE RISK IN CASE CONTROL STUDIES - A REVIEW - REPLY SO STATISTICS IN MEDICINE LA English DT Letter ID ASSIGNED SHARES; PROBABILITY; CAUSATION RP BENICHOU, J (reprint author), NCI,6130 EXECUT BLVD,EPN 403,ROCKVILLE,MD 20892, USA. NR 10 TC 2 Z9 2 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD JAN 15 PY 1993 VL 12 IS 1 BP 94 EP 96 PG 3 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA KK378 UT WOS:A1993KK37800008 ER PT J AU LAZAREVSKI, G VINKOVIC, M KOBREHEL, G DOKIC, S METELKO, B VIKICTOPIC, D AF LAZAREVSKI, G VINKOVIC, M KOBREHEL, G DOKIC, S METELKO, B VIKICTOPIC, D TI CONFORMATIONAL-ANALYSIS OF AZITHROMYCIN BY NUCLEAR-MAGNETIC-RESONANCE SPECTROSCOPY AND MOLECULAR MODELING SO TETRAHEDRON LA English DT Article DE AZITHROMYCIN; CONFORMATIONAL ANALYSIS; NMR SPECTROSCOPY; MOLECULAR MODELING ID ERYTHROMYCIN-A AB The conformation of azithromycin 1 in the solution was determined by NMR spectroscopy and molecular mechanics calculations and compared with its crystal structure and with some erythromycin derivatives. In solution 1 exists predominantly in a ''folded-in '' conformation in the C-3 to C-5 region. whereas its crystal state conformation is ''folded-out''. C1 RUDJER BOSKOVIC INST, 41000 ZAGREB, CROATIA. NIDDK, ANALYT CHEM LAB, BETHESDA, MD 20892 USA. RP LAZAREVSKI, G (reprint author), PLIVA, PHARMACEUT CHEM FOOD & COSMET IND RES INST, BARUNA FILIPOVICA 89, 41000 ZAGREB, CROATIA. NR 18 TC 28 Z9 28 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0040-4020 J9 TETRAHEDRON JI Tetrahedron PD JAN 15 PY 1993 VL 49 IS 3 BP 721 EP 730 DI 10.1016/S0040-4020(01)86274-8 PG 10 WC Chemistry, Organic SC Chemistry GA KE370 UT WOS:A1993KE37000019 ER PT J AU MCKEE, TC CARDELLINA, JH TISCHLER, M SNADER, KM BOYD, MR AF MCKEE, TC CARDELLINA, JH TISCHLER, M SNADER, KM BOYD, MR TI HIV-INHIBITORY NATURAL-PRODUCTS .9. IBISTEROL SULFATE, A NOVEL HIV-INHIBITORY SULFATED STEROL FROM THE DEEP-WATER SPONGE TOPSENTIA SP SO TETRAHEDRON LETTERS LA English DT Article ID CUCUMBER PSOLUS-FABRICII; SIDE-CHAIN ALKYLATION; MARINE LIPIDS; DELTA-9(11)-STEROLS; BIOSYNTHESIS AB The novel sulfated sterol ibisterol sulfate (1) was isolated from the deep water Caribbean sponge Topsentia sp. The combination of both a DELTA9(11) olefin and a methyl group at C-14 has not previously been reported in sponge sterols. C1 NCI,DRUG DISCOVERY RES & DEV LAB,BLDG 1052,ROOM 121,FREDERICK,MD 21702. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,NAT PROD BRANCH,FREDERICK,MD 21702. NR 12 TC 38 Z9 40 U1 0 U2 0 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 JAN 15 PY 1993 VL 34 IS 3 BP 389 EP 392 DI 10.1016/0040-4039(93)85083-9 PG 4 WC Chemistry, Organic SC Chemistry GA KG548 UT WOS:A1993KG54800004 ER PT J AU DANIELPOUR, D AF DANIELPOUR, D TI IMPROVED SANDWICH ENZYME-LINKED IMMUNOSORBENT ASSAYS FOR TRANSFORMING GROWTH FACTOR-BETA-1 SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE ELISA; TRANSFORMING GROWTH FACTOR-BETA-1; ANTI-TRANSFORMING GROWTH FACTOR-BETA-1 ANTIBODY; RETINOIC ACID; FIBROSARCOMA CELL, HUMAN; SUBMAXILLARY GLAND; (SPLEEN) ID FACTOR-BETA; DIFFERENTIAL REGULATION; RETINOIC ACID; EXPRESSION; CELLS; TGF-BETA-1; PURIFICATION; TISSUES; FORMS; ADULT AB Transforming growth factor betas (TGF-betas), a highly homologous family of 25 kDa dimers, function as both paracrine and autocrine growth modulators which relay a broad spectrum of critical biological functions. Although sensitive bioassays for TGF-betas have been described, their interference by other growth modulators have limited their application. We have previously described a highly sensitive (20-50 pg/ml) and specific sandwich enzyme-linked immunosorbent assay (SELISA) for TGF-beta1, based on use of rabbit anti-TGF-beta1, as the capture antibody. Widespread use of this assay was limited by the availability of this rather low-titer antibody. This report describes improved TGF-beta1 SELISAs with comparable sensitivities to the above assay based on available sources of commercial monoclonal and polyclonal antibodies. These newly developed SELISAs are the most sensitive, specific, precise and convenient methods for the quantitation of TGF-beta1 in complex biological fluids. RP DANIELPOUR, D (reprint author), NCI,CHEMOPREVENT LAB,BLDG 41,ROOM C629,BETHESDA,MD 20892, USA. NR 20 TC 114 Z9 115 U1 1 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD JAN 14 PY 1993 VL 158 IS 1 BP 17 EP 25 DI 10.1016/0022-1759(93)90254-5 PG 9 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA KJ742 UT WOS:A1993KJ74200003 PM 8429213 ER PT J AU KONDO, T KIRSCHENBAUM, LJ KIM, H RIESZ, P AF KONDO, T KIRSCHENBAUM, LJ KIM, H RIESZ, P TI SONOLYSIS OF DIMETHYL-SULFOXIDE WATER MIXTURES - A SPIN-TRAPPING STUDY SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID ISOTOPE-EXCHANGE-REACTIONS; AQUEOUS-SOLUTIONS; ORGANIC SONOCHEMISTRY; THERMAL-DECOMPOSITION; HYDROXYL RADICALS; HYDROGEN-ATOMS; RATE CONSTANTS; ULTRASOUND; CHEMISTRY; PYROLYSIS AB The 50-kHz sonolysis of argon-saturated dimethyl sulfoxide (DMSO)-water mixtures was investigated by ESR and spin trapping with 3,5-dibromo-4-nitrosobenzenesulfonate (DBNBS). Two distinct product regions are observed. At low DMSO concentrations, methyl radicals are formed due to the reaction of hydroxyl radicals, generated by the thermal decomposition of water vapor in collapsing cavitation bubbles, which escape into the bulk of the solution and react with DMSO. The maximum CH3-DBNBS yield is observed near 0.1% DMSO (v/v). An apparent maximum in the yield of the sulfur trioxide anion radical spin adduct of DBNBS (SO3-DBNBS) was found at 75% DMSO (v/v). Sulfur dioxide has previously been identified as a major product of the pyrolysis of DMSO vapor. In the presence of water, the SO2 produced in the collapsing cavitation bubbles is oxidized by DBNBS in the bulk of the solution to SO3.-, which subsequently forms stable SO3-DBNBS adducts. Whereas for previous sonolysis studies with aqueous mixtures of solvents more volatile than water, spin-adduct yields decrease at high mole fractions, because of decreasing effective gamma = C(p)/C(v) in the imploding argon cavitation bubbles, the thermolysis product of DMSO formed by sonolysis increases with increasing DMSO concentration. C1 FUKUI MED SCH,DEPT EXPTL RADIOL & HLTH PHYS,FUKUI 91011,JAPAN. NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NR 57 TC 43 Z9 43 U1 1 U2 6 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 JAN 14 PY 1993 VL 97 IS 2 BP 522 EP 527 DI 10.1021/j100104a042 PG 6 WC Chemistry, Physical SC Chemistry GA KH404 UT WOS:A1993KH40400042 ER PT J AU DERR, LK STRATHERN, JN AF DERR, LK STRATHERN, JN TI A ROLE FOR REVERSE TRANSCRIPTS IN GENE CONVERSION SO NATURE LA English DT Article ID MITOTIC RECOMBINATION; YEAST; SELECTION AB RECOMBINATION between a diffusible reverse transcript and its homologous chromosomal allele has been proposed as a mechanism for the precise removal of introns from DNA and gene conversion of dispersed repeated sequences1,2. We have reported that RNA-mediated recombination occurs in the yeast Saccharomyces cerevisiae3. This recombination requires expression of the retro-transposon Ty, and results in intron loss from a plasmid-borne marker gene and the formation of pseudogenes. Because the pseudogenes are embedded in Ty sequences, chromosomal insertion could have been mediated by Ty integrase or by homologous recombination with endogenous Ty sequences. The structure of the chromosomal recombinants and the fact that plasmid and chromosomal recombination can have different requirements demanded a direct demonstration of RNA-mediated gene conversion of a chromosomal allele. Here we report the first demonstration, to our knowledge, of recombination between a reverse transcript and its chromosomal homologue and describe an assay that specifically detects this novel recombination pathway. RP DERR, LK (reprint author), NCI,FREDERICK CANC RES & DEV CTR,EUKARYOT GENE EXPRESS LAB,FREDERICK,MD 21701, USA. NR 13 TC 110 Z9 111 U1 2 U2 5 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JAN 14 PY 1993 VL 361 IS 6408 BP 170 EP 173 DI 10.1038/361170a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KG466 UT WOS:A1993KG46600065 PM 8380627 ER PT J AU RODGERS, GP DOVER, GJ UYESAKA, N NOGUCHI, CT SCHECHTER, AN NIENHUIS, AW AF RODGERS, GP DOVER, GJ UYESAKA, N NOGUCHI, CT SCHECHTER, AN NIENHUIS, AW TI AUGMENTATION OF ERYTHROPOIETIN OF THE FETAL-HEMOGLOBIN RESPONSE TO HYDROXYUREA IN SICKLE-CELL DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID RECOMBINANT-HUMAN-ERYTHROPOIETIN; NICKEL MESH; ANEMIA; POLYMERIZATION; STIMULATION; BABOONS AB Background. Hydroxyurea increases the production of fetal hemoglobin in patients with sickle cell anemia, inhibiting the polymerization of hemoglobin S and potentially improving vaso-occlusive manifestations and hemolysis. Recombinant erythropoietin increases the number of reticulocytes containing fetal hemoglobin in laboratory animals and in humans. We studied whether hydroxyurea and erythropoietin might have a potentiating effect on the production of fetal hemoglobin in patients with sickle cell disease. Methods. We treated four patients who were receiving hydroxyurea for sickle cell disease (three who were homozygous for sickle cell anemia and one with sickle beta0-thalassemia) with escalating doses of intravenous erythropoietin for seven weeks, along with oral iron sulfate. Doses of hydroxyurea on four consecutive days were alternated with doses of erythropoietin on three consecutive days. Results. There was a 28 percent increase in the number of reticulocytes containing fetal hemoglobin and a 48 percent increase in the percentage of fetal hemoglobin, as compared with the maximal values obtained with hydroxyurea alone. The percentage of erythrocytes containing fetal hemoglobin (F cells) increased from 64 to 78 percent. As compared with hydroxyurea alone, treatment with hydroxyurea and erythropoietin decreased the mean (+/-SD) serum indirect bilirubin level from 0.8+/-0.2 to 0.5+/-0.1 mg per deciliter (13.3+/-2.9 to 8.9+/-2.2 mumol per liter) (P = 0.02), suggesting a further decrease in hemolysis. Red-cell filterability improved. Conclusions. Intravenous recombinant erythropoietin with iron supplementation alternating with hydroxyurea elevates fetal-hemoglobin and F-cell levels more than hydroxyurea alone. Such increases decrease intracellular polymerization of hemoglobin S and improve the overall rheologic characteristics of erythrocytes. A reduced dosage of hydroxyurea alternating with erythropoietin may prove less myelotoxic than hydroxyurea given daily or in pulsed-dose regimens. It may also increase levels of fetal hemoglobin in patients with sickle cell disease who have not been helped by hydroxyurea alone. C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. NIPPON MED COLL,DEPT PHYSIOL,TOKYO 113,JAPAN. RP RODGERS, GP (reprint author), NIDDKD,CHEM BIOL LAB,BLDG 10,RM 9N-307,BETHESDA,MD 20892, USA. NR 36 TC 200 Z9 201 U1 1 U2 2 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 JAN 14 PY 1993 VL 328 IS 2 BP 73 EP 80 DI 10.1056/NEJM199301143280201 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA KG467 UT WOS:A1993KG46700001 PM 7677965 ER PT J AU CHESON, BD AF CHESON, BD TI THE MATURATION OF DIFFERENTIATION THERAPY (NEW-ENGLAND J MED, VOL 327, PG 422, 1992) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Correction, Addition RP CHESON, BD (reprint author), NCI,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 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 JAN 14 PY 1993 VL 328 IS 2 BP 141 EP 141 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA KG467 UT WOS:A1993KG46700026 ER PT J AU CAPRANICO, G TINELLI, S ZUNINO, F KOHN, KW POMMIER, Y AF CAPRANICO, G TINELLI, S ZUNINO, F KOHN, KW POMMIER, Y TI EFFECTS OF BASE MUTATIONS ON TOPOISOMERASE-II DNA CLEAVAGE STIMULATED BY MAMSA IN SHORT DNA OLIGOMERS SO BIOCHEMISTRY LA English DT Article ID ANTITUMOR DRUGS; SEQUENCE; SITES; IDENTIFICATION; CAMPTOTHECIN; CHROMATIN AB DNA cleavage by topoisomerase II in the absence or presence of mAMSA, and VM-26 was investigated in a series of oligonucleotides of 36 and 42 base pairs, which were derived from the DNA sequence of the major topoisomerase II cleavage site in the matrix-associated region of SV40 DNA. Topoisomerase II introduced strand cuts at several sites in the oligonucleotides, and the sequence selectivities of DNA cleavage with and without drugs were the same as in larger SV40 DNA fragments. A time course analysis showed that mAMSA specifically stimulated DNA cleavage at the 4263/4266 site, while DNA cleavage was specifically induced at the 4265/4268 site by the enzyme without drug or with VM-26. In agreement with recent findings on local nucleotide requirements in order for mAMSA to stimulate DNA cleavage, the 4263/4266 site had adenines at the two positions +1. This nucleotide requirement was challenged by mutating the bases 4263 and 4266 of the oligonucleotide representing the natural SV40 DNA sequence. New cleavage sites were not observed in the mutated oligonucleotides, and base mutations had an effect on DNA cleavage induced with and without the two drugs. This general effect was likely due to the sensitivity of topoisomerase II itself to the local DNA sequence. Nevertheless, effects of base mutations were more pronounced for mAMSA than for VM-26. Point mutations of either base 4263 or 4266, representing the two positions +1, reduced markedly the stimulative effect of DNA cleavage at the 4263/4266 site by mAMSA, and mutations of both bases completely abolised it. The effects of these base mutations on DNA cleavage at other sites varied depending on the site and the mutated base. In particular, a purine at position -2 of the 4265/4268 site increased cleavage at that site by the enzyme without drugs. A guanine at position +2 tended to favor topoisomerase II DNA cleavage with the studied drugs. A pyrimidine at position -1 of the 4259/4262 site allowed the stimulative effect of DNA cleavage by mAMSA at the site, while a purine did not. The results indicate that the dinucleotide cleaved by topoisomerase II is crucial for stimulation of DNA cleavage by mAMSA and that the in vitro DNA binding and cleavage by topoisomerase II is determined by nucleotides immediately surrounding the cleavage site. C1 NCI,DCT,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RP CAPRANICO, G (reprint author), IST NAZL STUDIO & CURA TUMORI,DIV ONCOL SPERIMENTALE B,VIA G VENEZIAN 1,I-20133 MILAN,ITALY. RI Capranico, Giovanni/K-1678-2014 OI Capranico, Giovanni/0000-0002-8708-6454 NR 29 TC 19 Z9 19 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JAN 12 PY 1993 VL 32 IS 1 BP 145 EP 152 DI 10.1021/bi00052a020 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG380 UT WOS:A1993KG38000020 PM 8380330 ER PT J AU WEINBERGER, M HOLLINGSWORTH, H FEUERSTEIN, IM YOUNG, NS PIZZO, PA AF WEINBERGER, M HOLLINGSWORTH, H FEUERSTEIN, IM YOUNG, NS PIZZO, PA TI SUCCESSFUL SURGICAL-MANAGEMENT OF NEUTROPENIC ENTEROCOLITIS IN 2 PATIENTS WITH SEVERE APLASTIC-ANEMIA - CASE-REPORTS AND REVIEW OF THE LITERATURE SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID CLOSTRIDIUM-SEPTICUM INFECTION; SUCCESSFUL MEDICAL-MANAGEMENT; LOWER QUADRANT PAIN; ACUTE-LEUKEMIA; NECROTIZING ENTEROCOLITIS; INDUCED AGRANULOCYTOSIS; CHILDHOOD LEUKEMIA; TYPHLITIS; COLITIS; CT AB We describe two patients with severe aplastic anemia in whom neutropenic enterocolitis developed while they were undergoing treatment at the National Institutes of Health. Both patients had progressive symptoms while receiving optimal medical management and both underwent and survived surgical intervention despite continued prolonged neutropenia in the perioperative period. This experience contrasts with six cases reported in the literature and suggests that surgery can be employed even in patients with profound neutropenia. Thus, in patients who remain persistently septic or who develop clinical deterioration despite medical management or who have other indications for surgical intervention, neutropenia should not be a contraindication to the appropriate or necessary procedure. C1 NCI,INFECT DIS SECT,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT RADIOL,WASHINGTON,DC. GEORGETOWN UNIV,WASHINGTON,DC 20057. NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 60 TC 22 Z9 23 U1 0 U2 3 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 JAN 11 PY 1993 VL 153 IS 1 BP 107 EP 113 DI 10.1001/archinte.153.1.107 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA KH226 UT WOS:A1993KH22600012 PM 8422192 ER PT J AU GRUBER, KA AF GRUBER, KA TI AN ENDOGENOUS DIGITALIS-LIKE SUBSTANCE - A CITATION-CLASSIC COMMENTARY ON ENDOGENOUS DIGITALIS-LIKE SUBSTANCE IN PLASMA OF VOLUME-EXPANDED DOGS BY GRUBER,K.A., WHITAKER,J.M. AND BUCKALEW,V.M. SO CURRENT CONTENTS/LIFE SCIENCES LA English DT Article ID NATRIURETIC FACTOR RP GRUBER, KA (reprint author), NIDOCD,DIV COMMUN SCI & DISORDERS,ROCKVILLE,MD 20853, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU INST SCI INFORM INC PI PHILADELPHIA PA 3501 MARKET ST, PHILADELPHIA, PA 19104 SN 0011-3409 J9 CC/LIFE SCI PD JAN 11 PY 1993 IS 2 BP 9 EP 9 PG 1 WC Multidisciplinary Sciences; Social Sciences, Interdisciplinary SC Science & Technology - Other Topics; Social Sciences - Other Topics GA KC971 UT WOS:A1993KC97100002 ER PT J AU GOLDSBOROUGH, AS HEALY, LE COPELAND, NG GILBERT, DJ JENKINS, NA WILLISON, KR ASHWORTH, A AF GOLDSBOROUGH, AS HEALY, LE COPELAND, NG GILBERT, DJ JENKINS, NA WILLISON, KR ASHWORTH, A TI CLONING, CHROMOSOMAL LOCALIZATION AND EXPRESSION PATTERN OF THE POU DOMAIN GENE OCT-11 SO NUCLEIC ACIDS RESEARCH LA English DT Article ID BINDING PROTEIN OCT-1; OCTAMER DNA MOTIF; HYBRID CELL-LINES; TRANSCRIPTION FACTOR; MOUSE MYELOMA; CAENORHABDITIS-ELEGANS; EMBRYONIC-CELLS; LINKAGE MAP; STEM-CELLS; C-MOS AB POU domain genes encode a family of highly conserved transacting factors that influence the transcriptional activity of several cell type-specific and ubiquitous genes. We have cloned and sequenced cDNAs encoding a novel mouse POU domain protein, Oct-11, that is closely related within the POU domain to the POU class II proteins, Oct-1 and Oct-2. Recombinant Oct-11 protein binds specifically to an octamer sequence in vitro. The Oct-11 gene is expressed during mouse embryogenesis and in the adult thymus and testis. In addition, it is abundant in the myeloma cell line P3/NS-1/1-Ag4.1. We describe the structure of Oct-11 and its chromosomal localization, and discuss the evidence that the POU class II gene family has evolved by duplication and divergence of a common ancestral gene. C1 INST CANC RES,CHESTER BEATTY LABS,FULHAM RD,LONDON SW3 6JB,ENGLAND. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 71 TC 43 Z9 45 U1 0 U2 2 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 JAN 11 PY 1993 VL 21 IS 1 BP 127 EP 134 DI 10.1093/nar/21.1.127 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KJ069 UT WOS:A1993KJ06900018 PM 8441607 ER PT J AU VANDEWOUDE, GF ZHOU, RP DAAR, I YEW, N MATTEN, W FUKASAWA, K SATHYANARAYANA, BK RUBIN, JR AF VANDEWOUDE, GF ZHOU, RP DAAR, I YEW, N MATTEN, W FUKASAWA, K SATHYANARAYANA, BK RUBIN, JR TI MOS PROTOONCOGENE AND CELL-CYCLE REGULATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 57 EP 57 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400182 ER PT J AU RICE, NR LOGEAT, F MACKICHAN, ML LEBAIL, O ISRAEL, A AF RICE, NR LOGEAT, F MACKICHAN, ML LEBAIL, O ISRAEL, A TI THE REL/NF-KAPPA-B FAMILY OF TRANSCRIPTION FACTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. INST PASTEUR,F-75724 PARIS 15,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 58 EP 58 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400186 ER PT J AU KIM, SJ WISNIEWSKI, J WISNIEWSKA, M LEWIS, MS WU, C AF KIM, SJ WISNIEWSKI, J WISNIEWSKA, M LEWIS, MS WU, C TI BIOPHYSICAL STUDIES ON THE STRUCTURE OF THE HEAT-SHOCK TRANSCRIPTION FACTOR IN DROSOPHILA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCRR,BEIP,BETHESDA,MD 20892. NCI,LB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 64 EP 64 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400206 ER PT J AU BOGAZZI, F DESVERGNE, B NIKODEM, V AF BOGAZZI, F DESVERGNE, B NIKODEM, V TI DIFFERENTIAL INTERACTION OF ALPHA-THYROID AND BETA-THYROID HORMONE RECEPTOR WITH DIRECT REPEAT AND INVERTED PALINDROME TRE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 67 EP 67 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400217 ER PT J AU GOLDSMITH, ME MADDEN, MJ MORROW, CS COWAN, KH AF GOLDSMITH, ME MADDEN, MJ MORROW, CS COWAN, KH TI A Y-BOX CONSENSUS SEQUENCE IS REQUIRED FOR BASAL EXPRESSION OF HUMAN MULTIDRUG RESISTANCE (MDR1) GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MED BRANCH,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 73 EP 73 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400241 ER PT J AU HAGER, GL ARCHER, T SMITH, C AF HAGER, GL ARCHER, T SMITH, C TI DIFFERENTIAL ACTIVATION OF TRANSCRIPTION BY GLUCOCORTICOID AND PROGESTERONE RECEPTORS ON CHROMATIN TEMPLATES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 75 EP 75 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400248 ER PT J AU LAN, MS GOTO, Y DESILVA, MG TOSCANI, A PRABHAKAR, BS NOTKINS, AL AF LAN, MS GOTO, Y DESILVA, MG TOSCANI, A PRABHAKAR, BS NOTKINS, AL TI A NOVEL HUMAN INSULINOMA-ASSOCIATED CDNA, IA-1, ENCODES A PROTEIN WITH ZINC-FINGER DNA-BINDING MOTIFS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,ORAL MED LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 82 EP 82 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400276 ER PT J AU NAKHAI, B BOLOS, A GOLDMAN, D NIELSEN, DA AF NAKHAI, B BOLOS, A GOLDMAN, D NIELSEN, DA TI SEROTONIN1A RECEPTOR GENE STRUCTURE AND TRANSCRIPTIONAL REGULATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAAA,LN,MOLEC GENET SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 85 EP 85 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400289 ER PT J AU RABINDRAN, SK HAROUN, RI WU, C AF RABINDRAN, SK HAROUN, RI WU, C TI REGULATION OF THE HUMAN HEAT-SHOCK RESPONSE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 89 EP 89 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400305 ER PT J AU SHIRAKATA, M PATERSON, BM AF SHIRAKATA, M PATERSON, BM TI A SIGLE AMINO-ACID CHANGE IN THE HELIX-1 DOMAIN OF THE HELIX-LOOP-HELIX TRANSCRIPTION FACTOR, E12, CHANGES ITS OLIGOMERIZATION SPECIFICITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 91 EP 91 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400314 ER PT J AU TOLEDANO, MB STORZ, G AF TOLEDANO, MB STORZ, G TI THE BACTERIAL TRANSCRIPTION FACTOR OXYR RECOGNIZES DNA THROUGH A DEGENERATE CODE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 94 EP 94 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400326 ER PT J AU TSUKIYAMA, T BECKER, PB WU, C AF TSUKIYAMA, T BECKER, PB WU, C TI INTERACTION OF TRANSCRIPTION FACTORS WITH CHROMATIN USING AN INVITRO NUCLEOSOME ASSEMBLY SYSTEM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. EMBL,GENE EXPRESS PROGRAM,W-6900 HEIDELBERG,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 95 EP 95 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400329 ER PT J AU WISNIEWSKI, J CLOS, J RABINDRAN, S WU, C AF WISNIEWSKI, J CLOS, J RABINDRAN, S WU, C TI ACTIVATION TEMPERATURE OF HUMAN HEAT-SHOCK FACTOR (HSF1) IS REPROGRAMMED IN DROSOPHILA CELL ENVIRONMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 97 EP 97 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400338 ER PT J AU BECKER, KG JEDLICKA, P OZATO, K AF BECKER, KG JEDLICKA, P OZATO, K TI FUNCTIONAL-CHARACTERIZATION OF THE TRANSCRIPTION FACTOR HUCRBP SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 100 EP 100 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400350 ER PT J AU RHYS, CMJA CARLSON, S REICHENBAUGH, S LUETHY, JD HOLBROOK, NJ AF RHYS, CMJA CARLSON, S REICHENBAUGH, S LUETHY, JD HOLBROOK, NJ TI EXPRESSION OF GADD153 AND OTHER MEMBERS OF THE C/EBP FAMILY IN RESPONSE TO ACUTE STRESS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,MOLEC GENET LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 100 EP 100 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400347 ER PT J AU BOVOLENTA, C DRIGGERS, PH MARKS, MS MEDIN, JA POLITIS, AD VOGEL, SN COLIGAN, JE OZATO, K AF BOVOLENTA, C DRIGGERS, PH MARKS, MS MEDIN, JA POLITIS, AD VOGEL, SN COLIGAN, JE OZATO, K TI ICSBP REQUIRES AN ACCESSORY MOLECULE FOR HIGH-AFFINITY DNA-BINDING AND MAY COMPLETE WITH ISGF3 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,LMGR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 102 EP 102 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400355 ER PT J AU BRINI, AT LEE, GM KINET, JP AF BRINI, AT LEE, GM KINET, JP TI ALU SEQUENCES ARE INVOLVED IN THE CELL-SPECIFIC TRANSCRIPTIONAL REGULATION OF THE CHAIN OF FC AND T-CELL RECEPTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 102 EP 102 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400356 ER PT J AU BURBELO, P UTANI, A YAMADA, Y AF BURBELO, P UTANI, A YAMADA, Y TI A MAMMALIAN SEQUENCE-SPECIFIC DNA-BINDING PROTEIN CONTAINS A PROTEIN DOMAIN SIMILAR TO BACTERIAL-DNA LIGASES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. RI Burbelo, Peter/B-1027-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 103 EP 103 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400361 ER PT J AU HALLECK, MM LIU, H HOLBROOK, NJ STEVENS, JL AF HALLECK, MM LIU, H HOLBROOK, NJ STEVENS, JL TI REDOX REGULATION OF GADD153 AND GRP78 STEADY-STATE MESSENGER-RNA BY DITHIOTHREITOL SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 W ALTON JONES CELL SCI CTR,LAKE PLACID,NY 12946. NIA,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 111 EP 111 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400391 ER PT J AU HOU, XY JOHNSON, AC ROSNER, MR AF HOU, XY JOHNSON, AC ROSNER, MR TI IDENTIFICATION OF A NEGATIVE CIS-ACTING ELEMENT AND ITS BINDING-PROTEINS IN EGF RECEPTOR GENE PROMOTER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CHICAGO,BEN MAY INST,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MOLEC GENET & CELL BIOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT PHARMACOL & PHYSIOL SCI,CHICAGO,IL 60637. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 112 EP 112 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400398 ER PT J AU JANE, SM GUMUCIO, DL NEY, PA CUNNINGHAM, JM NIENHUIS, AW AF JANE, SM GUMUCIO, DL NEY, PA CUNNINGHAM, JM NIENHUIS, AW TI THE EFFECT OF DNA METHYLATION ON PROTEIN-BINDING TO THE STAGE SELECTOR ELEMENT OF THE GAMMA-GLOBIN GENE PROMOTER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. UNIV MICHIGAN,DEPT ANAT & CELL BIOL,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 113 EP 113 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400400 ER PT J AU KANNO, Y OZATO, K AF KANNO, Y OZATO, K TI 5' REGULATORY REGION OF THE ICSBP GENE - AN INTERFERON-GAMMA RESPONSIVE ELEMENT CONSERVED IN GENES OF THE IRF FAMILY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 114 EP 114 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400405 ER PT J AU KASHANCHI, F DUVALL, JF LINDHOLM, PF RADONOVICH, MF BRADY, JN AF KASHANCHI, F DUVALL, JF LINDHOLM, PF RADONOVICH, MF BRADY, JN TI SEQUENCES DOWNSTREAM OF THE TRANSCRIPTION INITIATION SITE ARE IMPORTANT FOR HTLV-I BASAL GENE-EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 114 EP 114 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400404 ER PT J AU MCBRIDE, AA WINOKUR, P AF MCBRIDE, AA WINOKUR, P TI SEPARATION OF THE TRANSCRIPTIONAL ACTIVATION AND REPLICATION FUNCTIONS OF THE BOVINE PAPILLOMAVIRUS E2-PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 119 EP 119 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400423 ER PT J AU NELSON, N MARKS, MS DRIGGERS, PH OZATO, K AF NELSON, N MARKS, MS DRIGGERS, PH OZATO, K TI ICSBP A MEMBER OF THE IRF FAMILY SUPPRESSES IFN-INDUCED GENE-TRANSCRIPTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 121 EP 121 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400432 ER PT J AU MUNGER, K WU, EW CLEMENS, KE HECK, DV AF MUNGER, K WU, EW CLEMENS, KE HECK, DV TI THE HUMAN PAPILLOMARVIRUS-E7 ONCOPROTEIN AND THE CELLULAR TRANSCRIPTION FACTOR-E2F BIND TO SEPARATE SITES ON THE RETINOBLASTOMA TUMOR SUPPRESSOR PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 139 EP 139 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400502 ER PT J AU ZHAN, QM KASTAN, MB CARRIER, F HOLLANDER, MC FORNACE, AJ AF ZHAN, QM KASTAN, MB CARRIER, F HOLLANDER, MC FORNACE, AJ TI IDENTIFICATION OF A P53-REGULATED GENE INVOLVED IN A CELL-CYCLE CHECKPOINT ACTIVATED BY DNA DAMAGE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV HOSP,CTR ONCOL,BALTIMORE,MD 21205. RI Carrier, France/C-3063-2008 NR 3 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 141 EP 141 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400513 ER PT J AU LI, CCH RUSCETTI, FW RICE, N CHEN, E YANG, NS MIKOVITS, J LONGO, DL AF LI, CCH RUSCETTI, FW RICE, N CHEN, E YANG, NS MIKOVITS, J LONGO, DL TI DIFFERENTIAL EXPRESSION OF REL FAMILY MEMBERS IN HTLV-I INFECTED-CELLS - EVIDENCE FOR TRANSCRIPTIONAL ACTIVATION OF C-REL BY TAX PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,MOLEC VIROL & CARCINOGENESIS LAB,BRI BASIC RES PROGRAM,FREDERICK,MD 21702. DYNCORP INC,PROGRAM RESOURCES,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,MOLEC IMMUNOREGULAT LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 146 EP 146 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400531 ER PT J AU NEDOSPASOV, SA TURETSKAYA, RL UDALOVA, IA RICE, NR KUPRASH, DV AF NEDOSPASOV, SA TURETSKAYA, RL UDALOVA, IA RICE, NR KUPRASH, DV TI MULTIPLICITY OF NUCLEAR NF-KAPPA-B/REL COMPLEXES - TISSUE-SPECIFICITY, EFFECTS OF THE SEQUENCE CONTEXT OF THE EXTENDED KAPPA-B SITE AND RELATION TO PROTEIN-INDUCED DNA BENDING SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,LMVC,ABL BRP,FREDERICK,MD 21702. ENGELHARDT MOLEC BIOL INST,MOSCOW 117984,RUSSIA. NCI,FCRDC,LMI,BRMP,FREDERICK,MD 21702. RI Nedospasov, Sergei/J-5936-2013; Nedospasov, Sergei/L-1990-2015; Kuprash, Dmitry/O-4899-2015; Nedospasov, Sergei/Q-7319-2016 OI Kuprash, Dmitry/0000-0002-1488-4148; NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 147 EP 147 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400535 ER PT J AU NOLAN, GP FUJITA, T BHATIA, K HUPPI, C LIOU, HC SCOTT, ML BALTIMORE, D AF NOLAN, GP FUJITA, T BHATIA, K HUPPI, C LIOU, HC SCOTT, ML BALTIMORE, D TI THE BCL-3 PROTOONCOGENE IS A NUCLEAR-RESIDENT I-KAPPA-B-LIKE MOLECULE THAT PREFERENTIALLY REGULATES NF-KAPPA-B P50 AND P49 DNA-BINDING ACTIVITY IN A PHOSPHORYLATION-DEPENDENT MANNER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ROCKEFELLER UNIV,NEW YORK,NY 10021. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 147 EP 147 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400537 ER PT J AU ROULSTON, A RICE, N HISCOTT, J AF ROULSTON, A RICE, N HISCOTT, J TI DISTINCT NF-KAPPA-B BINDING ACTIVITIES INDUCED IN RESPONSE TO PHORBOL ESTER AND VIRAL-INFECTION OF MYELOMONOBLASTIC CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MCGILL UNIV,LADY DAVIS INST MED RES,MONTREAL H3A 2T5,QUEBEC,CANADA. NCI,FREDERICK CANC RES FACIL,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 148 EP 148 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400538 ER PT J AU CARLSON, SG FAWCETT, TW HOLBROOK, NJ AF CARLSON, SG FAWCETT, TW HOLBROOK, NJ TI REGULATION OF THE C/EBP-RELATED GENE, GADDI53, BY GLUCOSE DEPRIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,MOLEC GENET LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 153 EP 153 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400561 ER PT J AU CHIANG, PK DAVE, JR NICHOLSON, DE RHODES, C YAMADA, Y ZENG, GC AF CHIANG, PK DAVE, JR NICHOLSON, DE RHODES, C YAMADA, Y ZENG, GC TI INDUCTION OF DIFFERENTIATION OF 3T3-L1 FIBROBLASTS TO ADIPOCYTES BY 3-DEAZAADENOSINE OR INSULIN REQUIRES C-FOS PROTOONCOGENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. WALTER REED ARMY INST RES,WASHINGTON,DC 20307. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 154 EP 154 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400563 ER PT J AU CUDDIHY, AE BRENTS, LA KIRSCH, IR KUEHL, WM AF CUDDIHY, AE BRENTS, LA KIRSCH, IR KUEHL, WM TI THE ROLE OF NUCLEAR FACTORS (MYB, SCL AND ID) IN MEL CELL-DIFFERENTIATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20889. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 155 EP 155 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400568 ER PT J AU DEGUCHI, Y MURAGUCHI, A KEHRL, JH AF DEGUCHI, Y MURAGUCHI, A KEHRL, JH TI IDENTIFICATION OF SPECIFIC DNA-BINDING SEQUENCES FOR A DIVERGED HUMAN HOMEOPROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 TOYAMA MED & PHARMACEUT UNIV,DEPT IMMUNOL,TOYAMA,TOYAMA 93001,JAPAN. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 155 EP 155 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400569 ER PT J AU DUNN, B COGLIATI, T CULTRARO, C SEGAL, S AF DUNN, B COGLIATI, T CULTRARO, C SEGAL, S TI REGULATION OF MAX AND MYC IN DIFFERENTIATION OF MURINE ERYTHROLEUKEMIA-CELLS STABLY TRANSFECTED WITH MAX OR C-MYC, N-MYC AND L-MYC SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,NAVY MED ONCOL BRANCH,BETHESDA,MD 20889. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 156 EP 156 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400571 ER PT J AU FREDERIKSE, P PIATIGORSKY, J AF FREDERIKSE, P PIATIGORSKY, J TI CHARACTERIZATION OF THE ALPHA-B-CRYSTALLIN PROMOTER - EVIDENCE FOR A ROLE FOR HSF IN LENS EXPRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NEI,LMDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 157 EP 157 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400575 ER PT J AU LEE, IJ DRIGGERS, PH MEDIN, JA OZATO, K AF LEE, IJ DRIGGERS, PH MEDIN, JA OZATO, K TI ANALYSIS OF RETINOID X RECEPTOR (RXR-BETA) FUNCTION BY AN INVITRO TRANSCRIPTION ASSAY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 163 EP 163 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400601 ER PT J AU MEDIN, JA DRIGGERS, PH OZATO, K AF MEDIN, JA DRIGGERS, PH OZATO, K TI 9-CIS-RETINOIC ACID ALTERS THE DNA-BINDING CHARACTERISTICS OF RECOMBINANT RXR-BETA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 165 EP 165 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400608 ER PT J AU MINUCCI, S ZAND, DJ MARKS, MS NAGATA, T OZATO, K AF MINUCCI, S ZAND, DJ MARKS, MS NAGATA, T OZATO, K TI CHARACTERIZATION OF RXR-BETA DELETION MUTANTS AND ANALYSIS OF THEIR FUNCTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. RI Minucci, Saverio/J-9669-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 165 EP 165 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400607 ER PT J AU OHTAKAMARUYAMA, C DREW, LR PISANO, MM CHEPELINSKY, AB AF OHTAKAMARUYAMA, C DREW, LR PISANO, MM CHEPELINSKY, AB TI TRANSCRIPTIONAL REGULATION OF THE HUMAN MIP GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 167 EP 167 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400613 ER PT J AU OWEN, RD BARRETT, JC AF OWEN, RD BARRETT, JC TI DIFFERENTIAL GENE-REGULATION IN RESPONSE TO LOSS OF TUMOR SUPPRESSOR GENE-FUNCTION - COLLAGEN-II (ALPHA-1) AND H19 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,NATL TOXICOL PROGRAM,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 168 EP 168 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400617 ER PT J AU PEMRICK, SM STURZENBECKER, LJ ABARZUA, P KRATZEISEN, C MARKS, MS MEDIN, JA OZATO, K LEVIN, AA HUNZIKER, W GRIPPO, JF AF PEMRICK, SM STURZENBECKER, LJ ABARZUA, P KRATZEISEN, C MARKS, MS MEDIN, JA OZATO, K LEVIN, AA HUNZIKER, W GRIPPO, JF TI 1,25 DIHYDROXYVITAMIN-D3 INDUCTION OF A RETINOIC ACID RESPONSE ELEMENT BY A CHIMERIC RECEPTOR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HOFFMANN LA ROCHE INC,DEPT INVEST TOXICOL,NUTLEY,NJ 07110. HOFFMANN LA ROCHE INC,DEPT ONCOL,NUTLEY,NJ 07110. PHARMA RES,BASEL,SWITZERLAND. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 168 EP 168 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400618 ER PT J AU SAUNDERS, NA BERNACKI, SH GEORGE, MD JETTEN, AM AF SAUNDERS, NA BERNACKI, SH GEORGE, MD JETTEN, AM TI DIFFERENTIATION-SPECIFIC EXPRESSION OF TRANSGLUTAMINASE TYPE-I IN SQUAMOUS DIFFERENTIATING EPITHELIA - REGULATION BY RETINOIDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. RI saunders, nicholas/E-1544-2014 OI saunders, nicholas/0000-0002-2478-3420 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 172 EP 172 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400635 ER PT J AU SEGARS, J NAGATA, T DREW, P BOURS, V MEDIN, J AN, JB BECKER, K STEPHANY, D SIEBENLIST, U OZATO, K AF SEGARS, J NAGATA, T DREW, P BOURS, V MEDIN, J AN, JB BECKER, K STEPHANY, D SIEBENLIST, U OZATO, K TI INDUCTION OF MHC CLASS-I GENES IN RETINOIC-ACID TREATED NTERA2 CELLS - COACTIVATION OF RETINOID RECEPTORS AND P50/P65-NFKB FACTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 173 EP 173 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400637 ER PT J AU BEGUINOT, L JOHNSON, AC YAMAZAKI, H PASTAN, I AF BEGUINOT, L JOHNSON, AC YAMAZAKI, H PASTAN, I TI CHARACTERIZATION AND PHOSPHORYLATION PROPERTY OF THE HUMAN GCF, A TRANSCRIPTIONAL REGULATOR OF THE EGF RECEPTOR GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HS RAFFAELE,DIBIT,MOLEC ONCOL LAB,MILAN,ITALY. NIH,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 179 EP 179 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400662 ER PT J AU FARINA, AR DAVISSMITH, T GARDNER, K LEVENS, DL AF FARINA, AR DAVISSMITH, T GARDNER, K LEVENS, DL TI INDUCIBILITY OF JUN D BY A POSTTRANSCRIPTIONAL MECHANISM IN T-CELL SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV LAQUILA,DEPT MED SPERIMENTALE,I-67100 LAQUILA,ITALY. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 181 EP 181 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400669 ER PT J AU HAMEL, PA HANLEYHYDE, J AF HAMEL, PA HANLEYHYDE, J TI CYCLIN EXPRESSION OVERCOMES PROMOTER REPRESSION BY P110RB1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV TORONTO,DEPT PATHOL,TORONTO M5S 1A8,ONTARIO,CANADA. NCI,GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 182 EP 182 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400674 ER PT J AU ONEILL, EA FRANTZWATTLEY, B NORDBY, E PARSONS, JN TOCCI, MJ KINCAID, RL OKEEFE, SJ AF ONEILL, EA FRANTZWATTLEY, B NORDBY, E PARSONS, JN TOCCI, MJ KINCAID, RL OKEEFE, SJ TI CALCINEURIN REGULATES THE ACTIVITY OF MULTIPLE TRANSCRIPTION FACTORS IN T-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAAA,IMMUNOL SECT,ROCKVILLE,MD 20852. MERCK RES LABS,DEPT MOLEC IMMUNOL,RAHWAY,NJ 07065. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400685 ER PT J AU PATERSON, BM MITSUI, K SHIRAKATA, M AF PATERSON, BM MITSUI, K SHIRAKATA, M TI CHANGES IN THE PHOSPHORYLATION STATUS OF MYOD ALTER DIMERIZATION SPECIFICITY AND DNA-BINDING ACTIVITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 186 EP 186 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400688 ER PT J AU CYEKL, A KANTOROW, M KLEMENT, JF SAX, CM PIATIGORSKY, J AF CYEKL, A KANTOROW, M KLEMENT, JF SAX, CM PIATIGORSKY, J TI ANALYSIS OF CIS-ACTING ELEMENTS AND DNA-BINDING PROTEINS REGULATING TRANSCRIPTION OF MOUSE AND CHICKEN ALPHA-A-CRYSTALLIN GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NEI,LMDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 191 EP 191 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400710 ER PT J AU KAWAMOTO, S CHOPRA, RK KITAGAWA, G AF KAWAMOTO, S CHOPRA, RK KITAGAWA, G TI CELL TYPE-DEPENDENT REGULATION OF GENE-EXPRESSION OF A NONMUSCLE MYOSIN HEAVY-CHAIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 198 EP 198 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400735 ER PT J AU POLLET, RJ ELKEBBI, I BRADSHAW, S PAO, CI PHILLIPS, LS CUSHMAN, S WILSON, C AF POLLET, RJ ELKEBBI, I BRADSHAW, S PAO, CI PHILLIPS, LS CUSHMAN, S WILSON, C TI REGULATION OF GLUCOSE TRANSPORTER GENE-EXPRESSION, SYNTHESIS AND TRANSLOCATION IN CULTURED MUSCLE-CELLS BY INSULIN AND GLUCOSE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 EMORY UNIV,VA MED CTR,ATLANTA,GA 30033. NIDDKD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 206 EP 206 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400767 ER PT J AU SCHERLE, P HOLMES, K STAUDT, L AF SCHERLE, P HOLMES, K STAUDT, L TI STAGE-SPECIFIC CHANGES IN TRANSCRIPTION FACTOR EXPRESSION DURING NORMAL-B CELL-DEVELOPMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 208 EP 208 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400775 ER PT J AU SCHWARTZ, RC BRETZ, JD WILLIAMS, S JOHNSON, PF AF SCHWARTZ, RC BRETZ, JD WILLIAMS, S JOHNSON, PF TI EXPRESSION OF C/EBP-RELATED TRANSCRIPTION FACTORS CORRELATES WITH THE LINEAGE SWITCH OF TRANSFORMED-B CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MICHIGAN STATE UNIV,DEPT MICROBIOL,E LANSING,MI 48824. NCI,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. RI Johnson, Peter/A-1940-2012 OI Johnson, Peter/0000-0002-4145-4725 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 208 EP 208 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400776 ER PT J AU WANG, LQ BALAKIR, R PRECHT, P HORTON, WE AF WANG, LQ BALAKIR, R PRECHT, P HORTON, WE TI IDENTIFICATION OF NUCLEAR PROTEINS FROM DIFFERENTIATING CHONDROCYTES WHICH BIND TO THE ENHANCER OF COLLAGEN-II GENE AND REGULATE ITS TRANSCRIPTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 211 EP 211 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400788 ER PT J AU WEI, Q PATERSON, BM AF WEI, Q PATERSON, BM TI THE CHICKEN E12/E47 PROTEINS ARE NUCLEAR PHOSPHOPROTEINS WHICH ARE UP-REGULATED DURING MYOGENESIS AND ARE ASSOCIATED WITH CMD1 INVIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 211 EP 211 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400790 ER PT J AU OSIFCHIN, N SAKAI, T SCHUERER, D KIM, SJ ROBBINS, PD AF OSIFCHIN, N SAKAI, T SCHUERER, D KIM, SJ ROBBINS, PD TI THE REGULATION OF EXPRESSION OF THE RETINOBLASTOMA SUSCEPTIBILITY GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 KYOTO PREFECTURAL UNIV,DEPT PREVENTAT MED,KYOTO 602,JAPAN. UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 216 EP 216 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400807 ER PT J AU VANDEWOUDE, GF ZHOU, RP DAAR, I YEW, N MATTEN, W FUKASAWA, K SATHYANARAYANA, BK RUBIN, JR AF VANDEWOUDE, GF ZHOU, RP DAAR, I YEW, N MATTEN, W FUKASAWA, K SATHYANARAYANA, BK RUBIN, JR TI PROTOONCOGENE AND CELL-CYCLE REGULATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 223 EP 223 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400827 ER PT J AU SARTOR, O MCLELLAN, CA AF SARTOR, O MCLELLAN, CA TI SURAMIN INDUCES TYROSINE PHOSPHORYLATION AND INHIBITS CELLULAR PROLIFERATION IN A HUMAN B-LYMPHOBLAST CELL-LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 240 EP 240 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400889 ER PT J AU EVANS, GA KIRKEN, RA FARRAR, WL AF EVANS, GA KIRKEN, RA FARRAR, WL TI IL-2-DEPENDENT ACTIVATION OF RECEPTOR SPECIFIC AND MITOGENIC TYROSINE KINASE PATHWAYS - INCREASED ACTIVITY OF A P97 MITOGENIC PATHWAY IN HTLV-1 TRANSFORMED T-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DYNCORP,PROGRAM RESOURCES,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES FACIL,BIOL RESPONSE MODIFIERS PROGRAM,MOLEC IMMUNNOREGULAT LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 252 EP 252 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400935 ER PT J AU MATOSKOVA, B SAMESHIMA, JH SARTOR, O ROBBINS, K AF MATOSKOVA, B SAMESHIMA, JH SARTOR, O ROBBINS, K TI MAPPING BIOLOGIC AND BIOCHEMICAL-PROPERTIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NATL INST DENTAL RES,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 256 EP 256 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400950 ER PT J AU SAMELSON, LE EGERTON, M ASHE, OR CHEN, D DRUKER, BJ BURGESS, WH AF SAMELSON, LE EGERTON, M ASHE, OR CHEN, D DRUKER, BJ BURGESS, WH TI VCP, THE MAMMALIAN HOMOLOG OF CDC48, IS TYROSINE PHOSPHORYLATED IN RESPONSE TO T-CELL ANTIGEN RECEPTOR ACTIVATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC & CELLULAR BIOL,BOSTON,MA 02115. NICHHD,CELL BIOL METAB BRANCH,BETHESDA,MD 20892. AMER RED CROSS,HOLLAND LAB,ROCKVILLE,MD 20850. