FN Thomson Reuters Web of Science™ VR 1.0 PT J AU CRAXTON, A ALI, N SHEARS, SB AF CRAXTON, A ALI, N SHEARS, SB TI COMPARISON OF THE ACTIVITIES OF A MULTIPLE INOSITOL POLYPHOSPHATE PHOSPHATASE OBTAINED FROM SEVERAL SOURCES - A SEARCH FOR HETEROGENEITY IN THIS ENZYME SO BIOCHEMICAL JOURNAL LA English DT Article ID HUMAN-ERYTHROCYTE-MEMBRANE; ENDOPLASMIC-RETICULUM; 1,3,4,5-TETRAKISPHOSPHATE 3-PHOSPHATASE; RAT-LIVER; 1,4,5-TRISPHOSPHATE; PROTEINS; BINDING; BRAIN AB A multiple inositol polyphosphate phosphatase (formerly known as inositol 1,3,4,5-tetrakisphosphate 3-phosphatase) was purified approx. 22 000-fold from rat liver. The final preparation migrated on SDS/PAGE as a doublet with a mean apparent molecular mass of 47 kDa. Upon size-exclusion chromatography, the enzyme was eluted with an apparent molecular mass of 36 kDa. This enzyme was approximately evenly distributed between the 'rough' and 'smooth' subfractions of endoplasmic reticulum. There was a 20-fold range of specific activities of this phosphatase in CHAPS-solubilized particulate fractions prepared from the following rat tissues: liver, heart, kidney, testis and brain. However, each of these extracts contained different amounts of endogenous inhibitors of enzyme activity. After removal of these inhibitors by MonoQ anion-exchange chromatography, there was only a 2.5-fold range of specific activities; kidney contained the most and brain contained the least. We prepared and characterized polyclonal antiserum to the hepatic phosphatase, which immunoprecipitated 85-100% of both particulate and soluble phosphatase activities. The antiserum also immunoprecipitated, with equivalent efficacy, CHAPS-solubilized phosphatase activities from heart, kidney, testis, brain and erythrocytes (all prepared from rat). Our data strengthen the case that the function of the mammalian phosphatase is unrelated to the metabolism of Ca2+-mobilizing cellular signals. The CHAPS-solubilized phosphatase from turkey erythrocytes was not immunoprecipitated by the polyclonal antiserum, and is therefore an isoform that is structurally distinct, and possibly functionally unique. RP CRAXTON, A (reprint author), NIEHS,CELLULAR & MOLEC PHARMACOL LAB,INOSITOL LIPID SECT,RES TRIANGLE PK,NC 27709, USA. NR 29 TC 21 Z9 21 U1 0 U2 3 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD JAN 15 PY 1995 VL 305 BP 491 EP 498 PN 2 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QC431 UT WOS:A1995QC43100023 PM 7832765 ER PT J AU ALI, N CRAXTON, A SUMNER, M SHEARS, SB AF ALI, N CRAXTON, A SUMNER, M SHEARS, SB TI EFFECTS OF ALUMINUM ON THE HEPATIC INOSITOL POLYPHOSPHATE PHOSPHATASE SO BIOCHEMICAL JOURNAL LA English DT Article ID NEUROBLASTOMA-CELLS; HEXAKISPHOSPHATE; HEPATOCYTES; 1,3,4,5,6-PENTAKISPHOSPHATE; 3-PHOSPHATASE; METABOLISM AB There is speculation that some of the toxic effects of Al3+ may originate from it perturbing inositol phosphate/Ca2+ signalling. For example, in permeabilized L1210 mouse lymphoma cells, 10-50 mu M Al3+ activated Ins(1,3,4,5)P-4-dependent Ca2+ mobilization and Ins(1,3,4,5)P-4 3-phosphatase activity [Loomis-Husselbee, Cullen,Irvine and Dawson (1991) Biochem. J. 277, 883-885]. Ins(1,3,4,5)P-4 3-phosphatase activity is performed by a multiple inositol polyphosphate phosphatase (MIPP) that also attacks Ins(1,3,4,5,6)P-5 and InsP(6), [Craxton, Ali and Shears (1995) Biochem. J. 305, 491-498] : 5-50 mu M Al3+ increased MIPP activity towards both Ins(1,3,4,5)P-4 (by 30%) and Ins(1,3,4,5,6)P-5 (by up to 500 %), without affecting metabolism of InsP(6). Higher concentrations of Al3+ inhibited metabolism of all three substrates, and in the case of InsP(6), Al3+ altered the pattern of accumulating products. When 1-50 mu M Al3+ was present, InsP(6) became a less effective inhibitor of Ins(1,3,4,5)P-4 3-phosphatase activity; this effect did not depend on the presence of cellular membranes, contrary to a previous proposal. The latter phenomenon largely explains how, in a cell-free system where Ins(1,3,4,5)P-4 3-phosphatase is inhibited by endogenous InsP(6), the addition of Al3+ can apparently increase the enzyme activity. However, there was no effect of either 10 or 25 mu M Al3+ (in either the presence or absence of apotransferrin) on inositol phosphate profiles in either Jurkat E6-1 lymphoma cells or AR4-2J pancreatoma cells. RP ALI, N (reprint author), NIEHS, INOSITOL LIPID SECT, CELLULAR & MOLEC PHARMACOL LAB, POB 12233, RES TRIANGLE PK, NC 27709 USA. NR 21 TC 11 Z9 11 U1 0 U2 1 PU PORTLAND PRESS LTD PI LONDON PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD JAN 15 PY 1995 VL 305 BP 557 EP 561 PN 2 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QC431 UT WOS:A1995QC43100032 PM 7832774 ER PT J AU GEORGE, DT NUTT, DJ RAWLINGS, RR PHILLIPS, MJM ECKARDT, MJ POTTER, WZ LINNOILA, M AF GEORGE, DT NUTT, DJ RAWLINGS, RR PHILLIPS, MJM ECKARDT, MJ POTTER, WZ LINNOILA, M TI BEHAVIORAL AND ENDOCRINE RESPONSES TO CLOMIPRAMINE IN PANIC DISORDER PATIENTS WITH OR WITHOUT ALCOHOLISM SO BIOLOGICAL PSYCHIATRY LA English DT Article DE CLOMIPRAMINE; COMORBIDITY; ALCOHOLISM; PANIC DISORDER; SEROTONIN; TYPE I TYPE II ALCOHOLICS ID DEPRESSED-PATIENTS; HEALTHY-SUBJECTS; INTRAVENOUS CLOMIPRAMINE; SEROTONIN FUNCTION; 5-HT RECEPTORS; GROWTH-HORMONE; PREFERRING P; ANXIETY; ETHANOL; RATS AB Central nervous system serotonin functions may differ between certain subgroups of alcoholics, patients with panic disorder, and healthy volunteers. To investigate these possibilities we administered the serotonin uptake inhibitor, clomipramine (12.5 mg, IV), to patients, with alcohol dependence, patients with panic disorder with or without alcohol dependence, and healthy volunteers. Alcoholics did nor differ from healthy volunteers in their neuroendocrine or behavioral responses. In contrast patients with panic disorder exhibited marked dysphoric reactions and/or panic attacks following low-dose IV clomipramine, whereas their neuroendocrine responses were similar to the other two groups. Patients with panic disorder may have super-sensitive postsynaptic serotonin receptors in areas of their central nervous system, which are important for mood regulation. C1 UNIV BRISTOL SCH MED,PSYCHOPHARMACOL UNIT,BRISTOL,AVON,ENGLAND. NIMH,CLIN PHARMACOL SECT,CLIN SCI LAB,BETHESDA,MD. RP GEORGE, DT (reprint author), NIAAA,DICBR,CLIN STUDIES LAB,BLDG 10,ROOM 3B-19,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 47 TC 22 Z9 22 U1 2 U2 4 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiat. PD JAN 15 PY 1995 VL 37 IS 2 BP 112 EP 119 DI 10.1016/0006-3223(94)00156-W PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QC584 UT WOS:A1995QC58400006 PM 7718674 ER PT J AU BERGSAGEL, PL SMITH, AM SZCZEPEK, A MANT, MJ BELCH, AR PILARSKI, LM AF BERGSAGEL, PL SMITH, AM SZCZEPEK, A MANT, MJ BELCH, AR PILARSKI, LM TI IN MULTIPLE-MYELOMA, CLONOTYPIC B-LYMPHOCYTES ARE DETECTABLE AMONG CD19(+) PERIPHERAL-BLOOD CELLS EXPRESSING CD38, CD56, AND MONOTYPIC IG LIGHT-CHAIN SO BLOOD LA English DT Article ID LINEAGE CELLS; BONE-MARROW; PLASMA-CELL; CD45 ISOFORMS; ANTIGEN; DIFFERENTIATION; POPULATIONS; MATURATION; SPLEEN; GENES AB Multiple myeloma (MM) is characterized by a plasma cell infiltrate of the hone marrow (BM). However, late-stage monotypic B cells have been detected in the blood. This work analyzes the effects of clinical treatment on late stage CD19(+) B cells present in 752 blood samples from 152 MM patients. MM patients have 2 to 8 times as many circulating CD19(+) cells as do normal donors. Analysis of the Ig heavy chain (IgH) gene rearrangements using polymerase chain reaction indicates that the CD19(+) population includes cells sharing the same clonotypic CDR3 region as is detected in the BM plasma cells, for patients analyzed during chemotherapy or in relapse. They are also monotypic as defined by their cytoplasmic or surface expression of Ig kappa- or lambda light chain. The light chain restriction is the same as that of the BM plasma cells. Individual patients observed over 1- to 2-year periods exhibit considerable variation in the number of B cells present in blood; this number does not correlate with the concentration of serum monoclonal Ig. The monoclonal blood CD19(+) cells are not eliminated by any of the chemotherapy regimens analyzed and remain at high levels during transient remissions. Patients in the progressive phase of disease or in relapse have significantly higher numbers of B cells than do patients in transient remission or untreated patients. During periods when the quantity of blood B cells approaches normal, phenotypically their quality is highly abnormal, with physical and phenotypic heterogeneity. Most B cells express CD45R0, a high density of CD38, and CD56 characteristic of late-stage B or pre-plasma cells. CD38(hi) blood B cells had a cyclical presence. We conclude that monoclonal B cells in the blood of myeloma patient populations include drug-resistant reservoirs of clonotypic cells that may underlie relapse. (C) 1995 by The American Society of Hematology. C1 UNIV ALBERTA,DEPT IMMUNOL,EDMONTON,AB T6G 2H7,CANADA. UNIV ALBERTA,DEPT ONCOL,EDMONTON,AB,CANADA. NCI,USN,MED ONCOL BRANCH,BETHESDA,MD. RI Bergsagel, Peter/A-7842-2011 OI Bergsagel, Peter/0000-0003-1523-7388 NR 39 TC 155 Z9 156 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 1995 VL 85 IS 2 BP 436 EP 447 PG 12 WC Hematology SC Hematology GA QB546 UT WOS:A1995QB54600017 PM 7529064 ER PT J AU TRICOT, G JAGANNATH, S VESOLE, D NELSON, J TINDLE, S MILLER, L CHESON, B CROWLEY, J BARLOGIE, B AF TRICOT, G JAGANNATH, S VESOLE, D NELSON, J TINDLE, S MILLER, L CHESON, B CROWLEY, J BARLOGIE, B TI PERIPHERAL-BLOOD STEM-CELL TRANSPLANTS FOR MULTIPLE-MYELOMA - IDENTIFICATION OF FAVORABLE VARIABLES FOR RAPID ENGRAFTMENT IN 225 PATIENTS SO BLOOD LA English DT Article ID COLONY-STIMULATING FACTOR; HIGH-DOSE CYCLOPHOSPHAMIDE; AUTOLOGOUS TRANSPLANTATION; INTENSIVE THERAPY; BONE-MARROW; MELPHALAN; CHEMOTHERAPY; MOBILIZATION; COLLECTION; CSF AB Transfusion of autologous peripheral blood stem cells (PBSCs) of good quality ensures fast hematopoietic engraftment after myeloablative therapy with a decrease in procedure-related morbidity and mortality. We have analyzed variables influencing the kinetics of engraftment, and therefore reflecting the quality of PBSC collections, in 225 patients with newly diagnosed or refractory multiple myeloma (MM) who received an autotransplant in support of high dose melphalan (200 mg/m(2)); 132 of these patients also completed a second transplant. All PBSCs were collected before the first transplant after high-dose cyclophosphamide (6 g/m(2)) and hematopoietic growth factors, mainly granulocyte-macrophage colony-stimulating factor. PBSCs were administered either alone (91 patients) or with bone marrow (134 patients). A highly significant correlation was observed between the number of CD34(+) cells per kilogram infused and prompt recovery of both granulocytes (P = .0001) and platelets (P = .0001). After correction for the proportion of patients with greater than or equal to 2 x 10(6)/kg CD34 PBSCs infused and with less than or equal to 12 months of prior therapy, no difference in engraftment kinetics was seen between patients receiving PBSCs only and those also receiving bone marrow. Exposure to chemotherapy, even to less than or equal to 6 months of alkylating agents, significantly delayed hematopoietic recovery posttransplantation. The threshold dose of CD34 cells necessary for prompt engraftment was greater than or equal to 2.0 x 10(6)/kg for patients with less than or equal to 24 months of chemotherapy before the first transplant, whereas greater than 5 x 10(6)/kg CD34 cells were required to assure rapid recovery also in those with longer exposure. Such quantities, easily collected in the large majority of patients with shorter exposure (91%), were obtained in only 28% of patients with more than 24 months of prior chemotherapy. Rapid platelet recovery within a narrow range of time (before day 14) was almost invariably seen (94%) when greater than 5 x 10(6)/kg CD34 cells were infused, irrespective of the duration of prior therapy, whereas the range widened progressively when less CD34 cells were infused. In the absence of CD34 measurements, fast recovery of platelets to greater than 50 x 10(9)/L within 14 days after high-dose cyclophosphamide and less than or equal to 12 months of prior chemotherapy were the best predictors of early engraftment. Prudent use of stem cell-damaging agents, such as melphalan and nitrosoureas, is recommended in MM patients who might be candidates for autotransplantation. Alternatively, PBSCs should be collected early after diagnosis. (C) 1995 by The American Society of Hematology. C1 UNIV ARKANSAS MED SCI HOSP,ARKANSAS CANC RES CTR,LITTLE ROCK,AR 72205. NCI,BETHESDA,MD 20892. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. RP TRICOT, G (reprint author), UNIV ARKANSAS MED SCI HOSP,DIV HEMATOL ONCOL,4301 W MARKHAM,SLOT 508,LITTLE ROCK,AR 72205, USA. FU NCI NIH HHS [CA55819, CA59340] NR 29 TC 382 Z9 386 U1 0 U2 4 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 1995 VL 85 IS 2 BP 588 EP 596 PG 9 WC Hematology SC Hematology GA QB546 UT WOS:A1995QB54600035 PM 7529066 ER PT J AU HONG, MK LASKIN, WB HERMAN, BE JOHNSTON, MH VARGO, JJ STEINBERG, SM ALLEGRA, CJ JOHNSTON, PG AF HONG, MK LASKIN, WB HERMAN, BE JOHNSTON, MH VARGO, JJ STEINBERG, SM ALLEGRA, CJ JOHNSTON, PG TI EXPANSION OF THE KI-67 PROLIFERATIVE COMPARTMENT CORRELATES WITH DEGREE OF DYSPLASIA IN BARRETTS-ESOPHAGUS SO CANCER LA English DT Article DE BARRETTS ESOPHAGUS; KI-67; MIB-1; PROLIFERATION; IMMUNOHISTOCHEMISTRY ID CELL NUCLEAR ANTIGEN; MONOCLONAL-ANTIBODY KI-67; FLOW-CYTOMETRIC ANALYSIS; HIGH-GRADE DYSPLASIA; ENDOSCOPIC SURVEILLANCE; EARLY ADENOCARCINOMA; EXPRESSION; RISK; CLASSIFICATION; PROGRESSION AB Background. Barrett's esophagus is a histologically defined premalignant lesion of the esophagus in which normal squamous epithelium is replaced by intestinalized columnar epithelium. In a multistep progression from Barrett's esophagus to fully developed carcinoma, accelerated proliferation may indicate or precede genomic instability and, therefore, may be an important factor in the pathogenesis and/or prediction of malignant transformation. Ki-67 is a nuclear antigen expressed in proliferating cells, (G(1), S, G(2), and M phases) but not in resting cells (G, phase). This study was undertaken to determine if Ki-67 expression correlates with the degree of dysplasia and if Ki-67 expression can help to differentiate those patients with or without dysplasia. Methods. The Ki-67 proliferation fraction in 87 paraffin embedded esophageal biopsies from 43 patients with the Ki-67 antibody (MIB-1) was analyzed using immunohistochemistry. Using a computerized proliferation index program (QNA v2.54, Becton Dickinson Cellular Imaging Systems, Inc., Elmhurst, IL), a Ki-67 score was derived for the luminal surface, upper esophageal crypt, lower crypt, and underlying glandular zone of the columnar-lined esophagus. Results. Significant differences in Ki-67 scores were noted in each zone among different histologic categories: normal gastric ([NG] n = 17); Barrett's without dysplasia ([ND] n = 17); low grade dysplasia ([LG] n = 21); high grade dysplasia ([HG] n = 14); and adenocarcinoma ([CA] n = 5). The pattern of Ki-67 expression was associated strongly ith each histologic category. The percentage of Ki-67 positive nuclei in each mucosal zone statistically separated high grade from low grade dysplasia (P < 0.001). In high grade dysplastic tissues, the Ki-67 positive nuclei were found predominantly on the surface epithelium and upper crypt zones, whereas in low grade dysplasia, the majority of Ki-67 positive nuclei were found in the lower crypt zone. The number of Ki-67 positive nuclei in each mucosal component also was significantly different in Barrett's esophagus without dysplasia when compared with Barrett's esophagus with low grade dysplastic tissues. (P < 0.001) Staining patterns of indefinite for dysplasia by H & E staining separated into several distinct patterns (five LG, seven ND, one NG) whereas six biopsies with low grade dysplasia had a Ki-67 expression pattern more consistent with that of high grade dysplasia. Conclusion. The Ki-67 staining pattern correlated with histologic findings in Barrett's esophagus and may represent an additional parameter for differentiating patients with or without dysplasia. C1 NCI, DIV CANC TREATMENT, NAVY MED ONCOL BRANCH, BETHESDA, MD 20892 USA. NCI, BIOSTAT & DATA MANAGEMENT SECT, BETHESDA, MD 20892 USA. NATL NAVAL MED CTR, DEPT PATHOL, BETHESDA, MD USA. NATL NAVAL MED CTR, DEPT GASTROENTEROL, BETHESDA, MD USA. OI Vargo, John/0000-0001-7638-5283 NR 38 TC 118 Z9 121 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 1995 VL 75 IS 2 BP 423 EP 429 DI 10.1002/1097-0142(19950115)75:2<423::AID-CNCR2820750202>3.0.CO;2-5 PG 7 WC Oncology SC Oncology GA QA968 UT WOS:A1995QA96800001 PM 7812911 ER PT J AU MELLEMKJAER, L OLSEN, JH LINET, MS GRIDLEY, G MCLAUGHLIN, JK AF MELLEMKJAER, L OLSEN, JH LINET, MS GRIDLEY, G MCLAUGHLIN, JK TI CANCER RISK AFTER SPLENECTOMY SO CANCER LA English DT Article DE SPLENECTOMY; NEOPLASMS; COHORT STUDY; HOSPITAL RECORDS ID NON-HODGKINS-LYMPHOMA; 2ND CANCERS; POSTTRAUMATIC SPLENECTOMY; LYMPHOCYTIC-LEUKEMIA; POLYCYTHEMIA-VERA; PEPTIC-ULCER; LUNG-CANCER; DISEASE; DISORDERS; SEPSIS AB Background. Splenectomy may have an impact on immunologic function. To the authors' knowledge, the only previous epidemiologic study investigating cancer risk among patients splenectomized because of trauma reported no increased cancer risk. In contrast, several investigations have suggested that splenectomy in patients with Hodgkin's disease increases the risk for secondary leukemia independent of treatment. Methods. To evaluate the cancer risk of patients who underwent splenectomy after traumatic rupture of the spleen, 1103 patients were identified between 1977 and 1989 through Danish hospital discharge records. Another 5212 splenectomized patients also were identified to perform additional analyses for assessing cancer risk subsequent to splenectomy for nontraumatic indications including benign and malignant conditions. Cancer occurrence was determined by performing a linkage to the Danish Cancer Registry. For comparison, expected numbers of cases of cancer were calculated from national cancer incidence rates. Results. The number of cancer cases observed among posttraumatic splenectomized patients matched the expected number (relative risk = 1.0; n = 20; 95% confidence interval = 0.6-1.6) in an average follow-up of 6.8 years. Additional analyses identified possible excesses of a number of site-specific neoplasms among certain subgroups of patients undergoing splenectomy for nontraumatic reasons, but the numbers in the subgroup analyses were small. Conclusions. No increased risk for cancer was observed among patients who underwent splenectomy because of trauma. However, an increased risk for some specific cancer sites was found in patients who underwent splenectomy for nontraumatic reasons, although the effect of treatments for underlying disease and lifestyle habits such as cigarette smoking could not be ruled out in explaining these excess risks. C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. RP MELLEMKJAER, L (reprint author), DANISH CANC SOC,DIV CANC EPIDEMIOL,STRANDBLVD 49,BOX 839,DK-2100 COPENHAGEN O,DENMARK. FU NCI NIH HHS [N01-CP-85639-04] NR 49 TC 63 Z9 68 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 1995 VL 75 IS 2 BP 577 EP 583 DI 10.1002/1097-0142(19950115)75:2<577::AID-CNCR2820750222>3.0.CO;2-K PG 7 WC Oncology SC Oncology GA QA968 UT WOS:A1995QA96800021 PM 7812926 ER PT J AU SHIMIZU, T OCONNOR, PM KOHN, KW POMMIER, Y AF SHIMIZU, T OCONNOR, PM KOHN, KW POMMIER, Y TI UNSCHEDULED ACTIVATION OF CYCLIN B1/CDC2 KINASE IN HUMAN PROMYELOCYTIC LEUKEMIA-CELL LINE HL-60 CELLS UNDERGOING APOPTOSIS INDUCED BY DNA-DAMAGE SO CANCER RESEARCH LA English DT Note ID TOPOISOMERASE-II INHIBITORS; HAMSTER OVARY CELLS; P34CDC2 KINASE; ANTITUMOR AGENTS; HL-60 CELLS; G2 ARREST; CAMPTOTHECIN; INDUCTION; ETOPOSIDE; EXPRESSION AB We have studied changes in cyclin A- and B1-dependent kinases during apoptosis induced in human promyelocytic leukemia (HL60) cells treated with the topoisomerase I inhibitor camptothecin. We found that cyclin B1/Cdc2 kinase activity transiently increases within 30 min after camptothecin treatment. This increase is followed by a rapid inactivation of the cyclin B1/Cdc2 kinase that is associated with Cdc2 tyrosine phosphorylation without any change in Cdc2 or cyclin B1 protein levels. The DNA polymerase inhibitor aphidicolin abrogates camptothecin-induced changes in cyclin B1/Cdc2 kinase activity, indicating that DNA replication-induced DNA damage is essential for both Cdc2 alterations and apoptosis activation. Apoptosis and the initial cyclin B1/Cdc2 kinase activation were amplified using synchronized S-phase cells, and cyclin A/cdk2 kinase did not change under these conditions. The same transient activation and subsequent inactivation of cyclin B1/Cdc2 kinase were observed after DNA damage by etoposide or bis-(2-chloroethyl)methylamine hydrochloride. These observations suggest that DNA damage promotes the transient and unscheduled stimulation of cyclin B1/Cdc2 kinase activity in HL60 cells prior to apoptosis. C1 NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 28 TC 170 Z9 171 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 1995 VL 55 IS 2 BP 228 EP 231 PG 4 WC Oncology SC Oncology GA QB808 UT WOS:A1995QB80800005 PM 7812949 ER PT J AU OLSEN, JH SCHULGEN, G BOICE, JD WHYSNER, J TRAVIS, LB WILLIAMS, GM JOHNSON, FB MCGEE, JO AF OLSEN, JH SCHULGEN, G BOICE, JD WHYSNER, J TRAVIS, LB WILLIAMS, GM JOHNSON, FB MCGEE, JO TI ANTIEPILEPTIC TREATMENT AND RISK FOR HEPATOBILIARY CANCER AND MALIGNANT-LYMPHOMA SO CANCER RESEARCH LA English DT Article ID ANTICONVULSANT DRUGS; ENHANCEMENT; COHORT AB The possible influence of phenobarbital and phenytoin treatment on cancer risk was investigated in a case-control study nested in a cohort of 8004 epileptic patients in Denmark. Information on anticonvulsive treatments was abstracted for 95% of 60 patients with cancers of the liver and biliary tract or malignant lymphoma and for 94% of 171 cancer-free control patients. Use of anticonvulsive drugs was correlated with angiographic procedures that used Thorotrast, a well-known human liver carcinogen. After exclusion of study subjects exposed to Thorotrast, no association was seen between treatment with phenobarbital and cancer of the liver (odds ratio, 1.0; 95% confidence interval, 0.1-8.0) or biliary tract (odds ratio, 0.8; 95% confidence interval, 0.1-4.2). Furthermore, a histopathological evaluation of slides from 7 of 9 liver cancer patients not treated with Thorotrast revealed that 3 of the 4 cases of hepatocellular carcinoma involved cirrhosis of the liver, which suggested an etiological role for alcohol or viral hepatitis. A possible link was observed between use of phenytoin and risk for non-Hodgkin's lymphoma (1.8; 0.5-6.6), with a rising trend in risk with increasing dose. Our results suggest that the increased risk for cancers of the liver and biliary tract among Danish epileptic patients is likely to be due to Thorotrast administration and factors associated with cirrhosis of the liver rather than to anticonvulsive treatment. C1 UNIV FREIBURG, INST MED BIOMETRIE & INFORMAT, D-79104 FREIBURG, GERMANY. NCI, RADIAT EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. AMER HLTH FDN, DIV PATHOL & TOXICOL, VALHALLA, NY 10595 USA. ARMED FORCES INST PATHOL, DEPT CHEM PATHOL, WASHINGTON, DC 20306 USA. UNIV OXFORD, JOHN RADCLIFFE HOSP, NUFFIELD DEPT PATHOL & BACTERIOL, OXFORD OX3 9DU, ENGLAND. RP OLSEN, JH (reprint author), DANISH CANC SOC, DIV CANC EPIDEMIOL, DK-2100 COPENHAGEN O, DENMARK. NR 20 TC 63 Z9 63 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1995 VL 55 IS 2 BP 294 EP 297 PG 4 WC Oncology SC Oncology GA QB808 UT WOS:A1995QB80800016 PM 7812960 ER PT J AU WEBBER, KO KREITMAN, RJ PASTAN, I AF WEBBER, KO KREITMAN, RJ PASTAN, I TI RAPID AND SPECIFIC UPTAKE OF ANTI-TAC DISULFIDE-STABILIZED FV BY INTERLEUKIN-2 RECEPTOR-BEARING TUMORS SO CANCER RESEARCH LA English DT Article ID SINGLE-CHAIN-FV; MONOCLONAL-ANTIBODIES; SOLID TUMORS; FRAGMENTS; PROTEINS; BINDING; IN-111; RADIOIMMUNODETECTION; BIODISTRIBUTION; IMMUNOTOXINS AB The disulfide-stabilized Fv (dsFv) is a novel form of a variable-region fragment (Fv) of an antibody which is stabilized by an interchain disulfide bond. As a consequence, it is more stable than its Fv analogue. Anti-Tac(dsFv) is derived from anti-Tac(IgG) which specifically binds to the p55 subunit of the interleukin-2 receptor (IL2R alpha). The receptor is found in large numbers on activated T cells and many T-cell leukemias. The biodistribution patterns of I-125-anti-Tac(dsFv) and I-125-anti-Tac(IgG) were determined in. athymic nude mice bearing two s.c. tumors, one expressing a stably transfected plasmid encoding IL2R alpha (ATAC4) and one composed of parental untransfected A431 epidermoid carcinoma cells. Anti-Tac(dsFv), which has a molecular weight of 25,000, was specifically captured by the ATAC4 tumors but not by control A431 tumors. The antigen-specific tumors accumulated >2% of the injected dose/g within 15-45 min after i.v. injection. The level of radioactivity in the ATAC4 tumors was maintained at >1% of the injected dose/g for nearly 6 h, at which time the ATAC4 tumors contained ii-fold more I-125-anti-Tac(dsFv) than did the A431 tumors. Unbound I-125-anti-Tac(dsFv) was rapidly cleared from the blood with apparently biphasic pharmacokinetics (alpha t(1/2) = <10 min; beta t(1/2) = similar to 5.5 h). Initially, the bulk of the I-125-anti-Tac(dsFv) appeared in the kidneys. In contrast, I-125-anti-Tac(IgG) showed no tumor- or tissue-specific uptake over the 24-h time course of the experiments and remained primarily in the blood stream (blood clearance t(1/2) = similar to 12 h). This is the first report of the biodistribution of a dsFv fragment. Because of its rapid uptake by IL2 receptor-bearing tumors, short serum half-life, and increased stability, radiolabeled anti-Tac(dsFv) may be useful for the imaging and therapy of neoplasias expressing the IL2 receptor. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 31 TC 21 Z9 21 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 1995 VL 55 IS 2 BP 318 EP 323 PG 6 WC Oncology SC Oncology GA QB808 UT WOS:A1995QB80800021 PM 7812965 ER PT J AU NAKANISHI, H TAYLOR, RM CHREST, FJ MASUI, T UTSUMI, K TATEMATSU, M PASSANITI, A AF NAKANISHI, H TAYLOR, RM CHREST, FJ MASUI, T UTSUMI, K TATEMATSU, M PASSANITI, A TI PROGRESSION OF HORMONE-DEPENDENT ADENOCARCINOMA CELLS TO HORMONE-INDEPENDENT SPINDLE CARCINOMA-CELLS IN-VITRO IN A CLONAL SPONTANEOUS RAT MAMMARY-TUMOR CELL-LINE SO CANCER RESEARCH LA English DT Article ID FIBROBLAST GROWTH-FACTOR; BREAST-CANCER; PHOSPHOTRANSFERASE GENE; ESTROGEN-RECEPTOR; EPITHELIAL-CELLS; C-MYC; EXPRESSION; VIMENTIN; ASSOCIATION; METASTASIS AB A hormone-dependent, clonal carcinoma cell line, designated RM22-F5, was derived from a malignant mammary mixed tumor spontaneously arising in an outbred old female Wistar rat. These cells expressed keratin and desmosomal protein and formed epithelial monolayers in a growth factor and hormone-supplemented medium (LHC-8) containing 10% fetal bovine serum (E-type cells). Cells subcultured for 6 to 8 passages in RPMI 1640 medium containing 10% fetal bovine serum without supplements appeared to be fibroblastic and expressed vimentin (F-type cells). The shift to a fibroblast-like morphology was associated with a more malignant phenotype which included rapid, hormone-independent growth and invasive sarcoma-like character in nude mice. F-type cells were no longer able to express their original epithelial phenotype in LHC-8 medium. Cytogenetic analysis revealed that both E- and F-type cells had essentially the same karyotype. Analysis of PCR-amplified DNA further demonstrated a point mutation of the H-ras-1 gene at codon 12 and loss of the normal H-ras-1 allele in both cell types. Genetic tagging of E-type cells with the neomycin-resistance gene resulted in the generation of F-type cells with neomycin resistance in RPMI 1640 medium, suggesting that F-type cells are a malignant variant of E-type cells arising during ira vitro culture, Somatic cell fusion between E- and F-type cells revealed that with most hybrid clones tested, the fibroblast like phenotype was greatly suppressed, These results suggest that an irreversible phenotypic transition, representative of tumor progression from hormone-dependent adenocarcinoma to more malignant hormone independent spindle carcinoma cells, is a recessive event and may involve loss of a suppressor function. C1 NIA,GERONTOL RES CTR,BIOL CHEM LAB,BALTIMORE,MD 21224. NIA,GERONTOL RES CTR,CLIN IMMUNOL LAB,BALTIMORE,MD 21224. JOHNS HOPKINS MED INST,DEPT PATHOL & DERMATOL,BALTIMORE,MD 21224. AICHI CANC CTR,RES INST,PATHOL LAB,CHIKUSA KU,NAGOYA,AICHI 464,JAPAN. AICHI CANC CTR,RES INST,ULTRASTRUCT RES LAB,CHIKUSA KU,NAGOYA,AICHI 464,JAPAN. NR 38 TC 19 Z9 19 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 15 PY 1995 VL 55 IS 2 BP 399 EP 407 PG 9 WC Oncology SC Oncology GA QB808 UT WOS:A1995QB80800033 PM 7529136 ER PT J AU VILNER, BJ JOHN, CS BOWEN, WD AF VILNER, BJ JOHN, CS BOWEN, WD TI SIGMA-1 AND SIGMA-2 RECEPTORS ARE EXPRESSED IN A WIDE VARIETY OF HUMAN AND RODENT TUMOR-CELL LINES SO CANCER RESEARCH LA English DT Article ID GUINEA-PIG BRAIN; BINDING-SITES; AFFINITY; SUGGEST; NCB-20 AB Thirteen tumor-derived cell lines of human and nonhuman origin and from various tissues were examined for the presence and density of sigma-1 and sigma-2 receptors. Sigma-1 receptors of a crude membrane fraction were labeled using [H-3](+)-pentazocine, and sigma-2 receptors were labeled with [H-3]1,3-di-o-tolylguanidine ([H-3]DTG); in the presence or absence of dextrallorphan. [H-3](+)-Pentazocine-binding sites were heterogeneous. In rodent cell lines (e.g., C6 glioma, N1E-115 neuroblastoma, and NG108-15 neuroblastoma x glioma hybrid), human T47D breast ductal carcinoma, human NCI-H727 lung carcinoid, and human A375 melanoma, [H-3](+)-pentazocine bound to high- and low-affinity sites with K(d)1 = 0.67-7.0 nM, B(max)1 = 25.5-108 fmol/mg protein, K(d)2 = 127-600 nM, and B(max)2 = 942-5431 fmol/mg protein. However, [H-3](+)-pentazocine bound to a single site in other cell lines. In human U-138MG glioblastoma, SK-N-SH neuroblastoma, and LNCaP.FGC prostate, K-d = 28-61 nM and B-max = 975-1196 fmol/mg protein, whereas in ThP-1 leukemia K-d = 146 nM and B-max = 1411 fmol/mg protein. The sigma-1-like nature of [H-3](+)-pentazocine-binding sites was confirmed by competition studies which revealed high affinity for haloperidol and enantioselectivity for (+)-pentazocine over (-)-pentazocine. Interestingly, human MCF-7 breast adenocarcinoma showed little or no specific binding of [H-3](+)pentazocine, suggesting the absence of sigma-1 receptors in this cell line. All cell lines examined expressed a high density of sigma-2 receptors with K-d values for [H-3]DTG ranging from 20 to 101 nM and B-max values of 491 to 7324 fmol/mg protein. Competition studies indicated possible heterogeneity of sigma-2 receptors. While sites labeled by [H-3]DTG in all cell lines tested exhibited affinity for haloperidol and preference for (-)-pentazocine over the (+)-enantiomer, human cell lines generally showed 4- to 7-fold lower affinity for haloperidol and approximately 10-fold lower affinity for (-)-pentazocine compared with the rodent cell lines. The high density of sigma-1 and sigma 2-binding sites in these cell lines suggests important cellular functions in cancer, as well as potential diagnostic utility for tumor-imaging agents which target sigma sites. These cell lines may be useful as model systems in which to study the functions of sigma sites in normal tissues, as well as their possible role in tumor biology. C1 NIDDKD,MED CHEM LAB,RECEPTOR BIOCHEM & PHARMACOL UNIT,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,MED CTR,DEPT RADIOL,RADIOPHARMACEUT CHEM SECT,WASHINGTON,DC 20037. NR 25 TC 328 Z9 335 U1 3 U2 16 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 1995 VL 55 IS 2 BP 408 EP 413 PG 6 WC Oncology SC Oncology GA QB808 UT WOS:A1995QB80800034 PM 7812973 ER PT J AU DUVERGER, N RADER, D IKEWAKI, K NISHIWAKI, M SAKAMOTO, T ISHIKAWA, T NAGANO, M NAKAMURA, H BREWER, HB AF DUVERGER, N RADER, D IKEWAKI, K NISHIWAKI, M SAKAMOTO, T ISHIKAWA, T NAGANO, M NAKAMURA, H BREWER, HB TI CHARACTERIZATION OF HIGH-DENSITY APOLIPOPROTEIN PARTICLES A-I AND A-I-A-II ISOLATED FROM HUMANS WITH CHOLESTERYL ESTER TRANSFER PROTEIN-DEFICIENCY SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article DE IMMUNOAFFINITY CHROMATOGRAPHY; APOLIPOPROTEIN AI; APOLIPOPROTEIN A II; HEPG2 CELLS ID CONTAINING LIPOPROTEIN PARTICLES; IMMUNOSORBENT-ASSAY ELISA; LIPID TRANSFER PROTEINS; HUMAN-PLASMA; TRANSGENIC MICE; IMMUNOAFFINITY CHROMATOGRAPHY; MONOCLONAL-ANTIBODIES; ADIPOSE-CELLS; SUBCLASSES; METABOLISM AB The cholesteryl ester transfer protein (CETP) plays an important role in metabolism of high-density lipoprotein and reverse cholesterol transport in humans. The two major classes of high-density lipoprotein particles are those containing apolipoprotein A-I (LpA-I) and those containing both apoA-I and apoA-II (LpA-I:A-II). We isolated and characterized the apoA-I-containing lipoprotein particles from three subjects with homozygous CETP deficiency (CETP-D) and compared the results with those from normolipidemic control subjects. Plasma concentrations of apoA-I in both LpA-I and LpA-I:A-II were significantly elevated in CETP-D subjects. Both LpA-I and LpA-I:A-II from these subjects were larger and contained more cholesteryl ester per particle than control particles. In CETP-D, subpopulations of LpA-I and LpA-I:A-II with an unusually large size (Stokes diameters 13.8 nm and 12.6 nm, respectively) not detected in normal subjects were isolated. The molar ratio of apoA-I to apoA-II in LpA-I:A-II isolated from CETP-D subjects was higher (mean 2.4) than those of controls (mean 1.4). ApoE was primarily associated with LpA-I:A-II in CETP-D subjects. A subclass of LpA-I with pre-beta migration on agarose electrophoresis was increased in CETP-D subjects. Both LpA-I and LpA-I:A-II from CETP-D subjects bound with higher affinity but less capacity to HepG2 cells compared with control particles, and were internalized to a lesser extent than control particles. These data suggest that the absence of CETP in humans significantly affects the plasma concentration, size, composition, and cellular interaction of both major classes of apoA-I-containing lipoprotein particles. C1 NHLBI, MOLEC DIS BRANCH, BETHESDA, MD USA. NATL DEF MED COLL, DEPT INTERNAL MED 1, TOKOROZAWA, SAITAMA 359, JAPAN. JIKEI UNIV, AOTO HOSP, SCH MED, DEPT INTERNAL MED, TOKYO, JAPAN. NR 64 TC 20 Z9 20 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD JAN 15 PY 1995 VL 227 IS 1-2 BP 123 EP 129 DI 10.1111/j.1432-1033.1995.tb20367.x PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QB851 UT WOS:A1995QB85100014 PM 7851377 ER PT J AU CHANG, AC SALOMON, DR WADSWORTH, S HONG, MJP MOJCIK, CF OTTO, S SHEVACH, EM COLIGAN, JE AF CHANG, AC SALOMON, DR WADSWORTH, S HONG, MJP MOJCIK, CF OTTO, S SHEVACH, EM COLIGAN, JE TI ALPHA(3)BETA(1) AND ALPHA(6)BETA(1) INTEGRINS MEDIATE LAMININ MEROSIN BINDING AND FUNCTION AS COSTIMULATORY MOLECULES FOR HUMAN THYMOCYTE PROLIFERATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PROTEIN-KINASE-C; EXTRACELLULAR-MATRIX COMPONENTS; BASEMENT-MEMBRANE PROTEINS; CELL-ADHESION; T-CELLS; FIBRONECTIN RECEPTOR; REGULATED EXPRESSION; DIVALENT-CATIONS; FOCAL ADHESIONS; CALPHOSTIN-C AB Integrins comprise a superfamily of ap heterodimers that serve as cell signaling as well as adhesion molecules. We demonstrate that the alpha(3) beta(1) and alpha(6) beta(1) integrins are laminin/merosin receptors expressed in human thymocytes. By reverse transcriptase-PCR analysis, we determined that the alpha(3A)beta(1), but not the alpha(3B)beta(1), cytoplasmic structural variant of alpha(3) beta(1) is expressed in thymocytes. In contrast, both alpha(6A)beta(1) and alpha(6B)beta(1) cytoplasmic structural variants of alpha(6) beta(1) are expressed. A small percentage (10 to 15%) of human thymocytes bind to immobilized laminin, and even fewer (3 to 5%) bind to merosin, the laminin isoform normally present in the thymus. This binding, however, can be increased to 39 to 41% after activation of thymocytes with Mn2+ (or PMA). Binding to either laminin or merosin is completely inhibited by anti-beta(1) mAb or by a mixture of anti-alpha(3) and anti-alpha(6) mAbs, indicating that both alpha(3) beta(1) and alpha(6) beta(1) participate in thymocyte adhesion to the laminin family of extracellular matrix proteins. The protein kinase C inhibitors, calphostin C and staurosporine, inhibit Mn2+-enhanced thymocyte binding, suggesting that protein kinase C activity is crucial for the binding. Furthermore, the data indicate that at least two divalent cation binding sites serve to regulate integrin binding activity. Finally, we show that both immobilized laminin and merosin have costimulatory function for anti-CD3-induced thymocyte proliferation, and both anti-alpha(3) and anti-alpha(6) mAbs can block this proliferative response. The cooperative function of alpha(3) beta(1) and alpha(6) beta(1) evidenced in the laminin/merosin binding and proliferation assays suggests that thymocyte-merosin interactions may play an important role in thymic T cell development. C1 NIAID,MOLEC STRUCT LAB,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,CELLULAR IMMUNOL SECT,BETHESDA,MD 20892. RI Salomon, Daniel/E-9380-2012 FU NIDDK NIH HHS [DK1820] NR 73 TC 57 Z9 58 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 1995 VL 154 IS 2 BP 500 EP 510 PG 11 WC Immunology SC Immunology GA QA636 UT WOS:A1995QA63600003 PM 7814863 ER PT J AU COX, JH GALARDY, P BENNINK, JR YEWDELL, JW AF COX, JH GALARDY, P BENNINK, JR YEWDELL, JW TI PRESENTATION OF ENDOGENOUS AND EXOGENOUS ANTIGENS IS NOT AFFECTED BY INACTIVATION OF E(1) UBIQUITIN-ACTIVATING ENZYME IN TEMPERATURE-SENSITIVE CELL-LINES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; MOUSE Y-CHROMOSOME; CLASS-I MOLECULES; ENDOPLASMIC-RETICULUM; VACCINIA VIRUS; PROTEIN; RECOGNITION; PATHWAY; GENE; CLONING AB Little is known regarding the mechanism by which MHC class I-associated peptides are generated. Proteins can be targeted for degradation by the covalent attachment of ubiquitin. The first step in ubiquitin conjugation to proteins is its binding to E(1) ubiquitin-activating enzyme. To study the role of ubiquitin-targeted protein degradation in Ag processing, we used two mutant cell lines with temperature-sensitive E(1) proteins, and a recombinant vaccinia virus expressing wild-type human E(1). One of the cell lines examined (hamster ts20 cells) was previously reported to have a minimal capacity after a 1-h incubation at 41 degrees C to present osmotically loaded OVA to a T cell hybridoma, as assessed by IL-2 release. Even after incubating the same cells for 1 h at 43 degrees C, we failed to detect an E(1)-related decrease in the presentation of biosynthesized or osmotically loaded OVA to splenic T cells, as measured by target cell lysis. We introduce the use of mouse tsA1S9 cells to Ag-processing studies and provide the initial biochemical characterization of their defect in protein ubiquitination. Relative to parental L929 cells, after thermal inactivation of E(1), these cells actually demonstrate enhanced presentation of endogenous or exogenous viral Ags to T cells. Our findings do not support a role for protein ubiquitination in Ag processing, and indicate that either the temperature-sensitive cell lines examined do not exhibit a sufficient reduction in ubiquitin-conjugating activity to affect the generation of antigenic peptides, or that ubiquitin-targeted proteolysis is not essential for processing the two exogenous and six endogenous Ags examined. C1 NIAID, VIRAL DIS LAB, BETHESDA, MD 20892 USA. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 42 TC 74 Z9 74 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 EI 1550-6606 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1995 VL 154 IS 2 BP 511 EP 519 PG 9 WC Immunology SC Immunology GA QA636 UT WOS:A1995QA63600004 PM 7814864 ER PT J AU GUERY, JC SETTE, A APPELLA, E ADORINI, L AF GUERY, JC SETTE, A APPELLA, E ADORINI, L TI CONSTITUTIVE PRESENTATION OF DOMINANT EPITOPES FROM ENDOGENOUS NATURALLY PROCESSED SELF-BETA(2)-MICROGLOBULIN TO CLASS II-RESTRICTED T-CELLS LEADS TO SELF-TOLERANCE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTIGEN PRESENTATION; POSITIVE SELECTION; AUTOPHAGIC VACUOLE; MHC MOLECULES; ACIDIC PH; PEPTIDES; BINDING; IA; MECHANISMS; THYMUS AB The mouse beta(2)-microglobulin (m beta(2)-m) peptide corresponding to residues 25-40 binds to the MHC class II molecules I-A(d) and I-E(d) and is immunogenic in BALB/c beta(2)-m-deficient but not in normal BALB/c mice. The self-m beta(2)-m peptide 25-40 is presented by both I-A(d) and I-E(d) class II molecules as demonstrated by the activation of T cell hybridomas specific for this sequence obtained from beta(2)-m knock-out mice. By analyzing the effect of N- and C-terminal truncations of m beta(2)-m25-40 on binding to class II molecules and on activation of T cell hybridomas, the minimum epitopes recognized by I-A(d) and I-E(d) -restricted T cells are included within amino acid residues 26-39 and 24-36, respectively. Both sets of T hybridomas are also activated by the corresponding naturally processed self-epitope presented by APC from BALB/c mice and from other H-2(d) strains, irrespective of their Mls phenotype. Therefore, the sequence 25-40 contains dominant naturally processed self-epitopes of the mouse beta(2)-m. Processing of endogenous m beta(2)-m is sensitive to protease inhibitors and lysosomotropic amines, and is not caused by reuptake of shed or released protein. These results indicate that self-beta(2)-m-peptide-MHC class II complexes derive from constitutive processing of the endogenous intracellular pool of m beta(2)-m in an acidic endosomal compartment. Antigenic complexes between m beta(2)-m peptides and I-A(d) or I-E(d) class II molecules are constitutively expressed by APC of different tissues, including the thymus, and they are able to induce T cell tolerance, as shown by the lack of T cell response to m beta(2)-m25-40 in BALB/c mice. C1 ROCHE MILANO RIC,I-20132 MILAN,ITALY. CYTEL CORP,SAN DIEGO,CA 92121. NCI,BETHESDA,MD 20892. RI GUERY, Jean-Charles/G-1452-2013 OI GUERY, Jean-Charles/0000-0003-4499-3270 FU PHS HHS [I18634] NR 47 TC 35 Z9 35 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 15 PY 1995 VL 154 IS 2 BP 545 EP 554 PG 10 WC Immunology SC Immunology GA QA636 UT WOS:A1995QA63600008 PM 7814867 ER PT J AU STEVENS, EJ JACKNIN, L ROBBINS, PF KAWAKAMI, Y ELGAMIL, M ROSENBERG, SA YANNELLI, JR AF STEVENS, EJ JACKNIN, L ROBBINS, PF KAWAKAMI, Y ELGAMIL, M ROSENBERG, SA YANNELLI, JR TI GENERATION OF TUMOR-SPECIFIC CTLS FROM MELANOMA PATIENTS BY USING PERIPHERAL-BLOOD STIMULATED WITH ALLOGENEIC MELANOMA TUMOR-CELL LINES - FINE SPECIFICITY AND MART-1 MELANOMA ANTIGEN RECOGNITION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INFILTRATING HUMAN MELANOMAS; TOXIC LYMPHOCYTES-T; AUTOLOGOUS MELANOMA; HLA-A; METASTATIC MELANOMA; INTERLEUKIN-2; IMMUNOTHERAPY; RESTRICTION AB PBLs were isolated from 13 patients with metastatic melanoma. Mixed lymphocyte tumor cell cultures (ML TCs) were established (15 times) by using irradiated HLA-matched (one class I locus) allogeneic melanoma tumor cell lines (13 times) or autologous melanoma tumor cell lines (two times) in medium containing 120 IU/ml IL-2 and 100 IU/ml IL-4. PBLs grew to levels that could be assessed for functional reactivity 9 of 15 times. In seven of nine cases, CD3(+)CD8(+) CTLs grew from MLTCs that were tumor specific; five were restricted by HLA-A2 and two were restricted by HLA-A24. Four of the tumor-specific CTL lines lysed autologous fresh tumor cells. Tumor-specific CTLs from two of three patients had cytolytic activity identical with tumor-infiltrating lymphocytes (TIL) derived from tumor biopsies removed earlier and grown in high concentrations (6000 IU/ml) of IL-2. Three of the HLA-A2-restricted tumor-specific CTLs were shown to recognize 293 cells transfected with HLA-A2.1 cDNA and the gene encoding the melanoma Ag, MART-1. In addition, these CTLs recognized the T2 cell line pulsed exogenously with the peptide MART-1(27-35), which is the nine-amino acid immunodominant epitope of the MART-1 Ag recognized on melanoma tumor cells by nearly all HLA-A2-restricted TIL. Thus, we have demonstrated the ability to generate tumor-specific CTLs from PBLs that are similar in their reactivity to TIL. This technique obviates the need for autologous tumor tissue and suggests that PBLs contain sufficient CTL precursors for use in generating antitumor CTLs for cellular immunotherapy trials. C1 NCI,SURG BRANCH,BETHESDA,MD 20892. RI Kawakami, Yutaka /E-7429-2013 OI Kawakami, Yutaka /0000-0003-4836-2855 NR 31 TC 85 Z9 86 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 1995 VL 154 IS 2 BP 762 EP 771 PG 10 WC Immunology SC Immunology GA QA636 UT WOS:A1995QA63600030 PM 7814882 ER PT J AU MARTIN, DF DEBARGE, LR NUSSENBLATT, RB CHAN, CC ROBERGE, FG AF MARTIN, DF DEBARGE, LR NUSSENBLATT, RB CHAN, CC ROBERGE, FG TI SYNERGISTIC EFFECT OF RAPAMYCIN AND CYCLOSPORINE-A IN THE TREATMENT OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID P70 S6 KINASE; ALLOGRAFT-REJECTION; IMMUNE PERFORMANCES; RENAL-FUNCTION; LYMPHOCYTES-T; UVEITIS; RAT; ACTIVATION; HEART; KIDNEY AB Immunosuppressive drugs currently available for the treatment of autoimmune diseases display a narrow therapeutic window between efficacy and toxic side effects. The use of combinations of drugs that have a synergistic effect may expand this window and reduce the risk of toxicity. We evaluated the combination effect of rapamycin (Rapa) and cyclosporin A (CsA) in an autoimmune disease model of the eye. The dose-effect relationship of Rapa with CsA was measured in vitro on the inhibition of proliferation of retinal S-Ag-primed lymphocytes. A median effect analysis was performed and a combination index (Cl) calculated for 50% inhibition of proliferation. Rapa and CsA were markedly synergistic over a wide dose range (lowest Cl = 0.31). Calculated dose reduction factors indicated that Rapa could be reduced nine-fold and CsA reduced five-fold when these drugs were used in combination. These reduced doses were tested in vivo for the treatment of experimental autoimmune uveoretinitis (EAU). Twelve of 15 rats treated with CsA, 2 mg/kg/day, developed EAU with a median severity of 2.5. Fourteen of 15 rats treated with Rapa, 0.01 mg/kg/day, developed EAU with a median severity of 3.25. Complete inhibition of EAU was achieved in all 15 animals treated with the combination of Rapa and CsA (combined vs CsA alone, p < 0.0002; combined vs Rapa alone, p < 0.00001). The demonstrated synergistic relationship between Rapa and CsA will allow the use of reduced doses of each drug to achieve a therapeutic effect. The use of lower doses may reduce the toxicity of these drugs for the treatment of autoimmune uveitis. C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 45 TC 52 Z9 52 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 1995 VL 154 IS 2 BP 922 EP 927 PG 6 WC Immunology SC Immunology GA QA636 UT WOS:A1995QA63600046 PM 7814893 ER PT J AU FARAGGI, D SIMON, R AF FARAGGI, D SIMON, R TI A NEURAL-NETWORK MODEL FOR SURVIVAL-DATA SO STATISTICS IN MEDICINE LA English DT Article ID CANCER-PATIENTS; REGRESSION; LENGTH; STAY AB Neural networks have received considerable attention recently, mostly by non-statisticians. They are considered by many to be very promising tools for classification and prediction. In this paper we present an approach to modelling censored survival data using the input-output relationship associated with a simple feed-forward neural network as the basis for a non-linear proportional hazards model. This approach can be extended to other models used with censored survival data. The proportional hazards neural network parameters are estimated using the method of maximum likelihood. These maximum likelihood based models can be compared, using readily available techniques such as the likelihood ratio test and the Akaike criterion. The neural network models are illustrated using data on the survival of men with prostatic carcinoma. A method of interpreting the neural network predictions based on the factorial contrasts is presented. RP FARAGGI, D (reprint author), NCI, BIOMETR RES BRANCH, 6130 EXECUT BLVD, ROOM 739, ROCKVILLE, MD 20852 USA. NR 29 TC 72 Z9 77 U1 4 U2 4 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0277-6715 EI 1097-0258 J9 STAT MED JI Stat. Med. PD JAN 15 PY 1995 VL 14 IS 1 BP 73 EP 82 DI 10.1002/sim.4780140108 PG 10 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 QF708 UT WOS:A1995QF70800006 PM 7701159 ER PT J AU LEE, CC YAMADA, KM AF LEE, CC YAMADA, KM TI ALTERNATIVELY SPLICED JUXTAMEMBRANE DOMAIN OF A TYROSINE KINASE RECEPTOR IS A MULTIFUNCTIONAL REGULATORY SITE - DELETION ALTERS CELLULAR TYROSINE PHOSPHORYLATION PATTERN AND FACILITATES BINDING OF PHOSPHATIDYLINOSITOL-3-OH KINASE TO THE HEPATOCYTE GROWTH-FACTOR RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID SCATTER FACTOR-RECEPTOR; 3-KINASE AB The hepatocyte growth factor (HGF) receptor is a tyrosine kinase receptor that mediates signal transduction upon ligand stimulation, This receptor is present in mouse tissues as two major isoforms differing by a 47-amino acid segment in the juxtamembrane domain, an alternatively spliced cytoplasmic region adjacent to the transmembrane domain of the receptor. We report here that the juxtamembrane domain of the receptor is involved in the regulation of downstream signal transduction, The two receptor isoforms were transiently expressed in COS-7 cells, Both exogenous receptors underwent autophosphorylation and subsequently stimulated a set of protein tyrosine phosphorylations that were not present in control cells. Comparisons of phosphotyrosine profiles of transfected cell lysates induced by receptor isoforms demonstrated that at least three phosphorylated proteins of similar to 62, similar to 35, and similar to 30 kDa were differentially induced by the receptor isoforms, suggesting that the juxtamembrane domain of a kinase receptor can play a role in selective signal transduction, Furthermore, the p85 subunit of phosphatidylinositol-3-OH kinase (PI3 kinase) co-precipitated with the small isoform of the HGF receptor, and this association was dramatically inhibited by treatment with 12-O-tetradecanoylphorbol-13-acetate. Since removal of the juxtamembrane domain facilitates the binding of p85 to the receptor, it is likely that the juxtamembrane region plays a role in negative regulation of the binding of PI3 kinase to the HGF receptor, Our study establishes novel molecular sequelae of alternative splicing of an intracellular domain of the HGF receptor. C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 22 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 13 PY 1995 VL 270 IS 2 BP 507 EP 510 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QB816 UT WOS:A1995QB81600002 PM 7822270 ER PT J AU TAKADA, T IIDA, K MOSS, J AF TAKADA, T IIDA, K MOSS, J TI CONSERVATION OF A COMMON MOTIF IN ENZYMES CATALYZING ADP-RIBOSE TRANSFER - IDENTIFICATION OF DOMAINS IN MAMMALIAN TRANSFERASES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEAT-LABILE ENTEROTOXIN; NAD-BINDING-SITE; ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; DIPHTHERIA-TOXIN; SKELETAL-MUSCLE; POLY(ADP-RIBOSE) POLYMERASE; RIBOSYLTRANSFERASE ACTIVITY; CRYSTAL-STRUCTURE; CHOLERA-TOXIN AB Bacterial toxin ADP-ribosyltransferases, e.g. diphtheria toxin (DT) and pertussis toxin, have in common consensus sequences involved in catalytic activity, which are localized to three regions, Region I is notable for a histidine or arginine; region II, similar to 50-75 amino acids downstream, is rich in aromatic/hydrophobic amino acids; and region III, further downstream has a glutamate and other acidic amino acids, A similar motif was observed in the sequence of the glycosylphosphatidylinositol-linked muscle ADP-ribosyltransferase. Site-directed mutagenesis was performed to verify the role of this motif, Proteins were expressed in rat adenocarcinoma cells, released from the cell with phosphatidylinositol-specific phospholipase C, and quantified with polyclonal antibodies, Transferase His(114) in region I aligned with His(21) of DT; as with DT, the H114N mutant was active. Aromatic/hydrophobic amino acids (region II) were found similar to 30-50 amino acids downstream of this histidine, Although transferase has a Glu(278)-Tyr-Ile sequence characteristic of region III in DT, Glu(278) was not critical for activity, In an alternative region III containing Glu(238)-Glu(239)-Glu(240), Glu(238) and Glu(240) but not Glu(239) were critical, Glu(240) aligned with critical glutamates in DT, Pseudomonas exotoxin, and C3 transferase. Thus, the mammalian ADP-ribosyltransferases have motifs similar to toxin ADP-ribosyltransferases, suggesting that these sequences are important in ADP-ribose transfer reactions. RP NHLBI, PULM & CRIT CARE MED BRANCH, RM 5N-307, BLDG 10, BETHESDA, MD 20892 USA. NR 34 TC 59 Z9 59 U1 0 U2 1 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 13 PY 1995 VL 270 IS 2 BP 541 EP 544 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QB816 UT WOS:A1995QB81600009 PM 7822277 ER PT J AU TONG, ZB NELSON, LM DEAN, J AF TONG, ZB NELSON, LM DEAN, J TI INHIBITION OF ZONA-PELLUCIDA GENE-EXPRESSION BY ANTISENSE OLIGONUCLEOTIDES INJECTED INTO MOUSE OOCYTES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MATERNAL MESSENGER-RNAS; SPERM RECEPTOR; DEVELOPMENTAL REGULATION; MONOCLONAL-ANTIBODIES; POLYACRYLAMIDE GELS; OOGENESIS; PROTEINS; BIOSYNTHESIS; TRANSLATION; ZP3 AB During murine oogenesis, the zona pellucida proteins (ZP1, ZP2, and ZP3) are synthesized and secreted to form an extracellular matrix that surrounds the oocyte and mediates specific biological functions essential to mammalian fertilization and early development. To investigate the relationship among the zona proteins during zona matrix assembly, we have undertaken to inhibit de novo biosynthesis of specific zona proteins with antisense oligonucleotides complementary to the 5'-ends of ZP2 (nucleotide position 19-42) and ZP3 (nucleotide 21-44) mRNAs, When injected into the cytoplasm of growing mouse oocytes, the antisense oligonucleotides targeted specific zona mRNAs for degradation, as confirmed by a RNase protection assay, Individual zona pellucida protein synthesis was followed by immunoprecipitation with ZP2- and ZP3-specific monoclonal antibodies, New zona protein synthesis from the targeted mRNA was abolished, but nontargeted zona protein continued to be synthesized, Interestingly, abolishment of either ZP2 or ZP3 protein synthesis prevented the incorporation of the other protein into the extracellular zona matrix, These results suggest that ZP2 and ZP3 proteins are independent of each other in their biosynthesis but are dependent upon each other for their incorporation into the zona pellucida matrix, This study provides an experimental system in which destruction of a targeted mRNA generates a transient loss-of-expression phenotype during mouse oocyte growth. C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP TONG, ZB (reprint author), NIDDK,CELLULAR & DEV BIOL LAB,BLDG 6,RM B1-26,6 CTR DR,MSC 2715,BETHESDA,MD 20892, USA. NR 35 TC 37 Z9 38 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 13 PY 1995 VL 270 IS 2 BP 849 EP 853 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QB816 UT WOS:A1995QB81600055 PM 7822321 ER PT J AU MITCHELL, J GUTIERREZ, J NORTHUP, JK AF MITCHELL, J GUTIERREZ, J NORTHUP, JK TI PURIFICATION, CHARACTERIZATION, AND PARTIAL AMINO-ACID-SEQUENCE OF A G-PROTEIN-ACTIVATED PHOSPHOLIPASE-C FROM SQUID PHOTORECEPTORS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LIMULUS VENTRAL PHOTORECEPTORS; GUANINE-NUCLEOTIDE BINDING; VISUAL EXCITATION; ALPHA-SUBUNITS; IMMUNOLOGICAL IDENTIFICATION; INVERTEBRATE PHOTORECEPTORS; BOVINE BRAIN; DROSOPHILA; LIGHT; MEMBRANES AB Invertebrate visual transduction is thought to be initiated by photoactivation of rhodopsin and its subsequent interaction with a guanyl nucleotide-binding protein (G protein), The identities of the G protein and its target effector have remained elusive, although evidence suggests the involvement of a phospholipase C (PLC). We have identified a phosphatidylinositol-specific PLC from the cytosol of squid retina, The enzyme was purified to near-homogeneity by a combination of carboxymethyl-Sepharose and heparin-Sepharose chromatography. The purified PLC, identified as an approximately 140-kDa protein by sodium dodecyl sulfate-polyacrylamide gels, hydrolyzed phosphatidylinositol 4,5-bisphosphate (PIP2) at a rate of 10-15 mu mol/min/mg of protein with 1 mu M Ca2+. The partial amino acid sequence of the protein showed homology with a PLC cloned from a Drosophila head library (PLC21) and lesser homology with Drosophila norpA protein and mammalian PLC beta isozymes. Reconstitution of purified squid PLC with an AIF(-)-activated 44-kDa G protein a subunit extracted from squid photoreceptor membranes resulted in a significant increase in PIP2 hydrolysis over a range of Ca2+ concentrations while reconstitution with mammalian G(t) alpha or G(i)1 alpha was without effect, These results suggest that cephalopod phototransduction is mediated by G alpha-44 activation of a 140-kDa cytosolic PLC. C1 NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA. RP MITCHELL, J (reprint author), UNIV TORONTO, DEPT PHARMACOL, MED SCI BLDG, TORONTO, ON M5S 1A8, CANADA. NR 43 TC 30 Z9 30 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 13 PY 1995 VL 270 IS 2 BP 854 EP 859 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QB816 UT WOS:A1995QB81600056 PM 7822322 ER PT J AU WANGE, RL ISAKOV, N BURKE, TR OTAKA, A ROLLER, PP WATTS, JD AEBERSOLD, R SAMELSON, LE AF WANGE, RL ISAKOV, N BURKE, TR OTAKA, A ROLLER, PP WATTS, JD AEBERSOLD, R SAMELSON, LE TI F-2(PMP)(2)-TAM-ZETA(3), A NOVEL COMPETITIVE INHIBITOR OF THE BINDING OF ZAP-70 TO THE T-CELL ANTIGEN RECEPTOR, BLOCKS EARLY T-CELL SIGNALING SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ZETA-CHAIN; TYROSINE PHOSPHORYLATION; PHOSPHOLIPASE C-GAMMA-1; SH2 DOMAINS; ACTIVATION; PROTEIN; KINASE; CD3-EPSILON; STIMULATION; RESIDUES AB Signaling by the T cell antigen receptor (TCR) is mediated by 17-residue tyrosine-based activation motifs (TAM) present in the cytoplasmic tails of the TCR zeta and CD3 chains. TAMs become tyrosine-phosphorylated upon TCR stimulation, creating a high affinity binding site for the tandem SH2 domains of ZAP-70. In permeabilized T cells, the association of TCR and ZAP-70 was inhibited by a protein tyrosine phosphatase (PTPase)resistant TAM peptide analog, in which difluorophosphonomethyl phenylalanyl (F(2)Pmp) residues replaced phosphotyrosine. Inhibition of this association prevented TCR-stimulated tyrosine phosphorylation of ZAP-70 and reduced ZAP-70 kinase activity to basal levels. The reduction in ZAP-70 activity coincided with reduced tyrosine phosphorylation of a number of substrates. Such PTPase-resistant peptides, capable of disrupting SH2 domain-mediated protein-protein interactions, should prove useful in further dissection of multiple signaling pathways and may serve as models for rationally designed chemotherapeutic agents for the treatment of autoimmune and neoplastic disorders. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NCI,DCT,DTP,MED CHEM LAB,BETHESDA,MD 20892. UNIV BRITISH COLUMBIA,BIOMED RES CTR,VANCOUVER,BC V6T 1Z3,CANADA. RI Burke, Terrence/N-2601-2014 NR 43 TC 85 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 13 PY 1995 VL 270 IS 2 BP 944 EP 948 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QB816 UT WOS:A1995QB81600069 PM 7822334 ER PT J AU DELUCA, D BLUESTONE, JA SHULTZ, LD SHARROW, SO TATSUMI, Y AF DELUCA, D BLUESTONE, JA SHULTZ, LD SHARROW, SO TATSUMI, Y TI PROGRAMMED DIFFERENTIATION OF MURINE THYMOCYTES DURING FETAL THYMUS ORGAN-CULTURE SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE T CELL DEVELOPMENT; FETAL THYMUS; ORGAN CULTURE ID T-CELL RECEPTOR; POSITIVE NONLYMPHOID CELLS; GAMMA-DELTA CELLS; ALPHA-BETA; EMBRYONIC THYMUS; SCID MICE; ANTIBODIES; SELECTION; LYMPHOCYTES; MATURATION AB Fetal thymus organ culture (FTOC) has become widely used to investigate the impact of immunomodulators on T cell development. However, these studies have given variable results among different laboratories. In this study, we have found that fetal tissue age and mouse strain differences can affect the development of T cell phenotypes in this system. T cell development in FTOC occurred in two 'waves', defined as peaks of cell recovery. The first wave consisted initially of CD4(-)CD8(-) double negative (DN) cells and CD4(-)CD8(+) single positive (SP) T cells expressing gamma delta T cell receptor (TCR). CD4(+)CD8(+) double positive (DP) cells expressing low levels of alpha beta TCR were produced soon thereafter; and these cells dominated the cultures for the balance of the first wave. Prolonged FTOC resulted in the production of another wave of T cells which were relatively enriched for CD4 or CD8 SP cells expressing high levels of alpha beta TCR, as well as DN cells and CD4(-)CD8(+) SP T cells expressing high levels of gamma delta TCR. As defined by cell number and differentiation of alpha beta TCR SP cells, development was delayed in FTOC using fetal thymus tissue from younger fetuses relative to that observed when older fetal thymus tissue was used. The degree of development of T cells in FTOC was also strain dependent. Organ cultures derived from 14 gestation days (gd) C.B-17 scid/scid fetal thymus did not generate TCR-bearing mature SP cells, but they did produce TCR-negative CD4 and CD8 SP cells likely to be precursors of DP thymocytes. Such cultures made from 18 gd tissue did not produce SP cells. Negative selection in FTOC was also evaluated. Mtv-specific V(beta)3 cells were deleted in FTOC of C3H/HeN tissue. Deletion occurred only in late FTOC, suggesting a late encounter between the Mtv deleting elements and susceptible T cells during ontogeny. These results show that while FTOC recapitulates normal thymic development by a variety of criteria, results can be influenced by the length of culture, as well as by the age and strain of fetal thymus tissue utilized. C1 UNIV CHICAGO,BEN MAY INST,CHICAGO,IL 60637. JACKSON LAB,BAR HARBOR,ME 04609. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP DELUCA, D (reprint author), UNIV ARIZONA,DEPT MICROBIOL & IMMUNOL,BLDG 90,TUCSON,AZ 85721, USA. FU NIAID NIH HHS [R01 AI29407]; NIGMS NIH HHS [R01 GM35968]; PHS HHS [R01 A19260] NR 38 TC 36 Z9 38 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 13 PY 1995 VL 178 IS 1 BP 13 EP 29 DI 10.1016/0022-1759(94)00236-P PG 17 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA QC783 UT WOS:A1995QC78300002 PM 7829862 ER PT J AU VOWELLS, SJ SEKHSARIA, S MALECH, HL SHALIT, M FLEISHER, TA AF VOWELLS, SJ SEKHSARIA, S MALECH, HL SHALIT, M FLEISHER, TA TI FLOW CYTOMETRIC ANALYSIS OF THE GRANULOCYTE RESPIRATORY BURST - A COMPARISON STUDY OF FLUORESCENT-PROBES SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE CHRONIC GRANULOMATOUS DISEASE; PHAGOCYTE; REACTIVE OXYGEN SPECIES ID OXIDATIVE BURST; WHOLE-BLOOD; NEUTROPHILS; PHAGOCYTOSIS; DISEASES AB Chronic granulomatous disease (CGD) is a rare recessive disorder caused by defects in the NADPH oxidase enzyme complex of phagocytes (neutrophils, eosinophils and monocytes). CGD phagocytes fail to produce superox ide and other reactive oxygen species following cell activation (Malech, 1993). The products of oxidase activation can be measured in individual cells by flow cytometry using specific fluorescent probes that increase fluorescence upon oxidation (Trinkle et al., 1987). This approach can be used to confirm a diagnosis of CGD, and to detect the normal/abnormal phagocyte mixture that characterizes the X-linked CGD carrier state. Three fluorescent probes have been described as useful for this purpose: 2'7'-dichlorofluorescin diacetate (DCF) (Bass et al., 1983), 5,6-carboxy-2'7'-dichlorofluorescein diacetate, bis(acetoxymethyl) ester (C-DCF) (Hockenbery et al., 1993) and dihydrorhodamine 123 (DHR) (Rothe et al., 1988; Kinsey et al., 1987). A direct comparison between these three probes has not been reported. In this study we performed a direct comparison between these three probes, evaluating their ability in flow cytometric analysis to maximize fluorescent separation between activated CGD patient and normal granulocytes. Using a whole blood technique with phorbol myristate acetate (PMA) as an activator, it was found that DHR loaded normal granulocytes had a fluorescence intensity which, upon activation, was 48-fold higher than that of C-DCF loaded granulocytes and seven-fold higher than DCF loaded granulocytes (P < 0.001). Use of sodium azide to decrease the catabolism of H2O2 enhanced the fluorescence of DCF by 140%, C-DCF by 45% and DHR by 25%, suggesting that DCF is primarily sensitive to H2O2. DCF and DHR were then evaluated for sensitivity in the detection of small percentages of normal cells in a CGD/normal granulocyte mixture. Normal sub-populations as small as 0.1% could clearly be distinguished using DHR, while DCF was insensitive at this level. Based on these findings, we used DHR in an effort to detect normal granulocytes in a CGD patient following therapeutic granulocyte transfusion. We were able to detect normal granulocytes in the circulation for up to 18 h after transfusion. With these data we show that DHR is the most sensitive flow cytometric indicator for the detection of oxygen reactive species in activated granulocytes and is the best probe for evaluating CGD patients and carriers. In addition, our data suggest that DHR is a useful tool for monitoring circulating normal granulocytes in CGD patients following transfusion, and potentially will be a sensitive probe for assessing the success of such future technologies as gene therapy for CGD. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,SERV IMMUNOL,BETHESDA,MD 20892. NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 14 TC 302 Z9 309 U1 1 U2 10 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 13 PY 1995 VL 178 IS 1 BP 89 EP 97 DI 10.1016/0022-1759(94)00247-T PG 9 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA QC783 UT WOS:A1995QC78300009 PM 7829869 ER PT J AU GOLDMAN, D LONG, J AF GOLDMAN, D LONG, J TI MORE ON DNA TYPING DISPUTE SO NATURE LA English DT Letter RP GOLDMAN, D (reprint author), NIAAA,INTRAMURAL RES PROGRAM,ROCKVILLE,MD 20852, USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 3 TC 0 Z9 0 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD JAN 12 PY 1995 VL 373 IS 6510 BP 99 EP 99 DI 10.1038/373099a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QB063 UT WOS:A1995QB06300024 PM 7816113 ER PT J AU ZUBER, M HOOVER, TA COURT, DL AF ZUBER, M HOOVER, TA COURT, DL TI CLONING, SEQUENCING AND EXPRESSION OF THE DNAJ GENE OF COXIELLA-BURNETII SO GENE LA English DT Article DE HEAT-SHOCK PROTEIN; MOLECULAR CHAPERONE; GENETIC COMPLEMENTATION; IMMUNO-CROSS-REACTIVITY ID ESCHERICHIA-COLI; VIRULENCE; PROTEINS; CELLS; GRPE AB A 6-kb EcoRI genomic DNA fragment of Coxiella burnetii, isolated from a recombinant bacteriophage lambda ZapII library, allowed heterologous genetic complementation of Escherichia coli deleted for its dnaJ gene. The C. burnetii dnaJ gene was expressed in E. coli and identified by Western blot analysis using polyclonal antibodies raised against purified E. coli DnaJ protein. Deletion mapping and genetic complementation demonstrated that C. burnetii dnaJ is present on a 2-kb EcoRI-HindIII genomic DNA fragment, from which the nt sequence of the C. burnetii dnaJ gene was determined. C1 USA,MED RES INST INFECT DIS,DIV TOXICOL,FT DETRICK,MD 21702. USA,MED RES INST INFECT DIS,DIV BACTERIOL,FT DETRICK,MD 21702. RP ZUBER, M (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,CHROMOSOME BIOL LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 22 TC 11 Z9 12 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD JAN 11 PY 1995 VL 152 IS 1 BP 99 EP 102 DI 10.1016/0378-1119(94)00687-N PG 4 WC Genetics & Heredity SC Genetics & Heredity GA QC927 UT WOS:A1995QC92700017 PM 7828937 ER PT J AU MCLAUGHLIN, JK FRAUMENI, JF NYREN, O ADAMI, HO AF MCLAUGHLIN, JK FRAUMENI, JF NYREN, O ADAMI, HO TI SILICONE BREAST IMPLANTS AND RISK OF CANCER SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter ID AUGMENTATION C1 UNIV UPPSALA,UPPSALA,SWEDEN. RP MCLAUGHLIN, JK (reprint author), NCI,BETHESDA,MD 20892, USA. NR 4 TC 21 Z9 21 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 11 PY 1995 VL 273 IS 2 BP 116 EP 116 DI 10.1001/jama.273.2.116 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA PZ687 UT WOS:A1995PZ68700023 PM 7799490 ER PT J AU FRIEDMAN, TC GORDON, VM LEPPLA, SH KLIMPEL, KR BIRCH, NP LOH, YP AF FRIEDMAN, TC GORDON, VM LEPPLA, SH KLIMPEL, KR BIRCH, NP LOH, YP TI IN-VITRO PROCESSING OF ANTHRAX TOXIN PROTECTIVE ANTIGEN BY RECOMBINANT PC1(SPC3) AND BOVINE INTERMEDIATE LOBE SECRETORY VESICLE MEMBRANES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE PROTEIN PROCESSING; TETRABASIC RESIDUES; PROHORMONE CONVERTASES; BACILLUS ANTHRACIS; L-CELLS; PROTECTIVE ANTIGEN ID OPIOMELANOCORTIN-CONVERTING ENZYME; KEX2-LIKE ENDOPROTEASE; FUNCTIONAL EXPRESSION; PROPROTEIN CONVERTASE; PRECURSOR CLEAVAGE; MAMMALIAN-CELLS; LETHAL FACTOR; GH4C1 CELLS; YEAST KEX2; PROTEASE AB Protective antigen (PA), an 83-kDa protein produced by Bacillus anthracis, requires proteolytic activation at a tetrabasic site (RKKR(167)) before it can combine with either edema factor or lethal factor on the cell surface. The complex is then endocytosed and the target cell intoxicated, Previous work has demonstrated that furin, a ubiquitously distributed, subtilisin-like protease, can perform this cleavage. In this study, another member of the furin family, PC1 (SPC3), was tested as a putative processing enzyme for PA, Recombinant PC1, partially purified from the medium of stably transfected L-cells, cleaved PA to a 63-kDa fragment (PA63) and a 20-kDa fragment (PA20). Amino-terminal sequence analysis of the 63 kDa product demonstrated that cleavage occurred between Arg(167) and Ser(168). The pH optimum for in vitro PA cleavage was 6.0 and the enzymatic activity was calcium-dependent. Medium from untransfected L-cells did not cleave PA, Site-directed mutagenesis of the tetrabasic cleavage site revealed that PC1 preferred to cleave sequences containing basic residues at positions -1 and -4 relative to the wild-type cleavage site, demonstrating that PC1 can cleave substrates at a monobasic residue site in vitro. Substrates having basic residues at the -1 and -2 positions were cleaved with approximately twofold less efficiency than wild-type PA. Mutants of PA containing basic residues in positions -1 and either -2 or -4 of the cleavage site were predicted to be substrates for PC1 and were more toxic to L-cells expressing PC1 than to untransfected L-cells, These results demonstrate that PA is cleaved by PC1 in vivo, Membranes from bovine intermediate lobe secretory vesicles which contain both prohormone convertases, PC1 and PC2, also cleaved PA to PA63 with a pH optimum of 5.5, Immunodepletion studies using antisera against PC1 and PC2 showed that these are the enzymes primarily responsible for the cleavage of PA in the membrane preparation, Thus, both recombinant PC1 and a membrane preparation containing endogenous PC1 can activate PA. (C) 1995 Academic Press, Inc. C1 NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. UNIV AUCKLAND,SCH BIOL SCI,AUCKLAND,NEW ZEALAND. RP FRIEDMAN, TC (reprint author), NICHHD,DEV NEUROBIOL LAB,CELLULAR NEUROBIOL SECT,BLDG 49,RM 5A-38,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Birch, Nigel/H-2498-2011 OI Birch, Nigel/0000-0002-8417-3587 NR 50 TC 14 Z9 14 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN 10 PY 1995 VL 316 IS 1 BP 5 EP 13 DI 10.1006/abbi.1995.1002 PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QJ933 UT WOS:A1995QJ93300002 PM 7840657 ER PT J AU CHAMULITRAT, W JORDAN, SJ MASON, RP LITTON, AL WILSON, JG WOOD, ER WOLBERG, G VEDIA, LMY AF CHAMULITRAT, W JORDAN, SJ MASON, RP LITTON, AL WILSON, JG WOOD, ER WOLBERG, G VEDIA, LMY TI TARGETS OF NITRIC-OXIDE IN A MOUSE MODEL OF LIVER INFLAMMATION BY CORYNEBACTERIUM-PARVUM SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE EPR; NITRIC OXIDE; CORYNEBACTERIUM PARVUM; LIPOPOLYSACCHARIDE; NONHEME IRON NITROSYL COMPLEX; CYTOCHROME P420 NITROSYL COMPLEX ID L-ARGININE; NITROGEN-OXIDES; PROTEIN-SYNTHESIS; RAT HEPATOCYTES; HEPATIC-INJURY; FREE-RADICALS; SYNTHASE; ENDOTOXIN; CYTOCHROME-P-450; MACROPHAGES AB Treatment of mice with Corynebacterium parvum induces chronic inflammation. This treatment followed by an injection of lipopolysaccharide (LPS) produces hepatic necrosis and death. We examined liver tissue by using electron paramagnetic resonance (EPR) spectroscopy and found that, in addition to the previously reported nonheme nitrosyl complexes, heme nitrosyl complexes were also formed. Hemoglobin nitrosyl complexes measured in the whole blood of mice treated with C. parvum were not increased after additional LPS treatment. However, this treatment significantly increased the heme nitrosyl complexes in the liver, whereas the nonheme nitrosyl complex concentration was unaffected. EPR signals from whole blood and liver tissues from mice treated with C. parvum and C. parvum + LPS were inhibited by prolonged treatment with N-G-monomethyl-L-arginine (L-NMA). Nitric oxide ((NO)-N-.) is known to bind to cytochrome P450 heme, and we consistently found a suppression of EPR signals attributable to ferric low-spin cytochrome P450/P420 peaks in the livers of mice treated with C. parvum and C. parvum + LPS. By performing analyses of EPR spectra obtained from hepatocytes exposed to (NO)-N-., we were able to unambiguously identify EPR signals attributable to cytochrome P420 and nonheme nitrosyl complexes in the livers of both treatments. Deconvolution of the composite in vivo EPR spectra indicated that hemoglobin nitrosyl complexes contributed weakly in the C. parvum livers, but threefold more in the C. parvum + LPS livers, suggesting that hemorrhage may have occurred. Experiments with L-NMA treatment revealed that this additional (NO)-N-. production did not correlate with hepatic necrosis and onset of death. Immunoprecipitation of liver cytosols from C. parvum- and (C. parvum + LPS)-treated mice using an antibody against mouse inducible nitric oxide synthase showed that this enzyme was indeed present in the cytosolic fractions and was absent in those from control livers. Our novel detection of cytochrome P420 nitrosyl complex in vivo may be linked to any role of hepatic P450's functions during liver inflammation. (C) 1995 Academic Press, Inc. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. WELLCOME RES LABS,RES TRIANGLE PK,NC 27709. NR 42 TC 36 Z9 39 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN 10 PY 1995 VL 316 IS 1 BP 30 EP 37 DI 10.1006/abbi.1995.1006 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QJ933 UT WOS:A1995QJ93300006 PM 7840629 ER PT J AU SHEU, FS HUANG, FL HUANG, KP AF SHEU, FS HUANG, FL HUANG, KP TI DIFFERENTIAL RESPONSES OF PROTEIN-KINASE-C SUBSTRATES (MARCKS, NEUROMODULIN, AND NEUROGRANIN) PHOSPHORYLATION TO CALMODULIN AND S100 SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE PROTEIN KINASE C; NEUROMODULIN; NEUROGRANIN; MARCKS; CALMODULIN; S100 ID MAJOR SPECIFIC SUBSTRATE; PROMINENT CELLULAR SUBSTRATE; GROWTH-ASSOCIATED PROTEIN; ADULT-RAT BRAIN; BINDING-PROTEIN; PHORBOL ESTERS; 87-KDA PROTEIN; MEMBRANE PHOSPHOLIPIDS; BOVINE BRAIN; PURIFICATION AB Phosphorylation of three physiological substrates of protein kinase C (PKC), MARCKS, neuromodulin (Nm), and neurogranin (Ng), was analyzed to determine their relative efficacy as substrates of PKC alpha, beta, and gamma and sensitivities to inhibition by calmodulin (CaM) and S100. Comparison of the V-max/K-m of the phosphorylation of each individual substrate indicated the order of efficacy as PKC substrate was MARCKS > Nm > Ng. Phosphorylation of these proteins in a mixture by PKC beta and gamma was indistinguishable from that when each individual substrate was phosphorylated by these two isozymes, In contrast, the rates of PKC alpha-catalyzed phosphorylation of Nm and Ng in a mixture also containing MARCKS were significantly reduced as compared to that when Nm or Ng was individually phosphorylated by this isozyme. When these substrates were present in a mixture, both CaM and S100 inhibited the PKC-catalyzed phosphorylation of MARCKS to a higher degree than that of Nm or Ng. Protease-activated catalytic fragment of PKC (PKM) was used to determine the effects of Ca2+ and phospholipid on the CaM and S100-mediated inhibition of PKC substrate phosphorylation. CaM and S100 inhibited the PKM-catalyzed phosphorylation of MARCKS only in the presence of Ca2+ and addition of phosphatidylserine (PS)/dioleoylglycerol (DG) did not influence the inhibitory effect. Phosphorylation of Nm or Ng by PKM was inhibited by CaM to a higher degree in the absence than in the presence of Ca2+. S100 was ineffective in inhibiting the phosphorylation of Nm and Ng without Ca2+ and only poorly effective in the presence of Ca2+. The CaM-mediated inhibition of Nm or Ng phosphorylation by PKM was also not affected by PS/DG either with or without Ca2+. The results presented here demonstrate that MARCKS is a preferred substrate of PKC and its phosphorylation by PKC is most sensitive to inhibition by regulatory proteins such as CaM and S100. (C) 1995 Academic Press, Inc. C1 NICHHD, ENDOCRINOL & REPROD RES BRANCH, METAB REGULAT SECT, BETHESDA, MD 20892 USA. RI SHEU, Fwu-Shan/G-6435-2011 OI SHEU, Fwu-Shan/0000-0002-2784-2529 NR 59 TC 44 Z9 45 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0003-9861 EI 1096-0384 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN 10 PY 1995 VL 316 IS 1 BP 335 EP 342 DI 10.1006/abbi.1995.1045 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QJ933 UT WOS:A1995QJ93300045 PM 7840634 ER PT J AU GUNTHER, MR HANNA, PM MASON, RP COHEN, MS AF GUNTHER, MR HANNA, PM MASON, RP COHEN, MS TI HYDROXYL RADICAL FORMATION FROM CUPROUS ION AND HYDROGEN-PEROXIDE - A SPIN-TRAPPING STUDY SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE HYDROXYL RADICAL; COPPER; SPIN-TRAPPING; ESR; H2O2; 4-POBN; ME(2)SO ID DNA DAMAGE; LIPID-PEROXIDATION; DEPENDENT HYDROXYL; AQUEOUS-SOLUTIONS; COPPER(II) ION; COMPLEXES; ADDUCTS; ULTRASOUND; METABOLISM; OXIDATION AB Copper toxicity has been presumed to involve catalytic hydroxyl radical ((OH)-O-.) formation from hydrogen peroxide. Addition of Cu1+ to a solution containing ethanol or dimethylsulfoxide (Me(2)SO) and the spin-trapping agent alpha(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) results in formation of the ol-hydroxyethyl radical or methyl radical adduct of 4-POBN, respectively. Adduct formation was prevented by inclusion of catalase, but not by superoxide dismutase. Inclusion of exogenous H2O2 in the reaction mixture increased the yield of ethanol- or Me(2)SO-derived radical adduct and also enhanced the formation of secondary radical adducts, including 4-POBN/H-. and the methyl radical adduct of 2-methyl-2-nitrosopropane. The alpha-hydroxyethyl adduct of 4-POBN is rapidly decomposed in the presence of copper, but not iron salts, whereas the methyl radical adduct is relatively stable in the presence of inorganic copper. The total concentration of radical adduct detected from the reaction between Cu1+ and H2O2, determined by comparison of the integrated spectral intensity with that of the stable 2,2,6,6-tetramethyl-1-piperidinyloxy free radical, was only 1-5% of the maximum amount predicted assuming radical adduct formation from all of the added copper, A variety of copper chelators inhibit formation of carbon-centered radical adducts of 4-POBN, including penicillamine and triethylenetetramine, which are the primary drugs used to treat the copper metabolism disorder Wilson's disease, The results provide clear evidence for hydroxyl radical formation from Cu1+ and H2O2 (either added or formed during the autoxidation of reduced copper). (C) 1995 Academic Press, Inc. C1 UNIV N CAROLINA,DEPT MED,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT MICROBIOL,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT IMMUNOL,CHAPEL HILL,NC 27599. RP GUNTHER, MR (reprint author), NIEHS,LAB MOLEC BIOPHYS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 45 TC 106 Z9 106 U1 2 U2 15 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN 10 PY 1995 VL 316 IS 1 BP 515 EP 522 DI 10.1006/abbi.1995.1068 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QJ933 UT WOS:A1995QJ93300068 PM 7840659 ER PT J AU SAWAKI, K BAUM, BJ AMBUDKAR, IS AF SAWAKI, K BAUM, BJ AMBUDKAR, IS TI ALPHA(1)-ADRENERGIC AND M(3)-MUSCARINIC RECEPTOR STIMULATION OF PHOSPHATIDYLINOSITOL 4,5-BISPHOSPHATE-SPECIFIC PHOSPHOLIPASE-C ARE INDEPENDENTLY MEDIATED BY G(ALPHA-Q/11) IN RAT PAROTID-GLAND MEMBRANES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE ADRENERGIC RECEPTOR; MUSCARINIC RECEPTOR; G-PROTEIN; PHOSPHOLIPASE C; PAROTID GLAND ID ACINAR-CELLS; G-PROTEIN; ALPHA-SUBUNITS; ACTIVATION; EXPRESSION; SECRETION; ISOZYMES; CALCIUM; CLONING AB Stimulation of ms-muscarinic cholinergic receptors (m(3)AChR) in the rat parotid gland increases the hydrolysis of phosphatidylinositol 4, 5-bisphosphate (PIP2) via activation of the G(alpha q/11) family of G-proteins (Sawaki et al. (1993) Arch. Biochem. Biophys., 546-550). Herein we report that alpha(1)-adrenergic receptor (alpha(1)-AR) stimulation of PIP2 hydrolysis is also mediated via alpha subunits of the G(q/11) family of G-proteins. The alpha(1)-AR agonist, epinephrine, induced a dose-dependent increase (1.5-fold maximum) of exogenously added PIP2 in the presence of guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S), which was inhibited by the (alpha(1)-AR antagonist, phentolamine, but not by the beta-adrenergic receptor antagonist, propranolol. The epinephrine-stimulated component of PIP2 hydrolysis was significantly inhibited by pretreating the membranes with an antiserum against G(alpha q/11). When carbachol and epinephrine were present simultaneously (with GTP gamma S), the increase in PIP2 hydrolysis obtained was not significantly different from the sum of the increases in PIP2 hydrolysis obtained with each agonist alone. PIP2 hydrolysis stimulated in the presence of carbachol and epinephrine was inhibited by alpha(1)-AR and m(3)AChR antagonists, phentolamine and atropine respectively, to the level obtained with each agonist alone. Notably, in the presence of both agonists the inhibition of PIP2 hydrolysis by anti-G(alpha q/11) antiserum was not significantly different from the sum of the inhibitions obtained with each agonist alone. These results indicate that m(3)AChR and alpha(1)-AR stimulation of PIP2 hydrolysis in rat parotid gland membranes are independently mediated by the G(alpha q/11) family of G-proteins. (C) 1995 Academic Press, Inc. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. NR 21 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD JAN 10 PY 1995 VL 316 IS 1 BP 535 EP 540 DI 10.1006/abbi.1995.1071 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QJ933 UT WOS:A1995QJ93300071 PM 7840663 ER PT J AU JUST, I SEHR, P JUNG, M VANDAMME, J PUYPE, M VANDEKERCKHOVE, J MOSS, J AKTORIES, K AF JUST, I SEHR, P JUNG, M VANDAMME, J PUYPE, M VANDEKERCKHOVE, J MOSS, J AKTORIES, K TI ADP-RIBOSYLTRANSFERASE TYPE-A FROM TURKEY ERYTHROCYTES MODIFIES ACTIN AT ARG-95 AND ARG-372 SO BIOCHEMISTRY LA English DT Article ID PERFRINGENS-IOTA-TOXIN; BOTULINUM C2 TOXIN; CLOSTRIDIUM-SPIROFORME; BINDING PROTEINS; DIVALENT-CATION; SKELETAL-MUSCLE; AMINO ACID; RIBOSYLATION; PURIFICATION; INHIBITION AB Turkey erythrocyte ADP-ribosyltransferase A catalyzes the transfer of ADP-ribose from NAD to both monomeric and polymeric skeletal muscle alpha-actin with the incorporation of 2 mol of ADP-ribose per mol of actin. In contrast, Clostridium perfringens iota toxin ADP-ribosylates only G-actin, with modification at arginine-177 [Vandekerckhove, J., et al. (1987) FEES Lett. 255, 48-42]. Transferase A-catalyzed modifications are sensitive to 0.5 M neutral hydroxylamine, consistent with the arginine side chain modification. Radiolabeled peptides ADP-ribosylated by transferase A were generated by tryptic digestion and purified by reversed phase high performance Liquid chromatography. Amino acid sequence and molecular mass analysis identified the ADP-ribosylation sites as Arg-95 and Arg-372 of actin; both residues are located within subdomain-1 of the actin 3D structure [Kabsch, W., et al. (1990) Nature 347, 37-44]. ADP-ribosylation did not affect cytochalasin D-stimulated G-actin ATPase, the binding of actin to DNase I or to gelsolin, or the ability of actin to polymerize. Following ADP-ribosylation, however, a prolonged delay in polymerization was observed, consistent with a decreased rate of nucleation. C1 STATE UNIV GHENT,PHYSIOL CHEM LAB,B-9000 GHENT,BELGIUM. NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. RP JUST, I (reprint author), UNIV SAARLAND,INST PHARMAKOL & TOXIKOL,D-66421 HOMBURG,GERMANY. RI Jung, Martin/D-2207-2012 OI Jung, Martin/0000-0002-1482-7020 NR 48 TC 15 Z9 15 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JAN 10 PY 1995 VL 34 IS 1 BP 326 EP 333 DI 10.1021/bi00001a040 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QB155 UT WOS:A1995QB15500041 PM 7819215 ER PT J AU CZUB, M MCATEE, FJ CZUB, S LYNCH, WP PORTIS, JL AF CZUB, M MCATEE, FJ CZUB, S LYNCH, WP PORTIS, JL TI PREVENTION OF RETROVIRUS-INDUCED NEUROLOGICAL DISEASE BY INFECTION WITH A NONNEUROPATHOGENIC RETROVIRUS SO VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; AMINO-ACID TRANSPORTER; MOUSE ECOTROPIC RETROVIRUS; CELL-SURFACE RECEPTOR; LONG TERMINAL REPEAT; FRIEND-LEUKEMIA; HOST RANGE; HIV TYPE-1; WILD MICE; RESISTANCE AB Perinatal infection of susceptible mice with the neurotropic retrovirus CasBrE leads to a noninflammatory spongiform degeneration of the central nervous system with a long incubation period of up to 1 year. Virus replication in infected animals can be suppressed by administration of antiviral antibodies, cytotoxic T cells, or by AZT treatment, which results in partial to complete protection from neurological disease. A highly neuropathogenic chimeric retrovirus, FrCas(E), which contains the envelope gene of CasBrE, induces rapid neurodegeneration within only 16 days. Here we report that this fatal disease could be prevented if a nonneuropathogenic Friend murine leukemia virus was administered to mice prior to their infection with FrCas(E). This double inoculation led to a substantial reduction of the replication level of FrCas(E) in spleen and CNS. Only live but not heat-inactivated nonneuropathogenic virus was able to protect from FrCas(E)-induced neurological disease. The extent of protection was influenced by the viral envelope gene and the kinetics of replication of the nonneuropathogenic virus. These observations in addition to the rapidity of the effect make it likely that competition for replication sites through the mechanism of viral interference is responsible for the protection. Resistance was demonstrable in vivo even when the ''protecting'' and ''challenge'' virus belonged to different in vitro interference groups. However, the protection was considerably weaker than that seen between viruses belonging to the same interference group. (C) 1995 Academic Press, Inc. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 51 TC 12 Z9 13 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JAN 10 PY 1995 VL 206 IS 1 BP 372 EP 380 DI 10.1016/S0042-6822(95)80052-2 PG 9 WC Virology SC Virology GA QD149 UT WOS:A1995QD14900040 PM 7831792 ER PT J AU ANDERSON, S MOMOEDA, M KAWASE, M KAJIGAYA, S YOUNG, NS AF ANDERSON, S MOMOEDA, M KAWASE, M KAJIGAYA, S YOUNG, NS TI PEPTIDES DERIVED FROM THE UNIQUE REGION OF B19 PARVOVIRUS MINOR CAPSID PROTEIN ELICIT NEUTRALIZING ANTIBODIES IN RABBITS SO VIROLOGY LA English DT Article ID B-CELL EPITOPES; CANINE PARVOVIRUS; HYDROPS FETALIS; IMMUNE-RESPONSE; INFECTION; SERUM; IDENTIFICATION; SURFACE; VACCINE; HUMANS AB B19 parvovirus is pathogenic in humans. The virus propagates in the bone marrow, where it is cytotoxic to erythroid progenitor cells. Antibodies appear in blood after infection and neutralize virus in vitro; infection appears to confer lasting immunity. The predominant immune response on immunoblot is to the minor capsid protein (VP1), which differs from the major capsid protein (VP2) by an additional 227 amino acids. We previously demonstrated that antisera directed to a fusion protein containing this unique region or to more limited fusion peptides of 50-100 amino acids each neutralized virus. In the current work, we tested synthetic peptides of about 20 amino acids derived from the VP1 unique region for their ability to elicit a neutralizing antibody response in rabbits. Individual peptides were covalently linked to a lysine core to produce a multivalent antigen. Animals produced antibodies to all 13 synthetic peptides, as determined by ELISA At 12 weeks, animals injected with one of three peptides - two from the far amino terminus and the third from the center of the unique region - had produced antibodies that completely neutralized virus; by 16 weeks, antisera elicited with another four peptides also were effective. In summary, we identified regions containing neutralizing epitopes within the first 80 amino acids and amino acids 148-205 of the unique region. Our data suggest that synthetic peptides might be useful vaccine reagents for protection against parvovirus infection in humans. (C) 1995 Academic Press, Inc. RP ANDERSON, S (reprint author), NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892, USA. NR 41 TC 37 Z9 37 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JAN 10 PY 1995 VL 206 IS 1 BP 626 EP 632 DI 10.1016/S0042-6822(95)80079-4 PG 7 WC Virology SC Virology GA QD149 UT WOS:A1995QD14900067 PM 7530397 ER PT J AU MALYKH, A REITZ, MS LOUIE, A HALL, L LORI, F AF MALYKH, A REITZ, MS LOUIE, A HALL, L LORI, F TI MULTIPLE DETERMINANTS FOR GROWTH OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 IN MONOCYTE-MACROPHAGES SO VIROLOGY LA English DT Note ID NEUTRALIZING MONOCLONAL-ANTIBODY; PRODUCTIVE INFECTION; MONONUCLEAR PHAGOCYTES; ENVELOPE GLYCOPROTEIN; LANGERHANS CELLS; VIRAL ENVELOPE; BRAIN-TISSUE; V3 LOOP; TROPISM; HIV-1 AB Attempts to define the genetic determinants required for efficient growth of human immunodeficiency virus type 1 (HIV-1) in monocyte-macrophages were made by constructing chimeras between two infectious clones of HIV-1 (HXB2 and LW/C), which despite only minor differences in their DNA sequence have striking differences in cell tropism. Although both of them replicate efficiently in peripheral blood mononuclear cells, HXB2 replicates extensively in permanent T cell lines but poorly in primary monocyte macrophages (T cell line tropic); the reverse is true for LW/C (macrophage tropic). The envelope proved to contain the major determinants of macrophage tropism. However, tropism determinants appeared to be scattered along the envelope. In particular, the Vs loop alone appeared to be neither necessary nor sufficient for growth in macrophages. Both vpr and nef genes appeared to play a less significant role to improve viral replication in macrophages, but only in the presence of the proper envelope sequences. HIV-1 macrophage tropism thus appears to result from the contribution of several different determinants. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 39 TC 26 Z9 26 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD JAN 10 PY 1995 VL 206 IS 1 BP 646 EP 650 DI 10.1016/S0042-6822(95)80082-4 PG 5 WC Virology SC Virology GA QD149 UT WOS:A1995QD14900070 PM 7831820 ER PT J AU LEWIS, RA CLOGSTON, P FAINSTEIN, V GROSS, R SAMO, T TUTTLE, C JABS, DA APUZZO, L BARTLETT, J COLESON, L DUNN, JP ELDRED, L FEINBERG, J FLYNN, T KING, R LESLIE, J BARRON, B GREENSPAN, D LECOUNT, C PEYMAN, G FRANKLIN, R HEINEMANN, MH POLSKY, B SQUIRES, K WISECAMPBELL, S FRIEDMAN, AH CHEUNG, TW JUSTIN, N TEICH, S SACKS, H SEVERIN, C FRIEDBERG, DN ADDESSI, A DIETERICH, D FROST, K WEINBERG, D JAMPOL, L MURPHY, R NAUGHTON, K HENDERLY, D HOLLAND, GN CHAFEY, S FALL, H HARDY, WD KIMBRELL, C MACARTHUR, LJ FREEMAN, WR MEIXNERT, L PETERSON, TJ QUICENO, JI RICKMAN, L SIMANELLO, MA SPECTOR, S ODONNELL, J HOFFMAN, J IRVINE, A JACOBSON, M LARSON, J SEIFF, S WANNER, M DAVIS, J CHUANG, E ESPINAL, M MENDEZ, P VANDENBROUCKE, R CHEESEMAN, SH GITTINGER, J HAUBRICH, R KACHADOORIAN, H TOLSON, K KLINE, JM KLEMM, AC STEVENS, M WEBB, R BROWNBELLAMY, J MARKOWITZ, JA MEINERT, CL BINDER, KL BROOKMEYER, R BROWN, VE COLLISON, BJ DODGE, J DONITHAN, M FINK, N GERCZAK, C HOLBROOK, JT ISAACSON, MR JONES, CP LEVINE, CR MIN, YI MEINERT, JL OWENS, RM NOWAKOWSKI, DJ SAAH, A SANDFORD, GR SINGER, S SMITH, M STERNBERG, AL TONASCIA, J VANNATTA, ML DAVID, MD AGRESSEGAL, M ARMSTRONG, J BROTHERS, R FREITAG, G HUBBARD, L HURLBURT, D KASTORFF, L MAGLI, Y MINER, K THOMAS, S VANDERHOOFYOUNG, M STEWART, G HUGHES, R WELCH, L MOWERY, R ELLENBERG, S KORVICK, J DAVIS, MD CLARK, T CLOGSTON, PS FREEMAN, W SATTLER, F JORDAN, C MILLS, J BROWN, BW CONWAY, B GRIZZLE, J NUSSENBLATT, R PHAIR, J SMITH, H AF LEWIS, RA CLOGSTON, P FAINSTEIN, V GROSS, R SAMO, T TUTTLE, C JABS, DA APUZZO, L BARTLETT, J COLESON, L DUNN, JP ELDRED, L FEINBERG, J FLYNN, T KING, R LESLIE, J BARRON, B GREENSPAN, D LECOUNT, C PEYMAN, G FRANKLIN, R HEINEMANN, MH POLSKY, B SQUIRES, K WISECAMPBELL, S FRIEDMAN, AH CHEUNG, TW JUSTIN, N TEICH, S SACKS, H SEVERIN, C FRIEDBERG, DN ADDESSI, A DIETERICH, D FROST, K WEINBERG, D JAMPOL, L MURPHY, R NAUGHTON, K HENDERLY, D HOLLAND, GN CHAFEY, S FALL, H HARDY, WD KIMBRELL, C MACARTHUR, LJ FREEMAN, WR MEIXNERT, L PETERSON, TJ QUICENO, JI RICKMAN, L SIMANELLO, MA SPECTOR, S ODONNELL, J HOFFMAN, J IRVINE, A JACOBSON, M LARSON, J SEIFF, S WANNER, M DAVIS, J CHUANG, E ESPINAL, M MENDEZ, P VANDENBROUCKE, R CHEESEMAN, SH GITTINGER, J HAUBRICH, R KACHADOORIAN, H TOLSON, K KLINE, JM KLEMM, AC STEVENS, M WEBB, R BROWNBELLAMY, J MARKOWITZ, JA MEINERT, CL BINDER, KL BROOKMEYER, R BROWN, VE COLLISON, BJ DODGE, J DONITHAN, M FINK, N GERCZAK, C HOLBROOK, JT ISAACSON, MR JONES, CP LEVINE, CR MIN, YI MEINERT, JL OWENS, RM NOWAKOWSKI, DJ SAAH, A SANDFORD, GR SINGER, S SMITH, M STERNBERG, AL TONASCIA, J VANNATTA, ML DAVID, MD AGRESSEGAL, M ARMSTRONG, J BROTHERS, R FREITAG, G HUBBARD, L HURLBURT, D KASTORFF, L MAGLI, Y MINER, K THOMAS, S VANDERHOOFYOUNG, M STEWART, G HUGHES, R WELCH, L MOWERY, R ELLENBERG, S KORVICK, J DAVIS, MD CLARK, T CLOGSTON, PS FREEMAN, W SATTLER, F JORDAN, C MILLS, J BROWN, BW CONWAY, B GRIZZLE, J NUSSENBLATT, R PHAIR, J SMITH, H TI MORBIDITY AND TOXIC EFFECTS ASSOCIATED WITH GANCICLOVIR OR FOSCARNET THERAPY IN A RANDOMIZED CYTOMEGALOVIRUS RETINITIS TRIAL SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID IMMUNE-DEFICIENCY-SYNDROME; ACQUIRED IMMUNODEFICIENCY SYNDROME; VIRUS RETINITIS; PENILE ULCERATION; NATURAL-HISTORY; DISEASE; RETINOPATHY; AIDS; MANIFESTATIONS; ZIDOVUDINE AB Background: The Foscarnet-Ganciclovir Cytomegalovirus Retinitis Trial compared the use of either ganciclovir or foscarnet for the initial treatment of cytomegalovirus retinitis in patients with the acquired immunodeficiency syndrome. We previously reported that patients treated with foscarnet lived longer but were more likely to have their treatment switched, the latter suggesting foscarnet may not have been as well tolerated as ganciclovir. This study compared the morbidity and toxic reactions reported during the trial. Methods: Two hundred thirty-four patients with the acquired immunodeficiency syndrome and preciously untreated cytomegalovirus retinitis at 11 university centers were randomly assigned to receive intravenously either foscarnet (n = 107) or ganciclovir (n = 127). Medical histories, laboratory tests, and drug treatment histories during the first 6 months of treatment were analyzed. Results: Neutropenia was more common in patients assigned to ganciclovir than to foscarnet (34% vs 14%; P = .001). Patients assigned to foscarnet reported more infusion-related symptoms (58% vs 24%; P < .001) and, in male patients, more genitourinary symptoms (36% vs 16%; P > .001); they also experienced a trend toward more nephrotoxic effects (13% vs 6%; P = .082) and electrolyte abnormalities. The incidence of seizures was similar in both groups (foscarnet, 12%; ganciclovir, 9%; P = .511). Patients assigned to foscarnet were more likely to be switched to the alternative treatment (foscarnet to ganciclovir, 46%; ganciclovir to foscarnet, 11%, P < .001), and most of this excess was attributable to toxic reactions. In 88% of cases in which treatment was snitched as a result of toxic reactions and in which follow-up data were available, the toxic reaction resolved after the switch. No permanent disability or death resulted from toxic reactions. Conclusions: Compared with ganciclovir, the use of foscarnet was more frequently limited by the occurrence of toxic reactions. However, these toxic reactions rarely had long-term sequelae. In light of the previously reported survival benefit seen in patients treated with foscarnet, these data support the use of foscarnet for the initial treatment of cytomegalovirus retinitis. C1 SOCA CHAIRMANS OFF,RES GRP,BALTIMORE,MD 21205. BAYLOR COLL MED,CULLEN EYE INST,HOUSTON,TX 77030. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. LOUISIANA STATE UNIV,MED CTR,NEW ORLEANS,LA. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. CORNELL UNIV,MED CTR,NEW YORK HOSP,NEW YORK,NY 10021. CUNY MT SINAI SCH MED,NEW YORK,NY. NYU,MED CTR,NEW YORK,NY. NORTHWESTERN UNIV,CHICAGO,IL. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. UNIV CALIF SAN DIEGO,SAN DIEGO,CA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA. UNIV MIAMI,SCH MED,MIAMI,FL. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD. UNIV WISCONSIN,CTR FUNDUS PHOTOG READING,MADISON,WI. ERC BIOSERV CORP,CTR DRUG DISTRIBUT,ROCKVILLE,MD. NEI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NR 43 TC 29 Z9 30 U1 1 U2 1 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 9 PY 1995 VL 155 IS 1 BP 65 EP 74 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA QA058 UT WOS:A1995QA05800008 ER PT J AU WOLFE, MS LEE, NR ZATZ, M AF WOLFE, MS LEE, NR ZATZ, M TI PROPERTIES OF CLOCK-CONTROLLED AND CONSTITUTIVE N-ACETYLTRANSFERASES FROM CHICK PINEAL CELLS SO BRAIN RESEARCH LA English DT Article DE ACETYL-COA; SEROTONIN N-ACETYLTRANSFERASE; ACETYL-COA; ARYLAMINE N-ACETYLTRANSFERASE; CIRCADIAN RHYTHM; MELATONIN ID PHOTOENDOCRINE TRANSDUCTION; MELATONIN RHYTHM; GLAND; ARYLAMINE; LIVER; FORSKOLIN; RAT AB The pineal gland synthesizes its hormone melatonin (O-methyl-N-acetylserotonin) from serotonin. Acetyl-CoA: serotonin N-acetyltransferase (SNAT), the enzyme that catalyzes the committed step in this biosynthesis, is largely restricted to the pineal gland and is regulated by adrenergic and circadian mechanisms. Another enzyme, acetyl-CoA: arylamine N-acetyltransferase (ANAT), having an apparently similar activity, is also present in the pineal. This enzyme, however, is not rhythmically regulated. SNAT activity of cultured chick pineal cells was obtained without ANAT after ammonium sulfate precipitation. ANAT activity was retained without SNAT activity after pre-incubation at 37 degrees C. Thus, each enzyme could be examined independently. Overlap in substrate specificity between the two enzymes was minimal. Kinetic analysis of the separated enzyme activities revealed that while SNAT operates via a random or ordered bi bi mechanism, ANAT catalysis occurs through a ping pong bi bi mechanism with substrate inhibition by acetyl-CoA. By size-exclusion chromatography, ANAT was confirmed to be 30-35 kDa, and SNAT was estimated at 15-20 kDa. Taken together, these results indicate that the two enzymes differ in their structure, reactivity, stability, and mechanism of catalysis. C1 NIMH,CELL BIOL LAB,BIOCHEM PHARMACOL SECT,BETHESDA,MD 20892. NR 29 TC 6 Z9 6 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 9 PY 1995 VL 669 IS 1 BP 100 EP 106 DI 10.1016/0006-8993(94)01267-L PG 7 WC Neurosciences SC Neurosciences & Neurology GA QB729 UT WOS:A1995QB72900014 PM 7712152 ER PT J AU LEE, KB PARKER, RJ REED, E AF LEE, KB PARKER, RJ REED, E TI EFFECT OF CADMIUM ON HUMAN OVARIAN-CANCER CELLS WITH ACQUIRED CISPLATIN RESISTANCE SO CANCER LETTERS LA English DT Article DE CADMIUM DICHLORIDE; CIS-DIAMMINEDICHLOROPLATINUM; DNA-ADDUCT ID CHINESE-HAMSTER CELLS; MAMMALIAN-CELLS; METALLOTHIONEIN; CHLORIDE; RAT; CARCINOGENICITY; INDUCTION; REPAIR; ZINC; OVEREXPRESSION AB Cadmium (Cd) dichloride is a compound that has teratogenic, mutagenic, and carcinogenic properties. Recent reports have suggested the possibility that this compound may also have tumor suppressive properties in some settings. For these reasons, we have studied the subcellular pharmacological profile of elemental cadmium in human ovarian cancer cells, when administered as cadmium dichloride. The cell lines A2780 and A2780/CP70 were used, which are well characterized with respect to their cellular response to platinum-based compounds. Cd was measured in all experiments with the use of atomic absorbance spectrometry with Zeeman background correction. In both cell lines, there were direct relationships between; drug dose and cellular accumulation of drug; cellular accumulation of drug and DNA damage levels; and DNA damage levels and cytotoxicity. These cell lines differed in that the cisplatin-resistant A2780/CP70 cell line, was also comparatively resistant to cadmium dichloride. This enhanced cellular resistance appeared to be mediated through decreased drug accumulation, and increased cellular tolerance to higher levels of DNA damage. Total genomic DNA repair and cytosolic inactivation of drug appeared not to differ substantively between these two cell lines. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NR 38 TC 16 Z9 16 U1 0 U2 1 PU ELSEVIER SCI PUBL 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 6 PY 1995 VL 88 IS 1 BP 57 EP 66 DI 10.1016/0304-3835(94)03626-T PG 10 WC Oncology SC Oncology GA QG088 UT WOS:A1995QG08800009 PM 7850774 ER PT J AU ZHANG, GF PATTON, WA LEE, FJS LIYANAGE, M HAN, JS RHEE, SG MOSS, J VAUGHAN, M AF ZHANG, GF PATTON, WA LEE, FJS LIYANAGE, M HAN, JS RHEE, SG MOSS, J VAUGHAN, M TI DIFFERENT ARF DOMAINS ARE REQUIRED FOR THE ACTIVATION OF CHOLERA-TOXIN AND PHOSPHOLIPASE-D SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID ADP-RIBOSYLATION FACTOR; GTP-BINDING PROTEIN; GOLGI MEMBRANES; DROSOPHILA; TRANSPORT; COP AB ADP-ribosylation factors (ARE's), initially described as activators of cholera toxin ADP-ribosyltransferase activity, regulate intracellular vesicular membrane trafficking and stimulate a phospholipase D (PLD) isoform, ARF-like (ARL) proteins are structurally related to ARFs but do not activate cholera toxin and have relatively little effect on PLD. A new human ARL gene termed hARL1, which shares 57% amino acid identity with hARF1, was identified using a polymerase chain reaction based cloning method. To determine whether different structural elements are responsible for the activation of the A subunit of cholera toxin and PLD, chimeric proteins were constructed by switching the amino-terminal 73 amino acids of ARF1 and ARL1. The recombinant rL73/F protein, in which the amino-terminal 73 amino acids of ARL1 replaced those of ARF1, activated the A subunit of cholera toxin, whereas the rF73/L protein, in which the NH2-terminal 73 amino acids of ARF1 replaced those of ARL1, was inactive. The two chimeric proteins had quite opposite effects on PLD activity, rF73/L activated PLD as effectively as rARF1, whereas rL73/F protein activated PLD only slightly. It appears that the amino terminal region of ARF1 is not critical for its action as a GTP-dependent activator of cholera toxin, whereas it is necessary for activation of the putative effector enzyme, PLD. C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RP ZHANG, GF (reprint author), NHLBI,PULM CRIT CARE MED BRANCH,RM 5N307,BLDG 10,BETHESDA,MD 20892, USA. OI LEE, FANG-JEN/0000-0002-2167-2426 NR 25 TC 51 Z9 55 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 6 PY 1995 VL 270 IS 1 BP 21 EP 24 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QA287 UT WOS:A1995QA28700006 PM 7814376 ER PT J AU KAHN, RA CLARK, J RULKA, C STEARNS, T ZHANG, CJ RANDAZZO, PA TERUI, T CAVENAGH, M AF KAHN, RA CLARK, J RULKA, C STEARNS, T ZHANG, CJ RANDAZZO, PA TERUI, T CAVENAGH, M TI MUTATIONAL ANALYSIS OF SACCHAROMYCES-CEREVISIAE ARF1 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ADP-RIBOSYLATION FACTOR; STIMULATORY REGULATORY COMPONENT; GTP-BINDING-PROTEIN; ADENYLATE-CYCLASE; CHOLERA-TOXIN; CATALYTIC SUBUNIT; ESCHERICHIA-COLI; ALPHA-SUBUNIT; YEAST; COFACTOR AB Wild type and eight point mutants of Saccharomyces cerevisiae ARF1 were expressed in yeast and bacteria to determine the roles of specific residues in in vivo and in vitro activities. Mutations at either Gly(2) or Asp(26) resulted in recessive loss of function. It was concluded that N-myristoylation is required for Arf action in cells but not for either nucleotide exchange or cofactor activities in vitro. Asp(26) (homologous to Gly(12) of p21(ras)) was essential for the binding of the activating nucleotide, guanosine 5'-3-O-(thio)triphosphate. This is in marked contrast to results obtained after mutagenesis of the homologous residue in p21(ras) or G(s) alpha, and suggests a fundamental difference in the guanine nucleotide binding site of Arf with respect to these other GTP binding proteins. Two dominant alleles were also identified, one activating dominant ([Q71L]Arf1) and the other ([N126I]) a negative dominant. A conditional allele, [W66R]Arf1, was characterized and shown to have approximate to 300-fold lower specific activity in an in vitro Arf assay. Two high-copy suppressors of this conditional phenotype were cloned and sequenced. One of these suppressors, SFS4, was found to be identical to PBS2/HOG4, recently shown to encode a microtubule associated protein kinase kinase in yeast. C1 NCI, DIV CANC TREATMENT, DEV THERAPEUT PROGRAM, BIOL CHEM LAB, BETHESDA, MD 20892 USA. STANFORD UNIV, DEPT BIOL SCI, STANFORD, CA 94305 USA. NR 48 TC 69 Z9 71 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 6 PY 1995 VL 270 IS 1 BP 143 EP 150 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QA287 UT WOS:A1995QA28700026 PM 7814365 ER PT J AU KIESEWETTER, DO LEE, JT LANG, LX PARK, SG PAIK, CH ECKELMAN, WC AF KIESEWETTER, DO LEE, JT LANG, LX PARK, SG PAIK, CH ECKELMAN, WC TI PREPARATION OF F-18 LABELED MUSCARINIC AGONIST WITH M2 SELECTIVITY SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Note ID RECEPTORS; SITES; BINDING; SUBTYPE; M1 C1 NIH,DEPT NUCL MED,BETHESDA,MD 20892. RP KIESEWETTER, DO (reprint author), NIH,CTR CLIN,DEPT POSITRON EMISS TOMOG,PET BLDG 10,RM 1C401,10 CTR DR MSC 1180,BETHESDA,MD 20892, USA. NR 20 TC 37 Z9 37 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD JAN 6 PY 1995 VL 38 IS 1 BP 5 EP 8 DI 10.1021/jm00001a002 PG 4 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA QB227 UT WOS:A1995QB22700002 PM 7837240 ER PT J AU MOODY, TW VENUGOPAL, R ZIA, F PATIERNO, S LEBAN, JJ MCDERMED, J AF MOODY, TW VENUGOPAL, R ZIA, F PATIERNO, S LEBAN, JJ MCDERMED, J TI BW2258U89 - A GRP RECEPTOR ANTAGONIST WHICH INHIBITS SMALL-CELL LUNG-CANCER GROWTH SO LIFE SCIENCES LA English DT Article DE BOMBESIN; GRP RECEPTOR; SMALL CELL LUNG CANCER; GROWTH; CALCIUM ID GASTRIN-RELEASING PEPTIDE; SWISS 3T3 CELLS; NEUROMEDIN-B; BOMBESIN ANTAGONIST; CYTOSOLIC CALCIUM; ANALOGS FUNCTION; HIGH-AFFINITY; LINES; CARCINOMA; INVITRO AB The ability of reduced peptide bond analogues of gastrin releasing peptide (GRP) to antagonize small cell lung cancer (SCLC) GRP receptors was investigated. BW462U89, BW1023U90, BW2123U89 and BW2258U89 inhibited binding of (I-125-Tyr(4)) BN to NCI-H345 cells with IC50 values of 5, 6, 140 and 10 nM respectively. The GRP analogues had no effect on basal cytosolic Ca2+ but inhibited the increase caused by 10 nM BN. BW462U89 reversibly blocked the increase in cytosolic Ca2+ caused by BN. The GRP analogues (1 mu M) inhibited NCI-H345 colony formation in the absence or presence of 10 nM BN. Also, BW2258U89 (0.4 mg/kg, s.c. daily) inhibited xenograft growth in nude mice. These data indicate that BW2258U89 inhibits SCLC growth in vitro and in vivo. C1 GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT BIOCHEM & MOLEC BIOL,WASHINGTON,DC 20037. GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT MICROBIOL,WASHINGTON,DC 20037. GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT PHARMACOL,WASHINGTON,DC 20037. BURROUGHS WELLCOME CO,DIV ORGAN CHEM,RES TRIANGLE PK,NC 27709. RP MOODY, TW (reprint author), NCI,BIOMARKERS & PREVENT RES BRANCH,9610 MED CTR DR,BLDG C,ROOM 300,ROCKVILLE,MD 20850, USA. FU NCI NIH HHS [CA-53477] NR 22 TC 16 Z9 16 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PD JAN 6 PY 1995 VL 56 IS 7 BP 521 EP 529 DI 10.1016/0024-3205(94)00481-7 PG 9 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA QA168 UT WOS:A1995QA16800006 PM 7869832 ER PT J AU LAROCHE, SD SHAFER, BK STRATHERN, JN AF LAROCHE, SD SHAFER, BK STRATHERN, JN TI A STE12-ALLELE HAVING A DIFFERENTIAL EFFECT ON A VERSUS ALPHA-CELLS SO MOLECULAR AND GENERAL GENETICS LA English DT Article DE STE12; TRANSCRIPTIONAL REGULATION; YEAST MATING-TYPE CONTROL ID MATING-TYPE LOCUS; AFFECTING SEXUAL CONJUGATION; PHEROMONE RESPONSE ELEMENTS; SACCHAROMYCES-CEREVISIAE; SIGNAL TRANSDUCTION; G-PROTEIN; TRANSCRIPTIONAL ACTIVATION; NONMATING MUTANTS; GAMMA-SUBUNITS; DNA-SEQUENCE AB The transcriptional activator ste12p is a key component of the yeast pheromone response pathway: phosphorylated as a consequence of signal transduction, it activates transcription of genes that promote mating and the subsequent fusion of the two cell types a and alpha. Activation by Ste12p requires three types of protein-protein interaction between DNA-binding activator proteins: (1) Ste12p by itself can induce non-cell-type-specific genes involved in mating; (2) cooperation of the transactivator Mcm1p with Ste12p induces a-specific genes; and (3) formation of a complex of the activator proteins Mcm1p and alpha 1 (a transcriptional activator of alpha-specific genes) with Ste12p is believed to induced alpha-specific genes. We isolated and characterized a partially functional ste12 allele (ste12-T50), that is defective only in the activation of alpha-specific genes. ste12-T50 was isolated as a second-site mutation conferring the a mating phenotype on mat alpha 2 mutant cells. In mat alpha 2 cells, where due to the lack of repressor, alpha 2, both sets of cell-type-specific genes are expressed. ste12-T50 apparently tips the balance in favor of a-specific gene expression. Thus, mat alpha 2 ste12-T50 cells mate like a cells. Additional ste12 mutants that confer the a mating phenotype on mat alpha 2 cells have also been isolated. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, EUKARYOT GENE EXPRESS LAB, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74101] NR 49 TC 4 Z9 4 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD JAN 6 PY 1995 VL 246 IS 1 BP 80 EP 90 PG 11 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA QC123 UT WOS:A1995QC12300010 PM 7823915 ER PT J AU MISHINA, Y SUZUKI, A GILBERT, DJ COPELAND, NG JENKINS, NA UENO, N BEHRINGER, RR AF MISHINA, Y SUZUKI, A GILBERT, DJ COPELAND, NG JENKINS, NA UENO, N BEHRINGER, RR TI GENOMIC ORGANIZATION AND CHROMOSOMAL LOCATION OF THE MOUSE TYPE-I BMP-2/4 RECEPTOR SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID SERINE THREONINE KINASE; BONE MORPHOGENETIC PROTEIN-4; DAUER LARVA DEVELOPMENT; ACTIVIN RECEPTOR; VENTRALIZING FACTOR; EXPRESSION CLONING; GENE; IDENTIFICATION; ELEGANS; INDUCTION AB We have characterized the structure of a mouse bone morphogenetic protein (BMP) type I receptor gene that can bind both BMP-2 and BMP-4. The mouse BMP-2/4 receptor gene is encoded by 11 exons and spans approximately 38-kb. Most of the intron/exon boundaries are not conserved compared to the kinase domain of the related, activin type II receptor. In addition, whereas the activin type II receptor gene contains large introns (>40 kb), the largest intron of the BMP-2/4 receptor gene is only 6.4-kb. The BMP-2/4 receptor gene (Bmpr) was mapped to mouse chromosome 14. Bmpr is closely linked to Rbp3 in the region containing pugnose, a mutation that alters bone development. Knowledge of the genomic structure of Bmpr provides important information to create Bmpr-deficient mice. (C) 1995 Academic Press, Inc. C1 UNIV TEXAS, MD ANDERSON CANC CTR, DEPT MOLEC GENET, HOUSTON, TX 77030 USA. HOKKAIDO UNIV, FAC PHARMACEUT SCI, SAPPORO, HOKKAIDO 060, JAPAN. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MAMMALIAN GENET LAB, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74101, CA16672]; NICHD NIH HHS [HD30284] NR 34 TC 27 Z9 32 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X EI 1090-2104 J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD JAN 5 PY 1995 VL 206 IS 1 BP 310 EP 317 DI 10.1006/bbrc.1995.1043 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QA375 UT WOS:A1995QA37500043 PM 7818535 ER PT J AU CARPER, DA HOHMAN, TC OLD, SE AF CARPER, DA HOHMAN, TC OLD, SE TI RESIDUES AFFECTING THE CATALYSIS AND INHIBITION OF RAT LENS ALDOSE REDUCTASE SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEIN STRUCTURE AND MOLECULAR ENZYMOLOGY LA English DT Article DE SITE-DIRECTED MUTAGENESIS; ALDOSE REDUCTASE; INHIBITION; KINETICS; POLYOL PATHWAY; DIABETES; RAT LENS ID SITE-DIRECTED MUTAGENESIS; DIABETIC COMPLICATIONS; CRYSTAL-STRUCTURE; NERVE FUNCTION; ACTIVE-SITE; BINDING; SORBINIL; INVOLVEMENT; NEUROPATHY; TOLRESTAT AB Aldose reductase (AR), the first enzyme of the polyol pathway, has been implicated in diabetic complications. Results of recent clinical studies have shown that compounds that inhibit aldose reductase (ARIs) and block the flux of glucose through the polyol pathway have provided benefit to diabetic neuropathic patients. Since many ARIs show broad substrate specificity, emphasis on the structure-function properties of the AR enzyme will help in the refinement and design of future inhibitors. To this end, catalysis and inhibition of rat lens aldose reductase was examined following site-directed mutagenesis. Replacement of tyrosine 48 with phenylalanine (Y48F) resulted in an enzyme form with less than 0.25% activity with DL-glyceraldehyde and no detectable activity with p-nitrobenzaldehyde or xylose, although circular dichroism spectra and NADPH binding affinity were similar to wild-type AR. Mutation of histidine 110 to glutamine (H110Q) also resulted in a less active protein with an approximate 3-fold decrease in k(cat) for the reduction of DL-glyceraldehyde; slight or no activity was measured with other substrates and an increase of 195-fold over wild type was observed in the K-m for glyceraldehyde. H110Q was less sensitive to inhibition by aldose reductase inhibitors. The most dramatic change was seen with imeristat, which showed an 1800-fold increase in IC50. Mutation of cysteine 298 to serine (C298S) affected enzyme function by increasing k(cat) 2- to 4-fold and increasing K-m 15- to 48-fold, with DL-glyceraldehyde, p-nitrobenzaldehyde or xylose as substrates. As a result k(cat)/K-m, catalytic efficiency, dropped to approx. 10% of control. Inhibition of C298S was not noticeably different from wild type. Substitution of histidine 187 or 200 with glutamine (H187Q, H200Q) had little effect on AR catalysis or inhibition. Based on structural and mutagenesis studies of human AR and the conservation of amino acids between human and rat, these data would indicate that Y48, H110, and C298 are important residues in the active site of rat AR and that Y48 is most likely the proton donor during substrate reduction by rat lens aldose reductase. In addition, these studies indicate that mutagenesis of H110 also affects aldose reductase inhibition. C1 WYETH AYERST LABS,PRINCETON,NJ 08540. RP CARPER, DA (reprint author), NEI,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 52 TC 22 Z9 22 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4838 J9 BBA-PROTEIN STRUCT M JI Biochim. Biophys. Acta-Protein Struct. Molec. Enzym. PD JAN 5 PY 1995 VL 1246 IS 1 BP 67 EP 73 DI 10.1016/0167-4838(94)00182-G PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QA913 UT WOS:A1995QA91300011 PM 7811733 ER PT J AU WANG, WL CONE, EJ AF WANG, WL CONE, EJ TI TESTING HUMAN HAIR FOR DRUGS OF ABUSE .4. ENVIRONMENTAL COCAINE CONTAMINATION AND WASHING EFFECTS SO FORENSIC SCIENCE INTERNATIONAL LA English DT Article; Proceedings Paper CT Workshop on Hair Analysis in Forensic Toxicology, at the XVIth Congress of the International-Academy-of-Legal-Medicine-and-Social-Medicine CY MAY 31-JUN 02, 1994 CL STRASBOURG, FRANCE SP INT ACAD LEGAL MED & SOCIAL MED DE HAIR ANALYSIS; COCAINE; BENZOYLECGONINE; TOXICOLOGY; CONTAMINATION; DECONTAMINATION; FORENSICS AB Active cocaine use results in sequestration of parent drug in hair. In addition, hair has unique physicochemical properties that permit absorption of cocaine from the environment. When hair is tested for evidence of cocaine, it is important to consider whether the positive test resulted from active drug use or environmental contamination. In a series of laboratory experiments, it was found that exposure of 'cut' hair to cocaine vapor ('crack' smoke) and to aqueous solutions of cocaine hydrochloride resulted in significant contamination of hair samples, Similar results were obtained with two subjects who were exposed to cocaine vapor in an unventilated room. The amount of contamination adsorbed by hair depended upon both time and extent of exposure. Washing the hair samples with methanol removed > 70% of the cocaine contaminant after cocaine vapor exposure, but was less effective (< 50%) following contamination with aqueous cocaine. Shampoo treatment cycles (overnight soaking) progressively removed increasing amounts of cocaine from the contaminated hair, but residual cocaine remained after 10 cycles. Studies were also performed to determine the usefulness of benzoylecgonine as a marker of active cocaine administration. Small amounts of benzoylecgonine (ca, 1 ng/mg) were formed in hair as a result of environmental contamination with cocaine. Also, it was found that benzoylecgonine could be adsorbed from illicit cocaine contaminated with benzoylecgonine. It was concluded that positive hair test results should be interpreted cautiously due to the possibility of environmental contamination from cocaine and related constituents. C1 NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. NR 7 TC 55 Z9 57 U1 1 U2 8 PU ELSEVIER SCI PUBL IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0379-0738 J9 FORENSIC SCI INT JI Forensic Sci.Int. PD JAN 5 PY 1995 VL 70 IS 1-3 BP 39 EP 51 DI 10.1016/0379-0738(94)01616-D PG 13 WC Medicine, Legal SC Legal Medicine GA QB224 UT WOS:A1995QB22400004 PM 7860035 ER PT J AU BEGUINOT, L VASS, WC MILOSO, M AF BEGUINOT, L VASS, WC MILOSO, M TI SHC IS CONSTITUTIVELY ACTIVATED BY A TRANSFORMING EGF RECEPTOR MUTANT WITH A POINT MUTATION IN THE TRANSMEMBRANE DOMAIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,MOLEC ONCOL LAB,BETHESDA,MD 20892. HS RAFFAELE,MOLEC ONCOL LAB,MILAN,ITALY. 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 5 PY 1995 SU 19A BP 11 EP 11 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700028 ER PT J AU COUCHMAN, G WALMER, D MCLACHLAN, J NELSON, K AF COUCHMAN, G WALMER, D MCLACHLAN, J NELSON, K TI IDENTIFICATION AND CHARACTERIZATION OF HUMAN ENDOMETRIAL PROTEIN-TYROSINE KINASES - EXPRESSION OF LYN, A SRC-FAMILY TYROSINE KINASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DURHAM,NC 27710. NIEHS,REPROD & DEV TOXICOL 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 5 PY 1995 SU 19A BP 13 EP 13 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700038 ER PT J AU CRESPO, P XU, NZ SIMONDS, WF GUTKIND, JS AF CRESPO, P XU, NZ SIMONDS, WF GUTKIND, JS TI MAP KINASE ACTIVATION BY BETA-ADRENERGIC RECEPTORS AND BY LPA INVOLVES BETA-GAMMA-SUBUNITS OF HETEROTRIMERIC G-PROTEINS ACTING ON P21RAS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,METABOL DIS BRANCH,BETHESDA,MD 20892. NIDR,CELLULAR DEV & ONCOL LAB,MOLEC SIGNALLING UNIT,BETHESDA,MD 20892. RI Gutkind, J. Silvio/A-1053-2009; Crespo, Piero/M-3273-2014 OI Crespo, Piero/0000-0003-2825-7783 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 5 PY 1995 SU 19A BP 13 EP 13 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700037 ER PT J AU GOLDSTEIN, DJ STAEBLER, AE SCHLEGEL, R PIERCE, JH AF GOLDSTEIN, DJ STAEBLER, AE SCHLEGEL, R PIERCE, JH TI SPECIFIC TRANSMEMBRANE INTERACTIONS MEDIATE THE ACTIVATION OF THE PDGF RECEPTOR BY THE BPV-1 E5 ONCOPROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,SCH MED,DEPT OBSTET GYNECOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC 20007. 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 5 PY 1995 SU 19A BP 17 EP 17 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700052 ER PT J AU MARCILLA, A AGARWAL, A RIVEROLEZCANO, OM ROBBINS, KC AF MARCILLA, A AGARWAL, A RIVEROLEZCANO, OM ROBBINS, KC TI IDENTIFICATION OF THE MAJOR TYROSINE-PHOSPHORYLATED SUBSTRATE IN SIGNALING COMPLEXES FORMED AFTER ENGAGEMENT OF FC-BETA RECEPTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. RI marcilla, antonio/F-9996-2010 OI marcilla, antonio/0000-0003-0004-0531 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 5 PY 1995 SU 19A BP 22 EP 22 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700073 ER PT J AU RHODES, N AFSHARI, CA INNES, CL MUDRYJ, M PAULES, RS AF RHODES, N AFSHARI, CA INNES, CL MUDRYJ, M PAULES, RS TI ALTERED REGULATION OF CELL-CYCLE CONTROL PROTEINS IN MOS TRANSFORMED-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,GROWTH CONTROL & CANC GRP,RES TRIANGLE PK,NC 27709. DUKE UNIV,MED CTR,CTR AGING,DURHAM,NC 27710. 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 5 PY 1995 SU 19A BP 27 EP 27 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700092 ER PT J AU CUTLER, ML MASUELLI, L MARINETTI, MR TSUDA, T AF CUTLER, ML MASUELLI, L MARINETTI, MR TSUDA, T TI HIGH-LEVEL EXPRESSION OF RSU-1 INHIBITS THE GAP ACTIVITY OF NEUROFIBROMIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR IMMUNOL & 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 5 PY 1995 SU 19A BP 32 EP 32 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700112 ER PT J AU EVANS, GA JOHNSTON, JA OSHEA, JJ ERWIN, R HOWARD, OMZ FARRAR, WL AF EVANS, GA JOHNSTON, JA OSHEA, JJ ERWIN, R HOWARD, OMZ FARRAR, WL TI A STUDY OF IL-2-DEPENDENT SIGNAL-TRANSDUCTION THROUGH THE ADAPTER PROTEIN SHC - ANALYSIS OF TYROSINE PHOSPHORYLATION AND RECEPTOR ASSOCIATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MOLEC IMMUNOREGULAT LAB,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 5 PY 1995 SU 19A BP 33 EP 33 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700116 ER PT J AU KANNO, T FRANZOSO, G SIEBENLIST, U AF KANNO, T FRANZOSO, G SIEBENLIST, U TI HTLV-I TAX-MEDIATED ACTIVATION OF NF-KAPPA-B FROM NOVEL P100 (NF-KAPPA-B2)-INHIBITED CYTOPLASMIC RESERVOIRS 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 5 PY 1995 SU 19A BP 37 EP 37 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700132 ER PT J AU KANNO, Y SCHUBERT, M OZATO, K AF KANNO, Y SCHUBERT, M OZATO, K TI REPRESSION OF HOST-CELL TRANSCRIPTION BY THE VSV-MATRIX PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NIH,VIRAL & MOLEC PATHOGENESIS 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 5 PY 1995 SU 19A BP 37 EP 37 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700134 ER PT J AU KIRKEN, RA RUI, H MALABARBA, MG KAWAMURA, M OSHEA, JJ FARRAR, WL AF KIRKEN, RA RUI, H MALABARBA, MG KAWAMURA, M OSHEA, JJ FARRAR, WL TI INTERACTION OF JAK1 AND JAK3 TYROSINE KINASES WITH THE IL2 RECEPTOR COMPLEX SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,CYTOKINE MOLEC MECH SECT,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. NCI,FCRDC,PRI DYNCORP,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,BRMP,LEUKOCYTE CELL BIOL SECT,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. RI Malabarba, Maria Grazia/L-4805-2015 OI Malabarba, Maria Grazia/0000-0002-9457-2047 NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 5 PY 1995 SU 19A BP 38 EP 38 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700135 ER PT J AU KUPRASH, DV RICE, NR NEDOSPASOV, SA AF KUPRASH, DV RICE, NR NEDOSPASOV, SA TI DNA-BINDING BY NF-KAPPA-B/REL PROTEINS IS DIFFERENTIALLY MODULATED BY CONFORMATIONAL CONTEXT OF THE BINDING-SITE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,BRMP,PRI DYNCORP,BCDP,FREDERICK,MD 21701. ENGELHARDT MOLEC BIOL INST,MOSCOW,RUSSIA. NCI,FCRDC,ABL-BRP,FREDERICK,MD 21701. 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 5 PY 1995 SU 19A BP 39 EP 39 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700141 ER PT J AU LI, CCH DAI, RM CHEN, E LONGO, DL AF LI, CCH DAI, RM CHEN, E LONGO, DL TI PHOSPHORYLATION OF NFKB1-P50 IS INVOLVED IN NF-KAPPA-B ACTIVATION AND STABLE DNA-BINDING SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,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 5 PY 1995 SU 19A BP 39 EP 39 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700142 ER PT J AU BOUKAMP, P POPP, S PETER, W BLEUEL, K STANBRIDGE, EJ HARRIS, CC FUSENIG, NE AF BOUKAMP, P POPP, S PETER, W BLEUEL, K STANBRIDGE, EJ HARRIS, CC FUSENIG, NE TI INVOLVEMENT OF P53, RAS ONCOGENE AND LOSS OF CHROMOSOME-15 IN HUMAN SKIN CARCINOGENESIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GERMAN CANC RES CTR,D-69120 HEIDELBERG,GERMANY. UNIV CALIF IRVINE,IRVINE,CA 92717. NCI,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 5 PY 1995 SU 19A BP 48 EP 48 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700174 ER PT J AU DELWEL, R HOL, S VANKAN, Y LOWENBERG, B IHLE, JN COPELAND, NG HAGEMEIJER, A VALK, P AF DELWEL, R HOL, S VANKAN, Y LOWENBERG, B IHLE, JN COPELAND, NG HAGEMEIJER, A VALK, P TI THE CANNABINOID RECEPTOR-2 GENE IS LOCATED IN A COMMON VIRUS INTEGRATION SITE IN 2 MOUSE LEUKEMIAS AND AT A BREAKPOINT INVOLVING CHROMOSOME 1P36 IN A HUMAN AML SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ERASMUS UNIV ROTTERDAM,VALK INST HEMATOL,3000 DR ROTTERDAM,NETHERLANDS. ERASMUS UNIV ROTTERDAM,INST GENET,3000 DR ROTTERDAM,NETHERLANDS. ST JUDE CHILDREN RES HOSP,DEPT BIOCHEM,MEMPHIS,TN. NCI,FREDERICK CANC RES & DEV CTR,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 5 PY 1995 SU 19A BP 50 EP 50 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700185 ER PT J AU GAUWERKY, C RAFFELD, M CROCE, C AF GAUWERKY, C RAFFELD, M CROCE, C TI GENETICS OF TUMOR PROGRESSION IN B-CELL NEOPLASM - BCL-3 AT CHR-17Q22 - TISSUE-SPECIFICITY AND CLONING OF TRANSLOCATION BREAKPOINTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,PHILADELPHIA,PA 19107. NCI,DEPT PATHOL,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 5 PY 1995 SU 19A BP 52 EP 52 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700191 ER PT J AU MALABARBA, MG KIRKEN, RA RUI, H KAWAMURA, M OSHEA, JJ FARRAR, WL AF MALABARBA, MG KIRKEN, RA RUI, H KAWAMURA, M OSHEA, JJ FARRAR, WL TI INTERACTION OF JAK3 AND JAK1 TYROSINE KINASES WITH THE IL4 RECEPTOR COMPLEX SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,MOLEC IMMUNOREGULAT LAB,CYTOKINE MOLEC MECH SECT,FREDERICK,MD 21702. NCI,FCRDC,EXPTL IMMUNOL LAB,LEUKOCYTE CELL BIOL SECT,FREDERICK,MD 21702. RI Malabarba, Maria Grazia/L-4805-2015 OI Malabarba, Maria Grazia/0000-0002-9457-2047 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 5 PY 1995 SU 19A BP 55 EP 55 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700204 ER PT J AU RUI, H ERWIN, RA KIRKEN, RA FARRAR, WL AF RUI, H ERWIN, RA KIRKEN, RA FARRAR, WL TI GENISTEIN AND STAUROSPORINE BLOCK PROLACTIN-INDUCED TYROSINE PHOSPHORYLATION OF SHC WITHOUT INHIBITING JAK2 - EVIDENCE FOR SHC PHOSPHORYLATION BY A DOWNSTREAM TYROSINE KINASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP & BIOL,CARCINOGENESIS DEV PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,LMI,CYTOKINE MOLEC MECH SECT,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 5 PY 1995 SU 19A BP 60 EP 60 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700222 ER PT J AU TOPOL, LZ MARX, M CALOTHY, G BLAIR, DG AF TOPOL, LZ MARX, M CALOTHY, G BLAIR, DG TI ACTIVATION OF THE MAP KINASE CASCADE CORRELATES WITH V-MOS TRANSFORMATION IN BOTH MOS-RESISTANT REVERTANTS AND TS-TRANSFORMED CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. CTR UNIV ORSAY,INST CURIE BIOL,F-91405 ORSAY,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 5 PY 1995 SU 19A BP 63 EP 63 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700234 ER PT J AU WONG, WT BIESOVA, Z AROCA, P SANTOS, E MATOSKOVA, B DIFIORE, PP AF WONG, WT BIESOVA, Z AROCA, P SANTOS, E MATOSKOVA, B DIFIORE, PP TI IDENTIFICATION AND CHARACTERIZATION OF 2 RELATED PROTEINS, E3B35 AND E3B78, THAT BIND TO THE SH3 DOMAIN OF EPS-8 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN 5 PY 1995 SU 19A BP 65 EP 65 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700242 ER PT J AU AMUNDADOTTIR, LT JOHNSON, MD SMITH, GH MERLINO, G DICKSON, RB AF AMUNDADOTTIR, LT JOHNSON, MD SMITH, GH MERLINO, G DICKSON, RB TI THE INTERACTION OF TRANSFORMING GROWTH-FACTOR-ALPHA AND C-MYC IN MOUSE MAMMARY-GLAND TUMORIGENESIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,TUMOR IMMUNOL & 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 5 PY 1995 SU 19A BP 66 EP 66 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700246 ER PT J AU LIU, P HAJRA, A GREGORY, P WIJMENGA, C BLAKE, T COLLINS, F AF LIU, P HAJRA, A GREGORY, P WIJMENGA, C BLAKE, T COLLINS, F TI ANALYSIS OF THE FUSION GENE GENERATED BY CHROMOSOME-16 INVERSION IN LEUKEMIA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,NCHGR,LGT,BETHESDA,MD 20892. RI Liu, Paul/A-7976-2012 OI Liu, Paul/0000-0002-6779-025X 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 5 PY 1995 SU 19A BP 69 EP 69 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700260 ER PT J AU TOMONAGA, T LEVENS, D AF TOMONAGA, T LEVENS, D TI HETEROGENEOUS RIBONUCLEOPROTEIN PARTICLE PROTEIN-K IS A DNA-BINDING TRANSACTIVATOR 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 5 PY 1995 SU 19A BP 80 EP 80 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700305 ER PT J AU LI, WQ PIERCE, JH AF LI, WQ PIERCE, JH TI STIMULATION OF THE PDGF-BETA RECEPTOR SIGNALING PATHWAY ACTIVATES PKC-DELTA 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 5 PY 1995 SU 19A BP 86 EP 86 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700326 ER PT J AU HILL, S KUZMINOV, A MYERS, R STAHL, MM TARKOWSKI, T THOMASON, LC STAHL, FW AF HILL, S KUZMINOV, A MYERS, R STAHL, MM TARKOWSKI, T THOMASON, LC STAHL, FW TI PHAGE-LAMBDA RECOMBINATION IN-VIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,ROCKY MT LABS,HAMILTON,MT 59840. UNIV OREGON,INST MOLEC BIOL,EUGENE,OR 97403. 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 5 PY 1995 SU 19A BP 91 EP 91 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700337 ER PT J AU AUSTIN, S BRENDLER, T ABELES, A AF AUSTIN, S BRENDLER, T ABELES, A TI P1 PLASMID MAINTENANCE - CONTROL OF REPLICATION AND PARTITION IN THE ESCHERICHIA-COLI CELL-CYCLE 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 5 PY 1995 SU 19A BP 94 EP 94 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700347 ER PT J AU BRENDLER, TG ABELES, AL AUSTIN, SJ AF BRENDLER, TG ABELES, AL AUSTIN, SJ TI A PROTEIN THAT BINDS TO THE P1 ORIGIN CORE AND ORIC 13-MER REGION IN A METHYLATION-SPECIFIC FASHION IS THE PRODUCT OF THE HOST SEQA GENE 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 5 PY 1995 SU 19A BP 100 EP 100 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700368 ER PT J AU LOBOCKA, M YARMOLINSKY, M AF LOBOCKA, M YARMOLINSKY, M TI P1 PLASMID PARTITION - MUTATIONS IN PARB THAT AFFECT INTERACTIONS OF PARB WITH PARS AND PARA 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 5 PY 1995 SU 19A BP 112 EP 112 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700415 ER PT J AU SAWITZKE, JA RADNEDGE, L DAVIS, MA AUSTIN, SJ AF SAWITZKE, JA RADNEDGE, L DAVIS, MA AUSTIN, SJ TI FUNCTIONS NECESSARY FOR PARTITION OF PLASMID P1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,CELL CYCLE REGULAT SECT,FREDERICK,MD 21702. 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 5 PY 1995 SU 19A BP 117 EP 117 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700435 ER PT J AU SLESAREV, AI LAKE, JA KOZYAVKIN, SA AF SLESAREV, AI LAKE, JA KOZYAVKIN, SA TI CLONING AND SEQUENCE-ANALYSIS OF METHANOPYRUS-KANDLERI TOP5, THE GENE ENCODING TOPOISOMERASE-V SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. NIH,BETHESDA,MD 20892. 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 5 PY 1995 SU 19A BP 118 EP 118 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700437 ER PT J AU DEDRICK, RL MORRISON, PF FLESSNER, MF LASKE, DW OLDFIELD, EH AF DEDRICK, RL MORRISON, PF FLESSNER, MF LASKE, DW OLDFIELD, EH TI PHARMACOKINETICS AND REGIONAL DELIVERY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV ROCHESTER,ROCHESTER,NY 14627. RI Kipke, Daryl/A-2167-2009 NR 4 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 5 PY 1995 SU 19A BP 166 EP 166 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700596 ER PT J AU SUNG, C VANOSDOL, WW WEINSTEN, JN DEDRICK, RL AF SUNG, C VANOSDOL, WW WEINSTEN, JN DEDRICK, RL TI APPLICATION OF STREPTAVIDIN-BIOTIN BINDING IN 2-STEP ANTIBODY-BASED TUMOR TARGETING PROTOCOLS 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 5 PY 1995 SU 19A BP 172 EP 172 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700615 ER PT J AU ROBERTS, DD GUO, NH KRUTZSCH, HC INMAN, JK AF ROBERTS, DD GUO, NH KRUTZSCH, HC INMAN, JK TI INHIBITION OF TUMOR-GROWTH IN-VITRO AND IN-VIVO BY STABLE ANALOGS OF THROMBOSPONDIN TYPE-1 REPEAT PEPTIDES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 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 5 PY 1995 SU 19A BP 178 EP 178 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700634 ER PT J AU FORNACE, AJ AF FORNACE, AJ TI INDUCTION BY GENOTOXIC STRESS OF MAMMALIAN GENES ASSOCIATED WITH GROWTH-ARREST AND APOPTOSIS, AND THE ROLE FOR THE P53 TUMOR-SUPPRESSOR IN THEIR REGULATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,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 5 PY 1995 SU 19A BP 184 EP 184 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700645 ER PT J AU EPSTEIN, CJ HUANG, TT CARLSON, E CHAN, PH PHILLIPS, JP CADET, JL AF EPSTEIN, CJ HUANG, TT CARLSON, E CHAN, PH PHILLIPS, JP CADET, JL TI THE EFFECTS OF INCREASED EXPRESSION OF CUZN-SUPEROXIDE DISMUTASE IN TRANSGENIC MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. UNIV GUELPH,GUELPH,ON N1G 2W1,CANADA. NIDA,CTR ADDICT RES,LEXINGTON,KY 40583. 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 5 PY 1995 SU 19A BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700647 ER PT J AU GONZALEZ, FJ AF GONZALEZ, FJ TI ROLE OF XENOBIOTIC-METABOLIZING ENZYMES IN CANCER SUSCEPTIBILITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC 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 5 PY 1995 SU 19A BP 187 EP 187 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700654 ER PT J AU EASTMAN, HB HOLBROOK, NJ AF EASTMAN, HB HOLBROOK, NJ TI ACTIVATION OF GADD153 BY DNA-DAMAGING AGENTS IN CISPLATIN-RESISTANT AND PARENTAL HELA-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,GENE EXPRESS & AGING UNIT,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 5 PY 1995 SU 19A BP 189 EP 189 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700659 ER PT J AU GUYTON, KZ HOLBROOK, NJ AF GUYTON, KZ HOLBROOK, NJ TI ACTIVATION OF THE MAMMALIAN STRESS-RESPONSE GENE GADD153 BY OXIDATIVE STRESS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,GENE EXPRESS & AGING UNIT,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 5 PY 1995 SU 19A BP 189 EP 189 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700662 ER PT J AU SILVERMAN, JA HILL, BA AF SILVERMAN, JA HILL, BA TI TRANSCRIPTIONAL REGULATION OF THE RAT MDRLB GENE BY CARCINOGENS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EXPTL 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 5 PY 1995 SU 19A BP 191 EP 191 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700669 ER PT J AU DUNNICK, JK ELWELL, MR AF DUNNICK, JK ELWELL, MR TI EXPERIMENTAL STUDIES OF THE TOXICITY AND CARCINOGENICITY OF NICKEL SULFATE, NICKEL SUBSULFIDE, AND NICKEL-OXIDE 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 5 PY 1995 SU 19A BP 196 EP 196 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700685 ER PT J AU BERNSTEIN, SL KEMPNER, ES AF BERNSTEIN, SL KEMPNER, ES TI RADIATION TARGET ANALYSIS OF RIBOZYMES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NEI,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 5 PY 1995 SU 19A BP 214 EP 214 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700746 ER PT J AU KELSALL, BL STROBER, W AF KELSALL, BL STROBER, W TI IN-SITU IDENTIFICATION OF MURINE PEYERS PATCH DENDRITIC CELLS - A UNIQUE POPULATION OF N418+ CELLS IS PRESENT IN THE SUBEPITHELIAL DOME SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,CLIN INVEST 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 5 PY 1995 SU 19A BP 247 EP 247 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700856 ER PT J AU WAKATSUKI, Y MATSUNAGA, Y USUI, T KITA, T STROBER, W AF WAKATSUKI, Y MATSUNAGA, Y USUI, T KITA, T STROBER, W TI ANALYSIS OF COSTIMULATION REQUIREMENTS FOR IG ISOTYPE DIFFERENTIATION AND TERMINAL DIFFERENTIATION OF PEYERS PATCH B-LYMPHOCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 KYOTO UNIV,FAC MED,KYOTO 606,JAPAN. NIAID,MUCOSAL IMMUN 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 5 PY 1995 SU 19A BP 253 EP 253 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700879 ER PT J AU MURPHY, BR CROWE, JE BUI, PT ELKINS, WR FIRESTONE, CY CHANOCK, RM LUBECK, MD KARRON, R CLEMENTS, ML WRIGHT, PF SIBER, GR AF MURPHY, BR CROWE, JE BUI, PT ELKINS, WR FIRESTONE, CY CHANOCK, RM LUBECK, MD KARRON, R CLEMENTS, ML WRIGHT, PF SIBER, GR TI PROGRESS TOWARD THE DEVELOPMENT OF A LIVE ATTENUATED RESPIRATORY SYNCYTIAL VIRUS (RSV) VACCINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. WYETH AYERST RES,RADNOR,PA 19101. JOHNS HOPKINS UNIV,BALTIMORE,MD 21205. VANDERBILT UNIV,MED CTR,SCH MED,NASHVILLE,TN 37232. MASSACHUSETTS PUBL HLTH BIOL LABS,BOSTON,MA 02130. RI Crowe, James/B-5549-2009 OI Crowe, James/0000-0002-0049-1079 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 5 PY 1995 SU 19A BP 274 EP 274 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700947 ER PT J AU BENNINK, JR ANTON, L LINK, HT YEWDELL, JW AF BENNINK, JR ANTON, L LINK, HT YEWDELL, JW TI GENERATION OF VIRAL PEPTIDES RECOGNIZED BY MHC CLASS I-RESTRICTED T-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 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 5 PY 1995 SU 19A BP 278 EP 278 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700957 ER PT J AU BERZOFSKY, JA AF BERZOFSKY, JA TI DEVELOPMENT OF SYNTHETIC PEPTIDE VACCINES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES 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 5 PY 1995 SU 19A BP 278 EP 278 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99700958 ER PT J AU KASHANCHI, F PIRAS, G DUVALL, JF RADONOVICH, MF CVEKL, A BRADY, JN AF KASHANCHI, F PIRAS, G DUVALL, JF RADONOVICH, MF CVEKL, A BRADY, JN TI TRANSCRIPTION AND TAX1 TRANSACTIVATION OF THE HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I PROMOTER BY AN ALPHA-AMANITIN RESISTANT POLYMERASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,MOLEC VIROL LAB,BETHESDA,MD 20892. NIH,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 5 PY 1995 SU 19A BP 291 EP 291 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701001 ER PT J AU REITZ, MS WATKINS, BA LOUIE, A GALLO, RC ROBERTGUROFF, M AF REITZ, MS WATKINS, BA LOUIE, A GALLO, RC ROBERTGUROFF, M TI BROADLY NEUTRALIZING ANTIBODIES TO HIV-1 IN INFECTED INDIVIDUALS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU 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 5 PY 1995 SU 19A BP 301 EP 301 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701042 ER PT J AU KARUPIAH, G HARRIS, N AF KARUPIAH, G HARRIS, N TI MACROPHAGE-DERIVED NITRIC OXIDE-MEDIATED INHIBITION OF VIRUS-REPLICATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS 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 5 PY 1995 SU 19A BP 307 EP 307 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701061 ER PT J AU LAPHAM, CK GOLDING, H INMAN, J BLACKBURN, R GOLDING, B AF LAPHAM, CK GOLDING, H INMAN, J BLACKBURN, R GOLDING, B TI CONJUGATION OF A PEPTIDE FROM THE V3 LOOP OF HIV GP120 TO THE VACCINE CARRIER BRUCELLA-ABORTUS INDUCES A SPECIFIC, MHC-RESTRICTED CYTOTOXIC RESPONSE AGAINST HIV GP120 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 US FDA,CBER DIV VIRAL PROD,BETHESDA,MD 20014. US FDA,CBER,DIV HEMATOL,BETHESDA,MD 20014. 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 5 PY 1995 SU 19A BP 312 EP 312 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701081 ER PT J AU LODMELL, DL SMITH, J EWALT, LC AF LODMELL, DL SMITH, J EWALT, LC TI RABIES VIRUS GLYCOPROTEIN EXPRESSED IN A VACCINIA VIRUS RECOMBINANT VACCINE CROSS PROTECTS MICE AGAINST UNIQUE GENETIC-VARIANTS OF RABIES VIRUSES ISOLATED WORLDWIDE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,PERSISTANT VIRAL DIS LAB,ROCKY MT LABS,HAMILTON,MT 59840. CTR DIS CONTROL,DIV INFECT DIS,VIRAL & RICKETTSIAL ZOONOSES BRANCH,RABIES LAB,ATLANTA,GA 30333. 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 5 PY 1995 SU 19A BP 312 EP 312 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701083 ER PT J AU PALUMBO, GJ STERN, R GLASGOW, WC MARTINEZ, L BULLER, RM MOYER, RW AF PALUMBO, GJ STERN, R GLASGOW, WC MARTINEZ, L BULLER, RM MOYER, RW TI RABBITPOX PS/HR (VV-WR-B5R ORF) GENE-PRODUCT INHIBITS THE GENERATION OF AN INFLAMMATORY RESPONSE IN-VIVO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV OKLAHOMA,HLTH SCI CTR,DEPT MICROBIOL,OKLAHOMA CITY,OK 73190. UNIV OKLAHOMA,HLTH SCI CTR,DEPT IMMUNOL,OKLAHOMA CITY,OK 73190. UNIV FLORIDA,DEPT IMMUNOL & MED MICROBIOL,GAINESVILLE,FL 32610. NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. ST LOUIS UNIV,DEPT MOLEC MICROBIOL & IMMUNOL,ST LOUIS,MO 63104. 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 5 PY 1995 SU 19A BP 317 EP 317 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701103 ER PT J AU BIDDISON, WE PARKER, KC COLIGAN, JE JACOBSON, S UTZ, U AF BIDDISON, WE PARKER, KC COLIGAN, JE JACOBSON, S UTZ, U TI HTLV-1 TAX-SPECIFIC CTL FROM HAM/TSP PATIENTS CROSS-REACT ON A SELF MYELIN-ASSOCIATED GLYCOPROTEIN-DERIVED PEPTIDE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. NIAID,MOLEC STRUCT 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 5 PY 1995 SU 19A BP 320 EP 320 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701111 ER PT J AU GOLDING, H KASLOW, RA BLACKBURN, R AF GOLDING, H KASLOW, RA BLACKBURN, R TI ANTI-HLA CROSS-REACTIVE AUTOANTIBODIES IN HIV-INFECTED INDIVIDUALS - CORRELATION WITH DISEASE PROGRESSION IN MACS STUDY PATIENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 US FDA,CBER,DIV VIROL PROD,BETHESDA,MD 20892. NIH,DMID,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 5 PY 1995 SU 19A BP 320 EP 320 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701114 ER PT J AU CARBONE, M RIZZO, P PROCOPIO, A MEW, DJY GIULIANO, MT STEINBERG, SM LEVINE, AS GRIMLY, P PASS, HI AF CARBONE, M RIZZO, P PROCOPIO, A MEW, DJY GIULIANO, MT STEINBERG, SM LEVINE, AS GRIMLY, P PASS, HI TI SV40 LARGE T-ANTIGEN AND P53 RELATIONSHIP IN PLEURAL MESOTHELIOMA SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV CHICAGO,DEPT PATHOL,CHICAGO,IL 60637. NICHHD,DNA REPAIR REPLICAT & MUTAGENESIS SECT,BETHESDA,MD 20892. NCI,THORAC ONCOL SECT,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. USUHS,DEPT PATHOL,BETHESDA,MD 20892. UNIV CHIETI,FISIOPATOL MOLEC LAB,CHIETI,ITALY. 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 5 PY 1995 SU 19A BP 321 EP 321 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701117 ER PT J AU BALINTKURTI, P GINSBURG, G KIMMEL, A AF BALINTKURTI, P GINSBURG, G KIMMEL, A TI RZIP, A TRANSCRIPTION FACTOR HOMOLOG INVOLVED IN CELL-DIFFERENTIATION AND PATTERNING DURING THE DEVELOPMENT OF DICTYOSTELIUM-DISCOIDEUM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,CELLULAR & 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 5 PY 1995 SU 19A BP 334 EP 334 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701151 ER PT J AU BYERS, S PISHVAIEN, M ORFORD, K SOMMERS, C LECHLEIDER, R AF BYERS, S PISHVAIEN, M ORFORD, K SOMMERS, C LECHLEIDER, R TI AN INTERACTIVE NETWORK OF RETINOID, SERINE AND TYROSINE KINASE SIGNALING PATHWAYS MODULATES BETA-CATENIN HOMEOSTASIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,DEPT CELL BIOL,WASHINGTON,DC 20007. 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 5 PY 1995 SU 19A BP 335 EP 335 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701157 ER PT J AU RICHARDSON, DL LOOMIS, WF KIMMEL, AR AF RICHARDSON, DL LOOMIS, WF KIMMEL, AR TI THE WAVE OF SPORULATION INDUCTION IN DICTYOSTELIUM IS MEDIATED BY A POSITIVE TRANSCRIPTIONAL ELEMENT SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,CELLULAR & 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 5 PY 1995 SU 19A BP 342 EP 342 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701185 ER PT J AU TACHIBANA, M URABE, K MEYERS, KA TAKEDA, K AARONSON, SA AF TACHIBANA, M URABE, K MEYERS, KA TAKEDA, K AARONSON, SA TI MITF (MICROPHTHALMIA-ASSOCIATED TRANSCRIPTION FACTOR) REGULATES MELANOCYTE-SPECIFIC GENES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDCD,LMG,BETHESDA,MD. NCI,LCB,BETHESDA,MD 20892. NCI,LCMB,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 5 PY 1995 SU 19A BP 344 EP 344 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701193 ER PT J AU YUAN, DS IWAI, Y DANCIS, A KLAUSNER, RD AF YUAN, DS IWAI, Y DANCIS, A KLAUSNER, RD TI REGULATORY CIRCUITS GOVERNING COPPER AND IRON-METABOLISM IN YEAST 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 5 PY 1995 SU 19A BP 345 EP 345 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QQ997 UT WOS:A1995QQ99701196 ER PT J AU THOMAS, A AF THOMAS, A TI RESEARCH INTEGRITY SO NATURE LA English DT Letter RP THOMAS, A (reprint author), NIH,BLDG 10,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD JAN 5 PY 1995 VL 373 IS 6509 BP 10 EP 10 DI 10.1038/373010c0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QA239 UT WOS:A1995QA23900020 PM 7800026 ER PT J AU FRANCOMANO, CA AF FRANCOMANO, CA TI THE GENETIC-BASIS OF DWARFISM SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID GROWTH-FACTOR RECEPTOR; FIBROBLAST RP FRANCOMANO, CA (reprint author), NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892, USA. NR 10 TC 26 Z9 27 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JAN 5 PY 1995 VL 332 IS 1 BP 58 EP 59 DI 10.1056/NEJM199501053320113 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA PZ497 UT WOS:A1995PZ49700013 PM 7990869 ER PT J AU FUKASAWA, K SHEN, RL RESAU, J DASILVA, PP VANDEWOUDE, GF AF FUKASAWA, K SHEN, RL RESAU, J DASILVA, PP VANDEWOUDE, GF TI OVEREXPRESSION OF MOS ONCOGENE PRODUCT IN SWISS 3T3 CELLS INDUCES APOPTOSIS PREFERENTIALLY DURING S-PHASE SO ONCOGENE LA English DT Article DE APOPTOSIS; MOS ONCOGENE; CELL CYCLE; S-PHASE ID MURINE SARCOMA-VIRUS; MEIOTIC MATURATION; XENOPUS-OOCYTES; MAP KINASE; PROTO-ONCOGENE; EARLY EVENT; DEATH; ENDONUCLEASE; INVITRO; FIBROBLASTS AB When Swiss 3T3 cells are acutely infected with Moloney murine sarcoma virus containing the v-mos oncogene, 90% of the cells round up and detach from the monolayer (floating cells) and express high levels of v-Mos. The majority of the floating cells are generated between 30 and 70 h post infection when the cellular level of Mos reaches similar to 0.1% of the total protein. Seventy percent of the floating cells exclude trypan blue but are growth arrested with 2C or 4C DNA content, whereas the remaining floating cells with <2C DNA content, are dead or dying, and show characteristic apoptotic phenotypes. The apoptotic cells are most likely generated from cells in S-phase since these cells are absent from the viable floating cell population and the percentage of cells with <2C DNA approximated the expected S-phase fraction of logarithmically growing cells. In addition, 5'-bromo-2'-deoxyuridine-labeling studies showed that similar to 50% of the floating cells with typical apoptotic phenotypes were metabolically-labeled with the drug. These analyses show that cell populations in different stages of the cell cycle are differently affected by high levels of v-Mos expression and cells in S-phase appear to be uniquely sensitive and undergo apoptosis. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,DIV CANC BIOL DIAG & CTR,INTRAMURAL RES PROGRAM,MATH BIOL LAB,MEMBRANE BIOL SECT,FREDERICK,MD 21702. RI Shen, Rulong/E-4079-2011 FU NCI NIH HHS [N01-CO-74101] NR 40 TC 36 Z9 38 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN 5 PY 1995 VL 10 IS 1 BP 1 EP 8 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA QA980 UT WOS:A1995QA98000001 PM 7824263 ER PT J AU LYMAN, SD JAMES, L ESCOBAR, S DOWNEY, H DEVRIES, P BRASEL, K STOCKING, K BECKMANN, MP COPELAND, NG CLEVELAND, LS JENKINS, NA BELMONT, JW DAVISON, BL AF LYMAN, SD JAMES, L ESCOBAR, S DOWNEY, H DEVRIES, P BRASEL, K STOCKING, K BECKMANN, MP COPELAND, NG CLEVELAND, LS JENKINS, NA BELMONT, JW DAVISON, BL TI IDENTIFICATION OF SOLUBLE AND MEMBRANE-BOUND ISOFORMS OF THE MURINE FLT3 LIGAND GENERATED BY ALTERNATIVE SPLICING OF MESSENGER-RNAS SO ONCOGENE LA English DT Article DE FT13 LIGAND; GROWTH FACTOR; GENE LOCATION; TYROSINE KINASE RECEPTOR; HEMATOPOIESIS ID COLONY-STIMULATING FACTOR; MESSENGER-RNA PRECURSORS; CELL GROWTH-FACTOR; KIT-LIGAND; MOLECULAR-CLONING; HUMAN CSF-1; GENE; MOUSE; TRANSMEMBRANE; ORGANIZATION AB We have recently described a novel hematopoietic growth factor, referred to as the flt3 ligand, that stimulates the proliferation of sub-populations of hematopoietic cells that are enriched for stem and progenitor cells, This factor is a transmembrane protein that undergoes proteolytic cleavage to generate a soluble form of the protein. We have isolated additional flt3 ligand isoforms by PCR that contain an extra exon and encode what are predicted to be either a soluble form of the ligand or a longer version of the transmembrane protein. We have also isolated cDNAs from murine T cell libraries that encode an isoform of the flt3 ligand that has an unusual C-terminus, This isoform results from a failure to splice out an intron during mRNA processing. The protein encoded by this cDNA is expressed on the cell surface, where it is biologically active. However, this novel isoform does not appear to give rise to a soluble form of the protein, Regulation of mRNA splicing is likely to control the generation of cell bound or soluble forms of this hematopoietic growth factor, Genetic mapping studies localize the gene encoding the flt3 ligand to the proximal portion of mouse chromosome 7 and to human chromosome 19q13.3. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. BAYLOR COLL MED,INST MOLEC GENET,HOUSTON,TX 77030. RP LYMAN, SD (reprint author), IMMUNEX RES & DEV CORP,51 UNIV ST,SEATTLE,WA 98101, USA. FU NCI NIH HHS [N01-CO-74101] NR 32 TC 72 Z9 74 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN 5 PY 1995 VL 10 IS 1 BP 149 EP 157 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA QA980 UT WOS:A1995QA98000017 PM 7824267 ER PT J AU BENNETT, JE AF BENNETT, JE TI FUNGI AS A CAUSE OF OTITIS - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP BENNETT, JE (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JAN 4 PY 1995 VL 273 IS 1 BP 25 EP 25 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA PZ042 UT WOS:A1995PZ04200020 ER PT J AU BRANCH, W DUCAT, L FANTEL, A LOW, WC ZHOU, FC DAYTON, DH GILL, TJ AF BRANCH, W DUCAT, L FANTEL, A LOW, WC ZHOU, FC DAYTON, DH GILL, TJ TI SUITABILITY OF FETAL TISSUES FROM SPONTANEOUS-ABORTIONS AND FROM ECTOPIC PREGNANCIES FOR TRANSPLANTATION SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Note AB Objective.-To assess the potential availability and utility of fetal tissues obtained from spontaneous abortions and from ectopic pregnancies for human transplantation therapy. Design.-Tissue collection and analysis by personnel skilled in tissue banking. Setting.-Procurement programs in five tissue banks located in diverse geographical areas that are funded by the National Institutes of Health. Patients.-All women entering obstetric clinics during 1993 who consented to participate in the study. Interventions.-None. Main Outcome Measures.-Evaluation of the products of conception by standard developmental, histological, microbiological, and cytogenetic criteria. Results.-From 22 235 obstetric admissions, 1250 spontaneously aborted embryos and 247 products of ectopic pregnancies were obtained. Of these, seven embryos (0.5%) were potentially useful for human transplantation therapy. Conclusion.-Fetal tissues from spontaneous abortions and from ectopic pregnancies are quite limited as feasible sources for human transplantation therapy, C1 UNIV PITTSBURGH,SCH MED,DEPT PATHOL,PITTSBURGH,PA 15261. UNIV UTAH,SCH MED,DEPT OBSTET & GYNECOL,SALT LAKE CITY,UT 84132. NATL DIS RES INTERCHANGE,PHILADELPHIA,PA. UNIV WASHINGTON,DEPT PEDIAT,SEATTLE,WA 98195. UNIV MINNESOTA,DEPT NEUROSURG,MINNEAPOLIS,MN 55455. INDIANA UNIV,DEPT ANAT,INDIANAPOLIS,IN. NICHHD,GENET & TERATOL BRANCH,BETHESDA,MD 20892. NR 8 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 4 PY 1995 VL 273 IS 1 BP 66 EP 68 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA PZ042 UT WOS:A1995PZ04200030 ER PT J AU NYREN, O MCLAUGHLIN, JK GRIDLEY, G EKBOM, A JOHNELL, O FRAUMENI, JF ADAMI, HO AF NYREN, O MCLAUGHLIN, JK GRIDLEY, G EKBOM, A JOHNELL, O FRAUMENI, JF ADAMI, HO TI CANCER RISK AFTER HIP-REPLACEMENT WITH METAL IMPLANTS - A POPULATION-BASED COHORT STUDY IN SWEDEN SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID HELICOBACTER-PYLORI INFECTION; RENAL-CELL CARCINOMA; LARGE-BOWEL CANCER; NEW-SOUTH-WALES; OSTEO-ARTHRITIS; ASPIRIN USE; GASTRIC ADENOCARCINOMA; JOINT REPLACEMENT; PROSTATE-CANCER; COLON CANCER AB Background: Joint replacement with metal implants has been the standard procedure for surgical treatment of irreversible degeneration of hip and knee joints for more than two decades, However, reports of local malignancy after joint replacement and experimental studies that suggest a carcinogenic action of metal ions and polymethylmethacrylate (an acrylic compound used to stabilize the implant in the host) have raised concern about the possible long-term risks associated with metal implants, Purpose: Our aim was to study cancer risk in a Swedish cohort of patients who had hip replacement surgery during the period 1965 through 1983, Methods: We studied the risk of cancer in a cohort of 39 154 patients (14 869 men and 24 285 women), identified in the nationwide Swedish Inpatient Register with at least one hip replacement during the period 1965 through 1983, The patients were followed through 1989 by means of record linkage to the Swedish Cancer Register, The cohort contributed a total of 327 922 person-years at risk, Standardized incidence ratios (SIRs) were computed using age-, sex-, and period-specific incidence rates derived from the entire Swedish population, Results: The overall relative risk of cancer was increased by only 3%, Bone cancer-the focus of previous concerns-occurred in six cases versus 4.3 expected, and connective tissue cancer occurred in 28 cases versus 25.9 expected, Increased risks were observed for kidney cancer (SIR = 1.31; 95% confidence interval [CI] = 1.13-1.51), prostate cancer (SIR = 1.13; 95% CI = 1.04-1.22), and melanoma (SIR = 1.23; 95% CI = 1.00-1.50), The relative risk of gastric cancer steadily declined with increasing follow-up time, in both men and women (SIR = 0.58; 95% CI = 0.39-0.84 more than 10 years after hip replacement). Conclusion: In this study, the largest study to date to evaluate hip replacement and subsequent cancer risk, the overall cancer risk appears to be negligible from a public health perspective, and our results have not produced any strong evidence against the continued use of these devices. Nevertheless, the small but statistically significant increases in kidney and prostate cancers and the decrease in gastric cancer deserve further study. C1 NCI,BETHESDA,MD 20892. MALMO GEN HOSP,DEPT ORTHOPAED,MALMO,SWEDEN. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. RP NYREN, O (reprint author), UNIV UPPSALA HOSP,DEPT CANC EPIDEMIOL,S-75185 UPPSALA,SWEDEN. NR 74 TC 140 Z9 141 U1 1 U2 9 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 4 PY 1995 VL 87 IS 1 BP 28 EP 33 DI 10.1093/jnci/87.1.28 PG 6 WC Oncology SC Oncology GA PZ215 UT WOS:A1995PZ21500008 PM 7666459 ER PT J AU SENDEROWICZ, AMJ KAUR, G SAINZ, E LAING, C INMAN, WD RODRIGUEZ, J CREWS, P MALSPEIS, L GREVER, MR SAUSVILLE, EA DUNCAN, KLK AF SENDEROWICZ, AMJ KAUR, G SAINZ, E LAING, C INMAN, WD RODRIGUEZ, J CREWS, P MALSPEIS, L GREVER, MR SAUSVILLE, EA DUNCAN, KLK TI JASPLAKINOLIDES INHIBITION OF THE GROWTH OF PROSTATE CARCINOMA-CELLS IN-VITRO WITH DISRUPTION OF THE ACTIN CYTOSKELETON SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID MARINE SPONGE; AMINO-ACIDS; CYCLODEPSIPEPTIDE; CYTOCHALASIN; JASPAMIDE; (+)-JASPLAKINOLIDE; ESTABLISHMENT; PEPTIDE; CANCER AB Background: Jasplakinolide, a cyclodepsipeptide produced by an Indo-Pacific sponge, Jaspis johnstoni, has been reported to inhibit the growth of breast cancer cells. Purpose: The effects of jasplakinolide on the proliferation of three human immortalized prostate carcinoma cell lines (PC-3, LNCaP, and TSU-Pr1) were studied. The growth-inhibitory effect of jasplakinolide on the PC-3 cell line was studied in detail to elucidate its mechanism of action. Methods: Cell counts mere used to study growth inhibition, a protein-based microplate assay was used to assess the time of exposure needed to cause persistent growth inhibition and to study the effects of jasplakinolide analogues. Metabolic changes were assessed by following the incorporation of radiolabeled precursors. The effects of jasplakinolide on the cytoskeleton were studied by fluorescent microscopy, using rhodamine phalloidin (RP) and antibodies to cytoskeletal components. Changes in RP binding were quantified by extracting bound fluorescent material from fixed cells and measuring the amount of fluorescence in a spectrofluorometer. Results: The growth of PC-3, LNCaP, and TSU-Pr1 cells was potently inhibited by exposure to jasplakinolide for 48 hours; doses of jasplakinolide that led to 50% growth inhibition were 65 nM for PC-3 cells, 41 nM for LNCaP cells, and 170 nhl for TSU-Pr1 cells. In PC-3 cells, exposure to 160 nM for 48 hours led to total growth inhibition, which persisted for several days even after drug removal. Several jasplakinolide analogues also inhibited the growth of PC-3 cells, although analogues in which the rigidity of the macrolide ring was altered were ineffective. No early changes in the synthesis of DNA, RNA, or protein or in intracellular adenosine triphosphate levels were seen in the PC-3 cells after exposure to jasplakinolide. Growth inhibition by jasplakinolide was accompanied by striking morphologic changes. Exposure for several doublings led to multinucleated cells. Further investigation of these changes in the PC-3 cells revealed a dramatic and early disruption of the actin cytoskeleton and a statistically significant decrease in RP binding. The doses of jasplakinolide, the time of exposure, and the pattern of growth inhibition by structural analogues corresponded with the changes seen in actin distribution. Conclusions: Jasplakinolide represents a novel marine natural product with patent in vitro antiproliferative activity against human prostate carcinoma cell lines, and it appears to target the actin cytoskeleton. Implications: Jasplakinolide is a potential candidate for further preclinical development and a lead structure for a novel class of therapeutic agents that can disrupt the actin cytoskeleton in mammalian cells. C1 NIH,BETHESDA,MD 20892. NCI,BIOL CHEM LAB,BETHESDA,MD 20892. NCI,PHARMACEUT CHEM LAB,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. UNIV CALIF SANTA CRUZ,DEPT CHEM & BIOCHEM,SANTA CRUZ,CA 95064. UNIV CALIF SANTA CRUZ,INST MARINE SCI,SANTA CRUZ,CA 95064. RI Duncan, Kimberly /C-3655-2013; Rodriguez, Jaime/G-8984-2015 OI Rodriguez, Jaime/0000-0001-5348-6970 FU NCI NIH HHS [CA52955] NR 35 TC 112 Z9 114 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 4 PY 1995 VL 87 IS 1 BP 46 EP 51 DI 10.1093/jnci/87.1.46 PG 6 WC Oncology SC Oncology GA PZ215 UT WOS:A1995PZ21500011 PM 7666463 ER PT J AU MEROPOL, NJ CREAVEN, PJ PETRELLI, NJ WHITE, RM ARBUCK, SG AF MEROPOL, NJ CREAVEN, PJ PETRELLI, NJ WHITE, RM ARBUCK, SG TI SEIZURES ASSOCIATED WITH LEUCOVORIN ADMINISTRATION IN CANCER-PATIENTS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter ID NEUROTOXICITY; FOLATE C1 ROSWELL PK CANC INST,DEPT SURG,BUFFALO,NY 14263. US FDA,DIV ONCOL DRUGS & PULM PROD,ROCKVILLE,MD 20857. NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892. RP MEROPOL, NJ (reprint author), ROSWELL PK CANC INST,DEPT MED,BUFFALO,NY 14263, USA. NR 15 TC 14 Z9 14 U1 0 U2 1 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JAN 4 PY 1995 VL 87 IS 1 BP 56 EP 58 DI 10.1093/jnci/87.1.56 PG 3 WC Oncology SC Oncology GA PZ215 UT WOS:A1995PZ21500013 PM 7666465 ER PT J AU TRAVIS, LB CURTIS, RE INSKIP, PD HANKEY, BF AF TRAVIS, LB CURTIS, RE INSKIP, PD HANKEY, BF TI LUNG-CANCER RISK AND RADIATION-DOSE AMONG WOMEN TREATED FOR BREAST-CANCER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter C1 NCI,DIV CANC PREVENT & CONTROL,CANC STAT BRANCH,BETHESDA,MD 20892. RP TRAVIS, LB (reprint author), NCI,DIV CANC ETIOL,RADIAT EPIDEMIOL BRANCH,EXECUT PLAZA N,RM 408,BETHESDA,MD 20892, USA. NR 4 TC 18 Z9 18 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 4 PY 1995 VL 87 IS 1 BP 60 EP 61 PG 2 WC Oncology SC Oncology GA PZ215 UT WOS:A1995PZ21500015 PM 7666469 ER PT J AU JINDRICH, J PITHA, J LINDBERG, B SEFFERS, P HARATA, K AF JINDRICH, J PITHA, J LINDBERG, B SEFFERS, P HARATA, K TI REGIOSELECTIVITY OF ALKYLATION OF CYCLOMALTOHEPTAOSE (BETA-CYCLODEXTRIN) AND SYNTHESIS OF ITS MONO-2-O-METHYL, MONO-2-O-ETHYL, MONO-2-O-ALLYL, AND MONO-2-O-PROPYL DERIVATIVES SO CARBOHYDRATE RESEARCH LA English DT Article DE CYCLOMALTOHEPTAOSE (BETA-CYCLODEXTRIN), DERIVATIVES OF; CYCLODEXTRIN, BETA- (CYCLOMALTOHEPTAOSE); SYNTHESIS ID NMR-SPECTRA; SUBSTITUENTS; ASSIGNMENT AB Mono-2-O-methyl-, -2-O-ethyl-, and -2-O-allyl-cyclomaltoheptaose were prepared by alkylations of cyclomaltoheptaose in dilute aqueous alkali, and mono-2-O-propylcyclomaltoheptaose was obtained by hydrogenation of the allyl derivative. Ah the 2-O-alkyl derivatives were less soluble in water than was cyclomaltoheptaose. All formed inclusion complexes with toluene in aqueous solution, but only the methyl ether was less soluble in the water-toluene system than in water. The solubilities of the other ethers in water were enhanced by the addition of toluene. Partial methylation of cyclomaltoheptaose with C-13-enriched dimethyl sulfate in dilute aqueous alkali yielded mixtures of products. The substitution patterns were analyzed by GLC-MS of the alditol acetates, prepared by hydrolysis, reduction, and acetylation, and by C-13 NMR after complete permethylation with nonenriched reagent. The results showed that methylation at O-2 is a predominant but not an exclusive reaction; as expected, the regioselectivity decreases with increasing degree of methylation. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. UNIV STOCKHOLM,ARRHENIUS LAB,DEPT ORGAN CHEM,S-10691 STOCKHOLM,SWEDEN. NATL INST BIOSCI & HUMAN TECHNOL,DEPT BIOMOLEC,TSUKUBA,IBARAKI 305,JAPAN. RI Jindrich, Jindrich/A-3527-2008 OI Jindrich, Jindrich/0000-0003-3770-0214 NR 15 TC 29 Z9 35 U1 0 U2 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD JAN 3 PY 1995 VL 266 IS 1 BP 75 EP 80 DI 10.1016/0008-6215(94)00251-A PG 6 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA QC250 UT WOS:A1995QC25000007 PM 7697652 ER PT J AU DALY, JW AF DALY, JW TI THE CHEMISTRY OF POISONS IN AMPHIBIAN SKIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article; Proceedings Paper CT Colloquium on Chemical Ecology - The Chemistry of Biotic Interaction CY MAR 25-26, 1994 CL NATL ACAD SCI, WASHINGTON, DC SP NATL ACAD SCI HO NATL ACAD SCI ID FROGS DENDROBATIDAE; ALKALOIDS; PEPTIDES; MYOBATRACHIDAE; PUMILIOTOXINS; DEFENSE AB Poisons are common in nature, where they often serve the organism in chemical defense. Such poisons either are produced de novo or are sequestered from dietary sources or symbiotic organisms. Among vertebrates, amphibians are notable for the wide range of noxious agents that are contained in granular skin glands. These compounds include amines, peptides, proteins, steroids, and both water-soluble and lipid-soluble alkaloids. With the exception of the alkaloids, most seem to be produced de novo by the amphibian. The skin of amphibians contains many structural classes of alkaloids previously unknown in nature. These include the batrachotoxins, which have recently been discovered to also occur in skin and feathers of a bird, the histrionicotoxins, the gephyrotoxins, the decahydroquinolines, the pumiliotoxins and homopumiliotoxins, epibatidine, and the samandarines. Some amphibian skin alkaloids are clearly sequestered from the diet, which consists mainly of small arthropods. These include pyrrolizidine and indolizidine alkaloids from ants, tricyclic coccinellines from beetles, and pyrrolizidine oximes, presumably from millipedes. The sources of other alkaloids in amphibian skin, including the batrachotoxins, the decahydroquinolines, the histrionicotoxins, the pumiliotoxins, and epibatidine, are unknown. While it is possible that these are produced de novo or by symbiotic microorganisms, it appears more likely that they are sequestered by the amphibians from as yet unknown dietary sources. RP DALY, JW (reprint author), NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892, USA. NR 36 TC 131 Z9 141 U1 1 U2 25 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 3 PY 1995 VL 92 IS 1 BP 9 EP 13 DI 10.1073/pnas.92.1.9 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QB238 UT WOS:A1995QB23800004 PM 7816854 ER PT J AU LISITSYN, NA LISITSINA, NM DALBAGNI, G BARKER, P SANCHEZ, CA GNARRA, J LINEHAN, WM REID, BJ WIGLER, MH AF LISITSYN, NA LISITSINA, NM DALBAGNI, G BARKER, P SANCHEZ, CA GNARRA, J LINEHAN, WM REID, BJ WIGLER, MH TI COMPARATIVE GENOMIC ANALYSIS OF TUMORS - DETECTION OF DNA LOSSES AND AMPLIFICATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CANCER; ONCOGENES; DIFFERENCE ANALYSIS; POLYMERASE CHAIN REACTION ID HUMAN CANCER AB We demonstrate the use of representational difference analysis for cloning probes that detect DNA loss and amplification in tumors. Using DNA isolated from human tumor cell lines to drive hybridization against matched normal DNA, we were able to identify six genomic regions that are homozygously deleted in cultured cancer cells. When this method was applied in the reverse way, using normal DNA to drive hybridization against tumor cell DNA, we readily isolated probes detecting amplification. Representational difference analysis was also performed on DNAs derived from tumor biopsies, and we thereby discovered a probe detecting very frequent homozygous loss in colon cancer cell lines and located on chromosome 3p. C1 COLD SPRING HARBOR LAB,COLD SPRING HARBOR,NY 11724. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. NCI,SURG BRANCH,BETHESDA,MD 20892. OI Wigler, Michael/0000-0003-4396-1971 FU NCI NIH HHS [5P30-CA45508-07] NR 11 TC 108 Z9 110 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 3 PY 1995 VL 92 IS 1 BP 151 EP 155 DI 10.1073/pnas.92.1.151 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QB238 UT WOS:A1995QB23800031 PM 7816807 ER PT J AU KOSTROUCH, Z KOSTROUCHOVA, M RALL, JE AF KOSTROUCH, Z KOSTROUCHOVA, M RALL, JE TI STEROID THYROID-HORMONE RECEPTOR GENES IN CAENORHABDITIS-ELEGANS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ZINC-FINGER; TRANSCRIPTION FACTORS; SUPERFAMILY; MEMBER; IDENTIFICATION; TRANSPORTER; NUR77; ACID; DHR3 AB The large family of steroid/thyroid hormone receptor (STR) genes has been extensively studied in vertebrates and insects but little information is available on it in more primitive organisms. All members possess a DNA binding domain of zinc fingers of the C2, C2 type. We have used the polymerase chain reaction with degenerate oligonucleotide primers covering this region to clone three distinct members of this family from the nematode Caenorhabditis elegans. All three belong to the retinoic acid receptor (RAR), thyroid hormone receptor subfamily of genes. The cDNA of one of these clones shows such a high homology to DHR3, an early ecdysone response gene found in Drosophila, and MHR3, identified in Manduca sexta, that we have termed it CHR3. Furthermore, the C-terminal portion of the deduced protein sequence shows a box containing eight identical amino acids among CHR3, DHR3, and MHR3 suggesting an identical specific ligand for these proteins. CNR8 shows homology to NAk1, and CNR14 has homology to both the RAR-gamma 1 gene and to another ecdysone response gene, E78A. Neither of the latter two cDNAs is a clear homologue of any known gene and each is distinctive. All of these genes are expressed varyingly in both larval and adult stages of nematode development as shown by Northern blot analyses. These data demonstrate that the STR family of genes is represented in a nematode whose ancestor appeared well before the branching that gave rise to the Arthropoda and Chordata. C1 NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 26 TC 44 Z9 52 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 3 PY 1995 VL 92 IS 1 BP 156 EP 159 DI 10.1073/pnas.92.1.156 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QB238 UT WOS:A1995QB23800032 PM 7816808 ER PT J AU MAYERS, DL MIKOVITS, JA JOSHI, B HEWLETT, IK ESTRADA, JS WOLFE, AD GARCIA, GE DOCTOR, BP BURKE, DS GORDON, RK LANE, JR CHIANG, PK AF MAYERS, DL MIKOVITS, JA JOSHI, B HEWLETT, IK ESTRADA, JS WOLFE, AD GARCIA, GE DOCTOR, BP BURKE, DS GORDON, RK LANE, JR CHIANG, PK TI ANTI-HUMAN-IMMUNODEFICIENCY-VIRUS-1 (HIV-1) ACTIVITIES OF 3-DEAZAADENOSINE ANALOGS - INCREASED POTENCY AGAINST 3'-AZIDO-3'-DEOXYTHYMIDINE-RESISTANT HIV-1 STRAINS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID S-ADENOSYLHOMOCYSTEINE HYDROLASE; INHIBITOR; CELL; TARGET; AP-1; PERTURBATIONS; METHYLATION; ACTIVATION; EXPRESSION; METABOLISM AB 3-Deazaadenosine (DZA), 3-deaza-(+/-)aristeromycin (DZAri), and 3-deazaneplanocin A (DZNep) are powerful modulators of cellular processes. When tested against H9 cells infected acutely with two different strains of human immunodeficiency virus 1 (HIV-1) and in the chronically infected monocytoid cell lines U1 and THP-1, the 3-deazanucleosides caused a marked reduction in p24 antigen production. Similar reductions in p24 antigen were seen in phytohemagglutinin-stimulated peripheral blood mononuclear cells infected with clinical HIV-1 isolates. Strikingly, in comparing the therapeutic indices between the paired pre- and post-3'-azido-3'-deoxythymidine (AZT) treatment HIV-1 isolates, DZNep and neplanocin A showed an increase of 3- to 18-fold in their potency against AZT-resistant HIV-1 isolates. In H9 cells treated with DZNep and DZAri, the formation of triphosphate nucleotides of DZNep and DZAri was observed. The mode of action of DZNep and DZAri appears complex, at least in part, at the level of infectivity as shown by decreases in syncytia formation in HIV-1-infected H9 cells and at the level of transcription as both drugs inhibited the expression of basal or tat-induced HIV-1 long terminal repeat chloramphenicol acetyltransferase activity in stably transfected cell lines. Since DZNep induced in H9 cells a rapid expression of nuclear binding factors that recognize the AP-1 transcription site, the anti-HIV-1 activity of the DZA analogs could partly be the induction of critical factors in the host cells. Thus, the 3-deazanucleoside drugs belong to an unusual class of anti-HIV-1 drugs, which may have therapeutic potential, in particular against AZT-resistant strains. C1 WALTER REED ARMY INST RES,WASHINGTON,DC 20307. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702. US FDA,ROCKVILLE,MD 20852. SRA TECHNOL,ROCKVILLE,MD 20850. OI /0000-0002-5704-8094 FU NCI NIH HHS [N01-CO-74102] NR 35 TC 49 Z9 50 U1 0 U2 2 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 3 PY 1995 VL 92 IS 1 BP 215 EP 219 DI 10.1073/pnas.92.1.215 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QB238 UT WOS:A1995QB23800044 PM 7816820 ER PT J AU KRUK, PA RAMPINO, NJ BOHR, VA AF KRUK, PA RAMPINO, NJ BOHR, VA TI DNA-DAMAGE AND REPAIR IN TELOMERES - RELATION TO AGING SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HUMAN TELOMERES ID HUMAN-FIBROBLASTS; XERODERMA-PIGMENTOSUM; PYRIMIDINE DIMERS; NUCLEAR MATRIX; YEAST TELOMERE; GROUP-C; CELLS; GENE; RADIATION; CAPACITY AB We have established a method for the detection of DNA damage and its repair in human telomeres, the natural ends of chromosomes which are necessary for replication and critical for chromosomal stability. We find that ultraviolet light-induced pyrimidine dimers in telomeric DNA are repaired less efficiently than endogenous genes but more efficiently than inactive, noncoding regions. We have also measured telomeric length, telomeric DNA damage, and its repair in relation to the progression of aging. Telomeres are shorter in fibroblasts from an old donor compared to fibroblasts from a young donor, shortest in cells from a patient with the progeroid disorder Werner syndrome, and relatively long in fibroblasts from a patient with Alzheimer disease. Telomeric DNA repair efficiency is lower in cells from an old donor than in cells from a young donor, normal in Alzheimer cells, and slightly lower in Werner cells. It is possible that this decline in telomeric repair with aging is of functional significance to an age-related decline in genomic stability. RP KRUK, PA (reprint author), NIA,GERONTOL RES CTR,MOLEC GENET LAB,BALTIMORE,MD 21224, USA. RI Kruk, Patricia/I-6489-2012 NR 35 TC 220 Z9 227 U1 1 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 JAN 3 PY 1995 VL 92 IS 1 BP 258 EP 262 DI 10.1073/pnas.92.1.258 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QB238 UT WOS:A1995QB23800053 PM 7816828 ER PT J AU DIMITROV, S WOLFFE, AP AF DIMITROV, S WOLFFE, AP TI CHROMATIN AND NUCLEAR ASSEMBLY - EXPERIMENTAL APPROACHES TOWARDS THE RECONSTITUTION OF TRANSCRIPTIONALLY ACTIVE AND SILENT STATES SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Review DE NUCLEOSOME; CHROMATIN FIBER; CHROMOSOME DOMAIN; TRANSCRIPTIONAL CONTROL; NUCLEAR LAMINA AND MEMBRANE ID POSITION-EFFECT VARIEGATION; DNA-REPLICATION INVITRO; RNA POLYMERASE-II; XENOPUS-LAEVIS OOCYTES; NUCLEOSOME CORE PARTICLE; ONE H2A.H2B DIMER; CELL-FREE SYSTEM; HISTONE ACETYLATION; SACCHAROMYCES-CEREVISIAE; LAMIN-A C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. RI dimitrov, stefan/M-7697-2013 NR 157 TC 28 Z9 29 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD JAN 2 PY 1995 VL 1260 IS 1 BP 1 EP 13 DI 10.1016/0167-4781(94)00182-3 PG 13 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QG045 UT WOS:A1995QG04500001 PM 7999782 ER PT J AU ZNAMENSKAYA, LV GABDRAKHMANOVA, LA CHERNOKALSKAYA, EB LESHCHINSKAYA, IB HARTLEY, RW AF ZNAMENSKAYA, LV GABDRAKHMANOVA, LA CHERNOKALSKAYA, EB LESHCHINSKAYA, IB HARTLEY, RW TI PHOSPHATE REGULATION OF BIOSYNTHESIS OF EXTRACELLULAR RNASES OF ENDOSPORE-FORMING BACTERIA SO FEBS LETTERS LA English DT Article DE BARNASE; BINASE; RIBONUCLEASE BP; GENE CLONING; PHO BOX; INORGANIC PHOSPHATE ID DNA AB The gene for the extracellular ribonuclease of B. pumilus KMM62 (RNase Bp) has been cloned and sequenced, The structural gene for this enzyme is similar to those of the extracellular ribonucleases of B. intermedius 7P (binase) and B. amyloliquefaciens H2 (barnase), as are the regulatory regions of binase and RNase Bp, The regulatory region of the barnase gene, however, is quite different from the other two, In the promoter of the genes for binase and RNase Bp, but not in that for barnase, is a region similar to the Pho box of E. coli. We have established that inorganic phosphate suppresses the synthesis of the binase and RNase Bp, but does not effect the synthesis of barnase. C1 NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. RP ZNAMENSKAYA, LV (reprint author), KAZAN VI LENIN STATE UNIV,DEPT MICROBIOL,LENIN ST 18,KAZAN 420008,RUSSIA. NR 13 TC 15 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD JAN 2 PY 1995 VL 357 IS 1 BP 16 EP 18 DI 10.1016/0014-5793(94)01316-S PG 3 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA PZ573 UT WOS:A1995PZ57300004 PM 8001670 ER PT J AU VALLE, A KINET, JP AF VALLE, A KINET, JP TI N-ACETYL-L-CYSTEINE INHIBITS ANTIGEN-MEDIATED SYK, BUT NOT LYN TYROSINE KINASE ACTIVATION IN MAST-CELLS SO FEBS LETTERS LA English DT Article DE N-ACETYL-L-CYSTEINE; FC-EPSILON-RI RECEPTOR; TYROSINE KINASE ID BASOPHILIC LEUKEMIA-CELLS; PHOSPHOLIPASE C-GAMMA-1; PHOSPHORYLATION; RECEPTOR; DEPHOSPHORYLATION; STIMULATION; ENGAGEMENT; RESIDUES; COMPLEX; H2O2 AB High affinity IgE receptors (alpha beta gamma(2)) mediate the activation of the non-receptor tyrosine kinases Lyn and Syk. Here we show that the antioxidant drug N-acetyl-L-cysteine (NAG) inhibits antigen-mediated Syk activation whereas Lyn activation and phosphorylation of beta and gamma is maintained. Furthermore, NAC inhibits antigen-mediated calcium mobilization and exocytosis in a dose-dependent manner, but does not inhibit ionomycin-induced exocytosis. These data support a model in which the activation of Lyn is responsible for receptor phosphorylation and precedes the activation of Syk, The inhibition of Syk activation by NAC may be relevant to B and T cell antigen receptors, which are also linked to Syk/ZAP70 tyrosine kinases. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. NR 33 TC 19 Z9 19 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD JAN 2 PY 1995 VL 357 IS 1 BP 41 EP 44 DI 10.1016/0014-5793(94)01329-Y PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA PZ573 UT WOS:A1995PZ57300010 PM 8001675 ER PT B AU VRHEL, M LEE, C UNSER, M AF VRHEL, M LEE, C UNSER, M GP IEEE TI FAST CONTINUOUS WAVELET TRANSFORM SO 1995 INTERNATIONAL CONFERENCE ON ACOUSTICS, SPEECH, AND SIGNAL PROCESSING - CONFERENCE PROCEEDINGS, VOLS 1-5 LA English DT Proceedings Paper CT 1995 International Conference on Acoustics, Speech, and Signal Processing CY MAY 09-12, 1995 CL DETROIT, MI SP IEEE, Signal Proc Soc C1 NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU I E E E PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 BN 0-7803-2432-3 J9 INT CONF ACOUST SPEE PY 1995 BP 1165 EP 1168 PG 4 WC Acoustics; Automation & Control Systems; Computer Science, Artificial Intelligence; Engineering, Electrical & Electronic; Optics; Telecommunications SC Acoustics; Automation & Control Systems; Computer Science; Engineering; Optics; Telecommunications GA BD41X UT WOS:A1995BD41X00292 ER PT B AU THEVENAZ, P UNSER, M AF THEVENAZ, P UNSER, M GP IEEE TI EFFICIENT GEOMETRIC TRANSFORMATIONS AND 3-D IMAGE REGISTRATION SO 1995 INTERNATIONAL CONFERENCE ON ACOUSTICS, SPEECH, AND SIGNAL PROCESSING - CONFERENCE PROCEEDINGS, VOLS 1-5 LA English DT Proceedings Paper CT 1995 International Conference on Acoustics, Speech, and Signal Processing CY MAY 09-12, 1995 CL DETROIT, MI SP IEEE, Signal Proc Soc C1 NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU I E E E PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 BN 0-7803-2432-3 J9 INT CONF ACOUST SPEE PY 1995 BP 2919 EP 2922 PG 4 WC Acoustics; Automation & Control Systems; Computer Science, Artificial Intelligence; Engineering, Electrical & Electronic; Optics; Telecommunications SC Acoustics; Automation & Control Systems; Computer Science; Engineering; Optics; Telecommunications GA BD41X UT WOS:A1995BD41X00729 ER PT B AU MARQUEZ, VE LEE, J SHARMA, R LEWIN, NE BLUMBERG, PM MILNE, GWA WANG, SM AF MARQUEZ, VE LEE, J SHARMA, R LEWIN, NE BLUMBERG, PM MILNE, GWA WANG, SM BE Ordax, FA Arrizabalaga, A Barrio, R TI The design of ultrapotent protein kinase C (PK-C) agonists based on a constrained diacylglycerol (DAG) template SO 25TH BIANNUAL MEETING OF THE SPANISH ROYAL SOCIETY FOR CHEMISTRY 1994, PLENARY CONFERENCE LA English DT Proceedings Paper CT 25th Biannual Meeting of Real-Sociedad-Espanola-de-Quimica CY SEP 25-29, 1994 CL VITORIA, SPAIN SP Real Soc Espanola Quim C1 NCI,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU DIPUTACION FORAL ALAVA SERVICIO PUBLICACIONES PI VITORIA PA PZA PROVINCIA 5, 01001 VITORIA, SPAIN BN 84-7821-218-3 PY 1995 BP 285 EP 288 PG 4 WC Chemistry, Multidisciplinary SC Chemistry GA BD85R UT WOS:A1995BD85R00021 ER PT B AU Zink, S AF Zink, S BE Purdy, JA Emami, B TI 3-D radiation treatment planning: NCI perspective SO 3-D RADIATION TREATMENT PLANNING AND CONFORMAL THERAPY LA English DT Proceedings Paper CT International Conference on 3-D Radiation Treatment Planning and Conformal Therapy CY APR 21-23, 1993 CL ST LOUIS, MO SP Radiat Oncol Ctr, Mallinckrodt Inst Radiol, Washington Univ Sch Med St Louis C1 NCI,RADIAT RES PROGRAM,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MEDICAL PHYSICS PUBLISHING PI MADISON PA 4513 VERNON BLVD, MADISON, WI 53705 BN 0-944838-51-0 PY 1995 BP 1 EP 10 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA BF57B UT WOS:A1995BF57B00001 ER PT B AU Kolobow, T Giacomini, M AF Kolobow, T Giacomini, M BE Roussos, C Armaganidis, A Papadatos, J Papandonatos, D Rasidakis, A TI Intratracheal pulmonary ventilation SO 8TH EUROPEAN CONGRESS OF INTENSIVE CARE MEDICINE, I AND II: I: MAIN LECTURES; II: FREE PAPERS LA English DT Proceedings Paper CT 8th European Congress of Intensive Care Medicine CY OCT 18-22, 1995 CL ATHENS, GREECE SP European Soc Intens Care Med C1 NHLBI,NIH,PULM CRIT CARE MED BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MONDUZZI EDITORE PI 40128 BOLOGNA PA VIA FERRARESE 119/2, 40128 BOLOGNA, ITALY BN 88-323-1018-1 PY 1995 BP A617 EP A624 PG 8 WC Emergency Medicine; Medicine, General & Internal SC Emergency Medicine; General & Internal Medicine GA BE79H UT WOS:A1995BE79H00086 ER PT B AU Kolobow, T RealiForster, C Giacomini, M AF Kolobow, T RealiForster, C Giacomini, M BE Roussos, C Armaganidis, A Papadatos, J Papandonatos, D Rasidakis, A TI New endotracheal tubes to decrease tracheal injury during mechanical ventilation SO 8TH EUROPEAN CONGRESS OF INTENSIVE CARE MEDICINE, I AND II: I: MAIN LECTURES; II: FREE PAPERS LA English DT Proceedings Paper CT 8th European Congress of Intensive Care Medicine CY OCT 18-22, 1995 CL ATHENS, GREECE SP European Soc Intens Care Med C1 NHLBI,NIH,PCCM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MONDUZZI EDITORE PI 40128 BOLOGNA PA VIA FERRARESE 119/2, 40128 BOLOGNA, ITALY BN 88-323-1018-1 PY 1995 BP A403 EP A409 PG 7 WC Emergency Medicine; Medicine, General & Internal SC Emergency Medicine; General & Internal Medicine GA BE79H UT WOS:A1995BE79H00055 ER PT J AU FROIO, J ABRAHAM, EH SONI, R EPSTEIN, A OKUNIEFF, P AF FROIO, J ABRAHAM, EH SONI, R EPSTEIN, A OKUNIEFF, P TI EFFECT OF INTRAPERITONEAL ATP ON TUMOR-GROWTH AND BONE-MARROW RADIATION TOLERANCE SO ACTA ONCOLOGICA LA English DT Article; Proceedings Paper CT International Workshop on the Tumour Microenvironment - Its Characterization, Modification and Clinical Implications CY SEP 23-25, 1994 CL UNIV GRANADA, FAC MED, GRANADA, SPAIN HO UNIV GRANADA, FAC MED ID MURINE FIBRO-SARCOMA; ADENINE-NUCLEOTIDES; ADENOSINE 5'-TRIPHOSPHATE; EXTRACELLULAR ADENOSINE; ANTICANCER ACTIVITIES; CELLS; THERMOCHEMOTHERAPY; TRIPHOSPHATE; TEMPERATURES; INHIBITION AB Transplants of a spontaneous murine fibrosarcoma (FSaII) treated with intraperitoneal ATP were studied in vitro, and in both C3H and nu/nu mice. Daily ATP treatment prolonged tumor volume doubling time in vivo and in vitro. Daily ATP treatments at the maximally tolerated dose (2 mmol/kg i.p.) did not significantly affect the pH or the PCr/P-i, or beta ATP/P-i ratios (measured by MRS). In contrast to the reduced tumor growth rate, there was no change in bone marrow recovery after whole body irradiation. ATP is minimally toxic to animals at active dose levels. It slows tumor growth rate without adversely affecting bone marrow radiation tolerance. ATP might therefore be useful as a biological modifier of chemotherapy or radiation therapy. C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NR 23 TC 12 Z9 12 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0284-186X J9 ACTA ONCOL JI Acta Oncol. PY 1995 VL 34 IS 3 BP 419 EP 422 PG 4 WC Oncology SC Oncology GA RB020 UT WOS:A1995RB02000026 PM 7779434 ER PT J AU OKUNIEFF, P ABRAHAM, EH MOINI, M SNYDER, ML GLOE, TR CAPOGROSSI, MC DING, I AF OKUNIEFF, P ABRAHAM, EH MOINI, M SNYDER, ML GLOE, TR CAPOGROSSI, MC DING, I TI BASIC FIBROBLAST GROWTH-FACTOR RADIOPROTECTS BONE-MARROW AND NOT RIF1 TUMOR SO ACTA ONCOLOGICA LA English DT Article; Proceedings Paper CT International Workshop on the Tumour Microenvironment - Its Characterization, Modification and Clinical Implications CY SEP 23-25, 1994 CL UNIV GRANADA, FAC MED, GRANADA, SPAIN HO UNIV GRANADA, FAC MED ID CELLS; INVITRO; LUNG; FGF AB We examined the potential of bFGF to function as a radioprotector of bone marrow (BM). Total intravenous doses of bFGF ranged from 1 to 24 mu g/mouse, in 2 divided doses. Whole body radiation (WBI) was given in a single fraction to C3H mice. Histologic observations were performed on femur BM at various times after bFGF (or placebo) treatment. Thigh radiation in thigh-tumor bearing mice was delivered in a single fraction, bFGF increased the LD(50/30) of mice in a dose dependent fashion, with an apparent maximum protection obtained with greater than or equal to 6 mu g given half 24 h and half 4 h before irradiation. BM histology shows prominent recovery of megakaryocytes and all cell lineages along with less loss in cellularity compared to control irradiated animals. No radioprotection of RIF1 tumors after bFGF was detected. These results indicate that bFGF may be a selective radioprotector of normal tissue. C1 NIA,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. RP OKUNIEFF, P (reprint author), NCI,RADIAT ONCOL BRANCH,9000 ROCKVILLE PIKE,BLDG 10 RM B3B69,BETHESDA,MD 20892, USA. NR 21 TC 13 Z9 13 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0284-186X J9 ACTA ONCOL JI Acta Oncol. PY 1995 VL 34 IS 3 BP 435 EP 438 PG 4 WC Oncology SC Oncology GA RB020 UT WOS:A1995RB02000029 PM 7779437 ER PT J AU CLARK, WH TUCKER, MA GOLDSTEIN, AM AF CLARK, WH TUCKER, MA GOLDSTEIN, AM TI PARENCHYMAL-STROMAL INTERACTIONS IN NEOPLASIA - THEORETICAL CONSIDERATIONS AND OBSERVATIONS IN MELANOCYTIC NEOPLASIA SO ACTA ONCOLOGICA LA English DT Article ID TUMOR PROGRESSION; EXTRACELLULAR-MATRIX; CANCER GROWTH; MELANOMA; LIMB AB The paper briefly reviews the reciprocal and continuous reciprocal interactions between epithelia, mesenchyme, and extracellular matrix in the development and maintenance of organismal form in multicellular organisms in the animal kingdom and describes the progressive changes in parenchymal-stromal interactions in melanocytic neoplastic development and progression, In addition to the parenchymal stromal form in non-lesional skin seven different and unique stromal patterns are described. These have been termed: 1) The stroma (diff-regress) of programmed differentiation leading to lesional regression characteristic of common nevi; 2) Concentric eosinophilic fibroplasia (cef), the hallmark of precursor nevi (dyplastic nevi) with and without melanocytic nuclear atypia; 3) Fibroplasia with angiogenesis (fa) commonly seen in superficial spreading melanoma without metastic competence (SSM); 4) Lamellar fibroplasia (If) seen in precursor nevi and melanomas with and without metastatic competence; 5) Diffuse fibroplasia with angiogenesis (dfa), 6) Narrow, uniform concentric eosinophilic fibroplasia (nucef), 7) No parenchymal-stromal interaction (nopsi); the last three being seen in the heterogeneous stroma of melanomas of the superficial spreading type with metastatic competence, The changes in neoplastic stroma proceed in concert with the changes in the parenchyma characteristic of melanocytic tumor progression. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,PATHOL SERV INC,DEPT PATHOL,CAMBRIDGE,MA 02138. UNIV PENN,SCH MED,PIGMENTED LES GRP,PHILADELPHIA,PA 19104. NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892. RI Tucker, Margaret/B-4297-2015 FU NCI NIH HHS [CA-25298, CA-58845] NR 25 TC 23 Z9 24 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0284-186X J9 ACTA ONCOL JI Acta Oncol. PY 1995 VL 34 IS 6 BP 749 EP 757 PG 9 WC Oncology SC Oncology GA RZ612 UT WOS:A1995RZ61200008 PM 7576741 ER PT J AU WU, GC ZHU, JM CAO, XD AF WU, GC ZHU, JM CAO, XD TI INVOLVEMENT OF OPIOID-PEPTIDES OF THE PREOPTIC AREA DURING ELECTROACUPUNCTURE ANALGESIA SO ACUPUNCTURE & ELECTRO-THERAPEUTICS RESEARCH LA English DT Article DE ACUPUNCTURE ANALGESIA; PREOPTIC AREA; OPIOID PEPTIDES; NORADRENALINE AB The present work was to study the roles of opioid peptides in the preoptic area on electroacupuncture analgesia (EA), and the effects of opioid peptides on noradrenaline (NA) release in the preoptic area during EA. It was found that the pain threshold and the level of [Leu(5)] enkephalin (L-EK) or beta-endorphin (beta-EP) release in the perfusate were increased during EA, but the NA release from the preoptic area was decreased. Naloxone (15 mu M) perfusion significantly reversed the increased pain threshold and the decreased NA release induced by acupuncture. The reversal of pain threshold and NA release by naloxone was dose-dependent. Multimicropipettes and microiontophoresis were also used to study the effect of acupuncture. The inhibition of nociceptive neuronal discharges produced by electroacupuncture was closely related to the etorphine-sensitive neurons, and reversed by microiontophoretic application of naloxone. The results suggest that the inhibitory effect induced by electroacupuncture may be mediated by opioid peptides in the preoptic area. RP WU, GC (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,E1-O1,POB 12233,RES TRIANGLE PK,NC 27713, USA. NR 0 TC 16 Z9 17 U1 0 U2 2 PU COGNIZANT COMMUNICATION CORP PI ELMSFORD PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 SN 0360-1293 J9 ACUPUNCTURE ELECTRO JI Acupunct. Electro-Ther. Res. PD JAN-MAR PY 1995 VL 20 IS 1 BP 1 EP 6 PG 6 WC Integrative & Complementary Medicine; Neurosciences SC Integrative & Complementary Medicine; Neurosciences & Neurology GA QZ055 UT WOS:A1995QZ05500001 PM 7572327 ER PT J AU Chilcoat, HD Schutz, CG AF Chilcoat, HD Schutz, CG TI Racial ethnic and age differences in crack use within neighborhoods SO ADDICTION RESEARCH LA English DT Article DE crack cocaine; socioeconomic factors; Blacks; Hispanic Americans; Whites ID COCAINE SMOKING AB Summ. overviews of crack use in the U.S. indicate that the lifetime prevalence of crack use for African-Americans is 2-3 times that of White-Americans. However, a recent study that used interview data from the 1988 National Household Survey of Drug Abuse (NHSDA) found no racial/ethnic differences, once neighborhood was held constant. In light of an observed increase in crack use among African-Americans since 1988, we set out to determine whether differences existed between race/ethnicities, using data from the 1990 NHSDA. Employing a post-stratification procedure, we found no overall differences in lifetime prevalence of crack use for African-Americans relative to White-Americans (RO = 1.37, 95% CI = 0.82-2.29) but found that Hispanic Americans had lower odds than whites (RO = 0.52, 95% CI = 0.28-0.96). However, stratification by age group indicated that African-Americans 30-34 years old had significantly higher odds of lifetime crack use than White-Americans in the same age strata when neighborhood is held constant (RO = 2.51, 95% CI = 1.10-5.74). Crack use in the year prior to interview was common among African-Americans in this age group who had ever used crack in their lifetime (63%), whereas it was unlikely among similarly aged White- or Hispanic-Americans with a lifetime history of crack use (14% and 0%, respectively). Generalized Additive Models (GAMs) were used to examine trends in the age-specific prevalence of lifetime crack use between 1988 and 1990 by rate/ethnicity. The overall increase in lifetime crack use among African-Americans is explained by an increase in prevalence for African-Americans who are approximately 30 years old-from 5% in 1988 to 8% in 1990. No change was observed for African-Americans of other ages. These findings point to the importance of studying factors specific to older African-Americans (i.e., 30-34 years old) that might have placed them at greater risk than similarly aged individuals of other racial/ethnic groups. RP Chilcoat, HD (reprint author), NIDA,ADDICT RES CTR,ETIOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA. NR 15 TC 4 Z9 4 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1058-6989 J9 ADDICT RES JI Addict. Res. PY 1995 VL 3 IS 2 BP 103 EP 111 DI 10.3109/16066359509005229 PG 9 WC Substance Abuse; Social Issues SC Substance Abuse; Social Issues GA TM192 UT WOS:A1995TM19200004 ER PT J AU HICKEY, JE SUESS, PE NEWLIN, DB SPURGEON, L PORGES, SW AF HICKEY, JE SUESS, PE NEWLIN, DB SPURGEON, L PORGES, SW TI VAGAL TONE REGULATION DURING SUSTAINED ATTENTION IN BOYS EXPOSED TO OPIATES IN-UTERO SO ADDICTIVE BEHAVIORS LA English DT Article ID CHILDREN; INFANTS; ADOLESCENTS; NARCOTICS; MOTHERS AB Attention and learning problems among children exposed to opiates in utero have been previously reported but are difficult to interpret due to imprecise measurement and inadequate control of postnatal factors. In this study, we used a behavior-based measure of attention (continuous-performance tasks) and a physiological index of sustained attention (cardiac vagal tone) to measure more precisely the process of sustained attention. Boys, aged 7 to 12, exposed to opiates in utero, were compared to boys whose mothers began using illicit substances after the child's birth (environmental controls), and boys whose mothers were non-drug users. This three-group design was intended to isolate in utero effects from postnatal environmental influences. Vagal tone, a measure of heart-rate variability sensitive to vagal influences on the heart, was measured pre- and postbaseline and during the three tasks of the Gordon Diagnostic System (Delay, Vigilance, and Distractibility). Vagal tone has been found to be sensitive to changes in environmental demand for sustained attention in infants, school-age children, and adults. Results indicated that when distractors were added to the vigilance task (Distractibility task), opiate-exposed boys failed to suppress vagal tone compared to both control groups. However, both the opiate-exposed boys and the environmental controls made fewer correct responses than non-drug-exposed controls on this task. These results indicate that normal physiological responses to increased attentional demand may be impaired in boys exposed in utero to opiates in this age range. However, the poor Distractibility scores of both the opiate-exposed and environmental controls suggests an important role of environmental influences on attentional performance. C1 NIDA,ETIOL BRANCH,INTRAMURAL RES PROGRAM,POB 5180,BALTIMORE,MD 21224. DEPT SERV CHILDREN YOUTH & THEIR FAMILIES,WILMINGTON,DE. UNIV MARYLAND,COLLEGE PK,MD 20742. ADDICT RES CTR,BALTIMORE,MD. NR 27 TC 16 Z9 17 U1 3 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4603 J9 ADDICT BEHAV JI Addict. Behav. PD JAN-FEB PY 1995 VL 20 IS 1 BP 43 EP 59 DI 10.1016/0306-4603(94)00044-Y PG 17 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA QD907 UT WOS:A1995QD90700003 PM 7785481 ER PT B AU JACOBSON, MA AF JACOBSON, MA BE Belardinelli, L Pelleg, A TI Molecular biology of adenosine receptors SO ADENOSINE AND ADENINE NUCLEOTIDES: FROM MOLECULAR BIOLOGY TO INTEGRATIVE PHYSIOLOGY LA English DT Proceedings Paper CT 5th International Symposium on Adenosine and Adenine Nucleotides CY MAY 09-13, 1994 CL PHILADELPHIA, PA SP Fujisawa Pharm Co, Medco Res Inc C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 0 TC 23 Z9 23 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-3190-7 PY 1995 BP 5 EP 13 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD52W UT WOS:A1995BD52W00001 ER PT B AU JACOBSON, KA FISCHER, B MAILLARD, M BOYER, JL HOYLE, CHV HARDEN, TK BURNSTOCK, G AF JACOBSON, KA FISCHER, B MAILLARD, M BOYER, JL HOYLE, CHV HARDEN, TK BURNSTOCK, G BE Belardinelli, L Pelleg, A TI Novel ATP agonists reveal receptor heterogeneity within P-2x and P-2y subtypes SO ADENOSINE AND ADENINE NUCLEOTIDES: FROM MOLECULAR BIOLOGY TO INTEGRATIVE PHYSIOLOGY LA English DT Proceedings Paper CT 5th International Symposium on Adenosine and Adenine Nucleotides CY MAY 09-13, 1994 CL PHILADELPHIA, PA SP Fujisawa Pharm Co, Medco Res Inc C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 0 TC 9 Z9 9 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-3190-7 PY 1995 BP 149 EP 156 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD52W UT WOS:A1995BD52W00018 ER PT B AU DALY, JW JACOBSON, KA AF DALY, JW JACOBSON, KA BE Belardinelli, L Pelleg, A TI Adenosine receptors: Selective agonists and antagonists SO ADENOSINE AND ADENINE NUCLEOTIDES: FROM MOLECULAR BIOLOGY TO INTEGRATIVE PHYSIOLOGY LA English DT Proceedings Paper CT 5th International Symposium on Adenosine and Adenine Nucleotides CY MAY 09-13, 1994 CL PHILADELPHIA, PA SP Fujisawa Pharm Co, Medco Res Inc C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 0 TC 24 Z9 24 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-3190-7 PY 1995 BP 157 EP 166 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD52W UT WOS:A1995BD52W00019 ER PT B AU ABRAHAM, EH AF ABRAHAM, EH BE Belardinelli, L Pelleg, A TI P-glycoprotein serves as a transporter of cellular ATP SO ADENOSINE AND ADENINE NUCLEOTIDES: FROM MOLECULAR BIOLOGY TO INTEGRATIVE PHYSIOLOGY LA English DT Proceedings Paper CT 5th International Symposium on Adenosine and Adenine Nucleotides CY MAY 09-13, 1994 CL PHILADELPHIA, PA SP Fujisawa Pharm Co, Medco Res Inc C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-3190-7 PY 1995 BP 189 EP 192 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD52W UT WOS:A1995BD52W00022 ER PT B AU VONLUBITZ, DKJE JACOBSON, KA AF VONLUBITZ, DKJE JACOBSON, KA BE Belardinelli, L Pelleg, A TI Behavioral effects of adenosine receptor stimulation SO ADENOSINE AND ADENINE NUCLEOTIDES: FROM MOLECULAR BIOLOGY TO INTEGRATIVE PHYSIOLOGY LA English DT Proceedings Paper CT 5th International Symposium on Adenosine and Adenine Nucleotides CY MAY 09-13, 1994 CL PHILADELPHIA, PA SP Fujisawa Pharm Co, Medco Res Inc C1 NIDDK,BIOORGAN CHEM LAB,MOLEC RECOGNIT SECT,BETHESDA,MD 20892. NR 0 TC 16 Z9 16 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-3190-7 PY 1995 BP 489 EP 498 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD52W UT WOS:A1995BD52W00052 ER PT J AU KOLENBRANDER, PE AF KOLENBRANDER, PE TI COAGGREGATIONS AMONG ORAL BACTERIA SO ADHESION OF MICROBIAL PATHOGENS SE METHODS IN ENZYMOLOGY LA English DT Review ID ACTINOMYCES-NAESLUNDII PK606; BACTEROIDES-LOESCHEII PK1295; STREPTOCOCCUS-SANGUIS; CELL-INTERACTIONS; SURFACE; HYDROXYAPATITE; ADHESIN; GENE RP KOLENBRANDER, PE (reprint author), NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892, USA. NR 14 TC 27 Z9 28 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 253 BP 385 EP 397 PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE08D UT WOS:A1995BE08D00031 PM 7476402 ER PT S AU LONDON, J AF LONDON, J BE Doyle, RJ Ofek, I TI IDENTIFYING AND ISOLATING FIMBRIAL-ASSOCIATED ADHESINS OF ORAL GRAM-NEGATIVE BACTERIA SO ADHESION OF MICROBIAL PATHOGENS SE Methods in Enzymology LA English DT Review ID BACTEROIDES-LOESCHEII PK1295; MONOCLONAL-ANTIBODIES RP LONDON, J (reprint author), NIDR, MICROBIAL ECOL LAB, BETHESDA, MD 20892 USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-182154-4 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 253 BP 397 EP 403 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE08D UT WOS:A1995BE08D00032 PM 7476403 ER PT J AU TOMER, KB DETERDING, LJ PARKER, CE AF TOMER, KB DETERDING, LJ PARKER, CE TI CAPILLARY ELECTROPHORESIS COUPLED WITH MASS-SPECTROMETRY SO ADVANCES IN CHROMATOGRAPHY, VOL 35 SE ADVANCES IN CHROMATOGRAPHY LA English DT Article ID FAST-ATOM-BOMBARDMENT; ELECTROSPRAY IONIZATION INTERFACE; LASER DESORPTION IONIZATION; ION SPRAY INTERFACE; ZONE ELECTROPHORESIS; LIQUID-CHROMATOGRAPHY; NANOSCALE SEPARATIONS; ATMOSPHERIC-PRESSURE; PROTEIN-ANALYSIS; PEPTIDES RP TOMER, KB (reprint author), NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709, USA. RI Tomer, Kenneth/E-8018-2013 NR 95 TC 14 Z9 15 U1 0 U2 1 PU MARCEL DEKKER PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0065-2415 J9 ADV CHROMATOGR PY 1995 VL 35 BP 53 EP 99 PG 47 WC Chemistry, Analytical SC Chemistry GA BD04G UT WOS:A1995BD04G00002 ER PT J AU ISSAQ, HJ JANINI, GM CHAN, KC ELRASSI, Z AF ISSAQ, HJ JANINI, GM CHAN, KC ELRASSI, Z TI APPROACHES FOR THE OPTIMIZATION OF EXPERIMENTAL PARAMETERS IN CAPILLARY ZONE ELECTROPHORESIS SO ADVANCES IN CHROMATOGRAPHY, VOL 35 SE ADVANCES IN CHROMATOGRAPHY LA English DT Review ID FUSED-SILICA CAPILLARIES; OPEN-TUBULAR CAPILLARY; MICELLAR ELECTROKINETIC CHROMATOGRAPHY; MASS-SPECTROMETRIC DETECTION; ELECTROOSMOTIC FLOW-CONTROL; HOST-GUEST COMPLEXATION; APPLIED RADIAL VOLTAGE; LIQUID-CHROMATOGRAPHY; STATIONARY PHASES; INFLUENCE MOBILITY C1 OKLAHOMA STATE UNIV,DEPT CHEM,STILLWATER,OK 74078. RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,DEPT CHEM SYNTH & ANAL,FREDERICK,MD 21702, USA. NR 193 TC 21 Z9 21 U1 1 U2 3 PU MARCEL DEKKER PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0065-2415 J9 ADV CHROMATOGR PY 1995 VL 35 BP 101 EP 169 PG 69 WC Chemistry, Analytical SC Chemistry GA BD04G UT WOS:A1995BD04G00003 PM 7879669 ER PT J AU NOTTELMANN, ED JENSEN, PS AF NOTTELMANN, ED JENSEN, PS TI COMORBIDITY OF DISORDERS IN CHILDREN AND ADOLESCENTS - DEVELOPMENTAL PERSPECTIVES SO ADVANCES IN CLINICAL CHILD PSYCHOLOGY, VOL 17 SE ADVANCES IN CLINICAL CHILD PSYCHOLOGY LA English DT Article ID ATTENTION-DEFICIT DISORDER; DSM-III DISORDERS; OPPOSITIONAL DEFIANT DISORDER; BEHAVIOR PROBLEM SYNDROMES; CONDUCT DISORDER; PSYCHIATRIC-DISORDERS; COMMUNITY SAMPLE; DEPRESSIVE-DISORDERS; ANXIETY DISORDERS; FOLLOW-UP RP NOTTELMANN, ED (reprint author), NIMH,ROCKVILLE,MD 20857, USA. NR 72 TC 92 Z9 92 U1 5 U2 17 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0149-4732 J9 ADV CLIN CHILD PSYCH PY 1995 VL 17 BP 109 EP 155 PG 47 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA BB79W UT WOS:A1995BB79W00003 ER PT S AU STUBBS, M VEECH, RL GRIFFITHS, JR AF STUBBS, M VEECH, RL GRIFFITHS, JR BE Weber, G TI TUMOR METABOLISM - THE LESSONS OF MAGNETIC-RESONANCE SPECTROSCOPY SO ADVANCES IN ENZYME REGULATION, VOL 35 SE ADVANCES IN ENZYME REGULATION LA English DT Article; Proceedings Paper CT 35th Symposium on Regulation of Enzyme Activity and Synthesis in Normal and Neoplastic Tissues CY OCT 03-04, 1994 CL INDIANA UNIV SCH MED, INDIANAPOLIS, IN HO INDIANA UNIV SCH MED ID RAT-TUMORS; INTRACELLULAR PH; CANCER-CELLS; SOLID TUMORS; BLOOD-FLOW; P-31-NMR SPECTROSCOPY; LACTATE-DEHYDROGENASE; INVIVO; NMR; OXYGENATION C1 NIAAA,METAB LAB,ROCKVILLE,MD 20852. RP STUBBS, M (reprint author), ST GEORGE HOSP,SCH MED,DIV BIOCHEM,CANC RES CAMPAIGN BIOMED MR RES GRP,CRANMER TERRACE,LONDON SW17 0RE,ENGLAND. RI Griffiths, John/F-2853-2010 NR 52 TC 47 Z9 50 U1 0 U2 0 PU PERGAMON PRESS LTD PI OXFORD PA THE BOULEVARD LANGFORD LANE KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0065-2571 BN 0-08-042639-5 J9 ADV ENZYME REGUL PY 1995 VL 35 BP 101 EP 115 DI 10.1016/0065-2571(94)00016-V PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BD26C UT WOS:A1995BD26C00008 PM 7572338 ER PT B AU BASILE, AS GU, ZQ YURDAYDIN, CH HARRISON, PM HUGHES, RD PANNELL, L MCKINNEY, A JONES, EA WILLIAMS, R AF BASILE, AS GU, ZQ YURDAYDIN, CH HARRISON, PM HUGHES, RD PANNELL, L MCKINNEY, A JONES, EA WILLIAMS, R BE Capocaccia, L Merli, M Riggio, O TI THE RELATIONSHIP BETWEEN BENZODIAZEPINE RECEPTOR LIGAND CONCENTRATIONS AND THE SEVERITY OF HEPATIC ENCEPHALOPATHY IN HUMANS AND AN ANIMAL MODEL OF ACUTE LIVER FAILURE SO ADVANCES IN HEPATIC ENCEPHALOPATHY AND METABOLIC NITROGEN EXCHANGE LA English DT Proceedings Paper CT 8th International Symposium on Ammonia - Advances in Hepatic Encephalopathy and Metabolic Nitrogen Exchange CY MAY 06-09, 1993 CL ROME, ITALY SP ZYMA, Banca Roma C1 NIDDKD,NEUROSCI LAB,DIGEST DIS BRANCH,LIVER DIS SECT,BETHESDA,MD. RI Harrison, Phillip/D-5374-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-8493-8964-X PY 1995 BP 193 EP 197 PG 5 WC Cell Biology; Gastroenterology & Hepatology; Clinical Neurology SC Cell Biology; Gastroenterology & Hepatology; Neurosciences & Neurology GA BD26Q UT WOS:A1995BD26Q00032 ER PT B AU YURDAYDIN, C WALSH, TJ ENGLER, H BASILE, AS JONES, EA AF YURDAYDIN, C WALSH, TJ ENGLER, H BASILE, AS JONES, EA BE Capocaccia, L Merli, M Riggio, O TI THE ROLE OF GUT BACTERIA IN THE ACCUMULATION OF BENZODIAZEPINE RECEPTOR LIGANDS IN HEPATIC ENCEPHALOPATHY SO ADVANCES IN HEPATIC ENCEPHALOPATHY AND METABOLIC NITROGEN EXCHANGE LA English DT Proceedings Paper CT 8th International Symposium on Ammonia - Advances in Hepatic Encephalopathy and Metabolic Nitrogen Exchange CY MAY 06-09, 1993 CL ROME, ITALY SP ZYMA, Banca Roma C1 NIDDKD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-8493-8964-X PY 1995 BP 198 EP 202 PG 5 WC Cell Biology; Gastroenterology & Hepatology; Clinical Neurology SC Cell Biology; Gastroenterology & Hepatology; Neurosciences & Neurology GA BD26Q UT WOS:A1995BD26Q00033 ER PT B AU JONES, EA YURDAYDIN, C BASILE, AS AF JONES, EA YURDAYDIN, C BASILE, AS BE Capocaccia, L Merli, M Riggio, O TI BENZODIAZEPINE ANTAGONISTS AND THE MANAGEMENT OF HEPATIC ENCEPHALOPATHY SO ADVANCES IN HEPATIC ENCEPHALOPATHY AND METABOLIC NITROGEN EXCHANGE LA English DT Proceedings Paper CT 8th International Symposium on Ammonia - Advances in Hepatic Encephalopathy and Metabolic Nitrogen Exchange CY MAY 06-09, 1993 CL ROME, ITALY SP ZYMA, Banca Roma C1 NIDDKD,LIVER DIS SECT,DIGEST DIS BRANCH,BETHESDA,MD. NR 0 TC 2 Z9 2 U1 0 U2 0 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-8493-8964-X PY 1995 BP 549 EP 563 PG 15 WC Cell Biology; Gastroenterology & Hepatology; Clinical Neurology SC Cell Biology; Gastroenterology & Hepatology; Neurosciences & Neurology GA BD26Q UT WOS:A1995BD26Q00084 ER PT B AU GANDJBAKHCHE, A WEISS, GH AF GANDJBAKHCHE, A WEISS, GH BE Alfano, RR Katzir, A TI RANDOM WALK ANALYSIS OF THE EFFECTS OF THE PRESENCE OF ABNORMALITIES IN A TURBID MEDIUM ON EXPRESSIONS FOR THE TIME-OF-FLIGHT SO ADVANCES IN LASER AND LIGHT SPECTROSCOPY TO DIAGNOSE CANCER AND OTHER DISEASES II, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Advances in Laser and Light Spectroscopy to Diagnose Cancer and Other Diseases II CY FEB 07-08, 1995 CL SAN JOSE, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS DE TIME-RESOLVED IMAGING; TUMOR SCREENING; INVERSE METHOD C1 NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1734-3 J9 P SOC PHOTO-OPT INS PY 1995 VL 2387 BP 102 EP 110 DI 10.1117/12.206810 PG 9 WC Oncology; Engineering, Biomedical; Optics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Oncology; Engineering; Optics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA BD04U UT WOS:A1995BD04U00012 ER PT B AU GANDJBAKHCHE, AH NOSSAL, R DADMARZ, R SCHWARTZENTRUBER, D BONNER, RF AF GANDJBAKHCHE, AH NOSSAL, R DADMARZ, R SCHWARTZENTRUBER, D BONNER, RF BE Alfano, RR Katzir, A TI EXPECTED RESOLUTION AND DETECTABILITY OF ADENOCARCINOMA TUMORS WITHIN HUMAN BREAST IN TIME-RESOLVED IMAGES SO ADVANCES IN LASER AND LIGHT SPECTROSCOPY TO DIAGNOSE CANCER AND OTHER DISEASES II, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Advances in Laser and Light Spectroscopy to Diagnose Cancer and Other Diseases II CY FEB 07-08, 1995 CL SAN JOSE, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS DE BREAST SCREENING; TIME-RESOLVED IMAGING; SPATIAL RESOLUTION; ADENOCARCINOMA C1 NIH,BETHESDA,MD 20892. RI Bonner, Robert/C-6783-2015 NR 0 TC 4 Z9 4 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1734-3 J9 P SOC PHOTO-OPT INS PY 1995 VL 2387 BP 111 EP 118 DI 10.1117/12.206811 PG 8 WC Oncology; Engineering, Biomedical; Optics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Oncology; Engineering; Optics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA BD04U UT WOS:A1995BD04U00013 ER PT B AU YADLOWSKY, MJ SCHMITT, JM BONNER, RF AF YADLOWSKY, MJ SCHMITT, JM BONNER, RF BE Alfano, RR Katzir, A TI CONTRAST AND RESOLUTION IN THE OPTICAL COHERENCE MICROSCOPY OF DENSE BIOLOGICAL TISSUE SO ADVANCES IN LASER AND LIGHT SPECTROSCOPY TO DIAGNOSE CANCER AND OTHER DISEASES II, PROCEEDINGS OF SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Advances in Laser and Light Spectroscopy to Diagnose Cancer and Other Diseases II CY FEB 07-08, 1995 CL SAN JOSE, CA SP SOC PHOTO OPT INSTRUMENTAT ENGINEERS DE OPTICAL COHERENCE MICROSCOPY; LOW COHERENCE INTERFEROMETRY; MULTIPLE SCATTERING; MONTE-CARLO; DETECTABILITY; TISSUE OPTICS; BIOMEDICAL IMAGING; SPECKLE C1 NIH,NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RI Bonner, Robert/C-6783-2015 NR 0 TC 12 Z9 12 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1734-3 J9 P SOC PHOTO-OPT INS PY 1995 VL 2387 BP 193 EP 203 DI 10.1117/12.206822 PG 11 WC Oncology; Engineering, Biomedical; Optics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Oncology; Engineering; Optics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA BD04U UT WOS:A1995BD04U00024 ER PT S AU BRAUNELWERT, L MULLIN, GE JAMES, SP AF BRAUNELWERT, L MULLIN, GE JAMES, SP BE Mestecky, J Russell, MW Jackson, S Michalek, SM TlaskalovaHogenova, H Sterzl, J TI Lymphokine mRNA expression in the human intestinal mucosa and PBL determined by quantitative RT/PCR SO ADVANCES IN MUCOSAL IMMUNOLOGY, PTS A AND B SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 7th International Congress of Mucosal Immunology CY AUG 16-20, 1992 CL PRAGUE, CZECH REPUBLIC SP Soc Mucosal Immunol RP NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45012-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 371 BP 27 EP 30 PN A-B PG 4 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BD67X UT WOS:A1995BD67X00006 PM 8525922 ER PT S AU EISENSTEIN, EM STROBER, W AF EISENSTEIN, EM STROBER, W BE Mestecky, J Russell, MW Jackson, S Michalek, SM TlaskalovaHogenova, H Sterzl, J TI Evidence for a generalized signaling abnormality in B cells from patients with common variable immunodeficiency SO ADVANCES IN MUCOSAL IMMUNOLOGY, PTS A AND B SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 7th International Congress of Mucosal Immunology CY AUG 16-20, 1992 CL PRAGUE, CZECH REPUBLIC SP Soc Mucosal Immunol RP NIH,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 15 Z9 15 U1 0 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45012-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 371 BP 699 EP 704 PN A-B PG 4 WC Cell Biology; Immunology SC Cell Biology; Immunology GA BD67X UT WOS:A1995BD67X00149 PM 7502879 ER PT J AU Ptitsyn, OB AF Ptitsyn, OB TI Molten globule and protein folding SO ADVANCES IN PROTEIN CHEMISTRY, VOL 47 SE ADVANCES IN PROTEIN CHEMISTRY LA English DT Review ID NUCLEAR-MAGNETIC-RESONANCE; HUMAN ALPHA-LACTALBUMIN; PANCREATIC TRYPSIN-INHIBITOR; SITE-DIRECTED MUTAGENESIS; CARBONIC-ANHYDRASE-B; HEAT-SHOCK PROTEINS; EGG-WHITE LYSOZYME; TAIL SPIKE PROTEIN; FOLDED APOMYOGLOBIN INTERMEDIATE; MITOCHONDRIAL PRECURSOR PROTEIN C1 NCI,MATH BIOL LAB,BETHESDA,MD 20892. RP Ptitsyn, OB (reprint author), RUSSIAN ACAD SCI,INST PROT RES,PUSHCHINO 142292,RUSSIA. NR 454 TC 1045 Z9 1060 U1 7 U2 63 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0065-3233 J9 ADV PROTEIN CHEM JI Adv.Protein Chem. PY 1995 VL 47 BP 83 EP 229 DI 10.1016/S0065-3233(08)60546-X PG 147 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA BE40Q UT WOS:A1995BE40Q00002 PM 8561052 ER PT B AU BLAIR, A ZAHM, SH AF BLAIR, A ZAHM, SH BE McDuffie, HH Dosman, JA Semchuk, KM Olenchock, SA Senthilselvan, A TI Epidemiologic studies of cancer among agricultural populations SO AGRICULTURAL HEALTH AND SAFETY: WORKPLACE, ENVIRONMENT, SUSTAINABILITY LA English DT Proceedings Paper CT 3rd International Symposium on Issues in Health, Safety and Agriculture CY MAY 10-15, 1992 CL SASKATOON, CANADA SP UNIV SASKATCHEWAN, CTR AGR MED, NATL INST OCCUPAT SAFETY & HLTH, INT COMMISS OCCUPAT HLTH, SCI COMM OCCUPAT HLTH AGR C1 NCI,OCCUPAT STUDIES SECT,BETHESDA,MD 20892. RI Zahm, Shelia/B-5025-2015 NR 0 TC 2 Z9 2 U1 0 U2 0 PU LEWIS PUBLISHERS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-87371-617-5 PY 1995 BP 111 EP 117 PG 7 WC Agricultural Economics & Policy; Agronomy; Public, Environmental & Occupational Health SC Agriculture; Public, Environmental & Occupational Health GA BD12L UT WOS:A1995BD12L00023 ER PT B AU ZAHM, SH WEISENBURGER, DD SAAL, RC VAUGHT, JB BABBITT, PA BLAIR, A AF ZAHM, SH WEISENBURGER, DD SAAL, RC VAUGHT, JB BABBITT, PA BLAIR, A BE McDuffie, HH Dosman, JA Semchuk, KM Olenchock, SA Senthilselvan, A TI Pesticide use, genetic susceptibility, and non-Hodgkin's lymphoma in women SO AGRICULTURAL HEALTH AND SAFETY: WORKPLACE, ENVIRONMENT, SUSTAINABILITY LA English DT Proceedings Paper CT 3rd International Symposium on Issues in Health, Safety and Agriculture CY MAY 10-15, 1992 CL SASKATOON, CANADA SP UNIV SASKATCHEWAN, CTR AGR MED, NATL INST OCCUPAT SAFETY & HLTH, INT COMMISS OCCUPAT HLTH, SCI COMM OCCUPAT HLTH AGR C1 NCI,ENVIRONM EPIDEMIOL BRANCH,OCCUPAT STUDIES SECT,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LEWIS PUBLISHERS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-87371-617-5 PY 1995 BP 127 EP 133 PG 7 WC Agricultural Economics & Policy; Agronomy; Public, Environmental & Occupational Health SC Agriculture; Public, Environmental & Occupational Health GA BD12L UT WOS:A1995BD12L00025 ER PT B AU WARD, MH ZAHM, SH WEISENBURGER, DD CANTOR, KP SAAL, RC BLAIR, A AF WARD, MH ZAHM, SH WEISENBURGER, DD CANTOR, KP SAAL, RC BLAIR, A BE McDuffie, HH Dosman, JA Semchuk, KM Olenchock, SA Senthilselvan, A TI Diet and drinking water source: Association with non-Hodgkin's lymphoma in Eastern Nebraska SO AGRICULTURAL HEALTH AND SAFETY: WORKPLACE, ENVIRONMENT, SUSTAINABILITY LA English DT Proceedings Paper CT 3rd International Symposium on Issues in Health, Safety and Agriculture CY MAY 10-15, 1992 CL SASKATOON, CANADA SP UNIV SASKATCHEWAN, CTR AGR MED, NATL INST OCCUPAT SAFETY & HLTH, INT COMMISS OCCUPAT HLTH, SCI COMM OCCUPAT HLTH AGR C1 NATL CANC INST,ENVIRONM EPIDEMIOL BRANCH,ROCKVILLE,MD. NR 0 TC 1 Z9 2 U1 0 U2 0 PU LEWIS PUBLISHERS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-87371-617-5 PY 1995 BP 143 EP 150 PG 8 WC Agricultural Economics & Policy; Agronomy; Public, Environmental & Occupational Health SC Agriculture; Public, Environmental & Occupational Health GA BD12L UT WOS:A1995BD12L00027 ER PT B AU ZAHM, SH WEISENBURGER, DD CANTOR, KP HOLMES, FF BLAIR, A AF ZAHM, SH WEISENBURGER, DD CANTOR, KP HOLMES, FF BLAIR, A BE McDuffie, HH Dosman, JA Semchuk, KM Olenchock, SA Senthilselvan, A TI Non-Hodgkin's lymphoma and the use of atrazine: Results from three case-control studies SO AGRICULTURAL HEALTH AND SAFETY: WORKPLACE, ENVIRONMENT, SUSTAINABILITY LA English DT Proceedings Paper CT 3rd International Symposium on Issues in Health, Safety and Agriculture CY MAY 10-15, 1992 CL SASKATOON, CANADA SP UNIV SASKATCHEWAN, CTR AGR MED, NATL INST OCCUPAT SAFETY & HLTH, INT COMMISS OCCUPAT HLTH, SCI COMM OCCUPAT HLTH AGR C1 NATL CANC INST,ENVIRONM EPIDEMIOL BRANCH,ROCKVILLE,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LEWIS PUBLISHERS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, BOCA RATON, FL 33431 BN 0-87371-617-5 PY 1995 BP 151 EP 156 PG 6 WC Agricultural Economics & Policy; Agronomy; Public, Environmental & Occupational Health SC Agriculture; Public, Environmental & Occupational Health GA BD12L UT WOS:A1995BD12L00028 ER PT J AU MITCHELL, WM TORRES, J JOHNSON, PR HIRSCH, V YILMA, T GARDNER, MB ROBINSON, WE AF MITCHELL, WM TORRES, J JOHNSON, PR HIRSCH, V YILMA, T GARDNER, MB ROBINSON, WE TI ANTIBODIES TO THE PUTATIVE SIV INFECTION-ENHANCING DOMAIN DIMINISH BENEFICIAL-EFFECTS OF AN SIV GP160 VACCINE IN RHESUS MACAQUES SO AIDS LA English DT Article DE ANTIBODY-DEPENDENT ENHANCEMENT; HIV; SIV; VACCINES; COMPLEMENT; ANIMAL MODELS; AIDS; PATHOGENESIS; TRANSMEMBRANE GLYCOPROTEIN ID HUMAN-IMMUNODEFICIENCY-VIRUS; DEPENDENT ENHANCEMENT; GLYCOPROTEIN GP41; TRANSMEMBRANE GLYCOPROTEIN; IMMUNODOMINANT DOMAIN; TYPE-1 INFECTION; HIV INFECTION; RECOMBINANT; INVITRO; PROTECTION AB Objective: To demonstrate that antibodies against amino acids (aa) 603-622 of the SIV gp41 transmembrane glycoprotein enhance infection of SIV in vivo. Design: A synthetic peptide derived from aa 603-622 of SIVmac251 gp41 was synthesized and tested for immunogenicity in rabbits and SIV-infected rhesus macaques. Next, SIV-naive animals were immunized with either a recombinant vaccinia virus expressing the SIV gp160 envelope glycoprotein (VVrgp160) and boosted three times with aa 603-622 (group 1,four animals), wild-type vaccinia virus and boosted with aa 603-622 (group 2, two animals), or VVrgp160 followed by three doses of an irrelevant peptide (group 3, two animals). Animals were challenged with SIVmac251. Results: Peptide aa 603-622 was immunogenic in rabbits. SIV-infected rhesus monkeys immunized with the peptide developed two-three log increases in antibodies to this peptide and antibodies that could enhance SIV infection in vitro. SIV-naive rhesus macaques in group 1 had higher levels of antibody to the peptide by enzyme-linked immunosorbent assay and higher levels of enhancing antibodies at the time of SIV challenge than the animals in groups 2 or 3. Following challenge with SIVmac251 the group 1 animals had detectable p27 antigen longer than animals in group 2 and 3 and died of simian AIDS before the respective animals in the two control groups (P<0.05 by log-rank test). Conclusions: aa 603-622 of SIV gp41, like aa 579-613 of HIV gp41, can stimulate production of antibodies that enhance SIV and HIV infection in vitro. Furthermore, immunization with this peptide suppressed beneficial effects of a gp160 vaccine and appeared to enhance SIV infection in vivo. C1 UNIV CALIF IRVINE, DEPT PATHOL, IRVINE, CA 92717 USA. VANDERBILT UNIV, DEPT PATHOL, NASHVILLE, TN USA. UNIV CALIF DAVIS, DEPT MICROBIOL & IMMUNOL, DAVIS, CA 95616 USA. CHILDRENS HOSP, DEPT PEDIAT, INFECT DIS SECT, COLUMBUS, OH 43205 USA. NIH, INFECT DIS LAB, ROCKVILLE, MD USA. UNIV CALIF DAVIS, DEPT PATHOL, DAVIS, CA 95616 USA. UNIV CALIF IRVINE, DEPT MICROBIOL & MOLEC GENET, IRVINE, CA 92717 USA. RI Johnson, Philip/A-6892-2009 FU NIAID NIH HHS [AI29398, AI31371] NR 48 TC 22 Z9 22 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0269-9370 EI 1473-5571 J9 AIDS JI Aids PD JAN PY 1995 VL 9 IS 1 BP 27 EP 34 DI 10.1097/00002030-199501000-00004 PG 8 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA QB059 UT WOS:A1995QB05900004 PM 7893438 ER PT J AU PURI, RK LELAND, P AGGARWAL, BB AF PURI, RK LELAND, P AGGARWAL, BB TI CONSTITUTIVE EXPRESSION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TAT GENE INHIBITS INTERLEUKIN-2 AND INTERLEUKIN-2 RECEPTOR EXPRESSION IN A HUMAN CD4(+) T-LYMPHOID (H9) CELL-LINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID TRANS-ACTIVATOR GENE; IL-2 RECEPTOR; HTLV-III; ENVELOPE PROTEIN; SELECTIVE LOSS; HIV-INFECTION; MESSENGER-RNA; GROWTH; GP120; AIDS AB Human immunodeficiency virus (HIV-1) tat, a trans-activator of the HIV long terminal repeat, is essential for HIV replication and causes inhibition of antigen-mediated T cell proliferation. To understand the mechanism of inhibition of T cell proliferation, we have investigated the regulation of IL-2 production and its receptor expression on a human CD4(+) T lymphoid cell line (H9) transfected with HIV-1 tat gene. When cells were activated by mitogens, as compared to control cells, a significant decrease in both IL-2 mRNA and protein was observed in tat-transfected cells. Similarly, mitogen-induced IL-2R alpha and IL-2R beta mRNA and surface expression of IL-2R alpha and IL-2R beta chains were also significantly decreased in tat-transfected cells compared to control cells. Only IL-2 receptor density was decreased; the affinity of the ligand for the receptor appeared to be unchanged. In contrast to our previous studies with B-lymphoblastoid cell line (purl RK and Aggarwal BB: Cancer Res 1992;52:3787-3790), IL-4R expression was unaltered by HIV tat transfection in the H9 T cell line, indicating a cell type-specific phenomenon. Owing to the central role of IL-2 in immunoregulation, our data suggest that immunosuppressive effects of HIV-1 tat may be mediated at least in part through the inhibition of both IL-2 production and IL-2 receptor expression. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT CLIN IMMUNOL & BIOL THERAPY,CYTOKINE RES STN,HOUSTON,TX 77030. RP PURI, RK (reprint author), NIH,US FDA,CBER,DIV CELLULAR & GENE THERAPIES,MOLEC TUMOR BIOL LAB,BLDG 29A,ROOM 2B23,BETHESDA,MD 20892, USA. RI Aggarwal, Bharat/G-3388-2013 NR 64 TC 32 Z9 32 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 1995 VL 11 IS 1 BP 31 EP 40 DI 10.1089/aid.1995.11.31 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA QE701 UT WOS:A1995QE70100005 PM 7734194 ER PT J AU HODGE, DR CHEN, YMA SAMUEL, KP AF HODGE, DR CHEN, YMA SAMUEL, KP TI OLIGOMERIZATION OF THE HIV TYPE-2 NEF PROTEIN - MUTATIONAL ANALYSIS OF THE HEPTAD LEUCINE REPEAT MOTIF AND CYSTEINE RESIDUES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; FOS-JUN INTERACTION; HUMAN T-CELLS; TRANSMEMBRANE PROTEIN; MONOCLONAL-ANTIBODIES; POLYACRYLAMIDE GELS; NUCLEOTIDE BINDING; ESCHERICHIA-COLI; GENE-PRODUCTS; ZIPPER AB The human immunodeficiency virus type 2 (HIV-2) Nef protein expressed in Escherichia coli forms highly stable homooligomeric complexes in vitro. Similarly, the native protein synthesized in the persistently infected H9 T cell line also forms stable homooligomers in vivo. To determine whether homooligomer formation is mediated by the leucine zipper-type sequence located in the middle region of the protein, site-directed mutagenesis was used to introduce double and triple point mutations at heptad leucine positions L1, L2, and L4 within the HIV-2(NIHZ) Nef protein sequence. Here, we show that substitution of a serine residue for the L1 (residue 108) and L2 (residue 115) heptad leucines, and a glutamine residue for the L4 (residue 129) heptad leucine, did not prevent Nef homooligomer formation in vitro. However, a more drastic substitution of alpha-helix-breaking proline residue for the L2 and L4 heptad leucines significantly abrogated ability of the protein to form stable homooligomers. In addition, because significantly higher levels of the Nef oligomers were consistently observed under the nonreducing SDS-PAGE condition, site-specific mutagenesis was also used to examine the role of cysteine residues in generating disulfide-linked Nef dimers in vitro. Here, we also show that single cysteine-to-glycine substitutions at positions 28, 32, or 55 drastically reduced covalent Nef dimer formation and thermal stability of the Nef protein in vitro. Therefore, these results demonstrate that; the leucine zipper-type motif in the HIV-2 Nef protein mediates stable homooligomer formation in vitro, and also establish a role for covalent disulfide bonds in the formation of linked Nef dimers and thermal stability of the monomer Nef in vitro. C1 NCI, FREDERICK CANC RES & DEV CTR, PROGRAM RESOURCES INC DYNCORP, CELLULAR BIOCHEM LAB, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, MOLEC ONCOL LAB, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74102] NR 63 TC 11 Z9 11 U1 0 U2 1 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0889-2229 EI 1931-8405 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JAN PY 1995 VL 11 IS 1 BP 65 EP 79 DI 10.1089/aid.1995.11.65 PG 15 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA QE701 UT WOS:A1995QE70100009 PM 7734198 ER PT J AU MAZUMDER, A GUPTA, M PERRIN, DM SIGMAN, DS RABINOVITZ, M POMMIER, Y AF MAZUMDER, A GUPTA, M PERRIN, DM SIGMAN, DS RABINOVITZ, M POMMIER, Y TI INHIBITION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INTEGRASE BY A HYDROPHOBIC CATION - THE PHENANTHROLINE-CUPROUS COMPLEX SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID CHEMICAL NUCLEASES; HIV DNA; PROTEIN; INVITRO; CELLS; 2,9-DIMETHYL-1,10-PHENANTHROLINE; FUNCTIONALIZATION; NEOCUPROINE; POLYMERASE; ENZYME AB The human immunodeficiency virus type 1 integrase (HIV-1 integrase) is required for integration of a double-stranded DNA copy of the viral RNA genome into a host chromosome and for HIV replication. We have examined the effects of 2:1 1,10-phenanthroline-cuprous complexes on purified HIV-1 integrase. Although the uncomplexed phenanthrolines are not active below 100 mu M, four of the cuprous complexes (neocuproine, 4-phenyl neocuproine, 2,3,4,7,8,9-hexamethyl phenanthroline, and 2,3,4,7,8-pentamethyl phenanthroline) have a 50% inhibitory concentration (IC50) for integration ranging between 1 and 10 mu M. Disintegration is also inhibited by these phenanthroline-cuprous complexes at slightly higher concentrations (between 10 and 40 mu M). Dialysis experiments showed that the inhibition is reversible and kinetic analyses revealed that the mode of inhibition by these cuprous complexes appears to be noncompetitive with respect to the substrate DNA. Consistent with these findings, binding assays demonstrate that, although these complexes can inhibit binding to DNA at high concentrations, they do not inhibit binding of integrase to the DNA substrate at their IC50 values. Because these complexes do not bind to B-DNA below 50 mu M, inhibition via binding to a specific region on the enzyme was examined. Using deletion mutants of integrase, it was determined that neither the amino-terminal (zinc finger) nor the carboxy-terminal (DNA-binding) integrase domain is required for inhibition by the phenanthroline-cuprous complexes. Therefore, inhibition via binding to the enzyme catalytic core or to the interface between the enzyme and a noncanonical DNA structure generated during the enzymatic reaction is the probable mechanism. These results suggest the utility of neocuproine-cuprous complexes in developing inhibitors of HIV-1 integrase as well as probes for drug-bending sites and enzymatic reaction mechanism. C1 NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOL CHEM,LOS ANGELES,CA 90024. NR 32 TC 29 Z9 29 U1 1 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JAN PY 1995 VL 11 IS 1 BP 115 EP 125 DI 10.1089/aid.1995.11.115 PG 11 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA QE701 UT WOS:A1995QE70100014 PM 7734185 ER PT J AU GALLO, RC AF GALLO, RC TI INTRODUCTION TO ANNUAL LABORATORY MEETING - 1995 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material RP GALLO, RC (reprint author), NCI,TUMOR CELL BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP R5 EP R5 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900001 ER PT J AU ABIMIKU, AG WANG, A KYARI, S AKINSETE, I GALLO, RC ROBERTGUROFF, M AF ABIMIKU, AG WANG, A KYARI, S AKINSETE, I GALLO, RC ROBERTGUROFF, M TI RAPID MOLECULAR CHARACTERIZATION OF HIV-1 CLADES IN NIGERIA USING FILTER BLOOD DOTS AND THE HETERODUPLEX MOBILITY ASSAY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ICSC,WORLD LAB,AIDS RES CTR,JOS,NIGERIA. LUTH,LAGOS,NIGERIA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S144 EP S144 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900318 ER PT J AU ALEXANDERMILLER, MA PARKER, KC LEGGATT, GR TSUKUI, T PENDLETON, CD COLIGAN, JE BERZOFSKY, JA AF ALEXANDERMILLER, MA PARKER, KC LEGGATT, GR TSUKUI, T PENDLETON, CD COLIGAN, JE BERZOFSKY, JA TI SIMILAR PRESENTATION OF A PROMISCUOUS HIV-1 PEPTIDE BY HUMAN AND MURINE CLASS-I MHC MOLECULES, AND ABILITY OF PEPTIDE-INDUCED MURINE CTL TO CLEAR VIRUS-INFECTION IN SCID MICE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NIAID,MOLEC STRUCT LAB,BETHESDA,MD. RI Leggatt, Graham/G-1924-2010 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S133 EP S133 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900274 ER PT J AU ALHARTHI, L GARZINODEMO, A PENG, B ARYA, SK AF ALHARTHI, L GARZINODEMO, A PENG, B ARYA, SK TI CELL-TYPE INDEPENDENT AND DOSE-DEPENDENT INHIBITION OF HIV-1 BY HIV-2 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S113 EP S113 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900197 ER PT J AU ARTHUR, LO BESS, J HENDERSON, L URBAN, R MANN, D BENVENISTE, R AF ARTHUR, LO BESS, J HENDERSON, L URBAN, R MANN, D BENVENISTE, R TI VIRAL ASSOCIATED CELLULAR ANTIGENS AS IMMUNOGENS TO PROTECT FROM SIV-INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 SAIC FREDERICK,AIDS VACCINE PROGRAM,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. HARVARD UNIV,DEPT BIOCHEM MOLEC BIOL,CAMBRIDGE,MA 02138. RI Bess, Jr., Julian/B-5343-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S137 EP S137 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900291 ER PT J AU BAMFORD, RN BATTIATA, AP WALDMANN, TA AF BAMFORD, RN BATTIATA, AP WALDMANN, TA TI IL-1S/IL-T PRODUCTION BY HUT-102 CELLS IS ASSOCIATED WITH AN HTLV-I-R/IL-15 FUSION MESSAGE THAT LACKS MANY UPSTREAM AUGS THAT NORMALLY ATTENUATE IL-15 MESSENGER-RNA TRANSLATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S121 EP S121 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900226 ER PT J AU BARABITSKAYA, O MALYKH, A EMELJANOV, A KURBATOVA, T YAROSLAVTSEVA, N KARAMOV, E FARZADEGAN, H REITZ, MS KOZLOV, A AF BARABITSKAYA, O MALYKH, A EMELJANOV, A KURBATOVA, T YAROSLAVTSEVA, N KARAMOV, E FARZADEGAN, H REITZ, MS KOZLOV, A TI MOLECULAR EPIDEMIOLOGY OF HIV-1 IN ST PETERSBURG, RUSSIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RES INST PURE BIOCHEM,ST PETERSBURG,RUSSIA. DI IVANOVSKII INST VIROL,MOSCOW,RUSSIA. JOHNS HOPKINS UNIV,SCH PUBL HLTH,BALTIMORE,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S145 EP S145 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900324 ER PT J AU BELSHE, RB BOLOGNESI, D CLEMENTS, ML COREY, L FAST, P GRAHAM, B KEEFER, M MESTECKY, J MULLIGAN, M AF BELSHE, RB BOLOGNESI, D CLEMENTS, ML COREY, L FAST, P GRAHAM, B KEEFER, M MESTECKY, J MULLIGAN, M TI STUDIES ON HIV-1 VACCINES BY THE AIDS VACCINE EVALUATION GROUP (AVEG) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,AVEG,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S138 EP S138 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900297 ER PT J AU BENSON, J CHOUGNET, C TARTAGLIA, J SHEARER, G PAOLETTI, E GALLO, R FRANCHINI, G AF BENSON, J CHOUGNET, C TARTAGLIA, J SHEARER, G PAOLETTI, E GALLO, R FRANCHINI, G TI IMMUNOGENICITY OF A NYVAC/SIV VACCINE IN COMBINATION WITH IL-12 AND IL-2 IN RHESUS MACAQUES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. VIROGENET CORP,TROY,NY 12180. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S147 EP S147 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900333 ER PT J AU BERNEMAN, ZN SAXINGER, C HALL, L GALLO, RC REITZ, MS AF BERNEMAN, ZN SAXINGER, C HALL, L GALLO, RC REITZ, MS TI SEQUENCE-ANALYSIS AND MAPPING OF THE GENOME OF HUMAN HERPESVIRUS 7 (HHV-7) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV ANTWERP,EXPTL HEMATOL LAB,B-2650 EDEGEM,BELGIUM. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S101 EP S101 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900148 ER PT J AU BIGGAR, RJ MIOTTI, P MTIMIVALYE, L WATERS, D TAHA, T AF BIGGAR, RJ MIOTTI, P MTIMIVALYE, L WATERS, D TAHA, T TI AN INTERVENTION TRIAL TO REDUCE MOTHER-TO-CHILD HIV TRANSMISSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. UNIV MALAWI,SCH MED,ZOMBA,MALAWI. FREDERICK CANC RES & DEV CTR,FREDERICK,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S78 EP S78 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900058 ER PT J AU BLATTNER, WA AF BLATTNER, WA TI AIDS EPIDEMIOLOGY - 1995 AND BEYOND SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VEB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S128 EP S128 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900254 ER PT J AU BLAUVELT, A SAVILLE, MW ASADA, H KLAUSKOVTUN, V YARCHOAN, R KATZ, SI AF BLAUVELT, A SAVILLE, MW ASADA, H KLAUSKOVTUN, V YARCHOAN, R KATZ, SI TI CULTURED DENDRITIC CELLS CAN BE INFECTED WITH HIV AND CAN EFFICIENTLY TRANSFER HIV TO CD4+ T-CELLS DURING THE GENERATION OF IMMUNE-RESPONSES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S113 EP S113 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900194 ER PT J AU BLUMENTHAL, R AF BLUMENTHAL, R TI MOLECULAR MECHANISMS OF VIRAL ENVELOPE PROTEIN-MEDIATED MEMBRANE-FUSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S82 EP S82 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900074 ER PT J AU BROWN, K GERSTBERGER, S CARLSON, L FRANZOSO, G SIEBENLIST, U AF BROWN, K GERSTBERGER, S CARLSON, L FRANZOSO, G SIEBENLIST, U TI CONTROL OF I-KAPPA-B-ALPHA PROTEOLYSIS BY SITE-SPECIFIC, SIGNAL-INDUCED PHOSPHORYLATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 1 U2 4 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S118 EP S118 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900215 ER PT J AU BUGE, SL ABIMIKU, AG KYARI, S GALLO, RC ROBERTGUROFF, M AF BUGE, SL ABIMIKU, AG KYARI, S GALLO, RC ROBERTGUROFF, M TI NEUTRALIZATION OF HIV-1 SUBTYPE-B AND SUBTYPE-G ISOLATES BY NIGERIAN SERA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ICSC,WORLD LAB,AIDS RES CTR,JOS,NIGERIA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S147 EP S147 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900331 ER PT J AU BUNNELL, BA MUUL, LM BLAESE, RM MORGAN, RA AF BUNNELL, BA MUUL, LM BLAESE, RM MORGAN, RA TI HIGH-EFFICIENCY RETROVIRAL-MEDIATED GENE-TRANSFER INTO HUMAN PERIPHERAL-BLOOD LYMPHOCYTES FOR HIV-1 GENE-THERAPY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NATL CTR HUMAN GENOME RES,CLIN GENE THERAPY BRANCH,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 6 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S156 EP S156 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900368 ER PT J AU BURDETT, LA GENDELMAN, HE LAUTENBERGER, JA AF BURDETT, LA GENDELMAN, HE LAUTENBERGER, JA TI IDENTIFICATION OF HIV-1 MODULATED CELLULAR GENES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. UNIV NEBRASKA,SCH MED,DEPT PATHOL,OMAHA,NE 68198. UNIV NEBRASKA,SCH MED,DEPT MICROBIOL,OMAHA,NE 68198. UNIV NEBRASKA,SCH MED,DEPT INTERNAL MED,OMAHA,NE 68198. UNIV NEBRASKA,SCH MED,EPPLEY INST RES CANC & RELATED DIS,OMAHA,NE 68198. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S118 EP S118 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900214 ER PT J AU CARA, A CERESETO, A GALLO, RC REITZ, M LORI, F AF CARA, A CERESETO, A GALLO, RC REITZ, M LORI, F TI IN-VITRO TRANSCRIPTIONAL ACTIVITY OF THE EXTRA CHROMOSOMAL FORMS OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Cara, Andrea/M-4865-2015 OI Cara, Andrea/0000-0003-4967-1895 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S115 EP S115 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900205 ER PT J AU CARPENTER, M BROWN, EW JOHNSON, WE BROUSSET, D OBRIEN, SJ AF CARPENTER, M BROWN, EW JOHNSON, WE BROUSSET, D OBRIEN, SJ TI VARIATION IN THE POL GENE OF FELINE IMMUNODEFICIENCY VIRUS IN PUMAS FROM NORTH, CENTRAL AND SOUTH-AMERICA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 SAIC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. USDA,DEPT MICROBIAL GENET,CHARLESTON,WV. UNIV NACL AUTONOMA MEXICO,COYOACAN,DF,MEXICO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S94 EP S94 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900119 ER PT J AU CERESETO, A DIELLA, F MULLOY, JC CARA, A GALLO, RC GRASSMAN, R FRANCHINI, G KLOTMAN, ME AF CERESETO, A DIELLA, F MULLOY, JC CARA, A GALLO, RC GRASSMAN, R FRANCHINI, G KLOTMAN, ME TI CONSTITUTIVE HIGH EXPRESSION OF P21WAF1/CIP1 IN HTLV-I-INFECTED T-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,TUMOR IMMUNOL BIOL LAB,BETHESDA,MD 20892. INST KLIN & MOLEK VIROL SCHLOSSGARTEN,ERLANGEN,GERMANY. RI klotman, mary/A-1921-2016; Cara, Andrea/M-4865-2015 OI Cara, Andrea/0000-0003-4967-1895 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S125 EP S125 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900243 ER PT J AU CHANA, HK SAMANIEGO, F BUONAGURO, L NAIR, BC GALLO, RC ENSOLI, B AF CHANA, HK SAMANIEGO, F BUONAGURO, L NAIR, BC GALLO, RC ENSOLI, B TI EXTRACELLULAR TAT BINDS HEPARIN-SULFATE COMPLEXES OF THE CELL-SURFACE AND EXTRACELLULAR-MATRIX (ECM) THROUGH THE BASIC REGION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. INST NAZL TUMORI FDN G PASCALE,DIV VIRAL ONCOL,I-80131 NAPLES,ITALY. ADV BIOSCI LABS INC,KENSINGTON,MD 20895. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S116 EP S116 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900208 ER PT J AU CHERTOVA, E HENDERSON, LE SOWDER, RC JOHNSON, DG COREN, LV KANE, BP CASASFINET, JR OTT, DE RICE, WG ARTHUR, LO AF CHERTOVA, E HENDERSON, LE SOWDER, RC JOHNSON, DG COREN, LV KANE, BP CASASFINET, JR OTT, DE RICE, WG ARTHUR, LO TI ANTI RETROVIRAL MECHANISMS OF THIURAMS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S160 EP S160 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900384 ER PT J AU COHEN, DI KOLESNITCHENKO, V TIAN, H ORENSTEIN, J RAFFELD, M SAMELSON, LE AF COHEN, DI KOLESNITCHENKO, V TIAN, H ORENSTEIN, J RAFFELD, M SAMELSON, LE TI CELL-CYCLE DISREGULATION DURING HIV-1 INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,DCBCD,BETHESDA,MD. NICHHD,CBMB,BETHESDA,MD. NIAID,LIR,BETHESDA,MD. GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S88 EP S88 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900096 ER PT J AU COLOMBINI, S BIBERFELD, P REITZ, MS SADOWSKA, M FRANCHINI, G ENSOLI, B GALLO, RC AF COLOMBINI, S BIBERFELD, P REITZ, MS SADOWSKA, M FRANCHINI, G ENSOLI, B GALLO, RC TI DETECTION OF HHV 8-LIKE DNA-SEQUENCES IN CYNOMOLGUS MONKEYS DEVELOPING B-CELL LYMPHOMAS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. KAROLINSKA INST,DEPT PATHOL,S-10401 STOCKHOLM,SWEDEN. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 3 TC 4 Z9 4 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S75 EP S75 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900045 ER PT J AU DEBRE, P OUAAZ, F RUSCETTI, FW MOSSALAYI, MD AF DEBRE, P OUAAZ, F RUSCETTI, FW MOSSALAYI, MD TI NITRIC-OXIDE (NO) INDUCES VIH REPLICATION IN MONOCYTIC CELLS - A ROLE FOR CD23 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HOP LA PITIE SALPETRIERE,F-75013 PARIS,FRANCE. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S85 EP S85 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900084 ER PT J AU DIGILIO, L GIRI, A FULLEN, J GALLO, RC FRANCHINI, G AF DIGILIO, L GIRI, A FULLEN, J GALLO, RC FRANCHINI, G TI MOLECULAR AND BIOLOGICAL CHARACTERIZATION OF STLV(PAN-P), A NOVEL INFECTIOUS RETROVIRUS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S141 EP S141 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900308 ER PT J AU DIMITROV, DS ENGLUND, G SHRAGER, R SPOUGE, J AF DIMITROV, DS ENGLUND, G SHRAGER, R SPOUGE, J TI MATHEMATICAL-MODELING OF HIV-1 INFECTION IN TISSUE-CULTURES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. NATL LIB MED,BETHESDA,MD. NIH,DCRT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S117 EP S117 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900210 ER PT J AU EIDEN, LE DACUNHA, A RAUSCH, DM MURRAY, EA REINHART, T HAASE, A AF EIDEN, LE DACUNHA, A RAUSCH, DM MURRAY, EA REINHART, T HAASE, A TI PATHOGENESIS OF ENCEPHALOPATHY IN THE SIV-INFECTED RHESUS-MONKEY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. UNIV MINNESOTA,DEPT MICROBIOL,SE MINNEAPOLIS,MN 55455. NR 3 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S151 EP S151 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900349 ER PT J AU EKMAN, M KAAYA, EE SCHALLING, M COLOMBINI, S ENSOLI, B GALLO, RC BIBERFELD, P AF EKMAN, M KAAYA, EE SCHALLING, M COLOMBINI, S ENSOLI, B GALLO, RC BIBERFELD, P TI HERPES-VIRUS LIKE (KSHV) DNA IN VARIOUS FORMS OF KAPOSIS-SARCOMA (KS) AND MALIGNANT-LYMPHOMA (ML) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 KAROLINSKA HOSP & INST,DEPT PATHOL,IMMUNOPATHOL LAB,STOCKHOLM,SWEDEN. KAROLINSKA HOSP & INST,DEPT MOLEC MED,NEUROSCI LAB,STOCKHOLM,SWEDEN. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Schalling, Martin/F-1518-2015; Ensoli, Barbara/J-9169-2016 OI Schalling, Martin/0000-0001-5011-2922; Ensoli, Barbara/0000-0002-0545-8737 NR 1 TC 4 Z9 4 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S74 EP S74 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900044 ER PT J AU ENSOLI, B BARILLARI, G FIORELLI, V SAMANIEGO, F GENDELMAN, R CHANG, HC COLOMBINI, S WATANABE, Y KAO, V NAIR, BC MARKHAM, P GALLO, RC AF ENSOLI, B BARILLARI, G FIORELLI, V SAMANIEGO, F GENDELMAN, R CHANG, HC COLOMBINI, S WATANABE, Y KAO, V NAIR, BC MARKHAM, P GALLO, RC TI HIV-1 TAT PROTEIN MIMICS THE EFFECT OF EXTRACELLULAR-MATRIX (ECM) PROTEIN ON VASCULAR CELL-GROWTH AND ANGIOGENESIS - IMPLICATIONS FOR AIDS-KAPOSIS SARCOMA (AIDS-KS) PATHOGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV ROMA TOR VERGATA,ROME,ITALY. ABL,KENSINGTON,MD. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S75 EP S75 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900047 ER PT J AU FAUCI, AS AF FAUCI, AS TI HOST FACTORS IN THE PATHOGENESIS OF HIV DISEASE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S84 EP S84 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900080 ER PT J AU FELBER, BK VALENTIN, A TABERNERO, C ZOLOTUKHIN, AS VONGEGERFELT, A BEAR, J PAVLAKIS, GN AF FELBER, BK VALENTIN, A TABERNERO, C ZOLOTUKHIN, AS VONGEGERFELT, A BEAR, J PAVLAKIS, GN TI PROPAGATION OF REV/RRE-INDEPENDENT HIV-1 IN PRIMATE CELLS - ROLE OF REV IN VIRUS-REPLICATION AND PATHOGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,HUMAN RETROVIRUS PATHOGENESIS GRP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S89 EP S89 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900099 ER PT J AU FIORELLI, V GENDELMAN, R MARKHAM, P GALLO, RC ENSOLI, B AF FIORELLI, V GENDELMAN, R MARKHAM, P GALLO, RC ENSOLI, B TI GAMMA-IFN INDUCES ENDOTHELIAL-CELLS TO ACQUIRE THE IN-VITRO AND IN-VIVO FEATURES OF KAPOSIS-SARCOMA SPINDLE CELLS INCLUDING THE ANGIOGENIC ACTIVITY AND THE RESPONSIVENESS TO THE HIV-1 TAT PROTEIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S76 EP S76 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900048 ER PT J AU FISHER, RJ FIVASH, M BLADEN, S GULNIK, S MAJHER, P LAUTENBERGER, J ERICKSON, J AF FISHER, RJ FIVASH, M BLADEN, S GULNIK, S MAJHER, P LAUTENBERGER, J ERICKSON, J TI BINDING OF HIV PROTEASE TO AN IMMOBILIZED INHIBITOR - A REAL-TIME KINETIC-STUDY UTILIZING SURFACE-PLASMON RESONANCE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,CELLULAR BIOCHEM LAB,FREDERICK,MD 21702. NCI,DATA MANAGEMENT SERV INC,FREDERICK,MD 21702. NCI,SAIC FREDERICK,FREDERICK BIOMED SUPERCOMP CTR,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702. NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702. RI Fisher, Robert/B-1431-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S161 EP S161 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900389 ER PT J AU FRANZOSO, G CARLSON, L BROWN, K DAUCHER, M BRESSLER, P SIEBENLIST, U AF FRANZOSO, G CARLSON, L BROWN, K DAUCHER, M BRESSLER, P SIEBENLIST, U TI PHYSICAL INTERACTION AND FUNCTIONAL SYNERGY OF NF-KAPPA-B AND THE SERUM RESPONSE FACTOR (SRF) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S117 EP S117 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900213 ER PT J AU GAJDUSEK, DC AF GAJDUSEK, DC TI VILIUISK ENCEPHALOMYELITIS - EXPANDING EPIDEMICITY OF AN ALWAYS FATAL INFECTION IN IAKUT SIBERIANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S71 EP S71 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900033 ER PT J AU GAO, WY JOHNS, DG AHLUWALIA, G MITSUYA, H AF GAO, WY JOHNS, DG AHLUWALIA, G MITSUYA, H TI ENHANCEMENT OF THE ANTI-HIV-1 ACTIVITY OF 2',3'-DIDEHYDRO-2',3'-DIDEOXYTHYMIDINE (D4T) BY THE THYMIDYLATE SYNTHETASE INHIBITOR FUDR - AN ANTI-HIV STRATEGY WITH A HOST-CELL TARGET SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,DTP,MED CHEM LAB,BETHESDA,MD 20892. NCI,DTP,MED BRANCH,EXPTL RETROVIROL SECT,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S161 EP S161 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900387 ER PT J AU GOEBEL, PB DRUMMOND, J WATERS, D BESS, J SOWDER, R HENDERSON, L ARTHUR, L AF GOEBEL, PB DRUMMOND, J WATERS, D BESS, J SOWDER, R HENDERSON, L ARTHUR, L TI AN UPDATE ON THE DEVELOPMENT OF A HIV-1 NUCLEOCAPSID PROTEIN CAPTURE ASSAY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC,FREDERICK,MD 21702. RI Bess, Jr., Julian/B-5343-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S145 EP S145 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900322 ER PT J AU GOLDING, H LAPHAM, CK MANISCHEWITZ, J BRODER, CC ROBINSON, J FABIAN, S LITTMAN, DR DIMITROV, DS AF GOLDING, H LAPHAM, CK MANISCHEWITZ, J BRODER, CC ROBINSON, J FABIAN, S LITTMAN, DR DIMITROV, DS TI PMA-INDUCED MODULATION OF ACCESSORY FUSION-RELATED COMPONENTS IN CD4-EXPRESSING CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD. NCI,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. UNIV CONNECTICUT,HLTH SCI CTR,FARMINGTON,CT. UNIV CALIF SAN FRANCISCO,SCH MED,SAN FRANCISCO,CA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S103 EP S103 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900157 ER PT J AU GORELICK, RJ GAGLIARDI, TD BOSCHE, WJ HENDERSON, LE ARTHUR, LO AF GORELICK, RJ GAGLIARDI, TD BOSCHE, WJ HENDERSON, LE ARTHUR, LO TI HIV-1 NC MUTANTS WITH STEROID-HORMONE RECEPTOR AND CLASSICAL TYPE ZINC-FINGER SUBSTITUTIONS - EFFECTS ON RNA PACKAGING AND INFECTIVITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,AIDS VACCINE PROGRAM,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S105 EP S105 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900163 ER PT J AU GOREN, I SEMMES, OJ JEANG, KT MOELLING, K AF GOREN, I SEMMES, OJ JEANG, KT MOELLING, K TI AMINOTERMINUS FOR INTERACTION WITH CREB SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV ZURICH,INST MED VIROL,CH-8028 ZURICH,SWITZERLAND. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S140 EP S140 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900303 ER PT J AU HAIGWOOD, NL MISHER, L SUTTON, W WATSON, A MCCLURE, J RANCHALIS, J TRAVIS, B LEWIS, A VOSS, G LETVIN, N HU, SL HIRSCH, V JOHNSON, P AF HAIGWOOD, NL MISHER, L SUTTON, W WATSON, A MCCLURE, J RANCHALIS, J TRAVIS, B LEWIS, A VOSS, G LETVIN, N HU, SL HIRSCH, V JOHNSON, P TI EVIDENCE FOR VIRUS CONTROL BY IMMUNE-RESPONSES - EARLY PASSIVE IMMUNE GLOBULIN THERAPY IN SIV-INFECTED MACAQUES DELAYS DISEASE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 BRISTOL MYERS SQUIBB CO,SEATTLE,WA 98121. NIAID,LID,ROCKVILLE,MD 20852. BETH ISRAEL HOSP,BOSTON,MA 02215. CHILDRENS HOSP RES FDN,COLUMBUS,OH 43205. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S130 EP S130 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900264 ER PT J AU HARRISKELSON, T ROBERTGUROFF, M ROLLER, P ALDRICH, K BATINIC, D ROBEY, FA AF HARRISKELSON, T ROBERTGUROFF, M ROLLER, P ALDRICH, K BATINIC, D ROBEY, FA TI A CONFORMATIONAL EPITOPE FROM THE C4 DOMAIN OF HIV GP120 THAT BINDS TO CD4 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S82 EP S82 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900071 ER PT J AU HERMANS, P PICARD, O LUNARDIISKANDAR, Y BRYANT, J PONCIN, M CLUMECK, N GALLO, RC AF HERMANS, P PICARD, O LUNARDIISKANDAR, Y BRYANT, J PONCIN, M CLUMECK, N GALLO, RC TI PRELIMINARY-RESULTS ON CLINICAL USE OF HUMAN CHORIONIC-GONADOTROPIN HORMONE (HCG) IN HIV PATIENTS (P) WITH KAPOSIS-SARCOMA (KS) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ST PIERRE HOSP,BRUSSELS,BELGIUM. HOP ST ANTOINE,F-75571 PARIS,FRANCE. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S96 EP S96 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900127 ER PT J AU HU, SL POLACINO, P KLANIECKI, J TRAVIS, B WREY, T PENNATHUR, S STALLARD, V KORNAS, H LANGLOIS, AJ MORTON, WR BENVENISTE, RE AF HU, SL POLACINO, P KLANIECKI, J TRAVIS, B WREY, T PENNATHUR, S STALLARD, V KORNAS, H LANGLOIS, AJ MORTON, WR BENVENISTE, RE TI SIMIAN MODELS FOR THE EVALUATION OF RECOMBINANT VACCINE APPROACHES AGAINST AIDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 BRISTOL MYERS SQUIBB,SEATTLE,WA. WASHINGTON REG PRIMATE RES CTR,SEATTLE,WA. NCI,FREDERICK,MD 21701. DUKE UNIV,DURHAM,NC 27706. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S136 EP S136 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900289 ER PT J AU HUANG, RCC GNABRE, JH GIZA, P BRADY, JN CLANTON, DJ AF HUANG, RCC GNABRE, JH GIZA, P BRADY, JN CLANTON, DJ TI INHIBITION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TRANSCRIPTION AND REPLICATION BY DNA-SEQUENCE SPECIFIC PLANT LIGNANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,DEPT BIOL,BALTIMORE,MD 21218. NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 1 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S168 EP S168 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900413 ER PT J AU HUMPHREY, RW SAVILLE, MW MITSUYA, H YARCHOAN, R AF HUMPHREY, RW SAVILLE, MW MITSUYA, H YARCHOAN, R TI HIV-1 PROTEASE FUNCTION PRIOR TO VIRAL BUDDING IS ESSENTIAL FOR THE PRODUCTION OF INFECTIOUS VIRIONS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S162 EP S162 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900392 ER PT J AU HUMPHREY, RW NISHIHARA, H SAVILLE, MW STRAUS, SE YARCHOAN, R AF HUMPHREY, RW NISHIHARA, H SAVILLE, MW STRAUS, SE YARCHOAN, R TI DETECTION OF KAPOSIS-SARCOMA-ASSOCIATED HERPES-VIRUS (KSHV) DNA-SEQUENCES IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS (PBMC) OBTAINED FROM HIV KAPOSIS-SARCOMA (KS) PATIENTS WITHOUT AND DURING THERAPY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MED BRANCH,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NR 2 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S98 EP S98 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900137 ER PT J AU JIMOH, AG WISE, DL BARTELS, CJ YANG, JC TRANTOLO, DJ GUPTA, R FRIDEN, PM RASMUSSEN, RA RUPRECHT, RM AF JIMOH, AG WISE, DL BARTELS, CJ YANG, JC TRANTOLO, DJ GUPTA, R FRIDEN, PM RASMUSSEN, RA RUPRECHT, RM TI RELEASE OF ANTIGENS FROM BIODEGRADABLE MICROPARTICLES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NORTHEASTERN UNIV,CTR BIOTECHNOL,DEPT CHEM ENGN,BOSTON,MA 02115. NCI,BETHESDA,MD 20892. CAMBRIDGE SCI INC,BELMONT,MA 02178. MASSACHUSETTS DEPT PUBL HLTH,BOSTON,MA 02130. PERIODONTIX INC,WATERTOWN,MA 02172. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S147 EP S147 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900330 ER PT J AU KAJIYAMA, W DICKIE, P KLOTMAN, PE KOPP, JB AF KAJIYAMA, W DICKIE, P KLOTMAN, PE KOPP, JB TI HIV-1 GENES ARE EXPRESSED IN GLOMERULAR EPITHELIAL AND TUBULAR EPITHELIAL-CELLS IN HIV-TRANSGENIC MOUSE KIDNEY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDDK,KIDNEY DIS SECT,BETHESDA,MD. MMID,GLAXO HERITAGE RES INST,EDMONTON,AB,CANADA. MT SINAI SCH MED,DIV RENAL,NEW YORK,NY. NR 1 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S153 EP S153 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900356 ER PT J AU KELLY, K WARD, Y AF KELLY, K WARD, Y TI THE ROLE OF T-CELL EARLY RESPONSE GENES IN SIGNAL-TRANSDUCTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S123 EP S123 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900237 ER PT J AU KIM, WK TANG, Y CHATTOPADHYAY, Y MORSE, HC AF KIM, WK TANG, Y CHATTOPADHYAY, Y MORSE, HC TI ABERRANT CELL SIGNALING IN MAIDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,LIP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S94 EP S94 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900121 ER PT J AU KINDT, TJ ROBINSON, MA BOWERS, FS ZHAO, TM AF KINDT, TJ ROBINSON, MA BOWERS, FS ZHAO, TM TI CHIMERIC MOLECULAR CLONES OF HTLV-I DERIVED FROM LEUKEMOGENIC AND NON LEUKEMOGENIC RABBIT-CELL LINES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S127 EP S127 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900252 ER PT J AU LENO, M HAGUE, B TELLER, R KINDT, TJ AF LENO, M HAGUE, B TELLER, R KINDT, TJ TI THE HUMAN CD4 MOLECULE DEPENDENCE FOR HIV-1 MEDIATED APOPTOSIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S118 EP S118 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900217 ER PT J AU LEVIN, A BRUBAKER, G SHAO, JS KUMBY, D OBRIEN, TR GOEDERT, JJ STRAUSS, KW BLATTNER, WA HANNET, I AF LEVIN, A BRUBAKER, G SHAO, JS KUMBY, D OBRIEN, TR GOEDERT, JJ STRAUSS, KW BLATTNER, WA HANNET, I TI DETERMINATION OF T-LYMPHOCYTE SUBSETS ON SITE IN HIV-I INFECTED AND NONINFECTED INDIVIDUALS IN RURAL TANZANIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ST BARTHOLOMEWS HOSP,COLL MED,RTI UNIT,LONDON,ENGLAND. SHIRATI HOSP,SHIRATI,TANZANIA. KILIMANJARO CHRISTIAN MED CTR,MOSHI,TANZANIA. NCI,VIRAL EPIDEMIOL BRANCH,ROCKVILLE,MD. BECTON DICKINSON,EREMBODEGEM,BELGIUM. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S146 EP S146 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900327 ER PT J AU LI, WQ PIERCE, JH AF LI, WQ PIERCE, JH TI PROTEIN-KINASE C-DELTA, AN IMPORTANT SIGNALING MOLECULE IN THE PLATELET-DERIVED GROWTH-FACTOR-BETA RECEPTOR PATHWAY SO AIDS RESEARCH AND HUMAN RETROVIRUSES 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 MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S122 EP S122 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900231 ER PT J AU LIEBERMAN, J SKOLNIK, PR PARKERSON, GR FABRY, JA FONG, DM BEYER, D WANG, A LANDRY, B AF LIEBERMAN, J SKOLNIK, PR PARKERSON, GR FABRY, JA FONG, DM BEYER, D WANG, A LANDRY, B TI IMMUNOTHERAPY WITH EX VIVO-EXPANDED HIV-SPECIFIC CYTOTOXIC T-LYMPHOCYTES IN SUBJECTS WITH CD4 COUNTS OF 100-400/MM(3) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. TUFTS UNIV NEW ENGLAND MED CTR,DEPT MED,BOSTON,MA 02111. NIH,DIV AIDS,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S132 EP S132 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900271 ER PT J AU LIN, JX MIGONE, TS TSANG, M FRIEDMANN, M WEATHERBEE, JA ZHOU, L YAMAUCHI, A BLOOM, ET MIETZ, J JOHN, S LEONARD, WJ AF LIN, JX MIGONE, TS TSANG, M FRIEDMANN, M WEATHERBEE, JA ZHOU, L YAMAUCHI, A BLOOM, ET MIETZ, J JOHN, S LEONARD, WJ TI ROLE OF SHARED RECEPTOR MOTIFS IN THE INDUCTION OF COMMON STAT PROTEINS - POTENTIAL CONTRIBUTION IN DETERMINING CYTOKINE SPECIFICITY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,MOLEC IMMUNOL LAB,BETHESDA,MD 20892. RES & DEV SYST,MINNEAPOLIS,MN 55413. US FDA,CBER,DIV CELL & GENE THERAPY,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S124 EP S124 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900238 ER PT J AU LISZIEWICZ, J SUN, D ENSOLI, B GALLO, RC AF LISZIEWICZ, J SUN, D ENSOLI, B GALLO, RC TI ANTITAT GENE-THERAPY - EFFECTIVENESS IN THE PRESENCE OF INFLAMMATORY CYTOKINES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S156 EP S156 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900369 ER PT J AU LOUIS, JM WONDRAK, EM NASHED, NT AF LOUIS, JM WONDRAK, EM NASHED, NT TI PROTEOLYTIC PROCESSING MECHANISM OF HUMAN-IMMUNODEFICIENCY-VIRUS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIDDK,CELLULAR & DEV BIOL LAB,BETHESDA,MD. NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S162 EP S162 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900390 ER PT J AU LOWY, DR DECLUE, JE VASS, WC PAPAGEORGE, AG NIELSEN, KH WILLUMSEN, BM AF LOWY, DR DECLUE, JE VASS, WC PAPAGEORGE, AG NIELSEN, KH WILLUMSEN, BM TI REGULATION OF RAS ACTIVITY IN CELLULAR SIGNALING SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV COPENHAGEN,DEPT MOLEC & CELL BIOL,COPENHAGEN,DENMARK. NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S64 EP S64 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900006 ER PT J AU LUSSO, P CROWLEY, RW SECCHIERO, P SOUTHERS, JL MARKHAM, PD FRANCHINI, G GALLO, RC AF LUSSO, P CROWLEY, RW SECCHIERO, P SOUTHERS, JL MARKHAM, PD FRANCHINI, G GALLO, RC TI EXPERIMENTAL COINFECTION IN-VIVO BY SIVSM AND HHV-6(GS) IN MACACA-NEMESTRINA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD. RI secchiero, paola/G-9689-2015 OI secchiero, paola/0000-0003-4101-7987 NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S100 EP S100 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900142 ER PT J AU LUSSO, P CROWLEY, RW SOUTHERS, JL MARKHAM, PD SECCHIERO, P GALLO, RC AF LUSSO, P CROWLEY, RW SOUTHERS, JL MARKHAM, PD SECCHIERO, P GALLO, RC TI EXPERIMENTAL CONFECTION IN-VIVO BY SIVSM AND HHY-6(GS) IN MACACA-NEMESTRINA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD. RI secchiero, paola/G-9689-2015 OI secchiero, paola/0000-0003-4101-7987 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S171 EP S171 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900425 ER PT J AU MALYKH, A WEINBERG, MA THORNTON, A GALLO, RC LORI, F AF MALYKH, A WEINBERG, MA THORNTON, A GALLO, RC LORI, F TI COMBINED INHIBITION OF CELLULAR AND VIRAL TARGETS - HYDROXYUREA REVERSES THE RESISTANCE OF HIV-1 MUTANTS TO NUCLEOSIDE ANALOGS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. MCGILL UNIV,MONTREAL,PQ,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S170 EP S170 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900422 ER PT J AU MALYKH, A BIGGAR, R REITZ, MS AF MALYKH, A BIGGAR, R REITZ, MS TI HIV-1 NEF SEQUENCES IN-VIVO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20853. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20853. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S108 EP S108 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900177 ER PT J AU MANN, DL KASLOW, RA APPLE, R CARRINGTON, K GOEDERT, J OBRIEN, SJ WINKLER, C AF MANN, DL KASLOW, RA APPLE, R CARRINGTON, K GOEDERT, J OBRIEN, SJ WINKLER, C TI HLA CLASS-I, CLASS-II, AND TAP GENES STRONGLY INFLUENCE THE COURSE OF HIV-INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NIAID,EBB,BETHESDA,MD 20892. ROCHE MOLEC SYST INC,ALAMEDA,CA 94501. NCI,FREDERICK CANC RES & DEV CTR,SAIC,BCDP,FREDERICK,MD 21702. NCI,VEB,BETHESDA,MD 20892. RI apple, raymond/I-4506-2012 OI apple, raymond/0000-0002-8007-0345 NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S85 EP S85 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900085 ER PT J AU MARKHAM, P KAO, V FIORELLI, V GENDELMAN, R ZON, G GALLO, RC ENSOLI, B AF MARKHAM, P KAO, V FIORELLI, V GENDELMAN, R ZON, G GALLO, RC ENSOLI, B TI ANTISENSE OLIGONUCLEOTIDE TARGETING BASIC FIBROBLAST GROWTH-FACTOR (BFGF) BLOCK GROWTH AND ANGIOGENESIS OF AIDS-KAPOSIS SARCOMA (KS) CELLS AND CYTOKINE-ACTIVATED ENDOTHELIAL-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,GAITHERSBURG,MD. LYNX THERAPEUT INC,HAYWARD,CA. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 5 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S96 EP S96 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900128 ER PT J AU MENZO, S PAOLUCCI, S BAGNARELLI, P COHEN, O PANTALEO, G CLEMENTI, M AF MENZO, S PAOLUCCI, S BAGNARELLI, P COHEN, O PANTALEO, G CLEMENTI, M TI HIV-1 QUASI-SPECIES IN LONG-TERM NONPROGRESSORS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV ANCONA,IST MICROBIOL,ANCONA,ITALY. NIAID,LIR,BETHESDA,MD 20892. UNIV TRIESTE,DIPARTIMENTO SCI BIOMED,TRIESTE,ITALY. RI Clementi, Massimo/F-6646-2013; Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S110 EP S110 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900184 ER PT J AU MIGONE, TS LIN, JX CERESETO, A MULLOY, JC OSHEA, JJ FRANCHINI, G LEONARD, WJ AF MIGONE, TS LIN, JX CERESETO, A MULLOY, JC OSHEA, JJ FRANCHINI, G LEONARD, WJ TI CONSTITUTIVELY ACTIVATED JAK-STAT PATHWAY FOLLOWING TRANSFORMATION OF T-CELLS WITH HTLV-I SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,MOLEC IMMUNOL LAB,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIAMS,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S139 EP S139 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900300 ER PT J AU MILEY, WJ BIGGAR, B BLATTNER, B TAHA, T MIOTTI, P BUTCHER, A WATERS, D AF MILEY, WJ BIGGAR, B BLATTNER, B TAHA, T MIOTTI, P BUTCHER, A WATERS, D TI MALAWI HIV-1 PERINATAL TRANSMISSION STUDY - PCR AMPLICOR(TM) DETECTION OF HIV-INFECTED INFANTS FROM BLOOD DRIED ON FILTER MATS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD. NCI,BETHESDA,MD 20892. JOHNS HOPKINS,BLANTYRE,MALAWI. ROCHE MOLEC SYST,SOMERVILLE,NJ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S146 EP S146 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900328 ER PT J AU MIRESKANDARI, A REID, RL KASHANCHI, F DITTMER, J BRADY, JN AF MIRESKANDARI, A REID, RL KASHANCHI, F DITTMER, J BRADY, JN TI INTERACTION OF TAX(1) WITH A NOVEL LYMPHOCYTE-SPECIFIC PROTEIN ASSOCIATED WITH THE CDC2/CYCLIN-B COMPLEX SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,DIV CLIN TRIAL DESIGN & ANAL,ONCOL BRANCH,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S125 EP S125 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900244 ER PT J AU MORGAN, RA CHUAH, M VANDENDRIESSCHE, T BUNNELL, B BRESSLER, P WALKER, R LANE, C BLAESE, RM AF MORGAN, RA CHUAH, M VANDENDRIESSCHE, T BUNNELL, B BRESSLER, P WALKER, R LANE, C BLAESE, RM TI COMPARISON OF ANTI-HIV-1 RETROVIRAL VECTORS AND THEIR USE IN AN AIDS GENE-THERAPY TRIAL IN IDENTICAL-TWINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NATL CTR HUMAN GENOME RES,BETHESDA,MD. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 4 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S157 EP S157 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900372 ER PT J AU MULLEY, MC CROWLEY, R MIGONE, TS CIMINALE, V FULLEN, J TON, N GALLO, RC LEONARD, WJ FRANCHINI, G AF MULLEY, MC CROWLEY, R MIGONE, TS CIMINALE, V FULLEN, J TON, N GALLO, RC LEONARD, WJ FRANCHINI, G TI ACTIVATION OF THE INTERLEUKIN-2 RECEPTOR PATHWAY IN HTLV-I AND HTLV-II INFECTED-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,MOLEC IMMUNOL LAB,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV PADUA,INST ONCOL,MOLEC PATHOL LAB,I-35128 PADUA,ITALY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S126 EP S126 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900246 ER PT J AU MURALIDHAR, S DONIGER, J MENDELSON, E ARAUJO, J BRADY, J ROSENTHAL, LJ AF MURALIDHAR, S DONIGER, J MENDELSON, E ARAUJO, J BRADY, J ROSENTHAL, LJ TI HUMAN CYTOMEGALOVIRUS 79AA ORF ONCOPROTEIN BINDS TO P53 AND RB AND DOWN-REGULATES P53 ACTIVATED TRANSCRIPTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 GEORGETOWN UNIV,WASHINGTON,DC. NCI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S100 EP S100 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900143 ER PT J AU MYAGKIKH, M SGAGIAS, MK DANFORTH, DN GUROFF, MR AF MYAGKIKH, M SGAGIAS, MK DANFORTH, DN GUROFF, MR TI PREFERENTIAL EXPRESSION OF HERV-K-RELATED SEQUENCES IN BREAST-CANCER SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S103 EP S103 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900156 ER PT J AU NARA, PL AF NARA, PL TI OTHER DETERMINANTS OF HIV-1 ENTRY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,DCE,BCP,LTCB,VBS,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S135 EP S135 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900284 ER PT J AU NERURKAR, VR DASHWOOD, WM HEATHCHIOZZI, ME YANAGIHARA, R AF NERURKAR, VR DASHWOOD, WM HEATHCHIOZZI, ME YANAGIHARA, R TI MOLECULAR EPIDEMIOLOGY OF HIV-I INFECTION IN HAWAII SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV HAWAII,RETROVIROL RES LAB,HONOLULU,HI 96822. NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S146 EP S146 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900326 ER PT J AU NGUYEN, BY CLERICI, M BAUZA, S BAILEY, J LONGO, D MURPHY, W GESUNDHEIT, N VENZON, D SHEARER, G YARCHOAN, R AF NGUYEN, BY CLERICI, M BAUZA, S BAILEY, J LONGO, D MURPHY, W GESUNDHEIT, N VENZON, D SHEARER, G YARCHOAN, R TI IMMUNOLOGICAL EFFECTS OF RECOMBINANT HUMAN INSULIN-LIKE GROWTH-FACTOR (RHIGF-1) AND RECOMBINANT HUMAN GROWTH-HORMONE (RHGH) IN HIV-INFECTED PATIENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. GENENTECH INC,S SAN FRANCISCO,CA 94080. RI Venzon, David/B-3078-2008 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S164 EP S164 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900398 ER PT J AU NUNN, M MARSH, J AF NUNN, M MARSH, J TI IDENTIFICATION OF PROTEINS ASSOCIATED WITH THE HIV-1 NEF GENE-PRODUCT - CHARACTERIZATION OF A 65,000 DALTON KINASE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S122 EP S122 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900233 ER PT J AU OROSZLAN, S SHULENIN, S YOUNG, M GORELICK, RJ BRIGGS, CJ AF OROSZLAN, S SHULENIN, S YOUNG, M GORELICK, RJ BRIGGS, CJ TI BIOCHEMISTRY OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) REPLICATION - THE ROLE OF THE VIRAL PROTEASE IN THE EARLY PHASE OF INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,LMVC,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S164 EP S164 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900399 ER PT J AU OSHEA, JJ KAWAMURA, M CHEN, YQ HANSEN, E TORTOLANI, J RIEDY, M BACON, C JOHNSTON, J AF OSHEA, JJ KAWAMURA, M CHEN, YQ HANSEN, E TORTOLANI, J RIEDY, M BACON, C JOHNSTON, J TI SIGNALING BY IL-2 AND IL-12 - ROLE OF JAKS AND STATS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAMS,ARTHRIT & RHEUMATISM BRANCH,LEUKOCYTE CELL BIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S124 EP S124 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900240 ER PT J AU OTT, D COREN, L JOHNSON, D SOWDER, R ARTHUR, L HENDERSON, L AF OTT, D COREN, L JOHNSON, D SOWDER, R ARTHUR, L HENDERSON, L TI PROTEIN-ANALYSIS OF IMMUNOPHILINS FOUND IN HUMAN AND SIMIAN IMMUNODEFICIENCY VIRUSES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S106 EP S106 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900166 ER PT J AU PANTALEO, G DEMAREST, JF VACCAREZZA, M DAUCHER, M GRAZIOSI, C COHEN, OC SCHNITTMANN, SM PERIN, L TAMBUSS, G SHAW, GM SEKALY, RP COREY, L FAUCI, AS AF PANTALEO, G DEMAREST, JF VACCAREZZA, M DAUCHER, M GRAZIOSI, C COHEN, OC SCHNITTMANN, SM PERIN, L TAMBUSS, G SHAW, GM SEKALY, RP COREY, L FAUCI, AS TI PRIMARY IMMUNE-RESPONSE TO HIV-INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. UNIV GENEVA,GENEVA,SWITZERLAND. SAN RAFFAELE INST,MILAN,ITALY. UNIV ALABAMA,UNIVERSITY,AL 35486. IRCM,MONTREAL,PQ,CANADA. UNIV WASHINGTON,SEATTLE,WA 98195. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S149 EP S149 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900339 ER PT J AU PAPAS, TS ROMANOSPICA, V GEORGIOU, P SUZUKI, H BHAT, NK AF PAPAS, TS ROMANOSPICA, V GEORGIOU, P SUZUKI, H BHAT, NK TI ROLE OF ETS1 IN IL-2 GENE-EXPRESSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,CTR MOLEC & STRUCT BIOL,CHARLESTON,SC. NCI,MOLEC ONCOL LAB,FREDERICK,MD. FREDERICK CANC RES & DEV CTR,SAIC INC,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S65 EP S65 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900011 ER PT J AU POTTER, M MULLER, J JANZ, S JONES, G AF POTTER, M MULLER, J JANZ, S JONES, G TI TIME AND SITE OF ORIGIN OF C-MYC-IG HEAVY-CHAIN SWITCH REGION ILLEGITIMATE RECOMBINATIONS IN MOUSE PERITONEAL PLASMACYTOMAGENESIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,GENET LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S67 EP S67 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900018 ER PT J AU PURI, A MORRIS, SJ JONES, P AF PURI, A MORRIS, SJ JONES, P TI HEAT-RESISTANT FACTORS IN HUMAN ERYTHROCYTE-MEMBRANES MEDIATE CD4-DEPENDENT FUSION WITH CELLS EXPRESSING HIV-1 ENVELOPE GLYCOPROTEINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S106 EP S106 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900167 ER PT J AU RABKIN, CS BIGGAR, RJ COLEMAN, A MUSABA, E CHIBWE, G JANZ, S AF RABKIN, CS BIGGAR, RJ COLEMAN, A MUSABA, E CHIBWE, G JANZ, S TI CLONALITY OF AIDS-RELATED KAPOSIS-SARCOMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD. UTH,LUSAKA,ZAMBIA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S74 EP S74 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900042 ER PT J AU REITZ, MS NICHOLAS, J HALL, L LUSSO, P GALLO, RC BERNEMAN, Z AF REITZ, MS NICHOLAS, J HALL, L LUSSO, P GALLO, RC BERNEMAN, Z TI IDENTIFICATION AND COMPARISON OF GLYCOPROTEINS GB AND GH FROM HUMAN HERPESVIRUS TYPE-7 (HHV-7) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD. UNIV ANTWERP HOSP,EDEGEM,BELGIUM. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S101 EP S101 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900147 ER PT J AU RICE, WG TURPIN, JA DOMAGALA, J BADER, JP ARTHUR, LO HENDERSON, LE AF RICE, WG TURPIN, JA DOMAGALA, J BADER, JP ARTHUR, LO HENDERSON, LE TI NOVEL INHIBITORS OF RETROVIRAL NUCLEOCAPSID PROTEIN ZINC FINGERS AS CANDIDATES FOR THE TREATMENT OF HIV-1 INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ANTIVIRAL DRUG MECH LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. PARKE DAVIS PHARMACEUT CO,ANN ARBOR,MI 48105. NCI,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S161 EP S161 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900388 ER PT J AU ROBERTGUROFF, M NATUK, RJ MYAGKIKH, M ALDRICH, K ALIPANAH, S KALYAN, N MURTHY, SCS WADE, MS SINANGIL, F STEIMER, K NIGIDA, SM ARTHUR, LO MARKHAM, PD GALLO, RC EICHBERG, JW LUBECK, MD AF ROBERTGUROFF, M NATUK, RJ MYAGKIKH, M ALDRICH, K ALIPANAH, S KALYAN, N MURTHY, SCS WADE, MS SINANGIL, F STEIMER, K NIGIDA, SM ARTHUR, LO MARKHAM, PD GALLO, RC EICHBERG, JW LUBECK, MD TI ADENOVIRUS-HIV-1(MN) ENV RECOMBINANTS AND A SF2 GP120 BOOST PROTECT CHIMPANZEES FROM A SF2 CHALLENGE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. WYETH AYERST RES,RADNOR,PA. CHIRON CORP,EMERYVILLE,CA 94608. NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD. ADV BIOSCI LABS INC,KENSINGTON,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S136 EP S136 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900286 ER PT J AU ROBERTS, DD GUO, NH BROWNING, PJ ZABRENETZKY, VS INMAN, JK KRUTZSCH, HC AF ROBERTS, DD GUO, NH BROWNING, PJ ZABRENETZKY, VS INMAN, JK KRUTZSCH, HC TI MODULATION OF TUMOR-GROWTH IN-VITRO AND IN-VIVO BY STABLE ANALOGS OF THROMBOSPONDIN PEPTIDES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. VANDERBILT UNIV,CTR CANC,NASHVILLE,TN 37232. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S73 EP S73 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900040 ER PT J AU RUPPACH, H VONBRIESEN, H NARA, P RUBSAMENWAIGMANN, H DIETRICH, U AF RUPPACH, H VONBRIESEN, H NARA, P RUBSAMENWAIGMANN, H DIETRICH, U TI OPTIMIZATION OF AN IN-VITRO SYSTEM FOR THE INFECTION OF MONOCYTES/MACROPHAGES WITH HIV SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 BAYER AG,INST VIROL,D-42096 WUPPERTAL,GERMANY. NCI,FREDERICK,MD 21701. GEORG SPEYER HAUS,D-60595 FRANKFURT,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S119 EP S119 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900221 ER PT J AU RYAN, J NELMS, K WANG, HY KEEGAN, AD PAUL, WE AF RYAN, J NELMS, K WANG, HY KEEGAN, AD PAUL, WE TI IL-4 RECEPTOR - DISTINCT DOMAINS PRINCIPALLY REGULATE GROWTH AND DIFFERENTIATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 AMER RED CROSS,HOLLAND LABS,ROCKVILLE,MD 20855. NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S121 EP S121 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900229 ER PT J AU SAMANIEGO, F MARKHAM, PD STURZL, M GENDELMAN, R FERRARA, N KAO, V KOWALSKI, K ENSOLI, B GALLO, RC AF SAMANIEGO, F MARKHAM, PD STURZL, M GENDELMAN, R FERRARA, N KAO, V KOWALSKI, K ENSOLI, B GALLO, RC TI VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) IS EXPRESSED BY AIDS-KAPOSIS SARCOMA (KS) CELLS AND SYNERGIZES WITH BFGF TO FORM KS-LIKE LESIONS IN NUDE-MICE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD 20895. MAX PLANCK INST BIOCHEM,W-8033 MARTINSRIED,GERMANY. GENENTECH INC,S SAN FRANCISCO,CA 94080. RI Sturzl, Michael/B-3019-2015; Ensoli, Barbara/J-9169-2016 OI Sturzl, Michael/0000-0002-9276-2824; Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S95 EP S95 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900125 ER PT J AU SAMANIEGO, F BRYANT, JL ZEMAN, RA THIERRY, A JUDDE, JG GALLO, RC LUNARDIISKANDAR, Y AF SAMANIEGO, F BRYANT, JL ZEMAN, RA THIERRY, A JUDDE, JG GALLO, RC LUNARDIISKANDAR, Y TI HUMAN CHORIONIC-GONADOTROPIN (HCG) PREVENTS DEVELOPMENT OF KAPOSIS-SARCOMA (AIDS-KS Y-1) TUMORS BY INDUCING APOPTOSIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIDR,ANIM CARE UNIT,BETHESDA,MD 20892. RI thierry, alain/F-9492-2014 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S76 EP S76 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900051 ER PT J AU SAVILLE, MW LIETZAU, J PLUDA, JM WILSON, W FEIGAL, E FEUERSTEIN, I ODOM, J HUMPHREY, R BRODER, S YARCHOAN, R AF SAVILLE, MW LIETZAU, J PLUDA, JM WILSON, W FEIGAL, E FEUERSTEIN, I ODOM, J HUMPHREY, R BRODER, S YARCHOAN, R TI ACTIVITY OF PACLITAXEL (TAXOL(TM)) FOR THE TREATMENT OF HIV-ASSOCIATED KAPOSIS SARCOMA (KS) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD. NIH,CTR CANC,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S77 EP S77 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900052 ER PT J AU SCHILLING, B QUAN, E CHOKEKIJCHAI, S MITSUYA, H STAUDT, L ZEICHNER, SL AF SCHILLING, B QUAN, E CHOKEKIJCHAI, S MITSUYA, H STAUDT, L ZEICHNER, SL TI ACUTE HIV-1 INFECTION OF H-9 CELLS LEADS TO DISTINCT TEMPORAL PATTERNS OF CELLULAR GENE-EXPRESSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. NCI,METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S114 EP S114 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900199 ER PT J AU SCHUBERT, U HENKLEIN, P BOUR, S FERRERMONTIEL, AV OBLATTMONTAL, M MONTAL, M STREBEL, K AF SCHUBERT, U HENKLEIN, P BOUR, S FERRERMONTIEL, AV OBLATTMONTAL, M MONTAL, M STREBEL, K TI VIRUS RELEASE FROM HIV-1-INFECTED CELLS IS REGULATED BY AN ION-CHANNEL ACTIVITY OF VPU SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. HUMBOLDT UNIV BERLIN,BERLIN,GERMANY. UNIV CALIF SAN DIEGO,DEPT BIOL,SAN DIEGO,CA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S114 EP S114 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900201 ER PT J AU SECCHIERO, P NICHOLAS, J DENG, H XIAOPENG, T VANLOON, N RUVOLO, V BERNEMAN, ZN REITZ, MS DEWHURST, S AF SECCHIERO, P NICHOLAS, J DENG, H XIAOPENG, T VANLOON, N RUVOLO, V BERNEMAN, ZN REITZ, MS DEWHURST, S TI STRUCTURAL-ANALYSIS OF THE GENOME TERMINI OF HHV-7 - IDENTIFICATION OF HUMAN TELOMERIC REPEAT MOTIFS AND PUTATIVE PACKAGING SIGNALS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD 21231. UNIV ROCHESTER,MED CTR,DEPT MICROBIOL & IMMUNOL,ROCHESTER,NY 14642. UNIV ANTWERP HOSP,B-2650 EDEGEM,BELGIUM. RI secchiero, paola/G-9689-2015 OI secchiero, paola/0000-0003-4101-7987 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S102 EP S102 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900150 ER PT J AU SHEARER, GM CLERICI, M AF SHEARER, GM CLERICI, M TI PROTECTIVE IMMUNITY AGAINST HIV AIDS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. UNIV MILAN,CATTEDRA IMMUNOL,MILAN,ITALY. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S131 EP S131 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900267 ER PT J AU SIMPSON, RM LENO, M HUBBARD, BAS BOWERS, FS TELLER, R DAVIS, CY ZHAO, TM KINDT, TJ AF SIMPSON, RM LENO, M HUBBARD, BAS BOWERS, FS TELLER, R DAVIS, CY ZHAO, TM KINDT, TJ TI CUTANEOUS MANIFESTATIONS OF HTLV-I INFECTION IN EXPERIMENTAL ADULT T-CELL LEUKEMIA (ATLL) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 1 Z9 1 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S140 EP S140 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900305 ER PT J AU SIRIANNI, MC UCCINI, S GENDELMAN, R MEZZAROMA, I BARDUAGNI, O CERIMELE, D ANGELICI, A BARONI, CD ENSOLI, B AIUTI, F AF SIRIANNI, MC UCCINI, S GENDELMAN, R MEZZAROMA, I BARDUAGNI, O CERIMELE, D ANGELICI, A BARONI, CD ENSOLI, B AIUTI, F TI PREFERENTIAL EXPRESSION OF GAMMA-INTERFERON IN SKIN BIOPSIES FROM KAPOSIS-SARCOMA PATIENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV ROMA LA SAPIENZA,DEPT CLIN IMMUNOL,ROME,ITALY. UNIV ROMA LA SAPIENZA,DEPT PATHOL ANAT 2,ROME,ITALY. UNIV ROMA LA SAPIENZA,DEPT SURG 4,ROME,ITALY. UNIV ROMA LA SAPIENZA,DEPT DERMATOL,ROME,ITALY. CATHOLIC UNIV ROME,DEPT DERMATOL,ROME,ITALY. NIH,LTCB,BETHESDA,MD. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S76 EP S76 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900049 ER PT J AU SOGOCIO, KM ANDERSON, B KAVLICK, M SAVILLE, W WAINBERG, MA CHERRINGTON, JM MITSUYA, H YARCHOAN, R AF SOGOCIO, KM ANDERSON, B KAVLICK, M SAVILLE, W WAINBERG, MA CHERRINGTON, JM MITSUYA, H YARCHOAN, R TI HIV-1 DEVELOPS REDUCED SENSITIVITY TO 9-(2-PHOSPHONYLMETHOXYETHYL) ADENINE (PMEA) IN-VITRO THROUGH ACQUISITION OF K65R SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MCGILL UNIV,AIDS CTR,MONTREAL,PQ,CANADA. NCI,BETHESDA,MD 20892. GILEAD SCI INC,FOSTER CITY,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S164 EP S164 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900400 ER PT J AU STERN, T BUGE, S ROBINSON, J ROBERTGUROFF, M AF STERN, T BUGE, S ROBINSON, J ROBERTGUROFF, M TI STUDIES OF HIV-1 ESCAPE MUTANTS AND REVERTANTS EMPHASIZE CRUCIAL ROLE OF LEUCINE-ZIPPER REGION FOR ENVELOPE STRUCTURE AND FUNCTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. UNIV CONNECTICUT,HLTH SCI CTR,FARMINGTON,CT. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S106 EP S106 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900168 ER PT J AU STREICHER, HZ AF STREICHER, HZ TI SUPPRESSION OF LYMPHOCYTE-PROLIFERATION BY KAPOSIS-SARCOMA (KS) CELL-LINES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S96 EP S96 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900129 ER PT J AU THIERRY, AR AKSENTIJEVICH, I LUNARDIISKANDAR, Y BRYANT, JL PENG, B GOTTESMAN, MM MAHAN, LC GALLO, RC AF THIERRY, AR AKSENTIJEVICH, I LUNARDIISKANDAR, Y BRYANT, JL PENG, B GOTTESMAN, MM MAHAN, LC GALLO, RC TI SYSTEMIC GENE-THERAPY - LONG-TERM TRANSGENE EXPRESSION IN MICE AND IN MOUSE BONE-MARROW PROGENITOR CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD. NCI,CELL BIOL LAB,BETHESDA,MD. NIDR,ANIM CARE UNIT,BETHESDA,MD 20892. NINCDS,NEUROCHEM LAB,BETHESDA,MD 20892. RI thierry, alain/F-9492-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S155 EP S155 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900364 ER PT J AU THOMSON, MM HOLLAND, M ALHARTHI, L ZON, G GALLO, RC KLOTMAN, ME AF THOMSON, MM HOLLAND, M ALHARTHI, L ZON, G GALLO, RC KLOTMAN, ME TI ANTISENSE PHOSPHOROTHIOATE OLIGODEOXYNUCLEOTIDES (S-ODNS) TARGETED TO THE LEADER SEQUENCE OF HIV-1 RNAS SHOW STRONG INHIBITION OF HIV-1 REPLICATION IN A TRANSIENT TRANSFECTION ASSAY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. LYNX THERAPEUT,HAYWARD,CA. MT SINAI MED CTR,NEW YORK,NY. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S160 EP S160 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900382 ER PT J AU THOMSON, MM REITZ, M BIGGAR, R GALLO, RC KLOTMAN, ME AF THOMSON, MM REITZ, M BIGGAR, R GALLO, RC KLOTMAN, ME TI IN-VIVO VARIABILITY OF HIV-1 TAT, REV AND NEF RNA EXPRESSION AND SPLICING REVEALED BY REVERSE TRANSCRIPTION-PCR SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. MT SINAI MED CTR,NEW YORK,NY 10029. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S111 EP S111 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900189 ER PT J AU VENKATESHAN, CN LAGRENADE, L DE, SK GOKULANATHAN, P BACHHUYNH, TG POMEROY, KL JOHNSON, BK STONE, GA MANNS, A HANCHARD, B RODGERSJOHNSON, P MARSH, JW ASHER, DM BLATTNER, W GAJDUSEK, DC GIBBS, CJ AF VENKATESHAN, CN LAGRENADE, L DE, SK GOKULANATHAN, P BACHHUYNH, TG POMEROY, KL JOHNSON, BK STONE, GA MANNS, A HANCHARD, B RODGERSJOHNSON, P MARSH, JW ASHER, DM BLATTNER, W GAJDUSEK, DC GIBBS, CJ TI OVEREXPRESSION OF PROINFLAMMATORY AND ANTIINFLAMMATORY CYTOKINES BY CULTURED KERATINOCYTES FROM HTLV-I-ASSOCIATED FAMILIAL INFECTIVE DERMATITIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV W INDIES,DEPT MED,MONA,JAMAICA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S143 EP S143 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900317 ER PT J AU WALKER, RE CARTER, CS MUUL, L NATARAJAN, V HERPIN, BR LEITMAN, SF KLEIN, HG FALLOON, J DAVEY, RT KOVACS, JA POLIS, MA MASUR, H BLAESE, RM LANE, HC AF WALKER, RE CARTER, CS MUUL, L NATARAJAN, V HERPIN, BR LEITMAN, SF KLEIN, HG FALLOON, J DAVEY, RT KOVACS, JA POLIS, MA MASUR, H BLAESE, RM LANE, HC TI SURVIVAL AND DISTRIBUTION OF GENETICALLY-MODIFIED CELLS IN IDENTICAL-TWINS DISCORDANT FOR HIV-1 INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NIH,CTR CLIN,BETHESDA,MD 20892. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. SAIC FREDERICK,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S166 EP S166 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900408 ER PT J AU WARNER, GL DRUMMOND, JE NARA, PL ARTHUR, LO WATERS, DJ AF WARNER, GL DRUMMOND, JE NARA, PL ARTHUR, LO WATERS, DJ TI SYNTHETIC PEPTIDE COMPETITION ELISA PREDICTS AN ANTISERUMS ABILITY TO NEUTRALIZE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 IN A LAB-STRAIN SPECIFIC MANNER SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S150 EP S150 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900344 ER PT J AU WATERS, D BRINING, S BLATTNER, W ARTHUR, L DERSE, D AF WATERS, D BRINING, S BLATTNER, W ARTHUR, L DERSE, D TI COMPARISON AND CHARACTERIZATION OF CELL-FREE INFECTION OF RHESUS LUNG-CELL (B5) WITH A HTLV-I MOLECULAR CLONE (PCS) AND A GAG MUTANT OF P15P, NUCLEIC-ACID BINDING-PROTEIN (NC) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,AIDS VACCINE PROGRAM,FREDERICK,MD. NCI,BETHESDA,MD 20892. BRMP,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S139 EP S139 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900299 ER PT J AU WATKINS, BA DAVIS, AE FIORENTINI, S REITZ, MS AF WATKINS, BA DAVIS, AE FIORENTINI, S REITZ, MS TI RECOMBINANT HUMAN-ANTIBODY FRAGMENTS TO THE HIV-1 GP120 CD4 BINDING-SITE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S134 EP S134 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900280 ER PT J AU WEICHOLD, FF LITTLE, R ZELLA, D MACIEJEWSKI, JP YOUNG, NS AF WEICHOLD, FF LITTLE, R ZELLA, D MACIEJEWSKI, JP YOUNG, NS TI HIV DOES NOT INFECT BONE-MARROW STEM-CELLS AS ASSESSED BY LTCICS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S156 EP S156 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900366 ER PT J AU WEICHOLD, FF MACIEJEWSKI, JP SAXINGER, C WAINBERG, MA YOUNG, NS AF WEICHOLD, FF MACIEJEWSKI, JP SAXINGER, C WAINBERG, MA YOUNG, NS TI INTRACELLULAR IMMUNIZATION WITH ANTI-RT ANTIBODY FRAGMENT PROTECTS PBLS FROM INFECTION WITH HIV SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. MCGILL UNIV,JEWISH GEN HOSP,MCGILL AIDS CTR,MONTREAL,PQ H3T 1E2,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S156 EP S156 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900367 ER PT J AU WEICHOLD, FF SLOAND, EM KUMAR, P YOUNG, NS MACIEJEWSKI, JP AF WEICHOLD, FF SLOAND, EM KUMAR, P YOUNG, NS MACIEJEWSKI, JP TI FAS MEDIATED DEPICTION OF CD4+ T-CELLS IN HIV-INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S80 EP S80 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900066 ER PT J AU WU, SC SPOUGE, J CONLEY, S TSAI, WP MERGES, M NARA, P AF WU, SC SPOUGE, J CONLEY, S TSAI, WP MERGES, M NARA, P TI HUMAN PLASMA ENHANCES THE INFECTIVITY OF PRIMARY HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ISOLATES IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS AND MONOCYTE-DERIVED MACROPHAGES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. NCI,FREDERICK CANC RES & DEV CTR,VIRUS BIOL SECT,TUMOR CELL BIOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOCHEM PHYSIOL LAB,BRMP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S151 EP S151 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900348 ER PT J AU ZELLA, D CROWLEY, RW SECCHIERO, P THORNTON, A REITZ, MS GALLO, RC AF ZELLA, D CROWLEY, RW SECCHIERO, P THORNTON, A REITZ, MS GALLO, RC TI HIV-1 INFECTION AND T-CELL ACTIVATION STATES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI secchiero, paola/G-9689-2015 OI secchiero, paola/0000-0003-4101-7987 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PY 1995 VL 11 SU 1 BP S107 EP S107 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RQ689 UT WOS:A1995RQ68900172 ER PT J AU GORDIS, E AF GORDIS, E TI THE NATIONAL-INSTITUTE-ON-ALCOHOL-ABUSE-AND-ALCOHOLISM - PAST ACCOMPLISHMENTS AND FUTURE GOALS SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article DE GOVERNMENT AGENCY; AOD ABUSE; AOD DEPENDENCE; RESEARCH FUNDING ID ETHANOL; DEPENDENCE; INHERITANCE; NALTREXONE; TOLERANCE; EXPOSURE; YOUTH; RISK; MICE AB Thanks largely to support from the National Institute on Alcohol Abuse and Alcoholism, alcoholism researchers have made significant strides in understanding the causes, prevention, and treatment of alcoholism and its consequences. Ongoing research will extend this knowledge. RP GORDIS, E (reprint author), NIAAA,BETHESDA,MD 20892, USA. NR 64 TC 3 Z9 3 U1 3 U2 3 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 1 BP 5 EP 11 PG 7 WC Substance Abuse SC Substance Abuse GA QV609 UT WOS:A1995QV60900001 ER PT J AU HEWITT, BG AF HEWITT, BG TI THE CREATION OF THE NATIONAL-INSTITUTE-ON-ALCOHOL-ABUSE-AND-ALCOHOLISM - RESPONDING TO AMERICA ALCOHOL PROBLEM SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article DE GOVERNMENT AGENCY; AOD ABUSE; AOD DEPENDENCE; HISTORY; AOD-RELATED (AODR) PROBLEMS; LEGISLATION AB Although they had founded their own national society and their own treatment program, people recovering from alcoholism in the 1960's realized that Americans did not recognize the alcohol-dependent person's plight, Thus, a few dedicated individuals set out to establish, through Federal legislation, a nationwide effort to combat alcoholism. RP HEWITT, BG (reprint author), NIAAA,BETHESDA,MD 20892, USA. NR 7 TC 3 Z9 3 U1 0 U2 1 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 1 BP 12 EP 16 PG 5 WC Substance Abuse SC Substance Abuse GA QV609 UT WOS:A1995QV60900002 ER PT J AU CHAFETZ, ME NOBLE, EP ARCHER, L MAYER, WE NIVEN, RG GORDIS, E AF CHAFETZ, ME NOBLE, EP ARCHER, L MAYER, WE NIVEN, RG GORDIS, E TI REFLECTIONS - NIAAAS DIRECTORS LOOK BACK ON 25 YEARS SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Editorial Material DE GOVERNMENT AGENCY INTERVIEW; PUBLIC POLICY ON AOD; AOD DEPENDENCY; AOD ABUSE; RESEARCH AB During its 25 years of existence, the National Institute on Alcohol Abuse and Alcoholism (NIAAA) has been influenced by many individuals and organizations. Among those shaping NIAAA's missions and their implementations, the Institute's directors played and continue to play a pivotal role. In return, the position as director of NIAAA had an impact on these men and their careers. Alcohol Health & Research World contacted the former and current directors to record their personal recollections and impressions of the alcohol field and NIAAA's role in it. C1 UNIV CALIF LOS ANGELES,ALCOHOL RES CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,ALCOHOL & DRUG TREATMENT PROGRAM,LOS ANGELES,CA. NIAAA,ROCKVILLE,MD 20852. WAYNE STATE UNIV,SCH MED,DETROIT,MI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 1 BP 17 EP 27 PG 11 WC Substance Abuse SC Substance Abuse GA QV609 UT WOS:A1995QV60900003 ER PT J AU GOLDMAN, D AF GOLDMAN, D TI ALDEHYDE DEHYDROGENASE-DEFICIENCY AS CAUSE OF FACIAL FLUSHING REACTION TO ALCOHOL IN JAPANESE - COMMENT SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Note DE ALDEHYDE DEHYDROGENASE; ALCOHOL FLUSH REACTION; ASIAN; METABOLISM; ACETALDEHYDE; GENETICS AND HEREDITY; AOD DEPENDENCE RP GOLDMAN, D (reprint author), NIAAA,DIV INTRAMURAL CLIN & BIOL RES,NEUROGENET LAB,BETHESDA,MD 20892, USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 7 TC 3 Z9 3 U1 0 U2 0 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 1 BP 48 EP 49 PG 2 WC Substance Abuse SC Substance Abuse GA QV609 UT WOS:A1995QV60900014 ER PT J AU LINNOILA, M COLBURN, TR PETERSEN, RC AF LINNOILA, M COLBURN, TR PETERSEN, RC TI ON THE RESEARCH FRONT - THE NIAAA INTRAMURAL RESEARCH-PROGRAM SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article DE AOD DEPENDENCE; AOD EFFECTS (AODE); BASIC RESEARCH; CLINICAL STUDY; GOVERNMENT AGENCY; EDUCATION AND TRAINING AB Intramural research at the National Institute on Alcohol Abuse and Alcoholism delves into many aspects of biological science relating to alcoholism, from the genetics of alcoholism to the imaging of alcohol-abusing patients' brains. Drawing on the unique resources within the National Institutes of Health, the Intramural Research Program plans to continue its commitment to conducting cutting-edge research. C1 NIAAA,ROCKVILLE,MD 20852. RP LINNOILA, M (reprint author), NIAAA,DIV INTRAMURAL CLIN & BIOL RES,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 1 BP 60 EP & PG 0 WC Substance Abuse SC Substance Abuse GA QV609 UT WOS:A1995QV60900020 ER PT J AU DUFOUR, MC AF DUFOUR, MC TI 25 YEARS OF ALCOHOL EPIDEMIOLOGY - TRENDS, TECHNIQUES, AND TRANSITIONS SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article DE AOD CONSUMPTION; AOD-RELATED (AODR) PROBLEMS; AOD DEPENDENCE EPIDEMIOLOGY; RESEARCH; TREND; AODR MORTALITY; GOVERNMENT AGENCY ID UNITED-STATES AB Alcohol epidemiology has developed as a discipline only in the second half of this century. The recognition of alcoholism as a diagnosable disease has permitted extensive studies of trends in alcohol consumption and its consequences throughout the United States. RP DUFOUR, MC (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,BETHESDA,MD 20892, USA. NR 24 TC 5 Z9 5 U1 0 U2 0 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 1 BP 77 EP 84 PG 8 WC Substance Abuse SC Substance Abuse GA QV609 UT WOS:A1995QV60900023 ER PT J AU INGLE, KG WEINGARTNER, HJ AF INGLE, KG WEINGARTNER, HJ TI COGNITIVE DEFICITS IN ALCOHOLISM - APPROACHES TO THEORETICAL MODELING SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article DE COGNITIVE PROCESS; AOD DEPENDENCE; LITERATURE REVIEW; AOD IMPAIRMENT; BRAIN IMAGING; PERFORMANCE TEST; SCIENTIFIC MODEL; TREATMENT ID MEMORY C1 NIAAA,CLIN STUDIES LAB,COGNIT NEUROSCI SECT,BETHESDA,MD. RP INGLE, KG (reprint author), ALCOHOL HLTH & RES WORLD,WASHINGTON,DC, USA. NR 22 TC 1 Z9 1 U1 1 U2 1 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 2 BP 155 EP 158 PG 4 WC Substance Abuse SC Substance Abuse GA TH280 UT WOS:A1995TH28000011 ER PT J AU Collins, FS Fink, L AF Collins, FS Fink, L TI The Human Genome Project SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article DE genome; genetic mapping; DNA; applied research; molecular genetics AB The Human Genome Project is an ambitious research effort aimed at deciphering the chemical makeup of the entire human genetic code (i.e., the genome). The primary work of the project is to develop three research tools that will allow scientists to identify genes involved in both rare and common diseases. Another project priority is to examine the ethical, legal, and social implications of new genetic technologies-and to educate the public about these issues, Although if has been in existence for less than 6 years, the Human Genome Project already has produced results that are permeating basic biological research and clinical medicine. For example, researchers have successfully mapped the mouse genome, and work is well under way to develop a genetic map of the rat, a useful model for studying complex disorders such as hypertension, diabetes, and alcoholism. RP Collins, FS (reprint author), NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892, USA. NR 10 TC 2 Z9 2 U1 0 U2 0 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 3 BP 190 EP 195 PG 6 WC Substance Abuse SC Substance Abuse GA UP637 UT WOS:A1995UP63700006 ER PT J AU Higley, JD AF Higley, JD TI Primates in alcohol research SO ALCOHOL HEALTH & RESEARCH WORLD LA English DT Article DE animal model; AOD dependence; research; hereditary factors; environmental factors; Cloninger's typology ID RHESUS-MONKEYS; CONSUMPTION AB The genetic similarity to humans of nonhuman primates makes them well suited to serve as models of complex human disorders such as alcoholism. Like humans, nonhuman primates vary with respect to their alcohol consumption, even within the same species. Studies of the origins of high consumption among nonhuman primates have suggested that both genetic and environmental factors play a role in their drinking. In fact, researchers have found some support for multiple subtypes of alcoholism among nonhuman primates. RP Higley, JD (reprint author), NIAAA,CLIN STUDIES LAB,PRIMATE UNIT,POOLESVILLE,MD 20837, USA. NR 16 TC 0 Z9 0 U1 0 U2 0 PU NATL INST ALCOHOL ABUSE ALCOHOLISM PI ROCKVILLE PA 6000 EXECUTIVE BLVD, ROCKVILLE, MD 20892-7003 SN 0090-838X J9 ALCOHOL HEALTH RES W JI Alcohol Health Res. World PY 1995 VL 19 IS 3 BP 213 EP 216 PG 4 WC Substance Abuse SC Substance Abuse GA UP637 UT WOS:A1995UP63700010 ER PT J AU CAPRON, M GOUNNI, AS MORITA, M TRUONG, MJ PRIN, L KINET, JP CAPRON, A AF CAPRON, M GOUNNI, AS MORITA, M TRUONG, MJ PRIN, L KINET, JP CAPRON, A TI EOSINOPHILS - FROM LOW-AFFINITY TO HIGH-AFFINITY IMMUNOGLOBULIN-E RECEPTORS SO ALLERGY LA English DT Article; Proceedings Paper CT Parallel Symposium on Basic Allergy - Immunoglobulin E Synthesis, Inflammation and Therapy, at the ICACI XV/EAACI 94 CY JUN 28, 1994 CL STOCKHOLM, SWEDEN SP European Acad Allerg & Clin Immunol, Pharm Allergy Res Fdn DE EOSINAPHILS; FC-EPSILON RII; FC-EPSILON RI; IGE BINDING PROTEINS; PATHOLOGY; PROTECTION ID IGE; RELEASE AB Several experimental approaches have been used to identify immunoglobulin (IgE) binding molecules expressed by human eosinophils. After the description that Fc epsilon RII/CD23 identified on eosinophils could participate in IgE binding and IgE-mediated cytotoxicity, Mac2/epsilon binding proteins belonging to the S-type lectin family were also detected on human eosinophils. Anti-Mac2 monoclonal antibodies inhibited eosinophil-dependent cytotoxicity towards parasitic targets. More recently, Fc epsilon RI was demonstrated on human eosinophils from hypereosinophilic patients. The 3 components of Fc epsilon RI, alpha, beta and gamma chains, were detected in eosinophils. The alpha chain of Fc epsilon RI was shown to be involved in IgE binding to eosinophils and in the selective release of eosinophil peroxidase. The participation of Fc epsilon RI-bearing eosinophils in a protective immune response against a parasitic infection indicates a so far unsuspected function of Fc epsilon RI. The interactions between the different types of IgE binding molecules are discussed. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. RP CAPRON, M (reprint author), INST PASTEUR,CTR IMMUNOL & BIOL PARASITAIRE,INSERM,U167,1 RUE PROF A CALMETTE,BP 245,F-59019 LILLE,FRANCE. NR 11 TC 22 Z9 22 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0105-4538 J9 ALLERGY JI Allergy PY 1995 VL 50 IS 25 SU S BP 20 EP 23 DI 10.1111/j.1398-9995.1995.tb04270.x PG 4 WC Allergy; Immunology SC Allergy; Immunology GA RF682 UT WOS:A1995RF68200005 PM 7677229 ER PT B AU ODonovan, MJ AF ODonovan, MJ BE Taylor, A Gladden, MH Durbaba, R TI Critique of papers on motoneurone inputs SO ALPHA AND GAMMA MOTOR SYSTEMS LA English DT Proceedings Paper CT Symposium on Alpha and Gamma Motor Systems CY JUL 11-14, 1994 CL LONDON, ENGLAND C1 NINCDS,NIH,NEURAL CONTROL LAB,SECT DEV NEUROBIOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45186-7 PY 1995 BP 37 EP 41 PG 5 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA BE59T UT WOS:A1995BE59T00006 ER PT B AU ODonovan, MJ Ritter, A AF ODonovan, MJ Ritter, A BE Taylor, A Gladden, MH Durbaba, R TI Optical recording and lesioning of spinal neurones during rhythmic activity in the chick embryo spinal cord SO ALPHA AND GAMMA MOTOR SYSTEMS LA English DT Proceedings Paper CT Symposium on Alpha and Gamma Motor Systems CY JUL 11-14, 1994 CL LONDON, ENGLAND C1 NINCDS,SECT DEV NEUROBIOL,NEURAL CONTROL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 BN 0-306-45186-7 PY 1995 BP 557 EP 563 PG 7 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA BE59T UT WOS:A1995BE59T00122 ER PT J AU SHIOTA, T JONES, M VALDESCRUZ, LM SHANDAS, R YAMADA, I SAHN, DJ AF SHIOTA, T JONES, M VALDESCRUZ, LM SHANDAS, R YAMADA, I SAHN, DJ TI COLOR-FLOW DOPPLER DETERMINATION OF TRANSMITRAL FLOW AND ORIFICE AREA IN MITRAL-STENOSIS - EXPERIMENTAL EVALUATION OF THE PROXIMAL FLOW-CONVERGENCE METHOD SO AMERICAN HEART JOURNAL LA English DT Article ID PRESSURE HALF-TIME; VENTRICULAR SEPTAL-DEFECT; VALVE AREA; REGURGITANT ORIFICE; BLOOD-FLOW; INVITRO; REGION; QUANTIFICATION; SURFACE; IMPACT AB To evaluate the in vivo accuracy of color Doppler flow-convergence methods for determining transmitral flow volumes and effective orifice areas in mitral stenosis, we studied two models for flow-convergence surface geometry, a hemispheric (HS) model and an oblate hemispheroid (OH) modes in a chronic animal model with quantifiable mitral flows. Color Doppler flow mapping of the proximal flow-convergence region has been reported to be useful for evaluation of intracardiac flows. Flow-convergence methods in patients with mitral stenosis that use HS assumption for the isovelocity surface have resulted in underestimation of actual flows. Chronic mitral stenosis was created surgically in six sheep with annuloplasty rings (group 1) and in 11 sheep with bioprosthetic porcine valves (group 2). Hemodynamic and echocardiographic/Doppler studies (n = 18 in group 1; n = 21 in group 2) were performed 20 to 34 weeks later. Left ventricular inflow obstruction was of varied severity, with mean transmitral valve gradients in group 1 ranging from 1.3 to 18 mm Hg and in group 2 ranging from 6.3 to 25.6 mm Hg. Although transmitral flows derived by both geometric flow convergence models showed significant correlations with reference cardiac outputs, the correlations for the OH model were better than those for the HS model (group 1, r = 0.86 for the OH model vs r = 0.72 for the HS model; group 2; r = 0.84 for the OH model vs r = 0.62 for the HS model). The OH model was also superior to the HS model in determining effective orifice areas compared to reference orifice areas determined by postmortem planimetry of anatomic orifices (group 1 only, r = 0.64 for OH vs 0.58 for HS), by the Gorlin and Gorlin formula (group 1, r = 0.63 for OH vs 0.72 for HS; group 2, r = 0.82 for OH vs 0.76 for HS), and by the Doppler pressure half-time method (group 1, r = 0.76 for OH vs 0.69 for HS; group 2, r = 0.84 for OH vs 0.62 far HS). The percentage differences between the reference values and calculated data with the OH model were significantly smaller for transmitral flows (-5.8% vs -59% in group 1 and -13% vs -63% in group 2) and for effective orifice areas in both groups, p < 0.0001 (-21% vs -56% for mitral orifice area by postmortem planimetry in group 1; -28% vs -61% in group 1 and -24% vs -68% in group 2 for mitral orifice area by the Gorlin and Gorlin formula; and -18% vs -57% in group 1 and -27% vs -71% in group 2 for the pressure half-time method, p < 0.0001 for each comparison). These studies demonstrate that flow convergence principles applied to color Doppler flow mapping permit estimation of transvalvular flow volumes and orifice areas in mitral stenosis. However, in the presence of orifices that are not infinitesimally small and when it is not clinically feasible to sample at substantial distances proximal to the orifice, determination of flows and areas with flow convergence principles results in underestimation relative to reference standards. This underestimation can be minimized by applying an OH geometric model to the flow convergence surface area rather than a strictly HS model. C1 NHLBI,BETHESDA,MD 20892. MAIMONIDES HOSP,DIV PEDIAT CARDIOL,BROOKLYN,NY. OREGON HLTH SCI UNIV,CLIN CARE CTR CONGENITAL HEART DIS,PORTLAND,OR 97201. CALTECH,PASADENA,CA 91125. OI Shandas, Robin/0000-0002-9473-7542 NR 47 TC 26 Z9 26 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD JAN PY 1995 VL 129 IS 1 BP 114 EP 123 DI 10.1016/0002-8703(95)90051-9 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QB188 UT WOS:A1995QB18800018 PM 7817904 ER PT J AU CASINO, PR KILCOYNE, CM CANNON, RO QUYYUMI, AA PANZA, JA AF CASINO, PR KILCOYNE, CM CANNON, RO QUYYUMI, AA PANZA, JA TI IMPAIRED ENDOTHELIUM-DEPENDENT VASCULAR RELAXATION IN PATIENTS WITH HYPERCHOLESTEROLEMIA EXTENDS BEYOND THE MUSCARINIC RECEPTOR SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID FOREARM RESISTANCE VESSELS; CORONARY-ARTERIES; SMOOTH-MUSCLE; SUBSTANCE-P; L-ARGININE; ACETYLCHOLINE; VASODILATION; DYSFUNCTION; HUMANS; ATHEROSCLEROSIS AB Patients with hypercholesterolemia have impaired endothelium-dependent vasodilation. However, previous human studies have invariably used muscarinic agents to assess endothelial function. The purpose of this investigation was to determine whether impaired endothelium-dependent vasodilation of hypercholesterolemic patients is related to a specific and isolated defect of the muscarinic receptor, or to a broader abnormality of the endothelial cells. The forearm vascular responses to the endothelium-dependent agents acetylch;oline (7.5, 15, and 30 mu g/min) and substance P (1, 2, and 4 pmol/min), and to the direct smooth muscle dilator sodium nitroprusside (0.8, 1.6, and 3.2 mu g/min) were studied in 16 hypercholesterolemic patients (8 men and 8 women; age [mean +/- SD] 50 +/- 7 years; serum cholesterol >250 mg/dl) and 16 normal volunteers (8 men and 8 women; age 47 +/- 8 years; serum cholesterol <200 mg/dl). Drugs were infused into the brachial artery and the response of the forearm vasculature was measured by strain-gauge plethysmography. The vasodilator response to acetylcholine was reduced in hypercholesterolemic patients compared with normal controls; at the highest dose (30 mu g/min) tile increase in forearm blood flow was 13.5 +/- 7 ml/min/100 mt in controls and 7.54 +/- 6 in patients (p <0.05). The response to substance P was also blunted in hypercholesterolemic patients; at the highest dose (4 pmol/min), the increase in forearm blood flow was 12.1 +/- 5 ml/ min/100 ml in controls and 7.6 + 4 in patients (p <0.03). A significant correlation was found between the highest blood flow responses with acetylcholine and with substance P (r = 0.58; p <0.001). No difference was found between the 2 groups in their response to sodium nitroprusside. These findings indicate that impaired endothelium-dependent vasodilation in hypercholesterolemia is not due to an isolated defect of the muscarinic receptor, and suggest either a more generalized endothelial abnormality or a defect in the final common pathway that regulates the endothelial modulation of vascular tone. C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 27 TC 69 Z9 71 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD JAN 1 PY 1995 VL 75 IS 1 BP 40 EP 44 DI 10.1016/S0002-9149(99)80524-4 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA PY937 UT WOS:A1995PY93700009 PM 7528464 ER PT J AU DENG, QS FANG, ZC YIN, Y AF DENG, QS FANG, ZC YIN, Y TI IONIC MECHANISM OF ACUPUNCTURE ON IMPROVEMENT OF LEARNING AND MEMORY IN AGED MAMMALS SO AMERICAN JOURNAL OF CHINESE MEDICINE LA English DT Article AB Memory impairment is one of the most frustrating problems for older people. Several acupoints were used for the treatment of memory loss in old rats, and the elemental mechanism of acupuncture therapy was studied with Inductively Coupled Plasma Spectroscopy. The result indicates that acupuncture improves learning and memory ability significantly in aged animals when compared with controls. This study demonstrated that elevations of eight essential elements (B, Ca, Cu, Fe, K, Mg, Na, and P) in the brain are the ionic basis for the therapeutic effect of acupuncture. A hypothetical model of the mechanism of acupuncture therapy is described. RP DENG, QS (reprint author), NIH,NEUROSCI LAB,BLDG 10,RM 6C-103,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 8 U1 0 U2 0 PU INST ADV RES ASIAN SCI & MED PI CHESTNUT HILL PA PO BOX 67336, CHESTNUT HILL, MA 02167 SN 0192-415X J9 AM J CHINESE MED JI Am. J. Chin. Med. PY 1995 VL 23 IS 1 BP 1 EP 9 DI 10.1142/S0192415X9500002X PG 9 WC Integrative & Complementary Medicine; Medicine, General & Internal SC Integrative & Complementary Medicine; General & Internal Medicine GA QR103 UT WOS:A1995QR10300001 PM 7598086 ER PT J AU KANT, AK GRAUBARD, BI SCHATZKIN, A BALLARDBARBASH, R AF KANT, AK GRAUBARD, BI SCHATZKIN, A BALLARDBARBASH, R TI PROPORTION OF ENERGY-INTAKE FROM FAT AND SUBSEQUENT WEIGHT CHANGE IN THE NHANES-I EPIDEMIOLOGIC FOLLOW-UP-STUDY SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE BODY WEIGHT; DIETARY FAT; OBESITY; NHANES I; NHEFS; WEIGHT CHANGE; DIET COMPOSITION; NUTRITION SURVEYS; ENERGY REQUIREMENTS ID MIDDLE-AGED MEN; DIETARY-FAT; BODY-WEIGHT; NATIONAL-HEALTH; FOOD-INTAKE; WOMEN; NUTRITION; OBESITY; COHORT; ADULTS AB We examined the association of percent energy intake from fat with subsequent weight change in 2580 men and 4567 women, using data from the National Health and Nutrition Examination Survey (NHANES)I Epidemiologic Follow-up Study (NHEFS). Weight change was defined as the difference between the follow-up weight (NHEFS, 1982-1984) and the baseline weight (NHANES I, 1971-1974). Fat intake was estimated from a 24-h dietary recall obtained at baseline. Regression analyses adjusted for potential confounders showed no significant association of percent fat energy with weight change in men. Among women aged <50 y, the inverse relation of percent fat energy with weight change was significant (beta = -0.052, P = 0.04). After exclusion of respondents with any morbidity from the analytic cohort, percent fat energy and weight change were positively associated in men (beta = 0.046, P = 0.05), but not in women. In conclusion, percent fat energy intake and weight change were inversely related in women aged <50 y in the NHEFS cohort, but positively associated in men without any morbidity. C1 NCI,BETHESDA,MD. RP KANT, AK (reprint author), CUNY QUEENS COLL,REMSEN HALL,ROOM 306E,65-30 KISSENA BLVD,FLUSHING,NY 11367, USA. NR 32 TC 58 Z9 61 U1 0 U2 1 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1995 VL 61 IS 1 BP 11 EP 17 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QA888 UT WOS:A1995QA88800002 PM 7825520 ER PT J AU OSGANIAN, SK NICKLAS, T STONE, E NICHAMAN, M EBZERY, MK LYTLE, L NADER, PR AF OSGANIAN, SK NICKLAS, T STONE, E NICHAMAN, M EBZERY, MK LYTLE, L NADER, PR TI PERSPECTIVES ON THE SCHOOL NUTRITION DIETARY ASSESSMENT STUDY FROM THE CHILD AND ADOLESCENT TRIAL FOR CARDIOVASCULAR HEALTH SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE NATIONAL SCHOOL LUNCH PROGRAM; SCHOOL BREAKFAST PROGRAM; CHILD AND ADOLESCENT TRIAL FOR CARDIOVASCULAR HEALTH; CATCH ID CORONARY HEART-DISEASE; RISK-FACTORS AB The School Nutrition Dietary Assessment Study provides current data on the nutritional quality and adequacy of the National School Lunch Program (NSLP) and the School Breakfast Program (SBP) as well as on the dietary intakes of students participating in these programs. The study demonstrates that the NSLP and SBP meals and children's total diets do not conform to the recommendations of the US Department of Agriculture and the National Research Council and confirms the need to improve the nutritional quality of the nation's school meal program and student's overall dietary intakes. In this regard, the Child and Adolescent Trial for Cardiovascular Health (CATCH) is the first collaborative, school-based field trial that tests the effectiveness of a multilevel intervention designed to reduce the fat, saturated fat, and sodium content of school meals and student's diets. This commentary highlights the findings and questions raised by the School Nutrition Dietary Assessment Study and presents an overview of CATCH, including the implications and significant questions that can be addressed by this intervention study. C1 TULANE UNIV, SCH PUBL HLTH & TROP MED, NEW ORLEANS, LA 70118 USA. NHLBI, BETHESDA, MD 20892 USA. UNIV TEXAS, HLTH SCI CTR, HOUSTON, TX USA. UNIV MINNESOTA, MINNEAPOLIS, MN 55455 USA. UNIV CALIF SAN DIEGO, SAN DIEGO, CA 92103 USA. RP OSGANIAN, SK (reprint author), NEW ENGLAND RES INST, 9 GALEN ST, WATERTOWN, MA 02172 USA. FU NHLBI NIH HHS [U01-HL-39852, U01-HL-39880, U01-HL-39906] NR 28 TC 8 Z9 8 U1 0 U2 1 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JAN PY 1995 VL 61 IS 1 SU S BP 241S EP 244S PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QB956 UT WOS:A1995QB95600010 PM 7832171 ER PT J AU COVI, L HESS, JM KREITER, NA HAERTZEN, CA AF COVI, L HESS, JM KREITER, NA HAERTZEN, CA TI EFFECTS OF COMBINED FLUOXETINE AND COUNSELING IN THE OUTPATIENT TREATMENT OF COCAINE ABUSERS SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article; Proceedings Paper CT 55th Annual Scientific Meeting of the College-on-Problems-of-Drug-Dependence CY JUN 16-17, 1993 CL TORONTO, CANADA SP Coll Problems Drug Dependence ID PLASMA-CONCENTRATIONS; ADDICTION; PSYCHOTHERAPY; DESIPRAMINE; DEPENDENCE; URGES; RATS AB Three methods of analysis were used to determine the effects of the combination of counseling with fluoxetine (20, 40, or 60 mg) and ''active'' placebo (diphenhydramine, 12.5 mg) randomly assigned. Forty-five cocaine-only dependent subjects were treated as outpatients with ''interpersonal'' counseling, medication, and drug use monitoring three times per week for up to 12 weeks. Treatment effects were analyzed: first, by comparing the three original assignments and placebo; second, by comparing the placebo group to fluoxetine subjects with detectable fluoxetine/norfluoxetine blood levels and those with no detectable medication blood level; third, by examining relapse prevention versus use cessation through stratifying the subjects into four groups according to fluoxetine or placebo assignment and initial urine cocaine positivity or negativity. All three analyses showed improvement on some measures over time regardless of group assignment. The 60-mg fluoxetine group showed least effectiveness, the group with detectable blood levels had less cravings, and the fluoxetine subjects who were abstinent at the start of treatment were somewhat less likely to avoid relapse than those on placebo. RP COVI, L (reprint author), NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 27 TC 65 Z9 65 U1 0 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 1995 VL 21 IS 3 BP 327 EP 344 DI 10.3109/00952999509002701 PG 18 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA RL986 UT WOS:A1995RL98600004 PM 7484983 ER PT J AU FRIEDMAN, AS GRANICK, S BRANSFIELD, S KREISHER, C KHALSA, J AF FRIEDMAN, AS GRANICK, S BRANSFIELD, S KREISHER, C KHALSA, J TI GENDER DIFFERENCES IN EARLY-LIFE RISK-FACTORS FOR SUBSTANCE USE ABUSE - A STUDY OF AN AFRICAN-AMERICAN SAMPLE SO AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE LA English DT Article ID DRUG-USE; ALCOHOLISM; BEHAVIOR AB Gender differences in risk and protective factors for substance use/abuse in early adulthood were studied. Comprehensive systematic data on African-American males (N = 318) and females (N = 322), from birth to 7 years of age, were available from the National Collaborative Perinatal Study. These subjects were retrieved for assessment at average age 24. There are more differences between males and females than there are similarities in regard to the early childhood variables that predict substance use in early adulthood. However, high activity and intensity of response during infancy (measured at 8 months of age) was found to predict later substance use for both males and females. This type of behavior is considered by us to be a trait of temperament and to suggest the possibility of a genetic predisposition. More risk factors were found for female than for males. The risk factors for females were primarily of two types: 1) Related to experiences with mother and with the family environment; and 2) Poor levels of intellectual functioning and academic performance, and abnormal mental status. C1 NIDA,DIV EPIDEMIOL & PREVENT RES,BETHESDA,MD. RP FRIEDMAN, AS (reprint author), BELMONT CTR COMPREHENS TREATMENT,RES CTR,4081 FORD RD,PHILADELPHIA,PA 19131, USA. FU NIDA NIH HHS [5-RO1-DA04414] NR 24 TC 7 Z9 7 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0095-2990 J9 AM J DRUG ALCOHOL AB JI Am. J. Drug Alcohol Abuse PY 1995 VL 21 IS 4 BP 511 EP 531 DI 10.3109/00952999509002713 PG 21 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA RZ482 UT WOS:A1995RZ48200006 PM 8561100 ER PT J AU ORNATO, JP ATKINS, JM HORAN, M MURRAY, J RAMZY, AJ RODRIGUE, RB SHADE, B BRADLEY, JC HAND, MM AF ORNATO, JP ATKINS, JM HORAN, M MURRAY, J RAMZY, AJ RODRIGUE, RB SHADE, B BRADLEY, JC HAND, MM TI STAFFING AND EQUIPPING EMERGENCY MEDICAL-SERVICES SYSTEMS - RAPID IDENTIFICATION AND TREATMENT OF ACUTE MYOCARDIAL-INFARCTION SO AMERICAN JOURNAL OF EMERGENCY MEDICINE LA English DT Review DE MYOCARDIAL INFARCTION; CARDIOPULMONARY RESUSCITATION; ELECTRIC DEFIBRILLATION; CARDIAC ARREST; EMERGENCY MEDICAL SERVICES; EMERGENCY MEDICAL TECHNICIANS; PARAMEDIC; AMBULANCES; THROMBOLYTIC THERAPY; ELECTROCARDIOGRAPHY AB Each year, about 1,250,000 people in the United States experience an acute myocardial infarction (AMI). Emergency medical services (EMS) systems play a key part in the prehospital care and transportation of AMI patients. Rapid, state-of-the-art treatment by EMS personnel is essential for improving AMI survival and outcomes, as dramatized by the patient who is the victim of out-of-hospital cardiac arrest. In order to improve the prehospital care provided to AMI patients, this article by the Access to Care Subcommittee of the National Heart Attack Alert Program Coordinating Committee makes a number of recommendations regarding the staffing and equipping of EMS systems. The recommendations cover the ''chain of survival'' concept, universal and enhanced 9-1-1, emergency medical dispatching, ground ambulance specifications, automated external defibrillators, advanced life support coverage, medical direction, 12-lead electrocardiograms, and prehospital thrombolysis. C1 NHLBI,NATL HEART ATTACK ALERT PROGRAM,31 CTR DR,MSC 2480,ROOM 4A18,BETHESDA,MD 20892. NR 0 TC 24 Z9 24 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0735-6757 J9 AM J EMERG MED JI Am. J. Emerg. Med. PD JAN PY 1995 VL 13 IS 1 BP 58 EP 66 PG 9 WC Emergency Medicine SC Emergency Medicine GA QE698 UT WOS:A1995QE69800017 ER PT J AU CLAWSON, JJ ATKINS, JM FRANCIS, CK GLASS, C HURTADO, F RYAN, S SCOTT, J BRADLEY, JC HAND, MM HORAN, M AF CLAWSON, JJ ATKINS, JM FRANCIS, CK GLASS, C HURTADO, F RYAN, S SCOTT, J BRADLEY, JC HAND, MM HORAN, M TI EMERGENCY MEDICAL DISPATCHING - RAPID IDENTIFICATION AND TREATMENT OF ACUTE MYOCARDIAL-INFARCTION SO AMERICAN JOURNAL OF EMERGENCY MEDICINE LA English DT Review DE EMERGENCY MEDICAL SERVICES; EMS COMMUNICATION SYSTEMS; MYOCARDIAL INFARCTION; CARDIOPULMONARY RESUSCITATION AB Emergency medical telephone calls (ie, those made to 9-1 or 7-digit emergency numbers) are directed to emergency medical dispatchers (EMDs) who are responsible for quickly obtaining critical pieces of information from the caller, then activating an appropriate level of emergency medical services (EMS) response and providing the caller with patient care instructions until medical help arrives. The impact of well-trained, medically managed EMDs on the early care of potential acute myocardial infarction (AMI) patients is believed to be beneficial. However standards for emergency medical dispatching vary widely across the nation. To improve emergency medical dispatching for AMI patients in the United States, this article by the Acces to Care Subcommittee on behalf of the National Heart Attack Alert Program makes a number of recommendations regarding the use of medical dispatch protocols, provision of dispatch life support, EMD training, EMD certification, and emergency medical dispatch quality control and improvement processes. (C) 1995 by W.B. Saunders Company) C1 NHLBI,NATL HEART ATTACK ALERT PROGRAM,31 CTR DR,MSC 2480,BETHESDA,MD 20892. NR 0 TC 25 Z9 26 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0735-6757 J9 AM J EMERG MED JI Am. J. Emerg. Med. PD JAN PY 1995 VL 13 IS 1 BP 67 EP 73 PG 7 WC Emergency Medicine SC Emergency Medicine GA QE698 UT WOS:A1995QE69800018 ER PT J AU CHILCOAT, HD DISHION, TJ ANTHONY, JC AF CHILCOAT, HD DISHION, TJ ANTHONY, JC TI PARENT MONITORING AND THE INCIDENCE OF DRUG SAMPLING IN URBAN ELEMENTARY-SCHOOL-CHILDREN SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE CHILD; PARENTING; SUBSTANCE ABUSE ID SUBSTANCE USE; ADOLESCENCE; PREDICTORS; BEHAVIORS; STUDENTS AB An epidemiologic study of urban-dwelling children aged 8-10 years in Baltimore, Maryland, was undertaken to test the hypothesis that close monitoring and supervision by parents might signal a reduced risk of drug use in the elementary school years. Drug use, monitoring by parents, peer drug use, and other suspected risk factors for early drug use were first assessed in 1989, identifying 947 children with no prior history of drug use. One year later, 4.2 percent of these children were found to have started using alcohol, tobacco, or other drugs on their own for the first time during the follow-up observation interval. Risk of starting drug use was higher for children with lower levels of parent monitoring (relative risk = 4.39, 95% confidence interval 1.48-13.0). In addition, for children with declining levels of parent monitoring, there was an increased risk of starting to use drugs on their own. C1 NIDA,ADDICT RES CTR,ETIOL BRANCH,BALTIMORE,MD 21224. OREGON SOCIAL LEARNING CTR,EUGENE,OR 97401. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MENTAL HYG,BALTIMORE,MD. FU NIDA NIH HHS [DA04392]; NIMH NIH HHS [P50 MH38752, T32 MH14592] NR 21 TC 109 Z9 109 U1 2 U2 3 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JAN 1 PY 1995 VL 141 IS 1 BP 25 EP 31 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QA339 UT WOS:A1995QA33900006 PM 7801962 ER PT J AU BALLARDBARBASH, R KREBSSMITH, S SUBAR, AF AF BALLARDBARBASH, R KREBSSMITH, S SUBAR, AF TI VEGETABLES, FRUIT AND COLON-CANCER IN THE IOWA WOMENS HEALTH STUDY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter RP BALLARDBARBASH, R (reprint author), NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,BETHESDA,MD 20892, USA. NR 3 TC 1 Z9 1 U1 0 U2 2 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JAN 1 PY 1995 VL 141 IS 1 BP 84 EP 85 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QA339 UT WOS:A1995QA33900015 PM 7801971 ER PT J AU TELL, GS EVANS, GW SHIMAKAWA, T FOLSOM, AR CARPENTER, MA HEISS, G AF TELL, GS EVANS, GW SHIMAKAWA, T FOLSOM, AR CARPENTER, MA HEISS, G TI DIETARY-FAT INTAKE AND CAROTID-ARTERY WALL THICKNESS - THE ATHEROSCLEROSIS RISK IN COMMUNITIES (ARIC) STUDY - REPLY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter C1 NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20894. UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55454. UNIV N CAROLINA,SCH PUBL HLTH,DEPT BIOSTAT,CHAPEL HILL,NC 27599. UNIV N CAROLINA,SCH PUBL HLTH,DEPT EPIDEMIOL,CHAPEL HILL,NC 27599. RP TELL, GS (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,300 S HAWTHORNE RD,WINSTON SALEM,NC 27157, USA. RI Tell, Grethe/G-5639-2015 OI Tell, Grethe/0000-0003-1386-1638 NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JAN 1 PY 1995 VL 141 IS 1 BP 84 EP 84 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QA339 UT WOS:A1995QA33900014 ER PT J AU HIRUMA, H NOGUCHI, CT UYESAKA, N HASEGAWA, S BLANCHETTEMACKIE, EJ SCHECHTER, AN RODGERS, GP AF HIRUMA, H NOGUCHI, CT UYESAKA, N HASEGAWA, S BLANCHETTEMACKIE, EJ SCHECHTER, AN RODGERS, GP TI SICKLE-CELL RHEOLOGY IS DETERMINED BY POLYMER FRACTION - NOT CELL MORPHOLOGY SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE SICKLE CELL DISEASE; INTRACELLULAR SICKLE HEMOGLOBIN; POLYMER FRACTION ID HEMOGLOBIN POLYMERIZATION; INTRACELLULAR POLYMERIZATION; ERYTHROCYTES; DEFORMABILITY; MEMBRANE; DISEASE; DEOXYGENATION; BLOOD; HETEROGENEITY; FILTRATION AB Sickle cell disease pathophysiology is mediated by acute and chronic impairment of cell flexibility due to the formation of intracellular sickle hemoglobin (Hb S) polymer as cells are partially deoxygenated in the microcirculation. We have recently developed a method to measure the relationship between the formation of intracellular polymerized Hb S and cell filtration. In this study, we have used this method to examine whether sickle cell morphology, independent of Hb S polymer fraction, had an effect on cell theology, We primarily use sickle trait (AS) and Hb S-beta(+)-thalassemia (S-beta(+)-thal) erythrocytes with low hemoglobin F levels, which have normal membranes and few or no dense cells, to remove these confounding effects. We find that the relationship between filtration and the percentages of each ''type'' of morphological deformation of AS erythrocytes was different from that of the S-beta(+)-thal erythrocytes. In addition, we find that white the filtration of AS erythrocytes as a function of oxygen saturation was similar, whether measured during deoxygenation or reoxygenation, the relationship between the percentages of each type of deformed erythrocyte and oxygen saturation demonstrated hysteresis during oxygenation-deoxygenation experiments. Transmission electron microscopy, for both elongated and irregularly shaped cells, showed that similarly distorted cells could have very different amounts and alignment of polymer. These results suggests that cell morphology per se is not strongly related to filtration, whereas calculated intracellular Hb S polymer fraction predicts loss of filtration of AS and S-beta(+)-thal erythrocytes well. Measured or calculated polymer fraction values would appear to be a better parameter for the study of sickle cell disease pathophysiology and response to treatment than cell morphology studies. (C) 1995 Wiley-Liss, Inc.* C1 NIDDKD,BIOL CHEM LAB,BETHESDA,MD 20892. NIDDKD,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. NIPPON MED COLL,DEPT PHYSIOL,TOKYO,JAPAN. OI Schechter, Alan N/0000-0002-5235-9408 NR 41 TC 14 Z9 15 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 1995 VL 48 IS 1 BP 19 EP 28 DI 10.1002/ajh.2830480105 PG 10 WC Hematology SC Hematology GA QE290 UT WOS:A1995QE29000004 PM 7832188 ER PT J AU KAPLAN, NL HILL, WG WEIR, BS AF KAPLAN, NL HILL, WG WEIR, BS TI LIKELIHOOD METHODS FOR LOCATING DISEASE GENES IN NONEQUILIBRIUM POPULATIONS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID CYSTIC-FIBROSIS LOCUS; LINKAGE DISEQUILIBRIUM; FRIEDREICH ATAXIA; HUNTINGTONS-DISEASE; NONUNIFORM RECOMBINATION; EXTENDED HAPLOTYPES; ITALIAN FAMILIES; REGION; POLYMORPHISMS; LOCALIZATION AB Until recently, attempts to map disease genes on the basis of population associations with linked markers have been based on expected values of linkage disequilibrium. These methods suffer from the large variances imposed on disequilibrium measures by the evolutionary process, but a more serious problem for many diseases is that they assume an equilibrium population. For diseases that arose only a few hundred generations ago, it is more appropriate to concentrate on the initial growth phase of the disease. We invoke a Poisson branching process for this early growth, and estimate the likelihood for the recombination fraction between marker and disease loci, on the basis of simulated disease populations. The limits of the resulting support intervals for the recombination fraction vary inversely with the age of the disease in generations. We illustrate the procedure with data on cystic fibrosis and diastrophic dysplasia, for which the method appears appropriate, and for Friedreich ataxia and Huntington disease, for which it does not. A valuable aspect of the method is the ability in some cases to compare likelihoods of the three orders for a disease locus and two linked marker loci. C1 N CAROLINA STATE UNIV, DEPT STAT, PROGRAM STAT GENET, RALEIGH, NC 27695 USA. NIEHS, STAT & BIOMATH BRANCH, RES TRIANGLE PK, NC 27709 USA. UNIV EDINBURGH, INST CELL ANIM & POPULAT BIOL, EDINBURGH, MIDLOTHIAN, SCOTLAND. FU NIGMS NIH HHS [GM45344] NR 43 TC 127 Z9 128 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JAN PY 1995 VL 56 IS 1 BP 18 EP 32 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA QC101 UT WOS:A1995QC10100004 PM 7825575 ER PT J AU LALWANI, AK BRISTER, JR FEX, J GRUNDFAST, KM PLOPLIS, B SANAGUSTIN, TB WILCOX, ER AF LALWANI, AK BRISTER, JR FEX, J GRUNDFAST, KM PLOPLIS, B SANAGUSTIN, TB WILCOX, ER TI FURTHER ELUCIDATION OF THE GENOMIC STRUCTURE OF PAX3, AND IDENTIFICATION OF 2 DIFFERENT POINT MUTATIONS WITHIN THE PAX3 HOMEOBOX THAT CAUSE WAARDENBURG SYNDROME TYPE-I IN 2 FAMILIES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID TUMOR ALVEOLAR RHABDOMYOSARCOMA; MAGNETIC-RESONANCE SPECTROSCOPY; HOMEODOMAIN-DNA INTERACTIONS; HUP2 PAIRED DOMAIN; MOUSE MUTANT; CRYSTAL-STRUCTURE; BINDING DOMAIN; HUMAN HOMOLOG; BOX GENE; DROSOPHILA AB Waardenburg syndrome is an autosomal dominant disorder characterized by sensorineural deafness and pigmentary disturbances. Previous work has linked the disease to PAX3 on chromosome 2, and several mutations within the highly conserved paired-box and octapeptide motifs, but not the homeobox, have been reported. In this report, we have used the published cDNA sequence to further define the genomic structure of PAX3, using inverse PCR. We have identified exon/intron boundaries between exons 5 and 6 and between exons 6 and 7. Further, we have identified the first two mutations within the homeobox in two different families with type 1 Waardenburg syndrome. The first is a point mutation (G-->T) at the first base of exon 6, which substitutes phenylalanine for valine. In another family, we have identified a point mutation (C-->G) within the homeobox, in exon 6, which substitutes a glycine for arginine at a highly conserved site. The homeodomain is important in binding of DNA and in effecting transcriptional control. These mutations likely result in structural change within the homeodomain that either change the DNA-binding specificity of the homeodomain or reduce the affinity of the PAX3 protein for DNA. These homeodomain mutations should aid in elucidating the role of the homeodomain in the function of the PAX3 protein. C1 NIDOCD,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 46 TC 45 Z9 46 U1 0 U2 1 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 1995 VL 56 IS 1 BP 75 EP 83 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA QC101 UT WOS:A1995QC10100010 PM 7825605 ER PT J AU RABEN, N EXELBERT, R SPIEGEL, R SHERMAN, JB NAKAJIMA, H PLOTZ, P HEINISCH, J AF RABEN, N EXELBERT, R SPIEGEL, R SHERMAN, JB NAKAJIMA, H PLOTZ, P HEINISCH, J TI FUNCTIONAL EXPRESSION OF HUMAN MUTANT PHOSPHOFRUCTOKINASE IN YEAST - GENETIC-DEFECTS IN FRENCH-CANADIAN AND SWISS PATIENTS WITH PHOSPHOFRUCTOKINASE DEFICIENCY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID RABBIT MUSCLE PHOSPHOFRUCTOKINASE; GRADIENT GEL-ELECTROPHORESIS; HEMOPHILIA-B; REGION; SUBSTITUTIONS; ASSIGNMENT; PROMOTER; ISOZYMES; MUTATION; CLONING AB Human phosphofructokinase (PFK) is a tetrameric enzyme, encoded by muscle, liver, and platelet genes. Deficiency of muscle PFK (PFK-M), glycogenosis type VII (Tarui disease), is an autosomal recessive disorder characterized by an exertional myopathy and hemolytic syndrome. Several disease-causing mutations have been identified in the PFK-M gene in Japanese, Ashkenazi Jewish, and Italian patients. We describe the genetic defects in French Canadian and Swiss patients with the disease, and we use a genetically well-defined yeast system devoid of endogenous PFK for structure-function studies of the mutant PFKs. A G-to-A transition at codon 209-in exon 8 of the PFK-M gene, changing an encoded Gly to Asp, is responsible for the disease in a homozygous French Canadian patient. Gly-209-mutated protein is completely inactive in the yeast system. The Swiss patient is a genetic compound, carrying a G-to-A transition at codon 100 in exon 6 (Arg to Gin) and a G-to-A transition at codon 696 in exon 22 (Arg to His). The mutants expressed in yeast generate functional enzyme with modest changes in thermal stability. The advantages and limitations of the yeast system for expression of human mutant PFKs are discussed. C1 UNIV ZURICH,INST MED GENET,ZURICH,SWITZERLAND. OSAKA UNIV,SCH MED,DEPT INTERNAL MED 2,SUITA,OSAKA 565,JAPAN. INST MICROBIOL,DUSSELDORF,GERMANY. RP RABEN, N (reprint author), NIAMSD,ARTHRITIS & RHEUMATISM BRANCH,10-9N244,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 49 TC 46 Z9 48 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 1995 VL 56 IS 1 BP 131 EP 141 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA QC101 UT WOS:A1995QC10100017 PM 7825568 ER PT J AU NAROD, SA FORD, D DEVILEE, P BARKARDOTTIR, RB LYNCH, HT SMITH, SA PONDER, BAJ WEBER, BL GARBER, JE BIRCH, JM CORNELIS, RS KELSELL, DP SPURR, NK SMYTH, E HAITES, N SOBOL, H BIGNON, YJ CHANGCLAUDE, J HAMANN, U LINDBLOM, A BORG, A PIVER, MS GALLION, HH STRUEWING, JP WHITTEMORE, A TONIN, P GOLDGAR, DE EASTON, DF MILNER, B ALLAN, L SIMARD, J ROMMENS, J MCGILLIVRAY, B GREEN, R IVES, E BOYD, N ROSEN, B COLE, D MORGAN, K MOSLEHI, R PONDER, B PETO, J SMITH, S STRATTON, M DICIOCCIO, RA GALLION, H SANTIBANEZKOREF, MS TEARE, MD EVANS, DG STOPPALYONNET, D LALLE, P BONAITI, C ESSIOUX, L GIRODET, C MAUGARDLOUBOUTIN, C NICOLLEAU, G LONGY, M TOULOUSE, C HORSTEIN, I BIRNBAUM, D EISINGER, F KARENGUEVEN, F NOGUCHI, T HARDOUIN, A RIO, P MACHELARDROUMAGNAC, M NOGUES, C COHENHAGUENAUER, O LORTHOLARY, A BAY, JO ARASON, A BARKDARDOTTIR, RB EGILSSON, V BISHOP, DT KELSELL, D MURDAY, VA SOLOMON, E SPURR, N TURNER, G LENOIR, G FEUNTEUN, J LYNCH, H LYNCH, J WATSON, P CONWAY, T BONNARDEL, C SEROVA, O TORCHARD, D LARSSON, C VASEN, H VANLEEUWEN, I CORNELISSE, CJ STEEL, M PORTER, D COHEN, BB CAROTHERS, A CANNONALBRIGHT, LA GOLDGAR, D SKOLNICK, M BECHER, H JOHANNSSON, O WEBER, B COLLINS, F BOEHNKE, M GARBER, J LI, F AF NAROD, SA FORD, D DEVILEE, P BARKARDOTTIR, RB LYNCH, HT SMITH, SA PONDER, BAJ WEBER, BL GARBER, JE BIRCH, JM CORNELIS, RS KELSELL, DP SPURR, NK SMYTH, E HAITES, N SOBOL, H BIGNON, YJ CHANGCLAUDE, J HAMANN, U LINDBLOM, A BORG, A PIVER, MS GALLION, HH STRUEWING, JP WHITTEMORE, A TONIN, P GOLDGAR, DE EASTON, DF MILNER, B ALLAN, L SIMARD, J ROMMENS, J MCGILLIVRAY, B GREEN, R IVES, E BOYD, N ROSEN, B COLE, D MORGAN, K MOSLEHI, R PONDER, B PETO, J SMITH, S STRATTON, M DICIOCCIO, RA GALLION, H SANTIBANEZKOREF, MS TEARE, MD EVANS, DG STOPPALYONNET, D LALLE, P BONAITI, C ESSIOUX, L GIRODET, C MAUGARDLOUBOUTIN, C NICOLLEAU, G LONGY, M TOULOUSE, C HORSTEIN, I BIRNBAUM, D EISINGER, F KARENGUEVEN, F NOGUCHI, T HARDOUIN, A RIO, P MACHELARDROUMAGNAC, M NOGUES, C COHENHAGUENAUER, O LORTHOLARY, A BAY, JO ARASON, A BARKDARDOTTIR, RB EGILSSON, V BISHOP, DT KELSELL, D MURDAY, VA SOLOMON, E SPURR, N TURNER, G LENOIR, G FEUNTEUN, J LYNCH, H LYNCH, J WATSON, P CONWAY, T BONNARDEL, C SEROVA, O TORCHARD, D LARSSON, C VASEN, H VANLEEUWEN, I CORNELISSE, CJ STEEL, M PORTER, D COHEN, BB CAROTHERS, A CANNONALBRIGHT, LA GOLDGAR, D SKOLNICK, M BECHER, H JOHANNSSON, O WEBER, B COLLINS, F BOEHNKE, M GARBER, J LI, F TI AN EVALUATION OF GENETIC-HETEROGENEITY IN 145 BREAST-CANCER OVARIAN-CANCER FAMILIES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID BRCA1 REGION; ALLELE LOSS; CHROMOSOME-17Q21; SUSCEPTIBILITY; LINKAGE; ONSET; MAPS; INTERVAL; MARKERS; RISKS AB The breast-ovary cancer-family syndrome is a dominant predisposition to cancer of the breast and ovaries which has been mapped to chromosome region 17q12-q21. The majority, but not all, of breast-ovary cancer families show linkage to this susceptibility locus, designated BRCA1. We report here the results of a linkage analysis of 145 families with both breast and ovarian cancer. These families contain either a total of three or more cases of early-onset (before age 60 years) breast cancer or ovarian cancer. All families contained at least one case of ovarian cancer, Overall, an estimated 76% of the 145 families are linked to the BRCA1 locus. None of 13 families with cases of male breast cancer appear to be linked, but it is estimated that 92% (95% confidence interval 76%-100%) of families with no male breast cancer and with two or more ovarian cancers are linked to BRCA1. These data suggest that the breast-ovarian cancer-family syndrome is genetically heterogeneous. However, the large majority of families with early-onset breast cancer and with two or more cases of ovarian cancer are likely to be due to BRCA1 mutations. C1 MCGILL UNIV,DEPT MED,DIV MED GENET,MONTREAL,PQ,CANADA. MCGILL UNIV,DEPT HUMAN GENET,MONTREAL,PQ,CANADA. INST CANC RES,EPIDEMIOL SECT,SUTTON,SURREY,ENGLAND. LEIDEN UNIV,DEPT PATHOL,LEIDEN,NETHERLANDS. LEIDEN UNIV,DEPT HUMAN GENET,LEIDEN,NETHERLANDS. UNIV HOSP ICELAND,DEPT PATHOL,REYKJAVIK,ICELAND. CREIGHTON UNIV,SCH MED,DEPT PREVENT MED & PUBL HLTH,OMAHA,NE 68178. UNIV CAMBRIDGE,DEPT PATHOL,HUMAN CANC GENET RES GRP,CANC RES CAMPAIGN,CAMBRIDGE,ENGLAND. UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,ANN ARBOR,MI. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MANCHESTER,PEDIAT & FAMILIAL CANC RES GRP,CANC RES CAMPAIGN,MANCHESTER,LANCS,ENGLAND. IMPERIAL CANC RES FUND,HUMAN GENET RESOURCES LAB,POTTERS BAR,HERTS,ENGLAND. WESTERN GEN HOSP,HUMAN GENET UNIT,MRC,EDINBURGH,MIDLOTHIAN,SCOTLAND. UNIV ABERDEEN,DEPT MOLEC & CELL BIOL,ABERDEEN,SCOTLAND. INST J PAOLI I CALMETTES,DEPT ONCOL GENET,MARSEILLE,FRANCE. CTR JEAN PERRIN,MOLEC ONCOL LAB,CLERMONT FERRAND,FRANCE. GERMAN CANC RES CTR,DIV EPIDEMIOL,HEIDELBERG,GERMANY. KAROLINSKA HOSP,DEPT CLIN GENET,S-10401 STOCKHOLM,SWEDEN. UNIV LUND HOSP,LUND,SWEDEN. ROSWELL PK CANC INST,BUFFALO,NY. NIH,GENET EPIDEMIOL BRANCH,BETHESDA,MD. STANFORD UNIV,SCH MED,DIV EPIDEMIOL,STANFORD,CA. UNIV UTAH,GENET EPIDEMIOL GRP,SALT LAKE CITY,UT. RI Struewing, Jeffery/C-3221-2008; Struewing, Jeffery/I-7502-2013 OI Struewing, Jeffery/0000-0002-4848-3334 NR 39 TC 242 Z9 243 U1 1 U2 6 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 1995 VL 56 IS 1 BP 254 EP 264 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA QC101 UT WOS:A1995QC10100033 PM 7825586 ER PT J AU JACOBSON, HR STRIKER, GE AF JACOBSON, HR STRIKER, GE TI REPORT ON A WORKSHOP TO DEVELOP MANAGEMENT RECOMMENDATIONS FOR THE PREVENTION OF PROGRESSION IN CHRONIC RENAL-DISEASE SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Editorial Material C1 NIDDKD,DIV KIDNEY UROL & HEMATOL DIS,BETHESDA,MD 20892. NR 4 TC 56 Z9 56 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 1995 VL 25 IS 1 BP 103 EP 106 DI 10.1016/0272-6386(95)90635-5 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA QA345 UT WOS:A1995QA34500020 PM 7810515 ER PT J AU BENNETT, PH HAFFNER, S KASISKE, BL KEANE, WF MOGENSEN, CE PARVING, HH STEFFES, MW STRIKER, GE AF BENNETT, PH HAFFNER, S KASISKE, BL KEANE, WF MOGENSEN, CE PARVING, HH STEFFES, MW STRIKER, GE TI SCREENING AND MANAGEMENT OF MICROALBUMINURIA IN PATIENTS WITH DIABETES-MELLITUS - RECOMMENDATIONS TO THE SCIENTIFIC-ADVISORY-BOARD OF THE NATIONAL-KIDNEY-FOUNDATION FROM AN AD-HOC-COMMITTEE OF THE COUNCIL-ON DIABETES-MELLITUS OF THE NATIONAL-KIDNEY-FOUNDATION SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE NEPHROPATHY; KIDNEY DISEASE; ALBUMINURIA; PROTEINURIA AB All individuals with diabetes mellitus should be screened yearly with a spot urine albumin:creatinine ratio to identify those who are at increased risk for the development of complications of diabetes mellitus, including nephropathy, retinopathy, and cardiovascular disease. Once these high-risk individuals are appropriately identified, it is recommended that therapy with an angiotensin-converting enzyme (ACE) inhibitor be initiated. In addition, cardiovascular risk factors should be investigated, and when appropriate, therapeutic interventions should be initiated according to existing recommendations. (C) 1995 by the National Kidney Foundation, Inc. C1 UNIV MINNESOTA,SCH MED,HENNEPIN CTY MED CTR,DEPT MED,DIV NEPHROL,MINNEAPOLIS,MN 55415. NIDDKD,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AARHUS UNIV HOSP,DK-8000 AARHUS,DENMARK. STENO DIABET CTR,COPENHAGEN,DENMARK. UNIV MINNESOTA HOSP & CLIN,MINNEAPOLIS,MN. NR 7 TC 254 Z9 261 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 1995 VL 25 IS 1 BP 107 EP 112 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA QA345 UT WOS:A1995QA34500021 PM 7810516 ER PT J AU AGODOA, LY EGGERS, PW AF AGODOA, LY EGGERS, PW TI RENAL REPLACEMENT THERAPY IN THE UNITED-STATES - DATA FROM THE UNITED-STATES RENAL DATA SYSTEM SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article; Proceedings Paper CT Symposium on Renal Replacement Therapy Throughout the World - The Registries CY DEC 09-11, 1993 CL MILAN, ITALY DE RENAL REGISTRIES; UNITED STATES RENAL DATA SYSTEM; END-STAGE RENAL DISEASE; RENAL REPLACEMENT THERAPY; INCIDENCE; PREVALENCE; MORBIDITY; MORTALITY; SURVIVAL; HEMODIALYSIS; CONTINUOUS AMBULATORY PERITONEAL DIALYSIS ID DIALYSIS; FAILURE AB This report is a summary of the discussion on the United States Renal Data System and its data contents, as presented at the Symposium on World Renal Registries on December 10, 1993, The United States Renal Data System is a national database that collects and analyzes information on the incidence, prevalence, morbidity, and mortality, as well as the modalities of therapy of patients with end-stage renal disease (ESRD) in the United States. The database is funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health, Data on the patients are provided by the Health Care Financing Administration Medicare Program, The coordinating center for the database, operated through a contract mechanism, was formerly at the Urban Institute in Washington, DC, but is currently located at the University of Michigan, Ann Arbor, MI. The data system contains information on over 462,000 patients with more than 4 million dialysis records, 2.3 million inpatient records, 94,000 transplant reports, and more than 290,000 follow-up reports, The incidence rate of ESRD is approximately 180 per million population, However, the rate is higher in African-Americans (430) and Native Americans (281) than in whites (153) and Asian/Pacific Islanders (133). The gross mortality rate of the entire ESRD population is approximately 168 deaths per 1,000 patient-years at risk. The death rate is higher in diabetic than in nondiabetic ESRD patients. It is also higher in ESRD patients older than 65 years (357) than in patients in the 45- to 64-year-old age group (158) or those in the 20- to 44-year-old age group (62). (C) 1995 by the National Kidney Foundation, Inc. C1 HLTH CARE FINANCING ADM,OFF RES DEMONSTRAT,BALTIMORE,MD. RP AGODOA, LY (reprint author), NIDDK,DIV KIDNEY UROL & HEMATOL DIS,USRDS,WESTWOOD BLDG,ROOM 3A11,BETHESDA,MD 20892, USA. NR 12 TC 85 Z9 89 U1 0 U2 1 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 1995 VL 25 IS 1 BP 119 EP 133 DI 10.1016/0272-6386(95)90638-X PG 15 WC Urology & Nephrology SC Urology & Nephrology GA QA345 UT WOS:A1995QA34500023 PM 7810518 ER PT J AU MOUL, DE WEHR, TA FRANK, JA AF MOUL, DE WEHR, TA FRANK, JA TI POSSIBLE SEASONAL-CHANGES IN PITUITARY SIZE SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Letter C1 NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. NIH,OFF INTRAMURAL RES,DIAGNOST RADIOL RES LAB,BETHESDA,MD 20892. RP MOUL, DE (reprint author), NIMH,EPIDEMIOL & PSYCHOPATHOL RES BRANCH,ROCKVILLE,MD 20857, USA. NR 1 TC 4 Z9 4 U1 0 U2 1 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 PY 1995 VL 16 IS 1 BP 214 EP 215 PG 2 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA QB206 UT WOS:A1995QB20600038 PM 7900597 ER PT J AU SHIONO, PH KLEBANOFF, MA NUGENT, RP COTCH, MF WILKINS, DG ROLLINS, DE CAREY, JC BEHRMAN, RE AF SHIONO, PH KLEBANOFF, MA NUGENT, RP COTCH, MF WILKINS, DG ROLLINS, DE CAREY, JC BEHRMAN, RE TI THE IMPACT OF COCAINE AND MARIJUANA USE ON LOW-BIRTH-WEIGHT AND PRETERM BIRTH - A MULTICENTER STUDY SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE COCAINE; MARIJUANA; PREGNANCY; PRENATAL CARE ID IONIZATION MASS-SPECTROMETRY; PREGNANCY; POPULATION; NEWBORNS; METABOLITES; PREVALENCE; EXPOSURE AB OBJECTIVE: Our aim was to evaluate prospectively the effects of cocaine and marijuana use on pregnancy outcomes. STUDY DESIGN: A prospective multicenter cohort study was conducted at seven university-based prenatal clinics in the United States from 1984 to 1989. The cohort described herein consisted of a multiethnic population of 7470 pregnant women. Information on the use of drugs was obtained from personal interviews at entry to the study and assays of serum obtained during pregnancy. Pregnancy outcome data (low birth weight [< 2500 gm], preterm birth [< 37 weeks' gestation], and abruptio placentae) were obtained with a standardized study protocol. RESULTS: A total of 2.3% of the women used cocaine and 11.0% used marijuana during pregnancy. Cocaine use was not associated with having a low-birth-weight infant (adjusted odds ratio 0.7, 95% confidence interval 0.4 to 1.3) or a preterm birth (1.3, 0.9 to 2.0). There was no association between short-term exposure to cocaine and preterm delivery (1.1, 0.3 to 4.0). However, cocaine use was strongly associated with abruptio placentae (adjusted odds ratio 4.2, 1.9 to 9.5). Marijuana use was not associated with low birth weight (1.1, 0.9 to 1.5), preterm delivery (1.1, 0.8 to 1.3) or abruptio placentae (1.3, 0.6 to 2.8). By comparison, 35% of the women smoked cigarettes during pregnancy, and cigarette smoking was positively associated with low birth weight (1.5, 1.2 to 1.8). CONCLUSIONS: In this population of women receiving prenatal care, cocaine use was uncommon and was not related to most adverse birth outcomes. Marijuana use was relatively common and was not related to adverse pregnancy outcomes. Tobacco is still the most commonly abused drug during pregnancy, 15% of all cases of low birth weight in this study could have been prevented if women did not smoke cigarettes during pregnancy. C1 NICHHD,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. UNIV UTAH,CTR HUMAN TOXICOL,SALT LAKE CITY,UT 84112. UNIV OKLAHOMA,DEPT OBSTET & GYNECOL,NORMAN,OK 73019. RP SHIONO, PH (reprint author), DAVID & LUCILE PACKARD FDN,CTR FUTURE CHILDREN,300 2ND ST,SUITE 102,LOS ALTOS,CA 94022, USA. OI Cotch, Mary Frances/0000-0002-2046-4350 FU Intramural NIH HHS [Z99 EY999999]; NICHD NIH HHS [HD-3-2834, HD-3-2832, HD-3-2833] NR 25 TC 96 Z9 96 U1 1 U2 6 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 1995 VL 172 IS 1 BP 19 EP 27 DI 10.1016/0002-9378(95)90078-0 PN 1 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QE785 UT WOS:A1995QE78500003 PM 7847533 ER PT J AU HORNSBY, PP WILCOX, AJ HERBST, AL AF HORNSBY, PP WILCOX, AJ HERBST, AL TI ONSET OF MENOPAUSE IN WOMEN EXPOSED TO DIETHYLSTILBESTROL IN-UTERO SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE DIETHYLSTILBESTROL; MENOPAUSE; HOT FLASHES; PREMATURE OVARIAN FAILURE ID FEMALE GUINEA-PIG; PREGNANCY; DAUGHTERS; DES; CYCLOPHOSPHAMIDE; EXPERIENCE; FERTILITY; MOUSE AB OBJECTIVES: As part of a larger health survey, we sought to determine whether prenatal exposure to diethylstilbestrol is associated with onset of early menopause or menopausal symptoms. STUDY DESIGN: Diagnosis of premature ovarian failure and symptoms of menopause were determined in a telephone interview with 542 women whose mothers participated in a randomized clinical trial of the use of diethylstilbestrol in pregnancy in the early 1950s. These women were aged 37 to 39 at the time of the interview. Medical records were obtained to confirm diagnosis of premature ovarian failure. RESULTS: The prevalence of menopausal symptoms (specifically hot flashes and night sweats) did not differ for exposed and unexposed women. One exposed woman and no unexposed women had a medically confirmed diagnosis of premature ovarian failure. CONCLUSIONS: Prenatal diethylstilbestrol exposure was not related to diagnosis or symptoms of menopause in this study. Further follow-up will be necessary to determine if a difference in age at menopause emerges as these women become older. C1 UNIV CHICAGO,DEPT OBSTET & GYNECOL,CHICAGO,IL 60637. NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709. OI Wilcox, Allen/0000-0002-3376-1311 NR 24 TC 8 Z9 8 U1 0 U2 1 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 1995 VL 172 IS 1 BP 92 EP 95 DI 10.1016/0002-9378(95)90090-X PN 1 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QE785 UT WOS:A1995QE78500015 PM 7847565 ER PT J AU HARLOW, BL FRIGOLETTO, FD CRAMER, DW EVANS, JK BAIN, RP EWIGMAN, B MCNELLIS, D LEFEVRE, M CORNELISON, S BOYER, L HORMAN, D PLATTNER, M CRANE, JP KANE, D WINBORN, R CRAWFORD, B BOYD, L TURLINGTON, T BURROWS, PK YAFFE, S CATZ, C AF HARLOW, BL FRIGOLETTO, FD CRAMER, DW EVANS, JK BAIN, RP EWIGMAN, B MCNELLIS, D LEFEVRE, M CORNELISON, S BOYER, L HORMAN, D PLATTNER, M CRANE, JP KANE, D WINBORN, R CRAWFORD, B BOYD, L TURLINGTON, T BURROWS, PK YAFFE, S CATZ, C TI EPIDEMIOLOGIC PREDICTORS OF CESAREAN-SECTION IN NULLIPAROUS PATIENTS AT LOW-RISK SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE CESAREAN SECTION; COHORT STUDIES; RISK FACTORS; ANTHROPOMETRY ID MATERNAL AGE; SHOE SIZE; PREGNANCY; DELIVERY; WEIGHT; HEIGHT AB OBJECTIVES: We sought to determine whether certain maternal and fetal characteristics influenced the risk of maternal- and fetal-indicated cesarean sections in pregnant women at low risk for adverse perinatal outcomes. STUDY DESIGN: From a cohort of 6393 low-risk nulliparous patients maternal and fetal indicated cesarean section rates with 95% confidence intervals were calculated and stratified by demographic, anthropometric, and clinical tests and measurements. The strongest risk factors were modeled by means of multiple logistic regression. RESULTS: Few risk factors distinguished maternal from fetal characteristics preceding cesarean delivery. Maternal age was associated with increased cesarean section risk in the tallest group of women only, and cesarean section rates decreased with increasing height, increased with higher prepregnancy weights, and was highest in women carrying male fetuses. Higher first prenatal visit diastolic blood pressure, increasing numbers of nonstress tests, greater than or equal to 2+ prenatal urine protein, late sonograms, geographic region, and practice type were statistically significant risk factors as well. Interestingly, results of prenatal visit tests and measurements contributed less to the prevalence of cesarean section than did age, fetal sex, and anthropometric parameters. However, the generalizability of these results is limited to low-risk (predominantly white) populations. CONCLUSIONS: Of the risk factors we were able to assess, a large proportion of the incidence of cesarean section in this population of nulliparous patients at low risk was attributable to age, sex of fetus, and anthropometric patient profiles. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET GYNECOL & REPROD BIOL,BOSTON,MA 02115. GEORGE WASHINGTON UNIV,CTR BIOSTAT,DEPT STAT COMP & INFORMAT SYST,WASHINGTON,DC 20052. UNIV MISSOURI,SCH MED,DEPT FAMILY & COMMUNITY MED,COLUMBIA,MO. NICHHD,BETHESDA,MD 20892. RP HARLOW, BL (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR OBSTET & GYNECOL EPIDEMIOL,221 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NICHD NIH HHS [HD 19897, HD 21017, HD 21140] NR 20 TC 42 Z9 42 U1 0 U2 0 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 1995 VL 172 IS 1 BP 156 EP 162 DI 10.1016/0002-9378(95)90106-X PN 1 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QE785 UT WOS:A1995QE78500031 PM 7847528 ER PT J AU QUINTERO, RA HUME, R SMITH, C JOHNSON, MP COTTON, DB ROMERO, R EVANS, MI AF QUINTERO, RA HUME, R SMITH, C JOHNSON, MP COTTON, DB ROMERO, R EVANS, MI TI PERCUTANEOUS FETAL CYSTOSCOPY AND ENDOSCOPIC FULGURATION OF POSTERIOR URETHRAL VALVES SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Note DE FETOSCOPY; POSTERIOR URETHRAL VALVES; FETAL THERAPY; MINIMALLY INVASIVE SURGERY AB Percutaneous fetal cystoscopy was performed in a male fetus with ultrasonographic evidence of lower urinary tract obstruction at 19 weeks of gestation. The diagnosis of posterior urethral valves was confirmed. Percutaneous endoscopic fulguration of the valves was successfully performed at 22 weeks of gestation, and urethral patency was established. This case illustrates the feasibility of performing diagnostic and therapeutic endoscopic procedures within the human fetus for the management of a congenital anomaly. While we believe that fetal cystoscopy may improve our diagnostic, prognostic, and therapeutic capabilities in the management of fetuses with lower obstructive uropathy, studies are needed to establish the actual value, risks, and limitations of this new approach in fetal medicine. C1 WAYNE STATE UNIV,DEPT OBSTET & GYNECOL,DETROIT,MI 48202. WAYNE STATE UNIV,CHILDRENS HOSP,DEPT PEDIAT UROL,DETROIT,MI 48202. NICHHD,PERINATAL RES BRANCH,BETHESDA,MD 20892. RP QUINTERO, RA (reprint author), HUTZEL HOSP,CTR FETAL DIAGNOSIS & THERAPY,FETAL ENDOSCOPY PROGRAM,4707 ST ANTOINE BLVD,DETROIT,MI 48201, USA. NR 4 TC 89 Z9 93 U1 0 U2 1 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 1995 VL 172 IS 1 BP 206 EP 209 DI 10.1016/0002-9378(95)90115-9 PN 1 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QE785 UT WOS:A1995QE78500040 PM 7847537 ER PT J AU CARITIS, SN THOM, E MCNELLIS, D AF CARITIS, SN THOM, E MCNELLIS, D TI COMMENT ON THE EFFECTIVENESS OF INDUCTION OF LABOR FOR POSTTERM PREGNANCY - REPLY SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Letter C1 BIOSTAT CTR,ROCKVILLE,MD 20852. NICHHD,PREGNANCY & PERINATOL BRANCH,BETHESDA,MD 20892. RP CARITIS, SN (reprint author), UNIV PITTSBURGH,MAGEE WOMENS HOSP,DEPT OBSTET & GYNECOL,FORBES & HALKET ST,PITTSBURGH,PA 15213, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 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 1995 VL 172 IS 1 BP 241 EP 241 DI 10.1016/0002-9378(95)90131-0 PN 1 PG 1 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QE785 UT WOS:A1995QE78500056 ER PT J AU GREINER, TC RAFFELD, M LUTZ, C DICK, F JAFFE, ES AF GREINER, TC RAFFELD, M LUTZ, C DICK, F JAFFE, ES TI ANALYSIS OF T-CELL RECEPTOR-GAMMA GENE REARRANGEMENTS BY DENATURING GRADIENT GEL-ELECTROPHORESIS OF GC-CLAMPED POLYMERASE CHAIN-REACTION PRODUCTS - CORRELATION WITH TUMOR-SPECIFIC SEQUENCES SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID MINIMAL RESIDUAL DISEASE; ACUTE LYMPHOBLASTIC-LEUKEMIA; SINGLE-BASE CHANGES; INVITRO AMPLIFICATION; JUNCTIONAL SEQUENCES; LIMITED DIVERSITY; MYCOSIS-FUNGOIDES; DNA; IMMUNOGLOBULIN; MUTATIONS AB We describe a modified denaturing gradient gel electrophoresis (DGGE) procedure with a 40-nucleotide GC clamp in the polymerase chain reaction to improve resolution in amplifying T cell receptor-gamma (TCR-gamma) rearrangements. DNA from 46 cases of lymphoblastic leukemia/lymphoma, 5 T cell lines, 2 B cell lines, 7 normal lymphocytes, and 3 cases of Hodgkin's disease was amplified by polymerase chain reaction. In addition, 20 cases of paraffin-embedded T cell lymphomas and 5 cases of reactive hyperplasia were also studied. Clonal TCR-gamma rearrangements were identified on DGGE by the presence of a predominant band. Results obtained from 5 T cell lines and 12 lymphoblastic leukemia/lymphomas containing known TCR-gamma gene rearrangements revealed 100% concordance in detecting clonal rearrangements between DGGE and traditional Southern blot analysis. Of the remaining 34 lymphoblastic leukemia/lymphoma cases studied by DGGE alone, 30 were positive. DGGE analysis of 10 lymphoblastic leukemia/lymphoma cases with known group IV gamma to J gamma 1 or J gamma 2 rearrangement sequences confirmed that the electrophoretic migration was dependent on the tumor-specific rearranged TCR-gamma sequence. In addition, 17 of 20 cases of paraffin-embedded T cell lymphomas were positive by DGGE, 6 of which had the clonal population also identified in fresh tissue DNA. DGGE analysis of GC-clamped polymerase chain reaction products can provide a way to more accurately detect TCR-gamma clonality of lymphoid tumors and can be applied to archival tissues. C1 NCI,HEMATOPATHOL SECT,PATHOL LAB,BETHESDA,MD 20892. UNIV IOWA,DEPT PATHOL,IOWA CITY,IA. NR 37 TC 124 Z9 128 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JAN PY 1995 VL 146 IS 1 BP 46 EP 55 PG 10 WC Pathology SC Pathology GA QA902 UT WOS:A1995QA90200008 PM 7856738 ER PT J AU VADILLOORTEGA, F GONZALEZAVILA, G FURTH, EE LEI, HQ MUSCHEL, RJ STETLERSTEVENSON, WG STRAUSS, JF AF VADILLOORTEGA, F GONZALEZAVILA, G FURTH, EE LEI, HQ MUSCHEL, RJ STETLERSTEVENSON, WG STRAUSS, JF TI 92-KD TYPE-IV COLLAGENASE (MATRIX METALLOPROTEINASE-9) ACTIVITY IN HUMAN AMNIOCHORION INCREASES WITH LABOR SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID HUMAN CHORIONIC CELLS; PREMATURE RUPTURE; AMNIOTIC MEMBRANES; PROTEINS; BIOSYNTHESIS; METABOLISM; INHIBITION AB To determine whether specific collagenolytic enzymes are expressed in human fetal membranes with labor, we examined gelatinase activity ill extracts of amniochorion by zymography. The 99-kd gelatinase (MMP-9) was barely detectable in extracts of fetal membranes before the onset of labor but was readily demonstrable in extracts prepared from membranes isolated from laboring women or membranes collected immediately after delivery, In contrast, the 72-kd gelatinase (MMP-2) was detectable ill extracts from pre- and post-labor membranes, Ethylenediaminetetracetic acid and the tissue inhibitor of metalloproteinases, TIMP-1, inhibited the gelatinase activities detected by zymography, confirming that the enzymes are metalloproteinases, Assay of amniochorion gelatinase activity using a radiolabeled denatured collagen substrate revealed a more than twofold increase in activity comparing prelabor with post-labor fetal membrane extracts. A function-blocking anti-MMP-9 monoclonal antibody inhibited pre-labor membrane gelatinase activity by similar to 11.5%, which was only slightly greater inhibition than observed with irrelevant monoclonal antibodies, However, post-labor membrane gelatinase activity was reduced by 53% by the function-blocking antibody, indicating that MMP-9 is a major contributor to the increased gelatinase activity extractable from post-labor membranes, Western blot analyses demonstrated increased MMP-9 protein in amniochorion extracts after onset of labor MMP-9 protein and mRNA were co-localized irt amnion epithelium, underlying macrophages and chorion laeve trophoblast and decidual cells after labor We conclude that I) MMP-9 activity and protein in human amniochorion increases with labor and 2) MMP-9 is expressed by amnion epithelium, macrophages and chorion laeve trophoblast and decidual cells, Tbe increased expression of MMP-9 may result in degradation of the extracellular matrix of the fetal membranes and facilitate their rupture under both physiological and pathological conditions. C1 UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA. NCI,PATHOL LAB,BETHESDA,MD. RP VADILLOORTEGA, F (reprint author), UNIV PENN,SCH MED,DEPT OBSTET & GYNECOL,778 CLIN RES BLDG,422 CURIE BLVD,PHILADELPHIA,PA 19104, USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NICHD NIH HHS [HD-06274] NR 22 TC 162 Z9 164 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JAN PY 1995 VL 146 IS 1 BP 148 EP 156 PG 9 WC Pathology SC Pathology GA QA902 UT WOS:A1995QA90200019 PM 7856724 ER PT J AU KULKARNI, AB WARD, JM YASWEN, L MACKALL, CL BAUER, SR HUH, CG GRESS, RE KARLSSON, S AF KULKARNI, AB WARD, JM YASWEN, L MACKALL, CL BAUER, SR HUH, CG GRESS, RE KARLSSON, S TI TRANSFORMING GROWTH-FACTOR-BETA-1 NULL MICE - AN ANIMAL-MODEL FOR INFLAMMATORY DISORDERS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID BETA TGF-BETA; MONOCLONAL-ANTIBODIES; AUTOIMMUNE-DISEASES; T-CELLS; B-CELLS; EXPRESSION; ANTIGENS; MOUSE; GENE; GROWTH-FACTOR-BETA-1 AB Approximately 40% of transforming growth factor-beta 1 null (knockout) mice generated in our laboratory develop normally to term, but 60% die in utero. The animals appear normal during the first 2 weeks of life but develop a rapid wasting syndrome and die by 3 to 4 weeks of age. All of the knockout mice have a multifocal inflammatory disease in many tissues. The heart and lungs are most severely affected. Increased adhesion of leukocytes to the endothelium of pulmonary veins is the initial lesion seen at day 8 postnatally and is soon followed by perivascular cuffing as well as inflammatory infiltrates in lung parenchyma. The lesions in the heart begin as endocarditis and then progress to myocarditis and pericarditis. Within the lung, chronic inflammatory infiltrates consist of T and B lymphocytes, including plasma cells, whereas macrophages are the primary inflammatory cell type in the heart. Increased expression of major histocompatibility complex class I and II proteins in seen in pulmonary vascular endothelium as early as day 8. An immunoblastic response in mediastinal and mandibular lymphnodes and spleen is also seen. In the absence of any pathogens, this massive inflammatory disease, together with overexpression of major histocompatibility complex class I and II proteins and overproduction of immunoglobulins by lymphocytes, offers circumstantial evidence for an autoimmune etiology. C1 NINCDS,MOLEC & MED GENET SECT,DEV & METAB NEUROL BRANCH,BETHESDA,MD 20892. NCI,VET & TUMOR PATHOL SECT,OFF LAB ANIM SCI,FREDERICK,MD. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,DIV CELLULAR & GENE THERAPIES,BETHESDA,MD. RI Bauer, Steven/G-5559-2012 FU NCI NIH HHS [N0-1-CO-74102] NR 36 TC 133 Z9 138 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JAN PY 1995 VL 146 IS 1 BP 264 EP 275 PG 12 WC Pathology SC Pathology GA QA902 UT WOS:A1995QA90200030 PM 7856732 ER PT J AU SHERER, DM METLAY, LA WOODS, JR AF SHERER, DM METLAY, LA WOODS, JR TI LACK OF MANDIBULAR MOVEMENT MANIFESTED BY ABSENT FETAL SWALLOWING - A POSSIBLE FACTOR IN THE PATHOGENESIS OF MICROGNATHIA SO AMERICAN JOURNAL OF PERINATOLOGY LA English DT Article DE PRENATAL ULTRASOUND; FETAL SWALLOWING; POLYHYDRAMNIOS; MICROGNATHIA AB This study was performed to assess the association of lack of mandibular movement as manifested by absent fetal swallowing and micrognathia in a nonrestrictive intrauterine environment. Over a 5-year period, 14 fetuses with sonographic findings of polyhydramnios (amniotic fluid index [AFI] more than 20 cm), absent mandibular movement, and a nonvisualized fetal stomach, all consistent with absent fetal swallowing, were followed. A group of 14 fetuses, each with polyhydramnios (AFI more than 20 cm) yet with sonographic detection of fetal swallowing, served as controls. All gravidas in both groups were normoglycemic throughout gestation. Subsequent mandibular development was assessed at delivery or autopsy. Analysis of the data revealed th at in the study group, 12 of these infants were liveborn, and two were stillborn. Eleven of the liveborn infants had an early neonatal death. All 14 infants of the study group demonstrated micrognathia. None of the control infants (all of whom survived) had micrognathia. In conclusion, this study supports the concept that normal mandibular growth may depend on the presence of mandibular movement during intrauterine development. RP SHERER, DM (reprint author), GEORGETOWN UNIV,MED CTR,DEPT OBSTET & GYNECOL,NICHD,DIV INTRAMURAL,PERINATOL RES BRANCH,3PHC,WASHINGTON,DC 20007, USA. NR 0 TC 15 Z9 18 U1 1 U2 1 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0735-1631 J9 AM J PERINAT JI Am. J. Perinatol. PD JAN PY 1995 VL 12 IS 1 BP 30 EP 33 DI 10.1055/s-2007-994395 PG 4 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA QF098 UT WOS:A1995QF09800009 PM 7710573 ER PT J AU SHERER, DM ALLEN, TA GHEZZI, F EPSTEIN, LG AF SHERER, DM ALLEN, TA GHEZZI, F EPSTEIN, LG TI PRENATAL-DIAGNOSIS OF MODERATE UNILATERAL HYDROCEPHALUS SUBSEQUENTLY NOT REQUIRING NEONATAL DECOMPRESSION SO AMERICAN JOURNAL OF PERINATOLOGY LA English DT Article DE PRENATAL DIAGNOSIS; PRENATAL ULTRASONOGRAPHY; UNILATERAL HYDROCEPHALUS AB Prenatal diagnosis of unilateral hydrocephalus is unusual. In the past most such cases have been treated with neonatal shunting procedures. We present an unusual case in which moderate unilateral hydrocephalus was diagnosed prenatally at 30 weeks' gestation. Despite prenatal and neonatal sonographic signs of both cortical thinning and mild displacement of midline intracranial structures, confirmed by computed tomography, neonatal shunting was not required. The findings and course in this unusual case suggest that infrequently some of the milder cases of idiopathic non progressive unilateral hydrocephalus discovered later in life may possibly represent late detection of this preexisting condition. RP SHERER, DM (reprint author), GEORGETOWN UNIV,MED CTR,DEPT OBSTET & GYNECOL,NICHD,DIV INTRAMURAL,PERINATOL RES BRANCH,3PHC,WASHINGTON,DC 20007, USA. OI Ghezzi, Fabio/0000-0003-3949-5410 NR 0 TC 8 Z9 9 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0735-1631 J9 AM J PERINAT JI Am. J. Perinatol. PD JAN PY 1995 VL 12 IS 1 BP 50 EP 52 DI 10.1055/s-2007-994400 PG 3 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA QF098 UT WOS:A1995QF09800014 PM 7710578 ER PT J AU GLOTH, FM WALSTON, J MEYER, J PEARSON, J AF GLOTH, FM WALSTON, J MEYER, J PEARSON, J TI RELIABILITY AND VALIDITY OF THE FRAIL ELDERLY FUNCTIONAL ASSESSMENT QUESTIONNAIRE SO AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION LA English DT Article DE FUNCTIONAL ASSESSMENT; FRAILTY; PHYSICAL ACTIVITY ID MINI-MENTAL-STATE AB Measuring functional activity for elderly at very low functional levels remains a challenge because many functional instruments have not been standardized in a frail elderly population. The Frail Elderly Functional Assessment questionnaire (FEFA) is a 19-item, interviewer-administered questionnaire designed to assess function in frail elderly at a very low activity level. The purpose of this study was to determine the reliability and validity of this instrument in a frail elderly population. Two groups of subjects over 65 yr old were selected to test the reliability and validity of this questionnaire. Test-retest reliability was determined by correlating the responses of 29 homebound (including nursing home-bound) subjects who answered the questionnaire on two occasions 2 wk apart. To assess the validity of the FEFA, the questionnaire was administered to 23 frail, homebound (including nursing home-bound) elderly subjects who had a Mini-Mental State Examination score of greater than or equal to 18. Validity was determined by correlating patient responses to direct observations by the investigators of tasks addressed in the questionnaire. Correlation was also determined against the Katz's Activity of Daily Living index, Lawton's Instrumental Activity of Daily Living index, and the Barthel index. The reliability coefficient was 0.82. Correlation between the FEFA questionnaire and direct observation of questionnaire task performance was 0.90. Construct validity against the Katz's Activity of Daily Living, Lawton's Instrumental Activity of Daily Living, and the Barthel index showed correlations of 0.86, 0.67 and 0.91, respectively. Initial data indicate that the FEFA is a valid and reliable instrument that may be useful in assessing function in frail elderly people. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV GERIATR MED & GERONTOL,BALTIMORE,MD 21205. HOPKINS BAYVIEW MED CTR,BALTIMORE,MD. NIA,GERONTOL RES CTR,APPL PHYSIOL SECT,BALTIMORE,MD 21224. NIA,GERONTOL RES CTR,LONGITUDINAL STUDIES BRANCH,BALTIMORE,MD 21224. RP GLOTH, FM (reprint author), UNION MEM HOSP,DIV GERIATR,201 E UNIV PKWY,BALTIMORE,MD 21218, USA. NR 17 TC 26 Z9 26 U1 3 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0894-9115 J9 AM J PHYS MED REHAB JI Am. J. Phys. Med. Rehabil. PD JAN-FEB PY 1995 VL 74 IS 1 BP 45 EP 53 DI 10.1097/00002060-199501000-00008 PG 9 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA QK132 UT WOS:A1995QK13200007 PM 7873113 ER PT J AU TIAN, Y BALLA, T BAUKAL, AJ CATT, KJ AF TIAN, Y BALLA, T BAUKAL, AJ CATT, KJ TI GROWTH-RESPONSES TO ANGIOTENSIN-II IN BOVINE ADRENAL GLOMERULOSA CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE AT(1) RECEPTOR; CELL CYCLE; PROLIFERATION; LYSOPHOSPHATIDIC ACID ID SMOOTH-MUSCLE CELLS; PROTEIN-KINASE-C; RECEPTOR SUBTYPES; ADRENOCORTICAL-CELLS; ALDOSTERONE PRODUCTION; GENE-EXPRESSION; STIMULATION; CALCIUM; METABOLISM; BINDING AB The effects of angiotensin II (ANG II) on growth responses of primary cultures of bovine adrenal glomerulosa cells were studied to explore the mechanism(s) by which ANG II leads to hyperplasia and hypertrophy of the glomerulosa layer in sodium deficiency. ANG II did not increase [H-3]thymidine incorporation during the first 5 days of culture, but mitogenic responses to ANG II became evident after longer periods of culture and were most prominent between 8 and 11 days after seeding. At this time, cell cycle analysis showed that ANG II increased the proportion of cells in the 8 phase and did not cause accumulation of cells in the G(2) phase. Consistent with this finding, ANG II also stimulated proliferation of glomerulosa cells during treatment for 3 days in the presence of 1% serum. The mitogenic effect of ANG II was not inhibited by pretreatment with pertussis toxin and was mediated by AT(1) receptors as indicated by its sensitivity to the subtype-selective antagonist DuP-753. Also, there was no emergence of AT(2) receptors in glomerulosa cells during prolonged culture. These results indicate that intracellular mechanisms that mediate growth responses become more active during prolonged culture of glomerulosa cells. Thus, in addition to regulating the steroidogenic and secretory functions of the tons glomerulosa, ANG II exerts mitogenic actions that depend on the functional state of the glomerulosa cells. C1 NICHHD, ENDOCRINOL & REPROD RES BRANCH, BETHESDA, MD 20892 USA. NR 35 TC 48 Z9 48 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD JAN PY 1995 VL 268 IS 1 BP E135 EP E144 PG 10 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA QB491 UT WOS:A1995QB49100020 PM 7840171 ER PT J AU SCHOLZ, TD LAUGHLIN, MR BALABAN, RS KUPRIYANOV, VV HEINEMAN, FW AF SCHOLZ, TD LAUGHLIN, MR BALABAN, RS KUPRIYANOV, VV HEINEMAN, FW TI EFFECT OF SUBSTRATE ON MITOCHONDRIAL NADH, CYTOSOLIC REDOX STATE, AND PHOSPHORYLATED COMPOUNDS IN ISOLATED HEARTS SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE FLUORESCENCE; NUCLEAR MAGNETIC RESONANCE; GLYCEROL 3-PHOSPHATE; PHOSPHORYLATION POTENTIAL ID PERFUSED RAT-HEART; P-31 NMR; OXIDATIVE-PHOSPHORYLATION; DEHYDROGENASE-ACTIVITY; OXYGEN-CONSUMPTION; FREE MAGNESIUM; WORKING HEART; RABBIT HEART; LIVER CELLS; GUINEA-PIG AB The effect of metabolic substrates on the relation among cytosolic redox state (NADH(c)/NAD(c)(+)), mitochondrial NADH (NADH(m)), and [ATP]/([ADP] x [P-i]) was studied in isolated working rabbit hearts. Substrates were varied from 5.6 mM glucose alone to glucose in combination with 10 mM lactate and/or 10 mM pyruvate while afterload and preload were held constant. Changes in NADH, were determined from epicardial NADH fluorescence. The ratio of glycerol 3-phosphate (G-3-P) to dihydroxyacetone phosphate (DHAP), determined from tissue extracts, was used as an index of cytosolic redox. Myocardial P-31 metabolites were measured using nuclear magnetic resonance spectroscopy. The addition of pyruvate to the perfusion medium caused increases in myocardial oxygen consumption (MVO(2)), NADH(m) fluorescence, phosphocreatine (PCr), and [ATP]/([ADP] x [P-i]) and a decrease in NADH(c)/NAD(c)(+) (decreased G-3-P/DHAP). Although the addition of lactate to the perfusion medium caused an increase in NADdH(m) similar to pyruvate, MVO(2) and PCr did not change significantly, [ATP]/([ADP] x [P-i]) increased less than with pyruvate, and there was an increase in NADH(c)/NAD(c)(+). The findings suggest that variations in the cytosolic redox state do not necessarily result in obligatory changes in either the mitochondrial redox state or in the [ATP]I([ADP] x [P-i]). This implies that under the conditions of this study an equilibrium is not maintained between [ATP]/([ADP] x [P-i]) and NADH(c)/NAD(c)(+). Furthermore, similar levels of NADH, can be associated with different values for [ATP]/([ADP] x [P-i]) and MVO(2), depending on the substrates available to the heart. C1 NHLBI, CARDIAC ENERGET LAB, BETHESDA, MD 20892 USA. RI Balaban, Robert/A-7459-2009 OI Balaban, Robert/0000-0003-4086-0948 NR 40 TC 80 Z9 81 U1 1 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD JAN PY 1995 VL 268 IS 1 BP H82 EP H91 PG 10 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA QB488 UT WOS:A1995QB48800013 PM 7840306 ER PT J AU FLAMION, B SPRING, KR ABRAMOW, M AF FLAMION, B SPRING, KR ABRAMOW, M TI ADAPTATION OF INNER MEDULLARY COLLECTING DUCT TO DEHYDRATION INVOLVES ST PARACELLULAR PATHWAY SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE WATER PERMEABILITY; SUCROSE PERMEABILITY; VASOPRESSIN; CELL MEMBRANES ID WATER PERMEABILITY; TIGHT JUNCTIONS; RAT-KIDNEY; VASOPRESSIN; CHANNEL; TUBULES; MEMBRANE; HETEROGENEITY; ACTIVATION; TRANSPORT AB Prolonged fluid restriction in rats is accompanied by functional modifications of the terminal part of the inner medullary collecting duct (IMCD) revealed by a sustained increase in arginine vasopressin (AVP)-independent transepithelial osmotic water permeability (P-TE) in vitro. The cellular basis of this adaptation was explored in isolated and perfused terminal IMCDs of Sprague-Dawley rats using video and fluorescence microscopy. Basolateral membrane osmotic water permeability (P-osm), transcellular P-osm, and P-TE were measured in quick sequence in every tubule. They were expressed per unit area of basolateral membrane corrected for infoldings, based on previous stereological studies and assuming no major change in membrane surface area between hydrated and dehydrated animals. Compared with IMCDs of rats with a high water intake, IMCDs of rats deprived of fluid for 36 h displayed a significantly higher basal P-TE (24.9 +/- 5.1 vs. 6.1 +/- 0.6 mu m/s), a similar basolateral P-osm, and a higher transcellular P-osm, implying a higher permeability of the apical membrane, despite the absence of exogenous AVP. However, when IMCDs of thirsted rats were exposed to AVP in vitro, their transcellular P-osm (36.0 +/- 2.4 mu m/s) was significantly smaller than their P-TE determined simultaneously (51.8 +/- 7.1 mu m/s), suggesting that part of the water flow may follow a paracellular route. A change in paracellular pathways was supported by higher apparent permeabilities to [C-14]sucrose (0.85 +/- 0.27 vs. 0.28 +/- 0.04 x 10(-5) cm/s) and to [methoxy-H-3]inulin (0.25 +/- 0.04 vs. 0.14 +/- 0.03 x 10(-5) cm/s) in IMCDs of thirsted rats. The nonelectrolyte permeabilities were affected neither by AVP nor by urea-rich bathing solutions. We conclude that in vivo factors related to dehydration produce a conditioning effect on terminal IMCD, which includes stabilization of the apical membrane in a state of high P-osm and opening up of paracellular pathways revealed by a higher permeability to water and nonelectrolytes. The role of these adaptive phenomena remains unclear but may pertain to the sudden transitions between antidiuresis and diuresis. C1 NHLBI, KIDNEY & ELECTROLYTE METAB LAB, BETHESDA, MD 20892 USA. RP FLAMION, B (reprint author), FREE UNIV BRUSSELS, PATHOPHYSIOL LAB, BAT E24108, 808 ROUTE LENNIK, B-1070 BRUSSELS, BELGIUM. NR 31 TC 11 Z9 11 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrol. Physiol. PD JAN PY 1995 VL 268 IS 1 BP F53 EP F63 PG 11 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA QB702 UT WOS:A1995QB70200007 PM 7840248 ER PT J AU SCHRAMM, U FRICKER, G WENGER, R MILLER, DS AF SCHRAMM, U FRICKER, G WENGER, R MILLER, DS TI P-GLYCOPROTEIN-MEDIATED SECRETION OF A FLUORESCENT CYCLOSPORINE ANALOG BY TELEOST RENAL PROXIMAL TUBULES SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE FLUORESCENCE MICROSCOPY; MULTIDRUG RESISTANCE TRANSPORTER; TELEOST FISH; VIDEO IMAGE ANALYSIS ID MULTIDRUG-RESISTANCE GENE; BINDING-PROTEIN; ORGANIC ANION; TRANSPORT; KIDNEY; DIGOXIN; IDENTIFICATION; INHIBITION; EXPRESSION; MECHANISMS AB The transport of a fluorescent cyclosporin analogue was measured in killifish (Fundulus heteroclitus) proximal tubules by means of epifluorescence microscopy and digital image analysis. Renal cells rapidly accumulated the cyclosporin analogue from the medium and attained steady state within 60 min; luminal fluorescence increased over the first 60-90 min. At steady state, luminal fluorescence intensity was two to three times higher than cellular. Cellular fluorescence intensity was a linear function of medium substrate concentration and was not affected by any treatment used. In contrast, luminal fluorescence exhibited a saturable component as the medium concentration of the cyclosporin was increased. Secretion into the lumen was blocked by metabolic inhibitors, vanadate, other cyclosporins, such as cyclosporin A and cyclosporin G, and substrates for P-glycoprotein (verapamil, vinblastine, and quinine) but not by substrates for the renal organic anion or organic cation transport systems, such asp-aminohippurate or tetraethylammonium. The data are consistent with the fluorescent cyclosporin analogue entering proximal tubule cells by simple diffusion and then being pumped into the tubular lumen by P-glycoprotein. C1 NIEHS, CELLULAR & MOLEC PHARMACOL LAB, RES TRIANGLE PK, NC 27709 USA. SANDOZ PHARMA AG, CH-4002 BASEL, SWITZERLAND. MT DESERT ISL BIOL LAB, SALSBURY COVE, ME 04672 USA. NR 35 TC 74 Z9 75 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrol. Physiol. PD JAN PY 1995 VL 268 IS 1 BP F46 EP F52 PG 7 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA QB702 UT WOS:A1995QB70200006 PM 7840247 ER PT J AU CLARKE, AS BOINSKI, S AF CLARKE, AS BOINSKI, S TI TEMPERAMENT IN NONHUMAN-PRIMATES SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article DE TEMPERAMENT; PERSONALITY; BEHAVIORAL TRAITS; REACTIVITY; INDIVIDUAL DIFFERENCES; SPECIES DIFFERENCES ID RHESUS-MONKEY INFANTS; SQUIRREL-MONKEYS; SOCIAL-BEHAVIOR; MACACA-MULATTA; PRENATAL STRESS; PERSONALITY-TRAITS; REARING CONDITIONS; LONGITUDINAL TWIN; SAIMIRI-OERSTEDI; VERVET MONKEYS AB Formerly applied to studies of responsivity in children, in more recent years the concept of temperament has been applied to nonhuman primates at the individual, species, and now population levels. While the concepts of temperament and personality have been less distinguished in nonhuman primate studies than in the human literature, temperamental and personality differences have now been identified among individual primates and among primate species in a number of studies. At the individual level, certain temperamental characteristics have been associated with age, sex, and most frequently rank. At the species level, temperamental profiles have been linked to intraspecific differences in social systems, sociodemographics, and features of life history and ecology. In this report we discuss the application of the temperament concept to nonhuman primates and review findings from studies of primate temperament at the individual, population, and species level. We also cite evidence for genetic and experiential influences on temperament in primates, outline concepts related to possible evolutionary influences on temperament, and discuss the possible relation of temperamental characteristics to social behavior and ecology in selected species. (C) 1995 Wiley-Liss, Inc. C1 NORTHWESTERN UNIV,SCH MED,ASHER CTR STUDY & TREATMENT DEPRESS DISORDERS,CHICAGO,IL. UNIV FLORIDA,DEPT ANTHROPOL,GAINESVILLE,FL. UNIV FLORIDA,DIV COMPARAT MED,GAINESVILLE,FL. NICHHD,CTR ANIM,COMPARAT ETHOL LAB,POOLESVILLE,MD. RP CLARKE, AS (reprint author), UNIV WISCONSIN,HARLOW PRIMATE LAB,22 N CHARTER ST,MADISON,WI 53711, USA. NR 156 TC 108 Z9 111 U1 0 U2 24 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1995 VL 37 IS 2 BP 103 EP 125 DI 10.1002/ajp.1350370205 PG 23 WC Zoology SC Zoology GA RW315 UT WOS:A1995RW31500004 ER PT J AU TIMME, A AF TIMME, A TI SEX-DIFFERENCES IN INFANT INTEGRATION IN A SEMIFREE-RANGING GROUP OF BARBARY MACAQUES (MACACA-SYLVANUS, L 1758) AT SALEM, GERMANY SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article DE SEMIFREE-RANGING BARBARY MACAQUES; SEX-SPECIFIC INFANT INTEGRATION; FEMALE PHILOPATRY MALE DISPERSAL ID BEHAVIOR AB Sixteen multiparous Barbary macaque females with newborns were studied over a 16 month period within the context of their naturally formed group. Analysis of their social behavior revealed 1) triadic interactions involving focal females, their newborns, and other group members occurred mainly with other females; and 2) mothers with female newborns interacted mainly with females of their own matriline, while mothers with male newborns interacted mainly with nonmatriline females. Observed in two successive birth seasons, this pattern indicates that partners of maternal interactions chose each other according to the sex of the newborn. Measures of distance from the mother also reflected differences between infants of different sex. At about five months of age, female infants were observed close to their mothers significantly more often than males. This finding follows the pattern of a sex-specific infant socialization process which integrates female infants into the network of their matrilines and male infants into the broader group. This sex-specific integration pattern is interpreted as supporting female philopatry and male dispersal. (C) 1995 Wiley-Liss, Inc. C1 UNIV GOTTINGEN,INST ANTHROPOL,W-3400 GOTTINGEN,GERMANY. FREE UNIV BERLIN,INST VERHALTENSBIOL,BERLIN,GERMANY. NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD. NR 21 TC 7 Z9 9 U1 2 U2 9 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1995 VL 37 IS 3 BP 221 EP 231 DI 10.1002/ajp.1350370304 PG 11 WC Zoology SC Zoology GA RZ897 UT WOS:A1995RZ89700003 ER PT J AU BOINSKI, S MITCHELL, CL AF BOINSKI, S MITCHELL, CL TI WILD SQUIRREL-MONKEY (SAIMIRI-SCIUREUS) CAREGIVER CALLS - CONTEXTS AND ACOUSTIC STRUCTURE SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Note DE PRIMATE VOCAL COMMUNICATION; MATERNAL BEHAVIOR; SAIMIRI SCIUREUS; ACOUSTIC STRUCTURE ID VOCAL BEHAVIOR AB A field study of the vocal behavior of 22 wild adult female squirrel monkeys (Saimiri sciureus) in Parque Nacional del Manu, Peru, found that 21% of vocalizations were ''caregiver'' calls. Caregiver calls are brief, low frequency calls, often with numerous harmonies, that are addressed by caregivers to their own infants in three contexts: 1) prenurse, signalling the caregiver's location and willingness to nurse; 2) nurse, while nursing; and 3) end nurse, indicating the end of the nursing bout. Three measures (start, end, and peak frequency) of the acoustic structure of the fundamental frequency of the caregiver calls significantly differed across the contexts. Duration of caregiver calls, however, was not distinguished by context. Compared to other primate taxa, the specificity and importance of caregiver calls in squirrel monkey vocal behavior appears unusual, if not unique. That S. sciureus caregiver calls are highly developed and employed so extensively probably follows from an unusual combination of ecological and life history factors. These factors include delayed weaning and large infant body size, high levels of indirect foraging competition which encourages spatial separation, susceptibility to predation, and specialization on a densely foliated, branch-end microhabitat in which visual contact is often impeded. (C) 1995 Wiley-Liss, Inc. C1 NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD. AMAZON BIODIVERS PROJECT,CUZCO,PERU. RP BOINSKI, S (reprint author), UNIV FLORIDA,DEPT ANTHROPOL,1350 TURLINGTON,GAINESVILLE,FL 32611, USA. NR 24 TC 17 Z9 17 U1 4 U2 8 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1995 VL 35 IS 2 BP 129 EP 137 DI 10.1002/ajp.1350350205 PG 9 WC Zoology SC Zoology GA QE268 UT WOS:A1995QE26800004 ER PT J AU WEINDRUCH, R MARRIOTT, BM CONWAY, J KNAPKA, JJ LANE, MA CUTLER, RG ROTH, GS INGRAM, DK AF WEINDRUCH, R MARRIOTT, BM CONWAY, J KNAPKA, JJ LANE, MA CUTLER, RG ROTH, GS INGRAM, DK TI MEASURES OF BODY-SIZE AND GROWTH IN RHESUS AND SQUIRREL-MONKEYS SUBJECTED TO LONG-TERM DIETARY RESTRICTION SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article DE NUTRITION; OBESITY; ADIPOSITY; DEVELOPMENT; AGING; MORPHOMETRY; SKIN-FOLD THICKNESS; MACACA MULATTA; SAIMIRI SP ID FOOD RESTRICTION; PHYSICAL GROWTH; ENERGY-INTAKE; BABOONS; MALNUTRITION; WEIGHT; MICE; NUTRITION; PRIMATES; BIRTH AB Although many studies have reported the robust effects of dietary restriction (DR) in retarding numerous aging processes in rodents, little is known about the outcomes of reducing caloric intake of a nutritious diet on aging in primates. Most primate studies have concerned the effects of malnutrition. We hypothesized that DR influences aging processes in primate species as it does in rodents. In the present study, 24 male rhesus (Macaca mulatta) monkeys (ages 0.6-5 years) and 25 male squirrel (Saimiri sp.) monkeys (ages 0.3-10 years) were provided diets formulated differently for each species but both fortified with vitamins and minerals (40% above recommended levels) as controls (approximating ad libitum levels) or experimentals (about 30% below the level of diet provided controls of comparable age and body weight). The results reported here concern the hypothesis that DR imposed during various developmental stages in these two primate species would affect morphometric parameters obtained at different occasions during the first 5 years of the study. Groups of older monkeys (rhesus: 18-25 years, n = 3; squirrel: 10-15 years, n = 4) were also included as controls for comparative purposes. Among groups of rhesus monkeys begun on DR prior to 6 years of age, growth in body weight and crown-rump length was reduced about 10-20% beginning after 1 year on the diet, with estimated food intake being reduced about 30-35% over this period. Measures of skin-fold thickness and various body circumference measures were also reduced in experimental groups of rhesus monkeys. In contrast, the DR regimen involving a different diet produced little impact on comparable measures in squirrel monkeys, with the estimated food intake being reduced only about 20-25% over this period. However, evidence of divergence in some morphometric parameters in squirrel monkeys was beginning to emerge in young groups (<5 years) after 3 years on the diet. (C) 1995 Wiley-Liss, Inc.* C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI. NATL ACAD SCI,FOOD & NUTR BOARD,WASHINGTON,DC 20418. USDA,BELTSVILLE HUMAN NUTR RES CTR,ENERGY & PROT NUTR LAB,BELTSVILLE,MD 20705. NIH,NATL CTR RES RESOURCES,BETHESDA,MD 20892. NIA,HOPKINS BAYVIEW MED CTR,CTR GERONTOL RES,MOLEC PHYSIOL & GENET SECT,BALTIMORE,MD 21224. NR 47 TC 25 Z9 25 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 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1995 VL 35 IS 3 BP 207 EP 228 DI 10.1002/ajp.1350350304 PG 22 WC Zoology SC Zoology GA QJ092 UT WOS:A1995QJ09200003 ER PT J AU BYRNE, GF SUOMI, SJ AF BYRNE, GF SUOMI, SJ TI DEVELOPMENT OF ACTIVITY PATTERNS, SOCIAL INTERACTIONS, AND EXPLORATORY-BEHAVIOR IN INFANT TUFTED CAPUCHINS (CEBUS-APELLA) SO AMERICAN JOURNAL OF PRIMATOLOGY LA English DT Article DE CAPUCHIN; CEBUS; DEVELOPMENT; ACTIVITY; SOCIAL BEHAVIOR ID GROUP-BORN INFANTS; SQUIRREL-MONKEYS; BIRTH; CAPTIVITY; LIFE AB Early organization of activity states was studied in 17 tufted capuchin (Cebus apella) infants from birth to 11 weeks of age. Development of exploration and interactions with mothers and other group members were studied in 14 of these infants up to the age of 1 year. Activity profiles changed from 3 to 8 weeks as infants began to move off mothers;and explore their environments. From 2 to 6 months time with mothers decreased; time alone increased correspondingly. Time spent with other group members did not vary significantly over the first year. By 7-9 months capuchin infants spent more time alone or with other group members than with mothers, although weaning was still not completed by the end of the first year. Simple environmental exploration began in the 2nd month and reached stable levels by 4 months. Complex manipulation of food and objects first began at 3-4 months and increased to stable levels in the second half of the first year. Some preliminary differences were evident between infants living in indoor cages and those living in indoor/outdoor runs. Infants in cages spent less time in dorsal contact with mothers, and less time in social play and proximity to other animals than those in runs. Instead, infants in cages spent more time alone and engaged in more manipulation of food. Some measures of social and exploratory behavior showed a high degree of variability which may he useful in exploring individual differences in infant temperarament or reactivity. (C) 1995 Wiley-Liss, Inc.* RP BYRNE, GF (reprint author), NICHHD,CTR ANIM,COMPARAT ETHOL LAB,POOLESVILLE,MD 20837, USA. NR 16 TC 22 Z9 22 U1 1 U2 13 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0275-2565 J9 AM J PRIMATOL JI Am. J. Primatol. PY 1995 VL 35 IS 4 BP 255 EP 270 DI 10.1002/ajp.1350350402 PG 16 WC Zoology SC Zoology GA QP297 UT WOS:A1995QP29700001 ER PT J AU ECKARDT, MJ STAPLETON, JM RAWLINGS, RR DAVIS, EZ GRODIN, DM AF ECKARDT, MJ STAPLETON, JM RAWLINGS, RR DAVIS, EZ GRODIN, DM TI NEUROPSYCHOLOGICAL FUNCTIONING IN DETOXIFIED ALCOHOLICS BETWEEN 18 AND 35 YEARS OF AGE SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID MINIMAL BRAIN-DYSFUNCTION; LONG-TERM ALCOHOLICS; SOCIAL DRINKERS; FAMILIAL ALCOHOLISM; PERFORMANCE; MEN; QUESTIONNAIRE; SYMPTOMS; HISTORY; CONSUMPTION AB Objective: The authors determined 1) cognitive functioning in detoxified alcoholics who had alcohol-related problems for a relatively brief time and 2) relationships between neuropsychological test scores and recent and chronic alcohol consumption patterns, childhood symptoms of hyperactivity/minimal brain dysfunction, and extent of familial alcoholism. Method: The subjects were 101 detoxified, drug-free alcoholics between 18 and 35 years of age who had consumed excessive amounts of alcohol (average of 114 g four to five times per week) for an average of 6 years. An average of 39 days after the last drink each alcoholic was given an extensive battery of neuropsychological tests assessing language skills, attention, motor skills, intelligence, memory, and cognitive functioning related to the frontal regions of the brain. Results: Only four individuals evidenced mild cognitive dysfunction. Current psychiatric condition, anxiety and depressive states, and liver dysfunction were not related to cognition. Relationships of cognition to lifetime estimates of alcohol consumption (average of 189 kg) and number of days from last drink to testing were determined to be nonlinear and suggested that greater lifetime consumption predicted worse performance and that longer abstinence predicted better performance. Neither extent of familial alcoholism nor number of childhood signs and symptoms of hyperactivity/minimal brain dysfunction was predictive of cognition except that more antisocial behavior predicted poorer cognitive functioning. Conclusions: Cognition an young alcoholics, averaging 6 years of excessive alcohol consumption, was within normal limits, evert though greater lifetime consumption predicted lower test scores and longer abstinence predicted higher scores. C1 NATL NAVAL MED CTR, DEPT TRI SERV ALCOHOLISM RECOVERY, BETHESDA, MD USA. RP ECKARDT, MJ (reprint author), NIAAA, CLIN STUDIES LAB,RM 3B19,NIH BLDG 10,10 CTR DR, MSC-1250, BETHESDA, MD 20892 USA. NR 46 TC 42 Z9 43 U1 0 U2 6 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JAN PY 1995 VL 152 IS 1 BP 53 EP 59 PG 7 WC Psychiatry SC Psychiatry GA PZ934 UT WOS:A1995PZ93400009 PM 7802120 ER PT J AU PERSICO, AM WANG, ZW BLACK, DW ANDREASEN, NC UHL, GR CROWE, RR AF PERSICO, AM WANG, ZW BLACK, DW ANDREASEN, NC UHL, GR CROWE, RR TI EXCLUSION OF CLOSE LINKAGE OF THE DOPAMINE TRANSPORTER GENE WITH SCHIZOPHRENIA SPECTRUM DISORDERS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Note ID DISPLAYS; VALIDITY; SCALES AB Objective: Involvement of genetic factors in the pathogenesis of schizophrenia spectrum disorders has been indicated in twin, adoption, and familial aggregation studies; the pivotal role played by the dopamine transporter in dopaminergic neurotransmission makes it a candidate gene for these disorders. Detection of close linkage between a dopamine transporter marker and schizophrenia spectrum disorders would strongly support the existence of causal relationships between genetic mutations at the dopamine transporter focus and the disease phenotype. Method: The authors assessed the linkage between this gene and schizophrenia spectrum disorders by using polymorphic dopamine transporter gene markers in 156 subjects from 16 multiplex pedigrees with schizophrenia as well as schizophreniform, schizoaffective, and schizotypal disorders and mood-incongruent psychotic depression. Results: Complete (theta=0.0) linkage to the schizophrenia spectrum was excluded under both dominant and recessive models. Conclusions: These results indicate that allelic variants at the dopamine transporter focus do not provide major genetic contributions to the etiology of schizophrenia and related disorders in these pedigrees. C1 NIDA,ADDICT RES CTR,MOLEC NEUROBIOL BRANCH,BALTIMORE,MD 21224. UNIV IOWA,COLL MED,DEPT PSYCHIAT,IOWA CITY,IA. FU NIMH NIH HHS [MH-00735, MH-43212] NR 16 TC 32 Z9 32 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JAN PY 1995 VL 152 IS 1 BP 134 EP 136 PG 3 WC Psychiatry SC Psychiatry GA PZ934 UT WOS:A1995PZ93400024 PM 7802105 ER PT J AU NELSON, DE GIOVINO, GA SHOPLAND, DR MOWERY, PD MILLS, SL ERIKSEN, MP AF NELSON, DE GIOVINO, GA SHOPLAND, DR MOWERY, PD MILLS, SL ERIKSEN, MP TI TRENDS IN CIGARETTE-SMOKING AMONG US ADOLESCENTS, 1974 THROUGH 1991 SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID GENDER DIFFERENCES; PREVENTION; CHILDREN; VALIDITY; PROGRAMS; COHORT; CAMEL; SALES AB Objectives. The purpose of this study was to determine national trends in adolescent cigarette smoking prevalence. Methods. We conducted trend analyses based on 1974 through 1991 current smoking prevalence data among persons aged 12 through 19 years from the National Household Surveys on Drug Abuse, High School Seniors Surveys, and National Health interview Surveys. Results. Overall smoking prevalence declined much more rapidly from 1974 through 1980 (1.9 percent age points annually among younger adolescents; the range among surveys of older adolescents was 0.2 to 2.0 percentage points annually) than from 1985 through 1991 (0 to 0.5 percentage points annually among all adolescents). Since 1980, smoking has generally declined at a slightly faster rate among older female adolescents than among male adolescents. Smoking among Black adolescents of all ages declined in nearly every survey population during each study period (range among surveys: 1974-1985 = 1.0 to 2.9 percentage points; 1985-1991 = 0.7 to 1.5 percentage points annually); for White adolescents, only minimal declines in smoking have occurred since 1985. Conclusions. Since 1974, major changes in adolescent smoking patterns have occurred, especially among Blacks. The overall slowing rate of decline in smoking prevalence since 1985 may indicate success of increased tobacco advertising and promotional activities targeted at adolescents or inadequate antitobacco education efforts. C1 CTR DIS CONTROL & PREVENT,OFF SMOKING & HLTH,ATLANTA,GA 30341. NCI,BETHESDA,MD 20892. BATTELLE INC,ARLINGTON,VA. RP NELSON, DE (reprint author), CTR DIS CONTROL & PREVENT,OFF SURVEILLANCE & ANAL,4770 BUFORD HIGHWAY,MAILSTOP K-30,ATLANTA,GA 30341, USA. NR 81 TC 173 Z9 173 U1 3 U2 4 PU AMER PUBLIC HEALTH ASSN INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 1995 VL 85 IS 1 BP 34 EP 40 DI 10.2105/AJPH.85.1.34 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QD559 UT WOS:A1995QD55900009 PM 7832259 ER PT J AU ARCHER, L GRANT, BF DAWSON, DA AF ARCHER, L GRANT, BF DAWSON, DA TI WHAT IF AMERICANS DRANK LESS - THE POTENTIAL EFFECT ON THE PREVALENCE OF ALCOHOL-ABUSE AND DEPENDENCE SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID CORONARY-DISEASE; CONSUMPTION; MORTALITY; RISK AB Objectives. Several advisory committees have recently recommended that alcohol consumption be limited to moderate levels. Moderate drinking has been defined generally as not more than two drinks per day for healthy men and not more than one drink per day for healthy, nonpregnant women. The impact of reducing alcohol consumption to within the recommended guidelines on the prevalence of two serious alcohol-related problems was examined by modeling the relationship between average daily ethanol intake and alcohol abuse and dependence. Methods. The recommended drinking guidelines, both in their existing form and modified by a measure of impairment, were applied to the observed distribution of consumption derived from a large representative survey of the US general population. Results. The results demonstrated that restricting drinking to the maximum allowable levels under the existing and the modified guide lines would reduce the prevalence of alcohol abuse and dependence by 14.2% and 47.1%, respectively, in the adult US general population. Conclusions. Implications of these findings are discussed in terms of the validity of the assumptions underlying the models and the nature and direction of future research that would form the basis of newly developed guidelines for safe drinking limits. C1 NIAAA,ROCKVILLE,MD 20892. NR 33 TC 24 Z9 24 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSN INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 1995 VL 85 IS 1 BP 61 EP 66 DI 10.2105/AJPH.85.1.61 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QD559 UT WOS:A1995QD55900013 PM 7832263 ER PT J AU HARTEL, DM SCHOENBAUM, EE SELWYN, PA KLINE, J DAVENNY, K KLEIN, RS FRIEDLAND, GH AF HARTEL, DM SCHOENBAUM, EE SELWYN, PA KLINE, J DAVENNY, K KLEIN, RS FRIEDLAND, GH TI HEROIN USE DURING METHADONE-MAINTENANCE TREATMENT - THE IMPORTANCE OF METHADONE DOSE AND COCAINE USE SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID INTRAVENOUS DRUG-USERS; STIMULANTS; INFECTION; PLASMA; ABUSE; RISK; AIDS AB Objectives. The purpose of this study was to examine factors associated with heroin use during methadone maintenance treatment. Methods. Logistic regression statistical models were used to examine data obtained in a cross-sectional sample of 652 methadone patients. Results. Heroin use during the 3 months prior to interview was shown to be greatest among (1) patients maintained on methadone dosages of less than 70 mg/day (adjusted odds ratio [OR] = 2.1, 95% confidence interval [CI]= 1 3, 3.4) and (2) patients who used cocaine during treatment (adjusted OR = 5.9, 95% CI = 3.8, 9.1). These results were independent of treatment duration, treatment compliance, alcohol use, and socioeconomic factors. Cocaine users were more likely than nonusers of cocaine to use heroin at all methadone dosage levels. Conclusions. This study confirms and extends past research showing high-dose methadone maintenance to be important to heroin abstinence. Further investigation of the independent association between heroin use and cocaine use is needed. C1 YALE UNIV,SCH MED,AIDS PROGRAM,NEW HAVEN,CT. COLUMBIA UNIV,NEW YORK STATE PSYCHIAT INST,NEW YORK,NY 10032. COLUMBIA UNIV,SERGIEVSKY CTR,NEW YORK,NY. NIDA,BETHESDA,MD. RP HARTEL, DM (reprint author), MONTEFIORE MED CTR,ALBERT EINSTEIN COLL MED,111 E 210TH ST,BRONX,NY 10467, USA. FU PHS HHS [U62-CCU200714]; SAMHSA HHS [R01-OA04347] NR 36 TC 129 Z9 131 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSN INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JAN PY 1995 VL 85 IS 1 BP 83 EP 88 DI 10.2105/AJPH.85.1.83 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QD559 UT WOS:A1995QD55900017 PM 7832267 ER PT J AU BUSSE, WW KIECOLTGLASER, JK COE, C MARTIN, RJ WEISS, ST PARKER, SR AF BUSSE, WW KIECOLTGLASER, JK COE, C MARTIN, RJ WEISS, ST PARKER, SR TI STRESS AND ASTHMA SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Editorial Material C1 NHLBI,DIV LUNG DIS,BETHESDA,MD 20912. RI Kiecolt-Glaser, Janice/A-3236-2009 OI Kiecolt-Glaser, Janice/0000-0003-4900-9578 NR 16 TC 80 Z9 83 U1 1 U2 4 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD JAN PY 1995 VL 151 IS 1 BP 249 EP 252 PG 4 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA QA903 UT WOS:A1995QA90300039 PM 7812562 ER PT J AU KNEBEL, A AF KNEBEL, A TI BREATHING COMFORT DURING WEANING WITH 2 VENTILATORY MODES SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Letter RP KNEBEL, A (reprint author), NIH,CTR CLIN,DEPT NURSING,BETHESDA,MD, USA. NR 4 TC 0 Z9 0 U1 0 U2 2 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD JAN PY 1995 VL 151 IS 1 BP 254 EP 255 PG 2 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA QA903 UT WOS:A1995QA90300046 ER PT J AU OSORNIOVARGAS, AR GOODELL, AL HERNANDEZRODRIGUEZ, NA BRODY, AR COIN, PG BADGETT, A BONNER, JC AF OSORNIOVARGAS, AR GOODELL, AL HERNANDEZRODRIGUEZ, NA BRODY, AR COIN, PG BADGETT, A BONNER, JC TI PLATELET-DERIVED GROWTH-FACTOR (PDGF)-AA, (PDGF)-AB, AND (PDGF)-BB INDUCE DIFFERENTIAL CHEMOTAXIS OF EARLY-PASSAGE RAT LUNG FIBROBLASTS IN-VITRO SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID SMOOTH-MUSCLE CELLS; IDIOPATHIC PULMONARY FIBROSIS; CONNECTIVE-TISSUE CELLS; PDGF ALPHA-RECEPTOR; ALVEOLAR MACROPHAGES; UP-REGULATION; GENE-EXPRESSION; FACTOR-BETA; ISOFORMS; AA AB Platelet-derived growth factor (PDGF) isoforms are chemoattractants and mitogens for cells of mesenchymal origin that could be important mediators of pulmonary fibrogenesis. We have previously reported that particle-activated alveolar macrophages secrete homologues of PDGF that are composed of all three PDGF isoforms (PDGF-AA, -AB, and -BB). This mixture of macrophage-derived PDGF, once dissociated from the PDGF-alpha-macroglobulin complex, induces chemotaxis of rat lung fibroblasts (RLF) in the nanomolar range, In addition, we have reported that PDGF isoforms induce differential proliferation of RLF (PDGF-BB > PDGF-AB > PDGF-AA), In the present study, we sought to determine the relative chemotactic potency of the three PDGF isoforms and correlate these responses to the relative abundance of the two types of PDGF cell-surface receptors: PDGF-alpha receptor (PDGF-R alpha) and PDGF-beta receptor (PDGF-R beta), We also investigated the chemotactic activity of combinations of two PDGF isoforms simultaneously. Isolates of early-passage RLF were assayed for chemotaxis in 48-microwell chambers. Swiss mouse 3T3 cells were assayed in parallel as a positive control cell line for PDGF-R alpha and PDGF-R beta expression, RLF responded differentially to the PDGF isoforms: PDGF-AB and PDGF-BB were potent chemoattractants and stimulated maximal chemotactic responses between 4 and 8 ng/ml PDGF whereas PDGF-AA elicited a weak chemotactic response that was maximally 15% of that obtained with either B-chain isoform, PDGF-AB End PDGF-BB were also the most potent chemoattractants for Swiss 3T3 cells, and their response to these B-chain isoforms was similar to 40% greater than that obtained for RLF Swiss 3T3 cells showed a 3-fold greater response to PDGF-AA when compared with RLF Northern analysis demonstrated that RLF strongly expressed a 5.2 kb PDGF-R beta transcript and only a weak expression for a 6.5 kb PDGF-alpha transcript, In contrast, Swiss 3T3 cells strongly expressed both PDGF-R beta and PDGF-R alpha. Radioligand binding assays for [I-125]PDGF-BB showed that RLF possessed mainly PDGF-R beta at the cell surface (B-max = similar to 70 fmol/10(6) cells; K-d = 0.1 nM), and preincubation with 50 ng/ml PDGF-AA prior to binding decreased receptor number < 10%, indicating a low level of cell-surface PDGF-R alpha. Swiss 3T3 cells also bound [I-125]PDGF-BB with a K-d of 0.1 nM, but possessed a B-max of similar to 175 fmol/10(6) cells, and preincubation with 50 ng/ml PDGF-AA reduced the B-max to similar to 80 fmol/10(6) cells while increasing receptor affinity 3-fold. Further analysis of the radioligand binding data showed that Swiss 3T3 cells possessed approximately equal numbers of cell-surface PDGF-R alpha and PDGF-R beta subunits. Finally, we observed that combinations of two different PDGF isoforms mixed at equal concentrations produced additive chemotactic effects, These data indicate that all three PDGF isoforms are chemoattractants for fibroblasts, and the chemotactic response to PDGF-AA, as well as PDGF-AB and PDGF-BB, depends on the abundance of cell-surface PDGF-R alpha relative to PDGF-R beta. C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NATL CANC INST,DIV CLIN INVEST,TLALPAN,MEXICO. RI Osornio Vargas, Alvaro/D-4012-2009; Osornio Vargas, Alvaro/B-4645-2010 OI Osornio Vargas, Alvaro/0000-0001-8287-7102 NR 42 TC 32 Z9 32 U1 0 U2 2 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD JAN PY 1995 VL 12 IS 1 BP 33 EP 40 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA QB325 UT WOS:A1995QB32500006 PM 7811469 ER PT J AU COPPENHAVER, DH SINGH, IP SARZOTTI, M LEVY, HB BARON, S AF COPPENHAVER, DH SINGH, IP SARZOTTI, M LEVY, HB BARON, S TI TREATMENT OF INTRACRANIAL ALPHAVIRUS INFECTIONS IN MICE BY A COMBINATION OF SPECIFIC ANTIBODIES AND AN INTERFERON INDUCER SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID SIMPLEX VIRUS-INFECTION; CENTRAL-NERVOUS-SYSTEM; THERAPY AB Finding an effective treatment for viral infections that cause encephalitis remains an important problem. A model of human alphavirus infections, Semliki Forest virus, causes lethal encephalitis in weanling mice. Mice are viremic within 24 hr of an intraperitoneal challenge with the equivalent of three 75% lethal doses of Semliki Forest virus. Virus reaches the brain by 48 hr, and mortality results in all mice in 5-7 days. Introduction of virus intracranially accelerates the course of the infection. Neither anti-Semliki Forest virus hyperimmune serum nor the potent interferon inducer poly I:CLC given intraperitoneally are protective when used therapeutically after an intracranial virus infection, but a combination of 1,000 U hyperimmune serum and 80 mu g/mouse of poly I:CLC results in a 50% survival rate. This combination treatment of intracranial Semliki Forest virus infection eliminates detectable viremia and reduces virus load in the brain over the course of the infection. These data show that when combined, specific antibody and an interferon inducer can interact synergistically to protect mice from alphavirus infections of the central nervous system even when given after the virus is replicating in the target organ. C1 VET ADM MED CTR,BALTIMORE,MD 21218. NIAID,BETHESDA,MD 20892. RP COPPENHAVER, DH (reprint author), UNIV TEXAS,MED BRANCH,DEPT MICROBIOL & IMMUNOL,GALVESTON,TX 77555, USA. NR 27 TC 20 Z9 23 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD JAN PY 1995 VL 52 IS 1 BP 34 EP 40 PG 7 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA QH643 UT WOS:A1995QH64300007 PM 7531956 ER PT J AU BERMAN, PW AF BERMAN, PW TI BROTHERS AND SISTERS - A SPECIAL PART OF EXCEPTIONAL FAMILIES - POWELL,TH, GALLAGHER,PA SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Book Review RP BERMAN, PW (reprint author), NICHHD,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN MENTAL RETARDATION PI WASHINGTON PA 444 N CAPITOL ST, NW, STE 846, WASHINGTON, DC 20001-1512 SN 0895-8017 J9 AM J MENT RETARD JI Am. J. Ment. Retard. PD JAN PY 1995 VL 99 IS 4 BP 445 EP 446 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA QC798 UT WOS:A1995QC79800012 ER PT B AU Brock, DB AF Brock, DB GP AMER STAT ASSOC TI Employment opportunities for biostatisticians in the Federal Government SO AMERICAN STATISTICAL ASSOCIATION - 1995 PROCEEDINGS OF THE SECTION ON STATISTICAL EDUCATION LA English DT Proceedings Paper CT Annual Meeting of Section on Statistical Education of the American-Statistical-Association CY AUG 13-17, 1995 CL ORLANDO, FL SP Amer Stat Assoc, Sect Stat Edu DE biostatistics; agencies; careers RP Brock, DB (reprint author), NIA,7201 WISCONSIN AVE,SUITE 3C309,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 BN 1-883276-24-1 PY 1995 BP 218 EP 222 PG 5 WC Education & Educational Research; Education, Scientific Disciplines; Statistics & Probability SC Education & Educational Research; Mathematics GA BJ20D UT WOS:A1995BJ20D00044 ER PT J AU ZAKHAROV, SF GARNER, MM CHRAMBACH, A AF ZAKHAROV, SF GARNER, MM CHRAMBACH, A TI FLUORESCENT LABELING OF DNA WITH ETHIDIUM HOMODIMER WITHOUT MEASURABLE DECREASE IN DNA MOBILITY - APPLICATION TO AUTOMATED GEL-ELECTROPHORESIS APPARATUS SO ANALYTICAL BIOCHEMISTRY LA English DT Article AB Mobilities of DNA, fluorescently labeled with ethidium homodimer (EtD), and normalized to the mobility of the 50-bp fragment [R(f(50))], are constant with time of electrophoresis, permitting one to conduct studies on DNA mobility in an automated electrophoresis apparatus with fluorescence detection. DNA mobility decreases with an increasing binding density of ethidium homodimer, as previously reported by others and expected since the dye decreases both the net charge and the conformational flexibility of the DNA. However, it was found that this effect of ethidium binding on electrophoretic mobility becomes undetectable at binding densities less than 1 EtD/40 bp. This implies that for the purposes of electrophoretic analysis in an apparatus with fluorescence detector, DNA with ethidium homo-dimer intercalated at dye-DNA ratios less than 1/40 bp behaves like unlabeled DNA and may be assumed to be in a conformation similar to that of the unliganded DNA. Necessarily, the low labeling ratio lowers the sensitivity of detection and, in particular, increases the load requirement for a full-scale band height required for the analysis of bandwidth and band shape during electrophoresis. (C) 1995 Academic Press, Inc. C1 NICHHD,THEORET & PHYS BIOL LAB,MACROMOLEC ANAL SECT,BETHESDA,MD 20892. NR 7 TC 6 Z9 6 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD JAN 1 PY 1995 VL 224 IS 1 BP 195 EP 198 DI 10.1006/abio.1995.1029 PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QB306 UT WOS:A1995QB30600029 PM 7710071 ER PT J AU SHETTY, HU HOLLOWAY, HW RAPOPORT, SI AF SHETTY, HU HOLLOWAY, HW RAPOPORT, SI TI CAPILLARY GAS-CHROMATOGRAPHY COMBINED WITH ION-TRAP DETECTION FOR QUANTITATIVE PROFILING OF POLYOLS IN CEREBROSPINAL-FLUID AND PLASMA SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID OSMOLYTES AB Polyol species in cerebrospinal fluid and plasma-ribitol, arabitol, xylitol, 1,5-anhydrosorbitol, myo-inositol, mannitol, sorbitol, and galactitol-simultaneously were quantitated by a capillary gas chromatography/ion trap (mass spectrometric) detection method. The details of the methodology are discussed and the results of analysis of polyols in healthy human subjects are reported. Microliter volumes of cerebrospinal fluid or plasma were mixed with internal standard (deuterium labeled myoinositol), deproteinized, and evaporated to dryness. Polyols were acetylated in the presence of pyridine catalyst and washed with sodium bicarbonate solution and the acetate derivatives were recovered. Standard curve solutions were similarly treated. The polyol components were resolved on a capillary column bonded with 50% phenyl-50% methyl polysiloxane. Chemical ionization mass spectra for the acetate derivatives of polyols were generated in an ion trap using acetonitrile as reagent gas. Each polyol yielded a fragment ion in 100% abundance arising probably from the loss of one acetate moiety from the protonated molecule. These ions were monitored. The relative standard deviation (within-day) for quantitation of polyols was not greater than 8% for cerebrospinal fluid and 15% for plasma matrix. A polyol profile in cerebrospinal fluid and plasma was determined in healthy human subjects and a cerebrospinal fluid/plasma concentration ratio larger than 1.0 was found for all polyol species except 1,5-anhydrosorbitol and xylitol. This assay technique will be used to study the role of polyols in central nervous system diseases. (C) 1998 Academic Press, Inc. RP SHETTY, HU (reprint author), NIA,NEUROSCI LAB,BLDG 10,ROOM 6C103,BETHESDA,MD 20892, USA. NR 21 TC 32 Z9 32 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD JAN 1 PY 1995 VL 224 IS 1 BP 279 EP 285 DI 10.1006/abio.1995.1041 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QB306 UT WOS:A1995QB30600041 PM 7710082 ER PT J AU HARMON, PA HENDLER, RW FRIAUF, WS LEVIN, IW AF HARMON, PA HENDLER, RW FRIAUF, WS LEVIN, IW TI COMBINATION OF POTENTIOMETRY AND RESONANCE RAMAN-SPECTROSCOPY FOR THE ANALYSIS OF A REDOX PROTEIN SO ANALYTICAL BIOCHEMISTRY LA English DT Article AB This paper describes apparatus and procedures for combining resonance Raman and optical absorption spectroscopies with potentiometry for the study of redox-active heme proteins. A specially designed anaerobic titration cell is described which allows for the laser excitation of the sample and the monitoring of both Raman scattered light and directly transmitted light from an optical source. New procedures for utilization of A/D and D/A converters on a standard I/O computer card are described, which allow for computer-controlled potentiometry and coulometry. The system was tested with cytochrome c, a well-characterized respiratory protein. The correct values for the midpoint potential and electron number of the Nernst equation were obtained both by the optical absorption and resonance Raman measurements. (C) 1995 Academic Press, Inc. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 8 TC 1 Z9 1 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD JAN 1 PY 1995 VL 224 IS 1 BP 309 EP 314 DI 10.1006/abio.1995.1045 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QB306 UT WOS:A1995QB30600045 PM 7710087 ER PT J AU DONALDSON, DJ MAHAN, JT YANG, H YAMADA, KM AF DONALDSON, DJ MAHAN, JT YANG, H YAMADA, KM TI INTEGRIN AND PHOSPHOTYROSINE EXPRESSION IN NORMAL AND MIGRATING NEWT KERATINOCYTES SO ANATOMICAL RECORD LA English DT Article DE KERATINOCYTE; INTEGRIN; PHOSPHOTYROSINE; NEWT; WOUND HEALING; EPIDERMAL ID PROTEIN TYROSINE PHOSPHORYLATION; EPIDERMAL-CELL MIGRATION; EXTRACELLULAR-MATRIX; FIBRONECTIN RECEPTOR; SIGNAL TRANSDUCTION; HUMAN-SKIN; ADHESION; SURFACE; ALPHA-3-BETA-1; HEMIDESMOSOMES AB Background: Cells interact with the extracellular matrix through a family of cell surface receptors known as integrins. Ligand specificity of a given integrin is determined in part by the type of alpha and the type of beta subunit comprising it. Accumulating evidence suggests that integrin-ligand binding in some systems influences cell behavior through tyrosine phosphorylation of intracellular proteins. Methods: In this study, we utilized immunohistochemistry to examine the expression of beta(1) and beta(4) integrin subunits as well as tyrosine phosphorylation in normal keratinocytes and in keratinocytes migrating to form a wound epithelium. An adhesion assay was used to determine if freshly isolated keratinocytes could interact with fibronectin and collagen. Polyacrylamide gel electrophoresis followed by immunoblotting was employed to compare beta(1) integrins in migrating and nonmigrating keratinocytes. Results: In normal epidermis, beta(1) and beta(4) localized primarily to basal cells, where both subunits were generally distributed over all parts of the cell periphery. Except for a modest presence in suprabasal cells and a minimal presence adjacent to the epidermal basement membrane, phosphotyrosine (ptyr) had a similar distribution. In migrating keratinocytes, beta(1), beta(4), and ptyr localized most heavily at the interface between the forming wound epithelium and the wound bed. Adhesion assays using keratinocytes from normal epidermis revealed a population of cells that could specifically adhere and spread on fibronectin and type I collagen. Immunoblots of beta(1) subunits from normal and migrating keratinocytes showed no increase in amount of beta(1), nor did the apparent size of beta(1) change in migrating compared to normal cells. Conclusions: The heavy accumulation of beta(1) and beta(4) at the wound bed interface in migrating cells suggests that these subunits may be involved in attachments of migrating cells to extracellular matrix proteins in the wound. The accumulation of ptyr in the same region further suggests that integrin-ligand interaction in keratinocytes modulates cell behavior through phosphorylated proteins. The fact that freshly isolated newt keratinocytes could adhere and spread on fibronectin or collagen shows that these cells are constitutively activated. This view is supported by the absence of any evidence that the beta(1) in migrating keratinocytes is larger and therefore more mature than beta(1) in normal keratinocytes. By comparison, beta(1) integrins on human keratinocytes are not constitutively activated (Takashima and Grinnell, 1985; Toda ct al., 1987; Guo et al., 1990, 1991), a difference that may explain why epidermal wound healing is faster in newts than in humans. (C) 1995 Wiley-Liss, Inc. C1 NIH,DEV BIOL LAB,BETHESDA,MD 20892. RP DONALDSON, DJ (reprint author), UNIV TENNESSEE,CTR HLTH SCI,DEPT ANAT & NEUROBIOL,855 MONROE AVE,MEMPHIS,TN 38163, USA. OI Yamada, Kenneth/0000-0003-1512-6805 FU NIAMS NIH HHS [AR27940] NR 39 TC 11 Z9 11 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 0003-276X J9 ANAT REC JI Anat. Rec. PD JAN PY 1995 VL 241 IS 1 BP 49 EP 58 DI 10.1002/ar.1092410108 PG 10 WC Anatomy & Morphology SC Anatomy & Morphology GA QF983 UT WOS:A1995QF98300007 PM 7533482 ER PT J AU LYON, GR AF LYON, GR TI TOWARD A DEFINITION OF DYSLEXIA SO ANNALS OF DYSLEXIA LA English DT Review ID SPEECH PRODUCTION DEFICITS; LEARNING-DISABILITIES; PHONOLOGICAL AWARENESS; DEVELOPMENTAL DYSLEXIA; READING-DISABILITY; INDIVIDUAL-DIFFERENCES; PHONEMIC AWARENESS; WORD-RECOGNITION; CHILDREN; SKILLS RP LYON, GR (reprint author), NIH,BLDG 10,BETHESDA,MD 20892, USA. NR 136 TC 226 Z9 230 U1 3 U2 21 PU ORTON DYSLEXIA SOC PI BALTIMORE PA CHESTER BUILDING, STE 382, 8600 LA SALLE RD, BALTIMORE, MD 21204-6020 SN 0736-9387 J9 ANN DYSLEXIA JI Ann. Dyslexia PY 1995 VL 45 BP 3 EP 27 PG 25 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA TK293 UT WOS:A1995TK29300002 ER PT J AU FISCHL, MA STANLEY, K COLLIER, AC ARDUINO, JM STEIN, DS FEINBERG, JE ALLAN, JD GOLDSMITH, JC POWDERLY, WG RAINES, CP MAYJO, KJ KERULY, JC CRAVEN, D HIRSHORN, L HIRSCH, MS JAYAWEERA, DT YOUNG, SW PATRONEREESE, J BRETTLER, D SPERBER, K GERITS, P SEREMETIS, S GILL, JC GELB, LD MCGUIRE, ML STIFFLER, T LEDERMAN, MM CAREY, JT WALLACE, M MACARTHUR, RD BERGE, P MILDVAN, D COREY, L COOMBS, RW CUMMINGS, DK SCHOOLEY, RT RAY, MG WAITE, V KURITZKES, DR FUHRER, J TENZLER, RJ DONLON, W VANDERHORST, CM TROIANI, L HORTON, J LANE, TW MURPHY, RR PHAIR, JP KESSLER, HA BENSON, CA ROSENWALD, V YONREN, S VALENTINE, F HASLETT, P MITSUYASU, RT GUERRO, M GOETZ, MB MATHISEN, GE FRAME, PT BRINKDOPKE, J POWELL, T HOELLE, M MERIGAN, TC SHAFER, R CAIN, P FESSELL, J HENRY, K RHAME, F CHRISTENSON, J STRYKE, D ZINGMAN, B KAHL, P SOEIRO, R CHOI, YS REICHMAN, RL REID, J BLAIR, DC STEIGBIGEL, RT HEWITT, RG CAMERON, ML DONNELLY, MA PACKARD, MV BARTLETT, JA FIFE, KH ZWICKL, BW BORUM, J BURACK, JH DYBECK, KA COLEMAN, RL JOHNSON, WR MCKINLEY, GF GRIECO, MH KOLATCH, BR SEPKOWITZ, K PONTICELLO, L GIORDANO, MF MURRAY, HW GOCKE, DJ FASS, RJ PARA, MF STERN, JS DREW, LJ SPECTOR, SA HAVLIR, DV NUFFER, KL RICHMAN, DD CONNOR, EM KLOSER, PC PICARDI, JM VANMATERMINER, C LEEDOM, JM HOLTOM, PD RICHARDSON, W EHMANN, WC ZURLO, JJ KREHER, M EYSTER, ME HYSLOP, NE MUSHATT, DM HOADLEY, DJ ZACHARY, JA SIMON, GL PARENTI, DM LELACHEUR, S SCHUCK, S HO, MT MCMAHON, DK PAZIN, GJ ROSENER, R CHEESEMAN, SH MANGINI, LA SANDS, MG KAZIAL, K JONES, G PETTINELLI, CB LANDRY, B MARTINEZ, AI AF FISCHL, MA STANLEY, K COLLIER, AC ARDUINO, JM STEIN, DS FEINBERG, JE ALLAN, JD GOLDSMITH, JC POWDERLY, WG RAINES, CP MAYJO, KJ KERULY, JC CRAVEN, D HIRSHORN, L HIRSCH, MS JAYAWEERA, DT YOUNG, SW PATRONEREESE, J BRETTLER, D SPERBER, K GERITS, P SEREMETIS, S GILL, JC GELB, LD MCGUIRE, ML STIFFLER, T LEDERMAN, MM CAREY, JT WALLACE, M MACARTHUR, RD BERGE, P MILDVAN, D COREY, L COOMBS, RW CUMMINGS, DK SCHOOLEY, RT RAY, MG WAITE, V KURITZKES, DR FUHRER, J TENZLER, RJ DONLON, W VANDERHORST, CM TROIANI, L HORTON, J LANE, TW MURPHY, RR PHAIR, JP KESSLER, HA BENSON, CA ROSENWALD, V YONREN, S VALENTINE, F HASLETT, P MITSUYASU, RT GUERRO, M GOETZ, MB MATHISEN, GE FRAME, PT BRINKDOPKE, J POWELL, T HOELLE, M MERIGAN, TC SHAFER, R CAIN, P FESSELL, J HENRY, K RHAME, F CHRISTENSON, J STRYKE, D ZINGMAN, B KAHL, P SOEIRO, R CHOI, YS REICHMAN, RL REID, J BLAIR, DC STEIGBIGEL, RT HEWITT, RG CAMERON, ML DONNELLY, MA PACKARD, MV BARTLETT, JA FIFE, KH ZWICKL, BW BORUM, J BURACK, JH DYBECK, KA COLEMAN, RL JOHNSON, WR MCKINLEY, GF GRIECO, MH KOLATCH, BR SEPKOWITZ, K PONTICELLO, L GIORDANO, MF MURRAY, HW GOCKE, DJ FASS, RJ PARA, MF STERN, JS DREW, LJ SPECTOR, SA HAVLIR, DV NUFFER, KL RICHMAN, DD CONNOR, EM KLOSER, PC PICARDI, JM VANMATERMINER, C LEEDOM, JM HOLTOM, PD RICHARDSON, W EHMANN, WC ZURLO, JJ KREHER, M EYSTER, ME HYSLOP, NE MUSHATT, DM HOADLEY, DJ ZACHARY, JA SIMON, GL PARENTI, DM LELACHEUR, S SCHUCK, S HO, MT MCMAHON, DK PAZIN, GJ ROSENER, R CHEESEMAN, SH MANGINI, LA SANDS, MG KAZIAL, K JONES, G PETTINELLI, CB LANDRY, B MARTINEZ, AI TI COMBINATION AND MONOTHERAPY WITH ZIDOVUDINE AND ZALCITABINE IN PATIENTS WITH ADVANCED HIV DISEASE SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE HIV INFECTIONS; ZIDOVUDINE; ZALCITABINE; DRUG THERAPY, COMBINATION; ANTIGENS, CD4 ID IMMUNODEFICIENCY-VIRUS-INFECTION; AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; PHASE-I TRIAL; 2',3'-DIDEOXYINOSINE DDI; DOUBLE-BLIND; 2',3'-DIDEOXYCYTIDINE; AZT; DIDEOXYCYTIDINE; EFFICACY AB Objective: To compare the safety and efficacy of continuing zidovudine therapy with that of zalcitabine alone or zalcitabine and zidovudine used together. Design: A randomized, double-blind, controlled trial. Setting: AIDS Clinical Trials units and National Hemophilia Foundation sites. Patients: 1001 patients with symptomatic human immunodeficiency (HIV) disease and 300 or fewer CD4 cells/mm(3) or asymptomatic HIV disease and 200 or fewer CD4 cells/mm(3) who had tolerated zidovudine therapy for 6 months or more. Intervention: Patients were randomly assigned to receive zidovudine, 600 mg/d; zalcitabine, 2.25 mg/d; or zidovudine, 600 mg/d, and zalcitabine, 2.25 mg/d. Measurements: The primary end point was time to disease progression or death. Results: The median follow-up time was 17.7 months. The estimated 72-month event-free rates were 70%, 67%, and 73%, respectively, for the zidovudine, zalcitabine, and combination groups (P = 0.26). A trend analysis showed significantly lower progression rates for combination therapy compared with zidovudine therapy as the pretreatment CD4 cell count increased (P = 0.027). For patients with 150 or more CD4 cells/ mm(3), those receiving combination therapy were less likely to have disease progression or to die than were those receiving zidovudine (relative risk, 0.51; 95% Cl, 0.28 to 0.93; P = 0.029). We observed no difference between the zalcitabine and zidovudine groups (relative risk, 0.74; Cl, 0.40 to 1.36; P = 0.33). For patients with 50 to 150 CD4 cells/mm(3) or fewer than 50 CD4 cells/mm(3), we found no differences among the treatment groups (P = 0.69 and P = 0.57, respectively). Severe toxic effects occurred less frequently among patients with 150 or more CD4 cells/mm(3). Conclusions: We found no overall benefits of zalcitabine used alone or with zidovudine. However, a trend analysis suggested a better outcome for combination therapy compared with zidovudine as the pretreatment CD4 cell count increased. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. UNIV WASHINGTON,HARBORVIEW MED CTR,SEATTLE,WA 98104. ALBANY MED COLL,ALBANY,NY 12208. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,NIAID,CLIN TRIALS GRP,BALTIMORE,MD. BETH ISRAEL HOSP,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MEM HOSP,NEW ENGLAND AREA COMPREHENS HEMOPHILIA CTR,WORCESTER,MA. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. MT SINAI HEMOPHILIA CTR,NEW YORK,NY. GREAT LAKES HEMOPHILIA CTR,MILWAUKEE,WI. WASHINGTON UNIV,ST LOUIS,MO. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. MED COLL OHIO,TOLEDO,OH 43699. BETH ISRAEL HOSP,NEW YORK,NY. UNIV WASHINGTON,SEATTLE,WA 98195. UNIV COLORADO,HLTH SCI CTR,DENVER,CO. SUNY STONY BROOK,STONY BROOK,NY. UNIV N CAROLINA,CHAPEL HILL,NC. CAROLINAS MED CTR,CHARLOTTE,NC 28203. MOSES CONE MEM HOSP,GREENSBORO,NC. NORTHWESTERN UNIV,CHICAGO,IL 60611. RUSH PRESBYTERIAN HOSP,CHICAGO,IL. NYU,MED CTR,NEW YORK,NY. UNIV CALIF LOS ANGELES,CTR CARE,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,HARBOR MED CTR,LOS ANGELES,CA 90024. SEPULVEDA VET ADM HOSP,LOS ANGELES,CA. OLIVE VIEW MED CTR,LOS ANGELES,CA. UNIV CINCINNATI,CINCINNATI,OH. STANFORD UNIV,STANFORD,CA 94305. KAISER PERMANENTE MED CTR,SAN FRANCISCO,CA. ST PAUL RAMSEY MED CTR,MINNEAPOLIS,MN. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. RIVERSIDE MED CTR,MINNEAPOLIS,MN. MONTEFIORE HOSP & MED CTR,BRONX,NY. ALBERT EINSTEIN COLL MED,BRONX,NY 10467. BRONX MUNICIPAL HOSP CTR,BRONX,NY. UNIV ROCHESTER,ROCHESTER,NY. SUNY SYRACUSE,SYRACUSE,NY. SUNY BUFFALO,BUFFALO,NY. DUKE UNIV,MED CTR,DURHAM,NC. INDIANA UNIV,INDIANAPOLIS,IN 46204. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,SAN FRANCISCO,CA. COLUMBIA UNIV,ST LUKES ROOSEVELT HOSP CTR,NEW YORK,NY. CORNELL UNIV,COLL MED,NEW YORK,NY. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,NEW BRUNSWICK,NJ. OHIO STATE UNIV,COLUMBUS,OH 43210. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,NEWARK,NJ 07103. UNIV SO CALIF,LOS ANGELES,CA. PENN STATE UNIV,COLL MED,HERSHEY,PA. TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. LOUISIANA STATE UNIV,MED CTR,SCH MED,NEW ORLEANS,LA 70112. GEORGE WASHINGTON UNIV,WASHINGTON,DC. UNIV PITTSBURGH,PITTSBURGH,PA. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA. BAYSTATE MED CTR,SPRINGFIELD,MA 01107. FRONTIER SCI & TECHNOL RES FDN INC,AMHERST,NY. NIAID,BETHESDA,MD 20892. RP FISCHL, MA (reprint author), UNIV MIAMI,SCH MED,DEPT MED,R-60A,POB 016960,MIAMI,FL 33101, USA. NR 25 TC 109 Z9 110 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JAN 1 PY 1995 VL 122 IS 1 BP 24 EP 32 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA PY502 UT WOS:A1995PY50200004 PM 7985892 ER PT J AU LEROITH, D BASERGA, R HELMAN, L ROBERTS, CT AF LEROITH, D BASERGA, R HELMAN, L ROBERTS, CT TI INSULIN-LIKE GROWTH-FACTORS AND CANCER SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID MESSENGER RIBONUCLEIC-ACID; NONISLET CELL TUMORS; HUMAN-BREAST CANCER; FACTOR-II GENE; WILMS-TUMOR; PROTEIN SECRETION; BINDING PROTEINS; IGF-I; EXPRESSION; RECEPTOR AB The insulin-like growth factor (IGF) family of peptides, binding proteins, and receptors are important for normal human growth and development and are involved in the specialized functions of most physiologic systems. Most members of the IGF system are expressed by different cancer cells and may play an important role in the propagation of these malignancies. New therapies aimed at modulating various components of the IGF system could affect the progression and metastasis of cancer. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,JEFFERSON CANC CTR,PHILADELPHIA,PA 19107. NCI,PEDIAT BRANCH,MOLEC ONCOL SECT,BETHESDA,MD 20892. RP LEROITH, D (reprint author), NIDDKD,DIABET BRANCH,MOLEC & CELLULAR PHYSIOL SECT,BLDG 10,ROOM 8S-239,BETHESDA,MD 20892, USA. OI Roberts, Charles/0000-0003-1756-5772 NR 53 TC 246 Z9 248 U1 0 U2 4 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JAN 1 PY 1995 VL 122 IS 1 BP 54 EP 59 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA PY502 UT WOS:A1995PY50200009 PM 7619109 ER PT J AU BENVENGA, S AF BENVENGA, S TI RESTRICTION ISOTYPING OF APOLIPOPROTEIN-E SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP BENVENGA, S (reprint author), NIDDKD,BETHESDA,MD 20892, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JAN 1 PY 1995 VL 122 IS 1 BP 68 EP 68 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA PY502 UT WOS:A1995PY50200014 PM 7985900 ER PT J AU SADATO, N ZEFFIRO, TA CAMPBELL, G KONISHI, J SHIBASAKI, H HALLETT, M AF SADATO, N ZEFFIRO, TA CAMPBELL, G KONISHI, J SHIBASAKI, H HALLETT, M TI REGIONAL CEREBRAL BLOOD-FLOW CHANGES IN MOTOR CORTICAL AREAS AFTER TRANSIENT ANESTHESIA OF THE FOREARM SO ANNALS OF NEUROLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; MAGNETIC STIMULATION; SOMATOSENSORY CORTEX; FUNCTIONAL-ANATOMY; PREMOTOR CORTEX; PET IMAGES; MOVEMENTS; REORGANIZATION; ORGANIZATION; BRAIN AB To study the effect of deafferentation on cortical areas activated by movement of the proximal muscles, we measured regional cerebral blood flow with positron emission tomography and O-15-labeled water. Flexion-extension movements of the right elbow before deafferentation were associated with an increase of regional cerebral blood flow in the primary sensorimotor area bilaterally, posterior supplementary motor area bilaterally, ipsilateral cerebellum, contralateral putamen, premotor area, anterior cingulate area, and posterior parietal region. Transient anesthesia of the right forearm induced by ischemic block caused an increase of regional cerebral blood flow in the primary sensorimotor area bilaterally at rest, but there was no change of regional cerebral blood flow with movement, indicating that the movement-related change in cerebral blood how was reduced. These findings are consistent with increased excitability of neurons as a result of deafferentation. In the supplementary motor area, anesthesia did not induce any change in regional cerebral blood flow at rest, but there was a decline with movement, again indicating a reduction of the change in cerebral blood flow related to movement. This might be due to a reduction in sensory feedback because of the anesthesia. C1 NINCDS,HUMAN MOTOR CONTROL SECT,MED NEUROL BRANCH,BETHESDA,MD 20892. NINCDS,BIOMETRY & FIELD STUDIES BRANCH,BETHESDA,MD. NIA,NEUROSCI LAB,BETHESDA,MD. KYOTO UNIV,FAC MED,DEPT NUCL MED,KYOTO,JAPAN. KYOTO UNIV,FAC MED,DEPT BRAIN PATHOPHYSIOL,KYOTO,JAPAN. NR 49 TC 59 Z9 60 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JAN PY 1995 VL 37 IS 1 BP 74 EP 81 DI 10.1002/ana.410370114 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA QB842 UT WOS:A1995QB84200012 PM 7818261 ER PT J AU Ferguson, JH AF Ferguson, JH TI Patient participation in medical consensus conferences SO ANNALS OF ONCOLOGY LA English DT Editorial Material RP Ferguson, JH (reprint author), NIH,OFF MED APPLICAT RES,FED BLDG,BETHESDA,MD 20892, USA. NR 2 TC 3 Z9 3 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PY 1995 VL 6 SU 2 BP 3 EP 4 PG 2 WC Oncology SC Oncology GA TQ504 UT WOS:A1995TQ50400002 PM 8547193 ER PT J AU CRAGG, GM BOYD, MR GREVER, MR SCHEPARTZ, S AF CRAGG, GM BOYD, MR GREVER, MR SCHEPARTZ, S TI PHARMACEUTICAL PROSPECTING AND THE POTENTIAL FOR PHARMACEUTICAL CROPS, NATURAL PRODUCT DRUG DISCOVERY AND DEVELOPMENT AT THE UNITED-STATES NATIONAL-CANCER-INSTITUTE SO ANNALS OF THE MISSOURI BOTANICAL GARDEN LA English DT Article; Proceedings Paper CT 40th Annual Systematics Symposium of the Missouri-Botanical-Garden on Economic Botany CY OCT 08-09, 1993 CL ST LOUIS, MO SP MISSOURI BOTAN GARDEN, NATL SCI FDN ID ANTICANCER; AGENTS; PLANTS; TAXOL AB Chemically-complex natural product drugs are not readily synthesized, and large-scale production for clinical and commercial development often involves isolation from the natural source. The rapidly escalating demand for taxol, originally isolated from the bark of Taxus brevifolia, has emphasized the need for alternative sources to the wild plant, and the National Cancer Institute (NCI) has developed policies for exploring such sources at the early stages of preclinical development of potential new drugs. The potential for pharmaceutical crop development in the case of several possible anti-AIDS agents will be discussed. RP CRAGG, GM (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892, USA. NR 27 TC 5 Z9 5 U1 0 U2 1 PU MISSOURI BOTANICAL GARDEN PI ST LOUIS PA 2345 TOWER GROVE AVENUE, ST LOUIS, MO 63110 SN 0026-6493 J9 ANN MO BOT GARD JI Ann. Mo. Bot. Gard. PY 1995 VL 82 IS 1 BP 47 EP 53 DI 10.2307/2399979 PG 7 WC Plant Sciences SC Plant Sciences GA QJ948 UT WOS:A1995QJ94800006 ER PT J AU SUN, PD DAVIES, DR AF SUN, PD DAVIES, DR TI THE CYSTINE-KNOT GROWTH-FACTOR SUPERFAMILY SO ANNUAL REVIEW OF BIOPHYSICS AND BIOMOLECULAR STRUCTURE LA English DT Review DE X-RAY STRUCTURE; COMMON CYTOKINE FOLD; COMPARISON OF TGF-BETA, PDGF, NGF, AND HCG; DISULFIDE MOTIF ID HUMAN TRANSFORMING GROWTH-FACTOR-BETA-2; DEOXYRIBONUCLEIC-ACID CLONING; MESSENGER RIBONUCLEIC-ACID; REFINED CRYSTAL-STRUCTURE; OVARIAN FOLLICULAR-FLUID; MOLECULAR-WEIGHT COMPLEX; FACTOR-BETA FAMILY; TGF-BETA; 3-DIMENSIONAL STRUCTURE; NEUROTROPHIC FACTOR AB Four recent crystal structures of growth factors-nerve growth factor, transforming growth factor-beta, platelet-derived growth factor, and human chorionic gonadotropin-from four separate superfamilies revealed that these proteins are structurally related and share a common overall topology. These proteins have very little sequence homology, but they all have an unusual arrangement of six cysteines linked to form a ''cystine-knot'' conformation. The active forms of these proteins are dimers, either homo- or heterodimers. Despite the overall topological similarity between the monomers, the interfaces used to form the dimer are in each case quite different. Because the surfaces used for dimer formation are mostly hydrophobic, the uniqueness of each dimer accounts for the lack of sequence homology and raises questions about the effectiveness of reverse sequence fitting in this kind of structure as a predictor of structural homology. C1 NIDDKD, BETHESDA, MD 20892 USA. RP SUN, PD (reprint author), NIAID, BETHESDA, MD 20892 USA. NR 104 TC 212 Z9 216 U1 1 U2 21 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 1056-8700 J9 ANNU REV BIOPH BIOM JI Annu. Rev. Biophys. Biomolec. Struct. PY 1995 VL 24 BP 269 EP 291 DI 10.1146/annurev.bb.24.060195.001413 PG 23 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RD912 UT WOS:A1995RD91200011 PM 7663117 ER PT J AU Wu, C AF Wu, C TI Heat shock transcription factors: Structure and regulation SO ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY LA English DT Review DE heat shock response; regulators; DNA binding; coiled coil; transactivation ID DNA-BINDING ACTIVITY; RNA POLYMERASE-II; SACCHAROMYCES-CEREVISIAE; MOLECULAR CHAPERONES; ACTIVATOR PROTEIN; FACTOR CONTAINS; COILED-COIL; HSP70 GENE; SCHIZOSACCHAROMYCES-POMBE; DROSOPHILA-MELANOGASTER AB Organisms respond to elevated temperatures and to chemical and physiological stresses by an increase in the synthesis of heat shock proteins. The regulation of heat shock gene expression in eukaryotes is mediated by the conserved heat shock transcription factor (HSF). HSF is present in a latent state under normal conditions; it is activated upon heat stress by induction of trimerization and high-affinity binding to DNA and by exposure of domains for transcriptional activity. Analysis of HSF cDNA clones from many species has defined structural and regulatory regions responsible for the inducible activities. The heat stress signal is thought to be transduced to HSF by changes in the physical environment, in the activity of HSF-modifying enzymes, or by changes in the intracellular level of heat shock proteins. RP Wu, C (reprint author), NCI,NIH,BIOCHEM LAB,BLDG 37,ROOM 4C-09,BETHESDA,MD 20892, USA. NR 157 TC 768 Z9 820 U1 8 U2 91 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 1081-0706 J9 ANNU REV CELL DEV BI JI Annu. Rev. Cell Dev. Biol. PY 1995 VL 11 BP 441 EP 469 DI 10.1146/annurev.cellbio.11.1.441 PG 29 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA TY448 UT WOS:A1995TY44800016 PM 8689565 ER PT J AU Kennison, JA AF Kennison, JA TI The Polycomb and trithorax group proteins of Drosophila: Trans-regulators of homeotic gene function SO ANNUAL REVIEW OF GENETICS LA English DT Review DE polycomb; trithorax; homeotic; brahma; zeste ID POSITION-EFFECT VARIEGATION; DOSAGE-DEPENDENT MODIFIERS; HETEROCHROMATIN-ASSOCIATED PROTEIN; POSTERIOR-SEX COMBS; BITHORAX COMPLEX; TRANSCRIPTIONAL ACTIVATION; SEQUENCE SIMILARITY; HOMOEOTIC MUTATIONS; MELANOGASTER; ZESTE AB The Polycomb and trithorax group genes encode trans-regulators of homeotic gene function in Drosophila. The Polycomb group genes encode transcriptional repressors, while the trithorax group proteins are positive factors required for homeotic gene function. Among the Polycomb group proteins, the POLYCOMB protein has been most extensively characterized. The POLYCOMB protein contains a chromodomain, a conserved domain found in a Drosophila protein with effects on position-effect variegation. Among the trithorax group proteins characterized, the BRAHMA protein appears to be a subunit of a protein complex conserved from yeast to man (the SNF/SWI complex) that modifies chromatin to facilitate the transcriptional activation by gene-specific DNA-binding proteins. The ZESTE protein may help to activate transcription by bringing distant cis-regulatory elements closer to promoter-bound proteins. RP Kennison, JA (reprint author), NICHHD,GENET MOLEC LAB,BETHESDA,MD 20892, USA. NR 82 TC 318 Z9 328 U1 1 U2 6 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4197 J9 ANNU REV GENET JI Annu. Rev. Genet. PY 1995 VL 29 BP 289 EP 303 DI 10.1146/annurev.ge.29.120195.001445 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA TL719 UT WOS:A1995TL71900011 PM 8825476 ER PT J AU Lichten, M Goldman, ASH AF Lichten, M Goldman, ASH TI Meiotic recombination hotspots SO ANNUAL REVIEW OF GENETICS LA English DT Review DE crossing-over; gene conversion; meiosis; chromosome structure; chiasmata ID DOUBLE-STRAND BREAKS; MAJOR HISTOCOMPATIBILITY COMPLEX; YEAST SACCHAROMYCES-CEREVISIAE; GENE CONVERSION GRADIENT; CAENORHABDITIS-ELEGANS; HOT-SPOT; CHIASMA DISTRIBUTION; INITIATION SITE; HIS4 LOCUS; SCHIZOSACCHAROMYCES-POMBE AB Meiotic recombination occurs more frequently in some regions of the eukaryotic genome than in others, with variations of several orders of magnitude observed in frequencies of meiotic exchange per unit physical distance. This article reviews what is known about meiotic recombination hotspots loci, or regions that display a greater than average frequency of meiotic exchange. Hotspots have been most intensively studied in Saccharomyces cerevisiae, which is a major focus of this article. Also reviewed is the current state of knowledge regarding hotspots in other fungi, in maize, in nematodes, in mice, and in humans. RP Lichten, M (reprint author), NCI,DIAGNOSIS & CTR,DIV CANC BIOL,BIOCHEM LAB,BETHESDA,MD 20892, USA. RI Lichten, Michael/C-5795-2013 OI Lichten, Michael/0000-0001-9707-2956 NR 155 TC 244 Z9 252 U1 2 U2 22 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4197 J9 ANNU REV GENET JI Annu. Rev. Genet. PY 1995 VL 29 BP 423 EP 444 DI 10.1146/annurev.ge.29.120195.002231 PG 22 WC Genetics & Heredity SC Genetics & Heredity GA TL719 UT WOS:A1995TL71900017 PM 8825482 ER PT J AU CameriniOtero, RD Hsieh, P AF CameriniOtero, RD Hsieh, P TI Homologous recombination proteins in prokaryotes and eukaryotes SO ANNUAL REVIEW OF GENETICS LA English DT Review DE recombination; RecA; homologous pairing; meiosis; synapsis ID SINGLE-STRANDED-DNA; ESCHERICHIA-COLI RECA; SITE-SPECIFIC RECOMBINATION; SYNTHETIC HOLLIDAY JUNCTIONS; SACCHAROMYCES-CEREVISIAE; GENETIC-RECOMBINATION; BINDING-PROTEIN; BRANCH MIGRATION; BACTERIOPHAGE-LAMBDA; NUCLEOTIDE-SEQUENCE AB Genetic recombination is common to all forms of life and involves the exchange of DNA sequences between two chromosomes or DNA molecules. Such exchanges contribute to the generation of genetic diversity and the repair of damaged DNA. There are two major classes of recombination, site-specific recombination and general or homologous recombination. In homologous recombination the joining of the DNA duplexes exhibits a similar degree of precision or fidelity but, generally speaking, does not take place at specific sites. Since exchange can occur anywhere along the length of two homologous chromosomes, it follows that the proteins that catalyze homologous recombination are not sequence- or site-specific binding proteins. This review focuses on genetic and biochemical analyses of homologous recombination proteins that carry out conjugational recombination in E, coli and meiotic recombination in eukaryotes. RP CameriniOtero, RD (reprint author), NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892, USA. NR 259 TC 119 Z9 122 U1 4 U2 12 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4197 J9 ANNU REV GENET JI Annu. Rev. Genet. PY 1995 VL 29 BP 509 EP 552 DI 10.1146/annurev.genet.29.1.509 PG 44 WC Genetics & Heredity SC Genetics & Heredity GA TL719 UT WOS:A1995TL71900020 PM 8825485 ER PT J AU Gottesman, MM Hrycyna, CA Schoenlein, PV Germann, UA Pastan, I AF Gottesman, MM Hrycyna, CA Schoenlein, PV Germann, UA Pastan, I TI Genetic analysis of the multidrug transporter SO ANNUAL REVIEW OF GENETICS LA English DT Review DE multidrug resistance; P-glycoprotein; chemotherapy; episomes; gene therapy ID PROTEIN-KINASE-C; P-GLYCOPROTEIN GENE; RESISTANT CHINESE-HAMSTER; KB CARCINOMA-CELLS; HUMAN MDR1 GENE; DIHYDROFOLATE-REDUCTASE GENES; PREDICTED TRANSMEMBRANE DOMAIN; DOUBLE MINUTE CHROMOSOMES; MULTIPLE-DRUG RESISTANCE; ATP-DEPENDENT TRANSPORT AB The analysis of how human cancers evade chemotherapy has revealed a rich variety of cell-based genetic changes resulting in drug resistance. One of the best studied of these genetic alterations is increased expression of an ATP-dependent plasma membrane transport system known as P-glycoprotein, or the multidrug transporter. This transporter actively effluxes a large number of natural product, hydrophobic, cytotoxic drugs, including many important anticancer agents. This review focuses on the genetic and molecular genetic analysis of the human multidrug transporter, including structure-function analysis, pre- and posttranslational regulation of expression, the role of gene amplification in increased expression, and the properties of transgenic and ''knock-out'' mice. One important feature of the MDR gene is its potential for the development of new selectable vectors for human gene therapy. C1 MED COLL GEORGIA, AUGUSTA, GA 30912 USA. VERTEX PHARMACEUT INC, CAMBRIDGE, MA 02139 USA. NCI, MOLEC BIOL LAB, BETHESDA, MD 20892 USA. RP Gottesman, MM (reprint author), NCI, CELL BIOL LAB, BETHESDA, MD 20892 USA. NR 258 TC 407 Z9 415 U1 1 U2 4 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0066-4197 EI 1545-2948 J9 ANNU REV GENET JI Annu. Rev. Genet. PY 1995 VL 29 BP 607 EP 649 PG 43 WC Genetics & Heredity SC Genetics & Heredity GA TL719 UT WOS:A1995TL71900023 PM 8825488 ER PT J AU WILDER, RL AF WILDER, RL TI NEUROENDOCRINE-IMMUNE SYSTEM INTERACTIONS AND AUTOIMMUNITY SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE STRESS RESPONSE; THYMUS; CORTICOSTEROIDS; HYPOTHALAMIC-PITUITARY-ADRENAL AXIS; HYPOTHALAMIC-PITUITARY-GONADAL AXIS ID CORTICOTROPIN-RELEASING HORMONE; PITUITARY-ADRENAL AXIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; BLOOD MONONUCLEAR-CELLS; GLUCOCORTICOID-INDUCED APOPTOSIS; INTERLEUKIN-6 MESSENGER-RNA; THYMIC EPITHELIAL-CELLS; SUSCEPTIBLE LEWIS RATS; AGE-ASSOCIATED DECLINE; TUMOR-NECROSIS-FACTOR AB The concept of an integrated bidirectionally regulated neuroendocrine-immune adaptive response to stress has strong experimental support; The quality and intensity of this coordinated response to stress varies depending upon age, gender, reproductive status, and other genetically determined factors as well as the types and magnitudes of environmental challenges. These factors and dysfunctional communication between the nervous, endocrine, and immune systems appear to contribute to the development of autoimmune diseases in the Lewis and BE rats, the OS chicken, and the NOD, MRL, NZB, NZW, and NZB/NZW F1 mice. Neuroendocrine-immune dysfunction also contributes to the pathogenesis of human autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, thyroid diseases, and others. This review highlights these concepts. It includes discussions on various aspects of the stress response, the hypothalamic-pituitary-adrenal and -gonadal axes, corticotropin releasing hormone, luteinizing hormone releasing hormone, interleukin-1 and -6, corticosteroids, estrogens, testosterone, dehydroepiandrosterone, growth hormone, prolactin, and thyroid hormone. The role of the nervous and endocrine systems in regulating thymopoiesis and T cell development is also emphasized. RP WILDER, RL (reprint author), NIH,ARTHRIT & RHEUMAT BRANCH,INFLAMMATORY JOINT DIS SECT,BETHESDA,MD 20892, USA. NR 220 TC 363 Z9 372 U1 1 U2 18 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1995 VL 13 BP 307 EP 338 PG 32 WC Immunology SC Immunology GA QV290 UT WOS:A1995QV29000012 PM 7612226 ER PT J AU PANTALEO, G FAUCI, AS AF PANTALEO, G FAUCI, AS TI NEW CONCEPTS IN THE IMMUNOPATHOGENESIS OF HIV-INFECTION SO ANNUAL REVIEW OF IMMUNOLOGY LA English DT Review DE LYMPHOID ORGANS; PRIMARY IMMUNE RESPONSE; IMMUNE ACTIVATION; LONG-TERM NONPROGRESSORS ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMMUNE-SYSTEM ACTIVATION; PROGRAMMED CELL-DEATH; RECEPTOR BETA-CHAIN; T-CELL; INTERLEUKIN-2 RECEPTORS; TYPE-1 INFECTION; LYMPHOID ORGANS; LYMPHOCYTES-T; REGION GENES AB The typical course of HIV infection is characterized by multiple phases that occur over a period of eight to ten years, A critical event in the initial establishment of HIV infection is the localization of HIV in lymphoid organs that serve as major reservoirs for HIV and as primary sites for virus replication. Despite the fact that the majority of HIV-infected individuals do not show any clinical signs of disease activity for extended periods of time, HIV disease is active and progressive in lymphoid organs during this clinically latent period, Persistence of virus in lymphoid organs causes a chronic stimulation of the immune system that ultimately leads to destruction of the lymphoid tissue and loss of the ability to respond to HIV and/or other pathogens. Major expansions of restricted subsets of CD8(+) T cells determined by the usage Of certain variable domains (V) of the beta (beta) chain of the T cell receptor (TCR) occur in certain patients during primary HIV infection. These restricted expansions of CD8(+) VB subsets are oligoclonal and represent HIV-specific immune responses with cytolytic T cell activity, Although only limited numbers of patients were studied thus far, certain patterns have emerged that appear to correlate with the subsequent clinical outcome. It is conceivable that immunologic and virologic events associated with primary infection have a major impact on the ultimate course of HIV disease, Histopathologic, virologic, and immunologic studies of long-term nonprogressors (LTNP) indicate that a small proportion of patients who have been HIV-infected for approximately 10 years have normal lymph node architecture, brisk HIV-specific humoral and cellular immune responses, and high and stable CD4(+) T cell counts serially determined over years. Viral burden and expression are low in these patients; however, low levels of viremia are present, and virus derived from mononuclear cells is replication competent and infectious in most patients. Studies of events associated with primary HIV infection, examination of lymphoid tissue at various stages of disease, and dissection of the immunologic and virologic components of LTNP should contribute substantially to our understanding of the pathogenesis of HIV disease. RP PANTALEO, G (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,BETHESDA,MD 20892, USA. RI Pantaleo, Giuseppe/K-6163-2016 NR 83 TC 247 Z9 254 U1 0 U2 17 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0732-0582 J9 ANNU REV IMMUNOL JI Annu. Rev. Immunol. PY 1995 VL 13 BP 487 EP 512 DI 10.1146/annurev.immunol.13.1.487 PG 26 WC Immunology SC Immunology GA QV290 UT WOS:A1995QV29000019 PM 7612232 ER PT J AU KOTRLA, KJ WEINBERGER, DR AF KOTRLA, KJ WEINBERGER, DR TI BRAIN IMAGING SCHIZOPHRENIA SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE MAGNETIC RESONANCE IMAGING (MRI); POSITION EMISSION TOMOGRAPHY (PET); SINGLE PHOTON EMISSION COMPUTED TOMOGRAPHY (SPECT); FUNCTIONAL MRI ID CEREBRAL BLOOD-FLOW; DORSOLATERAL PREFRONTAL CORTEX; POSITRON EMISSION TOMOGRAPHY; TEMPORAL-LOBE; COMPUTED-TOMOGRAPHY; PHYSIOLOGICAL DYSFUNCTION; STRUCTURAL ABNORMALITIES; CORTICAL DEVELOPMENT; MONOZYGOTIC TWINS; VENTRICULAR SIZE AB Neuroimaging provides an unprecedented means by which to study psychiatric disorders. Structural imaging methods, i.e. computerized tomography (CT) and magnetic resonance imaging (MRI), have revealed subtle differences in the brains of schizophrenic patients that appear to be present before symptom onset. Radionuclide functional methods such as single photon emission computed tomography (SPECT) and positron emission tomography (PET) have led to hypotheses about dysfunction in specific neuronal networks in schizophrenia. New advances in MRT allow functional data to be obtained noninvasively in a single individual using conventional MRI scanners. This chapter discusses the parallels between the historical technical developments in neuroimaging and the deepening understanding of the etiology and manifestations of schizophrenia. RP KOTRLA, KJ (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. NR 62 TC 47 Z9 47 U1 3 U2 5 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1995 VL 46 BP 113 EP 122 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA QT175 UT WOS:A1995QT17500011 PM 7598448 ER PT J AU DUFOUR, M FULLER, RK AF DUFOUR, M FULLER, RK TI ALCOHOL IN THE ELDERLY SO ANNUAL REVIEW OF MEDICINE LA English DT Review DE ALCOHOLISM; PREVALENCE; DIAGNOSIS; TREATMENT ID SUBSTANCE-ABUSE; 216 INPATIENTS; UNITED-STATES; DRINKING; DIAGNOSIS; PATIENT AB Although older individuals drink less and report fewer alcohol-related problems than do younger individuals, alcohol use and abuse are significant health issues for older patients. The signs and symptoms of alcohol problems and dependence in the elderly may not only differ from those of young problem drinkers, but may also be present at lower levels of alcohol consumption. Older alcoholics do well in alcohol treatment. Therefore, discussion of alcohol consumption is a critical part of every history and physical examination for all patients, including older individuals. RP DUFOUR, M (reprint author), NIAAA,ROCKVILLE,MD 20892, USA. NR 30 TC 85 Z9 87 U1 2 U2 6 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4219 J9 ANNU REV MED JI Annu. Rev. Med. PY 1995 VL 46 BP 123 EP 132 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA QT175 UT WOS:A1995QT17500012 PM 7598449 ER PT J AU DESIMONE, R DUNCAN, J AF DESIMONE, R DUNCAN, J TI NEURAL MECHANISMS OF SELECTIVE VISUAL-ATTENTION SO ANNUAL REVIEW OF NEUROSCIENCE LA English DT Review DE VISION; CORTEX; PRIMATES; VISUAL SEARCH; NEGLECT ID INFERIOR TEMPORAL CORTEX; SHORT-TERM-MEMORY; DELAYED-RESPONSE PERFORMANCE; MONKEY SUPERIOR COLLICULUS; POSTERIOR PARIETAL CORTEX; BEHAVING RHESUS-MONKEY; FRONTAL EYE FIELDS; PREFRONTAL CORTEX; MACAQUE MONKEY; RECOGNITION MEMORY C1 MRC,APPL PSYCHOL UNIT,CAMBRIDGE CB2 2EF,ENGLAND. RP DESIMONE, R (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 49,ROOM 1B80,BETHESDA,MD 20892, USA. NR 164 TC 3929 Z9 4013 U1 57 U2 454 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0147-006X J9 ANNU REV NEUROSCI JI Annu. Rev. Neurosci. PY 1995 VL 18 BP 193 EP 222 DI 10.1146/annurev.neuro.18.1.193 PG 30 WC Neurosciences SC Neurosciences & Neurology GA QN293 UT WOS:A1995QN29300008 PM 7605061 ER PT J AU GONZALEZ, FJ KORZEKWA, KR AF GONZALEZ, FJ KORZEKWA, KR TI CYTOCHROMES P450 EXPRESSION SYSTEMS SO ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY LA English DT Review DE CDNA EXPRESSION; NADPH-P450 OXIDOREDUCTASE; CYTOCHROME B5; YEAST; COS CELLS; VACCINIA VIRUS; BACULOVIRUS; RETROVIRUS; B LYMPHOBLASTOID CELLS ID CDNA-DIRECTED EXPRESSION; CHINESE-HAMSTER CELLS; YEAST SACCHAROMYCES-CEREVISIAE; BACILLUS-MEGATERIUM CYTOCHROME-P-450BM-3; HUMAN NADPH-P450 OXIDOREDUCTASE; HIGH-LEVEL EXPRESSION; HUMAN LIVER P-450; ESCHERICHIA-COLI; STABLE EXPRESSION; CATALYTIC ACTIVITIES AB Catalytically active cytochrome P450 enzymes have been successfully expressed in bacterial, yeast, and mammalian cells. A variety of expression vectors have been used, resulting in both transient and stable expression. The system of choice depends on the goals of a particular project. Factors such as expense, ease of use, and yields required should govern the decision whether to use bacterial, yeast, insect, or mammalian cDNA expression. High-level expression of mammalian P450s in bacteria usually requires modifications of the amino-terminal region of the enzyme. The Escherichia coli P450-OR fusion proteins may also come of age for use in fermentation-production processes for the chemical industry. Many cytochromes P450 have been expressed in yeast, with variable levels of expression. Baculovirus, albeit somewhat tedious in having to individualize expression conditions, can produce high levels of enzyme. The standard mammalian cell expression systems, both transient and stable, have been of tremendous value to drug metabolism and carcinogenesis research and will continue to play a role in these areas. RP GONZALEZ, FJ (reprint author), NCI, MOLEC CARCINOGENESIS LAB, BETHESDA, MD 20892 USA. NR 139 TC 130 Z9 138 U1 1 U2 19 PU ANNUAL REVIEWS PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA SN 0362-1642 J9 ANNU REV PHARMACOL JI Annu. Rev. Pharmacol. Toxicol. PY 1995 VL 35 BP 369 EP 390 PG 22 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA QV291 UT WOS:A1995QV29100015 PM 7598499 ER PT J AU JACKSON, MB YAKEL, JL AF JACKSON, MB YAKEL, JL TI THE 5-HT3 RECEPTOR-CHANNEL SO ANNUAL REVIEW OF PHYSIOLOGY LA English DT Review DE LIGAND-GATED CHANNELS; SEROTONIN RECEPTOR; SYNAPTIC RECEPTOR; DESENSITIZATION; ION PERMEATION; ION CHANNELS ID NEURO-BLASTOMA CELLS; N1E-115 NEUROBLASTOMA-CELLS; MEDIATED ION CURRENT; NICOTINIC ACETYLCHOLINE-RECEPTORS; NUCLEUS-TRACTUS-SOLITARIUS; SUPERIOR CERVICAL-GANGLION; RADIOLIGAND BINDING; FUNCTIONAL EXPRESSION; SEROTONIN RECEPTORS; RECOGNITION SITES C1 NIEHS,RES TRIANGLE PK,NC 27709. RP JACKSON, MB (reprint author), UNIV WISCONSIN,SCH MED,DEPT PHYSIOL,MADISON,WI 53706, USA. FU NINDS NIH HHS [NS23512] NR 78 TC 162 Z9 162 U1 0 U2 1 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0066-4278 J9 ANNU REV PHYSIOL JI Annu. Rev. Physiol. PY 1995 VL 57 BP 447 EP 468 PG 22 WC Physiology SC Physiology GA QN292 UT WOS:A1995QN29200022 PM 7539990 ER PT J AU SCHAPER, C FLEMING, TR SELF, SG RIDA, WN AF SCHAPER, C FLEMING, TR SELF, SG RIDA, WN TI STATISTICAL ISSUES IN THE DESIGN OF HIV VACCINE TRIALS SO ANNUAL REVIEW OF PUBLIC HEALTH LA English DT Review DE HIV VACCINE; VACCINE EFFICACY; FIELD EFFICACY; SURROGATE MARKER; BEHAVIORAL INTERVENTION ID IMMUNODEFICIENCY-VIRUS INFECTION; EVALUATING BEHAVIORAL INTERVENTIONS; PLACEBO-CONTROLLED TRIAL; SURROGATE END-POINTS; AIDS-RELATED COMPLEX; CONTROL-OF-SEX.; CLINICAL-TRIALS; SEXUAL-BEHAVIOR; PSYCHOLOGICAL INTERVENTIONS; ANTIRETROVIRAL THERAPY AB HIV vaccine trials present significant challenges related to trial endpoints, vaccine efficacy measurement, and the role of nonvaccine interventions. Infection is a valid endpoint for detecting sterilizing immunity. But if the vaccine prevents AIDS without preventing infection, infection may be a misleading surrogate. Appropriate endpoints must be defined for other mechanisms of vaccine action. Direct, indirect, behavioral, and biological effects all determine vaccine efficacy. False security among HIV-vaccine recipients may make negative behavioral effects an important component of vaccine performance. Both biological potency and a more comprehensive program effectiveness should be measured. These goals may require unblinded designs or community randomization. Nonvaccine interventions are currently the only HIV-prevention strategy. Support for larger scale implementation requires more rigorous evaluation that is less dependent on self-reported behavioral changes. The vaccine trial cohorts provide a unique opportunity to cost-effectively evaluate behavioral interventions. C1 FRED HUTCHINSON CANC RES CTR,PROGRAM BIOSTAT,SEATTLE,WA 98104. NIAID,DIV AIDS,BETHESDA,MD 20892. RP SCHAPER, C (reprint author), UNIV WASHINGTON,DEPT BIOSTAT,SEATTLE,WA 98195, USA. NR 96 TC 15 Z9 15 U1 0 U2 1 PU ANNUAL REVIEWS INC PI PALO ALTO PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 SN 0163-7525 J9 ANNU REV PUBL HEALTH JI Annu. Rev. Public Health PY 1995 VL 16 BP 1 EP 22 PG 22 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QZ046 UT WOS:A1995QZ04600002 PM 7639865 ER PT S AU POMMIER, Y AF POMMIER, Y BE Priebe, W TI DNA TOPOISOMERASES AND THEIR INHIBITION BY ANTHRACYCLINES SO ANTHRACYCLINE ANTIBIOTICS: NEW ANALOGUES, METHODS OF DELIVERY, AND MECHANISMS OF ACTION SE ACS SYMPOSIUM SERIES LA English DT Article; Proceedings Paper CT Symposium on Anthracycline Antibiotics - New Analogues, Methods of Delivery, and Mechanisms and Action, at the 205th National Meeting of the American-Chemical-Society CY MAR 28-APR 02, 1993 CL DENVER, CO SP AMER CHEM SOC, DIV CARBOHYDRATE CHEM ID SISTER CHROMATID EXCHANGES; ACUTE MYELOID-LEUKEMIA; HAMSTER OVARY CELLS; DOUBLE-STRAND BREAKS; CYTO-TOXICITY; II INHIBITORS; MAMMALIAN-CELLS; ANTITUMOR AGENT; POINT MUTATION; EUKARYOTIC TOPOISOMERASE AB Several of the most active anticancer drugs, including anthracyclines, poison cellular DNA topoisomerase II (top2). The genomic sites of top2 inhibition differ for each class of drug, thereby providing a rationale that may help to explain the mechanisms of drug inhibition (''stacking model'') and the differential activity of top2 inhibitors in the clinic. Resistance to anthracyclines is often associated with top2 alterations and increased drug efflux by the P-glycoprotein(MDR). Different parts of the anthracycline molecules are probably involved in top2 inhibition, recognition by the P-glycoprotein(MDR), and generation of free radicals. Therefore, it should be possible to design more morpholinyldoxorubicin, inhibits topoisomerase I (top1) rather than top2, it may be also be possible to find top1 inhibitors among anthracyclines. RP POMMIER, Y (reprint author), NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892, USA. NR 195 TC 14 Z9 14 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 SN 0097-6156 BN 0-8412-3040-4 J9 ACS SYM SER PY 1995 VL 574 BP 183 EP 203 PG 21 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry, Multidisciplinary; Immunology; Infectious Diseases; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry; Immunology; Infectious Diseases GA BB95Z UT WOS:A1995BB95Z00012 ER PT J AU SUPKO, JG MALSPEIS, L AF SUPKO, JG MALSPEIS, L TI PHARMACOKINETICS OF MICHELLAMINE B, A NAPHTHYLISOQUINOLINE ALKALOID WITH IN-VITRO ACTIVITY AGAINST HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 AND TYPE-2, IN THE MOUSE AND DOG SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID HIV AB Michellamine B (MB) is a naturally occurring naphthylisoquinoline alkaloid of novel chemical structure with activity against human immunodeficiency virus (HIV) types 1 and 2 in vitro. In conjunction with its preclinical evaluation, the plasma pharmacokinetics of MB was characterized in mice and dogs treated by intravenous infusions of 1- and 15-min durations, respectively. At doses ranging from 1 to 9 mg/kg of body weight, the drug exhibited apparent first-order kinetics in both species, affording triexponential plasma concentration-time profiles. Treatment with doses of 5 to 9 mg/kg provided peak plasma levels within the range that completely inhibits the cytopathic effects of HN upon cultured human lymphoblastoid cells (50 to 100 mu g/ml) without evidence of toxicity. MB had a biological half-life of 2.8 +/- 0.8 h in mice, with a mean residence time of 2.1 +/- 0.3 h, and a total plasma clearance of 2.4 +/- 0.5 ml/min/kg (mean +/- standard deviation; n = 3); however, the terminal-phase contribution to the area under the plasma profile from time zero to infinity was 44.6% +/- 12.9%. In contrast, the terminal phase was the primary determinant of drug disposition in dogs, accounting for 74.1% +/- 2.8% (n = 3) of the area under the curve. Furthermore, the systemic duration of MB was significantly longer in the dogs than in mice, as indicated by mean values of the apparent half-life (11.6 +/- 1.2 h), mean residence time (12.3 +/- 1.8 h), and clearance (0.50 +/- 0.08 ml/min/kg). However, there was no statistical difference between its apparent volume of distribution in the mice (0.60 +/- 0.08 liters/kg) and dogs (0.50 +/- 0.07 liters/kg). A single dog was also treated with a total dose of 97 mg/kg given as a 72-h constant-rate intravenous infusion, since prolonged systemic exposure to potentially therapeutic drug concentrations will very likely be required for clinical anti-HIV effects. Within 4 h after starting the infusion, the plasma MB concentration exceeded 18 mu g/ml, its reported 50% effective concentration against HIV in vitro, and subsequently increased to 41 mu g/ml at the end of the infusion. There were no clinical or pathological indications of toxicity. Whereas the total plasma clearance (0.48 ml/min/kg) was within the range observed for dogs treated by 15-min infusion, extension of the postinfusion sampling period from 24 h to 4 days facilitated better definition of the terminal exponential phase, yielding a value of 25.6 h for the biological half-life of MB. The amount of drug excreted by dogs unchanged in the urine ranged from 3.7 to 11.1% of the administered dose. Thus, the major pathways by which the drug is eliminated from the body remain to be identified. On the basis of these findings, continued development of MB as a novel lead compound for the treatment of BTV infection is warranted. RP SUPKO, JG (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,PHARMACEUT CHEM LAB,FREDERICK,MD 21701, USA. NR 15 TC 9 Z9 9 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD JAN PY 1995 VL 39 IS 1 BP 9 EP 14 PG 6 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA PY869 UT WOS:A1995PY86900002 PM 7695336 ER PT S AU Plowe, CV Wellems, TE AF Plowe, CV Wellems, TE BE Jungkind, DL Mortensen, JE Fraimow, HS Calandra, GB TI Molecular approaches to the spreading problem of drug resistant malaria SO ANTIMICROBIAL RESISTANCE: A CRISIS IN HEALTH CARE SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT Symposium on Antimicrobial Resistance: A Crisis in Healthcare - Clinical Laboratory and Epidemiologic Considerations CY NOV 11-12, 1993 CL PHILADELPHIA, PA SP Amer Soc Microbiol, E Penn Branch, Lederle Labs, Merck Inc, Miles Pharm, Pfizer Roerig Div, MetPath, Becton Dickinson, Pfizer Labs, Ortho Pharm, Remel Microbiol Prod, Baxter Microscan, Penn Dept Hlth, Gwynedd Mercy Coll, Hahnemann Univ, Natl Lab Training Network, Penn Coll Podiatr Med, Philadelphia Coll Osteopath Med, St Christophers Hosp, Temple Univ Sch Med, Thomas Jefferson Univ, Univ Penn ID UNCOMPLICATED FALCIPARUM-MALARIA; THYMIDYLATE SYNTHASE GENE; PLASMODIUM-FALCIPARUM; CHLOROQUINE-RESISTANCE; PYRIMETHAMINE RESISTANCE; RIBOSOMAL-RNA; ANTIMALARIAL; AMPLIFICATION; TETRACYCLINE; DESIPRAMINE RP Plowe, CV (reprint author), NIAID,MALARIA RES LAB,NIH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 48 TC 19 Z9 19 U1 0 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-45207-3 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 390 BP 197 EP 209 PG 13 WC Medicine, Research & Experimental; Microbiology SC Research & Experimental Medicine; Microbiology GA BF46X UT WOS:A1995BF46X00017 PM 8718614 ER PT B AU LEE, C UNSER, M KETTER, TA AF LEE, C UNSER, M KETTER, TA BE Tescher, AG TI Automatic recognition of corpus callosum from sagittal brain MR images SO APPLICATIONS OF DIGITAL IMAGE PROCESSING XVIII SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT 1995 Symposium on Applications of Digital Image Processing XVIII CY JUL 12-14, 1995 CL SAN DIEGO, CA SP Soc Photo Opt Instrumentat Engineers DE OBJECT RECOGNITION; MAGNETIC RESONANCE IMAGES (MRI); THRESHOLDING; CORPUS CALLOSUM; MEDICAL IMAGING; REGION MATCHING; DIRECTED WINDOW REGION GROWING C1 NIH,NCRR,BEIP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPIE - INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA PO BOX 10, BELLINGHAM, WA 98227-0010 BN 0-8194-1923-0 J9 P SOC PHOTO-OPT INS PY 1995 VL 2564 BP 528 EP 534 DI 10.1117/12.217439 PG 7 WC Computer Science, Hardware & Architecture; Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Optics SC Computer Science; Optics GA BD96W UT WOS:A1995BD96W00055 ER PT J AU HE, CY MERRICK, BA PATTERSON, RM SELKIRK, JK AF HE, CY MERRICK, BA PATTERSON, RM SELKIRK, JK TI ALTERED PROTEIN-SYNTHESIS IN P53 NULL AND HEMIZYGOTIC TRANSGENIC MOUSE EMBRYONIC FIBROBLASTS SO APPLIED AND THEORETICAL ELECTROPHORESIS LA English DT Article DE P53; TRANSGENIC MICE; FIBROBLAST; PROTEIN; 2D-PAGE; IMAGE ANALYSIS ID WILD-TYPE P53; 2-DIMENSIONAL GEL-ELECTROPHORESIS; TUMOR SUPPRESSOR PROTEIN; CELL-CYCLE CONTROL; ERYTHROLEUKEMIA-CELLS; SV40-TRANSFORMED CELLS; P53-DEFICIENT MICE; TRANSFORMED-CELLS; RAS ONCOGENE; ANTIGEN AB Embryonic fibroblasts derived from p53-deficient transgenic mice showed distinct phenotypic and biological changes in vitro. In this study, we investigated the possible impact of p53 on the synthesis of other cellular proteins by comparing the protein profiles of p53 null (-/-), hemizygous (+/-) and p53 positive homozygous (+/+) cells using high resolution two dimensional gel electrophoresis. A total of more than 850 proteins were detected in each cell line labeled with S-35-methionine by using computerized image analysis, and a number of proteins were detected with qualitative or quantitative changes in p53 -/ - cells and to a lesser extent in p53 +/- cells. Specifically, seven proteins became undetectable, and no new proteins were detected in p53 -/- cells. Neither newly expressed nor absent proteins were detected in p53 +/- cell line. Quantitatively, a total of 97 and 59 proteins were detected with significant quantitative changes (3 fold or greater) in p53 -/- and p53 +/- cells, respectively. Generally, most protein changes fell into one of the following four patterns: 1) progressively decreased synthesis in cells from p53 +/+ to p53 +/- to p53 -/- cells; 2) progressively increased synthesis in cells from p53 +/+ to p53 +/- to p53 -/- cells; 3) decreased synthesis only in p53 -/- cells; and 4) increased synthesis only in p53 -/- cells. A 70 kD heat shock protein (Hsp70) was identified and showed a greater than 1,000-fold increase in p53 -/- cells compared to that in p53 +/+ cells. Transferrin, tropomyosin, and proliferating cell nuclear antigen (PCNA) have also been identified and measured in this study. Synthesis of transferrin and tropomyosin was significantly increased or decreased, respectively in p53 -/ - cells, whereas expression of PCNA showed no significant change in p53 -/- cells despite their much higher (3-4 times) proliferation rate than the other two cell lines (p53 +/+ and p53 +/- cells). We conclude that disruption of a single important gene, p53, results in a cascade of protein changes which are related to the loss of p53 mediated negative growth effects on cell cycle control. C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 53 TC 6 Z9 6 U1 0 U2 0 PU ALLEN PRESS INC PI LAWRENCE PA C/O ELECTROPHORESIS SOC PO BOX 1897, LAWRENCE, KS 66044 SN 0954-6642 J9 APPL THEOR ELECTROPH JI Appl. Theor. Electrophor. PY 1995 VL 5 IS 1 BP 15 EP 24 PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RV023 UT WOS:A1995RV02300003 PM 8534750 ER PT J AU ZAKHAROV, SF GARNER, MM CHRAMBACH, A AF ZAKHAROV, SF GARNER, MM CHRAMBACH, A TI RECOVERY OF SDS-PROTEIN AND DNA USING COMMERCIAL AUTOMATED GEL-ELECTROPHORESIS APPARATUS SO APPLIED AND THEORETICAL ELECTROPHORESIS LA English DT Article DE ELECTROPHORESIS; PREPARATIVE; AUTOMATED; PROTEIN; DNA ID POLYACRYLAMIDE AB The HPGE-1000 apparatus (LabIntelligence, Menlo Park, CA) is a gel electrophoresis instrument with intermittent fluorescence scanning of the migration path and with preparative capability. An electroelution cup sealed with gel is placed onto the band of interest, identified and located under computer control, and the band is electroeluted into the cup at a right angle to the orientation of the resolving gel. The correct location of the eluted band and the degree of its recovery into the elution cup are then verified on the gel pattern, visualized on the computer screen. Using that procedure, SDS-conalbumin-FLUOS was electrophoresed at 5, V/cm in a discontinuous tricinate-chloride- Tris system at loads of 0.25 to 20 mu g, using 5% agarose (MetaPhor, FMC), 0.03% SDS gel at 5 degrees C. The horizontal gel was partitioned at the sample loading slit between a gel in Tris-tricinate (prepared at the concentrations of an operative phase ZETA) and in Tris-chloride (prepared as phase BETA). The elution cup was sealed with the latter gel and overlayered with buffer of the composition of the former, This arrangement should provide for electroelution of the band as a highly concentrated stack. At electroelution times of 2, 3.5, 4-5, 12, 15 and 15 min at 15 V/cm yields were 58, 60, 54-76, 99, 99 and 84% for loads of 0.25, 0.5, 1, 4, 10 and 20 mu g, respectively. At the most sensitive scale of detection (13), a full-scale peak was obtained at a load of 1.7 mu g when the fluorophore (FLUOS, Boehringer-Mannheim) to protein ratio was 10:1. Similarly, homogeneous nucleosomal DNA (146 bp), electrophoresed in 0.2 x TBE buffer at a load of 5 mu g, was near-quantitatively recovered into the same buffer by electroelution at 15 V/cm for 2.5 or 6 min. C1 NICHHD,THEORET & PHYS BIOL LAB,MACROMOLEC ANAL SECT,BETHESDA,MD 20892. NR 10 TC 21 Z9 21 U1 1 U2 2 PU ALLEN PRESS INC PI LAWRENCE PA C/O ELECTROPHORESIS SOC PO BOX 1897, LAWRENCE, KS 66044 SN 0954-6642 J9 APPL THEOR ELECTROPH JI Appl. Theor. Electrophor. PY 1995 VL 5 IS 1 BP 25 EP 29 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RV023 UT WOS:A1995RV02300004 PM 8534751 ER PT J AU ALDROUBI, A ZAKHAROV, SF CHRAMBACH, A AF ALDROUBI, A ZAKHAROV, SF CHRAMBACH, A TI A COMPUTER-PROGRAM FOR PREDICTING RECOVERY OF SDS-PROTEIN IN THE AUTOMATED HPGE-1000 APPARATUS SO APPLIED AND THEORETICAL ELECTROPHORESIS LA English DT Article DE AUTOMATED GEL ELECTROPHORESIS; RECOVERY PROGRAM AB The commercial automated gel electrophoresis apparatus (HPGE-1000 of LabIntelligence, Menlo Park, CA) allows one to recover the material migrating and visualized as a fluorescent-labeled band by electrophoresis into a collection cup located above the band at a right angle to the orientation of the separation path. The degree of recovery is a function of sample load (peak area), electrophoresis time at constant field strength, the mobility of the material and band width. Neglecting the latter, recovery of several SDS-proteins was measured as a function of the first three parameters. These measurements were used as a data base for a computer program capable of predicting, by interpolation of the experimental values, the time of electrophoresis needed to obtain a specified degree of recovery, or the degree of recovery obtained after a desired time of electrophoresis into the collection cup. C1 NICHHD,NATL CTR RES RESOURCES,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NICHHD,THEORET & PHYS BIOL LAB,MACROMOLEC ANAL SECT,BETHESDA,MD 20892. RI Aldroubi, Akram/J-7186-2012 NR 11 TC 13 Z9 13 U1 0 U2 0 PU ALLEN PRESS INC PI LAWRENCE PA C/O ELECTROPHORESIS SOC PO BOX 1897, LAWRENCE, KS 66044 SN 0954-6642 J9 APPL THEOR ELECTROPH JI Appl. Theor. Electrophor. PY 1995 VL 5 IS 1 BP 31 EP 34 PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RV023 UT WOS:A1995RV02300005 PM 8534752 ER PT J AU MERRIL, CR GOLDSTEIN, MP MYRICK, JE CREED, GJ LEMKIN, PF AF MERRIL, CR GOLDSTEIN, MP MYRICK, JE CREED, GJ LEMKIN, PF TI THE PROTEIN DISEASE DATABASE OF HUMAN-BODY FLUIDS .1. RATIONALE FOR THE DEVELOPMENT OF THIS DATABASE SO APPLIED AND THEORETICAL ELECTROPHORESIS LA English DT Article DE ELECTROPHORESIS; GEL; 2-DIMENSIONAL; HUMAN; DATABASE; PROTEIN; DISEASE; BODY FLUIDS; ELECTROPHORETIC; DIAGNOSTIC; ALZHEIMERS DISEASE; SCHIZOPHRENIA; ACUTE PHASE PROTEINS; SERUM; PLASMA; URINE; CEREBROSPINAL FLUID ID PHASE PLASMA-PROTEINS; TUMOR-NECROSIS-FACTOR; CEREBROSPINAL-FLUID; ALZHEIMERS-DISEASE; 2-DIMENSIONAL ELECTROPHORESIS; CYTOKINES; ALPHA-1-ANTICHYMOTRYPSIN; INTERLEUKIN-1; SCHIZOPHRENIA; DEPRESSION AB We are developing a relational database to facilitate quantitative and qualitative comparisons of proteins in human body fluids in normal and disease states, For decades researchers and clinicians have been studying proteins in body fluids such as serum, plasma, cerebrospinal fluid and urine, Currently, most clinicians evaluate only a few specific proteins in a body fluid such as plasma when they suspect that a patient has a disease. Now, however, high resolution two-dimensional protein electrophoresis allows the simultaneous evaluation of 1,500 to 3,000 proteins in complex solutions, such as the body fluids, This and other high resolution methods have encouraged us to collect the clinical data for the body fluid proteins into an easily accessed database, For this reason, it has been constructed on the Internet World Wide Web (WWW) under the title Protein Disease Database (PDD), In addition, this database will provide a linkage between the disease-associated protein alterations and images of the appropriate proteins on high-resolution electrophoretic gels of the body fluids, This effort requires the normalization of data to account for variations in methods of measurement, Initial efforts in the establishment of the PDD have been concentrated on alterations in the acute-phase proteins in individuals with acute and chronic diseases, Even at this early stage in the development of our database, it has proven to be useful as we have found that there appear to be several common acute-phase protein alterations in the plasma and cerebrospinal fluid from patients with Alzheimer's disease, schizophrenia and major depression, Our goal is to provide access to the PDD so that systematic correlations and relationships between disease states can be examined and extended. C1 NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,BIOCHEM GENET LAB,WASHINGTON,DC 20032. CTR DIS CONTROL & PREVENT,NATL CTR ENVIRONM HLTH,DIV ENVIRONM HLTH LAB SCI,ATLANTA,GA 30341. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 41 TC 11 Z9 11 U1 0 U2 0 PU ALLEN PRESS INC PI LAWRENCE PA C/O ELECTROPHORESIS SOC PO BOX 1897, LAWRENCE, KS 66044 SN 0954-6642 J9 APPL THEOR ELECTROPH JI Appl. Theor. Electrophor. PY 1995 VL 5 IS 2 BP 49 EP 54 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TG260 UT WOS:A1995TG26000001 PM 8573599 ER PT J AU LEMKIN, PF ORR, GA GOLDSTEIN, MP CREED, GJ MYRICK, JE MERRIL, CR AF LEMKIN, PF ORR, GA GOLDSTEIN, MP CREED, GJ MYRICK, JE MERRIL, CR TI THE PROTEIN DISEASE DATABASE OF HUMAN-BODY FLUIDS .2. COMPUTER METHODS AND DATA ISSUES SO APPLIED AND THEORETICAL ELECTROPHORESIS LA English DT Article DE PROTEIN DISEASE DATABASE; PDD; WORLD-WIDE-WEB; HYPERTEXT; INTERNET; RELATIONAL DATABASE; FOLD CHANGE; 2-DIMENSIONAL ELECTROPHORESIS; ACUTE PHASE PROTEINS; DATABASES; FACTUAL STANDARDS; PROTEINS GENETICS; HUMAN; ELECTROPHORESIS; GEL; 2-DIMENSIONAL; BLOOD PROTEINS ANALYSIS; CSF PROTEINS ANALYSIS; URINARY PROTEINS ANALYSIS AB The Protein Disease Database (PDD) is a relational database of proteins and diseases, With this database it is possible to screen for quantitative protein abnormalities associated with disease states, These quantitative relationships use data drawn from the peer-reviewed biomedical literature, Assays may also include those observed in high-resolution electrophoretic gels that offer the potential to quantitate many proteins in a single test as well as data gathered by enzymatic or immunologic assays. We are using the Internet World Wide Web (WWW) and the Web browser paradigm as an access method for wide distribution and querying of the Protein Disease Database, The WWW hypertext transfer protocol and its Common Gateway Interface make it possible to build powerful graphical user interfaces that can support easy-to-use data retrieval using query specification forms or images, The details of these interactions are totally transparent to the users of these forms, Using a client-server SQL relational database, user query access, initial data entry and database maintenance are all performed over the Internet with a Web browser, We discuss the underlying design issues, mapping mechanisms and assumptions that we used in constructing the system, data entry, access to the database server, security, and synthesis of derived two-dimensional gel image maps and hypertext documents resulting from SQL database searches. C1 NCI,FREDERICK CANC RES & DEV CTR,IMAGE PROC SECT,LMMB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD 21702. MONOCLONET INT,HOUSTON,TX. NIMH,CTR NEUROSCI,WASHINGTON,DC 20032. NCEH,CDCP,DIV ENVIRONM HLTH LAB SCI,ATLANTA,GA. NR 28 TC 7 Z9 7 U1 1 U2 1 PU ALLEN PRESS INC PI LAWRENCE PA C/O ELECTROPHORESIS SOC PO BOX 1897, LAWRENCE, KS 66044 SN 0954-6642 J9 APPL THEOR ELECTROPH JI Appl. Theor. Electrophor. PY 1995 VL 5 IS 2 BP 55 EP 72 PG 18 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TG260 UT WOS:A1995TG26000002 PM 8573600 ER PT J AU CHANG, HT CHRAMBACH, A AF CHANG, HT CHRAMBACH, A TI FEASIBILITY OF ELECTROPHORESIS OF A SUBCELLULAR-SIZED PARTICLE IN POLYMER-SOLUTIONS, USING AUTOMATED HORIZONTAL GEL APPARATUS SO APPLIED AND THEORETICAL ELECTROPHORESIS LA English DT Article DE POLYMER SOLUTION; HORIZONTAL APPARATUS; AUTOMATED DETECTION AB Electrophoresis in polymer solutions of a fluorescently labeled polystyrene carboxylate particle of 46.5 nm radius was carried out in a horizontal gel electrophoresis apparatus with intermittent scanning of the migration path, Polymers of the order of 10(6) (dextran, polyvinylpyrrolidone, polyacrylamide and polyethyleneglycol) and 10(5) (hydroxyethylcellulose, polyethyleneglycol) M(r) were used, In each application, bands formed, became symmetric and narrowed with increasing polymer concentration, The decrease in dispersion coefficients, D', with polymer concentration was sharpest with the polymers of M(r) 10(6); but significant differences in the effectiveness of polymers within that group also exist which are not accounted for. Provided that the demonstrated feasibility of banding in concentrated polymer solutions will allow for separations similar to those achieved at low polymer concentrations in CZE, the method promises to overcome the inherent shortcomings of capillary electrophoresis in polymer solutions with regard to inaccessibility of bands for immunological and affinity detection as well as to preparative scale and preparative instrumental complexity. C1 NICHHD,THEORET & PHYS BIOL LAB,MACROMOLEC ANAL SECT,BETHESDA,MD 20892. NR 9 TC 10 Z9 10 U1 0 U2 0 PU ALLEN PRESS INC PI LAWRENCE PA C/O ELECTROPHORESIS SOC PO BOX 1897, LAWRENCE, KS 66044 SN 0954-6642 J9 APPL THEOR ELECTROPH JI Appl. Theor. Electrophor. PY 1995 VL 5 IS 2 BP 73 EP 77 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TG260 UT WOS:A1995TG26000003 PM 8573601 ER PT J AU RADKO, SP CHRAMBACH, A AF RADKO, SP CHRAMBACH, A TI MOLECULAR-SIEVING BY POLYMER-SOLUTIONS - DEPENDENCE ON PARTICLE AND POLYMER SIZE, INDEPENDENCE OF POLYMER ENTANGLEMENT SO APPLIED AND THEORETICAL ELECTROPHORESIS LA English DT Article DE MOLECULAR SIEVING; MECHANISM; POLYMER SOLUTIONS; POLYMER WEIGHT; RETARDATION COEFFICIENT ID GEL-ELECTROPHORESIS; MOBILITY DATA; DNA; SEPARATION AB The previous postulate of collision and displacement mechanisms of molecular sieving based on a biphasic plot of retardation coefficient vs particle radius (''R-plot'') was extended and modified in four ways: i) A wider size range of particles and polymers confirmed the biphasic nature of the R-plot and, in addition, revealed a third mechanistic phase in the largest size range of particles and polymers which exhibits a positive slope in plots of retardation coefficient vs log (particle or polymer size), presumably denoting a collision mechanism, ii) Peaks of retardation in polyethyleneglycol (PEG) solutions were found with a particle M(r) of 10(7) independently of the M(r) of PEG, and with a PEG M(r) of 4 x 10(5) independently of particle Mr showing that the retardation mechanism is not qualitatively a function of the particle/polymer size ratio as postulated previously, although quantitatively retardation is directly related to the size of particle and polymer, iii) Items i) and ii) were confirmed using band width in lieu of mobility measurement, iv) The entanglement threshold, c*, was found to decrease monotonically across the entire polymer size range in which the triphasic retardation takes place, Thus, c* cannot be the sole cause for a non-monotonic change of retardation or normalized relative bandwidth with polymer size and particle size, Moreover, Ferguson plots across c* do not reflect it in any way. C1 NICHHD,THEORET & PHYS BIOL LAB,MACROMOLEC ANAL SECT,BETHESDA,MD 20892. NR 21 TC 8 Z9 8 U1 0 U2 1 PU ALLEN PRESS INC PI LAWRENCE PA C/O ELECTROPHORESIS SOC PO BOX 1897, LAWRENCE, KS 66044 SN 0954-6642 J9 APPL THEOR ELECTROPH JI Appl. Theor. Electrophor. PY 1995 VL 5 IS 2 BP 79 EP 87 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TG260 UT WOS:A1995TG26000004 PM 8573602 ER PT J AU TIETZ, D AF TIETZ, D TI BENEFITS OF ADVANCED GEL-ELECTROPHORESIS DATA-ANALYSIS METHODS SO APPLIED AND THEORETICAL ELECTROPHORESIS LA English DT Article DE ANOMALOUS ELECTROPHORETIC MIGRATION; BENT KINETOPLAST DNA; CHARGE AND SIZE ISOMERS; COMPUTER MODELING; CONJUGATED VACCINES; EXTENDED OGSTON MODEL; IMAGE PROCESSING; NUCLEOSOME CORE PARTICLES ID FERGUSON PLOTS; DNA FRAGMENTS; FREE MOBILITY; PORE-SIZE; PARTICLES; ELECTROPHEROGRAMS; COMPUTERS AB Significantly more information can be obtained if sample mobilities are measured at several gel concentrations (%T) and evaluated on the basis of a mathematical-physical model, This allows one to exploit differences in particle size, charge and shape, and results in the following advantages: (i) Charge and size isomers of proteins can be detected, It is possible to separate components of similar size, but different surface net charge density, (ii) Samples yielding patterns with no discernible peaks can be evaluated to produce size and charge distribution profiles, as shown for protein-conjugated meningitis vaccines, Particle distributions are calculated from 2-D Serwer-type gels, (iii) Different DNA conformations are recognized and reasonable size estimates are available for anomalously migrating DNA species (e,g,, bent kinetoplast DNA) or DNA complexes (nucleosome core particles). C1 NIH,BETHESDA,MD 20892. NR 24 TC 4 Z9 4 U1 0 U2 0 PU ALLEN PRESS INC PI LAWRENCE PA C/O ELECTROPHORESIS SOC PO BOX 1897, LAWRENCE, KS 66044 SN 0954-6642 J9 APPL THEOR ELECTROPH JI Appl. Theor. Electrophor. PY 1995 VL 5 IS 2 BP 107 EP 111 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TG260 UT WOS:A1995TG26000007 PM 8573597 ER PT J AU JENSEN, P ROPER, M FISHER, P PIACENTINI, J CANINO, G RICHTERS, J RUBIOSTIPEC, M DULCAN, M GOODMAN, S DAVIES, M RAE, D SHAFFER, D BIRD, H LAHEY, B SCHWABSTONE, M AF JENSEN, P ROPER, M FISHER, P PIACENTINI, J CANINO, G RICHTERS, J RUBIOSTIPEC, M DULCAN, M GOODMAN, S DAVIES, M RAE, D SHAFFER, D BIRD, H LAHEY, B SCHWABSTONE, M TI TEST-RETEST RELIABILITY OF THE DIAGNOSTIC INTERVIEW SCHEDULE FOR CHILDREN (DISC-2.1) - PARENT, CHILD, AND COMBINED ALGORITHMS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PSYCHIATRIC-DIAGNOSIS; AFFECTIVE-DISORDERS; ADOLESCENTS; POPULATION; AGREEMENT; VALIDITY AB Background: Previous research has not compared the psychometric properties of diagnostic interviews of community samples and clinically referred subjects within a single Study. As part of a multisite cooperative agreement study funded by the National Institute of Mental Health, 97 families with clinically referred children and 278 families identified through community sampling procedures participated in a test-retest study of version 2.1 of the Diagnostic Interview Schedule for Children (DISC 2.1). Methods: The DISC was separately administered to children and parents, and diagnoses were derived from computer algorithms keyed to DSM-III-R criteria. Three sets of diagnoses were obtained, based on parent information only (DISC-P), child information only (DISC-C), and information from either or both (DISC-PC). Results: Test-retest reliabilities of the DISC-PC ranged from moderate to substantial for diagnoses in the clinical sample. Test-retest kappa coefficients were higher for the clinical sample than for the community sample. The DISC-PC algorithm generally had higher reliabilities than the algorithms that relied on single informants. Unreliability was primarily due to diagnostic attenuation at time 2. Attenuation was greatest among child informants and less severe cases and in the community sample. Conclusions: Test-retest reliability findings were consistent with or superior to those reported in previous studies. Results support the usefulness of the DISC in further clinical and epidemiologic research; however, closely spaced or repeated DISC interviews may result in significant diagnostic attenuation on retest. Further studies of the test-retest attenuation phenomena are needed, including careful examination of the child, family, and illness characteristics of diagnostic stability. C1 NEW YORK STATE PSYCHIAT INST & HOSP,DIV CHILD & ADOLESCENT PSYCHIAT,NEW YORK,NY. COLUMBIA UNIV,COLL PHYS & SURG,NEW YORK,NY. UNIV PUERTO RICO,DEPT PSYCHIAT,SAN JUAN,PR 00936. EMORY UNIV,SCH MED,DEPT PSYCHIAT,ATLANTA,GA 30322. UNIV MIAMI,SCH MED,DEPT PSYCHIAT,MIAMI,FL 33152. YALE UNIV,SCH MED,YALE CHILD STUDY CTR,NEW HAVEN,CT. RP JENSEN, P (reprint author), NIMH,CHILD & ADOLESCENT DISORDERS RES BRANCH,PARKLAWN BLDG,5600 FISHERS LN,ROCKVILLE,MD 20857, USA. RI Piacentini, John/C-4645-2011; OI Richters, John/0000-0002-6780-1828; Jensen, Peter/0000-0003-2387-0650 FU NIMH NIH HHS [UO1 MH46725, UO1 MH46717, UO1 MH46718] NR 34 TC 198 Z9 199 U1 2 U2 6 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD JAN PY 1995 VL 52 IS 1 BP 61 EP 71 PG 11 WC Psychiatry SC Psychiatry GA QB300 UT WOS:A1995QB30000006 PM 7811163 ER PT J AU BROUWERS, P DECARLI, C CIVITELLO, L MOSS, H WOLTERS, P PIZZO, P AF BROUWERS, P DECARLI, C CIVITELLO, L MOSS, H WOLTERS, P PIZZO, P TI CORRELATION BETWEEN COMPUTED TOMOGRAPHIC BRAIN-SCAN ABNORMALITIES AND NEUROPSYCHOLOGICAL FUNCTION IN CHILDREN WITH SYMPTOMATIC HUMAN-IMMUNODEFICIENCY-VIRUS DISEASE SO ARCHIVES OF NEUROLOGY LA English DT Article ID NEUROLOGIC MANIFESTATIONS; PEDIATRIC AIDS; HIV-INFECTION; BASAL GANGLIA; CALCIFICATION; ZIDOVUDINE; INFANTS; CT AB Objective: To evaluate the clinical significance of computed tomographic brain scan abnormalities observed in children with symptomatic human immunodeficiency virus disease. Patients: Eighty-seven previously untreated children with symptomatic human immunodeficiency virus type 1 disease. Methods: General levels of cognitive functioning, obtained from age-appropriate intelligence tests, and social-emotional behavior were correlated with computed tomographic brain scan abnormality ratings. Results: A significant relation between computed tomographic brain scan abnormalities and cognitive dysfunction as well as aberrant behavior was found, which appeared stronger in (younger) vertically infected children compared with transfusion-infected patients. Calcifications, independent from the degree of brain atrophy, were associated with significantly greater delays in neurocognitive development. Conclusion: Computed tomographic brain scan abnormalities, even when mild, were of clinical significance, suggesting that human immunodeficiency virus-associated central nervous system compromise is a continuous process and that scans may be helpful at baseline in defining patients at risk and for monitoring them during therapy. C1 NINCDS,EPILEPSY RES BRANCH,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,WASHINGTON,DC 20010. MED ILLNESS COUNSELING CTR,CHEVY CHASE,MD. RP BROUWERS, P (reprint author), NCI,CTR CLIN,PEDIAT BRANCH,ROOM 13N240,BETHESDA,MD 20892, USA. RI DeCarli, Charles/B-5541-2009 NR 27 TC 45 Z9 47 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD JAN PY 1995 VL 52 IS 1 BP 39 EP 44 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA QB190 UT WOS:A1995QB19000007 PM 7826274 ER PT J AU CHEW, EY KLEIN, ML MURPHY, RP REMALEY, NA FERRIS, FL AF CHEW, EY KLEIN, ML MURPHY, RP REMALEY, NA FERRIS, FL TI EFFECTS OF ASPIRIN ON VITREOUS PRERETINAL HEMORRHAGE IN PATIENTS WITH DIABETES-MELLITUS - EARLY TREATMENT DIABETIC-RETINOPATHY STUDY REPORT NO-20 SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID FOLLOW-UP; MORTALITY AB Objective: To assess whether the use of aspirin exacerbates the severity or duration of vitreous/preretinal hemorrhages in patients with diabetic retinopathy. Design: The Early Treatment Diabetic Retinopathy Study (ETDRS), a multicenter randomized clinical trial, was designed to assess the effect of photocoagulation and aspirin on 3711 patients with mild to severe nonproliferative or early proliferative diabetic retinopathy. Intervention: Patients were randomly assigned to either an aspirin (650 mg/d) or a placebo group. One eye of each patient was randomly assigned to early photocoagulation and the other to deferral of photocoagulation. Main Outcome Measures: The severity and duration of the vitreous/preretinal hemorrhages were determined from gradings of the annual, seven standard stereoscopic field, fundus photographs. Clinical examinations scheduled every 4 months also provided information on the presence and duration of hemorrhages. Results: Annual fundus photographs of eyes assigned to deferral of photocoagulation revealed vitreous/preretinal hemorrhages at some time during follow-up in 564 patients (30%) assigned to the placebo group and 585 patients (32%) assigned to the aspirin group (P=.48). Based on gradings of fundus photographs, there were no statistical differences in the severity of vitreous/preretinal hemorrhages (P=.11) or their rate of resolution (P=.86) between the groups. Clinical examination of eyes assigned to deferral of photocoagulation revealed 721 eyes (39%) assigned to the aspirin group and 689 (37%) assigned to the placebo group that had vitreous/preretinal hemorrhages during the course of the study (P=.30). Again, no statistically significant difference was found between the rates of resolution, as assessed clinically, between the two treatment groups (P=.43). Conclusions: As previously reported, the use of aspirin did not increase the occurrence of vitreous/preretinal hemorrhages in patients enrolled in the ETDRS. The data presented in this report demonstrate that the severity and duration of these hemorrhages were not significantly affected by the use of aspirin and that there were no ocular contraindications to its use (650 mg/d) in persons with diabetes who require it for treatment of cardiovascular disease or for other medical indications. C1 OREGON HLTH SCI UNIV,CASEY EYE INST,PORTLAND,OR 97201. RETINA INST MARYLAND,BALTIMORE,MD. RP CHEW, EY (reprint author), NEI,BIOMETRY & EPIDEMIOL PROGRAM,BLDG 31,ROOM 6A-52,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU Intramural NIH HHS [Z99 EY999999] NR 19 TC 50 Z9 53 U1 1 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD JAN PY 1995 VL 113 IS 1 BP 52 EP 55 PG 4 WC Ophthalmology SC Ophthalmology GA QA884 UT WOS:A1995QA88400011 PM 7826294 ER PT J AU WOODS, GL WITEBSKY, FG AF WOODS, GL WITEBSKY, FG TI COLLEGE-OF-AMERICAN-PATHOLOGISTS MYCOBACTERIOLOGY-E - PROFICIENCY TESTING SURVEY - SUMMARY OF PARTICIPANT PERFORMANCE, 1979-1992 SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID TUBERCULOSIS AB The College of American Pathologists first offered a program of proficiency testing in mycobacteriology in 1969 to laboratories that offered any extent of diagnostic service. This program was intended to provide a mechanism for evaluation of methods of staining, culture, identification, and susceptibility testing. From 1979 to 1992, the period covered by this review, participation in the Mycobacteriology E Survey increased almost sixfold. On graded smears to be stained for detection of acid-fast bacilli, more than 85% of Extent 4 and Extent 3 laboratories and more than 80% of Extent 2 laboratories responded correctly to all specimens except one. Performance on specimens that contained Mycobacterium tuberculosis was similar for Extent 4 and Extent 3 laboratories. For all specimens containing M tuberculosis, a mean of more than 90% of Extent 4 and Extent 3 laboratories provided a correct identification each year except 1979, when a mean of 83% of Extent 3 laboratories responded correctly. Only Extent 4 laboratories were required to identify isolates other than M tuberculosis to the species level. For specimens that contained nontuberculous mycobacteria,the means of the yearly averages of correct responses for Extent 4 laboratories were 90% or greater for M kansasii, M marinum, M avium complex, and M fortuitum-chelonae complex and less than 85% for M bovis, M simiae, M scrofulaceum, M szulgai, M flavescens, M xenopi, M terrae complex, and M gastri. In general, on these same specimens, a slightly higher percentage of Extent 3 laboratories (which were required to identify only M tuberculosis to the species or complex level) gave correct or acceptable responses, and the performance of Extent 2 laboratories (which were only required to report whether or not a mycobacterium was present) was the best of all extents. The data suggext that laboratory performance improved somewhat after initial experience with uncommonly encountered organisms. For the most part, however, performance with a given species changed minimally from year to year. C1 NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,MICROBIOL SERV,BETHESDA,MD 20892. RP WOODS, GL (reprint author), UNIV TEXAS,MED BRANCH,DEPT PATHOL,GALVESTON,TX 77555, USA. NR 8 TC 4 Z9 4 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD JAN PY 1995 VL 119 IS 1 BP 17 EP 22 PG 6 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA PZ996 UT WOS:A1995PZ99600005 PM 7802547 ER PT J AU PIKIS, A AKRAM, S DONKERSLOOT, JA CAMPOS, JM RODRIGUEZ, WJ AF PIKIS, A AKRAM, S DONKERSLOOT, JA CAMPOS, JM RODRIGUEZ, WJ TI PENICILLIN-RESISTANT PNEUMOCOCCI FROM PEDIATRIC-PATIENTS IN THE WASHINGTON, DC, AREA SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID STREPTOCOCCUS-PNEUMONIAE MENINGITIS; ANTIMICROBIAL RESISTANCE; BLOOD CULTURES; CO-TRIMOXAZOLE; DAY-CARE; ANTIBIOTICS; SUSCEPTIBILITY; CHILDREN; PREVALENCE; DIAGNOSIS AB Objective: To assess the prevalence and antimicrobial susceptibility of penicillin-resistant pneumococci (PRP) isolated from patients in a pediatric hospital. Methods: All (108) isolates of Streptococcus pneumoniae recovered from usually sterile body sites between June 1, 1992, and May 31, 1993, were screened for susceptibility to penicillin by the E-test method. Minimum inhibitory concentrations of penicillin and other antibiotics were also determined by an agar dilution method for 10 PRP and 22 penicillin-susceptible strains. Results: Fourteen isolates (12.9%) were PRP by the E-test; nine of these (8.3%) were intermediately resistant and five (4.6%) were highly resistant. All strains were sensitive to rifampin and vancomycin. Increased frequency of resistance to oral and parenteral cephalosporins and carbapenems was found among PRP; for most of these antibiotics, resistance exceeded 40% of the PRP. In addition, 20% of the PRP were resistant to macrolides and all penicillin-susceptible and PRP were resistant to a combination of trimethoprim and sulfamethoxazole. Conclusions: The decreased susceptibility to oral and parenteral cephalosporins, macrolides, a combination of trimethoprim and sulfamethoxazole, and carbapenems creates a significant problem in the treatment of pneumococcal infections in bath ambulatory and hospitalized patients. C1 CHILDRENS NATL MED CTR,RES FDN,WASHINGTON,DC 20010. CHILDRENS NATL MED CTR,MED LAB,WASHINGTON,DC 20010. NIDR,MICROBIAL ECOL LAB,BETHESDA,MD. GEORGE WASHINGTON UNIV,MED CTR,DEPT PEDIAT,WASHINGTON,DC. GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC. GEORGE WASHINGTON UNIV,MED CTR,DEPT MICROBIOL & IMMUNOL,WASHINGTON,DC. RP PIKIS, A (reprint author), CHILDRENS NATL MED CTR,DEPT INFECT DIS,111 MICHIGAN AVE NW,WASHINGTON,DC 20010, USA. NR 40 TC 18 Z9 18 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD JAN PY 1995 VL 149 IS 1 BP 30 EP 35 PG 6 WC Pediatrics SC Pediatrics GA QC103 UT WOS:A1995QC10300006 PM 7827656 ER PT J AU ACKERMANN, HW ELZANOWSKI, A FOBO, G STEWART, G AF ACKERMANN, HW ELZANOWSKI, A FOBO, G STEWART, G TI RELATIONSHIPS OF TAILED PHAGES - A SURVEY OF PROTEIN-SEQUENCE IDENTITY SO ARCHIVES OF VIROLOGY LA English DT Note ID SITE-SPECIFIC INTEGRATION; NUCLEOTIDE-SEQUENCE; TEMPERATE BACTERIOPHAGE; DNA-POLYMERASES; RNA-POLYMERASE; LACTOBACILLUS-BULGARICUS; ENCODING GENE; EXPRESSION; CLASSIFICATION; LYSIS AB Using a multiple alignment program, we surveyed about 150 proteins from 35 tailed phages and calculated identity percentages. Sequence similarities are generally weak, indicating an extensive diversification of tailed phages. Related proteins occur in phages of different morphology and host range. DNA and RNA polymerases, integrases, muramidases, and several other tailed phage proteins appear to be acquired from bacteria. Tailed phages seem to be a monophyletic group and to constitute a polythetic order. Proteins common to all tailed phages may be detected by comparing the three-dimensional structure of major head and tail proteins. Amino acid alignments have presently no impact on the definition of high-level taxa of tailed phages. C1 NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. MAX PLANCK INST BIOCHEM,D-82512 MARTINSRIED,GERMANY. UNIV LAVAL,FAC AGR,STELA RES CTR,ST FOY,PQ G1K 7P4,CANADA. RP ACKERMANN, HW (reprint author), UNIV LAVAL,FAC MED,DEPT MICROBIOL,FELIX HERELLE REFERENCE CTR BACTERIAL VIRUSES,ST FOY,PQ G1K 7P4,CANADA. NR 65 TC 10 Z9 10 U1 0 U2 2 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1995 VL 140 IS 10 BP 1871 EP 1884 DI 10.1007/BF01384350 PG 14 WC Virology SC Virology GA TD158 UT WOS:A1995TD15800017 PM 7503687 ER PT J AU AGOSTINI, HT BRUBAKER, GR SHAO, J LEVIN, A RYSHKEWITSCH, CF BLATTNER, WA STONER, GL AF AGOSTINI, HT BRUBAKER, GR SHAO, J LEVIN, A RYSHKEWITSCH, CF BLATTNER, WA STONER, GL TI BK VIRUS AND A NEW-TYPE OF JC VIRUS EXCRETED BY HIV-1 POSITIVE PATIENTS IN RURAL TANZANIA SO ARCHIVES OF VIROLOGY LA English DT Article ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; POLYMERASE CHAIN-REACTION; HUMAN POLYOMAVIRUS; NUCLEOTIDE-SEQUENCE; REGULATORY REGION; VARIANTS; BRAIN; URINE; PAPOVAVIRUS; DNA AB HIV-1 positive patients from Tanzanian villages near Shirati were examined for urinary excretion of the human polyomaviruses JC and BK using the polymerase chain reaction (PCR). BK virus (BKV) was detected in 11 of 23 individuals tested. The BKV DNA sequences were all closely related to prototype Gardner strain and BKV (DUN). In contrast, a new type of JCV, termed Type 3 [or JCV (Shi)], was identified in seven of these same 23 individuals by comparison with Type 1 and Type 2 sequences of the VP1/intergenic/T antigen region of U.S., European and Asian strains. This suggests that JCV and BKV, although closely related, have different evolutionary histories within the African population. The six BKV regulatory regions amplified all showed the archetypal configuration. However, two of the seven JCV regulatory regions showed rearrangements: a small deletion and an inverted repeat. JCV causes a fatal demyelinating disease, progressive multifocal leukoencephalopathy (PML), in about 5% of AIDS patients in Europe and the U.S.A., but only one case has been reported in Africa. Our results suggest that this rarity of PML is not due to the absence of JCV in the African population. C1 NATL INST HLTH,NINDS,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. UNIV DAR ES SALAAM,MUHIMBILI MED CTR,DAR ES SALAAM,TANZANIA. SHIRATI HOSP,SHIRATI,TANZANIA. NATL INST HLTH,NATL CANC INST,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. ST BARTHOLOMEWS HOSP,COLL MED,RES TRIANGLE INST,RTI UNIT,LONDON,ENGLAND. FU NCI NIH HHS [N01-CP-33005] NR 47 TC 69 Z9 70 U1 0 U2 1 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0304-8608 J9 ARCH VIROL JI Arch. Virol. PY 1995 VL 140 IS 11 BP 1919 EP 1934 DI 10.1007/BF01322682 PG 16 WC Virology SC Virology GA TG910 UT WOS:A1995TG91000003 PM 7503691 ER PT J AU MCDERMOTT, M KASTNER, DL HOLLOMAN, JD SCHMIDTWOLF, G LUNDBERG, AS SINHA, AA HSU, C CASHIN, P MOLLOY, MG MULCAHY, B OGARA, F MCCONNELL, FI ADAMS, C KHAN, MA WOLFE, F RUBIN, LA CLEGG, DO HUSEBYE, D AMOS, CI WARD, RH MCDEVITT, HO AF MCDERMOTT, M KASTNER, DL HOLLOMAN, JD SCHMIDTWOLF, G LUNDBERG, AS SINHA, AA HSU, C CASHIN, P MOLLOY, MG MULCAHY, B OGARA, F MCCONNELL, FI ADAMS, C KHAN, MA WOLFE, F RUBIN, LA CLEGG, DO HUSEBYE, D AMOS, CI WARD, RH MCDEVITT, HO TI THE ROLE OF T-CELL RECEPTOR-BETA CHAIN GENES IN SUSCEPTIBILITY TO RHEUMATOID-ARTHRITIS SO ARTHRITIS AND RHEUMATISM LA English DT Article ID FRAGMENT-LENGTH-POLYMORPHISMS; ASSOCIATION; HAPLOTYPES AB Objective. To evaluate the role of the T cell receptor beta chain locus (TCRB) in genetic susceptibility to rheumatoid arthritis (RA). Methods. Twenty-eight multiplex RA families were recruited from 3 rheumatology outpatient departments. All members were genotyped for a highly informative microsatellite (V(beta)6.7), a V(beta)12.2 SSCP marker, and a biallelic C-beta restriction fragment length polymorphism. Data were analyzed by the SIBPAL program to assess identity-by-descent in affected sib-pairs. Results. Using the V(beta)12.2 marker, there was suggestive evidence of increased sib-pair sharing (P = 0.005) in affected offspring (a P value of 0.001 is generally taken to establish linkage). Data for V(beta)6.7 and C-beta yielded significance levels of 0.06 and 0.19, respectively. Conclusion. These data suggest that a gene in or linked to the TCRB complex may confer genetic susceptibility to RA in these families. Confirmation in a larger panel of families is required. C1 NIAMS,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD. STANFORD UNIV,STANFORD,CA 94305. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. UNIV KANSAS,WICHITA,KS. UNIV TORONTO,WOMENS COLL HOSP,TORONTO,ON,CANADA. UNIV UTAH,SCH MED,SALT LAKE CITY,UT. UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX. RP MCDERMOTT, M (reprint author), NATL UNIV IRELAND UNIV COLL CORK,DEPT MICROBIOL,CORK,IRELAND. FU NCI NIH HHS [CA-49734]; NIAMS NIH HHS [AR-40057] NR 13 TC 26 Z9 26 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD JAN PY 1995 VL 38 IS 1 BP 91 EP 95 DI 10.1002/art.1780380114 PG 5 WC Rheumatology SC Rheumatology GA QB696 UT WOS:A1995QB69600013 PM 7818578 ER PT S AU TARASOVA, N DENSLOW, ND PARTEN, BF TRAN, N NHUYEN, HP JONES, A ROBERTS, NB DUNN, BM AF TARASOVA, N DENSLOW, ND PARTEN, BF TRAN, N NHUYEN, HP JONES, A ROBERTS, NB DUNN, BM BE Takahashi, K TI A comparative study on amino acid sequences of three major isoforms of human pepsin A SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,POB B,FREDERICK,MD 21702, USA. RI Jones, Arwyn/E-4787-2010 OI Jones, Arwyn/0000-0003-2781-8905 FU NCI NIH HHS [N01-CO-74101]; PHS HHS [18865] 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 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 77 EP 81 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00008 PM 8540383 ER PT S AU ERICKSON, JW BALDWIN, ET BHAT, TN GULNIK, S AF ERICKSON, JW BALDWIN, ET BHAT, TN GULNIK, S BE Takahashi, K TI Structure of human cathepsin D: Comparison of inhibitor binding and subdomain displacement with other aspartic proteases SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702, USA. NR 0 TC 4 Z9 4 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 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 181 EP 192 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00022 PM 8540317 ER PT S AU BHAT, TN BALDWIN, ET LIU, B CHENG, YSE ERICKSON, JW AF BHAT, TN BALDWIN, ET LIU, B CHENG, YSE ERICKSON, JW BE Takahashi, K TI X-ray structure of a tethered dimer for HIV-1 protease SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK BIOMED SUPERCOMP CTR,STRUCT BIOCHEM CTR,FREDERICK,MD 21702, USA. NR 0 TC 3 Z9 3 U1 0 U2 2 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 439 EP 444 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00056 PM 8540354 ER PT S AU BALDWIN, ET BHAT, TN GULNIK, S LIU, BS KISO, Y MITSUYA, H ERICKSON, JW AF BALDWIN, ET BHAT, TN GULNIK, S LIU, BS KISO, Y MITSUYA, H ERICKSON, JW BE Takahashi, K TI Structure of HIV-1 protease with KNI-272: A transition state mimetic inhibitor containing allophenylnorstatine SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702, USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 445 EP 449 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00057 PM 8540355 ER PT S AU SILVA, AM CACHAU, RE BALDWIN, ET GULNIK, S SHAM, HL ERICKSON, JW AF SILVA, AM CACHAU, RE BALDWIN, ET GULNIK, S SHAM, HL ERICKSON, JW BE Takahashi, K TI Molecular dynamics of HIV-1 protease in complex with a difluoroketone-containing inhibitor: Implications for the catalytic mechanism SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 451 EP 454 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00058 PM 8540356 ER PT S AU COLLINS, JR BURT, SK ERICKSON, JW AF COLLINS, JR BURT, SK ERICKSON, JW BE Takahashi, K TI Activated dynamics of flap opening in HIV-1 protease SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK BIOMED SUPERCOMP CTR,FREDERICK,MD 21702, USA. NR 0 TC 9 Z9 9 U1 0 U2 1 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 455 EP 460 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00059 PM 8540357 ER PT S AU CACHAU, RE TOPOL, IA BURT, SK SILVA, AM ERICKSON, JW AF CACHAU, RE TOPOL, IA BURT, SK SILVA, AM ERICKSON, JW BE Takahashi, K TI Computer simulation and analysis of the reaction pathway for the decomposition of the hydrated peptide bond in aspartic proteases SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01CO-74102] NR 0 TC 1 Z9 1 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 461 EP 465 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00060 PM 8540358 ER PT S AU GUSTCHINA, A AF GUSTCHINA, A BE Takahashi, K TI Molecular modeling of the structure of FIV protease SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 479 EP 484 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00063 PM 8540361 ER PT S AU LOH, YP CAWLEY, NX FRIEDMAN, TC PU, LP AF LOH, YP CAWLEY, NX FRIEDMAN, TC PU, LP BE Takahashi, K TI Yeast and mammalian basic residue-specific aspartic proteases in prohormone conversion SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NICHHD,DEV NEUROBIOL LAB,CELLULAR NEUROBIOL SECT,BETHESDA,MD 20892, USA. NR 0 TC 6 Z9 6 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 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 519 EP 527 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00068 PM 8540366 ER PT S AU TOPOL, IA CACHAU, RE BURT, SK ERICKSON, JW AF TOPOL, IA CACHAU, RE BURT, SK ERICKSON, JW BE Takahashi, K TI Quantum mechanical model of the hydration and acidity of the active site in aspartic proteases SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK BIOMED SUPERCOMP CTR,FREDERICK,MD 21702, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0065-2598 BN 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 549 EP 554 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00071 PM 8540370 ER PT S AU AZARYAN, AV FRIEDMAN, TC CAWLEY, NX LOH, YP AF AZARYAN, AV FRIEDMAN, TC CAWLEY, NX LOH, YP BE Takahashi, K TI Characteristics of YAP3, a new prohormone processing aspartic protease from S-cerevisiae SO ASPARTIC PROTEINASES: STRUCTURE, FUNCTION, BIOLOGY, AND BIOMEDICAL IMPLICATIONS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 5th International Conference on Aspartic Proteinases CY SEP 19-24, 1993 CL KAWASHIMACHO, JAPAN SP Naito Museum Pharm Sci & Ind, Int Sci Fdn RP NICHHD,DEV NEUROBIOL LAB,CELLULAR NEUROBIOL SECT,BETHESDA,MD 20892, USA. NR 0 TC 4 Z9 4 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 0-306-44830-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 362 BP 569 EP 572 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD70Y UT WOS:A1995BD70Y00075 PM 8540374 ER PT B AU Suomi, SJ AF Suomi, SJ BE Goldberg, S Muir, R Kerr, J TI Influence of attachment theory on ethological studies of biobehavioral development in nonhuman primates SO ATTACHMENT THEORY: SOCIAL, DEVELOPMENTAL, AND CLINICAL PERSPECTIVES LA English DT Proceedings Paper CT Conference on Attachment Theory - Social, Developmental, and Clinical Perspectives CY OCT, 1993 CL TORONTO, CANADA SP C M Hincks Inst, Univ Toronto, Ontario Inst Studies Educ C1 NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD 20892. NR 0 TC 35 Z9 35 U1 0 U2 2 PU ANALYTIC PRESS PI HILLSDALE PA 365 BROADWAY, HILLSDALE, NJ 07642 BN 0-88163-184-1 PY 1995 BP 185 EP 201 PG 17 WC Psychiatry SC Psychiatry GA BF35P UT WOS:A1995BF35P00007 ER PT B AU ENGEL, BT AF ENGEL, BT BE Kikuchi, T Sakuma, H Saito, I Tsuboi, K TI Behaviorist's view of behavioral medicine SO BIOBEHAVIORAL SELF-REGULATION: EASTERN AND WESTERN PERSPECTIVES LA English DT Proceedings Paper CT 3rd International Conference on Biobehavioral Self-Regulation and Health - Biobehavioral Self-Regulation in the East and West CY SEP 21-24, 1993 CL TOKYO, JAPAN DE BEHAVIOR; BEHAVIORAL MEDICINE C1 NIA,GERONTOL RES CTR,BEHAV SCI LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG PI TOKYO PA 37-3, HONGO 3-CHOME BONKYO-KU, TOKYO 113, JAPAN BN 4-431-70153-2 PY 1995 BP 355 EP 361 PG 7 WC Psychology, Clinical; Psychology, Applied; Psychiatry; Psychology SC Psychology; Psychiatry GA BD89H UT WOS:A1995BD89H00065 ER PT J AU OKAZAKI, IJ ZOLKIEWSKA, A TAKADA, T MOSS, J AF OKAZAKI, IJ ZOLKIEWSKA, A TAKADA, T MOSS, J TI CHARACTERIZATION OF MAMMALIAN ADP-RIBOSYLATION CYCLES SO BIOCHIMIE LA English DT Article; Proceedings Paper CT 11th International Symposium on ADP-ribosylation CY SEP 17-21, 1994 CL BISCHENBERG-STRASBOURG, FRANCE SP Commiss European Communities, EEC Concerted Act DNA Repair & Canc, INSERM, Univ Louis Pasteur, Strasbourg, CNRS DE ADP-RIBOSYLATION; MONO-ADP-RIBOSYLTRANSFERASE; RT6.2 PROTEIN; GLYCOSYLPHOSPHATIDYLINOSITOL ANCHOR; ADP-RIBOSYLARGININE HYDROLASE ID SKELETAL-MUSCLE CELLS; AMINO-ACID-SEQUENCE; TURKEY ERYTHROCYTES; ESCHERICHIA-COLI; RIBOSYLARGININE HYDROLASE; PSEUDOMONAS-AERUGINOSA; ENZYMATIC-ACTIVITY; GLUTAMIC ACID-553; CHOLERA-TOXIN; EXOTOXIN-A AB NAD:arginine ADP-ribosyltransferases catalyze the transfer of the ADP-ribose moiety from NAD to an arginine in an acceptor protein, whereas ADP-ribosylarginine hydrolases remove ADP-ribose, regenerating free arginine and completing an ADP-ribosylation cycle. A family of four mono-ADP-ribosyltransferases was isolated and characterized from turkey erythrocytes. Transferases from rabbit and human skeletal muscle were cloned. The muscle transferases are glycosylphosphatidylinositol-anchored proteins and highly conserved across mammalian species. The rat T cell alloantigen RT6.2 has significant amino acid sequence identity to the muscle ADP-ribosyltransferase. Mammalian cells transformed with the RT6.2 coding region cDNA expressed NAD glycohydrolase activity. Sequences of RT6.2, rabbit muscle transferase and several of the bacterial toxin ADP-ribosyltransferases contain regions of amino acid similarity which, in the bacterial toxin ADP-ribosyltransferases, form the NAD-binding and active-site domains. ADP-ribosylarginine hydrolase, initially purified from turkey erythrocytes, was cloned from rat, mouse, and human brain. Deduced amino acid sequences of the rat and mouse hydrolases were 94% identical with five conserved cysteines whereas the human hydrolase sequence was 83% identical to that of the rat, with four conserved cysteines. It is unclear how an intracellular hydrolase acts in concert with a surface ADP-ribosyltransferase. RP NHLBI, PULM CRIT CARE MED BRANCH, BLDG 10, ROOM 5N307, BETHESDA, MD 20892 USA. NR 43 TC 11 Z9 12 U1 0 U2 2 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0300-9084 EI 1638-6183 J9 BIOCHIMIE JI Biochimie PY 1995 VL 77 IS 5 BP 319 EP 325 DI 10.1016/0300-9084(96)88141-7 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RK563 UT WOS:A1995RK56300003 PM 8527484 ER PT J AU Laufs, J Jupin, I David, C Schumacher, S HeyraudNitschke, F Gronenborn, B AF Laufs, J Jupin, I David, C Schumacher, S HeyraudNitschke, F Gronenborn, B TI Geminivirus replication: Genetic and biochemical characterization of Rep protein function, a review SO BIOCHIMIE LA English DT Article; Proceedings Paper CT 1st National Meeting on the Convergence of the 3Rs CY JUN 06-09, 1995 CL VILLEJUIF, FRANCE SP CNRS, INSERM, Commissariat Energie Atom, Assoc Rech Canc, Assoc Francaise Myopathies, Comite Org Avec Noms DE plant virus; DNA replication; ATPase; DNA binding; endonuclease ID GOLDEN MOSAIC-VIRUS; SINGLE-STRANDED-DNA; WHEAT DWARF VIRUS; MAIZE STREAK VIRUS; ROLLING-CIRCLE REPLICATION; NUCLEOTIDE-SEQUENCE; MUTATIONAL ANALYSIS; INITIATOR PROTEINS; BINDING-PROTEIN; ONE-COMPONENT AB Replication of the single-stranded DNA genome of plant geminiviruses follows a rolling circle mechanism. It strictly depends on a 'replication initiator protein' (Rep) which is the sole viral protein essential for replication. Rep protein catalyzes multiple reactions during the reproductive cycle of the virus. Here we summarize the recent advances of in vivo and in vitro analyses of the various Rep protein activities in a model for replication initiation and termination. In addition, the position of the geminivirus Rep protein within a general context of bacterial and mammalian replication initiator proteins is discussed. C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. MAX PLANCK INST ZUCHTUNGSFORSCH,D-50829 COLOGNE,GERMANY. RP Laufs, J (reprint author), CNRS,INST SCI VEGETALES,AVE TERRASSE,F-91198 GIF SUR YVETTE,FRANCE. NR 85 TC 73 Z9 76 U1 2 U2 8 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0300-9084 J9 BIOCHIMIE JI Biochimie PY 1995 VL 77 IS 10 BP 765 EP 773 DI 10.1016/0300-9084(96)88194-6 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TQ323 UT WOS:A1995TQ32300003 PM 8824773 ER PT J AU RHEE, CK LEVY, LA LONDON, RE AF RHEE, CK LEVY, LA LONDON, RE TI FLUORINATED O-AMINOPHENOL DERIVATIVES FOR MEASUREMENT OF INTRACELLULAR PH SO BIOCONJUGATE CHEMISTRY LA English DT Article ID F-19 NMR; MAGNETIC-RESONANCE; P-31 NMR; INDICATORS; ACIDS AB The simple 2-aminophenol group which serves as a building block for many cationic indicators has been modified to yield a series of pH sensitive probes. This approach is based on the replacement of one of the N-acetate groups of the chelator APTRA (o-aminophenol N,N,O-triacetate) by an N-ethyl group. The resulting series of (N-ethylamino)phenol (NEAP) compounds exhibit pK values in the physiological range and negligible affinity far physiological levels of other ions. Three fluorinated analogs have been prepared: N-ethyl-5-fluoro-2-aminophenol N,O-diacetate (5F NEAP), N-ethyl-2-((2-fluoro-4-carboxybenzyl)oxy)-4-fluoroaniline-N-acetic acid (5F NEAP-2), and 1-(2-(N-ethylamino)-5-fluorophenoxy)-2-(2-fluoro-4-aminophenoxy)ethane-N,N',N'-triacetic acid (5F NEAP-3). These derivatives exhibit total titration shifts of-ii ppm. NEAP-2 and NEAP-3 contain an additional fluorine to serve as an internal chemical shift reference, and NEAP-3, the most highly charged analog prepared, was designed in order to minimize leakage. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NR 21 TC 11 Z9 11 U1 2 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD JAN-FEB PY 1995 VL 6 IS 1 BP 77 EP 81 DI 10.1021/bc00031a008 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA QK410 UT WOS:A1995QK41000009 PM 7711108 ER PT J AU DELAROSA, A WILLIAMS, RL STEEG, PS AF DELAROSA, A WILLIAMS, RL STEEG, PS TI NM23 NUCLEOSIDE DIPHOSPHATE KINASE - TOWARD A STRUCTURAL AND BIOCHEMICAL UNDERSTANDING OF ITS BIOLOGICAL FUNCTIONS SO BIOESSAYS LA English DT Article ID GTP-BINDING PROTEINS; MYXOCOCCUS-XANTHUS; NM23 GENE; TUMOR-METASTASIS; DROSOPHILA DEVELOPMENT; BREAST-CANCER; EXPRESSION; CELLS; RAT; SUPPRESSOR AB The nm23 gene, a putative metastasis suppressor gene, was originally identified by its reduced expression in highly metastatic K-1735 murine melanoma cell lines, as compared to related, low metastatic melanoma cell lines, Transfection of nm23 cDNA has been reported to suppress malignant progression in Drosophila and mammalian cells. Highly conserved homologues of nm23 have been found in organisms ranging from the prokaryote Myxococcus xanthus to Drosophila, where the gene is involved in normal development and differentiation. The product of the nm23 gene exhibits a nucleoside diphosphate kinase activity, yet the nucleoside diphosphate kinase activity of Nm23 does not correlate with its apparent biological functions. We review recent cellular, genetic, biochemical and Xray crystallographic data to formulate and evaluate hypotheses concerning the molecular mechanism of nm23 action. C1 MRC CTR,CTR PROT ENGN,CAMBRIDGE CB2 2QH,ENGLAND. RP DELAROSA, A (reprint author), NCI,WOMENS CANC SECT,PATHOL LAB,BETHESDA,MD 20892, USA. FU Medical Research Council [MC_U105184308] NR 57 TC 198 Z9 202 U1 0 U2 5 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD JAN PY 1995 VL 17 IS 1 BP 53 EP 62 DI 10.1002/bies.950170111 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA QD935 UT WOS:A1995QD93500009 PM 7702594 ER PT J AU Gladyshev, VN Lecchi, P AF Gladyshev, VN Lecchi, P TI Identification of molybdopterins in molybdenum- and selenium-containing enzymes SO BIOFACTORS LA English DT Article AB Selenium is coordinated to a molybdenum atom in nicotinic acid hydroxylase (NAH) from Clostridium barkeri and formate dehydrogenase H (FDH) from Escherichia coli. Selenium is present in FDH in a selenocysteine residue whereas in NAH it occurs in an unidentified labile cofactor. In this paper we describe a simple procedure for isolation and identification of molybdopterins from Mo-containing enzymes. The molybdopterin, after release from the protein with guanidine-hydrochloride, is reduced with KBH4, alkylated with iodoacetamide and separated on a reversed-phase HPLC column. The carboxamidomethylated pterin compound is further characterized by UV spectroscopy and mass-spectrometry. We found that FDH contains molybdopterin guanine dinucleotide whereas NAH contains molybdopterin cytosine dinucleotide. C1 NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA. NIDDKD, Analyt Chem Lab, NIH, Bethesda, MD 20892 USA. RP Gladyshev, VN (reprint author), NHLBI, Biochem Lab, NIH, 9000 Rockville Pike,Bldg 3,Rm 103, Bethesda, MD 20892 USA. NR 21 TC 8 Z9 8 U1 0 U2 0 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0951-6433 J9 BIOFACTORS JI Biofactors PY 1995 VL 5 IS 2 BP 93 EP 97 PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA V3216 UT WOS:000171895800005 PM 8722123 ER PT J AU Tamura, T Gladyshev, V Liu, SY Stadtman, TC AF Tamura, T Gladyshev, V Liu, SY Stadtman, TC TI The mutual sparing effects of selenium and vitamin E in animal nutrition may be further explained by the discovery that mammalian thioredoxin reductase is a selenoenzyme SO BIOFACTORS LA English DT Review AB The recent discovery that mammalian thioredoxin reductase is a selenoprotein furnishes an additional explanation of the mutual sparing roles of selenium and vitamin E in cellular antioxidant systems. Thioredoxin reductases isolated from human lung adenocarcinoma cells, human Jurkat T-cells and HeLa cells contain selenocysteine which is located in a C- terminal tripeptide, -Cys-SeCys-Gly. C1 NHLBI, Biochem Lab, IR, NIH, Bethesda, MD 20892 USA. Okayama Univ, Fac Agr, Okayama 700, Japan. RP Stadtman, TC (reprint author), NHLBI, Biochem Lab, IR, NIH, Bldg 3,Room 108,3 Ctr Dr MSC 0320, Bethesda, MD 20892 USA. NR 42 TC 27 Z9 27 U1 1 U2 1 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0951-6433 J9 BIOFACTORS JI Biofactors PY 1995 VL 5 IS 2 BP 99 EP 102 PG 4 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA V3216 UT WOS:000171895800006 PM 8722124 ER PT B AU BIANCHINE, PJ METCALFE, DD AF BIANCHINE, PJ METCALFE, DD BE Kitamura, Y Yamamoto, S Galli, SJ Greaves, MW TI Adhesion molecules and their relevance in understanding the biology of the mast cell SO BIOLOGICAL AND MOLECULAR ASPECTS OF MAST CELL AND BASOPHIL DIFFERENTIATION AND FUNCTION LA English DT Proceedings Paper CT International Symposium on Biological and Molecular Aspects of Mast Cell and Basophil Differentiation and Function CY JUN 16-18, 1994 CL HIROSHIMA, JAPAN SP Bayer Yukuhin Ltd, Daiichi Pharm Co Ltd, Dainippon Pharm Co Ltd, Eisai Co Ltd, Fujisawa Pharm Co Ltd, Hitachi Chem Co Ltd, Kabi Pharm Diagnost K K, Kaken Pharm Co Ltd, Kanebo Ltd, Kissei Pharm Co Ltd, Kowa Co Ltd, Kojin Kai, Kyowa Hakko Kogyo Co Ltd, Lederle Japan Ltd, Marion Merrell Dow K K, Minophagen Pharm Co, Mitsubishi Kasei Co, Mochida Pharm Co Ltd, Nippon 'Boehringer Ingelheim Co Ltd, Nippon Glaxo Ltd, Nippon Roche K K, Nippon Shoji K K, Nippon Upjohn K K, Nippon Wellcome K K, Nov Co Ltd, Ono Pharm Co Ltd, Otsuka Pharm Co Ltd, Ryokuhu Kai, Sandoz Pharm Ltd, Sankyo Co Ltd, Sansho Kai, Shionogi Co Ltd, Taiho Pharm Co Ltd, Tekeda Chem Ind Ltd, Tanabe Seiyaku Co Ltd, Tokyo Tanabe Co Ltd, Torii & Co Ltd, Toyobo Co, Tsumura Co Ltd RP NIAID,CLIN INVEST LAB,ALLERG DIS SECT,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU RAVEN PRESS PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 BN 0-7817-0314-X PY 1995 BP 139 EP 147 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA BD27M UT WOS:A1995BD27M00012 ER PT B AU GNARRA, JR LERMAN, MI ZBAR, B LINEHAN, WM AF GNARRA, JR LERMAN, MI ZBAR, B LINEHAN, WM BE Bukowski, RM Finke, JH Klein, EA TI Molecular studies of the VHL tumor suppressor gene in renal cell carcinoma SO BIOLOGY OF RENAL CELL CARCINOMA LA English DT Proceedings Paper CT International Symposium on Renal Cell Carcinoma CY MAR, 1994 CL CLEVELAND, OH SP Cleveland Clin Fdn C1 NCI,SURG BRANCH,UROL ONCOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 BN 0-387-94503-2 PY 1995 BP 33 EP 39 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Oncology; Cell Biology GA BE19Q UT WOS:A1995BE19Q00004 ER PT B AU ZEA, AH LONGO, DL FINKE, JH BUKOWSKI, RM OCHOA, AC AF ZEA, AH LONGO, DL FINKE, JH BUKOWSKI, RM OCHOA, AC BE Bukowski, RM Finke, JH Klein, EA TI Alterations in signal transduction in T cells from cancer patients SO BIOLOGY OF RENAL CELL CARCINOMA LA English DT Proceedings Paper CT International Symposium on Renal Cell Carcinoma CY MAR, 1994 CL CLEVELAND, OH SP Cleveland Clin Fdn C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,CLIN SERV PROGRAM,IMMUNOTHERAPY LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 BN 0-387-94503-2 PY 1995 BP 65 EP 71 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Oncology; Cell Biology GA BE19Q UT WOS:A1995BE19Q00007 ER PT B AU WILTROUT, RH GHOSH, P FRANCO, JL MORI, M FENTON, RG LONGO, DL MURPHY, WJ GRZEGORZEWSKI, K KELVIN, DJ KOMSCHLIES, KL AF WILTROUT, RH GHOSH, P FRANCO, JL MORI, M FENTON, RG LONGO, DL MURPHY, WJ GRZEGORZEWSKI, K KELVIN, DJ KOMSCHLIES, KL BE Bukowski, RM Finke, JH Klein, EA TI Cellular and molecular considerations for the treatment of murine renal cancer SO BIOLOGY OF RENAL CELL CARCINOMA LA English DT Proceedings Paper CT International Symposium on Renal Cell Carcinoma CY MAR, 1994 CL CLEVELAND, OH SP Cleveland Clin Fdn C1 NCI,EXPTL IMMUNOL LAB,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 BN 0-387-94503-2 PY 1995 BP 123 EP 132 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Oncology; Cell Biology GA BE19Q UT WOS:A1995BE19Q00012 ER PT J AU FULCHER, KD MORI, C WELCH, JE OBRIEN, DA KLAPPER, DG EDDY, EM AF FULCHER, KD MORI, C WELCH, JE OBRIEN, DA KLAPPER, DG EDDY, EM TI CHARACTERIZATION OF FSC1 CDNA FOR A MOUSE SPERM FIBROUS SHEATH COMPONENT SO BIOLOGY OF REPRODUCTION LA English DT Article ID MESSENGER-RIBONUCLEIC-ACID; SPERMATOGENIC CELLS; MORPHOLOGICAL CHARACTERIZATION; EXPRESSION; PROTEINS; GENE; LOCALIZATION; FLAGELLUM; INSITU; RT7 AB The fibrous sheath is a major cytoskeletal structure in the principal piece of the mammalian sperm flagellum. We have cloned a cDNA and used it to characterize the expression of mRNA for a mouse sperm fibrous sheath protein. Peptides from a tryptic digest of fibrous sheath proteins were separated by HPLC and a 31 amino acid sequence was obtained from one of the peptides. Through the use of degenerate oligonucleotide polymerase chain reaction (PCR) primers predicted from this sequence, an 80-bp product was amplified from mouse testis first-strand cDNA. This was utilized as a probe to isolate a 2.9-kb cDNA clone from a mouse round spermatid cDNA library. Sequence analysis of the cDNA clone showed that it encodes a protein with an open reading frame of 849 amino acids and includes the original peptide sequence. The predicted protein has a molecular weight of 93 795 and contains 32 cysteine residues and 32 potential phosphorylation sites. It has no significant homology with other known cytoskeletal proteins. Northern blot analysis detected an mRNA of similar to 3 kb that was abundant in round spermatids of the mouse and in testes from six other mammalian species, but not in twelve somatic tissues from the mouse. In situ hybridization analysis indicated that the mRNA is first detected in step I-G spermatids, is most abundant in step 8-12 spermatids, and decreases in amount in step 13-15 spermatids, suggesting that expression of the mRNA occurs in the postmeiotic phase of spermatogenesis. In addition, monoclonal antibody 5A8, which recognizes proteins of the mouse fibrous sheath, was used to isolate cDNAs from a mouse spermatid expression library that were found by PCR analysis to be homologous to the original cDNA clone. These results suggest that the similar to 3-kb mRNA encodes a major structural component of the mouse fibrous sheath that appears to be a unique cytoskeletal protein of spermatogenic cells. We designate the cDNA for this fibrous sheath component Fsc1. C1 NIEHS,REPROD & DEV TOXICOL LAB,GAMETE BIOL SECT,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT MICROBIOL & IMMUNOL,CHAPEL HILL,NC 27599. UNIV N CAROLINA,REPROD BIOL LABS,CHAPEL HILL,NC 27599. FU NCI NIH HHS [CA16086]; NICHD NIH HHS [HD26485, P30-HD18968, R01 HD026485] NR 33 TC 77 Z9 78 U1 0 U2 2 PU SOC STUDY REPRODUCTION PI MADISON PA 1526 JEFFERSON ST, MADISON, WI 53711-2106 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD JAN PY 1995 VL 52 IS 1 BP 41 EP 49 DI 10.1095/biolreprod52.1.41 PG 9 WC Reproductive Biology SC Reproductive Biology GA PX592 UT WOS:A1995PX59200005 PM 7711182 ER PT J AU WELCH, JE BROWN, PR EDDY, EM AF WELCH, JE BROWN, PR EDDY, EM TI GENOMIC ORGANIZATION OF THE HUMAN GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE (GAPD-S) GENE SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 US EPA,REPROD TOXICOL BRANCH,RES TRIANGLE PK,NC 27711. NIEHS,GAMETE BIOL SECT,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1526 JEFFERSON ST, MADISON, WI 53711-2106 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1995 VL 52 SU 1 BP 102 EP 102 PG 1 WC Reproductive Biology SC Reproductive Biology GA RD902 UT WOS:A1995RD90200183 ER PT J AU TILLY, JL FLAWS, JA DESANTI, A KUGU, K RUBIN, JS HIRSHFIELD, AN AF TILLY, JL FLAWS, JA DESANTI, A KUGU, K RUBIN, JS HIRSHFIELD, AN TI ROLE OF INTRAFOLLICULAR GROWTH-FACTORS IN MATURATION AND ATRESIA OF RAT OVARIAN FOLLICLES SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,DEPT POPULAT DYNAM,DIV REPROD BIOL,BALTIMORE,MD 21218. UNIV MARYLAND,SCH MED,DEPT ANAT,BALTIMORE,MD 21201. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 7 Z9 7 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1526 JEFFERSON ST, MADISON, WI 53711-2106 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1995 VL 52 SU 1 BP 159 EP 159 PG 1 WC Reproductive Biology SC Reproductive Biology GA RD902 UT WOS:A1995RD90200410 ER PT J AU SLAYDEN, OD MURRAY, G IZUMI, S RUBIN, JS CHEDID, M BRENNER, RM AF SLAYDEN, OD MURRAY, G IZUMI, S RUBIN, JS CHEDID, M BRENNER, RM TI STEROIDS REGULATE HEPATOCYTE GROWTH-FACTOR (HGF) MESSENGER-RNA IN THE REPRODUCTIVE-TRACT OF RHESUS MACAQUES SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 OREGON REG PRIMATE RES CTR,DIV REPROD SCI,BEAVERTON,OR 97006. NAGASAKI UNIV,SCH MED,DEPT ANAT 3,NAGASAKI 852,JAPAN. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1526 JEFFERSON ST, MADISON, WI 53711-2106 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1995 VL 52 SU 1 BP 161 EP 161 PG 1 WC Reproductive Biology SC Reproductive Biology GA RD902 UT WOS:A1995RD90200417 ER PT J AU DAVIS, BJ FLAGLER, ND CORNIFFE, G TRAVLOS, GS WILSON, R MARONPOT, RR AF DAVIS, BJ FLAGLER, ND CORNIFFE, G TRAVLOS, GS WILSON, R MARONPOT, RR TI ETHYLENE-GLYCOL MONOMETHYL ETHER DISRUPTS OVARIAN ENDOCRINE FUNCTION SO BIOLOGY OF REPRODUCTION LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NCSU,COLL VET MED,RALEIGH,NC 27606. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1526 JEFFERSON ST, MADISON, WI 53711-2106 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PY 1995 VL 52 SU 1 BP 170 EP 170 PG 1 WC Reproductive Biology SC Reproductive Biology GA RD902 UT WOS:A1995RD90200454 ER PT B AU OLDEN, K AF OLDEN, K BE Mendelsohn, ML Peeters, JP Normandy, MJ TI The role of the NIEHS in the development of a national program for environmental health science research SO BIOMARKERS AND OCCUPATIONAL HEALTH: PROGRESS AND PERSPECTIVES LA English DT Proceedings Paper CT International Workshop on the Development and Applications of Biomarkers CY APR 26-29, 1994 CL SANTA FE, NM SP US DOE, Environm Safety & Hlth, US DOE, Energy Res, US DOE, Environm Management C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL ACADEMY PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, PO BOX 285, WASHINGTON, DC 20055 BN 0-309-05187-8 PY 1995 BP 25 EP 34 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA BD69J UT WOS:A1995BD69J00004 ER PT B AU ROTHMAN, N STEWART, WF RABKIN, CS SCHULTE, PA AF ROTHMAN, N STEWART, WF RABKIN, CS SCHULTE, PA BE Mendelsohn, ML Peeters, JP Normandy, MJ TI The development, validation and application of biomarkers for early biologic effects SO BIOMARKERS AND OCCUPATIONAL HEALTH: PROGRESS AND PERSPECTIVES LA English DT Proceedings Paper CT International Workshop on the Development and Applications of Biomarkers CY APR 26-29, 1994 CL SANTA FE, NM SP US DOE, Environm Safety & Hlth, US DOE, Energy Res, US DOE, Environm Management C1 NCI,OCCUPAT STUDIES SECT,ROCKVILLE,MD 20892. NR 0 TC 5 Z9 5 U1 0 U2 0 PU NATL ACADEMY PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, PO BOX 285, WASHINGTON, DC 20055 BN 0-309-05187-8 PY 1995 BP 109 EP 115 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA BD69J UT WOS:A1995BD69J00012 ER PT B AU RABKIN, CS ROTHMAN, N AF RABKIN, CS ROTHMAN, N BE Mendelsohn, ML Peeters, JP Normandy, MJ TI The development, validation, and application of biomarkers for HIV SO BIOMARKERS AND OCCUPATIONAL HEALTH: PROGRESS AND PERSPECTIVES LA English DT Proceedings Paper CT International Workshop on the Development and Applications of Biomarkers CY APR 26-29, 1994 CL SANTA FE, NM SP US DOE, Environm Safety & Hlth, US DOE, Energy Res, US DOE, Environm Management C1 NIH,VIRAL EPIDEMIOL BRANCH,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL ACADEMY PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, PO BOX 285, WASHINGTON, DC 20055 BN 0-309-05187-8 PY 1995 BP 116 EP 119 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA BD69J UT WOS:A1995BD69J00013 ER PT B AU GONZALEZ, FJ AF GONZALEZ, FJ BE Mendelsohn, ML Peeters, JP Normandy, MJ TI Xenobiotic/metabolizing enzymes in biomarker research SO BIOMARKERS AND OCCUPATIONAL HEALTH: PROGRESS AND PERSPECTIVES LA English DT Proceedings Paper CT International Workshop on the Development and Applications of Biomarkers CY APR 26-29, 1994 CL SANTA FE, NM SP US DOE, Environm Safety & Hlth, US DOE, Energy Res, US DOE, Environm Management C1 NCI,ROCKVILLE,MD 20852. NR 0 TC 3 Z9 3 U1 0 U2 0 PU NATL ACADEMY PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, PO BOX 285, WASHINGTON, DC 20055 BN 0-309-05187-8 PY 1995 BP 238 EP 256 PG 3 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA BD69J UT WOS:A1995BD69J00023 ER PT J AU BENICHOU, J AF BENICHOU, J TI A COMPLETE ANALYSIS OF VARIABILITY FOR ESTIMATES OF ABSOLUTE RISK FROM A POPULATION-BASED CASE-CONTROL STUDY ON BREAST-CANCER SO BIOMETRICAL JOURNAL LA English DT Article DE ABSOLUTE RISK; POPULATION-BASED CASE-CONTROL STUDY; BREAST CANCER; COMPONENTS OF VARIABILITY; IMPLICIT DELTA-METHOD; SUBSAMPLING ID INDIVIDUALIZED PROBABILITIES; MODELS AB The absolute risk is the probability of developing a given disease over a specified time interval given age and risk factors. GAIL et al. (1989) obtained point estimates for the absolute risk of breast cancer from a population-based case-control study, the Breast Cancer Detection and Demonstration Project (BCDDP). They combined relative risk estimates obtained from the case-control data and based on four risk factors and age, and composite hazard estimates from the cohort data. In this paper, we present a complete analysis of variability for breast cancer absolute risk estimates. Our proposed variance estimator takes into account all components of variability, namely the variances of relative risk estimates and of baseline hazard estimates as well as the covariance between the two, the latter terms being based on implicit delta-method arguments (Benichou and Gail, 1989). Our variance estimator also takes into account the specifics of the BCDDP study, namely the subsampling of cases and controls. We provide full details of the variance calculations because we anticipate that, in future studies, subsampling will also occur. We also present numerical illustration based on the BCDDP data. These calculations have been used in a recently developed program that computes point estimates and confidence intervals for the absolute risk of breast cancer based on the BCDDP data (Benichou, 1993). RP BENICHOU, J (reprint author), NCI,ROCKVILLE,MD 20892, USA. NR 20 TC 3 Z9 3 U1 0 U2 1 PU AKADEMIE VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0323-3847 J9 BIOMETRICAL J JI Biom. J. PY 1995 VL 37 IS 1 BP 3 EP 24 PG 22 WC Mathematical & Computational Biology; Statistics & Probability SC Mathematical & Computational Biology; Mathematics GA QF031 UT WOS:A1995QF03100001 ER PT J AU NAM, JM AF NAM, JM TI CONFIDENCE-LIMITS FOR THE RATIO OF 2 BINOMIAL PROPORTIONS BASED ON LIKELIHOOD SCORES - NONITERATIVE METHOD SO BIOMETRICAL JOURNAL LA English DT Article DE CONFIDENCE LIMITS; RELATIVE RISK; RELATIVE DIFFERENCE; NONITERATIVE METHOD ID RELATIVE DIFFERENCE; RISK RATIO; INTERVALS AB The interval estimation of the ratio of two binomial proportions based on the score statistic is superior over other methods. Iterative algorithms for calculating the approximate confidence interval have been provided by, e.g., KOOPMAN (1984, Biometrics 40:513-517) and GART and NAM (1988a, Biometrics 44:323-338). This note presents the analytical solutions for upper and lower confidence limits in a closed form and gives examples for numerical illustration. The non-iterative method is generally more desirable than the iterative method. C1 NCI,BIOSTAT BRANCH,ROCKVILLE,MD 20892. NR 13 TC 14 Z9 15 U1 0 U2 0 PU AKADEMIE VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0323-3847 J9 BIOMETRICAL J JI Biom. J. PY 1995 VL 37 IS 3 BP 375 EP 379 DI 10.1002/bimj.4710370311 PG 5 WC Mathematical & Computational Biology; Statistics & Probability SC Mathematical & Computational Biology; Mathematics GA QZ658 UT WOS:A1995QZ65800007 ER PT J AU FARAGGI, D SIMON, R AF FARAGGI, D SIMON, R TI MAXIMUM-LIKELIHOOD NEURAL-NETWORK PREDICTION MODELS SO BIOMETRICAL JOURNAL LA English DT Article DE FEEDFORWARD NEURAL NETWORKS; MAXIMUM LIKELIHOOD; NONLINEAR REGRESSION AB Neural networks have received much attention in recent years mostly by non-statisticians. The purpose of this paper is to incorporate neural networks in a non-linear regression model and obtain maximum likelihood estimates of the network parameters using a standard Newton-Raphson algorithm. We use maximum likelihood estimators instead of the usual back-propagation technique and compare the neural network predictions with predictions of quadratic regression models and with non-parametric nearest neighbor predictions. These comparisons are made using data generated from a variety of functions. Because of the number of parameters involved, neural network models can easily over-fit the data, hence validation of results is crucial. C1 NCI,BIOMETR RES BRANCH,ROCKVILLE,MD 20852. NR 15 TC 2 Z9 2 U1 0 U2 0 PU AKADEMIE VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0323-3847 J9 BIOMETRICAL J JI Biom. J. PY 1995 VL 37 IS 6 BP 713 EP 725 DI 10.1002/bimj.4710370607 PG 13 WC Mathematical & Computational Biology; Statistics & Probability SC Mathematical & Computational Biology; Mathematics GA RP959 UT WOS:A1995RP95900006 ER PT J AU LANTZ, LM HOLMES, KL AF LANTZ, LM HOLMES, KL TI IMPROVED NONRADIOACTIVE CELL-SURFACE LABELING TECHNIQUE FOR IMMUNOPRECIPITATION SO BIOTECHNIQUES LA English DT Note ID PROTEINS C1 NIAID,LMS,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,WASHINGTON,DC. NR 9 TC 12 Z9 12 U1 0 U2 1 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD JAN PY 1995 VL 18 IS 1 BP 56 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QA601 UT WOS:A1995QA60100012 PM 7702854 ER PT J AU TING, CC LIANG, SM WANG, J CHEN, YY HARGROVE, ME XU, NS AF TING, CC LIANG, SM WANG, J CHEN, YY HARGROVE, ME XU, NS TI IL-4-REGULATION OF PERFORIN GENE-EXPRESSION AND BLT-ESTERASE PRODUCTION IN ALPHA-CD3-INDUCED ACTIVATED KILLER-CELLS SO BIOTECHNOLOGY THERAPEUTICS LA English DT Article DE IL-4; KILLER CELLS; PERFORIN GENE ID STIMULATORY FACTOR-I; LYMPHOCYTE-T PRECURSORS; MONOCLONAL-ANTIBODY; CYTO-TOXICITY; CYTOPLASMIC GRANULES; INTERFERON-GAMMA; IL-4 REGULATION; PROTEIN-KINASE; INTERLEUKIN-4; INVIVO AB This present study examines Il-4 regulation of perforin gene expression and cytolytic granule production in alpha CD3-induced activated killer cells CD3-AK. After stimulation of resting T cells with alpha CD3, proliferative response could be detected at 1 day after activation. The expression of perforin mRNA and production of cytolytic granules (using BLT-E as indicator) was detected on days 2-4, and this time course correlated with the generation of lyric CD3-AK cells. These findings indicate that killer cells generation is a late event during the course of alpha CD3 activation. Generation of CD3-AK cells is primarily PKC dependent and is blocked by the depletion or inhibition of PKC by PMA or SSP. These changes are accompanied by the suppression of perforin gene expression (mRNA) and BLT-E production. However, adding IL-4 into the cultures restored the perforin mRNA expression and BLT-E production, and also the cytolytic activity of the CD3-AK cells. Furthermore, for preactivated CD3-AK cells cultured in IL-2, SSP also suppressed the perforin mRNA and BLT-E with the concomitant reduction of cytolytic activity. Similar to the resting T cells, in the SSP-maintained preactivated CD3-AK cells, switching the cytokine from IL-2 to IL-4/IL-2 restored perforin mRNA expression and BLT-E production, with concomitant restoration of the cytolytic activity. In contrast, switching from IL-4/IL-2 gave the opposite effect. These results could be reproduced by using amiloride which also inhibited PKC activity but did not affect the growth of preactivated CDS-AK cells. These findings indicate that IL-4 may play a role in the late stage of alpha CD3 activation to regulate the expression of perforin gene and probably the translation process during the generation of activated killer cells. C1 N AMER VACCINE INC,BELTSVILLE,MD 20705. NIDR,CELL DEV & ONCOL LAB,BETHESDA,MD 20892. RP TING, CC (reprint author), NCI,DIV CANC BIOL DIAG & CTR,OFF DIRECTOR,BLDG 10,ROOM 4B17,BETHESDA,MD 20892, USA. NR 36 TC 1 Z9 1 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0898-2848 J9 BIOTECHNOL THER JI Biotechnol. Ther. PY 1995 VL 5 IS 3-4 BP 99 EP 115 PG 17 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA TJ072 UT WOS:A1995TJ07200001 ER PT J AU COOK, JA MITCHELL, JB AF COOK, JA MITCHELL, JB TI MEASUREMENT OF THIOLS IN CELL-POPULATIONS FROM TUMOR AND NORMAL TISSUE SO BIOTHIOLS, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID GLUTATHIONE S-TRANSFERASES; SOLID TUMORS; MONOCHLOROBIMANE; SULFOXIMINE; CARCINOMA; INVITRO RP COOK, JA (reprint author), NCI,RADIAT BIOL BRANCH,BLDG 10,BETHESDA,MD 20892, USA. NR 26 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 251 BP 203 EP 212 PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD46P UT WOS:A1995BD46P00017 PM 7651198 ER PT J AU SIMONS, SS PRATT, WB AF SIMONS, SS PRATT, WB TI GLUCOCORTICOID RECEPTOR THIOLS AND STEROID-BINDING ACTIVITY SO BIOTHIOLS, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID HEAT-SHOCK PROTEIN; RAT-LIVER CYTOSOL; TISSUE-CULTURE CELLS; DEXAMETHASONE 21-MESYLATE; SULFHYDRYL-GROUPS; HORMONE-BINDING; DNA-BINDING; COVALENT MODIFICATION; ACTIVATING FACTOR; MODIFYING AGENTS C1 UNIV MICHIGAN,SCH MED,DEPT PHARMACOL,ANN ARBOR,MI 48109. RP SIMONS, SS (reprint author), NIDDKD,STEROID HORMONES SECT,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. FU NIDDK NIH HHS [DK31573] NR 69 TC 39 Z9 39 U1 0 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 251 BP 406 EP 422 PG 17 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BD46P UT WOS:A1995BD46P00039 PM 7651222 ER PT J AU GLASS, RS STADTMAN, TC AF GLASS, RS STADTMAN, TC TI SELENOPHOSPHATE SO BIOTHIOLS, PT B SE METHODS IN ENZYMOLOGY LA English DT Review ID SELD GENE-PRODUCT; ESCHERICHIA-COLI; SELENIUM DONOR; TRANSFER-RNAS; 5-METHYLAMINOMETHYL-2-SELENOURIDINE C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RP GLASS, RS (reprint author), UNIV ARIZONA,DEPT CHEM,TUCSON,AZ 85721, USA. NR 16 TC 9 Z9 9 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1995 VL 252 BP 309 EP 315 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA BE08C UT WOS:A1995BE08C00031 PM 7476367 ER PT J AU COLLINS, AF PEARSON, HA GIARDINA, P MCDONAGH, KT BRUSILOW, SW DOVER, GJ AF COLLINS, AF PEARSON, HA GIARDINA, P MCDONAGH, KT BRUSILOW, SW DOVER, GJ TI ORAL SODIUM PHENYLBUTYRATE THERAPY IN HOMOZYGOUS BETA-THALASSEMIA - A CLINICAL-TRIAL SO BLOOD LA English DT Article ID GLOBIN GENE-EXPRESSION; FETAL HEMOGLOBIN; BUTYRIC-ACID; DIFFERENTIATION; INDUCTION; CELLS; ADULT; 4-PHENYLBUTYRATE; ERYTHROPOIETIN; 5-AZACYTIDINE AB Butyrate analogues have been shown to increase fetal hemoglobin (HbF) production in vitro and in vivo. Sodium phenylbutyrate (SPB), an oral agent used to treat individuals with urea-cycle disorders, has been shown to increase HbF in nonanemic individuals and in individuals with sickle cell disease. We have treated eleven patients with homozygous beta thalassemia (three transfusion dependent) and one sickle-beta-thalassemia patient with 20 g/d (forty 500-mg tablets) of SPB far 41 to 460 days. All patients showed an increase in the percent of F reticulocytes associated with treatment, but only four patients responded by increasing their Hb levels by greater than 1 g/dL (mean increase, 2.1 g/dL; range, 1.2 to 2.8 g/dL). None of the transfusion-dependent thalassemia subjects responded. Increase in Hb was associated with an increase in red blood cell number (mean increase, 0.62 x 10(12)/L), and mean corpuscular volume (mean increase, 6 fL). Changes in percent HbF, absolute HbF levels, or alpha- to non-alpha-globin ratios as measured by levels of mRNA and globin protein in peripheral blood did not correlate with response to treatment. Response to treatment was not associated with the type of beta-globin mutation, but baseline erythropoietin levels of greater than 120 mU/mL was seen in all responders and only two of eight nonresponders to SPB. Compliance with treatment was greater than 90% as measured by pill counts. Side effects of the drug included weight gain and/ or edema caused by increase salt load in 2/12, transient epigastric discomfort in 7/12, and abnormal body odor in 3/12 subjects. Two splenectomized patients who were not on prophylactic antibiotics developed sepsis while on treatment. We conclude that SPB increases Hb in some patients with thalassemia, but the precise mechanism of action is unknown. (C) 1995 by The American Society of Hematology. C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. YALE UNIV,SCH MED,NEW HAVEN,CT. NEW YORK HOSP,CORNELL MED CTR,NEW YORK,NY. NHLBI,BETHESDA,MD. FU NHLBI NIH HHS [HL 28028]; NICHD NIH HHS [HD 11134, HD 26358] NR 42 TC 188 Z9 191 U1 0 U2 4 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 1 PY 1995 VL 85 IS 1 BP 43 EP 49 PG 7 WC Hematology SC Hematology GA QA032 UT WOS:A1995QA03200006 PM 7528572 ER PT J AU TREISMAN, J HWU, P MINAMOTO, S SHAFER, GE COWHERD, R MORGAN, RA ROSENBERG, SA AF TREISMAN, J HWU, P MINAMOTO, S SHAFER, GE COWHERD, R MORGAN, RA ROSENBERG, SA TI INTERLEUKIN-2-TRANSDUCED LYMPHOCYTES GROW IN AN AUTOCRINE FASHION AND REMAIN RESPONSIVE TO ANTIGEN SO BLOOD LA English DT Article ID TUMOR-INFILTRATING LYMPHOCYTES; GENE-TRANSFER; MOLECULAR CHARACTERIZATION; RETROVIRAL VECTORS; T-LYMPHOCYTES; CELL-GROWTH; IL-2 GENE; TUMORIGENICITY; EXPRESSION; LINE AB The maintenance of T lymphocytes in vivo after adoptive transfer for immunotherapy requires the systemic administration of interleukin-2 (IL-2), but prolonged administration of IL-2 is associated with substantial toxicity. The constitutive production of IL-2 by T cells may be an alternative method to prolong T-cell survival and potentially augment antitumor responses. To study the effects of constitutive production of IL-2 on the growth and antigen reactivity of a murine T cell, the sperm-whale myoglobin (SWM) specific T-cell line 14.1 was retrovirally transduced with the cDNA for IL-2. Cells that were transduced with vectors without an internal promoter were able to proliferate in the absence of exogenously added IL-2, and to grow in an autocrine fashion. These vectors used an internal ribosomal entry site (IRES) to allow translation of the neomycin phosphotransferase (neo') gene. In contrast, the cells transduced with an IL-2 vector in which the neo' gene was under the transcriptional control of an internal SV-40 promoter failed to proliferate or grow in the absence of exogenously added IL-2. The proliferation of the cells growing without IL-2 could be inhibited with antibodies to the IL-2 receptor or to human IL-2, indicating that they were still IL-2 dependent. Despite their autocrine growth, no tumor formation was observed in syngeneic mice injected subcutaneously with the transduced cells, and the cells retained their antigen reactivity and specificity. These results suggest that autocrine growth of T cells for therapy will not interfere with effector function. (C) 1995 by The American Society of Hematology. RP TREISMAN, J (reprint author), NCI,SURG BRANCH,BLDG 10,ROOM 2B42,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 31 TC 60 Z9 60 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 1 PY 1995 VL 85 IS 1 BP 139 EP 145 PG 7 WC Hematology SC Hematology GA QA032 UT WOS:A1995QA03200018 PM 7803791 ER PT J AU SCHNEIDER, E COWAN, KH BADER, H TOOMEY, S SCHWARTZ, GN KARP, JE BURKE, PJ KAUFMANN, SH AF SCHNEIDER, E COWAN, KH BADER, H TOOMEY, S SCHWARTZ, GN KARP, JE BURKE, PJ KAUFMANN, SH TI INCREASED EXPRESSION OF THE MULTIDRUG RESISTANCE-ASSOCIATED PROTEIN GENE IN RELAPSED ACUTE-LEUKEMIA SO BLOOD LA English DT Article ID P-GLYCOPROTEIN EXPRESSION; ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; CELL-LINES; CYTOTOXICITY; TRANSPORTER; ACCUMULATION; INVITRO; MRP AB Quantitative reverse transcriptase polymerase chain reaction (RT-PCR) was used to determine relative levels of transcripts for MDR1 and the recently described multidrug resistance-associated protein (MRP) in normal lymphohematopoietic cells and in 62 bone marrow aspirates of newly diagnosed and recurrent acute leukemia. Levels of MRP expression in newly diagnosed AML samples were similar to those observed in normal bone marrow cells (CD34-negative and CD34-positive) and in unselected HF60 human promyelocytic leukemia cells, which were used as an internal control throughout this study. In contrast, samples of AML obtained at the time of relapse contained approximately twofold higher levels of MRP RNA (P < .01). Analysis of paired samples, the first obtained at diagnosis and the second at relapse, from 13 acute myelogenous leukemia (AML) and four acute lymphocytic leukemia (ALL) patients showed that MRP expression was increased at the time of relapse in greater than 80% of patients. In contrast, no consistent changes of MDR1 expression at relapse were observed. These results raise the possibility that increased MRP expression might contribute to leukemic relapse. This is a US government work. There are no restrictions on its use. C1 JOHNS HOPKINS UNIV HOSP,CTR ONCOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205. RP SCHNEIDER, E (reprint author), NCI,MED BRANCH,BLDG 10,RM 12N226,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 45 TC 173 Z9 175 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JAN 1 PY 1995 VL 85 IS 1 BP 186 EP 193 PG 8 WC Hematology SC Hematology GA QA032 UT WOS:A1995QA03200024 PM 7528566 ER PT J AU WHANGPENG, J KNUTSEN, T JAFFE, ES STEINBERG, SM RAFFELD, M ZHAO, WP DUFFEY, P CONDRON, K YANO, T LONGO, DL AF WHANGPENG, J KNUTSEN, T JAFFE, ES STEINBERG, SM RAFFELD, M ZHAO, WP DUFFEY, P CONDRON, K YANO, T LONGO, DL TI SEQUENTIAL-ANALYSIS OF 43 PATIENTS WITH NON-HODGKINS-LYMPHOMA - CLINICAL CORRELATIONS WITH CYTOGENETIC, HISTOLOGIC, IMMUNOPHENOTYPING, AND MOLECULAR STUDIES SO BLOOD LA English DT Article ID CONSECUTIVELY ASCERTAINED SPECIMENS; CHROMOSOMAL-ABNORMALITIES; CELL LYMPHOMAS; TRANSLOCATION; SERIES; GENE AB Few reports correlating specific cytogenetic abnormalities with distinct subtypes of lymphoma have performed serial studies at diagnosis and at tumor recurrence or progression. In our file of 325 cytogenetically analyzed non-Hodgkin's lymphoma (NHL) patients studied over the past decade, 43 had serial biopsies, 39 of whom had at least two successful preparations; of the 43, nine had one and 32 had two or more cytogenetically abnormal specimens. In this study, we correlated cytogenetic, histopathologic, molecular, and clinical parameters. Patients with low-grade lymphomas were as likely as patients with intermediate- or high-grade lymphomas to acquire new chromosomal abnormalities with time (16 of 23 patients as compared with 7 of 16; P-2 = .11, chi(2) test). In four patients, originally diagnosed indolent disease progressed to aggressive disease; all had t(14;18), all gained additional chromosomal abnormalities with disease progression, and three of the four expressed abnormalities associated with disease progression and/or short survival: der(18), +7, and/or +12. Cytogenetic results from early disease were compared with those obtained later in disease: in the t(14;18) group, the most common abnormalities were +7 (eight patients) and der(18) (five patients), both seen later in disease. The most common abnormalities in patients without t(14;18) were 6q deletions; they were seen in both early and late disease and were associated with significantly shorter survivals (P-2 = .0014) compared with all patients without 69 deletions. Secondary chromosomal abnormalities, observed after at least one previous abnormal study, were seen in 19 of 22 t(14;18) patients and in 11 of 21 patients without t(14;18) and were associated with a poor survival (P-2 = .13) compared with patients without any secondary chromosomal abnormalities. Chromosome 1 abnormalities were seen in almost half of the patients and were observed in initial specimens and early in disease as well as late in disease and as secondary abnormalities; 19 involvement was more frequent than 1p (15 versus eight patients) and was significantly associated with poor survival only in patients with intermediate-/high-grade disease; the most common breakpoints were 1q21-q22 (nine patients) and 1p36 (six patients). Breakpoints at 2q21 and 3q27-q29 were limited to patients with t(14;18) and were almost exclusively secondary in nature. Molecular studies in 24 of our patients showed discrepancies with the cytogenetic results in only three patients: two had t(14;18) but no molecular rearrangements while two patients had no visible t(14;18) but were positive for major breakpoint region (MBR) rearrangement. The presence of MBR or minor breakpoint cluster (MCR) rearrangement had no apparent effect on survival. The most significant prognostic indicator was low-grade lymphoma (P-2 < .0001). Age (P-2 = .012) and the presence of 1q (P-2 = .0026) in intermediate-/high-grade disease, and the presence of t(14;18) in low-grade lymphoma (P-2 = .035) were prominent prognostic variables in the two grade categories. This is a US government work. There are no restrictions on its use. C1 NCI,MED BRANCH,CYTOGENET ONCOL SECT,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NCI,BIOL RESPONSE MODIFIERS PROGRAM,BETHESDA,MD 20892. NR 32 TC 97 Z9 97 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 1 PY 1995 VL 85 IS 1 BP 203 EP 216 PG 14 WC Hematology SC Hematology GA QA032 UT WOS:A1995QA03200026 PM 7803794 ER PT J AU LIU, JM KIM, S WALSH, CE AF LIU, JM KIM, S WALSH, CE TI RETROVIRAL-MEDIATED TRANSDUCTION OF THE FANCONI-ANEMIA-C COMPLEMENTING (FACC) GENE IN 2 MURINE TRANSPLANTATION MODELS SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Article DE FANCONI ANEMIA; GENE TRANSDUCTION; MOUSE BONE MARROW TRANSPLANTATION ID HUMAN ADENOSINE-DEAMINASE; MOUSE; EXPRESSION; CLONING; MARROW; CELLS; MICE AB Fanconi anemia (FA) is a well-known genetic syndrome manifested by bone marrow failure, variable physical anomalies, and cancer susceptibility. This disorder is marked by genotypic and phenotypic heterogeneity and consists of four distinct complementation groups A, B, C, and D. The defective gene responsible for the C group of FA, FACC, was identified by cDNA complementation cloning, and we have recently proposed a trial of gene therapy for group C FA. No animal model yet exists for FA. Consequently, we have studied the effects of constitutive expression of human FACC in two murine transplantation models. In the first model, we demonstrated transduction of FACC to reconstituting stem cells of mutant W/W-V mice. In the second model, we demonstrated transduction of FACC to hematopoietic cells transplanted to the bone marrows and spleens of non-myeloablated BALB/c mice. Our data suggest that retroviral-mediated transfer of the normal human FACC cDNA to hematopoietic progenitor and stem cells of mice is feasible and not associated with direct harmful effects to the hematopoietic organ. C1 NIH,CPD,CTR CLIN,SERV HEMATOL,BETHESDA,MD 20892. RP LIU, JM (reprint author), NHLBI,HEMATOL BRANCH,BLDG 10,RM 7C103,BETHESDA,MD 20892, USA. NR 31 TC 5 Z9 5 U1 0 U2 0 PU BLOOD CELLS FOUNDATION PI LA LOLLA PA C/O ERNEST BEUTLER SCRIPPS RES INST, DEPT MOLECULAR EXP MEDICINE, LA LOLLA, CA 92037 SN 1079-9796 J9 BLOOD CELL MOL DIS JI Blood Cell Mol. Dis. PY 1995 VL 21 IS 1 BP 56 EP 63 DI 10.1006/bcmd.1995.0009 PG 8 WC Hematology SC Hematology GA RP697 UT WOS:A1995RP69700008 PM 7544677 ER PT J AU GOANS, RE ABRAMS, SA VIEIRA, NE MARINI, JC PEREZ, MD YERGEY, AL AF GOANS, RE ABRAMS, SA VIEIRA, NE MARINI, JC PEREZ, MD YERGEY, AL TI A 3-HOUR MEASUREMENT TO EVALUATE BONE CALCIUM TURNOVER SO BONE LA English DT Article DE CALCIUM; KINETICS; ACCRETION; BONE TURNOVER; POWER FUNCTION; OSTEOPOROSIS; OSTEOGENESIS IMPERFECTA ID PLASMA CALCIUM; DERMATOMYOSITIS; POLYMYOSITIS; METABOLISM; KINETICS AB It is well established that short-term clearance of an intravenous calcium load in vivo reflects bone uptake. Using results from isotope-dilution experiments with Ca-42, a 3-h test has been developed to measure-a quantity, gamma, related to bone accretion. This test is proposed as a useful, clinically applicable measure of bone status. For early times, t, after a bolus of Ca-42, plasma tracer dilution was well approximated by t(-gamma), where gamma is related to the fractional rate of loss of tracer, q, from blood into bone ((l/q)(dq/dt) = -gamma/t). Gamma was evaluated from kinetic measurements on 91 normal female children, adolescents, and adult women in the age range 4-50 years. For t less than or equal to 3 h, all clearance curves were well fit by a power function. Gamma was found to vary from 0.244 +/- 0.031 for adult premenopausal women (N = 22) to 0.392 +/- 0.056 for prepubertal children (N = 29). Using the Spearman rank order correlation test, gamma was correlated with bone accretion measured from classic calcium kinetic studies with a correlation coefficient of 0.721, significant at p < 0.005. In those cases in which accretion and resorption remain tightly linked, gamma also provides information on the state of calcium loss from bone. Gamma was evaluated in 14 subjects with bone disease characterised by increased resorption (osteoporosis, Paget's disease) and in 27 subjects with decreased accretion (osteogenesis imperfecta, types I, III, IV; steroid-treated juvenile dermatomyositis). All subjects with Paget's disease and with osteoporosis showed increased gamma, consistent with high bone turnover. The osteoporotic patients furthermore exhibited gamma increasing monotonically by approximately 1% per year after age 55. The osteogenesis imperfecta patients consistently showed either normal or decreased gamma, depending upon the severity of the disease. The steroid-treated dermatomyositis patients had consistently decreased gamma, in concordance with previous studies demonstrating decreased accretion in disease states requiring steroid medication. C1 NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. USDA ARS,CHILDRENS NUTR RES CTR,HOUSTON,TX. BAYLOR COLL MED,DEPT PEDIAT,HOUSTON,TX 77030. NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. NR 39 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 8756-3282 J9 BONE JI Bone PD JAN PY 1995 VL 16 IS 1 BP 33 EP 38 DI 10.1016/8756-3282(95)80008-E PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA RB631 UT WOS:A1995RB63100005 PM 7742080 ER PT S AU Barrett, JA AF Barrett, JA BE Sackstein, R Janssen, WE Elfenbein, GJ TI Strategies to enhance the graft-versus-malignancy effect in allogeneic transplants SO BONE MARROW TRANSPLANTATION: FOUNDATIONS FOR THE 21ST CENTURY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Bone Marrow Transplantation in the 90s - Into the 21st-Century CY MAR 15-18, 1995 CL ORLANDO, FL SP New York Acad Sci, AMGEN Inc, H Lee Moffitt Canc Ctr & Res Inst, Bristol Myers Squibb, Sandoz Pharm Corp, Alpha Therapeut Corp, Armour Pharm Co, Bayer Corp, Chiron Therapeut, Coulter Corp, Genentech Inc, Glaxo Inc, Hoffmann La Roche Inc, Immunex Corp, Integrated Therapeut Corp, NIH, NCI, Oncol Biotech, Ortho Biotech, Pfizer Inc, Upjohn Co, Xoma Corp ID BONE-MARROW TRANSPLANTATION; CHRONIC MYELOGENOUS LEUKEMIA; MINOR HISTOCOMPATIBILITY ANTIGENS; T-CELL DEPLETION; HOST-DISEASE; RELAPSE; INTERLEUKIN-2; DETERMINANTS; SURVIVAL RP Barrett, JA (reprint author), NHLBI,HEMATOL BRANCH,BONE MARROW TRANSPLANT UNIT,BETHESDA,MD 20892, USA. NR 45 TC 0 Z9 0 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 0-89766-994-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 770 BP 203 EP 212 DI 10.1111/j.1749-6632.1995.tb31056.x PG 10 WC Oncology; Hematology; Multidisciplinary Sciences; Transplantation SC Oncology; Hematology; Science & Technology - Other Topics; Transplantation GA BF30X UT WOS:A1995BF30X00018 PM 8597361 ER PT S AU Eckelman, WC AF Eckelman, WC BE Ochi, H Konishi, J Yonekura, Y Fukuchi, M Nishimura, T Tamaki, N Inoue, Y Shiomi, S Tsumura, M Okamura, T TI Advances in the uses of PET radiotracers SO BRAIN, HEART AND TUMOR IMAGING: UPDATED PET AND MRI SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 2nd International Osaka-City-University Symposium on Brain, Heart and Tumor Imaging CY OCT 02-04, 1994 CL OSAKA, JAPAN SP Japanese Soc Nucl Med, Osaka City, Osaka City Univ, Osaka City Univ Med Sch, Uehara Mem Fdn, Osaka Pharm Manufacturers Assoc, Osaka Med Assoc C1 NIH,PET DEPT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-82155-4 J9 INT CONGR SER PY 1995 VL 1090 BP 11 EP 15 PG 5 WC Oncology; Cardiac & Cardiovascular Systems; Neurosciences; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Cardiovascular System & Cardiology; Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA BE50V UT WOS:A1995BE50V00002 ER PT S AU CHUANG, RY CHUANG, LF LI, Y KUNG, HF KILLAM, KF AF CHUANG, RY CHUANG, LF LI, Y KUNG, HF KILLAM, KF BE Sharp, BM Eisenstein, TK Madden, JJ Friedman, H TI SIV mutations detected in morphine-treated Macaca mulatta following SIV mac239 infection SO BRAIN IMMUNE AXIS AND SUBSTANCE ABUSE SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Proceedings Paper CT 2nd Annual Symposium on Brain-Immune Axis and Substance Abuse CY JUN 16-18, 1994 CL PALM BEACH, FL ID SIMIAN IMMUNODEFICIENCY VIRUS C1 UNIV MARYLAND,DEPT MICROBIOL & IMMUNOL,BALTIMORE,MD 21201. NCI,FREDERICK,MD 21701. RP UNIV CALIF DAVIS,SCH MED,DEPT MED PHARMACOL & TOXICOL,DAVIS,CA 95616, USA. FU NIDA NIH HHS [DA 05901] NR 11 TC 7 Z9 7 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 0-306-45017-8 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1995 VL 373 BP 175 EP 181 PG 7 WC Substance Abuse; Immunology; Neurosciences SC Substance Abuse; Immunology; Neurosciences & Neurology GA BD36W UT WOS:A1995BD36W00024 PM 7668149 ER PT J AU GEHRMANN, J YAO, DL BONETTI, B BRENNER, M BONDY, C WEKERLE, H KREUTZBERG, GW WEBSTER, HD AF GEHRMANN, J YAO, DL BONETTI, B BRENNER, M BONDY, C WEKERLE, H KREUTZBERG, GW WEBSTER, HD TI ASTROCYTES UP-REGULATE GLIAL FIBRILLARY ACIDIC PROTEIN (GFAP), BUT NOT INSULIN-LIKE GROWTH-FACTOR-I (IGF-I) DURING EXPERIMENTAL AUTOIMMUNE NEURITIS (EAN) SO BRAIN PATHOLOGY LA English DT Article ID EXPERIMENTAL ALLERGIC NEURITIS; RECEPTOR GENE-EXPRESSION; SPINAL-CORD MICROGLIA; T-CELL LINES; RAT-BRAIN; FACIAL NUCLEUS; MATURATION; ISCHEMIA; PATTERN; NEURONS AB T cell-mediated autoimmune neuritis produces rapid activation of spinal cord microglia. To determine whether this microglial response upregulates astrocytic expression of IGF-related proteins, we induced EAN and used in situ hybridization and immunocytochemistry to examine the mRNAs and peptides for glial fibrillary acidic protein (GEAR), insulin-like growth factor-I (IGF-I), IGF-I receptor (IGFR-I) and IGF binding protein-2 (IGFBP-2). Relative levels of GFAP mRNA and peptide were highest in the lumbar spinal cord 4-10 d following T cell transfer and significant GFAP elevations were still present after three weeks. The astrocytes expressing GEAR mRNA and peptide were localized around motoneurons which were related topographically to axons in peripheral nerve inflammatory lesions. In the nucleus gracilis, where terminals of dorsal root ganglion neurons are located, astrocytic levels of GFAP mRNA and peptide rose later and did not reach their highest levels until 21 d after T cell transfer. Even though microglia were activated in both locations 2-4 d after transfer, astrocytic levels of IGF-I, IGFR-I and IGFBP-2 mRNA and peptide did not differ significantly from those observed in controls. The dissociation of GFAP and IGF-I expression in EAN suggests that these astrocytic responses may be independently regulated. We also suggest that the type and severity of remote neuronal injury are probably more important inducers and regulators of these astrocytic responses than microglial cell activation. C1 NINCDS,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. MAX PLANCK INST PSYCHIAT,D-82152 MARTINSRIED,GERMANY. NINCDS,STROKE BRANCH,BETHESDA,MD 20892. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP GEHRMANN, J (reprint author), UNIV ZURICH HOSP,INST NEUROPATHOL,DEPT PATHOL,CH-8091 ZURICH,SWITZERLAND. NR 51 TC 8 Z9 8 U1 0 U2 1 PU INT SOC NEUROPATHOLOGY PI ZURICH PA ISN JOURNAL PO BOX, CH-8033 ZURICH, SWITZERLAND SN 1015-6305 J9 BRAIN PATHOL JI Brain Pathol. PD JAN PY 1995 VL 5 IS 1 BP 1 EP 10 DI 10.1111/j.1750-3639.1995.tb00570.x PG 10 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA QJ684 UT WOS:A1995QJ68400001 PM 7539325 ER PT J AU EGAN, MF FERGUSON, JN HYDE, TM AF EGAN, MF FERGUSON, JN HYDE, TM TI EFFECTS OF CHRONIC NALOXONE ADMINISTRATION ON VACUOUS CHEWING MOVEMENTS AND CATALEPSY IN RATS TREATED WITH LONG-TERM HALOPERIDOL DECANOATE SO BRAIN RESEARCH BULLETIN LA English DT Article DE NALOXONE; VACUOUS CHEWING MOVEMENTS; HALOPERIDOL; TARDIVE DYSKINESIA ID VENTRAL TEGMENTAL AREA; RECEPTOR UP-REGULATION; NUCLEUS-ACCUMBENS; TARDIVE-DYSKINESIA; DOPAMINE RELEASE; BEHAVIORAL SUPERSENSITIVITY; INDUCED HYPERMOTILITY; NEUROLEPTIC TREATMENT; PARKINSONS-DISEASE; LOCOMOTOR-ACTIVITY AB Most antipsychotic medications produce motoric side effects, including parkinsonism and tardive dyskinesia (TD). Correlates of these behaviors in rats (catalepsy and vacuous chewing movements, respectively) were used as a model to assess the usefulness of chronic naloxone administration in symptom reduction. Previous studies have suggested that increased neurotransmission in the endogenous opioid system modulates neuroleptic-induced motoric side effects. Rats were treated with haloperidol decanoate or vehicle for 27 weeks, and withdrawn for 30 weeks. Subsequently, naloxone (0.5 to 2.0 mg/kg SC twice daily) was given for 5 weeks. Long-term haloperidol treatment produced a syndrome of vacuous chewing movements (VCMs) that persisted during the drug withdrawal period. Catalepsy developed rapidly and also persisted. Naloxone treatment had little effect on VCMs but increased catalepsy scores in both haloperidol and vehicle treated groups. Naloxone reduced rearing and grooming in haloperidol rats while increasing these measures in vehicle treated rats. The results indicate that neuroleptic-induced motoric side effects are not reversed by naloxone in rats. Furthermore, they suggest that increased opioid neurotransmission may not underlie the expression of VCMs. This does not rule out the possibility that endogenous opioid system may be involved in the development of VCMs. To the extent that this animal model is valid, naloxone may not be effective in treating TD and neuroleptic-induced parkinsonism in humans. C1 NIMH,NEUROSCI RES CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. RP EGAN, MF (reprint author), NIMH,NEUROSCI RES CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,2700 ML KING JR AVE SE,WASHINGTON,DC 20032, USA. NR 67 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 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1995 VL 38 IS 4 BP 355 EP 363 DI 10.1016/0361-9230(95)00108-Q PG 9 WC Neurosciences SC Neurosciences & Neurology GA RV808 UT WOS:A1995RV80800008 PM 8535858 ER PT J AU ISRAEL, A STROMBERG, C TSUTSUMI, K GARRIDO, MD TORRES, M SAAVEDRA, JM AF ISRAEL, A STROMBERG, C TSUTSUMI, K GARRIDO, MD TORRES, M SAAVEDRA, JM TI ANGIOTENSIN-II RECEPTOR SUBTYPES AND PHOSPHOINOSITIDE HYDROLYSIS IN RAT ADRENAL-MEDULLA SO BRAIN RESEARCH BULLETIN LA English DT Article DE PHOSPHOINOSITIDE TURNOVER; CGMP; RAT ADRENAL MEDULLA; ANGIOTENSIN II RECEPTOR SUBTYPES; LOSARTAN ID CHROMAFFIN CELLS; INOSITOL TRISPHOSPHATE; PHEOCHROMOCYTOMA CELLS; GLOMERULOSA CELLS; BINDING; BRAIN; STIMULATION; DUP-753; CALCIUM; AT2 AB Angiotensin II (ANG) receptor subtypes were characterized by quantitative autoradiography after incubation with the ANG agonist [I-125]Sar(1)-ANG in rat adrenal medulla. ANG receptors are highly localized in adrenal medulla. Specific binding was displaced by 4% and by 95% with the AT(1) receptor blocker losartan and the AT(2) receptor competitor CGP 42112A, respectively. Analysis of competition curves indicated relative binding potencies for the AT(2) population of CGP 42112A>PD 123319> PD 123177. ANG stimulated inositol phosphate formation in a dose-dependent manner in rat adrenal medulla. Losartan at concentrations of 10(-9) to 10(-5) M antagonized the effect of ANG, whereas PD 123177 or PD 123319 had no antagonistic action, However, at a higher concentration (10(-5) M) PD 123177 or PD 123319 potentiated the effect of ANG on InsP(1)-accumulation. In the presence of PO 123319 (10(-5) M) ANG dose-response curve was shifted to the left with no change in the maximal effect. This affect was blocked by the addition of losartan (10(-5) M). On the contrary, the addition of CGP 42112A (10(-6) M) inhibited ANG-induced increase in InsP(1)-accumulation. On the other hand, ANG and CGP 42112A reduced basal cyclic GMP formation, this effect was partially reverted by sodium orthovanadate, a phosphotyrosine phosphatase inhibitor, Our results further demonstrate the presence of two ANG receptor subtypes in adrenal medulla: ANG binding to AT(1) receptor stimulates inositol phospholipid metabolism, whereas ANG binding to AT(2) receptors decreases both inositol phosphate production and cGMP formation. C1 NIMH,CLIN SCI LAB,PHARMACOL SECT,BETHESDA,MD 20892. NR 46 TC 41 Z9 41 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1995 VL 38 IS 5 BP 441 EP 446 DI 10.1016/0361-9230(95)02011-F PG 6 WC Neurosciences SC Neurosciences & Neurology GA RY852 UT WOS:A1995RY85200005 PM 8665267 ER PT J AU OSTROWSKI, NL PERT, A AF OSTROWSKI, NL PERT, A TI SUBSTANTIA-NIGRA OPIATE RECEPTORS ON BASAL GANGLIA EFFERENTS SO BRAIN RESEARCH BULLETIN LA English DT Article DE NALOXONE; SUBSTANTIA NIGRA; PARS COMPACTA; PARS RETICULATA; OPIATE RECEPTORS; INTERNAL CAPSULE; GLOBUS PALLIDUS; STRIATUM; RAT; SUBSTANTIA NIGRA AFFERENTS; [H-3] NALOXONE; MU OPIOID RECEPTORS; DELTA OPIOID RECEPTORS; DOPAMINE; GABA; VENTRAL MESENCEPHALON ID VENTRAL TEGMENTAL AREA; DOPAMINE NEURONS; RAT-BRAIN; AUTORADIOGRAPHIC LOCALIZATION; NUCLEUS ACCUMBENS; OPIOID RECEPTORS; MU-OPIATE; MORPHINE; STRIATUM; ENKEPHALIN AB Many behavioral effects of opiate narcotics and peptides have been linked to effects on dopamine neurons originating in the substantia nigra pars compacta and ventral tegmental area. Selective brain lesions were combined with quantitative autoradiography to determine whether opiate receptors are on dopaminergic somata and/or processes in the substantia nigra pars compacta and ventral tegmental area. 6-Hydroxydopamine lesions that eliminated dopamine neurons produced little change in the pattern or density of [H-3]-naloxone binding in the substantia nigra pars compacta or ventral tegmental area. Radiofrequency lesions of the internal capsule or globus pallidus and kainic acid lesions of the striatum markedly decreased [H-3]-naloxone binding in the pars compacta and pars reticulata. These results are consistent with a dense distribution of opiate receptors on pallido-nigral and/or striato-nigral fibers and strengthen the likelihood that local effects of opiates on dopamine function in the nigrostriatal pathway are mediated indirectly by actions on nondopaminergic processes. C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. NR 65 TC 13 Z9 13 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1995 VL 38 IS 6 BP 513 EP 523 DI 10.1016/0361-9230(95)02014-4 PG 11 WC Neurosciences SC Neurosciences & Neurology GA TF570 UT WOS:A1995TF57000001 PM 8590072 ER PT J AU REILLY, JJ NARDOZZI, J SCHULKIN, J AF REILLY, JJ NARDOZZI, J SCHULKIN, J TI THE INGESTION OF CALCIUM IN MULTIPAROUS AND VIRGIN FEMALE RATS SO BRAIN RESEARCH BULLETIN LA English DT Article DE CALCIUM INGESTION; FEMALES; VIRGINS; MULTIPAROUS RATS ID BRAIN; SEX AB The present experiments demonstrate that multiparous females ingest more calcium that virgin females. In two experiments, we demonstrated that multiparous females ingested more calcium than virgin females, and both ingested larger amounts than males. The biological basis for this enhanced avidity for calcium lie in the greater needs for calcium during reproduction. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. NR 16 TC 8 Z9 8 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1995 VL 37 IS 3 BP 301 EP 303 DI 10.1016/0361-9230(95)00036-E PG 3 WC Neurosciences SC Neurosciences & Neurology GA QT037 UT WOS:A1995QT03700012 PM 7627574 ER PT J AU WAN, XM FU, TC FUNK, A LONDON, RE AF WAN, XM FU, TC FUNK, A LONDON, RE TI DIFFERENTIAL CLEARANCE OF NITROXIDE MRI CONTRAST AGENTS FROM RAT CEREBRAL-VENTRICLES SO BRAIN RESEARCH BULLETIN LA English DT Article DE CEREBRAL VENTRICLES; MRI; NITROXIDES; CONTRAST AGENTS ID NUCLEAR MAGNETIC-RESONANCE; SPIN LABELS; REDUCTION; METABOLISM; CELLS; LIVER; PHARMACOKINETICS; PERMEABILITY AB Seven stable nitroxides have been evaluated as contrast agents in MRI studies of the rat cerebroventricular system. Because the contrast enhancement is primarily confined to the cerebral ventricles, nitroxides can be used to examine the ventricular structure. On the other hand, based on the absence of reducing agents in the rat CSF and on the fact that nitroxides can be reduced intracellularly, the relative reduction in contrast subsequent to an intracerebral injection provides information on the relationship of chemical structure to transmembrane flux in vivo. Observed rate constants and rate constants due to reduction have been analyzed quantitatively by modeling the effects of flow with GdDTPA, which is not subject to reduction. Five-membered ring nitroxides, in general, were reduced at much slower rates than six-membered ring nitroxides. The presence of a positive charge in the structure can substantially slow down the transmembrane flux. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NATL TAIWAN UNIV,COLL MED,DEPT PHYSIOL,TAIPEI,TAIWAN. NR 30 TC 7 Z9 7 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1995 VL 36 IS 1 BP 91 EP 96 DI 10.1016/0361-9230(94)00170-6 PG 6 WC Neurosciences SC Neurosciences & Neurology GA PT245 UT WOS:A1995PT24500014 PM 7882056 ER PT J AU KRESSE, A JACOBOWITZ, DM SKOFITSCH, G AF KRESSE, A JACOBOWITZ, DM SKOFITSCH, G TI DETAILED MAPPING OF CGRP MESSENGER-RNA EXPRESSION IN THE RAT CENTRAL-NERVOUS-SYSTEM - COMPARISON WITH PREVIOUS IMMUNOCYTOCHEMICAL FINDINGS SO BRAIN RESEARCH BULLETIN LA English DT Article DE CALCITONIN GENE-RELATED PEPTIDE; IN SITU HYBRIDIZATION; HISTOCHEMICAL NEUROANATOMY; CRANIAL MOTONEURONS ID GENE-RELATED PEPTIDE; DORSAL-ROOT GANGLIA; INSITU HYBRIDIZATION HISTOCHEMISTRY; NICOTINIC ACETYLCHOLINE-RECEPTOR; CALCITONIN-GENE; SPINAL-CORD; MESSENGER-RNAS; SUBSTANCE-P; BRAIN-STEM; CHOLINE-ACETYLTRANSFERASE AB The localization of CGRP mRNA in neurons of the rat brain and spinal cord was assessed by in situ hybridization histochemistry (ISH) using a radiolabeled synthetic 57-mer oligodeoxynucleotide probe complementary to the rat prepro CGRP mRNA, Results were compared with previously published findings of CGRP-immunoreactive (CGRP-IR) cell bodies revealed by an indirect immunofluorescence technique. The highest numbers of CGRP mRNA expressing neurons as well as the greatest intensity of staining were found in the lateral hypothalamic area, the parabrachial nuclei, and among the cranial motor nuclei, especially in the nuclei of the 7th and 12th nerve and the ambiguus nucleus, which is generally in good agreement with findings assessed by immunocytochemistry (ICH), However, some mismatches between the localization of the peptide by ICH and the localization of the CGRP mRNA were also observed. Thus, ISH was not able to confirm CGRP-IR in cells of the amygdaloid complex and parts of the medial hypothalamus, the central gray, and the inferior colliculus, but ISH revealed considerably more CGRP mRNA expressing cells in the lateral hypothalamic area, arcuate nucleus, posterior and peripeduncular thalamic nuclei, and all cranial motor nuclei than CGRP-IR containing cells found by ICH. Moreover, ISH also revealed CGRP mRNA synthesis in the nucleus of the lateral olfactory tract and in the perihypoglossal nuclei that were devoid of CGRP-IR. The reasons for the observed mismatches still remain to be elucidated; however, intracerebroventricular colchicine pretreatment used to increase immunocytochemical signals also might have induced or suppressed gene expression in certain brain regions in an unpredictable matter, On the other hand, detection of only the mRNA in a certain region does not necessarily mean that also the active peptide is synthesized there. C1 GRAZ UNIV,DEPT ZOOL,HISTOPHARMACOL UNIT,A-8010 GRAZ,AUSTRIA. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. NR 89 TC 48 Z9 50 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1995 VL 36 IS 3 BP 261 EP 274 DI 10.1016/0361-9230(94)00201-B PG 14 WC Neurosciences SC Neurosciences & Neurology GA PY930 UT WOS:A1995PY93000009 PM 7697380 ER PT J AU ISAACS, KR ABBOTT, LC AF ISAACS, KR ABBOTT, LC TI CEREBELLAR VOLUME DECREASES IN THE TOTTERING MOUSE ARE SPECIFIC TO THE MOLECULAR LAYER SO BRAIN RESEARCH BULLETIN LA English DT Article DE BISECTOR METHOD; CAVALIERI METHOD; STEREOLOGY; MOLECULAR LAYER; PURKINJE CELL ID MUTANT MOUSE; PURKINJE-CELLS; TYROSINE-HYDROXYLASE; RAT-BRAIN; UNDERNUTRITION; EPILEPSY; GROWTH; MALNUTRITION; EXPRESSION; SEIZURES AB The volume of the cerebellum as a whole and the volume of the molecular layer per Purkinje cell in adult tottering (tg/tg) and tottering/leaner (tg/tg(la)) mice were reduced when compared with normal age-matched wild type mice (+/+). No changes in the volume of the granule cell layer or white matter layer were detected, suggesting that the mutation effects were limited to the molecular layer of the cerebellum. The density of Purkinje cells and the total number of Purkinje cells did not vary between groups. The cerebellar and body weights were decreased in tg/tg and tg/tg(la) mice compared with +/+ mice. C1 UNIV ILLINOIS,COLL VET MED,URBANA,IL 61801. RP ISAACS, KR (reprint author), NIMH,CLIN SCI LAB,HISTOPHARMACOL SECT,BLDG 10,RM 3D-48,BETHESDA,MD 20892, USA. NR 35 TC 19 Z9 20 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PY 1995 VL 36 IS 3 BP 309 EP 314 DI 10.1016/0361-9230(94)00207-H PG 6 WC Neurosciences SC Neurosciences & Neurology GA PY930 UT WOS:A1995PY93000014 PM 7697385 ER PT J AU LYNCH, HT WATSON, P CONWAY, T LYNCH, J BOYD, J AF LYNCH, HT WATSON, P CONWAY, T LYNCH, J BOYD, J TI BREAST-CANCER AND IMPORTANCE OF ZYGOSITY DETERMINATION IN TRIPLET SISTERS SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Note DE BREAST CANCER; PARAFFIN EMBEDDED TUMOR BLOCKS; TRIPLETS; ZYGOSITY ID OVARIAN-CANCER; FAMILIAL BREAST; CHROMOSOME-17Q21; LINKAGE AB This study is the first to examine the genetic risk in a breast cancer-prone family wherein two of three triplet sisters and their mother manifested breast cancer. The unaffected triplet, the proband, was found to be monozygotic with her deceased sister through DNA testing of tumor blocks and dizygotic to her living affected sister. Genetic counseling implications are discussed. C1 NIEHS,GENE EXPRESS SECT,RES TRIANGLE PK,NC. RP LYNCH, HT (reprint author), CREIGHTON UNIV,SCH MED,DEPT PREVENT MED,2500 CALIF PLAZA,OMAHA,NE 68178, USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 1995 VL 36 IS 3 BP 315 EP 317 DI 10.1007/BF00713403 PG 3 WC Oncology SC Oncology GA RX145 UT WOS:A1995RX14500005 PM 8573714 ER PT J AU OSHAUGHNESSY, JA COWAN, KH AF OSHAUGHNESSY, JA COWAN, KH TI CURRENT STATUS OF PACLITAXEL IN THE TREATMENT OF BREAST-CANCER SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE PACLITAXEL; TAXOL(R); COMBINATIONS; TREATMENT; DRUG RESISTANCE ID COLONY-STIMULATING FACTOR; CELL-LINES; TAXOL; RESISTANCE; DRUG AB Paclitaxel is a highly active single agent as therapy for previously untreated as well as doxorubicin-refractory metastatic breast cancer, with associated response rates of 62% and 20-48%, respectively. Complete responses with paclitaxel occur chiefly in breast cancer patients whose metastatic disease has not been previously treated with chemotherapy. Early data suggest a possible dose-response relationship for paclitaxel in metastatic breast cancer, but the optimal dose has not yet been defined. The optimal duration of infusional paclitaxel treatment is also not yet known. A study of 96-hour infusional paclitaxel in the treatment of doxorubicin- or mitoxantrone-refractory metastatic breast cancer patients has demonstrated a 48% response rate suggesting that prolonged exposures to paclitaxel may offer a therapeutic advantage. Randomized trials of 3- vs 96-hour paclitaxel are ongoing or planned. The relative efficacy of paclitaxel versus standard chemotherapy as front-line or salvage therapy for metastatic breast cancer is currently under study, In addition, two randomized trials are under way in node positive breast cancer patients to study whether treatment with paclitaxel following standard or high dose doxorubicin and cyclophosphamide adjuvant therapy results in improved patient benefit. Combining paclitaxel with other active agents in the treatment of metastatic breast cancer is an area of active investigation. Combined paclitaxel and doxorubicin, administered concurrently or sequentially, is associated with modest complete response rates in metastatic breast cancer patients, Sequential paclitaxel-->doxorubicin administration is associated with more mucositis than is doxorubicin-->paclitaxel when paclitaxel is administered over 24 hours. High doses of cyclophosphamide can be combined with 24- or 72-hour infusional paclitaxel, and phase II studies of this combination are warranted. Early data suggest that administering biweekly paclitaxel and cisplatin to previously untreated metastatic breast cancer patients is associated with high response rates, and confirmatory studies of this combination and schedule are planned, Preclinical data suggest that cell cycle considerations may be important in combining doxorubicin and possibly other agents with paclitaxel. Paclitaxel is an excellent substrate for P-glycoprotein, the protein product of the multidrug resistance-1 (mdr-l) gene, and phase I trials are under way combining paclitaxel with several known blockers of Pgp function, Finally, pilot studies are under way to determine whether the radiation sensitizing effects of paclitaxel can be exploited as part of radiation therapy for patients with locally advanced breast cancer. RP OSHAUGHNESSY, JA (reprint author), NCI,MED BRANCH,MED BREAST CANC SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 12N226,BETHESDA,MD 20892, USA. NR 28 TC 11 Z9 11 U1 1 U2 7 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD JAN PY 1995 VL 33 IS 1 BP 27 EP 37 DI 10.1007/BF00666068 PG 11 WC Oncology SC Oncology GA PZ324 UT WOS:A1995PZ32400003 PM 7749130 ER PT J AU MULCAHY, D AF MULCAHY, D TI ASYMPTOMATIC ISCHEMIA DURING DAILY-LIFE IN STABLE CORONARY-ARTERY DISEASE - RELEVANT OR REDUNDANT - REPLY SO BRITISH HEART JOURNAL LA English DT Letter RP MULCAHY, D (reprint author), NHLBI,PUBL HLTH SERV,DEPT HLTH & HUMAN SERV,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-0769 J9 BRIT HEART J JI Br. Heart J. PD JAN PY 1995 VL 73 IS 1 BP 101 EP 101 PG 1 WC Cardiac & Cardiovascular Systems; History & Philosophy Of Science SC Cardiovascular System & Cardiology; History & Philosophy of Science GA QC427 UT WOS:A1995QC42700024 ER PT J AU DOYLE, LA ROSS, DD SRIDHARA, R FOJO, AT KAUFMANN, SH LEE, EJ SCHIFFER, CA AF DOYLE, LA ROSS, DD SRIDHARA, R FOJO, AT KAUFMANN, SH LEE, EJ SCHIFFER, CA TI EXPRESSION OF A 95-KDA MEMBRANE-PROTEIN IS ASSOCIATED WITH LOW DAUNORUBICIN ACCUMULATION IN LEUKEMIC BLAST CELLS SO BRITISH JOURNAL OF CANCER LA English DT Article DE MULTIDRUG RESISTANCE; ANTHRACYCLINE; PROTEIN; ACUTE MYELOID LEUKEMIA ID HUMAN-TUMOR-CELLS; MULTIDRUG-RESISTANCE; P-GLYCOPROTEIN; GENE-EXPRESSION; HL60 CELLS; LEUKEMIA; OVEREXPRESSION; TOPOISOMERASE; AMPLIFICATION; CYTOTOXICITY AB A 95 kDa membrane protein (P-95) has been previously noted to be overexpressed in a doxorubicin-resistant subline of the MCF-7 breast cancer line and in clinical samples obtained from patients with solid tumours refractory to doxorubicin. We performed Western blotting on blast cell lysates from adults with acute myeloid leukaemia, using antisera to P-95. Concomitant flow cytometric assays measured daunorubicin accumulation and retention. Blasts from 16/46 patient samples had detectable P-95 and had reduced accumulation of daunorubicin compared with the negative marrows. Experiments with the P-95 positive MCF-7 multidrug-resistant subline demonstrated decreased daunorubicin accumulation and retention relative to the sensitive parent line. AML blast cells positive for P-95 also demonstrated greater overall in vitro survival in the presence of daunorubicin relative to the P-95-negative samples. The expression of P-95 did not correlate with failure to achieve an initial complete remission with daunorubicin and cytarabine induction chemotherapy. We conclude that the P-95 protein may possess an efflux transporter function, and may represent another mechanism responsible for anthracycline resistance in acute myeloid leukaemia. C1 UNIV MARYLAND,SCH MED,DEPT MED,DIV HEMATOL & ONCOL,BALTIMORE,MD 21201. NCI,MED BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,CTR ONCOL,BALTIMORE,MD 21287. RP DOYLE, LA (reprint author), UNIV MARYLAND,SCH MED,CTR CANC,22 S GREENE ST,BALTIMORE,MD 21201, USA. FU NCI NIH HHS [CA 52178] NR 26 TC 31 Z9 31 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD JAN PY 1995 VL 71 IS 1 BP 52 EP 58 DI 10.1038/bjc.1995.11 PG 7 WC Oncology SC Oncology GA QA578 UT WOS:A1995QA57800011 PM 7819048 ER PT J AU PUTNAM, FW AF PUTNAM, FW TI INVESTIGATING MULTIPLE PERSONALITY-DISORDER SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Letter RP PUTNAM, FW (reprint author), NIMH,BETHESDA,MD 20892, USA. NR 4 TC 3 Z9 3 U1 0 U2 0 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD JAN PY 1995 VL 166 BP 122 EP 123 DI 10.1192/bjp.166.1.122 PG 2 WC Psychiatry SC Psychiatry GA QB796 UT WOS:A1995QB79600033 PM 7894867 ER PT J AU LINDBERG, DAB AF LINDBERG, DAB TI SYMPOSIUM - BUILDING THE NATIONAL-HEALTH INFORMATION INFRASTRUCTURE - THE ROLE OF HIGH-PERFORMANCE COMPUTING AND COMMUNICATIONS - INTRODUCTION SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Editorial Material RP LINDBERG, DAB (reprint author), NATL LIB MED,OFF PRESIDENT,OFF SCI & TECHNOL POLICY,HPCC NATL COORDINAT OFF,8600 ROCKVILLE PK,BETHESDA,MD 20894, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD JAN PY 1995 VL 83 IS 1 BP 28 EP 28 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA QC122 UT WOS:A1995QC12200005 ER PT J AU LINDBERG, DAB AF LINDBERG, DAB TI HPCC AND THE NATIONAL INFORMATION INFRASTRUCTURE - AN OVERVIEW SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article; Proceedings Paper CT Conference on Building the National Health Information Infrastructure - The Role of High Performance Computing and Communications CY MAY 19, 1994 CL SAN ANTONIO, TX SP MED LIB ASSOC, MED INFORMAT SECT, HIGH PERFORMANCE COMP & COMMUN, NATL COORDINAT OFF AB The National Information Infrastructure (NII) or ''information superhighway'' is a high-priority federal initiative to combine communications networks, computers, databases, and consumer electronics to deliver information services to all U.S. citizens. The NII will be used to improve government and social services while cutting administrative costs. Operated by the private sector, the NII will rely on advanced technologies developed under the direction of the federal High Performance Computing and Communications (HPCC) Program. These include computing systems capable of performing trillions of operations (teraops) per second and networks capable of transmitting billions of bits (gigabits) per second. Among other activities, the HPCC Program supports the national supercomputer research centers, the federal portion of the Internet, and the development of interface software, such as Mosaic, that facilitates access to network information services. Health care has been identified as a critical demonstration area for HPCC technology and an important application area for the NII. As an HPCC participant, the National Library of Medicine (NLM) assists hospitals and medical centers to connect to the Internet through projects directed by the Regional Medical Libraries and through an Internet Connections Program cosponsored by the National Science Foundation. In addition to using the Internet to provide enhanced access to its own information services, NLM sponsors health-related applications of HPCC technology. Examples include the ''Visible Human'' project and recently awarded contracts for test-bed networks to share patient data and medical images, telemedicine projects to provide consultation and medical care to patients in rural areas, and advanced computer simulations of human anatomy for training in ''virtual surgery.'' RP LINDBERG, DAB (reprint author), NATL LIB MED,OFF PRESIDENT,OFF SCI & TECHNOL POLICY,NATL COORDINAT OFF,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 2 TC 6 Z9 6 U1 1 U2 4 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD JAN PY 1995 VL 83 IS 1 BP 29 EP 31 PG 3 WC Information Science & Library Science SC Information Science & Library Science GA QC122 UT WOS:A1995QC12200006 PM 7703935 ER PT J AU Ellwein, LB Kupfer, C AF Ellwein, LB Kupfer, C TI Strategic issues in preventing cataract blindness in developing countries SO BULLETIN OF THE WORLD HEALTH ORGANIZATION LA English DT Article ID SURGERY; NEPAL AB Cataract blindness is a public health problem of major proportions in developing countries. intracapsular cataract extraction with aphakic spectacles has been the standard surgical technique for restoring sight. Because of image magnification in the operated eye, however, the result in unilaterally blind patients is less than satisfactory. Fortunately, with the availability of low-cost intraocular lenses (IOL) and ophthalmologists trained in extracapsular surgery, it is now practical to intervene successfully in the unilateral case. The need for increased attention on the quality of the visual outcome is only one of three important strategic issues in cataract blindness control. The existing high prevalence of cataract blindness in developing countries and an increasing cataract incidence due to an aging population require substantial increases in surgical volume. The third issue relates to cost. If significant increases in surgical volume and quality of outcomes are to be realized without an increased need for external funding, service delivery must be made more efficient. The expansion of IOL surgery for unilateral blindness is a favourable trend in ensuring financial sustainability of delivery systems; patients can be operated on while still economically productive and able to pay rather than waiting for bilateral blindness and a less favourable economic and social impact. If the quality, volume, and cost issues are to be successfully addressed, operational and structural changes to eye care delivery systems are necessary. These changes can be effected through training technology introduction, management of facilities, social marketing, organizational partnerships, and evaluation. With improved understanding of the critical factors in successful models their widespread replication will be facilitated. RP Ellwein, LB (reprint author), NEI,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 21 TC 24 Z9 28 U1 0 U2 2 PU WORLD HEALTH ORGANIZATION PI GENEVA 27 PA DISTRIBUTION AND SALES, CH-1211 GENEVA 27, SWITZERLAND SN 0042-9686 J9 B WORLD HEALTH ORGAN JI Bull. World Health Organ. PY 1995 VL 73 IS 5 BP 681 EP 690 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TN134 UT WOS:A1995TN13400014 PM 8846495 ER PT J AU GREENWALD, P KELLOFF, G BURCHWHITMAN, C KRAMER, BS AF GREENWALD, P KELLOFF, G BURCHWHITMAN, C KRAMER, BS TI CHEMOPREVENTION SO CA-A CANCER JOURNAL FOR CLINICIANS LA English DT Article AB Chemoprevention has been shown to be an extremely promising approach to the prevention of invasive cancer. Through the identification of chemopreventive agents that inhibit or reverse the process of carcinogenesis, new strategies of early intervention can be developed for patients at high risk that potentially prevent the onset of invasive and metastatic phases of cancer. This articles reviews the present efforts in chemoprevention research, including the identification of promising agents, screening, and preclinical and clinical evaluations. RP GREENWALD, P (reprint author), NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892, USA. NR 0 TC 89 Z9 92 U1 0 U2 2 PU AMER CANCER SOC PI NEW YORK PA C/O JB LIPPINCOTT CO 1180 AVE OF THE AMERICAS 6TH FLOOR, NEW YORK, NY 10036 SN 0007-9235 J9 CA-CANCER J CLIN JI CA-Cancer J. Clin. PD JAN-FEB PY 1995 VL 45 IS 1 BP 31 EP & DI 10.3322/canjclin.45.1.31 PG 0 WC Oncology SC Oncology GA QD850 UT WOS:A1995QD85000003 PM 7804897 ER PT J AU FEDARKO, NS VETTER, UK ROBEY, PG AF FEDARKO, NS VETTER, UK ROBEY, PG TI AGE-RELATED-CHANGES IN BONE-MATRIX STRUCTURE IN-VITRO SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article; Proceedings Paper CT NIA/NIDR Workshop on Human Models of Skeletal Aging CY MAR 01-02, 1994 CL WASHINGTON, DC SP NIA, NIDR ID CELLS-INVITRO; EXTRACELLULAR-MATRIX; COLLAGEN; HYALURONAN; TISSUES; PROTEIN; DECORIN; SPARC C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV GERIATR MED & GERONTOL,BONE METAB RES LAB,BALTIMORE,MD 21224. HUMBOLDT UNIV BERLIN,DEPT PEDIAT,BERLIN,GERMANY. RP FEDARKO, NS (reprint author), NIDR,BONE RES BRANCH,BETHESDA,MD 20892, USA. RI Robey, Pamela/H-1429-2011; OI Robey, Pamela/0000-0002-5316-5576; Fedarko, Neal/0000-0001-6055-6279 NR 16 TC 10 Z9 10 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 1995 VL 56 SU 1 BP S41 EP S43 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QE653 UT WOS:A1995QE65300018 PM 7719986 ER PT J AU FRIEDENSTEIN, AJ AF FRIEDENSTEIN, AJ TI MARROW STROMAL FIBROBLASTS SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article; Proceedings Paper CT NIA/NIDR Workshop on Human Models of Skeletal Aging CY MAR 01-02, 1994 CL WASHINGTON, DC SP NIA, NIDR ID BONE-MARROW; CELLS; INVITRO C1 NF GAMALEI INST EPIDEMIOL & MICROBIOL,MOSCOW 123098,RUSSIA. RP FRIEDENSTEIN, AJ (reprint author), NIDR,BONE RES BRANCH,BLDG 30,ROOM 106,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 8 TC 43 Z9 46 U1 1 U2 4 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 1995 VL 56 SU 1 BP S17 EP S17 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QE653 UT WOS:A1995QE65300008 PM 7719975 ER PT J AU ROBEY, PG SHERMAN, S AF ROBEY, PG SHERMAN, S TI HUMAN MODELS OF SKELETAL AGING - INTRODUCTION SO CALCIFIED TISSUE INTERNATIONAL LA English DT Editorial Material C1 NIA,GERIATR PROGRAM,BETHESDA,MD 20892. RP ROBEY, PG (reprint author), NIDR,BONE RES BRANCH,BLDG 30,ROOM 106,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 0 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 1995 VL 56 SU 1 BP S2 EP S2 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QE653 UT WOS:A1995QE65300002 PM 25773026 ER PT J AU ROBEY, PG AF ROBEY, PG TI COLLAGENASE-TREATED TRABECULAR BONE FRAGMENTS - A REPRODUCIBLE SOURCE OF CELLS IN THE OSTEOBLASTIC LINEAGE SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article; Proceedings Paper CT NIA/NIDR Workshop on Human Models of Skeletal Aging CY MAR 01-02, 1994 CL WASHINGTON, DC SP NIA, NIDR ID INVITRO; HETEROGENEITY; PURIFICATION; EXPRESSION RP ROBEY, PG (reprint author), NIDR,BONE RES BRANCH,BETHESDA,MD 20014, USA. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 21 TC 20 Z9 20 U1 0 U2 5 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 1995 VL 56 SU 1 BP S11 EP S12 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QE653 UT WOS:A1995QE65300006 PM 7719973 ER PT J AU SHERMAN, S ROBEY, PG HADLEY, EC AF SHERMAN, S ROBEY, PG HADLEY, EC TI AGING AND THE HUMAN SKELETON - RECOMMENDATIONS FOR RESEARCH SO CALCIFIED TISSUE INTERNATIONAL LA English DT Editorial Material C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. RP SHERMAN, S (reprint author), NIA,GERIATR PROGRAM,7201 WISCONSIN AVE,BETHESDA,MD 20892, USA. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 0 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 1995 VL 56 SU 1 BP S3 EP S4 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QE653 UT WOS:A1995QE65300003 PM 7719982 ER PT J AU YOUNG, MF AF YOUNG, MF TI TRANSCRIPTION AND AGING OF HUMAN BONE TISSUE SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article; Proceedings Paper CT NIA/NIDR Workshop on Human Models of Skeletal Aging CY MAR 01-02, 1994 CL WASHINGTON, DC SP NIA, NIDR ID C-FOS; EXPRESSION; RECEPTORS; ESTROGEN; CELLS; MICE RP YOUNG, MF (reprint author), NIDR,BONE RES BRANCH,BETHESDA,MD 20892, USA. NR 11 TC 0 Z9 0 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 1995 VL 56 SU 1 BP S39 EP S40 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QE653 UT WOS:A1995QE65300017 PM 7719985 ER PT S AU SPEKSNIJDER, JE MCDOUGAL, A SARDET, C GUALTIERI, R JEFFERY, WR BERRIDGE, MJ WILLIAMS, RJP THOMAS, AP PUTNEY, JW AF SPEKSNIJDER, JE MCDOUGAL, A SARDET, C GUALTIERI, R JEFFERY, WR BERRIDGE, MJ WILLIAMS, RJP THOMAS, AP PUTNEY, JW BE Bock, GR Ackrill, K TI CALCIUM SIGNALING AND LOCALIZATION OF ENDOPLASMIC-RETICULUM IN ASCIDIAN EMBRYOS SO CALCIUM WAVES, GRADIENTS AND OSCILLATIONS SE CIBA FOUNDATION SYMPOSIA LA English DT Discussion CT Symposium on Calcium Waves, Gradients and Oscillations CY APR 26-28, 1994 CL CIBA FDN, LONDON, ENGLAND SP CIBA FDN HO CIBA FDN ID OOPLASMIC SEGREGATION; EGG; FERTILIZATION; POLARITY; WAVES C1 UNIV CAMBRIDGE,BABRAHAM INST,DEPT ZOOL,MOLEC SIGNALLING LAB,CAMBRIDGE CB2 3EJ,ENGLAND. UNIV OXFORD,INORGAN CHEM LAB,OXFORD OX1 3QR,ENGLAND. THOMAS JEFFERSON UNIV,DEPT PATHOL & CELL BIOL,PHILADELPHIA,PA 19107. NIEHS,CALCIUM REGULAT SECT,RES TRIANGLE PK,NC 27709. RP SPEKSNIJDER, JE (reprint author), UNIV GRONINGEN,CTR BIOL SCI,DEPT GENET,KERKLAAN 30,9751 NN HAREN,NETHERLANDS. NR 9 TC 1 Z9 1 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA BAFFINS LANE, CHICHESTER, ENGLAND PO19 7UD SN 0300-5208 BN 0-471-95234-6 J9 CIBA F SYMP PY 1995 VL 188 BP 141 EP 145 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA BD06E UT WOS:A1995BD06E00009 ER PT S AU CANNELL, M CHENG, H PUTNEY, JW JAFFE, LF PETERSEN, OH BERRIDGE, MJ THOMAS, AP AF CANNELL, M CHENG, H PUTNEY, JW JAFFE, LF PETERSEN, OH BERRIDGE, MJ THOMAS, AP BE Bock, GR Ackrill, K TI CALCIUM SPARKS IN CARDIAC-MUSCLE SO CALCIUM WAVES, GRADIENTS AND OSCILLATIONS SE CIBA FOUNDATION SYMPOSIA LA English DT Discussion CT Symposium on Calcium Waves, Gradients and Oscillations CY APR 26-28, 1994 CL CIBA FDN, LONDON, ENGLAND SP CIBA FDN HO CIBA FDN ID CONTRACTION C1 NIEHS, CALCIUM REGULAT SECT, RES TRIANGLE PK, NC 27709 USA. MARINE BIOL LAB, WOODS HOLE, MA 02543 USA. UNIV LIVERPOOL, PHYSIOL LAB, MRC, SECRETORY CONTROL RES GRP, LIVERPOOL L69 3BX, MERSEYSIDE, ENGLAND. UNIV CAMBRIDGE, BABRAHAM INST, DEPT ZOOL, MOLEC SIGNALLING LAB, CAMBRIDGE CB2 3EJ, ENGLAND. THOMAS JEFFERSON UNIV, DEPT PATHOL & CELL BIOL, PHILADELPHIA, PA 19107 USA. RP ST GEORGE HOSP, SCH MED, DEPT PHARMACOL & CLIN PHARMACOL, CRANMER TERRACE, LONDON SW17 0PE, ENGLAND. NR 7 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-95234-6 J9 CIBA F SYMP PY 1995 VL 188 BP 165 EP 174 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA BD06E UT WOS:A1995BD06E00011 ER PT J AU BROWNSON, RC LOY, TS INGRAM, E MYERS, JL ALAVANJA, MCR SHARP, DJ CHANG, JC AF BROWNSON, RC LOY, TS INGRAM, E MYERS, JL ALAVANJA, MCR SHARP, DJ CHANG, JC TI LUNG-CANCER IN NONSMOKING WOMEN - HISTOLOGY AND SURVIVAL PATTERNS SO CANCER LA English DT Article DE ACCURACY; HISTOLOGY; LUNG NEOPLASMS; NONSMOKERS; PATHOLOGY; WOMEN ID RISK-FACTORS; MISSOURI AB Background. Despite the widespread view that important clinical and etiologic differences exist between histologic categories of lung cancer, few studies have examined the accuracy of hospital-reported pathologic diagnoses of lung cancer. Methods. A review of pathologic material and an assessment of survival patterns were conducted in conjunction with a recently completed case-control study of lung cancer among nonsmoking women in Missouri. Using established protocols, tissue slides from tumors of 482 patients were reviewed by 3 pathologists. Results. Adenocarcinoma was the most common histologic type among former smokers and lifetime nonsmokers. The overall agreement rate between the original and review diagnoses was 65.6%. The positive predictive value ranged from 0.33 for bronchioalveolar carcinomas to 0.84 for adenocarcinomas. Agreement rates for small, medium, and large hospitals were 63.1, 66.6, and 66.2%, respectively. Survival rates were highest for bronchioalveolar carcinoma and lowest for small cell carcinoma. Conclusion. Given the importance of lung cancer to public health and the need to examine risk by histologic type, these data indicate that pathologic review of registry-reported lung cancer cases may be an important component of large scale studies of etiology. C1 MISSOURI DEPT HLTH,DIV CHRON DIS PREVENT & HLTH PROMOT,COLUMBIA,MO. UNIV MISSOURI,SCH MED,DEPT PATHOL,COLUMBIA,MO 65212. MAYO CLIN & MAYO FDN,DEPT LAB MED & PATHOL,ROCHESTER,MN 55905. NCI,EPIDEMIOL & BIOSTAT PROGRAM,ROCKVILLE,MD. CTR DIS CONTROL & PREVENT,EPIDEMIOL PROGRAM OFF,EPIDEM INTELLIGENCE SERV,ATLANTA,GA 30341. RP BROWNSON, RC (reprint author), ST LOUIS UNIV,SCH PUBL HLTH,3663 LINDELL BLVD,ST LOUIS,MO 63108, USA. FU NCI NIH HHS [N01-CP7-1096-02, N01-CP7-1096-01] NR 20 TC 52 Z9 52 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 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1995 VL 75 IS 1 BP 29 EP 33 DI 10.1002/1097-0142(19950101)75:1<29::AID-CNCR2820750107>3.0.CO;2-Q PG 5 WC Oncology SC Oncology GA QA657 UT WOS:A1995QA65700006 PM 7804973 ER PT J AU PERCY, C MUIR, C AF PERCY, C MUIR, C TI DEDICATION TO DR STEWART,HAROLD,L SO CANCER LA English DT Item About an Individual RP PERCY, C (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 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 1 PY 1995 VL 75 IS 1 SU S BP 139 EP 139 PG 1 WC Oncology SC Oncology GA QB791 UT WOS:A1995QB79100001 ER PT J AU PERCY, C YOUNG, JL MUIR, C RIES, L HANKEY, BF SOBIN, LH BERG, JW AF PERCY, C YOUNG, JL MUIR, C RIES, L HANKEY, BF SOBIN, LH BERG, JW TI HISTOLOGY OF CANCER INCIDENCE AND PROGNOSIS - SEER POPULATION-BASED DATA, 1973-1987 - INTRODUCTION SO CANCER LA English DT Editorial Material DE HISTOLOGY; SEER; INCIDENCE; PROGNOSIS AB This supplement presents the study of various histologic types of cancers diagnosed in the populations covered by the Surveillance, Epidemiology, and End Results (SEER) Program. It describes the SEER program and the coding of histologic type by the International Classification of Diseases for Oncology. Each of the 19 articles deals with the histologic types of cancer found in major sites or with specific histologic types, such as lymphomas or melanomas. Histologic types have been grouped based on those developed by Dr. John Berg. Data presented in this supplement are based on more than one million microscopically proven invasive cancers and 98,000 in situ cancers diagnosed during the period 1973-1987 in areas covered by the SEER Program. C1 CALIF DEPT HLTH SERV,CANC SURVEILLANCE SECT,SACRAMENTO,CA. SCOTTISH HLTH SERV,DIV INFORMAT & STAT,EDINBURGH,MIDLOTHIAN,SCOTLAND. ARMED FORCES INST PATHOL,DEPT HEPAT & GASTROINTESTINAL PATHOL,WASHINGTON,DC 20306. UNIV COLORADO,DEPT PATHOL & PREVENT MED,DENVER,CO 80202. RP PERCY, C (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC STAT BRANCH,EPN 343J,6130 EXECUT BLVD,MSC 7352,BETHESDA,MD 20892, USA. NR 25 TC 40 Z9 40 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1995 VL 75 IS 1 SU S BP 140 EP 146 DI 10.1002/1097-0142(19950101)75:1+<140::AID-CNCR2820751303>3.0.CO;2-H PG 7 WC Oncology SC Oncology GA QB791 UT WOS:A1995QB79100002 PM 8000992 ER PT J AU CARRIAGA, MT HENSON, DE AF CARRIAGA, MT HENSON, DE TI LIVER, GALLBLADDER, EXTRAHEPATIC BILE-DUCTS, AND PANCREAS SO CANCER LA English DT Review DE CANCER; BILE DUCTS; EPIDEMIOLOGY; GALLBLADDER; HISTOLOGIC TYPE; LIVER; PANCREAS; SEER; STAGING; SURVIVAL ID HEPATITIS-B VIRUS; UNDIFFERENTIATED EMBRYONAL SARCOMA; ACINAR CELL CYSTADENOCARCINOMA; CHRONIC ULCERATIVE-COLITIS; HEPATOCELLULAR-CARCINOMA; ADENOSQUAMOUS-CARCINOMA; EPITHELIOID HEMANGIOENDOTHELIOMA; PROGNOSTIC-SIGNIFICANCE; OPISTHORCHIS-VIVERRINI; PRECURSOR LESIONS AB Background. The liver, gallbladder, bile ducts, and pancreas have a common embryologic origin; cancers that arise from these sites therefore are expected to share a similar spectrum of histologic types. These cancers are known for their extremely poor prognoses. Methods. Data from the Surveillance, Epidemiology, and End Results Program regarding the incidence, distribution of histologic types, stage of disease, and survival for cancers of the gallbladder (n = 4412), extrahepatic bile ducts (n = 3486), pancreas (n = 23,116), and liver (n = 6,391) were reviewed. The most common histologic types are discussed, and the frequency of rare types is reported. Results. The incidence of biliary cancer decreased, while the incidence of hepatic and pancreatic cancer rose slightly over the 15-year period from 1973 to 1987. Age and sex distributions varied by histologic type. Greater than 98% of pancreatic and biliary cancers were carcinomas, and adenocarcinoma (not otherwise specified) was the most common histologic type recorded. In the liver, hepatocellular carcinoma was the most common type, followed by intrahepatic cholangiocarcinoma. The overall 5-year relative survival rates for these cancers were very low: gallbladder, 12.3%; extrahepatic bile duct, 12.7%; liver 3.1%; and pancreas 2.5% (all stages combined, 1978-1986). Conclusions. This review confirmed that these carcinomas are associated with a very poor outcome; however, survival was influenced by stage of disease and histologic type. In the gallbladder and extrahepatic bile ducts, papillary adenocarcinoma was associated with the best outcome of all histologic types, and in the exocrine pancreas, mucinous cystadenocarcinoma was associated with the best prognosis. C1 NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC. NR 144 TC 274 Z9 283 U1 0 U2 7 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1995 VL 75 IS 1 SU S BP 171 EP 190 DI 10.1002/1097-0142(19950101)75:1+<171::AID-CNCR2820751306>3.0.CO;2-2 PG 20 WC Oncology SC Oncology GA QB791 UT WOS:A1995QB79100005 PM 8000995 ER PT J AU TRAVIS, WD TRAVIS, LB DEVESA, SS AF TRAVIS, WD TRAVIS, LB DEVESA, SS TI LUNG-CANCER SO CANCER LA English DT Article DE SEER; LUNG CARCINOMA; SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; LARGE CELL CARCINOMA; SMALL CELL CARCINOMA; BRONCHIOLOALVEOLAR CARCINOMA; SURVIVAL; INCIDENCE; WORLD HEALTH ORGANIZATION CLASSIFICATION ID RAS ONCOGENE ACTIVATION; BRONCHOGENIC-CARCINOMA; UNITED-STATES; PATIENTS YOUNGER; PASSIVE SMOKING; CELL TYPE; TUMORS; SCAR; ADENOCARCINOMA; RADON AB Background. Lung cancer is the most common cause of cancer death in the United States, and its incidence has been rising for at least 50 years, Shifts in histologic type and differences in sex and race distribution have accompanied the increased incidence of lung malignancies. Methods. Population-based data regarding lung cancer reported to the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program for the 15-year period 1973-1987 were analyzed. Results. Results indicate that from 1973-1977 to 1983-1987, the age-adjusted rates of lung cancer increased by 30%, with the gain markedly greater in women (70%) than in men (17%). The largest percentage increases in age-adjusted rates were observed for small cell carcinoma and adenocarcinoma (approximately 60% each), with a more modest change for squamous cell carcinoma (+14%). For squamous cell carcinoma, the age-adjusted rates increased substantially for black (65%) and white (70%) women and only slightly for black men (10%), whereas it decreased slightly in recent years for white men. Conclusions. In recent years, adenocarcinoma has replaced squamous cell carcinoma as the most frequent histologic subtype for all sexes and races combined; These shifts in histologic types by sex and race may be related to differences in exposure to tobacco products, dietary factors, environmental or occupational carcinogens, and host characteristics. Increased use of transbronchial and needle biopsy may have also influenced these trends to some extent, Over the study period, 5-year relative survival rate did not change appreciably for lung cancer, suggesting that therapeutic advances have had little effect. C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. RP TRAVIS, WD (reprint author), ARMED FORCES INST PATHOL,DEPT PULM & MEDIASTINAL PATHOL,WASHINGTON,DC 20306, USA. NR 47 TC 500 Z9 521 U1 5 U2 28 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1995 VL 75 IS 1 SU S BP 191 EP 202 DI 10.1002/1097-0142(19950101)75:1+<191::AID-CNCR2820751307>3.0.CO;2-Y PG 12 WC Oncology SC Oncology GA QB791 UT WOS:A1995QB79100006 PM 8000996 ER PT J AU MEDEIROS, LJ GREINER, TC AF MEDEIROS, LJ GREINER, TC TI HODGKINS-DISEASE SO CANCER LA English DT Article DE HODGKINS DISEASE; SEER; 1973-1987; EPIDEMIOLOGY ID EPSTEIN-BARR-VIRUS; REED-STERNBERG CELLS; TUMOR-CELLS; ASSOCIATION; EXPRESSION; DIAGNOSIS; INFECTION; LYMPHOMA; PATTERNS; TISSUES AB Background. Over three time periods, 1973-1977, 1978-1982, and 1983-1987, the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute collected all cases of Hodgkin's disease in designated geographic regions representative of the United States as a whole. Methods. The authors reviewed the data pertaining to 9418 microscopically confirmed cases of Hodgkin's disease and focused on trends that emerged over the time intervals of this study. Results. Hodgkin's disease had a bimodal distribution of age-specific incidence rates with two peaks in the age groups of 15-34 years and older than 55 years. Since 1973, the incidence of Hodgkin's disease in the younger age group increased progressively as a result of a marked increase in the incidence of the nodular sclerosis subtype. From the period 1973-1977 to 1983-1987, the age-adjusted incidence rate of nodular sclerosis rose from 1.1 to 1.6 per 100,000. In 1983-1987, nodular sclerosis represented 57.7% of Hodgkin's disease and occurred most often in whites, with an equal sex ratio. In females, this increase in incidence over time was most dramatic in young adult women. The overall incidence of the mixed cellularity subtype, 23.4% of Hodgkin's disease, remained stable although the age-specific incidence rate increased progressively in black males older than age 40 years. The incidence of the lymphocytic predominance subtype, 6.0% of Hodgkin's disease, remained stable over time, with a slight increase in adults older than age 50 years. The lymphocytic depletion subtype, 3.8% of Hodgkin's disease, occurred predominantly in the elderly; its incidence decreased, most likely the result of changes in diagnostic criteria, with many cases being reclassified as non-Hodgkin's lymphoma (NHL). Similarly, unclassifiable cases of Hodgkin's disease designated as miscellaneous, 9.1% of Hodgkin's disease, decreased over time, probably the result of improved classification. Nevertheless, a subset of cases of Hodgkin's disease remained difficult to subclassify. The human immunodeficiency virus (HIV) epidemic appears to be associated with an increased incidence of Hodgkin's disease in San Francisco County in adult males age 30-49 years, a population known to have a high prevalence of HIV infection. Conclusion. The SEER data suggest that Hodgkin's disease is a heterogeneous entity composed of at least two different diseases-nodular sclerosis and mixed cellularity. Over the time course of this study, the incidence of nodular sclerosis increased dramatically, particularly in adolescents and young adults, whereas mixed cellularity remained stable. The incidence of Hodgkin's disease in the elderly decreased, most likely the result of our improved ability to diagnose both Hodgkin's disease and NHL and the realization that many cases of NHL had been misclassified as Hodgkin's disease. This decrease in Hodgkin's disease occurred predominantly in the lymphocytic depletion and miscellaneous groups. C1 BROWN UNIV, SCH MED, PROVIDENCE, RI 02912 USA. NCI, PATHOL LAB, HEMATOPATHOL SECT, BETHESDA, MD 20892 USA. RP RHODE ISL HOSP, DEPT PATHOL, 593 EDDY ST, PROVIDENCE, RI 02903 USA. NR 39 TC 68 Z9 68 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0008-543X EI 1097-0142 J9 CANCER-AM CANCER SOC JI Cancer PD JAN 1 PY 1995 VL 75 IS 1 SU S BP 357 EP 369 DI 10.1002/1097-0142(19950101)75:1+<357::AID-CNCR2820751318>3.0.CO;2-A PG 13 WC Oncology SC Oncology GA QB791 UT WOS:A1995QB79100017 PM 8001007 ER PT J AU GREINER, TC MEDEIROS, LJ JAFFE, ES AF GREINER, TC MEDEIROS, LJ JAFFE, ES TI NON-HODGKINS-LYMPHOMA SO CANCER LA English DT Article DE LYMPHOMA; NON-HODGKINS; INCIDENCE; EPIDEMIOLOGY; ACQUIRED IMMUNODEFICIENCY SYNDROME ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; B-CELL LYMPHOMA; PRIMARY GASTRIC LYMPHOMA; INCREASING INCIDENCE; MALIGNANT-LYMPHOMAS; HOMOSEXUAL MEN; RISK; TISSUE; EPIDEMIOLOGY; LESIONS AB Background. Significant advances in the understanding of non-Hodgkin's lymphoma (NHL) have occurred in the past two decades, resulting in changes in terminology and classification practices, which may affect the analysis of the Surveillance, Epidemiology, and End Results (SEER) data. Methods. The incidence rates for each subgroup of NHL in the Working Formulation were reviewed from the National Cancer Institute's SEER data during three time periods: 1973-1977, 1978-1982, and 1983-1987. Results. NHL has significantly increased by 50% from 1973 to 1988. The most frequently occurring NHL is diffuse large cell lymphoma, constituting nearly 30% of all lymphomas. Increased incidence rates for large cell immunoblastic and small noncleaved cell NHL observed during the 1980s are attributable largely to the acquired immunodeficiency syndrome epidemic. Exposure to environmental agents such as herbicides and hair coloring dyes have recently been identified as factors that increase the risk of NHL, but the overall contribution of these factors remains to be identified. The increase in extranodal lymphomas is in part a consequence of the application of modern immunophenotypic and genotypic methods, which lead to the reclassification of pseudolymphomas as monoclonal B-cell neoplasms. The apparent dramatic decline in the incidence of diffuse small cleaved NHL appears to be artifactual, as well, secondary to changes in classification of NHL. Conclusions. With the enhanced ability of pathologists to delineate new clinicopathologic entities by immunophenotypic and molecular biologic studies, future modifications to the collection of SEER data may be appropriate, Such an approach will address the limitations of the Working Formulation and lead to a more accurate data base for the evaluation of epidemiologic trends. C1 BROWN UNIV,RHODE ISL HOSP,SCH MED,DEPT PATHOL,PROVIDENCE,RI 02903. RP GREINER, TC (reprint author), NCI,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892, USA. NR 51 TC 91 Z9 95 U1 3 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1995 VL 75 IS 1 SU S BP 370 EP 380 DI 10.1002/1097-0142(19950101)75:1+<370::AID-CNCR2820751319>3.0.CO;2-Q PG 11 WC Oncology SC Oncology GA QB791 UT WOS:A1995QB79100018 PM 8001008 ER PT J AU MILLER, RW YOUNG, JL NOVAKOVIC, B AF MILLER, RW YOUNG, JL NOVAKOVIC, B TI CHILDHOOD-CANCER SO CANCER LA English DT Article DE INCIDENCE; CHILDHOOD; CANCER; HISTOLOGY; SURVEILLANCE, EPIDEMIOLOGY, AND END RESULTS ID LEUKEMIA AB Background. Cancers of individual organs generally are composed of various histologic types, each with its own frequency and demographic patterns. For childhood cancers in particular, a classification of cancers by histologic type is important for understanding the etiology and progression of the disease. Methods. Data from the Surveillance, Epidemiology, and End Results (SEER) Program on 9308 microscopically confirmed malignant neoplasms in children younger than age 15, newly diagnosed during 1973-1987, were made available for analysis. Tumors were grouped histologically according to a classification previously utilized in an international volume of childhood cancer incidence. Results. The most frequent histologic types were acute lymphocytic leukemia (23.6%), astrocytoma (9.6%), neuroblastoma (6.6%), and Wilms' tumor (6.4%). Acute lymphocytic leukemia accounted for 75% of childhood leukemia, The most common form of Hodgkin's disease was the nodular sclerosing subtype, which was diagnosed in 56% of all cases. Burkitt's and Burkitt-like disease accounted for approximately one third of non-Hodgkin's lymphoma, the sex ratio (male to female) being unusually high (5.7). Among the brain tumors, glioma was of interest because 198 cases (excluded from this analysis) were diagnosed without histologic confirmation-due, no doubt, to their inaccessibility for biopsy because they were located in the brain stem. The most common histologic type of soft tissue sarcoma was rhabdomyosarcoma, which accounted for 51% of the total, more than half of which were of the embryonal type. To the authors' knowledge, this report offers for the first time the relative frequencies of rare types of leukemias, such as megakaryoblastic leukemia, in childhood. This report also includes the frequencies of 21 rarer forms of soft tissue sarcoma. Five forms of childhood cancer had a B-year relative survival rate of 85% or better, Of the cancers with the poorest outcome, three had relative survival rates of 46.5-49%; the relative survival rate for acute myelogenous leukemia was only 26.4%. The trends in survival over time for 21 types of childhood cancer also are included in this report. Conclusions. Further refinements in classification now are available through laboratory techniques utilizing molecular biology, immunology, and cytogenetics, which are of importance in etiologic studies, diagnosis, treatment, and prognosis. It would be important in the future for cancer registries to record the results of relevant laboratory tests for further analysis by subtype. C1 NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. CALIF DEPT HLTH SERV,CANC SURVEILLANCE SECT,SACRAMENTO,CA. RP MILLER, RW (reprint author), NCI,CLIN EPIDEMIOL BRANCH,EPN-400,BETHESDA,MD 20892, USA. NR 29 TC 274 Z9 289 U1 0 U2 8 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1995 VL 75 IS 1 SU S BP 395 EP 405 DI 10.1002/1097-0142(19950101)75:1+<395::AID-CNCR2820751321>3.0.CO;2-W PG 11 WC Oncology SC Oncology GA QB791 UT WOS:A1995QB79100020 PM 8001010 ER PT J AU CARRIAGA, MT HENSON, DE AF CARRIAGA, MT HENSON, DE TI THE HISTOLOGIC GRADING OF CANCER SO CANCER LA English DT Review DE CANCER; EPIDEMIOLOGY; GRADING; HISTOLOGIC GRADE; HISTOLOGIC TYPE; SEER; STAGING; SURVIVAL ID SOFT-TISSUE SARCOMAS; INVASIVE BREAST-CANCER; EPITHELIAL OVARIAN-CARCINOMA; SUPERFICIAL BLADDER-CANCER; SURGICAL ADJUVANT BREAST; SQUAMOUS-CELL CARCINOMA; LONG-TERM SURVIVAL; PROGNOSTIC FACTORS; ENDOMETRIAL CANCER; MULTIVARIATE-ANALYSIS AB Background. The histologic grade of a tumor provides prognostic information in addition to that provided by stage of disease. Poorly differentiated tumors are known to pursue a more aggressive course than their well differentiated counterparts. Methods. The frequency of grading and the relationship of grade to outcome was investigated for 793,649 cases of cancer from 15 anatomic sites as recorded in the Surveillance, Epidemiology, and End Results Program. Results. For all cancers, the frequency of grading increased from 1973 to 1987 and varied by anatomic site and histologic type. Survival decreased with advancing grade, and within each stage, grading separated cases into at least three distinct prognostic subgroups. For some cancers, regional stage cases assigned Grade 1 or 2 had higher survival rates than did localized stage cases assigned Grade 3 or 4. Therefore, grading allowed the identification of high and low risk subgroups within each stage grouping. Conclusions. The tumor grade was a strong prognostic indicator for cancers of the urinary bladder, endometrium, and prostate-sites most often graded by pathologists, The histologic grade was also an important determinant of outcome for cancers of the brain, soft tissue, and breast; however, only a small percentage of these tumors were graded. The results are important because no common criteria for grading were established among the many contributing pathologists. Therefore, observer variation did not alter the known relationship of histologic grade to outcome. This review demonstrates that the histologic grade is a strong predictor of outcome that refines the prognostic information provided by the stage of disease. C1 NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT PATHOL,WASHINGTON,DC. NR 123 TC 60 Z9 60 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 1 PY 1995 VL 75 IS 1 SU S BP 406 EP 421 DI 10.1002/1097-0142(19950101)75:1+<406::AID-CNCR2820751322>3.0.CO;2-W PG 16 WC Oncology SC Oncology GA QB791 UT WOS:A1995QB79100021 PM 8001011 ER PT J AU Janz, S Shacter, E AF Janz, S Shacter, E TI Disposition of the plasmacytomagenic alkane pristane (2,6,10,14-tetramethylpentadecane) in mice SO CANCER BIOCHEMISTRY BIOPHYSICS LA English DT Article DE alkanes; pristane; disposition; metabolism; mouse; plasmacytoma ID CELLS; RAT; LYMPHOCYTES; FLUIDITY; BILAYERS; DNA AB The intraperitoneal administration of pristane (2,6,10,14-tetramethylpentadecane) induces peritoneal plasmacytomas in genetically susceptible BALB/c mice. The purpose of this study was to estimate the disposition of an amount of intraperitoneally injected pristane that would conventionally be used in a tumor induction protocol. The distribution of H-3-labeled pristane in various tissues was monitored by liquid scintillation counting at different times after injection. The data show that pristane is present in the blood and detectable in all tested tissues during an observation period of one to 64 days. The levels of pristane fluctuate in some tissues such as lymph node and bone marrow but show a clear tendency to accumulate in others such as liver, spleen and kidney. Evidence is also presented for the in vivo metabolism of pristane based on the observed urinary excretion of tritium and on the high levels of radioactivity in the gall bladder fluid. It is concluded that intraperitoneally administered pristane is distributed throughout the mouse and is stored in tissues in sufficient amounts to allow interactions with the cells residing there. C1 US FDA,CTR BIOL EVALUAT & RES,IMMUNOL LAB,BETHESDA,MD 20892. RP Janz, S (reprint author), NCI,GENET LAB,BLDG 37,ROOM 2B09,BETHESDA,MD 20892, USA. NR 23 TC 5 Z9 5 U1 0 U2 0 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0305-7232 J9 CANCER BIOCHEM BIOPH JI Cancer Biochem. Biophys. PY 1995 VL 15 IS 1 BP 25 EP 34 PG 10 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA TM193 UT WOS:A1995TM19300004 PM 8536217 ER PT J AU DORGAN, JF REICHMAN, ME JUDD, JT BROWN, C LONGCOPE, C SCHATZKIN, A ALBANES, D CAMPBELL, WS FRANZ, C KAHLE, L TAYLOR, PR AF DORGAN, JF REICHMAN, ME JUDD, JT BROWN, C LONGCOPE, C SCHATZKIN, A ALBANES, D CAMPBELL, WS FRANZ, C KAHLE, L TAYLOR, PR TI THE RELATION OF BODY-SIZE TO PLASMA-LEVELS OF ESTROGENS AND ANDROGENS IN PREMENOPAUSAL WOMEN (MARYLAND, UNITED-STATES) SO CANCER CAUSES & CONTROL LA English DT Article DE ANDROGENS; ESTROGENS; HEIGHT; WEIGHT; UNITED-STATES ID BREAST-CANCER RISK; SEX-HORMONES; FAT DISTRIBUTION; POSTMENOPAUSAL WOMEN; FREE TESTOSTERONE; OBESE WOMEN; HEIGHT; WEIGHT; AGE; MASS AB We analyzed data from a cross-sectional study of 107 premenopausal women to evaluated the relations of height, weight, and body mass index (BMI) with plasma hormone levels. Participants were 20- to 40-year old women residing in Maryland (United States), whose reported menstrual cycle lengths were not more than 35 days and whose measured weights for height were 85 to 130 percent of 'desirable' based on 1983 Metropolitan Life Insurance tables. Fasting blood specimens were collected on each of days 5-7, 12-15, and 21-23 of every participant's menstrual cycle and pooled to create follicular, midcycle, and luteal phase samples, respectively, for analysis. Adjusted for age, taller women had significantly higher follicular-phase plasma-estradiol levels (percent difference/cm = 1.5, 95 percent confidence interval [CI] = 0.3-2.7, and heavier women had significantly lower plasma sex-hormone binding globulin (SHBG) levels averaged across the menstrual cycle phases (percent difference/kg = -1.2; CI = -1.9-0.6). Body weight within the range studied, however, was not related significantly to the concentration of SHBG-bound estradiol during any phase of the menstrual cycle. The results of this cross-sectional study suggest a possible mechanism by which height may influence breast cancer risk. C1 USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,BELTSVILLE,MD 20705. INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. UNIV MASSACHUSETTS,SCH MED,DEPT OBSTET & GYNECOL,WORCESTER,MA 01605. UNIV MASSACHUSETTS,SCH MED,DEPT MED,WORCESTER,MA 01605. RP DORGAN, JF (reprint author), NCI,DIV CANC PREVENT & CONTROL,EXECUT PLAZA N,ROOM 211,BETHESDA,MD 20892, USA. RI Perez , Claudio Alejandro/F-8310-2010; Albanes, Demetrius/B-9749-2015 OI Perez , Claudio Alejandro/0000-0001-9688-184X; NR 40 TC 43 Z9 44 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD JAN PY 1995 VL 6 IS 1 BP 3 EP 8 DI 10.1007/BF00051674 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA QK412 UT WOS:A1995QK41200001 PM 7718732 ER PT S AU Parkinson, DR Pluda, JM Cazenave, L Liu, JM Ho, P Sorensen, JM Christian, MC Sznol, M AF Parkinson, DR Pluda, JM Cazenave, L Liu, JM Ho, P Sorensen, JM Christian, MC Sznol, M BE Kimura, K Ota, K Yamada, K Saito, H Ogawa, M TI Investigational anti-cancer agents under development in the United States by the National Cancer Institute SO CANCER CHEMOTHERAPY: CHALLENGES FOR THE FUTURE, VOL 10 SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 10th Nagoya International Symposium on Cancer Treatment - Challenges for Today and New Targets for Tomorrow CY SEP 16-17, 1994 CL NAGOYA, JAPAN RP Parkinson, DR (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,INVEST DRUG BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-82320-4 J9 INT CONGR SER PY 1995 VL 1110 BP 278 EP 293 PG 16 WC Oncology SC Oncology GA BG91L UT WOS:A1995BG91L00022 ER PT J AU JOHNSON, ES OVERBY, L PHILPOT, R AF JOHNSON, ES OVERBY, L PHILPOT, R TI DETECTION OF ANTIBODIES TO AVIAN LEUKOSIS/SARCOMA VIRUSES AND RETICULOENDOTHELIOSIS VIRUSES IN HUMANS BY WESTERN-BLOT ASSAY SO CANCER DETECTION AND PREVENTION LA English DT Article DE SEROLOGY; POULTRY ONCOGENIC VIRUSES; RETROVIRUSES AB Serologic evidence of antibodies in humans to avian leukosis/sarcoma viruses (ALSV) and reticuloendotheliosis viruses (REV) has in general been negative. Because of the difficulty in infecting mammalian cells in vitro with these viruses, it is generally held that they do not infect humans. We first provided presumptive evidence of serologic response to these viruses in human sera of workers in poultry slaughtering plants, using an ELISA. We now provide confirmatory evidence using Western blot assay. Our results show that exposed poultry workers and subjects with no occupational exposure to these viruses have antibodies in their sera specifically directed against ALSV p27, p19, p15, and p12 antigens. In addition, we demonstrate evidence of serologic response to REV. This is the first time definitive evidence of exposure to ALSV or REV has been demonstrated in human sera. The significance of this is not known. Further investigation into whether these findings mean that virus has been integrated into the human genome is needed, to assess the public health implications of these results. C1 NIEHS,EPIDEMIOL BRANCH,ENVIRONM & MOLEC EPIDEMIOL SECT,RES TRIANGLE PK,NC 27709. NR 0 TC 23 Z9 27 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 1995 VL 19 IS 6 BP 472 EP 486 PG 15 WC Oncology SC Oncology GA TG504 UT WOS:A1995TG50400002 PM 8925516 ER PT J AU BENNETT, WP AF BENNETT, WP TI P53 ALTERATIONS IN PROGENITOR LESIONS OF THE BRONCHUS, ESOPHAGUS, ORAL CAVITY, AND COLON SO CANCER DETECTION AND PREVENTION LA English DT Review DE TUMOR SUPPRESSOR; MULTISTAGE CARCINOGENESIS; IMMUNOHISTOCHEMISTRY; EARLY DIAGNOSIS AB Human cancers are believed to develop in multiple stages. There is morphologic evidence for this in many tissues, including cancers of the lung, esophagus, head and neck, skin, colon, cervix, and bladder; and corresponding genetic models are developing. This article summarizes reports describing the timing and frequency of p53 alterations (i.e., mutation and/or protein accumulation) in progenitor lesions of human lung, esophagus (both squamous and Barrett's), head and neck, and colon. In squamous lesions of the lung, esophagus, and head and neck, there is evidence for p53 alteration in a minority of the earliest dysplasias and in a majority of the late or severe dysplasias. It is not known whether all of the alterations are caused by mutations or by epigenetic factors. In sporadic colonic adenomas, there is also evidence for p53 protein accumulation in early adenomas, but it is clear that p53 mutations occur mostly in the stage of late adenoma or carcinoma. The causes of the protein accumulation in the earlier stages are not clear. Strategies for early diagnosis based on detecting p53 mutations in body fluids including sputum, urine, and stool have been published (Sidransky D. J. Natl Cancer Inst 1994; 86:995-956).(1) Although substantial technical hurdles remain, the high frequency and early occurrence of these mutations make the p53 tumor suppressor gene an attractive target for early detection and early therapeutic intervention in many common human cancers. RP BENNETT, WP (reprint author), NCI,HUMAN CARCINOGENESIS LAB,BLDG 37,ROOM 2C25,37 CONVENT DR,MSC 4255,BETHESDA,MD 20892, USA. NR 0 TC 17 Z9 17 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 1995 VL 19 IS 6 BP 503 EP 511 PG 9 WC Oncology SC Oncology GA TG504 UT WOS:A1995TG50400005 PM 8925519 ER PT J AU KELLOFF, GJ JOHNSON, JR CROWELL, JA BOONE, CW DEGEORGE, JJ STEELE, VE MEHTA, MU TEMECK, JW SCHMIDT, WJ BURKE, G GREENWALD, P TEMPLE, RJ AF KELLOFF, GJ JOHNSON, JR CROWELL, JA BOONE, CW DEGEORGE, JJ STEELE, VE MEHTA, MU TEMECK, JW SCHMIDT, WJ BURKE, G GREENWALD, P TEMPLE, RJ TI APPROACHES TO THE DEVELOPMENT AND MARKETING APPROVAL OF DRUGS THAT PREVENT CANCER SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Review ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ORNITHINE DECARBOXYLASE INDUCTION; PANCREATIC DUCTAL ADENOCARCINOMAS; POTENTIAL CHEMOPREVENTIVE AGENT; PROLIFERATIVE BREAST DISEASE; TRACHEAL EPITHELIAL-CELLS; MOUSE SKIN PAPILLOMAS; I CLINICAL-TRIALS; SERUM VITAMIN-E; COLON-CANCER AB The broad concept of chemoprevention applies to the prevention of clinical cancer by the administration of chemical agents. Current approaches to the development and marketing approval of drugs to prevent cancer are described by a Working Group from the National Cancer Institute and the Food and Drug Administration. A strategy is presented that identifies candidate drugs, with examples that illustrate how drugs are characterized for efficacy through in vitro transformation modulation and mechanistic assays, and in vivo tumor modulation models of carcinogenesis. Requirements and recommendations for safety evaluation in toxicology testing are given, and the evaluation of pharmacokinetic and pharmacodynamic drug effects and potential surrogate end point biomarkers in Phase I trials are discussed. Appropriate subject populations are identified. Phase II trials should emphasize the evaluation of surrogate end point biomarkers that are highly correlated with cancer incidence and may serve as an estimate of cancer incidence reduction. In Phase III trials the interim analysis of a validated surrogate end point of cancer incidence may facilitate timely and cost-effective marketing of efficacious drugs. C1 NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. FDA,CTR DRUG EVALUAT & RES,ROCKVILLE,MD 20857. NR 114 TC 100 Z9 103 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1995 VL 4 IS 1 BP 1 EP 10 PG 10 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA QA971 UT WOS:A1995QA97100001 PM 7894318 ER PT J AU HARTGE, P HOLLY, EA HALPERN, A SAGEBIEL, R GUERRY, D ELDER, D CLARK, W HANSON, L HARRISON, C TARONE, R TUCKER, MA AF HARTGE, P HOLLY, EA HALPERN, A SAGEBIEL, R GUERRY, D ELDER, D CLARK, W HANSON, L HARRISON, C TARONE, R TUCKER, MA TI RECOGNITION AND CLASSIFICATION OF CLINICALLY DYSPLASTIC NEVI FROM PHOTOGRAPHS - A STUDY OF INTEROBSERVER VARIATION SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID MALIGNANT-MELANOMA; RISK-FACTOR; DIAGNOSES AB The recognition of dysplastic nevi from photographs can aid in population surveys of nevi and in epidemiological studies of melanoma risk. The reproducibility of techniques for recognizing nevi as dysplastic or for scoring them according to the degree of dysplasia has not been measured. Using photographs of 300 nevi taken in the course of a case-control study of melanoma, we assessed the agreement among six clinicians in independently categorizing nevi as dysplastic and in grading the degree of dysplasia. On average, reviewers agreed with each other 77% of the time in classifying a nevus as dysplastic or normal. Pairwise agreement within one point on a six-point scale occurred 87% of the time on average. These results suggest that criteria for recognizing nevi as clinically dysplastic from photographs can be applied reproducibly. C1 NCI,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,MED CTR,SAN FRANCISCO,CA 94143. UNIV PENN,PHILADELPHIA,PA 19104. WESTAT CORP,ROCKVILLE,MD 20850. RI Tucker, Margaret/B-4297-2015 NR 13 TC 19 Z9 19 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1995 VL 4 IS 1 BP 37 EP 40 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA QA971 UT WOS:A1995QA97100005 PM 7894322 ER PT J AU SHAW, GL FALK, RT DESLAURIERS, J FRAME, JN NESBITT, JC PASS, HI ISSAQ, HJ HOOVER, RN TUCKER, MA AF SHAW, GL FALK, RT DESLAURIERS, J FRAME, JN NESBITT, JC PASS, HI ISSAQ, HJ HOOVER, RN TUCKER, MA TI DEBRISOQUINE METABOLISM AND LUNG-CANCER RISK SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; GENETIC-POLYMORPHISM; OXIDATION; HYDROXYLATION; SUSCEPTIBILITY; POPULATION; PHENOTYPES; HUMANS; FAMILY; URINE AB Previous reports of the association between the debrisoquine metabolic polymorphism and lung cancer risk have been conflicting. We examined the hypothesis that the genetically determined ability to metabolize debrisoquine identifies individuals at increased risk for lung cancer in a study designed to address some of the methodological criticisms of previous studies. A case-control study of 335 incident Caucasian lung cancer patients and 373 controls matched for age, race, sex, and hospital, was conducted at the National Naval Medical Center (Bethesda, MD) and at the Laval Hospital (Sainte-Foy, Quebec, Canada). Debrisoquine metabolic phenotype was determined by debrisoquine administration and analysis of debrisoquine and 4-hydroxydebrisoquine in the subsequent 8-h urine collected. Stratified and logistic regression analyses were used to evaluate the association between extensive or intermediate debrisoquine metabolism and lung cancer risk. We found no increased risk among extensive or intermediate metabolizers (odds ratio, 0.6; 95% confidence interval, 0.3-1.2). The lack of an association was not confounded by control diagnoses, medications used within 1 month of debrisoquine administration, smoking, stage, or histology of lung cancer. No relationship was found among either heavy smokers or light and nonsmokers. Our results do not support the role of debrisoquine metabolism as a marker for lung cancer risk. While the concept that polymorphisms of metabolism may account for differential susceptibility to lung cancer is sound, debrisoquine metabolic phenotype was not associated with lung cancer risk in these data. C1 NCI, BETHESDA, MD 20892 USA. LAVAL HOSP, ST FOY, PQ, CANADA. NATL NAVAL MED CTR, BETHESDA, MD 20814 USA. DYNCORP, PROGRAM RESOURCES INC, NATL CANC INST, FREDERICK CANC RES & DEV CTR, FREDERICK, MD 21702 USA. RI Tucker, Margaret/B-4297-2015 FU NCI NIH HHS [N01-CP1-5672, N01-CPO-5684] NR 34 TC 24 Z9 25 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1995 VL 4 IS 1 BP 41 EP 48 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA QA971 UT WOS:A1995QA97100006 PM 7894323 ER PT J AU DEBENEDETTI, VMG WELSH, JA TRIVERS, GE HARPSTER, A PARKINSON, AJ LANIER, AP MCMAHON, BJ BENNETT, WP AF DEBENEDETTI, VMG WELSH, JA TRIVERS, GE HARPSTER, A PARKINSON, AJ LANIER, AP MCMAHON, BJ BENNETT, WP TI P53 IS NOT MUTATED IN HEPATOCELLULAR CARCINOMAS FROM ALASKA NATIVES SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Note ID LIVER-CANCER; CELL-LINES; GENE; MUTATIONS; POLYMORPHISM; FREQUENCY AB Hepatocellular carcinoma is common among Alaska Natives. The known risk factor in this population is hepatitis B viral infection; fungal toxins, including aflatoxin B1, have not been detected in foodstuffs. In this series of 14 patients (including 4 siblings and 2 second cousins), 3 patients were less than 12 years old at diagnosis of hepatocellular carcinoma, 8 patients were 13-24 years old, and 3 patients were more than 60 years old. Since p53 mutations occur in 29% of hepatocellular carcinomas worldwide, we tested the tumors for p53 mutations and serum samples for anti-p53 antibodies. Serum samples from these 14 patients did not contain detectable levels of anti-p53 antibodies. Loss of heterozygosity within the p53 locus was not detected in any of 9 informative cases. Immunohistochemical analysis for p53 protein accumulation was negative in all of 11 tumors. DNA sequence analysis of 12 tumor samples showed no evidence of p53 mutation in the highly conserved regions included in exons 5-8. These data, combined with one case from a previous report, indicate a mutation frequency of 0 of 13, which differs significantly from the worldwide frequency of 29% (CHI2 3.9; P = 0.048). These results indicate that liver carcinogenesis among Alaska Natives occurs independently of a traditional p53 pathway. The familial clustering and early onset in this population strongly suggest an inherited genetic predisposition to develop liver cancer. Germline mutations in a tumor suppressor or a cancer susceptibility gene are likely. Future studies of these samples should include investigations of candidate suppressor or susceptibility genes which map to chromosomal regions commonly deleted in liver cancers. C1 NCI,HUMAN CARCINOGENESIS LAB,BLDG 37,ROOM 2C25,37 CONVENT DR,MSC 4255,BETHESDA,MD 20892. NATL CTR INFECT DIS,ARCT INVEST PROGRAM,ANCHORAGE,AK 99510. ALASKA AREA NATIVE HLTH SERV,ANCHORAGE,AK 99510. NR 30 TC 25 Z9 27 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 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN-FEB PY 1995 VL 4 IS 1 BP 79 EP 82 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA QA971 UT WOS:A1995QA97100011 PM 7894327 ER PT J AU DADMARZ, R SGAGIAS, MK ROSENBERG, SA SCHWARTZENTRUBER, DJ AF DADMARZ, R SGAGIAS, MK ROSENBERG, SA SCHWARTZENTRUBER, DJ TI CD4(+) T-LYMPHOCYTES INFILTRATING HUMAN BREAST-CANCER RECOGNIZE AUTOLOGOUS TUMOR IN AN MHC-CLASS-II RESTRICTED FASHION SO CANCER IMMUNOLOGY IMMUNOTHERAPY LA English DT Article DE BREAST CANCER; CD4(+); T CELLS; MHC CLASS-II RESTRICTION; CYTOKINE SECRETION ID COLONY-STIMULATING FACTOR; NECROSIS-FACTOR-ALPHA; B-CELL LINES; CYTOKINE SECRETION; BLOOD-LYMPHOCYTES; MALIGNANT BREAST; HLA ANTIGENS; MELANOMAS; EXPANSION; TISSUE AB Tumor-infiltrating lymphocytes (TIL) were derived from primary breast tumors, metastatic lymph nodes and malignant pleural effusions from 34 patients with breast cancer. TIL were cultured for approximately 30 days and studied for phenotype, cytotoxicity, and the ability to secrete cytokines in response to autologous tumor stimulation. Tumor specimens were obtained from two different sites in 7 patients, resulting in 41 samples from which 38 TIL cultures were established. In addition to screening 38 bulk TIL cultures, TIL from 21 patients were separated into CD4(+) and CD8(+) subsets and extensively studied. Three CD4(+) TIL were found specifically to secrete granulocyte macrophage-colony-stimulating factor and tumor necrosis factor a when stimulated by autologous tumor and not by a large panel of stimulators (24-34) consisting of autologous normal cells, allogeneic breast or melanoma tumors and EBV-B cells. This cytokine release was found to be MHC-class-II-restricted, as it was inhibited by the anti-HLA-DR antibody L243. These 3 patients' EBV-B cells, when pulsed with tumor lysates, were unable to act as antigen-presenting cells and induce cytokine secretion by their respective CD4(+) TIL. These findings demonstrate that MHC-class-II-restricted CD4(+) T cells recognising tumor-associated antigens can be detected in some breast cancer patients. RP DADMARZ, R (reprint author), NCI,SURG BRANCH,BLDG 10,ROOM 2B04,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 31 TC 44 Z9 46 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-7004 J9 CANCER IMMUNOL IMMUN JI Cancer Immunol. Immunother. PD JAN PY 1995 VL 40 IS 1 BP 1 EP 9 PG 9 WC Oncology; Immunology SC Oncology; Immunology GA QD304 UT WOS:A1995QD30400001 PM 7828162 ER PT J AU TOLCHER, AW GIUSTI, RM OSHAUGHNESSY, JA COWAN, KH AF TOLCHER, AW GIUSTI, RM OSHAUGHNESSY, JA COWAN, KH TI ARTERIAL THROMBOSIS ASSOCIATED WITH GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR (GM-CSF) ADMINISTRATION IN BREAST-CANCER PATIENTS TREATED WITH DOSE-INTENSIVE CHEMOTHERAPY - A REPORT OF 2 CASES SO CANCER INVESTIGATION LA English DT Note ID TUMOR-NECROSIS-FACTOR; PATENT FORAMEN OVALE; ENDOTHELIAL-CELLS; ACTIVATION; MYELOSUPPRESSION; DOXORUBICIN; VINBLASTINE; COAGULATION; TOXICITY; THERAPY AB The occurrence of arterial thrombosis reported in other breast cancer series has largely been confined to the upper extremities, ipsilateral to a previous mastectomy site and clinically manifest as cerebral vascular accidents. This case report describes 2 patients who experienced iliac artery thrombosis temporally related to receiving granulocyte-macrophage colony-stimulating factor (GM-CSF) and dose-intensive chemotherapy for metastatic breast cancer. A review of the literature concerning arterial thrombosis as relevant to breast cancer treatment and GM-CSF is included. C1 NCI,DIV CANC TREATMENT,MED BRANCH,MED BREAST CANC SECT,BETHESDA,MD 20892. NR 31 TC 18 Z9 18 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1995 VL 13 IS 2 BP 188 EP 192 DI 10.3109/07357909509011689 PG 5 WC Oncology SC Oncology GA QM826 UT WOS:A1995QM82600008 PM 7874573 ER PT J AU GUADAGNI, F ROSELLI, M COSIMELLI, M FERRONI, P SPILA, A CAVALIERE, F CASALDI, V WAPPNER, G ABBOLITO, MR GREINER, JW SCHLOM, J AF GUADAGNI, F ROSELLI, M COSIMELLI, M FERRONI, P SPILA, A CAVALIERE, F CASALDI, V WAPPNER, G ABBOLITO, MR GREINER, JW SCHLOM, J TI CA-72-4 SERUM MARKER - A NEW TOOL IN THE MANAGEMENT OF CARCINOMA PATIENTS SO CANCER INVESTIGATION LA English DT Review ID MONOCLONAL-ANTIBODY B72.3; TUMOR-ASSOCIATED ANTIGEN; CARCINOEMBRYONIC ANTIGEN; OVARIAN-CANCER; COLORECTAL-CANCER; GASTROINTESTINAL CARCINOMA; CA-72-4 RADIOIMMUNOASSAY; GLYCOPROTEIN TAG-72; MONITORING PATIENTS; GASTRIC-CANCER AB Among the new tumor markers that have been recently proposed, CA 72-4 is of particular interest, not only for its capabilities in diagnosing and monitoring certain neoplastic diseases, but also for its excellent specificity. Several studies focused on the potential clinical usefulness of CA 72-4 in gastrointestinal (GI) and gynecological cancer, showing a sensitivity of approximately 40% in colorectal and gastric cancer and 50% in ovarian cancer, with an overall specificity of more than 95%. Longitudinal evaluations of patients with either GI or gynecological malignant diseases demonstrated that significant elevations of CA 72-4 serum levels may be predictive of recurrent disease. Moreover, the combination of CA 72-4 with other known serum markers, such as CEA and CA 19-9 for GI cancer or CA 125 for ovarian cancer, indicated that an increase in the sensitivity can be achieved without substantial changes in the overall specificity, improving the possibility of monitoring these patients. In conclusion, these results provide a strong argument for the use of CA 72-4 in the management of these neoplastic diseases. C1 UNIV ROMA TOR VERGATA,DEPT SURG,ROME,ITALY. UNIV ROMA LA SAPIENZA,DEPT EXPTL MED,I-00185 ROME,ITALY. NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. RP GUADAGNI, F (reprint author), REGINA ELENA INST CANC RES,VIALE REGINA ELENA 291,I-00161 ROME,ITALY. RI Guadagni, Fiorella/J-4432-2013; Cavaliere, Francesco/J-7635-2016; Ferroni, Patrizia/C-2705-2017 OI Guadagni, Fiorella/0000-0003-3652-0457; Cavaliere, Francesco/0000-0001-6501-8648; Ferroni, Patrizia/0000-0002-9877-8712 NR 47 TC 28 Z9 30 U1 0 U2 3 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1995 VL 13 IS 2 BP 227 EP 238 DI 10.3109/07357909509011692 PG 12 WC Oncology SC Oncology GA QM826 UT WOS:A1995QM82600011 PM 7874576 ER PT J AU KASPRZAK, KS AF KASPRZAK, KS TI POSSIBLE ROLE OF OXIDATIVE DAMAGE IN METAL-INDUCED CARCINOGENESIS SO CANCER INVESTIGATION LA English DT Review ID HYDROXYL RADICAL FORMATION; HAMSTER OVARY CELLS; DNA-BASE DAMAGE; REMOVES 8-HYDROXYGUANINE RESIDUES; SUPEROXIDE-DISMUTASE ACTIVITY; MODEL LIPID HYDROPEROXIDES; SISTER-CHROMATID EXCHANGES; SITE-SPECIFIC MUTAGENESIS; OXYGEN FREE-RADICALS; PROTEIN CROSS-LINKS AB This review presents and evaluates evidence relevant to the mechanisms of metal carcinogenicity with special emphasis on the emerging hypothesis of the oxidative nature of metals' effect on DNA. The carcinogenic transition metals are capable of in vivo binding with the cell nucleus and causing promutagenic damage that includes DNA base modifications, inter- and intramolecular crosslinking of DNA and proteins, DNA strand breaks, rearrangements, and depurination. The chemistry of that damage and the resulting mutations observed in vitro and in metal-induced tumors are both characteristic for oxidative attack on DNA. The underlying mechanism involves various kinds of active oxygen and other radical species arising from metal-catalyzed redox reactions of O-2, H2O2, lipid peroxides, and others, with certain amino acids, peptides, and proteins. Other metal-mediated pathogenic effects, such as enhancement of lipid peroxidation, stimulation of inflammation, inhibition of cellular antioxidant defenses, and inhibition of DNA repair, may also contribute to that mechanism. Thus far, published data revealing the oxidative character of metal-induced promutagenic DNA alterations are particularly strong for two of the most powerful human metal carcinogens, chromium and nickel. However, without excluding contribution of other effects, the promotion of oxidative damage tends to take the leading role in explaining mechanisms of carcinogenicity and acute toxicity of certain other metals as well. RP KASPRZAK, KS (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,BLDG 538,ROOM 205,FREDERICK,MD 21702, USA. NR 275 TC 206 Z9 213 U1 1 U2 4 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1995 VL 13 IS 4 BP 411 EP 430 DI 10.3109/07357909509031921 PG 20 WC Oncology SC Oncology GA RK581 UT WOS:A1995RK58100008 PM 7627727 ER PT J AU WALDMANN, TA AF WALDMANN, TA TI THE METABOLISM BRANCH - AN EXEMPLAR OF PATIENT-ORIENTED RESEARCH SO CANCER INVESTIGATION LA English DT Editorial Material RP WALDMANN, TA (reprint author), NCI,METAB BRANCH,BLDG 10,ROOM 4N115,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1995 VL 13 IS 6 BP 662 EP 663 DI 10.3109/07357909509024938 PG 2 WC Oncology SC Oncology GA TG153 UT WOS:A1995TG15300016 PM 7583719 ER PT S AU Greenwald, P AF Greenwald, P BE Bradlow, HL Osborne, MP Veronesi, U TI Preventive clinical trials - An overview SO CANCER PREVENTION: FROM THE LABORATORY TO THE CLINIC: IMPLICATIONS OF GENETIC, MOLECULAR, AND PREVENTIVE RESEARCH SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT International Conference on Cancer Prevention - From the Laboratory to the Clinic: Implications to Genetic, Molecular, and Preventive Research CY SEP 22-24, 1994 CL NEW YORK, NY SP Strang Canc Prevent Ctr, European Sch Oncol, Cornell Univ Med Coll ID NUTRITION INTERVENTION TRIALS; DISEASE-SPECIFIC MORTALITY; BREAST-CANCER; CHEMOPREVENTION RESEARCH; ABNORMAL-CYTOLOGY; LOW-FAT; SUPPLEMENTATION; DYSPLASIA; HISTORY; LINXIAN RP Greenwald, P (reprint author), NCI,DIV CANC PREVENT & CONTROL,NIH,BETHESDA,MD 20892, USA. NR 41 TC 7 Z9 7 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 0-89766-947-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 768 BP 129 EP 140 DI 10.1111/j.1749-6632.1995.tb12116.x PG 12 WC Oncology; Multidisciplinary Sciences SC Oncology; Science & Technology - Other Topics GA BE92E UT WOS:A1995BE92E00013 PM 8526342 ER PT S AU Gormley, GJ Brawley, O Thompson, I AF Gormley, GJ Brawley, O Thompson, I BE Bradlow, HL Osborne, MP Veronesi, U TI The potential application of finasteride for chemoprevention of prostate cancer SO CANCER PREVENTION: FROM THE LABORATORY TO THE CLINIC: IMPLICATIONS OF GENETIC, MOLECULAR, AND PREVENTIVE RESEARCH SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT International Conference on Cancer Prevention - From the Laboratory to the Clinic: Implications to Genetic, Molecular, and Preventive Research CY SEP 22-24, 1994 CL NEW YORK, NY SP Strang Canc Prevent Ctr, European Sch Oncol, Cornell Univ Med Coll ID MALE PSEUDOHERMAPHRODITISM; DIHYDROTESTOSTERONE; 5-ALPHA-REDUCTASE C1 NCI,ROCKVILLE,MD 20852. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. RP Gormley, GJ (reprint author), MERCK RES LABS,RAHWAY,NJ 07065, USA. NR 22 TC 13 Z9 15 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 0-89766-947-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 768 BP 163 EP 169 DI 10.1111/j.1749-6632.1995.tb12119.x PG 7 WC Oncology; Multidisciplinary Sciences SC Oncology; Science & Technology - Other Topics GA BE92E UT WOS:A1995BE92E00016 PM 8526345 ER PT S AU Ambrosone, CB Freudenheim, JL Marshall, JR Graham, S Vena, JE Brasure, JR Michalek, AM Laughlin, R Nemoto, T Shields, PG AF Ambrosone, CB Freudenheim, JL Marshall, JR Graham, S Vena, JE Brasure, JR Michalek, AM Laughlin, R Nemoto, T Shields, PG BE Bradlow, HL Osborne, MP Veronesi, U TI The association of polymorphic N-acetyltransferase (NAT2) with breast cancer risk SO CANCER PREVENTION: FROM THE LABORATORY TO THE CLINIC: IMPLICATIONS OF GENETIC, MOLECULAR, AND PREVENTIVE RESEARCH SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT International Conference on Cancer Prevention - From the Laboratory to the Clinic: Implications to Genetic, Molecular, and Preventive Research CY SEP 22-24, 1994 CL NEW YORK, NY SP Strang Canc Prevent Ctr, European Sch Oncol, Cornell Univ Med Coll ID EPIDEMIOLOGY; GENOTYPE C1 NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. RP Ambrosone, CB (reprint author), SUNY BUFFALO,DEPT SOCIAL & PREVENT MED,BUFFALO,NY 14214, USA. RI Shields, Peter/I-1644-2012 NR 11 TC 11 Z9 11 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 0-89766-947-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1995 VL 768 BP 250 EP 252 DI 10.1111/j.1749-6632.1995.tb12132.x PG 3 WC Oncology; Multidisciplinary Sciences SC Oncology; Science & Technology - Other Topics GA BE92E UT WOS:A1995BE92E00029 PM 8526358 ER PT J AU KAUFMANN, WK LEVEDAKOU, EN GRADY, HL PAULES, RS STEIN, GH AF KAUFMANN, WK LEVEDAKOU, EN GRADY, HL PAULES, RS STEIN, GH TI ATTENUATION OF G(2) CHECKPOINT FUNCTION PRECEDES HUMAN CELL IMMORTALIZATION SO CANCER RESEARCH LA English DT Note ID HUMAN-FIBROBLASTS; GENE; MECHANISMS; COMPLEXES; PROTEIN; ARREST; P53 AB We have investigated the hypothesis that attenuation of the G(2) checkpoint, which delays entry into mitosis in response to damage to DNA and protects against clastogenesis, may contribute to the genetic instability of immortal human cell lines, IMR-90 normal human fibroblasts displayed stringent G(2) checkpoint response to gamma-radiation-induced DNA damage, Irradiation with 1.5 Gy induced 98% inhibition of mitosis and 79% inhibition of cyclin B1/p34(CDC2) kinase activity within 2 h, SV40-transformed IMR-90 cells with extended in vitro proliferative lifespan and immortal derivative cells displayed significantly less radiation-induced G, delay (60-70%) and less inhibition of cyclin B1/p34(CDC2) protein kinase activity (43-46%) than was seen in normal cells, Two other SV40-transformed lines and a fibrosarcoma line displayed a similar attenuation of G, checkpoint function, The attenuation of G, checkpoint function in SV40 transformed IMR-90 cells was associated with elevated levels of expression of cyclin B1 (8-fold greater) and p34(CDC2) (2.5-fold greater), By allowing cells with damaged chromatids to enter mitosis, an attenuation of G, checkpoint function In finite lifespan cells may promote the genetic alterations necessary for the conversion to immortality. C1 UNIV N CAROLINA,DEPT PATHOL,CHAPEL HILL,NC 27599. NIEHS,GROWTH CONTROL & CANC GRP,RES TRIANGLE PK,NC 27709. UNIV COLORADO,DEPT MOLEC CELLULAR & DEV BIOL,BOULDER,CO 80309. RP KAUFMANN, WK (reprint author), UNIV N CAROLINA,LINEBERGER COMPREHENS CANC CTR,CB 7295,CHAPEL HILL,NC 27599, USA. FU NCI NIH HHS [CA42765, P01 CA042765]; NIA NIH HHS [AG00947] NR 20 TC 71 Z9 75 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1995 VL 55 IS 1 BP 7 EP 11 PG 5 WC Oncology SC Oncology GA PZ268 UT WOS:A1995PZ26800002 PM 7805043 ER PT J AU KIHARA, A PASTAN, I AF KIHARA, A PASTAN, I TI CYTOTOXIC ACTIVITY OF CHIMERIC TOXINS CONTAINING THE EPIDERMAL GROWTH FACTOR-LIKE DOMAIN OF HEREGULINS FUSED TO PE38KDEL, A TRUNCATED RECOMBINANT FORM OF PSEUDOMONAS EXOTOXIN SO CANCER RESEARCH LA English DT Article ID SINGLE-CHAIN IMMUNOTOXINS; FACTOR RECEPTOR FAMILY; TYROSINE KINASE; HUMAN-BREAST; PROTO-ONCOGENE; FACTOR-ALPHA; CANCER; LIGAND; GENE; CELLS AB The EGF-like domains of heregulin alpha, beta 1, beta 2, and beta 3 were fused to a truncated form of Pseudomonas exotoxin (PE38KDEL), which contains a modified carboxyl-terminal sequence, KDEL, that increases that toxin activity. The resulting chimeric toxins were produced in Escherichia coli, purified to near homogeneity, and shown to be cytotoxic to target cells with very high activity on HTB2O, N-87 MCF-7, and HepG2 cells; high activity on A431 and MDA-MB468 cells; and low activity toward SK-OW, L929, and KB cells. The fact that cytotoxicity did not correlate with the levels of erbBZ expression indicated that another receptor in the erb family might be involved. Accordingly, cytotoxicity assays were performed on NIH/3T3 cell lines transfected with EGFR, ErbB2, ErbB3, or ErbB4. The results indicate that the heregulin toxins target ErbB4 or possibly ErbB3 but not ErbB2. C1 NCI,DIV CANC BIOL & DIAG,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 32 TC 22 Z9 25 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1995 VL 55 IS 1 BP 71 EP 77 PG 7 WC Oncology SC Oncology GA PZ268 UT WOS:A1995PZ26800015 PM 7805044 ER PT J AU Zbar, B AF Zbar, B TI Von Hippel-Lindau disease and sporadic renal cell carcinoma SO CANCER SURVEYS LA English DT Article ID TUMOR-SUPPRESSOR GENE; SHORT ARM; CHROMOSOME-3; LOCUS; TRANSLOCATION; DELETION; IDENTIFICATION; LOCALIZATION; REGION RP Zbar, B (reprint author), NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702, USA. NR 32 TC 39 Z9 39 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1995 VL 25 BP 219 EP 232 PG 14 WC Oncology SC Oncology GA TW073 UT WOS:A1995TW07300013 PM 8718521 ER PT J AU Greenblatt, MS Harris, CC AF Greenblatt, MS Harris, CC TI Molecular genetics of lung cancer SO CANCER SURVEYS LA English DT Review ID BRONCHIAL EPITHELIAL-CELLS; GLUTATHIONE-S-TRANSFERASE; BOMBESIN-LIKE PEPTIDES; TUMOR-SUPPRESSOR GENE; ASYMPTOMATIC CIGARETTE SMOKERS; RAS ONCOGENE ACTIVATION; P53 MUTATIONS; GROWTH-FACTOR; POOR-PROGNOSIS; URANIUM MINERS RP Greenblatt, MS (reprint author), NCI,NIH,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 141 TC 17 Z9 17 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1995 VL 25 BP 293 EP 313 PG 21 WC Oncology SC Oncology GA TW073 UT WOS:A1995TW07300016 PM 8718524 ER EF