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 258 EP 258 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400959 ER PT J AU WIRTH, PJ LUO, L AF WIRTH, PJ LUO, L TI ANALYSIS OF TRANSFORMING GROWTH-FACTOR BETA-1 SIGNAL TRANSDUCTION IN RAT-LIVER EPITHELIAL-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPT CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 263 EP 263 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46400977 ER PT J AU SONG, L ADLER, WH CHUNG, S KIM, YH COLLINS, GD NAGEL, JE AF SONG, L ADLER, WH CHUNG, S KIM, YH COLLINS, GD NAGEL, JE TI TYROSINE PHOSPHORYLATION OF A 42-KDA ERK2 KINASE IS ASSOCIATED WITH MAXIMAL IL-2 PRODUCTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,GRC,CLIN IMMUNOL SECT,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 276 EP 276 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401029 ER PT J AU MIKI, T SMITH, CL FLEMING, TP AF MIKI, T SMITH, CL FLEMING, TP TI EXPRESSION CLONING OF CDNAS FOR A NOVEL ONCOGENE, ECT2, ENCODING A CANDIDATE ACTIVATOR OF SMALL GTP-BINDING PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 280 EP 280 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401047 ER PT J AU CRAXTON, A NOGIMORI, K SHEARS, SB AF CRAXTON, A NOGIMORI, K SHEARS, SB TI INS(1,3,4,5)P4/INS(1,3,4,5,6)P5 3-PHOSPHATASE - A TARGET FOR REGULATION BY PROTEIN-PHOSPHORYLATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,INOSITOL LIPIDS SECT,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 284 EP 284 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401060 ER PT J AU GUTKIND, JS KALINEC, G XU, NZ AF GUTKIND, JS KALINEC, G XU, NZ TI ROLE OF PROTEIN-KINASES AND PHOSPHOLIPID-KINASES IN CELL-GROWTH AND TRANSFORMATION INDUCED BY G-PROTEINS AND THEIR COUPLED RECEPTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,CELLULAR DEV & ONCOL,MOLEC SIGNALLING GRP,BETHESDA,MD 20892. RI Gutkind, J. Silvio/A-1053-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 286 EP 286 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401068 ER PT J AU ALCORTA, D AFSHARI, C BARRETT, JC AF ALCORTA, D AFSHARI, C BARRETT, JC TI ROLE OF SIGNAL TRANSDUCTION KINASES PHOSPHATASES IN THE INDUCTION OF DNA-SYNTHESIS IN SENESCENT PRIMARY FIBROBLASTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 290 EP 290 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401087 ER PT J AU KANG, WK HA, MJ MYERS, CE TREPEL, JB AF KANG, WK HA, MJ MYERS, CE TREPEL, JB TI LOVASTATIN, AN INHIBITOR OF HMG-COA REDUCTASE, CAN BLOCK BOTH S-PHASE ENTRY AND EXIT FROM G2/M IN MITOGEN-ACTIVATED HUMAN PERIPHERAL-BLOOD LYMPHOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 293 EP 293 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401099 ER PT J AU RHODES, N INNES, C HICKS, R KASENALLY, A PROPST, F PAULES, RS AF RHODES, N INNES, C HICKS, R KASENALLY, A PROPST, F PAULES, RS TI CELL-CYCLE CONTROL MECHANISMS IN MOS TRANSFORMED-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ICRF,LONDON W2 1PG,ENGLAND. ST MARYS HOSP,SCH MED,LUDWIG INST CANC RES,LONDON W2 1PG,ENGLAND. NIEHS,MAMMALIAN MOLEC GENET GRP,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 296 EP 296 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401109 ER PT J AU ADNANE, J SHAO, ZH KIM, SJ ROBBINS, PD AF ADNANE, J SHAO, ZH KIM, SJ ROBBINS, PD TI THE REGULATION OF TRANSCRIPTION BY THE RETINOBLASTOMA SUSCEPTIBILITY GENE-PRODUCT AND CYCLINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 297 EP 297 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401112 ER PT J AU LINDHOLM, PF REID, RL KASHANCHI, F BRADY, JN AF LINDHOLM, PF REID, RL KASHANCHI, F BRADY, JN TI THE HTLV-I TAX1 PROTEIN ASSOCIATES WITH PROTEIN-KINASE-C SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 300 EP 300 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401125 ER PT J AU NORMAN, SA THOMPSON, DB MOTT, D AF NORMAN, SA THOMPSON, DB MOTT, D TI REGULATION OF HUMAN SKELETAL-MUSCLE PP-1 GENE-EXPRESSION BY INSULIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract ID PHOSPHATASE-ACTIVITY; CATALYTIC SUBUNIT C1 NIH,PHOENIX,AZ 85016. NR 5 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 302 EP 302 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401132 ER PT J AU SCHERLE, P BEHRENS, T STAUDT, L AF SCHERLE, P BEHRENS, T STAUDT, L TI LY-GDI, A LYMPHOID-SPECIFIC GDP GTP EXCHANGE PROTEIN FOR P21RHO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 304 EP 304 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401140 ER PT J AU ADAMCZEWSKI, M KORETZKY, GA KINET, JP AF ADAMCZEWSKI, M KORETZKY, GA KINET, JP TI CD45 CONTROLS PHOSPHORYLATION AND SIGNAL TRANSDUCTION OF THE HIGH-AFFINITY IGE-RECEPTOR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV IOWA,COLL MED,DEPT INTERNAL MED,IOWA CITY,IA 52242. NIAID,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 307 EP 307 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401152 ER PT J AU ISHIBASHI, T BOTTARO, DP CHAN, AML MIKI, T AARONSON, SA AF ISHIBASHI, T BOTTARO, DP CHAN, AML MIKI, T AARONSON, SA TI EXPRESSION CLONING OF A NOVEL HUMAN DUAL SPECIFICITY PHOSPHATASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. RI Bottaro, Donald/F-8550-2010 OI Bottaro, Donald/0000-0002-5057-5334 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 311 EP 311 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401168 ER PT J AU LU, J GOTO, Y NOTKINS, AL LAN, MS AF LU, J GOTO, Y NOTKINS, AL LAN, MS TI CLONING AND SEQUENCE-ANALYSIS OF A NOVEL CDNA ISOLATED FROM HUMAN INSULINOMA THAT ENCODES A PUTATIVE PROTEIN TYROSINE PHOSPHATASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,ORAL MED LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 312 EP 312 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401172 ER PT J AU MOSINGER, B WESTPHAL, H AF MOSINGER, B WESTPHAL, H TI CHARACTERIZATION OF THE MURINE INTRACELLULAR PHOSPHOTYROSINE PHOSPHATASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MAMMALIAN GENES & DEV LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 313 EP 313 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401177 ER PT J AU OKEEFE, SJ PARSONS, JN FRANTZWATTLEY, B NORDBY, E TOCCI, MJ TAMURA, J KINCAID, RL ONEILL, EA AF OKEEFE, SJ PARSONS, JN FRANTZWATTLEY, B NORDBY, E TOCCI, MJ TAMURA, J KINCAID, RL ONEILL, EA TI CALCINEURIN (PROTEIN PHOSPHATASE-2B) IS THE FK-506-SENSITIVE COMPONENT OF THE T-CELL SIGNAL TRANSDUCTION PATHWAY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MERCK SHARP & DOHME LTD,DEPT MOLEC IMMUNOL,RES LABS,RAHWAY,NJ 07065. NIAAA,IMMUNOL SECT,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 313 EP 313 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401179 ER PT J AU DELAROSA, A MACDONALD, NJ BENEDICT, MA FREIJE, JMP STEEG, PS AF DELAROSA, A MACDONALD, NJ BENEDICT, MA FREIJE, JMP STEEG, PS TI PHOSPHORYLATION AND BIOCHEMICAL-ANALYSIS OF NM23 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 316 EP 316 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401191 ER PT J AU HA, MJ KANG, WK BANG, YJ JENSEN, RT FANG, WG SHENKER, A SPIEGEL, AM PARK, DJ KOENIG, ML PIRNIA, F MYERS, CE GOLDSMITH, PK NIKLINSKI, WT TREPEL, JB AF HA, MJ KANG, WK BANG, YJ JENSEN, RT FANG, WG SHENKER, A SPIEGEL, AM PARK, DJ KOENIG, ML PIRNIA, F MYERS, CE GOLDSMITH, PK NIKLINSKI, WT TREPEL, JB TI UNCOUPLING OF PURINERGIC RECEPTORS FROM PHOSPHOLIPASE-C IS ASSOCIATED WITH LOSS OF GROWTH-REGULATION IN A PROSTATE CARCINOMA CELL-LINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NIDDKS,DIGEST DIS BRANCH,BETHESDA,MD 20892. NIDDKS,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. WALTER REED ARMY INST RES,INST MED NEUROSCI,WASHINGTON,DC 20307. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 317 EP 317 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401195 ER PT J AU LARSEN, RD CARLSON, LM PICKEL, J SCHULTZ, T LOWE, JB THOMPSON, CB LEE, KP AF LARSEN, RD CARLSON, LM PICKEL, J SCHULTZ, T LOWE, JB THOMPSON, CB LEE, KP TI EXPRESSION OF LEWIS-X AND SIALYL LEWIS-X EPITOPES IN AVIAN LYMPHOCYTE-B DEVELOPMENT CORRELATES WITH TISSUE SPECIFIC LOCALIZATION OF IMMUNE CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HENRY M JACKSON FDN,BETHESDA,MD 20814. MEDIMMUNE INC,GAITHERSBURG,MD 20877. NCI,FREDERICK CANC RES PROGRAM,FREDERICK,MD 21702. HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. GLYCOMED INC,ALAMEDA,CA 94501. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 331 EP 331 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401232 ER PT J AU CHANG, AC WADSWORTH, S COLIGAN, JE AF CHANG, AC WADSWORTH, S COLIGAN, JE TI EXPRESSION OF MEROSIN IN MOUSE THYMUS AND ITS INTERACTION WITH THYMOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 337 EP 337 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401253 ER PT J AU PILI, R CORDA, S PASSANITI, A ZIEGELSTEIN, RC CAPOGROSSI, MC AF PILI, R CORDA, S PASSANITI, A ZIEGELSTEIN, RC CAPOGROSSI, MC TI ENDOTHELIAL-CELL CA-2+ MODULATES TUMOR-CELL ADHESION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 352 EP 352 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401313 ER PT J AU RACKE, MK SCOTT, D QUIGLEY, L MCFARLIN, DE AF RACKE, MK SCOTT, D QUIGLEY, L MCFARLIN, DE TI MODIFICATION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS BY ADMINISTRATION OF ANTIBODIES TO LFA-1 AND ICAM-1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. NIAMS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 355 EP 355 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401325 ER PT J AU POZSGAY, V GLAUDEMANS, CPJ ROBBINS, JB SCHNEERSON, R AF POZSGAY, V GLAUDEMANS, CPJ ROBBINS, JB SCHNEERSON, R TI SYNTHESIS OF EXTENDED FRAGMENTS OF THE O-POLYSACCHARIDE OF SHIGELLA-DYSENTERIAE TYPE-1 AND THEIR INTERACTIONS WITH A MONOCLONAL-ANTIBODY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIADDKD,BETHESDA,MD 20892. NICHHD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 9 PY 1993 SU 17A BP 369 EP 369 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KN464 UT WOS:A1993KN46401364 ER PT J AU BRENNER, MK RILL, DR MOEN, RC KRANCE, RA MIRRO, J ANDERSON, WF IHLE, JN AF BRENNER, MK RILL, DR MOEN, RC KRANCE, RA MIRRO, J ANDERSON, WF IHLE, JN TI GENE-MARKING TO TRACE ORIGIN OF RELAPSE AFTER AUTOLOGOUS BONE-MARROW TRANSPLANTATION SO LANCET LA English DT Note ID LEUKEMIA AB Bone marrow harvested for autologous bone-marrow transplantation may contain residual malignant cells even when it is judged to be in remission. Genetic marking and subsequent detection of these cells in recipients would give useful information about the origin of relapse after transplantation. We transferred the neomycin-resistance gene into bone-marrow cells harvested from children with acute myeloid leukaemia in remission. Two patients have relapsed since reinfusion of the marked cells. In both, the resurgent blast cells contained the neomycin-resistance gene marker; thus, remission marrow can contribute to disease recurrence. This method of tracking malignant cells should enable the development of better marrow purging strategies. C1 GENET THERAPY INC, CLIN LABS, GAITHERSBURG, MD USA. CHILDRENS HOSP PITTSBURGH, DIV HEMATOL ONCOL, PITTSBURGH, PA USA. ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, MEMPHIS, TN 38101 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT PEDIAT, MEMPHIS, TN 38163 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT MED, MEMPHIS, TN 38163 USA. NHLBI, BETHESDA, MD 20892 USA. FU NCI NIH HHS [5 P01 CA 20180, CA 21765] NR 9 TC 880 Z9 887 U1 0 U2 5 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0140-6736 J9 LANCET JI Lancet PD JAN 9 PY 1993 VL 341 IS 8837 BP 85 EP 86 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KF870 UT WOS:A1993KF87000007 PM 8093407 ER PT J AU DACUNHA, A JEFFERSON, JJ TYOR, WR GLASS, JD JANNOTTA, FS VITKOVIC, L AF DACUNHA, A JEFFERSON, JJ TYOR, WR GLASS, JD JANNOTTA, FS VITKOVIC, L TI GLIOSIS IN HUMAN BRAIN - RELATIONSHIP TO SIZE BUT NOT OTHER PROPERTIES OF ASTROCYTES SO BRAIN RESEARCH LA English DT Article DE ASTROCYTE; GLIAL FIBRILLARY ACIDIC PROTEIN; GLIOSIS; HYPERPLASIA; HYPERTROPHY ID FIBRILLARY ACIDIC PROTEIN; HUMAN CEREBRAL-CORTEX; RAT-BRAIN; REACTIVE ASTROCYTES; ENCEPHALOMYELITIS; INTERLEUKIN-1; INJURY; GFA AB Gliosis is the most frequent and therefore important neurocellular reaction to brain insult occurring in diseases ranging from AIDS to infarction. Neuropathological diagnosis of gliosis is based on morphological changes of brain glial cells. Changes commonly agreed to reflect gliosis are qualitative increases in size, number and glial fibrillary acidic protein (GFAP) immunoreactivity of astrocytes. These parameters were morphometrically quantified in brain tissues of 22 individuals who died with 7 diseases and statistically compared to the extent of gliosis independently determined by 3 qualified observers. The data indicate that the extent of gliosis correlated with the increase in size of astrocytes in white matter (rho = 0.67) and this relationship was statistically significant (P = 0.0006). In contrast, the extent of gliosis was not correlated with the density of astrocytes nor the intensity of GFAP staining. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,DEPT NEUROPATHOL,BALTIMORE,MD 21287. NCI,PATHOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,DEPT NEUROL,BALTIMORE,MD 21287. GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20037. FU PHS HHS [P0-126643] NR 35 TC 45 Z9 45 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JAN 8 PY 1993 VL 600 IS 1 BP 161 EP 165 DI 10.1016/0006-8993(93)90415-J PG 5 WC Neurosciences SC Neurosciences & Neurology GA KG540 UT WOS:A1993KG54000022 PM 8422583 ER PT J AU RABINDRAN, SK HAROUN, RI CLOS, J WISNIEWSKI, J WU, C AF RABINDRAN, SK HAROUN, RI CLOS, J WISNIEWSKI, J WU, C TI REGULATION OF HEAT-SHOCK FACTOR TRIMER FORMATION - ROLE OF A CONSERVED LEUCINE ZIPPER SO SCIENCE LA English DT Article ID DNA-BINDING; TRANSCRIPTION FACTOR; ACTIVATION; CLONING; GENE AB The human and Drosophila heat shock transcription factors (HSFs) are multi-zipper proteins with high-affinity binding to DNA that is regulated by heat shock-induced trimerization. Formation of HSF trimers is dependent on hydrophobic heptad repeats located in the amino-terminal region of the protein. Two subregions at the carboxyl-terminal end of human HSF1 were identified that maintain the monomeric form of the protein under normal conditions. One of these contains a leucine zipper motif that is conserved between vertebrate and insect HSFs. These results suggest that the carboxyl-terminal zipper may suppress formation of trimers by the amino-terminal HSF zipper elements by means of intramolecular coiled-coil interactions that are sensitive to heat shock. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 38 TC 356 Z9 366 U1 1 U2 8 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD JAN 8 PY 1993 VL 259 IS 5092 BP 230 EP 234 DI 10.1126/science.8421783 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KF719 UT WOS:A1993KF71900032 PM 8421783 ER PT J AU CARROLL, FI ABRAHAM, P KUZEMKO, MA GRAY, JL LEWIN, AH BOJA, JW KUHAR, MJ AF CARROLL, FI ABRAHAM, P KUZEMKO, MA GRAY, JL LEWIN, AH BOJA, JW KUHAR, MJ TI SYNTHESIS AND COCAINE RECEPTOR AFFINITIES OF 3-PHENYL-2-(3'-METHYL-1,2,4-OXADIAZOLE-5'-YL)TROPANE ISOMERS SO JOURNAL OF THE CHEMICAL SOCIETY-CHEMICAL COMMUNICATIONS LA English DT Article ID LIGAND-BINDING; ANALOGS AB This study reports the synthesis and binding affinities at the cocaine receptor of all four isomers of 3-phenyl-2-(3-methyl-1,2,4-oxadiazole-5-yl)tropane derivable from natural (-)-cocaine. C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224. RP CARROLL, FI (reprint author), RES TRIANGLE INST,POB 12194,RES TRIANGLE PK,NC 27709, USA. NR 19 TC 15 Z9 15 U1 0 U2 1 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK MILTON ROAD, CAMBRIDGE, CAMBS, ENGLAND CB4 4WF SN 0022-4936 J9 J CHEM SOC CHEM COMM JI J. Chem. Soc.-Chem. Commun. PD JAN 7 PY 1993 IS 1 BP 44 EP 46 DI 10.1039/c39930000044 PG 3 WC Chemistry, Multidisciplinary SC Chemistry GA KH239 UT WOS:A1993KH23900021 ER PT J AU TANAKA, Y ADAMS, DH HUBSCHER, S HIRANO, H SIEBENLIST, U SHAW, S AF TANAKA, Y ADAMS, DH HUBSCHER, S HIRANO, H SIEBENLIST, U SHAW, S TI T-CELL ADHESION INDUCED BY PROTEOGLYCAN-IMMOBILIZED CYTOKINE MIP-1-BETA SO NATURE LA English DT Article ID LYMPHOCYTES-T; CD44; PROTEIN; ACTIVATION; RECEPTOR; FAMILY; GLYCOSAMINOGLYCANS; HYALURONATE; MOLECULE-1; ADHERENCE AB LYMPHOCYTE migration from blood into tissue depends on integrin-mediated adhesion to endothelium1-4. Adhesion requires not only integrin ligands on the endothelium, but also activation signals because T-cell integrins cannot bind well until they are activated. The physiological 'triggers' for T-cell adhesion are unknown, but cytokines may be good candidates as they are released during inflammation and trigger adhesion in neutrophils and monocytes2,5,6. We have identified a cytokine, macrophage inflammatory protein-1beta (MIP-1beta),that induces both chemotaxis and adhesion of T cells; MIP-1beta is most effective at augmenting adhesion of CD8+ T cells to the vascular cell adhesion molecule VCAM-1. We reasoned that, as cytokines in vivo will be rapidly washed away, MIP-1beta might be bound to endothelial surfaces and so induce adhesion in its immobilized form. Here we show that: (1) MIP-1beta is present on lymph node endothelium; (2) immobilized MIP-1beta induces binding of T cells to VCAM-1 in vitro. MIP-1beta was immobilized by binding to proteoglycan: a conjugate of heparin with bovine serum albumin and cellular proteoglycan CD44 were both effective. We propose that MIP-1beta and other cytokines with glycosaminoglycan-binding sites will bind to and be presented by endothelial proteoglycans to trigger adhesion selectively not only of lymphocyte subsets, but also of other cell types. C1 UNIV BIRMINGHAM,DEPT PATHOL,BIRMINGHAM B15 2TT,W MIDLANDS,ENGLAND. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP TANAKA, Y (reprint author), NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892, USA. RI Adams, David/C-9092-2009 NR 40 TC 776 Z9 781 U1 3 U2 10 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JAN 7 PY 1993 VL 361 IS 6407 BP 79 EP 82 DI 10.1038/361079a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KF718 UT WOS:A1993KF71800053 PM 7678446 ER PT J AU TANG, AM AMAGAI, M GRANGER, LG STANLEY, JR UDEY, MC AF TANG, AM AMAGAI, M GRANGER, LG STANLEY, JR UDEY, MC TI ADHESION OF EPIDERMAL LANGERHANS CELLS TO KERATINOCYTES MEDIATED BY E-CADHERIN SO NATURE LA English DT Article ID DENDRITIC CELLS; BONE-MARROW; MOLECULES; FAMILY; EXPRESSION; DIFFERENTIATION; GLYCOPROTEIN; DESMOCOLLINS; DESMOGLEIN; MEMBER AB LANGERHANS cells (LC) are the principal accessory cells present in epidermis1. Because LC have limited capacity for self-renewal2, epidermis is continually repopulated by as-yet uncharacterized bone marrow-derived LC progenitors3,4. In addition, although LC persist in epidermis for extended periods, LC are induced to migrate from skin to regional lymph nodes after antigen exposure5. To begin to elucidate mechanisms involved in LC trafficking, we characterized LC-keratinocyte (KC) interactions. Here we report that fresh murine LC express cadherins, and that LC adhere to KC in vitro through E-cadherin. Cultured LC (which may bear a phenotypic and functional relationship to LC that have migrated to lymph nodes6,7) express lower levels of E-cadherin and exhibit decreased affinity for KC. These results suggest that expression of E-cadherin by LC promotes persistence of these cells in epidermis, and that cadherins may play important and unanticipated roles in interactions between leukocytes and epithelia. C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RI Amagai, Masayuki/K-5325-2013 OI Amagai, Masayuki/0000-0003-3314-7052 NR 29 TC 368 Z9 370 U1 0 U2 4 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD JAN 7 PY 1993 VL 361 IS 6407 BP 82 EP 85 DI 10.1038/361082a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA KF718 UT WOS:A1993KF71800054 PM 8421498 ER PT J AU PAI, LH AF PAI, LH TI IMMUNOTOXIN THERAPY FOR CANCER SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID HUMAN OVARIAN-CANCER; RICIN-A CHAIN; PSEUDOMONAS EXOTOXIN; MONOCLONAL-ANTIBODY; ESCHERICHIA-COLI; DIPHTHERIA-TOXIN; MOUSE MODEL; RECEPTOR; DOMAINS; CELLS RP PAI, LH (reprint author), NCI,MOLEC BIOL LAB,BLDG 37,ROOM 4E16,BETHESDA,MD 20892, USA. NR 26 TC 50 Z9 52 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 JAN 6 PY 1993 VL 269 IS 1 BP 78 EP 81 DI 10.1001/jama.269.1.78 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA KF026 UT WOS:A1993KF02600032 PM 8416411 ER PT J AU GALETTO, G LEVINE, A AF GALETTO, G LEVINE, A TI AIDS-ASSOCIATED PRIMARY CENTRAL-NERVOUS-SYSTEM LYMPHOMA SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID HUMAN-IMMUNODEFICIENCY-VIRUS; RADIATION-THERAPY; CHEMOTHERAPY; RISK C1 NIAID,DIV AIDS,AIDS CLIN TRIALS GRP,ONCOL CORE COMM,BETHESDA,MD 20892. RP GALETTO, G (reprint author), UNIV SO CALIF,SCH MED,1441 EASTLAKE AVE,LOS ANGELES,CA 90033, USA. NR 14 TC 18 Z9 18 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 JAN 6 PY 1993 VL 269 IS 1 BP 92 EP 93 DI 10.1001/jama.269.1.92 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA KF026 UT WOS:A1993KF02600035 PM 8416414 ER PT J AU BOICE, JD AF BOICE, JD TI 2ND CANCER AFTER HODGKINS-DISEASE - THE PRICE OF SUCCESS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID THERAPY; BREAST; RISK RP BOICE, JD (reprint author), NCI,DIV CANC ETIOL,RADIAT EPIDEMIOL BRANCH,6130 EXECUT BLVD,EXECUT PLAZA N,RM 408,ROCKVILLE,MD 20852, USA. NR 16 TC 22 Z9 22 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 JAN 6 PY 1993 VL 85 IS 1 BP 4 EP 5 DI 10.1093/jnci/85.1.4 PG 2 WC Oncology SC Oncology GA KF029 UT WOS:A1993KF02900002 PM 8416254 ER PT J AU HANCOCK, SL TUCKER, MA HOPPE, RT AF HANCOCK, SL TUCKER, MA HOPPE, RT TI BREAST-CANCER AFTER TREATMENT OF HODGKINS-DISEASE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID 2ND CANCERS; WOMEN; RISK; TUBERCULOSIS; RADIOTHERAPY; IRRADIATION; MORTALITY; CARCINOMA; THERAPY AB Background: Most studies of survivors of Hodgkin's disease have shown a low risk for subsequent breast cancer, even though much lower doses of radiation than those used for Hodgkin's disease have been shown to induce breast cancer in other settings. Purpose: This study quantifies the risk of breast cancer following Hodgkin's disease treatment according to age at treatment and type of treatment. Methods: To evaluate the risk of breast cancer from irradiation, we reviewed records of 885 women treated for Hodgkin's disease between 1961 and 1990 (mean follow-up, 10 years). Risks for breast cancer incidence and mortality were calculated by comparison with expected rates for a general female population matched by age and race. Results: Twenty-five patients have developed invasive breast cancer, yielding a relative risk (RR) of 4.1 (95% confidence interval [CI] = 2.5-5.7). An additional patient developed multifocal carcinoma in situ. Age at irradiation strongly influenced risk: RR was 136 for women treated before 15 years of age (95% CI = 34-371). RR declined with age at irradiation (P for trend <.0001), but the elevation remained statistically significant for subjects less than 30 years old at the time of irradiation (for those 15-24, RR = 19 [95% CI = 10.3-32]; for those 24-29, RR = 7 [95% CI = 3.2-14.4]). In women above 30 years of age, the risk was not elevated (RR = 0.7; 95% CI = 0.2-1.8). Risk of breast cancer increased significantly with time since treatment (P for trend <.0001). The RR was 2.0 (95% CI = 1.0-3.5) with follow-up under 15 years and 13.6 (95% CI = 7.9-18.2) with follow-up equal to or exceeding 15 years. The addition of mechlorethamine, vincristine, procarbazine, and prednisone chemotherapy to irradiation increased the risk within the first 15 years. Most breast cancers (22 of 26) arose within or at the margin of the radiation field and were infiltrating ductal carcinomas. Stage distribution and outcome suggest that the increased incidence was not solely attributable to vigilant screening. RR of death from breast cancer was 5.1 (95% CI = 2.2-10.0). Conclusions: Women treated for Hodgkin's disease with radiation before 30 years of age are at markedly increased risk for breast cancer, with risk increasing dramatically more than 15 years after therapy. Implications: The high RR for development of breast cancer in women exposed to therapeutic radiation under 30 years of age raises important issues about optimal treatment strategies for patients with Hodgkin's disease, breast cancer, and other cancers. C1 STANFORD UNIV,MED CTR,SCH MED,DEPT RADIAT ONCOL,STANFORD,CA 94305. NCI,DIV CANC ETIOL,BETHESDA,MD 20892. RI Tucker, Margaret/B-4297-2015 FU NCI NIH HHS [P0CA-34233] NR 28 TC 381 Z9 388 U1 0 U2 4 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 JAN 6 PY 1993 VL 85 IS 1 BP 25 EP 31 DI 10.1093/jnci/85.1.25 PG 7 WC Oncology SC Oncology GA KF029 UT WOS:A1993KF02900011 PM 8416252 ER PT J AU GORI, GB AF GORI, GB TI ENVIRONMENTAL TOBACCO-SMOKE - THE PRICE OF SCIENTIFIC UNCERTAINTY SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter ID LUNG-CANCER C1 NCI,DIV CANC CAUSES & PREVENT,BETHESDA,MD 20892. NR 9 TC 0 Z9 0 U1 1 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 JAN 6 PY 1993 VL 85 IS 1 BP 66 EP 66 DI 10.1093/jnci/85.1.66 PG 1 WC Oncology SC Oncology GA KF029 UT WOS:A1993KF02900019 PM 8416258 ER PT J AU HUFF, CA YUSPA, SH ROSENTHAL, D AF HUFF, CA YUSPA, SH ROSENTHAL, D TI IDENTIFICATION OF CONTROL ELEMENTS 3' TO THE HUMAN KERATIN-1 GENE THAT REGULATE CELL TYPE AND DIFFERENTIATION-SPECIFIC EXPRESSION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MOUSE EPIDERMAL-CELLS; BETA-GLOBIN GENE; TISSUE-SPECIFIC EXPRESSION; HUMAN TYPE-I; TERMINAL DIFFERENTIATION; TRANSCRIPTIONAL ENHANCER; CYTOKERATIN GENES; SILENCER ELEMENTS; TRANSGENIC MICE; C-FOS AB To define DNA regulatory elements that mediate the response of the keratin 1 (K1) gene to Ca2+-induced differentiation, regions spanning the 5'- and 3'-flanking sequences, coding regions, and introns from the human K1 gene were cloned into vectors containing the chloramphenicol acetyltransferase (CAT) reporter gene and transfected into cultured mouse keratinocytes. A 4.3-kilobase (kb) region located 3' to the K1 gene stimulated CAT activity in response to increasing Ca2+ concentrations from 0.05 mM (basal cells) to 1.2 mm (differentiated cells). The 4.3-kb fragment was also active in human epidermal cells but inactive in NIH 3T3 cells and primary mouse fibroblasts. Deletion analysis localized the activity to the terminal 1682 base pairs (bp) of the flanking sequence which retained Ca2+ sensitivity in epidermal cells but was not active in mesenchymal cells. Removal of a 207-base pair element created an enhancer which was active in both epidermal and mesenchumal cells but was still Ca2+-inducible. Further deletions identified two elements which functioned synergistically to give maximal Ca2+-sensitive activity. Stably transfected epidermal cell lines expressed CAT under the direction of these elements when grafted onto nude mice to reconstitute an intact epidermis. Previously reported keratin regulatory motifs were not contained in the 1682-bp fragment, but an AP-1 site was identified in one of the synergistic subunits. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NR 73 TC 63 Z9 63 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 JAN 5 PY 1993 VL 268 IS 1 BP 377 EP 384 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KE603 UT WOS:A1993KE60300058 PM 7677999 ER PT J AU BLOBE, GC SACHS, CW KHAN, WA FABBRO, D STABEL, S WETSEL, WC OBEID, LM FINE, RL HANNUN, YA AF BLOBE, GC SACHS, CW KHAN, WA FABBRO, D STABEL, S WETSEL, WC OBEID, LM FINE, RL HANNUN, YA TI SELECTIVE REGULATION OF EXPRESSION OF PROTEIN-KINASE-C (PKC) ISOENZYMES IN MULTIDRUG-RESISTANT MCF-7 CELLS - FUNCTIONAL-SIGNIFICANCE OF ENHANCED EXPRESSION OF PKC-ALPHA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID P-GLYCOPROTEIN; PHORBOL ESTERS; LEUKEMIA-CELLS; ADRIAMYCIN; PHOSPHORYLATION; FORMS; RNA AB The multidrug resistance (MDR) phenotype induces cross-resistance to many chemotherapeutic agents in cancer cells. Protein kinase C (PKC) has been implicated in the regulation of the MDR phenotype. In order to determine the role of specific PKC isoenzymes in regulating the MDR phenotype, the expression and activity of PKC isoenzymes in the human breast cancer cell line, MCF-7-WT, and an MDR subline, MCF-7-MDR, were examined. The MDR phenotype was associated with a 10-fold increase in calcium-dependent PKC activity as well as a 10-fold decrease in calcium-independent activity. The increase in calcium-dependent activity was due to a selective increase in the expression of PKC alpha as determined by Western blot analysis and hydroxylapatite chromatography. This increase in expression of PKC alpha was regulated at the message level as demonstrated by Northern blot analysis. The decrease in calcium-independent activity was caused by a decrease in the expression of PKC delta and epsilon. The significance of the increase in PKC alpha expression was then demonstrated by a commensurate 11-fold increase in the basal and stimulated phosphorylation of the myristolated alanine-rich C kinase substrate. Phosphorylation of P-glycoprotein, the cellular mediator of the MDR phenotype, was increased >20-fold in the unstimulated MCF-7-MDR cell line and its phosphorylation was further increased 2-fold in response to phorbol 12-myristate 13-acetate. These changes paralleled the increases in P-glycoprotein pump function and the MDR phenotype underscoring the role for PKC alpha in regulating P-glycoprotein phosphorylation and function. C1 MAX PLANCK GESELL, MAX DELBRUCK LAB, W-5000 COLOGNE 30, GERMANY. NIEHS, MOLEC & INTEGRATED NEUROSCI LAB, RES TRIANGLE PK, NC 27709 USA. DUKE UNIV, DIV HEMATOL ONCOL, DURHAM, NC 27710 USA. DUKE UNIV, DIV GERIATR, DURHAM, NC 27710 USA. DUKE UNIV, DEPT MED, DURHAM, NC 27710 USA. DUKE UNIV, DEPT CELL BIOL, DURHAM, NC 27710 USA. VET ADM MED CTR, DURHAM, NC 27705 USA. CIBA GEIGY AG, DIV PHARMACEUT, DEPT RES, CH-4002 BASEL, SWITZERLAND. FU NCI NIH HHS [5U01-CA-46738]; NHLBI NIH HHS [HL-43707] NR 29 TC 170 Z9 175 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 JAN 5 PY 1993 VL 268 IS 1 BP 658 EP 664 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KE603 UT WOS:A1993KE60300099 PM 8093247 ER PT J AU YOSHIMURA, K CHU, CS CRYSTAL, RG AF YOSHIMURA, K CHU, CS CRYSTAL, RG TI ALTERNATIVE SPLICING OF INTRON-23 OF THE HUMAN CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR GENE RESULTING IN A NOVEL EXON AND TRANSCRIPT CODING FOR A SHORTENED INTRACYTOPLASMIC-C TERMINUS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHLORIDE CHANNEL; EPITHELIAL-CELLS; DNA; EXPRESSION; IDENTIFICATION; CFTR; SEQUENCES; FRAGMENTS; MUTATIONS; INVITRO AB The cystic fibrosis transmembrane conductance regulator (CFTR) gene, the gene responsible for the lethal hereditary disorder cystic fibrosis, codes for a membrane protein functioning as a cAMP-regulated Cl- channel. Evaluation of human CFTR mRNA transcripts from epithelial and nonepithelial cells demonstrated a CFTR cDNA containing a 260-base pair (bp) insertion between the known CFTR exons 23 and 24, introducing a premature stop codon that would result in a CFTR protein shortened by 61 amino acids at the carboxyl terminus compared to that expected from the normal reported human CFTR coding sequences. Sequence analysis of intron 23 of the CFTR gene demonstrated that the 260-bp insertion (named exon 24a), a part of the reported intron 23 and located consecutive to exon 24, is likely generated by an alternative splice acceptor site. The exon 24a+ CFTR mRNA transcripts represented 3-16% of the total CFTR transcripts in epithelial and nonepithelial cells. These observations suggest an unexpected plasticity of expression of the CFTR gene, where alternative splicing of precursor CFTR mRNA transcripts permits the use of an alternative exon derived from a genomic segment previously believed to function as an intron. RP YOSHIMURA, K (reprint author), NHLBI,PULM BRANCH,BETHESDA,MD 20892, USA. NR 41 TC 15 Z9 15 U1 1 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 JAN 5 PY 1993 VL 268 IS 1 BP 686 EP 690 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KE603 UT WOS:A1993KE60300103 PM 7678008 ER PT J AU DRAKE, JW AF DRAKE, JW TI GENERAL ANTIMUTATORS ARE IMPROBABLE SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Note DE ANTIMUTATOR MUTATIONS; BACTERIOPHAGE-T4; EVOLUTION; MUTATOR MUTATIONS ID BACTERIOPHAGE-T4 DNA-POLYMERASE; HERPES-SIMPLEX VIRUS; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE; SPONTANEOUS MUTATION; BIOCHEMICAL BASIS; NUCLEOTIDE SELECTION; INDUCED MUTAGENESIS; MUTANTS; SENSITIVITY RP DRAKE, JW (reprint author), NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709, USA. NR 51 TC 43 Z9 43 U1 0 U2 2 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 JAN 5 PY 1993 VL 229 IS 1 BP 8 EP 13 DI 10.1006/jmbi.1993.1002 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG623 UT WOS:A1993KG62300002 PM 8421317 ER PT J AU HAN, YH AUSTIN, MJF POMMIER, Y POVIRK, LF AF HAN, YH AUSTIN, MJF POMMIER, Y POVIRK, LF TI SMALL DELETION AND INSERTION MUTATIONS INDUCED BY THE TOPOISOMERASE-II INHIBITOR TENIPOSIDE IN CHO CELLS AND COMPARISON WITH SITES OF DRUG-STIMULATED DNA CLEAVAGE INVITRO SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE APRT GENE; VM-26; ILLEGITIMATE RECOMBINATION; CLEAVABLE COMPLEX; SEQUENCE SPECIFICITY ID HAMSTER OVARY CELLS; SISTER CHROMATID EXCHANGES; APRT LOCUS; STRAND CLEAVAGE; SEQUENCE; RECOMBINATION; GENE; MUTANTS C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA08950, CA40615] NR 35 TC 56 Z9 57 U1 0 U2 0 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 JAN 5 PY 1993 VL 229 IS 1 BP 52 EP 66 DI 10.1006/jmbi.1993.1007 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG623 UT WOS:A1993KG62300007 PM 8380617 ER PT J AU ALVORD, WG ROSSIO, JL AF ALVORD, WG ROSSIO, JL TI DETERMINING CONFIDENCE-LIMITS FOR DRUG POTENCY IN IMMUNOASSAY SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE INVERSE REGRESSION; INVERSE CONFIDENCE INTERVAL; NONLINEAR REGRESSION; BIOASSAY; DRUG POTENCY DETERMINATION AB Nonlinear models have frequently been used to characterize dose-response data obtained from biological assays. The effect of a bioactive agent is observed and the model allows prediction of the dose required to obtain the observed effect (the 'inverse prediction'). The precision of this estimate is important in potency determination. Here, a general method is presented for calculating the inverse confidence intervals for estimates of dose potencies obtained from nonlinear models often used to describe these tests. The approach is demonstrated with application of data sets to the negative exponential and four-parameter logistic regression models. Necessary theory is presented and followed by detailed discussion in which estimation strategies are explained and intermediate quantities calculated. C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,CLIN IMMUNOL SERV,FREDERICK,MD 21702. RP ALVORD, WG (reprint author), DATA MANAGEMENT SERV INC,BLDG 362,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74103, N01-CO-74102] NR 14 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD JAN 4 PY 1993 VL 157 IS 1-2 BP 155 EP 163 PG 9 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA KJ505 UT WOS:A1993KJ50500020 PM 8423359 ER PT J AU HOLLSTEIN, MC WILD, CP BLEICHER, F CHUTIMATAEWIN, S HARRIS, CC SRIVATANAKUL, P MONTESANO, R AF HOLLSTEIN, MC WILD, CP BLEICHER, F CHUTIMATAEWIN, S HARRIS, CC SRIVATANAKUL, P MONTESANO, R TI P53 MUTATIONS AND AFLATOXIN-B1 EXPOSURE IN HEPATOCELLULAR-CARCINOMA PATIENTS FROM THAILAND SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID HEPATITIS-B VIRUS; LIVER-CANCER; GENE; INFECTION; ADDUCTS; CHINA AB The prevalence and type of mutations in the p53 tumour-suppressor gene have been determined in 15 hepatocellular carcinomas (HCC) originating from Thailand. Direct sequencing of exons 5-8 revealed 2 mutations. an AGG to AGT (Arg --> Ser) transversion at codon 249, and an ATC --> AAC (Ile --> Asn) transversion at codon 254. Samples from the Thai patients were analyzed for the presence of aflatoxin-liver DNA and aflatoxin-serum albumin adducts, and all but one were found negative. All the patients were genotyped for glutathione-S-transferase (GST) mu, an enzyme possibly involved in the detoxification of AFB1, and 12 out of 15 had the null genotype. In general, the level of aflatoxin-albumin adducts in sera and the prevalence of p53 mutation at codon 249 in HCC were lower than in other areas at high risk of HCC, including southern China and parts of Africa. C1 INT AGCY RES CANC,MECHANISMS CARCINOGENESIS UNIT,150 COURS ALBERT THOMAS,F-69372 LYON,FRANCE. NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. NCI,BANGKOK 10400,THAILAND. FU NCI NIH HHS [5 U01 CA48409-05] NR 30 TC 90 Z9 93 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JAN 2 PY 1993 VL 53 IS 1 BP 51 EP 55 DI 10.1002/ijc.2910530111 PG 5 WC Oncology SC Oncology GA KD949 UT WOS:A1993KD94900010 PM 8380058 ER PT J AU SLAVINCHIORINI, DC HAND, PH KASHMIRI, SVS CALVO, B ZAREMBA, S SCHLOM, J AF SLAVINCHIORINI, DC HAND, PH KASHMIRI, SVS CALVO, B ZAREMBA, S SCHLOM, J TI BIOLOGIC PROPERTIES OF A CH2 DOMAIN-DELETED RECOMBINANT IMMUNOGLOBULIN SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID MONOCLONAL-ANTIBODY B72.3; COLORECTAL-CARCINOMA; TUMOR-LOCALIZATION; ESCHERICHIA-COLI; CANCER-PATIENTS; CELLS; IMMUNOSCINTIGRAPHY; EXPRESSION; BINDING; RADIOLOCALIZATION AB Monoclonal antibody (MAb) B72.3 reacts with TAG-72, a high-molecular-weight mucin expressed on several types of human carcinoma, and is currently being used in clinical trials for the diagnosis and therapy of human carcinoma. An expression construct containing cDNA encoding an immunoglobulin (Ig) heavy chain, with the variable region of murine MAb B72.3 and a human Ig constant region with a deletion of the C(H)2 domain, was generated. Immunoglobulin from the transfectoma with the highest expression of the TAG-72 immunoreactive antibody was designated MAb chimeric (c) B72.3DELTAC(H)2. The pharmacokinetics of serum clearance of iodine-labeled MAbs cB72.3DELTAC(H)2 and the intact cB72.3 were compared in athymic mice. By 24 hr, less than 1 % of the cB72.3DELTAC(H)2 was left in the plasma, while 36% of the cB72.3 still remained. The T1/2alpha values of the cB72.3DELTAC(H)2 and cB72.3 MAbs were 1.7 and 2.4 hr, respectively. The T1/2beta values were 7.8 hr for the domain-deleted cMAb and 48.9 hr for cB72.3. Biodistribution studies in athymic mice bearing LS-174T xenografts showed a reduction in the percentage of injected dose per gram in tumor with I-131-cB72.3DELTAC(H)2; however, the I-131-cB72.3DELTAC(H)2 both localized to tumors faster and cleared from the blood faster than the I-125-cB72.3 MAb. Only trace amounts of the I-131-cB72.3DELTAC(H)2 were detected in normal tissues, including kidney. The faster clearance rate, more rapid tumor targeting and lack of metabolic uptake in normal tissues demonstrated with the iodine-labeled C(H)2 domain-deleted cMAb may be an advantage for certain clinical protocols. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BLDG 10,ROOM 8B07,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 35 TC 37 Z9 38 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JAN 2 PY 1993 VL 53 IS 1 BP 97 EP 103 DI 10.1002/ijc.2910530119 PG 7 WC Oncology SC Oncology GA KD949 UT WOS:A1993KD94900018 PM 8416208 ER PT J AU CERUTTI, P HIRT, B NABHOLZ, M NIGG, E HANAWALT, PC HOEIJMAKERS, JHJ WEEDA, G TROELSTRA, C KOKEN, MHM VANDERSPEK, PJ BOOTSMA, D MAHER, VM CHEN, RH MCGREGOR, WG WANG, YC LUKASH, L MAH, MCM BOLDT, J MCCORMICK, JJ AGUILAR, F POURZAND, C HUSSAIN, P ALBERTINI, RJ NICKLAS, JA ONEILL, JP HARRIS, CC BENNETT, WP LEHMANN, TA FORRESTER, K FELLEYBOSCO, E GERWIN, BI HOLLSTEIN, MC RAUSCHER, FJ CURRAN, T XANTHOUDAKIS, S HERRLICH, P SACHSENMAIER, C GEBEL, S RADLERPOHL, A AUER, HP KRAMER, M RAHMSDORF, HJ AARONSON, SA MARSHALL, CJ ASHWORTH, A HOWE, LR LEEVERS, SJ PATERSON, HF THORNEYCROFT, SG GOMEZ, N NAKIELNY, S TRAVERSE, S COHEN, P AYER, D BLACKWOOD, EM KRETZNER, L TIETJE, K EISENMAN, RN DAYAN, S GALLANT, P KREK, W MARIDOR, G PETER, M MOSES, HL DAGNINO, L FREXESSTEED, M JOHNSON, MD NIGRO, JM PIERCE, DF SOLOMON, E BORROW, J FREEMONT, P GILLARD, E GODDARD, A HOWE, K BERNSTEIN, A ZHANG, LQ LEE, J BERNS, A AF CERUTTI, P HIRT, B NABHOLZ, M NIGG, E HANAWALT, PC HOEIJMAKERS, JHJ WEEDA, G TROELSTRA, C KOKEN, MHM VANDERSPEK, PJ BOOTSMA, D MAHER, VM CHEN, RH MCGREGOR, WG WANG, YC LUKASH, L MAH, MCM BOLDT, J MCCORMICK, JJ AGUILAR, F POURZAND, C HUSSAIN, P ALBERTINI, RJ NICKLAS, JA ONEILL, JP HARRIS, CC BENNETT, WP LEHMANN, TA FORRESTER, K FELLEYBOSCO, E GERWIN, BI HOLLSTEIN, MC RAUSCHER, FJ CURRAN, T XANTHOUDAKIS, S HERRLICH, P SACHSENMAIER, C GEBEL, S RADLERPOHL, A AUER, HP KRAMER, M RAHMSDORF, HJ AARONSON, SA MARSHALL, CJ ASHWORTH, A HOWE, LR LEEVERS, SJ PATERSON, HF THORNEYCROFT, SG GOMEZ, N NAKIELNY, S TRAVERSE, S COHEN, P AYER, D BLACKWOOD, EM KRETZNER, L TIETJE, K EISENMAN, RN DAYAN, S GALLANT, P KREK, W MARIDOR, G PETER, M MOSES, HL DAGNINO, L FREXESSTEED, M JOHNSON, MD NIGRO, JM PIERCE, DF SOLOMON, E BORROW, J FREEMONT, P GILLARD, E GODDARD, A HOWE, K BERNSTEIN, A ZHANG, LQ LEE, J BERNS, A TI GENETIC-DAMAGE AND ESCAPE FROM PROLIFERATION CONTROL - CONFERENCE HELD AT EPALINGES LAUSANNE, SWITZERLAND, JANUARY 14-15, 1993 SO INTERNATIONAL JOURNAL OF CANCER LA English DT Editorial Material ID ACUTE PROMYELOCYTIC LEUKEMIA; IMMUNODEFICIENCY VIRUS TYPE-1; DEPENDENT STRAND BIAS; DNA-BINDING ACTIVITY; WILMS-TUMOR GENE; EXCISION REPAIR; RETINOIC ACID; CELL-CYCLE; HPRT GENE; P53 GENE C1 STANFORD UNIV, DEPT BIOL SCI, STANFORD, CA 94305 USA. ERASMUS UNIV, CTR MED GENET, DEPT CELL BIOL & GENET, 3000 DR ROTTERDAM, NETHERLANDS. MICHIGAN STATE UNIV, DEPT BIOCHEM, CARCINOGENESIS LAB, E LANSING, MI 48824 USA. MICHIGAN STATE UNIV, DEPT MICROBIOL, E LANSING, MI 48824 USA. PENN STATE UNIV, MILTON S HERSHEY MED CTR, HERSHEY, PA 17033 USA. SWISS INST EXPTL CANC RES, DEPT CARCINOGENESIS, CH-1066 EPALINGES, SWITZERLAND. UNIV VERMONT, VCC GENET LAB, BURLINGTON, VT 05401 USA. NCI, HUMAN CARCINOGENESIS LAB, BETHESDA, MD 20892 USA. IARC, LYON, FRANCE. WISTAR INST, PHILADELPHIA, PA 19104 USA. ROCHE INST MOLEC BIOL, RES CTR, DEPT MOLEC ONCOL & VIROL, NUTLEY, NJ 07110 USA. KERNFORSCHUNGSZENTRUM KARLSRUHE GMBH, INST GENET & TOXIKOL, W-7500 KARLSRUHE 1, GERMANY. NCI, CELLULAR & MOLEC BIOL LAB, BETHESDA, MD 20892 USA. INST CANC RES, CHESTER BEATTY LABS, CELL & MOLEC BIOL SECT, LONDON SW3 6JB, ENGLAND. UNIV DUNDEE, DEPT BIOCHEM, MRC, PROT PHOSPHORYLAT UNIT, DUNDEE DD1 4HN, SCOTLAND. FRED HUTCHINSON CANC RES CTR, DIV BASIC SCI, SEATTLE, WA 98104 USA. VANDERBILT UNIV, MED CTR, SCH MED, DEPT CELL BIOL, NASHVILLE, TN 37232 USA. ICRF, LONDON, ENGLAND. MT SINAI HOSP, SAMUEL LUNENFELD RES INST, DIV MOLEC & DEV BIOL, TORONTO M5G 1X5, ONTARIO, CANADA. NETHERLANDS CANC INST, DIV MOLEC GENET, 1066 CX AMSTERDAM, NETHERLANDS. RP CERUTTI, P (reprint author), SWISS INST EXPTL CANC RES, CH-1011 LAUSANNE, SWITZERLAND. RI koken, marcel/J-8154-2012; Curran, Tom/C-1164-2008; Curran, Tom/D-7515-2011; Pourzand, Charareh/L-8853-2016 OI koken, marcel/0000-0002-0839-0125; Curran, Tom/0000-0003-1444-7551; NR 100 TC 0 Z9 0 U1 0 U2 10 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0020-7136 EI 1097-0215 J9 INT J CANCER JI Int. J. Cancer PD JAN 2 PY 1993 VL 53 IS 1 BP 161 EP 177 DI 10.1002/ijc.2910530129 PG 17 WC Oncology SC Oncology GA KD949 UT WOS:A1993KD94900028 ER PT J AU KLEINMAN, A STRAUS, SE AF KLEINMAN, A STRAUS, SE TI CHRONIC FATIGUE SYNDROME - INTRODUCTION SO CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material C1 HARVARD UNIV, SCH MED, DEPT SOCIAL MED, BOSTON, MA 02115 USA. NIAID, CLIN INVEST LAB, BETHESDA, MD 20892 USA. RP KLEINMAN, A (reprint author), HARVARD UNIV, DEPT ANTHROPOL, 25 SHATTUCK ST, BOSTON, MA 02115 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1993 VL 173 BP 1 EP 5 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA KL866 UT WOS:A1993KL86600001 ER PT J AU STRAUS, SE AF STRAUS, SE TI STUDIES OF HERPESVIRUS-INFECTION IN CHRONIC FATIGUE SYNDROME SO CIBA FOUNDATION SYMPOSIA LA English DT Article ID EPSTEIN-BARR-VIRUS; EARLY ANTIGEN; HHV-6; MONONUCLEOSIS; PERSISTENT; ANTIBODY; ILLNESS; HBLV AB The relationship of herpesviruses to chronic fatigue syndrome has received considerable attention over the past decade. Data suggesting an association fall into three major categories. First, among acute precipitants of the syndrome are primary infections with some herpesviruses, most notably Epstein-Barr virus and cytomegalovirus. Second, a series of studies have detailed elevations of antibodies to most herpesviruses in selected chronic fatigue syndrome populations, with Epstein-Barr virus and human herpes type 6 being the objects of most scrutiny. Third, one recent study reported a greater ease of recovery of human herpes virus type 6 from chronic fatigue syndrome patients. This review article critically examines the cumulative data regarding an association between one or more herpesviruses and the chronic fatigue syndrome in the context of the known biology and epidemiology of these agents. In view of these, and additional considerations regarding study methodologies, the conclusion is drawn that herpesviruses are not dominant causes of the chronic fatigue syndrome and may not even be necessary to the perpetuation of the illness, but it is premature to dismiss entirely this latter possibility. RP STRAUS, SE (reprint author), NIAID, CLIN INVEST LAB, BLDG 10, RM 11N228, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 34 TC 0 Z9 0 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1993 VL 173 BP 132 EP 145 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA KL866 UT WOS:A1993KL86600008 ER PT J AU LLOYD, AR WAKEFIELD, D HICKIE, I AF LLOYD, AR WAKEFIELD, D HICKIE, I TI IMMUNITY AND THE PATHOPHYSIOLOGY OF CHRONIC FATIGUE SYNDROME SO CIBA FOUNDATION SYMPOSIA LA English DT Article ID EPSTEIN-BARR VIRUS; HUMAN IMMUNODEFICIENCY VIRUS; IMMUNOLOGICAL ABNORMALITIES; DEPRESSIVE-DISORDERS; B-CELLS; INTERFERON; INFECTION; MONONUCLEOSIS; DYSFUNCTION; BEREAVEMENT AB The pathophysiology of chronic fatigue syndrome (CFS) remains unknown. The syndrome often follows a recognized or presumed infection and the disorder may therefore result from a disordered immune response to a precipitating infection or antigenic challenge. Abnormalities of both humoral and cellular immunity have been demonstrated in a substantial proportion of patients with CFS. The most consistent findings are of impaired lymphocyte responses to mitogen and reduced natural killer cell cytotoxicity. Cutaneous anergy and immunoglobulin G subclass deficiencies have also been found. Further studies are needed examining cytokine levels in serum and cerebrospinal fluid, and cytokine production in vitro in patients with CFS. Interpretation of the findings of published studies of immunity is limited by probable heterogeneity in the patient groups studied, and by the lack of standardization and reproducibility in the assays used. The pattern of abnormalities reported in immunological testing in patients with CFS is consistent with the changes seen during the resolving phases of acute viral infection. These data provide circumstantial support for the hypothesis that CFS results from a disordered immune response to an infection. Longitudinal studies of immunity in patients developing CFS after defined infectious illnesses will provide the best means of further examining this hypothesis. C1 NCI, MOLEC IMMUNOREGULAT LAB, FREDERICK, MD 21702 USA. PRINCE HENRY HOSP, DEPT IMMUNOPATHOL, SYDNEY, NSW 2036, AUSTRALIA. PRINCE HENRY HOSP, DIV PSYCHIAT, MOOD DISORDERS UNIT, SYDNEY, NSW 2036, AUSTRALIA. NR 55 TC 0 Z9 0 U1 2 U2 2 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1993 VL 173 BP 176 EP 192 PG 17 WC Medicine, General & Internal SC General & Internal Medicine GA KL866 UT WOS:A1993KL86600011 ER PT B AU MOSCICKI, EK AF MOSCICKI, EK GP WORLD CONF ON INJURY CONTROL TI Advances in suicide prevention: An overview SO 2ND WORLD CONFERENCE ON INJURY CONTROL, 1993 - PROCEEDINGS OF THE PLENARY SESSIONS LA English DT Proceedings Paper CT 2nd World Conference on Injury Control CY MAY 20-23, 1993 CL ATLANTA, GA SP Assoc Adv Automot Med, Assoc Adv Injury Control, Natl Council Disabil, US Dept Transportat, Natl Highway Traff Safety Adm, WHO, Pan Amer Hlth Org, US Consumer Prod Safety Commiss, US Dept HHS, Agcy Hlth Care Policy & Res, Hlth Resources & Serv Adm, Indian Hlth Serv, NIH, HICHHD, Ctr Dis Control & Prevent C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSOC ADVANCEMENT AUTOMOTIVE MEDICINE PI DES PLAINES PA 2340 DES PLAINES AVE, STE 106, DES PLAINES, IL 60018 PY 1993 BP 77 EP 83 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA BD85Q UT WOS:A1993BD85Q00017 ER PT J AU CRAGG, GM BOYD, MR CARDELLINA, JH GREVER, MR SCHEPARTZ, SA SNADER, KM SUFFNESS, M AF CRAGG, GM BOYD, MR CARDELLINA, JH GREVER, MR SCHEPARTZ, SA SNADER, KM SUFFNESS, M TI ROLE OF PLANTS IN THE NATIONAL-CANCER-INSTITUTE DRUG DISCOVERY AND DEVELOPMENT PROGRAM SO ACS SYMPOSIUM SERIES LA English DT Review ID PHASE-II; NATURAL-PRODUCTS; ANTITUMOR AGENTS; TAXOL; HIV-1; LUNG; CAMPTOTHECIN; 4-IPOMEANOL; ANALOGS AB Over the past 30 years the National Cancer Institute (NCI) has developed a number of plant-derived drugs which have undergone clinical trials. Prior to 1986, plant collections were generally restricted to temperate areas of the world. Since then, collections have focused on tropical, primarily rainforest, regions, and to date over 28,000 plant samples have been collected from over 20 countries. Policies have been formulated aimed at establishing collaborations with scientists in these countries and providing long-term compensation to source countries for drugs which are developed as marketable products. The various facets of the NCI drug discovery and development program are discussed, including future plans for the large-scale production of biomass for the isolation of promising new anticancer and antiviral natural products. RP CRAGG, GM (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892, USA. NR 44 TC 29 Z9 29 U1 1 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0097-6156 J9 ACS SYM SER PY 1993 VL 534 BP 80 EP 95 PG 16 WC Chemistry, Multidisciplinary SC Chemistry GA LX112 UT WOS:A1993LX11200007 ER PT J AU CARDELLINA, JH GUSTAFSON, KR BEUTLER, JA MCKEE, TC HALLOCK, YF FULLER, RW BOYD, MR AF CARDELLINA, JH GUSTAFSON, KR BEUTLER, JA MCKEE, TC HALLOCK, YF FULLER, RW BOYD, MR TI NATIONAL-CANCER-INSTITUTE INTRAMURAL RESEARCH ON HUMAN-IMMUNODEFICIENCY-VIRUS INHIBITORY AND ANTITUMOR PLANT NATURAL-PRODUCTS SO ACS SYMPOSIUM SERIES LA English DT Review ID TUMOR-CELL-LINES; NONPROMOTING PHORBOL; DERIVATIVES; ALKALOIDS; HIV-1 AB The natural products drug discovery program of the United States National Cancer Institute (NCI) was dramatically reorganized and revitalized during the mid-to-late 1980's. One component of the overall strategic approach was the creation of the first-ever intramural, interdisciplinary research unit, the Laboratory of Drug Discovery Research and Development (LDDRD), with a central focus on natural products. LDDRD scientists identify leads from extracts housed in the NCI Natural Products Repository and screened in the high throughput in vitro antitumor and AIDS-antiviral bioassays, isolate and identify the antitumor and/or antiviral agents through bioassay-guided fractionation and spectral analyses, and examine in detail the biological activity of the isolated compounds. This report focuses on some selected illustrative examples of LDDRD research on HIV-inhibitory and antitumor plant natural products. RP CARDELLINA, JH (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702, USA. RI Beutler, John/B-1141-2009 OI Beutler, John/0000-0002-4646-1924 NR 22 TC 11 Z9 11 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0097-6156 J9 ACS SYM SER PY 1993 VL 534 BP 218 EP 227 PG 10 WC Chemistry, Multidisciplinary SC Chemistry GA LX112 UT WOS:A1993LX11200015 ER PT J AU GLAUDEMANS, CPJ BENNETT, LG BHATTACHARJEE, AK NASHED, EM ZIEGLER, T AF GLAUDEMANS, CPJ BENNETT, LG BHATTACHARJEE, AK NASHED, EM ZIEGLER, T TI DISTINGUISHING ANTIBODIES THAT BIND INTERNAL ANTIGENIC DETERMINANTS FROM THOSE THAT BIND THE ANTIGENIC CHAIN-TERMINUS ONLY SO ACS SYMPOSIUM SERIES LA English DT Review ID MYELOMA PROTEINS; DEXTRAN; SPECIFICITY; SUBSITES; SITES AB The binding of monoclonal antibodies to polymeric antigens is discussed. Once the immuno-determinant, and its affinity for the antibody, is known, a measurement using the entire polymeric antigen and the Fab or Fab' fragment of the antibody can quickly establish if the antibody can read that determinant at any position in the antigen's polymeric chain, or if it is limited to binding that determinant only when it is located at the chain terminus. RP GLAUDEMANS, CPJ (reprint author), NIDDKD,CARBOHYDRATES SECT,BETHESDA,MD 20892, USA. NR 24 TC 4 Z9 4 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0097-6156 J9 ACS SYM SER PY 1993 VL 519 BP 72 EP 79 PG 8 WC Chemistry, Multidisciplinary SC Chemistry GA KH055 UT WOS:A1993KH05500006 ER PT J AU SHERMAN, ME WEINSTEIN, M SUGHAYER, M CAPPELLARI, JO ORR, JE EROZAN, YS SCHIFFMAN, MH KURMAN, RJ AF SHERMAN, ME WEINSTEIN, M SUGHAYER, M CAPPELLARI, JO ORR, JE EROZAN, YS SCHIFFMAN, MH KURMAN, RJ TI THE BETHESDA SYSTEM - IMPACT ON REPORTING CERVICOVAGINAL SPECIMENS AND REPRODUCIBILITY OF CRITERIA FOR ASSESSING ENDOCERVICAL SAMPLING SO ACTA CYTOLOGICA LA English DT Article ID CERVICAL SMEARS; CELLULAR COMPOSITION; PAPANICOLAOU SMEARS; CELLS; DIAGNOSIS; CYTOLOGY; WOMEN AB This study examined the impact of applying the Bethesda System guidelines for specimen adequacy on cytopathologic diagnosis at the Johns Hopkins Hospital laboratory of cytopathology during a one-year period. Application of the Bethesda guidelines resulted in a 1.3% unsatisfactory rate. In addition, 3.8% of specimens were satisfactory but contained an inadequate endocervical component (IEC). Smears obtained after a cone biopsy or an initial IEC smear were IEC in 16.5% and 18.7% of cases, respectively. The IEC rate following an initial smear lacking an endocervical component was 11.8% in repeat specimens obtained with an endocervical brush as compared to 29.4% in those obtained with a spatula alone. The reproducibility of the Bethesda criteria for assessing endocervical sampling was evaluated by comparing the level of agreement between three independent reviewers examining 40 test cases. Three-way agreement was achieved in 75% of cases. Two-way agreement ranged from 80.0% to 87.5%. We conclude that implementation of the Bethesda System guidelines for assessing specimen adequacy should produce a minimal impact on cytopathologic reporting and gynecologic practice. Repeat specimens lacking an endocervical component may be encountered relatively frequently in certain subsets of patients. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. RP SHERMAN, ME (reprint author), JOHNS HOPKINS UNIV HOSP,406 PATHOL,600 N WOLFE ST,BALTIMORE,MD 21205, USA. NR 20 TC 10 Z9 10 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 0001-5547 J9 ACTA CYTOL JI Acta Cytol. PD JAN-FEB PY 1993 VL 37 IS 1 BP 55 EP 60 PG 6 WC Pathology SC Pathology GA KZ885 UT WOS:A1993KZ88500010 PM 8434497 ER PT J AU WAKAYAMA, I NERURKAR, VR GARRUTO, RM AF WAKAYAMA, I NERURKAR, VR GARRUTO, RM TI IMMUNOCYTOCHEMICAL AND ULTRASTRUCTURAL EVIDENCE OF DENDRITIC DEGENERATION IN MOTOR NEURONS OF ALUMINUM-INTOXICATED RABBITS SO ACTA NEUROPATHOLOGICA LA English DT Article DE ALUMINUM; SPINAL MOTOR NEURON; DENDRITE; MICROTUBULE-ASSOCIATED PROTEIN-2; NEUROFILAMENT ID EXPERIMENTAL NEUROFIBRILLARY CHANGES; MICROTUBULE-ASSOCIATED PROTEIN-2; SYSTEMIC ALUMINUM; CHRONIC ANIMALS; BRAIN; TANGLES; ACCUMULATION; EXPRESSION; MYELOPATHY; PATHOLOGY AB Using immunocytochemical and ultrastructural methods, we observed extensive and characteristic dendritic changes in motor neurons of rabbits inoculated intracisternally with aluminum phosphate. Anti-microtubule-associated protein 2 immunostaining revealed markedly reduced immunoreactivity in motor neuron dendrites and a reduced number of dendritic trees in aluminum phosphate-intoxicated rabbits. These dendritic changes were confirmed at the ultrastructural level; neurofilamentous accumulations, membranous inclusions and disrupted microtubules were common features of motor neuron dendrites, but less prominent in motor neuron axons. These observations suggest that dendrites are characteristically involved in aluminum intoxication in addition to the widely reported accumulation of phosphorylated neurofilament in perikarya and axons. C1 NATL INST NEUROL DISORDERS & STROKE,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. NR 41 TC 7 Z9 8 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0001-6322 J9 ACTA NEUROPATHOL JI Acta Neuropathol. PD JAN PY 1993 VL 85 IS 2 BP 122 EP 128 PG 7 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA KJ618 UT WOS:A1993KJ61800002 PM 8442404 ER PT J AU NAKAMURA, A KUMAZAWA, T LIM, DJ DEMARIA, TF VANBLITTERSWIJK, CA AF NAKAMURA, A KUMAZAWA, T LIM, DJ DEMARIA, TF VANBLITTERSWIJK, CA TI CULTURE OF MIDDLE-EAR EPITHELIUM - A REVIEW SO ACTA OTO-LARYNGOLOGICA LA English DT Review DE TISSUE CULTURE; EPITHELIAL CELL; EAR RESEARCH AB We discuss several techniques of culturing middle ear epithelium from several species, which was formerly difficult but is now possible because of recent advances in culture methods. The three main methods of initiating a culture are organ culture, primary explant culture, and cell culture. Although each method has both advantages and disadvantages, investigators can choose the method most suitable to their purpose. A few researchers, including ourselves, have succeeded in obtaining serial culture of middle ear epithelium. Using 3T3 feeder layer technique or conditioned medium enabled us to develop a fibroblast-free cultured middle ear epithelium. The availability of cultured middle ear epithelium provides a potential tool in future middle ear research. C1 NIDCD,DIV INTRAMURAL PROGRAM,BETHESDA,MD. OHIO STATE UNIV,COLL MED,OTOL RES LABS,COLUMBUS,OH 43210. LEIDEN UNIV,DEPT OTOLARYNGOL,2300 RA LEIDEN,NETHERLANDS. RP NAKAMURA, A (reprint author), KANSAI MED UNIV,DEPT OTOLARYNGOL,MORIGUCHI,OSAKA 570,JAPAN. OI van Blitterswijk, Clemens/0000-0003-2371-4615 NR 24 TC 6 Z9 6 U1 0 U2 2 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6489 J9 ACTA OTO-LARYNGOL JI Acta Oto-Laryngol. PY 1993 SU 500 BP 75 EP 79 PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA KL237 UT WOS:A1993KL23700021 ER PT J AU SCHULSINGER, C MEDNICK, BR KLEBANOFF, MA SECHER, NJ TEASDALE, TW BAKER, RL AF SCHULSINGER, C MEDNICK, BR KLEBANOFF, MA SECHER, NJ TEASDALE, TW BAKER, RL TI DELIVERY OF PRETERM AND SMALL-FOR-GESTATIONAL-AGE INFANTS ACROSS GENERATIONS SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE PERINATAL HEALTH; RISK FACTOR; LONGITUDINAL STUDY; PREMATURE BIRTH; LOW BIRTH WEIGHT AB Two generations of women were studied to clarify the influence of a woman's own preterm delivery or intrauterine growth retardation on her later risk of delivering preterm or growth-retarded infants. The first generation consists of the cohort of women who gave birth at the National University Hospital (Rigshospitalet) in Copenhagen from 1959 to 1961 and the second, those of their daughters that have delivered themselves. The background of the study and the procedures involved are described. The percentage of data obtained and the preliminary findings concerning the relationship between social and demographic factors and the willingness of subjects to participate are included. C1 COPENHAGEN HLTH SERV,INST PREVENT MED,COPENHAGEN,DENMARK. UNIV COPENHAGEN,REHABIL CTR BRAIN DAMAGE,DK-1168 COPENHAGEN,DENMARK. NICHHD,BETHESDA,MD 20892. UNIV SO CALIF,DEPT EDUC PSYCHOL,LOS ANGELES,CA 90089. AARHUS UNIV,AARHUS KOMMUNE HOSP,DEPT GYNAECOL,DK-8000 AARHUS,DENMARK. NR 11 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-690X J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PY 1993 VL 87 SU 370 BP 62 EP 66 DI 10.1111/j.1600-0447.1993.tb05362.x PG 5 WC Psychiatry SC Psychiatry GA KQ213 UT WOS:A1993KQ21300010 ER PT J AU DAWSON, DA AF DAWSON, DA TI PATTERNS OF ALCOHOL-CONSUMPTION - BEVERAGE EFFECTS ON GENDER DIFFERENCES SO ADDICTION LA English DT Article AB This Data Note reports findings from 22 102 current drinkers who responded in the US National Interview Survey in 1988. Mean estimated alcohol intake of males exceeded that of females by a factor of two. Males drank more per occasion (ratio 1.45) and drank on more occasions (1.41). Mean ethanol content per drink was slightly less for males (ratio 0.95) attributable to a decreased proportion of drinks being wine and liquor. When beverage preferences were taken into account, the drinking patterns of males and females showed no meaningful differences among persons with similar levels of overall ethanol intake. The results do not support the view that the difference between ethanol consumption of males and females are due primarily to males drinking more per occasion. Apparent differences in drinking patterns are attributable to differences in preferred beverage. RP DAWSON, DA (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 7 TC 27 Z9 27 U1 0 U2 1 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0965-2140 J9 ADDICTION JI Addiction PD JAN PY 1993 VL 88 IS 1 BP 133 EP 138 DI 10.1111/j.1360-0443.1993.tb02771.x PG 6 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA KM838 UT WOS:A1993KM83800023 PM 8448504 ER PT J AU MANDERSCHEID, RW AF MANDERSCHEID, RW TI DEVELOPMENTS IN MENTAL-HEALTH STATISTICS SO ADMINISTRATION AND POLICY IN MENTAL HEALTH LA English DT Article RP MANDERSCHEID, RW (reprint author), NIMH,CTR MENTAL HLTH SERV,SURVEY & ANAL BRANCH,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 0 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 JAN PY 1993 VL 20 IS 3 BP 193 EP 196 DI 10.1007/BF00713956 PG 4 WC Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA KM227 UT WOS:A1993KM22700006 ER PT J AU CHIN, KV PASTAN, I GOTTESMAN, MM AF CHIN, KV PASTAN, I GOTTESMAN, MM TI FUNCTION AND REGULATION OF THE HUMAN MULTIDRUG-RESISTANCE GENE SO ADVANCES IN CANCER RESEARCH LA English DT Review ID P-GLYCOPROTEIN GENE; KB CARCINOMA-CELLS; REGENERATING RAT-LIVER; HAMSTER OVARY CELLS; HUMAN MDR1 GENE; DRUG-RESISTANCE; TRANSGENIC MICE; PROTEIN-KINASE; TUMOR-CELLS; BONE-MARROW C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RI Chin, Khew-Voon/F-2670-2013 NR 107 TC 185 Z9 189 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0065-230X J9 ADV CANCER RES JI Adv. Cancer Res. PY 1993 VL 60 BP 157 EP 180 PG 24 WC Oncology SC Oncology GA MC970 UT WOS:A1993MC97000005 PM 8417499 ER PT J AU GREENWALD, P MALONE, WF CERNY, ME STERN, HR AF GREENWALD, P MALONE, WF CERNY, ME STERN, HR TI CANCER PREVENTION RESEARCH TRIALS SO ADVANCES IN CANCER RESEARCH, VOL 61 SE ADVANCES IN CANCER RESEARCH LA English DT Review ID EPITHELIAL-CELL PROLIFERATION; FAMILIAL ADENOMATOUS POLYPOSIS; INTERMEDIATE END-POINTS; DIETARY WHEAT BRAN; LARGE-BOWEL CANCER; COLON CANCER; COLORECTAL-CANCER; BREAST-CANCER; CHEMOPREVENTION RESEARCH; ANIMAL-MODELS C1 PROSPECT ASSOCIATES,ROCKVILLE,MD 20852. RP GREENWALD, P (reprint author), NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892, USA. NR 74 TC 25 Z9 25 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0065-230X J9 ADV CANCER RES JI Adv.Cancer Res. PY 1993 VL 61 BP 1 EP 23 PG 23 WC Oncology SC Oncology GA BZ72Z UT WOS:A1993BZ72Z00001 PM 8346716 ER PT B AU DOSZKOCS, TE SASS, RK AF DOSZKOCS, TE SASS, RK BE Fidel, R Kwasnik, BH Smith, PJ TI AN ASSOCIATIVE SEMANTIC NETWORK FOR MACHINE-AIDED INDEXING, CLASSIFICATION AND SEARCHING SO ADVANCES IN CLASSIFICATION RESEARCH, VOL 3: PROCEEDINGS OF THE 3RD ASIS SIG/CR CLASSIFICATION RESEARCH WORKSHOP SE ASIS MONOGRAPH SERIES LA English DT Proceedings Paper CT 3rd ASIS SIG/CR Classification Research Workshop CY OCT 25, 1992 CL PITTSBURGH, PA SP AMER SOC INFORMAT SCI, SPECIAL INTEREST GRP CLASSIFICAT RES C1 NATL LIB MED,OFF COMP & COMMUN SYST,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INFORMATION TODAY INC PI MEDFORD PA 143 OLD MARLTON PIKE, MEDFORD, NJ 08055 BN 0-938734-79-2 J9 ASIS MONOGR PY 1993 BP 15 EP 35 PG 21 WC Information Science & Library Science SC Information Science & Library Science GA BB37T UT WOS:A1993BB37T00002 ER PT B AU HUMPHREY, SM AF HUMPHREY, SM BE Fidel, R Kwasnik, BH Smith, PJ TI CONTEXTUAL HIERARCHIES IN CLASSIFICATION SCHEMES SO ADVANCES IN CLASSIFICATION RESEARCH, VOL 3: PROCEEDINGS OF THE 3RD ASIS SIG/CR CLASSIFICATION RESEARCH WORKSHOP SE ASIS MONOGRAPH SERIES LA English DT Proceedings Paper CT 3rd ASIS SIG/CR Classification Research Workshop CY OCT 25, 1992 CL PITTSBURGH, PA SP AMER SOC INFORMAT SCI, SPECIAL INTEREST GRP CLASSIFICAT RES C1 NATL LIB MED,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INFORMATION TODAY INC PI MEDFORD PA 143 OLD MARLTON PIKE, MEDFORD, NJ 08055 BN 0-938734-79-2 J9 ASIS MONOGR PY 1993 BP 47 EP 60 PG 14 WC Information Science & Library Science SC Information Science & Library Science GA BB37T UT WOS:A1993BB37T00004 ER PT J AU KAUFMAN, S AF KAUFMAN, S TI THE PHENYLALANINE HYDROXYLATING SYSTEM SO ADVANCES IN ENZYMOLOGY AND RELATED AREAS OF MOLECULAR BIOLOGY, VOL 67 SE ADVANCES IN ENZYMOLOGY AND RELATED AREAS OF MOLECULAR BIOLOGY LA English DT Review ID DIHYDROPTERIDINE REDUCTASE DEFICIENCY; ADRENAL TYROSINE-HYDROXYLASE; DEPENDENT PROTEIN-KINASE; AMINO-ACID-SEQUENCE; RAT-LIVER CELLS; NON-HEME IRON; PARTIAL-PURIFICATION; LIMITED PROTEOLYSIS; CELLULAR-REGULATION; HUMAN-PLATELETS RP KAUFMAN, S (reprint author), NIMH,NEUROCHEM LAB,BETHESDA,MD 20892, USA. NR 308 TC 133 Z9 133 U1 1 U2 13 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 3RD AVE, NEW YORK, NY 10016 SN 0065-258X J9 ADV ENZYMOL RAMB PY 1993 VL 67 BP 77 EP 264 PG 188 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BB86W UT WOS:A1993BB86W00002 PM 8322620 ER PT S AU SAX, CM PIATIGORSKY, J AF SAX, CM PIATIGORSKY, J BE Meister, A TI EXPRESSION OF THE ALPHA-CRYSTALLIN SMALL HEAT-SHOCK PROTEIN MOLECULAR CHAPERONE GENES IN THE LENS AND OTHER TISSUES SO ADVANCES IN ENZYMOLOGY AND RELATED AREAS OF MOLECULAR BIOLOGY, VOL 69 SE ADVANCES IN ENZYMOLOGY AND RELATED AREAS OF MOLECULAR BIOLOGY LA English DT Review ID NF-KAPPA-B; MAJOR HISTOCOMPATIBILITY COMPLEX; CREUTZFELDT-JAKOB DISEASE; NON-LENTICULAR TISSUES; TATA-BINDING PROTEIN; NIH 3T3 FIBROBLASTS; A-CRYSTALLIN; TRANSGENIC MICE; SKELETAL-MUSCLE; NUCLEAR PROTEINS RP NEI, MOLEC & DEV BIOL LAB, BETHESDA, MD 20892 USA. NR 176 TC 1 Z9 1 U1 1 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0065-258X BN 0-471-01767-1 J9 ADV ENZYMOL RAMB JI Adv. Enzymol. Relat. Areas Mol. Biol. PY 1993 VL 69 BP 155 EP 201 PG 47 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BB39K UT WOS:A1993BB39K00005 ER PT S AU PAUL, WE SEDER, RA PLAUT, M AF PAUL, WE SEDER, RA PLAUT, M BE Dixon, FJ TI LYMPHOKINE AND CYTOKINE PRODUCTION BY FC-EPSILON-RI(+) CELLS SO ADVANCES IN IMMUNOLOGY, VOL 53 SE Advances in Immunology LA English DT Review ID CONNECTIVE-TISSUE-TYPE; NON-T CELLS; STIMULATORY FACTOR-I; MOUSE MAST-CELLS; FC-EPSILON-RI; SPLENIC NON-B; RECEPTOR-MEDIATED ACTIVATION; HIGH-AFFINITY RECEPTOR; NECROSIS-FACTOR-ALPHA; MURINE IMMUNE-SYSTEM C1 NIAID, ASTHMA & ALLERGY BRANCH, BETHESDA, MD 20892 USA. RP NIAID, IMMUNOL LAB, BETHESDA, MD 20892 USA. NR 97 TC 105 Z9 105 U1 1 U2 1 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0065-2776 BN 0-12-022453-4 J9 ADV IMMUNOL JI Adv.Immunol. PY 1993 VL 53 BP 1 EP 29 DI 10.1016/S0065-2776(08)60496-4 PG 29 WC Immunology SC Immunology GA BZ73D UT WOS:A1993BZ73D00001 PM 8512033 ER PT J AU STANLEY, JR AF STANLEY, JR TI CELL-ADHESION MOLECULES AS TARGETS OF AUTOANTIBODIES IN PEMPHIGUS AND PEMPHIGOID, BULLOUS DISEASES DUE TO DEFECTIVE EPIDERMAL-CELL ADHESION SO ADVANCES IN IMMUNOLOGY, VOL 53 SE ADVANCES IN IMMUNOLOGY LA English DT Review ID UVOMORULIN-CATENIN COMPLEX; CALCIUM-SENSITIVE EPITOPE; DIFFERENT ANTIGEN SOURCES; MEMBRANE ZONE ANTIBODIES; ULTRASTRUCTURAL-LOCALIZATION; FOLIACEUS ANTIGEN; DESMOPLAKIN-I; DESMOSOMAL GLYCOPROTEIN; HUMAN KERATINOCYTES; STRUCTURAL-ANALYSIS RP STANLEY, JR (reprint author), NCI,DERMATOL BRANCH,BETHESDA,MD 20892, USA. NR 145 TC 204 Z9 211 U1 1 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0065-2776 J9 ADV IMMUNOL JI Adv.Immunol. PY 1993 VL 53 BP 291 EP 325 DI 10.1016/S0065-2776(08)60503-9 PG 35 WC Immunology SC Immunology GA BZ73D UT WOS:A1993BZ73D00008 PM 8512037 ER PT J AU DACUNHA, A EIDEN, LE AF DACUNHA, A EIDEN, LE TI NEURO-AIDS - PRIMATE LENTIVIRUS INFECTION AND THE BRAIN SO ADVANCES IN NEUROIMMUNOLOGY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR-NECROSIS-FACTOR; CENTRAL-NERVOUS-SYSTEM; TRANSFORMING GROWTH-FACTOR; IMMUNE-DEFICIENCY-SYNDROME; MAJOR HISTOCOMPATIBILITY COMPLEX; CORTICOTROPIN-RELEASING FACTOR; HTLV-III; CEREBROSPINAL-FLUID; DEMENTIA COMPLEX RP DACUNHA, A (reprint author), NIMH,CELL BIOL LAB,MOLEC NEUROSCI SECT,BETHESDA,MD 20892, USA. OI Eiden, Lee/0000-0001-7524-944X NR 182 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-5428 J9 ADV NEUROIMMUNOL JI Adv. Neuroimmunol. PY 1993 VL 3 IS 2 BP 97 EP 127 DI 10.1016/S0960-5428(06)80042-2 PG 31 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA LK278 UT WOS:A1993LK27800003 ER PT J AU WATSON, RR GOTTESFELD, Z AF WATSON, RR GOTTESFELD, Z TI NEUROIMMUNE EFFECTS OF ALCOHOL AND ITS ROLE IN AIDS SO ADVANCES IN NEUROIMMUNOLOGY LA English DT Review ID CORTICOTROPIN-RELEASING FACTOR; PITUITARY-ADRENAL AXIS; NORADRENERGIC SYNAPTIC TRANSMISSION; TUMOR-NECROSIS-FACTOR; FREELY-MOVING RATS; ADRENOCORTICOTROPIC HORMONE; ETHANOL-CONSUMPTION; FETAL ALCOHOL; IMMUNE-SYSTEM; ACTH RELEASE C1 UNIV TEXAS,SCH MED,DEPT NEUROBIOL & ANAT,HOUSTON,TX 77225. RP WATSON, RR (reprint author), UNIV ARIZONA,SCH MED,NIAAA,ALCOHOL RES CTR,DEPT FAMILY & COMMUNITY MED,TUCSON,AZ 85724, USA. NR 107 TC 8 Z9 8 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-5428 J9 ADV NEUROIMMUNOL JI Adv. Neuroimmunol. PY 1993 VL 3 IS 2 BP 151 EP 162 DI 10.1016/S0960-5428(06)80045-8 PG 12 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA LK278 UT WOS:A1993LK27800006 ER PT S AU AARONSON, SA MIKI, T MEYERS, K CHAN, A AF AARONSON, SA MIKI, T MEYERS, K CHAN, A BE Zappia, V Salvatore, M DellaRagione, R TI GROWTH-FACTORS AND MALIGNANT TRANSFORMATION SO ADVANCES IN NUTRITION AND CANCER SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Review CT International Conference on Nutrition and Cancer CY NOV 20-21, 1992 CL NATL TUMOR INST FDN PASCALE, NAPLES, ITALY SP CNR, SOC ITALIANA BIOCHIM, CTR INT STUDI ALIMENTAZ, CNR, IST SCI ALIMENTAZ AVELLINO, BECKMAN ANAL S P A, PIERREL S P A HO NATL TUMOR INST FDN PASCALE RP AARONSON, SA (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44670-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1993 VL 348 BP 7 EP 22 PG 16 WC Oncology; Public, Environmental & Occupational Health; Nutrition & Dietetics SC Oncology; Public, Environmental & Occupational Health; Nutrition & Dietetics GA BZ51U UT WOS:A1993BZ51U00001 PM 8172024 ER PT J AU KINCAID, R AF KINCAID, R TI CALMODULIN-DEPENDENT PROTEIN PHOSPHATASES FROM MICROORGANISMS TO MAN - A STUDY IN STRUCTURAL CONSERVATISM AND BIOLOGICAL DIVERSITY SO ADVANCES IN SECOND MESSENGER AND PHOSPHOPROTEIN RESEARCH LA English DT Review ID RABBIT SKELETAL-MUSCLE; CATALYTIC SUBUNIT; CALCINEURIN-A; PHOSPHOPROTEIN PHOSPHATASE; DICTYOSTELIUM-DISCOIDEUM; BINDING PROTEINS; SACCHAROMYCES-CEREVISIAE; CELLULAR-REGULATION; PROBABLE IDENTITY; MAMMALIAN BRAIN RP KINCAID, R (reprint author), NIAAA,IMMUNOL SECT,ROCKVILLE,MD 20852, USA. NR 61 TC 67 Z9 68 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1040-7952 J9 ADV SEC MESS PHOSPH JI Adv. Second Messenger Phosphoprot. Res. PY 1993 VL 27 BP 1 EP 23 PG 23 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KG219 UT WOS:A1993KG21900001 PM 8380326 ER PT J AU CLERICI, M AF CLERICI, M TI CELL-MEDIATED-IMMUNITY IN HIV-INFECTION SO AIDS LA English DT Article DE HIV; T-LYMPHOCYTES; LYMPHOKINES; IMMUNE RESPONSE ID HUMAN-IMMUNODEFICIENCY-VIRUS; TOXIC LYMPHOCYTE-T; SELECTIVE LOSS; HELPER CELL; SEROPOSITIVE INDIVIDUALS; CYTOKINE PRODUCTION; SYNTHETIC PEPTIDES; RESPONSES; TYPE-1; SUPPRESSION RP CLERICI, M (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B-17,BETHESDA,MD 20892, USA. NR 65 TC 15 Z9 15 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PY 1993 VL 7 SU 1 BP S135 EP S140 DI 10.1097/00002030-199301001-00018 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LE916 UT WOS:A1993LE91600018 PM 8363777 ER PT J AU FAST, PE WALKER, MC AF FAST, PE WALKER, MC TI HUMAN TRIALS OF EXPERIMENTAL AIDS VACCINES SO AIDS LA English DT Review DE AIDS; HIV-1; HIV VACCINES; VACCINE CLINICAL TRIALS ID HUMAN-IMMUNODEFICIENCY-VIRUS; TOXIC LYMPHOCYTES-T; NEUTRALIZING ANTIBODIES; SEROPOSITIVE INDIVIDUALS; ENVELOPE GLYCOPROTEIN; SYNTHETIC PEPTIDES; RECOMBINANT GP160; PROLIFERATIVE RESPONSES; CANDIDATE VACCINE; INFECTED CELLS RP FAST, PE (reprint author), NIAID,DIV AIDS,VACCINE RES & DEV BRANCH,SOLAR BLDG,ROOM 2B-06,BETHESDA,MD 20892, USA. NR 124 TC 42 Z9 42 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PY 1993 VL 7 SU 1 BP S147 EP S159 DI 10.1097/00002030-199301001-00020 PG 13 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LE916 UT WOS:A1993LE91600020 PM 8363779 ER PT J AU FELBER, BK PAVLAKIS, GN AF FELBER, BK PAVLAKIS, GN TI MOLECULAR-BIOLOGY OF HIV-1 - POSITIVE AND NEGATIVE REGULATORY ELEMENTS IMPORTANT FOR VIRUS EXPRESSION SO AIDS LA English DT Review DE GENE REGULATION; TAT; REV; INHIBITORY INSTABILITY ELEMENTS (INS); RNA STABILITY; TRANSCRIPTIONAL AND POSTTRANSCRIPTIONAL REGULATION ID HUMAN-IMMUNODEFICIENCY-VIRUS; LONG TERMINAL REPEAT; HTLV-I REX; STRUCTURAL GENE-EXPRESSION; RNA RESPONSE ELEMENTS; VIRAL MESSENGER-RNA; TRANS-ACTIVATOR GENE; TAR RNA; TYPE-1 REV; TRANSCRIPTIONAL REGULATION C1 NCI, FREDERICK CANC RES & DEV CTR, HUMAN RETROVIRUS SECT, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, HUMAN RETROVIRUS PATHOGENESIS GRP, FREDERICK, MD 21701 USA. FU NCI NIH HHS [N01-CO-74101] NR 137 TC 36 Z9 37 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0269-9370 J9 AIDS JI Aids PY 1993 VL 7 SU 1 BP S51 EP S62 DI 10.1097/00002030-199301001-00007 PG 12 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LE916 UT WOS:A1993LE91600007 PM 8363803 ER PT J AU GIRARD, MP SHEARER, GM AF GIRARD, MP SHEARER, GM TI VACCINES AND IMMUNOLOGY - OVERVIEW SO AIDS LA English DT Editorial Material C1 NCI,DIV CANC BIOL DIAG & CTR,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B-17,BETHESDA,MD 20892. INST PASTEUR,F-75724 PARIS 15,FRANCE. NR 2 TC 1 Z9 1 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PY 1993 VL 7 SU 1 BP S115 EP S116 DI 10.1097/00002030-199301001-00015 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LE916 UT WOS:A1993LE91600015 PM 8363776 ER PT J AU PANTALEO, G GRAZIOSI, C FAUCI, AS AF PANTALEO, G GRAZIOSI, C FAUCI, AS TI THE ROLE OF LYMPHOID ORGANS IN THE IMMUNOPATHOGENESIS OF HIV-INFECTION SO AIDS LA English DT Article DE HIV; VIRAL BURDEN; TISSUE DISTRIBUTION; LYMPHOID ORGANS; HISTOPATHOLOGIC ALTERATIONS; FOLLICULAR DENDRITIC CELLS ID HUMAN-IMMUNODEFICIENCY-VIRUS; FOLLICULAR DENDRITIC CELLS; ACCESSORY CELLS; AIDS; LYMPHADENOPATHY; LYMPHOCYTES; INDIVIDUALS; MECHANISMS; RESERVOIRS; NODES RP PANTALEO, G (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM IIB13,BETHESDA,MD 20892, USA. RI Pantaleo, Giuseppe/K-6163-2016 NR 29 TC 38 Z9 38 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PY 1993 VL 7 SU 1 BP S19 EP S23 DI 10.1097/00002030-199301001-00003 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LE916 UT WOS:A1993LE91600003 PM 8363784 ER PT J AU SCHULTZ, AM HU, SL AF SCHULTZ, AM HU, SL TI PRIMATE MODELS FOR HIV VACCINES SO AIDS LA English DT Article DE VACCINE; CHIMPANZEE; MACAQUE; SIMIAN IMMUNODEFICIENCY VIRUS (SIV); HIV; ANIMAL MODEL; AIDS ID SIMIAN IMMUNODEFICIENCY VIRUS; AFRICAN-GREEN MONKEYS; SOOTY MANGABEY MONKEYS; RHESUS-MONKEYS; EXPERIMENTAL-INFECTION; CYNOMOLGUS MONKEYS; MACAQUE MONKEYS; PROVIRAL DNA; PROTECTION; CHIMPANZEES C1 BRISTOL MYERS SQUIBB PHARMACEUT RES INST, SEATTLE, WA USA. RP SCHULTZ, AM (reprint author), NIAID, DIV AIDS, VACCINE RES & DEV BRANCH, ROOM 2B-01, 6003 EXECUT BLVD, BETHESDA, MD 20892 USA. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 NR 102 TC 30 Z9 30 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0269-9370 J9 AIDS JI Aids PY 1993 VL 7 SU 1 BP S161 EP S170 DI 10.1097/00002030-199301001-00021 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA LE916 UT WOS:A1993LE91600021 PM 8363780 ER PT J AU BOERI, E GESSAIN, A GARIN, B KAZADI, K DETHE, G FRANCHINI, G AF BOERI, E GESSAIN, A GARIN, B KAZADI, K DETHE, G FRANCHINI, G TI QUALITATIVE CHANGES IN THE HUMAN T-CELL LEUKEMIA LYMPHOTROPIC VIRUS TYPE-I ENV GENE SEQUENCE IN THE SPASTIC VERSUS NONSPASTIC TROPICAL PARAPARESIS ARE NOT CORRELATED WITH DISEASE SPECIFICITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Note ID NUCLEOTIDE-SEQUENCE; HTLV-I; ANTIBODIES; VARIABILITY; MYELOPATHY; CLUSTER C1 NCI,TUMOR CELL BIOL LAB,BLDG 37,ROOM 6A01,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. INST PASTEUR,F-75724 PARIS 15,FRANCE. INST RECH BIOMED,GOMBE KINSHASA,ZAIRE. UNIV KINSHASA,CTR NATL NEUROPSYCHOPATHOL,KINSHASA,ZAIRE. NR 18 TC 17 Z9 17 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JAN PY 1993 VL 9 IS 1 BP 1 EP 5 DI 10.1089/aid.1993.9.1 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA KL618 UT WOS:A1993KL61800001 PM 8427713 ER PT J AU WATSON, RR AF WATSON, RR TI ALCOHOL NUTRIENT INTERACTIONS - A CRITICAL COMPONENT OF PHYSIOLOGICAL CHANGE SO ALCOHOL AND ALCOHOLISM LA English DT Editorial Material RP WATSON, RR (reprint author), UNIV ARIZONA,ARIZONA HLTH SCI CTR,DEPT FAMILY & COMMUNITY MED,NIAAA,ALCOHOL RES CTR,TUCSON,AZ 85724, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0735-0414 J9 ALCOHOL ALCOHOLISM JI Alcohol Alcohol. PD JAN PY 1993 VL 28 IS 1 BP 57 EP 58 PG 2 WC Substance Abuse SC Substance Abuse GA KW261 UT WOS:A1993KW26100007 PM 8471087 ER PT J AU ESKELSON, CD ODELEYE, OE WATSON, RR EARNEST, DL MUFTI, SI AF ESKELSON, CD ODELEYE, OE WATSON, RR EARNEST, DL MUFTI, SI TI MODULATION OF CANCER GROWTH BY VITAMIN-E AND ALCOHOL SO ALCOHOL AND ALCOHOLISM LA English DT Article ID COD LIVER OIL; LIPID-PEROXIDATION; ETHANOL-CONSUMPTION; RATS; SUPPLEMENTATION; RISK AB Seventy-five percent of esophageal cancers are alcohol related, yet alcohol is not a carcinogen. Ethanol may promote carcinogenesis via increased free radical products during its metabolism, as indicated by data from this and other studies. Ethanol is oxidized to acetaldehyde by alcohol dehydrogenase, catalase and the microsomal ethanol oxidizing system (MEOS). Free radicals (FR) are released during the oxidation of ethanol by the MEOS. An increased formation of FR in tissues would increase their oxidative stress and may increase their susceptibility for developing chemically induced cancers. FR and some FR products can rapidly react with biological materials, i.e. lipids, proteins and nucleic acids, forming toxic products. This study focuses on the effects of FR and/or FR products on cancer promotion during alcohol metabolism. Eight groups of mice were fed nutritionally adequate diets supplemented with vitamin E and/or ethanol. Some groups of mice were also orally gavaged with N-nitrosomethylbenzylamine (NMBzA), an esophageal carcinogen. Following the feeding of the various diets for 22 weeks, livers and esophagi were removed and the FR burden in the liver measured by the presence of lipid peroxide products and the number of tumors in each esophagus determined. These studies indicate that a linear relationship exists between the increasing number of esophageal tumors and increasing levels of lipid peroxide products that are formed during FR activity. These results show that FR and/or FR products are the cancer promoters during ethanol metabolism, since diets supplemented with high levels of vitamin E, which inhibits ethanol-induced FR activity and the formation of FR products, suppress the promotion of cancer by ethanol. Therefore, we conclude that FRs produced during ethanol metabolism and/or the products of FR activity are the cancer promoters attributed to ethanol. C1 UNIV ARIZONA,HLTH SCI CTR,DEPT FAMILY & COMMUNITY MED,TUCSON,AZ 85724. UNIV ARIZONA,HLTH SCI CTR,DEPT INTERNAL MED,TUCSON,AZ 85724. UNIV ARIZONA,HLTH SCI CTR,DEPT PHARMACOL & TOXICOL,TUCSON,AZ 85724. UNIV ARIZONA,HLTH SCI CTR,NIAAA,ALCOHOL RES CTR,TUCSON,AZ 85724. RP ESKELSON, CD (reprint author), UNIV ARIZONA,HLTH SCI CTR,DEPT SURG,TUCSON,AZ 85724, USA. FU NCPDCID CDC HHS [NCI 51088]; NIAAA NIH HHS [AA08037] NR 32 TC 42 Z9 42 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0735-0414 J9 ALCOHOL ALCOHOLISM JI Alcohol Alcohol. PD JAN PY 1993 VL 28 IS 1 BP 117 EP 125 PG 9 WC Substance Abuse SC Substance Abuse GA KW261 UT WOS:A1993KW26100014 PM 8471082 ER PT B AU SALEM, N WARD, G AF SALEM, N WARD, G BE Alling, C Diamond, I Leslie, SW Sun, GY Wood, WG TI THE EFFECTS OF ETHANOL ON POLYUNSATURATED FATTY-ACID COMPOSITION SO ALCOHOL, CELL MEMBRANES, AND SIGNAL TRANSDUCTION IN BRAIN LA English DT Proceedings Paper CT Marcus Wallenberg Symposium on Alcohol, Cell Membranes, and Signal Transduction in Brain CY JUN 28-JUL 01, 1992 CL LUND, SWEDEN SP MARCUS WALLENBERG FDN INT SCI EXCHANGE, NIAAA, SWEDISH MED RES COUNCIL C1 NIAAA,DICBR,MEMBRANE BIOCHEM & BIOPHYS LAB,BETHESDA,MD 20892. NR 0 TC 11 Z9 11 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44583-2 PY 1993 BP 33 EP 46 PG 14 WC Substance Abuse; Neurosciences; Physiology SC Substance Abuse; Neurosciences & Neurology; Physiology GA BZ52R UT WOS:A1993BZ52R00003 ER PT B AU WEIGHT, FF PEOPLES, RW WRIGHT, JM LI, C AGUAYO, LG LOVINGER, DM WHITE, G AF WEIGHT, FF PEOPLES, RW WRIGHT, JM LI, C AGUAYO, LG LOVINGER, DM WHITE, G BE Alling, C Diamond, I Leslie, SW Sun, GY Wood, WG TI NEUROTRANSMITTER-GATED ION CHANNELS AS MOLECULAR SITES OF ALCOHOL ACTION SO ALCOHOL, CELL MEMBRANES, AND SIGNAL TRANSDUCTION IN BRAIN LA English DT Proceedings Paper CT Marcus Wallenberg Symposium on Alcohol, Cell Membranes, and Signal Transduction in Brain CY JUN 28-JUL 01, 1992 CL LUND, SWEDEN SP MARCUS WALLENBERG FDN INT SCI EXCHANGE, NIAAA, SWEDISH MED RES COUNCIL C1 NIAAA,MOLEC & CELLULAR NEUROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 9 Z9 9 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-44583-2 PY 1993 BP 107 EP 122 PG 16 WC Substance Abuse; Neurosciences; Physiology SC Substance Abuse; Neurosciences & Neurology; Physiology GA BZ52R UT WOS:A1993BZ52R00010 ER PT J AU JENSEN, RT METZ, DC KOVIACK, PD FEIGENBAUM, KM AF JENSEN, RT METZ, DC KOVIACK, PD FEIGENBAUM, KM TI PROSPECTIVE-STUDY OF THE LONG-TERM EFFICACY AND SAFETY OF LANSOPRAZOLE IN PATIENTS WITH THE ZOLLINGER-ELLISON SYNDROME SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS LA English DT Article; Proceedings Paper CT 1ST INTERNATIONAL SYMP ON LANSOPRAZOLE - TREATMENT OF ACID PEPTIC DISEASE : FOCUS ON PROTON PUMP INHIBITORS CY SEP 24, 1992 CL ATHENS, GREECE ID GASTRIC-ACID SECRETION; PUMP INHIBITOR AG-1749; HYPERSECRETORY STATES; OMEPRAZOLE; THERAPY; RANITIDINE; CIMETIDINE; MANAGEMENT; ULCER; CELLS AB The long-term safety and efficacy of lansoprazole were studied in 21 patients with Zollinger-Ellison syndrome. The initial maintenance dose was determined by acid inhibition studies. In all patients lansoprazole controlled gastric acid hypersecretion and peptic symptoms in both the short and long term. Patients were treated for a mean of 31 months (range 1-43 months) with all but 4 patients followed for > 18 months. The mean initial dose was 60 mg/day, with 2 patients requiring a twice daily dose and the others a single daily dose. During long-term treatment 6 patients required an increased dosage, 5 within the first year. Long-term maintenance doses were reduced in 5 of the 6 patients in whom this was attempted. No changes in serum gastrin concentration, haematological parameters, liver function studies or other biochemical parameters occurred due to lansoprazole. No patient developed a gastric carcinoid tumour while being treated with lansoprazole. These results demonstrate that long-term treatment with lansoprazole is both safe and effective in patients with Zollinger-Ellison syndrome, and suggest that this drug will be useful in such patients. Furthermore, maintenance doses of lansoprazole, determined by the currently recommended method of acute acid titration studies in patients with Zollinger-Ellison syndrome, are too high. RP JENSEN, RT (reprint author), NIDDKD,DIGEST DIS BRANCH,BLDG 10,ROOM 9C-103,BETHESDA,MD 20892, USA. NR 39 TC 31 Z9 32 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-2813 J9 ALIMENT PHARM THERAP JI Aliment. Pharmacol. Ther. PY 1993 VL 7 SU 1 BP 41 EP 50 PG 10 WC Gastroenterology & Hepatology; Pharmacology & Pharmacy SC Gastroenterology & Hepatology; Pharmacology & Pharmacy GA KY358 UT WOS:A1993KY35800007 PM 8490079 ER PT J AU COHEN, SG AF COHEN, SG TI SPAIN, PORTUGAL, COLUMBUS,CHRISTOPHER, AND THE JEWISH PHYSICIAN .1. SO ALLERGY PROCEEDINGS LA English DT Article RP COHEN, SG (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 SN 1046-9354 J9 ALLERGY PROC JI Allergy Proc. PD JAN-FEB PY 1993 VL 14 IS 1 BP 71 EP 83 DI 10.2500/108854193778816761 PG 13 WC Allergy SC Allergy GA KU119 UT WOS:A1993KU11900014 PM 8462865 ER PT S AU FELDER, CC MA, AL BRILEY, EM AXELROD, J AF FELDER, CC MA, AL BRILEY, EM AXELROD, J BE Nitsch, RM Growdon, JH Corkin, S Wurtman, RJ TI MUSCARINIC ACETYLCHOLINE-RECEPTOR SUBTYPES ASSOCIATED WITH RELEASE OF ALZHEIMER AMYLOID PRECURSOR DERIVATIVES ACTIVATE MULTIPLE SIGNAL-TRANSDUCTION PATHWAYS SO ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Meeting of the International-Study-Group-on-the-Pharmacology-of-Memory-Disorders-Associ ated-with-Aging: Alzheimers Disease CY FEB 12-14, 1993 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOC AGING ID CELLS AB Five subtypes of muscarinic acetylcholine receptors have been identified and designated m1-m5. The m1 and m3 receptors have recently been shown to stimulate APP processing. The m1 and m3 receptors couple to a variety of signal transduction pathways in both tissue slices and a variety of cell lines endogenously expressing either or both subtypes. In contrast, the m2 and m4 receptors have been primarily associated with inhibition of adenylate cyclase. We have transfected all five subtypes of muscarinic receptors into a variety of mammalian cell lines in order to investigate the signaling associated with single receptor subtypes. The m1, m3, or m5 receptors stimulate phospholipase A(2), C, and D, adenylate cylase, receptor-operated calcium channels, and tyrosine kinase activity simultaneously. The m2 or m4 receptor inhibits cAMP accumulation and augments a previously stimulated release of arachidonic acid and calcium influx. RP FELDER, CC (reprint author), NIMH,CELL BIOL LAB,BLDG 36 RM 3A-15,BETHESDA,MD 20892, USA. NR 6 TC 13 Z9 13 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-853-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 695 BP 15 EP 18 DI 10.1111/j.1749-6632.1993.tb23020.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BZ92T UT WOS:A1993BZ92T00003 PM 8239275 ER PT S AU JOSEPH, JA CUTLER, R ROTH, GS AF JOSEPH, JA CUTLER, R ROTH, GS BE Nitsch, RM Growdon, JH Corkin, S Wurtman, RJ TI CHANGES IN G-PROTEIN-MEDIATED SIGNAL-TRANSDUCTION IN AGING AND ALZHEIMERS-DISEASE SO ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Meeting of the International-Study-Group-on-the-Pharmacology-of-Memory-Disorders-Associ ated-with-Aging: Alzheimers Disease CY FEB 12-14, 1993 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOC AGING ID AGED RAT AB Previous reports have shown that there are age-related reductions in muscarinic receptor (mAChR) sensitivity to agonist stimulation. Our research has elucidated the mechanisms involved in this loss. These studies have shown that this decline is the result of decreases in mAChR concentration, reductions in the number of neuronal cells, and altered phosphoinositide (PI)-mediated signal transduction (ST). The decrements in PI-mediated ST are observed as a reduced ability of muscarinic (m) agonists to enhance K+-evoked release of DA (K(+)ERDA) from striatal slices from old rats. Additional experiments indicated that the locus of the ST deficits appears to be at the mAChR-G protein interface, since attempts to bypass this interface reduced m-enhanced K(+)ERDA deficits in the striata from old rats. Moreover, it appears that the ability of mAChR to decouple from their respective G proteins is reduced as a function of age, since carbachol-stimulated low K-M GTPase activity was found to be reduced in hippocampal and striatal tissue obtained from old rats. Similar findings were observed in this parameter in AD hippocampus and basal ganglia. Further reductions were seen in carbachol-stimulated low K-M GTPase as a function of the duration of the disease. Results are discussed in terms of structural membrane alterations in aging and disease that may lead to reductions in the efficacy of receptor-G protein coupling/uncoupling. RP JOSEPH, JA (reprint author), NIA,GERONTOL RES CTR,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 5 TC 23 Z9 25 U1 1 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-853-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 695 BP 42 EP 45 DI 10.1111/j.1749-6632.1993.tb23024.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BZ92T UT WOS:A1993BZ92T00007 PM 8239310 ER PT S AU NITSCH, RM SLACK, BE FARBER, SA BORGHESANI, PR SCHULZ, JG KIM, C FELDER, CC GROWDON, JH WURTMAN, RJ AF NITSCH, RM SLACK, BE FARBER, SA BORGHESANI, PR SCHULZ, JG KIM, C FELDER, CC GROWDON, JH WURTMAN, RJ BE Nitsch, RM Growdon, JH Corkin, S Wurtman, RJ TI RECEPTOR-COUPLED AMYLOID PRECURSOR PROTEIN PROCESSING SO ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Meeting of the International-Study-Group-on-the-Pharmacology-of-Memory-Disorders-Associ ated-with-Aging: Alzheimers Disease CY FEB 12-14, 1993 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOC AGING ID ALZHEIMERS-DISEASE; PHOSPHORYLATION; DERIVATIVES; HYDROLYSIS; ACTIVATION; SECRETION; RELEASE; CELLS AB The family of beta-amyloid protein precursors (APP) can be processed via several alternative proteolytic pathways. Some generate potentially amyloidogenic APP derivatives, whereas others preclude the formation of such fragments. The cellular mechanisms regulating the relative activities of these pathways are thus important in determining the factors contributing to the formation of amyloidogenic APP derivatives. In order to investigate whether cell-surface receptor activity can regulate APP processing, HEK 293 cell lines stably expressing human muscarinic acetylcholine receptors (mAChR; subtypes mi, m2, m3, m4) were stimulated with the muscarinic agonist carbachol, and the release of APP derivatives was measured. Carbachol increased the release of large amino-terminal APP-fragments 4- to 6-fold in cell lines expressing the m1 or m3 receptors but not in those expressing m2 or m4 subtypes. This increase was blocked by various protein kinase inhibitors and mimicked by phorbol esters, indicating that it is mediated by protein kinase activation, presumably by protein kinase C (PKC). To determine whether additional cell-surface receptor types linked to this signal transduction pathway could also regulate APP processing, we stimulated differentiated PC-12 cells with bradykinin and found that this neuropeptide also increased the secretion of amino-terminal APP derivatives. We next investigated the possibility that neuronal depolarization might affect APP processing in mammalian brain. Electrically stimulated rat hippocampal slices released two times more amino-terminal APP derivatives than unstimulated control slices. This release increased with increasing stimulation frequencies in the physiological firing range of hippocampal pyramidal cells, and was blocked by tetrodotoxin. These results suggest that, in brain, APP processing is regulated by neuronal activity. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP NITSCH, RM (reprint author), MIT,DEPT BRAIN & COGNIT SCI,E25-604,CAMBRIDGE,MA 02139, USA. RI Schulz, Joachim/H-2430-2011; Farber, Steven/G-5851-2012 OI Farber, Steven/0000-0002-8037-7312 NR 15 TC 26 Z9 26 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-853-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 695 BP 122 EP 127 DI 10.1111/j.1749-6632.1993.tb23039.x PG 6 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BZ92T UT WOS:A1993BZ92T00022 PM 8239269 ER PT S AU POLLARD, HB ROJAS, E ARISPE, N AF POLLARD, HB ROJAS, E ARISPE, N BE Nitsch, RM Growdon, JH Corkin, S Wurtman, RJ TI A NEW HYPOTHESIS FOR THE MECHANISM OF AMYLOID TOXICITY, BASED ON THE CALCIUM-CHANNEL ACTIVITY OF AMYLOID-BETA PROTEIN (A-BETA-P) IN PHOSPHOLIPID-BILAYER MEMBRANES SO ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION SE Annals of the New York Academy of Sciences LA English DT Article ID ALZHEIMERS-DISEASE; DEMENTIA; STATES AB Amyloid beta protein (A beta P) is the 40-42 residue polypeptide implicated in the pathogenesis of Alzheimer's disease (AD). We have reconstituted this peptide into phosphatidylserine liposomes and then fused the liposomes with a planar lipid bilayer. When incorporated into this bilayer, the A beta P forms cation selective channels capable of transporting calcium and some monovalent cations including cesium, lithium, potassium, and sodium. The channels behave in an ohmic fashion and single channels can be shown to exhibit multiple subconductance states. Hitherto, A beta P has been presumed to be neurotoxic, although direct demonstration of toxicity has proved elusive. On the basis of the present data we suggest that the ion channel activity of the polypeptide may be the basis of its neurotoxic effects. RP POLLARD, HB (reprint author), NIDDK, DEPT CELL BIOL & GENET, BLDG 8, RM 401, BETHESDA, MD 20892 USA. NR 18 TC 58 Z9 60 U1 0 U2 11 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 0-89766-854-5; 0-89766-853-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 695 BP 165 EP 168 DI 10.1111/j.1749-6632.1993.tb23046.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BZ92T UT WOS:A1993BZ92T00029 PM 8239277 ER PT S AU JOHNSON, G REFOLO, LM WALLACE, W AF JOHNSON, G REFOLO, LM WALLACE, W BE Nitsch, RM Growdon, JH Corkin, S Wurtman, RJ TI HEAT-SHOCKED NEURONAL PC12 CELLS REVEAL ALZHEIMERS-DISEASE - ASSOCIATED ALTERATIONS IN AMYLOID PRECURSOR PROTEIN AND TAU SO ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 7th Meeting of the International-Study-Group-on-the-Pharmacology-of-Memory-Disorders-Associ ated-with-Aging: Alzheimers Disease CY FEB 12-14, 1993 CL ZURICH, SWITZERLAND SP INT STUDY GRP PHARM MEMORY DISORDERS ASSOC AGING AB The Alzheimer's disease (AD) brain contains many abnormal protein modifications. These include the abnormal processing of amyloid precursor protein (APP) to form the amyloidogenic beta/A4 peptide and the abnormal phosphorylation of tau to form A68, the major constituent of the neurofibrillary tangle. In addition, many of the biochemical alterations found in the AD brain are also found in heat-shocked or stressed cells. We used heat-shocked neuronal PC12 cells to investigate the effects of stress on APP and tau. We found that by simply exposing neuronal PC12 cells to an elevated temperature (45 degrees C) for 30 minutes, they exhibited several features characteristic of the heat shock response. These included a 45% reduction in total protein synthesis, the induction of heat shock protein (hsp) 72, and increased phosphorylation of the protein synthesis initiation factor eIE-2 alpha. The heat-shocked cells also exhibited alterations in the metabolism and phosphorylation of APP. Under heat shock conditions, we found two additional APP-like polypeptides not present in controls and a significant decrease in the phosphorylation state of APP. We also found that an A68-like protein is formed in neuronal PC12 cells when subjected to elevated temperature. This A68-like protein was formed with heat shock even in the absence of protein synthesis, suggesting that its production occurred post-translationally The tau/A68 polypeptides were identified as phosphoproteins, and the phosphorylation of tau to form A68 was reversed with recovery of the cells from heat shock. Immunoprecipitation of lysates from heat shocked cells with antibodies to hsp72/73 resulted in co-precipitation of tau, but not A68 with hsp72 indicating a stable complex formation between these two proteins. These results suggest that heat shock proteins may play either a protective or promoting role in the formation of A68 and/or the amyloidogenic C-terminal fragment of APP. C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,BIOCHIM GENET LAB,WASHINGTON,DC 20032. MOLEC GERIATR INC,LAKE BLUFF,IL 60044. NR 7 TC 9 Z9 10 U1 1 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 SN 0077-8923 BN 0-89766-853-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1993 VL 695 BP 194 EP 197 DI 10.1111/j.1749-6632.1993.tb23051.x PG 4 WC Biochemistry & Molecular Biology; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Science & Technology - Other Topics; Neurosciences & Neurology GA BZ92T UT WOS:A1993BZ92T00034 PM 8239282 ER PT J AU MAIL, PD JOHNSON, S AF MAIL, PD JOHNSON, S TI BOOZING, SNIFFING, AND TOKING - AN OVERVIEW OF THE PAST, PRESENT, AND FUTURE OF SUBSTANCE USE BY AMERICAN-INDIANS SO AMERICAN INDIAN AND ALASKA NATIVE MENTAL HEALTH RESEARCH LA English DT Article; Proceedings Paper CT American Indian Firefighters Drug Free Work Place Conference CY 1991 CL TUCSON, AZ SP UNIV ARIZONA, COLL MED, NATIVE AMER RES & TRAINING CTR ID FETAL ALCOHOL SYNDROME; DRUG-USE; NATIVE AMERICANS; ADOLESCENTS; PREVENTION; PROGRAM; ABUSE; PATTERNS AB This paper provides an overview of Indian peoples, alcohol misuse, and the prevalence of drug and inhalant experience. Early use of alcohol among North American Native peoples may represent early chemical warfare to gain European advantage over an ''enemy.'' The magnitude of the present-day problem of alcohol and substance misuse is described in mortality rates and proportionate use reports. The use of other drugs and substances, such as inhalants, amphetamines, sedatives, and hallucinogens is examined. A brief overview of the history and complex relationships between American Indians and alcohol from the time of initial contact to the present is sketched out before approaches to primary, secondary and tertiary prevention are considered. The issue of potential conflict between tribal statutes and health objectives is noted. Some possible solutions are proposed. RP MAIL, PD (reprint author), NIAAA,ALCOHOL DRUG ABUSE & MENTAL HLTH ADM,22 MONROE ST,SUITE 301,ROCKVILLE,MD 20850, USA. NR 84 TC 32 Z9 32 U1 2 U2 2 PU UNIVERSITY PRESS COLORADO PI NIWOT PA PO BOX 849, NIWOT, CO 80544 SN 0893-5394 J9 AM INDIAN ALASKA NAT JI Am. Indian Alsk. Nativ. Ment. Health Res. PY 1993 VL 5 IS 2 BP 1 EP 33 PG 33 WC Psychology, Clinical SC Psychology GA MQ944 UT WOS:A1993MQ94400002 PM 8130311 ER PT J AU RUBINS, HB ROBINS, SJ IWANE, MK BODEN, WE ELAM, MB FYE, CL GORDON, DJ SCHAEFER, EJ SCHECTMAN, G WITTES, JT KARVONEN, J COLLINS, D BARTOZZI, R CUSHING, C DERRICO, J NEWVINE, K SATHER, MR DRAGO, M FETTER, R GAGNE, W MCNAMARA, JR CROW, RS SWANSON, C SMITH, K PEARSON, TA GOTTO, AM BAILEY, KR DAVIS, BR PARISI, AF RIFKIND, BM ZELIS, R WILT, TJ CROW, R DEMOTS, H LINARES, E RUTAN, G LAKSHMAN, R KOU, W MANCINI, GBJ SAMPLE, S CHAMPAGNE, N CHAPIN, C GILROY, D AICARDI, N PAPP, MA STANFORD, S MONREAL, S WEXLER, LF SHAFFER, J SNOW, E JOHNSON, K DEEDWANIA, PC MURPHY, E KING, J MANN, DL KUO, P TYLER, C ESPADAS, D TOUCHON, RC PEART, K BABB, M ANDERSON, JW SMITH, B BUCHANAN, L LOGAN, JE FAAS, FH THOMAS, S RIDINGS, K KASHYAP, ML DOWNEY, N KNIGHT, R SALEH, JR JOSEPH, SA SAMOLS, E KINNY, D PIGNATORA, L MAYOSMITH, M NICE, C CARSON, M LAVOIE, L RUTAN, G HARRIS, L PINSON, J CHILDRESS, R RISTOW, S PARKER, C WILT, TJ SCHLASNER, L ROOTES, D DEMOTS, H GRAY, L BAGNOLI, S IRANMANESH, A RUSSELL, DC CLARY, S WERTZ, L LINARES, E VELAZQUEZ, MS CRUZ, MD PAPADEMETRIOU, V METCALFE, M DANDENAU, P HERSHMAN, JM SINGH, BN MCCLOY, P GODDART, K AF RUBINS, HB ROBINS, SJ IWANE, MK BODEN, WE ELAM, MB FYE, CL GORDON, DJ SCHAEFER, EJ SCHECTMAN, G WITTES, JT KARVONEN, J COLLINS, D BARTOZZI, R CUSHING, C DERRICO, J NEWVINE, K SATHER, MR DRAGO, M FETTER, R GAGNE, W MCNAMARA, JR CROW, RS SWANSON, C SMITH, K PEARSON, TA GOTTO, AM BAILEY, KR DAVIS, BR PARISI, AF RIFKIND, BM ZELIS, R WILT, TJ CROW, R DEMOTS, H LINARES, E RUTAN, G LAKSHMAN, R KOU, W MANCINI, GBJ SAMPLE, S CHAMPAGNE, N CHAPIN, C GILROY, D AICARDI, N PAPP, MA STANFORD, S MONREAL, S WEXLER, LF SHAFFER, J SNOW, E JOHNSON, K DEEDWANIA, PC MURPHY, E KING, J MANN, DL KUO, P TYLER, C ESPADAS, D TOUCHON, RC PEART, K BABB, M ANDERSON, JW SMITH, B BUCHANAN, L LOGAN, JE FAAS, FH THOMAS, S RIDINGS, K KASHYAP, ML DOWNEY, N KNIGHT, R SALEH, JR JOSEPH, SA SAMOLS, E KINNY, D PIGNATORA, L MAYOSMITH, M NICE, C CARSON, M LAVOIE, L RUTAN, G HARRIS, L PINSON, J CHILDRESS, R RISTOW, S PARKER, C WILT, TJ SCHLASNER, L ROOTES, D DEMOTS, H GRAY, L BAGNOLI, S IRANMANESH, A RUSSELL, DC CLARY, S WERTZ, L LINARES, E VELAZQUEZ, MS CRUZ, MD PAPADEMETRIOU, V METCALFE, M DANDENAU, P HERSHMAN, JM SINGH, BN MCCLOY, P GODDART, K TI RATIONALE AND DESIGN OF THE DEPARTMENT-OF-VETERANS-AFFAIRS HIGH-DENSITY-LIPOPROTEIN CHOLESTEROL INTERVENTION TRIAL (HIT) FOR SECONDARY PREVENTION OF CORONARY-ARTERY DISEASE IN MEN WITH LOW HIGH-DENSITY-LIPOPROTEIN CHOLESTEROL AND DESIRABLE LOW-DENSITY-LIPOPROTEIN CHOLESTEROL SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID HEART-DISEASE; MYOCARDIAL-INFARCTION; CARDIOVASCULAR-DISEASE; LOWERING CHOLESTEROL; RISK-FACTORS; PLASMA; MORTALITY; FRAMINGHAM; ATHEROGENESIS; GEMFIBROZIL AB Although a large body of epidemiologic evidence suggests that low levels of high-density lipoprotein (HDL) cholesterol are strongly associated with an increased risk of coronary artery disease (CAD), no large-scale clinical trials focusing on this association have been reported. This report describes the rationale and design of the Department of Veterans Affairs HDL Intervention Trial (HIT), a multicenter, randomized, controlled clinical trial designed to determine whether lipid therapy reduces the combined incidence of CAD death and nonfatal myocardial infarction in men with established CAD who have low levels of HDL cholesterol with ''desirable'' levels of low-density lipoprotein (LDL) cholesterol. Twenty-five hundred men with CAD and HDL cholesterol less-than-or-equal-to 40 mg/dl, LDL cholesterol less-than-or-equal-to 140 mg/dl, and triglycerides less-than-or-equal-to 300 mg/dl are being recruited at 20 Department of Veterans Affairs medical centers, randomized to either gemfibrozil or placebo, and followed in a double-blind manner for an average of 6 years. In this population, gemfibrozil is expected to increase HDL cholesterol by 10 to 15%, have a negligible effect on LDL cholesterol, and lower triglycerides by 30 to 40%. Because an estimated 20 to 30% of patients with CAD have a low HDL cholesterol as their primary lipid abnormality, the results of this trial are expected to have far-reaching clinical implications. C1 DEPT VET AFFAIRS MED RES SERV,COOPERAT STUDIES PROGRAM,BOSTON,MA. DEPT VET AFFAIRS MED RES SERV,COOPERAT STUDIES PROGRAM,MINNEAPOLIS,MN. DEPT VET AFFAIRS MED RES SERV,COOPERAT STUDIES PROGRAM,MEMPHIS,TN. UNIV MINNESOTA,SCH MED,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. DEPT MED,MINNEAPOLIS,MN. DEPT MED,BOSTON,MA. DEPT MED,MEMPHIS,TN. MILWAUKEE DEPT VET AFFAIRS MED CTR,MILWAUKEE,WI. UNIV MINNESOTA,SCH MED,DEPT MED,MINNEAPOLIS,MN 55455. BOSTON UNIV,SCH MED,DEPT MED,BOSTON,MA 02118. TUFTS UNIV,SCH MED,DEPT MED,BOSTON,MA 02111. UNIV TENNESSEE,CTR HLTH SCI,COLL MED,DEPT MED,MEMPHIS,TN 38163. MED COLL WISCONSIN,DEPT MED,MILWAUKEE,WI 53226. NHLBI,LIPID METAB ATHEROGENESIS BRANCH,BETHESDA,MD 20892. NEW ENGLAND MED CTR,DEPT MED,DIV ENDOCRINOL,LIPID RES LAB,BOSTON,MA. DEPT VET AFFAIRS MED CTR,BOSTON,MA. DEPT VET AFFAIRS MED CTR,RICHMOND,VA. DEPT VET AFFAIRS MED CTR,MINNEAPOLIS,MN. RP RUBINS, HB (reprint author), VET ADM MED CTR 1110,MINNEAPOLIS,MN 55417, USA. NR 56 TC 80 Z9 80 U1 0 U2 3 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD JAN 1 PY 1993 VL 71 IS 1 BP 45 EP 52 DI 10.1016/0002-9149(93)90708-K PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA KG288 UT WOS:A1993KG28800009 PM 8420235 ER PT J AU MCAULIFFE, WE ASHERY, RS AF MCAULIFFE, WE ASHERY, RS TI IMPLEMENTATION ISSUES AND TECHNIQUES IN RANDOMIZED TRIALS OF OUTPATIENT PSYCHOSOCIAL TREATMENTS FOR DRUG-ABUSERS .2. CLINICAL AND ADMINISTRATIVE ISSUES SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID TERM INTERPERSONAL PSYCHOTHERAPY; MAINTAINED OPIATE ADDICTS; CONDUCTING FAMILY-THERAPY; 2.5-YEAR FOLLOW-UP; OPIOID ADDICTS; ONE-PERSON; INTERVENTION; BENEFITS; CONJOINT; HELP AB This paper focuses on implementation problems in randomized trials of outpatient psychosocial treatments for drug abusers. The authors examined these problems in nine clinical trial studies and drew on published literature and their own research experiences. Common problems faced by principal investigators include the need for midstream treatment protocol and research design modifications based on the response of both clients and clinical staff, tension between research and clinical requirements, and the need to administer a large, complex organization over a substantial period of time. Solutions include conducting a pilot study, employing advanced research and analysis methods that can incorporate complex design variations, fostering a team spirit between diverse staffs, and employing special management structures. C1 NIDA,COMMUNITY RES BRANCH,ROCKVILLE,MD 20857. RP MCAULIFFE, WE (reprint author), HARVARD UNIV,CAMBRIDGE HOSP,SCH MED,DEPT PSYCHIAT,1493 CAMBRIDGE ST,CAMBRIDGE,MA 02139, USA. FU NIDA NIH HHS [DA03075, DA04418, DA02798] NR 38 TC 3 Z9 3 U1 1 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1993 VL 19 IS 1 BP 35 EP 50 DI 10.3109/00952999309002664 PG 16 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA KL892 UT WOS:A1993KL89200003 PM 8438830 ER PT J AU SCHMITZ, J DEJONG, J ROY, A GARNETT, D MOORE, V LAMPARSKI, D WAXMAN, R LINNOILA, M AF SCHMITZ, J DEJONG, J ROY, A GARNETT, D MOORE, V LAMPARSKI, D WAXMAN, R LINNOILA, M TI SUBSTANCE-ABUSE AMONG SUBJECTS SCREENED OUT FROM AN ALCOHOLISM RESEARCH-PROGRAM SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID DRUG-ABUSE; CLINICAL IMPLICATIONS; MENTAL-DISORDERS; PSYCHOPATHOLOGY; PREVALENCE; ONSET; AGE AB Three hundred and eight subjects were screened over the phone for admission to an inpatient alcohol treatment research unit. Using a structured interview, the prospective patients were asked questions regarding demographics, drinking history, previous treatments, physical health, family history, and a detailed history of past and present substance use. Drug use was studied as regular use versus no use or brief experimental use of five drug categories: cannabinoids, stimulants, sedatives, opiates, and hallucinogens. Fifty-one percent of the men and 48% of the women reported regular use of one or more of the drugs in addition to alcohol. For women, the amount of alcohol intake was positively correlated with use of stimulants (r = .32, p = .001), cannabinoids (r = .24, p = .019), sedatives (r = .30, p = .003), and hallucinogens (r = .30, p = .003). For men, correlations between the amount of alcohol intake and drug use were weaker but significant for stimulants (r = .21, p = .002), opiates (r = .15, p = .028), and hallucinogens (r = .15, p = .029). Women with alcoholic mothers displayed higher alcohol intake than women with nonalcoholic in others (p = .02) and also showed more frequent use of most drugs. Although men with alcoholic fathers also showed greater alcohol intake compared to men with nonalcoholic fathers, the two groups did not differ in drug use. Younger subjects of both sexes were more likely to use cannabinoids, stimulants, opiates, and hallucinogens. Alcohol and sedative use was relatively constant across all age groups. RP SCHMITZ, J (reprint author), NIAAA,CLIN STUDIES LAB,9000 ROCKVILLE PIKE,BLDG 10,ROOM 3B19,ROCKVILLE,MD 20852, USA. NR 29 TC 3 Z9 3 U1 2 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1993 VL 19 IS 3 BP 359 EP 368 DI 10.3109/00952999309001625 PG 10 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA LU642 UT WOS:A1993LU64200009 PM 8213699 ER PT J AU DAWES, MA FRANK, S ROST, K AF DAWES, MA FRANK, S ROST, K TI CLINICIAN ASSESSMENT OF PSYCHIATRIC COMORBIDITY AND ALCOHOLISM SEVERITY IN ADULT ALCOHOLIC INPATIENTS SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID SELF-REPORTS; DRINKING BEHAVIOR; SUBSTANCE ABUSE; DRUG-ABUSE; RECOGNITION; RELIABILITY; PREVALENCE; VALIDITY; POPULATIONS AB Although psychiatric comorbidity and alcoholism severity are risk factors for poor outcomes in treating alcoholism, little is known about whether clinicians assess these conditions accurately. In this study we evaluated four clinicians' assessments of two indicators of alcoholism severity and three psychiatric comorbidities in 78 inpatients in their third to seventh day of hospitalization in alcohol treatment programs. Clinicians overestimated the number of days drinking in 28% of subjects, and the number of drinks per drinking day in 37% of subjects. Clinicians underestimated alcohol consumption for patients with higher incomes. Clinicians correctly diagnosed 67% of 18 subjects with antisocial personality disorder, 65% of 26 with major depression, and 89% of 28 with drug abuse. These preliminary results need to be replicated in larger samples of clinicians to determine whether interventions are needed to improve the recognition of important prognostic factors in the treatment of alcoholic patients. C1 UNIV ARKANSAS MED SCI HOSP,DEPT PSYCHIAT,VA,HSR&D FIELD PROGRAM MENTAL HLTH,NIMH,LITTLE ROCK,AR 72205. NR 30 TC 7 Z9 7 U1 1 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1993 VL 19 IS 3 BP 377 EP 386 DI 10.3109/00952999309001627 PG 10 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA LU642 UT WOS:A1993LU64200011 PM 8213701 ER PT J AU WEINBERG, CR AF WEINBERG, CR TI TOWARD A CLEARER DEFINITION OF CONFOUNDING SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE BIAS (EPIDEMIOLOGY); CASE-CONTROL STUDIES; COHORT STUDIES; CONFOUNDING FACTORS (EPIDEMIOLOGY); EFFECT MODIFIERS (EPIDEMIOLOGY); EPIDEMIOLOGIC METHODS; RESEARCH DESIGN ID CANCER AB Epidemiologists are aware that the estimated effect of an exposure can be biased if the investigator fails to adjust for confounding factors when analyzing either a prospective or retrospective etiologic study. Standard texts warn, however, that intervening factors are an exception: one should not adjust for any factor which is intermediate on the causal pathway between the exposure and the disease. Other factors which are not on the causal pathway but are caused in part by the exposure are often adjusted for in epidemiologic studies. This paper illustrates that bias can result when adjustment is made for any factor which is caused in part by the exposure under study and is also correlated with the outcome under study. Intervening variables are only one example of this phenomenon. The misleading effects of this practice are illustrated with examples. RP WEINBERG, CR (reprint author), NIEHS,POB 12233,MD B3-02,RES TRIANGLE PK,NC 27709, USA. NR 11 TC 237 Z9 238 U1 0 U2 11 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JAN 1 PY 1993 VL 137 IS 1 BP 1 EP 8 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KP916 UT WOS:A1993KP91600001 PM 8434568 ER PT J AU BRITTENHAM, GM COHEN, AR MCLAREN, CE MARTIN, MB GRIFFITH, PM NIENHUIS, AW YOUNG, NS ALLEN, CJ FARRELL, DE HARRIS, JW AF BRITTENHAM, GM COHEN, AR MCLAREN, CE MARTIN, MB GRIFFITH, PM NIENHUIS, AW YOUNG, NS ALLEN, CJ FARRELL, DE HARRIS, JW TI HEPATIC IRON STORES AND PLASMA FERRITIN CONCENTRATION IN PATIENTS WITH SICKLE-CELL-ANEMIA AND THALASSEMIA MAJOR SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE DEFEROXAMINE; CHELATING AGENTS; MAGNETOMETRY ID OVERLOAD; HEMOCHROMATOSIS; CHELATION; BINDING; SERUM AB To examine the relationship between hepatic iron stores and plasma ferritin concentration in individuals treated with red cell transfusion and iron chelation therapy, 37 patients with sickle cell anemia and 74 patients with thalassemia major were studied. In each patient, hepatic iron stores were measured by an independently validated noninvasive magnetic method, and plasma ferritin was determined by immunoassay. The correlation between hepatic iron and plasma ferritin was significant both in patients with sickle cell anemia (R = 0.75, P < 0.0001) and in those with thalassemia major (R = 0.76, P < 0.0001). Regression analysis showed no significant difference between the two groups in the linear relationships between hepatic iron stores and plasma ferritin. Considering all 111 transfused patients as a group, the coefficient of correlation between hepatic iron stores and plasma ferritin was highly significant (R = 0.76, P < 0.0001). Regression analysis found that variation in body iron stores, as assessed by magnetic determinations of hepatic iron, accounted for only approximately 57% of the variation in plasma ferritin, suggesting that the remainder was the result of other factors, such as hemolysis, ineffective erythropoiesis, ascorbate deficiency, inflammation, and liver disease. The 95% prediction intervals for hepatic iron concentration, given the plasma ferritin, were so broad as to make a single determination of plasma ferritin an unreliable predictor of body iron stores. Variability resulting from factors other than iron status limits the clinical usefulness of the plasma ferritin concentration as a predictor of body iron stores. C1 CASE WESTERN RESERVE UNIV,DEPT MED,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,DEPT PHYS,CLEVELAND,OH 44106. CHILDRENS HOSP,DIV HEMATOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PEDIAT,PHILADELPHIA,PA 19104. NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. MOORHEAD STATE UNIV,DEPT MATH,MOORHEAD,MN. FU NHLBI NIH HHS [HL24198]; NIADDK NIH HHS [AM25105]; NIDDK NIH HHS [DK14370] NR 18 TC 181 Z9 181 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD JAN PY 1993 VL 42 IS 1 BP 81 EP 85 DI 10.1002/ajh.2830420116 PG 5 WC Hematology SC Hematology GA KC197 UT WOS:A1993KC19700015 PM 8416302 ER PT J AU PEARSON, JD JAMES, GD BROWN, DE AF PEARSON, JD JAMES, GD BROWN, DE TI STRESS AND CHANGING LIFE-STYLES IN THE PACIFIC - PHYSIOLOGICAL STRESS RESPONSES OF SAMOANS IN RURAL AND URBAN SETTINGS SO AMERICAN JOURNAL OF HUMAN BIOLOGY LA English DT Article ID CATECHOLAMINE EXCRETION RATES; INTER-POPULATION COMPARISONS; BLOOD-PRESSURE; URINARY CATECHOLAMINES; MEN; MODERNIZATION AB The lifestyles and social environments of Pacific Islanders have changed profoundly as a result of local development and migration to urban, cosmopolitan centers. These changes have often been accompanied by an increase in chronic diseases, alcoholism, and suicide. As a result, the health effects of psychological and physiological stress have become an increasing concern in Pacific Island nations and in countries with significant Pacific migrant communities. Several studies in the Samoan Studies Project have examined catecholamine excretion rates in order to understand how the behavioral, psychological, and environmental changes of modernization affect the physiological stress responses of young Samoan adults. The results of studies in rural and urban Western Samoa, American Samoa, and Honolulu, Hawaii show that several complex factors associated with urban, more cosmopolitan lifestyles tend to increase stress hormone levels. Specifically, lifestyle differences in physical activity, diet, and social interaction have significant independent and interactive contributions. These behavioral factors can lead to a high degree of day-to-day variability in catecholamine excretion. The implications of these findings for future research designs are discussed. However, the data suggest that it is a complex interaction of lifestyle factors, not any specific single factor, that determines the physiological stress responses of Samoans in different environments. C1 CORNELL UNIV,MED CTR,CTR CARDIOVASC,NEW YORK,NY 10021. UNIV HAWAII,DEPT ANTHROPOL,HILO,HI 96720. RP PEARSON, JD (reprint author), NIA,LONGITUDINAL STUDIES BRANCH,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 50 TC 26 Z9 26 U1 1 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1042-0533 J9 AM J HUM BIOL JI Am. J. Hum. Biol. PY 1993 VL 5 IS 1 BP 49 EP 60 DI 10.1002/ajhb.1310050109 PG 12 WC Anthropology; Biology SC Anthropology; Life Sciences & Biomedicine - Other Topics GA KL836 UT WOS:A1993KL83600006 ER PT J AU PEARSON, JD MORRELL, CH FLEG, JL BRANT, LJ AF PEARSON, JD MORRELL, CH FLEG, JL BRANT, LJ TI AGE-ASSOCIATED CHANGES IN BLOOD-PRESSURE AMONG MEN AND WOMEN IN THE BALTIMORE LONGITUDINAL-STUDY OF AGING SO AMERICAN JOURNAL OF HUMAN BIOLOGY LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1042-0533 J9 AM J HUM BIOL JI Am. J. Hum. Biol. PY 1993 VL 5 IS 1 BP 138 EP 138 PG 1 WC Anthropology; Biology SC Anthropology; Life Sciences & Biomedicine - Other Topics GA KL836 UT WOS:A1993KL83600041 ER PT J AU HEARING, VJ AF HEARING, VJ TI UNRAVELING THE MELANOCYTE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Editorial Material ID NEGATIVE OCULOCUTANEOUS ALBINISM; TYROSINASE-RELATED PROTEIN; SINGLE BASE INSERTION; COAT COLOR LOCUS; MOUSE CHROMOSOME-10; GENE; MUTATIONS; MAPS; EXPRESSION; PIGMENTATION RP HEARING, VJ (reprint author), NCI,CELL BIOL LAB,BLDG 37,ROOM 1B22,BETHESDA,MD 20892, USA. NR 48 TC 63 Z9 64 U1 2 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 JAN PY 1993 VL 52 IS 1 BP 1 EP 7 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA KK908 UT WOS:A1993KK90800001 PM 8434579 ER PT J AU CHRISTIAN, JC NORMAN, JE AF CHRISTIAN, JC NORMAN, JE TI ROBINETTE,CHARLES,DENNIS (1935-92) - IN MEMORIAM SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Item About an Individual C1 NHLBI,BETHESDA,MD 20892. RP CHRISTIAN, JC (reprint author), INDIANA UNIV,SCH MED,DEPT MED & MOLEC GENET,INDIANAPOLIS,IN 46202, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JAN PY 1993 VL 52 IS 1 BP 204 EP 204 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA KK908 UT WOS:A1993KK90800023 ER PT J AU AMOS, CI WILLIAMSON, JA AF AMOS, CI WILLIAMSON, JA TI ROBUSTNESS OF THE MAXIMUM-LIKELIHOOD (LOD) METHOD FOR DETECTING LINKAGE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Letter C1 UNIV COLORADO,PROGRAM BIOCHEM & DRUG METAB,BOULDER,CO 80309. RP AMOS, CI (reprint author), NATL INST ARTHRITIS MUSCULOSKELETAL & SKIN DIS,GENET STUDIES SECT,BETHESDA,MD, USA. NR 3 TC 12 Z9 12 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JAN PY 1993 VL 52 IS 1 BP 213 EP 214 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA KK908 UT WOS:A1993KK90800031 PM 8434591 ER PT J AU FREIMUTH, VS VANNEVEL, JP AF FREIMUTH, VS VANNEVEL, JP TI CHANNELS AND VEHICLES OF COMMUNICATION - THE ASBESTOS AWARENESS CAMPAIGN SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article; Proceedings Paper CT WORKSHOP ON THE METHODOLOGY OF WORKER NOTIFICATION CY AUG 01-02, 1991 CL VAIL, CO SP NIOSH DE WORKER NOTIFICATION; RISK COMMUNICATION; ASBESTOS EXPOSURE; MASS MEDIA; GATEKEEPERS; PUBLIC SERVICE ANNOUNCEMENTS; PRETESTING; BOUNCEBACK POSTCARDS; BROADCAST ADVERTISER REPORTS AB In April 1978, the U.S. Department of Health, Education, and Welfare launched a multimedia campaign to inform doctors, workers, and others about the increased risks of asbestos exposure. Unlike most worker notification efforts, this one had no lists of workers or even of workplaces but faced the challenge of locating people who had worked in the shipbuilding industries more than 30 years earlier. Multiple mass media channels were used, but since most messages were distributed as public service announcements, gatekeepers were critical to the success of the campaign. Some campaign messages were aired, but mostly at hours other than prime time, and the coverage focused more on the controversial, fast-breaking events rather than on estimates of risk or on behaviors to reduce risk. The campaign was effective in increasing the number of people who believed they were at risk, but was less successful with older Americans than with manual laborers. C1 NCI,OFF CANC COMMUN,BETHESDA,MD 20892. RP FREIMUTH, VS (reprint author), UNIV MARYLAND,DEPT SPEECH COMMUN,2701 OXFORD CIRCLE,UPPER MARLBORO,MD 20772, USA. NR 2 TC 1 Z9 1 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD JAN PY 1993 VL 23 IS 1 BP 105 EP 111 DI 10.1002/ajim.4700230116 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA KE654 UT WOS:A1993KE65400015 PM 8422039 ER PT J AU STRIKER, GE SCHERBENSKE, MJ AF STRIKER, GE SCHERBENSKE, MJ TI PROCEEDINGS FROM THE WORKSHOP ON THE MORBIDITY AND MORTALITY OF END-STAGE RENAL-DISEASE - SPONSORED BY THE NATIONAL-INSTITUTES-OF-HEALTH MIAMI, FL - FEBRUARY 27-29, 1992 - DKUHD PERSPECTIVES IN END-STAGE RENAL-DISEASE SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Editorial Material RP STRIKER, GE (reprint author), NIDDK,DKUHD,RENAL PHYSIOL CELL BIOL PROGRAM,BETHESDA,MD, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD JAN PY 1993 VL 21 IS 1 BP 71 EP 71 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA KG849 UT WOS:A1993KG84900014 ER PT J AU JONES, CA EGGERS, PW AF JONES, CA EGGERS, PW TI EPIDEMIOLOGY WORKING GROUP ON MORBIDITY AND MORTALITY OF END-STAGE RENAL-DISEASE SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Editorial Material RP JONES, CA (reprint author), NIDDK,DKUHD,WESTWOOD BLDG,ROOM 3A-07,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD JAN PY 1993 VL 21 IS 1 BP 111 EP 113 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA KG849 UT WOS:A1993KG84900024 PM 8418614 ER PT J AU BAILEYWILSON, JE PLATO, CC ELSTON, RC GARRUTO, RM AF BAILEYWILSON, JE PLATO, CC ELSTON, RC GARRUTO, RM TI POTENTIAL ROLE OF AN ADDITIVE GENETIC COMPONENT IN THE CAUSE OF AMYOTROPHIC-LATERAL-SCLEROSIS AND PARKINSONISM-DEMENTIA IN THE WESTERN PACIFIC SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE AMYOTROPHIC LATERAL SCLEROSIS; PARKINSONISM DEMENTIA; SEGREGATION ANALYSIS; FAMILY STUDIES; GENETIC LIABILITY ID SEGREGATION ANALYSIS; UNLIKELY CAUSE; GUAM; DISORDERS; MIGRANTS; CALCIUM; ACID AB Amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia (PD) are neurological degenerative disorders that occur in three high incidence foci in the western Pacific: among the Chamorros of Guam and the Commonwealth of the Northern Marianas Islands, among Japanese on the Kii peninsula of Honshu Island, and among the Auyu and Jakai peoples of southern West New Guinea. Previous studies have implicated both genetic susceptibility and environmental risk factors in the causation and familial clustering of these disorders. The data analyzed consist of 2,026 individuals in nuclear families ascertained on Guam through two mechanisms: (1) nuclear families were included in the study if one or both parents in the family were affected with ALS or PD or both; and (2) a group of ''controls'' was selected by obtaining nuclear families where neither parent was affected and both had lived through the age of risk. Clinically, ALS and PD are two distinct disorders. However, preliminary analyses indicated that combining all three diagnoses into one affected diagnosis for genetic analyses (thereby assuming any genetic effect on susceptibility to the two disorders was due to the same genetic mechanism) was reasonable. An age, sex and birth cohort-specific liability was defined and segregation analysis was performed under both logistic and normal models for this liability at the time of disease onset. Under either model, purely environmental, Mendelian dominant and Mendelian recessive hypotheses could be rejected, but a two-allele additive major locus hypothesis could not be rejected. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NIH,BETHESDA,MD 20892. RP BAILEYWILSON, JE (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,1901 PERDIDO ST,NEW ORLEANS,LA 70112, USA. OI Bailey-Wilson, Joan/0000-0002-9153-2920 FU NCRR NIH HHS [1 P41 RR03655]; NIGMS NIH HHS [GM28356] NR 35 TC 34 Z9 35 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 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JAN 1 PY 1993 VL 45 IS 1 BP 68 EP 76 DI 10.1002/ajmg.1320450118 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA KR915 UT WOS:A1993KR91500016 PM 8418664 ER PT J AU MILLER, DL AF MILLER, DL TI DIRECT ORIGIN OF THE ARTERY OF THE CERVICAL ENLARGEMENT FROM THE LEFT SUBCLAVIAN ARTERY SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE ARTERIES, ABNORMALITIES AND ANOMALIES; ARTERIES, ANATOMY; ARTERIES, SPINAL AB An anatomic variation is described in which the principal radiculomedullary artery to the cervical spinal cord, the artery of the cervical enlargement, arises directly from the left subclavian artery. This anomaly is important clinically because it may be necessary to catheterize this vessel selectively during spinal arteriography, and also because unintentional injection of this vessel can be associated with complications. C1 GEORGETOWN UNIV,MED CTR,DEPT RADIOL,WASHINGTON,DC 20007. RP MILLER, DL (reprint author), NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BLDG 10,BETHESDA,MD 20892, USA. NR 9 TC 4 Z9 4 U1 0 U2 0 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD JAN-FEB PY 1993 VL 14 IS 1 BP 242 EP 244 PG 3 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA KJ756 UT WOS:A1993KJ75600043 PM 8427098 ER PT J AU CNATTINGIUS, S FORMAN, MR BERENDES, HW GRAUBARD, BI ISOTALO, L AF CNATTINGIUS, S FORMAN, MR BERENDES, HW GRAUBARD, BI ISOTALO, L TI EFFECT OF AGE, PARITY, AND SMOKING ON PREGNANCY OUTCOME - A POPULATION-BASED STUDY SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE MATERNAL AGE; PARITY; SMOKING; LOW BIRTH WEIGHT; SMALL-FOR-GESTATIONAL-AGE; PRETERM DELIVERY ID GESTATIONAL-AGE; MATERNAL AGE; BIRTH-WEIGHT; FETAL GROWTH; MORTALITY; SWEDEN AB OBJECTIVES: The purpose of our study was to investigate the combined interactive effects of maternal age, parity, and smoking on pregnancy outcome. STUDY DESIGN: This was a population-based Swedish study (n = 538,829). RESULTS: Multiple logistic regression analysis showed that the smoking-related effect on the relative increase in the odds ratio of low birth weight and preterm delivery was significantly greater among multiparous patients than nulliparous; among multiparas, smoking increased the odds ratios for low birth weight and preterm delivery by 2.4 and 1.6; the corresponding relative increases in the odds ratios among nulliparas were 1.7 and 1.1, respectively. With advancing maternal age there was a smoking-related relative increase in the odds ratios for small-for-gestational-age births. Moreover, the age effect on the relative increase of low birth weight, preterm delivery, and small-for-gestational-age births was greater among nulliparas than multiparas. CONCLUSIONS: Older smokers are at an especially high risk for small-for-gestational-age births, and parous smokers are at an especially high risk for low birth weight and preterm delivery. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. NCI,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. NCI,BIOMETRY BRANCH,BETHESDA,MD 20892. NR 26 TC 106 Z9 106 U1 2 U2 7 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD JAN PY 1993 VL 168 IS 1 BP 16 EP 21 PN 1 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA KH569 UT WOS:A1993KH56900004 PM 8420320 ER EF